March 2017 vol3 issue1

ANAESTHESIOLOGYANAESTHESIOLOGYANAESTHESIOLOGY
M.P.M.P.
Editor: Dr. Meenu Chadha
Co-editor: Dr. Harsha Desai Phulambrikar
?March 2017 Volume 3? ?Issue 1

Anaesthesiology M.P. 1
CONTENTS
Exective Body of
M.P. State 2016-2017
EDITOR
CO-EDITOR
Dr. Harsha Desai Phulambrikar
EDITORIAl BOARD
Dr. Ashwin Soni, Dr. Suman Gupta,
Dr. Ruchi Tandon, Dr. Ashish Sethi
Dr. Harsh Mangal
Dr. Meenu Chadha
Senior Anaesthesiologist,
& Pain Physician
CHL Hospital Indore.
chadha.meenu@gmail.com
9977161035
Consultant Anaesthesiologist
Greater Kailash Hospitals, Indore
harshaphulambrikar@gmail.com
Dr. Meenu Chadha
From Editor's Desk - Smoking and back pain
021
Dr. P.N.Jain
A rational approach to cancer pain management
042
Dr. Harsh Kasliwal, Dr. M.M. Neema,
Dr. Tejinder Singh Ajmani
Evaluation of Thiopentone Sodium, Propofol and
Midazolam for modified electro convulsive therapy
08
3
Dr. Suman Gupta, Dr. Preeti Goyal, Dr. Bhanu Choudhary
Documentation of Anaesthesia Records-
A Prerequisite for good Anaesthesiologists.
164
Dr. Gyanesh Namjoshi
Case report: Aortic Valve replacement in a patient of
Parkinson's disease with deep brain stimulator
225
Dr. Kriti Vig, Dr. Kunal Waghmare, Dr. Gyanesh Namjoshi
Dr. R. Nalgirkar
Post Myocardial Infarction Ventricular Septal defect
276
Dr. Teena Desai, Shaila Kamat, Deepa
Comparison of Acute Physiology and Chronic Health
Evaluation-II (APACHE-II) Score and sequential organ
Failure Assessment (SOFA) Score ... Pneumonia (VAP
337
Dr. Sadhana Sanwatsarkar, Dr. Dipit Saxena, Dr Vibhu Gupta
Neurosurgery and Pregnancy : A Unique
Anaesthetic Challenge
438
Dr. Jyotsna Agarwal
A Tribute to Dr. Chandy Varghese
479
President
Dr. Sanjay Khanna
Senior Pain Consultant, Jabalpur
dr_khannahp@gmail.com
9826186423
Vice President
Dr. Avtar Singh Yadav
Assoc. Professor
Dept. of Anaesthesiology
S.S. Medical College, Rewa
dravtaryadav@gmail.com
9861599520
Hon. Secretary
Dr. Surendra Raikwar
Assoc. Professor
Gandhi Medical College, Bhopal
drskraikwar@gmail.com
94065 33300
Hon. Treasurer
Dr. R.P. Kaushal
Professor Cardiac Anaesthesiologist,
Gandhi Medical College, Bhopal
rpkaushal@rediffmail.com
9617377134
ADVISORS
Dr. T.C. Kriplani, Dr. V.M. Agnihotri
Dr. R.C. Agarwal, Dr. V.K. Joshi
Dr. M.M. Neema, Dr. Bhanu Ved
Dr. K.G. Vijayan, Dr. K.K. Arora
Dr. Shikha Mehrotra, Dr. Aditya Agarwal
Dr. Dilip Kothari, Dr. Sadhana Sanwatsarkar
DR. Sudhakar Diwedi

ow back pain is one of the leading causes of
disability all over the world. There is lot ofLresearch being done on the impact of smoking on
back pain. Smoking is found to be one of the major
causes of musculoskeletal pains. Besides causing
various medical conditions like lung cancer,
chronic bronchitis and coronary artery disease
smoking is also the root cause of many
musculoskeletalproblems.Itmaycausechangesin
the pain process and may also result in structural
changes in other systems that will predispose to
powerfulmusculoskeletalconditions.
Epidemiologically smoking alters the pain
process so patients have more pain. Long term
exposuretonicotinecausesacetylcholinereceptor
desensitization and causes tolerance to nicotine
induced antinociception. Further stopping
smoking (withdrawal from nicotine) causes
hyperalgesia. A Norwegian study has shown that
smokers with musculoskeletal disorders had
1
increased pain as compared to nonsmokers . .
Smoking also causes changes in other systems that
predispose to increased pain. It also accelerates
2
degenerative process and increases risk of injury .
Smokers have increased disc degeneration,
impaired healing, increased risk of injury and
impaired pain pathways. This may be due to
impairmentofoxygendeliverybecauseofincrease
in sympathetic outflow and carboxyhaemoglobin
level.
Another study has shown that though smokers
had increased pain scores and required more
hydrocodone but still they had lower hydrocodone
levels than nonsmokers. Smoking also decreases
bone mineral content and increases incidence of
fracture and delayed fracture healing. Research
has shown that smoking is associated with low
3
back pain independent of other cofactors .
Psychological factors and depression also
contribute to interaction between smoking and
chronicpain(Fig1).
Fig 1- Potential mechanism of chronic pain in
smokers
An Australian review of twin studies has shown
that genetics also plays a dose response role, with
genetic factors contributing to chronic and
4
disabling pain than to acute pain . A Turkish study
of risk factors also found a strong association
between back pain and illiteracy, low
socioeconomic strata and labor intensive
5
occupation inadditiontosmoking.
Thus those patients who stopped smoking
Anaesthesiology M.P.2
SMOKING AND BACK PAIN
EDITORIAL
DR. Meenu Chadha

during their care had greater improvement than
those who continued smoking and patients who
did not quit smoking had no improvement in back
pain despite a treatment program for back pain.
Therefore to maximize the effectiveness of the
pain treatment for back pain, stopping smoking is
essential.
"We conclude that smoking increases risk of
transitioning to chronic back pain, an effect
mediated by corticostriatal circuitry involved in
addictivebehaviorandmotivatedlearning."
1. Eriksen WB, Brage S, Brusgaard D. Does
smoking aggravate musculoskeletal pain?
ScandJRheumatol1997;26(1):49-54
Refrences:
2. Shi Y, Weingarten TN, Mantilla CB, Hooten WM,
WarnerDO.Smokingandpainpathophysiology
and clinical implications. Anesthesiology
2010;113(4):977-992.
3. Abate M, Vanni E, Pantelone A, Salini V.
Cigarette smoking and musculoskeletal
disorders. Muscles Ligaments Tendons J.
2013:3(2):63-69
4. Ferreira PH, Beckenkamp P, Maher CG, Hopper
JL, Ferreira ML. Nature or nurture in low back
pin? Results of systematic review of studies
based on twin samples. Eur J Pain
2013;17(7):957-971
5. UndeAyat P, Aydin ON, Ogurlu M. Risk factors
associated with lower back pain un the
Polyclinic of Algology. Agri 2012;24 (4);165-
170.

1. Professor, Dept. ofAnesthesiology, Critical Care & Pain, Head Division of Pain
Tata Memorial Hospital, Mumbai
Magnitude of the problem
1
Prevalence of pain:
In India, about 1 million new cancer
patients are diagnosed every year. A stastistical
data suggests that approximately 60-80%
patients, when they are diagnosed, are advanced
cases & hence incurable. Often, their major
symptom is moderate to severe pain. According to
present estimates, about 56% cancer patients
require relief of symptoms (palliative care) at any
given time in India, however, only 28% are
provided some sort of palliative care before they
die. There is an immediate need to address this
issue at all levels. Clinicians should reassure
patients & their families that most pain can be
relieved throughout the course of illness. Health
professionals should encourage patients to be
active participants in pain management. State
regulatorybodies should not hamper the supply &
collaborate with patients and their families taking
the costs of the drugs & technologies into
accounts in selecting pain management
strategies.
A systematic review (2007) of 6000 patients
including 54 studies during 1964-2005 found
following prevalence of cancer pain. Despite clear
World Health Organization guidelines (1986) pain
stillisamajorproblem.
• Painaftercurativetreatment,33%
A RATIONALAPPROACH TO CANCER PAIN
MANAGEMENT
1
lDr. P.N. Jain
• Painduringactiveanticancertherapy59%
• Duringadvanceddisease64%
• Atalldiseasestages53%
• >33% patients grade their pain as moderate or
severe
Pain control merits high priority for two
reasons. First under-relieved pain causes
unnecessary suffering. Because pain diminishes
activity, appetite, and sleep, it can further weaken
an already debilitated patient. The psychological
effectofcancerpaincanbedevastating. Pain
is defined as 'an unpleasant sensory & emotional
experience associated with actual or potential
tissue damage or described in terms of such
damage'(InternationalAssociationfortheStudyof
Pain 1979). The perception of pain is modulated
by the patient's mood, morale & the meaning of
the pain for the patient. Pain in cancer may be
caused by the cancer itself or by its treatment
(radiation, chemotherapy & surgery) or its related
debilityorconcurrentdisorder.
• Functional (physiological e.g. cramp,
myofascialpain,colic)
• Organic(pathologicale.g.trauma,cancer)
Importance of controlling cancer pain:
Classification of pain:
Nociceptive :

· Somatic pain arising from the covering of the
body,i.e.skin,subcutaneoustissue.
Visceralpainarisesfromviscera.
· Nervecompression(e.g.sciatica)
· Neuralinjury
· Peripheral(e.g.postherpeticneuralgia)
· Centralsympatheticallymaintainedpain
Bone pain is the most common kind of pain
causedby cancer. Upto 85% of patients dying from
breast, prostate or lung cancer demonstrate bone
involvement at autopsy. Bone pain affects 28%
hospice in-patients, 34% in cancer pain clinic &
45% advanced patients at home. The gold
standardtreatmentisradiotherapy.
Neuropathic Pain: Defined as pain arising due
to lesion or disease in the somatosensory nervous
system(NeuPSIG2008).Itcanbecausedbycancer
directly invading the nervous system or cancer
treatment itself causing pain e.g chemotherapy
induced peripheral neuropathy (CIPN),
radiotherapy induced pain or pain caused by
surgery i.e. phantom limb pain. Neuropathic
cancer pain is caused by cancer directly while
neuropathic pain in cancer is caused by treatment
or due to co-morbid conditions e.g diabetic
neuropathy, post herpetic neuralgia. Now
treatment guidelines have been released by the
International neuropathic pain group (neuPSIG,
2
2015).
Relief of pain may be achieved by the following
methods:
· Explanation
· Modificationofpathologicalprocess
· Elevationofpainthreshold
·
Non-Nociceptive (Neuropathic) :
Bone Metastases:
Principles of pain management:
· Interruptionofpainpathways
· Modification oflifestyle &immobilization
· Reliefatnight
· Reliefatrestduringtheday
· Relief on movement (this is not always
completelypossible)
Assess relief in relation to each pain. Whether
pain is somatic, visceral or neuropathic or mixed
assess different components of each pain. If
marked anxiety and/or depression, it may take 2-4
weeks to achieve optimum results. Pain score
should be assessed on 0-10 numerical rating scale
(NRS), where 0 is “no pain” and 10 is “worst
possible pain”. Reassessment is a continuing
necessity. Various QOL scales are available e.g. Mc
GillPainquestionnaire,Briefpaininventory(BPI).
Useofanalgesics:
“By the mouth”-The oral route is the preferred
routeforanalgesics,includingmorphine.
“By the clock”- Persistent pain relief requires
preventive therapy. This means that analgesics
should be given regularly & prophylactically. “ As
needed”medicationisirrational&inhumane.
“By the ladder”-use a three-step WHO
analgesicladder:
Step1:nonnarcotics(NSAIDS)
Step2:mildopioids(Codeine,pentazocine)
Step3:strongopioids(morphine)
If a drug falls to relieve, move up the ladder. Do
notmovelaterallyinthesameefficacygroup.
“For the individual”-The right dose of an
Goals of pain management:
Pain Assessment:
Pharmacotherapy of pain: WHO ladder
Approach

analgesicisthedosethatrelievesthepain.
“Monitored treatment”-The response to
treatment must be monitored to ensure that
benefits of treatment are maximized & adverse
effectsminimized.
“Use adjuvant drugs”-A laxative is almost
always necessary with an opioid: > 50% of patients
needananti-emetic.
3
Oral analgesics are the mainstay of
therapy for cancer pain. An estimated 70-90% of
patients can be rendered relatively free of pain,
when rational principles of pharmacological
management are applied in a thorough & careful
manner. The World Health Organization has
adopted a 'ladder' approach to cancer pain
management that relies exclusively on the
4
administrationoforalanalgesia.
These agents are effective when administered
as the sole drug treatment for mild pain. They may
be combined with opioids to treat moderate to
severepain.
Paracetamol is a safe step 1 WHO ladder
analgesics. NSAID's have analgesic, anti-
inflammatory & antipyretic activity. They can be
given orally, rectally, intramuscularly as well as by
topical application and are the first line agents for
mild to moderate cancer pain. There is increasing
evidence to suggest that these drugs may have
uniqueroleinmanagementofcertainkindsofpain
from bone metastases. Side effects of NSAIDs
should be carefully monitored. Cox-2 NSAIDs (e.g.
Celecoxib, Etoricoxib) have been introduced in
practice, which are considered relatively safe in
termsofgastricmucosaandplatelets.
They are the mainstay treatment in moderate
Oral Analgesics:
I) Non-opioid ( Non-narcotic ) analgesics :
II) Opioids :
to severe cancer pain because of their
effectiveness, ease of titration & favorable risk-to-
benefitratio.Opioidsdonothaveaceilingeffectto
their analgesic efficacy & will not reverse or
antagonise the effects of other opioids within this
classgivensimultaneously.Side effects include
constipation, nausea, vomiting, itching, urinary
retention, confusion, sedation & rarely respiratory
depression if patient is not opioid naïve. Drug
tolerance, physical dependence, addiction are no
morebigclinicalissues.
Morphine is the most commonly used opioid
for moderate to severe pain because of it's
availabilityin a widevarietyof dosageand forms. It
has well characterized pharmacokinetic &
pharmacodynamic profile & relatively low cost.
Recommended starting dose is usually 10 mg 4
hourly.
Guidelines for the use of opioids in the
managementofcancerpain–
1. Start with a specific drug for a specific type of
pain.
2. Know the pharmacologyof the drug prescribed
verywell.
3. Adjust the route & dose of the drug as per
patient'sneed&comfort.
4. Use drug combination for additive effects &
reducesideeffects
5. Anticipate&treatthesideeffectsaggressively.
6. Prevent acute withdrawal by slowly tapering
doses.
7. Anticipate & manage complications like
overdose,seizures&myoclonusetc.
Adjuvants play a major role for pains that
are insensitive to opioids. They are also useful in
counteracting the side effects of the pain
III. Adjuvant Drugs:

medications like nausea, vomiting, itching,
dyspepsia, constipation etc. The mainly used
adjuvantsareasfollows:
1 Corticosteroids
2 Antidepressants(amitryptyline)
3 Anticonvulsants(gabapentin)
4 Other drugs: Antacids, H2 blockers, laxatives,
stool softeners, antiemetics, antihistaminics &
antipsychotic drugs etc. Radiopharmaceutical
agents like bisphosphonates may be used in
once a week infusion in bone metastasis with
good relief. Inj calcitonin also has a role in pain
reliefdueosteolyticlesions.
1. Van den Beuken-van Everdingen MH, de Rijke
JM, Kessels AG, Schouten HC, van Kleef M,
References
Patijn J. Prevalence of pain in patients with
cancer: a systematic review of the past 40
years.AnnOncol.2007:18(9):1437-49.
2. Nanna B Finnerup, Nadine Attal, Simon
Haroutounian, Ewan McNicol et al
Pharmacotherapy for neuropathic pain in
adults: a systematic review and meta-analysis
LancetNeurology2015;143(2):162–173
3. Bennett MI, Rayment C, Hjermstad M, Aass N,
CaraceniA, KaasaSPrevalenceandaetiologyof
neuropathic pain in cancer patients: a
systematicreview.Pain.2012:153(2):359-65.
4. ZechDF,GrondS,LynchJ,HertelD,LehmannKA
Validation of World Health Organization
Guidelines for cancer pain relief: a 10-year
prospectivestudy.Pain.1995;63(1):65-76.

ABSTRACT:
Modified Electroconvulsive therapy (MECT),is
anevidencebased,safeandestablishedtreatment
for various psychiatric diseases that includes
acute mania, major depressive disorder,
schizophrenia, suicidal tendency and many more
conditions.Government of India and World health
organization has mandated use of sedative /
anesthetic drug to make MECT an acceptable
methodoftreatment.
MECT is administered under anesthesia to
control acute cardiovascular, cerebrovascular and
musculoskeletal changes occurring subsequent to
delivery of electric current across the cerebral
cortex. This also prevents respiratory and
traumaticcomplications.
In the present clinical observational study we
analyzed 113 MECT administrations for evaluating
suitability of thiopentone sodium, propofol and
midazolam with succinyl choline chloride; on 45
patients belonging to ASA grade II with no
associatedsystemicdiseases.
We observed the induction characteristics,
induction and recovery time, associated changes
in hemodynamic parameters during and after
procedure, duration and energy required to
inducemuscularconvulsionsandchangesinserum
potassiumlevel.
Our observations indicates that induction was
quicker with propofol than with thiopentone 43.67
± 9.13v/s 61.31± 15.58 seconds and recovery time
was also quicker with propofol than
thiopentone518.73 ± 69.67 v/s 595.25 ± 112.68
seconds . Only on one occasion in thiopentone
groupinductionwasturbulent.
Acute but short lasting changes in heart rate,
systolic, diastolic and mean arterial pressure was
observed in both thiopentone and propofol
groups. The energy requirement was less than 100
joules on 34 sittings in thiopentone group while in
propofol group it was observed on 47 sittings. In
thiopentone group on 17occasionenergyrequired
were more than 100 joules and 5 occassions in
propofol group. There was transient elevation of
mean serum potassium of 0.55 meq/lit after MECT
in all patients. Midazolam did not produce
satisfactory condition in dose of 5 mg and needed
thiopentonesupplementon10occasions.
The findings allowed us to conclude that both
thiopentone and propofol along with sub-paralytic
dose of succinyl choline chloride produced
satisfactory conditions for MECT sittings without
EVALUATION OF THIOPENTONE SODIUM,
PROPOFOLAND MIDAZOLAM FOR
MODIFIED ELECTRO CONVULSIVE
THERAPAY
1 2 3
lDr. Harsh Kasliwal , Dr. M.M. Neema , Dr. Tejinder Singh Ajmani ,
1.Assistant Professor 2. Professor and Head 3. Postgraduate Student
Department ofAnesthesiology , R.D. Gardi Medical College, Ujjain

complications. However propofol provided quick
induction and recovery and lesser energy
requirement.
MECT, Thiopentone, Propofol, Midazolam
Anaesthesia
In early 1900s, Meduna, Father of convulsive
therapy for the cure of psychiatric diseases like
acute mania, schizophrenia and depressive
disordersusedchemicals (Camphor, leptazol,
insulin etc.) to induce convulsions in his patients.
His assumptions were based on principle of
biological antagonism that, epilepsy and
1
schizophreniadonotco-exist.
Later on Ugocerelleti and Luci Binni (1939)
after animal and human experiments established
that convulsions can be easily and reliably induced
by application of appropriate strength of electric
current to the cerebral cortex and called this
2
methodas“ElectroConvulsiveTherapy”(ECT).
Direct application of current to the cerebral
cortex results in acute and short lasting changes in
body physiology which involves almost all body
systems including cardiovascular, cerebrovascular,
muscle injuries, bone fractures and joint
dislocations. Accidental airway choking is also
reported.Itisnotapleasantsitetolookatfrothing,
convulsing a patient held by robust persons to
avoidinjuries.
Electroconvulsive therapy is an effective
physical treatment supported by evidences for
treating variety of psychiatric ailments such as
drug resistant major depressive disorder,
schizophrenia, acute mania, suicidal tendency,
endogenous depression and many more clinical
3
conditions.
BecauseMECTisashortprocedure thatcauses
involvement of almost all body systems after
Key words:
INTRODUCTION
delivery of electric current; therefore anesthesia
requirements for electroconvulsive therapy are
unique and intended towards quick induction and
recovery, attenuation of cardiovascular,
cerebrovascular and musculoskeletal changes and
avoidance of physical injuries and upper airway
c h o k i n g . H e n c e w h i l e p l a n n i n g
sedation/anesthesia for conducting MECT these
objectives are to be kept in mind besides
1,3
availabilityofresuscitationfacilities.
Proper conduct of ECT in operation theatre
with anesthesia machine, resuscitation facilities
and the use of sedatives or anestheticsis called
modifiedelectroconvulsivetherapy(MECT).
Government of India (2010) and World Health
Organization (1960) have mandated the use of
some form of sedation or anesthesia to make ECT
safeandacceptableprocedureforthepatients.
• The present study was conducted on 45
patients divided in three groups as
Thiopentone group (group-A), Propofol group
(group-B), and Midazolam group (group-C),
who received multiple sittings of MECT after
approvalofinstitutionalethicscommittee.
• Informed consent of blood relative was
obtained and was instructed to observe that
patient does not take any thing by mouth at
leastfor6hoursbeforetheprocedure.
• Antipsychotic medication was allowed to
continue
• Theobservationsweremadeon113sittings.
• In the operating room intravenous drip with
normalsalinewassetupandmultiparamonitor
applied for continuous monitoring of heart
rate, electrocardiogram, pulse oximeter and
noninvasivebloodpressure.
METHOD

• All patients received Injection Atropine
sulphate 0.6 mg intravenously along with pre-
oxygenation for 5 minutes before induction of
anesthesia.
• Patients received either thiopentone sodium,
(Max. dose 250 mg) Group A, propofol (Max.
dose 80 mg) Group B or midazolam (Max. dose
5 mg) Group C with sub paralytic dose of
succinylcholinechloride(50mg).
• After relaxation, psychiatrist was allowed to
deliver electric current trans-cutaneously
acrosscerebralcortex.
• Assisted breathing with 100 % oxygen after
delivery of electric current till the return of
adequate rate and depth of spontaneous
breathingandmonitoredcontinuously
• The patients shifted to recovery room after the
patients were conscious with stable vitals and
responding to verbal commands for further
observation.
• On every MECT sitting patient received the
sameinductionagent.
• Patients were monitored continuously on
multipara for ECG,NIBP, SpO2 and heart rate
during the entire procedure and continued
with similar observations in recovery room till
patientmetthedischargecriteria.
• Patients were shifted to their wards with
necessaryinstructions.
• Continuous Numeric Data: Presented as Mean
withstandarddeviation.
• Significance of observations analyzed by
independentsample’t’test.
• Significancelimit:P<0.05
• Complication Rate&ratio presented as number
STATISTICAL METHOD
of patients exhibiting and significance was
foundbychisquaretest.
• Observations presented as graphs and line
diagram.
We are presenting our observations made on
113 MECT sittings on 45 patients of physical status
II as per American society of Anesthesiologists’
classification of physical status. All study subjects
were free from concurrent systemic
cardiovascular,cerebrovascularorotherdiseases.
Table 1 shows the demographic profile and
mean number of MECT sittings with each study
drug.
Observations:
Table number 1
Parameter GroupA GroupB GroupC
Meanage 32.4 28.2 29.0
ofpatients
(inyrs.)
Male:Female 11:9 14:6 3:2
Meannumber 2.50 2.55 2.0
ofMECTsittings
perpatient
Table 2 shows the induction characteristic,
induction and recovery time with thiopentone,
propofol and midazolam. It was smooth on all
sittings except on one occasion (less than 1%) in
thiopentonegroup.Howevermidazolamindoseof
5 mg intravenously did not produce smooth
induction in all 10 sittings and required
supplement dose of thiopentone 100 – 150 mg .
Use of midazolam was dropped for further sittings
asobjectedbypsychiatrist.
Meaninductiontimewasshorterwithpropofol
(43.67 seconds) as compared with thiopentone
(61.47 seconds), the change is statistically highly

significant. Induction time was calculated as time
fromtheinjectionofdrugtilllossofverbalcontact.
Both induction and recovery was quicker with
propofol than with thiopentone (highly significant
value). The mean recovery time in propofol group
(518.73±69.67 seconds) was shorter than with
thiopentone (595.25 ±112.68 seconds) which was
highlysignificant.
Table 3 shows the energy requirement in both
thiopentone and propofol groups . It revealed that
energy required to induce muscular convulsions
was statistically highly significant in thiopentone
group. More than 100 joules was needed in 17
sittingswiththiopentone.
Thiopentone 25sittings 09sittings 17sittings
Propofol 26sittings 21sittings 05sittings
Pvalue P=0.03
(chisquaretest)
Table 4 shows the duration of muscular
convulsions in both thiopentone and propofol
group the difference was insignificant (20.76 ±
9.09 v/s 24.44 ± 9.84 seconds; P = 0.053 Not
Significant) but of shorter duration with
thiopentone.
Table 2
Table 3
Study
group Joules joules 100joules
Upto50 51-100 Morethan
Table 4
Table 5
Table 6
Table 5 shows that insignificant rise of serum
potassium occurred in both groups of patient.
Mean rise was higher for propofol group. (0.55 ±
0.35v/s0.68±0.68MEq/lit).
Table 6 shows that the hemodynamic parameter
and ECG recorded before anesthesia were within
normalrangeinallpatientsincludedinthestudy.
Line Diagram 1 to 4 shows the changes in
hemodynamic parameters before and after
delivery of MECT. All patients showed changes in
hemodynamic parameter as described by Perin
(1960). There are period of initial parasympathetic
overactivity followed by sympathetic overactivity
Induction Thiopentone Propofol Midazolam
character group group group
Smooth 50 52 00
Turbulent 01 00 10
Mean 61.47± 43.67± P=<0.01(HS)
induction 15.58Sec 9.13sec
time
Mean 595.25± 518.73± P=<0.01(HS)
recovery 112.68sec 69.67Sec
time
A 20.76 ±9.09 =0.052
B 24.44 ±9.84
Study Mean Standard P
group Deviation
A Mean 4.06 4.59 0.55
Standard
Deviation ±0.50 ±0.45 0.35
Mean 4.02 4.74 0.68
B Standard
Deviation ±0.49 ±0.52 0.36
Study Pre Post Increase p-value
Ictal Ictal for
increase
MeansystolicBlood 116.0 115.5 110.0
Pressure(mmHg)
MeanDiastolicBlood
Pressure(mmHg)
ECG WNL WNL WNL
Parameter GroupA GroupB GroupC
MeanPulseRate(bpm) 81.1 85.05 76.4

Line Diagram 4
Table 8
Table 8 shows the incidence of ECG changes
observed. A brief period of bradycardia and
lowering of systolic, diastolic and mean arterial
blood pressure occurs during 2 – 4 minute period
thatreturnedtobaselinevalueswithin30minutes.
Table 9 shows the comparison of time to
discharge in minutes using PADSS score. Patients
who received propofol achieved safe PADSS score
significantly earlier than those who received
thiopentone.
and finally the tone of both systems returned to
baseline tone.Initial parasympathetic over activity
occurring in first 15 – 20 seconds cannot be
recorded with usual monitoring equipment’s
available.
Line Diagram 1
Line Diagram 2
Line Diagram 3
WNL ST SB WNL ST SB
Pre Induction 37 13 1 44 6 2
Post Induction 12 39 0 15 37 0
One Minute 11 40 0 6 46 0
Two Minutes 17 16 18 29 0 23
Three Minutes 6 32 13 3 49 0
Four Minutes 3 48 0 7 45 0
Five Minutes 21 29 1 11 41 0
Ten Minutes 44 7 0 40 12 0
GroupA Group B

Table number 9
StudyGroup Mean Standard P
Deviation
A 22.55 4.83
B 16.44 2.68 <0.01
MECT is a widely recognized and effective
treatment for various psychiatric illnesses. Use of
anesthetics reduced psychological trauma while
succinylcholinechloridereducedtheincidencesof
1
physical trauma(Wanderdel) and atropine
supports the periods of parasympathetic over
activity.
In present study we used hypnotic doses of
thiopentone, propofol and midazolam so that
induction agent does not interfere with ECT
inducedcerebralseizures.
In present study induction, recovery time and
time to discharge was shorter with propofol in
comparisonwith thiopentone thatwas statistically
significant. Induction was smooth with both
thiopentone and propofol, however with
midazolam in dose of 5 mg did not produce
satisfactory condition there was resistance to
apply electrode and needed supplement with
thiopentone.
Findings of present study do not tally with
findings of many authors who reported on
adequacy of sedation with midazolam for MECT
3
{Pratibha Jain Shah et al 2010, ArvindArya,
4
Manpreet Singh , A.K Gurwara (2008) ; N Loimer, P
5
Hoffman , H.R. Chaudhry (1992). All authors
reportedadequatesedationwithmidazolam.
Reason for getting inadequate sedation could
be employment of lower doses in range of 0.09-
0.1mg/kg body weight,whereasPratibhaJain Shah
3 4
et al 2010 , ArvindArya, Manpreet Singh (2008)
usedmidazolaminthedoseof0.2mg/kg.
DISCUSSION:
N.Lomier, P. Hoffman and H.R Chaudhary
5
(1992) compared midazolam anaesthesia with
thiopentone plus succinyl choline, midazolam
significantly reduces seizure duration that was not
therapeutically desirable and concluded that
midazolam anaesthesia offers no advantage over
standard anaesthetic drugs for ECT with
thiopentoneandsuccinylcholinechloride.
In present study a short mean duration of
muscle convulsion was observed with thiopentone
i.e 20.76±9.09 seconds as compared to propofol
which was 24.44±9.84 seconds (P = 0.052). The
statistical comparison showed the change in
duration of muscle seizures as not significant;but
sufficient to produce therapeutically effective
duration of muscle convulsion. Our findings
correlate with Alok Kumar and others (2012) who
noted shorter mean seizure duration with
6
thiopentonethanpropofol.
6
Manpreetsingh and others (2008) observed
shortest duration of muscle seizure with
midazolam (21.6 ± 4.23 sec), followed by propofol
(28.76 ± 3.38 sec) and longest with thiopentone
(37.63±5.83sec)
In present study a small insignificant rise of
0.55 and 0.68 meq/L in thiopentone and propofol
groups respectively was observed (P=0.055).
Changes in serum potassium observed are
inconsequential in healthy individuals while this
changemayassumeclinicallysignificantinpatients
with heart diseases and electrolyte imbalance.Bali
7,8
IM and Agrawal R Verma, Doshi, Kaur, G. D
Shukla, Shrivastav; also found similar insignificant
riseofserumpotassium.
Changes in heart rate, systolic, diastolic, mean
arterial pressure occurred with both induction
agents and caused attenuation of hemodynamic
response after MECT delivery but the rate and
pressure responses were better suppressed with
propofol than with thiopentone. Extent of

attenuation of these acute cardiovascular
responses is character of intravenous anaesthetics
1
and co-administered drugs given to the patients.
Mean Arterial Pressure (MAP) was similar in both
groupsatalltimesofobservations.KanakoLwasaki
9
et al (2002) did not observe significant change in
MAP with two drugs that is propofol and
thiopentone.
Significant difference was observed in present
study in the mean time of recovery. With
thiopentone, was found to be 595.25±112.68
seconds which was significantly higher than
propofol518.73±69.67seconds(P<0.01).
Observations made in the present study
correlate with the observations of Pratibha Jain
3
Shah et al (2010)- Nadeem A Zaidi, Fauzia Khan
10 11
(2000) , Rolly G et al (1985) - In year (2008)T M
Omprakash, MohdInayat Ali, B Anand, M
12
Gouridevi, P Surrender . All authors reported a
shorter recovery time with propofol than with
thiopentoneormidazolam.
Incidence of postoperative nausea, vomiting,
postictalagitationwasnotobserved.
3
Pratibha Jain Shah et al 2010 reported
occurrence of headache, nausea, vomiting,
pyrexia, delerium, sensitivity, thrombophlebitis,
apnea, tachycardia in her study as side effects and
complicationsafteranaesthesia.
Observations made in the present study allow
ustoconcludethat
• Clear first choice as replacement of
Methohexitoneispropofol
• Thiopentone has its own pros and cons but can
s a f e l y b e u s e d b y e x p e r i e n c e d
anesthesiologist.
• Methohexitone is still a gold standard but it is
difficulttoprocure
Conculsions:
References:-
1. John L. Beyer, M.D., Andrew D. Krystal Mehul V.
Mankad Richard D. Weiner – Clinical Manual of
ECT, first edition 2010 ,chapters , introduction
to ECT History of Electroconvulsive Therapy
page - 3 to 8. Anaesthetics and other
medications 81-96 ictalmotor response 97-
104, ictal encephalographic response, 105 –
128,Cardiovascularresponse129-138.
2. Channapattana W. The origins of
electroconvulsive therpy. J psychiatry
associationThailand2000;45:371-80
3. Pratibha Jain Shah, Kamta Prasad Dubey,
C h h a t a r a p a l W a t t i , a n d J a y a
LalwaniEffectiveness of thiopentone, propofol
and Midazolam as an ideal intravenous
a n a e s t h e t i c a g e n t f o r m o d i f i e d
electroconvulsive therapy: A comparative
study; Indian J Anaesth. 2010 Jul-Aug; 54(4):
296–301
4. ArvindArya, ManpreetSingh , A.K Gurwara :
Comparison of Thiopentone sodium, propofol
and Midazolam for electrocomvulsive therapy:
J o u r n a l a n a e s t h e s i a c l i n i c a l
pharmacology:200824(3)pp291-294.
5. Loimer N1, Hofmann P, Chaudhry HR. 1992.
Midazolam shortens seizure durationfollowing
electroconvulsive therapy; Jornal of Psychiatric
researchApr;26(2):97-101
6. Alok Kumar, Devendra Kumar Sharma,
Raghunandan Mani: A comparison of propofol
and thiopentone for electroconvulsive
therapy; Journal of anaesthesiology: Clinical
Pharmacology 2012 Volume : 28 Issue : 3, 353-
35
7. Bali and Dandi – British Journal of Anaesthesia
197547(3)398-401
8.AggarwalR,KatyalS,SinghA,KaulTK.Changesin

serum potassium after electroconvulsive
therapy.JAnaesthesia2002;18;35-39
9. Kanako Iwasaki, Atsuhiro Sakamoto, Takeshi
Hoshino et al. Canadian Journal of Anaesthesia
49:2002;324-325
10. Nadeem A. Zaidi,Fauzia A. Khan Comparison of
thiopentone Sodium and Propofol for Electro
Convulsive therapy. Journal of Pakistan
MedicalAssociation50:60,2000
11. Rolly G, Versichelen L. Comparison of propofol
and thiopentone for induction of anaesthesia
i n p r e m e d i c a t e d p a t i e n t s .
Anaesthesia.1985;40:945-48
12. TM Omprakash, MohdInayat Ali, B Anand, M
Gowri Devi, P SurenderComparison of
thiopentone sodium and propofol in ECT
anaesthesia. Indian Journal of psychological
Medicine2008Volume:30Issue:1:48-51

1. AssistantProfessor. 2. AssociateProfessor3.Professor&HOD
DepartmentofAnaesthesia,GajraRajaMedicalCollege,Gwalior,M.P.
DOCUMENTATION OF ANAESTHESIA
RECORDS –A PREREQUISITE FOR A GOOD
ANAESTHESIOLOGIST
1 2 3
Dr. Suman Gupta , Dr. Preeti Goyal ,Dr. Bhanu Choudhary
ABSTRACT
INTRODUCTION
In this era of evidenced based medicine,
documentation is the sort of real time
authentication by the practicing Anaesth-
esiologists of what was done and what was not
done to the patient right from the preanaesthetic
visitup tilldischargefrom hospital,eitheron paper
orelectronicrecord.
In 1846 W.T.G.Morton demonstrated the
effective surgical anesthesia following the
discovery of inhaled Diethyl ether. Although Dr.
John Snow (1813-1858), Joseph Clover (1825-
1882) and Mounier (1855) demonstrated the
importance of monitoring the pulse and
respiration during anaesthesia, but the historians
believe that the first consistent recording of
physiological variable during anaesthesia was the
work of surgeons E.A. Codman(1869-1940) and
Harvey Cushing (1869-1939) when they were
‘junior house pupils’ at Massachusetts General
Hospital in 1895. They established the practice of
keeping a written record (on graph paper) of the
patient’s pulse and respiration during operation as
1
shownin some early records (FIGURE 1.). In 1901,
they started including measurement of arterial
bloodpressureusingnewlydescribedapparatusof
Scipione Riva-Rocci (1863-1937) as shown in
2
(FIGURE 2.) .A.J. wright describes how record
keeping of vital signs gradually spread into
3
everydayanaesthesiapractice.
The record generally serves as a concise
FIGURE.1. TWO SIDES OF HISTORICAL
ANAESTHESIA CHART.(1)
FIGURE 2.Front and Back of early anesthesia
2
recordsmonitoringpulserateandbloodpressure.

ANAESTHETIC DATAFIELD REQUIREMENT SCORE
DOCUMENTATION
PREOPERATIVEENCOUNTER NameGenderWeight Documentationonpreand 4
intraoperativedocuments.
Date Ofpreoperativeassessment 1
andprocedure
NameandSignature Onpreandintraoperative 1
encounter
Procedure Briefdescription 2
Medicalstatus ASAscore 1
Medicationandallergy Onpreanaestheticassessment 1
Previousanaesthesia Listandissues 1
document of the relevant preoperative
assessment, intraoperative anaesthetic
administration and physiological data, as well as
anaesthesiologists orders for the immediate
4
postoperative management. The Australian and
New Zealand college of Anaesthetists
5
( A N ZC A ) ,T h e A m e r i ca n S o c i et y o f
6
Anaesthesiologists(ASA) ,and Canadian
7
Anaesthesiologist Society (CSA) has laid down
certain guidelinesfordocumentation.
Good documentation and implicit quality care
provided to the patient serve for future reference
also and medicolegally protect from false
accusation of negligence. Accurate and through
documentation is an essential element of high
quality and safe medical care, and a basic
DISCUSSION
responsibility of physician anaesthesiologists.
Anaesthesia care is a continuum including three
p h a s e s o f c a r e ; p r e a n a e s t h e t i c ,
intraoperative/intraprocedural and post
8
anaesthesiacare. Ascoring system was designed
for objective assessment of the adequacy of the
4
records as shown in Table 1, Where maximum
scoring is with preoperative encounter
emphasizing the importance of data field such as
documentation of name, gender, weight, brief
descriptionof procedure,presenceandseverityof
gastro esophageal reflux disease(GERD) and
airway assessment. Thus importance of
maintaining an adequate, accurate and legible
anaesthetic record has been emphasized by
ANZCA comprising of wholesome information of
5
patientcare. .[AnnexureA]
TABLE1.A scoring system for objective assessment of the adequacy of the records

Airway,Dentition,GERD Mallampatiscore,thyromental 3
distance,anylooseor
missingandfalsetooth,presence
ofGERDanditsseverity
Premedication Ifappropriate 1
Anaestheticplan Briefdescription 1
Risk Briefdescription 1
INTRAOPERATIVEENCOUNTER Anaesthetictechnique Fulldetail(general/regional) 1
Drugsadministered Timeanddose 1
Airway Sizeandtype 1
Breathingsystem Flowandmodeofventilation 1
Monitoringmethod Listanddetails(sizeandsite 1
ofIAL,CVC)
VascularaccessandIVT Siteandsize,typeandvolumeof 1
fluidinfused
Significantbloodloss Mustbedocumentedin 1
intracavitary,majorgynecological
orthopedic,cesareansection
andurologyprocedures
POSTOPERATIVE Postoperativerecovery Painprotocol 1
INSTRUCTIONS analgesia
Postoperativeward Documentedonoperative 1
analgesia recordormedicationchart
Postoperativefluid Tocoverover24hours 1

5
ANNEXURE A
1. Basic Information
2. Pre-anaesthesia Consultation Information
TheAnaesthesiaRecordshouldinclude:
1.1 The name of the patient and the hospital,
the hospital record number, the age, gender
andweightofthepatient.
1.2 The dates of the pre-anaesthesia
consultationandoftheanaesthesia.
1.3 Thename(s)oftheanaesthetists(s).
1.4 The name of the surgeon or other
proceduralist.
1.5 A brief description of the procedure actually
performed.
2.1 Documentation of the pre-anaesthesia
assessmentofthepatient.Thiswillnormally
include:
2.1.1 A summary of general medical status by
relevantsystemsanddiseases.
2.1.2 Concurrent therapy and any known drug or
othersensitivities.
2.1.3 The history of previous anaesthesia and
relevantsurgery.
2.1.4 An assessment of the airway, dental
condition and risk of gastric reflux, where
appropriate.
2.1.5 Results of relevant laboratory data and
otherinvestigations.
2.2 Any pre-medicant drugs, time given, route
of administration and description of any
unusualresponse
2.3 An outline of the anaesthesia plan, if
appropriate.
2.4 Documentation of discussion with the
patient or guardian on the anaesthesia plan,
possible therapies and possible outcomes
andrisks
3.1 Technique:Thefulldetailsoftheanaesthetic
technique used, whether general, regional
or sedation with monitored anaesthesia
care.
3.2 Medication: The details of administration of
all drugs including any used by the surgeon,
andadescriptionofanyunusualresponse.
3.3 Airway: The size and type of any artificial
airway used a description of any airway
problems encountered and the method of
theirsolution.
3.4 Anaesthesia Breathing System: Details of
the anaesthesia circuit, gas flows, and
controlledventilationtechniques.
3.5 Monitoring: The monitoring methods used
and regular documentation of relevant
information obtained. Information provided
as a monitor print-out must have correct
patientidentification
3.6.1 Intravenous infusion: Details of intravenous
solutions including the site, size of cannula
andthenatureandvolumeoffluidsinfused.
3.6.2 Detailsofcentralvenousandarterialaccess.
3.7 Blood loss: An estimate of blood and fluid
losswhereappropriate.
3.8 Position: The position of the patient during
the procedure and, where appropriate, any
protectivemeasuresemployed.
3.9 Time: The time of significant anaesthesia
and operative events, observations and
interventions including administration of
drugs.
3. Anaesthesia Information
3.6 Fluid Therapy and Vascular Access:

3.10 Complications or problems: A detailed
description of any complications or
problemsencountered.
3.11 Other information that the anaesthetist
considers is particularly relevant to a
particularcaseshouldalsoberecorded.
4.1 Respiratory, cardio-vascular and
neurological status and any other relevant
information.
4.2 Incidents arising during this period and their
management.
4.3 Planforpainmanagement,fluidtherapyand
oxygen therapy for first 24 hours if
appropriate, but certainly for guidance of
RecoveryRoomStaff.
4.4 Time and discharge destination on transfer
fromoperatingtheatreorrecoveryroom.
4.5 Space for documentation of the post-
anaesthesiavisit.
4.6 Space for documentation of outcome data,
including Clinical Indicators, audit and
quality assurance information as decided by
theanaesthesiadepartment/anaesthetists.
With advancing technology, Anesthesia
Information Management Systems (AIMS) is a
newly introduced method which allows the
automatic and reliable collection, storage, and
presentation of patient data during the
perioperativeperiod.Theyarespecializedformsof
electronic health record (EHR) systems that in
addition to providing basic record-keeping
functions, typically provide end users with ready
access to summary data that can be used to
facilitate quality assurance and research
9
functions. Figure 3.shows documentation of an
airway as a part of AIMS method of record
maintenanceinanaesthesia.
4. Post-Anaesthesia Information
Figure 3.showing the documentation of airway
management as a ,part of AIMS, with reference
link to airway flow chart A, airway documentation
check BUTTON C, and smart logic button B, which
highlight automatically the sections not
10
completed.
Systematic application of process
improvement methodologies can improve
documentation and are also effective in improving
other areas of anesthesia clinical practice. Every
institute and department should develop a
protocol according to local factors for
documentation
1. Two sides of anesthesia chart by E.A,
CordmanM.D.November 30.1894. From
Beecher Hk. The first anesthesia record
(Codman, Cushing,) 1990.surg, gynecol,
&obstet.71:689-693.
2. Anesthesia record from Noseworthy M.D.A
Method of keeping Anesthesia records and
assessing results. British journal Anesthesia
1943;18(4):160-179.
3. www.asahq.org
CONCLUSION
REFERENCES

4. ElhalawaniI, Jenkins, Newman N, Perioperative
anaesthetic documentation; Adherence to
current Australian guidelines. J Anaesthesiol
clinpharmacol2013;29:211-5.
5. Australian and New Zealand college of
Anaesthetists. The anaesthesia record.
Recommendation on the recording of an
episode of anaesthesia care.ps06.Revised
2 0 0 6 . A c c e s s e d f r o m ;
http://www,anzcz.edu.au/resources/professi
onal-documents/ps9hlml.
6. The American society of Anaesthesiologists,
statement on documentation of anaesthesia
care. Approved 2008. Available from
http://www.asahq.org/for-members/
standards-guidelinesandstatements.aspx
7. Merchant R. Bosenber C, Brown K,Chartrand D,
Dain s, Dobodon J, etal. Guidelines on the
practice of anaesthesia. Revised 2010. Can
J.Anaesth2010;57-87.
8. Statement on documentation of anaesthesia
care; Approved by the ASA House of Delegates
onoct.15.lastamendedonoctober28.2015.
9. Ehrenfeld JM,Rehman M A.Anaesthesia
information management systems: A Review of
functionality and installation considerations. J
Clin MonitComput 2011:25(1); 71-
79.doi:10.1007/s10877-010-9256-y
10.L. Kelsey McCarty, Daniel Saddawi-Konefka,
Lauren M. Gargan, B.S., William D. Driscoll,
John L. Walsh, Robert A. Peterfreund.
Application of Process Improvement
Principlesto Increase the Frequency of
C o m p l e t e A i r w a y M a n a g e m e n t
Documentation. Anesthesiology 2014;
121:1166-74.

Fig 1. Deep brain stimulator
Patients with Parkinson’s disease and
implanted DBS, who require cardiac surgery, are
complex cases that require a multidisciplinary
approach. Adequate preoperative planning
regarding optimization of pharmacological
therapy is very important to minimize
postoperative complications related to the
disease. DBS can potentially generate
inappropriate stimulation due to interference
between electrocautery and deep brain
4
stimulator . Risks of brain damage from
h a e m o r r h a g i c c o m p l i c a t i o n s d u r i n g
cardiopulmonary bypass are very high. Brain
electrodes present a substantial risk for cerebral
haematoma when anticoagulation therapy is
needed. Thus, potential operational safety and
efficacyissuesmustalsobedefined.
1. ConsultantCardiothoracicAnaesthetist,Essex,Basildon,UK
CASE REPORT:
AORTIC VALVE REPLACEMENT IN A
PATIENT OF PARKINSON'S DISEASE WITH
DEEP BRAIN STIMULATOR
1
Dr. Gyanesh Namjoshi
Background
Parkinson’s disease (PD) is a chronic
neurodegenerative disease which has a
prevalence of 5-346 per 100,000 per year in the
1
European population . This is a condition of varied
etiology characterized by tremors, rigidity,
dyskinesiaandposturaldisturbances.
These patients respond well to treatment with
Levodopa when given in combination with
peripheral decarboxylase inhibitors. Ergot derived
dopamine receptor agonists like Pergolide and
cabergoline have also been used for the control of
symptoms effectively. Heart valve lesions are the
main side effect of these dopamine receptor
2,3
agonists Other adjuncts to pharmacological
therapy are COMT inhibitors (Talcopone,
Entacapone), anticholinergic drugs, and non-ergot
dopamine receptor agonists like Ropinirol and
Rotigotinetransdermalpatches.
Stereotactic neurosurgery and the use of brain
stimulation technology can improve quality of life,
withrestorationofmobilityinneurologicdisorders
with intractable tremor such as Parkinson’s
disease. Thalamic Deep Brain Stimulation implants
(DBS), also known as the “pacemaker of the brain”,
have shown good control over dystonia and
dyskinetic movements in drug refractory
Parkinson’sdisease(Fig.1).

We report a case of severe Parkinson’s disease
with DBS implant, who presented with aortic valve
regurgitation possibly because of long term
treatment with dopamine receptor agonist agent,
requiring aortic valve replacement surgery. We
also discuss her successful perioperative
management including pharmacological
optimisation using transdermal Rotigotine
patchesandNGsupplementedLevodopa.
A 55 year old Caucasian woman was diagnosed
with Parkinson’s disease. Initially she was treated
with Levodopa and Talcopone (COMT inhibitor).
Two years later Cabergoline (Dopamine
antagonist) was added to the treatment because
of worsening symptoms. After 4 years patient
underwent DBS implantation for her worsening
dyskinesia and severe motor fluctuations, which
improvedhersymptoms.
Six years after DBS implantation, patient was
admitted to hospital with profound dystonia and
difficulty in breathing. (NYHA Class III).
Echocardiography revealed moderate Aortic
regurgitation (peak gradient 1.54) with mild mitral
and tricuspid regurgitation, mild pulmonary
hypertension and dilated left ventricle with
ejection fraction of 40%. Angiographic studies
confirmednormalcoronaries.
At this point (and due to already described
relationship between Cabergoline and valvular
disease) Cabergoline was stopped and Ropinerol
was added to the anti-PD drugs. After
multidisciplinary reviews and discussions amongst
surgeons, anaesthetists / intensivists,
neurophysiologists, pharmacists and nursing staff
and physiotherapists the patient was planned for
aorticvalvereplacement.
Careful anaesthetic assessment showed
increased dyskinesia. It was decided that she
Case report
should be changed from oral Ropinirole to
transdermal Rotigotine patches as compliance
would be better and changes in plasma levels of
dopamine can be minimised. A Parkinson’s
specialist nurse was involved during the
perioperative period for anti-PD drugs and DBS
management.
Patient was fasted overnight and in the
morning of surgery she received all her anti-PD
medication.Rotigotinepatcheswereremovedand
DBS was switched off using a magnetically
controlledswitch.Priortoanaestheticinductionof
the patient a nasogastric (NG) tube was inserted
for intraoperative levodopa supplementation.
Grounding pad was placed on the back and
monopolar electrocautery was used during the
surgery. After routine sternotomy, and careful
dosing of heparin, cardiopulmonary bypass was
instituted in a routine fashion and size 21 tissue
aortic valve prosthesis was implanted under
generalanaesthesia.
Patient was taken to Intensive care unit
immediately after the surgery. Rotigotine patches
were reapplied and DBS was restored to the pre-
operative settings. Anti-PD drugs (Levodopa)
weregiventhroughtheNGtube.After5hours,and
once wehad confirmed thatthere were no signs of
muscular rigidity, the patient was extubated. Oral
fluid intake was encouraged and oral doses of anti-
PDdrugswererecommencedonthesameday.The
physiotherapy team ensured that patient gets
chestphysiotherapyandstartearlymobilisationto
reducetherespiratorycomplications.
The patient showed good recovery and at the
st
end of 1 postoperative day she was discharged to
the ward. She was subsequently sent home on the
th
6 postoperativeday.
After 18 days the patient was seen in clinic,
where a minimal pleural effusion was noted.
Although the patient was not clinically

compromised, she was readmitted for drainage.
Shewasthendischargedhomeafter5days.
Parkinson’s disease (PD) is the most common
neuro-degenerative disease of old age. Several
studies and case reports strongly support a
relationship between the occurrence of drug-
induced “restrictive” valvular heart disease and
treatment with the ergot-derived dopamine
receptor agonist mainly used to treat PD. These
abnormalities closely resemble carcinoid –related
5
valvopathies .
It has been proposed that the valvular damage
induced by these agents may be mediated by the
serotoninergicsystem.Thedrugshavehighaffinity
for, and are full or partial agonists of, the serotonin
receptor subtype 5-HT2B, which is expressed in
6
heart valves and is known to cause mitogenesis .
Proliferation of fibroblasts may occur within valve
tissuewhenthisreceptorisstimulated.
FordisabledpatientswithPDDBStechnologyis
used. The electrode is connected via a tunnelled
extension lead to an implanted pulse generator.
Stimulation can be performed continuously or
intermittently, and can deliver a variety of
electrical field patterns. This mode of treatment
although effective is not free of adverse effects.
Inappropriate stimulation may cause aggressive
behaviourorpyramidalsyndromes.
Increasingnumberofcasesarepresentingfora
variety of major elective and emergency surgical
procedures. Prognosis of these patients depends
on carefully planned perioperative management,
severity of disease, type of surgery and efficient
ITUmanagement7
Deep brain stimulator is very effective in
controlling tremors in drug refractory severe PD.
Intraoperative use of electro cautery during
surgery can cause inappropriate stimulation of
Discussion
8
DBS resulting in behaviour disorder. This is
because of damage to the pulse generator or
reprogramming of the pacemaker. Bipolar leads
are much more resistant to the conducted
electromagnetic interference than are unipolar
leads. However in cardiac surgery bipolar
electrocautery is not very efficient. An alternative
in these patients could be the use of an ultrasonic
scalpel. With this device there is minimal transfer
of energy or no transfer of electrical energy to the
tissues. Pre operatively DBS can be switched off
using magnetic switch to enable the use of
monopolar electrocautery. Disconnection of DBS
under local anaesthesia prior to surgery has also
9
beenreported .
There is relatively small risk of cerebral
10
haemorrhage with DBS, but not insignificant .
Cardiopulmonary bypass can be safely performed
after 6 months after the DBS implantation. The
presence of brain electrodes poses a significant
risk for cerebral haematoma when long-term
anticoagulation therapy is needed. For this reason
the authors in this case employed the use of a
bioprosthesis for aortic valve replacement,
because anticoagulation therapy can be avoided,
although the authors are aware of the controversy
surrounding the choice of bioprosthesis for the
aorticpositionina55-year-oldpatient.
Interruption of Levodopa even for small period
can cause severe skeletal muscle rigidity because
of its short half life of 1-3 hours. Various case
reports describe successful management of PD
patients with intraoperative nasogastric (NG)
11, 12
supplementation of LD . In this case we also
used recently licensed dopamine agonist
Rotigotine transdermal patches. Rotigotine helps
to prevent the symptoms when the effect of
levodopa wears off(on offperiod) or when there is
fluctuations in the levodopa levels. These patches
contain aluminium foil; hence removal of patches

is recommended prior to surgery, cardioversion
andMRI,topreventskinburns.
A potential problem in patients with DBS
implantis the use of cardiac pacemaker which may
be required following aortic valve replacement
surgery. Concerns about the possible
electromagnetic interaction between two devices
have been raised. Two case reports show
successful use of these two devices without any
13,14
complication
Because of poorly compliant lung these
patients can be difficult to wean from the
ventilator. Post extubation they are at increased
risk of atelectasis, chest infection and pneumonia
due to poor ventilation and weak cough.
Aggressive chest physiotherapy and early
mobilisation is indicated in these patients. For this
reason it is very important that administration of
the anti-parkinsonian medication is continued
throughout the entire procedure and recovery
period either with NG administration or oral when
thisbecomespossible.
We propose a plan of management for elective
or emergency major surgery for patients with
Parkinson’s disease. These patients should be
assessed by a multidisciplinary team prior to
surgery. Pre admission anaesthetic assessment,
liaison with Parkinson’s disease specialist
physician and DBS technician will allow careful
planning of the best intraoperative strategy.
Communication with ITU staff, pharmacists,
dieticians and physiotherapists will avoid
unnecessary prolonged hospital stay, as we have
shown in the case described. In terms of the
symptomatic management of Parkinson’s disease,
DBS should be temporarily switched off to prevent
inappropriate stimulation and interference and it
should be restarted soon after the procedure;
intraoperative supplementation of levodopa and
use of Rotigotine transdermal patches for better
control over the symptoms should also be done.
Advanced planning and early involvement of all
those teams involved in the care of these patients
during their stay in hospital can allow a smooth
recovery without complications and an early
dischargehome.
1. Von Campenhausen S, Bornschein B, Wick R et
al Prevalence and incidence of Parkinson’s
d i s e a s e i n E u r o p e . E u r
Neuropsychopharmacol.2005;15(4):473-90
2. Renzo Zanettini, et al: valvular heart disease
and the use of Dopamine agonist for
Parkinson’s disease. N Engl J Med 356; 1,
January4,2007.
3. Rene Schade et al: Dopamine agonist and the
risk of cardiac valve regurgitation. N Engl J Med
356;1,January4,2007.
4. Lozano AM, Mahant N: Deep brain stimulation
surgery for Parkinson’s disease; Mechanism
and consequences. Parkinsonism Related
Disorder1:S49-S57,2004(suppl)
5. Redfield MM, Nicholson WJ, Edwards WD, Tajik
AJ. Valve disease associated with ergot
alkaloid use: echocardiographic and pathologic
correlations.AnnInternMed1992;117:50-52
6. Rothman RB, Bauman MH, Savage JE, at al.
evidence for possible involvement of 5-HT2B
receptors in the cardiac valvulopathy
associated with fenfluramine and other
serotoninergic medications. Circulation 2000;
102:2836-2841
7. William D freeman, K Meng Tan, GA Glass et al.
ICU management of patients with Parkinson’s
disease or Parkinsonism; Current anaesthesia
&criticalcare(2007)18,227-236
8. Beric A, Kelly PJ et all : complications of deep
brain stimulation surgery; Stereotact Funct
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Neurosurg7;73-78,2001
9. Xavier Benoit D’Journo et al: Scheduled
cardiothoracic surgery and Parkinson’s
disease: how to deal with deep brain
stimulation. Journal of Cardiothoracic and
vascular anaesthesia, Vol 20, No 5(Oct) 2006:
pp707-708
10. Binder DK, Rau G, Star PA: Haemorrhagic
complications of microelectrode guided deep
brain stimulation, Stereotact Funct Neurosurg
80;28-31,2003
11.Navdeep Goyal, Lalita Chaudhary, Aruna Jain:
Pa r k i n s o n ’s d i s e a s e : A n a e s t h e t i c
considerations. The Internet Journal of
Anaesthesiology.2007.Volume13Number
12.Furuya, Ryousuke MD; Hirai, Akiko MD; Andoh,
Tomio MD, PhD; Kudoh, Ichidai MD, PhD;
Okumura, Fukuichiro MD, PhD: Successful
Perioperative Management of a Patient with
Parkinson’s Disease by Enteral Levodopa
Administration under Propofol Anesthesia,
Anesthesiology:Volume 89(1)July 1998pp 261-
263
13.Alois A Obwegeser, et al : Simultaneous
thalamic deep brain stimulation and
implantable cardioverter-defibrillator ; Mayo
ClinProc,2001;76:87-89
14.Patric B Sennatus et al.: Implantation of
bilateraldeepbrainstimulatorsinpatientswith
Parkinson disease and pre-existing cardiac
pacemakers: Report of twocases;J.Neurosurg.
2004vol.101,pp1073-1077

EssexCardiothoracicCentre,BAsildon,UK
POST MYOCARDIAL INFARCTION
VENTRICULAR SEPTAL DEFECT
1 2 3 4 5
Dr. Kriti Vig , Dr. Kunal Waghmare , Dr. Gyanesh Namjoshi , Dr. R Nalgirkar , Dr. Mr Sudhir Bhusari
INTRODUCTION
POST MI VSD
A ventricular septal defect (VSD) is an opening
in the ventricular septum which causes mixing of
the oxygenated blood from the left ventricle with
thedeoxygenatedbloodintherightventricle.
VSDcanbeCongenitalorAcquired.
MostcommoncausesofacquiredVSDare
1) Postmyocardialinfarction(MI)
2) Post transcatheter aortic valve
implantation(TAVI)
3) Po st S e p ta l M yo m e c to my fo r
hypertrophiedcardiomyopathy
· Typically occurs 3-8 days after an acute
myocardial infarction (MI). It may, however,
develop within the first 24 hours or as late as
twoweeks.
· Often presents as sudden worsening
hemodynamics due to cardiogenic shock and
biventricularfailure.
· The differential diagnosis of post infarction
cardiogenic shock should exclude free
ventricular wall rupture and rupture of the
papillarymuscles.
· Relevantanatomy
The septal blood supply comes from branches
of the left anterior descending (LAD) coronary
artery, the posterior descending branch of the
right coronary artery, or the circumflex artery
whenitisdominant.
The size of the defect determines the
magnitude of left-to-right shunting, which in turn
affectsthelikelihoodofsurvival.
· Transmural/muscularpartoftheseptum.
· It’s more likely to occur in the anterior or apical
septum (with anterior MI)(60%) than in the
posterior septum at the base (with inferior
MI)(40%).
· Rupture develops at the margin of the necrotic
andnon-necroticmyocardium.
· Theperforationisusuallysingleandvariesfrom
onetofewcentimetresinsize.
1. Singlevesseldisease,especiallyLAD
2. Extensivemyocardialdamage
3. Poorseptalcollateralcirculation
4. Firstinfarction
5. Rightventricularinfarction
1. Ventricularaneurysm.
2. Mitral valve insufficiency secondary to
papillarymuscleinfarctionordysfunction.
Site of rupture -
· Risk Factors
· Associated Lesions
CASE-REPORT

· Surgical Intervention
CASE DETAILS
1. The success of surgical therapy depends on
prompt medical stabilization of the patient and
preventionofcardiogenicshock
2. Immediate surgery is usually indicated.The
high surgical risk of early repair is accepted
because of the even higher risk of death
withoutsurgeryundersuchcircumstances.
3. The relative safety of repair 2-3 weeks or more
after perforation has been established, as the
edges of the defect have become firmer and
fibroticenablingamoresecurerepair.
4. A successful clinical outcome is related to the
adequacyoftheclosureoftheVSR
A 65 years old gentleman, (with a background
history of IHD, COPD, recent pneumonia, liver
cirrhosis, and high alcohol intake and lupus
disease) was admitted to a District General
Hospital with presenting complaints of fall and a
brief loss of consciousness. ECG performed
showed anterolateral ST segement elevation
myocardial infarction (STEMI) and hence patient
was referred to our tertiary care ESSEX
CardiothoracicCentre,Basildon.
Initially the patient was admitted to the
cardiologyward.Atransthoracicechoexamination
was done which showed moderate LV function
with a large apical VSD (1.4cm).Coronary
angiogram showed occlusion of mid segment of
LAD and disease of Circumflex branch of left
coronaryastery(LCX)andOM.
Initial optimisation wasachieved by starting
diureticsandbyinsertionof Intraortic ballonpump
(ABP). However, during this period, he developed
chest infection (S. aureus) followed by Type 1
respiratory failure and acute renal failure. Hence
patient was admitted to ITU, 7 days after initial
presentation,forfurtherstabilisation.
Respiratory support was provided with non-
invasive ventilation-CPAP; hemodynamic support
was maintained with infusion of inotropes,
noradrenaline and dobutamine, in addition to
IABP, while doing invasive blood pressure
measurement and Continous Veno-venous
hemofiltraion (CVVH) was commenced for renal
support. A broad spectrum antibiotic,Meropenem
was started to combat sepsis. He also underwent
USGguideddrainageofpleuraleffusion.
The case was discussed with the cardiac
surgeons and a collective decision was made to
optimise the patient and scheduled for surgery 3
weeksaftertheinitialpresentation.
Onthescheduleddateofsurgery,thepatientwas
transferredtotheatresonIABPandinotropeswhile
CVVH was temporarily discontinued. In the
anaesthetic room, he was premedicated with
midazolam 4mg iv and fentanyl 250 mcg iv. After
preoxygenating for 3 minutes, anaesthesia was
induced with 30mg propofol and after check
ventilation, Rocuronium 80mg iv was given for
neuromuscular blockade. Direct laryngoscopy was
performedandthetracheawasintubatedwithasize
7 oral endotracheal tube(grade 2 intubation). The
tube position was confirmed by a continuous
capnographytraceandvisiblechestriseandthetube
was secured in place. Teicoplanin and gentamycin
wasgivenforperioperativeantibioticcover.
The anaesthetic depth was maintained with iv
infusions of Propofol and fentanyl and with
Isoflurane 1% inhalation, with boluses of
Rocuronium as needed. The surgical procedure
was performed under continuous monitoring of
ECG, Invasive BP, etCO2, Temperature, SaO2, CVP,
FiO2, and inhalational gases concentration.
Arterial blood gases, ACT, TEG and urine output
were amongst the other measurements done
periodically.
Hemodynamic support was maintained with
ongoing IABP and amongst inotropes,
Pre Cardiopulmonary by pass (CPB)

noradrenaline infusion was continued whereas
Dobutamine was weaned off and Milrinone
started.PreCPBperiodwasuneventful.
Transoesophageal echocardiography was
performed beforeCPB, during weaningoffCPB and
postCPB.
1)Apicalseptumdefect seen
2) Colourflowacrossthedefect
A)Defectinseptumintransgastricview
B) Colourflowacrossthedefect
On CPB :
·
· 1.3litresfiltered
· Isoflurane1%
· CPBtime77minutes
· Aorticcrossclamptime52minutes
· UrineoutputonCPB100ml
Post CPB : 1 pool of platelets, 3 units Fresh
Frozen Plasma and 600 ml cell saved blood
transfused.
1) VSDPATCHREPAIR
2)VSDPATCHREPAIRWITHCOLOUR
Patient was transferred back to ITU for post-
operative care. Sedation was stopped, respiratory
support weaned off and once the patient was fully
awake and oriented, he was extubated following
4unitsofRBCgiven

day. IABP was taken out on the next day of surgery;
he came off CVVH on postoperative day 3 whereas
it took him 5 days to completely wean off from
noradrenaline.Patient was given a course of
Ceftazidine, Linezolid and Gentamicin to further
take care of his sepsis during his ITU stay. He was
discharged from the ITU to the ward on 5th post-
operativeday.
His recovery in the step down ward was
without any significant post-operative
complications. However, the recovery was
hindered by his low mood and depression due to
which he had to be encouraged to eat and drink
and to take self-care. He had postural hypotension
and tachycardia for the initial few days in ward,
which responded to oral fluids and hydration.
During his stay in the ward, he received inputs and
advice from the psychiatric team, from the alcohol
liaison services suggesting referral to social care
community, from the physiotherapist and the
dietician. He suffered from urinary incontinence
and had to be discharged with a long term urinary
catheter in situ and long term medications for
treatmentofheartfailure.
Rupture of the ventricular chamber (septum or
free wall), after myocardial infarction, is a
relatively infrequent condition, with high
mortality. These conditions, resulting from
transmural infarction, may cause rapid
hemodynamic compromise and early death
precluding surgical repair. Free wall rupture can
result in tamponade and sudden cardiovascular
collapse. In ventricular septal rupture, there is a
variable amount of left-to-right shunting, but such
defects typically lead to symptoms of heart failure.
The clinical presentation ranges from an
asymptomatic murmur to cardiogenic shock and
suddendeath.
Since 1988, in the UK, an average of 165
DISCUSSION:
patientsperyearhaveundergonesurgicalrepairof
post MI interventricular septal rupture(Cardiac
surgical registry of the Society of Cardiothoracic
Surgeons of Great Britain and Ireland). From
anaesthetist and surgeon’s viewpoint this
operation is a rare event. Given that there are now
around 200 consultant cardiac surgeons in the UK,
the current workload averages out at less than one
casepersurgeonperyear.
The overall hospital mortality of patients
undergoing surgical repair in the UK in the same
time period was 38%. So it is not only a rare
operation but it is also difficult to end up with a
survivor. The national figures suggest that hospital
mortality has increased with time (fig 1 1). In
addition, the number of patients undergoing
repair has decreased in the last five years. These
two statistics are almost certainly associated with
the increasing use of thrombolytic agents in the
management of patients with acute myocardial
infarction.
The current guidelines of the American College
of Cardiology/American Heart Association
recommend immediate surgical intervention to
prevent further hemodynamic deterioration in
7
patientwithVSR .Inductionofgeneralanaesthesia
for a patient with VSR and coronary artery disease
is challenging. If systemic vascular resistance (SVR)
increases with sympathetic stimuli because of
trachealintubation,italsoincreasestheshuntflow
apart from increasing the oxygen demand.
Therefore, induction of general anaesthesia and
tracheal intubation must be accomplished with
minimal or no hemodynamic changes. In our
patient, induction of anaesthesia was performed
with a combination of anaesthetic drugs,
Midazolam, Propofol and Fentanyl in appropriate
titration.
One of the most important concerns in
anaesthetic management of VSD after its closure is

to reduce LV afterload while maintaining
hemodynamics. Reduction of afterload is required
to prevent tension in the suture line of newly
repaired septum during the post-bypass
period.Milrinone infusion was started to maintain
systemicBPwithoutincreasingSVR.
Volatile anaesthetics were administered to the
patient as they have myocardial protective effects
and afterload reduction properties which are
beneficial in patient with VSD. Maintaining
optimum pulmonary vascular resistance (PVR) is
equally important to SVR in patients with VSR.
Anaesthesiologists must avoid techniques that
tend to decrease PVR/SVR ratio such as
hypocapnia and hyperoxemia. Efforts should be
made to maintain normocapnia and normoxia by
controlled respiratory parameters like rate and
inspired oxygen concentration.. However, it may
be difficult to maintain low inspired oxygen
concentration (FiO2) when the patient has
pulmonarycongestionduetoleft-torightshunt.
Surgical closure of ventricular septal rupture
following myocardial infarction is an infrequent
operation with a very high operative risk.
Nonetheless, early surgical intervention offers the
only realistic chance of survival and this
opportunity should not be denied to patients.
Thrombolysis for myocardial infarction has altered
the pattern of the condition, reducing the
incidence but providing the surgeon with an even
greater challenge. Immediate intra-aortic balloon
counter pulsation provides some haemodynamic
optimisation while preparations are made for
surgery. The good long term outcome for survivors
makesthehighearlymortalityworthwhile.
Department of Cardiothoracic Anaesthesia
and Surgery, theatre and Intensive care unit at
CONCLUSION
ACKNOWLEDGEMENT
EssexCardiothoracicCentre,Basildon,UK.
1. Sanders RJ, Kern WH, Blount SG. Perforation of
the interventricular septum complicating
myocardial infarction. Am Heart J
1956;51:736–48.
2. Edwards BS, Edwards WD, Edwards JE.
Ventricular septal rupture complicating acute
myocardial infarction: identification of simple
and complex types in 53 autopsied hearts. Am J
Cardiol1984;54:1201–4.
3. Mann JM, Roberts WC. Acquired ventricular
septal defect during acute myocardial
infarction: analysis of 38 unoperated necropsy
patients and comparison with 50 unoperated
necropsy patients without rupture. Am J
Cardiol1988;62:8–19.
4. Skehan JD, Carey C, Norrell MS, et al. Patterns
of coronary artery disease in post-infarction
ventricular septal rupture. Br Heart J
1989;62:268–72.
5. Pretre R, Rickli H, Qing Y, et al. Frequency of
collateral blood flow in the infarct-related
coronary artery in rupture of the ventricular
septum after acute myocardial infarction. Am J
Cardiol2000;85:497–9.
6. Parry G, Goudevenos J, Adams PC, et al. Septal
rupture after myocardial infarction: is very
early surgery really worthwhile? Eur Heart J
1992;13:373–82.
7. Crenshaw BS, Granger CB, Birnbaum Y, et al.
Risk factors, angiographic patterns, and
outcomes in patients with ventricular septal
defect complicating acute myocardial
infarction.Circulation2000;100:27.
8. Rhydwen GR, Charman S, Schofield PM.
Influence of thrombolytic therapy on the
patterns of ventricular septal rupture after
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acute myocardial infarction. Postgrad Med J
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mortality after surgical repair of postinfarction
ventricular septal rupture: importance of rupture
location.AnnThoracSurg1996;61:1752–8.
10. Heitmiller R, Jacobs ML, Daggett WM.
Surgical management of postinfarction ventricular
septalrupture.AnnThoracSurg1986;41:683–91.
11. Konstantinides S, Geibel A, Kasper W, et al.
Noninvasive estimation of right ventricular systolic
pressure in postinfarctionseptal rupture: an
assessment of two Doppler echocardiographic
methods.CritCareMed1997;25:1167–74.
12. Norell MS, Gershlick AH, Pillai R, et al.
Ventricularseptalrupturecomplicatingmyocardial
infarction: is earlier surgery justified? Eur Heart J
1987;8:1281–6.
13. Moore CA, Nygaard TW, Kaiser DL, et al.
Postinfarction ventricular septal rupture: the
importance of location of infarction and right
ventricular function in determining survival.
Circulation1986;74:45–55.
14. Fananpazir L, Bray CL, Dark JF, et al. Right
ventricular dysfunction and surgical outcome in
postinfarction ventricular septal defect. Eur Heart J
1983;4:155–67.

Comparison of Acute Physiology and Chronic
Health Evaluation-II (APACHE-II) Score And
Sequential Organ Failure Assessment (SOFA)
Score in predicting the outcome of patients with
Ventilator-Associated Pneumonia (VAP)
1 2 3
lTeena Desai , Shaila Kamart, Deepa C,
ABSTRACT
Ventilator-associated pneumonia (VAP) is a
common nosocomial infection in intensive care
units (ICU) and results in high mortality, prolonged
1
ICU stay and increased costs of health care . One
important component of treating patients with
pneumonia is the initial assessment of the severity
of disease. Scoring systems for use in the intensive
care unit (ICU) have been developed for the past
many years. The use of these prognostic models
help in providing meaningful information to
physicians when discussing patient prognosis with
thepatient’srelatives.Ourstudyfocusesonmainly
Acute Physiology and Chronic Health Evaluation II
(APACHE II) score and Sequential Organ Failure
Assessment (SOFA) scores. A prospective
observational study was conducted in an8 bedded
Intensive care unit of Goa Medical College, from
January 2013 to March 2014, after obtaining
approval from institutional ethics committee.
Patients aged more than 12 years, who were
mechanically ventilated in Intensive Care Unit for
more than 48 hours were included in the study.
The study population included surgical as well as
medical cases. Diagnosis of VAP (ventilator
associated pneumonia) was done based on CPIS
(clinical pulmonary infection) score. CPIS score of
more than 6 was diagnostic of VAP. On the day of
diagnosis of VAP, APACHE II and SOFA score were
calculated for assessing the outcome in these
2
patients . The outcomes measured were duration
of mechanical ventilation, duration of ICU stay and
mortality. Discrimination was tested using the
receiver operating characteristic (ROC) curves and
3
by evaluating area under the curve (AUC) . All
analyses were performed using SPSS (Statistical
Package for the Social Sciences) software .P -value
of <0.05 was considered to be statistically
significant. We observed that the mean APACHE II
score at the onset of VAP was higher in non-
survivors than in survivors. These findings were
consistent with the study carried out by Gursel et
2
al Although APACHE II score determined at the
time of diagnosis of VAP was higher in non-
survivors than in survivors it was not statistically
significant (P>0.05).The mean SOFA score
measured at the onset of VAP was observed to be
higher in non-survivors than in survivors and was
statistically significant (P>0.05).Although, the
APACHE II score carried a higher sensitivity
1. SeniorResident 2. Professor&HOD 3.Lecturer,DepartmentofAnaesthesiologyandCriticalCare
GoaMedicalCollege,Bambolim-Goa

(sensitivity=88.24) at the selected cut-off (APACHE
II e”16), the specificity of this score was very low
(specificity = 42.86).The sensitivity of the SOFA
score at the selected cut-off (SOFA e”10) was low
(sensitivity=47.06) but specificity was high
(specificity =100) with a positive predictive value
of 100.To conclude, the SOFA score determined at
the onset of VAP is a better predictor of mortality
thanAPACHEIIscoreinpatientswhodevelopVAP.
KEY WORDS: Ventilator Associated
Pneumonia,APACHE-II,SOFA.
Ventilator-Associated Pneumonia (VAP) is
defined as pneumonia that develops after
endotracheal tube intubation/mechanical
ventilation (MV) for more than 48 hrs. It is a
common nosocomial infection in intensive care
units (ICU) and results in high mortality, prolonged
ICUstayandincreasedcostsofhealthcare.
VAP that occurs within 48 to 72 hours of MV is
termed as early onset VAP. VAP that occurs after
this period is considered late onset VAP.VAP
accounts for approximately 8 to 20% of all hospital
acquired infections and 27% of infections in
medicalintensivecareunits.
86% of nosocomial pneumonias are associated
with mechanical ventilation. The mortality rate
4
variesfrom27to76%.
One important component of treating patients
with pneumonia is the initial assessment of the
severity of disease. Even though several scores are
availabletoevaluateseverityandtopredicttherisk
of mortality for patients with community-acquired
pneumonia, no specific score has been developed
toevaluatemortalityriskinpatientswithVAP.
Scoring systems for use in the intensive care
unit (ICU) have been developed for past many
years. They are widely used in the field of critical
care medicine. The use of these prognostic models
INTRODUCTION
help in providing meaningful information to
physicians when discussing patient prognosis with
the patient’s relatives. There are many scores
available at present. But our study focuses on
mainly Acute Physiology and Chronic Health
Evaluation II (APACHE II) score and Sequential
OrganFailureAssessment(SOFA)scores.
A prospective observational study was
conducted in 8 bedded Intensive care unit, from
January 2013 to March 2014 after obtaining
approval from institutional ethics committee.
Patients aged more than 12yrs admitted in
intensive care unit during the study period who
were on mechanical ventilation for more than
48hrs were included in the study. The study
population included surgical as well as medical
cases.
Age>12years
Patient admitted to ICU who were intubated
and mechanically ventilated for more than 48
hours
Age<12years
Patientswho were on mechanicalventilationin
otherhospitalandlatershiftedtoourinstitute
Pneumoniapriortoendotrachealintubation
History of blunt chest trauma with or without
historyofchesttubeinsertion
Historyofaspiration
Lungmalignancyprimaryandsecondary
1.Completehemogram
2. Renal function tests – Blood Urea and Serum
Creatinine
Materials & Methods
Inclusion criteria:
Exclusion criteria:
On daily basis

3.Serumelectrolytes–SodiumandPotassium
4.Arterialbloodgases
1.ChestX-ray
2.Serumbilirubin
Along with the above mentioned blood
investigations following clinical parameters were
monitored:
GlasgowComaScale
Temperature
Heartrate
Meanarterialpressure
Respiratory rate and ventilator rate
subsequently
Urineoutput
Diagnosis of VAP (ventilator associated
pneumonia) was done based on CPIS (Clinical
Pulmonary Infection Score). CPIS score of more
than 6 was diagnostic of VAP. Once the patient had
crossed 48 hours on mechanical ventilation, the
CPIS score was assessed daily using variables like
white blood cell count, temperature, quantity and
nature of secretions and PaO2/FiO2 ratio. Chest X-
ray would be taken routinely every 72hrs as a part
of ICU protocol or if CPIS >4 based on above
variables.
If the CPIS was more than 4 based on above
mentioned variables, with or without Chest X-ray
infiltrates,endotrachealaspiratewascollectedina
mucus extractor and sent for gram stain,
qualitative culture and sensitivity. CPIS was
reassessed after obtaining endotracheal aspirate
culture report. On the day of diagnosis of VAP,
APACHE II and SOFA score were calculated for
assessing the outcome in these patients. The
outcomes measured were duration of mechanical
ventilation,durationofICUstayandmortality.
Every 72 hours
Statistical Analysis
RESULTS
Equality of variances and equality of means
were tested using Levene’s test and single-tailed
t-test respectively. Cut-offs for APACHE II and
SOFA scores were calculated using the maximum
value for Youden’s index, where Youden’s index =
sensitivity – (1-specificity). Discrimination was
tested using the ROC curves and by evaluating
area under the curve (AUC). All analyses were
performed using SPSS (Statistical Package for the
Social Sciences) software .P -value of <0.05 was
consideredtobestatisticallysignificant.
There were a total of 812 admissions in 8
bedded ICU over a period of 15 months from
January 2013 to March 2014. Out of which 182
fulfilled the inclusion criteria and were enrolled in
the study. Among these patients 24 developed
VAP as per CPIS score whose APACHE II and SOFA
scoresattheonsetofVAPwereassessed.
In our study,patients wereinagegroup of 18–
76 years with mean age of 44 ± 17.Out of the 24
VAP cases,17 expired and 7 were dischargedfrom
ICU.Thepatientsincludedweremedicalaswellas
surgicalcases.
Both APACHE II and SOFA scores at the onset
of VAP were higher in non-survivors than in
survivors. The mean APACHE II score in non-
survivors was 24±7 and in survivors was 19±8
FIGURE NO: 1

(p=0.07).The mean SOFA score in non-survivors
was10±3andinsurvivorswas7±2(p=0.031).
Duration of mechanical ventilation and
duration of ICU stay was greater in patients
diagnosed of VAP with lower APACHE II and SOFA
scores.
Themeandurationofmechanicalventilationin
VAP patients with APACHE II e”16 was 18±10 days
(P= 0.003) and with APACHE II <16 was 45±32 days
(P=0.191). The mean duration of length of ICU stay
in VAP patients with APACHE e” 16 was 18±10 days
(P=0.002) and with APACHE II < 16 was 47±30 days
(P=0.158).
Themeandurationofmechanicalventilationin
VAP patients with SOFA e”10 was 20±11 days and
withSOFA<10was25±22days(P=0.45).Themean
duration of length of ICU stay in VAP patients with
FIGURE NO: 2
TABLE NO: 1
SOFA e”10 was 20±11 days and with SOFA < 10 was
26±22days(P=0.36).
Majority (67%) of the patients were found to
have late onset VAP. Most common organism
isolated in this group was Acinetobacterbaumanii.
29% of the population was affected with MDR
Acinetobacterbaumanii. Equal distribution of 15%
TABLE NO: 2
FIGURE NO: 3
FIGURE NO: 4
Duration of mechanical ventilation
N Mean Std. Std. Error
Deviation Mean
Apache >16 20 17.75 9.797287 2.247652
<16 4 44.5 31.638584 18.266545
Sofa >10 11 19.181818 10.52443 3.328117
<10 13 24.769231 22.207933 6.410878
Duration of Length of ICU stay
N Mean Std. Std. Error
Deviation Mean
Apache >16 20 18.4 10.28233 2.358929
<16 4 46.75 30.368569 17.533302
Sofa >10 11 19.454545 10.727196 3.392237
<10 13 26.230769 22.417084 6.471255

was seen with MDR Klebsiella and MDR
Pseudomonas aeruginosa.Where as in patients
with APACHE <16 causative organism isolated
were Acinetobacterbaumanii (50%), Klebsiella
(33%) and Pseudomonas aeruginosa (17%). All the
aboveorganismsshowedantibioticsensitivity.
Most common organism isolated in patients
with SOFA e”10 was Acinetobacterbaumanii, 33%
of which were MDR. Other organisms isolated
were Klebsiella (26%), Pseudomonas aeruginosa
(7%), Enterobacter (7%) and Staphylococcus
aureus(7%).
In majority of patients with SOFA <10 causative
organism for VAP was Acinetobacterbaumanii
(44%),followedbypseudomonasaeruginosa.
For the two scoring systems tested, the
sensitivity and specificity values were calculated,
and cut-off points for the mortality were
determined. From table no.3 it could be inferred
that the cut-off point for APACHE II score is e”16
(sensitivity=88.2, specificity=42.86). APACHE II
e”16wasassociatedwithhighermortality.
Fromthetableno.4itcouldbeinferredthatthe
cut-off for SOFA score is e”10 (sensitivity=47.06,
specificity=100). SOFA e”10 was associated with
FIGURE NO: 5
highermortality.
The ROC (Receiver Operating Characteristic)
curves for APACHE II and SOFA score are shown in
fig10.Area under the curve(AUC) is greater for
SOFA (AUC=0.75) than for APACHE II (AUC=0.67)
and is statistically significant(p=0.01). APACHE II
score e” 16 had a positive predictor value of 78.9
and negative predictor value of 60. SOFA score e”
10hadpositivepredictorvalueof100andnegative
predictor value of 43.7. SOFA had greater
specificitythanAPACHEII.
Discrimination power of SOFA was statistically
significant (AUC=0.75, CI=0.53-0.90, p =0.01) but
not significant for APACHE II (AUC=0.67, CI= 0.45-
0.85,p=0.17)(fig10).
Ventilator-associated pneumonia (VAP) is the
most frequent hospital acquired infection. It is the
leading cause of mortality associated with
nosocomial infection. Prediction of its outcome is
important in the decision-making process. It
results in high mortality, prolonged ICU stay and
increased costs of health care. It accounts for 8 to
1
20%ofallhospitalacquiredinfections .
FIGURE 6
DISCUSSION

The mortality rate in patients developing VAP
ranges from 33 to 70%. This depends on patient-
specific characteristics, diagnostic criteria, and the
pathogens involved; however, the directly
attributablemortalityremainscontroversial.
Previous studies have not clearly
5
demonstrated that pneumonia is indeed
responsible for the higher mortality rate of these
patients. Two independent factors make it difficult
to assign responsibility unambiguously. The first is
the difficulty in establishing a firm diagnosis, that
is, to clearly identify patients with VAP. Second,
studies have demonstrated that severe underlying
Criterion Sensitivity 95% CI Specificity 95% CI +PV -PV
e”7 100.00 80.5 - 100.0 0.00 0.0 - 41.0 70.8
>7 100.00 80.5 - 100.0 14.29 0.4 - 57.9 73.9 100.0
>12 94.12 71.3 - 99.9 14.29 0.4 - 57.9 72.7 50.0
>13 94.12 71.3 - 99.9 28.57 3.7 - 71.0 76.2 66.7
>14 88.24 63.6 - 98.5 28.57 3.7 - 71.0 75.0 50.0
>16 88.24 63.6 - 98.5 42.86 9.9 - 81.6 78.9 60.0
>18 76.47 50.1 - 93.2 42.86 9.9 - 81.6 76.5 42.9
>19 70.59 44.0 - 89.7 57.14 18.4 - 90.1 80.0 44.4
>20 64.71 38.3 - 85.8 57.14 18.4 - 90.1 78.6 40.0
>22 58.82 32.9 - 81.6 71.43 29.0 - 96.3 83.3 41.7
>24 41.18 18.4 - 67.1 71.43 29.0 - 96.3 77.8 33.3
>26 35.29 14.2 - 61.7 85.71 42.1 - 99.6 85.7 35.3
>30 17.65 3.8 - 43.4 85.71 42.1 - 99.6 75.0 30.0
>31 17.65 3.8 - 43.4 100.00 59.0 - 100.0 100.0 33.3
>37 0.00 0.0 - 19.5 100.00 59.0 - 100.0 29.2
TABLE NO: 3
Criterion Sensitivity 95% CI Specificity 95% CI +PV -PV
e”4 100.00 80.5 - 100.0 0.00 0.0 - 41.0 70.8
>4 94.12 71.3 - 99.9 14.29 0.4 - 57.9 72.7 50.0
>6 88.24 63.6 - 98.5 28.57 3.7 - 71.0 75.0 50.0
>7 76.47 50.1 - 93.2 42.86 9.9 - 81.6 76.5 42.9
>8 64.71 38.3 - 85.8 71.43 29.0 - 96.3 84.6 45.5
>9 58.82 32.9 - 81.6 85.71 42.1 - 99.6 90.9 46.2
>10 47.06 23.0 - 72.2 100.00 59.0 - 100.0 100.0 43.7
>16 0.00 0.0 - 19.5 100.00 59.0 - 100.0 29.2
TABLE NO: 4

illness predisposes patients in the ICU to the
development of pneumonia, and their mortality
7
rates are, consequently high . Therefore, it is
difficult to determine whether such patients
wouldhavesurvivedifVAPhadnotoccurred.
In contrast , in patients with extremely severe
medical conditions, such as those surviving
cardiac arrest, or young patients with no
underlying disease, such as those admitted after
8,9
trauma
Nosocomial pneumonia does not seem to
significantly affect prognosis. Similarly, VAP does
not appear to markedly influence overall survival
of patients with ARDS, as documented by several
10,11,12
studies . Despite these difficulties and
limitations, the results of several studies support
the notion that the presence of VAP is an
important determinant of the poor prognosis of
patients treated with mechanical ventilation.53
13,14,15,16
other studies were in agreement with our
findings with respect to SOFA score that differed
significantly between survivors and non-
survivors.
A model’s discrimination (the ability of the
model to distinguish patients who died from
those who survive) was assessed by numerically
examining the AuROC (Area under receiver
operating curve). An AuROC of 1 means a perfect
discrimination while 0.5 is a random chance. A
model is considered acceptable if the AuROC is
e”0.7 and is considered excellent if the AuROC is
17,18,19.
e”0.9
Discriminatory power in outcome prediction
as estimated by the AuROC was acceptable for
initial SOFA score (AuROC=0.75) but less
satisfactory for APACHE II score (AuROC=0.67).
Thus it could be inferred that among the two
scores calculated at the onset of VAP, SOFA score
wasabetterpredictor.
TheAPACHEIIscorecarriedahighersensitivity
(sensitivity=88.24) at the selected cut-off (APACHE
II e”16), but the specificity of this score was very
low (specificity = 42.86).The sensitivity of the SOFA
score at the selected cut-off (SOFA e”10) was low
(sensitivity=47.06) but specificity was the highest
(specificity=100)withapositivepredictivevalueof
20
100. Similarly, in a study by Halimet al. SOFA
scoringsystemwasbetterthanAPACHEIIsystemin
predicting mortality in ICU surgical patients. Serial
measurements of SOFA score significantly
improvedthepredictiveaccuracy.
SOFA-based prognostic models provide insight
into the dynamics of organ failures and their
relation to mortality. Its simplicity and feasibility
makes it a preferred choice over other ICU
prediction scores such as APACHE score, which
provides only an admission risk factor
2,13
profile compared APACHE II and SOFA scores at
onset of VAP in 63 pulmonary patients; found that
APACHE II score is a better predictor in comparison
to SOFA score in pulmonary patients who
developed VAP. Our results were not consistent
with this study. The opposing results could be
attributed to the different 54 study population, as
our study included medicalas well as surgicalcases
andsmallersamplesizeofourstudy.
The scoring system used regularly in most ICUs
is the APACHE II score. However, several other
studies revealed a few weaknesses in its ability to
predict outcomes in patients with sepsis and
peritonitis. (110, 111, 112, 113, 114) APACHE II
score has also been consistently less accurate in
21,22,23
predictingtheoutcomesoftraumapatients.
Patients with unstable hemodynamic which
24
require invasive cardiovascular monitoring, and
25
post cardiopulmonary bypass surgery .The
APACHE II score is quite cumbersome to perform
and with less satisfactory prediction accuracy in
manysurgicalcasesasdescribedabove.
The SOFA score has several desirable

characteristics,becauseitiseasytocalculateatthe
bedside and includes clinical and laboratory data
that are routinely available in the ICU. The SOFA
scoreismorepractical,includesonlyvitalsignsand
laboratory data that are routinely available and
does not require a definitive final diagnosis of the
acuteprocess.
These facts, in addition to the equivalent
performance of the SOFA score observed in this
study, suggest that it may be preferred more than
APACHE II score for risk stratification and
prognosis.
Our results suggested that it might be possible
to use this scoring system to predict mortality in
patients with VAP. Even though the primary aim of
the SOFA score is not to predict mortality, a
relationship exists between organ failure and
death, and thus between morbidity and
26
mortality.
Other outcomes observed in our study were
the duration of mechanical ventilation and
duration of ICU stay. Duration of mechanical
ventilation and length of ICU stay was shorter in
patientswhodevelopedVAPwithhigherAPACHEII
i.e. e”16 and higher SOFA e”10.These findings
werenotinagreementwithfindingsbyLauplandet
27
al and J.M.A˜nón etal (121) in which the APACHE
II and SOFA scores were higher among the patients
subjectedtoprolongedventilation.
Furthermore, mortality was influenced by type
of organism isolated. We observed that majority
(59%) of patients with higher APACHE II score were
affected by MDR organisms as evident from fig.
Similar trend was seen in patients with higher
SOFA score, MDR organisms being more prevalent
in these patients (fig. 9). Some studies have
claimed increased mortality rates associated with
bacteraemia, especially with Pseudomonas
aeruginosa or Acinetobacter species, medical
rather than surgical illness, and treatment with
18,19
ineffectiveantibiotictherapy.
Acinetobacterbaumanii and Pseudomonas
aeruginosa were the most common organisms
isolated in patients who developed VAP. Among
the 24 patients diagnosed of VAP, 67% had late
onset type of VAP (fig.8). Both these factors are
related with higher mortality. Our results showed
shorterdurationofMVandICUstayinVAPpatients
with higher APACHE II and SOFA scores. This could
be attributed to higher mortality among these
patients, hence shorter duration of MV and ICU
stay.
Outcome studies suggest that several factors
such as age, co-morbidity, sepsis, resistant
microorganisms and appropriateness of the
antibiotic therapy are related to the mortality rate
28
in VAP . A number of underlying chronic diseases
and co-morbidities impact on the eventual
outcome in patients with VAP. Immu-
nosuppression, hypotension, multilobar lung
infiltrates, and thrombocytopenia have been
previously demonstrated as risk factors for
mortality in patients with community acquired
29,30,31
pneumoniaandinpatientswithVAP
Studies of the effect of length of stay in the
hospital, length of stay in the intensive care unit, or
prior days on a ventilator have indicated that
patients who developed late-onset VAP are at an
increasedriskforpooroutcomes.
1. The small sample size was the foremost
limitation of the study since it influences the
evaluation of calibration and discrimination of
thescores.
2. As the study was performed within a single ICU,
the results cannot be extended to other
treatmentsettings.
3. Since severity of underlying disease, age of the
patients and therapy protocols are different
Limitations of our study

from one ICU to the next, each ICU needs to
determine their own cut-off points for each
scoreevenfordifferentpatientgroups.
4. Repetitivescoreswerelackinginthisstudy.
To conclude, the SOFA score determined at the
onset of VAP is a better predictor of mortality than
APACHE II score in patients who develop VAP.
Higher APACHE II and higher SOFA score was
associated with shorter duration of mechanical
ventilation and length of ICU stay possibly due to
higher mortality in these patients secondary to
factors like age, co-morbidity, sepsis, resistant
microorganisms and appropriateness of the
antibiotic therapy. However, due to the limited
number of patients in this study, further studies
with greater number of patients are required to
improvetheaccuracy.
1. Safdar N, Dezfulian C, Collard HR, Saint S.
Clinical and economic consequences of
ventilator-associated pneumonia: a systematic
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2. Gursel G, Demirtas S. Value of APACHE II, SOFA
and CPIS scores in predicting prognosis in
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in intubated trauma patients. Microbiology and
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10.Chastre J, Trouillet JL, Vuagnat A, Joly-Guillou
ML, Clavier H, Dombret MC et al Nosocomial
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1999;159:1249-1256
11.Delclaux C,Roupie E, Blot F, Brochard L, Lemaire
F, Brun-Buisson C. Lower respiratory tract
colonization and infection during severe acute
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diagnosis. Am J RespirCrit Care Med 1997; 156:
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12.Markowicz P, Wolff M, Djedaini K, Cohen Y,
Chastre J, Delclaux C, et al. Multicenter
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30:1705–1711.
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Case Report
NEUROSURGERY AND PREGNANCY: A
UNIQUE ANAESTHETIC CHALLENGE
1 2 3
lDr Sadhana Sanwatsarkar, Dr. Dipti Saxena, Dr. Vibhu Gupta,
1. ProfessorandHead
2. AssociateProfessor
3. PGresident
DepartmentofAnaesthesiologyandcriticalcare,SAIMS,Indore.

r Chandy Varghese was born in Trissur,
Kerala. Following schooling from variousDschools in India, he graduated from Madras
Medical College, Madras in 1974. His grandfather
had also graduated from the same college in 1907
and served as a general surgeon in British Army
MedicalService.ChandyVarghesewasalsorelated
to ShriVarghese Kurien, father of “White
Revolution” in India. During his college days,
Chandy Varghese was actively involved in sports.
He led his college basketball team as Vice captain
to win the state championship and was an ardent
snookerplayertoo.
After completing his medical graduation, he
workedasamedicalofficerinKeralateaplantation
hospital for almost a year. In 1976, DrChandy
VarghesemigratedtoUK.
In UK, he initially joined as a house officer in
medicine, but later moved as registrar in
department of anaesthesia at Royal Gwent
hospital and Taunton hospital. at British Royal
Infirmary, Dr Chandy got the chance to work under
the doyens of anaesthesia Cedric Prys-Roberts and
Peter Baskett, leading to an academic stimulation
to his clinical mind. He gradually progressed to the
post of lecturer in the academic unit of Royal
London.
At Royal London, Dr. Varghese first met Dr.
Archie Brain, and happened to witness the
insertion of Brain's Laryngeal Mask Airway (LMA)
undertopicalanaesthesia.Itwasfollowingthisand
many more meetingsthattheir associationled toa
revolutionary development in the field of airway
management. Chandy Varghese later became the
senior Lecturer and Honorary Consultant and Dr
Brain worked as Locum Consultantat Newham,
RoyalLondon.
In 1987, Dr Chandy joined the Royal Berkshire
in Reading as Consultant Anaesthetist, whereDr
Brain also finally got financial support for his work,
from Robert Gaines-Cooper and Panter and it was
this opportunity that paved the way to
pathbreaking evolution in airway management
methodologies.
Late Andranik Ovassapian once wrote 'Dr.
Brain's innovation is a gift of life to patients and
anesthesiologists alike..” In a private house near
Royal Berkshire, Dr. Brain constantly made new
prototypes, which Dr. Varghese would put to
clinical test on patients in hospital, and the
promising models would undergo further formal
clinical trials and assessments. Thus, the LMA
family grew from simple classic LMA to the second
generation supraglottic devices(SGD) and
intubatingLMAs.
Along with development of newer LMA
congeners, Dr Varghese also hugely contributed in
promoting the use of LMAs and SGDs for securing
airway in various difficult airway scenarios
including prone position, neonates, intensive care
A TRIBUTE TO DR. CHANDY VARGHESE
1. Assistant Professor, Anaesthesiology and Critical Care, Army College of Medical Sciences and Base
Hospital,DelhiCantt.
1
lCompiled by Dr. Jyotsna Agarwal,

units etc., which saved many lives and potential
catastrophes.He would travel across globe to
impart knowledge and training on use of LMA.His
another clinically very significant contribution to
airway management is the “Chandy Manoeuver”,
which maximizes the chances of intubation
throughIntubatingLMA(ILMA).
th
Founder member and 9 president of Society
of Airway Management, USA, Chandy Varghese
released his own video demonstrating airway
blocks and awake intubation using ILMA on
himself in 2008. The video gained widespread
popularity and has been viewed more than 47000
times till now. Dr. Chandy Varghese was conferred
with the prestigious DAS Mcewen medal in 2011
for his outstanding contributions to the airway
society.
He was known tobe a passionate teacher and a
very fine human being. Extremely soft spoken and
g r o u n d e d , D r Va r g h e s e r e m a i n e d
unpresumptuoustoallthefameheacquired.Inhis
later years, Chandy Varghese was not keeping well
th
and the great soul left us for heavenly abode on 5
March2017.
The anaesthesiologists and Airway society all
over the world will miss Dr Chandy Varghese
dearly.
1. Difficult Airway Society-Citation for 2011 DAS
medal.
2. Friends and close associates of DrChandy
Varghese
References

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