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TETRAMINE (TMA)

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Tetramine is tetramethylammonium hydroxide. It is a quaternary ammonium compound whose distribution in nature is still being investigated, but it has been found in several gastropods, some plants, and some cephalopods. It has been isolated as a toxic fraction from the sea anemone Actinia equina.
    B) Tetramine is an autonomic ganglionic blocking agent.

Specific Substances

    1) Tetramine
    2) Tetramethylammonium hydroxide
    3) TMA
    4) Molecular Formula: C4-H12-N.H-O
    5) CAS 75-59-2
    6) SEA SNAILS
    7) SNAILS, SEA
    8) TMA (TETRAMINE)

Available Forms Sources

    A) SOURCES
    1) The whelk Neptunea antiqua is known to contain this toxin in the salivary gland and the rest of the animal (Anthoni et al, 1989). This marine gastropod is considered edible by many, but has been associated with a number of cases of poisoning (Fange, 1960; Emmelin & Fange, 1958; Halstead, 1978). Tetramine was also discovered as the toxic agent responsible for poisonings from Neptunea arthritica (Asano & Ito, 1959).
    2) Other marine species which contain tetramine include:
    1) Actinia equina (a sea anemone with about 1500 to
    2)
    a) 2000 micrograms per gram of tentacle, with the
    b) rest of the body having about one half this
    c) concentration) (Ackermann, 1923; Mathias et al,
    d) 1960; Halstead, 1978)
    3) Cellaria fistulosa (A. byrozoan) (Anthoni et al,
    4)
    a) 1989a)
    5) Cellaria salicornioides (A. bryozoan) (Anthoni
    6)
    a) et al, 1989a)
    7) Cellaria sinuosa (A. bryozoan) (Anthoni et al,
    8)
    a) 1989a)
    9) Condylactis gigantea (Walsh & Prock, 1958)
    10) Courbonia virgata (all parts of this Sudanese
    11)
    a) plant of the Capparidaceae family) (Henry &
    b) Grindley, 1949)
    12) Cyanea capillata (Walsh & Prock, 1958)
    13) Dosidocus gigas is a squid with TMA as a
    14)
    a) constituent of the axoplasm of the giant nerve
    b) fibers. Its concentration was about 0.04% of
    c) the dialyzable solutes of the axoplasma
    d) (Deffner, 1961).
    15) Fusitriton oregonensis, a snail, has the tetramine
    16)
    a) in its salivary gland at concentrations of 5.5
    b) to 9 mg/g of gland (Asano & Itoh, 1960).
    17) Hydra littoralis (Walsh & Prock, 1958)
    18) Metridium dianthus (Walsh & Prock, 1958)
    19) Neptunea antiqua, a snail, has the material
    20)
    a) throughout the animal in concentrations of 0.03%
    b) wet weight, and concentrated in the salivary
    c) gland (0.4% to 0.9%) (Fange, 1960; Anthoni et al,
    d) 1989)
    21) Neptunea arthritica, a snail had concentrations in
    22)
    a) the salivary gland of 4 to 7.5 mg/gram of gland
    b) (Asano & Itoh, 1960).
    23) Neptunea intersculpta, a snail with concentrations
    24)
    a) in the salivary gland of 3 to 4 mg/g of gland
    b) (Asano & Itoh, 1960).
    25) Physalia physalis (Walsh & Prock, 1958)
    26) Plexaura flexuosa (Walsh & Prock, 1958)

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Tetramine is an autonomic ganglionic blocking agent. Initial symptoms start about 30 minutes after ingestion and persist for a few hours. There may be vomiting, various visual disorders, dizziness, motion sickness, and headache.
    B) Humans most often become exposed after ingesting gastropods (snails) such as Neptunea species. For some species this may be avoided by removing the salivary gland, but in N. antiqua, there is sufficient TMA in the tissues to produce symptoms.
    C) Clinically, poisonings should resemble those seen with nicotine. The parasympathetic ganglia and cholinergic nerve endings are activated, resulting in an increase in tone and motor activity of the GI tract. When combined with vagal stimulation of the afferent nerves of the upper GI, this leads to salivation, nausea, and vomiting.
    0.2.4) HEENT
    A) Blindness, photophobia, tearing, amblyopia, and diplopia have been reported after eating snails containing these agents.
    0.2.5) CARDIOVASCULAR
    A) Hypotension and decreased cardiac output may occur with severe poisoning.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Respiratory arrest may occur in serious cases due to paralysis of the respiratory muscles.
    0.2.7) NEUROLOGIC
    A) Dizziness and headache have been reported in human cases. Muscle fasciculations and paralysis may occur in severe cases. Seizures have occurred in poisoned animals.
    0.2.8) GASTROINTESTINAL
    A) Hypersalivation, nausea, vomiting, and paralytic ileus may occur in human toxicity cases.
    0.2.14) DERMATOLOGIC
    A) Urticaria was reported in one case.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) Monitor vital signs, particularly for decreased blood pressure.
    B) Monitor respiratory function: pulse oximetry and/or arterial blood gases may be indicated.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Inducing emesis is NOT recommended as seizures may occur and absorption after ingestion is very rapid.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 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) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 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).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.

Range Of Toxicity

    A) Ingestion of one or two snails containing tetramine may be sufficient to cause poisoning.
    B) An estimated lethal dose in humans is 250 to 1000 mg, or 3 to 4 milligrams per kilogram.

Clinical Effects

Summary Of Exposure

    A) Tetramine is an autonomic ganglionic blocking agent. Initial symptoms start about 30 minutes after ingestion and persist for a few hours. There may be vomiting, various visual disorders, dizziness, motion sickness, and headache.
    B) Humans most often become exposed after ingesting gastropods (snails) such as Neptunea species. For some species this may be avoided by removing the salivary gland, but in N. antiqua, there is sufficient TMA in the tissues to produce symptoms.
    C) Clinically, poisonings should resemble those seen with nicotine. The parasympathetic ganglia and cholinergic nerve endings are activated, resulting in an increase in tone and motor activity of the GI tract. When combined with vagal stimulation of the afferent nerves of the upper GI, this leads to salivation, nausea, and vomiting.

Heent

    3.4.1) SUMMARY
    A) Blindness, photophobia, tearing, amblyopia, and diplopia have been reported after eating snails containing these agents.
    3.4.3) EYES
    A) Temporary blindness may occur after ingestion of tetramine (Anthoni et al, 1989).
    B) Diplopia, blurred vision and impaired visual accommodation have been reported after ingestion of animal tissue containing TMA (Anthoni et al, 1989; Halstead, 1978).
    C) Photophobia has been reported after ingestion of TMA containing N. arthritica (Asano, 1952; Asano & Ito, 1959).
    D) Amblyopia may occur after ingestion of TMA containing N. intersculpa (Asano & Itoh, 1960).
    E) Excessive lacrimation may occur (Anthoni et al, 1989a).

Cardiovascular

    3.5.1) SUMMARY
    A) Hypotension and decreased cardiac output may occur with severe poisoning.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) Severe poisonings may result in decreased blood pressure and decreased cardiac output (Halstead, 1978).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Respiratory arrest may occur in serious cases due to paralysis of the respiratory muscles.
    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) Paralysis of the respiratory muscles with resultant apnea is the usual cause of death in poisoning by tetramine (Jodlbauer, 1900; (Henry & Grindley, 1949; Henry, 1948).
    b) TETRAMETHYLAMMONIUM HYDROXIDE: A 39-year-old man was found dead approximately 1 hour following occupational dermal exposure to a pallet cleaning solution containing 35% of a 25% tetramethylammonium hydroxide (TMAH) solution. An autopsy revealed second degree burns on 12% of his skin. There were no other apparent complications that were attributed to his death. Because it is rare that burns on 12% of skin without complications would cause death, it is believed that TMAH may have caused ganglion blockage via dermal absorption, resulting in respiratory failure (Park et al, 2013).

Neurologic

    3.7.1) SUMMARY
    A) Dizziness and headache have been reported in human cases. Muscle fasciculations and paralysis may occur in severe cases. Seizures have occurred in poisoned animals.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Severe headache may occur after ingestion of TMA in animal tissue (Anthoni et al, 1989).
    B) DIZZINESS
    1) Vertigo and a feeling similar to that of intoxication may occur after ingestion of animal tissue containing TMA. This may result in an unsteady or reeling gait (Anthoni et al, 1989). Weakness, fatigue and dizziness may occur following tetramine ingestions (Halstead, 1978).
    C) PARALYSIS
    1) Paralysis of the respiratory muscles with resultant apnea is the usual cause of death in poisoning by tetramine (Jodlbauer, 1900) (Henry & Grindley, 1949; Henry, 1948).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) Animals given per os doses of 50 and 100 mg Me4N+/kg died as a result of excessive seizures within 120 to 180 minutes and 45 to 47 minutes respectively (Anthoni et al, 1989).
    2) PARALYSIS
    a) Animal studies have shown that TMA causes fasciculations leading to paralysis of the skeletal muscles (Albuquerque et al, 1968; Bacq & Brown, 1937).

Gastrointestinal

    3.8.1) SUMMARY
    A) Hypersalivation, nausea, vomiting, and paralytic ileus may occur in human toxicity cases.
    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) Nausea, vomiting and a feeling like that of seasickness have been reported after ingestion of TMA (Anthoni et al, 1989; Halstead, 1978). Gastrointestinal motility may become disturbed, resulting in diarrhea, and in some cases, constipation. Paralytic ileus may occur (Halstead, 1978).
    B) EXCESSIVE SALIVATION
    1) Excessive salivation may occur shortly after an exposure (Anthoni et al, 1989a).
    C) APTYALISM
    1) Dry mouth may occur following ingestions as a result of the autonomic ganglionic blocking action of tetramine (Halstead, 1978).

Dermatologic

    3.14.1) SUMMARY
    A) Urticaria was reported in one case.
    3.14.2) CLINICAL EFFECTS
    A) URTICARIA
    1) WITH POISONING/EXPOSURE
    a) Urticaria has been reported after ingestion of N. arthritica (Asano, 1952; Asano & Ito, 1959).
    B) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) TETRAMETHYLAMMONIUM HYDROXIDE: A 39-year-old man was found dead approximately 1 hour following occupational dermal exposure to a pallet cleaning solution containing 35% of a 25% tetramethylammonium hydroxide (TMAH) solution. An autopsy revealed second degree burns on 12% of his skin. There were no other apparent complications that were attributed to his death. Because it is rare that burns on 12% of skin without complications would cause death, it is believed that TMAH may have caused ganglion blockage via dermal absorption, resulting in respiratory failure (Park et al, 2013).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS75-59-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, particularly for decreased blood pressure.
    B) Monitor respiratory function: pulse oximetry and/or arterial blood gases may be indicated.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Plasma tetramine laboratory tests are not commonly available, and toxic levels have not been established.
    2) Monitor CPK levels in patients with prolonged seizures.
    B) ACID/BASE
    1) Monitor pulse oximetry and/or arterial blood gases in patients with muscle weakness or paralysis.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor pulse, blood pressure and respiratory function.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Various methods have been identified, but the most rapid and accurate methods involve proton nuclear magnetic resonance spectroscopy or mass spectrometry (Anthoni et al, 1989a) Anthoni et al, 1989). Neither of these methods are particularly clinically useful, and non-toxic versus toxic tetramine levels have not been determined.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor vital signs, particularly for decreased blood pressure.
    B) Monitor respiratory function: pulse oximetry and/or arterial blood gases may be indicated.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED-
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for seizures.
    B) ACTIVATED CHARCOAL -
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    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).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Due to the risk of seizures, inducing emesis is NOT recommended. Tetramine is rapidly absorbed and distributed, also making induced emesis unlikely to be effective unless performed almost immediately after ingestion. Absorption is slowed by the presence of food in the stomach.
    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) Most exposures occur after ingestion of tetramine in a biologic being used as food. Patients are not usually seen until the tetramine is absorbed and is causing symptoms. There is no specific antidote; treatment is supportive and symptomatic. Special care should be taken to monitor respiratory function as respiratory paralysis is the primary cause of death. Endotracheal intubation and mechanical ventilation may be necessary. Duration of symptoms is generally just a few hours.
    B) SEIZURE
    1) 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 .
    2) 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).
    3) 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).
    4) 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).
    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).
    C) 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).

Enhanced Elimination

    A) SUMMARY
    1) Extracorporeal elimination methods have not been tried and because of the short distribution and elimination half-lives, would not be indicated.

Abstracts

Case Reports

    A) ADULT
    1) A 31-year-old purchased two N. antiqua gastropods for food. They were boiled for only 30 minutes, instead of the recommended two hours. Shortly after ingestion, the patient experienced short periods of blurred vision and blindness, as well as reeling gait, vertigo, and a feeling of intoxication. She also vomited and had a headache. She was well again after 30 minutes (Anthoni et al, 1989).

Range Of Toxicity

Summary

    A) Ingestion of one or two snails containing tetramine may be sufficient to cause poisoning.
    B) An estimated lethal dose in humans is 250 to 1000 mg, or 3 to 4 milligrams per kilogram.

Minimum Lethal Exposure

    A) ACUTE
    1) An estimated lethal dose of TMA in a human is 250 to 1000 milligrams (3 to 4 milligrams/kilogram), but smaller amounts will produce symptoms (Henry, 1948; Anthoni et al, 1989a).
    B) A lethal case of TMA poisoning was reported after ingestion of Courbonia virgata (plant) (Henry, 1948), with an estimated lethal dose of 3 to 4 milligrams/kilogram.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Ingestion of one or two snails containing TMA may cause symptoms (Anthoni et al, 1989).

Workplace Standards

    A) ACGIH TLV Values for CAS75-59-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS75-59-2 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS75-59-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS75-59-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIMAL DATA
    1) LD50- (INTRAPERITONEAL)RAT:
    a) 15 mg/kg (Anthoni et al, 1989)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) TMA has a direct action on nicotinic and muscarinic receptors which increases the conduction of the ganglion cells used for depolarization, firing, and impulse transmission. This increased conductance results in an increase in intracellular sodium ions which activates an electrogenic sodium ion pump which in turn increases membrane potential and causes reduced excitability of the ganglion (Anthoni et al, 1989a).
    B) TMA induces a nerve transmission block by ganglionic depolarization, a period of recovery from block during the falling phase of depolarization, and a recurring of ganglionic blockade associated with ganglionic hyperpolarization (Gebber & Volle, 1966).

Toxicologic Mechanism

    A) TMA has a definite muscarinic effect on receptors at postganglionic nerves in smooth muscle, cardiac muscle, and exocrine glands (Bolton & Clark, 1981; Hobbiger et al, 1969; Mitchelson, 1971).
    B) Although symptoms such as headache, dizziness, and gait abnormality would indicate some CNS toxicity, it has not been established that tetramine crosses the blood-brain barrier to any extent (Anthoni et al, 1989a).

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