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 »  Abstract
 »  Introduction
 »  Material and methods
 »  Results
 »  Discussion
 »  References

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Year : 2001  |  Volume : 49  |  Issue : 1  |  Page : 25-8

Management of respiratory failure in severe neuroparalytic snake envenomation.

Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012, India.

Correspondence Address:
Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012, India.

  »  Abstract

Fourteen patients with severe neuroparalytic snake envenomation, resulting in acute type II respiratory failure, admitted to respiratory critical care unit for mechanical ventilation during one year period, were studied. Ventilatory requirements, amount of anti snake venom (ASV) infused, period of neurological recovery and hospital survival were evaluated. All patients had severe manifestations such as ptosis, extraocular muscle paresis and limb weakness along with dyspnoea. Seven patients (50%) had additional complaints of dysphagia and dysphonia. ASV was administered to all, with a median requirement of 900 ml. Mechanical ventilation was required for a median duration of 17 hours and all except one patient, who had suffered irreversible hypoxic cerebral injury prior to resuscitation, survived with complete neurological recovery. We conclude, that the timely institution of ventilatory support and anti-venom therapy in such patients, is associated with an excellent outcome.

How to cite this article:
Agrawal P N, Aggarwal A N, Gupta D, Behera D, Prabhakar S, Jindal S K. Management of respiratory failure in severe neuroparalytic snake envenomation. Neurol India 2001;49:25

How to cite this URL:
Agrawal P N, Aggarwal A N, Gupta D, Behera D, Prabhakar S, Jindal S K. Management of respiratory failure in severe neuroparalytic snake envenomation. Neurol India [serial online] 2001 [cited 2023 Oct 5];49:25. Available from:

   »   Introduction Top

In India, approximately 15,000 persons die of bites by
poisonous snakes every year.1 The systemic effects of
venom of elapid snakes (cobra and krait) are
predominantly neurotoxic, causing a selective neuromuscular
block, affecting mainly the muscles of eyes,
tongue, throat and chest leading to respiratory
failure.[2] These patients require ventilatory assistance
in addition to administration of anti-snake venom
(ASV) and other supportive measures. We present our
experience with management of patients with severe
neuroparalytic manifestations and acute ventilatory

   »   Material and methods Top

The study was conducted at the respiratory intensive
care unit (RICU) of Postgraduate Institute of Medical
Education and Research, Chandigarh. All consecutive
patients seen during one year period, who required
mechanical ventilation for respiratory muscle
paralysis, secondary to snake envenomation, were
included. Snake bite victims with mild neuromuscular
weakness not requiring ventilatory assistance, as also
patients with systemic manifestations other than
neuroparalysis, were excluded from the study.
Detailed history and physical examination, including
the onset and nature of symptoms, site of bite, local
reaction at the bite site and general and systemic
manifestations, were recorded for each patient.
Laboratory investigations performed at admission
included arterial blood gas (ABG) analysis,
electrocardiogram (ECG), chest radiograph, serum
biochemistry, haemogram and coagulogram.
All patients were transferred to RICU from the
emergency service and ventilated using Puritan
Bennett 7200ae ventilators. Initially, control mode
ventilation (CMV) was used; patients were gradually
switched to synchronized intermittent mandatory
ventilation (SIMV) with pressure support as
neuroparalysis recovered. Meticulous attention was
paid to asepsis, nutrition, humidification of inspired
air, regular endotracheal toiletting and continuous
monitoring of haemodynamic and respiratory
(including ABG and respiratory mechanics) variables.
An effort was made to maintain oxygen fraction in
inspired air (FiO2) at <0.5, while maintaining
adequate oxygenation (pO2 >60 mm Hg). Weaning
was accomplished by gradual reduction in the SIMV
rate and the level of pressure support, once adequate
respiratory effort had reappeared. A short T-piece trial
was given and patients were extubated if they had
normal bulbar reflexes and did not show any
worsening during the period of T-piece trial.
Polyvalent ASV (Haffkine Institute, Bombay) was
administered in a loading dose of 100 ml over 2 hours,
followed by a continuous infusion at a rate of 100 ml
ASV every 6 hours, until recovery of neurological
manifestations. Ultimate outcome measure studied
was hospital survival. Duration of ventilation, period
of neuromuscular recovery and ventilator associated
complications (if any) were also recorded.

   »   Results Top

Twenty three victims, bitten by various snakes were
admitted to this Institute during the study period, of
whom 14 patients (13 males and one female) with
ventilatory failure were managed at RICU. Their age
ranged between 12 to 60 years. All the 14 cases had
severe neuroparalytic manifestations [Table I]. Bite
marks were seen in 10 (71.4%) and local swelling
around the site of bite was present in 3 (21.4%)
patients. On admission, all patients had evidence of
type II respiratory failure as evidenced by hypercapnia
(pCO2 > 45 mm Hg) with or without severe
hypoxaemia (pO2 < 60 mm Hg) [Table I].
ASV was administered in a median dose of 900 ml
(range 400 to 1400 ml) for a median duration of 36
hours (range 8 to 60 hours). Four of the 14 patients
(28.6%) developed urticaria during ASV infusion
which was easily controlled after slowing the infusion
rate and administration of epinephrine. Neostigmine
or other cholinesterase inhibitors were not
administered to any victim.
The median duration of mechanical ventilation was 17
hours [Table II]. 60% of the patients required assisted
ventilation for less than 24 hours. One patient, who
had sustained irreversible neurological damage before
reaching the hospital, was ventilated for 20 days.
However, he succumbed to complications related to
aspiration pneumonia and septicaemia. All other
patients improved and were discharged. None of the
other patients had any ventilator associated
complications like pneumonia or barotrauma.
The median duration of neurological recovery was 76
hours (range 10 to 120 hours) in 13 patients who
survived. None of these patients had any residual
neurological deficit at the time of discharge from
hospital. Serum sickness was notably absent in all the
9 patients, who reported for follow up 4 weeks after

   »   Discussion Top

Neuroparalysis leading to type II respiratory failure is
the most important cause of morbidity and mortality
in victims bitten by venomous snakes of elapidae
family.[3],[4],[5] Indian cobra (Naja naja) and common
Indian krait (Bungarus ceruleus) are two important
species of elapid snakes responsible for neurotoxic
symptoms in the victims in India.1 Post-synaptic
neurotoxins in snake venom (such as -bungarotoxin
and cobrotoxin) bind to acetylcholine receptors at
motor end plate, while pre-synaptic neurotoxins (such
as -bungarotoxin, crotoxin and taipoxin) prevent
release of acetylcholine at the neuromuscular
junction. Cobra and krait venom affect mainly the
muscles of eyes, tongue, throat and chest, leading to
respiratory failure.[2] Severity of envenomation and
progression to respiratory failure is related to several
factors such as dose of venom injected (which
depends on the mechanical efficiency of bite species
and size of snake, condition of fangs, and whether the
snake has recently fed or is injured), potency of
venom (which depends on species, age and health of
snake), anatomic location of bite (whether proximal or
distal), age, health, size and possibly immune status of
victim, and the nature and timing of first-aid and
medical treatment.[4],[5] In all such patients, timely
administration of ASV and institution of cardiorespiratory
support is associated with an excellent
All except one patient, in this study, had completely
recovered. The only patient who died, had sustained
irreversible hypoxic-ischaemic cerebral injury
because of delay in reaching the hospital. Delayed
arrival in hospital is an important factor contributing
to a fatal outcome in such victims.[5] Immediate
endotracheal intubation is necessary for airway
protection and prevention of aspiration in patients
with bulbar involvement.[11] Mechanical ventilation,
generally is easy and without complications in such
patients, as the lungs are not diseased and have normal
mechanics. In this study, the median duration of
ventilation was 17 hours. The duration of mechanical
ventilation in snake bite victims is usually short since
neuroparalysis reverses quickly with prompt
administration of ASV.[11] Infact, our aim was to wean
patients as quickly as possible because the fear of
increased risk of ventilator associated pneumonia with
prolonged ventilation. One of our patients had
developed this complication, as he was ventilated for
a very long period.
The use of ASV is mandatory, as it is the only
effective treatment for neutralisation of venom that
has entered the circulation. It is most effective when
administered within 1-4 hours after envenomation.[6]
Patients with severe poisoning require higher doses of
ASV.[4] Recently, Tariang and coworkers have also
observed that patients with neuroparalysis require
higher doses of ASV as compared to patients with
haematological complications only.[12] In the present
study, we used a median of 900 ml ASV, and could
salvage all except one patient. This dose is higher than
the one recommended in literature.[4] However, in the
absence of any clear guidelines, and in view of severe
neuroparalytic envenomation, higher doses were used
in the hope of early recovery.
Few investigators have also advocated the use of
neostigmine and related anticholinesterase drugs as a
supportive measure in the management of these
victims.13 However, there is no consensus over the
routine of such drugs.[13],[14] Anticholinesterases will act
only against the post-synaptic toxins that induce a
myasthenia-like block. They are not active against
toxins acting presynaptically. They are also not useful
if administered late, as binding of toxin to
acetylcholine receptors becomes relatively
irreversible with time. None of the patients studied in
this report received such drugs.
From these observations, we conclude that
mechanical ventilatory support, along with ASV
therapy, forms the backbone of management in
patients with respiratory failure due to severe
neuroparalytic snake envenomation. The ultimate
outcome is excellent if therapy is administered
adequately and in time.

  »   References Top

1.Banerjee RN : Poisonous snakes of India, their venoms, symptomatology and treatment of envenomation. In: Progress in clinical medicine in India. Vol. 2 Ahuja MMS (ed). Arnold Heinmann Publishers. New Delhi 1978; 136-179.  Back to cited text no. 1    
2.Mitra S : Snake bite in India and its management. J Indian Med Assoc 1987; 85 : 129-131.  Back to cited text no. 2    
3.Warrell DA : Injuries, poisoning and allergic reactions causes by animals. In: Oxford textbook of medicine. Weatherall DJ, Ledingham JGG, Warrell DA (eds): Oxford University Press, Oxford. 1984; 6.35-6.47.  Back to cited text no. 3    
4.Warrell DA : Animal toxins. In : Manson's tropical diseases. Cook G (ed): W.B. Saunders, London. 1996; 468-515.  Back to cited text no. 4    
5.Looareesuwan S, Viravan C, Warrell DA : Factors contributing to fatal snake bite in the rural tropics: analysis of 46 cases in Thailand. Tramuctiom of Royal Society of Tropical Medicine and Hygiene 1988; 82 : 930-934.  Back to cited text no. 5    
6.Udwadia FE : Critical care in envenomation. In : Principles of critical care. Udwadia FE (ed). Oxford University Press. Delhi 1995; 607-611.  Back to cited text no. 6    
7.Mehta SS, Kelkar PN, Parikh NN : Respiratory failure after snake bite poisoning successfully treated with prolonged artificial ventilation. Indian J Anaesth 1968; 16 : 273-275.  Back to cited text no. 7    
8.Bhatnagar NS : Artificial respiration in snake bite. J Indian Med Assoc 1969; 52 : 476-477.  Back to cited text no. 8    
9.Pawar DK, Singh S : Elapid snake bite. Br J Anaesth 1987;59 : 385-387.  Back to cited text no. 9    
10.Casale FF, Patel SM : Elapid snake bite. A report of two cases. Br J Anaesthesia1974; 46 : 181-183.  Back to cited text no. 10    
11.Vijayendra HS, Puri GD, Bharadwaj N et al : Management of snake bites in north India. Indian J Anaesthesia 1998; 42:65-67.  Back to cited text no. 11    
12.Tariang DD, Philip PJ, Alexander G et al : Randomized controlled trial on the effective dose of anti-snake venom in cases of snake bite with systemic envenomation. J Assoc Phy India 1999; 47 : 369-372.  Back to cited text no. 12    
13.Watt G, Theakston RDG, Hayes CG et al : Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). N Engl J Med1986; 315 :1444-1447.  Back to cited text no. 13    
14.Sethi PK, Rastogi JK : Neurologic aspects of ophitoxemia (Indian krait) - a clinico-electromyographic study. Indian J Med Res 1981; 73 : 269-276.  Back to cited text no. 14    


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