2. Anaesthesiology M.P. 1
CONTENTS
ANAESTHESIOLOGY
M.P
Dr. Meenu Chadha
From Editor's Desk - Bioterrorism A Challenge for the
Anaesthesiologist
021EDITOR
Dr. Meenu Chadha
CO-EDITOR
Dr. Alok Biyani
EDITORIAl BOARD
Dr. Harsha Desai Phulambrikar
Dr. Ashwin Soni
Dr. Suman Gupta
Dr. Ruchi Tandon
Dr. Ashish Sethi
Dr. Harsh Mangal
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
Chief Anaesthetist,
Pain Physician &
OT Suprintendent
Vishesh Hospital Indore.
chadha.meenu@gmail.com
9977161035
Consultant
Apollo Hospitals
Indore
drolokbiyani@gmail.com
9329548444
Dr. Gyanesh Namjoshi, Dr. Maria Rita Maccaroni
Temperature Management after Cardiac Arrest
042
Dr. Suman Gupta, Dr. Preeti Goyal, Dr. Neelima Tandon,
Dr. Bhanu Choudhary
Symmetrical Chest rise and bilateral equal air entry
could be falsity, for assessment of correct tracheal
intubation in neonatal age group - Case Report.
133
Dr. Ruchi Tandon, Dr. Sonal Awasya
Congenital Fibroepithelial Polyp; A case report of
difficult airway
194
Dr. Shailendra Singh Chauhan
A Comparison of Classical Postero-Lateral Approach
and Transdiscal Approach for Hypogastric Plexus
Block in Patients with Chronic Pelvic Pain
215
Dr. Lini Shrivastava, Dr. Monika Gandhi,
Dr. Ravi Shrivastava, Dr. K. K. Arora, Dr. Vilas Niwasker
Anesthetic Management in A Case of Childhood
Odontogenic Myxoma
306
3. The devastating consequences of the nine
eleven attacks in the United States have
drawn attention worldwide on the potential
complications of a successful terrorist attack.
Before the nine eleven attack terrorism was
rarely on the forefront of American mind but
today terrorism is reported and analyzed in
almost every media outlet. Whether the attack
is a hoax, a small food borne outbreak, a lethal
aerosol cloud moving silently through the city at
night or introduction of contagious disease, the
possibility of biological warfare is rapidly
becomingareality.
Standardized protocols have been made in
the United States to manage accidental release
1,2,3
of the hazardous material (HAZMAT) which
provides detailed information to emergency
services above the action and management of
toxic substances when in use or during
4,5,6
transit . HAZMAT database provides
i n f o r m a t i o n f o r p r o t e c t i o n a n d
decontamination and clinical management
7,8
protocols . This system deals with both
accidentalanddeliberatereleases.
The severity of the chemical and biological
weapon (CBW) attack depends on the dispersal
method used. CBW release into the water and
food supply is less hazardous than what results
from airborne release. Though water and food
may be contaminated secondarily even after
airbornerelease.
Anaesthetists and intensivists routinely deal
with sick patients and are very well versed with
the pathophysiology and pharmacology, so they
arethebestpeopletodealwiththeaftermathof
a terrorist or CBW attack. Most of the
anaesthesiologists do not have full information
of the CBW agents. White has produced a useful
comprehensive document elaborating a wide
range of chemicals, toxins and organisms that
are suspected to be used in warfare and the
9
terrorist’s attacks . He has also classified CBW
agents as weapons of mass injury and not of
destructionwhichisamorerealistictermforthe
anaesthesiologist. Personal safety is very
important. Anaesthesiologists who are part of
the primary response team should be trained to
use Level C personal protective equipment i.e. a
full face mask or half face mask, air purifying
respirators, hooded chemical resistant clothing
(splash suits), chemical resistant gloves and
boots. Exposure of anaesthetists can also be
reduced by decontamination of the patient
before admission. Decontamination means
removal or neutralization of the CBW’S to limit
human exposure. This prevents further damage
in patients and protects the health care workers
from injury. Decontamination in the ambulance
is ideal because it will minimize the exposure in
thehospital.
Some biological agents are very infectious so
continued personal protection is needed even
Anaesthesiology M.P.2
BIOTERRORISM A CHALLENGE
FOR THE ANAESTHESIOLOGIST
EDITORIAL
DR. Meenu Chadha
4. Anaesthesiology M.P. 3
after decontamination. Life saving treatment,
both due to the effect of CBW’s and of
concomitanttraumamayberequiredbeforethe
patients are decontaminated. Resuscitation
may be difficult because the type of CBW used is
not known and there may be lack of antidotes.
Treatment may require prolonged ventilation
andsupportivetreatmentintheICU.
There is an alarming statistics which is
quoted for significant chemical or biological
weapon attack, but the mortality is low.
Morbidity is however is high because of the
unpreparedness for the event. There is an
increased recognition that medical outcome
may be improved by implementation of specific
CBW mass casualty procedures in conjunction
with the dissemination of irrelevantinformation
concerningclinicalmanagement.
It is important that anaesthesia societies
t a ke i n t e r e s t a n d ex p l a i n t o t h e
anesthesiologists that they have an important
role to play in the management of chemical
injury. Most of the general public is still unaware
thatan anaesthesiologist is a medicalpractioner
so it will be a revelation to them. Training and
close integration of the anaesthesiologist into
toxic emergency response team is needed and
training for this is essential. The speciality must
bring out clear and positive message about the
real dangers of the CBW, and appropriate
protocols should be formed to provide some
comforttothegeneralpublic.
1. Baker DJ. The pre hospital management of
injury following mass toxic release; a
comparison of military and civil approaches.
Resuscitation1999;42:155–9
REFERENCES-
2. HAZMAT. Emergency Response Guidebook,
2000,eversion:http://www.tc.gc.ca/canutec
/erg_gmu/erg2000_menu.htm
3. Moles TM. Emergency medical services
systems and HAZMAT major incidents.
Resuscitation1999;42:103–16
4. Borak J, Callan M, Abbot W. Hazardous
Materials Eposure ; Emergency Response
and PatientCare, New Jersy; Prentice Hall Inc
,1991.
5. Moles TM. Emergency Medical Services
Systems and HAZMAT major incidents.
Resucitation 1999;42:103-16 .
6. Organisation of Economic Cooperation and
Development ( OECD) . Health Aspects of
Chemical Accidents : Guidance on Chemical
Accident Awareness. Preparedness and
Response for Helath Professionals and
Emergency Responders .Paris : OECD
Environment Monograph No. 81
(OCDE/GD(94)I)1994.
7. Bronstein AC, Currance PL. Emergency Care
for Hazardous Materials Eposure 2ndEdn.
MosbyLifeline:1994.
8. US Dept of Health and Human Services (
Agency for Toxic substances and Disease
Registry): M a n a g i n g H a z a r d o u s
Materials–Vols1-3.1996
9. White SM. Chemicaland biologicalweapons:
implications for anesthetic and intensive
care.BrJAnaesth2002;89:30624.
10. Brennan RJ, Waeckerle JF, Sharp TW,
Lillibrirge SR. Chemical warfare agents:
emergency medical and emergency public
health issues. Ann Emerg Med 1999;34:
191–204
5. 1-2. Consultant CardiothoracicAnaesthetist, Essex CTC, Basildon, U.K.
gyanesh.namjoshi@gmail.com; mariarita.maccaroni@gmail.com
Introduction
Sudden cardiac arrest is one of the major
causes of death in the whole world. The global
incidence of Out of Hospital Cardiac Arrest
(OOHCA) is about 82.9 per 100,000 populations in
all age group and about 213.1 per 100,000 in adult
1
age group. Return of spontaneous circulation
2,
(ROSC)is observed in 25% to40 % of the patients.
3
. Global brain ischemia and reperfusion injury
following resuscitation are the major reasons for
pooroutcomeandhighmortalityafterROSC.
After OOHCA, improvement of neurological
outcomes and survival is related to the post-
resuscitation care, which includes optimising
oxygenation and ventilation, avoiding
hypotension, treating immediate precipitants of
cardiac arrest such as acute coronary ischemia,
and the management of temperature where it is
notcontraindicated.
The use of Mild Therapeutic
Hypothermia (MTH) to 32-34 C° for 12- 24 hours is
adopted for the treatment of unconscious adult
patients with ROSC. Two randomized control
studies (RCTs) have shown the beneficial effect of
MTH in the improvement of survival and
neurological outcomes of patients following
4,5
cardiac arrest. In 2010, European resuscitation
council (ERC) and European society of intensive
care medicine (ESICM) collaborated to produce
guidelines to recognise the importance of high
5,6
qualitypost-resuscitationcare.
According to a systematic review of global
incidence of OOHCA, the incidence of treated
OHCAs was higher in North America (54.6) than in
Europe (35.0), Asia (28.3), and Australia (44.0). In
Asia, the percentage of ventricular fibrillation (VF)
and survival to discharge rates were lower (11%
and 2%, respectively) than those in Europe (35%
and9%,respectively),NorthAmerica(28%and6%,
respectively), or Australia (40% and 11%,
6
respectively.
The MTH was recommended by the
international guidelines to protect the brain
against the global ischemia that occurs during the
cardiac arrest. This became the standard
management of unconscious patients with ROSC
untilrecently.
A randomized trial by Nielsen et al, published
in the New England Journal of Medicine
0
comparedtheoutcomesofcoolingpatientsto33 C
0
with those to 36 C. The survival and the
neurological outcomes were not statistically
different in the two groups of patients. The key
message is that we need to avoid hyperthermia in
24
the patients who have had a cardiac arrest . The
MTH is not superior to the target temperature
0
management to 36 C in terms of outcomes but it is
associated with side effects such as coagulopathy
Anaesthesiology M.P.4
TEMPERATURE MANAGEMENT AFTER
CARDIAC ARREST
1 2
lDr. Gyanesh Namjoshi , Dr. Maria Rita Maccaroni
Anaesthesiology M.P.4
6. andhemodynamicinstability.
Hypothermia has been described as a therapy
7
in medicine. It dates back to about 5000 years .
However, its use has become widespread since
2002, following the demonstration of safety and
rationale of cooling as a technique of
neuroprotection in different clinical scenarios,
such as post- cardiac arrest, traumatic brain injury
8-12
spinal cord injury, and stroke. In 1950s Bigelow
et al. documented the positive effect on the brain
13
during cardiac surgery in animals models.
Rosomoff demonstrated that hypothermia
reduced cerebral blood flow and oxygen
14
consumption In 1958 the first clinical trial was
published considering hypothermia in the
treatment of unconscious patients following
15
cardiacarrest .
Despite the good survival, the use of
therapeutic hypothermia in clinical practice was
abandoned due to the side effects such as
arrhythmias, coagulopathy and infections. In
2002, two prospective randomized controlled
trails demonstrated the benefit of therapeutic
hypothermiainpatients,cooledfor12-24hoursto
0
32-34 C within few hours from ROSC following an
OOHCAwithVF/VTfirstrhythm.Thesetwostudies
compared mild hypothermia with normothermia
in comatose survivors of OOHCA. The studies
demonstrated improved survival and neurological
outcomes in patients treated with mild
hypothermia compared with normothermic
group. Survival to hospital discharge to home was
49% in the hypothermia group and 26% in the
16,17
normothermicgroup .
Mild hypothermia provided significant
functional neurological recovery at hospital
discharge (55% vs 39%) and the 6–months
mortality was lower compared with patients that
18,19
were not cooled (41% vs 55%) . Following the
Hypothermia
results of these two randomized studies, in 2003,
the International Liaison Committee on
Resuscitation(ILCOR)hasrecommendedtheuseof
mild hypothermic therapy for the treatment of
OOHCA patients with VF and VT cardiac arrest. The
same recommendation was confirmed in the
Guidelines for the Cardiopulmonary Resuscitation
20
in2010.
The prevalence of VF/VT in OOHCA is 25-30%,
while the prevalence of non VF-VT cardiac arrest is
higher (70-75%).The evidence in the literature
abouttheuseofMTHinthesekindofrhythmisless
clear. Despite the lack of evidence, the guidelines
have suggested to use MTH in patients with non
21,22,23
VF-VTcardiacarrest .
In 2013, a cardiac study studied the targeted
0 0
temperature management at 33 C versus 36 C.
The cardiac study enrolled 950 patients and found
that survival and neurological outcomes were not
0
statistically different in patients cooled to 33 C
0
compared with those cooled to 36 C. This
randomised trial found the same good outcomes
0
withanewtargettemperatureat36 C,withoutthe
24
sideeffectsrelatedwiththemildhypothermia .
Inducing mild therapeutic hypothermia in
patients successfully resuscitated from cardiac
arrest improves neurologic survival in the short
term. This beneficial effect appears to be
independent of the method used to induce
hypothermia. Hypothermia can affect many
p at hways , w h i c h a re i m p o r ta nt fo r
neuroprotection like reactions of inflammation,
apoptosisandintracerebralmetabolism.
During cerebral ischemia, there is deficiency in
oxygen, adenosine triphosphate (ATP) and
glucose. Cerebral metabolic rate is a principal
Neuroprotection with Mild Therapeutic
Hypothermia:
Decrease in Cerebral metabolism
Anaesthesiology M.P. 5
7. Anaesthesiology M.P.6
26
determinantincerebralperfusion .
Following a period of ischemia-reperfusion,
the cells can be destroyed or enter a pathway
leading to programmed cell death a process called
apoptosis. It is related to the release of
26
intracellular caspase enzymes Mild hypothermia
seems to inhibit the caspase enzyme activation
and decreases p53 proteins levels - a protein that
activates genes of apoptosis and pro-apoptosis
27
levelsinthebrain.
Followinga period of ischemia with low level of
O2 in the brain, the level of ATP decreases and the
intracellular metabolism becomes anaerobic
leading to an increase in intracellular levels of
inorganic phosphate, lactate and hydrogen
resulting in both intra and extra-cellular acidosis
28,29
and movement of calcium into the cell. . As
calcium increases mitochondria sequesters it,
causingmitochondrialdysfunction.
Calcium activates intracellular enzymes,
leading to neuronal cell membrane depolarization
and releasing excitatory neurotransmitters such as
glutamate. Excitatory amino acids act on NMDA
receptor. The NMDA receptor requires the
presence of glycine to be activated, and glycine
30
acceleratesthefunctionofthesereceptors .
The activation of excitatory receptors leads to
an influx of sodium and chloride into the cells and
further influx of calcium into the cells; this causes
influx of water resulting in intracellular edema and
cellulardeath.
This cycle is called neuroexcitatory cascade i.e.
there is increase in intracellular calcium,
accumulation of glutamate and activation of
glutamate receptors. Mild hypothermia can
modify the neuroexcitatory cascade. The release
of excitatory neurotransmitters such as glutamate
Apoptosis
Neuro-excitotoxicity
31
and aspartate is temperature dependent .
Hypothermia decreases the release of excitatory
32
aminoacidsanddecreasestheglycinelevels .
Following an ischemia –reperfusion injury
there occurs activation of immunological
inflammatoryresponseand releaseoffreeoxygen
radicals such as superoxide, peroxynitrite,
hydrogenperoxideandhydroxylradicalsleadingto
peroxidation of lipids, proteins and nucleic acids
33,34,35,
that means damage of cellular components .
Under hypothermic conditions, the quantity of
free radicals significantly reduces, allowing lower
cellular damage and better neuroprotection. Mild
hypothermia reduces the inflammatory products
such as cytokines, interleukins and arachidonoic
36,37
cascade
Ischemic-reperfusion causes disruption in the
blood-brain barrier integrity that can lead to
38,39
cerebral oedema . Mild hypothermia attenuates
the destructive process related with the anoxic
brain injury such as integrity of the membrane,
failure of ion pumps, mitochondrial dysfunction,
intracellular enzymes, and cellular hyperactivity.
Allthesefactorsreducebloodbrainbarrier disruptions
40,41
anddecreasesvascularpermeability .
After cardiac arrest there is immunological and
inflammation activation causing coagulation
activation with intra-vascular formation.
Hypothermia has anticoagulant effects, leading to
mild platelet dysfunction and inhibition of
42,43
coagulationcascade .
CARDIVASCULAREFFECTS
Hypothermia can cause hypovolemia due to
Inflammation and free radical production
Cerebral oedema
Coagulation
PHYSIOLOGICAL CHANGES RELATED WITH
THERAPEUTIC HYPOTHERMIA
8. Anaesthesiology M.P. 7
“colddiuresis” through a combination of increased
venous return secondary to peripheral veno-
constriction, decreased level of antidiuretic
hormone receptor levels and activation of atrial
44
natriuretic peptide . Hypovolemia if not
corrected, can cause hypotension and electrolyte
45
imbalance . Mild hypothermia decreases the
heart rate by reducing the rate of spontaneous
depolarization of cardiac myocytes, as well as
prolongation of the duration of action potentials
and a mild decrease in the speed of myocardial
impulse conduction. Hypothermia can prolong the
PR interval, the QT interval and widen the QRS
43
complex . Mild hypothermia induces coronary
vasodilatation, increases myocardial perfusion
43
andreducesmetabolicrate .
In contrast, deep hypothermia can induce
vasoconstriction in atherosclerotic coronary
arteries, shivering, tachycardia and increase in the
46,47
metabolic rate . We need larger data to
understand the mechanism of hypothermia on the
coronaryperfusion.
Mild hypothermia can cause platelet
dysfunction and mild decrease in platelet
48,49
count . Mild hypothermia can cause dysfunction
in the synthesis and action of clotting enzymes.
Though mild hypothermia is associated with mild
coagulopathy, it is not associated with severe
bleeding
Mild hypothermia causes reduction in the
cytochrome p450 functional activity. Hypothermia
affects the rates of tubular secretion and
reabsorption causing reduction in drug
50
clearance . The serum amylase concentration is
increased during hypothermia but the significance
of this is unclear. The clearance of sedative drugs
and neuromuscular blockers is reduced by up to
COAGULATION
LIVER FUNCTION AND METABOLISM
0 51
30%atthecoretemperatureof34 C.
The Hypothermia therapy can be divided into
threephases:
1.Induction
2.Maintenance
3.Re-warming
1. The induction phase: The patients, who qualify
for MTH, should be intubated, sedated and
maintained on controlled ventilation. Internal
or external cooling techniques can be used.
Cooling should commence rapidly and as early
as possible with the aim to get core
temperature down to targeted level as quickly
as possible (within 4-6 hours of cardiac arrest).
This phase is related toseveral side effects such
as hypovolemia, electrolyte disorders, and
52
hyperglycaemia.
2. The maintenance phase consists of control of
core temperature and effective temperature
monitoring. This can be done with a thermistor
placedinthebladderand/orintheoesophagus
that avoids temperature fluctuations
0
(maximum 0.2-0.5 C) and overcooling. There
are several methods of inducing and
maintaining the target temperature like; Ice
packs, cooling blankets, water or air circulating
blankets, transnasal evaporative cooling,
intravascular heat exchanger and
extracorporeal circulation. Vasopressors may
be required to maintain the MAP >65 mm of
Hg. Aim for avoidance of hypoxemia, and
maintain a normal pH and PaCO2levels. Ensure
that patient is adequately sedated and
consider anticonvulsant therapy if seizure
activity is noted. Observe and manage cardiac
arrhythmias, replace electrolytes and look for
the signs of infection. 2-4 hourly skin and
pressure area assessment is also very
Maintenance of MTH and re-warming
9. Anaesthesiology M.P.8
important, as, hypothermia increases the risk
of skin breakdown due to reduced blood flow
53,54
totheperipheries.
3. The goal of rewarming is to achieve
normothermia i.e. to avoid rebound
hyperthermia. After 24 hours of maintenance
phase, patients are gradually rewarmed to
0
36 C. The re-warming phase should be slow
and controlled. The optimal rate of rewarming
is uncertain, but the consensus is currently
0
about 0.25- 0.50 C rewarming per hour (ILCOR
recommendation). It usually takes about 8
hours for controlled rewarming. The
rewarming phase is very critical as, the
constricted peripheral vascular beds start to
dilate and it may cause hypotension.
Rewarming can cause electrolyte imbalance
such as hyperkalemia due to shift of K+ from
the intracellular to the extra-cellular
compartment and Insulin sensitivity can
56
increasecausinghypoglycaemia .
Neurological evaluation should be performed
53,54
atleast72hoursaftercompletionofTTM.
Therapeutic hypothermia has shown to
improve outcome after out-of-hospital cardiac
arrest. With initial shockable rhythm, it is now
recommended in international resuscitation
guidelines and its use has been extended to
cardiac arrest following other causes as well as in
hospital cardiac arrests. However, several issues
such as optimal level of temperature or correct
method of cooling still remains unexplained.
Unconscious survivors of OOHCA have a high risk
ofdeathorpoorneurologicalfunction.
In 2013, publication of the large international
multicentre randomised TTM trial, by Nielsen et
0 0
all, compared 33 C with 36 C in unconscious
survivors of OOHCA and with minimum follow-up
0 0
33 C vs. 36 C –TTM trial
24
of 6 months. . At the end of the trial, 235 of 473
patients in the 33°C group (50%) and 225 of 466
patientsinthe36°Cgroup(48%)haddied.Thistrial
demonstrated that there were no significant
differences between the two groups in overall
mortality or in the poor neurologic function or
death at 180 days. Trial proposed that, based on
these results, decisions about which temperature
to target after out-of-hospital cardiac arrest
requirescarefulconsideration.
Nicolas Deye et all performed an international
survey in 2015 to observe the impact on change in
practice, after the publication of Nielson's study in
57
New England Journal of medicine . Based on the
518 responders from 264 ICU from 11 countries,
they concluded, “The TTM trial publication has
induced a modification of current practices in one-
third of respondents, whereas the 32–34°C target
temperatureremainedunchangedfor56%.
Considering debates after various large trials,
ILCOR experts published a new recommendation
regarding the TTM use after cardiac arrest. They
suggested that the clinicians should provide post
resuscitation care based on current
recommendationsandlocaldecisionscanbemade
0
to use the target temperature of 36 C pending
55
furtherguidancefromILCOR .
There is wide variability in survival rate among
hospitals and caringfor patients after resuscitation
from cardiac arrest. This depends on variation in
duration of transport to the hospital and
inconsistency in quality of post cardiac arrest care.
There is also evidence of improved survival after
out-of-hospital cardiac arrest in large hospitals
with cardiac catheterization facilities compared
with smaller hospitals with no cardiac catheter
facilities.
European Resuscitation Council (ERC) and
Discussion
10. Anaesthesiology M.P. 9
European Society of Intensive Care Medicine
(ESICM) collaborate and every 5 year they produce
update on post-resuscitation care guidelines,
which recognise the importance of high-quality
post-resuscitationcareasavitallinkintheChain of
Survival. The most important changes in the 2015
guidelines are that, now there is greater emphasis
on the need for urgent coronary catheterisation
and percutaneous coronary intervention (PCI)
following out-of-hospital cardiac arrest of likely
cardiaccause.Targetedtemperaturemanagement
remains important but there is now an option to
0
target a temperature of 36 C instead of the
0
previously recommended 32–34 C. There is now a
better multimodal strategy to assess neurological
recovery and rehabilitation after the cardiac
56
arrest.
The key message to take from the plethora of
available published data is that, the targeted
0 0
temperature management (33 C – 36 C) remains
an important component of post resuscitation
care of the unconscious cardiac arrest patient. In
future, further studies will evaluate the impact on
patient outcome of these practices and results will
translate into better knowledge and formation of
guidelineforbetterclinicalpractice.
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14. 1.Assistant Professor, 2.Associate Professor, 3.Associate Professor, 4. Professor and HOD
Department ofAnaesthesia, Gajra Raja Medical College Gwalior (M.P.).
Newly born needs tracheal intubation during
resuscitation post delivery, in Neonatal
Intensive Care Unit (NICU) or to provide general
anasthesia for various neonatal surgeries like
Tr a c h e o - e s o p h a g e a l F i s t u l a ( T E F ) ,
Meningomyelocele, Diaphragmatic hernia,
ompahalocele etc. Correct endotracheal
tube(ETT) placement in this subset of age is of
utmost importance, as their airways varies from
adult airways in many aspects like narrow nares,
large head and tongue, small pharynx, floppy
epiglottis and higher anterior funnel shape larynx,
.ETT intubation has an approximately failure rate
1
of 8%. Developing proficiency at intubation
2
requires a significant amount of experience.
Unrecognized intubation of the esophagus is
3
followed by morbidity and mortality. Tochen’s
rule alone would lead to inadequate tube
placement in 47% of infants. Auscultation allows
adequate placement in only three-fourths of
4,5,6
patients. To avoid all these mishap various
methods have been used to identify correct tube
placementfromtimesinceETTinsertionisdonein
newborn to till date where newer technology has
7
penetrated it., as shown in (Table.1) . Thus an
array of techniques are available for confirming
correct tube placement in new born, which varies
depending upon the availability in particular
institution.
15-days old term neonate, weighing 2.4kg
with huge Occipital Meningomyelocele as shown
in (Figure. 1), was scheduled for surgical repair
under general anesthesia. As per institutional
CASE REPORT
“If that's what you think, you've got another thing coming up…an ultrasound verification of correct tube
placementinneonatalagegroup.”
Anaesthesiology M.P. 13
SYMMETRICAL CHEST RISE AND
BILATERAL EQUALAIR ENTRY
COULD BE FALSITY, FOR ASSESSMENT OF
CORRECT TRACHEAL
INTUBATION IN NEONATALAGE GROUP
1 2 3 4
lDr. Suman Gupta , Dr. Preeti Goyal , Dr. Neelima Tandon , Dr. Bhanu Choudhary
Fig1: A neonate with huge occipital Meningomyelocele
15. pulse oximetry, ECG, temperature probe were
applied after ensuring adequate ventilation inj.
succinylcholine 2mg/kg was administered I/V,
Trachea was intubated with portex uncuffed ETT
3.0 tube using straight Miller blade for direct
laryngoscopy. Soon after intubation, ventilation
was commenced and the chest was auscultated to
confirm correct endotracheal intubation. A good
chest rise and air entry could be heard bilaterally,
but saturation start falling gradually from 100% to
34%, suspecting esophageal intubation ,abdomen
was auscultated, equally similar breath sounds
couldbeheard,Saturationwasstilldeclining, heart
rate declined from 160/min to 48/min, baby
cyanotic, Cardiac massage was started and inj.
atropine given and decision was made to
reattempt intubation, heart rate improved, baby
turned pink and saturation improved. after rapid
intubation thus auscultation and chest rise
misguided us that tube is in the correct place. The
rest of the intraoperative course went uneventful
andbabywasextubatedattheendofthesurgery.
Incidence of esophageal intubation is more
DISCUSSIONS
norms baby underwent preanaesthetic
examination. Birth history revealed, baby was
th
delivered at 36 wk of gestation via lower segment
cesarean section. A thorough pediatric clinical
examination was done and any other congenital
anomalywasnotpresentapartfromthis.Thebaby
was subjected to base line investigations i.e
Hbgm%, TLC, Chest X-ray, all were found to be
normal for that age group. Our concern was
difficult airway because of restricted cervical spine
mobility owing to presence of occipital
Meningomyelocele.
Baby was shifted from NICU where it was on
pediatric fluid regime along with expelled breast
milksupplementunderthecoverofoxygen.
Preoperatively baby was kept warm and blood
was arranged for dealing with unwarned
emergency. Because of huge occipital
Meningomyelocele, it was difficult to achieve
neutral head positioning for intubation, hence
decided to intubate in lateral position. General
anaesthesia was induced with inhaled halothane
with 100% 02,an intravenous catheter was placed,
all the monitors including precordial stethoscope,
Anaesthesiology M.P.14
7
Table 1 Timeline: Evolution of ETT placement in newborn infants
1834 Digital intubation and external digital tracheal palpation
1895 Modern laryngoscope was invented
1964 Chest was auscultated while blowing into the tube
1966 Carbon di oxide monitoring
1971 Chest radiograph
1972 Flexible fiber optic laryngoscope
1974 Using respiratory function
1979 Calculations to correctly position oropharyngeal and nasophayngeal tube
1986 First study describing ultrasound to confirm correct tube position
1992 Colorimetric CO2 detectors
1990 Magnetically detectable tracheal tubes
2000 Video laryngoscope technique for intubation
2006 Respiratory function to detect correct tube placement
2007 Studies examining ultrasound to detect correct tube placement
16. than the incidence of inability to intubate . In
mishaps like brain hypoxic injury and vegetative
state, esophageal intubation is one of the main
causes of accidents leading to death or
8
neurological damage There are primary and
secondary verification methods of endotracheal
intubation. Primary verification is defined as
procedure performed before endotracheal tube is
secured i.e direct observation of the tube going
through the glottis, and indirect methods of
identifying as, the rise of chest, presence of
condensationofvaporsinthetube,auscultationof
breath sounds in stomach and lung region,
quantative waveform capnograph measurement.
Bedside upper airway ultrasound is a method that
8
observes the upper airway trachea in real time,
Secondary verification is like chest x-ray to
determine the ETT is inside the airway after
9
primaryverification.
Since endotracheal intubation commenced,
myriadsoftechniqueshadbeenusedtoconfirmits
correct placement to avoid unnoticed esophageal
intubation, Ultrasonography (USG) was
introduced for tracheal tube placement from 2007
10,11
onwards. Tracheal Rapid Ultrasound Exam
(TRUE)forconfirmingendotrchealtubeplacement
during emergency intubation required the median
12
operating time of 9.0 sec Whereas median time
required for confirming endotracheal intubation
via capnography versus clinical determination of
the tube placement in a study was 9.0sec and
13
35secrespectively.
Various advantages of this USG technique are
apparent as it is easily portable, painless, no
radiation, less handling, potential to determine
the tube position in the delivery room and earlier
7
detection of complication and malposition. It is
advantageous in situations involving
cardiovascular and broncho constriction where
ULTRSONOGRAPHY
14
capnography or EtCo2 may be faulty, . As
recommended by Chun and colleagues, there is
an enormous potential in the use of USG in
extreme environment like aeromedicine and
disasters where usual equipment to verify ETT
15
position is difficult, . A study conducted in Taiwan
concluded that the use of TRUE is a timeless novel
approach to determine endotracheal tube
location during intubation and can be performed
12
quickly. .Using a protocol TRUE, Trachea was
identified as hyper echoic air-mucosa with a
reverberation artifacts where as esophagus as
8,9,12
doubleairwaytractsign
Marciniak et al showed that sonography was
100% sensitive and 100%specific in determining
the tracheal position of the tube during
16
intubation.
Pfeiffer et al in their study showed that
ETT placement with ultrasound is faster than the
standard method of auscultation and
17
capnography and is as fast as auscultation alone
Ultrasound that has been used to confirm ETT
placement, can be divided into direct and indirect
methods, Direct methods involve viewing trachea
where as indirect methods involves viewing
intercostals and subxiphoid windows or dia-
phragm based on pleural sliding or diaphragmatic
movement but nevertheless these movement
involve positive pressure movement. USG
assessmentcanalsobedoneinadynamicorstatic
9
manner Only constraints are anatomical neck
distortion, as distorted anatomy of the neck
9
makesUSGinterpretationimpossible.
American Heart association in its
recommendation for neonatal resuscitation
international guidelines recommended,thatafter
endotracheal intubation and administration of
positive pressure ventilation a prompt increase in
a heat rate is the best indicator that the tube is in
CLINICAL SIGNS
Anaesthesiology M.P. 15
17. the tracheal bronchial tree and providing effective
18
ventilation. Other clinical sign recommended for
correct tube placement are tube condensation,
chest movement, presence of equal breath sound
bilaterally, but these indicators have not been
18
systematicallyevaluatedinneonates.
Tube condensation and chest rise is not the
criterion for identifying correct endotracheal tube
as it canoccur with oesophaeal intubation as well,
as happened in our case .i.e movement of chest
wall similar to as if ventilating lung can occur with
19
oesphgeal intubation. Clinically auscultation of
chest is routinely the first and foremost to assure
correct tube placement, but few studies quote
thatnormalbreathsoundswerepresentevenwith
ventilation with esophageal tube in situ, as air
passing through the esophagus, resembles coarse
20
and tubular breath sounds Thus using clinical
signs it takes long time to identify oesphageal
intubation,
Although EtCO2 is a simple and gold standard
criterion for detecting correct tube placement yet
capnographyyieldsfalsenegativeresultsincardiac
arrest, low cardiac output, acute pulmonary
embolism, when there is hypothermia, or apnea,
airway obstruction, hyperventilation, pregnancy,
bronchospasm and kinked tracheal tube and
8,21
technicalerror(hoseleak,calibrationerror)
A new focused ultrasound airway check
combined to Rapid Sequence Induction (RSI) and
nd th
tracheal intubation, lung sliding(betweenn2 - 4
Inter Costal Space, Mid Clavicular Line ) movement
of the pleura , lung pulse,(visualization of pleura
movement b/s of myocardial movement or
21
contraction,canbeseen
C.Sites in 1972 first described the use of
fiberoptic laryngoscope for endotracheal
CAPNOGRAPHY
FIBEROPTICDEVICES
22
intubation. Apaediatric bronchoscopehas been
used to asses correct tracheal tube placement in
23
new born Although fiberoptic is a very promising
way of confirming neonatal intubation but it need
expertise skill to operate in paediatric age and is
notreadilyavailableinmanysetups.
John Robinson first described the use of
airway pressure and gas flow waves via flow
sensor in oesophageal and tracheal flow waves to
24
identify correct tube placement. If the gas flow
can be observed in both direction, the tube is in
the trachea, and if only inspiratory gas flow is
observed, the tube is most likely in the
oesophagus. However, neither gas flow nor
airway pressure monitor can distinguish tube
placement in the trachea from one of the main
5
bronchi,asamajorlimitation.
IR measures the electrical conductivity of
thorax, A single test that is simple, inexpensive,
reliable,and quick toperform, may be of the great
25
interest to paediatric anaesthetist. Mehta et al
studied thoracic impedence plethysmography
was found to be 100% specific and 100% sensitive
in 79 patients studied for the detection of both
26
trachealandoesophagealtubeplacement
IR has its own potential problems, detection
might be more difficult in the emergency setting
as it might not be possible to determine the best
position of electrode, especially in an apneic child
25
andtherefore,interpretationmaybedifficult.
Another method to detect ETT intubation is
diaphragm motion in right subcostal ultrasound
view is a sensitive and specific. Secondary
confirmation method for diagnosis of ETT in
27
place. Measuring endotrcheal tube cuff
pressure, for distinguishing esophageal from
endotracheal intubation also have its own
RESPIRATORY FUNCTION MONITOR
IMPEDENCE RESPIROMETRY (IR)
Anaesthesiology M.P.16
18. 28
limitation The standard method used at present
are direct vision and capnography in combination,
this combination is also not infailiable and, it has
been shown that it may fail to detect in 40
29
esophagealintubationsinneonates.
USG confirmation can be used to identify
oesophageal intubation even before pumping air
tothe patient and preventingunintended stomach
ventilation. But the anaesthesiologist mind set is
withEtCO2anditwilltakelongtochangeittoUSG,
Since technology is moving fast, so we should
adapt newer technology and save patient from
complication of incidental. or accidental
oesophogeal intubation. This reduces incidence of
unrecognized oeophaeal intubation which is
sometime difficult to detect but may cause
substantialmorbidityandmortality.
To conclude can say that sonography is an
operator dependent technique, sonographic
guidance of the tube placement should be
considered by anesthesiologist. The use of
sonogrphy to confirm tracheal intubation is
attractive for several reasons. It is useful, quick,
repeatable, noninvasive, pain free, portable and
direct method of assessment of tracheal tube
position, which is not affected by very low
pulmnory flow. With further studies USG may
proveouttobegoldstandard.
1. Grmec S. Comparison of three different
methods to confirm tracheal tube placement in
emergency intubation. Intensive care Med. 2002;
28:701-4
2. Leone TA, Rich W, Finer NN. Neonatal
intubation success of pediatric trainees. j Pediatr.
2005; 146:638-41.
3. Clyburn P, Rosen M. Accidental oesophageal
intubation.Br.J.Anaesth1994;73:55-63
Conclusion
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15. Chun R, Kirkpatrick AW, Sirois M, Sargasyn
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17. Pfeiffer P. Rudolph SS,Borglum J, Isbye DL.
Temporal comparison of ultrasound Vs
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19. Birmingham PK. Cheney FW,Ward RJU.
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Anaesthesiology M.P.18
20. 1. AssistantProfessor.
2. SeniorResident,
DepartmentofAnaesthesiology,GandhiMedicalCollege,Bhopal.
CONGENITAL FIBROEPITHELIAL POLYP;
A CASE REPORT OF DIFFICULT AIRWAY
1 2
Dr. Ruchi Tandon , Dr. Sonal Awasya
Abstract
Keywords:
Introduction
Case Report
A 9 month old child presented with a growth in
theoropharynxforremoval.
Only complaint was distressed breathing on
crying. It turned out to be a case of difficult
paediatric airway that was managed well. A
diagnoses of oesophageal fibro-epithelial polyp
wasmadeafterhistopathologicalexamination.
Neonatal, paediatric anaesthesia, difficult
airway,congenitalpolyp
As anaesthesiologists we are aware that many
a times, paediatric intubations turn out to be
difficult, and we may land up with an
unanticipated difficult airway. Paediatric
population is more at risk for hypoventilation and
hypoxia if intubation during anaesthesia is delayed
and ventilation is inadequate. An expected
“normal airway and intubation” may take an
ominousturntoCVCI.
We are reporting a very unusual case of the
same.
A child of 9 months with normal vaginal
delivery presented with history of difficulty in
breathing especially while crying and choking kind
of sound when coughing. But when child was calm,
quiet and asleep there are no complaints and the
babywascomfortable.
She was otherwise apparently normal and
activewithnodelayinmilestones.
A pre-anaesthetic checkup was done. All
routineinvestigationswerewithinnormallimits.
Patient was posted for removal of the lesion,
afterinformedconsentfromtheparents.
Patient was premedicated with Inj.
Glycopyrrolate, Inj Midazolam and Inj Fentanyl and
Course of anaesthesia:
Anaesthesiology M.P. 19
21. anaesthesia was induced with InjThiopentone
sodium in appropriate doses with Inj. Succinyl
choline to facilitate intubation. However, it was
difficult to ventilate the patient during the period
of apnoea. On laryngoscopy, the resident was not
able to visualize the larynx and intubation was
unsuccessful. Second attempt of direct
laryngoscopy was done and still larynx was not
visualized.Attemptsatventilationwereonlypartly
successful.
Patient soon came out of scoline apnoea and
we decided to intubate the patient under
inhalational anaesthesia with halothane (as
available).
When adequate plane of anaesthesia was
reached, laryngoscopy was done and and a small
fleshy structure was seen obstructing more than
two third of the larynx. It was gently pushed aside
using the endotracheal tube itself but it fell back
into place over the larynx on shifting the
endotracheal tube even slightly. Intubation was
successful in the second attempt. After confirming
correct placement of the ETT the patient was
administered Inj Atracurium in doses required.
After the ETT was secured we held the fleshy mass
with a Magills forceps and found it to be rather
long , more like a worm and similar in diameter to
the ETT in situ. It was probably arising from upper
endofoesophagus.
Thegrowthwasligatedbythesurgeonandsent
forHPE.
The subsequent course of anaesthesia and
post reversal recovery were uneventful.
Postoperatively,thepatientdidwell.
No difficulty in airway was anticipated in this
case. However in paediatric cases, even a short
delay in ventilating the patient during scoline
apnoea may lead to rapid oxygen desaturation
Discussion
with considerable fall in SPO2 on the monitor. In
this case, probably, the tip of the growth
obliterated the larynx and made it difficult to mask
ventilate the patient. Due to the same reason it
was difficult to visualize the larynx during
laryngoscopy. Keeping a cool head under such
circumstances and avoiding chaos is of prime
importance. Luckily return of spontaneous
respiration was not delayed and we were able to
ventilate the patient and maintain the SPO2 in
spite of partial obstruction of larynx. Secondly,
instrument manipulation by the surgeon in the
same restricted field is a cause for concern in such
cases. Accidental extubation of trachea and even
endobronchial intubation should be watched for
veryvigilantlyduringanaestheticmanagement.
1) CardwellM;WalkerRWM.
Management of difficult paediatric airway. BJA
CEPDReviews2003;3:167-70.
2) RiaziJ.
The difficult paediatric airway. AnesthClin
NorthAm1998;16:707-923
3) Gupta S, Sharma R, Jain D Airway Assessment:
Predictorsofdifficultairways.
IndianJ.Anaesth.200549(4):257–262
4) American Society of Anesthesiologists Task
ForceonDifficultAirway
Management. Practice Guidelines for
Management of the Difficult Airway: An
Updated Report by the American Society of
AnesthesiologistsTaskForceon
Management of the Difficult Airway.
Anesthesiology200398:1269-1277
5) Jimenez N, Posner KL, Cheney FW et al. An
updateonpediatricanesthesia
liability: a closed claims analysis. AnesthAnalg
2007104:147–153
6) Paediatric Anaesthesia: The paediatric airway.
Themededition.200919:1-197
References:
Anaesthesiology M.P.20
22. patient satisfaction were evaluated before the
procedure, at 24 hrs. and then every month for 3
months after the procedure. In addition duration
of procedure,adequacy of block,volume of
neurolytic solution and VAS score during
procedurewasalsonoted.
In group A the final position of needle on
one side could not be achieved in 2 patients while
disc puncture was performed without difficulty in
all the patients of group B and the difference was
statistically significant {p<.05 }. Duration of the
procedure was longer and VAS score was higher in
group A as compared to group B. In group A 7
patients had statistically significant pain relief
immediatelyafterblockascomparedto8patients
in group B{p <.05 }. In group A 8 patients were
satisfied after the block and their daily analgesic
requirements decreased significantly as
compared to all 10 patients in group B and the
difference was statistically significant {p<.05 }.In
group A 2 patients reported complaints of bowel
discomfort,constipation and decrease in apetite
whilenocomplicationswerereportedingroupB.
RESULTS
Summary
BACKGROUND AND OBJECTIVES:
METHODS
Hypograstricplexusblockhasbeenconsidered
a safe and effective alternative to treat patients
with chronic pelvic pain. In this study we have
performed HPB using classical postero-lateral
approach & transdiscal approach in 10 patients
each, diagnosed with chronic pelvic pain because
of cancer Published studies available at MedLine
on the subject were included and evaluated in this
review.
In this prospective randomized trial 20
patients undergoing Hypogastric plexus block
(HPB) were divided in two groups. Group A [n=10]
received HPB via classical postero-lateral
approach. 8 ml of 10% aqueous phenol was
injected after confirming the position with spread
of non ionic contrast TAZOGRAF.Same procedure
was repeated on the other side. Group B [n=10]
received Hypogastric plexus block via transdiscal
approach.After verifying position with spread of
dye, 5 ml of 10% aqueous phenol was injected.
The VAS values, daily analgesic requirements and
A COMPARISON OF CLASSICAL POSTERO-
LATERALAPPROACH AND TRANSDISCAL
APPROACH FOR HYPOGASTRIC PLEXUS
BLOCK IN PATIENTS WITH CHRONIC
PELVIC PAIN
1
lDr Shailendra Singh Chauhan
1. Consultant Anesthesiology & Interventional Pain, Director SPINE [Spine pain intervention N Endoscopy] centre,
Jabalpur, MP, INDIA
Anaesthesiology M.P. 21
23. been described to block superior hypogastric
plexus sympathetic nervous system, such as
clinical response to local anesthetic injection using
external anatomic references, those guided by
5-10
fluoroscopy or CT-scan . Patients with neoplasias
and extensive pelvic involvement are also affected
by severe chronic pain, often refractory to oral and
parenteral drugs. Oncologic pelvic pain is a chronic
condition related to visceral involvement by the
tumor (visceral pain), to the impairment of pelvic
muscular structures (somatic pain) and/or to the
involvement of nervous structures (neuropathic
11
pain) . Some studies emphasize that anesthetic or
neurolytic superior hypogastric plexus block is
11-12
effective torelief chronic pelvic cancerpain and
12
non-oncologicchronicpain.
The purpose of this study was to evaluate the
efficacy of Superior hypogastric plexus block and
tocomparethetwodifferentapproaches.
10
In 1990, Plancarte et al. have described 28
pelvic cancer patients who received to superior
hypogastric plexus block for pain relief. In 1993, de
4
Leon-Casasola et al. has evaluated 26 advanced
gynecologic, colorectal or genito-urinary cancer
patients suffering from disabling chronic pelvic
11
pain. In 1997, Plancarte et al. has performed the
largest longitudinal multicenteric study on
superior hypogastric plexus block. In 2002,
12
Mercadante et al. have evaluated pain
mechanisms in pancreatic or pelvis cancerpatients
and the possible indication of celiac and superior
hypogastric plexus block,respectively. In 2004, de
13
Oliveira et al. have studied 60 patients with
history of chronic oncologic pelvic pain, especially
visceral pain, secondary to inoperable cancer or
metastases. Traditionally, superior hypogastric
plexus block is guided by fluoroscopy with bilateral
10 6-9-14
needles . Six studies have described
EVOLUTION OF BLOCK
CONCLUSION
INTRODUCTION
Transdiscal approach to Hypogastric plexus
blockappearstobemoresafeandeffective,easyto
perform,more quick,requires single injection and
has no complications as compared to classical
approach. However prospective randomized
controlled studies comparingdifferentapproaches
areneededtoincreaseourknowledgeofHPB.
Studentttestappliedp<.05significant
The blockade of nervous transmission through
sympathetic nervous system have been proposed
1,2
to treat chronic pain of different origins .
Classically, stellate ganglion blockade (C6-T1) has
been used to treat upper limb, face and cervical
pain; celiac plexus (T12-L1) block to relieve upper
abdominal pain; and lumbar sympathetic chain
1,2
block to treat lower limb pain . Several
anaesthetic or neurolytic techniques to block
sympathetic ganglia have been described and
evaluated in the last decades with prospective
studies. Celiac plexus block is probably the most
widely investigated method to treat pancreatic
1,2
neoplastic pain . However, the blockade of other
plexuses, such as superior hypogastric plexus, has
received minor attention and few studies were
carried out on the subject. Superior hypogastric
plexus is a retroperitoneal structure bilaterally
located in L5 lower third and S1 upper third, close
to the sacral promontory and common iliac veins
3
bifurcation . Superior hypogastric plexus transmits
visceral painful stimulation from right colon,
3,4
uterus, cervix, tubes, upper vagina and bladder .
Superiorhypogastricanestheticorneurolyticblock
has been proposed as an effective alternative to
treat different pain syndromes, such as oncologic
pelvic pain (visceral pain), chronic non-oncologic
pelvic pain (endometriosis) and refractory penile
1,2
pain, among others . Several techniques have
Anaesthesiology M.P.22
24. alternative techniques to approach superior
hypogastric plexus, such as anterior approach with
14 7
single needle guided by CT-scan or fluoroscopy ,
6
coaxial technique and technique guided by
8
microlaparoscopy . These studies, however, are
purely descriptive and there is no comparison
among different techniques. Other superior
hypogastric plexus approaches, such as pre-sacral
15
neurectomy, have been described , especially in
non-oncologic conditions, but again prospective
and controlled studies are needed to recommend
33
suchprocedure .
To know the efficacy of HPB block in chronic
pelvic pain secondary to cancer & to compare the
classicaltechniqueandtransdiscalapproach
It was a preliminary,prospective randomized
trial on 20 patients which were randomly divided
in 2 groups. Group A [ N=10] received block via
Classical ie postero-lateral approach and Group B
[N=10] received block via Trans-discal L5-S1
approach.
1. Patients with chronic pelvic pain secondary to
cancerwithnodocumentedmetastasis
2. Thosesufferingfrompainwithintensity of >
4/10 according to VAS scale despite of i/v
analgesicsincludingopioids
3. Those who had no contraindications to
regional techniques and sympathetic
block
4. Those who understood and gave informed
consent
1. Those who had documented metastasis and
paininotherareasalso
AIMS & OBJECTIVES
STUDY DESIGN
INCLUSION CRITERIA
EXCLUSION CRITERIA
2. Those who had contraindications to
regional techniques and sympathetic
block
3. Thosewhodidnotgaveinformedconsent
4. Those who were having psychological
issues.
20 patients were arbitrarily selected for the
study & randomly divided in two groups. 8 [40%]
patients were suffering from cervical cancer, 6
[30%[ from endometrial cancer, 4 [20%] from
prostatecancer&2[10%]fromtesticularcancer
All the patients were taken in operation
theatre after informed consent. Fasting protocols
were followed. Premedication was with I/V
Midazolam 0.05 mg/kg & fentanyl 1mg/kg.
Patients were preloaded with 10ml/kg Ringer
lactated and received I/V Ceftriaxone 1.0 gm pre
procedure. Continous monitoring of HR, EKG, NIBP
and SPO2 was done. Procedures done under
sterileconditionsandfluoroscopicguidance
The patient was put in prone position and L4-5
intervertebral space was identified under
fluoroscopy. A 22 G 20 cm long spinal needle
DISTRIBUTION OF PATIENTS
TECHNIQUE
CLASSICAL TECHNIQUE
Anaesthesiology M.P. 23
25. SURETECH was inserted 5-7 cm from midline
0 0
around 30 caudal & 45 medially. The tip of the
needle is directed towards the antero-lateral
aspect of the lower border of L5 vertebra. After
touching the bone needle is gradually grazed and
advanced in lateral view 1 cm past L5 vertebral
body in the retroperitoneal space.The spread of
non ionic radiocontrast dye should show smooth
posterior contour corresponding to anterior psoas
fascia in lateral view and vertical spread lateral to
midline in AP view.After confirming the accurate
placement of needle tip diagnostic block with 5 ml
of 1% xylocard was given.After waiting for 5
minutes some pain relef was confirmed and if no
motor block is observed then neurolysis was done
with 8 ml 10% aqueous phenol.Same procedure
wasrepeatedon theothersidealso.
TRANS-DISCAL TECHNIQUE
The patient was put in prone position With the
C-arm properly aligned in oblique view, there is a
small triangular window through which the needle
must pass to reach the anterolateral margin of the
lumbosacral junction. The triangle is bounded
superiorly by the transverse process of L5, laterally
by the iliac crest, and medially by the L5/SI facet
joint. A skin entry point is made over the lowest
point of this triangle and typically overlies the iliac
crest, 5 to 7 cm from midline at the level of the L5
spinous process. A 22-gauge, 15 cm long needle
SURETECH is advanced using fluoroscopic
guidance to lie anterolateral to the L5/S1
intervertebral disc or the inferior margin of the L5
vertebral body . A small volume (2 to 3 ml) of
radiographic contrast material is seen to spread
Anaesthesiology M.P.24
26. along the anterior surface of the lumbosacral
junction in lateral view, confirming correct needle
position. After confirming the accurate placement
of needle tip diagnostic block with 5 ml of 1%
xylocard was given.After waiting for 5 minutes
some pain relef was confirmed and if no motor
block is observed then neurolysis was done with 5
ml 10% aqueous phenol. After neurolysis 0.5 ml of
saline is pushed to prevent deposition of phenol
insidethedisc.
Anaesthesiology M.P. 25
27. PARAMETERS EVALUATED
OBSERVATIONS & RESULTS
1. ADEQUACY OF BLOCK
2. DURATION OF PROCEDURE
1. The VAS values, daily analgesic requirements
and patient satisfaction were evaluated before
the procedure, at 24 hrs and then every month
for3monthsaftertheprocedure.
2. In addition adequacy of procedure, duration of
procedure,volume of drug used, VAS score
duringprocedureandearlycomplicationswere
alsonoted
In group A the final position of needle on one
side could not be achieved in 2 patients while disc
puncture was performed without difficulty in all
the patients of group B and the difference was
statisticallysignificant{p<.05}
Duration of the procedure was longer in group
A as compared to group B & difference was
statistically significant [p<.05].Duration included
timing from entry to exit of patient from operation
theatre.
VAS score during the procedure was higher in
group A as compared to group B & difference was
notstatisticallysignificant[p>.05].
Average 16 ml of aqueous phenol was used in
group A while 5 ml in group B,leading to 69.75%
3. VAS DURING PROCEDURE
4. VOLUME OF NEUROLYTIC SOLUTION
Anaesthesiology M.P.26
28. reduction in volume and the difference was
statistically significant [p<.05]
In group A 8 patients were satisfied after the
block and their daily analgesic requirements
decreased significantly as compared to all 10
patients in group B and the difference was
statisticallysignificant{p<.05}.
5 DAILY ANALGESIC REQUIREMENT
6 PATIENT SATISFACTION SCORE
In group A 8 patients were satisfied after the block
as compared to all 10 patients in group B and the
differencewasstatisticallysignificant{p<.05}.
In group A 7 patients had statistically
significant pain relief immediately after block as
compared to 8 patients in group B{p <.05 } Group B
hadlowerVASScoresupto3monthsthanGroupA.
In group A, 2 patients reported
complaints of bowel discomfort, constipation and
decrease in apetite while no complications were
reported in group B. No incidence of discitis
reportedingroupBupto3months.
7. VISUAL ANALOGUE SCORE
8. INCIDENCE OF EARLY COMPLICATIONS
UP TO THREE MONTHS
DURING THE PROCEDURE
Anaesthesiology M.P. 27
%ofpatients
29. DISCUSSION
Sympathetic neurolysis is effective and safe for
the treatment of pancreatic and pelvic visceral
pain in cancer and is a useful adjunct to oral
therapy.It should be offered as an adjuvant to
reduceanalgesicconsumption.
The classical procedure described by Plancarte
10
et al [1990] is directed to the region where
hypogastric plexus has already divided into its left
& right trunk,hence needs two needle placement
to target both.While in transdiscal approach
bilateral spread in lower volumes is achieved with
singleneedleplacement.
Ina et al. [1992] were the first investigators to
report successful SHP block using paramedian
16
transdiscal approach . This approach has been
used for celiac plexus and lumbar sympathetic
block. Ina et al, 1996, Ohno and oshita, 1997 have
regarded it as safe & simpler than other
approaches. The incidence of discitis is low [1-2%]
andstrictaseptictechniqueisrecommended..
In our study we found transdiscal technique
[Group B] more adequate as in 2 patients
procedure could not be completed in classical
technique [Group A] & the difference was
7
statistically significant [p<.05]. Both the patients
were in severe pain & could not lie prone for more
than 10 minutes.Since oversedation has to be
avoidedprocedure was abandoned & later on they
receivedblockviatransdiscaltechnique.
In our study duration of procedure was shorter
in patients with transdiscal technique [Group
B].Average duration in group B was 24 minutes
with 58 minutes in Group A & difference was
statistically significant [p<.05] This may be the
reason that patients tolerated the procedure
betteringroupB.
An important observation was done to assess
which procedure is less painful by seeing VAS
during the procedure.Average VAS in group A was
6.5 while in group B it was 5.Since transdiscal
technique is performed by single needle
placement and duration of procedure was
significantly shorter patients in group B found it
16
lesspainful .
In our study we observed that in group A
significantly high volumes of aqueous phenol [16
ml] were used as in group B [5ml] , p<.05 to
16
achieve almost same results. Since its safer to
use minimum volume of neurolytic agents we
foundtransdiscalapproachbetter.
In our study we also observed patient
satisfaction score during the procedure and at 24
hrs, 1, 2 & 3 month post procedure by filling a
proforma which included 3 questions: 1. Was the
procedure painful 2. Was it difficult to lie down
for long time in prone position during the
procedure & 3. Did you had any complications
after or during the procedure. Since the duration
was shorter & procedure was less painfulin group
B & moreover 2 patients knew that there
procedure could not be completed, the overall
satisfactionscorewasbetteringroupB[p<.05]
In our study we observed daily analgesic
requirement pre procedure,24 hrs after the
procedure&then at1,2&3months.Wecouldnot
find much difference amongst the two groups at
allintervals.Thisstronglysuggeststhatresultsare
comparableintwogroups.
In our study we observed pain relief by
comparing VAS scores preprocedure,24 hrs after
the procedure & then at 1,2,&3 months. We
found that VAS scores were slightly higher in
group B but that can be attributed to pre-existing
higher VAS score in group B. At 1,2 & 3 months
follow up we found lower VAS scores in group B
suggesting that block was more adequate in
group B.Since we could not find much difference
in analgesic requirements at the same intervals in
Anaesthesiology M.P.28
30. both the groups this suggests that neurolytic
blocks cant take care of complete pain & they
should be utilized as early as possible as adjuvants
9
tooraltherapyinthesepatients .
In our study we noticed early minor
complications in 2 patients [20%] in group A.These
patients complained of bowel discomfort,
constipation & loss of apetite. The obvious reason
could not be traced out and patients recovered
within a week with conservative management.In
group B no complication was reported.Discitis can
beaseverecomplicationinanyintraortrans-discal
17
procedure but incidence is very low[1-2%]. With
this observation we can suggest that transdiscal
approachismoresaferthanclassicalapproach.
We believe that Hypogastric plexus neurolysis
reliably treats intractable chronic pelvic pain
secondary to cancer & it should be indicated as an
adjuncttooraltherapyinearlycourseofdisease.
Hypogastric plexus neurolysis can be achieved
via various techniques.In this study we compared
classicalpostero-lateralapproachwithtrans-discal
approachandconcludedthattransdiscalapproach
is easier, takes less time,safer, effective,requires
single injection & less volume of neurolytic
solution.
This technique has two significant advantages
over classical technique: Single injection is
sufficientfor a successfulblock and sometimes it is
difficult for patient to lie in prone position because
of severe pain and this technique can be
performed in prone as well as lateral
position.However a large well controlled study is
needed to establish safety & efficacy of transdiscal
overclassicaltechnique
1. Bonica JJ - The management of pain of
malignant disease with nerve blocks.
CONCLUSION
REFERENCES
Anesthesiology,1954;15:134-135.
2. Bonica JJ - Autonomic innervation of the
viscera in relation to nerve block.
Anesthesiology,1968;29:793-813.
3. Rapkin AJ - Neuroanatomy, neurophysiology,
and neuro- pharmacology of pelvic pain. Clin
ObstetGynecol,1990;33:119-129.
4. De Leon-Casasola OA, Kent E, Lema MJ -
Neurolytic superior hypogastric plexus block
for chronic pelvic pain associated with cancer.
Pain,1993;54:145-151.
5. Wechsler RJ, Maurer PM, Halpern EJ - Superior
hypogastric plexus block for chronic pelvic pain
in the presence of endometriosis: CT
techniques and results. Radiology,
1995;196:103-106.
6. Stevens DS, Balatbat GR, Lee FM - Coaxial
imaging technique for superior hypogastric
plexus block. Reg Anesth Pain Med,
2000;25:643-647.
7. Kanazi GE, Perkins FM, Thakur R - New
technique for superior hypogastric plexus
block.RegAnesthPainMed,1999;24:473-476.
8. Steege JF - Superior hypogastric block during
micro- laparoscopic pain mapping. J Am Assoc
GynecolLaparosc,1998;5:265-267.
9. Rosenberg SK, Tewari R, Boswell MV - Superior
hypogastric plexus block successfully treats
severe penile pain after transurethral resection
of prostate. Reg Anesth Pain Med,
1998;23:618-620.
10. Plancarte R, Amescua C, Patt RB - Superior
hypogastric plexus for pelvic cancer pain.
Anesthesiology,1990;73:236-239.
11. Plancarte R, de Leon-Casasola OA, El-Helaly M -
Neurolytic superior hypogastric plexus block
for chronic pelvic pain associated with cancer.
RegAnesth,1997;22:562-568.
Anaesthesiology M.P. 29
31. Anaesthesiology M.P.30
12. Mercadante S, Fulfaro F, Casuccio A - Pain
mechanisms involved and outcome in
advanced cancer patients with possible
indications for celiac plexus block and superior
hypogastric plexus block. Tumori,
2002;88:243-245.
13. de Oliveira R, dos Reis MP, Prado WA - The
effects of early or late neurolytic sympathetic
plexus block on the management of abdominal
orpelviccancerpain.Pain,2004;110:400-408.
14. Cariati M, De Martini G, Pretolesi F CT-guided
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15. Stones RW, Mountfield J - Interventions for
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block:
32. Introduction
Case report
Odontogenic myxoma is an uncommon tumor,
seldom encountered in patients before their
1
second decade of life, and rarely in females. It is
generally believed to originate from the primitive
mesenchymal portion of the tooth follicles. The
tumor proliferates slowly, but owing to its local
aggressiveness and high recurrence rate , radical
management is recommended.These patients can
present a challenge to the anesthesiologist due to
mass effect , leading to difficult mask ventilation
and intubation. We report a case of odontogenic
myxoma in a 12 year old female child posted for
hemimandibulectomy. The perioperative
managementofthiscaseisdiscussed.
A 12 year old female weighing 30 kg presented
to our institute with a 2 years history of swelling
over the right mandible. This had been
progressively increasing in size since 2 years and
lately she complained of pain in swelling since 1
month. On examination, a large extra oral swelling
was present , extending from angle of the right
mandible to para symphysis. Intra orally , firm and
tender swelling extending from the angle of
mandible to para symphysis measuring 8 X 6 cm
was seen. Overlying skin was healthy .Oral hygiene
was very poor. Pus was draining from involved
gingival sulcus. Preoperative investigations
revealed hemoglobin to be 11 gm%, INR 1.12,
blood urea to be 16 mg%, blood sugar 91 mg%.
There was no significant past medical or surgical
history. There was no history of any chemo or
radiation therapy. Computed tomographic scan
showed“Honeycomb”patternofradiolucency.
At the preoperative assessment, patient was
awake and alert. The patient’s heart rate was
86/min, regular and noninvasive blood pressure
was 118/70 mmHg in right upper limb. . On airway
1
examination, mouth opening was / fingers and a2
swelling was present on right mandible and
retromolar region deviating tongue to the left side
and backwards . Oral cavity on the right side of
uvula was completely occupied by the mass.
Case Report
ANESTHETIC MANAGEMENT IN A CASE
OF CHILDHOOD ODONTOGENIC
MYXOMA.
1 2 3 4 5
lDr Lini Srivastava , Dr. Monika Gandhi, Dr. Ravi Shrivastava, Dr K.K. Arora, Dr. Vilas Niwasker
nd
1. 2 YearPostGraduateResident.
2. AssociateProfessor.
rd
3. 3 YearPostGraduateResident.
4. Dr.K.K.Arora,ProfessorandHeadofDepartment,
DepartmentofAnaesthesiology,M.G.M.MedicalCollegeandM.Y.Hospital,Indore
5. Dr.VilasNiwasker,Professorand HeadofDepartment,
DepartmentofOral&MaxillofacialSurgery,GovernmentDentalCollegeandM.Y.Hospital,Indore
Anaesthesiology M.P. 31
33. Thyromental distance was 5 cm and tempero-
mandibular joint movement was adequate. The
patienthadamallampatigradeof4.Bilateralnares
werepatentbutnasalcavitywasnarrow..
/2 fingers and a swelling was present on right
mandible and retromolar region deviating tongue
to the left side and backwards . Oral cavity on the
right side of uvula was completely occupied by the
mass. Thyromental distance was 5 cm and
tempero-mandibular joint movement was
adequate. The patient had a mallampati grade of
4. Bilateral nares were patent but nasal cavity was
narrow..
Patient was fasted for 8 hours. Consent of
anesthesia and surgery was obtained. Parents and
patient were properly counselled about the
intubation procedure. Patient was monitored
with pulse oximeter , NIBP and ECG .As difficult
mask ventilation and intubation was anticipated, a
difficult airway cart with bougie , laryngeal mask
airway of size 2 and laryngoscope blades of
different sizes was kept ready. Premedication was
done with i.v. midazolam at a dose of 0.03 mg/ kg
body weight and i.v. glycopyrollate 20
micrograms/kg body weight. Nasal packing was
done through right nare with 2% lidocaine with
adrenaline soaked gauze. After 10 minutes pack
was removed. Meanwhile bilateral superior
laryngeal nerve block and trans laryngeal block
with 2% lidocaine were given .The upper airway
was anaesthetized with lidocaine 4% spray over
approximately 10 minutes. Cotton pads were kept
on left cheek to form proper seal for mask
ventilation. Still some leak was present and so
mask ventilation was done with the help of an
assistant. Patient was sedated with i.v. fentanyl 1
microgram per kg body weight. Endotracheal tube
size 5 mm uncuffed, was gently advanced through
right nostril till it reached pharynx. Laryngoscopy
was attempted, but Cormack Lehane grade 4 was
observed. So awake blind nasal intubation was
planned. Listening to the breath sounds , tube was
guided through the vocal cords by the anesthetist.
Circuit was connected and ventilation was done.
After ensuring proper bilateral air entry, tube was
fixed .Inj succinylcholine i.v. 2 mg/kg was given.
Throat pack was inserted. Dexamethasone i.v. 0.4
mg/kg was given. Patient was maintained on
nitrous oxide and oxygen (1:1) mixture, inj
atracurium with loading dose of 0.5 mg/kg and
maintenance dose of 0.1 mg/kg and intermittent
Patient with Odontogenic myxoma and Limited
mouthopening
Picture Showing tumour intra-operatively
Anaesthesiology M.P.32
34. bolus doses of inj propofol was given. Adequate
analgesia was maintained with inj paracetamol i.v
15mg/kg.Intraoperativeperiodwasuneventful.
A tumor of size approximately 8 X 6 X 6 cm
involving right mandible was removed .Mandible
reconstruction was scheduled for later. Throat
pack was removed and suction of blood and
secretions was done properly. Reversal was done
with inj. neostigmine i.v . 0.05mg/kg and inj
glycopyrollate 0.01 mg/kg. After patient started
following commands, extubation was done on
table, and shifted to recovery .Adequate
postoperative analgesia was given with inj
diclofenac1.5mg/kgi.v.
Myxomas are nonencapsulated benign locally
aggressive tumors which may occur in both the
soft tissues and bone. Macroscopically myxoma
appears as a mass of characteristically mucoid or
slimy material. Microscopically, as first described
2
by Virchow , it consists of stellate cells with long
intertwining processes in amorphous mucoid
ground substance. It is believed to arise from
3,4,5
odontogenic epithelium. Some authors believe
myxomas to arise from myxomatous
DISCUSSION
6,7
degeneration of fibrous stroma . Others regard it
8
to arise from primitive mesenchyme . They may
have appearance of malignant tumor or may
present as typical benign odontogenic tumor or
even as a cyst. The tumor may progress slowly or
may have sudden enlargement. Paresthesia or
9
complete anesthesia may be present . Treatment
of odontogenic myxomas is still a matter of
debate. While some authors recommend
resection of area of mandible involved, others
9,10
recommendcurettage .
Large odontogenic myxoma of mandible can
distort the facial contour and make mask
ventilation difficult, so awake intubation was
planned with local blocks. A nasotracheal tube
was preferred as it was oral surgery. Other
methods of intubation in such patient include
tracheostomy and transtracheal jet ventilation in
1
emergency situation . Various methods of awake
intubation include blind nasal, fiberoptic and
retrograde intubation after appropriate airway
1
anesthesia . In massive mandible tumors with
extension into oral cavity, awake fiberoptic
intubation is the technique of choice as it is
minimaly stimulating, helps to assess airway ,
sucks blood and secretions and supplements
PictureShowingexcisedmandibulartumor Picture showing patient after tumorhas been
excised
Anaesthesiology M.P. 33
35. oxygen. But fiberoptic intubating scope was not
available at that time. Blind nasal intubation
requires no special equipments but requires skill
and expertise. However risk of bleeding from nose
and tumor exists. Retrograde intubation can be
safely used to retrieve the catheter. It may be
especially useful in patients with limited neck
mobility, airway trauma or in presence of
oropharyngeal bleed which may obscure the
fiberoptic field. But since it’s easier to retrieve
catheter orally than nasally, so this method was
1
notpreferred.
At the end of surgery, prior to reversal oral
cavity should be cleared of secretions and blood.
The postoperative presence of airway edema can
cause airway obstruction and in such situations, it
may be wise to leave endo tracheal tube in the
place. Also care must be taken that the patient
must be fully awake and all airway reflexes have
returnedtonormalbeforeextubation.
1. Hasleton PS, Simpson PW, Craig RDP: Myxoma
of the mandible: a fibroblastic tumor. Oral Surg
46:396-406,1978
2. Virchow RLK: Die krankhaften Geschw(ilste,
Bd. 1. Berlin, Germany; Verlag w~n August
Hirschwald,1863pp369-434
References:
3.LucasRB:PathologyofTumorsoftheOralTissues
,3rd ed.Edinburgh;Churchill-Livingstone, 1976
pp174-77
4. Goldblatt LI:Ultrastructural study of an
odontogenic myxoma.Oral Surg 42;206-
20,1976
5. Harrison JD:Odontogenic myxoma
:ultrastructuralandhistochemicalstudies:JClin
Pathol26:570-82,1973
6. Lund BA, Waite DB: Mandibular myxoma:
reportofacase.JOralSurg24:454-59,1966
7. Whitman RA, Stewart S, Stoopack JG, Jerrold
TL: Myxomaof the mandible: report of a case.
OralSurg29:63-70,1971
8. Bernier JL: The Management of Oral Disease,
2nded.StLouis;CVMosbyCo,1959.
9. Gundlach KKH, Schultz A: Odontogenic
myxoma: clinical concept and morphological
studies.JOralPathol6:343-58,1977
10.Zimmerman DC, Dahlin DC: Myxomatous
tumorsofthejaws.OralSurg11:1069-80,1958
11.Dureja J,Balhara S Saini , S Ghai A.Airway
Management in Ameloblastoma-A Case
Re p o r t . J A n a e st h C l i n P h a r m a co l
2005;21(3):31719
Anaesthesiology M.P.34