Snake Envenomation

Abstract

SNAKE ENVENOMATION REPRESENTS AN IMPORTANT HEALTH PROBLEM IN much of the world. In 2009, it was recognized by the World Health Organization (WHO) as a neglected tropical disease, and in 2017, it was elevated into Category A of the Neglected Tropical Diseases list, further expanding access to funding for research and antivenoms. However, snake envenomation occurs in both tropical and temperate climates and on all continents except Antarctica. Worldwide, the estimated number of annual deaths due to snake envenomation (80,000 to 130,000) is similar to the estimate for drug-resistant tuberculosis and for multiple myeloma.^, 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. Venomous snakes kept as pets are not rare, and physicians anywhere might be called on to manage envenomation by a nonnative snake. Important advances have occurred in our understanding of the biology of venom and the management of snake envenomation since this topic was last addressed in the Journal two decades ago. For the general provider, it is important to understand the spectrum of snake envenomation effects and approaches to management and to obtain specific guidance, when needed.

Figure 1.. Venom Delivery Systems of Snakes.

All venom delivery systems involve either venom glands or, in the case of colubrids, Duvernoy’s glands, which unlike venom glands, do not have a large reservoir of venom. Venom glands are attached to tubular fangs through a duct. In Viperidae, Elapidae, and Atracta-spidinae (Panels A, B, and C, respectively), contraction of muscles around the venom glands propels the venom into the fangs and eventually into bitten tissue through openings near the tips. In Colubridae (Panel D), low-pressure channeling of venom into the bite site through grooved fangs occurs. All snakes have teeth on the lower jaw for better tissue purchase.

Figure 2.. Neurotoxic Effects of Snake Venom.

Neurotoxins generally cause a progressive, descending paralysis, beginning with bulbar muscles (ptosis and dysarthria) and progressing to respiratory compromise.

Figure 3.. Clinical Appearance, Assessment, and Management of Snakebites.

After a snakebite, a break in the skin is usually seen. This may be a scratch, a single or double puncture, or multiple punctures. Teeth in the lower jaw may also produce multiple, linear punctures (Panel A). Pain, swelling, and progressive edema with a leading edge may be seen with cytotoxic venoms, a finding that may be more tactile than visual (Panel B). Blisters may form at the bite site and elsewhere on the bitten extremity, and ecchymosis and bruising may occur as a result of coagulopathy (Panel C). Fasciotomy is a disfiguring procedure without a demonstrated benefit (Panel D).

Figure 4.. IgG and IgG Fragments Developed against Snake Venom Components.

The mammalian IgG molecule (Panel A) consists of an Fc (heavy) chain, a hinge, and two Fab (light) chains. The light chains have constant and variable regions, which allow the IgG to bind to certain antigens (Ag), such as venom components. When the IgG is treated with pepsin, the IgG molecule is cleaved below the hinge (comprising two disulfide bridges), and an F(ab′)₂ fragment is produced (Panel B). When the IgG is treated with papain, the cleavage occurs above the hinge, and two Fab fragments are produced (Panel C). The Fc remnant or chain, which is more immunogenic than the Fab chains, can be removed from the remaining solution by means of various purification techniques.