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Management of respiratory failure in severe neuroparalytic snake envenomation.
Correspondence Address:
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.
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 failure.
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.
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 discharge.
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 outcome.[6],[7],[8],[9],[10] 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.
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