Sea Snake Toxicity

Etiology

Sea snakes are not inherently aggressive, although bites can occur when the animal is threatened or startled. Fishermen represent the highest-risk population, as contact frequently occurs during the removal of sea snakes from fishing nets. Similar to terrestrial snakes, not all bites result in envenomation.[3] Sea snakes possess small fangs and often deliver painless bites, which may go unnoticed until systemic symptoms develop.

Epidemiology

An estimated 5.4 million snake bites occur annually, with less than 50% resulting in envenomation.[4] Although sea snake bites are less common than terrestrial snake bites, the venom’s potent neurotoxic effects contribute to a high risk of morbidity and, if untreated, mortality.[5]

Pathophysiology

Sea snake venom contains a potent neurotoxin characterized by low LD50 values. Several enzymes contribute to the toxicity of this poisonous molecule, including acetylcholinesterase, hyaluronidase, leucine aminopeptidase, 5'-nucleotidase, phosphomonoesterase, phosphodiesterase, and phospholipase A.

Neurotoxicity occurs at both presynaptic and postsynaptic sites. The presynaptic effect, largely attributed to phospholipase A, initially promotes the release of acetylcholine but ultimately inhibits its release, leading to neuromuscular blockade. The postsynaptic neurotoxin is a small protein, approximately 6,000 to 8,000 Da, that binds almost irreversibly to acetylcholine receptor sites at the postsynaptic membrane.

The combined presynaptic and postsynaptic actions inhibit neural transmission and can result in flaccid skeletal muscle paralysis, including respiratory muscle and diaphragmatic involvement. In addition to neurotoxicity, phospholipase A and other venom components can induce myonecrosis, leading to muscle breakdown, myoglobinuria, and elevated levels of creatinine and creatine kinase.

Toxicokinetics

Sea snake venom is highly stable under extreme conditions. Experimental studies have demonstrated that boiling the venom for 30 minutes or dissolving it in solutions with pH values ranging from 1 to 11 does not significantly alter its LD50 in animal models. Thus, hot water immersion, commonly used for marine envenomations, is not recommended for sea snake bites. This intervention may exacerbate toxicity by increasing local blood flow and facilitating systemic absorption of venom.

History and Physical

Careful history-taking is essential and should include possible or confirmed exposure to sea snakes, time of injury, and the presence of symptoms such as localized pain, swelling, or erythema. Physical examination findings primarily reflect neurotoxicity and muscle injury. Clinical features may include paralysis, dysphagia, muscle spasms, dysarthria, and respiratory arrest. The leading cause of death following sea snake envenomation is respiratory failure from diaphragmatic paralysis or drowning due to flaccid skeletal muscle paralysis.

Bite marks may be difficult to appreciate because sea snakes have small fangs, and victims may not realize they have been bitten until systemic symptoms develop. In general, the absence of neurologic findings or muscle pain within several hours suggests the possibility of a dry bite. Approximately 50% of sea snake bites do not result in envenomation, and clinically significant envenomation occurs in only about half of exposures.[6]

Evaluation

Phospholipase A-induced myonecrosis may result in elevated serum creatine kinase levels and myoglobinuria. Diagnosis is clinical and based on a history of sea snake exposure and characteristic signs and symptoms. No specific laboratory or imaging studies are required to confirm the diagnosis. However, serum electrolytes and creatinine levels may be useful to assess for renal injury secondary to rhabdomyolysis, although these tests are not essential for initial evaluation.[7]

Treatment / Management

Treatment is primarily supportive and includes prompt administration of antivenom once symptoms of envenomation are identified. Immediate removal from the water is critical, as skeletal muscle paralysis may lead to drowning. Respiratory compromise can also occur due to diaphragmatic paralysis, necessitating endotracheal intubation and mechanical ventilation until antivenom neutralizes the circulating venom.

Incision, drainage, or suctioning of the bite site is not recommended. These interventions are unlikely to remove significant venom and carry additional risks of tissue damage and secondary infection. A pressure-immobilization bandage may be considered to delay systemic venom absorption.

Monitoring urine output is important for detecting myoglobinuria. Serum creatinine and electrolyte levels should be assessed frequently, with correction of electrolyte disturbances as needed. Hemodialysis may be considered in settings where antivenom is unavailable. Although not standard, this intervention is theoretically beneficial in refractory cases due to the small molecular size of the neurotoxin (6,000 to 8,000 Da), which may allow partial clearance.

Differential Diagnosis

Several conditions may mimic sea snake envenomation due to overlapping neurologic or myotoxic features. The differential diagnosis includes both venomous snakebites and nonenvenomation syndromes presenting with paralysis or rhabdomyolysis. 

• Cobra (Naja spp.) envenomation
• Coral snake (Micrurus spp.) envenomation
• Copperhead (Agkistrodon contortrix) and cottonmouth (Agkistrodon piscivorus) envenomation
• Mojave rattlesnake (Crotalus scutulatus) envenomation
• Other rattlesnake (Crotalus spp) envenomations
• Guillain-Barré syndrome
• Rhabdomyolysis of nontoxicologic origin

Accurate diagnosis relies on careful evaluation of exposure history, bite characteristics, and progression of symptoms. Neurotoxic envenomations such as those from cobra or coral snakes may present similarly but differ in geographic distribution and antivenom specificity. Guillain-Barré syndrome and other nontoxicologic causes of rhabdomyolysis, such as traumatic muscle injury and metabolic disorders, should be considered in the absence of a clear exposure history.

Prognosis

The low LD50 of sea snake venom contributes to significant morbidity and mortality in the absence of prompt treatment. However, the overall prognosis is favorable with early supportive care, including mechanical ventilation for respiratory failure and timely administration of antivenom.

Complications

Complications of sea snake envenomation include muscle necrosis and myoglobinuria secondary to phospholipase A-induced myotoxicity. Extensive muscle breakdown may result in elevated serum creatinine levels and acute kidney injury. Severe morbidity may occur without prompt antivenom administration, including death from respiratory failure or drowning.