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Australian College of Rural & Remote Medicine
Rural Clinical Guidelines
DERMATOLOGY
TIPS & TECHNIQUES
Australian College of Rural and Remote Medicine
Rural Clinical Guidelines
ACRRM – July 2012
Note: As these guidelines have been specifically designed to be used on a mobile/smartphone device
or as an online activity on https://www.rrmeo.com you will find that there are numerous hyperlinks that
you will not be able to access in this .pdf document.
To further enhance the usability of the guidelines this .pdf version now has hyperlinks ‘from and back
to’ the ‘Table of Contents’ and is suitable to download onto your computer or any of the smaller iPad,
Tablet, Notebook etc. using your e-reader.
As each discipline is a separate file it is suggested that you also download the ‘Alphabetical List’ of
the guidelines to enable easy cross reference to guidelines in other disciplines.
For a list of all the abbreviations used in these guidelines download the ‘Abbreviations List’.
Table of Contents
End-user licence agreement for ACRRM Mobile Device Clinical Guidelines ............................................................................ 3
List of amendments in this update ............................................................................................................................................. 4
RRMEO Modules ...................................................................................................................................................................... 5
ACKNOWLEDGEMENTS ......................................................................................................................................................... 9
ACNE TYPICAL TREATMENT REGIMES .............................................................................................................................. 10
BIOPSY OF A DIFFICULT SITE ............................................................................................................................................. 25
CONCHAL BOWL BIOPSY ..................................................................................................................................................... 27
CRYOTHERAPY ..................................................................................................................................................................... 30
CURETTAGE .......................................................................................................................................................................... 45
DRUG ERUPTIONS ................................................................................................................................................................ 52
EFUDIX - A USERS GUIDE .................................................................................................................................................... 56
ITCH IN THE ELDERLY .......................................................................................................................................................... 69
MARINI SUTURE .................................................................................................................................................................... 74
PULLEY SUTURE ................................................................................................................................................................... 78
PUNCH BIOPSY ..................................................................................................................................................................... 82
REMOVE AN EAR CYST IN UNDER 6 mins .......................................................................................................................... 86
SECOND INTENTION HEALING ............................................................................................................................................ 88
SHAVE BIOPSY ...................................................................................................................................................................... 93
SKIN BIOPSY .......................................................................................................................................................................... 99
SKIN CHECK ........................................................................................................................................................................ 101
SKIN TAGS ........................................................................................................................................................................... 105
SOLAR KERATOSIS ............................................................................................................................................................. 108
STEROIDS ............................................................................................................................................................................ 117
THE BAND-AID SIGN ........................................................................................................................................................... 122
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
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End-user licence agreement for ACRRM Mobile Device Clinical Guidelines
1. Introduction
(i) The terms and conditions stated here are in addition to the terms and conditions of the End-User
Licence Agreement for licensees of ACRRM software (Software Licence Agreement) which also apply
to your use of these Mobile Device Rural Clinical Guidelines (Guidelines).
2. Acknowledgement
(i) The Guidelines were developed by the Australian College of Rural and Remote Medicine (ACRRM).
3. Intellectual property rights
(i) The Software Licence Agreement is a legal agreement between the customer and ACRRM which
sets out the terms and conditions of this legal agreement. By clicking on 'Accept' and downloading the
Guidelines you have agreed to be bound by the terms and conditions of the Software Licence
Agreement.
4. Permitted users
(i) The Guidelines are for use only by health professionals who are currently enrolled in the ACRRM
Clinical Guidelines for PDA User Group on ACRRM's www.rrmeo.com website (Permitted Users). The
Guidelines may not be transmitted to or distributed to or used by other persons.
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(i) A Permitted User may download, store in a cache, display, print and copy the material in unaltered
form only. The Guidelines may not be transmitted, distributed or used by any other person, or
commercialised without the prior written permission of ACRRM.
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(i) The Guidelines may be updated from time to time. We may advise you by email from time to time if
new versions of the Guidelines become available however you are responsible for checking whether
you have the most recent version. The most recent version of the Guidelines is available on the
ACRRM Clinical Guidelines for PDA User Group webpage on www.rrmeo.com. We disclaim all liability
arising from your failure to download updates of the Guidelines.
7. Seek independent advice
(i) The Guidelines are intended to aid Permitted Users in the management of their patients but do not
provide explanations as to the conditions or treatments outlined. There may be clinical or other
reasons for using different therapy. In all cases, users should understand the individual situation and
exercise independent professional judgment when assessing therapy based on these Guidelines.
Users should seek independent advice.
(ii) The Guidelines do not include comprehensive drug information. Drug usage and doses should
always be checked prior to administering drugs to patients.
(iii) Every effort has been made to ensure the validity and accuracy of the information in this
adaptation of the Guidelines however Permitted Users should at all times exercise good clinical
judgment and seek professional advice where necessary. Treatment must be altered if not clinically
appropriate.
(iv) This adaptation of the Guidelines is presented as an information source only and provided solely
on the basis that users will be responsible for making their own assessment of the matters presented
herein. Users are advised to formally verify all relevant representations, statements and information
from appropriate advisers as it does not constitute professional advice and should not be relied upon
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(v) To the extent permitted by law, ACRRM expressly disclaims any responsibility and all warranties,
express or implied, and excludes liability for all loss (including consequential loss) whatsoever that
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Process: For detailed referencing of the guideline sources, please see the acknowledgements page in
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ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 3 of 123
DERMATOLOGY TIPS and TECHNIQUES
List of amendments in this update
No amendments in this update
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ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 4 of 123
DERMATOLOGY TIPS and TECHNIQUES
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RRMEO Modules
Note: This section of the 'ACRRM Clinical Guidelines' is for the sole purpose of assisting users to locate other
educational resources relevant to the ACRRM Curricula statements and to use them as a reference tool only.
You are again reminded that your knowledge acquisition must still be via the directives set out in each of the
ACRRM curricula statements.
This list of modules can be accessed via RRMEO
- to enrol go to RRMEO: https://www.rrmeo.com - Educational Inventory/RRMEO Modules
Note: Abbreviations used:
ATSI = Aboriginal and Torres Strait Islander Health
AIM = Adult Internal Medicine
Anaes = Anaesthesia (JCCA, advanced rural skills)
EM = Emergency Medicine
GEM = Generalist Emergency Medicine (GEM) (Post-Fellowship program)
MH = Mental Health
Obs = Obstetrics and Gynaecology (DRANZCOG Advanced)
Paeds = Paediatrics
Pop = Population Health
RM = Remote Medicine
Surg = Rural Generalist Surgery
Module Name
Suggested Curricula relevance
An Introduction to Digital Photography and Videography
ATSI
AIM
Anaes
EM
GEM
MH
Obs
Paeds
Pop
RM
Surg
Antenatal Care
ATSI
MH
Obs
RM
Best Care Guide to Stroke Management in General Practice:
Module 1
- Transient Ischaemic Attack (TIA) and Early Assessment
Module 2
- Antiplatelet Therapy for Secondary Stroke Prevention
Module 3
- Preventing Fatal and Disabling Stroke in Patients with Atrial Fibrillation
ATSI
AIM
EM
GEM
MH
RM
Breast Cancer
- How not to miss a breast cancer / the triple test in practice
Breast cancer diagnosis
- What now?
Breast cancer treatment
- Managing the impact
Breast cancer treatment is over
- What's next?
ATSI
AIM
EM
GEM
MH
Obs
RM
Surg
Education Program in Cancer Care
(EPICC)
Module 1A
- General Principles of Cancer Care
Module 1B
- Types of Cancer Treatment
ATSI
AIM
Anaes
EM
GEM
MH
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Module 1C
- Cancer Diagnosis
Module 1D
- Multidisciplinary Care Teams
Module 2
- Side Effects of Treatment and Symptom Management
Module 3
- Oncological Emergencies
Module 4
- Psychosocial Care
Module 5
- Follow Up
Obs
Paeds
RM
Surg
General Practitioners Guide to Parkinson's Disease
ATSI
AIM
EM
GEM
MH
Obs
Paeds
RM
Introduction to
Cultural Awareness
ATSI
Pop
RM
Introduction to
Dental Emergencies
ATSI
Anaes
EM
GEM
Paeds
RM
Surg
Introduction to
Population Health
ATSI
EM
GEM
MH
Obs
Paeds
Pop
RM
Mx of Autism Spectrum Disorders in Childhood and Adolescence
Module 1
- Clinical Aspects and Diagnosis
Module 2
- Treatment and Ongoing Management
Module 3
- Special Challenges
ATSI
Paeds
RM
Mx of
Secondary Lymphoedema
ATSI
AIM
Paeds
RM
Surg
Non-Directive Pregnancy Support Counselling Training
ATSI
Obs
RM
Opioid Medication in Palliative Care
ATSI
AIM
Anaes
EM
GEM
MH
Paeds
RM
Surg
Palliative Care
- Choose Your Own Adventure
ATSI
AIM
MH
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Paeds
RM
Palliative Care in
Aged Care Homes
- Palliative Care Australia
ATSI
AIM
MH
RM
Radiology Online
ATSI
AIM
Anaes
EM
GEM
Obs
Paeds
RM
Surg
RANZCP - IMG Orientation
Module 01
- Components of Australian health care
Module 02
- Subspecialties of psychiatry
Module 03
- Professional expectations, your responsibilities & rights
Module 04
- Patient & community expectations
Module 05
- Mental health care in a multicultural community
Module 06
- Aboriginal & Torres Strait Islander mental health care
Module 07
- Gender & sexuality
Module 08
- Mental health in rural & remote Australia
Module 09
- Funding & payments
Module 10
- Mental health legislation & regulation
Module 11
- Psychiatric treatment in Australia
Module 12
- Current issues in mental health policy & Australian psychiatry
ATSI
AIM
EM
GEM
MH
Paeds
Pop
RM
Renal Failure
ATSI
AIM
Anaes
EM
GEM
Paeds
RM
Surg
Retrieval Medicine
- Advanced
- Basic
ATSI
AIM
Anaes
EM
GEM
MH
Obs
Paeds
Pop
RM
Surg
RVTS
Mental Health Disorders Package
for
Rural Practice Core
ATSI
AIM
EM
GEM
MH
Paeds
Pop
RM
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Sexual Health
- taking a sexual history and managing STI's
ATSI
AIM
EM
GEM
MH
Obs
RM
Tele-Derm National
ATSI
Anaes
EM
GEM
Obs
Paeds
Pop
RM
Surg
Tele-Tox
ATSI
AIM
Anaes
EM
GEM
Obs
Paeds
Pop
RM
Surg
The Beginnings of
Practice Management
RM
Women's Health
- Contraceptive Options in the Bush
ATSI
Obs
RM
(Back to Top)
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ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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Page 8 of 123
DERMATOLOGY TIPS and TECHNIQUES
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ACKNOWLEDGEMENTS
These dermatology ' Tips and Techniques' are re-formatted copies from 'Jim's Tips' in 'Other Resources' on the
RRMEO Tele-Derm National module. To find this module log on to: https://www.rrmeo.com (using your user
name and password) and from the 'Educational Inventory' select 'RRMEO Modules' then scroll down to 'TeleDerm National' and enrol.
Our thanks to Dr Jim Muir who is the resident Dermatologist on the RRMEO Tele-Derm National site and
provides free advice on diagnosis and management of cases submitted to the forums. Dr Muir is a graduate of the
University of Queensland and received his fellowship of the Australasian College of Dermatologists in 1994. He is
the visiting dermatologist to the Mater hospital, South Brisbane as well as running a private practice. His special
interest areas include; acne, cutaneous malignancy, skin and systemic disease, psychiatric disease and the skin,
medical education and medico-legal issues. He is chairman of the Brisbane Hospitals Dermatology Group.
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ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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ACNE TYPICAL TREATMENT REGIMES
Treatment of Acne
Special Problems
Acne in Pregnancy and Lactation
Typical Treatment Regimes
'Acne Dilemma' Case Studies
"YOUR ACNE TREAMENT SUCKS"
It is a quiet Tuesday afternoon and a teenage acne patient returns for review
- you had prescribed treatment at your previous meeting
- when asked how he is going, the reply is "your acne treatment sucks!"
An all too real scenario
- what are you to do?
- the first question to answer is whether or not your treatment really does suck
- has the patient improved but is still unhappy anyway or are they indeed no better or even worse?
- hopefully your original notes give a good idea of the acne severity at your last meeting
- this can be via a written description of the amount of inflammation, pustulation, presence of cysts and scarring
etc
- a simple sketch showing the extent and severity of involvement is a useful aide memoir
- for the more technologically minded a digital photo is extremely useful in this situation
- it is quite common for patients, especially adolescents, not to remember how badly they were affected
Your examination will reveal one of two situations
- they may have had obvious improvement but are still unhappy or their skin is indeed no better!
- depending on the situation your job is to look for underlying reasons
There are many reasons why a patient may be unhappy despite an obvious improvement in their skin
Unrealistic expectations
Unhappy with the treatment
Big Event Anxiety
Career Problems
Psychiatric illnesses
(i) They may have unrealistic expectations of what can be achieved
- unless specifically told, many patients mistake treatment for an attempt to cure
- if there is any ongoing acne at all they will be unhappy
- some may have expected any scarring to disappear with your treatment!
- before initiating treatment it is vital to outline what you are trying to achieve
- you will be suppressing their acne not curing it
- hopefully they will go into remission but most likely they will need some form of ongoing acne treatment for some
time
- the vast majority of people 'grow out' of acne in their early twenties
- unfortunately 3% of men and 5% of women aged 40 to 49 still suffer with acne
- scarring is permanent and will not disappear with treatment of active acne
- it is best to point these facts out to the patient before embarking on therapy
(ii) They may be unhappy with the treatment prescribed
- male patients are said to prefer systemic treatment in general
- the drying effects of topical therapy may be upsetting them
- the time required to treat their skin may be resented
(iii) "Big Event Anxiety" is a common problem
- perfect skin is essential for a variety of situations
- the common ones Dr Muir encounters are the females who have a school formal, duty as a bride’s maid or,
worst of all, their own wedding on the horizon
- they will often be unhappy with anything less than perfect skin
(iv) "Career Problems"
- Dr Muir has had a number of patients wanting to pursue modeling jobs who were intolerant of even the smallest
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acne blemish
- an even more common problem is the patient about to undergo the medical for joining the army
(acne can preclude entry into the military)
(v) A variety of psychiatric illnesses can manifest in this way
- depression, anxiety and obsessive compulsive disorders need to be considered
- dysmorphophobia is also worth thinking of
If they are indeed no better, a reason needs to be found
- unfortunately there are many possibilities
Time
Patient characteristics
Compliance
Interference with treatment
Exacerbants
Bacterial problems
Hormonal Problems
Mis-diagnosis
HIV
1. Time is probably the commonest reason
Acne treatment in general takes two to three months to work
- i tell my patients 'your treatment will not work by this time next tuesday
- it will take at least three months before we know whether it will work or not
- do not call me and tell me i am an idiot before then"
- a wrinkle to this is the patient who does not fill the prescription for some weeks after the appointment
- at review they may have been on the treatment for a short while only despite not having been seen for three
months
2. Patient characteristics influence response
- adolescent males with truncal acne are the most resistant to treatment
3. Compliance is a huge problem in treating acne
- as we will see acne treatment requires a considerable amount of time and effort on behalf of the patient
- non-compliance may be deliberate or inadvertent
Reasons include;
a) Side effects
(e.g. nausea from antibiotics, drying and irritation from topical's, photosensitivity from retinoids or doxycycline,
antibiotic induced thrush etc.)
b) Time constraints
- applying two different topicals and taking an oral antibiotic does take a certain amount of time which some
patients just don't seem to be able to find
c) Expense needs to be considered
- the topical retinoids and antibiotics we use are not subsidised by the PBS and thus may be unaffordable to some
- this is especially so if attempting to treat large areas such as the trunk
d) Embarrassment or stigmatisation
- teasing by siblings or school mates in the boarding school situation can prevent patients using their treatment
e) Laziness is a definite issue
- some are not prepared to put in any effort to treating their skin and thus get no benefit from the prescribed
treatment
- Dr Muir tells them "this treatment will not work if it stays on the bathroom shelf!"
f) Poor advice
- topicals need to be applied to all affected areas of skin not just the inflamed lesions
- unless told most patients will understandably only treat the pimples
g) Under dosing
- despite written instructions it is common for patients to take half the required dose of antibiotic or apply a topical
once rather then twice daily
h) Lack of supplies
- when treating a chronic skin disease the patient needs a prescription that will ensure therapy can be treated as
long as desired
- an authority prescription (1800 888 333) will be needed for the antibiotics and repeats on the topicals
- a common problem, even so, is the patient will fail to get the repeat filled unless specifically told to!
i) When did they start treatment?
- some do not get the prescription filled for some time after the initial consultation
- at review they may have only been on the treatment for a few weeks
j) Did they initially improve and then stop treatment and then deteriorate?
- this is a not uncommon event in my experience
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- remember unless told they will assume your treatment is designed as a permanent cure and logically will stop
when clear
k) Other reasons never cease to amaze Dr Muir
- he has had people claim they are unable to swallow tablets, even when crushed!
4. Interference with treatment
- food, milk, antacids, iron, zinc, bismuth, cimetidine and sodium bicarbonate all reduce tetracycline absorption
5. Exacerbants
- are they in some way causing their acne to worsen or persist?
a) Oily topicals such as some emollients or sun blocks
b) Environmental factors such as exposure to heat for chefs / dishwashers or oil and grease for mechanics
c) Tropical acne so called where people flare in a hot and humid climate
d) Leisure activities which cause excess perspiration
e) Acne mechanica where comedones are seen under occlusive head gear, straps and even musical instruments
such as violins
f) Acne detergicans is a complication of excessive face washing
- remember the myth persists that acne is due to dirt
g) Hair oil and pomades can result in forehead acne
h) Prescribed medications can exacerbate acne
examples include:
- androgens
- anabolic steroids
- androgenic progesterones
- prednisone
- inhaled and topical steroids
- dilantin
- lithium
- cyclosporin
- PUVA
- isoniazid
- rifampicin
- halogens
- quinine
- thiouracil
- thiourea
- chloral hydrate
- disulfiram
(to name a few!)
i) Non-prescribed medications i.e. illicit anabolic steroids
- beware the angry patient, as many of these people are
j) Patient activity
- i.e. acne excoriee where patients with relatively mild acne usually have a lot of skin changes secondary to
picking and squeezing
k) Dermatitis artefacta is rare in this situation
- these patients deliberately damage their skin to produce an illness
- this may be done consciously or unconsciously and the motivation may not be readily apparent
l) Underlying conditions associated with acne such as epilepsy or schizophrenia
6. Bacterial problems
a) Antibiotic resistant bacteria
this is an increasingly common problem but does not mean treatment failure in all cases by any means
b) Gram negative bacterial super infection
c) Coagulase negative staphylococcal folliculitis
7. Hormonal Problems
a) Exogenous hormones with androgenic effects
b) Anabolic steroids
c) Endogenous androgen excess e.g. HAIR-AN (hyperandrogenism, insulin resistance, acanthosis nigricans)
syndrome, polycystic ovary disease, Cushing's syndrome and Aperts
- many patients seem to have end organ hyper-responsiveness to androgen rather then androgen excess
8. Mis-Diagnosis is not as uncommon as one would think especially with truncal involvement
A number of conditions can mimic acne
These include; Darier's disease, bacterial or pityrosporum folliculitis, steroid acne (which is a form of folliculitis as
opposed to steroid induced exacerbation of acne, see case 159), steatocystoma multiplex suppurativa,
hidradenitis suppurativa, rosacea, halogen acne, solar comedones (see case 138), furunculosis, dental sinus,
milia, familial comedones (autosomal dominant disorder with polyporus comedones and sebaceous cysts),
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demodex folliculitis, facial plane warts, a rare form of dermatitis herpetiformis causing facial pustules and acne
necrotica
9. HIV
Acne is a manifestation of early stage disease i.e. severe acne is seen in HIV infected persons with high CD4
counts and a low viral load
as the disease progresses acne becomes less common and less severe
there are reports in the literature of facial demodicidosis i.e. demodex mite infestation mimicking acne and
clearing with 5% permethrin cream
<top>
TREATMENT of ACNE
Topical Therapy
Systemic Therapy
Oral Antibiotic Therapy
Anti-Androgen Therapy
Physical Therapy
Diet
As with any disease acne treatment needs to be directed at the causal factors
- currently there are felt to be four major pathological features causing acne;
(i) Hyperkeratotic follicular occlusion resulting in comedone formation
(ii) Excess sebum production
(iii) Bacterial overgrowth, predominantly of propionibacterium acnes
(iv) Inflammation as a result of the above
Treatment will not be successful unless it addresses all or most of these factors
- the commonest mistake made with acne treatment is to only target one of these factors at a time
- best results are seen if all four pathogenic factors are attacked simultaneously
- the treatment you prescribe will depend on many factors
- best results will be seen if as many pathogenic features as possible are addressed for sufficient duration
- improvement is unlikely in less than two months with any treatment
1. TOPICAL THERAPY
Topical Retinoids
Benzoyl Peroxide
Topical Erythromycin
Topical Clindamycin
Azelaic Acid
Topical Keratolytics
Tea Tree Oil
Sulphur
Steroids
(i) Topical Retinoids
These are the mainstay of acne treatment as they are anti-comedonal
- any acne regime which does not target follicular occlusion is unlikely to be successful
- in Australia we have available tretinoin (0.025, 0.05 and 0.1%), isotretinoin (0.05%) and adapalene (0.1%)
- all are effective and the studies dispute the relative merits of one over the others
- adapalene tends to be the least irritating of the three
- some feel that 0.05% tretinoin is more effective then 0.1% adapalene
- they need to be applied to all the affected skin not just visible lesions as they act to prevent comedone formation
- effects may not be seen for some time and Dr Muir encourages patients to persevere for at least 8-12 weeks
All can irritate with the patients likely to complain of redness and drying of the skin
- photosensitivity is also a potential hazard although probably less likely with adapalene
- to minimise side effects apply the chosen preparation to the skin in the evening and wash off the next morning
- use a non-greasy emollient for any dryness (e.g. cetaphil)
It is important to realise that the base used to deliver an agent to the skin can be a major source of any irritant
effect
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- thus merely changing the base may result in greater tolerance
- for instance the cream preparation of adapalene may be better tolerated then the gel
All topical retinoids are listed as Category D drugs
(i.e. drugs that have caused, are suspected to have caused or may be expected to cause, an increased incidence
of human foetal malformation when used during gestation)
- there are studies showing that topical application of retinoids do not effect plasma retinoid levels
- similarly two large studies showed no increase in birth defects in women exposed to topical retinoids during the
first trimester
- retinoids are not advised during pregnancy but if there is exposure there is probably no increased risk
(ii) Benzoyl Peroxide
A useful treatment which, till recently, was under utilised
- it causes a dramatic reduction in the number of bacteria (p. acnes and staph. epidermidis) in the skin
- some feel it has comedolytic and anti-inflammatory effects also
- use results in decreased numbers of inflammatory and non-inflammatory lesions
- it is often used concomitantly with antibiotics (topical and oral) as it delivers a greater drop in bacterial numbers,
better clinical results and decreases the emergence of bacterial resistance
- in fact there are commercial preparations available overseas containing 1% clindamycin or 3% erythromycin with
5% benzoyl peroxide
Available in concentrations ranging from 2.5-10% and as a gel, cream, lotion or wash
- concentrations above 5% are probably no more efficacious and are certainly more irritating
- mostly used twice daily
- the wash preparation (Benzac AC wash) is useful for treating large areas on the trunk
Side effects include irritant and allergic contact dermatitis as well as bleaching of clothes and hair
- interestingly it can also cause photosensitivity
- it is said that irritation is reduced by combining with a topical antibiotic
(iii) Topical Erythromycin
A widely used and useful treatment with both antibiotic and anti-inflammatory effects
- available in Australia as a 2% gel and applied twice daily
- it promotes emergence of resistant strains of p.acnes and staphylococcal organisms
- this is reduced by combining with topical benzoyl peroxide
- addition of 1.2% zinc acetate to the solution can increase efficacy
(iv) Topical Clindamycin
Similar efficacy and mechanism of action to topical erythromycin
- there are studies showing superior efficacy to oral antibiotics
- bacterial resistance is a problem and if resistant to erythromycin the organisms are usually resistant to
clindamycin and vice versa
- if suspect resistance to one there is no point substituting the other
- irritant effects are common with clindamycin but allergy is rare
- gram negative folliculitis reported
- when the hydrochloride form was used, which is better absorbed than the currently used phosphate, there were
even rare cases of pseudomembranous colitis
(v) Azelaic Acid
Used as a 20% cream (Skinoren and Acnederm) twice daily
- it is felt to be anti-inflammatory, bacteriostatic to p.acnes and comedolytic
- there are studies showing equal efficacy with 0.05% tretinoin
- efficacy is enhanced by combining with benzoyl peroxide, tretinoin or topical antibiotics
- there is no development of bacterial resistance
In practice Dr Muir has not found it to be as useful as studies suggest
- it is a very safe drug and has recently been approved for use in rosacea as well
(vi) Topical Keratolytics
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Used to unblock pores, these agents can be useful when trying to treat large areas where topical retinoids would
be impractical
- salicylic acid is the most widely used
- most dermatologists have their own preferred 'brew'
- for the trunk Dr Muir uses 5% salicylic acid, 10% propylene glycol in 50-60% ethanol b.d.
(200 mls and rpt's x 2 )
- this is of course flammable so no smoking and the higher the amount of ethanol the more likely there is to be
irritation
There are various commercial preparations containing 2-5% salicylic acid for use on the face
- it is important to have a light base such as aqueous cream or cetaphil lotion to avoid exacerbating the acne
(vii) Tea Tree Oil
In Dr Muir's opinion a treatment looking for a disease!
- it is however popular with the lay public
- a 1990 study in the Medical Journal of Australia showed equal efficacy of a 5% tea tree oil gel to benzoyl
peroxide with fewer side effects
- a recent review stated that there was no compelling evidence to show that tea tree oil was efficacious in any
dermatological condition
- this paper emanated from the Dept. of Complementary Medicine at the University of Exeter
- it is quite a good allergen with lots of reports of contact dermatitis and even one case of anaphylaxis with topical
use!
(viii) Sulphur
A time honoured treatment but does it work and if so how?
- felt to be primarily comedolytic either by an irritant effect or by producing hydrogen sulfide
- there are studies showing it to be comedogenic!
(it is rather smelly)
- there are a variety of extemporaneous solutions prescribed with concentrations from 2-10% combined with
resorcinol, zinc sulphate, thymol and others
- bases used include alcohol, calamine and aqueous cream
- it is an ingredient in 'Clearasil' and 'Neomedrol'
Dr Muir does not use it at all but many dermatologists prescribe it routinely
(ix) Steroids
Topical steroids have no role in the routine management of acne
- occasionally topical application of a potent steroid to a severely inflamed 'cyst' might be contemplated
Intralesional steroid is a very useful measure for acute treatment of inflamed 'cysts'
- most use triamcinolone acetonide 2.5-10mg/ml with a 1 ml syringe and 30 gauge needle
- there is a study showing 0.63mg/ml to be just as useful as 2.5mg/ml
- Dr Muir tends to use 2.5 mg/ml as it is effective and reduces the risk of side effects
- ideally place the steroid in the middle of the lesion causing slight distension
- usually only need 0.1 of a ml of solution
- Dr Muir does not do this unless the patient is on oral antibiotics
- Dr Muir does not have any data to support this but it would seem a sensible precaution
- complications include atrophy both locally and along the draining lymphatics
<top>
2. SYSTEMIC THERAPY
Systemic agents used include;
(i) Antibiotics;
- Tetracycline, doxycycline, minocycline, erythromycin, erythromycin ethylsuccinate, cotrimoxazole and
trimethoprim
(ii) Anti-androgen therapy;
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- spironolactone, cyproterone acetate, drospirenone, oestrogen and steroids used as an adrenosuppressant
(iii) Isotretinoin
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3. ORAL ANTIBIOTIC THERAPY
The antibiotics used in acne work by reducing bacterial numbers in the skin and via an anti-inflammatory
mechanism aimed primarily at neutrophils
- the main errors made in treating acne with oral antibiotics is to prescribe too low a dose for too short a period of
time and not combining with topical therapy aimed at comedones
- a minimum course of at least two months is needed before one can say the drug is not working
- the patient will need an authority prescription for adequate supplies (1800 888 333)
Of the commonly prescribed antibiotics in acne there is little evidence that any have major therapeutic advantages
over the rest
- a recent Cochrane review specifically makes the point that minocycline is no better then other tetracycline group
antibiotics
Doxycycline
Tetracycline
Minocycline
Erythromycin
Erythromycin Ethyl Succinate
Cotrimoxazole
Trimethoprim
(i) Doxycycline
Popular, usually well tolerated although can cause phototoxicity
- dosage is usually 100mg/day and can be taken with meals
(ii) Tetracycline
Usually 500mg b.d.,
- Dr Muir tends to use the 250 mg tablets as the patient can reduce the dose to 750mg/day if getting nausea
- has to be given on an empty stomach
- this agent is said to be the most likely to cause nausea, vomiting, diarrhoea and vulvovaginal candidiasis
(iii) Minocycline
Dr Muir avoids this drug due to its side effect profile
- it can cause drug induced lupus, a serum sickness like syndrome, autoimmune hepatitis, pseudotumor cerebri,
pneumonitis, pigmentation of skin, mucosa and alveolar bone
- the pseudotumor cerebri tends to be seen within the first 8 weeks of treatment and can result in visual field loss
- there are reports of patients dying from minocycline induced hepatitis or needing liver transplant
- the autoimmune hepatitis associated with a lupus like syndrome tends to be seen after very prolonged treatment
(i.e. >1 year a hypersensitivity hepatitis with eosinophilia and exfoliative dermatitis occurs within the first month)
- for all that severe adverse reactions to minocycline are rare but it is a substantially greater risk than for the other
antibiotics with no evidence of greater efficacy
- minocycline should be a second line drug only
- if used, a dose of 100 mg/day is usual
NONE OF THE TETRACYCLINE GROUP CAN BE USED WITH ISOTRETINOIN DUE TO THE RISK OF
PSEUDOTUMOUR CEREBRI
(iv) Erythromycin
- is used in a dose of 500mg b.d.
- once again the 250mg tablets are best as the dose can be titrated to lessen side effects
(v) Erythromycin Ethyl Succinate
- is administered at a dose of 400 mg, two tablets b.d.
- it can be given with meals and is usually very well tolerated
- Dr Muir tends to mainly use this agent as with most people he sees, he is considering isotretinoin, and
erythromycin is not associated with causing raised intracranial pressure
(vi) Cotrimoxazole
- is used by many but Dr Muir tends to avoid as it is associated with a greater incidence of side effects including
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toxic epidermal necrolysis
- it is however an effective agent and is also useful in gram negative folliculitis
(vii) Trimethoprim
- is preferred to cotrimoxazole due to its better side effect profile
- it is used in those unresponsive to or intolerant of tetracycline or erythromycin
- the dose is 300 mg b.d.
- it is felt to be equally effective as tetracycline
Other antibiotics are described but rarely used
Clindamycin is said to be very useful due to its high lipid solubility but the risk of pseudomembranous colitis
precludes routine use
Roxithromycin and azithromycin are getting written up in the literature as effective agents
- they are expensive and as azithromycin is used as prophylaxis against mycobacterium avium complex in HIV
and other serious infections Dr Muir would avoid its use in acne due to the risk of encouraging resistance
<top>
4. ANTI-ANDROGEN THERAPY
Most women with acne have no clinical or biochemical evidence of androgen excess
- androgens are however a pre-requisite for the development of acne
- even women with irregular menses or hirsuitism may reveal no abnormalities on testing
- women with acne will respond to anti-androgen treatment even in the absence of abnormal hormone levels i.e.
there does not need to be demonstrable hyperandrogenism before considering anti-androgen therapy
Suspect androgen abnormalities if there is; a history of pre-menstrual flaring, an irregular menstrual cycle,
spotting, insulin resistance or infertility
- clinical features include obesity, pattern alopecia, hirsuitism, acanthosis nigricans and clitoromegaly
- it is said that jaw line acne is more likely to respond to anti-androgen treatment
I have never been able to get a sensible answer on appropriate investigation of the female patient with suspected
hyperandrogenism
- a reasonable screen includes LH / FSH, free testosterone, DHEAS and androstenedione
- some add prolactin and ovarian ultrasound
- others only do a free testosterone
- these investigations are done in the second half of the cycle when not on the oral contraceptive pill
- in the majority of cases no abnormality is found
When embarking on hormonal treatment response is slow
- there is little chance of improvement before six weeks and six to twelve months is a not unusual duration
- the mechanism of action seems to be via decreases in sebum production and comedogenesis
Spironolactone
Oral Contraceptive Pill
Systemic Steroids
(i) Spironolactone
This agent blocks androgen receptors and decreases androgen synthesis
- usually given at a dose of 50-100 mg/day it can be very effective either as a sole or adjuvant treatment
- it can be used at doses of up to 200 mg/day
- six months would probably be needed in most cases
- in a study of 85 females, two thirds either cleared or were substantially improved
- most tolerate it well
- the commonest complaint is of menstrual irregularities (17.5%), or lethargy, fatigue, dizziness or headaches
(16%)
- other reported side effects include breast tenderness, diuresis, postural hypotension and nausea
- rises in potassium can be seen but are mostly clinically insignificant
- reported benefits in this study included decreased facial oiliness and endometriosis pain and increased libido
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It is important to remember that most adverse effects with spironolactone are dose dependent and menstrual
irregularities can be decreased by dropping the dose
- alternatively the drug can be given cyclically
(i.e. 21 days on and 7 off)
- combining with the oral contraceptive pill is common
- in animal studies it causes breast cancer albeit at high doses
- it is recommended that it not be used in women genetically predisposed to breast cancer
- it crosses the placenta and enters breast milk
- it is category B3 and could potentially feminise a male foetus
- Dr Muir would not use it in a patient at risk of pregnancy or one who is breast feeding
(ii) Oral Contraceptive Pill
The pill can have a neutral, detrimental or beneficial effect on acne
- most contain an oestrogen and a progestin
- oestrogens increase sex hormone binding globulin and decrease free testosterone
- the progestins used have a range of androgenic effects
Low androgenic progestins include:
- desogestrel
- norgestimate
- gestodene
Moderately androgenic progestins include:
- norethindrone
- ethinodyol diacetate
High androgenic progestins include:
- levonorgestrel
- norgestrel
- norethindrone acetate
Anti-androgenic progestins include:
- cyproterone acetate
- drospirenone
Progestogen only contraceptives both oral and injectable can be expected to worsen acne
If a patient is to be on the pill anyway it is logical to select a low or anti androgenic progestin if possible
- effects can take 6 months to become apparent
- they can improve acne, prevent comedone formation and reduce the oiliness of the skin
Pills containing 2 mg of cyproterone acetate and 35 micrograms of ethinyl oestradiol (Diane, Brenda) have a
similar contraceptive efficacy and side effect profile to other oral contraceptives
- weight gain may be more of a risk as well as mood swings and breast tenderness
- there does not seem to be any evidence of feminisatin of male foetuses in the event of pregnancy whilst on this
agent
If a cyproterone acetate containing pill is ineffective or you wish to have greater anti-androgen effect due to the
presence of hirsuitism, extra cyproterone acetate can be prescribed
- this is given on days 5 through 14 of the cycle
- doses used vary from 25 to 100 mg/day
The latest contraceptive wonder drug is 'Yasmin' which contains drospirenone as a progestogen and 30 mg of
ethinyloestradiol
- drospirenone is an analogue of spironolactone and has anti androgenic and anti mineralocorticoid actions
- it can improve acne, decrease fluid retention, alleviate premenstrual dysphoric disorder, does not cause weight
gain and is apparently a contraceptive!!
Other then rifampin there is no evidence that antibiotics lower the efficacy of oral contraceptives in the absence of
vomiting or diarrhoea
- there are large studies that have been successfully used in the American courts stating that there is no need to
advise back up contraception when using antibiotics with the pill
- Dr Muir states that he must admit that he still advises them of the theoretical risk
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(iii) Systemic Steroids
Prednisone can be used as an anti-inflammatory agent in acute, severe forms of acne
- it is also used on occasion as an 'emergency treatment' to clear acne quickly, albeit temporarily, for a big event
such as a wedding
- this is usually given at a dose of 0.4-0.5 mg/kg/day
It has also been used as an 'adrenosuppressant' in females
- in this situation a steroid is given at night to suppress adrenal hormone production
- the usual dose used was 5-15 mg/day of prednisone or 0.25-0.5 mg/day of dexamethasone
- this can suppress female testosterone levels and improve acne
- in the studies, which are quite old now, women with elevated testosterone levels, which dropped with treatment,
showed the greatest improvement of acne
- however pre-treatment elevation was not a pre-requisite for response
Dr Muir has not used this treatment nor has he seen it used
<top>
5. PHYSICAL THERAPY
Personally I don't perform any form of physical therapy in managing my acne patients
- other dermatologists swear by a variety of interventions
Comedone extractor
Electrocautery
Microdermabrasion
Cryotherapy
Light Treatment
Photodynamic Therapy
Superficial X-Ray Therapy
(i) Comedone extractor
This is a small curette like instrument with a small hole in the base of the spoon
- the hole is placed around a comedone and firm downward pressure expels the keratin plug
- you then move on to the next comedone
- useful for getting rid of the occasional troublesome comedone but labour intensive if used extensively
(ii) Electrocautery
This has been used for macro-whiteheads and blackheads up to 1.5 mm diameter
- the instrument is used at a low setting with EMLA topical local anaesthetic
- there is supposed to be little pain and good results with no sequelae
- not something Dr Muir has ever been called upon to do
(iii) Microdermabrasion
Once very popular with the lay public and those who owned the equipment this treatment is little heard of now
- there is surprisingly little in the literature considering how widespread was its use
- considering the mechanism of action there is little likelihood that this intervention would make a major impact on
acne
(iv) Cryotherapy
This is mentioned in the major texts as a possible intervention in acne
(Dr Muir includes it here for completeness sake)
- it is a described treatment for 'cysts'
- it is used on older lesions as two 15 second freezes with liquid nitrogen
- the resultant inflammation causes destruction of the fibrotic 'cyst' lining
- it works best on older lesions rather then acutely inflamed nodules
- Dr Muir has never seen it used and the only references for it stem from the early 1970's
- personally Dr Muir would not recommend it
(v) Light Treatment
This is a new treatment modality
- a variety of light sources are described including blue and blue and red combined
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- the rationale is that p.acnes produce their own coproporphyrin III irradiation of which produces singlet oxygen
and bacterial death
- there are studies showing a decrease in the number of inflammatory lesions with twice weekly treatment for 5-12
weeks
- there seems to be a lesser effect on comedone numbers
(vi) Photodynamic Therapy
This uses application of aminolevulinic acid to the affected skin followed by exposure to light 3 hours later
- it results in sebaceous gland damage on histology, reduced sebum production and p.acnes numbers
- the papers claim an improvement in clinical appearance
- it can result in pain, desquamation, folliculitis and hyperpigmentation
Both the above mentioned light treatments are new and there is not a huge amount of published material on them
as yet
- the consensus seems to be that they can be moderately useful
- it will be interesting to see if they become part of the armamentarium of acne management or yet another
footnote
(vii) Superficial X-Ray Therapy
This was once a widely used and effective modality
- it is rarely used now since the advent of oral retinoids
- Dr Muir has never seen it used in acne
- it has been suggested that no long term harm is likely if the total dose is kept to less then 8.1g
- a typical regime is 0.9g three times a week at three week intervals for three cycles
- side effects seen include increased incidence of BCC and thyroid cancer
- Dr Muir could imagine using this but only as a last resort
<top>
6. DIET
Most patients and many doctors believe that diet plays a role in the pathogenesis of acne
- at the moment "there is no strong evidence to support a causal relationship between ingestion of certain
foodstuffs and the causation or exacerbation of acne"
- the role of diet in acne is currently being re-evaluated
There are epidemiological studies showing an absence of acne amongst hunter gatherer societies in Paraguay
and New Guinea
- the authors speculate that diet is a probable explanation
(Dr Muir can count on one hand the number of hunter-gatherers he has seen with acne!)
- a recent paper explored the possible causative role of foods with a high glycaemic index in acne
- there is a lot of evidence that metformin used in HAIR-AN syndrome results in lowered insulin and androgen
levels and improvement in acne
- thus it would seem logical that any method resulting in decreasing elevated insulin levels may improve acne
There are studies showing no relationship between diet and acne
- many would argue that these studies were badly designed
- Dr Muir points out to his patients that the dietary intake of a nine year old, a sixteen year old and a twenty six
year old are not wildly different
- the relative incidence of acne between these age groups is
In short Dr Muir thinks the jury is still out on diet and acne
- he does not use diet as a therapeutic intervention beyond advising a healthy, well balanced intake
- he warns against using very restrictive diets in the vain hope that it will improve their skin
- if they feel that chocolate exacerbates their acne then avoid chocolate
<top>
SPECIAL PROBLEMS
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Gram negative folliculitis
Coagulase negative staphylococcal folliculitis
Antibiotic resistance
(I) Gram Negative Folliculitis
This is nearly always a complication of long term antibiotic use in acne and on occasion rosacea
- it presents as a sudden deterioration of previously well controlled acne
- typically one sees multiple, small, follicular based pustules or more uncommonly deep seated nodular lesions
- swabs reveal causative organisms such as klebsiella, e.coli, proteus and pseudomonas
- these can be grown from the pustules but also from the skin and nares
- one study revealed that all affected patients had some form of immune dysfunction in their series
- these included decreased IgM and alpha 1 antitrypsin or elevated IgE
If suspected stop the current antibiotic
- take swabs for culture and substitute ampicillin 250mg q.i.d. or trimethoprim 300 mg b.d.
- swabs should be taken from multiple sites as many pustules will be sterile
- as gram negatives are susceptible to desiccation make sure the samples are transported quickly
- the lab needs to be notified as these organisms require special culture media
Many feel that the treatment of choice is isotretinoin which probably works by making the skin and nasal
environment untenable for these organisms
(ii) Coagulase Negative Staphylococcal Folliculitis
This presents in a similar way to gram negative folliculitis
- it occurs de novo or complicates antibiotic therapy especially tetracycline
- interestingly it responds to benzoyl peroxide
(iii) Antibiotic Resistance
An increasingly common problem
- the use of long term antibiotics is a source of major concern for the infectious diseases community due to the
risk of producing pathogenic resistant organisms
There are multiple articles documenting the increase in prevalence of resistant P.acnes
Erythromycin resistance in vitro is seen in over 50% of patients
- this compares to a figure of only 20% in 1978
- there is normally cross resistance to clindamycin
- resistance to the tetracycline group especially minocycline is much less common
It is common to isolate resistant P.acnes from patients who have not previously received treatment
- with antibiotic treatment the prevalence of resistance increases
- interestingly resistant coagulase negative staphylococcus is very common
Although there has been an enormous increase in the prevalence of antibiotic resistant P.acnes this has not been
accompanied by a surge in treatment resistant acne
- there are a number of possible reasons for this:
- perhaps the role of bacteria in acne is overstated, this is unlikely
- antibiotics work more by their anti-inflammatory than their antibiotic effects
- in vitro resistance does not always mean in vivo resistance and vice versa
- for the prescribed antibiotic to kill bacteria its concentration in the pilosebaceous unit must exceed the minimal
inhibitory concentration
- the concentration of antibiotic achieved clinically is affected by multiple variables
(i.e. dose, compliance, absorption and metabolism rates, lipid solubility, sebum flow rates etc)
- in the event of treatment failure one cannot assume that antibiotic resistance is the cause
- in a study from the late 80's of a group of non-responding acne patients, 65% had no microbiological abnormality
- just under 20% had a resistant p.acnes and 16% a gram negative folliculitis
- interestingly 8% of untreated controls had a resistant P.acnes
- in other words most cases or resistant acne were for reasons other then microbiological
Suspect antibiotic resistance if there is treatment failure, relapse while on treatment, recurrent relapses or a
poorly compliant patient
- swabs should be taken and the lab notified of your suspicions as P.acnes is difficult to culture
- if antibiotic resistance is detected in the setting of treatment failure another antibiotic could be substituted guided
by sensitivities
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- minocycline resistance is rare but increasing
- in some cases simply increasing the dose of the current antibiotic can work
- application of benzoyl peroxide can actually restore antibiotic sensitivity
- other non-antibiotic treatments could be considered
(e.g. isotretinoin or anti-androgens)
To prevent resistance emerging use the following stratagems:
- avoid antibiotics where possible
- combine antibiotics with other treatments
(concomitant benzoyl peroxide reduces the emergence of resistance)
- do not use a topical antibiotic different to the oral
- use topical antibiotics to all the skin not just pimples
- limit systemic antibiotics to 6 months
- if they do well on a particular antibiotic and then relapse use the same drug again
- consider anti-androgen therapies in females
- if recurrently relapse isotretinoin may be indicated
<top>
ACNE IN PREGNANCY AND LACTATION
Acne can improve, deteriorate or remain the same in pregnancy
- many patients will refuse any and all medication during pregnancy for fear of harming the child
- most of the available treatments are not Category A
- Dr Muir has been asked on occasion for an absolute assurance that his prescribed treatment carries no risk to
the mother or child
- this is of course impossible to give even with a Category A drug
There has been some concern over erythromycin even though it is listed as being safe in pregnancy
- there has recently been a Swedish study published (reprod toxicol 2005 July-Aug 20 (2): 209-14) showing an
increased risk for cardiovascular malformations and pyloric stenosis in the offspring of women exposed to
erythromycin in early pregnancy
- there are other papers disputing this finding
Category A Treatments
Category B Treatments
Category D Treatments
(i) Category A Treatments
Erythromycin and clindamycin are both Cat A
- it will be interesting to see if further research into erythromycin results in a change in classification
- erythromycin is considered compatible with nursing even though breast milk contains 50% of the level reached
in serum
Benzoyl peroxide is not classified in MIMS
- 5% of applied benzoyl peroxide is absorbed, the metabolised drug enters the circulation as benzoate and is then
excreted in the urine
- this small amount of benzoate is easily handled by the kidneys so systemic or foetal effects are not expected
- the drug is felt to be safe in pregnancy
- a 1998 New England Journal of Medicine review considers topical erythromycin, clindamycin or benzoyl
peroxide the treatments of choice for acne in pregnancy
(ii) Category B Treatments
Azelaic acid is B1 and almost certainly safe in pregnancy and lactation
- there is no evidence of harm in animal studies and systemic absorption is minimal
(iii) Category D Treatments
All forms of topical retinoid fall into this category
- having said that, you probably get greater systemic exposure to Vitamin A from eating carrots
- some texts discuss use of topical retinoids in pregnancy after the first trimester
- personally Dr Muir would not prescribe them at all during pregnancy
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- if someone using a topical retinoid became pregnant there is little chance that the foetus would be adversely
affected
- they should stop the agent and their obstetrician should be notified
There are of course individual case reports of birth defects in children after maternal exposure to topical retinoids
- animal studies with tretinoin in lactation have not shown any problems and minimal amounts are found in human
milk after topical use
All the topical retinoids list pregnancy as a contraindication and mention lactation in precautions
Tetracycline, minocycline and doxycycline are all Category D
- tetracycline binds strongly with calcium orthophosphate and is deposited in bones and teeth undergoing
calcification
- in teeth this is permanent
- children exposed to tetracycline after the fourth month of pregnancy will have yellow staining of their deciduous
teeth which will darken over time
Calcification of permanent teeth begins 4-6 months after birth and continues till age 5-12
- therefore maternal ingestion of tetracycline during pregnancy should not effect permanent dentition
- similarly first trimester tetracycline ingestion, prior to calcification, should not discolour deciduous teeth
This group of drugs differ in their ability to bind calcium and hence in their ability to stain teeth
- tetracycline is thus more likely to stain teeth then doxycycline and minocycline is least likely
- all can result in teeth discolouration however
- once it was felt that enamel hypoplasia and increased dental caries would result but this has been refuted
- the possibility of maternal tetracycline ingestion causing reduced bone growth, cataracts in infancy and
teratogenicity have been raised over the years but their is apparently no good evidence to support these claims
Tetracycline ingestion in pregnancy is associated with potentially fatal acute fatty liver
- this is mostly seen in women with renal disease on high doses in the second trimester and beyond
Tetracycline is excreted in breast milk in small amounts only
- as it is strongly bound to calcium it has a low bioavailability and the concentration in infant serum remains low
In conclusion tetracycline can be used in women of child bearing age but they should avoid pregnancy
- if they do become pregnant as long as the drug is ceased in the first trimester there are unlikely to be any
problems
- these drugs should not be used routinely during lactation
- the W.H.O. states that infant risk is low if maternal use is less then 7-10 days
- obviously such a short course of treatment would not be used in acne
<top>
TYPICAL TREATMENT REGIMES
Predominantly comedonal acne
Comedonal acne with scattered pustules
Comedonal acnes with papules, pustules and occasional nodule
Severe acne with comedones, papules, pustules and numerous nodules
Female with moderately severe acne
(i) Predominantly comedonal acne across the forehead and cheeks
- topical retinoid at bed time washed off in the morning
- use a gel if oily and a cream if dry skin
- Cetaphil lotion or cream if gets dryness
- consider adding a benzoyl peroxide wash if tolerates the retinoid
- review after 2-3 months
(ii) Comedonal acne with scattered pustules and occasional small papules
- topical retinoid combined with either topical benzoyl peroxide cream b.d. or topical antibiotic (erythromycin or
Clindamycin) and Benzac AC wash
- review after 2-3 months
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(iii) Comedonal acnes with papules, pustules and occasional nodule
- topical retinoid and oral antibiotic (tetracycline, doxycycline or erythromycin) at appropriate dose
- combine with a topical benzoyl peroxide product
- Dr Muir tends to use the wash
(iv) Severe acne with comedones, papules, pustules and numerous nodules
- consider oral erythromycin and referral for consideration of isotretinoin
- topicals may not be tolerated when very inflamed
- in this situation Dr Muir will often wait a few weeks till the oral antibiotic has taken effect and then add topicals
(v) Female with moderately severe acne
- consider trial of low androgenic or anti androgenic oral contraceptive
<top>
'Acne Dilemma' - Case Studies
Cases from Tele-Derms Online Case Studies
- See: Case 207, Case 208, Case 209, Case 210, Case 211and Case 212
To access these case studies go to: Tele-Derm National - Online Cases
- see below for details
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
<top>
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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BIOPSY OF A DIFFICULT SITE
Other Skin Biopsy Procedures:
Conchal Bowl biopsy
Punch biopsy
Shave biopsy
You will occasionally need to biopsy a lesion in a difficult to reach site
- these can be awkward to reach and placing a suture difficult
- the two spots that present Dr Muir with the most problems are the inner canthi and the conchal bowl
- the usual indication is for biopsy of a lesion suspicious for malignancy thus a shave is all that is needed
- these sites have limited access and the skin around the eye is loose and resists cutting by a scalpel
This is where a Stiefel curette comes in very handy
- the long, thin handle makes it easier to reach these sites than with a hand held blade or one mounted on a
scalpel handle
- the cutting action is different to a blade as you can 'pull' from behind the lesion
- these have the advantage over a reusable curette as they are extremely sharp
(i) An elderly sun damaged man with an irritating, occasionally bleeding papule deep under the orbital ridge
- the skin is sun damaged and 'loose'
- a simple shave should give us the diagnosis and if the lesion is benign solve the problem
- a good indication for a Stiefel curette shave biopsy
(ii) After infiltrating local anaesthetic perform your shave
- note that the hand gripping the curette has complete freedom of movement
- the other hand is applying traction to allow the blade to cut
- the cutting action should be directed away from the eye
- if the patient closes their eyes it tends to throw the skin into folds and makes getting a clean shave difficult
(iii) The final defect
- a nice, clean and exact cut with no damage to the surrounding skin
- as you can see the defect is just below the level of the surrounding skin
- this is because Dr Muir used the curette to 'scoop' as well as shave to ensure that he had dermis as well
- the lesion had a dermal component clinically
- if it had been a purely epidermal lesion such as seborrhoeic or solar keratosis shaving level with the surrounding
skin would have been sufficient
- this was dressed with a small square of calcium alginate (Kaltostat)
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(iv) The lesion sits nicely within the curette for transfer to the sample bottle
- minimal chance of crushing
(v) The business end of the instrument
- note that only the narrow, tapered edge is sharp
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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CONCHAL BOWL BIOPSY
Other Skin Biopsy Procedures:
Biopsy of a difficult site
Punch biopsy
Shave biopsy
In the Australian population it is not uncommon to see solar related skin problems in relatively sun protected sites
such as the conchal bowl
- this is an area where surgery is relatively difficult but the consequences of missing a malignancy can be
catastrophic
This is the ear of a man in his late sixties
- he has had numerous non-melanoma skin cancers and solar keratoses over the years
- the lesion shown has been frozen in the past only to recur
- it is itchy and has bled
- in this situation we need both a diagnosis and treatment
Any treatment that does not produce histology is contraindicated as this could be a well differentiated SCC
- therefore the following should not be used:
-- cryotherapy
-- imiquimod
-- photodynamic therapy
-- 5 flurouracil cream
-- diclofenac
- the more likely diagnosis is a solar keratosis for which excision would be overkill
- repair of an excision defect in this site can be difficult requiring a graft, prolonged second intention healing or
other procedures
(beyond Dr Muir's skill and time limit)
A punch biopsy will only sample the lesion in which case further treatment will be needed even if it reveals solar
keratosis only
A deeper then average shave will give a very good specimen for histology and result in cure of the lesion if it is a
solar keratosis only
- if histology revealed an intraepidermal carcinoma or squamous cell carcinoma then further treatment will be
needed
Usually Dr Muir does a shave excision with a 15 blade held in gloved hand
- getting into a restricted area like this can be difficult
- biopsy here is made much easier with a Stiefel disposable curette
- the images illustrate the procedure
- Dr Muir has everted the conchal bowl with pressure on the posterior aspect of the ear
- this makes the lesion more accessible and creates haemostasis
- these curettes are much sharper then reusable ones and shave these lesions out easily
- the resultant defect can be left to heal by second intention
- as the defect is superficial it can be expected to heal far more quickly then after an excision
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Histology showed a moderately dysplastic solar keratosis
- this should require no further treatment other than review at 3 months or so
- it would be a rare patient indeed with a solar keratosis in the conchal bowl who did not have more problems with
skin cancer then you could poke a stick at so they'd need regular review anyway
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Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
CRYOTHERAPY
Cryotherapy for Skin Malignancy
How does it work
Liquid Nitrogen Delivery
Freezing techniques with liquid nitrogen
What cure rates can be expected
Complications
Contraindications
(NOTE: For more information see 'Cryotherapy' in the Video Vault from 'Jim's Tips' on the RRMEO Tele-Derm
National module - see 'Reference' below)
1. Cryotherapy for skin malignancy
Cryotherapy is used for a range of benign, malignant and pre-malignant skin conditions
- a number of freezing agents have been used over the years
These include:
- carbon dioxide, boiling point of minus 79oC
- nitrous oxide, boiling point of minus 90oC
- fluorocarbon liquid, boiling point of minus 60 oC
- liquid nitrogen, boiling point of minus 196oC
Because of it's ease of storage and delivery and very low temperature liquid nitrogen is the only cryogen (freezing
agent) in common use by dermatologists
(when the term cryotherapy is used in this article it refers to liquid nitrogen)
The literature is replete with reports of the use of cryotherapy in an enormous range of conditions
- in many it has been superseded by other treatments
- it remains an extremely useful modality with excellent cure rates and good cosmesis when used appropriately
Benign conditions where good results can be achieved with cryotherapy include:
- solar and simple lentigos
- a variety of vascular lesions
(venous lakes, cherry haemangiomas, angiokeratomas, spider naevi etc)
- milia
- benign adnexal tumours
(syringomas, trichoepitheliomas, small hidrocystomas)
- skin tags
- a variety of benign lesions characterised by epidermal hyperkeratosis
(seborrhoeic keratoses, lichenoid keratoses, stucco keratoses, dermatosis papulosa nigra, acrokeratosis
verruciformis of Hopf)
- some epidermal naevi
- sebaceous hyperplasia
- and a range of other lesions
Ophthalmologists use cryotherapy for eyelid trichiasis
Liquid nitrogen cryotherapy has long been a mainstay of treatment of viral warts
- it is not however uniformly successful
There is a body of literature supporting it's use in keloid scars both as a sole modality and in combination with
intralesional steroid injection
It's use has been advocated in a number of benign conditions where Dr Muir admits he would not use it
These include:
- acne cysts
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- hidradenitis suppurativa
- rhinophyma
- xanthelasma
- alopecia areata
- elastosis perforans serpiginosa
- dermatofibromas
- angiofibromas
- tattoos
- port wine stains
- and more
Cryotherapy remains the most commonly used treatment modality for solar keratosis
- it achieves good cure rates and variable cosmesis
Over the years cryotherapy has been used to treat a range of skin malignancies
- it was a commonly used modality and achieved acceptable results for AIDS related Kaposi's sarcoma
- it is still widely used for intraepidermal squamous cell carcinoma (Bowen's disease), superficial and nodular
basal cell carcinoma
- given good tumour selection and treatment technique cure rates with liquid nitrogen cryotherapy are equivalent
to any other modality except Mohs surgery
Although well described in the treatment of invasive squamous cell carcinoma with documented cure rates
equivalent to simple surgery, cryotherapy is not as often used for this indication compared to previously
- as these lesions carry the risk of metastasis cryotherapy is restricted to low risk lesions in carefully selected
patients
Keratoacanthomas have been treated with cryotherapy but are more resistant than SCC
- they tend to be bulky lesions with a thick keratin plug, features that resist destruction by freezing
Lentigo maligna has been treated with cryotherapy with some series showing excellent cure rates of more then
90%
- other series showed cases of recurrent nodular melanoma within treatment fields during ten year follow up
- once again patient and tumour selection coupled with appropriate technique are essential to success for this
condition
- palliation of cutaneous deposits of metastatic melanoma is another indication for cryotherapy
<top>
2. How does It work?
It is thought that freezing causes cell death by the following sequence of events:
(i) Extracellular ice formation, which begins once minus 10-15oC is reached, leads to concentration of extracellular
solutes as water is lost to ice
(ii) The resultant osmotic gradient created draws water out of the cells
- at the same time damage to cell membranes by the ice crystals increases this outward flow of water from the
cells
- thus intracellular solute concentration results
(iii) Intracellular ice formation occurs with resultant damage to mitochondria and endoplasmic reticulum
(remember them?)
(iv) Vasoconstriction is triggered by the drop in temperature
- at minus 15oC there is damage to endothelium, platelet aggregation and thrombus formation
- this leads to ischaemic necrosis of tissue
(v) With thawing there is a reactive hyperaemia followed by inflammation secondary to tissue damage
- this contributes to ongoing injury
Histologically change first becomes apparent at about thirty minutes post freezing
- at two hours one sees oedema, capillary damage, bleeding and microthrombi
- at eight hours segmental blood vessel necrosis is seen
Cells vary in their relative susceptibility to damage from freezing
- Melanocytes are the most sensitive dying at minus 4-7oC compared to keratinocytes which can tolerate up to
minus 30oC
- Basal cells are between these two in terms of sensitivity
- after keratinocytes in order of increasing resistance to death from freezing come:
-- bacteria
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-- connective tissue
-- nerve sheath
-- vascular endothelium
-- and then viruses
<top>
3. Liquid Nitrogen Delivery
A variety of suppliers will deliver liquid nitrogen to your practice
- this is because it boils at minus 196oC and the resultant vapour build up will cause an explosion in a totally air
tight container
- this evaporation will lead to loss of liquid nitrogen
- greater volumes can be stored for longer periods than smaller
For instance a store of:
- 5 litres of liquid nitrogen has a static holding time of 6 days
- 25 litres 110 days
- 50 litres 125 days
Hand held flasks are used when treating patients
- the liquid nitrogen can be transferred to these by the simple expedient of pouring from the storage container or
with pressure head withdrawal device
- this transfer generates clouds of vapour and hence wastage
- the pressure head device reduces this
On average a hand held flask will retain the liquid nitrogen for six to twelve hours if unused
- once again these are not vapour tight and have a pressure relief valve to prevent excess build up of vapour
Liquid nitrogen storage dewar
Note protective gloves and pressure head device for extracting contents
- Dr Muir's is refilled about once a week
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The lid of the dewar does not create an air tight seal
- as the pressure builds up within the stopper rises up to release it otherwise..........
KABOOM!!/
A typical cryotherapy gun
Note the trigger mechanism, pressure release valve at the back and interchangeable nozzle
- once filled this would last for a whole consulting day usually
Transfer of liquid nitrogen from the dewar to a cryo-gun using the pressure head device
Note the protective gloves.
- he is also wearing goggles
<top>
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4. Freezing Techniques with Liquid Nitrogen
When Dr Muir first started in dermatology it was still common to see dermatologists use a cotton wool tipped
applicator when freezing lesions with liquid nitrogen
- cotton wool is wrapped loosely around an orange stick and dipped into a container of liquid nitrogen
- the cotton wool tip is then applied directly to the lesion
- pre-prepared cotton wool tipped sticks are no good as the volume of cryogen carried is too little
- the tip is held in contact with the lesion for the desired time
(usually until a small halo of ice forms on the surrounding skin)
- if pressed firmly this gives a greater area of contact and squeezes liquid (water/blood) out of the lesion allowing
lower temperatures to be reached
- several applications may be needed with the tipped re dipped in between
This is a relatively slow and inconvenient method and not one that Dr Muir ever uses
- to do this you need to decant liquid nitrogen into a small container, often a plastic specimen jar
- this is so you do not contaminate your main reservoir with infectious particles from the patient
- interestingly adenovirus has been shown to survive liquid nitrogen so others may as well
- another potential hazard is the increased risk of spillage and burns as you have the cryogen in an open
container
- it is more wasteful of cryogen then newer delivery methods
Nearly all cryotherapy is now performed with a 'cryogun'
- this is an insulated, robust vacuum flask which is refilled daily or more often from the main storage reservoir
- it has a trigger activated release mechanism which allows you to direct a stream of liquid nitrogen onto the skin
- the size of the stream delivered can be modified with interchangeable nozzles
- this is termed the 'open spray technique'
A standard selection of nozzle tips and attachments
Dr Muir mainly uses a 'B' nozzle
(he has never used the thing for shooting around corners!)
Nozzle tips are easily changed dependent on your preference
With a small lesion less then about 2 cm in diameter the nozzle is held above the centre of the lesion
- the radius of frozen skin approximately equals the maximum depth of freeze
- this unsurprisingly is called the 'spot technique'
- where a larger field is being treated the nozzle is moved over the field while spraying cryogen
- some use a paint brush technique going back and forth across the treatment field
- others begin freezing centrally and then spiral the spray outwards to cover the entire field
(in this instance of course the depth of freeze will be much less then the width)
The spot technique is commonly used on
- solar keratoses
- warts
- small intraepidermal carcinomas
- superficial BCC's
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- nodular BCC's
When larger lesions are to be treated then the spiral or paint brush method is used
eg. if a 5 cm diameter IEC was to be treated, the depth of freeze would not need to be anywhere near that of the
radius of the frozen zone
On occasion a cone may be used
- these , as the name suggests, are horizontally truncated cones
- the narrow aperture fits around the lesion to be frozen while the spray is directed down the other end
- this allows an intense freeze of the lesion plus a safety margin of clinically uninvolved skin and a greater depth
of freeze while leaving other adjacent structures alone
In action!
Metal cryoprobes are also available
- these are attached to the nozzle of the cryogun and cooled by liquid nitrogen flowing through them
- Vaseline is applied to the lesion to be treated and the frozen probe is then pressed onto the lesion
- this allows extremely accurate freezing
(they are not used often)
By far the commonest technique in use today is the open spray using a spot or spiral/paint brush technique
depending on the lesion size
The commonest question Dr Muir is asked is "how long should I spray the lesion for?"
- unfortunately there is no simple answer for this
The duration of a spray will depend on many variables:
- lesion diameter
- thickness and histology
- how far from the skin the nozzle is
- and so on
When talking about freezing times people are often referring to different things
- one technique is to commence timing from the moment spraying starts
- while the most commonly used method is to measure the duration of freeze from the moment the entire
treatment field is fully frozen
If you read texts on this topic they discuss using various temperature monitoring devices but this is rarely done or
indeed needed in clinical practice
The simplest method is the 'spot freeze technique'
- this is only done on treatment fields of less then 2 cm diameter
- if treating a bigger field than this the edges will not get cold enough
- bigger lesions are thus done in sections with overlapping fields
The recommended technique is as follows;
(i) The area to be treated is marked out on the skin
- this will include the lesion and a safety margin of normal skin
- markings are useful as the tumour margins will be difficult to see once frozen
(ii) Using a full cryogun to ensure an even flow of liquid nitrogen and holding the nozzle 1 cm above the skin
surface spray the centre of the treatment field till frozen
- this is best detected by palpation
- the resultant ice ball will feel hard and will involve the entire field up to the inked margins
- timing of the freeze begins once the field is fully frozen
(iii) This ice ball is maintained with the spray for the desired length of time by spraying the centre of the field as
needed
- spraying then ceases
- if this technique was used to treat a lesion that needed a total freeze time of 15 seconds, timing would not
commence till the entire treatment field had been turned into an ice ball
- the ice ball would then be maintained by careful spraying until a period of fifteen seconds had elapsed
- spraying would then cease and the lesion would be left to thaw
- so some of the lesion would be 'frozen' for longer then 15 seconds and actual spraying of liquid nitrogen onto the
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lesion would not continue for the whole 15 seconds
(confusing isn't it!)
(iv) If two freeze-thaw cycles are needed the lesion must be allowed to completely thaw before the second freeze
to obtain best results
- once again determination of thawing is best done by palpation
If the treatment field was 6 cm in diameter, the field would be frozen in 2 cm diameter sections, which would
overlap each other
Interestingly many people tolerate even fairly brutal freezes without anaesthesia
- if needed, local infiltration with lignocaine or application of a topical local anaesthetic such as EMLA, can be
done
A superficial BCC on the upper back
Lesion extent and treatment field marked out
- in a BCC: a 5 mm margin of normal skin is frozen
The resultant ice ball
- this will need to be maintained for thirty seconds for a BCC before being allowed to thaw
Palpation allows determination of ice ball formation
- it should feel quite solid
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- remember timing of freeze duration does not begin till the treatment field is fully frozen
- the ice ball is maintained by top up sprays till the desired duration is reached
Fully thawed and second freeze can be done in the same way as the first
- it is important to wait till the lesion is completely thawed if you want to achieve the best cure rates
Another lesion being treated with the aid of a cone
A 1995 review recommends the following freeze times:
(i) Solar keratosis
- a single 5-15 second freeze, with a 1 mm margin of normal skin
(Dr Muir would err towards the shorter duration)
(ii) Intraepidermal carcinoma
- a single 15-30 second freeze with a 3 mm margin of normal skin
(iii) Basal cell carcinoma
- a double freeze thaw cycle of 30 second duration each treating a 5 mm margin of normal skin
(iv) Squamous cell carcinoma
- is the same as for BCC but this modality is used less now than previously for this lesion
Documentation of a freeze can be done as follows:
IEC L distal, radial forearm LiqN2 20 sec 1xFTC 2 fields of 2cm diameter
Which translates as:
- an 'intraepidermal carcinoma on the left distal, radial forearm treated with liquid nitrogen cryotherapy
- a single freeze/thaw cycle was used and a total freeze time of 20 seconds was delivered to the lesion by treating
in two sections of 2 cm diameter
<top>
5. What cure rates can be expected?
Solar Keratoses
Intraepidermal Carcinoma (Bowen's Disease)
Basal Cell Carcinoma
Squamous Cell Carcinoma
Other Skin Malignancies
There are many published studies on cure rates comparing the different treatment modalities for solar keratosis
and 'non-melanoma skin cancer'
- these show that cryotherapy can achieve results comparable with modalities such as surgery and radiotherapy
- this is however highly dependent on lesion selection and technique
- commonly these studies use different follow up times
- this will result in results showing cure rates of 98% at three months, 92% at twelve and 87% at five years for
example
Dr Muir personally finds this hard to reconcile.
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- if 98% are 'cured' at 3 months how can a significant number of these become 'uncured' by five years
- a better way is to compare relapse rates
(i.e. 2% relapse at three months and 13% at five years)
(i) Solar keratoses
Cure rates should be very high
- some studies quote results of around the 99% mark
- freeze times will vary with each lesion treated
- a hyperkeratotic lesion will resist destruction
- the flip side of a high cure rate is that this may well be accompanied by a higher complication rate
When treating a solar keratosis it is important to realise that these lesions do not arise from 'virgin' skin
- new solar keratoses will develop in the area over time
- whether this is recurrence or a new lesion can be hard to decide
There is a push to classify solar keratoses as squamous cell carcinomas
- this emanates from the United States and is not widely accepted here, as yet
- most still consider these to be pre-malignant lesions
- the chances of an individual lesion transforming into a malignancy is low but when, as is often the case, a
patient has dozens of visible lesions the risk of some transforming is high
- which one and when remain difficult questions
- as the cosmetic result is better with a lighter freeze then a heavier it is usually reasonable when treating solar
keratoses not to be too heavy handed
- as these lesions are restricted to the epidermis they will need much less of a spray time than lesions with a
dermal component such as BCC
- if the lesion persists the treatment can always be repeated
- it is very common to see patients whose sun exposed skin is a mass of white cryotherapy scars but still having
numerous solar keratoses
When treating solar keratoses Dr Muir warns the patient about the potential side effects
(that there is a chance of treatment failure and that new lesions will continue to develop over time regardless)
- he tends to freeze mainly those lesions that he can feel rather then merely see
- between visits he gets the patient to sun protect and apply a moisturising keratolytic twice daily
- the strength varies with the site, the degree of solar damage and the patient's tolerance
- typically for the face he will use 5% salicylic acid in aqueous cream b.d. and for the forearms 8%.
(on the scalp he may go up to 12%)
- he also uses glycolic acid, lactic acid, urea or propylene glycol
- regular use of keratolytic and strict sun protection has been shown to reduce the number of solar keratoses
forming and to cause regression of existing lesions
If they have never had cryotherapy in the past he will usually only do a few lesions on the first visit to see how
they tolerate it and what the cosmetic results are
- the reason for this is that some people will blister very readily with cryotherapy and others have a marked
tendency to de pigmentation
- cryotherapy on the cutaneous upper lip will readily cause hypo pigmentation in women
(this produces an extremely poor cosmetic result so he tends to avoid using it here)
(ii) Intraepidermal carcinoma (Bowen's disease)
Cryotherapy is often used to treat these lesions
- they require a shorter freeze time than BCC as there is no dermal component
- a 3mm margin of healthy skin should also be treated
- studies give very high cure rates of over 98% with a single 30 second freeze
- results in everyday practice do not seem to be as high
(warning Muir anecdote)
Dr Muir suspects the two main reasons for treatment failure are under treatment of the lesions in terms of duration
of freeze and extent
30 seconds is a long time
- he suspects that many practitioners do not time their freezes and as this is a fairly uncomfortable procedure
there is a tendency to cease spraying early
- determining the lateral extent of an IEC in sun damaged skin is not easy and so even with a margin of
supposedly uninvolved skin, tumour at the edge is often left out of the treatment field
- at review one will see a nice white cryotherapy scar with a penumbra of IEC
- this should not be classified as recurrence but rather as persistence as it was never treated in the first instance
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Some studies talk about using a 15 second freeze time for IEC below the knee
- this is an attempt to reduce morbidity but is of course at the expense of lower cure rates
- freezing below the knee carries a high risk of ulceration and slow or indeed non-healing
- freezing produces a lot more oedema and damage to the underlying dermis than other techniques hence the
healing problems
IEC can invade down hair follicles
- this means that there will be cancer cells anatomically much deeper in the skin then the epidermis and so
beyond the reach of your cryogen
- it is said that freezing will still cure IEC on hairy skin as the entire hair follicle is shed after cryotherapy
- Dr Muir is however still wary of using cryotherapy or curettage for lesions involving terminal hair and will usually
opt for a different modality
(iii) Basal cell carcinoma
Readily available current treatments for BCC include;
- cryotherapy
- curettage and cautery
- excision with or without margin control
- radiotherapy
- CO2 laser ablation
- topical imiquimod
- photodynamic therapy
There are more in the pipeline
- this tells us that there is no single treatment suitable for all BCC's in all people
Depending on the study, cure rates of over 95% can be achieved when treating BCC with cryotherapy
- these results can only be achieved if the lesion selected is appropriate and the treatment technique is good
Cryotherapy will readily treat to 3mm depth
- it is rare for a BCC to be thicker than this
(<5% in some studies)
- the depth of freeze in the centre of the lesion approximates to the radius of the frozen area when the spot freeze
technique is used
- as a margin of 5 mm of normal skin is used with BCC most treatment fields will deliver a tumoricidal freeze to the
base of most BCC's
- if there is doubt about the lesion thickness a punch biopsy can be performed
(this will give you some idea of depth but it may not be accurate due to sampling error)
- in general if you think you are dealing with a thick lesion it may be best to opt for surgical treatment or
radiotherapy
Not all histological types of BCC are suited to cryotherapy
- mostly it's use is restricted to superficial and small nodular BCC
- lesions recurrent in scars or with aggressive histology are unlikely to respond and another modality should be
selected
(eg. morphoeic, micronodular, infiltrative, basi-squamous, perineural involvement etc)
- what can only be termed heroic freezing techniques have been used in the past on aggressive BCC's
- morbidity is huge and even then cure rates are mostly not as good as the alternatives
The typical BCC to be treated with cryotherapy would have the following characteristics
- it would be a small (<2cm) diameter lesion invading to less then 3mm depth
- it would be clinically well defined, not fixed to underlying structures and have had no previous treatment
- histology would be either superficial or nodular
- it would be on the back
- there would be no closely underlying anatomical structures of note
A poor choice for cryotherapy would be a larger lesion over 2 cm wide or 3 mm thick
- these can and have been treated but there is a drop in cure rate and the short and long term morbidity of a
curative freeze is much greater
- Dr Muir would consider aggressive histology (micronodular, infiltrative, morphoeic etc), recurrent lesions, fixation
to underlying structures, location on a free margin such as the ala to be absolute contraindications except in
extraordinary circumstances
- he would not treat a facial BCC with cryotherapy
- if you treat one arising in hair bearing skin the resultant scar will result in an area of alopecia
- if the patient is unhappy with the outcome from previous freezes he would avoid this modality
- the darker the patients skin the more noticeable the cryotherapy scar
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It is interesting that BCC's arising in radiation treatment fields heal well after cryotherapy while surgical
procedures may heal only with difficulty
The treatment regime is outlined above
- as with an IEC determining the lateral extent of these lesions can be difficult
- underestimation of its width will result in under treatment
With thicker lesions, some debulk the lesion first by curettage, this also provides an accurate determination of the
lateral extent of the lesion
- the curetted site is then treated in the standard way with cryotherapy
(iv) Squamous cell carcinoma
Dr Muir does not treat SCC's with cryotherapy
- this is by no means a universal prejudice amongst dermatologists
- the NHMRC guidelines for treatment of non-melanoma skin cancer state "SCC of low risk type can be similarly
treated by cryosurgery"
They define low risk SCC as: small, well differentiated, primary tumours, clinically well defined arising on the limbs
and trunk
- they state that histological confirmation and analysis for high risk features is essential prior to cryosurgery
- Dr Muir feels it is usually not much harder to excise a small low risk SCC then to biopsy it
- this will mean the patient only has to go through one procedure
Having said that cure rates of 95% are reported for cryotherapy of suitable SCC
- lesions which are large, less well differentiated, recurrent or arising on the head and neck are more likely to
recur
(especially lips, ears, periorbital and scalp lesions)
- treatment failure carries a risk of metastasis
- in one study around 77% of cutaneous SCC metastases arose from a primary on the head or neck
Having said that it is certain that numerous small well differentiated SCC's are treated successfully with
cryotherapy in the mistaken belief that they are solar keratoses
(v) Other skin malignancies
Cryotherapy was often used for Kaposi's sarcoma during the early days of the HIV epidemic
- they were quite sensitive to freezing requiring only a single freeze with a 3mm margin of 15-30 seconds duration
- it could be used on lesions recurrent after cryotherapy
- as expected lesions which are thin and small do best
Lentigo maligna and lentigo maligna melanoma have been treated with cryotherapy
Melanocytes are killed much more readily by cryotherapy then keratinocytes
- there are only small published series with variable follow up periods but they claim cure rates of 90% and better
- these lesions are deceptive in that they penetrate hair follicles
- this means that the freezing has to cause epilation
The recommended regime is two 30 second freezes with a 1 cm margin of normal skin
- this means that all lesions need to be treated with more then one 2 cm diameter field
- these lesions often show extensive and irregular subclinical extension laterally
- thus even with a 1 cm margin the entire extent of the lesion may not be frozen
- as these lesions characteristically occur on the face the cosmetic outcome is likely to be suboptimal
Dr Muir has never been involved in using this treatment modality for this indication
- he would only consider it after other options such as excision and radiotherapy had been deemed to be
contraindicated
- he would very carefully obtain and document informed consent
- the NHMRC guidelines for management of cutaneous melanoma do not even mention cryotherapy as an option
- having said that a lentigo maligna left untreated has a significant risk of transforming into invasive melanoma
Cryosurgery can achieve cure
<top>
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6. Complications
Cryotherapy is a destructive modality and has a not insignificant morbidity and complication rate
- having said that most patients tolerate it well and happily submit to multiple treatments over the years
- some of these effects are inevitable with the heavy freezes required for cutaneous malignancy
- for instance acute pain and oedema with resultant long term pigment loss will be seen with freezing of a BCC
with curative intent unless it is done incorrectly
- on the other hand some people experience idiosyncratic reactions to cryotherapy
- Dr Muir has had a few patients over the years who developed large bullae with only a very light freeze of a solar
keratosis
- similarly some patients seem especially prone to pigment loss
Side effects are usually divided into acute or immediate, short term or delayed and chronic or prolonged
Acute Side Effects
Short Term Side Effects
Temporary Side Effects
Permanent Side Effects
(i) Acute Side Effects
Pain is obviously inevitable
- there is a wide range of tolerance
- the pain varies in character with patients describing a burning and stinging sensation while the spraying is going
on and then a throbbing sensation while thawing
- freezing on the scalp/temple often precipitates headaches
- similarly cryotherapy of peri-ungual lesions is often poorly tolerated
- intralesional or topical local anaesthetic can be used pre-treatment and oral analgesia if needed
Syncopal reactions to the pain are by no means uncommon
- the patient should be treated in a position where if fainting does occur he (it is usually a young 'he') will not injure
himself
Bleeding can occur acutely
- especially if the lesion has been recently traumatised
- some people do a diagnostic biopsy and then freeze immediately, this can result in bleeding
- simple measures such as pressure and elevation will stem the flow
Oedema is inevitable and blistering very common with cryotherapy for skin malignancy
- obviously this effect is more marked with harder freezes
- some anatomical sites are very prone to excess swelling
- the classical site being the periorbital skin of the sun damaged
- below the knee the action of gravity results in much greater swelling then above
(this can cause delayed healing)
Vigorous freezing on the bridge of the nose can result in bilateral periorbital oedema
A hard freeze on the penis can cause so much oedema to necessitate passing a catheter
- Dr Muir avoids using cryotherapy at these sites for this and other reasons
- many patients will defer freezing till after an important social event because of this swelling
- if a tense blister arises Dr Muir leaves them intact if small but if they are getting in the way or painful draining is
indicated
To minimise swelling many apply a potent steroid ointment to the treatment site immediately post freeze
(eg. Diprosone, Elocon, Betnovate etc)
Insufflation is one acute side effect that Dr Muir has never seen but which is well described
- this complicates spray delivery of the cryogen onto broken skin such as a non-healed biopsy site or ulcer
- the gas travels through the skin above the sub-cutis
- this presents as an immediate swelling around the site
- it is most likely to complicate freezing around the orbit
- the gas resorbs over a few days without sequelae apparently
**Dr Muir was always told, when a registrar, to avoid freezing near the external auditory meatus as this can cause
a vagal response and sudden death!
A febrile reaction to cryotherapy within the first 24 hours can be seen but is rare
- when Dr Muir worked in the UK they used to occasionally admit people and treat multiple lesions simultaneously
with cryotherapy
- a fever was often seen
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(ii) Short Term Side Effects
Infection is uncommon
Bleeding can occur as the frozen tumour undergoes necrosis
- this will be seen at day 10-14 post treatment
- apparently capillaries and venules undergo intravascular thrombosis but arterial flow is maintained and it is from
these that the necrotic tumour bleeds
Excess granulation [proud flesh], pyogenic granuloma and pseudoepitheliomatous hyperplasia can
complicate freezing
- these occur during the healing phase
- when Dr Muir was a registrar he had a keratoacanthoma develop on the site of cryotherapy treated, biopsy
proven superficial BCC
(iii) Temporary Side Effects
Some long term side effects improve over time while others are permanent
- interestingly hyperpigmentation can be seen especially in people with darker skin
- it will usually fade over some months
Any blister arising at the dermo-epidermal junction can result in milia formation and cryotherapy is no exception
- these will usually disappear over time or can be treated with a variety of techniques
Hypertrophic scars can be seen especially on the nose, lip, forehead, chest and back
- it would be unusual to see cryotherapy for skin cancer on the face these days
- one can expect these scars to settle over time
- the process can be hastened with topical or intralesional steroids or silica gel dressings and other techniques
- mostly they are left to improve by themselves
Neuropathy is uncommon but well documented
- nerve tissue itself is much more sensitive to freezing than is the neural sheath
The classic site to see this complication is on the lateral side of the digits
- it is described at multiple other sites where nerves lie superficially
(the ulnar fossa of the elbow and radial wrist for instance but also the facial nerve)
Touch, pain and cold sensation can all be affected and recovery time can be very prolonged up to 18 months
- in a reported case where freezing of a wart overlying the ulnar nerve at the elbow was accompanied by
neuropathy motor as well as sensory function was affected
(the patient had pronounced wasting of muscles innervated by the nerve but did recover full function over two
years apparently)
(iv) Permanent Side Effects
As melanocytes are much more sensitive to cryotherapy than other skin cells hypopigmentation is inevitable
with skin cancer cryotherapy
- having said that people do vary a lot in their susceptibility to this side effect
- some repigmentation can occur over time
- obviously the darker the patient's skin the more obvious the area of hypopigmentation
- the stark contrast between treatment site and surrounding skin can be minimised by feathering which means
lightly spraying the margin of the treatment field
A typical cryotherapy scar after treatment of a superficial BCC some years previously
- there is an excision scar adjacent for comparison
(if you do not see hypopigmentation after freezing a BCC you have not done it properly!)
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Close up of the scars
Alopecia always complicates skin cancer cryotherapy and can occur idiosyncratically with light freezes
- as this hair loss is permanent one usually avoids treating significant lesions on the scalp or beard area
- with cryotherapy of lesions that often involve hair follicles (e.g. lentigo maligna and intraepidermal carcinoma) an
alopecia inducing freeze is a prerequisite for treatment success
Fibroblasts and collagen fibres are more resistant to freezing damage
- this means that scarring usually does not occur if the duration of ice ball formation is less then 30 seconds
- longer freeze times can result in scarring and subsequent contracture and distortion
The texts talk about ectropion and eyelid notching after treating malignancies on the eyelid margin
Similarly distortion of the lip or ala can complicate cancer cryotherapy at these sites
- it would be rare for cryotherapy to be used in these sites now
Interestingly, cartilage resists freezing damage to such an extent that a double freeze-thaw cycle can be done on
the nose or ear without creating any distortion on healing
- obviously this is not true if the lesion has invaded cartilage but cryotherapy would not be used in this instance
now
<top>
7. Contraindications
Cryotherapy is avoided with a number of intercurrent illnesses
- the presence of cryoprecipitants (cryoglobulins, cryofibrinogen) is an obvious one
- cold precipitated vascular disorders such as Raynauds or cold urticaria is another
- blood dyscrasias of unknown origin and agammaglobulinaemia are listed
- as pyoderma gangrenosum shows pathergy cryotherapy or indeed any trauma to the skin can result in a lesion
arising at the treatment site
Although aggressive and high risk lesions have been treated with cryotherapy the resultant morbidity and
increased risk of treatment failure means this modality is not used as widely as it once was
- it would rarely be used now on the face, nose, eyelids, lips or ears for malignancy
- cryotherapy below the knee carries a high risk of ulceration
- use over the lateral fingers or other sites where nerves lie superficially carries a significant risk of neuropathy
and so another modality will be used in preference
- lesions with a higher risk of recurrence such as previously treated tumours, sclerosing BCC and other
aggressive histologies, large lesions (>3cm diameter) and lesions showing perineural invasion are mainly treated
with another modality
- patients in whom the resultant hypopigmented scar is likely to be cosmetically unacceptable may be best treated
with some other therapy
Although used widely in the past on a variety of lesions, the main use for cryotherapy in skin malignancy these
days amongst most practitioners Dr Muir knows is for:
-- intraepidermal carcinoma
-- superficial and small nodular BCC on the back, upper limbs and thighs
- small low risk SCC are treated but most favour other techniques
The most important contraindication to using cryotherapy is a practitioner who lacks the training and skills to
ensure that the best modality has been chosen and that the treatment is carried out adequately
<top>
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Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 44 of 123
DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
CURETTAGE
A typical Queensland back with two superficial BCC's
They are outlined with a solid line
- some of the other red smudges you can see are also BCC's
- if you excise them all you are going to run out of skin
- this is a job for "Curette Man (or Woman)"!!
A close up
- the dotted line encloses a hypertrophic scar
A simple procedure useful in the management of a variety of both benign and malignant skin disease
Indications include;
- viral warts
- molluscum contagiosum
- seborrhoeic keratoses
- pyogenic granulomas
- solar keratoses
- intra-epidermal carcinomas
- basal cell carcinomas
- keratoacanthomas
- small well differentiated squamous cell carcinomas in non high risk sites
When used for treatment of malignant lesions it is combined with cautery
All of these lesions tend to be more friable than normal skin and so can be readily scraped away with a suitable
curette
- these instruments have an edge but are not sharp like a scalpel
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The set up:
- 1% plain lignocaine
- specimen jar
- gauze
- curette
- cautery
- skin prep
The commonest use in Dr Muir's practice is in the management of superficial BCC's on the back
Here is how he treats a superficial BCC on the back
You will need:
- a suitable skin curette
- local anaesthetic
(Dr Muir uses 1% plain lignocaine as it stings less and the cautery stops any bleeding)
- a formalin filled specimen jar for your curetted material
- surgical skin prep
(povidone iodine or chlorhexidine etc)
- remember as you will be using cautery a fire hazard exists with alcoholic prep
- gauze squares
- a cautery device
(Dr Muir uses a hyfrecator as shown)
- hot wire cautery was used traditionally
(Dr Muir still uses this if they have a pacemaker in situ)
- a dressing
(a bit of calcium alginate [e.g. kaltostat] and some micropore tape will do)
- gloves and eye protection
- an informed patient with a suitable BCC
Dr Muir's hyfrecator
- note the disposable, single use sleeve
- the tips are removed and autoclaved
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The local goes in
- note how the red smudge that is the BCC is disappearing
- always mark the site beforehand
Outline your lesion with skin marker and infiltrate with local anaesthetic
- they tend to disappear when the local goes in
- once the area is numb scrape vigorously with your curette
(personally Dr Muir thinks the secret of a good curette is; you should be able to hear a scraping noise from across
the room)
Only the tumour will spoon out
- the adjacent normal skin will remain intact
(try it and you will see)
- be sure to scrape in a number of different directions
Down to business
- note the fingers "tensioning" the skin
(this makes curettage easier)
- remember do it in all directions, vigorously so you can hear it and scrape the margin
- stop looking at the scar!
(Dr Muir will explain that later)
Now you're cooking!
- note the gauze square used to sop up any excess blood which will prevent cautery
- people often mention the smell at this stage
- Dr Muir tells them it varies with the quality of the meat being cooked!
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End result of the first cycle
- now wipe with skin prep and repeat
Then cauterise
- Dr Muir chars the margin as well
- then wipe the area down with skin prep and repeat the procedure
- this makes the second pass easier
- some texts suggest using a smaller curette for this second scraping but this is rarely done in practice
- some operators do 3 cycles of curette and cautery
(Dr Muir does not)
Apply your dressing and they can go
- the whole process rarely takes more than 5 minutes
The second curettage
- note the fresh prep, Dr Muir finds the charred material scoops out more easily if it is wet
Second curette done and ready for cautery
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Another round of cautery and almost done
The usual complications of surgery can ensue
- infection is rare
- hypertrophic or keloid scars surprisingly uncommon
- the resultant scar is usually flat, white, about the same size as the treated lesion and cosmetically acceptable
- Dr Muir tells his patients that one advantage of curettage is that if they are unhappy with the scar we can always
have the area excised and substitute an excision scar for a curettage scar
(no one has ever taken him up on this offer - maybe they've seen his excision scars!)
The end result, ready for a dressing
It is extremely useful in patients on anti-coagulants as these do not have to be stopped
- Dr Muir uses it often in his immuno suppressed organ transplant patients
- it is extremely useful in those all too common patients with multiple superficial BCC's on the back
- with this process little normal skin is lost and multiple lesions can be treated at one sitting for little cost
- Dr Muir has a patient who was exposed to arsenic and he curettes 6 intra-epidermal carcinomas from her every
3-6 weeks
(this has been going on now for over 5 years!)
All dressed up and ready to go
It is not suitable for tumours with an aggressive histological pattern
(morphoeic, micronodular, perineural spread etc)
- do not use on BCC's recurrent after previous therapy
- Dr Muir does not use it for facial or ear BCC's
(although when he was a registrar, back in the last millennium, they routinely used this technique for selected
facial lesions with good results)
- Dr Muir will use it elsewhere including below the knee
- beware of IEC's arising in terminal hair bearing skin as tumour can extend down the hair follicle and thus escape
your curette
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This a typical curettage scar, from elsewhere on this mans back
- very acceptable
Dr Muir will use it on small nodular BCC's but normally prefers excision
- the bigger the superficial BCC the lower the cure rate
- in one study, a cure rate of 98.8% was achieved for those less then 1 cm, 95.5% for 1-2 cm lesions and only
84% for lesions greater then 2 cm
- Dr Muir has treated a 7cm diameter lesion on the shoulder and 6 years on there is still no sign of recurrence
Although simple it is like any procedure dependent on tumour selection and operator technique to achieve best
results
This sort of result is the commonest, especially if they have lots of sun damage
Common Questions:
How do I know I've got it all?
- this technique has the same cure rate when done correctly as excision
(i.e. around the 90-95% mark)
- with an excision, a pathologists report of clear margins does not always mean you got it all
- otherwise the recurrence rate for excision would be zero
How will I know when to stop?
- your 'spoon' will tell you
- tissue will cease to come away as you pass from BCC into normal skin
What if I go through into fat?
- this probably means the tumour has penetrated through the dermis into fat and so you will need to get your
scalpel out and excise the area
What is the item number?
- 30196
These Stiefel curettes are good
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- single use only and very sharp
For further information have a look at the NHMRC guidelines for non-melanoma skin cancer
- http://www.nhmrc.gov.au/publications/synopses/cp87syn.htm
If you wish to gain some supervised experience with this technique please contact Dr Muir
(via Tele-Derm National on RRMEO - see below)
- although simple, training is still required
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 51 of 123
DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
DRUG ERUPTIONS
How Not to Miss A Drug Eruption
A common referral often ends with the words
"I am concerned this rash may be due to his medications"
- drug eruptions are a bit like syphilis they can look like anything
- drug eruptions are of course available to popular and unpopular alike
Rashes with a drug aetiology can exactly mimic common dermatoses such as:
- psoriasis, eczema and lichen planus
- equally they can look absolutely bizarre
- to make life difficult they can resolve despite continuation of the causative agent and then just to really mess you
up they can recur
Skin changes related to drug ingestion are many and they are by no means all related to allergy
Some are an expected part of the course of treatment
(e.g. dry skin/mucosa with isotretinoin and alopecia with chemotherapy)
- steroid acne, a typical dermatology misnomer, is a predictable complication of higher doses of prednisone
Some drugs can exacerbate pre-existing dermatoses
(e.g. prednisone, beta blockers and ACE inhibitors are able to worsen psoriasis)
- lithium can make acne, lupus and psoriasis flare
Others may be a manifestation of incorrect dosage such as:
- purpura with anticoagulation
Some individuals have an inherent susceptibility to drug side effects
for example:
- procainamide induced lupus is more common in slow acetylators of n-acetyltransferase
Prolonged use of a drug can result in skin and mucosal discoloration
for example:
- minocycline and hydroxychloroquine
Drug induced phototoxicity causing a sun burn like reaction requires a sufficient dose of both medication and drug
to occur
- so a Victorian teenager on doxycycline may only have problems when his family holidays in Noosa
Drug induced mast cell degranulation by non-immune mechanisms can result in urticaria and itch
- the classic culprit being aspirin
but other agents include:
- alcohol, opiates and tubocurare
Antibiotics can allow the overgrowth of non-sensitive organisms resulting in vulval candidiasis
The Jarisch-Herxheimer reaction,
characterised by:
- fever
- adenopathy
- arthralgia
- urticaria
- and exacerbation of existing lesions
is seen with antibiotic therapy for:
- syphilis
- systemic treatment of tinea
- and of course onchocerciasis
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Patients with infectious mononucleosis will get an ampicillin induced eruption but can be usually re-exposed with
no problems
None of these are allergic reactions
Drug induced allergic reactions seen in the skin include;
- urticaria
- angioedema
- immune complex vasculitis
- morbilliform drug eruptions
- lichenoid
- photoallergic
- photolichenoid
- fixed drug
Acute generalised exanthematous pustulosis is particularly dramatic and toxic epidermal necrolysis is of course
threatening to health, life and sight
Suspect a drug aetiology whenever someone has a sudden onset of a new eruption or a deterioration in a preexisting skin condition
Certain clinical scenarios increase the chances of a drug eruption occurring
e.g. higher starting doses are associated with an increased drug eruption risk with:
- minocycline
- lamotrigine
- phenytoin
Concurrent medications can increase the risk of a severe reaction such as
- Stevens Johnson syndrome [SJS] and toxic epidermal necrolysis [TEN]
Starting lamotrigine in a person on sodium valproate or any SJS/TEN associated drug in a patient on
corticosteroids increases the chances of these severe drug eruptions
- patients with renal or hepatic impairment are more likely to react to allopurinol when started at normal doses
- patients with HIV / AIDS, lymphoma or SLE have a higher incidence of drug eruption
The two big challenges in managing drug eruptions are:
- firstly realising the problem has a drug aetiology and
- secondly working out which medication is responsible
(i) The first can be at least partially addressed by always including drugs in your differential diagnosis
(ii) The second is harder, here is why:
- drug histories are notoriously inaccurate
- patients commonly do not remember all the medications they ingest
- ask specifically about prescribed, non-prescribed, borrowed, 'natural' (oh it can't be that, it's natural), tonics, over
the counter and especially intermittent drug use
- drugs used for period pain, swollen ankles, migraines etc are often used when needed and forgotten when a
history is taken
- do not forget immunisations and radiological contrast
(iii) Illicit drugs need to be considered
for example:
- anabolic steroid use and acne
- there is a recent report of guttate psoriasis precipitated by 'ecstasy'
- whether it was the drug itself responsible or an unidentified contaminant is unknown
- if you do not specifically ask this information will not be volunteered
Ask about recently ceased medications as drug eruptions can begin after an agent has been stopped and can
extend and worsen after drug cessation
- even then drug histories dribble out over weeks
Do not believe the computer generated print out from another doctor
- it may be out of date and include drugs they no longer take or have never taken and often leaves out recently
prescribed medicaments or the ones prescribed elsewhere
The exact time course is desirable but often unobtainable, the term 'ages' can signify any period of time from
more than a week to decades
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It is not always the new drug that is the culprit
- lichenoid drug eruptions often do not occur for months after commencing the agent and equally they can take a
long time to resolve after cessation
- photosensitive drug eruptions may not be triggered till the patient gets enough light exposure
- witness the Victorian tourist
Anaphylaxis occurs within minutes of exposure,
- IgE mediated urticaria and fixed drug eruption within hours
- angioedema to ACE inhibitors can occur within minutes to years after first exposure
- exanthemas and SJS/TEN take days to a few weeks usually
(occasionally TEN can occur after months or years of exposure to the causative drug)
- drug induced lupus can have it's onset years after commencement
- there is considerable overlap and the time course will be at best a rough guide to causality only especially in the
all too common state of polypharmacy
Having said that most drug reactions are due to agents commenced within the last six weeks
A condition known to be caused by drugs may have a host of other causes
for example:
- erythema multiforme and erythema nodosum have drugs as one of multiple possible aetiologies
Drug induced lupus uncommonly has skin manifestations but will be clinically indistinguishable from typical LE
- similarly lichen planus induced by a drug may be indistinguishable both clinically and histologically from the 'wild'
form
Patients history of drug allergy is often inaccurate,
- witness the number of people 'allergic' to penicillin who fainted after an IMI injection
- or their morphine 'allergy' makes them sleepy
- or their erythromycin 'allergy' causes nausea
If they say they are allergic to drug 'x' always inquire as to the nature of the 'allergy'
- this is important due to the possibility of cross reactivity to current medications or even re-exposure to the same
drug
Having said that, it would seem that sulpha based drug cross reactivity and that between cephalosporins and
penicillin's is not nearly as frequent as once thought
- if however a person has TEN Dr Muir would not risk re-exposing them to any drug related to the triggering agent
To get an accurate history may mean combing through hospital records and talking to relatives, pharmacists and
doctors
Precisely characterising the reaction type may help you identify which of multiple drugs the patient is on is causal
- then again it may not with the patient being on a multitude of possible offenders
Individual drugs can be associated with a host of different skin reactions
Thiazide diuretics can cause:
- urticaria
- fixed drug eruptions
- Sweets syndrome
- vasculitis
- exanthematous drug eruptions
- erythema multiforme
- photoallergic and phototoxic reactions
- drug induced lupus
- erythema nodosum and TEN
If a patient is on more then one agent known to cause their drug reaction it isn't necessarily the most common
aetiological agent nor the most recently started drug responsible
There is no single test which will reliably diagnose a rash as being drug related or identify the culprit
- the diagnosis is mainly clinical and identifying the likely culprit relies on classifying the type of reaction and
determining the likelihood of which drug is responsible from the time course of use and the type of reaction
- unfortunately biopsies are often non-specific and the pathologist will not be able to see 'frusemide bodies' or
'phenytoin inclusions' to give you the causative agent
- also many drug eruptions share a similar histology
- lupus, lichenoid, lichen planus like drug eruptions and erythema multiforme all show lichenoid changes under the
microscope
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How Not to Miss A Drug Eruption
- include drug eruption in your differential of any rash seen
- take an accurate, comprehensive drug history
- determine what type of drug eruption the patient has
(this is done mainly on clinical signs rather then biopsy)
- from the time course of their medication use, the type of drug eruption and past history determine which drug is
most likely to be responsible
- be prepared to reconsider your diagnosis of both the nature of a rash and why it has occurred
- the number of drug eruptions on tele-derm is slowly increasing
- hopefully these will aid you in managing your own patients
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 55 of 123
DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
EFUDIX - A USERS GUIDE
How Does Efudix Work?
Side Effects
When Should I Use Efudix?
When Shouldn't I Use Efudix?
What Should I Do Before Using Efudix?
How Do I Start Efudix?
Special Areas
Efudix and Intraepidermal Carcinoma (IEC)
What about Methotrexate and Efudix??
Efudix Images
There is a host of ways to treat solar or actinic keratoses
- as usual with any one condition which has multiple treatments none are perfect
- an extremely useful modality is 5% 5 fluorouracil cream
- in Australia we have only the one brand 'Efudix'
(at the time of writing)
- Dr Muir will therefore use this term from now on
There are new formulations available overseas
Efudix is part of a group of treatments known as ‘field therapies’
- these are used to treat a wide area of solar damaged skin which contains multiple solar keratoses
- these differ from spot treatments such as cryotherapy or surgical removal, which treat one individual lesion at a
time
- the advantage of field therapies is that they treat sub-clinical as well as obvious solar keratoses at the same time
- in the main, they are much less likely to cause scarring or pigment disturbance, than cryotherapy
Other field therapies include;
- topical tretinoin
- topical keratolytics
- topical imiquimod (Aldara) cream
- a variety of chemical peels
- CO2 laser resurfacing; and
- photodynamic therapy
Other treatments may become available soon
- for example: topical diclofenac cream
1. How Does Efudix Work?
It is a structural analogue of thymine with fluorine replacing the 5-methyl group
- it is incorporated in RNA and blocks thymidylate synthetase and hence inhibits DNA formation
- this of course results in the death of a dividing cell i.e. it is cytotoxic
Interestingly, 5 FU was and is used systemically in the treatment of various malignancies
- in 1963 it was noted that sun damaged people, receiving the drug intravenously, developed inflammation and
subsequent clearing of their solar keratoses
- Dr Muir has seen a number of people over the years get substantial clearing of their solar keratoses after
systemic treatment of a malignancy
Dose ranging studies using concentrations from 0.5-20% were done with varying periods of total application time
- it was found from these that 5%, twice daily in a cream base for three weeks, was optimal as far as balancing
results with side effects
The major side effects of its use are inflammation and irritation
- interestingly, when applied to the skin, often only the solar keratoses themselves will become inflamed
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- it has been shown that the drug penetrates abnormal skin more readily then normal
- presumably the numbers of mitosing cells are higher in a solar keratosis and hence cell death and subsequent
inflammation will be greater also
- having said that, the exact cause of the inflammatory reaction is unknown
- evidently, despite the lack of inflammation clinically, ultrastructural changes are seen in skin that appears
unaffected
2. Side Effects
The main side effects are:
- local irritation
- inflammation
- itch acutely
Dr Muir is always surprised by how well most people tolerate it even with very severe inflammation
- ulceration can develop
- crusting can be a problem
In the long term they can develop hyper or hypo pigmentation
- telangiectasias are a known side effect and Dr Muir has seen them on a few occasions
- allergic contact dermatitis is well documented although he has never seen a case
- photosensitivity is seen also
- presumably a clue to this would be a severe reaction everywhere the cream is applied not just the solar
keratoses
- of course many Queensland patients are basically wall to wall sun spot and will develop wall to wall inflammation
Management of these effects is usually simple
- most people seem to settle without any need for treatment
- if very inflamed some topical steroid can help
- Dr Muir uses 1% hydrocortisone, desonide lotion or on occasion more potent steroids depending on the severity
of the symptoms and signs
- this can be combined with cool, wet compresses and bland emollients
(e.g. emulsifying ointment)
Nail loss and nail dystrophy are reported but these are mainly a complication of use of Efudix on the nail area
Only 6% of an applied dose is absorbed systemically
- as expected absorption is higher from abnormal than normal skin
Systemic side effects include:
- nausea
- stomatitis
- diarrhoea
- bone marrow suppression
- hair loss
cardiac/neurological toxicity
This is extremely unlikely with topical use but explains why the product information advises not treating an area
greater then 500 square centimetres
(23x23 cm)
- there have been only seven reports of possible systemic side effects with efudix, mainly marrow suppression
- considering the amount of efudix used this statistic reflects very well on its safety
Dr Muir found an interesting case report out of Israel of a woman who developed angina after applying 5 FU
cream to a forehead BCC
- re challenge resulted in recurrence of the chest pain
- interestingly (and Dr Muir says) bravely, they carried on but used a nitroglycerin patch before application and
completed a month of treatment
(Int J Cardiol 1995 May; 49(3) 282-3)
3. When Should I Use Efudix?
Dr Muir tends to avoid using it in summer
- this is not so much for the photosensitivity but rather for the patients comfort when dealing with extremely
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inflamed facial skin
- itch will be greater in summer
- hopefully, use in winter will lessen the risk of post-inflammatory hyperpigmentation
Dr Muir will use it occasionally in the hotter months on the scalp as they can wear a hat or cap and the degree of
symptomatology is generally much less
4. When Shouldn't I Use Efudix?
There is an extremely rare autosomal codominant syndrome which results in deficiency of the enzyme
dihydropyrimidine dehydrogenase
- 3-5% of the population is heterozygous for this
- this enzyme metabolises most of absorbed 5 FU
- if deficient in DHD toxicity can result especially with systemic use
- there is a case report of a DHD deficient patient who developed life threatening systemic toxicity with topical 5
FU
- the patient was homozygous for the gene and had diarrhoea, stomatitis, rash, neutropenia and
thrombocytopenia
- with cessation of the 5 FU recovery was complete
- this is not screened for by anyone but obviously with documented deficiency of the enzyme should avoid 5 FU
Obviously allergy to 5 FU itself or the excipients (parahydroxybenzoate, propylene glycol, stearyl alcohol) in the
cream will preclude use
Pregnancy is an absolute contraindication obviously
- Dr Muir tells his male patients not to get anyone pregnant while using it either
(pretty hard to when you think of what their skin looks like!)
He avoids it in summer
- use on already inflamed skin can be difficult
- for instance people with facial rosacea or seborrhoeic dermatitis may not tolerate it at all
- Dr Muir has seen rosacea flare badly with this
He would be rather nervous about using it in patients with a history of post inflammatory hyperpigmentation
5. What Should I Do Before Using Efudix?
The typical patient will be a sun damaged individual over fifty with multiple facial solar keratoses
Dr Muir does the following;
- complete a full skin check
- biopsy and treat any lesions suspicious for skin malignancy in the proposed treatment area
- discuss the treatment options with the patient including the various efudix treatment regimes
(i.e. pulse dosing, segmental treatment etc)
- show them photos of what to expect when using efudix
- warn them about the potential side effects
- warn them of the limitations of treatment
- give them a brochure on the therapy and arrange review
- if at review they are happy to go ahead he starts treatment than
- he rarely starts treatment at an initial consultation
- due to the severity of the inflammatory reaction informed consent is vital
- the patient needs time to consider the pros and cons of the various treatment options
6. How Do I Start Efudix?
Dr Muir has an Efudix season stretching from late April through to the end of October
- the treatment is much better tolerated in these cooler months
- he explains to his patients that it takes some years to develop solar keratoses so a few months won’t matter
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Dr Muir uses a variety of regimes
- every dermatologist he has ever spoken to about this topic has their own regime
- typical approaches include the following:
(i) With a stoical patient, especially one who has used efudix before, Dr Muir will use it twice a day to all the skin
of the face
- he will review at two weeks
- depending on the degree of inflammation seen he will then determine how long to keep going
- occasionally they are very inflamed at two weeks and he will stop then
- in most cases he will keep going for the full three weeks and rarely, if there is little reaction, 4 weeks or more
(ii) Dr Muir tells the patient to apply the cream to all the affected skin not just the visible keratoses
- that way they will pick up clinical and sub-clinical lesions
- if they are concerned by the level of inflammation, they can reduce the frequency of application or stop
altogether and call me
- we can always recommence after all
(iii) With a ‘nervous’ patient or one with a lot of solar keratoses Dr Muir will use pulse therapy
- this is where one applies efudix twice a day two days per week
- the other five days are treatment free days
- if they get too inflamed they can apply some topical steroid ointment on the non-efudix days
- they should apply the efudix on those days when they will be getting the least amount of sun
For instance:
- if they play cricket on Sunday he gets them to apply it on Monday and Tuesday thereby minimizing the amount
of inflammation when they are outdoors
- ideally of course they would avoid sun exposure altogether
Dr Muir will keep this up for 6-16 weeks depending on how they go
- he warns them that the clearance rate with this may well be lower then with the ‘usual’ b.d. for three week
regime
- they are reviewed at fortnightly intervals to see how they are getting on and treatment may be modified
according to response
- you will see studies stating this technique does not work
- there are others that say it does
- Dr Muir finds it useful
(Muir anecdote)
(iv) Oftentimes Dr Muir will start with ‘pulse therapy’ but at review the patient will have decided it is not so bad and
then increase to the standard regime
(v) Another treatment is to start with a pulse regime and then as the individual sun spots light up just treat them
twice daily with no cream applied to the intervening skin
- this is a technique Dr Muir uses when patients have a co-existent inflammatory dermatosis such as rosacea or
seborrhoeic dermatitis
(vi) There is a study where they used efudix till the lesions became inflamed
(i.e. about a week and then froze them with liquid nitrogen)
Dr Muir feels that seems like an odd approach
- good results were claimed
- a US dermatologist uses efudix for a while and then does a chemical peel
- she claims good results and less morbidity
(vii) There are other described techniques;
- once daily for four weeks only
- two cycles of treatment some months apart b.d. for two weeks each
- cosmetic unit treatment
i.e. only doing a single cosmetic unit of the face at a time
(e.g. the forehead, and then once that has settled, the cheeks and later the nose)
Dr Muir does this a fair bit
- especially with bald men
- the scalp is done first, then the forehead and later the cheeks
- they are allowed to fully recover from one treatment before starting the next
- this is useful as it allows the patient to get an idea of the side effects before using it on the more sensitive facial
skin
Another interesting regime is:
- daily for seven days followed by 2-4 weeks rest
- then daily for two weeks with 8 weeks rest
- finally b.d. for two weeks
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The idea being that with this method the severity of the final reaction will be much less
(Dr Muir has not used this method but it seems logical)
As can be readily seen there are numerous published regimes and probably a lot more unpublished
- most of the alternate regimes to b.d. for 3-4 weeks are trying to achieve efficacy without preventing people from
living their normal lives
As with most things in dermatology the more inconvenient the treatment the better it works
- the greater the inflammatory response the better the therapeutic and cosmetic result
As stated previously Dr Muir is very flexible with efudix
- if a few solar keratoses slip through the net does it really matter?
- we can always go back and get them later!
If in doubt or with an anxious patient start ‘low and slow’
- in other words do a small area of less sensitive skin
(i.e. the forehead rather then the cheeks and use two day a week pulsing)
- review at two weeks and modify the treatment as the situation demands if needed
7. Special Areas
The Bald Scalp
The Forearms
The Lower Lip
The Bald Scalp
Efudix is very useful here especially as freezing and photodynamic therapy are often poorly tolerated
- if the keratoses are thick shave off the thicker ones and soften up the rest with a keratolytic
- Dr Muir uses 40% propylene glycol in sorbolene or aqueous cream b.d. for a month or two prior
- then you will usually get away with twice a day for 3-6 weeks depending on response
The Forearms
Efudix never seems to work as well off the face as on it
- the forearms will certainly light up with treatment but Dr Muir has always found the eventual results disappointing
compared to the face or scalp
- most suggest going for a lot longer duration
The Lower Lip
This is popular with some dermatologists as a cheap alternative to CO2 laser for actinic cheilitis
- most use b.d. for 2 weeks
(Dr Muir finds people cannot tolerate it)
- great results are claimed however
As with all efudix treatments but especially on the lip it is vital to exclude SCC prior to treatment
- if they have a history of herpes they will need to be covered with an oral anti viral
8. Efudix and Intraepidermal Carcinoma (IEC)
This medication has long been used in the treatment of IEC
- there is a surprising lack of published trial work documenting its efficacy however
- Dr Muir uses it routinely in selected patients
- it is especially useful on the face and lower limb
- cosmetic results are excellent and healing is not a problem
A usual treatment is 4-12 weeks b.d. depending on response
- they need to be reviewed during therapy and followed for at least two years after
Dr Muir does not use it where there is probable extension down terminal hair follicles
- he would not usually use it in an IEC recurrent after surgery or cryotherapy
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There are trials demonstrating efficacy in superficial BCC with b.d. application for 6 weeks
- it is not licensed for this indication here but is in the USA however
- Dr Muir has never used it for BCC
9. What about Methotrexate and Efudix??
Dr Muir is often asked whether you can use topical efudix in a patient on methotrexate
- the product information states that ‘methotrexate………may interfere with efudix’
Dr Muir has written to the manufacturers and they state that 'they are going to take this out of the product
information'
- the interaction is seen when both agents are used systemically
- the manufacturers state that there is 'little or no evidence of an interaction when efudix is used topically as so
little is absorbed'
- there are two case reports only apparently
- the manufacturers consider the interaction clinically insignificant
As can be seen, efudix is a useful treatment for solar keratoses and selected intraepidermal carcinomas
- what regime you use will depend on many variables
These include:
- the area to be treated
- the patient’s skin type
- the degree of solar damage
- the patient’s occupation
- the climate
- the patient's past experience with the preparation
- the severity of the reaction and so on
Good results can be achieved but side effects are seen
- follow up monitoring of the patient under treatment is essential
10. The following images illustrate the points made
Efudix Images
Face
Scalp
Forearm
Eyelid IEC
Neck IEC
Forearm IEC
Nail Fold IEC
Lip
Philtrum
Nasolabial
Efudix Crust
Too Much Efudix
Face
A moderate reaction after two weeks of b.d. application of efudix
- note the characteristic sparing of skin adjacent to the inflamed solar keratoses
- we continued for a further week
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Scalp
This is a typical scalp about three weeks into treatment
- the large numbers of inflamed solar keratoses illustrate the futility of trying to treat with liquid nitrogen
(where do you stop spraying?)
- inflammation on the scalp is usually less than on the face
- mostly it is also better tolerated
It is always possible to get a confluent erythema as on this scalp
- this patient was only using the cream over the temples
- he suffered little discomfort and completed the course of treatment with a good outcome
This was after three weeks of b.d. efudix
- time to stop
The same area a year later
- a nice result
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Forearm
This is a forearm after three weeks of treatment
- the patient had a total of six weeks therapy but results were disappointing as far as clearance went
- she tolerated it well and there was no pigment disturbance
Eyelid IEC
This is an IEC of the eyelid with adjacent hidrocystomas
- this is not a case for efudix
- at this site you really want a cure as there is only so much eyelid to go around
- this was treated with margin controlled excision
Neck IEC
This is a biopsy proven intra epidermal carcinoma on the neck of an elderly man
Options for treatment include:;
- excision
- curettage
- cryotherapy
- topical imiquimod
(it is not licensed for this as yet in Australia)
- photodynamic therapy
- radiotherapy or efudix cream
Excision would be difficult as the margins are indistinct and the lesion is quite broad
- a graft may well be needed to effect a repair
- curettage and cryotherapy would leave a hypopigmented scar with a lot of short term morbidity
- topical imiquimod is more expensive then efudix as is photodynamic therapy
- radiotherapy would be logistically demanding as well as concerns over proximity of the thyroid gland
- Dr Muir decided to use efudix b.d.
You must obtain informed consent before embarking on this treatment
- prolonged follow up is essential
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At review two weeks later
- this illustrates the fact that IEC's do not arise from 'virgin' skin
- there will be solar keratoses and probably foci of IEC adjacent
- with a field therapy these can be incorporated in the treatment area with minimal extra expense or morbidity
- within the area you can see scars from previous cryotherapy
Nail Fold IEC
This is IEC of the nail fold
- this is a difficult problem as the IEC can extend widely including onto the inferior aspect of the nail fold
- Dr Muir would be wary of field treatments although he has seen it done
After treatment a beautiful result
- the marking tattoo can be seen for his radiotherapy
- this finger belongs to the man with the central lip IEC treated with efudix
Forearm IEC
A biopsy proven IEC on the forearm of a man in his fifties
- histology demonstrated intrafollicular extension
- it had been frozen in the distant past also
- this can easily be excised and the presence of follicular extension and previous ablative treatment mean that
field therapies are unlikely to work
( eg. efudix, aldara, photodynamic therapy)
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Lip
(i) Before treatment
- small solar keratoses on the upper lip
- not a good area for cryotherapy as high risk of white marks
(ii) Two weeks of b.d. efudix
- minimal inflammation
- we pushed on and reviewed at four weeks
(iii) 4 weeks of b.d. and now it is time to stop
- looks sore but she still manages a smile!
(iv) The same area about a year later
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Philtrum
(i) A biopsy proven IEC over the central upper lip of a man in his sixties
What are your treatment options?
- excision would leave a difficult repair
- cryotherapy or curettage would be cosmetically poor
- radiotherapy would result in hair loss as would freezing if done properly
- as it is in hair bearing skin there is a possibility of intrafollicular extension of the IEC
- this means field treatments such as efudix, aldara or photodynamic therapy may not treat the follicular
involvement
After much discussion we decided to use efudix
- biopsy had not shown any follicular extension
(for what that is worth)
(ii) This is the same area after three weeks of efudix
- inflamed and crusted but not bothering him too much
- in a patient with a history of herpes labialis you may want to cover with an oral antiviral
(iii) The same area about a year later
- an excellent cosmetic result with no sign of any IEC
- he is now four years post treatment and remains clear
- Dr Muir would not use this treatment in a patient likely to be lost to follow up
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Nasolabial
It is quite common to see a more severe reaction in the naso-labial groove then elsewhere
- this image also shows how one often sees confluent erythema rather then the more usual mix of spared and
inflamed skin
- this will settle by itself or you could prescribe some topical steroid
- Dr Muir would usually use desonide lotion in this situation
- cool, wet compresses are also useful
This is the same area a few months later
- a very nice result
Efudix Crust
(i) A typical sun damaged forehead in an elderly bald man
- a good indication for efudix
(ii) Three weeks into treatment this patient presented with the changes seen
- this is just adherent crust and was scraped off with a wooden spatula after applying a wet compress for 20
minutes
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(iii)The same forehead immediately after scraping off the crust
(iv)The end result three months later!
Too Much
This is a forehead of an elderly gentleman who kept using efudix for 6 weeks
- there is significant erosion
- he should have been reviewed at two or three weeks but wasn't
- he probably continued for about two weeks too long
- amazingly it did not bother him too much
Dr Muir would take swabs and get him to apply saline compresses four times a day
- if culture was positive then oral antibiotics might be needed if he failed to improve
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ITCH IN THE ELDERLY
'I'm Old and I'm Itchy'
Causes
Ix
Tx
What are you going to do about it?
A number of studies have claimed that itch is the most common skin complaint of those over 65.
The second may well be dry skin aka xerosis which is of course a very common cause of itch.
As the proportion of over 65’s is only going to increase this is a problem that will be seen more and more.
What are the two most important things to know when evaluating an itchy elder?
- is there an associated rash?
- is the itch localised or generalised?
Obviously those patients presenting with a rash that itches present less of a diagnostic issue
Common itchy rashes in the elderly include but are not limited to;
- endogenous dermatitis
(atopic, seborrhoeic, nummular, pompholyx)
- psoriasis
- contact dermatitis
(allergic and irritant)
- tinea
- scabies
- venous insufficiency dermatitis
- mycosis fungoides
- bullous pemphigoid
- other autoimmune blistering disorders
With these the approach is simple as resolution of the rash will be accompanied by resolution of the itch in the
vast majority
- diagnosis of the eruption can usually be made on clinical and/or histological grounds
- most are amenable to therapy
Difficulty increases with itch that is unaccompanied by a rash
(i) localised itch without rash is most common with nostalgia paraesthetica and brachioradial pruritus
(ii) the latter affecting the outer aspect of the upper limb whilst the former hits between the shoulder blades
(iii) localised itch can complicate other diverse neurological pathologies such as:
- strokes
- brain tumours
- brain abscesses
- multiple sclerosis
- transverse myelitis
- diabetes
Causes:
The list of causes of generalised itch without rash is long and getting longer
The classics are:
- renal, liver or thyroid dysfunction
- iron deficiency
- myeloproliferative disorders
(esp. lymphoma, myeloma, polycythaemia)
- solid malignancies
Others that people forget to think of include:
- HIV
- dermatomyositis
- medication induced itch
- anorexia nervosa
Don’t forget psychiatric disease:
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- the patient with a delusion of parasitosis may not admit to it
Physical urticaria's may not have a rash at presentation but cause itch
(e.g. dermographism and pressure urticaria)
Aquagenic pruritus is usually recognised as such by the victim
There are conditions that will usually give some form of visible skin changes but occasionally don’t such as:
- scabies (especially if previously treated)
- fibreglass dermatitis
No cause may be found
There is a theory of an age related sub-clinical neuropathy that results in itch
So how to manage an older person presenting with itch but no rash?
As with all aspects of medicine an accurate diagnosis is essential
Step 1 - is a thorough history
An itch history is basically the same as one for pain
So we want to know:
- when and where did it start?
- how bad is it?
- does it wake you from sleep, stop you from working etc?
- when do you get it and does anything bring it on?
- are there any recognisable relieving or exacerbating factors?
- what comes in contact with your skin?
( this includes their ‘skin care’ regime as well as exposure to irritants etc.)
- treatment to date and their effect
(it is very important to find out what they have used in the few days prior to presentation especially if potent topical
or systemic steroids as this may obscure any clinical features)
- past medical history
(especially of any conditions known to be associated with itch and risk factors for same)
- family history
- medications including:
-- prescribed
-- non-prescribed
-- borrowed
-- otc
-- natural
-- systemic
-- topical
-- inhaled
It is vital that this is taken accurately
- do not believe the referral letter especially if computer generated
(typically these include drugs they are not on and omit ones they are taking)
- alcohol and tobacco and illicit drug use
(remember the flower child of the sixties is now in their 60’s or older!)
- anyone at home itchy?
- any possible contacts with itchy people?
- social situation
- exposure to animals
(never cease to be amazed by how rare it is for people’s own dogs or cats to have fleas - all do of course)
- risk factors for any of the myriad of possible causes of itch without rash
- a careful systems review
All aspects of the history need to be taken with the list of possible causes of itch in mind
To illustrate
- the itch of renal or liver failure is usually insidious in onset compared to the acute onset of scabetic itch or a drug
cause
- a common error is to equate nocturnal exacerbation with scabetic infestation
- as with pain most itch is worse at night when the distractions of the day are gone
On a similar note
- just because itch is worse after a shower it does not mean that the diagnosis is one of aquagenic pruritus
Raised temperature
- will make the itch of eczema or indeed most aetiologies worse
(it is said that xerotic skin is typically more itchy after exposure to water)
Cervical or thoracic spine arthritis is associated with
- brachioradial pruritus and nostalgia paraesthetica respectively
Risk factors for causes of liver disease or internal malignancy etc are many but worth seeking.
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Simply asking the patient what they think is causing their itch may be revealing especially if they respond with
‘well I think it is bugs’
By the time you have taken a comprehensive history you may well be none the wiser.
A careful physical examination is essential
This includes checking:
- all the skin and the scalp
- mucosa
- nails etc.
Male genital skin is commonly involved in scabies
- a full physical examination can’t hurt
Obviously if systems review reveals anything suggestive of underlying disease these should be looked for.
A history of night sweats and weight loss should trigger a search for:
- lymphadenopathy and organomegaly
Don’t miss
- an enlarged thyroid etc.
Secondary changes from scratching (erosions, lichenification etc)] can obscure the underlying picture.
Scratching changes will be absent or at least far less prominent on inaccessible skin such as the central back.
Some rashes are intermittent and won’t be apparent on the day e.g. urticaria.
Dermatographism can be demonstrated by scratching the back with a blunt object.
Scabies can have very little in the way of rash or be so obscured by scratching and gouging that the diagnosis is
not considered.
(if they have been recently treated finding a mite or a burrow can be very tricky)
Typically by the time you get to the end of this process the diagnosis will be either easily made or utterly obscure
- this latter outcome is most likely in the previously well elderly patient with no visible rash
Often all that will be found is that the patient has generalised dry skin
- if so it is reasonable in the absence of any other suspicious features to treat this with emollients and soap
avoidance and see what happens
- if the itch resolves no further investigation is needed
All too often they are either not all that dry or have not been helped by moisturiser.
Then what?
If there is no rash to be found then biopsy is not indicated
- however it just might help if there is any rash at all
- it is often good for public relations also
('You’ll never believe it doc but my first dermatologist didn’t even do a biopsy and my friend said that her doctor
fixed her after a skin biopsy')
Ix:
Given the range of possible underlying causes there are clearly a heap of investigations that could be ordered
Although renal and liver disease commonly cause itch without a rash it is extremely unusual for this symptom to
be the presentation
- typically these patients are already known to have the disease
In the usual case of itch without rash where the above has failed to yield any clues to a cause order the following;
(i) FBE
- which will pick up or at least hint at myeloproliferative disease, anaemia, polycythaemia, maybe iron deficiency,
perhaps HIV (if you are lucky)
- Eosinophilia may be seen with scabies, pemphigoid, bowel parasites etc.
(ii) U and E’s / LFT which will exclude:
- renal and liver problems
- perhaps diabetes
(although this is not a cause of generalised pruritus)
- hypercalcaemia
(iii) ESR may be elevated in all sorts of conditions including:
- myeloma
- malignancy
- occult infection etc.
(remember the normal range in the elderly is a lot higher)
(iv)TFT can pick up:
- sub-clinical thyroid dysfunction
(v) Dr Muir might do an EPP
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(vi) also an IgE level if he suspects adult onset atopic dermatitis
(vii) chest x-ray for lymphoma or cancer
Other tests are guided by what is found on history and examination
- age appropriate cancer screening should be considered
- how long and hard you look will be determined by suspicion based on history, examination, test results and
severity/persistence of the symptom
- a lot of patients will have no cause found despite careful history, examination and lots of tests
(it is worth following them and re-evaluating especially if new symptoms develop)
- Dr Muir was always taught that the itch of Hodgkin's lymphoma can precede the diagnosis by years
(one study he read suggested that up to 10% of patients will eventually reveal a cause after initial negative
screening - the absolute figure does not matter when dealing with an individual)
A usual case referred to him will be an elderly patient with multiple co-morbidities taking numerous medications
- they will have dry skin and loads of changes secondary to scratching, rubbing and gouging
- they will have tried a number of different treatments usually including some half hearted scabies treatment
- there will be no definite evidence of a primary dermatosis and nothing on history to pin your hopes on
- blood tests might reveal a bit of renal compromise but it is usually long standing
- a monoclonal gammopathy of uncertain significance is also not rare
(the haematologists only monitor these anyway)
- biopsy will show excoriation or lichenification only
Tx:
Dr Muir's approach is to treat the complications of scratching with:
- emollients
- wet wraps
- and potent topical steroid ointments often under occlusion
- scratching alone triggered by a systemic cause of itch can result in eczematous changes in this patient group
- if the itch persists after resolution of a rash it is worth looking for a systemic cause
(Dr Muir suggests admission especially in the very old without home support - he re-examines on several
occasions and re-investigates as prompted by events)
It is worth remembering that multiple causes may be contributing to a patients complaint of itch
i.e.
- dry skin
- renal compromise
- their medications
- what they are applying to their skin
- a bit of iron deficiency and hypothyroidism
- some depression
- poor sleep
(any symptom is harder to cope with if you are sleeping poorly)
In the all too common patient where itch remains a problem despite treatment of secondary changes and
exclusion / treatment of underlying causes the following measures can be considered:
(i) Continue emollients but avoid allergens especially perfumes
- use the greasiest they will tolerate
- cheap is better as quantity is the main determinant of efficacy
- aim at slightly oily skin
(ii) Avoid anything that will dry the skin - i.e.
- long hot baths / showers
- soap
- shampoo
- degreasers
- petrol
- frictional irritants etc etc.
(these patients will often have active lives and hobbies that may expose them to irritants)
(iii) Internal heating dries out the skin
(iv) Antipruritic's
(a popular one being 1% menthol in aqueous cream)
- avoid topical antihistamines
(steroids won’t help in the absence of inflammation - although Dr Muir does have luck with them in brachioradial
pruritus, anecdote!!)
(v) Avoid sedating oral antihistamines as they really only help through sedation and this can be a big problem in
the elderly
- a trial of a non-sedating one can be tried but don’t hold your breath
(vi) The experts always mention capsaicin for localised itch but Dr Muir says he has yet to see it work
- people stop due to the symptoms
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(vii) Dr Muir has used a TENS machine in nostalgia paraesthetica with success
(viii) UVB phototherapy is safe and certainly can benefit renal failure itch and urticaria etc.
(it is worth a shot in idiopathic)
(ix) Anecdotes and small studies abound using agents such as:
- amitriptyline
- cyclosporine
- doxepin
- paroxetine
- anti-epileptics
- gabapentin
- thalidomide and others
(Dr Muir remains to be convinced and would apply the principle of ‘primum non nocere’)
(x) The opioid antagonist naloxone has been used
- the mechanism of action thought to be by blocking the inhibition of itch suppressing fibres by endogenous
opioids in the spinothalamic tract
(it has been used in all sorts of itchy skin)
A difficult problem and unfortunately all too common. Having said that most can be managed by:
- looking for and treating the underlying cause
- reversing and preventing recurrence of xerosis
- treating any inflammatory component; and
- keeping the patient under review
The patients Dr Muir has had where a serious underlying cause has been found and where treatment resulted in
the resolution of the symptom were of a different degree and character to those where mere xerosis was
responsible.
(a significant minority remain a diagnostic dilemma but happily can usually be controlled symptomatically)
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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MARINI SUTURE
Dr Muir's surgically orientated colleagues advise using sub-cutaneous sutures when closing a surgical defect
- these supply the strength to your repair and so reduce the risk of tram tracking (see image 1and 2) and wound
dehiscence
- they also reduce stretching of scars as they provide support after surface sutures are removed and the healing
process is still ongoing
This is a simple running suture used to close a leg wound
- it was done without any sub-cutaneous support
- the operator has used a thickish calibre (4/0) and left the stitch in for 2 weeks
- thus all the tension is taken up by the wound surface
- the inflammation seen is probably a foreign body reaction rather then infection
- this is extremely likely to give cross hatching and a stretched wound
Cross hatching or tram tracking due to external sutures
- buried sutures will reduce the risk of this
If done well they can be used without the need for external sutures
- Dr Muir found doing sub-cutaneous sutures well a bit of a struggle till someone showed him the marini suture
- this is very simple to do especially in tight wounds where placing a buried interrupted suture is beyond his limited
dexterity
Dr Muir only uses this technique on the back
(i) Excise the lesion in the usual way
(ii) Undermine around the wound
- not everyone does this
(iii) Pass suture up through fat and exit the skin
- Dr Muir uses 3/0 Maxon, an absorbable monofilament suture
(iv) Turn the needle around, go back through the same hole passing horizontally so you exit the skin as high as
possible in the dermis
(v) Now introduce the needle through the directly opposite wound margin
- enter at the dermo-epidermal junction
- exit through the epidermis
- the exit sites are placed about 5mm from the wound margin
(vi) Turn the needle around back through the same hole and exit through sub-cutis
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- try to keep the levels even on either side
(vii) Tie your knot
- the knot will be deep in the wound
- monofilaments tend to slip a bit so be careful with your knot tying
- cut the suture so there are no loose ends protruding from the wound
(viii) Continue till the wound is closed
- steri-strip the skin edges together
When you first start doing these you may find the wound edges are too far apart to oppose without surface
sutures
- if so, as almost all the tension is taken up by your sub-cutaneous stitch, you will be able to get away with a finer
suture than usual and will only need to leave it in for a shorter period
(Dr Muir uses a 5/0 Dyloc.)
Undermine around your wound
Pass your suture up through fat and out via the epidermis
Turn the needle around and go back through the same hole
Exit horizontally in the upper dermis
(Note how close the exit point is to the epidermis)
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Cross the wound horizontally and pass your needle through the upper dermis and exit through the epidermis
- this should be a mirror image of the other side of the wound
Turn the needle around and back through the same hole
Exit through sub cutis, level with your original entry point on the opposite side
Tie your knot
(Note how closely opposed the skin edges are)
The end result
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- Tinct Benz Co applied on either side as extra adhesion for steri-strips
- wound edges closely approximated so no need for external sutures
- the needle holes disappear without a trace usually
- there is a hump running along the wound, this disappears as the suture is absorbed
What Dr Muir uses for external support
The end result, ready for a dressing
This can be used to close the entire wound or just when you have difficulty doing a usual sub cutaneous suture
This suture requires little skill
- it eliminates the need for suture removal,
(as there are no external sutures, infection rates are lower and cosmesis is improved)
- warn your patients that absorbable sutures do on occasion 'spit' through the wound
The doctors, Dr Muir knows, doing dermatological surgery are often very dogmatic about which absorbable suture
to use
- some swear by monocryl, others refuse anything other then PDS
- most have specific preferences for different situations
- ask your supplier for some samples and make up your own mind
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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PULLEY SUTURE
A rapidly growing lesion on the lower calf
- clinically a keratoacanthoma
- for excision
Occasionally you are faced with a surgical defect which turns out to be harder to close then you banked on
- the edges won't oppose no matter how hard you pull or the suture snaps
- if, like Dr Muir, you have limited surgical skills, this is where the pulley suture is invaluable
By crossing a wound twice with a stitch you gain a mechanical advantage which will often allow a wound to be
closed with surprising ease
- this technique is popular in scalp reduction surgery where the bald skin is excised and the hair bearing skin then
pulled together!
(Leaves you with a very natural head of hair - Not!)
The main instance Dr Muir uses this technique is on the lower leg, especially the shin, where the skin can be very
tight
- on occasion it has got him out of trouble on the back in barrel chested men and on 'tight' scalps
- as Dr Muir doesn't do grafts it has saved him the embarrassment of calling in one of his surgically inclined
colleagues
(Nothing worse then looking bad in front of a 'surgeon')
Margins outlined and local in
Note the blanching effect from the adrenaline, this was taken 7 minutes after infiltration
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To remember how to do it just memorise the phrase
- 'near-far, far-near stitch'
Dr Muir usually uses a 3/0 dyloc on the lower leg
First do the NEAR step
- pass the stitch through the skin, via the epidermis, about 3 mm from the wound edge, usually at the mid-point of
the defect
- the needle exits through fat, crosses the defect entering fat on the opposite side at the same level and exiting
through the epidermis about 9mm from the wound edge
That is the first FAR step
The first step
- the needle has been passed through the skin near to the left hand side of the wound
- we are using 3/0 dyloc
The suture is passing through the skin far from the right hand side of the wound
Back to the left hand side and through far from the wound margin in line with the previous pass
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The suture is passing through the skin near the right hand side of the wound
The needle is then passed straight back across the wound and inserted through the skin on the same side you
started and in line with the other passes
- this time, however, you enter the skin about 9mm from the wound margin
- you have now done the second FAR step
The needle exits through the sub cutis re-crosses the wound at the same level and then out through fat and skin
to complete the final NEAR step exiting about 3 mm from the wound margin
Now pull on your suture in the usual way, the mechanical advantage will be obvious
- tie your knot
Usually only one pulley suture will be needed
- some will put in buried sutures on either side and then close the wound
- some remove the pulley suture at the end once the wound is fully closed
(Dr Muir doesn't - if it isn't broken don't fix it!!)
When removing the pulley suture do it so that the exposed suture is not dragged back through the wound as this
is an infection hazard
If you still can't close the wound you may need:
- to do a graft,
- alter your closure
- consider second intention healing
- or seek help
Tie the knot in the usual way
The end result, only the middle one is a pulley suture
- ignore the dog ears, they will settle
- if they don't you can always tidy them up later
Dr Muir's maxim is:
- "anything you have not done you can always do but anything you have done cannot be undone!"
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A firm dressing is a good idea at the end
Mild erythema and scale will disappear over the next few days
- some tape the wound for added support at suture removal
Compare the dog ears left at surgery and the result at suture removal
Dr Muir routinely leaves dog ears behind above the elbow and below the knee
- they settle
- inform your patient, so if tidy up is needed they do not get a surprise
(Dr Muir has never had to go back and remove one)
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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PUNCH BIOPSY
Skin biopsy aims
Other Skin Biopsy Procedures:
Biopsy of a difficult site
Conchal Bowl biopsy
Shave biopsy
How to do a Punch Biopsy
Typical lesion requiring a punch biopsy for diagnosis
This elderly gentleman has a well circumscribed erythematous scaling plaque on his calf
- he has been previously diagnosed with cutaneous T-cell lymphoma (CTCL) on his trunk
- numerous non-melanoma skin cancers have been treated over the years
- to cap things off he delights in having a good old pick at his skin
This could be a plaque of CTCL, an area of intraepidermal squamous cell carcinoma, a patch of lichen simplex
chronicus or even discoid eczema
- a biopsy is indicated
HOW TO DO A PUNCH BIOPSY
You will need:
(i) a suitable punch biopsy
- usually 3mm
(ii) local anaesthetic and needle
- use 1% plain lignocaine as it hurts less
- the haemostatic effect of adrenaline takes 7-15 minutes to kick in
(iii) gauze squares
(iv) surgical skin prep
(v) a 15 scalpel blade or other cutting tool to free the specimen at the base
(vi) suture and suturing equipment
- use 5/0 dyloc
(Dr Muir always sutures but this is not universal)
- the cosmetic result is superior then allowing second intention healing
(vii) a skin marking pencil
(viii) gloves and eye protection
(ix) a 'suitable' skin disorder
Set up
- Formalin container
- local anaesthetic
- swabs
- scalpel or scissors
- suture and needle holders
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- Explain what you are about to do to the patient
- Warn re scarring, infection etc.
- Mark your intended biopsy site or it will disappear with the local
- Prep the skin and infiltrate with local anaesthetic
Mark your target
- the intended biopsy site will disappear when the local goes in
- go for where you are most likely to find pathology
( Note no normal skin included)
Skin prep then local
- 1% plain lignocaine is preference
A punch is round and you will need to leave a slightly elliptical defect
- to achieve this stretch the skin at right angles to the direction you want your ellipse to lie
- so if you want a North/South ellipse stretch the skin East/West
- try to lay the ellipse along skin tension lines or wrinkles
While stretching the skin drill the punch in by rotating it between thumb and forefinger
- you will need to reach fat, so usually penetrate to the hilt
- be mindful of underlying anatomical structures of importance
Down to business
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Note the skin is being 'tensioned' at right angles to the way you want the final ellipse to run
- on the lower limb try to run your scars vertically
- just drill the punch in by twirling between thumb and forefinger
In to the hilt so we should be down to fat
Now lay the punch on its side and sweep around 360 degrees
- this will often free the core of tissue from underlying tissue allowing easy extraction
- remove the punch
- press on the skin around the biopsy site and the core will pop up and out with a bit of luck
- if it is still attached, separate with your scalpel
- if you can't see a core of tissue it is probably 'up the spout'. If so it will usually shake out
- transfer the sample to a suitable specimen container without crushing
- slide a toothed forceps under it and carry it to the container or push it onto a piece of gauze
(Do not grip it!)
- ensure the details on the container match your patients
A perfect sample
Merely pressing down on the surrounding skin after sweeping the punch around will often cause your specimen to
pop out like this
- this avoids any need for forceps and so no risk of crushing and ruining your biopsy
Ease the specimen onto a piece of gauze with your (gloved) finger or use your forceps to push it on
Then transfer to the specimen jar and reverse the process
- do not crush it or the pathologist will be extremely sarcastic
Suture and apply a dressing
(not everyone will put on a dressing)
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Now suture
Dr Muir suggests using 5/0 dyloc
- note the vague elliptical shape of the wound
- this will result in a cosmetically superior result
Sutured and ready for a dressing
Dr Muir often uses just a piece of calcium alginate (e.g. Kaltostat etc) and some micropore tape
- sutures out at 7 - 10 days usually
The pathologists report for this biopsy read 'cutaneous T-cell lymphoma'
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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REMOVE AN EAR CYST IN UNDER 6 mins
How To Treat In Under 6 minutes or 'While the Next Patient Is Getting Undressed!'
Dr Muir says that he is not what one would call surgically orientated
- nevertheless he does upwards of ten procedures per consulting day
- rarely do these take longer then 6 minutes from putting knife to skin to asking his nurse to dress the wound
- many skin problems can be treated in this time
This is the ear of a man in his seventies
- as can be seen he has had extensive surgery in the area some years ago
- the visible nodule has been present for some time and interferes with his sleep as it causes discomfort when he
lies on that side
- it is firm and slightly mobile
- clinically it is an epidermoid cyst and has probably arisen as a result of the previous surgery
- the black spot is a pen mark
How best to treat?
- clearly it needs to be removed
- excisions on the ear are technically more demanding then elsewhere
- he wanted Dr Muir to do it but can it be done with my limited surgical skills and within my 6 minute time limit?
The answer is 'yes' and 'easily'
- with luck these things can be easily extracted with little chance of recurrence
- this is especially so on the ear where there is so little dermis
- a proviso to this is if they have been inflamed previously
- this will result in scarring and tethering to the surrounding skin
HOW TO REMOVE!
(i) Infiltrate the area with local anaesthetic but without piercing the cyst wall
- Dr Muir used plain lignocaine as he did not have time to wait for the adrenaline effect and bleeding should not be
a problem
(ii) Incise through the skin and the cyst wall
- firm pressure either side with your fingers will keep the lesion in place
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(iii) Express/extract the cyst contents which is basically keratin
- these are not sebaceous cysts but epidermoid
- as you can see the cyst lining is still visible at the wound edge
(iv) Then grip the cyst lining firmly with some non-toothed forceps and slowly extract the cyst hopefully intact
- it came out very readily and in one piece
- if it does not come out in one piece it is not a disaster
- just use your forceps to grab as much as the lining as possible
- the resultant healing will usually be unaffected but the recurrence rate seems to be higher
(v) The resultant wound will have a bit of redundant skin from the stretching effect of the cyst
- Dr Muir would not suture as this sits together nicely and there is no lateral traction across the wound
- Dr Muir just had the patient apply pressure for a few minutes and then steri stripped the wound
Total duration 5.5 minutes!
This technique will not work as well on the back where they are more firmly attached to the surrounding dermis
- it can be tried however and if not successful go onto the more usual removal technique
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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SECOND INTENTION HEALING
One of the interesting things about dermatology is that nearly every skin problem can be successfully treated in
more then one way
Not all excision sites have to be closed primarily or grafted
- a useful option is second intention healing
Dr Muir uses this technique often especially on:
- bald scalps
- upper back and
- lower leg
- it can be used elsewhere
Dr Muir has seen it used with excellent results in:
- the conchal fossa
- medial canthus and
- on concave parts of the nose
Cure rates and patient satisfaction are equal to other techniques in properly selected cases
It requires a minimum of equipment and only basic surgical skills
- the procedure rarely takes more then a few minutes so can be done there and then
- excision margins are determined by the nature of the lesion being treated
- a minimum of uninvolved skin is removed compared with a traditional ellipse
- healing times are longer but infection is uncommon and haematomas cannot form
All one does is excise the lesion 'in the round' and then allow the surgical defect to granulate up and heal
- excision margins are determined by the nature of the lesion being treated
- due to wound contracture the resultant scar is about the same size or even smaller than the lesion removed
Obviously this procedure should not be done near a free margin such as:
- vermillion of lip
- eyelid
- eyebrow
- free margin of ear or nose
--> due to distortion risk
If a split skin graft fails to take, the wound is often left to heal rather then a further graft being applied
Why not cut out the middle man?
- the most common complaint patients make after a split skin graft is about the discomfort from the donor site
- second intention healing has only the one wound
- the cosmetic result is usually superior to a graft
- many severely sun damaged patients with a history of multiple non-melanoma skin cancers on the lower leg
prefer this technique
Before performing this procedure Dr Muir tells his patients that he can always go back and excise the scar if they
are unhappy with the result
- no one has ever taken me up on this offer
What you will need
(i) a suitable lesion and an informed patient
(ii) dressing pack
- skin prep
- surgical gloves and
- skin marking pencil
(iii) specimen jar
(iv) local anaesthetic, in these as with an elliptical excision Dr Muir uses lignocaine with adrenaline
- he uses one part 1% lignocaine with adrenaline diluted with 4 parts plain
- this reduces the discomfort of infiltration while still giving good vasoconstriction and haemostasis
(v) a 15 scalpel blade and handle
(vi) a skin hook or suitable forceps
(vii) some system for cautery if needed
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(keep cautery to a minimum)
(viii) a suitable dressing,
(Dr Muir usually uses calcium alginate)
Mark out your excision line in a circle around the lesion
- prep the area
- infiltrate with local
- the full vasoconstrictive effect will take at least 7 minutes
- incise along your marked margins
Dr Muir will go down into fat, or, on the back with its thick skin, down to deep reticular dermis
- at this level he likes to see a layer of fibrous tissue with 'buds' of adipose poking through
(obviously with any malignancy you need to ensure lateral as well as deep clearance)
Lift up one edge of the specimen with your skin hook and dissect it away from the underlying tissue
- place the specimen in your formalin jar
- do not crush your specimen
- establish haemostasis and dress
Further management will depend on the histology
- review at 3-6 months or sooner if needed
Procedure for excision of nodular BCC
This elderly and severely sun damaged patient has a lesion as shown on his anterior scalp
- tender and indurated at the base a diagnosis of SCC rather then inflamed solar keratosis was made
- although a standard ellipse could have been done his skin was quite tight and the resultant closure would have
been under some tension
- it was quite symptomatic and he wanted rid of it rather then coming back on another day
- we therefore excised it in the round and allowed second intention healing
Excision margins marked and local anaesthetic going in
Cut along the dotted line
Dissecting the lesion away from underlying tissue
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- note the skin hook, no chance of crushing the specimen
Almost free
The resultant wound
- note the cautery sites
- the little bit of bleeding stopped with brief pressure
- ready for a dressing
The result at two months follow up
- histology reported as "
--> 'a well differentiated SCC arising in a solar keratosis, margins well clear'
Cheap, simple, convenient and cured
- the entire procedure should take no more than twelve minutes including waiting for local to work
Excision of a nodular BCC
Clinically a nodular BCC
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- excision margin outlined and local in
- note the slight pallor due to vasoconstrictive effect of adrenaline
The incision along the dotted line
Skin hook supplying traction and lift while the lesion is dissected out
The final defect ready for dressing
- note fat visible in the base but still a bit of reticular dermis in situ
- heals more quickly
- once again done in minutes and histology reported as
--> 'adequately excised nodular BCC'
This is the scar from excision and second intention healing of a pigmented BCC 18 months earlier
- the erythema has faded and she is left with a cosmetically acceptable white maculae
- as you can see this is a woman's deltoid and so at high risk of keloid
- the more sun damage the less exuberant the scarring process
Not the same case
- but this scar is also on the upper back three months after a BCC was excised and allowed to heal by second
intention
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- not perfect, but not bad
--> most importantly the histological margins were clear and the patient is happy
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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DERMATOLOGY TIPS and TECHNIQUES
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SHAVE BIOPSY
Other Skin Biopsy Procedures:
Biopsy of a difficult site
Conchal Bowl biopsy
Punch biopsy
A very useful procedure
- it is used for both diagnostic and therapeutic purposes
- it needs minimal equipment and takes very little time
(Dr Muir does these while his next patient is getting undressed)
- the secret is to keep the shave superficial but deep enough to obtain a diagnostic specimen and use no cautery
How Dr Muir does a shave biopsy
Dr Muir uses shaves in the following situations:
(in almost all instances these lesions are located in the superficial dermis or epidermis)
A perfect indication for a shave biopsy
Pre-operative photo allows easy localisation
- histology micronodular BCC
(i) Biopsy of suspected non-melanoma skin cancer where the diagnosis is in doubt
- Dr Muir uses this method routinely from the scalp, to the lip, to the foot
(ii) Confirmation of clinical diagnosis on a cosmetically sensitive site or where healing will be difficult
- nothing worse then having a wound complication or poor cosmetic result when the treated tumour turns out to
have been benign
(iii) If the treatment to be used on a tumour will not provide material for histology
(eg. cryotherapy, radiation treatment, imiquimod or photodynamic therapy)
(iv) Where you need to know the histological sub-type to help decide on treatment modalities
(eg. - is it a micronodular or solid BCC?)
(v) A mapping procedure to determine how extensive a tumour is
- this is a not uncommon indication with large areas of BCC or intraepidermal carcinoma on the head and neck
(vi) Large macular pigmented lesions where the differential falls between a benign lentigo or a lentigo maligna /
Hutchinsons melanotic freckle etc
- in these cases the lesions are too large to easily excise
- in this and the last instance one can easily take multiple samples and so reduce the chance of sampling error
(vii) With small pigmented lesions or skin cancers Dr Muir will do a deep and wide shave to remove the lesion in
toto
- this will usually result in a complete excision
(viii) As definitive treatment of hyperkeratotic or cryotherapy resistant solar keratoses
- this will remove the lesion and exclude the presence of SCC
(ix) For treating solar keratoses where Dr Muir thinks cryotherapy is likely to leave a cosmetically unacceptable
result and the lesion is too thick for topical creams such as 5 flurouracil or imiquimod
- in other words on the upper lip or eyelid
(x) For removal of any and all manner of benign skin lesions for cosmetic or 'nuisance' reasons
- it is especially useful for awkward placed seborrhoeic keratoses, viral warts, benign naevi, molluscum
contagiosum etc.
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Another good indication
- this solar keratosis has been frozen twice
- Dr Muir did a deep shave to exclude SCC
- histology confirmed a solar keratosis
Is that a BCC in the conchal fossa or just the result of his picking?
- a simple shave confirmed a BCC
A good example of mapping biopsies on this extensive hyperkeratotic plaque on the shin
- Dr Muir was very worried about invasive SCC but all three shave biopsies and another four since show
intraepidermal carcinoma only
-this lady healed easily and we can now work out a suitable treatment plan
The black mark is on a small recurrently bleeding papule
- the area had been previously frozen by another doctor
- Dr Muir's differential diagnosis included a BCC or an area of chronic inflammation and irritation
- a shave biopsy was done
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The biopsy showed an area of chronic inflammation centred on a ruptured milium
- this is the same site one year down the track
- she has had no further problems
- a reasonable cosmetic result, cancer excluded and symptoms gone after shave biopsy
A common problem
- two areas of irritation on a sun damaged nose with significant rosacea
(Note the scar of previous BCC excision - are these lesions rosacea papules or skin cancer?)
- a job for shave biopsy person
The same nose 18 months later
- the upper lesion showed rosacea only
- the lower a completely excised intraepidermal carcinoma
- she is happy with the cosmetic result
HOW DR MUIR DOES A SHAVE BIOPSY
You will need:
(i) a 15 scalpel blade
- some use a 10 but Dr Muir finds them too big
(ii) skin prep
(iii) a few gauze squares
(iv) 1% plain lignocaine and a needle
(v) a formalin jar
(Dr Muir submits all removed specimens for histology regardless)
(vi) a calcium alginate dressing (e.g. kaltostat) and some adhesive tape
(vii) gloves and eye protection
(viii) a suitable lesion and a informed patient
Mark the intended lesion if needed
- wipe down with skin prep and infiltrate with local anaesthetic
- tension the surrounding skin and holding the blade parallel to the skin surface slice through the lesion
- the resultant wound should have little depth to it and show only pin-point bleeding spots
- the specimen will usually sit on your blade allowing easy transport to your correctly labeled specimen jar
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- Dr Muir will often then hold the blade, sharp edge perpendicular to the skin, to use as a abrasive to 'sand' off any
residual lesion and blur the margin with the neighbouring skin
- DO NOT CAUTERIZE
- apply your calcium alginate dressing and then get the patient to apply pressure
(Cautery greatly increases pigment loss and scarring)
Done!!
A perfect indication for a shave
- this typical seborrhoeic keratosis catches on this lady's jewellery
- a purely epidermal lesion so easily shaved
What you will need
Note: the specimen jar is mislabeled, should be right neck
- Always check!
In goes the local
- try to raise the lesion up a bit with your bleb, makes the shave easier
- 1% plain lignocaine, about 0.1 of a ml is ample
Slicing away with the 15 blade parallel to the skin surface
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The specimen comes off in one piece and transferred easily to the formalin jar
- no chance of crushing!
Note the pin point bleeding spots therefore Dr Muir is in the papillary dermis and scarring should be minimal
Now hold the blade vertically and lightly sand off any remaining keratosis
Note how with any cutting Dr Muir is tensioning the skin
On goes some calcium alginate which stops any residual bleeding
- bleeding is not a problem even if they are anticoagulated
The final dressing, just to get them home really
- white micropore costs less than brown!
If Dr Muir thinks it will be difficult to find the site at follow up he will take a digital photograph
- this is especially important with sampling suspected facial skin cancers as it is commonly impossible to see any
evidence of the biopsy at follow up even a week later
- these photos are also very handy when Dr Muir sends patients off to a surgeon so they can find the tumour
Dr Muir uses plain lignocaine as it hurts less, haemostasis is almost never a problem and he is unable to wait 7
minutes for the adrenaline to take affect
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When correctly done this technique supplies excellent histological samples and very good cosmetic results
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 98 of 123
DERMATOLOGY TIPS and TECHNIQUES
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SKIN BIOPSY
Any doctor involved in the management of skin disease must be able to perform a competent skin biopsy
- an accurate diagnosis is crucial in dermatology
- a biopsy can help achieve this
Aim
Biopsy of a Rash
Biopsy of a Suspected Malignancy
Procedures:
Biopsy of a difficult site
Conchal Bowl biopsy
Punch biopsy
Shave biopsy
AIM
For the biopsy to be useful a number of requirements must be met
(i) It must be representative of the pathology
- most skin cancers arise in the epidermis and superficial dermis so a shave biopsy will usually be sufficient
- with a rash the pathologist will need to see the whole depth of skin from epidermis down to and including fat
- this means either a punch or incisional biopsy
(ii) Collection of the biopsy needs to be done in such a way that artefact is avoided
- in other words don't crush it!!
(iii) Use a pathologist who is used to dealing with skin disease
- this is especially true in the case of inflammatory dermatoses
- dermatopathology is a sub-specialty in its own right
- not all pathologists are equally comfortable in dealing with skin disease
(iv) Give the lab as much clinical and historical detail of the condition as you can
- for instance if you suspect a drug eruption list the medications they are on
- if they have had treatment especially systemic or topical steroids outline this
- do you suspect photosensitivity?
- supply a clinical differential diagnosis
- with difficult cases call the pathologist to discuss your suspicions
- occasionally you will need to supply specimens for culture, immunofluorescence or marker studies
- these will need to be forwarded fresh or in special transport media
- discuss this with the lab
(v) Ensure that the details on the specimen container match those of your patient
- mention the anatomical site
BIOPSY OF A RASH
Ideally biopsy a fresh lesion which has been neither excoriated nor treated
- if it is an extensive rash avoid biopsying below the knee, on the dominant upper limb or in a cosmetically
sensitive area
- if they have been using corticosteroids it may be worth reassessing the patient after a few days to a week
- steroids will alter both the clinical and histological appearance and thus increase the chances of misdiagnosis
Usually a 3mm punch biopsy will be sufficient
- this may require doing a small ellipse rather then a punch
- the end of the ellipse can be removed and submitted for immunofluorescence
2mm diameter biopsies are unpopular with pathologists dealing with inflammatory dermatoses
- they are difficult to process and harder to interpret
- having said that Dr Muir uses one for a deep biopsy of a suspected skin cancer, especially on the nose
4mm diameter punches are usually overkill
- these larger diameter instruments can be useful for excising tiny BCC's
Although it is mentioned in texts and propagated by some, there is usually no need to include adjacent normal
skin
- pathologists know what normal skin looks like
- there are some relatively rare conditions causing subtle alteration to collagen, elastin, other dermal components
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or adipose where including adjacent normal skin is needed for diagnosis
At the time of biopsy you may want to do bacterial swabs or fungal cultures if indicated
BIOPSY OF A SUSPECTED MALIGNANCY
It is rare for Dr Muir to do anything other then a shave biopsy when trying to exclude skin malignancy
- this is because the pathologist will usually need only epidermis and superficial dermis to make the diagnosis
A shave biopsy is an extremely useful technique requiring little training and minimal equipment
- the cosmetic results are usually excellent
- in fact Dr Muir does a pre-biopsy digital photo so he can find the site again at review
One thing you will realise when you start regularly biopsying skin lesions is that skin cancer can be extremely
difficult to diagnose clinically
- a shave will reduce sampling error compared to punch biopsy as you can take a bigger and hopefully more
representative sample
- a shave of a solar keratosis or even an intraepidermal carcinoma will often be both diagnostic and therapeutic
removing these non-invasive lesions in toto
- even with invasive lesions it is quite common for no residual tumour to be found with definitive excision
Anatomical sites where shave biopsy is particularly useful include;
- the nose
- upper cutaneous lip
- the vermillion
- the inner canthi
(anywhere on the face really)
- the conchal fossa
- below the knee
Ideally a shave should be only into papillary dermis
- at this level you will see pin point bleeding spots representing the transected ends of vessels within the dermal
papillae
- you may wish to go deeper then this on occasion
- the deeper you go the more scarring you will cause
Suspected malignant leg ulcers represent a special case
Chronic leg ulcers can be complicated by malignant degeneration
- they can be lesions of pyoderma gangrenosum, atypical infection or due to an underlying vasculitis or other
pathology
- thus a biopsy is needed
- the usual fear expressed to Dr Muir by his registrars is that biopsy may cause a leg ulcer
- he reply's that they already have one and without a diagnosis treatment is likely to be unsuccessful
The way Dr Muir biopsies a leg ulcer is to incise a reverse 'slice of cake' shaped piece of tissue vertically from the
ulcer margin
- this extends from normal skin into the ulcer bed with the narrow apex being in the normal skin and the base in
the ulcer itself
- the removed tissue can then be divided for histological and microbiological assessment
- a couple of stitches are used to oppose the defect margins in the normal skin
- the wound in the ulcer is left alone
- this almost invariably heals without incident
The biopsy will only tell you what the biopsy is!
If the histology does not match your suspicions do not hesitate to re-biopsy
- this is especially true for skin malignancy
(Just because pathologists get first class honours at Med school does not mean they are infallible!!)
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
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DERMATOLOGY TIPS and TECHNIQUES
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SKIN CHECK
A common presentation is the patient seeking a skin check
- this may be precipitated by concern over a specific lesion or just in the way of a preventative health measure
- the major group Dr Muir sees are people sent along as they have recently had a skin cancer treated by their GP
How to go about it
Areas where skin cancers can be easily missed
How to go about it?
This is what Dr Muir does:
Ideally a dedicated appointment should be made
- do not fall into the trap of:
"Oh, while I'm here could you quickly check my moles?"
(i) Firstly take a history
Dr Muir basically does a mini hospital admission
You will need to know their:
- medical
- social
- drug
- tobacco
- alcohol and
- family history
Ask specifically re allergies to or problems with:
- local anaesthetic
- dressings and
- antibiotics
--> all of which may be needed if you perform any surgery
Have they had problems with previous treatments?
- some people blister easily or depigment readily with cryotherapy
- others have a tendency to wound infection or keloid scarring after surgery
- some people will need prophylactic antibiotics for surgery if they have joint prostheses, artificial heart valves etc
(ii) Enquire after skin cancer risk factors
- where did they spend their childhood?
- have they been sunburnt and how often?
(if they are white Queenslanders and say 'no' you can assume the rest of their history is probably unreliable too!)
- are they immunosuppressed?
- have they ever had radiotherapy or phototherapy?
- is there any family history of skin cancer?
- are they currently spending a lot of time outdoors?
- is there any personal history of skin malignancy?
--> if so what type?
- when, how and by whom were they treated?
(iii) Find out if the lesion they are complaining of has been previously treated
- cryotherapy can make the malignant look benign and the benign look malignant
(iv) Take this information with a grain of salt
- people will often state they have had melanoma's excised when it was in fact a non-melanoma skin cancer or
merely a benign nevus
- similarly they will report that treatment was adequate
- if asked how they know, they reply; 'the doctor would have rung me if there was anything wrong'
- Dr Muir then asks if they have seen the doctor since
- if not Dr Muir replies 'perhaps he's dead! - he wouldn't call you then would he?"
Dr Muir tells his patients 'if it is worth having a test done it is worth finding out the result'
- it is common to see people with histological reports documenting inadequate excision margins where no further
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action has been taken
- similarly details of family history can be inaccurate
If possible try to get copies of any previous histology
Dr Muir is not saying 'don't believe your patient' but knowledge is power
- having an accurate history can save both you and the patient a lot of grief
(v) Ask about any skin lesions that are concerning them
- Dr Muir asks 'has anything on your skin been itching, crusting, oozing,bleeding, changing, staying out late or
otherwise bothering you?'
(vi) If a particular spot worries them, ask why
- it is common for a single mole to be identified with the comment 'this one worries me!'
- when asked to elaborate it transpires that it has been present all their life, never changed but it is dark and they
have been told that the darker the more dangerous
(vii) Dr Muir finds it very difficult to ignore a good history of change in a single nevus, even if it looks totally benign
- to make life difficult you will get the occasional patient who will give a vague history of change in multiple naevi
(viii) By now you should have all the information needed to do a check
- people joke that you would have to get them back on another day after going through all that
- it should take you no more then 5 minutes
(ix) Ask them to get undressed down to their underwear
- if they query this Dr Muir explains that most skin cancers he finds, people don't know they have them
- on the flip side the lesion they are worried about is often nothing
- it doesn't hurt to look
- if they still refuse he does not push the issue but documents that they declined a full skin check
(x) You will need a good light, magnification
(Dr Muir uses loupes on a head band to leave his hands free)
- and preferably a powered examination couch to save your back
- a dermatoscope is essential to his practice
- in trained hands these instruments increase accuracy
(in untrained they have been shown to decrease accuracy)
(xi) Dr Muir sits the patient on the edge of the couch facing him
- the entire skin surface needs to be examined
- this includes the scalp, palms, soles, nails and mucosal surfaces
- obviously get an escort when examining the genitals
(with his female patients he suggests that they have their genital skin examined during pap smears etc)
(xii)The examination needs to be systematic
- start with the left hand, go up and across the chest and down to the right hand
- then they lie down and the bed level is raised so you don't have to bend too much
- the anterior torso is then checked
- then peruse the lower limbs, parting the toes
- the patient is then asked to roll over and start at the soles and work your way up
(xiii) Once you reach the neck the patient is sat up
- the head and neck area is then assessed
- ask them to raise their arms and check the axillae
(xiv) Check all previous treatment sites
- assess the lymph nodes, liver and spleen if indicated
(xv) always look at the lesion that concerns them last
- that way if it is something bad you don't forget to examine the rest of them
Areas where skin cancers can be easily missed are:
- the apex of the naso-labial groove
- the inner canthus
- posterior aspect of the pinna
- the scalp 'part line'
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- and of course the nooks, crannies
- and covered skin
One of Dr Muir's patients developed a malignant melanoma on the conjunctival surface of his upper eyelid!!
- this was found only when it bled
- check inside the mouth,
(Dr Muir has found one case of oral melanoma and a number of SCC's)
In short the best tip Dr Muir ever had on how to do a skin check is the adage:
- 'more is missed by not looking than not knowing'
If a lesion bleeds spontaneously or with minor trauma it is cancer till proven otherwise
If a keratotic lesion is tender and has palpable dermal involvement SCC is more likely then solar keratosis
A solar keratosis that fails to respond to cryotherapy may be malignant
There is a basal cell carcinoma on this chest
- can you see it?
show me
If an erythematous area is still present after 3 months it may well be a skin cancer
Any lesions found Dr Muir documents on a sketch and numbers
- cryotherapy is done as you go along
Discuss your findings and possible course of action with the patient
- ask if they have any questions
To finish
- advise them on sun protection
- the warning signs of malignant change
- skin self examination and
- when they should next be checked
Document the above
- the whole process should take no more then 15 minutes
(Next patient, please!)
Answer to show me
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A typical superficial BCC deep in the infra-mammary fold
- the patient was unaware of its existence
- if you don't look you won't find
Only small so easy to treat
<Back>
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 104 of 123
DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
SKIN TAGS
These lesions are on the lateral neck of moderately overweight woman
- she finds them very annoying' especially in summer when some become inflamed and itchy
- they catch on her jewellery and collar
- these are commonly misdiagnosed as 'skin tags' when if you look closely they have a verrucous surface
- they are, in fact, pedunculated seborrhoeic keratoses
She would like treatment
- there are a number of possible therapies
Dr Muir sometimes just snips them off
- this is done without anaesthetic with a small pair of forceps to apply traction and a sharp pair of scissors
- local anaesthetic is not needed
- it produces multiple small bleeding points which are a bit of a fiddle to dress
- healing is usually not a problem and the cosmetic result is mostly excellent
Some use their electrocautery machine to fulgurate them
- Dr Muir finds that a bit tricky and is painful for the patient
A simple technique is cryotherapy
- this needs to be done in such a way that the lesion alone is frozen
- leaving the surrounding skin untouched
- a frozen lesion will turn black and fall off in about a fortnight
If the surrounding skin is frozen as well the morbidity and discomfort are greatly increased
- the cosmetic result is inferior due to increased hypopigmentation
Dr Muir uses two simple tricks
1. Pour some liquid nitrogen into a fresh plastic specimen container
- place two pairs of broad forceps in the nitrogen
- wait 60 seconds or so and use the forceps to grip individual lesions
- you want to see an ice ball involving down to the base of the stalk but not the adjacent skin
- if you supply a little bit of traction there is virtually no discomfort
- repeat on the next one
- after a while the forceps will have warmed enough that no ice ball will form
- you then swap that pair for the one in the container
- this way you will not have to wait for your forceps to cool down
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Two pairs of forceps sitting in a liquid nitrogen bath ready for use
- the handles may be too cold to use without protection, just use some folded gauze
Gripping a 'tag' whilst applying a bit of traction which seems to reduce discomfort
- you should be able to do three or four before needing to swap forceps
- Note the ice ball extending down to the base
2. Grab the lesion with a pair of forceps and gently pull it away from the skin
- using your cryotherapy gun to freeze it by directing the spray in such a way that the surrounding skin is spared
- once again your ice ball should be restricted to the lesion alone
- you will find that your forceps will stick on occasion
- there is minimal discomfort
The grab and spray technique
- the stream of liquid nitrogen is directed away from the surrounding skin
If the patient has never had this done before Dr Muir tends to do just a few in the first session
- this is to ensure they tolerate it and get a good cosmetic result
- larger lesions may need two freezes with either technique
Unlike the open spray technique there is little post-treatment inflammation or weeping
- this is important in the areas these lesions occur
(i.e. neck, groin and axillae)
The lesions are almost always removed with no visible mark
- warn the patients that they may get a mark and that it may not work especially on the larger ones
- they will continue to get new lesions also
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With either technique this is the desired end result
- the entire lesion is an ice ball but the neighbouring skin is unaffected
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
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Page 107 of 123
DERMATOLOGY TIPS and TECHNIQUES
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SOLAR KERATOSIS
Any doctor dealing with skin disease will spend a major part of each day dealing with solar keratoses
They are incredibly common with some studies suggesting a prevalence of greater then 50% in Caucasian
Australians over 40
Treatment Options
Conclusion
Examples
There are numerous described treatments:
- keratolytics
- topical retinoids
- chemical peels
- cryotherapy
- phenol
- curettage/shaving
- excision
- topical 5 fluorouracil cream
- imiquimod cream
- diclofenac cream
- photodynamic therapy
- ablative lasers
- superficial x-ray
- and others
Why so many?
For the usual reason that none are uniformly effective and choice of treatment varies with:
- the patient
- the anatomical site
- the number and size of lesions; and
- with the practitioner and practice!
Why do we treat them?
The usual reason given is that they are pre-malignant
- indeed in some circles they are considered to be in situ malignancy
- Dr Muir is yet to be convinced that labeling these almost ubiquitous lesions as malignancy is either accurate or
helpful
What are the chances of an individual solar keratosis becoming an invasive squamous cell carcinoma?
It is very hard to give an exact answer
(that can be translated as impossible)
- studies show that most cutaneous SCC's arise from a pre-existing solar keratosis or at least have features of
solar keratosis within them or in close proximity
- this does not tell us what the chances are for an individual solar keratosis becoming malignant
Is it 100%, 1% or something else?
- surprisingly there is little work on the topic
A recent Dutch review [Eur J Dermatol 2006 Jul-Aug;16(4):335-9] could only identify one study that examined the
percentage of malignant transformation and it came up with a rate of between 0.025 and 20% per lesion per
year!!
- the latter figure is clearly far too high and the former probably too low
An Australian study suggested the rate of malignant transformation was less then 1 in 1000 per year
(if you ‘do the math’ this may mean that a person with 7.7 solar keratoses has a 10% probability of one
transforming within 10 years!)
Suffice to say it is, in practical terms, impossible to give a patient a risk analysis for any particular solar keratosis
- Dr Muir tells his severely sun damaged patients that the chances of any individual sun spot becoming an
invasive SCC are small
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- the chances of one of their many solar keratoses becoming an invasive SCC are high but which one and when?
Who knows?
A malignant skin lesion will grow, function abnormally and elicit an immune response
- thus a lesion which is large (>1cm diameter), rapidly growing, indurated, inflamed, ulcerated, painful, tender
and/or bleeding is more likely to be malignant
- having said that the more biopsies you do the more you will realise how innocuous some SCC's can be
(Dr Muir adds to the above list that, any lesion which resists appropriate solar keratosis treatment should be
considered malignant till proven otherwise)
Why else do people seek treatment?
- many find that their solar damage/keratoses are symptomatic
- it is very common for people to complain of itch and even tenderness especially with high temperatures and
physical exertion
- Dr Muir has a large number of bald men with severe scalp sun damage who complain bitterly of these symptoms
especially in summer
- another common concern is cosmesis especially with facial and hand lesions
- some people find them non-specifically annoying and pick and squeeze them and when they fail to go, seek
treatment
Then of course there are the many patients who decline treatment
- Dr Muir has a lot of people on his books who have been treated for solar keratoses for years
(and have the scars to prove it) who decline treatment except for those lesions which are malignant or annoying
- provided they are educated and kept under regular surveillance this is a not unreasonable approach
When confronted with a patient with solar keratosis what should our approach be?
- as with most conditions treatment is individualised but regardless of the final decision a few aspects of
management are common to all:
(i) Education
- the nature of solar keratosis needs to be explained to them
- the small but real risk of malignant transformation and symptoms and signs thereof elucidated
- patients will understandably assume that their solar keratoses are cancers
- should they develop a suspicious lesion they need to inform their doctor
Although solar keratoses are a product of life time sun exposure, adequate sun protection from now on will result
in the development of fewer solar keratoses and perhaps the resolution of some existing ones
Ideally they should have regular full skin examinations as they are at increased risk of both non melanoma and
melanoma skin cancer
- the frequency will vary with the individual patient and whether they are getting skin cancer as well
(ii) Treatment Options
Once they have been educated about solar keratosis they need to decide what they want to do about their lesions
It is important to realise that solar keratoses do not arise from virgin skin
- by this Dr Muir means that the easily seen, palpable solar keratoses will be arising adjacent to smaller often
clinically inapparent solar keratoses
- if you freeze 20 or so solar keratoses on the forearms and face of a 60 year old concretor there are probably still
dozens of lesions left behind
- for this reason he tends to not get too heroic with his freezing
- similarly this fact makes the so called ‘field treatments’ an attractive option
<top>
TREATMENT OPTIONS
Doing Nothing
Topical Keratolytics
Topical Vitamin A
Liquid Nitrogen Cryotherapy
Topical 5% 5-Fluorouracil Cream
Imiquimod
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Cold Steel
Photodynamic Therapy
Diclofenac Gel
Chemical Peels and CO2 Laser Resurfacing
Oral Retinoids
(i) Doing “Nothing”
Can this be justified?
(by nothing Dr Muir means):
- education
- emollient and/or keratolytic, if they can be bothered
- sun protection and
- regular review
Solar keratoses spontaneously resolve at a rate of 15-25% per year
- couple this with a low risk of malignant transformation and a lack of wonderful treatments this is a reasonable
approach
The emollient, placebo arm of various topical treatments (masoprocol, diclofenac) have shown significant rates of
solar keratosis ‘resolution’
(or at least a reduction in the keratotic build up to such an extent to make the lesion invisible)
- continuing this theme, studies show a greater reduction in solar keratosis counts with daily sun block than with
simple emollient
(ii) Topical Keratolytics
A useful intervention is use of a topical keratolytic cream on a regular basis
- this can reduce the number of visible solar keratoses and relieve itch associated with dry skin
- what you use will vary with the severity and site
- similarly the base chosen will vary
- you may like to use a lighter base in summer than winter
Dr Muir uses the following depending on circumstance:
a) 5-12% acid sal in aqueous (less greasy) or sorbolene (more greasy) cream
- the weaker strengths for the face and the stronger for the arms/scalp
b) 10-20 % urea cream
- this can be bought over the counter
- useful on arms and face in some if it doesn't irritate
c) 5-15% lactic acid in aqueous cream for similar indications to salicylic acid
d) glycolic acid is available in a host of different 'over the counter' preparations in a variety of concentrations and
bases
e) 40% propylene glycol in aqueous cream
- Dr Muir uses this on bald scalps if they are very hyperkeratotic
- it can sting and is a known allergen
f) ammonium lactate which is available as a 17.5% cream called ‘lanate’
There are numerous other keratolytics
With regular use of these sort of preparations, combined with sun protection, the total number of solar keratoses a
patient develops can be reduced
(iii) Topical Vitamin A
Tretinoin was a very popular intervention in the early 90’s
- it can certainly work with studies showing reduction of solar keratosis counts, with daily to twice daily use for
months
- it does not seem to be hugely more effective then emollient and sun block however
- response is dose dependent with higher concentrations working best
- it can of course irritate and is a photosensitiser
(more reason to stay out of the sun)
- it does seem to help with fine wrinkling and pigment disturbance also
- if you use it, the patient will need to be motivated and continue for at least 6 months and ideally a lot longer
- cost precludes use on more then just the face and perhaps the back of the hands
(iv) Liquid Nitrogen Cryotherapy
30192, the item number of choice for the fashionable skin doctor
- other forms of cryotherapy have fallen by the wayside due to a lack of efficiency
- there is not a huge amount of ‘Cochranista’ evidence for it but we know it works - don’t we?
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- in a PDT study where cryotherapy was used as comparator, the complete response rate for it was 75% albeit
with a double freeze thaw cycle
- another study with the more usual single freeze gave only a 68% response rate
Thick hyperkeratotic solar keratoses are often resistant
Personally Dr Muir thinks people freeze too many solar keratoses
- he tries to restrict himself to the palpable lesions and those that annoy the patient
- efficacy is extremely user and lesion dependent and so Dr Muir doubts very much that published studies relate
to his individual practice
- in his hands most lesions he chooses to freeze go
- thick lesions he tends to shave off especially if they are below the knee
- solar keratoses do not arise from ‘virgin’ skin, so skin adjacent will harbour next years sun spot
Pigment loss is not uncommon especially on the upper lip
(v) Topical 5% 5-Fluorouracil Cream
A personal favourite (of Dr Muir's) that has been around for decades
- it works by blocking DNA and possibly RNA synthesis by inhibition of thymidylate synthetase
- significant inflammation is inseparable from it’s use and in fact many claim that without inflammation it won’t
work
Once again the 'Cochranista’s' would not be happy with the level of evidence for this medicament
- only a small number of trials were controlled or had adequate numbers or durations of follow up
- many of the trials use different concentrations, vehicles, frequencies and durations of follow up
- nevertheless it does work well but the reduction in numbers is by no means permanent with treatments often
needing to be repeated after a few years
Facial does better then non-facial skin which often requires longer durations
- the more inflamed they get usually the better they do
- attempts to reduce the inflammation with pulse dosing
(i.e. 2 days on followed by 5 days rest for up to 12 weeks have probably sacrificed efficacy on the altar of
tolerance)
It has been used in combination with topical tretinoin or cryotherapy with claimed added benefit
(vi) Imiquimod
Not licensed as yet for this indication in Australia, it is an effective treatment
- studies are few, with small numbers of patients, different regimes and limited follow up
- they do show reasonable response rates of 50% complete clearance on clinical examination
- regimes used vary, but 3 times a week application for 12-16 weeks is popular
- a duration Dr Muir has found hard to understand as BCC's only need 6 weeks
- side effects are not dissimilar to 5 fluorouracil (erythema, erosion, crust and ulceration)
- as with 5 fluorouracil the more you suffer the better you do
Dr Muir does not use it for solar keratoses as there seems to be little therapeutic advantage over 5 fluorouracil
and it is far more expensive
(19 times more expensive gram for gram!)
(vii) Cold Steel
Surgical treatment Dr Muir reserves for:
- thick hyperkeratotic lesions,
- those that resist other treatments
(as this may mean that his diagnosis was wrong); and
- those where the diagnosis is in doubt
Dr Muir usually does a shave and the depth will vary with the thickness of the lesion but rarely is deeper then the
papillary dermis
- he finds this useful for lesions on the lower leg
(where cryotherapy sites can be much slower to heal)
- he will often shave thicker solar keratoses of the upper lip
(as topical treatments won’t work and cryotherapy has a high chance of causing pigment loss)
(viii) Photodynamic Therapy
The 'next to newest kid' on the block!
This involves application of a photosensitising agent (5-aminolevulinic acid or 5-methylaminolevulinate) to the
affected area of skin after initial superficial debridement followed by illumination with a dedicated light source 3
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hours later
- it can give very good results which are dependent on patient selection and initial skin preparation
- thicker lesions do not respond well especially if the initial debridement is inadequate
- cosmesis is usually good, but it does hurt during the illumination and they can be quite inflamed and swollen
after!
Personally Dr Muir does not think it is markedly better then 5 fluorouracil and it is very expensive by comparison
- in his practice they do not use it nearly as often for this indication as for BCC or IEC
(ix) Diclofenac Gel
This, 'the newest kid' on the block, is a non-steroidal anti-inflammatory agent used in a 3% concentration in a
base containing 2.5% hyaluronic acid
- the trials show good response of 50-70% achieving total clinical clearance albeit with very short follow ups
- the duration of treatment is quite long
(i.e. 60-90 days)
- it does cause itch and inflammation but to a lesser extent than 5 fluorouracil or imiquimod
(x) Chemical Peels and CO2 Laser Resurfacing
Peels can be done as a series of low strength peels over weeks or more aggressive single treatments
- this is a superficially destructive process and so needs to be done carefully and by an experienced practitioner
- one study comparing a 35% trichloroacetic acid peel on one side of the face with 5 fluorouracil on the other
showed similar efficacy with improvement at 12 months but not at 32
CO2 laser resurfacing also gets rid of wrinkling as well as solar keratoses
- it can be efficacious but is obviously more expensive with a greater risk of scarring and of limited availability
- other lasers are also used
- Dr Muir occasionally refers people for aggressive peels or laser but mostly that is people who are looking for
cosmetic outcomes as the main aim rather then just getting rid of solar keratoses
(xi) Oral Retinoids
In Australia, oral acitretion is licensed and subsidised for the treatment of disorders of keratinisation and sun
damage is a recognised indication
- mainly it is used for chemoprophylaxis in people with a tendency to keratoacanthomas / SCC's as well as
multiple solar keratoses
- this form of chemoprophylaxis is especially likely to be used in transplant patients
- the dose employed varies but side effects make higher dosages hard to tolerate
<top>
CONCLUSION
Solar keratoses are very common
- they can undergo malignant transformation but mostly do not
- their presence means that the patient is at increased risk of malignancy elsewhere on their skin
- they can be unsightly and symptomatic
- treatments are many and none are perfect
Management is individualised and may range from benign neglect to the latest in laser modalities
- sadly no matter what treatment you select your patient will continue to develop new lesions
<top>
EXAMPLES
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A typical set of severely affected Queensland forearms
- which bit isn't a solar keratosis is more to the point
- there are numerous solar keratoses of variable thickness
- some are a bit inflamed
- there is scarring from previous procedures
Dr Muir's approach here would be:
- education
- long sleeves
- freeze the ones that are palpable and look like they will respond and shave off the thicker ones
- any that resist freezing shave off
- once those sites have healed use a keratolytic, say 15% lactic acid in aqueous cream b.d.
- he needs regular review anyway as he gets skin cancer as well
Dr Muir would not treat every single solar keratosis he has just the palpable ones
(some doctors would use 5% 5 fluorouracil cream but Dr Muir advises that he doesn't get much joy with it off the
face)
- photodynamic therapy could be tried but would be quite expensive
- other field treatments such as diclofenac or imiquimod could be used
A typical severely sun damaged bald scalp
- there is a mix of keratoacanthomas or SCC's
(domed lesions left posterior and right anterior)
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- thick and thin solar keratoses
- sun damage and scarring from previous procedures
A reasonable approach would be to treat the obvious malignancies by excision
- biopsy any lesions suspicious of malignancy and treat depending on their results
- shave off any thick solar keratoses and freeze any that look like they will respond
- once these large lesions are dealt with a field treatment could be tried
Dr Muir would use 40% propylene glycol in aqueous cream for a month or so to get rid of some of the
hyperkeratosis and then 5% 5 fluorouracil cream for 3-6 weeks
(scalps usually need longer than faces)
- photodynamic therapy or imiquimod could also be used
- any lesions that fail to go, freeze or shave, depending on their thickness and how certain you are they are not
SCC's
Another option considering the presence of malignancies is radiotherapy
- similarly chemical peels could be done
(but you would still need to get rid of the thick ones)
Diffuse solar damage over the cheek with multiple solar keratoses
- often symptomatic but better approached with a field treatment rather then a spot treatment like cryotherapy
- Dr Muir would use 5 FU but PDT, diclofenac or imiquimod are alternatives
- long term tretinoin can help
This image shows the benefit of sun protection
- note the difference between his trunk and forearms
- there is also actinic purpura
- sun protection, keratolytic and selective cryotherapy to thicker lesions would be Dr Muir's approach
- a field treatment could be attempted
(5FU, diclofenac, PDT etc)
Severe sun damage and an eroded lesion
- you would worry that this could be a malignancy
(SCC or IEC)
- if it is indurated and tender then malignancy even more likely
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Dr Muir has a low threshold for getting histology on these lesions
- having said that, a traumatised solar keratosis can look like this also
Wall to wall sun spot
- note how nice the skin is where the watch usually sits
Dr Muir's approach would be:
- education
- sun protection
- keratolytic and cryotherapy to selected thicker lesions
Field treatments (5FU, PDT, diclofenac, imiquimod) could all be tried if desired
These hands show a lot of sun damage and some small flat solar keratoses
- Dr Muir would just sun protect and use a suitable keratolytic
(e.g. 8% lactic acid in aqueous cream b.d.)
- cryotherapy for any lesions that are palpable but ones that he can merely see rather then feel he tends to leave
- this lady needs to be educated as to the signs of malignancy and have her skin checked regularly
These solar keratoses are arising either side of a previous cryotherapy attempt
- whether they are recurrences or new lesions is problematic and probably makes little difference
They are too thick to easily freeze as the depth of freeze will cause a lot of oedema and discomfort and resultant
depigmented scar
- Dr Muir would shave them both
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This hand belongs to a very elderly lady with awful skin
She declines treatment of her solar keratosis except when they annoy her or are likely to be SCC's
- the thick lesion over her second metacarpophalangeal joint is far too thick to freeze and obviously won't respond
to anything other then surgical removal
- a perfect lesion for shaving
- these heal very well on skin like this
<top>
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 116 of 123
DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
STEROIDS
‘This Steroid Doesn't work!’
A common scenario is the patient returning to complain that the topical steroid prescribed for their skin condition
has not worked.
A common response to this is to change the treatment to another steroid or to add a topical antifungal
A better approach is to consider why your prescribed steroid was ineffective.
The following should be considered:
Wrong Diagnosis
Wrong Treatment
Wrong Preparation
Wrong Amount
Patient Anxiety
Inappropriate Strength
Steroid Side Effects
Tachyphylaxis
Expense
Sloth/Lack of Faith/Non-compliance
Lack of Penetration
Patient Is Unrealistic
Variable Response
Used Alone
Wrong Diagnosis
- if your diagnosis is incorrect then it is likely that your treatment will not work (although often it will)
- Tinea treated with a steroid will transiently appear to improve as the inflammation and itch subsides
- once the steroid is stopped the problem will recur and can be more extensive
- neoplastic conditions such as skin cancer can be inflamed and look eczematous
--> this is especially so of intraepidermal carcinoma (IEC)
- topical steroids will of course have no effect
- Scabies will show steroid responsive eczematous change but until the mite is eradicated the condition will
persist
- Pruritus due to systemic causes such as renal or liver failure can result in eczematous changes from scratching
- an unrecognised drug eruption will not respond to topical steroids till the causative agent is ceased
- there are a number of inflammatory disorders of the skin where topical steroids are of little use
(e.g. pityriasis lichenoides and pityriasis rubra pilaris)
Topical steroids, especially potent ones, can alter the clinical and histological appearance of a skin condition.
If you suspect that the diagnosis is wrong often the best thing to do is stop treatment and review after a week or
so.
Wrong Treatment
(i.e. conditions for which steroids are prescribed inappropriately)
- acne
- rosacea
- folliculitis
- pigmented purpuric dermatosis
- pityriasis rubra pilaris
--> all look like they might respond to topical steroids but usually won’t
(steroids may have no discernible effect or as in the case of rosacea and acne actually make the condition worse)
Wrong Preparation
- steroids come in a variety of formulations
- treatment success can be dependent on which you choose
Ointments v. Creams
This is the commonest error seen by Dr Muir
- ointments in general work better then creams
(the reason being that they promote penetration of the steroid molecule into the skin due to their occlusive effect)
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- any disorder characterised by dry skin will likely be worsened by the drying effect of a cream and helped by the
emollient effect of a steroid ointment
By contrast an exudative eczema is best treated with a cream
- a creams drying effect will reduce exudation
(as the condition dries out ideally an ointment is substituted)
Areas of skin that are in general moist will usually do better with a cream then an ointment such as:
- the groin
- axillae
- and sub-mammary areas
In the scalp use of an ointment will be unacceptable to the patient due to the mess involved
(also a lot of it will end up stuck in the patients hair)
- a lotion is usually a better choice
(Dr Muir will often use a cream here but get the patient to dampen the hair and pull it out of the way so that it can
be applied to the scalp skin)
Some conditions will do better with intralesional rather then topical steroid
- the classic example being a keloid scar
Wrong Amount
Widespread disease needs large quantities of steroid
If you don’t give the patient enough they will be sparing in use and thus have little chance of response
A “finger tip unit” (ftu) is the amount of ointment expressed from a 5mm diameter nozzle sufficient to cover the
palmar skin of the distal phalanx of the index finger
- 1 ftu in a man weighs 0.49gm and covers 312 sq cm
- 1 ftu in a woman weighs 0.43gm and covers 257 sq cm
In a adult to cover the whole body you will need 40.5ftu
i.e.
- 19.85gm in a man
or
- 17.2gm in a woman
To cover the adult trunk daily you will need
- 14 ftu or 7gm
This refers to careful application, patients will often misapply
- thus one 15gm tube will not last long
Get An Authority!!
If a patient has a widespread rash and all that is prescribed is a single 15gm tube of ointment there is no chance it
will work
- you are better off prescribing too great an amount than too little
(at least then you will have given your treatment a chance to work)
The other thing to do is get an authority for a potent steroid and then after 5-7 days have the patient reduce to
something like:
- Celestone M
(a milder steroid which comes in a 100 gm tube)
Whenever you issue an authority it is important to warn the patient about side effects and that they should not
keep using the steroid unless under medical supervision
- always try to get them to make a follow up appointment
Patient Anxiety
A ‘side effect’ of explaining potential side effects is the patient will become so anxious that they will not apply your
prescribed steroid preparation
- in most instances the more potent steroids will not be needed for prolonged periods
- the patient needs to be educated about steroid side effects and advised on how to avoid them
- point out to them that with many skin conditions not treating the rash will damage the skin
(most of the horror stories with steroids emanate from the days when people used potent steroids for too long on
inappropriate sites needlessly)
Prescribe the appropriate strength steroid for the condition and anatomical site to be treated
- explain that as the condition improves they can reduce the frequency and/or the potency of the steroid applied
- in the long term if they are applying a steroid less then two or three times a week to any particular site they are
unlikely to get side effects
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- this does not mean that they can’t use the steroid daily long term
(just that they should not use it to exact same site - if they need to then they should be reviewed)
Inappropriate Strength
Prescribe a steroid that has a chance of working
- the potency chosen will depend on the severity and nature of the condition to be treated and the anatomical site
- Hydrocortisone is almost useless off face/genitals
(while a weak steroid will work well on these sites it will be ineffective for the same rash on the trunk or forearm)
(Dr Muir mostly initiates treatment with a potent steroid and then reduces to a milder steroid)
- if you initiate treatment with a weak steroid it may be that the condition is steroid responsive but your treatment
will not work as the agent chosen is too weak
The following is a list of the topical steroids Dr Muir uses:
Betamethasone dipropionate
Mometasone
Methylprednisolone aceponate
Betamethasone valerate
Desonide
Hydrocortisone
(i) Betamethasone dipropionate in optimised vehicle (Diprosone OV)
- this is the strongest topical steroid readily available in Australia
- Dr Muir rarely uses it as it is not on the PBS
- it is reserved for ‘stubborn conditions’
(ii) Mometasone (Elocon and Novasone)
- a strong steroid
- commonly used on the limbs and trunk
- it would rarely be used on the face/genitals/flexures
- Dr Muir uses it for facial cutaneous lupus
(iii) Methylprednisolone aceponate (Advantan)
- this is a potent steroid which is claimed to be less likely to cause side effects
- Dr Muir finds that it may not work as well in certain conditions as other potent steroids
- it is very popular with most dermatologists
(iv) Betamethasone valerate 0.02% (Celestone M or Betnovate 1/5)
(the ‘M’ stands for ‘maintenance’)
- Dr Muir uses this a lot as it comes in a 100gm tube
- it is considered a mild/moderate strength steroid
- it is useful in managing widespread eczema
- it can still cause significant side effects
(v) Desonide (Desowen) lotion
- this is a steroid that is said to be significantly stronger than hydrocortisone but with the same side effect profile
- Dr Muir finds it useful for facial eczema where hydrocortisone has not worked
(vi) Hydrocortisone (Sigmacort, Egocort etc)
- this is considered a weak steroid and is useful on faces, flexures and genitals due to it’s lesser side effect profile
There are numerous other steroids available
- the big thing is to use as little steroid as possible and to use the weakest one that will do the job
Steroid Side Effects
Topical steroids can cause side effects that may be mistaken for the condition they were prescribed for
- the commonest example of this is when a patient is prescribed a potent steroid for facial seborrhoeic dermatitis
(after a while this induces perioral dermatitis)
- a similar scenario can be seen with use on the perianal area or genitals
- steroid induced atrophy and telangiectasia can be mistaken for almost cleared psoriasis or eczema
- the patient keeps using the steroid to get rid of this last remnant only to make the problem worse
Topical steroids can induce:
- folliculitis
- miliaria
- purpura
- hypertrichosis
- and even ulceration
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In the nappy area they can cause a gluteal granuloma
- these can be mistaken for manifestations of the original problem
When stopping topical or more commonly oral steroids the treated condition, especially eczema and psoriasis,
can undergo a rebound flare
Topical steroid preparations can be irritant
- this is especially so with creams due to the preservatives they contain
- Mometasone and ‘Diprosone OV’ contain propylene glycol which is also an irritant
In recent years there has been increasing incidence of allergy to a variety of steroid molecules
- this can result in an allergic contact dermatitis
People also become allergic to the preservatives and other excipients in topical steroids
Tachyphylaxis
This is the acute development of tolerance
- this is the situation where increasing amount of drug is required to achieve the same therapeutic benefit.
- this is most described with psoriasis although some argue that it is less common then previously thought
Expense
Some patients will not get prescriptions filled if they feel they are too expensive
- on occasion they will not tell you this and just claim that your prescription did not help
(presumably in the hope that you will prescribe something cheaper)
- an authority can help
Generics may be cheaper but are they equi efficacious?
- they are supposed to be but there is some literature disputing that notion
Sloth/Lack of Faith/Non-compliance
Good old fashioned poor compliance is a very common cause for ‘non-response’
- clues to this will be the patient who still has ‘plenty of cream left’ or the patient who is vague about the treatment
regime used
- when asked they might say ‘I did what you told me to’
- another clue is the patient who has no idea of the name of the steroid being applied
- you have to “sell” the treatment and give clear even written instructions for them to follow
Lack of Penetration
If the condition you are trying to treat is:
- on thick skin (e.g. the palm or sole)
- is complicated by lichenification,
- characterised by thick overlying scale or crust or
- is centred on the deeper dermis rather then the epidermis
--> then a topical steroid may not work as the molecule cannot penetrate to where the disease process is
A common example of a dermal inflammatory process is granuloma annulare
- this will often respond to topical steroid with occlusion while mere application alone will have no effect
Simple steps to enhance penetration include:
(i) Application after a shower or bath and wet wrap or ‘Glad Wrap’ occlusion for 30 minutes to an hour
- also apply zinc paste to small lesions after some topical steroid has been applied
(ii) Another technique is to apply:
- a potent steroid ointment and then cover with a hydrocolloid dressing such as ‘Duoderm’ for 5-7 days
- this is especially useful in lichen simplex chronicus
- here penetration and hence therapeutic effect is enhanced and the skin is protected from scratching and rubbing
(iii) Addition of a penetrant to the ointment base is commonly done
- e.g. propylene glycol is the penetrant that converts Diprosone to Diprosone O.V.
(with the ‘OV’ standing for ‘optimised vehicle’)
(iv) Removal of overlying scale and crust either manually or with keratolytic creams etc is also of use
Enhancing penetration will increase the risk of side effects as well as response
Patient Fails To Avoid Exacerbants/Precipitants
Various skin disorders can be worsened by a variety of exacerbants
If these are not ceased then the rash will be unlikely to improve
- a common example would be the patient with a drug rash who continues to take the causal agent
Other examples include:
- sun exposure in lupus
- house dust mite in some atopic eczema
- continued use of drugs that worsen psoriasis
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(lithium, beta blockers, ACE inhibitors etc) and
- failure to avoid irritants such as soap and detergents in hand dermatitis
Patient Is Unrealistic
This is a common one
- these patients will tell you that their eczema has never been helped by topical steroids
- when questioned what they mean is that it has not been cured
- they will admit that it improved but recurred
- many steroid responsive rashes are not curable
- they are however eminently treatable
In conditions such as atopic or seborrhoeic dermatitis or psoriasis it is important to tell the patient that these
conditions will always recur and that the topical steroids will relieve symptoms and reduce or even eliminate the
eruption but that it will recur.
Variable Response
Some conditions will respond to topical steroids in some cases only:
- lupus
- lichen planus
- alopecia areata
- vitiligo
- Pityriasis Rosea etc.
--> will often respond
In other patients they will be of no use
- with the individual in front of you it is impossible to accurately predict which will be helped and which won’t
- in these patients it is worth pointing this out to them
- if the topical steroids fail other modalities can be used
Used Alone
It is important not to use steroids alone
- they will treat the inflammatory and proliferative components of a rash but other features need to be addressed
as well
- dryness being the common one
- when treating eczema for instance emollients are at least as important as topical steroids
Interestingly when eczema is secondarily infected a topical steroid alone will often result in clearing of the rash
- presumably because the bacteria die as the steroid reverses the erythema and serous ooze in the skin
Steroids can be used in combination with the following when treating psoriasis:
- tar
- dithranol
- calcipotriol
- phototherapy
Combination treatment will usually give better results and allow less use of potent steroids
On a similar note use of a topical steroid will often allow lower doses of systemic medications such as:
- Acitretin
- Methotrexate
- Cyclosporine etc.
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 121 of 123
DERMATOLOGY TIPS and TECHNIQUES
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
THE BAND-AID SIGN
Beware the patient with the bandage or band aid!
These can and do cover some nasty surprises
This man presented for review of a long standing, widespread pruritic skin condition
- on asking what the bandage was covering he replied:
'Just a boil or carbuncle'
He had been applying some 'drawing ointment' to it
When asked he admitted that it was not painful and had been present for six weeks
- neither bit of history supports a diagnosis of 'boil'
With some reluctance he allowed Dr Muir to remove the bandage to reveal the 'boil'
- as you can see it is a fairly typical keratoacanthoma although an SCC cannot be excluded on clinical grounds
- excision is indicated
This is a not uncommon approach to skin malignancies by the general public
- i.e. cover it up and hope it goes away
Most instances that Dr Muir has seen have been men or very elderly patients
As a young registrar Dr Muir very nearly sent a man with a band aid covered nodular melanoma home as the
patient assured him that the covered lesion was an 'ulcer'
One of the best dermatologists Dr Muir ever worked with used to say:
- 'more is missed by not looking than not knowing'
The following is a nice example of same
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Below you can see this lesion had an adhesive dressing covering it
- it was being treated as an 'ulcer' by staff at the nursing home
- Histology revealed it to be a largely amelanotic malignant melanoma
Reference:
This guideline is copied from 'Jim's Tips' in 'Other Resources' on the RRMEO Tele-Derm National module. To
find this module log on to: https://www.rrmeo.com - using your user name and password and from the
'Educational Inventory' select 'RRMEO Modules' - scroll down to 'Tele-Derm National' and enrol.
Back to TABLE OF CONTENTS / Dermatology Tips and Techniques
ACRRM Clinical Guidelines Version July 2012
(*Expires July 2013 - check RRMEO for latest version)
ACRRM Rural Clinical Guidelines – Dermatology Tips & Techniques – Version July 2012
Page 123 of 123