Snake Bite


Most snakebites are innocuous and are delivered by nonpoisonous species. Twenty-five species of poisonous snakes make North America their home. Worldwide, only about 15% of the more than 3000 species of snakes are considered dangerous to humans. The family Viperidae is the largest family of venomous snakes, and members of this family can be found in Africa, Europe, Asia, and the Americas. The family Elapidae is the next largest family of venomous snakes. In North America the venomous species are members of the families Elapidae, and Viperidae, subfamily Crotalidae.

The subfamily Crotalidae (pit vipers) includes rattlesnakes (Crotalus and Sistrurus), cottonmouths (Agkistrodon), and copperheads (Agkistrodon). The Western diamondback, timber, and prairie rattlesnakes are pit vipers (see Image 1). A triangular-shaped head, nostril pits (heat-sensing organs), elliptical pupils, and subcaudal plates arranged in a single row are characteristic features of Crotalidae. They may be found in all regions of the country, and their habitat varies by species. Cottonmouths reside near swamps or rivers. Copperheads are found in aquatic and dry environments, and rattlesnakes prefer dry grasslands and rocky hillsides.

Elapidae includes the coral snakes (Micrurus fulvius fulvius and Micrurus fulvius tenere; see Image 2). The eastern and western species that inhabit the United States are smaller and brightly colored with red, yellow, and black rings. The nonvenomous king snakes share the same colors but not in the same order. A common warning is "red on yellow, kill a fellow; red on black, venom lack." Coral snake pupils are round, and their subcaudal scales are arranged in double rows. The southern and southwestern states provide the dry sandy conditions (and often a body of water) that coral snakes prefer.

Cobras, mambas, and kraits also are also members of the family Elapidae but are not indigenous to the Americas. However, an increasing number of exotic species are kept by both zoos and private collectors making bites by non-indigenous species increasingly common.


Venom is produced and stored in paired glands below the eye. It is discharged from hollow fangs located in the upper jaw. Fangs can grow to 20 mm in large rattlesnakes. Venom dosage per bite depends on the elapsed time since the last bite, the degree of threat the snake feels, and the size of the prey. The nostril pits respond to the heat emission of the prey, which may enable the snake to vary the amount of venom delivered.

Coral snakes have shorter fangs and smaller mouths. This allows them less opportunity for envenomation than the crotalids, and their bites more closely resemble chewing rather than the strike for which the pit vipers are famous. Both methods inject venom into the victim to immobilize it quickly and begin digestion.

Venom is mostly water. Enzymatic proteins in venom impart its destructive properties. Proteases, collagenase, and arginine ester hydrolase have been identified in pit viper venom. Neurotoxins comprise the majority of coral snake venom. Specific details are known for several enzymes as follows: (1) hyaluronidase allows rapid spread of venom through subcutaneous tissues by disrupting mucopolysaccharides; (2) phospholipase A2 plays a major role in hemolysis secondary to the esterolytic effect on red cell membranes and promotes muscle necrosis; and (3) thrombogenic enzymes promote the formation of a weak fibrin clot, which, in turn, activates plasmin and results in a consumptive coagulopathy and its hemorrhagic consequences.

Enzyme concentrations vary among species, thereby causing dissimilar envenomations. Copperhead bites generally are limited to local tissue destruction. Rattlesnakes can leave impressive wounds and cause systemic toxicity. Coral snakes may leave small wounds that later result in respiratory failure from the typical systemic neuromuscular blockade.

The local effects of venom serve as a reminder of the potential systemic disruption of organ system function. One effect is local bleeding; coagulopathies are not uncommon with severe envenomations. Another effect, local edema, increases capillary leak and interstitial fluid in the lungs. Pulmonary mechanics may be altered significantly. The final effect, local cell death, increases lactic acid concentration secondary to changes in volume status and requires increased minute ventilation. The effects of neuromuscular blockade result in poor diaphragmatic excursion. Cardiac failure can result from hypotension and acidosis. Myonecrosis raises concerns about myoglobinuria and renal damage.

  • Deaths secondary to snake bites are rare. With the proper use of antivenin, they are becoming rarer still. The national average has been less than 4 deaths per year for the last several years.
  • A review of morbidity associated with snakebites from Kentucky was published. Most bites were from copperheads and resulted in 8 days of pain, 11 days of extremity edema, and 14 days of missed work.1 A review specifically of copperhead bites in West Virginia described similar outcomes and noted that the peak effects of envenomation were not present until over 4 hours from the bite.2
  • Local tissue destruction rarely contributes to long-term morbidity. Occasionally, skin grafting is required to close a defect from fasciotomy, but wounds requiring fasciotomy to reduce compartment pressures from muscle edema are infrequent.
  • Data gathered in a 5-year retrospective chart review from the University of Tennessee Medical Center at Knoxville (UTMCK), a level-I trauma center, focused on 25 bites. Of these, 4 required fasciotomy and 2 subsequently needed split-thickness skin grafting. The average length of stay was 3.2 days. No deaths occurred, and morbidity was limited to the local wounds.


History usually can be obtained from the patient. Most cases result from attempting to handle snakes, so the genus usually is known. Knowledge of indigenous fauna also is important.

The time elapsed since the bite is a necessary component of the history. This allows assessment of the temporal effects of the bite to determine if the process is confined locally or if systemic signs have developed.

  • Obtain a description of the snake or capture it, if possible, to determine its color, pattern, or the existence of a rattle.
  • Most snakes remain within 20 feet after biting.
  • Assess the timing of events and onset of symptoms. Inquire about the time the bite occurred and details about the onset of pain. Early and intense pain implies significant envenomation.
  • Local swelling, pain, and paresthesias may be present.
  • Systemic symptoms include nausea, syncope, and difficulty swallowing or breathing.
  • Determine history of prior exposure to antivenin or snakebite.
  • Determine history of allergies to medicines because antibiotics may be required.
  • Determine history of comorbid conditions (eg, cardiac, pulmonary, and renal disease) or medications (eg, aspirin, anticoagulants such as warfarin (Coumadin) or GPIIb/IIIa inhibitors, beta-blockers).


Follow the established routine for a complete comprehensive examination.

  • Vital signs, airway, breathing, circulation
  • Fang marks or scratches (determine coral snake bite pattern by expressing blood from the suspected wound)
  • Local tissue destruction
  1. Soft pitting edema that generally develops over 6-12 hours but may start within 5 minutes
  2. Bullae
  3. Streaking
  4. Erythema or discoloration
  5. Contusions
  • Systemic toxicity
  1. Hypotension
  2. Petechiae, epistaxis, hemoptysis
  3. Paresthesias and dysthesias - Forewarn neuromuscular blockade and respiratory distress (more common with coral snakes)


* In the United States, more than 40% of victims put themselves in danger by either handling pets or attempting to capture reptiles in the wild. The popularity of keeping exotic species has increased the number of envenomations by nonnative species.
* UTMCK data support this by reporting that 15 of 25 patients were bitten handling snakes; 2 of these were involved in religious ceremonies.

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