Marine envenomations; Part 1: Vertebrates

The Journal of Emergency Medicine, Vol. 9, pp 497-502, 1991

PrInted In the USA. CopyrIght Q 1991 Pergamon Press plc

MARINE ENVENOMATIONS; PART 1: VERTEBRATES John McGoldrick,

MD,

and John A. Marx,

MD

Department of Emergency Medicine, Denver General Hospital, Denver, Colorado Reprint address: John McGoldrick, MD, Department of Emergency Medicine, Denver General Hospital , 777 Bannock St., Denver CO, 80204

0 Abstract - As more people travel to the oceans for sport diving and other marine related activities, the incidence of marine envenomations has risen. This article is designed to give the emergency physician an overview of varying marine envenomations, their clinical presentation, and recommended treatment. Part 1 of this article addresses general wound management and vertebrate envenomations. Part 2 will concentrate on invertebrate envenomations.

acid for coelenterate envenomation), all wounds should be irrigated with a sterile diluent, such as normal saline. Crushed and devitalized tissue should be excised with sharp dissection and any foreign bodies should be removed. Closure of wounds should take into consideration the need for hemostasis and cosmesis. However, the propensity of marine acquired wounds to become infected dictates that most wounds should be left to heal secondarily. These wounds have been immersed in sea water and sometimes contaminated with bottom sediment and the oral flora of marine animals (2). There is a wide variety of bacteria that have been cultured from sea water, marine sediment, marine animals, and infected wounds of marine origin (2,4-7). Where cosmesis is a particular concern, the principle of delayed primary wound closure may be applied. If a wound becomes infected or sepsis is present, the laboratory should be notified that a marine acquired organism may be present. Special culture media is required for isolation of certain marine organisms (8). Infected wounds should also be cultured for routine aerobes and anaerobes. Management of marine acquired infections should include therapy against Vibrio species. Any patient with a marine acquired wound who develops rapidly progressive cellulitis or myositis should be suspected of having Vibrio parahemolyticus or Vibrio vulnificus infection (8-12). Third generation cephalosporins provide excellent coverage (13). Proper tetanus prophylaxis is indicated.

0 Keywords - marine envenomations; vertebrates; marine antivenins; detoxification

INTRODUCTION Most hazardous marine organisms are found in temperate or tropical oceans, particularly in the Indo-Pacific region. With more people traveling to exotic locales for sport diving and other marine-related activities, and with the increase in private salt water aquariums, the incidence of marine envenomations has risen (1,2). When treating a marine envenomation or wound, the general principles of emergency medicine apply. Occasionally, an envenomation will be accompanied by an allergic reaction and treatment for anaphylaxis will be necessary (3).

GENERAL

WOUND MANAGEMENT

Most envenomations will be secondary to a bite, spine puncture, or abrasion. Table 1 provides a summary of treatment modalities. After any specific detoxification (such as hot water for stingray envenomation or acetic

RECEIVED: 7 August 1990; FINAL SUBMISSIONRECEIVED:27 ACCEPTED: 16 December 1990

VERTEBRATES Table 2 lists the three classes of hazardous marine life.

November

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1990;

0736-4679/91

vertebrate

$3.00 + .OO

John McGoldrick

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Table 1. Treatment of Marine Envenomatlons: Vertebrates Detoxification

Marine Organism Stingray

Catfish Weeverfish

Scorpionfish (Stonefish)

Sea Snake

ED Treatment

Hot water (105°F)

Irrigation with normal saline. Exploration and debridement. Observation for S-4 h to rule out systemic envenomation. Same as outlined for Hot water, 40.5% (105°F) stingray. Hot water, 405°C Same as outlined for stingray. IV calcium (105°F) gluconate if pain persists. Hot water, 405°C Same as outlined for stingray. Stonefish (105°F) antivenin for severe systemic reactions. Limb immobilized in Give polyvalent sea dependent position. snake antivenin for Pressure any evidence of envenomation. immobilization Monitor respiratory bandage. and renal function, and support as needed. If no signs of envenomation after 8 h, patient can be discharged.

Stingrays and Sharks

The order Rajiformes includes the skates and rays (see Figure l), which are fishes having the gills confined to the ventral surface of their bodies (14). They inhabit all

and John A. Marx

temperate and tropical seas and are primarily bottom dwellers. There are 11 species of stingrays found in US coastal waters and an estimated 1500 stingray injuries per year in this country (1). The venom mechanism consists of a bilaterally retroserrate dentinal spine and its enveloping integumentary sheath. Along either edge of the spine are two glandular grooves that house the venom glands. The spine can measure up to 37 cm long. Stingray venom contains many protein fractions including serotonin, 5’-nucleotidase, and phosphodiesterase (1). Venomous sharks include the dogfish shark (Squalus acarhias) and the Port Jackson shark (Heterodontus portusjacksoni). They carry envenomating spines anterior to the two dorsal fins (14,15). It is the sting from the spine that is venomous, not the bite of the shark. CEinical Presenrarion. The clinical syndrome produced by venomous rays and sharks is similar. Stingrays (see Figure 1) are bottom feeders and generally sting in defense when handled, cornered, or stepped on. The tail of the ray thrusts the caudal spine into the victim. A stingray wound can be a significant traumatic injury as well as an envenomation (2). The force of the blow depends on the size of the ray, but it generally produces a puncture wound or jagged laceration. As the spine penetrates the victim, the integumentary sheath covering the spine ruptures releasing venom into the wound (14). Pieces of sheath, fragments of spine, and mucus are frequently left in the wound. Usually the lower extremities of the victim are involved. Fatalities have been reported following thoracic or intraabdomi-

Flgure 1. Stlngray.

Marine

499

Envenomations

Table 2. Hazardous Marine Llfe Phylum Chordata Subphylum Vertebrata (Vertebrates) Class Chondrichthyes; Stingrays, Skates, Sharks Class Osteichthyes: Bony Fishes Catfish, Weeverfish, Scorpionfish Class Reptilia Sea Snakes

Table 3. Marine Antlvenlns” Marine Organism sea snake

(Enhydrina schistosa)

sea snake (E

schistosa)

nal penetration (16-18). Following a sting, there is usually immediate intense local pain out of proportion to the size of the wound. Untreated, the pain may last up to 48 hours. Systemic manifestations of envenomation include weakness, nausea, vomiting, diarrhea, vertigo, tachycardia, headache, syncope, seizures, muscle cramps, fasciculations, hypotension, dysrhythmias, and death (14,19,20). Therapy should attempt to reverse the local and systemic effects of the venom, alleviate pain, and prevent infection. The success of therapy is related to the rapidity with which it is undertaken. The wound should be irrigated with whatever diluent is at hand. In the field this is usually sea water. Any visible pieces of sheath or spine should be removed to decrease the extent of envenomation. Radiographs may be useful in identifying retained pieces of spine (1). As soon as possible, the wound should be soaked in nonscalding hot water to the patient’s tolerance (about 40.5”C [ lOYF]). This is thought to inactivate any heat labile components of the venom and perhaps to help reverse local toxin-induced vasospasm and tissue ischemia (21). This should be continued for 30 to 90 minutes or until the pain is relieved (1,16,22,23). If pain is not controlled with the hot water soak, a regional nerve block or local infiltration with bupivicaine can be performed. The wound should be reirrigated with sterile diluent, explored, and debrided of all necrotic tissue and foreign material. Wounds should be left open for delayed primary closure or healing by secondary intention. Prophylactic antibiotics are controversial, but should be considered in high-risk wounds (19). Highrisk wounds are generally considered to be puncture wounds of the extremities, particularly the hands and feet, and wounds in immunocompromised individuals. If a person is to be treated and released, they should be observed for 3 to 4 hours from the time of envenomation to detect a systemic reaction (1,2). Treatment.

Catfish

There are over 1000 species of catfish (Siluroidei nematognathi). Most of these are freshwater fish, but a few

stonefish

(Syanceja trahynis)

Source Commonwealth Serum Laboratories (CSL) Melbourne, Australia Haffkine Institute, Bombay, India CSL

Comment A polyvalent sea snake antivenin from hyperimmune horse globulin

A monovalent antivenin used to neutralize the bite of most sea snakes antivenin for stonefish and scorpionfish from hyperimmune horse globulin

‘In the United States these antivenins can be obtained from: Health Services Department, Sea World, San Diego, CA.; Sea World, Aurora, OH; Steinhart Aquarium, San Francisco, CA.

are marine (14). The catfish derives its name from the sensory barbels or whiskers around the mouth and possesses a slimy skin without any true scales. The fish range in size from the 275 kg Siluras glanis to the small urinophilus, an Amazonian catfish noted for its ability to penetrate the urethral orifice of mammals, including man (1,2,24). The Egyptian catfish (Malaptem) has electrical organs capable of giving a severe jolt (14). Plotosus linearus, a marine catfish found along the coasts of East Africa, Southeast Asia, Japan, Philippines, Malay archipelago, and Northern Australia, is one of the most dangerous venomous fishes known, and envenomation has caused many fatalities (14). The venom apparatus consists of the dorsal and pectoral fin spines and the axillary venom glands. Both the dorsal and pectoral spines can be locked into an extended position. The spine is enveloped in an integumentary sheath with venom glands beneath the sheath. The axillary glands secrete onto the dorsal aspect of the pectoral spine base. The venom, which has been poorly characterized, contains vasoconstrictive, dermatonectrotic, and other fractions (14,25). Clinical Presentation. Most stings occur when a fish is handled and thus involve the victim’s upper extremities. When the spine penetrates the skin, the integumentary sheath is tom and the glandular venom tissue is exposed. The wound is usually immediately painful, with radiation up the involved extremity. As in stingray envenomations, the pain is out of proportion to the direct mechanical tissue damage (1). A mild envenomation may cause pain for 30 to 60 minutes, while pain may last for 48 hours in a more severe case (26). Described systemic effects include local muscle spasm, fasciculations, diaphoresis, hypotension, syncope, respiratory distress, and death (2,14).

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Treatment. The treatment is the same as outlined for stingray envenomations. Specific antitoxin is unavailable. Weeverj?sh Weeverfish (family Truchinidue) are a group of small marine fishes found in the Mediterranean Sea, eastern Atlantic Ocean, and European coastal areas. They are considered one of the more dangerous venomous fishes, and their stings are extremely painful and sometimes fatal (14). They are generally found hiding in the sand along shallow sandy bottoms. The venom apparatus consists of a series of dorsal spines and two opercular spines located on either side of the head. These spines are enveloped by an integumentary sheath covering the underlying glandular tissue that produces the venom. The venom has been incompletely characterized, but contains several peptides, histamine, catecholamines, and mucopolysaccharide components (27). Weeverfish can survive for hours out of water. Moreover, the toxin remains potent for hours in dead fish (14). Clinical Presentation. It is usually a fisherman handling the fish or an unwary bather swimming or wading along sandy coastal areas who is envenomated. When the spine penetrates the skin the integumentary sheath is tom and the venom glands are exposed. The sting immediately produces severe pain which radiates to the entire limb. The pain usually peaks in 30 minutes and subsides in 24 hours, but may last for days. Systemic manifestations include diaphoresis, nausea, vomiting, headache, delirium, seizures, hypotension, dysrhythmias, syncope, and death (1,14,28). Treatment. The treatment is the same as that outlined for stingray envenomations. Intravenous calcium gluconate has been described as being effective in relieving pain in a case where intravenous narcotics failed (14). Scorpionfish Scorpionfish (family Scorpuenidue) are found in tropical and temperate oceans. There are several hundred species divided into three groups on the basis of venom organ structure: 1) Zebrafish (Pterois), includes the lionfish and turkeyfish; 2) Scorpionfish (Scorpuenu); and 3) Stonefish (Synunceju). The Zebrafish are beautiful coral reef fish that are usually found swimming in shallow water. Scorpionfish live on the bottom in shallow water, bays, and coral reefs. Stonefish live in shallow water, often in tide pools and among reefs.

They are usually found in coral crevices or holes, or are buried in the sand (15,22,29). The venom apparatus consists of 12 to 13 dorsal, 2 pelvic, and 3 anal spines. The pectoral spines are frequently plumelike and ornate, but are not associated with venom glands (14). Each venomous spine is covered with an integumentary sheath, under which venom runs along grooves from the paired venom glands at the base of the spine. It is generally accepted that the most potent venom is that of the stonefish; it has been compared in toxicity to cobra snake venom (26). The principal action of stonefish venom appears to be direct muscle toxicity resulting in paralysis of involuntary and skeletal muscle (30). Envenomation occurs when a spine punctures the skin, tearing the sheath and exposing the venom. The venom retains full potency for at least 24 to 48 hours after the death of the fish (14,31). Clinical Presentation. A sting is usually the result of an unwary diver or fisherman who steps on or handles the fish. In a recent study from the San Francisco Bay Regional Poison Center, there were 51 cases of Scorpaenidae envenomation reported over 5 years. Fortyfive of these were lionfish stings to aquarium owners or fish handlers (31). The puncture wound is immediately painful, with radiation up the affected extremity. The pain usually peaks in 60 to 90 minutes, and resolves in 6 to 12 hours. Pain from a stonefish envenomation may persist for days. The severity of the envenomation varies depending on the species, the amount of venom released, and the age and underlying health of the victim. Systemic manifestations described include anxiety, headache, tremors, maculopapular skin rash, nausea, vomiting, diarrhea, diaphoresis, delirium, seizures, abdominal pain, arthralgia, fever, hypertension, dysrhythmias, syncope, and death (14,32). Treatment. The treatment of the wound is similar to that of stingray injuries. A stonefish antivenin is available for cases of severe systemic reactions. It is a hyperimmune horseserum with 1 mL capable of neutralizing about two stings. It has cross reactivity with other scorpionfish, but is rarely needed outside of stonefish envenomations. The antivenin should be used for any severe systemic manifestations of envenomation. It is manufactured by the Commonwealth Serum Laboratories in Melbourne, Australia (1,2,29) (Table 3). As with any horseserum product, the risks of serum sickness and anaphylaxis must be considered. Sea Snakes There are 52 species of sea snakes, all of which are venomous (14). They are distributed in the tropical and

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temperate Pacific and Indian oceans with the highest number of envenomations in southeast Asia, Malaysia, and the Persian Gulf. There are no sea snakes in the Atlantic Ocean or Caribbean Sea. It is generally thought that sea snakes are docile, but can become aggressive during mating season and when cornered or handled. The venom apparatus consists of 2 to 4 hollow maxillary fangs and a pair of associated venom glands. The venom consists of a variety of protein fractions that have neurotoxic, hemolytic, and myotoxic properties. This results in intravascular hemolysis, skeletal muscle necrosis, and subsequent renal tubular damage (14, 32,33). Clinical Presentation. Most bites are sustained by fisherman who handle snakes caught in their nets or by waders who accidently step on them. It is thought that about one-third to one-half of all sea snake bites do not result in envenomation (14). A sea snake bite characteristically is not painful initially. There are fang marks consisting of multiple pinhead size puncture wounds, usually 1 to 4, but potentially up to 20. The characteristic symptoms of envenomation include painful muscle movement, extremity paralysis, trismus, and ptosis. Symptoms are usually present within one hour, but can be delayed up to 6 to 8 hours. If no symptoms have occurred by 6 to 8 hours, envenomation has not occurred. Severe envenomation is marked by progressively intense symptoms. Myoglobinuria usually becomes evident 3 to 4 hours after envenomation. Respiratory distress, bulbar paralysis, aspiration-related hypoxia, electrolyte disturbances, and acute renal failure all contribute to the ultimate demise. Mortality is 25% in pa-

tients who do not receive antivenin and 3% overall (1,29,32,34). Treatment. The treatment of sea snake envenomation is similar to that of terrestrial snake envenomation. The affected limb should be immobilized and maintained in a dependent position. A pressure immobilization technique for venom sequestration has been popularized in Australia and thought to be effective (35). If the location of the bite permits, a thick gauze pad should be placed directly over the bite wound and held firmly in place by a wide circumferential bandage applied at lymphatic-venous occlusive pressure (70 tort). The arterial circulation should not be occluded, and arterial pulsations and proper capillary refill should be checked frequently. The bandage should be released after two hours or after the victim has been brought to proper medical attention and supportive care is available (1,2, 35). Incision and suction therapy is controversial and is generally not thought to be of value after the initial 5 minutes (1). With any evidence of envenomation, polyvalent sea snake antivenin should be administered intravenously. The amount of antivenin needed depends on the amount of venom injected, but generally 3 to 10 ampules are needed (29). This is a horse serum derivative. Therefore, signs and symptoms of anaphylaxis and serum sickness should be watched for. Respiratory and renal function should be closely monitored and supported as necessary (14). The antivenin is available from the Commonwealth Serum Laboratories in Melbourne, Australia, and the Haffkine Institute in Bombay, India (14,29) (Table 3).

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10. Howard RT, Pessa ME, Brennaman BH, Ramphal R. Necrotizing soft-tissue infection caused by marine vibrios. Surgery. 1985;98:126. 11. Jenkins RD, Johnston JM. Inland presentation of vibrio vulnificus primary septicemia and necrotizing fasciitis. West J Med. 1986;144:78. 12. Johnston JM, Becker SF, McFarland LM. Vibro vulnificus: man and the sea. JAMA. 1985;253:2850. 13. Morris JG, Tenney J. Antibiotic therapy for Vibro vulnificus infection. JAMA. 1985;253:1121. 14. Halstead BW. Poisonous and venomous marine animals of the world. Princeton, NJ. Darwin Press; 1978. 15. Sutherland SK. Venomous creatures of australia. Melbourne: Oxford University Press; 1981. 16. Cross TB. An unusual stingray injury - the skin diver at risk. Med J Aust. 1976;2:947-8. 17. Rathjen WF, Halstead BW. Report on two fatalities due to stingrays. Toxicon. 1969;6:301-2. 18. Ronka EKF, Roe WF. Cardiac wound caused by the spine of the stingray (suborder Musricuru). Milit Surg. 1945;97: 135-7. 19. Grainger CR. Sting ray injuries. Trans R Sot Trop Med Hyg. 1985;79:443-4.

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20. Barss P. Wound necrosis caused by the venom of stingrays. Med J Aust. 1984;141:854. 21. Patten BM. More on catfish stings. JAMA. 1975;232:248. 22. Kiter KW. Marine envenomations. J Toxic01 Clin Toxicol. 1983-84;21:527-55. 23. Rosco MD. Cutaneous manifestations of marine animal injuries including diagnosis and treatment. Cutis. 1977;19:507-10. 24. Scoggin CH. Catfish stings. JAMA. 1975;23:17677. 25. Calton GJ, Burnett JW. Catfish (Icralurus cams) fin venom. Toxicon. 1975;13:39943. 26. Fisher AA. Altas of aquatic dermatology. New York: Grune and Stratton; 1978. 27. Russell FE. Weeverfish sting: the last word. Br Med J. 1983;287: 981-2. 28. Cain D. Weeverfish sting: an unusual problem. Br Med J. 1983;287:406-7.

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29. Auerbach PS. Hazardous marine animals. Emerg Med Clin North Am. 1984;2:5314. 30. Goetz CG. Pharmacology of animal neurotoxins. Clin Neuropharmacol. 1982;5:231-8. 31. Kizer KW, McKinney HE, Auerbach PS. Scorpaendae envenomation: a five year poison center experience. JAMA. 1985;253: 807-10. 32. Southcott RV. Australian venomous and poisonous fishes. Clin Toxicol. 1977;10:291-325. 33. Audley I. A case of sea snake envenomation. Med J Aust. 1985;143:532. 34. Linaweaver PG. Toxic marine life. Milit Med. 1967;113:43742. 35. Anker RC, Straffer WG, Loiselle DS, Anker KM. Retarding the uptake of “mock venoms” in humans: comparison of three first-aid treatments. Med J Aust. 1982;1:212-14.