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  3. Clinical entry: Sea snakes

Clinic: Sea snakes

Examine for venom effects

Local Effects

  • Pain
  • Tender local (spreading) swelling

Neurological effects

  • Descending flaccid paralysis (rarely progresses to involve bulbar and respiratory muscles):
    • Ptosis (not to be mixed up with tiredness / drowsiness; test: lid retraction with upward gaze).
    • Double vision (external ophthalmoplegia)
    • Difficulties to swallow (dysphagia) (bulbar paralysis) > inhalation of vomitus!
    • Difficulties to lift the head when lying on the back (‘broken neck syndrome’)
    • Cyanosis, shallow breathing, respiratory arrest (respiratory paralysis); respiratory arrest may be precipitated by obstruction of the upper airway by the paralysed tongue or inhaled vomitus. 
    • Weakness or loss of voluntary movement; movements of digits may still be possible, allowing the patient to communicate.
    • Loss of consciousness and generalized convulsions caused by hypoxaemia in patients who have respiratory paralysis.  

Muscular effects

  • Generalized rhabdomyolysis:
    • Muscles pain and tenderness, painful on passive stretching, muscle stiffness, trismus
    • Bulbar and respiratory muscle weakness.
    • Dark brown urine. 
    • Renal failure
    • Laboratory: Generalized rhabdomyolysis: defined by a serum creatine kinase level > 10,000 U/l
    • ECG: Signs of hyperkalaemia.

Species-specific envenoming pattern

The assessment of the envenoming pattern is based on the data from publication in which the identification of the snakes is clearly specified and in accordance with accepted criteria. 

   Local
effects1
 		 Neurological effects2 Musular effects3

Hydrophis cyanocinctus

      

Hydrophis schistosus (described as Enhydrina schistosa)

      

Hydrophis semperi

   ?  ? 

Hydrophis spiralis

      
Hydrophis stokesii (described as Astrotia stokesii)   ?

Hydrophis zweifeli (described as Enhydrina schistosa, Australia)

      

Laticauda colubrina

      

The largest series of patients with sea snake envenoming is described from Penang/Malaysia (Reid 1975a,b,c):
Patients were included in the clinical part of this study if they had systemic symptoms of envenoming after E. schistosa (=Hydrophis schistosus) (16 patients), Hydrophis cyanocinctus (3 patients) and Hydrophis spiralis (3 patients) bites.
The great majority of bites were caused by E. schistosa (=Hydrophis schistosus). In the years 1957–1964, 101 patients who had suffered bites conclusively determined as being caused by a sea snake were cared for under the direction of A. Reid, most in Penang General Hospital. In only 10 cases was the snake available for identification: E. schistosa (=Hydrophis schistosus) 7, H. cyanocinctus 1, H. spiralis 1, Kerilia jerdoni (=Hydrophis jerdoni) 1. 71 patients identified the snake that had bitten them by choosing from amongst live sea snakes that were shown to them. This gave the following results: E. schistosa (=Hydrophis schistosus) 55/101, H. cyanocinctus 14/101, H. spiralis 9/101, K. jerdoni 1/101 (=Hydrophis jerdoni), Lapemis hardwickii 2/101, not identified 20/101.

Time interval between the bite and admission to hospital:
≤0.5 h: 5/101; 1 of whom died,
0.5–1 h: 8/101; 1 of whom died,
1–2 h: 15/101; no deaths,
2–4 h: 27/101; no deaths,
4–6 h: 27/101; no deaths,
6–10 h: 11/101; 3 of whom died,
>10 h: 8/101; 3 of whom died. 

Species suspected of using brackish waters is based, but without confirmation in the literature, on Murphy (2012): Pseudonaja spp, Tropidechis spp.. This could lead to misclassification of evenoming in brakish waters. 

1Local effect

“The bite is usually painless and may not be noticed by the wader or swimmer. Minimal or no local swelling.” (Warrell 2023).
Initial stabbing pain (Reid 1975a, 1979) 

2Neurological effects

Neurological effects are rarely reported, predominately from Australia (Johnston et al. 2022; Mercer et al. 1996; Tiemensma et al. 2021). 

3Muscular effects

"Generalized rhabdomyolysis is the dominant effect of envenoming. Generalized aching, stiffness and tenderness of the muscles becomes noticeable between 30 minutes and 3.5 hours after the bite. Trismus is common. Passive stretching of the muscles is painful. Later, there is progressive flaccid paralysis starting with ptosis, as in elapid envenoming. The patient remains conscious until the respiratory muscles are sufficiently affected to cause respiratory failure. Myoglobinaemia and myoglobinuria develop 3–8 hours after the bite. These are suspected when the serum/plasma appears brownish and the urine dark reddish brown (‘Coca-Cola-coloured’). ‘Stix’ tests will appear positive for haemoglobin/blood in urine containing myoglobin. Myoglobin and potassium released from damaged skeletal muscles may cause renal failure, while hyperkalaemia developing within 6–12 hours of the bite may precipitate diastolic cardiac arrest.“ (Warrell 1994, 2023)
Cardiac dysrhythmias and renal failure secondary to ‘Muscular effects’ (Reid 1975a,b,c, 1979).
Also: Johnston et al. (2022), Marsden and Reid (1961), Reid (1961b)
In the 13 cases described by Johnston et al. (2022) from Australia, in only two was the culprit identified (Hydrophis zweifeli). One patient had non-specific systemic symptoms, and one patient was not envenomed.

Publications reporting broadly on Australian sea snake envenoming and treatment

Johnston et al. (2022), Sutherland and Tibballs (2001), Warrell (1994), White (1995). 

Species-specific publications 
see ‘References’ at the end of the file.

Clinical management

See also Clinical Management: sea snakes

for advice on post-First Aid measures, diagnosis (clinical, laboratory) and treatment (supportive, antivenom).

First Aid

Any type of tourniquet follow link above.

Local treatment

Pain control
Tetanus prophylaxis
Standard wound care
WHO (2010) 

Systemic supportive treatment

A general understanding of emergency medicine is required, or can be found in emergency medicine guidelines, e.g. ABCDE approach, WHO-ICRC Basic Emergency Care.

Follow SAMPLE & ABCDE ApproAch

Obey Seasnake - specific features

see

  • 'Species-specific envenoming pattern above'.

and

Key issues

Respiratory failure

  • Airway management
  • Breathing: Oxygen ⇨ assisted ventilation ⇨ mechanical ventilation

ABCDE-approch is lifesaving as supportive treatment until the antivenom applied acts or when antivenom is not available or fails.

Rhabdomyolysis, hyperkalaemia and hypercalcaemia

See footnote 3 above.

Specific treatment (antivenoms)

Guidance and guidelines

References

  • Chiew AL, Buckley NA, Graudins A, Munir VL. Review article: Up (to) date for Australian Toxicology and Toxinology guidelines. Emerg Med Australas. 2021 Feb;33(1):6-8. Epub 2020 Oct 29. PMID: 33124195. https://doi.org/10.1111/1742-6723.13663
  • Isbister GK, Brown SG, Page CB, McCoubrie DL, Greene SL, Buckley NA. Snakebite in Australia: a practical approach to diagnosis and treatment. Med J Aust. 2013 Dec 16;199(11):763-8. PMID: 24329653. https://doi.org/10.5694/mja12.11172
  • Isbister GK. The critical time period for administering antivenom: golden hours and missed opportunities. Clin Toxicol (Phila). 2024 May;62(5):277-279. Epub 2024 May 28. PMID: 38804828. https://doi.org/10.1080/15563650.2024.2352026
  • Isbister GK. Antivenom availability, delays and use in Australia. Toxicon X. 2022 Dec 8;17:100145. PMID: 36523639; PMCID: PMC9747507. https://doi.org/10.1016/j.toxcx.2022.100145
  • Johnston CI, Tasoulis T, Isbister GK. Australian Sea Snake Envenoming Causes Myotoxicity and Non-Specific Systemic Symptoms - Australian Snakebite Project (ASP-24). Front Pharmacol. 2022 Mar 21;13:816795. PMID: 35387331; PMCID: PMC8977552. https://doi.org/10.3389/fphar.2022.816795
  • MARSDEN AT, REID HA. Pathology of sea-snake poisoning. Br Med J. 1961 May 6;1(5235):1290-3. PMID: 13767157; PMCID: PMC1954083. https://doi.org/10.1136/bmj.1.5235.1290
  • Mercer HP, McGill JJ, Ibrahim RA. Envenomation by sea snake in Queensland. Med J Aust. 1981 Feb 7;1(3):130-2. PMID: 7219284. https://doi.org/10.5694/j.1326-5377.1981.tb135383.x
  • Murphy JC. Marine invasions by non-sea snakes, with thoughts on terrestrial-aquatic-marine transitions. Integr Comp Biol. 2012 Aug;52(2):217-26. Epub 2012 May 10. PMID: 22576813. https://doi.org/10.1093/icb/ics060
  • REID HA. Myoglobinuria and sea-snake-bite poisoning. Br Med J. 1961b May 6;1(5235):1284-9. PMID: 13740487; PMCID: PMC1954109. https://doi.org/10.1136/bmj.1.5235.1284
  • Reid HA. Epidemiology of sea-snake bites. J Trop Med Hyg. 1975a May;78(5):106-13.PMID: 1152101.
  • Reid HA. Antivenom in sea-snake bite poisoning. Lancet. 1975b Mar 15;1(7907):622-3. PMID: 47960. https://doi.org/10.1016/s0140-6736(75)91897-8
  • Reid, H.A., 1975c. Epidemiology and clinical aspects of sea snake bites. In:Dunson, W.A., (Ed.), The Biology of Sea Snakes,University Park Press, Baltimore, pp. 417–462
  • Reid, H.A. (1979) Symptomatology, Pathology and Treatment of the Bites of Sea Snakes. In: Lee, CY. (eds) Snake Venoms. Handbook of Experimental Pharmacology, vol 52. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66913-2_25
  • Snakebite. In: Toxicology and Toxinology. Therapeutic Guidelines. 3rd ed. Melbourne: Therapeutic Guidelines Ltd; 2020.
  • Sutherland and Tibballs. Australian animal toxins: the creatures, their toxins, and care of the poisoned patient. Second ed. South Melbourne: Oxford University Press; 2001.
  •  Tiemensma M, Byard RW. Fatal Sea Snake Envenomation. Am J Forensic Med Pathol. 2021 Dec 1;42(4):401-404. PMID: 33833198. https://doi.org/10.1097/paf.0000000000000679
  • Warrell DA. Sea snakebites in the Asia-Pacific region. In: Gopalkrishnakone P, editor. Sea Snake Toxinology. Singapore: Singapore University Press; 1994:1–36.
  • Warrell DA. Venomous and poisonous animals. In: Farrar J, Garcia PJ, Hotez T, Junghanss T, Kang G, Laloo D (eds.).Manson’s tropical diseases. 24th ed. Elsevier; 2023.
  • Warrell DA, Williams DJ. Clinical aspects of snakebite envenoming and its treatment in low-resource settings. Lancet. 2023 Apr 22;401(10385):1382-1398. PMID: 36931290. https://doi.org/10.1016/s0140-6736(23)00002-8
  • White J. Clinical toxicology of snakebite in Australia and New Guinea. In: Meier J, White J, editors. Handbook of clinical toxicology of animal venoms and poisons. New York: CRC Press, 1995: 595-618.
  • WHO ABCDE Approach. https://cdn.who.int/media/docs/default-source/integrated-health-services-(ihs)/csy/bec-quick-cards/becp-edu29-pdf-en-finl.pdf?sfvrsn=2532d61b_2
  • WHO-ICRC Basic Emergency Care: approach to the acutely ill and injured. https://www.who.int/publications-detail-redirect/basic-emergency-care-approach-to-the-acutely-ill-and-injured. https://cdn.who.int/media/docs/default-source/integrated-health-services-(ihs)/csy/bec-quick-cards/becp-edu29-pdf-en-finl.pdf?sfvrsn=2532d61b_2
  • WHO Snakebite Information and Data Platform. https://www.who.int/teams/control-of-neglected-tropical-diseases/snakebite-envenoming/snakebite-information-and-data-platform
  • WHO (2010) Wound and lymphoedema management. WHO/HTM/NTD/GBUI/20101 I. 2010. https://www.who.int/publications/i/item/9789241599139
  • WHO (2016) Guidelines for the management of snakebites. 2nd edition (Australasian elapids)  https://www.who.int/publications/i/item/9789290225300

Species-specific evidence

Hydrophis schistosus (described as Enhydrina schistosa), Hydrophis cyanocinctus, Hydrophis spiralis

Malaysia (Penang)

  • Reid (1975a,b,c)  
    Patients were included in the clinical part of this study if they had systemic symptoms of envenoming after E. schistosa (=Hydrophis schistosus) (16 patients), Hydrophis cyanocinctus (3 patients) and Hydrophis spiralis (3 patients) bites.
    The great majority of bites were caused by E. schistosa (=Hydrophis schistosus). In the years 1957–1964, 101 patients who had suffered bites conclusively determined as being caused by a sea snake were cared for under the direction of A. Reid, most in Penang General Hospital. In only 10 cases was the snake available for identification: E. schistosa (=Hydrophis schistosus) 7, H. cyanocinctus 1, H. spiralis 1, K. jerdoni (=Hydrophis jerdoni) 1. 71 patients identified the snake that had bitten them by choosing from amongst live sea snakes that were shown to them. This gave the following results: E. schistosa 55/101, H. cyanocinctus 14/101, H. spiralis 9/101, K. jerdoni 1/101, Lapemis hardwickii 2/101, not identified 20/101.
    Proportion of the individual genera of 4,735 sea snakes that were caught over a distance of up to 10 miles from the coast of Penang Island between 1960 and 1963: E. schistosa (=Hydrophis schistosus) 2,403, H. cyanocinctus 1,074, H. spiralis 349, K. jerdoni 188, L. hardwickii 115.
    Circumstances of the bite: only 12/101 patients were not fishermen. Of these 12, 10 were bitten while swimming, although all 10 were not actually swimming but rather wading at the time they were bitten.
    Classification: for the definition of no/mild/severe/fatal envenoming, see below "Signs and symptoms".
    Enhydrina schistosa (=Hydrophis schistosus)
    No envenoming: 39/55,
    Mild envenoming: 4/55,
    Severe envenoming: 5/55,
    Fatal envenoming: 7/55.
    For comparison, cases of envenoming caused by the other genera:
    Hydrophis cyanocinctus
    No envenoming: 11/14, mild envenoming: 2/14, severe envenoming: 1/14.
    Hydrophis spiralis
    No envenoming: 6/9, mild envenoming: 3/9.
    Kerilia jerdoni (=Hydrophis jerdoni)
    No envenoming: 1/1.
    Lapemis hardwickii
    No envenoming: 2/2.
    Not identified
    No envenoming: 9/20, mild envenoming: 2/20, severe envenoming: 8/20, fatal envenoming: 1/20.
    Time interval between the bite and admission to hospital:
    ≤0.5 h: 5/101; 1 of whom died,
    0.5–1 h: 8/101; 1 of whom died,
    1–2 h: 15/101; no deaths,
    2–4 h: 27/101; no deaths,
    4–6 h: 27/101; no deaths,
    6–10 h: 11/101; 3 of whom died,
    >10 h: 8/101; 3 of whom died.
  • Reid (1957)
    Enhydrina schistosa (=Hydrophis schistosus)
    Identification: morphological; Reid himself was bitten.
  •  Reid (1962)  
    Enhydrina schistosa (=Hydrophis schistosus)
    Identification: morphological.

Signs & symptoms

Enhydrina schistosa (=Hydrophis schistosus), (Hydrophis cyanocinctus, Hydrophis spiralis)

Local effects
Apart from an initial stabbing pain, no local signs or symptoms! (Reid 1975a,b,c, 1979).

Muskular effects
Mild envenoming
In most cases no clinical signs or symptoms apart from elevated serum AST (see below "Laboratory and physical investigations").
In some cases onset of myalgia within 0.5–3.5 h after the bite. Myalgia never very marked and remains localised in around half the cases, in the other half it becomes generalised within 0.5 h. 1–4 h after the bite moderate pain may be caused by passive movement of the skeletal musculature. Symptoms disappear completely within 1–3 days.

Severe envenoming
In these cases the latency period before the onset of symptoms of envenoming is always <2 h (if no efficient tourniquet was applied after the bite). The symptoms correspond to those of mild envenoming with the difference that they start earlier and are more severe. Symptoms become generalised after 0.5 h. Dysphagia and dysphonia very marked.
At the physical investigation 1–2 h after the bite the patient lies in bed with arms bent and legs outstretched. Passive movements are very painful. Neurological investigations (grip and pinch strength, deep tendon reflexes) are normal in most cases.
Dark, red, brown or black urine first becomes evident after 3–8 h.
After several more hours actual (flaccid) paralysis (of the peripheral type) may occur: ptosis, ophthalmoplegia, inability to stick out the tongue or swallow and to keep the head upright. Posture can no longer be controlled. Deep tendon reflexes can no longer be elicited. Respiratory distress may occur due to the impairment of the respiratory musculature. However, patients are generally fully conscious.

Course (if no antivenom administered)
The myalgia and myoglobinuria reach a maximum 1 week after the bite. Paralyses continue to deteriorate during this period. Grip and pinch strength returns in the 3rd week, anddeep tendon reflexes in the 3rd or 4th week.

Fatal envenoming
Aspiration may occur due to glossopharyngeal paralysis. Respiratory failure due to paralysis of the respiratory musculature can occur between several and up to 60 h after the bite.
Hyperkalaemiain the early stages of envenoming (myonecrosis)
Cardiac effects and acute renal failure somewhat later in the course of envenoming may also cause severe complications and death (Reid 1975a, 1979).

Cardiac effects
Cardiac dysrhythmias (secondary, see above "Muscular effects") (Reid 1975ab,c, 1979).

Renal effects
Renal failure (secondary, see above "Muscular effects") (Reid 1975a,b,c, 1979).

Other signs and symptoms
Nausea, vomiting, headache (Reid 1975a,b,c, 1979).

Morbidity

Without antivenom it can take several months for a patient who suffers severe envenoming to be restored to full health. In the first month after the bite the symptoms are similar to those of a muscular dystrophy. Later on the patient is able to make a firm fist and to raise themselves from a lying to a sitting position. Even after 1.5 years there may be mild residual muscle weakness. Irreversible damage of the skeletal musculature is possible, particularly if the muscles are used again too soon and the preserved sarcolemmal sheaths, which are crucial structures for muscle regeneration, are torn.
Renal failure (Reid 1975a,b,c).

Case fatality rate

7/55 patients who were bitten by E. schistosa according to the above-mentioned criteria.
At the time when no antivenom was available, mortality from sea snake bites was estimated at 10%. However, if only the cases of severe envenoming (see above for definition) are considered, around 50% (6/11) died in the pre-antivenom era. Once antivenom became available, 20% (2/10) of the patients with severe envenoming died, although these patients were already moribund upon arrival at hospital (Reid 1975a,b,c).

Laboratory and physical investigations

Leucocytes
In severe envenoming generally >20,000/mm³ (Reid 1975a,b,c). 
Serum urea, creatinine 
Elevated as a consequence of myonecrosis and acute renal insufficiency (Reid 1975a,b,c). 
Serum potassium 
Elevated as a consequence of myonecrosis and acute renal insufficiency (Reid 1975a,b,c). 
AST (GOT), CPK
These enzymes are released from the damaged skeletal muscles and are very sensitive indicators of sea snake envenoming. Their levels do not correlate with the severity of envenoming.
Mild envenoming: serum AST significantly increased over 1–3 days (Reid 1975a,b,c).
CPK isoenzymes: 93,200 IU/l (MM 100%, MB 0%, BB 0%) (Hydrophis cyanocinctus; Higa et al. 1990).
Myoglobin
Detectable in serum and urine (Reid 1975a, b). 
Serum myoglobin: 11,200 ng/ml (normal <70 ng/ml) (Hydrophis cyanocinctus; Higa et al. 1990). 
Myoglobin in the urine: 660 ng/ml (normal <20 ng/ml) (Hydrophis cyanocinctus; Higa et al. 1990).

ECG
Signs of hyperkalaemia (Reid 1975a,b,c).

Muscle biopsy - histology
Extensive hyaline necrosis. Individual muscle fibres may be affected while directly adjacent fibres remain undamaged. Within a single muscle fibre only one to a few segments are affected. There is usually an abrupt transition between damaged and undamaged segments within a single muscle fibre. The sarcolemma remains intact (E. schistosa ((=Hydrophis schistosus)) Marsden and Reid 1961). The autopsied cases had all been bitten by E. schistosa (=Hydrophis schistosus) according to the above-mentioned criteria.

Renal biopsy - histology
Acute tubular necrosis (Marsden and Reid 1961: the autopsied cases had all been bitten by E. schistosa according to the above-mentioned criteria)

Treatment (supportive)

  1. Immobilisation to guarantee undisturbed regeneration of the skeletal musculature.
  2. Maintenance of sufficient hydration levels and diuresis. 
  3. Lowering of increased serum potassium.
  4. Endotracheal intubation, artificial respiration.
  5. Dialysis. Besides the renal insufficiency, dialysis also improved the symptoms in the skeletal musculature (Sitprija et al. 1971: the species of sea snake that caused the accidents were not identified).
  6. Neostigmine appears to be ineffective in the cases observed by Reid. 

Japan

  • Higa et al. (1990) 
    Hydrophis cyanocinctus
    Identification: morphological.

Sri Lanka

  • Kularatne SA, Hettiarachchi R, Dalpathadu J, Mendis AS, Appuhamy PD, Zoysa HD, Maduwage K, Weerasinghe VS, de Silva A. Enhydrina schistosa (Elapidae: Hydrophiinae) the most dangerous sea snake in Sri Lanka: three case studies of severe envenoming. Toxicon. 2014 Jan;77:78-86. Epub 2013 Nov 12. PMID: 24239658. https://doi.org/10.1016/j.toxicon.2013.10.031
    3 cases, 1/3 fatal case.

Hydrophis semperi

Philippines (Lake Taal: freshwater lake!)

  • Watt and Theakston (1985)
    8 patients were retrospectively identified as having been bitten by H. semperi. Criteria: the patients stated that the bite was caused by a sea snake. 
    In 3/5 antibodies to H. cyanocinctus (ELISA) (Theakston et al. 1981) were found in the blood.
    Only H. semperi Hydrophiidae were found in Lake Taal. It was reported that one patient died several days after being bitten by a sea snake.

Signs & symptoms
Muscular effects
Myalgia 5/8, pareses 4/8 (Watt and Theakston 1985).
The data from this study do not make it possible to clearly attribute the pareses to a myotoxic and/or neurotoxic effect of the venom.

Hydrophis stokesii (described as Astrotia stokesii)

Australia

  • Audley (1985) 
    1 A. stokesii bite. Identification: morphological.
  • Mercer et al. (1981)
    Case description
    1 A. stokesii bite. Identification: morphological.

Signs & symptoms

Neurological effects

Ptosis developed within 30 s after the mother loosened her grip on the child's lower leg, which had obviously acted like a tourniquet. Directly afterwards respiratory distress developed. Only 4 min after the onset of symptoms (20 min after the bite) the child was cyanotic, unconscious and displayed tonic movements of the extremities. After intubation and under adequate respiration with good circulatory and respiratory conditions, flaccid paralysis and hyperreflexia were present, but not the Babinski sign. 14 h after the bite, after initial improvement of the neurological symptoms under antivenom treatment, spasmodic generalised tonic cramps as soon as the child was touched (Mercer et al. 1981).
Diplopia (Audley 1985).

Muscular effects
After approximately 50 h (after the paralysis of the respiratory musculature had been corrected and the child had already been extubated for approx. 24 h) a marked instability of the lower extremities occurred simultaneously with the maximum CPK level and myoglobinuria (see below). The gait disorder improved within 2 weeks. One month after the bite the child was functioning completely normally again except for an unstable gait when tired (Mercer et al. 1981).

Other signs and symptoms
Hallucinations (Mercer et al. 1981), cerebral confusion (Audley 1985).

Laboratory and physical investigations
Leucocytes
Leucocytosis 27,200/mm³ (Mercer et al. 1981).
Myolysis
Serum enymes changes reflecting skeletal muscle damage (without myocardial involvement), maximum approx. 50 h after the bite. At this point myoglobinuria also developed (Mercer et al. 1981).
ECG
Normal (Mercer et al. 1981).

First Aid

The mother's firm grip on the child's lower leg acted as an efficient tourniquet. Thirty seconds after she loosened her grip the full neurological effects of the venom became apparent (Mercer et al. 1981).

Hydrophis zweifeli

Australia

  • Johnston et al. (2022)
    Report on myotoxicity and non-specific systemic symptoms caused by Australian sea snake envenoming 

Laticauda colubrina

  • Tiemensma and Byard (2021)
    1 patient with fatal outcome.

References

  • Audley I. A case of sea-snake envenomation. Med J Aust. 1985 Nov 25;143(11):532. PMID: 4069058. https://doi.org/10.5694/j.1326-5377.1985.tb119935.x
  • Higa, H., H. Uezato, Y. Araki (1990) A case of sea snake bite in Okinava, Japan. Snake 22: 100-105
  • Johnston CI, Tasoulis T, Isbister GK. Australian Sea Snake Envenoming Causes Myotoxicity and Non-Specific Systemic Symptoms - Australian Snakebite Project (ASP-24). Front Pharmacol. 2022 Mar 21;13:816795. PMID: 35387331; PMCID: PMC8977552. https://doi.org/10.3389/fphar.2022.816795
  • Kularatne SA, Hettiarachchi R, Dalpathadu J, Mendis AS, Appuhamy PD, Zoysa HD, Maduwage K, Weerasinghe VS, de Silva A. Enhydrina schistosa (Elapidae: Hydrophiinae) the most dangerous sea snake in Sri Lanka: three case studies of severe envenoming. Toxicon. 2014 Jan;77:78-86. Epub 2013 Nov 12. PMID: 24239658. https://doi.org/10.1016/j.toxicon.2013.10.031
  • MARSDEN AT, REID HA. Pathology of sea-snake poisoning. Br Med J. 1961 May 6;1(5235):1290-3. PMID: 13767157; PMCID: PMC1954083. https://doi.org/10.1136/bmj.1.5235.1290
  • Mercer HP, McGill JJ, Ibrahim RA. Envenomation by sea snake in Queensland. Med J Aust. 1981 Feb 7;1(3):130-2. PMID: 7219284. https://doi.org/10.5694/j.1326-5377.1981.tb135383.x
  • REID, H. A. (1956a). Sea snake bites. BMJ, 2, 73.
  • REID HA. Sea-snake bite research. Trans R Soc Trop Med Hyg. 1956b Nov;50(6):517-38; discussion, 539-42. PMID: 13391905.
  • Reid, H. A. (1956c) Three fatal cases of sea snakebite. In Buckley, E. E., N. Porges: Venoms. American association for the advancement of science, Washington 44: 367-371 https://doi.org/10.1016/0035-9203(56)90057-8
  • REID HA. Antivenene reaction following accidental sea-snake bite. Br Med J. 1957 Jul 6;2(5035):26-9. PMID: 13436851; PMCID: PMC1961644. https://doi.org/10.1136/bmj.2.5035.26
  • REID HA. Diagnosis, prognosis, and treatment of sea-snake bite. Lancet. 1961a Aug 19;2(7199):399-402. PMID: 13740486 https://doi.org/10.1016/s0140-6736(61)92483-7 
  • REID HA. Myoglobinuria and sea-snake-bite poisoning. Br Med J. 1961b May 6;1(5235):1284-9. PMID: 13740487; PMCID: PMC1954109. https://doi.org/10.1136/bmj.1.5235.1284
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