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Management of Snake Bite Victims


with Respiratory Paralysis in ICU

Dr. T.R. Chandrashekar


Director Critical Care
K.R.Hospital
Bangalore

www.themegallery.com
DR TRC/ KRH
Management of Snake Bite Victims
with Respiratory Paralysis in ICU
 Facts given
 Snake bite which has lead to Respiratory
Paralysis
 Patient in ICU
 Answer
 Management aspects
How to prevent snake bites?
 A world free of snakes

 Nearly a quarter of us would go hungry


 Are The
important elements
bottom line in
is the
wefood
needchain to
control the rodent
snakes population- Which destroy all
to survive
major crops.
Epidemiology
 India estimates in the region of 200,000 bites
and 15-20,000 snake bite deaths per year
 Originally made in the last century, are still
quoted. No reliable national statistics are
available.
 Males are bitten almost twice as often as
females
 Majority of the bites being on the lower
extremities.
 50% of bites by venomous snakes are dry bites.
that result in negligible envenomation.
FAB FOUR
 In India, more than 200 species of snakes but only 52
are poisonous. Majority of bites
 Saw-scaled viper (Echis carinatus) Nearly 70-80%
Hemotoxin
 Russell’s viper (Daboia russelii) Vasculotoxin
 Common krait (Bungarus caeruleus)
 Indian cobra (Naja naja) Neurotoxic

1 2 3 4
Species: Medical Implications
Signs/Symptoms Russell’s
Cobra Krait Saw Scaled Other
and Potential Viper
Viper Vipers
Treatments

Local pain/ Tissue


Damage
Yes No Yes Yes Yes

Ptosis/Neurotoxicity Yes Yes Yes! NO No

Coagulation No No Yes Yes Yes

Renal Problems No No Yes NO Yes


Neostigmine &
Atropine Yes No? No? NO No
Syndromic approach
 No local signs with Neuro-toxicity- Krait
 With or with out local signs and Neuo-toxicity-Cobra
 With or with out Neurotoxicity and local signs and
hemotoxicity-Rusell’s Viper
 Local signs with hemotoxicity-Saw Scaled Viper
Snake bite
Majority is by non-venomous snakes

Venomous snakes
About 50% of bites are dry

Anti snake venom


ASV -severe adverse reactions, Costly, Limited supply.
Used- benefits of ASV treatment is considered to exceed
the risks.
Our statistics

1998-2008 45 snake bite admissions


8 Neuotoxic bites 6 required MV
33 Hemotoxic bites 20 required MV

Causes
 ARF, DIC, Shock, Pulmonary edema,
Sepsis
Snake bite and Respiratory paralysis
More cases why ?
Neurotoxic
MV for respiratory ASV
paralysis MV as Supportive care

Neuromuscular paralysis- Bulbar paralysis-Aspiration


blockade of neuromuscular
Sepsis,
transmission.
Cobra- post-synaptic DIC-shock
Krait- pre-synaptic ARF-Pulmonary edema
NEUROTOXICITY HEMOTOXICITY
 Starts early- many die before  Starts late hence most of them
they reach hospitals reach hospitals
 Many reverse very well with  Many organ involvement hence
ASV if started early MV is mostly supportive to buy
 Less number of cases time for organs to recover
 More number of cases
70-80%

20-30%
Case scenario…….
 34 yr old male shifted from rural health center with H/O
snake bite 6 hrs back has ptosis, respiratory distress, RR
35/mt, BP 120/60, oral secretions present, absent gag
and cough reflex shifted to ICU for teritary care.
 On ASV 100ml stat, & 50ml in NS over 6 hrs
 Oxygen 3l/mt
Patient is comfortable, vitals stable
No ptosis, distress

Patient received
in casualty
Patient is dead –what do you think
went wrong ?
Patient is dead –what do you think went wrong ?

 What could have been done better ?


 Bulbar signs-probably aspirated and died
 Endotracheal intubation can be placed on T-piece
Ambuing or Transport Ventilator
 Anticholienesterases
 Neostigmine with atropine
Case scenario…….
 34 yr old male shifted from rural health center with H/O
snake bite 6 hrs back has ptosis, respiratory distress, RR
35/mt, BP 120/60, oral secretions present, absent gag
and cough reflex shifted to ICU for teritary care.
 On ASV 100ml stat, & 50ml in NS over 6 hrs
 Oxygen 3l/mt
What are the Management issues?

Why does
Neurotoxicity occur ASV, Anticholineesterases,
MV…
Snake venom components
Krait- Pre-synaptic action
Beta-bungarotoxin- Phospholipases A2

1) Inhibiting the release of


acetylcholine from the presynaptic
membrane
2) Presynaptic nerve terminals
exhibited signs of irreversible physical
damage and are devoid of synaptic
vesicles

3) Antivenoms & anticholinesterases


have no effect

Paralysis lasts several weeks and frequently requires prolonged MV.


Recovery is dependent upon regeneration of the terminal axon.
Cobra –post-synaptic
 alpha-neurotoxins

“Curare-mimetic toxins’’

Bind specifically to acetylcholine


receptors, preventing the interaction
between acetylcholine and receptors
on postsynaptic membrane.

Prevents the opening of the


sodium channel associated with the
acetylcholine receptor and results in
neuromuscular blockade.

 ASV -rapid reversal of paralysis.

 Dissociation of the toxin-receptor


complex, which leads to a reversal of
Paralysis
Anticholinesterases reverse the neuromuscular blockade
Snake envenomation in a north Indian hospital

Ptosis

Ophthalmoplegia

RS
r
Bulba ss involvement
e
weakn

N Sharma, S Chauhan, S Faruqi, P Bhat, S Varma, Emerg Med J 2005;22:118–120


Neurotoxic envenoming-Examination
•Ask the patient to look up and observe whether the upper
lids retract fully.
•Test eye movements for evidence of early external
ophthalmoplegia .
•Check the size and reaction of the pupils.
•Krait can cause fixed, dilated non reactive pupils
simulating brain stem death – however, it can recover fully
•Ask the patient to open their mouth wide and protrude
their tongue; early restriction often paralysis of pterygoid
muscles.
• The muscles flexing the neck may be paralysed, giving
the “broken neck sign
Bulbar paralysis
 Can the patient swallow or are secretions accumulating
in the pharynx- an early sign of bulbar paralysis?
 Ask the patient to take deep breaths in and out.
“Paradoxical respiration”.
 Objective measurement of ventilatory capacity is very
useful. Use a peak flow metre, spirometer (FEV1 and
FVC)
 Ask the patient to blow into the tube of a
sphygmomanometer to record the maximum expiratory
pressure (mmHg).
Local examination
 During the initial evaluation, the bite site
should be examined for signs of local
envenomation (edema, petechiae, bullae,
oozing from the wound, etc) and for the extent
of swelling.
 The bite site and at least two other, more
proximal, locations should be marked and the
circumference of the bitten limb should be
measured every 15 min thereafter, until the
swelling is no longer progressing.
Treatment
 Anti Snake Venom
 Polyvalent /Monovalent
 Dose-large vs small
 Timing
 Repeat dose
 Hypersensitivity
 Anticholinesterases- Tensilon test
 Mechanical ventilation
ASV
 The decision to treat a snake bite with antivenin is
largely based on clinical parameters.
 Trying to capture, kill, or transport a snake for
identification purposes seems of little value and
possibly dangerous

ASV is polyvalent
Syndromic approach helps in examination
and investigations and outcome predictions
Skin testing for ASV
 Skin/conjunctival hypersensitivity testing does not
reliably predict early or late antivenom reactions
and is not recommended.
What is ASV?
 Antivenom is immunoglobulin (usually the enzyme
refined F(ab)2 fragment of IgG) purified from the serum
or plasma of a horse or sheep that has been immunised
with the venoms of one or more species of snake.
 Monovalent or monospecific antivenom neutralises the
venom
 of only one species of snake
 Polyvalent or polyspecific antivenom neutralises the
venoms of several different species of snakes
 The ASV that is available in India is a polyvalent type
which is active against the commonly found snakes in
India including the FAB Four.
Indications for ASV
 Neurotoxicity
 ARF
 Bleeding/coagulopathy
 Myoglobinuria/haemoglobinuria
 Cardiac toxicity
 Local swelling involving more than half of the bitten limb
 Rapid extension of swelling
 Development of an enlarged tender lymph node draining
the bitten limb
Timing of ASV
 There is no consensus as to the outer limit of time of
administration of antivenom. Best effects are observed
within four hours of bite .
 It has been noted to be effective in symptomatic patients
even when administered up to 48 hours after bite.
 Reports suggest that antivenom is efficacious even 6-7
days after the bite from vipers
 When there are signs of local envenoming, without
systemic envenoming, antivenom will be effective only if
it can be given within the first few hours after the bite
Dose

5 vials(50ml)

5-10 vials
(50-100ml)

10-20 vials
(100-200ml)
Large vs small dose
High dose group 100ml stat and 100 ml every 6 hrs
Low dose group 100ml stat and 50 ml every 6 hrs
Until recovery of neurological signs

Low dose of snake antivenom is as effective as high dose in


patients with severe neurotoxic snake envenoming
Agarwal, Aggarwal, Gupta, et al
Emerg Med J 2005;22:397–399.
High vs low ASV
 When a person is bitten by a snake, the major part of the
toxin gets fixed to the tissues and only a relatively small
part remains in the cirulation by the time the patient is
brought to the hospital.

 Though it is useful and essential to neutralize the


circulating toxin, it is more important to treat the systems
involved effectively and aggressively.
Repeat dose
 Signs of systemic envenoming may recur within 24-48 hrs
 Criteria for repeating the initial dose of antivenom
 Persistence or recurrence of blood incoagulability after 1-2
hr
 Deteriorating neurotoxic or cardiovascular signs after 1-2 hr
Causes
 Continuing absorption- due to improved blood supply
following correction of shock, hypovolaemia etc,
 After elimination of antivenom
 A redistribution of venom from the tissues into the vascular
space.
Observation of the response to
Antivenom
Cobra bites-Post synaptic
May begin to improve as early as 30 minutes
after anti-venom, but usually take several hours.

Krait and sea snakes- Pre synaptic


Depends on the timing of ASV administration
If delayed may not produce any action or
Minimal delayed action
Antivenom reactions
 Complement activation by IgG aggregates or residual
Fc fragments or direct stimulation of mast cells or
basophils by antivenom protein are more likely
mechanisms for these reactions.
 20%, of patients, usually more than develop a reaction
Types
 Early anaphylactic reactions- within 10-180 min
 Pyrogenic (endotoxin) reactions- develop 1-2 hours
 Late (serum sickness type) reactions- develop 1-12
(mean 7) days.

Fatal reactions have probably been under-reported as


death after snake bite is usually attributed to the venom.
Antivenom reactions
 At the earliest sign of a reaction:
 Antivenom administration must be temporarily suspended
5-day course of oral antihistamine/ Prednisolone.
Serum
 Adrenaline-0.1% solution, 1 in21,000, 1 mg/ml is the
Chlorpheniramine: mg six hourly
sickness
effective treatment for early5 mg
Prednisolone: anaphylactic
six hourly reactions.
 IV hydrocortisone (adults 100 mg, children 2 mg/kg body
weight). The corticosteroid is unlikely to act for several
hours, but may prevent recurrent anaphylaxis
 There is increasing evidence for anti H2 antihistamines-
Ranitidine – adults 50 mg, children 1 mg/kg.
 Pyrogenic reactions require- antipyretics.
 In case of circulatory collapse- start fluids, inotropes along
with IV adrenaline
Trial of anticholinesterase
Anticholinesterase (“Tensilon”/Edrophonium) test
 Record baseline parameters
 Give atropine IV
 Give anticholinesterase drug edrophonium chloride
(adults 10 mg, childrenNeostigmine
0.25 mg/kg25µg/kr/hr
body weight) given
Dose of Neostigmine 0.5 mg / 6 hr
intravenously
Neostigmine
over 3 or 4 minutes
IV atropine 0.5 mg / 12 hr
Observe
Negative response
Positive response Tearing, salivation,
Improvement in
ptosis, Respiratory muscle fasciculation,
distress, better cough abdominal cramp,
effort, decrease in bronchospasm,
RR bradycardia, cardiac
arrest Atropine IV
Neostigmine
34 yr old male shifted from rural health center with
H/O snake bite 6 hrs back has ptosis, respiratory
distress, RR 35/mt, BP 120/60, oral secretions
present, absent gag and cough reflex shifted to ICU
for tertiary care.
On ASV 100ml stat, & 50ml in NS over 6 hrs
Oxygen 3l/mt
Is given neostigmine 0.6mg and 0.6 mg atropine iv

You can have alive but a sicker patient Cobra

You can have dead patient Krait


Alive but a sicker patient

Shifted to ICU placed on a Ventilator lot of secretions


Do we continue anticholinesterases ?
Issues to consider
Increased secretions
Increased incidence of VAP ?
We rarely use these drugs once the patient is in the
ICU under observation
Repeat dose
 Signs of systemic envenoming may recur within 24-48 hrs
 Criteria for repeating the initial dose of antivenom
 Persistence or recurrence of blood incoagulability after 1-2
hr
 Deteriorating neurotoxic or cardiovascular signs after 1-2 hr
 Continuing absorption of venom from the “depot” at the site
of the bite, due to improved blood supply following
correction of shock, hypovolaemia etc,
 After elimination of antivenom
 A redistribution of venom from the tissues into the vascular
space, as the result of antivenom treatment
Mechanical ventilation
 If patient has respiratory distress or bulbar paralysis-
intubate and ventilate.
 If delayed can cause aspiration or hypoxia and cardiac
arrest.
 Even if the facility for MV is not available
Ambuing can save the day.
 This helps even during transport.
 MV is not complicated is like ventilating a patient with
curare over-dosage
ASV and children
 Dose of antivenom
 Snakes inject the same dose of venom into children and
adults.
 Children must therefore be given exactly the same dose
of antivenom as adults.
Pregnancy and snake bite
 Pregnant patient is treated the same manner as the
nonpregnant patient. Spontaneous abortion, bleeding,
fetal death & malformations are common.
 Lactating mothers can continue lactating
 Fetal demise is difficult to predict because of associated
symptoms, such as coagulopathy or hypotension, and
complications of treatment including anaphylaxis.
 Generally speaking, the severity of the mother's clinical
course seems to be the best indicator of the fetal
survival.
Treatment issues in non
Neurotoxic respiratory paralysis
 Aspiration can complicate MV
 Respiratory paralysis due to Shock, ARF, Sepsis, etc..
MV is instituted to buy time till the organs recover
Treatment is directed towards the cause
ASV
Antibiotics
Source control-Fasciotomies ?
Dialysis
Inotropes
Blood and blood products
 A 25 yr old male with snake bite has signs of
compartment syndrome and the pressure is 60 mmHg is
undergoing surgery has a Hb of 6 gm%, is hypotensive
100/60, on noradrenalin, acidotic,coagulation profile is
normal
 Blood is started
 After 15 mts of surgical time patient develops
 Dark colored urine Treatment
 Bp drops to 80/60 Fluids, Mannitol,
Alkalinize the urine,
 What are the possibilities ? Manage electrolytes
Fasciotomy
RRT
Rhabdomyolysis
Mismatched Blood transfusion
Krait
 Bites by krait, coral snake, and some cobras are
associated with minimal local changes;
 However, bite by the Indian cobra (Naja naja)
results in tender local swelling, blistering, and
necrosis. Local necrosis causes a picture of wet
gangrene with a characteristic putrid smell due to
the direct cytolytic action of the venom.
 Skip lesions are typical findings
Viper
 Viper bite is primarily vasculotoxic. It causes
rapidly developing swelling of the bitten part.
 Local necrosis is mainly ischemic as thrombosis
blocks the local blood vessels and causes a dry
gangrene
Clinical features of a compartmental syndrome

• Disproportionately severe pain


• Weakness of intracompartmental muscles
• Pain on passive stretching of intracompartmental muscles
• Hypoaesthesia of areas of skin supplied by nerves running
through the compartment
• Obvious
Earlytenseness
treatmentofwith
theantivenom
compartment on palpation
remains the best
way of preventing irreversible muscle damage

Criteria for fasciotomy in snake-bitten limbs

Haemostatic abnormalities have been corrected


(antivenom, with or without clotting factors)
• Clinical evidence of an intracompartmental syndrome
• Intracompartmental pressure >40 mmHg (in adults)
Summary
 Snake bites may be by an non venomous snake or a dry
bite
 Not all snake bites require ASV
 ASV is the main stay in the treatment of snake bites
 ASV must be initiated if indicated at the earliest
 Respiratory paralysis can be because of different
reasons-Neurotoxicity, shock, sepsis, ARF…
 MV may be main stay of treatment or just supportive
depending on the cause of failure.
Fasciotomy
 Fasciotomy should not be carried out in snake
bite patients unless or until haemostatic
abnormalities have been corrected.
 Clinical features of an intracompartmental
syndrome are present and a high
intracompartmental pressure has been confirmed
by direct measurement
High-Dose Anti-Snake Venom Versus Low-Dose Anti-
Snake Venom in The Treatment of Poisonous Snake
Bites — A Critical Study

 Results :
 In the low-dose group
 Mortality rate of 10%, 18% required dialysis and 6%
required ventilatory support. LOS 8.42 days
 In the high-dose group
 Mortality rate of 14%, 26% required dialysis 6% required
ventilatory support.LOS 9.02 days
 Conclusion : While there was no additional advantage in
following a high-dose regime for snake bite cases, there
was considerable financial gain by following the low-dose
regime,
 Most of the parameters showed a beneficial trend for
the low-dose group though the differences were not
statistically significant
JAPI • VOL. 52 • JANUARY 2004
High vs low ASV
 Repeated high doses of ASV to restore the clotting time
to normal within the shortest time, do not seem to be
necessary to reduce the ultimate morbidity and mortality.
 A smaller dose sufficient to make the clotting time graph
take a downward trend is sufficient.
 The body’s detoxifying system will bring down the clotting
time eventually though it may take a slightly longer time.
 This delay does not seem to affect the morbidity and
mortality as shown by the results of this trial.