Sea Snake Envenomation 

Updated: Jun 15, 2018
Author: Dimitrios Papanagnou, MD, MPH; Chief Editor: Joe Alcock, MD, MS 



Sea snakes, venomous elapid snakes that inhabit marine environments, are the most abundant and widely dispersed group of poisonous reptiles in the world.[1] They comprise approximately 70 species, 50 of which are members of the family Hydrophiidae. Sea snakes are characterized by laterally compressed bodies and vertically flattened tails and nostrils with valve-like flaps, giving them an eel-like appearance. Their most characteristic feature is a paddle-like tail, which increases their swimming ability.[2] Unlike eels, however, sea snakes have scales but lack gills or fins. Although they spend much of their time underwater, they must surface regularly to breathe.[3] They are typically about 1 m in length, but some species may grow to 3 m. See the image below.

Yellow-belly pelagic sea snake. Illustration by Da Yellow-belly pelagic sea snake. Illustration by David Kirshner.

Sea snakes are found in warm coastal waters, predominantly in tropical and subtropical waters in the western Pacific and Indian Oceans.[4, 5] They are usually found in protected coastal waters and near river mouths. However, they are able to thrive in a variety of habitats, ranging from muddy or turbid water, to clear waters and coral reefs. Most species prefer shallow waters not far from land, around islands. The pelagic sea snake, Pelamis platurus, has a remarkably wide geographic range, reaching the western coasts of North America and South America from the Baja peninsula to Ecuador, along with the waters around Hawaii. Sea snakes are not found in the Atlantic Ocean, the Caribbean, or along the North American coast north of Baja.

Generally, sea snakes are not aggressive with gentle dispositions. They are not thought to bite humans unless provoked, and they typically do not actively pursue swimming prey. Sea snakes have been noted to become quite aggressive, when they are taken out of water, exhibiting erratic movements and striking anything near them that moves.[6]


Among this group are species with some of the most potent venoms of all snakes. The venom apparatus of sea snakes is fairly rudimentary, consisting of 2-4 short hollow maxillary fangs associated with a pair of venom-producing glands. The venom ducts open near the tips of the fangs. The fangs are dislodged easily from their sockets and may remain embedded in the skin of victims.

Nearly 80% of sea snake bites fail to produce significant envenomation, and bites may be inconspicuous, painless, and free of edema. Usually, little or no swelling is involved, and it is rare for any nearby lymph nodes to be affected. However, sea snake venom is extremely potent, and a complete envenomation by an adult sea snake may contain enough venom to kill 3 adult people.

The clinically relevant toxins in sea snake venom are neurotoxins and myotoxins. The primary neurotoxin causes peripheral paralysis by competitively binding to postsynaptic nicotinic acetylcholine receptors at the neuromuscular junction. Potent myotoxins account for the significant muscle necrosis, with consequent myoglobinemia and hyperkalemia that may occur following envenomation. Sea snake venom does not affect blood coagulation to a significant degree.

Sea snakes are closely related to Australian elapids; therefore, some paraspecificity exists between sea snake antivenom and Australian elapid antivenom.


The following exposures may lead to sea snake envenomation:

  • Occupational exposure - Usually fishermen handling nets

  • Accidental exposure - Stepping on sea snakes in shallow water

  • Nonaccidental exposure - Intentionally handling sea snakes (eg, home aquariums)



United States

Hawaii is the only US state where sea snakes are found.


Sea snake envenomations occur throughout the serpents' geographic ranges, but accurate data about the incidence of envenomation are not available. Victims most commonly are fishermen bitten while handling nets or after stepping on a snake.


No inherent racial predilection exists for sea snake bites; however, the best-represented races in areas with endemic sea snake populations are the most commonly bitten.


Males are bitten much more commonly than females, with a male-to-female ratio of approximately 4:1, because of the increased occupational exposure to sea snakes by male fishermen.


Age is a factor in determining sea snake bites only insofar as it occurs with potential recreational or occupational exposure to the serpents.


Before the development of sea snake antivenom, the mortality rate associated with sea snake bites was approximately 10%, but approximately 50% for clinically significant envenomations. With timely administration of antivenom and aggressive supportive care, the mortality rate currently is much lower, although accurate numbers are not available.

Although sea snake venoms contain extremely potent toxins, as many as 80% of sea snake bites do not produce clinically significant envenomation.[7] Therefore, the overall prognosis for people bitten by sea snakes is good.

In fatal cases, death has been reported as early as 2.5 hours and as late as 24 days after envenomation.

Patient Education

In areas with endemic sea snake populations, public education about the identification and avoidance of sea snakes may be useful.




The diagnosis of sea snake envenomation requires the establishment of the potential for exposure to a sea snake (eg, exposure to water in an area known to harbor sea snakes), identification of symptoms of envenomation, and demonstration of evidence of a bite (eg, multiple puncture wounds or reliable history of observed bite).

Symptoms are attributable to multiple organ systems, with neurological symptoms predominating. They may occur as early as 5 minutes or as late as 8 hours following the bite, but they usually occur within 2 hours. Initial symptoms include generalized aching, stiffness and tenderness of all muscle groups, as well as pain with passive muscle stretching. Trismus is also common. This is followed by progressive flaccid paralysis, starting with ptosis and paralysis of voluntary muscles. Paralysis of muscles responsible for swallowing and respiration can be fatal. Within 8 hours of envenomation, myoglobin, as a result of muscle breakdown, begins to rise in blood plasma; this eventually leads to myoglobinuria with resultant acute renal failure.[8] If muscle breakdown is severe, hyperkalemia may ensue, possibly leading to cardiac arrest.

  • Euphoria

  • Anxiety

  • Malaise

  • Drowsiness or mild confusion

  • Headache

  • Myalgias (typically worse with movement, usually beginning in the afflicted extremity, as well as the neck, within 30-60 min after envenomation)

  • Arthralgias

  • Ptosis

  • Mydriasis with sluggish reaction to light

  • Ophthalmoplegia, leading to diplopia

  • Failing vision (usually a terminal symptom)

  • Sialorrhea

  • Trismus

  • Facial paralysis

  • Muscle paralysis (usually ascending, may be flaccid or spastic)

  • Dyspnea

  • Nausea, vomiting, abdominal pain, and cramping

  • Change in urine color (dusky yellow to reddish brown)

  • Oliguria

  • Thirst

Physical Examination

Physical examination findings of sea snake envenomation may include the following:

  • Fang marks (usually two or more small circular dots, which may be difficult to initially identify)

  • Local tissue reaction (usually absent or minimal)

  • Paralysis (typically ascending)

  • Hyporeflexia (progressing to loss of reflexes)

  • Hypersalivation

  • Trismus

  • Bulbar paralysis

  • Ptosis

  • External ophthalmoplegia

  • Dysarthria and slurred speech

  • Dysphagia

  • Respiratory distress or respiratory failure

  • Tachypnea

  • Cyanosis

  • Apnea

  • Cardiac arrest (secondary to hyperkalemia)

  • Fever (variable)

  • Lymphadenopathy (involving the nodes responsible for draining the site of envenomation)


Complications of sea snake envenomation may include the following:

  • Respiratory failure

  • Cardiovascular collapse and shock

  • Allergic reactions (eg, anaphylaxis), in response to sea snake envenomation or antivenom administration[9]

  • Serum sickness following antivenom administration (usually between 5 d and 3 wk), characterized by urticaria, fever, lymphadenopathy, and arthritis

  • Renal failure, most commonly due to necrosis in the distal tubules

  • Hyperkalemia

  • Dysrhythmias (secondary to hyperkalemia)





Laboratory Studies

Obtain arterial blood gas (ABG) measurements if the patient's respiratory status is questionable.

Myoglobinuria may be found on urinalysis, typically 3-6 hours following envenomation. The urine may test positive for protein and occult blood 1 hour before myoglobin is detected.

Creatine kinase (CK) level may be elevated secondary to muscle damage.

Serum glutamic-oxaloacetic transaminase (SGOT) level may be elevated secondary to muscle damage.

Electrolyte levels may reveal hyperkalemia from myonecrosis.

Assess blood urea nitrogen (BUN) and creatine levels to monitor renal function.

Obtain a CBC count. A leukocytosis higher than 20,000 cells/µL suggests significant envenomation.

Imaging Studies

The following imaging studies may be useful:

  • Chest radiography: This is useful to exclude other causes of respiratory distress and is mandatory in patients requiring intubation and mechanical ventilation.

  • Soft tissue and bone films of the bitten extremity: Radiographs may reveal embedded fangs and/or underlying osseous injury.

  • Bedside ultrasonography: As ultrasonography is becoming a more useful adjunct to physical examination in the emergency department, bedside imaging may facilitate identifying retained fangs at the site of venomous inoculation.

Other Tests

An electrocardiogram (ECG) is useful to look for signs of hyperkalemia, including peaked T waves, a widened QRS complex, or ventricular arrhythmias.

Before antivenom administration, if time permits, skin testing to assess for allergy to horse serum is indicated, but it is not mandatory if the patient is unstable. The results of skin testing are not completely reliable. Intradermal injection of 0.02-0.03 mL of a 1:10 dilution of normal horse serum is the most commonly described technique; however, the test is more accurate if a 1:10 dilution of actual reconstituted antivenom is used. Skin test results are positive if a wheal develops in 5-30 minutes.



Prehospital Care

The critical components of prehospital care for sea snake bites are initial stabilization with airway control, pressure immobilization of the bitten extremity, and prompt transport to a facility capable of providing advanced medical care (including antivenom administration).[10]

A brief attempt to visually identify the offending snake is warranted, but prolonged attempts to kill or capture the snake should be avoided. The bite reflex persists for up to an hour even after the snake is decapitated, making it possible for dead snakes to inflict a serious bite.

If needed, institute supportive measures, including endotracheal intubation and mechanical ventilation, as clinically indicated.

Apply pressure immobilization of the bitten extremity as quickly as possible because it may impede venom spread. Rapidly wrap the limb with a broad pressure bandage, starting at the wound site and extending as high up the extremity as possible. The bandage should be wrapped to venous occlusive pressure (approximately 70 mm Hg) in a manner similar to wrapping a sprained ankle. An extremity splint completes the immobilization. See the images below.

Technique for application of pressure immobilizati Technique for application of pressure immobilization in field management of sea snake bites. Figure 1, Apply a broad-pressure bandage over the bite site as soon as possible. Do not take off jeans because the movement of doing so assists venom to enter the bloodstream. Keep the bitten leg still. Figure 2, The bandage should be as tight as would be applied to a sprained ankle. Figure 3, Extend the bandage as high as possible.
Technique for application of pressure immobilizati Technique for application of pressure immobilization in field management of sea snake bites. Figure 4, Apply a splint to the leg. Figure 5, Bind the splint firmly to as much of the leg as possible. If the bandages and splint are applied correctly, they will be comfortable and may be left on for several hours. They should not be taken off until the patient has reached medical care. The doctor will decide when to remove the bandages. If venom has been injected, it will move into the bloodstream quickly once the bandages are removed. The doctor should leave the bandages and splint in position until he or she has assembled appropriate antivenom and drugs that may need to be used when the dressings and splint are removed. Figure 6, For bites on a hand or forearm, bind to the elbow with bandages, use a splint to the elbow, and use a sling.

Avoid incision, ice, or other cooling measures.

Suction is unlikely to be beneficial and only should be attempted if a mechanical suction device is immediately available.

Emergency Department Care

Initial treatment is as follows:

  • Stabilization of airway, breathing, and circulation (ABCs)

  • Intravenous access

  • Cardiac monitoring and continuous pulse oximetry

  • Tetanus prophylaxis

Manage all symptomatic sea snake envenomations on an inpatient basis. Given the potentially serious nature of envenomation and the risks associated with antivenin administration, most patients require admission to an intensive care unit.

Monitor patients treated with antivenom for allergic reactions and treat appropriately.

Transfer is appropriate if it is required to provide antivenom administration, intensive monitoring, or critical care that is not available at the institution to which the patient initially presents.

Antivenom administration

Antivenom administration is indicated for any patient with signs of envenomation.[10, 11] The agent of choice is polyvalent sea snake antivenom (Commonwealth Serum Laboratories, Melbourne, Australia). Alternatively, tiger snake (Notechis scutatus) antivenom can be substituted because of the close relationship of tiger snake and sea snake venoms.[12, 13]

Indications for antivenom use include shock, respiratory distress or failure, generalized myalgias, trismus, moderate-to-severe pain with passive movement of extremities, myoglobinuria, elevated creatine kinase level (>600 IU/l), altered level of consciousness, hyperkalemia, or leukocytosis.

Administer antivenom as soon as possible. Benefits may be observed up to 36 hours after the bite.

For early mild-to-moderate envenomation, use one ampule of antivenom (1000 U). Later or severe envenomation typically requires 3-10 ampules (3000-10,000 U) of antivenom, respectively.

If antivenom is not available, consider dialysis. Sea snake neurotoxin is of low enough molecular weight to be dialyzable. Furthermore, dialysis may be life saving in cases of severe hyperkalemia.

Aggressive hydration with diuresis can help promote renal myoglobin clearance. Urine alkalinization may be of some benefit in cases of myoglobinuria.

In-patient admission for observation, especially if the patient is to receive antivenom as allergic/anaphylactic reactions are common.


Poison control centers, zoos, or experts in snake envenomation may help guide the management of sea snake envenomations and assist with the location of antivenom.

In cases of serious envenomation, an internist or intensivist should be consulted for admission to the hospital or intensive care unit, respectively.


Patients should avoid waters known to harbor sea snakes.

Patients should avoid approaching, handling, or provoking sea snakes.

Children playing or swimming in waters within the typical geographic ranges of sea snakes should be carefully supervised.

Long-Term Monitoring

Before discharge, describe the signs and symptoms of delayed serum sickness to patients who receive antivenom and advise them to seek prompt medical care if any such symptoms occur.

Patients who are asymptomatic (ie, experience no pain with passive muscle movement 2 hours after a sea snake bite) are extremely unlikely to have experienced a significant envenomation and may be safely discharged with close follow-up monitoring. However, patients may have delayed symptoms if the bite site was immobilized and treated with a pressure bandage or venous tourniquet, and they should be observed in the hospital.



Medication Summary

The mainstay of medical therapy for sea snake venom poisoning is antivenom. If time permits, a skin test for sensitivity to horse serum may be performed before antivenom administration. The purpose of skin testing is to try to predict possible anaphylaxis, rather than determine whether antivenom should be used. Omit skin testing if the patient clearly needs antivenom because skin testing reliability is low. Closely monitor the patient during antivenom administration and begin aggressive treatment if any evidence of allergic reaction is observed.


Class Summary

Antivenom conveys passive immunity to patients with sea snake bite.

Antivenin polyvalent sea snake

This can be obtained from Commonwealth Serum Laboratories, Melbourne, Australia. It is the drug of choice for the treatment of symptomatic sea snake envenomation. It is a hyperimmune horse globulin prepared against the venoms of Enhydrina schistosa and N scutatus and is efficacious in the treatment of all sea snake envenomations.

An alternative to polyvalent sea snake antivenom is monovalent sea snake antivenom (Haffkine Institute, Bombay, India), prepared against the venom of E schistosa, which is effective against most sea snake venoms. Finally, tiger snake (N scutatus) antivenom (Commonwealth Serum Laboratories, Melbourne, Australia) displays substantial activity against sea snake venoms because of a close relationship between tiger snake and sea snake venoms.

Early or mild envenomation can be treated with 1 ampule, while late and/or severe envenomations should be treated with 3-10 ampules. Snake antivenom only is administered intravenously.

The intravenous infusion should be started at a slow rate, which may be increased if no evidence of significant allergic reaction exists. Most authorities recommend premedication with diphenhydramine.


Class Summary

These agents are used to treat minor allergic reactions and anaphylaxis.

Diphenhydramine (Benadryl)

Diphenhydramine  may be used to pretreat patients with prior documentation of minor allergic reactions. It is used as a prophylactic treatment and for the treatment of allergic reactions to antivenom.


Class Summary

Active immunity can prevent hypersensitivity reactions and neutralize toxoids.

Diphtheria & tetanus toxoids (Decavac, DT, Td)

This is used to induce active immunity against tetanus in selected patients. The immunizing agents of choice for most adults and children older than 7 years are 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, may administer into the deltoid or midlateral thigh muscles. In infants, the preferred site of administration is the mid thigh laterally.

The tetanus immunization status should be updated for any patient bitten by a sea snake. The precise formulation used is dependent on the patient's age and prior immunization status.

Cardiovascular agents

Class Summary

These agents are useful for treatment or prophylaxis of acute allergic reactions and for support of blood pressure in patients with shock.

Epinephrine (Epi-Pen, Adrenaline)

Epinephrine is the drug of choice for the treatment of anaphylactoid reactions and should be considered as pretreatment before giving antivenom. It has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Its beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.


Class Summary

Anti-inflammatory agents are useful in the management of acute and delayed allergic reactions to sea snake envenomation or antivenom administration.

Methylprednisolone (Solu-Medrol, Depo-Medrol)

Steroids ameliorate delayed effects of anaphylactoid reactions and may limit biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may be beneficial to reduce inflammatory effects of this immune-complex mediated disease.

Prednisone (Deltasone, Orasone, Meticorten)

Prednisone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.