Glossary Terms
Coagulopathy: A defect in the blood-clotting mechanism. After a crotalid envenomation, this disorder is often recognized by an elevated prothrombin time (PT) and/or a decreased fibrinogen concentration on blood laboratory analysis.
Disseminated intravascular coagulation (DIC):”ž A pathologic condition in which clotting occurs unchecked and clotting factors are consumed. The clotting within organs leads to multisystem organ failure; once clotting factors are consumed, patients may bleed uncontrollably.Fasciotomy:surgical procedure to cut the fascia surrounding muscle compartments in order to relieve pressure within the compartment. The increased pressure typically results from bleeding or swelling within the compartment.
Myoglobinuria:”ž A pathologic condition in which myoglobin (a muscle protein) is found in the urine.Ptosis:Drooping of the upper eyelid due to paralysis or weakness.
Rhabdomyolysis:”ž The breakdown of muscle fibers leading to the release of myoglobin in the blood and eventually in the urine. This can lead to renal damage.
Thrombocytopenia:”ž An abnormal decrease in the number of circulating platelets in the blood (<150,000/mm3).
Venom Components
Anticoagulants:”ž Prevents blood coagulation (largely the result of fibrinogen and fibrin destruction).
Cardiotoxins: Responsible for hypotension and decreased cardiac output.
Fibrinolysins: Responsible for the inappropriate breakdown of fibrinogen and fibrin, which results in a coagulopathy.
Hemorrhagins: Responsible for bleeding, resulting in ecchymosis, hemorrhagic bleb formation and swelling.
Hemotoxins: Responsible for low platelet counts, low fibrinogen levels and bleeding. This component includes the anticoagulants, fibrinolysins and hemorrhagins.
Neurotoxins: Responsible for cranial nerve deficits, muscle weakness and paralysis, and muscle fasciculations.
While hiking with friends, a 20-year-old man encounters a rattlesnake. Curious, he attempts to touch the reptile and is bitten on the right index finger. The man and his friends hike two hours back to their car before they can call for help.
On EMS arrival, the crew finds the patient in acute pain but without respiratory complaints. Vital signs include BP 100/p and pulse 110 bpm. An IV is quickly established, and after a liter of normal saline, the patient’s blood pressure improves to 110/p.
A quick assessment of his right upper extremity reveals extensive swelling in his entire hand and forearm. The swelling appears most impressive when compared with his unaffected left hand. A 1_1 cm hemorrhagic bleb on his index finger is noted, and only one puncture wound is located immediately adjacent to the bleb.
The puncture wound shows minimal blood oozing, and his entire index finger is ecchymotic. Any palpation of his right arm creates severe pain. The patient is also noted to be tender in his right axilla, despite no swelling in that area. All his digits are warm and pink with normal capillary refill. The crew places sterile gauze over the bleeding wound, and the patient’s right arm is immobilized in complete extension and hung from an IV pole in order to maximally elevate the hand.
En route, the patient receives another liter of normal saline and several doses of morphine for pain. After serial exams, providers note the bleb is unchanged and the swelling has progressed to his axilla, but the swelling in his hand appears decreased. His fingers maintain good perfusion.
On hospital arrival, the patient has extensive swelling from his hand to his axilla, with ecchymosis extending from his index finger to his forearm. The bleb now covers a large portion of the dorsal aspect of his finger. Laboratory results demonstrate a platelet count of 20,000/mm3 (NL = 350,000à150,000/mm3) and a prothrombin time of > 90 seconds (NL = 9à11 seconds). However, the patient has no signs of active bleeding.
After several more liters of IV fluids and multiple doses of morphine, the patient’s BP is 125/75 and pulse is 85 bpm. In the meantime, CroFab antivenin is mixed and administered. His laboratory results improve with antivenin therapy, and his swelling and hemorrhagic bleb stabilize.
Epidemiology
In the United States, approximately 6,000 snake envenomations occur each year, and even more bites occur from non-venomous snakes. Distinguishing venomous from non-venomous encounters can be extremely difficult and requires astute clinical skills by the prehospital provider.
About 99% of the venomous snakebites occur as the result of crotalinae, or pit vipers. The”žcrotalinae include rattlesnakes (Crotalus spp), copperheads, water moccasins/cottonmouths (Agkistrodon spp), and the massasauga (Sistrurus spp). The remaining 1% occur as the result of the coral snake (Micruroides spp and Micrurus spp).
Because snakes hibernate in the winter, the majority of envenomations occur during the summer months, although a few occur during the winter months in southern states. The most commonly envenomated demographic is men intentionally handling snakes, and alcohol is frequently involved. This demographic can pose a treatment problem if extremely inebriated. Not surprisingly, the upper extremity is the most common location for bites, followed by the lower extremity. On rare occasion, facial or tongue bites have occurred from handlers attempting to kiss a snake.
Mortality rates from snake envenomations in the U.S. are considered low (< 1%), but the morbidity, particularly from crotalids, can be severe. It would not be uncommon to have significant tissue necrosis with the loss of fingers or toes.
Although beyond the scope of this article, providers should also be aware that a significant number of exotic snakes are purchased and owned illegally in the U.S. and may be associated with different types of envenomations and treatments.
Venomous snake identification”ž”ž
Crotalids are well-adapted snakes found throughout the U.S. in a wide range of environments except in Maine, Alaska and Hawaii. Among the crotalid subfamily, rattlesnakes have the most distinctive feature due to their boisterous rattle. Only copperheads and water moccasins/cottonmouths (Agkistrodon spp) don’t possess a rattle. However, the rattle doesn’t typically offer enough warning to prevent the accidental close encounter. Snakes have poor eyesight and are easily startled from close proximity. Most accidental rattlesnake envenomation victims never hear a rattle before the strike.
Although they don’t all have rattles, all crotalinae have similar head features (see Figure 1). The crotalid head is triangle-shaped with elliptical pupils, heat-sensing pits just anterior to their eyes, and very long fangs (as long as 3à4 cm). Additionally, copperheads have gold-brown coloration to their head, and cottonmouths have a white mouth.
Coral snakes are brightly colored with characteristic yellow, black and red stripes (see photo). The coral snake, unfortunately, is easily confused with the non-venomous king snake due to their similar coloration. What distinguishes the coral from the king snake is the color sequence. A common rhyme to remember the pattern is “red on yellow kills a fellow; red on black, venom lack.” Also, the coral snake has a black snout, whereas the king snake has a red one.
Coral snakes have a much more limited geographic range than the crotalid. The Sonoran coral snake (Micruroides euryxanthus) is found largely in Arizona, the Texas coral snake (Micrurus fulvius tenere) is found in Texas and the Gulf states, and the Eastern coral snake (Micrurus fulvius fulvius) is found in coastal states from Louisiana to North Carolina.
It’s often impossible to characterize an envenomation without confirming the snake’s identity. However, prehospital personnel are never recommended to capture a potentially venomous snake. Safety of the care provider is always paramount. Unsuspecting care providers have been envenomated by decapitated snakes that were thought to be considered safely “dead.” Never assume a dead snake is a safe snake.
Pathophysiology
Snake venom is often referred to as a “mosaic of antigens.” It’s a mixture of various proteins, peptides, lipids, carbohydrates and enzymes Æ’ many of which aren’t clearly identified. Extensive variability occurs in venoms between and within species. The age, health, diet and geographic range can affect the potency and clinical differences seen from snake envenomations within the same species.
Crotalid envenomations: In general, approximately 20% of crotalid bites are “dry,” which means no venom is injected.6 However, a single snake can have enough venom to strike up to four consecutive times with significant envenomations on each strike.
The hallmark and most obvious prehospital finding of crotalid envenomations are localized tissue damage and swelling (see photos). Within minutes of the bite, the patient can experience significant swelling and pain. Within minutes to hours, ecchymosis, hemorrhagic blebs and tissue necrosis can develop. The skin and muscle necrosis can be extensive and result in”žrhabdomyolysis and the loss of fingers and toes. Counting the number of fang marks or attempting to find and measure fang marks offer only a distraction and shouldn’t be of concern. Because crotalid fangs are hinged, wider than expected puncture wounds have been characterized.
The crotalid envenomation is a dynamic process that can progress rapidly, appear to stop, and then continue to progress. The full extent of the envenomation may not be known for hours or days. If no swelling, tissue damage, lymph node tenderness or laboratory abnormality occur within 12 hours of a bite, then a “dry” bite can be assumed.
Crotalids usually deposit their venom into the subcutaneous space. The venom then disseminates via lymphatics and venous channels. Tender lymph nodes proximal to the bite site are a telltale sign of envenomation. After the venom is deposited and tissue damage occurs, the venom slowly diffuses into systemic circulation. For this reason, systemic findings tend to follow the localized tissue damage.
However, there is much variability in the onset of systemic signs. On rare occasion, the venom is injected intravascularly. Because the venom is then quickly distributed away from the bite site, it typically results in profound systemic symptoms without the localized tissue swelling and necrosis. Particularly for intravascular injections, systemic findings can occur almost immediately with or without the localized tissue swelling. Fatalities are more likely to occur as the result of intravascular envenomations due to the rapidity and severity of systemic signs.
Systemic effects from crotalinae are varied. Signs and symptoms include nausea and vomiting, diarrhea, abdominal cramping, generalized weakness, hypotension, tachycardia, headache, strange metallic taste, sweating and confusion. It can be difficult to distinguish true venom effects from the fear and anxiety of the snake encounter or the pain from the localized tissue damage. Regardless, treatment remains the same.
Renal failure can also occur as a systemic effect but is most often the result of”žmyoglobinuria from rhabdomyolysis. Lastly,”ždisseminated intravascular coagulation (DIC) occurs rarely, but it has been reported and is extremely life-threatening with the possibility of severe end-organ damage if prompt and aggressive treatment isn’t initiated.
Among the crotalinae, the Mojave rattle snake (Crotalus scutulatus) has a unique toxicity due to its neurotoxins. This rattlesnake is largely found in the desert southwest from Texas across New Mexico, Arizona and California. The neurotoxin found in the Mojave rattlesnake can cause generalized weakness, cranial nerve dysfunction (e.g., eyelid”žptosis), and respiratory depression. The Mojave snakes that cause neurotoxicity usually lack the ability to cause localized tissue damage.
The timber rattler (Crotalus horridus horridus) has unique neurologic effects as well.This snake is found from the East Coast to the Midwest and Gulf states. The timber rattler can cause”žmyokymia, a wave-like motion of muscle fibers. It’s often confused with fasciculations, which look similar, but it has distinctive myography different from fasciculations.
Coagulopathy and”žthrombocytopenia are common findings from crotalid envenomations. Within hours of the bite, platelet counts fall due to platelet aggregate inducers and inhibitors. Independently, a coagulopathy develops from a complex mixture of anticoagulants, fibrinolysins and hemorrhagins. The coagulopathy results in a low serum fibrinogen and elevated prothrombin time (PT) on laboratory analysis. These findings are often confused with DIC. Interestingly, the coagulopathy and thrombocytopenia rarely result in significant bleeding problems. For prehospital personnel, bleeding will not likely be an issue unless trauma is involved. Commonly, patients have bleeding from the bite site, but it rarely amounts to significant blood loss.
Rarely, anaphylaxis can occur from crotalid venom. This most typically results from prior exposure to crotalid snakes, including eating crotalid meat. Also, snake handlers can unknowingly inhale or make skin contact with small amounts of aerosolized snake venom and develop sensitization. Anaphylaxis from crotalid envenomation is no different than other anaphylactic reactions. Patients can suffer life-threatening anaphylaxis Æ’ including hives, itching and wheezing Æ’ without any signs typical of crotalid envenomation. Symptoms quickly respond to standard treatment (e.g., antihistamines, steroids and epinephrine).
Elapid envenomations: Unlike the crotalinae, coral snakes tend to lack the impressive outward signs of envenomation. Coral snakes manifest their toxicity via neurotoxins, much like that of the Mojave rattlesnake. As much as 60% of these snakebites are “dry” due to the much smaller fixed fangs and poor venom delivery apparatus.
Clinical signs of these envenomations can be delayed for more than 12 hours, so the lack of signs or symptoms shouldn’t preclude rapid assessment and treatment. The characteristics of coral snake envenomation make prehospital evaluation much more difficult, and bites from these snakes shouldn’t be taken lightly. Envenomation from the Sonoran coral snake is much less severe than envenomations from the Texas and eastern coral snakes.
Although typically delayed, the systemic effects of coral snake envenomation can occur suddenly. Generally, these snakes cause muscle weakness from their curare-like effects. The most severe sign is respiratory depression from neuromuscular weakness. Even without antivenin, the clinical effects of coral snake envenomation will resolve without consequence over several days with adequate respiratory support (e.g., intubation with mechanical ventilation). Other signs and symptoms from coral snake envenomations include paresthesias (35%), vomiting (25%), dizziness (10%), dyspnea (10%), diaphoresis (10%), fasciculations (5%), confusion (5%) and other symptoms.
Assessment & treatment
As with other biological/environmental exposures, scene safety is the first priority. Patients and prehospital providers often feel the need to capture the snake in order to identify it and make appropriate treatment suggestions based on the snake’s specific identification. In North America, however, only the two families of snakes discussed in this article have shown potential for significant toxicity, and crotalinae are by far the more common of the two.
Additionally, the clinical manifestations make the treatment plan obvious despite having no snake to identify. Prehospital providers should never place themselves at risk and should be certain to move the patient to a safe location prior to treatment initiation.
Crotalinae: Once scene safety has been addressed, the standard evaluation of the ABCs should ensue. Although rare, airway compromise and cardiovascular collapse can occur. Airway emergencies can result from anaphylaxis, neurotoxicity (from the Mojave rattlesnake), or direct face and neck bites.
As mentioned earlier, anaphylactic reactions from crotalids are treated as any other anaphylaxis. Antihistamines and steroids are used for minor symptoms, and epinephrine is reserved for signs of airway distress and wheezing. Antivenin has no place in the treatment of anaphylaxis.
In the most severe Mojave rattlesnake envenomations, its neurotoxic venom can cause muscle weakness and respiratory distress. Patients have required intubation from Mojave envenomation. Other than airway support with assisted ventilations, no specific field treatment is effective in terms of correcting respiratory muscle weakness. Once the airway has been cleared and oxygen administered, assisted ventilation or intubation may be necessary.
Direct face, tongue and neck bites are imminent airway emergencies. The airway will need to be addressed early in these cases. The swelling is so profound from crotalid envenomations that prophylactic oral (for those who have drugs available for rapid sequence induction) or nasotracheal intubation should be attempted before swelling progresses. In these cases, the airway management performed by prehospital personnel will be critical.
All crotalid snakebite victims should receive IV access. Hypotension most commonly results from IV fluid loss into the swollen extremity. It’s not uncommon to have several liters of intravascular volume loss in a swollen extremity after a crotalid envenomation. Hypotension in these cases will typically respond with IV fluids, although multiple boluses may be required.
Less commonly, hypotension is the direct result of the venom. Indications that the venom is the source of hypotension are the lack of swelling and hypotension unresponsive to fluid administration. When 2à3 L of crystalloid (or 40à60 mL/Kg in a child) fail to improve hemodynamics, dopamine or epinephrine infusions should be started during hospital transport. Cases of hypotension not responsive to IV fluids and vasopressors will often respond within minutes of antivenin initiation, which makes rapid hospital transport imperative.
Routine use of IV fluids is good practice for crotalid envenomations even in the absence of hypotension. Fluid administration is also good treatment of venom-induced rhabdomyolysis and renal failure. Plus, the IV offers a means to administer pain medications.
The majority of treatment is focused on the localized tissue destruction. The patient is much more likely to lose a finger, toe or limb than lose their life due to crotalid envenomations. Thus, treatment should focus on reducing tissue damage. No first aid treatment has been shown to improve outcome for crotalid envenomation, but certain treatments should be avoided in order to prevent further tissue damage. Rapid assessment and transport to the hospital for antivenin initiation is the best way to reduce morbidity. Because patients often require wilderness extraction prior to transport, prehospital providers familiar with snakebite care are crucial during potential delays to definitive care.
Once the ABCs are addressed, the most important prehospital treatment should focus on wound care and swelling. Any bleeding or open wounds should be dressed with sterile gauze. Careful assessment for extremity blood flow becomes an important triage factor. Monitoring for decreased perfusion should be closely watched with serial exams. Any signs of decreased capillary refill or cyanotic digits should increase your suspicion for compartment syndrome.
Direct measurement of pulses is often difficult due to the severity of the swelling. The severe swelling and pain associated with crotalid envenomations leads the novice observer to believe that compartment syndrome is imminent. However, patients rarely require a”žfasciotomy to relieve compartment pressures and fasciotomies actually worsened tissue damage in a porcine model.
After the initial assessment, the affected limb should be immobilized to prevent rapid systemic venom absorption from increased physical activity. Animal studies have shown that immobilizing a limb improves survival. This may be unrealistic for a leg bite that requires the patient to ambulate to help, rather than be carried. Most crotalid envenomations do well if medical treatment is sought within several hours of the bite, so immobilization should not delay hospital transport.
The bitten extremity should be immobilized in full extension and elevated above the heart. As opposed to splinting a broken bone in the position of comfort, immobilizing in full extension is preferred to prevent the pooling of venom in the antecubital or popliteal fossae with subsequent necrosis developing in those areas. Elevating the extremity helps reduce swelling in the dependant portion, increase perfusion distally and reduce pain.
Often, generous analgesics may be required throughout assessment. Administration of pain medication should be based on local protocols and as directed by online medical control. Appropriate starting doses include 2 mg of IV morphine and titrating to effect. Providers may have access to patient-administered nitrous oxide. Regardless of pain treatment plans, patients may require generous doses for adequate pain control. The severity of swelling is largely responsible for the amount of pain and can be used as a guide for pain treatment.
In the past, pressure immobilization or tourniquets were advocated to reduce systemic absorption of the venom. Pressure immobilization is a technique advocated for use in Australian snakebites. In this technique, an elastic bandage is applied over the bite site and wrapped proximally. Once applied, lymphatics are compressed and systemic venom distribution is retarded while blood flow remains uninhibited. This technique has been shown to increase survival time from crotalid venom in a pig model. However, pigs frequently die from crotalid envenomation while humans do not.
This model, therefore, is not evidence in favor of pressure immobilization for crotalid bites. This study merely demonstrates the fact that systemic venom absorption is inhibited with pressure immobilization. Tourniquets, on the other hand, are tightened to the point of completely obstructing blood flow. Tourniquet use was considered standard prehospital practice in the 1950s. Unfortunately, pressure immobilization and tourniquets merely confine the venom to the area of the bite and lead to greater tissue necrosis and swelling. Thus, the use of pressure immobilization and tourniquets should not be generalized for use in North American snake envenomations.
Incision and suction are not recommended either. Incisions can lead to more tissue damage and the opportunity to sever blood vessels, nerves and tendons. Mouth suction is of no yield and has the potential only to introduce mouth bacteria into a sterile wound. Crotalid snake venom is sterile, and their bites rarely get infected when mouth suction isn’t performed. Commercially available suction devices with suction cups and plungers are also available, but they haven’t been shown to improve outcome or remove substantial amounts of venom. Typically, attempting to use these commercial suction devices leads to a delay in appropriate care of the patient.
Other treatments that seem far-fetched are still part of our cultural mindset. Electric-shock treatment resurfaced as a treatment in the mid-1980s due to a letter published in”žThe Lancet. Plus, lore surrounds the use of this therapy among snake handlers. The technique usually involves attaching cables to a car battery in order to neutralize the venom via electric shocks. The poorly performed research published by Guderian in”žThe Lancet”ž was never reproduced in well-controlled experiments performed later. The risks associated with this treatment are well documented.
Other therapies, such as cryotherapy, and ice and heat application, offer theoretical benefits but aren’t advocated. Cryotherapy is aggressive wound cooling via carbon dioxide fire extinguishers, dry ice or air-conditioning coolants. Cooling techniques would theoretically decrease venom activity and subsequent tissue damage, whereas heat application would increase blood flow to the wound, disseminate the venom and decrease localized tissue destruction. However, no benefit has been found with these techniques in animal models. Instead, the author has seen thermal injury from use of these techniques, which complicates the existing damage. Severe pain from the snakebite will mask any further pain and tissue damage done by thermal injury inflicted by the care provider.
Except for fang marks and minimal local swelling directly from the crotalid bite, no progressive swelling or lymph tenderness proximal to the bite site will likely be noted in a dry bite. In addition, laboratory results, such as platelet counts, fibrinogen level and prothrombin time, would remain normal. Because evaluation of thrombocytopenia and coagulopathy are not easily assessed in the field, all patients are encouraged to undergo hospital evaluation. Coagulopathy and thrombocytopenia can last for weeks, and patients need to know if they’re at increased risk for internal bleeding with close hospital follow-up until their laboratory results return to normal. Even without outward signs of envenomation, patients can develop severe thrombocytopenia and coagulopathy.
The effects of crotalid venom typically are delayed no longer than 12 hours. Hand, foot and upper extremity bites tend to develop signs of envenomation earlier than leg bites. The author has seen cases of severe envenomation delayed many hours after a leg bite when initial physical and laboratory findings were unremarkable. Short hospital admissions are standard for all leg bites regardless of presenting signs so there will be no delay in administering antivenin therapy should delayed signs develop. This becomes important for the prehospital provider to always recommend hospital transport for crotalid bites, even if the patient “feels fine.”
Definitive treatment for crotalid envenomation is antivenin. Prehospital providers should know which hospitals regularly stock antivenin. Regional variations in hospital pharmacy practices make generalizations difficult to make. When in doubt about local hospital antivenin supplies, diversion to a tertiary care trauma center would be most appropriate to ensure timely access to antivenin.
Antivenin can reverse systemic signs and symptoms, as well as coagulopathy and thrombocytopenia, but it cannot reverse the swelling and tissue necrosis. It can, however, halt the progression of tissue necrosis. This is why hospital transport is of utmost importance. In addition to the wound care items discussed above, the best way to limit tissue necrosis is to administer antivenin as soon as possible. Moreover, other systemic signs, such as vomiting and hypotension, may be difficult to manage in the prehospital setting with standard antiemetics, IV fluids and vasopressors, but usually resolve shortly after antivenin initiation.
Indications of antivenin therapy are vague, but include progressive swelling, profound coagulopathy or thrombocytopenia, neuromuscular toxicity and hemodynamic compromise. Two antivenins are available for crotalid envenomations Æ’ Antivenin Crotalidae Polyvalent (ACP) from Wyeth Laboratories and CroFab from Protherics Inc. Both products are antibody-derived in order to bind and neutralize circulating venom, but neither are perfect therapies. Complications include immediate and delayed allergic reactions in ACP and “recurrence” of venom effects due to the shorter duration of action for CroFab. CroFab is more specifically formulated to treat North American crotalinae, as opposed to crotalids found elsewhere, and can be given again if the patient happens to get bitten on another encounter.
Some patients are followed for weeks with recurrent blood draws until coagulation studies and platelet counts return to normal. Typically, retreatment with antivenin is reserved only for severely abnormal laboratory findings or signs of bleeding. Much debate persists about what to do with “recurrence.”
Elapidae:”ž Coral snake envenomations lack the tissue destruction seen with the crotalinae. However, the relatively benign outward clinical findings should not preclude aggressive prehospital management. Any patient with skin penetration and a known coral snake encounter should empirically receive antivenin therapy even before the onset of symptoms. Because recovery can be lengthy if antivenin is delayed, even suspected but unidentified coral snake encounters will require a minimum of 24 hours of hospitalization for observation.
As mentioned, coral snake envenomation treatment focuses on the ABCs. Because the neurotoxicity of coral snake envenomations can happen unexpectedly and progress rapidly, all patients should receive IV access in anticipation of such deterioration.6 The worst-case scenario would result in respiratory depression from muscle weakness. Because IV access has already been obtained, concentration can focus on managing the airway and breathing with supplemental oxygen, assisted respirations, and intubation if necessary. Coral snake envenomations can be fatal, but one study reported good outcome in nearly 40 coral snake envenomations with adequate airway treatment, including intubation.
The ultimate treatment is antivenin. The exception is the Sonoran coral snake found in Arizona; no cases of severe toxicity requiring antivenin treatment have been reported with this species. In all other cases, Wyeth Laboratories makes a coral snake-specific antivenin, which carries similar advantages and disadvantages as its crotalid antivenin.
Summary
Field treatment of snakebite victims can be difficult when prolonged wilderness extraction is required, and the prehospital provider is crucial in the rapid treatment and transport of these patients. Incident information obtained by prehospital personnel may be pivotal in setting a streamlined course toward definitive treatment. Many of the folklore remedies for snakebites actually increase tissue damage and morbidity. Appropriate prehospital care will be the backbone of patient support, field guidance, adequate pain control and expedited transport.
Anthony F. Pizon, MD, is a professor with the University of Pittsburgh School of Medicine”s Division of Medical Toxicology. He has published several articles and has extensive experience in treating snakebites. Dr. Pizon has two years” experience as a prehospital care physician, serving on the physician response unit and as crew with STAT MedEvac. Contact him at pizonaf@upmc.edu.
This continuing education activity is approved by the Center for Emergency Medicine of Western Pennsylvania Inc., an organization accredited by the Continuing
