Snake Bite, Rhabdomyolysis, and Renal Failure

Abstract

APPROXIMATELY 5 million snake bites, scorpion stings, and anaphylactic reactions to insect stings occur worldwide annually, causing over 100,000 human deaths each year.1 Snake bites are estimated to cause 30,000 deaths annually in Asia and 1,000 deaths each in Africa and South America. By contrast, in Australia and the United States, the number of deaths is minimal. The animal toxin can cause a spectrum of effects, from local reaction with pain and swelling to severe systemic response and vital organ involvement. Intravascular hemolysis, disseminated intravascular coagulation, rhabdomyolysis, and muscular paralysis are common and can lead to or contribute to devastating hemodynamic effects. Myoglobinuria and hemoglobinuria are often observed. In the tropics, animal toxins are an important cause of rhabdomyolysis. Insect stings (wasps, hornets, and bees) and snake bites are the most common cause of myoglobinuric acute renal failure (ARF). Examination of renal biopsy specimens using immunoperoxidase staining techniques has revealed myoglobin in the renal tubules of 60% of patients with various tropical diseases, yet clinical myoglobinuria is observed in only 9%. Snakes known to have toxins with myotoxicity include Notechis scutatus (Australian tiger snake), Oxyuranus scutellatus (Australian Taipan snake), Bungarus multicinctus (Taiwanese krait), Bungarus caeruleus (Indian krait), Crotalus durissus terrificus (South American rattlesnake), Micropechis ikeheka (small-eyed snake of New Guinea), Pseudechis australis (Mulga snake), Pseudechis colletti (Collett’s snake), Pseudechis affinis (Dugite snake), Pseudechis porphyriacus (red-bellied black snake), Pseudonaja textitis (common brown snake), Tropidechis carinatus (rough-scaled snake), Austrelaps superbus (copperhead), Cryptophis nigrescens (smalleyed snake), Vipera russelli pulchella (Sri Lankan Russell’s viper), and sea snakes. All myotoxic snake venoms contain phospholipase A2, which is responsible for the rhabdomyolysis. The venoms also have neurotoxin components. Some have presynaptic effects, while a few have predilection for postsynaptic action. Postsynaptic neurotoxins account for approximately 60% of the toxic protein of sea snakes (Enhydrina schistosa). Nevertheless, the clinical picture of poisoning is predominantly myotoxic rather than neurotoxic.2 Muscular pains and myoglobinuria are the most characteristic symptoms in human snake bite victims. Myalgia starts after the bite, reaches a peak a few days later, and usually lasts for 1 week. Muscular pains are associated with myoglobinuria, muscular paresis, and areflexia. Myoglobinuria lasts for approximately 1 week, while muscular paresis and areflexia can last as long as 3 weeks. ARF occurs in the majority of patients. Hyperkalemia, hyperuricemia, hypocalcemia, hyperphosphatemia, and a low ratio of serum urea nitrogen to serum creatinine concentrations are common laboratory findings. Serum creatine phosphokinase and lactate dehydrogenase levels are variable. Of clinical interest is the observation that hemodialysis in sea snake (Enhydrina schistosa) bite victims improves the muscular symptoms, including paresis. Although the clinical aspects of the Australian elapid and sea snake bites are well described, little is known about the sequential pathologic changes of the effects of myoglobinuria in the kidney. A recent renal pathologic study in mice at