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Article Last Updated: Oct 9, 2008
Alcohol-related psychosis is a secondary psychosis with predominant hallucinations occurring in many alcohol-related conditions, including acute intoxication, withdrawal, after a major decrease in alcohol consumption, and alcohol idiosyncratic intoxication. Alcohol is a neurotoxin that affects the brain in a complex manner through prolonged exposure and repeated withdrawal, resulting in significant morbidity and mortality. Alcohol-related psychosis is often an indication of chronic alcoholism; thus, it is associated with medical, neurological, and psychosocial complications.
Alcohol-related psychosis spontaneously clears with discontinuation of alcohol use and may resume during repeated alcohol exposure. Although distinguishing alcohol-related psychosis from schizophrenia through clinical presentation often is difficult, it is generally accepted that alcohol-related psychosis remits with abstinence, unlike schizophrenia. If persistent psychosis develops, diagnostic confusion can result. Comorbid psychotic disorders, eg, schizophrenia and bipolar affective disorder, may exist, resulting in the psychosis being attributed to the wrong etiology.
Alcohol idiosyncratic intoxication is an unusual condition that occurs when a small amount of alcohol produces intoxication that results in aggression, impaired consciousness, prolonged sleep, transient hallucinations, illusions, and delusions. These episodes occur rapidly, can last from only a few minutes to hours, and are followed by amnesia. Alcohol idiosyncratic intoxication often occurs in elderly persons and those with impaired impulse control.
Unlike alcoholism, alcohol-related psychosis lacks the in-depth research needed to understand its pathophysiology, demographics, characteristics, and treatment. This article will attempt to provide as much possible information for adequate knowledge of alcohol-related psychosis and the most up-to-date treatment.
For related information, see Medscape's Addiction Resource Center.
Alcohol-related psychosis most likely relates to dopamine in the limbic and possibly other systems. The dopamine hypothesis often is applied to psychosis involving excessive activity of the dopaminergic system. Animal studies have shown dopaminergic activity to increase with increased release of dopamine when alcohol is administered. On the other hand, alcohol withdrawal generates a decrease in the firing of dopaminergic neurons in the ventral tegmental area and a decrease in release of dopamine from the neuron.
The pathophysiological systems of intoxication, withdrawal, and alcohol idiosyncratic intoxication all are different, and their relationships to psychosis are unclear. To some degree, they all involve the neurotoxicity of alcohol with resultant neurological, genetic, biochemical, and physiological pathology.
Alcohol intoxication results in disinhibition, sedation, and anesthesia. Acute depression of the cerebral cortex and reticular activating system results. The pathophysiology of alcoholism involves alterations in short-term membrane regulation and long-term effects on gene expression.
In patients who are dependent on alcohol, alcohol withdrawal results in adrenergic hypersensitivity of the limbic system and brainstem. Thiamine deficiency also is a contributing factor and is known to be associated with more severe episodes of withdrawal psychosis, which may present as a delirious state known as Wernicke-Korsakoff syndrome (WKS). Psychosis is not considered a symptom in uncomplicated alcohol withdrawal in patients who are not dependent on alcohol. The psychosis often is self-limited and recurs with subsequent withdrawals.
Roughly 3% of persons with alcoholism experience psychosis during acute intoxication or withdrawal. Approximately 10% of patients who are dependent on alcohol who are in withdrawal experience severe withdrawal symptomatology, including psychosis. Twins studies have shown concordance rates for alcohol-related psychosis to be 17.3% in monozygotic twins and 4.8% in dizygotic twins.1
In as much as 50% of Japanese, Chinese, and Korean populations, the likelihood of alcohol-related disorders occurring is less because of the absence of aldehyde dehydrogenase. This causes an Antabuse-type reaction involving facial flushing and palpitations.
Studies of the Soviet Slavic republic of Belarus from 1970-2005 suggest a correlation between cultural and social context of alcohol consumption and alcohol-related suicides and alcohol-induced psychosis.2
The appearance of alcohol-related psychosis occurs with long-term alcohol abuse; therefore, it is associated with the same morbidity and mortality of long-term alcoholism. Alcohol-related psychosis is a serious indicator of medical, neurological, and psychosocial complications, which hinder appropriate treatment and outcome. Prognosis with treatment is considered good, with only 10-20% of psychosis cases becoming chronic. Alcohol-related psychosis itself does not have specific morbidity or mortality; instead, it correlates with a cluster of risk factors that indicate higher morbidity and mortality in patients with alcoholism.3
Psychiatric complications of alcohol-related psychosis include higher rates of depression and suicide. The potential for violence also exists.
Alcohol-related psychosis may indicate undiagnosed schizophrenia or other psychotic disorders. The use of alcohol may potentiate or initiate psychosis through kindling, a process where repetitive neurologic insult results in greater expression of the disease.
Some of the medical complications observed with alcohol-related psychosis include liver disease, pulmonary tuberculosis, diabetes mellitus, musculoskeletal injury, hypertension, and cerebrovascular disease.
Cultural influences on alcohol-related psychosis stem from cultural norms about alcohol. Irish males who traditionally drink to the point of intoxication are at higher risk, while Jewish males who traditionally shun intoxication have lower risks. Considering the relationship of thiamine to Wernicke-Korsakoff syndrome, cultures that have a low intake of thiamine and high rates of alcohol abuse also are at higher risk for the complication of Wernicke-Korsakoff syndrome.
Alcohol abuse and dependency has a male-to-female ratio of 5:1. Females develop alcohol-related disorders later in life because they start heavy use later then males.
Alcohol-related psychosis occurs after extended periods of alcohol abuse that result in an alteration of neuronal membranes, genetic expression, and thiamine deficiency. Early-onset alcoholism results in a greater chance of complications earlier in life and an outcome that is influenced by psychosocial function. Late-onset alcoholism only delays the onset of complications. As a general rule, alcohol-related psychosis occurs more frequently in older populations. Most alcohol-related disorders occur in persons aged 35-40 years.
Alcohol-related psychosis can be confused with other psychiatric disorders resulting from other substance abuse disorders and from other medical, neurologic, and psychological etiologies. The cause of alcohol-related psychosis can be determined by the patient history and family genealogy.
The Diagnostic Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) provides criteria for the diagnosis of substance-induced psychotic disorder and should be helpful in clarifying etiology.6
During the initial examination of every psychiatric patient, a full physical and neurological examination is required. When a patient presents as psychotic or intoxicated, also assess the risk of dangerous behavior.
Possible causes or contributors to alcohol-related psychosis include the following:
Because most cases of alcoholic psychosis are self-limiting, removal of alcohol should suffice. Initial treatment should include medically stabilizing the patient by assessing respiratory, circulatory, and neurological systems. A patient intoxicated to the point of psychosis is considered a medical emergency because of the risk of unconsciousness, seizures, and delirium tremens. Medical treatment should focus on the effect of alcohol on the body as a whole. A patient with head trauma may be misdiagnosed with Wernicke-Korsakoff syndrome, and a neurologic examination should always be considered. Alcohol withdrawal requires inpatient hospitalization for more than 72 hours after the risk of delirium tremens has subsided. Remember, although self-limited, it carries with it significant morbidity and mortality.
No specific dietary restrictions are necessary, only the recommendation for a regular diet. However, if a patient has a thiamine-poor diet, further dietary intake should be normalized.
A patient intoxicated with alcohol is dangerous. Limit the activity of such patients until symptoms have been resolved.
Benzodiazepines protect patients from the effects of alcohol withdrawal, and they control psychotic symptoms. Flexibility of administration (eg, PO/IV/IM), rapid onset of action, and efficacy in sedating aggressive patients effectively provide treatment in emergencies. Risk of behavioral disinhibition and liver failure require caution.
Antipsychotics that lower seizure threshold increase risk of seizures associated with alcohol withdrawal. Typical antipsychotics (eg, haloperidol) effectively treat acute psychosis because they have been found to be helpful for rapid tranquilization. Evidence indicating that atypical antipsychotics would have similar rapid effects is insufficient. High-potency antipsychotics are recommended for rapid tranquilization; lower-potency antipsychotics might require higher doses. The medication also should be available in IM form; this eliminates all atypical antipsychotics and some typical antipsychotics (eg, molindone, thioridazine, pimozide). If long-term psychosis develops, the atypical antipsychotics (eg, risperidone, olanzapine, quetiapine) that are more tolerable can be used.
Other medications used in the treatment of alcohol-related psychosis are disulfiram for enforced abstinence, naltrexone or topiramate to dampen cravings, and naloxone if opiate overdose is suspected.
Topiramate doses of up to 300 mg have been studied for treating alcohol dependence. No literature is available to support its use.
By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmissions and other inhibitory transmitters.
| Drug Name | Lorazepam (Ativan) |
|---|---|
| Description | Preferred over chlordiazepoxide because half-life in liver disease is more predictable. Does not undergo oxidative metabolism by the liver. Accumulation of drug or its active metabolites does not occur. Available in PO, IV, and IM forms. |
| Adult Dose | 5-10 mg/d PO/IV/IM in single or divided doses Elderly/debilitated: Initial dose of 1-2 mg PO/IV/IM Detoxification protocol: 1-2 mg PO/IV/IM q6h for 1 d, 1-2 mg PO/IV/IM q8h for 1 d, 1 mg PO/IV/IM bid for 1 d; 1 mg PO/IV/IM qhs on a tapering schedule may be used Symptom-triggered dosing using structured assessment scales, such as the Clinical Institute Withdrawal Assessment-Alcohol (CIWA-A) withdrawal symptoms, can be well controlled and the total dose of the drug can be reduced |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; acute angle-closure glaucoma |
| Interactions | Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, narcotic analgesics, scopolamine, barbiturates, and MAOIs |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in renal or liver failure, myasthenia gravis, organic brain syndrome, or Parkinson disease; paradoxical excitement resulting in rage behavior; depressed patients with suicidal tendencies |
| Drug Name | Chlordiazepoxide (Librium) |
|---|---|
| Description | Provides rapid onset and efficacy in sedating aggressive patients. Longer half-life, providing a steady withdrawal. Available in PO, IV, and IM forms. |
| Adult Dose | 50-100 mg/d PO/IV/IM in a single or divided dose Elderly/debilitated: Initial dose of 10 mg PO/IV/IM Detoxification protocol: 25 mg PO/IV/IM q6h for 1 d, 25 mg PO/IV/IM q8h for 1 d, 25 mg PO/IV/IM q12h for 1 d, 25 mg PO/IV/IM qhs for 1 d During taper: If BP is greater than or equal to 140/90 and pulse is greater than or equal to 100, use 25 mg PO/IV/IM prn |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | Coadministration with alcohol, phenothiazines, barbiturates, and MAOIs increases CNS toxicity; cisapride can significantly increase levels |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in liver failure; paradoxical excitement resulting in rage behavior; depressed patients at risk for suicide; respiratory arrest can occur if doses exceed those needed to control withdrawal; caution in patients receiving other CNS depressants or diagnosed with low albumin levels |
High-potency agents (eg, haloperidol, droperidol) provide rapid, predictable, and effective sedation in the management of acutely psychotic patients. They are less sedating and are more easily titrated but are more likely to cause EPS than the lower-potency agents. They often are combined in the same syringe with a benzodiazepine (eg, lorazepam, diazepam) for better sedation and anxiolysis and less dystonia or akathisia. They are given IM or IV, or, in a less acute setting, they are given PO (haloperidol only). Haloperidol also has a monthly depot form (Haldol Decanoate). Depot antipsychotics are not intended for use in the acute setting.
| Drug Name | Haloperidol (Haldol) |
|---|---|
| Description | Controls psychosis and provides rapid tranquilization. Administer with a benzodiazepine to protect against lowered seizure threshold. In emergencies, select high-potency antipsychotic available in tab, liquid, or IM form. |
| Adult Dose | 2-5 mg PO/IM |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; extrapyramidal symptoms; Parkinson disease |
| Interactions | Serum plasma levels decreased by rifampin; potentiates effects of CNS depressants (eg, alcohol, opiates, anesthetics); lithium has induced an encephalopathic syndrome |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Severe neurotoxicity manifesting as rigidity or inability to walk or talk may occur in patients with thyrotoxicosis also receiving antipsychotics; if administered IV/IM, watch for hypotension; caution in diagnosed CNS depression or cardiac disease; if history of seizures, benefits must outweigh risks; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if occurs) Ventricular arrhythmias such as torsade de pointes have been reported in patients, especially those with cardiac disease and in those given high doses of IV haloperidol |
| Drug Name | Thiothixene (Navane) |
|---|---|
| Description | Blocks postsynaptic blockade of CNS dopamine receptors, inhibiting dopamine-mediated effects. Provides rapid tranquilization in PO and IM forms. |
| Adult Dose | 5-20 mg/d PO/IM in a single or divided dose |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; breastfeeding; CNS depression; blood dyscrasias |
| Interactions | Decreases effects of guanethidine; increases toxicity of CNS depressants, anticholinergics, and alcohol |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in narrow-angle glaucoma, severe liver disease, seizures, bone marrow suppression, cardiac disease; extrapyramidal symptoms (eg, muscle rigidity, inability to walk or talk, akathisia, dystonia); opisthotonos and oculogyric crisis; circulatory collapse; coma |
A patient who is highly motivated to participate in an abstinence program may benefit from the use of disulfiram. Disulfiram inhibits the metabolism of alcohol, causing increased levels of acetaldehyde, resulting in flushing, nausea, and multiple other noxious symptoms. Compliance can be determined through detecting diethylamine (disulfiram metabolite) in the urine. Naltrexone is an agent helpful in decreasing the craving for alcohol. It has been shown to be superior to placebo when used in combination with supportive psychotherapy. Naltrexone's mechanism of action is thought to be through blocking the opioid system, which is thought to be involved in alcohol craving. Acamprosate is the newest approved drug. Its mechanism of action is not fully understood, but it is hypothesized to restore neuronal excitation and inhibition balance. In 3 placebo-controlled trials, acamprosate was superior to placebo in maintaining alcohol abstinence as part of a comprehensive management program.
| Drug Name | Disulfiram (Antabuse) |
|---|---|
| Description | Used to enforce abstinence but does not cure alcoholism. Often used in conjunction with psychotherapy and AA meetings. |
| Adult Dose | 500 mg PO qd for up to 2 wk; 250 mg PO qd; not to exceed 500 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; ethanol intoxication; psychosis; cardiac disease, coronary occlusion |
| Interactions | Increases effects of diazepam and chlordiazepoxide; metronidazole, isoniazid, and phenytoin may increase toxicity; coadministration with warfarin may increase prothrombin time |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Requires >12 h abstinence before administration; caution in hypothyroidism, diabetes, hepatic cirrhosis or insufficiency, and seizure disorders Because disulfiram also inhibits dopamine-beta-hydroxylase activity, caution should be used in those with comorbid schizophrenia. |
| Drug Name | Naltrexone (ReVia) |
|---|---|
| Description | Used primarily to block the opioid receptors and prevent euphoria (thus decreasing craving) in those who abuse opiates. Theoretically, when a person with alcoholism craves alcohol, the opioid system is stimulated and the opioid receptors are antagonized, thus, the craving is dampened. |
| Adult Dose | 25-50 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; patients who have had opiates within past 7-10 d |
| Interactions | Inhibits effects of opiates |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Liver function should be established prior to use; higher than approved doses have led to hepatotoxicity; caution in those at risk for suicide (overdose can lead to liver failure) |
| Drug Name | Acamprosate (Campral) |
|---|---|
| Description | Synthetic compound with a chemical structure similar to that of the endogenous amino acid homotaurine (structural analogue of gamma-aminobutyric acid [GABA]). The mechanism of action to maintain alcohol abstinence is not completely understood. Hypothesized to interact with glutamate and GABA neurotransmitters centrally to restore neuronal excitation and inhibition balance. Not associated with tolerance or dependence development. Use does not eliminate or diminish alcohol withdrawal symptoms. Indicated to maintain alcohol abstinence as part of a comprehensive management program that includes psychosocial support. Available as a 333-mg tab. |
| Adult Dose | 666 mg PO tid; initiate as soon as possible after alcohol withdrawal when abstinence has been achieved; if <60 kg, may need to decrease dose by 333-666 mg/d CrCl 30-50 mL/min: 333 mg PO tid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; severe renal impairment (ie, CrCl <30 mL/min) |
| Interactions | Coadministration with naltrexone increases acamprosate Cmax and AUC, but no dosage adjustments are necessary |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Common adverse effects include headache, diarrhea, flatulence, and nausea; depression and anxiety incidence slightly higher than that of placebo in 1 study |
These agents provide a number of major improvements over the traditional agents, including the following: fewer adverse anticholinergic effects, less dystonia and parkinsonism, very low risk of tardive dyskinesia, and potential reversal of many negative symptoms (eg, affective blunting, alogia, withdrawal, avolition). These agents affect dopamine receptors but also affect serotonin receptors involved with frontal lobe functions.
| Drug Name | Aripiprazole (Abilify) |
|---|---|
| Description | Improves positive and negative schizophrenic symptoms. The mechanism of action is unknown but is hypothesized to work differently than other antipsychotics. Aripiprazole is thought to be a partial dopamine (D2) and serotonin (5HT1A) agonist, and antagonize serotonin (5HT2A). Additionally, no QTc interval prolongation was noted in clinical trials. Available as tab, orally disintegrating tab, or oral solution. |
| Adult Dose | 10-15 mg PO qd; if needed, may increase dose gradually q2wk, not to exceed 30 mg/d Alternatively, 9.75 mg IM initially (dose range 5.25-15 mg); may give second dose after minimum of 2 h; not to exceed total cumulative dose of 30 mg/d; replace injection with oral dose (10-30 mg/d) as soon as possible |
| Pediatric Dose | <13 years: Not established >13 years: 2 mg PO qd initially; after 48 h, may titrate upward to 5 mg/d and then after another 48 h to 10 mg/d; subsequent dose increases should be in 5 mg/d increments; not to exceed 30 mg/d |
| Contraindications | Documented hypersensitivity |
| Interactions | CYP450 3A4 and 2D6 isoenzyme substrate, thus, inhibitors (ie, ketoconazole, quinidine, fluoxetine, paroxetine) or inducers (ie, carbamazepine) may increase or decrease serum levels respectively; decrease dose by one-half when coadministered with strong CYP450 3A4 inhibitors (eg, ketoconazole, clarithromycin) or 2D6 inhibitors (eg, quinidine, fluoxetine, paroxetine); dose should be doubled when coadministered with strong CYP3A4 inducers (eg, carbamazepine, rifampin) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Common adverse effects include headache, anxiety, somnolence, or insomnia; rare reports of tardive dyskinesia and neuroleptic malignant syndrome; may cause orthostatic hypotension, seizure, dysphagia, or suicidal ideation; hyperglycemia may occur and in some cases be extreme, resulting in ketoacidosis, hyperosmolar coma, or death |
| Drug Name | Olanzapine (Zyprexa) |
|---|---|
| Description | May inhibit serotonin, muscarinic, and dopamine effects. Efficacy similar to risperidone, fewer dose-dependent adverse effects but more concern about weight gain. |
| Adult Dose | 5-20 mg/d PO in divided doses |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | Fluvoxamine may increase effects; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease effects |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration |
| Drug Name | Quetiapine (Seroquel) |
|---|---|
| Description | May act by antagonizing dopamine and serotonin effects. Efficacy similar to risperidone and olanzapine. Fewer dose-dependent adverse effects and less concern of weight gain. |
| Adult Dose | 25 mg PO bid; titrate to 150-750 mg/d PO; not to exceed 800 mg/d |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | May antagonize levodopa and dopamine agonists; phenytoin, thioridazine, and other liver enzyme inducers may reduce levels |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | May induce orthostatic hypotension associated with dizziness, tachycardia, and syncope; neuroleptic malignant syndrome has been associated with this treatment; cataracts may develop (perform eye examination every 6 mo) |
| Drug Name | Risperidone (Risperdal) |
|---|---|
| Description | Unlike haloperidol, has serotonergic blocking effects that alleviate negative symptoms of psychosis (eg, anhedonia, avolition, amotivational, flat effect). Well tolerated with fewer adverse extrapyramidal effects than with typical antipsychotics. Doses > 6 mg/d increase risk of extrapyramidal effects. No atypical antipsychotic agent is preferred in treating alcohol-related psychosis. |
| Adult Dose | 2-14 mg/d PO in divided doses |
| Pediatric Dose | Children: Not established Adolescents: Administer as in adults |
| Contraindications | Documented hypersensitivity |
| Interactions | Coadministration with carbamazepine may decrease effects; may inhibit effects of levodopa; clozapine may increase levels |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | May cause extrapyramidal reactions, hypotension, tachycardia, and arrhythmias |
Naloxone acts similar to naltrexone as an opiate receptor antagonist but has significant differences, restricting it to emergency situations of opiate overdose. Also should be considered in patients with alcoholism who have altered mental status due to overdose of opiates. Naloxone is poorly absorbed PO and should be administered IM or IV.
| Drug Name | Naloxone (Narcan) |
|---|---|
| Description | Used in emergencies in which narcotic overdose results in respiratory depression. Available in IV, IM, and SC forms. |
| Adult Dose | 0.4-2 mg IV; if no improvement, repeat q2-3min; not to exceed 10 mg; if no response observed after 10 mg, question the diagnosis; if IV unavailable, use IM or SC route |
| Pediatric Dose | <20 kg or < 5 years: 0.1 mg/kg IV; if no improvement, repeat q2-3min >20 kg or > 5 years: 2 mg IV; if no improvement, repeat q2-3min If IV unavailable, use IM or SC route |
| Contraindications | Documented hypersensitivity |
| Interactions | Decreases effects of narcotic analgesics |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Caution in cardiovascular disease; may precipitate withdrawal symptoms in patients addicted to opiates |
Admit for observation if further withdrawal, cognitive impairment, psychosis, and medical complications occur.
Alcohol-Related Psychosis excerpt
Article Last Updated: Oct 9, 2008