Download BAOHNS Cancer Management Guidelines

EFFECTIVE
HEAD AND NECK CANCER
MANAGEMENT
BAO-HNS Document 6
•
Autumn 2002
Third Consensus Document • 2002
British Association of Otorhinolaryngologists
Head and Neck Surgeons
at The Royal College of Surgeons of England
35 - 43 Lincoln’s Inn Fields • London WC2A 3PE • U.K.
Tel: 020-7404 8373
•
[email protected]
•
www.orl-baohns.org
•
Fax: 020-7404 4200
CONTENTS
Page
PREFACE
ACKNOWLEDGEMENTS
1
2
SECTIONS
1
NATURE OF HEAD AND NECK CANCER
Editor: Mr P Bradley
Chapter
2
3
1.1
1.2
1.3
5
3
6
10
DIAGNOSTIC APPROACHES
34
Editors: Miss Louise Clark, Mr John Watkinson
Chapter
2.1
Role of Imaging
2.2
Pathology Datasets
34
54
SERVICE PROVISION
59
Editor: Mr Richard Wight
Chapter
3.1
3.2
3.3
3.4
3.5
3.6
4
Head and Neck Cancer in the UK
Staging and Clinical Datasets
AJCC Staging
Prevention
Role of Multidisciplinary Team
One Stop Clinics – Quick & Early Diagnosis
Quality Assurance
Radiotherapy
Chemoradiation
59
63
66
69
74
77
BEYOND PRIMARY TREATMENT
80
Editor: Mr Andrew Parker
Chapter
4.1
4.2
4.3
4.4
4.5
80
85
93
104
107
Quality of Life Assessment
Rehabilitation of Speech and Swallowing
Nutritional Aspects
Current Patient Issues
Palliative Care
CLINICAL GUIDELINES
Editor: Mr Andrew Robson
Chapter
5.1
5.2
5.3
129
Neck
Oral Cavity and Lip
Hypopharynx
129
136
144
Oropharynx
Larynx
149
153
Salivary Glands
Nose and Sinuses
Nasopharynx
Ear and Temporal Bone
160
165
171
174
Thyroid
Non Melanotic Skin Tumours
178
191
Editor: Mr Ken McKenzie
Chapter
5.4
5.5
Editor: Mr Graham Cox
Chapter
5.6
5.7
5.8
5.9
Editor: Mr Andy Welch
Chapter
5.10
5.11
PREFACE
The British Association of Otorhinolaryngologists – Head and Neck Surgeons remains committed to
raising standards and providing the best possible care for patients with head and neck cancer and, to this
end, the first Consensus Document was published by the BAO-HNS in 1998.
I am pleased to introduce this third Consensus Document to you. It updates the 2000 issue , but retains a
multidisciplinary authorship. This expanded edition has a greater emphasis on the evidence base for
management decisions and has been able to draw on the teams of reviewers who contributed to the NOTO
annual EBM conferences, co-ordinated by Andrew Robson. Also new to this edition is the introduction
of a team of Section Editors, who have streamlined the production process.
The Association did consider deferring publication until the latest UK Guidance was published, but this
document will not appear until 2003 at the earliest. Developments in Head and Neck cancer progress
rapidly, and we feel that an updated version of this widely used handbook is now timely.
IAN S. MACKAY FRCS
President
1
ACKNOWLEDGEMENTS & CONTRIBUTORS
This document has been produced by the British Association of Otorhinolaryngologists - Head and Neck Surgeons.
The Association gratefully acknowledge the efforts of the many contributors who include Otolaryngologists,
maxillofacial surgeons, radiologists, clinical oncologists, pathologists, dieticians, speech pathologies, palliative care
practitioners, and not forgetting our patient representatives, many officiated to the National Association of
Laryngectomee Clubs.
We also gratefully acknowledge permission via Mr Pat Bradley, Section Editor, from the AJCC and Springer Verlag
to include the latest version of the TNM Staging System for Head and Neck Cancer.
General Editor
Professor Janet A Wilson
Section Editors
Nature of Head and Neck Cancer
Diagnostic Approaches
Service Provision
Beyond Primary Treatment
Clinical Guidelines
Mr Pat Bradley
Ms Louise Clark, Mr John Watkinson
Mr Richard Wight
Mr Andy Parker
Mr Andrew Robson, Mr Ken McKenzie,
Mr Graham Cox, Mr Andy Welch
Contributors
Staging and Clinical Datasets
Role of Imaging
Pathology Datasets
Prevention
Role of Multidisciplinary Team
One Stop Clinics – Quick & Early Diagnosis
Quality Assurance
Non Surgical Therapy - Radiotherapy
Non Surgical Therapy -Chemoradiation
Quality of Life Assessment
Rehabilitation of Speech and Swallowing
Nutritional Aspects
Current Patient Issues
Palliative Care
Clinical Guidelines
1
Mr Nick Roland
Ms Julie Olliff, Mr Giles Roditti, Mr Julian Keballa,
Dr Ivan Zammit
Dr Ken McLennan, Prof Tim Helliwell, Dr Julie Woolgar
Mr Peter Clark
Ms Noleen Hunter, Ms Georgia Partridge, Ms Shannon Rees
Mr Colin Fielder
Mr Martin Birchall
Dr David Morgan, Dr Martin Robinson
Mr Adele Resouly, Dr David Boote
Mr Simon Rogers, Ms Kaye Radford
Dr Paul Carding, Ms Jo Patterson, Ms Fiona Richardson,
Mr Peter Samuel, Ms Janet Thornton, Ms Yvonne Edels,
Ms Anne Hurren, Ms Mary Jackson, Ms Jane Machin,
Ms Sarah Owen, Ms Helen Woods
Mr Alan Torrance, Ms Jane Wilson, Mr Jarod Homer
Mr & Mrs Culling, Mr & Mrs Fraser
Dr Claude Regnard
Mr Mark Watson, Mr Martin Robinson, Mr Ian Martin,
Mr Graham Putnam, Mr Kim Ah-See, Mr Ian Smith,
Prof Valerie Lund, Mr Rob Sanderson, Mr Jean Pierre Jeannon,
Mr Chris Milford, Mr Andy Pritchard, Mr Tom Lennard,
Mr Rob Sudderick, Mr Duncan Ingram, Dr Ujjal Mallick,
Mr Simon Watts, Prof Nick Jones, Mr Akhtar Hussain.
EBM Day Teams: M Gleeson, A Munro, A Batchelor,
R Wight, M Gaze, J Langdon, A Jones, J Soames, K McKenzie,
J Watkinson, J Olliff, A Parker, J Brown, T Helliwell, G Robertson,
J Glaholm, D Howard, G Buckley, M Birchall, D Soutar, R Evans,
J Eveson, D Courtney, C Kerawella, F Calman, I Camilleri,
C Hopper, N Slevin, N McLean, S Rogers, P Bradley, I Zammit,
L Clark, N Brookes C Kelly, J Dempster, G Cox, T Lovell.
NATURE OF HEAD AND NECK CANCER
Requests for additional copies should be addressed to the: BAO-HNS Office, Royal College of Surgeons, 35-43 Lincoln
Inn Fields, London WC2A 3PN. Tel: 020 7404 8373. Fax: 020 7404 4200
2
Chapter 1
Head and Neck Cancer in the UK
Cancer of the head and neck does not refer to a single histological diagnosis or organ of origin. Rather, it
refers to malignant tumours arising from the upper aerodigestive tract (UADT), salivary glands, thyroid
and parathyroid glands, Paranasal sinuses, and the skin of the head and neck. Because of this
heterogeneity, a wide spectrum of aetiologies, disease presentations, and clinical characteristics must be
considered when caring for these patients. However the term “head and neck cancer” usually refers to
squamous cell carcinomas arising from the mucosal surfaces of the upper aerodigestive tract. These
tumours make up more than 95% of the cases of head and neck cancer. Head and neck cancers comprise
3.0% of all new cancers in the UK per year. . In the UK the major head and neck sites are the larynx, oral
cavity, hypopharynx and oropharynx, which together account for 90% of head and neck squamous cell carcinoma.
Head and neck cancer in the past was predominantly a disease of men and of urban areas. The main
identifiable causes of head and neck squamous cell carcinoma are smoking and excessive alcohol
consumption. Other factors such as poor dentition and dietary factors may also increase the risk of oral
cancer. There is more recently identified a subgroup of patients without the traditional risk factors [1,2].
Recent clinical and molecular investigations suggest that there are distinctive clinical entities, particularly
affecting young patients with cancers of the oral tongue and oropharynx. It is therefore possible to prevent
the development of cancer by reducing the use of tobacco and alcohol intake. The NHS Cancer Plan [3]
and the DOH “Smoking Kills” [4] are investing millions of pounds annually on a rolling programme to
reduce cancer overall. There is no mention of head and neck cancer by tumour site in either of these
documents! A recent study [5] on delays in diagnosis in head and neck cancers recommends that special
educational iniatives should be directed to those patients most at risk and their general practitioners. There
continues to be reported evidence that general practitioners, medical and dental, are still in need of further
education on the aetiology and health education of patients who may be at risk of developing head and
neck cancer [6-8]. The absence of definite early warning signs for most head and neck cancers suggests
the need to develop essential screening criteria [9]. It is essential to define the population that is at high
risk for head and neck cancer and to subject it to aggressive screening protocols [10].
Making the diagnosis of head and neck cancer is based on clinical symptoms and signs, confirmation of
the presence of cancer by histopathology [11]. The current staging of the disease, now universally
involves each patient undergoing radiological imaging with computer tomography [CT] and/or magnetic
resonance imaging [MRI] to assess the true extent of the disease. Positron emission tomography [PET]
me help by evaluation of tumour biological aggression, and, thus, improved staging PET detection of
residual or recurrent tumour activity following definitive treatment, by surgery or radiotherapy, may aid
with treatment planning [12]. Developments in histopathology have improved the ability to predict which
areas of pre-malignancy [leukoplakia] in the oral cavity and the larynx are likely to progress to
malignancy and require aggressive therapy and be given long-term follow up clinic observation [13-14].
A recent study [15]of UK waiting times during the management of head and neck tumours showed that
there was an inordinate delay in time to radiology, 4.1 – 5.5 weeks, and primary radiotherapy - 10.3
weeks and to surgery – 5.5 weeks. It is recognised that the provision of a head and neck oncology service,
currently not widely recognised or resourced in the UK, will require appropriate funding and staffing
which is sustainable and recurrent [16].
The untreated head and neck cancer patient is seldom encountered nowadays, but a report from Brazil on
808 patients diagnosed and followed up between 1953 and 1990, showed that approximately 50% of
untreated patients died within 4 months, but the remaining patients survived up to 4 or more years
following diagnosis [17].
3
Treatment for head and neck squamous cell carcinomas in the UK is currently by surgery or radiotherapy
or a combination of both. In early disease the treatment is tending to move from radiotherapy to
conservation surgery [18], while in advanced disease the treatment in the main is surgery with adjuvant
radiotherapy. Combined chemoradiation has steadily grown in popularity.
The evidence base for head and neck cancers is low with relatively few randomised controlled trials of the
two main treatments. In a review of treatments in three large areas of England, the patterns of surgery and
radiotherapy treatments for head and neck cancers were studied and their effects on survival [19]. There
was evidence of regional variations in the treatments given and four patients in ten did not receive
currently recommended treatments. Better survival was associated with surgery for the mouth cancers,
radiotherapy for laryngeal cancers and with a combined treatment regimefor pharyngeal cancers
independent of tumour and demographic factors. The use of altered fraction schedules of radiotherapy and
the addition of chemotherapeutic agents to standard treatments in advanced disease needs to be further
explored by the inclusion of patients in randomised controlled trials. A greater research culture in UK
head and neck cancer management is required before the practice develops in a haphazard, unregulated
fashion [20-22]. The results of aggressive primary treatment including surgery, radiotherapy, or both
show that more than 60% of these patients develop loco regional recurrence or distant metastases.
Survival rates for recurrent disease are very poor, despite further surgery, radiation therapy, or
chemotherapy [23]. The other difficulty with the management of head and neck squamous cell carcinoma
patients is the presence of synchronous primary tumours which are present in 1 – 15% and are most
commonly associated with an index tumour of the larynx. There is also the continued risk of developing a
metachronous second primary malignancy of 4 – 7% per year of survival [24].
Ultimately it is the quantity and quality of the patient’s survival that is the aim of treatment interventions.
Where once there was little demonstrable improvement in survival of patients over several decades,
recent evidence has been provided which shows improved outcomes [25]. It is of utmost importance to
audit and review activity [26] and to evaluate the quality of life [QoL] [27] of all patients who are
definitively treated for head and neck cancer.
It is now recognised since the reorganisation of cancer services that care provision is best provided by a
structured and weekly run multidisciplinary clinic [MDC] [28]. These clinics require resourcing adequate space, staff and equipment, to provided optimum convenience and minimal disruption to the
patient and their carers where they can be informed of their diagnosis and plan of treatment once the
diagnosis of head and neck cancer has been confirmed. It is also recognised that the staff require
resources in communication skills training in oncology [29]. Currently, there is a need to define who and
what personnel are essential to attend the MDC, and the optimum scheduling of the care discussion and
the presence of the patient [30].
To summarise: Head and neck cancer is an uncommon cancer, seldom recognised in the early stages by
the patients and their “carers”, and thus requires widespread public health education of its existence to aid
with earlier stage disease detection. To diagnose the cancer requires pathologists and radiologists to aid
with staging and planning of treatment. The treatment of patients requires a co-ordination of clinicians surgeons, radiotherapists and oncologists to minimise delays and interruptions to planned treatments.
These patients subsequently require rehabilitation of their breathing, eating, swallowing and voice, as well
as clinical follow up to detect recurrent, persistent or new disease.
The current 5 year survival outlook for a patient diagnosed with a head and neck cancer is more than
60%.
4
References:
1
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15
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19
20
21
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23
24
25
26
27
28
29
30
Lingen,M., Sturgis, E.M., and Kies, M.S., Squamous cell carcinoma of the head and neck in non-smokers. Curr
Opin Oncol 2001:13; 176 – 182.
Koch, W.M., McQuone, S., Clinical and Molecular Aspects of Squamous Cell Carcinoma of the Head and Neck in
the non-smoking and non-drinker. Curr Opin Oncol 1997: 9 ; 257 – 261.
The NHS Cancer Plan. Department of Health. London 2001
Smoking Kills. A White paper on Smoking. Department of Health. London 1998.
Amir, Z., Kwan, S.Y., Landes, D., Feber, T., Diagnostic Delays in Head and Neck Cancers. Eur J Cancer Care.
1999:8; 198 – 203.
Smith, S.E., Warnakulasuriya, K.A.A.S., Feyeraband, C., Belcher, M., Cooper, D.J., Johnson, N.W., A Smoking
Cessation Programme Conducted Through Dental Practices in the U.K. Br Dental J. 1998: 185; 299 – 303.
Warnakulsuriya, K.A., Johnson, N.W. Dentists and oral cancer prevention in the UK. Oral Diseases. 1999:5; 10 –
4
Hollows, P., McAndrew, P.G., Perini, M.G., Delays in the Referral and Treatment of Oral Squamous Cell
Carcinoma. Br Dental J. 2000:188; 262 – 5.
Dolan, R.W., Vaughan, C.W., Fuleihan, N., Symptoms in early head and neck cancer: An inadequate indicator.
Otolaryngol Head Neck Surg 1998:119; 463 – 7.
O’Hara, J., Bradley, P.J. Head and Neck Cancer: A Screening Strategy! Clinical Otolaryngol 2002: 27;133-134
Ferlito, A., Boccato, P., Shaha, A.R., et al The art of Diagnosis in Head and Neck Tumours, Acta Otolaryngol
2001:121; 324 – 328.
Greven, K., McGuirt, W.F., The emerging role of positron emission tomography in the management of head and
neck cancer. Curr Opin Otolaryngol Head Neck Surg 1999:7; 48 – 51.
Sudbo, J., Kildal, W., Risberg, B., Koppang, H.S., Danielsen, H.E., Reith, A: DNA content as a prognostic marker
in patients with oral leukoplakia. N Engl J Med 2001:344;1270 – 8.
Gallo, A., de Vincentiis, M., Rocco, C.D., Moi, R., Simonelli, M., Minni, A., Shaha, A.R., Evolution of
Precancerous Laryngeal lesions: A Clinicopathologic Study with Long-Term Follow-up on 259 Patients. Head
Neck 2001:23; 42 – 47.
Jones, T.M., Hargrove, O., Lancaster, J., Fenton, J., Shenoy, A., Roland, N.J., Waiting times during the
management of Head and Neck Tumours. J Laryngol Otol. 2002: 116 ; 275 – 279.
Corbridge,R., Cox, G., The Cost of Running a Multidisciplinary Head and Neck Oncology Service – an Audit.
Rev Laryngol Otol Rhinol 2000: 121; 151 – 153.
Kowalski, L.P., Carvalho, A.L., Natural History of Untreated Head and Neck Cancer. Eur J Cancer 2000; 36:1032
– 1037.
Ferlito, A., Silver, C.E., Howard, D.J., Laccourreye, O., Rinaldo, A., Owen, R., The role of partial laryngeal
resection in current management of laryngeal cancer; a collective review. Acta Otolaryngol 2000; 120:456 – 465.
Edwards, D.E., Johnson, N.W., Treatment of upper aerodigestive tract cancers in England and its effects on
survival. Br J Cancer. 1999:81; 323 – 329.
Mendenhall, W.M., Amdur, R.J., Siemann, D.W., Parsons, J.T., Altered fractionation in definitive irradiation of
squamous cell carcinoma of the head and neck. Curr Opin Oncol 2000; 12: 207 – 214.
Robbins, K.T. The RADPLAT treatment technique for advanced squamous cell carcinoma of the upper
aerodigestive tract. Curr Opinion Otolaryngol Head Neck Surg 1998; 6:113 – 119.
Weissler, M.C., Combined chemotherapy and radiation therapy for advanced squamous cell cancer of the head
and neck. Curr Opinion Otolaryngol Head Neck Surg 1998; 6:120 – 123.
Ingrams D.R., Rhys-Evans, P., Strategies for the Management of Recurrent Head and Neck Squamous Cell
Carcinoma. Curr Opin Otolaryngol Head Neck Surg 2001; 9:109 – 113.
Sood, S., Bradley, P.J., Quraishi, M.S., Second Primary Tumours in Squamous Cell Carcinoma of the Head and
Neck – Incidence, Site, Location and Prevention. Curr Opin Otolaryngol Head Neck Surg 2000; 8:87 – 90.
Jones, A.S., Houghton, D.J., Beasley, N.J.P., Husband, D.J., Improved survival in patients with head and neck
cancer in the 1990’s. Clin Otolaryngol. 1998; 23:319 – 325.
Nicholls, C., Ilankovan, V., An audit of oral and dental health regimes practised in the management of
oropharyngeal cancer. Br J Oral Maxfac surgery. 1998; 36:63 – 66.
Liat, M.A., Stracks, J., Evaluation of Quality of Life in patients definitively treated for squamous carcinoma of the
head and neck. Curr Opin Oncol 2000; 15: 215 – 220.
Provision and Quality Assurance for head and neck cancer care in the United Kingdom.London. The British
Association of Head and Neck Oncologists. August 1998.
Baile, W.F., Kudelka, A.P., Beale, E.A., Glober, E.G. et al. Communication Skills Training in Oncology. Cancer
1999; 86: 887 – 97.
Bradley, P.J., Chairman. Practice Care Guidance for Clinicians Participating in the Management of Head and
Neck Cancer Patients in the UK. Eur J Surg Oncol 2001; 27:S1 – S18.
5
31
Section 1
Chapter 2
Staging and Clinical Guidelines
DATASETS
In the 1998 edition of Effective Head and Neck Cancer Management, it was recognised that the single
most major deficiency in the United Kingdom head and neck cancer management had been the absence of
accurate systematic prospective data collection. A prototype minimum dataset was proposed for the UK,
to assist in:− accreditation of cancer service providers
− prospective audit
− more accurate prognosis
− long term population based observational studies
The minimum dataset seeks to record the minimum amount of data to allow an individual patient and
groups of patients to be identified, their management quantified and analysis made of simple defined
outcomes.
The essential outcomes being :− survival
− complications of treatment
− quality of life measures eg University of Washington QOL
Utilising the minimum of data improves speed of entry, compliance, and accuracy. However every
clinician is free to collect additional data to meet local needs and research needs.
Within the dataset standard coding practice should be followed, to allow cross comparison of data.
Development of unified datasets for professions managing head and neck cancer:
Clinicians from all specialities managing head and neck cancer, representatives from the cancer registries,
Office for National Statistics, Department of Health and coding advisors met in March 1998 under the
auspices of BAHNO (British Association of Head and Neck Oncologists). From this emerged a multi –
agency working group, who built upon the BAO-HNS initiatives outlined above, to define a
multidisciplinary dataset to be utilised by all professions managing head and neck cancer. This
incorporated the 1998 Report from The Royal College of Pathologists in which a minimum dataset for
histopathology reporting in head and neck cancer was described. This group’s report was published in
June 1999 – BAHNO NATIONAL MINIMUM AND ADVISORY HEAD AND NECK CANCER
DATA SETS, which utilised wherever possible international classifications of coding to allow crosscomparison of data. The BAHNO minimum and advisory data sets were formally adopted by BAHNO’s
Council and its membership in 1999, and a recent survey has shown a steady rise in their usage. The full
text document is available on the BAO-HNS website - www.orl-baohns.org .
It was thus appropriate that BAHNO in May 2000, formed one of the four established clinical areas (lung,
colon, breast and head and neck) who contributed to the evolution of a National Cancer Dataset with the
aim to provide a generic core common to all cancers, with a site specific extension designed to meet the
needs of professionals managing head and neck cancer.
The work was commissioned by the National Cancer Director in conjunction with the National Health
Service Information Authority (NHSIA) and was delivered by a working group to which BAHNO’s
representative contributed and linked to the BAHNO Data Set Working Group.
6
The National Cancer Dataset delivers both the information for performance management required by
the NHS, as well as matching the requirements set out above, to achieve co-ordinated data collection,
across cancer networks and nationally, meet the requirements for Cancer Registration, and assist clinical
teams to better follow the patients journey.
The latest iteration Version 1.1ISB can be found on the NHSIA website at www.nhsia.nhs.uk/cancer and
has now successfully received draft NHS Information Standards Board Approval, which is the first step to
becoming mandated for all NHS providers to use and report on.
It is accompanied on the website above by a head and neck cancer data manual jointly developed with
BAHNO defining all items and codes, for head and neck cancer. The Cancer Dataset is intended to be
used for all patients identified as having cancer; and all stages of cancer should be included i.e. primary,
secondary/recurrences, second primaries. Within this data manual, site specific items for head and neck
cancer which fall outside the generic core National Cancer Dataset are defined. These are of two types,
those fields common to most cancers’ staging but with their head and neck subsite variants described, and
those items felt to be specifically relevant only to head and neck cancer. The latter have been derived
from the original BAHNO data set and have been re-evaluated by the dataset working group to ensure
their purpose remains and their continuation is justified. Item codes have been modified if required as
well as aligning smoking history with the lung group, but including other tobacco usage. A new section
has been created on nutrition confirming the aims to reflect a multidisciplinary approach, whilst a section on
surgical voice restoration is in preparation.
An addendum to the manual will be issued to meet any specific requirements from thyroid cancer, which are
being examined by a multi-speciality group, with reporting expected in early 2003. Companion
developments in lymphoma and skin cancer will need to be accommodated.
KEY SECTIONS IN THE NATIONAL CORE CANCER DATASET for HEAD AND NECK
CANCER (see www.nhsia.nhs.uk/cancer) for latest details
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
Demographics
Referrals
Imaging
Diagnosis
Cancer Care Plan
Staging
Surgery an other procedures
Pathology details –both diagnostic and resective matching to RCPath reporting
Chemotherapy and other drugs
Radiotherapy
Brachytherapy
Palliative care (in development)
Clinical trials
Clinical status assessment
Death details
HEAD AND NECK SPECIFIC ITEMS SECTION
History non head and neck cancer
Smoking and alcohol history
Quality of life
Family history of cancer
Nutritional support
7
It is recognised that the development and implementation of this dataset is a significant undertaking for all
those involved in the management and delivery of cancer services. It is also recognised that until
appropriate IT systems are in place, collection of some data items will be more difficult than others.
However, the National Cancer Dataset is a significant step in the drive to improve cancer services and it is
only through its collection and use that further development can take place.
The timetable for implementation of the National Cancer dataset is now becoming clearer, with a three
phase introduction:PHASE 1 – focuses on waiting times information to key referral, diagnosis and treatment points.
Information on head and neck cancer will be required to be reported by September 2003.
PHASE 2 – is based on subset of the full dataset to provide National Comparative Clinical Audit, with
waiting times as a component. Introduction will occur between 2003 and 2005 support from the National
Clinical support program. Initial piloting of DAHNO (DAta for Head and Neck Oncology) will
commence in spring 2003, and then be progressively made available across England. Regular updates will
be provided at the BAHNO website. (www.bahno.org) Separate arrangements will apply for Scotland,
Wales and Northern Ireland with the exact timing for head and neck cancer yet to be confirmed.
PHASE 3 – is the implementation of all remaining items.
By 2004 all cancer data will be transmitted to registries electronically.
All colleagues managing head and neck cancer are requested to consider moving to use the National
Cancer Dataset for Head and Neck as soon as is practicable. This will support both the move towards
universal high quality data collection for every head and neck cancer patient throughout their cancer
journey and to achieve the aims of true prospective audit on a routine basis.
A migratory map is available for those wishing to transfer previous NMDS/NADS data to the latest
format, as well as paper proformas for those not able to enter electronically at the point of contact.(see
NHSIA website)
DEFINING RESPONSIBILITIES IN HEAD AND NECK CANCER DATA COLLECTION
To achieve the overall aim of comprehensive head and neck cancer data collection, collation and analysis,
wide scale support and ultimately financial provision will be needed. The agenda requires a recognition of
the responsibilities outlined below:that BAO-HNS will :− Continue to liaise with BAHNO in future development of the head and neck specific elements of the
National Core Cancer Dataset
− Recommend all its members to follow the National Core Cancer Dataset
− Encourage development of common standards for data transfer to support National Comparative audit
− Liaise with National Clinical Audit support program (NCASP) to develop statistical analysis and
regional/central collation
that EACH TRUST/ CANCER NETWORK will:− develop a cancer information strategy by Autumn 2002
− Seek to provide hardware /software/provision for data collection input at the point of patient contact
− assist the unit in its responsibilities by providing technical support in computing
− seek solutions to support data transfer where the patients path moves across unit and centre
that EACH HEAD and NECK UNIT will :− accept responsibility for organising data collection along the patient pathway/collation / validation /
presentation and assist in interpretation for central/regional reporting
8
that EACH HEAD AND NECK SURGEON/ONCOLOGIST will :− facilitate data collection by leading other professionals by example
− ensure data is correct and true
− hold regular local/regional meetings to review surgeon/unit specific data
USEFUL ADDRESSES AND SOURCES OF INFORMATION:
NHS Information Authority website – for details of National core cancer dataset for head and neck,
cancer data manual and up to date details on implementation http://www.nhsia.nhs.uk/cancer
Royal College of Pathologists Minimum data set for head and neck carcinoma histopathology reports,
November 1998. Royal College of Pathologists, 2 Carlton House Terrace, London, SW1Y 5AF.
www.rcpath.org
BAHNO National Minimum and Advisory Head and Neck Cancer Data Sets Version 1.0 June 1999
Available at www.orl-baohns.org
-ICD-10. International Statistical Classification of Diseases and Related Health Problems.
10th revision
World Health Organisation 1992
-ICD-O. International Classification of Diseases for Oncology second edition 1990. The morphology
codes are included in Volume 1 of ICD 10 as a reference source.
-OPCS-4. Tabular list of the classification of surgical operations and procedures. Fourth revision Office
of Population Censuses and Surveys HMSO 1990.
9
Section 1
Larynx
Chapter 3
TNM Classification: AJCC 2002-3
(Nonepithelial tumours such as those of lymphoid tissue, soft tissue, bone and cartilage are not included.)
C10.1 Anterior (lingual) surface of epiglottis
C32.0 Glottis
C32.1 Supraglottis (laryngeal surface)
C32.2 Subglottis
C32.3 Laryngeal cartilage
C32.8 Overlapping lesion
C32.9 Larynx, NOS
ANATOMY
Primary Site. The following anatomic definition of the larynx allows classification of carcinomas arising in the
encompassed mucous membranes but excludes cancers arising on the lateral or posterior pharyngeal wall, pyriform
fossa, postcricoid area, or base of tongue. The anterior limit of the larynx is composed of the anterior or lingual
surface of the suprahyoid epiglottis, the thyrohyoid membrane, the anterior commissure, and the anterior wall of the
subglottic region, which is composed of the thyroid cartilage, the cricothyroid membrane, and the anterior arch of
the cricoid cartilage. The posterior and lateral limits include the laryngeal aspect of the aryepiglottic folds, the
arytenoid region, the interarytenoid space, and the posterior surface of the subglottic space, represented by the
mucous membrane covering the surface of the cricoid cartilage. The superolateral limits are composed of the tip
and the lateral borders of the epiglottis. The inferior limits are made up of the plane passing through the inferior
edge of the cricoid cartilage. For purposes of this clinical stage classification, the larynx is divided into three
regions: supraglottis, glottis, and subglottis. The supraglottis is composed of the epiglottis (both its lingual and
laryngeal aspects), aryepiglottic folds (laryngeal aspect), arytenoids, and ventricular bands (false cords). The
epiglottis is divided for staging purposes into suprahyoid and infrahyoid portions by a plane at the level of the hyoid
bone. The inferior boundary of the supraglottis is a horizontal plane passing through the lateral margin of the
ventricle at its junction with the superior surface of the vocal cord. The glottis is composed of the true vocal cords,
including the anterior and posterior commissures, superior and inferior surfaces. It occupies a horizontal plane 1cm
in thickness, extending inferiorly from the lateral margin of the ventricle. The subglottis is the region extending
from the lower boundary of the glottis to the lower margin of the cricoid cartilage.
The division of the larynx is summarized in the following table:
Site
Supraglottis
Glottis
Subglottis
Subsite
Suprahyoid epiglottis
Infrahyoid epiglottis
Aryepiglottic folds (laryngeal aspect)
Arytenoids
Ventricular bands (false cords)
True vocal cords including anterior and posterior commissures
Subglottis
Regional Lymph Nodes. The incidence and distribution of cervical nodal metastases from cancer of the larynx
varies with the site of origin and the “T” classification of the primary tumour. The true vocal cords are nearly
devoid of lymphatics and tumours of that site alone rarely spread to regional nodes.
On the contrary, the supraglottis has a rich and bilaterally interconnected lymphatic network and primary
supraglottic cancers are commonly accompanied by regional lymph node spread.
Glottic tumours may spread directly to adjacent soft tissues and prelaryngeal, pretracheal, paralaryngeal and
paratracheal nodes as well as upper, mid and lower jugular nodes.
Supraglottic tumours commonly spread to upper and midjugular nodes, considerably less commonly to submental or
submandibular nodes, but occasionally to retropharyngeal nodes.
10
The rare subglottic primary tumours spread first to adjacent soft tissues and prelaryngeal, pretracheal, paralaryngeal
and paratracheal nodes, then to mid and lower jugular nodes.
Contralateral lymphatic spread is common. It is recognized that most masses over 3 cm in diameter are not single
nodes but are confluent nodes or tumour in soft tissues of the neck. There are three categories of clinically positive
nodes: N1, N2, and N3. Midline nodes are considered ipsilateral nodes
Metastatic Sites: Distant spread is common only for patients who have bulky adenopathy. When distant
metastases occur, spread to the lungs is most common; skeletal or hepatic metastases occur less often. Mediastinal
lymph node metastases are considered distant metastases.
RULES FOR CLASSIFICATION
Clinical Staging. The assessment of the larynx is accomplished primarily by inspection, using indirect mirror and
direct endoscopic examination. The tumour must be confirmed histologically and any other data obtained by
biopsies may be included. Cross-sectional imaging in laryngeal carcinoma is recommended when the primary
tumour extent is in question based upon clinical examination. Radiologic nodal staging should be done
simultaneously to supplement clinical examination. Complete endoscopy under general anesthesia is usually
performed after completion of other diagnostic studies to accurately assess, document and biopsy the tumour.
Pathological Staging. Pathologic staging requires the use of all information obtained in the clinical staging in
addition to histologic study of the surgically resected specimen. The surgeon’s evaluation of gross unresected
residual tumour must also be included. Specimens that are resected after radiation or chemotherapy need to be
identified and considered in context. The pathologic description of any lymphadenectomy specimen should describe
size, number, position of the involved node(s), and the presence or absence of extracapsular extension
DEFINITION OF TNM
Primary Tumour (T)
TX
T0
Tis
Primary tumour cannot be assessed
No evidence of primary tumour
Carcinoma in situ
Supraglottis
T1
Tumour limited to one subsite of supraglottis with normal vocal cord mobility
T2
Tumour invades mucosa of more than one adjacent subsite of supraglottis or glottis or region outside the
supraglottis (e.g. mucosa of base of tongue, vallecula, medial wall of pyriform sinus) without fixation of
the larynx.
T3
Tumour limited to larynx with vocal cord fixation and./or invades any of the following
postcricoid area, pre-epiglottic tissues, paraglottic space, and/or minor thyroid cartilage erosion
(e.g. inner cortex)..
T4A
Tumour invades through the thyroid cartilage and or invades tissues beyond the larynx (e.g., trachea, soft
tissues of neck including deep extrinsic muscle of the tongue, strap muscles, thyroid, or esophagus).
T4B
Tumour invades prevertebral space or encases carotid artery or invades mediastinal structures
Glottis
T1
Tumour limited to the vocal cord(s) (may involve anterior or posterior commissure with normal mobility
T1a
Tumour limited to one vocal cord
T1b
Tumour involves both vocal cords
T2
Tumour extends to supraglottis and/or subglottis, and/or with impaired vocal cord mobility
T3
Tumour limited to the larynx with vocal cord fixation, and/or invades paraglottic space, and or minor
thyroid cartilage erosion (e.g. inner cortex).
Tumour invades through the thyroid cartilage and/or invades tissues beyond the larynx (e.g., trachea, soft
tissues of neck including deep extrinsic muscle of the tongue, strap muscles, thyroid or esophagus)
Tumour invades prevertebral space or encases carotid artery or invades mediastinal structures
T4a
T4b
11
T1
T2
T3
T4a
T4b
Subglottis
Tumour limited to the subglottis
Tumour extends to vocal cord(s) with normal or impaired mobility
Tumour limited to larynx with vocal cord fixation
Tumour invades cricoid or thyroid cartilage and/or invades tissues beyond the larynx
(e.g., trachea, soft tissues of neck including deep extrinsic muscles of the tongue, strap muscles, thyroid or
esophagus)
Tumour invades prevertebral space or encases carotid artery or invades mediastinal structures
STAGE GROUPING
Stage 0
Stage I
Stage II
Stage III
Stage IVA
`
Stage IVB
Stage IVC
Tis
T1
T2
T3
T1
T2
T3
T4a
T4a
T1
T2
T3
T4a
T4b
Any T
Any T
N0
N0
N0
N0
N1
N1
N1
N0
N1
N2
N2
N2
N2
Any N
N3
Any N
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M1
HISTOPATHOLOGIC TYPE
The predominant cancer is squamous cell carcinoma. The staging guidelines are applicable to all forms of
carcinoma. Nonepithelial tumours such as those of lymphoid tissue, soft tissue, bone and cartilage (i.e., lymphoma,
melanoma, and sarcoma) are not included. Histologic confirmation of diagnosis is required.
Histopathologic grading of squamous carcinoma is recommended: the grade is subjective and uses a descriptive as
well as numerical form, i.e., well differentiated, moderately differentiated, and poorly differentiated, depending
upon the degree of closeness to or deviation from squamous epithelium in mucosal sites. Also recommended where
feasible is a quantitative evaluation of depth of invasion of the primary tumour and the presence or absence of
vascular invasion and perineural invasion. Although the grade of tumour does not enter into the staging of the
tumour, it should be recorded. The pathologic description of any lymphadenectomy specimen should describe the
size, number, position of the involved node(s) and the presence or absence of extracapsular extension.
HISTOPATHOLOGIC GRADE (G)
GX
G1
G2
G3
Grade cannot be assessed
Well differentiated
Moderately differentiated
Poorly differentiated
12
TNM Classification: AJCC 2002-3
Head and Neck Sites
The T classifications indicating the extent of the head and neck primary tumour differ in specific details. The N
classification for cervical lymph node metastasis is uniform for all mucosal sites except nasopharynx. The N
classifications for thyroid and nasopharynx are unique to those sites and are based upon tumour behaviour and
prognosis. The clinical staging systems presented in this section are all clinical staging, based on the best possible
estimate of the extent of the disease before first treatment. Imaging techniques (computed tomography (CT),
magnetic resonance imaging (MRI), ultrasonography) may be applied, and in more advanced tumour stages, have
added to the accuracy of primary (T) and nodal (N) staging, especially in the nasopharyngeal, paranasal sinuses and
regional lymph nodal areas. Appropriate imaging studies should be obtained whenever the clinical findings are
uncertain. Similarly, endoscopic evaluation of the primary tumour, when appropriate, is desirable for detailed
assessment of the primary tumour for accurate “T” staging. Fine needle aspiration biopsy (FNAB) may confirm the
presence of tumour and its histopathologic nature, but cannot rule out the presence of tumour.
Any diagnostic information which contributes to the overall accuracy of the pretreatment assessment should be
considered in clinical staging and treatment planning. When surgical treatment is carried out, cancer of the head and
neck can be staged (pathologic stage (pTNM) using all information available from clinical assessment as well as
from the pathologic study of the resected specimen. The pathologic stage does not replace the clinical stage, which
should be reported as well.
In reviewing the staging systems, several changes in the T classifications as well as stage groupings are made to
reflect current practices of treatment, clinical relevance and contemporary data. Uniform “T” staging for oral cavity,
oropharynx, salivary and thyroid cancers greatly simplifies the system and will improve compliance by clinicians.
T4 tumours are subdivided into advanced resectable (T4a) and advanced unresectable (T4b) categories.
Regrouping of Stage IV disease for all sites into advanced resectable (Stage IVA), advanced unresectable (Stage
IVB), and distant metastatic (Stage IVC) also simplifies advanced disease staging.
A major revision of the nasopharynx classification has been stimulated by clinical experience from several Asian
sources.
Regional Lymph Nodes. The status of the regional lymph nodes in head and neck cancer is of such prognostic
importance that the cervical nodes must be assessed for each patient and tumour. The lymph nodes may be
subdivided into specific anatomic subsites and grouped into seven levels for ease of description.
Level I:
Level II:
Level III:
Level IV:
Level V:
Level VI:
Level VII:
Other groups:
Submental
Submandibular
Upper jugular
Midjugular
Lower jugular
Posterior triangle (Spinal accessory and transverse cervical)
(Upper, mid and lower, corresponding to the levels that define upper,
mid, and lower jugular nodes)
Prelaryngeal (Delphian)
Pretracheal
Paratracheal
Upper mediastinal
Retropharyngeal
Parapharyngeal
Buccinator (facial)
Preauricular
13
FIG. 1/2 Schematic diagram indicating the location of the lymph node levels in the neck as described in the text.
The location of the lymph node levels conforms to the following clinical descriptions which also correlate with
surgical landmarks at the time of surgical neck exploration .
Level I:
Contains the submental and submandibular triangles bounded by
the anterior and
posterior bellies of the digastric muscle, the hyoid bone inferiorly and the body of the mandible
superiorly.
Level II:
Contains the upper jugular lymph nodes and extends from the level of the skull base superiorly to
the hyoid bone inferiorly.
Level III:
Contains the middle jugular lymph nodes from the hyoid bone superiorly to the level of
the lower border of the cricoid cartilage inferiorly.
Level IV:
Contains the lower jugular lymph nodes from the level of the cricoid cartilage superiorly to the
clavicle inferiorly.
Contains the lymph nodes in the posterior triangle bounded by the anterior border of the
trapezius muscle posteriorly, the posterior border of the sternocleidomastoid muscle anteriorly,
and the clavicle inferiorly. For descriptive purposes, Level V may be further subdivided into
upper, middle, or lower levels corresponding to the superior and inferior planes that define Levels
II, III, and IV.
Level V:
Level VI:
Contains the lymph nodes of the anterior central compartment from the hyoid bone superiorly to
the suprasternal notch inferiorly. On each side, the lateral boundary is formed by the medial
border of the carotid sheath.
Level VII:
Contains the lymph nodes inferior to the suprasternal notch in the superior mediastinum.
The pattern of the lymphatic drainage varies for different anatomic sites. However, the location of the lymph node
metastases has prognostic significance in patients with squamous cell carcinoma of the head and neck. Survival is
significantly worse when metastases involve lymph nodes beyond the first echelon of lymphatic drainage and,
particularly, lymph nodes in the lower regions of the neck, i.e. Level IV and Level V (supraclavicular region).
Consequently, it is recommended that each “N” staging category be recorded to show, in addition to the established
parameters, whether the nodes involved are located in the upper (U) or lower (L) regions of the neck, depending
upon their location above or below the level of the cricoid cartilage.
The natural history and response to treatment of cervical nodal metastases from nasopharynx primary sites is
different, in terms of its impact on prognosis, and, therefore, justifies a different “N” classification scheme.
Regional node metastases from well differentiated thyroid cancer do not significantly impact upon the ultimate
prognosis and, therefore, also justify a unique staging system for thyroid cancers.
Histopathologic examination is necessary to exclude the presence of tumour in lymph nodes. No imaging study (as
yet) can identify microscopic tumour foci in regional nodes or distinguish between small reactive nodes and small
malignant nodes.
When enlarged lymph nodes are detected, the actual size of the nodal mass(es) should be measured. It is recognized
that most masses over 3 cm in diameter are not single nodes but are confluent nodes or tumour in soft tissues of the
neck. Imaging studies showing amorphous spiculated margins of involved nodes or involvement of internodal fat
resulting in loss of normal oval to round nodal shape strongly suggest extracapsular (extranodal) tumour spread.
Pathologic examination is necessary for documentation of tumour extent in terms of the location or level of the
lymph node(s) involved, the number of nodes containing metastases and the presence or absence of extracapsular
spread of tumour.
14
For pN, a selective neck dissection will ordinarily include 6 or more lymph nodes and a radical or modified radical
neck dissection will ordinarily include 10 or more lymph nodes. Negative pathologic examination of a lesser
number of nosed still mandates a pN0 designation.
Metastatic Sites. The most common sites of distant spread are in the lungs and bones; hepatic or brain metastases
occur less often. Mediastinal lymph node metastases are considered distant metastases.
Regional Lymph Nodes (N)
NX
Regional lymph nodes cannot be assessed
N0
No regional lymph node metastasis
N1
U
L
Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension
N2
U
L
Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than
6 cm in greatest dimension; or in multiple ipsilateral lymph nodes, none more than 6 cm
in greatest dimension; or in bilateral or contralateral lymph nodes, none more than 6 cm
in greatest dimension
N2a
Metastasis in single ipsilateral lymph node more than 3 cm but not more than 6 cm in
greatest dimension
N2b
Metastasis in multiple ipsilateral lymph nodes, none more than 6
cm in greatest dimension
N2c
Metastasis in bilateral or contralateral lymph nodes, none more than 6 cm in greatest
dimension
N3
U
U
L
=
=
L
Metastasis in a lymph node more than 6 cm in greatest dimension
Upper neck: Metastasis located above the level of the cricoid cartilage
Lower neck: Metastasis located below the level of the cricoid cartilage
Distant Metastasis (M)
MX
M0
M1
Distant metastasis cannot be assessed
No distant metastasis
Distant metastasis
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
Percy C, Van Holten V, Muir C (eds>) International Classification of Disease for Oncology, 2nd Edition. Geneva,
Switzerland: World Health Organization, 1990.
Beahrs O, Henson DE, Hutter RVP, Kennedy BJ, eds. American Joint committee on Cancer: manual for Staging of Cancer,
4th Edition, Philadelphia, PA: JB Lippincott, 1992.
Hillsamer PJ, Schuller DE, McGhee RB, et al. Improving diagnostic accuracy of cervical metastases with CT and MRI
imaging. Arch Otolaryngo Head Neck Surg, 1990, 116: 2297-1301.
Kowalski LP, Bagietto R, Lara JR, et al. Prognostic significance of the distribution of neck node metastasis from oral
carcinoma. Head Neck, 2000, 22:207-214.
Medina JE. A rational classification of neck dissections. Otolaryngol Head Neck Surg, 1989, 100:169-176.
Picirillo JF. Inclusion of comorbidity in a staging system for head and neck cancer. Oncology, 1995, 9:831-836.
Richard JM, Sancho-Gamier H, Michaeu C, et al. Prognostic factors in cervical lymph node metastasis in upper respiratory
and digestive tract carcinomas: study of 1713 cases during a 15-year period. Laryngoscope, 1987, 97:97-101.
Robbins KT. Neck dissection: classification and incisions. In Shockley WW, Pillsbury HC , (Eds.), The neck: diagnosis
and surgery, St. Louis: Mosby; 1994, pp. 381-391.
Stell PM, Morton RP, Singh SD. Cervical lymph node metastases: the significance of the level of the lymph node. Clin
Oncol, 1983, 9: 101-107.
15
FIG 1 & 2
16
TNM Classification: AJCC 2002 –3
Lip and Oral Cavity
(Nonepithelial tumours such as those of lymphoid tissue, soft tissue, bone, and cartilage are not included.)
Anatomical Sites and Subsites
Lip
External upper lip (vermilion border ) (C00.0)
External lower lip (vermilion border) (C00.1)
Commissures (C00.6)
Oral cavity
Buccal mucosa
- mucosa of the upper and lower lips (C00.3, 4)
- cheek mucosa (C06.0)
- retromolar areas (C06.2)
- bucco-alveolar sulci, upper and lower (vestibule of mouth) (C06.1)
Upper alveolus and gingiva (upper gum) (C03.0)
Lower alveolus and gingiva (lower gum) (C03.1)
Hard palate (C05.0)
Tongue
- dorsal surface and lateral borders anterior to vallate papillae (anterior two-thirds) (C02.0, 1).
- inferior (ventral) surface (C02.2)
Floor of mouth (C04)
ANATOMY
Primary Site. The oral cavity extends from the skin-vermilion junction of the lips to the junction of the hard and
soft palate above and to the line of circumvallate papillae below and is divided into the following specific areas:
Mucosal Lip. The lip begins at the junction of the vermilion border with the skin and includes only the vermilion
surface or that portion of the lip that comes into contact with the opposing lip. It is well defined into an upper and
lower lip joined at the commissures of the mouth.
Buccal Mucosa. This includes all the membrane lining of the inner surface of the cheeks and lips from the line of
contact of the opposing lips to the line of attachment of mucosa of the alveolar ridge (upper and lower) and pterygomandibular raphe.
Lower Alveolar Ridge. This refers to the mucosa overlying the alveolar process of the mandible which extends
from the line of attachment of mucosa in the buccal gutter to the line of free mucosa of the floor of the mouth.
Posteriorly it extends to the ascending ramus of the mandible.
Upper Alveolar Ridge. This refers to the mucosa overlying the alveolar process of the maxilla which extends from
the line of attachment of mucosa in the upper gingival buccal gutter to the junction of the hard palate. Its posterior
margin is the upper end of the pterygopalatine arch.
Retromolar Gingiva (Retromolar Trigone). This is the attached mucosa overlying the ascending ramus of the
mandible from the level of the posterior surface of the last molar tooth to the apex superiorly, adjacent to the
tuberosity of the maxilla.
Floor of the Mouth. This is a semilunar space over the mylohyoid and hyoglossus muscles, extending from the
inner surface of the lower alveolar ridge to the undersurface of the tongue. Its posterior boundary is the base of the
anterior pillar of the tonsil. It is divided into two sides by the frenulum of the tongue and contains the ostia of the
submaxillary and sublingual salivary glands.
17
Hard Palate. This is the semilunar area between the upper alveolar ridge and the mucous membrane covering the
palatine process of the maxillary palatine bones. It extends from the inner surface of the superior alveolar ridge to
the posterior edge of the palatine bone.
Anterior Two-Thirds of the Tongue (Oral Tongue). This is a freely mobile portion of the tongue that extends
anteriorly from the line of circumvallate papillae to the undersurface of the tongue at the junction of the floor of the
mouth. It is composed of four areas: the tip, the lateral borders, the dorsum, and the undersurface (nonvillous ventral
surface of the tongue). The undersurface of the tongue is considered as a separate category by the World Health
Organization (WHO).
Regional Lymph Nodes. Mucosal cancer of the oral cavity may spread to regional lymph node(s). Tumours of each
anatomic site have their own predictable patterns of regional spread. The risk of regional metastasis generally relates
to the T category and probably more importantly to the depth of infiltration of the primary tumours. Cancer of the lip
carries a low metastatic risk and initially involves adjacent submental and submandibular nodes, then jugular nodes.
Cancers of the hard palate and alveolar ridge likewise have a low metastatic potential and involve buccinator,
submandibular, jugular and occasionally retropharyngeal nodes. Other oral cancers will primarily spread to
submandibular and jugular nodes, uncommonly posterior triangle/supraclavicular nodes. Cancer of the anterior oral
tongue may spread directly to lower jugular nodes. The closer to the midline the primary, the greater the risk of
bilateral cervical nodal spread. Any previous treatment to the neck, surgical and/or radiation, may alter normal
lymphatic drainage patterns resulting in unusual distribution of regional spread of disease to the cervical lymph
nodes. In general, cervical lymph node involvement from oral cavity primary sites is predictable and orderly,
spreading from the primary to upper, then middle, and subsequently lower cervical nodes. However, disease in the
anterior oral cavity may also spread directly to the midcervical lymph nodes. The risk of distant metastasis is more
dependent upon the "N" than the "T" status of the head and neck cancer.
Metastatic Sites. The lungs are the commonest site of distant metastases; skeletal or hepatic metastases occur less
often. Mediastinal lymph node metastases are considered distant metastases.
RULES FOR CLASSIFICATION
Clinical Staging. The assessment of the primary tumour is based upon inspection and palpation of the oral cavity
and neck. Additional studies may include CT or MRI. When imaging is utilized one study will generally suffice to
evaluate primary and nodal tumour extent. Clinical assessment of extent of mucosal involvement is more accurate
than is radiographic assessment. The radiographic estimate of deep tissue extent and of regional lymph node involvement is usually more accurate than clinical assessment. MRI is generally more revealing of extent of soft
tissue, perivascular and perineural spread, skull base involvement and intracranial tumour extension.
On the other hand, high resolution CT with contrast will often provide similar information if carefully done and will
provide better images of bone and larynx detail and is minimally affected by motion. CT or MR imaging may be
more useful in evaluation of advanced tumours for assessment of bone invasion (mandible or maxilla) and deep
tissue invasion (deep extrinsic tongue muscles, midline tongue, soft tissues of neck). Clinical examination
supplemented with dental films or panoramic X-rays may be helpful in determining cortical bone involvement. If
CT or MR imaging is undertaken for primary tumour evaluation, radiologic assessment of nodal involvement should
also be done simultaneously. For lesions of an advanced extent appropriate screening for distant metastases should
be considered.
Ultrasonography may be helpful in assessment of major vascular invasion as an adjunctive test. The tumour must be
confirmed histologically. All clinical, imaging, and pathologic data available prior to first definitive treatment may
be used for clinical staging.
Pathologic Staging. Complete resection of the primary site and/or regional nodal dissections followed by pathologic
examination of the resected specimen(s) allow the use of this designation for pT and/or pN, respectively.
Specimens that are resected after radiation or chemotherapy need to be identified and considered in context. pT is
derived from the actual measurement of the unfixed tumour in the surgical specimen. It should be noted, however,
that up to 30% shrinkage of soft tissues may occur in the resected specimen. Pathological staging represents
additional and important information and should be included as such in staging, but does not supplant clinical
staging as the primary staging scheme.
18
DEFINITION OF TNM
Primary Tumour (T)
TX
T0
Tis
T1
T2
T3
T4 (lip)
Primary tumour cannot be assessed
No evidence of primary tumour
Carcinoma in situ
Tumour 2 cm or less in greatest dimension
Tumour more than 2 cm but not more than 4 cm. in greatest dimension
Tumour more than 4 cm in greatest dimension
Tumour invades adjacent structures (e.g., through cortical bone, inferior alveolar nerve,
floor of mouth, skin of face, i.e. chin or nose)
T4a (oral cavity) Tumour invades adjacent structures (e.g., through cortical bone, into deep [extrinsic]
muscle of tongue (genioglossus, hyoglossus, palatoglossus, and styloglossus), maxillary sinus,
skin of face. Superficial erosion alone of bone/tooth socket by gingival primary is not sufficient to
classify as T4)
T4b
Tumour invades masticator space, pterygoid plates, skull base and internal carotid artery
NOTE: Superficial erosion alone of bone/tooth socket by gingival primary is not sufficient to classify a tumour as
T4.
STAGE GROUPING – Identical to Larynx
HISTOPATHOLOGIC TYPE
The predominant cancer is squamous cell carcinoma. The staging guidelines are applicable to all forms of
carcinoma.
Nonepithelial tumours such as those of lymphoid tissue, soft tissue, bone and cartilage (i.e., lymphoma, melanoma,
and sarcoma) are not included. Histologic confirmation of diagnosis is required. Histopathologic grading of
squamous carcinoma is recommended; the grade is subjective and uses a descriptive as well as numerical form, i.e.,
well, moderately well, and poorly differentiated, depending upon the degree of closeness to or deviation from squamous epithelium in mucosal sites. Also recommended is a quantitative evaluation of depth of invasion of the
primary tumour and the presence or absence of vascular invasion and perineural invasion.
Characteristics of Tumours
Endophytic. The measurement using an ocular micrometer is taken perpendicular from the surface of the invasive
squamous cell carcinoma (A) to the deepest area of involvement (B) and recorded in millimeters. The measurement
should not be done on tangential sections or in lesions without a clearly recognizable surface component.
Exophytic. The measurement which is better characterized as tumour thickness rather than depth of invasion is
taken from the surface (A) to the deepest area (B).
Ulcerated. The measurement is taken from the ulcer base (A) to the deepest area (B) as well as from the surface of
the most lateral extent of the invasive carcinoma (C) to the deepest area (D).
Depth of tumour invasion (mm) should be recorded. Depth is NOT used for T staging.
Although the grade of the tumour does not enter into staging of the tumour, it should be recorded. The pathologic
description of any lymphadenectomy specimen should describe the size, number, and position of involved lymph
node(s), and the presence or absence of extracapsular extension.
HISTOPATHOLOGIC GRADE (G)
GX
G1
G2
G3
Grade cannot be assessed
Well differentiated
Moderately differentiated
Poorly differentiated
19
PROGNOSTIC FACTORS
In addition to the importance of the TNM factors outlined previously, the overall health of these patients clearly
influences outcome. Comorbidity can be classified by more general measures, such as the Karnofsky Performance
status (KPS), or more specific measures, such as the Kaplan-Feinstein Index. The KPS provides a uniform, objective
assessment of an individual’s functional status. The scale, in 10 point increments from 0 (dead) to 100 (normal, no
complaints, no evidence of disease), was devised in 1948 by David A. Karnofsky. The KPS is a reliable,
independent predictor of survival outcome for patients with solid tumors and, therefore, is a required baseline
assessment in clinical protocols in head and neck and other cancers.
The AJCC strongly recommends recording of KPS along with standard staging information.
Karnofsky Scale: Criteria of Performance Status (PS)
100
90
80
70
60
50
Normal; no complaints; no evidence of disease.
Able to carry on normal activity; minor signs or symptoms of disease
Able to carry on normal activity with effort; some signs or symptoms of disease
Cares for self; unable to carry on normal activity or do active work.
Requires occasional assistance but is able to care for most of own needs.
Requires considerable assistance and frequent medical care.
Disabled; requires special care and assistance.
Diagnosis and treatment of depression may also aid in symptom control and improved quality of life. Continued
exposure to carcinogens, such as alcohol and tobacco smoke, likely also affects patients' outcome adversely.
20
TNM Classification: AJCC 2002 –3
Major Salivary Glands
(Parotid, Submandibular and Sublingual)
C07.9 Parotid gland
C08.0 Submandibular gland
C08.1 Sublingual gland
C08.8 Overlapping lesion of major salivary glands
C08.9 Major salivary gland, NOS
This staging system is based on an extensive retrospective review of the world literature regarding malignant tumors
of the major salivary glands.
Numerous factors affect patient survival, including the histologic diagnosis, cellular differentiation of the tumor
(grade), site, size, degree of fixation, or local extension, facial nerve involvement and the status of regional lymph
nodes as well as distant metastases. The classification here proposed involves the four dominant clinical variables:
tumor size, local extension of the tumor, nodal metastasis, and distant metastasis. The T4 category has been
subdivided (T4a, T4b), T4a indicates advanced lesions which are resectable with grossly clear margins; T4b reflects
extension to areas which preclude resection with clear margins. Histologic grade, patient age and tumor site are
important additional factors that should be recorded for future analysis and potential inclusion in the staging system.
ANATOMY
Primary Site The major salivary glands include the parotid, submandibular and sublingual glands.
Tumors arising in minor salivary glands (mucous-secreting glands in the lining membrane of the upper aerodigestive
tract) are properly staged according to the anatomic site of origin (e.g., oral cavity, sinuses, etc). Primary tumors of
the parotid comprise the largest proportion of salivary gland tumors. Sublingual primary cancers are rare and may
be difficult to distinguish with certainty from minor salivary gland primary tumors of the anterior floor of the mouth.
Regional Lymph Nodes Regional lymphatic spread from salivary gland cancer is less common than from head and
neck mucosal squamous cancers and varies according to the histology and size of the primary tumor. Most nodal
metastases will be clinically apparent on initial evaluation. Low-grade tumors rarely metastasize to regional nodes,
while the risk of regional spread is substantially higher from the high-grade cancers. Regional dissemination tends
to be orderly, progressing from intraglandular to adjacent (periparotid, submandibular nodes) then to upper and
midjugular, and occasionally retropharyngeal nodes. Bilateral lymphatic spread is rare.
Metastatic Sites. Distant spread is most frequently to the lungs.
RULES FOR CLASSIFICATION
Clinical Staging The assessment of primary salivary gland tumors includes a pertinent history (pain, trismus, etc),
inspection, palpation and evaluation of the cranial nerves. Radiologic studies may add valuable information for
staging. The soft tissues of the neck from the skull base to the hyoid bone must be studied with the lower neck
included whenever lymph node metastases are suspected. Images of the intratemporal facial nerve are critical to the
identification of perineural tumor in this area. Cancers of the submandibular and sublingual salivary glands merit
cross-sectional imaging. Computed tomography (CT) or MRI may be useful in assessing extent of deep
extraglandular tumor, bone invasion, deep tissue extent (extrinsic tongue muscle and/or soft tissues of the neck).
Pathologic staging. The surgical pathology report and all other available data should be used to assign a pathologic
classification to those patients who have resection of the cancer.
21
DEFINITION OF TNM
Primary Tumor (T)
TX
T0
T1
T2
T3
T4a
T4b
Primary tumor cannot be assessed
No evidence of primary tumor
Tumor 2 cm or less in greatest dimension without extraparenchymal extension*
Tumor more than 2 cm but not more than 4 cm in greatest dimension without extraparenchymal extension*
Tumor more than 4 cm and/or tumor having extraparenchymal extension*
Tumor invades skin, mandible, ear canal, and/or facial nerve
Tumor invades skull base, pterygoid plates, and/or carotid artery
Note:
Extraparenchymal extension is clinical or macroscopic evidence of invasion of soft tissues or facial Nerve.
STAGE GROUPING - Identical to Larynx
HISTOPATHOLOGIC TYPE
The suggested histopathologic typing is that proposed by the World Health
Organization.
Acinic cell carcinoma
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Polymorphous low grade adenocarcinoma
Epithelial-myoepithelial carcinoma
Basal cell adenocarcinoma
Sebaceous carcinoma
Papillary cystadenocarcinoma
Mucinous adenocarcinoma
Oncocytic carcinoma
Salivary duct carcinoma
Adenocarcinoma
Myoepithelial carcinoma
Carcinoma ex pleomorphic adenoma
Squamous cell carcinoma
Small cell carcinoma
Other carcinomas
22
HISTOLOGIC GRADE (G)
Histologic grading is applicable only to some types of salivary cancer:
Mucoepidermoid carcinoma, adenocarcinoma not otherwise specified, or when either of these is the carcinomatous
element of carcinoma ex pleomorphic adenoma.
In most instances, the histologic type defines the grade (i.e. salivary duct carcinoma is
high grade; basal cell adenocarcinoma is low grade).
TNM Classification: AJCC 2002 -3
Paranasal Sinuses
(Nonepithelial tumours such as those of lymphoid tissue, soft tissue, bone and cartilage are not included)
C30.0 Nasal cavity
C31.0 Maxillary sinus
C31.1 Ethmoid sinus
ANATOMY
Primary Sites. Cancer of the maxillary sinus is the most common of the sinonasal malignancies. Ethmoid sinus
and nasal cavity cancers are equal in frequency, but considerably less common than maxillary sinus cancers.
Tumours of the sphenoid and frontal sinuses are so rare as not to warrant staging.
The location, as well as the extent, of the mucosal lesion within the maxillary antrum has prognostic significance.
Historically, Ohngren’s line, connecting the medial canthus of the eye to the angle of the mandible, is used to divide
the maxillary antrum into an anteroinferior portion (infrastructure) which is associated with a good prognosis and a
superoposterior portion (suprastructure) which has a poor prognosis (Fig. 1 a&b). The poorer outcome associated
with superoposterior cancers reflects early access of these tumours to critical structures including the eye, skull base,
pterygoids, and infratemporal fossa.
For the purpose of staging, the nasoethmoidal complex is divided into two sites, nasal cavity and ethmoid sinuses.
The ethmoids are further subdivided two sub-sites, left and right, separated by the nasal septum. The nasal cavity is
divided into four sub-sites, the septum, floor, lateral wall and vestibule.
Site
Subsite
Nasal Cavity
Septum
Floor
Lateral wall
Vestibule
Ethmoid sinus
Left
Right
23
Regional Lymph Nodes. Regional lymph node spread from cancer of paranasal origin is relatively uncommon.
Involvement of buccinator, submandibular, upper jugular and occasionally retropharyngeal nodes may occur with
advanced maxillary sinus cancer, particularly those extending beyond the sinus walls to involve adjacent structures
including soft tissues of the cheek, upper alveolus, palate, and buccal mucosa. Ethmoid sinus cancers are less prone
to regional lymphatic spread. When only one side of the neck in involved, it should be considered ipsilateral.
Bilateral spread may occur with advanced primary cancer, particularly with spread of the primary beyond the
midline.
Metastatic Sites. Distant spread to lungs is most common; occasionally there is spread to bone.
RULES FOR CLASSIFICATION
Clinical Staging. The assessment of primary maxillary antrum, nasal cavity and ethmoid tumours is based on
inspection and palpation including examination of the orbits, nasal and oral cavities, nasopharynx, and neurologic
evaluation of the cranial nerves. Nasal endoscopy with rigid or fibreoptic flexible instruments is recommended.
Radiological assessment with magnetic resonance imagining (MRI) or computed tomography (CT) is mandatory for
accurate pretreatment staging of malignant tumor of the sinuses. If available, MRI more accurately depicts skull
base and intracranial involvement and differentiation of fluid from solid tumor. Neck nodes are assessed by
palpation +/- imaging. Imaging for possible nodal metastases is probably unnecessary in the presence of a clinically
negative neck. Examinations for distant metastases include appropriate radiographs, blood chemistries, blood count
and other routine studies as indicated.
Pathological Staging. Pathologic staging requires the use of all information obtained in the clinical staging in
addition to histologic study of the surgically resected specimen.
The surgeon’s evaluation of gross unresected residual tumor must also be included. Specimens that are resected
after radiation or chemotherapy need to be identified and considered in context. The pathologic description of the
lymphadenectomy specimen should describe the size, number, position of the involved node(s), and the presence or
absence of extracapsular extension.
DEFINITION OF TNM
Maxillary Sinus
Primary Tumor (T)
TX
T0
Tis
T1
T2
T3
T4a
T4b
Primary tumor cannot be assessed
No evidence of primary tumor
Carcinoma in situ
Tumor limited to the antral mucosa with no erosion or destruction of bone
Tumor causing bone erosion or destruction including extension into the hard palate and/or middle nasal
meatus, except extension to posterior antral wall of maxillary sinus and pterygoid plates
Tumor invades any of the following: bone of the posterior wall of maxillary sinus, subcutaneous tissues,
floor or medial wall of orbit, pterygoid fossa, ethmoid sinuses
Tumor invades anterior orbital contents, skin of cheek, pterygoid plates, infratemporal fossa, cribriform
plate, sphenoid or frontal sinuses
Tumor invades any of the following: orbital apex, dura, brain, middle cranial fossa, cranial nerves other
than maxillary division of trigeminal nerve, nasopharynx, and/or clivus
24
Nasal Cavity and Ethmoid Sinus
Primary Tumor (T)
Tx
T0
Tis
T1
T2
T3
T4a
T4b
Primary tumor cannot be assessed
No evidence of primary tumor
Carcinoma in situ
Tumor restricted to any one sub-site, with or without bony invasion
Tumor invading two sub-sites in a single region or extending to involve an adjacent region within
the nasoethmoidal complex, with or without bony invasion
Tumor extends to invade the medial wall or floor of the orbit, maxillary sinus, palate, or cribriform plate
Tumor invades any of the following: anterior orbital contents, skin of nose or cheek, minimal extension to
anterior cranial fossa, pterygoid plates, sphenoid or frontal sinuses
Tumor invades any of the following: orbital apex, dura, brain, middle cranial fossa, cranial nerves other
than nasopharynx, or clivus
STAGE GROUPING - Identical to Larynx
HISTOPATHOLOGIC TYPE
The predominant cancer is squamous cell carcinoma. The staging guidelines are applicable to all forms of
carcinoma. Nonepithelial tumours such as those of lymphoid tissue, soft tissue, bone and cartilage are not included.
Histologic confirmation of diagnosis is required. Histopathologic grading of squamous carcinoma is recommended.
The grade is subjective and uses descriptive as well as a numerical i.e., well differentiated, moderately
differentiated, and poorly differentiated depending upon the degree of closeness to, or deviation from, squamous
epithelium in mucosal sites. Also recommended where feasible is a quantitative evaluation of depth of invasion of
the primary tumor and the presence or absence of vascular invasion and perineural invasion. Although the grade of
the tumor does not enter into the staging of the tumor, it should be recorded. The pathologic description of any
lymphadenectomy specimen should describe the size, number, position of the involved node(s), and the presence or
absence of extracapsular extension.
HISTOPATHOLOGIC GRADE (G)
GX
G1
G2
G3
Grade cannot be assessed
Well differentiated
Moderately differentiated
Poorly differentiated
PROGNOSTIC FACTORS
In addition to the importance of the TNM factors outlined previously, the overall health of these patients clearly
influences outcome.
Comorbidity can be classified by more general measures, such as the Karnofsky performance score, or more specific
measures such as the Kaplan-Feinstein Index or the Charlson Index, and increase in incidence and severity with
increasing age. Continued exposure to carcinogens such as alcohol and tobacco smoke likely also affects patient’s
outcomes adversely.
25
TNM Classification: AJCC 2002 –3
Pharynx
.(Including base of tongue, soft palate and uvula)
(Nonepithelial tumours such as those of lymphoid tissue, soft tissue, bone, and cartilage are not
included.)
C01.9 Base of tongue, NOS
C02.4 Lingual tonsil
C05.1 Soft palate, NOS
C05.2 Uvula
C09.0
C09.1
C09.8
C09.9
Tonsillar fossa
Tonsillar pillar
Overlapping lesion
Tonsil, NOS
C11.0 Superior wall of
nasopharynx
C11.1 Posterior wall of
nasopharynx
C11.2 Lateral wall of
nasopharynx
C11.3 Anterior wall of
nasopharynx
C11.8 Overlapping lesion
C11.9 Nasopharynx, NOS
C12.9 Pyriform sinus
C10.0 Vallecula
C10.2 Lateral wall of oropharynx
C13.0 Postcricoid region
C13.1 Hypopharyngeal aspect of aryepicglottic
fold
C13.2 Posterior wall of
hypopharynx
C13.8 Overlapping lesion
C13.9 Hypopharynx, NOS
C14.0
C14.1
C14.2
C14.8
Pharynx, NOS
Laryngopharynx
Waldeyer’s ring
Overlapping lesion of
lip, oral cavity and
pharynx
C10.4 Branchial cleft
C10.8 Overlapping lesion
C10.9 Oropharynx, NOS
ANATOMY
Primary Sites and Subsites. The pharynx (including base of tongue, soft palate, and uvula) is divided into three
regions: nasopharynx, oropharynx and hypopharynx. Each region is further subdivided into specific sites as
summarized in the following:
Nasopharynx. The nasopharynx begins anteriorly at the posterior choana and extends along the plane of the airway
to the level of the free border of the soft palate. It includes the vault, the lateral walls including the fossae of
Rosenmuller and the mucosa covering the torus tubaris forming the eustachian tube orifice, and the posterior wall.
The floor is the superior surface of the soft palate. The posterior margins of the choanal orifices and of the nasal
septum are included in the nasal fossa.
Parapharyngeal involvement denotes postero-lateral infiltration of tumour beyond the pharyngobasilar fascia.
Involvement of the masticator space denotes extension of tumour beyond the anterior surface of the lateral
pterygoid muscle, or lateral extension beyond the postero-lateral wall of the maxillary antrum, pterygo-maxillary
fissure.
Oropharynx. The oropharynx is the portion of the continuity of the pharynx extending from the plane of the
superior surface of the soft palate to the superior surface of the hyoid bone (or floor of the vallecula) and includes
the base of tongue, the inferior surface of the soft palate and the uvula, the anterior and posterior tonsillar pillars, the
glossotonsillar sulci, the pharyngeal tonsils; the lateral and posteriors walls.
Hypopharynx. The hypopharynx is that portion of the pharynx extending from the plane of the superior border of
the hyoid bone (or floor of the vallecula) to the plane corresponding to the lower border of the cricoid cartilage and
includes the pyriform fossae (right and left), the lateral and posterior hypopharyngeal walls, and the postcricoid
region.
26
The post cricoid area extends from the level of the arytenoid cartilages and connecting folds to the inferior border of
the cricoid cartilage and connects the two pyriform sinuses thus forming the anterior wall of the hypopharynx.
The pyriform sinus extends from the pharyngoepiglottic fold to the upper end of the esophagus at the lower border
of the cricoid cartilage and is bounded laterally by the lateral pharyngeal wall and medially by the lateral surface of
the aryepiglottic fold, arytenoid and cricoid cartilages. The posterior pharyngeal wall extends from the level of the
superior surface of the hyoid bone (or floor of the vallecula) to the inferior border of the cricoid cartilage and from
the apex of one pyriform sinus to the other.
Regional Lymph Nodes. The risk of regional nodal spread from cancers of the pharynx is high. Primary
nasopharyngeal tumours commonly spread to retropharyngeal, upper jugular, and spinal accessory nodes, often
bilaterally.
Oropharyngeal cancers involve upper and mid-jugular lymph nodes, less likely
submental/submandibular nodes. Hypopharyngeal cancers spread to adjacent parapharyngeal, paratracheal and midand lower jugular nodes. Bilateral lymphatic drainage is common.
In clinical evaluation the maximum size of the nodal mass should be measured. It is recognized that most masses
over 3 cm in diameter are not single nodes but are confluent nodes or tumour in soft tissues of the neck. There are
three categories of clinically involved nodes for the nasopharynx, oropharynx, and hypopharynx: N1, N2, and N3.
The use of subgroups a, b and c is not required, but is recommended.
For pN, a selective neck dissection will ordinarily include 6 or more lymph nodes and a radical or modified radical
neck dissection will ordinarily include 10 or more lymph nodes. Negative pathologic examination of a lesser
number of nodes still mandates a pN0 designation.
Metastatic Sites. The lungs are the commonest sites of distant metastases; skeletal or hepatic metastases occur less
often. Mediastinal lymph node metastases are considered distant metastases.
RULES FOR CLASSIFICATION
Clinical Staging. Clinical staging is generally employed for squamous cell carcinomas of the pharynx. Assessment
is based primarily on inspection, and by indirect and direct endoscopy. Palpation of sites (when feasible) and of
neck nodes is essential. Neurologic evaluation of all cranial nerves is required. Imaging studies are essential in
clinical staging of pharynx tumours.
Cross-sectional imaging in nasopharyngeal cancer is mandatory to complete the staging process. Magnetic
resonance imaging (MRI) often is the study of choice because of its multiplanar capability, superior soft tissue
contrast and its sensitivity to skull base and intracranial tumour spread. Computed tomography (CT) staging with
axial and coronal thin section technique with contrast is alternative. Radiologic nodal staging should be done to
assess adequately the retropharyngeal and cervical nodal status.
Cross-sectional imaging in oropharyngeal carcinoma is recommended when the deep tissue extent of the primary
tumour is in question. CT or MRI may be employed. Radiologic nodal staging should also be done simultaneously.
Cross-sectional imaging of hypopharyngeal carcinoma is recommended when the extent of the primary tumour is in
doubt, particularly its deep extent in relationship to adjacent structures (i.e., larynx, thyroid, cervical vertebrae, and
carotid sheath). CT is preferred currently because of less motion artifact than MRI. Radiologic nodal staging
should be done simultaneously.
Complete endoscopy, usually under general anesthesia, is performed after completion of other staging studies, to
accurately assess the surface extent of the tumour and to assess deep involvement by palpation for muscle resistance
and to facilitate biopsy. A careful search for other primary tumours of the upper aerodigestive tract is indicated
because of the incidence of multiple independent primary tumours occurring simultaneously.
Pathologic Staging. Pathologic staging requires the use of all information obtained in clinical staging in addition to
histologic study of the surgically resected specimen. The surgeon’s evaluation of gross unresected residual tumour
must also be included. The pathologic description of any lymphadenectomy specimen should describe the size,
number and level of any involved nodes.
27
DEFINITION OF TNM
Primary Tumour (T)
TX
T0
Tis
Primary tumour cannot be assessed
No evidence of primary tumour
Carcinoma in situ
Nasopharynx
T1
T2
T2a
T2b
T3
T4
Tumour confined to the nasopharynx
Tumour extends to soft tissues
Tumour extends to the oropharynx and/or nasal cavity without parapharyngeal extension *
Any tumour with parapharyngeal extension *
Tumour involves bony structures and/or paranasal sinuses
Tumour with intracranial extension and/or involvement of cranial nerves, infratemporal fossa,
hypopharynx, orbit, or masticator space
*Note: Parapharyngeal extension denotes posterolateral infiltration of tumour beyond the pharyngobasilar fascia.
Oropharynx
T1
T2
T3
T4a
T4b
Tumour 2cm or less in greatest dimension
Tumour more than 2cm but not more than 4cm in greatest dimension
Tumour more than 4cm in greatest dimension
Tumour invades the larynx, deep/extrinsic muscle of tongue, medial pterygoid, hard palate, or mandible.
Tumour invades lateral pterygoid muscle, pterygoid plates, lateral nasopharynx, skull base, or carotid
artery.
Hypopharynx
T1
T2
T3
T4a
T4b
Tumour limited to one subsite of hypopharynx and 2 cm or less in greatest dimension
Tumour invades more than one subsite of hypopharynx or an adjacent site, or measures more than 2 cm but
not more than 4 cm in greatest diameter without fixation of hemilarynx
Tumour measures more than 4 cm in greatest dimension or with fixation of hemilarynx
Tumour invades thyroid/cricoid cartilage, hyoid bone, thyroid gland, esophagus or central compartment
soft tissue. *
Tumour invades prevertebral fascia, encases carotid artery, or invades mediastinal structures.
*Note: Central compartment soft tissue includes prelaryngeal strap muscles and subcutaneous fat.
Regional Lymph Nodes (N): Nasopharynx
The distribution and the prognostic impact of regional lymph node spread from nasopharynx cancer, particularly of
the undifferentiated type, is different than that of other head and neck mucosal cancers and justifies use of a different
N classification scheme.
NX
N0
N1
N2
N3
N3a
N3b
Regional lymph nodes cannot be assessed
No regional lymph node metastasis
Unilateral metastasis in lymph node(s). 6 cm or less in greatest dimension, above the supraclavicular fossa*
Bilateral metastasis in lymph node(s), 6 cm or less in greatest dimension, above the supraclavicular fossa*
Metastasis in a lymph node(s)
greater than 6 cm in dimension
extension to the supraclavicular fossa*
* Midline nodes are considered ipsilateral nodes.
28
Supraclavicular zone or fossa is relevant to the staging of nasopharyngeal carcinoma and is the triangular region
originally described by Ho. It is defined by three points: (1) the superior margin of the sternal end of the clavicle;
(2) the superior margin of the lateral end of the clavicle; (3) the point where the neck meets the shoulder (see Fig. 42). Note that this would include caudal portions of Levels IV and V. All cases with lymph nodes (whole or part) in
the fossa are considered N3b.
STAGE GROUPING: Nasopharynx
Stage 0
Stage I
Stage IIA
Stage IIB
Tis
T1
T2a
T1
T2
T2a
T2b
T2b
T1
T2a
T2b
T3
T3
N0
N0
N0
N1
N1
N1
N0
N1
N2
N2
N2
N0
N1
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
Stage IVA
T3
T4
N2
N0
M0
M0
Stage IVB
Stage IVC
T4
T4
Any T
Any T
N1
N2
N3
Any N
M0
M0
M0
M1
StageIII
STAGE GROUPING: Oropharynx, Hypopharynx: Identical to Larynx
HISTOPATHOLOGIC TYPE
The predominant cancer type is squamous cell carcinoma for all pharyngeal sites. Nonepithelial tumours such as
those of lymphoid tissue, soft tissue, bone and cartilage are not included in this system.
For nasopharyngeal carcinomas it is recommended that the World Health Organization (WHO) Classification be
used (Table 4.1). Histologic diagnosis is required to use this classification.
HISTOPATHOLOGIC GRADE (G): Oropharynx, Hypopharynx
GX
G1
G2
G3
Grade cannot be assessed
Well differentiated
Moderately differentiated
Poorly differentiated
PROGNOSTIC FACTORS
In addition to the importance of the TNM factors outlined previously, the overall health of these patients clearly
influences outcome. Comorbidity can be classified by more general measures, such as the Karnofsky performance
score, or more specific measures, such as the Kaplan-Feinstein Index.
Continued exposure to carcinogens, such as alcohol and tobacco smoke, likely also affects patients’ outcome
adversely.
29
Table 4-1. Classification of Nasopharyngeal Carcinoma
WHO Classification
Former Terminology
Type 1. Squamous
cell carcinoma
Squamous cell carcinoma
Type 2.
Nonkera-tinizing carcinoma
without lymphoid
stroma
with lymphoid
stroma
Type 3. Undifferentiated carcinoma
without lymphoid
stroma
with lymphoid
stroma
Transitional cell carcinoma
Intermediate cell carcinoma
Lymphoepithelial cell
carcinoma (Regaud)
Anaplastic carcinoma, clear
cell carcinoma
Lymphoepithelial carcinoma
(Schminke)
30
TNM Classification: AJCC 2002 –3
Thyroid Gland
Although staging for cancers in other head and neck sites is based entirely on the anatomic extent of disease, it is not
possible to follow this pattern for the unique group of malignant tumors that arise in the thyroid gland. Both the
histologic diagnosis and the age of the patient are of such importance in the behaviour and prognosis of thyroid
cancer that these factors are included in this staging system
ANATOMY
Primary Site.
The thyroid gland ordinarily is composed of a right and a left lobe lying adjacent and lateral to the upper trachea and
oesophagus.
An isthmus connects the two lobes and in some cases a pyramidal lobe is present extending upward anterior to the
thyroid cartilage.
Regional Lymph Nodes.
Regional lymph node spread from thyroid cancer is common but of less prognostic significance in the generally
well-differentiated tumors (papillary, follicular) than in medullary cancers. The first echelon of nodal metastasis is
the paralaryngeal, paratracheal, and prelaryngeal (Delphian) nodes adjacent to the thyroid gland in the central
compartment of the neck generally described as Level VI. Although involvement of these lymph nodes has minimal
prognostic significance, it is usually observed in the older age group. Metastasis secondarily involves the mid and
lower jugular, supraclavicular and, much less commonly, the upper deep jugular and spinal accessory lymph nodes.
Lymph node metastasis to submandibular and submental lymph nodes is indeed very rare. Upper mediastinal (Level
VII) nodal spread occurs frequently both anteriorly and posteriorly. Retropharyngeal nodal metastasis may be seen
usually in the presence of extensive lateral cervical metastasis. Bilateral nodal spread is common. The components
of the N category are described as first echelon (central compartment/Level VI), N1a and lateral cervical and/or
superior mediastinal as N1b. The lymph node metastasis should also be described according to the Level of the
neck that is involved. Nodal metastases from medullary thyroid cancer carry a much more ominous prognosis
although they follow a similar pattern of spread.
Metastatic Sites.
Distant spread occurs by hematogenous routes, for example to lungs and bones, but many other sites may
be involved.
RULES FOR CLASSIFICATION
Clinical Staging.
The assessment of a thyroid tumor depends on inspection and palpation of the thyroid gland and regional lymph
nodes. Indirect laryngoscopy to evaluate vocal cord motion is essential. A variety of imaging procedures can
provide additional useful information. These include radioisotope thyroid scans, ultrasonography, computed
tomography scans (CT), and magnetic resonance imaging (MRI) scans. When cross-sectional imaging is utilized,
MRI is recommended so as to avoid contamination of the body with the iodinated contrast medium generally used
with CT. Iodinated contrast media will delay the possibility of administering radioactive iodine-131
postoperatively. The diagnosis of thyroid cancer must be confirmed by needle biopsy or open biopsy of the tumor.
Further information for clinical staging may be obtained by biopsy of lymph nodes or other areas of suspected local
or distant spread. All information available prior to first treatment should be used.
31
Pathologic Staging.
Pathologic staging requires the use of all information obtained in the clinical staging in addition to histologic study
of the surgically resected specimen. The surgeon’s description of gross unresected residual tumor must also be
included.
DEFINITION OF TNM
Primary Tumor (T)
Note: All categories may be subdivided: (a) solitary tumor, (b) multifocal tumor (the largest determines the
classification).
TX
T0
T1
T2
T3
T4a
T4b
Primary tumor cannot be assessed
No evidence of primary tumor
Tumor 2 cm or less in greatest dimension limited to the thyroid
Tumor more than 2 cm but not more than 4 cm in greatest dimension limited to the thyroid
Tumor more than 4 cm in greatest dimension limited to the thyroid or any tumor with minimal extrathyroid
extension (e.g. extension to sternothyroid muscle or perithyroid soft tissues).
Tumor of any size extending beyond the thyroid capsule to invade subcutaneous soft tissues, larynx,
trachea, oesophagus, or recurrent laryngeal nerve.
Tumor invades prevertebral fascia, carotid artery or mediastinal vessels
All anaplastic carcinomas are considered T4 tumors.
T4a
T4b
Intrathyroidal anaplastic carcinoma – surgically resectable.
Extrathyroidal anaplastic carcinoma – surgically unresectable
Regional Lymph Nodes (N)
Regional lymph nodes are the central compartment, lateral cervical, and upper mediastinal lymph nodes.
NX
N0
Regional lymph nodes cannot be assessed.
No regional lymph node metastasis
N1
Regional lymph node metastasis
N1a
N1b
Metastasis to Level VI (pretracheal, paratracheal, and prelaryngeal/Delphian lymph nodes)
Metastasis to unilateral, bilateral or contralateral cervical or superior mediastinal lymph nodes.
HISTOPATHOLOGIC TYPE
There are four major histopathologic types:
Papillary carcinoma (including follicular variant of papillary carcinoma)
Follicular carcinoma (including Hurthle cell carcinoma)
Medullary carcinoma
Undifferentiated (anaplastic) carcinoma
32
STAGE GROUPING
Separate stage groupings are recommended for papillary follicular, medullary or undifferentiated (anaplastic)
carcinoma.
Papillary or Follicular
Under 45 years
Stage I
Stage II
Any T, Any N, M0
Any T, Any N, M1
Papillary or Follicular
45 years and older
Stage I
T1, N0, M0
Stage II
T2, N0, M0
Stage III
T3, N0, M0
T1. N1a, M0
T2, N1a, M0
T3, N1a, M0
Stage IV-A
T4a, N0, M0
T4a, N1a, M0
T1, N1b, M0
T2, N1b, M0
T3, N1b, M0
Stage IV-B
Stage IV-C
T4a, N1b, M0
T4b, Any N, M0
Any T, Any N, M1
Medullary Carcinoma
Stage I
Stage II
Stage III
Stage IV-A
Stage IV-B
Stage IV-C
T1, N0, M0
T2, N0, M0
T3, N0, M0
T1, N1a, M0
T2, N1a, M0
T3, N1a, M0
T4a, N0, M0
T4a, N1a, M0
T1, N1b, M0
T2, N1b, M0
T3, N1b, M0
T4a, N1b, M0
T4b, Any N, M0
Any T, Any N, M1
Anaplastic Carcinoma
All anaplastic carcinomas are considered Stage IV
Stage IV-A
Stage IV-B
T4a, Any N, M0
T4b, Any N, M0
Stage IV-C
Any T, Any N, M1
33
2
DIAGNOSTIC APPROACHES
Chapter 1
Role Of Imaging
INTRODUCTION
Within the head and neck there are requirements for imaging which are specific to each subsite and those
which apply to evaluation of head and neck tumours in general. The common aims of baseline head and
neck imaging are clarified and augmented with site specific protocols, taking into account the
development of the Royal College of Radiologists guidelines/protocols. Squamous cell carcinoma is the
commonest head and neck cancer and because it arises from mucosal surfaces is usually diagnosed by
direct visualisation and biopsy. Clinical assessment of mucosal disease of the primary tumour is
significantly superior to any radiological technique - the clinical estimate of the mucosal extent of the
primary tumour exceeds the radiographic estimate. Conversely, cross sectional imaging is essential for
evaluating the deep extent of the disease.
Imaging in patients with head and neck malignant disease is crucial for various reasons. It is
important to ascertain the location and relationship to neighbouring structures of the primary
disease. This is particularly important in surgical planning. The initial imaging will also indicate tumour
size and the status of the rest of the neck. In order to stage certain head and neck tumours fully,
information may also be required as to the metastatic status in other areas, notably the chest and the
skeletal system/liver.
Imaging is important in monitoring the response to treatments, particularly in respect of recurrent disease,
further spread or the development of a second primary. In some instances imaging can be useful in
enabling optimal function to be obtained following treatment or as a baseline before treatment, e.g. the
use of swallowing investigations and those associated with dental/maxillofacial function. The use of
imaging therefore forms an important part of pre and post treatment work up and each unit should have
access to CT/MRI scanning, ultrasonography, radio isotope imaging and more simple plain x-ray
techniques such as a simple chest radiograph and an orthopantomogram (although the use of this form of
radiograph is controversial and most now prefer CT scanning). Contrast examinations such as a
barium/water soluble swallow may also be required. Ultrasonographic techniques can also be combined
with the use of fine needle aspiration and this is considered further. Imaging is useful for detecting and
monitoring post treatment complications, and rehabilitation.
Various reports in the world literature have shown a positive correlation between tumour volume and
prognosis for all sites (1, 2, 3 ). Imaging has rendered T staging a lot more precise. Various methods of
determining tumour volume from e.g. CT scans have been devised such as the summation of areas
technique in various planes (4) and errors of volume calculations using this technique are within 5-10 %
when compared with volumes determined by excision and examination. Most of the studies dealing with
tumour volume and clinical progression arise from series of patients with laryngeal and oropharyngeal
disorder and in the one by Gilbert et al (3) it was shown that the tumour volume determined from pretreatment CT scans was the most important predictor for a successful outcome with radiotherapy.
Volume measurement, however, in other sites is probably less important. Olmi et al (5) and Cellai et al
(6) showed that tumour volume in nasopharyngeal carcinoma has only a minor influence on prognosis.
Pameijer et al (7) in a study investigating variability of tumour volumes in T3 staged head and neck
tumours showed considerable variability of tumour volumes in conventionally staged T3 head and neck
tumours and proposed incorporation of tumour volume data to the TNM classification system, in view of
the potential as a prognostic indicator.
34
CT SCANNING
Although it is appreciated that all imaging departments are under a great deal of pressure imaging should
be carried out ideally within two weeks of referral and preferably before biopsy. If imaging is performed
after biopsy then this should ideally be carried out 7-10 days later as the biopsy may result in air pockets
and possibly result in the disease being upstaged.
Computerised axial tomographic scanning or CT scanning uses conventional x-rays with computer
processing of digital information obtained from layer or spiral tomographs. It is particularly useful in
evaluating the relationship of tumours with bone and can also be useful for evaluating malignant disease
in relation to cartilage infiltration.
Assessment of the tumour in relation to spread into cartilage is useful in, for example, laryngeal tumours
where significant upstaging can result from invasion into or through the thyroid cartilage. Radiotherapy
tends to lose its effectiveness if tumour invades cartilage.
CT PROTOCOL
3-5 mm collimation sections using intravenous contrast (100mls of 300mg/ml) should be obtained to
include the skull base to sternal notch. Intravenous contrast helps increase the conspicuity of the primary
tumour and is essential for evaluating cervical nodal metastases. The patient should lie supine with the
neck comfortably extended and the head immobilised in a suitable support. Patients are told not to
swallow during the examination and to breathe quietly. A lateral scout view should be obtained from
which the examination is planned. Spiral or dynamic modes should be used if possible as this reduces
motion artefact and optimises use of iv contrast. Direct coronal sections or reconstruction (if using spiral
CT) may be necessary to assess tumour extension to the skull base and cranial fossa. Soft tissue and bone
reconstruction algorithm should be used.
For the nasopharynx, sections parallel to the hard palate from the level of the cavernous sinus to sternal
notch are obtained.
Proper gantry angle is essential in the oropharynx and oral cavity to avoid dental related artefacts and if
necessary the gantry angle should be changed to optimise visualisation of the oral tongue and tongue
base.
For the larynx and hypopharynx, sections must be obtained parallel to the true vocal cords and this is
approximately parallel to a disc space or the plane of the hyoid bone.
The advantages of CT scanning over and above MRI is that the acquisition times are faster and thereby
there is less motion artefact. Bone detail is better. It is cheaper than MRI scanning and nonclaustrophobic. It is also noted to be easier to use.
Co-morbidity is very important and probably to date has not been fully addressed in head and neck
practice. At least in some UK regions, the detection of unspecified pulmonary metastatic disease, even for
small T stages is expensive and the rate not sufficiently high to warrant routine use. There are also
specific sites [thyroid, sinus] and tumour types [high grade salivary] where chest CT is advisable in any
case. For patients already in the scanning room, the marginal cost of additional chest CT is very little
more than the previously "routine" chest x-ray, and can also be used by the anaesthetist. But if there is no
spiral scanner, on the other hand, scanning the chest in addition to the primary site and neck drainage
areas would significantly extend scanner time.
A screening chest CT following examination of the head and neck to detect pulmonary metastatic disease
or synchronous primary in bronchogenic carcinoma has been advocated by some authors (8, 9, 10). Other
authors have not found this to be justified (11,12).
35
This remains a controversial area, since one has to bear in mind the expense and the low pick up rate and
the risk of added ionising radiation. CT guided needle biopsy of pulmonary lesions is also potentially
useful.
MAGNETIC RESONANCE IMAGING
Magnetic resonance imaging uses the magnetic properties of biological materials and generates images
without the use of ionising radiation.
MRI PROTOCOL
T1W and T2W or STIR sequences in at least two planes, preferably axial and coronal, and T1W FSE or
Fat Suppressed images post gadolinium. The use of contrast is particularly useful in identifying perineural
spread and leptomeningeal involvement. Although images of the nasopharynx can be obtained with a
head coil, a combined head and neck coil is necessary to allow assessment of cervical lymph nodes. The
ideal section thickness is 3-4mm with at most a 10% gap. Fat saturation images permit better
identification of the tumour margins as the method helps separate the enhancing tumour margins from
background fat.
MRI scanning has distinct advantages over CT. There is no ionising radiation, there is multiplanar
capability and no dental amalgam artefact. Soft tissue contrast is superior and there is no requirement for
iodinated contrast media. In addition MR angiography may also provide information about the
relationship of the major vascular structures to the mass lesion.
ULTRASONOGRAPHY
Ultrasonography has proved useful in evaluation of lymphadenopathy and particularly useful in respect of
accurate insertion of needles for biopsy. Differentiation between benign and malignant disease, however,
has not otherwise been easy and CT/ MRI scanning is generally considered to be superior, being able to
also stage the primary tumour. Ultrasonographic criteria have been evaluated and assessed to assist in this
differentiation in the study by Vassallo et al 1992 (17). It is widely accepted that ultrasonography is more
sensitive than simple palpation for the detection of enlarged lymph nodes (14, 15 & 16). High resolution
ultrasound probes have been shown to differentiate between the hilus and cortex of a lymph node where
changes in the usual relationship suggest the presence of malignant disease. It has also been useful in
assessing infiltration of blood vessels by nodal metastasis (17). In the study by Vassallo et al 1992 (17)
204 patients with suspected lymphadenopathy underwent ultrasonography and a result obtained using
various parameters concerning the shape and relationship of hilar/cortex.
This was compared with subsequent histological evaluation. Nodal size was found not to be a reliable
criterion for differentiating benign from malignant nodes but of relevance in monitoring response to
treatment.
Differences were found in the longitudinal-transverse diameter ratio and the presence of eccentric cortical
widening was seen only in malignant nodes. The accuracy of ultrasonography can be increased by fine
needle aspiration cytology performed at the same time. It is usually not possible to stage the primary
tumour with ultrasonography, it is highly dependent upon operator experience and
in general there are no significant advantages over CT/MRI scanning other than cost.
The aims therefore of imaging in patients with head and neck malignant disease can therefore be
summarised in table 1. It is assumed that each unit has rapid access to CT scanning, orthopantography,
ultrasonograpny and fine needle aspiration cytology.
36
RATIONALE FOR THE BASELINE HEAD AND NECK PROTOCOL
The key issue in tumour staging is the question of tumour volume, but there is as yet no standard
volumetric method. The cross sectional area or maximum diameter of the primary tumour should be
routinely reported.
The neck should be scanned 1] to assess the contralateral nodes, 2] because at the time of imaging the
primary treatment is not known. If the neck is ultimately treated non surgically, no staging neck dissection
information will be available.
(i) IMAGING OF NECK NODES
The diagnosis of pathological neck nodes in patients with squamous cell cancer of the head and neck is
made either on size criteria or on the recognition of central nodal necrosis. This causes rim enhancement
with central low density following IV contrast enhanced CT. If this is seen in a patient with squamous cell
cancer of the head and neck, it is highly specific for the presence of a pathological neck node whatever
the size of that node. It has been said to have an accuracy of 100% (18). The presence of central necrosis
is recognised on MRI either by heterogeneity of signal intensity on T2 weighted scans or by rim
enhancement following the use of IV Gadolinium. There is debate amongst authors whether IV
Gadolinium is necessary or whether T2 weighted images alone will be sufficient (18,19). Different
authors have used different size criteria. A minimal axial size of 10mm (11 mm in a subdigastric region)
was felt to be the most effective (19). Groups of 3 or more borderline nodes also increases the sensitivity
of detecting pathological neck nodes and does not significantly decrease the specificity (18,19). Other
authors have used a minimal axial diameter of 8 mm as the cut off (20). Comparing CT with MRI some
authors have found CT to perform better than MRI (21, 18).
A meta-analysis of CT versus physical examination using a 15 year Medline review with 647 neck
dissections showed CT to have a sensitivity of 84%, specificity of 83% and accuracy of 83% with
physical examination having a sensitivity of 74%, specificity of 81% and accuracy of 77%. It was found
that the diagnostic modalities were additive with CT significantly enhancing detection rates of physical
examination alone. Overall physical examination detected 75% but this increased to 91% with the use of
CT (22).
Ultrasound guided fine needle aspiration cytology may also be used to detect pathological neck nodes.
Some have found it to be more accurate than CT (23) but other authors have not found an advantage (24).
Ultrasound alone does not have any advantage over CT and is unable to stage the primary tumour.
The role of positron emission tomography in staging the primary tumour and nodal disease in the initial
staging is uncertain. It is expensive and lacks the spatial resolution of other cross-sectional imaging
modalities. It is best reserved for problem patients or in the setting of recurrent disease.
(ii) SITE SPECIFIC ASPECTS
The radiological criteria used for diagnosing a lymph node as malignant on CT include:
1. nodal size, central necrosis
2. extracapsular extensions
3. obliteration of perivascular fat planes
37
The criteria for malignant node on MRI include:
1. Evidence of central necrosis.
2. Minimal axial diameter greater than 11 mm in the subdigastric area or greater than 10 mm in other
areas.
3. Grouping of three or more borderline nodes in the lymph nodes draining region of the primary tumour.
With the above criteria, these results are an improvement on those reported in the literature for CT or
MRI and of great importance in enabling the detection of occult metastatic disease in the neck.
Intravenous contrast is important in the head and neck to allow recognition of pathological rim
enhancement in nodes of normal size. Anatomical staging terms understood by clinician and radiologist
should be used. The node number, size (CSA/max diameter) and levels should be reported on an agreed
standard proforma, preferably with a diagram number.
PARANASAL SINUSES AND NASOPHARYNX
Tumours arising in the paranasal sinuses and nasopharynx often involve critical structures, their deep
extent is not visible at nasoendoscopy and thus radiological imaging is essential in staging. The
commonest tumours can be grouped as to their type and site and the imaging issues related to these are
discussed.
CT technique
The complex nature of paranasal sinus anatomy means that imaging in more than one plane is often vital
to an appreciation of disease extent, thus where helical CT is available it is recommended that the scan be
performed with axial helical acquisition and reformats obtained for coronal images. This avoids patient
repositioning and repeat scanning (plus dental artefact is minimised). Thin collimation (1mm) is required
covering from the top of the frontal sinuses to the maxillary teeth and the image data should be
reconstructed at 1mm increments (or less) in order to allow reformation of good quality true coronal
images (perpendicular to the hard palate). Sagittal reformations may also be helpful to the surgeon for
lesions involving the frontal recess region. Axial scanning has the further benefit that repositioning of the
patient is not required in order to scan the neck to stage lymphatic spread and this should be performed as
for any other head and neck neoplasm.
MRI technique
MRI of the paranasal sinuses must be performed with thin sections (3 - 4 mm), no gap, small field of
view and high image matrix (512 reconstruction) in the head coil in order to maximise spatial resolution
and SNR. Fast spin-echo imaging is helpful for T2 in order to reduce acquisition time; this is less of an
advantage for T1 imaging. T1 images in both coronal and axial planes should be obtained. The choice of
which plane is used for T2 is according to individual preference. Gadolinium contrast enhancement is
strongly recommended to demonstrate skull base involvement and intracranial extension (25, 26) but must
be performed with fat suppression and the same coverage/parameters as non-fat suppressed pre-contrast
T1 imaging to enable direct comparison.
Additional sagittal imaging is helpful for posterior nasal and PNS lesions. If there is frank invasion of the
skull base then a supplementary examination of the whole brain is prudent. As elsewhere an overview
coronal STIR sequence of the neck will help in staging lymphadenopathy.
38
BENIGN PARANASAL SINUS TUMOURS
Benign tumours such as osteoma, ossifying fibroma and dentigerous cysts are usually adequately imaged
by standard unenhanced CT sinus protocols though as imaging in both the axial and coronal planes is
helpful then helical scanning is recommended where available.
Inverting papilloma requires more extensive imaging as there may be malignant degeneration and even
with benign localised disease it is helpful to distinguish between the tumour mass and any retained
secretions. Thus with CT, contrast enhancement should be employed and the neck scanned to exclude
lymphadenopathy. MRI may be more productive in differentiating tumour from retained secretions and
better help to determine local soft tissue extent (27).
Juvenile angiofibroma may be localised but often invades through the sphenopalatine foramen to the
pterygopalatine fossa as well as to the infratemporal fossa. The extent at presentation must be known, as
full excision is the key to minimising recurrence (28). MRI is recommended and the addition of sagittal
imaging is suggested to show the anteroposterior extent of the lesion. It may also show sphenopalatine
extension to advantage. Contrast enhanced MR angiography can usefully show the extent of major vessel
vascular supply - this is best performed in the sagittal plane using the head coil with thin partitions and
small field of view to maximise spatial resolution.
MALIGNANT PARANASAL SINUS TUMOURS Malignant paranasal sinus tumours are uncommon and include SCC (the commonest and usually
maxillary sinus in origin), lymphoma and minor salivary gland tumours (including adenoid cystic and
mucoepidermoid carcinomas). Tumours arising from bone and/or cartilage such as
myeloma/plasamacytoma, osteosarcoma & chondrosarcoma also occur but are rare. Aside from the
finding of calcification in the matrix of the sarcomas the features of these tumours are similar as they
manifest as local soft tissue masses with local bone destruction. Malignant paranasal sinus tumours are
best initially staged by MRI due to its superior sensitivity to the extent of tumour spread, particularly
intracranial and perineural spread. Axial imaging best evaluates pterygopalatine and infratemporal fossa
extension while coronal images are superior for evaluating orbital and intracranial extensions. Lymphatic
spread of these tumours is initially to the retrophayngeal nodes and thence the upper deep cervical chain these areas should thus be carefully evaluated.
TABLE 1 - IMAGING CHECK LIST FOR PARANASAL SINUS TUMOURS
•
Identification of primary tumour, differentiation from retained secretions
•
Assessment of extent of bone destruction
•
Involvement of hard palate and middle meatus for maxillary tumours (i.e. the infrastructure as defined
by Ohngren’s line)
•
Extension to pterygoid plates, retroantral fat and pterygopalatine fossa
•
Any orbital involvement
•
Identification of perineural involvement, skull base invasion and extension to anterior or middle
cranial fossa
•
Nodal involvement looking first to retropharyngeal nodes.
39
NASOPHARYNGEAL SCC
The ideal protocol for the primary tumour and neck is MRI scanning and if there is any uncertainty in
respect of disease involvement of the base of skull then CT may provide better bone detail. MRI is more
accurate than CT in evaluating primary nasopharyngeal malignancy, primarily due to the relative
immobility of the nasopharynx. Motion artefact is thereby minimised allowing MR to capitalise on its
inherent superior soft tissue contrast relative to CT.
Deep infiltration of the tumour appears to be a more important prognostic factor in nasopharyngeal
carcinoma than tumour volume, hence the importance of MRI. In recent studies MRI has proved better
than CT in identifying obliteration of the pharyngobasilar fascia, invasion of the sinus of Morgagni,
(through which the cartilaginous portion of the eustachian tube and the levator veli palatini muscle pass),
metastases to lymph nodes in the carotid and retropharyngeal spaces (29, 30) and invasion of the skull
base (29, 30, 31).
If nodal spread is confirmed the chest should be imaged, preferably by CT scan as there is a significant
incidence of thoracic nodal and pulmonary parenchymal spread (32). Important radiological features are
as shown in table 3.
TABLE 2 - IMAGING CHECK LIST FOR NASOPHARYNGEAL TUMOUR (33,34)
•
Identification of primary tumour looking closely at any asymmetry in Fossa of Rosenmuller.
•
Any involvement of the deep spaces (parapharyngeal, carotid, prevertebral and masticator) indicating
violation of the pharyngobasilar fascia and other deep fascial layers.
•
Identification of skull base invasion
•
Any perineural tumour spread is critical as this upstages the tumour to T4 and requires an increase in
radiotherapy dose.
•
Any involvement of nasal cavity, maxillary, ethmoid or sphenoid sinuses.
•
Any orbital involvement- direct involvement is rare but orbit may be invaded via the pterygopalatine
fossa, inferior orbital fissure and ethmoid/sphenoid sinuses.
•
Nodal involvement looking closely at retropharyngeal nodes.
IMAGING FOR SKULL BASED NEOPLASMS (32,36)
Aim
1. Diagnosis.
2. Define extent and size.
3. Perineural spread.
4. Pre-Operative staging
5. Surgical and DXT planning
6. Post-operative assessment
Modalities
1.CT Scan
2. MRI/MRA
3. Angiogram
4. PET scan
40
CT Scan
Axial/coronal scans.
Spiral CT with volume acquisition & multiplanar reformats.
Slice thickness 3mm or less.
Contrast. 50-100 cc IV.
Soft and Bone algorithms.
CT Scan better than MR at assessing bone involvement.
MRI
T1 axial & Coronals.
5mm slice or less.
STIR axial/coronals.
Pre and Gadolinium Post contrast T1 fat suppressed scans. 3-5mm slice thickness.
T2 and Proton density scans to assess sinus/mastoid secretions.
MR excellent at detecting
1. Intracranial involvement.
2. Dural/leptomeningeal involvement.
3. Perinerual spread. This is associated with decreased survival.
4. Marrow infiltration.
Arteriography.
1. Cerebral angiography. Carotid/vertebral angiograms.
2. For diagnosis and evaluation of vascularity.
3. For endovascular therapy.
4. Trial carotid occlusion.
PET Scans
FDG PET commonly used agent.
All Hospitals may not have access.
Post op. Assessment.
Differentiate scar/granulation tissue from recurrent/residual tumour.
Limitations of PET to be borne in mind.
ORAL CAVITY AND OROPHARYNX
Cross sectional imaging has significantly altered the treatment and management of these oral and
oropharyngeal malignancies, but often underestimates the extent of gingival and hard palate tumours.
A comparison of CT and MRI in T and N staging of primary and recurrent SCC of the oral cavity and
oropharynx was performed in 33 patients (51 episodes) by Leslie et al 1999 (37).
This showed that for T staging, MRI is overall more accurate than CT. If degraded images on CT due to
dental amalgam and T1 tumours are however excluded, the techniques are comparable. MRI is
oversensitive for recurrent disease in the post operative neck as non specific high signal from previous
surgery and radiotherapy can mimic recurrent disease. For N staging all methods failed to detect small
metastatic deposits. The presence of an irregular outline of nodes on MRI in this study suggested the
presence of extracapsular spread but other authors (38) have found it of limited value. Wide et al 1999
(39) have also shown that MRI lacks sufficient sensitivity and specificity to replace elective neck
dissection for both staging and prognostic purposes.
41
The oral cavity has an extensive lymphatic drainage system with metastasis most frequently to Levels I, II
and III. The presence of cervical metastases in patients with SCC of the oral cavity is a vital prognostic
indicator.
Positron Emission Tomography (PET) has been evaluated by Myers and Wax 1998 (40) in the N0 neck in
patients with SCC of the oral cavity and correlated with pathologic examination of neck dissections. PET
in 11 patients and 19 neck dissections was found to have an overall sensitivity, specificity, positive
predictive value and accuracy of 100%. Although promising, the numbers in this study are small and PET
scanning is not freely available. Thallous Chloride Tl201-Labelled Single Photon Emission Computed
Tomography Scanning in Head and Neck Cancer was shown by Gregor et al(41) to be useful in detecting
occult primary lesions in the oropharynx.
The most commonly performed surgical procedure for treatment of squamous cell carcinoma of the
tongue is a partial glossectomy, a procedure that requires preservation of one lingual artery and
hypoglossal nerve. Information from imaging that will directly affect the surgical approach includes
whether the tumour involves the ipsilateral neurovascular bundle, submucosal involvement in adjacent
areas including the floor of the mouth and whether the tumour crosses the midline. If the tumour crosses
the midline, its relationship to the contralateral lingual neurovascular bundle precludes a partial
glossectomy and requires a total glossectomy, which is often unacceptable. Treatment of tonsillar and soft
palate carcinomas depends on lesion size and involvement of surrounding structures. Extension to involve
the parapharyngeal and masticator spaces, requires resection of portions of the tongue base, mandible and
maxilla. Important radiological features are as shown in tables 3 and 4.
TABLE 3 -IMAGING CHECK LIST FOR OROPHARYNGEAL TUMOUR
(1) Tongue base carcinoma
Extension to floor of mouth and surrounding structures
Relationship to ipsilateral lingual neurovascular bundle
Extension across midline and relationship to contralateral neurovascular bundle
(2) Tonsil, soft palate and posterior pharyngeal wall carcinoma
Submucosal extension into parapharyngeal space and nasopharynx
Tongue base invasion
Encasement of carotid artery
Bone erosion
Pre vertebral muscle invasion
TABLE 4 -IMAGING CHECK LIST FOR ORAL CAVITY TUMOURS (other than nodal
involvement)
(1) Lip Carcinoma
Bone erosion
Soft tissue invasion
(2) Floor of Mouth Carcinoma
Extent of bone erosion
Deep invasion along the mylohyoid and hyoglossus muscles
Relationship to ipsilateral lingual neurovascular bundle
Extension across midline and relationship to contralateral neurovascular bundle
Tongue base invasion
Extension into the soft tissues of neck
42
(3) Oral Tongue carcinoma
Invasion of ipsilateral lingual neurovascular bundle
Extension across midline and relationship to contralateral neurovascular bundle
Invasion of floor of mouth and associated bone erosion
(4) Buccal carcinoma
Submucosal extension
Bone erosion
(5) Gingival and hard palate carcinoma
Bone erosion
Perineural invasion of the incisive canal and greater and lesser palatine foramen
(6) Retromolar trigone carcinoma
Bone erosion
Submucosal spread
Perineural invasion
LARYNX
The larynx is divided into the supraglottis, glottis and subglottis. The supraglottic larynx is located above
the true vocal cords and extends from the tongue base and valleculae to a laryngeal ventricle.
Imaging of Laryngeal Tumours
The Royal College of Radiology is developing guidelines for all head and neck sites and these have been
integrated into this section. They are evidence based and the level of evidence and recommendation are
given below.
Summarised results
from each of the cited
references
Conclusion
Evidence level classified I – IV
Investigation
Recommendation *
Grade of Recommendation
A–C
Comment
MRI is better than CT for T staging prior to partial laryngectomy (42,43,44)
due to direct coronal imaging capability. MRI is more sensitive but is less
specific than CT for cartilage involvement (45, 44) but both acceptable and
may be complementary (46). MRI is preferred for T staging if the patient is
cooperative (42) or tongue base is involved (43). CT is good at assessing
anterior and posterior commissures and fat spaces when compared to
histopathology, but is less good for assessing cartilage involvement,
extralaryngeal spread and N stage (47). CT combined with clinical evaluation
is better than either alone, particularly for supra- and trans-glottic tumours
(48). CT is as good as MRI for N staging (44) or better (43).
MRI has advantages over CT for T staging in certain situations, and is
otherwise equal, so MRI is preferable where available, though CT is
acceptable. CT is as good as or better than MRI for N staging. US can be
used for T and N staging and follow-up of laryngeal cancer by centres with
appropriate expertise.
IIb – III for CT/MR and III for ultrsound
CT or MRI. Ultrasound.
CT or MRI are indicated but ultrasound is a specialised investigation.
B
Where available, MRI preferable to CT for T staging. Either for N staging.
Ultrasound can be used for T and N staging and follow-up in centres with
appropriate expertise.
43
CT of the neck should be performed with the gantry angled to the true cords. This may be approximated
by using the position of the hyoid bone on a lateral scout view to determine the correct angling of the
gantry. CT sections should be taken at least 5mm, preferably 3mm, intervals through the larynx. The area
scanned should include nodal stations likely to be involved by the primary tumour, i.e. level 2 superiorly
and scanned inferiorly to examine the subglottic region, i.e. to the root of the neck. Scans should be
obtained following a bolus of intravenous iodinated contrast agent (at least 100 ml).
Intravenous contrast agent helps to increase the conspicuity of the primary tumour and is necessary for
evaluating neck nodes. CT scans should be evaluated at soft tissue settings. Scans through the region of
the laryngeal cartilage should also be evaluated using a bony algorithm and bony window settings.
MR imaging should be performed using a neck coil or other suitable surface coil. MR imaging should be
performed in both the axial and coronal planes with a slice thickness of 4 mm or less. T1 and T2 weighted
spin echo images should be obtained. STIR (Short Time Inversion Recovery) images may be useful for
the evaluation of laryngeal cartilage involvement. The STIR sequence takes out the fat signal which
appears as black with water as white. These scans however have poor spatial discrimination and are not
used in isolation. If intravenous contrast agent is given, T1 weighted fat saturated scans may be useful
following this. The role of intravenous Gadolinium enhanced MRI in the staging of the primary tumour
and neck nodes in laryngeal carcinomas is less clear than that of intravenous iodinated contrast enhanced
CT (18), (19). Important radiological features are as shown in table 5.
TABLE 5 - IMAGING CHECK LIST FOR LARYNGEAL TUMOURS
Key Imaging Findings
1.Transglottic extension of tumour.
1.Piriform sinus invasion.
2.Cartilage invasion.
3.Spread outside the larynx.
Glottic and Supraglottic Tumours
Transglottic extension.
Subglottic extension and relationship to cricoid cartilage.
Cartilage invasion.
Involvement of the anterior commissure.
Involvement of the crico-arytenoid joint.
Extension to the posterior commissure.
Deep invasion of the paraglottic fat.
Tumour volume.
Subglottic Tumours
Primary subglottic tumours are uncommon.
Inferior extent.
Cartilage invasion.
State of tracheal lumen, particularly in respect of ability to intubate.
Tumour volume.
44
HYPOPHARYNX
The hypopharynx extends from the hyoid bone to the inferior aspect of the cricoid cartilage and is
anatomically divided into the pyriform sinuses, post cricoid region and posterior pharyngeal wall.
Imaging includes CT, MRI, barium swallow and PET scanning. There is little if any role for ultrasound
to specifically assess the primary tumour but it may be of some use in detecting local tumour recurrence
(49). Various authors (50, 51, 52) stress the importance of CT and MRI to assess deep tumour extension
into the pre-epiglottic space, para-glottic space and laryngeal framework. The primary tumour is
inaccurately staged by clinical examination in 35-47% of cases while CT/MRI upstages up to 40% of
cases (53). PET scanning is at present of limited use in staging because of poor anatomical detail. CT has
an accuracy of 65%-73% for hypopharyngeal cancer while a combination of clinical examination and CT
results in accuracy rates for staging ranging from 73-88%. Comparison of conventional and single slice
spiral CT by Kosling (54) showed no significant difference in the TMN staging of oro- and
hypyopharyngeal tumours. The addition of the valsalva manoeuvre in CT is a supportive method in
evaluating pyriform fossa tumours (55). 3D and CT virtual endoscopy are promising techniques that are
still being evaluated.
Zbaren (50) specifically comparing CT and MRI in the pretherapeutic staging of hypopharyngeal
carcinoma concluded that there was no difference in the staging accuracy between CT and MRI. Held
(56) comparing CT with ultrafast MR sequences in all pharyngeal tumours showed that functional
imaging with phonation and valsalva manoeuvre was particularly useful in the case of hypopharyngeal
tumours. MRI in this study was shown to have a higher false positive rate and CT a higher false negative
rate. Held (57) showed improved tumour detection on MRI with provocative manoeuvres (accuracy
95.5%) when compared with MRI during quiet respiration (accuracy 80%). The use of intravenous
gadolinium has also been shown to be more useful in assessing the extent of tumour and laryngeal
cartilage invasion (58, 59).
Mukherji (60) and Pameijer (61) prefer CT for hypopharyngeal staging but in around 10% of cases feel
that MRI is also needed to resolve issues such as prevertebral muscle invasion and submucosal spread
towards the oesophageal verge.
Various studies (65, 66, 67, 68) have shown that PET may be more accurate than CT or MRI for detecting
local recurrence post treatment for a variety of head and neck cancers with sensitivity of 50-100% and
specificity of 71-73%.
Follow up neck CT is particularly useful in detecting local failures in those patients initially identified as
high risk (69). Thoracic CT is useful for symptomatic and asymptomatic post treatment patients with
Stage 3 or 4 disease but only useful in Stage 1 or 2 patients who present with clinical recurrences (10).
Imaging is otherwise as for larynx but with the possible addition of barium swallow to assess the lower
extent of the lesion and for detection of a synchronous oesophageal primary (62-64). This is important
clinical information since some hypopharyngeal tumours are treated surgically with preservation of the
cervical oesophagus while others require its removal.
TABLE 6 - IMAGING CHECK LIST FOR HYPOPHARYNGEAL TUMOURS
Key Imaging Features
1.Extension across the midline.
2.Apical involvement.
3.Extension into the oesophageal inlet.
4.Extension into chest.
5.Cartilage invasion.
6.Anterior extension into the para-glottic space.
45
PAROTID/SUBMANDIBULAR REGION
Ultrasound, CT and MRI are all useful in evaluating the salivary glands, particularly for neoplasia. MRI is
probably better than CT. It should be pointed out that some clinicians do not image salivary gland
tumours at all if they are superficial and mobile and particularly in the tail of the parotid gland.
i.CT Technique
5mm iv contrast enhanced images (75-100 mls of 300mg/ml contrast) from the level of the pinna to
hyoid bone. The plane of section may need to be altered to avoid artefacts from dental amalgam. Patient is
asked not to swallow and to breathe quietly. With this technique there is less claustrophobia than MRI
scanning.
ii.MR Technique
Head and neck coil may be necessary for full coverage. Axial and coronal planes with 4-5mm slice
thickness, T1W and T2W or STIR sequences. Intravenous contrast is rarely necessary unless adenoid
cystic tumour is suspected because of the potential for perineural spread of disease.
Summarised results
from each of the cited references
Conclusion
Evidence level classified I - IV
Investigation
Recommendation *
Grade of Recommendation
A–C
Comment
Both CT and MRI can be used for staging parotid tumours (71, 72). Corr
et al (73) reserve CT for staging deep lesions, using US to stage small,
superficial ones. Soler et al (74) consider MRI important for staging and
follow-up. Freling et al (75) found MRI good for staging malignant
tumours, and Kamal et al (76) demonstrated MRI to be better than CT for
staging parotid tumours.
Corr et al (73) found US better than CT for the detection and
characterisation of parotid masses and Shimizu et al (77) demonstrated
that the shape and distibution of internal echoes can predict the nature of a
parotid mass. Schick et al (10) found pulsed and colour Doppler
sonography a useful adjunct to grey scale images for differentiating
benign from malignant lesions.
McGuirt et al (71), Banerjee et al (72) and Kamal et al (76) all found that
FNAC improved the diagnostic accuracy of other methods of assessment clinical or imaging
MRI is preferred to CT for staging of parotid tumours, although either is
acceptable, particularly for deep lesions. US +/- Doppler can suggest the
nature of a parotid mass in addition to its detection. FNAC improves
diagnostic accuracy further.
III for US and IIb – III for CT/MRI
CT, MRI and US
Indicated
B
CT and MRI are particularly for deep lesions and prior to complex
surgery. MRI preferred if available. Ultrasound is good for the detection
of superficial lesions, and can often characterise them. FNAC improves
diagnostic accuracy.
Important radiological features are shown in table 7.
46
TABLE 7 - IMAGING CHECK LIST FOR PAROTID GLAND TUMOURS
Location of mass in superficial or deep lobe of parotid gland
Identify any occult mass in same gland or opposite gland
Identify relationship to facial nerve using styloid process, posterior belly of digastric and
retromandibular vein as reference
Has mass smooth or infiltrative margins?
Is the mass solid or cystic?
Is the mass confined to gland?
EXTERNAL MEATUS AND MIDDLE EAR
Imaging should show primary site and metastatic fields. CT scan should include the neck with contrast.
Raw data should be acquired to reconstruct relevant images on sharp bone algorithm.
MR scanning should include gadolinium enhancement to exclude intracranial involvement.
THYROID
Ultrasound, isotope scans, CT and MRI are all used for imaging the thyroid and guidelines are outlined
here for diagnosis, staging and follow-up, taking into account the Royal College of Radiologists
guidelines which are being drawn up.
Diagnosis
Summarised results
from each of the cited references
Statement (= the conclusion
drawn from E)
Evidence level classified I – IV
Investigation
Recommendation *
Grade of Recommendation
A–C
Comment
US alone is not reliable in differentiating benign from malignant nodules
(79), but used to guide or in combination with FNAC, US-FNAC is the
best available technique (80, 81, 82, 83, 84, 85, 86,87), although it is
unreliable for follicular and Hurthle-cell nodules (88). It is useful for the
detection of residual/recurrent disease at the primary site and in
locoregional lymph nodes after thyroidectomy (89, 79), and can again be
combined with FNAC (87).
US-FNAC for diagnosis, but unreliable for follicular and Hurthle-cell
nodules.
IIb – III
US
Indicated
B
Used in combination with or to guide FNAC.
47
Staging
Summarised results
from each of the cited references
Conclusion
Evidence level classified I – IV
Investigation
Recommendation *
Grade of Recommendation
A–C
Comment
Summarised results
from each of the cited references
Conclusion
Evidence level classified I – IV
Investigation
Recommendation *
Grade of Recommendation
A–C
Comment
US better than MRI for staging small primary tumours, multifocal disease
and lymphadenopathy. (80,83,90). Hay and Klee (91) specify tumour
extent and lymph nodes and James et al (87) concentrate on
lymphadenopathy and recurrent disease. Shimamoto et al (92) obtained
82% accuracy for T staging, but only 48% accuracy for N stage due to a
low sensitivity, and consider US limited in assessing extracapsular extent
of tumour and lymph node involvement.
US useful for staging small primary tumours and lymph nodes.
IIb – III
US
Indicated
B
Where appropriate expertise is available, the investigation of choice for
locoregional staging.
MRI (90), CT (80, 89), or either (82, 83, 84, 86, 79) for the demonstration
extrathyroidal/extracapsular and mediastinal extension. Peritracheal
disease (87) and tracheal compression (82) can be demonstrated by either
modality. MRI to demonstrate lymphadenopathy if US is not available
(82, 93), particularly for medullary thyroid carcinoma with 93% accuracy
(81). CT or MRI are required for the staging of medullary thyroid
carcinoma to look for other tumours in MEN syndromes (83, 89), and for
assessment of recurrent disease (79). Distant metastases can be shown by
CT for lung (80), MRI (89) or either (79).
The extent of large primary tumours, detection of distant metastases and
staging of medullary thyroid carcinoma in MEN syndromes can be
performed using CT or MRI
IIb – III
CT or MRI
Indicated
B
To assess large primary tumours, detect distant metastases, and for
medullary thyroid carcinoma in MEN syndromes.
48
Follow up
Summarised results
from each of the cited references
Conclusion
Evidence level classified I – IV
Investigation
Recommendation *
Grade of Recommendation
A–C
Comment
NM mainly used for demonstration of residual/recurrent differentiated
cancer after thyroidectomy (80, 88, 84, 89, 91, 94, 79), including
medullary thyroid carcinoma. [18F]-2-deoxy-2-FDG PET has 82%
sensitivity for demonstrating residual/recurrent differentiated carcinoma
after thyroidectomy (79).
Follow-up of differentiated carcinomas after thyroidectomy.
Lib
NM
Indicated
B
For the detection of residual/recurrent disease after thyroidectomy. See
Cancer Section L05.
POST TREATMENT IMAGING OF THE NECK
A potentially difficult area is imaging the post operative neck where surgery can lead to significant
alteration in the normal anatomy. It is important therefore that the reporting radiologist has some
familiarity with the various forms of neck dissection that are now performed from the original radical
neck dissection described by Crile to the modified varieties (96,95). The situation may be complicated
since reconstructive techniques can also produce anatomical confusion. This is principally by use of
various skin flaps and/or visceral transposition. A useful review of these and typical and radiological
representations are as described by Som et al (97).
This team recommends imaging 4-8 weeks post operatively, during which time a baseline can be obtained
and periodic imaging thereafter over at least the first three years at 4-6 monthly intervals. Yearly intervals
thereafter for at least two more years are also advised. These recommendations are probably not in
accordance with most British practice which tends to centre around clinical suspicion of recurrence with
appropriate investigation and imaging thereafter. Som et al (97) point out, however, that the imaging
findings on this regime altered the post operative salvage plan in 25% of cases where recurrence occurred
and that clinical occult disease was found at sectional imaging in 17%.
Both CT and MRI can be difficult to interpret and the imaging modality chosen depends on pre operative/
radiotherapy work up. Other imaging such as nuclear medicine procedures have been tested. Although for
staging purposes, PET is limited by its lack of anatomical detail, it compares favourably with CT and
MRI in detecting recurrent/residual cancer (65, 98). Thallium 201 SPECT is particularly useful in
assessing recurrences (41, 99). PET-FDG has also been shown to be more accurate than CT/MRI for
identifying recurrent tumours. This area is reviewed more fully by Hanasono et al (68).
References:
1.
2.
3.
4.
5.
6.
7.
Kleinsasser O Revision of classification of laryngeal cancer - is it long overdue? J of Laryngol Otol 1987; 106: 197 – 204
Johnson C.R., Thames H.D., Huang D.T., Schmidt-Ullrich R.K. The tumour volume and clonogen number relationship:
Tumour control predictions based upon tumour volume estimates derived from computed tomography Int J Radiat Oncol
Biol Phys 1995; 33: 281-187.
Gilbert R W, Birt D, Shulman H et al Correlation of tumour volume with local control in laryngeal carcinoma treated by
radiotherapy Ann Otol, Rhinol Laryngol 1987; 96 : 514 – 518.
Breiman R S, Beck J W, Korobkin M et al Volume determinations using computer tomography A J Radiol 1982; 138 : 329 –
333.
Olmi P, Cellai E, Shiavacci A et al Computer tomography in nasopharyngeal carcinoma part I: T stage conversion with CT
staging Int J Radiat Oncol Biol Phys 1990; 19 : 1171 – 1175.
Cellai E, Olmi P, Shiavacci A et al Computer tomography in nasopharyngeal carcinoma part II: impact on survival Int J
Radiat Oncol Biol Phys 1990; 19 : 1177 – 1182.
Pameijer F.A., Balm A.J.M. et al. Variability of tumour volumes inT3 staged head and neck tumours Head & Neck 1997,
49
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
161: 6-13.
Reiner B. Siegel E. Sawyer R. The impact of routine CT of the chest on the diagnosis and management of newly diagnosed
squamous cell carcinoma of the head and neck AJR. 169:667-71, 1997.
Houghton DJ. Hughes ML. Garvey C, et al. Role of chest CT scanning in the management of patients presenting with head
and neck cancer Head & Neck. 20 614-8, 1998.
Mercader VP. Gatenby RA. Mohr RM, et al. CT surveillance of the thorax in patients with squamous cell carcinoma of the
head and neck: a preliminary experience’J Comput Ass Tomog. 21:412-7, 1997.
Tan L. Greener CC. Seikaly H. Rassekh CH. Calhoun KH. Role of screening chest computed tomography in patients with
advanced head and neck cancer. Otolaryngol - Head & Neck Surgery. 120:689-92, 1999.
Nilssen EL. Murthy P. McClymont L. Denholm S. Radiological staging of the chest and abdomen in head and neck
squamous cell carcinoma--are computed tomography and ultrasound necessary? J Laryngol Otol. 113:152-4, 1999.
Hajek P C, Salomonowitz E & Turk R Lymph nodes of the neck ; evaluation with ultrasonography Radiology 1986; 158 :
739 – 742.
Sutton R T, Reading C C, Sharbononeau J W Ultrasound guided biopsy of neck masses in post operative management of
patients with thyroid cancer Radiology 1988; 168 : 769 – 772.
Bruneton J N, Roux P, Caramella E Ear nose & throat cancer : ultrasound diagnosis of metastases to cervical lymph nodes
Radiology 1994; 152 : 771 – 773.
Greitzmann N, Taxler M & Grasl M Advanced laryngeal cancer: sonographic assessment Radiology 1989; 171 : 171 – 175.
VassalloP. Wernecke K. Roos N. and Peter PE. Differentiation of benign from malignant superficial lymphadenopathy : the
role of high-resolution US. Radiology 183 : 215-220.
Yousem DM. Som PM. Hackney DB, et al. Central nodal necrosis and extra-capsular neoplastic spread in cervical lymph
nodes: MR imaging versus CT. Radiology 182:753-9, 1992.
Van den Brekel MW. Castelijns JA. Stel HV, et al. Detection and characterisation of metastatic cervical adenopathy by MR
imaging: comparison of different MR techniques J Comp Ass Tomog. 14:581-9, 1990.
Steinkamp HJ. Hosten N. Richter C, et al. ‘Enlarged cervical lymph nodes at helical CT’ Radiology. 191:795-8, 1994.
Curtin HD. et al. Comparison of CT and MR imaging in staging of neck metastases Radiology. 207:123-30, 1998.
Merritt RM. Williams MF. James TH, et al. Detection of cervical metastasis. A meta-analysis comparing computed
tomography with physical examination. Arch Otolaryngol – Head Neck Surg. 123:149-52, 1997
Atula TS. Varpula MJ. Kurki TJ, et al. Assessment of cervical lymph nodes status in head and neck cancer patients:
palpation, computed tomography and low field magnetic resonance imaging compared with ultrasound-guided fine-needle
aspiration cytology. Eur J Radiol. 25:152-61, 1997.
Righi PD. Kopecky KK. Caldemeyer KS, et al. Comparison of ultrasound-fine needle aspiration and computed tomography
in patients undergoing elective neck dissection Head Neck. 19:604-10 1997.
Van Tassel P, Lee YY. Gd-DTPA enhanced MR for detecting intracranial extension of sinonasal malignancies. J Comput
Assist Tomog 1991;15:387-92
Yamamoto S. Takano H. Motoori K et al. Detection of nasopharyngeal carcinoma: fast short time inversion recovery
images compared with fat suppression, contrast enhanced T(1) weighted spin echo images. Br J Radiol. 74:805-10, 2001.
Petit P, Vivarrat-Perrin L, Champsaur P, et al. Radiological follow-up of inverted papilloma. Eur Radiol 2000; 10: 11841189.
Lloyd G, Howard D, Lund V J, Savy L. Imaging for juvenile angiofibroma. Laryngol Otolol 2000; 114: 727-730.
Sakata K et al. Prognostic Factors of Nasopharynx Tumours investigated by MR Imaging in The Newly Published TNM
Staging Int J Radiat Oncol Biol Phys 1999. 43: 273-278.
Ng S.H., Chang T.C., Ko S.F. et al. Nasopharyngeal carcinoma: MRI and CT assessment Neuroradiol 1997; 39: 741-746.
Chong V. F. H. & Fan Y. F. Skull Base Erosion in Nasopharyngeal Carcinoma; Detection by CT and MRI Clin Radiol
1996. 51: 625-631.
Daly BD, Leung SF, Cheung H, Metreweli C. Thoracic metastases from carcinoma of the nasopharynx: high frequency of
hilar and mediastinal lymphadenopathy. AJR 1993;160:241-4
Wakisaka M, Mori H, Fuwa N, Matsumoto A. MR analysis of nasopharyngeal carcinoma: correlation of the pattern of
tumor extent at the primary site with the distribution of metastasized cervical lymph nodes. Preliminary results. Eur
Radiology 2000; 10: 970-977.
King AD, Lam WW, Leung SF, Chan YL, Teo P, Metreweli C. MRI of local disease in nasopharyngeal carcinoma: tumour
extent vs tumour stage. Br J Radiol 1999;72:734-41
Keyes JW, Watson NE, Williams DW: FDG PET in head and neck cancer. AJR169:1663-1669, 1997.
Durden DD’ Williams DW. Radiology of skull base neoplasms. Otolaryg.Clin of North AM. 34: 1043-1064, 2001
Leslie A., Fyfe E., Guest P., Goddard P., Kabala J.E. Staging of Squamous Cell Carcinoma of the Oral Cavity and
Oropharynx: A Comparison of MRI and CT in T and N Staging J Comp Assist Tomog. 1999; 23: 43-49.
Van den Breckel M.W.M., Castelijins J.A., Snow G.B. Imaging of cervical lymphadenopathy Head Neck Imaging 1996; 6:
417-434.
Wide J.M., White D.W., Woolgar J. A., Brown J. S., Vaughan E. D., Lewis-Jones H. G. Magnetic Resonance Imaging in the
Assessment of Cervical Nodal; Metastasis in Oral Squamous Cell Carcinoma Clin Radiol 1999; 54: 90-94.
Myers L.L. & Wax M.K. Positron Emission Tomography in the Evaluation of the Negative Neck in Patients with Oral
Cavity Cancer J Otolaryng. 1998; 27:342-347.
Gregor R.T., Valdes Olmos R., Koops W., Balm A.J.M., Hilgers F. J. M., Hoefnagel C.A. Preliminary Experience With
Thallous Chloride Tl 201-Labelled Single Photon Emission Computed Tomography Scanning in Head and Neck Cancer
50
Arch Otolaryngol Head Neck Surg 1996; 122: 509-514.
42. Castelijns JA. Hermans R. van den Brekel MW. Mukherji SK. Imaging of laryngeal cancer. Seminars in Ultrasound, CT &
MR. 1998. 19:492-504.
43. Williams Dw 3rd. Imaging of Laryngeal Cancer. Otolaryngol Clin North Am 1997, 30:35-58.
44. Giron J. Joffre P. Serres-Cousine O. Senac JP. CT and MR evaluation of laryngeal carcinomas. J Otolaryngol. 1993, 22:
284-93.
45. Becker M. Neoplastic invasion of laryngeal cartilage: radiologic diagnosis and therapeutic implications. Eur J Radiol. 2000,
33: 216-29.
46. Hermans R.Op de Beeck K. Delaere PR. Marchal G. Computed tomography and magnetic resonance imaging of laryngeal
tumours. Acta Oto-Rhino-Laryngologica Belgica. 1999, 53:79-86.
47. Kazkayasi M. Onder T. Ozkaptan Y. Can C. Pabuscu Y. Comparison of preoperative computed tomographic findings with
postoperative histo-pathological findings in laryngeal cancers. European Arch of Oto-Rhino-Laryngol. 1995, 252:325-31.
48. Thabet HM. Sessions DG. Gado MH. Gnepp DA. Harvey JE. Talaat M. Comparison of clinical evaluation and computed
tomographic diagnostic accuracy for tumors of the larynx and hypopharynx. Laryngoscope. 1996, 106:589-594.
49. Lee JH, Sohn JE, Choe DH et al. Sonographic findings of the neopharynx after total laryngectomy: comparison with CT.
Am J Neuroradiol 2000; 21: 823-7.
50. Zbaren P, Becker M, Lang H. Pretherapeutic staging of hypopharyngeal carcinoma: clinical findings, computed
tomography and magnetic resonance imaging compared with histopathologic evaluation. Arch Otolaryngol Head Neck Surg
1997; 123: 908-13.
51. Thabet HM, Sessions DG, Gado MH et al. Comparison of clinical evaluation and computed tomographic diagnostic
accuracy for tumours of the larynx and hypopharynx. Laryngoscope 1996; 106: 589-94
52. Sulfaro S, Barzan L, Qurein F, Lutman M, Caruso G. T staging of the laryngopharyngeal carcinoma. Arch Otolaryngol
Head Neck Surg 1989; 115: 613-20.
53. Aspestrand F, Kolbenstvedt A, Boysen M. Carcinoma of the Hypopharynx: CT staging. J Comput Assist Tomogr 1990; 14:
72-6
54. Kosling S, Schmidtke M, Vothel F et al. The value of spiral CT in the staging of carcinomas of the oral cavity and of the
oro-and hypopharynx. Radiol 2000; 40: 632-9.
55. Yamamoto S, Yasuda S, Kimura S et al. The purpose of this study is to determine the clinical usefulness of Valsalva
manoeuvre (VM) to evaluate pyriform fossae lesions on helical CT. Jpn J Clin Radiol 1997; 42: 759-62
56. Held P, Breit A. MRI and CT of tumours of the pharynx: Comparison of the two imaging procedures including fast and
ultrafast MR Sequences. Eur J Radiol 1994: 18: 81-91.
57. Held P, Fellner C, Seitz J, Geissler A, Bonkowsky V. MRI of the hypopharynx with provocative manoeuvres. Clinical
Imaging 1998; 22: 26-33
58. Einspieler R, Ebner F, Posawetz W et al. MR-imaging with Gd-DTPA in carcinomas of tongue, oro- and Hypopharynx. Eur
J Radiol 1991; 13: 21-6.
59. Sakai F, Sone S, Kiyon K et al. MR evaluation of laryngohypopharyngeal cancer: value of gadopentate dimeglumine
enhancement. Am J Neuroradiol 1993; 14:1059-69
60. Mukherji SK, Mancuso AA, Kotzur Im et al. Radiologic appearance of the irradiated larynx. Part 11. Primary site response.
Radiology 1994; 193: 149-54
61. Pameijer FA, Mancuso AA, Mendenhall WM et al. Evaluation of pretreatment computed tomography as a predictor of local
control in T1/T2 pyriform sinus carcinoma treated with definitive radiotherapy. Head Neck 1998; 20: 159-68
62. Keberle M, Kenn W, Tschammler A et al. Current value of double-contrast pharyngography and of computed tomography
for the detection and for staging of hypopharyngeal, oropharyngeal and supraglottic tumours. Eur Radiol 1999; 9: 1843-50.
63. Catic DZ Lovrincevic A. Correlation of computed tomography and conventional hypopharyngography finding in
hypopharyngeal tumours. Eur J Radiol 1985; 5: 178-80.
64. Peng J, Xu Y, Li G. Magnetic resonance imaging of hypopharyngeal and cervical oesophageal cancer. Lin Chuang Erh Pi
Yen Hou Ko Tsa Chih J Clin Otorhinol 1998; 12: 150-2.
65. Wong W.L., Chevretton E.B., McGurk M. et al. ‘A prospective study of PET -FDG imaging for the assessment of head and
neck squamous cell carcinoma’ Clin Otolaryngol 1997; 22: 209-214.
66. Stokkel MP, Terhaard CH, Hordijk Gj, van Rijk PP. The detection of local recurrent head and neck cancer with flourine-18
fluordeoxyglucose dual head positron emission tomography. Eur J Nucl Med 1999; 26: 767-73
67. Paulus P, Sambon A, Vivegnis D et al. 18 FDG-PET for the assessment of primary head and neck tumours: clinical,
computed tomography and histopathological correlation in 38 patients. Laryngoscope 1998; 108 1578-83
68. Hanasono M.H. Kunda L.D. Segall G.M. Ku G.H. Terris D.J. Uses and Limitations of FDG Positron Emission Tomography
in Patients With Head and Neck Cancer Laryngoscope 1999; 109: 880-885.
69. Hermans R, Pameijer FA, Mancuso AA, Parsons JT, Mendenhall WM. Laryngeal or hypopharyngeal squamous cell
carcinoma: can follow-up CT after definitive radiation therapy be used to detect local failure earlier than clinical
examination alone? Radiology 2000; 214: 683-687
70. Mercader VP, Gatenby RA, Mohr RM, Fisher MS, Caroline DF. CT surveillance of the thorax in patients with squamous
cell carcinoma of the head and neck: a preliminary experience. J Comput Assist Tomogr 1997; 21: 412-7.
71. McGuirt WF. Keyes JW Jr. Greven KM. Williams DW 3rd. Watson NE Jr. Cappellari JO. Preoperative identification of
benign versus malignant parotid masses: a comparative study including positron emission tomography. Laryngoscope. 1995;
105:579-84.
72. Banerjee AK. Ubhi CS. Pegg CA. Diagnostic approaches to parotid swellings. Br J Hosp Med. 1994;51:516-21.
51
73. Corr P. Cheng P. Metreweli C. The role of ultrasound and computed tomography in the evaluation of parotid masses.
Austral Radiol 1993; 37:195-7.
74. Soler R. Bargiela A. Requejo I. Rodriguez E. Rey JL. Sancristan F. Pictorial review: MR imaging of parotid tumours.
Clinical Radiology. 1997; 52:269-75.
75. Freling NJM. Molenaar WM. Vermey A. Mooyaart EL. Panders AK. Annyas AA. Thijn CJP. Malignant parotid tumors:
clinical use of MR imaging and histologic correlation. Radiology. 1992;185,691-6.
76. Kamal SA. Othman EO. Diagnosis and treatment of parotid tumours. J Laryngol Otol. 1997;111:316-21.
77. Shimizu M. Ussmuller J. Hartwein J. Donath K. Kinukawa N. Statistical study for sonographic differential diagnosis of
tumorous lesions in the parotid gland. Oral Surgery, Oral Medicine, Oral Pathol, Oral Radiol, & Endodontics.
1999;88:226-33.
78. Schick S. Steiner E. Gahleitner A. Bohm P. Helbich T. Ba-Ssalamah A. Mostbeck G. Differentiation of benign and
malignant tumors of the parotid gland: value of pulsed Doppler and color Doppler sonography European Radiology.
1998;8:1462-7.
79. James C. Starks M. MacGillivray DC. White J. The use of imaging studies in the diagnosis and management of thyroid
cancer and hyperpara-thyroidism. Surg Oncol Clin of North Am. 1999, 8: 145-69.
80. Jana S. Abdel-Dayem HM. Young I. Nuclear medicine and thyroid cancer [editorial]. Eur J Nuc Med. 1999, 26:1528-32.
81. Wang Q. Takashima S. Fukuda H. Takayama F. Kobayashi S. Sone S. Detection of medullary thyroid carcinoma and
regional lymph node metastases by magnetic resonance imaging. Archives of Otolaryngology -- Head & Neck Surgery.
82. Singer PA. Thyroid nodules: malignant or benign? Hospital Practice (Office Edition)1998, 33:143-4, 147-8, 153-6.
83. Pelizzo MR. Bernante P. Toniato A. Piotto A. Gemo G. Pagetta C. Bernardi C. Guidelines for the diagnosis of thyroid
carcinoma. J Exper Clin Cancer Res .1997; 16:427-8.
84. Danese D. Centanni M. Farsetti A. Andreoli M. Diagnosis of thyroid carcinoma. Journal of Exper Clin Cancer Res. 1997;
16:337-47.
85. Lin JD. Huang BY. Weng HF. Jeng LB. Hsueh C. Thyroid ultrasonography with fine-needle aspiration cytology for the
diagnosis of thyroid cancer. J Clin Ultrasound. 1997;25:11-8
86. Goldman ND. Coniglio JU. Falk SA. Thyroid cancers. I. Papillary, follicular, and Hurthle cell. Otolaryngol Clin North
Am.1996; 29:593-609.
87. Lin JD. Diagnosis of papillary and follicular thyroid cancers. Chang-Keng i Hsueh Tsa Chih. 1999;22:348-61.
88. Galloway RJ. Smallridge RC. Imaging in thyroid cancer. Endocrinology & Metabolism Clinics of North Am. 1996; 25:93113.
89. King AD. Ahuja AT. To EW. Tse GM. Metreweli C. Staging papillary carcinoma of the thyroid: magnetic resonance
imaging vs ultrasound of the neck. Clin Radiol. 200; 55:222-6.
90. Hay ID. Klee GG. Thyroid cancer diagnosis and management. Clin Lab Med. 1993; 13:725-34.
91. Shimamoto K. Satake H. Sawaki A. Ishigaki T. Funahashi H. Imai T. Preoperative staging of thyroid papillary carcinoma
with ultrasonography. Eur JRadiol. 1998; 29:4-10.
92. Takashima S. Sone S. Takayama F. Wang Q. Kobayashi T. Horii A. Yoshida JI. Papillary thyroid carcinoma: MR diagnosis
of lymph node metastasis. Am J Neuroradiol. 1998; 19:509-13.
93. Krausz Y. Rosler A. Guttmann H. Ish-Shalom S. Shibley N. Chisin R. Glaser B. Somatostatin receptor scintigraphy for early
detection of regional and distant metastases of medullary carcinoma of the thyroid. Clin Nuc Med. 1999; 24:256-60.
94. Crile G. Landmark article Dec 1, 1906: Excision of cancer of the head and neck. With special reference to the plan of
dissection based on one hundred and thirty-two operations. By George Crile. [Biography. Classical Article. Historical
Article. Journal Article] JAMA. 258:3286-93, 1987 Dec 11.
95. Robbins KT. Medina JE. Woolfe GT. Levine PE. Sessions RB. And Pruet CW. Standardising neck dissection terminology.
Arch Otolaryngol, Head Neck Surg 1991: 117; 601-605.
96. Som P M, Urken M L, Biller H & Lidov M Imaging the post operative neck Radiology 1993; 187 : 593 – 603.
97. Paulus P. Sambon A. Vivegnis D. et al. ‘18 FDG-PET for the Assessment of Primary Head and Neck Tumours: Clinical,
Computed Tomography, and Histopathological Correlation in 38 Patients Laryngoscope 1998; 108: 1578-1583.
99. Valdes Olmos R.O., Balm A.J.M., Hilgers F.J.M. et al. ‘Thallium 201 SPECT in the diagnosis of
head and neck cancer. J Nuc Med 1997; 38:873-879.
Other useful references
Becker M. et al. Neoplastic invasion of the laryngeal cartilage : comparison of MR imaging and CT with
histopathological correlation Radiology 1995, 196: 476-479.
Becker M. Zbaren P. Laeng H, et al. Neoplastic invasion of the laryngeal cartilage: comparison of MR
imaging and CT with histopathologic correlation Radiology. 294:661-669, 1995.
Castelijns J A, Gerristen G J, Kaser Invasion of laryngeal cartilage by cancer: comparison of CT and MR
imaging Radiology 1988; 167: 199 – 206.
Chong V.F.H., Fan Y.F., Toh K.H., Khoo J.B.H. Lim T.A. Magnetic resonance imaging and computed
52
tomography features of nasopharyngeal carcinoma with maxillary sinus involvement Aust Radiol 1995; 39: 2-9.
Chong V.F.H.,Fan Y.F., Khoo J.B.K. Retropharyngeal lymphadenopathy in nasopharyngeal carcinoma
Eur J Radiol 1995; 21: 100-105.
Chong VFH, Mukherji SK, Ng SHH, Ginsberg LE, Wee JTS, Sham ST, O’Sullivan B. Nasopharyngeal
carcinoma: Review of how imaging affects staging JCAT 1999;23,6, 984-993.
Howaldt H P, Frenz M, Pitz H ‘Proposal for a modified T classification for oral cancer’ J
Craniomaxillofacial Surgery 1992; 21 : 96 – 101
Wong WL, Chevretton EB, McGurk M et al. A prospective study of PET-FDG imaging for the
assessment of head and neck squamous cell carcinoma. Clin Otolaryngol 1997; 22: 209-214.
Hanasono MM, Kunda LD, Segall GM, Ku GH, Terris DJ. Uses and limitations of FDG positron
emission tomography in patients with head and neck cancer. Laryngoscope 1999; 109: 880-5.
Pameijer FA, Mukherji SK, Balm AJ van der Laan BF. Imaging of squamous cell carcinoma of the
hypopharynx. Sem Ultrasound CT MRI 1998; 19: 476-91.
53
Section 2
Chapter 2
Pathology Datasets
Pathology Services – Staffing: A Consultant Histopathologist and a Consultant Cytopathologist with
special interest in head and neck diseases are essential members of the multidisciplinary clinical oncology
team. Appropriate cover for periods of leave should be included in the service budget. The
Cytopathologist may attend the early diagnosis clinics to provide a 'one-stop' service. Local circumstances
may dictate that this is not an efficient use of the Consultant resource and cytological specimens may be
sent to the laboratory for reporting. The turnaround time for reports will depend upon the nature of the
diagnostic problem and the work required to reach a diagnosis. Consultant Pathologists should participate
in an appropriate, accredited, diagnostic EQA scheme.
Laboratory Facilities: Space for the preparation and reporting of cytological specimens is required if a
'one-stop' clinic service is provided. The laboratory service should participate in technical EQA and
should be accredited by Clinical Pathology Accreditation (UK) Ltd or to a similar standard.
A minimum dataset for histopathology reports on cases of head and neck squamous carcinomas has been
published by The Royal College of Pathologists, and will be updated during 2002-3 to include a section
on salivary neoplasms. The current document can be downloaded from College website
[www.rcpath.org]. The aims of this document are to:
•
•
•
enhance and make more consistent the information provided for patient management through the use
of a proforma report or checklist
facilitate the monitoring of changing pattern of disease
allow equitable comparison of surgical units and of patients in clinical trials
The Royal College of Pathologists has commissioned minimum datasets for the histopathology reports on
thyroid neoplasms and is considering salivary neoplasms; the broad outlines of their likely composition
are included for guidance.
MINIMUM DATASET FOR SQUAMOUS CARCINOMAS
This minimum dataset is for squamous carcinomas, is evidence-based and the contents are summarised
here.
The content of the histopathology report will include clinical information (that should be provided by the
surgeon or oncologist), data on the primary carcinoma and data on the extent of nodal involvement (if
dissected).
1. Clinical data
1.1. Primary carcinoma
• Site(s) and side(s) of the carcinoma(s) recorded according to the UICC nomenclature.
• Type of resection specimen e.g., total or partial glossectomy, laryngectomy.
• Clinical TNM stage. The final pathological T coding at some sites e.g., the larynx, will be determined
by clinical features such as vocal cord mobility (2)
• Previous radiotherapy or chemotherapy (this may influence the histological interpretation).
• Illustrative diagrams of the primary resection specimen are invaluable to the pathologist in some
situations, and their use is to be encouraged. Some centres provide pre-printed request forms that
include such diagrams.
• Where the orientation of the specimen is critical e.g. for assessment of marginal status, the surgeon
and pathologist should agree a protocol for marking the specimens with clips or sutures.
54
•
For some sites e.g. mucosal resection and partial laryngectomy specimens, specimens may be pinned
onto cork or polystyrene boards to preserve the anatomical relationships and minimise distortion
during fixation (3).
1.2. Neck dissections
• The type of neck dissection should be specified as either comprehensive or selective.
• Node levels present in the specimen.
• Nodes in addition to the main groups e.g. parapharyngeal nodes, should be sent as separate
specimens.
• Specimens should be pinned onto cork or polystyrene boards to preserve the anatomical relationships
and minimise distortion during fixation. The surgeon and pathologist should agree a protocol for
marking the specimens with clips or sutures to indicate node levels.
2. Pathological data for the primary carcinoma
• Maximum diameter of tumour (millimetres).
• Maximum depth of invasion (millimetres) below the luminal aspect of surface.
• Histological type of carcinoma. The guidelines specifically apply to typical squamous carcinomas.
Subtypes of squamous carcinoma, such as papillary, verrucous, basaloid, adenosquamous and spindle
cell carcinomas, should be recognised [4]
• Degree of differentiation. Grading of the most aggressive area is based on the WHO classification (4)
into well, moderately or poorly-differentiated carcinomas. Anaplastic or undifferentiated carcinomas
are also recognised. This system is prognostically useful, even though it suffers from inter-observer
variability and sampling problems (5,6).
• Invasive front of the carcinoma. The pattern of invasion by the carcinoma at its deep margin is of
proven prognostic value for oral carcinomas (7,8,9). The few published studies of tumours at other
sites suggest that a similar approach may be of value (10). Scoring systems for histopathological
features of squamous carcinomas have the potential to improve the consistency of reporting, but are
not in widespread use and do not form part of the minimum dataset.
• Distance from invasive carcinoma to mucosal and deep margins (millimetres).
• Vascular invasion.
• Perineural invasion ahead of the invasive front of the carcinoma is especially important for
carcinomas of the lip.
• Bone invasion.
• Severe dysplasia/in situ carcinoma is associated with a high risk of progression to carcinoma and its
presence both adjacent to the primary carcinoma and at the resection margins should be recorded
(11,12).
Other features that may be reported
It should be emphasised that this is a minimum dataset and individual centres may wish to record
features in addition to those listed above. Some features should be included as part of a comprehensive
description of a carcinoma and the surrounding tissues, but are considered to be of uncertain prognostic
significance at most sites in the head and neck region.
1.
Type and intensity of inflammatory infiltrate and desmoplastic stromal response.
2.
Involvement of a tracheostomy (if present).
3.
Response to previous therapy (if applicable).
4.
Results of other investigations e.g. flow cytometry, molecular and immunohistochemical studies.
The diagnostic role of immunohistochemical techniques
A wide range of antibodies is available to help resolve diagnostic problems. Most antibodies lack a
precise tissue of neoplastic specificity, so that a combination of appropriate results is required to make a
diagnosis.
55
Molecular markers of prognosis or prediction of therapeutic response.
Markers including measures of cell proliferation and nuclear DNA content, the expression of involucrin,
blood group antigens, cell adhesion molecules and oncogenes, and the intensity of neoangiogenesis have
been investigated as potential prognostic factors. These features generally correlate with cellular
differentiation but do not provide any consistent independent prognostic information (7,13,14).
The tumour suppressor genes p53 and p16 and the oncogene cylinD1 have been studied in squamous cell
carcinoma of the head and neck. p53 mutation per se may not be of prognostic significance (15), but null
mutations do appear to be of prognostic value (16). Likewise combinations of genetic alterations are
being identified which carry prognostic significance (17). At present it is unclear as to whether or not
molecular staging or classification of cancers are clinically relevant and multicentre trials are underway
(18,19). In the UK, this type of staging may not be possible or practical with current funding of
pathology laboratories. Thus, while molecular markers predictive of tumour behaviour or response to
therapy may be required pathological data in the future, current surgical practice does not demand their
inclusion in the minimum data set.
3. Pathological data from the neck dissection specimen
The extent of nodal involvement is a major prognostic factor for head and neck squamous carcinomas.
The following data items should be recorded:
• At each anatomical level, record the total number of nodes identified and number of nodes involved
by carcinoma.
• Size of largest metastatic deposit. The size of the largest metastasis is a determinant in the TNM
staging (2).
• Presence or absence of extra-capsular rupture and the node level(s) showing this feature.
Extracapsular spread is a manifestation of the aggressiveness of a carcinoma and is associated with a
poor prognosis (20,21). Although the prognostic significance of micrometastases (<3mm. diameter) is
not determined (22), their presence should be included in the number of involved nodes.
Other features that should be included as part of a comprehensive description, but are considered to be of
uncertain prognostic significance at most sites in the head and neck region.
1. Presence of other pathology in cervical nodes.
2. Presence of evidence of response of tumour e.g. keratin debris, to previous therapy
Sentinel node biopsy
The clinical utility of sentinel node biopsy is controversial and the most appropriate method of handling
such specimens has not been defined. The current guidelines from the ADASP (23) indicate that:
Intaoperative frozen section diagnosis is only appropriate where the result will change clinical
management. Only routine, H&E stains should be used except for experimental situations.
The whole node should be processed for paraffin sections and ‘more than one section’ taken from each
block. There are no evidence-based guidelines to indicate how many sections should be used.
It is unclear whether or not immunocytochemical staining adds clinically relevant information [falsepositive results can occur].
4. Diagnostic coding of primary carcinomas and metastases
• pT and pN status should be recorded according to the UICC guidelines (2).
• SNOMED T and M codes should be recorded for both primary site(s) and for nodes.
56
MINIMUM DATASET FOR THYROID NEOPLASMS
A minimum dataset for pathology reports is being prepared for the Royal College of Pathologists (details
may be obtained from Dr Ann Marie McNicol, University Department of Pathology, Glasgow Royal
Infirmary, GLASGOW G4 0SF). The pathological features likely to be included in this document include:
•
•
•
•
•
•
•
•
specimen type (thyroidectomy or lobectomy), size and weight
histological type of neoplasm
macroscopic size and degree of encapsulation of the neoplasm
presence or absence of invasion of the thyroid capsule or surrounding tissues and distance from
resection margin
presence or absence of vascular invasion
microscopic distance from excision margin
extent of lymph node involvement
diagnostic coding of primary carcinomas and metastases (UICC and SNOMED)
MINIMUM DATASET FOR SALIVARY TUMOURS
A minimum dataset for pathology reports will form part of the updated Head and Neck Carcinoma
pathology.
The following features should be recorded for salivary neoplasms:
• size of tumour
• distance from tumour to resection margins [macroscopic distance confirmed histologically]
• histological type of neoplasm [and subtype for adenoid cystic carcinomas]
• grade of malignance
• presence of perineural or vascular invasion
• extent of lymph node involvement
• diagnostic coding of primary carcinomas and metastases (UICC and SNOMED).
Other features should be included as part of a comprehensive description, but are considered to be of
uncertain prognostic significance:
• whether tumour is solitary or multifocal
• nature of tumour margin [encapsulated or ill-defined]
• solid or cystic tumour
• mitotic index
• microscopic changes in the macroscopically normal salivary tissue
References:
1. Helliwell TR, Woolgar JA: Minimum datset for the reporting of Head and Neck Carcinomas. London: The Royal College of
Pathologists, 1998.
2. Sobin LH, Wittekind C: TNM Classification of Malignant Tumours. (5th ed.) New York: John Wiley & Sons, Inc., 1997.
3. Helliwell TR. ACP Broadsheet. Guidelines for the laboratory handling of laryngectomy specimens. Journal of Clinical
Pathology 2000;53;171-176.
4. Pindborg JJ, Reichart PA, Smith CJ, van der Waal I: Histological Typing of Cancer and Precancer of the Oral Mucosa. (2
ed.) Berlin: Springer, 1997. International Histological Classification of tumours;
5. Henson DE: The histological grading of neoplasms. Arch. Pathol. 1988;112:1091-1096.
6. Roland NJ, Caslin AW, Nash J, Stell PM: Value of grading squamous cell carcinoma of the head and neck. Head Neck
1992;14:224-229.
7. Bryne M, Nielsen K, Koppang HS, Dabelsteen E: Reproducibility of two malignancy grading systems with reportedly
prognostic value for oral cancer patients. J. Oral Pathol. Med. 1991;20:369-372.
8. Crissman JD, Liu WY, Gluckman JL, Cummings G: Prognostic value of histologic parameters in squamous cell carcinoma of
the oropharynx. Cancer 1984;54:2995-3001.
9. Odell EW, Jani P, Sherriff M, et al.: The prognostic value of individual grading parameters in small lingual squamous cell
carcinomas. Cancer 1994;74:789-794
57
10. Jakobsson PA, Eneroth CM, Killander D, Moberger G, Martensson B: Histologic classification and grading of malignancy in
carcinoma of the larynx. Acta Radiol. 1973;12:1-8.
11. Hellquist H, Lundgren J, Olofsson J: Hyperplasia, keratosis, dysplasia and carcinoma in situ of the vocal cords - a follow-up
study. Clin. Otolaryngol. 1982;7:11-27.
12. Lumerman H, Freedman P, Kerpel S: Oral epithelial dysplasia and the development of invasive squamous cell carcinoma.
Oral Surg. Oral Med. Oral Pathol. 1995;79:321-329.
13. Bryne M: Prognostic value of various molecular and cellular features in oral squamous cell carcinomas: a review. J. Oral
Pathol. Med. 1991;20:413-420.
14. Carter RL: Pathology of squamous carcinomas of the head and neck. Curr. Opin. Oncol. 1993;5:491-495.
15. Kearsley JH, Thomas S: Prognostic markers in cancers of the head and neck region. Anticancer Drugs 1993;4:419-429.
16. Saunders ME, MacKenzie R, Shipman R, Fransen E, Gilbert R, Jordan CK.: Patterns of p53 gene mutations in head and neck
cancer: full-length gene sequencing and results of primary radiotherapy. Clinical Cancer Research 1999; 5:2455-2463.
17. Hashimoto T, Tokuchi Y, Hayashi M, Kobayashi Y, Nishida K, Hayashi S, Ishikawa Y, Tsuchiya S, Nakagawa K, Hayashi J
and Tsuchiya E: p53 null mutations undetected by immunohistochemical staining predict a poor outcome with early-stage
non-small cell lung carcinomas. Cancer Research 1999;59;5572-5577.
18. Bova RJ, Quinn DI, Nankervis JS, Cole IE, Sheridan BF, Jensen MJ, Morgan GJ, Hughes CJ, and Sutherland RL. Clinical
Cancer Research. 1999;5:2810-2819.
19. Golub TR, Slonim DK, Tamayo P, Huard C, Gaasenbeek M, Mesirov JP, Coller H, Loh ML, Downing JR, Caligiuri MA,
Bloomfield CD and Lander ES. Molecular classification of cancer:class discovery and class prediction by gene expression
monitoring. Science 1999:286;531-537.
20. Brennan JA, Sidransky D: Molecular staging of head and neck squamous cell carcinoma. Cancer and Metastasis Reviews.
1999; 15;3-10.
21. Woolgar JA: Detailed topography of cervical lymph-node metastases from oral squamous cell carcinoma. International
Journal of Oral & Maxillofacial Surgery 1997;26:3-9.
22. Van den Brekel MWM, Stel HV, van der Valk P, van der Waal I, Meyer CJLM, Snow GB: Micrometastases from squamous
cell carcinoma in neck dissection specimens. Eur. Arch. Otorhinolaryngol. 1992;249:349-353.
23. Lawrence WD. ADASP recommendations for processing and reporting of lymph node specimens submitted for evaluation
for metastatic disease. Virchows Archiv 2001;439;601-603.
58
3
SERVICE PROVISION
Chapter 1
Prevention
Key Points
•
Tobacco exposure is the important risk factor for the development of upper aerodigestive tract
squamous cell carcinoma.
•
Excessive alcohol has a synergistic effect with tobacco use.
•
There is no evidence that screening leads to a reduction in mortality or morbidity.
•
Preventative intervention must concentrate on modifying smoking habits.
•
Optimal treatment for tobacco dependence consists of structural behavioural support involving
multiple sessions combined with nicotine replacement or bupropion.
•
Chemo prevention remains a promising area for future research, but the current evidence shows no
benefit for the prevention of second primary cancers.
Introduction
The most important risk factor for the development of upper aerodigestive tract squamous cell carcinoma
is tobacco exposure. Alcohol is also an independent risk factor although the exact inter-relationship is
hard to quantify because intake of the two is so highly correlated. Tobacco and alcohol together, however,
synergistically influence the development of head and neck cancer, with heavy smokers and heavy
drinkers having 38 times the risk of oral cancer than abstainers of both (1).
Other risk factors are of lesser significance when controlling for alcohol and tobacco consumption and so
preventative interventions for head and neck cancer must concentrate on modifying smoking habits. Other
preventative interventions include screening and chemo prevention. The usefulness of general population
screening is limited by the low prevalence and incidence of the disease, the potential for false positive
diagnoses and the poor compliance with screening and referral (2). There is no evidence that screening of
the general population or high risk groups leads to a reduction in mortality or morbidity. Chemo
prevention is an attractive proposition. However, there is inadequate evidence to support the use of any
chemo preventative drug or other agent.
Modifying tobacco and alcohol intake
Tobacco is clearly the most preventable cause of head and neck cancer. This was recognised for laryngeal
cancer (3) and continues to be a constant finding with smokers of more than one packet of cigarettes per
day having a risk of head and neck cancer that is 13 times higher than that of non smokers (4). Tobacco
smoking and alcohol drinking each contribute to the risk of second cancers with the effects of smoking
being more pronounced (5).
Tobacco use also adversely influences cancer patients’ survival – after controlling for age, race, alcohol
use and histological grade, smokers had a lower rate of survival than non smokers with risk ratios of 1.55
for males and 1.43 for females (6).
59
Trigg et al (7) have also shown that smokers present with higher grades of cancers – patients diagnosed
with stage III or IV laryngeal cancers smoked a significantly greater amount and were also more likely to
be heavy drinkers.
Given these facts, the moderation of alcohol consumption and the cessation of smoking should be a high
priority in head and neck cancer prevention.
Few medical interventions of any kind have the same potential as smoking cessation to both improve
health and prolong life and arguably be cost effective. Smoking halves the chance of survival to 70 years
and accounted for 120,000 deaths in the UK in 1995. In a group of 1445 male smokers aged 40 to 59, an
intervention group received individual advice on the relationship between smoking and health and over a
20 year period total mortality was seven per cent lower in this group, fatal coronary artery disease 13 per
cent lower and lung cancer 11 per cent lower (8). Similar studies in head and neck cancer have shown a
substantial drop in oral and pharyngeal cancers.
Table 1
Effect of smoking cessation on risk of oral and pharyngeal cancer in 1114 cases, 1268 controls (1)
Odds Ration
Male
Female
Current smoker
1-9y ex smoker
10-19y ex smoker
20y + ex smoker
3.4
1.1
1.1
0.7
4.7
1.8
0.8
0.4
An Italian study (9) confirms the reduction in Table 1 with an overall odds ration after allowance for age,
sex, education and alcohol consumption of 8.4 for current smokers, 6.2 for those who had stopped
smoking for less than two years, 4.5 for those who had stopped smoking for three to five years and 1.6 for
those who had stopped for ten to 14 years. The risk of premalignant lesions such as leukoplakia is also
found to be reduced following smoking cessation (10).
The effect of reducing alcohol intake is less clear and it is difficult to assess the effects of reducing
alcohol intake independently of reducing smoking. Franceschi (11) does however show a reduced odds
ratio for the development of oral and pharyngeal cancer from 11.6 for current drinkers to 1.9 for former
drinkers.
Facilitating smoking cessation
Interest in smoking cessation is high in patients with head and neck cancer, and although the
diagnosis of a tobacco related malignancy clearly represents a strong catalyst for stopping
smoking, a sizeable subgroup of patients continue to smoke (12). More than 132,000 people used
smoking cessation services in England between April 2000 and March 2001 with 49 per cent
giving up for at least a month after setting a ‘quit’ date.
♣
Behavioural therapy
Data from 188 randomised controlled trials suggest that encouragement and advice given by a
doctor during a single consultation resulted in two per cent of all smokers stopping without relapse
for up to a year (13) Recent studies looking at intervention by ward nurses (14) or midwives (15)
have no effect at six weeks or one year. Intervention may trigger an attempt to quit, but the subsequent
treatment is important. A Cochrane review shows that behavioural support and counselling increases a
smokers chances of achieving lasting abstinence (16).
60
•
Nicotine replacement
Nicotine replacement attempts to replace nicotine in the body with gradual weaning to reduce the
pharmacological sequelae of the chemical addiction. Nicotine is absorbed through the cheek from gum or
lozenges, transdermally via patches or transmucosally via inhalers or sprays, though these latter may also
become addictive. Patches are available on prescription and increase the odds ratio of abstinence to 1.71
(17).
•
Bupropion
Available on prescription as Zyban this drug reduces the withdrawal symptoms and has been shown to
improve abstinence rates over six months in people with cardiovascular disease (18).
Optimal treatment for tobacco dependence consists of structural behavioural support involving multiple
sessions combined with nicotine replacement or bupropion (19).
Chemo prevention
Chemo prevention may be defined as the use of chemical agents to prevent the development of cancer.
The epithelium of the upper aerodigestive tract has a rapid turnover and is exposed to ingested and
inhaled carcinogens This, along with a genetic susceptibility predisposes to the development of
premalignant lesions, cancers and second primary cancers. The idea that a chemo preventative drug could
arrest the progression of premalignancy to invasion, or prevent the development of a metachronous
primary is an attractive one. Laboratory and epidemiological studies suggest that dietary carotenoids are
inhibitors of epithelial carcinogenesis with inverse associations between beta carotene intake and risk of
laryngeal cancers (20). Low vitamin A and C intake also appears to increase the risk of oral cancer(21)
and case controlled studies show that oral cancer patients have lower consumption of fruit and vegetables
(22). In vitro studies have shown that retinoids block tumour promotion by inhibiting proliferation,
inducing apoptosis and inducing differentiation (23). Work with nude mice suggests that retinoids and
interferon alpha are synergistic anti-angiogenic agents (24).
Both vitamin A derivatives and N-acetyl cystine showed some early promise though toxicity was a
significant concern with dose related dry skin, cheilitis, conjunctivitis and arthralgia being the main side
effects. Disappointingly, however, the EUROSCAN multicentre trials of 2592 patients showed no
statistically significant benefit for these interventions (25). Equally, topical vitamin A showed no benefit
in the treatment of leukoplakia (26).
Chemo prevention remains a promising area for future research, but the current evidence shows no benefit
for the prevention of second primary cancers.
Vitamin A analogues may reduce the incidence of malignant change in premalignant lesions, but there
remain considerable problems with toxicity therefore limiting their use at present.
References:
1.
2.
3.
4.
5.
Blot WJ, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston-Martin S, et al. Smoking and drinking in relation to
oral and pharyngeal cancer. Cancer Res 1988;48:3282-7.
Hawkins RJ, Wang EE, Leake JL. Preventive health care, 1999 update: prevention of oral cancer mortality. The Canadian
Task Force on Preventive Health Care. J Can Dent Assoc 1999;65:617.
Wynder EL, Bross IJ, Day E. Epidemiological approach to etiology of cancer of the larynx. JAMA 1956;160:1384-91.
Andre K, Schraub S, Mercier M, Bontemps P. Role of alcohol and tobacco in the aetiology of head and neck cancer: a casecontrol study in the Doubs region of France. Eur J Cancer B Oral Oncol 1995;31B:301-9.
Day GL, Blot WJ, Shore RE, McLaughlin JK, Austin DF, Greenberg R, Liff JM, Preston-Martin S, Sarkar S, Schoenberg
JB, et al. Second cancers following oral and pharyngeal cancers: role of tobacco and alcohol. J Natl Cancer Inst
1994;86:131-7.
61
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
Yu GP, Ostroff JS, Zhang ZF, Tang J, Schantz SP. Smoking history and cancer patient survival: a hospital cancer registry
study. Cancer Detect Prev 1997;21:497-509.
Trigg DJ, Lait M, Wenig BL. Influence of tobacco and alcohol on the stage of laryngeal cancer at diagnosis. Laryngoscope
2000;110 (3 Pt1):408-11.
Rose G, Colwell L. Randomised controlled trial of anti smoking advice: final [20 year] results. J Epidemiol and Comm
Health 1992;46:75-7.
Vecchia C, Franceschi S, Bosetti C, Levi F, Talamini R, Negri E. Time since stopping smoking and the risk of oral and
pharyngeal cancers. J Natl Cancer Inst 1999;91:726-8.
Gupta PC, Murti PR, Bhonsie RB, Mehta FS, Pindborg JJ. Effect of cessation of tobacco use on the incidence of oral
mucosal lesions in a 10-yr follow-up study of 12,212 users. Oral Dis 1995;1:54-8.
Franceschi S, Levi F, Dal Maso L, Talamini R, Conti E, Negri E, La Vecchia C. Cessation of alcohol drinking and risk of
cancer of the oral cavity and pharynx. Int J Cancer 2000;85:787-90.
Ostroff JS, Jacobsen PB, Moadel AB, Spiro RH, Shah JP, Strong EW, Kraus DH, Schantz SP. Prevalence and predictors of
continued tobacco use after treatment of patients with head and neck cancer. Cancer 1995;75:569-76.
Law M, Tang JL. An analysis of the effectiveness of interventions intended to help people stop smoking. Arch Intern Med
1995;155:1933-41.
Hajek P, Taylor TZ, Mills P. Brief intervention during hospital admission to help patients to give up smoking after
myocardial infarction and bypass surgery: randomised controlled trial. BMJ 2002;324:87-9.
Hajek P, West R, Lee A, Foulds J, Owen L, Eiser JR, et al. Randomised controlled trial of a midwife-delivered brief
smoking cessation intervention in pregnancy. Addiction 2001;96:485-94.
Lancaster T, Stead LF. Individual behavioural counselling for smoking cessation. Cochrane Database Syst Rev
2001;3:CD003086.
Silagy C, Mant D, Fowler G, Lodge. Meta-analysis on efficacy of nicotine replacement therapies in smoking cessation. M.
Lancet 1994;343:139-42.
West R. Helping patients in hospital to quit smoking. BMJ 2002;324:64.
West R, McNeill A, Raw M. National smoking cessation guidelines for health professionals: an update. Thorax
2000;55:987-99.
Tavani A, Negri E, et al. Attributable risk for laryngeal cancer in Northern Italy. Cancer Epidemiol Biomarkers prev
1994;3:121-5
Marshall J, Graham S et al Diet in the epidemiology of oral cancer. Nutr Cancer 1982;3:145-9
La Vecchia C, Negri E et al Dietary indicators of oral and pharyngeal cancer. Int J Epidemiol 1991;20:39-44
Niles R. Recent advances in the use of vitamin a in the prevention and treatment of cancer. Nutrition 2000;16:1084-9
Lingen M, Polverini P and Bouck N Retinoic acid and interferon alpha act synergistically as antiangiogenic agents against
human head and neck squamous cell carcinoma. Cancer Res 1998;58:5551-8
van Zandwijk n, Dalesio et al EUROSCAN, a randomised trial of vitamin A and N-acetylcysteine in patients with head and
neck cancer or lung cancer. For the European Organisation for Research and Treatment of Head and neck and lung Cancer
Cooperative Groups. J Natl Cancer Inst. 2000;92:959-60
Epstein J and Gorsky M Topical application of vitamin A to oral leukoplakia: A clinical case series. Cancer 1999;86:921-7
62
Section 3
Chapter 2 Role of Multidisciplinary Team
All patients with a diagnosis of cancer of the head and neck must be seen in a multidisciplinary clinic.
The recommended staffing structure is:
Present in clinic
Available throughout clinic
Affiliated to clinic
Head and Neck Surgeon (1 of 2)
Clinical oncologist (1 of 2)
Reconstructive Surgeon (1 of 2)
Head and Neck Nurse Specialist
Dietitian
Speech pathologist (voice)
MDT Co-ordinator
Speech pathologist (dysphagia)
Restorative Dental Practitioner
Palliative Care Physician
Dental hygenist
Pathologist – head and neck focus
Prosthodontist
Cytologist
Radiologist – head and neck focus
GI surgeon/physician
Physiotherapist
Social Worker
Psychologist
The particular skills of an Otolaryngologist which makes him/her a key member of the surgical team are
in:
• diagnostic endoscopy/video documentation
• primary therapy
• management of acute and chronic upper airway compromise
• management of associated disorders/treatment complications e.g. otologic
The key to delivery of multidisciplinary care is the careful co-ordination of the combined oncology clinic
as well as its consistent delivery throughout the year. The Clinic co-ordinator is responsible for
preparatory work for the clinic including assembly of results, as well as keeping an attendance register,
ensuring liaison between members , supporting data capture and facilitating further appointments and
treatments.
Head and neck cancer patients represent a significant challenge in achieving and maintaining optimal
nutritional status, with around two thirds of diagnosed patients experiencing moderate to severe
malnutrition. (1,2,3,4). Early intervention is essential to prevent deterioration of nutritional status in this
high risk group. (5) The Dietician is a key attendee at the combined oncology clinic to provide nutritional
assessment, advice and support from diagnosis, and regular monitoring through the patients cancer
journey and in liasing with relevant professionals across the secondary care and community. See section
Beyond Primary Treatment
Most patients benefit from the service of a Speech and Language Therapist (SALT)(Pathologist). The
SALT, as a permanent member of the multidisciplinary team provides assessment and ongoing advice on
swallowing, speech and overall communication, which may include advice and/or provision of
appropriate communication aids. Their patient contact will normally have begun preoperatively, and
supports the patients’ journey involving radiotherapy, and major head and neck surgery including
surgical voice restoration. The multidisciplinary clinic provides an appropriate environment for regular
patient review and monitoring of progress/change.
The role of nurse specialists is multifaceted and is a core function of the multidisciplinary team (6,7), in
co-ordinating professionals across secondary and primary care to give seamless care.
The nurse specialist shares information with the patient and relative at the multidisciplinary clinic.
Patients fail to retain half of medical information given(8): therefore nurse specialists can help amplify
the consultation outcome, and provide contact telephone numbers to each patient and relative for future
use.
63
Their skills encompass expertise in pain and symptom management and the ability to discuss treatment
options. Specialist nurses utilise counselling skills and act as the patient’s advocate from diagnosis and
throughout the cancer journey, independent of treatment outcome.
All patients should have a general dental/prosthodontic assessment because of the impact of both
radiotherapy and surgery on dentition. Continued support through treatment and in palliative care is
important. The dental hygienist educates patients in self care, and prevents possible post treatment
problems by improving oral hygiene, as well as encouraging visits to their own dentist or Community
dental scheme if appropriate
Some patients, especially after radical neck dissection, or with coexistent chest disease, will benefit from
physiotherapy. Close liaison with specialist head and neck pathology and radiology services, and an
affiliated gastrointestinal team with an interest in gastric mobilisation and jejunal harvest, and where
necessary, percutaneous gastrostomy, is desirable.
The advantages of working from a multiprofessional combined oncology clinic for both patient and
professional are as follows:Advantages of Centralised Multidisciplinary Clinics
• Avoids attendances at multiple appointments with different professionals
• Avoids reduplication of information from various members of the MDT
• Ensure professionals work “together”, rather than “alongside” each other
• Increases knowledge, development and understanding among professionals
• Potential sharing of certain advisory roles and thus provide some cover for staff absence
• Peer support
• Continuity of care
• Cost effective for both time and resources
These outweigh the potential disadvantages:Disadvantages of Centralised Interdisciplinary Clinics
• Sub optimal use of specialist time
• Intimidating atmosphere from team size
• Pressure on room space
• Brief consultation times, especially if patient well
• Increased complexity to run clinic to schedule
• Longer distances to travel
• Appointment dates potentially inflexible
Many of these drawbacks can be addressed by increased resources, in particular having multiple rooms
available and a surplus of personnel. To assist in the smooth running of the clinic, some groups find it
helpful to divide new and follow up patients into quite separate clinic times, minimising extended waits
for the patient and reducing the number of clinicians needed throughout the clinic.
Continuous engagement of patient views on the configuration of the multidisciplinary clinic should be
sought.
64
References:
1.
2.
3.
4.
5.
6.
7.
8.
Hearne BE, Duaj J M, Daly JM, Strong EW, Vikram B, LePorte BJ, De Cosse JJ . Enteral nutrition support in head & neck
cancer: Tube versus oral feeding during radiation therapy. Journal of the American Dietetic Association 1985, 85 669-677
Lees J Nasogastric & percutaneous endoscopic gastrostomy feeding in head & neck cancer patients receiving radiotherapy
treatment at a regional oncology unit: a two-year study.
European Journal of Cancer Care 1997, 6 45-49
Goodwin WRJ & Byers PM Nutritional management of the head & neck cancer patient (Review) Medical Clinics of North
America. 1993, 597-610
Grant m, Rhinder M, Padilla GV Nutritional management in the head & neck cancer patient .Seminars in Oncology Nursing
5. 1989, 195-204
Oncology Group of the British Dietetic Association (Feb 1997) Guidelines for Nutrition & Dietetic Services in the
Oncology Setting - Response to the Calman Report on Cancer Services. Position Paper.
Birchall M, Nettlefield P, Richardson A, Lee 1 (2000) Finding their voices: a focus study group of patients with head &
neck cancer & their carers. South West Regional Cancer organisation. Bristol
Edwards D (1997) Face to Face. Patient, family & professional perspective of head & neck cancer care
London. Kings Fund Publishing
Buckman R (1994) How to break bad news. A guide for health professionals. London. Pan Books
65
Section 3
Chapter 3
ONE STOP CLINICS - Quick and Early Diagnosis
The “NHS Cancer Plan” (1) was presented to Parliament by the Secretary of State for Health in
September 2000. The plan applies to England only but similar plans have been published in Scotland,
Wales and Northern Ireland (2). The “NHS Cancer Plan” builds on previous government publications
including “The New NHS: modern, dependable” (Dec.1997) (3), “The NHS Plan” (July 2000) (4) and its
main features are summarised in the short guide for patients/users “Your guide to the NHS” (Feb 2001)
(5). It sets ambitious targets for waiting times for investigation and treatment of patients with cancer or
symptoms suggestive of cancer. It also states that these targets can only be achieved with an expansion of
capacity and investment in new facilities, equipment and staff: and reform of cancer delivery services.
“The New NHS” target, to be achieved by December 2000, was that all patients with suspected cancer
should be seen by a specialist, within 2 weeks of their GP deciding that they need to be seen urgently and
requesting an appointment (in Wales, within 10 working days of receipt of the referral by the hospital).
By 2005 the maximum wait from diagnosis to treatment should be one month. The maximum wait from
GP referral to treatment should be two months with an ultimate goal of one month (which is currently the
standard for all paediatric and testicular cancers).
Ambitious targets have also been set for routine referrals. By 2005 the maximum wait for routine
outpatients should be 3 months (average 5 weeks) and the maximum wait for routine inpatient procedures
should be 6 months (average 7 weeks). “Your Guide to the NHS” states that “waiting lists for all hospital
appointments and admissions will be replaced by booking systems that allow you to choose a convenient
date and time with a guaranteed maximum waiting time.”
The concept of QED (quick and early diagnosis) was presented in the Lancet in 1996 (6) outlining the
procedures in the QED unit in Birmingham. The unit provides centralised facilities and administration for
a variety of specialities and/or symptoms. The actual work of the unit is no different to that of
conventional clinics but the process is efficient and streamlined. The most important features are:
•
•
•
•
•
Neck lumps should be referred to head and neck clinicians who can adequately examine the upper
aerodigestive tract before proceeding to further investigations
Referral by telephone with immediate provision of date and time of appointment to patient and GP
One-stop approach for examination, endoscopy, radiology and pathology
‘Real time’ computer documentation of the whole process
Regular demographic and clinical audit.
Can ‘QED/rapid access/one-stop’, be successful in the head and neck cancer setting?
Three UK departments have published initial results of such services (7,8,9).
Fine needle aspiration cytology and fibreoptic endoscopy have been known to be diagnostically reliable
and reproducible in the outpatient setting for over 17 years in the UK (10,11) and 26 years in the USA.
The major difficulties for most departments will be:
•
•
providing experienced and skilled staff for regular, rapid access clinics, every week of the year
the number of referrals
This second point is highlighted in the recent Commission for Health Improvement, National Service
Framework Assessment Number 1, (12), which states “…more resources are probably spent on checking
patients who do not have cancer than treating those who do.”
66
The second edition of this document (13) estimated 50,000 new dysphonia referrals to UK otolaryngology
clinics with a cancer detection rate of 5%. Our own district audit, if extrapolated, would suggest 111,000
referrals with a cancer detection rate of only 2% for laryngeal cancer. Resouly et al (Dec 2001) (9)
suggest much stricter referral criteria to their dysphonia clinic than those published in the Department of
Health “Referral Guidelines for Suspected Cancer” (14). Even so, their cancer rate was 1 in 34 referrals
(3%). The Glasgow experience (15) shows that, even with referral by fax, it is not possible to achieve the
2 week waiting time target with current staffing levels.
QED: the future
There are many possible reasons for setting up QED services.
1) Early diagnosis leads to improved survival and/or quality of life.
2) Rapid access to diagnostic and treatment services reduces anxiety and uncertainty in patients with
symptoms suspicious of cancer and is the preferred choice of patients.
3) The Patients Charter requires that patients with a possible diagnosis of cancer be seen within 2 weeks
of referral.
The first point, while clinically the most important, lacks evidence. Early stage disease has a better
prognosis than late stage and it is tempting to extrapolate from this that survival from head and neck
cancer will be improved with the introduction of rapid access services. Unfortunately, no such evidence
has been reported in head and neck cancer. In breast cancer, where high quality screening and
symptomatic services are available (and funded), mortality has fallen with the associated service
improvements. The Eurocare Working Group report (16), suggests that the UK has lower survival rates
for cancers: “unexpectedly lower than rates of nearest nations, often below the European average”.
Reducing the outpatient waiting time for cancer symptoms from the current average of 4 to 6 weeks to the
target of 2 weeks on the face of it may only produce a small improvement in survival. However, small
improvements at every stage of the cancer patients journey may have an impact. A lack of direct evidence
should not prevent common sense being used as an argument for funding an improved service that most
multidisciplinary staff as well as patients and politicians would like available.
The second point is obvious in that all patients with worrying symptoms would like to be seen promptly.
One stop and other rapid access services are popular with patients and score well on satisfaction surveys.
The third point is the most easily dealt with. The NHS plan is absolutely clear that cancer patients or
patients with suspicious symptoms must be seen quickly, whether or not evidence exists that this will
improve survival. Funding is currently available to allow the development of innovative cancer services
and cancer is at the moment the first priority for booked appointments.
Developing a QED service
Major differences in facilities and staffing in different hospitals make it difficult to advise on the exact
structure of a QED service for head and neck cancer symptoms.
The cancer network multidisciplinary head and neck team must approve and be part of the model.
The MDT should agree how patients are managed and treated by the most appropriate specialities.
A recent report in the British Medical Journal suggests the use of the collaborative improvement model to
enhance services and reduce delays in cancer treatment in the UK (17). National Service Framework
documents and NICE “improving outcomes in cancer” documents, specifically targeting head and neck
cancer, should be published in 2003 and are available on the internet (18,19).
A possible ‘gold standard’ model is described, providing an integrated service.
•
•
•
Plan to deliver at least one clinic each week (typical population covered 500,000)
At least 2 consultant head and neck surgeons and specialist registrars to allow for leave
Cytopathology service including technicians and consultant pathologists (within clinic)
67
•
•
•
•
Consultant radiologists providing ultrasound scanning of the neck, with guided FNA where necessary
(within clinic)
Central office receiving telephoned or faxed requests for appointments
Full documentation of both process and clinical details of the consultation, ultimately ‘real-time’ on
computer
Other members of the MDT as deemed appropriate: nurse specialist, speech therapist, dental
hygienist, to support the clinic.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
The NHS Cancer Plan. Department of Health, September 2000 (available at www.doh.gov.uk/cancer)
NHS Wales Quality Care and Clinical Excellence: Putting patients first. Welsh Office, Jan 1998 and HMSO (CM 3841)
The New NHS: modern: dependable (CM 3807) HMSO Dec 1997
The NHS Plan (CM 4818-I) HMSO July 2000
Your Guide to the NHS. Department of Health, February 2001 (available at www.nhs.uk/nhsguide)
Kendall M.J., Toescu V., Wallace D. QED: quick and early diagnosis.Lancet 1996; 348: 528-529.
Vowles R., Ghiacy S., Jefferis A. A clinic for the rapid processing of patients with neck masses.
Journal of Laryngology and Otology 1998; 112: 1061-1064.
Murray A., Stewart C., McGarry G., MacKenzie K. Patients with neck lumps: can they be managed in a ‘one-stop’ clinic
setting? Clinical Otolaryngology 2000; 25: 471-475.
Resouly A., Hope A. Thomas S. A rapid access husky voice clinic: useful in diagnosing laryngeal pathology. Journal of
Laryngology and Otology 2001; 115: 978-980.
Lancer J. and Jones A.S. Flexible fibreoptic rhinolaryngoscopy. Results of 338 consecutive examinations.
JLO 1985, 99: 771-773.
Wilson J. et al. The diagnostic value of fine needle aspiration cytology in the head and neck.
J R Coll Surg Edinb 1985, 30: 375-379.
NHS Cancer Care in England and Wales, National Service Framework Assessment Number 1 (Commission for Health
Improvement December 2001) (also at www.chi.nhs.uk/cancer/index.htm)
British Association of Otolaryngology – Head and Neck Surgery Consensus Document on the Management of Head and
Neck Cancer, Second Edition 2000
Referral guidelines for suspected cancer (available at www.doh.gov.uk/cancer)
Kishore A., Stewart C., McGarry G., MacKenzie K. One-stop neck lump clinic: phase 2 of audit. How are we doing?
Clinical Otolaryngology 2001;26: 495-497.
Vercelli M., Capocaccia R., Quaglia A., Casella C., Puppo A., Coebergh J., EUROCARE Working Group. Relative survival
in elderly cancer patients: evidence for health care inequalities.Critical Reviews in Oncology/Haematology 2000; 35:161179.
Kerr D., Bevan H., Gowland B., Penny J., Berwick D. Redesigning cancer care.
British Medical Journal 2002; 324: 164-166
NICE “Improving Outcomes in Cancer” series (available at www.doh.gov.uk/cancer)
National Service Frameworks (available at www.doh.gov.uk/nsf/cancer.htm)
Search Strategy for Chapter
Medline Search (1966 to present) using search terms: QED, rapid access, one stop, dysphonia, neck
lump, dysphagia, larynx, cancer, anxiety, diagnosis. Manual search of the index of JLO and Clin.Otol.
1996 to 2001. Review of government publications 1997 to 2001.
68
Section 3
Chapter 4
Quality Assurance
In April, 2001, the NHS sponsored a ‘proposal generating event’ in Harrogate consisting of
multidisciplinary groups from all over the UK working to determine what an ideal head and neck service
would look like. Since then, a team at NICE has been using this as a basis for new COG guidelines which
should include much that would be covered by this section in future years. However, at the time of
writing, the emergence of the COG document has been delayed until at least September 2003. Therefore,
we feel that the standards below are likely to remain relevant until the 4th Edition of this book in 2004.
Quality
This is a ‘degree of excellence’. The use of this term has different implications in different contexts. In
industry, it is associated with a philosophical viewpoint and the use of a wide range of tools and
techniques, not all of which are of use in the service sector. In the service sector, including health care,
quality assurance has moved from being an ill-defined process of assessing client satisfaction, to a
comprehensive and, where possible, quantitative process.
Standards
Standards are the cornerstone of quality assurance. They are precise and authoritative statements of the
criteria necessary to ensure that a process is fit for the purpose for which it is intended. Standards are
drawn up with the co-operation of and consensus, or general approval of, interested parties. They are
based on the consolidated results of science and experience, aimed at the promotion of optimum
community benefits and approved by a body recognised on a national (in this case, the BAO-HNS),
regional or international level. Standardisation is an activity to improve efficiency by bringing
consistency to services. In the present context, this could be seen as an attempt to reduce so called ‘postcode’
variation.
Standards
are
essential
for
audit,
bench-marking
and
accreditation/certification/designation of cancer centres.
In preparing this section on quality assurance, we do not seek to limit the judgement of individual
clinicians or teams in how to manage individual patients. Rather, we hope the standards provided will
form a common framework for the delivery of the head and neck care process and a mechanism for
continuous improvement, including providing evidence for better service provision by health authorities
and hospital Trusts.
Accreditation
The accreditation process is now widespread in head and neck cancer care, with each region (and
nationally, in Scotland) producing its own set of standards. Third-party accreditation has been used as part
of this process in some regions. It is hoped that the present standards (themselves subject to regular
review), will assist in the continuing audit and re-accreditation cycles in these regions, as well as assisting
those regions wishing to embark on such a process.
Derivation of standards
The quality section of the first edition of Effective Head and Neck Cancer Management (1998) was used
as the template. This was modified using recent research, as well as by comparison with other national
and regional standards. The most important modifier was the result of an extensive patient and carer
exercise. Where professional and patient/carer standards disagreed significantly, the patient/carer
viewpoint has been taken as the default position.
69
References:
1.
2.
3.
4.
5.
Effective Head and Neck Cancer Management. 1st Ed. London; BAO-HNS, Royal College of Surgeons of England, 1998. This is the
first edition of the present document and used widespread national consensus within Otolaryngology.
Provision and quality assurance for head and neck cancer care in the United Kingdom: a nationally co-ordinated multidisciplinary
approach. Birmingham; The British Association of Head and Neck Oncologists, 1995. This is a concise multidisciplinary document
providing broad guidelines for practice.
Head and neck cancer : consensus standards for the process of care. Bristol; South and West Regional Cancer Organisation, 1997.
This regional document used an extensive formal multidisciplinary consensus process to define detailed standards for all parts of the
process of head and neck cancer care. Updating is overdue, however.
Birchall M, Richardson A, Lee L. Eliciting views of patients with head and neck cancer and carers on professionally derived standrads
for care. BMJ 2002 Mar 2;324 (7336):516
Referral guidelines for suspected cancer – consultation document. London, DoH. November, 1999. This, prepared with the help of
BAHNO, set out the “two-week wait” for high risk symptoms and patients.
MINIMUM TEMPORAL STANDARDS IN THE PROCESS OF HEAD AND NECK CANCER CARE
Interval
GP/GDP to first outpatients
clinic note to GP/GDP
Fine-needle or other biopsy arrival in pathology
time for frozen section result
biopsy to report issue
Patient to be seen in MHNC from being told of
diagnosis of cancer
general clinic to MHNC
MHNC to EUA/panendoscopy/dental/prosthetic
MHNC to radiotherapy, chemotherapy
(curative intent)
All patients notified of start and finishing dates of their
treatment
Radiotherapy start from planning
MHNC to radiotherapy, chemotherapy
(palliative intent)
MHNC to ablative surgery
Within radiotherapy/chemotherapy course
primary treatment to rehabilitation
(speech, swallowing, needs assessment)
treatment to first follow-up clinic
GP
GDP
MHNC
Standard
14 days
7 days
no wait
30 minutes for one, 45 for multiple
7 days
7 days
7 days
7 days
14 days to planning for radiotherapy
14 days to start chemotherapy
Within 48 hours
90% within one month
7 days to planning
14 days
as planned and documented
no delay
one month
= General Practitioner
= General Dental Practitioner
= Multidisciplinary head and neck clinic
STANDARDS FOR AUDIT AND ACCREDITATION
Activity
Task
Standard
All activities
co-ordination
100% of centres should have a named head and neck specialist responsible
for co-ordinating the local provision of care.
100% of centres should have a 100% specialist head and neck liaison nurse
(e.g. Macmillan), whose contact details should be provided to all patients at
the earliest opportunity in all cases.
100% of centres should have a list of consultants accredited to provide
head and neck cancer care at that centre
70
Communication
Issue referral letters
issuing of discharge
summaries
should arrive at hospital within 48 hours of dictation [e.g. fax]
Centres need a written protocol and or/checklist to include:
•
•
•
•
Information
documentation of
patient and carer
information
patient support
information
Pre treatment advice
Information
technology
BRIEF overview of the inpatient care received
name and contact details of head and neck specialist liaison nurse for
GP and patient/carers
diagnosis, procedures, complications, with dates
follow-up arrangements
100% of patient notes document what the patient and his/her carers have
been told about the diagnosis, prognosis and treatment
two leaflets available in 100% head and neck clinics and wards:
1. a general one on head and neck cancer; 2. a list of support
organisations (national and local), and details of where to get extra
information. One document on the list must be the current set of national
standards (in lay terms). Register of patients willing to visit should be
offered to all patients
100 patients should be given the opportunity to meet a previous patient who
has similar treatment (including radiotherapy). All specialist nurses should
keep a register of such persons locally.
100% centres have a computerised database containing the BAHNO
minimum data-set. 95% patients’ entries must be updated a minimum of
annually / until death
First hospital
outpatient visit
prioritisation
95% by a Consultant
consultation
90% with a consultant, the remainder to have a consultant available in
the building for advice
Interdisciplinary head
and neck clinic
time-tabling
These should be held weekly in each centre
consultation
100% with a consultant
100% with a 100% specialist head and neck liaison nurse (e.g. Macmillan)
environment
there should be no talking in the background during consultations
bad news should be broken in a manner consistent with King’s Fund
guidelines 100%*
staffing
Head and Neck specialist surgeon(s) with skills in endoscopy and dental
assessment 100%
Oncologist with a special interest in Head and Neck Oncology 100%
Plastic and Reconstructive surgeon 50%
Palliative care team representative 50%
Specialist head and neck nurse 100%
treatment planning
both a surgeon and an oncologist involved in the consultation and planning
in 100% of cases
the team should use a written protocol and a bench mark to manage coordinated care
the aim of treatment (cure/palliation) should be documented at the first
combined clinic in 80% of cases
the treatment plan should be communicated to the patient and carers
verbally, and to the GP in writing, within 3 days in 75% of cases.
80% of plans should include actual dates of admission and radiotherapy
patient selection
95% of all new head of neck cancer patients seen in a combined head and
neck clinic prior to treatment
71
Diagnosis and
staging
responsibility
95% of staging by a head and neck specialist whoever is responsible for the
initial diagnosis
TNM staging in 100% (includes TxNxMx)
examination under
anaesthesia
90% of all tumours
radiology
Primary Therapy
a standard imaging protocol should be applied by a radiologist with special
expertise in H & N
CT-scan of chest in 90% of cases prior to treatment planning
biopsy
100% of new cases require a histological diagnosis of cancer pre planning
fine-needle aspiration
biopsy
95% of neck masses and parotids
guidelines
Interpretation by a named cytologist with a head and neck interest
Agreed national guidelines should be adhered to
surgery
Skill standards should include clear surgical margins in radical [nonpalliative ] surgery in 95% of cases
oncology
Standards have still to be developed, but are expected to include:
- delay prior to onset of treatment
- treatment morbidity
- nutritional input / gastrostomy usage
- functional outcomes
30 day and 3 year relative survival to be recorded in 98% of patients
outcome
Follow up
panendoscopy 90% of all tumours
GP
GP’s should be faxed a typed discharge summary within 48hours of
discharge from hospital in 90% cases
Centres must have a named speech therapist with at least 25% of time
dedicated to head and neck cancer work and with specialist laryngectomy
skills
Videofluoroscopy must be available in all centres
Rehabilitation of
speech and
swallowing
staffing
Dental and
prosthodontic care
pre-treatment
assessment and
treatment
95% of patients with maxilla/orbital tumours
restorative/prosthetic team member before surgery
attention during
radiotherapy
at least 75% see a hygienist
scheduling
Monthly year one, tailing to annually by year 5
Follow-up
should
see
a
a dental practitioner and or hygienist should see 100% of patients
90% prescribed fluoride mouthwashes
At year 5, patients to be given the option of annual visits
Research and
audit
clinical trials
All centres should be encouraged to take part in national trials. A
comprehensive directory of local centre Network trial participation should
be available on–site.
Notification of and recruitment to clinical trials should take place as part of
the treatment-planning process, with the same 3-day standard.
clinical audit
There should be 100% participation in process and outcome audit, with at
least one active head and neck project at all times
Participation in national head and neck audit (e.g.Royal College of
Surgeons/Radiologists) in 100% of centres
The results of audit (local and national) should be published and made
available to purchasers [Cancer Commissioning Groups]
72
Palliative care
medicine *
hospital medical and
nursing staffing
all centres have written guidelines agreed with the local palliative care
consultant
100% of staff should know route of referral to palliative care (person, place,
method)
Breaking bad news
This should be done in accordance with Kings Fund guidance
crisis planning
100% of centres and hospices dealing with head and neck cancer patients
should have protocols for tracheostomy blockage and major vessel ‘blowout’ 90% of ward nurses should know the protocols
Patients at risk of these crises and their carers to be made aware of warning
signs 100%
living with cancer
notification of death
Patients and carers request that new standards be established to include:
-
contact with specialist nurses, clinical psychologists and support
groups
-
provision for returning to primary care as main source of support
-
financial and social support
For patients dying in hospital, the patient’s GP should be informed within
one working day in 100% of cases.
For patients dying at home or in a hospice, the patient’ s Consultant
should be informed of the date and location of death within 10 working days
in 80% of cases
* See:
Breaking Bad News: Guidelines and Patient Information Card. May, 1996. The King’s Fund, 11-13 Cavendish Square, London W1M
0AN. Tel.: 0171-307-2672.
73
Section 3
Chapter 5
Head and Neck Radiotherapy
Radiotherapy for head & neck cancer has, like most radiotherapy, traditionally been delivered in daily
fractions, five days a week. Fractionation practices vary considerably between UK centres, whereas the
majority of North American and European radiotherapy (and many British centres) have used single
fractions of 2Gy per day (for brevity, we can call this “conventional” fractionation). A number of clinical
trials in recent years have suggested that using more, smaller fractions, without reducing total dose
(hyperfractionation), and with some reduction in overall time (acceleration), or simply employing either
strategy, leads to better results than “conventional” fractionation1-3. At the same time (vide infra), results
from combining chemotherapy with “conventional” fractionation have also yielded benefits4. The strategy
of combining modified fractionation with chemotherapy, perhaps the next logical step, remains
inadequately tested, but “conventional” fractionation alone can no longer be regarded as “state of the art”
except, perhaps, for very early lesions.
Radiotherapy for head & neck cancer requires great precision and this must be reproduced daily for
several weeks. A complex process of immobilisation (usually using individually-made thermoplastic
shells) and imaging (usually CT, performed with the immobilisation device in place) is thus necessary as
a preliminary to the actual radiotherapy planning process, which in itself is quite time-consuming.
Technical advances in imaging, mechanics and computing have resulted in the real possibility of
improving radiotherapy techniques by more precisely defining which areas to irradiate, which to spare,
and to be able to achieve this with complex three-dimensional (“conformal”) planning. This is a rapidlyevolving field, one of the most exciting areas currently being the use of intensity-modulated radiotherapy
(“IMRT”), where the radiation fluence across an individual beam is actually varied during treatment.
Interstitial radiotherapy (the insertion of radioactive sources directly into tumours), also often referred to
as “brachytherapy”, is an effective form of treatment for small accessible tumours. Usually in treating
head & neck cancer it is performed using wires of iridium-192, which are left in place for approximately a
week. This entails significant risks of radiation exposure for staff, and comprehensive radiation
protection procedures must be rigorously enforced. Its place in relation to other forms of local treatment –
surgery or external beam radiotherapy – has however, never been properly assessed. A recent publication
of the Royal College of Radiologists advises that this treatment should only be performed in centres with
adequate volume of work5.
Radiotherapy is also a very effective treatment for palliation of certain symptoms in incurable patients,
notably bone pain associated with metastases, but the place of radiotherapy as a palliative measure for
incurable, locally-advanced disease is debatable.
Radiotherapy should be delivered in an accredited department. This will have undergone assessment
according to the national radiotherapy standards defined in the Manual of Cancer Services6
These ensure that radiotherapy services are of a high quality through:
1) Clearly defined leadership and organisational arrangements.
2) Provision of adequate professional staffing and equipment.
Treatment should be planned by a specialist Clinical Oncologist with access to a mould room, 3D
planning facilities, beam blocking techniques and portal imaging so as to ensure to geometric
accuracy and reproducibility of planning, with minimisation of dose to neighbouring normal but
radiosensitive structures.
74
3) Minimising delays for treatment and breaks in treatment. This is particularly important for
squamous head and neck cancer where unscheduled prolongation of overall treatment time
reduces the cure rate by at least 1% per extra day. Not more than 10% of radical courses
should be prolonged by unscheduled breaks. Where treatment gaps are unavoidable they
should be managed using the Royal College of Radiologist guidelines7.
4) Use of standardised processes for prescribing and checking radiotherapy treatments.
5) Use of standard principles for the delivery of radiotherapy.
6) Clear documentation of treatments delivered.
7) Quality assurance processes for radiotherapy treatments. An externally reviewed quality
assurance programme is likely to be in place to ensure that these principles are covered. An
example of this is ISO 9000:2002.
8) Implementation of protocols to minimise treatment toxicity. These should:
a) adequately inform patients of common toxicities.
b) ensure that dentate patients are assessed pre-radiotherapy by a restorative
dentist/hygienist.
c) ensure weekly review of all cases by clinician/specialist health care professional and
dietician.
9) Participation in network agreed clinical trials, especially those involving quality
assurance and peer review.
The Joint Council for Clinical Oncology recommended that for radical courses of radiotherapy the delay
from deciding to treat to the actual start of treatment should not exceed four weeks, and this
recommendation has been adopted by the Manual of Cancer Services6. To complete the preparatory work
and planning within this time scale is challenging, but must be the standard that radiotherapy strives to
achieve.
Some of the more pressing gaps in evidence-based knowledge in the field of head & neck cancer
are:
•
•
•
•
•
What are the relative roles of radiotherapy (including brachytherapy) and conservative surgery in the
management of early disease?
Can the strategies of chemoradiation and modified fractionation, both of which have been shown
independently to be superior to “conventional” fractionation alone, be combined?
In combining chemotherapy and radiotherapy, what are the best drugs, what is the best route (arterial
or venous), and what is the best scheduling of drugs in respect to radiation?
To what extent do the improved results obtained with altered fractionation and chemoradiation make
organ preserving strategies (i.e. non-surgical primary approaches to advanced disease) more widely
applicable?
Is radiotherapy useful as a palliative tool for incurable, locally-advanced disease, and if so, for which
patients?
75
References:
1. Horiot JC, Le Fur R, N’Guyen et al. Hyperfractionation versus conventional fractionation in oropharyngeal carcinoma: final
analysis of a randomized trial of the EORTC Co-operative Group for Radiotherapy. Radiother Oncol 1992; 25: 231-41.
2. Fu KK. Pajak TF. Trotti A et al.. A Radiation Therapy Oncology Group (RTOG) phase III randomized study to compare
hyperfractionation and two variants of accelerated fractionation to standard fractionation radiotherapy for head and neck
squamous cell carcinomas: first report of RTOG 9003. Intl J Radiat Oncol, Bioly, Phys. 2000; 48:7-16, 2000
3. Overgaard J, Alsner J, Erikson J, Horsman MR, Grau C. Department of experimental clinical oncology. Importance of
overall treatment time for the response to radiotherapy in patients with squamous cell carcinoma of the head and neck. 2000,
25:313-9.
4. Pignon JP, Bourhis J, Domenge C, Designé L. Chemotherapy added to locoregional treatment for head and neck squamouscell carcinoma: three meta-analyses of updated individual data. MACH-NC Collaborative Group. Meta-Analysis of
Chemotherapy on Head and Neck Cancer. Lancet 2000; 355: 949-55.
5. Royal College of Radiologists (2001) The Role and Development of Brachytherapy Services in the United Kingdom. London:
RCR.
6. Manual of Cancer Services NHS Executive 2001. www.doh.gov.uk/cancer
7. Royal College of Radiologists (1996) Guidelines for the Management of Unscheduled Interruption or Prolongation of a
radical Course of Radiotherapy. London: RCR.
76
Section 3
Chapter 6
Chemoradiation
Chemotherapy is likely to play an increasing role in the management of advanced head and neck cancer.
Three meta-analyses have shown that chemotherapy can improve survival when added to radiotherapy (13). The improvement is modest, and at the cost of increased acute toxicity.
What meta-analysis cannot identify is the “optimal” chemoradiation schedule. The combination of
cisplatin and fluorouracil is the most widely-accepted “standard” chemotherapy, but evidence to support
its use above other drugs or combinations is not conclusive.
The best timing of drug administration in relation to radiotherapy is also an unresolved issue.
Chemotherapy can be combined with surgery and radiotherapy in three main ways:I.
II.
III.
Neoadjuvant (induction) chemotherapy – given prior to radiotherapy or surgery. This improves
local control but does not have a significant effect on overall survival. It does however allow
greater organ preservation.
Concurrent chemoradiotherapy – only concurrent chemoradiotherapy has been shown to be
consistently associated with a significant survival advantage. The most recent meta-analysis
showed an 8% absolute survival benefit from chemotherapy (3).
Adjuvant chemotherapy – given after radiotherapy or surgery. This should only be given in the
context of a clinical trial for patients at very high risk of recurrence.
Although the trend is moving from neoadjuvant (induction) chemotherapy towards concurrent
chemoradiotherapy, delays in starting radiotherapy treatments in the UK at the moment mean that good
performance patients may benefit from both neoadjuvant and concurrent chemotherapy.
(a) LOCALLY ADVANCED UNRESECTABLE DISEASE
Four recently published randomised trials comparing concurrent chemoradiotherapy with radiotherapy
alone have shown significant differences in both loco-regional control and survival (4-7).
The absolute survival benefit was between 9% and 24% for chemoradiotherapy.
Concurrent chemoradiotherapy should be considered for good performance status patients with locally
advanced unresectable disease. Poor performance status patients should receive radiotherapy alone.
(b) LOCALLY ADVANCED RESECTABLE DISEASE
A recent study in advanced laryngeal cancer demonstrated that 88% of patients preserved their larynx at 2
years with concurrent chemoradiotherapy compared to 69% in patients treated with radiotherapy alone
(8). Another study in advanced oropharyngeal cancer reported a 20-25% absolute improvement in local
control and survival when chemotherapy was given concurrently with radiotherapy (9). Concurrent
chemoradiotherapy is an alternative for good performance status patients who would prefer to avoid
surgery in stage III and IV cancer of the larynx and oropharynx (10-12).
(c) NASOPHARYNGEAL CARCINOMA
Concurrent chemoradiotherapy has proved superior to radiotherapy alone for advanced disease (13). AlSarraf et al (14) demonstrated an increase in 5-year survival from 47% to 78% when chemotherapy was
added to radiotherapy.
77
(d) CHOICE OF REGIMEN
The choice of cytotoxic and the optimum regimen are not well-defined. The most commonly used drugs
are Cisplatin, 5-FU and Methotrexate. Recent very promising results have been seen with the addition of
newer drugs such as Taxanes to Cisplatin and 5-FU (15-19).
DELIVERING CHEMOTHERAPY
Chemotherapy should only be delivered by centres/units fulfilling the national chemotherapy standards.
These ensure that chemotherapy services are of a high quality through:
(1)
(2)
(3)
(4)
(5)
(6)
Clearly defined leadership and organisational arrangements.
Provision of dedicated and suitably equipped areas for the administration of chemotherapy.
Co-ordination and control over the use of specified chemotherapy regimens within a network.
Supervision of chemotherapy by appropriate specialists (clinicians and pharmacists)
Administration of chemotherapy by appropriately trained staff.
Use of guidelines for the prevention and treatment of side effects and implications of
chemotherapy.
Minimising delays in starting treatments.
Provision of facilities for aseptic reconstitution of cytotoxic agents.
Clear and comprehensive documentation of chemotherapy delivery.
(7)
(8)
(9)
Photodynamic Therapy
Requires the systemic administration or topical application of a photosensitizing agent, which is activated
by a specific wavelength of light related to the physical properties of the sensitizing agent.
The photosensitiser acts as a vehicle to allow the transfer of energy to produce highly reactive singlet
oxygen, which causes cellular damage and vascular shut down resulting in tissue necrosis.
Second generation systemic photosensitisers are highly efficient generators of singlet oxygen and can be
activated by simple to use computer controlled diode lasers. Light may be administered directly onto the
tumour surface where the degree of tissue penetrance is related to the wavelength of the administered
light. The longer the wavelength of light the greater the tissue penetrance. Red light of 652nm will
penetrate soft tissue reliably up to 1cm. Light may also be delivered to a tumour via interstitial methods
and accurate calculations of tumour necrosis made.
Photodynamic therapy may be used for management of low volume disease of the head and neck as well
as palliation of end stage disease.
Currently Photofrin and Foscan are licensed for photodynamic therapy for squamous cell carcinoma in the
head and neck.
References:
1.
2.
3.
4.
Munro AJ. An overview of randomised controlled trials of adjuvant chemotherapy in head and neck cancer. Br J
Cancer. 1995;71:83-91.
El-Sayed S, Nelson N. Adjuvant and adjunctive chemotherapy in the management of squamous cell carcinoma of the
head and neck region. A meta-analysis of prospective and randomised trials. J Clin Oncol. 1996;14:838-847.
Pignon JP, Bourhis J, Domenge C, Designe L, for the MACH-NC Collaborative Group. Chemotherapy added to
locoregional treatment for head and neck squamous cell carcinoma: three meta-analyses of updated individual data.
Lancet. 2000;355:949-955.
Merlano M, Benasso M, Corvo R, et al. Five-year update of a randomised trial of alternating radiotherapy and
chemotherapy compared with radiotherapy alone in treatment of unresectable squamous cell carcinoma of the head and
neck. J Natl Cancer Inst 1996;88:583-589.
78
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19
Adelstein DJ, Adams GL, Li Y, et al. A phase III comparison of standard radiation therapy (RT) versus RT plus
concurrent Cisplatin (DDP) versus split-course RT plus concurrent DDP and 5-fluorouracil (5FU) in patients with
unresectable squamous cell head and neck cancer (SCHNC): an Intergroup Study. Proc Am Soc Clin Oncol.
2000;19:411a. Abstract 1624.
Wendt TG, Grabenbauer GG, Rodel CM, et al. Simultaneous radiochemotherapy versus radiotherapy alone in
advanced head and neck cancer: a randomised multicenter study. J Clin Oncol. 1998;16:1318-1324.
Brizel DM, Albers ME, Fisher SR, et al. Hyperfractionated irradiation with or without concurrent chemotherapy for
locally advanced head and neck cancer. N Engl J Med. 1998;338:1798-1804.
Forastiere AA, Berkey B, Maor M, et al. Phase III trial to preserve the larynx: induction chemotherapy and
radiotherapy versus concomitant chemoradiotherapy versus radiotherapy alone, Intergroup trial R91-11. Proc Am Soc
Clin Oncol 2001;20:2a abstract.
Calais G, Alfonsi M, Bardet E, et al. Randomized trial of radiation therapy versus concomitant chemotherapy and
radiation therapy for advanced-stage oropharynx carcinoma. J Natl Cancer Inst. 1999;91:2081-2086.
Tobias JS, Ball D. Synchronous chemoradiation of squamous carcinoma: this has become the gold standard – whatever
the primary site. BMJ 2001 2001;322:676-7.
Lamont EB, Vokes EE. Chemotherapy in the management of squamous-cell carcinoma of the head and neck. Lancet
Oncology.2001;2:261-269.
Forastiere A, Koch W, Trotti A, et al. Head and Neck cancer. N Engl J Med 2001;345:1890-1900.
Chan AT, Teo PM, Ngan RK, et al. A phase III randomised trial comparing concurrent chemoradiotherapy with
radiotherapy alone in locoregionally advanced nasopharyngeal carcinoma. Proc A, Soc Clin Oncol. 2000;19:1637.
Al-Sarraf M, Pajak TF, Cooper JS, et al. Chemo-radiotherapy in patients with locally advanced nasopharyngeal
carcinoma: a Radiation Therapy Oncology Group study. J Clin Oncol. 1990;8:1342-1351.
Colevas AD, Busse PM, Norris CM, et al. Induction chemotherapy with docetaxel, Cisplatin, fluorouracil, and
leucovorin for squamous cell carcinoma of the head and neck: a phase I/II trial. J Clin Oncol. 1998;16:1331-1339.
Colevas AD, Norris CM, Tishier RB, et al. Phase II trial of docetaxel, Cisplatin, fluorouracil, and leucovorin as
induction for squamous cell carcinoma of the head and neck. J Clin Oncol. 1999;17:3505-3511.
Posner MR, Glisson B, Frenette G, et al. Multicenter phase I-II trial of docetaxel, Cisplatin and Fluorouracil Induction
Chemotherapy for patients with locally advanced squamous cell cancer of the head and nec. J Clin Oncol.
2001;19:1096-1104.
Boote D, Mellor T, Resouly A, et al. Neoadjuvant docetaxel, Cisplatin and 5FU followed by radiotherapy for locally
advanced carcinoma of the head and neck. The first European conference of head and neck cancer. 2001;abstract.
Gibson BS, Murphy BA, Frenchette G, Khuri FR, Farastiere AA. Phase II Trial of docetaxel
cisplatin carbination chemotherapy in patients with squamous cell carcinoma of the head and neck. J Clin Oncol 2002
20:1593-9
79
4
BEYOND PRIMARY TREATMENT
Chapter 1 Quality of Life Assessment
The evaluation of the quality of life (QOL) in people with head and neck cancer is integral to best patient
care (1). Survival may be the initial primary concern of patients (2), (3) however after treatment there
tends to be a shift towards maintaining or improving their quality of life (4). Health-related quality of life
(HRQOL) is an important measure of outcome as different treatments sometimes can confer relatively
small gains in survival but at the cost of disrupting the most basic of human functions such as speech,
appearance, swallowing, chewing and social interaction.
Health-related quality of life will be considered in the following sections:
1.
2.
3.
4.
5.
6.
What is quality of life?
Why should we measure quality of life?
Who should measure quality of life?
How should it be measured?
When should it be measured?
What are the key issues?
WHAT IS QUALITY OF LIFE?
The available literature supports the difficulty in defining and measuring quality of life. (5), (6) It is a
broad concept that incorporates all aspects of an individual’s existence. Aaronson et al describe QOL as
essentially having four core dimensions functional status, physical complaints (such as symptoms of
disease), psychological distress, and social interaction. (7) The term ‘health-related quality of life’ is more
focused and points to those aspects of life that are affected by healthcare interventions. (8).
WHY SHOULD WE MEASURE QUALITY OF LIFE?
The inclusion of ‘quality of life’ into treatment planning and appraisal has many potential benefits. It
encourages multidisciplinary team working, helps identify poor outcome groups, gives better information
for the patient and their carers and the opportunity to identify problem areas and so target support and
intervention. (9).
When two methods of treatment produce equivalent cure rates one of the major factors determining which
treatment should be chosen is the post-treatment quality of life. The principle of HRQOL measurement
forms part of the national head and neck advisory datasets. (The British Association of Head and Neck
Oncologists and the British Association of Otorhinolaryngologists Head Neck Surgeons).
WHO SHOULD MEASURE QUALITY OF LIFE?
The literature supports the view that HRQOL should be recorded from the patient’s individual
perspective. There are significant differences when health care professionals rather than patients measure
quality of life (10). The simplest way to measure HRQOL is by patient self-completed questionnaire
although other methods include open and semi-structured interview. One member of the multidisciplinary team should have clear and agreed responsibility to collect HRQOL data.
The results for an individual and for groups of patients should be communicated to the rest of the team in
order for appropriate action to be taken such as psychosocial support, treatment for depression and the
adjustment of treatment protocols. An interesting development is the inclusion of the patients rating of the
‘most important’ domains (11).
80
It may be that the combination of changes in individual domain scores linked with the importance rating
will serve to highlight the complex functional alterations that occur with treatment and provide an
indication for targeted therapeutic interventions.
HOW SHOULD IT BE MEASURED?
Questionnaires give a structured insight into the patients’ perspective. The choice of questionnaire
depends on many factors including the aim of the study, its design and the available resources. If the
measure is for patient self-completion it needs to be easily understood and take less than 10 minutes to
complete (12). A different questionnaire would be appropriate to use in routine practice as a basic
indicator of HRQOL as compared to that in a research setting. Although there are at least 14 validated
head and neck questionnaires most workers in this field recognise that there is no one instrument ideal for
all purposes (13), (8).They are each different in style and content and should be selected after consultation
with the multi-disciplinary team so that a consensus is reached. If the intention is for data to be compared
with other units or nationally it is important that there is a common questionnaire in use.
The questionnaires most commonly in use are:
University of Washington Head and Neck cancer Questionnaire (UW-QOL)
The UW-QOL has undergone three major revisions since it was first published. In version 2, an
importance-rating scale was added. In version 3 two new domains (taste, saliva) were added and the
employment domain dropped and in the latest version mood and anxiety has been included. There is no
charge for use and it is in the published domain.
The questionnaire is available at the University of Washington website.
(www.depts.washington.edu/soar/projects/dxcat/hnca/qol_uw.htm)
Postal address: Surgical Outcomes & Research (SOAR)
1660 South Columbian Way
HS 112 OTO
Seattle WA 98108
USA
European Organization for Research and Treatment of Cancer (EORTC)
This is a modular approach with assessment of generic aspects of QOL (30 questions) and a module
specific to head and neck (35 items). Both the QLQ-C30 and the QLQ-H&N35 are copyrighted
instruments and require the completion of a User's Agreement form. There is no charge for academic use
but if the study is sponsored there is a royalty fee.
Further information is available at the following web address: www.eortc.be/home/qol/
Postal address: EORTC Data Centre
QOL Unit, Ave. E. Mounier 83, B-11
1200 Brussels, Belgium
Functional Assessment of Chronic Illness Therapy (FACIT)
The FACIT scales are modular with the general version (FACT-G, 27 questions) used with patients of
any tumour type and a head and neck cancer component (FACT-H&N, 11 questions).
Translations in a range of languages are available. All collaborators must complete a collaborators’
project information form prior to use of any FACIT scales. There is no charge.
Further information is available at the following web address: www.facit.org/facit_questionnair.htm
81
Postal address: Kimberley A Webster
Director of Communications
Center on Outcomes, Research & Education (CORE)
1001 University Place, Suite 100
Evanston, IL 60201
USA
WHEN SHOULD IT BE MEASURED?
Questionnaires can be administered as part of either a cross sectional or longitudinal study.
Longitudinal data from pre-treatment has the distinct advantage of allowing the measurement of change
and also recording HRQOL during the different phases of treatment. The HRQOL at baseline gives an
indication of outcome in different clinic-demographic groups such as size of tumour, combine treatments
(surgery +/- adjvant radiotherapy) (14).
It is a logistical challenge to ensure patients self-complete questionnaires before treatment and at regular
intervals subsequently. However, prospective study allows for comparison over time for the same
individual and this can be used to trigger interventions. The poorest scores are seen at 3 months and 6
months following primary treatment (15), whilst HRQOL at 1 year gives an indication of long-term
outcome (16).
The frequency of data collection will depend on how the data is being used in clinical practice and the
resources available. It is recommended that where possible questionnaires are completed at pre-treatment,
6 months and 1 year.
WHAT ARE THE KEY ISSUES?
There are a large number of articles published each year reporting HRQOL in patients with head and
cancer. Key issues relate to tumour site, treatment options, and a variety of other HRQOL issues.
TUMOUR SITES
Published studies have demonstrated a difference in HRQOL profile between cancer sites. Generally the
worst groups are oropharynx and hypopharynx as many domains are affected. (15)(17), (18), (19), (20).
TREATMENT OPTIONS
There are very few studies that have attempted to compare surgery and radiotherapy in matched groups
(21), (22), (23) however in general HRQOL outcome has been found to be much better following single
modality treatment (24). Combined treatments involving both surgery and radiotherapy confer much
poorer HRQOL than single modality treatment. (15), (25), (26).
Some of the major themes are summarised in the list below and for brevity there are only two references
cited:
Coping
(27), (28)
Dental status (29), (30)
Disfigurement (31), (32)
Emotion
(33), (34)
Speech
(35), (36)
Oral Rehab
(37), (38)
Swallowing
(39), (40)
Shoulder
(41), (42)
Social support (43), (44)
82
CONCLUSION
To date very few centres in the UK are routinely measuring HRQOL in their caseload of patients either by
cross sectional or prospective study. The reasons are multifactorial and include the lack of guidance on
which measure to use, emphasis on other measures of outcome such as survival and complication rates,
time constraints and manpower restrictions. There is a need for clinicians to derive positive gain from
acquiring HRQOL data in order to inform clinical practice and have direct relevance to improving patient
care. It is only by overcoming these problems that progress can be made. The adoption of a common
questionnaire would allow for multicentre HRQOL data collection and facilitate both specific sub-site and
treatment analysis which is not possible with single site data collection.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
Weymuller,E.A., Jr.,Yueh, B.,Deleyiannis, F.W.,Kuntz, A.L.,Alsarraf, R.,& .era MD. Quality of life in head and neck
cancer, Laryngoscope, 2000 110: 4-7
List,M.A., Stracks, J.,Colangelo, L.,Butler, P.,Ganzenko, N.,Lundy, D., livan P, Haraf, D., Kies, M., Goodwin, W.,& Vokes,
E. E. How Do head and neck cancer patients prioritise treatment outcomes before initiating treatment?. J Clin Oncol 2000.
18: 877-884.
Sharp, H. M.,List, M., MacCracken, E., Stenson, K., Stocking, C.,& Siegler, M. Patients' priorities among treatment effects
in head and neck cancer: evaluation of a new assessment tool, Head & Neck 1999. 21:538-546.
Ware, J. E. Methodology in behavioural and psychosocial cancer research. Conceptualising disease impact and treatment
outcomes, Cancer 1984. 53:2316-2326.
Gotay, C. C. & Moore, T. D. Assessing quality of life in head and neck cancer. Quality of Life Research 1992. 1:5-17.
Gill, T. M. & Feinstein, A. R. A critical appraisal of the quality of quality-of-life measurements. JAMA 1994. 272:619-626.
Aaronson, N. K. Quality of life: what is it? How should it be measured? Oncology (Huntington) 1988. 2:69-76.
Ringash, J. & Bezjak, A. A structured review of quality of life instruments for head and neck cancer patients. Head & Neck
2001. 23:201-213.
Hammerlid, E., Persson, L. O., Sullivan, M., & Westin, T.Quality-of-life effects of psychosocial intervention in patients
with head and neck cancer. Otolaryngology - Head & Neck Surgery 1999. 120:507-516.
Mohide, E. A., Archibald, S. D., Tew, M., Young, J. E., & Haines, T. Postlaryngectomy quality-of-life dimensions identified
by patients and health care professionals. Am J Surg. 1992:64:619-622.
Rogers, S.N., Laher, S., Overend, L., Lowe, D. Domain importance-rating using the UW-QOL questionnaire in patients
treated by primary surgery for oral and oropharyngeal cancer. J Cranio-Maxillofacial Surgery (in press).
Sadura, A., Pater, J., Osoba, D., Levine, M., Palmer, M., & Bennett, K. Quality-of-life assessment: patient compliance with
questionnaire completion. J National Cancer Institute. 1992. 84:1023-1026.
Rogers, S. N., Fisher, S. E., & Woolgar, J. A. A review of quality of life assessment in oral cancer. Int J Oral &
Maxillofacial Surgery 1999. 28:99-117.
Rogers, S. N., Lowe, D., Humphris, G. Distinct patient groups in oral cancer? A prospective study of perceived health status
following primary surgery, Oral Oncology. 2000. 36:529-538.
Rogers, S. N., Lowe, D., Brown, J. S., & Vaughan, E. D. The University of Washington head and neck cancer measure as a
predictor of outcome following primary surgery for oral cancer. Head & Neck. 1999. 21:394-401.
Rogers, S. N., Hannah, L., Lowe, D., & Magennis, P. Quality of life 5-10 years after primary surgery for oral and oropharyngeal cancer. J Cranio-Maxillo-Facial Surgery. 1999. 27:187-191.
DeSanto, L. W., Olsen, K. D., Perry, W. C., Rohe, D. E., & Keith, R. L. Quality of life after surgical treatment of cancer of
the larynx. Annals of Otology, Rhinology & Laryngology. 1995. 104:763-769.
de Graeff, A., de Leeuw, J. R., Ros, W. J., Hordijk, G. J., Blijham, G. H., & Winnubst, J. A prospective study on quality of
life of patients with cancer of the oral cavity or oropharynx treated with surgery with or without radiotherapy. Oral
Oncology. 1999. 35: 27-32.
Bjordal, K., de Graeff, A., Fayers, P. M., et al. S. A 12 country field study of the EORTC QLQ-C30 (version 3.0) and the
head and neck cancer specific module (EORTC QLQ-H&N35) in head and neck patients. EORTC Quality of Life Group.
European Journal of Cancer 2000. 36:1796-1807.
Weymuller, E. A., Yueh, B., Deleyiannis, F. W., Kuntz, A. L., Alsarraf, R., & .MD. Quality of life in patients with head and
neck cancer: lessons learned from 549 prospectively evaluated patients. Archives of Otolaryngology -- Head & Neck
Surgery. 2000. 126:329-335.
Harrison, L. B., Zelefsky, M. J., Armstrong, J. G., Carper, E., Gaynor, J. J., & Sessions, R. B. Performance status after
treatment for squamous cell cancer of the base of tongue--a comparison of primary radiation therapy versus primary surgery.
International Journal of Radiation Oncology, Biology, Physics. 1994. 30:953-957.
Deleyiannis, F. W., Weymuller, E. A., Jr., Coltrera, M. D., & Futran, N.Quality of life after laryngectomy: are functional
disabilities important? Head & Neck. 1999. 21:319-324.
Moore, G. J., Parsons, J. T., & Mendenhall, W. M. Quality of life outcomes after primary radiotherapy for squamous cell
carcinoma of the base of tongue. International Journal of Radiation Oncology, Biology, Physics. 1996. 36:351-354.
83
24. Succo G., Bramardi F., Airoldi M., Gabriele P., Riva F., Moletto M., Rosso S., Caiazzo A., Sartoris A. 1997 “QOL after
treatment in patients with laryngeal carcinoma” Acta Otorhinolaryngologica Italica 17 32-44.
25. List, M. A., Ritter-Sterr, C. A., Baker, T. M., Colangelo, L. A., Matz, G., Pauloski, B., & Logemann, J. A. Longitudinal
assessment of quality of life in laryngeal cancer patients. Head & Neck 1996. 18:1-10.
26. Terrell J.,Fisher SG.,Wolf GT. Long Term QOL after treatment of laryngeal cancer. Arch Otolaryngol & Head & Neck
Surgery. 1996. 12:964-971
27. Owen, C., Watkinson JC., Pracy, P., Glaholm J. The psychosocial impact of head & neck cancer. Clinical Otolaryngol.
26:351-6
28. De Boer, M. F., McCormick, L. K., Pruyn, J. F., Ryckman, R. M., & van den Borne, B. W. Physical and psychosocial
correlates of head and neck cancer: a review of the literature. Otolaryngology - Head & Neck Surgery. 1999. 120:427-436.
29. Beeken, L. & Calman, F. A return to "normal eating" after curative treatment for oral cancer. What are the long-term
prospects? European Journal of Cancer. 1994. Part B, Oral Oncology. 30B:387-392.
30. Allison, P. J., Locker, D., & Feine, J. S. The relationship between dental status and health-related quality of life in upper
aerodigestive tract cancer patients. Oral Oncology. 1999. 35:138-143.
31. Dropkin, M. J. Body image and quality of life after head and neck cancer surgery. Cancer Practice. 1999. 7:309-313.
32. Katz, M. R., Irish, J. C., Devins, G. M., Rodin, G. M., & Gullane, P. J. Reliability and validity of an observer-rated
disfigurement scale for head and neck cancer patients. Head & Neck. 2000. 22:132-141.
33. de Leeuw, J. R., de Graeff, A., Ros, W. J., Blijham, G. H., Hordijk, G. J., & Winnubst, J. Prediction of depression 6 months
to 3 years after treatment of head and neck cancer. 2001. Head & Neck. 23: 892-898.
34. de Graeff, A., de Leeuw, J. R., Ros, W. J., Hordijk, G. J., Blijham, G. H., & Winnubst, J. Pretreatment factors predicting
quality of life after treatment for head and neck cancer. Head & Neck. 2000. 22:398-407.
35. Karnell, L. H., Funk, G. F., & Hoffman, H. T. Assessing head and neck cancer patient outcome domains. Head & Neck.
2000. 22:6-11.
36. Schliephake, H., Schmelzeisen, R., Schonweiler, R., Schneller, T., & Henbernd, C. Speech, deglutition and life quality after
intraoral tumour resection. A prospective study. International Journal of Oral & Maxillofacial Surgery. 1998. 27:99-105.
37. Moroi, H. H., Okimoto, K., & Terada, Y.The effect of an oral prosthesis on the quality of life for head and neck cancer
patients. Journal of Oral Rehabilitation. 1999. 26:265-273.
38. Rogers, S. N., McNally, D., Mahmoud, M., Chan, M. F., & Humphris, G. M. Psychologic response of the edentulous patient
after primary surgery for oral cancer: A cross-sectional study. Journal of Prosthetic Dentistry. 1999. 82:317-321.
39. Harrison, L. B., Zelefsky, M. J., Pfister, D. G., Carper, E., Raben, A., Kraus, D. H. Detailed quality of life assessment in
patients treated with primary radiotherapy for squamous cell cancer of the base of the tongue. Head & Neck. 1997. 19:169175.
40. Logemann, J. A., Pauloski, B. R., Rademaker, A. W., & Colangelo, L. A. Speech and swallowing rehabilitation for head and
neck cancer patients. Oncology (Huntington). 1997. 11:651-656.
41. Kuntz, A. L. & Weymuller, E. A., Jr. Impact of neck dissection on quality of life. Laryngoscope. 1999. 109:1334-1338.
42. Terrell, J. E., Welsh, D. E., Bradford, C. R., Chepeha, D. B., Esclamado, R. M., .N ND, & Wolf, G. T. Pain, quality of life,
and spinal accessory nerve status after neck dissection. Laryngoscope. 2000. 110:620-626.
43. Herranz, J. & Gavilan, J. Psychosocial adjustment after laryngeal cancer surgery. Annals of Otology, Rhinology &
Laryngology. 1999. 108:990-997.
44. Stam ,H., Koopmans, J., Mathieson, C. The psychosocial impact of laryngectomy: a comprehensive assessment. Journal
Psych. Soc. Oncol. 1991. 9:37-58
84
Section 4
Chapter 2
Rehabilitation of Speech and Swallowing
INTRODUCTION
There have been major advances in speech, swallowing and voice rehabilitation for patients with head and
neck cancer in recent years (1-5). Effective rehabilitation allows the patient to minimise the disability of
the surgical and or radiotherapy/chemoradiation treatment by finding alternative or compensatory
strategies. Speech, swallowing and voice rehabilitation should be available to patients with head and
neck cancer. Rehabilitation should be team orientated, with the specialist speech and language therapist
assigned the key worker role, in these aspects of head and neck cancer care.
Active rehabilitation should aim to:
•
assess and manage speech and swallowing difficulties, ensuring treatment is specifically aimed at
maximising residual function and introducing compensatory strategies where appropriate
•
facilitate neuromuscular recovery wherever possible (i.e. post-radiotherapy)
•
provide compensatory aids to assist or replace function
•
teach patients and carers how to manage speech/voice/swallowing difficulties within the realistic
confines of their disability
•
help the patient and their carers to cope with the consequences of a major life-changing situation.
•
help the patient and their immediate family/carer to adjust to the huge changes from their pre-morbid
function, and where realistic assist in restoring as much of the pre-morbid lifestyle as possible
•
promote choice and autonomy in partnership with patients and carers
Service Delivery
•
The lead specialist speech and language therapist in head and neck cancer should be highly skilled,
have significant clinical experience in the field and have appropriate post graduate training. The
specialist speech & language therapist should be responsible for setting standards, devising local
policies and developing pathways of care. The therapist will adhere to Clinical Guidelines in Head &
Neck Cancer published by the Royal College of Speech & Language Therapists (RCSLT).
•
Appropriate staffing levels are essential to delivering a quality rehabilitation service that allows for
intensive therapy, multidisciplinary liaison, audit etc. (1-6).
•
Speech and language therapists working in the field, will participate in peer review to ensure best
practice and adherence to guidelines. This may be done locally or regionally.
•
In cases of transfer to local speech and language therapy services the clinician should have an
adequate level of skill and access to specialist advice and training.
Communication should be two-way with close liaison to ensure continuity of care within the extended
MDT. Discussion of this complex issue is beyond the scope of this document (see future directives
section at the end of this chapter).
•
Time and funding should be made available for the continuing professional development.
85
•
There should be an active teaching and training policy within the Unit to achieve a cohesive
multidisciplinary approach. This continuing education programme should be available to all members
of the team and they should be familiar with how to access it.
•
There should be a commitment from speech and language therapy to training non- specialist speech
and language therapists and other health professionals in the community.
RESOURCES
•
Sufficient funding should be available for all communication aids, SVR and swallowing equipment
prescribed by the speech and language therapist.
•
The specialist speech & language therapist will have adequate access to equipment and expertise for
the assessment of speech, voice & swallowing e.g. Fibreoptic Evaluation of Swallowing,
Videofluroscopy. (7, 8, 9, 10).
•
Tracheostoma valves should be offered to all laryngectomy patients who undergo SVR and are
assessed as suitable candidates. A choice of tracheostoma valves should be available.
THE REHABILITATION PROCESS
a. Pre-treatment period
•
The speech and language therapist should be present at the combined clinic treatment planning
meeting in order to discuss rehabilitation issues. All patients who are likely to experience significant
speech swallowing/voice problems should be seen by speech and language therapy.
•
The speech & language therapist requires information regarding the extent of the resection as this
may be correlated to the extent of speech, voice & swallowing impairment (11, 12, 13, 14, 15, 16)
The nature of the surgical reconstruction may also affect the patient’s functional ability
postoperatively (12,17).
•
The aims of the initial appointments are to:
1 . Carry out appropriate assessments of speech, swallowing and voice within a psychosocial
context.
2. Provide information on speech, swallowing and voice to the patient/carer.
3 . Specific communication needs should be taken into account, e.g. people with literacy/visual
problems will have access to video/audio information.
•
Where ever possible realistic aims and goals are discussed with the patient and family.
b. Early post-treatment period
•
All patients require a post-treatment re-evaluation of baseline rehabilitation needs – e.g. swallowing,
voice and speech status.
•
In the surgically treated patient, speech and language therapy begins when the surgeon indicates that
the patient’s healing has progressed to the point where there is no danger to the suture lines.
•
It is important to recognise that the rehabilitation options should be tailored to meet the needs of the
patient
86
•
This stage is often the optimum time for speech & language therapists to direct swallowing
management techniques and range of motion exercises in order to achieve the goal of re-establishing
safe oral feeding, or if this is not possible to determine whether a patient needs total or supplementary
non-oral feeding. (Ref. 15,18) Refer also to NICE Guidelines. These factors should be taken into
consideration when planning discharge and early discharge should be avoided at the cost of
compromising optimal swallowing and nutritional care.
•
Therapeutic work should be commenced prior to sutures healing e.g. work on intelligibility with
silent mouthing or work with carers and patients to assist them in coping with the frustration of
communication breakdown.
c. In-patient discharge
•
Discharge is potentially the most difficult time for the patient (6). Discharge should be planned and
agreed by all members of the rehabilitation team. Care should be made to prepare the patients for
discharge and appropriate support networks should be in place.
•
The timing of the discharge should be made known to all the relevant parties (i.e. GP. Social worker
etc).
•
There should be liaison between the rehabilitation team with Community staff and Support Services
including Hospice care, to ensure a seamless continuity of care (2).
•
The patient should be quite clear of how and where to get further advice before the follow-up visit.
•
or patients whose long term communication remains poor, family members may find lip reading skills
and training helpful. Consideration should be given to methods of telephone communication,
summoning emergency aid etc.
d. On going care
•
Out patient therapy will be tailored to patient’s individual need.
•
The specialist speech & language therapist will be aware of the potential side affects (temporary and
chronic) from radiation and chemoradiation treatments for head & neck cancer.
The speech & language therapist and patient will remain in contact throughout the period of treatment
and thereafter. If the patient suffers with side affects that prevent regular rehabilitation management,
progress needs to be monitored and active treatment reinstated as soon as the patient is able to comply
(19, 20, 21, 22).
•
The multidisciplinary and community team will be kept updated regarding the patient’s progress and
prognosis in therapy.
•
Patients should be made aware that there is open access after discharge and know how to re-refer.
87
SPECIFIC CONSIDERATIONS FOR LARYNGECTOMY PATIENTS
•
The surgeon and speech & language therapist should plan the most appropriate vocal rehabilitation oesophageal voice, the use of tracheo-oesophageal voice prosthesis, an artificial larynx or a
combination. It is important to respect the patient’s preference in the planning process.
•
The speech and language therapist should be the key worker with laryngectomy patients in terms of
rehabilitation of voice and swallowing and prosthesis selection. Nurses also have an important role,
especially in out of hours cover for patients with voice prostheses.
•
An active programme of surgical voice rehabilitation is essential in every centre where laryngectomy
is performed (1,3,7,8). Primary SVR, i.e. a puncture undertaken at the time of primary surgery is now
accepted as the gold standard for rehabilitation, if the patient is judged as a suitable candidate by both
the ENT Consultant and the Speech and Language Therapist (23, 24, 25,). Patients should only be
deselected for primary puncture when there are clear contraindications, these should be assessed by
both the ENT Consultant and Speech and Language Therapist.
•
Considerable expertise is required from both the surgeon and speech and language therapist to
provide a SVR service appropriately and there should be a commitment to continuing education and
clinical audit.
•
A choice of indwelling and exdwelling valves and valve brands should be offered at all units in order
that valve selection can be tailored to patient’s needs and preference. Only a small number of studies
have been carried out comparing voice prostheses and their pros and cons. Further studies are needed
(26, 27).
•
A 24-hour SVR service is essential for all units, as urgent problems with valves are inevitable. A
rolling training programme should be offered for ward nurses and junior medical staff as they are first
in line for out of hours emergencies.
•
All units should have access to videofluoroscopy with audio recording to assess pe segment function.
This may be in house or as a tertiary referral. This should include access to botulinum toxin injections
under videofluoroscopic guidance to treat spasm or marked hypertonicity of the p-e segment (28, 29).
•
Primary myotomy or neurectomy is recommended as a routine part of surgery to maximise the chance
of successful voice outcome.
This includes patients deselected for SVR as it creates optimal conditions for the
oesophageal voice (30).
acquisition of functional
•
Manometry (to measure tracheal air pressure) should be available to assess patient suitability for a
“hands free” tracheostoma valve and to train patients to minimise back pressure when voicing with
this type of valve (31).
•
Patients should be retained on an inactive caseload once routine rehabilitation and review ceases.
SVR patients should attend for annual review. Electrolarynx and communication aid users should
return their aid for an annual safety check to be carried out by the electronics department at each unit.
88
Specific Considerations for Tumours of the Oral / Oropharynx and Laryngeal
Conservation Treatment
•
The precise functional effects of the treatment are generally difficult to predict generally cannot be
provided in detail for the individual during preoperative counselling.
Counselling focuses on informing the individual that there are likely to be changes in speech and
swallowing after treatment. (15, 33). Patients are informed about the rehabilitation process and that
it will be their responsibility to practise and follow rehabilitation strategies.
•
A multi-disciplinary team discussion regarding alternative/augmentative feeding is required when
patients are anticipated to have considerable problems maintaining adequate oral intake either
because of the tumour or the expected outcome of their treatment (34).
•
There is evidence to demonstrate the benefits of speech & language therapy interventions to improve
function for both speech and swallowing post radiotherapy (15). Currently there is under resourcing
of specialist speech & language therapy services nationally, with particular limitations in radiotherapy
units.
•
Therapy continues until a patients swallow has reached a point where the speech & language therapist
and the patient agree that maximum goals have been attained. Often the ultimate functional outcome
cannot be determined until several months post treatment and then involves discussions between the
various members of the team seeing the patient (15).
SPECIFIC CONSIDERATIONS FOR PALLIATIVE CARE
Orally feeding the dysphagic patient at the end stage of life
The Speech and Language Therapist has a role in ensuring that appropriate information is given about the
choices and risks facing dysphagic patients on their caseload, who may wish to continue orally feeding in
the end stage of life. Decision making and reviews should be made in the context of the Multidisciplinary
Team. In terminal care this team could be the Cancer Centre Multidisciplinary Team, community
GP/Macmillan Nursing team, or hospice team. Community Speech and Language Therapists should agree
shared goals with their Primary care team, and have access to cancer centre specialist Speech and
Language Therapists, if necessary, for support and advice where shared care, or onward referral has taken
place. More consensus needs to be reached by Royal College of Speech & Language Therapists on this
issue.
OUTCOME MEASURES
Currently there is no guidance or agreement nationally, regarding which parameters should be measured
for both clinical or research purposes, or indeed, who should be collecting the data and at what time
intervals. Many units do not have adequate speech & language therapy staff to enable them to collect
outcomes routinely, even for clinical practice. A number of the quality of life tools such as the SF36,
Washington and EORTC also include measurements of some of these parameters and this section should
be read in conjunction with the quality of life chapter. In addition to these tools there is a widely known
speech & language therapy outcome measurement package – the Enderby Therapy Outcome Measures
(TOMS) (35) which rate Impairment, Handicap, Disability and Distress. There are sections for dysarthria,
dysphonia, dysphagia and laryngectomy. A number of clinicians are also using outcome measurement
packages that have been devised locally or that are not specifically designed for head and neck cancer.
Others may be using modified versions of standardised tools, which affects the validity of any
information collected. There are currently no assessments for dysphagia post- laryngectomy or consensus
on a “normal” versus disordered swallowing after this type of surgery.
89
This is one of many areas that require more research to develop evidence based practice. A range of
speech, laryngeal voice, alaryngeal voice and swallowing parameters, and perceptual and instrumental
tools used to measure them are listed below:
Speech
Parameters
Speech intelligibility
Range, Strength,
accuracy of articulation
Laryngeal voice
Parameters
Voice quality
Perceptual measures
Instrumental measures
Assessment of Intelligibility of Dysarthric Spectography
Speech
SF 36
Frenchay Dysarthia Assessment
Spectography
Electro-palatography
Perceptual measures
GRBAS
Vocal Profile Analysis
Buffalo
Instrumental measures
Acoustic analysis
Laryngograph
Patient ratings of
function / acceptability
SF 36
Vocal handicap Index
Patient questionnaire of vocal performance
Laryngeal function
Fibreoptic profiles
Stroboscopy profiles
Laryngeal voice
Parameters
Voice
quality / intelligibility
Perceptual measures
Wepman
Semantic 7 point scale
Patient ratings of
Function / acceptability
Vocal handicap Index
Acceptability ratings
Instrumental measures
Spectrography
P.E. Segment function
Swallowing
Parameters
Videofluoroscopy
Manometry
Perceptual measures
Instrumental measures
Swallowing
Function
Penetration-Aspiration Scale
Videofluoroscopy
(VFSS)
Fibreoptic Endoscopic
Evaluation of Swallow
Study (FEES)
Patient ratings of
Function/ acceptability
SWAL-QOL
A full reference list is available from Speech and Language Therapy Departments at Sunderland Royal
Hospital or Freeman Road Hospital, Newcastle-upon-Tyne. Email: [email protected]
[email protected]
90
IDEAS FOR FUTURE DIRECTIONS
1. There is a need for collecting information concerning functional outcomes nationally for Head &
Neck Cancer patients. There needs to be more consensus regarding appropriate outcome
measures and methods of collection and analysis. This can be a time consuming process and can
only be achieved with adequate staffing. This information can be used for establishing best
practice.
2. There is a need for a national strategy for prioritising and coordinating a research and audit plan
in speech, voice and swallowing in head and neck cancer.
3. There are currently differences in levels of service provision and skill amongst non-specialist
SaLTs across the UK. The degree of responsibility for patient care differs according to local
agreement. As a profession we need to define skill level, competencies, guidelines for education
and training as outlined by the National Cancer Plan.
We also need a consensus on access to appropriate support, clinical supervision and peer review.
Roles, responsibilities and standards for provision of service between hospital-based specialist speech
and language therapists and non-specialist community-based therapists needs clarification. This will
require planning at a local and national level in keeping with RCSLT and NICE guidelines.
4. Patient and carer involvement should remain at the core of planning speech & language therapy
services.
Core References:
1.
2.
3.
4.
5.
6.
Casper JK and Colton R (1998) Clinical Manual for Laryngectomy and Head and Neck Rehabilitation. 2nd edition. Singular
Publishing Group Inc, San Diego, London. ISBN 1-56593-959-X.
Communicating Quality II (1997). Royal College of Speech and Language Therapists, London.
Blom ED, Singer MI and Hamaker RC (1998) Tracheosophageal Voice Restoration following Total Laryngectomy. Singular
Publishing Group Inc, San Diego, London ISBN 1-56593-908-5
Sullivan PA, Guilford AM (1999) Swallowing Intervention in Oncology. Singular Publishing Group Inc, San Diego,
London ISBN 1-56593-751-1
Appleton J and Machin J (1995) Working with Oral Cancer. Winslow Press, Bicester Oxon. ISBN 0-86388-129-7.
Edels Y (1983). Laryngectomy: Diagnosis to Rehabilitation. Croom Helm, London and Sydney. ISBN 0-7099-09071
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Logemann et al The impact of the diagnostic procedure on outcome measures of swallowing rehabilitation in head & neck
cancer patients. Dysphagia 1992;7:179-186
Humphreys B et al Videofluroscopic & scientigraphic analysis of dysphagia in the head & neck patient. Laryngoscope
1987;97:25-32
Logemann. Aspiration in head & neck surgical patients. Ann Otol Rhinol Laryngol 1985;94:373-376
Furia et al Videofluroscopic evaluation after glossectomy. Arch Otolaryngol Head and Neck Surgery 2000;126:378-383
Colango et al T Stage and Functional Outcome in Oral and Oropharyngeal Cancer patients. Head & Neck 1996;18:259-268
Pauloski BR, Logemann JA, Colangelo LA, Rademaker AW, McConnel FM, Heiser MA, Cardinale S, Shedd D, Stein D,
Beery Q, Myers E, Lewin J, Haxer M, Esclamado R. Surgical variables affecting speech in treated patients with oral and
oropharyngeal cancer. Laryngoscope. 1998 ;108(6):908-16
McConnel et al Surgical variables affecting postoperative swallowing efficiency in oral cancer patients: A pilot study
Laryngoscope;1994;104:87-90
Kronenberger & Meyers Dysphagia following head & neck surgery. Dysphagia 1994;9:236-244
Logemann J Evaluation and treatment of Swallowing Disorders 2nd edition. Austin, TX: Pro-ed; 1998
Hirano et al Dysphagia following various degrees of surgical resection for oral cancer. Ann Otol Rhinol Laryngol
1992;101:138-141
Brown J Zuydam A Jones D Rogers S Vaughan E. Functional Outcome in Soft Palate Reconstruction using a Radial
Forearm Free Flap in conjunction with a superiorly based Pharyngeal Flap. Head & Neck 1997;19:524-534
Logemann J. Pauloski B Rademaker A Colangelo L Speech & swallowing rehabilitation in head & neck cancer patients.
Oncology 1997;11:651-656
Hughes et al Dysphagia in treated nasopharyngeal cancer. Head & Neck 2000;22:393-397
91
14. Schliephake H, Schmelzeisen R, Schonweiler R, Schneller T, Altenbernd C. Speech, deglutition and life quality after
intraoral tumour resection. A prospective study. Int J Oral Maxillofac Surg. 1998 Apr;27:99-105.
15. Logemann J Smith C Pauloski B Rademaker A et al Effects of xerostomia on perception and performance of swallow
function. Head & Neck 2001;23:317-321
16. Lazarus C Logemann J Kahrilas P Mittal B Swallowing recovery in an oral cancer patient following surgery, radiotherapy
and hyperthermia. Head & Neck 1994;16:259-265
17. Yoshida, GY, Hamaker, R.C, Singer, M.I., Blom, E.D., and Charles, G.A. Primary voice restoration at laryngectomy: 1989
update. Laryngoscope 1989 99:1093-1095
18. Mahieu H.F. Secondary t-E puncture: A Method of second choice? Paper presented at 2nd EGFL conference 6th International
congress of Surgical and Prosthetic Voice Restoration after total laryngectomy, San Sebastien, Spain 1995
19. Freeman, SB, and Hamaker, M.D., Tracheoesophageal Voice Restoration at the time of Laryngectomy in
Tracheoesophageal voice restoration following Laryngectomy. Blom ED, Singer, M.D., 1998 Singular Publishing: San
Diego
20. Issing, W.J, Fuchshuber, S. and Wehner, M. Incidence of tracheo-oesophageal fistulas after primary voice rehabilitation
with the Provox or the Eska – Herrmann voice prosthesis. Eur Arch Otorhinolaryngol 2001 258:240-242
21. Delsupehe, K., Zink, I., Lejaegere, S.T., and Delaer, P. Prospective Randomized Comparative Study of Trachoeoesophageal
Voice Prosthesis: Blom-Singer versus Provox. Laryngoscope 1998 108:1561- 1565
22. Hoffman, H.T., and McCulloch, T.M., Botulinum Neurotoxin for Trachoeoesphageal Voice Failure in Tracheoesophageal
voice restoration following Laryngectomy. Blom, ED, Singer, M.D., 1998 Singular Publishing: San Diego
23. Lewin JS, Bishop-Leone JK, Forman, AD, and Diaz, EM. Further xxperience with botox injection for tracheoesophageal
speech failure. Head and Neck 2001 23:456-460
24. Hamaker, RC and Cheesman AD. Surgical Management of Pharyngeal Constrictor Muscle Hypertonicity in
Tracheoesophageal voice restoration following Laryngectomy. Blom, E.D., Singer, M.D., 1998 Singular Publishing: San
Diego
25. Blom ED. Tracheostoma Valve fitting and Instruction in Tracheoesophageal voice restoration following Laryngectomy..
Blom E.D., Singer, M.D., 1998 Singular Publishing: San Diego
26. Colango et al T Stage and Functional outcome in oral and Oropharyngeal cancer patients. Head & Neck 1996;18:259-268
27. McConnel et al Surgical variables affecting postoperative swallowing efficiency in oral cancer patients: A pilot study.
Laryngoscope;1994;104:87-90
28. Machin & Shaw A multidisciplinary approach to head & neck cancer. Eur J Cancer Care 1998;7:93-96
29. Enderby P and John A. Therapy Outcome Measures. Speech and Language Therapy. Singular. 1997
92
Section 4
Chapter 3
Nutritional Aspects
Introduction
The role of nutrition in both the amelioration and treatment of the head and neck cancer patient
has become increasingly recognised in recent years. Most of the data linking symptom control
and therapy have been largely epidemiological however recent advances in molecular biology
and genetics are now allowing a greater focus on “cause and effect”.1 It is possible that as many
as 80% of cancer cases may be lifestyle related. In this context diet, tobacco use and/or alcohol
consumption are likely to be significant risk factors in the development of head and neck cancer.
Advances in technology enhance the ability for earlier diagnosis and treatment with reduced morbidity.
In addition increased survival rates mean that patients are now living long enough for deleterious long
term effects of therapy to occur including the development of secondary malignancies. These present
new challenges in the provision of nutritional support and a greater understanding the pathophysiology of
cancer cachexia.
These patients, due to the position of tumours, are particularly susceptible to malnutrition and which if
untreated can progress to cachexia. Although the syndrome of cachexia results in a profound loss of both
adipose tissue and skeletal muscle mass, it is the latter which determines both the quality of life and
overall survival.
Nutrition has become an increasingly important quality of life issue surrounding the psychosocial and
rehabilitative needs of many head and neck cancer patients. Quality of appetite and the ability to eat are
often regarded as crucial components in patients’ definitions of their physical well-being and symptom
control.2 Nutrition should be considered an integral part of treatment irrespective of whether the
therapeutic intent is cure or palliation. It is essential to remember that intervention is likely to be of most
benefit and arguably most cost effective when concurrent clinical treatment is being undertaken. The
moribund patient is unlikely to benefit to any significant extent from nutritional support. Professional
carers “have a duty to prolong life, but not to inappropriately prolong dying”.3
Effects of Treatment on Nutritional Status
Surgery
Although multimodal treatment approaches have evolved and improved markedly over recent years
surgery remains the primary and often the only cure for some tumours. Any surgery results in varying
degrees of catabolic stress and increases the risk of compromising nutritional status. When surgery is
undertaken for non systemic pathological conditions in otherwise healthy, well nourished patients,
nutrition is usually not a risk factor, at least not in the immediate post-operative period. However when a
patient is malnourished and debilitated by an ongoing disease process, complications or associated
therapy nutritional status becomes a significant risk factor in clinical outcome.4
Even minor oropharyngeal surgery may lead to the development of impaired taste and smell and impaired
chewing and swallowing which can temporarily, or in some cases, permanently render patients unable to
maintain an adequate dietary intake.
The majority of patients undergoing a radical resection are likely to require enteral or occasional
parenteral nutrition certainly in the immediate post operative period and often for several weeks
thereafter.5 It is important to ensure that appropriate protocols are planned in advance and in place so that
the nutritional requirements of patients can be met to best effect.6
93
This will involve a co-ordinated interdisciplinary approach, otherwise there is a risk of patients being
overlooked, particularly in the current environment of shorter hospital admissions and out patient follow
up. Long term changes in nutritional requirements may be necessary as a result of surgery. Wound
healing and the integrity of grafts are markedly affected by nutritional status. This is an important
consideration in the rehabilitation process.7
While surgery for the purposes of reducing tumour bulk or the resection of metastatic disease does not in
itself present nutritional risks which are different from those for other similar surgical procedures;
nevertheless nutritional requirements will be affected to a certain extent. For example head and neck
surgery and its effects may lead to changes in activity levels and in body composition. Some patients will
expend increased levels of energy during rehabilitation and adaptation while others may become
relatively sedentary.
Additionally one of the main aims of reconstructive and rehabilitative head and neck surgery will
wherever possible be to restore the patient to normal or near normal oral function. Even if this is not
entirely possible any symptomatic relief will enhance a patient’s quality of life and significantly improve
the chances of an adequate nutritional intake being achieved. When food can be eaten normally the
psychological benefits of improved self-image are considerable.8
Radiotherapy
The negative effects of radiotherapy on nutritional status and oral feeding are well documented.9 These
can be ameliorated by establishing nutritional support at the beginning of (or preferably before)
irradiation. Early and ongoing nutritional support improves the chances of patients completing full
courses of therapy and may reduce morbidity in the head and neck group. 10,11
Much of the effect of radiotherapy on nutritional status is related to the location of the tumour which can
also determine the type and amount of radiation delivered (or possible).
Brachytherapy may result in local complications such as dysphagia and odynophagia particularly in the
oropharynx.
The effect of any radiation injury can be acute or chronic and generally depends on whether single or
cumulative doses are being administered. The common effects of radiotherapy and nutritional status in
head and neck cancer are listed in Table 1.
Table 1 - Effects of radiotherapy in the head & neck region on nutritional status
Oropharyngeal Irradiation
• Impaired taste and smell accompanied by food aversions
• Stomatitis
• Xerostomia
• Mucositis
• Trismus
• Dental caries
• Mandibular osteonecrosis
Oesophageal Irradiation
• Dysphagia
• Oesophagitis
• Oesophageal stricture
• Odynophagia
94
Xerostomia is usually the most immediate and lasting side effect of radiotherapy to the head and neck. It
can be induced by as little as 6-7 Gray (Gy) units given in two or three doses. If the parotid glands (or at
least one gland) can be spared during irradiation and parotid function preserved there is evidence to
suggest that xerostomia may be prevented or minimised; and that consequently oral intake and body
weight can be maintained particularly with early stage tumours.12
At a cumulative dose of about 20 Gy mucositis and loss of taste usually occur. At this stage oral intake
becomes not only mechanically difficult and painful but also pleasureless. Additional problems such as
alterations in the viscosity of saliva and in oral pH with an increased oral bacterial concentration may
predispose to a greater risk of dental caries. Any oesophageal involvement is likely to result in significant
dysphagia. 13
Chemotherapy
The gastrointestinal epithelium is particularly susceptible to the effects of chemotherapeutic agents.14
The most common and immediate side effects of chemotherapy are nausea, vomiting and anorexia. If
untreated this will lead inevitably to a decreased oral intake, fluid and electrolyte imbalances, general
malaise and weight loss. The level of toxicity of the chemotherapy depends on the agent used, the single
and cumulative doses, drug metabolism and excretion rates, other concurrent treatments and individual
patient tolerance. For example combined use of carboplatin and cisplatin in the treatment of head and
neck tumours presents a number of challenges in the nutritional management of patients. Although
carboplatin has a spectrum of activity similar to that of cisplatin it is less toxic and better tolerated with
reduced levels of nausea and vomiting and nephrotoxicity which may afford greater ability and desire to
achieve an enhanced nutritional intake.
Common side effects associated with cisplatin and 5-fluorouracil (5-FU) additionally include mucositis
and anaemia.
The side effects of newer chemotherapeutic drugs, such as taxanes and retinoids, on nutritional status
have yet to be fully established. 15, 16 However, it is likely that these will be similar to other agents and
will be dose related. Mucosal toxicity (particularly of the oral mucosa) stomatitis, ulceration, cheilosis,
glossitis and pharyngitis will all interfere with the ability to maintain an adequate oral intake.
Dehydration and malnutrition will often occur rapidly as a result.
Agents that induce transient xerostomia and acidification of the saliva may have implications on dental
health and consequently nutritional status.
Combined-Modality Therapy
Although chemotherapy appears to be most effective when it is administered concurrently with
radiotherapy it also exacerbates the radiation reaction. Adelstein et al have reported the concurrent use of
5-FU, cisplatin and radiation therapy in a study involving squamous cell head and neck cancer patients
resulted in a significant increase in the incidence of acute mucositis, tube feeding and greater weight
loss.17
Generally acute mucositis is significantly increased when more than one chemotherapeutic agent is used
in addition to radiotherapy.18
Radioprotective agents (e.g. amifostine), growth factors and cytokines which can reduce the toxicity of
combined modality therapy may play an important future role in ameliorating the side effects of treatment
which interfere with nutritional intake.
95
Practical aspects of nutrition in the head and neck cancer patient
Nutritional Assessment
It is essential for all head and neck cancer patients to undergo nutritional screening in order to identify
those individuals who have, or are at risk of developing malnutrition19 . There is, howeer, no single
anthropometric or biochemical marker that can identify the nutritional status of an individual20.
Head and Neck Cancer patients frequently will have already encountered periods of malnutrition prior to
Hospital admission21. Nutritional assessment is likely to be most effective if carried out by means of a
team approach.
Nutritional screening is the first step in the process of identifying those who would benefit from
specialised dietetic assessment. Screening may be carried out by nursing or medical staff and should be
conducted on admission, to facilitate early nutritional intervention. To date there is no valid screening
tool for cancer patients,22 however, there are a number of tools in use, mainly based on the Subjective
Global Assessment tool. Recent weight loss, dietary intake, body composition, anthropometry,
biochemical status and functional ability should all be considered. Any identified chewing and
swallowing problems must be taken into consideration in order that the most appropriate and effective
dietary programme is designed.
Patients who have unintentionally lost more than 10% of their weight in 6 months, or more than 5% in the
one month before admission to hospital are likely to be clinically at risk 20, 23. Early nutritional screening
and counselling from a Dietitian, are essential to provide nutritional support tailored to the patients'
needs24. This will improve the patient life outcome prospects.
Table 2 – Recommended energy & protein requirements
Energy
25-35 Kcal/Kg/24 hours
35-45 Kcal/Kg/24 hours
maintenance
repletion
Protein
0.8-1.2 g/Kg/24 hours
1.2-1.5 g/Kg /24 hours
maintenance
repletion
Table 3 – Recommended micronutrient requirements
Vitamins
A complete range of water and fat soluble vitamins
especially vitamin K, B1 and B6
Antioxidants (vitamins A, C and E)
Trace Elements
A complete range of trace elements
especially zinc and selenium
As previously stated many head and neck cancer patients have a poor nutritional state on the initial
presentation of their diagnosis, thus early assessment and nutritional support will aim to prevent further
weight loss and/or improve nutritional state.
Nutritional Monitoring
Monitoring is an essential step to ensuring the patient does not develop a compromised nutritional state,
contributing to outcome 25. Re-screening of patients on a weekly basis or on each admission as an inpatient is essential.
96
As part of the re-screening, patients should have their weight checked weekly, or on admission. Any
individual's weight which has decreased by more than 2 kg over a two week period must be re-referred to
the dietetic team.
The biochemical state must be closely monitored. This is especially important at the early states of enteral
feeding, where re-feeding syndrome may occur 21.
During the treatment, whether that is radiotherapy, chemotherapy or combined, it is vital to support the
patient nutritionally, allowing adaptation of nutritional advice depending on the side effects of the
treatment. This adaptation of advice should involve the following.
First line intervention:
meal fortification – allowing an increase in energy (Kcal) and protein through food consumption and
snacks.
Second line intervention:
the use of oral nutritional supplements.
Third line intervention:
non-oral feeding. This is ideally enteral feeding whether that is nasogastric feeding or gastrostomy
feeding.
Nutritional Management
Oral Nutritional Support
Where possible patients should be encouraged and laser assisted to take food orally.
As previously outlined, maintaining a normal eating pattern is important psychologically to both patients
and their carers.9
An early evaluation of current dietary intake should be undertaken. Any identified chewing and
swallowing problems must be taken into consideration in order that the most appropriate and effective
dietary programme is designed.
Nutritional Support
Nutritional support should achieve and maintain a desirable body weight within a targeted weight range
and correct or prevent nutritional deficiency. 19 It must be tailored to individual patient requirements.
Dysphagia
The primary aim in dysphagia management, once the underlying cause has been identified, is to utilise
strategies and postures to ensure patients can maintain an intake of as much of a normal food consistency
as possible. A full swallowing assessment should be carried out by a Speech and Language Therapist
who will determine the most appropriate food consistencies to use as part of ongoing therapy.
97
Table 4 – Clinical symptoms affecting oral intake
1.
Loss of teeth
2.
Dry mouth
3.
Poor dentition and caries
4.
Excess saliva
5.
Sore mouth (mucositis, oesophagitis)
6.
Food Disinterest and Aversion
7.
Anorexia
8.
Weight Loss
9.
Diarrhoea
10. Constipation
11. Aversion to Taste
12. Preference for Cold Foods
13. Nausea
14. Pain
15. Swallowing Difficulties
16. Fatigue
17.
Loneliness
Enteral Feeding
In situations where oral intake is inadequate or not possible enteral feeding should be considered without
undue delay, otherwise compromised nutritional status will rapidly occur. If it is envisaged that the
effects of surgery may lead to ongoing feeding difficulties careful planning of appropriate nutritional
management should be carried out preoperatively.
Nasogastric Feeding
In the short term (≤ 14 days) most patients requiring enteral nutrition will receive this by means of a
nasogastric tube. The choice of tube is likely to depend on individual circumstances, personal preference
and experience. Fine bore feeding tubes improve patient comfort and reduce tube associated
complications such as pharyngitis and oesophagitis.20 On the other hand wide bore tubes may facilitate
98
bolus as opposed to continuous feeding regimens and allow for easier administration of drugs if this is
necessary.
Although there is a perceived increased risk of pulmonary aspiration when wide bore tubes are used this
is not borne out in clinical practice.21 The risk of aspiration can be reduced by ensuring the patient is fed
in an upright position or at least having the head and shoulders raised by 30-40 degrees. In addition to
problems with mucosal erosion and nasopharyngeal irritation, the likelihood of tube displacement and the
resultant difficulties in replacement in the head and neck patient ultimately limit the nasogastric route as a
long term feeding option.
Gastrostomy 29-37
When enteral feeding is likely to be needed for periods of more than 14 days, there is an inability to
tolerate a naso-gastric tube or the tube itself is contraindicated due to the presence of an oesophageal
abnormality, the placement of a PEG tube should be considered. The assessment process, ideally carried
out by a specialist team, must also take into account the acceptability of the PEG to the patient and his/her
family and carers and the patient’s long term prognosis
The advantages of gastrostomy over prolonged NGT feeding are broadly speaking two-fold. It provides
the patient with a more socially acceptable facial appearance and it avoids problems caused by the NGT
itself. These include the impedance of swallowing rehabilitation, arytenoid oedema, aspiration, the
prolongation of radiation mucositis, sinonasal infection and discomfort.
There are three methods of gastrostomy tube placement:
1.
Percutaneous Endoscopic Gastrostomy (PEG). Using the usual "pull" technique, the endoscope is
used to introduce a pull cord into the stomach percutaneously. This is then used to pull the
PEG catheter perorally into the stomach and out percutaneously. Variations exist whereby the
PEG catheter is pushed out or the stomach directly punctured but all methods involve the
endoscope being passed through the upper aerodigestive tract.
2.
Percutaneous Fluoroscopic (or Radiologic) Gastrostomy. Under fluoroscopic control, a
guidewire and dilator is introduced directly into the stomach. Some methods involve gastropexy
using two or three T-fasteners. It is preferable to pass a nasogastric tube to use this method, but
this can be circumvented.
In the case of head and neck tumours the placement of a percutaneous radiological gastrostomy (PRG)
is preferred and recommended for two principal reasons. Firstly the radiological procedure does not
involve endoscopy which can be difficult due to access and secondly there is a high risk of transferring
tumour cells from the oral maxillary region to the stoma site which can then colonise in/or adjacent to the
stoma, if an endoscope is used.38 If an nasogastric tube is already in situ this can normally be used to
administer barium contrast (approx 200 ml) to aid radiological visualisation. Administration of a
prophylatic antibiotic regimen prior to the procedure is now standard practice in most units.39
In most cases full feeding using proprietary enteral feeds can be established within 24-48 hours post PRG
placement.
Surgical gastrostomy. This can be achieved either laparoscopically or by an open laparotomy under
general anaesthesia. It is usually reserved for failed percutaneous gastrostomy or in patients with a
contraindication to a percutaneous technique.
The clinical situations in which a gastrostomy should be considered are:
99
Surgical patients: patients in whom oral diet is not possible in the medium or long term because of postoperative dysphagia, aspiration, odonophagia or limited/painful mastication, particularly if post-operative
radiotherapy is planned.
A low threshold for gastrostomy should be maintained after open partial laryngeal/pharyngeal surgery
because its placement greatly assists swallowing rehabilitation and reduces the psychological pressure and
frustration by inferring that the expectation of its use is medium term. A further post-operative indication
is the development of a fistula necessitating a prolonged period of NBM.
Radiotherapy patients: patients due to have high intensity radiotherapy or chemo-radiotherapy for locally
advanced tumours are particularly likely to have swallowing difficulties, and patients who are likely to
need a gastostomy can be predicted by virtue of their tumour site, stage and comorbidities29. Ideally, such
patients should be identified before treatment so arrangements can be made for gastrostomy, in order to
avoid interruptions in radiotherapy or chemoradiotherapy30-31.
Palliation: gastrostomy placement is an integral component of a comprehensive palliative care package
for patients with no or little oral nutrition.
Minor complications of percutaneous gastrostomy tube placement occur both in the short and long term
and are relatively common (10-15%). These include skin leakage, wound infection, blockage or
dislodgment of tubes. It is essential for patients outside hospital to have liaison with a head and neck
nurse who can deal with long term minor complications, which usually necessitate a tube change. Major
complications include local complications such as peritonitis due to abdominal sepsis, visceral leakage,
tube misplacement or early dislodgment, gastric haemorrhage, major wound infection/dehiscence. Other
major complications include aspiration and cardio-pulmonary events during the procedure. In general
terms, most series report a major complication rate of 2-9% 32-35. The definition of a complication as
“major” is not fixed and accounts for some variation. The mortality due to the procedure is around 0.51%32-35
No matter whichever method is used and who the operator is (radiologist, gastroenterologist, general
surgeon, head and neck surgeon), agreed protocols and responsibilities need to developed to detect and
deal with complications that arise in hospital.
Areas of controversy:
Which method of gastrostomy?
Gastrostomy should be performed percutaneously where possible. The choice between radiologic and
endoscopic methods is determined by the following issues:
•
Situations in which it is impossible or not desirable to pass an endoscope: examples of this are
patients with severe dysphagia, a post-operative fistula or in a patient with either recent or delicate
reconstruction. In these situations, radiologic methods are preferred.
•
Metastatic deposition. There are now over 20 case reports of stomal seeding of head and neck
cancers. This complication is well recognised now and many cases probably therefore not reported.
The most accepted school of thought is that the tumour is seeded directly using endoscopic
techniques, especially the “pull” technique, before tumour resection or treatment. Some authors have
suggested either using a radiologic technique or using an alternative to the “pull” technique for PEG
placement in this situation36.
100
•
Safety issues: Complication rates for either percutaneous method vary widely and probably reflect
local expertise and strict adherence to a thought-out protocol rather than the technique per se.
Therefore, when either percutaneous method is applicable, the one with the lowest complication rate
in the unit concerned should be used. Regular audit of complication rates should take place.
The timing of gastrostomy
As a general rule, if a patient will require a gastrostomy tube, it should be done as early as possible. It is
certainly better to adopt a prophylactic policy for radiotherapy patients to avoid interruptions in treatment.
On the other hand, adopting an expectant policy will reduce the number of gastrostomies performed. For
surgical patients, the timing may be influenced by the particular method used. Radiologic percutaneous
gastrostomies are more amenable to an expectant policy. PEG’s, on the other hand, may be difficult to
perform in the early post-operative period and be associated with more complications37. If a PEG is to be
performed prophylactically, it is more practical and safer to perform it per-operatively after tumour
resection and before reconstruction37. This also avoids possible tumour stomal seeding.
In conclusion, the provision of a gastrostomy service is essential in the treatment of patients with head
and neck cancer. Head and neck surgeons and oncologists need to have close liaison with endoscopists,
radiologists and general surgeons. Nursing support in the community is required for longer term problems
associated with gastrostomy tubes. Finally, it should be noted that this procedure carries an associated
mortality of 0.5-1% and protocols to deal with major complications need to be developed and audited.
Home Enteral Nutrition (HEN)
Careful discharge planning incorporating regular follow up is essential if feeding problems are to be
minimised and compliance achieved.
Ideally ongoing close liaison with patients and their carers should be arranged through inter-disciplinary
teams. For the majority of patients where gastrointestinal function is satisfactory and once feeding has
been fully established, a bolus feeding regimen will be the preferred option. This prevents the need for
periods of continuous pump feeding and may facilitate the transition to oral feeding and regulate appetite.
Immunonutrition
There has been a growing interest in the concept that qualitative modulation of specific nutritional
substrates may influence nutritional and immunological status without enhancing tumour growth in head
and neck cancer. Ideally substrate supplementation should enhance immunogenic response, replete
protein stores and possibly sensitise tumours to specific treatments.40-42 Glutamine due to its role as the
preferential amino acid substrate for rapidly dividing cells such as lymphocytes, macrophages and
intestinal epithelial cells has been explored in several studies investigating chemotherapy induced
toxicity.
Jebb et al found no benefit in administering a low dose of glutamine (16g/day) on the degree of mucositis
in patients with gastrointestinal cancer receiving 5-FU/calcium folinate (Leucovorin) combination
therapy43 However, in a similar cross over study Skubitz and Anderson demonstrated a significant
decrease in mucositis when glutamine (8g/day) was given orally over a 28 period of chemotherapy.44
Similarly arginine is known to exhibit a number of immunomodulatory actions although its benefits in
head and neck cancer have not been documented.
The most promising developments involve the use of new lipid formulations containing Omega-3 fatty
acids in particular eicosapentaenoic acid derived from fish oils. Omega-3 polyunsaturated fatty acids
(PUFA) appear to have protective effects on the development of carcinogen-induced tumours, the growth
of solid tumours, cachexia and metastatic disease.45
101
Dietary supplementation has been tested in several clinical trials. The principal findings include
significant weight gain, improved performance status and enhanced appetite.46-48
Additionally the immunomodulating effect of Omega 3 PUFA may prolong survival rates.49
Although these studies have been carried out predominately in pancreatic cancer there are encouraging
early indications that similar effects of Omega 3 PUFA are applicable across a range of different cancers.
Summary
Malnutrition is prevalent in head and neck cancer patients and is associated with an impaired quality of
life and a reduced survival in many cases. It results from a number of multifactorial events such as an
inadequate dietary intake, alterations of taste and smell, metabolic disturbances, inflammatory responses
and the side effects of concurrent anti-cancer treatments.
Nutritional assessment will determine the initial nutrition therapy and on-going management. Early
dietetic and speech therapy intervention is essential to ensure that the oral nutrition plan is both
appropriate and safe and that regular monitoring of nutritional status is facilitated effectively. If oral
feeding is not possible nutritional requirements can be adequately met by means of enteral tube feeding.
Current research is focusing on the effects of immunonutrition on the host-tumour relationship and how it
may influence metabolic response. Further studies are needed to determine the efficacy of specific
nutrients in terms of overall nutritional and oncological objectives and whether there are real cost
benefits, in outcome, to be gained on the length and quality of life.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Greenwald P, Clifford CK & Milner JA. Diet and cancer prevention. Eur J Cancer 2001. 37:948-965.
Hammerlid E, Bjordal K et al. A prospective study of quality of life in head and neck cancer patients.Part 1: At
Diagnosis.Laryngoscope 2001. 111: 669-680.
Lennard-Jones JE. Legal and Ethical Aspects of Hydration and Nutrition. BAPEN PO Box 422, Maidenhead, Berks. 1998; 6
Bassett MR, Dobie RA. Patterns of nutritional deficiency in head and neck cancer. Otolaryngol Head Neck Surg 1983.
91:119-125.
Gardine RL, Kokal WA et al. Predicting the need for prolonged enteral supplementation in the patient with head and neck
cancer.Am J of Surg 1988.156: 63-65.
Batty J. Head and Neck Oncology Nursing, Feber T(ed) London. Whurr Publishers Ltd 2000. 176-177.
Van Bokhorst-De Vander Schueren MAE, Van Le Euwen PAM et al. Assessment of malnutrition parameters in head and
neck cancer and their relation to post operative complications. Head Neck 1997. 19: 419-425.
Van Bokhorst-De Van Der Schueren MAE, Langendoen SI et al. Perioperative enteral nutrition and quality of Life of
severely malnourished head and neck cancer patients: A Randomised Clinical Trial. Clin Nutr 2000.19: 437-444.
Donaldson SS. Nutritional support as an adjunct to radiation therapy. JPEN 1984. 8:302-310.
Goodwin WJ, Byers PM. Nutritional management of the head and neck cancer patient. Med Clin North Am 1993. 77: 597610.
Lopez MJ, Robinson P et al. Nutritional support and prognosis in patients with head and neck cancer. J Surg Oncol 1994.
55: 33-36.
Reddy SP, Leman CR et al. Parotid-Sparing irradiation for cancer of the oral cavity: maintenance of oral nutrition and body
weight by preserving parotid function. Am J Clin Oncol: Can Clin Trials 2001. 24:341-346.
Zlotolow I, Toth B et al. Minimizing oral complications of cancer treatment (Review) Oncology 1995. 9: 858-864.
Sonis ST. Oral complications of cancer therapy in: Devita VT, Hellman S, Rosenberg SA (eds).Cancer: Principles and
Practice of Oncology, 4th ed Philadelphia: JB Lippincott; 1993: 2385-2394.
Dreyfuss AI, Clark JR et al. Docetaxel: An active drug for squamous cell carcinoma of the neck. J Clin Oncol 1996. 14:
672-1678.
Niles RM. Recent advances in the use of Vitamin A (Retinoids) in the prevention and treatment of cancer. Nutrition 2000.16
: 1084-1089.
Adelstein DJ, Saxton JP et al. A Phase III Radomised Trial comparing concurrent chemotherapy and radiotherapy with
radiotherapy alone in resectable stage III and IV squamous cell head and neck cancer: Preliminary Results. Head & Neck
1997.19:567-575.
Sprinzl GM, Galvan O et al. Local application of granulocyte-macrophage colony stimulating factor (GM-CSF) for the
treatment of oral mucositis. Eur J Cancer 2001. 37:2003-2009.
102
19. Klein S, Kinney J et al. Nutritional support in clinical practice: Review of published data and recommendations for future
research directions. Summary of a conference sponsored by the nutritional institutes of health, American society for
parenteral and enteral nutrition and American society for clinical nutrition. Am J Clin.1997.66:683-706.
20. Corish A, Kennedy, NP. Protein-Energy Undernutrition in hospital in-patients. Br J Nut 2000. 83:573-591.
21. Shadaba A, Paine J et al. Re feeding syndrome. J Laryngol Otol 2001. 115:755-756.
22. Shaw C. Current thinking: Nutrition and Cancer. 2000. Pub Novartis Consumer Health, Horsham, West Sussex.
23. Blackburn GL, Bistrian BR et al. Nutritional and Metabolic Assessment of the Hospitalised Patient. JPEN 1977. 1:11-22.
24. Nitenberg G, Raynard B, Nutritional support of the cancer patient: Issues and dilemmas. Crit Rev Oncol Haematol 2000.
34:137-168.
25. Dechelotte P. Nutritional therapy in cancer patients. Nut Clin Metab. 2000.14:241-249.
26. Kouba J. Nutritional care of the individual with cancer (Review). Nut Clin Prac 1988. 5: 175-182.
27. Newton M, Burnham WR et al. Morbidity, mortaility and risk factors for esophagitis in Hospital patients. J Clin
Gastroenterol 2000. 30: 264-269.
28. Sands JA. Incidence of pulmonary aspiration in intobated patients receiving enteral nutrition through wide and narrow bore
nasogastric feeding tubes. Heart Lung J Crit Care 1991. 20: 75-80.
29. Beaver,ME, Matheny,KE, Roberts,DB, Myers,JN. Predictors of weight loss during radiation therapy. Otolaryngol.Head
Neck Surg. 2001;125:645-648.
30. Scolapio,JS, Spangler,PR, Romano,MM, McLaughlin,MP, Salassa,JR. Prophylactic placement of gastrostomy feeding tubes
before radiotherapy in patients with head and neck cancer: is it worthwhile? J.Clin.Gastroenterol. 2001;33:215-217.
31. Lee,JH, Machtay,M, Unger,LD et al. Prophylactic gastrostomy tubes in patients undergoing intensive irradiation for cancer
of the head and neck. Arch.Otolaryngol.Head Neck Surg. 1998;124:871-875.
32. Lin,HS, Ibrahim,HZ, Kheng,JW, Fee,WE, Terris,DJ. Percutaneous endoscopic gastrostomy: strategies for prevention and
management of complications. Laryngoscope. 2001;111:1847-1852.
33. de Baere,T, Chapot,R, Kuoch,V et al. Percutaneous gastrostomy with fluoroscopic guidance: single-center experience in 500
consecutive cancer patients. Radiology. 1999;210:651-654.
34. Beaver,ME, Myers,JN, Griffenberg,L, Waugh,K. Percutaneous fluoroscopic gastrostomy tube placement in patients with
head and neck cancer. Arch.Otolaryngol.Head Neck Surg. 1998;124:1141-1144.
35. Wollman,B, D'Agostino,HB, Walus-Wigle,JR, Easter,DW, Beale,A. Radiologic, endoscopic, and surgical gastrostomy: an
institutional evaluation and meta-analysis of the literature. Radiology. 1995;197:699-704.
36. Sinclair,JJ, Scolapio,JS, Stark,ME, Hinder,RA. Metastasis of head and neck carcinoma to the site of percutaneous
endoscopic gastrostomy: case report and literature review. J.Parenter.Enteral Nutr. 2001;25:282-285.
37. Schweinfurth,JM, Boger,GN, Feustel,PJ. Preoperative risk assessment for gastrostomy tube placement in head and neck
cancer patients. Head Neck. 2001;23:376-382.
38. Thorburn D, Karin SN et al. Tumour seeding following percutaneous endoscopic gastrostomy placement in head and neck
cancer. Post Grad Med J 1997. 73: 430-432.
39. Preclik G, Grune S et al. Prospective, randomised, double blind trial of prophylaxis with single dose of co-amoxiclav before
percutaneous endoscopic gastrostomy. BMJ 1999. 319: 881-884.
40. Laviano A, Meguid MM. Nutritional issues in cancer management. Nutrition 1996. 12: 358-371.
41. Heys SD, Gough DB et al. Is Nutritional support in patients with cancer undergoing surgery beneficial? Eur J Surg Oncol
1996. 22: 292-297.
42. Dechelotte P. Pharmacological nutrition and immune nutrition in cancer patients. In: Cynober L, Furst P, Lawin P,
Editors.Pharmacological Nutrition, Immune Nutrition. New York: Verlag 1995. 122-134.
43. Jebb SA, Osborne RJ et al. 5-Fluorouracil and folinic acid-induced mucositis: No effect of oral glutamine supplementation.
Br J Cancer 1994. 70: 732-735.
44. Skubitz KM, Anderson PM. Oral glutamine to prevent chemotherapy induced stamatitis: A Pilot Study. J Lab Clin Med
1996. 127: 223-228.
45. Karmali RA. Historical perspective and potential use of n-3 fatty acids in therapy of cancer cachexia. Nutrition 1996.12:
52-4.
46. Wigmore SJ, Ross JA et al. The effect of polyunsaturated fatty acids on the progress of cachexia in patients with pancreatic
cancer. Nutrition 1996. 12: S27-30.
47. Barber MD, Ross JA et al. The effect of an oral Nutritional supplement enriched with fish oil on weight-loss in patients with
pancreatic cancer. Br J Cancer 1999. 81: 80-86.
48. Wigmore SJ, Barber MD et al. Effect of oral eicosapentaenoic acid on weight loss in patients with pancreatic cancer.
Nutrition & Cancer 2000. 36: 177-184.
49. Gogos CA, Ginopoulos P et al. Dietary Oemga-3 Polyunsaturated Fatty Acids plus Vitamin E restore immunodeficiency and
prolong survival for severely ill patients with generalised malignancy: A Randomised Control Trial Cancer 1998. 82: 395402.
103
Section 4
Chapter 4
Current Patient Issues
Principal Patient Concerns
Patients priorities are that all patients, carers and families should be supported throughout the patient
journey.
a) Planning for discharge should begin at admission – all patients should be assessed by a
multidisciplinary team, fully conversant with all aspects of head & neck care, professionals will begin
the journey along the route which will produce the most patient centred outcome.
b) Patients feel that to ensure good outcomes co-ordination between secondary, primary, social Care and
the principal carer is essential. This hopefully should ensure that support (for patient and carer) is
available at the time of need, this is particularly true in the benefits scenario. Patients should be
encouraged to seek support of a trained benefits advisor conversant with head and neck issues (see
National Association of Laryngectomee Club’s benefits pack as a possible role model). It is
extremely important that all professionals recognise that patients may have social problems not
always obvious in the medical setting.
c) Patients must be given information in a timely manner and in an accessible format appropriate to their
needs.
To enable this there should be screening/ recognition of existing disabilities or language
barriers.
d) All Health Care Trusts must ensure that all aspects of pre and post registration staff training are
inclusive of all aspects of head and neck care, particularly around resuscitation of neck breathers. To
support this aim it is essential that new (neck breather inclusive) resuscitation mannequins are
developed and that all National Health Service staff, carers and families receive training in
resuscitation techniques.
e) There is a clear need for ongoing training to include speech disability awareness and skills. This could
perhaps be rolled out to include carers and families of head and neck patients.
f)
Patients feel that the British Association of Otolaryngologists - Head and Neck Surgeons should be
encouraged to consult with National Patient Support Associations to enable appropriate protocols for
head and neck care to be established nationally.
g) The availability of pre treatment counselling for new head and neck patients is felt to be highly
advisable. Wherever possible, befriending partnerships should be offered to both the patient and
family. It is, however, essential for the well being of both parties that befrienders are supported, and
whenever possible trained to undertake this role.
h) Concern has been expressed that patients undergoing radiotherapy may not receive adequate levels of
support at that time. The National Laryngectomee Club recognises its limitations in this role, given
the potential risks of non-Laryngectomee patients feeling that treatment could fail at a later stage,
were Laryngectomees to be involved in support at this time.
It is recognised that there may well be an enhanced role at this time for the head and neck specialist nurse,
particularly in stoma care.
104
i)
Patients look to advances in treatment regimes to reduce the side effects of radiotherapy. However
they do feel that greater use of complimentary/alternative therapies may reduce the effect upon the
patient.
j)
Patients should all have access to equipment appropriate to their medical/social needs – i.e.
nebulisers, suction and humidifier machines, bathing aids, Servox, voice enhancer and telephonic
equipment.
k) Follow up – directly as a result of the relative rarity of head and neck cancer it is felt that specialist
follow up should be open ended. Patients do, however, feel that where non specialist Consultant
clinics are held in district hospitals, those facilities could be used for this purpose for the 5 year+ post
operative patient.
l)
Patients feel strongly that no Laryngectomy should be undertaken without the patient being enabled
to access, together with professionals a full choice, of voice restoration methodology. Similarly all
head and neck patients must have access to a full range of cosmetic surgery and speech therapy as
appropriate. Contracts between commissioners and providers must be fully inclusive of these items.
m) Research should be promoted into new treatments/therapies, and into the potential risk to laryngeal
health of the papilloma virus.
n) Serious consideration should be given to an effective screening methodology for high risk groups;
this may well result in a need to update primary care practitioners’ information of potential risk
factors. Patients and carers recognise that for progress in this area there is a need for further research
into all possible causes of head and neck cancers.
o) Patients and their carers are particularly aware of the risk factors for patients with speech impairment.
The Social Services Inspectorates have produced standard guidelines for communication support for
deaf, hard of hearing and deaf/blind people. Research has indicated quite clearly that no similar
support is available for those with speech impairment. In fact great difficulty is being experienced in
finding researchers to undertake the initial research required. Speech support groups recognise that
this matter is now urgent given the requirements of the Disability Discrimination Act and Human
Rights Acts and the responsibilities placed on the statutory sector, in particular, as a result.
p) Difficulties with communication should, patients feel, be taken into account whenever staffing issues
are reviewed. Laryngectomees, older patients in particular, do appear to experience difficulties when
staff have poor English skills, with stressful episodes being more difficult where there is an additional
language barrier.
q) Specialist Care needs and communication problems would indicate that head and neck patients’ care
may require unit staffing to include at least one head and neck specialist nurse practitioner, with
wards being organised to allow for all head and neckpatients to share that care even where admissions
are for other specialist areas.
r)
The role of the specialist nurse practitioner, supported in many cases by at least one head and neck
specialist nurse, is seen by patients to be vital to ensuring that ongoing care in both secondary (centre
and district) and primary settings is of the standard required by the National Support Federation
guidelines. Patients envisage an enlarged training role for these specialist staff members.
s) Patients continue to face difficulties with direct ambulance admission.
medical conditions may be compromised long term by these difficulties.
105
Many feel that patient’s
Patients and their carers feel that new protocols should be in place to ensure assessment by head and neck
clinicians as soon as possible after arrival at Accident and Emergency departments .
Whilst we recognise that for many units this may prove difficult in practice, we do feel that paramedic
units attending emergency calls are sufficiently skilled to ensure appropriate screening of patients.
Useful Addresses
Macmillan Cancer Relief
89 Albert Embankment
London SE1 7UQ
Tel 0207-840-7840
[email protected]
Marie Curie Cancer Care
28 Belgrave Sq.
London SW1X 8QG
Tel 0207-235-3325
www.mariecurie.org.uk
Cancer BACUP
3 Bath Place
Rivington St.
London EC2A 3JR
Tel. 0207 696 9003
www.cancerbacup.org.uk
NALC (National Association of Laryngectomee Clubs)
6 Ground Floor
Rickett St.
Fulham
London Tel:0207 381 9993
Fax: 0207 381 0025
www.communicationsforum.org.uk/organisations/nalc.shtm
106
Section 4
Chapter 5
Supportive and Palliative Care
Definitions
Although head and neck tumours can be curable if caught early, many patients present with advanced
malignancies. Supportive and palliative care becomes appropriate in these patients and also in patients
who have failed treatment to their head and neck tumours.
Supportive and palliative care is the care of patients with life-threatening illness, their partners and carers.
Its focus is the quality of their lives with the aim of maintaining comfort and dignity from diagnosis,
through treatment to the end of the patient’s life, and of the carer’s comfort and dignity throughout this
time and into bereavement.
Effective supportive care, backed by palliative care, has become a key feature of the Calman-Hine
commissioning of cancer services.
• Supportive care
= good quality communication and symptom control that is the right of every person and the duty of
every professional
• Palliative interventions
= treatments used to palliate symptoms (eg. surgery, radiotherapy)
• Palliative care
= care delivered by clinicians with specialist training as part of an interdisciplinary care for patients
with severe or complex problems.
Supportive and palliative care start as soon as they are needed.
Supportive care
All care professionals should offer effective supportive care, but palliative care help will be needed for
some patients, partners and relatives. The nurses, family, surgeons and oncologists will give most of the
supportive care.
Palliative interventions
Palliative interventions are not palliative care. Surgery, radiotherapy and chemotherapy all have the
potential for palliation. A neck dissection to control nodes in the neck and stop them fungating is an
acceptable palliative procedure. In contrast, major resections when cure is not possible can cause great
morbidity and distress at the end of life, resulting in a poor quality of life. Palliative radiotherapy
Palliative Care
Some patients have severe or complex physical or psychological symptoms, and some partners and
relatives and difficult psychosocial problems. These are likely to need help from palliative care which has
the following key elements:
•
•
•
•
•
Provided by accredited clinicians
Life-threatening illness
Interdisciplinary working (medical, nursing, physio, OT, social worker)
Rehabilitation (readaptation)
Evaluation, research, education
107
Palliative care services are available in hospital, hospice and community
•
•
•
•
•
•
•
•
specialist medical advice (all settings)
specialist nursing support (all settings)
day hospice
home care
inpatient care
telephone advice
education and research
Partnerships in care
Establishing principles of palliative care in Head and Neck Cancer
The effects of cancer invade patients, partners and carers alike. Although some will grow from the
experience, it remains a distressing experience for all. For the patient, everyday activities become a source
of distress and irritation, while the partners and family feel shut out by the patient and unprepared for the
ordeal.
The sense of isolation in patients and carers is reflected in professionals who, faced with multiple
physical, psychological, spiritual and social issues can find it difficult to find logical and appropriate
treatments with consequent distress to themselves.
Although such distress can seem insurmountable, supportive and palliative care is well established as an
effective means of managing this distress. It cannot remove all distress, but provides a path through the
distress and confusion, helping achieve a worthwhile quality of life for patient, family, partner and
professional alike.
Information sources and learning materials
•
PCF2: Palliative Care Formulary, 2nd ed.
Twycross RG, Wilcock A, Charlesworth S. Oxford: Radcliffe Medical Press, 2002.
Also: www.palliativedrugs.com
•
Symptom Management in Advanced Cancer, 3rd edition.
Twycross RG, Wilcock A. Oxford: Radcliffe Medical Press, 2001.
•
The Oxford Textbook of Palliative Medicine, 3rd edition. 2002.
Calman K, Doyle D, Hanks GWC eds. Oxford: Oxford Medical Publications.
•
CLiP (Current Learning in Palliative Care) 15 minute worksheets.
Regnard C, ed. Oxford: Radcliffe Medical Press, 2002.
•
A Clinical Decision Guide to Symptom Relief in Palliative Care, 5th edition, 2002.
Regnard C, Hockley J. Oxford: Radcliffe Medical Press, 2002.
•
Supportive and Palliative Care: an Introduction Regnard C, Kindlen M. Oxford: Radcliffe Medical
Press, 2002.
For clinical information and advice contact your local specialist palliative care service.
For information on palliative care services contact St. Christopher’s Hospice Information Service
on www.hospiceinformation.info
108
Symptom management key clinical decisions
Checklist ‘CueCards’
These summarise the key clinical decisions required in a range of situations. More details on
management details are to be found in the information sources mentioned previously.
Tel: 0191 285 0063
Fax: 0191 284 8004
e-mail: [email protected]
videoconferencing number: 0191 284 1313
Coleman Education Centre
St. Oswald’s Hospice
Newcastle upon Tyne
Cue Cards
Current
Learning
in
Palliative Care
Cue Cards
Do not wait for a patient to complain- ask and observe.
Accurately diagnose the cause of the problem
•
•
Treat concurrent symptoms
•
These CueCards are designed to help you follow these
principles in a logical way, while adapting your
approach to the individual person
Empathy, understanding, diversion and elevation of mood are
essential adjuncts.
Re-assess repeatedly and regularly
•
•
Set realistic goals
Administer drugs regularly in doses titrated to each individual, that
ensure the symptom does not return.
Do not delay starting treatment.
•
•
•
Clinical estimates of symptom severity are highly subjective and are
a poor basis for choosing a treatment
Establish a partnership with the patient, the partner and family
•
•
Create a ‘safe place to suffer’
Ensure adequate team skills, knowledge, attitudes and
communication
Effective palliative care is the right of every patient and
partner, and the duty of every professional.
•
•
•
Principles of symptom control
CLIP
The Oxford Textbook of Palliative Medicine, 3rd edition. 2002. Calman
K, Doyle D, Hanks GWC eds. Oxford: Oxford Medical Publications.
Association for Palliative Medicine
www.palliative-medicine.org
Palliative Drugs: advice on drugs relevant to palliative care.
CLiP (Current Learning in Palliative Care) 15 minute worksheets.
Regnard C, ed. Oxford: Radcliffe Medical Press, 2002.
Reference text
www.palliativedrugs.com
Learning materials
Mailbase: a site for discussion groups and now containing a palliative
medicine mailbase
www.mailbase.org.uk/lists/palliative-medicine
Symptom Management in Advanced Cancer, 3rd edition.
Twycross RG, Wilcock A. Oxford: Radcliffe Medical Press, 2001.
Clinical Decision Guide to Symptom Relief in Palliative Care, 5th edition,
2002. Regnard C, Hockley J. Oxford: Radcliffe Medical Press, 2002.
PaPaS (Pain, Palliative Care and Supportive Care): special interest
group of the Cochrane Collaboration
www.jr2.ox.ac.uk/Cochrane
Information on palliative care services in the UK and overseas.
www.hospiceinformation.info
Dundee palliative care program
www.dundee.ac.uk/MedEd/welcome.htm
Palliative care internet/web sites
Further Resources
PCF2: Palliative Care Formulary, 2nd ed.
Twycross RG, Wilcock A, Charlesworth S. Oxford: Radcliffe Medical
Press, 2002. Also: www.palliativedrugs.com
Guides
Supportive and Palliative Care: an Introduction
Regnard C, Kindlen M. Oxford: Radcliffe Medical Press, 2002.
Introductory text
Contact your local hospice, or community/hospital palliative care team
for advice and help.
Local Palliative Care Team
Resources and Reading
Cue
Card
See over for notes
Is the person accepting the news?
Is the person very distressed?
Is the person holding on to unrealistic expectations?
Is the patient and/or family colluding?
NB. It is not the professional’s task to decide whether or not to tell,
but to find out what the person wants to know.
• Do you need more help?
Check for reactions (yes, no, unsure).
If more information is wanted then use the
Warn – Pause – Check method
Some distress is normal.
• Does the person want to know more?
at present?
• Does the person have all the information they need
• Is the person able to understand?
• Is the setting appropriate?
1: Breaking difficult news
CLIP
Current
Learning
in
Palliative Care
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
More help: Ask for help if a person is very distressed, strongly colluding,
or if they are so unrealistic that they are having difficulty accepting
treatment.
Denial is a good coping mechanism for many people. It is unusual for it
to be difficult to obtain informed consent for treatment.
Warn – Pause – Check: If they want to know more
Warn eg. "The results were more serious than we hoped"
Pause to see response and give time for the person to respond.
Check if person wants more information.
Repeat as needed.
Knowing more: Most people are clear whether or not they want to know
more. If a person does not want to know or is unsure, acknowledge this
and offer to answer their questions if they ask again in the future.
What do they know? Many people have already guessed the
seriousness of the situation.
Understanding: Check that problems like deafness or severe anxiety will
not prevent understanding.
Setting: Corridors are not appropriate!
Difficult news: You cannot assume that news is good or bad until you
have spoken to the person to find out what they know and whether they
want to know more.
1: Notes on breaking difficult news
Cue
Card
See over for notes
NB. Difficult questions have to be answered, but clear
answers are not always possible- being honest about
uncertainty is acceptable!
• Is the answer difficult news?
• Is a clear answer difficult?
-have they misunderstood?
-were you unprepared ?
-were you unwilling to listen?
-are you uncomfortable with the question?
-does the person want to stop the interview?
• Is the person reluctant to pursue the question?
– accepted the setting may not be ideal
– acknowledged the importance of the question
– checked why the question is being asked
• Have you done these first?
2: Handling difficult questions
CLIP
Current
Learning
in
Palliative Care
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Is it difficult news?
See CueCard 1 on Breaking Difficult News
Clear answer difficult: Some questions (eg. ‘How long have I got?’) are
impossible to answer with accuracy. Giving probabilities or being honest
about not knowing are acceptable. It’s OK to be uncertain!
Reluctance:
Check for deafness, drowsiness or confusion.
If you weren’t listening, apologise and acknowledge the importance of
the question.
It is helpful to say ‘I’m finding that difficult to answer’.
Honesty is allowed. If you can’t answer ask if there is someone else they
would like to talk to.
If the person wants to stop going any further, let them. Inform them they
are free to ask again in the future.
Checking why the question is being asked
ensures both of you are on the same wavelength.
Acknowledging the question’s importance
Because it may have taken the person much
time and courage to ask it
First steps:
Difficult questions need to be answered immediately, even if the setting
is not ideal.
2: Notes on handling difficult questions
Cue
Card
is
is
is
is
there unresolved fear, anger or depression?
the compliance poor?
this a new pain?
the analgesic inappropriate or incorrectly administered?
See over for notes
-
• Is the pain persisting?
- on inspiration ? pleurisy or rib metastases
– periodic ? colic from bowel, bladder, or ureter
- related to eating ? oral, pharyngeal, gastric or duodenal problems
- unpleasant sensory changes at rest ? neuropathic pain (eg.
neuralgia)
- supplied by a peripheral nerve ? nerve compression
• Is the pain present at rest?
-by the slightest passive movement ? fracture
-by bone strain on examination ? bone metastases
-by active movement only ? muscle strain or spasm
-related to joints, infiltration or distension?
• Is the pain related to movement?
• Is this breakthrough pain?
3: Diagnosing pain in advanced disease
CLIP
Current
Learning
in
Palliative Care
Breakthrough pain
Pain related to movement
Pain present at rest
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Pleuritic pain: due to local inflammation. Check for a rub.
Periodic pain (colic): regular episodes of pain lasting a few minutes.
Bowel the commonest, followed by bladder and ureter.
Pain related to a procedure: painful procedures produce fear and pain
with future procedures.
Pain related to eating: consider inflammation of the mucosa of the
mouth, pharynx, oesophagus or stomach. Remember related
structures, eg. teeth.
Inflammation or infiltration: local pressure or movement often
precipitates pain.
Associated skin changes: eg. ulcers due to pressure, malignancy or
vascular disease.
Unpleasant sensory changes at rest: neuropathic pain (eg. zoster
neuralgia) can occur after any nerve damage. Features: altered
sensation (reduced, hypersensitive, or painful to touch), an
unpleasant sensation (eg. burning, stabbing).
Pain in an area supplied by a peripheral nerve: eg. sciatica.
•
Fracture: movement of the affected part by the examiner will usually
result in severe pain on the slightest movement.
Bone metastases or infection: best picked up on bone scan (myeloma
and renal carcinoma may show better up on X-rays).
Muscle pain: Myofascial pain: has a tender spot when pressed with band
of muscle in spasm beneath (= trigger point).
Skeletal muscle strain usually occurs suddenly during exertion.
Severe soft tissue inflammation: overlying skin is red and swollen (deep
infections or in AIDS may have few signs).
Other causes: structures that are inflamed, infected or distended.
•
This is pain occurring despite regular analgesia.
•
3: Notes on diagnosing pain
Cue
Card
Neuropathic pain
Start and titrate a strong opioid. Arrange for radiotherapy. If no
improvement: add a NSAID (eg, diclofenac). Consider regular
pamidronate infusions.
Continued over
Contact pain or palliative care specialist if pain persists.
Hyoscine butylbromide (Buscopan) 10-20mg SC.
Colic
Start and titrate a strong opioid. Consider dexamethasone (8mg once
daily) or local nerve block.
Local tumour distension
Treat infection if present. Consider a NSAID. If pain localised to 1-3
dermatomes, try an intercostal block.
Pleuritic pain
If trigger point present- inject TP with 3-5mls 0.25% bupivacaine (or use
TENS). Muscle strain: TENS or local cooling.
Muscle pain
Use non-adherent, silicone-dressings (eg. Mepitel).
Bone metastases
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press
NB. Contact pain or palliative care specialist
if pain persists.
A complete reassessment is necessary.
Persistent pain
Start and titrate a strong opioid. Exclude skeletal instability (eg. vertebral
collapse). Treat bone metastases. Consider dexamethasone 8mg daily.
Nerve compression pain
Amitriptyline 10mg at night, titrated up to 50mg if tolerated. If no better,
add gabapentin100mg 8-hourly, titrated daily to control pain (up to 900mg
8-hourly).
Skin ulcer pain
Mucosal pain in mouth or oesophagus: treat infection. Consider
benzydamine (Difflam) mouthwash or benzocaine lozenge.
Gastritis: ranitidine or omeprazole.
Pain related to eating
Change technique. Consider: 4-hourly dose of usual analgesic or sedation
with midazolam (1-5mg titrated IV or 2.5 - 5mg SC).
Pain during a procedure
4: Pain treatments in advanced
disease (cont)
Immobilise. See CueCard 14. Arrange X-ray.
Fracture
Give usual 4-hourly dose of regular analgesic, but in instant-release
form. If this helps, consider increasing regular dose. If there is no
response after 3 breakthrough doses, reconsider the cause of pain.
Breakthrough pain
4: Pain treatments in advanced disease
CLIP
Current
Learning
in
Palliative Care
Cue
Card
If poor renal function: use morphine and diamorphine with care.
Alternatives are hydromorphone PO in mild impairment or fentanyl *
If poor hepatic function: continue on codeine or morphine
If non-oral route needed: use diamorphine SC or fentanyl *
* Transdermal fentanyl is not suitable for titration or in unstable pain
See over for notes
For breakthrough pain (‘as required’ or ‘PRN’):
Use instant-release opioid (4-hourly preparation)
Divide 24 hour dose by 6 to give the required breakthrough dose
Once daily: morphine XL or SR caps
Frequency and titration:
• Increase dose by 50% every other day Regular prescribing prevents
pain returning
• Review daily
• If oral route impossible, convert to parenteral
4 hourly: morphine tabs or soln, hydromorphone, oxycodone
12 hourly: morphine SR tabs, granules or caps, hydromorphone SR
caps, oxycodone SR caps
Doses: see CueCard 6 for equivalents. Use low doses in elderly.
Typical daily oral morphine dose range = 30 - 600mg daily
•
•
•
If already on paracetamol: add codeine 30mg 4-hrly
If already on a weak opioid: change to oral morphine 5 – 10mg 4-hrly
If already on morphine: increase by 50% and continue titration as below
5: Using opioids in advanced disease
CLIP
Current
Learning
in
Palliative Care
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Breakthrough doses
‘As required’ or ‘PRN’ prescribing for pain control must be used with
regular prescribing, never on its own (‘PRN’ = Pain Relief Nil!). For most
opioids, using the 4-hourly equivalent is a suitable dose. For
breakthrough pain whilst on fentanyl use dextromoramide,
hydromorphone, morphine or diamorphine in equivalent of 4-hourly doses
(see Conversion Card).
Titrating strong opioids
The aim is to prevent the pain returning by prescribing the opioid regularly
and titrating the dose until the patient is comfortable throughout the dosing
interval. Opioids are normally increased by 50% every other day. They
can be increased faster in severe pain, but at the expense of adverse
effects such as drowsiness.
Doses
There are no fixed dose ranges for strong opioids, but most patients are
managed on 30 - 600mg oral morphine / 24 hours. Elderly patients should
start on low doses eg. some people over 75 years will not tolerate a
morphine starting dose over 20mg daily.
Choosing the right opioid
In renal failure the active metabolites of morphine accumulate- this is less
of a problem with hydromorphone and does not seem to be a problem with
fentanyl.
The WHO analgesic ladder
This stepped approach only applies to choosing an analgesic for opioid
responsive pain. Weak opioids are a useful step if strong opioids are
difficult to obtain, or patients are too fearful of strong opioids. These steps
should be used in conjunction with co-analgesics such as NSAIDs.
5: Notes on using opioids
Cue
Card
(see over for more information)
So, 60mg/24 hrs oral morphine ≡ 20mg /24 hrs SC diamorphine
Example Oral morphine to diamorphine infusion: conversion factor is [÷ 3]
6: Changing opioids
CLIP
Current
Learning
in
Palliative Care
Calculate the 24 hour dose of opioid
Find the starting opioid and route in the columns at the TOP
Find the opioid and route you are changing to on the RIGHT
Where the column and line crosses, read the conversion
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
If in doubt, contact pain or palliative care specialist
For fentanyl: check manufacturer’s conversion tables
(quick conversion: oral morphine in mg/24hrs ÷ 3
≈ SC or TD fentanyl in microg/hr)
Conversions from weak opioids to potent opioids (and vice versa) are not
recommended eg. codeine to fentanyl.
More potent opioids or routes DO NOT provide greater efficacy. eg. a pain
that is not responsive to titrated oral morphine, will not respond to
injectable diamorphine either, even though this route and drug are 3 times
as potent.
Rules of opioid conversions:
Conversion factors are only approximations so:
1. Know your opioid
2. Use a conversion factor with which you are familiar.
3. Be prepared to re-titrate the dose.
x multiply by this factor
÷ divide by this factor
nr this conversion is not recommended
•
•
•
•
6: Notes on changing opioids
Fear of opioid: addiction is rare because psychological dependence and
tolerance to analgesia are rare. The belief in the ‘double effect’ is due to
ignorance of analgesic use- it is not an issue with good palliative care.
Confusion: confusion in advanced disease is often due to infection, other
drugs or biochemical disturbances (eg. hypercalcaemia). If the opioid is
the cause, it is usually due to sedation and this will wear off in a few days.
Persistent and troublesome confusion due to opioids requires an opioid or
dose change.
Fear of opioid: Information (psychological dependence, respiratory
depression and tolerance are rare, the ‘double-effect’ is not seen with
good palliative care).
Confusion / nightmares:
If due to sedation: treat as above.
If persistent or troublesome: reduce dose, or change to hydromorphone
or fentanyl.
Myoclonus: a sign of opioid toxicity (along with pin-point pupils,
drowsiness, confusion).
Respiratory depression: this is rare with chronic opioid usage.
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Urinary retention: Rare. Reduce dose, or change opioid.
Myoclonus: Reduce dose, or change opioid.
See over for notes
Hallucination: reduce dose, or change opioid.
Opioids are poor sedatives: tolerance develops rapidly and there is a risk
of increased agitation and myoclonus with inappropriately increased
doses.
Sedation: tolerance develops within a few days. Persistent sedation
usually has other causes. In patients on morphine or diamorphine, check
the renal function, since their active metabolites are renally excreted.
Sedation: Usually mild and self-limiting (2-5 days). If troublesome,
exclude other causes (drugs, hypercalcaemia). If due to opioid consider
hydromorphone or fentanyl.
NB. opioids should not be used for sedating a patient
Dry mouth: Local measures or pilocarpine PO 5mg 8-hrly
Nausea and vomiting:
If gastric stasis (large volume vomiting):
Metoclopramide or domperidone
In other cases:
Haloperidol SC or PO 1.5-3mg once at night for 2 weeks.
Nausea and vomiting: Gastric stasis causes large volume vomiting with
brief nausea, and may be accompanied by fullness, heartburn, early
satiation and hiccups. Other cases are caused by stimulation of the area
postrema and respond to the dopamine antagonist haloperidol (in low
doses it is an effective antiemetic for chemical causes of nausea and
vomiting with few adverse effects).
Constipation: Regular laxative (eg. senna + docusate)
7: Notes on opioid adverse effects
Constipation occurs in nearly all patients on morphine and diamorphine.
Fentanyl may be less constipating.
Cue
Card
7: Managing opioid adverse effects
CLIP
Current
Learning
in
Palliative Care
Cue
Card
Can thirst be helped by non-oral routes?
•
See over for notes
Can anorexia be helped by corticosteroids?
– anxiety or depression
– swallowing problems
– weakness or disability preventing intake
– constipation
– nausea and vomiting
–infection or odour
– appetite suppressant drugs
– drugs causing nausea, mucosal irritation or gastric
– poor food presentation
Exclude the following as causes:
•
•
stasis.
–is deterioration day-to-day?
– does the patient want to continue hydration and feeding?
– does the partner, family and staff agree with patient?
• Is hydration or feeding necessary?
8: Reduced hydration and feeding
CLIP
Current
Learning
in
Palliative Care
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Non-oral routes: as an alternative to IV consider:
For hydration: SC infusions in amounts of 1 – 3 l/24 hours.
For nutrition a gastrostomy (endoscopic or under X-ray control) are the
best long-term solutions. NG routes are not well tolerated for more than 12 weeks (even with fine bore tubes) and may increase the risk of
aspiration.
Corticosteroids: useful if brief (1-4 week) effect is wanted.
Dexamethasone 2 – 4mg once in the morning, has the fewest adverse
effects and is convenient.
Exclude causes of reduced hydration and feeding: a wide range of
causes can reduce intake. Check these before prescribing appetite
stimulants.
Discussions should be around the need for hydration and feeding as
comfort and health measures, not as life-prolonging measures.
If the partner, family or staff disagree with patient arrange meeting with all
parties (including patient). If necessary ask help from palliative care team.
Feeding is necessary for comfort, pleasure or if further treatment is
awaited.
Hydration is usually necessary in most other situations.
Usually unnecessary in coma or semi-coma due to advanced disease in
the context of day-to-day deterioration. No distress results from this
approach if good nursing care continues
Check the patient’s wishes
Necessity of hydration and feeding:
8: Notes on reduced hydration
and feeding
Cue
Card
See over for notes
From: A Clinical Decision Guide to Symptom Relief in Palliative
Care. Radcliffe Medical Press, 2002
Persisting nausea and vomiting:
– exclude anxiety and gastritis.
– if not already tried, try levomepromazine as above
– ask for help from a palliative care specialist
NB. Treatments used in chemotherapy emesis are often
ineffective in palliative care emesis.
-is fear or anxiety present?
-is gastritis present?
-would low dose levomepromazine be helpful?
-is specialist help needed?
Other causes: start with cyclizine 50mg 8-hourly PO or SC (or
150mg / 24 hours SC infusion).
If nausea and vomiting persist try:
levomepromazine (Nozinan) 3-6mg PO or 2.5-5mg SC once
at night.
Bowel obstruction:
– treat obstruction if possible.
– inoperable: start cyclizine 150mg / 24 hrs SC infusion
– consider adding haloperidol 2.5mg SC once at night
– contact palliative care specialist for further advice
Chemical causes: eg. morphine, toxins, hypercalcaemia
Use haloperidol 2.5mg SC or 3mg PO once at night.
Mainly vomiting:
Regurgitation: suggests partial or complete pharyngeal or
oesophageal obstruction.
Large volume vomiting: suggests delayed gastric emptying. Give
metoclopramide 10-20mg 8-hrly given initially by SC or IV
route, then later PO
Raised intracranial pressure: use cyclizine 50mg 8-hrly.
9: Notes on nausea and vomiting
• Is the nausea and vomiting persisting?
• Is this bowel obstruction?
to cyclizine?
• Could there be vagal stimulation that would respond
very low dose haloperidol?
• Is there a drug or toxic cause that would respond to
-is this regurgitation?
-is there reduced gastric emptying which would respond to a
prokinetic agent?
-is there raised intracranial pressure?
• Is patient mainly vomiting?
9: Nausea and vomiting
CLIP
Current
Learning
in
Palliative Care
Cue
Card
See over for notes
NB. Add new drugs only if there is no other option
-are abnormal experiences present that would respond to
haloperidol or levomepromazine?
-is fear the main feature that would respond to lorazepam or
midazolam?
• Has behaviour altered?
• Is control of disturbance urgent?
psychiatric illness?
• Is patient hallucinating due to a toxic state or
altered alertness?
• Is patient misinterpreting external events due to
depression?
• Is concentration impaired due to anxiety, pain or
state?
• Has alertness changed due to an acute confusional
dementia?
• Is memory failure present that would suggest a
10: Confusion
CLIP
Current
Learning
in
Palliative Care
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Urgent control of disturbance: See CueCard 15 on Severe Agitation.
Altered behaviour: eg. paranoid, euphoria, dysphoria
Exclude: causes of memory failure, drugs (especially corticosteroids) and
psychiatric illness.
Hallucinations: consider drugs, chemical withdrawal, and psychiatric
illness.
Misinterpretations: common in causes of altered alertness.
Impaired concentration: consider anxiety state, depression, pain.
Change in alertness: typical of acute confusional states (alertness may
be increased or decreased). Exclude / treat: infection (chest, urine), drugs
(started or stopped), chemical withdrawal, biochemical causes
(hypercalcaemia, uraemia), cardiac disease, hypoxia, trauma (long bone
fracture, subdural).
Memory failure:
Dementia: suggested by little fluctuation in confusion, no change in
alertness and history lasting months.
Cerebral tumour: uncommon cause, which may respond to
dexamethasone and cranial irradiation.
10: Notes on confusion
Cue
Card
See over for notes
NB. Depression is common in advanced disease, but is
only one of several causes of withdrawal. It can respond
rapidly to treatment
• Is specialist help needed?
• Is this a clinical depression?
• Could this have an organic cause?
• Is there a confusional state?
• Is patient refusing help?
Acknowledge the behaviour
(‘You seem much quieter than usual’)
• Is this the patient’s usual behaviour?
11: The withdrawn patient
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Persisting low mood: ask for specialist help. Referral for cognitive
behavioural therapy reduces relapses.
Responses can occur within 2 weeks.
Start lofepramine 70mg at night, increasing to 70mg 12 hrly or if
necessary 70mg mane, 140mg nocte. Alternatively consider venlafaxine
or citalopram.
Clinical depression: indicated by
–persistent low mood for > 2 weeks, for > 50% of time
– unlike their usual mood
– difficult to distract them out of mood
– 4 other depressive symptoms (eg. early morning wakening,
diurnal variation, loss of enjoyment, undue guilt, hopelessness.)
Fears, guilt or shame: clarify their concerns and check if these feelings
a realistic. Ask for specialist help if necessary.
Organic causes: consider Parkinson’s, drugs causing Parkinson-like
symptoms, or severe fatigue due to the illness. If this is the only cause
these patients will not express a low mood.
Confusional state: manage as in CueCard 10.
Refusing help: This is their right. Acknowledge the refusal and offer
willingness to help in the future.
Usual behaviour: some people are normally introverted or quiet. Offer
time to establish trust.
11: Notes on the withdrawn patient
Cue
Card
Is there an underlying depression?
See over for notes
NB. Anxiety and depression commonly co-exist
• Is specialist help needed?
•
• Are panics or phobias a feature?
-is sedation needed?
• Is the person functioning poorly?
• Is this an anxiety state?
• Would simple supportive measures help?
Acknowledge the anxiety
(‘You seem to be worried.’)
anxiety?
• Is this a drug-induced dyskinesia mimicking
12: The anxious person
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From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Persistent anxiety:
– consider depression (the two often co-exist). See CueCard 11.
– ask for specialist help. The response to cognitive behavioural
therapy can be rapid (six sessions or less).
Panics and phobias: consider clomipramine 25mg at bedtime
(10mg if > 70 years)
Poor functioning:
Mild disorganisation (able to care for self):
– during day lorazepam 0.5mg – 1mg 6-hourly
– at bedtime temazepam 10-30mhg
Severe disorganisation (unable to care for self):
-haloperidol 5-20mg at night.
–for more sedation change to levomepromazine (Nozinan) 1050mg at night.
Anxiety state: indicated by
– persistent apprehension for > 2 weeks for > 50% of time
– unlike their usual mood
– 4 other anxiety related symptoms (eg. rumination, irritability,
insomnia, tremor, tachycardia, sweating)
Simple measures: empathy, offering information if wanted, exploring
causes of concern, reviewing procedures causing anxiety.
Drugs: drug-induced dyskinesia causing restlessness can seem like
anxiety, but if this is the only cause, patients are clear that anxiety is not
the main problem.
12: Notes on the anxious person
Cue
Card
See over for notes
NB. If you acknowledge the anger and are clear in your
willingness to help, anger should start to defuse in the
first few minutes
-is this normal behaviour?
-is specialist help needed?
• Is the anger persisting
• Is their anger causing isolation?
• Is the person depressed?
-can the person contain their anger? (If not, leave the room)
• Is the anger escalating?
• Is the anger correctly directed?
• Is the person controlled and contained?
Acknowledge the anger
(‘I can see you’re angry, how can I help?)
• Do you know how anger affects you?
13: The angry person
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From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Persisting anger: this may be normal behaviour or due to causes
unconnected to illness. Consider specialist help.
Isolation: acknowledge anger and explore the effects on relationships.
Depression: anger can be a feature. See CueCard 11.
Escalating anger: if anger is not defusing or is worsening
– position yourself near exit door
– set limits (‘I can only continue if you can control your anger’)
If person cannot accept limits = pathological anger
Stop interview and leave room immediately.
Appropriateness of anger:
– misdirected: check this and explore the causes.
– correctly directed: show understanding without being defensive.
Apologise if it is your fault, but do not apologise for others.
Patient is controlled and contained:
– if you’re the only angry person, you need to withdraw.
– some patients express passive anger: acknowledge the anger, discuss
the cause and encourage its expression.
Anger and you: when facing an angry person
– if you get angry: you need to be more restrained
– if you tend to withdraw: you need to be more assertive
13: Notes on the angry person
Cue
Card
See over for notes
Within 24 hours
Ensure a good night’s sleep with sedatives if necessary
If pain is localised (eg. fracture): consider referral for spinal analgesia or
nerve block.
Within 4 hours
If still in pain: convert to oral morphine PO or diamorphine SC and
increase dose by 50%. Review in 2 hours- if still in pain, contact pain or
palliative care specialist.
If treatment is to be delayed for 6 hours or more: ask for advice.
Consider diamorphine equivalent (see opposite), plus lorazepam
500microg. sublingual or PO.
Within 1 hour
Exclude: myocardial infarction, pulmonary embolus.
For back pain: exclude cord compression.
If pathological fracture: decide if patient is able to travel for X-ray.
If still in pain: repeat above dose of diamorphine.
Check through CueCard 3 on Diagnosing Pain
Immediate
For fracture: immobilise.
For agitation that prevents assessment: midazolam
(1-5mg titrated IV or 2.5 - 5mg SC).
For colic: hyoscine butylbromide 20mg IV, IM or SC
For severe pain at rest: give diamorphine IV or IM (5mg if not on opioid,
otherwise equivalent of usual 4-hourly dose). Repeat every 20mins SC if
necessary (up to 3 doses).
14: Managing severe pain in advanced disease
CLIP
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From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Psychological issues: although the agitation may settle, low mood,
anxiety and exhaustion may persist. This persistence of psychological
problems will delay the resolution of the pain for several weeks and to
avoid disappointment this needs to be understood by patient, partner and
staff.
The advice of palliative care, pain and oncology colleagues can be
invaluable.
In situations when a procedure is to be delayed (eg. in the night), or
where a patient is deteriorating rapidly, titrated sedation is appropriate.
Fractures: simple treatments for some pathological fractures are possible
eg. splinting for a humeral neck fracture, or intercostal nerve block for a
rib fracture. An intercostal block of bupivacaine and methylprednisolone
(as DepoMedrone) gives analgesia for as long as radiotherapy. Other
fractures (eg. vertebra, femoral shaft) may need referral for local nerve
blocks or spinal analgesia.
Agitation that is driven by fear and pain will ease with titrated midazolamsome patients will require no more than 2.5mg (eg. ill patients or those
who have slept little in the previous 24 hours), others will require more
than 10mg (eg. younger patients or those previously on benzodiazepines).
The most immediate goal is to reduce pain at rest and to allow the
patient to settle sufficiently to allow adequate assessment.
14: Notes on managing severe pain
Cue
Card
See over for notes
NB. Do not use opioids to control agitation- they can
make agitation worse
-are abnormal experiences present that would respond
to haloperidol or levomepromazine?
-is fear the main feature that would respond to
lorazepam or midazolam?
• Is control of disturbance necessary?
-have the clinical decisions for confusion been
considered?
From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Control of disturbance:
Ensure well lit, quiet, constant environment.
In absence of abnormal experience or behaviour:
- minimal sedation use lorazepam 0.5mg PO or SL
- for sedation use midazolam 2-10mg SC, IM or PR (or 20 – 120mg
SC infusion per 24 hours)
In presence of abnormal experience or behaviour:
- minimal sedation use haloperidol 2.5 – 10mg once
at night PO or SC
- for sedation use thioridazine 25 – 50mg PO at night or
levomepromazine 25 – 100mg at night PO or SC
(or 50 – 200mg SC infusion per 24 hours)
Confusional state: see CueCard 10.
Simple measures: try gentle explanation of the situation. Many confused
patient’s fear about what is happening can be eased by explaining what is
happening.
Hypoxia: can cause or worsen agitation. Give 100% through facemask
(NB. if there is a history of pulmonary disease with CO2 retention give no
more than 24%).
• Would simple measures help?
• Is a confusional state present?
Do not use opioids to treat agitation
(They can make agitation worse)
Urgent control:
eg. irreversible haemorrhage, prevention of injury
–midazolam 2-10mg titrated IV, or 5mg IM
(repeated until settled)
– ensure environment is safe
– do not leave patient unattended
15: Notes on managing severe
agitation
• Is hypoxia present?
eg. irreversible haemorrhage, prevention of injury
• Is control of the agitation urgent?
15: Severe agitation
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Cue
Card
See over for notes
NB. Clarity about the cause of deterioration is
important- do not assume it is irreversible
- would it help to consult with partner or family?
- would it help to consult with the care team?
- would it help to wait a few hours or days before deciding?
• Is the need for treatment uncertain?
• Is a delay in treatment likely?
- is sedation required?
- is analgesia required?
• Is the treatment indicated for comfort only ?
• Are drugs the cause?
16: Unexpected deteriorationdeciding about treatment
CLIP
Current
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From: A Clinical Decision Guide to Symptom Relief in Palliative Care.
Radcliffe Medical Press, 2002
Uncertainty about treatment:
Consult with the partner or family about patient’s previous wishes.
Consult with care team about history, rate of deterioration,
availability of treatment and previous quality of life.
If need for treatment is still uncertain use rule of 3:
– hour by hour deterioration, review in 3 hours
– day by day deterioration, review in 3 days.
If further deterioration has occurred, treat for comfort only.
If no further deterioration, or improvement, consider treating.
Delay in treatment: if distressed give sedation.
See CueCard 15.
Comfort only: eg. rapid deterioration with irreversible cause, very short
prognosis (hour by hour deterioration), or patient refusing treatment.
– sedation if agitated. See CueCard 15
– analgesia if in severe pain. See CueCard 14
Support patient, partner, family and staff (including you!).
Drugs as the cause: reduce dose, but if ventilation has been
seriously compromised (<5 resps/min) do the following:
Opioid: dilute 400microg naloxone in 10mls 0.9% saline and titrate IV at
2ml/min until improved, followed by naloxone infusion (do not fully reverse
all the opioid or severe pain and agitation will result).
Benzodiazepine: flumazenil IV 200 microg over 15 seconds followed by
100 microg/min up to 1000 microg (1mg)
16: Notes on unexpected deterioration
Cue
Card
Advice from outside the team is invaluable eg. primary health care team, palliative
care team, chaplain, social worker, BMA and UKCC advice lines, local ethics
committee.
From: A Clinical Decision Guide to Symptom Relief in Palliative Care. Radcliffe
Medical Press, 2002
See over for notes
Asking patients and relatives is uncomfortable but is easier if they have the
information they want about the situation and they are allowed time to make their
decision.
Providing resuscitation can be less distressing than withholding it against
the wishes of patient and relatives.
The consultant responsible for the patient has the final decision, but it is wise to
reach a consensus with staff and relatives.
Both offering and witholding resuscitation can have immediate and long term
benefits, ie do not assume one is good and the other is bad.
The only exceptions are if the patient is not comptetent, death is an expected and
inevitable outcome, or the patient does not want to discuss the matter.
The consultant responsible for the patient has the final decision, but it is wise to
reach a consensus with staff and relatives.
Both offering and withholding resuscitation can have immediate and long-term
benefits, ie do not assume one is good and the other is bad.
Advice points
The patient’s view is paramount, ie. decisions cannot be made without them. The
only exceptions are if the patient is not competent, death is an expected and
inevitable outcome, or the patient does not want to discuss the matter.
These are resuscitation measures: Cardiac massage and artificial respiration
(CPR). These measures are instituted immediately and in full following an
unexpected collapse, and in the absence of a DNAR order.
These are comfort and palliative treatment measures: Analgesia, antibiotics, drugs
for symptom control, feeding, hydration, oxygen, seizure/status control, suction,
treatment for choking. Comfort and treatment measures are instituted after
assessment, consultation with patient and family, and on the basis of clinical need.
Competency: competent patients are able to understand the results of their
decisions, and are free from depression or undue influence.
CPR cannot be offered if it is not expected to succeed.
Uncertainty can result in distressing attempts to resuscitate someone who has
collapsed, or inappropriate withdrawal of treatment.
17: Notes on deciding a ‘DNR’ order
6. Any change in decision needs a new DNAR form
5. Reassess the wish for resuscitation regularly
While this does not mean burdening the patient and family with a
difficult decision every day, it does require staff to be sensitive in picking
up any change of views during discussions with the patient, partner or
family. The frequency will depend on the clinical situation, eg. week-byweek deterioration needs a weekly review.
4. Assume that any patient without a DNAR order is for
resuscitation and act accordingly in the presence of collapse or a
major, life-threatening bleed.
3. Document the DNAR order in the notes.
2. Consider the consequences of discussion about CPR with the
patient and family: if the patient’s intent is clear and they are
competent for this decision, document their decision in the notes. If the
patient agrees, explain the decision with partner, family and
multidisciplinary staff (including advocate and keyworker). If patient’s
intent is unclear for this decision (ie. they are not competent or unwilling
to discuss matter), talk to family and staff to develop clear consensus on
the DNAR order.
1. Decide if it is possible to offer CPR: CPR is not an option in a
terminally ill patient where CPR is not expected to succeed. A DNAR
decision needs to be documented, but permission from partners or
relatives is not needed for a treatment that cannot succeed.
17. ‘Do Not Attempt Resuscitation’ (DNAR)
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5
CLINICAL GUIDELINES
Chapter 1
Neck
This section has been updated and modified taking into account the conclusions reached at the 3rd
Evidence Based Consensus Conference on Head & Neck Cancer, entitled ‘The Management of the Neck
in Squamous Head & Neck Cancer’, held at the Freeman hospital, Newcastle upon Tyne on 24th
November 1999 (see www.noto.org), and again following a further literature review in January 2002.
Key points
The available level of evidence for managing nodal disease in the neck is poor with an almost complete
lack of good randomised controlled clinical trials.
•
The status of the cervical lymph nodes is the single most important prognostic factor.
•
When a single nodal metastasis exists at presentation or subsequently develops, the cure rate halves1.
•
Prognosis is affected by the number of metastases, the level in the neck, the tumour load, the presence
of extracapsular spread, the presence of perineural and/or vascular invasion, previous treatment by
surgery or radiotherapy and resectability2,3.
•
A large number of malignant nodes will measure less than 10 mm in diameter (micrometastases) and
extranodal spread will occur in a substantial percentage of smaller nodes, as small as 2mm4.
•
The incidence of nodal metastases depends mainly on the site and the size of the primary tumour.
This figure may be as low as 1% for early glottic tumours or as high as 80% for nasopharyngeal
carcinomas 5.
The majority of tumours will metastasise in a predictable manner to certain nodal groups but it should
be remembered that certain tumours will fast track to remote sites ( i.e. nasopharyngeal cancers to
level V, tongue cancers to jugulo-omohyoid nodes) and the pattern of spread will be disrupted by
previous surgery or radiotherapy.
•
•
The possibility of bilateral nodal disease should be considered especially when the primary site
involves the tongue base, nasopharynx or supraglottic larynx.
•
There is no evidence that control of metastatic disease in the neck leads to improved survival and
issues of function and quality of life have to be considered in the management.
•
Standardised reporting of neck dissection specimens according to the Royal College of Pathologists is
essential.
Assessment
Clinical Palpation is generally regarded as inaccurate (sensitivity and specificity 60% – 70%), due to a
number of factors including shape of neck and the recognised incidence of micrometastases.
CT scanning has a higher sensitivity in detecting metastatic disease [69-93%] than the 70% sensitivity of
physical examination6,7. Overall the accuracy of CT is slightly better than MRI in the N0 neck.
129
Ultrasound Guided Fine Needle Aspiration Cytology: US-guided FNAC requires both expertise and
experience, and is a useful technique when available. It has a sensitivity of 76% and a specificity of
100% in necks that were clinically negative by palpation alone8.
TREATMENT OPTIONS
Treatment of cervical lymph nodes is either elective (in the clinically negative neck) or therapeutic (in
the
clinically positive neck).
Clinically Negative Neck (N0)
The rationale for elective treatment of the N0 neck is based on the following:
Occult disease in the neck will inevitably develop into clinically manifest disease9.
Despite close regular follow up, some patients will develop inoperable disease in the neck with a wait and
see policy9.
Untreated occult disease in the neck may predispose to the development of distant metastases17.
•
Although a survival advantage from elective treatment of the N0 neck in squamous carcinoma has
not so far been demonstrated by controlled trials, some multivariate analyses of retrospective data
suggest a significant benefit in N0 tongue tumours10.
•
Elective neck dissection provides useful histological information on which to base future research as
well as prognostic information for the patient. Weiss et al11 used a decision analysis model to
propose that tumours that carry a risk of occult metastases of >20% should undergo elective
treatment of the neck. This paper was based on data of variable quality. It is now a widely held view
that the neck should be treated in cases with a high probability of micrometastases. The evidence to
support this is stronger in oral cavity primaries9 than in laryngeal or hypopharyngeal primaries.
The arguments against elective treatment of the neck are:
•
Where the risk of occult neck disease is low, a large number of patients will undergo unnecessary
treatment.
•
Such treatment destroys a barrier to cancer spread which may be important if recurrence in the
primary site occurs at a later date.
• A close follow-up regime to ensure early detection of metastatic disease will improve salvage rates if
a ‘wait and see’ policy is adopted. Adding US-guided FNAC to clinical follow-up may provide an
alternative strategy to elective neck dissection12.
•
There is some morbidity and mortality associated with elective treatment13.
•
The evidence to support elective neck treatment is retrospective and of variable quality.
Indications for elective treatment of the N0 neck
•
High likelihood of occult nodal metastases (over 20%). Most sites and stages of squamous cell
carcinoma in the head and neck, specifically excluding lip, early glottic cancers and lower alveolar
ridge SCC, qualify for elective treatment because the incidence of occult nodal metastases is over
20%11, 14. Whilst this is generally accepted practice, it is not supported by strong evidence and should
be the subject of clinical trials.
•
The status of the cervical lymph nodes cannot be adequately assessed.
•
The patient will be unavailable for regular follow up.
•
The neck needs to be entered for surgical access to the primary tumour and/or for microvascular
anastomosis.
There is good evidence that elective irradiation of the neck is as effective as elective surgical treatment15.
The choice of neck treatment should, therefore, be influenced by the mode of treatment for the primary.
130
Elective Neck Dissection
The committee of Head and Neck Surgery and Oncology of the American Academy of Otolaryngology
and Head and Neck Surgery has produced a standardised neck dissection terminology (Table 1)16.
Table 1
Radical neck dissection
Modified radical neck dissection
Selective neck dissection
Extended radical neck dissection
Classification of neck dissection techniques
is the fundamental procedure by which any other neck dissection is
compared. Levels I-V dissected; accessory nerve, internal jugular vein and
sternomastoid muscle resected.
denotes preservation of one or more of the accessory nerve, internal jugular
vein or sternomastoid muscle (types I, II, III respectively), levels I-V dissected.
denotes preservation of one or more group(s) of lymph nodes.
denotes removal of one or more additional lymphatic and/or non-lymphatic
structure(s)
The classical radical neck dissection (RND) has no role to play in elective treatment of the N0 neck. The
choice lies between a modified RND or a selective neck dissection (SND). A recent prospective study
has suggested that SND is just as effective as MRND type III31. As initially stated, most tumours will
metastasise in a predictable manner and it is possible to tailor the dissection accordingly. Sentinel node
biopsy has been shown to be feasible in head and neck tumours, and may become an alternative to
elective neck dissection, at least for oral cavity tumours32,33. In oral cavity and oropharyngeal tumours a
selective neck dissection of levels I to IV should be performed due to the possibility of skip lesions in
level IV3,36, although level IV metastases are considered rare by some authors34,35. In laryngeal and
hypopharyngeal tumours a selective neck dissection of levels II-IV should be performed. Adjuvant
postoperative radiotherapy should certainly be used when nodes are found to be involved and bad
prognostic factors are present (>1 positive node, presence of extracapsular spread, perivascular or
perineural infiltration) and may be beneficial if any node involvement at all is found37.
Elective Radiotherapy
When the primary tumour is treated with radiotherapy, the lymph node regions at the greatest risk of
harbouring occult disease are included in the treatment field. Elective irradiation is reported to eliminate
95% of nodal metastases with less morbidity than radical surgery17 and is, therefore, preferred when both
sides of the neck are to be treated, such as in nasopharyngeal cancers18.
Clinically Positive Neck (N1-3)
Treatment of the positive neck will involve surgery, radiotherapy or a combination of the two.
Single modality treatment may be sufficient for N1 disease (especially where the primary tumour arises
from the tonsil), but combined modality treatment (surgery plus post-operative radiotherapy) will
generally be indicated for stage N2 and N3 necks38.
The previously stated criteria for post-operative radiotherapy will apply. The dose should be varied
according to the bulk of the disease.
The classical RND has traditionally been the gold standard for treating clinically node positive necks, but
has a significant cosmetic and functional morbidity. Shoulder function is reportedly better following
MRND than classical RND (and SND better than either)13 . MRND appears to be as oncologically
effective as RND, even for N2/N3 disease, when combined with postoperative radiotherapy38. MRND
type I is now the standard technique for management of the node positive neck in many centres39. The
need for comprehensive (i.e. levels I-V) neck dissection in the node positive neck has been questioned:
for instance, it may not be necessary to dissect level I for laryngeal tumours40,41. Level V involvement is
uncommon.
131
However, if a MRND is being performed and there is involvement of non-lymphatic structures (accessory
nerve, internal jugular vein or sternomastoid muscle) then conversion to RND is generally advised.
Where bad prognostic features are found by the pathologist, postoperative radiotherapy is indicated (as
above)19.
Management of the Neck in cases of an Occult Primary Tumour
The patient will present with palpable disease in the neck in the absence of a primary site. No more than
5% of patients with head and neck cancer genuinely fall into this category as the primary site can nearly
always be identified. Any metastatic lymph node containing SCC in the neck apart from supraclavicular
fossa nodes should be considered to be a metastasis from an upper aerodigestive tract primary.
Supraclavicular fossa nodes are more likely to arise from outwith the head and neck.
Diagnosis
•
Careful upper aerodigestive tract examination is mandatory and will identify primary tumours in 4050% of patients presenting with a metastatic cervical lymph node and no other symptoms21.
•
General Examination. Examination of the breasts, the chest, the abdomen and central nervous system
should be performed.
•
Fine needle aspiration cytology is mandatory, but this is only immediately useful if positive for
carcinoma. If negative repeat attempts should be considered.
•
Radiology – Chest X ray should be performed to look for chest metastases and an obvious bronchial
primary. A CT or MRI scan of the head and neck should be performed prior to any biopsy in an
attempt to identify a primary site. The consensus among head & neck oncologists is that a CT scan of
the chest should be carried out in such circumstances. PET scanning may be useful if it is available.
•
Endoscopy under general anaesthetic. Panendoscopy should include examination of the oral cavity,
pharynx (naso/oro/ and hypo/) the larynx, and upper oesophagus. If there is still no obvious tumour
present, biopsies should be taken of the nasopharynx, the ipsilateral tonsil removed and the tongue
base biopsied. The primary will be found to be arising from the tonsil or tongue base in up to 33% of
such cases22. Bilateral tonsillectomy has been advocated as there is a 10% incidence of contralateral
node metastasis from an occult tonsillar primary45.
•
Where no primary is identified serology for EBV IgA/Early Antigen (and possibly Viral Capsid
Antigen) should be taken. If positive it is highly predictive for NPC and multiple biopsies should be
taken of the postnasal space23.
Management of the Neck in the Occult Primary
Following this protocol, it is reported that in only 5% will the primary site remain truly occult24. The
evidence supporting the management options is retrospective and of variable quality. However it is
apparent that surgical salvage after failed RT is not effective in terms of survival25 . The consensus
approach is as follows;
If the FNA is positive for SCC a neck dissection should be performed. If the tumour is staged N1, RT
should be given for poor prognostic features, and the neck observed if there are good pathological
prognostic features. For N2+ necks, combined modality treatment (surgery and RT) and possibly cisplatin
based chemotherapy should be administered.
If the FNA is negative an excision biopsy is performed. A frozen section may be performed and, if
positive, a neck dissection (MRND or RND) is carried out. If bad prognostic features are present on
histology, postoperative radiotherapy (RT) should be given. When only excision biopsy has been
performed for N1/NX disease this is always followed by RT.
For N2+ disease, a neck dissection is performed with adjuvant postoperative RT and possibly cisplatin
based chemotherapy. Chemotherapy should be administered within a clinical trial26.
132
Treatment of the likely Primary Sites
The site of cervical lymph node should be considered when trying to identify the primary tumour.
Squamous carcinomas of the head and neck region do have a typical cervical node region to which they
tend to metastasise.
Evidence for elective mucosal irradiation (EMI) is divided into papers advocating EMI on the basis of
reduced occurrence of primary site disease27 and those opposing EMI because observation demonstrated
only a small percentage of patients developing primaries27. Treatment should be individualised bearing in
mind the potential for severe morbidity and the fact that many patients may be treated unnecessarily. EMI
does not improve survival. Ipsilateral mucosal irradiation is advocated as an alternative with less
morbidity42.
Recurrence after combined treatment
Recurrence in the neck after surgery and radiotherapy carries a very poor prognosis and is often
associated with distant metastases28. However, the neck recurrence causes distressing symptoms, such as
pain, bleeding, offensive fungation and contracture. In selected cases retreatment by means of excision of
as much as possible of the tumour, brachytherapy and replacement of the overlying skin with a distant
skin or myocutaneous flap is worth considering as a palliative procedure30.
RADIOTHERAPY TECHNIQUES AND DOSES
Radical radiotherapy
Radiotherapy should be delivered within an accredited department as described in section 3. Modern
treatment will use of megavoltage photons from a linear accelerator (typical energies 4- 6 MV).
Adequate irradiation of the neck often requires the use of multiple phases of treatment using photons and
electrons of appropriate energy with patients immobilised during the treatment. In early cancer of the oral
cavity, oropharynx, hypopharynx and larynx first station nodes are treated in continuity with the primary.
The same principles should be used for selecting the nodes for radiotherapy treatment as are described
above for surgery. The probability of microscopic involvement of the other nodal groups rises with
increasing T-stage and will require the use of large matched fields to encompass these areas. Commonly
this may involve the use of asymmetric fields to ensure accurate junctioning between the anterior lower
neck field and those treating the primary site.
The number of fields and energy of photons/electrons used will depend on the exact geometry of the
individual patient. This information is best obtained by performing a CT scan in the treatment position.
The morbidity of neck irradiation is higher in the patient who has undergone a radical neck dissection. In
the future implementation of intensity modulated radiotherapy techniques may be of value in reducing
these side effects in the unexplored neck. There is now good evidence that the use of concomitant
chemo-radiotherapy may improve progression free survival in head neck cancer and this is being
increasingly used although it is associated with increased acute morbidity.
The use of elective nodal irradiation achieves ninety to ninety five percent local control with doses of
50Gy in 25 fractions or equivalent.
The indications for postoperative radiotherapy in the neck are derived from careful pathological
examination of the neck dissection specimen. Multiple nodal level involvement and extracapsular spread
are definite indications for treatment.
An increased risk of recurrence is associated with oral cavity primaries, presence of perineural invasion
around the primary site. A randomised trial carried out in advanced head and neck cancer at the MD
Anderson found no significant dose-response relationship for total doses ranging from 57.6Gy to 68.4Gy
-given in 1.8Gy fractions43.
133
A follow on trial demonstrated the importance of completing post-operative radiotherapy within 11 weeks
of surgery in the high risk group44. There may be a role for accelerated radiotherapy schedules in order to
achieve this. This question is being addressed by the current CHARTWEL trial being run in the UK.
Palliative treatment
Incurable nodal disease may be treated with either palliative chemotherapy or radiotherapy.
Available chemotherapy agents include cisplatin, 5FU and methotrexate.
Palliative radiotherapy should be delivered using simple field arrangements, by lateral parallel
pair or a single anterior field. Doses used will be lower than in radical treatment, but up to 45 Gy
or occasionally more may be required for useful disease control.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
Spiro RH, Alfonso AE, Farr HW, Strong EW. Cervical node metastases from epidermoid carcinoma of the oral cavity and
oropharynx. A critical assessment of current staging. Am J Surg 974;128:562-567.
Myers EN, Fagan JJ Treatment of the N+ Neck in Squamous cell carcinoma of the upper aerodigestive tract. Otolaryngol
Clin North Am 1998; 31: 671 – 686.
Woolgar JA. Micrometastases in oral/oropharyngeal squamous cell carcinoma; incidence, histopathological features and
clinical implications. Br. J Oral Maxillofac Surg 1999; 37:181-6.
Don-DM; Anzai-Y; Lufkin-RB; Fu-YS; Calcaterra-TC Evaluation of cervical lymph node metastases in squamous cell
carcinoma of the head and neck. Laryngoscope. 1995; 105: 669-74.
Snow GB, Patel P, Lemma’s CR, Toward R Management of cervical lymph nodes in patients with head and neck cancer.
EW Arch ORL. 1992; 249:187-194.
Stern WBR, Silver CE, Heifer BA, Perky MS, Heeler KS. Computed tomography of the clinically negative neck. Head
&Neck 1990; 12:109-113.
Stevens MH, Harnsberger HR, Mancusco AA et al. Computed tomography of cervical lymph nodes. Staging and
management of head and neck cancer. Arch Otolaryngol Head & Neck Surg 1985; 111: 735-9.
Van den Brekel MWM, Castelijns JA, Stel HV, Luth WJ, Valk J, Waal I van der, Snow GB Occult metastatic neck
disease: detection with ultrasound and ultrasound-guided fine needle aspiration cytology. Radiology 1991; 180 :457-461 .
Van den Brekel MWM, Snow GB: Assessment of lymph node metastases in the neck. Oral Oncol Eur J Cancer 1994; 30:88
Haddadin KJ, Soutar DS, Oliver RJ, Webster MH, Robertson AG, MacDonald DG Improved survival for patients with
clinically T1/T2, N0 tongue tumors undergoing a prophylactic neck dissection. Head & Neck 1999; 21:517-25.
Weiss MH, Harrison LB, Isaacs RS. Use of decision analysis in planning a management strategy for the N0 neck. Arch
Otolaryngol Head Neck Surg 1994;120:699-702.
Van den Brekel MWM, Castelijns JA, Reitsman LC et al. Outcome of observing the N0 neck using ultrasonographicguided cytology for follow up. Arch Otolaryngol Head & Neck Surg 1999; 125:153-156.
Kuntz AL, Weymuller EA. Impact of neck dissection on quality of life. Laryngoscope 1999; 109: 1334-1338.
Weber PC, Johnson JT, Meyers EN. The impact of bilateral neck dissection on patterns of recurrence and survival in
supraglottic cancer. Arch Otolaryngol Head Neck Surg. 1994; 120: 703-706.
August M, Gianetti K. Elective neck irradiation versus observation of the clinically negative neck of patients with oral
cancer. J Oral Maxillofacial Surg 1996; 54: 1050-1055.
Robbins KT, Medina JE, Wolfe GT, Levine PA, Sessions RB, Pruet CW Standardising neck dissection terminology
official report of the Academy's Committee for Head and Neck Surgery and Oncology. 1991 Arch Otolaryngol Head Neck
Surg 1991; 117:601-605.
Fletcher GL. The place of irradiation in the management of metastatic neck disease. Front Radiat Ther Oncol. 1988;
22:111-120.
Lee AWM, Sham JST, Poon YF, Ho JHC. Treatment of stage I nasopharyngeal carcinoma: analysis of the patterns of
relapse and the results of withholding elective neck irradiation. Int Radiat Oncol Biol Phys 1989;17:1183-1190.
Davidson BJ, Spiro RH, Patel S, Patel K, Shah JP. Cervical metastases of occult origin; the impact of combined modality
therapy. 1994. Am J Surg. 1994; 168: 395-9.
Buckley JG, Maclennan K. Cervical node metastases in laryngeal and hypopharyngeal cancer. A prospective analysis of
prevalence and distribution. Head & Neck 2000:22; 380-385
Mendenhall WM, Mancuso AA, Parsons JT, Stringer SP, Cassisi NJ. Diagnostic evaluation of squamous cell carcinoma
metastatic to cervical lymph nodes from an unknown head and neck primary site. Head & Neck 1998; 20:739-44.
Righi P, Sofferman R. Screening unilateral tonsillectomy in the unknown primary. Laryngoscope 1995; 105:548-550.
Chew CT. Early diagnosis of nasopharyngeal carcinoma. Ann of the Acad of Med in Singapore. 1990; 19:270-274.
Harwick RD. Cervical metastases from an occult primary site. Semin Surg Oncol 1991; 7:2-8.
Wang RC, Goepfert H, Barber AE, Wolf P. Unknown primary squamous cell carcinoma metastatic to the neck. Arch
Otolaryngol Head Neck Surg 1990; 116: 1388-1393.
134
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45
Jeramic B, Zivic DJ, Matovic M, Marinkovic J. Cisplatin and 5-fluoruracil as induction chemotherapy followed by
radiation therapy in metastatic squamous cell carcinoma of an unknown primary tumour localised to the neck. A phase II
study. J Chemother 1993; 5: 262-265.
Reddy SP et al. Metastatic carcinoma in the cervical lymph nodes from an unknown primary site; results of bilateral neck
plus mucosal irradiation vs. ipsilateral neck irradiation. Int. J. Radiat. Oncol. Biol. Phys. 1997 ;37: 797-802.
Glynne-Jones RG et al. Metastatic carcinoma in the cervical lymph nodes from an occult primary; a conservative approach
to the role of radiotherapy. Int. J. Radiat. Oncol. Biol. Phys 1990; 18: 289-294.
Ridge JA: Squamous cancer of the head and neck: Surgical treatment of local and regional recurrence. Semin Oncol 1993;
20:419.
Comes P, Cox HJ, Rhys-Evans PR et al. Salvage treatment for inoperable neck nodes in head and neck cancer using
combined iridium-192 brachytherapy and surgical reconstruction. Br J Surg 1996, 1620-2.
Brazilian Head and Neck Cancer Study Group. End results of a prospective trial on elective lateral neck dissection vs type
III modified radical neck dissection in the management of supraglottic and transglottic carcinomas. Head & Neck 1999;
21:694-702.
Taylor RJ, Wahl RL, Sharma PK, et al. Sentinel node Localization in oral cavity and oropharyngeal squamous cell cancer.
Arch Otolaryngol Head Neck Surg 2001; 127:970-974.
Shoaib T, Soutar DS, MacDonald DG, et al. The accuracy of head and neck carcinoma sentinel lymph node biopsy in the
clinically N0 neck. Cancer 2001; 91:2077-2083.
Khafif A, Lopez-Garza JR, Medina JE. Is dissection of level IV necessary in patients with T1-T3 N0 tongue cancer?
Laryngoscope 2001; 111:1088-1090.
Ambrosch P, Kron M, Pradier O, Steiner W. Efficacy of selective neck dissection: A review of 503 cases of elective and
therapeutic treatment of the neck in squamous cell carcinoma of the upper aerodigestive tract. Otolaryngol Head Neck
Surg 2001; 124:180-7.
Ferlito A, Mannara GM, Rinaldo A, et al. Is extended supraomohyoid Neck Dissection Indicated for treatment of oral
cancer with clinically negative neck? Acta Otolaryngol 2000; 120:792-795.
Byers RM, Clayman GL, McGill D, et al. Selective neck dissections for squamous carcinoma of the upper aerodigestive
tract: Patterns of regional failure. Head Neck 1999; 21:499-505.
Richards BL, Spiro JD. Controlling advanced neck disease: Efficacy of neck dissection and radiotherapy. Laryngoscope
2000; 110:1124-1127.
England RJA, Stafford ND. Conservative neck surgery in squamous cell carcinoma. Surgical Oncology 1999; 7:91-94.
Buckley JG, Feber T. Surgical treatment of cervical node metastases from squamous carcinoma of the upper aerodigestive
tract: Evaluation of the evidence for modifications of neck dissection. Head Neck 2001; 23:907-915.
Santos CR, Filho JG, Magrin J, et al. Involvement of level I neck lymph nodes in advanced squamous carcinoma of the
larynx. Ann Otol Rhinol Laryngol 2001; 110:982-984.
Friesland S, Lind MG, Lundgren J. Outcome of ipsilateral treatment for patients with metastases to neck nodes of
unknown origin. Acta Oncologica 2001; 40:24-28.
Peters IJ, Goepfert H, Ang KK, et al. Evaluation of the dose for postoperative radiation therapy of head and neck cancer:
First report of a prospective randomised trial. Int J Radiat Oncol Biol Phys 1993; 26:3-11.
Ang KK, Trotti A, Brown BW et al. Randomized trial addressing risk factors and time factors of surgery plus radiotherapy
in advanced head and neck cancer. Int J Radiat Oncol Biol Phys 2001;51:571-578.
Koch WM, Bhatti N, Williams MF, Eisele DW. Oncologic rationale for bilateral tonsillectomy in head and neck squamous
cell carcinoma of unknown primary source. Otolaryngol Head Neck Surg 2001;124:331-333.
135
Section 5
Chapter 2 Oral Cavity and Lip
This chapter has been written using the conclusions from the NOTO EBM day, ‘Management of Oral
cavity carcinoma’ in November 2000. The reference list is substantial and can be found in full on the
NOTO website www.noto.org.
CONFIRMATION OF DIAGNOSIS
EUA/endoscopy and biopsy
•
Careful physical examination is mandatory and has not been superceded by imaging..
Examination should include either fibreoptic or direct examination of pharynx, larynx and
postnasal space.
•
EUA - direct palpation to adequately assess floor of mouth, tongue and neck.
•
Panendoscopy for second primary, in those at high risk.
•
Tumour sites and areas of field cancerisation should be carefully documented using standardized
tumour maps
•
Biopsy report should include degree of differentiation, tumour thickness, vascular and peri-neural
invasion
Specific imaging
•
Superficial low-volume lesions do not require radiological studies.
•
Deep invasion, mandibular invasion and nodal status may be assessed by CT or, in selected cases,
by MRI. No single imaging modality exists with adequate sensitivity and specificity to accurately
assess mandibular invasion. A variety of techniques including MRI, CT, plain radiography and
radioisotope scans may be necessary to accurately assess neoplastic disease in the mandible.
•
All imaging methods, including specialist dental films, may not show early mandibular invasion.
The patient’s dentition is evaluated by a combination of orthopantography and standard dental
views.
CONSULTATIONS
All patients with a diagnosis of head and neck cancer must be seen in a multidisciplinary team meeting to
allow adequate discussion of the case and appropriate decision-making.
Team members should include:
•
Oncologist specializing in head & neck cancer
•
Appropriately trained head & neck surgeons with skills encompassing ablation and reconstruction
including free tissue transfer
•
Specialist head and neck nurse
•
Appropriately trained dental surgeon to assess the status of the dentition and make
recommendations in relation to the dentition in respect of radiation therapy. The evaluating
clinician should be aware of the treatment portals planned for radiotherapy.
136
Additionally prosthetic support may be required both perioperatively and in the post operative
phase for example obturation of surgical defects. An appropriately equipped and staffed oral &
maxillofacial laboratory is required to support this aspect of care
•
Speech and language therapists for pre-operative counseling regarding possible post-operative
speech and swallowing rehabilitation. To assess nutritional status and need for percutaneous
gastrostomies.
•
Internal medicine, cardiology, respiratory medicine, or anaesthetics as needed to evaluate comorbidities that may preclude or increase the risk of general anaesthesia.
•
Smoking and alcohol cessation counseling
Data regarding the cancer care spell and follow up should be collected prospectively in an appropriate
electronic database. Pooling of data and analysis would provide a powerful tool to advance the care of
patients with head & neck cancer.
Early Oral Cancer1, 2, 3,
•
T1/smaller T2 - this may be treated effectively by single modality therapy, either surgery
including ablative transoral laser treatment or radiotherapy (both external beam megavoltage and
interstitial techniques). In contrast, larger T2 lesions (>3 cm) require combination therapy.
Smaller lesions may be allowed to heal following excision by a primary repair or by secondary
infection.
•
For anterior tongue, buccal mucosa and floor of mouth surgery is preferred if tumour invades the
periosteum.
•
Radiation therapy is preferred if the oral commissure is involved and for lesions confined to the
soft palate.
•
Most gingival/palatal lesions are treated surgically.
•
Brachytherapy close to the submandibular salivary gland duct can cause scarring requiring
surgical intervention to relieve outflow obstruction. Surgical treatment with an ablative laser may
reduce this type of problem.
•
There is evidence supporting the use of photodynamic therapy as an alternative for low volume
disease with complete remission rates and maintenance of response similar to other treatment
modalities. It may have a further role in the management of field change cancerisation26, 27
•
Moh's micrographic surgery has also been used for low volume disease of the lips.
•
Trans-oral laser resection of the primary disease with the use of an operating microscope is being
increasingly advocated in some centres.
•
Discontinuous neck dissection is often carried out at a separate operative procedure to manage the
neck allowing the margins of the primary resection to be histologically assessed and further
treatment to the primary site carried out if appropriate. Survival rates compare favourably with
conventional surgery with improved functional results.
The surgical treatment includes:
•
Frozen section evaluation of margins as needed to ensure adequate resection.
•
Tracheostomy at the discretion of the surgeon.
137
•
Dental extractions if necessary.
•
Insertion of a feeding tube or gastrostomy (optional).
•
Orientation of the primary and neck dissection specimen for the pathologist, by the surgeon.
RADIOTHERAPY
•
Radiotherapy affects function in different ways to surgery. Radiotherapy may be an appropriate
option, especially in the older age group, and in those where anaesthesia is a particular risk.
Equivalent survival rates can be achieved compared to excision and repair in T1 and low volume
T2 tumours of the dorsum of the tongue, the lateral border of the middle third of the tongue, and
the floor of mouth.
•
As at other head and neck sites, verrucous tumours are treated like any SCC. Tongue tip tumours
should be excised. The above only applies if some or the entire radiation dose is given by
brachytherapy. Surgery is preferable if the facilities for brachytherapy are not available, or the
patient should be referred to a centre where brachytherapy can be offered.
•
The only situation where external beam radiotherapy alone is a valid alternative to surgery is in
early lesions of the retro-molar trigone.
Disadvantages of external beam irradiation:
•
Cannot be used again at or near same site.
•
Salvage surgery for radiation failure is associated with low survival and high morbidity.
•
Side effects include xerostomia, mucositis and osteo-radionecrosis.
•
Patients may require full dental clearance prior to treatment.
Large volume T2, T3 and T4
These tumours should be treated with combination surgery/post-operative radiotherapy if the patient
is fit enough and there is confidence that the tumour can be completely excised macroscopically and
repaired with satisfactory functional results.
Special Surgical Considerations 21, 22, 23, 24
•
Mandible A marginal/segmental mandibulectomy is carried out where invasion of the bone has
occurred. The key to a successful outcome is adequate assessment and accurate resection bearing
in mind both over and underestimates from existing imaging modalities.
•
The use of smears from the resected mandible margins has a high predictive value in the
assessment of tumour status.
•
The surgeon must be aware of the patterns of tumour invasion, which differ between dentate and
edentulous patients. Previous radiotherapy alters the pattern of invasion. It is difficult for good
functional results to be achieved after excision of the largest tumours.
•
Dental rehabilitation should be considered for patients with mandibular reconstruction. This may
include the use of osseointegrated implants.
•
Reconstruction Primary closure if possible is the method of choice but significant functional
impairment may result from the over zealous use of this technique.
138
•
The complex three dimensional and composite nature of many oral defects means that a variety of
reconstructive techniques may be indicated. These include:
•
Local skin flaps, skin grafts, vascularised free tissue transfer (including composite flaps) with
myocutaneous flaps less commonly used due to their higher morbidity.
•
Reconstruction of the mandible can be carried out using a suitable plating system (for short lateral
defects) or free tissue transfer for more extensive defects (including the anterior mandible). The
most appropriate bone flaps for mandibular reconstruction include the fibula and deep circumflex
iliac artery free flaps. Consideration should be given to the soft tissue defect when assessing the
bone flap best suited to the defect. The composite radial free flap produces excellent soft tissue
for mucosal reconstruction but has limitations in bone quantity and volume. There is an
associated incidence of fracture of the osteotomised radius that may be reduced with the use of
prophylactic plating. The best reconstruction may be achieved by the use of more than one flap
but consideration must be given to the patients general condition and the potential greater
morbidity associated with this approach
•
There are a number of plating systems available to aid reconstruction of the mandible and the
surgeon should be familiar with the indications for their use.
•
The selection of a flap to be used for oral reconstruction must consider the type of defect to be
encountered, the impact upon function of the reconstruction and the donor site morbidity. For
oro-pharyngeal soft tissue defects requiring free tissue transfer the fasciocutaneous radial forearm
flap is a versatile, reliable and robust flap. It enables a large volume of pliable thin soft tissue to
be harvested with a long pedicle and good-sized vessels for anastamosis. It is suited to a two-team
approach to surgery thus minimizing operative time and has a low donor site morbidity. Where
more bulk is required the rectus abdominus flap provides an abundant volume of skin and muscle
or muscle only for reconstruction. Vessels are again of a good size with minimal donor site
morbidity.
TREATMENT OF THE NECK 5, 15-20
•
N0 - The incidence of occult metastasis is approximately 34% according to most series,
therefore expectant management of the N0 neck is not recommended. Necks becoming
positive during a “wait and see policy” often do so at high pathological stage with poor
salvage rates.
•
Elective radiotherapy may be used, but the advantage of surgery for the N0 neck is that the
specimen is sent for histopathological examination, providing significant prognostic
information and objective assessment of adequacy of resection (elective selective staging
neck dissection). This surgical staging of the N0 neck is preferable in T2 and non-infiltrating
T3 tumours, high grade T1 lesions and low-grade T2 and T3 lesions.
•
Because of lymphatic crossover and retrograde flow, especially with anterior lesions and
those that are located at or near the mid-line, consideration should be given to treatment of
the neck bilaterally, whether radiotherapeutic or selective neck dissection.
•
Primary oral tongue lesions may have a different biological behaviour than other oral cavity
sub sites, metastasising more frequently to levels II and III than level I. In addition to levels I
to III, level IV is also at significant risk of skip lesions from primary oral tongue tumours.
Peppering of nodes at multiple levels may also occur in up to 10% of patients with primary
lesions of the tongue. Therefore, a selective neck dissection, including levels I to IV, is the
most appropriate type of neck dissection for oral tongue primary tumours.
139
•
The N+ Neck With palpable neck node involvement or evidence following imaging of the
neck, surgical treatment is required which may be in the form of a modified radical neck
dissection, radical neck dissection or extended radical neck dissection. In most instances,
post-operative irradiation is indicated.
CRITERIA FOR POST-OPERATIVE RADIOTHERAPY
Primary Site
•
Any stage with microscopically positive margins.
•
Large T2, all T3 and T4, irrespective of nodal status
•
Peri-neural or intra-vascular invasion
•
Poorly differentiated tumours.
Radiation therapy should begin as soon as possible and not > 6 weeks post surgery. It may include a
brachytherapy boost when indicated by pathological findings such as unsatisfactory margins.
LIP 6-14
Upper lip & commissures Rare, but less well-differentiated, lymphatic metastases earlier and more
diffuse. Upper lip may spread to pre-auricular and parotid nodes.
Lower lip Common - > 90% of cases.
Clinical evaluation.
•
Complete history, including history of sun exposure and tobacco usage
•
Complete examination of the head and neck. Include examination of the lip and skin of the head
and neck, entire oral cavity and oropharynx mucosa, indirect or direct fibreoptic laryngoscopy of
the larynx and hypopharynx. Evidence of neural involvement of the lower lip musculature
(marginal nerve weakness) or hyperaesthesia of the mental nerve should be documented.
Biopsy - presence of peri-neural invasion significantly decreases survival.
Specific Imaging Studies
Orthopantomogram - indicated if evidence of neural or bony involvement is present or when appropriate
to evaluate the patient's dentition prior to radiation therapy.
CONSULTATIONS
•
Dermatology - in consideration for dermatological treatment of malignant or pre-malignant
lesions or Moh’s surgery for the primary lesion.
•
Medicine or anaesthetics - as needed to evaluate existing conditions that may preclude or increase
the risk of general anaesthesia.
•
Dental assessment - in consideration for pre-radiation extractions, restorations or prophylactic
treatment.
140
DEFINITIVE TREATMENT
Treatment of Primary Tumour
Surgery
Adequate surgical excision is generally the preferred initial treatment modality. Margins should be
assessed with frozen section, as needed to ensure adequate resection. Most early lesions may be excised
under local anaesthesia +/- intravenous sedation. Adjacent pre-malignant tissue should also be excised.
Superficial lesions of the vermillion may be treated with thermal laser ablation or PDT
Full thickness lip lesion defects can be repaired by:
•
< 1/3 of lip - closed primarily with V-lip or W-lip technique.
•
>1/3 – 2/3 of lower lip - local flap reconstruction with Abbe Estlander flap, Bernard flap or
Karapandizic flap.
•
>2/3 of lower lip - usually requires micro-vascular free tissue transfer or pedicled regional flap
reconstruction.
•
Approximation of the tumour to the mandible without evidence of erosion or invasion may
require marginal mandibulectomy. Evidence of bone or neural foramina invasion should be
removed with segmental resection. Free tissue transfer offers the best reconstruction of the
anterior mandible defect.
Radiation and chemoradiation 25
T1, T2, N0
Fewer than 6% of T1 and T2 lesions are N+. Radiation therapy is a satisfactory treatment for cancer of
the lower lip, particularly for patients where the anticipated functional and cosmetic outcome is
unsatisfactory with surgery, as well as for those patients medically unfit to undergo surgery.
Treatment by external beam radiotherapy, brachytherapy or a combination of the two is employed as
dictated by the size and location of the tumour. Gingival shielding will reduce mucositis. External beam
may be electron or megavoltage (250-300 kV) photon fields.
T3, T4, N+
Generally only indicated as primary treatment modality in patients medically unfit to undergo surgical
excision and necessary reconstruction.
In some advanced cases, radiation therapy may be utilised as primary therapy if the cosmetic and
functional results from surgery are felt to be inferior to that anticipated with radiation alone. 60-70 Gy
should be utilised to treat the primary, in 1.8-2 Gy fractions.
Treatment of the Neck Surgery
N0
•
T1 - 5% risk of nodes - no treatment
141
•
T2 - 15-35% chance of nodes - controversial - usual spectrum of opinion ranging from support of
almost routine selective neck dissection to total lack of support for any form of elective
management. No firm evidence.
•
For poorly-differentiated high risk or T3/T4 lesions unilateral or bilateral selective neck
dissections levels l – lll.
N1
•
Ipsilateral modified radical neck dissection encompassing levels I-V with or without contra-lateral
supra-omohyoid neck dissection.
•
N2, N3 Ipsilateral or bilateral radical or modified radical neck dissection. The spinal accessory nerve
should be preserved if not involved or approximated in tumour.
The jugular vein should be preserved on at least one side.
•
Radiation
•
May be used in N0 neck patient at high risk for metastases (poorly differentiated or advanced
primary) or in patients unable to undergo general anaesthesia. Approximately 50 Gy in 1.82.0 Gy fractions should be utilised for N0 neck patients. For N1 patients, a radiation dose of
60-70 Gy should be utilised.
Post-operative radiation
• Beneficial to patients with close or positive primary resection margins, extensive peri-neural
invasion, extra-capsular spread or positive nodes.
• Radiation is initiated after healing has occurred, preferably not > 6 weeks post-operatively.
Recurrence
• Best managed with aggressive surgical resection with frozen section control. Elective neck
dissection advocated as 25% have occult metastases. High success rate in management of local
recurrence, 75-85%.
References
Assessment
1.
Jones KR, Lodge-Rigal D, Reddick RL, Tudo GE & Shockley WW. Prognostic factors in the recurrence of stage I and
II squamous cell cancer of the oral cavity. Arch Otolaryngol Head & Neck Surgery 1992 118: 483-485.
Tongue
2.
3.
4.
5.
Morton RP, Ferguson CM, Lambie NK & Whitlock RML. Tumour thickness in early tongue cancer. Arch Otolaryngol
Head Neck Surg 1994 120: 717-7203
Lydiatt DD, Robbins KT, Byers RM & Wolf PF. Treatment of stage I and II oral tongue cancer. Head & Neck 1993
115: 308-312.
Haughey BH. Tongue reconstruction concepts and practice. Laryngoscope 1993 103: 1132-1141.
Byers RM, Wever RS, Andrews T, McGill D, Karl R & Wolf P. Frequency and therapeutic implications of 'skip
metastasis' in the neck from squamous carcinoma of the oral tongue. Head & Neck 1997 19: 14-19.
Lip
6.
7.
Hosal IN, Onerci M, Kaya S & Turan E. Squamous cell carcinoma of the lower lip. Am J Otolaryngol 1992 13(6): 363365.
Stepnick DW. Cancer of the lip. In Current Therapy in Otolaryngology - Head & Neck Surgery, 5th Edition, Mosby, St
Louis 1994 257-261
142
8.
9.
10.
11.
12.
13.
14.
Mehregan DA & Roenigk RK. Management of superficial squamous cell carcinoma of the lip with Moh's micrographic
surgery. Cancer 1990 66: 463-468.
Fein DA, Mendenhall WM, Parson JT et al. Carcinoma of the oral tongue: a comparison of results and complications of
treatment with radiotherapy and/or surgery. Head & Neck 1994 16: 358-365.
Sykes AJ, Allan E & Irwin C. Squamous carcinoma of the lip: the role of electron treatment. Clin Oncol 1996 8: 384-386.
Knabel MR, Koranda FC, Panje WR et al. Squamous carcinoma of the upper lip. J Dermatol Surg Oncol 1982 8: 487.
Byers RM, Bland KI & Wasder J. The therapeutic and prognostic implications of nerve invasion in cancer of the lower lip.
Int J Radiat Oncol Biol 1978; 4: 215
Baker SR & Krause CJ. Carcinoma of the lip. Laryngoscope 1980 90: 19-27.
Cruse CW & Radocha RF. Squamous cell carcinoma of the lip. Plast Reconstr Surg 1987 80: 787-791.
Neck
15. Ho CM, Lam KH, Wei WI, Lau SK & Lam LK. Occult lymph node metastasis in small oral tongue cancers. Head & Neck
1992 14: 359-363.
16. DiNardo LJ. Lymphatics of the submandibular space: a study with applications to floor of mouth carcinoma. Laryngoscope
1998 108: 206-214.
17. Yuen APW, Wei WI, Wong YM, Tang CT, Elective neck dissection versus observation in the treatment of early oral tongue
carcinoma Head & Neck 1997 19:583-588
18. Andersen PE, Cambronero E, Shaha AR, Shah JP The extent of neck disease after regional failure during observation of the
NO neck Am J Surg 1996 172: 689-691
19. Woolgar JA, Scott J,.Prediction of cervical lymph node metastasis in squamous cell carcinoma of the tongue/floor of mouth
Head & Neck 1995 17: 463-472
20. Haddadin KJ, Soutar DS, Oliver RJ, Webster MH, Robertson AG, MacDonald DG,.Improved survival for patients with
clinically T1/T2 N0 tongue tumours undergoing a prophylactic neck dissection Head & Neck 1999 21: 517-5
Mandible
21. Urken ML, Weinberg H, Vickery C et al. Oromandibular reconstruction using micro-vascular composite free flaps. Arch
Otolaryngol Head Neck Surg 1991 117: 733-744.
22. McGregor AD, McDonald DG. Patterns of spread of squamous cell carcinoma within the mandible. Head Neck Surgery
1989 11:457-461
23. Brown JS, Griffith JF, Phelps PD, Browne RM. A comparison of different imaging modalities and direct inspection after
periosteal stripping in predicting the invasion of the mandible by oral squamous cell carcinoma. British Journal of Oral &
Maxillofacial Surgery 1994 32:347-59.
24. van den Brekel MW, Runne RW, Smeele LE, Tiwari RM, Snow GB, Castelijns JA. Assessment of tumour invasion into the
mandible: the value of different imaging techniques. European Radiology 1998 8:1552-7.
Radiotherapy and chemotherapy
25. Benasso M, Merlano M, Sanguinetti G et al., Gemcitabine. Cisplatin and radiation in advanced unresectable squamous cell
carcinoma of the head and neck: a feasibility study. Am J Oncol 2001 24618-22
Photodynamic therapy
26. Gluckman JL & Portugal LG. Photodynamic therapy for cancer of head and neck. Cancer Treat Res 1995 74: 159-171
27. Kubler A, de Carpentier J, Hopper C, eonard A, Putnam G,. Treatment of squamous cell carcinoma of the lip using Foscan
mediated photodynamic therapy. Int J Oral Maxillofac Surg 2001 30: 504-9
143
Section 5
Chapter 3
Hypopharynx
This chapter has been updated and modified using the work carried out by the faculty of the 5th Evidence
based Management Consensus Conference on Head & Neck Cancer in 2001 as well as the conclusions
emanating from the discussion. The abstracts and full reference list supporting the meeting is available on
the NOTO website (www.noto.org).
EVALUATION
Endoscopy. The tumour site and extent are recorded using staging diagrams and a biopsy taken for
histological examination. Oesophagoscopy is currently the best way to eliminate synchronous primary
tumours (1,2). Bronchoscopy may be useful to exclude tracheal invasion in those tumours extending to
the upper oesophagus. Tumours should be staged according to the UICC TNM Classification of
Malignant tumours (2002). It may be appropriate to perform a Percutaneous Endoscopic Gastrostomy
(PEG) at this stage.
Chest x-ray is better than bronchoscopy in defining a second primary. Chest CT is preferable.
Spiral CT and Magnetic resonance imaging (MRI) are complementary. Cross sectional imaging should
be performed in all cases due to the upstaging that these investigations lead to in a significant proportion
of cases (3). CT has the benefit of speed and may be the best technique to assess the presence of thyroid
cartilage invasion. MRI may offer better soft tissue imaging and may be better at assessing the extent of
cartilage invasion. CT including the chest is adequate for most tumours with the addition of MRI in
difficult cases (3 - 5).
Pulmonary function testing is occasionally useful prior to partial resections involving the supraglottic
larynx.
Thyroid function. This is useful as a baseline. If the thyroid is included in the radiation field there is a
high incidence of late thyroid failure (6).
TREATMENT
Treatment planning takes the patient’s physical and mental state and their wishes into consideration and
recommendations may be modified according to individual circumstances. There is a consensus that
optimal treatment for all except the earliest stage tumours is combined surgery and radiotherapy, although
there is little in the way of evidence. The validity of survival as a parameter to compare the effectiveness
of primary treatment is hindered by the high incidence of regional and distant metastases. Local control
appears to be improved by combined surgery and radiotherapy according to the little comparative data
that are available (7-10). This may improve quality of survival but more data on functional outcomes of
treatment is needed. The nature of the surgery principally depends on the site of the tumour. Conservation
surgical techniques are preferable in early stage disease if feasible. Precise treatment depends on the site
of the tumour. Some tumours may be suitable for endoscopic resection (11). The use of different
modalities to treat the primary tumour and cervical nodes is appropriate in some circumstances. Resection
should be wide enough to provide clear margins because positive margins have a poor prognostic factor.
Submucosal spread of tumour is more extensive in piriform sinus carcinoma (c.10mm) than postcricoid
carcinoma (c.5mm) (12)
Patients should be counselled to stop smoking because of the adverse effect on response to radiotherapy
and survival (13).
144
The use of neoadjuvant chemotherapy to increase laryngeal preservation has been the subject of
investigation (14) but at the present time there is insufficient evidence of improvement in either
locoregional control or survival to recommend it outside the setting of a clinical trial (15-17).
Evidence based recommendations for treatment are hindered by the lack of high quality evidence and the
absence of any evidence on function and quality of life after any intervention. In view of the fact that the
survival figures for each modality of treatment are broadly similar the treatment modality that is expected
to produce the best quality of life should be used.
Surgery
T1 and T2 tumours are very infrequent. Single modality treatment of the primary tumour by partial
pharyngolaryngectomy, radiotherapy or endoscopic resection has been reported but there is insufficient
evidence to distinguish between them on the basis of local control or survival (11, 18). There appears to
be a worse survival if the piriform sinus apex is involved and if disease is bulky. Radiotherapy appears to
be less effective in such circumstances (19).
T3-4 tumours are likely to be optimally controlled by combining radical surgery with post-operative
radiotherapy. The nature of the surgery depends on the site and extent of the tumour. Some advanced
tumours may be suitable for more extensive conservation or endoscopic surgery (11) but most require
total laryngectomy with partial pharyngectomy or total pharyngolaryngectomy. Studies concerning
conservation surgery (near total laryngectomy and supracricoid hemilaryngopharngectomy) have reported
highly selected cases but good functional results in terms of voice function have been described (20, 21).
Resection and reconstruction
It is difficult to be dogmatic about individual techniques in the absence of good quality data on functional
outcomes. Endoscopic resection is particularly suited to some early posterior wall and pyriform fossa
tumours and is likely to offer the best functional results and lowest morbidity (11). Partial pharyngectomy
with or without partial laryngectomy may be used for more advanced tumours. Reconstructive options
range from none (small posterior wall defects) through primary closure to flaps. Radial forearm,
myofascial, myocutaneous and jejunal patch flaps have all been successfully used to reconstruct partial
pharyngectomy defects. Reconstruction of total pharyngolaryngectomy by single stage techniques is the
accepted standard. Free jejunal transfer is the technique that is best supported by the literature (22,23) but
tubed free radial forearm free flaps are an appropriate alternative with less donor site morbidity. More
extensive defects involving the oesophagus may require gastric transposition.
Radiotherapy
Primary radiotherapy with salvage surgery, although only effective in a small number of patients, is a
recognised treatment in the UK and is used in some centres. Primary radiotherapy is an appropriate
treatment for small hypopharyngeal tumours (5). It is also indicated in those patients who are medically
unfit for surgery and can obviate the need for pharyngo-laryngectomy in some circumstances.
The dose given when using primary radical radiotherapy as initial treatment varies from 55 Gy in a short
overall treatment time of four weeks, to 70 Gy in seven weeks depending on the site, volume irradiated
and the treatment philosophy of different cancer centres.
Whilst primary radiotherapy for advanced tumours does not produce as good survival figures as radical
surgery, the quality of studies is impaired by selection bias in favour of surgery for fitter patients.
Postoperative radiotherapy
Postoperative radiotherapy is indicated for
• T3-T4, N0-N3 tumours
• T1-T2 N0 tumours if histology shows:
- Microscopically positive margins
- Vascular invasion
145
- Perineural invasion
- Extracapsular spread
- If neck dissection has not been performed (pNX)
Radiotherapy should be initiated within 6 weeks. The dose for adjuvant radiotherapy is in the range 45 Gy
in 18 fractions to 50 Gy in 20 fractions, well below a radical dose. The philosophy in giving adjuvant
radiotherapy does differ from that in giving primary radiotherapy where the dose has to be radical or cure
will not be achieved. If there is macroscopic or extensive microscopic disease left in the neck then a
radical course of radiotherapy should be given. An adjuvant course should be given if there is no
indication that there is any gross disease left but that there may be some microscopic residuum.
Lymph node metastases
Approximately 2/3 of patients are N+ at presentation. Occult metastases are found in about 40% of neck
dissections for N0 staged disease (24). Pathological studies show spread in the N0 neck occurs to levels II
- IV and rarely to levels I or V (25-27). Spread is bilateral in midline or bilateral tumours. Level VI
involvement may occur in apical pyriform fossa or post-cricoid tumours (28).
N0 Neck
There is very little good randomised control trial or even retrospective evidence on how to manage the
node negative neck most effectively. If a patient is having primary radiotherapy then first echelon nodes
can be covered with the radiotherapy field. If surgical treatment is used then selective neck dissection of
levels II, III, IV as a minimum is recommended, with the inclusion of level VI in those tumours that
extend to the postcricoid region or apex of the pyriform fossa. If there is oropharyngeal extension then
level I should be included. Bilateral dissection is required for central tumours.
N1-3 Neck
Comprehensive neck dissection has been the accepted standard for the N+ staged neck. The pattern of
invasion of the nodes will dictate whether radical or modified radical dissection is required. This would
usually mean a modified radical (functional) dissection for N1-2 disease. Pathological studies suggest that
selective neck dissection of levels II - IV may be adequate for N1 disease (23-27). Although its use is
controversial, there is some comparative evidence of its clinical effectiveness (29). The available
evidence on functional and quality of life outcomes suggests that selective neck dissection is superior to
comprehensive dissection (30, 31). The use of supradose cis-platinum and radiotherapy is being trialled
for advanced and inoperable neck disease.
Recurrent or residual disease
In general surgery should be used for recurrent disease if it is resectable. Post-operative radiotherapy is
used if it has not been given before. Chemotherapy may have a palliative role.
Rehabilitation
The help of the speech therapist is invaluable for restoring normal swallowing and speech after partial
surgery. Consideration should be given to surgical voice restoration as either a primary or secondary
procedure. Low-pressure valves are necessary when free tissue transfer has been used for reconstruction.
These patients can have quite marked nutritional problems and the input of a dietician is important.
In some circumstances the long term use of gastrostomy feeding may be required. PEG feeding is usually
required during radical or adjuvant radiotherapy.
Palliation
Approximately one third of patients are incurable at presentation. The specialist palliative care team
should be involved as early as possible in the disease process. Pain can be controlled and local protocols
should be followed. Percutaneous endoscopic gastrostomies (PEGs) placed early can help maintain
nutrition in an acceptable manner.
146
Palliative radiotherapy can produce tumour shrinkage and hence symptom relief. Dysphagia and
dyspnoea due to obstruction and pain due to infiltration may all help. Doses approaching radical doses are
often required. However, 40Gy given in 10 fractions three times weekly is also helpful.
Re-treatment with radiotherapy and especially using superficial electrons to recurrent neck disease might
be useful. Total cord doses have to be carefully assessed in this situation. Endoscopic tumour debulking
with the laser may help relieve obstructive symptoms. In inoperable cervical node recurrence further
surgery and brachytherapy are sometimes very effective. For bone metastases standard radiotherapy
techniques are used. Palliative radiotherapy is not indicated for asymptomatic distant extension or spread
since it will cause iatrogenic symptoms and will not produce cure. The role of chemotherapy as adjuvant
or neo-adjuvant treatment is not supported by randomised controlled trials. Toxicity due to palliative
chemotherapy is unacceptable. Carboplatin plus or minus 5 fluorouracil is a reasonable palliative regime.
Taxanes may have a role to play in fitter patients. In the absence of a response, persistence is not rational.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
Fitzpatrick PJ, Tepperman BS, Deboer G: Multiple primary squamous cell carcinomas in the upper digestive tract. Int J
Radiat Oncol, Biol, Phys 1984. 10: 2273-2279.
Black RJ, Gluckman JL, Shumrick DA: Multiple primary tumors of the upper aerodigestive tract. Clin Otolaryngol 1983.
8:277-281.
Zbaren P, Becker M, Lang H: Pretherapeutic staging of hypopharyngeal carcinoma: clinical findings, computed
tomography, and magnetic resonance imaging compared with histopathologic evaluation. Arch Otolaryngol, Head Neck
Surg 1997. 123:908-913.
Becker M. Larynx and hypopharynx. Radiol Clin North Am. 1998. 36:891-920.
Pameijer FA; Mukherji SK; Balm AJ; van der Laan BF. Imaging of squamous cell carcinoma of the hypopharynx. Semin
Ultrasound CT MR 1998. 19:476-91.
Turner SL, Tiver KW, Boyages SC: Thyroid dysfunction following radiotherapy for head and neck cancer. Int J Radiat
Oncol, Biol, Phys. 1995. 31:279-283.
Van den Bogaert W. Ostyn F. van der Schueren E. Hypopharyngeal cancer: results of treatment with radiotherapy alone and
combinations of surgery and radiotherapy. Radiother & Oncol. 1985. 3:311-8.
Arriagada R. Eschwege F. Cachin Y. Richard JM. The value of combining radiotherapy with surgery hypopharyngeal and
laryngeal cancers. Cancer. 1983. 51:1819-25.
Elias MM. Hilgers FJ. Keus RB. Gregor RT. Hart AA. Balm AJ. Carcinoma of the pyriform sinus: a retrospective analysis
of treatment results over a 20-year period. Clin Otolaryngol 1995. 20:249-53.
Pingree TF. Davis RK. Reichman O. Derrick L. Treatment of hypopharyngeal carcinoma: a 10-year review of 1,362 cases.
Laryngoscope. 1987. 97:901-4.
Steiner W. Ambrosch P, Hess CF, Kron M. Organ preservation by transoral laser microsurgery in piriform sinus carcinoma.
Otolaryngol Head Neck Surg 2001. 124:58-67
Batsakis JG. Surgical margins; a pathologists perspective. Adv Anatom Pathol 1999. 6:140-148.
Browman GP, Wong G, Hodson I, et al.: Influence of cigarette smoking on the efficacy of radiation therapy in head and
neck cancer. New England Journal of Medicine 1993. 328:159-163.
Lefebvre JL, Chevalier D, Luboinsky B, et al.: Larynx preservation in pyriform sinus cancer: preliminary results of a
European Organization for Research and Treatment of Cancer phase III trial. J Nat Cancer Inst 1996. 88:890-899.
Harari PM: Why has induction chemotherapy for advanced head and neck cancer become a United States community
standard of practice? J Clin Oncol 1997. 15:2050-2055.
Beauvillain C, Mahe M, Bourdin S, et al.: Final results of a randomized trial comparing chemotherapy plus radiotherapy
with chemotherapy plus surgery plus radiotherapy in locally advanced resectable hypopharyngeal carcinomas.
Laryngoscope 1997. 107:648-653.
Head and Neck Contracts Program: Adjuvant chemotherapy for advanced head and neck squamous carcinoma: final report
of the Head and Neck Contracts Program. Cancer 1987. 60:301-311.
Pameijer FA, Mancuso AA, Mendenhall WM et al, Evaluation of pretreatment computed tomography as a predictor of local
control in T1/T2 pyriform sinus carcinoma treated with definitive radiotherapy. Head Neck 1998. 20:159-68.
Mendenhall WM, Parsons JT, Devine JW, et al.: Squamous cell carcinoma of the pyriform sinus treated with surgery and/or
radiotherapy. Head and Neck Surgery 1987. 10:88-92.
Pearson BW, DeSanto LW, Olsen KD, Salassa JR. Results of near-total laryngectomy. Ann Otol Rhinol Laryngol. 1998.
107:820-5.
Laccourreye H, Lacau St Guily J, Brasnu D, Fabre A, Menard M. Supracricoid hemilaryngopharyngectomy. Analysis of 240
cases. Ann Otol Rhinol Laryngol 1987. 96:217-21.
Coleman JJ 3rd. Reconstruction of the pharynx and cervical esophagus. Seminars in Surgical Oncology. 1995. 11:208-20.
Theile DR, Robinson DW, Theile DE, Coman WB. Free jejunal interposition reconstruction after pharyngolaryngectomy:
201 consecutive cases. Head and Neck 1995. 17:83-8.
147
24. Shah JP. Shaha AR. Spiro RH. Strong EW. Carcinoma of the hypopharynx. Am J Surg. 1976. 132:439-43.
25. Shah JP. Patterns of cervical lymph node metastases from squamous carcinomas of the upper aerodigestive tract. Am J Surg.
1990. 160:405-409.
26. Byers RM. Modified neck dissection: a study of 967 cases from 1970 to 1980. A J Surg 1985. 150:414-421.
27. Candela FC, Kothari K, Shah JP. Patterns of cervical node metastases from squamous carcinoma of the oropharynx and
hypopharynx. Head Neck Surg. 1990. 12:197-203.
28. Buckley JG, MacLennan K. Cervical node metastases in laryngeal and hypopharyngeal cancer: A prospective analysis of
prevalence and distribution. Head and Neck 2000 22:380-5.
29. Pelliteri PK, Robbins KT, Neuman T. Extended application of selective neck dissection with regard to nodal status. Head
and Neck. 1997.19:260-265.
30. Kuntz AL. Weymuller EA Jr. Impact of neck dissection on quality of life. Laryngoscope. 1999 109:1334-8.
31. Leipzig B, Suen JY, English JL, Barnes J, Hooper M. Functional evaluation of the spinal accessory nerve after neck
dissection. Am J Surg 1983. 146:526-529-32
148
Section 5
Chapter 4
Oropharynx
GENERAL
When considering tumours in this subsite it should be remembered that there are significant differences in
management for each of the anatomical areas which may be involved (1).
The principle areas for registration of index tumours are tonsil, base of tongue, soft palate and pharyngeal
wall. As with many areas of the head and neck it is frequently difficult to determine the index site of large
indeterminate tumours.
The main effects of treatment are on the functions of speech and swallowing and are at their greatest
when the soft palate and tongue are involved.
ASSESSMENT OF TUMOUR/CONFIRMATION OF DIAGNOSIS
Although full assessment in the outpatient setting is of value in giving an appreciation of the extent of the
tumour it is mandatory to carry out an EUA and biopsy of the tumour. This will:
•
•
•
•
•
•
•
determine the histological diagnosis
enable staging
assess extent of surgical resection; with respect to extension across the midline of the tongue base,
involvement of the mandible, larynx, or prevertebral muscles.
give indication of type and extent of reconstruction required
allow assessment of potential airway compromise/requirement for tracheostomy
exclude synchcronous head and neck tumours
assess/treat dentition
INVESTIGATIONS
These are principally imaging. Assessment of the primary is best achieved by either CT or MR scanning
with the latter being the preferred option. The use of imaging allows further assessment of the neck and
chest, which is of importance in this group as oropharynx has the highest incidence of distant metastases
of all the head and neck tumours (2). If there is further doubt about the neck status ultrasound with FNAC
can be performed, an orthopantomogram is frequently required when assessing the dentition.
CONSULTATIONS
•
Dietary; most of the tumours involving the tongue base, tonsil, or pharyngeal wall will require dietary
support to correct the frequently encountered cachexia and for continuing support during treatment.
Although there should be a low threshold for gastrostomy insertion, either by endoscopic or
radiological techniques, it carries the potential for additional morbidity (3).
•
Speech and Language Therapy; Early referral is required to allow management of
communication and swallowing problems.
•
Oral Surgery; Treatment of caries must be complete in view of potential mandibular surgery and/or
radiotherapy.
In view of the significant differences between subsites, each will be considered in turn.
149
both
TONSIL
Tonsil carcinoma may be found as part of the diagnostic workup of a patient presenting with SCC
lymphadenopathy. The tonsil dissection for such a T1 lesion is sufficient as the initial treatment but
radiotherapy will be required post operatively
T1/T2 lesions can be treated by transoral surgery or radical radiotherapy
T3/T4 lesions require radical resection, frequently some form of clearance of the ipsilateral neck,
reconstruction and radical radiotherapy.
To ensure adequate exposure of the tumour ipsilateral paramedian mandibulotomy is generally the most
effective and when carried out in the most appropriate site results in little morbidity.
Irrespective of the neck status neck dissection is performed to facilitate the reconstruction of the defect,
this will range from a selective neck dissection to a modified radical neck dissection.
Reconstruction is by either pectoralis major myocutaneous flap or free radial flap with little conclusive
evidence of a better functional result with one than the other (4). If resection of the mandible is required,
for example due to involvement of the retromolar trigone every effort should be made to preserve at least
the rim of the mandible as the functional result is superior to that if a segmental resection is required. If it
is necessary then a free fibula flap will be required for the defect.
BASE OF TONGUE
Although T1 lesions can be treated by surgery, for example via a transhyoid approach, there has been
increasing interest in the use of endoscopic laser techniques. There is little evidence in the relative value
of any of these techniques or methods of reconstruction. They can however be treated equally well by
radical radiotherapy. T2,T3 and T4 lesions require radical treatment, the principal decision being
between the use of brachytherapy in conjunction with bilateral neck dissections or external beam
radiotherapy possibly in conjunction with chemotherapy (5-8). There are various chemotherapy regimes
which can be used, but in general they include the platinum based drugs, carboplatin or cisplatin, and 5FU
(9-13). If there is recurrence, or if the extent of the original tumour is deemed incurable by the above
techniques, total glossectomy with laryngectomy may be considered. This has extremely high morbidity,
but with careful counselling and extensive rehabilitation it can be performed in an appropriate group of
patients.
SOFT PALATE
Tumours in this area tend to appear on the free edge of the soft palate or uvula, are predominantly T1 or
T2 at presentation, and can be treated effectively by either endoscopic resection, with or without the CO2
laser, or by radical radiotherapy. If they are larger and radical resection is employed effective, functional
reconstruction is a challenge and frequently results in significant morbidity.
POSTERIOR PHARYNGEAL WALL
T1/T2 lesions can be treated by either endoscopic resection or by radical radiotherapy.
If more extensive than this then they will tend to involve the lateral pharyngeal wall and so treatment will
be very similar to that for tonsillar tumours. If more advanced then to effect a cure is difficult , however to
attempt this or to maximise palliation radical radiotherapy +/- chemotherapy can be used.
150
Difficulty in swallowing and aspiration occur in most patients, with little evidence in support of any
combination in treatments reducing this morbidity.
NECK
As base of tongue, posterior pharyngeal wall, and palatal lesions predominantly affect the midline then
spread to lymph nodes on both sides of the neck must be considered when planning treatment. (14-17). In
the N0 neck consideration should be given to elective treatment, either by radical radiotherapy or by
selective neck dissection if open resection is being employed (18). In T1/T2 lesions levels I-III are
cleared, whereas with more extensive lesions level IV is also included. In the last few years there has been
increasing interest in the use of sentinel node biopsy. Although it shows promise, either on its own or in
combination with imaging such as ultrasound, its use can be regarded as research based at present. (19,
20).
The N1 neck is treated by neck clearance either by selective or type I modified radical neck
dissection, depending on the treatment of the primary. In early lesions radical radiotherapy may be used.
In N2/N3 necks a type I modified radical neck dissection is indicated but may not be possible depending
on the site of the disease in N2 and the extent in N3. Post operative radical radiotherapy is indicated if
more than one node is involved or if extracapsular spread is present.
RADIOTHERAPY
This may be indicated in the following circumstances:
Postoperatively to the index site following excision of large tumours and to the neck if more than one
node is involved.
To the index tumour in the case of T1/T2 lesions with a curative aim or in T3/T4 lesions, with or without
chemotherapy, as either with a curative or palliative aim.
The dose and fractionation is determined by local factors, from 50Gy being used electively for the N0
neck, 60/65 Gy for the index site to 68Gy for advanced base of tongue lesions in conjunction with
chemotherapy.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Bradley PJ. – Management of squamous cell carcinoma of the oropharynx. Current Opinion in Otolaryngology & Head &
Neck Surgery. 2000. 8:80-86.
Goodwin WJ. Distant metastases from oropharyngeal cancer. Journal of Oto-Rhino-Laryngology & Its Related Specialties.
2001. 63:222-3.
Magne N., Marcy PY., Foa C., Falewee MN., Schneider M., Demard F., Bensadoun RJ. – Comparison between nasogastric
tube feeding and percutaneous fluoroscopic gastrostomy in advanced head and neck cancer patients. Eur Arch Oto-RhinoLaryngol. 2001.258:89-92.
Klozar J., Lischkeova B., Betka J. - Subjective functional results 1 year after surgery and postoperative radiation for
oropharyngeal carcinoma. Eur Arch Oto-Rhino-Laryngol. 2001. 258:546-551.
Robertson ML., Gleich LL., Barrett WL., Gluckman JL. – Base of tongue cancer: survival, function and quality of life after
external-beam irradiation and brachytherapy. Laryngoscope. 2001. 11:1362-5.
Grabenbauer GG., Rodel C., Brunner T., Schulze-Mosgau S., Strnad V., Muller RG., Iro H., Sauer R. – Interstitial
brachytherapy with Ir-192 low-dose-rate in the treatment of primary and recurrent cancer of the oral cavity and
oropharynx> Review of 318 patients treated between 1985 and 1997. Stralentherapie und Onkologie. 2001.177:338-44.
Kaylie DM., Stevens KR Jr., Kang MY., Cohen JI., Wax MK., Anderson PE. – External beam radiation followed by
planned neck dissection and brachytherapy for base of tongue squamous cell carcinoma. Laryngoscope 2000. 110:1733-6.
Mazeron JJ., Noe G., Simon JM. - Head and neck brachytherapy. Seminars in Radiation Oncology. 2002.12:95-109.
Mantz CA., Vokes EE., Stenson K., Kies MS., Mittal B., Witt ME., List MA., Weichselbaum RR., Haraf DJ. – Induction
chemotherapy followed by concomitant chemoradiotherapy in the treatment of locoregionally advanced oropharyngeal
cancer. 2001 Cancer Journal 7:140-8.
Kokubo M., Nagata Y., Nishimura Y., Kimura H., Shoji K., Asato R., Sasai K., Hiroaka M. – Concurrent
chemoradiotherapy for oropharyngeal carcinoma. Am J Clin Oncol 2001. 24:71-6.
Domenge C., Hill C., Lefebvre JL., De Raucourt D., Rhein B., Wibault P., Marandas P., Coche-Dequeant B., StromboniLuboiski M., Sancho-Garnier H., Luboinski B. Randomized trial of neoadjuvant chemotherapy in oropharyngeal
carcinoma. French Groupe d’Etude des Tumeurs de la Tet et du Cou (GETTEC). Br J Cancer. 2000. 83:1595-8.
151
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
Urba SG., Wolf GT., Bradford CR., Thornton AF., Eisbruch A., Terrell JE., Carpenter V., Miller T., Strawderman M. –
Neoadjuvent therapy for organ preservation in head and neck cancer. Laryngoscope 2000.110:2074-80.
Giralt JL., Gonzalez J., del Campo JM., Maldonado J., Sanz X., Pamias J., Eraso A., Bescos S., Rapsall G. – Preoperative
induction chemotherapy followed by concurrent chemoradiotherapy in advanced carcinoma of the oral cavity and
oropharynx. Cancer 2000. 89:939-945.
Mukherji SK., Armao D., Joshi VM – Cervical node metastases in squamous cell carcinoma of the head and neck: what to
expect. Head & Neck. 2001.23:995-1005.
Ferlito A., Shaha AR., Rinaldo A. – The incidence of lymph node micro-metastases in patients pathologically staged N0 in
cancer of oral cavity and oropharynx. Oral Oncology. 2002. 38:3-5.
Gray L., Woolgar J., Broan J. – A functional map of cervical metastases from oral squamous cell carcinoma. Acta OtoLaryngologica. 2000. 120: 885- 890.
Ambrosch P., Kron M., Pradier O., Steiner W. – Efficacy of selective neck dissection: a review of 503 cases of elective and
therapeutic treatment of the neck in squamous cell carcinoma of the upper aerodigestive tract. Otolaryngology – Head &
Neck Surgery. 2001.124: 180-7.
Shoaib T., Soutar DS., MacDonald DG., Camilleri IG., Dunaway DJ., Gray HW., McCurrach GM., Bessent RG., MacLeod
TI., Robertson AG. – The accuracy of head and neck carcinoma sentinel lymph node biopsy in the clinically N0 neck.
Cancer 2001. 91:2077-83.
Colnot DR., Nieuwenhuis EJC., Van den Brekel MWM., Pijpers R., Brakenhoff RH., Snow GB., Castelijns JA. – Head and
neck squamous cell carcinoma: Us-guided fine needle aspiration of sentinel lymph nodes for improved staging – Initial
experience. Radiology. 2001. 218:289-293.
Staar S., Rudat V., Stuetzer H., Dietz A., Volling P., Schroeder M., Flentje M., Eckel HE., Meuller RP – Intensified
hyperfractionated accelerated radiotherapy limits the additional benefit of simultaneous chemotherapy – results of a
multicentric randomized German trial in advanced head-and-neck cancer. Int J Radiat Oncol, Biology, Physics. 2001.
50:1161-71.
Rudat V., Wannemacher . – Role of multimodal treatment in oropharynx, larynx, and hypopharynx cancer. Seminars in
Surgical Oncology. 2001. 20:66-74.
Johansen LV., Grau C., Overguard J. – Squamous cell carcinoma of the oropharynx – an analysis of treatment results in
289 consecutive patients. Acta Oncologica.2000. 29:985-94.
Zuydam AC., Rogers SN., Brown JS., Vaughan ED., Magennis P. – Swallowing rehabilitation after oro-pharyngeal
resection for squamous cell carcinoma. Br J Oral & Maxfac Surg. 2000. 28:513-8.
Licitra L., Bernier J., Grandi C., Merlano M., Bruzzi P., Lefebvre JL. – Cancer of the oropharynx. Critical Reviews in
Oncology-Hematology. 2002. 41:107-122.
Cizmarevic B., Lanisnik B., Didanovic V., Kramberger K. – Combined therapy for oral cavity and oropharyngeal
squamous cell carcinoma: Depth of invasion as prognostic factor. Radiology & Oncology. 2001. 35:255-258.
Gupta NK., Swindell R. – concomitant methotrexate and radiotherapy in advanced head and neck cancer: 15-year followup of a randomized clinical trial. Clin Oncol. 2001.13:339-344.
Cappeillo J., Bolzoni A., Piazza C., Balzabelli C., Nicolai P., Antonelli AR. – Oncologic results and quality of life after
reconstructive surgery for advanced oral cavity and oropharyngeal cancer. Rivista Italiana di Chirurgia Plastica.2000.
32:145-151.
Wax MK., Myers LL., Anderson Pe., Cohen JI. – The effect of head and neck reconstruction on quality of life. Current
Opinion In Otolaryngology & Head & Neck Surgery. 1999.7:180-184.
Hosal AS., Carrau RL., Johnson JT., Myers EN. – Selective neck dissection in the management of the clinical nodenegative neck. Laryngoscopy. 2000.10:2037-2040.
Pignon JP., Bourhis J., Domenge C., Designe L. – chemotherapy added to locoregional treatment for head and neck
squamous cell carcinoma: three meta-analyses of updated individual data. Lancet. 2000.355:949-955.
Bouthis J., Pignon JP. – Meta-analyses in head and neck squamous cell carcinoma: What is the role of chemotherapy?
Hematology - Oncology Clinics of North America. 1999.13:769-775.
152
Section 5
Chapter 5
Larynx
CONFIRMATION OF DIAGNOSIS
Clinical and radiological evaluation are necessary for accurate staging. Laryngoscopy or
microlaryngoscopy and pharyngoscopy are supplemented with oesophagoscopy and bronchoscopy where
necessary. Hopkin’s rods should be used in assessing the subglottis. If available, photo documentation is a
valuable record of the lesion for the case record. PET (positron emission tomography) has shown promise
in detecting primary and recurrent laryngeal disease (1).
TREATMENT
An accurate anatomical description of the tumour extent is essential to stage the tumour, and to allow the
best treatment selection. All patients must be accurately staged clinically and radiologically. It is
essential that this information is recorded. Glottic, supraglottic and subglottic tumours differ significantly
in patterns of behaviour and are considered separately. Even tumours involving different anatomical subsites within the same region may behave differently. These tumour related factors, as well as the medical
condition and the needs of the individual patient, all require consideration in formulating a treatment
strategy. In general, radiotherapy and conservation surgery alone are options for T1-2, N0 lesions, and
combined surgery and radiotherapy is used for advanced (high volume T3 and 4) and N+ disease (2). The
UK standard practice for treating T1 and T2 laryngeal cancer is currently radiotherapy.
The sole use of radical radiotherapy, or sole use of surgery for all T stages of laryngeal cancer is not
acceptable.
It is no longer acceptable for surgeons to manage patients laryngeal cancer on the basis of only one
surgical option (total laryngectomy)
No patient should be subjected to laryngectomy in the absence of modern methods of voice restoration
including valved speech.
The surgeon’s repertoire must include conservation techniques, including laser surgery, partial
laryngectomy, selective neck dissection, and surgical voice restoration.
Early glottic cancer
The goal of treatment in glottic cancer is to effect a cure and preserve a normal voice without impairing
breathing or swallowing. To select the appropriate treatment modality for early glottic cancer is difficult
in the face of extensive conflicting literature supporting different approaches (3,4) Early glottic cancer is
potentially curable with either surgery or radiotherapy (5) Single modality treatment is recommended.
Endoscopic or open resection (partial laryngectomy), or radiotherapy are the treatment options. There is a
need for a randomised control trial to evaluate (a) disease control, (b) functional outcomes, (c) treatment
morbidity. Tumour distribution and the age and performance status of the patient determine the choice of
treatment.
A comparison of outcomes in Canada and the US suggested better larynx preservation in treatment plans
consisting of primary radiotherapy with salvage surgery. Survival was the same (6).
Tis: Evidence suggests carcinoma-in-situ can be reversible with cessation of smoking (7) Excision
biopsy is probably the treatment of choice although excellent control rates can be achieved with both
endolaryngeal microsurgery and radiotherapy.
Excision with preservation of the vocal ligament if possible is probably the best option, if not then an
initial biopsy followed by definitive treatment is indicated. Close follow-up where possible by the same
treatment team is important (8).
T1a – T1a: A large amount of literature, almost exclusively case series, reports that radiotherapy or
endoscopic laser resection offer comparable local control rates for accessible lesions.
153
Similar local control rates can be achieved with partial laryngectomy (9) although voice results are
radiotherapy and laser surgery seem better (10).
Cost analysis shows endolaryngeal laser surgery to be more cost-effective that radiotherapy.
T1b: Treatment options here are the same as T1a (Radiotherapy, Laser surgery and Partial
laryngectomy) In the UK radiotherapy remains the overall treatment of choice. Involvement of the
anterior commissure in some series correlates with poorer outcome for both radiotherapy and laser
therapy. This may however relate to under-staging of the disease at diagnosis (11,12).
For partial laryngectomy satisfactory functional results can be achieved if more than half of the
contralateral cord is preserved.
The literature supports the belief that continued smoking and alcohol consumption during and after
radiotherapy worsens the outcome in terms of local control (13,14)
T2: Superficial tumours without restricted cord mobility (T2a) can be treated by radiotherapy or
surgery. Radiotherapy may be preferable for extensive superficial tumours because of better functional
results. Tumours impairing cord movement (T2b) can be treated with radiotherapy or partial
laryngectomy (15). One recent paper reports high local control rates (93.8-95.7%) in patients undergoing
induction chemotherapy and partial laryngectomy for T2 glottic carcinoma (16) In the absence of
randomised controlled trial evidence however the impact of combined versus single modality therapy in
early glottic cancer remains unclear.
Advanced glottic cancer
T3: Large variations in tumour volume affect treatment outcome in similarly staged tumours
(17).Treatment needs to be individualised. It may be that some T3 tumours are under-staged and are really
T4 due to unsuspected cartilage invasion. Treatment options are surgery or radiotherapy or combined
therapy. Partial laryngectomy may be suitable for small volume tumours while radiotherapy may be the
preferred option for medically unfit patients and can give better voice outcomes.
The role for combination therapy including chemotherapy is unclear at the present time. Overall survival
is comparable with all treatment options although laryngeal preservation is obviously higher in those
patients undergoing primary non-surgical treatment. Loco-regional control may however be better in the
surgically treated patient. One non-randomised study from India reported higher 4 year survival rates in
the Surgery and radiotherapy group compared with the Radiotherapy and salvage surgery group (18). A
review of prognostic factors in T3 laryngeal cancers concluded that glottic lesions, female patients and N0
disease did better with primary radiotherapy and salvage surgery while patients with pre-operative
tracheostomy or N+ disease did better with primary surgery (19)
Salvage surgery generally implies total laryngectomy however some authors now report good results
with salvage partial laryngectomy (20,21)
As the role of chemotherapy remains unclear in advanced disease its use should be confined to the setting
of a clinical trial.
T4.: Primary surgery with post-operative radiotherapy may be the treatment of choice since authors
report higher disease-free survival compared with primary radiotherapy (22). Patients who are not fit for
or refuse surgery may be candidates for radiotherapy and/or chemotherapy.
A randomised controlled trial of alternating chemo-radiotherapy compared with radiotherapy alone in
patients with advanced inoperable head and neck cancer ( including laryngeal) reported higher diseasefree and overall survival in the combined treatment group (23).
Supraglottic Tumours
Treatment should take into account the high incidence of overt and occult metastatic disease. T staging
does not correlate well with tumour volume, suitability for partial laryngectomy, or prognosis. In general
early stage tumours are treated with a single modality, advanced tumours with combined surgery and
radiotherapy. Surgery may offer better local control for early stage supraglottic cancer (24,25) but not all
patients are medically suitable, with the risk of post-operative swallowing problems and aspiration.
154
Early Supraglottic Tumours – T1-2
Conservation surgery (including endolaryngeal resection) or radiotherapy are alternatives. The choice
depends on the tumour distribution and performance status. Consideration should be given to bilateral
elective neck treatment.
Advanced Supraglottic Tumours – T3-4
The only prospective randomised trial for advanced laryngeal cancer suggests that total laryngectomy
with post operative radiotherapy confers no survival advantage when compared to induction
chemotherapy followed by radiotherapy, and if necessary salvage laryngectomy (26). Other studies have
suggested there is no survival advantage for T3 laryngeal cancers in performing laryngectomy with or
without follow up radiotherapy, compared to radical radiotherapy with salvage surgery (27,28), but that
primary laryngectomy with follow up radiotherapy does confer a significant survival advantage in T4
laryngeal disease compared to radical radiotherapy, with if necessary, salvage surgery (22). This may
suggest chemoradiation to be the treatment of choice in low volume T3 laryngeal disease, but that
primary surgery with follow up radiotherapy should be considered for high volume T3 supraglottic
disease. Primary surgery does have the advantage of allowing access to the neck nodes. Midline cancers
must have both sides of the neck treated (29). Patients with supraglottic tumours involving the preepiglottic space or upper piriform fossae may be suitable for an extended supraglottic or subtotal
laryngectomy rather than total laryngectomy (30). To perform conservation laryngeal surgery the patient
must have good health and pulmonary function otherwise total laryngectomy is the surgical option of
choice.
Subglottic Tumours
Most tumours are indistinguishable from glottic tumours with subglottic extension. Radiotherapy may be
suitable for early tumours, but most present at a late stage often with stridor, and treatment with total
laryngectomy and post-operative radiotherapy is indicated.
MANAGEMENT OF THE NECK IN LARYNGEAL CANCER
N0
In early glottic cancer (T1-T2), there should be no need for elective neck treatment as the risk for occult
neck metastases is low.
There is no Level I or II evidence that elective treatment of the N0 neck in laryngeal cancer improves
survival. Elective treatment of the neck inevitably carries some morbidity. Elective neck irradiation is as
effective as elective neck dissection. Some groups adopt an aggressive surgical policy for the N0 neck
(31).
However, with advanced glottic cancer (T3-T4), transglottic, all T stages of supraglottic cancer, and
subglottic cancer there is at the present time a consensus that the neck needs to be treated electively.
Treatment of the primary site will determine how the neck is treated. If the primary site is treated with
radiotherapy then elective neck radiation should be performed. If the primary site is treated with surgery
then an appropriate elective neck dissection should be performed. Glottic cancer would be treated with an
ipsilateral selective neck dissection, and a bilateral selective neck dissection for supraglottic cancer.
Levels II, III, IV are at greatest risk. Subglottic extension of glottic cancers and subglottic cancer tend to
spread to the paratracheal nodes (level VI) and these should be included in the bilateral neck dissection
(32) If the paratracheal nodes are positive then the mediastinum should be included in the post-operative
radiotherapy fields. If histopathology demonstrates multiple nodal metastases, or extra capsular spread,
post-operative radiotherapy of the neck is indicated.
In Salvage surgery treatment of the N0 neck should always be considered (33).
N+
If radiotherapy (with or without chemotherapy) is used to treat the primary tumour both sides of the neck
should be included in the irradiation fields.
155
If post radiotherapy assessment at 6 weeks demonstrates, on clinical examination or CT scan, residual
neck disease, then this should be treated with a modified or radical neck dissection.
If the primary tumour is treated with surgery then a modified radical neck dissection(s) is performed with
post-operative radiotherapy for multiple positive nodes, or nodes demonstrating extra capsular spread.
Histological positive paratracheal nodes would indicate post-operative radiotherapy to the mediastinum.
Bilateral dissection is arguably required for all supraglottic disease, but is essential when the disease
crosses the midline.
Special Circumstances
The patient presenting with stridor presents a difficult problem. Most have advanced disease that dictates
combined modality treatment. Endoscopic debulking is carried out when possible. This can be with the
microdebridor or laser (34) Tracheostomy, although not desirable, may be necessary. Emergency
laryngectomy should be used only in exceptional circumstances. The diagnosis being established with
frozen section.
Recurrent or Residual Disease
The treatment will depend on whether the patient has been treated with initial irradiation or surgery.
Recurrence after previous irradiation is managed with salvage surgery. The surgical approach for
recurrent disease is planned according to the site and extent of the original lesion. Total laryngectomy is
the most commonly performed salvage surgery, although conservation laryngeal procedures are still
appropriate in carefully selected cases (20). Unresectable post-surgical recurrences are treated with
radiation, with or without chemotherapy. Stomal recurrence, particularly if arising superiorly may be
resectable, requiring mediastinal resection and possible pharyngeal replacement.
CHEMOTHERAPY IN LARYNGEAL CANCER
The role of chemotherapy in the management of laryngeal cancer is evolving through mounting evidence
from randomised trials and non-randomised studies.
The contribution of chemotherapy must be judged by its effect on laryngeal preservation, disease free and
overall survival, and on levels of treatment related morbidity.
Studies of chemotherapy on laryngeal preservation have shown that the larynx could be preserved in a
quarter to a third of cases without detriment to overall survival. The American VA trial, which has the
longest follow-up (median follow-up over 8 years) confirms the larynx can be preserved in up to 2/3 of
patients achieving complete or partial response to induction chemotherapy without jeopardising survival
(26).
The EORTC trial (of larynx preservation in patients with hypopharyngeal cancers) showed a similar
effect (35). An interim report on a French randomised trial (GETTEC) concerning just 68 patients of a
planned 300 accrual showed a worse survival outcome for those receiving induction chemotherapy (36).
Meta-analysis of all three trials demonstrated there was no differences in overall or disease free survival,
but a functional larynx was preserved in two thirds of surviving patients (37). A more recent authoritative
meta-analysis (Meta-Analysis of Chemotherapy on Head and Neck Cancer Collaborative Group, MACHNC) confirms a significance benefit from cisplatin and fluorouracil given concurrently with radiotherapy
– absolute 2 year survival benefit=7% (38). Such benefits however must be balanced against the sideeffects of the chemotherapy.
Combining chemotherapy concurrently with radiotherapy may be superior to induction or neo-adjuvant
chemotherapy in advanced head and neck cancers, and may improve overall survival. Two randomised
trials have shown improved local control and survival in over 5 years of follow-up in patients receiving an
alternating chemo-radiotherapy regime (23).
156
The role of chemotherapy in laryngeal cancer continues to evolve. Carefully controlled trials of
chemotherapy with other treatment modalities should be supported. Patients treated with chemotherapy in
conjunction with other modalities outside of trials should be managed in strictly controlled situations.
•
•
•
•
•
High response rates to chemotherapy are achievable in laryngeal cancers.
Chemotherapy with radiotherapy may improve larynx preservation rates but remains under
investigation.
The effect of concurrent chemo-radiotherapy may be to increase toxicity but the impact on survival
remains unclear.
The optimal combinations of chemotherapy with differing schedules of radiotherapy have yet to be
determined.
Further studies and trials are required and should be supported.
References:
1. Lowe VJ. Kim H. Boyd JH. Eisenbeis JF. Dunphy FR. Fletcher JW. Primary and recurrent early stage laryngeal cancer:
preliminary results of 2-[fluorine 18]fluoro-2-deoxy-D-glucose PET imaging.Radiology. 1999. 212:799-802
2. Tupchong L, Phil D, Scott CB, et al.: Randomised study of preoperative versus postoperative radiation therapy in advanced
head and neck carcinoma: long-term follow-up of RTOG study 73-03. Int J Radiat Oncol Biol Phys. 1991. 20: 21-28.
3. Hoffmann HT, Karnell LK. Laryngeal cancer. In Steele GD and others, editors: National cancer data base annual review of
patient care 1995. Atlanta, 1995, American Cancer Society.
4. Morris MR, Canonico D, Blank C. A critical review of radiotherapy in the management of T1 glottic carcinoma. Am J
Otolaryngol. 1994. 15:276.
5. Ton-Van J, Lefebvre J-L, Stern JC, Buisset E, Coche-Dequeant B, Vankemmel B. Comparison of surgery and radiotherapy in
T1 and T2 glottic carcinomas. Am J Surg.1991. 162:337-340.
6. Groome PA. O'Sullivan B. Irish JC. Rothwell DM. Math KS. Bissett RJ. Dixon PR. Eapen LJ. Gulavita SP. Hammond
JA. Hodson DI. Mackenzie RG. Schneider KM. Warde PR. Mackillop WJ. Glottic cancer in Ontario, Canada and the
SEER areas of the United States. Do different management philosophies produce different outcome profiles? J Clin Epidem.
2001. 54:301-15.
7. Hellquist H, Lundgren J, Olofsson J. Hyperplasia, keratosis, dysplasia and carcinoma in situ of the vocal cords - A follow-up
study. Clin Otolaryngol. 1982. 7:11-27.
8. Spayne JA. Warde P. O'Sullivan B. Payne D. Liu FF. Waldron J. Gullane PJ. Cummings BJ. Carcinoma-in-situ of the
glottic larynx: results of treatment with radiation therapy. International J of Radiat Oncol,, Biol, Phys. 2001. 49:1235-8.
9. Chevalier D.Beatse V.Darras JA.Desaulty A.Piquet JJ. Surgical treatment of T1-T2 glottic carcinomas. Acta Oto-RhinoLaryngologica Belgica. 1999. 53:179-80.
10. Rosier JF. Gregoire V. Counoy H.Octave-Prignot M. Rombaut P. Scalliet P. Vanderlinden F. Hamoir M. Comparison of
external radiotherapy, laser microsurgery and partial laryngectomy for the treatment of T1N0M0 glottic carcinomas: a
retrospective evaluation. Radiotherapy & Oncology. 1998. 48:175-83.
11. Maheshwar AA Gaffney CC. Radiotherapy for T1 glottic carcinoma: impact of anterior commissure involvement. Journal of
Laryngology & Otology. 2001. 115:298-301.
12. Persky MS. Lagmay VM. Cooper J. Constantinides M. O'Leary R. Curative radiotherapy for anterior commissure laryngeal
carcinoma. Ann of Otol,Rhinol & Laryngol. 2000. 109:156-9..
13. Brouha XD. Op De Coul B. Terhaard CH. Hordijk GJ.Does waiting time for radiotherapy affect local control of T1N0M0
glottic laryngeal carcinoma? Clin Otolaryngol. 2000. 25:215-8.
14. Terhaard CH et al. Radiotherapy in T1 laryngeal cancer: prognostic factors for locoregional control and survival, uni – and
multivariate analysis. Int J Rad Onc Bio Phys 1991. 21:1179-86
15. Glanz H, Kimmich T, Eichhorn T, Kleinsasser O. Results of treatment of 584 laryngeal cancers at the Ear-Nose-Throat Clinic
of Marburg University. 1989. HNO. 37:1-10.
16. Laccourreye O. Diaz EM Jr. Bassot V. Muscatello L. Garcia D. Brasnu D. A multimodal strategy for the treatment of patients
with T2 invasive squamous cell carcinoma of the glottis. Cancer. 1999. 85:40-6.
17. Pameijer, FA,Balm, AJM, Hilgers, FJM, Muller, SH. Variability of tumour volumes in T3 staged head and neck tumours.
Head and Neck. 1997. 19:6-13.
18. Thakar A. Bahadur S. Mohanti BK Nivsarkar S. Clinically staged T3N0M0 laryngeal cancer: how is it best treated?
Definitive radiotherapy with salvage surgery v/s combined surgery and radiotherapy. J of Laryngol & Otol. 2000. 114:10812.
19. Manni J J et al. Prognostic factors for survival in patients with T3 laryngeal carcinoma. Am J Surgery 1992. 164:682-7
20. Watters GW. Patel SG. Rhys-Evans PH. Partial laryngectomy for recurrent laryngeal carcinoma. Clin Otolaryngol.2000.
25:146-52.
21. Lavey and Calcaterra. Partial laryngectomy for glottic cancer after high dose radiotherapy. Am J Surg 1991.162, 341-4
157
22. Finizia C, Geterud A, Holmberg E, Lindstrom J, Lundgren J, Kuylenstierna R, Rylander R, Biorklund A, Rydell R, Anderson
I, Mercke C. Advanced laryngeal cancer T3-T4 in Sweden: a retrospective study 1986-1990. Survival and locoregional
control related to treatment. Acta Oto-Laryngologica. 1996.116 :906-12.
23. Merlano M, Benasso M, Corvo et al. Five year update of a randomised trial of alternating radiotherapy and chemotherapy
compared with radiotherapy alone in the treatment of unresectable squamous cell carcinoma of the head and neck. J Natl
Cancer Inst 1996. 88:583-589
24. Mendenhall, WM., Parsons, JT., Mancuso, AA. et al. Radiotherapy for carcinoma of the supraglottic larynx: An alternative to
surgery. Head and Neck. 1996.18:24-35.
25. Robbins, KT., Davidson, W., Peters, LJ., Goepfort, H. Conservation surgery for T2 and T3 carcinomas of the supraglottic
larynx. Arch Otolaryngol Head Neck Surg. 1988.114:421-426.
26. The department of Veterans Affairs laryngeal cancer study group. Induction chemotherapy plus radiation compared with
surgery plus radiation in patients with advanced laryngeal cancer. New Engl J Med. 1991.324:1685-90.
27. Jones AS, Cook JA, Phillips DE, Soler Lluch E. Treatment of T3 carcinoma of the larynx by surgery or radiotherapy. Clin
Otolaryngol. 1992.17: 433-6.
28. Terhaard CH. Hordijk GJ, van den Broek P, de Jong PC, Snow GB, Hilgers FJ, Annyas BA, Tijho-Heslinga RE, de Jong JM.
T3 laryngeal cancer: a retrospective study of the Dutch Head and Neck Oncology Cooperative Group: study design and
general results (Review) (45 refs) Clin Otolaryngol. 1992.17:393-402.
29. Hoekstra CJM et al. Squamous cell carcinoma of the supraglottic larynx without clinically altered lymph node metastases,
problem of local relapse and overall treatment time. Int J Rad Onc Bio Phys 1990.18:13-21.
30. Lima RA et al. New-total laryngectomy for treatment of advanced laryngeal cancer. Am J Surg. 1997. 174:490-1.
31. Myers EN. Fagan JF. Management of the neck in cancer of the larynx. Annals of Otology, Rhinology & Laryngology.
1999.108:828-32
32. Hicks WL,JR Kollmorgen Dr, Kuriakose MA, Orner J, Bakamjian VY, Winston J, Loree TR. Patterns of nodal metastasis
and surgical management of the neck in supraglottic laryngeal carcinoma. Otolaryngol – Head & Neck Surg. 1999. 121:
57-61.
33. Wax MK. Touma BJ. Management of the N0 neck during salvage laryngectomy. Laryngoscope. 1999. 109:4-7.
34. Laccourreye O. Lawson G. Muscatello L. Biacabe B. Laccourreye L. Brasnu D.Carbon dioxide laser debulking for
obstructing endolaryngeal carcinoma: a 10-year experience. Ann of Otol, Rhinol & Laryngol. 1999. 108:490-4.
35. Lefebvre J, ChevalierD, Luboinski B et al. Larynx preservation in pyriform sinus cancer: Preliminary results of a European
organisation for research and treatment of cancer phase III trial. J Natl Cancer Inst. 1996. 88:890-899.
36. Richard J, Sancho-Garnier H, Pessey J et al. Randomised trial of induction chemotherapy in larynx carcinoma. Oral Oncol.
1998. 34:224-228.
37. Forastier A. Larynx preservation trials: a critical appraisal. Semin Rad Oncol 1998. 8:254-261.
38. Pignon JP,Bourhis J, Domenge C, Designe. Chemotherapy added to locoregional treatment for head and neck squamous-cell
carcinoma: three meta analysis of updated individual data. MACH-NC Collaborative Group. 2000. Lancet 355:949-955.
Additional References:
I. Dickens WJ, Cassisi NJ, Million RR, Bova FJ. Treatment of early vocal cord carcinoma: a comparison of apples and
apples. Laryngoscope. 1983;93:216-9.
II. Steiner W: Results of curative laser microsurgery of laryngeal carcinomas. Am J Otolaryngol 1993. 14: 116-121.
III. Lee, NK. Goepfort, H., Wendt, CD. Supraglottic laryngectomy for intermediate - stage cancer: U.T.M.D. Anderson
Cancer Centre experience with combined therapy. Laryngoscope. 1990. 100:831-836.
IV. Bocca E, Pignataro O, Oldini C, Sambataro G, Cappa C. Extended supraglottic laryngectomy. Review of 84 cases.
Ann Otol Rhinol Laryngol. 1987. 96:384-6.
V. Shah JP. et al. Patterns for care for cancer of the larynx in the United States. Arch Otolaryngol Head Neck Surg. 1997.
123:475-483.
VI. Bocca, E., Pignataro, O., Oldini, C. Supraglottic laryngectomy: 30 years of experience. Ann. Otol. Rhinol. Laryngol.
1983. 92:14-18.
VII. Mendenhall WM, Parsons JP, Stringer SP, Cassisi NJ, Million RR, Stage T3 squamous cell carcinoma of the glottic
larynx: a comparison of laryngectomy and irradiation. Int j Radiat Oncol Biol Phys 1992. 23:725-32.
VIII. Yuen AP. Wei WI, Wong SH. Critical appraisal of watchful waiting policy in the management of N0 neck of advanced
laryngeal carcinoma. Arch Otolaryngol – Head & neck Surg. 1996. 122 :742-5.
IX. Lavertu P. Aldestein DJ, Saxton JP, Secis M, Wannamaker JR, Eliachar I, Wood BG, Strome M. Management of the
neck in a randomised trial comparing concurrent chemotherapy and radiotherapy with radiotherapy alone in resectable
stage III and IV squamous cell head and neck cancer. Head & Neck 1997. 19: 559-66.
X . Simpson D, Robertson AG, Lamont D. A comparison of radiotherapy and surgery as primary treatment in the
management of T3 N0 M0 glottic tumours. J of Laryngol & Otolol. 1993. 107:912-5, 1993
XI. De Andres L, Brunet J, Lopez-Pousa A et al. Function preservation in stage III squamous laryngeal carcinoma: results
with an induction chemotherapy protocol. Laryngoscope 1995;105:822-826.
XII. Giglio R, Mickiewicz E, Roth B et al. Organ preservation (LP) in resectable stage III and IV epidermoid carcinoma of
the larynx (LC) with sequential chemotherapy (CT) + radiation therapy (RT). Proceedings Am Soc Clin Oncol
1993;12:282.
158
XIII. Laccourreye O, Bassot V, Menard M et al. Preservation of the larynx following neo-adjuvant chemotherapy. A
preliminary report. In Neo-adjuvant chemotherapy. Banzet P, Holland JF, Khavat D, Weil M eds. Paris:SpringerVerlag;1991:28-31.
XIV. Pfister DG, Strong E, Harrison L et al. Larynx preservation with combined chemotherapy and radiation therapy in
advanced but resectable head and neck cancer. J Clin Oncol 1991. 9:850-859.
XV. Shirinian MH, Weber RS, Lippman SM et al. Laryngeal preservation by induction chemotherapy plus radiation
therapy in locally advanced head and neck cancer: the MD Anderson cancer centre experience. Head Neck 1994;16:3944.
XVI. Mendenhall WM, Tannehill SP, Hotz MA, Kasler M, Remenar E. Should chemotherapy alone be the initial treatment
for glottic squamous cell carcinoma? Eur J Cancer 1999;35:1309-1313
159
Section 5
Chapter 6 Salivary Glands
This section has been updated and modified with reference to the ‘Evidence Based Conference of the
Management of Salivary Gland Neoplasms’ held at the Freeman Hospital, Newcastle upon Tyne on the
19th November 1998. A full reference list from the meeting is available on the NOTO website –
www.noto.org (1)
Salivary gland malignancies are rare and present a diverse range of histology and clinical behaviour. The
original 1972 WHO histological classification of salivary gland tumours consisted of four subgroups:
Epithelial tumours, Non-epithelial tumours, unclassified tumours and allied conditions of which the
epithelial group was the larger in number. This was modified in 1991 (2) such that tumours of similar
pathology are now grouped together even though they may have differing prognoses. Under the new
system there are seven categories:
a.
b.
c.
d.
e.
f.
g.
Adenomas
Carcinomas
Non Epithelial tumours
Malignant Lymphomas
Secondary tumours
Unclassified tumours
Tumour -like disorders
Carcinomas are often further classified as high grade, low grade or mixed, the latter inferring a variable
behaviour depending on the histological picture. Except in the case of mucoepidermoid tumours
however, clinicopathological correlation has proved to be unreliable and often the clinical behaviour
rather than the histology of a tumour provides a better guide for treatment. Although, overall, tumours are
more common in the parotid, the incidence of malignancy is higher in the submandibular, sublingual and
minor salivary glands (3). The more common adenomas and carcinomas are shown below:
Adenomas
• Pleomorphic adenoma
• Myoepithelial (myoepithelian adenoma)
• Basal cell adenoma
• Warthin’s tumour (adenolymphoma)
• Ductal Papilloma
• Cystadenoma
Carcinomas
• Acinic cell carcinoma
• Mucoepidermoid carcinoma
• Adenoid cystic carcinoma
• Polymorphous low-grade (terminal duct)
• Papillary cystadenocarcinoma
• Mucinous adenocarcinoma
• Adenocarcinoma
• Carcinoma in pleomorphic adenoma
• (malignant mixed tumour)
• Squamous cell carcinoma
• Undifferentiated carcinoma
CONFIRMATION OF DIAGNOSIS
Malignant tumours may be clinically indistinguishable from benign lesions and definitive histology is
usually unavailable until after surgical resection. Diagnosis is therefore based on:
Clinical presentation - pain, rapid growth, fixation, nerve involvement or neck metastasis all suggestive
of malignancy.
160
FNAC - useful for major salivary gland lesions - must be examined by cystopathologist experienced in
the diagnosis of salivary gland disease. This should distinguish malignant from benign disease in 90% of
cases (4,5).
MRI scanning - non-homogeneity, muscle infiltration or suspicious regional lymph node appearance
suggests malignancy.
Open biopsy - this should not be done for major salivary gland lesions because of tumour spillage
although it may be indicated for minor salivary gland lesions where the overlying epithelium will be
excised at the time of surgery.
Frozen section - accurate diagnosis often difficult and false negative rates significant and therefore
should not be relied on. (6)
SUBMANDIBULAR GLAND
TREATMENT POLICY
SURGERY
Primary Tumour
• A total excision is appropriate for most tumours confined to the gland. Some argue in favour of wider
resection for adenoid cystic tumours including the lingual, hypoglossal and marginal mandibular
nerve if there is any suspicion of involvement by tumour (7), but evidence is not strong, and the
advice is counter to recommendations for the uninvolved facial nerve in parotid disease. Clinically
high-grade tumours in young individuals should be treated more aggressively with excision of the
gland plus a 2cm margin of apparently healthy tissue (8).
• Large Tumours with bone involvement - composite resection of tumour, adjacent soft tissue cuff and
segmental mandibulectomy.
Neck Disease
• All Patients - clearance of nodes in suprahyoid region. Clinically high-grade tumours or suspicious
MRI appearance should have an elective supra-omohyoid dissection.
• Patients with clinically confirmed neck metastasis should have a radical or modified radical neck
dissection (8,9).
RADIOTHERAPY
•
Inoperable tumours where palliation can be achieved.
Post-operative (7,10)
Indications:
• High grade or advanced stage tumours with a high risk of local recurrence
• Residual neck disease or microscopic extra-capsular spread from lymph nodes
• Surgery for recurrent disease
• Adenoid cystic tumours
• Radiotherapy should be commenced within six weeks of surgery.
161
PAROTID GLAND
TREATMENT POLICY
SURGERY
Primary Tumour
• Apart from lymphomas, surgery is the treatment of choice. A conservative parotidectomy should be
performed with preservation of the facial nerve providing there is no tumour invasion. For deep lobe
tumours this will involve a total parotidectomy plus resection of adjacent structures if necessary to
achieve an en-bloc resection. Any part of the facial nerve not infiltrated by tumour should be
preserved (11,12). Primary nerve grafting should be considered if microscopic clearance of the main
trunk and peripheral branches can be achieved.
• Adenoid cystic carcinoma requires a total parotidectomy with sacrifice of any part of the nerve
involved by tumour (7).
• Resection of an intact nerve has been shown to improve local disease control but will not improve
survival (13). It is unlikely that nerve grafting will compromise outcome and therefore could be
considered particularly if combined with post-operative radiotherapy.
Neck
• Neck dissection should be performed in patients with evidence of nodal disease either clinically or on
MRI scanning.
•
A prophylactic neck dissection should be considered for patients with clinically high grade tumours,
i.e. adenocarcinoma, squamous and undifferentiated. (14)
RADIOTHERAPY (7,12,15)
Post-operative
• As for the submandibular gland plus any patient in whom the facial nerve has been preserved despite
close approximation of the tumour.
Recurrent Disease
• Requires careful evaluation of the patient with repeat imaging and a review of the histology from the
initial excision. This will usually require more radical surgery with sacrifice of the nerve and
overlying skin if any suspicion of involvement by tumour. Super-radical resections of skull base have
not to date shown convincing evidence of improved survival. Consider chemotherapy and/or
radiotherapy for palliation.
MINOR SALIVARY GLANDS
Confirmation of diagnosis
Clinical history and examination with particular reference to palate and nasal cavity. Open biopsy
permissible to confirm diagnosis. The prognosis for these patients is more closely related to stage of
disease rather than histology (16).
Treatment
En-bloc resection with depth of excision equal to width to ensure adequate resection margins. Significant
defects are repaired as appropriate if necessary.
Neck
Therapeutic neck dissection indicated for lymph node involvement.
Elective neck dissection indicated for adenocarcinoma, carcinoma in pleomorphic adenoma and
undifferentiated carcinoma.
162
Radiotherapy Indications: (16)
• Post-operative
• Microscopic residual disease
• Adenoid cystic tumours
• Aggressive undifferentiated tumours
NATURAL HISTORY OF COMMON TUMOURS
Acinic cell carcinoma
• Accounts for about 3% of parotid tumours where it occurs most commonly. Peak incidence 5th
decade
• Demonstrates a variable histological pattern and can be multifocal in origin and occasionally bilateral.
• Determinate survival rates of 90% at five years and 55% at 20 years
• Lymph node metastases occur in approximately 10% of cases (11)
• Total parotidectomy with preservation of uninvolved nerves recommended. Elective neck dissection
not indicated.
Mucoepidermoid Tumour (11)
• A tumour of variable malignancy with low-grade lesions showing a ‘benign’ nature
• Most common major salivary gland tumour (4%-9%) >90% in the parotid but overall more frequent
in minor salivary glands
• Commonest malignant salivary gland tumour in children
• Highest incidence third to fifth decade M=F
• Almost always in the superficial lobe of the parotid
• Histological division into low, intermediate and high-grade shows correlation with prognosis;
although so called ‘low-grade’ tumours can on occasion be aggressive. Five year survival varies
between 86% for low-grade to 22% for high-grade tumours
• 40% incidence of lymph node metastases in intermediate and high-grade tumours
• Low-grade tumours require local resection with adjuvant radiotherapy indicated for high-grade
tumours
Adenoid Cystic Carcinoma (17)
• Most common salivary gland malignancy - mucosal sites more frequent than major salivary gland
• 2-6% of parotid and approximately 15% of submandibular tumours
• Slow, pervasive growth and a high incidence of perineural infiltration
• Variable histologic appearance but difficult to correlate with clinical behaviour
• High rate of morbidity due to recurrence both locally and at distant sites particularly lung. Note 20%
with pulmonary metastases survive more than 5 years
• Slow growth rate make five year survival unreliable. Spiro reports 5-year survival of 60% and 20year survival of 20%
•
Treat by widest local excision with preservation of uninvolved major nerves. Adjuvant postoperative radiotherapy indicated.
Adenocarcinoma
• Uncommon tumour most frequently found in the parotid gland
• M=F affects any age and is one of the commoner tumours seen in children
• Histologic appearance varies between low-grade well-differentiated papillary or mucinous patterns to
high-grade, undifferentiated lesions
• The incidence of distant metastases is about 40% for high-grade tumours and is directly related to
survival rates - 75% 5-year survival for low-grade tumours and 19% 5-year survival for high-grade
tumours
• Treatment is by wide local resection with elective neck dissection and adjuvant radiotherapy for
clinically high-grade tumours.
163
Malignant Mixed Tumour
99% arise from a pleomorphic adenoma usually after a period of 10-15 years. Frequency varies
between 2% and 5%
• The most aggressive of all malignant neoplasms with a high incidence of haematogenous metastases
and 5-, 10- and 15-year cure rates of 40%, 24% and 19% respectively
• Radical resection with adjuvant radiotherapy offer the best form of management
•
Squamous cell carcinoma
• M:F = 2:1
• A rare tumour often mistaken for either a high-grade mucoepidermoid lesion or metastasis from
another primary site
• Tends to occur in the elderly - 7th decade
• Very bad prognosis - Should be treated as high-grade mucoepidermoid lesions.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Robson AR. The management of salivary gland neoplasms. Proceedings of an evidence based concensus conference. Clin
Otol. 1998
Seifert,G.,Sobin, L.H. Histological classification of salivary gland tumours. World Health Organisation, International
classification of tumours. Berlin Springer – Verlag. 1991
Eveson J.W., & Cawson R.A. Salivary gland tumours. A Review of 2410 cases with particular reference to histological
types, site, age and sex distribution. J Pathol. 1985. 46: 265a
Eneroth C.M., Franzen S., & Zajicek J. Cystologic diagnosis on aspirate from 1000 salivary gland tumours. Acta
Otolaryngologica Supplementum. 1967.I244168-171
Boccato P., Altavilla G., & Blandamura S. Fine needle aspiration biopsy of salivary gland lesions. Acta Cytologica.1998.
42:888-898
Hillel A.D., & Fee W.E. Evaluation of frozen section in parotid gland surgery. Arch Otolaryngol. 1983.109:230-232
Garden A.S., Weber R.S., Morrison W.H., Ang K.K., & Peters L.J. The influence of positive margins and nerve invasion in
adenoid cystic carcinoma of the head and neck treated with surgery and radiation. Int. J. Radiation Oncol Biol
Phys.1995.32:619-626
Spiro R.H. Salivary neoplasms: Overview of a 35-year experience with 2807 patients. Head Neck Surg.1986. 8:177-184
Spiro R.H., Armstrong J., Harrison L., Geller N.L., Shiow-Yun Lin & Strong E.W. Carcinoma of major salivary glands.
Arch.Otolaryngol. Head Neck Surg. 1989.115:316-321
Fu K.K., Leibel S.A., Levine M.L., Friedlander L.M., Boles R., & Phillips T.L. Carcinoma of the major and minor salivary
glands. Cancer.1977. 40: 2882-2890
Renehan A., Gleave E.N., Hancock B.D., Smith P., & McGurk M Long-term follow-up of over 1000 patients with salivary
gland tumours treated in a single centre. Br J Surg.1966. 83:750-1754
Spiro R.H., Huvos A.G., & Strong E.W. Cancer of the parotid gland. Am J Surg 1975.130: 452-459
Frankenthaler R.A., Luna M.A., Sang Sook Lee, Kei-Kian Ang, Byers R.M., Guillamondegui O.M., Wolf P., & Goepfert H.
Prognostic variables in parotid gland cancer Arch. Otolaryngol Head Neck Surg. 1991. 117:1251-1256
Casler J.D., & Conley J.J. Surgical management of adenoid cystic carcinoma in the parotid gland. Arch. Otolaryngol Head
Neck Surg. 1992 106:332-338
Spiro I.J., Wang C.C., & Montgomery W.W. Carcinoma of the parotid gland. Analysis of treatment results and patterns of
failure after combined surgery and radiation therapy. Cancer. 1992.71:2699-2705
Parsons J.T., Mendenhall W.M., Stringer S.P., Cassisi N.J., Million R.R. Management of minor salivary gland carcinomas.
Int J Radiation Oncology Biol Phys. 996. 35:443-454
Spiro R.H., Huvos A.G., & Strong E.W.Adenoid cystic carcinoma of salivary origin. A clinicopathologic study of 242
cases. Am J Surg. 1974. 128:512-520
164
Section 5
Chapter 7
Nose and Sinuses
TUMOURS INCLUDED
Tumours in the sinonasal region are rare, affecting <1/100,000 people per year but it represents the area
of greatest histological diversity in the body. Although squamous cell carcinoma remains the commonest
tumour, every tissue type may occur. The commoner epithelial tumours include adenocarcinoma,
olfactory neuroblastoma, adenoid cystic carcinoma and malignant melanoma. Sarcomas include
chondrosarcoma and rhabdomyosarcoma. All areas of the nasal cavity and paranasal sinuses can be
affected but the lateral wall, ethmoids and maxillary sinus are the most common primary sites. The
sphenoid and frontal sinuses are rarely primarily affected for reasons that are unknown.
CONFIRMATION OF DIAGNOSIS
Biopsy (optimally performed under general anaesthesia to obtain representative tissue. An experienced
histopathologist is essential as up to 1 in 5 cases may have their diagnosis modified after expert review).
An endonasal endoscopic approach should be used to avoid transgression of normal tissue planes.9
Imaging (experienced radiologist) 27, 17
CT - direct coronal and axial cuts with intravenous contrast enhancement
MRI - three planar T1 pre- and post-gadolinium DTPA, +/- T2, fat suppression & MRA as appropriate
CONSULTATION
• Oral and orbital prosthetic rehabilitation
• Neurosurgical expertise
• Medical oncology
TREATMENT OPTIONS
Can only be determined following biopsy and imaging.
• Surgery alone or in combination with radiotherapy is required in the majority of cases.
• Radiotherapy may be given before or after surgery. The patient should be immobilised in a beam
directing shell. The target volume is determined on the basis of CT and MR images and clinical
and/or surgical assessment. Planning may be done with orthogonal simulator pictures using bony
landmarks, or the patient may be CT planned. Care should be taken to shield the brain stem, optic
pathways, eyeball, lacrimal gland and orbit wherever possible. Megavoltage photons should be used.
The usual dose will be 60-66Gy in 30-33 fractions over 6-6_ weeks, treating five days a week.
Alternative established fractionation schedules are acceptable. The neck nodes do not require
prophylactic treatment.
• The use of concomitant chemotherapy with radiotherapy is increasingly indicated in both the
preoperative and postoperative situation for patients with squamous cell carcinoma, other tumours
such as embryonal rhabdomyosarcoma, and advanced lymphoma.
• Topical chemotherapy (5-FU) combined with repeated meticulous surgical debulking has been
advocated for squamous cell carcinoma and adenocarcinoma in two centres but their results have not
been replicated elsewhere.15,30 Success for the technique requires careful adherence to the established
protocol and is best reserved for those centres who have carefully studied it. It is, however, not
without its problems.
• Brachytherapy may be used for squamous cell carcinoma of the columella and anterior nasal septum.
• Radiotherapy alone is required for tumours such as lymphoma19, or for palliation.
165
Primary Tumour
Surgery
(a) Craniofacial Resection
• tumours commonly treated by craniofacial resection include adenocarcinoma, olfactory
neuroblastoma, chondrosarcoma and squamous cell carcinoma
• tumours involving the skull base requiring surgery may be performed via an extended lateral
rhinotomy or a combined midfacial degloving and bifrontal craniotomy through a bicoronal flap or
spectacle incision. 1,3,21,31
• may be extended to include a maxillectomy and resection of orbital structures.
• neurosurgical expertise may be required
(b) Maxillectomy
• squamous cell carcinoma is commonest indication for this procedure.
• tumours involving the palate and/or extending through the posterior wall to involve the pterygoid
region and infratemporal fossa
• via a midfacial degloving, lateral rhinotomy or Weber-Fergusson/Diffenbach incisions
• medial, subtotal, total, extended
• may be combined with clearance of the orbit or extended to craniofacial resection.
• immediate prosthetic rehabilitation with modified denture and gutta percha is optimal. The
postoperative care may be reduced where an obturator cannot be fitted, by insertion of a free flap eg.
rectus abdominis.
(c) Lateral rhinotomy (partial or medial maxillectomy)
• commoner indications include malignant melanoma of the nasal mucosa
• tumours involving the nasal septum and lateral wall (i.e.medial maxilla, ethmoids and frontal sinus)
of the nose, up to but not including the anterior skull base
• offers rapid access with reasonable cosmesis e.g. elderly patients
(d) Midfacial degloving11
procedure used
• alone to access both maxilla, ethmoids and sphenoid and nasal cavity
• combined with a bicoronal incision for access to the skull base for craniofacial resection
(e) Orbit (see attached algorithm) : resection with (exenteration) or without (clearance) of the eyelids
(f)
•
•
•
Total rhinectomy and tumours of the cartilaginous nasal skeleton
required for extensive tumours of the anterior cartilaginous septum and nasal dorsum
commonest indication is for squamous cell carcinoma
prosthetic or local flap reconstruction
(g) Endoscopic endonasal approaches
Suitable for selected cases of benign neoplasia e.g. inverted papilloma. 23,36,33, and a small number of
malignant tumours e.g. malignant melanoma. 6,34There are insufficient numbers and/or follow-up to
justify an exclusive endoscopic approach in the majority of malignant tumours at present though it
may be combined with other approaches e.g. bifrontal craniotomy.35
(h)Neck dissection is only indicated in the presence of cervical metastases. 24
166
HISTOLOGY
Expert histology with frozen section service is required. When in doubt, services of a superspecialist
laboratory eg Royal National Throat, Nose & Ear Hospital may be useful.
Individual histologies
Squamous cell carcinoma
Maxilla or antro-ethmoid, rarely nasal vestibule, columella & septum
Combined surgery and radiotherapy (may be given pre or post-operatively)
Five year actuarial survival 32%, ten years 32% , 7,13,21
Adenocarcinoma associated with hard wood exposure though not exclusive29
Ethmoid or antro-ethmoid
Surgery (craniofacial +/- maxillectomy) +/- DXT
Five year actuarial survival 43%, ten year actuarial survival 38% 21
87% five year survival claimed for 5FU/debulking 15
Adenoid cystic carcinoma
Widespread local dissemination by perineural lymphatic and embolic dissemination.
Blood borne metastasis to lungs common.
Locally extensive surgery + post-operative radiotherapy. The addition of radiotherapy delays
local recurrence but does not affect overall prognosis.
Five year actuarial survival 53-73%, ten year survival 7-41%, twenty year survival
< 8%.10,21
Olfactory neuroblastoma
Arises olfactory epithelium e.g. superior nasal cavity with frequent involvement of anterior
cranial fossa via olfactory tract 8
Craniofacial resection to stage disease, followed by radiotherapy (or chemotherapy) if anterior
cranial fossa involvement present
Five year actuarial survival 62-78%, ten year survival 47-71% 5,21,28
In patients with cervical metastases (5%) survival was 29% compared with 64% for patients
with N0 disease (odds ration 5.1)
Chondrosarcoma
Involves perpendicular plate of ethmoid and skull base
Surgery (repeated as required) eg craniofacial resection, midfacial resection , lateral rhinotomy
Five year actuarial survival 62%, ten year survival 47% 21
Malignant melanoma
Arises from melanocytes, most frequently within nasal cavity
Behaviour - capricious and unpredictable with disseminated metastatic and local recurrence
possible at any time. Outcome not determined by depth of invasion as in cutaneous lesions
Wide surgical excision primarily
Post-operative radiotherapy shows tendency to delay recurrence but no statistical benefit
demonstrated 2,22
Chemotherapy & immunotherapy not shown to be effective25
Chordoma
Embrological remnant of notochord
Surgery + post-operative radiotherapy.
167
Inverted papilloma
Typically arises in middle meatus, extending into maxillary sinus, ethmoid and frontal
sinuses;
may invade adjacent bone leading to frequent ‘recurrence’
Potential for malignant transformation in 1-2% of cases
Surgical excision, approach determined by extent eg endoscopic , midfacial degloving, lateral
rhinotomy..16,23,36,32
Angiofibroma
Arises sphenopalatine region with erosion of medial pterygoid plate and extension into
nasopharynx, sphenoid, pterygo-palatine canal and infratemporal fossa.17
Surgery eg mid-facial degloving11 +/- radiotherapy for recurrence. Recurrence significantly
reduced by drilling out of basisphenoid.12. Endoscopic excision combined with embolisation
also possible. 14,26
FOLLOW UP
• Imaging: (ideally MRI; T1 pre- and post-gadolinium DTPA) baseline at three months, then at four to
six monthly as appropriate to histology. 20
• EUA and decrusting of cavity initially three to four monthly, then six monthly as appropriate to
individual patient and histology.
SINONASAL MALGNANCY AND THE ORBIT
Biopsy/Imaging
Craniofacial
Resection
Lamina papyracea
Eroded
Tumour through
periosteum
Orbital Clearance
Tumour adjacent to
periosteum
Resect periosteum
Frozen section
Recurrence
168
Lamina papyracea
Intact
Periosteum clear
Orbital preservation
References:
1. Bilsky MH. Kraus DH. Strong EW, et al. Extended anterior craniofacial resection for intracranial extension of malignant
tumours. Am J Surg. 174:565-8, 1997 (Level 3)
2. Brandwein MS, Rothstein WL, Bodian C, Urken ML. Sinonasal melanoma. A clinicopathologic study of 25 cases and
literature. Meta analysis. Archives of Otolaryngol Head and Neck Surg 1997 123:290-296 (Level 3)
3. Catlano PJ, Hecht CS, Biller HF et al. Craniofacial resection. An analysis of 73 cases. Archives Of Otolaryngol Head and
Neck Surg 1994 120:1203-1208 (Level 3)
4. Dulguerov P, Allal AS, Calcatera TC. Esthesinoneuroblastoma: a meta-analysis and review. Lancet Oncology 2001 2:683690 (Level 3)
5. Eden BV, Debo RF, Lamer JM et al. Esthesioneuroblastoma. Long term outcome and patterns of failure - the University of
Virgina experience. Cancer 1994 73:2556-2562 (Level 3)
6. Goffart Y, Jorissen M, Daele J, Vandr Poorten V, Born J, Deneufbourgh J-M, Zicot A-Fr, Remacle J-M. Minimally invasive
endoscopic management of malignant sinus tumours. Acta Oto-rhino-laryngologica Belg 2000 54:221-232 (Level 4)
7. Harbo G. Grau C. Bundgaard T, et al. Cancer of the nasal cavity and paranasal sinuses. A clinico-pathological study of 277
patients. Acta Oncol 1997 36:45-50 (Level 3)
8. Harrison DFN. Surgical pathology of olfactory neuroblastoma. Head and Neck Surg 1984 7:60-64 (Level 3)
9. Homer JJ. Jones NS. Bradley PJ. The role of endoscopy in the management of nasal neoplasia. Am J Rhinol. 1997 11:417,1997 (Level 4)
10. Howard DJ, Lund VJ. Reflections on the management of adenoid cystic carcinoma of the nasal cavity and paranasal
sinuses. Otolaryngol Head and Neck Surg 1985 93:338-341 (Level 3)
11. Howard DJ, Lund VJ. The role of midfacial degloving in modern rhinological practice. J of Laryngol and Otol 1999
113:885-887 (Level 3)
12. Howard DJ, Lloyd G, Lund VJ. Recurrence and its avoidance in juvenile angiofibroma. Laryngoscope 2001 111: 1509-151
(Level 2b)
13. Jakobsen MH. Larsen SK. Kirkegaard J, et al. Cancer of the nasal cavity and paranasal sinuses. Prognosis and outcome of
treatment. Acta Oncologica. 1997 36:27-31 (Level 3)
14. Jorissen M, Eloy Ph, Rombaux Ph, Bachert Cl, Daele J. Endoscopic sinus surgery for junvenile nasopharyngeal
angiofibroma. Acta Oto-rhino-laryngologica Belg 2000 54: 201-219 (Level 3)
15. Knegt PP, Ah-See KW, vd Velden LA, Kerrebijn J. Adenocarcinoma of the ethmoid sinus complex: surgical debulking and
topical fluorouracil may be the optimal treatment. Archives of Otolaryngol - Head and Neck Surg 2001 127:141-146
(Level 3)
16. Lawson W, Ho BT, Shaari CM, Biller HF. Inverted papilloma. A report of 112 cases. Laryngoscope 1995 105:282-288
(Level 3)
17. Lloyd G., Howard DJ, Phelps P, Cheesman A. Juvenile angiofibroma the lessions of 20 years of modern imaging. J of
Laryngol and Otology.1999 113:127-134 (Level 3)
18. Lloyd GAS, Lund VJ, Howard DJ, Savy L. Optimum imaging for sinonasal malignancy. J of Laryngol and Otology 2000
114:557-562 (Level 3)
19. Logsdon MD. Ha CS. Kavadi VS, et al. Lymphoma of the nasal cavity and paranasal sinuses:imoroved outcome and altered
prognostic factors with combined modality therapy. Cancer. 1997 80:477-88 (Level 3)
20. Lund VJ, Lloyd GAS, Howard DJ, Cheesman AD, Phelps PD. Enhanced magnetic resonance imaging and substraction
techniques in the post-operative evaluation of craniofacial resection for sinonasal malignancy. Laryngosocope 1996
106:553-558 (Level 3)
21. Lund VJ. Howard DJ. Wei WI. Cheesman AD. Craniofacial resection for tumours of the nasal cavity and paranasal sinusesa 17 year experience. Head & Neck. 1998 20:97-105 (Level 3)
22. Lund VJ, Howard DJ, Harding L, Wei W. Management options and survival in malignant melanoma of the sinonasal
mucosa. Laryngoscope 1999 109:208-211 (Level 3)
23. Lund VJ. Optimum management of inverted papilloma. J of Laryngol and Otology 2000 114:194-197 (Level 3)
24. Lund VJ. Distant metastases from sinonasal cancer. In Distant Metastases from Head and Neck Cancer: a multiinstitutional view. Editor A Ferlito. ORL 2001 63:212-213 (Level 3)
25. Nandapalan V,Roland NJ, Helliwell TR, Williams EMI, Hamilton JW, Jones AS. Mucosal melanoma of the head and neck.
Clin Otolaryngol 1998 23:107-116 (Level 3)
26. Newlands SD, Weymuller Jr, EA. Endoscopic treatment of juvenile nasopharyngeal angiofibroma. Am J of Rhinol 1999 13:
213-219 (Level 4)
27. Phillips CD. Current status and new developments in techniques for imaging the nose and sinuses. Otolaryngol Clin North
Am. 1997 30:371-87 (Level 4)
28. Rinaldo A, Ferlito A, Shaha AR, Wei WI, Lund VJ. Esthesioneuroblastoma and cervical lymph node metastases: clinical
and therapeutic implications. Acta Oto-Laryngologica 2002 122:215-221 (Level 3)
29. Robinson CF. Peterson M. Seiber WK, et al. Mortality of Carpenter’s Union members employed in the US construction or
wood products industries, 1987-1990. Am J Indust Med 1996 30:674-94 (Level 2)
30. Sakai S, Honki A, Fuchihata DD, Tanaka Y. Multidisciplinary treatment of maxillary sinus cancer. Cancer 1983 52:13601364 (Level 3)
31. Shah JP, Kraus H, Arbit E et al. Craniofacial resection for tumours involving the anterior skull base. Otolaryngol Head and
Neck Surg 1991 106:387-391 (Level 3)
169
32. Savy L, Lloyd G, Lund VJ, Howard DH. Optimum imaging and diagnosis for inverted papilloma. J of L a r y n g o l
and
Otology 2000 114: 891-893
33. Sham CL,Woo JKS, van Hasselt CA. Endoscopic resection of inverted papilloma of the nose and paranasalsinus. J of
Laryngol and Otolaryngol 1998 112:758-764 (Level 3)
34. Stammberger H, Andrhuber W, Walch Ch Papaefthymiou G. Possibilities and limitation sof endoscopic management of
nasal and paranasal sinus malignancies. Acta Oto-Rhino-Laryngologica Belg 1999 53:199-205 (Level 3)
35. Thaler ER, Kotapka M, Lanza D, Kennedy DW. Endoscopically assisted anterior cranial skull base resection of sinonasal
tumours. Am J of Rhinology 1999 13:303-310 (Level 4)
36. Waitz G, Wigand ME. Results of endoscopic sinus surgery for the treatment of inverted papillomas. Laryngoscope, 1992
102:917-922 (Level 3)
37. Yu KH, Yu SC. Teo PM, et al. Nasal lymphoma:results of local radiotherapy with or without chemotherapy. Head & Neck.
1997 19:251-9 (Level 3)
170
Section 5
Chapter 8
Nasopharynx
DIAGNOSIS AND STAGING
Common presenting symptoms include:•
Nasal blockage
•
Conductive deafness due to an obstructing primary tumour
•
Cranial nerve palsies due to skull base invasion
•
Cervical lymphadenopathy.
Tumour within the nasopharynx may be either obvious or undetectable on examination in the outpatient
clinic. Either way, examination under anaesthesia and biopsy is essential to confirm the diagnosis and to
stage the disease. Carcinoma needs to be distinguished from lymphoma and other rarer tumours, which
can also occur at this site but are managed differently. In the patient who presents with cervical
lymphadenopathy only, the finding of Epstein-Barr virus (EBV) titres in serum, e.g. IgA antibodies to
early antigen - diffuse (Ead) and viral capsid antigen (VCA) and anti Epstein-Barr nuclear antigen
(EBNA) may help in confirming the diagnosis. If available, biopsy material may be tested for genomic
material by amplification of DNA with a polymerase chain reaction thereby providing strong evidence to
support a diagnosis of a nasopharyngeal primary tumour.
Even if the nasopharynx appears normal at EUA in the investigation of cervical lymphadenopathy, blind
biopsies should be taken from the nasopharynx (as well as from the tongue base and an ipsilateral
tonsillectomy should also be performed) to detect an occult primary tumour. CT scanning and MRI
provide complementary information in staging the local extent of disease. Because there is a significantly
greater incidence of distant metastases at presentation in patients with nasopharyngeal carcinoma
compared with those with tumours at other head and neck primary sites, all patients should be fully staged
to exclude the presence of bone, liver and lung metastases. Patients with suspected or confirmed
nasopharyngeal carcinoma, should be jointly assessed by a head and neck surgeon and an oncologist in a
combined clinic.
TREATMENT OPTIONS IN LOCALISED DISEASE
Radiotherapy
High dose radiation therapy with or without chemotherapy is the primary treatment of nasopharyngeal
carcinoma both for the primary tumour site and both sides of the neck even in patients without palpable
neck disease and regardless of T stage. Radiation therapy dose and field margins are individually tailored
to the location and the size of the primary tumour and lymph nodes. Although most tumours are treated
with external beam irradiation exclusively, in some tumours radiation therapy may be boosted by
intracavitary or interstitial implants when clinical expertise is available and the anatomy is suitable.
Chemotherapy
There is now level I evidence, in addition to a substantial body of less strong evidence, to show that
platinum based chemoradiotherapy produces better results than radiotherapy alone, albeit at a cost in
terms of toxicity. Not all randomised controlled trials comparing radiotherapy and chemotherapy with
radiotherapy alone for nasopharyngeal carcinoma have shown improved outcome, however.
Nonetheless, most oncologists will choose to use chemotherapy as well, especially in more advanced
disease.
Surgery
Surgery has no place in the initial management of nasopharyngeal carcinoma, other than to obtain tissue
for diagnosis.
171
It is reserved for the salvage, when feasible, of patients with nodes that fail to regress after radiotherapy,
or whose nodes reappear following complete clinical response, and in highly selected cases of localised
recurrence at the primary site.
METASTATIC DISEASE
Patients with distant metastases at presentation are probably incurable by any means, nonetheless
relatively aggressive systemic treatment with chemotherapy is often beneficial in fit patients and can
result in prolonged remissions. Consolidation of an early response with high dose radiotherapy to the
primary site and neck may then be indicated to provide durable symptom control.
RECURRENT NASOPHARYNGEAL CANCER TREATMENT OPTIONS
Selected patients who either have failed primary treatment with radiotherapy of postnasal space
carcinoma or have a recurrence of disease may be treated with further external beam or interstitial
radiotherapy, or be considered for surgical resection. Most experience has been with the surgical
implantation of gold grains into the nasopharynx either by a palatal split or under direct vision. Five-year
survival rates have been reported as 79.1% for residual disease and 53.6% for recurrent disease. Patients
however who had evidence of disease extension outside the nasopharynx had lower control rates. Surgical
resection can also be considered for persistent or recurrent disease in the nasopharynx, and this is
particularly applicable to disease that has spread into the paranasopharyngeal space but not yet involved
the internal carotid artery. Five-year survival rates have been reported as high as 73% in selected cases
with a transpalatal, transmaxillary and/or transcervical approach. Most experience is with the
transmaxillary approach. Neck dissection is also indicated for nodal recurrence. If a patients has
metastatic disease or local recurrence no longer amenable to surgical or radiation treatment palliative
chemotherapy may be an option.
MORBIDITY
Radical treatment is associated with substantial mucositis, which can compromise nutrition, and PEG
feeding may be beneficial. Chemoradiotherapy with cisplatin and inevitable irradiation of the petrous
temporal bone makes sensorineural deafness common. Carboplatin may be less ototoxic but there are
fewer data about its efficacy. The parotid salivary glands are inevitably irradiated and xerostomia is
universal. Oral pilocarpine benefits a few patients. Dentition is at risk in the absence of saliva. Meticulous
attention to oral hygiene is therefore necessary to prevent accelerated dental decay. If extractions of
carious teeth become necessary there is the added risk of osteoradionecrosis. Thyroid function testing
should be performed prior to therapy and as part of follow up as about one third of patients may develop
primary hypothyroidism following neck irradiation. Reirradiation may lead to temporal lobe and temporal
bone necrosis.
OUTCOME
Small localised cancers of the nasopharynx, although rare, are highly curable by radiation treatment with
5 year survival rates approaching 80 to 90 percent. Moderately advanced lesions without clinical evidence
of spread to lymph nodes are often curable with survival rates of 50 to 70 percent.
Patients with advanced lesions especially those associated with clinically positive cervical lymph nodes,
cranial nerve involvement and bone destruction are poorly controlled locally by radiation treatment, with
or without surgery and often develop distant metastases despite local control. Most recurrences occur
within 5 years of diagnosis.
References:
1.
2.
3.
Fee W E, et al. Surgical management of recurrent nasopharyngeal carcinoma after radiation failure at the primary site.
Laryngoscope 1988; 98: 1220-1226.
Grandi C, et al. Analysis of prognostic factors and proposal of a new classification for nasopharyngeal cancer. Head Neck
1990. 12: 31-40.
Fandi A, et al. Nasopharyngeal Cancer: Epidemiology, staging, and treatment. Semin Oncol. 1994; 21: 382-397.
172
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
Lee A W M, et al. Retrospective analysis of 5037 patients with nasopharyngeal carcinoma treated during 1976-1985: overall
survival and patterns of failure. Int. J Radiat. Oncol. Biol Phys. 1992; 23: 261-270.
Munro A J. Head and Neck. Nasopharynx. pp 329-336. In The Treatment of Cancer. 3rd edition. 1995 Editors Price P and
Sikora K. Chapman and Hall publ. London ISBN 0 412 56010.0.
Schantz S P, et al. Tumours of the nasal cavity and paranasal sinuses, nasopharynx, oral cavity and oropharynx. In: De Vita
V T, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology. Philadelphia: J B Lippincott Company,
4th edition, 1993, pp 574-630.
Dobbs J, Barrett A and Ash D. Practical radiotherapy planning: Third edition 1999. Chapter 9. Nasopharynx. pp 94-100.
Arnold publ. London.
Neel H B, et al. Antibodies to Epstein-Barr virus in patients with nasopharyngeal carcinoma and in comparison groups. Ann
Otol, Rhinol and Laryngol 1984. 93 (5, part 1): 477-482.
National Cancer Institute. Physicians Data Query (PDQ) on nasopharyngeal cancer. www.cancernet.nci.nih.gov. Last
modified 04/2000.
Teo PML, et al. Intracavitary brachytherapy significantly enhances local control of early T stage nasopharyngeal carcinoma:
the existence of a dose-tumor-control relationship above conventional tumoricidal dose. Int. J. Radiat. Oncol. Biol. Phys.
2000; 46: 445-458.
Wolden SL, et al. Improved long-term survival with combined modality therapy for pediatric nasopharynx cancer. Int. J.
Radiat. Oncol. Biol. Phys. 2000; 46: 859-864.
Lee AWM, et al. Total biological effect on late reactive tissues following re-irradiation for recurrent nasopharyngeal
carcinoma. Int. J. Radiat. Oncol. Biol. Phys. 2000; 46: 865-872.
Al Sharraf M, et al. Chemoradiotherapy versus radiotherapy in patients with advanced nasopharyngeal cancer: phase III
randomised intergroup study 0099. J. Clin. Oncol. 1998; 16: 1310-1317.
Chua DT, et al. Preliminary report of the Asian-Oceanian Clinical Oncology Association randomised trial comparing
cisplatin and epirubicin followed by radiotherapy versus radiotherapy alone in the treatment of patients with locoregionally
advanced nasopharyngeal cancer. Cancer 1998; 83: 2270-2283.
Chan ATC, et al. A prospective randomised study of chemotherapy adjunctive to definitive radiotherapy in advanced
nasopharyngeal carcinoma. Int. J. Radiat. Oncol. Biol. Phys. 1995; 33: 569-577.
International Nasopharynx Study Group. Preliminary results of a randomised trial comparing neoadjuvant chemotherapy
(cisplatin, epirubicin, bleomycin) plus radiotherapy vs. radiotherapy alone in stage IV (> or = N2, M0) undifferentiated
nasopharyngeal carcinoma: a positive effect on progression free survival. VUMCA I trial. Int. J. Radiat. Oncol. Biol. Phys
1996; 35: 463-469.
Kwong DL, et al. Long term results of radioactive gold grain implantation for the treatment of persistent and recurrent
nasopharyngeal carcinoma. Cancer 2001 Mar 15:91:1105-1113.
Wei WI, Nasopharyngeal cancer: current status of management: a New York Head and Neck Society lecture. Arch
Otolaryngol Head Neck Surg 2001 Jul:127:766-769.
Fee WE Jr et al. Nasopharyngectomy for recurrent Nasopharyngeal Cancer: A 2-to 17-Year Follow-up. Arch Otolaryngol
Head Neck Surg 2002 Mar;128 :280-284
Hao SP et al. Salvage Surgery for recurrent nasopharyngeal carcinoma. Arch Otolaryngol Head Neck Surgery 2002 Jan;
128: 63-67
173
Section 5
Chapter 9
Ear and Temporal Bone
In reviewing the current literature on this subject, both Medline & PubMed were used to search the
literature, and papers reviewed using a 15 year limit (although some earlier papers were sourced by
reviewing references noted in recent papers). In the available literature there are no prospective
randomised or nonrandomised trials evaluating the treatment options, and no uniformity in terms of
treatment exists.
Introduction.
Cancers arising in the structures of the temporal bone are extremely rare accounting for only 0.05% of
head and neck cancers (1). In a study from England & Wales, the age-adjusted incidence remained stable
at about 1 / 1000,000 per year for women and 0.8 / 1,000,000 for men from 1968 to 1977 (2).
In several large series approximately 70% of malignancies arose from the auricle, 20 % from the external
auditory canal, and 10% from the middle ear and mastoid (3).
Tumours may involve the ear in the following ways:
•
•
•
Primary cancers involving the ear can arise from the auricle, the external auditory canal
2w(EAC), or the middle ear and temporal bone. More than 70% of ear cancers originate on
the pinna (4).
Tumours from adjacent sites can extend into the structures of the temporal bone. These
include malignancies arising from the parotid gland, temporomandibular joint (TMJ), and
skin of the preauricular area or postauricular sulcus.
Metastases from tumours arising in the breast, kidney, lung, prostate, and other sites have
been documented (5).
Optimal setting & team membership.
A multidisciplinary approach is required for all types of cancer involving the ear, and management may
involve one or more of the following:
•
•
•
•
•
•
•
•
•
Surgical oncologist (usually an otolaryngologist re EAC/Temporal bone)
Neurosurgeon (for those more extensive tumours with dural involvement)
Plastic & reconstructive surgeon (for more extensive tumours of the auricle and reconstruction of
larger resection defects)
Clinical oncologist
Neuroradiologist
Cytopathologist with an interest in Head & Neck pathology
Macmillan specialist nurse
Speech therapist
Dietitian
Confirmation of diagnosis.
Histologic confirmation of the diagnosis is usually required before the planning of definitive treatment
and this may be obtained under local or general anaesthetic. Some lesions on the pinna may be suitable
for excisional biopsy, which will prove to be the definitive treatment.
In the case of parotid tumours invading the ear (and secondarily involved lymph nodes), fine needle
aspiration cytology should distinguish benign from malignant disease in 90% of cases (6).
174
Imaging
Tumours of the pinna may require no imaging unless there is associated cervical lymphadenopathy.
However, for those tumours involving the EAC high-resolution computed tomography (CT) is the
investigation of choice for assessing the bony anatomy of the temporal bone. Arriaga et al (7) investigated
the utility of preoperative CT and concluded that the pathologic extent of tumour growth can be
accurately assessed with this modality.
Magnetic resonance imaging (MRI) is more useful to define the tumour from brain and from the reactive /
inflammatory changes that may occur, and gives information regarding internal carotid artery (ICA) and
sigmoid sinus patency, by the presence or absence of flow void signals.
Carotid angiography may however be necessary to establish unequivocally involvement of the carotid
artery. If involvement of the ICA is suspected on angiography, then its sacrifice (or reconstruction) may
be considered by some surgeons as part of the resection. Under these circumstances some assessment of
the effect of ICA occlusion on intracranial circulation is required – in the UK this would usually involve a
test balloon occlusion of the ICA under local anaesthetic in order to assess any neurologic sequelae.
Staging
The American Joint Committee on Cancer (AJCC) states that the goal of a staging system is to evaluate
the efficacy of treatment and to provide a sound basis for therapeutic planning in cancer patients, by
describing in comparable form the survival and results of treatment of different patient groups. Currently
no staging system for malignancies involving the ear is accepted by either the International Union
Against Cancer (UICC) or the AJCC.
Treatment Guidelines
1. Cutaneous carcinoma of the pinna.
The most common method of treatment for auricular skin cancer is surgical resection. Resection can be
accomplished in a traditional fashion or with Mohs micrographic technique (8). If there are involved
nodes then this surgery may need to be performed together with a parotidectomy and neck dissection.
Surgical treatment of auricular skin cancer poses several anatomic challenges that are unique to the ear.
The greatest challenge comes in dealing with the underlying cartilaginous skeleton of the external ear. A
judgment must be made whether auricular cartilage must be sacrificed.
Reconstruction of the pinna would normally require the input of a plastic and reconstructive surgeon, and
there are occasions when the use of a prosthetic ear is the most suitable option.
Radiotherapy can offer an excellent cure rate for smaller carcinomas of the ear. Concerns about
radiotherapy centre on the uncertainty of tumour margin control, the possibility of radiation necrosis, and
questionable efficacy if cartilaginous and bony invasion are present (9).
2. Carcinoma involving the EAC / Temporal bone.
The lack of an accepted staging system, the rarity of malignancy involving the EAC and temporal bone
and the wide variety of treatment plans that have been employed make it difficult to extract definitive
information from the literature regarding the optimal treatment and prognosis. Clinical experience
therefore dictates management decisions and complete surgical resection with a clear microscopic margin
must be the preferred initial primary treatment goal in a patient with a resectable cancer.
The steps in the decision making process involve the following:
• Histopathologic confirmation of malignancy.
• Radiologic determination of disease extent and metastatic spread.
• A realistic assessment of whether surgery is aimed at palliation or cure.
• The need to include the parotid , TMJ, infratemporal fossa, neck exploration, carotid artery, and
dural or cerebral resection or reconstruction as part of the planned resection.
175
•
•
•
The necessity or type of reconstructive options.
An opinion from a clinical oncologist regarding adjuvant radiotherapy.
A neurosurgical opinion if a more formal skull base resection is required
A widely accepted operative concept is to free the involved temporal bone from its surrounding venous
sinuses, protect the internal carotid artery and brainstem, and avoid injury to cranial nerves if they are still
functioning.
A number of surgical approaches (that largely depend on the extent of the tumour) are available that
satisfy these criteria and they include:
•
•
•
•
Mastoidectomy – includes all types of modified radical and radical mastoidectomy.
Lateral temporal bone resection (TBR) – removal of the osseous and cartilaginous external
auditory canal, tympanic membrane, malleus and incus.
Subtotal TBR – includes the additional removal of the otic capsule.
Total TBR – involves the additional removal of the petrous apex
The above procedures may be combined with superficial parotidectomy and neck dissection dependent on
the extent of the local disease and the presence of associated lymphadenopathy.
Involvement of dura or brain, have led some workers to perform extended temporal bone resections. No
groups have shown any impact on survival with this approach except Moffat et al (10). Moffat performed
salvage surgery in 15 cases with a 47% 5 year survival.
Surgical resection and reconstruction of carcinomatous involvement of the ICA is also controversial, with
no studies able to show an improved survival with this aggressive approach.
Radiotherapy is seldom advocated as the sole treatment modality. The precise role of preoperative or
postoperative radiotherapy is unclear. A review by Prasad & Janecka (11) has indicated that the addition
of radiotherapy to patients with disease confined to the EAC and treated with lateral TBR confers no
survival advantage. The role of radiotherapy in patients treated with subtotal TBR was unclear.
Guidelines from the American Society for Head & Neck Surgery and The Society of Head & Neck
Surgeons (12) for postoperative radiotherapy include:
•
•
•
Close resection margins (less than 5 mm), when proximity of tumour to important structures such
as ICA or facial nerve preclude wide margins.
Positive resection margins.
Perineural invasion.
These conditions apply to the majority of resections for temporal bone carcinoma thus postoperative
radiotherapy is indicated in most cases.
Prognosis.
Cutaneous carcinoma of the pinna has been described by several authors as having a higher rate of
recurrence and a worse prognosis than with other skin cancers.
Byers & colleagues (13) in a review of 486 patients with squamous cell carcinoma of the ear reported a
local recurrence rate of 14% with death in 2.5% from local failure.
The prognosis in carcinoma involving the EAC / Temporal bone where the disease is confined to the EAC
is approximately 50% 5 year survival but falls to approximately 29% with middle ear involvement (11).
176
Summary
Carcinoma involving the temporal bone is a rare disease. Lack of prospective randomised or nonrandomised trials evaluating the treatment options, means that clinical experience currently dictates
management decisions. Complete surgical resection with a clear microscopic margin must be the
preferred initial primary treatment goal in a patient with a resectable cancer. In patients with disease
confined to the EAC this would involve lateral TBR.
The precise role of preoperative or postoperative radiotherapy is unclear. Postoperative radiotherapy is
indicated in the most cases.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Arena S, Keen M. Carcinoma of the middle ear and temporal bone. Am J Otolaryngol 1998 ; 9: 351 – 356.
Morton RP, Stell PM, Derrick PPO. Epidemiology of cancer of the middle ear cleft. Cancer.1984.53: 1612-1617.
Conley J, Sculler K. Malignancies of the ear. Laryngoscope. 1976.86:1147-1163.
Marfatia P.Malignant tumors of the ear. A review of 57 cases.Laryngoscope.1966.76:1591-1595.
Cumberworth VL, Friedmann I, Glover GW. Late metastasis of breast carcinoma to the external auditory canal. J Laryngol
Otol 1994. 108 : 808-810.
Boccato P, Altavilla G, Blandamura S. Fine needle aspiration biopsy of salivary gland lesions. Acta Cytologica 1998. 42:
888-898.
Arriaga M, Curtin H,Takahashi H, Hirsch BE, Kamerer DB. Staging proposal for external auditory meatus carcinoma on
preoperative clinical examination and computed tomography findings. Ann Otol Rhinol Laryngol 1990. 99 : 714 – 721.
Niparko JK, Swanson NA, Baker SR, Telian SA, Sullivan MJ, Kemink JL. Local control of auricular , periauricular , and
external canal cutaneous malignancies with Mohs surgery. Laryngoscope 1990. 100: 1047 – 1051.
Goodwin W, Jesse R. Malignant neoplasms of the external auditory canal and temporal bone. Arch Otolaryngol 1988. 9(5):
393-398.
Moffat DA, Grey P, Ballagh RH, Hardy DG. Extended temporal bone resection for squamous cell carcinoma. Otolaryngol
Head & Neck Surg.1997. 116: 617-623.
Prasad S, Janecka IP. Efficacy of surgical treatments for squamous cell carcinoma of the temporal bone: A literature review.
Otolaryngol Head Neck Surg 1994. 110:270-280.
The American Society for Head and Neck Surgery and The Society of Head and Neck Surgeons. Clinical practice guidelines
for the diagnosis and management of cancer of the head and neck. The American Society for Head and Neck Surgery and
The Society of Head and Neck Surgeons.1996.
Byers R, Kesler K, Redmon B. Squamous carcinoma of the external ear. Am J Surg. 1980.146: 447-452.
177
Section
5
Chapter 10
Thyroid
Introduction
Approximately 8% of the UK population have nodular thyroid disease. A significant proportion are
clinically solitary. Thyroid nodules are more common in women with increasing age. In contrast, thyroid
cancer is rare (2 to 3 cases per 100,000 per annum in the UK). The commonest presentation is as a
solitary thyroid nodule in a euthyroid patient and in that group, the incidence of malignancy is between 10
and 20%. The majority are differentiated thyroid cancer, and most have an excellent prognosis. A
minority present with local and distant metastases e.g. with metastatic neck disease, airway and pharyngooesophageal obstruction, and bony or pulmonary secondaries. Differentiated thyroid cancer (90% of all
thyroid cancer) consists of papillary or mixed papillary and follicular (80%) and follicular cancer (10%).
There have been no prospective randomised studies investigating treatment outcomes for this condition,
so that the consensus view expressed in these guidelines is formed predominantly from retrospective
analyses (level II-III evidence).
Optimal Setting and Team Membership
Multidisciplinary thyroid clinic to include:
Endocrinologist (ideally 2 for leave cover)
Specialist Surgeon (ideally 2 for leave cover)
Specialist in Thyroid Cytology and Pathology
Specialist Radiologist
Clinical Oncologist
MacMillan Specialist Nurse
Diagnostic evaluation
History should include past history of :Ionizing radiation to the head or neck
Family history of thyroid cancer
Personal history of previous thyroid disease
In addition, patients should be asked whether they have developed a hoarse voice, difficulty in
swallowing or breathing.
Examination includes not only neck evaluation but also vocal cord function
Initial investigations
• All patients should have baseline thyroid function tests (TSH, and free T4 with free T3 as appropriate).
Suppression of TSH is a common and non-specific finding in subjects with goitre. Overt thyroid
dysfunction, indicated by raised serum concentrations of free T4 and T3 or biochemical
hypothyroidism, is frequently associated with a goitre and such patients do not generally require
further investigation. Assessment of thyroid antibody status may assist in the diagnosis of chronic
lymphocyte thyroiditis, predict postoperative hypothyroidism and aid the interpretation of both thyroid
function and serum thyroglobulin measurements.
• All euthyroid patients presenting with thyroid enlargement should have fine needle aspiration cytology
(FNAC) as a mandatory initial investigation. It is important to document which side and what part of
the goitre has been aspirated. Fine needle aspiration cytology results are reported and classified as
inadequate, benign, suspicious, or frankly malignant. A strategy for the evaluation of the solitary or
dominant thyroid nodule is shown in the appendix.
The following are not routine, but may be of value following initial evaluation if the diagnosis is not
clear, or when the diagnosis of cancer has been established.
178
• Radiological Imaging
Chest x-ray may demonstrate tracheal deviation, mediastinal extension of disease or lymphadenopathy,
and pulmonary metastases or associated co-morbidity. Soft tissue x-rays of the neck and thoracic inlet
may show tracheal deviation and compression but are less accurate than respiratory flow loop studies.
Anatomical imaging with CT or MRI can be used to evaluate the thyroid, neck, midline visceral
compartment, mediastinum, chest and abdomen.
• Ultrasound of the neck
This can be helpful in differentiating a solitary from a multinodular swelling, in measuring tumour size
and assessing the contralateral lobe. It may be used to evaluated complex cysts and distinguish purely
cystic nodules from complex cysts with a solid component, but it is unable to differentiate reliably
between benign and malignant disease.
• Thyroid scintigraphy
The commonest investigation currently used is scanning with Technetium (Tc99m) pertechnetate. This test
is poorly specific and sensitive in the diagnosis of thyroid cancer. This is, in part, because technetium is
trapped and not organified by the thyroid and since some cancers retain the ability to trap and not
organify, (and also have a high blood flow), “cold” nodules may appear “hot” using this technique.
However, scintigraphy can be useful to assess the state of the thyroid bed following previous surgery, to
measure tumour size and assess the contralateral lobe. The best way to evaluate whether or not a thyroid
nodule is truly functioning is to use I123 scintigraphy. Truly functioning nodules, (ie “hot”) are unlikely to
be malignant (less than 1%) and in those nodules with a suspicious FNA (hyperplasia versus low grade
neoplasia), I123 scintigraphy may in the future be an alternative in some cases to a diagnostic lobectomy.
Treatment Guidelines
• The following treatment modalities are available for thyroid cancer.
Surgery
Radioactive iodine
External beam radiotherapy
Thyroxine therapy
Chemotherapy
• The main stay of treatment for differentiated and medullary thyroid cancer is surgery
• All differentiated and medullary thyroid cancers should be TNM staged
• There are a number of prognostic factors associated with differentiated thyroid cancer:
Patient factors Age, gender
Tumour factors Stage and histology
Management factors Delay in therapy, extent of surgery, experience of the surgeon, thyroid hormone
therapy and treatment with radioiodine post-operatively.
• Patients should be given proper informed consent and the opportunity to contribute openly and freely
in any management discussions. Patient information leaflets should be readily available.
Papillary Thyroid Cancer
Primary Tumour
• The aim of treatment is to remove all macroscopic and microscopic disease with minimum morbidity.
The minimum operation that should be performed on a solitary thyroid nodule is a diagnostic
lobectomy (or isthmusectomy for a midline lesion).
• Although there is no prospective evidence, a consensus view based on retrospective data suggests that
risk stratification treatment for differentiated thyroid cancer can be based on the TNM (tumour, nodes,
distant metastases) classification combined with patient gender. This is shown below.
179
Risk stratification treatment based on TNM classification including gender, age, stage and histology
(GASH)
• Age (less or more than 45 years)
• Gender (males carry a worse prognosis than females)
• Tumour size
• Tumour histology
• Nodal and distant metastases
Selection of a treatment policy for differentiated thyroid cancer by allocation into risk groups depending
on gender, age, stage and histology facilitates surgical treatment which is shown in Figure 1.
Table 1 - Surgical treatment of differentiated thyroid cancer
Low risk patient with low risk tumour
=
lobectomy
Low risk patient with high risk tumour
=
? lobectomy or TT
High risk patient with low risk tumour
=
? lobectomy or TT
High risk patient with high risk tumour
=
total thyroidectomy
= Intermediate group
TT
= Total thyroidectomy
Low risk patients include females under the age of 45
High risk patients include all males, and females over 45
Low risk tumours include papillary carcinomas less than 1cm in size, and minimally invasive follicular
carcinomas less than 1cm in size.
High risk tumours include papillary and follicular carcinomas greater than 1cm in size. Also included is
any tumour associated with significant multifocality, or local or distant spread.
Patients under 16 with a diagnosis of cancer should be regarded as high risk and, are usually best treated
aggressively.
Papillary thyroid carcinoma (PT1)
Solitary papillary thyroid cancers which measure less than 1cm in size (PT1) and which are surrounded
by an adequate margin of normal thyroid tissue, in the absence of cervical or distant metastases, can be
treated by unilateral lobectomy, subsequent TSH suppression with thyroxine and thyroglobulin
surveillance. Tumours in the isthmus can similarly be treated by an isthmusectomy and a 1cm margin of
resection of normal tissue.
Papillary thyroid carcinoma (PT2)
The treatment of this lesion (1-4cm in size) is controversial. Low risk patients, that is females under 45
years of age with solitary, non metastatic tumours greater than 1cm but less than 3cm in size (small PT2
N0 M0 tumours) can also probably be safely treated with lobectomy, TSH suppression with thyroxine and
subsequent monitoring of the serum thyroglobulin. However, in men, and women with larger tumours, the
risk of recurrence is higher. Such patients should have total thyroidectomy, postoperative radio-iodine
ablation of residual thyroid tissue, TSH suppression with thyroxine and monitoring of the serum
thyroglobulin.
Papillary thyroid carcinoma (tumours greater than 4cm in size, PT3)
All patients with tumours greater than 4cm in size and any tumour where there is significant multi- focal
disease, extracapsular spread, lymph node or distant metastases should have a total thyroidectomy, with
preservation of both recurrent laryngeal nerves (and external laryngeal nerves where possible) selective
neck dissection as required to clear disease, followed by radio-iodine ablation of residual tissue. Longterm TSH suppression with thyroxine and serial measurements of serum thyroglobulin are important.
180
For many patients with thyroid cancer, total thyroidectomy with parathyroid preservation will be the
operation of choice. If there is any concern regarding the morbidity resulting from a truly total
thyroidectomy, a near-total thyroidectomy can be performed in the absence of contralateral disease. In
this procedure, a sliver of the contralateral lobe including the parathyroids is preserved. The remnant of
normal thyroid tissue can then be ablated with radioiodine.
During thyroidectomy, the use of the nerve stimulator to identify the recurrent laryngeal nerve is not
routinely recommended but may be of value in re-do surgery, and also when attempts to identify the
external laryngeal nerve prove difficult.
Postoperative hypocalcaemia should be managed in line with local protocols.
Papillary thyroid cancer arising in a thyroglossal duct cyst can be managed conservatively as long as the
patient has undergone Sistrunk’s operation, that the resection has been microscopically complete and that
the remaining thyroid gland is normal both on palpation and on investigation by ultrasound or
radioscintigraphy. Postoperatively, treatment is with TSH suppression with thyroxine and sequential
measurement of the serum thyroglobulin.
When an unsuspected papillary thyroid carcinoma is discovered in a multinodular goitre resected by
either lobectomy, near- total or total thyroidectomy, if excision margins are free of disease, then treatment
is TSH suppression with thyroxine and monitoring of the serum thyroglobulin. If clearance is
questionable, or a follicular or multifocal component present, then completion thyroidectomy and post
operative radioiodine ablation are necessary.
The Neck
Node negative disease (N0)
The extent of nodal surgery is determined by the degree of lymphatic involvement. In the clinically N0
neck, level 6 should be routinely dissected and levels 2 to 5 and 7 palpated at the time of surgery.
Suspicious nodes can be subjected to frozen section and if involved, a selective neck dissection (at least
levels 2 to 4) should be performed.
Node positive disease (N+)
Clinically palpable disease in levels 2 to 5 indicates the need for at least a selective neck dissection
involving these levels and depending on the size and extent of disease, a modified radical, radical or
extended radical neck dissection may be required.
The aim of combined total thyroidectomy and limited lymphadenectomy is to remove all microscopic
malignant cervical lymphadenopathy with minimum associated co-morbidity ie, the preservation of nonlymphatic structures such as the internal jugular vein, the sternomastoid muscle and the accessory nerve.
Follicular thyroid cancer
The management of follicular adenocarcinoma is similar to that of papillary tumours. The mainstay of
treatment is surgery. All follicular adenomas and small follicular cell carcinomas < 1cm with minimal
vascular invasion (PT1) can be managed safely by lobectomy alone. Surgery should be followed by TSH
suppression with thyroxine and sequential measurement of the serum thyroglobulin.
For the more advanced tumours, surgery usually entails a near-total or total thyroidectomy although some
patients in the intermediate group with tumours less than 3cm in size with minimal invasion (as for
papillary cancer) may be treated conservatively with hemithyroidectomy. The neck and the mediastinum
are managed as described for papillary carcinoma.
In advanced cases of differentiated thyroid cancer, invasion of local visceral structures by continuity and
contiguity may indicate that, after appropriate imaging, extensive extirpative surgery is appropriate to
181
include total laryngectomy, tracheal resection, partial or complete pharyngectomy and neck dissection. It
is important to exclude any major vessel involvement prior to surgery and the help of a cardiothoracic
surgeon may be required for mediastinal access.
Hürthle cell adenomas may be treated by lobectomy alone. Hürthle cell carcinomas represent variants of
follicular cell carcinoma but are more aggressive and are less likely to concentrate radioiodine and
therefore, should be managed more aggressively with total thyroidectomy.
Radiotherapy for differentiated thyroid cancer.
Radioiodine ablation and therapy
•
I131 (Radio-iodine) is used following surgery for a differentiated thyroid cancer to ablate residual
normal thyroid tissue and to search for and treat any metastatic disease. The protocol to be followed
for both ablation of residual normal thyroid tissue and treatment of any functioning local residual
disease or distant metastases is shown in Figure 2.
131
• The therapeutic isotope used is I
• Patients should be admitted to hospital and accommodated in a single room equipped for radiation
protection.
• As many patients with thyroid cancer are women of child bearing age, the possibility of pregnancy
must be excluded before radioiodine therapy is given.
• The patient must be off thyroxione for 4 weeks, Liothyronine (T3) for 10 days to allow exogenous
TSH levels to rise and stimulate uptake of iodine. In the future, administration of human recombinant
TSH may be useful in preventing iatrogenic hypothyroidism.
• The TSH levels should be measured before radioiodine therapy.
• The protocol for therapy should be followed and serum thyroglobulin sequentially measured as
indicated.
External beam radiotherapy
This may be appropriate in differentiated thyroid cancer when macroscopic disease has been left behind
following surgery, when ablative radioiodine therapy has been ineffective, or when tumours are
inoperable.
Chemotherapy
There is no role for chemotherapy in the management of differentiated thyroid cancer.
Management of lung and bone metastases.
Long term survival may be achieved after radioiodine treatment of lung metastases. Caution must be
taken in the treatment of miliary nodules because of the risk of radiation pneumonitis and subsequent
fibrosis. Fractionated radioiodine dosage is recommended. Soft tissue extradural spinal metastases,
considered unsuitable for surgical management, should be treated similarly in order to minimise the risk
of spinal cord compression.
Bone metastases are associated with a poor prognosis because of their relatively low level of radioiodine
uptake. Some are suitable for resection. Pre-surgical embolisation may be required, particularly in the
axial skeleton, in order to reduce vascularity.
Following surgery patients should be considered for radioiodine therapy and external beam radiotherapy
to the resection bed. This approach may offer long term disease free survival.
Monitoring of serum thyroglobulin
Thyroglobulin (Tg) is a serum protein which is the key substrate for the biosynthesis and storage of
thyroid hormones. In differentiated thyroid cancer, thyroglobulin is a specific, sensitive and therefore
extremely useful tumour marker. It is secreted by both normal and cancerous thyroid cells.
Following near-total or total thyroidectomy and I131 ablation, the measurement of serum thyroglobulin
when TSH has been suppressed by T4 therapy is helpful since Tg secretion from normal thyroid tissue is
182
more TSH - dependent than Tg secretion from neoplastic tissue. Thus, a detectable serum thyroglobulin is
highly indicative of residual or recurrent disease. In such patients, the diagnostic sensitivity of serum Tg
measurement is enhanced by the elevation of TSH so measurement of Tg after thyroid hormone
withdrawal prior to I131 scanning and ablation may be useful. Thyroglobulin is measured by a specific
radioimmunoassay; results should be interpreted with caution if endogenous Tg antibodies are present.
Follow up
After initial successful treatment, patients should be followed up by clinical evaluation and serial
thyroglobulin measurements (Figure 1). They should be seen 6 monthly for 18 months and then yearly for
life.
183
Figure 1 - Treatment of differentiated thyroid carcinoma Birmingham oncology centre protocol
“TOTAL” THYROIDECTOMY
Liothyronine (T3) 20
Micrograms tds stop 2 weeks
before I-131
Avoid iodine containing medicines, fish,
added salt & x-ray contrast examinations
I-131 Ablation 3GBq
day 3 check Thyroglobulin (Tg) & TSH
Thyroxine (T4)
for 6 weeks only
6 Weeks out-patient
appt.
check Tg, TSH, T4
Change to T3
20 micrograms tds for 2 weeks
(stop 2 weeks before I-131)
10 Weeks
I-131 Diagnostic scan 200 MBq check Tg and
TSH
Scan positive
Thyroglobulin raised
Metastases
Scan negative
Thyroglobulin < 10 micrograms/L
No metastases
Recommence T3
20 micrograms
tds for 2 weeks
(stop 2 weeks before I131)
Commence T4
Follow-up check
Tg, TSH, T4
(6-12 monthly appt.)
14 weeks
I-131 therapy dose
5.5GBq day 3
scan
184
Medullary thyroid carcinoma (MTC)
This cancer is rare with 75-80% being sporadic tumours, the remainder a familial syndrome. Multiple
endocrine neoplasia (MEN) syndrome 2A consists of MTC in association with phaeochromocytomas and
occasionally primary hyperparathyroidism. MEN2B consists of MTC together with neuromas of the lips,
tongue and conjunctivae, ganglioneuromatoses of the bowel, a Marfanoid appearance and occasionally
phaeochromocytomas. It is usually a new mutation with no obvious previous family history. The third
condition is familial MTC in isolation. All 3 familial disorders have been linked to abnormalities of the
RET proto-oncogene. MEN2B is a much more aggressive disorder usually presenting in childhood. In
MEN2A and familial MTC the clinical disorder usually presents in adult life. Surgery for this disease
should be performed in a unit with access to facilities for appropriate biochemical investigations and to
clinical and molecular genetics.
Making the diagnosis
Clinical evaluation
• A family history of thyroid, parathyroid or adrenal tumours or renal stones
• Any history or presence of any evidence of hyperparathyroidism or phaeochromocytoma
• Any history of neuromas of the lips, tongue or conjunctivae or gastrointestinal tract.
Head and Neck Examination
• Evaluation of the thyroid, and its relation to visceral structures.
• Any evidence of extrathyroid extension
• The presence or absence of any lymph nodes including their number, size and level
• Examination of vocal cord function.
General examination
This should include assessment of the chest and abdomen (including the liver). Look for evidence of a
Marfanoid appearance or any evidence of neuromas of the lips, tongue or conjunctivae.
Genetic studies
In excess of 90% of patients with any form of familial MTC have been shown to have a mutation of the
RET proto-oncogene. Moreover, 98% of cases of MEN2A have mutations in one of just 6 codons. These
plus mutations in an additional two codons have been found in isolated familial MTC while just one
single different mutation has been found in 95% of all cases of MEN2B. Such a restricted range of
mutations means that selective analysis of the RET gene is a very feasible and useful technique.
Screening for familial MTC
It is important to identify the apparently sporadic case which in fact is an index case of a familial form of
the disease. The finding of multiple foci of tumours together with definite ‘C’ cell hyperplasia virtually
guarantees the diagnosis of familial disease although their absence does not exclude it. A family history
of any of the tumours associated with MEN2 should raise suspicion.
In likely sporadic cases, family screening should not be undertaken initially and the emphasis should be
on increasing the certainty that the case is sporadic. If the clinical information is inconclusive, a limited
analysis of the RET proto-oncogene should be undertaken. If this is normal, the likelihood of familial
disease is < 0.5%. If a genetic abnormality is found, then this should be used to screen other family
members. Patients with likely MEN2B should also have their RET proto-oncogene analysed expecting to
find an abnormality which can be used to screen offspring.
Stimulated calcitonin measurements which previously were the mainstay of diagnosis. The test has been
replaced by genetic testing. They should only be considered where there is very strong suspicion of
familial disease and a normal genetic analysis in the affected case.
185
It is strongly advised that family screening and genetic counselling is done by, or in close association
with, a clinical genetics department so that everyone is aware of the implications of the tests before they
are undertaken.
Imaging studies
Chest radiograph (If CT not performed)
CT to evaluate the thyroid bed, any extension into the midline visceral structures, metastatic neck
disease, evidence of disease in the mediastinum as well as the chest. Abdominal CT to assess both the
liver and adrenals to exclude phaeochromocytoma (if MEN 2A is suspected). The adrenals are
probably best evaluated with MRI.
99m
• Whole body imaging with Tc
(v) dimercaptosuccinic acid (Pentavalent DMSA) together with
conventional Tc99m MDP bone scanning may be necessary to evaluate, localise and stage systemic
spread.
123
• Imaging with I
- MIBG (Metiodobenzylguanidine) may be useful to evaluate and stage systemic
spread, and to confirm or refute the diagnosis of a phaeochromocytoma.
•
•
Laboratory tests
These should include:
• Thyroid function tests
• basal serum calcitonin levels.
• Serum calcium (if this is elevated, then a parathyroid hormone level should be obtained)
• Serum albumin
• 24 hour urine catecholamine excretion (If MEN 2A is suspected).
Prognostic factors
• TNM stage
• Pre - and postoperative calcitonin levels
• Previous surgery
Treatment
Surgery
• The primary tumour
All patients should undergo a total thyroidectomy, with preservation of both recurrent laryngeal nerves
(and external laryngeal nerves where possible). An attempt should be made to preserve all the
parathyroids but if there is any evidence of tumour involvement, these should be removed.
• The Neck
Node negative disease (N0).
In combination with a total thyroidectomy, the medial compartment of the neck (levels 6) should be
dissected from the level of the hyoid down to the brachiocephalic vein, and from one carotid sheath to
another. In addition, nodes in levels 2, 3 and 4 should be palpated and any suspicious ones sent for frozen
section. The presence of positive disease at the time of surgery indicates the need for at least a selective
neck dissection (levels 2-5).
Node positive disease (N+)
In those instances where there is either radiological or clinical evidence of cervical nodal spread, then the
appropriate neck dissection should be performed.
This should be as conservative as possible and at least levels 2 to 5 should be dissected with preservation
of the accessory nerve, the internal jugular vein and the sternomastoid muscle wherever possible.
Occasionally, either a modified radical or radical neck dissection may be required.
186
Radiotherapy
Since MTC does not concentrate iodine, there is no role in this disease for post-operative radio- iodine
ablation and therapy. In those cases where tumour excision has been complete, no further treatment is
indicated. If there is microscopic evidence of residual disease, then external beam radiation therapy may
be beneficial in the following instances
• Multiple large nodal metastases with extracapsular extension.
• Residual macroscopic disease
As an alternative to radiotherapy (or in conjunction with it), some patients who concentrate I123 MIBG
should be considered for therapeutic treatment with I131 MIBG.
Associated phaeochromocytoma
Any evidence of a phaeochromocytoma which is discovered during the preoperative work up of a patient
with MTC should be treated and resected first, by a specialist endocrine surgeon before definitive
treatment of the thyroid tumour.
Chemotherapy
There is no established role for chemotherapy in the management of patients with MTC
The role of parathyroidectomy
In patients who have the MEN 2A syndrome, parathyroid hyperplasia is common and may occur in 30 40% of patients. In this situation, a subtotal or total parathyroidectomy with auto transplantation may be
necessary at the time of initial surgery. This avoids the need of having to re- operate later with potential
risk for damage to both recurrent laryngeal nerves. Those parathyroids that are removed can be
cryopreserved so that if hypoparathyroidism subsequently develops, these glands can be reimplanted.
Follow up
Patients should be followed up for life. The particular schedule for each patient should be tailored to their
initial clinical course and subsequent risk of recurrent disease but the following protocol is recommended.
• Six monthly for 5 years
• Then yearly for life.
• Patients should have a head and neck examination and a once yearly measurement of thyroid function
• Yearly serum calcium levels and urine catecholamines should be done in patients with familial MTC
• The role of routine postoperative measurements for serum calcitonin is controversial. If the pre
operative calcitonin drops post-treatment to an undetectable level, then this is a good prognostic sign.
The presence of an elevated serum calcitonin postoperatively indicates residual or recurrent disease
which is highly likely to be incurable. In this situation, there is little evidence that subsequent regular
routine measurements of calcitonin and the search for residual and recurrent disease makes any
difference to long term prognosis.
Patients should be followed up clinically, and any significant symptoms or signs investigated
appropriately. Recurrent disease should be then treated on its merits.
Thyroid Lymphoma
This rare condition presents with a rapidly expanding thyroid mass and often coexistent dysphagia and
stridor. There may be a preceeding Hashimoto’s thyroiditis. FNAC may suggest lymphoma. A tru-cut or
open biopsy is then required for histological evaluation.
This condition needs to be differentiated from anaplastic carcinoma. Formal lymphoma staging is
required by a designated clinical oncologist and the subsequent treatment protocol will include
chemotherapy plus or minus radiotherapy. The outlook is generally good.
Investigations required.
•
Thyroid function tests
187
•
•
•
•
•
Thyroid antibodies
FNAC and open biopsy (or tru-cut)
Whole body CT
Bone marrow and trephine
ESR, LDH.
Anaplastic thyroid cancer
This condition presents in a similar way to thyroid lymphoma with a rapidly expanding mass, dysphagia
and airway obstruction in an elderly patient. Clinical examination usually reveals a firm, fixed, infiltrating
mass. There is often a past history of a goitre. An open biopsy is usually required to make the diagnosis
and differentiate this condition from lymphoma. Further surgery is not usually indicated other than an
isthmusectomy to relieve airway obstruction when a tracheostomy may also be necessary. Subsequent
treatment is with external beam radiotherapy. Chemotherapy has no role. The outlook is generally very
poor and most patients survive less than 12 months.
Investigations required
• Thyroid function tests
• Thyroid antibodies
• FNAC and open biopsy (or tru-cut)
• Neck and chest CT (or chest x-ray).
Data Collection
Surgeons carrying out thyroid surgery should collect their data using standardised information packages
in line with local guidelines and also audit their results.
Surgical workload
Surgeons carrying out this sort of work should be performing at least 30 cases per year (which includes
benign and malignant disease). It is recommended that the surgical management of advanced disease,
(total thyroidectomy for cancer, neck dissection etc) is performed in centres by recognised experts.
Outcome measurements
There are a number of performance indicators which can be used to monitor effective management of
thyroid cancer and they are listed below.
• Adequate primary surgery
• Incidence of vocal cord paralysis
• Incidence of hypoparathyroidism (temporary and permanent)
• Achievement of TSH suppression
• Provision and treatment with radioiodine postoperatively when indicated.
• Regular monitoring of serum thyroglobulin
• Abnormal thyroglobulin acted upon
• Quality of life
• Disease free interval
• Survival
188
Appendix
A DIAGNOSTIC STRATEGY TO EVALUATE THE
“SOLITARY” OR “DOMINANT”
THYROID NODULE
FNAC
Malignant
Surgery
or
Suspicious
(Hyperplasia
or low grade
neoplasia)
Consider
Scintigraphy
Benign
Watch.
Discharge after 2
negative FNAC’s
Inadequate sample
Repeat FNAC
I123 Scan
“Hot”
Observe
“Warm” or “Cold”
Surgery
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
Brierley, J.D. Panzaerlla, T. Tsang, R.W., Gospodarowicz, M.K. and O’Sullivan, B A comparison of different staging
systems. Predictability of patient outcome. Thyroid carcinoma as an example Cancer, 1997. 79: 2414-2423
Cady, B and Rossi, R. An Expanded view of Risk-Group Definition in Differentiated Thyroid Carcinoma. Surgery.
1988. 104: 947-953
Ellenhorn, JDI., Shah, JP. And Brennan, MF. Impact of therapeutic regional lymph node dissection for medullary
carcinoma of the thyroid gland. Surgery. 1993. 114: 1078-1082
Hay, ID, Bergstralh, E.J, Goellner, JR and Grant CS. Predicting outcome in Papillary Thyroid Carcinoma:
Development of a reliable prognostic scoring system in a cohort of 1779 patients surgically treated at one institution
during 1940 through 1989. Surgery 1993. 114: 1050-1058
Hay ID, Grant CS, Taylor WF and McConahey, WM. Ipsilateral lobectomy versus bilateral lobar resection in papillary
thyroid carcinoma: A retrospective analysis of surgical outcome using a novel programme scoring system Surgery.
1987. 102: 1088-1095
Kumar. H, Daykin. J, Holder. R, Watkinson. J C, Sheppard. MC, and Franklyn. JA. Gender, Clinical Findings, and
Serum. Thyrotropin measurements in the prediction of thyroid neoplasia in 1005 patients presenting with thyroid
enlargement and investigated by fine-needle aspiration cytology. Thyroid 1999. 11: 1105-1109.
Mazzaferri, EL.Management of solitary thyroid nodule (Editorial) New Engl J Med. 1993. 382: 553-559.
Mazzaferri, EL and Jhiang. Long term impact of initial surgical and medical therapy on papillary and follicular thyroid
cancer. Am J Med 1997. 97: 418-428
Mazzaferri, EL. An overview of the management of papillary and follicular thyroid cancer. Thyroid. 1999..9: 421-427
189
10. Moley, JF.,Wells, SA., Dilley WG and Tissell, LE. Re-operation for recurrent or persistent medullary thyroid cancer.
Surgery. 1993. 114: 1090-1096
11. Shah, JP, Loree, TR, Dharker, D et al. Prognostic factors in differentiated carcinoma of the thyroid gland. Am J Surg
1992.164:658-661
12. Shah, JP, Loree, TR, Dharker, D and Strong, EW. Lobectomy versus total thyroidectomy for differentiated carcinoma
of the thyroid: A matched-pair analysis. Am J Surg. 1993. 166:331-334
13. Shah, J, Loree, TR Thyroid and Parathyroids. In Head and Neck Surgery (2nd Edition). Mosby Wolfe, New York. 1996.
10:393-240
14. Shaha, AR, Loree, TR. and Shah, JP. Intermediate Risk Group and Differentiated Carcinoma of the Thyroid
Surgery.1994. 116:1036-1041
15. UICC (1997) Sobin, L.H and Willekind, C.H (eds) TNM Classification of Malignant Tumours. Fifth Edition, WileyLiss. New York
16. Walsh, R, Watkinson, J C and Franklyn, J. The management of the solitary thyroid nodule. A review. Clin Otolaryngol.
1999. 24:388-397.
190
Section 5
Chapter 11
Non Melanotic Skin Tumours
Introduction
Non-melanotic skin tumours (NMST) encompass an array of malignancies including epithelial, vascular,
adventitial, neuroendocrine, haematologic and adnexal. They account for more newly diagnosed cancer
cases annually than any other tumour group with the rate rising at between 4% and 8% a year. The vast
majority of these tumours are represented by two epithelial malignancies, namely basal cell carcinoma
(BCC) and squamous cell carcinomas (SCC)1
In the USA, the incidence of basal-cell carcinoma is 300 per 1000002 and 38.8 per 100000 for squamous
carcinoma3 . Of these, up to 90% present within the head and neck region4
The histologic morphology of BCC is divided into different patterns with the nodular BCC accounting for
the majority of lesions (75%) followed by superficial BCC (10%)5 There are many histological patterns
of SCC lesions as1
Presentation and diagnosis
Most ENT centres within the UK rely heavily on a good working relationship with their respective
dermatology departments. With this in mind, however, it should be stated that the diagnosis of skin
tumours still remains very much in the domain of the dermatologist.
The major predisposing factors for the development of BCC are UV radiation and severe sunburn during
childhood. Other factors include Fitzpatrick skin types 1-11 red hair, freckling in childhood, ionising
radiation, immunosuppression and a family history of skin cancer6 The Fittzpatric Skin Type Scale is
based on a combination of genetic disposition, reaction to such exposure and tanning habits (see
appendix). There are also some dermatological conditions that predispose individuals to BCC formation
including albinism, linear epidermal naevii and xeroderma pigmentosum. The above factors all predispose
to the development of SCC as well. In addition, the following factors also predispose to the formation of
SCC, namely osteomyelitis, HPV, arsenic exposure and chronic skin conditions (discoid lupus, chronic
ulcers, dyskeratosis)7 Diagnosis of the vast majority of these lesions is by clinical evaluation taking into
account the risk factors mentioned above. Where there is doubt, an intra-lesional biopsy may be required
to gain a diagnosis. To date there is no system available for NMST staging.
Treatment
Treatment options depend on several criteria, namely tumour type, patient profile, size and location of
tumour, recurrence, physician experience and patient preference8. The management of both SCC and
BCC can be divided into surgical and non-surgical treatments with a combination of the two approaches
needed in certain cases.
1. Surgical
This modality can be subdivided into destruction or excision of the lesion:
• Destruction
BCC
Curettage and cautery is used for small (< 4mm), well-defined BCC lesions with non-aggressive
histology in non-critical sites with a 5-year cure rate of up to 97%. This decreases dramatically to 60% for
treatment of recurrent BCC9.
191
Cryosurgery can be used for single or multiple BCC lesions and the same principles for selection apply as
shown above. Again, it is less effective for recurrent lesions11 but, on the whole, it is well tolerated on an
outpatient basis producing good cosmetic results10.
Carbon dioxide laser is not widely used but can be useful for large or multiple superficial lesions12.
SCC
Non-excisional modalities can be used in small SCC lesions less than 1cm.
•
Excision
Surgical excision is either radical excision with predetermined surgical margins or excision under total
microscopic control – Mohs micrographic surgery (MMS)13
BCC
In the excision of small, well-defined BCC lesions, 2-3mm margins will clear 85% of cases13 but in the
larger or morpheaform BCC's wider margins of 5mm enable an 82% clearance rate14.
According to Thissen et al15, the 5-year recurrence rates of BCC after MMS and surgical excision are 1%
and 5.3% respectively. The indications for MMS is for tumours with indistinct margins, in areas where
maximum tissue preservation is important (nose, lips) and in cases there is a high risk of recurrence (>
2cm, midface/ears, aggressive histology, long duration).
SCC
Treatment is similar to BCC treatment with a few differences. Metastasis to lymphatics and other organs
must be evaluated and excluded. Tumours at high risk for local or distant spread are those larger than 2cm
or deeper than 6mm, recurrences, poor differentiation, immunosuppressive host and perineural invasion.
Excision is the commonest form of treatment with a 4mm margin for low risk lesions and 6mm for high
risk ones. MMS is advised in the high-risk group.
Incomplete Margins of Excision
The treatment of incompletely excised lesions is controversial. An expectant policy is appropriate where
the residual tumour is on the lateral margin(s) only, sparing the deep margin. Added to this, nonaggressive histology, a non-critical anatomical site and a previously non-recurrent tumour are also
considered to be suitable for this approach. The study by Sarma et al16 revealed that only 7% of
incompletely excised lesions contained residual tumour upon re-excision, thus justifying a "watch and
wait" policy.
Re-treatment would be the most appropriate course of action if the lesion were present on the deep
margins, aggressive histologically, in a critical anatomical site or previously a recurrence.
Bieley et al17 in their study demonstrated residual tumour in 55% of cases where BCC was incompletely
excised.
Liu et al used radiotherapy to treat lesions with residual tumour demonstrating a 91% 5-year survival
rate18.
2. Non-Surgical
• Radiotherapy
BCC
This is a useful mode of treatment for BCC barring those that are so large that the radiation dose
approaches the maximum tissue tolerance19. A review of studies since 1947 showed a 5-year survival rate
of 91.3% for primary lesions and 90.2% for recurrences11.
192
SCC
In the treatment of SCC it may be appropriate for lesions in the elderly and/or those with
contraindications to anaesthesia or surgery. The dosage is 4000Gy given in 5-16 fractions.
There are certain cases where radiotherapy is not appropriate:
- Lesions previously treated with radiotherapy
- Young patients: increased incidence of late onset cutaneous atrophy and telangiectasia.
- Lesions close to the eye: increased incidence of epiphora and ectropion plus cataract formation20.
- Verrucous carcinoma
Some suggest that recurrent BCC previously radiated behave more aggressively but this may simply
reflect that the lesion was highly infiltrative and aggressive from the start21.
Treatments under Investigation
There are some treatment modalities that are still under investigation but are mentioned along with
references to preliminary work that has been done.
These include:
. Topical therapy with 5-fluorocytosine. This is used primarily in the treatment of the
pre-malignant condition, Bowens disease.
. Intralesional interferon22.
. Photodynamic therapy23.
. Retinoids24.
. Chemotherapy25.
Metastases
Cervical metastatic disease from these tumours is rare but is a much commoner occurrence in SCC (0.3 13.7%) than in BCC (0.0028 - 0.4%)4.
Certain high-risk lesions predisposing to metastatic spread include those > 2cm in diameter and / or >
6mm thickness, perineural/vascular invasion, local recurrence, poor tumour differentiation, invasion of
auricular cartilage and invasive lip disease plus involvement of the commissure or upper lip26.
Parotid nodal metastases arise from cutaneous malignancies more than from any other cancer and, when
present, demonstrate a poor 5-year survival rate of 27.8% if single modality treatment is used26. Cassisi et
al27 showed that the majority of parotid metastases occurred within 1 year of treatment of the primary
tumour and it was controlled in 89% of cases with a combination of surgery and radiotherapy to the
parotid region plus neck27.
Follow-up
Metastases to the neck in facial SCC are relatively low as shown previously in this paper. Tavin et al28
and Netterville et al29 showed that primary cutaneous tumours in the preauricular region and cheek tended
to metastasise most frequently of all the facial SCC.
The average time to development of the delayed metastases was 19 months28 and 11 months29. It would
thus seem reasonable to follow these cases for 3 years post treatment.
The follow-up regime for BCC is different to that for SCC, as recurrences are not as common. The
majority of single, nodular or superficial lesions are followed up once post treatment to ensure that the
site of excision has healed with a cosmetically acceptable result.
193
However, patients considered high risk (as previously discussed) plus patients presenting with multiple
BCC are followed routinely for 5 years as studies show that over 80% of recurrences will present within 5
years of treatment30.
References:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
Skidmore RA; Flowers FP. Non-melanoma skin cancer. Med Clin of North Am. 1998.82:1309-1323.
Lear JT; Smith AG Basal cell carcinoma. Postgraduate Med J. 1997. 73:538 - 42.
Brodland DG; Zitelli JA. Surgical margins for excision of primary cutaneous cell carcinoma. J Am Acad Dermatol. 1992.27:
241-8.
Brown RO; Osguthorpe JD. Management of the neck in nonmelanotic cutaneous carcinomas. Otolaryn Clin of North Am.
1998. 31(5): 841-57.
Harrist TJ. Basal cell carcinoma and squamous cell carcinoma: Histologic diagnosis and clinical correlation. In 'Basal Cell
and Squamous Cell Carcinomas of the Head and Neck. Baltimore, Williams & Wilkins: 1996. 9-24
Leffell DJ, Fitzgerald DA Basal cell carcinoma. In: Freedberg IM et al. Fitzpatrick's Dermatology in General Medicine, 5th
edition. McGraw-Hill, 1999:857-864.
Bernstein SC; Lim KK; Brodland DG. Heidelberg KA. The many faces of squamous cell carcinoma. Dermatol Surg. 1996.
22: 243-54.
Bagheri MM, Safai B. Cutaneous Malignancies of Keratinocytic Origin. Clin in Dermatol. 2001. 19: 244-252.
Silverman MK; Kopf AW; GrinCM; Bart RS; Levenstein MJ. Recurrence rates of treated basal cell carcinomas. J Dermatol
Surg Oncol. 1991.17:720-26.
Holt PJ. Cryotherapy for skin cancer: results over a 5-year period using liquid nitrogen spray cryosurgery. Br J Dermatol.
1988.119: 231-40.
Rowe DE; Carroll RJ; Day CL. Long term recurrence rates in previously untreated basal cell carcinoma: implications for
patient follow-up. J Dermatol Surg Oncol. 1989. 15:315-28.
Wheland RG; Bailin PG; Roenigk RK; Ratz JL. CO2 laser vapourisation and curettage in the treatment of large or multiple
superficial basal cell carcinomas. J Dermatol Surg Oncol. 1987. 13: 119-25.
Telfer NR Mohs micrographic surgery for cutaneous squamous cell carcinoma: practical considerations. (Editorial) Br J
Dermatol 2000. 142:631-5.
Breuninger H; Dietz K. Prediction of subclinical tumour infiltration in basal cell carcinoma. J Dermatol Surg Oncol. 1991.
17: 574-8.
Thissen MR, Neumann MH, Schouten LJ A systematic review of treatment modalities for primary BCC. Arch
Dermatol.1999. 135: 177-83.
Sarma DP; Griffing CC; Weilbaecher TG. Observations on the inadequately excised basal cell carcinoma. J Surg Oncol.
1984. 25: 79-80.
Bieley HC; Kirsner RS; Reyes BA; Garland LD. The use of Mohs Micrographic surgery for the determination of residual
tumour in incompletely excised basal cell carcinoma. J Am Acad Dermatol. 1992. 26: 754-56.
Liu FF; Maki R; Warde P; Payne D; Fitzpatrick P. A management approach to incompletely excised basal cell carcinomas
of the skin. Int J Radiat Oncol Biol Phys. 1991. 20: 423-8.
Cooper JS. Radiotherapy in the treatment of skin cancers. In Cancer of the skin. Philadelphia: WB Saunders. 1991. 553-568.
Orton CI.The treatment of basal cell carcinoma by radiotherapy. Clin Oncol.1978. 4: 317-22.
Smith SP; Grande DJ.Basal cell carcinoma recurring after radiotherapy: a unique difficult treatment subclass of recurrent
basal cell carcinoma. J Dermatol Surg Oncol. 1991. 17: 26-30.
Cornell RC; Greenway HT; Tucker SB. Intralesional interferon therapy for basal cell carcinoma. J Am Acad Dermatol.1990.
23: 694-700.
Wilson BD; Mang TS; Stoll H. 1992) Photodynamic therapy for the treatment of basal cell carcinoma. Arch Dermatol. 128:
1597-601.
Hodak E; Ginzburg A; David M. Etretinate treatment of nevoid basal cell carcinoma syndrome. Theraputic and
chemopreventive effect. Int J Dermatol. 1987. 26: 606-9.
Guthrie TH; Porubsky ES; Luxenberg MN. Cisplatin-based chemotherapy is advanced basal cell and squamous cell
carcinomas of the skin: results in 28 patients including 13 patients receiving multi-modality therapy. J Clin Oncol. 1990. 8:
342-6.
Rowe DE; Carroll RJ; Clay CL. Prognostic factors for local recurrence, metastasis and survival ratesin squamous carcinoma
of the skin, ear and lip. J Am Acad Dermatol. 1992. 26: 976-990.
Cassisi NJ; Million RR. Management of head and neck cancer: A multidisciplinary approach. Ed 2. Philadelphia, JB
Lippincott. 1994.
Tavin E; Persky M. Metastatic cutaneous squamous cell carcinoma of the head and neck region. Laryngoscope. 1996. 106:
156-58.
Netterville JL; Sinard RJ; Bryant GL; Burkey BB. Delayed regional metastases from midfacial squamous carcinomas. Head
Neck. 1998. 20: 328-33.
Hauben DJ; Zirkin H; Mahler D; Sacks M. The biologic behaviour of basal cell carcinoma: analysis of recurrence in excised
basal cell carcinoma: Part 2. Plast Reconstr Surg. 1982. 69: 110-16.
194
Fitzpatrick Skin Type Quiz
This information will help our office to better evaluate your skin type so the laser treatment will be more
effective. Skin type is often categorised according to the Fitzpatrick skin type scale which ranges from
very fair (skin type I) to very dark (skin type VI). The two main factors that influence skin type and the
treatment program devised by your practitioner are:
•
•
Genetic disposition
Reaction to sun exposure and tanning habits
Skin type is determined genetically and is one of the many aspects of your overall appearance, which also
includes the colour of your eyes, hair, etc. The way your skin responds to sun exposure is another way of
correctly assessing your skin type. Recent tanning, whether by the sun or an artificial tanning booth, even
tanning creams, can have a major impact on your skin colour evaluation. By using the information you
provide on this form, we can be better prepared to provide you with the best care. Please take a few
minutes to fill out this questionnaire.
Mark 0 through 4 for each question.
Genetic Disposition
Score
0
1
2
3
4
Your eye colour?
Light blue,
Grey, green
Sandy, red
Blue, grey or
green
Blond
Blue
Dark brown
Brownish black
Dark brown
Brownish black
Reddish
Very pale
Light brown
Dark brown
Many
Several
Chestnut, dark
blond
Pale with beige
tint
Few
Incidental
None
Natural colour of
your hair?
Colour of your skin
non-exposed?
Do you have
freckles
on
unexposed areas?
Total score for genetic disposition: _____
195
Reaction to Sun Exposure
Score
0
1
2
3
4
What happens
when you stay
too long in the
sun?
To what degree
do you turn
brown?
Do you turn
brown within
several hours
after
sun
exposure?
How does your
face react to the
sun?
Painful redness,
blistering,
peeling
Blistering,
followed
peeling
Rarely burns
Never burns
Hardly or not at
all
Light colour tan
Burns
sometimes,
followed by
peeling
Reasonable tan
Tan very easily
Turn
dark
brown quickly
Never
Seldom
Sometimes
Often
Always
Very sensitive
Sensitive
Normal
Very resistant
Never had
problem
by
a
Total score for reaction to sun exposure: _____
Tanning Habits
Score
0
1
2
3
4
When did you
last expose your
body to sun or
tanning
booth/cream?
Did you expose
the area to be
treated to the
sun?
More than 3
months ago
2-3 months ago
1-2 months ago
Less than one
month ago
Less than
weeks ago
Never
Hardly ever
Sometimes
Often
Always
2
Total score for tanning habits: _____
Summary
Add up the total scores for each section for your Skin Type Score to give you a better evaluation of your
skin type.
_____ Total score for Genetic Disposition
_____ Total score for Reaction to Sun Exposure
_____ Total score for Tanning Habits
_____ SKIN TYPE SCORE
196
Your Fitzpatrick Skin Type:
Skin Type Score
0-7
8-16
17-25
25-30
Over 30
Fitzpatrick Skin Type
I
II
III
IV
V-VI
Name: __________________________________________________Date: _____________________
Which of the following best describes your skin type?
Please circle one:
1- always burn, never tan
2- always burn, sometimes tan
3- sometimes burn, tan somewhat
3- rarely burn, tan with ease
4- moderately pigmented, tans very easily
5- deeply pigmented, never burn
Ethnic background is of importance when considering skin colour and laser hair removal. If known what
is your ethnic background:
197