You are in: eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Toxicology Toxicity, SeafoodArticle Last Updated: Jun 21, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 6
  Author: David Pledger, MD, BScHC, FRCP(C), Staff Physician, Department of Emergency Medicine, Greater Victoria Hospital Society David Pledger is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada Coauthor(s): Michael E Mullins, MD, Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine Editors: Michael E Mullins, MD, Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center; Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System; Maureen Strafford, MD, Arnold P Gold Foundation Associate Professor, Departments of Anesthesiology and Pediatrics, Tufts University and Tufts-New England Medical Center Author and Editor Disclosure Synonyms and related keywords: seafood toxicity, seafood poisoning, ciguatera toxicity, ciguatera poisoning, scombroid toxicity, scombroid poisoning, pufferfish toxicity, pufferfish poisoning, tetrodotoxin, TTX, Tetrodon, blowfish toxicity, blowfish poisoning, fugu, sardine toxicity, sardine poisoning, hallucinogenic fish toxicity, hallucinogenic fish poisoning, shellfish toxicity, shellfish poisoning, paralytic shellfish toxicity, paralytic shellfish poisoning, PSP, neurotoxic shellfish toxicity, neurotoxic shellfish poisoning, NSP, brevotoxic shellfish toxicity, brevotoxic shellfish poisoning, diarrheal shellfish toxicity, diarrheal shellfish poisoning, DSP, amnestic shellfish toxicity, amnestic shellfish poisoning, ASP, oyster, abalone, red whelk, echinoderm toxicity, echinoderm poisoning, sea urchin, starfish, asteriotoxin INTRODUCTIONSection 2 of 6
  Seafood poisoning occurs as a result of consumption of fish flesh. Patients with seafood poisoning have highly variable presentations. Ingestion of fish normally known to be safe may occasionally induce illness, and some species of fish cause different syndromes at different periods in time. Severity of symptoms also may be geographically dependent. The scope of seafood poisoning is vast. The intent of this article is not to exhaustively cover all types of seafood poisoning but rather to provide a general overview. Poisoning by viral and bacterial contamination of seafood is not considered here. For excellent patient education resources, visit eMedicine's Poisoning - First Aid and Emergency Center and Wilderness Emergencies Center. FISH POISONINGSection 3 of 6
Ciguatera Ciguatera comprises over 50% of all reported cases of seafood poisoning. This poisoning is endemic in warm waters, spans the globe, and generally is observed between latitudes within 35° of the equator. Ninety percent of cases in the United States occur in Florida and Hawaii. Ciguatera, while once believed to occur only in dark meat fish, occurs in many species; however, it is restricted to larger-sized fish because of the dynamics of the marine food chain. Ciguatera toxin is found in blue-green algae, protozoans, and dinoflagellates. These organisms are ingested by herbivorous fish, which, in turn, are eaten by larger fish. Ciguatera is concentrated in the flesh, adipose tissue, and organs of the larger fish. The toxin is odorless and tasteless, and contaminated fish taste normal. The toxin is heat stable and, thus, may affect people even if fish are prepared properly. Ciguatera toxin is secreted into breast milk and freely crosses the placenta. The toxin is a polyether ladder that binds to and increases the permeability of sodium channels. Symptoms usually are evident within 2-6 hours after ingestion and may last as long as 48 hours. Symptoms generally consist of diaphoresis, abdominal cramps, nausea, vomiting, profuse watery diarrhea, myalgias, arthralgias, weakness, and dysuria. Dyspareunia following intercourse with males who are infected with ciguatera-affected has been reported. Neurologic symptoms tend to occur later (up to 72 h) and may persist for months. These are predominantly paresthesias, but a myriad of other sometimes bizarre neurologic symptoms also may be observed, including sensation of loose painful teeth, tingling in the lips, tongue, throat, and perioral tissues, metallic taste, reversal of temperature sensation, and the sensation of heat in the superficial tissues of the extremities with concomitant sensation of cold in the deeper tissues. Further neurologic symptoms can include vertigo, ataxia, visual changes, and seizures. The widely disparate symptoms make ciguatera poisoning difficult to understand. Symptoms may be more serious in subsequent exposures and with ingestion of alcohol, nuts, and co-ingestion of other noncontaminated fish. The effects of ciguatera may persist for years. In more severe poisonings, bradycardia with hypotension and cardiovascular collapse may occur. Akin to neurologic symptoms, cardiovascular symptoms can persist for months. While ciguatera poisoning can result in death, no fatalities in the United States have been documented. Direct treatment of ciguatera poisoning primarily toward the management of airway, breathing, and circulation (ABC). Charcoal may be of benefit if the patient presents early after exposure. Atropine for symptomatic bradycardia as well as sympathomimetics for cardiovascular support may be necessary. Mannitol has been demonstrated to markedly decrease neurologic and muscular symptoms if administered within 24 hours of exposure. Several mechanisms have been postulated; however, how mannitol helps minimize the effects of neurologic sequelae in ciguatera poisoning is simply not understood. GI symptoms are resistant to treatment with mannitol. Other therapies have been tried with inconsistent results. Both an enzyme-linked immunosorbent assay (ELISA) and high-performance liquid chromatography (HPLC) test are available to confirm the diagnosis of ciguatera poisoning. Scombroid Ingestion of improperly stored seafood causes scombroid poisoning. Decarboxylation of histidine, naturally found on fish, into biogenic amines, such as histamine, occurs at temperatures greater than 15°C. Histamine is not inactivated by heat; therefore, proper cooking is not a remedy for improper storage. Patients sometimes describe a peppery or bitter taste to the fish, but often the fish tastes completely normal. A constellation of symptoms, including skin flushing, throbbing headache, oral burning, abdominal cramps, nausea, diarrhea, palpitations, a sense of unease, and, rarely, prostration or loss of vision characterize scombroid. Symptoms usually occur within 10-30 minutes of ingesting fish and generally are self-limited. Physical signs may include a diffuse blanching erythema, tachycardia, wheezing, and hypotension or hypertension. Persons who are very young or elderly are at particular risk because of lower physiologic reserve. Additionally, persons with asthma are vulnerable because they may experience acute exacerbation of their asthma. Scombroid is second in incidence only to ciguatera poisoning; however, it often is misdiagnosed because it resembles an allergic reaction. The diagnosis is usually made on the basis of the history and physical examination. Laboratory tests are available to measure the concentration of histamine on fish; however, these are generally unnecessary. If blood pressure is abnormal, an ECG may be warranted. Treatment is directed toward supportive care (eg, oxygen, monitor fluids). Histamine1- and histamine2-blockers diminish the effects of histamine. Epinephrine rarely is necessary as the full cascade of mediators of allergic reactions does not occur; thus, symptoms usually are less serious. In rare instances in which patients are seriously ill and present acutely, administering activated charcoal may be of some benefit. Pufferfish poisoning Tetrodotoxin (TTX) causes pufferfish (Tetrodon) poisoning, also known as blowfish poisoning or fugu. TTX is one of the most potent nonprotein poisons found in nature, and exposure can result in rapid death. Symptoms occur within 15 minutes of ingestion but may be observed as late as several hours later. More rapid onset of symptoms is associated with higher levels of toxin ingestion. Symptoms principally are neurologic and cardiovascular in nature and may include perioral tingling, a floating sensation, a feeling of overall warmth, weakness, incoordination, slurred speech, bradycardia, hypotension, and dyspnea. Decreased levels of consciousness, seizures, and death have occurred in as few as 17 minutes. TTX is concentrated in organ meat and gonads. TTX binds specifically to and blocks nerve cell sodium channels. Currently, no antidote exists for TTX. Care is supportive. Gastric lavage and charcoal are indicated in cases of early presentation. Some clinicians have used anticholinesterases (eg, neostigmine, edrophonium) with varying success. Atropine, pressors, and IV fluids can be used for cardiovascular instability. Patients who present with mild symptoms may be observed and discharged at 8 hours if symptoms have diminished. Remember that exposure to TTX does not result in alteration of sensorium; therefore, do not overlook sedation. The incidence of pufferfish poisoning is decreasing, presumably because of heightened awareness and proper preparation of fish. Sardine poisoning Sardine poisoning is rare and episodic. While poorly understood, large numbers of sardines may become toxic at the same time. Anchovies and sprats also may be affected. Geographic distribution is widespread. A feeling of anxiety, bizarre behavior, and skin desquamation may occur. Violent GI symptoms precede paresthesias, muscular contractions, and seizures. Marked dysrhythmias and cardiac arrest have been reported. Mortality may approach 40%. No toxin has been identified, and currently no antidote exists. Treatment is restricted to supportive care. Hallucinogenic fish poisoning Hallucinogenic fish poisoning can occur with the ingestion of a number of fish species. Indoles with similar effects to lysergic acid diethylamide (LSD) have been implicated with sources in algae and plankton. Hallucinations occur in isolation with no other symptomatology. SHELLFISH POISONINGSection 4 of 6
The bulk of shellfish poisonings are infectious in nature. This can be bacterial or viral in nature, with the Norwalk virus likely accounting for the bulk of the gastroenteritides; however, 4 separate types of toxic ingestion have been identified. They are paralytic, neurologic, diarrheal, and amnestic shellfish poisonings. Toxins are found in microscopic diatoms and dinoflagellates with concentrations occurring in filter feeding bivalves, such as clams or mollusks. Contrary to common belief, algal blooms (red tides) are not well correlated to outbreaks of shellfish poisoning. Shellfish poisoning can occur in the absence of a red tide; conversely, red tides do not necessarily mean that shellfish are poisonous. Despite folklore that contends that shellfish are universally safe if eaten during months containing the letter r, correlation between outbreaks of shellfish poisoning and water temperature is poor. The incidence of shellfish poisoning has been declining, most likely because of careful monitoring, beach closures, and improved public awareness. Treatment of shellfish poisoning primarily is supportive but may include the use of isotonic bicarbonate because shellfish toxins are less potent in an alkaline environment. All shellfish toxins are heat stable. Paralytic shellfish poisoning Paralytic shellfish poisoning (PSP) causes the most severe symptoms of all the shellfish poisonings. The causative agent is saxitoxin. PSP usually occurs in outbreaks and is observed most commonly in recreational diggers. PSP exerts its toxicity through sodium channel blockade. Symptoms include paresthesias of the mouth, face, and limbs with nausea, vomiting, and diarrhea. A floating sensation often is described. Dysphonia, ataxia, weakness, and respiratory paralysis can occur within 2-12 hours and may persist for as long as 72 hours. The incidence of requirement for ventilation is 3-6% with a 1-12% fatality rate. Animal research shows some promise for the use of 4-aminopyridine. Carnivorous gastropods accumulate toxins, presumably from the ingestion of toxic bivalves and, in turn, may be a source of toxicity. Neurotoxic shellfish poisoning Neurotoxic shellfish poisoning (NSP), also referred to as brevotoxic shellfish poisoning, is associated with mild GI symptoms as well as facial and limb paresthesias, myalgias, and temperature reversal. No cases of paralysis or death from NSP have been reported. Onset is within 15 minutes but may occur as late as 18 hours with a mean time of 3 hours. Symptoms may persist for several days. NSP is unique in that it aerosolizes in conditions of heavy surf or spray. Symptoms in this setting resemble an upper respiratory tract infection. Diarrheal shellfish poisoning Diarrheal shellfish poisoning (DSP) is a mild poisoning with symptoms restricted to nausea, vomiting, diarrhea, and abdominal pain. Onset is within 30 minutes and may persist for 1 day. Symptoms are self-limited and mild. No cases of death from DSP have been reported. Amnestic shellfish poisoning Amnestic shellfish poisoning (ASP) is a potentially serious poisoning. Diatoms produce domoic acid, which is the causative agent and exhibits glutamatelike activity. Exposure to domoic acid has been demonstrated to cause cellular death in the hippocampus. Symptoms of ASP include nausea, vomiting, diarrhea, loss of cognitive ability, coma, and seizures. A 1987 outbreak of ASP in Canada's eastern province of Prince Edward Island affected more than 100 people. Approximately 50% of patients experienced severe headache, and 25% of patients suffered short-term memory loss, which, for many, was permanent. Of those afflicted, 3% died. Miscellaneous shellfish poisonings Other shellfish poisonings include oyster, abalone, and red whelk poisoning. ECHINODERM POISONINGSection 5 of 6
Sea urchin gonads contain an acetylcholinelike substance that produces the expected constellation of signs and symptoms, including salivation, nausea, vomiting, diarrhea, and abdominal pain. Starfish ingestion may be associated with nausea and vomiting as a result of asteriotoxin. REFERENCESSection 6 of 6
Article Last Updated: Jun 21, 2006 |
