Download Document 8923652

MIDDLE EAST JOURNAL OF ANESTHESIOLOGY
Department of Anesthesiology
American University of Beirut Medical Center
P.O. Box 11-0236. Beirut 1107-2020, Lebanon
Editorial Executive Board
Consultant Editors
Editor-In-Chief:
Ghassan Kanazi
Assem Abdel-Razik
(Egypt)
Executive Editors
Fouad Salim Haddad
[email protected]
Maurice A. Baroody
Bassam Barzangi
(Iraq)
Izdiyad Bedran
(Jordan)
Chakib Ayoub
Marie Aouad
Sahar Siddik-Sayyid
Dhafir Al-Khudhairi
(Saudi Arabia)
Mohammad Seraj
(Saudi Arabia)
Managing Editor
Mohamad El-Khatib
[email protected]
Abdul-Hamid Samarkandi
(Saudi Arabia)
Founding Editor
Bernard Brandstater
Mohamad Takrouri
(Saudi Arabia)
Bourhan E. Abed
(Syria)
Mohamed Salah Ben Ammar
(Tunis)
Ramiz M. Salem
(USA)
Elizabeth A.M. Frost
(USA)
Halim Habr
(USA)
Editors
Emeritus Editor-In-Chief Anis Baraka
Honorary Editors
Nicholas Greene
Musa Muallem
Webmaster
Rabi Moukalled
Secretary
Alice Demirdjian
[email protected]
The Middle East Journal of Anesthesiology is a
publication of the Department of Anesthesiology of
the American University of Beirut, founded in 1966 by
Dr. Bernard Brandstater who coined its famous motto:
“For some must watch, while some must sleep”
(Hamlet-Act. III, Sc. ii).
and gave it the symbol of the poppy flower (Papaver
somniferum), it being the first cultivated flower in
the Middle East which has given unique service to
the suffering humanity for thousands of years. The
Journal’s cover design depicts The Lebanese Cedar
Tree, with’s Lebanon unique geographical location
between East and West. Graphic designer Rabi
Moukalled
The Journal is published three times a year (February,
June and October) The volume consists of a two year
indexed six issues. The Journal has also an electronic
issue accessed at www.aub.edu.lb/meja
The Journal is indexed in the Index Medicus and
MEDLARS SYSTEM.
E-mail: [email protected]
Fax: +961 - (0)1-754249
All accepted articles will be subject to a US $ 100.00
(net) fee that should be paid prior to publishing the
accepted manuscript
Please send dues via:
WESTERN UNION
To Mrs. Alice Artin Demirjian
Secretary, Middle East Journal of Anesthesiology
OR TO
Credit Libanaise SAL
AG: Gefinor.Ras.Beyrouth
Swift: CLIBLBBX
Name of Beneficent
Middle East Journal of Anesthesiology
Acc. No. 017.001.190 0005320 00 2
(Please inform Mrs. Demirjian [email protected]
- Name and Code of article
- Transfer No. and date (WESTERN UNION)
- Receipt of transfer to (Credit Libanaise SAL)
Personal checks, credit cards and cash, are not
acceptable
“For some must watch, while some must sleep”
(Hamlet-Act. III, Sc. ii)
SYMPOSIUM ANNOUNCEMENT
29th Annual Symposium
Clinical Update in Anesthesiology, Surgery and Perioperative Medicine
January 16-21, 2011
St. Martin, French West Indies
BROCHURE, ABSTRACT, POSTER AND PAPERS INFORMATION:
(Deadline – October 25, 2010)
Helen Philips
Mount Sinai Medical Center
1 Gustave L. Levy Place
Box 1010, Dept. of Anesthesiology
New York, NY 10029-6574
Phone: 212 – 241 – 7467
Fax: 212 – 426 – 2009
Email: [email protected]
134
Kingdom of Saudi Arabiah
National Guard Health Affairs
DEPARTMENT OF INTENSIVE CARE
The National Guard Health Affairs is considered a flagship facility in the Middle East,
providing primary and tertiary healthcare services to the National Guard forces, their
dependents and civilian employees. The National Guard group comprises of four major
hospitals and sixty healthcare center, which operate to American JCI standards. As a
Center Of Excellence, it performs all major surgeries-including cardiac surgery, liver
transplants and conjoined twin separation. We are currently inciting applications for
the following post:
•
Staff Physician – ICU
Riyadh
Our requirements in terms of academics and experience are
as follows:
MBBS/MD/Masters with Min 3 years experience in ICU/
Critical within a recognized healthcare facility.
We in turn can offer a generous tax-free salary, generous holidays, annual flights and
exceptional benefits.
If you are interested send your CV with copies of your certificates to the recruitment
office of the KAMC for the attention of John Quinn at Email: [email protected], or
fax# +966-1-2520056. Yoyr application will be treated in strictest of confidence and all
initial enquiries or requests for mor information are welcomed. For mor information
please visit our website at www.ngha.med.sa
Middle East Journal of Anesthesiology
Vol. 20, No. 6, October 2010
CONTENTS
EDITORIAL
“ROUTINE” PREOXYGENATION BEFORE INDUCTION OF AND RECOVERY FROM ANESTHESIA (A SAFETY
PRECAUTION)
����������������������������������������������������������������������������������������������������������������������������� Anis Baraka
769
REVIEW ARTICLES
ANESTHETIC MANAGEMENT Of PATIENTS WITH CORNELIA DE LANGE SYNDROME
��������������������������������������������������������������������������������� Veronica Washington and Alan D. Kaye
PERIOPERATIVE MANAGEMENT OF THE PATIENT WITH GOODPASTURE’S SYNDROME
773
������������������������������������������������������������������������������������������ Keri Copponex and Alan D. Kaye
779
SCIENTIFIC ARTICLES
TARGET-CONTROLLED INFUSION VERSUS MANUALLY CONTROLLED INFUSION ANESTHESIA WITH
PROPOFOL AND REMIFENTANIL IN MASTOIDECTOMY
�����������������������������������������������������������������������������������������Nasser Yeganeh, Bahman Roshani,
Mitra Yari and Afshin Almasi
Airway Management And Hemodynamic Response To Laryngoscopy And Intubation In
Supine And Left Lateral Positions
������������������������������������������������������������������������� Muhammad Faisal Khan, Fawzia Anis Khan
and Fawzia Nasim Minai
Fentanyl Pretreatment For Alleviation Of Perineal Symptoms Following Preoperative
Administration Of Intravenous Dexamethasone Sodium Phosphate – A Prospective,
Randomized, Double Blind, Placebo Controlled Study
������������������������������������������������ Vimi Rewari, Rakesh Garg, Anjan Trikha and Chandralekha
Transient Neurological Symptoms Following Spinal Anesthesia For Cesarean Section
785
795
803
������������������������������������������������������������������������������������������Edomwonyi, N.P. and Isesele, T.O.
Perioperative Cardiac Arrest – Analysis of Anesthetics over a 14–year Period
809
�����������������������������������������������������������������������Farouk M. Messahel and Mary June Gregorio
Efficacy Of Ultrasound-Guided Transversus Abdominis Plane (TAP) Block For PostCesarean Section Delivery Analgesia – A Double-Blind, Placebo- Controlled, Randomized
Study
��������������������������������������������������������������� Jumana M. Baaj, Raed A. AlSatli, Hayan A. Majaj,
Zainab A. Babay and Ahmed K. Thallaj
COMPLICATIONS AND INTERVENTIONS ASSOCIATED WITH EPIDURAL ANALGESIA FOR POSTOPERATIVE
PAIN RELIEF IN A TERTIARY CARE HOSPITAL
������������������������������������������������������������ Faraz Shafiq, Mohammad Hamid and Khalid Samad
CARDIOVASCULAR RESPONSES TO OROTRACHEAL INTUBATION IN PATIENTS UNDERGOING CORONARY
ARTERY BYPASS GRAFT SURGERY
��������������������������������������������������������� Nahid Aghdaii, Rasoul Azarfarin, Forouzan Yazdanian
and Seyede Zahra Faritus
EFFECTS OF INTRAOPERATIVE INTRATHECAL SUFENTANIL INJECTION ON POSTOPERATIVE PAIN
MANAGEMENT AFTER SINGLE LEVEL LUMBAR DISCECTOMY
������������������������������������������������������������������� Saeid Abrishamkar, Mohammad Hossein Karimi
Mohammad Reza Safavi, Azim Honarmand and Afshin Safavi
815
767
821
827
833
839
M.E.J. ANESTH 20 (6), 2010
The EFFECTS OF DURATION OF PROPOFOL INJECTION ON HEMODYNAMICS
����������������������������������������������������������������������������������������� Abdul Zahoor and Nauman Ahmed
CONTINUAL INFUSION OF INTRATHECAL BACLOFEN (ITB) LONG TERM EFFECT ON SPASTICITY
845
����������������������������������������������������������������� Dhafir Al-Khudhairi, Abdulrahman Shug’a Aldin,
Yousef Hamdan, Abdullah Rababah, Mona Mathana,
Jiri Pazdirek and Jalal Abdulsalam
851
CASE REPORTS
THE VIDEO LARYNGOSCOPES BLIND SPOTS AND POSSIBLE LINGUAL NERVE INJURY BY THE GLIDERITE
RIGID STYLET – Case Report and Review of Literature
�������������������������������������������������������������������������������������������Magboul Magboul and Shaw Joel
Subclavian Vein Injury And Massive Hemothorax Requiring Thoracotomy Following
Insertion Of Tunneled Dialysis Catheter – A Case Report and Literature Review –
�������������������������������������������������������������������������������������������Qutaiba Tawfic, Pradipta Bhakta,
Ahmed Khamis, Jasvinder Sharma
Cesarean Section Under Spinal Anesthesia In A Patient With Ankylosing Spondylitis
– A Case Report –
���������������������������������������������������������������������������������������������G. Ulufer Sivrikaya, Ayse Hansi,
Hale Dobrucali and Aylin Yalcinkaya
Levosimendan AS A Rescue Adjunct In Amlodipine Intoxication – A Case Report –
���������������������������������������������������������������� M. Gokhan Teker, Haluk Ozdemir, Leyla Saidoglu,
Kerem Erkalp and Gokcen Basaranoglu
SUCCESSFUL MANAGEMENT OF HIGH DOSE METFORMIN INTOXICATION – ROLE OF VASOPRESSIN IN THE
MANAGEMENT OF SEVERE LACTIC ACIDOSIS
����������������������������������������������������������������������������������������Yasin Al-Makadma and Tamer Riad
AWAKE CRANIOTOMY USING INITIAL SLEEP WITH LARYNGEAL MASK AIRWAY IN A DEPRESSED AND
AGITATED PATIENT
���������������������������������������������������������������������������������������������������������������������� Khalid Al-Suaibi
CARDIAC ARRYTHMIA AFTER SUCCINYLCHOLINE ADMINISTRATION IN A PATIENT WITH GUILLAN-BARRE
SYNDROME
��������������������������������������������������������������������������������������������������������������������������� Jyh Yung Hor
CONSCIOUS SEDATION FOR AWAKE CRANIOTOMY IN INTRA-OPERATIVE MAGNETIC RESONANCE IMAGING
OPERATING THEATRE (IMRI-OT) ENVIRONMENT
������������������������������������������������������������ Mohamad Takrouri, Firas Shubbak, Aisha Al-Hajjaj,
Ronaldo Delmaaestro, Lahbib Soualmi,
Mashael Al-Khodair, Abrar Al-Duraibi and Najeeb Ghanem
EFFECTIVE AWAKE THORACIC EPIDURAL ANESTHETIC FOR MAJOR ABDOMINAL SURGERY IN TWO HIGHRISK PATIENTS WITH SEVERE PULMONARY DISEASE – Case Report –
�����������������������������������������������������������������������E. Abd Elrazek, M. Thornton and A. Lannigan
VARIANTS OF PHEOCHROMOCYTOMA AND THEIR ANESTHETIC IMPLICATIONS
– A Case Report and Literature Review –
������������������������������������������������� Kathryn Dortzbach, Daniel Gainsburg, and Elizabeth Frost
Anesthetic Management Of Achondroplastic Dwarf Undergoing Cesarean Section
– A Case Report –
����������������������������������������������������������������������������������������� Banu Cevic and Serhan Colakoglu
768
857
861
865
869
873
877
881
885
891
897
907
EDITORIAL
“ROUTINE” PREOXYGENATION BEFORE
INDUCTION OF AND RECOVERY
FROM ANESTHESIA
(A SAFETY PRECAUTION)
Whenever you travel by air “fasten your seat belt” is the “minimum safety precaution” during
take off and landing. Similar to air flying, the risk to patients undergoing general anesthesia is
highest at induction (take off) and recovery (landing) and hence “routine” preoxygenation during
these two critical periods, can be considered a “safety precaution”1-3.
The potential for oxygen desaturation in otherwise smooth induction of anesthesia in healthy
patients has led to previous calls for “routine” preoxygenation. Although it can be argued that such
desaturation does not necessarily generate mortality or morbidity, there appears to be an overall
weight of benefit favoring this practice1-3.
Since the inception of the ASA Closed Claims project, adverse respiratory events have
constituted the single largest source of injury4. Just three mechanisms of injury accounted for
nearly three fourths of all claims for adverse respiratory events. These mechanisms are inadequate
ventilation (38%), esophageal intubation (18%) and difficult tracheal intubation (17%). Most of
these adverse respiratory events (72%) are readily diagnosed by pulse oximetry and end-tidal
capnography. Also, the consequent hypoxemia can be ameliorated by the “routine” preoxygenation.
Recent investigations have highlighted risk factors for the rapid development of hypoxemia
during apneic episodes. These risk factors are additive. It included reduced functional residual
capacity (FRC), increased oxygen consumption and/or airway obstruction. It also includes
hypoventilation prior to apnea or inadequate preoxygenation. Patients with a combination of these
factors are liable to develop rapid desaturation during apnea5.
Preoxygenation will always be mandatory in the context of “rapid-sequence induction”
of general anesthesia in patients with full stomach, and arguably so in an additional range of
scenarios as the predictable “difficult airway”. Imperative preoxygenation exists for those patients
who will not tolerate a fall in PO2 such as ischemic heart disease or atopic individuals. “Routine”
preoxygenation would also be strongly advisable when FRC is low and oxygen consumption is
high (the pregnant, the obese and children), as well as in patients with already low PO2 such as lung
disease or right-to-left shunt2.
In the absence of any of the above factors, “routine” preoxygenation offers identifiable
“safety benefits” during induction of general anesthesia1-3, since many conditions may be
unpredictable such as the “difficult intubation-difficult ventilation scenario”. Also, many adverse
drug reactions can follow induction of anesthesia such as drug-induced anaphylaxis, hypotension
and hypoventilation. Thus, the recommendation of “routine” preoxygenation will be in line with
the promotion of patient safety. However, “routine” preoxygenation must be used as an adjunct
rather than an alternative to a sequence of fundamental preoperative precautions than minimize
adverse sequalae2.
769
M.E.J. ANESTH 20 (6), 2010
770
Anis BARAKA
Recovery from anesthesia and tracheal extubation
have received limited critical safety measures compared
with attention to the identification and management of
potentially difficult intubation, despite the observation
that airway complications are more likely to be
associated with tracheal extubation than intubation6,7.
The American Society of Anesthesiologists (ASA)
Task Force on Management of the Difficult Airway
recommended that each anesthesiologist must have a
pre-formulated strategy for extubation of the difficult
airway, and an airway management plan for dealing
with post extubation hypoventilation8. “High-risk”
extubation is defined as a situation where in reestablishing a lost airway, be it due to failure of
oxygenation, ventilation or loss of airway patency is
likely to be difficult or incomplete without significant
risk.
Even routine discontinuation of anesthesia,
reversal of neuromuscular block and tracheal
extubation can be complicated with hypoxemia,
hypoventilation and loss of airway patency.
Hypoventilation and hypoxemia can result from the
residual effects of anesthetics as well as the incomplete
reversal of neuromuscular block9. Residual anesthesia
and neuromuscular block can decrease the functional
activity of the pharyngeal muscles resulting in
upper airway obstruction and in fourfold to fivefold
increase in the risk of aspiration10. The residual effects
of anesthesia and relaxants can also decrease the
contractions of the respiratory muscles resulting in
hypoventilation, as well as inability of deep breathing
and effective coughing which predispose to atelectasis.
It can also obtund the hypoxic drive by the peripheral
chemoreceptors11. In addition, Baraka has shown that
adequate oxygenation must be ensured before reversal
of neuromuscular block by neostigmine in order to
achieve safe reversal and minimize neostigmineinduced cardiac arrhythmia12,13. Jacoby et al have
shown that cardiac response to vagal stimulation is
more frequent and serious in the presence of hypoxia14.
There is evidence that “routine” preoxygenation
with 100% oxygen prior to reversal of neuromuscular
block and tracheal extubation is recommended not
only to ensure safe reversal of neuromuscular block
by neostigmine12,13 but also to improve the margin of
safety, given the potential of unpredictable airway and
ventilation problems.
Preoxygenation of the awake patient before
induction of general anesthesia increases the alveolar
oxygen and decreases the alveolar nitrogen in a parallel
fashion. “Denitrogenation” of the functional residual
capacity (FRC) of the lungs is 95% complete within
3 minutes when the subject is breathing a normal tidal
volume from a circle absorber system using a fresh gas
flow equals to the alveolar ventilation volume about
5 L/min15. A higher oxygen flow up to 10 L/min is
required whenever the alveolar ventilation volume is
high as observed during pregnancy. Also, a high oxygen
flow is required whenever “rapid” preoxygenation is
achieved by the 8 deep breaths’ technique within 60
seconds16,17. In the anesthetized patient on intermittent
positive pressure ventilation, preoxygenation during
recovery from anesthesia can be also achieved by either
the normal tidal volume ventilation for 3 minutes, or
by the 8 deep breath technique for 60 seconds.
The
effectiveness
of
preoxygenation
(denitrogenation) can be checked by an end-tidal
oxygen >80%. The achievement of SpO2 100% is not
a reason to stop denitrogenation and may occur before
the lungs are adequately denitrogenated. Conversely,
failure of SpO2 to increase substantially does not
necessarily indicate failure of denitrogenation18.
In conclusion, “routine” preoxygenation with
100% oxygen can be considered as a “safety” measure
during induction of and recovery from general
anesthesia. However, it must be used as an adjunct
rather than an alternative to a sequence of fundamental
precautions that minimized adverse sequalae.
Baraka, MD,FRCA (Hon)
Emeritus Editor-in-Chief
Middle East Journal of Anesthesiology
“ROUTINE” PREOXYGENATION BEFORE INDUCTION OF AND RECOVERY FROM ANESTHESIA
(A SAFETY PRECAUTION)
771
References
1.Kung MC, Hung CT, Ng KP, et al. Arterial desaturation during
induction in healthy adults; should preoxygenation be a routine?
Anaesthesia and Intensive Care; 1991, 19:192-196.
2.Bell MDD: Routine preoxygenation-a new “minimum standard” of
care. Anaesthesia; 2004, 59:943-945.
3.Baraka A: Routine preoxygenation. Anaesthesia; 2006, 61:612613.
4.Caplan RA: Adverse respiratory events in anesthesia: a closed claim
analysis. Anesthesiology; 1990, 72:828-833.
5.Hardman JG, Wills JS, Aitkenhead AR: Factors determining the
onset and course of hypoxemia during apnea. An investigation using
physiological modeling. Anesth Analg; 2000, 38:96-102.
6.Miller KA, Harkin CO, Bailey PL: Postoperative tracheal
extubation. Anesth Analg; 1995, 80:149-172.
7.Asai T, Koga K, Voughan RS: Respiratory complications associated
with tracheal intubation and extubation. Br J Anaesth; 1998, 80:767775.
8. American Society of Anesthesiologists. Practice Guidelines for
Management of the Difficult Airway. An update report by the
American Society of Anesthesiologists Task Force on Management
of the Difficult Airway. Anesthesiology; 2003, 98:1269-1277.
9.Baraka A: Irreversible tubocurarine neuromuscular block in the
human. Br J Anaesth; 1967, 39:891-893.
10.Eriksson LI, Sundman E, Olsson R, et al: Functional assessment
at rest and during swallowing in partially paralyzed humans.
Simultaneous videomanometry and mechanography of awake
human volunteers. Anesthesiology; 1997, 87:1035-1043.
11.Eriksson LI: The effects of residual neuromuscular blockade and
volatile anesthetics on the control of ventilation. Anesth Analg;
1999, 89:243-251.
12.Baraka A: Safe reversal (1) atropine followed by neostigmine-an
electrocardiographic study. Brit J Anaesth; 1968, 40:27-29.
13.Baraka A: Safe reversal (2) atropine-neostigmine mixture. An
electrocardiographic study. Brit J Anaesth; 1968, 40:30-36.
14.Jacoby J, Ziegler C, Hamelberg W, et al: Cardiac arrhythmia: effect
of vagal stimulation and hypoxia. Anesthesiology; 1955, 16:1004.
15.Hamilton WK, Eastwood DW: A study of denitrogenation with
some inhalation anesthetic systems. Anesthesiology; 1955, 16:861867.
16.Baraka AS, Taha SK, Aouad MT, et al: Preoxygenation.
Comparison of maximal breathing and tidal volume breathing
techniques. Anesthesiology; 1999, 91:612-615.
17.Benumof JL: Preoxygenation. Best method for both efficacy and
efficiency (Editorial). Anesthesiology; 1999, 91:603-605.
18.McCahon RA, Hardman JG: Fighting for breath: apnea vs the
anaesthetized. Anaesthesia; 2007, 62:105-108.
M.E.J. ANESTH 20 (6), 2010
review articles
ANESTHETIC MANAGEMENT IN A PATIENT
WITH CORNELIA DE LANGE SYNDROME
Veronica Washington* And Alan David Kaye**
Introduction
Cornelia de Lange syndrome (CdLS), also known as Brachmann−de Lange syndrome, is a
syndrome of multiple congenital anomalies of variable severity. This rare syndrome is genetically
heterogeneous and sporadic, with an estimated prevalence of 1 in 10,000 to 30,000. First described
by Cornelia de Lange as a diagnostic entity in 1933, Vrolik and Brachmann reported isolated
cases in severely affected infants between 1849 and 1916. The syndrome is best characterized
by distinctive facial appearance, prenatal and postnatal growth deficiency, psychomotor delay,
and upper limb malformations. Although almost all organ systems can be affected, individuals
with CdLS most notably display deficits in the development of neurosensory, craniofacial,
musculoskeletal, cardiac and gastrointestinal systems. There is no known cure but the syndrome
can be managed by treating associated clinical symptoms. Sixty six percent of CdLS individuals
die before the first year of life1. Mortality occurs primarily from aspiration in infancy and from
infection and bowel obstruction there after1.
Pathogenesis
Several genes have been discovered in CdLS (NIPBL, SMC1A, SMC3), all of which are
involved in sister chromatid cohesion. Cohesion proteins are involved in chromosome segregation,
regulation of gene expression, DNA repair and maintenance of genome stability. Mutations in
NIPBL on chromosome 5 account for~ 60% of CdLS cases, while mutations in SMC1A on the
inactivated X chromosome, and SMC3 on chromosome 10 account for ~5%2. NIPBL and SMC3
mutations are both believed to have an autosomal dominant inheritance. SMC1A mutations are
believed to have an X-linked dominant pattern of inheritance, however males and females are
affected similarly. The genotype-phenotype correlation reveals that mutations in NIPBL result in
more severe phenotypes than mutations in SMCA1 and SMC3 genes2. Moreover, the associated
phenotype in NIPBL mutations increases in severity as the severity of the mutation increases. More
severe mutations occur in NIPBL deletions or truncations, while milder forms of CdLS occur in
patients with NIPBL missense mutations. SMCA1 and SMC3 gene mutations are predominantly
missense and small in-frame deletions. The phenotype in patients with SMCA1 and SMC3
mutations is milder, consisting mainly of mild to moderate mental retardation, without associated
severe growth retardation, limb or systemic involvement3,4. Although mutations in these genes are
implicated in 65% of patients, the pathogenesis of most cases of CdLS is sporadic and dominant2.
*
**
MD, MPH, Resident, LSU Dept. of Family Practice at Bogalusa Medical Center, Mississipi.
MD PhD DABPM, Professor and Chairman, Department of Anesthesiology and Professor, Depart. of Pharmacology,
LSU School of Medicine, Room 656, 1542 Tulane Ave. New Orleans, Louisiana, 70112.
For additional information, contact Dr. Alan D. Kaye, MD PhD DABPM, Professor and Chairman, Department of
Anesthesiology, LSU School of Medicine, 1542 Tulane Ave, New Orleans, Louisiana, U.S.A. Tel: 504-568-2319, E-mail:
[email protected].
773
M.E.J. ANESTH 20 (6), 2010
774
V. Washington & A. D. Kaye
Clinical Manifestations
CdLS is diagnosed based on clinical signs and symptoms (Table 1).
Table 1
Diagnostic Criteria for Cornelia de Lange Syndrome
Body category
No.
(1) Facial
(2) Growth
>2 of
(3) Development
>1 of
(4) Behavior
>2 of
Main criteria
With
Secondary criteria
Synophrys (arched, fine eyebrows)
and >3 of Long eyelashes
Short nose, anteverted nares
Long, prominent philtrum
Broad or depressed nasal bridge
Small or square chin
Thin lips, down-turned corners
High palate
Widely spaced or absent teeth
(6) Neurosensory/
Skin
>3 of
Weight below 5th centile for age
Height or length below 5th centile for age
OFC below 2nd centile for age
Developmental delays or mental retardation
Learning disabilitites
Attention deficit disorder ± hyperactivity
Obsessive-compulsive characteristics
Anxiety
Constant roaming
Aggression
Self-injurious behavior
Extreme shyness or withdrawal
Autistic-like features
Reduction defects with absent forearms
alone
Small hands and/or feet (below 3rd centile) or and >2 of
Oligodactyly
None of these
and >3 of 5th finger clinodactyly
Abnormal palmar crease
Radial head dislocation/abnormal
elbow extension
Short 1st metacarpal/proximally
placed thumb
Bunion
Partial 2,3 syndactyly toes
Scoliosis
Pectus excavatum
Hip dislocation or dysplasia
Ptosis
(7) Other major
systems
>3 of
Tear duct malformation or blepharitis
Myopia -6.00 D
Major eye malformation or peripapillary
pigmentation
Deafness or hearing loss
Seizures
Cutis marmarata
Hirsutism, generalized
Small nipples and/or umbilicus
Gastrointestinal malformation/malrotation
(5) Musculoskeletal
OR
OR
Diaphragmatic hernia
Gastroesophageal reflux disease
Cleft palate or submucous cleft palate
Congenital heart defect
Micropenis
Hypospadias
Cryptorchidism
Renal or urinary tract malformation
OFC = head circumference. Diagnosis: (1) Positive mutation on CdLS gene testing; or (2) Facial findings and meet criteria from two
of the growth, development or behavior categories; or (3) Facial findings and meet criteria for three other categories, including one
from growth, development or behavior, and two from the other categories (see notes). Adapted from Kline AD et al. Cornelia de Lange
syndrome: Clinical review, diagnostic and scoring systems, and Anticipatory guidance. American journal of medical genetics part A
2007; 143A: 1287-1296.
ANESTHETIC MANAGEMENT IN A PATIENT WITH CORNELIA DE LANGE SYNDROME
775
Table 2
Anesthetic Considerations in CdLS
Cardiac Anomalies
Provide endocarditis prophylaxis.
Pulmonary Anomalies
Increase risk of respiratory infections, irritable airway, hypoxia, and hypercapnia.
Renal dysfunction
Renally dose drugs
Airway
Risk of aspiration, and occlusion of airway. Prepare for difficult intubation.
Contraindicated drugs
Halothane and nitrous oxide
Recommended induction agents
Sevoflurane, isoflurane, ketamine, etomidate, and narcotics
Malignant Hyperthermia
Associated with paralysis in the presence of strabismus.
Cranio facial
Facial features are the most distinctive clinical
feature. The head is microcephalic, with a low hairline
on the forehead and posterior neck. Eyebrows are
confluent and well defined, extend down to the nasal
ridge and are highly arched in 98%5. Eyelashes are
thick and long with an exaggerated upward curve of
upper eyelashes and an exaggerated downward curve
of bottom eyelashes. Hypertelorism and antimongoloid
slant of the eyes are also noted. The midface has a
flattened appearance with a short nose and anteverted
nares. The nasal bridge is usually broad or depressed.
The philtrum is long, smooth, and prominent, while
the lips are thin with downturned corners. These
patients also have micrognathia or square chin with
a high arched palate and cleft palate in 30%5. Dental
anomalies include widely spaced small teeth, absent
teeth, and crowded teeth. Ears are low set, posteriorly
rotated, and often hirsute.
Cardiovascular
The incidence of congenital heart disease is as
high as 20 – 30%, compared to 0.8% for all births5. The
most common abnormalities include (in descending
order): ventricular septal defects, atrial septal defects,
pulmonic stenosis, tetralogy of Fallot, hypoplastic left
heart syndrome, and tricuspid aortic valve. Some heart
defects have obvious signs and symptoms at birth that
will prompt an evaluation by a pediatric cardiologist.
Other defects are subtle and are not always recognized at
birth; therefore detection of congenital heart disease in
CdLS patients may be delayed. It is recommended that
every CdLS patient be evaluated by echocardiogram.
Musculoskeletal
Along with the distinctive craniofacial features,
specific extremity findings help in establishing a
diagnosis of CdLS. Although lower extremity findings
are less common, over 80% of affected individuals
have partial syndactyly of toes 2 and 35. Hands and
feet are small in measurement in over 90%, and
single palmar creases are observed in over 50%5.
Fifth finger clinodactyly is observed in 74%, as well
as bradydactyly5. The first metacarpal is usually
disproportionately shortened with a proximally placed
thumb6. Upper extremity malformations are observed
in up to 30% of patients, and range from oligodactyly
to ulnar deficiency to absent forearm, with digit(s)
present distal to the elbow6. Other common extremity
findings include radial head dislocation with abnormal
elbow extension, clubbed feet and poikilothermia.
Pectus excavatum, scoliosis and hip dislocation or
dyplasia are other common musculoskeletal findings.
Gastrointestinal
Gastroesophageal reflux disease (GERD) is the
most common GI complication in CdLS patients, with
an incidence of over 90%6. Esophagitis, aspiration,
chemical pneumonitis, and irritability are complications
of GERD that can be avoided by diagnosis and treatment
in the neonatal period. Pyloric stenosis has been
reported, and may contribute to malnutrition and poor
weight gain during the newborn period. Malrotation
occurs in at least 10% and is associated with an
increase risk of volvulus6. Congenital diaphragmatic
hernia also occurs, however the reported incidence
varies and may be underestimated secondary to infants
who die in the perinatal period.
Genitourinary
Up to 40% of CdLS patients have structural
kidney and/or urinary tract anomalies, the most
M.E.J. ANESTH 20 (6), 2010
776
common are vesiculoureteral reflux, pelvic dilation
and renal dysplasia, with the possibility of deficient
renal function6. Genitalia malformations have also
been reported in many CdLS cases. Crytorchidism has
been reported in up to 73% of males, in addition to
hypoplastic and micropenis in 57% and hypospadias6.
Females may have small labia majora and abnormally
formed uteri.
Auditory and Vision
Up to 60% of affected individuals have hearing
loss, including both sensorineural and conductive6. Ear
canals are narrow if not stenotic, which predisposes
these patients to otits media and sinusitis6. The most
common ophthalmologic findings are peripapillary
pigmentations, high myopia, ptosis, microcornia, and
blepharitis. Rare ophthalmologic findings include
nasolacrimal duct obstruction, nystagmus, cataract and
glaucoma.
Neuropsychiatric
Behavioral issues in CdLS patients are speculated
to be secondary to frustration from an inability
to communicate. Many individuals demonstrate
behavior consistent with depression and attention
deficit hyperactivity disorder, and display obsessivecompulsive behavior, autistic behavior, including selfdestructive tendencies, defiance, extreme shyness and
avoidance of social interactions.
Growth and Developmental Retardation
Growth failure occurs in over 95% of patients with
CdLS6. Proportionate small stature begins prenatally,
although most significant by six months of age, and
continues throughout life. Although growth in CdLS
parallels standard growth curves, mean height and
weight remain below the 5th percentile6. Developmental
delay is observed in over 95%6. Patients with classic
CdLS experience profound to severe developmental
delays. The overall IQ ranges from below 30 to 102,
with an average of 537,8. Patients with mild forms of
CdLS have higher functioning with IQ ranging from
normal to borderline IQ with learning disabilities9.
However, most individuals experience disabilities in
speech and language.
V. Washington & A. D. Kaye
Anesthetic Considerations
Pharmacology
General anesthesia is often necessary in CdLS
patients due to non-cooperative and hyperactive
behavior. However, perioperative sedation should be
light due the possibility of upper airway obstruction
and unpredictable responses to drugs secondary to
endocrine disorders10. In cases in which rapid induction
of anesthesia is necessary, ketamine or etomidate are
often recommended due to limited cardiac depressant
effects 10. In patients with suspected or confirmed
pulmonary hypertension inhalational agents and
narcotics are recommended10. Newer inhalation
agents, including desflurane and sevoflurane, allow for
faster recovery than older agents such as halothane.
Nitrous oxide should be avoided since it can increase
pulmonary vascular resistance10. Also, caution with
induction of paralysis in patients with strabismus
is warranted, as there is a reported association of
malignant hyperthermia in these patients10.
Cardiorespiratory
Preanesthetic examination to access for
cardiorespiratory system is extremely important and
often difficult. Many have previously undiagnosed
congenital cardiac anomalies including tetralogy
of Fallot, pulmonary or aortic stenosis, atrial septal
defect, ventricular septal defect, pulmonary ductus
arteriosus, hypoplasia of the left ventricle and
abnormal electrocardiographic findings (i.e. AV block,
left ventricular hypertrophy, and right ventricular
hypertrophy) that are unveiled during anesthetic
management. Cases of right bundle branch block, with
and without murmur, first observed during anesthetic
management have been reported10. Confirmation of any
of these cardiac anomalies necessitates administration
of antibiotics for endocarditis prohylaxis10.
Postoperative complications in such patients include
unstable cardiac function and marked susceptibility
to infections. In patients with both cardiac anomalies
and repeated episodes of upper airway obstruction
secondary to macroglossia and micrognathia,
pulmonary hypertension may develop, which may
complicate anesthesia with the development of
hypoxia and hypercapnia10. Successful perioperative
ANESTHETIC MANAGEMENT IN A PATIENT WITH CORNELIA DE LANGE SYNDROME
management of such cases may include increasing
FiO2 to achieve adequate O2 saturations, and if
warranted, prostaglandins, and even nitric oxide10.
Pulmonary hypoplasia and lobular anomalies
predispose CdLS patients to respiratory infections.
The most common causes of death in such patients
are acute pneumonia and bronchitis11. The airway is
considered to be irritable and the administration of
intravenous hydrocortisone has been shown to relieve
asthma-like symptoms that occurred during general
anesthesia11.
Renal/Endocrine
Endocrine disorders and renal dysfunction,
secondary to immaturity and malformation, necessitate
preanesthetic evaluation to determine renal function and
preparation for potential postoperative complications.
Dosing of drugs excreted by the kidneys, should be
carefully assessed.
Airway
Anesthetic management may pose a serious
problem due to aspiration complications, and difficult
intubation secondary to craniofacial anomalies
characteristic of CdLS. The risk of aspiration secondary
to GERD may be managed with premeditation
including famotidine, metoclopramide and/or sodium
bicitrate, and utilizing a rapid sequence induction with
succinylcholine to offer some protection form stomach
content aspiration.
Intubation in patients with CdLS almost always
requires a tube of smaller size than that which is
age appropriate due to the immature development
of airway structures, most notably the presence of a
hypoplastic larynx11. The craniofacial features that
pose a risk of difficult intubation include macroglossia,
cleft lip/palate, midface hypoplasia, high arched
palate, and mandibular hypoplasia. In the case of
macroglossia, the enlarged tongue fills the oral cavity,
which obstructs the airway and impedes visualization
of the larynx. Obstruction by the tongue can also
occur in individuals with cleft palates. In this case,
the nasal airway is obstructed if the tongue falls into
the cleft, and oropharynx will be completely occluded
777
if the tongue falls posteriorly with relaxation of the
oropharyngeal musculature12. In midface hypoplasia,
the palate is high and arched, and the nasal passages
are small, therefore these individuals are primarily
mouth breathers, which can potentially pose a problem
during mask ventilation12. When the mouth is closed,
the tongue occludes the small oral cavity and the small
nasal passage creates resistance to nasal airflow, which
can be overcome by holding the mouth open during
induction12. Craniofacial dysostosis makes mask fit
difficult; therefore maintaining a good mask seal is
paramount12. In mandibular hypoplasia the anterior
mandibular space is decreased, thereby decreasing
the space into which the tongue is displaced during
laryngoscopy, and making tracheal intubation more
difficult12. Such patients should be managed with
fiberoptic intubation, glide scope, or other advanced
airway techniques. In general, difficult intubations
encountered in CdLS are best managed by having an
introducer, laryngeal mask or fiberoptic bronchoscope
readily available. A laryngeal mask airway is
recommended as an alternative to mask ventilation or
tracheal intubation, and as a tool in fiberoptic scope
assisted tracheal intubation13. Laryngeal mask airway
is also beneficial in that it does not require paralysis,
which may be relevant in individuals with strabismus,
which can be associated with malignant hyperthermia13.
Some literature advocates corticosteroid application
prior to intubation to prevent airway trauma and edema
from potential multiple intubation attempts14.
Conclusion
Although specific gene mutations can be found
in some patients, genetic testing is usually reserved to
confirm an already highly suspected CdLS diagnosis.
At present there is no cure for CdLS. Treatment is
symptomatic and therapy based. Early intervention
by means of medical and surgical care are necessary
for feeding difficulties, congenital heart disease,
urinary, auditory and visual abnormalities, as well as
psychomotor delay. In summary, the anesthetic care of
the patient with CDLS is often challenging and a well
thought out perioperative plan can potentially reduce
morbidity and mortality.
M.E.J. ANESTH 20 (6), 2010
778
V. Washington & A. D. Kaye
References
1. Sargent, WW: Anesthetic management of a patient with Cornelia de
Lange syndrome. Anesthesiology; 1991, 74:1162-1163.
2. Revekova E, Focarelli ML, Susani L, et al: Cornelia de Lange
mutations in SMC1A or SMC3 affect binding to DNA. Human
Molecular Genetics; 2009, 18: 418-427.
3. DeardoffM, Kaur M, Yaeger D, et al: Mutations in cohesion
complex members SMC3 and SMC1A casue a mild variant of
Cornelia de Lange syndrome with predominant mental retardation.
American Journal of Human Genetics; 2007, 80:485-494. 16.
4. Musio A, Selicorni A, Focarelli ML, et al: X-linked Cornelia de
Lange syndrome owing to SMC1L1 mutations. Nature Genetics;
2006, 38:528-530.
5. Jackson L, Kline AD, Barr MA, Koch S: De Lange syndrome: a
clinical review of 310 individuals. American Journal of Medical
Genetics; 1993, 47:940–946.
6. Kline AD, Krantz ID, Sommer A, Kliewer M., Jackson LG,
Fitzpatrick DR, Levin AV, Selicorni A: Cornelia de Lange
syndrome: Clinical review, diagnostic and scoring systems, and
Anticipatory guidance. American journal of medical genetics part
A; 2007, 143A:1287-1296. 6.
7. Kline AD, Stanley C, Belevich J, Brodsky K, Barr M, Jackson
LG. Developmental data on individuals with the Brachmann-de
Lange syndrome. American Journal of Medical Genetics; 1993,
47:1053–8.
8. Saal HM, Samango-Sprouse CA, Rodnan LA, Rosenbaum KN,
Custer DA: Brachmann-de Lange syndrome with normal IQ.
American Journal of Medical Genetics; 1993, 47:995–8.
9. Moeschler JB, Graham JM Jr: Mild Brachmann-de Lange
syndrome. Phenotypic and developmental characteristics of mildly
affected individuals. American Journal of Medical Genetics; 1993,
47:969–76.
10.Corsini LM, Stefano GD, Porras MC, Galindo S, Palencia J:
Anaesthetic implications of Cornelia de Lange syndrome. Paediatric
Anaesthesia; 1998, 8:159-162.
11.Takeshita T, Akita S, Kawahara M: Anesthetic management of a
patient with Cornelia de Lange syndrome. Anesthesia Progress;
1987, 34: 63-65.
12.Nargozian C: The airway in patients with craniofacial abnormalities.
Pediatric Anesthesia; 2004, 14:53-59.
13.Garcia RF, Mencia TP, Gutierrez-Jodra A, Garcia AL: Anesthetic
management with laryngeal mask in a child with Brachmann de
Lange syndrome. Pediatric Anesthesia; 2006, 16:698-700.
14.Küçükyavuz Z, Özkaynak Ö, Tüzüner AM, Kisnisçi R. Difficulties
in anesthetic management of patients with micrognathia: report of a
patient with Stickler Syndrome. Oral surgery, oral medicine, oral
pathology, oral radiology, and endodontics; 2006, 102; e33-e36.
PERIOPERATIVE MANAGEMENT OF THE PATIENT
WITH GOODPASTURE’S SYNDROME
Keri Copponex * and Alan David. Kaye **
Introduction
Goodpasture’s Syndrome (GS) is characterized by the classic triad of diffuse pulmonary
hemorrhage, glomerulonephritis, and circulating anti-basement membrane antibodies1. It is an
uncommon disorder, with an incidence estimated to be 0.3 cases per 100,000 people per year2.
There is a male predominance, with a male to female ratio between 2:1 and 9:13. The disease
may present at any age, although it most commonly manifests between the ages of 20 and 30
years1. Goodpasture first described the pulmonary renal syndrome in 1919 during the influenza
epidemic. However, it was not until 1958 that Stanton and Tange referenced Goodpasture’s original
description in their report of young men with pulmonary hemorrhage and glomerulonephritis1. The
role of anti-GBM antibodies in the pathogenesis of GS was discovered in 19671. Reported risk
factors for the development of GS include exposure to hydrocarbons, cigarette smoking, and a
preceding viral illness, especially influenza2.
Clinical Manifestations
While there is considerable variation in the clinical presentation of GS, the initial symptoms
most cases include progressive dyspnea and hemoptysis (seen in 80% to 95%), which may range
in severity from blood-tinged sputum to massive hemorrhage4. Additionally, some patients have
alveolar hemorrhage, evident only on biopsy or bronchoalveolar lavage1. Between 20% and 40%
of patients have only renal disease, and less than 10% have only pulmonary disease1. Patients
may present initially with hemoptysis only, then develop glomerulonephritis months or years
later. Alternatively, some patients may present with glomerulonephritis and either later develop
pulmonary hemorrhage or never develop pulmonary hemorrhage2. Unlike systemic inflammatory
disorders, GS typically does not cause clinical signs of inflammation, although some patients may
have prodromal symptoms such as nausea, vomiting, fatigue, and weight loss.
Continuous pulmonary hemorrhaging can result in hypoxemia and significant iron deficiency,
with decreased levels of serum iron and ferritin1. If massive hemoptysis occurs, the alveolar spaces
are rapidly flooded with blood, resulting in respiratory failure. Acute pulmonary hemorrhage is seen
as bilateral patchy areas of dense alveolar infiltrates on chest radiographs, and air bronchograms are
also often present2. The apices and costophrenic angles are generally not involved3. Some patients
may have a normal chest radiograph; however, CT scan may reveal parenchymal abnormalities3.
After a patient has an acute episode of pulmonary hemorrhage, serial chest radiographs demonstrate
a predictable change in pattern. Within 2 to 3 days, the initial patchy areas of consolidation disappear
and a reticulonodular pattern becomes evident3. The pattern becomes distinctly reticular within 1
week, and the chest radiograph usually returns to normal in 10 to 12 days3.
*
**
MD, Resident, Department of Anesthesiology, Louisiana State University School of Medicine in New Orleans.
MD, PhD, Professor and Chairman, Department of Anesthesiology and Professor, Department of Pharmacology,
Louisiana State University School of Medicine in New Orleans.
Address Correspondence to: Alan D. Kaye, MD., Ph.D., DABPM, Professor and Chairman, Department of Anesthesiology,
Louisiana State University School of Medicine, 1542 Tulane Ave, Room 656, New Orleans, LA 70112. Tele: (504) 5682319, Fax: (504) 568-2317, E-mail: [email protected]
779
M.E.J. ANESTH 20 (6), 2010
780
GS patients with renal disease usually have
rapidly progressive glomerulonephritis (RPGN).
Renal dysfunction causes azotemia, as well as
proteinuria, hematuria, and red blood cell casts are
seen on urinalysis. 1 Without treatment, end-stage renal
failure may occur within days to weeks after the onset
of symptoms2.
Pathogenesis
Genetics are likely involved in the pathogenesis of
GS, given that there is a strong association between the
disease and HLA-DR2. There is an increased incidence
of HLA-DR2 in patients with GS when compared to
the general population5. However, additional factors
must also be involved, as most cases are sporadic. GS
is defined by the presence of antibodies that target the
carboxyl-terminal region of the alpha-3 chain of type
IV collagen1. Only the lungs and kidneys, are involved
despite the presence of type IV collagen throughout
the body. This effect may be explained because the
antigen is more accessible to the antibody in the
alveoli and glomeruli or because of the predominance
of the alpha-3 chain in the alveoli and glomeruli rather
than in other tissues1. Structural differences between
the alveoli and glomeruli may explain why some
patients develop only alveolar hemorrhage or only
glomerulonephritis, as opposed to the combination
of the two pathologies. One such difference is the
presence of fenestrae in the glomerular endothelium,
which grant greater accessibility of the antibodies to
the basement membrane1. These fenestrae are absent
in the alveolar endothelium3.
Diagnosis
Microscopic abnormalities associated with
GS include intra-alveolar blood, hemosiderin-laden
macrophages in the alveoli and interstitium, interstitial
fibrosis, and type II cell hyperplasia1. Occasionally,
there may be a lymphocytic interstitial infiltrate.
Results of electron microscopy have been inconsistent,
with findings ranging from no abnormalities to
thickening, splitting, discontinuity, or smudging of the
basement membrane1. However, none of these findings
is diagnostic of GS. Confirmation of the diagnosis is
accomplished by performing a renal biopsy and proving
the presence of tissue-bound anti-basement membrane
K. Copponex & A. D. Kaye
antibodies by enzyme-linked immunosorbent assay
(ELISA)3. If a biopsy is contraindicated, the diagnosis
can be made by serologic testing and demonstration
of the presence of anti-basement membrane antibodies
in the serum with either indirect immunofluorescence
or ELISA. Focal or diffuse crescentic and necrotizing
glomerulonephritis is seen on light microscopic
examination of kidney tissue, and immunofluorescence
shows linear staining of IgG along the glomerular
basement membrane3. Immunofluorescence of lung
tissue demonstrates diffuse linear staining along the
alveolar wall, usually attributable to IgG.
Pulmonary function testing is not useful in
diagnosing GS, but may help in monitoring the course
of the disease4. Patients generally demonstrate a
restrictive pattern, along with a decreased diffusing
capacity and a decrease in resting PaO2, which may exist
even during remission of the disease3. The diffusing
capacity of the lung for carbon monoxide (DLCO)
may be increased due to intraalveolar blood binding
to carbon monoxide4. When measured throughout
the disease, the Diffusing Capacity of the Lung for
Carbon Monoxide (DLCO) may help to identify an
acute pulmonary hemorrhage versus other causes of
radiographic opacities4.
Prognosis and Treatment
Prior to the development of immunosuppressive
therapy and plasmapheresis, GS was usually fatal,
secondary to either lung hemorrhage or renal failure.
However, corticosteroids, immunosuppressants, and
plasmapheresis have greatly improved outcome,
although some patients remain dependent on dialysis1.
Three to six months of treatment are usually required,
though symptoms begin to resolve within two
months5. Plasmapheresis rapidly decreases the level of
circulating anti-basement membrane antibody, while
corticosteroids and immunosuppressants (namely,
prednisone and cyclophosphamide) decrease the
production of antibody6. If irreversible kidney damage
has taken place at the time of diagnosis, the patient
may receive a kidney transplant only after the antibasement membrane antibodies have been cleared
from the serum3. Otherwise, if irreversible kidney
damage has not occurred when the diagnosis is made,
chronic immunosuppression can prevent progression
PERIOPERATIVE MANAGEMENt OF THE PATIENT WITH GOODPASTURE’S SYNDROME
of renal damage and a kidney transplant often is not
necessary3.
Anesthetic Considerations
Preoperative Assessment
Elective surgery should be delayed until the
disease is in an inactive state5. Chest radiographs,
pulmonary function studies, and arterial blood gases
can be used to evaluate the patient’s pulmonary status,
while renal function studies, urinalysis, and blood
chemistries indicate renal function5. Causes of renal
insufficiency, other than glomerulonephritis, should
also be sought. Prerenal factors such as hypovolemia
and decreased cardiac output can compound the GSinduced renal dysfunction, and should be corrected
to avoid further kidney damage. Dialysis-dependent
patients should be dialyzed shortly before surgery to
correct volume overload, hyperkalemia, and acidosis5.
Renal failure often demands that drug selection and
dosing be modified. In general, the technique of choice
when applicable would be the use of local anesthetics
for local or regional blockade whenever possible
with careful sedation. However, there are significant
considerations in the delivery of anesthetics to GS
patients.
Pulmonary
Due to the alveolar hemorrhage that occurs in
GS, oxygenation of the patient during surgery is the
principal challenge of the anesthesiologist5. Blood in
the alveoli makes gas exchange difficult. Furthermore,
continuous alveolar hemorrhaging results in anemia,
which plays an additional role in diminished tissue
oxygen delivery5. A larger than normal sized
endotracheal tube should be used to intubate to allow
for better pulmonary suction. Care should be taken to
avoid high airway pressure, increased oxygen tension,
and other stresses on the lungs, as this may worsen
antibody-mediated lung injury5.
Renal
Renal failure in GS, as in all cases of renal failure,
can affect the volume of distribution, metabolism,
and excretion of certain anesthetic drugs. Watersoluble metabolites that are minimally active may
781
accumulate and prolong the effects of the parent drug7.
The elimination half-life of drugs that are excreted
unchanged by the kidneys can be prolonged in renal
failure. The protein loss and uremia that occur in renal
failure may potentiate the effects of drugs that are
typically protein-bound7.
Thiopental requires a decreased induction dose
because its free fraction is nearly doubled in renal
failure8. The dosing of ketamine, on the other hand,
does not need to be altered because it is not highly
protein-bound and its free fraction is minimally
affected by renal failure9. Etomidate exhibits less
protein binding in renal failure patients than it does in
normal patients, but the larger free fraction does not
appear to alter its clinical effects10. Propofol is quickly
metabolized by the liver into inactive metabolites that
are then excreted by the kidney; thus renal failure does
not result in extension of its clinical effects11. The
plasma free fraction of benzodiazepines is increased by
renal failure because these drugs are normally highly
protein-bound. Additionally, benzodiazepines have
active metabolites that can accumulate after repeated
doses in renal failure and lead to prolonged sedation7.
Midazolam is metabolized to an active alpha-hydroxy
compound, and 60-80% of the drug is excreted in this
form12. The metabolite accumulates after long-term
infusions in renal failure, therefore causing a longer
time of sedation13. Renal failure patients are more
sensitive to the sedative effects of alprazolam because
it has less protein binding and an increased free
fraction when compared to individuals with normal
renal function14. Dexmedetomidine is hepatically
metabolized. When given to patients with impaired
renal function, sedation was longer when compared to
patients with normal renal function, likely due to less
protein binding in the presence of renal dysfunction15.
While the pharmacokinetics of a single dose
of morphine are unaffected in a chronic renal failure
patient, long-term administration causes its active
metabolite morphine-6-glucuronide to accumulate and
exert potent analgesic and sedative effects16. Thus, the
dose of morphine should be decreased in the presence
of renal dysfunction. Meperidine is metabolized to
the neurotoxic compound normeperidine, which
must be excreted by the kidneys and therefore should
not be administered to patients with renal failure7.
M.E.J. ANESTH 20 (6), 2010
782
Hydromorphone’s active metabolite hydromorphone3-glucuronide also accumulates in renal failure patients
and can cause cognitive dysfunction and myoclonus17.
Renal failure patients have a longer elimination time
for oxycodone, thus repeated doses cause prolonged
effects18. Codeine is not recommended for long-term
use in patients with renal dysfunction because it can
also cause prolonged narcosis16. Because fentanyl
does not have active metabolites, has an unchanged
free fraction, and has a short redistribution phase, it
is well-tolerated and is a good choice19. Alfentanil
has decreased protein binding in the presence of
renal disease, but because its elimination half-life
and clearance are unaffected, the total dose should be
similar to that for patients without renal disease20.
With the exception of succinylcholine,
atracurium, cis-atracurium, and mivacurium, muscle
relaxants rely heavily on renal excretion and therefore
result in prolonged effects in patients with chronic
renal failure7. In renal failure, most nondepolarizing
muscle relaxants must be either excreted by the liver
or metabolized to inactive forms7. Some muscle
relaxants, such as vecuronium, are metabolized to
active compounds that must be excreted by the kidneys,
resulting in prolonged effects in GS patients7. Because
succinylcholine does not result in a major prolongation
of clinical effects, it may be used for rapid-sequence
intubation.
Due to the shorter duration of action, the
intermediate-acting atracurium, cis-atracurium, and
K. Copponex & A. D. Kaye
rocuronium are preferred over the long-acting muscle
relaxants for patients with renal failure5. Atracurium
and cis-atracurium are recommended because their
metabolites do not depend on renal clearance and
the elimination half-life, clearance, and duration of
action are not affected by renal failure21. Vecuronium
exhibits prolonged effects in patients with renal
dysfunction due to decreased plasma clearance and
increased elimination half-life22. An additional cause
for lengthening of the clinical duration of vecuronium
is that it is metabolized to 3-desmethylvecuronium, an
active compound that accumulates in renal failure23.
Mivacurium is a short-acting muscle relaxant that, like
succinylcholine, is eliminated by pseudocholinesterase.
In renal failure patients with a lower level of plasma
pseudocholinesterase, recovery from a dose of
mivacurium is slower24.
Conclusion
Although it is uncommon, Goodpasture’s
Syndrome is a disease that anesthesiologists may
encounter and which poses many challenges. The
extensive renal involvement dictates which drugs
should be administered and which avoided. Complex
pulmonary manifestations require that special care be
taken in management of the airway. Patients should be
treated with corticosteroids, immunosuppressants, and
plasmapheresis to render the disease dormant before
elective surgery is performed.
PERIOPERATIVE MANAGEMEnT OF THE PATIENT WITH GOODPASTURE’S SYNDROME
783
References
1.Ball JA, Young Jr KR: Pulmonary Manifestations of Goodpasture’s
Syndrome. Clinics in Chest Medicine; 1998 Dec. (19)4:777-791.
2.Homer RJ: “Depositional Diseases of the Lungs”. Fishman’s
Pulmonary Diseases and Disorders, vol. 1, 4th ed. Ed. Fishman AP,
Elias JA, Fishman JA, Grippi MA, Senior RM, Pack AI. New York,
NY: McGraw-Hill; 2008, 1239-1241, 1287-1288.
3.Fraser RS, Colman N, Muller NL, Paré PD: Fraser and Paré’s
Diagnosis of Diseases of the Chest. vol. 3, 4th ed. Philadelphia, PA:
W.B. Saunders Company; 1999, 1757-1765.
4.Morris DG, Botway MB, Homer RJ, Noble PW, Reynolds HY,
Matthay RA: “Diffuse Parenchymal and Alveolar Lung Diseases”.
Chest Medicine: Essentials of Pulmonary and Critical Care. 5th ed.
Ed. George RB, Light RW, Matthay MA, Matthay RA. Philadelphia,
PA: Lippincott, Williams & Wilkins; 2005, 265-266.
5.Cartagena R, Passannante A, Rock P: “Respiratory Diseases”.
Anesthesia and Uncommon Diseases. 5th ed. Ed. Fleisher LA.
Philadelphia, PA: W. B. Saunders Company; 2006, 136-137.
6.Levy JB, Turner AN, Rees AJ, Pusey CD: Long-term outcome
of anti-glomerular basement membrane antibody disease treated
with plasma exchange and immunosuppression. Annals of Internal
Medicine; 2001, 134:1033.
7.Stafford-Smith M, Shaw A, George R, Muir H: “The Renal
System and Anesthesia for Urologic Surgery”. Clinical Anesthesia,
6th ed. Ed. Barash PG, Cullen BF, Stoelting, RK. Philadelphia, PA:
Lippincott, Williams & Wilkins; 2009, 1356-1358.
8.Burch PG, Stanski DR: Decreased Protein Binding and Thiopental
Kinetics. Clinical Pharmacology & Therapeutics; 1982, 32:212.
9.Reich DL, Silvay G: Ketamine: An update on the first twenty-five
years of clinical experience. Canadian Journal of Anaesthesia;
1989, 36:186.
10.Carlos R, Calvo R, Erill S: Plasma protein binding of etomidate
in patients with renal failure or hepatic cirrhosis. Clinical
Pharmacokinetics; 1979, 4:144.
11.Kirvela M, Olkkola KT, Rosenberg PH, et al: Pharmacokinetics
of Propofol and Haemodynamic Changes during Induction of
Anaesthesia in Uraemic Patients. British Journal of Anaesthesia;
1992, 68:178.
12.Vinik HR, Reves JG, Greenblatt DJ, et al: The pharmacokinetics
of midazolam in chronic renal failure patients. Anesthesiology;
1983, 59:390.
13.Driessen JJ, Vree TB, Guelen PJ: The effects of acute changes in
renal function on the pharmacokinetics of midazolam during longterm infusion in ICU patients. Acta Anaesthesiologica Belgica;
1991, 42:149.
14.Schmith VD, Piraino B, Smith RB, et al: Alprazolam in end-stage
renal disease. II. Pharmacodynamics. Clinical Pharmacology &
Therapeutics; 1992, 51:533.
15.De Wolf AM, Fragen RJ, Avram MJ, et al: The pharmacokinetics
of dexmedetomidine in volunteers with severe renal impairment.
Anesthesia and Analgesia; 2001, 93:1205.
16.Chan GL, Matzke GR: Effects of Renal Insufficiency on the
Pharmacokinetics and Pharmacodynamics of Opioid Analgesics.
Drug Intelligence & Clinical Pharmacy; 1987, 21:773.
17.Babul N, Darke AC, Hagen N: Hydromorphone Metabolite
Accumulation in Renal Failure. Journal of Pain and Symptom
Management; 1995, 10:184.
18.Kirvela M, Lindgren L, Seppala T, et al: The pharmacokinetics
of oxycodone in uremic patients undergoing renal transplantation.
Journal of Clinical Anesthesia; 1996, 8:13.
19.Sear JW: Kidney Transplants: Induction and Analgesic Agents.
International Anesthesiology Clinics; 1995, 33:45.
20.Davis PJ, Stiller RL, Cook DR, et al: Effects of cholestatic hepatic
disease and chronic renal failure on alfentanil pharmacokinetics in
children. Anesthesia and Analgesia; 1989, 68:579.
21.Boyd AH, Eastwood NB, Parker CJ, et al: Pharmacodynamics
of the 1R cis-1’R cis isomer of atracurium (51W89) in health and
chronic renal failure. British Journal of Anaesthesia; 1995, 74:400.
22.Lynam DP, Cronnelly R, Castagnoli KP, et al: The
pharmacodynamics and pharmacokinetics of vecuronium in patients
anesthetized with isoflurane with normal renal function or with renal
failure. Anesthesiology; 1988, 69:227.
23.Segredo V, Caldwell JE, Matthay MA, et al: Persistent paralysis in
critically ill patients after long-term administration of vecuronium.
New England Journal of Medicine; 1992, 20(327):524.
24.Cook DR, Freeman JA, Lai AA, et al: Pharmacokinetics of
mivacurium in normal patients and in those with hepatic or renal
failure. British Journal of Anaesthesia; 1992, 69:580.
M.E.J. ANESTH 20 (6), 2010
TARGET-CONTROLLED INFUSION ANESTHESIA
WITH PROPOFOL AND REMIFENTANIL
COMPARED WITH MANUALLY
CONTROLLED INFUSION ANESTHESIA
IN MASTOIDECTOMY SURGERIES
Naser Yeganeh*, Bahman Roshani*,
Mitra Yari* and Afshin Almasi**
Abstract
Target-controlled infusion (TCI) system is increasingly used in anesthesia to control
the concentration of selected drugs in the plasma or at the site of drug effect (effect-site). The
performance of propofol TCI delivery when combined with remifentanil in patients undergoing
elective surgeries has been investigated. Our aim in this study was to assess the anesthesia profile
of the propofol and remifentanil target controlled infusion (TCI) anesthesia as compared to the
manually controlled infusion (MCI), in mastoidectomy surgery, where a bloodless field is of utmost
importance to the surgeon. Sixty patients, aged 18-60 years ASA I-II enrolled in the study, were
divided into two equal groups. Group MCI received propofol and remifentanil by conventionaldose-weight infusion method, and Group TCI received propofol 4 µg/ml and remifentanil 4 ng/ml
as effect-site target concentration. The hemodynamic variability, recovery profile, postoperative
nausea and vomiting (PONV), surgeons satisfaction were assessed. Results were analyzed by SPSS
version 11.5. The two groups were comparable with respect to age, ASA class, sex, weight, basal
vital signs, operation time. The blood pressure and pulse were above desired levels in some data
points in the MCI Group (P ≤ 0.05). The PACU stay time to reach Aldret score of 10 was longer
in the MCI Group (42.54 ± 8 vs 59.01 ± 6 min) (P ≤ 0.05). The PONV was more common in the
MCI Group (P ≤ 0.05). Surgeon’s satisfaction of the surgical field showed no significant differences
except when described as “good”, more common in the TCI Group. TCI is capable to induce and
maintain anesthesia as well as MCI. In some stages of anesthesia, the TCI control of vital signs are
better than the MCI. In some stages of anesthesia, the TCI control of vital signs are beter than the
MCI. Recovery profile and complication rate and surgeon’s satisfactions are more acceptable in the
TCI than in the MCI. Group.
Keywords: Target-controlled infusion anesthesia, manually controlled infusion anesthesia,
remifentanil, propofol, mastoidectomy.
* MD, Associate professor of anesthesia, Department of Anesthesiology and Intensive Care, Imam Khomeini Hospital,
Kermanshah University of Medical Sciences, Iran.
** Assistant professor of anesthesia.
***MSc, Master of Science in Biostatistics, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Corresponding Author: Deputy of Education and Research in Imam Reza Hospital, Kermanshah University of Medical
Sciences, Kermanshah, Iran. Tel: +98 9121459654, Fax: +98 831 427 6355, E-mail: [email protected].
785
M.E.J. ANESTH 20 (6), 2010
786
Introduction
Target controlled infusion (TCI) is increasingly
used in anesthesia. This method of infusion of
intravenous anesthetic drugs has been investigated
for its ability to achieve targeted blood or effect site
concentrations for selected drugs. Maintaining a
constant plasma or effect compartment concentration
of an IV anesthetic requires continuous adjustment
of the infusion rate according to the pharmacokinetic
properties of the drugs which can be achieved by
commercially available target controlled infusion
pumps. The main advantage of this infusion
method among the other advantages is prompt
response to signs of inappropriate anesthesia depth
without any need to mathematical calculations for
anesthesiologists1.
Total intravenous anesthesia based on the
administration of propofol combined with an opioid,
has become a popular anesthesia technique. It allows
independent modulation of the different components
of anesthesia: unconsciousness, amnesia and loss of
response, to noxious stimuli the first two components
are controlled by hypnotics and the third by opioids.
Remifentanil appears to be an ideal analgesic for
total IV anesthesia (TIVA) in combination with
propofol, because of its independent pathway from
that of propofol as well as its rapid elimination
and favorable controllability. The performance of
propofol TCI delivery when combined with opioid
in patients undergoing elective surgery has been
investigated2-4.
In the TCI system of delivery, the
anesthesiologist, depending on the appearance of
noxious stimuli, can adjust the target concentrations
of propofol or remifentanil and change the infusion
rate. Surgeons performing mastoidectomies as well
as other otolaryngological procedures when working
microscopically under high power visual field, request
asanguinous surgical field. Decrease of bleeding could
be accomplished by targeting higher plasma or effect
site concentration of hypnotic and opioid by the TCI
system. In contradistinction, the changes in infusion
rates in the manually controlled infusion (MCI), could
be difficult, inaccurate and time consuming.
Our aim in this study was to assess the clinical
effects of propofol and remifentanil target controlled
N. Yeganeh et al
infusion (TCI) and compare them to the manually
controlled infusion (MCI), in mastoid or similar
surgeries.
Results
There were no statistical difference between the
two groups regarding ASA class, age, sex, weight,
basal vital signs and surgery duration (Table 1). Two
anesthesiologists performed 60 anesthesias and 6
surgeons performed the surgery.
Table 1
Patient demographics and characteristics
(Mean and SD in parenthesis)
MCI
TCI
(n=30)
(n=30)
*P
Value
Sex (M/F)
18/12
17/13
0.55
Age (Y)
28.03
(9.79)
26.67 (8.73)
0.57
Weight (kg)
62.00
(9.70)
63.33
(12.90)
0.34
BMI (kg/m2)
23.65
(2.52)
23.50 (3.85)
0.66
BSA (m2)
1.58 (0.15)
1.65 (0.18)
0.054
ASA (I-II)
19 / 11
17 / 13
0.081
Surgery duration(min)
73.60
(17.66)
81.67
(19.63)
0.08
Baseline Systolic
BP(mmHg)
125.13
(8.72)
121.27
(10.55)
0.67
Baseline Diastolic
BP(mmHg)
79.37
(6.39)
79.67 (8.08)
0.69
Baseline Mean
BP(mmHg)
86.60
(6.44)
84.50 (7.59)
0.98
Baseline Mean HR
(Beats/min)
76.20
(8.32)
79.12 (7.61)
0.74
* P value < 0.05 is significant.
The systolic and mean arterial pressure at T4 and
systolic arterial pressure at T5 data points were higher
in the MCI group (P value ≤ 0.05) and no statistical
differences were remarkable in the other data points
(Fig. 1). There were also no statistical difference in
heart rates in data points (Fig. 2).
The least BIS value recorded in data points were
significantly lower in T4 and T5 data points in the MCI
group (Fig. 3).
TARGET-CONTROLLED INFUSION ANESTHESIA WITH PROPOFOL AND REMIFENTANIL COMPARED WITH
MANUALLY CONTROLLED INFUSION ANESTHESIA IN MASTOIDECTOMY SURGERIES
Fig. 1
Systolic, Mean and Diastolic arterial pressure in different data
points in two groups (Mean±SD)
787
Fig. 2
Heart rate during different data points
in two groups (Mean ± SD)
110
180
170
100
150
140
130
TCI
MCI
120
110
100
Heart rate (per min)
Systolic Blood Pressure(mmHg)
160
90
90
TCI
MCI
80
70
60
80
70
50
60
T1
T2
T3
T4*
T5*
T6
T1
T7
T2
T3
T4*
T5*
T6
T7
Data points
Data points
*Significant difference between two groups
Fig. 3
BIS changes during different data points in two groups
(Mean±SD).
90
80
100
TCI
MCI
70
60
50
40
T1
T2
T3
T4*
T5*
T6
90
80
Bispectral index(BIS)
Diastolic Blood Pressure(mmHg)
100
T7
Data points
70
60
TCI
MCI
50
40
30
Mean Blood Pressure (mmHg)
20
140
10
130
0
T1
120
T2
T3
T4*
T5*
T6
T7
Data points
110
*Significant difference between two groups
100
TCI
MCI
90
80
70
60
50
Table 2
Duration of post anesthesia care unit (PACU) residence,
incidence of postoperative side effects and recovery
characteristics (Mean and standard deviation in parenthesis).
40
T1
T2
T3
T4*
T5*
T6
T7
Data points
* Significant difference between two groups.
In the PACU, though there were no statistical
differences between the Aldrete score between the
two groups, yet the staying time for acquiring score
of 10 was longer in the MCI group. The nausea and
vomiting incidences were higher in the MCI group and
same symptoms continued higher in the surgical ward
(Table 2).
The total consumption and rate of consumption
of Remifentanil and propofol were significantly higher
in the MCI when compared to the TCI group (Table 3).
There were no differences in the time from the
end of administration of anesthetics to eye opening
PACU
Length of stay (min)
Aldrete Scoring receiving
PACU
Nausea (n of patients)
Vomiting (n of patients)
Shivering (n of patients)
Ward
Nausea (n of Patients)
Vomiting (n of patients)
Shivering (n of patients)
*P value < 0.05 is significant
TCI
(n=30)
MCI
(n=30)
*P
value
42.54
(8)
7.2
(1.0)
6
(18%)
3 (9%)
59.01
(6)
6.4 (0.4)
0.00
0.00
9
(27%)
14
(42%)
11
(33%)
10
(30%)
10
(30%)
2 (6%)
0
17
(51%)
6 (18%)
1 (3%)
0.01
0.06
0.00
0.40
0.00
0.50
M.E.J. ANESTH 20 (6), 2010
788
N. Yeganeh et al
Table 3
Propofol and remifentanil consumed in two groups (Mean and
standard deviations in parenthesis)
*P
MCI
TCI
Value
Total Propofol administered 1178.83 872.73
0.000
(mg)
(187.86) (274.05)
Propofol used per weight and 138.81
107.84
0.007
(20.17) (25.09)
time ( µg / kg / min )
Total
remifentanil 1324.23 955.07
0.005
administered (mg)
(189.18) (285.14)
Remifentanil used per weight
0.33
0.19
0.001
(0.04)
(0.04)
and time ( µg / kg / min )
*
P value < 0.05 is significant.
Table 4
Prediction of awakening time by pump, eye opening time, obey
to commands time (extubation time) , time to reach Aldrete
score 10 and drug costs in two groups (Mean and standard
deviation in parenthesis).
*P
MCI
TCI
Value
Prediction of awakening
8.33
8.83 (2.53)
0.43
(min)
(2.92)
8.76
Eye opening time (min) 9.00 (2.24)
0.72
(2.81)
Obey to commands time
9.11
9.26 (2.19)
0.82
(min)
(2.89)
Time to reach Aldrete
59.01
42.54
0.00
score 10
(6.77)
(8.32)
35.35
(6.53)
Total cost of drugs ($)
Cost per minute ($)
0.57 (0.10)
* P value < 0.05 is significant.
29.09
(7.80)
0.45
(0.08)
0.00
0.00
(awakening time) and to extubation time (obey to
commands time) in the two groups (Table 4).
The costs of anesthetic drugs (propofol and
remifentanil) and cost of one minute of anesthesia, was
higher in the MCI than in the TCI group (0.57 ± 0.10
dollar vs 0.45 ± 0.08 dollar) (Table 4).
Materials and Methods
Following approval of the Ethics Committee of
our institution and patient written informed consent,
60 patients 18-60 years. ASA I-II scheduled for
mastoidectomy with a planned duration of what than 30
minutes, were included in the study. Exclusion criteria
consisted of patients under 18 and above 60 years, ASA
physical status more than II, hypertriglyceridemia,
alcohol or opium dependence or drug abuse and use
of beta adrenergic receptor blocking agents or α2
adrenergic receptor agonists.
All patients were unpremedicated. Patients
were randomly allocated into two groups (30 each)
by sealed envelop technique; group target controlled
infusion group (TCI) and group B or manually
controlled infusion group (MCI). On arrival to the OR
the weight of patients were measured by electronic
weighing-machine and then, electrocardiogram leads,
pulse oximetry and noninvasive blood pressure,
were attached. A 20 gauge IV cannula was inserted
in antecubital vein in all patients. Ringer solution
10 cc/kg of body weight was infused intravenously
before induction of anesthesia. Bi-refferential
electroencephalogram (EEG) leads (Aspect medical
system BIS-XP version 3.23, USA) were attached after
skin preparation and disinfection with alcohol and
slight rubbing. When electrode impedance exceeded
10 KΩ, the electrode was replaced and skin preparation
was repeated.
In (TCI) group anesthesia was induced with
propofol 1% (Braun Melsungen, Germany) and
remifentanil 50 µg/ml (GSK, UK) simultaneously
administered by two separate modules of a continuous
computer assisted TCI system (Fresenius Kabi
Company, Base Prima and DPS Module System,
France). Before induction of anesthesia, patients'
weight and height, age, sex and target of effect site
concentration of propofol and remifentanil were
entered into the TCI system. The initial effect site
target of propofol was set at 4 µg/ml, titrated against
clinical effect and BIS values, and the initial effect site
target of remifentanil was 4 ng/ml, titrated against vital
signs. We used Schnider and Minto three compartments
pharmacokinetic models for propofol and remifentanil
respectively (5-6). The goal of propofol administration
was to maintain BIS level from 45 to 60.
After hypnosis (lack of eyelid reflex), atracurium
(0.5 mg/kg) was administered IV slowly to achieve
muscle relaxation for endotracheal intubation. The
atracurium dose was repeated to maintain post tetanic
count zero. After intubation the effect site concentration
of propofol and remifentanil were adjusted to maintain
the BIS level from 45 to 60 and 55 < MAP > 85
mmHg. BIS values beyond the desired levels were
managed with increasing or decreasing 1 µg/ml from
propofol effect site target concentration, and MAP far
from desired levels also managed with increasing or
TARGET-CONTROLLED INFUSION ANESTHESIA WITH PROPOFOL AND REMIFENTANIL COMPARED WITH
MANUALLY CONTROLLED INFUSION ANESTHESIA IN MASTOIDECTOMY SURGERIES
Fig. 4
Satisfaction of surgeons about surgical field.
* In good condition difference between two groups is significant.
decreasing 0.5 ng/ml to effect site target concentration
of remifentanil (Flowchart1).
With decreasing of MAP < 55 mmHg, crystalloids
(Ringer solution) were infused and until a clinically
adequate volume load was achieved a vasopressor
789
(Ephedrine) 2.5 mg i.v was administered to restore
MAP immediately. With increasing MAP > 85 mmHg
increasing the effect site concentration of remifentanil
was repeated step by step until reaching remifentanil
target to 10 ng/ml and if this failed to reduce MAP <
85 mmHg, infusion of trinitroglycerine 5 µg/min was
added.
In the MCI group anesthesia was induced with
bolus propofol infusion 1 mg/kg and after that 170 µg/
kg/min for 10 minutes, and then 130 µg/kg/min for 10
minutes and finally 100 µg/kg/min for maintenance of
anesthesia. This method of propofol infusion produces
and maintains propofol plasmatic concentration about
4 µg/ml7. Remifentanil infusion was started with
Flowchart 1
Anesthetics administration algorithm in TCI group
M.E.J. ANESTH 20 (6), 2010
790
N. Yeganeh et al
Flowchart 2
Anesthetics administration algorithm in MCI group
slow bolus dose of 1 µg/kg and then was continued
0.5 µg/kg/min. After loss of consciousness atracurium
was administered, repeated and managed as the same
manner as in TCI group. The goals of anesthesia were
the same as in TCI group. BIS values and MAP out
of the desired range was managed with increasing
or decreasing of propofol and remifentanil infusion
rate 10 µg/kg/min and 0.25 µg/kg/min respectively
(Flowchart 2).
In both groups patients were ventilated to
maintain normocapnia (ETCO2 between 36-44 mmHg
with mixture of oxygen in air (FIO2 40%). In all patients
the continuous infusion of propofol and remifentanil
were stopped at the beginning of skin closure when 2
mg morphine sulphate and 4 mg ondansetrone were
administered intravenously for postoperative analgesia
and prophylaxia of nausea and vomiting.
The time from stopping the infusion until
patients opened their eyes (eye opening time), obeyed
to commands and underwent tracheal extubation
(extubation time) and the time from stopping the
infusion until Aldrete score of 10 were documented and
compared in two the groups8. Six different surgeons
blinded to anesthesia method conducted were asked
TARGET-CONTROLLED INFUSION ANESTHESIA WITH PROPOFOL AND REMIFENTANIL COMPARED WITH
MANUALLY CONTROLLED INFUSION ANESTHESIA IN MASTOIDECTOMY SURGERIES
about their satisfaction about asanguineous surgical
field which was described as good (without disturbing
bleeding), moderate (minimal bleeding not disturbing
surgery) and poor (bleeding disturbing surgery).
Seven data points were defined for monitoring
and documentation of vital signs and BIS: T1, before
the induction of anesthesia; T2, before intubation;
T3, three minutes after tracheal intubation; T4, three
minutes after skin incision; T5, during mastoidectomy;
T6, during tympanic membrane placement and T7,
before skin closure.
The costs of intravenous anesthetic drugs
(disposables, nursing, staff, oxygen, air, vasopressors
and antiemetics were not included) were taken from
hospital pharmacy list.
Data were presented as mean with standard
deviation in parenthesis unless otherwise stated. For
statistical analysis SPSS software (version 11.5)
was used. Hemodynamic variables were analyzed
with two factorial analysis of variance for repeated
measurements. Student's t-test was applied at the
end point of each measurement. In case of multiple
comparisons, P values were corrected according to
Bonferroni. Fisher's exact tests, X² tests, leven tests,
Mann-Whitney U-tests, or nonpaired student's t-tests
were used when appropriate. P values < 0.05 were
considered significant.
Discussion
In this study we used propofol as hypnotic
together with remifentanil as analgesic for induction
and maintenance of anesthesia. Propofol is presently
the most common intravenous anesthetic used for total
intravenous anesthesia. Pharmacokinetic model-driven
infusion of propofol has become widely available
worldwide. In addition, remifentanil is the newest
μ-agonist available for administration as an analgesic
during surgery and it is best administered as an infusion
because of its metabolism by general body esterases.
Interaction of these two drugs in preventing
responses to noxious stimulation is investigated.
Increasing the duration of the infusion has minimal
impact on recovery time if the optimal dose of
remifentanil is not used9. Hence combination of these
two drugs has become more popular for intravenous
791
anesthesia. Regardless of the kind of surgery,
remifentanil improves intraoperative hemodynamic
stability when compared to other opioids: Twersky
reported better hemodynamic control when remifentanil
used compared with fentanyl10 and Mackey confirmed
better control of tachycardia and hypertension in very
high risk outpatients laryngoscopies with remifentanil
as compared to fentanyl11. In our study remifentanil was
used as an analgesic in both TCI and MCI, however,
the TCI group when surgical stimuli were profound
showed more stable hemodynamic parameters in
different data points at T4 (three minutes after skin
incision) and T5 (during mastoidectomy). This is
very important in mastoidectomy operations because
bleeding in surgical field is directly related to blood
pressure and even when minimal bleeding may disturb
the ideal condition for surgery.
Remifentanil is associated with faster recovery
and extubation time because of its rapid hydrolysis
and decreased hypnotic requirements. This can affect
early and late recovery and discharge time of patients
from operating table to the (PACU) and eventually to
surgical wards and finally to home. Remifentanil as an
anesthetic used as TCI method has showed superiority
to the conventional manually controlled infusion
(MCI).
Various studies have shown that hemodynamic
stability, recovery time, and discharge time have
improved by the use of TCI for the administration
of remifentanil and propofol in the induction and
maintenance of anesthesia12-13. Despite these findings
other authors could not show significant hemodynamic
differences between TCI and MCI group during
induction and maintenance of anesthesia14-15.
We think the findings in our study are the result
of administration both hypnotic and analgesic with
TCI technique which allows fine titration of effectsite target concentration counter effecting the noxious
stimuli. The TCI enables anesthesiologist to rapidly
change the effect-site target concentration of desired
drug for desired response without need to timeoccupying mathematical calculation to adjust infusion
rate for body mass of the patient. Also our findings
demonstrated the efficacy of TCI in controlling
anesthesia depth during different stages of surgery
as well as MCI. Although all patients were received
M.E.J. ANESTH 20 (6), 2010
792
to PACU with comparable Aldrete score, the MCI
patients, however, stayed more in this unit to reach
Aldrete score 10. In other word, intermediate recovery
time (discharge from PACU to surgical ward) was
longer in the MCI group. This correlates with total
propofol and remifentanil consumed during anesthesia
observed more in the MCI group.
Although we found less drug consummation and
decreased drug cost in the TCI group, literature review
is contradictory, Suttner found that TCI using propofol
and remifentanil was the most expensive anesthesia
regimen, with total intraoperative costs almost two
fold compared with the standard IV propofol regimen
and almost four times larger compared with a standard
inhaled anesthetic with isoflurane in sixty patients
undergoing elective laparoscopic cholecystectomies12.
Fombeur and coworkers described a standard regimen
of desflurane was more cost-effective than TCI
propofol for anesthesia maintenance in achieving
post operative nausea and vomiting free episodes in
otlogical surgeries16 Russell and coworkers17 found
significantly more propofol was administered during
both induction and maintenance of anesthesia with the
target controlled system while no clinically significant
difference in heart rate and hemodynamic variables
were observed. On the other hand De castro and
coworkers reported significantly smaller requirements
of remifentanil without a difference in propofol
requirement and at the same time more common
intraoperative hypotension episodes in MCI group
patients than TCI group18.
Limitation of our study lies in the fact that our
data collection was not performed continuously in
all times of the operation but in selected data points
in which hemodynamic imbalance episodes were
more probable. Despite this limitation data in the
N. Yeganeh et al
postoperative time were collected continuously in
which the PONV and the shorter staying time in
recovery room to reach Aldrete score of 10 the TCI
group.
The possible explanations can explain the
contradictory results with the tel system, consiste
that studies used only hypnotic or analgesic and in
others both been administered by TCI. Fine titration
of hypnotic and/or analgesic target concentration
against clinical effects can rapidly produce desired
clinical situation without time delay and uncontrolled
hemodynamic changes. Changing effect-site target
concentration of every drug and attention to drug
pharmacodynamic instead of drug pharmacokinetic
can result to more stable hemodynamic variables, less
drug consumption and shorter recovery time19. On the
other hand biovariabilty plays an important role in
different responses to identical target concentration
in various studies20. Several models have been
proposed and validated for their ability to predict drug
concentration in the plasma or effect site compartment
for propofol and remifentanil. Biovariability and
severeal pharmacokinetic models produces different
results when TCI is used. In summary remifentanilpropofol TCI-based anesthesia achieved better
hemodynamic stability through the stages, better
recovery profile, decreases drug costs of anesthetics
and more satisfaction of surgeons about surgical field
condition, as compared to the manually controlled
infusion (MCI) anesthesia, in mastoidectomy surgeries.
Acknowledgement
We would like to thank the research authorities
of Kermanshah University of Medical Sciences and
Health Services for funding this study.
TARGET-CONTROLLED INFUSION ANESTHESIA WITH PROPOFOL AND REMIFENTANIL COMPARED WITH
MANUALLY CONTROLLED INFUSION ANESTHESIA IN MASTOIDECTOMY SURGERIES
793
References
1. Holas A: total intravenous anesthesia: Target-controlled anesthesia.
2005/5/21. Available at http://www.anesthesia.at/anesthesiology/
tiva3.html.
2. Gale T, Leslie K, Kluger M: propofol anesthesia via targetcontrolled infusion or manually controlled infusion: Effects on the
bispectral index as a measure of anesthetic depth. Anaesth Intensive
Care; 2001, 29:579-584.
3. Schraags S, Mohl U, Hirsch M, Stolberg E, Geaorgieff M:
Recovery from opioid anesthesia: The clinical implication of
context-sensitive half-times. Anesthesiology; 1998, 86:184-190.
4. Vuyk J, Engbers FH: The pharmacodynamics interaction of
propofol and alfentanil during lower abdominal surgery in women.
Anesthesiology; 1995, 83: 8-22.
5. Schnider TW, Minto CF, Shafer SL, Gambus PL, Anderson
C, Goodale DB, Youngs EJ: The influence of age on propofol
pharmacodynamics. Anesthesiology; 1999, 90:1502-1516.
6. Minto CF, Schnider TW, Egan TD, Shafer SL: The influence of
age and gender on the pharmacokinetics and pharmacodynamics of
remifentanil.I. Model development. Anesthesiology; 1997, 86:1023.
7. Glass PS, Shafer SL, Reves JG: Intravenous drug delivery system.
In: Miller RD Anesthesia. New York: Churchill Livingstone; 2005,
p. 461.
8. Aldrete JA: The post-anesthesia recovery score revisited. Clin
Anesth; 1995, 7:89-91.
9. Vuyk J, Mertens MJ, Olofsen E: Propofol anesthesia and
rational opioid selection: Determination of optimal EC50-EC95
concentrations that assure adequate anesthesia and a rapid return of
consciousness. Anesthesiology; 1997, 87:1594-1562.
10.Twersky RS, Jamerson B, Warner DS: Hemodynamic and
emergence profile of remifentanil versus fentanyl prospectly
compared in a large population of surgical patients. J Clin Anesth;
2001, 13:407-16.
11.Mackey JJ, Parker SD, Nass CM: Effectiveness of remifentanil
versus traditional fentanyl-based anesthesia in high-risk outpatient
surgery. J Clin Anesth; 2000, 12:427-32.
12.Suttner S, Boldt J, Schmidt C: Cost analysis of target-controlled
infusion based anesthesia compared with standard anesthesia
regimen. Anesth Analg; 1999, 88:77-82.
13.Yeganeh N, Roshani B: A Bispectral index guided comparison of
target-controlled versus manually-controlled infusion of propofol
and remifentanil for attenuation of pressor response to laryngoscopy
and tracheal intubation in non cardiac surgery. JRMS; 2006,
11(5):302-308.
14.Lehmann A, Boldt J, Thaler E, Piper S, Weisse U: Bispectral index
in patients with target-controlled infusion of propofol. Anesth Analg;
2002, 95:639-44.
15.Breslin DS, Mirakhur RK, Reid JE, Kyle A: Manuall versus targetcontrolled infusion of propofol. Anesthesia; 2004, 59:1059-1063.
16.Fombeur PO, Patrick R, Beaussier TM, Lorente C, Yazid L,
Lienhart AH: Cost-effectiveness of propofol anesthesia using
target-controlled infusion compared with a standard regimen using
desflurane. Am J Health-sys Pharm; 2002, 59(14):1344-1350.
17.Russell D, Wilkes M, Hunter SG, Glen JB, Hutton PK, Kenny
GN: Manual compared with target-controlled infusion of propofol.
Br J Anaesth; 1995, 75:562-6.
18.De Castro V, Godet G, Menica G, Raux M, Coriat P: Targetcontrolled infusion for remifentanil in vascular patients improves
hemodynamics and decreases remifentanil requirements. Anesth
Analg; 2003, 96:33-8.
19.Vuyk J: Pharmacokinetic and pharmacodynamic interaction
between opioid and propofol. J Clin Anesth; 1997, 9(6 suppl):23s6s.
20.Pandin PC, Cantrain F, Ewalenko P, Deneu SC, Coussaert E,
Hollander A: Predictive accuracy of target-controlled propofol and
sufentanil co-infusion in long lasting surgery. Anesthesiology; 2000,
93:653-661.
M.E.J. ANESTH 20 (6), 2010
AIRWAY MANAGEMENT AND HEMODYNAMIC
RESPONSE TO LARYNGOSCOPY AND INTUBATION IN
SUPINE AND LEFT LATERAL POSITIONS
Muhamad Faisal Khan*, Fawzia Anis Khan**
and Fawzia N asim M inai ***
Abstract
Introduction: Intubation in the lateral position is desirable in several conditions. We
compared the technical ease and hemodynamic response to laryngoscopy and intubation in the
lateral (group L) and supine (group S) positions in 120 patients with normal airway in a prospective
randomized controlled study.
Methods: This was a randomized, controlled observational study. All intubations were
performed by a single investigator experienced in lateral intubation. Ventilation score with bag
and mask ventilation, laryngoscopy duration and attempts, application of external pressure and
Cormac & Lehane grade were measured. Blood pressure and heart rate were observed before and
after induction of anesthesia, after laryngoscopy/intubation and then at one minute interval for 6
minutes.
Results: 90% of patients in group S were ventilated by a single operator compared to 17% in
group L. Duration of laryngoscopy was significantly longer in group L (32 seconds) compared to
group S (12 seconds) [p<0.001]. 78% of the patients in group S had Cormack and Lehane grade 1
versus nil in group L. External pressure was required in 58% patients in group L and 5% in group S.
In intra-group comparison at specified time lines no difference was observed in HR but the changes
in BP were significantly higher in the lateral position (P-value <0.001).
Conclusion: Ventilation and intubation in lateral position was more difficult technically than
in the suprine position, and the BP response was exaggerated in the lateral position.
Keywords: Laryngoscopy; intubation; supine; lateral; hemodynamic response.
*
FCPS (Pak), Senior Instructor, Department of Anaesthesia, Aga Khan University, P.O. Box 3500, Karachi 74800, Pakistan.
** FRCA (UK), Professor, Department of Anaesthesia, Aga Khan University, P.O. Box 3500, Karachi 74800, Pakistan.
*** FCPS (Pak), Assistant Professor, Department of Anaesthesia, Aga Khan University, P.O. Box 3500, Karachi 74800,
Pakistan.
Author for Correspondence: Dr. Muhammad Faisal Khan, Senior Instructor, Department of Anaesthesia, Aga Khan University,
Stadium Road, P.O. Box 3500, Karachi-74800, Pakistan. Telephone: (92) 21 486-4639, Fax: (92) 21 493-4294, 493-2095,
E-mail: [email protected]
795
M.E.J. ANESTH 20 (6), 2010
796
Introduction
Anaesthesiologists should be able to performs
tracheal intubations in the lateral position as this
position may be encountered in trauma, accidental
airway loss during surgery, in posteriorly located
pathology, or in patients with oral bleed.
The published literature on this topic is deficient.
A recent randomized control trial has looked at the
technical ease of tracheal intubation in the lateral
position1, others have compared the use of different
airway devices other than tracheal tube in supine
versus lateral positions2,3. The aim of this study was to
compare the technical ease and hemodynamic response
of laryngoscopy and intubation in lateral and supine
position in patients undergoing elective surgery under
general anesthesia. All of these patients had a low
predictive risk of difficult airway. Our rationale was that
in the lateral position gravity will aid the laryngoscopist
by displacing the tongue and this less force may be
require thus altering the hemodynamic response.
Methods
After institutional ethical committee approval,
written informed consent was obtained from 120
surgical patients scheduled to undergo general
anesthesia for elective surgery for this prospective
randomized controlled trial. The sealed opaque
envelope technique was used to divide the patients
into two groups of 60 patients each; a control group,
where tracheal intubation was carried out in the supine
position (S) and the study group in whom the tracheal
intubation was performed in the lateral position (L).
The inclusion criteria was American Society of
Anesthesiology (ASA) class 1 and 2, adults of either
sex 18 to 55 years of age with no predictors of difficult
mask ventilation or difficult intubation.
Detailed airway assessment was conducted on
each enrolled patient by one of the primary investigators.
The preoperative difficult airway predictors used were
Langeron’s criteria of difficult mask ventilation4,
Mallampati class, Wilson score5, and sub mandibular
space assessment. Patients who had Langeron Difficult
Mask Ventilation (DMV) score more than or equal to
2, Mallampatti class 2, 3 or 4, Wilsons score more than
4, thyromental distance less than 6 cm, mentohyoid
Muhamad Faisal Khan et al
distance less than 4 cm, or inadequate jaw protrusion,
were excluded. Other patients who were excluded
were those with facial trauma, emergency surgery,
history of gastro-esophageal reflux, pregnancy, raised
intracranial pressure, cervical spine disease, dental
abnormalities, and obesity. Patients with hypertension,
cardiovascular disease or atherosclerotic disease were
also excluded.
All patients were premedicated with 0.15 mgkg-1
of oral midazolam one hour before surgery. On arrival
to the operating room patients were monitored with
CM 5 lead for measuring the heart rate (HR) and ST
segment changes. An 18 gauge iv catheter was inserted
in an upper extremity vein. Blood pressure (BP) was
measured at preset intervals by oscillotonometry
using Datex Ohmeda monitor (AS 3; Datex, Helsinki
Finland). Oxygen saturation using a finger pulse
oximeter and EtCO2 were measured continuously.
The BP and HR readings were taken preinduction
(baseline), after a rest period of five minutes, one
minute after induction and then every minute following
laryngoscopy and intubation for six minutes by an
anesthesiologist unconnected with the study.
Prior to induction patients in group L were placed
in the left lateral position with a pillow under the head
and the head and neck in the sniffing position. Baseline
readings were obtained. Those in group S stayed supine
with a pillow under the occiput. The height of the table
was adjusted so that the top of patients head was at the
xiphisternum of the anesthesiologist in both groups.
All patients were pre oxygenated with 4 liters
of oxygen/min. Fentanyl 1.5 µgkg-1 was administered
intravenously over a period of 5 sec. Anesthsia was
induced with thiopentone 4mg kg-1 administered over
a period of 30 seconds, and muscle relaxation was
achieved with atracurium 0.6 mgkg-1 administered
over a period of 10 secs. The lungs of all patients
were ventilated with N2O/O2 60:40 mixture and
1% isoflurane. Hand ventilation was assessed by a
ventilation score. This score looked at how the airway
was maintained before tracheal tube insertion. A note
was made whether a single operator could maintain
the airway without insertion of oropharangeal airway,
single operator along with insertion of oropharangeal
airway, two operators without insertion of oral airway,
or two operators with insertion of oral airway. All
AIRWAY MANAGEMENT AND HEMODYNAMIC RESPONSE TO LARYNGOSCOPY AND INTUBATION IN SUPINE
AND LEFT LATERAL POSITIONS
induction and tracheal intubations were performed
by a single investigator with anesthesia experience of
seven years who underwent a learning curve for lateral
intubation. Intubating conditions were assessed by
ulnar nerve stimulation. Laryngoscopy was performed
at train of four count zero with a size 3 Macintosh
laryngoscope blade.
Difficulty of intubation was graded I-IV
according to Cormac and Lehane classification. A note
was also made of the number of intubation attempts
and application of any external pressure. Pressure
was be applied at the level of cricoid cartilage. A size
7.5mm polyvinyl chloride tracheal tube was used in
females and size 8.5mm in male patients. The time
from insertion of laryngoscope to successful insertion
of tracheal tube (appearance of capnograph on manual
ventilation) was monitored by a stop watch by another
anesthesiologist not connected to the study. Mucosal
trauma and lip or dental injuries were also recorded. In
case of failure of appearance of capnograph for three
consecutive manual breaths, the tube was withdrawn
and reinserted. Number of attempts of laryngoscopy
for correct tracheal tube placement were noted.
Any disturbance of cardiac rhythm, rate, inability to
maintain the oxygen saturation of 95% or more, any ST
segment depression of more than 1mm during the study
period was also noted. In case of failure to intubate in
the lateral position, with more than 3 attempts or more
than five minutes, or desaturation to less than 92% the
protocol required the patients to be turned supine and
intubation performed in the supine position.
For intubation in the left lateral position the
laryngoscope was held in the left hand and inserted from
the right side of the mouth, and the tracheal tube was
held in the right hand. The duration of laryngoscopy was
defined as the time from insertion of the laryngoscope
to the time of appearance of capnograph trace with
positive pressure ventilation. The end point of the study
was six minutes after intubation.
Results
Demograhphic characteristics and baseline
hemodynamic parameters
There were 60 patients in each group. The
demographic characteristics of the two groups are
shown in Table 1.
797
Table 1
Demographic characteristics and baseline haemodynamic
parameters of the two groups Mean (SD)
Group S
Group L
P value
Age: years
35.8 (12.8)
35.0 (11.3)
0.71
Weight: kg
69.0 (9.8)
66.7 (10.5)
0.22
Gender: m/f
38/22
38/22
1.0
SAP
126.6 (14.6)
119.8 (13.8)
0.009
DAP
78.9 (8.3)
72.5 (10.3)
<0.001
MAP
64.4 (9.4)
86.6 (9.8)
<0.001
HR
80.5 (16.4)
77.03 (12)
0.32
SD: Standard deviation; SAP: Systolic arterial pressure; DAP:
Diastolic blood pressure; MAP: Mean arterial pressure; HR:
Heart rate
No significant difference was observed in age (p = 0.71), weight
(p = 0.22) and gender (p = 1.0). Significant difference was
observed between baseline systolic blood pressure (p = 0.009),
diastolic (p <0.001), and mean arterial pressure (p <0.001)
between the two groups. No difference was observed in heart
rate (p = 0.32).
Preoperative Airway Assessment
The comparison is shown in Table 2.
Table 2
Comparison of preoperative airway assessment between the
two groups (SD deviation)
Groups
Airway assessment
S
L
p value
DMV Score
0
1
2
45
11
4
45
13
2
0.65
Wilson’s Score
0
1
58
2
55
5
0.41
Mean TM distance
9 . 8 6
(2.25)
10.13
(2.02)
0.49
Mean MH distance
7 . 5 0
(1.46)
7 . 2 7
(1.50)
0.39
DMV
: Difficult mask ventilation
TM distance
: Temperomandibular distance
MH distance
: Mentohyoid distance
No significant difference was observed between the two groups.
Ease of mask ventilation
54 patients (90%) in group S were ventilated
by a single operator, versus 10 (17%) in group L.
M.E.J. ANESTH 20 (6), 2010
798
Muhamad Faisal Khan et al
One patient in each group required two operators
to ventilate. Five patients in group S needed one
operator + oropharangeal airway versus 42 in group
L. None of the patients in group S needed 2 operator +
oropharangeal airway versus 7 in group L (p = <0.001).
None of the patients required turning from lateral
to supine position.
Number of intubation attempts and
applications of external pressure
A significant difference in SAP, DAP and
MAP was seen in the baseline parameters inspite of
randomization. Average percentage change from
baseline was therefore calculated in both groups
for comparison. The trend was initial decrease from
baseline blood pressures after induction, then increase
after laryngoscopy and intubation, remaining high for
three minutes and thereafter decreasing to baseline
values. This difference was significant (p <0.001) when
the percentage change from baseline was compared at
different timelines in the same group. A significant
difference was observed between the two groups with
the values being higher in the lateral group (p <0.001).
Similar changes were observed for SAP, DAP and
MAP (Figures 1, 2 and 3).
All patients in group S were intubated by a single
attempt versus 41 in group L (68%). Nineteen patients
in group L required two attempts. (CI 1.2, 1.44). In
three (5%) patients in group S and, 35 (58%) in group
L external laryngeal pressure was required to bring
vocal cords in view.
Duration of laryngoscopy
Mean duration of laryngoscopy in group S was
12.9 seconds, SD 4.2 (95% CI 11.8 – 14.0), compared
to 32 seconds, SD 12.7 (95% CI: 28.7-35.3) in group
L. This difference was significant (p <0.001).
Grade of intubation
Forty seven patients (78%) in group S had
Cormack and Lehane (C & L) grade 1 versus none in
group L. Eleven patients in group S had C & L grade
2a and two were grade 2b. Eighteen patients in group L
were C&L2a, and 39 were 2b. Three patients in group
L were grade 3 C&L compared to none in group S.
Fig. 1
Mean percentage change in systolic blood
pressure associated with tracheal intubation at
specified time points in the supine (●) and lateral
(o) groups, with 95% confidence intervals.
*P<0.05 between groups
Hemodynamic Changes
Blood pressure
Heart rate
There was no difference in baseline heart rate
between the two groups. A significant difference was
observed compared to baseline in both groups within
intra group comparison (p <0.001). On inter group
comparison the difference was significant at all time
points with the readings being higher in the L group
(Figure 4).
AIRWAY MANAGEMENT AND HEMODYNAMIC RESPONSE TO LARYNGOSCOPY AND INTUBATION IN SUPINE
AND LEFT LATERAL POSITIONS
799
Fig. 2
Mean percentage change in diastolic blood pressure
associated with tracheal intubation at specified time
points in the supine (●) and lateral (o) groups with
95% confidence intervals. *P<0.05 between groups
Fig. 3
Mean percentage change in mean arterial blood
pressure between groups associated with tracheal
intubation at specified time points in the supine
(●) and lateral (o) groups with 95% confidence
intervals. *P<0.05 between groups
Fig. 4
Mean percentage change in heart rate associated
with tracheal intubation at specified time points
in the supine (●) and lateral (o) groups with 95%
confidence intervals. *P <0.05 between groups
M.E.J. ANESTH 20 (6), 2010
800
Complications
None of the patients in either group had a heart
rate of less than 60 beats/minutes during the study
period. No desaturation below 95%, as measured by
pulse oximetry or ST segment changes were observed
in either group. Esophageal intubation was not
observed in either group. No mucosal or dental injury
was reported.
Discussion
Supine position is the conventional position used
for tracheal intubation, however intubation in left
lateral position is recommended by some authorities
in failed intubation drills6 and as a safer position
for post tonsillectomy hemorrhage7. It may also be
helpful in posteriorly located pathology like cervical
meningomylocele, injuries, abscesses, and in large
goiters.
The left lateral position prevents the laryngeal
structures from collapsing8; it also decreases upper
airway obstruction in anesthetized adults and in
children with sleep apnea9. McCaul recently looked
at the airway management in the lateral position and
subsequent use of tracheal tube or LMA1. The left lateral
position resulted in deterioration of laryngoscopic
view in 35% of patients. In eight out of 39 patients
there was failure of tracheal tube insertion compared
to one out of 30 in the LMA group. The paper did not
mention whether the anesthetists were trained or felt
comfortable in intubating in the lateral position. The
exact duration of training to learn this technique is
also not clear. In a study by Nathanson the reduction
in intubation time from first to third attempt was 12%
versus, 27% for supine and lateral positions10, but there
are no universal recommendations. The intubation
time in our study was 32 + 12.7 seconds in lateral
position compared to 12.9 + 4.2 seconds in the supine
position. We did not have any failed intubation. This
difference in success of intubation in lateral position
was probably due to the experience of the principle
investigator who underwent a formal training period
till he felt comfortable in airway management in the
lateral position.
Majority of our patients in supine position (90%)
required a single operator for bag mask ventilation
Muhamad Faisal Khan et al
following muscle relaxation versus 17% in the lateral
position. The laryngoscopic view also deteriorated in
lateral position and 58% of the patients in this group
required external pressure to bring vocal cords in view
and tracheal intubation took significantly longer Time.
Our results are similar to McCaul et al1, in this respect.
Nathanson10 et al reported a higher rate of esophageal
intubation in lateral position, whereas we did not
encounter any esophageal intubation in our series.
Other studies have compared alternate airway
devices besides tracheal tubes in both supine and
lateral positions e.g. intubating laryngeal mask airway
(ILMA)11, LMA1 fiber optic laryngscope8, and light
wand3. Both LMA and light wand provided reliable
airway control in the lateral position. None of these
studies looked at the hemodynamic responses.
Laryngoscopy and intubation lead to
hemodynamic instability due to sympathetic
stimulation. The major stimulus is said to be the force
exerted by the laryngoscope12. Our rationale to look
at this response was that the force maybe different
in the two positions as gravity aids the movement
of the tongue and lesser laryngoscopic force maybe
needed in the lateral position hence leading to a lesser
hemodynamic response.
There was a significant difference in the baseline
systolic, diastolic and mean blood pressure in our
groups inspite of random allocation. This has also
been pointed out in a study by Whiteman et al13 who
found cardiac output to be higher in the left lateral
position compared to supine or right lateral position.
Similar results were seen by Nakao et al14 in animals
where cardiac output increased from supine to left
lateral position. In order to overcome the difference
in the baseline blood pressure we only compared the
percentage rise in the values rather then the absolute
rise. No change in the heart rate was observed. Our
findings were similar with higher blood pressure
recorded in left lateral position but the heart rate
remained the same.
The hemodynamic response to laryngoscopy
and intubation was exaggerated in the lateral position
compared to supine position. In supine position
all readings post intubation were within 20% of
baseline. In lateral position the parameters remained
above 20% of baseline until three minutes post
AIRWAY MANAGEMENT AND HEMODYNAMIC RESPONSE TO LARYNGOSCOPY AND INTUBATION IN SUPINE
AND LEFT LATERAL POSITIONS
intubation. A prolonged intubation time and a higher
number of multiple attempts in lateral position could
have exaggerated the response further. Duration of
laryngoscopy is one of the factors that increase this
response15. This could be a limitation in our study.
Another limitation of our study is that an
experienced user inserted the tracheal tube in the
lateral position and our results may not be applicable
to inexperienced users. Thirdly although patients were
randomly assigned, double blinding was not practical
in our study.
We recommend that tracheal intubation in lateral
position be formally taught in the training program
but the exaggerated hemodynamic response should
be kept in mind. This response still occurred inspite
of giving fentanyl 1.5 micrograms kg-1 and though
attenuated, but could be detrimental in patients with
pre-existing ischemic heart diseases, hypertension
or cerebrovascular pathology; and manipulating the
airway in the lateral position in such patients may not
be desirable. The hemodynamic response also needs to
801
be studied with other airway devices recommended for
insertion in the lateral position. More work needs to be
done on the teaching curve required to learn this skill.
Conclusion
Our study indicates that both mask ventilation
and intubation are more difficult in the lateral position
compared to supine, probably due to alteration in
larangeal anatomy. The blood pressure response is
also exaggerated in the lateral position but there is no
change in the heart rate response. We recommend that
lateral intubation should be formally taught as a skill
in the residency programs and further work needs to be
done in this area.
Acknowledgement
We would like to acknowledge the contribution
of Mr. Iqbal Azam, Associate Professor for his support
in designing the study and in statistical analysis of the
results.
M.E.J. ANESTH 20 (6), 2010
802
Muhamad Faisal Khan et al
References
1. McCaul CL, Harney D, Ryan M, Moran C, Kavanagh BP, Boylan
JF: Airway management in lateral position: A randomized controlled
trial. Anesth Analg; 2005, 101:1221-25.
2. Biswas BK, Agarwal B, Bhattacharyya P, Badhani UK, Bhattarai
B: Intubating laryngeal mask for airway management in lateral
decubitus state: Comparative study of right and left lateral positions.
Br J Anaesth; 2005, 95:715-18.
3. Dimitriou V, Voyagis GS, Iatrou C, Brimcombe J: Flexible
lighwand-guided intubation using the intubating laryngeal mask
airway in the supine, right and left lateral positions in healthy
patients by experienced users. Anesth Analg; 2003, 96:896-98.
4. Langeron O, Masso E, Huraux C et al: Prediction of difficult mask
ventilation. Anesthesiology; 2000, 92:1229-36.
5. Wilson ME, Spiegelhalter D, Robertson JA, Lesser P: Predicting
difficult intubation. Br J Anaesth; 1988, 61:211-16.
6. Hawthorne L, Wilson R, Lyons G, Dresner M: Failed intubation
revisited: 17-years experience in teaching maternity unit. Br J
Anaesth; 1996; 76:680-84.
7. Nimmo AF, Spence AA: Postoperative recovery and oxygen therapy.
In: Nimmo WS, Rowbotham D and Smith G (Ed.). Anaesthesia,
Wiley Blackwell. 1995, 740-56.
8. Adachi YU, Satomoto M, Higuchi H: Fiberoptic orotracheal
intubation in the left semilateral position (Correspondence). Anesth
Analg; 2002, 94:477-78.
9. Litman RS, Wake N, Chan LM et al: Effect of lateral positioning
on upper airway size and morphology in sedated children.
Anesthesiology; 2005, 3:484-88.
10.Nathanson MH, Gajraj NM, Newson CD: Tracheal intubation
in manikin: comparison of supine and left lateral positions. Br J
Anaesth; 1994, 73:690-91.
11.Komatsu R, Nagata O, Sessler Dl, Ozaki M: The intubating
laryngeal mask airway facilitates tracheal intubation in the lateral
position. Anesth Analg; 2004, 98:858-61.
12.Shribman AJ, Smith G, Achola KJ: Cardiovascular and
catecholamine response to laryngoscopy with and witout tracheal
intubation. Br J Anaesth; 1987, 59:295-99.
13.Whitman GR, Howaniak DL, Verga TS: Comparison of cardiac
output measurement in 20-degree supine and 20-degree right and
left lateral recumbent position. Heart Lung; 1982, 11:256.
14.Nakao S, Come PC, Miller MJ et al: Effects of supine and
lateral positions on cardiac output and intracardiac pressures: an
experimental study. Circulation; 1986, 73:579-85.
15.Stoelting RK: Circulatory changes during direct laryngoscopy and
tracheal intubation: Influence of duration of laryngoscopy with or
without prior lidocaine. Anesthesiology; 1977, 47:381-83.
FENTANYL PRETREATMENT FOR ALLEVIATION
OF PERINEAL SYMPTOMS FOLLOWING
PREOPERATIVE ADMINISTRATION OF INTRAVENOUS
DEXAMETHASONE SODIUM PHOSPHATE
A prospective, randomized, double blind, placebo controlled study
Vimi Rewari*, Rakesh Garg**, Anjan Trikha***
and C handralekha ****
Abstract
Background: Corticosteroids have anti-inflammatory, analgesic and antiemetic effects but
causes severe perineal symptoms when given intravenously. Simultaneous administration of
dexamethasone and fentanyl have been known to decrease the duration of perineal pain but its
role in alleviating perineal pain has not been studied. Therefore, we hypothesized that fentanyl
pretreatment could prevent the perineal symptoms associated with the dexamethasone.
Material and Methods: This prospective, randomized, double blind, placebo controlled study
was done in 200 patients undergoing elective surgery requiring dexamethasone. The patients were
randomized into two groups of 100 each. Group BD received 5 ml normal saline followed, 5
minutes later, by 8 mg dexamethasone bolus intravenously. Group FD received 1 µg/kg fentanyl
diluted in saline to a volume of 5 ml followed by 8 mg dexamethasone bolus 5 minutes later. The
time of onset, intensity, site, duration and nature of the pain after the drug administration were
recorded.
Results: The demographic profile was comparable in the two groups. The incidence and
severity of pain was more in females as compared to males (p value = 0). The pain was located
especially in the perineal region and was expressed as itching (62%), burning (13%) or both (25%).
The incidence of pain, its duration and severity were significantly reduced after pretreatment with
fentanyl (p value = 0).
Discussion: Our study showed that the intravenous administration of dexamethasone sodium
phosphate leads to significant perineal symptoms. These symptoms are alleviated by pretreatment
with fentanyl (1 µg/kg) (incidence, severity and duration). The pharmacological mechanism
explaining perineal pain with intravenous administration of dexamethasone remains poorly
understood, but could be related to the phosphate ester.
Department of Anaesthesiology and Intensive Care, All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110029,
India.
*
Associate Professor.
** Senior Resident.
***Professor.
****Professor and Head.
Corresponding Author: Dr Vimi Rewari, Department of Anaesthesiology and Intensive Care, All India Institute of Medical
Sciences, Ansari Nagar, New Delhi-110029, India. Phone: 91-11-9818304880, 91-11-9868397802, Email: [email protected]
The paper was presented as poster in the 1st International Conference on Recent Advances in Anaesthesiology-INCRAA 2009,
AIIMS, New Delhi, India on 1st Feb 2009 and was declared best clinical study.
803
M.E.J. ANESTH 20 (6), 2010
804
We conclude, that intravenous administration
of dexamethasone sodium phosphate is associated
with perineal pain and can be alleviated effectively by
pretreatment with 1 µg/kg of fentanyl.
Key Words: Corticosteroids, Dexamethasone;
Pain, Perineal; Fentanyl
Introduction
Corticosteroids play an important role in the
perioperative period because of their diverse antiinflammatory, analgesic and antiemetic effects1-3.
Dexamethasone sodium phosphate is a water
soluble inorganic ester of dexamethasone which is
commonly used in the perioperative period because
of its prolonged duration of action as well as lack
of mineralocorticoid effect. In fact, it is now an
established agent for the multimodal management of
postoperative nausea and vomiting4,5.
Timing of the treatment with dexamethasone is
an integral part of the concept of preemptive analgesia
and needs to be administered prior to anesthetic
induction for its optimal effect6-9. This may be
related to the presumed mechanism of action (on an
intracellular receptor in the central nervous system),
allowing sufficient time for dexamethasone to reach
the effect site. Dexamethasone can be administered
after induction of anesthesia, but this might limit the
efficacy of dexamethasone to prevent postoperative
nausea and vomiting as well as postoperative pain10.
However, one of the disadvantages of
administering dexamethasone in the preinduction
period is that it leads to severe perineal symptoms
like pruritis, burning and pain following a bolus
intravenous injection that could be very distressing for
an awake patient.
Literature cites isolated case reports or case
series related to perineal pain after intravenous
administration of dexamethasone4,10-16. Till to date
there is no randomized controlled trial evaluating
the perineal symptoms caused by the administration
of intravenous dexamethasone. It has been reported
that simultaneous administration of dexamethasone
and fentanyl may reduce the duration of pain but its
role in alleviating perineal pain has not been studied11.
Therefore, we hypothesize that the analgesic effect of
Vimi Rewari et al
fentanyl, a potent opioid could prevent the perineal
symptoms associated with the dexamethasone.
This study was planned to estimate the incidence
of perineal symptoms (pruritis, burning, pain) after
intravenous dexamethasone administered in the
preoperative period and to evaluate the effect of
fentanyl pretreatment for alleviation of these perineal
symptoms.
Material and Methods
This prospective, double blind, placebo
controlled, randomized study was done after obtaining
the approval of the institutional ethics committee and
a written informed consent from 200 ASA physical
status I-III patients undergoing elective surgery at
a tertiary care centre (All India Institute of Medical
Sciences, New Delhi, India) requiring dexamethasone
for multimodal management of postoperative nausea
and vomiting (PONV) or postoperative analgesia.
A thorough preanesthetic work up of all patients
with clinical evaluation and relevant laboratory
investigations was carried out. Patients were eligible
for participation, if they were more than14 years of
age and could cooperate and understand the Visual
analogue score (VAS) scale. Only those patients,
who were at increased risk for postoperative nausea
and vomiting (laparoscopic procedures, gynaecologic
procedures, middle ear surgery, and squint surgery) or
in need for dexamethasone as multimodal analgesic
requirement were included. Patients who were on
regular medications with analgesic or analgesic use
within 24 hours of anesthesia, drug or alcohol abuse,
contraindications to steroid use [diabetes mellitus /
impaired glucose tolerance, peptic ulcer disease,
endocrine disorder, morbid obesity (BMI >30)] were
excluded from the study.
Patients were explained about the use of VAS for
grading the severity of pain on a scale of 0 to 10.
In the operating room, after attaching routine
monitors (ECG, non invasive blood pressure, pulse
oximeter), an 18 G intravenous cannula was secured
on the dorsum of the left hand.
The patients were randomized into two groups
of 100 each based on computer generated random
number list.
FENTANYL PRETREATMENT FOR ALLEVIATION OF PERINEAL SYMPTOMS FOLLOWING PREOPERATIVE
ADMINISTRATION OF INTRAVENOUS DEXAMETHASONE SODIUM PHOSPHATE
(I) Group BD: Intravenous administration of 5 ml
normal saline followed by 8 mg dexamethasone bolus
5 minutes later.
(II) Group FD: Intravenous administration of 1
µg/kg fentanyl diluted in saline to a volume of 5 ml
followed by 8 mg dexamethasone bolus 5 minutes
later.
The randomization was not disclosed to any
of the personnel (those administering drugs, those
observing study parameters, data analysts) or
the patient throughout the study. An independent
investigator not involved in the observation prepared
the study drug. The effects of the drugs were observed
by an investigator who was unaware of the drugs
administered. The patient was observed for the next
ten minutes and the rest of the anesthetic procedure
was allowed to proceed.
The following parameters were recorded
continuously following the drug administration:
=The time of onset and intensity (VAS) of
the perineal symptoms after the end of the drug
administration.
805
=The site of pain or other symptoms.
=The duration of the symptoms.
=The nature of the symptoms (pruritis, burning,
pain).
In the absence of any previous study, the sample
size was calculated based on the case series by Perron
et al4 with perineal symptoms as primary outcome and
with an aim of 50% decrease in the symptoms with
pretreatment with fentanyl, with a power of 90% and
α-0.05.
The comparison of sex and occurrence of pain
was carried out using chi square test. The age, weight,
onset and duration of pain and VAS was compared
using independent t test. The p value <0.05 was taken
as significant.
Results
A total of 227 patients were assessed for eligibility
and 200 patients were enrolled in the study (Fig. 1).
The demographic profile was comparable in the
two groups (Table 1).
Fig. 1
Flow chart showing patient enrollment for the study
M.E.J. ANESTH 20 (6), 2010
806
Vimi Rewari et al
Table 1
Demographic Profile
Age (years)
Sex (M:F) (%)
Weight (kg)
Group BD (n=100)
Group FD (n=100)
P value
35.6 ± 12.9 (14-75)
35.8 ± 11.4 (14-65)
0.906
40:60 (40:60)
38:62 (38:62)
0.085
58.3 ± 10.5 (37-93)
59.3 ± 9 (38-80)
0.487
Values as mean ± SD (Range)
The incidence and severity of pain was more in
females as compared to males (p value 0.001) (Table 2).
The pain was located especially in the perineal
region and was expressed as itching (62%), burning
(13%) or both (25%). One patient mentioned
generalized tingling sensation all over the body and
another patient reported dizziness. The incidence,
duration and severity of the perineal symptoms were
significantly reduced following pretreatment with
fentanyl (p value 0.001) (Table 3).
Discussion
Our study showed that the intravenous
administration of dexamethasone sodium phosphate
causes pain and itching in the perineal region. These
symptoms were observed to be more severe and of
a longer duration in females as compared to males.
The pretreatment with fentanyl in a dose of 1 µg/kg
reduced the pain and itching (incidence, severity and
duration) caused by intravenous administration of
dexamethasone.
Table 2
Incidence of dexamethasone induced pain among males and females
Male (n = 40)
Female (n = 60)
Pain (n) (%)
P value
15/40 (37.5%)
56/60 (93.3%)
0.001
Pain Onset (sec)
25.7 ± 7.3 (20-40)
24.3 ± 7 (10-45)
0.505
Pain Duration (sec)
28.7 ± 19.2 (10-80)
77.8 ± 31 (21-120)
0.001
Pain VAS (median)
4 (3-6)
7 (4-9)
0.001
Values as mean ± SD (Range) or as otherwise stated
Table 3
Effect of Fentanyl pretreatment on pain with intravenous dexamethasone
n
Group BD
n
Group FD
P a i n
perceived
(n) (%)
Pain Onset
(sec)
P a i n
Duration
(sec)
Pain VAS
(median)
P value
Total
100
71/100 (71%)
100
25/100 (25%)
0.001
Male
40
15/40 (37.5%)
38
0/38 (0%)
0.001
Female
60
56/60 (93.3%)
62
25/62 (40.3%)
0.001
Total
100
24.6 ± 7 (10-45)
100
17.6 ± 6 (10-35)
0.001
Male
40
25.7 ± 7.3 (20-40)
38
-
-
Female
60
24.3 ± 7 (10-45)
62
17.6 ± 6 (10-35)
0.001
Total
100
67.4 ± 35.2 (10-120)
100
11.6 ± 4 (5-20)
0.001
Male
40
28.7 ± 19.2 (10-80)
38
-
-
Female
60
77.8 ± 31 (20-120)
62
11.6 ± 4 (5-20)
0.001
Total
100
7 (3-9)
100
2 (1-3)
0.001
Male
40
4 (3-6)
38
0
0.001
7 (4-9)
62
2 (1-3)
0.001
Female
60
Values as mean ± SD or otherwise as stated
FENTANYL PRETREATMENT FOR ALLEVIATION OF PERINEAL SYMPTOMS FOLLOWING PREOPERATIVE
ADMINISTRATION OF INTRAVENOUS DEXAMETHASONE SODIUM PHOSPHATE
The pharmacological mechanism explaining
perineal pain with intravenous administration of
dexamethasone remains poorly understood, but could
be related to the phosphate ester of the corticosteroid
(dexamethasone sodium phosphate) since perineal
irritation has been described with hydrocortisone21-phosphate sodium and prednisolone phosphate
as well4,11,12,15. The symptoms lasted only for a short
period till the drug was hydrolysed into phosphate ions
and dexamethasone.
Opioids (fentanyl, remifentanil, alfentanil,
tramadol) have been used to alleviate the pain of
propofol intravenous administration17,21.
Opioid receptors are found in the dorsal root
ganglia, the central terminals of primary afferent
nerves and peripheral sensory nerve fibres and their
terminals. Opioids show their effects either centrally
or peripherally. The reduction in pain due to propofol
injection has been attributed to the interaction with
peripheral m-opioid receptors17,22. It has also been
suggested that prevention of propofol injection pain by
opioids may be mediated via central opioid receptors21.
In view of propofol pain being decreased by
pretreatment with opioids, we thought of using it for
alleviating pain with dexamethasone administration.
Of interest in the perioperative setting is the
decreased release of bradykinin, tumour necrosis
factor, interleukin-1, interleukin-2 and interleukin-6
and decreased production of prostaglandins after
administration of steroids. There is decreased
transmission of impulses in C fibres23. So, we think that
fentanyl probably acts via central action for alleviating
dexamethasone pain.
807
sodium phosphate equivalent to 4 mg dexamethasone
phosphate or 3.33 mg dexamethasone. The pH of
both concentrations is 7.0-8.5. Other ingredients
include methylparaben and propylparaben added as
preservatives. The implication of methylparaben,
propylparaben for causing perineal pain has not been
reported25,26.
The type of pain mentioned includes itching,
burning and squeezing11. Perron reported perineal
burning, itching and tingling after intravenous
dexamethasone4. In our study, we observed the
symptoms as burning and itching mainly and one
patient complained of tingling and dizziness.
Various measures to prevent perineal discomfort
include administration of dexamethasone after
induction of anesthesia, dilution of dexamethasone and
giving it as a slow bolus11,12,14,27. Most of the effects
of glucocorticoids are mediated through an altered
protein synthesis3. So, onset of biological action is
generally one to two hours. Wang et al designed a
study to test the hypothesis that dexamethasone was
more effective in preventing PONV when administered
before the induction of anesthesia than at the end of
anesthesia7. They observed that the administration of
dexamethasone at the end of anesthesia did not provide
an effective antiemetic effect during the immediate
postoperative period of 0-2 hours. Based on this finding,
they suggested that the onset time of dexamethasone
antiemetic effect may be approximately two hours6.
Though dexamethasone can cause side effects
such as increased incidence and severity of infection,
adrenal suppression and delayed healing in surgical
patients, a single dose has not been reported to cause
any such adverse effects3,29-31.
Adverse effects reported in association with
dexamethasone include perineal pain associated
with intravenous injection. The incidence of this
complication is unclear, with females at increased risk
compared to men. The speed of injection and the dose
may also influence the severity.
Our study is limited by the fact that the use of
fentanyl as pretreatment for alleviating dexamethasone
pain can be used in the perioperative settings where
fentanyl is a part of anesthetic management. Its
use cannot be justified in other settings where
dexamethasone is being used such as chemotherapy.
Epidural administration of dexamethasone has
not been associated with perineal pain24.
We conclude, intravenous administration of
dexamethasone sodium phosphate is associated with
perineal pain which can be alleviated effectively by
pretreatment with 1 µg/kg of fentanyl.
Each milliliter of dexamethasone sodium
phosphate injection, 4 mg/mL, contains dexamethasone
M.E.J. ANESTH 20 (6), 2010
808
Vimi Rewari et al
References
1.Filho JRL, Maurette PE, Allals M, Cotinho M, fernandes C:
Clinical comparative study of the effectiveness of two dosages
of dexamethasone to control postoperative swelling, trismus and
pain after the surgical extraction of the mandibular impacted third
molars. Med Oral Patol Oral Cir Bucal; 13:129-32, 2008.
2.Gupta P, Khanna J, Mitramustafi AK, Bhartia VK: Role of
preoperative dexamethasone as prophylaxis for postoperative
nausea and vomiting in laparoscopic surgery. J Min Access Surg;
2:12-16, 2006.
3.Bisgaard T, Klarskov B, Kehlet H, Rosenberg J: Preoperative
dexamethasone improves surgical outcome after laparoscopic
cholecystectomy-a randomized double blind placebo controlled
trial. Ann Surg; 238:651-60, 2003.
4.Perron G, Dolbec P, Germain J, Bechard P: Perineal pruritis after
iv dexamethasone administration. Can J Anesth; 50:749-750, 2003.
5.Jensen K, Kehlet H, Lund CM: Postoperative recovery profile after
laparoscopic cholecystectomy: a prospective, observational studt of
a multimodal anaesthestic regime. Acta Anaesthesiol scand; 51:46471, 2007.
6.Wang JJ, Ho ST, Tzeng JI, Tang CS: The effect of timing of
dexamethasone administration on its efficacy as a prophylactic
antiemetic for postoperative nausea and vomiting. Anesth Analg;
91:136-139, 2000.
7.Elhakim M, Nafie M, Mahmoud K, Atef A: Dexamethasone 8 mg
in combination with ondansetron 4 mg appears to be the optimal
dose for the prevention of nausea and vomiting after laparoscopic
cholecystectomy. Can J Anaesth; 49:922-926, 2002.
8.Gan TJ, Meyer T, Apfel CC, Chung F, Davis PJ, Eubanks S,
Kovac A, Philip BK, Sessler DI, Temo J, Tramer MR, Watcha
M: Consensus guidelines for managing postoperative nausea and
vomiting. Anesth Analg; 97:62-71, 2003.
9.Fujii Y, Nakayama M: dexamethasone for reduction of nausea,
vomiting and analgesic use after gynecologic laparoscopic surgery.
Internat J Gyn Obst; 100:27-30, 2007.
10.Crandell JT, Deer R: Perineal pruritis after the administration of iv
dexamethasone. Can J Anesth; 51:398, 2004.
11.Neff SPW, Stapelberg E, Warmington A: Excruciating perineal
pain after intravenous dexamethasone. Anaesth Intensive Care;
30:370-371, 2002.
12.Thomas VL: More on dexamethasone-induced perineal irritation. N
Engl J Med; 314:1643–4, 1986.
13.Klygis LM: Dexamethasone-induced perineal irritation in head
injury (Letter). Am J Emerg Med; 10:268, 1992.
14.Andrews D, Grunau VJ: An uncommon adverse effect following
bolus administration of intravenous dexamethasone. J Can Dent
Assoc; 52:309-11, 1986.
15.Taleb N, Geahchan N, Ghosn M, Brihi E, Sacre P: Vulvar pruritus
after high-dose dexamethasone. Eur J Cancer Clin Oncol; 24:495,
1988.
16.Kuczkowski KM: Perineal pruritis and dexamethasone. Anaesthesia;
59:308, 2004.
17.Kwak K, Kim J, Park S, Lim D, Kim S, Baek W, Jeon Y: Reduction
od pain on injection of propofol: combination of pretreatment
of remifentanil and premixture of lidocaine with propofol. Eur J
Anaesthesiol; 24:746-750, 2007.
18.Roehm KD, Piper SN, Maleck WH, Boldt J: Prevention of propofol
induced injection pain by remifentanil: a placebo controlled
comparison with lidocaine. Anaesthesia; 58:165-170, 2008.
19.Rahman AA, Al-Mujai H, Ivanova MP, Marzouk HM, Batra
YK, Al-Qattan AR: Prevention of pain on injection of propofol:
a comparison of remifentanil with alfentanil in children. Minerva
Anestesiol; 73:219-223, 2007.
20.Aouad MT, Sayyid SMS, Al-Alami AA, Baraka AS: Multimodal
analgesia to prevent propofol-induced pain: pretreatment with
remifentanil and lidocaine versus remifentanil orlidocaine alone.
Anesth Analg; 104:1540-4, 2007.
21.Lee JR, Jung CW, Lee YH: Reduction of pain during induction with
target controlled propofol and remifentanil. Br J Anaesth; 99:876880, 2007.
22.Iyilikci L, Balkan BK, Gokel E, Gunerli A, Ellidokuz H: The
effects of alfentanil or remifentanil pretreatment on propofol
injection pain. J Clin Anesth; 16:499-502, 2004.
23.Werner MU, Lassen B, Kehlet H: Analgesic effects of
dexamethasone in burn injury. Reg Anesth & Pain Med; 27(3):25460, 2002.
24.Thomas S, Beevi S: Epidural dexamethasone reduces postoperative
pain and analgesic requirements. Can J Anesth; 53:899-905, 2006.
25.Soni MG, Taylor SL, Greenberg NA, Burdock GA: Evaluation
of the health aspects of methyl paraben: a review of the published
literature. Food and Chemical Toxicology; 40:1335-1373, 2002.
26.Soni MG, Taylor SL, Greenberg NA, Burdock GA: Safety aspects
of propylparaben:: a review of the published literature. Food and
Chemical Toxicology; 39:513-532, 2001.
27.Singh M, Mohta M, Sethi AK, Tyagi A: Efficacy of dexamethasone
pretreatment for alleviation of propofol injection pain. Eur J
Anaesthesiol; 22:887-894, 2005.
28.Czerwinski AW, Czerwinski AB, Whitsett TL, Clark ML: Effects
of a single, large, intravenous injection ofdexamethasone. Clin
Pharmacol Ther; 13:638-42, 1972.
29.Wattwil M, Thorn SE, Lovqvist A, Wattwil L, Gupta A, Liljeqren
G: Dexamethasone is as effective as ondansetron for the prevention
of postoperative nausea and vomiting following breast surgery. Acta
Anaesthesiol Scand; 47:823-827, 2003.
30.Splinter W, Roberts J: Prophylaxis for vomiting by children after
tonsillectomy: dexamethasone versus perphenazine. Anesth Analg;
85:534-537, 1997.
31.Wang JJ, Ho ST, Liu YH, Lee SC, Liu YC, Liao YC, Ho CM:
Dexamethasone reduces nausea and vomiting after laparoscopic
cholecystectomy. Br J Anaesth; 83:773-775, 1999.
TRANSIENT NEUROLOGICAL SYMPTOMS FOLLOWING
SPINAL ANESTHESIA FOR CESAREAN SECTION
Edomwonyi NP* and Isesele TO *
Abstract
Background
Transient neurological symptoms (TNS) are defined as symmetrical bilateral pain in the back
or buttocks or pain radiating to the lower extremities after recovery from spinal anesthesia. About
80-85% of cesarean sections are performed under spinal anesthesia in our centre.
Our aim was to determine the incidence of TNS, risk factors and outcome of management in
pregnant women undergoing cesarean section.
Patients and Methods
Approval was obtained from the hospital ethic’s committee, and consent from the patients.
ASA 1 and 2 pregnant women undergoing cesarean section under spinal anesthesia formed the
subjects of this prospective study. They were evaluated and pre-medicated by the attending
anesthetists. Spinal anesthesia was performed at the L2-3 or L3-4 interspaces, using a 25G Quincke
or 25G pencil point spinal needle with 0.5% heavy bupivacaine. The investigators interviewed the
patients in the ward for three consecutive days, in order to identify those that developed TNS.
Results
One hundred and twenty consecutive patients were studied. TNS were documented in 12
(10%) patients. Backache was recorded in 8 patients (6.6%), pain in the thighs in 2 (1.7%) and pain
in the buttocks in 2 (1.7%). Onset time of symptoms was recorded as 6-12 hrs in 5 (4.2%) patients,
12-24 hrs in 5 (4.2%) and 24-48 hrs in 2 (1.6%). The patients that developed TNS were managed
accordingly with satisfactory outcome.
Conclusion
A follow-up for all patients that receive spinal anesthesia for cesarean section should constitute
a standard practice.
Key words: Anesthetic technique: spinal anesthesia, anesthetics-local: bupivacaine,
hyperbaric, surgery: cesarean section, complications: neurological.
*
MD, Obstetric Unit, Department of Anaesthesia, University of Benin Teaching Hospital, Benin City, Edo State, Nigeria.
Corresponding Author: Dr. NP Edomwonyi, Department of Anaesthesia, University of Benin Teaching Hospital, PMB
1111, Benin City, Nigeria.
809
M.E.J. ANESTH 20 (6), 2010
810
Introduction
Transient neurological symptoms (TNS) are
defined as symmetrical bilateral pain in the back or
buttocks or pain radiating to the lower extremities after
recovery from spinal anesthesia1. The first report of
TNS with 5% lignocaine by Schneider and colleagues
in 19931 was confirmed later by several other studies2-4.
It is thought that a localized local anesthetic toxic
effect may be an important contributing factor in the
development of transient neurological symptoms after
spinal anesthesia with concentrated solutions5,6. The
occurrence of this complication is rare after the use
of 0.5% bupivacaine for spinal anesthesia7,8. Hiller
et al reported 3% incidence of TNS following the
use of 0.5% bupivacaine against 30% after the use of
mepivacaine9.
The aim of our study was to determine the
incidence of transient neurological symptoms after
spinal anesthesia for cesarean section, the risk factors
and outcome of management.
Patients and Methods
This was a prospective study carried out
form February to October, 2007 after approval was
obtained from the institutional Ethic’s committee, and
consent from the patients. One hundred and twenty
consecutive, ASA 1and 2 pregnant women who
presented for cesarean section formed the subjects
of study. Exclusion criteria were ASA 3 and above,
patients with neurological diseases, presence of back
ache and pain in the buttocks and legs (as a result of
pressure from the fetal presentation). They were all
seen, reviewed and pre-medicated by the anesthetists
in attendance.
Premedication consisted of 30 ml of mixture
magnesium trisilicate, intravenous metoclopramide,
10 mg and 50 mg Ranitidine.
In the theatre, multiparameter monitor was
attached, after obtaining baseline vital signs (pulse rate,
blood pressure and oxygen saturation), intravenous
access was established with 18 gauge cannulae.
Preloading of the circulation was achieved with 10-15
ml of 0.9% normal saline.
Spinal anesthesia was performed at the L2-3 or
L3-4 interspace with the patient in the sitting position,
Edomwonyi NP & Isesele TO
using a 25G Quincke spinal needle or 25G pencil point
(SIMS Portex). 0.5% heavy bupivacaine, 2.2-2.5 ml
was injected and patient repositioned supine with a
15o left lateral tilt and slight head up tilt. Vital signs
were continuously monitored during the operation.
After the delivery of the fetuses, the patients were
repositioned supine. Intraoperative complications,
such as hypotension, bradycardia, shivering were
managed accordingly.
Standard questionnaire was used to document
patients’ characteristics, intraoperative clinical data,
duration of anesthesia and surgery recovery room
and complications in the ward, attempts at lumbar
puncture. The type of spinal needle used was not by
choice but was determined by what was available at
the time of study.
The investigators were anesthetists not primarily
responsible for the conduct of the anesthesia.
They interviewed the patients in the ward 24
hrs postoperatively, again at 48 hrs and 72 hrs
postoperatively to identify those patients that developed
transient neurological symptoms, the location of pain,
and onset of pain after recovery of block, duration
of pain after recovery of block, management and its
outcome.
Results
One hundred and twenty patients were recruited
in the study. Table 1 showed their demographic
characteristics. Twelve (10%) patients complained of
transient neurological symptoms. Variables of spinal
anesthesia are shown in Table 2.Quincke spinal needle
was used in 55 (45.8%) patients and pencil point in 65
(54.2%) patients. The mean dose of bupivacaine (ml)
was 2.468 (0.29). The mean duration of surgery in
minutes was 59.92 (21.86). Block height was T2-T10
with T6 as median range.
Table 1
Demographic Characteristics
Mean/Sd
Age (yrs)
33.08 (3.94)
Weight (kg)
76.5 (9.76)
Height (cm)
160.172 (3.49)
TRANSIENT NEUROLOGICAL SYMPTOMS FOLLOWING SPINAL ANESTHESIA FOR CESAREAN SECTION
Table 2
Variables of Spinal Anaesthesia
Needle type/size
No of patients
Quincke/2555
Pencil point/ 25
65
Mean duration of
Surgery (minutes)
-59.92 (21.86)
Mean Volume of 0.5%
Heavy bupivacaine (mls) -2.468 (0.29)
Two attempts were made in 9 (75%) patients.
Three attempts were made in two (16.7%) patients
that reported severe pain. Ten (67%) out of the twelve
patients complained of mild to moderate pain while 2
(33%) complained of severe pain.
Table 3 shows onset of pain after recovery of
block while Table 4 shows sites of symptoms.
Table 3
Onset of pain after recovery of block (hr)
6-12 hrs5- (41.7%) patients
12-24 hrs-5 (41.7%)
24-48 hrs-2 (16.6%)
Table 4
Location of pain
Buttocks-2 (16.7%)
Thighs-2 (16.7%)
Back ache-8 (66.6%)
Total-12 (100%)
Quincke needle was used in ten (83%) of the
patients that complained of symptoms against 2
(17%) in the pencil point group. The difference was
considered statistically significant using Fisher’s exact
test P = 0.0116, 95% CI: 1.462 to 33.513. With regard to
the grade of the anesthetists who performed the block,
11 (91.7%) were done by residents (registrar1and
senior registrars) while one (8.3%) was performed by a
consultant. The difference was statistically significant,
P = 0.0253, 95% CI: 0.01009 to 0.8192. The duration
of pain in the thighs and back lasted for 24-72 hours
and the pain in the buttocks lasted for 96 hrs.
The risk factors for the development of TNS
were the use of cutting spinal needle (Quincke),
811
number of attempts at lumbar puncture and the grade
of anesthetist. Six (50%) patients were managed with
non-steroidal anti-inflammatory drug, Ketorolac 30 mg
6 hourly while 3 (25%) were given opioid, tramadol
hydrochloride 100mg, 8 hourly. Both drugs were
administered intramuscularly. Three (25%) patients
required no analgesics. The outcome of management
was satisfactory.
Discussion
Although spinal anesthesia offers many
advantages for cesarean section, it is not without
complications, including transient neurological
deficits. Previous control trials have reported a
low incidence of 0-8% TNS in women undergoing
cesarean section10 or postpartum tubal ligation (3%)11.
Our study showed a slightly higher incidence of
10% TNS. In Great Britain, a number of high profile
legal cases in the 1950s concerning complications of
neuraxial techniques led to its decline for more than
two decade12. Albert Woolley and Cecil Roe were
healthy, middle aged men who became paraplegic after
spinal anesthesia for minor surgery in 1947 in Britain.
Phenol, in which the ampoules of local anesthetic had
been immersed, had contaminated the local anesthetic
through invisible cracks13.
Transient neurological symptoms were also
described as conditions characterized by back pain
radiating to the lower extremities without sensory
or motor deficits, which resolved spontaneously14,15.
Injury may result from direct needle trauma to nervous
tissues at the level of the spinal cord, nerve root or
peripheral nerve, from spinal cord ischemia, from
accidental injection of neurotoxic drugs or chemicals,
from introduction of bacteria into the subarachnoid or
epidural space or rarely from epidural hematoma16-18
and positioning (lithotomy). Avidan and colleagues,
reported details of magnetic resonance imaging of a
patient with TNS after spinal lidocaine. It indicated
a local inflammatory process as the possible etiology
for the symptoms, and concluded that TNS in some
cases results in permanent neurological deficit19. In
many cases, deficits are the results of administration
of neurotoxic doses of local anesthetic or result from
trauma after multiple attempts necessary to establish a
technically difficult block10,20.
M.E.J. ANESTH 20 (6), 2010
812
The risk factors for the development of TNS,
identified in this study were the use of cutting spinal
needle (Quincke), number of attempts at lumbar
puncture and the grade of anesthetists who performed
the block. A greater occurrence of neurological
symptoms was associated with the use of cutting spinal
needles. Three attempts were made in two patients that
reported severe pain. Our findings showed that spinal
anesthesia was performed by a registrar grade level
in eight patients that complained of TNS. Although
neurological complications may be secondary to the
labour and delivery process, the neural block is usually
considered causative until proven otherwise21.
Auroy et al prospectively monitored neurologic
complications in more than 103,000 regional
anesthesia, all deficits were present within 48 hours
after anesthesia. Most were transient with recovery
occurring between two days and three months16.
In a similar study involving 123,000 regional
anesthetics in parturients, 46 cases of single nerve root
neuropathies were reported (3.7/10,000) with complete
recovery in all patients by three months22. Most of our
patients reported an onset time of 12 to 24 hours after
cesarean section and recovery lasted for two to four
days. This is in agreement with previous study16.
There is a suggestion that certain patients may
have a predisposition to developing neurological
deficit after spinal anesthesia23. It is best to avoid the
technique in such cases as recommended nearly half a
Edomwonyi NP & Isesele TO
century ago24.
Current therapeutic options include opioids, nonsteroidal anti-inflammatory drugs (NSAID), muscle
relaxants and, symptomatic therapy25. One of the
most successful classes of drugs for treating TNS has
been the NSAID. Ibuprofen, naproxen and ketorolac
have all been used successfully. Significant muscle
spasm can be relieved with muscle relaxant, such as
cyclobenzaprine. Symptomatic therapy, including leg
elevation on pillows and heating pads, may provide an
additional measure of patients’ comfort25. The patients
that complained of transient neurological symptoms in
our study were treated with NSAID and opioid with
satisfactory outcome.
Conclusion
A follow-up for all patients that receive spinal
anesthesia for cesarean section should constitute a
standard practice in order to identify and manage
associated complications.
Aknowledgement
We thank the resident doctors in the department
of Anesthesia and the nurses in the maternity ward
for their cooperation during the study. We are grateful
to Abieyuwa Ima-Edomwonyi for her assistance in
preparing the manuscript.
TRANSIENT NEUROLOGICAL SYMPTOMS FOLLOWING SPINAL ANESTHESIA FOR CESAREAN SECTION
813
References
1.Schneider M, Ettlin T, Kaufmann M, Schumacher P, Urwyler A,
Hampl K, Von Hochstetter A: Transient neurologic toxicity after
hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesthesia
and Analgesia; 76:1154-1157, 1993.
2.Hampl KF, Schneider M, Drasner K, Stotz G, Drewe J: 5%
hyperbaric lidocaine: A risk factor for transient radicular irritation?
Anesthesiology; 79:3A, A875, 1993.
3.Tarkkila P, Huhtala J, Tuominen M: Transient radicular irritation
after spinal anaesthesia with hyperbaric 5% lignocaine. Br J Anaes;
74:328-329, 1995.
4.Salmela L, Aromaa U, Cozanitis DA: Leg and back pain after
spinal anaesthesia involving hyperbaric 5% lignocaine. Anaesthesia;
51:391-393, 1996.
5.Lambert LA, Lambert DH, Strichartz GR: Irreversible conduction
block in isolated nerve by high concentrations of local anesthetics.
Anesthesiology; 80:1082-1093, 1994.
6.Bainton C, Strichartz G: Concentration dependence of lidocaineinduced irreversible conduction loss in frog nerve. Anesthesiology;
81:657-667, 1994.
7.Hampl K, Schneider M, Ummenhofer W, Drewe: Transient
neurologic symptoms after spinal anaesthesia. Anaes and Analg;
81:1148-1149, 1993.
8.Tarkkila P, Huhtala J, Tuominen M: Transient radicular irritation
after bupivacaine spinal anesthesia. Reg Anaes; 21:26-29, 1996.
9. A Hiller and PH: Rosenberg, Transient neurological symptoms after
spinal anaesthesia with 4% mepivacaine and 0.5% bupivacaine. Br J
Anaes, 79:301-305, 1997.
10.Aouad M, Siddik S, Jalbout M, Baraka A: Does pregnancy
protect against intrathecal lidocaine-induced transient neurologic
symptoms. Anesth Analg; 92:401-404, 2001.
11.Philip J, Sharma S, Gottumukkla V, Perez B, Slay-Maker E, Wiley
J: Transient neurologic symptoms after spinal anaesthesia with
lidocaine in obstetric patients. Anesth Analg; 92:405-409, 2001.
12.Cope RW: The Wooley and Roe Case. Anesthesia; 50:162-173,
1995.
13.Maltby JR, Hutter CDD, Clayton KC: The Woolley and Roe Case.
Anaesthesia; 84:121-126, 2000.
14.Hodgson PS, Liu SS: New developments in spinal anesthesia.
Anesthesiol Clin North America; 18:235-249, 2000.
15.Horlocker TT: Complications of spinal and epidural anesthesia.
Anesthesiol Clin North America; 18:235-249, 2000.
16.Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K: Serious
complications related to regional anesthesia: results of a prospective
survey in France. Anesthesiology; 87:479-486, 1997.
17.Wlody D: Complications of regional anesthesia in obstetrics. Clin
Obstet Gynecol; 46:667-678, 2003.
18.Zaric D, Christiansen C, Pace NL, Punjasawadwon Y: Transient
neurologic symptoms TNS following spinal anaesthesia with
lidocaine versus other local anaesthetics. Cochrane Database Syst
Rev; CD003006, 2003.
19.Avidan A; Gomori M, Davidson E: Nerve root inflammation
demonstrated by magnetic resonance imaging in a patient with
transient neurologic symptoms after intrathecal injection of
lidocaine. Anesthesiology; 97:257-8, 2002.
20.Dahlgren N, Tornebrandt K: Neurological complications after
anaesthesia. A follow-up of 18,000 spinal and epidural anaesthetics
performed over three years. Acta Anaesthesiol Scand; 39:872-880,
1995.
21.Chestnut DH: Anesthesia and maternal mortality. Anesthesiology;
86:273-276, 1997.
22.Scott DB, Tunstall ME: Serious complications associated with
epidural/spinal blockade in obstetrics:a two year prospective study.
Int J. Obstet Anesth; 4:133-139, 1995.
23.Aldrete JA: Anaesthetic substances in the spine. In Arachnoiditis:the
silent Epidemic J. Aldrete (ed). Futuremed: Denver, CO, 77-101,
2000.
24.Vandam LD, Dripps RD: Exacerbation of pre-existing neurological
disease after spinal anaesthesia with lidocaine. N Engl J Med;
255:843 (Medline), 1956.
25Pullock JE: Transient Neurologic Symptoms: Etiology, Risk
Factors, and Management. Regional Anesthesia and Pain Medicine,
vol. 27, no. 6 (November-December), pp. 581-586, 2002.
M.E.J. ANESTH 20 (6), 2010
INCIDENCE OF PERIOPERATIVE
CARDIAC ARREST:
Analysis of anesthetics over 18-year period.
Farouk M Messahel* and Ali S Al-Qahtani**
Abstract
Objective: Several studies have surveyed perioperative cardiac arrests and their outcomes,
regardless of whether patients were successfully resuscitated or died. No such studies have
originated from the Kingdom of Saudi Arabia. This is a study of perioperative cardiac arrests and
their outcome in a Saudi General Hospital, over an 18-year period.
Methods: Armed Forces Hospital, Wadi Al-Dawasir, Kingdom of Saudi Arabia, serves
military personnel and their families, in addition to eligible civilian members of the community.
Operating theaters’ records were examined to collect details of patients who underwent some form
of surgical procedure since the commission of the Hospital on 12.07.1992 up until 30.09.2010.
Those surgical cases were traced in the Medical Records Department and the outcome of each
case was reviewed. The numbers and causes of cardiac arrests and death occurring during the
intraoperative and within the first postoperative 24 hours, were noted.
Results: There were 15,832 patients received anesthesia during the 18-year period. Five
patients died during this period (an incidence of 0.03%), all were emergency cases and were due to
non-anesthetic causes; four of them died intraoperatively and the fifth died within the first 24 hour
postoperatively.
Conclusion: There were 5 non-anesthetic deaths in the perioperative period during the
18-year period. The absence of anesthesia-related cardiac arrests in such patient population has
demonstrated that adopting quality improvement measures, teamwork approach and applying strict,
but updated and evidence-based, guidelines are essential in the prevention of such catastrophes. A
multicentre similar survey is needed to include all types of surgical operations.
Key words: anesthesia; complications, cardiac arrest; outcomes.
*
DA, FRCA, Senior Consultant: Anesthesia & Intensive Care, Director: Continuous Quality Improvement & Patient Safety,
Armed Forces Hospitals, Southern Region, Khamis Mushayt, Saudi Arabia.
** DLO, KSUF, Vice-Dean and Consultant ENT/Head & Neck Surgeon, College of Medicine, King Khalid University, Abha,
Saudi Arabia.
Corresponding author: Dr. Farouk M Messahel, Armed Forces Hospitals, Southern Region. P.O. Box 101, Khamis Mushayt,
Saudi Arabia., Mobile: 0503434653, E-mail: [email protected]
815
M.E.J. ANESTH 20 (6), 2010
816
Introduction
The incidence and causes of perioperative cardiac
arrests related to anesthesia have been studied over
the last two decades by many authors from Australia1,
Brazil2, Canada3, France4,5, Japan6,7, Sweden8, Taiwan9,
Thailand10, The Netherlands11, and the USA12,13,14,15.
This period has seen the introduction of new anesthetic
agents, improvements in anesthetic and monitoring
techniques, optimization of patients' condition prior to
surgery, the adoption of medical practice guidelines,
and the implementation of quality standards in the
healthcare service. This has led many researchers to
believe that the frequency of anesthesia-related cardiac
arrests have declined13,16,17,18. But although the risk of
death attributable to anesthesia has fallen appreciably
over the years, the number of perioperative deaths
remains static19. However, a recent review questioned if
there any change has happened over the last decades20.
There are no data on the subject in the Saudi Medical
Literature. This study is looking at the incidence and
outcome of cardiac arrests in a surgical population as
a result of anesthesia over an 18-year period in a Saudi
general hospital.
Methods
Armed Forces Hospital at Wadi Al-Dawasir,
Kingdom of Saudi Arabia, provides both primary
and secondary medical care to military personnel and
their dependants, and receives entitled patients from
the civilian population. It acts as a referral centre for
other hospitals in the region including major trauma
cases. It is the first hospital in the Kingdom of Saudi
Arabia to obtain the ISO 9000 (International Standard
Organization) Certificate in 1997. It is also the first
hospital in Saudi Arabia and among all military
hospitals in the Kingdom to apply Total Quality
Management standards in 2003. The hospital has
facilities for all types of surgery except open heart
operations and major neonatal and pediatric surgery.
Following approval of the local Scientific and
Ethics Committee, surgical records of the operating
theater were examined since the commission of the
hospital on 13.07.1992 until 30.09.2010. In addition
to demographic data, the nature and type of surgery,
whether elective or emergency, type of anesthetic
administered (general, regional or local) was recorded
F. M. Messahel & M. J. Gregorio
in special forms. The medical records of all surgical
cases during that period were traced in the Medical
Records Department and the outcome of each case was
observed. The causes of cardiac arrests and deaths were
assigned to one of four groups2: (i) totally anesthesiarelated when anesthesia was only or the major
contributory factor; (ii) partially related to anesthesia
when patient condition or surgical procedure were
contributory factors, but anesthesia represented an
additional factor; (iii) totally surgery-related; or (iv)
totally related to patient disease or condition.
Results
There were 15,832 surgical procedures
performed during that period, of which 7561 were
males (47.8%) and 8271 females (52.2%), a ratio of
0.9 M: 1.0 F. Age group ranged from one day to 104
years old (average 28.1-yr old). General anesthesia
was administered to 10983 (69.4%) cases, 3769
(23.8%) received regional anesthesia (spinal, epidural
or caudal), and 1080 (6.8%) plexus, nerve or regional
intravenous IV (Bier’s) block. There were 4 intra- and
one postoperative death during this period. All 4 cases
were emergencies. The first case was a 29-yr old known
case of placenta previa who was admitted in labour.
Due to mis-communication the locum member of
staff overlooked cross matching the necessary units of
blood needed in these situations. When the patient bled
profusely, attempts at circulatory resuscitation were not
successful. The second intraoperative death occurred
in a 67-yr old patient with massive hematemesis due to
advanced liver cirrhosis. The third was a victim of road
traffic accident who suffered irreversible circulatory
shock as a result of pelvic fracture and extended deep
rectal laceration. His heart came to standstill during
surgical exploration. the fourth was 73-yr old patient
who had a cardiac arrest 24 hrs following removal
of chicken breast bone impacted in his hypopharynx.
On admission, the patient was already showing
signs of mediastinitis as a result of perforation of the
pharynx. The fifth patient was a 54-yr old male run
over by a motor vehicle and suffered crush injury to
the right lower limb and penetrating perineal wound.
Patient developed DIC (Dissiminated Intravascular
Coagulopathy), was resuscitated by massive plasma
expander, blood transfusion and fresh frozen plasma,
PERIOPERATIVE CARDIAC ARREST
and was on maximum inotropic circulatory support,
but his heart stopped during surgical exploration of the
wounds.
Discussion
There are considerable differences between
previous studies regarding the definition of the
perioperative period. While some defined it as, the
intraoperative period only6,7,8,11,12,13, others defined
it as the intraoperative and either the recovery from
anesthesia period15, or the first 24 hr postoperatively14.
In this study we adopted the last definition.
Preoperative cardiac arrests may be due to patient
disease/condition, surgical factors, or to adverse
events related to anesthesia. The rate of anesthesia
related mortality has been stable over the past decade
at approximately 1 death per 13000 anesthetics20.
Anesthesia-attributable cardiac arrests are mainly the
result of airway management. But also they may be
due to cardiovascular depression or medication-errors.
The type of the anesthetic is at the discretion of the
anesthetist with patient approval if there is a choice. The
vast majority of cases in our study (69.4%) received
general anesthesia, 23.8% received regional anesthesia
(spinal, epidural or caudal), and 6.8% plexus, nerve
or regional intravenous IV (Bier’s) block. Previous
studies suggest that the incidence of cardiac arrest is
8.3-fold higher in general than in neuraxial (spinal
and epidural) anesthesia15. Recent survey of cardiac
arrest incidence during neuraxial anesthesia reported
2.7 cardiac arrests per 10000 anesthetics21. This is
lower than an earlier study22. The improvement here is
mainly due to the better knowledge of neuraxial block
physiology and the use of new local anesthetic drugs
with fewer side-effects, associated with more routinely
used cardiac and oxygen monitoring.
Increasing grades of surgical trauma and
general anesthesia can initiate inflammatory and
hypercoagulable states23. These factors may have a
direct role in initiating plaque fissuring and acute
coronary thrombosis24,25.
The stress state associated with anesthesia and
surgery involves increased levels of catecholamines
and cortisol. Their levels increase with general
anesthesia, anesthetic reversal, extubation, increasing
817
pain scores, increasing grades of surgical trauma,
anemia, fasting and hypothermia26. Increased stress
hormone levels result in increases in blood pressure,
heart rate, coronary artery shear stress, relative insulin
deficiency and free fatty acid levels27. Coronary artery
shear stress may trigger plaque fissuring and acute
coronary thrombosis26. The other factors increase
oxygen demand and can result in perioperative
myocardial ischemia, which is strongly associated
with perioperative myocardial infarction28,29,30.
Factors that can initiate a hypoxic state
include anemia, hypothermia (through shivering),
and anesthesia and analgesia (through suppression
of breathing). Perioperative hypoxia can result
in myocardial ischemia in the setting of a
hemodynamically significant coronary artery stenosis.
These factors were taken into consideration
when the anesthetic service at our hospital. We believe
that the low incidence of perioperative deaths in our
series is due to many factors which we are following
in our hospital. International specialty standards,
approved guidelines, evidence-based practices,
implementation of quality improvement standards, are
all meticulously applied. Members of the anesthetic
staff are experienced and have continuous practice
in anesthesia. Trainees are well selected and closely
supervised by senior members of staff. The use of
modern anesthetic equipment and monitoring systems
in the perioperative period which detect changes in
ST segment of the electrocardiogram, and which
are regularly checked and serviced, together with
stringent measures of checking drugs and blood for
transfusion before administration have all contributed
to this favorable outcome. We would like also to
emphasize that periodic morbidity and mortality
meetings and the enforcement of the ISO and Total
Quality Management roles which necessitate regular
auditing of departmental activities are essential
elements in persistently providing a quality patient
service.
We strongly believe in good teamworking. One of
the 5 principles of the Institute of Medicine’s report “To
Err is Human” concludes that healthcare organizations
need to “promote effective team functioning”31. It has
been shown that surgical teams who exhibited good
team work had better outcomes than patients of teams
M.E.J. ANESTH 20 (6), 2010
818
with poor teamwork32. Patients on the elective list are
visited and assessed by the anesthetist at least 24 hours
preoperatively. Patients with associated non-surgical
findings are referred to the appropriate specialty for
management and optimization of their condition
before surgery. The case may be postponed until the
maximum possible improvement has been reached.
In emergency cases, at least 75% of patients should
be seen and assessed prior to their surgery. Such cases
are also assessed by the appropriate specialty teams.
If there is any possibility of optimizing the co-morbid
condition of the patient prior to surgery it will be
initiated, otherwise the benefit/risk ratio is applied.
F. M Messahel & M. J. Gregorio
This study is the first of its kind in the Kingdom
of Saudi Arabia and it looked at the incidence and
outcome of perioperative cardiac arrests in a military
general hospital. One factor which might have
contributed to this favorable outcome is that military
personnel tend to be younger and fitter than the general
public. Similar studies need to be conducted in Saudi
tertiary hospitals, but better still in multicenters to
include all types of surgery and to compare results with
those from other institutions4,6,7,9.
Acknowledgment: The authors wish to thank
staff nurse Mary June Gregorio of the operating theater
for her help and assistance.
PERIOPERATIVE CARDIAC ARREST
819
References
1. Morgan CA, Webb RK, Cockings J, Williamson JA: The Australan
Incident Monitoring Study Cardiac Arrest: an analysis of 2000
incident report. Anaesth Intensive Care; 1993, 21:626-637.
2. Braz GL, Módolo NSP, do Nascimento P Jr, Bruscchi BAM,
Castiglia YMM, de Carvalho LR, et al: Perioperative cardiac
arrest: a study of 53718 anaesthetics over 9 yr from a Brazilian
teaching hospital. Br J Anaesth; 2006, 96:569-575.
3. Cohen MM, Duncan PG, Pope WD, Wolkenstein C: A survey
of 112,000 anaesthetics at one teaching hospital (1975-83). Can
Anaesth Soc J; 1986, 33:22-31.
4. Tiret L, Desmonts JM, Hatton F, Vourc’h G: Complications
associated with anaesthesia: a prospective survey in France. Can
Aaesth Soc J; 1986, 3:336-344.
5. Biboulet P, Aubas P, Dubourdieu J, Rubenovitch J, Capdevila X,
d'Athis F
: Fatal and non-fatal cardiac arrests related to anaesthesia.
Can J Anesth; 2001, 48:426-332.
6. Kubota Y, Toyoda Y, Kubota H, Ueda Y, Asada A, Okamoto T, et
al: Frequency of anesthetic cardiac arrest and death in the operating
room at a single general hospital over a 30-year period. J Clin
Anesth; 1994, 6:227-238.
7. Kawashima Y, Takahashi S, Suzki M, Morita K, Irita K, Iwao Y, et
al: Anaesthesia-related mortality and morbidity over a 5-year period
in 2,363,038 patients in Japan. Acta Anaesthesiol Scand; 2003,
47:809-817.
8. Olsson GL, Hallen B: Cardiac arrest during anaesthesia. A
computer-aided study in 250,543 anaesthetics. Acta Anaesthesiol
Scand; 1988, 32:653-664.
9. Wu KH, Rau RH, Lin CF, Chan YL: Cardiac arrest during anesthesia
in a teaching hospital. A 4 year survey. Int Surg; 1997, 82:254-256.
10.Aroonpruksakul N, Raksakiatisak M, Thapenthai Y, Wangtawesaup
K, Chaiwat O, Vasharaksa K, et al: Perioperative cardiac arrest at
Siriraj Hospital between 1999-2001. J Med Assoc Thai; 2002, 85
(Suppl 3): S993-999.
11.Chopra V, Bovill JG, Spierdijk J: Accidents, near accidents and
complications during anaesthesia. A retrospective analysis of a 10year period in a teaching hospital. Anaesthesia; 1990, 45:3-6.
12.Keenan RL, Boyan CP: Cardiac arrest due to anesthesia. A study of
incidence and causes. JAMA; 1985, 253:2372-2377.
13.Keenan RL, Boyan CP: Decreasing frequency of anesthetic cardiac
arrests. J Clin Aneth; 1991, 3:354-457.
14.Newland MC, Ellis SJ, Lydiatt CA, Peters KR, Tinker JH,
Romberger DJ, et al: Anesthetic-related cardiac arrest and its
mortality: a report covering 72,959 anesthetics over 10 years from a
US teaching hospital. Anesthesiology; 2002, 97:108-115.
15.Sprung J, Warner ME, Contreras MG, Schroeder DR, Beighly
CM, Wilson GA, et al. Predictors of survival following cardiac
arrest in patients undergoing noncardiac surgery: a study of 518,294
patients at a tertiary referral center. Anesthesiology; 2003, 99:259269.
16.Tikkanen J, Hovi-Viander M: Death associated with anaesthesia
and surgery in Finland in 1986 compared to 1975. Acta Anaesthesiol
Scand; 1995, 39:262-267.
17.Gaba DM: Anaesthesiology as a model for patient safety in health
care. Br Med J; 2000, 320:785-788.
18.Cooper JB, Gaba D: No myth: anesthesia is a model for addressing
patient safety. Anesthesiology; 2002, 97:1335-1337.
19.National confidential Enquiry into perioperative deaths (2000) Then
and Now-1990-2000. General Data 1-16. London, www.ncepod.org.
uk
20.Lagasse RS: Anesthesia safety: model or myth? A review of
the published literature and analysis of current original data.
Anesthesiology; 2002, 97:1609-1617.
21.Auroy Y, Benhamou D, Bargues L, Ecofffey C, Fallissard B,
Mercier FJ, et al: Major complications of regional anesthesia
in France: The SOS Regional Anesthesia Hotline Service.
Anesthesiology; 2002, 97:1274-1280.
22.Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K: Serious
complications related to regional anesthesia: results of a prospective
survey in France. Anesthsiology; 1997, 87:479-486.
23.Rosenfeld BA, Beattie C, Christopherson R, Nortis EJ, Frank
SM, Breslow MJ, et al: The effects of different anesthetic regimens
on fibrinolysis and the development of postoperative arterial
thrombosis. Perioperative Ischemia Randomized Anesthesia Trial
Study Group. Anesthesiology; 1993, 79:435-43.
24.Blake GJ, Ridker PM: Inflammatory bio-markers and cardiovascular
risk prediction. J Intern Med; 2002, 252:283-94.
25.Baxevanis CN, Papilas K, Dedoussis GV, Pavlis T, Papamichail M:
Abnormal cytokine serum levels correlate with impaired cellular
immune responses after surgery. Clin Immunol Immunopathol;
1994, 71:82-8.
26.Priebe HJ: Triggers of perioperative myocardial ischaemia and
Infarction. Br J Anesth; 2004, 93:9-20.
27.Parker SD, Breslow MJ, Frank SM, Resenfeld BA, Norris EJ,
Christopherson R, et al: Catecholamine and cortisol responses
to lower extremity revascularization: correlation with outcome
variables. Perioperative Ischemia Randomized Anesthesia Trial
Study Group. Crit Care Med; 1995, 23:1954-61.
28.Fleisher LA, Nelson AH, Rosenbaum SH: Postoperative
myocardial ischemia: etiology of cardiac morbility or manifestation
of underlying disease? J Clin Anesth; 1995, 7:97-102.
29.Landesberg G, Mosseri M, Zahger D, Wolf Y, Perouansky M,
Anner H, et al: Myocardial infarction after vascular surgery: the
role of prolonged stress-induced, ST depression-type ischemia. J Am
Coll Cardiol; 2001, 37:1839-45.
30.Mangano DT, Browner WS, Hollenberg M, London MJ, Tubau
JF, Tateo IM: Association of perioperative myocardial ischemia
with cardiac morbidity and mortality in men undergoing noncardiac
surgery. The Study of Perioperative Ischemia Research Group. N
Engl J Med; 1990, 323:1781-8.
31.Kohn LT, Corrigan JM, Donaldon MD. Eds. To Err Is Human.
Washington DC: National Acaemy Press; 2000.
32.Mazzocco K, Petitti DB, Fong KT, et al: Surgical team behavior
and patient outcomes. The American Journal of Surgery; 2009,
197:679-685.
M.E.J. ANESTH 20 (6), 2010
EFFICACY OF ULTRASOUND-GUIDED TRANSVERSus
ABDOMINIS PLANE (TAP) BLOCK FOR POSTCESAREAN SECTION DELIVERY ANALGESIA
- A Double-Blind, Placebo-Controlled, Randomized Study -
Jumana M Baaj*, Raed A Alsatli**, Hayan A Majaj***, Zainab A
Babay**** and Ahmed K Thallaj*****
Abstract
Background: Ultrasound-guided transversus abdominis plane (TAP) block has been used
for intra-operative and postoperative analgesia. Here we evaluate the efficacy of TAP block for
postoperative cesarean delivery analgesia.
Method: A randomized, double-blind, placebo-controlled trial was performed at King Khalid
University Hospital on 40 patients undergoing cesarean delivery under spinal anesthesia with
bupivacaine and fentanyl. At the end of surgery they received bilateral ultrasound-guided TAP
block either with bupivacaine 0.25% (B group) 20 patients, or saline (S group, or placebo group)
20 patients, followed by patient controlled analgesia with IV morphine only. Each patient was
assessed 24 hours after delivery for pain, morphine consumption, nausea, vomiting, sedation,
patient’s satisfaction, and also pain relief during mobilization (24 hours post-cesarean section).
Results: All 40 participants completed the study. Total morphine consumption was reduced
more than 60% in the bupivacaine group; the bupivacaine group also reported improved satisfaction
with their pain relief over 24 hours after surgery, reduced morphine consumption, less nausea,
vomiting, and better patient’s satisfaction.
Conclusion: Ultrasound-guided TAP block improved postoperative analgesia, reduced
morphine consumption and improved patient’s satisfaction regarding analgesia after cesarean
delivery.
Key words: Ultrasound guided (USG), transversus abdominis plane (TAP), (U S) ultrasound.
external oblique muscle (EOM), internal oblique muscle (IOM), transversus abdominis muscle
(TAM), visual analogue scale (VAS), cesarean section C/S.
From the Departments of Anaesthesia, Cardiac Science Obstetrics & Gynaecology, College of Medicine and King Khalid
University Hospital, King Saud University, Riyadh, Saudi Arabia.
*
MD, Arab Board. Consultant Anesthesiologist, Department of Anaesthesia.
** MD, Facharzt, Assistant Professor and Consultant Cardiac Anaesthetist, Department of Cardiac Science, Cardiac
Anaesthesia.
*** MD, Arab Board, Senior Registrar, Department of Anaesthesia.
****MBBS, ABOG, Professor and Consultant, Obstetrician, Gynecologist and Perinatologist, Department of Obstetrics &
Gynaecology.
*****MD, Arab Board, Assistant Professor and Consultant Anaesthesiologist, Department of Anaesthesia.
Address Correspondence to: Dr. Jumana BM Baaj, Consultant Anaesthetist, Department of Anaesthesia, College of
Medicine, P.O Box: 2925, Riyadh 11461, Kingdom of Saudi Arabia. Tel: (+9661) 4692019/4692194, Fax: (+9661)
4692366, E-mail: [email protected]
821
M.E.J. ANESTH 20 (6), 2010
822
J. M. Baaj et al
Introduction
half way between costal margin and iliac crest.
Post-cesarian section pain and discomfort may be
anticipated due to skin incision, uterine incision and
uterine contraction. The aim of this study is to evaluate
the analgesic efficacy of ultrasound-guided TAP block
for postoperative period.
The satisfactory image was aimed to visualize
the subcutaneous fat, external oblique muscle, internal
oblique muscle, transversus abdominis muscle,
peritoneum, and intraperitoneal cavity (Fig. 1).
We hypothesized that the TAP block, as an
analgesic regimen, would result in improved analgesia,
decreased opioid consumption in the first 24 hours after
cesarean delivery compared with placebo, facilitated
early mobilization, and improved postoperative
patient’s satisfaction.
Fig. 1
Transversus abdominis plane, EOM (external oblique
muscle), IOM (internal oblique muscle),
TAM (transversus abdominis muscle)
Method
The study was performed in the period May 2009
to April 2010, in King Khalid University Hospital. It
was approved by our institution’s Ethics Committee
and a written informed consent was obtained from
each patient. We studied 40 ASA I-II women having
cesarean delivery at term in a randomized, doubleblind, placebo-controlled trial. A control group of 20
patients received saline for TAP block (S group), while
other 20 patients received bupivacaine (B group). All
participants were above 18 years old.
Exclusion Criteria: Patients who were (ASA)
classification III-IV, patients with contraindications to
spinal anesthesia or history of allergy to bupivacaine,
patients who received analgesics in the past 24 hours,
and obese patients with a BMI >40 were not included
in the study.
A 100 mm long 20G short bevel needle
(Stimuplex A B/BRAUN Melsungen AG, Germany)
was inserted in plane to the probe of the ultrasound
anteriorly to lie between internal oblique muscle
and transversus abdominis muscle, a total of 20 ml
study solution was injected in each side (left and
right). Successful injection was obtained when an
echoluescent lens-shape appeared between the two
muscles (Fig. 2a and 2b).
Fig. 2a
Transverse ultrasound view of the EOM, IOM, and TAM at the
beginning of local anesthetic injection, between the inner two
muscles IOM and TAM
All participants received spinal anesthesia using
hyperbaric 0.5%, bupivacaine 10 mg, and fentanyl 20
µg. Antiemetics were not routinely administered but if
required, metoclopromide 10 mg i.v. was given.
An ultrasound-guided TAP block was performed
at the end of surgery, skin was prepared with 2%
chlorhexidine solution and a high-frequency (13-6
MHz) ultrasound probe (SonoSite M-Turbo Sonosite
Inc., Bothel) was used.
The injectate syringes were prepared under
aseptic technique; syringes contained either normal
saline 40 ml (placebo group) or bupivacaine 0.25% 40
ml. Investigators were blinded to the injected solution.
Ultrasound probe was positioned in mid-axillary line
Fig. 2b
Transverse ultrasound view of the EOAM, IOAM, and TAM at
the end of local anaesthetic injection
EFFICACY OF ULTRASOUND-GUIDED TRANSVERSus ABDOMINIS PLANE (TAP) BLOCK FOR POST-CESAREAN
SECTION DELIVERY ANALGESIA
All patients received morphine patient-controlled
analgesia with dose of 1mg bolus, and 10 minutes
lock-out time for 24 hours postoperatively. The
primary outcome was the total morphine consumption
over 24 hours after surgery. Data were obtained from
PCA pump. Accumulative morphine doses at 6, 10, 12,
18, 24 hours post-surgery were recorded, participants
were asked about their pain experience on 10mm
visual analogue scale (VAS) during the 24 hours
postoperatively and during mobilization 24 hours after
surgery. Satisfaction with pain relief was reported
over 24 hours. Participants were asked for severity of
nausea, vomiting, and sedation.
The calculation assumed the use of Fisher’s exact
test. Chi-square test was used to compare between
patients in bupivacaine group and placebo group for
nominal variables, i.e. sedation, satisfaction, postoperative nausea and vomiting, previous cesarean and
previous surgical operations.
823
Table 2
Previous caesarean section (C/S) showing no significant
difference between both groups of patients
Parameter
Bupivacaine
group
No. (%)
Control
group
No. (%)
P value
No C/S
12 (63.2%)
9 (45%)
Previous C/S
7 (36.8%)
11 (55%)
0.415
The TAP block with bupivacaine 0.25% compared
with placebo reduced postoperative pain (Fig. 3).
Fig. 3
The TAP block with bupivacaine reduced postoperative visual
analog scale by 25% (± SD) compared with control group
Student’s t-test was used for independent groups
to compare between both groups for measurable
variables, i.e. age, BMI, weight, height, morphine
consumptions and visual analogue score.
We assumed there was a statistically significant
difference when P-value is less than 0.05
Results
Forty patients were included in the study, all
participants had elective cesarean deliveries, the
baseline characteristics of the two groups were not
significantly different (Table 1); ultrasound views were
satisfactory in all participants, no blood aspiration
occurred in all TAP block cases, no side effects
were observed during and after 24 hours of surgery.
Regarding previous cesarean sections there was no
statistical difference between both groups (Table 2).
Table 1
Baseline characteristic of the study participants; no
statistically significant differences between the groups for all
baseline characteristics
Parameter
Age (yrs) {mean range}
Bupivacaine
group
Control group
Total morphine requirements in the first
postoperative 24 hours were also reduced in the
bupivacaine group compared with the placebo group
(25.89 ± 5.13 mg versus 62 ± 4.78, p <0.05) (Table 3,
Fig. 4).
Table 3
Postoperative morphine consumption in 24 hours period post
surgery is reduced in Bupivacaine group compared to control
group. Data are presented as mean ± (SD)
Cumulative
morphine dose at:
Bupivacaine
group
Control
group
6hr(mg) {mean(sd)}
3.89 ± 2.97
16.25 ± 2.99
10hr
8.3 ± 3.14
28.95 ± 4.5
12hr
13.11 ± 4.3
36.5 ±.28
29
30.75
Height (cm) {mean (SD)}
156.53 ± 4.12
155.25 ± 5.09
BWT(kg) {mean (SD)}
78.27 ± 9.33
75.7 ± 7.56
18hr
19.05 ± 3.97
50.4 ± 3.73
BM I {mean (SD)}
32.0 ± 2.91
31.35 ± 3.23
24hr
25. 79 ± 5.14
62.55 ± 4.72
M.E.J. ANESTH 20 (6), 2010
824
J. M. Baaj et al
Fig. 4
Postoperative morphine consumption in 24 hours period postsurgery. Data are presented as mean (SD)
There was less nausea and vomiting in bupivacaine
group than placebo group; two patients from placebo
group received antiemetic during 24 hours period, but
only one patient from bupivacaine group received an
antiemetic drug in the same period (Fig. 5).
Fig. 5
Postoperative nausea and vomiting was less in the
Bupivacaine group compared to control group.
Fig. 6
Patient’s satisfaction with pain relief was significantly higher
in Bupivacaine group.
muscle and anteriorly by external oblique muscle.
TAP block provides motoric and sensory block
to anterior and lateral abdominal wall, it has been used
for intra-operative and postoperative analgesia, either
by anatomical landmarks or ultrasound-guided. It has
been performed for the following procedures: caesarean
delivery2, hysterectomy3, retropubic prostatectomy4,
appendectomy5, laparoscopic cholecystectomy6, and
laparoscopic hernia repair with mesh.
The efficacy of TAP block was also studied by
Belavy et al7 using Ropivacaine 0.5% as one tool of
multimodal analgesia in addition to PCA morphine,
paracetamol and NSAIDs regularly, but in this study,
morphine is the single analgesic given to the patient
if postoperative analgesia was required. Efficacy of
block was evaluated by assessing pain level with VAS,
and the postoperative morphine consumption.
Patient’s satisfaction with pain relief was
significantly higher in bupivacaine group (Fig. 6).
Discussion
TAP block is relatively a new regional anesthesiaanalgesia technique1; it was initiated by Raffi as a
landmark-based technique within the iliolumbar
triangle of Petit. The triangle of Petit was bounded
inferiorly by iliac crest, posteriorly by latissimus dorsi
Though ultrasonographic guidance enable exact
placement of local anesthetics between internal oblique
and transversus abdominis muscle, the safety of TAP
block has been discussed by Zorica et al8. There are
reports of visceral damage when the needle went too
far like liver injury9, colon rupture10-11, and another
reported complication is transient femoral nerve
palsy12. Accidental intravascular injection of local
anesthetic, infection, and catheter breakage should
also be considered as potential complications of TAP
block13.
There are several suggestions to minimize
such complications: (i) by using a fine-gauge, blunttipped, short-bevel needle to minimize risk of visceral
EFFICACY OF ULTRASOUND-GUIDED TRANSVERSus ABDOMINIS PLANE (TAP) BLOCK FOR POST-CESAREAN
SECTION DELIVERY ANALGESIA
825
damage, and (ii) directing the needle obliquely instead
of perpendicularly to increase the resistance of each
aponeurosis, and using smaller volume of local
anesthetic to decrease the incidence of femoral nerve
block.
improved patient’s satisfaction and quality of pain
relief.
Conclusion
Further research is essential to determine the ideal
injected dose, volume of local anesthetics, duration of
the block according to local anesthetic serum level,
and the use of TAP block as intraoperative anesthetic
technique for other procedures.
This study demonstrates the analgesic efficacy
of ultrasound-guided TAP block after cesarean
delivery. The block reduced the postoperative pain,
total morphine consumption, antiemetic drugs, and
We recommend this block for all women
undergoing cesarean delivery who are not given longacting neuroaxial opioids.
M.E.J. ANESTH 20 (6), 2010
826
J. M. Baaj et al
References
1. McDonnell JG, O'Donnell BD, Farrell T, Gough N, Tuite D,
Power C, Laffey JG: Transversus abdominis plane block: a cadaveric
and radiological evaluation. Reg Anesth Pain Med; 32(5):399-404,
2007.
2. McDonnell JG, Curley G, Carney J, Benton A, Costello J,
Maharaj CH, Laffey JG: The analgesic efficacy of transversus
abdominis plane block after cesarean delivery: a randomized
controlled trial. Anesth Analg; 106(1):186-191, 2008.
3. McDonnell JG, O'Donnell B, Curley G, Heffernan A, Power C,
Laffey JG: The analgesic efficacy of transversus abdominis plane
block after abdominal surgery: a prospective randomized controlled
trial. Anesth Analg; 104(5):193-197, 2007.
4. O'Donnell BD, McDonnell JG, McShane AJ: The transversus
abdominis plane (TAP) block in open retropubic prostatectomy. Reg
Anesth Pain Med; 31(1):91, 2006.
5. Niraj G, Searle A, Mathews M, Misra V, Baban M, Kiani S, Wong
M: Analgesic efficacy of ultrasound-guided transversus abdominis
plane block in patients undergoing open appendicectomy Br J
Anaesth; 103(4):601-605, 2009.
6. El-Dawlatly AA, Turkistani A, Kettner SC, Machata AM,
Delvi MB, Thallaj A, Kapral A, Marhofer P: Ultrasound-guided
transversus abdominis plane block: description of a new technique
and comparison with conventional systemic analgesia during
laparoscopic cholecystectomy. Br J Anaesth; 102(6):763-767, 2009.
7. Belavy D, Cowlishaw PJ, Howes M, Phillips F: Ultrasound-guided
transversus abdominis plane block for analgesia after Caesarean
delivery. Br J Anaesth; 103(5):726-730, 2009.
8. Jankovic Z, Ahmad N, Ravishankar N, Archer F: Transversus
abdominis plane block: how safe is it? Anesth Analg; 107(5):17581759, 2008.
9. Farooq M, Carey M: A case of liver trauma with a blunt regional
anesthesia needle while performing transversus abdominis plane
block. Reg Anesth Pain Med; 33(3):274-275, 2008.
10.Jöhr M, Sossair: Colonic puncture during ilioinguinal nerve block
in a child. Anesth Analg; 88(5):1051-1052, 1999.
11.Frigon C, Mai R, Valois-Gomez T, Desparmet J: Bowel hematoma
following an iliohypogastric-ilioinguinal nerve block. Paediatr
Anaesth; 16(9):993-996, 2006.
12.Walter EJ, Smith P, Albertyn R, Uncles DR: Ultrasound imaging
for transversus abdominis blocks. Anaesthesia; 63(2):211, 2008.
13.Weintraud M, Marhofer P, Bösenberg A, Kapral S, Willschke
H, Felfernig M, Kettner S: Ilioinguinal/iliohypogastric blocks in
children: where do we administer the local anesthetic without direct
visualization? Anesth Analg; 106(1):89-93, 2008.
COMPLICATIONS AND INTERVENTIONS ASSOCIATED
WITH EPIDURAL ANALGESIA FOR POSTOPERATIVE
PAIN RELIEF IN A TERTIARY CARE HOSPITAL
Faraz Shafiq*, Mohammad Hamid**
and K halid S amad ***
Introduction
Epidural analgesia is one of the commonly used methods of postoperative pain control despite
its associated complications. Early recognition and intervention is required to minimize the effect
of these complications. Present audit was conducted to find out the incidence of complications and
type of interventions required to change the outcome.
Methodology
The record of all the patients who had epidural catheter placed for postoperative pain
management reviewed from the departmental acute pain management register. Parameters included
level of insertion, drugs used, number of days infusion continued and complications like nausea,
vomiting, motor block, sedation, dural tap, catheter pull out, hypotension and itching. In addition,
the intervention done to manage these complications was also recorded.
Results
Total 1706 entries of epidurals were recorded in study period 2001 to 2007. The overall
incidence of the complication was 26.6%. The common complications were motor block (13.4%),
dural tap (1.2%), ineffective pain control (2.4%), accidental catheter pull outs (3.8%) and problems
associated with the delivery system of drug (1.7%).
The 12% of patients required intervention for the particular complications. The regime
was discontinued in 28%, drug concentration changed in 21.5% while the other modes of pain
management were used in 19% of patients. 0.9% of patients required epidural blood patch while
2% of patients required catheterization for urinary retention.
Conclusion
This audit shows the importance of regular assessment and early intervention to manage
epidural related complications in improving outcome.
Key words: Pain management, epidural, complication.
* MCPS, FCPS, Resident.
** MD, Associate Professor.
*** MCPS, FCPS, Assistant Professor.
Department of Anaesthesia, Aga Khan University Hospital, Karachi, Pakistan.
Correspondence: Dr. Faraz Shafiq MCPS, FCPS, Resident, Department of Anaesthesia, Aga Khan University Hospital Karachi,
Pakistan. Mobile: +92-03453179095, E-mail: [email protected], [email protected]
827
M.E.J. ANESTH 20 (6), 2010
828
Introduction
Acute pain may be defined as pain that is
present in patients because of preexisting diseases,
the surgical procedure or the combination of disease
or surgery related sources1. Acute pain in the
postoperative period may be the worst experience in
a life of patient, as most of them perceive it as one
of the most ominous aspect of surgery. Inadequate
postoperative pain relief is associated with increase
in morbidity and mortality after surgery2. At our
institution, we are using different modalities for
acute pain management in the postoperative surgical
patients. The epidural analgesia is the frequently
used modality amongst them.
Epidural analgesia is used for continuous
administration of local anesthetic (LA) agent alone
or in combination with narcotic agents in the epidural
space. It has got the potential to reduce or eliminate
the perioperative stress responses to the surgery. It
also decreases the incidence of post operative surgical
complications3 leading to the better outcome4. Pain
management with the epidural analgesia is not free
from side effects. The therapy can be made effective
and safe by giving particular attention to the clinical
assessment of the patient in terms of pain control
and complications. Importance should be given to
the educational and organizational aspects related
to the delivery of pain relief modality. Regular
audits and review of problematic areas are helpful
in the identification and reduction of complications
associated with the technique.
The objective of the audit was to identify the
complications associated with epidural analgesia in the
postoperative period and interventions required for the
associated complications by acute pain management
service (APMS).
Material and Methods
The data of patients having epidural analgesia
was reviewed retrospectively. It included all patients
enrolled in the acute pain service from 2001 to 2006,
requiring epidural catheter placement for postoperative
pain management. Thoracic, labor and caudal epidurals
were excluded. Similarly pediatric patients and data
which was incomplete or missing was also excluded.
F. Shafiq et al
The record of all the patients who had epidural
catheter for postoperative pain management was
reviewed from the departmental APMS register
by the primary investigator. The dedicated APMS
organized the rounds, patients’ evaluation and other
organizational aspects of the acute pain service
in our hospital. The departmental APMS register
is helpful in organizing patient’s record keeping
in terms of medical record number, location and
comorbids. The parameters which we recorded in
the register also includes surgical procedure, level
of catheter insertion, concentration of LA used. In
our setup pharmacy prepared 100 ml piggy bags of
three different concentrations of bupivicaine that is,
M1-0.1%, M2-0.125%, M3-0.0625% with 2µg/ml
of fentanyl respectively. Complications like nausea,
vomiting, sedation, and unilateral/bilateral motor
blocks which are common, have dedicated columns
for their entries. Other complications which are rare
or unusual as ineffective pain control, accidental
catheter pull outs, hypotension, itching etc. are
recorded in the miscellaneous column if they
occurred. The assessment of pain, nausea, vomiting
and sedation is based on the fixed proctols designed
by the acute pain management service. Numerical
pain rating scale of 0-3 is used to evaluate these
parameters with 0 being no occurrence while the
score of 3 indicates severity of the mentioned
problem. Similarly numerical score of 0-3 is used for
the evaluation of unilateral motor block (UMB) or
bilateral motor block (BMB). The score of 0 indicates
no motor block, while score of 3 is the motor block
impairing the movement of limbs. Nurses record the
patient’s status in dedicated monitoring forms. The
APMS is 24hrs on call service, available to manage
any particular complication associated with the
pain relief modalities. Interventions and necessary
action taken for the particular complications are also
mentioned in the register. The team manages the
particular complications on predesigned protocols
as decreasing the concentration or rate of LA for
BMB or pulling out of epidural catheter to a certain
extent in the presence of UMB. Patient tilting to
a lateral position that is the block side up is also
followed for the UMB. Other complications are
usually managed according to the cause and at the
discretion of physician judgment.
COMPLICATIONS AND INTERVENTIONS ASSOCIATED WITH EPIDURAL ANALGESIA FOR POSTOPERATIVE
PAIN RELIEF IN A TERTIARY CARE HOSPITAL
Results
Total 1706 entries of epidurals were recorded.
The lumbar intervertebral space was selected in 88%
patients while the thoracic level was used in 11% of
patients. Epidural was inserted for the perioperative
pain management in different surgical procedures
as shown in figure 1. The obstetric patients were
the largest among group that receive epidural that is
32%. The different concentrations of LA were used
as mentioned in table 1. Over all 63.54% of patients
received M 2 regime in the infusion form. In 50%
of patients the epidural was continued for 3 days, in
33% of patients it was continued for 2 days while in
17% the epidural was discontinued after 1 day, see
figure 2. The regime was discontinued prematurely
for different reasons in 3.8% of patients. The overall
incidence of the complications as shown in table 2, in
our audit was 26.5%. Common complications were
UMB and BMB. Dural tap was occurred in 1.2%
of patients while 0.17% of patients complained of
moderate to severe post dural puncture head ache
Fig. 1
Different Surgical Procedures
32%
24%
22%
Table 1
Concentration of LA used
Epidural Drug
Percent%
No. of Pts (n)
M1
17.29
295
M2
63.54
1084
M3
19.1
327
Table 2
Complications of epidural Analgesia
Complications
Percentage
Number
%
(n) 453
Unilateral motor Block
(RT)
5.33
91
Unilateral motor Block
(LT)
4.74
81
Bilateral motor Block
3.04
52
Dural Tap
1.23
21
Pull out
3.75
64
Filter Dislodgement
0.82
14
Hypotension
1.34
23
Nausea and Vomiting
0.29
5
Itching
0.35
6
Ineffective
2.4
41
Severe pain
0.4
7
Urinary retention
0.4
7
Head ache
0.17
3
System faults
1.69
29
Others
0.52
9
12%
8%
Table 3
Interventions done by APMS team
Intervention
Percentage
Number
%
(n)
2%
17%
33%
Total
12.77
218
Discontinued
28.4
62
Change of regime
19.2
42
21.55
47
Pull out of catheter
6.42
14
Rate decrease
3.21
7
Holding of infusion
5.0
11
Change
concentration
Fig. 2
Number for days for which epidural used
50%
829
in
1 Day
Positioning
5.96
13
2 Days
Epidural Bolus
6.42
14
3 Days
Blood patch
0.9
2
Catheterization
1.83
4
Others
0.9
2
M.E.J. ANESTH 20 (6), 2010
830
(PDPH). In 2.4% of patients epidural analgesia was
ineffective. Systems fault leading to ineffective drug
delivery were present in 1.7% of patients. The epidural
catheter pull outs and filter dislodgement were the
common causes of premature discontinuation of
epidural infusions.
Overall 12.1% of patients in the audit required
intervention by the APMS team for the particular
complications. Interventions done are shown in
table 3 UMB and BMB were the common reasons for
intervention. 21.5% of patients required change of LA
regime to a lower concentration for this reason while
6.4% of patient required epidural catheter pulls out for
unilateral motor blockade. 5.9% of patients require
change of positioning for UMB. 19.2% of patients
require change of regime due to ineffective pain relief.
Discussion
The epidural analgesia is the commonly used
modality for the perioperative pain management and it
has shown proven benefit particularly in dynamic pain
control. The effective use of epidural analgesia in the
postoperative period requires careful assessment of the
patient physiological status, pain control and associated
complications. It is also very important to monitor the
functioning status of epidural drug delivery system and
the location of catheter tip in the epidural space. The
audit helped in the identification of common technical
problems and complications in local population.
Unilateral or bilateral motor block, hypotension,
nausea, vomiting and itching were the frequent
complications found. The problems associated with the
epidural drug delivery system like catheter dislodgment
and the filter disconnection were also identified.
Use of LA agents in epidural space cause
differential nerve blockage depending upon the
concentration of LA agent and the fibers blocked.
The more dilute the agent the chance of getting motor
blockade will be low. The target is to achieve pain
control in terms of minimal motor blockade. The motor
block interfering with the lower limbs movement may
be associated with higher incidence of pressure sores
and deep vein thrombosis and if remain persist, despite
of appropriate intervention may be the indicator of
epidural hematoma or abscess. The overall incidence
of BMB in our study was 3.0%. The incidence reported
F. Shafiq et al
by Scott DA et al in their prospective study was 3.0%5,
with the combination of fentanyl and bupivicaine
infusion. The incidence of UMB was higher in our
patients as compared to bilateral (4.74-5.33 vs. 3.0%).
The cause of which may be the increased length of
catheter in epidural space. The usual practice in our
hospital is to have a length of 3-5 cm of catheter in
epidural space.
The neuronal blockade at the level of T1-T4
involving cardiac sympathetic chain may be associated
with the occurrence of hypotension and bradycardia.
The concentration of LA agent and height of block
which is planned to be achieved are additional factors
associated with this hemodynamic instability. The
reported incidence in literature is 0.7-3%6. In our
patients the incidence was comparable that is 0.7%. The
63.5% of patients in our audit received bupiviacaine
0.125%, which may be reason of lower incidence of
hypotension and bradycardia in this audit.
Epidural administered opioids achieve analgesia
via pre and post synaptic effects in dorsal horn of
spinal cord. They also interfere with the nociceptive
input but do not cause neuronal blockade. The use of
opioids in epidural infusion is responsible for effects
like respiratory depression, sedation, nausea, vomiting
and itching. The reported incidence of respiratory
depression is 0.24%7 depending upon the type of
narcotic used. The incidence reduces with the use of
more lipophilic agents like fentanyl. In our audit we
didn’t find any report of respiratory depression due
to the epidural infusion. We routinely monitor the
sedation level and respiratory rate of the patients having
epidural analgesia in progress. The narcotic we use in
combination of LA is fentanyl 2µg\ml which may be
the reason of undetectable incidence of respiratory
depression in our patients.
The nausea and vomiting associated with the
opioids is the major cause of patient dissatisfaction.
The opioid present in the epidural infusion stimulates
the chemoreceptor trigger zone which in turn causes
nausea and vomiting. The incidence was 024% in
our patients which may be due to the low dose of
fentanyl used. Itching is mu receptor mediated adverse
effect of epidurally adminsitered opioids. It involves
usually the face and upper chest. The incidence in our
postoperative patients was 0.35%.
COMPLICATIONS AND INTERVENTIONS ASSOCIATED WITH EPIDURAL ANALGESIA FOR POSTOPERATIVE
PAIN RELIEF IN A TERTIARY CARE HOSPITAL
The rare but most feared complications of
epidural analgesia are epidural abscess, meningitis
and epidural hematoma. No such cases were detected
in this audit. The reported incidence in literature is
1-1000 to 1-500008. In a retrospective audit of 8100
epidural during six year period Christieet al9 identified
six cases of epidural abscess, three of meningitis and
three of epidural hematoma. Symptoms of epidural
abscess or meningitis developed a median of 5 days
after epidural catheter removal. Methicillin resistant
Staphylococcus aureus was the predominant pathogen.
In our hospital we usually discontinued epidural at the
third postoperative day. Detection of motor power of
leg is crucial in the presence of epidural analgesia10
which may be the sign of impending neurological
deficit.
The other area of concern was the premature
catheter pull outs and filter disconnections due
to negligence in catheter management. Alternate
analgesia in the form of PCIA or intravenous narcotics
was provided to these patients. The APMS service is
actively involved in the teaching of paramedics and
nursing staff to prevent such complications. But the
compliance during different period varied. 2.4% of
patients had ineffective pain relief for which regime
was changed. The cause of which may be multi
factorial including technical errors the findings of
831
which was not our objective.
Different interventions were done for particular
complications specially those for which APMS service
was called. Over all 12.77% of patients required
interventions. The motor block was the most common
complication in our study for which the step wise
approach has been followed as mentioned in the
methodology like change of positioning or pulling
out of epidural catheter to a certain length. For severe
PDPH not responding to the conventional therapy only
0.9% of patients required epidural blood patch.
The limitation of this study was the retrospective
review, so the chance of getting missed data and
incomplete information may be the source of error as
the compliance of maintaining the pain management
register is also noted to be varied at different times, but
again the common problems were highlighted.
Conclusion
This audit helped us in identification of problems
associated with epidural analgesia technique and
emphasizes the effectiveness of early interventions
done by APMS team. It also shows the importance of
regular monitoring, multidisciplinary approach and
early intervention to reduce disastrous complication
and improve patient satisfaction.
M.E.J. ANESTH 20 (6), 2010
832
F. Shafiq et al
References
1. Practice guide line for acute pain management in perioperative setting.
An updated report by the American society of Anesthesiology; 2004,
100:1573-8.
2.Sharrock NE, Cazan MG, Hargett MJ, Williams-Russo P, Wilson
PD Jr: Changes in mortality after total hip and knee arthroplasty
over a ten-year period. Anesth Analg; 1995, 80:242-248.
3.Grass JA: The role of epidural anesthesia and analgesia in
postoperative outcome. Anesthesiol Clin North America; 2000,
18:407-428.
4.Park WY, Thompson JS, Lee KK: Effect of epidural anesthesia and
analgesia on peri-operative outcome. Ann Surg; 2001, 234:560-571.
5.Scott DA, Beilby DS, Mc Clymont C: Postoperative analgesia
using epidural infusions of fentanyl with bubivicaine. Aprospective
analysis of 1,014 patients. Anesthesiology; 1995, 83:727-37.
6.Tsui SL, Irwin MG, Wong CM, et al: An audit of the safety of an
acute pain service. Anesthesia; 1997, 52:1042-7.
7.Burstal R, Wegener F, Hayes C, Lantry G: Epidural analgesia:
prospective audit of 1062 patients. Anaesth Intensive Care; 1998,
26(2):165-72.
8.Moen V, Dahlgren N, Irestedt L: Severe neurological complications
after central neuraxial blockade in Sweden 1990-99. Anesthesiology;
2004, 101:950-9.
9.Christie I W, Mc Cabe S: Major complications of epidural analgesia
after surgery: Results of a six-year survey. Anaesthesia; 2007, 62,
pages 335-341.
10.Breivik H: Safe perioperative spinal and epidural analgesia. Acta
Anaesthesiologica Scandinavica; 1995, 39:869-71.
CARDIOVASCULAR RESPONSES TO OROTRACHEAL
INTUBATION IN PATIENTS UNDERGOING CORONARY
ARTERY BYPASS GRAFTING SURGERY
Comparing Fiberoptic Bronchoscopy With Direct Laryngoscopy
Nahid Aghdaii*, Rasoul Azarfarin**, Forouzan Yazdanian***
and S eyede Z ahra Faritus ***
Abstract
Background: The intubation by using fiberoptic brochoscop (FOB) can avoid the mechanical
stimulus to oropharyngolaryngeal structures thereby it is likely to attenuate hemodynamic response
during orotracheal intubation. Based on this hypothesis, we compared the hemodynamic responses
to orotracheal intubation using an FOB and direct laryngoscope (DLS) in patients undergoing
general anesthesia for coronary artery bypass grafting (CABG) surgery.
Methods: Fifty patients with ASA physical status II and Mallampati score I and II were
scheduled for elective CABG surgery under general anesthesia requiring orotracheal intubation
were randomly allocated to either DLS group (n = 25) or FOB group (n = 25). The same protocol
of anesthetic medications was used. Invasive systolic and diastolic blood pressure (SBP & DBP)
and heart rate (HR) were recorded before and after anesthesia induction, during intubation and in
the first and second minutes after intubation. The differences among the hemodynamic variables
recorded over time and differences in the circulatory variables between the two study groups were
compared.
Results: Duration of intubation was shorter in DLS group (19.3 ± 4.7 sec) compared with
FOB group (34.9 ± 9.8 sec; p = 0.0001). In both study groups basic SBP and DBP and HR were
not significantly different (P >0.05). During the observation, there were no significant differences
between the two groups in BP or HR at any time points or in their maximal values (all p values
>0.05).
Conclusion: We conclude that the FOB had no advantage in attenuating the hemodynamic
responses to orotracheal intubation in patients undergoing CABG surgery.
Keywords: Laryngoscopy-Hemodynamic responses-Fiberoptic bronchoscope-Orotracheal
intubation.
*
MD, Associated Professor of Anesthesiology, Department of Anesthesiology, Shahid Rajaii cardiovascular Medical Center,
Iran University of Medical Sciences, Tehran, Iran.
** MD, Associated Professor of Anesthesiology, Fellow in Cardiac Anesthesia, Cardiovascular Research Center, Madani Heart
hospital, Tabriz University of Medical Sciences, Tabriz, Iran.
*** MD, Assistant Professor of Anesthesiology.
Correspondence and Reprints to: Rasoul Azarfarin MD, Cardiovascular Research Center, Madani Heart Hospital, Tabriz
University of Medical Sciences, Tabriz, Iran. Tel: +98 411 3373950, Fax: +98 411 3373950,
E-mail: [email protected], razarfarin@ yahoo.com
833
M.E.J. ANESTH 20 (6), 2010
834
Introduction
The cardiovascular response to laryngoscopy
and tracheal intubation has been extensively studied
during the past three decades. Direct laryngoscopy
and passage of a tracheal tube are noxious stimuli that
can provoke adverse responses in the cardiovascular,
respiratory, and other physiologic systems. Tracheal
intubation causes a reflex increase in sympathetic
activity that may result in hypertension, tachycardia,
and arrhythmia1-3. The magnitude of the response
is affected by many factors: the technique of
laryngoscopy and tracheal intubation4-6, and the
use of various airway instruments, like flexible
fiberoptic bronchoscope and light wand intubating
device1,3. Premedication and induction drugs may
attenuate the circulatory response7-10, many drugs and
techniques have been tried in an effort to attenuate
adverse hemodynamic responses to laryngoscopy
and endotracheal intubation1-3,6-11. A patient’s medical
condition affects his physiologic response7-13. The
cardiovascular response to tracheal intubation,
include elevation in arterial pressure and typically
starts within 5 seconds of laryngoscopy, peaks in 1
to 2 minutes, and returns to control levels within 5
minutes. Such hemodynamic changes can result in
myocardial ischemia but seem to cause little harm
to most patients. However they are undesirable in
patients with cardiac disease. There are limited studies
comparing differences in the circulatory responses
to DLS and FOB in cardiac patients and we cannot
find the previously published study on patients who
undergoing coronary artery bypass graft (CABG)
surgery. However, Tsubaki et al14 demonstrated that
fiberoptic intubation should be used in patients with
difficult airway, hypertension, ischemic heart disease,
or cerebrovascular atherosclerosis. In this randomized
clinical trial, we compared the circulatory responses
to either direct laryngoscopy (DLS) or fiberoptic
bronchoschopy (FOB) to determine whether there is
a clinically relevant difference between the circulatory
responses to FOB and DLS in patients undergoing
CABG surgery.
Methods
After the study protocol was approved by the
Division Ethics Committee of our institute, all of the
N. Aghdaii et al
50 adult patients signed informed written consent to
participate in this study. These patients were ASA
physical status II, 35-65 years old and ejection fraction
(EF) ≥40% and scheduled for elective coronary
artery bypass graft surgery under general anesthesia
and orotracheal intubation. No difficulties with their
airway management or intubation were predicted
during preoperative visits (Table1). Exclusion
criteria were a history of reactive airway disease,
gastroesophageal reflux, morbid obesity, co-existing
cardiovascular diseases except coronary artery
disease and opium addiction. The patients taking
their medications before surgery had similar protocol.
All of them were taking metoprolol, nitrocontin and
aspirin. Patients were randomly allocated to either the
FOB group (n = 25) or the DLS group (n = 25) using
online randomization software (URL: http://www.
graphpad.com). Patients in the first group underwent
orotracheal intubation using fiberoptic bronchoscope.
For intubation in FOB group, after placing the
patient's head in the sniffing position, a jaw thrust was
performed by an experienced assistant. He placed the
fingers behind the posterior ramus of the mandible,
at the same time the thrust directed upward and the
thumbs opened the mouth. After exposure of the
glottis, the FOB was passed between the vocal cords
and downward into the trachea. To avoid stimulation
of the carina, we advanced the tip of the FOB into
the trachea no more than 3-4 cm below the glottis.
A tracheal tube was then advanced over the FOB
while rotated counterclockwise. After insertion of the
tracheal tube into the trachea, the jaw thrust maneuver
was stopped. The FOB was then removed after
confirmation of the correct tracheal tube placement
by auscultation of both lungs. All of patients in DLS
group underwent conventional orotracheal intubation
using a rigid Macintosh 3 (in women) or 4 (in men)
laryngoscope blade. Fiberoptic and laryngoscopy
intubations were performed by one anesthesiologist
who was experienced in both methods.
Before the induction of anesthesia, all patients
were premedicated with intramuscular lorazepam
1 mg and morphine sulfate 0.1 mg/kg 1 hour before
entering the operating room. Then, in the operating
room, the electrocardiogram, invasive blood pressure,
and arterial oxygen saturation by pulse oximetry were
monitored. The electrodes of nerve stimulator were
CARDIOVASCULAR RESPONSES TO OROTRACHEAL INTUBATION IN PATIENTS UNDERGOING CORONARY
ARTERY BYPASS GRAFTING SURGERY
applied at the volar side of the wrist for stimulation of
the ulnar nerve. With placement of these electrodes,
electrical stimulation normally elicits only finger
flexion and thumb adduction. Induction of anesthesia
with Etomidate 0.2 mg/kg, sufentanil 2.5 µg/kg and
cisatracurium 0.2 mg/kg in both groups was done.
After achieving hypnosis, determined as a loss of
any response to verbal command and before muscle
relaxant was injected, the mode of nerve stimulation
was changed to TOF (train of four). Then, cisatracurium
(0.2 mg/kg) was administered. Trachea was intubated
when the response to TOF stimulation disappeared.
Procedures were then started according to the study
protocol. During the observation, a third person acted
as the time keeper using a digital stopwatch, time
zero was (zero seconds) when the response to TOF
stimulation disappeared and facemask was removed
from the patient. When the jaw thrust maneuver was
stopped and ventilation was restarted through the
tracheal tube and carbon dioxide was detected by
capnography, this was recorded as total intubation
time. Blood pressure and heart rate were measured
and recorded before induction (T0), post induction
(T1), at endotracheal intubation (T2), 1 and 2 minutes
afterwards (T3, T4).
The statistical analysis of data was performed
with SPSS Version 15.0 statistical software (SPSS Inc,
Chicago, IL). The intragroup differences among the
circulatory variables recorded over time were analyzed
using the repeated measures analysis of variance.
Differences in mean values of circulatory variables
were analyzed by using independent samples t test. The
categorical variables in the two groups were analyzed
by using Chi-square test or Fisher's exact test as
appropriate. The differences in circulatory parameters
in "the two consequent times" were analyzed by
using paired t test. The hypothesis of this study was
that there would be a clinically meaningful difference
in the hemodynamic responses to two fiberoptic and
laryngoscopy intubation methods. The quantitative
data were expressed as mean ± SD. A P value of ≤0.05
was considered statistically significant for all tests.
Results
There were no significant differences between
the two groups regarding the patients’ gender, age,
835
Mallampati score or ejection fraction. No significant
differences were seen in the baseline values of BPs and
HRs. The time required for intubation was significantly
longer for the fiberoptic method compared with
conventional intubation with laryngoscopy (34.9 ± 9.8
versus 19.3 ± 4.7 seconds, P = 0.0001; Table 1).
Table 1
Clinical characteristics of the patients
DLS
N = 25
FOB*
N = 25
P
Age (yr)
53.0 ± 7.8
53.1 ± 6.9
0.970
Gender (male)
17 (68%)
16 (64%)
0.373
Ejection
fraction
46.2 ± 3.9
47.4 ± 5.4
1.000
Mallampati
score (I/II)
22/3
21/4
?
Intubation
time(sec)
19.3 ± 4.7
34.9 ± 9.8
0.0001
= FOB: Fiberoptic bronchoscopy
= DLS: Direct laryngoscopy
After anesthesia induction, systolic and
diastolic BP in the two groups decreased significantly
compared with baseline values (p = 0.001). There
was no statistically significant change in HR in FOB
and DLS groups. Also, postinduction values of BP
and HR were not significantly different between
the two groups (p values >0.05). Compared with
postinduction values, both FOB and DLS resulted in
statistically significant increase in BP but not in HR
(Fig. 1 and 2). There were no significant differences in
the blood pressure or heart rate from before intubation
to immediately after intubation between the FOB and
DLS groups. At the second minute after intubation,
no significant difference was observed between the
two groups. BP and HR during intubation (T2) and
after intubation were similar in both FOB and DLS
group (p values> 0.05). The maximum values of SBP,
DBP and HR during the observed periods were not
statistically significantly different in the two study
groups. During the observation, the times required to
reach maximum values of SBP and HR were similar
in the two groups, but the times required for recovery
of SBP and HR to reach to the postinduction values
were significantly slower in the FOB group than in
the DLS group (Fig. 1 and 2).
M.E.J. ANESTH 20 (6), 2010
836
Fig. 1
Variation in systolic (SBP) and diastolic blood pressure (DBP)
in patients undergoing direct laryngoscopy or fiberoptic
brnchoscopy (FOB) for orotracheal intubation
Fig. 2
Variation in heart rate in direct laryngoscopy and fiberoptic
brnchoscopy groups
Discussion
One advantage of the fiberoptic intubation is that
it can avoid the mechanical stimulus to the base of
tongue, epiglottis and the receptors in the pharyngeal
muscles exerted by direct laryngoscope. Some studies
have shown that the cardiovascular responses to
tracheal intubation are greatly inhibited by attenuating
or avoiding the oropharyngolaryngeal stimuli15-18. The
primary goal of this investigation was to determine
whether there is a clinically relevant difference
between the circulatory responses to FOB and DLS in
coronary artery disease patients anesthetized for CABG
surgery. We examined whether fiberoptic intubation
attenuated hemodynamic responses to orotracheal
intubation, compared with those that occurred with
N. Aghdaii et al
laryngoscopy. The results of this investigation suggest
that bronchoscopy do not suppress the hemodynamic
response to endotracheal intubation more than the
response to laryngoscopy. It is well known that the
stimuli to airway structures are the main causes
of circulatory responses to tracheal intubation19.
Laryngoscopy itself is one of the most invasive
stimuli during orotracheal intubation20-21. Many
anesthesiologists agree that a skilled anesthesiologist
applies only a small force to the patient’s larynx when
using a laryngoscope and that reducing the force on
the larynx might prevent excessive hyperdynamic
responses to orotracheal intubation22-24. It is possible to
separate the factors that contribute to the hemodynamic
responses to orotracheal intubation21. The first is the
response to laryngoscopy and the second is the response
to endotracheal intubation. Hemodynamic changes
start within seconds of direct laryngoscopy, and there
is a further increase in heart rate and blood pressure
with passage of the tracheal tube. It is not known which
component is more responsible for the hyperdynamic
response to orotracheal intubation. Although we
attempted to reduce the hyperdynamic responses to
intubation by using fiberoptic bronchoscopy without
deep insertion in the trachea, there was no statistically
significant difference in the cardiovascular variables
between the fiberoptic bronchoscopy (FOB) and
direct laryngoscopy (DLS) groups. The results of
our study correspond with those of other previous
studies25-29. whereas other investigators demonstrated
the effectiveness of avoiding laryngoscopy using
new devices4,13-17,22-25. This study shows that under the
general anesthesia orotracheal intubation using the
FOB and DLS caused similar increases in BPs and
HRs. This suggests that the FOB can not attenuate
the cardiovascular responses to orotracheal intubation
compared to the DLS. This can be due to the longer
intubation time in FOB group that cause hypercapnia,
which can result in hypertention and tachycardia7,29,
the airway clearance maneuver (jaw thrust maneuver)
that is necessary for FOB intubation, or irritation
of trachea by insertion and removal of FOB. In our
study, the mean intubation time is significantly longer
in the FOB group than in the DLS group. The lifting
of the jaw upward to make a clear passage for the
FOB and for the tracheal tube to enter the glottis can
cause cardiovascular responses. Hirabayashi et al30.
CARDIOVASCULAR RESPONSES TO OROTRACHEAL INTUBATION IN PATIENTS UNDERGOING CORONARY
ARTERY BYPASS GRAFTING SURGERY
demonstrated that, in anesthetized adults receiving
lightwand-guided tracheal intubation, the magnitude of
stimulus from the jaw thrust maneuver was sufficient
to cause circulatory responses similar to those observed
in laryngoscopic intubation. Thus, one might argue that
the differences in nociceptive stimulation from the jaw
thrust maneuver cause the differences in the circulatory
responses between the fiberoptic and laryngoscopic
intubation methods. In addition, the successful
intubation (the advancement of the tracheal tube over
the FOB) often requires some specific maneuvers e.g.
rotating the tracheal tube, further lifting jaw upward
and adjusting the patient's head-neck position. All these
procedures are blind and invasive, and may further
837
stimulate pharyngolaryngeal structures and the trachea.
In contrast, with the direct laryngoscopic intubation,
only the tracheal tube is inserted into the trachea under
direct vision. The laryngoscopy produces a balanced
stimulation of vagal and cardiac accelerator fibers,
whereas the intratracheal manipulation produces less
vagal stimulation31.
In conclusion, our study demonstrated that
the orotracheal intubations using a FOB and a DLS
produced similar hemodynamic responses. The FOB
had no special advantage in attenuating hemodynamic
responses to orotracheal intubation compared to the
DLS.
M.E.J. ANESTH 20 (6), 2010
838
N. Aghdaii et al
References
1.McCoy EP, Mirakhur RK, McCloskey BV: A comparison of the
stress response to laryngoscopy. The Macintosh versus the McCoy
blade. Anaesthesia; 1995, 50:943-946.
2.Shinji T, Taro M, Masayuki M, Hidenori T: Hemodynamic
responses to tracheal intubation with laryngoscope versus lightwand
intubating device (Trachlight®) in adults with normal airway. Anesth
Analg; 2002, 95:480-4.
3.Choyce A, Avidan MS, Harvey A, et al: The cardiovascular
response to insertion of the intubating laryngeal mask airway.
Anaesthesia; 2002, 57:330-333.
4.Yoshihiro H, Shuji D: Differences in cardiovascular response to
airway stimulation at different sites and blockade of the responses
by lidocaine. Anesthesiology; 2000, 93:95-103.
5.Latorre F, Hofmann M, Kleemann PP, Dick WF: Stress response to
nasotracheal intubation: a comparative evaluation of fiberendoscopic
vs. laryngoscopic intubation with and without topical anaesthesia of
the larynx. Anaesthetist; 1993, 42:423-6.
6.Rose DK, Cohen MM: The airway: Problems and predictions in
18,500 patients. Can J Anaesth; 1994, 41:372-383.
7.Takita K, Morimoto Y, Kemmotsu O: Tracheal lidocaine attenuates
the cardiovascular response to endotracheal intubation. Can J
Anaesth; 2001, 48:732-736.
8.Schaefer HG, Marsch SC, Strebel SP, Drewe J: Cardiovascular
effects of fibreoptic oral intubation. A comparison of a total
intravenous and a balanced volatile technique. Anaesthesia; 1992,
47:1034-1036.
9.Mustola ST, Baer GA, Metsa-Ketela T, Laippala P: Haemodynamic
and plasma catecholamine responses during total intravenous
anaesthesia for laryngomicroscopy. Thiopentone compared with
propofol. Anaesthesia; 1995, 50:108-113.
10.Maguire AM, Kumar N, Parker JL, Rowbotham DJ, Thompson
JP: Comparison of effects of remifentanil and alfentanil on
cardiovascular response to tracheal intubation in hypertensive
patients. Br J Anaesth; 2001, 86:90-3.
11.Neidhart PP, Champion P, Vogel J, Zsigmond EK, Tassonyi E: A
comparison of pipecuronium with pancuronium on haemodynamic
variables and plasma catecholamines in coronary artery bypass
patients. Can J Anaesth; 1994, 41:469-474.
12.Kirvela M, Scheinin M, Lindgren L: Haemodynamic and
catecholamine responses to induction of anaesthesia and tracheal
intubation in diabetic and non-diabetic uraemic patients. Br J
Anaesth; 1995, 74:60-65.
13.Nishikawa K, Omote K, Kawana S, Namiki A: A comparison of
hemodynamic changes after endotracheal intubation by using
the lightwand device and the laryngoscope in normotensive and
hypertensive patients. Anesth Analg; 2000, 90:1203-7.
14.Tsubaki T, Aono K, Nakajima T, Shigematsu A: A Blood pressure,
heart rate and catecholamine response during fiberoptic nasotracheal
intubation under general anesthesia. J Anesth; 1992, Oct. 6(4):4749.
15.Hawkyard SJ, Morrison A, Doyle LA, Croton RS, Wake PN:
Attenuating the hypertensive response to laryngoscopy and
endotracheal intubation using awake fiberoptic intubation. Acta
Anaesthesiol Scand; 1992, 36:1-4.
16.Kitamura T, Yamada Y, Chinzei M, Du HL, Hamaoka K:
Attenuation of haemodynamic responses to tracheal intubation by
the StyletScope. Br J Anaesth; 2001, 86:275-7.
17.Nishikawa K, Kawana S, Namiki A: Comparison of the lightwand
technique with direct laryngoscopy for awake endotracheal
intubation in emergency cases. J Clin Anesth; 2001, 13:259-63.
18.Kimura A, Yamakage M, Chen X, Kamada Y, Namiki A: Use of
the fibreoptic stylet scope (Styletscope) reduces the hemodynamic
response to intubation in normotensive and hypertensive patients.
Can J Anaesth; 2001, 48:919-23.
19.Xue FS, Li CW, Liu KP, Sun HT, Zhang GH, Xu YC, Liu Y:
Circulatory Responses to Fiberoptic Intubation in Anesthetized
Children: A Comparison of Oral and Nasal Routes. Anesth Analg;
2007, 104:283-288.
20.Kovak AL: Controlling the hemodynamic response to laryngoscopy
and endotracheal intubation. J Clin Anesth; 1996, 8:63-79.
21.Adachi YU, Satomoto M, Higuchi H, Watanabe K: Fentanyl
attenuates the hemodynamic response to endotracheal intubation
more than the response to laryngoscopy. Anesth Analg; 2002, Jul.
95(1):233-7, table of contents.
22.Bishop MJ, Harrington RM, Tencer AF: Force applied during
tracheal intubation. Anesth Analg; 1992, 74:411-4.
23.Bucx MJ, Snijders CJ, Van Geel RT, et al: Forces acting on the
maxillary incisor teeth during laryngoscopy using the Macintosh
laryngoscope. Anaesthesia; 1994, 49:1064-70.
24.Tong JL, Ashworth DR, Smith JE: Cardiovascular responses
following laryngoscope assisted, fibreoptic orotracheal intubation.
Anaesthesia; 2005, 60:754-8.
25.Adachi YU, Takamatsu I, Watanabe K, Uchihashi Y, Higuchi H,
Satoh T: Evaluation of the cardiovascular responses to fiberoptic
orotracheal intubation with television monitoring: comparison with
conventional direct laryngoscopy. J Clin Anesth; 2000, 12:503-8.
26.Barak M, Ziser A, Greenberg A, Lischinsky S, Rosenberg
B: Hemodynamic and catecholamine response to tracheal
intubation:direct laryngoscopy compared with fiberoptic intubation.
Journal of Clinical anesthesia; 2003, 15:132-6.
27.Xue FS, Zhang GH, Li XY, Sun HT, Li P, Li CW, Liu KP:
Comparison of hemodynamic responses to orotracheal intubation
with the GlideScope videolaryngoscope and the Macintosh direct
laryngoscope. J Clin Anesth; 2007, Jun, 19(4):245-50.
28.Xue FS, Zhang GH, Sun HT, Li CW, Li P, Liu KP, Xu YC, Liu Y, Liu
J: A comparative study of hemodynamic responses to orotracheal
intubation with fiberoptic bronchoscope and laryngoscope in
children. Paediatr Anaesth; 2006, Jul. 6(7):743-7.
29.Xue FS, Zhang GH, Li XY, Sun HT, Li P, Sun HY, et al: Comparison
of haemodynamic responses to orotracheal intubation with
glidescope (R) videolaryngoscope and fibreoptic bronchoscope. Eur
J Anaesthesiol; 2006, 23:522-526.
30.Hirabayashi Y, Hiruta M, Kawakami T, Inoue S, Fukuda H, Saitoh
K, Shimizu R: Effects of lightwand (Trachlight) compared with
direct laryngoscopy on circulatory responses to tracheal intubation.
Br J Anaesth; 1998, 81:253-5.
31.Shribman AJ, Smith G, Achola KJ: Cardiovascular and
catecholamine responses to laryngoscopy with and without tracheal
intubation. Br J Anaesth; 1987, 59:295-9.
EFFECTS OF INTRAOPERATIVE-INTRATHECAL
SUFENTANIL INJECTION ON POSTOPERATIVE
PAIN MANAGEMENT AFTER SINGLE
LEVEL LUMBAR DISCECTOMY
Saeid Abrishamkar*, Mohammadhossein Karimi**,
Mohammadreza Safavi***, Azim Honarmand***
and A fshin S afavi ****
Abstract
Background: For lumbar disc operation a chain of painful procedures including skin incision,
muscle dissection and sometimes laminectomy should be performed. The combination of these
manoeuvres results in significant post-operative pain.
The standard way to reduce post-operative pain consist of intra-operative injection of local
anaesthetic (Bupivicaine or Lidocaine) to the superficial tissues and intravenous, oral or rectal
prescription of Opioid analgesics or other analgesics after operation, but inadequate analgesia,
constipation and delayed mobilisation are frequent side effect of those treatments. The goal of
this study was to reduce postoperative pain of patients which causes a reduction in analgesic
consumption and eventually shortened hospital stay and acceleration in physical therapy programs
and ambulation.
Materials and Methods: After ethical comitte approval, patients allocated in two groups
A and B. Each group consisted 30 patients which all of them underwent general anesthesia. All
of operations performed by same surgeon... After discectomy and at the end of surgerybased on
patients odd or even number of hospital admission, one group (group-A) received sufentanil
(Iranian pharmaceutic company) 0.05/kg intrathecaly injected in surgical level and the placebo
group (group-B) normal saline was injected. In recovery room when patients were sufficiently
awake for pain assessment, patients were asked to score pain on the verbal pain assessment score In
both groups we compaired pain scores pre and postoperativly. The total dose of opioid requirement
for patients and its time after operation was recorded.
From the Departments of Neurosurgery, Anesthesiology and Intensive Care units, Isfahan University of Medical Sciences,
Isfahan, Iran.
*
MD, Associate Professor of Neurosurgery, and Intensive Care Unit.
**
MD, Neurosurgery and Intensive Care Unit.
*** MD, Assistant Professor of Anesthesia and Intensive Care Unit.
**** MD, Anesthesiology and Intensive Care Unit.
Corresponding Author: Mohammadreza Safavi, MD, Assistant Professor of Anesthesia and Intensive Care, Department of
Anesthesiology and Intensive Care Unit, Isfahan University of Medical Sciences, Isfahan, Iran. Tel: 00989133152416, Fax: 0098
(311)2732659, E-mail: [email protected]
839
M.E.J. ANESTH 20 (6), 2010
840
S. Abrishamkar Et Al
Results:
Introduction
Of the 60 patients (ASA classes I and II) entering
the study, no one excluded during our study. 30
patients received intrathecal injection of sufentanil
as group-A or case and 30 patients normal saline as
group-B or control. Mean age between two groups
showed no significant difference. 45.7 year (SD
= 11.5) for group-A and 44.3 year (SD = 9.9) for
group-B which did not differ between two groups (P
= 0.617). Urinary retension happened in 3 patients of
group-A and 3 patients of group-B (P = 1). Pruritis
happened in 1 patient of group-A and no patient in
group-B (P = 0.15). Patients in group-A had reduced
analgesic requirments (P = 0.01). Preoperative low
back pain based on NPS (numerical pain scores)
criteria in group-A shows score 1, (n = 7) score 2, (n
= 10) score 3, (n = 11) and score 4 (n = 2) (mean =
2.2667 and SD = 0.9072). These scores in group-B
showed score 2 (n = 4) score 3 (n = 16) and score 4
(n = 10) (mean = 3.2 and SD = 0.6644) (P <0.001).
After surgery low back pain assessment in two groups
shows in group-A three patients had score 1, score 2,
(n = 7) score 3, (n = 11) score 4, (n = 8) score 5 (n =
1) (mean = 2.9 and SD = 1.0289) and in group-B score
4 (n = 17) score 5 (n = 13) (mean = 4.4333 and SD
= 0.5040) (P <0.001). Preoperative lower extremity
radicular pain assessment in two groups shows a mean
pain score of 8.3 with SD = 0.9523 in group-A and
a mean of 8.3448 with SD = 1.1109 in group-B and
after operation a mean pain score of 1.7333 with SD
= 0.8277 in group-A and a mean of 4.1667 with SD =
0.7466 in group-B. In walking ability assessments pre
and postoperatively based on Mann-Whitney test it is
shown that in group-A walking ability is better than
group-B (P <0.001).
Lumbar disc herniation surgery is a common
surgical procedure performed within neurosurgical
and some orthopedics departments. It is usually carried
out for lumbar degenerative condition mostly affecting
those patients between 30 to 40 years old1. For lumbar
disc operation a chain of painful procedures including
skin incision, muscle dissection and sometimes
laminectomy should be performed. The combination
of these maneuvers results in significant post-operative
pain.
Conclusion: In this study we studied the efficacy
of intraoperative-intrathecal sufentanil injection versus
placebo on post operative pain management. Our
study showed that intrathecal (IT) sufentanil provided
more effective analgesia postoperatively after single
level disccectomy. Urinary retention was equal in two
groups. For more exact conclusions it is better to do a
similar study on more patients.
Key words: intrathecal sufentanil -postoperative
pain-lumbar discectomy.
The standard way to reduce post-operative
pain consist of intra-operative injection of local
anaesthetic (Bupivicaine or Lidocaine) to the
superficial tissues and intravenous, oral or rectal
prescription of Opioid analgesics or other analgesics
after operation, but inadequate analgesia, constipation
and delayed mobilization are frequent side effect of
these treatments1,3. Lumbar intrathecal (IT) opioids
have been used as an adjunct to post thoracotomy
analgesia4,5,6,7 but the available literature6 has not
clearly demonstrated the clinical usefulness of this
technique for pain reduction in lumbar disc operaiton.
Intrathecal analgesia has been used after “lumbar spine
procedures”7, spinal fusion8, laminectomy, discectomy,
hemilaminotomy, and foraminotomy9.
Epidural analgesia was used after lumbar
laminectomy10, posterior, anterior or combined fusion11,
posterior fusion2,4 with or without decompression10,
and after posterior or anterior-posterior lumbar fusion3.
For continuous postoperative analgesia, epidural
administration is an established and safe method used
routinely for other operative procedures. Epidural
opioids10, ropivacaine3,4, or a combination of opioids
with bupivacaine2,11, have been reported to be useful
after spine surgery. Patients’ postoperative functional
rehabilitation is hampered by intense postoperative
pain. Although fairly high doses of IV opioids are
typically necessary, epidural analgesia may result in
fewer side effects. The goal of this study was to reduce
postoperative pain of patients which causes a reduction
in analgesic consumption and eventually shortened
hospital stay and acceleration in physical therapy
programs and ambulation.
EFFECTS OF INTRAOPERATIVE-INTRATHECAL SUFENTANIL INJECTION ON POSTOPERATIVE PAIN MANAGEMENT
AFTER SINGLE LEVEL LUMBAR DISCECTOMY
Materials and Methods
The ethical committee of our university approved
this interventional double blind &case series study.
This study was performed on patients which needed
a surgical intervention for lumbar disc herniation in
ayatollah kashani hospital of Isfahan university of
medical sciences. Number of patients allocated for this
study was based on 1% of general population which
experience low back pain during their life and 10% of
them which may need surgical intervention (0.0001
of general population). Patients were excluded if they
had more than one level disc herniation, previously
underwent operation for disc herniation, age more
than 60 years, spinal canal stenosis, patients refusal
for intrathecal injection and patients who encountered
a surgical complication (eg. nerve root injury, thecal or
sac laceration…).
Based on these statistical information and
exclusive criteria 60 patients entered our study which
were divided in to two 30 patients groups based on
their hospital admission number. In all patients general
anesthesia was induced with thiopental(5-7 mg/kg)
and fentanyl (1-1.5 microgm/kg). Atracurium (0.6
mg/kg) was administrated to facilitate endotracheal
intubation. Anesthesia was maintained with Nitrous
Oxide (N20/O2 ratio50% /50%) and Isoflurane (up
to1.3 MAC). Atracurium increments were used to
facilitate mechanical ventilation of the lung. Also
morphine (0.15 mg/kg administrated intravenously at
the start of surgery. Whenever the blood pressure or
heart rate increased by more than 30%, so that depth
of anesthesia was judged inadequate, hemodynamic
control was ensured with incremental doses of IV
fentanyl (50-100 microgm). All operations were
performed by the same surgeon. After discectomy
and at the end of surgery based on patients number
of hospital admission, one group (group-A) received
sufentanil (Iranian pharmaceutic company) 0.05/kg
intrathecaly injected in surgical level and the placebo
group (group-B) normal saline was injected. Resident
which should control post operative pain scores
questionare don’t knows which substance is injected.
Then it was blinded to type of injection. In recovery
room when patients were sufficiently awake for pain
assessment, patients were asked to score pain on the
verbal pain assessment score (Table 1).
841
Table 1
Numerical pain score
Score
Quality of Pain
1
No pain
2
Mild pain
3
Pain that cause the patient discomfort
4
Pain that cause the patient searching medical
care
5
Moderate pain that is still supportable
6
Pain that make the patient fill completely
discomfort
7
Pain that cause the patient to stop all
activities
8
Severe pain rarely have been experienced
9
Very severe pain
10
Pain as worst as possible
The motor ability of patients was assessed
based on 1-5 criteria. Pain assessment was performed
every 12 hours for first two postoperative days and
morphine was administrated if pain score was greater
than 9 (0.05 mg/kg). Most of patients were discharged
after two days of hospitalization. In both groups we
compared pain scores pre and postoperativly. The total
dose of opioid requirement for patients and its time
after operation was recorded. Hemodynamic variables,
vertigo, pruritis and urinary retention were recorded
in two groups of study. All of these probable side
effects were monitored in post operation period and
if happened recorded. The primary outcome measure
was a visual analogue pain score which recorded
in recovery, on the first and second post-operative
days. Secondary outcome measures were length of
post-operative hospital stay, post-operative analgesia
required-total dose and types per 24 hours for first
two days. All opiod analgesics will be converted
to morphine equivalents and side effects by day 2
including urinary retention, nausea, vomiting and
pruritis and hemodynamic variables.
Statistical Analysis
Pain scores were ranked data that should be
distributed in a normal distribution. Analysis was
therefore by a Mann Whitney rank sum test.
Length of hospital stay was continuous data so
the t test was used for analyzing.
M.E.J. ANESTH 20 (6), 2010
842
S. Abrishamkar Et Al
The prevalence of side effects will be analysed
using a Chi2 test. The total intra and post-operative
analgesia requirement was converted to morphine
equivalents and I\IIanalyzed using a t test. No subgroup
analysis was undertaken.
Trial termination
The trial ended when the last patient was
discharged from hospital
Results
Sixty patients were included, 30 in Group A
and 30 in Group B. No patient was excluded from
the study. The two groups were similar with respect
to demographic variables, duration of surgery and
anesthesia (Table 1).
Table 1
Demographic and intra-operative data (ASA I\II)
Group A
(n = 30)
Group B
(n = 30)
45.7 ± 11.5
44.3 ± 9.9
21/9
19/11
Weight (kg)
82/3 ± 11.1
77.8 ± 12.3
Duration of anesthesia (min)
54.0 ± 7.1
52.7 ± 7.4
Duration of surgery (min)
39.0 ± 5.6
36.8 ± 5.8
Age (yr)
Gender (M/F)
Data are presented as mean± SD or number of patients.
There was no significant difference between two groups.
Three patients in each group had urinary retention
(P = 1.0). One patient in group A and no patient in group
B had pruritus (P = 0.15). The postoperative morphine
requirements were significantly less in group A when
compared with group B (5 mg vs 20. mg, P = 0.01).
Preoperatively, there was no significant difference in
mean (± SD) NPS score at rest in two groups (3.0 ±
0.5 in group A vs. 3.1 ± 0.6 in group B, P = 0.64). After
surgery, mean (± SD) NPS score was significantly
less in group A compared with group B (2.9 ± 1.03 in
group A vs. 4.4 ± 0.5 in group B, P < 0.001). Incidence
of different NPS scores in two groups was shown in
figure 1.
Preoperatively, there was no significant
difference in mean (± SD) lower extremity radicular
pain assessment score (NPS score) in two groups (8.3
± 0.9 in group-A vs. 8.3 ± 1.1 in group-B, P = 0.803).
After surgery, mean (± SD) lower extremity radicular
pain assessment score (NPS score) was significantly
Fig. 1
The incidence of different NPS scores in
group A and group B
Group A
Group B
18
16
14
12
10
8
6
4
2
0
1
2
3
4
5
6
7
8
9
10
less in group-A compared with group-B (1.7 ±
0.8 in group-A vs. 4.2 ± 0.7 in group-B, P <0.000).
Incidence of different lower extremity radicular pain
assessment score (NPS score) in two groups was
shown in figure 2. In walking ability assessments pre
and postoperatively based on Mann-Whitney test it is
shown that in group-A walking ability is better than
group-B (P <0.001). Walking ability of patients was
assessed based on scores listed in table 1.
1
Table 1
Walking ability scores after lumbar discectomy
Patient is returned to near normal lifestyle and normal
movements with no significant pain.
2
Significant improvement in patients’ movements with
mild restriction due to low back pain and some degree
of pain in extremities.
3
Partial improvement in patients movements with some
intermediate pain and discomfort but the patient is able
to walk.
4
Only mild improvement in movements and pain that
make the patient fill completely discomfort.
5
There is no difference between preoperative and post
operative pain and walking ability.
Discussion
The aim of postoperative pain relief is to
provide subjective comfort in addition to inhibiting
nociceptive impulses. Autonomic and somatic reflexes
responses to pain can be blunted, allowing the patient
to breathe, cough and move more easily. It is not only
the humanitarian feature of pain that must be assessed
but also its ability to restore normal function. It is
therefore necessary to assess and treat pain not only
at rest but also during activity. In this study we studied
the efficacy of intraoperative-intrathecal sufentanil
injection versus placebo on post operative pain
EFFECTS OF INTRAOPERATIVE-INTRATHECAL SUFENTANIL INJECTION ON POSTOPERATIVE PAIN MANAGEMENT
AFTER SINGLE LEVEL LUMBAR DISCECTOMY
management.
Our study showed that intrathecal (IT) sufentanil
provided more effective analgesia postoperatively
after single level disccectomy. Urinary retention was
equal in two groups of sufentanil and distilled water
IT injection. Urinary retention has not been studied in
previous7 studies. Pruritis happened in one of patients
in group-A which was mild and spontaneously releafed
and would be an expected side effect of opioids. In
the study of Schenk et al on Postoperative Analgesia
After Major Spine Surgery after intrathecal morphin
injection on 72 patients 5 experienced pruritis1. Patients
in group-A had reduced pain scores and analgesic
requirments in comparision with group-B which only
received distilled water as placebo. Mean pain scores in
group-A which received IT sufentanil was 2.2667 but
in group-B our study showed a higher score of about2,3.
In the study of Riad et al Patients in the morphine group
had significantly lower median numerical rating score
(NRS) for pain on movement at 4h [0 versus 3.5] (P =
0.0008) and 8h [0 versus 4] (P = 0.0083)12. In addition,
median PCA morphine consumption was significantly
reduced at 4h [0 versus 1] (P = 0.0005), 8h [0.5 versus
6] (P = 0.0063) and 12h [3 versus 8.5] (P = 0.0426)
843
in the morphine group12. After surgery low back pain
assessment in two groups shows that in n group-A
the mean pain score is 2.9 compared with 4.43 in
group-B. Preoperative lower extremity radicular pain
assessment in two groups shows a mean pain score of
8.3 with SD = 0.9523 in group-A and a mean of 8.3448
with SD = 1.1109 in group-B which shows an equlity.
After operation a mean pain score of 1.7333 with
SD = 0.8277 in group-A and a mean of 4.1667 with
SD = 0.7466 in group-B that shows a very effective
pain reduction with sufentanil. In walking ability
assessments pre and postoperatively based on MannWhitney test it is shown that in group-A scores are
better than group-B. (P <0.001) which means a better
quality of walking ability between patients reaciving
sufentanil inntraoperativly. As a final conclusion from
this study it is obviated that intrathecal sufentanil
causes better pain tolerance and eventually reduction
of post operative analgesic needs and more satisfaction
and better walking abilities after surgery compaired
with patients who have reacived placebo. Side effects
like pruritis or urinary retention were negligible for
patients. For more exact conclusions it is better to do a
similar study on more patients.
M.E.J. ANESTH 20 (6), 2010
844
S. Abrishamkar Et Al
References
1.Schenk MR, Putzier M, Kugler B, Tohtz S, Voigt K, Schink T,
et al: Postoperative analgesia after major spine surgery: patientcontrolled epidural analgesia versus patient-controlled intravenous
analgesia. Anesth Analg; 2006, 103(5):1311-1317.
2.Gottschalk A, Freitag M, Liehr K, Domke A, Schuster M, Standl
T: [Does patient satisfaction correlate with pain level during patientmonitored epidural analgesia. Evaluation of data from postoperative
pain service]. Schmerz; 2004, 18(2):145-150.
3.Bernards CM, Shen DD, Sterling ES, Adkins JE, Risler L, Phillips
B, et al: Epidural, cerebrospinal fluid, and plasma pharmacokinetics
of epidural opioids (part 2): effect of epinephrine. Anesthesiology;
2003, 99(2):466-475.
4.Bernards CM, Shen DD, Sterling ES, Adkins JE, Risler L,
Phillips B, et al: Epidural, cerebrospinal fluid, and plasma
pharmacokinetics of epidural opioids (part 1): differences among
opioids. Anesthesiology; 2003, 99(2):455-465.
5.Bonhomme V, Doll A, Dewandre PY, Brichant JF, Ghassempour K,
Hans P: Epidural administration of low-dose morphine combined
with clonidine for postoperative analgesia after lumbar disc surgery.
J Neurosurg Anesthesiol; 2002, 14(1):1-6.
6.Capogna G, Parpaglioni R, Lyons G, Columb M, Celleno D:
Minimum analgesic dose of epidural sufentanil for first-stage labor
analgesia: a comparison between spontaneous and prostaglandin-
induced labors in nulliparous women. Anesthesiology; 2001,
94(5):740-744.
7.Liu N, Kuhlman G, Dalibon N, Moutafis M, Levron JC, Fischler
M: A randomized, double-blinded comparison of intrathecal
morphine, sufentanil and their combination versus IV morphine
patient-controlled analgesia for postthoracotomy pain. Anesth
Analg; 2001, 92(1):31-36.
8.Hormann C, Langmayr J, Schalow S, Benzer A: Low-dose
sufentanil increases cerebrospinal fluid pressure in human
volunteers. J Neurosurg Anesthesiol; 1995, 7(1):7-11.
9.Hansdottir V, Hedner T, Woestenborghs R, Nordberg G: The
CSF and plasma pharmacokinetics of sufentanil after intrathecal
administration. Anesthesiology; 1991, 74(2):264-269.
10.Bernards CM, Shen DD, Sterling ES, Adkins JE, Risler L, Phillips
B, et al: Epidural, cerebrospinal fluid, and plasma pharmacokinetics
of epidural opioids (part 2): effect of epinephrine. Anesthesiology;
2003, 99(2):466-475.
11.Wiebalck A, Brodner G, Van AH: The effects of adding sufentanil
to bupivacaine for postoperative patient controlled epidural
analgesia. Anesth Analg; 1997, 85(1):124-129.
12.Riad T, Williams B, Musson J, Wheatley B: Intrathecal morphine
compared with diamorphine for postoperative analgesia following
unilateral knee arthroplasty. Acute Pain; volume 4, Issue1, page 5.
THE EFFECTS OF DURATION OF PROPOFOL
INJECTION ON HEMODYNAMICS
Abdul Zahoor* and Nauman Ahmed**
Abstract
Objectives: The aim of study was to see whether increasing the time of injection of standard
dose of Propofol during induction can prevent fall in blood pressure in female patients; as is
commonly observed with this anesthetic agent.
Design: Comparative, non-interventional, prospective, and randomized and single blind
study.
Place and duration: The study was carried out on female in-patients admitted and surgically
operated at a specialized, tertiary care hospital and was completed with in 6-months.
Patients and methods: The hemodynamic effects of Propofol were compared in three groups
of patients undergoing minor surgical procedures. Each group comprised of 25 patients. A 2 mg/kg
Propofol was administered for 30, 60 and 120 seconds in patients of group-A, group-B and group-C
respectively. Baseline heart rate, systolic blood pressure, diastolic blood pressure and mean arterial
blood pressures were recorded before induction of anesthesia. The same hemodynamic variables
were recorded after induction at one-minute intervals for 10-minutes. Anesthesia was maintained
with 1.5% enflurane and 60% nitrous oxide in oxygen. Complications such as pain on injection,
dystonic movements, erythema, laryngeal spasm, episodes of desaturation, hypoventilation and the
number of additional boluses required to induce hypnosis were also recorded.
Results: The fall in blood pressure was statistically insignificant between the three groups of
patients. The incidence of dystonic movements was the highest in group-A while pain on injection
was highest in group-C. Additional boluses of Propofol to induce hypnosis were required for
patients in group-B and group-C.
Conclusion: Varying the speed of injection of Propofol during induction of anesthesia in adult
female patients does not cause any major difference in the drop of their heart rate, systolic blood
pressure, diastolic pressure and mean arterial pressure.
Key words: Anesthetics, intravenous, Propofol, hemodynamics.
* MD, FCPS.
** MBBS, FCPS.
Department of Anesthesia, King Khaled Eye Specialist Hospital, PO Box 7191, Riyadh 11462, Kingdom of Saudi Arabia
Corresponding Author: Abdul Zahoor, MD, FCPS, Consultant Anesthesiologist, King Khaled Eye Specialist Hospital. P.O Box:
7191, Riyadh 11462, Kingdom of Saudi Arabia. Phone; Mobile +966509003709, Phone: +966-1-4821234, ext. 3995, Fax: +9661-4821908, E-mail: [email protected] and [email protected].
845
M.E.J. ANESTH 20 (6), 2010
846
Introduction
Propofol is a well accepted intravenously
administered anesthetic agent and, by virtue of
its pharmacodynamic properties, is considered a
popular choice both for the induction as well as in
the maintenance of anesthesia1. Propofol was first
introduced into clinical practice in about two decades
back. Over the years, extensive clinical experiences
with Propofol in a wide variety of patients during
different surgical procedures have demonstrated its
effectiveness2.
Propofol has been claimed to be the best available
drug because of its rapid and smooth induction, short
duration of action and a swift and clear headed recovery3.
The standard Propofol dose of 2 mg/kg given over the
recommended time of 30-seconds to pre-medicated
patients is associated with a few disadvantages. The
patients may experience pain during injection of
Propofol, some patients exhibit dystonic movements
and in majority of patients, there is a significant drop in
blood pressure on induction1,4,5. The pain on Propofol
injection can be treated in different ways, including
mixing Propofol with Lidocaine, injecting Lidocaine
into the same vein before injecting Propofol, injecting
cold saline before the injection or refrigerating the
emulsion before injection. The pain on Propofol
injection can also be reduced by selecting large size
veins for administration of the drug6-9. Dystonic
movements occur in a small percentage of patients,
which are usually transient10.
The fall in blood pressure in patients remains
a major problem during induction with Propofol,
especially in hypertensive patients, patients having
ischemic heart disease and those with cerebro-vascular
disease, where a fall in blood pressure can lead to
myocardial or cerebral ischemia. The aim of this study
was to see whether increasing the time of injection of
a standard dose of Propofol prevents the fall in blood
pressure.
Methods
The study was initiated after approval from the
hospital’s project review board and ethics committee.
Seventy five American society of anesthesiologists
(ASA) grade I & II patients undergoing dilatation and
A. Zahoor & N. Ahmed
curettage (D & C) were randomly allocated to one of
the three groups of patients. Patients with an ASA classIII or higher, patients with history of hypertension,
peripheral vascular disease, diabetes and those with
a history of sensitivity to egg proteins were excluded
from the study. A written consent was obtained from
all the patients who participated in the study. Patient
demographics, including age, height and weight were
recorded.
All the patients were pre-medicated orally with
3 – 4 mg Lorazepam, 2 hours before administering
anesthesia. Baseline measurement of heart rate,
systolic blood pressure, diastolic blood pressure and
mean arterial pressure were recorded with a noninvasive automatic blood pressure measuring machine
(Dinamap Pro 400 V2, GE healthcare, USA). One
18 gauge canula was inserted into a large peripheral
vein in one of the patient’s forearm. Two-milliliters
of 2% Lidocaine was injected through the same vein
before starting the injection of Propofol. The patients
in group-A, group-B and group-C were administered a
2 mg/kg dose of Propofol for 30, 60 and 120 seconds
respectively, using an infusion pump (Imed Gemini
PC-1, Alaris Medical systems, San Diego, CA, USA).
The heart rate, systolic blood pressure, diastolic blood
pressure and arterial pressures were recorded every
minute after induction of anesthesia for 10 minutes.
In all the groups, after the loss of verbal contact
with patient, anesthesia was maintained with 1.5%
enflurane and 60% nitrous oxide in oxygen via face
mask. An additional 10 mg bolus of Propofol was
given to patients with whom verbal contact was not
lost after a full induction dose of Propofol. The number
of boluses required in each group were noted. Pain on
injection and any other side effect including erythema
at the site of injection or dystonic movement were
also documented. Endotracheal intubations, patient’s
positioning and surgery were delayed for 10 – 12
minutes after induction in order to avoid any kind
of stimulus which could affect the hemodynamics.
The quality of anesthesia was ensured by monitoring
laryngo-spasm, episodes of apnea, desaturation,
hypoventilation and any abnormal movements.
SPSS version 14 was used to analyze the data of
the study. Numerical data was analyzed by one way
analysis of variance (ANOVA) and expressed as mean
THE EFFECTS OF DURATION OF PROPOFOL INJECTION ON HEMODYNAMICS
and standard deviation. Non-parametric data were
compared with chi-square test. The values of statistical
significance were taken as p < 0.05.
Results
The data was successfully obtained in all cases.
The demographic data was comparable between the
three groups. No statistically significant differences
were found between the groups with respect to age,
weight and height (Table I). The baseline hemodynamic
variables including the heart rate, systolic blood
pressure, diastolic blood pressure and mean arterial
pressure were also comparable and statistically
insignificant (Table II).
Soon after induction of anesthesia, a 15 – 20%
decrease in the heart rate from the base line was generally
observed in all patients. The drop in the heart rate was
comparable between the three groups and there was no
statistically significant difference between them (p >
0.05) (Fig. 1A).The systolic blood pressure decreased
generally by 20 – 25% from the base line in patients
of all groups and no statistically significant difference
was observed between the three groups (p > 0.05) (Fig.
1B). The diastolic blood pressure in patients of all
groups also decreased after induction of anesthesia by
22 – 28% from the base line. The decrease in diastolic
847
blood pressure was gradual and a maximum decrease
was observed at the last minute of recording. There was
no statistically significant difference in the decrease of
diastolic blood pressure among the three groups (p >
0.05). However, the percent decrease in mean diastolic
pressure was slightly different (22 – 28 %) than the
percent decrease in mean systolic blood pressure (20
– 25%) among the three groups of patients (Fig. 1C).
A general decrease in the mean arterial pressure by 20
– 25% from the base line was also noted parallel to
the decrease in systolic and diastolic blood pressures,
but no statistically significant difference was noted
between the three groups (p > 0.05) (Fig. 1D).
Moderate to severe pain was observed on injection
of Propofol in 8 (32%) patients in group-A, 9 (36%) in
group-B and 11 (44%) in group-C. This was despite the
fact that all these patients were injected with Lidocaine
in the same vein before the injection of Propofol.
Erythema at the site of injection was noted in only one
patient in group-C. Dystonic movements were observed
in 6 (24%) patients in group-A, 4 (16%) in group-B and
3 (12%) in group-C. Other complications including
laryngeal spasm, apnea (longer than 30 seconds),
desaturation (SpO2 < 90%) and hypoventilation (End
tidal carbon dioxide > 45 mmHg) were not observed
in any patient among the three groups. Verbal contact
by the end of 2 mg/kg Propofol injection was lost with
Table I
Demographics of patients included in the study
Group A
Group B
Group C
P-Value
Age (Years)
28.68 ±4.5
29.0 ± 6.1
28.91 ± 6.1
0.95
Weight (Kilograms)
62.1 ± 8.1
62.30 ± 9.34
59.4 ± 6.1
0.34
Height (Centimeters)
153.96 ± 6.5
154.28 ± 6.6
154.0 ± 6.2
0.98
The data is the mean ± standard deviation (SD) of 25 patients (n = 25) in each group.
Table II
Baseline hemodynamic variables included in the study
Group A
Group B
Group C
P-Value
Heart Rate min-1
93
90
88
0.99
Systolic blood pressure (mmHg)
120
127
116
0.98
Diastolic blood pressure (mmHg)
77
79
73
0.92
Mean Arterial pressure (mmHg)
88
93
85
0.90
The data is the mean of at least three readings from each of the 25 patients.
M.E.J. ANESTH 20 (6), 2010
848
A. Zahoor & N. Ahmed
Fig. 1
Heart rate (Fig. 1-A), Systolic blood pressure (Fig. 1-B), Diastolic blood pressure (Fig. 1-C) and Mean Arterial pressure (Fig. 1-D)
were recorded in female patients for 10 minutes after induction with Propofol in patients in group-1 (―■―), group- 2 (---∆---) and
group-3 (―▼―).
all patients in group-A. However, 3 patients in group-B
and 5 patients in group-C required additional boluses
of 10 mg and 20 mg of Propofol respectively before
they lost verbal contact.
Discussion
Propofol induced hypotension has been thought
to act by different mechanisms. Propofol may lead
to a reduction in the systemic vascular resistance and
cardiac output is decreased by less than 20%4. Propofol
induced hypotension is mediated by inhibition of the
sympathetic nervous system and impairment of the
baroreflex regulatory mechanism11. Similarly Propofol
is considered to have a direct relaxant effect on venous
smooth muscles and in this way an increase in venous
capacitance may contribute to the hypotension in
patients12. Propofol also has a negative inotropic
effect on the heart and moderately depresses cardiac
function (more than thiopentone and ketamine). The
mechanism is thought to be the attenuation of the autoregulation of the heart which also leads to coronary
vasodilatation13.
In our study, no significant difference between the
three groups of patients was observed with respect to the
established hemodynamic effects of propofol, while a
fall in systolic blood pressure, diastolic blood pressure
and mean arterial pressures were comparable to other
reported studies14. Rapid administration of Propofol
probably results in an early peak drug concentration in
plasma, thus providing a larger gradient for Propofol
uptake into the central nervous system and for drug
redistribution to other body tissues. This observation
was studied by Rolly et al, 1985 who failed to induce
THE EFFECTS OF DURATION OF PROPOFOL INJECTION ON HEMODYNAMICS
anesthesia in 10% of his non-premedicated patients
who received 2 mg/kg Propofol injected over 60
seconds, whereas the same dose was effective in all
patients when injected for over five seconds15. This
explains the need for additional boluses in our study
in some patients in group-B and group-C. On the other
hand, the slow increase in plasma drug concentration
associated with a slow infusion provides a lower but
more sustained gradient for uniform drug delivery
throughout the central nervous system. However, by
slow infusion a larger total dose may be required to
maintain a sustained gradient of drug delivery into
central nervous system.
Increasing the duration of induction delayed the
loss of verbal contact in some patients in group-B
and group-C in the present study, however, the
hemodynamic response was similar in all the three
groups of patients. Our results confirm the reported
observations of Gillies and Lees, 1989 where they
found that 2.5 mg/kg Propofol injected over 20,
40 or 80 seconds resulted in a significantly slower
induction compared to Etomidate (0.3 mg/kg) injected
at equivalent rates16. They also found that although
increasing the length of injection resulted in a slower
induction, the hemodynamic response was not
different between the 20, 40 and 80 seconds groups of
the Propofol administered patients.
Some studies have observed an initial tachycardia
in patients after Propofol administration. However,
most of the studies reported no change or decrease
in the heart rate of patients after a bolus or infusion
of Propofol15. In our study, the heart rate generally
decreased by 15 – 20% in all groups of patients, which
may be due to the absence of baroreflex activity and
direct vagotonic effects of Propofol17.
The overall reported incidence of pain on injecting
Propofol is 17.5 – 74%, however, the incidence varies
with the technique of administration18. The size and
site of the vein, temperature and concentration of the
solution and the use of Lidocaine can help in pain
reduction in patients injected with Propofol to 34%1819
. In our study, the incidence of pain in group-A and
849
Group-B was comparable with the generally accepted
incidence, however the frequency was higher in
group-C compared to other studies5. Theoretically,
patients in group-A and B had a lower incidence of
pain because the effect was transient due to shorter
duration of induction. However, patients in group-C
had a delayed loss of consciousness due to longer
period of induction and therefore experience of pain
was also probably longer.
The reported incidence of excitatory effects,
including spontaneous movements, twitching,
tremor, hypertonus and hiccups in patients as a result
of Propofol induction is 14%1. We noticed similar
complications among 6 (24%) patients in group-A,
4 (16%) in group-B and 3 (12%) in group-C. The
incidence of excitatory effects was comparable in
group-B and C but was slightly higher in-group-A.
These observations indicate towards the possibility of
an indirect correlation between the speed of injection
of Propofol and dystonic movements. Further studies
with larger sample size may be required to firmly
correlate the incidence of pain on injection and dystonic
movements with the speed of injection of Propofol.
Conclusions
Propofol is a well accepted intravenously
administered anesthetic agent but it causes a significant
drop in blood pressure on induction. From the results
obtained in this study we may conclude that varying
the speed of injection of Propofol for induction of
anesthesia in adult female patients does not prevent
the decrease in heart rate, systolic blood pressure,
diastolic blood pressure and mean arterial pressure.
Administration of induction dose of Propofol (2 mg/
kg) in 60 seconds and 120 seconds is associated with
increased requirement for additional boluses to induce
complete hypnosis. Incidence of pain at the site of
injection is also higher in this group of patients, while
injecting the same dose of Propofol in 30 seconds
is associated with a relatively higher incidence of
dystonic movements.
M.E.J. ANESTH 20 (6), 2010
850
A. Zahoor & N. Ahmed
References
1. Shafer SL: Advances in propofol pharmacokinetics and
pharmacodynamics. J Clin Anesth; 1993, 5:14S–21S.
2. Overbaugh R, Jones P, Nguyen A, Swaney G: Effect of mixed versus
unmixed lidocaine with propofol. Internet J Anesthesiol; 2003, Vol.
7(2).
3. Picard P, Tramèr MR: Prevention of pain on injection with propofol:
a quantitative systematic review. Anesth Analg; 2000, 90:963-9.
4. Barker P, Langton JA, Murphy P, Rowbotham DJ: Effect of prior
administration of cold saline on pain during propofol injection.
A comparison with cold propofol and propofol with lignocaine.
Anesthesia; 1991, 46:1069-70.
5. Tariq MA, Kamran M: Incidence of pain on Propofol injection
and efficacy of addition of lignocaine or selecting big vein or both
combined in reducing it: A randomized control trial. J Postgrad Med
Inst; 2006, 20:8–11.
6. Claey MA, Gepts E, Camu F: Hemodynamic changes during
anesthesia induced and maintained with propofol. Br J Anesth;
1988, 60:3-9.
7. Ebert TJ, Muzi.M, Berens R, Goff D, Kampine JP: Sympathetic
responses to induction of anesthesia in humans with propofol or
etomidate. Anesthesiology; 1992, 76:725-33.
8. Muzi M, Berens RA, Kampine JP, Ebert TJ: Venodilation contributes
to propofol mediated hypotension in humans. Anesth Analg; 1992,
72:877-83.
9. Stowe DF, Bosnjak ZJ, Kampine JP: Comparison of etomidate,
ketamine, midazolam, propofol and thiopentone on function and
metabolism of isolated hearts. Anesth Analg; 1992, 74:547-48.
10.Kobayashi Y, Tsuchida A, Kamada Y, Seki S, Ichimiya T, Namiki A:
Effects of speed of injection on anesthesia induction with propofol
and fentanyl. Masui; 1999, 48:847-57.
11.Rolly G, Versichelen L, Huyghe L, Mungroop H: Effects of speed
of injection on induction of anesthesia using propofol. Br J Anesth;
1985, 57:743-6.
12.Gillies GWA, Lees NW: The effects of speed of injection on
induction with propofol. A comparison with etomidate. Anesthesia;
1989, 44:386-8.
13.Malyshev VD, Zhdanov AM, Andriukhin IM, Omarov Kh T,
Kheĭmets GI, Sviridov SV, Vedenina IV, Orudzheva SA: The effects
of diprivan on the indices of central hemodynamics and the heart
conduction system. Anesteziol Reanimatol; 1993, 4:11-14.
14.Stokes DN, Robson N, Hutton P: Effects of diluting propofol on
the incidence of pain on injection and venous sequelae. Br J Anesth;
1989, 62:202-3.
15.Tham CS, Khoo ST: Modulating effects of lignocaine on propofol.
Anesth Intensive Care; 1995, 23:154-7.
16.McCulloch MJ, Lees NW: Assessment and modification of pain on
induction with propofol (Diprivan). Anesthesia; 1985, 40:1117-20.
17.Stark RD, Binks SM, Dutka VN, O'Connor KM, Arnstein MJ,
Glen JB: A review of the safety and tolerance of propofol. Postgrad
Med J; 1985, 61:152-6.
18.Fulton B, Sorkin EM: Propofol: An overview of its pharmacology
and a review of its clinical efficacy in intensive care sedation. Drugs;
1995, 50:636-57.
19.Ananthanarayan C: Dystonic reaction after anesthesia. Can J
Anaesth; 2001, 48:101-3.
CONTINUAL INFUSION OF INTRATHECAL BACLOFEN (ITB):
LONG TERM EFFECT ON SPASTICITY
Dhafir Al Khudhairi*, Abdulrahman Shug’a Aldin**,
Yousef Hamdan***, Abdullah Rababah****,
Mona Hafez Matthana*****, Jiri Pazdirek******
and J alal A bdulsalam *******
Abstract
Background: Spasticity is a disorder of muscular function causing muscular tightness or
spasm which occurs when there is damage to the central nervous system whether it is of spinal
cord or brain origin. This insult could be either pathological or traumatic.
Method: Thirty-three patients had intrathecal Baclofen pumps implanted for severe spasticity.
These patients either did not respond to or tolerate oral medications.
Results: All patients showed significant improvement in their spasms following the procedure.
Improvement was noted not only in spasticity, but also in pain, management of sleep disturbance,
activities of daily living, indoor and outdoor mobility and behavior.
Conclusion: The number of complications was acceptable, and generally were not lifethreatening. Infection was the significant complication in two patients and this led to explantation
of their pumps. Patient satisfaction was very high and was related to improvement in the quality of
life for the patients.
*
Fellow of the Faculty of Anaesthesia of the Royal College of Surgeons of Ireland, Director of Anaesthesia and Critical
Care, Prince Sultan Cardiac Centre Consultant Chronic Pain Management, Riyadh Military Hospital and Sultan Bin
Abdulaziz Humanitarian City.
**
MBBS, Doctor of Medicine.
***
Ba GP, Consultant Physiatrist.
**** MBBS, Consultant Physiatrist.
***** MBChB, Ms, PhD, Consultant Physiatrist.
****** MD, Board in Orthopedics, Board in Physical Medicine and Rehabilitation Consultant Physiatrist.
*******MD, Ms in Physical Medicine and Rehabilitation.
Corresponding Author: Dr. Dhafir Al Khudhairi, FFARSCI, Director of Anaesthesia Department, Prince Sultan Cardiac Centre,
Consultant Chronic Pain Management, Riyadh Armed Forces Hospital, Consultant Chronic Pain Management, Sultan Bin
Abdulaziz Humanitarian City. Tel: +9661-4791000, ext: 8554, Fax: +9661-4760543, P.O. Box: 7897, Riyadh 11159, Kingdom of
Saudi Arabia, E-mail: [email protected]
851
M.E.J. ANESTH 20 (6), 2010
852
D. Al Khudhairi et al
Introduction
depressant properties.
Spasticity is a disorder of muscle function
causing muscle tightness or spasm which occurs
when there is damage to the central nervous system.
Spasticity is a major disorder characterized by a
velocity-dependant increase in tonic stretch reflex
(muscle tone) with exaggerated tendon jerks resulting
from hyperexcitability of the stretch reflexes as one
component of the upper motor neurone syndrome1.
This damage may result from spinal cord injury,
traumatic brain injury, stroke, tumour, cerebral palsy
or multiple sclerosis2,3,4,5,6,7.
When spasticity cannot be managed efficiently,
some of the associated problems can be dealt with in a
number of ways, in addition severe, late and long term
spasticity could be managed with periodic injections of
Botulinum toxin or Phenol into the spastic muscle, or
implantation devices like intrathecal pumps. Surgery
is also indicated and performed in very severe and late
cases.
In a clinical setting severe spasticity not only
reduces rehabilitation goals but produces ailments
such as joint contractures leading to bad posture,
pressure sores, detrusor-sphinctre dyssynergia and
impaired motor function. Some workers have reported
25-35% rates of such seriously effected patients8.
Spasticity can be debilitating and causes suffering in
many ways such as muscle spasms, limited functional
movement, impaired functional capacity, scissoring
(involuntary crossing of legs), altered personal hygiene
and pain. The pain may be neuropathic, resulting from
deafferentation, central collateral sprouting or neural
disinhibition. The pain may also be nociceptive/
somatic directly due to muscle spasm.
Uncontrolled
spasticity
causes
multiple
problems, for example orthopaedic deformities, such
as hip dislocation, contractures or scoliosis. It impairs
personal hygiene and effects many other activities of
daily living. In addition to all of the above, spasm can
interfere with sleep and can result in depression.
Spasticity is usually managed by a combination
of oral medication with antispastic agents such as
Baclofen, Tizanidine or Diazepam and physiotherapy
and rehabilitation.
Most of the mild to moderate spasticity cases are
effectively managed with the conservative measures
and available oral therapy mentioned, but cases of
severe spasticity are less responsive.
Since unacceptable CNS effects often occur when
high doses of Baclofen are taken orally the therapeutic
effect usually cannot be improved by an increase in
dose. Sedation, somnolence, ataxia and respiratory
and cardiovascular depression are the drug’s CNS
The most effective treatment, with the least side
effects is intrathecal Baclofen (ITB) and this therapy
can be used if oral medications fail and this consists of
long term delivery of Baclofen to the intrathecal space.
It was first carried out by Penn and Kroin in 19842.
ITB therapy gained US FDA approval for managing
severe spasticity of spinal origin in 1992, and for
severe spasticity of cerebral origin in 1996. Since then,
several studies supporting this have been published by
various authors9,10.
The abundance of GABA-B receptors in the
superficial layers of spinal cord means that intrathecal
administration of Baclofen results in a greater than
four-fold increase in the cerebrospinal fluid level
with 1% of the oral dose3. This treatment can be
very effective. The benefits of ITB typically include
reduced tone, spasm and pain and also increased
mobility. The use of ITB therapy as a treatment for
spasticity requires a four phase approach: (1) patient
selection, (2) screening, (3) implantation, and (4) dose
adjustment and maintenance.
Materials and Methods
Between April 2004 until June 2009, 33 patients
with severe spasticity had intrathecal Baclofen pumps
implanted.
Thirty-three patients out of the 45 tested proved
positive to the intrathecal Baclofen drug test, 9 female
and 24 male, ages ranging from 12 to 57 years. There
were 18 spinal injury patients, 6 with demyelination
disease and 9 with brain insult.
The pumps implanted were all Medtronic and
we used 5 pumps of 20cc Synchromed II, 27 of 40cc
Synchromed II and one of 20cc Synchromed L.
When patients have persistent and uncontrollable
spasticity despite oral antispasmodic medications, they
CONTINUAL INFUSION OF INTRATHECAL BACLOFEN (ITB): LONG TERM EFFECT ON SPASTICITY
will be offered implantation of intrathecal Baclofen
pumps. As mentioned, selection of patients is the first
step to plan screening and see if intrathecal diagnostic
tests will be of benefit to the patient. If this is successful
then the next step is implantation and later on dose
adjustment.
In our institute we give a bolus dose of 50-100µg
of Baclofen injected intrathecally in the diagnostic
phase and spasticity is assessed over the next 10 hours,
although the significant effect of intrathecal Baclofen
would occur four hours after injection.
The spasticity is assessed according to the
Ashworth Score and when the Score improved
(reduced) by around two scales then the patient was
considered eligible for implantation.
There are two choices of pump size, 20ml and
40ml capacity, depending on the size of the patient
and also on the anticipated daily dose of intrathecal
Baclofen and the estimated refill intervals.
When the decision is made to implant the
Baclofen pump, the patient is usually put under general
anaesthesia and with the patient on his side, a catheter
is tunneled through a needle inserted through the L3-4
space, preferably in a paramedical approach and the
catheter is guided upwards to the higher thoracic
vertebrae and checked on fluoroscopy. The catheter
which will be connected to the pump is then tunneled
beneath the skin around the flank of the patient to the
subcostal area. The pump is then implanted just beneath
the skin in the subcutaneous fatty tissue which lies
above the abdominal muscles of the lower abdomen.
Usually the pump is prepared and filled with
Baclofen before implantation and the surgical incision
closed properly in layers and the patient given
prophylactic antibiotic cover for 48 hours.
Results
All 33 patients who passed screening, showed
significant improvement following pump implantation.
The mean preoperative Ashworth Scale was reduced
from 3.9 to 1.7. In addition to improvement of
spasticity, there was significant clear improvement in
patient behavior and activities of daily living. Also
bladder and bowel functions were improved. It was
noticed that after initiation of intraspinal treatment
853
most patients had an immediate reduction of muscle
tone to normal levels and spontaneous spasms were
eliminated. Many patients experienced less discomfort,
significant pain relief, and daily activities were more
easily accomplished.
In our group of patients the intrathecal daily
dose after adjustment was variable, between 50 and
850µg per day. We noticed small doses were needed
for patients with demyelination disease, whereas larger
doses were necessary to control spasticity in those with
brain insult. One patient had Morphine and Baclofen
mixed in the pump for both spasticity and pain.
The pumps in two patients were explanted due to
infection, one after three months and the other after four
years. One patient had a damaged (broken) intrathecal
catheter which was replaced. Other complications
were minor, headache, swelling and pain at the site of
the pump, but these were resolved within a few days.
We found a definite improvement after the use
of intrathecal Baclofen in patients with supraspinal
spasticity and this has been reported by others11,12,13.
Discussion
The site of action of Baclofen in the spinal cord
is not clear and Baclofen was first used in humans
in 197414. It is a gamma-amino butyric acid (like
GABA) analogue that binds to the GABA-B receptor
resulting in inhibition of calcium influx at pre-synaptic
terminals and thus suppressing release of excitary
neuro transmitters. These GABA receptor sites occur
widely throughout the central nervous system15,16,17.
As complications are related to operator
inexperience it is recommended that specific personnel
or a specific centre should perform this procedure,
where protocols can be standardised and long term
results properly evaluated. Therefore the programme
requires specific team designated leadership and
identified co-ordination to ensure smooth transition
between the different stages of therapy and effective
long term follow up. Rehabilitation therapists,
particularly Physical and Occupational Therapists are
essential team members who can help monitor patients’
response to treatment and changing functional status
over time. The team also involves a very experienced
surgeon who should be actively involved with the
M.E.J. ANESTH 20 (6), 2010
854
D. Al Khudhairi et al
team for system-related problems which could arise
at any time. ITB therapy could replace a number of
orthopaedic and neurosurgical interventions for those
cases suffering with irreversible, severe spasticity-with
or without contractures.
catheter breakage and the catheter was replaced after
three years of implantation. We had four patients
with headache and dizziness after the test dose and
implantation, but these side effects were temporary
and were resolved easily.
There are several risks involved with placement
of Baclofen pumps. A comprehensive study of ITB
complications in a survey of 40 centres with a total
of 1002 test doses and 936 pump placements was
published17. Common test dose complications were
nausea/vomiting (2.6%) and sedation (2.2%). Pump
complications included CFS collection (3.3%),
constipation (2.9%) and headache (2.4%). Common
long-term complications were catheter kink or
migration (4.5) and infection (1.2%).
Intrathecal Baclofen is approximately 100 times
more effective than oral alternatives and produces
fewer side effects than large oral doses which can lead
to drowsiness, sedation, ataxia, weakness and fatigue
due to Baclofen crossing the blood-brain barrier.
Other studies showed that complication rates
ranged from 20-50%18,19.
Even with safe surgical techniques, some common
complications of Baclofen pump implantation still
occur. Excessive swelling may be a sign of developing
seroma, sometimes requiring percutaneous drainage.
CSF leak may be detected by spongy swelling on the
incision site on the back.
Intrathecal use of Baclofen does not completely
eradicate the central risks. The most frequent drugrelated side effects of ITB include drowsiness,
dizziness, constipation and muscle hypertonia.
Baclofen withdrawal is a serious risk if there is
an abrupt decrease in drug infusion; causes include
catheter failure (eg-obstruction, fracture or dislodging
of the intrathecal catheter), pump malfunction or low
pump reserves. Symptoms include pruritis without a
rash, hyperthermia, hypertension, changes in mental
status and aggravation of spasticity, immediate and
active intensive treatment and care should be instituted
with doses of Benzodiazepines and try to recommence
intrathecal Baclofen infusion.
In our study there were 2 out of 33 pumps
explanted due to infection, and one patient needed
significantly increasing doses; this was diagnosed as
Although Intrathecal Baclofen is an alternative
method requiring considerable initial outlay for the
start up course, this can be reduced in the long term20.
Nursing care and mobilization after Baclofen pump
implantation become much easier with improvement
in activities and daily living2,21. It also resulted
in a decrease in the average length of subsequent
hospitalisations21.
As a whole, IBT can improve the quality of life in
carefully selected patients and can be cost effective22,23.
In our study we have demonstrated that ITB is an
effective technique for relieving spasticity in patients
who do not respond to conventional therapy.
Conclusion
Spasticity secondary to spinal cord injury and
other central nervous system damage is common
with clinical manifestations of hypertonicity, spastic
paralysis and hyper-reflexia. Multimodal treatment
should be aimed at preventing exacerbating factors,
daily physical therapy with stretching, medications,
contracture release and denervation of the motor
neuron endplate. The most effective oral therapy for
spasticity is Baclofen, Diazepam and Tizanidine,
though all have limitations. Denervation of the motor
neuron endplate with Phenol or Botulinum toxin can
be effective, but the most effective treatment, with the
least side effects, is intrathecal Baclofen, which should
be considered when conservative methods fail.
CONTINUAL INFUSION OF INTRATHECAL BACLOFEN (ITB): LONG TERM EFFECT ON SPASTICITY
855
References
1.Feldman RG, Young RR, Koella WP, Lace JW: Symposium
synopsis: spasticity-disordered motor control. Chicago: Year Book
Medical Publishers; 1980, p. 485.
2.Penn RD: Intrathecal baclofen for spasticity of spinal origin: 7 years
of experience. J Neurosurg; 1992, 77:236-40.
3.Coffey JR, Cahill D, Steers W, et al: Intrathecal baclofen
for intractable spasticity of spinal origin: results of a long term
multicenter study. J Neurosurg; 1993, 78:226-32.
4.Albright AL, Barry MJ, Painter MJ, et al: Infusion of intrathecal
baclofen for generalized dystonia in cerebral palsy. J Neurosurg;
1998, 88:73-6.
5.Albright AL, Kriel RL, Gilmartin RC, et al: Hip status in cerebral
palsy after one year of continuous intrathecal baclofen infusion.
Pediatr Neurol; 2004, Mar. 30(3):163-8.
6.Albright AL, Gilmartin R, Swift D, Krach LE, et al: Long term
intrathecal baclofen therapy for sever spasticity of cerebral origin. J
Neurosurg; 2003, Feb. 98(2):291-5.
7.Metz L: Multiple sclerosis: symptomatic therapies. Semin neurol;
1998, 18:389-95.
8.Corston RN, Johnson F, Goodwin-Austen RB: The assessment of
drug treatment of spastic gait. J Neurol Neurosurg Psychiatry; 1981,
44:1035-9.
9.Penn RD, Kroin JS: Intrathecal baclofen alleviates spinal cord
spasticity. Lancet; 1984, 1:1078.
10.Zierski J, Muller H, Dralle D, Wurdinger T: Implanted pump
system for treatment of spasticity. Acta Neurochir Supp;l 1998,
43:94-9.
11.Milan R, Dimitrijevic: Spasticity. Scientific basis of clinical
neurology. New York: Churchill Livingstone; 1985, pp. 108-15.
12.Saltuari K, Kronenberg M, Marosi MJ, Kofler M, Russegger
L, Rifici C, et al: Long-term intrathecal baclofen treatment in
supraspinal spasticity. Acta Neurol; 1992, 14:195-207.
13.Rifici C, Kofler M, Kronenberg M, Kofler A, Bramanti P,
Saltuari L: Intrathecal baclofen application in patients with
supraspinal spasticity secondary to severe traumatic brain injury.
Funct Neurol; 1994, Jan-Feb. (1):29-34.
14.Pederson S, Arlien-Soberg P, Mai J: The mode of action of the
FABA derivative baclofen in human spasticity. Acta Neurol Scand;
1994, 50:665-80.
15.Bowrey NG, Price GW, Hudson AL, Hill DR, Wilkin GP, Turnbull
MJ: GABA receptor multiplicity: visualisation of different receptor
types in the mammalian CNS. Neuropharmacology; 1984, 23:21931.
16.Davies J: Selective depression of synaptic excitation in cat spinal
neurons by baclofen: an iontophoretic study. Br J Pharmacol; 1981,
72:373-84
17.Stempen, et al. Am J Med Rehab; 2000.
18.Follet K. Neuromodulation; 2003, 6(1):32-41.
19.Teddy P, Jamous A, Gardner B, et al. Br J Neurosurg, 1992,
6(2):115-18.
20.Ordia JI, Fischer E, Adamski E, Spatz E: Chronic intrathecal
delivery of baclofen by programmable pump for the treatment of
severe spasticity. J Neuro Surg; 1996, vol. 85:452-7.
21.Azouri P, Mane M, Thiebaut NB, Denys P, Remy-Neris O, Bussel
B: Intrathecal baclofen administration for control of severe spinal
spasticity: functional improvement and long term follow-up. Arch
Phys Med Rehabil; 1996, 77:35-9.
22.Sampson FC, et al: Functional benefits and cost/benefit analysis
of continuous intrathecal baclofen infusion for the management of
severe spasticity. J Neurosurg; 2002, 96:1052-7.
23.Becker WJ, et al: Long-term intrathecal baclofen therapy in patients
with intractable spasticity. Can J Neurol Sci; 1995, 22:208-17.
M.E.J. ANESTH 20 (6), 2010
CASE REPORTS
THE VIDEO LARYNGOSCOPES BLIND SPOTS
AND POSSIBLE LINGUAL NERVE INJURY BY THE
GLIDERITE® RIGID STYLET
- Case Presentation and Review of literature -
Magboul MA Magboul* and Shaw Joel**
Summary
We report the first case of near serious lingual nerve injury in an 80-y-old female caused by
the Rigid GlideScope Stylet. This complication was discovered during oral surgery and may have
been missed if the site of surgery was not oral cavity.
Introduction
The GlideScope Video Laryngoscope is a relatively new intubating device designed to
provide better view of the glottis without alignment of the oral, pharyngeal and tracheal axes. The
aim of this case presentation is to increase awareness for possible serious complications that may
arise with increase popularity and usage of video laryngoscopes, and their Rigid Stylet.
Key words: Glide Rite, Glide Scope, Complications, Lingual nerve injury.
Case Presentation
A morbidly obese 80-y-old female (Wt.102.1 kg, Ht. 157.5 cm, BMI of 41) presented with
mouth pain and multiple carious teeth was scheduled for teeth extraction with an alveoplasty. Past
Medical history of CVA, TIA, CHF, hypertension, and MI. ECG showed first degree heart block,
prolonged QT with and anterolateral infarct. ECHO showed an ejection fraction of 45-50%, left
atrial enlargement, mild pulmonary hypertension, and trace mitral regurgitation.
Pre-operative airway assessment revealed a Mallampati score of IV, three finger breadth
mouth opening, slight limitation of neck movement, and loose carious teeth. With this assessment
the patient was predicted to be difficult to intubate. The anesthetic plan included management of
the predicted difficult intubation with the GlideScope.
Anesthesia was induced with fentanyl 150 micro grams, lidocaine 100 mg, propofol 150 mg
and succinylcholine 100 mg.
*
**
MD, FFARCSI, Chief of Anesthesia VA Medical Center, Iowa City. Clinical Assistant Professor of Anesthesia, University
of Iowa, College of Medicine, Iowa City, USA.
BSN, SRNA, Student RN Anesthetist, University of Iowa, College of Medicine, Iowa City, USA.
Correspondence: Magboul MA Magboul, MD, FFARCSI, Chief of anesthesia VA Medical Center Iowa City. Clinical
Assistant Professor Anesthesia, University of Iowa, college of Medicine, Department of Anesthesia-6JCP, 200 Hawkins
Drive, Iowa City, Iowa 52242-1009, USA. Tel: (319) 356 8497 (Office), Tel: (319) 356-2633 (Department), Tel: (319) 356
7471 (Sec. office), Fax: (319) 356 2940 (Department), E-mail: [email protected]
857
M.E.J. ANESTH 20 (6), 2010
858
The GlideScope blade tip was placed in the
vallecula and the vocal cords and epiglottis were seen.
A size 7 ETT was mounted in the GlideRite® Rigid
stylet (Figure 2a, b) and then passed into the oral
cavity for intubation. The ETT appeared to slide into
the oropharynx with relative ease and the endotracheal
tube was placed into the trachea. The stylet was
removed, positive ETCO2 and equal bilateral breath
sounds was confirmed. A successful GlideScope
intubation was assumed.
As the surgeon began the procedure he noticed
that the endotracheal tube had pierced and entered the
tissue of the Retromolar trigonum [the same space
which holds the lingual nerve], and then proceeded to
pass through the oropharyngeal space and re-enter the
vocal cords (Figure 1a, b).
Fig. 1a
ETT had pierced into Retromolar Trigonum tissues, and then
entered the vocal cords
M. MA Magboul & S. Joel
We decided to remove the endotracheal tube to
avoid trauma to Lingual nerve, and re-insert another
size 7 endotracheal tube with the aid of the GlideScope
camera. Positive ETCO2 and equal bilateral breath
sounds was confirmed. Surgery was completed
uneventfully; however, the surgeon stated multiple
times that the patient’s oral mucosa was very fragile
and easily torn. The patient was easily extubated and
transferred to PACU.
The PACU staff was instructed to look for signs
of lingual nerve injury (loss of tongue sensation,
difficulty breathing, slurred speech, or bleeding from
her oral cavity).
The PACU stay was uneventful, the patient
denied any of the above mentioned symptoms, and
was discharged.
Discussion
The GlideScope and other video laryngoscope
have improved tracheal intubation especially in
patients with difficult Airway1.
The GlideRite® Rigid stylet (Figure 2a, b)
was introduced to over come difficulties found with
intubation with GlideScope and other similar video
laryngoscope and help reduce patient trauma2,5.
Fig. 2a
The GlideRite® Rigid Stylet is specifically designed to work
with GlideScope® Video Laryngoscopes.
Fig. 1b
ETT had pierced into Retromolar Trigonum tissues, and then
entered the vocal cords
THE VIDEO LARYNGOSCOPES BLIND SPOTS, AND POSSIBLE LINGUAL NERVE INJURY BY THE GLIDERITE
RIGID STYLET
Figure 2b
The GlideRite® Rigid Stylet is specifically designed to work
with GlideScope® Video Laryngoscopes.
859
penetrating injury of the soft Palate during
GlideScope® intubation17 Malik, and Frogel reported.
The first Anterior tonsillar pillar perforation during
Glidescope® Video laryngoscopy18.
This is the first reported case of near serious
lingual nerve injury by The Rigid GlideScope Stylet.
Accidently discovered during oral surgery.
Decision to reintubate, rather than cutting the
oropharyngeal tissues to release the tube, has avoided
a serious injury to the lingual nerve. Injuries to lingual
nerve are now frequently reported with upper airway
intubation and instrumentation. Lingual nerve injury
was even reported with the use of LMA, Cuffed
oropharyngeal airway, oropharyngeal airway, Proseal
LMA, and conventional endotracheal intubation. Both
unilateral and bilateral injuries have been reported.
Potential predisposing factors included the use of
nitrous oxide6,7,8,9,10,14,16 using an LMA that was too
small6,9,11,12,13,16 and excessive pressure.
Study by Tukstra et al showed that the dedicated
GlideScope rigid stylet and the standard malleable ETT
stylet are equally effective in facilitating endotracheal
intubation4,5.The Flex-It® Stylet was no more effective
in facilitating endotracheal intubation than the standard
malleable endotracheal tube stylet3,5.
In our case the Rigid stylet converted the
endotracheal tube tip into a sharp knife like weapon
that cut through the patient oral tissues.
When Intubating with video laryngoscope the
operator usually concentrate on the perfect image of
the cords. The path of the tube from the mouth opening
to the vocal cords is a “blind spot” to the intubating
person.
Hsu, Huang, and Chen reported the first
We concluded that injuries from video
laryngoscopes intubation aids could be avoided by
careful attention to the following steps:
The ETT must be passed close to the scope and
away from the corners of the mouth. Close attention to
the path of the tube from mouth entering to vocal cord
intubation.
The tube course must be re-inspected by the
video scopes on the way out after intubation.
When using rigid stylet, ETT with softer tips
must be used. The parker ETT has a soft malleable tip
and maybe helpful in these situations. The tip of the
conventional ETT, if dipped into warm saline, will turn
softer and less traumatic.
We recommend the use of soft stylets and Soft
tipped ETT to prevent such traumatic injuries.
M.E.J. ANESTH 20 (6), 2010
860
M. MA Magboul & S. Joel
References
1. RM Cooper, JA Pacey, MJ Bishop and SA McCluskey: Early
clinical experience with a new videolaryngoscope (GlideScope) in
728 patients. Can J Anaesth; 2005, 52, pp. 191-198. Full Text via
Cross Ref View Record in Scopus Cited By in Scopus (108).
2.Timothy Turkstra MDa, Christopher Jones MDa: Comparison of
GlideScope-specific rigid stylet to standard malleable stylet. Journal
of Clinical Anesthesia, Volume 20, Issue 1, February 2008, Page 75.
3. JV Cuchillo and MA: Rodriguez, Considerations aimed at
facilitating the use of the new GlideScope videolaryngoscope
[Letter], Can J Anaesth; 52 (2005), p. 661. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (18).
4. PM Jones, TP Turkstra and KP: Armstrong, Effect of stylet
angulation and endotracheal tube camber, Can J Anaesth; 54 (2007),
pp. 21–27. Full Text via CrossRef | View Record in Scopus | Cited
By in Scopus (12).
5. Comparison of Flex-It Stylet to Malleable Stylet for GlideScope
Intubation: A Randomized Controlled Trial Timothy Turkstra MDa,
Christopher Jones MDa.
6. Ahmad NS, Yentis SM: Laryngeal mask airway and lingual nerve
injury. Anaesthesia; 1996, 51:707.
7. Laxton CH, Kipling R: Lingual nerve paralysis following the use of
the laryngeal mask airway. Anaesthesia; 1996, 51:869-70.
8. Majumder S, Hopkins PM: Bilateral lingual nerve injure following
the use of the laryngeal mask airway. Anaesthesia; 1998, 53:184-6.
9. Gaylard D: Lingual nerve injury following the use of the laryngeal
mask airway. Anaesth Intens Care; 1999, 27:668.
10.King C, Street MK: Twelfth cranial nerve paralysis following use
of a laryngeal mask airway. Anaesthesia; 1994, 49:786-7.
11.Stewart A, Lindsay WA: Bilateral hypoglossal nerve injury
following the use of the laryngeal mask airway. Anaesthesia; 2002,
57:264-5.
12.Sommer M, Schuldt M, Runge U, Gielen W, Marcus MA: Bilateral
hypoglossal nerve injury following the use of the laryngeal mask
without the use of nitrous oxide. Acta Anaesthesiol Scand; 2004,
48:377-8.
13.Morikawa M: [Vocal cord paralysis after use of the LM]. J Clin
Anesth (Rinsho-Masui); 1992, 16:1194.
14.Inomata S, Nishikawa T, Suga A, Yamashita S: Transient bilateral
vocal cord paralysis after insertion of a laryngeal mask airway.
Anesthesiology; 1995; 82:787-8.
15.Daya H, Fawcett W, Weir N: Vocal cord palsy after use of the
laryngeal mask airway. J Laryngol Otol; 1996, 110:383-4.
16.Laffon M, Ferrandiere M, Mercier C, Fusciardi J: Transient
lingual and glossopharyngeal nerve injury: a complication of cuffed
oropharyngeal airway. Anesthesiology; 2001, 94:719-20.
17. Hsu W-T, Hsu S-C, Lee Y-L, Huang J-S, Chen C-L: Penetrating
injury of the soft palate during GlideScope® intubation. Anesth
Analg; 2007, 104:1609-10.
18.Malik AM, Frogel JK: Anterior tonsillar pillar perforation during
Glidescope® Video laryngoscopy. Anesth Analg; 2007, 104:1610-1.
SUBCLAVIAN VEIN INJURY AND MASSIVE
HEMOTHORAX REQUIRING THORACOTOMY
FOLLOWING INSERTION OF TUNNELED
DIALYSIS CATHETER
- A Case Report and Review of Literature -
Ahmed
Qutaiba A. Tawfic*, Pradipta Bhakta**,
Khamis Mohammed*** and Jasvinder Sharma****
Abstract
Tunneled dialysis catheters are widely used for hemodialysis. Large caliber dilator is used for
insertion of such catheter which can result in serious vascular injury leading to haemothorax. Here
we report such an inadvertent central venous injury requiring thoracotomy following blind dilator
advancement along with review of literature and recommendation to prevent such complication.
Key words: Subclavian vein injury; Haemothorax; Tunneled dialysis catheter.
Background
Tunneled dialysis catheters (TDC) are widely used for hemodialysis1,2. Insertion of such
catheters requires large caliber dilator which can cause devastating vascular injury leading to
cardiac arrest or even death particularly if there are anatomical abnormalities, stenosis, history of
previous multiple insertion attempts.1,3-5 Here we report such a case of vascular injury leading to
hemo-pneumothorax requiring thoracotomy following TDC insertion.
Case Report
A 54 year old female patient with end-stage renal disease (ESRD), hypertension, diabetes
mellitus, cardiomyopathy, and left ventricular failure was admitted to our hospital. Patient was on
irregular hemodialysis. This time she was admitted with respiratory distress and features of fluid
overload. Consultant nephrologist decided to resume hemodialysis using TDC (Quinton Permcath,
Kendall, Tyco Healthcare, USA). Informed consent was taken after explaining the procedure.
Pulse oximetry, electrocardiogram and blood pressure (BP) monitoring were started. Right internal
jugular vein (RIJV) was punctured after lignocaine infiltration under aseptic precaution using
From Sultan Qaboos University Hospital, Muscat, Oman.
*
FICMS, MBChB, Registrar.
** MD, DNB, MNAMS, FCARCSI-I, Senior Registrar.
*** FICMS, MBChB, Registrar.
****MD, Senior Registrar.
Correspondong author: Dr. Pradipta Bhakta (MD, DNB, MNAMS, FCARCSI-I), Senior Registrar, Department of Anaesthesia,
Sultan Qaboos University Hospital, Al-Khoud, P.O. Box No: 38, Muscat, Oman. Zip Code: 123. Phone: (H) 00968-24414622,
(M) 00968-95036291, (Fax) 00968-24144710, E-mail: [email protected]
861
M.E.J. ANESTH 20 (6), 2010
862
ultrasound (Site Rite 5, BARD, USA). After obtaining
free flowing dark coloured blood, a guidewire was
inserted under ultrasound guidance till arrhythmia
was noted. Guidewire was then withdrawn a little bit.
Skin was infiltrated once again with lignocaine for
subcutaneous tunneling of TDC. Then a 12 French
dilator with the sheath was introduced over the
guidewire. While doing so guidewire came out a bit,
but it was still inside the vein. The dilator was then
pushed blindly to its full length. After that the dilator
was pulled out and TDC was introduced through the
sheath. At this time patient complained of shearing
pain and shortness of breath. Further advancement
of catheter was stopped. On aspiration back flow of
blood was obtained only from the proximal lumen.
Immediately intravenous portion of TDC along with
sheath was removed and pressure was applied. At this
time fluoroscopy was used which showed right sided
pneumothorax. Patient became more tachypneic and
hypoxic, so a chest tube was inserted. This resulted
in some clinical improvement. Femoral catheter (FC)
insertion was planned as she needed urgent dialysis.
During FC insertion she became more dyspneic, irritable
and hypotensive. Vascular injury was suspected and
the radiologist performed an angiogram through FC
which showed minor spillage of dye into pleural cavity
indicating pleural tear (Fig. 1). She was shifted to ICU
for further observation. She became more unstable
with increasing breathlessness, desaturation, and
hypotension. She was resuscitated with fluids and put
on oxygen by mask. Routine blood investigations were
sent and cardiothoracic opinion was sought. Repeat
chest X-ray revealed complete whitening of the right
hemi-thorax (Fig. 2). A new chest tube was inserted as
previous one was not working well. Immediately about
400ml of blood came out. Her hemoglobin dropped
from 11.4 to 5.2gm/dL. Dopamine (10µg/kg/min) was
started for maintenance of BP. Cardiothoracic surgeon
decided to do urgent thoracotomy because of suspicion
of continued vascular leak. A large clot amounting to
1.5 liter of blood along with tear in right subclavian vein
was found during thoracotomy. After surgery she was
shifted back to ICU for observation and mechanical
ventilation. She received seven packed red blood
cells perioperatively and her hemoglobin improved to
10.7gm/dL. Her BP improved and she could be weaned
off from inotrope and ventilator. Hemodyalysis was
Q. A. Tawfic et al
started through FC. Later she developed thrombosis
of right femoral vein due to longer stay of FC. So the
FC was removed and she was put on enoxaparin and
warfarin. Afterwards arterio-venous fistula (AVF) was
created for regular dialysis and she is doing fine with
that.
Fig. 1
An angiogram done via femoral catheter (which is clearely
visible coming up from inferior vena cava) revealing leak of
dye in pleural cavity.
1. Right tunneled catheter in situ (which was not fully removed
from subcutaneous tunnel, but was removed from the vein).
2. Angiography catheter passed through femoral vein for doing
venography.
3. Spillage of dye into pleural cavity.
4. Receeding of lung mergin due to pneumothorax.
5. Intial pigtail catheter inserted to drain pneumothorax.
Fig. 2
Right sided haemothorax with whitening of right chest cavity
(Chest drain tube in situ)
1. Spillage of dye into pleural cavity.
2. Whitening of right hemi thorax due to haemo-pneumothorax.
3. Standard chest drain tube in situ.
SUBCLAVIAN VEIN INJURY AND MASSIVE HEMOTHORAX REQUIRING THORACOTOMY FOLLOWING INSERTION
OF TUNNELED DIALYSIS CATHETER
Discussion
RIJV is often selected as ideal vein for hemodialysis
access because of its straight course, reduced risk
of malposition and thrombosis2,3,6. Central venous
catheter (CVC) insertion and dilator manipulation
can lead to complications like pneumothorax,
subcutaneous emphysema, thoracic duct injury,
arterial puncture, hemothorax, pericardial tamponade,
and mediastinal hematoma2-5,7-10. In majority of reports
hemothorax resulted from arterial injury, and rarely
from venous injury due to faulty insertion of needle
or catheter2-5,8,10. Venous injury is most commonly
reported to occur during left sided CVC insertion and
arterial injury during right sided CVC insertion2-5. Very
rarely it has been reported to occur from dilator5. Too
deep insertion of dilator can result in injury of vessel
or heart5. Because of its stiff texture it can cause more
serious vascular injury than needle or catheter5. Safer
dilator design and insertion technique have also been
recommended to prevent such complication5. In our
case the dilator was blindly and mistakenly inserted
to full length, even though the guidewire came out
partially, which probably had resulted in venous injury.
This is very dangerous maneuver and should never be
attempted. Also undue force should never be applied
while advancing the dilator. Direction of dilator
advancement is also important as RIJV maintains a
medial course while draining to superior vena cava. So
the dilator should always be advanced along the course
of the vein. Use of real-time sonography or fluoroscopy
is recommended especially in difficult cases during
insertion of the needle and dilator for prevention
863
of such complication1-4,6,7. Venography before or
after CVC insertion may help to detect unexpected
central venous anomalies, minimize the risk of
complications and extravasal placement (as in our
case)1,2,4,7. Postprocedure X-ray, CT Scan, ultrasound
or echocardiography are recommended to detect such
complication2-4,9,10. This is specifically indicated if
patient complains of retrosternal pain and respiratory
distress during insertion or aspiration of blood2,5.
Management of vascular injury includes endovascular
repair, stent placement, embolization and or balloon
tamponade3,7,10. Even emergency thoracotomy like in
our case may be needed to evacuate the hematoma and
repair the vascular tear9,10. Rare occurrence of dilator
induced venous injury leading to hemo-pneumothorax
requiring emergency thoracotomy prompted us to
report this case. Our purpose to report this case was
to notify that this type of misadventure can lead to
serious consequences.
Inadvertent and blind insertion of large caliber
dilator can result in serious vascular injury. Such
dilator should never be inserted for a length more than
necessary. We propose that graduated dilator with
markings indicating the safe and dangerous lengths
and should be used under real-time fluoroscopic and/
or ultrasound guidance.
Acknowledgement
We are thankful to Dr. Arvind Narayanan (MD),
Mrs. Paromita Bose (MA, M. Phil) for editing our
paper and to Dr. Amisha Bhakta (MSc, PhD) for
editing the figures.
M.E.J. ANESTH 20 (6), 2010
864
Q. A. Tawfic et al
References
1. Taal MW, Chesterton LJ, McIntyre CW: Venography at insertion
of tunnelled internal jugular vein dialysis catheters reveals significant
occult stenosis. Nephrol Dial Transplant; 2004, 19:1542-5.
2. Tong MK, Siu YP, Ng YY, Kwan TH, Au TC: Misplacement of a right
internal jugular vein haemodialysis catheter into the mediastinum.
Hong Kong Med J; 2004, 10:135-8.
3. Kusminsky RE: Complication of central venous catheterization. J
Am Coll Surg; 2007, 204:681-96.
4. Schummer W, Schummer C, Fritz H. [Perforation of the superior
vena cava due to unrecognized stenosis. Case report of a lethal
complication of central venous catheterization]. Anaesthesist; 2001,
50:772-7.
5. Oropello JM, Leibowitz AB, Manasia A, Del Guidice R, Benjamin
E. Dilator-associated complications of central vein catheter insertion:
possible mechanisms of injury and suggestions for prevention. J
Cardiothorac Vasc Anesth; 1996, 10:634-7.
6. Schillinger F, Schillinger D, Montagnac R, Milcent T:
Post catheterization vein stenosis in haemodialysis: comparative
angiographic study of 50 subclavian and 50 internal jugular accesses.
Nephrol Dial Transplant; 1991, 6:722-4.
7. Sandhu NS: Transpectoral ultrasound-guided catheterization of the
axillary vein: an alternative to standard catheterization of the subclavian
vein. Anesth Analg; 2004, 99:183-7.
8. Hama Y, Kaji T, Fujii M, Kosuda S: Internal mammary artery injury
following subclavian catheterization. Emerg Radiol; 2005, 11:170-2.
9. Fangio P, Mourgeon E, Romelaer A, Goarin JP, Coriat P, Rouby
JJ: Aortic injury and cardiac tamponade as a complication of subclavian
venous catheterization. Anesthesiology; 2002, 96:1520-2.
10.Guilbert MC, Elkouri S, Bracco D, Corriveau MM, Beaudoin
N, Dubois MJ, et al: Arterial trauma during central venous catheter
insertion: case series, review and proposed algorithm. J Vasc Surg;
2008, 48:918-25.
CESAREAN SECTION UNDER SPINAL ANESTHESIA
IN A PATIENT WITH ANKYLOSING SPONDYLITIS
- A Case Report -
G. Ulufer Sivrikaya*, Ayse Hanci**, Hale Dobrucali*
and Aylin Yalcinkaya *
Abstract
Introduction: It is generally accepted that neuraxial anesthesia is difficult to establish in
patients with ankylosing spondylitis. General anesthesia also has some disadvantages, especially
with respect to airway control in patients with ankylosing spondylitis. We present herein a gravida
with ankylosing spondylitis who had a cesarean delivery performed under spinal anesthesia.
Case: A 30-yr-old gravida at 38 weeks gestation with a 9 yr history of ankylosing spondylitis
was admitted to our hospital in labor. She was scheduled for an elective repeat cesarean delivery.
Spinal anesthesia was induced using a 22-gauge Quincke spinal needle with 1.8 mL of 0.5% heavy
bupivacaine + 0.2 mL (10µg) of fentanyl at the L3-4 interspace in the left lateral position by the
median approach. Adequate sensory and motor blockade were achieved. The postoperative period
was uneventful and she was discharged home on postoperative day 3.
Conclusion: We suggest that spinal anesthesia can be safely and effectively used as an
alternative to general anesthesia in patients with ankylosing spondylitis. Neuraxial techniques
should not be regarded as unachievable in such patients; however, all necessary precautions should
be taken to avoid complications of spinal anesthesia, and facilities to secure the airway should be
available.
Introduction
Ankylosing spondylitis (AS) is a seronegative spondyloarthropathy; it is a chronic and usually
progressive inflammatory disease. The primary sites of involvement are the sacroiliac joints and
the spine1,2. The disease prevalence varies ranging between 0.1 and 1.1% in different populations3,4.
Patients with AS may require surgery of any type and these patients present specific challenges
to the anesthesiologist. Both airway management and neuraxial access may prove to be difficult1,5.
Pregnancy may also occur in patients with AS. Although most pregnant patients with AS have a
normal spontaneous vaginal delivery, the manifestations of the disease may interfere with labor
and delivery as well as the administration of general and regional anesthesia6. There are but a few
reports on the use of anesthesia in gravidas with AS6-9.
*
**
MD, Staff Anesthesiologist.
MD, Chief of the Anesthesiology and Reanimation Department.
GUS, AH, HD: Sisli Etfal Training and Research Hospital, Department of 2nd Anesthesiology and Reanimation, Istanbul,
TURKEY; AY: Dr. Munif Islamoğlu State Hospital, Department of Anesthesiology, Kastamonu, TURKEY.
Corresponding author: G. Ulufer SIVRIKAYA, Kucukbahce Sk. No:28/34 Sisli. Istanbul-TURKEY. Telephone number:
+90.532.2924173, Fax number: +90.212.2472576, E-mail: [email protected]
865
M.E.J. ANESTH 20 (6), 2010
866
Herein, we present a case of a gravida with AS
who had a cesarean section under spinal anesthesia.
Case Report
A 30-yr-old gravida 3 para 2, at 38 weeks
gestation with a weight of 66 kg and a height of 164
cm, was admitted to our hospital in labor. She had a 9
yr history of AS. The history and physical examination
were consistent with moderate cervical AS involving
the thoraco-lumbar vertebral column with kyphosis,
but without lower limb neurologic involvement. She
required two pillows to support her head and four
pillows to support her back due to the disease process
and curvature of the cervical and thoraco lumbar
spines. An elective repeat cesarean section had been
planned. She had undergone two cesarean deliveries
12 and 11 years previously under general anesthesia.
Since AS had not been diagnosed at the time of her
prior cesarean deliveries, the two general anesthesia
experiences were uneventful.
Her medical history was benign other than
the AS. Her current medications were infliximab,
indomethacin, and salicylazosulfapyridine. She could
open her mouth 5 cm; physical examination revealed a
Grade III Mallampati score. The problems of general
anesthesia, with particular reference to difficult
intubation, were explained to the patient and she opted
for a regional anesthesia technique.
Preoperative laboratory data were within normal
limits. The patient was premedicated with ranitidine
HCl (50 mg iv) and metoclopramide HCl (10 mg iv)
30 minutes before the planned surgery. In the operating
room, an ECG, non-invasive blood pressure, and
peripheral oxygen saturation were monitored and an
intravenous infusion of Lactated Ringer’s solution
was started. Spinal anesthesia was planned, but since
the patient was a candidate for difficult endotracheal
intubation, airway management devices for emergent
use, including a percutaneous tracheostomy set, were
kept ready.
With the patient in the sitting position, two
unsuccessful attempts were made to insert a 22-gauge
Quincke spinal needle between the L3-4 intervertebral
space using a median technique. The patient was
then turned to the left lateral position. Free flow of
G. U. SIVRIKAYA et. al
cerebrospinal fluid was obtained using the midline
technique at the same level on the first attempt in
this position and 1.8 mL of 0.5% heavy bupivacaine
and 0.2 mL (10 µg) of fentanyl were injected into
this space. The patient was then returned to the
supine position with pillow support and the operating
table rotated toward the left in order to avoid supine
hypotensive syndrome. Spinal anesthesia resulted in a
complete sensory and motor block from T6 caudally.
The APGAR scores were 9 and 10 for the 1. and 5.
min respectively. Surgery was performed successfully
within 45 minutes. The patient recovered without any
complications and was discharged home following a
good recovery on the 3rd postoperative day.
Discussion
AS is often a self-limiting disease with unknown
etiology. It is a chronic and usually progressive
inflammatory disease involving the articulations of
the spine and adjacent soft tissues. It begins in the
sacroiliac joints and moves cranially. The degree of the
disease ranges from involvement of the sacroiliac joint
alone to complete ankylosis of the spine1,2,10.
The traditional anesthetic approach to patients
with AS is to secure the airway using awake intubation
because fusion of the vertebral column renders
neuraxial anesthesia difficult or impossible2. In patients
with a fixed cervical spine, it has been reported that it
is usually not possible to see any part of the laryngeal
inlet, emphasizing the difficulty with intubation3.
Since the number of patients with AS are not
adequate to perform a controlled study regarding the
best method of anesthesia, case reports concerning the
care of these patients have provided diverse anecdotal
experiences.
The largest series of patients with AS who
underwent anesthetic procedures was reported by
Schelew and Vaghadia2 as a retrospective analysis of
82 patients over 10 years. They reviewed the approach
to patients with AS having surgical procedures at one
institution to investigate the utilization of neuraxial
anesthesia and to determine whether the success rate
was acceptable, in an effort to make this a viable
alternative to general anesthesia. Neuraxial anesthesia
was planned in 19.5% (n=16) of the patients and
CESAREAN SECTION UNDER SPINAL ANESTHESIA IN A PATIENT WITH ANKYLOSING SPONDYLITIS
successful spinal anesthesia was achieved in 76.2%
(n=10) of those in whom it was planned. Their results
indicate that spinal anesthesia may be relatively
underutilized in patients with AS presenting for surgery.
In our review of the current literature, we found a
few reports on epidural or combined spinal-epidural
anesthesia11-13. In our patient, we preferred spinal
anesthesia after consideration of the consequences and
our anecdotal experience favored spinal anesthesia in
patients with AS undergoing cesarean section.
The presence of ossification in the interspinous
ligament would suggest better success with a
paramedian approach1. Kumar and Mehta14 reported
three cases in which patients with AS were successfully
administered spinal anesthesia using a paramedian
approach after failed attempts with a median approach.
Nevertheless, Schelew et al2. suggest that both
midline and paramedian methods may be attempted
with success. In our patient, spinal anesthesia was
successfully administered by the median approach in
the lateral position on the first attempt, but preceded
by two failed attempts by the median approach in the
sitting position.
From the anesthetic point of view, preoperative
assessment, including indirect laryngoscopy and
preparation to overcome anticipated problems, should
enable those patients with AS to be managed safely.
But, as in the two cases described in detail by Wittmann
et al3, the greatest danger occurs when patients present
for surgery which is unrelated to their condition and
867
difficulties are not anticipated. On the other hand, even
in the cases in which regional anesthesia is planned,
emergent securing of the airway can be required, such
as reported by Batra et al15. In the literature, total
spinal anesthesia was achieved following an epidural
test dose in a patient with AS undergoing total hip
replacement and after an unsuccessful attempt to
intubate the trachea with direct laryngoscopy, positive
pressure ventilation was restored by placing a size 4
laryngeal mask airway. Intubation could hardly be
achieved using a McCoy’s laryngoscope and a bougie
in the patient. These are the important reasons for
having intubating equipment ready for immediate use
in patients with AS3. Therefore full consideration of
airway control was included in our plan for anesthesia
in this patient.
In conclusion, patient anesthetic preference,
potential airway maintanence problems, and specific
requirements of the surgical intervention should all
be considered for the anesthetic approach in patients
with AS. If a central neuraxial blockade is chosen as
the anesthetic technique, the likelihood of successful
spinal anesthesia seems higher than other neuraxial
interventions. Airway intervention and equipment and
aids to secure the airway must be available.
Acknowledgements
Informed consent and approval were taken from
the patient for this case report.
M.E.J. ANESTH 20 (6), 2010
868
G. U. SIVRIKAYA et. al
References
1. McCARREN JP: Respiratory diseases. In: Benumof JL, ed.
Anesthesia & Uncommon Diseases, 4th edn. Philadelphia,
Pennsylvania: W.B.Saunders Company, 1998, 51-69.
2.Schelew BL, Vaghadia H: Ankylosing spondylitis and neuroaxial
anaesthesia-a 10 year review. Can J Anaesth; 1996, 43: 65-8.
3. Wittmann FW, Ring PA: Anaesthesia for hip replacement in
ankylosing spondylitis. J R Soc Med; 1986, 79:457-9.
4. Braun J, Bollow M, Remlinger G, Eggens U, Rudwaleid M,
Distler A, Sieper J: Prevalence of spondyloarthropathies in HLA
B27-positive and –negative blood donors. Arthritis Rheum; 1998,
41: 58-67.
5. Ahmad N, Channa AB, Mansoor A, Hussain A: Management of
difficult intubation in a patient with ankylosing spondylitis-a case
report. Middle East J Anaesthesiol; 2005, 18:379-84.
6. Bourlier RA, Bırnbach DJ: Anesthetic management of the
parturient with ankylosing spondylitis. Int J Obstet Anesth; 1995, 4:
244-7.
7. Mehrotra S, Gupta KL: Cesarean section in a patient with advanced
ankylosing spondylitis. Int J Gynaecol Obstet; 2005, 89:272-3.
8. Hiruta A, Fukuda H, Hiruta M, Hirabayashi Y, Kasuda H, Seo N:
Anesthetic management of caesarean section in a parturient with
ankylosing spondylitis complicated with severe cervical myelitis.
Masui; 2002, 51:759-61.
9. Broomhead CJ, Davies W, Higgins D: Awake oral fibreoptic
intubation for caesarean section. Int J Obstet Anesth; 1995, 4:172-4.
10.Sharrock NE, Savarese JJ: Anesthesia for Orthopedic Surgery. In:
Miller RD, ed. Anesthesia, 5th edn. USA: Churchill Livingstone
Inc., 2000, 2118-39.
11.Deboard JW, Ghia JN, Guilford WB: Caudal anesthesia in a patient
with ankylosing spondylitis for hip surgery. Anesthesiology; 1981,
54:164-6.
12.Hyderally HA: Epidural hematoma unrelated to combined spinalepidural anesthesia in a patient with ankylosing spondylitis receiving
aspirin after total hip replacement. Anesth Analg; 2005, 100:882-3.
13.Wulf H: Epidural anaesthesia and spinal haematoma. Can J
Anaesth; 1996, 43:1260-71.
14.Kumar CM, Mehta M: Ankylosing spondylitis: lateral approach
to spinal anaesthesia for lower limb surgery. Can J Anaesth; 1995,
42:73-6.
15.Batra YK, Sharma A, Rajeev S: Total spinal anaesthesia following
epidural test dose in an ankylosing spondylitic patient with
anticipated difficult airway undergoing total hip replacement. Eur J
Anaesthesiol; 2006, 23:897-8.
LEVOSIMENDAN AS A RESCUE ADJUNCT IN
AMLODIPINE INTOXICATION
– A Case Report –
M Gökhan Teker*, Haluk Özdemir*, Leyla Saidoglu*
Kerem Erkalp*and Gökçen Başaranoğlu
Introduction
Calcium channel blockers (CCB) are the cardiovascular medicines most commonly associated
with overdose death1. Amlodipine, a dihydropyridine CCB, can cause shock at overdose levels. The
hemodynamic shock is likely caused by calcium channel blockade in myocardial smooth muscle
and beta cells. This blockade leads to peripheral vasodilatation, hyperglycemia, hypoinsulinemia,
metabolic acidosis and shock2. Here we describe the use of levosimendan, a calcium sensitizing
agent, to treat a 16-year old woman who ingested 500 mg of amlodipine and failed to respond
to conventional therapies including calcium salts, inotrope infusions and hyperinsulinemiaeuglycemia therapy.
Case Report
A 16-year old woman with no past medical history or psychiatric disorders was admitted
to the intensive care unit of Private Hospital (Istanbul, Turkey) approximately 15 hours after
attempting suicide by ingesting 50 tablets of amlodipine 10 mg (500 mg total). She was a student
living with her family and denied tobacco and alcohol use. She had no known allergies and took
no regular medications.
She received gastric lavage and activated charcoal in the emergency department four hours
after ingestion. She was admitted to the intensive care unit with a blood pressure of 75/34 mm Hg
and a pulse of 125 bpm. She received intravenous crystalloid, intravenous dopamine 10 µg·kg1·min-1, and intravenous insulin 0.5 U·kg-1·h-1. Chest x-ray revealed pulmonary infiltration
suggestive of pulmonary edema. During her seven-hour intensive care unit stay, she had received
2700 mL of crystalloids, but her urine output was only 50 mL. Her blood glucose was normal at
each hourly check. For financial and logistics reasons, she was then transferred to the anesthesia
intensive care unit of our hospital.
Upon transfer, the patient was awake and conversant, with a Glascow Coma Scale (GCS)
score of 15. Her blood pressure was 87/36 mm Hg, heart rate was 112 bpm, temperature was 36.0ºC,
and oxygen saturation was 99% on oxygen 4 L/min by face mask. Her pupils were equal, round and
reactive to light. Her neurological, cardiovascular and gastrointestinal systems were unremarkable.
Laboratory tests disclosed the following values: sodium, 137 mmol/L (normal range 136-142);
*
MD, Department of Anesthesiology, Vakif Gureba Hospital, Istanbul, Turkey.
Corresponding Author: Kerem Erkalp, MD, Şenlikköy Mah. Ekşinar Cad. İncir Sok. Sarı Konaklar Sitesi, No:3, B-Blok,
Daire:6, Florya, Bakırköy, Istanbul, Turkey. Tel: 090 212 5346900, Fax: 090 212 6217580, E-mail: [email protected]
869
M.E.J. ANESTH 20 (6), 2010
870
potassium, 4.71 mmol/L (3.5-5.0); total calcium, 2.43
mmol/L (2.05-2.55) [9.7 mg/dL (8.2-10.2)]; ALT,
41 UL (10-14); AST, 40 (20-48). Her renal function
values and other liver function values were normal. An
electrocardiogram showed sinus tachycardia. Arterial
blood gas analyses showed a mild metabolic alkalosis.
Plasma amlodipine level was not measured.
Hyperinsulinemia-euglycemia (HIE) therapy
was provided with increasing rates of dopamine 10
µg·kg-1·min-1 and norepinephrine 0.2 µg·kg-1·min-1
delivery. Calcium chloride 10 g in serum saline over
3 hours was also given with the HIE therapy. On day
three, the patient developed shortness of breath and
subsequent respiratory arrest. Endotracheal intubation
and mechanical ventilation were performed. A repeat
chest x-ray showed uniform, diffuse pulmonary
infiltrates with a normal-appearing heart. Continious
ventilatory support and diuretic therapy for one day
were successful in resolving the pulmonary infiltrates,
metabolic alkalosis and fever.
On the same day, the patient developed a
leucocytosis of 28 cells/mL. Tracheal aspirates were
pink and foamy, suggesting pulmonary edema. An
echocardiogram revealed normal left ventricular
function, minimal aortic insufficiency, and mild
mitral insufficiency, making a cardiogenic cause for
pulmonary edema unlikely. The ejection fraction was
50% and cardiac enzymes were within normal ranges.
A subclavian catheter was inserted on the same day
and her central venous pressure (CVP) was 21 mm
Hg. Because the patient did not respond to initial
treatment, she underwent plasma exchange to clear the
amlodipine from her circulation. Dopamine 20 µg·kg1·min-1 and norepinephrine 15 µg·kg-1·min-1 were
administered for hemodynamic support.
On day four, she received levosimendan 12
µg·kg-1·min-1 for 10 min as a loading dose, then
levosimendan 0.1 µg·kg-1·min-1 for 12 hours, then
levosimendan 0.2 µg·kg-1·min-1 for 12 hours. The
patient responded to levosimendan therapy (blood
pressure and heart rate returned to normal levels)
and inotropes were decreased. On day five, inotropes
were stopped, and the patient was succesfully weaned
from the ventilator on day six. She was transferred
to the Internal Medicine ward after psychiatric
consultation.
M G. Teker et al
Discussion
In treating this patient, we searched the published
literature and found that HIE therapy is the generally
recommended treatment for CCB toxicity in the
critical care setting6-12. Supportive care including the
use of phosphodiesterase inhibitors, adrenergic agents,
cardiac pacing, balloon pump or extracorporeal bypass
is indicated if antidotal thearpy is ineffective17-19.
Because our patient did not respond to HIE therapy
and supportive treatment, we searched for alternative
treatement strategies.
A study by Buckley et al.20 discussed the use
of calcium to overcome amlodipine’s competitive
blockade of calcium channels in the cardiac conducting
system. The degree of hypercalcemia required to
overcome blockade depends on the degree of CCB
intoxication and the body’s response20. Buckley et al.20
recommend administering one gram of calcium salts
every two to three minutes until the cardiac block is
reversed on electrocardiogram. In their experience,
patients who were refractory to calcium therapy were
refractory to other treatments as well20,21.
Our patient received 14 g of calcium chloride,
with a resultant serum calcium level of 15 mg/dL (3.75
mmol/L). However, we found no obvious response to
this calcium therapy. Because CCBs are highly proteinbound, extensively distributed in tissues, and rapidly
metabolized by the liver to inactive metabolites22,
hemofiltration and dialysis are ineffective in the
management of overdose. One case report by
Ezidiegwu at al.23 described successful treatment of
amlodipine overdose with plasma exchange after nonresponsiveness to conventional therapy. However,
plasma exchange had no effect in our patient.
After four days of treatment, our patient remained
in shock with no evidence of improvement. We decided
to use levosimendan, a calcium-sensitizing agent
indicated for use in patients with acutely decompensated
heart failure26. Levosimendan sensitizes contractile
proteins to calcium by interacting with troponin in
cardiac muscle, which prolongs troponin’s effect on
contractile proteins26. Levosimendan also vasodilates
via ATP-dependent potassium channels27. We used the
intravenous levosimendan loading dose and infusion
rates that are approved for the short-term treatment
of acute severe decompensated heart failure26,28, and
LEVOSIMENDAN AS A RESCUE ADJUNCT IN AMLODIPINE INTOXICATION
observed blood pressure effects soon after initiating
treatment.
Conclusion
To the best of our knowledge, this is the first
report of using levosimendan to treat amlodipine
intoxication. In our opinion, levosimendan can be used
as a rescue adjunct in paitents with CCB overdoses
871
who fail to respond to conventional therapies such
as calcium salts, inotropes, and hyperinsulinemiaeuglycemia therapy. Given the long half-life of CCB
agents, levosimendan may be a useful alternative to
invasive therapies like intra-aortic balloon pump in
CCB overdoses17. Further clinical research is needed
to support the current findings opinion and evaluate
the role of levosimendan in calcium channel blocker
intoxication.
M.E.J. ANESTH 20 (6), 2010
872
M G. Teker et al
References
1.Bruca DA, William TB: Amlodipine overdose causes prolonged
calcium channel blocker toxicity: Am J Emerg Med; 16:527-8, 1998.
2.Vogt S, Mehlig A, Hunziker: Survival of severe amlodipine
intoxicarion due to medical intensive care. Forensic Sci Int;
161:216-20, 2006.
3.Katz AM: Cardiac ion channels: N Eng J Med; 328:1244-51, 1993.
4.Hockerman GH, Peterson BZ, Johnson BD, Catterall WA:
Molecular determinants of drug binding and action on L-type
calcium channels. Annu Rev Pharmacol Toxicol; 37:361-96, 1997.
5.Brunton LL, Lazo JS, Parker KL, Buxton IL, Blumenthal D,
editors. Goodman & Gilman’s The Pharmacological Basis of
Therapeutics, 11th edition. New York, McGraw-Hill, 2005.
6.Ramoska EA, Spiller HA, Winter M, Borys D: A one-year
evaluation of calcium channel blocker overdoses: toxicity and
treatment. Ann Emerg Med; 22:196-200, 1993.
7.Shepherd G, Klein-Schwartz W: High-dose insulin therapy for
calcium-channel blocker overdose. Ann Pharmacother; 39:923-30,
2005.
8.Megarbane B, Karyo S, Baud FJ: The role of insulin and glucose
(hyperinsulinaemia/euglycaemia) therapy in acute calcium channel
antagonist and beta-blocker poisoning. Toxicol Rev; 23:215-22,
2004.
9.Smith SW, Ferguson KL, Hoffman RS, Nelson LS, Greller HA:
Prolonged severe hypotension following combined amlodipine and
valsartan ingestion. Clin Toxicol (Phil); 46:470-4, 2008.
10.Greene SL, Gawarammana I, Wood DM, Jones AL, Dargan PI:
Relative safety of hyperinsulinemia/euglycaemia therapy in the
management of calcium channel blocker overdose:a prospective
observational study. Intensive Care Med; 33:2019-24, 2007.
11.Lheureux PER, Zahir S, Gris M, Derrey AS, Penaloza A: Benchto-bedside review: hyperinsulinaemia/euglycaemia therapy in the
management of overdose of calcium-channel blockers. Critical
Care; 10:212, 2006.
12.Harris NS: Case records of MassachusettsGeneral Hospital. Case
24-2006. A 40 year-old woman with hypotension after an overdose
of amlodipine. N Eng J Med; 355:602-11, 2006.
13.Yuan TH, Kerns WP II, Tomaszewski CA, Ford MD, Kline JA:
Insulin-glucose as adjunctive therapy for severe calcium channel
antagonist poisoning. J Toxicol Clin Toxicol; 36:463-74, 1999.
14.Kline JA, Raymond RM, Leonova ED, Williams TC, Watts JA:
Insulin improves heart function and metabolism during nonischemic cardiogenic shock in awake canines. Cardiovasc Res;
34:289-98, 1997.
15.Whitlow PL, Rogers WJ, Smith LR, McDaniel HG, Papapietro
SE, Mantle JA, et al: Enhancement of left ventricular function by
glucose-insulin-potassium infusion in acute myocardial infarction.
Am J Card; 49:811-20, 1982.
16.Rasmussen L, Husted SE, Johnsen SP: Severe intoxication after
an intentional overdose of amlodipine Acta Anaesthesiol Scand;
47:1038-40, 2003.
17.Janion M, Stepien A, Sielski J, Gutkowski W: Is the Intra-aortic
balloon pump a method of brain protection during cardiogenic shock
after drug intoxication? J Emerg Med; Apr 8 (Epub ahead of print),
2008.
18.Ross FD: Calcium channel blockers. In: Goldfrank LR, Flomenbaum
NE, Lewin NA, Hoffman RS, Nelson RS, editors. Goldfrank’s
Toxicologic Emergencies,7th edtion, New York, McGraw-Hill, pp.
762-74, 2002.
19.Salhanick SD, Shannon MW: Management of calcium channel
antagonist overdose. Drug Saf; 26:65-79, 2003.
20.Buckley NA, Dawson AH, Howarth DM, Whyte IM: Slow release
verapamil poisoning. Use of polyethylene glycol wholebowel lavage
and high-dose calcium. Med J Aust; 158:202-4, 1993.
21.Buckley NA, Whyte IM, Dawson AH: Overdose with calcium
channel blockers. BMJ; 308:1639, 1994.
22.Kenny J: Treating overdose with calcium channel blockers. BMJ;
308:992-3, 1994.
23.Ezidiegwu C, Spektor Z, Nasr MR, Kelly KC, Rosales LG: A case
report on the role of plasma exchange in the management of massive
amlodipine besylate intoxication. Ther Apher Dial; 12:180-4, 2008.
24.Humbert VH JR, Munn NJ, Hawkins RF: Noncardiogenic
pulmonary edema complicating massive diltiazem overdose. Chest;
99:258-9, 1991.
25.Stanek EJ, Nelson CE, DeNofrio D: Amlodipine overdose. Ann
Pharmacother; 31:853-6, 1997.
26.Toller WG, Stranz C: Levosimendan, a new inotropic and
vasodilator agent. Anesthesiology; 104:556-69, 2006.
27.Perrone SV, Kaplinsky EJ: Calcium sensitizer agents: a new class
of inotropic agents in the treatment of decompensated heart failure.
Int J Cardiol; 103:248-55, 2005.
28.Innes CA, Waqstaff AJ: Levosimendan: a review of its use in the
management of acute decompansated heart failure. Drugs; 63:265171, 2003.
SUCCESSFUL MANAGEMENT OF HIGH-DOSE
METFORMIN INTOXICATION.
ROLE OF VASOPRESSIN IN THE MANAGEMENT
OF SEVERE LACTIC ACIDOSIS
Yasin S Al-Makadma* and Tamer Riad**
Case Report
We report the case of a 49 year old, 100 kg male patient who, in a suicidal attempt, ingested
an estimated dose of 40 to 45 grammes of Metformin. Three hours he presented to AE Department.
Due to deterioration of consciousness and a marked irritability, he was sedated, intubated and
ventilated at the receiving hospital.
On induction of anesthesia (for intubation), the patient hemodynamics became very unstable
prompting the initiation of both Epinephrine and Nor-Epinephrine Intra-venous (IV) infusions.
Glucose 10% IV infusion and Insulin IV infusion were also started. The pre-transfer management
also included Hydrocortisone IV justified by the marked hemodynamic instability and mediocre
response to inotropic support. Arterial Blood Gas (ABG) analysis showed severe acidosis and
Lactate level of 34 mmol/l, in addition to a Hyperkalemia of 7 mmol/l. He was then transferred to
our Intensive Care Unit (ICU) to start Continuous Veno-Venous Hemofiltration (CVVH).
On arrival to the ICU, patient was sedated, ventilated. His pupils were dilated and non-reactive.
His hemodynamic was refractory, demanding significant inotropic support (at approximately
1mcg/kg/min of Nor-Epinephrine and Epinephrine). The systolic BP was at best 80 to 100 mmHg.
His CVP was 19 mmHg. Arterial blood gas revealed a PaO2 of 50 kPa, and a PaCO2 of more than
10 Kpa despite hyperventilation. The arterial blood pH remained as low as 6.8. Lactate level was
beyond the maximum titration limit of our ABG machine. ****Blood Sugar was at 11 g/l.
The administration of 500 mls of Molar Sodium Bicarbonate failed to improve the metabolic
acidosis and despite the initiation of CVVH, using Prisma System, the pH remained around 6.80
on repetitive analysis.
As Catecholamines requirements were increasing with limited benefit on hemodynamic
parameters, the decision to introduce Vasopressin IV infusion was taken. We used Pitressin*,
diluted in Dextrose 5% solution for a final concentration of 1 IU/ml. The initial dose was 6 IU/hour.
Rapid improvement of ABP parallel with rapid decrease of Epinephrine requirement allowed
to be stopped by the next morning, less than 12 hours from the introduction of Vasopressin. We also
noted a slow but consistent rise of the pH.
*
MD, FFA.
**FRCA.
Corresponding author: Dr. Yasin S. Al-Makadma, MD, CMU, FFA, FFPM, Security Forces Hospital, Riyadh, KSA, Co-author:
Dr. Tamer Riad, FFA, Mid-Yorkshire Hospitals, Dewsbury, UK.
873
M.E.J. ANESTH 20 (6), 2010
874
Y. S Al-Makadma & T. Riad
Table 1
pH and Base-Excess recorded first 48 hours of admission
Time (hours)
Base Deficit
pH
A&E
“OUT OF RANGE”
6.8
ICU admission
-28.3
6.79
4
-28.7
6.79
8
-26.7
6.86
16
-17.4
7.12
24
-16.8
7.13
28
-16.1
7.16
32
-15
7.17
40
-12.6
7.22
48
-9.8
7.28
The patient continued to rapidly improve from
hemodynamic point of view and the Nor-Epinephrine
was gradually weaned and stopped over few days. The
Vasopressin infusion was gradually decreased and
stopped as the stabilization of the hemodynamic state
was confirmed.
A Tracheostomy was performed followed by a
successful weaning of Ventilator three days later.
The patient was discharged to the HDU and then
to a medical ward before leaving the hospital.
Discussion
Metformin is a Biguanide oral anti-diabetic agent.
The pharmacological action of this molecule depends
on decreasing Glucose transit through intestinal
mucosal cells and decreasing gluconeogenesis as well
as increasing peripheral glucose utilization.
There are only few cases of Metformin overdose
in the literature. To our knowledge, the highest dose
reported as overdose was 25 g, at the time of our case.
Dell'Anglio et al reported, more recently, a suspected
much higher dose at 75 to 100 g1. Our patient's
overdose remains however very significant at, 40 to 45
g of Metformin.
Except in multiple drugs intoxication, combined
with Metformin and considering the mode of action
of Metformin, hypoglycemia is not a major issue1 in
either normal therapeutic range or overdose. Lactic
acidosis, however, is a well documented complication
of Metformin overdose1-5, with risk of fatal outcome in
over 50% of cases2. This risk is considerably increased
if treatment is initiated after cardiovascular collapse
occurs2. High plasmatic metformin level above 150
mcg/ml, high lactatemia and low pH would predict
increased risk of mortality2,3,4.
Lactic acidosis is not due to tissue hypoxemia and
anaerobic metabolism but to reduction of cell redox
function. The negative inotropism effect of Metformin
could also contribute to the ability of hepatocytes to
extract circulating lactate. This kind of Lactic acidosis,
in the absence of anaerobic metabolism is known as
type B Lactic acidosis. Prognosis of type B Lactic
acidosis does not necessarily correlate with the level
of lactatemia15.
Aggressive therapy should be initiated as a soon
as possible. The use of CVVH, when bicarbonate
administration fails to correct the acidosis remains a
corner stone in the management of its complication8,9,10.
With this severe acidosis, Metformin overdose
concomitantly presents with a refractory hemodynamic
status6,7, of which the support can be very difficult. Death
can be the unfortunate outcome in these overdoses if
the intensive therapy fails to reverse the general trend
of acidosis and circulatory failure. There is a vicious
circle that starts with the acidosis and continues with
the circulatory failure. A lot of emphasis is made for the
treatment of acidosis8,9,10, but less clear advice is given
for the modality of hemodynamic support. The use of
high amounts of Nor-Epinephrine and Epinephrine is
not always efficient in supporting the cardio-vascular
system in the context of severe metabolic acidosis.
We believe that our case supports that early use
of Vasopressin can be very useful in the treatment
of precarious haemodynamic states and circulatory
failure in relation with Metformin overdose and
probably in those circulatory failures linked to severe
acidosis. This role could be due to the fact that below
a pH of 6.9, the Catecholamines can be of limited
effect6. In addition, Vasopressin seems to compromise
regional perfusion less than does Noradrenaline. This
would help in limiting the aggravation of metabolic
acidosis as could be seen with Epinephrine and
Norepinephrine.
It is also well accepted that, in case of underutilization of lactate, like in Metformin overdose
cases, the treatment of the underlying cause is of a
major importance. The CVVH in such case is less
efficient than in cases of Mineral metabolic acidosis.
SUCCESSFUL MANAGEMENT OF HIGH-DOSE METFORMIN INTOXICATION. ROLE OF VASOPRESSIN IN THE
MANAGEMENT OF SEVERE LACTIC ACIDOSIS
The treatment of organic metabolic acidosis should be
geared towards the correction of the cause rather than
the symptoms8. This would mean that Renal dialysis
techniques are not necessarily the unique answer to
Lactic acidosis caused by Metformin overdose. Some
authors found, however, that CVVH is successful in
the treatment of such acidosis5. More recently, it is high
flow CVVH that was recommended for Metformin
overdose. In these circumstances, the CVVH would be
efficient in the treatment of Lactic acidosis either by
clearance of the Metformin or by the improvement of
hemodynamic state of the patient.
Why Vasopressin?
It is admitted that the sympathetic effects of
Catecholamines are less strong in acidotic conditions
(()). Although a range of pH between 7.4 and 7 is
considered, by some authors, to be compatible with
the activity of Catecholamines, these drugs would
875
loose their effect however if the pH decreases below
6.96,7.
In Metformin overdose complicated by a severe
lactic acidosis, the hemodynamic instability is mainly
due to the deep vasodilatation that occurs and not to
the effect of acidosis on the myocardium10.
Conclusion
Intoxication by high dose of Metformin could
lead to fatal outcome, mainly by the detrimental
effects on the hemodynamic function. In this scenario,
Catecholamines are not necessarily efficient. The
management of severe lactic acidosis associated
with Metformin overdose should include aggressive
hemodynamic support and early introduction of
Vasopressin. High flow, lactate-depleted CVVH could
also be beneficial in reversing the trend towards fatality.
References
1. Dell’aglio DM, Perino LJ, Todino JD, Algren DA, Morgan BW:
Metformin overdose with a resultant serum pH of 6.59: Survival
without sequalae; J Em Med, 2008, in press.
2. Perrone J, Phillips C, Gaieski D: Occult Metformin Toxicity
in Three Patients with Profound Lactic Acidosis, J Emergency
Medicine, 2008.
3. DM Dell’Aglio, LJ Perino, ZN Kazzi, BW Morgan, MD Schwartz
and RJ Geller: Mortality in acute metformin overdose is predicted
by serum pH, lactate, and metformin concentration, J Toxicol Clin
Toxicol; 44 (2006), p. 712.
4. Nisse P, Mathieu-Nolf M, Deveaux M, Forceville X, Combes: A
fatal case of metformin poisoning. AJ Toxicol Clin Toxicol; 2003,
41(7):1035-6.
5. Ben Harvey RSCN, Ceri Hickman RSCN, Gillian Hinson,
MRPharmS, Tanya Ralph RSCN, Anton Mayer MRCPCH: Severe
lactic acidosis complicating metformin overdose successfully treat-
ed with high-volume venovenous hemofiltration and aggressive alkalinization; Pediatr Crit Care Med; 2005, 6:598-601.
6. Smith NT, Corbascio AN: Myocardial resistance to metabolic acidosis. Arch Surg; 1966, 92:892-896.
7. Huang YG, Wong KC, Yip WH, et al: Cardiovascular responses to
graded doses of three catecholamines during lactic and hydrochloric
acidosis in dogs. Br J Anaesthesiol; 1995, 74:583-590.
8. Levraut J, Ciebiera JP, Jambou P, et al: Effect of continuous venovenous hemofiltration with dialysis on lactate clearance in critically
ill patients. Crit Care Med; 1997, 25:58-62.
9. Hilton PJ, Taylor J, Forni LG, et al: Bicarbonate-based haemofiltration in the management of acute renal failure with lactic acidosis.
Q J Med; 1998, 91:279-283.
10.Teale KFH, Devine A, Stewart H, Harper: The management of
metformin overdose, Case Report, NJH, Anaesthesia; July 1998,
53(7), pp. 698-701.
M.E.J. ANESTH 20 (6), 2010
AWAKE CRANIOTOMY USING INITIAL SLEEP
WITH LARYNGEAL MASK AIRWAY IN
DEPRESSED AGITATED PATIENT
- A Case Report -
Khalid M Al Shuaibi*
Abstract
Depressed patients with brain tumors are often not referred to awake craniotomy because of
concern of uncooperation which may increase the risk of perioperative complications. This report
describes an interesting case of Awake Craniotomy for frontal lobe glioma in 41 year old woman
undergoing language and motor mapping intra-operatively. As she was fearful and apprehensive
and was on antidepressant therapy to control depression the author adapted general anesthesia
with laryngeal mask airway during initial stage of skull pinning and craniotomy procedures.Then
patient reverted to awake state to continue the intended neurosurgical procedure. Patient tolerated
the situation satisfactory and was cooperative till the finish without any event.
Key words: craniotomy; awake. LMA. Parietal tumor.
Introduction
Intra-operative mapping, of targeted areas of brain resection, is an integral part of modern
neurosurgery. Intraoperative stimulation of near speech and motor regions may prevent un-necessary
nervous tissue damage. while using neuro navigation and intraoperative MRI (iMRI) allowing
maximum resection of the tumor. This procedure requires an awake, cooperative patient to assess
motor and verbal responses. Sometimes patient may be not cooperative during this procedure due
to psychological profile or extreme fear from the notion of being awake during initial surgical
intervention while the skull is fixed and then opened. This report describes the author’s experience
with awake craniotomy in a middle aged woman having anxiety and treated for depression, using
initial sleep and maintaining the airway by laryngeal mask airway initially then awake technique
before testing and to the end of the surgery.
*
MD, Pain Medicine Fellow.
Consultant of Anesthesiology, Pain Medicine &Chairman of Anesthesia, Department of Anesthesia, King Fahad Medical City,
Riyadh, Kingdom Saudi Arabia. E-mail: [email protected]
877
M.E.J. ANESTH 20 (6), 2010
878
Case Report
A 42 year old female (weight:59 kg. Hight:168
cm) presented to the Neuroscience Department at
King Fahad Medical City (KFMC), complaining of
progressively, increasing headaches of 18 months
duration. She was placed on anticonvulsant therapy:
valproic. Clinical history revealed reports of depression
since a long time related to overwhelming psychosocial problems at home. Clinical examinations
were unremarkable. Awake craniotomy was planned
including intra-operative mapping for language and
motor function. In the BrainSuite® Lab, intravenous
line was started and sedation using both midazolam 1-2
mg iv. and fentanyl 25-50 µg iv. Standard anesthetic
monitoring was initiated (ECG, NIBP and pulse
oximetry). A right radial arterial line was inserted,
under local anesthesia, for continuous blood pressure
measurement and serial blood gases monitoring.
A nasal cannula was placed in position. Scalp
Block was established, with the use of 80 ml of
0.125% bupivacaine and 5 µg.ml-1 of adrenaline, by
the surgeon. The patient was positioned in supine
position and her head was rotated to the left side. A
four-pin frame failed to fix after many trials due to
irritable patient. We gave 20-30 mg propofol bolus
with 25-50 µg fentanyl and still the patient was
uncooperative during the pins application. Anesthesia
was induced with propofol 2 mg.kg-1 and fentanyl 50
µg. iv. Laryngeal Mask Airway (LMA) size 3 was
inserted easily and after demonstration of proper deep
anesthesia. Airway and spontaneous breathing was
maintained using 4 L.min-1 of 50% 02 in air. Anesthesia
was maintained with combined continuous infusions
of propofol 1% 20-30 ml.h-1 and fentanyl 25 ug.h-1.
Patient then brought to the BrainSuite® Lab. for preoperative MRI and Neuronavigation. MRI- compatible
monitoring was included i/ e. ECG, IBP, Capnography,
Temperature and Pulse Oximetry.
Patient; urinary bladder was catheterized and
mannitol 0.5 mg.kg-1 was given in addition to
Dexamethazone 8 mg iv.
Surgery started and after the dura is opened the
propofol and fentanyl was gradually decreased and later
stopped. The patient became awake smoothly. LMA
was removed without complications. Oxygenation
was maintained with a nasal cannula. The patient
Khalid M Al Shuaibi
became completely awake, able to talk within 10
minutes following the removal of LMA. The surgery
was commenced again while the patient was fully
awake with proper intra-operative motor and language
assessments. The course of the surgery went uneventful.
Hemodynamic variables were thoroughly stable. There
were no desaturation or airway obstruction. Another
MRI study was done while patient was completely
awake. After surgery patient was transferred to SICU
with a good clinical condition.
Discussion
BrainSuite Lab is newly established at
KFMC. Two years have passed and various difficult
neurosurgical surgery operation with great success.
Awake craniotomy was done to benefit from
intraoperative MRi and navigation facilities1.
Awake craniotomy for seizure foci resection
is currently popular since a complete resolution of
seizures foci without increasing neurological deficit2,-4.
This requires “asleep, awake, asleep” anesthesia
technique to keep an awake, comfortable patient who
cooperates with intraoperative testing.
Drugs are used to manage this state. They are
selected according to their short half-lives and ease
of titration. Using such drugs concurrently can cause
powerful respiratory depression. Our selection of the
prescribed regimen in accordance of reported success
in literature2,5. Neuroanesthesia team should be vigilant
for such events like: hypoventilation, apnea, and chest
wall rigidity.
Several options are available for airway
management during awake craniotomy including
endotracheal intubation, LMA, nasal airway and non
intubation technique preserving natural airway.
Adverse events during awake craniotomy can
include nausea, intraoperative anxiety, seizures, and
brain engorgement6,7. Nausea and/or vomiting may
result in significant morbidity. We chose to reduce
this risk, by administering ranitidine, ondansetron,
metoclopramide, dexamethasone, and glycopyrrolate.
Appropriate patient selection is critical to
success. In this vase it was not an ideal patient for
the technique but detailed pre-operative explanation
of the anesthesia plan was important for operators
AWAKE CRANIOTOMY USING INITIAL SLEEP WITH LARYNGEAL MASK AIRWAY, IN DEPRESSED AGITATED PATIENT
to go ahead. Despite uncontrollable anxiety and
the concurrent state of depression we expected that
incorporation could still occur. Our efforts focus on
reassure the patient followed by supplements of sedoanalgesics regimen and we explained, to the patient,
that general anesthesia is possible for short period and
there would be no pain when she will be waken up for
testing. Intraoperative urgent intubation is technically
difficult and slow to secure. The anesthesiologist in
expectation of intraoperative seizers. Although, it
did not happened in this case, the plan for its control
swiftly should be in mind i.e. surgeon’s application of
ice water irrigation and discontinuation of stimulation,
anticonvulsants intravenously and if respiratory
instability occur, intubation and controlled ventilation.
Fig. 1
Briansuite ® settings: surgeon looking to mural screens
showing integrated iMRI an imaging with microscopic
operating field screen
879
In conclusion, a careful approach in handeling
psychological patient may tolerate the current
analgesia and anesthesia techniques during awake
craniotomy, this case may open the field to operate on
moderately disturbed patient and have more exposure
rather keeping awake craniotomy for fully co-operative
patient. Anesthesiologist should be malleable in his
plan to the immediate needs of his patient.
Acknowledgement
The author would like to thank neurosurgical
team lead by Dr Ahmad Larry for using information
derived from their patient and iMRI brainsuite staff
who performed the iMRI study.
Fig. 2
MRI vault: the patient is drapped and protected by head coil
before iMRI session
M.E.J. ANESTH 20 (6), 2010
880
Khalid M Al Shuaibi
References
1. M Said Maani Takrouri & OS Seif: Leap Into Future In Image
Navigation Neurosurgery: Visit to the BrainSuite at King Fahad
Medical City in Riyadh, KSA. The Internet Journal of Health; 2007,
Volume 6 Number 1.
2. Sarang A, Dinsmore J: Anaesthesia for awake craniotomy evolution
of a technique that facilitates awake neurological testing. Br J
Anaesth; 2003, 90:161-5.
3. Ebeling U, Schmid UD, Ying H, et al: Safe surgery of lesions near
the motor cortex using intra-operative mapping techniques: A report
on 50 patients. Acta Neurochir; (Wien) 1992, 119:23-28.
4. Sahjpaul RL: Awake craniotomy: controversies, indications and
techniques in the surgical treatment of temporal lobe epilepsy. Can J
Neurol Sci; 2000, 27(S1):S55-63.
5. McDougall RJ, Rosenfeld JV, Wrennall JA, et al: Awake
Craniotomy in an Adolescent. Anaesth Intensive Care; 2001,
29:423-425.
6. Archer DP, McKenna JM, Morin L, et al: Conscious-sedation
analgesia during craniotomy for intractable epilepsy: a review of
354 consecutive cases. Can J Anaesth; 1988, 35(4):338-344.
7. Young DA: Awake craniotomy using a modified nasal airway,
propofol, and remifentanil in an adolescent.
http://www.pedsanesthesia.org/meetings/2004winter/pdfs/2004_
P23.pdf [last access: oct.23rd 2009].
CARDIAC ARRHYTHMIA AFTER SUCCINYLCHOLINE
ADMINISTRATION IN A PATIENT WITH
GUILLAIN-BARRÉ SYNDROME
- A Case Report -
Jyh Yung Hor*
Abstract
We report a case of cardiac arrhythmia occurring in a Guillain-Barré syndrome (GBS)
patient after succinylcholine administration during third endotracheal intubation, on day 13 of
illness. The probable cause of arrhythmia is succinylcholine-induced hyperkalemia. Of interest,
this case demonstrated in the same patient that arrhythmia only occurred during third intubation,
when duration of illness is prolonged, and not during previous two intubation episodes, despite
succinylcholine was also being used. In GBS, muscle denervation resulted in up-regulation
of acetylcholine receptors at neuromuscular junctions, causing the muscle cell membrane to
become supersensitive to succinylcholine, leading to severe hyperkalemia and arrhythmia when
succinylcholine was administered.
Key words: Guillain-Barré syndrome, Succinylcholine, Cardiac arrhythmia, Endotracheal
intubation, Acetylcholine receptor up-regulation, Denervation.
Introduction
Succinylcholine-induced hyperkalemia causing life-threatening cardiac arrhythmia has been
reported in Guillain-Barré syndrome (GBS)1,2 and in chronic polyneuropathy3. Here, we present
a case of cardiac arrhythmia in a patient with GBS after succinylcholine administration during
the third endotracheal intubation, on day 13 of illness. Of interest, this case demonstrated in the
same patient that arrhythmia only occurred during third intubation, when the duration of illness
is prolonged, and not during previous two intubation episodes, despite succinylcholine was also
being used.
*
MD, Department of Internal Medicine, Sultanah Bahiyah Hospital, Alor Star, Kedah, Malaysia.
Corresponding Author: Jyh Yung Hor, MD, 5 Lebuh Batu Maung 6, 11960 Penang, Malaysia. Tel.: +60 12 4617842, Fax: +60 4
6563754, E-mail: [email protected]
881
M.E.J. ANESTH 20 (6), 2010
882
Case Report
A 30-year-old woman presented with 4-day
history of hands and feet numbness, followed by
weakness of upper and lower limbs that started distally.
One day prior to admission, she became unable to walk,
breathless, and having dysphagia. On presentation, she
was conscious, afebrile but tachypneic. Power of both
upper and lower limbs was 2/5, and with generalized
areflexia.
A clinical diagnosis of GBS was made. She
deteriorated fast and was intubated for respiratory
failure. Midazolam 5mg intravenous (i.v.) and
succinylcholine 100mg i.v. were given prior to
intubation. She was admitted to intensive care unit
(ICU) for mechanical ventilation, and was given i.v.
immunoglobulin 0.4g/kg/day for 5 days.
On day 6 of ICU stay (day 10 of illness), her
muscle power improved to 4/5 for upper limbs and 3/5
for lower limbs. She was extubated and put on oxygen
supplementation. However, 1 hour after extubation, she
became breathless and was unable to speak. She was
re-intubated, using i.v. midazolam and succinylcholine
as before. The potassium level prior to re-intubation
was 4.32 mmol/L.
On day 9 of ICU stay (day 13 of illness),
her condition has again improved clinically. She
was extubated and given oxygen supplementation.
However, 1.5 hour after extubation, she again became
tachypneic. Nevertheless, she remained conscious and
oxygen saturation by pulse oxymetry was maintained
at 99%. Re-intubation was decided. To facilitate
intubation, i.v. midazolam 5mg and i.v. succinylcholine
100mg were given. Just before attempt for intubation,
ventricular tachycardia (VT) was noted on cardiac
monitor. She was promptly intubated, and cardiopulmonary resuscitation (CPR) was immediately
initiated, and was continued for about 15 minutes.
During CPR, she was defibrillated 3 times for pulseless
VT, before being reverted to sinus tachycardia. Her
potassium level on that morning was 4.41mmol/L. The
potassium level repeated after CPR was 4.63 mmol/L.
On day 13 of ICU stay, there was a leak at the
endotracheal tube. She was extubated and given
non-invasive ventilation. She tolerated well and was
weaned off ventilator the next day. Her muscle power
Jyh Yung Hor
eventually returned to normal. She could walk, talk
and swallow well, and was discharged after 20 days of
hospitalisation.
Discussion
The probable cause of cardiac arrhythmia in
this patient is succinylcholine-induced hyperkalemia.
Noxious stimuli such as laryngoscopy and endotracheal
intubation may also trigger cardiac arrhythmia, but
in this case arrhythmia has occurred prior to such
manipulation.
Normally, serum potassium increases by 0.5 to 1
mmol/L after succinylcholine administration4. In GBS,
muscle denervation results in increased production
of acetylcholine receptors5,6. With this up-regulation,
the muscle cell membrane becomes supersensitive to
succinylcholine, resulting in a great efflux of potassium
upon succinylcholine administration, that may lead
to severe hyperkalemia and cardiac arrhythmia. This
supersensitivity increases dramatically by day 5,
and can continue for weeks or even longer5-7. This
explains why this patient did not develop arrhythmia
on admission day and on day 6 when succinylcholine
was used, but subsequently developed it on day 9 of
ICU stay (day 13 of illness). It is important to note that
prior to second intubation on day 6 and third intubation
on day 9, the potassium levels were 4.32mmol/L and
4.41mmol/L, respectively. Despite the very similar
potassium level, arrhythmia only happened on a later
occasion.
Succinylcholine-induced hyperkalemia is a
transient phenomenon, where potassium level peaked
at 3 - 5 minutes to around 8 or 9 mmol/L in denervated
muscle, then started decreasing over time, and
eventually back to normal range by 20 - 30 minutes3,7,8.
This may explain why severe hyperkalemia was not
seen in her post-CPR blood results, as blood was only
withdrawn about 30 minutes after onset of VT.
From the literature, succinylcholine-induced
hyperkalemia has not been reported in patients with
acquired pathologic states of < 4 days’ duration5.
This case re-affirms the observation, where cardiac
arrhythmia (most probably due to hyperkalemia)
only occurred at day 13 of illness, and not earlier
even though succinylcholine was used twice before
CARDIAC ARRHYTHMIA AFTER SUCCINYLCHOLINE ADMINISTRATION IN A PATIENT WITH GUILLAIN-BARRÉ
SYNDROME
that. Of particular interest, this case demonstrated in
the same patient that arrhythmia did not occur with
succinylcholine administration on days 1 and 6 of
admission, but happened on day 9 of admission during
third intubation, despite the very similar pre-intubation
potassium level of around 4.4mmol/L during each
occasion.
883
In conclusion, succinylcholine should be avoided
in GBS, as has been recommended by others1,2,
especially when the duration of illness was > 4 days5.
Instead, non-depolarizing muscle relaxant with
relatively more rapid onset such as rocuronium should
be considered.
References
1. Reilly M, Hutchinson M: Suxamethonium is contraindicated in the
Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry; 1991,
54:1018-1019.
2. Dalman JE, Verhagen WIM: Cardiac arrest in Gullain-Barré
syndrome and the use of suxamethonium. Acta Neurol Belg; 1994,
94:259-261.
3. Fergusson RJ, Wright DJ, Willey RF, Crompton GK, Grant
IWB: Suxamethonium is dangerous in polyneuropathy. BMJ; 1981,
282:298-299.
4. Bevan DR, Donati F: Muscle relaxants. In: Barash PG, Cullen
BF, Stoelting RK (eds): Clinical Anesthesia, 4th ed. Philadelphia:
Lippincott Williams & Wilkins; 2001, pp.419-447.
5. Martyn JAJ, Richtsfeld M: Succinylcholine-induced hyperkalemia
in acquired pathologic states: etiologic factors and molecular
mechanisms. Anesthesiology; 2006, 104:158-169.
6. Martyn JAJ, White DA, Gronert GA, Jaffe RS, Ward JM: Upand-down regulation of skeletal muscle acetylcholine receptors:
effects on neuromuscular blockers. Anesthesiology; 1992, 76:822843.
7. Gronert GA, Theye RA: Pathophysiology of hyperkalemia induced
by succinylcholine. Anesthesiology; 1975, 43:89-99.
8. Gronert GA, Lambert EH, Theye RA: The response of denervated
skeletal muscle to succinylcholine. Anesthesiology; 1973, 39:13-22.
M.E.J. ANESTH 20 (6), 2010
CONSCIOUS SEDATION FOR AWAKE CRANIOTOMY
IN INTRA-OPERATIVE Magnetic RESONANCE
IMAGING OPERATING THEATRE
(IMRI OT) ENVIRONMENT
Mohamad Said Maani Takrouri*, Firas A Shubbak**,
Aisha Al Hajjaj***, Rolando F Del Maaestro****,
Lahbib Soualmi*****, Mashael H Alkhodair******,
Abrar M Alduraibi****** and Najeeb Ghanem*******
Abstract
This technical report disrobes the first case in Intra-operative Magnatic Resonance Imaging
operating theatre (iMRI OT) (BrainSuite®), of Awake Craniotomy. The procedure was for frontal
lobe glioma excision in 24 y. old man. He was scheduled to undergo eloquent cortex language
mapping intra-operatively. He was motivated and was excited to see the operating theatre.
He requested to take his photos while operated upon. The authors adapted conscious sedation
technique with variable depth according to Ramsey’s scale , in order to revert to awake state to
perform the intended neurosurgical procedure. Patient tolerated the situation satisfactory and was
cooperative till the finish without any event. We elicit in this report the special environment of
iMRI OT for lengthy operation in pinned fixed patient having craniotomy. The text shows the
special environment, its demands and its possible difficulties.
Key words: Awake craniotomy; scalp block ; language mapping motor testing. Intra-operative
Magnatic Resonance Imaging operating theatre (iMRI OT); BrainSuite®: Coil head protection.
Neuroanesthesia; Neurosurgery.
Introduction
Intra-operative mapping, of intended areas of brain resection, constitutes an essential part
of modern neurosurgery1-4. It is well established that intra-operative stimulation of near speech
and motor regions. Also using neuro-navigation and intra-operative MRI (iMRI) allows maximum
resection of the tumor4,5. This procedure requires an awake, cooperative patient to assess motor
and verbal responses. Sometimes patient may be not cooperative during this procedure due to
psychological profile or extreme fear from the notion of being awake during surgical intervention
while the skull is fixed and then opened. The anesthetic technique has to satisfy three parties;
*
MB. ChB. FRCA (I), Consultant.
**
MD, CJBA, Assistant Consultant Anesthesiologist.
***
MD, Consultant Neurosurgeon and Neurointervention.
****
MD, PhD, FRCS(c), FRCE, DABNC, Profesor of Neurosurgery and Oncology.
***** PhD, Director of Neuronavigation Unit and Brain Suite.
****** BSc, SLP, Speech Language Pathologist II.
*******MD, Consultant Interventional Radiologist.
885
M.E.J. ANESTH 20 (6), 2010
886
patient, surgeon and anesthesiologist4. Many
anesthesia techniques may help to produce favorable
operating condition based on Scalp block with local
anesthesia and various sedation and anesthesia based
on propofol titrated sedation and short acting narcotics
(ramifentanil and fentanyl)5-20. This will allow stages
of sleep-awake-sleep or sedation-awake-sedation.
This report describes the authors experience with
(nine hours duration) of awake craniotomy, interrupted
by session of iMRI, on a man who was motivated to be
subjected to awake technique before and during testing
language mapping. It was carried out under conscious
sedation which was interrupted during sessions of
mapping then continued to the end of the surgery.
Case Report
A 24 year old male (weight: 69 kg. Hight:168 cm)
presented to the Neurosciences Department at King
Fahad Medical City (KFMC).He complained of one
sudden episode of seizure, for which a brain CT scanwas done reveling a left frontal lobe tumor. Awake
craniotomy was planned including intra-operative
brain mapping, for resection of epileptogenic foci
close to eloquent cortex, i.e. motor and speech areas of
the brain, for language and motor function.
In preoperative assessment he stated to be smoker
of 20 cigarettes a day. Medically he was known to have
mild intermittent bronchial asthma on treatment of β2
agonist (salbutamol nebulizer).
On examination; the patient was conscious,
oriented to place time and dates, alert, no signs of limbs
weakness nore speech abnormalities. He was already
seen by speech specialist and surgeon who informed
him about all the expected operation and his role to
reduce and prevent any side effects. Emphasis was put
on that he is going to be awake during testing and he
would have 2- 3 sessions of iMRI. Anesthesiologists
answer all the questions regarding pain and sedation
and being beside him all the operation. He was very
excited about being operated upon in BrainSuite®
theatre. He requested to have his pictures takrn during
the procedures and he gave consent to use it for medical
publications.
M. S. Maani Takrouri et. al
Vitals: HR:80 b.min-1, RR: 20 b.min-1, SPO2:
97% room air, BP: 130/80 mmHg, temp:36.9 Cº.
Laboratory investigations were all within normal
ranges.
In iMRI OT, intravenous line was established and
sedation using both propofol 1-2 mg iv. and fentanyl
25-50 µg iv. Standard, Monitoring was initiated (ECG,
NIBP , skin temperature and pulse oximetry).
The patient was placed in supine position.
Oxygenation while breathing air was enriched through
a nasal oxygen catheter, was delivering 2 l.min-1.
Conscious sedation was maintained with continuous
infusions of:
- Propofol (20-40) ug.kg-1.min-1.
- Fentanyl at the rate of 2 µg.kg-1.h-1 Infusion
rates.
Depth of sedation was adjusted by the attending
anesthesiologists according to patient comfort,
hemodynamic and respiratory parameters and was
kept ar 2-4 Ramsay’s sedation scale.
Scalp Block was established, with the use of 80
ml of 0.125% bupivacaine and 5 µg.ml-1 of adrenaline,
by the surgeon.
Concern in managing patient in iMRI theatre
environment.
MRI environment would dictate strict obedience
to instruction and wornings for MRI compatibility.
Fig. 1
The patient after scalp block and under conscious sedation
pinned to the table and drapped ready for craniotomy
CONSCIOUS SEDATION FOR AWAKE CRANIOTOMY IN INTRA-OPERATIVE MAGNETIC RESONANCE IMAGING
OPERATING THEATRE (IMRI OT) ENVIRONMENT
Fig. 2
Scalp incision under scalp block and conscious sedation
887
Fig. 5
Patient’s movement carried on surgical table top to and from
MRI tube with extreme care for connected monitored and
intravenous lines. One of the authors [FS]. is pictured in the far
right caring for the patient.
Fig. 3
Patient’s ears are plugged with earphones with recitation of
quean as he requested to help him coping with iMRI noise
Fig. 6a
Pre operative: Left frontal lobe mass lesion, low signal in T1
WI, and High signal intensities in T2 WI , with homogeneous
enhancement and necrotic area in Post Gad T1 WI
Fig. 4
Patient’s head covered with head shield (coil) after
ears are plugged with earphones with recitation of quean
as he requested to help him coping with iMRI noise.
The airway is protected by keeping the patient
in conscious sedation (Natural airway).
T1_WI_pre_op (A)
Left frontal lobe mass lesion showed
hypo intense signal intensity inT1 W
Image
T2_WI_pre_op (B)
Left frontal lobe mass lesion showed
high signal intensities in T2 W Image.
Post_Gad_T1_WI_pre_op (C)
Left frontal lobe mass showed
inhomogeneous enhancement and necrotic
area in Post Gad T1 W image
M.E.J. ANESTH 20 (6), 2010
888
M. S. Maani Takrouri et. al
Fig. 6b
Post Operative: Left frontal surgical cavity (
Encephalomalacia) at previously removed frontal lobe
mass in post GAD T1 WI with minimal linear enhancement
representing reactiveenhancement with no residual mass.
Pre-Operative language assessment:
Within the same week of surgery, a full language
and cognitive-linguistic assessments were done.
Additionally, a trial of intra-operative assessment using
pictures naming task (50 pictures or more) was done
the same day .Patient presented with normal receptive
and expressive language skills along with a normal
cognitive-linguistics skills .Results were documented
as patient's pre-operative baseline. After that patient
was counseled regarding the intra-operative assessment
that he will undergo.
Intra-operative language assessment:
T1_WI_post_op (D)
Left frontal surgical cavity
(Enchephalomalaxia) at previously
removed frontal lobe mass showed
low signal intensity (CSF intensity) in
T1 W image
T2_WI_post_op (E)
Left frontal surgical cavity
(Enchephalomalaxia) at
previously removed frontal lobe
mass showed high signal intensity
(CSF intensity) in T2 W image
Post_Gad_T1_WI__post_op (F)
Left
frontal
surgical
cavity
(Enchephalomalaxia) at previously
removed frontal lobe mass with
minimal linear enhancement in
post GAD T1 WI represent reactive
enhancement without residual mass.
Fig. 6
iMRI images with radiologist’s report
Patient before entering the MRI tube should wear
ear plugs to protect his ears from the noise. Also the
head would be covered by head shield coil to protedt it
from all possible contact inside the tube or incidental
projectiles.
The patient was planned for three iMRI sessions
and he was prepared this way each time.
Care was critically applied when the operating
table top was moved to and from the MRI tube.
Duration of the procedure: It took six hours
operation and mapping, and three hours iMRI sessions
Speech-Language pathologist ‘s role in Awake
Brain Mapping of Dominant hemisphere
protocol followed in this case
Speech-language pathologists attended the
surgery after the bone flap for the sensorimotor
mapping. Speech-language pathologist arranged with
the neurophysiologists and neurosurgeons regarding
the timing and type of stimulation. The patient was
asked to perform counting (regularly from 1 to 10
over and over) and provide naming (proceeded by
the carrier phrase "this is a……").The two tasks were
used to identify the essential language sites known
to be inhibited by stimulation. (SLPs were observing
for any disturbance in language functions during the
stimulations and alerting the surgeon to it). During
the tumor resection, patient continued to count and/or
name pictures when the resection became closer to the
subcortical language structures.
Post-operative language assessment:
The patient was assessed 2-days post surgery
by the speech-language pathologist using the same
language and cognitive-linguistics assessment tools
that were used preoperatively. Assessment showed
intact receptive and expressive language skills.
Discussion
The iMRI OT is newly established at KFMC21.
Two years have passed and various difficult
neurosurgical operations were performed with great
success5. Awake craniotomy was done to benefit from
intra-operative MRi and navigation facilities21. The
surgeon would operate with advantage of dynamic
imaging navigation allowing proper tumor tissue
resection with elimination of brain tissue shift effect,
which is experience in brian surgery. The updated
pictures are projected on wall mounted huge screen
CONSCIOUS SEDATION FOR AWAKE CRANIOTOMY IN INTRA-OPERATIVE MAGNETIC RESONANCE IMAGING
OPERATING THEATRE (IMRI OT) ENVIRONMENT
889
and satellite screens in front of the eye of the surgeon
and his assistants21.
Table 2
The key components of the BrainSuite® iMRI
Surgical team operate outside the effect of
MRI influence put again they should observe MRI
compatibility code.
1. Navigation System. Automatic Image Registration
Operating inside this environment necessitate
adaptation of MRI compatibility and other anesthesia
technique adjustments [Table 1, 2].
3. Data Billboard BrainSuite and Data Management System.
Awake craniotomy for seizure foci resection is
currently popular since it allows a complete resolution
of seizures foci without increasing neurological
deficit17-20. This requires “asleep, awake, asleep”
anesthesia technique to keep an awake, comfortable
patient who cooperates with intra-operative testing.
Anesthetic drugs are selected according to their
short half-lives and ease of titration. Propofol and
fentanyl were selected in this case in accordance of
reported success in literature17-20.
Table 1
Issues of concern to anesthesia staff in iMRI OT
Issues
Anaesthetic Considerations
Ferromagnetic Implant devices: Aneurismal clips.
Objects
Prosthetic heart valves. Tissue expanders
with metallic ports. Cardiac pacemakers.
Also antable defibrillators/cardioverters
and implantable infusion pumps. Metallic
based substancespens, key chains, scissors,
Noise
stethoscope, non lithium batteries etc.
It comes from scanner due to torque
of wire have gradient currents induced
in them during RF pulses. This cause
Occupational
vibration and audible noise.
There are no reports of harmful tissue
Exposure
Anaesthesia
contact with the magnetic fields.
Safety. Proper functioning in the magnetic
Machines
field. No effect on MRI image quality.
Ventillators
ECG Monitor
can cause image degradation of MRI scans
from the wire leads acting as antennas.
Pulse Oximetry Burn to finger.
Blood Pressure Adjustment and MRI compatible
Monitoring
measuring screens. Some irregular
measurements transmission.
Mohammad Bilal Delvi et al, MEJ ANESTH, 19 (1), 2007 [21].
Vector Vision software.
2. Microscope Zeiss OPMI Neuro NC4 MultiVision.
4. BrainSuite iMRI system: high-field MRI scanner (1.5 Tesla
Siemens Magnetom Espree).
5. Rotating Operating Room (OR) table with integrated
head clamp and coil.
6. Operating room (OR) lights with integrated video camera,
ceiling supply unit, anesthesia equipment.
7. BrainSuite iMRI RF shielded OR cabin.
MSM Takrouri, The Internet Journal of Health, 2007 Volume
6 [22].
Using such drugs concurrently can cause powerful
respiratory depression. Neuroanesthesia team should
be vigilant for such events like: hypoventilation,
apnea, and chest wall rigidity.
Several options are available for airway
management during awake craniotomy including
endotracheal intubation, LMA, nasal airway and non
intubation technique preserving natural airway23,24.
Adverse events during awake craniotomy can
include nausea, intraoperative anxiety, seizures, and
brain engorgement7,24.
Nausea and/or vomiting may result in
significant morbidity. We chose to reduce this
risk, by administering ranitidine, ondansetron,
metoclopramide, dexamethasone, and glycopyrrolate.
Appropriate patient selection is critical to
success. In this case it was an ideal patient for the
technique. Nevertheless a detailed pre-operative
explanation of the anesthesia plan was important for
operators to go ahead. Our efforts focus on reassure the
patient followed by supplements of sedo-analgesics
regimen and we explained, to the patient, that there
would be no pain when he will be subjected to testing.
Intraoperative urgent intubation is technically difficult
and slow to secure, in case of seizures, should be in the
mind of anesthesia team. Although, it did not happen
in this case, the plan for its control swiftly should be in
mind i.e. surgeon’s application of ice water irrigation
M.E.J. ANESTH 20 (6), 2010
890
and discontinuation of stimulation., anticonvulsants
intravenously and if respiratory instability occur,
intubation and controlled ventilation.
In conclusion, a careful approach by supporting
psychological aspect and motivation of the patient in
order to tolerate the procedure the current analgesia
and anesthesia techniques during awake craniotomy
can be adjusted quickly to the benefit to a controlled
operative time, this case may open the field to operate
on co-operative patient.
M. S. Maani Takrouri et. al
Acknowledgement:
This paper is based on Takrouri MM, Shubbak
FA, Al Hajjaj A, Del Maestro RF, Soualmi L, Alkhodari
MH, Alduraiby AM, Ghanem N. Conscious sedation for
awake craniotomy in intraoperative magnetic resonance
imaging operating theater. Anesth Essays Res [serial
online] 2010 [cited 2011 Mar 5];4:33-7. Available
from:
http://www.aeronline.org/tex.asp?2010/4/1/33/69306
References
1. Black PM, Ronner SF: Cortical mapping for defining the limits of
tumor resection. Neurosurgery; 1987, 20:914-9.
2. Ebeling U, Schmid UD, Ying H, Reulen HJ: Safe surgery of lesions
near the motor cortex using intra-operative mapping techniques: a
report on 50 patients. Acta Neurochir; (Wien), 1992, 119:23-8.
3. Haglund MM, Berger MS, Shamseldin M, Lettich E, Ojemann
GA: Cortical localization of temporal lobe language sites in patients
with gliomas. Neurosurgery; 1994, 34:567-76.
4. Khalifah N, Herrick I, Megyesi J, Parrent A, Steven D, Craen R:
Patient satisfaction following awake craniotomy. Saudi J Anaesth
[serial online] 2008 [cited 2010 Jan 1], 2:52-6. Available from:
http://www.saudija.org/text.asp?2008/2/2/52/51856
5. Sabbagh AJ, Al-Yamany M, Bunyan RF, Takrouri MS, Radwan
SM: Neuroanesthesia management of neurosurgery of brain stem
tumor requiring neurophysiology monitoring in an iMRI OT setting.
Saudi J Anaesth [serial online] 2009 [cited 2010 Jan 1], 3:91-3.
Available from: http://www.saudija.org/text.asp?2009/3/2/91/57877
[serial online] 2008 [cited 2010 Jan 1];2:52-6. Available from: http://
www.saudija.org/text.asp?2008/2/2/52/51856
6. Archer DP, McKenna JM, Morin L, Ravussin P: Conscioussedation analgesia during craniotomy for intractable epilepsy: a
review of 354 consecutive cases. Can J Anaesth; 1988; 35:338-44.
7. Sarang A, Dinsmore J: Anaesthesia for awake craniotomy evolution
of a technique that facilitates awake neurological testing. Br J
Anaesth; 2003, Feb, 90:161-5.
8. Danks RA, Rogers M, Aglio LS, Gugino LD, Black PM: Patient
tolerance of craniotomy performed with the patient under local
anesthesia and monitored conscious sedation. Neurosurgery; 1998,
42:28-34.
9. Herrick IA, Craen RA, Gelb AW, Miller LA, Kubu CS, Girvin JP,
Parrent AG, Eliasziw M, Kirkby J: Propofol sedation during awake
craniotomy for seizures: patient controlled administration versus
neurolept analgesia. Anesth.Analg; 1997, Jun, 84:1285-91.
10.Johnson KB, Egan TD: Remifentanil and propofol combination for
awake craniotomy: case report with pharmacokinetic simulations. J
Neurosurg Anesthesiol; 1998, Jan, 10:25-9.
11.Berkenstadt H, Perel A, Hadani M, Unofrievich I, Ram Z:
Monitored anesthesia care using remifentanil and propofol for
awake craniotomy. J Neurosurg Anesthesiol; 2001, Jul, 13:246-9.
12.Taylor MD, Bernstein M: Awake craniotomy with brain mapping as
the routine surgical approach to treating patients with supratentorial
intraaxial tumors: a prospective trial of 200 cases. J Neurosurg;
1999, 90:35-41.
13.Blanshard HJ, Chung F, Manninen PH, Taylor MD, Bernstein M:
Awake craniotomy for removal of intracranial tumor: considerations
for early discharge. Anesth Analg; 2001, 92:89-94.
14.Hogue CW, Jr., Bowdle TA, O'Leary C, Duncalf D, Miguel R,
Pitts M, Streisand J, Kirvassilis G, Jamerson B, McNeal S, et
al: A multicenter evaluation of total intravenous anesthesia with
remifentanil and propofol for elective inpatient surgery. Anesth
Analg; 1996, Aug, 83:279-85.
15.Vuyk J, Mertens MJ, Olofsen E, Burm AG, Bovill JG: Propofol
anesthesia and rational opioid selection: determination of optimal
EC50-EC95 propofol-opioid concentrations that assure adequate
anesthesia and a rapid return of consciousness. Anesthesiology;
1997, Dec, 87:1549-62.
16.Egan TD, Lemmens HJ, Fiset P, Hermann DJ, Muir KT, Stanski
DR, Shafer SL: The pharmacokinetics of the new short-acting
opioid remifentanil (GI87084B) in healthy adult male volunteers.
Anesthesiology; 1993, 79:881-92.
17.Egan TD: Remifentanil pharmacokinetics and pharmacodynamics.
A preliminary appraisal. Clin Pharmacokinet; 1995, 29:80-94.
18.Borgeat A, Wilder-Smith OH, Saiah M, Rifat K: Subhypnotic
doses of propofol possess direct antiemetic properties. Anesth
Analg; 1992, 74:539-41.
19.Smith I, Monk TG, White PF, Ding Y: Propofol infusion during
regional anesthesia: sedative, amnestic, and anxiolytic properties.
Anesth Analg; 1994, 79:313-9.
20.Herrick IA, Gelb AW: Anesthesia for temporal lobe epilepsy
surgery. Can J Neurol Sci; 2000, 27 Suppl, 1:S64 7, discussion S926.:S64-S67.
21.Delvi MB, Samarkandi A, Zahrani T, Faden A: Recovery profile
for magnetic resonance imaging in pediatric daycase-sevoflurane vs.
isoflurane. Middle East J Anesthesiol; 2007, Feb, 19(1):205-11.
22.Takrouri MSM & Seif OS: Leap Into Future In Image Navigation
Neurosurgery: Visit to the BrainSuite at King Fahad Medical City
in Riyadh, KSA. The Internet Journal of Health; 2007, Volume 6
Number 1.
23.Sahjpaul RL: Awake craniotomy: controversies, indications and
techniques in the surgical treatment of temporal lobe epilepsy. Can J
Neurol Sci; 2000, 27(S1):S55-63.
24.Young DA: Awake craniotomy using a modified nasal airway,
propofol, and remifentanil in an adolescent. http://www.
pedsanesthesia.org/meetings/2004winter/pdfs/2004_P23.pdf [last
access: oct.23rd 2009].
EFFECTIVE AWAKE THORACIC EPIDURAL
ANESTHETIC FOR MAJOR ABDOMINAL
SURGERY IN TWO HIGH-RISK PATIENTS
WITH SEVERE PULMONARY DISEASE
- A Case Report -
E Abd Elrazek*, M Thornton** and A Lannigan**
Summary
Awake thoracic epidural anaesthesia as the sole anaesthetic technique was successfully
employed for two high risk surgical patients with chronic obstructive pulmonary disease undergoing
abdominal surgery. The procedure was tolerated well and the anaesthetic technique which has
been shown to reduce intra-operative and post-operative cardiac, respiratory and gastrointestinal
complications, may have significantly contributed to the prompt, complication free recovery
experienced by both patients.
We report two cases of awake major abdominal surgery in two high-risk surgical patients
with severe pulmonary disease, performed effectively under thoracic epidural anaesthesia as a sole
technique. The first case was an elective open sigmoid colectomy in a sixty one year old cancerous
patient with chronic obstructive pulmonary disease [COPD] and recent thoracotomy for a wedge
resection of a bronchial adenocarcinoma [pT1NoMx]. The second case was an emergency open
cholecystectomy in an adult patient with end-stage COPD. Reviewing the literature, no similar
cases were reported recently.
First Case
A 61 year old male patient known to have end-stage COPD was diagnosed with a sigmoid
adenocarcinoma in January 2008. Pre-operative staging identified a spiculated mass lesion in his
right lung. A PET scan suggested that these were two independent primaries. In March 2008 he
underwent a right thoracotomy under a combined anaesthetic technique of general anaesthesia in
conjunction with a thoracic epidural. During surgery, it was difficult to ventilate him with secretions
in his dependent lung and a decision was taken to limit the operative procedure to a wedge resection
rather than a lobectomy. The first 10 post-operative days were complicated by atelectasis, reduced
oxygen saturation and rapid atrial fibrillation, which converted to sinus rhythm with Amiodarone.
At pre-anaesthetic assessment prior to colonic resection in July, the patient’s BMI was 32
and he was still smoking 4-5 per day, with a previous history of 50 packs per year. He had chronic
productive cough and was on four different inhalers; Bricanyl, Spiriva and Symbicort regularly
plus Salbutamol as required. Although his pre-operative chest xray was reported to be clear his
*
Consultant Anaesthetist, Wishaw General Hospital, Wishaw, UK.
** Consultant Surgeon, Wishaw General Hospital, Wishaw, UK.
Correspondence to: Dr. Essam Abd Elrazek ([email protected]).
891
M.E.J. ANESTH 20 (6), 2010
892
chest sounded generally wheezy with reduced air entry
bilaterally [Fig. 1]. The patient’s peak expiratory flow
rate [PEFR] was very low [250 L/M]. Pulmonary
function tests showed that his FEV1 was 1.5 liters
[54% predicted] with an FEV1/FVC ratio of 45%
pre and post bronchodilator. The six minutes walk
test [6MWT] detected an overall low level at 223
meters [predicted distance in health elderly = 631 ±
93 meters]1, and he was diagnosed to have moderately
irreversible COPD.
Second Case
A sixty six year old male ex-smoker was
admitted to the emergency department of Wishaw
General Hospital suffering from sudden onset
epigastric and right upper quadrant pain. He had
tenderness and guarding in the right upper quadrant
with obviously palpable gall bladder consistent with
acute cholecystitis. He had progressive shortness of
breath, generalized expiratory wheeze with bilateral
basal crepitations consistent with COPD for which he
used three different inhalers regularly; Salbutamol,
Seretide, and Spiriva. He could manage only 50 yards
on the flat and one flight of stairs, with a PEFR of
250 L/M. His most recent pulmonary function tests
showed that he had FEV1 of 1.14 L [45% predicted]
and FEV1/FVC ratio of 41% giving him the diagnosis
of moderate airflow obstruction with no significant
irreversibility, air trapping and severe reduction in
transfer factor. His chest x-ray showed COPD with
bilateral basal consolidation [Fig. 2]. He was also on
Amlodipine for a history of hypertension and Codydramol for osteoarthritis. On admission, his WCC
was raised with slightly elevated LDH, but CRP was
raised to over 300 which was settled to some extent
on IV antibiotics. An ultrasound confirmed gallstones
with acute inflammatory changes in the gallbladder.
Imaging and clinical impression suggested he was
developing a gallbladder empyema and concerns were
raised about the viability of the gallbladder, suggesting
surgery was necessary.
Anesthetic Technique
Pre-operatively, surgical and anaesthetic options
were discussed and we decided to proceed to open
E. Abd Elrazek et. al
surgery under awake thoracic epidural anaesthesia to
minimise potential chest complications. With each
patient’s consent, they have had their laparotomies
[case no. 1: lower abdominal for a sigmoid colectomy
and case no. 2: sub-costal for a cholecystectomy]
completed under thoracic epidural anaesthesia only.
Both patients were received an awake thoracic
epidural anaesthetic [case no. 1: T7-8 and case no.:
2: T6-7]. The technique was performed in a lateral
position under complete aseptic technique and basic
monitoring; heart rate (HR), arterial blood pressure
(ABP), and pulse oximetry (SpO2%). Light sedation
using 4-mg of Midazolam was given and Lignocaine
1% [5 ml] was used to infiltrate the chosen space. For
the block induction, a recipe of Lignocaine 2% with
Adrenaline 1:200.000 [total, 20 ml], Clonidine [150
ug] and Diamorphine [3 mg] were used. Up to T4 loss
of sensation was obtained bilaterally 5 minutes post
induction. This was confirmed using the ice test and
we were confident that the surgery should proceed.
Later, a bolus of 10 ml L-Bupivacaine 0.5% was given
followed by an infusion of 0.1% L-Bupivacaine with
Fentanyl, 2 ug/ml [10 – 15 ml / hour] to maintain the
block through out the operation. The analgesic and the
abdominal muscle relaxation conditions were optimum
and the Surgeons were very satisfied.
The two patients were conversing with the
operative teams during surgeries, while they remained
very comfortable, breathing spontaneously 4-6 L/M
O2 via Hudson face mask. Because of potential
complications, no further sedation was given. They
were haemodynamically and respiratorily stable
throughout the operations. The operation time was two
hours in the first case and one hour in the second. No
invasive monitoring was needed.
Post-operatively, patients were transferred
to the recovery room and, subsequently, to the
high dependency unit [HDU] for post-operative
observation, monitoring and continuous epidural
analgesia which was very effective in both cases. No
further analgesia was required. The upper level of the
epidural block was consistent with the epidural scoring
scale for arm movements of zero {ESSAM score =
0; able to perform a hand grip}2, and patients were
breathing comfortably and no respiratory support was
needed. Not having had a general anaesthetic, both
EFFECTIVE AWAKE THORACIC EPIDURAL ANESTHETIC FOR MAJOR ABDOMINAL SURGERY IN TWO
HIGH-RISK PATIENTS WITH SEVERE PULMONARY DISEASE
made a remarkable recovery and later were able to be
discharged home in good general condition. The first
patient went home only 6 days post-operatively with a
final diagnosis of a pT3 No adenocarcinoma, and was
reviewed 4 and 8 weeks post-discharge and found to
be well, having returned to all pre-operative activity
levels. The cholecystectomy patient had to stay in
hospital for 12 days post-operatively to optimise his
chronic chest condition with nebulisers, antibiotics
and physiotherapy. The postoperative histopathologic
examination of his specimen has confirmed the
diagnosis of acute diffuse suppurative cholecystitis
with numerous suppurative foci within the necrotic
gallbladder wall.
Discussion
General anesthesia in high risk surgical patients
with significant pulmonary disease can trigger some
adverse effects including; pneumonia, impaired cardiac
performance, neuromuscular problems, biotrauma and
barotrauma and subsequently intra and post-operative
hypoxemia3. Avoiding endotracheal intubation
decreases the risk of postoperative laryngospasm and
bronchospasm, especially in elderly COPD patients
with irritated upper and lower airway tracts. Awake
thoracic epidural anaesthesia has been reported to be a
safe technique in patients with end-stage COPD4.
In order to reduce the adverse effects of general
anaesthesia, thoracic epidural anaesthesia has been
recently employed to perform awake cardio- thoracic
surgery procedures, including coronary artery bypass
grafting, management of pueumothorax, resection
of pulmonary nodules and solitary metastases, lung
volume surgery, and trans-sternal thymectomy5,6.
Thoracic epidural anaesthesia blunts the decrease
of subcutaneous tissue oxygen tension caused by
surgical stress and adrenergic vasoconstriction during
major abdominal surgery providing sufficient tissue
oxygenation, and improving cardiac, respiratory
and gastrointestinal function and may decrease the
incidence of surgical wound infection7. Splanchnic
sympathetic nervous blockade results in reduced
inhibitory gastrointestinal tone and increased
intestinal blood flow, positive factors where a colonic
anastomosis is to be performed8.
Given that our two patients had end-stage COPD
893
and significant co-morbidity the advantages of epidural
anaesthesia may have been vital contributor to the
satisfactory recovery.
Post-operative myocardial infarctions are
reported to be significantly lower due to continuous
thoracic epidural analgesia9. Two systemic reviews
have found that epidural anaesthesia with or without
post-operative epidural analgesia reduce postoperative pulmonary infections compared with general
anaesthesia with or without post-operative systemic
analgesia10,11. Ballantyne et al confirmed that postoperative epidural pain control can significantly
decrease the incidence of pulmonary morbidity12.
Furthermore, a comparative study of major abdominal
surgery in the elderly reported that the epidural route
of post-operative analgesia provides better pain relief,
improved mental status and faster return of bowel
activity13. In patients undergoing lower abdominal
surgery, the neuroaxial blockade and surgical
anaesthesia achieved by epidural local anaesthetics
was associated with decreased post-operative analgesic
demands as seen with our patients14.
The pathophysiological response to surgical
trauma, especially when it is major, could include pain,
nausea, vomiting and ileus, stress-induced catabolism,
impaired pulmonary function, increased cardiac
demands, and risk of thromboembolism. Subsequently,
further complications, need for treatment, and delayed
recovery as well as discharge from hospital, could
occur. Development of safe anaesthetic and analgesic
techniques including regional anaesthesia have
provided an important tool for excellent quality of
surgery and enhanced recovery. We definitely agree
with Kehlet and Dahl’s opinion regarding the pivotal
role of the anasethetist facilitating early post-operative
recovery providing a minimally invasive anaesthesia
and analgesia and may be tailoring his anaesthetic
strategy to meet the surgical demand in view of the
patient’s general condition15.
In 1994, awake epidural anaesthesia has been
reported to be effective and safe technique in the highrisk colectomy patient16. Since then, there has been
a paucity of data in the literature on the procedure
performed under regional, especially awake epidural
anaesthesia, in patients with co-existing pulmonary
diseases. Also, awake laparoscopic cholecystectomy
M.E.J. ANESTH 20 (6), 2010
894
has been reported to be safely done under thoracic
epidural anaesthesia in COPD patients17. However,
this anaesthetic technique is still unrecorded for open
cholecystectomy, despite being known to adversely
affect the post-operative pulmonary function more
than the laparoscopic procedure18.
In this article, the two reported patients had
significant co-morbidity, presenting the need to
consider all surgical and anaesthetic options. Thoracic
epidural was preferred to combined spinal epidural
(CSE) anaesthesia because it is simple, less invasive
and more reliable. In a CSE technique, the clinician
has no chance to test the effectiveness of his epidural
until the effect of the spinal wears off, and it would
be too late if it is found to be ineffective or not
working at all and the only available option in this
case scenario would be putting the patient off to sleep,
the technique that the Anaesthetist initially tried to
avoid. In our technique, we started with Lignocaine
to speed up the block induction, but later, the longer
acting L-Bupivacaine was used19. Diamorphine20 and
Clonidine21 were added to improve the quality of the
analgesic effect of the epidural. The risk of inadvertent
high blockade post-operatively, may be reduced by
monitoring the patien’s arm movements using the
epidural scoring scale for arm movements [ESSAM],
E. Abd Elrazek et. al
which has been found to be very simple and reliable
method for the early detection of the cephalad spread
of thoracic epidural analgesia2.
Finally, we believe that thoracic epidural
anaesthesia and analgesia is very useful technique,
especially when it is used for selected patients
helping to avoid general anaesthesia when it is contraindicated. Encouraging this technique might help
increase the safety margin of the surgery offered to the
high-risk surgical co-morbid patients, especially those
with severe pulmonary diseases. It could also help
smooth the recovery period and enhance the discharge
rate of those patients, increase the turnover of surgical
cases, and subsequently, shorten the long waiting lists
for surgery in the NHS. Needless to say that optimum
anaesthetic and surgical experience as well as cooperation will be necessary in such circumstances.
Acknowledgement
The authors would like to thank Dr. Donald
MacLean, Dr. Alison Simpson and Dr. Marisa
Haetzman, Anaesthetic Consultants at Wishaw General
Hospital for reviewing this article. Also, we would like
to thank the theatre, HDU and physiotherapy staff for
their efficiency and co-operation.
EFFECTIVE AWAKE THORACIC EPIDURAL ANESTHETIC FOR MAJOR ABDOMINAL SURGERY IN TWO
HIGH-RISK PATIENTS WITH SEVERE PULMONARY DISEASE
895
References
1. Troosters T, Gosselink R, Decramer M: Six minutes walk distance
in healthy elderly subjects. European Respiratory Journal; 1999,
14: 270-274.
2. Abd Elrazek E, Scott NB, Vohra A: An epidural scoring scale
for arm movements (ESSAM) in patients receiving high thoracic
epidural analgesia for coronary artery bypass grafting. Anaesthesia;
1999, 54:1097-1109.
3. Jin F, Chung F: Minimising perioperative adverse events in the
elderly. British Journal Anaesthesia; 2001, 87:608-624.
4.Gruber EM, Tshernko EM, Kritzinger M, Deviatko E, Wisser
W, Zurakowski D, Haider W: The effects of thoracic Epidural
Analgesia with Bupivacaine 0.25% on Ventilatory Mechanics
in patients with Severe Chronic obstructive Pulmonary Disease.
Anesthesia & Analgesia; 2001, 92:1015-1019.
5. Mineo TC: Epidural anaesthesia in awake thoracic surgery. European
Journal Cardiothoracic Surgery; 2007, 32:13-19.
6. Noiseux N, Prieto I, Bracco D, Basile F, Hemmerling T: Coronary
artery bypass grafting in the awake patient combining high thoracic
epidural and femoral nerve block: first series of 15 patients. British
Journal Anaesthesia; 2008, 100:184-189.
7. Kabon B, Fleischmann E, Treschan T, Tguchi A, Kapral S, Kurz
A: Thoracic epidural anesthesia increases tissue oxygenation during
major abdominal surgery. Anesthesia and Analgesia; 2003, 97:18121817.
8. Veering BT, Cousins MJ: Cardiovascular and pulmonary effects of
epidural anaesthesia. Anaesthetic Intensive Care; 2000, 28:620-635.
9. Beattie SW: Epidural analgesia reduces postoperative myocardial
infarction: A meta-analysis. Anesthesia and Analgesia; 2001,
93:853-858.
10.Jayr C, Thomas H, Rey A, Farhat F, Lasser P, Bourgain JL:
Postoperative pulmonary complication: epidural analgesia using
bupivacaine and opioids versus parentral opioids. Anaesthesiology;
1993, 78:666-676.
11.Rodgers A, Walker N, Schug S, et al: Reduction of postoperative
mortality and morbidity with epidural or spinal anaesthesia: results
from overview of randomized trials. British Medical Journal; 2000,
321:1493-1497.
12.Ballantyne JC, Carr DB, deFerranti A, et al: The comparative
effects of postoperative analgesic therapies on pulmonary outcome:
cumulative meta-analysis of randomized controlled trials. Anesthesia
and Analgesia; 1998, 86:598-612.
13.Mann C, Pouzeratte Y, Boccara G, et al: Comparison of
Intravenous or epidural patient-controlled analgesia in the elderly
after major abdominal surgery. Anesthsiology; 2000, 92:433-441.
14.Shir Y, Raja SN, Frank SM: The effect of epidural versus general
anaesthesia on postoperative pain and analgesic requirements in
patients undergoing radical prostatectomy. Anesthesiology; 1994,
80:49-56.
15.Kehlet H, Dahl JB: Anaesthesia, surgery, and challenges in
postoperative recovery. Lancet; 2003, 362:1921-1928.
16.Koltun WA, McKenna K, Rung G: Awake epidural anaesthesia is
effective and safe in the high-risk colectomy patient. Diseases of the
Colon and Rectum; 1994, 37:1236-1241.
17.Pursnani KG, Bazza Y, Calleja M, Mughal MM: Laparoscopic
cholecystectomy under epidural anaesthesia in patients with chronic
respiratory disease. Surgical Endoscopy; 1998, 12:1082-1084.
18.Karayiannkis AJ, Makri GG, Mantzioka A, Karousos D, Karatzas
G: Postoperative pulmonary function after laparoscopic and open
cholecystectomy. British Journal Anaesthesia; 1996, 77:448-452.
19.McLeod IK: Local anaesthetics. http://www.emedicine.com/ent/
topic20.htm (accessed 17/11/2008).
20.Stoddart PA, Cooper A, Russel R, Reynolds F: A comparison of
epidural diamorphine with intravenous patient-controlled analgesia
using the Baxter infusor following Caesarean section. Anaesthesia;
1993, 48:1086-1090.
21.Dobrydnjov I, Axelsson K, Gupta A, Lundin A, Holström B,
Granath B: Improved analgesia with clonidine when added to local
anaesthetic during combined spinal-epidural anesthesia for hip
arthroplasty: a double-blind, randomized and placebo-controlled
study. Acta Anaesthesiolgica Scandinavica; 2005, 49:538-545.
M.E.J. ANESTH 20 (6), 2010
VARIANTS OF PHEOCHROMOCYTOMA AND
THEIR ANESTHETIC IMPLICATIONS
– A Case Report And Literature Review –
Kathryn Dortzbach, Daniel M Gainsburg*
and E lizabeth AM F rost **
Anesthesiologists are trained to appreciate and respond appropriately to the considerable
consequences of pheochromocytomas. It is however, less well appreciated that these tumors may
be associated with other syndromes that can also carry significant anesthetic risk. We describe the
case of a young man who had a rare disease in combination with multiple pheochromocytomas and
suffered a fatal outcome after anesthesia. Possible causes for this disaster are suggested.
Case History
A 23 year-old male with a past medical history significant for Von Hippel-Lindau (VHL)
syndrome presented for a laparoscopic right partial nephrectomy. The patient was diagnosed with
renal cell carcinoma (RCC), which was found incidentally on CT scan, originally performed to
assess for rib fractures after a motor vehicle accident. His past surgical history was significant
for craniotomy with tumor resection secondary to hemangiomas related to VHL, and a right total
adrenalectomy and left partial adrenalectomy both to remove pheochromocytomas. These surgeries
were performed nine and eight years prior, respectively. The patient showed no other recurrences
of lesions secondary to VHL other than the RCC. On preoperative assessment, the patient weighed
100 kg and stood 183cm tall. His blood pressure was 125/78 and his pulse was 80. Medications
included only a muscle relaxant, which he took for back spasms following the accident He was
otherwise asymptomatic. He reported a possible allergy to penicillin as a child.
In the operating room, induction was performed and an arterial cannula was placed following
intubation. Gentamycin 80mg and clindamycin 600mg were given as antibiotic prophylaxis. Tumor
resection was difficult due to its deep location. The case lasted over six hours and was otherwise
uneventful. Vital signs were stable throughout with a blood pressure ranging from 100-170/5080 and a pulse rate from 75-110. He received a total of fentanyl 925mcg, and was maintained
with isoflurane, oxygen and nitrous oxide. Urine output was 500 ml and the estimated blood loss
was 500 ml. Crystalloids, 4 liters were infused. At the end of the case, the patient was awakened
and extubated without difficulty. He was transported to the recovery room in stable condition.
Vital signs were blood pressure of 140/70, pulse rate 90, respiratory rate 20, temperature 37.4.
Chemistry panel was within normal limits and the hematocrit was 40.
Vital signs upon discharge from the recovery room five hours later were blood pressure
of 120/50, pulse rate 85, respiratory rate 14. The patient indicated at that time that he was not
experiencing pain.
Around 4:45 am, several hours after he was transferred to the ward, the patient was found
asystolic, pulseless and apneic and with evidence of emesis. Immediate resuscitation was performed
but the patient could not be revived.
Attending Anesthesiologist, New York Eye & Ear Infirmary, New York, NY.
*
MD, Assistant Professor.
** MD, Professor.
Dept of Anesthesiology, Mount Sinai Medical Center, New York NY.
897
M.E.J. ANESTH 20 (6), 2010
898
K. Dortzbach et. al
Introduction
Incidence and Epidemiology
Pheochromocytoma is one of the more
challenging medical conditions faced by the
anesthesiologist. Its hallmark paroxysmal hypertensive
crises and cardiac manifestations including sinus
tachycardia and bradycardia as well as arrhythmias,
require the anesthesiologist to exercise the highest
degree of vigilance. Significant improvements have
been made in the management of pheochromocytomas
since the first reports of their resection in the mid to
late 1920s. Today, the mortality rate is less than 5%1.
With greater awareness in diagnosing and treating
pheochromocytomas, anesthesiologists can work
perioperatively to reduce the mortality rate even further.
The greatest incidence of pheochromocytomas
occurs in the fourth and fifth decades.
Among patients diagnosed with hypertension,
roughly
0.1
percent
are
attributable
to
2
pheochromocytomas , a small but not insignificant
statistic given the incidence of hypertension. Also,
these patients have a medical condition, which in most
instances can be cured if diagnosed and treated correctly.
Patients who remain undiagnosed are at great risk
for further morbidity and high mortality, particularly
if they must undergo surgical procedures. Of those
patients with undiagnosed pheochromocytomas, as
many as 25-50% die from complications occurring
during induction of anesthesia or during anesthesia for
procedures for other medical conditions3.
Pheochromocytomas are very vascular tumors
comprised of chromaffin tissue, which secretes varying
quantities of epinephrine and norepinephrine which
account for the clinical presentation. These tumors
are most commonly found in the adrenal medulla
but can be found anywhere chromaffin cells reside
within or close to sympathetic ganglia, including the
spleen, broad ligament, bladder, right atrium and at the
bifurcation of the aorta3.
While isolated pheochromocytomas of a nonfamilial etiology comprise most cases, it is important
to understand the threat of a pheochromocytoma in
more complex clinical settings. Approximately 5%
of pheochromocytomas are associated with other
syndromes such as VHL3. Our case serves as an
example of one of many atypical contexts in which
pheochromocytomas arise. Pheochromocytomas in
the setting of VHL, and other familial syndromes, as
well as in the setting of recurrence and clinically silent
cases and the general management are presented.
In the adult population, roughly 80% of tumors
are solitary and unilateral, occurring in one of the
adrenal glands. The remaining 20% are divided
between bilateral lesions or extraadrenal masses.
“The rule of 10s” refers to the statistic that 10% of
tumors are extraadrenal, 10% are bilateral and 10% are
malignant. Malignant spread is most typically to the
liver via lymphatics and venous routes3. Recurrence is
estimated at 8%1. Five percent of pheochromocytomas
are inherited, either as an isolated phenomenon or as
part of a familial syndrome.
Symptoms
Catecholamine release from pheochromocytomas
accounts for most symptoms, usually headaches,
palpitations and sweating. Both epinephrine and
norepinephrine are synthesized, stored and secreted in
pheochromocytomas. However, every tumor releases
a different ratio of the two catecholamines and some
tumors contain only one catecholamine. Epinephrine
secreting tumors produce palpitations, sweating,
heat intolerance, tremulousness, pallor and flushing,
headache and weight loss. With the potential for very
strong beta-stimulation, these tumors can infrequently
cause severe hypotension or shock. Characteristically,
norepinephrine secreting tumors are associated with
more benign symptoms and can be misdiagnosed as
essential hypertension3.
Tumors that secrete both catecholamines exert
a wide spectrum of symptoms. Few patients are
asymptomatic. Around 50% of patients experience
nonparoxysmal hypertension, either sustained or
labile. The rest experience paroxysmal elevated blood
pressure with the worst symptoms associated with the
greatest fluctuations in plasma catecholamine levels.
The frequency of symptoms is also variable, as patients
may live for years without a recurrent attack while
others suffer over 20 attacks of sudden onset daily.
Most attacks last for a few minutes to a few hours but
some may be as short as several seconds and others
may persist for days1-3.
In addition to hypertension, pheochromocytomas
VARIANTS OF PHEOCHROMOCYTOMA AND THEIR ANESTHETIC IMPLICATIONS
can cause deleterious but less common cardiac
manifestations. Sinus tachycardia, sinus bradycardia,
supraventricular dysrhythmias and premature
ventricular contractions have all been reported. Patients
without a history of coronary artery disease may suffer
anginal pain and myocardial infarctions, believed to
be a result of catecholamine induced coronary artery
spasm. Electrocardiographic changes include right and
left bundle branch blocks, non-specific ST segment
and T wave changes and prominent U waves3.
Catecholamine cardiomyopathies are rare and
are presumed to be associated with a longer duration
of disease and exposure to catecholamines. In the
most severe cases, these cardiomyopathies can lead
to heart failure and death. The mechanism has not
been fully delineated but persistent hypertension
can cause a hypertrophic cardiomyopathy. Dilated
cardiomyopathies are less common4.
Other findings may include weight loss,
carbohydrate intolerance due to decreased insulin
production and increased hepatic glucose production.
Orthostatic hypotension may be seen in as many as
70% of patients. The exact mechanism is unknown but
may be due to desensitized alpha-adrenergic receptors
or sympathetic reflexes from the high amount of
circulating catecholamines or volume depletion related
to hypertension4. Patients with pheochromocytomas
in the bladder wall may present with hematuria and
bladder spasms with polyuria.
Diagnosis and Laboratory findings
The first step in diagnosis is often made
by measuring 24 hour urinary metanephrine
and vanillylmandelic acid levels and plasma
catecholamines. No test is perfect with each having
different degrees of sensitivity and specificity.
The sensitivity of plasma free metanephrines is
approximately 96-100%. Specificity is lower, between
82-96%. In comparison, urine metanephrines and
catecholamines have a greater specificity of 98% and
a lower sensitivity of 90%5. Any of the biochemical
markers could be negative despite positive clinical
findings and the presence of a tumor. Conversely, there
are several drugs that can lead to false positive results for
899
catecholamines and metanephrines, falsely suggesting
a diagnosis of pheochromocytoma. The list includes
antipsychotics, L-dopa, tricyclic antidepressants,
clonidine, phenoxybenzamine, caffeic acid (found
in decaffeinated coffee), ethanol, paracetamol and
substantial physical stress5. The clonidine suppression
test can be used to rule out a rise in catecholamines
due to other causes6. Because a pheochromocytoma
secretes catecholamines that are free from neurogenic
control, administration of clonidine will not result in
suppression. To confirm a diagnosis, imaging studies
include CT scan, magnetic resonance imaging (MRI)
and meta-iodobenzylguanidine scintiscan (MIBG). CT
and MRI are comparable in sensitivity, 98% and 100%
respectively but both have lower specificities, CT with
70% and MRI with 67%. MIBG has a specificity of
100% but a lower sensitivity of 78%7. All components
of an evaluation must be taken into account to arrive at
the correct diagnosis.
Familial Pheochromocytomas in Association
with Syndromes
Five percent of pheochromocytomas are
of familial origin, passed down as an autosomal
dominant trait as an isolated finding or in association
with a syndrome including VHL, Multiple
Endocrine Neoplasia (MEN) type 2a and type
2b, and von Recklinghausen neurofibromatosis.
For the anesthesiologist, pheochromocytoma is
generally the most threatening component of both
VHL and MENIIA/IIB8,9. Patients with any of these
syndromes should be evaluated preoperatively for
pheochromocytoma regardless of their medical history
and whether or not they show any signs or symptoms
of catecholamine secreting tumors.
Von Hippel-Lindau Syndrome is an autosomal
dominant disease that has variable expression and
incomplete penetrance (Fig. 1). The disease was first
described over 100 years ago. Eugen von Hippel
described angiomas in the eye in 190410. Arvid Lindau
described angiomas of the cerebellum and spine in
192711.
M.E.J. ANESTH 20 (6), 2010
900
Fig. 1
Von Hippel-Lindau Syndrome is an autosomal dominant
disease
Findings include capillary hemangioblastomas
of the retina (seen in 60-70% of patients), and
hemangioblastomas of the central nervous system
(CNS) (30-70% of patients). Most of the CNS lesions
are located in the cerebellum. Less commonly,
erythrocytosis, pancreatic and renal cysts, renal
cell carcinoma and hypernephroma are seen.
Pheochromocytoma occurs in about 10%12. and is more
likely to be bilateral and to recur13. VHL patients tend
to be younger at the age of diagnosis and have their
pheochromocytomas diagnosed early, likely because
of the higher level of suspicion for pheochromocytoma
and its known association with VHL. VHL results from
a mutation in the tumor-supressor gene on chromosome
3p25.314-19. As long as one copy of the VHL gene is
producing functional VHL protein in each cell, tumors
do not develop. If a mutation occurs in the second copy
of the VHL gene during a person's lifetime, the cell
has no working copies of the gene and produces no
functional VHL protein. A lack of this protein allows
tumors characteristic of von Hippel-Lindau syndrome
to develop. Since both alleles need to be mutated for
K. Dortzbach et. al
the disorder to develop, it would be likely to conclude
that the mutation is recessive. However, studying
the patterns of heredity,VHL is, paradoxically, an
autosomal dominant disorder because people who
have already inherited one mutated copy of the gene
have an extremely high probability of developing the
second mutation. An inherited mutation of the VHL
gene is responsible for about 80 percent of cases. In
about 20 percent of cases, however, the altered gene
is the result of a new mutation that occurs during the
formation of reproductive cells (eggs or sperm) or
early in fetal development. This is quite rare because
the probability of a mutation occuring in a cell where
both alleles are previously normal is quite small. Also,
the first mutation must be followed by a second for the
syndrome to develop.
VHL may be diagnosed when one of its associated
diseases causes discomfort20-26. Angiomatosis,
hemangioblastomas, pheochromocytoma, renal cell
carcinoma, pancreatic cysts and café au lait spots
are all associated with VHL. Angiomatosis occurs in
37.2% of patients presenting with VHL and usually
occurs in the retina, however other organs can be
affected. As a result, loss of vision is very common.
On average only about 20% of people with VHL get
pheochromocytomas. The risk of developing such
tumors (which are usually histologically benign)
appears to hinge on the precise nature of the mutation
responsible for VHL disease in a specific family. In
kindreds with VHL who demonstrate a deletion or
protein-truncating mutation of the VHL gene (type
1 VHL), the risk for pheochromocytoma is less than
10%. However, the risk is approximately 50% for
pheochromocytoma development in kindreds with a
missense mutation (type 2 VHL).
There is a wide variation in the age of onset of
the disease, the organ system affected and the severity
of effect suggesting that the second mutation can occur
in different types of cells and at various times of a
person's life.
If a patient with VHL has coexisting lesions or
disorders that require surgical correction in addition
to the removal of the pheochromocytoma, resection
of the pheochromocytoma is prioritized. In patients
with CNS lesions, potential complications exist. If the
intracranial mass is addressed first, the anesthesiologist
VARIANTS OF PHEOCHROMOCYTOMA AND THEIR ANESTHETIC IMPLICATIONS
is faced with the potential for extreme hypertension
leading to intracranial bleeding intraoperatively and
postoperatively. If the decision is made to resect the
pheochromocytoma first, required use of vasodilators
to control hypertension may increase cerebral blood
flow (CBF) and intracranial pressure which may be
offset initially by hyperventilation, placement of an
intraventricular drain or administration of mannitol
and/or furosemide. This dilemma must be discussed
with the operative team, to decide which procedure
takes precedence27.
Multiple endocrine neoplasias (MEN) comprise
three different familial syndromes inherited as autosomal
dominant traits8. MEN I does not have pheochromocytoma
as part of its profile and therefore does not pertain to this
case. MEN IIA (Sipple’s syndrome) includes medullary
thyroid cancer (97%), pheochromocytoma (50%) and
hyperparathyroidism (20%) and is thus more similar to
VHL regarding the presentation of pheochromocytoma.
MEN IIB, rarer than IIA, is associated with medullary
thyroid cancer, pheochromocytoma and a Marfanoid
body habitus and mucosal neuronal syndrome with
mucosal neuromas and intestinal ganglioneuromas. Also,
in MEN IIB, the tumor generally presents late and is
rarely malignant or bilateral9.
In the case of MEN IIA patients, if the
pheochromocytoma is resected before removal of the
parathyroid glands, the calcium level must be checked
as most patients have asymptomatic hypercalcemia.
Symptomatic patients may complain of fatigue,
weakness in general or proximal muscle weakness,
confusion, polyuria, and polydypsia. Patients may also
have findings of hyporeflexia, pseudogout, anemia,
subperiosteal bone resorption, and renal stones.
Abnormal EKG findings include a shortened QT interval
and prolonged PR interval8. Cardiac dysrhythmias
are the most important potential complication of
hypercalcemia. QT intervals do not necessarily
correlate with changes in calcium concentrations, thus
blood gas analyses must be done in conjunction with
blood calcium levels. Management of hypercalcemia
includes intravenous fluid administration with sodiumcontaining solutions, which dilute the calcium and
inhibit renal reabsorption. Urine output must be closely
monitored to assess renal dysfunction.
Other concerns for the anesthesiologist in these
901
cases include muscle relaxant dosing, positioning of
the patient and the potential for airway compromise.
Muscle relaxant effects may be enhanced by
hypercalcemia. Preoperative assessment of muscle
weakness must be documented to record baseline and
to tailor muscle relaxant administration to the patient’s
requirements. Careful positioning of the patient with
appropriate padding is important to avoid pathological
fractures from osteoporosis8. Although bilateral tumors
frequently occur with medullary thyroid cancer,
they are rarely large enough to compress the airway.
However, airway compromise must be considered and
a difficult airway cart made available.
For any patient with VHL or MENIIA/B presenting
for surgery, the diagnosis of pheochromocytoma should
be suspected even if the patient is asymptomatic.
Additionally, patients who have had a previously
resected pheochromocytoma, and are returning for
surgery, should be screened for recurrences and/or for
pheochromocytoma on the unresected side.
Asymptomatic Pheochromocytoma
A subset of pheochromocytomas known as
adrenal incidentalomas is clinically silent. These
tumors likely make a substantial contribution to the
statistic that fifty percent of pheochromocytomas
are discovered post-mortem6. With advancements in
imaging, these lesions are estimated at a prevalence of
almost 3% in middle age to nearly 10% in the elderly13.
These pheochromocytomas may be hormonally
active or inactive and therefore may not be detected
during screening12. While incidentalomas may secrete
catecholamines at a level that leaves the patient
asymptomatic, the lesions are not benign. There has
been an increasing trend to treat these subclinical
tumors given the uncertainty of their association with
increased morbidity.
The undiagnosed pheochromocytoma suspected
intraoperatively during surgery for another medical
condition can have devastating consequences. The
mortality rate is as high as 80%, during anesthesia.
Any hypertensive patient not taking antihypertensive
medications presenting for surgery who complains
of orthostatic hypotension, should be tested for a
diagnosis of pheochromocytoma. As many as 10%
of cases of orthostatic hypotension may be due to
M.E.J. ANESTH 20 (6), 2010
902
pheochromocytomas6,28. Also any patient for surgery
to remove an adrenal mass must be evaluated for
pheochromocytoma.
Preoperative Management
Part of the key to avoiding intraoperative
complications in the removal of pheochromocytomas
is to ensure preoperative optimization. The most
important goal is to achieve blood pressure
control prior to surgery. The alpha adrenergic
blocker, phenoxybenzamine is first line therapy.
Phenoxybenzamine is a non-selective alpha blocker
targeting both alpha 1 and alpha 2 receptors.
The blockade is noncompetitive and irreversible.
Phenoxybenzamine can be started at least two weeks
prior to the scheduled surgery on an outpatient basis
to allow for maximal alpha blockade and restoration
of blood volume given that chronic alpha constriction
causes volume depletion. The protocol for preoperative
alpha blockade requires initially phenoxybenzamine 40
mg per day followed by a gradual increase to 80 to 120
mg per day. Postural hypotension is the most common
side effect. While this relatively simple intervention
cannot promise the prevention of fluctuations in blood
pressure intraoperatively, it has been estimated to
decrease perioperative mortality from 45% to 3%6.
Even patients without cardiovascular symptoms
despite the diagnosis of pheochromocytoma may benefit
from alpha blockade treatment. Apparent preoperative
hemodynamic stability does not preclude severe
intraoperative hemodynamic fluctuations including
increased systemic vascular resistance following
induction of anesthesia and hypotension following
tumor resection. Calcium channel blockers have shown
benefit in patients who are generally normotensive
but with paroxysmal hypertension8. The advantage
is that they do not cause orthostatic hypotension;
however alpha blockers are still considered preferable
in preoperative management. Beta blockade is the
second component to preoperative preparation if the
patient has tachycardia, arrhythmias, or a history of
coronary artery disease. Alpha-adrenergic block must
be established prior to beta-blockade. If beta-blocking
agents are given first, unopposed alpha-blockade and
its consequential vasoconstriction could lead to a life
threatening hypertensive crisis. To ensure optimization
K. Dortzbach et. al
for surgery, it is highly recommended that the patient
meet the Roizen criteria for sufficient alpha blockade
(Table 1)29.
Table 1
Roizen’s Criteria for Appropriate Preoperative
Alpha Blockade and Surgical Optimization
• No in hospital pre-surgical blood pressures
measuring higher than 165/90 24 hours prior
to surgery.
• No orthostatic hypotension with blood
pressure measuring lower than 80/45.
• No EKG showing ST-T changes one week
prior to surgery.
• No more than one premature ventricular
contraction every five minutes.
An echocardiogram should be performed
preoperatively to assess catecholamine related
cardiomyopathy. In patients with cardiomyopathy,
a longer period of preoperative preparation, while
not always practical (some have suggested that as
long as six months treatment with alpha-blockade is
necessary) may help reverse myocardial dysfunction30.
Untreated, a heart stressed by high levels of circulating
catecholamines and arterial hypertension may not
compensate for postoperative hypotension due to
catecholamine withdrawal.
Intraoperative Management
Surgical resection cures 90% of patients.
Laparoscopic removal of pheochromocytomas has
become increasingly common, provided there is no
local invasion and the mass is less than 6cm. Large,
recurrent or invasive pheochromocytomas should
be removed by laparotomy31. While the laparoscopic
approach results in a shorter recovery time, both
laparoscopic and open approaches are equal in terms
of overall survival7. Neither approach has been proven
superior regarding anesthetic management.
The greatest intraoperative concern is the
release of catecholamines leading to life-threatening
hypertension. Hypertensive crises can cause
myocardial infarction, heart failure, dysrhythmias, and
cerebral hemorrhage. Severe hypertension can occur
at any time throughout the surgery but induction,
intubation and tumor palpation tend to be the times of
greatest catecholamine release.
VARIANTS OF PHEOCHROMOCYTOMA AND THEIR ANESTHETIC IMPLICATIONS
Premedication with an anxiolytic such as
midazolam decreases the stress response activating
the sympathetic nervous system. After entering the
operating room and placing standard ASA monitors,
obtaining intravenous access, preferably at two reliable
sites is desirable. Arterial cannulation is necessary
and should be in place prior to induction. The use
of central venous monitoring and pulmonary artery
catheterization depends upon the clinical condition
and should be used in cases of cardiomyopathy and
documented preoperative cardiac compromise.
Induction agents should be titrated slowly to
maintain normotension. A short acting narcotic such
as fentanyl, with its minimal myocardial depression,
in combination with a sedative/hypnotic is preferable
to a sedative/hypnotic agent alone. It is important
to achieve an adequate depth of anesthesia such
that the patient does not respond to the stimulus of
intubation8,31. Vecuronium or rocuronium may be
used for muscle relaxation as these agents have few
if any cardiovascular effects. Pancuronium should
be avoided because of its sympathomimetic effects.
Histamine release caused by atracurium can increase
the release of catecholamines. Succinylcholine should
theoretically be avoided because of its possible
potentiation of catecholamine release from contracting
skeletal muscle6,8. Inhalational agents (isoflurane,
sevoflurane, desflurane) may be used with or without
intravenous agents.
Intraoperatively, alpha blockade is continued
with phentolamine. Phentolamine is a competitive
alpha 1 and alpha 2 receptor blocker32 and is the
single best antihypertensive treatment in managing
hypertensive crises due to pheochromocytoma. Its
most common side effect is reflex tachycardia due to
the baroreceptor reflex following alpha 2 blockade.
Labetalol should be used to control tachycardia.
Calcium channel blockers and nitroprusside, while
sporadically helpful in controlling hemodynamic
fluctuations, do not have the same success as
phentolamine. Based upon the anesthesiologist’s
preference, intravenous nitroprusside (1-2 mcg/kg)
and sublingual nifedipine can be used as second line
therapies. However, the combination of phentolamine
and labetalol ideally render unnecessary the use of
other antihypertensives8.
903
Phentolamine should be titrated in 5 mg
increments intravenously. One technique is to inject
phentolamine 5mg after induction, and before the
tumor is mobilized. With close communication
between the surgeon and anesthesiologist, the
surgeon is asked to stop if necessary so that more
phentolamine can be administered. Thus, blood
pressure control is maintained during tumor resection8.
Over administration of phentolamine may lead to
transient hypotension. Cardiovascular instability may
be such that treatment of hypotension with a pressor
such as ephedrine or other beta adrenergic agents
may rarely lead to significant ventricular irritability
including ventricular tachycardia or even fibrillation.
Thus, careful dosing of phentolamine is extremely
important, however at times very difficult given the
unexpected extreme rises in blood pressure. Transient
hypotension induced by phentolamine may be treated
best with fluid administration and watchful waiting for
a natural rise and return of blood pressure to normal.
In severe symptomatic cases, a magnesium infusion
can be used in addition to phentolamine and labetalol.
Maintaining plasma levels < 2ug/ml (not to potentiate
muscle relaxation) decreases catecholamine levels and
hemodynamic fluctuations and blunts the effects of
stimulation during intubation6.
Following ligation of the vein draining the
pheochromocytoma, intravenous fluid administration
is essential for volume expansion. The sudden drop
in catecholamines can lead to significant hypotension,
requiring aggressive fluid replacement with a
combination of crystalloids and colloids. Pressors
may be necessary to maintain blood pressure in
severe hypotension but they are best avoided and
contraindicated if the patient is hypovolemic. Often
the hypotension of pheochromocytoma is refractory
to agents such as norepinephrine, epinephrine, and
dopamine because of the desensitization of sympathetic
receptors to the previously persistently high levels of
catecholamines8.
Throughout the case, aggressive intravenous fluid
resuscitation is important to account for chronic volume
depletion, hypotension following catecholamine
withdrawal, and intraoperative blood loss, which is
usually minimal with a laparoscopic approach.
The anesthesiologist should also monitor for
M.E.J. ANESTH 20 (6), 2010
904
K. Dortzbach et. al
glycemic changes. Hyperglycemia associated with
increased catecholamine secretion may require insulin.
It almost always resolves with removal of the tumor.
Hypoglycemia may follow tumor resection because of
rebound hyperinsulinism without the inhibitory effect
of norepinephrine on insulin secretion.
Medications That Trigger Catecholamine
Release
Several medications have been shown
to trigger the release of catecholamines from
pheochromocytomas (Table 2). The pressor effects
of metoclopramide are well established. Although
the mechanism by which it does this is unclear,
metoclopramide can cause a serious or even fatal
hypertensive crisis. It should be avoided not only
in patients with pheochromocytomas but also in all
patients with particularly labile blood pressure that
could very rarely be due to this tumor.
Table 2
Medications Reported to Trigger the Release of
Catecholamines in Pheochromocytomas
• Metoclopramide.
• Pentazocaine.
• Droperidol.
• Atracurium.
• SSRIs.
• MAO inhibitors.
• Imipramine.
• Beta-blockers.
• Opioids.
• Curare.
Many of the above medications particularly beta-blockers and opioids
have been used in cases with pheochromocytomas without incidence.
Patients must be treated on an individual basis.
Pentazocaine and droperidol can also increase
release and circulating levels of catecholamines.
Droperidol additionally inhibits the reuptake of
catecholamines into nerve terminals. Any medications
that induce histamine release should be avoided,
including morphine and atracurium. Even small amounts
of histamine can lead to large release of catecholamines
from pheochromocytomas, although practitioners have
used morphine and atracurium without repercussions.
Selective serotonin reuptake inhibitors (SSRI),
monoamine oxidase (MAO) inhibitors, imipramine,
and curare have all been implicated in provoking the
release of catecholamines12,33.
Conclusion
In the case of our 23 year-old male, post mortem
examination revealed an incidentaloma. It is possible
that the patient had episodes of postoperative pain, not
controlled by patient controlled analgesia, which caused
the release of catecholamines. These catecholamines
could have then caused either a hypertensive crises
or cardiac arrhythmias in turn leading to the patient’s
demise. Thus, an undiagnosed pheochromocytoma
should be included as one of the causes of the patient’s
death. It was not seen on radiographic images and the
patient had not been screened for biochemical markers
given he was asymptomatic and had had a history
of prior resection of bilateral pheochromocytomas.
This case raises the question of fully evaluating for
pheochromocytomas in every patient with VHL or with
MENIIA/B regardless of symptomatology or previous
history of pheochromocytoma. Such evaluation is not
a universally accepted standard of care but should be
considered.
Pheochromocytomas have variable ways in which
they may present beyond the well known text book case.
Clinicians must be prepared to identify and treat patients
with such atypical presentations, particularly with the
aging population and their increased incidence of these
tumors. In instances where anesthesiologists find great
lability in perioperative blood pressures, there should
be a higher level of suspicion for pheochromocytoma.
Our case especially emphasizes the need for careful
post-operative monitoring, possibly in an intensive
care unit setting for 24-48 hours.
VARIANTS OF PHEOCHROMOCYTOMA AND THEIR ANESTHETIC IMPLICATIONS
905
References
1. Williams DT, Dann S and Wheeler MH: Pheochromocytomaviews on current management. European Journal of Surgical
Oncology; 2003, 29:483-490.
2. Landsberg and Young JB: Pheochromocytoma. Harrison’s
Principles in Internal Medicine. 14th edition. 1998. TR Harrison.
McGraw-Hill. New York, 2057-2060.
3. Roizen MF: Anesthetic Implications of Concurrent Diseases.
Anesthesia. 5th edition. 2000. RD Miller. Churchill Livingstone.
New York, 924-925.
4. Munakata M, Aihara A, Imari Y, Noshiro T, Ito S, and Yoshinaga
K: Altered sympathetic and vagal modulations of the cardiovascular
system in patients with pheochromocytoma. American Journal of
Hypertension; 1999, 12:572-580.
5. Tahrani AA and Macleod AF: A diagnostic dilemma in diagnosing
and managing an incidental phaeochromocytoma. Exp Clin
Endocrinol Diabetes; 2006, 114:204-207.
6. Myklejord
DJ:
Undiagnosed
pheochromocytoma:
the
anesthesiologist nightmare. Clinical Medicine & Research; 2004,
2:59-62.
7. Bravo EL: Pheochromocytoma: current perspectives in the
pathogenesis, diagnosis, and management. Arq Bras Endocrinol
Metabol; 2004, 48:746-50.
8. Grant F: Anesthetic considerations in the multiple endocrine
neoplasia syndromes. Current Opinion in Anaesthesiology; 2005,
18:345-352.
9. Ailun L, Xiangyang G, Hongzhi R, Yuguang H, and Tiehu Y:
Clinical features and anesthetic management of multiple endocrine
neoplasia associated with pheochromocytoma. Chinese Medical
Journal; 2003, 116:208-211.
10.von Hippel E: Ueber eine sehr seltene Erkrankung der Netzhaut.
Albrecht von Graefes Arch Ophthal; 1904, 59:83-106.
11.Lindau A: Zur Frage der Angiomatosis Retinae und Ihrer
Hirncomplikation. Acta Ophthal; 1927, 4:193-226.
12.Gurunathan U and Korula G: Unsuspected pheochromocytoma: von
Hippel-Lindau disease. Journal of Neurosurgical Anesthesiology;
2004, 16:26-28.
13.Amar L, Servais A, Gimenez-Roqueplo AP, Zinzindohour
F, Chatellier G and Plouin PF: Year of diagnosis features
at presentation, and risk of recurrence in patients with
pheochromocytoma or secreting paraganglioma. The Journal of
Clinical Endocrinology & Metabolism; 2005, 90:2110-2116.
14.Wong WT, Agrón E, Coleman HR, et al: "Genotype-phenotype
correlation in von Hippel-Lindau disease with retinal angiomatosis".
Archives of ophthalmology; 2007, 125 (2):239-45.
15.Abbott MA, Nathanson KL, Nightingale S, Maher ER and
Greenstein RM: The von Hippel-Lindau (VHL) germline mutation
V84L manifests as early-onset bilateral pheochromocytoma. Am J
Med Genet A; 2006, 140:685-90.
16.Beroud C, Joly D, Gallou C, Staroz F, Orfanelli MT and Junien
C: Software and database for the analysis of mutations in the VHL
gene. Nucleic Acids Res; 1998, 26:256-8.
17.Bryant J, Farmer J, Kessler LJ, Townsend RR, and Nathanson KL:
Pheochromocytoma: the expanding genetic differential diagnosis. J
Natl Cancer Inst; 2003, 95:1196-204.
18.Glasker S: Central nervous system manifestations in VHL:
genetics, pathology and clinical phenotypic features. Fam Cancer;
2005, 4:37-42.
19.Maher ER and Eng C: The pressure rises: update on the genetics of
phaeochromocytoma. Hum Mol Genet; 2002, 11:2347-54.
20.Molino D, Sepe J, Anastasio P and De Santo NG: The history of
von Hippel-Lindau disease. J Nephrol; 2006, 19 Suppl, 10:S119-23.
21.Kreusel KM: Ophthalmological manifestations in VHL and NF 1:
pathological and diagnostic implications. Fam Cancer; 2005, 4:437.
22.Kreusel KM, Bechrakis NE, Krause L, Neumann HP and
Foerster MH: Retinal angiomatosis in von Hippel-Lindau disease:
a longitudinal ophthalmologic study. Ophthalmology; 2006,
113:1418-24.
23.Maher ER, Iselius L, Yates JR, Littler M, Benjamin C, Harris R,
Sampson J, Williams A, Ferguson-Smith MA and Morton N: Von
Hippel-Lindau disease: a genetic study. J Med Genet; 1991, 28:4437.
24.Molino D, Sepe J, Anastasio P and De Santo NG: The history of
von Hippel-Lindau disease. J Nephrol; 2006, 19 Suppl, 10:S119-23.
25.Wanebo JE, Lonser RR, Glenn GM and Oldfield EH. The natural
history of hemangioblastomas of the central nervous system in
patients with von Hippel-Lindau disease. J Neurosurg; 2003, 98:8294.
26.Webster AR, Maher ER and Moore AT: Clinical characteristics of
ocular angiomatosis in von Hippel-Lindau disease and correlation
with germline mutation. Arch Ophthalmol; 1999, 117:371-8.
27.Umgawar M, Rajender Y, Purohit A, Sastry RA, Sundaram C
and Rammurti S: Anesthetic management of von Hippel-Lindau
syndrome for excision of cerebellar hemangioblastoma and
pheochromocytoma surgery. Anesthesia & Analgesia; 1998, 86:673674.
28.Mansmann G, Lau J, Balk E, Rothberg M, Miyachi Y and
Bornstein SR: The clinically unapparent adrenal mass: update in
diagnosis and management. Endocrine Reviews; 2004, 25:309-340.
29.Roizen MF, Schreider BD and Hassan SZ: Anesthesia for patients
with pheochromocytoma. Anesthesiol Clin North Am; 1987, 5:26975.
30.Shupak RC: Difficult anesthetic management during
pheochromocytoma surgery. Journal of Clinical Anesthesia; 1999,
11:247-250.
31.Pederson LC and Lee JE: Pheochromocytoma. Current Treatment
Options in Oncology; 2003, 4:329-37.
32.Mycek MJ, Harvey RA and Chaupe PC: Lippincott’s Illustrated
Reviews Pharmacology, 2nd edition. Lippincott-Raven. Philadelphia;
1992, pp. 71-71.
33.Anon: Phaeochromocytoma unmasked by drug therapy. Prescrire
int; 2003, 12:181-2.
M.E.J. ANESTH 20 (6), 2010
ANESTHETIC MANAGEMENT OF ACHONDROPLASTIC
DWARF UNDERGOING CESAREAN SECTION
- A Case Report Banu Çevik* and Serhan Çolakoğlu*
Abstract
There are more than 100 different types of dwarfism. Achondroplasia is the most common
of these conditions. The aim of this report is to describe the anesthetic management of these
patient, discussing the anesthetic considerations and emphasizing the difficulties encountered.
A 32-year-old achondroplastic parturient underwent cesarean section under general anesthesia.
We did not encounter problems related with airway management. The operation went without
any complication. There are risks for both regional and general anesthesia in achondroplastic
patients. The most important point is the careful preoperative assessment. Anesthesia plan should
be specified to individual basis.
Introduction
Various uncommon disorders present in pregnant women can create a dilemma for obstetricians
and obstetric anesthesists as to how to best manage these patients. Achondroplastic dwarfism is
one of these disorders and the clinical management remains controversial1. Achondroplasia is
the commonest form of dwarfism, in which a large number of cases resulted from spontaneous
mutation. The incidence varies between 4 and 15 per 100,000 live births. Females are affected
more frequently than males2.
Achondroplastic patients present several problems for both general and regional anesthesia.
We describe a patient with achondroplasia undergoing Cesarean section and discuss the anesthetic
considerations in achondroplastic individuals.
Case Report
A 32-yr-old primagravid achondroplastic dwarf presented for elective Cesarean section at 37
weeks’ gestation. She had no previous history of anesthesia and her pregnancy had been uneventful.
Her history included no relevant conditions. She was taking prenatal vitamins and had no known
allergies.
Physical examination revealed a 49-kg, 135 cm, normal intelligent female with large head,
short limbs and mild kyphoscoliosis. She had short neck, large tongue, protruded chin, full set of
teeth. Mouth opening was adequate with Mallampati II airway and neck extention was not limited.
Examination of cardiorespiratory system revealed no problems and there was no neurological
abnormalities. Preoperative hemoglobin and electrolyte concentrations were within normal limits.
Ultrasonic measurements in utero suggested that the fetus was normally developed.
*
MD, Department of Anesthesiology and Reanimation, Dr. Lütfi Kirdar Kartal Training and Research Hospital, Istanbul,
Turkey.
Correspondong author: Banu Çevik, MD, Bağdat Cad., Noter Sok, Yazicioğlu Apt. 10/12 Erenköy/Istanbul/Turkey. Phone: (0216)
4413900/1298, E-mail: [email protected]
907
M.E.J. ANESTH 20 (6), 2010
908
The patient was very anxious and she did not
desire to be awake during procedure. Therefore, after
discussion of potential risk and written informed
consent, it was decided to performe the operation
under genral anesthesia. Appropriate sized facemasks,
tracheal tubes, stillettes, laryngeal mask airways
(LMATM) and intubating laryngeal mask airways
(ILMATM) were prepared for possible difficulty in
intubation.
No premedication was given and she was
monitored by non-invasive arterial pressure,
electrocardiogram (ECG) and pulse oxymetry on
arrival in the operating room. Anesthesia was induced
with thiopenthal and neuromuscular blockade was
achieved with succinylcholine. Trachea was intubated
at the first attempt with a 7.0-mm ID endotracheal
tube. Lower segment cesarean section proceeded
and a live baby was delivered weighing 3200 grams
with APGAR scores of 8 and 9 at the first and the
fifth minutes respectively. Maintenance of anesthesia
was provided by sevoflurane in 50% oxygen-nitrous
oxide mixture. Muscle relaxation was achieved with
vecuronium the patient was given oxytocin and
fentanyl after the umbilical cord was clamped. No
other medication was given during the procedure. The
total duration of anesthesia was 1h and all monitored
parameters (ECG, pulse oxymetry, endtidal CO2 and
non-invasive blood pressure) remained stable. At the
end of the operation, neuromuscular blockade was
reversed with neostigmine 0.05 mg.kg-1 and atropine
0.02 mg.kg-1 and the trachea was extubated when
the patient was fuly awake. The patient was taken to
postanesthesia care unit and administered 5 l.min-1 of
oxygen through a face mask until transferring to the
ward. The postoperative period was uneventful and the
patient and neonate were discharged on the fifth day.
Discussion
Achondroplastic
dwarfs
characteristically
have low fertility rates; however, they often require
delivery by cesarean section because the normal-sized
fetal head and smaller than normal maternal pelvic
diameter result in cephalopelvic disproportion during
the later stages of pregnancy3. These patients have a
number of anatomic and physiological abnormalities
that contribute to problems with the administration of
B. Çevik & S. Çolakoğlu
obstetric anesthesia.
Achondroplastic patients have facial features that
alert the anesthesists to potential problems in airway
management4. They have narrow nasal passages and
pharyngeal and maxillary hypoplasia. Maintenance
of a patent upper airway may be difficult because
of the presence of a large tongue and mandible. The
base of the skull is shorted (because of early fusion
of constituent bones) and angulated, yielding a
limited extension and making endotracheal intubation
potentially difficult1,5. On the other hand, not all
authors have encountered difficulties. Mayhew et al.6
reported no difficulty in airway management or direct
laryngoscopy in a series of 27 patients undergoing
36 anesthetic procedures. They also suggested that is
tracheal intubation was required, a small tracheal tubes
should have been selected. There are reports describing
the achondrplastic patients with classical symptoms
and signs of upper airway obstruction but no difficulty
encountered7-11.
We elected to use general anesthesia for two
reasons. First of all, the patient wanted to be asleep
because of her anxiety. Secondly, preoperative
examination suggested no possibility of a difficult
airway. Consequently, the intubation was completed in
the first attempt without any undesirable effects.
Several anatomical abnormalities found in
achondroplasia may complicate regional techniques.
Difficulties may result from kyphoscoliosis and
other spinal abnormalities, included narrowing of the
vertebral canal, shortening of the pedicles, reduced
interpedicular distance (particularly in the lower
lumbar spine) and osteophyte formation. Spinal
stenosis may impair cerebrospinal fluid flow, such that
identification of dural puncture is more difficult. Also
the presence of narrow epidural space make insertion
of catheter difficult12. Engorged epidural veins increase
the risk of venous puncture either by the Tuohy needle
or the catheter, and result in an unpredictable spread of
local anesthetic within the space13.
We found reports related with achondroplasia
which had successfully managed by regional
anesthesia. These are spinal14-17, epidural3,5,13,18-20 or
combined spino-epidural (CSE) techniques4.
In these reports, technically challenging problems
owing to skeletal abnormalities and the appropriate
ANESTHETIC MANAGEMENT OF ACHONDROPLASTIC DWARF UNDERGOING CESAREAN SECTION
dose of drugs were discussed. Ravenscroft et al.16 were
successful in one patient with the spinal anesthetic dose
decreased by 30%. DeRenzo et al.17 also reduced the
intracheal dose of bupivacaine from 12 to 10 mg with
the addition of 0.2 mg morphine for the relief of postcesarean section pain21. In that report, the patient had
experienced discomfort, requiring iv sedation for forty
minutes after delivery. The suggested that decreasing
the intracheal dose was not unreliable.
It’s suggested that epidural anesthesia was
theoretically preferable to spinal anesthesia because of
ability to titrate the level of block. Incremental doses
of anesthesia could be required due to maternal short
stature and kyphoscoliosis1,4. Trikha et al.4 preffered
CSE over a spinal or epidural technique because it
909
combines the rapid onset of spinal anesthesia with
the implantation of epidural catheter. This approach
provided prolonged anesthesia and excellent
postoperative analgesia. DeRenzo et al.17 also reported
that titratable techniques such as epidural, CSE,
continuous spinal would have been beter suited for
these paitents.
In conclusion, the risks of both regional and
general anesthesia in achondroplastic patients are
known. With the above factors taken into consideration,
a complete history and physical examination before
administration of anesthesia can help to reduce risks.
The anesthesia plan should be based on each indivdual
case and the potential risks must be discussed with the
patient.
M.E.J. ANESTH 20 (6), 2010
910
B. Çevik & S. Çolakoğlu
References
1. Kuczkowski KM: Labor analgesia for the parturient with an
uncommon disorder: A common dilemma in the delivery suite.
Obstet Gynecol Surv; 2003, 58(12):800-3.
2. Eisenach JC: Orthopedic disease. In: Obstetrical Anesthesia: The
Complicated Patient (James FM, Wheeler AS, Dewan DM eds) 2dn
ed. FA Davis Company. Philadelphia 1998, p. 239.
3. Brimacombe JR, Caunt JA: Anaesthesia in a gravid achondroplastic
dwarf. Anaesthesia; 1990, 45(2):132-4.
4. Trikha A, Goyal K, Sadera GS, Singh M: Combined spinal epidural
anaesthesia for vesicovaginal fistula repair in an achondroplastic
dwarf. Anaesth Intensive Care; 2002, 30(1):96-8.
5. Morrow MJ, Black IH: Epidural anaesthesia for caseran section in
an achondroplastic dwarf. Br J Anaesth; 81(4):619-21.
6. Mayhew JF, Katz J, Miner M, Leiman BC, Hall ID: Anaesthesia for
the achondroplastic dwarf. Can J Anaesth; 1986, 33(2):216-21.
7. Krishnan BS, Eipe N, Korula G: Anaesthetic management of a
patient with achondroplasia. Paediatr Anaesth; 2003, 13(6):547-9.
8. Kalla GN, Fening E, Obiaya MU: Anaesthetic management of
achondroplasia. Br J Anaesth; 1986, 58(1):117-9.
9. Monedero P, Garcia-Perdajas F, Coca I, Fernandez-Liesa
JI, Panadero A, de los Rios J: Is management of anesthesia in
achondroplastic dwarfs really a challenge? J Clin Anesth; 1997,
9:208-12.
10.Huang J, Babins N: Anesthesia for cesarean delivery in an
achondroplastic dwarf: a case report. AANAJ; 2008, 76(6):435-6.
11.Ghumman S, Goel N, Rajaram S, Singh KC, Kansal B, Dewan P:
Pregnancy in an achondroplastic dwarf: a case report. J Indian Med
Assoc; 2005, 103(10):536-8.
12.Berkowitz ID, Raja SN, Bendor KS, Kopits SE: Dwarfs:
Pathophysiology and anesthetic implications. Anesthesiology; 1990,
73:739-59.
13.Wardall GJ, Frame WT: Extradural anaesthesia for Cesarean
section in achondroplasia. Br J Anaesth; 1990, 64(3):367-70.
14.Crawford M, Dutton DA: Spinal anaesthesia for caeserean section
in an achondroplastic dwarf. Anaesthesia; 1992, 47(11):1007.
15.McGlothlen S: Anesthesia for cesarean section for achondroplastic
dwarf: a case report. AANA J; 2000, 68(4):305-7.
16.Ravenscroft A, Govender T, Rout C: Spinal anesthesia for
emergency cesarean section in an achondroplastic dwarf.
Anaesthesia; 1998, 53:1236-7.
17.DeRenzo JS, Vallejo MC, Ramanathan S: Failed regional
anesthesia with reduced spinal bupivacaine dosage in a parturient
with achondroplasia presenting for urgen cesarean section. Int J
Obstet Anesth; 2005, 14(2):175-8.
18.Cohen SE: Anesthesia for cesarean section in achondroplastic
dwarfs. Anesthesiology; 1980, 52(3):264-6.
19.Carstoniu J, Yee I, Halpern S: Epidural anaesthesia for cesarean
section in an achondroplastic dwarf. Can J Anaesth; 1992,
39(7):708-11.
20.Waltz IF, Finerman G, Wyatt GM: Anaesthesia for dwarfs and
other patients of pathological small stature. Can J Anaesth; 1975,
22(6):703-9.
21.Abboud TK, Dror A, Mosaad P et al: Mini-dose intracheal
morphine for the relief of post-cesarean section pain: safety, efficacy
and ventilatory responses to carbon dioxide. Anesth Analg; 1988,
67:137-43.
GUIDELINES FOR AUTHORS
The Middle East of Anesthesiology publishes original
work in the fields of anesthesiology, intensive care, pain, and
emergency medicine. This includes clinical or laboratory
investigations, review articles, case reports and letters to the
Editor.
Submission of manuscripts:
The Middle East Journal of Anesthesiology accepts
electronic submission of manuscripts as an e-mail attachment
only.
Manuscripts must
attachment to:
be
submitted
via
email
Editor-In-Chief,
Department of Anesthesiology,
American University of Beirut Medical Center
Beirut, Lebanon
E-mail: [email protected]
Human Subjects
Manuscripts describing investigations performed in
humans must state that the study was approved by the appropriate
Institutional Review Board and written informed consent was
obtained from all patients or parents of minors.
Language:
Articles are published in English.
Manuscript Preparation
Manuscript format required:
Double-spaced lines
Wide margins (1.5 inches or 3.8 cm)
Page numbers start on title page
Word count should reflect text only (excluding abstract,
references, figures and tables).
Editorial
1500
Abstract
250 (General articles)
100 (Case Reports)
Clinical or laboratory investigations:
The following structured format is required:
1. Cover Letter
7. Discussion
2. Title page
8. Acknowledgements
3. Abstract
9. References
4. Introduction
10. Tables
5. Methods
11. Figures
6. Results
1. Cover Letter
Manuscripts must be accompanied by a cover letter,
signed by all authors and stating that:
- All authors have contributed intellectually to the
manuscript and the manuscript has been read and
approved by all the authors.
- The manuscript has not been published, simultaneously
submitted or accepted for publication elsewhere.
2. Title Page
Starts at page 1 and includes:
- A concise and informative title (preferably less than 15
words). Authors should include all information in the
title that will make electronic retrieval of the article both
sensitive and specific.
- Authors listing: first name, middle initial and last name
with a superscript denoting the academic degrees as
footprints.
- The name of the department(s) and institutions(s) to
which the work should be attributed.
- The name, address, telephone, fax numbers and e-mail
address of the corresponding author.
- Disclose sources of financial support (grants, equipment,
drug etc…).
- Conflict of interest: disclosure of any financial
relationships between authors and commercial interests
with a vested interest in the outcome of the study.
- A running head, around 40 characters.
- Word count of the text only (excluding abstract,
acknowledgements, figure legends and references).
Review article
4000
Original article
3000
Case Reports
800
3. Abstract
Letter to Editor
500
Abstract should follow the title page. It should be
structured with background, methods, results and conclusion.
M.E.J. ANESTH 20 (6), 2010
It should state, the specific purpose of the research or
hypotheses tested by the study, basic procedures, main findings
and principal conclusions.
Provide separate word count for the abstract.
4. Introduction
Provide the nature of the problem and its significance.
State the specific purpose or research objectives or hypothesis
tested. Provide only directly pertinent references and do not
include data or conclusions from the work being reported.
5. Methods
A. Selection and description of participants:
- Describe selection of participants (including controls)
clearly, including eligibility and exclusion criteria.
B. Technical information:
-Identify the methods, apparatus (give the
manufacturer’s name and address in parentheses),
and procedure in sufficient detail to allow others
to reproduce the results. Give references to
established methods. Provide references and brief
descriptions for methods that have been published.
Identify precisely all drugs and chemicals used,
including generic names(s), dose(s) ands routes(s)
of administration.
C. Statistics-describe statistical methods with enough
detail to enable a knowledgeable reader with access to
the original date to verify the reported results. Define
statistical terms, abbreviations and most symbols.
Specify the computer software used. Provide a power
analysis for the study.
6. Results
Present your results in logical sequence in the text, tables
and illustrations, giving the main or most important findings
first. Do not repeat all the data in the tables or illustrations
in the text: emphasize or summarize only the most important
observations. Extra or supplementary materials and technical
details can be placed in an appendix.
7. Discussion
Emphasize the new and important findings of the study
and the conclusions that may be drawn.
Do not repeat in details data or other information given
in the Introduction or the Results sections. For experimental
studies, it is useful to begin the discussion by summarizing
briefly the main findings, then explore possible mechanisms or
explanations for these findings, compare and contrast the results
with other relevant studies. State the limitations of the study,
and explore the implications of the findings for future research
and for clinical practice. Link the conclusions with the goals of
the study, but avoid unjustified statements and conclusions not
adequately supported by the data.
8. Acknowledgements
They should be brief. Individuals named must be given
the opportunity to read the paper and approve their inclusion in
the acknowledgments.
9. References
- References should be indicated by Arabic numerals in
the text in the form of superscript and listed at the end
of the paper in the order of their appearance. Please be
accurate, giving the names of all authors and initials, the
exact title, the correct abbreviation of the journal, year of
publication, volume number and page numbers.
- The titles of journals should be abbreviated according
to the style used in the list of Journals Indexed for
MEDLINE.
Example: (1) from a journal (2) from a book.
1.SHAWW: AND ROOT B: Brachial plexus anesthesia
Comparatives study of agents and techniques. Am. J.
Surg.; 1951, 81:407.
2. ROBINSON JS: Modern Trends in Anaesthesia, Evans
and Gray Ch. 8, Butterworth Pub. Co., London 1967.
10. Tables
Tables capture information concisely and display it
efficiently: They also provide information at any desired level
of details and precision. Including data in tables rather than text
frequently makes it possible to reduce the length of the text.
- Type or print each table with double spacing on a separate
sheet of paper.
- Number tables consecutively in the order of their first
citation in the text.
- Supply a brief title for each.
- Place explanatory matter in footnotes, not in the
heading.
- Explain all nonstandard abbreviations in footnotes.
- Identify statistical measures of variations, such as
standard deviation and standard error of the mean.
11. Figures
- Figures should be submitted in JPEG or TIFF format
with a minimum of 150 DPI in resolution.
- Colored data if requested by author is chargeable.
- If a figure has been published previously, acknowledge
the original source and submit written permission from
the copyrights holder to produce the figure.
Abbreviations and symbols:
- Use only standard abbreviations.
- Avoid abbreviations in the title of the manuscript.
-The spelled-out abbreviations followed by the
abbreviation in parenthesis should be used in first
mention.