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  • Author: Brian J Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Joe Alcock, MD, MS  more...
Updated: Apr 08, 2016


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 snakesa Snakebite. Southern Copperhead snake, from

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 Lampropeltis Snakebite. 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.



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.

Some evidence suggests that the differences between venoms developed through a diet/prey directed evolution occurring over time.[1] 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.




United States

Snakebites frequently go unreported. Approximately 8,000 bites are reported in the United States annually, with approximately 2,000 delivered by venomous snakes. North Carolina has the highest frequency, with 19 bites per 100,000 persons. The national average is approximately 4 bites per 100,000 persons. Mortality from snakebites is rare, with no more than 12 cases of death due to venomous snake bites per year reported between the years of 1960 and 1990.[2]


Generally, only localized reporting of international data is available. Most snakebites and deaths due to snakebites are not reported, especially in the developing world. An estimated 1.8-2.5 million venomous snakebites occur worldwide each year, resulting in an estimated 100,000 to 125,000 annual deaths, but this may be underreported.[3] Worldwide, snakebites disproportionately affect low socioeconomic populations in more rural locations. They are often seen as bites to the lower extremities by farmers or workers who step on or disturb a snake in the field or rice paddies, or they can present as a bite to the head or trunk in individuals sleeping outside on the ground.[4, 5]


White males account for 76% of the victims.


National studies report a 9:1 male-to-female ratio. University of Tennessee Medical Center at Knoxville (UTMCK) studies report a 2.1:1 male-to-female ratio.


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, of which 56% were 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.[6]



Full recovery is the rule, though local complications from envenomation may occur. Death occurs in less than 1 bite in 5000.


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.[7] 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.[8] 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.[9]

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.


Patient Education

For excellent patient education resources, see eMedicineHealth's patient education article Snakebite.

A new web site (Australian Venom Research Unit) based at the University of Melbourne in Australia comprehensively outlines the species, first aid, and treatment of all venomous creatures indigenous to the region. The web site is easily navigated and sectionally divided for the practitioner, interested epidemiologists, snake fanciers, and children of Australia and the Asia/Pacific region.

Contributor Information and Disclosures

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

Disclosure: Nothing to disclose.


Sneha Bhat, MD Resident Physician, Department of Surgery, University of Tennessee Health Science Center College of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Chair of the Clinical Competency Committee, Pulmonary and Critical Care Fellowship Program, Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Health System; Chair, Guideline Oversight Committee, American College of Chest Physicians

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

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Lisa Kirkland, MD, FACP, FCCM, MSHA Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; Vice Chair, Department of Critical Care, ANW Intensivists, Abbott Northwestern Hospital

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

Disclosure: Nothing to disclose.

Chandler Long, MD Resident Physician, Department of Surgery, University of Tennessee Medical Center-Knoxville

Disclosure: Nothing to disclose.

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, Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

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Snakebite. Western diamondback rattlesnake.
Snakebite. Western coral snake.
Snakebite. Southern Copperhead snake, from
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.
Table 1. Snakebite Severity Scale
Criteria Signs/Symptoms Score
  No symptom/sign 0
  Dyspnea, minimal chest tightness, mild or vague discomfort, or respirations of 20-25 breaths/min 1
  Moderate respiratory distress (tachypnea, 26-40 breaths/min, accessory muscle use) 2
  Cyanosis, air hunger, extreme tachypnea, or respiratory insufficiency/failure 3
  No symptom/sign 0
  Tachycardia (100-125 beats/min), palpitations, generalized weakness, benign dysrhythmia, or hypertension 1
  Tachycardia (126-175 beats/min) or hypotension with systolic blood pressure < 100 mm Hg 2
  Extreme tachycardia (>175 beats/min) or hypotension with systolic blood pressure < 100 mm Hg, malignant dysrhythmia, or cardiac arrest 3
Local wound No symptom/sign (swelling or erythema < 2.5 cm of fang mark) 0
  Pain, swelling, or ecchymosis within 5-7.5 cm of bite site 1
  Pain, swelling, or ecchymosis involving less than half of the extremity (7.5 cm from site) 2
  Pain, swelling, or ecchymosis extending beyond affected extremity (>100 cm from site) 3
  No symptom/sign 0
  Pain, tenesmus, or nausea 1
  Vomiting or diarrhea 2
  Repeated vomiting or diarrhea, hematemesis, hematochezia 3
  No symptom/sign 0
  Coagulation parameters slightly abnormal (PTa < 20 seconds, PTTb < 50 seconds, platelets 100,000-150,000/µL, fibrinogen 100-150 mcg/mL) 1
  Coagulation parameters abnormal (PT < 20-50 seconds, PTT < 50-75 seconds, platelets 50,000-100,000/µL, fibrinogen 50-100 mcg/mL) 2
  Coagulation parameters abnormal (PT < 50-100 seconds, PTT < 75-100 seconds, platelets 20,000-50,000/µL, fibrinogen < 50 mcg/mL) 3
  Coagulation parameters markedly abnormal, with serious bleeding or threat of spontaneous bleeding (PT or PTT unmeasurable, platelets < 20,000/µL, fibrinogen undetectable), with severe abnormalities in other laboratory values, including venous clotting time 4
Central nervous system    
  No symptom/sign 0
  Minimal apprehension, headache, weakness, dizziness, chills, or paresthesia 1
  Moderate apprehension, headache, weakness, dizziness, chills, paresthesia, confusion, or fasciculation in area of bite site, ptosis, and dysphagia 2
  Severe confusion, lethargy, seizure, coma, psychosis, or generalized fasciculation 3
  Extremely severe envenomation leading to death 4
a PT = Prothrombin time.

b PTT = Partial thromboplastin time.

Table 2. Severity of Envenomation
Type of Signs/Symptoms Minimal Moderate Severe
Local Swelling, erythema, or ecchymosis confined to bite site Progression of swelling, erythema, or ecchymosis beyond bite site Rapid swelling, erythema, or ecchymosis involving the entire body part
Systemic No systemic signs or symptoms Non–life-threatening signs or symptoms (nausea/vomiting, mild hypotension, perioral paresthesias, myokymia) Markedly severe signs or symptoms (hypotension [systolic < 80 mm Hg], altered sensorium, tachycardia, tachypnea, and respiratory distress)
Coagulation No coagulation abnormalities or other laboratory abnormalities Mild abnormal coagulation profile without significant bleeding Abnormal coagulation profile with bleeding (INRa, aPTTb, fibrinogen, platelet count < 20,000/µL
Snakebite Severity Score 0-3 4-7 8-20
a INR = International normalized ratio.

b aPTT = Activated partial thromboplastin time.

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