Snakebite 

  • Author: Brian James Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Apr 14, 2010
 

Background

Most snakebites are innocuous and are delivered by nonpoisonous species. North America is home to 25 species of poisonous snakes. 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 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). A Southern copperhead is shown in the image below.

Snakebite. Southern Copperhead snake, from snakesaSnakebite. Southern Copperhead snake, from snakesandfrogs.com

The Western diamondback (shown in the image below), timber, and prairie rattlesnakes are pit vipers.

Snakebite. Western diamondback rattlesnake. Snakebite. Western diamondback rattlesnake.

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; this is shown in the image below).

Snakebite. Western coral snake. Snakebite. Western coral snake.

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 mnemonic to recall the order of bands is "red on yellow, kill a fellow; red on black, venom lack." These snakes are shown in the image below.

Snakebite. Comparison of the harmless LampropeltisSnakebite. Comparison of the harmless Lampropeltis triangulum annulata (Mexican milksnake) (top) with Micrurus tener (Texas coral snake) (bottom). Photo by Charles Alfaro.

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 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 nonindigenous species increasingly common.

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Pathophysiology

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 perceived by the snake, and size of the prey. 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 a smaller mouth. 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 a small wound that later results in respiratory failure from systemic neuromuscular blockade.

The local effects of venom serve as a reminder of the potential for systemic disruption of organ system function. One effect is local bleeding; coagulopathy is not uncommon with severe envenomation. 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.

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Epidemiology

Frequency

United States

Snakebites frequently go unreported. Approximately 4000-7000 bites are reported to national centers each year. North Carolina has the highest frequency, with 19 bites per 100,000 persons. The national average is approximately 4 bites per 100,000 persons.

International

Generally, only localized reporting of international data are available. Most snakebites and deaths due to snakebites are not reported, especially in the developing world.

Mortality/Morbidity

A 20-year review of data from the National Vital Statistics Systems identified 97 fatalities. The state of Texas had the most fatalities (17), followed by Florida (14), and Georgia (12).

  • Deaths secondary to snakebites are rare.[1] 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.[2] A review specifically of copperhead bites in West Virginia described similar outcomes and noted that the peak effects of envenomation were not present until longer than 4 hours after the bite.[3]
  • 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.

Race

White males account for 76% of the victims.

Sex

  • National studies report a 9:1 male-to-female ratio.
  • UTMCK studies report a 2.1:1 male-to-female ratio.

Age

  • National studies report 50% of patients were aged 18-28 years. UTMCK studies report 25% were aged 18-28 years, with a mean of 29.5 years.
  • National studies report 95% of bites were located on an extremity, especially the hand. UTMCK studies report 96% of bites were located on an extremity, 56% to the hand.
  • National studies report a seasonal occurrence of 90% from April to October. UTMCK studies report 100% occurrence from April to October (May: 1 bite out of 25 cases; June to August: 19 bites out of 25 cases; and September to October: 5 bites out of 25 cases).
  • In the pediatric population, most snakebites occurred in school-aged children and adolescents around the perimeter of the home during the afternoon in summer months. The most frequent wound sites were the lower limbs.[4]
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Contributor Information and Disclosures
Author

Brian James Daley, MD, MBA, FACS, FCCP, CNSC  Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine

Brian James Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Eastern Association for the Surgery of Trauma, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

A Mariah Alexander, MD  Resident Physician, Department of Surgery, University of Tennessee Graduate School of Medicine, Knoxville

A Mariah Alexander, MD is a member of the following medical societies: American College of Surgeons and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Lisa Kirkland, MD, FACP, CNSP, MSHA  Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Daniel R Ouellette, MD, FCCP  Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

References
  1. Weinstein S, Dart R, Staples A, White J. Envenomations: an overview of clinical toxinology for the primary care physician. Am Fam Physician. Oct 15 2009;80(8):793-802. [Medline].

  2. Spiller HA, Bosse GM. Prospective study of morbidity associated with snakebite envenomation. J Toxicol Clin Toxicol. 2003;41(2):125-30. [Medline].

  3. Scharman EJ, Noffsinger VD. Copperhead snakebites: clinical severity of local effects. Ann Emerg Med. Jul 2001;38(1):55-61. [Medline].

  4. Sotelo N. Review of treatment and complications in 79 children with rattlesnake bite. Clin Pediatr (Phila). Jun 2008;47(5):483-9. [Medline].

  5. Corneille MG, Larson S, Stewart RM, et al. A large single-center experience with treatment of patients with crotalid envenomations: outcomes with and evolution of antivenin therapy. Am J Surg. Dec 2006;192(6):848-52. [Medline].

  6. Dart RC, Seifert SA, Boyer LV, et al. A randomized multicenter trial of crotalinae polyvalent immune Fab (ovine) antivenom for the treatment for crotaline snakebite in the United States. Arch Intern Med. Sep 10 2001;161(16):2030-6. [Medline].

  7. Lavonas EJ, Gerardo CJ, O'Malley G, et al. Initial experience with Crotalidae polyvalent immune Fab (ovine) antivenom in the treatment of copperhead snakebite. Ann Emerg Med. Feb 2004;43(2):200-6. [Medline].

  8. Vohra R, Cantrell FL, Williams SR. Fasciculations after rattlesnake envenomations: a retrospective statewide poison control system study. Clin Toxicol (Phila). Feb 2008;46(2):117-21. [Medline].

  9. Richardson WH, Goto CS, Gutglass DJ, Williams SR, Clark RF. Rattlesnake envenomation with neurotoxicity refractory to treatment with crotaline Fab antivenom. Clin Toxicol (Phila). Jun-Aug 2007;45(5):472-5. [Medline].

  10. Cannon R, Ruha AM, Kashani J. Acute hypersensitivity reactions associated with administration of crotalidae polyvalent immune Fab antivenom. Ann Emerg Med. Apr 2008;51(4):407-11. [Medline].

  11. Cowles RA, Colletti LM. Presentation and treatment of venomous snakebites at a northern academic medical center. Am Surg. May 2003;69(5):445-9. [Medline].

  12. Holstege CP, Singletary EM. Images in emergency medicine. Skin damage following application of suction device for snakebite. Ann Emerg Med. Jul 2006;48(1):105, 113. [Medline].

  13. Hunsaker DM, Hunsaker JC 3rd, Clayton T, Spiller HA. Lethal envenomation: medicolegal aspects of snakebites and religious snake handlers in Kentucky: a report of three cases with comment on medical, legal, and public policy ramifications. J Ky Med Assoc. Nov 2005;103(11):542-56. [Medline].

  14. Jordan GH, Deitch EA, Britt LD. Management of Poisonous Snakebites. American College of Surgeons: Consensus statement. 1997.

  15. Kravitz J, Gerardo CJ. Copperhead snakebite treated with crotalidae polyvalent immune fab (ovine) antivenom in third trimester pregnancy. Clin Toxicol (Phila). 2006;44(3):353-4. [Medline].

  16. Kularatne SA, Kumarasiri PV, Pushpakumara SK, et al. Routine antibiotic therapy in the management of the local inflammatory swelling in venomous snakebites: results of a placebo-controlled study. Ceylon Med J. Dec 2005;50(4):151-5. [Medline].

  17. Lavonas EJ, Gerardo CJ, O'Malley G, et al. Initial experience with Crotalidae polyvalent immune Fab (ovine) antivenom in the treatment of copperhead snakebite. Ann Emerg Med. Feb 2004;43(2):200-6. [Medline].

  18. Schmidt JM. Antivenom therapy for snakebites in children: is there evidence?. Curr Opin Pediatr. Apr 2005;17(2):234-8. [Medline].

  19. Shires TG, Thal ER, Jones RC. Trauma. Principles of Surgery. 1994;6:183-5.

  20. Stewart RM, Page CP. Wounds, Bites, and Stings. Trauma. 1996;3:929-34.

  21. Sullivan JB, Wingert WA, Norris Jr RL. North American Venomous Reptile Bites. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 1995;3:680-709.

  22. Whitley RE. Conservative treatment of copperhead snakebites without antivenin. J Trauma. Aug 1996;41(2):219-21. [Medline].

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Snakebite. Western diamondback rattlesnake.
Snakebite. Western coral snake.
Snakebite. Southern Copperhead snake, from snakesandfrogs.com
Snakebite. Copperhead bite day 3; initial wounds to finger.
Snakebite. Copperhead bite day 3; initial wounds to finger.
Snakebite. Copperhead bite day 3; initial wounds to finger.
Snakebite. Comparison of the harmless Lampropeltis triangulum annulata (Mexican milksnake) (top) with Micrurus tener (Texas coral snake) (bottom). Photo by Charles Alfaro.
Snakebite. Juvenile southern Pacific rattlesnake (Crotalus oreganus helleri). Photo by Sean Bush, MD.
Snakebite. Moderate rattlesnake envenomation in a toddler after treatment with antivenom. Photo by Sean Bush, MD.
 
 
 
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