Approximately 40-50 species of venomous coral snakes exist in North America and South America, with the greatest variety from Mexico to northern South America. A number of African and Asian coral snake species also exist. All coral snakes belong to the family Elapidae; Micrurus fulvius (eastern coral snake) and Micrurus tener (Texas coral snake) are the most important species in the United States.
Another US coral snake, Micruroides euryxanthus (Sonoran or Arizona coral snake), is a small and relatively innocuous snake, and no deaths have been attributed to its bite.
Coral snakes tend to be relatively shy creatures, and bites are uncommon. Coral snakes account for less than 1% of venomous snakebites in the United States. Most people bitten by coral snakes are handling them intentionally. Most bites occur in the spring or fall. Deaths have been reported but are extremely rare.
Also see Physical Examination.
The vast majority of patients bitten by coral snakes report that a brightly colored snake bit them.
North of Mexico City, including the United States, the color pattern of the snake can be helpful in differentiating a coral snake from a harmless mimic (eg, nonvenomous milk snake). In this region, all coral snakes have a red, yellow, black, yellow, red banding pattern (every other band is yellow; red and yellow bands touching, and bands completely encircle the body; see the image below); most harmless mimics have a red, black, yellow, black, red pattern (every other band is black; red and yellow separated by black; and/or some bands do not completely encircle the body).[1] The mnemonic "Red on yellow, kill a fellow; red on black, venom lack," may be helpful in this region. South of Mexico City, this rule can not be used as the banding patterns are much different, and bicolor (red and black) species are also present.
History may include the following:
Onset of symptoms may be delayed up to 10-12 hours but may then be rapidly progressive.
Paucity of local complaints
Local paresthesias (may be painful)
Soft tissue swelling (usually mild)
Myalgias have been reported
Alteration of mental status
Complaints related to cranial nerve dysfunction (eg, diplopia, ptosis, difficulty swallowing)
Complications of snake bite may include the following:
Aspiration
Cardiovascular collapse
Prolonged neuromuscular weakness
No laboratory studies are of diagnostic benefit. Baseline laboratory studies (eg, complete blood count [CBC], electrolyte tests, renal function studies) may be obtained in severe bite cases or if the patient has significant underlying medical problems. Coagulation studies are not indicated.
An arterial blood gas (ABG) determination may be helpful if the patient's respiratory status is of concern.
A chest radiograph is beneficial in patients who have severe envenomation, who require intubation, or who show evidence of cardiopulmonary failure.
If available, pulmonary function testing such as negative inspiratory force (NIF) and forced vital capacity (FVC) can be used to determine if patients may have impending respiratory failure. Similarly, the single breath count (SBC) test can also be used. To perform the SBC: Ask the patient to take a deep breath and count as high as possible in their normal speaking voice without taking another breath. A normal SBC is approximately 50 and SBC < 20 is associated with the need for mechanical ventilation.[2]
See Prehospital Care, Emergency Department Care, and Medication.
Consult a toxicologist, poison control center, or an expert in snakebite management.
Complications
Antivenom-related complications may include anphylatic reactions, anphylactoid reactions and delayed serum sickness. These can range from mild (rash) to life-threatening (hypotension, shock).
Long-term monitoring
Muscle weakness can takes weeks to resolve. Follow up with primary care physicain or a medical toxicologist is recommended after discharge.
Prevention
Avoid handling venomous or unidentified snakes.
Use caution when placing bare hands or feet into areas where one cannot see and in which snakes may be seeking shelter.
The coral snake venom apparatus is composed of a pair of small, fixed, hollow fangs in the anterior aspect of the upper jaw through which the snake injects venom via a chewing motion (see the image below). Unlike pit vipers, such as rattlesnakes, copperheads, and cottonmouths, which strike quickly, coral snakes must hang on for a brief period to achieve significant envenomation in humans.
Coral snake venoms tend to have significant neurotoxicity, inducing neuromuscular dysfunction. Coral snake venom has components which inhibit pre-synaptic releast of acetylcholinesterase and post-synaptic binding of acetylcholinesterase. They have little enzymatic activity or necrotic potential compared with most vipers and pit vipers. These venoms tend to be some of the most potent found in snakes, yet the venom yield per animal is less than that of most vipers or pit vipers. Because of the relatively primitive venom delivery apparatus, as many as 60% of those bitten by North American coral snakes are not envenomed (ie, they receive a "dry bite").
United States
There were 76 alleged coral snake bites reported to the American Association of Poison Control Centers in 2020.[3]
International
No accurate information on international incidence is available, but there are no regions of the world where coral snake bites would be considered common.[4, 5]
With sound supportive care (eg, prevention of aspiration) and appropriate antivenom administration, when available, prognosis following coral snake envenomation is excellent and a full recovery is expected. This is generally true, even in the absence of an available, appropriate antivenom,[6] but the overall clinical course (including the need for prolonged intubation and respiratory support) will be longer. Patients who survive the bite may require respiratory support for up to a week and may suffer persistent weakness for weeks to months.
A single death has been reported due to a coral snake bite in the United States in the last 40 years (roughly, since coral snake antivenom became available).[7] Before that time, the estimated case-fatality rate was 10%, and the cause of death was respiratory or cardiovascular failure.
Impending respiratory failure signs and symptoms include the following:
Respiratory distress
Pharyngeal spasm
Hypersalivation
Cyanosis
Trismus
Neurologic dysfunction signs and symptoms include the following:
Altered mental status
Ptosis
Generalized weakness
Muscle fasciculations
Cardiovascular collapse signs and symptoms include the following:
Hypotension
Tachycardia
In addition to a brief generalized examination, the skin should be carefully examined in an effort to identify what may be very tiny puncture wounds at the bite site. These may be hard to see and many bite sites are never identified.. Generally, there is little in the way of other local findings (little bleeding, ecchymosis or swelling).
A careful neurological examination should be done in an effort to identify any evidence of early venom-induced dysfunction. Particular attention should be paid to the cranial nerves (watching for any evidence of bulbar weakness) and to motor strength (including respiratory muscles).
Any condition which causes acute, descending flaccid paralysis would need to be considered when evaluating a possible coral snake envenomation.
In the prehospital setting, the primary goal is prompt movement of the victim to a medical facility capable of rendering advanced care, including possible antivenom administration and airway support.
Briefly attempt to identify the snake (especially, note the color pattern). If possible, take a digital photo of the snake from a safe distance. Efforts to catch or kill the animal can result in wasted time and further bites.
Rapidly apply the Australian pressure immobilization technique in which a compressive bandage (eg, elastic bandage, crepe bandage, torn clothing) is wrapped around the bitten extremity, starting distally and progressing to encompass the entire limb.[8, 9] Wrap it as tightly as one would wrap a severely sprained joint. Then, splint the extremity and, if possible, keep it at approximately heart level. The victim must then be carried from the scene to the hospital (ie, without any ambulation, regardless of whether the bite is on an upper or lower extremity). This technique may significantly delay systemic absorption of elapid venoms, including coral snake venom. Research suggests, however, that in a simulated snakebite scenario, even after focused, intensive hands-on training, people tend to underestimate the application tension required for the technique to be effective.[10] See the images below.
No incisions are indicated.
Suction is of no benefit and may be harmful.
Avoid applying ice or initiating any other cooling measures.
Aggressively manage any signs of impending respiratory failure with endotracheal intubation to prevent aspiration.
Immediately institute cardiac and pulse oximetry monitoring.
Monitor vital signs closely.
Start at least one large-bore intravenous line of normal saline or Ringer's lactate at a maintenance rate. If evidence of hypotension or hypoperfusion is present, select an appropriate, faster rate.
Because of the lack of early signs and symptoms, the severity of coral snake bites may be underestimated at presentation. Maintain a high index of concern.
Historically, if the snake was positively identified as an eastern or Texas coral snake and the victim was asymptomatic, or if signs and symptoms of envenomation were already present, the recommendation was to obtain and immediately administer appropriate antivenom. However, recent data suggests that there adminstration of antivenom to asymptomatic patients is of no benefit. [6]
In the United States, the Food and Drug Administration (FDA) approved antivenom for coral snake envenomation is the North American Coral Snake Antivenin (Micrurus fulvius) (Equine Origin). However, production of this coral snake antivenom has ceased. The FDAhas extended the expiration date for the remaining of North American Coral Snake Antivenin through June 30, 2024.[11] After this time, unless stock remains and the expiration date is further extended, this country may find itself without a commercially available coral snake antivenom. Research is ongoing to find a suitable new antivenom for the treatment of coral snake bite victims in the United States and studies have demonstrated that some non-native elapid antivenom can neutralize North American coral snake venom. [12, 13] There is a possibility that coral snake antivenom production will resume in the United States at some point in the future. Until then, healthcare providers treating a coral snake bite victim should contact their regional poison control center for assistance.
Absent an available antivenom, victims can be managed with sound supportive care (as outlined above) with an expectation of excellent outcome as long as airway management and respiratory support are adequate, though ventilator dependence could persist for many days or weeks following serious bites.
Bites by Sonoran coral snakes tend to be very mild (there has never been a documented fatality) and are treated with supportive measures alone.
Admit all persons bitten by a coral snake to a closely monitored facility, whether or not antivenom is given.
Observe asymptomatic patients for at least 24 hours because delayed signs and symptoms may occur.
If an appropriate antivenom was available and administered, but resulted in an acute reaction, continue to administer systemic antihistamines and steroids as needed.
Patients should be monitored for 12-24 hours after the last dose of antivenom.
Generally, little or no risk of tissue necrosis is present following coral snake bites.
Inform patients who have received antivenom of the signs and symptoms of delayed serum sickness. If symptoms of serum sickness develop after discharge, promptly evaluate the patient for initiation of systemic steroids and diphenhydramine (see Medications).
Definitive therapy for coral snake envenomation is antivenom administration. Antivenom (usually derived from horses or sheep) is generally specific for closely related species of snake. While species-specific antivenom is preferred, cross reactivey exists due to conservation of venom components across genera. This is supported by evidence that Australian elapid antivenom and Mexician coral snake antivenom can neutralize the venom of North American coral snakes.[12, 13] Administering any antivenom can result in acute or delayed adverse reactions (eg, anaphylaxis, anaphylactoid reaction, or delayed serum sickness) and should be given only after expert consultation.
If antivenom is unavailable, compression and immobilization should be maintained, and the airway and respiratory status supported as necessary. An appropriately applied compression/immobilization device should be removed only after supportive measures are in place and antivenom, if available, is obtained.
In the United States, the product used to treat Micrurus bites for the last several decades, North American Coral Snake Antivenin (Micrurus fulvius) (equine orgin), is no longer in production and current stock is due to expire in June 30, 2024.[11] Other antivenoms are produced in other countries (eg, Brazil, Costa Rica) for non-North American coral snakes. Mexico produces an antivenom that appears effective for coral snake bites in the United States.[13] Foreign elapid antivenoms may prove useful for treatment of coral snake bites in the United States, and research in this area continues. Assistance in locating and securing an appropriate antivenom can be obtained by contacting a regional poison control center.
Any appropriate, available antivenom should be administered according to the manufacturer's instructions. For the North American Coral Snake Antivenin (Micrurus fulvius) (equine orgin), the dose would be 3-5 vials as needed, up to 10 vials.
In the absence of such an antivenom, care will be entirely supportive.
Neostigmine, a reversible cholinesterase inhibitor, has been used to treat South American coral snake envenomations.[14] It can improve muscle strength by antagonizing the post-synaptic acetylcholinesterase blockade that occurs with coral snake venom.
Care for persons bitten by Sonoran coral snakes is entirely supportive because no specific antivenom is available for this species.
As with any form of bite, tetanus status should be updated as necessary.
Antibiotic prophylaxis is not indicated. Because of the relative paucity of enzymatic necrotic components in their venoms, coral snake bites tend to cause little local tissue damage, and secondary infections are rare.
These agenst impart passive immunity to the patient against the venom components of the snake(s) for which it is manufactured. The heterologous antibodies administered bind with venom antigens and block their deleterious effects.
This historically is the drug of choice for significant bites by M fulvius (eastern coral snake) and M tener (Texas coral snake). Dose of 3-5 vials prn up to 10 vials are recommended. However, it is no longer being produced. Unless another known effective antivenom is available, care for victims bitten by coral snakes in the United States will have to rely entirely on supportive care (as per the text above), though the outcome should still be good.
H1 and H2 blockers may blunt or prevent acute allergic reaction when given before the administration of antivenom. If an anaphylactoid reaction occurs despite pretreatment, further antihistamine dosing may be required. They are also useful in managing pruritus in cases of delayed serum sickness, which may appear days to weeks following antivenom treatment.
Diphenhydramine is administered parenterally and often is the H1 blocker of choice in treating or preventing anaphylactic/anaphylactoid reactions. It is also effective in oral forms for treating itching associated with serum sickness.
Cimetidine is administered parenterally and often is the H2 blocker of choice in treating or preventing anaphylactoid reactions. Use this medication in addition to H1 antihistamines.
These agents are useful in treating acute allergic reactions that may occur with antivenom administration and in supporting the blood pressure and tissue perfusion of hypotensive patients with shock unresponsive to IV fluids and antivenom.
Epinephrine is the drug of choice for treating anaphylactoid reactions. It has alpha-agonist effects that increase peripheral vascular resistance and reverse peripheral vasodilatation, systemic hypotension, and vascular permeability. Conversely, the beta-agonist activity of epinephrine produces bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Dopamine may be required to support blood pressure with hypotension caused by an anaphylactoid reaction that is unresponsive to fluids and epinephrine or by direct coral snake venom effects that are unresponsive to fluids and antivenom.
Norepinephrine may be used as an alternative to dopamine to support blood pressure in the face of hypotension caused by an anaphylactoid reaction that is unresponsive to fluids and epinephrine.
Corticosteroids are essential for the management of acute and delayed allergic phenomena following antivenom administration. Steroids have no primary role in the management of snake envenomation.
Methylprednisolone ameliorates the delayed effects of anaphylactoid reactions and may limit biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may reduce the inflammatory effects of this immune-complex mediated disease.
This or other oral forms of corticosteroids (eg, prednisolone) are useful in managing mild-to-moderate serum sickness on an outpatient basis.
Immune globulins bind toxoids, stimulate an immune response, and offer transient protection while the host immune system develops antibodies.
Tetanus immune globulin is used for passive immunization if the wound might be contaminated with tetanus spores when the patient has no history of completing a primary tetanus immunization series.
This is used to induce active immunity against tetanus.
The immunizing agent of choice for most adults and children older than 7 years is tetanus and diphtheria toxoids. It is necessary to administer booster doses to maintain tetanus immunity throughout life. Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen-containing product. In children and adults, it may be administered into the deltoid or midlateral thigh muscles. In infants, the preferred site of administration is the mid thigh laterally.