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Bungarotoxin present in Bungarus caeruleus (BC) causes life threatening respiratory muscle paralysis. Deep coma and hypokalaemia have been observed in a significant proportion of patients, but the cause is unknown. We postulate the likely mechanism behind these two phenomena. We studied clinical details of two patients admitted with deep coma and p...
Citations
... This cation in response to the toxic enzymes in snake venom causing cell membrane rupture and also due to secondary effect of renal failure can be elevated in serum manifesting as hyperkalemia. However, there have been conflicting reports of hypokalemia being seen in cases of snakebite [9,10]. ...
... The bite of common Krait (Bungarus caeruleus) bite may not be painful and the local manifestations are barely discernible, but systemic symptoms and abdominal pain are the distinctive features of a krait envenomation, along with hypokalemia [10]. Following cobra and krait bite, there will be neuromuscular paralysis of palate, tongue, pharynx and respiratory muscles, coma and death occurs due to respiratory failure or shock. ...
... Kularatne et al., published a case report where the patient was in coma and later developed disseminated intravascular coagulation and acute respiratory distress within a week. Serial analysis of blood sample each day following admission in this patient consecutively for 5 days showed persistent low serum potassium in spite of potassium supplementation [10]. Hypokalemia is known to affect cardiac, skeletal and intestinal muscle cells and it is also a major risk factor for both ventricular and atrial arrhythmias. ...
... 81 Another report documented two victims of common krait bite, who developed deep coma and hypokalemia, with low renal potassium excretion and no evidence of gastrointestinal potassium loss (no diarrhea or ileus). 82 The authors proposed that hypokalemia occurred due to the intracellular shift in a mechanism similar to barium poisoning. Barium ions increase the activity of Na + -K + -ATPase enzyme and block potassium channels to interfere with its passive diffusion, leading to a drop in extracellular potassium. ...
Snake envenoming is a neglected, public health problem in tropical and subtropical regions. Local tissue necrosis, neurotoxic, and hemo-vasculotoxic effects are well-recognized features, whereas the endocrine and metabolic derangements are not as well known. In addition to contributing to morbidity, some of these manifestations can be potentially life-threatening if not recognized early. The most prominent endocrine manifestation is hypopituitarism (HP), which can manifest acutely or remain asymptomatic and present years later. Unexplained recurrent hypoglycemia and refractory hypotension are early clinical clues to suspect corticotroph axis involvement in acute settings. Chronic pituitary failure may present, like Sheehan's syndrome, several years after the bite. The occurrence of acute kidney injury, capillary leak syndrome, and disseminated intravascular coagulation are predictors of HP. Adrenal hemorrhages are documented in autopsy series; however, primary adrenal insufficiency is very rare and confounded by the presence of HP. Hyponatremia, hypokalemia or hyperkalemia, and dysglycemia can occur, but the mechanisms involved are only partially understood. Awareness, a high index of suspicion, correct interpretation of hormonal parameters, and timely treatment of these abnormalities can be lifesaving.
... All 51 children were referred from primary-and secondary-level health-care facilities of the four neighboring North Indian states. The mean (6SD) time lapse between the bite and first health-care contact, in rural and urban areas was 8.59 (6 5.01) and 5.87 (6 4.67) hours, respectively, which was not statistically significant (p ¼ 0. 19). ...
... The cause, at least in the three children who presented in cardiac arrest, could well have been hypoxia, but other possibilities like direct cardiac toxicity and dyselectrolytemia cannot be ruled out. Cardiac toxicity of viper and cobra bites is well documented, as is hypokalemia in krait bites [17][18][19]. ...
Objective:
Snake envenomation has been poorly studied in developing countries. 'Early morning neuroparalytic syndrome' (EMNS), the classical clinical constellation caused by krait bites, refers to nighttime, indoor bites where nonspecific symptoms progress to neuroparalysis. Literature regarding EMNS in children is scarce. This study was planned to describe the clinical profile, intensive care needs and predictors of outcome in children with EMNS.
Methods:
It is a retrospective study of children below 12 years admitted with a clinical diagnosis of snake envenomation to the pediatric intensive care unit (PICU) of a tertiary care hospital in North India. Patient records were reviewed from the electronic patient database manager. Comparison was made between the EMNS group and the non-EMNS group and between survivors and nonsurvivors within the EMNS group.
Results:
Of the 111 children with snake envenomation, 76 had neuroparalysis (68%) and 51 had EMNS. In the EMNS cohort, 37 (72.5%) belonged to rural areas, 46 (90.2%) had indoor bites and 39 (76.5%) were witnessed. Patients with EMNS were more likely to have absent fang marks, hypoxemia at admission, bulbar palsy and need for PICU admission. Mortality rate was 13.7% in EMNS; predictors included younger age, presence of ptosis, cardiac arrest at admission and nonavailability of PICU bed (univariable analysis) but none of them independently predicted mortality.
Conclusion:
Younger age, presence of ptosis, cardiac arrest at admission and nonavailability of intensive care beds increase the risk of mortality in children with EMNS. Timely recognition and respiratory support may reduce mortality in these children.
... Central neurological effects are rarely reported in snake envenoming, and are almost always due to indirect neurological effects of haemorrohagic or thrombotic toxicity in the central nervous system from snake venom procoagulant toxins [26][27][28][29][30]. Apparent deep coma reported after krait envenoming [23,31] suggests possible direct toxin-mediated central neurological effects. However, this may be explained as an extreme state of neuromuscular paralysis mimicking coma rather than actual coma [4,[31][32][33][34]. ...
... Central neurological effects are rarely reported in snake envenoming, and are almost always due to indirect neurological effects of haemorrohagic or thrombotic toxicity in the central nervous system from snake venom procoagulant toxins [26][27][28][29][30]. Apparent deep coma reported after krait envenoming [23,31] suggests possible direct toxin-mediated central neurological effects. However, this may be explained as an extreme state of neuromuscular paralysis mimicking coma rather than actual coma [4,[31][32][33][34]. ...
Antivenom therapy is currently the standard practice for treating neuromuscular dysfunction in snake envenoming. We reviewed the clinical and experimental evidence-base for the efficacy and effectiveness of antivenom in snakebite neurotoxicity. The main site of snake neurotoxins is the neuromuscular junction, and the majority are either: (1) pre-synaptic neurotoxins irreversibly damaging the presynaptic terminal; or (2) post-synaptic neurotoxins that bind to the nicotinic acetylcholine receptor. Pre-clinical tests of antivenom efficacy for neurotoxicity include rodent lethality tests, which are problematic, and in vitro pharmacological tests such as nerve-muscle preparation studies, that appear to provide more clinically meaningful information. We searched MEDLINE (from 1946) and EMBASE (from 1947) until March 2017 for clinical studies. The search yielded no randomised placebo-controlled trials of antivenom for neuromuscular dysfunction. There were several randomised and non-randomised comparative trials that compared two or more doses of the same or different antivenom, and numerous cohort studies and case reports. The majority of studies available had deficiencies including poor case definition, poor study design, small sample size or no objective measures of paralysis. A number of studies demonstrated the efficacy of antivenom in human envenoming by clearing circulating venom. Studies of snakes with primarily pre-synaptic neurotoxins, such as kraits (Bungarus spp.) and taipans (Oxyuranus spp.) suggest that antivenom does not reverse established neurotoxicity, but early administration may be associated with decreased severity or prevent neurotoxicity. Small studies of snakes with mainly post-synaptic neurotoxins, including some cobra species (Naja spp.), provide preliminary evidence that neurotoxicity may be reversed with antivenom, but placebo controlled studies with objective outcome measures are required to confirm this.
... Coma has been previously reported in common krait envenoming [7,33]. In one study, two patients with deep coma were reported to have electroencephalogram abnormalities, abnormal brain stem visual and auditory evoked potentials, leading to the conclusion that krait venom can cause cortical and brain stem effects [33]. ...
... Coma has been previously reported in common krait envenoming [7,33]. In one study, two patients with deep coma were reported to have electroencephalogram abnormalities, abnormal brain stem visual and auditory evoked potentials, leading to the conclusion that krait venom can cause cortical and brain stem effects [33]. However peptide and protein toxins are unlikely to cross the blood brain barrier making this theoretically unlikely. ...
Objective:
We aimed to investigate neurophysiological and clinical effects of common krait envenoming, including the time course and treatment response.
Methodology:
Patients with definite common krait (Bungarus caeruleus) bites were recruited from a Sri Lankan hospital. All patients had serial neurological examinations and stimulated concentric needle single-fibre electromyography (sfEMG) of orbicularis oculi in hospital at 6wk and 6-9mth post-bite.
Principal findings:
There were 33 patients enrolled (median age 35y; 24 males). Eight did not develop neurotoxicity and had normal sfEMG. Eight had mild neurotoxicity with ptosis, normal sfEMG; six received antivenom and all recovered within 20-32h. Seventeen patients developed severe neurotoxicity with rapidly descending paralysis, from ptosis to complete ophthalmoplegia, facial, bulbar and neck weakness. All 17 received Indian polyvalent antivenom a median 3.5h post-bite (2.8-7.2h), which cleared unbound venom from blood. Despite this, the paralysis worsened requiring intubation and ventilation within 7h post-bite. sfEMG showed markedly increased jitter and neuromuscular blocks within 12h. sfEMG abnormalities gradually improved over 24h, corresponding with clinical recovery. Muscle recovery occurred in ascending order. Myotoxicity was not evident, clinically or biochemically, in any of the patients. Patients were extubated a median 96h post-bite (54-216h). On discharge, median 8 days (4-12days) post-bite, patients were clinically normal but had mild sfEMG abnormalities which persisted at 6wk post-bite. There were no clinical or neurophysiological abnormalities at 6-9mth.
Conclusions:
Common krait envenoming causes rapid onset severe neuromuscular paralysis which takes days to recover clinically consistent with sfEMG. Subclinical neuromuscular dysfunction lasts weeks but was not permanent. Antivenom effectively cleared venom but did not prevent worsening or reverse neuromuscular paralysis.
... These complications are at least partly due to the presynaptic action of a neurotoxic phospholipase A 2 (b-bungarotoxin) present in the venom. The clinical manifestations are associated with delayed brain stem auditory and visual evoked potentials and abnormalities on electroencephalogram (Kularatne, 2002;Gawarammana et al., 2010). ...
Sri Lanka is a tropical developing island nation that endures significant economic and medical burden as a result of snakebite envenomation, having not only a high prevalence of envenomations, but also one of the highest incidence rates (200 snakebites/100,000 people/year) of venomous snakebite in the world (Kasturiratne et al., 2005). Ironically, the very snakes responsible for this human morbidity and mortality are a valuable a biomedical and ecological national resource, despite the medical and economic consequences of envenomation. Currently, no snake antivenom is produced using venoms from native Sri Lankan snakes as immunogens, and there is a true need for an efficacious Sri Lanka, poly-specific snake antivenom. An approach to fulfilling this need via combining the scientific, technological and economical resources from Costa Rica and the United States with the knowledge and talent of Sri Lankan official governmental agencies, legal counsels, environmental, medical and veterinary academic institutions, and religious and cultural leaders has been initiated, coordinated and funded by Animal Venom Research International (AVRI), a non-profit charity. This bridging of nations and the cooperative pooling of their resources represents a potential avenue for antivenom development in a developing country that suffers the consequences of few specific resources for the medical management of venomous snakebite. The desired final outcome of such an endeavor for Sri Lanka is, most importantly, improved medical outcomes for snakebite patients, with enhanced and expanded science and technology relating to snake venoms and antivenoms, and the collateral benefits of reduced economic cost for the country.
Neurologic dysfunction due to natural neurotoxins is an important, but neglected, public health hazard in many parts of the world, particularly in the tropics. These toxins are produced by or found among a variety of live forms that include venomous snakes, arthropods such as scorpions, spiders, centipedes, stinging insects (Hymenoptera), ticks, certain poisonous fish, shellfish, crabs, cone shells, skin secretions of dart-poison frogs, and bacterial poisons such as botulinum toxin. These toxins commonly act on neuromuscular transmission at the neuromuscular junction where acetylcholine is the neurotransmitter, but in certain situations the toxins interfere with neurotransmitters such as GABA, noradrenaline, adrenaline, dopamine, and γ-aminobutyrate. Of the toxins, α-toxins and κ-toxins (e.g., Chinese krait, Bungarus multicinctus) act on the postsynaptic membrane, blocking the receptors, whilst β-toxin (e.g., common krait, B. caeruleus) acts on the presynaptic membrane, causing impairment of acetylcholine release. Conversely, dendrotoxins of the African mamba enhance acetylcholine release. The toxins of scorpions and spiders commonly interfere with voltage-gated ion channels. Clinically, the cardinal manifestation is muscle paralysis. In severe cases respiratory paralysis could be fatal. Effective antivenoms are the mainstay of treatment of envenoming, but their lack of availability is the major concern in the regions of the globe where they are desperately needed. Interestingly, some toxins have proved to be valuable pharmaceutical agents, while some others are widely exploited to study neuromuscular physiology and pathology.
