Disorders Caused by Reptile Bites and Marine Animal Exposures

Reptile Bites

This chapter outlines general principles for evaluation and management of victims of envenomation by venomous snakes and marine creatures. Because the incidence of serious bites and stings is relatively low in developed nations, there remains a paucity of relevant clinical research, and therapeutic decision-making is often based on anecdotal information.

Venomous Snakebite

Venomous snakes of the world belong to the families Viperidae (subfamily Viperinae: Old World vipers; subfamily Crotalinae: New World and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes, and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family, of which most species are nonvenomous and only a few are dangerously toxic to humans). Bite rates are highest in temperate and tropical regions where the population subsists by manual agriculture. Estimates indicate >5 million bites annually by venomous snakes worldwide, with  more than 125,000 deaths.

Snake Anatomy/Identification
The typical snake-venom apparatus consists of bilateral venom glands located below and behind the eye and connected by ducts to hollow, anterior maxillary teeth. In viperids (vipers and pit vipers), these teeth are long mobile fangs that retract against the roof of the mouth when the animal is at rest. In elapids and sea snakes, the fangs are smaller and are relatively fixed in an erect position. In ~20% of pit viper bites and higher percentages of other snakebites (e.g., up to 75% for sea snakes), no venom is released ("dry" bites). Significant envenomation probably occurs in ~50% of all venomous snakebites.
Differentiation of venomous from nonvenomous snake species can be difficult. Viperids are characterized by somewhat triangular heads (a feature shared with many harmless snakes); elliptical pupils (also seen in some nonvenomous snakes, such as boas and pythons); enlarged maxillary fangs; and, in pit vipers, paired heat-sensing pits (foveal organs) on each side of the head. The New World rattlesnakes generally have a series of interlocking keratin plates (the rattle) on the tip of the tail; the rattle is used to warn potentially threatening intruders. Color pattern is notoriously misleading in identifying most venomous snakes. Many harmless snakes have color patterns that closely mimic venomous snakes found in the same region.

Venoms and Clinical Manifestations
Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and metal ions. Among the deleterious components are hemorrhagins that promote vascular leakage and cause both local and systemic bleeding. Proteolytic enzymes cause local tissue necrosis, affect the coagulation pathway at various steps, and impair organ function. Myocardial depressant factors reduce cardiac output, and neurotoxins act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms have multisystem effects in their victims.
Envenomations by most viperids and some elapids with necrotizing venoms typically cause progressive local swelling, pain, ecchymosis (Fig. 391-1), and (over a period of hours or days) hemorrhagic bullae and serum-filled vesicles. In serious bites, tissue loss can be significant (Fig. 391-2). Systemic findings can include changes in taste, mouth numbness, muscle fasciculations, tachycardia or bradycardia, hypotension, pulmonary edema, hemorrhage (from essentially any anatomic site), and renal dysfunction. Envenomations by neurotoxic elapids such as kraits (Bungarus spp.), many Australian elapids [e.g., death adders (Atractaspis spp.) and tiger snakes (Notechis spp.)], some cobras (Naja spp.), and some viperids [e.g., the South American rattlesnake (Crotalus durissus) and some Indian Russell's vipers (Daboia russelii)] cause neurologic dysfunction. Early findings may consist of cranial nerve weakness (e.g., manifested by ptosis) and altered mental status. Severe poisoning may result in paralysis, including the muscles of respiration, and lead to death due to respiratory failure and aspiration. After elapid bites, the time of onset of venom intoxication varies from minutes to hours depending on the species involved, the anatomic location of the bite, and the amount of venom injected. Sea snake envenomation usually causes local pain (variable), myalgias, rhabdomyolysis, and neurotoxicity; these manifestations are occasionally delayed for hours.

Figure 391-1
Figure 391-1
Figure 391-2 Early stages of severe, full-thickness necrosis 5 days after a Russell's viper (Daboia russelii) bite in southwestern India

 Venomous Snakebite: Treatment

Field Management
The most important aspect of prehospital care of a victim bitten by a venomous snake is rapid delivery to a medical facility equipped to provide supportive care (airway, breathing, and circulation) and antivenom administration. Most first aid recommendations made in the past are of little benefit, and some can actually worsen outcome. It is reasonable to apply a splint to the bitten extremity in order to lessen bleeding and discomfort and, if possible, to keep the extremity at approximately heart level. In developing regions, indigenous people should be encouraged to seek care quickly at health care facilities equipped with antivenoms as opposed to consulting traditional healers.
Although mechanical suction has been recommended in the field management of venomous snakebite for many years, there is now evidence that this intervention is of no benefit and can actually be deleterious in terms of local tissue damage.
Techniques or devices used for centuries in an effort to limit venom spread remain controversial. Lympho-occlusive bandages or tourniquets may limit spread only at the cost of greater local tissue damage, particularly with necrotic venoms. Because tourniquets lead to higher rates of amputation and loss of function, they absolutely should not be used. Elapid venoms that are primarily neurotoxic and have no significant local tissue effects may be localized by pressure-immobilization, in which the entire limb is immediately wrapped with a bandage (e.g., crepe or elastic) and then splinted. The wrap pressure must reach ~40–70 mmHg to be effective. Furthermore, if more than a few minutes from medical care, the victim must be carried out from the scene of the bite. Otherwise, muscular pumping will promote venom dispersal, even in bites to the upper extremities. In short, pressure-immobilization should be used only in cases where the offending snake is reliably identified and has a primarily neurotoxic venom, the rescuer is skilled in pressure-wrap application, and the victim can be carried to medical care—an uncommon combination of conditions. Besides tourniquets, other forbidden measures include incising or cooling the bite site, giving the victim alcoholic beverages, and applying electric shocks. The best first aid advice, as coined by Dr. Ian Simpson of the World Health Organization's Snakebite Treatment Group, is to "do it 'RIGHT'": reassure the victim, immobilize the extremity, get to the hospital, and inform the physician of telltale symptoms and signs.

Hospital Management
In the hospital, the victim should be closely monitored (vital signs, cardiac rhythm, oxygen saturation, urine output) while a history is quickly obtained and a rapid, thorough physical examination is performed. Victims of neurotoxic envenomation should be watched carefully for evidence of difficulty swallowing or respiratory insufficiency, which should prompt definitive securing of the airway by endotracheal intubation. To provide objective evidence of the progression of envenomation, the level of swelling in a bitten extremity should be marked and limb circumferences measured in several locations every 15 min until swelling has stabilized. Large-bore IV access in unaffected extremities should be established. Early hypotension is due to pooling of blood in the pulmonary and splanchnic vascular beds. Later, hemolysis and loss of intravascular volume into soft tissues may play important roles. Fluid resuscitation with isotonic saline should be initiated for clinical shock. If the blood pressure response to administration of crystalloid (20–40 mL/kg) is inadequate, a trial of 5% albumin (10–20 mL/kg) is prudent. If tissue perfusion fails to respond to volume resuscitation and antivenom infusion (see below), vasopressors (e.g., dopamine) can be added. Invasive hemodynamic monitoring (central venous and/or pulmonary arterial pressures) can be helpful in such cases, although obtaining access is risky if coagulopathy has developed.
Blood should be drawn for typing and cross-matching and for laboratory evaluation as soon as possible. Important studies include a complete blood count (to evaluate degree of hemorrhage or hemolysis and effects on platelet count), studies of renal and hepatic function, coagulation studies (to identify consumptive coagulopathy), and testing of urine for blood or myoglobin. In developing regions, the 20-min whole-blood clotting test (WBCT) can be used to diagnose coagulopathy reliably. A few milliliters of fresh blood are placed in a new, plain glass receptacle (e.g., test tube) and left undisturbed for 20 min. The tube is then tipped once to 45° to determine whether a clot has formed. If not, coagulopathy is diagnosed. In severe envenomations or with significant comorbidity, arterial blood gas studies, electrocardiography, and chest radiography may be helpful. Any arterial puncture in the setting of coagulopathy, however, requires great caution and must be performed at an anatomic site amenable to direct-pressure tamponade. After antivenom therapy (see below), laboratory values should be rechecked every 6 h until clinical stability is achieved.
The key to management of venomous snakebite is the administration of specific antivenom. Circulating venom components bind quickly with heterologous antibodies produced in animals immunized with the venom in question (or a very closely related venom). Antivenoms may be monospecific (for a particular snake species) or polyspecific (covering several medically important species in the region) but rarely offer cross-protection against snake species other than those used in their production unless the species are known to have homologous venoms. In the United States, assistance in finding antivenom can be obtained 24 h a day from regional poison control centers.
Indications for antivenom administration in victims of viperid bites include any evidence of systemic envenomation (systemic symptoms or signs; laboratory abnormalities) and (possibly) significant, progressive local findings (e.g., soft tissue swelling crossing a joint or involving more than half the bitten limb in the absence of a tourniquet). Care must be used in determining the significance of isolated soft-tissue swelling as, in many countries, the saliva of some relatively harmless snakes causes mild edema at the bite site. In such bites, antivenoms are unhelpful and unnecessary.
In the developing world (e.g., much of Asia and Africa), elapid bites are generally treated similarly to viperid bites. Systemic symptoms such as ptosis, other manifestations of cranial nerve impairment, or respiratory compromise constitute grounds for antivenom administration. Decisions about antivenom administration to victims with isolated local signs or symptoms are based on the criteria listed above for viperid bites.
Production of the only antivenom currently available in the United States for coral snake bites has been discontinued, and remaining stocks will be exhausted or will expire shortly. Until a suitable substitute is produced or imported, physicians caring for victims of Micrurus bites may have to rely on sound supportive care, especially airway management and respiratory support.
The package insert for the selected antivenom can be consulted regarding species covered, method of administration, starting dose, and need (if any) for re-dosing. The information in antivenom package inserts, however, is not always accurate and reliable. Whenever possible, it is advisable for treating physicians to seek advice from experts in snakebite management regarding indications for and dosing of antivenom. For viperid bites, antivenom administration should generally be continued as needed until the victim shows definite improvement (e.g., stabilized vital signs, reduced pain, restored coagulation). Neurotoxicity from elapid bites may be harder to reverse with antivenom. Once neurotoxicity is established and endotracheal intubation is required, further doses of antivenom are unlikely to be beneficial. In such cases, the victim must be maintained on mechanical ventilation until recovery occurs, which may take days to weeks.
The newest available antivenom in the United States (CroFab; Fougera, Melville, NY) is an ovine, Fab fragment antivenom that covers systemic venom effects of all North American pit viper species and carries a low risk of allergic sequelae. Table 391-1 compares the two antivenoms recently available for the treatment of pit viper bites in the United States. The manufacturer of Antivenin (Crotalidae) Polyvalent has recently discontinued its production, leaving CroFab as the current drug of choice for the management of indigenous pit viper envenomations in the United States. Use of any heterologous serum product carries a risk of anaphylactoid reactions and delayed-hypersensitivity reactions (serum sickness). Skin testing for potential allergy is insensitive and nonspecific and should be omitted. Worldwide, the quality and availability of antivenoms are highly variable. In many developing countries, antivenom resources are scarce, contributing to high morbidity and mortality rates in these regions. The rates of acute anaphylactoid reactions to some of these products exceed 50%. If the risk of allergic reaction is significant, pretreatment with appropriate loading doses of IV antihistamines (e.g., diphenhydramine, 1 mg/kg to a maximum of 100 mg; and cimetidine, 5–10 mg/kg to a maximum of 300 mg) may be considered. In some regions, a prophylactic SC or IM dose of epinephrine is given in an effort to reduce the risk of reaction. Further research is necessary to determine whether any pretreatment measures are truly beneficial. Modest expansion of the patient's intravascular volume with crystalloids could blunt an acute adverse reaction.

Table 391-1 Comparison of Antivenoms Recently Available for Treatment of Pit Viper Bites in the United States
Antivenin (Crotalidae) Polyvalenta
Available since
Snakes used in manufacture
Crotalus adamanteus
C. adamanteus
C. atrox
C. atrox
C. durissus terrificus
C. scutulatus
Bothrops atrox
Agkistrodon piscivorus
Snakes covered
All North, Central, and South American and some Asian pit vipers
All North American pit vipers (and possibly other Latin American pit vipers)
IgG, equine albumin
Fab fragments
Skin testing recommended by manufacturer
Pretreatment with antihistamines recommended
Dosing (for North American pit viper bites only)c
Dry bite
0 or 5 vials
4 vials
10 vials
4–6 vials
15–20 vials
6 vials
Repeat dosing
As needed
Repeat starting dose if patient fails to stabilize. After stabilization, give 2 vials q6h for 3 more doses. (Alternatively, re-dose on an as-needed basis with close observation for recurrence of abnormalities.)
Volume of diluent
1000 mLd
250 mL
Administer over
2 h
1 h
Incidence of anaphylactic/-oid reaction
Incidence of delayed serum sickness
  • aWyeth-Ayerst Laboratories, Philadelphia, PA.
  • bFougera, Melville, NY.
  • cDegrees of envenomation: mild = progressive local findings (no systemic findings and normal laboratory tests); moderate = local findings plus either mild systemic findings or mild laboratory abnormalities; and severe = local findings plus either severe systemic findings or severe laboratory abnormalities.
  • dReduce for children and for patients with congestive heart failure.
  • eSome reactions have been severe, and some have been fatal.
  • fTo date, all reactions have been relatively mild.
  • gIncidence is higher with larger doses.

Pretreatment is not recommended by the manufacturer of CroFab. Epinephrine should, however, always be immediately available, and the antivenom dose to be administered should be diluted in an appropriate volume of crystalloid according to the package insert. Antivenom should be given only by the IV route, and the infusion should be started slowly, with the physician at the bedside during the initial period to intervene immediately at the first signs of any acute reaction. The rate of infusion can be increased gradually in the absence of a reaction until the full starting dose has been administered (over a total period of ~1 h). Further antivenom may be necessary if the patient's clinical condition fails to stabilize or worsens. After stabilization, additional doses of CroFab are often recommended as the small-molecular-weight Fab fragments are rapidly cleared from the circulation. Larger, whole IgG or F(ab)2 antivenoms have longer half-lives that eliminate the need for re-dosing after initial stabilization unless definitive symptoms of envenomation reappear.
If the patient develops an acute reaction to antivenom, the infusion should be temporarily stopped and the reaction immediately treated with IM epinephrine and IV antihistamine and steroids. If the severity of envenomation warrants additional antivenom, the dose should be further diluted in isotonic saline and restarted as soon as possible. Rarely, in recalcitrant cases, a concomitant IV infusion of epinephrine may be required to hold allergic sequelae at bay while further antivenom is administered. The patient must be very closely monitored, preferably in an intensive care setting, during such therapy.
Blood products are rarely necessary in the management of the envenomated patient. The venoms of many snake species can cause a drop in platelet count or hematocrit and depletion of coagulation factors. Nevertheless, these components usually rebound within hours after administration of adequate antivenom. If the need for blood products is thought to be great (e.g., for a dangerously low platelet count in a hemorrhaging patient), these products still should be given only after adequate antivenom administration to avoid adding fuel to ongoing consumptive coagulopathy.
Rhabdomyolysis and hemolysis should be managed in standard fashion. Victims who develop acute renal failure should be evaluated by a nephrologist and referred for dialysis (peritoneal or hemodialysis) as needed. Such renal failure, usually due to acute tubular necrosis, is frequently reversible. If bilateral cortical necrosis occurs, however, the prognosis for renal recovery is more grim, and long-term dialysis with possible renal transplantation may be necessary.
Acetylcholinesterase inhibitors (e.g., edrophonium and neostigmine) may promote neurologic improvement in patients bitten by snakes with postsynaptic neurotoxins. Victims with objective evidence of neurologic dysfunction after snakebite should receive a trial of acetylcholinesterase inhibitors as outlined in Table 391-2. If they respond, additional doses of long-acting neostigmine can be continued as needed. Special vigilance is required to prevent aspiration if repetitive dosing of neostigmine is used in an attempt to obviate endotracheal intubation.

Table 391-2 Use of Acetylcholinesterase Inhibitors in Neurotoxic Snake Envenomation
1. Patients with clear, objective evidence of neurotoxicity after snakebite (e.g., ptosis or inability to maintain upward gaze) should receive a trial of edrophonium (if available) or neostigmine.
a. Pretreat with atropine: 0.6 mg IV (children, 0.02 mg/kg; minimum of 0.1 mg)
b. Follow with:
Edrophonium: 10 mg IV (children, 0.25 mg/kg)
Neostigmine: 1.5–2.0 mg IM (children, 0.025–0.08 mg/kg)
2. If objective improvement is evident at 5 min, continue neostigmine at a dose of 0.5 mg (children, 0.01 mg/kg) every 30 min as needed, with continued administration of atropine by continuous infusion of 0.6 mg over 8 h (children, 0.02 mg/kg over 8 h).
3. Maintain vigilance regarding aspiration risk, and secure the airway with endotracheal intubation as needed.

Care of the bite wound includes application of a dry sterile dressing and splinting of the extremity with padding between the digits. Once the administration of an indicated antivenom has been initiated, the extremity should be elevated above heart level to relieve edema. Tetanus immunization should be updated as appropriate. Prophylactic antibiotics are generally unnecessary after bites by North American snakes, as the incidence of secondary infection is low. Antibiotics can be considered, however, if misguided first-aid efforts have included incisions or mouth suction. In some regions of the world, secondary bacterial infection is more common and the consequences are dire. In these regions, prophylactic antibiotics (e.g., cephalosporins) are commonly used.
Most snake envenomations involve subcutaneous deposition of venom. On occasion, however, venom can be injected more deeply into muscle compartments. If swelling in the bitten extremity raises concern that subfascial muscle edema may be impeding tissue perfusion (muscle-compartment syndrome), intracompartmental pressures (ICPs) should be checked by any minimally invasive technique—e.g., wick catheter or ICP monitor (Stryker Instruments, Kalamazoo, MI). If any ICP is high (more than 30–40 mmHg), the extremity should be kept elevated while further antivenom is given. A dose of IV mannitol (1 g/kg) can be given in an effort to reduce muscle edema if the patient's hemodynamic status is stable. If, after 1 h of such therapy, the ICP remains elevated, a surgical consultation for possible fasciotomy should be obtained. While evidence from studies of animals suggests that fasciotomy may actually worsen myonecrosis, compartmental decompression is still required to preserve nerve function. Fortunately, the incidence of muscle-compartment syndrome is very low following snakebite.
Wound care in the days after the bite may require careful aseptic debridement of clearly necrotic tissue once coagulation has been restored. Intact serum-filled vesicles or hemorrhagic blebs should be left undisturbed. If ruptured, they should be debrided with sterile technique.
Physical therapy should be started when pain allows in order to return the victim to a functional state. The incidence of long-term loss of function (e.g., reduced range of motion, impaired sensory function) is unclear but is probably quite high (less than 30%), particularly after viperid bites.
Any patient with signs of venom poisoning should be observed in the hospital for at least 24 h. In North America, a patient with an apparently "dry" viperid bite should be watched for at least 8 h before discharge, as significant toxicity occasionally develops after a delay of several hours. The onset of systemic symptoms is commonly delayed for a number of hours after bites by several of the elapids (including coral snakes), some non–North American viperids [e.g., the hump-nosed pit viper (Hypnale hypnale)], and sea snakes. Patients bitten by these reptiles should be observed in the hospital for at least 24 h. Unstable patients should be admitted to a monitored setting.
At discharge, victims of venomous snakebite should be warned about signs and symptoms of wound infection and serum sickness as well as other potential long-term sequelae, such as pituitary insufficiency in Russell's viper (D. russelii) bites. If the victim had evidence of coagulopathy early on, this abnormality can recur during the first 2–3 weeks after the bite. Such victims should be warned to avoid elective surgery or activities posing a high risk of trauma during this period. Outpatient analgesic treatment and physical therapy should be continued.
In the event of serum sickness (fever, chills, urticaria, myalgias, arthralgias, and possibly renal or neurologic dysfunction developing 1–2 weeks after antivenom administration), the victim should be treated with systemic glucocorticoids (e.g., oral prednisone, 1–2 mg/kg daily) until all findings resolve, at which point the dose is tapered over 1–2 weeks. Oral antihistamines (e.g., diphenhydramine in standard doses) provide additional relief of symptoms.

Morbidity and Mortality
The overall mortality rates for venomous snakebite are low in areas with rapid access to medical care and appropriate antivenoms. In the United States, for example, the mortality rate is  less than 1% for victims who receive antivenom. Eastern and western diamondback rattlesnakes (Crotalus adamanteus and C. atrox, respectively) are responsible for the few snakebite deaths occurring in the United States. Snakes responsible for large numbers of deaths in other regions include cobras (Naja spp.), carpet and saw-scaled vipers (Echis spp.), Russell's vipers (D. russelii), large African vipers (Bitis spp.), lancehead pit vipers (Bothrops spp.), and tropical rattlesnakes (C. durissus).
The incidence of morbidity—defined as permanent functional loss in a bitten extremity—is difficult to estimate but is substantial. Morbidity may be due to muscle, nerve, or vascular injury or to scar contracture. In the United States, such loss tends to be more common and severe after rattlesnake bites than after bites by copperheads (Agkistrodon contortrix) or water moccasins (A. piscivorus).

Marine Envenomations
Management of venom poisoning by marine creatures is similar to that of venomous snakebite in that much of the treatment administered is supportive in nature. A specific marine antivenom can be used when appropriate.

Hydroids, fire coral, jellyfish, Portuguese man-of-war, and sea anemones possess specialized living stinging cells called cnidocytes, which encapsulate intracytoplasmic stinging organelles called cnidae (including nematocysts). The venoms from these organisms are mixtures of proteins, carbohydrates, and other components. Victims usually report immediate prickling or burning, pruritus, paresthesias, and painful throbbing with radiation. The skin becomes reddened, darkened, edematous, and/or blistered. A legion of neurologic, cardiovascular, respiratory, rheumatologic, gastrointestinal, renal, and ocular symptoms have been described. Anaphylaxis sometimes develops. During stabilization, the skin should immediately be decontaminated with a generous application of vinegar (5% acetic acid), which is the all-purpose agent most useful in inactivating the nematocysts. Rubbing alcohol (40–70% isopropyl alcohol), baking soda (sodium bicarbonate), papain (unseasoned meat tenderizer), fresh lemon or lime juice, household ammonia, olive oil, or sugar may be effective, depending on the species of stinging creature.
For the sting of the venomous box-jellyfish (Chironex fleckeri), vinegar should be used. Perfume, aftershave lotion, and high-proof ethanol are not efficacious and may be detrimental; formalin, ether, gasoline, and other organic solvents should not be used. Shaving the skin helps remove remaining nematocysts. Freshwater irrigation and rubbing lead to further stinging by adherent nematocysts and should be avoided. Commercial (chemical) cold packs or real ice packs applied over a thin dry cloth or plastic membrane have been shown to be effective in alleviating mild or moderate Physalia utriculus (bluebottle jellyfish) stings. Recent observations suggest that local application of heat [up to 45°C (113°F)] may be as effective as or more effective than application of cold. After decontamination, application of anesthetic ointment (lidocaine, benzocaine), antihistamine (diphenhydramine), or steroid (hydrocortisone) topical preparations may be helpful. Persistent severe pain after decontamination may be treated with morphine, meperidine, fentanyl, or another narcotic analgesic. Muscle spasms may respond to 10% calcium gluconate (5–10 mL) or diazepam (2–5 mg, titrated upward as necessary) given IV. An ovine-derived antivenom is available from Commonwealth Serum Laboratories (see section on antivenom sources, below) for stings from the box-jellyfish found in Australian and Indo-Pacific waters. As of this writing, this antivenom has not yet been used to treat envenomation by the box-shaped jellyfish (possibly of the genus Chiropsalmus) that has been found in Florida waters. The pressure-immobilization technique is no longer recommended for venom containment in the setting of a jellyfish sting. Safe Sea, a "jellyfish-safe" sunblock (www.nidaria.com) applied to the skin before an individual enters the water, inactivates the recognition and discharge mechanisms of nematocysts, has been tested successfully against a number of marine stingers, and may prevent or diminish the effects of coelenterate stings.
Touching a sea sponge may result in dermatitis. The afflicted skin should be gently dried and adhesive tape used to remove embedded spicules. Vinegar should be applied immediately and then for 10–30 min three or four times a day. Rubbing alcohol may be used if vinegar is unavailable. After spicule removal and skin decontamination, steroid or antihistamine cream may be applied to the skin. Severe vesiculation should be treated with a 2-week course of systemic glucocorticoids.
Annelid worms (bristleworms) possess rows of soft, cactus-like spines capable of inflicting painful stings. Contact results in symptoms similar to those of nematocyst envenomation. Without treatment, pain usually subsides over several hours, but inflammation may persist for up to a week. Victims should resist the urge to scratch, since scratching may fracture retrievable spines. Visible bristles should be removed with forceps and adhesive tape or a commercial facial peel; alternatively, a thin layer of rubber cement can be used to entrap the spines. Use of vinegar, rubbing alcohol, or dilute ammonia or a brief application of unseasoned meat tenderizer (papain) may provide additional relief. Local inflammation should be treated with topical or systemic glucocorticoids.
Sea urchins possess either hollow, venom-filled, calcified spines or triple-jawed, globiferous pedicellariae with venom glands. The venom contains toxic components, including steroid glycosides, hemolysins, proteases, serotonin, and cholinergic substances. Contact with either venom apparatus produces immediate and intensely painful stings. The affected part should be immersed immediately in hot water (see below). Accessible embedded spines should be removed but may break off and remain lodged in the victim. Residual dye from the surface of a spine remaining after the spine's removal may mimic a retained spine but is otherwise of no consequence. Soft tissue radiography or MRI can confirm the presence of retained spines, which may warrant referral for attempted surgical removal if the spines are located near vital structures (e.g., joints, neurovascular bundles). Retained spines may cause the formation of granulomas that are amenable to excision or to intralesional injection with triamcinolone hexacetonide (5 mg/mL). Local and diffuse neuropathies have been observed after penetration by multiple spines of the black sea urchin (Diadema spp.). The pathophysiology of this phenomenon has not yet been determined.
Serious envenomations and deaths have followed bites of the Australian blue-ringed octopuses (Octopus maculosus and O. lunulata). Although these animals rarely exceed 20 cm in length, their venom contains a potent neurotoxin (maculotoxin) that inhibits peripheral nerve transmission by blocking sodium conductance. Oral and facial numbness develop within several minutes of a serious envenomation and rapidly progress to total flaccid paralysis, including failure of respiratory muscles. Immediately after envenomation, a circumferential pressure-immobilization dressing 15 cm wide should be applied over a gauze pad (~7 x 7 x 2 cm) that has been placed directly over the sting. The dressing should be applied at venous-lymphatic pressure, with the preservation of distal arterial pulses. Once the victim has been transported to the nearest medical facility, the bandage can be released. Since there is no antidote, treatment is supportive. If respirations are assisted, the victim may remain awake although completely paralyzed. Even with serious envenomations, significant recovery often takes place within 4–10 h. Sequelae are uncommon unless related to hypoxia.

A stingray injury is both an envenomation and a traumatic wound. The venom, which contains serotonin, 5'-nucleotidase, and phosphodiesterase, causes immediate, intense pain that may last up to 48 h. The wound often becomes ischemic in appearance and heals poorly, with adjacent soft tissue swelling and prolonged disability. Systemic effects include weakness, diaphoresis, nausea, vomiting, diarrhea, dysrhythmias, syncope, hypotension, muscle cramps, fasciculations, paralysis, and (in rare cases) death.
The designation scorpionfish encompasses members of the family Scorpaenidae and includes not only scorpionfish but also lionfish and stonefish. A complex venom with neuromuscular toxicity is delivered through 12 or 13 dorsal, 2 pelvic, and 3 anal spines. In general, the sting of a stonefish is regarded as the most serious (severe to life-threatening); that of the scorpionfish is of intermediate seriousness; and that of the lionfish is the least serious. Like that of a stingray, the sting of a scorpionfish is immediately and intensely painful. Pain from a stonefish envenomation may last for days. Systemic manifestations of scorpionfish stings are similar to those of stingray envenomations but may be more pronounced, particularly in the case of a stonefish sting. The rare deaths following stonefish envenomation usually occur within 6–8 h.
Two species of marine catfish—Plotosus lineatus (the oriental catfish) and Galeichthys felis (the common sea catfish)—as well as several species of freshwater catfish are capable of stinging humans. Venom is delivered through a single dorsal spine and two pectoral spines. Clinically, a catfish sting is comparable to that of a stingray, although marine catfish envenomations are generally more severe than those of their freshwater counterparts. Surgeonfish (doctorfish, tang), weeverfish, ratfish, and horned venomous sharks have also envenomated humans.

Marine Vertebrate Stings: Treatment
The stings of all marine vertebrates are treated in a similar fashion. Except for stonefish and serious scorpionfish envenomations (see below), no antivenom is available. The affected part should be immersed immediately in nonscalding hot water (45°C/113°F) for 30–90 min or until there is significant relief of pain. Recurrent pain may respond to repeated hot-water treatment. Cryotherapy is contraindicated. Opiates will help alleviate the pain, as will local wound infiltration or regional nerve block with 1% lidocaine, 0.5% bupivacaine, and sodium bicarbonate mixed in a 5:5:1 ratio. After soaking and anesthetic administration, the wound must be explored and debrided. Radiography (in particular, MRI) may be helpful in identification of foreign bodies. After exploration and debridement, the wound should be vigorously irrigated with warm sterile water, saline, or 1% povidone-iodine in solution. Bleeding can usually be controlled by sustained local pressure for 10–15 min. In general, wounds should be left open to heal by secondary intention or treated by delayed primary closure. Tetanus immunization should be updated. Antibiotic treatment should be considered for serious wounds and for envenomation in immunocompromised hosts. The initial antibiotics should cover Staphylococcus and Streptococcus spp. If the victim is immunocompromised, if a wound is primarily repaired and is more than minor, or if an infection develops, antibiotic coverage should be broadened to include Vibrio spp.

Approach to the Patient: Marine Envenomations

It is useful to be familiar with the local marine fauna and to recognize patterns of injury.
A large puncture wound or jagged laceration (particularly on the lower extremity) that is more painful than one would expect from the size and configuration of the wound is likely to be a stingray envenomation. Smaller punctures, as described above, represent the activity of a sea urchin or starfish. Stony corals cause rough abrasions and, in rare instances, lacerations or puncture wounds.
Coelenterate (marine invertebrate) stings sometimes create diagnostic skin patterns. A diffuse urticarial rash on exposed skin is often indicative of exposure to fragmented hydroids or larval anemones. A linear, whiplike print pattern appears where a jellyfish tentacle has contacted the skin. In the case of the dreaded box-jellyfish (Fig. 391-3), a cross-hatched, sometimes frosted appearance, followed by development of dark purple coloration within a few hours of the sting, heralds skin necrosis. The frosted appearance may be augmented by aluminum salt–based remedies applied to the wound. An encounter with fire coral causes immediate pain and swollen red skin irritation in the pattern of contact, similar to but more severe than the imprint left by exposure to an intact feather hydroid. Seabather's eruption, caused by thimble jellyfishes and larval anemones, may produce a diffuse rash that consists of clusters of erythematous macules or raised papules, accompanied by intense itching (Fig. 391-4). Toxic sponges create a burning and painful red rash on exposed skin, which may blister and later desquamate. Virtually all marine stingers invoke the sequelae of inflammation, so that local erythema, swelling, and adenopathy are fairly nonspecific.

Figure 391-3
Skin lesions caused by Chironex fleckeri sting.
Figure 391-4 Erythematous, papular rash typical of seabather's eruption caused by thimble jellyfish and larval anemones.

Sources of Antivenoms and Other Assistance
The best way to locate a specific antivenom in the United States is to call a regional poison control center and ask for assistance. Divers Alert Network, a nonprofit organization designed to assist in the care of injured divers, may also help with the treatment of marine injuries. The network can be reached on the Internet at www.diversalertnetwork.org or by telephone 24 hours a day at (919) 684-8111. An antivenom for stonefish (and severe scorpionfish) envenomation is made in Australia by the Commonwealth Serum Laboratories (CSL; 45 Poplar Road, Parkville, Victoria, Australia 3052; www.csl.com.au; 61-3-389-1911). Polyvalent sea snake antivenom is also available from CSL. It is no longer recommended that tiger snake antivenom be used if sea snake antivenom is unavailable.

Marine Poisonings

Ciguatera poisoning is the most common nonbacterial food poisoning associated with fish in the United States; most U.S. cases occur in Florida and Hawaii. The poisoning almost exclusively involves tropical and semitropical marine coral reef fish common in the Indian Ocean, the South Pacific, and the Caribbean Sea. Of reported cases, 75% (except in Hawaii) involve the barracuda, snapper, jack, or grouper. The ciguatera syndrome is associated with at least five polyether sodium channel activator toxins that originate in photosynthetic dinoflagellates (such as Gambierdiscus toxicus) and accumulate in the food chain. Three major ciguatoxins are found in the flesh and viscera of ciguateric fishes: CTX-1, -2, and -3. Most, if not all, ciguatoxins are unaffected by freeze-drying, heat, cold, and gastric acid. None of the toxins affects the odor, color, or taste of fish. Cooking methods may alter the relative concentrations of the various toxins.
The onset of symptoms may come within 15–30 min of ingestion and typically takes place within 2–6 h. Symptoms increase in severity over the ensuing 4–6 h. Most victims develop symptoms within 12 h of ingestion, and virtually all are afflicted within 24 h. The >150 symptoms reported include abdominal pain, nausea, vomiting, diarrhea, chills, paresthesias, pruritus, tongue and throat numbness or burning, sensation of "carbonation" during swallowing, odontalgia or dental dysesthesias, dysphagia, dysuria, dyspnea, weakness, fatigue, tremor, fasciculations, athetosis, meningismus, aphonia, ataxia, vertigo, pain and weakness in the lower extremities, visual blurring, transient blindness, hyporeflexia, seizures, nasal congestion and dryness, conjunctivitis, maculopapular rash, skin vesiculations, dermatographism, sialorrhea, diaphoresis, headache, arthralgias, myalgias, insomnia, bradycardia, hypotension, central respiratory failure, and coma. Death is rare.
Diarrhea, vomiting, and abdominal pain usually develop 3–6 h after ingestion of a ciguatoxic fish. Symptoms may persist for 48 h and then generally resolve (even without treatment). A pathognomonic symptom is the reversal of hot and cold tactile perception, which develops in some persons after 3–5 days and may last for months. Tachycardia and hypertension have been described, in some cases after potentially severe transient bradycardia and hypotension. More severe reactions tend to occur in persons previously stricken with the disease. Persons who have ingested parrotfish (scaritoxin) may develop classic ciguatera poisoning as well as a "second-phase" syndrome (after 5–10 days' delay) of disequilibrium with locomotor ataxia, dysmetria, and resting or kinetic tremor. This syndrome may persist for 2–6 weeks.
The differential diagnosis of ciguatera includes paralytic shellfish poisoning, eosinophilic meningitis, type E botulism, organophosphate insecticide poisoning, tetrodotoxin poisoning, and psychogenic hyperventilation. At present, the diagnosis of ciguatera poisoning is made on clinical grounds because no routinely used laboratory test detects ciguatoxin in human blood. High-performance liquid chromatography (HPLC) is available for ciguatoxins and okadaic acid but is of limited clinical value because most health care institutions do not have the equipment needed to perform the test. A ciguatoxin enzyme immunoassay or radioimmunoassay may be used to test small portions of the suspected fish, but even these tests may not detect the very small amount of toxin (0.1 ppb) necessary to render fish flesh toxic.

Ciguatera Poisoning: Treatment
Therapy is supportive and based on symptoms. Nausea and vomiting may be controlled with an antiemetic, such as prochlorperazine (2.5–5 mg IV). Hypotension may require the administration of IV crystalloid and, in rare cases, a pressor drug. Bradyarrhythmias that lead to cardiac insufficiency and hypotension generally respond well to atropine (0.5 mg IV, up to 2 mg). Cool showers or the administration of hydroxyzine (25 mg PO every 6–8 h) may relieve pruritus. Amitriptyline (25 mg PO twice a day) reportedly ameliorates pruritus and dysesthesias. In three cases unresponsive to amitriptyline, tocainide appeared to be efficacious. Nifedipine has been used to treat headache. IV infusion of mannitol may be beneficial in moderate or severe cases, particularly for the relief of distressing neurologic or cardiovascular symptoms, although the efficacy of this therapy has been challenged and has not been definitively proven. The infusion is rendered initially as 1 g/kg per day over 45–60 min during the acute phase (days 1–5). If symptoms improve, a second dose may be given within 3–4 h and repeated on the following day. Care must be taken to avoid dehydration in the treated patient. The mechanism of the benefit against ciguatera intoxication is perhaps hyperosmotic water-drawing action, which reverses ciguatoxin-induced Schwann cell edema. Mannitol may also act in some fashion as a "hydroxyl scavenger" or may competitively inhibit ciguatoxin at the cell membrane.
During recovery from ciguatera poisoning, the victim should exclude the following from the diet: fish (fresh or preserved), fish sauces, shellfish, shellfish sauces, alcoholic beverages, nuts, and nut oils. Consumption of fish in ciguatera-endemic regions should be avoided. All oversized fish of any predacious reef species should be suspected of harboring ciguatoxin. Neither moray eels nor the viscera of tropical marine fish should ever be eaten.

Paralytic Shellfish Poisoning
Paralytic shellfish poisoning is induced by ingestion of any of a variety of feral or aquacultured filter-feeding organisms, including clams, oysters, scallops, mussels, chitons, limpets, starfish, and sand crabs. The origin of their toxicity is the chemical toxin they accumulate and concentrate by feeding on various planktonic dinoflagellates (e.g., Protogonyaulax, Ptychodiscus, and Gymnodinium) and protozoan organisms. The unicellular phytoplanktonic organisms form the foundation of the food chain, and in warm summer months these organisms "bloom" in nutrient-rich coastal temperate and semitropical waters. These planktonic species can release massive amounts of toxic metabolites into the water and cause mortality in bird and marine populations. The paralytic shellfish toxins are water-soluble as well as heat- and acid-stable; they cannot be destroyed by ordinary cooking. The best-characterized and most frequently identified paralytic shellfish toxin is saxitoxin, which takes its name from the Alaska butter clam Saxidomus giganteus. A toxin concentration of >75 g/100 g of foodstuff is considered hazardous to humans. In the 1972 New England "red tide," the concentration of saxitoxin in blue mussels exceeded 9000 g/100 g of foodstuff. Saxitoxin appears to block sodium conductance, inhibiting neuromuscular transmission at the axonal and muscle membrane levels.
The onset of intraoral and perioral paresthesias (notably of the lips, tongue, and gums) comes within minutes to a few hours after ingestion of contaminated shellfish, and these paresthesias progress rapidly to involve the neck and distal extremities. The tingling or burning sensation later changes to numbness. Other symptoms rapidly develop and include lightheadedness, disequilibrium, incoordination, weakness, hyperreflexia, incoherence, dysarthria, sialorrhea, dysphagia, thirst, diarrhea, abdominal pain, nausea, vomiting, nystagmus, dysmetria, headache, diaphoresis, loss of vision, chest pain, and tachycardia. Flaccid paralysis and respiratory insufficiency may follow 2–12 h after ingestion. In the absence of hypoxia, the victim often remains alert but paralyzed.

Paralytic Shellfish Poisoning: Treatment
Treatment is supportive and based on symptoms. If the victim comes to medical attention within the first few hours after poison ingestion, the stomach should be emptied by gastric lavage and then irrigated with 2 L (in 200-mL aliquots) of a solution of 2% sodium bicarbonate; this intervention has not been proved to be of benefit but is based on the notion that gastric acidity may enhance the potency of saxitoxin. Because breathing difficulty can be rapid in onset, induction of emesis is not advised. The administration of activated charcoal (50–100 g) and a cathartic (sorbitol, 20–50 g) makes empirical sense since these shellfish toxins are believed to bind well to charcoal. Some authors advise against administration of magnesium-based solutions (e.g., certain cathartics), cautioning that hypermagnesemia may contribute to suppression of nerve conduction.
The most serious problem is respiratory paralysis. The victim should be closely observed in a hospital for at least 24 h for respiratory distress. With prompt recognition of ventilatory failure, endotracheal intubation and assisted ventilation prevent anoxic myocardial and brain injury.
A direct human serum assay to identify the toxin responsible for paralytic shellfish poisoning is not yet clinically available; the mouse bioassay in widespread use may be replaced by an automated tissue culture bioassay. Polyclonal enzyme-linked immunosorbent assay (ELISA) to measure specific toxins is under development, as is fluorimetric HPLC.

Domoic Acid Intoxication (Amnestic Shellfish Poisoning)
In late 1987 in eastern Canada, an outbreak of gastrointestinal and neurologic symptoms (amnestic shellfish poisoning) was documented in persons who had consumed mussels found to be contaminated with domoic acid. In this outbreak, the source of the toxin was Nitzschia pungens, a diatom ingested by the mussels. In 1991, an epidemic of domoic acid poisoning in the state of Washington was attributed to the consumption of razor clams. A heat-stable neuroexcitatory amino acid whose biochemical analogues are kainic acid and glutamic acid, domoic acid binds to the kainate type of glutamate receptor with three times the affinity of kainic acid and is 20 times as powerful a toxin. Shellfish can be tested for domoic acid by mouse bioassay and HPLC. The regulatory limit for domoic acid in shellfish is 20 parts per million.
The abnormalities noted within 24 h of ingesting contaminated mussels (Mytilus edulis) include arousal, confusion, disorientation, and memory loss. The median time of onset is 5.5 h. Other prominent symptoms include severe headache, nausea, vomiting, diarrhea, abdominal cramps, hiccoughs, arrhythmias, hypotension, seizures, ophthalmoplegia, pupillary dilation, piloerection, hemiparesis, mutism, grimacing, agitation, emotional lability, coma, copious bronchial secretions, and pulmonary edema. Histologic study of brain tissue taken at autopsy has shown neuronal necrosis or cell loss and astrocytosis, most prominently in the hippocampus and the amygdaloid nucleus—findings similar to those in animals poisoned with kainic acid. Several months after the primary intoxication, victims still display chronic residual memory deficits and motor neuronopathy or axonopathy. Nonneurologic illness does not persist.

Domoic Acid Intoxication: Treatment
Therapy is supportive and based on symptoms. Since kainic acid neuropathology seems to be nearly entirely seizure-mediated, an emphasis should be placed on anticonvulsive therapy, for which diazepam appears to be as effective as any other drug.

Scombroid Poisoning
Scombroid (mackerel-like) fish include the albacore, bluefin, and yellowfin tuna; mackerel; saury; needlefish; wahoo; skipjack; and bonito. Nonscombroid fish that produce scombroid poisoning include the dolphinfish (Hawaiian mahimahi, Coryphaena hippurus), kahawai, sardine, black marlin, pilchard, anchovy, herring, amberjack, and Australian ocean salmon. In the northeastern and mid-Atlantic United States, bluefish (Pomatomus saltatrix) has been linked to scombroid poisoning. Because greater numbers of nonscombroid fish are being recognized as scombrotoxic, the syndrome may more appropriately be called pseudoallergic fish poisoning.
Under conditions of inadequate preservation or refrigeration, the musculature of these dark- or red-fleshed fish undergoes bacterial decomposition, which includes decarboxylation of the amino acid L-histidine to histamine, histamine phosphate, and histamine hydrochloride. Histamine levels of 20–50 mg/100 g are noted in toxic fish, with levels >400 mg/100 g on occasion. However, it is possible that some other compound may be responsible for this intoxication, since large doses of oral histamine do not reproduce the affliction. Whatever toxin(s) are involved are heat-stable and are not destroyed by domestic or commercial cooking. Affected fish typically have a sharply metallic or peppery taste; however, they may be normal in appearance, color, and flavor. Not all persons who eat a contaminated fish necessarily become ill, perhaps because of uneven distribution of decay within the fish.
Symptoms develop within 15–90 min of ingestion and include flushing (sharply demarcated; exacerbated by ultraviolet exposure; particularly pronounced on the face, neck, and upper trunk), a sensation of warmth without elevated core temperature, conjunctival hyperemia, pruritus, urticaria, angioneurotic edema, bronchospasm, nausea, vomiting, diarrhea, epigastric pain, abdominal cramps, dysphagia, headache, thirst, pharyngitis, gingival burning, palpitations, tachycardia, dizziness, and hypotension. Without treatment, the symptoms generally resolve within 8–12 h. Because of blockade of gastrointestinal tract histaminase, the reaction may be more severe in a person who is concurrently ingesting isoniazid.

Scombroid Poisoning: Treatment
Therapy is directed at reversing the histamine effect with antihistamines, either H-1 or H-2. If bronchospasm is severe, an inhaled bronchodilator—or in rare, extremely severe circumstances, injected epinephrine—may be used. Glucocorticoids are of no proven benefit. Protracted nausea and vomiting, which may empty the stomach of toxin, may be controlled with a specific antiemetic, such as prochlorperazine. The persistent headache of scombroid poisoning may respond to cimetidine or a similar antihistamine if standard analgesics are not effective.

Further Readings
  1. Auerbach PS (ed): Wilderness Medicine, 5th ed. St. Louis, Mosby, 2007
  2. Bush SP, Hardy DL: Immediate removal of Extractor is recommended. Ann Emerg Med 38:607, 2001 [PMID: 11679882]
  3.  et al: Effects of a negative pressure venom extraction device (Extractor) on local tissue injury after artificial rattlesnake envenomation in a porcine model. Acad Emerg Med 7:495, 2000
  4. Dart RC et al: A randomized multicenter trial of Crotalinae polyvalent immune Fab (ovine) antivenom for the treatment for crotaline snakebite in the United States. Arch Intern Med 161:2030, 2001 [PMID: 11525706] 
  5. Gold BS et al: Bites of venomous snakes. N Engl J Med 347:347, 2002 [PMID: 12151473]
  6. Mebs D: Venomous and Poisonous Animals. Boca Raton, FL, CRC Press, 2002
  7. Meier J, White J (eds): Handbook of Clinical Toxicology of Animal Venoms and Poisons. Boca Raton, FL, CRC Press, 1996, pp 89–176
  8. Meyer WP et al: First clinical experiences with a new ovine Fab Echis ocellatus snake bite antivenom in Nigeria: Randomized comparative trial with Institute Pasteur Serum (Ipser) Africa antivenom. Am J Trop Med Hyg 56:291, 1997 [PMID: 9129531]
  9. Pearn J: Neurology of ciguatera. J Neurol Neurosurg Psychiatry 70:4, 2001 [PMID: 11118239]
  10. Simpson ID, Norris RL: Snakes of medical importance in India: Is the "big 4" still relevant and useful? Wilderness Environ Med 18:2, 2007 [PMID: 17447706]
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