Sea Snake Toxicity

Etiology

Sea snakes are not aggressive, although if they feel threatened or surprised, a bite can occur. Fishermen are the most at-risk population for sea snake bites, as contact with sea snakes can occur when fishermen attempt to remove sea snakes from their netting. Much like terrestrial snakes, not all bites result in envenomation.[2] Importantly, sea snakes have small teeth, making it possible for a bite to occur without a person realizing they were bitten until symptoms begin.

Epidemiology

Sea snake bites occur far less frequently than terrestrial snake bites and most commonly occur when fishermen attempt to remove them from fishing nets. The true incidence of sea snake bites is not known as many bites likely occur at sea and in small fishing villages where reporting bites may be difficult. Although sea snake bites occur less frequently than terrestrial snake bites, the potent neurotoxin leads to a high rate of morbidity and, potentially, mortality if not treated rapidly.[3]

Pathophysiology

Sea snake venom contains a potent neurotoxin with low LD50 levels. Several enzymes are present in sea snake venom, including acetylcholinesterase, hyaluronidase, leucine aminopeptidase, 5'- nucleotidase, phosphomonoesterase, phosphodiesterase, and phospholipase A. Sea snake venom acts at both presynaptic and postsynaptic sites. The presynaptic toxin is thought to be due to phospholipase A. This toxin initially causes the release of acetylcholine but, ultimately, the inhibition of acetylcholine release. The postsynaptic neurotoxin is a small protein between 6,000 and 8,000 daltons. This neurotoxin binds nearly irreversibly to the postsynaptic membrane at acetylcholine receptor sites. The net effect of both the presynaptic and postsynaptic toxin is the inhibition of neural impulses which can lead to skeletal muscle paralysis, including paralysis of the respiratory muscles and diaphragm. Other toxins, such as phospholipase A, can cause myonecrosis with resultant muscle breakdown, myoglobinuria, and elevated creatinine and creatine kinase levels.[1]

Toxicokinetics

Sea snake venom is extremely stable. Research has shown that boiling for 30 minutes and dissolving venom in both acidic and basic solutions to a pH range of 1 to 11, respectively, did not significantly change LD50 levels after administration in rats.[1] Therefore, hot water is not indicated for this venom and may, in fact, worsen outcomes by increasing blood flow to the area with the toxins.

History and Physical

Physical exam findings revolve around the blockage of neural impulses and muscle breakdown. Paralysis, dysphagia, muscle spasm, respiratory arrest, and dysarthria can occur, and the most common cause of death in sea snake poisoning is respiratory arrest due to diaphragm paralysis or drowning secondary to skeletal muscle paralysis. Because sea snakes have small teeth, bite marks may be difficult to appreciate, and it can sometimes be difficult for the victim to realize they were bitten until symptoms occur. In general, if no symptoms occur within a few hours after the bite, including both neurologic symptoms and muscle pain from myonecrosis, it is possible that the bite was a dry bite with no envenomation.[2] Approximately 50% of bites are dry bites, and only 50% of the time is there a significant envenomation.[4]

Evaluation

Due to the potential for myonecrosis from phospholipase A, creatine kinase levels may be elevated and myoglobinuria present in urine. No specific laboratory or radiographic tests are required for the diagnosis as clinical history including contact with a sea snake, and typical symptomatology is all that is required for diagnosis. Serum electrolytes and creatinine levels may be helpful to monitor for resultant kidney injury but are not required for diagnosis.[5]

Treatment / Management

Treatment is supportive and requires the administration of antivenin as soon as possible when symptoms of envenomation are present. Removal of the patient from the water is paramount, as skeletal muscle paralysis can cause drowning. Respiratory compromise may also occur owing to diaphragmatic paralysis, and patients may require intubation and mechanical ventilation until antivenin is administered and can neutralize the venom. Incision, drainage, and suctioning of the bite area are not indicated as little venom is likely to be removed in this manner, and resultant damage to the skin and possible subsequent infection risks outweigh the benefit of any possible venom removal. A pressure-immobilization bandage can be considered to help prevent systemic circulation of venom. Monitoring urine output should also be considered to evaluate for myoglobinuria, and frequent measurement of serum creatinine and electrolytes should be evaluated, and electrolytes supplemented as needed. In the absence of antivenin, hemodialysis can be considered and, theoretically, could be helpful in refractory cases given the small protein size (6,000 to 8,000 daltons) of the neurotoxin.[1](B3)

Differential Diagnosis

• Cobra envenomation

• Copperhead and cotton mouth envenomation

• Coral snake envenomation

• Gillian-Barre syndrome

• Mojave Rattlesnake envenomation

• Rattlesnake envenomation

• Rhabdomyolysis

Prognosis

Due to the low LD50 of sea snake venom, morbidity, and mortality rates are high without appropriate treatment. However, if supportive care, including mechanical ventilation as needed for respiratory compromise and antivenin administration, is done early, the overall prognosis is good.

Complications

Complications of sea snake envenomation can include muscle necrosis and myoglobinuria due to phospholipase A. If significant muscle breakdown occurs, the resultant myoglobinuria can lead to elevated creatinine levels and kidney damage. If antivenin is not administered promptly, significant morbidity up to and including death from drowning or respiratory failure can occur.