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SEA SNAKES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sea snake venoms contain both myotoxins and neurotoxins. The neurotoxin component of the venom is very potent and of clinical significance. They are more toxic then the venoms of land snakes. Sea snake venom neurotoxins act on the neuromuscular junction causing paralysis in the victim.

Specific Substances

    A) SEA SNAKES
    1) Acalyptophis peronii
    2) Aipysurus apraefrontalis
    3) Aipysurus duboisii
    4) Aipysurus eydouxii
    5) Aipysurus foliosquama
    6) Aipysurus fuscus
    7) Aipysurus laevis (olive brown sea snake)
    8) Aipysurus tenuis
    9) Astrotia stokesii (Stoke's sea snake)
    10) Disteira kingii
    11) Disteira major
    12) Disteira nigrocincta
    13) Emydocephalus annulatus
    14) Emydocephalus ijimae
    15) Enhydrina schistosa (beaked sea snake)
    16) Ephalopis greyi
    17) Ephalopis mertoni
    18) Hydrelaps darwinensis
    19) Hydrophidae
    20) Hydrophis belcheri
    21) Hydrophis bituberculatus
    22) Hydrophis brookii
    23) Hydrophis caerulescens
    24) Hydrophis cantoris
    25) Hydrophis cyanocinctus (annulated sea snake)
    26) Hydrophis elegans
    27) Hydrophis fasciatus (banded small headed sea snake)
    28) Hydrophis gracilis (graceful small headed sea snake)
    29) Hydrophis inornatus
    30) Hydrophis klossi
    31) Hydrophis lapemoides
    32) Hydrophis mamillaris
    33) Hydrophis melanocephalus
    34) Hydrophis melanosoma
    35) Hydrophis obscurus
    36) Hydrophis ornatus (reef sea snake)
    37) Hydrophis parviceps
    38) Hydrophis semperi
    39) Hydrophis spiralis (yellow sea snake)
    40) Hydrophis stricticolis
    41) Hydrophis torquatus
    42) Kerilia jerdoni
    43) Kalpophis annandalei
    44) Lapemis curtus
    45) Lapemis hardwickii (Hardwicke's sea snake)
    46) Pelamis platurus (yellow bellied pelagic sea snake)
    47) Praescutata viperina
    48) Thalassophis anomalus
    49) Laticuada colubrina (yellow lipped sea krait)
    50) Laticuada crockeri
    51) Laticuada laticuadata
    52) Laticuada semifasciata
    53) Laticuada schistorhynchus
    54) Snake bite (sea snakes)

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Sea snakes are generally found either close to the shore or near coral reefs, with the exception of Pelamis platurus which can be found in deep areas of the ocean. They are found in the oceans around the eastern coasts of Africa and the Middle East, southern and eastern coasts of Asia, all but the southern coast of Australia, throughout Micronesia, Malaysia, and the Philippines, and the Pacific coasts of Central America, Ecuador, southern Columbia, and northern Peru.
    B) TOXICOLOGY: Sea snake venoms contain myotoxins and neurotoxins.
    C) EPIDEMIOLOGY: Bites are probably under reported and occur most commonly in small villages among fisherman who use traditional methods of fishing. In endemic areas of Malaysia, 3% of 68 positively identified venomous snake exposures involved sea snakes.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: About 80% of bites are believed to either be dry or result in trivial envenomation. There is little pain and no erythema or swelling at the bite site, although teeth or scratch marks may be seen.
    2) SEVERE ENVENOMATION: Muscle stiffness and pain, weakness, dizziness, dry mouth, diaphoresis, nausea and vomiting may develop early. Even with severe envenomation local tissue effects are minimal.
    a) MYOTOXIC EFFECTS: Myotoxicity includes myalgias with pain on active or passive muscle movement, muscle weakness secondary to pain, muscle stiffness and myoglobinuria. Acute renal failure may develop as a complication of severe muscle injury. Onset of muscle toxicity is generally within 30 minutes to 3.5 hours; in patients with severe envenomation evidence of myotoxicity generally develops within 2 hours. Myoglobinuria is generally evident within 3 to 6 hours after envenomation. Myotoxicity can cause increased CK, ALT, and in severe cases renal insufficiency and hyperkalemia.
    b) NEUROTOXIC EFFECTS: Neurotoxicity can cause ptosis, diplopia, ophthalmoplegia, dysarthria, and dysphagia. Strength in the extremities may be preserved initially, but limb weakness may develop later, and in severe cases it may progress to flaccid paralysis and respiratory failure. Onset can be as rapid as 5 minutes after envenomation or may appear 8 hours or more after the bite.

Laboratory Monitoring

    A) Monitor for evidence of neurotoxicity, including generalized weakness, cranial nerve palsies, depressed deep tendon reflexes, and respiratory compromise. Monitoring negative inspiratory force may provide an early marker for impending respiratory failure.
    B) Monitor renal function, electrolytes, and CK.
    C) Monitor urine output and qualitative urinary myoglobin. Myoglobinuria becomes evident 3 to 6 hours post bite; a dusky yellow color and positive protein and occult blood tests usually precede by an hour or so the red-brown color of spectroscopically positive myoglobinuria.
    D) Monitor ECG in patients with hyperkalemia or significant myotoxicity.

Treatment Overview

    0.4.7) BITES/STINGS
    A) NO OR MILD ENVENOMATION
    1) Patients who are asymptomatic or only have mild symptoms and no laboratory evidence of envenomation should be monitored for a minimum of 12 hours. If a compression bandage has been applied it may be removed when intravenous access is established and the patient is in a facility where intubation and mechanical ventilation can be performed if needed and where antivenom can be administered if needed.
    B) SEVERE ENVENOMATION
    1) Patients with severe symptoms or laboratory evidence of venom-induced myotoxicity or neurotoxicity should be treated with antivenom. If a compression bandage has been applied to a patient who already has symptoms, it should not be removed until the patient has receive antivenom.
    C) ANTIVENOM
    1) Patients with evidence of myotoxicity (muscle pain or tenderness, rhabdomyolysis or myoglobinuria) or neurotoxicity (cranial nerve palsies, muscle weakness, respiratory failure) should be treated with sea snake antivenom. The initial dose is 1 to 3 vials depending on the severity and rapidity of onset of symptoms. Dilute 1 to 10 in isotonic crystalloid and infuse each vial IV over 15 to 30 minutes. Monitor carefully for acute allergic reactions. If sea snake antivenom is unavailable, tiger snake antivenom may be use. Approximately 2 to 4 vials of tiger snake antivenom is considered equivalent to 1 vial of sea snake antivenom. If neither sea snake nor tiger snake antivenom is available, Australian polyvalent antivenom may be used. Be prepared to treat anaphylaxis.
    D) AIRWAY MANAGEMENT
    1) Monitor carefully for evidence of respiratory muscle weakness. Monitoring negative inspiratory force may provide an early marker for impending respiratory failure. Perform endotracheal intubation and provide mechanical ventilation as needed.
    E) RHABDOMYOLYSIS
    1) Administer sufficient 0.9% saline to maintain urine output of 2 to 3 mL/kg/hr. Monitor input and output, serum electrolytes, CK, and renal function. Diuretics may be necessary to maintain urine output. Urinary alkalinization is NOT routinely recommended.
    F) MONITORING OF PATIENT
    1) Monitor for evidence of neurotoxicity, including generalized weakness, cranial nerve palsies, depressed deep tendon reflexes, and respiratory compromise. Monitoring negative inspiratory force may provide an early marker for impending respiratory failure. Monitor renal function, electrolytes, and CK. Monitor urine output and qualitative urinary myoglobin. Myoglobinuria becomes evident 3 to 6 hours post bite; a dusky yellow color and positive protein and occult blood tests usually precede by an hour or so the red-brown color of spectroscopically positive myoglobinuria. Monitor ECG in patients with hyperkalemia or significant myotoxicity.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: There is no role for home management of a possible sea snake bite.
    2) OBSERVATION CRITERIA: All patients with suspected snake bite should be observed for at least 12 hours, with serial laboratory studies (ie, CK, electrolytes, renal function) on admission and every 6 hours thereafter, and careful clinical evaluation for myotoxicity or neurologic toxicity. If there is no clinical or laboratory evidence of envenomation after this time, the patient can be discharged.
    3) ADMISSION CRITERIA: Any patient who develops more than mild clinical signs and symptoms or who develops ANY evidence of myotoxicity or neurologic toxicity should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a clinical toxinologist, medical toxicologist or poison center for any patient with severe envenomation.
    H) TOXICOKINETICS
    1) Onset of envenomation can be quite rapid. Patients who develop systemic envenomation usually do so within 4 to 6 hours. Mild weakness may persist for several weeks.
    I) PITFALLS
    1) The snake is often not seen, so a high index of suspicion is necessary. If pressure immobilization has been applied it should only be removed after the patient has reached a facility where antivenom and the ability to intubate and ventilate the patient is available and an intravenous line established. If the patient has evidence of envenomation antivenom should be administered before the compression dressing is removed.
    J) DIFFERENTIAL DIAGNOSIS
    1) Blue ringed octopus bite, box jellyfish sting (usually painful), stonefish or lionfish stings (usually very painful and true paralysis rare).

Range Of Toxicity

    A) TOXICITY: About 80% of sea snake bites are dry or result in trivial envenomation. Of the remaining 20% of patients, up to 40% or more develop severe envenomation. A bite can be fatal, although fatalities are rare and patients generally survive if timely respiratory support is provided.

Clinical Effects

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) The blood picture is normal apart from leukocytosis (exceeding 20,000 per mm(3)) and changes from hemoconcentration (Reid, 1975).
    B) PLATELET AGGREGATION
    1) WITH POISONING/EXPOSURE
    a) ANIMAL DATA
    1) The venom from two species of Hydrophildae inhibited ADP-induced rabbit platelet aggregation, although with less effect than a variety of viperid and elapid snakes (Oyama & Takahashi, 2007).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SNAKE BITE - WOUND
    1) WITH POISONING/EXPOSURE
    a) Sea snake bites do not cause significant local tissue injury. Mild erythema and bite marks or scratches have been described (Senanayake et al, 2005), but significant swelling, bruising or blebs have not been reported.

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Myalgias are often a prominent complaint (Watt & Theakston, 1985; Patterson & Swallow, 1991). Pain is worse with passive or active movement (Acott, 1986). Muscle stiffness has also been reported.
    B) JOINT PAIN
    1) WITH POISONING/EXPOSURE
    a) Arthralgias have also been reported (Audley, 1985).
    C) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Muscle weakness is a common finding and may be so severe as to prohibit walking or sitting (Patterson & Swallow, 1991; Amarasekera et al, 1994; Watt & Theakston, 1985).
    b) After 6 hours, peripheral paresis may ensue, and later tendon reflexes become depressed then absent. The paresis becomes flaccid; "broken neck" syndrome (from paresis of neck muscles), and inability to sit up result (White, 1995). The patient is usually mentally alert until respiratory failure is far advanced.
    D) SPASM
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: An 18-year-old man was bitten while working on the deck of a fishing trawler. He rapidly developed muscle weakness, retching, and severe, nearly continuous muscle spasms. On arrival at the hospital 7 hours after the bite he had ptosis, a bite mark on his forearm, and intermittent tonic spasms. He received 2 ampoules of sea snake antivenom. He was transferred to an intensive care unit at another hospital about 30 hours after the bite, with persistent ptosis, and intermittent severe extensor spasms and opisthotonus that could be precipitated by stimulation. He had no weakness in between episodes of spasm. He received 2 vials of tiger snake antivenom and diazepam with no effect, and was then sedated with diazepam, paralyzed with pancuronium and ventilated for 2 days. At that time his spasms were less severe and less frequent, and they gradually resolved over the next 3 days. He did not develop myoglobinuria or renal insufficiency (Dobb, 1986).
    E) INJURY OF MUSCLE
    1) WITH POISONING/EXPOSURE
    a) ANIMAL DATA
    1) Phospholipase A2 (PLA2-H1) isolated from the venom of Hydrophis cyanocinctus, induced myonecrosis, and, when injected intraperitoneally, histopathological changes in other tissues, including the kidney, lung, and liver in albino rats and mice (Ali et al, 2000).

Summary Of Exposure

    A) BACKGROUND: Sea snakes are generally found either close to the shore or near coral reefs, with the exception of Pelamis platurus which can be found in deep areas of the ocean. They are found in the oceans around the eastern coasts of Africa and the Middle East, southern and eastern coasts of Asia, all but the southern coast of Australia, throughout Micronesia, Malaysia, and the Philippines, and the Pacific coasts of Central America, Ecuador, southern Columbia, and northern Peru.
    B) TOXICOLOGY: Sea snake venoms contain myotoxins and neurotoxins.
    C) EPIDEMIOLOGY: Bites are probably under reported and occur most commonly in small villages among fisherman who use traditional methods of fishing. In endemic areas of Malaysia, 3% of 68 positively identified venomous snake exposures involved sea snakes.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: About 80% of bites are believed to either be dry or result in trivial envenomation. There is little pain and no erythema or swelling at the bite site, although teeth or scratch marks may be seen.
    2) SEVERE ENVENOMATION: Muscle stiffness and pain, weakness, dizziness, dry mouth, diaphoresis, nausea and vomiting may develop early. Even with severe envenomation local tissue effects are minimal.
    a) MYOTOXIC EFFECTS: Myotoxicity includes myalgias with pain on active or passive muscle movement, muscle weakness secondary to pain, muscle stiffness and myoglobinuria. Acute renal failure may develop as a complication of severe muscle injury. Onset of muscle toxicity is generally within 30 minutes to 3.5 hours; in patients with severe envenomation evidence of myotoxicity generally develops within 2 hours. Myoglobinuria is generally evident within 3 to 6 hours after envenomation. Myotoxicity can cause increased CK, ALT, and in severe cases renal insufficiency and hyperkalemia.
    b) NEUROTOXIC EFFECTS: Neurotoxicity can cause ptosis, diplopia, ophthalmoplegia, dysarthria, and dysphagia. Strength in the extremities may be preserved initially, but limb weakness may develop later, and in severe cases it may progress to flaccid paralysis and respiratory failure. Onset can be as rapid as 5 minutes after envenomation or may appear 8 hours or more after the bite.

Vital Signs

    3.3.2) RESPIRATIONS
    A) Respiratory paralysis is the primary cause of early fatalities.
    3.3.3) TEMPERATURE
    A) FEVER has been reported after envenomation (Watt & Theakston, 1985).
    3.3.4) BLOOD PRESSURE
    A) In most cases of serious poisoning the blood pressure remains normal.

Heent

    3.4.3) EYES
    A) Pupils may be dilated. Failing vision is considered to be a terminal sign.
    B) Patients may report DIPLOPIA or blurred vision secondary to external ophthalmoplegia (Audley, 1985; Amarasekera et al, 1994). Ptosis is another early finding in patients with neurotoxic effects (Amarasekera et al, 1994).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) Some patients with severe myotoxicity may succumb to hyperkalemic cardiac arrest, although this has not been well described. The hyperkalemia is caused by potassium released from damaged muscle.
    B) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Tall peaked T-waves and QRS prolongation suggest severe hyperkalemia. Monitor ECG in patients with myotoxicity.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) Respiratory failure from muscle weakness may occur (Tu, 1987) from within a few hours to as long as 60 hours post bite.
    B) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea has been reported (Patterson & Swallow, 1991).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PARALYSIS
    a) In dogs and monkeys intravenous injection of sea snake venom (Hydrophis cyanocinctus, Enhydrina schistosa and Pelamis platurus) and actual bites by these snakes rapidly produced death by respiratory paralysis, without significant tissue damage or coagulopathy (Vick, 1994).
    b) PARENCHYMAL INJURY
    1) Phospholipase A2 (PLA2-H1) isolated from the venom of hydrophis cyanocinctus, when injected intraperitoneally, produced histopathological changes in the lung at 48 hours which included dilated bronchia and marked infiltration of inflammatory cells within alveoli in albino rats and mice (Ali et al, 2000).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) BULBAR PARALYSIS: Clinical findings may include ptosis, external ophthalmoplegia, diplopia, difficulty swallowing, and slurred speech (Patterson & Swallow, 1991; Amarasekera et al, 1994; Acott, 1986). This may progress to generalized weakness, inability to sit up, and depressed deep tendon reflexes. In severe cases flaccid paralysis and respiratory failure can develop (White, 1995).
    B) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Severe CNS depression is not common, but drowsiness or mild confusion may develop (Audley, 1985; Amarasekera et al, 1994).
    C) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has also been reported (Audley, 1985).
    D) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Numbness may develop in the bitten extremity (Watt & Theakston, 1985).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting and abdominal cramping may develop within minutes of envenomation (Patterson & Swallow, 1991).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) In the liver there are generally no specific changes. AST and LDH may be markedly elevated due to muscle damage (Tu, 1987).
    B) INJURY OF LIVER
    1) WITH POISONING/EXPOSURE
    a) ANIMAL EFFECTS
    1) Phospholipase A2 (PLA2-H1) isolated from the venom of Hydrophis cyanocinctus, when injected intraperitoneally, produced histopathological liver damage after 24 hours as evidenced by fatty infiltration in the parenchyma and squashed hepatocytes, and after 48 hours by fatty vacuolation of parenchyma in a generalized pattern in the liver of albino rats and mice (Ali et al, 2000).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) MYOGLOBINURIA
    1) WITH POISONING/EXPOSURE
    a) Myoglobinuria develops several hours post bite in severe cases (Tu, 1987).
    B) RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Renal failure often results from sea snake envenomation. Death 48 hours or more post-bite is usually due to acute renal failure.
    b) Distal tubular necrosis was found in 3 patients dying more than 48 hours post bite (Reid, 1975). After the first 3 to 4 days following the bite renal failure is the chief hazard. A "fixed" specific gravity of 1.010 to 1.013, together with a low urine volume output, myoglobinuria, and progressively rising blood urea are indicative acute renal failure in the setting of sea snake envenomation.
    C) TOXIC NEPHROPATHY
    1) WITH POISONING/EXPOSURE
    a) ANIMAL DATA
    1) Kidney damage was seen in mice following subcutaneous and intramuscular injections of Alpysurus laevis (Olive sea snake) venom. Renal function returned to normal within two months, but renal lesions persisted for up to 3 months. Renal injury was greater following intramuscular injection, possibly as a result of more rapid absorption (Ryan & Yong, 2002; Ryan & Yong, 1997).
    2) Phospholipase A2 (PLA2-H1) isolated from the venom of Hydrophis cyanocinctus, when injected intraperitoneally, produced severe histopathological changes as evidenced by focal tubular necrosis, complete desquamation of the epithelial lining, and epithelial degeneration of the renal tubules in albino rats and mice (Ali et al, 2000).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ANAPHYLACTOID REACTION
    1) WITH POISONING/EXPOSURE
    a) Some venoms have enzymes which cause the release of histamine, bradykinin and serotonin, which may trigger a serious anaphylactic reaction, but this has not been described with sea snake envenomation.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor for evidence of neurotoxicity, including generalized weakness, cranial nerve palsies, depressed deep tendon reflexes, and respiratory compromise. Monitoring negative inspiratory force may provide an early marker for impending respiratory failure.
    B) Monitor renal function, electrolytes, and CK.
    C) Monitor urine output and qualitative urinary myoglobin. Myoglobinuria becomes evident 3 to 6 hours post bite; a dusky yellow color and positive protein and occult blood tests usually precede by an hour or so the red-brown color of spectroscopically positive myoglobinuria.
    D) Monitor ECG in patients with hyperkalemia or significant myotoxicity.

Methods

    A) IMMUNOASSAY
    1) An ELISA has been developed for the detection of antibodies to Hydrophis cyanocinctus in blood, but is not available for clinical use (Watt & Theakston, 1985).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.6) DISPOSITION/BITE-STING EXPOSURE
    6.3.6.1) ADMISSION CRITERIA/BITE-STING
    A) Any patient who develops more than mild clinical signs and symptoms or who develops ANY evidence of myotoxicity or neurologic toxicity should be admitted to an intensive care setting.
    B) Patients who develop systemic envenomation usually do so within 4 to 6 hours (White, 1995a). Patients who sustain a sea snake bite should be observed in a facility with intensive care capability for 12 hours or more. If no evidence of systemic envenomation (myalgias, myoglobinuria, cranial nerve dysfunction, muscle weakness, etc.) develops during this time they can be discharged. Tourniquets may delay the onset of systemic envenomation (Reid, 1975). Patients in whom a tourniquet or compression bandage was applied should probably be observed for 12 hours after the removal of the tourniquet or compression bandage.
    6.3.6.2) HOME CRITERIA/BITE-STING
    A) There is no role for home management of a possible sea snake bite.
    B) Under no circumstances should the snake be handled. A severe bite may be inflicted for up to an hour, even after decapitation, due to a primitive bite reflex (Visser & Chapman, 1978).
    C) All patients should be taken to the nearest hospital to manage the patient's existing medical condition(s). Ideally, patients should be taken to the nearest hospital that stocks antivenom.
    6.3.6.3) CONSULT CRITERIA/BITE-STING
    A) Consult with a physician experienced in the management of envenomations, whenever possible. Consultation with a regional poison center is appropriate. Poison centers have access to the Online Antivenom Index site and can be reached at 1-800-222-1222 in the US.
    6.3.6.5) OBSERVATION CRITERIA/BITE-STING
    A) All patients with suspected snake bite should be observed for at least 12 hours, with serial laboratory studies (ie, CK, electrolytes, renal function) on admission and every 6 hours thereafter, and careful clinical evaluation for myotoxicity or neurologic toxicity. If there is no clinical or laboratory evidence of envenomation after this time, the patient can be discharged.

Monitoring

    A) Monitor for evidence of neurotoxicity, including generalized weakness, cranial nerve palsies, depressed deep tendon reflexes, and respiratory compromise. Monitoring negative inspiratory force may provide an early marker for impending respiratory failure.
    B) Monitor renal function, electrolytes, and CK.
    C) Monitor urine output and qualitative urinary myoglobin. Myoglobinuria becomes evident 3 to 6 hours post bite; a dusky yellow color and positive protein and occult blood tests usually precede by an hour or so the red-brown color of spectroscopically positive myoglobinuria.
    D) Monitor ECG in patients with hyperkalemia or significant myotoxicity.

Abstracts

Case Reports

    A) ADULT
    1) A 23-year-old man was bitten on the thumb by a black sea snake (later identified as Astrotia stokesii) while trying to remove it from a fishing net. Within 30 minutes he developed pain and numbness radiating up the arm, followed by diffuse joint pain, diplopia, blurred vision, frontal headache and drowsiness. Nine hours after the bite he had increasing drowsiness and confusion. He was treated with one ampoule of sea snake antivenom with little improvement, and then one ampoule of tiger snake antivenom, after which he recovered rapidly (Audley, 1985).
    2) An 18-year-old man was bitten on the forearm while pulling in a fishing net. About 10 minutes later he developed vomiting and muscle spasms. On arrival to medical care 7 hours after the bite, he had ptosis, a bite mark on his arm, intermittent tonic muscle spasms, and an INR of 1.2. He was treated with 2 vials of sea snake antivenom and transferred to another hospital. On arrival 18 hours after envenomation he had persistent ptosis and painful extensor spasms with opisthotonus every 10 to 20 minutes. He received 2 ampoules of tiger snake antivenom with minimal improvement. He was then sedated with benzodiazepines, paralyzed with pancuronium, intubated and mechanically ventilated. After 2 days the spasms were less severe and less frequent so he was extubated. Spasms gradually improved over the next 3 days and he was discharged (Dobb, 1986).
    3) A 19-year-old man was bitten on the right great toe while swimming. He developed immediate pain which spread up the leg, and was dragging the right leg when he came out of the water. Two fang marks were noted on the toe, and a lifeguard applied a pressure immobilization bandage. He developed diplopia, and was transferred to a hospital by ambulance, arriving about 90 minutes after the bite. On arrival at the hospital, he had pain in the right leg, weakness in the right leg and arm, slightly slurred speech, incomplete right facial weakness, and flat facial expression. There was no swelling, tenderness or erythema at the bite site. Weakness continued to progress, and he was given 3000 units of tiger snake antivenom and the compression bandage was then removed. After 30 minutes all weakness resolved. Blood and urine tests remained normal throughout (Fulde & Smith, 1984).
    B) PEDIATRIC
    1) CHILD: A 2-year-old girl was bitten on the left ankle by a sea snake (later identified as Astrotia stokesii) while wading. Her mother used her hands as a tourniquet on the child's leg and took her to an ambulance station. The child looked well, the wound was cleaned and the mother removed her hands from the girl's leg. The girl rapidly became drowsy and developed ptosis, and en route to the hospital vomited and developed respiratory distress. On arrival at the hospital 75 minutes after envenomation, the child was unresponsive, and tolerated laryngoscopy for endotracheal intubation without resistance. She had flaccid paralysis, and dilated sluggishly reactive pupils, and multiple fang marks and lacerations were noted on her foot. She received 1000 units of sea snake antivenom and was transferred to intensive care, where she received 2 further doses of 1000 units 2.5 and 3.5 hours after envenomation. After the third dose, pupils became reactive, she started moving her extremities and made some respiratory effort. Initial laboratory studies showed slightly prolonged coagulation times, leukocytosis, and rhabdomyolysis. About 14 hours after the bite, she had tonic generalized spasmodic movements when touched, and slightly decreased level of consciousness. She received 4 more ampoules of sea snake antivenom, improved and was extubated 22 hours after the bite. Spasms with stimulation continued intermittently and she was noted to hallucinate. CK peaked 2 days after envenomation. She had weakness and gait instability that gradually improved over several weeks (Mercer et al, 1981).
    2) ADOLESCENT: A 16-year-old fisherman was bitten on the hand. Within minutes he had weakness, difficulty walking, abdominal pain, muscle cramping, blurred vision, dyspnea and dysphagia. On hospital arrival 4.5 hours after the bite he had poor visual acuity and pain with passive and active muscle movement. He received 1000 units of sea snake antivenom after arrival and another 1000 units the next day. Symptoms improved after the second dose and he recovered completely (Patterson & Swallow, 1991).

Range Of Toxicity

Summary

    A) TOXICITY: About 80% of sea snake bites are dry or result in trivial envenomation. Of the remaining 20% of patients, up to 40% or more develop severe envenomation. A bite can be fatal, although fatalities are rare and patients generally survive if timely respiratory support is provided.

Minimum Lethal Exposure

    A) SUMMARY
    1) Sea snake venoms are highly toxic. One "drop" (about 0.03 mL) contains enough venom to kill 3 adult men (Reid, 1975). Some sea snake species can eject 7 to 8 such "drops" in a single bite. Taking the minimal lethal dose of E SCHISTOSA venom as 0.05 mg/kg for warm-blooded animals, it is estimated that the minimal lethal dosage for a 70 kg man would be 3.5 mg or about one-third of the venom injected by a fresh adult sea snake (Halstead, 1978).

Maximum Tolerated Exposure

    A) SUMMARY
    1) It is estimated approximately 80% of patients sustaining sea snake bites develop no or trivial envenomation. Of the remaining 20% of patients, up to 40% or more develop severe envenomation (White, 1995a). In endemic areas of Malaysia, 3% of 68 positively identified venomous snake exposures involved sea snakes (White, 1995a).
    2) CASE REPORTS: Sea snake bites were reported in a 7-year-old boy and a 39-year-old man. Other than mild redness at the envenomation site in the adult, both patients were asymptomatic (Senanayake et al, 2005).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) TOXIN A PELAMIS PLATURUS VENOM Mori et al, 1989
    B) TOXIN B PELAMIS PLATURUS VENOM Mori et al, 1989

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Neurotoxins include Erabutoxins (a) and (b).

Toxicologic Mechanism

    A) VENOMS - Sea snake venoms contain hyaluronidase, acetylcholinesterase, leucine aminopeptidase, 5'neucleotidase, phosphomonoesterase, phosphodiesterase, and phospholipase A (Takasaki, 1998; Tu, 1987).
    B) NEUROTOXINS
    1) The neurotoxins act by binding to the alpha subunit of the nicotinic acetylcholine receptors of the neuromuscular junction (Takasaki, 1998). They inhibit acetylcholine induced contraction of skeletal muscle. Sea snake toxins act at both presynaptic and postsynaptic sites (Tu, 1987).
    2) The postsynaptic neurotoxins in sea snake venom are relatively small, highly stable proteins with molecular weights between 6,000 and 8,000 daltons (Tu, 1987).
    3) PELAMIS PLATURUS - This venom contains several neurotoxins, the primary ones are Pelamis toxin a and b. Toxin b contains 60 amino acid residues (one amino acid different from Pelamis toxin a). Toxin b is a postsynaptic neurotoxin which binds to the acetylcholine receptor competitively (Mori et al, 1989).
    4) MYOTOXINS - Incremental doses of Aipysurus laevis (Olive sea snake) venom injected into mouse muscle showed coagulative necrosis and inflammation suggestive of direct myotoxicity (Ryan & Yong, 2002).

Physicochemical

Physical Characteristics

    A) Neurotoxins from sea snake venoms consist of either 60-62 or 70-74 amino acid residues (Tu, 1977).
    B) Sea snake venom is not only simpler in overall protein composition, but also contains fewer enzymes than the venom of land snakes (Tu, 1977).
    C) The phospholipases A2 from Hydrophis cyanocinctus venom were found to be thermostable (60 to 65 degrees C), with a compact folded structure stabilized by disulfide bridges (Ali et al, 2000).

Molecular Weight

    A) Snake venoms may contain dozens of components of varying molecular weights. Two phospholipases A2 from Hydrophis cyanocinctus venom (H1 and H2) were 13588.1 and 13247.2 daltons, respectively (Ali et al, 2000).

References

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