Last October, the American Heart Association and The Red Cross issued snakebite recommendations that have toxicologists shaking their heads.
Annually, more than 3,000 patients seek care in the United States following envenomation by poisonous snakes. Many of these envenomations are from Crotalinae such as rattlesnakes, cottonmouths, and copperheads, which mainly cause local tissue injury as opposed to a minority of bites from the Elapidae or coral snake which causes neuromuscular weakness leading to respiratory arrest. In October 2010, the American Heart Association and the American Red Cross issued their most recent first aid guidelines. Incorporated in these guidelines is a section titled “snakebites.” Among the recommendations provided is one for the routine use of a pressure immobilization device.
Following its publication in Circulation, these guidelines have generated considerable amount of discussion in the toxicology community. While the guidelines are well intended, it appears they are based upon a fundamental misunderstanding of Crotalidae (rattlesnakes, cottonomouths, and copperheads) toxicity. As a result, most toxicologists disagree with these recommendations.
Pressure immobilization was first described in the 1970s by Sutherland and colleagues for the management of Australian neurotoxic elapids. Due to long transport times, there was concern that patients with elapid envenomations may go into respiratory arrest before arriving at the hospital. The primary purpose of this pre-hospital treatment modality is to delay the systemic absorption of venom until the patient is at a facility capable of providing definitive care, including the administration of antivenom and airway management. This technique involves wrapping the entire envenomated extremity in a bandage followed by splint immobilization. Ideally, the wrap should generate a pressure between 40-70 mmHg in the upper extremity and 55-70 mmHg in the lower extremity to reduce systemic absorption of venom.
Animal models have demonstrated that successful application of a pressure immobilization device can delay both systemic absorption of venom and mortality following their application. Importantly, however, most humans do not die from Crotalidae envenomations. Occasionally, people may have an anaphylactic response to the venom or the venom may be directly injected into a vein. In these rare situations, patients suddenly become critically ill and pressure immobilization would likely not help. The primary toxicity from these envenomations is local tissue necrosis, rather than mortality from exsanguination or cardiovascular collapse. Therefore, the use of animal models whose primary endpoint is mortality is not a suitable endpoint for most human envenomations from Crotalinae. Sequestering the venom, which contains numerous proteolytic and cytotoxic components can result in increased tissue destruction and necrosis. Furthermore, applying pressure immobilization to a swine model of Crotalinae envenomation is associated with significant increased intracompartmental pressures to a potentially dangerous range.
Furthermore, while intuitively applying a pressure immobilizer is not a difficult concept, numerous studies have demonstrated poor skill retention, with misapplication occurring frequently. Most commonly, when applied incorrectly, the bandage is too loose, and inadequate pressure is applied, thereby decreasing the effectiveness of this device. Occasionally, however, the bandage is applied too tight, resulting in excessive external pressure. The later scenario can make the pressure immobilizer function as a tourniquet, with resultant limb ischemia and increased systemic absorption of venom.
Therefore, given that the primary toxicity of most snakebites in the US is not mortality but rather local tissue injury, the use of a pressure immobilizer cannot be recommended in the management of North American Crotalidae envenomations. These devices are unlikely to affect mortality, since most snakebite victims do not die, but may result in increased local tissue necrosis.
References
1. Bronstein AC, Spyker DA, Cantilena LR, et. al. 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 27th Annual Report. Clin Toxicol. 2010; 48:979-1178.
2. Markenson D, Ferguson JD, Chameides L, et. al. 2010 American Heart Association and American Red Cross Guidelines for first aid. Circulation. 2010; 122 (18 Suppl 3): S934-46.
3. Sutherland SK, Coulter AR, Harris RD. Rationalisation of first-aid measures for elapid snakebite. Lancet. 1979; 27:183-5
4. Howarth DM, Southee AE, Whyte IM. Lymphatic flow rates and first-aid in simulated peripheral snake or spider envenomation. Med J Aust. 1994; 161:695-700
5. Bush SP, Green SM, Laack TA, et al. Pressure immobilization delays mortality and increases intracompartmental pressure after artificial intramuscular rattlesnake envenomation in a porcine model. Ann Emerg Med. 2004;44:599-604.
6. German BT, Hack JB, Brewer K, et al. Pressure-immobilization bandages delay toxicity in a porcine model of Eastern coral snake (Micrurus fulvius fulvius) envenomation. Ann Emerg Med. 2005; 45:603-608
7. Sutherland SK, Coulter AR. Early management of bites by the Eastern diamondback rattlesnake (Crotalus adamanteus): studies in monkeys (Macaca fascicularis). Am J Trop Med Hyg. 1981; 30:497-200
8. Canale E, Isbister GK, Currie BJ. Investigating pressure bandaging for snakebite in a simulated setting: bandage type, training, and the effect of transport. Emerg Med Australas. 2009; 21:184-190.
9. Currie BJ, Canale E, Isbister GK. Effectiveness of pressure-immobilization first aid for snakebite requires further study. Emerg Med Australas. 2008; 20:267-270
10. Norris RL, Ngo J, Nolan K, et al. Physicians and lay people are unable to apply pressure immobilization properly in a simulated snakebite scenario. Wilderness Environ Med. 2005; 16:16-21.
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