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CLUPEOTOXIC FISH POISONING

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Cluepotoxism is a form of ichthyosarcotoxism (the toxin found within the flesh) caused by fishes of the order Clupeiformes, which includes the families Clupeidae, the herrings, and Engraulidae, the anchovies.

Specific Substances

    1) Clupeotoxism
    2) Ichthyosarcotoxism
    3) Clupeiformes
    4) Clupeidae
    5) Herring
    6) Engraulidae
    7) Anchovies
    8) Elopidae
    9) Tarpons
    10) Albulidae
    11) Bonefishes
    12) Pterothrissidae
    13) Deepsea bonefishes
    14) Alepocephalidae
    15) Deepsea slickheads
    16) FISH POISONING, CLUPEOTOXIC

Available Forms Sources

    A) SOURCES
    1) Clupeotoxin is believed to originate in the food chain since all fishes that have been incriminated in human biotoxications have a reputation as being edible.
    2) Cluepotoxism is a form of ichthyosarcotoxism (the toxin found within the flesh) caused by fishes of the order Clupeiformes, which includes the families Clupeidae, the herrings, and Engraulidae, the anchovies. These two families are most commonly incriminated in human intoxications.
    3) The families Elopidae, the tarpons, Albulidae, the bonefishes, Pterothrissidae, the deepsea bonefishes, and Alepocephalidae, the deepsea slickheads have been implicated.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DESCRIPTION: Clupeotoxism is a form of ichthyosarcotoxism (the toxin found within the flesh) caused by ingesting fishes of the order Clupeiformes (sardines, herrings, anchovies, tarpons, bone fishes, and slickheads).
    B) TOXICOLOGY: The exact nature of the toxin is unknown. Clupeotoxism results from eating contaminated fish especially the viscera.
    C) EPIDEMIOLOGY: Since clupeotoxism is not a reportable disease, there are no reliable data available regarding either the incidence or mortality rate. The incidence of clupeotoxism seems to be seasonal, occurring most often in the warm, summer months (July-September in northern latitudes). Cooking procedures, salting, and drying will not prevent intoxication. Clupeotoxism is an unpredictable public health problem of the tropical Atlantic Ocean, Caribbean Sea, and tropical Pacific Ocean. The mortality rate of clupeotoxism is thought to be much higher than that of other forms of ichthyosarcotoxism.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Initially, metallic taste followed by vomiting, dry mouth, excessive salivation, diarrhea, muscle cramps, and abdominal pain may occur. Pruritus, desquamation, ulceration, and cold,clammy skin have also been reported. Neurologic effects include violent headaches, malaise, numbness and tingling, and vertigo.
    2) SEVERE TOXICITY: Tachycardia, feeble pulse, hypotension, cyanosis, muscular paralysis, seizures, coma, and death have all been described. Death can occur within minutes of ingestion of contamination fish.

Laboratory Monitoring

    A) Specific testing for toxins are unavailable at this time.
    B) Monitor vital signs and mental status.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    D) Obtain an ECG, and institute continuous cardiac monitoring as necessary.
    E) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea and/or vomiting. Manage mild hypotension with IV fluids. Treat headaches with analgesics. Treat pruritus and urticarial dermatitis with antihistamines.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Support respiratory and cardiovascular function. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur.
    C) DECONTAMINATION
    1) PREHOSPITAL: ORAL EXPOSURE: Prehospital gastrointestinal decontamination is not recommended. DERMAL EXPOSURE: Remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists after washing. EYE EXPOSURE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. if irritation, pain swelling, lacrimation or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    2) HOSPITAL: Activated charcoal may be considered in very rare cases with severe toxicity that develops soon after ingestion, provided that the patient is not vomiting and the airway is protected. Gastric lavage or whole bowel irrigation are generally not recommended given the risk of complications including aspiration.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with CNS depression or respiratory failure secondary to muscle paralysis. Continuous pulse oximetry and end tidal CO2 monitoring should be employed.
    E) ANTIDOTE
    1) None.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with severe symptoms following an ingestion of fish of the order Clupeiformes should seek medical attention.
    2) OBSERVATION CRITERIA: Asymptomatic exposures can be discharged home after 4 to 6 hours of observation, given the usual rapid onset of symptoms.
    3) ADMISSION OF CRITERIA: Patients with cardiac or persistent symptoms should be admitted overnight for further monitoring.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing severe poisonings or differentiation of symptoms from other fish related poisonings.
    5) TRANSFER CRITERIA: Patients with severe toxicity or hemodynamic instability should be transferred to an intensive care setting.
    G) PITFALLS
    1) Clupeotoxic fish poisoning can be life-threatening and may warrant an intensive care setting. The onset of symptoms is rapid and may be fatal within minutes.
    H) TOXICOKINETICS
    1) Signs and symptoms may appear within a few minutes following ingestion.
    I) PREDISPOSING CONDITIONS
    1) Given the dose-response nature of the toxicity, small children may have higher risk, given the same dosage of toxin. Elderly patients with comorbid conditions, especially cardiovascular disease, may be at higher risk for cardiac failure.
    J) DIFFERENTIAL DIAGNOSIS
    1) Palytoxin, palytoxin analogues ("ostreocines"), ciguatera, scombroid, paralytic shellfish poisoning, gastroenteritis, enterotoxigenic infections (eg, shigellosis, hemolytic uremic-syndrome).

Range Of Toxicity

    A) TOXICITY: Toxicity is not dependent on the size of the fish. The viscera are the most toxic part of the fish.

Clinical Effects

Summary Of Exposure

    A) DESCRIPTION: Clupeotoxism is a form of ichthyosarcotoxism (the toxin found within the flesh) caused by ingesting fishes of the order Clupeiformes (sardines, herrings, anchovies, tarpons, bone fishes, and slickheads).
    B) TOXICOLOGY: The exact nature of the toxin is unknown. Clupeotoxism results from eating contaminated fish especially the viscera.
    C) EPIDEMIOLOGY: Since clupeotoxism is not a reportable disease, there are no reliable data available regarding either the incidence or mortality rate. The incidence of clupeotoxism seems to be seasonal, occurring most often in the warm, summer months (July-September in northern latitudes). Cooking procedures, salting, and drying will not prevent intoxication. Clupeotoxism is an unpredictable public health problem of the tropical Atlantic Ocean, Caribbean Sea, and tropical Pacific Ocean. The mortality rate of clupeotoxism is thought to be much higher than that of other forms of ichthyosarcotoxism.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Initially, metallic taste followed by vomiting, dry mouth, excessive salivation, diarrhea, muscle cramps, and abdominal pain may occur. Pruritus, desquamation, ulceration, and cold,clammy skin have also been reported. Neurologic effects include violent headaches, malaise, numbness and tingling, and vertigo.
    2) SEVERE TOXICITY: Tachycardia, feeble pulse, hypotension, cyanosis, muscular paralysis, seizures, coma, and death have all been described. Death can occur within minutes of ingestion of contamination fish.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) MYDRIASIS may be noted.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) A feeble pulse and tachycardia have been noted (Halstead, 1978).
    B) HYPOTENSIVE EPISODE
    1) Hypotension has been reported (Halstead, 1978).
    C) CYANOSIS
    1) Cyanosis may develop (Halstead, 1978).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Respiratory distress has been reported (Halstead, 1978).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Violent headaches have been noted (Halstead, 1978).
    B) PARESTHESIA
    1) Numbness and tingling have been noted (Halstead, 1978; Champetier De Ribes et al, 1997).
    C) FEELING NERVOUS
    1) Nervousness has been noted (Halstead, 1978).
    D) PARALYSIS
    1) Muscular paralysis has been noted (Halstead, 1978).
    E) SEIZURE
    1) Seizures have been noted in later phases of the illness (Halstead, 1978).
    F) COMA
    1) Coma has been reported in later phases of the illness (Halstead, 1978).
    G) DIZZINESS
    1) Vertigo may develop (Halstead, 1978).
    H) MALAISE
    1) Malaise may develop soon after ingestion (Halstead, 1978).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) TASTE SENSE ALTERED
    1) First indication is the sharp metallic taste which may be present upon ingestion of the fish (Halstead, 1978).
    B) VOMITING
    1) Vomiting is common and may be followed by dryness of the mouth, malaise, and abdominal pain (Helfrich, 1961; Champetier De Ribes et al, 1997).
    C) DIARRHEA
    1) Diarrhea and abdominal pain may develop (Randall, 1958).
    D) EXCESSIVE SALIVATION
    1) Hypersalivation may be seen, but dry mouth may also be noted (Halstead, 1978).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ITCHING OF SKIN
    1) Pruritus and various types of skin eruptions including desquamation and ulceration have been reported in victims who have survived the initial poison (Halstead, 1978).
    B) CHILL
    1) Cold, clammy skin may also occur (Halstead, 1978).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) Muscle cramps may occur (Halstead, 1978).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Specific testing for toxins are unavailable at this time.
    B) Monitor vital signs and mental status.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    D) Obtain an ECG, and institute continuous cardiac monitoring as necessary.
    E) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with cardiac or persistent symptoms should be admitted overnight for further monitoring.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with severe symptoms following an ingestion of fish of the order Clupeiformes should seek medical attention.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing severe poisonings or differentiation of symptoms from other fish related poisonings.
    6.3.1.4) PATIENT TRANSFER/ORAL
    A) Patients with severe toxicity or hemodynamic instability should be transferred to an intensive care setting.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Asymptomatic exposures can be discharged home after 4 to 6 hours of observation, given the usual rapid onset of symptoms.

Monitoring

    A) Specific testing for toxins are unavailable at this time.
    B) Monitor vital signs and mental status.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    D) Obtain an ECG, and institute continuous cardiac monitoring as necessary.
    E) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY: Activated charcoal may be considered in very rare cases with severe toxicity that develops soon after ingestion, provided that the patient is not vomiting and the airway is protected. Gastric lavage or whole bowel irrigation are generally not recommended given the risk of complications including aspiration.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea and/or vomiting. Manage mild hypotension with IV fluids. Treat headaches with analgesics. Treat pruritus and urticarial dermatitis with antihistamines.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Support respiratory and cardiovascular function. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur.
    B) MONITORING OF PATIENT
    1) Specific testing for toxins are unavailable at this time.
    2) Monitor vital signs and mental status.
    3) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    4) Obtain an ECG, and institute continuous cardiac monitoring as necessary.
    5) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).

Range Of Toxicity

Summary

    A) TOXICITY: Toxicity is not dependent on the size of the fish. The viscera are the most toxic part of the fish.

Pharmacology Toxicology

Toxicologic Mechanism

    A) The chemical and pharmacological properties of the poison are unknown. Whether clupeotoxism is caused by a biotoxin chemical distinct from ciguatoxin or whether the clinical evidence represents a quantitative difference in the amount of the poison ingested has not been determined.
    B) The incidence of Clupeotoxism seems to be seasonal, occurring most often in the warm, summer months (July-September in northern latitudes)-- at which time the fish move in close to shore and do their feeding. Cooking procedures, salting, and drying will not prevent intoxication.

References

General Bibliography

    1) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    2) Banner H & Helfrich P: The distribution of ciguatera in the tropical Pacific. Tech Rept no 3, Final Rept NIH Contr, SA-43-ph-3741, Hawaii Marine Lab, Univ Hawaii, Honolulu, HI, 1964, pp 48.
    3) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    4) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    5) Champetier De Ribes G, Rasolofonirina RN, & Ranaivoson G: [Intoxication by marine animal venoms in Madagascar (ichthyosarcotoxism and chelonitoxism): recent epidemiological data] (abstract). Bull Soc Pathol Exot 1997; 90:286-290.
    6) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    7) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    8) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    9) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    10) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    11) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    12) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    13) Halstead BW: Poisonous and Venomous Marine Animals of the World, The Darwin Press, Inc, Princeton, NJ, 1978.
    14) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    15) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    16) Helfrich P: Fish poisoning in the tropical pacific, Hawaii Marine Lab, Univ Hawaii, Manoa, HI, 1961, pp 16.
    17) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
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    19) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    20) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    21) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    22) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    23) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
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    27) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    28) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    29) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    30) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.