Clinical Pearls & Morning Reports
Published January 5, 2022
Snake envenomation represents an important health problem in much of the world. In countries with adequate resources, deaths are infrequent (e.g., <6 deaths per year in the United States, despite the occurrence of 7000 to 8000 bites), but in countries without adequate resources, deaths may number in the tens of thousands. Read the NEJM Review Article here.
Q: How often does a snake bite result in envenomation?
A: Not all bites by venomous snakes involve envenomation; “dry” bites occur in 2 to 50% of cases. When envenomation does occur, the clinical effects depend on the toxins in the venom.
Q: What are the important components of prehospital care in cases of snake envenomation?
A: Because of the wide variety of presentations and management challenges, expert assistance should be sought early. The primary priorities of the prehospital assessment and management of snakebite are, first, to get away from the snake and identify it, if possible; second, to loosely splint the bitten body part, with a default of heart-neutral positioning; third, to anticipate swelling (e.g., remove jewelry); and finally, to obtain transport (with personnel competent in advanced life support) to a capable health care facility.
A: Envenomation syndromes may vary widely among different species within a geographic region, and identification of a specific snake on the basis of envenomation effects may not be possible. Although venoms can derive from diverse genetic forebears, their effects may have many clinical similarities. Conversely, venoms from within a family, genus, or species may have substantially different clinical effects as a result of snake venomics, variable gene expression, and epigenetic factors. As examples, myotoxicity and neurotoxicity are typically seen in elapid envenomation but also occur in Crotalinae envenomation in Central and South America. Some Mojave rattlesnakes (Crotalus scutulatus) contain large amounts of Mojave toxin, a potent neurotoxin, whereas others have none at all. Even in the same snake, different venom effects are the result of ontogenic changes expressed over time, from newborn, to juvenile, to adult. Thus, knowledge of the family, genus, and species of an envenomating snake may not allow accurate prediction of the likelihood of venom-induced toxic effects.
A: Neuromuscular paralysis is one of the leading clinical disorders due to envenomation from elapids (snakes in the Elapidae family) such as naja, bungarus, and micrurus species and can also be seen with envenomation from other snake families such as Crotalinae in the United States and Hydrophiidae. Neurotoxic snake venoms may contain exclusively postneuromuscular or preneuromuscular synaptic toxins or a mixture of the two types. Postsynaptic neurotoxins bind to and block membrane receptors but remain extracellular. Presynaptic neurotoxins, such as alpha-bungarotoxin, are taken up into the presynaptic membrane and impair the release of neurotransmitters. Either type of neurotoxin may cause a descending, flaccid paralysis that progresses to airway compromise and life-threatening respiratory insufficiency. Progressive paralysis from postsynaptic neurotoxins may be reversed because they remain available to neutralization by antivenom. Progression of the paralytic effects of presynaptic toxins may be halted by antivenom, but because the neurotoxins are intracellular and no longer available for neutralization, the effects are not readily reversible.