Cases reported "Snake Bites"

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1/12. Krait bite requiring high dose antivenom: a case report.

    Anti snake venom (ASV) is the most specific therapy available for treatment of snakebite envenomation. The ASV available in nepal are polyvalent ASV produced in india and are effective against envenomation by cobra and krait, the two most common species found in Eastern nepal. Neurotoxic signs respond slowly and unconvincingly and continuous absorption of venom may cause recurrent neurotoxicity. Therefore, close observation and continuous administration of ASV is essential to save the victim. We report a case of neurotoxic envenomation due to bite by common krait (Bangarus caeruleus). The victim required very high dose of polyvalent ASV for reversal of neurological manifestations.
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2/12. Exotic snake bite: a challenge for the Scandinavian anesthesiologist?

    BACKGROUND: Venomous snake bites are uncommon in the Scandinavian countries. Envenomation from exotic snakes do however occur, mostly amongst snake handlers. This case report documents the effects and treatment for envenomation from Hoplocephalus bungaroides, or the Broad-Headed snake, native to eastern and southern australia. snakes of the genus Hoplocephalus have previously been described as of 'lesser medical importance' because of their rarity. methods: This case report describes the signs, symptoms and management of systemic envenomation in a previously healthy man. RESULTS: The patient developed signs of severe coagulopathy less than an hour after envenomation. There was also biochemical evidence of rhabdomyolysis, and cardiotoxicity. At no time did the patient develop respiratory insufficiency, neurotoxicity or renal failure. The patient was initially managed with i.v. crystalloids, plasma, corticosteroids and antifibrinolytics and by observation in the intensive care unit (ICU). Coagulopathy resolved after causal treatment with monovalent Tiger snake antivenom. CONCLUSION: The patient made good progress and was well on discharge from the ICU 26 h postenvenomation.
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3/12. Presentation and treatment of venomous snakebites at a northern academic medical center.

    Poisonous snakebites are relatively rare in the united states. The incidence of venomous snakebites is comparatively high in the southern states compared with the northern states and reports of these accidents from northern states is particularly uncommon. We report the experience with treatment of venomous snakebites at the University of michigan over a 25-year period from 1976 to 2001. Six cases were identified and are described in detail. All patients were male and all were bitten in the upper extremity by pit vipers. One patient suffered a moderate envenomation and was treated with antivenin. Four other cases of mild envenomation occurred and two of these cases required antivenin therapy. One case was considered to represent a "dry" bite and required only 24-hour observation. There were no severe envenomations and no mortalities. On short-term follow-up all patients recovered without sequelae. This report demonstrates that venomous snakebites can be treated effectively at low-volume centers.
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4/12. Conservative management of delayed, multicomponent coagulopathy following rattlesnake envenomation.

    BACKGROUND: Crotaline Fab therapy is recommended for controlling local tissue effects, coagulation abnormalities, and other systemic signs following mild-to-moderate N American Crotaline envenomations. Occasionally, coagulation abnormalities emerge after control of tissue effects has been achieved. These coagulation changes range from minor, single parameter abnormalities to multicomponent, critical value derangements. The bleeding risk associated with these abnormalities is unknown, and dosing guidelines for Crotaline Fab therapy in treating coagulation abnormalities that are severe or delayed-in-onset have not been clearly established. CASE REPORT: A 40-year-old man was envenomated in the right hand by a rattlesnake. Crotaline Fab therapy was started within 1 h of envenomation and arrest of edema progression was achieved by 48 h of admission. Although fibrinogen, platelet count, aPTT, and INR were all normal on initial assessment, hematologic changes were evolving over post-envenomation days 1 to 5 despite 32 vials of Crotaline Fab. The patient was transferred to our tertiary care center on the fifth postenvenomation day with a platelet count of 15,000/mm3 and unmeasurable values for fibrinogen, aPTT, and INR. The patient was managed with close observation alone, with no additional antivenom, and was discharged home on day 12 with no improvement in fibrinogen, aPTT or INR. Follow up lab assessment showed resolution of the hematologic effects sometime between day 17 and 37. CONCLUSION: We report a case of rattlesnake envenomation with profound, delayed hematologic effects that were resistant to 32 vials of Crotaline Fab given over post-envenomation days 1 to 4. After day 4, no further attempt was made to achieve normal lab indices using antivenom. Close observation alone may be adequate in cases of multicomponent, critical value coagulopathies following rattlesnake envenomation as long as there is no evidence of bleeding and local tissue effects and systemic effects have been adequately controlled.
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5/12. Occipital infarction revealed by quadranopsia following snakebite by bothrops lanceolatus.

    We report a case of snakebite in which envenomation was manifested through impairment of the visual field. The patient, a 46-year-old man, was bitten on the right thumb by bothrops lanceolatus. Treatment with a specific equine antivenom (Bothrofav) was administered one hour after the bite. With the exception of fang marks, the results of a clinical examination, particularly the neurologic component, were normal. The day after the bite, the patient developed an inferior left lateral homonymous quadranopsia with macular epargne. T2 magnetic resonance imaging showed a right occipital infarction. His condition improved clinically and biologically. This observation of snakebite is the first in which envenomation was accompanied exclusively by an impairment of the visual field. Envenomation by B. lanceolatus is distinct in its incidence of significant thrombotic complications at a distance from the site of the bite.
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6/12. 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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7/12. Timber rattlesnake venom-induced myokymia: evidence for peripheral nerve origin.

    Facial and limb myokymia occurred in four consecutive cases of timber rattlesnake envenomation and represents the "fasciculations" frequently reported in this entity. The facial myokymia disappears within hours of antivenin therapy and the limb myokymia by increasing serum ionized calcium. These observations suggest that the action of the venom is a biochemical one, increasing peripheral nerve excitability.
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8/12. Adder bites in children.

    16 children with adder bites were admitted to hospital in Southampton in the years 1969--77. Two children were severely poisoned; these 2, and a 3rd, fulfilled suggested criteria for antivenom administration but they recovered without it. Three children had no treatment, and 9 children no analgesia. Prolonged morbidity was not seen in these children. Careful observation in hospital was the most important factor in management, with early clinical improvement obviating the need for antivenom.
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9/12. Cross-reactivity of bardick snake venom with death adder antivenom.

    A case of a young man who was bitten by a bardick snake (Notechis curtus) and who, apart from marked local swelling, had neither signs of coagulopathy nor neurological symptoms, is reported. The bardick snake venom taken from the site of the bite reacted strongly with the death adder antivenom in the snake venom detection kit, but did not react with the Notechis antivenom. This anomalous reactivity was confirmed when dried bardick snake venom was used. In-vitro observations of the bardick snake venom showed that it had anticoagulant properties similar to those of death adder venom, and was not procoagulant as are the venoms of other snakes of the Notechis genus. The clinical importance of these findings is discussed.
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10/12. Clinical observations on glucocorticoids in cobra envenomation.

    A clinical trial of corticosteroid treatment in five cases of cobra, Naja naja, bite with systemic poisoning is reported. The results reveal that corticosteroid had no demonstrable beneficial effect in the neurotoxic poisoning of the cobra. Specific antivenom is the most important therapeutic agent for systemic poisoning. The combination of antivenom and corticosteroid had no effect on the development of local necrosis.
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