This chapter outlines general principles for the evaluation and management of victims of envenomation and poisoning by venomous snakes and marine creatures. Because the incidence of serious bites and stings is relatively low in developed nations, there is a paucity of relevant clinical research; as a result, therapeutic decision-making often is based on anecdotal information.
Venomous snakes belong to the families Viperidae (subfamily Viperinae: Old World vipers; subfamily Crotalinae: New World and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes, and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family in which most species are nonvenomous and only a few are dangerously toxic to humans). Bite rates are highest in temperate and tropical regions where populations subsist by manual agriculture. Recent estimates indicate somewhere between 1.2 million and 5.5 million snakebites worldwide each year, with 421,000–1,841,000 envenomations and 20,000–94,000 deaths. Such wide-ranging estimates bear testimony to two facts: collection of data is problematic in the regions most affected by venomous snakes (the "developing world"), and what constitutes a "snakebite" varies among researchers. Some count all snakebites (a figure that may include bites by nonvenomous snakes), whereas others count only apparent envenomations.
The typical snake-venom apparatus consists of bilateral venom glands situated below and behind the eye and connected by ducts to hollow anterior maxillary teeth. In viperids (vipers and pit vipers), those teeth are long mobile fangs that retract against the roof of the mouth when the animal is at rest. In elapids and sea snakes, the fangs are smaller and are relatively fixed in an erect position. In ∼20% of pit viper bites and higher percentages of other snakebites (up to 75% for sea snakes), no venom is released ("dry" bites). Significant envenomation probably occurs in ∼50% of all venomous snakebites.
Differentiation of venomous from nonvenomous snake species can be difficult. Viperids are characterized by somewhat triangular heads (a feature shared with many harmless snakes), elliptical pupils (also seen in some nonvenomous snakes, such as boas and pythons), enlarged maxillary fangs, and, in pit vipers, paired heat-sensing pits (foveal organs) on each side of the head. The New World rattlesnakes generally have a series of interlocking keratin plates (the rattle) on the tip of the tail; this rattle is used to dissuade potential threats. Color pattern is notoriously misleading in identifying most venomous snakes. Many harmless snakes have color patterns that closely mimic those of venomous snakes found in the same region.
Venoms and Clinical Manifestations
Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, metal ions, and other constituents. Among the deleterious components are hemorrhagins that promote vascular leakage and cause both local and systemic bleeding. Proteolytic enzymes cause local tissue necrosis, affect the coagulation pathway at various steps, and impair organ function. Myocardial depressant factors reduce cardiac output, and neurotoxins act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms have multisystem effects on their victims.
Envenomations by most viperids and some elapids with necrotizing venoms cause progressive local swelling, pain, ecchymosis (Fig. 396-1), and (over a period of hours or days) hemorrhagic bullae and serum-filled vesicles. In serious bites, tissue loss can be significant (Fig. 396-2). Systemic findings can include changes in taste, mouth numbness, muscle fasciculations, tachycardia or bradycardia, hypotension, pulmonary edema, hemorrhage (from essentially any anatomic site), and renal dysfunction. Envenomations by neurotoxic elapids such as kraits (Bungarus spp.), many Australian elapids [e.g., death adders (Atractaspis spp.) and tiger snakes (Notechis spp.)], some cobras (Naja spp.), and some viperids [e.g., the South American rattlesnake (Crotalus durissus) and some Indian Russell's vipers (Daboia russelii)] cause neurologic dysfunction. Early findings may consist of cranial nerve weakness (e.g., manifested by ptosis) and altered mental status. Severe envenomation may result in paralysis, including the muscles of respiration, and lead to death from respiratory failure and aspiration. After elapid bites, the time of onset of venom intoxication varies from minutes to hours, depending on the species involved, the anatomic location of the bite, and the amount of venom injected. Sea snake envenomation usually causes local pain (variable), myalgias, rhabdomyolysis, and neurotoxicity; these manifestations occasionally are delayed for hours.
Northern Pacific rattlesnake (Crotalus oreganus oreganus) envenomations.Top: Moderately severe envenomation. Note edema and early ecchymosis 2 h after a bite to the finger. Bottom: Severe envenomation. Note extensive ecchymosis 5 days after a bite to the ankle.
Early stages of severe, full-thickness necrosis 5 days after a Russell's viper (Daboia russelii) bite in southwestern India.
Treatment: Venomous Snakebite
The most important aspect of prehospital care of a person bitten by a venomous snake is rapid delivery to a medical facility equipped to provide supportive care (airway, breathing, and circulation) and antivenom administration. Most of the first-aid recommendations made in the past are of little benefit, and some actually worsen outcome. It is reasonable to apply a splint to the bitten extremity to lessen bleeding and discomfort and, if possible, to keep the extremity at approximately heart level. In developing regions, indigenous people should be encouraged to seek care quickly at health care facilities equipped with antivenoms as opposed to consulting traditional healers and thus incurring significant delays in reaching appropriate care.
Incising wounds and/or applying suction to the bite should be avoided, as these measures are ineffective and exacerbate local tissue damage. Similarly ineffective and ...