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Pulmonary Effects and Complications of SnakebitesSnakebites and the Lung FREE TO VIEW

Ariaranee Gnanathasan, MPhil, MD; Chaturaka Rodrigo, MD
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From the Department of Clinical Medicine, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka.

CORRESPONDENCE TO: Ariaranee Gnanathasan, MPhil, MD, Department of Clinical Medicine, Faculty of Medicine, University of Colombo, 25 Kynsey Rd, Colombo 08, Sri Lanka; e-mail: ariaranee2000@yahoo.com


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(5):1403-1412. doi:10.1378/chest.13-2674
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This review is on the pulmonary complications of snakebites, which can have fatal consequences. We identified three common themes as reported in the literature regarding envenomation: generalized neuromuscular paralysis affecting airway and respiratory muscles, pulmonary edema, and pulmonary hemorrhages or thrombosis due to coagulopathy. Respiratory paralysis and pulmonary edema can be due to either elapid or viper bites, whereas pulmonary complications of coagulopathy are exclusively reported with viper bites. The evidence for each complication, timeline of appearance, response to treatment, and details of pathophysiology are discussed.

Figures in this Article

The pulmonary complications of snakebites have had little focus in the medical literature, but a significant number of deaths from lung involvement due to systemic envenomation is plausible. In endemic areas, pulmonary involvement in snakebite is commonly encountered in clinical practice; therefore, it is surprising that the number of case reports and series are lacking. Perhaps in settings where clinicians have accepted it as the norm makes the condition not worth reporting. This review summarizes the effects of snakebite envenomation on lungs and the rest of the respiratory apparatus as reported in the literature to aid clinicians practicing in endemic regions.

This narrative review synthesizes PubMed and EMBASE searches with the following key words: “snake bite” in abstracts and (1) “pulmonary” in any field, (2) “ventil*” in any field, and (3) “lung” in any field. The same search strategies were repeated using the key word “snake” instead of “snake bite.” The search was then extended to involve more-specific key words based on the themes identified after the first round of searching (eg, “respiratory paralysis,” “pulmonary edema,” “thromboembolism”). Key words such as “paralysis,” “neurotoxicity,” “intubation,” “oedema” (“edema”), “anticholinesterases,” “neostigmine,” and names of specific snakes were used in a second search round. The search was restricted to articles published in the past 20 years to get the most recent information. There were 1,506 abstracts in this initial search. The software EndNote 3.0 (Thomson Reuters) was used to filter articles. Bibliographies of cited literature were also searched. All abstracts were read independently by the two authors, and key articles were identified based on a consensus. The final synthesis comprised 72 articles. These were mainly in form of case reports and case series.

Venomous snakes to humans are primarily divided into four families: (1) viperidae (> 200 species; responsible for a large number of human deaths; includes vipers, puff adder, and rattlesnakes), (2) elapidae (highly venomous species; includes cobras, sea snakes, coral snakes, and kraits), (3) colubridae (only a few species are potentially harmful), and (4) atractaspididae (a few species can produce cardiotoxic venom).1 Pulmonary involvement during envenomation has been reported in viper and elapid bites and can be categorized into three main themes: (1) respiratory paralysis, (2) pulmonary edema, and (3) hemorrhage and thrombosis involving the pulmonary vasculature.

Respiratory Paralysis

Respiratory paralysis, although part of a generalized neuromuscular dysfunction, has two consequent mechanisms specific to the respiratory system that lead to death: (1) accumulation of secretions and paralysis of tongue, causing upper airway obstruction, and (2) paralysis of the diaphragm and intercostal muscles, leading to impaired ventilation and hypoxia. The term “respiratory paralysis” in this article refers to upper airway obstruction by paralysis of oropharyngeal muscles (which can cause death by itself) as well as to paralysis of the ventilatory apparatus by dysfunction of the intercostal muscles and diaphragm. The snakes that cause neuromuscular junction dysfunction are mostly elapids, although vipers also account for a significant number of cases. The neurotoxins in snake venom are usually classified as α and β. α-Neurotoxins cause reversible postsynaptic blockage of acetylcholine receptors by a curare-like action (eg, irditoxin), whereas β-neurotoxins (eg, crotoxin, viperotoxin, taipoxin) cause more lengthy presynaptic blockade by interfering with acetylcholine release.1 Sometimes the venom causes irreversible damage to the presynaptic terminal, and new terminals must form before the effect wears off. Some snakes have both α- and β-neurotoxins in their venom (see next). Although respiratory paralysis is a well-known complication of snakebites, especially after elapid bites (eg, cobras, kraits), the number of cases reported in the literature are few.24

In a case series in Sri Lanka, Theakston et al4 described the clinical course of five patients bitten by common kraits (Bungarus caeruleus) and two patients bitten by Sri Lankan cobras (Naja naja naja). Respiratory paralysis developed in two patients in the series who had to undergo mechanical ventilation. Their symptoms reversed within 8 to 30 h. In another case series of 25 cobra bites in Sri Lanka, Kularatne et al5 described four patients (16%) needing ventilatory support (median duration, 24 h). A case series of 83 children aged 6 months to 12 years with snakebites in Malaysia reported four cases of respiratory failure needing mechanical ventilation. Two of these died, and the other two recovered. In another case series where four patients with cobra bites were managed without administration of antivenom but by mechanical ventilation alone, symptoms reversed within 36 to 72 h.6 Studies characterizing the venom of the Indian cobra (Naja naja), which is similar to its Sri Lankan counterpart, have shown the main venom component to be a phospholipase A2, which acts postsynaptically.7,8 This explains the relatively faster recovery from paralysis caused by cobra bites compared with krait bites.

Laothong and Sitprija9 described the course of three patients bitten by Malayan krait (Bungarus candidus) in whom respiratory failure developed. In the absence of specific antivenom, the patients were managed with mechanical ventilation. One died of cardiac arrest and the other two recovered after 4 and 30 days of mechanical ventilation. Administration of acetylcholine esterase inhibitors (neostigmine) was not associated with an immediately apparent benefit. However, this observation was in contrast to that of Warrell et al,10 who also described two patients envenomed by Malayan kraits needing respiratory support. One patient survived, showing a dramatic response to neostigmine. Malayan krait venom contains neurotoxins that cause predominantly presynaptic inhibition, explaining the prolonged course of respiratory paralysis. Two small randomized double-blind trials have shown a positive effect for edrophonium (a short-acting anticholinesterase) in reversing the neuroparalytic effects of Naja philippinensis bites.11,12 In a large prospective study in India, 72 patients with common krait envenoming were treated with antivenom and neostigmine (three doses of 2.5 mg at 30-min intervals).13 The mean time between bite and arrival at the hospital was 4.5 h. All patients proceeded to have respiratory paralysis requiring ventilatory support, and neostigmine did not seem to have an effect on improving the signs of paralysis. However, there was no control arm for comparing duration of ventilation and recovery times. This finding is explainable by looking at the mechanism of action of krait β-neurotoxins that act presynaptically. They lead to the depletion of acetylcholine vesicles, impaired acetylcholine-mediated neurotransmission, and loss of the nerve terminal some time later. Clinical recovery is slow and involves regeneration of the nerve terminal; thus, the patient must be supported with mechanical ventilation until such time. Antivenom and anticholinesterases are unlikely to help offset the effect of already-bound venom.14 The postsynaptically bound neurotoxins vary in their composition, but most produce a curare mimetic nondepolarizing blockage that is potentially reversible by antivenom and anticholinesterases.14 There are a few case reports of bites involving Asiatic cobra, the coral snake Micrurus frontalis, and death adder wherein anticholinesterases reversed neurologic paralysis. The dominant components of venom in these instances would have bound to the postsynaptic membrane.1518 Again, this is an oversimplification because some molecules (eg, α-bungarotoxin) bind more or less irreversibly to the postsynaptic membrane, and anticholinesterases will have little effect in reversing such envenomations despite the location of action being the postsynaptic membrane. However, several venom toxins (cobrotoxin, candotoxin) bind reversibly to the postsynaptic membrane, leaving a potential role for anticholinesterases. Snake venom comprises multiple molecules with variable actions on either side of the nerve terminals; thus, response to these agents can be highly variable.

In a Sri Lankan series of 88 common krait (B caeruleus) bites, Ariaratnam et al19 reported respiratory failure in 56 (64%) (Fig 1). Respiratory failure developed between 30 min and 13 h from the time of the bite. All patients were intubated and mechanically ventilated (mean duration, 5 days; range, 18 h-16 days). In a larger case series of 210 patients with common krait bites also from Sri Lanka, Kularatne et al20 showed that 48% needed respiratory support with mechanical ventilation. The mortality rate was 7.6%, and the duration of ventilator dependence varied between 12 h and 29 days (mode, 2 days). Those who were severely envenomed were treated with Indian polyspecific antivenom (Haffkine), but a higher dose of antivenom did not result in a significant reduction in duration of mechanical ventilation. Although the antivenom may clear the unbound venom in blood during the early phase of envenomation, it cannot reverse the damage incurred by the already-bound venom to nerve terminals. In cases of presynaptic inhibition, new nerve terminals must form to regain functionality, and repeated administration of antivenom is unlikely to help. In fact, it can be harmful because the patient remains at risk for hypersensitivity reactions to the antivenom. A study by Agarwal et al21 also confirmed that giving a higher dose of antivenom did not necessarily shorten the duration of ventilatory support of patients with severe envenomation. This trial had 55 patients with severe envenomation needing respiratory support, but unfortunately, species identification had been done for only three (kraits and cobras).

Figure Jump LinkFigure 1 –  Patient receiving supportive care for respiratory paralysis caused by envenomation by Bungarus caeruleus.Grahic Jump Location

Bungarus multicinctus is another venomous krait (Taiwanese or Chinese krait) prevalent in Southeast Asia. A case series from Vietnam in 60 consecutive patients with bites by this species showed that nearly 87% needed ventilatory support (mean duration, 8 days).22 However, this group was selected from an ICU and expected to have severe envenoming. These findings, therefore, cannot be generalized to B multicinctus bites as a whole. The mean duration of ICU stay was 12 days, and mortality was 7%. Bungarus niger (greater black krait) is a venomous snake found in India and its eastern neighbors of Bangladesh, Burma, and Nepal. Case reports of venomous bites are less frequent compared with other kraits, but respiratory paralysis needing ventilatory support has been reported.23

Because specific antivenom may only be helpful in early stages of envenomation and anticholinesterases are not always useful (especially with krait bites), the major management strategy in elapid bite envenomation is supportive care, including mechanical ventilation. Unfortunately, when such services are limited, mortality is high. It can be even higher when there are other confounding factors, such as difficulty in accessing health care, delays in identifying a bite, and not seeking timely treatment due to cultural beliefs or a desire for indigenous medication. In a case series of 30 elapid bites in rural India (23 krait and seven cobra), Bawaskar and Bawaskar24 described a higher mortality rate than other studies, possibly for these reasons. The mortality in their sample was 40% for patients with krait bites and 43% for those with cobra bites. Four patients were dead on admission. Of those surviving, eight needed ventilatory support.

Taipans are another group of extremely toxic elapids inhabiting the Australasian geographic area. A study of 166 patients with Papuan taipan (Oxyuranus scutellatus canni) bites showed that 37% needed mechanical ventilation.25 Neurotoxicity reached a peak within 24 h of the bite, and mean time to intubation was 13.5 h. Ventilatory support was needed in patients for up to 7.3 days (median, 3.6 days). Two deaths (1.2%) were attributed to respiratory arrest. The sole terrestrial venomous elapid snakes in the Americas are the coral species, which number > 70, but fatalities following coral snake bites are rare. However, case reports indicated that some species of coral snakes cause severe neurotoxic envenomation leading to respiratory paralysis.26

Studies do not report long-term complications following recovery from severe elapid envenoming, but patients may experience complications of prolonged mechanical ventilation. For example, a study in India assessing 59 snakebites (mostly krait bites) showed that 61% of the sample needed mechanical ventilation for a mean duration of 2.3 days (range, 1-6.2 days) and a rate of ventilator-associated pneumonia of 8.7%.27 In a retrospective audit of 533 patients in south India over 10 years, David et al28 showed that assisted ventilation was significantly associated with mortality (other predictors were acute kidney injury and hemotoxicity). Although part of this may be due to severe envenomation, complications of prolonged ventilation might have also added to the mortality rate. A randomized trial assessing two modes of overcoming endotracheal tube resistance in patients ventilated after snakebites (species not mentioned) showed that pressure support ventilation with automatic tube compensation would be a better option than pressure support ventilation alone because it leads to significantly faster weaning.29

Compared with elapid bites, reports of respiratory paralysis due to viper bites are few. In a series of 336 patients with Russell’s viper bits, Kularatne30 reported eight patients needing mechanical ventilation. Neurotoxicity resolved in these patients within 1 to 5 days. Ariaratnam et al31 studied 319 patients with Russell’s viper bites and observed respiratory muscle paralysis requiring mechanical ventilation in just seven (2%). Paret et al32 also described a case series of 37 envenomations with Vipera palaestine where respiratory compromise developed in two patients.

Many other studies have described respiratory paralysis due to elapid and (rarely) viper bites. They are summarized in Table 1.3353 Respiratory failure following sea snake bites has only been published as case reports.54

Table Graphic Jump Location
TABLE 1 ]  Respiratory Complications of Snakebites: Summary of Studies Not Discussed in Text

In summary, most reported cases of severe neurotoxic envenomation with respiratory paralysis are due to elapid bites. Kraits and cobras are the two most commonly cited elapids in this regard. Although the venom profile of some species has not been characterized, kraits usually have presynaptic neurotoxins that cause more permanent damage; hence, prolonged ventilatory support is needed. Cobra envenomation is relatively reversible because the toxin binds postsynaptically. When specific antivenom is available, early administration is recommended, but repeated dosing in absence of clinical improvement is not necessary because such manifestations are due to the already-bound venom, which is not affected by antivenom. Mechanical ventilation is needed in respiratory paralysis and is the most useful measure until the effect of venom wears off. Therefore, monitoring the progression of neurotoxicity in an ICU with objective measuring of vital capacity for early elective intubation can save lives. Anticholinesterases, such as neostigmine, may be useful when venom components predominantly reversibly bind to postsynaptic membranes. Because venom comprises a mixture of toxic proteins that may act on both sides of the membranes, the response to anticholinesterases may vary across individuals; thus, admission or transfer of a patient to a unit with facilities for assisted ventilation should not be delayed. Neostigmine should not be used in situations where it is likely to be ineffective, such as when venom proteins irreversibly bind to presynaptic membranes.

Pulmonary Edema

Pulmonary edema following envenomation is another complication of snakebites55 and has been reported for both viper and elapid bites.21,5658 Jeyarajah56 described a case series of Russell’s viper bites in 22 patients from Sri Lanka and found that pulmonary edema developed in eight (36.4%) and that all had acute renal failure. Four patients died, with the immediate cause of death attributed to severe pulmonary edema secondary to acute renal failure. Viper bites are known to cause neurogenic pulmonary edema as well.59 Joseph et al60 reported a case of pulmonary edema following a hump-nosed pit viper bite (Hypnale species) in Kerala, India. The venom of these vipers is known to cause acute renal failure, and pulmonary edema might have been secondary to this complication because the patient was dialysis dependent at the time this complication developed.

Elapid bites likely cause pulmonary edema secondary to autonomic dysfunction and cardiotoxicity; however, most related studies are isolated case reports. Describing two brown snake (Pseudonaja textilis) envenomations in Australia, Henderson et al61 reported pulmonary edema secondary to cardiorespiratory failure and coagulopathy; both patients had succumbed to the illness. Agarwal et al62 also described a case of pulmonary edema secondary to cardiac involvement after a common krait bite in India (B caeruleus). Cardiotoxicity following krait bites is rare, and its exact mechanism is yet unknown. During the period of severe envenomation in this particular patient, global hypokinesia was observed on echocardiography, which reversed with treatment. No alternative cause explained the pulmonary edema other than myocarditis secondary to venom cardiotoxicity. Pillai et al63 also reported an episode of pulmonary edema secondary to left ventricular dysfunction in a patient bitten by a Sind krait (Bungarus cf sindanus) in Maharashtra, India. Apart from a direct effect of envenomation, treatment with antivenom itself is known to precipitate pulmonary edema. However, such instances are rare. Singh et al64 reported an instance of noncardiogenic pulmonary edema in an 11-year-old boy secondary to antivenom therapy, which started 6 h after the infusion began.

Overall, pulmonary edema is a known complication of both viper and elapid bites. However, the reported incidence in the literature is limited to a few case reports. Pulmonary edema from viper bites is mostly due to effects of acute kidney injury, and the rate may be grossly underestimated given that a significant number of Russell’s viper and hump-nosed viper envenomations lead to renal failure.65 Elapid bites may cause cardiogenic pulmonary edema secondary to cardiotoxicity, but the exact venom profile and mechanism of action are yet unidentified. Expectation and early detection is the key to avoiding death. Monitoring of patients with acute kidney injury and initiation of timely dialysis will save lives. Once pulmonary edema sets in, ICU care with ventilatory support (if required) is necessary.

Thrombotic and Hemorrhagic Complications Affecting the Lung

Thrombotic and hemorrhagic complications have been almost exclusively reported following viper bites. Most of the case reports are for the pit vipers of Bothrops species, which are endemic to Central and South America. Bothrops venom has procoagulant as well as anticoagulant properties, and usually, the manifestations are due to pulmonary hemorrhage secondary to anticoagulant properties. However, Estrade et al66 reported a case of pulmonary embolism following disseminated intravascular coagulation (DIC) due to Bothrops lanceolatus bite. Widespread thromboses following B lanceolatus are repeatedly observed and usually start 2 days after a bite, even in patients with moderate envenomation. Malbranque et al67 reported another case of a B lanceolatus bite where diffuse thrombotic microangiopathy developed, affecting the patient’s cerebral, pulmonary, myocardial, and mesenteric vasculature. Thrombosis attributed to B lanceolatus envenomation is believed to be due to vascular endothelial injury. In most patients, the tests for coagulopathy are normal or minimally deranged apart from thrombocytopenia. How vascular endothelial injury occurs in these bites is still unclear. One possibility is that the metalloproteinases in the venom are responsible. Some authors hypothesize that activation of von Willebrand factor may give rise to a microangiopathic thrombosis as seen with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome spectrum. Makis et al68 reported another instance where pulmonary embolism followed a viper bite; however, the patient had a rare form of congenital anemia (Diamond-Blackfan anemia) and depended on transfusions with resulting iron overload. Iron overload itself is associated with a risk of thrombosis due to chronic oxidative damage to vessel endothelium.69 These background issues might have added to the patient’s prothrombotic state following envenomation.

Hemorrhagic manifestations are well-known following viper bites because of the combined effects of consumptive coagulopathy, platelet dysfunction, and direct action of hemorrhagins (metalloproteinases) in viper venom.70 Regarding the lungs, pulmonary hemorrhages have been frequently reported following Bothrops species bites.70,71 Most local and hemorrhagic manifestations of viper bites are attributable to zinc metalloproteinases, which cause hemorrhage, hypofibrogenemia, and inhibition of platelet aggregation. Inhibitors to metalloproteinases have shown some promise in counteracting some of the deleterious effects of Bothrops asper venom, confirming this hypothesis.72 In an animal model, several substances in B asper venom predisposed to bleeding tendency. Aspercetin caused a drop in platelet counts following injection, whereas jararhagin, a metalloproteinase, also contributed to this decline.73 Jararhagin has been demonstrated to induce pulmonary hemorrhage following injection in another animal study, and it is an important component in the venom of pit vipers.71 The proteinases Jararacussin-I and basparin-A, which are enzymes with procoagulant properties (serine proteinase and a prothrombin activator), also contribute to bleeding tendency by altering the checks and balances of clotting pathways.

Almost all cases of pulmonary involvement with bleeding and thrombosis have been reported for Bothrops species bites in Central and South America. However, there are abundant case reports of viper bites causing bleeding manifestations in other organs from all over the world. DIC is a well-known complication of viper bites, which may at times cause a thrombotic microangiopathy affecting small vasculature, including that of the lungs. In one of the largest case series of Russell’s viper bites described (of 336 patients), Kularatne et al30 showed that 77% of patients had evidence of coagulopathy as demonstrated by a nonclotting 20-min whole-blood clotting test. However, the numbers with actual bleeding manifestations were less, and none showed frank pulmonary hemorrhage. DIC was observed in only seven patients (2%).

The management of hemorrhagic or thrombotic manifestations is mainly supportive. However, when specific antivenom is available, it must be administered as early as possible. Unlike for neurotoxicity, repeated doses of antivenom may be necessary until the coagulopathy reverses. The 20-min whole-blood clotting test, which is a simple bedside test, is a good guide in this regard. Supportive care of bleeding tendency or DIC must always be carried out in consultation with a hematologist and would require frequent monitoring of prothrombin time, activated partial thromboplastin time, and serum fibrinogen levels for replacement of clotting factors. The lungs are a less likely target for organ damage due to hemotoxicity following viper bites. Physicians should be more alert to intracranial hemorrhages, infarctions, and renal damage, which are well-known causes for increased mortality and morbidity following viper bites.

This review identifies three main themes with respect to pulmonary involvement from snakebites. The most well-known effect is respiratory paralysis, which is predominantly due to the neurotoxicity of elapid bites, such as those of cobras, taipans, and kraits. However, viper bites are also known to cause fatal respiratory paralysis, although it is not as prominent a feature as with elapid bites. Pulmonary edema is the second fatal manifestation of snakebites and can occur with both viper and elapid bites. This can be secondary to acute kidney injury or myocarditis due to cardiotoxicity of the venom. Lung hemorrhages and thromboses due to alteration of clotting mechanisms and DIC are mostly reported for pit vipers that are endemic to Central and South America. Management is twofold for all these complications and can be summarized as (1) administration of a specific antivenom (if available) and (2) supportive care. For respiratory paralysis and pulmonary edema, supportive care is the cornerstone to management, and repeated dosing of antivenom is unlikely to reverse the neurologic manifestations due to already-bound venom to nerve terminals. However, damage from coagulopathy is more likely to be averted by antivenom (supplemented by supportive care), and repeated dosing is recommended as monitored by tests of coagulation.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

DIC

disseminated intravascular coagulation

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Kularatne SA. Epidemiology and clinical picture of the Russell’s viper (Daboia russelii russelii) bite in Anuradhapura, Sri Lanka: a prospective study of 336 patients. Southeast Asian J Trop Med Public Health. 2003;34(4):855-862. [PubMed]
 
Ariaratnam CA, Sheriff MH, Arambepola C, Theakston RD, Warrell DA. Syndromic approach to treatment of snake bite in Sri Lanka based on results of a prospective national hospital-based survey of patients envenomed by identified snakes. Am J Trop Med Hyg. 2009;81(4):725-731. [CrossRef] [PubMed]
 
Paret G, Ben-Abraham R, Ezra D, et al. Vipera palaestinaesnake envenomations: experience in children. Hum Exp Toxicol. 1997;16(11):683-687. [CrossRef] [PubMed]
 
Agrawal PN, Aggarwal AN, Gupta D, Behera D, Prabhakar S, Jindal SK. Management of respiratory failure in severe neuroparalytic snake envenomation. Neurol India. 2001;49(1):25-28. [PubMed]
 
Bawaskar HS, Bawaskar PH. Profile of snakebite envenoming in western Maharashtra, India. Trans R Soc Trop Med Hyg. 2002;96(1):79-84. [CrossRef] [PubMed]
 
Bawaskar HS, Bawaskar PH, Punde DP, Inamdar MK, Dongare RB, Bhoite RR. Profile of snakebite envenoming in rural Maharashtra, India. J Assoc Physicians India. 2008;56:88-95. [PubMed]
 
Brooks DE, Graeme KA, Ruha AM, Tanen DA. Respiratory compromise in patients with rattlesnake envenomation. J Emerg Med. 2002;23(4):329-332. [CrossRef] [PubMed]
 
Bucaretchi F, Hyslop S, Vieira RJ, Toledo AS, Madureira PR, de Capitani EM. Bites by coral snakes (Micrurusspp.) in Campinas, State of São Paulo, Southeastern Brazil. Rev Inst Med Trop Sao Paulo. 2006;48(3):141-145. [CrossRef] [PubMed]
 
Churchman A, O’Leary MA, Buckley NA, et al. Clinical effects of red-bellied black snake (Pseudechis porphyriacus) envenoming and correlation with venom concentrations: Australian Snakebite Project (ASP-11). Med J Aust. 2010;193(11-12):696-700. [PubMed]
 
Ha TH, Höjer J, Trinh XK, Nguyen TD. A controlled clinical trial of a novel antivenom in patients envenomed byBungarus multicinctusJ Med Toxicol. 2010;6(4):393-397. [CrossRef] [PubMed]
 
Johnston CI, O’Leary MA, Brown SG, et al; ASP Investigators. Death adder envenoming causes neurotoxicity not reversed by antivenom–Australian Snakebite Project (ASP-16). PLoS Negl Trop Dis. 2012;6(9):e1841. [CrossRef] [PubMed]
 
Kitchens CS, Van Mierop LH. Envenomation by the Eastern coral snake (Micrurus fulvius fulvius). A study of 39 victims. JAMA. 1987;258(12):1615-1618. [CrossRef] [PubMed]
 
Lalloo D, Trevett A, Black J, et al. Neurotoxicity and haemostatic disturbances in patients envenomed by the Papuan black snake (Pseudechis papuanus). Toxicon. 1994;32(8):927-936. [CrossRef] [PubMed]
 
Lalloo DG, Trevett AJ, Black J, et al. Neurotoxicity, anticoagulant activity and evidence of rhabdomyolysis in patients bitten by death adders (Acanthophissp.) in southern Papua New Guinea. QJM. 1996;89(1):25-35. [CrossRef] [PubMed]
 
Pe T, Myint T, Htut A, Htut T, Myint AA, Aung NN. Envenoming by Chinese krait (Bungarus multicinctus) and banded krait (B. fasciatus) in Myanmar. Trans R Soc Trop Med Hyg. 1997;91(6):686-688. [CrossRef] [PubMed]
 
Punde DP. Management of snake-bite in rural Maharashtra: a 10-year experience. Natl Med J India. 2005;18(2):71-75. [PubMed]
 
Scop J, Little M, Jelinek GA, Daly FF. Sixteen years of severe Tiger snake (Notechis) envenoming in Perth, Western Australia. Anaesth Intensive Care. 2009;37(4):613-618. [PubMed]
 
Seneviratne U, Dissanayake S. Neurological manifestations of snake bite in Sri Lanka. J Postgrad Med. 2002;48(4):275-278. [PubMed]
 
Sharma N, Chauhan S, Faruqi S, Bhat P, Varma S. Snake envenomation in a north Indian hospital. Emerg Med J. 2005;22(2):118-120. [CrossRef] [PubMed]
 
Watt G, Padre L, Tuazon L, Theakston RD, Laughlin L. Bites by the Philippine cobra (Naja naja philippinensis): prominent neurotoxicity with minimal local signs. Am J Trop Med Hyg. 1988;39(3):306-311. [PubMed]
 
Bhagat R, Sharma K, Sarode R, Shen YM. Delayed massive pulmonary thromboembolic phenomenon following envenomation by Mojave rattlesnake (Crotalus scutulatus). Thromb Haemost. 2010;104(1):186-188. [CrossRef] [PubMed]
 
Chani M, Abouzahir A, Larréché S, Mion G. Pulmonary embolism in the context of severe envenomation by a Moroccan viper [in French]. Bull Soc Pathol Exot. 2012;105(3):162-165. [CrossRef] [PubMed]
 
Karlson-Stiber C, Salmonson H, Persson H. A nationwide study ofVipera berusbites during one year-epidemiology and morbidity of 231 cases. Clin Toxicol (Phila). 2006;44(1):25-30. [CrossRef] [PubMed]
 
Thomas L, Tyburn B, Bucher B, et al; Research Group on Snake Bites in Martinique. Prevention of thromboses in human patients withBothrops lanceolatusenvenoming in Martinique: failure of anticoagulants and efficacy of a monospecific antivenom. Am J Trop Med Hyg. 1995;52(5):419-426. [PubMed]
 
Mercer HP, McGill JJ, Ibrahim RA. Envenomation by sea snake in Queensland. Med J Aust. 1981;1(3):130-132. [PubMed]
 
Caiaffa WT, Vlahov D, Antunes CM, de Oliveira HR, Diniz CR. Snake bite and antivenom complications in Belo Horizonte, Brazil. Trans R Soc Trop Med Hyg. 1994;88(1):81-85. [CrossRef] [PubMed]
 
Jeyarajah R. Russell’s viper bite in Sri Lanka. A study of 22 cases. Am J Trop Med Hyg. 1984;33(3):506-510. [PubMed]
 
Marsh NA, Whaler BC. The Gaboon viper (Bitis gabonica): its biology, venom components and toxinology. Toxicon. 1984;22(5):669-694. [CrossRef] [PubMed]
 
Hardy DL. Fatal rattlesnake envenomation in Arizona: 1969-1984. J Toxicol Clin Toxicol. 1986;24(1):1-10. [CrossRef] [PubMed]
 
Gupta S, Tewari A, Nair V. Cerebellar infarct with neurogenic pulmonary edema following viper bite. J Neurosci Rural Pract. 2012;3(1):74-76. [CrossRef] [PubMed]
 
Joseph JK, Simpson ID, Menon NC, et al. First authenticated cases of life-threatening envenoming by the hump-nosed pit viper (Hypnale hypnale) in India. Trans R Soc Trop Med Hyg. 2007;101(1):85-90. [CrossRef] [PubMed]
 
Henderson A, Baldwin LN, May C. Fatal brown snake (Pseudonaja textilis) envenomation despite the use of antivenom. Med J Aust. 1993;158(10):709-710. [PubMed]
 
Agarwal R, Singh AP, Aggarwal AN. Pulmonary oedema complicating snake bite due toBungarus caeruleusSingapore Med J. 2007;48(8):e227-e230. [PubMed]
 
Pillai LV, Ambike D, Husainy S, Khaire A, Captain A, Kuch U. Severe neurotoxic envenoming and cardiac complications after the bite of a Sind krait’ (Bungarus cf. sindanus) in Maharashtra, India. Trop Med Health. 2012;40(3):103-108. [CrossRef] [PubMed]
 
Singh A, Biswal N, Nalini P, Sethuraman, Badhe A. Acute pulmonary edema as a complication of anti-snake venom therapy. Indian J Pediatr. 2001;68(1):81-82. [CrossRef] [PubMed]
 
Herath N, Wazil A, Kularatne S, et al. Thrombotic microangiopathy and acute kidney injury in hump-nosed viper (Hypnalespecies) envenoming: a descriptive study in Sri Lanka. Toxicon. 2012;60(1):61-65. [CrossRef] [PubMed]
 
Estrade G, Garnier D, Bernasconi F, Donatien Y. Pulmonary embolism and disseminated intravascular coagulation after being bitten by aBothrops lanceolatussnake. Apropos of a case [in French]. Arch Mal Coeur Vaiss. 1989;82(11):1903-1905. [PubMed]
 
Malbranque S, Piercecchi-Marti MD, Thomas L, et al. Fatal diffuse thrombotic microangiopathy after a bite by the “Fer-de-Lance” pit viper (Bothrops lanceolatus) of Martinique. Am J Trop Med Hyg. 2008;78(6):856-861. [PubMed]
 
Makis A, Kattamis A, Grammeniatis V, et al. Pulmonary embolism after snake bite in a child with Diamond-Blackfan anemia. J Pediatr Hematol Oncol. 2011;33(1):68-70. [CrossRef] [PubMed]
 
Visudhiphan S, Ketsa-Ard K, Tumliang S, Piankijagum A. Significance of blood coagulation and platelet profiles in relation to pulmonary thrombosis in beta-thalassemia/Hb E. Southeast Asian J Trop Med Public Health. 1994;25(3):449-456. [PubMed]
 
Benvenuti LA, França FO, Barbaro KC, Nunes JR, Cardoso JL. Pulmonary haemorrhage causing rapid death afterBothrops jararacussusnakebite: a case report. Toxicon. 2003;42(3):331-334. [CrossRef] [PubMed]
 
Escalante T, Núñez J, Moura da Silva AM, Rucavado A, Theakston RD, Gutiérrez JM. Pulmonary hemorrhage induced by jararhagin, a metalloproteinase fromBothrops jararacasnake venom. Toxicol Appl Pharmacol. 2003;193(1):17-28. [CrossRef] [PubMed]
 
Rucavado A, Escalante T, Gutiérrez JM. Effect of the metalloproteinase inhibitor batimastat in the systemic toxicity induced byBothrops aspersnake venom: understanding the role of metalloproteinases in envenomation. Toxicon. 2004;43(4):417-424. [CrossRef] [PubMed]
 
Rucavado A, Soto M, Escalante T, Loría GD, Arni R, Gutiérrez JM. Thrombocytopenia and platelet hypoaggregation induced byBothrops aspersnake venom. Toxins involved and their contribution to metalloproteinase-induced pulmonary hemorrhage. Thromb Haemost. 2005;94(1):123-131. [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  Patient receiving supportive care for respiratory paralysis caused by envenomation by Bungarus caeruleus.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  Respiratory Complications of Snakebites: Summary of Studies Not Discussed in Text

References

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Kularatne SA, Budagoda BD, Gawarammana IB, Kularatne WK. Epidemiology, clinical profile and management issues of cobra (Naja naja) bites in Sri Lanka: first authenticated case series. Trans R Soc Trop Med Hyg. 2009;103(9):924-930. [CrossRef] [PubMed]
 
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Warrell DA, Looareesuwan S, White NJ, et al. Severe neurotoxic envenoming by the Malayan kraitBungarus candidus(Linnaeus): response to antivenom and anticholinesterase. Br Med J (Clin Res Ed). 1983;286(6366):678-680. [CrossRef] [PubMed]
 
Watt G, Theakston RD, Hayes CG, et al. Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study. N Engl J Med. 1986;315(23):1444-1448. [CrossRef] [PubMed]
 
Watt G, Meade BD, Theakston RD, et al. Comparison of Tensilon and antivenom for the treatment of cobra-bite paralysis. Trans R Soc Trop Med Hyg. 1989;83(4):570-573. [CrossRef] [PubMed]
 
Anil A, Singh S, Bhalla A, Sharma N, Agarwal R, Simpson ID. Role of neostigmine and polyvalent antivenom in Indian common krait (Bungarus caeruleus) bite. J Infect Public Health. 2010;3(2):83-87. [CrossRef] [PubMed]
 
Ranawaka UK, Lalloo DG, de Silva HJ. Neurotoxicity in snakebite—the limits of our knowledge. PLoS Negl Trop Dis. 2013;7(10):e2302. [CrossRef] [PubMed]
 
Lee SW, Jung IC, Yoon YH, et al. Anticholinesterase therapy for patients with ophthalmoplegia following snake bites: report of two cases. J Korean Med Sci. 2004;19(4):631-633. [CrossRef] [PubMed]
 
Gold BS. Neostigmine for the treatment of neurotoxicity following envenomation by the Asiatic cobra. Ann Emerg Med. 1996;28(1):87-89. [CrossRef] [PubMed]
 
Vital Brazil O, Vieira RJ. Neostigmine in the treatment of snake accidents caused by Micrurus frontalis: report of two cases (1). Rev Inst Med Trop Sao Paulo. 1996;38(1):61-67. [CrossRef] [PubMed]
 
Hudson BJ. Positive response to edrophonium in death adder (Acanthophis antarcticus) envenomation. Aust N Z J Med. 1988;18(6):792-794. [CrossRef] [PubMed]
 
Ariaratnam CA, Sheriff MH, Theakston RD, Warrell DA. Distinctive epidemiologic and clinical features of common krait (Bungarus caeruleus) bites in Sri Lanka. Am J Trop Med Hyg. 2008;79(3):458-462. [PubMed]
 
Kularatne SA. Common krait (Bungarus caeruleus) bite in Anuradhapura, Sri Lanka: a prospective clinical study, 1996-98. Postgrad Med J. 2002;78(919):276-280. [CrossRef] [PubMed]
 
Agarwal R, Aggarwal AN, Gupta D, Behera D, Jindal SK. Low dose of snake antivenom is as effective as high dose in patients with severe neurotoxic snake envenoming. Emerg Med J. 2005;22(6):397-399. [CrossRef] [PubMed]
 
Hung HT, Höjer J, Du NT. Clinical features of 60 consecutive ICU-treated patients envenomed byBungarus multicinctusSoutheast Asian J Trop Med Public Health. 2009;40(3):518-524. [PubMed]
 
Faiz A, Ghose A, Ahsan F, et al. The greater black krait (Bungarus niger), a newly recognized cause of neuro-myotoxic snake bite envenoming in Bangladesh. Brain. 2010;133(11):3181-3193. [CrossRef] [PubMed]
 
Bawaskar HS, Bawaskar PH. Envenoming by the common krait (Bungarus caeruleus) and Asian cobra (Naja naja): clinical manifestations and their management in a rural setting. Wilderness Environ Med. 2004;15(4):257-266. [CrossRef] [PubMed]
 
Lalloo DG, Trevett AJ, Korinhona A, et al. Snake bites by the Papuan taipan (Oxyuranus scutellatus canni): paralysis, hemostatic and electrocardiographic abnormalities, and effects of antivenom. Am J Trop Med Hyg. 1995;52(6):525-531. [PubMed]
 
Manock SR, Suarez G, Graham D, Avila-Aguero ML, Warrell DA. Neurotoxic envenoming by South American coral snake (Micrurus lemniscatus helleri): case report from eastern Ecuador and review. Trans R Soc Trop Med Hyg. 2008;102(11):1127-1132. [CrossRef] [PubMed]
 
Ahmed SM, Nadeem A, Islam MS, Agarwal S, Singh L. Retrospective analysis of snake victims in Northern India admitted in a tertiary level institute. J Anaesthesiol Clin Pharmacol. 2012;28(1):45-50. [CrossRef] [PubMed]
 
David S, Matathia S, Christopher S. Mortality predictors of snake bite envenomation in southern India—a ten-year retrospective audit of 533 patients. J Med Toxicol. 2012;8(2):118-123. [CrossRef] [PubMed]
 
Aggarwal AN, Agarwal R, Gupta D. Automatic tube compensation as an adjunct for weaning in patients with severe neuroparalytic snake envenomation requiring mechanical ventilation: a pilot randomized study. Respir Care. 2009;54(12):1697-1702. [PubMed]
 
Kularatne SA. Epidemiology and clinical picture of the Russell’s viper (Daboia russelii russelii) bite in Anuradhapura, Sri Lanka: a prospective study of 336 patients. Southeast Asian J Trop Med Public Health. 2003;34(4):855-862. [PubMed]
 
Ariaratnam CA, Sheriff MH, Arambepola C, Theakston RD, Warrell DA. Syndromic approach to treatment of snake bite in Sri Lanka based on results of a prospective national hospital-based survey of patients envenomed by identified snakes. Am J Trop Med Hyg. 2009;81(4):725-731. [CrossRef] [PubMed]
 
Paret G, Ben-Abraham R, Ezra D, et al. Vipera palaestinaesnake envenomations: experience in children. Hum Exp Toxicol. 1997;16(11):683-687. [CrossRef] [PubMed]
 
Agrawal PN, Aggarwal AN, Gupta D, Behera D, Prabhakar S, Jindal SK. Management of respiratory failure in severe neuroparalytic snake envenomation. Neurol India. 2001;49(1):25-28. [PubMed]
 
Bawaskar HS, Bawaskar PH. Profile of snakebite envenoming in western Maharashtra, India. Trans R Soc Trop Med Hyg. 2002;96(1):79-84. [CrossRef] [PubMed]
 
Bawaskar HS, Bawaskar PH, Punde DP, Inamdar MK, Dongare RB, Bhoite RR. Profile of snakebite envenoming in rural Maharashtra, India. J Assoc Physicians India. 2008;56:88-95. [PubMed]
 
Brooks DE, Graeme KA, Ruha AM, Tanen DA. Respiratory compromise in patients with rattlesnake envenomation. J Emerg Med. 2002;23(4):329-332. [CrossRef] [PubMed]
 
Bucaretchi F, Hyslop S, Vieira RJ, Toledo AS, Madureira PR, de Capitani EM. Bites by coral snakes (Micrurusspp.) in Campinas, State of São Paulo, Southeastern Brazil. Rev Inst Med Trop Sao Paulo. 2006;48(3):141-145. [CrossRef] [PubMed]
 
Churchman A, O’Leary MA, Buckley NA, et al. Clinical effects of red-bellied black snake (Pseudechis porphyriacus) envenoming and correlation with venom concentrations: Australian Snakebite Project (ASP-11). Med J Aust. 2010;193(11-12):696-700. [PubMed]
 
Ha TH, Höjer J, Trinh XK, Nguyen TD. A controlled clinical trial of a novel antivenom in patients envenomed byBungarus multicinctusJ Med Toxicol. 2010;6(4):393-397. [CrossRef] [PubMed]
 
Johnston CI, O’Leary MA, Brown SG, et al; ASP Investigators. Death adder envenoming causes neurotoxicity not reversed by antivenom–Australian Snakebite Project (ASP-16). PLoS Negl Trop Dis. 2012;6(9):e1841. [CrossRef] [PubMed]
 
Kitchens CS, Van Mierop LH. Envenomation by the Eastern coral snake (Micrurus fulvius fulvius). A study of 39 victims. JAMA. 1987;258(12):1615-1618. [CrossRef] [PubMed]
 
Lalloo D, Trevett A, Black J, et al. Neurotoxicity and haemostatic disturbances in patients envenomed by the Papuan black snake (Pseudechis papuanus). Toxicon. 1994;32(8):927-936. [CrossRef] [PubMed]
 
Lalloo DG, Trevett AJ, Black J, et al. Neurotoxicity, anticoagulant activity and evidence of rhabdomyolysis in patients bitten by death adders (Acanthophissp.) in southern Papua New Guinea. QJM. 1996;89(1):25-35. [CrossRef] [PubMed]
 
Pe T, Myint T, Htut A, Htut T, Myint AA, Aung NN. Envenoming by Chinese krait (Bungarus multicinctus) and banded krait (B. fasciatus) in Myanmar. Trans R Soc Trop Med Hyg. 1997;91(6):686-688. [CrossRef] [PubMed]
 
Punde DP. Management of snake-bite in rural Maharashtra: a 10-year experience. Natl Med J India. 2005;18(2):71-75. [PubMed]
 
Scop J, Little M, Jelinek GA, Daly FF. Sixteen years of severe Tiger snake (Notechis) envenoming in Perth, Western Australia. Anaesth Intensive Care. 2009;37(4):613-618. [PubMed]
 
Seneviratne U, Dissanayake S. Neurological manifestations of snake bite in Sri Lanka. J Postgrad Med. 2002;48(4):275-278. [PubMed]
 
Sharma N, Chauhan S, Faruqi S, Bhat P, Varma S. Snake envenomation in a north Indian hospital. Emerg Med J. 2005;22(2):118-120. [CrossRef] [PubMed]
 
Watt G, Padre L, Tuazon L, Theakston RD, Laughlin L. Bites by the Philippine cobra (Naja naja philippinensis): prominent neurotoxicity with minimal local signs. Am J Trop Med Hyg. 1988;39(3):306-311. [PubMed]
 
Bhagat R, Sharma K, Sarode R, Shen YM. Delayed massive pulmonary thromboembolic phenomenon following envenomation by Mojave rattlesnake (Crotalus scutulatus). Thromb Haemost. 2010;104(1):186-188. [CrossRef] [PubMed]
 
Chani M, Abouzahir A, Larréché S, Mion G. Pulmonary embolism in the context of severe envenomation by a Moroccan viper [in French]. Bull Soc Pathol Exot. 2012;105(3):162-165. [CrossRef] [PubMed]
 
Karlson-Stiber C, Salmonson H, Persson H. A nationwide study ofVipera berusbites during one year-epidemiology and morbidity of 231 cases. Clin Toxicol (Phila). 2006;44(1):25-30. [CrossRef] [PubMed]
 
Thomas L, Tyburn B, Bucher B, et al; Research Group on Snake Bites in Martinique. Prevention of thromboses in human patients withBothrops lanceolatusenvenoming in Martinique: failure of anticoagulants and efficacy of a monospecific antivenom. Am J Trop Med Hyg. 1995;52(5):419-426. [PubMed]
 
Mercer HP, McGill JJ, Ibrahim RA. Envenomation by sea snake in Queensland. Med J Aust. 1981;1(3):130-132. [PubMed]
 
Caiaffa WT, Vlahov D, Antunes CM, de Oliveira HR, Diniz CR. Snake bite and antivenom complications in Belo Horizonte, Brazil. Trans R Soc Trop Med Hyg. 1994;88(1):81-85. [CrossRef] [PubMed]
 
Jeyarajah R. Russell’s viper bite in Sri Lanka. A study of 22 cases. Am J Trop Med Hyg. 1984;33(3):506-510. [PubMed]
 
Marsh NA, Whaler BC. The Gaboon viper (Bitis gabonica): its biology, venom components and toxinology. Toxicon. 1984;22(5):669-694. [CrossRef] [PubMed]
 
Hardy DL. Fatal rattlesnake envenomation in Arizona: 1969-1984. J Toxicol Clin Toxicol. 1986;24(1):1-10. [CrossRef] [PubMed]
 
Gupta S, Tewari A, Nair V. Cerebellar infarct with neurogenic pulmonary edema following viper bite. J Neurosci Rural Pract. 2012;3(1):74-76. [CrossRef] [PubMed]
 
Joseph JK, Simpson ID, Menon NC, et al. First authenticated cases of life-threatening envenoming by the hump-nosed pit viper (Hypnale hypnale) in India. Trans R Soc Trop Med Hyg. 2007;101(1):85-90. [CrossRef] [PubMed]
 
Henderson A, Baldwin LN, May C. Fatal brown snake (Pseudonaja textilis) envenomation despite the use of antivenom. Med J Aust. 1993;158(10):709-710. [PubMed]
 
Agarwal R, Singh AP, Aggarwal AN. Pulmonary oedema complicating snake bite due toBungarus caeruleusSingapore Med J. 2007;48(8):e227-e230. [PubMed]
 
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[Acute renal failure caused by viper: report of 48 cases]. Zhonghua Wai Ke Za Zhi 1994;32(2):119-20.
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