In the US: thousands of snake bites annually, with very few (if any) deaths per year.
Worldwide: 5 million snake bites with 125,000 deaths globally.
There are five families of venomous snakes which include: viperidae, elapidae, hydrophiidae, atractaspididae, colubridae. In the US, the only two families of venomous snakes are the viperidae and elapidae. The Viperidae include rattlesnakes and vipers, whereas the elapidae include the coral snakes. The two families have different presentations and characteristics of envenomations thus we will address them separately.
Crotalinae, also known as pit vipers, or crotalids, are snakes with a triangular shaped head, elliptical pupils, and equipped with heat sensing pits. They are generally found throughout the US except Maine and Hawaii. for which most envenomations occurring between May and October (hibernate in the winter) in the afternoon hours
The striking distance of a crotalid is half of its length, and typically makes a subcutaneous envenomation. . Thus, the venom of crotalids spreads through the lymphatic system—they will rarely be intravenous envenomations. Most bites are from rattlesnakes, with the remaining bites from cottonmouths, water moccasins, and other species. Cottonmouths and water moccasins have generally less severe envenomations than rattlesnakes. A quarter of the bites from crotalids will be dry bites. However, those with real envenomation will experience severe pain and swelling within minutes, followed by ecchymosis and blistering between minutes to hours. Anaphylaxis can occur, albeit rare. Occasionally the severity of the envenomation can produce rhabdomyolysis. Systemic symptoms may include weakness, malaise, abdominal pain, anxiety, nausea, vomiting, and diarrhea with possible hypotension. Patients commonly develop coagulopathy and/or may develop neurotoxicity. Generally, if one doesn’t have symptoms within 6-8 hours, it is a dry bite (leg bites are the exception, may have delayed onset of symptoms), thus observation between 8-12 hours is reasonable.
Coagulopathy is a common, as victims will have low fibrinogen and platelet counts, and PT/PTT times being considerably prolonged. It is not unusual for the coagulation studies to be abnormal despite significant clinical improvement.
The immediately most concerning issues such as airway issues (analyphylaxis) are very rare, and the Mojave is the only North American crotalid that is neurotoxic (producing lethargy, cranial nerve deficits and respiratory failure through a neurotoxin that inhibits neurotransmitter release presynaptically). Bleeding from DIC is rare, and so is compartment syndrome, which is important to monitor for. While incredibly rare, documented cases do exist of anaphylaxis occurring to those who have been sensitized to crotalids. It is mediated through IgE like any other anaphylaxis case, but it may be difficult to distinguish from severe envenomation.
For crotalid envenomation, NEVER USE a tourniquet, ice, compression bandage, incision/suction, or venom extractors. None of these help. Like any sick patient, do the ABCs: manage their airway, give IV fluids, and pressors if hypotensive. Epinephrine is a popular choice for pressor. Elevate the extremity, fentanyl for pain control, and benzos for anxiety. Continue neurovascular checks, update tetanus status, and monitor the circumference of an extremity and indicate the extent of swelling on the extremity by time and date. Keep the extremity in extension, and place into a splint. Prophylactic antibiotics are unnecessary in these envenomations. There is significant swelling, and often many providers are concerned for compartment syndrome. As mentioned earlier, the envenomation is subcutaneous, although patients will complain of paresthesias, tense swelling, pain, and weakness, which is obviously concerning for compartment syndrome. The question of dermotomy or fasciotomy comes up, and when in doubt, check compartment pressures, however it is rarely needed. It was found that fasiotomies and subcutaneous decompression doesn’t prevent myonecrosis in animals receiving venom injections. They have even found that envenomations will increase arterial blood flow distal to the swelling, which is contrary to what we would expect in compartment syndrome. Once the swelling subsides, wound debridement occurs with surgery, usually in 3-6 days.
The most important labs include platelets, PTT and fibrinogen level. Blood products are not indicated in the absence of bleeding, and anything given for low platelets or coagulation factors will be consumed immediately after being given (since active venom is present), such that it is futile to administer blood products without concurrent administration of antivenom also. Trend coagulation studies after each antivenom bolus dose and prior to hospital discharge. Just remember that normalization of coagulation studies is not an endpoint, as coagulation studies may not completely normalize.
One can imagine, when do you give antivenom?!?! Consider the three possibilities:
1. Rapid progression of swelling
2. Significant coagulopathy or thrombocytopenia
3. Systemic symptoms (neurotoxicity, shock, etc)
The antivenom of choice is CroFab. It is a polyvalent immune Fab, where the Fc fragment is removed, leaving only the Fab component that binds to the venom. It is derived from sheep that were immunized with Mojave, western and eastern and cottonmouth snake venom. Studies have shown that Crofab stops progression of swelling, reverses hematologic toxicity, and likely reverses systemic symptoms,but there is still no evidence that prevents tissue loss.
Give 4-6 vials of CroFab, with normal saline over 1 hour Once the first 4-6 vials are done, repeat the 4-6 vials until clear improvement is appreciated in swelling, coagulopathy and platelet counts. Maintenance CroFab is then given with 2 vials every 6 hours for three total maintenance doses.
CroFab is not without its own limitations. A recurrence phenomena can occur where once the envenomation resolves with treatment, swelling or hematologic abnormalities (coagulopathy, thrombocytopenia) recur. The timeframe usually is several days after treatment, and if the patient is rebleeding, retreat with CroFab, however otherwise observe the patient. Beyond recurrence, CroFab is expensive, results in longer hospital stays, and outpatient follow-up required.
If patients are asymptomatic, observe for 6-8 hours for those suspected to be bitten by a pit viper. Be vigilant for subtle signs of envenomation
The other family of venomous snakes are the elapidae, which include coral snakes, cobras, mambas, tiger snakes, and taipan. Coral snakes are the elapidae encountered in the US. These are notorious for neurotoxicity, with minimal local findings, in contrast to the crotalids. The US is home to 3 coral snake species: The Eastern, Texas, and Sonoran coral snakes. They are often confused with king snakes which are nonvenomous. Coral snakes have black snouts. Additionally, many remember the color bands on the bodies of the snakes: “black on yellow, kill a fellow, red on black, venom lack.” Overall compared to the Crotalids, they are much more docile.
Elapidae envenomations can appear deceptively benign given that the pain is often minor. In comparison to crotalids where their fangs puncture deeper, coral snakes have shallower fangs with a ‘gnawing’ bite (and may not immediately let go), where removing the snake is akin to peeling off Velcro. Less than 40% of elapidae envenomations are clinically significant. In decreasing prevalence, local swelling, paresthesias, nausea, vomiting, euphoria, weakness, dizziness, diplopia, diaphoresis, and muscle tenderness occur. Severe envenomations have been reported with long asymptomatic periods >12 hours, and when they deteriorate, respiratory distress/failure and neurologic abnormalities occur with the major cause of immediate death is respiratory failure secondary to neuromuscular weakness. That said, ventilation and supportive care is effective as the weakness/paralysis is reversible over the course of couple days. Close observation for a day will be paramount for these patients.
Nelson L., et al. Goldfrank’s Toxicologic Emergencies