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ETHCHLORVYNOL

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ethchlorvynol is a tertiary alcohol (or acetylenic alcohol) hypnotic drug.
    B) Abbott and Banner Pharmacaps discontinued production of ethchlorvynol in 1999; it is no longer available in the United States.

Specific Substances

    1) 1-chloro-3-ethyl-pent-1-en-4-yn-3-ol
    2) Beta-Chlorovinyl Ethyl Ethynyl Carbinol
    3) E-Ethchlorvynol
    4) Molecular Formula: C7-H9-ClO
    5) CAS 113-18-8

Available Forms Sources

    A) FORMS
    1) Ethchlorvynol was available under the trade name Placidyl(R) (Abbott) and as generic ethchlorvynol (Banner Pharmacaps) in 100, 200, 500 and 750 mg capsules. Both companies discontinued production of the drug in 1999, and it is no longer available in the United States.
    2) Ethchlorvynol is a Schedule IV drug of the Controlled Substance Act (Yell, 1990).
    3) Ethchlorvynol was available as a gelatin capsule with 0.5 mL of liquid drug and a polyethylene glycol diluent.
    B) USES
    1) Ethchlorvynol is a short-term hypnotic and sedative agent with some anticonvulsant and muscle relaxant properties. Ethchlorvynol has been replaced by benzodiazepines for the treatment of insomnia (S Sweetman , 2001).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) Intoxications with ethchlorvynol are characterized by patient reports of mint-like taste, as well as slurred speech, ataxia, nystagmus, and lethargy. Severe intoxication is characterized by prolonged deep coma, hypotension, respiratory depression, and hypothermia.
    2) Coma of 17 days duration with full recovery has been reported. Flat EEG readings have been described during coma, hence supportive care should not be discontinued unless brain death is absolutely certain.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Nystagmus and mydriasis are relatively common.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Marked hypotension, relative bradycardia or tachycardia, and cardiac arrest may be noted.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Respiratory depression and non-cardiogenic pulmonary edema (most common following IV injection) may be noted.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Blurred vision, facial numbness, lethargy, headache, prolonged coma, hypothermia, dysarthria, and areflexia may be noted. Concurrent ingestion of alcohol or other sedative hypnotics will enhance the toxic effects of ethchlorvynol.
    0.2.8) GASTROINTESTINAL
    A) WITH THERAPEUTIC USE
    1) Nausea and vomiting are common.
    0.2.9) HEPATIC
    A) WITH POISONING/EXPOSURE
    1) Hepatotoxicity has been reported following an overdose.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Rhabdomyolysis has been reported following abuse of ethchlorvynol.
    2) Urinary retention has been reported following an overdose.
    0.2.13) HEMATOLOGIC
    A) WITH THERAPEUTIC USE
    1) Hemolysis and pancytopenia have been reported.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Bullous eruptions have been described following an overdose.
    0.2.20) REPRODUCTIVE
    A) Ethchlorvynol is classified as FDA pregnancy category C. Neonatal withdrawal following maternal ingestion has been reported.
    0.2.22) OTHER
    A) WITH POISONING/EXPOSURE
    1) Ethchlorvynol liquid is sometimes injected to achieve psychotropic effects, and thus has become a drug of abuse. Withdrawal symptoms (anxiety, seizures, diarrhea) may be noted following ingestion of 500 mg/day for 4 to 5 months. Jitteriness is common following withdrawal in neonates.

Laboratory Monitoring

    A) Ethchlorvynol blood levels may be helpful in establishing diagnosis and determining need for hemoperfusion.
    B) Serum levels of 19 mg/L or greater were associated with moderate symptoms in one study. Levels greater than 38 mg/L have been associated with coma.
    C) No specific lab work (CBC, electrolyte, urinalysis) is needed unless otherwise indicated. Patients with central nervous system depression should have an arterial blood gas and a chest x-ray.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) 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.
    C) MONITOR EKG AND VITAL SIGNS regularly. HYPOTHERMIA should be managed with temperature controlled blankets, warm IV fluids, and warm gastric lavage.
    D) HEMODIALYSIS - Although hemodialysis may shorten the half-life of ethchlorvynol, it has little effect on the duration of coma because of the large redistribution of drug from fat stores.
    E) CHARCOAL HEMOPERFUSION - Experience with several patients has demonstrated little benefit. It should be reserved for patients with massive ingestions with hypotension that is becoming increasingly refractory to pressors and fluid.
    F) WITHDRAWAL - May be managed with oral phenobarbital, or ethchlorvynol.

Range Of Toxicity

    A) Insufficient data in the literature to characterize the minimum toxic or lethal dose. Death has been reported in adults following the acute ingestion of 2.5 grams in combination with alcohol.
    B) As little as one capsule in a small child is likely to produce signs and symptoms of toxicity.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) Intoxications with ethchlorvynol are characterized by patient reports of mint-like taste, as well as slurred speech, ataxia, nystagmus, and lethargy. Severe intoxication is characterized by prolonged deep coma, hypotension, respiratory depression, and hypothermia.
    2) Coma of 17 days duration with full recovery has been reported. Flat EEG readings have been described during coma, hence supportive care should not be discontinued unless brain death is absolutely certain.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTHERMIA is a consistent feature (S Sweetman , 2001).

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nystagmus and mydriasis are relatively common.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) NYSTAGMUS - INCIDENCE - Nystagmus was present in 6 of 11 cases of pure ethchlorvynol ingestion (Kelner & Bailey, 1984). Nystagmus was also a common finding reported in 51 nonfatal cases of ethchlorvynol intoxication, 78% of whom had coingestants (S Sweetman , 2001; Bailey & Shaw, 1990).
    2) MYDRIASIS - INCIDENCE - Mydriasis was present in 6 of 11 cases of pure ethchlorvynol ingestion (Kelner & Bailey, 1984).
    3) WITHDRAWAL - Withdrawal may precipitate nystagmus, diplopia, macular degeneration, amblyopia, and chiasmal optic neuritis (Hudson, 1961), which are reversible (Reynolds, 1982).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Marked hypotension, relative bradycardia or tachycardia, and cardiac arrest may be noted.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension has been marked in some cases and has responded well to fluids and vasopressor agents (S Sweetman , 2001; Kelner & Bailey, 1984).
    B) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) Cardiac arrest and respiratory arrest have been noted.
    C) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE - Tachycardia was seen in 4 of 11 cases of pure ethchlorvynol ingestion (Kelner & Bailey, 1984). Tachycardia was a common finding reported in a review of 51 nonfatal cases of ethchlorvynol intoxication, 78% of whom had coingestants (Bailey & Shaw, 1990).
    D) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) A "relative" bradycardia in the setting of hypotension is common (S Sweetman , 2001; Kelner & Bailey, 1984).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Respiratory depression and non-cardiogenic pulmonary edema (most common following IV injection) may be noted.
    3.6.2) CLINICAL EFFECTS
    A) HYPOVENTILATION
    1) WITH POISONING/EXPOSURE
    a) Respiratory depression requiring prolonged assistance with artificial ventilation is common following a toxic ingestion (S Sweetman , 2001).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Non-cardiogenic pulmonary edema can develop following IV injection of ethchlorvynol in humans (S Sweetman , 2001; Conces et al, 1985; Glauser et al, 1976; Kurt et al, 1982(Suppl); Swearingen, 1976).
    b) In patients who have developed pulmonary edema after oral ingestion, the onset has been 24 to 48 hours in conjunction with large overdoses and prolonged coma.
    c) Pulmonary edema was rapid in onset after IV injection of relatively small amounts (within 1 to 3 hours of injection of 1.5 to 2.25 grams) (Schottstraedt et al, 1981;(Kurt et al, 1982(Suppl)).
    d) It was delayed in onset (24 to 48 hours) following oral ingestion (Schottstaedt et al, 1981).
    e) CASE REPORT - Adult pulmonary distress syndrome was described in a 22-year-old pregnant female who injected the contents of four 750 mg capsules intravenously. Dyspnea occurred shortly after injection. Within 18 hours, the patient developed severe hypoxemia which responded to PEEP (Burton et al, 1980).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY EDEMA
    a) ANIMAL STUDIES - In experimental animals, intravenous injection of ethchlorvynol causes increased pulmonary osmolar permeability (Glauser et al, 1977).
    2) PLEURAL EFFUSION
    a) ANIMAL STUDIES - A study conducted in rabbits demonstrated that pleural effusions can develop with ethchlorvynol induced pulmonary edema. It was postulated that fluid moved from the interstitium of the lung to the pleural space along a pressure gradient (Miller et al, 1989).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Blurred vision, facial numbness, lethargy, headache, prolonged coma, hypothermia, dysarthria, and areflexia may be noted. Concurrent ingestion of alcohol or other sedative hypnotics will enhance the toxic effects of ethchlorvynol.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma has been reported to last 17 days with recovery (Tozer et al, 1974) in a patient who ingested 80 grams or more. Flat EEG readings have been described during coma and; therefore, should not always indicate cessation of supportive care.
    b) The duration of coma in patients not treated with hemoperfusion is summarized below.
    Estimated ingested dose (grams)Coma duration (hours)Reference
    32Schottstaedt (1981)
    422Westervelt (1966)
    4.58Schottstaedt (1981)
    4.528Schottstaedt (1981)
    646Westervelt (1966)
    7.5 to 11.255Schottstaedt (1981)
    7.5 to 1518Schottstaedt (1981)
    92Schottstaedt (1981)
    10 to 25120 to 168Algeri (1962)
    1152*Westervelt (1966)
    11110*Westervelt (1966)
    1548Teehan (1970)
    20 to 25136Schultz (1966)
    25168*Teehan (1970)
    2558Teehan (1970)
    30144Teehan (1970)
    40>100*Welch (1972)
    45288Teehan (1970)
    5010.5Teehan (1970)
    80 to 12517 days* (408 hours)Tozer (1974)
    100 to 12517 days* (408 hours)Klock (1974)
    * = hemodialyzed

    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures may occur during ethchlorvynol withdrawal, as with other hypnotic/sedative agents. Cases that have been reported following acute intoxication have been in chronic abusers and occur as serum levels are falling (Cahn, 1959; Kelner & Bailey, 1984).
    C) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Toxic effects also include blurring of vision, drowsiness, fatigue, areflexia, dysarthria, headache, mental confusion, and ataxia (Bailey & Shaw, 1990). The neurologic effects of ethchlorvynol may be enhanced by alcohol or barbiturates.
    D) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) Peripheral neuropathy has been reported in patients with prolonged coma due to ethchlorvynol overdose and has been attributed to pressure ischemia (Teehan et al, 1970).
    E) AMNESIA
    1) WITH POISONING/EXPOSURE
    a) Retrograde amnesia following manic purposeful episodes are seen frequently.
    F) PSYCHOTIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) Psychiatric effects may include visual, auditory, and tactile hallucinations, schizophrenia, delirium, anxiety, and agitation (Marshall, 1982; Merrin, 1980).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Nausea and vomiting are common.
    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) WITH THERAPEUTIC USE
    a) SIDE EFFECTS - include an unpleasant after-taste (mint-like) and gastric discomfort followed by nausea and vomiting.

Hepatic

    3.9.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hepatotoxicity has been reported following an overdose.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) Hurwitz et al (1980) reported a case of ethchlorvynol overdose in which 3000 mg was administered intravenously with subsequent development of hypotension, pulmonary edema and liver damage. Hepatotoxicity has not been previously described after IV ethchlorvynol.

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Rhabdomyolysis has been reported following abuse of ethchlorvynol.
    2) Urinary retention has been reported following an overdose.
    3.10.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Rhabdomyolysis has been reported following IV injection of the contents of ethchlorvynol capsules (Kurt et al, 1982(Suppl)).
    B) RETENTION OF URINE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 75-year-old woman developed urinary retention following an ingestion of 2 grams of ethchlorvynol. There were no previous urinary tract symptoms, she was not taking other medications associated with retention, and symptoms abruptly resolved upon recovery (Voto & Drake, 1986).

Hematologic

    3.13.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Hemolysis and pancytopenia have been reported.
    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) WITH THERAPEUTIC USE
    a) Hemolysis and pancytopenia have been reported following ingestion and intravenous injection (S Sweetman , 2001; Klock, 1974; Kurt et al, 1982(Suppl)).
    B) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) Thrombocytopenia may be seen in overdose (S Sweetman , 2001; Westervelt, 1966).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Bullous eruptions have been described following an overdose.
    3.14.2) CLINICAL EFFECTS
    A) BULLOUS ERUPTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Extensive bullous eruptions over the trunk and extremities (not confined to pressure areas) were described in a 45-year-old male with prolonged coma (3 days) due to ethchlorvynol and ethanol overdose. Blister fluid ethchlorvynol levels were 8.2 mcg/dL (Brodin & Redmond, 1980).
    B) LYELL'S TOXIC EPIDERMAL NECROLYSIS, SUBEPIDERMAL TYPE
    1) WITH POISONING/EXPOSURE
    a) Sweat gland necrosis, epidermal necrosis, and subepidermal necrosis were noted on the lateral malleolus of the right foot and the medial aspect of the left foot in a 17-year-old male found in coma.
    1) The serum toxicology screen was positive for ethchlorvynol and the urine was positive for opiates, salicylates, and phencyclidine (Chamberlain et al, 1990).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH THERAPEUTIC USE
    a) Allergic reactions include skin rashes, urticaria, thrombocytopenia and cholestatic jaundice (S Sweetman , 2001).

Reproductive

    3.20.1) SUMMARY
    A) Ethchlorvynol is classified as FDA pregnancy category C. Neonatal withdrawal following maternal ingestion has been reported.
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY CATEGORY
    1) Ethchlorvynol is classified as FDA pregnancy category C (Prod Info Placidyl(R), 1994).
    B) WITHDRAWAL SYNDROME
    1) Withdrawal in a newborn following maternal ingestion of an amount appropriate for night time sedation has been described (Peters, 1981).
    2) Ingestion of 300 mg/kg produced peak concentrations in 90 minutes. Blood levels ranged from 3.5 to 6.5 mcg/mL, in both mother and child. Levels in amniotic fluid rose from 0 to 2.0 mcg/mL over 90 minutes, but then stabilized (Hume et al, 1971).
    3) NEONATE WITHDRAWAL - Within the first 20 minutes, hypotonia, poor suck, absent rooting reflex, and poor startle reflex may be seen. Within 24 to 48 hours, hunger behavior, irritability, and extreme jitteriness is seen (Rumack & Walravens, 1973).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Ethchlorvynol blood levels may be helpful in establishing diagnosis and determining need for hemoperfusion.
    B) Serum levels of 19 mg/L or greater were associated with moderate symptoms in one study. Levels greater than 38 mg/L have been associated with coma.
    C) No specific lab work (CBC, electrolyte, urinalysis) is needed unless otherwise indicated. Patients with central nervous system depression should have an arterial blood gas and a chest x-ray.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Ethchlorvynol blood levels may be helpful in establishing diagnosis and determining need for hemoperfusion.

Methods

    A) CHROMATOGRAPHY
    1) Quantitative analysis of ethchlorvynol in blood and tissues can be accomplished through gas-liquid chromatography(Winek et al, 1989; Winek et al, 1988; Winek et al, 1981).
    2) Time from ingestion to time of ethchlorvynol determination is an important consideration when evaluating concentration values; both tissue and blood have shown ethchlorvynol loss with elapsed time (Winek et al, 1981).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Ethchlorvynol blood levels may be helpful in establishing diagnosis and determining need for hemoperfusion.
    B) Serum levels of 19 mg/L or greater were associated with moderate symptoms in one study. Levels greater than 38 mg/L have been associated with coma.
    C) No specific lab work (CBC, electrolyte, urinalysis) is needed unless otherwise indicated. Patients with central nervous system depression should have an arterial blood gas and a chest x-ray.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) CNS depression occurs rapidly with ethchlorvynol overdose, usually within 1 to 2 hours (Lynn et al, 1979).
    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) CNS depression occurs rapidly with ethchlorvynol overdose, usually within 1 to 2 hours (Lynn et al, 1979).
    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) Attentive supportive and symptomatic care is the cornerstone of therapy (Skoutakis & Acchiardo, 1982).
    B) MONITORING OF PATIENT
    1) Monitor cardiac and respiratory function closely. Evaluate pulmonary status frequently. This may require arterial blood gases.
    2) Observe for hypothermia, hypotension, tachycardia, and respiratory complications (Yell, 1990).
    3) CBC should be done to assess anemia and thrombocytopenia. Coagulation studies are required to assess changes (Yell, 1990).
    4) Take baseline levels of amylase and calcium. These may aid in monitoring hypocalcemia or pancreatitis induced by hemoperfusion (Yell, 1990).
    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).
    D) HYPOTHERMIA
    1) Should be treated carefully with blankets or temperature-controlled water blankets. Consider warm intravenous fluids and/or warm gastric lavage if very low.
    E) ACUTE LUNG INJURY
    1) Following intravenous ethchlorvynol, non-cardiogenic pulmonary edema may occur and should be treated with end positive pressure in severe cases (Burton et al, 1980; Wysolmerski, 1985).
    2) Diuretics, digoxin, and unloading agents are probably not of benefit in the treatment of ethchlorvynol induced noncardiogenic pulmonary edema. PEEP is the standard treatment for non-cardiogenic pulmonary edema.
    3) Blanch et al (1992) propose that effects of PEEP in pulmonary edema is to restore tidal ventilation to a population of alveoli recruitable only at high airway pressures. This was surmised from ethchlorvynol-induced lung injury in canines and treatment with PEEP (Blanch et al, 1992).
    4) A study in mongrel dogs suggested that ibuprofen 12.5 mg/kg administered 60 minutes following ethchlorvynol induced unilateral lung injury improved the ventilation-perfusion relationship (Sprague et al, 1987).
    F) DRUG WITHDRAWAL
    1) Is probably best treated with either reinstitution of ethchlorvynol with gradual tapering, or with substitution of phenobarbital (Yell, 1990; Goth, 1984).
    2) PHENOBARBITAL
    a) Administer phenobarbital (100 or 200 mg initially). If within an hour signs of withdrawal have been decreased a second dose of 100 or 200 mg should be instituted.
    b) This should be continued at 1 to 2 hour intervals until the patient is comfortable.
    c) Administration of phenobarbital should then occur at 6 hour intervals until a dose has been reached stabilizing the patient when given every 6 hours.
    3) In general, a 30 mg dose of phenobarbital may be substituted for 100 mg of ethchlorvynol (Goth, 1984).
    4) A withdrawal schedule for phenobarbital is then set up cutting in half dose 1 and 3 for 2 days, then cutting in half doses 2 and 4 for 2 days and gradually reducing the phenobarbital over a 2 week time period.
    G) 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) 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).
    5) 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).
    6) If phenobarbital is unsuccessful, administer ethchlorvynol.
    H) DRUG WITHDRAWAL
    1) NEONATES
    a) Symptoms of neonatal withdrawal from ethchlorvynol may be present at birth or may be delayed up to 2 weeks (Rumack & Walravens, 1973).
    b) Treated with a short course of 3 to 5 mg/kg phenobarbital.

Enhanced Elimination

    A) HEMOPERFUSION
    1) RESIN
    a) Resin hemoperfusion has been the most effective method of enhancing elimination of ethchlorvynol in substantial overdoses, usually resulting in clinical neurological and hemodynamic improvement, and may lessen the duration of coma.
    b) Hemoperfusion should be considered in comatose patients with high blood concentrations.
    c) Complications of prolonged coma (pneumonia) have not been affected, however, in most cases it has been instituted too late in the course of intoxication to influence the development of complications.
    d) These benefits must be weighed against the low risks of the procedure (thrombocytopenia, anemia, hypocalcemia), which have necessitated blood transfusions in some cases.
    e) Clinical experience with patients intoxicated with ethchlorvynol has supported the use of resin hemoperfusion. In a total of 6 patients reported in the literature who were treated with Amberlite XAD-4 resin hemoperfusion, successful results were described.
    f) CASE REPORT
    1) In 3 patients where the estimated ingested dose was 12 to 15 grams (Lynn et al, 1979; Hull et al, 1980), hemoperfusion removed 4.9 grams (over 8 hours), 1.9 grams (over 4 hours) and 3.1 grams (over 10 hours).
    2) The duration of coma in these patients was 47 hours, 12 hours, and 53 hours. In patients not treated with hemoperfusion who ingested 7.5 to 15 grams, the duration of coma was 2, 18, 52, 55, and 110 hours.
    3) Patients treated with hemoperfusion who reportedly ingested larger amounts (22, 22.5 and 30 grams) (Benowitz et al, 1980; (Lynn et al, 1979; Dua et al, 1980), had coma lasting 168 hours, 80 hours, and greater than 48 hours.
    4) Nevertheless, a total of 6.6 grams, 3.73 grams, and 9 grams were removed in 15 hours, 3.5 hours, and 6 hours, respectively.
    5) The duration of coma in non-hemoperfused patients reportedly ingesting 20 to 25 grams has ranged from 58 to 168 hours.
    6) Comparison of total duration of coma in patients treated with hemoperfusion to non-perfused patients may be deceptive in evaluating the benefits of this therapy.
    7) In 4 of the 6 patients reported, resin hemoperfusion was initiated late in the course of intoxication; these patients were 16 hours or greater post-ingestion and had been in coma for most of that time.
    g) In one patient (Lynn et al, 1979) who ingested 15 grams and received hemoperfusion within 3 to 4 hours of ingestion, the total duration of coma was 12 hours.
    h) While the total duration of coma in patients treated with hemoperfusion has not been markedly different from patients treated with supportive care or hemodialysis, all of these patients had substantial clinical improvement shortly after initiation of hemoperfusion.
    1) Increased blood pressure and improved hemodynamic stability occurred within 1, 2, and 12 hours in 3 patients (Lynn et al, 1979; Hull et al, 1980).
    2) Return of deep tendon reflexes, spontaneous motor activity and withdrawal from painful stimuli occurred in 5 of 6 patients during the first course of hemoperfusion.
    3) All were in stage 4 coma at the start of the procedure and demonstrated improvement within 1 hour in 3 cases, 3 hours in 1 case, and 7 hours in 1 case.
    i) The removal of ethchlorvynol during resin hemoperfusion is summarized below:
    Estimated ingested doseDuration of perfusion (hours)Amount removed (% of dose) Reference
    12 grams 41.9 g (15.8%)Lynn (1979)
    15 grams 8 4.9 g (32.6%)Lynn (1979)
    15 grams 107.7 g (51.3%)Hull (1980)
    22 grams 156.6 g(30%)Lynn (1979)
    22.5 grams 3.53.73 gBenowitz (1980)
    30 grams 69 g (30%)Dua (1980)

    j) Complications of hemoperfusion in 6 patients reported were thrombocytopenia (all patients often not requiring treatment), hypocalcemia (2 patients), anemia requiring blood transfusion (2 patients), and pancreatitis (1 patient).
    k) Complications of ethchlorvynol overdose or prolonged coma (ie, pneumonia) occurred in 4 of 6 patients. In one patient pneumonia was present before hemoperfusion was initiated.
    l) ANIMALS
    1) In a study of 10 dogs given oral overdoses of 350 or 400 mg/kg, a four hour run of Amberlite XAD-4 resin hemoperfusion started five hours post-ingestion resulted in a mean of 37% of the ingested dose removed.
    2) This amount was twice the amount apparent from calculated plasma clearance. This experiment indicated that the bulk of the drug removed originated from extravascular compartments.
    3) The elimination of ethchlorvynol was linear in these dogs, and the half-life during hemoperfusion (mean 3.8 hours, range 2.4 to 6.9 hours) was significantly different from preperfusion half-life (mean 94.1 hours, range 29.9 to 445 hours).
    4) All dogs were in stage 4 coma at the start of hemoperfusion, awoke during the procedure, and remained arousable afterward. One nonperfused control animal remained in coma for 5 days (Zmuda, 1980).
    B) CHARCOAL
    a) Although resin hemoperfusion appears to be superior in removing ethchlorvynol, charcoal hemoperfusion has produced clinical benefits when initiated within 5 hours of ingestion (Kathpalia et al, 1983), and may be considered if resin hemoperfusion is unavailable.
    b) Total amounts of ethchlorvynol removed during charcoal hemoperfusion have been less than that reported for resin hemoperfusion (see table below). In one patient who received both modalities, charcoal hemoperfusion removed 3.1 grams in 4.5 hours and resin hemoperfusion removed 9 grams in 6 hours (Dua et al, 1980).
    Estimated ingested doseTotal removed (% of dose)Duration ofhemoperfusion (hrs)Reference
    Not stated2.4 g9Crome (1980)
    12.5 g941 mg (7.5%)4Kathpalia (1983)
    30 g3.1 g (10%)4.5Dua (1980)

    c) Clinical improvement was not demonstrated in 2 patients (de Torrente et al, 1979), and in 1 patient (Dua et al, 1980) following charcoal hemoperfusion which was initiated 72 hours, 20 hours, and 2 days post-ingestion, respectively.
    1) Blood ethchlorvynol levels were unchanged 6 hours after initiation of hemoperfusion in 8 patients.
    d) The time from ingestion to initiation of the procedure or clinical benefit was not stated (Koffler et al, 1978).
    C) HEMODIALYSIS
    1) Hemodialysis has not been successful in significantly enhancing elimination of ethchlorvynol (Tozer et al, 1974; Westervelt, 1966; Teehan et al, 1970; Schultz et al, 1966; Welch et al, 1972).
    2) In one patient reported to ingest 25 grams, the blood ethchlorvynol level was unchanged after 13 hours of hemodialysis; 50 mcg was recovered in the dialysate (Maher & Schreiner, 1963).
    3) In one patient who ingested 100 to 125 grams, hemodialysis was initiated on the third day. Fourteen grams was removed in 14 hours of dialysis. The blood pressure improved, but the patient remained comatose for 17 days (Klock, 1974).
    D) EXCHANGE TRANSFUSION
    1) Has been reported simultaneously with peritoneal dialysis in a 20 month old child who ingested 3.5 to 5 grams of ethchlorvynol. The author reported a dramatic response (spontaneous respiration after 1000 mL) but no post-procedure blood levels or calculated amount removed are documented (Hyde et al, 1968).

Abstracts

Case Reports

    A) ADULT
    1) ROUTE OF EXPOSURE
    a) INJECTION: Glauser et al (1976) reported a case of a 23-year-old female who injected the contents of 2 capsules (a total of 1.5 grams) of ethchlorvynol IV and immediately developed symptoms of mint-like flavor in the mouth, cough, and shortness of breath. The patient then fell asleep, but upon wakening approximately 20 hours later, noticed symptoms of shortness of breath, and a cough productive of a clear to yellowish sputum. Physical examination of the patient's chest revealed diffuse end bilateral inspiratory rales with a chest x-ray demonstrating bilateral diffuse alveolar infiltrates.
    1) A second patient, a 22-year-old male who injected 3 grams of ethchlorvynol IV over 10 minutes also immediately tasted a minty flavor followed by the development of severe shortness of breath. The patient then lost consciousness and upon awakening 17 hours later, had fever, marked shortness of breath, and a cough producing yellowish, blood-streaked sputum. Again, physical examination revealed inspiratory rales with a chest x-ray demonstrating diffuse bilateral alveolar infiltrates. Both patients recovered with supportive treatment and respiratory therapy with oxygen, IPPB and bronchodilators (Glauser et al, 1976).
    b) INJECTION: Van Swearingen (1976) report a case of a 26-year-old male who injected 1.5 grams of ethchlorvynol intravenously who immediately developed chest pain, shortness of breath, and vomiting which decreased over the next 4 hours.
    1) Physical exam revealed mid to end-expiratory rales but without any wheezing. The patient was also noted to be markedly dyspneic with a nonproductive cough. Chest x-rays revealed diffuse pulmonary infiltrates in all lung fields and blood gases revealed a pH of 7.42, pCO2 of 30.3, pO2 of 41.5 and an oxygen saturation of 65%.
    2) The patient was given oxygen, intermittent positive pressure breathing, and furosemide 40 mg, in addition to IV steroids and penicillin. The patient's condition improved rapidly and chest pain gradually resolved after 48 hours (Swearingen, 1976).
    c) INJECTION: Burton et al (1980) describe a case of acute respiratory distress syndrome following IV Placidyl(R) injection, responding dramatically to PEEP therapy (Burton et al, 1980).
    d) ORAL: A 29-year-old man ingested 100 to 125 grams (1.33 to 1.66 grams/kg) of ethchlorvynol in a suicide attempt. He became comatose, apneic, and hypotensive, and required assisted ventilation and pressor agents.
    1) Pancytopenia and hemolysis occurred on the third day postingestion. Hemodialysis was initiated on the third day and removed 14 grams in 14 hours. The patient was comatose for 17 days. The lowest blood count occurred on day 15. The highest ethchlorvynol serum level recorded was 27.5 mg/dL on day 3 (Klock, 1974).

Range Of Toxicity

Summary

    A) Insufficient data in the literature to characterize the minimum toxic or lethal dose. Death has been reported in adults following the acute ingestion of 2.5 grams in combination with alcohol.
    B) As little as one capsule in a small child is likely to produce signs and symptoms of toxicity.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) 500 to 1000 milligrams at bedtime. For patients awakening during the night or early morning, supplemental doses of 100 to 200 milligrams may be given at that time (Prod Info Placidyl(R), 1994).

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Fatalities have been reported following ingestion of 10 grams (156 mg/kg) (Algeri et al, 1962) to 49.5 grams of ethchlorvynol (Teehan et al, 1970).
    2) A death was reported after ingestion of 5 grams (Cravey & Baselt, 1968) and 2.5 grams in combination with alcohol (Harenko, 1967).
    3) Clearly a period of observation must occur following ingestion of even small overdosage.

Maximum Tolerated Exposure

    A) ACUTE
    1) Ingestions of 25 to 45 grams have been associated with survival (Teehan et al, 1970).

Serum Plasma Blood Concentrations

    7.5.1) THERAPEUTIC CONCENTRATIONS
    A) THERAPEUTIC CONCENTRATION LEVELS
    1) GENERAL
    a) THERAPEUTIC (SLEEP INDUCING) LEVELS - Are generally 1 to 2 mg/dL (Dawborn, 1972).
    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) TOXIC
    1) ADULT - A 33-year-old man who received ethchlorvynol 1 gram daily for 2 years had a serum level of 70 mcg/mL, and he was found somnolent but totally conscious. Nonlinear kinetics were seen in this patient with levels greater than 25 mcg/mL (Kolpek et al, 1986).
    2) PLASMA LEVELS
    a) A plasma concentration of 0.8 mg/dL at 15 hours after ingestion was demonstrated in a patient who was in coma for 48 hours (Teehan et al, 1970).
    b) A level of 2.2 mg/dL 4 hours after ingestion was demonstrated in a patient who was alert (Teehan et al, 1970).
    c) In 13 deaths due to overdose of ethchlorvynol, postmortem blood concentration averaged 11.9 mg/dL (range 1.4 to 40 mg/dL) (Rehling, 1967).
    d) The plasma level in one patient who was in coma for 288 hours was 8.5 mg/dL 5 hours after ingestion (Teehan et al, 1970).
    e) Nystagmus, lethargy, ataxia, and disorientation were reported in a 27-year-old woman with a serum level of 17 mg/L (Ropper, 1975).
    f) A plasma level of 13.5 milligrams/deciliter was demonstrated 12 hours after ingestion in a patient who was in coma for 144 hours (Teehan et al, 1970).
    g) In a report of 11 patients who overdosed on ethchlorvynol alone, serum levels greater than 38 mg/L were associated with grade 3 coma and respiratory depression in 2 patients.
    1) Levels of 19 mg/L or greater were associated with dysarthria (7 cases), mydriasis (6 cases), nystagmus (6 cases), and tachycardia (4 cases) (Kelner & Bailey, 1984a).
    h) The blood concentrations of the "pure" and "mixed" ethchlorvynol intoxications did not differ significantly among the 51 nonfatal cases (range, 3 to 115 mg/L).
    1) The 38 fatal cases had ethchlorvynol levels ranging from 5 to 258 mg/L which did not differ from those of the nonfatal ones (Bailey & Shaw, 1990).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (SUBCUTANEOUS)RAT:
    1) 200 mg/kg (RTECS, 2001)
    B) LD50- (INTRAPERITONEAL)MOUSE:
    1) 275 mg/kg (RTECS, 2001)
    C) LD50- (ORAL)MOUSE:
    1) 290 mg/kg (RTECS, 2001)
    D) LD50- (SUBCUTANEOUS)MOUSE:
    1) 240 mg/kg (RTECS, 2001)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Ethchlorvynol is a highly lipid soluble sedative hypnotic drug. It is capable of causing prolonged coma and is a hazard for addiction.
    B) It is known to have some muscle relaxant and anticonvulsant activity as well (Bertino, 1986).

Physicochemical

Physical Characteristics

    A) pungent vinyl-like odor
    B) pungent slightly bitter taste

Molecular Weight

    A) 144.6

References

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