Sea Snake Envenomation Clinical Presentation

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. 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 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)

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)

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
• 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)