Bites by puff-adder (Bitis arietans) in Nigeria, and value of antivenom. (25/243)

Ten patients bitten by the puff-adder (Bitis arietans) were studied in the North of Nigeria. Six showed severe local signs, and four also had evidence of systemic envenoming, including spontaneous bleeding with thrombocytopenia, hypotension, and bradycardia. Two patients died after developing circulatory collapse and renal failure. Antivenom and intravenous fluid restored blood pressure in two hypotensive patients, and antivenom probably prevented the development of local necrosis in four others with massive local swelling. Victims of B arietans who have swelling of more than half the bitten limb or show signs of systemic envenoming should be given at least 80 ml of specific polyvalent antivenom and watched carefully for signs of circulatory collapse. Debridement of necrotic tissue may be necessary.  (+info)

Common krait (Bungarus caeruleus) bite in Anuradhapura, Sri Lanka: a prospective clinical study, 1996-98. (26/243)

Common krait (Bungarus caeruleus) is the deadliest snake found commonly in the dry zone of Sri Lanka. In Anuradhapura, 210 farmers bitten by the common krait over a three year period were investigated prospectively from 1 January 1996. The sex ratio was equal, 110 (52%) patients were in the age group 10-30 years. One hundred and one (48%) patients were severely envenomed and needed mechanical ventilation from 12 hours to 29 days (mode two days). The bite occurred at night while the victims were asleep on the floor. In 99 (47%) situations killed specimens were available for identification. The cardinal symptom was abdominal pain developing within hours of the bite. Alteration in the level of consciousness was observed in 150 (71%) patients: drowsy in 91 (43%), semiconscious in 24 (11%), and deep coma in 35 (17%). Autonomic disturbances included transient hypertension, tachycardia, lacrimation, sweating, and salivation. These manifested in 139 (66%) patients with moderate to severe envenomation. One hundred and forty nine (71%) had hypokalaemia and 105 (50%) metabolic acidosis, anterograde memory loss in 84 (40%), and delayed neuropathy in 38 (22%) patients. Polyvalent antivenom had no significant benefit (t = 0.5) in reversing respiratory paralysis and preventing delayed neurological complications. Sixteen (7.6%) patients died and a submucosal haemorrhage in the stomach was seen at necropsy in three cases. Mortality could be minimised with early and free access to mechanical ventilation.  (+info)

Snakebites by Crotalus durissus ssp in children in Campinas, Sao Paulo, Brazil. (27/243)

From January, 1984 to March, 1999, 31 children under 15 y old (ages 1-14 y, median 8 y) were admitted after being bitten by rattlesnakes (Crotalus durissus ssp). One patient was classified as "dry-bite", 3 as mild envenoming, 9 as moderate envenoming and 18 as severe envenoming. Most patients had neuromuscular manifestations, such as palpebral ptosis (27/31), myalgia (23/31) and weakness (20/31). Laboratory tests suggesting rhabdomyolysis included an increase in total blood creatine kinase (CK, 28/29) and lactate dehydrogenase (LDH, 25/25) levels and myoglobinuria (14/15). The main local signs and symptoms were slight edema (20/31) and erythema (19/31). Before antivenom (AV) administration, blood coagulation disorders were observed in 20/25 children that received AV only at our hospital (incoagulable blood in 17/25). AV early reactions were observed in 20 of these 25 cases (9/9 patients not pretreated and 11/16 patients pretreated with hydrocortisone and histamine H1 and H2 antagonists). There were no significant differences in the frequency of patients with AV early reactions between the groups that were and were not pretreated (Fisher's exact test, p = 0.12). Patients admitted less than and more than 6 h after the bite showed the same risk of developing severe envenoming (Fisher's exact test, p = 1). No children of the first group (< 6 h) showed severe complications whereas 3/6 children admitted more than 6 h post-bite developed acute renal failure. Patients bitten in the legs had a higher risk of developing severe envenoming (Fisher's exact test, p = 0.04). There was a significant association between both total CK and LDH blood enzyme levels and severity (p < 0.001 for CK and p < 0.001 for LDH; Mann-Whitney U test). No deaths were recorded.  (+info)

Multiple cerebral infarctions following a snakebite by Bothrops caribbaeus. (28/243)

Bothrops caribbaeus, a species of the Bothrops complex, is found only in the island of Saint Lucia, West Indies. Snakebite from this pitviper is very rare. We report the case of a healthy 32-year-old Saint Lucian man who developed multiple cerebral infarctions following envenoming by this snake. This patient developed signs and symptoms very similar to those observed in patients envenomed by Bothrops lanceolatus, a snake found only in Martinique, the neighbor island of Saint Lucia. This clinical presentation differs dramatically from coagulopathies and systemic bleeding observed with the Central and South American bothropic envenomings. The exact mechanism of this thrombogenic phenomenon, leading to a unique envenoming syndrome, remains unknown.  (+info)

Neurological manifestations of snake bite in Sri Lanka. (29/243)

BACKGROUND AND AIMS: Snake bite is an important cause of mortality and morbidity in certain parts of Sri Lanka. This study was designed to determine the offending snakes, neurological manifestations, disease course, and outcome in neurotoxic envenomation. METHODS AND MATERIAL: Fifty six consecutive patients admitted with neurological manifestations following snake bite were studied prospectively. Data were obtained regarding the offending snakes, neurological symptoms, time taken for onset of symptoms, neurological signs, and time taken for recovery. RESULTS: The offending snake was Russell's viper in 27(48.2%), common and Sri Lankan krait in 19(33.9%), cobra in 3(5.4%), and unidentified in 7(12.5%). Ptosis was the commonest neurological manifestation seen in 48(85.7%) followed by ophthalmoplegia (75%), limb weakness (26.8%), respiratory failure (17.9%), palatal weakness (10.7%), neck muscle weakness (7.1%), and delayed sensory neuropathy (1.8%). Neurological symptoms were experienced usually within 6 hours after the bite. Following administration of antivenom, the signs of recovery became evident within a few hours to several days. The duration for complete recovery ranged from four hours to two weeks. CONCLUSIONS: Complete recovery of neuromuscular weakness was observed in all patients except for one who died with intracerebral haemorrhage shortly after admission.  (+info)

The calcium-dependent protease of Loxosceles gaucho venom acts preferentially upon red cell band 3 transmembrane protein. (30/243)

Eighty micrograms red blood cell (RBC) ghosts from patients who had previously exhibited the cutaneous form of loxoscelism (presenting localized dermonecrosis) and the viscerocutaneous form of loxoscelism (presenting dermonecrosis, hemoglobinuria, hematuria, and jaundice) and from controls were incubated with 2.5 microg crude Loxosceles gaucho venom in 5 mM phosphate buffer, pH 7.4, at 37 C. Among all membrane proteins, quantitative proteolysis of the important integral transmembrane protein 3 increased with venom dose and with incubation time from 30 to 120 min, as demonstrated by gel densitometry. Similar quantitative data were obtained for RBC ghosts from patients and from control subjects, a fact that argues against the possibility of genetic factors favoring the hemolytic viscerocutaneous form. These data suggest that the clinical forms may be different types of the same disease, with the viscerocutaneous form being the result of large amounts of intravascularly injected venom and the superficial form being the result of in situ venom action. Since protein 3 is a housekeeping integral membrane protein, whose genetic deficiency leads to hemolytic anemia, it is reasonable to relate it to the hemolysis which occurs in the viscerocutaneous form of loxoscelism. The venom protease responsible for the process was not inhibited after 120-min incubation by 0.2 mM paramethylsulfonyl fluoride or by 0.2 mM N-ethylmaleimide but was inhibited by 25 mM ethylenediaminetetraacetic acid (a calcium-chelating agent) in 5 mM phosphate buffer at pH 7.4, which suggests that the enzyme is a calcium-dependent metalloprotease.  (+info)

Multiple hemorrhagic brain infarcts after viper envenomation. (31/243)

We report the case of a 65-year-old woman who presented with severe neurologic complications after envenomation by a viper snake. A computed tomography (CE) scan revealed multiple brain hemorrhagic infarcts. Conservative treatment in this case proved to be sufficient and repetitive CT scans displayed a complete resolution of the radiologic findings. Possible mechanisms for the cerebral infarctions are discussed. The mechanism of infarctions in this case was believed to be the vasomotor and coagulation disorders caused by the toxins present in the snake's venom and was one of the reasons that led to conservative treatment.  (+info)

Case report: Extraocular muscle paresis caused by snakebite. (32/243)

A 51 year-old man presented with binocular diplopia on the three days after the snakebite in the fifth finger of the right hand by an Agkistrodon blomhoffi (mamushi). In the primary position he had an exotropia and right hypertropia, which became apparent when his head was tilted to the right. From ocular angle of deviation measured by synoptophore and Hess chart test, he was diagnosed as having medial rectus muscle paresis as well as inferior oblique muscle paresis of the left eye. Elevation deficit on right gaze in the left eye had remained during three days. Our case suggested that the occurrence of subjective binocular diplopia is an important clinical sign for the onset of general abnormalities caused by snakebite.  (+info)