A retrospective study of 40 victims of Crotalus snake bites: analysis of the hepatic necrosis observed in one patient

Abstract

Forty patients with a diagnosis of snake bite were studied at the Infectious and Parasitic Disease Service of the Faculty of Medicine of Botucatu. Thirty were males and 10 females, ranging in age from 16 to 70 years. All were farm laborers and 35 of them were bitten in the lower limbs. Two of the 9 patients seen more than 6 hours after the bite died. The low mortality rate (5%) observed could be explained by the early care provided, by the use of appropriate doses of anti-crotalus serum, parenteral hydration, urine alkalinization with sodium bicarbonate and induction of osmotic diuresis with a mannitol solution. Anatomopathological examination of one of the patients who died revealed extensive hepatic necrosis. The authors discuss the possibility of the effect of a factor of snake venom in the genesis of hepatic necrosis and in the increased transaminase levels.

Acute hepatotoxicity of Crotalus durissus terrificus (South American rattlesnake) venom in rats

“…The increased AST levels observed in the present work are similar to elevated serum activity of the same enzyme after human envenomations (24,11). Changes in serum levels of other enzymes, including creatine kinase (CK) and lactate dehydrogenase (LDH), have also been observed in human envenomations (11).…”

“…In humans, envenomation by C. d. terrificus causes hepatic lesions involving necrosis, effects attributed to release of pro-inflammatory cytokines (24)(25)(26)(27). Also, hepatic steatosis and increased serum aspartate aminotransferase (AST) levels were reported by Azevedo Marques et al (14) in patients bitten by C. d. terrificus and extensive hepatic necrosis by Barraviera et al (24).…”

Africanized honeybee stings: how to treat them

“…Acute renal failure, which occurs after massive attacks by AHB, results from toxic and ischemic mechanisms accompanied by hypovolemic and/or anaphylactic shock associated with tubular lesion caused by pigments released by muscular lesion (myoglobinuria), by hemolysis (hemoglobinuria), and by the direct toxic effect of the venom itself [33][34][35] . This type of accident is followed by complications such as hypotension, hemolysis, rhabdomyolysis, clotting disturbances, and hepatic involvement 34,52 . According to Gabriel et al 53 , four hypotheses must be considered to explain the pathogenesis of acute tubular necrosis: I) a direct toxic effect of AHB venom on renal tubules, especially proximal tubules; II) a toxic effect of myoglobin and hemoglobin on the tubules ( Figure 1E); III) an ischemic effect mediated by AHB or by substances released in the organism, or by a fall in cardiac output due to acute myocardial infarction-like lesions with a consequent fall in mean arterial pressure, reducing renal plasma flow; and iv) a stress-potentiating effect acting, for example, on nicotinamide adenine dinucleotide release in the myocardium, aggravating the cardiac ischemic component and consequently renal perfusion.…”

Epidemiologia dos acidentes ofídicos nos últimos 100 anos no Brasil: uma revisão

“…Artigos muito específicos, como os de , que tratam da epidemiologia e quadro clínico dos acidentes causados por serpentes adultas e filhotes da espé-cie Bothrops jararaca, assim como o de Barraviera et al (1989) to aos movimentos da serpente no momento da picada e após, explicitação do motivo de eventual demora na busca de atendimento e dos meios de locomoção utilizados no transporte do paciente. Caiaffa et al (1997) realizaram um estudo clínico-epidemiológico durante um período de sete anos em um hospital de emergências de Belo Horizonte, comparando 310 pacientes hospitalizados por acidentes ofídicos (casos) com 310 pacientes hospitalizados por outras causas (controles), pareados por idade e sexo.…”