a) Massive ingestion is often serious and sometimes fatal and may result in tachycardia, refractory hypotension, shock, dysrhythmias, circulatory collapse, pulmonary edema, respiratory depression, and prolonged coma (Buire et al, 2009).
b) Effects of meprobamate and phenprobamate poisoning include palpitations, dysrhythmias, tachycardia, and bradycardia (Tasdemir et al, 2002; Lhoste et al, 1977). Cardiac arrest with successful resuscitation has been reported (Tasdemir et al, 2002; Jacobsen et al, 1987). Acute cardiac failure may result from a direct action of meprobamate on cardiac muscle (Kintz et al, 1988). Cardiac failure and vasodilation leading to shock has been reported following the ingestion of 72 grams (Eeckhout et al, 1988) and 25 grams (Peyriere et al, 1998) of meprobamate.

a) Hypotension can be severe and persistent, leading to profound shock (Charron et al, 2005; Shane & Hirsch, 1956; Ferguson et al, 1960; Deisher, 1956; Scott et al, 1956; Bailey, 1981; Sauder et al, 1994; Lin et al, 1993; Peyriere et al, 1998; Tasdemir et al, 2002).
b) The development of hypotension due to meprobamate toxicity was associated with a significantly longer duration of mechanical ventilation in ICU patients (Charron et al, 2005).
c) INCIDENCE: In one series 13 of 38 patients (34%) developed hypotension (Sauder et al, 1994) due to meprobamate overdoses. In another series of 74 patients admitted to an ICU after meprobamate overdose, 29 (39%) developed hypotension (Charron et al, 2005).
d) Depressed myocardial activity is in large part responsible for the development of hypotension (Maddock & Bloomer, 1967; Kintz et al, 1988; Lhoste et al, 1977). In a retrospective study of 29 patients with hypotension after meprobamate overdose, echocardiography revealed depressed left ventricular (LV) stroke index, cardiac index and LV ejection fraction(Charron et al, 2005).
e) Hypotension may also be due to the direct effect of meprobamate on the vasomotor center causing vasomotor center depression (Ferguson et al, 1960; Peyriere et al, 1998).
f) CASE REPORT: A 45-year-old woman, with a history of depressive disorder, was found unresponsive in the street. Ten empty boxes of duloxetine, prazepam, and meprobamate were also found. The patient was lethargic (Glasgow coma scale [GCS] score: 11) and confused upon initial examination with normal vital signs; however, her mental status worsened (GCS score: 3) while being transported to the ED. Her blood pressure dropped (67/41 mmHg) and she was administered fluids and 10 mg of ephedrine without response. The patient remained hypotensive and venous blood gas analysis showed acute respiratory acidosis. Serum meprobamate concentration was 146.3 mg/L. Orotracheal intubation and resuscitation with boluses of crystalloids and norepinephrine were initiated. She was then transferred to the ICU and continuous venovenous hemodiafiltration (CVVHDF) was immediately performed. Arterial hypotension persisted despite fluid resuscitation and norepinephrine administration. CVVHDF was continued for 36 hours with the patient eventually recovered and was transferred to the psychiatric ward 2 days post-admission (Ceschi et al, 2013).

a) In a retrospective study of 29 patients with hypotension after meprobamate overdose, echocardiography revealed depressed left ventricular (LV) stroke index, cardiac index and LV ejection fraction(Charron et al, 2005).

a) A sufficiently high dose of meprobamate or phenprobamate can induce severe respiratory depression requiring mechanical ventilation (Charron et al, 2005; Schwartz, 1976; Allen et al, 1977; Eeckhout et al, 1988; Lin et al, 1993; Tasdemir et al, 2002), although the diaphragm is relatively resistant to the action of these drugs.
b) In one series, 27 of 38 patients (71%) required mechanical ventilation following meprobamate overdoses (Sauder et al, 1994).

a) Massive ingestion is often serious and sometimes fatal and may result in tachycardia, refractory hypotension, shock, dysrhythmias, circulatory collapse, pulmonary edema, respiratory depression, and prolonged coma (Buire et al, 2009).
b) Pulmonary edema can readily develop following therapy for meprobamate overdose (Axelson & Hagaman, 1977). Forced diuresis has precipitated severe pulmonary edema. In one patient cardiac failure developed in the setting of acute pulmonary edema, with death occurring shortly thereafter as a result of cardiogenic shock and refractory cardiac arrest following an ingestion of 25 grams of meprobamate (Peyriere et al, 1998).
c) CASE REPORT: Following a mixed drug overdose, including 14.8 grams phenprobamate, a 16-year-old male developed mild bilateral alveolar edema. The patient recovered following mechanical ventilation, hemoperfusion and supportive care (Tasdemir et al, 2002).

a) Bronchospasm has been reported (Gilman et al, 1990).

a) Aspiration pneumonia is common in patients with severe poisoning. In a series of 72 patients who were admitted to the ICU for respiratory support after meprobamate overdose, 65% developed aspiration pneumonia (Charron et al, 2005).

a) Meprobamate/phenprobamate exert depressant actions on the CNS similar to those produced by barbiturates. EEG changes are often seen (Tasdemir et al, 2002).
b) Meprobamate concentration between 60 and 120 mg/L is associated with moderate CNS depression. Deep/prolonged coma may develop with meprobamate concentrations greater than 120 mg/L (Buire et al, 2009).
c) A mixed drug overdose, including 14.8 grams of phenprobamate, resulted in coma unresponsive to painful stimuli. EEG remained normal. Level of consciousness improved after one session of hemoperfusion (Tasdemir et al, 2002).
d) Plasma levels between 100 to 200 mcg/mL are associated with deep coma and may be lethal (Maddock & Bloomer, 1967; Bailey, 1981). Coma has been reported to last from 1 to 73 hours (Ehlers, 1963).
e) Other CNS symptoms of meprobamate/phenprobamate intoxication may include slurred speech, headache, vertigo and weakness (Mouton et al, 1967).
f) In one series 36 of 38 patients (95%) were comatose (Sauder et al, 1994).
g) Patients presenting with prolonged meprobamate use of higher than recommended doses may exhibit ataxia, slurred speech, and vertigo (Prod Info Miltown(R), meprobamate, 1998).
h) One patient developed a Glasgow coma score less than 5 and reactive bilateral mydriasis following a 25 gram meprobamate ingestion (Peyriere et al, 1998).
i) CASE REPORT/PHENBROMATE: A 27-year-old woman developed neurotoxicity (hypotonia, ataxia, weakness, loss of muscle control, slow-down in motion, depressed reflexes, dizziness, drowsiness, fatigue, irritability, agitation, combativeness, impairment in thinking, and limited attention span) 2.5 hours after ingesting 8 grams of phenprobamate. Despite hemodialysis for 3 hours, her condition did not improve. Following supportive care, she recovered and was discharged on day 5 (Emet et al, 2009).
j) CASE REPORT: A 45-year-old woman, with a history of depressive disorder, was found unresponsive in the street. Ten empty boxes of duloxetine, prazepam, and meprobamate were also found. The patient was lethargic (Glasgow coma scale [GCS] score: 11) and confused upon initial examination with normal vital signs; however, her mental status worsened (GCS score: 3) while being transported to the ED. Her blood pressure dropped (67/41 mmHg) and she was administered fluids and 10 mg of ephedrine without response. The patient remained hypotensive and venous blood gas analysis showed acute respiratory acidosis. Serum meprobamate concentration was 146.3 mg/L. Orotracheal intubation and resuscitation with boluses of crystalloids and norepinephrine were initiated. She was then transferred to the ICU and continuous venovenous hemodiafiltration (CVVHDF) was immediately performed. Arterial hypotension persisted despite fluid resuscitation and norepinephrine administration. CVVHDF was continued for 36 hours with the patient eventually recovered and was transferred to the psychiatric ward 2 days post-admission (Ceschi et al, 2013).

a) Meprobamate may precipitate seizures in epileptic patients (Prod Info Miltown(R), meprobamate, 1998).

a) Areflexia was reported (Mouton et al, 1967).

a) Ataxia may occur (Allen et al, 1977).

a) Paresthesia has been noted (Mouton et al, 1967).

a) Euphoria and paradoxical CNS stimulation may occur during meprobamate intoxication, resulting in excitement and fast electroencephalographic activity. Hyperactive deep tendon reflexes, and bilateral ankle clonus have been described (Mouton et al, 1967).
b) Carisoprodol overdose has been noted to cause symptoms similar to serotonin syndrome. Features include hypertension, tachycardia, hyperreflexia, hyperthermia, myoclonus and altered mental status. It is unclear whether these findings result from the direct effects of carisoprodol or its metabolite, meprobamate. Patients in this series were found to have substantially higher meprobamate versus carisoprodol serum levels (Bramness et al, 2005).

a) Therapeutic use of meprobamate can induce anorexia, nausea, vomiting and diarrhea (Prod Info Miltown(R), meprobamate, 1998).

a) Bezoars containing large amounts of meprobamate may be formed (Schwartz, 1976; Jenis et al, 1969; Eeckhout et al, 1988). Relapse may occur after return of normotension and splanchnic blood flow as residual enteric meprobamate is absorbed (North & Krenzelok, 1982). Relapsing coma has also occurred without major fluctuations in blood pressure and presumed splanchnic perfusion (Davis et al, 2006).
b) Death from meprobamate poisoning has occurred following apparent recovery. A mass containing 25 g of meprobamate was found at autopsy in the stomach (Jenis et al, 1969). The authors speculate the residual enteric meprobamate was effectively absorbed from the GI tract after the return of normotension and splanchnic blood flow, thus resulting in a relapse phenomenon.
c) A patient who remained unconscious despite aggressive therapy was found, by gastroscopy, to have a large, gelatinous mass in the stomach; gastrotomy produced a 140 g tarry mass (Schwartz, 1976).

a) A 30-year-old woman developed a deep esophageal ulceration with purulent discharge, which was diagnosed as a tracheo-esophageal fistula, after meprobamate overdose complicated by protracted hypotension and respiratory failure (Lin et al, 1993). Death was due to complications of the fistula.

a) CASE REPORT: Mildly elevated alkaline phosphatase (142 International Units) and hyperbilirubinemia (1.48 mg/dL; range 0.3 to 1.2 mg/dL) developed in a 27-year-old woman who also experienced neurotoxicity 2.5 hours after ingesting 8 grams of phenprobamate. Despite hemodialysis for 3 hours, her condition did not improve. Following supportive care, including plasmapheresis using 12 Units of fresh frozen plasma for 2 days, she recovered and was discharged on day 5 (Emet et al, 2009).

a) Both respiratory and metabolic acidosis may develop in patients with hypotension and respiratory depression (Lin et al, 1993).
b) CASE REPORT: A 45-year-old woman, with a history of depressive disorder, was found unresponsive in the street. Ten empty boxes of duloxetine, prazepam, and meprobamate were also found. The patient was lethargic (Glasgow coma scale [GCS] score: 11) and confused upon initial examination with normal vital signs; however, her mental status worsened (GCS score: 3) while being transported to the ED. Her blood pressure dropped (67/41 mmHg) and she was administered fluids and 10 mg of ephedrine without response. The patient remained hypotensive and venous blood gas analysis showed acute respiratory acidosis (pH: 7.29; pCO2: 7.02 kPa; HCO3: 24.7 mmol/L). Serum meprobamate concentration was 146.3 mg/L. Orotracheal intubation and resuscitation with boluses of crystalloids and norepinephrine were initiated. She was then transferred to the ICU and continuous venovenous hemodiafiltration (CVVHDF) was immediately performed. Arterial hypotension persisted despite fluid resuscitation and norepinephrine administration. CVVHDF was continued for 36 hours with the patient eventually recovered and was transferred to the psychiatric ward 2 days post-admission (Ceschi et al, 2013).

a) Some major hematologic reactions that have occurred during meprobamate therapy include agranulocytosis, aplastic anemia, thrombocytopenic purpura, and leukopenia (Prod Info Miltown(R), meprobamate, 1998).

a) Mild transient leukopenia and thrombocytopenia were reported following an overdose (Lin et al, 1993).

a) CASE REPORT: Mild leukocytosis (17700/mcL) developed in a 27-year-old woman who also experienced neurotoxicity 2.5 hours after ingesting 8 grams of phenprobamate. Despite hemodialysis for 3 hours, her condition did not improve. Following supportive care, including plasmapheresis using 12 Units of fresh frozen plasma for 2 days, she recovered and was discharged on day 5 (Emet et al, 2009).

a) Meprobamate may exacerbate acute intermittent porphyria (Prod Info Miltown(R), meprobamate, 1998).

a) Cyanosis develops occasionally following overdose (Jenis et al, 1969).

a) Allergic reactions to meprobamate include pruritus, urticaria, and/or erythematous maculopapular rash, either generalized or confined to the groin (Peterson & Manick, 1967; Robbins & Brown, 1978). Bullous dermatitis has been seen.

a) Acute nonthrombocytopenic purpura has uncommonly been reported following therapeutic use (Gilman et al, 1990).

a) CASE REPORT: A 23-year-old drug abuser developed acute right hand ischemia after an intra-arterial injection of 2 mL of meprobamate solution (made by dissolving a 200-mg meprobamate tablet in hot water) into the antecubital fossa of his right forearm. Despite supportive therapy, including heparinization, low molecular-weight dextran infusion, corticosteroids, and hyperbaric oxygen therapy, he developed gangrenous necrosis on the distal tips of his right thumb, index finger, ring finger, and little finger. Surgical amputation to remove the gangrenous tissue was performed on day 18 (Seak et al, 2012).

a) Allergic reactions to meprobamate include pruritus, urticaria, and/or erythematous maculopapular rash, either generalized or confined to the groin (Peterson & Manick, 1967; Robbins & Brown, 1978). Bullous dermatitis has been seen.
b) Severe hypersensitivity reactions, including hyperpyrexia, chills, angioneurotic edema, bronchospasm, oliguria, anuria, anaphylaxis, erythema multiforme, exfoliative dermatitis, Stevens-Johnson syndrome, and bullous dermatitis may rarely occur (Prod Info meprobamate oral tablet, 2004).

a) A 27-year-old nursing woman taking 700 mg of carisoprodol daily had an average meprobamate concentration of 11.6 mg/mL. It was estimated that her infant consumed 4.1% of the daily dose of carisoprodol; absolute daily dose was calculated at 1.9 mg/kg. Although the infant remained asymptomatic during 6 months of breastfeeding, the authors recommended that breastfeeding should be stopped until more clinical data was available (Nordeng et al, 2001).

a) One study showed that arterial-venous differences in meprobamate levels exists early during the course of acute intoxications (Sato et al, 1986). The earlier the blood samples are taken, the higher the arterial-venous difference, particularly in massive intoxications.

a) Two children who had been in deep coma following ingestion of a meprobamate-containing combination product regained consciousness when their meprobamate plasma levels had dropped 144 mcg/mL and 158 mcg/mL (Dennison et al, 1985).

a) Bedside echocardiography has been used to guide therapy in patients with hypotension (Charron et al, 2005).

a) EEG may be monitored in symptomatic overdoses, especially in comatose patients.

a) Bezoar formation may be detected with abdominal CT scanning (Davis et al, 2006).

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.

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).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) WHOLE BOWEL IRRIGATION/INDICATIONS: Whole bowel irrigation with a polyethylene glycol balanced electrolyte solution appears to be a safe means of gastrointestinal decontamination. It is particularly useful when sustained release or enteric coated formulations, substances not adsorbed by activated charcoal, or substances known to form concretions or bezoars are involved in the overdose.
b) CONTRAINDICATIONS: This procedure should not be used in patients who are currently or are at risk for rapidly becoming obtunded, comatose, or seizing until the airway is secured by endotracheal intubation. Whole bowel irrigation should not be used in patients with bowel obstruction, bowel perforation, megacolon, ileus, uncontrolled vomiting, significant gastrointestinal bleeding, hemodynamic instability or inability to protect the airway (Tenenbein et al, 1987).
c) ADMINISTRATION: Polyethylene glycol balanced electrolyte solution (e.g. Colyte(R), Golytely(R)) is taken orally or by nasogastric tube. The patient should be seated and/or the head of the bed elevated to at least a 45 degree angle (Tenenbein et al, 1987). Optimum dose not established. ADULT: 2 liters initially followed by 1.5 to 2 liters per hour. CHILDREN 6 to 12 years: 1000 milliliters/hour. CHILDREN 9 months to 6 years: 500 milliliters/hour. Continue until rectal effluent is clear and there is no radiographic evidence of toxin in the gastrointestinal tract.
d) ADVERSE EFFECTS: Include nausea, vomiting, abdominal cramping, and bloating. Fluid and electrolyte status should be monitored, although severe fluid and electrolyte abnormalities have not been reported, minor electrolyte abnormalities may develop. Prolonged periods of irrigation may produce a mild metabolic acidosis. Patients with compromised airway protection are at risk for aspiration.

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).

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

a) DOSE: ADULT: Infuse at 5 to 10 micrograms/kilogram/minute IV. PEDIATRIC: Infuse at 2 to 20 micrograms/kilogram/minute IV or intraosseous, titrated to desired effect (Peberdy et al, 2010; Kleinman et al, 2010).
b) CAUTION: Decrease infusion rate if ventricular ectopy develops (Prod Info dobutamine HCl 5% dextrose intravenous injection, 2012).

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).

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 .

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).

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).

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).

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):

a) Estimate the patient's total daily dose of meprobamate. Convert that amount of meprobamate to an equivalent amount of phenobarbital. Use the conversion factor 30 milligrams of phenobarbital are equivalent to 400 milligrams of meprobamate.
b) Give as an initial dose 1/4 of the calculated phenobarbital equivalent. Then, every 6 hours, give that dose (or increase the dose to relieve any abstinence symptoms that may develop).
c) As soon as the patient has been asymptomatic for 48 hours on a particular maintenance dose of phenobarbital, gradually withdraw the phenobarbital over at least 10 to 14 days.
d) The phenobarbital withdrawal schedule should remain flexible, so that dosages are reduced without producing withdrawal symptoms.

1) Mean hemoperfusion clearances of 134 to 164 mL/min were achieved in 4 patients with severe meprobamate intoxication, compared to a mean renal clearance of 15 to 23 milliliters/minute (calculated in 2 cases).
2) The amount of meprobamate removed was 1.6 to 6.2 grams. Meprobamate half-life decreased from 8.3 to 2.6 hours in one patient (Jacobsen et al, 1987).

a) Up to 400 milligrams three or four times a day orally (Boyd, 1986; Prod Info Miltown(R), meprobamate, 1998).
b) Doses larger than 2400 milligrams per day are not recommended (Boyd, 1986; Prod Info Miltown(R), meprobamate, 1998).

a) Children 6 to 12 years - 100 to 200 milligrams given orally 2 or 3 times per day (Boyd, 1986).
b) Children less than 6 years - Not recommended (Boyd, 1986; Prod Info Miltown(R), meprobamate, 1998).

a) Therapeutic blood levels are reported to range from 0.5 to 2.0 mg% (Prod Info Miltown(R), meprobamate, 1998).
b) Therapeutic plasma levels have been reported to range up to 10 mcg/mL (Mangin et al, 1989).

a) Mild to moderate overdose symptoms (stupor or light coma) - blood levels are usually in the range of 3 to 10 mg% (Prod Info meprobamate oral tablet, 2004) or 60 to 120 mg/L (Buire et al, 2009; Dennison et al, 1985).
b) Severe overdose symptoms (deeper coma) - blood levels are usually in the range of 10 to 20 mg% (Prod Info meprobamate oral tablet, 2004) or 100 to 240 mg/L (Buire et al, 2009; Dennison et al, 1985; Maddock & Bloomer, 1967).
c) One study reported peak plasma concentrations of 800 (176), 816 (180), 863 (190) and 923 micromoles/L (203 mg/liter) in 4 patients, respectively, who survived without sequelae (Jacobsen et al, 1987).
d) PEDIATRICS: Plasma meprobamate concentrations exceeded 100 mg/liter in 2 pre-school children. A peak of 170 mg/liter and 158 mg/liter, respectively, was reported in a 2-year-old and a 2.5-year-old. Both children were comatose and recovered with conservative treatment (Dennison et al, 1985).

a) At levels greater than 20 mg%, more fatalities than survivals may be expected (Prod Info meprobamate oral tablet, 2004).
b) Fatalities have been reported with levels of 120 to 342 mcg/mL (Felby, 1970; Lambert et al, 1992). A fatality with a blood meprobamate level of 88.2 mcg/mL has been reported (Mangin et al, 1989).

a) 750 mg/kg (RTECS , 2002)

a) 794 mg/kg (RTECS , 2002)

a) 840 mg/kg (RTECS , 2002)

a) 275 mg/kg (RTECS , 2002)

a) 1110 mg/kg (RTECS , 2002)