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Alcohol-related crises are among the most prevalent psychiatric emergencies, accounting for 20% to 36% of visits to emergency departments (Walker, 1983) and nearly 40% of admissions to general medical and surgical wards (Hanke, 1984). Aside from the medical complications of alcoholism, these emergencies include alcohol intoxication, idiosyncratic intoxication, alcohol withdrawal, alcohol amnestic disorder, and alcohol hallucinosis,
An intoxicated patient exhibits a range of behaviors and physical symptoms, depending on the amount of alcohol in the blood.
Mild to moderate symptoms include loquacity, slurred speech, impaired judgment, shortened attention span, inappropriate emotional responses, and euphoria (Gallant, 1989). A more severely intoxicated patient may become irrational, angry, or violent; display progressively sluggish responses to environmental stimuli; and have the "dry heaves."
Physical findings in a patient with mild to moderate intoxication include alcohol on the breath, diminished motor coordination, dysmetria, ataxia, nystagmus, blurred vision, dizziness, flushed face. orthostatic hypotension, hematemesis, and stupor. In cases of severe intoxication, the patient has a decreased respiratory rate, slow pulse, low blood pressure, sluggish reflexes, and low body temperature; in the most serious cases, a patient can progress to shock and coma.
Depending on the patient's medical history and on clinical findings at the time of evaluation, laboratory studies may include a complete blood count (for hematemesis), an electrocardiogram (ECG) and electrolyte studies (for cardiac abnormalities), a hepatic profile (for jaundice), and a serum glucose level and computed tomography (CT) scan (for persistent stupor).
Alcohol intoxication can resemble many serious medical diseases, including diabetic ketoacidosis, hypoglycemia, intoxication with barbiturates or other sedative and hypnotic agents, subdural hematoma, multiple sclerosis, cerebellar ataxia, and Huntington's chorea (Dubin and Stolberg, 1981). If the patient is uncooperative and hostile, you can easily overlook potential medical complications of alcohol abuse, including cardiac arrhythmia, cardiac failure, upper and lower GI tract bleeding, pneumonia, liver failure or associated ascites, pancreatitis, anemia, subdural hematoma, seizures, and peripheral neuropathy (Schuckit, 1989). To elicit alcohol-related medical problems, Walker (1983) suggests asking the following questions:
Head injury is of special concern because intoxicated patients may be unable to feel the site of pain. Carefully examine the patient for bruises, cuts, and fractures, and closely examine the patient's scalp for evidence of traumatic head injury.
Perhaps no patient draws more negative response from hospital staff members than an intoxicated patient. Although such reactions are a normal response to the annoying behavior and mayhem created by an intoxicated person, you cannot allow these personal feelings to influence your professional judgments and actions.
Before interviewing a loud and boisterous patient, alert the hospital security force. Although security intervention is seldom required, you may find it reassuring to have the assistance ready. Conduct the interview in a large, comfortable room. Many alcoholic patients are claustrophobic, and you may be uncomfortable in an enclosed room with a potentially violent patient.
Assume a tolerant, nonthreatening manner. An authoritarian position is much more likely to precipitate a violent outburst (see Chapter 7, Violent Behavior). Also be prepared to tolerate insults and threats and not personalize them.
Approach the patient with an introductory handshake, and make no efforts to change the patient's behavior (Hackett, 1987). Listening to a patient's tirade and attempting to make sense of it is more effective than demanding that he speak more temperately, especially for uncovering a major grievance or misunderstanding. Try to avoid direct eye contact for more than a few seconds, because an intoxicated patient commonly interprets this as a challenge. Offering food, coffee, or juice may be helpful (Hackett, 1987); many patients are less aggressive after eating.
If the patient is excited or potentially assaultive, a benzodiazepine, such as diazepam (Valium) 5 mg orally every 30 to 60 minutes, is recommended (Hackett, 1987). If the patient is so agitated that he refuses to take oral medication, 1 to 2 mg of lorazepam (Ativan) may be given intramuscularly every hour until the patient is calm. Dosage requirements vary and commonly must be determined empirically. If the patient has a concomitant psychotic illness, a high-potency neuroleptic agent can be administered as an oral concentrate or intramuscularly every 30 to 60 minutes for up to six doses a day. Recommended doses are thiothixene (Navane), 10 mg I.M. or 20 mg concentrate; haloperidol (Haldol), 5 mg I.M. or 10 mg concentrate; and loxapine (Loxitane), 10 mg I.M. or 25 mg concentrate.
One of the cornerstones of treatment for alcohol addiction is educating the patient about the disease and its diverse effects on him and on his family and associates. Unfortunately, several factors inhibit educational efforts in the emergency setting: an intoxicated person is not receptive to learning, and an alcoholic who continues to drink usually denies his illness vehemently.
Because discharging an intoxicated patient is clinically and legally risky, the safe course is to give him time to "sleep it off' and then attempt educational interventions. If possible, have a representative of Alcoholics Anonymous speak with the patient to reduce his denial. When speaking with the patient yourself, cover the following points:
Because alcohol intoxication is a time-limited condition, most patients can be discharged to outpatient care. When possible, send the patient home in the company of family members or friends. with referral to an alcohol treatment program the next day. If the patient is already an active member of Alcoholics Anonymous (AA), obtain his permission to call the AA sponsor to arrange for immediate reinvolvement in AA.
No patient who remains ataxic should be discharged from the emergency setting, and hospitalization is recommended for intoxicated patients who have concomitant medical disorders, such as diabetes, dehydration, hypertension, or head injury, or who are suffering from medical complications of alcoholism.
The essential feature of idiosyncratic intoxication is altered behavior. usually aggression, caused by ingesting an amount of alcohol that would be insufficient to induce intoxication in most people. Anterograde amnesia (an inability to learn new information) usually occurs for the duration of the intoxication (DSM-llI-R, 1987). The patient's behavior during intoxication is atypical of his behavior when sober. Behavioral changes may last several hours or days and usually end in a prolonged sleep (Hackett, 1987).
Mental status findings in a patient who is idiosyncratically intoxicated include agitation, impulsiveness, and aggression. At times, the patient may be delusional or experience visual hallucinations. Hyperactivity, restlessness, and anxiousness are also common.
No characteristic physical findings are helpful in diagnosing idiosyncratic intoxication.
Useful tests for making the diagnosis are an electroencephalogram, drug screen, and CT head scan.
The differential diagnosis should exclude temporal lobe epilepsy, intoxication from other drugs, drug withdrawal, and malingering.
Because you cannot predict whether the patient will become aggressive, consider the patient dangerous and use caution during the initial examination. Gallant (1989) suggests the following guidelines for managing patients with idiosyncratic intoxication:
If the patient requires sedation, 10 mg of diazepam I.V. over 1 to 2 minutes or 1 to 2 mg of lorazepam I.V. over 1 to 2 minutes is recommended (Gallant, 1989). These doses can be repeated at 10minute intervals. An alternative would be 5 mg of haloperidol IX. repeated every hour if necessary (Schuckit, 1989).
Because amnesia usually accompanies idiosyncratic intoxication, reserve educational interventions until the patient is lucid and attentive. At that time, describe the patient's behavior to him in detail. Although your description may induce in him a sense of shame. the negative feeling may help him remain abstinent. Other messages about the disease of alcoholism may or may not be relevant, depending on his history. The typical patient with this disorder does not ingest much alcohol, but its dangers are nevertheless potent. Make this clear to the patient by saying, "Alcohol poisons your brain. You seem to be one of those people who cannot drink, even in small amounts. If you do, you are playing with fire."
Usually, the patient can be discharged once the episode is over. If the patient remains agitated or delusional, however, admit him for further psychiatric evaluation. Refer a patient who cannot control his drinking to an alcohol rehabilitation program.
Heavy drinkers experience various withdrawal symptoms when they stop drinking or drastically reduce alcohol intake. Withdrawal symptoms can be precipitated by severe physical stress, such as pneumonia, or the need for a major medical or surgical procedure for which the patient must be hospitalized, leading to a forced withdrawal.
Symptoms of uncomplicated alcohol withdrawal peak 24 to 48 hours after the last drink and subside within 5 to 7 days, even without treatment. However, mild irritability and insomnia may last for 10 days or more. Patients in withdrawal usually are depressed, irritable, and anxious and may experience transient hallucinations or illusions.
The mental status of a patient with alcohol withdrawal syndrome (a severe form of withdrawal formerly known as delirium tremens) is similar to that of a delirious patient. A patient typically experiences vivid visual hallucinations. Tactile, olfactory, and auditory hallucinations also can occur. Hallucinations usually are frightening-the patient sees and feels mice or lice crawling on the skin, or he sees animals, especially snakes, in threatening poses (Hacken. 1987). Other signs of alcohol withdrawal syndrome include disoriemation to time, place, or person; waxing and waning of symptoms; and intermittent agitation, commonly violent in nature.
Physical findings - the prominent feature of alcohol withdrawal and the most helpful in establishing the diagnosis - include tachycardia. sweating, elevated blood pressure, nausea, vomiting, malaise, weakness, tremulousness, hyperreflexia, orthostatic hypotension. and. occasionally, generalized seizures.
Left untreated, alcohol withdrawal syndrome can lead to death secondary to infections, fat emboli, or cardiac arrhythmias associated with hyperkalemia, hyperpyrexia, poor hydration, and hypertension (Frances and Franklin, 1987). The syndrome usually occurs in those with a 5- to 15-year history of heavy drinking who decrease their blood alcohol levels and who have a significant physical illness, such as infection, trauma, liver disease, or metabolic disorder (Frances and Franklin, 1987). Onset ranges from 24 to 72 hours after cessation of drinking.
The initial laboratory evaluation consists of blood glucose levels. serum drug levels, complete blood count (CBC), urinalysis. and serum electrolytes. Other laboratory studies that may be helpful are an ECG, chest X-ray, serum amylase, arterial blood gas (ABG) studies, and CT scan (if head trauma is suspected or found).
Differential diagnosis for alcohol withdrawal and for the more severe alcohol withdrawal syndrome must rule out concomitant medical illness (see Common nonalcoholic causes of delirium, page 44). After these medical illnesses are excluded, the primary differential diagnoses are essential tremor, withdrawal from sedative or hypnotic agents, hypoglycemia, and diabetic ketoacidosis (DSM-III-R. 1987). Hackett (1987) cautions that a clinician can easily overlook alcohol withdrawal as a diagnosis when the patient's manner, social position, or reputation belie the possibility of alcoholism.
Most patients undergoing mild alcohol withdrawal respond well to reassurance and acceptance. Staff members must treat these patients with tolerance and try to suppress any negative feelings they may have for patients with alcohol disorders. Additionally, relatives and friends can be a useful adjunct to treatment because they provide support and familiarity to the patient. Mild, pleasurable sensory stimulation, such as soft music, may further reduce the patient's agitation (Gallant, 1989).
Be clear and unambiguous with the patient at all times, identifying yourself as often as necessary and explaining the procedures that must be carried out (Tomb, 1988). Keep the patient in a well lighted room, under constant observation by staff, family members. or friends to prevent him from wandering or sustaining injury.
Unfortunately, interpersonal interventions have limited value for a patient with alcohol withdrawal syndrome, but you should try to be tolerant and supportive, minimize stimulation, identify yourself periodically, explain any procedures you must perform, and be clear, direct, and concise in your instructions.
The drug of choice for treating patients in alcohol withdrawal is a benzodiazepine (Schuckit, 1989). Other drugs-including clonidine (Catapres), propranolol (Inderal), atenolol (Tenormin), haloperidol, chlorpromazine (Thorazine), and hydroxyzine (Atarax)-have been used but are not recommended for routine therapy of alcohol withdrawal.
| Common Nonalcoholic Causes of Delirium |
| Medical (infection, thyrotoxicosis, hypoparathyroidism, congestive heart failure) |
| Surgical (head trauma, postanesthesia, confusional state, brain tumor, fat embolus, pancreatitis) |
| Metabolic (hypoxia, uremia, hypoglycemia, hepatic encephalopathy, water intoxication) |
| Drug ingestion (bromides, steroids, stimulants, atropine, psychedelics) |
| Drug withdrawal (barbiturates, tranquilizers, opiates) |
| Source: Usdin and Lewis, 1979, p. 329. Reprinted with permission of the publisher |
The primary decision in administering benzodiazepines is whether to use long- or short-acting medication. Long-acting medications, such as diazepam or chlordiazepoxide (Librium), ease withdrawal because of their long half-lives but can result in drug accumulation, which can cause lethargy, drowsiness, and ataxia, especially in a patient with hepatic impairment. Short-acting benzodiazepines, which are less likely to accumulate, must be administered more frequently because their short half-life results in rapid disappearance from the plasma, which can worsen alcohol with drawal syndrome and precipitate seizures.
Additionally, patients in alcohol withdrawal should receive vitamin and mineral supplements, because vitamin deficiencies are common in those with chronic alcoholism (Frances and Franklin, 1987). A suggested regimen consists ofthiamine (100 mg P.O. four times daily), folic acid (1 mg P.O. four times daily), a daily multivitamin, and magnesium sulfate (1 g I.M. every 6 hours for 2 days if status postwithdrawal seizures occur).
From 1% to 4% of patients in alcohol withdrawal experience seizures (Schuckit, 1989). These seizures, associated with long-term drinking, appear 7 to 38 hours after the last drink, with the average onset at 24 hours. More than 50% of patients with alcohol withdrawal seizures endure bursts of two to six generalized seizures, although less than 3% of these patients progress to status epilepticus (Frances and Franklin, 1987). Because alcohol withdrawal seizures do not represent a primary seizure disorder, a patient without such a disorder should not be routinely placed on anticonvulsant medication. Phenytoin (Dilantin) does not give added protection against seizures beyond that provided by the benzodiazepines. (See Drug treatment of alcohol withdrawal seizures.)
| Drug Treatment of Alcohol Withdrawal Seizures | |
| Drug | Intervention |
| diazepam (Valium) | Administer 10 mg I.V. over 1 to 2 minutes; repeat until the seizure clears. Do not exceed 30 mg of diazepam over 15 to 20 minutes. |
| amobarbital (Amytal) | Administer 100 to 150 mg/minute I.V. unless respiration is compromised. Repeat until the seizure clears. |
| phenytoin (Dilantin) | Administer 1,000 mg I.V. over 20 minutes (50 ml/minute in a glucose-free normal saline solution). |
| Source: Gallant, 1989; Frances and Franklin, 1988. | |
The primary pharmacologic intervention is sedation to attenuate the severity of the withdrawal. A regimen of benzodiazepines - including chlordiazepoxide, diazepam, oxazepam (Serax), and lorazepam - is usually advised. Neuroleptic medications should be used only for the most severe symptoms, such as agitation or hallucinations that do not respond to benzodiazepines. Neuroleptic agents do not increase incidence of seizures (Benforado and Hou-den, 1979; Lenchan et al., 1985). Neuroleptic doses are similar to those used in rapid tranquilization: haloperidol, 5 mg I.M. or 10 mg concentrate; thiothixene, 10 mg I.M. or 20 mg concentrate: loxapine, 10 mg I.M. or 25 mg concentrate; or fluphenazine (Pro-lixin), 5 mg I.M. or 10 mg concentrate.
| Managing Alcohol Withdrawal Syndrome | |
| Procedure | Considerations |
| Administer vitamins. | Thiamine, 100 mg I.M. followed by 100 mg P.O. for 3 consecutive days; folk; acid, 1 mg/day; multiple-vitamin tablets, 1/day. |
| Sedate the patient. | Benzodiazepines are recommended. |
| Administer fluids as needed. | Carefully individualize and titrate (over hydration is common). |
| Administer potassium chloride. | If serum potassium is low and the patient has normal kidney function, replace with potassium chloride. |
| Administer 50% magnesium sulfate, 2 to 4 ml I.M. every 8 hours for three doses. | Magnesium deficiency can contribute to lethargy and weakness and lower the patient's seizure threshold. |
| Consider anticonvulsants. | Anticonvulsants are necessary only if the patient has a history of seizures or is in status epilepticus. |
| Provide a high-carbohydrate diet. | Hypoglycemia is a significant danger in abstinent alcoholic patients. |
| Source: Walker, 1983. Adapted with permission of the publisher | |
Adjunct therapy consists of vitamins and minerals. Thiamine is necessary to prevent development of alcohol amnestic disorder. Potassium supplements are prescribed for fatigue and muscle weakness, and magnesium is given to raise the seizure threshold. No evidence suggests that anticonvulsants will protect a patient from withdrawal seizures; therefore, they should be prescribed only if the patient has an underlying seizure disorder. (See Managing alcohol withdrawal syndrome.)
Educational interventions for alcohol withdrawal are similar to those for alcohol intoxication (see page 38).
Outpatient medical detoxification is possible for most patients undergoing mild withdrawal, although close follow-up care, including daily visits, is essential to ensure adequate hydration and prevent complications. Outpatient treatment permits the patient to remain in work and social settings, and family members can provide muchneeded support. If possible, the patient should be discharged in the company of friends or relatives.
Hospitalization may be necessary if the patient has:
Note: Because alcohol withdrawal syndrome is life-threatening, a patient with this condition should be admitted to the hospital for aggressive medical intervention.
Alcohol amnestic disorder is associated with excessive alcohol consumption and a diet deficient in vitamins, especially thiamine. Although most often associated with alcoholism, this disorder can occur with malabsorption syndrome, severe anorexia, upper GI tract obstruction, prolonged intravenous feeding, thyrotoxicosis, and hemodialysis (Frances and Franklin, 1987).
Historically, alcohol amnestic disorder has been referred to as Wernicke-Korsakoff syndrome, which is actually two separate disorders: Wernicke's encephalopathy (characterized by neurologic dysfunction) and Korsakoffs psychosis (characterized by severe memory impairment). Korsakoffs psychosis, the amnestic disorder. usually follows an acute episode of Wernicke's encephalopathy.
Mental status findings characteristic of Korsakoffs psychosis are retrograde amnesia (an inability to remember events that occurred several years before onset of the illness) and anterograde amnesia (an inability to learn new information). In its acute stage, the deficiency is striking-patients cannot recall the day, time, or the examiner's first name, even after being given this information several times (Hackett, 1987). Patients usually are cheerful, pleasant. and unaware of the memory loss. Those with Wernicke's encephalopathy are disoriented and either apathetic or profoundly lethargic, at times progressing to coma.
Physical findings include cerebellar ataxia with a broad-based gait (the patient's legs are much wider apart when walking to maintain balance), inability to perform the finger-to-nose test, and oculomotor disturbances, which may include deficiency in conjugate gaze. horizontal and vertical nystagmus, and ptosis.
Standard tests include those for patients with organic disorders: a CBC, electrolyte studies, ECG, glucose, BUN level, and chest X-ray. Additionally, thiamine, folate, and vitamin B12 levels should be determined.
The chief differential diagnosis is between delirium and dementia. Patients with alcohol amnestic disorder do not experience a clouding of consciousness as do those with delirium and intoxication. Despite the memory loss, general intellectual ability remains intact, in contrast to alcohol dementia or Alzheimer's disease (Gallant. 1989).
The primary interpersonal intervention is careful observation :L prevent the patient from wandering or harming himself. Additionally, staff members should be supportive, reassuring, and tolerant.
Wernicke's encephalopathy is a medical emergency. Failure to treat the coma resulting from this disorder can increase risk of mortality. Further, the longer the coma remains untreated, the poorer the prognosis. Thus, the patient should receive 100 mg of thiamine I.M. daily for at least 3 days, followed by oral multivitamin preparations (Schuckit, 1989). The patient's oculomotor signs usually improve several hours after receiving thiamine. If not, they may be a result of hypomagnesemia (Frances and Franklin, 1987). In such instances. 1 to 2 ml of magnesium sulfate I.M. in a 50% solution should be administered. When any intoxicated patient is given I.V. glucose. thiamine should either be given I.M. or added to the I.V. solution to prevent the development of the amnestic disorder. The patient should also receive a balanced diet and 100 mg of oral thiamine three times daily.
Educational inteventions for alcohol amnestic disorder are similar to those for alcohol intoxication (see page 38).
In view of the potentially serious prognosis, a patient with alcohol amnestic disorder should be admitted to the hospital. In an inpatient setting, the patient can safely be withdrawn from alcohol and given aggressive treatment for vitamin and mineral deficiencies.
Alcohol hallucinosis is characterized by vivid and persistent hallucinations that develop in alcohol-dependent persons within 48 hours after they stop drinking or reduce their alcohol intake, although hallucinations can occur in patients who continue to drink (Hackett, 1987). The disorder, which can last for several weeks or months, primarily affects those who have been heavy drinkers for 10 or more years (DSM-llI-R, 1987).
Mental status findings include vivid auditory and visual hallucinations, the key features of alcohol hallucinosis. Auditory hallucinations are more common, typically in the form of voices discussing the patient. The voices may threaten or malign the patient, accusing men of homosexual practices or women of promiscuity, and the patient may respond to auditory commands. At times, a frightening delusion can develop in response to hallucinations, leading patients to call the police or arm themselves. In extreme cases, patients may commit suicide (Hackett, 1987). Chronic alcohol hallucinosis is identified by ideas of reference, poorly systematized persecutory delusions, tangential thinking, and inappropriate affect.
No physical findings specific to alcohol hallucinosis exist, although findings characteristic of alcohol abuse may be evident on examination.
No specific laboratory studies facilitate the diagnosis.
Alcohol hallucinosis can be differentiated from paranoid schizophrenia on the basis of heavy alcohol use, lack of formal thought disorder (unless it has progressed to a chronic stage), and lack of schizophrenia or mania as a part of the family history (Frances and Franklin, 1987). Hallucinations typical of this disorder, unlike those of alcohol withdrawal, occur despite intact orientation and memory' and lack of autonomic arousal (Frances and Franklin, 1987).
Patience and kindness are fundamental interpersonal interventions. Try to remain supportive and nonjudgmental when caring for these patients.
Although signs and symptoms resolve spontaneously within several weeks, neuroleptic drugs are useful for reducing agitation and promoting patient comfort until the psychosis clears (Schuckit, 1988). Recommended doses of oral neuroleptic agents include haloperidol. 2 to 5 mg; thiothixene, 5 to 10 mg; loxapine, 10 to 25 mg; or fluphenazine, 2 to 5 mg. All doses are given twice daily. Neuroleptic agents should not be given for more than 4 weeks; periodically reassess the patient so that medications can be discontinued when psychotic thinking abates.
Educational interventions for alcohol hallucinosis are similar to those for alcohol intoxication (see page 38).
A patient with alcohol hallucinosis should be admitted to the hospital and withdrawn from alcohol. Because of the frightening nature of the hallucinations, admit the patient for observation for 24 to 48 hours to prevent possible harm to the patient or others.
Alcoholic emergencies commonly involve two legal issues: competence and dangerousness. Usually, patients with idiosyncratic intoxication, alcohol withdrawal syndrome, amnestic disorders, or hallucinosis are not competent. Many such patients are uncooperative, combative, psychotic, or lacking insight, which further complicates treatment. You have a duty to ensure appropriate care for intoxicated patients and can initiate treatment without consent for patients in critical situations, such as those experiencing delirium or hallucinosis. When possible, ask family members to give their consent for treatment, additional patient history, and direct support to the patient.
Intoxicated persons are at great risk for harming themselves, others, or property, according to reports from the Drug Abuse Warning Network, which correlates alcohol and drug use with hospital emergency visits and deaths reported to county medical examiners (National Institute on Drug Abuse, 1987). Make every effort to detain an intoxicated patient until he is sober and to discharge the patient in the care of relatives, friends, or AA members. You can be held legally responsible for harm caused by an intoxicated patient you release too soon.