Cases reported "Snake Bites"

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1/11. A new monospecific ovine Fab fragment antivenom for treatment of envenoming by the Sri Lankan russell's viper (Daboia Russelii Russelii): a preliminary dose-finding and pharmacokinetic study.

    russell's viper is the most important cause of life-threatening snake bite and acute renal failure in sri lanka. Only equine polyspecific antivenoms imported from india are available. They have not proved effective clinically or in clearing venom antigenemia and they frequently cause reactions. In an attempt to reduce mortality and morbidity, a new monospecific ovine Fab fragment antivenom (PolongaTab; Therapeutic antibodies, Inc., london, United Kingdom) was raised against Sri Lankan russell's viper venom. In a preliminary dose-finding study in 35 patients, an initial dose of 3-4 g restored blood coagulability permanently and stopped systemic bleeding, even in severely envenomed patients. Venom antigenemia disappeared within 1 hr of antivenom treatment but recurred, probably as a result of continued absorption of venom from the site of the bite, after the rapid clearance of therapeutic antibody. Twelve patients (34%) experienced early reactions that were usually mild and always responded to epinephrine.
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2/11. Efficacy of Crotalidae polyvalent antivenin for the treatment of hognosed viper (Porthidium nasutum) envenomation.

    Envenomation from pit vipers native to north america can be treated successfully with either of the 2 commercially available antivenoms licensed in the united states. However, envenomations from imported snakes held in zoos or private collections often pose unique challenges to management because of the lack of specific antivenom and the unclear efficacy of the available licensed products. We report the case of a 37-year-old man who was envenomated on his left hand by his pet hognosed viper (Porthidium nasutum ). He had swelling at the wound site that progressively worsened over 3 to 4 hours. His symptom progression included the structural motor impairment of his fingers and a sensory deficit. Treatment with 8 vials of Antivenin (Crotalidae) polyvalent was associated with a halt of extremity swelling and restoration of neurologic and motor function of his hand. Limited experimental evidence provides support for antigenic cross-reactivity between Antivenin (Crotalidae) polyvalent and P nasutum venom.
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3/11. clinical trial of two antivenoms for the treatment of bothrops and Lachesis bites in the north eastern Amazon region of brazil.

    The efficacies of specific bothrops atrox-Lachesis and standard bothrops-Lachesis antivenoms were compared in the north eastern Amazon region of brazil. The main aim was to investigate whether a specific antivenom raised against the venom of B. atrox, the most important Amazon snake species from a medical point of view, was necessary for the treatment of patients in this region. Seventy-four patients with local and systemic effects of envenoming by bothrops or Lachesis snakes were randomly allocated to receive either specific (n = 38) or standard (n = 36) antivenoms. In 46 cases (24 in the standard antivenom group, 22 in the other) the snake was identified either by enzyme immunoassay or by examination of the dead snake, as B. atrox in 45, L. muta in one. patients were similar in all clinical and epidemiological respects before treatment. Results indicated that both antivenoms were equally effective in reversing all signs of envenoming detected both clinically and in the laboratory. Venom-induced haemostatic abnormalities were resolved within 24 h after the start of antivenom therapy in most patients. The extent of local complications, such as local skin necrosis and secondary infection, was similar in both groups. There were no deaths. The incidence of early anaphylactic reactions was 18% and 19%, respectively for specific and standard antivenoms; none was life-threatening. Measurement of serum venom concentrations by enzyme immunoassay (EIA) confirmed that both antivenoms cleared venom antigenaemia effectively. EIA also revealed that one patient had been bitten by Lachesis muta, although the clinical features in this case were not distinctive.
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4/11. life-threatening envenoming by the Saharan horned viper (Cerastes cerastes) causing micro-angiopathic haemolysis, coagulopathy and acute renal failure: clinical cases and review.

    BACKGROUND: The desert horned vipers (Cerastes cerastes and C. gasperettii) are the most familiar snakes of the great deserts of North africa and the middle east, including the plains of iraq. They are responsible for many human snake bites. In Western countries, they are popular among exotic-snake keepers. AIM: To investigate mechanisms of life-threatening envenoming and treatment. DESIGN: Clinical investigation. methods: Clinical and laboratory studies with measurement of serum venom antigen concentrations by enzyme immunoassay. RESULTS: Two men bitten while handling captive Saharan horned vipers (Cerastes cerastes) in europe developed extensive local swelling and life-threatening systemic envenoming, characterized by coagulopathy, increased fibrinolysis, thrombocytopenia, micro-angiopathic haemolytic anaemia and acute renal failure. The clinical picture is explicable by the presence in C. cerastes venom of several thrombin-like, Factor-X-activating, platelet-aggregating, haemorrhagic and nephrotoxic components. In one case, prophylactic use of subcutaneous epinephrine may have contributed to intracranial haemorrhage. The roles in treatment of heparin (rejected) and specific antivenom (recommended) are discussed. DISCUSSION: Cerastes cerastes is capable of life-threatening envenoming in humans. Optimal treatment of envenoming is by early administration of specific antivenom, and avoidance of ineffective and potentially-dangerous ancillary methods.
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5/11. Prolonged hypofibrinogenemia and protein c activation after envenoming by Echis carinatus sochureki.

    Following envenomization by Echis carinatus sochureki, a professional snake handler developed a profound coagulopathy manifested by hemorrhage from the bite site, venipuncture sites and gums; coagulation testing revealed prothrombin and partial thromboplastin times greater than 150 seconds, a fibrinogen of 0 mg%, and marked elevation of fibrin degradation products. In addition, protein c antigen levels were undetectable. The coagulopathy was treated with cryoprecipitate; two different antivenoms were also administered with uncertain benefit. Subsequently, the properties of the venom and antivenoms were studied. Venom did not directly clot fibrinogen; however, venom concentrations as low as 0.2 micrograms/ml caused significant prothrombin activation. In addition, venom activated protein c in the absence of thrombomodulin, and this activity was inhibited by hirudin. The ability of four commercial antivenoms to neutralize the venom prothrombinase and hemorrhagic activity was measured. Three of the four antivenoms partially neutralized venom-induced prothrombin activation. Extreme differences in efficacy were found among the four antivenoms in neutralizing venom hemorrhagic activity in mice. This case illustrates the difficulty in managing the complex coagulopathy that can result from exotic snake envenomization, and identifies a new coagulant property of Echis carinatus venom (protein c activation).
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6/11. Envenoming by the common krait (bungarus caeruleus) and Sri Lankan cobra (Naja naja naja): efficacy and complications of therapy with Haffkine antivenom.

    In Anuradhapura, sri lanka, 5 patients proved to have been bitten by common kraits (bungarus caeruelus) and 2 by Sri Lankan cobras (Naja naja naja) were investigated. In all the cases of krait bite the patients were bitten while they were asleep: local signs were negligible but 4 developed symptoms of systemic envenoming including paralysis, muscle pain and tenderness and abdominal pain. Mild myoglobinaemia was found in one case. Of the 2 patients bitten by cobras, one developed severe local swelling which progressed to necrosis and the other local swelling and respiratory paralysis. Response to polyspecific antivenom (Haffkine, india) was neither rapid nor convincing. Venom antigenaemia became undetectable within 2 h of the start of antivenom treatment, but recurred 25 and 65 h later in 2 cases. Among a group of 27 patients treated with this antivenom (including 21 bitten by Russell's vipers), the incidence of early anaphylactic and pyrogenic reactions was high at 52% and 65% respectively. Anticholinesterase did not improve paralysis in 2 patients bitten by kraits. The respiratory failure in 2 patients was successfully treated by mechanical ventilation for 8 and 30 h. These observations confirm the importance of neurotoxic symptoms following bites by these species but also suggest a contributory role of generalized rhabdomyolysis in krait victims and emphasize the problem of severe local tissue necrosis in cobra victims. There is a need for safer and more potent antivenoms for use in sri lanka.
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7/11. Contribution of focal haemorrhage and microvascular fibrin deposition to fatal envenoming by russell's viper (Vipera russelli siamensis) in Burma.

    In Burma, clinicopathological studies were carried out in three young farmers who died 15, 52 and 36 h after being bitten by Russell's vipers. Clinical features included local swelling, spontaneous systemic bleeding, defibrination, shock, cardiac arrhythmia, hypoglycaemia, coma and oliguria. On admission to hospital, 15, 48 and 21 h after the bites, serum venom antigen concentrations ranged from 50 to 130 ng/ml. Autopsies revealed widespread congestion and bleeding in the lungs, gastrointestinal and renal tracts, adrenals, heart, brain and anterior pituitary. There was histopathological evidence of focal haemorrhage and fibrin deposition at the site of the bite and in the pituitary, lungs and kidneys and acute tubular necrosis. Deposition of fibrin microthrombi results from the action of venom procoagulants. shock was attributed to increased capillary permeability, revealed clinically by conjunctival oedema. Acute pituitary/adrenal failure in one case was explained by fibrin deposition and haemorrhage in the anterior pituitary--resembling Sheehan's syndrome. Acute tubular necrosis resulted from ischaemia caused by fibrin deposition and to prerenal factors. An intractable cardiac tachyarrhythmia may have been caused by subendocardial and myocardial haemorrhages.
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8/11. King cobra (Ophiophagus hannah) bites in myanmar: venom antigen levels and development of venom antibodies.

    Venom, venom IgG and IgM antibody and total serum IgG levels following king cobra bites in two reptile handlers were measured by enzyme immunoassay. The patient in case 1 received antivenom while the patient in case 2 did not. Case 1 made a complete recovery following the bite and produced a high titre short-lived antibody. Venom antigen was not detected in the sample taken 11 hr after antivenom. Case 2 had experienced two recent minor king cobra bites and had received traditional immunization 4 weeks before the accident reported here. He had developed only local swelling and suffered no neurological symptoms. Venom antigen measured at 1.45 hr after the bite was 132 ng/ml; this rapidly fell to 45 ng/ml over the next 30 min, and was no longer detectable 14 hr after the bite. The pattern of venom IgG and IgM antibody responses in both cases was comparable, except that in case 2 the venom IgG peak was maintained for 13 days, compared with 1 day in case 1; in case 2 it subsequently fell to low levels 8 weeks after the bite. Venom IgM appeared 1 day after the bite, peaked at day 7-9, rapidly tailed off on day 12-16 and was then undetectable from day 20 onwards in both. Total IgG level remained within normal limits in both. It is possible that previous bites and recent immunization contributed to the boosting of the venom IgG response in case 2.
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9/11. Neurotoxicity, haemostatic disturbances and haemolytic anaemia after a bite by a Tunisian saw-scaled or carpet viper (Echis 'pyramidum'-complex): failure of antivenom treatment.

    A young man in germany was bitten by a large captive saw-scaled viper (Echis 'pyramidum'-complex) of Tunisian origin. During the first few hours after the bite he developed evidence of disseminated intravascular coagulation and fibrinolysis, and bled spontaneously. Despite being given a total of 310 ml of three different Echis-specific antivenoms (together with large amounts of fresh frozen plasma and concentrated clotting factors), venom antigenaemia (measured by enzyme immunoassay) and coagulopathy persisted for more than 10 days, and he developed a haemolytic anaemia and mild renal dysfunction. Transient bilateral ptosis was attributed to envenoming. The venom of the snake responsible for the bite was immunologically distinct from that of Nigerian E. ocellatus and was clearly not neutralised by the three monospecific antivenoms which had been administered. This case is another illustration of the geographical variation in snake venoms and the need for pooling venoms from snakes from different parts of the geographical range in the preparation of antivenoms. Envenoming by North African Echis species may not be reversible by available antivenoms.
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10/11. Accidental envenoming by a Gaboon viper (Bitis gabonica): the haemostatic disturbances observed and investigation of in vitro haemostatic properties of whole venom.

    We report the successful treatment of envenoming by the Gaboon viper (Bitis gabonica) and include results of in vitro investigations of the haemostatic properties of the whole venom. The patient was admitted to casualty soon after the bite with chest tightness, dizziness, nausea and swelling at the site of the bite and was treated immediately with polyspecific antivenom, hydrocortisone, chlorpheniramine and antibiotics. Results of haemostatic investigations were essentially normal on admission but on day 3 the thrombin time became prolonged and was associated with significant hypofibrinogenaemia and elevated D-dimers. Factors V and VIII, antithrombin iii and protein c levels and platelet number were not significantly reduced. The haemostatic disturbances persisted for more than 24 h despite treatment with blood products (16 units of cryoprecipitate, 2 units of fresh frozen plasma and 6 units of platelet concentrate). Resolution of the abnormalities occurred only after administration of a further dose of antivenom. The period of hypofibrinogenaemia occurred at a time when venom antigen was undetectable in plasma by enzyme-linked immunosorbent assay. Studies in vitro with whole venom and a panel of amidolytic substrates commonly employed for measurement of haemostatic proteins revealed significant activity of venom with substrates sensitive to kallikrein and plasmin. The venom inhibited washed platelet aggregation induced by collagen, thrombin, arachidonic acid and the calcium ionophore A23187 in a dose-dependent manner.
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