Approximately 10,000 poisonous snakebites occur each year in the U.S.
WHO estimates snake bites occur in 5.4 million people worldwide each year, with 2.7 million evenomations resulting in 81,000-130,000 deaths each year.
It is estimated that the number of annual deaths from snake envenomation is similar as for drug resistant tuberculosis and for multiple myeloma.
Snake envenomation occurs in both tropical and temperate climates and on all continents except Antarctica.
About half of all snakebites result in envenomation, which affects many organ system and is potentially life-threatening.
Fewer than 10 victims of snakebites die in the U.S. each year, despite 7000-8000 bite per year.
snakes are predators and mostly subdue their prey with constriction, aggressive biting and chewing or by using venom.
Snakes avoid human contact by hiding or retreating and many species have defense mechanisms such as the rattlesnake’s rattle and the cobras hooding to ward off threats.
Snakebites can occur for several reasons: accidental reaching or stepping, not being aware of the danger, rolling over a snake while sleeping, being unaware of the presence of a snake because of poor hearing or vision, careless handling of a venomous snake, failed attempts to capture or kill a snake, and intentional envenomation.
Approximately 95% of poisonous snakebites in the U.S. are caused by pit vipers comprising multiple species of rattlesnakes, water moccasins and copperheads.
Envenoming can cause neuromuscular paralysis, tissue necrosis, myolysis, cardiotoxicity, acute kidney injury, thrombosis and hypovolemic shock, and hemorrhage and prolonged disruption of hemostasis.
Globally, an estimated 81,000 to 138,000 people a year die from a snakebite, and around 400,000, are left with permanent disabilities.
Bites most commonly involve the extremities.
Unprovoked bites are more likely to involve females and lower extremities.
Provoked bites are more likely to involve male and upper extremities.
Not all bites by venomous snakes involve envenomation, as dry bites occur in 2 to 50% of cases.
The majority of bites in North America are from copperheads, cottonmouths and rattlesnakes.
Approximately 1-2% of U.S. cases involve coral snakes.
Approximately 2-3% inflicted by exotic snakes found in zoos or snake handlers.
Of extreme importance to identify type of snake involved as treatment and prognosis are dependent on this knowledge.
Species more important than the size of the snake.
Bites of pygmy rattlesnake not associated with death.
Envenomations by copperhead snakes and water moccasin result in moderate syndromes with death a rare event.
Eastern, Western diamondbacks and Mojave rattlesnake have higher degrees of toxicity and account for most deaths in the U.S.
Coral snakes has high mortality and severe neurotoxicity.
Coral snake neurotoxicity related to aspiration pneumonia and respiratory arrest.
For coral snakebites respiratory support is indicated until the process reverses at about 1 week.
Coral envenomation is without pain, swelling or discoloration.
80% of envenomations by pit vipers are not accidental and associated with poor judgment and alcohol, while 20% of cases are accidental.
All North American pit vipers have pupils like those of a cat, as opposed to round pupils, and have large fangs that are continually replaced.
Pit viper venom contains a number of proteolytic enzymes that digest protein, fat, connective tissue and nucleic acids.
Pit viper venom contains small peptides which accounts for autonomic symptoms that occur with a bite and include: tachycardia, sweating, diarrhea and vomiting
Pit viper venom has significant variability over time and among various species resulting in variation of symptoms and prognosis after envenomation because of various species of pit vipers.
The Eastern diamondback rattlesnake venom contains a thrombin like enzyme that partially cleaves fibrinogen and results in the production of fibrin degradation products, with moderate thrombocytopenia.
The Western diamondback rattlesnake venom activates plasminogen to plasmin with hyperfibrinolysis.
Bites of Eastern and Western diamondback rattlesnakes result in alterations in the prothrombin time and the partial thromboplastin time, but are associated with little bleeding.
Eastern or Western diamondback rattlesnake envenomation results in minimal serum creatine kinase elevation.
Canebrake rattlesnake envenomation results in my necrosis with marked elevation of CK and CK-MB without elevations in cardiac enzymes.
Mojave rattlesnake bites associated with my necrosis , neurological symptoms, but minimal coagulation abnormalities.
Timber rattlesnake bites associated with thrombocytopenia , refractory to platelet transfusions.
20% of pit viper bites are not associated with envenomation and the administration of antivenin is not indicated: dry bites indicated by absence of pain, swelling, or discoloration of the wound by 1-2 hours after the bite.
snake venom contains an array of toxins with clinical effects that can be local or systemic, and range from mild to fatal.
Local effects of venomous snake bites include swelling within two hours of the bite, blistering in 2-12 hours, and tissue necrosis with in a day.
Local tissue injury and inflammation are caused by enzymes search is hyaluronidase and collagenase as well as proteinases and phopholipases.
Local tissue injury results in pain and swelling.
Swelling can spread from the site of the bite and lead to bullae and dermal necrosis.
Local ecchymoses may result from coagulopathy and vascular permeability.
Snake venom metalloproteinases cause release of extracellular matrix derived peptides that have tissue effects causing additional tissue destruction, hemorrhage, skeletal muscle necrosis and lack of muscle restoration, blistering, dermal necrosis as well as inflammatory mediators accounting for pain, swelling and leukocyte infiltration.
The effects of venom can mimic the signs and symptoms of a true compartment syndrome.
Lymphangitis in local lymph node enlargement may occur.
Snake evenomination can injure lymphatic system with the development of edema.
Local signs with systemic coagulopathies and shock or sometimes indistinguishable from the effects of infection.
Procoagulant toxins in snake venom skin promote a consumption coagulopathy may result in spontaneous or uncontrolled bleeding.
Venom of different snakes vary in their affect on clotting factors.
A thrombotic microangiopathy me a company a venom induced consumption coagulopathy.
Sneak envenomation can result in myocardial infarction, stroke, other thrombotic effects.
In severe cases of envenomation thrombocytopenia can occur.
Neuromuscular paralysis due to envenomation can occur with a variety of snake families.
Neurotoxic snake venoms contain toxins that block post synaptic neurons, and presynaptic neurotoxins exist as well.
Neurotoxins can manifest as flaccid paralysis or life-threatening respiratory insufficiency.
Myotoxicity can result from the direct effect of venom on muscle disrupting integrity of the plasma membrane and provoking calcium influx.
Muscle damage can include the myocardium and skeletal muscle involvement with rhabdomyolysis, and respiratory compromise.
Hypotension may be a complication.
Other effects of venom can include nausea, vomiting, diarrhea, and diaphoresis.
Snakebites can result in acute kidney injury, which may progress to chronic kidney disease or renal failure related to snake venoms.
Nephrotoxicity can be result of the venom or can be a result of microangiopathy or from rhabdomyolysis, altered clearance of blood degradation products, immune complexes or from shock.
Supportive therapy with intravenous access and saline or crystalloid fluids to maintain volume and blood pressure are instituted.
It is necessary to estimate the severity of the bit to determine need and extent of antivenin treatment.
Determining the rate of change in signs and symptoms is required to establish the severity of the bite.
Efficacy of the antivenin treatment is a function of the time between bite and institution of the treatment.
Treatment with antivenin should be done as early as possible since the treatment cannot undo already existing damage.
Administration of the antivenin after 24 hours will not be helpful.
Dry bites require no treatment.
Prophylactic anabiotics are not beneficial, and are unnecessary following a rattlesnake bite.
Treatment of a snakebite may require: wound care and reconstructive surgery, cardio respiratory resuscitation, airway intubation, mechanical ventilation, and rehabilitation services.
Immunotherapy with anti-venom preparations can neutralize venom components but it does not reverse the physiological damage already caused.
Snake venom does not cross intact skin or mucous membranes.
Snake venom does not cross intact skin or mucous membranes.
The amount of venom injected varies and the degree of toxicity of a venom is related to its specific components which are a function of the genetic and epigenetic factors of the snake.
Envenomation syndromes vary among different species within a geographic region, and identification of a specific snake on the basis of envenomation effects may not be possible.
Prehospital assessment and management include identifying the snake, if possible, splinting the bitten body part with the heart neutral positioning, and anticipate swelling, and obtain transport to a healthcare facility.
Impairing lymphatic flow may slow the systemic effects of the venom, as the majority of venom enters the circulation through lymphatics: A compressive bandage, or blood pressure cuff please proximal to the bite should be applied.
Other interventions such as the use of arterial and venous tourniquet, incision, suction, heat, cold, electricity may delay access to definitive treatment and may result in additional trauma.