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Snake Envenomation, Sea

Author: Dimitrios Papanagnou, MD, MPH, Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center
Coauthor(s): Susi U Vassallo, MD, FACEP, FACMT, Assistant Professor of Emergency Medicine, New York University School of Medicine/Bellevue Hospital Center
Contributor Information and Disclosures

Updated: Nov 6, 2008

Introduction

Background

Sea snakes, venomous elapid snakes that inhabit marine environments, are the most abundant and widely dispersed group of poisonous reptiles in the world. 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.1 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. They are typically about 1 m in length, but some species may grow to 3 m.

Sea snakes are found in warm coastal waters, predominantly in tropical and subtropical waters in the western Pacific and Indian Oceans. 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.

Yellow-belly pelagic sea snake.

Yellow-belly pelagic sea snake.

Yellow-belly pelagic sea snake.

Yellow-belly pelagic sea snake.


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.2

Pathophysiology

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.

Frequency

United States

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

International

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.

Mortality/Morbidity

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

Race

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.

Sex

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

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

Clinical

History

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

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

  • Fang marks (usually 2 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)

Causes

  • Occupational exposure - Usually fishermen handling nets
  • Accidental exposure - Stepping on sea snakes in shallow water
  • Nonaccidental exposure - Intentionally handling sea snakes (eg, home aquariums)

More on Snake Envenomation, Sea

Overview: Snake Envenomation, Sea
Differential Diagnoses & Workup: Snake Envenomation, Sea
Treatment & Medication: Snake Envenomation, Sea
Follow-up: Snake Envenomation, Sea
Multimedia: Snake Envenomation, Sea
References

References

  1. Food and Agriculture Organization. Sea Snakes. United Nations; August 2007. [Full Text].

  2. Ditmars RL. The MacMillan Company. Reptiles of the World, Revised Edition. 1933:329, pp 89.

  3. Auerbach PS. Marine envenomations. N Engl J Med. Aug 15 1991;325(7):486-93. [Medline].

  4. Auerbach PS. Marine envenomations. In: Auerbach PS, ed. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 3rd ed. Mosby-Year Book; 1995:1327-74.

  5. Baxter EH, Gallichio HA. Cross-neutralization by tiger snake (Notechis scutatus) antivenene and sea snake (Enhydrina schistosa) antivenene against several sea snake venoms. Toxicon. May 1974;12(3):273-8. [Medline].

  6. Chetty N, Du A, Hodgson WC, et al. The in vitro neuromuscular activity of Indo-Pacific sea-snake venoms: efficacy of two commercially available antivenoms. Toxicon. Aug 2004;44(2):193-200. [Medline].

  7. Dunson WA. The Biology of Sea Snakes. Baltimore, Md: University Park Press; 1975.

  8. Guenin DG, Auerbach PS. Trauma and envenomations from marine fauna. In: Tintinalli, et al, eds. Emergency Medicine: A Comprehensive Study Guide. 4th ed. McGraw-Hill; 1996:868-73.

  9. Heatwole H. Sea Snakes. Krieger Publishing Company; 1999.

  10. Minton SA Jr. Paraspecific protection by elapid and sea snake antivenins. Toxicon. Jul 1967;5(1):47-55. [Medline].

  11. Pinney R. Sea snakes. Reptile & Amphibian. 1994;26:22-34.

  12. Reid HA. Antivenom in sea-snake bit poisoning. Lancet. Mar 15 1975;1(7907):622-3. [Medline].

  13. Reid HA. Epidemiology of sea-snake bites. J Trop Med Hyg. May 1975;78(5):106-13. [Medline].

  14. Reid HA, Chan KE. The paradox in therapeutic defibrination. Lancet. Mar 9 1968;1(7541):485-6. [Medline].

  15. Senanayake MP, Ariaratnam CA, Abeywickrema S. Two Sri Lankan cases of identified sea snake bites, without envenoming. Toxicon. Jun 1 2005;45(7):861-3. [Medline].

  16. Tu AT. Biotoxicology of sea snake venoms. Ann Emerg Med. Sep 1987;16(9):1023-8. [Medline].

  17. Tu AT, Fulde G. Sea snake bites. Clin Dermatol. Jul-Sep 1987;5(3):118-26. [Medline].

  18. Vick JA. Medical studies of poisonous land and sea snakes. J Clin Pharmacol. Jun 1994;34(6):709-12. [Medline].

Further Reading

Keywords

sea snake envenomation, sea snake bite, sea snakes, snake bite, Hydrophiidae, Pelamis platurus, P platurus, Enhydrina schistosa, E schistosa, sea snake venom, neurotoxins, myotoxins, snake envenomations, sea snake neurotoxin, sea snake wound

Contributor Information and Disclosures

Author

Dimitrios Papanagnou, MD, MPH, Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center
Dimitrios Papanagnou, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Student Association/Foundation, and Emergency Medicine Residents Association
Disclosure: Nothing to disclose.

Coauthor(s)

Susi U Vassallo, MD, FACEP, FACMT, Assistant Professor of Emergency Medicine, New York University School of Medicine/Bellevue Hospital Center
Susi U Vassallo, MD, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, New York Academy of Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert L Norris, MD, Associate Professor, Department of Surgery; Chief, Division of Emergency Medicine, Stanford University Medical Center
Robert L Norris, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, California Medical Association, International Society of Toxinology, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

James Steven Walker, DO, MS, Clinical Professor of Surgery, Department of Surgery, University of Oklahoma Health Sciences Center
James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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