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Meprobamate poisoning

Meprobamate poisoning
Literature review current through: Jan 2024.
This topic last updated: May 05, 2022.

INTRODUCTION — Meprobamate is a sedative and anxiolytic medication that was marketed for decades in the United States and Europe. The first case of meprobamate poisoning was described in 1956 [1]. Due to its substantial abuse potential, meprobamate is no longer recommended for treatment of insomnia and has been replaced by benzodiazepines and other agents. Although use of the drug is declining, significant meprobamate overdose remains a life-threatening emergency.

This topic will review the basic pharmacology, clinical presentation, and management of meprobamate poisoning. Discussions of the general approach to the management of poisoned patients and detailed management of other toxins are found elsewhere. (See "General approach to drug poisoning in adults" and "Initial management of the critically ill adult with an unknown overdose".)

EPIDEMIOLOGY — Meprobamate poisoning is rare and most cases involve suicide attempts [2]. In France, meprobamate has been used more widely and the drug was involved in approximately 7 percent of psychotropic poisonings in 2005 [3]. Mortality in cases of overdose has ranged between 1.7 and 5 percent [4-6]. Meprobamate ingestion is associated with an increased risk of intensive care unit (ICU) admission (adjusted odds ratio [OR] = 2.71; 95% CI: 1.27-5.81) [7].

PHARMACOLOGY — Meprobamate is a carbamate which acts primarily as a sedative by increasing GABAA-mediated neurotransmission in a manner similar to barbiturates [8,9]. Carisoprodol, prescribed as a centrally acting muscle relaxant, is mainly metabolized to meprobamate by cytochrome P450 2C19, shares properties with meprobamate, and also has significant potential for abuse [10-12].

PHARMACOKINETICS AND TOXICOKINETICS — After oral ingestion of a therapeutic dose, meprobamate is rapidly absorbed from the gastrointestinal tract and peak plasma concentrations are reached within one to three hours [13,14]. Protein binding is negligible (14 to 24 percent). The drug’s volume of distribution is reported to be 0.70 L/kg, and is not significantly altered in overdose. A standard single therapeutic dose for an adult ranges from 200 to 800 mg. Significant toxicity is likely with ingestions of 4 to 5 g or more [3,4].

Meprobamate is primarily metabolized in the liver to inactive metabolites [15,16], although 10 to 20 percent of the parent compound is excreted unmetabolized by the kidneys [16]. Elimination is by first order pharmacokinetics and reported elimination half-lives range between 6.4 and 16.6 hours with therapeutic doses [17,18] with little change in overdose [17,19].

CLINICAL FEATURES OF OVERDOSE

History — In the setting of a drug overdose, an accurate history can be difficult to obtain. However, whenever possible, the clinician should try to learn from the patient and any others who may be knowledgeable (eg, friends, paramedics) about the circumstances of the meprobamate ingestion. Features of special concern include other comorbidities (particularly heart failure or other cardiac disease), whether the ingestion was intentional, the amount ingested, the time elapsed since the ingestion, and whether other substances were also taken. There is no data that accurately describes the correlation between the amount ingested and the severity of symptoms, but the case fatality rate for meprobamate poisoning is low. Significant toxicity is likely with ingestions of 4 to 5 g or more [3,4]. Meprobamate is often ingested with benzodiazepine [4]. (See 'Epidemiology' above and "Benzodiazepine poisoning".)

Clinical symptoms and signs

Overview — The onset of symptoms from meprobamate poisoning usually occurs within 20 to 30 minutes of ingestion [2-6]. Most important among the signs of poisoning are hypotension and depressed mental status. Potential signs of poisoning are myriad but primarily related to depression of the central nervous, cardiovascular, and respiratory systems. Symptoms and signs may include: drowsiness, weakness, ataxia, paresthesias, headaches, vision disturbances, seizures, stupor, coma, nausea and vomiting, respiratory depression, pulmonary edema, respiratory arrest, arrhythmias (both bradycardia and tachycardia), and shock.

Cardiovascular — Hypotension is a hallmark of meprobamate poisoning and is generally ascribed to myocardial depression [3,5,20-23]; vasoplegia (decreased peripheral vascular resistance) is a less likely explanation. Hypotension can be profound, and death from meprobamate overdose is most often due to cardiovascular collapse.

Myocardial depression has been demonstrated on echocardiogram in a number of case reports. A case series of 74 patients with severe meprobamate poisoning requiring mechanical ventilation reported that 29 (40 percent) exhibited hypotension with a decreased left ventricular ejection fraction (LVEF, 45±15 percent) and decreased cardiac index (2.0±0.7 L/minute/m2) on echocardiography [3]. Twenty-eight of the 29 hypotensive patients required treatment with vasopressors.

Neurologic — Altered mental status with significant central nervous system (CNS) depression is frequently described in meprobamate poisoning [4,6]. In one retrospective case series of 146 cases, more than 80 percent of patients had a Glasgow Coma Scale (GCS) score ≤7, although most patients in this series had ingested additional sedatives (primarily aceprometazine) [6]. In another series of 59 confirmed meprobamate ingestions, the mean GCS was 7.1±1 [4]. The duration of coma can vary from an hour or two to a few days depending upon the severity of the overdose. Coma from severe meprobamate overdose associated with an absence of electrical brain activity (electroencephalographic silence) has been described in several case reports [24-26].

Other neurologic manifestations of meprobamate poisoning may include decreased muscle tone and loss of deep tendon reflexes [4,21].

Respiratory — Cases of respiratory failure and pulmonary edema associated with meprobamate poisoning have been reported [21,27,28]. In most cases, the cause of respiratory failure is likely multifactorial and may include direct depression of the respiratory centers of the brain, prolonged myocardial depression, aspiration, and the development of acute respiratory distress syndrome. In addition, patients with meprobamate poisoning have often ingested other agents that contribute to respiratory depression, such as benzodiazepines and alcohol.

Other manifestations — Cases of rhabdomyolysis [29], pancreatitis [30,31], and hypothermia have been described in association with meprobamate poisoning, but a causal relationship remains speculative. Bezoar formation can occur [32].

DIAGNOSTIC IMAGING — In cases of suspected meprobamate poisoning, a bedside transthoracic ultrasound or echocardiogram can assist with diagnosis by demonstrating depressed myocardial function (diminished ejection fraction). A plain chest radiograph should be obtained if pulmonary edema is suspected.

LABORATORY EVALUATION

Testing for meprobamate — Analytical methods for the identification and quantification of meprobamate in the blood and urine are available [33,34]. However, rapid laboratory testing in the emergency setting typically cannot be performed and thus plays no role in the management of acute overdose.

There is an association between the severity of central nervous system (CNS) depression and serum meprobamate concentrations [4]. In a review of 59 cases of meprobamate overdose, patients with a Glasgow Coma Scale (GCS) score of 13 to 15 (n = 8) had a mean concentration of 63 mg/L, patients whose GCS score ranged from 9 to 12 (n = 9) had a mean concentration of 81 mg/L, and patients whose GCS score ranged from 3 to 5 (n = 42) had a mean concentration of 111 mg/L [4]. Nevertheless, a clear correlation between clinical presentation and serum concentration is far from established, and concentrations are not required to guide therapy.

General evaluation — Routine laboratory evaluation of the patient with suspected meprobamate poisoning generally includes the following:

Complete blood count, basic serum electrolytes, and serum BUN and creatinine.

Fingerstick glucose, to rule out hypoglycemia as the cause of altered mental status.

Acetaminophen and salicylate levels, to rule out these common co-ingestants.

Electrocardiogram, to rule out conduction system abnormalities (eg, QRS or QTc interval prolongation).

Blood and urine samples for further toxicologic analyses if needed.

In patients with manifestations of a significant meprobamate poisoning (eg, hypotension, altered mental status), we obtain a serum lactate concentration, arterial or venous blood gas, liver transaminases (AST, ALT), lipase, and creatine phosphokinase.

DIAGNOSIS — Although a definitive diagnosis of meprobamate poisoning can be made with serum testing, typically such methods are not available to the emergency or critical care clinician managing the acutely ill patient. Most often, the diagnosis is made clinically on the basis of a history of ingestion (often intentional) when available and suggestive clinical findings, such as depressed mental status, hypotension from myocardial depression, and possibly depressed respiration. A transthoracic ultrasound or echocardiogram is useful for confirming myocardial depression as the cause of hypotension.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of meprobamate poisoning includes overdose with sedative-hypnotics, such as barbiturates and benzodiazepines, baclofen, alcohol, and other central nervous system (CNS) depressants. Although seldom an issue in clinical practice, medical conditions that cause both depressed mental status and hypotension without other prominent signs could be confused with meprobamate poisoning. Such conditions include severe hypothyroidism, adrenal insufficiency, and hypopituitarism. Common causes of depressed mental status, such as hypoglycemia, intracerebral hemorrhage, stroke, seizure (eg, postictal state), and sepsis should be considered in the differential diagnosis. These conditions can generally be distinguished readily from meprobamate poisoning on the basis of the history, examination findings (eg, focal neurologic deficits with stroke; signs of infection with sepsis), basic laboratory tests (eg, finger stick glucose), or when necessary diagnostic imaging. (See "General approach to drug poisoning in adults" and "Benzodiazepine poisoning" and "Ethanol intoxication in adults" and "Initial assessment and management of acute stroke" and "Evaluation and management of the first seizure in adults" and "Definition, classification, etiology, and pathophysiology of shock in adults".)

The combination of marked central nervous system depression, hypotension, and myocardial depression distinguishes meprobamate poisoning clinically from most other toxic ingestions, with the exception of barbiturate poisoning. Severe CNS depression, hypothermia, and respiratory depression are the characteristic signs of barbiturate poisoning. Cutaneous bullae (“barb blisters”) have been described in association with barbiturate poisoning [35,36], but blisters cannot reliably distinguish the two poisonings. When clear differentiation is necessary, serum concentration measurements are usually needed.

MANAGEMENT

Initial stabilization — Initial assessment of the poisoned patient is described separately; details related to the management of the patient with meprobamate poisoning are discussed here. (See "General approach to drug poisoning in adults", section on 'Initial evaluation and treatment' and "Initial management of the critically ill adult with an unknown overdose".)

Management begins with rapid assessment of the patient's airway, breathing, and circulation, and these are secured as necessary. Central nervous system depression is a hallmark of meprobamate poisoning and respiratory compromise can also occur, so early tracheal intubation may be required. Intubation is generally needed due to a decline in mental status and the resulting loss of airway protection, rather than isolated respiratory depression. Given the risk of myocardial depression and severe hypotension in these patients, etomidate and ketamine are the preferred induction agents for rapid sequence intubation. Common causes of altered mental status should be ruled out (eg, fingerstick glucose measurement for hypoglycemia). Continuous cardiac monitoring and pulse oximetry should be performed. (See "Rapid sequence intubation in adults for emergency medicine and critical care".)

Meprobamate poisoning is potentially life-threatening but the drug is readily removed by hemodialysis or other forms of extracorporeal elimination. Therefore, we recommend that immediate nephrology consultation be obtained for any patient with a severe meprobamate poisoning (eg, severely depressed mental status, respiratory problems requiring intubation, hypotension requiring treatment with a vasopressor). (See 'Enhanced elimination' below.)

Treatment of hypotension — As hypotension from meprobamate poisoning is due primarily to myocardial depression, clinicians must approach fluid resuscitation cautiously. Intravenous boluses of isotonic fluid are given to maintain intravascular volume, but fluid overload must be avoided. Vasopressor support may be needed to treat hypotension. In such cases, we suggest starting with dobutamine. If needed to maintain adequate mean arterial pressure, norepinephrine may be added. The authors prefer to avoid dopamine and epinephrine due to the risk of arrhythmia. (See "Use of vasopressors and inotropes" and "Inotropic agents in heart failure with reduced ejection fraction".)

Start a dobutamine infusion at 2.5 µg/kg per minute and titrate to effect, using mean arterial pressure, urine output, skin findings (eg, skin temperature, capillary refill), and serum lactate concentrations as markers for perfusion. The rate of the dobutamine infusion can be increased up to 10 µg/kg per minute. In the authors’ experience, larger doses have not improved outcomes. If necessary, norepinephrine can be added at a starting dose of 2 to 5 µg/minute and titrated upwards as needed. For shock that is refractory to intravascular volume repletion, dobutamine, and norepinephrine, additional treatments can include epinephrine (bolus doses and an infusion can be given) and mechanical assist devices such as an intra-aortic balloon pump or intraventricular pump. In cases of refractory hypotension, we recommend obtaining an echocardiogram to assess cardiac function.

Gastrointestinal decontamination — There are no controlled trials that explore the efficacy and safety of either gastric lavage or activated charcoal for the treatment of meprobamate poisoning. We do not routinely recommend gastric lavage but do suggest administration of a single dose of activated charcoal if the patient presents within one hour of a significant meprobamate ingestion (eg, patient is symptomatic; ingestion ≥4 to 5 g) and the airway is secure (ie, patient is alert or tracheal tube is in place).

We do not routinely suggest the use of multidose activated charcoal. However, a case series of two patients given two treatments each of activated charcoal reported an average elimination half-life of 4.5 hours [37], which is considerably shorter than those commonly reported in therapeutic dose and overdose [17-19].

Although rare, bezoar formation has been reported after ingestion of meprobamate [32,38,39]. Bezoar formation may be suspected following a massive overdose or in patients with persistent signs of poisoning (eg, prolonged refractory hypotension). Diagnosis may be made on the basis of imaging studies (plain abdominal radiograph, computed tomography, ultrasound). In addition, if such testing is available, serial serum meprobamate concentrations may be helpful as a consistently elevated or rising level would suggest the presence of a bezoar causing ongoing absorption of drug from the gastrointestinal tract. Consultation with a gastroenterologist and surgeon should be obtained if a bezoar is suspected or identified in order to arrange for endoscopic or surgical removal. (See "Gastric bezoars".)

Enhanced elimination — Meprobamate exhibits low protein binding and is efficiently removed by high flux hemodialysis and other forms of extracorporeal elimination [27]. We recommend that immediate nephrology consultation be obtained for any patient with a severe meprobamate poisoning (eg, severely depressed mental status, respiratory problems requiring intubation, hypotension requiring treatment with a vasopressor) in order to initiate extracorporeal removal as quickly as possible. The best method for removal will vary depending upon available resources and local expertise. (See "Enhanced elimination of poisons", section on 'Extracorporeal removal' and "Acute hemodialysis prescription".)

Although multiple techniques to enhance the elimination of meprobamate have been described, reports are largely limited to small case series. Proposed techniques include resin and charcoal hemoperfusion [19,40-42], hemodialysis [13,20,27], peritoneal dialysis [43], and combined hemodialysis-hemoperfusion [13]. The authors have used hemodiafiltration successfully to remove meprobamate from poisoned patients. Values reported for plasma clearance for charcoal hemoperfusion have ranged between 134 and 164 mL/minute [19], a range of 162 to 222 mL/minute was reported for resin hemoperfusion [41], and a rate of 62 mL/minute was reported for hemodialysis in one case [27].

Ongoing treatment and disposition — Ongoing treatment of meprobamate poisoning is largely supportive as no antidote is available. There are no controlled studies to inform treatment decisions. Airway protection and mechanical ventilation are vital in cases of significant central nervous system depression or respiratory compromise. The extent of any pulmonary injury and baseline function determine the approach to mechanical ventilation. (See "Mechanical ventilation of adults in the emergency department" and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Hypotension is managed with judicious administration of IV isotonic crystalloid and vasopressor support as needed. In case of refractory hypotension, we recommend obtaining an echocardiogram to assess cardiac function. Nephrology consultation should be obtained for any severe poisoning to expedite extracorporeal removal. (See 'Treatment of hypotension' above and 'Enhanced elimination' above.)

Any patient with signs of severe meprobamate poisoning should be admitted to an intensive care setting. There are no systematic data to guide the management of mildly symptomatic or asymptomatic patients with purported meprobamate ingestion. Patients with minor symptoms or signs (eg, mild drowsiness but airway reflexes intact and blood pressure stable) should be observed in a monitored setting until these findings resolve. We suggest close monitoring of such patients including pulse oximetry, cardiac monitor, and reassessment of vital signs and a focused neurologic evaluation every 30 to 60 minutes. Patients whose clinical status worsens should be transferred to an intensive care setting; those whose symptoms resolve should undergo a psychiatric evaluation.

With the exception of patients with a massive ingestion complicated by bezoar formation, patients who have ingested meprobamate should manifest symptoms within three hours, as gastrointestinal absorption is rapid and peak serum concentrations are achieved within one to three hours. Therefore, we suggest that asymptomatic patients with a reported meprobamate overdose be observed for four to six hours to provide a margin of safety; they may be discharged or referred for psychiatric evaluation if they remain without clinical signs or symptoms and their reexamination is unremarkable. Patients who develop signs of overdose are admitted to the appropriate monitored setting. Appropriate psychiatric evaluation is needed for all patients whose overdose was intentional.

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients who are critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have clinical and/or medical toxicologists available for bedside consultation and/or inpatient care. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment".)

SUMMARY AND RECOMMENDATIONS

EpidemiologyMeprobamate poisoning is rare and occurs most often from intentional overdose. (See 'Epidemiology' above.)

Clinical presentationMeprobamate poisoning causes central nervous system depression, which may result in coma, and myocardial depression, which can produce significant hypotension.

The onset of symptoms occurs within 20 to 30 minutes of ingestion. The most important signs of a significant poisoning are hypotension and depressed mental status. Other symptoms and signs may include: drowsiness, weakness, ataxia, headaches, vision disturbances, seizures, stupor, coma, vomiting, respiratory depression, pulmonary edema, respiratory arrest, arrhythmias (both bradycardia and tachycardia), and shock. (See 'Clinical features of overdose' above.)

Differential diagnosis – The differential diagnosis of meprobamate poisoning includes overdose of sedative-hypnotic drugs, such as benzodiazepines and barbiturates, drugs with sedative-like effects (eg, baclofen), alcohols, and medical conditions that cause coma and hypotension. (See 'Differential diagnosis' above.)

Laboratory evaluation and diagnostic imaging – The necessary laboratory workup is described in the text. We suggest performing echocardiography to assess myocardial depression in significant poisoning causing systemic hypotension. (See 'Laboratory evaluation' above and 'Diagnostic imaging' above.)

Management of severe overdose – Death from meprobamate overdose results from cardiovascular collapse or respiratory failure. Securing the airway early is crucial. Blood pressure is maintained by careful administration of IV crystalloids to maintain circulating volume, while avoiding fluid overload, and vasopressor support when necessary. We suggest initiating treatment with dobutamine, when vasopressor support is needed (Grade 2C). (See 'Initial stabilization' above and 'Treatment of hypotension' above and 'Gastrointestinal decontamination' above.)

Enhanced elimination including hemodialysisMeprobamate is efficiently removed by high flux hemodialysis and other forms of extracorporeal elimination. We recommend that immediate nephrology consultation be obtained for any patient with a severe meprobamate poisoning (eg, severely depressed mental status, respiratory problems requiring intubation, or hypotension requiring treatment with a vasopressor) in order to initiate extracorporeal removal as quickly as possible. (See 'Enhanced elimination' above.)

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