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Alcohol Intoxication and Withdrawal 

Alcohol Intoxication and Withdrawal
Chapter:
Alcohol Intoxication and Withdrawal
Author(s):

Sanjay Shewakramani

DOI:
10.1093/med/9780190862800.003.0092
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date: 24 November 2020

  1. A. Introduction. Alcohol use is important to consider in hospitalized patients for many reasons:

    1. a. Although modest alcohol intake (i.e., up to one serving daily) may have cardioprotective effects, heavier use contributes to multiple medical conditions. Acutely, intoxication can lead to pancreatitis, peptic ulcer disease, and arrhythmia, whereas chronic heavy intake can lead to cardiomyopathy, cirrhosis, nutritional deficiencies, and hypertension.

    2. b. Alcohol has a potent immunosuppressive effect. Its use increases the frequency and mortality of infectious diseases such as bacterial pneumonia.

    3. c. As opposed to patients withdrawing from opiates, patients with severe alcohol withdrawal (delirium tremens) are at a significant risk for death if not treated properly.

  2. B. Alcohol Intoxication. Tolerance occurs with chronic alcohol consumption. Thus, higher serum alcohol levels are needed to cause intoxication in long-term, heavy drinkers compared with first-time drinkers.

    1. a. Clinical manifestations of alcohol intoxication. Alcohol is a central nervous system (CNS) depressant. Alcohol intoxication results in a wide variety of responses that may include slurred speech, euphoria, disinhibition, uncontrolled mood swings, violence, nausea, ataxia, stupor, altered mental status, and respiratory depression.

    2. b. Approach to the patient

      1. i. Supportive care. The clinical approach depends on the degree of CNS and respiratory depression. Supportive care may mean as little as observation until the patient is clinically sober, or as much as intubation in a comatose patient who is unable to protect his or her airway. The cervical spine should be protected if there is any history of trauma. Physical restraints should be used cautiously and only with frequent reevaluation. Chemical restraints, such as benzodiazepines and antipsychotics, may worsen respiratory depression but may be necessary to prevent further harm to the patient as well as health care providers.

      2. ii. Glucose. Because of liver dysfunction, alcohol use without other nutritional intake may result in hypoglycemia. Early blood glucose assessment should be considered in all acutely intoxicated patients with altered mental status.

      3. iii. Blood alcohol level (BAL) peaks between 30 and 90 minutes after ingestion. In general, the legal BAL in the United States is 80 mg/dL. A BAL of 500 mg/dL is fatal to 50% of adults, although tolerant individuals may present with significantly higher levels. One can expect the BAL to decline by anywhere from 15 to 35 mg/dL per hour depending on the patient’s alcohol intake because frequent users metabolize alcohol more quickly. An altered mental status with a low alcohol level or one that fails to improve with time should prompt further evaluation such as a computed tomography (CT) scan of the brain, lumbar puncture or further metabolic and toxicologic assessment (see Chapter 81).

      4. iv. Toxic alcohol ingestion (e.g., methanol or ethylene glycol) should always be considered if an anion gap acidosis (see Chapter 42) is accompanied by an osmolar gap.

      5. v. Patients with isolated alcohol intoxication typically do not require admission to the hospital unless they have a comorbid condition or develop concerning signs of moderate to severe withdrawal. Those with evidence of mild withdrawal can potentially be treated as outpatients with the appropriate medications, assuming they have proper supervision and prompt follow-up.

  3. C. Alcohol Withdrawal

    1. a. Pathogenesis. Alcoholics may drink continually to avoid the discomfort of alcohol withdrawal. As physiologic tolerance develops, more alcohol is needed to avoid withdrawal. When an event occurs to interrupt their habit (such as an illness or hospitalization), alcoholics may develop withdrawal.

    2. b. Clinical manifestations of alcohol withdrawal. As the blood alcohol level decreases, symptoms and signs develop that are generally opposite in nature to the primary CNS depressant effects of the drug (i.e., generalized CNS arousal and hyperactivity). In chronic alcoholics, symptoms of withdrawal usually begin well before the BAL is zero. There are four alcohol withdrawal syndromes that may have differing time courses and clinical manifestations; however, substantial overlap may occur. If only one sign of withdrawal appears, consider other diagnoses.

      1. i. “The shakes.” Symptoms may appear within 3–12 hours of the patient’s last drink. Early symptoms include jitters or shakes, an intense craving for alcohol, anxiety, weakness, diaphoresis, nausea, and myalgias. The patient is often agitated, irritable, and hypervigilant. Common signs include tachycardia, hypertension, and a coarse tremor of the hands or tongue. Symptoms typically last 24–48 hours if they do not progress further.

      2. ii. Seizures. Withdrawal seizures are typically diffuse tonic-clonic seizures that often occur 12–48 hours after the patient’s last drink. Single seizures occur 50% of the time, with short bursts being most common when multiple seizures occur. The postictal period is often short, and status epilepticus is rare. However, other causes for seizures in chronic alcoholics (e.g., intracranial injury, infection) should always be considered because they are common in this population. Consider investigating other causes, especially if the patient is febrile, has a history or signs of head trauma, or has prolonged seizure activity or if the seizures begin more than 48 hours after the last drink.

      3. iii. Hallucinations are classically visual or tactile (e.g., bugs crawling on the skin or wall) but can also be auditory. Patients may become fearful or paranoid, which may further increase agitation. Hallucinations typically occur 24–48 hours after the last drink.

      4. iv. Delirium tremens is characterized by hallucinations, profound confusion, diaphoresis, fever, and tachycardia and occurs in approximately 5% of patients with alcohol withdrawal. Typically, delirium tremens begin 2–3 days after the patient’s last drink, peak on day 4, and may last 1–2 weeks. Approximately 5% of patients will die from delirium tremens, usually from arrhythmia or infection.

      5. v. Other illnesses to consider that mimic the autonomic hyperactivity that defines alcohol withdrawal are sepsis, thyrotoxicosis, heat stroke, hypoglycemia, intracranial hemorrhage, and cocaine intoxication.

        Hot Key

        When managing a patient who appears to be withdrawing from alcohol, always ask yourself: could this patient be septic?

    3. c. Approach to the patient

      1. i. Alleviate withdrawal symptoms

        1. 1. Supportive measures. Keep the patient in a quiet room. Restraining the patient may worsen paranoia and agitation. Restraints should be used only when necessary. Chemical restraints are preferred over physical restraints whenever possible. The patient’s status must be monitored frequently for changes in vital signs as well as neurologic function.

        2. 2. Pharmacologic therapy

        3. a. Benzodiazepines are the drugs of choice. They, like alcohol, act at the γ‎-aminobutyric acid (GABA) receptor to sedate the patient. Lorazepam (1–2 mg given by intravenous [IV] route every 30 minutes until symptoms resolve) is the preferred agent, especially in older adults, because of its short half-life and fast onset of action. The barbiturate phenobarbital is another option. If outpatient treatment is desired, diazepam, phenobarbital, or chlordiazepoxide are preferred agents due to their longer half-life, and are usually given in a tapering dose over 3 to 5 days. Ensure that the patient will have proper supervision (to avoid coingestion with alcohol, which can be fatal) as well as prompt follow-up with outpatient alcohol addiction services.

        4. b. β‎-Blockers and central α‎2-agonists (e.g., clonidine) block the hypertension and tachycardia of withdrawal but should not be used as monotherapy because they do not treat the underlying autonomic derangement and may thus potentially mask delirium tremens.

        5. c. Phenytoin should be used only to treat seizures not entirely attributable to alcohol.

      2. ii. Correct metabolic deficiencies

        1. 1. Fluid deficit should be replaced initially with normal saline, with appropriate adjustment in volume for renal insufficiency or heart failure.

        2. 2. Thiamine (100 mg IV) should be administered before infusing glucose to prevent the development of Wernicke’s encephalopathy. Other vitamins, including folic acid, can also be given.

        3. 3. Glucose may be infused as 50% dextrose or as part of the intravenous fluid rehydration (e.g., D5 normal saline) or as a good meal.

        4. 4. Potassium, magnesium, and phosphorus tend to be low in chronic alcoholics and should be repleted. Pre-mixed IV bags containing normal saline, potassium, magnesium, thiamine, folic acid, and other vitamins are given to patients with alcohol intoxication, and are commonly referred to as a "banana bag."

        5. 5. Vitamin K may be considered if the prothrombin time (PT) is prolonged.

      3. iii. Manage associated medical conditions. Perform a complete history and physical examination to look for associated medical conditions and to rule out other causes of altered mental status and autonomic hyperactivity. A head CT scan, chest radiograph, and lumbar puncture are often necessary in patients with fever, persistent altered mental status, seizures, or abnormal neurologic examination findings.

      4. iv. Attempt rehabilitation. The patient should be referred to a social worker, an alcohol rehabilitation center, Alcoholics Anonymous, or an outpatient mental health center.

  4. D. Alcoholism. Alcohol plays a role in more than 80,000 deaths and costs the US economy more than $250 billion annually. Men at risk for alcohol abuse are defined as individuals who consume 14 drinks per week or 4 drinks per occasion. Women at risk are defined as those who consume 7 drinks per week or 3 per occasion.

    1. a. Detection. Screening recommendations include asking patients about whether they drink beer, wine, liquor, or distilled spirits. The CAGE questions—In the last 12 months, have you ever felt that you should cut down on your drinking? Have people ever annoyed you by criticizing your drinking? Have you ever felt bad or guilty about your drinking? Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (an eye-opener)?—have a sensitivity of 75% and specificity of 88% for at-risk drinkers when one or more responses are positive for women and two or more are positive for men.

    2. b. Approach to the patient

      1. i. Brief negotiated interview (BNI). The BNI is a short method by which the practitioner attempts to facilitate awareness and change in the drinker. The process consists of five steps.

        1. 1. Establish rapport with the patient.

        2. 2. Ask the patient’s permission and then discuss the pros and cons of alcohol use.

        3. 3. Summarize what the patient has said.

        4. 4. Ask the patient to describe (e.g., on a scale from 1 to 10) his or her readiness to change.

        5. 5. Negotiate with the patient based on the perception of readiness. If the patient is ready, approaches to quitting might be brainstormed; if the patient is unsure, then pros and cons might be further explored.

      2. ii. Medications used in alcohol treatment include disulfiram (Antabuse), which induces symptoms of a hangover when patients drink alcohol, and naltrexone, helping curb the urge to drink.

      3. iii. In all cases, the patient should be provided a list of resources and referrals. If the patient is ready to accept referral, a hospital staff member may be able to assist in arranging an appointment or entry into a treatment program.

  5. E. Alcoholic Ketoacidosis

    1. a. Pathogenesis. Alcoholic ketoacidosis (AKA) typically occurs after a period of heavy drinking associated with “relative starvation” when vomiting or limited food intake has reduced the amount of glucose available for metabolism. In response, the body produces ketones as an alternative source of energy.

    2. b. Clinical manifestations. No physical findings point definitively to AKA. Most commonly, patients complain of nausea, vomiting, and abdominal pain. They are often tachycardic and tachypneic and have mild, diffuse abdominal tenderness. An increased anion gap must be present to diagnose AKA. Other simultaneous conditions such as fever or contraction alkalosis may produce a mixed acid-base disorder and thus may mask acidosis. Testing urine for ketosis may be of limited value because β‎-hydroxybutyrate (which most urine dip sticks do not demonstrate) is far more abundant than acetoacetate in AKA. Blood glucose may be low, normal, or slightly elevated but is almost always less than 300 mg/dL.

    3. c. Approach to the patient

      1. i. Fluid rehydration and glucose administration. Patients typically are not hyperosmolar, and aggressive fluid resuscitation can be performed with less concern for cerebral edema than exists with diabetic ketoacidosis. Typically, normal saline containing dextrose (D5NS) can be used to replete volume and promote endogenous insulin secretion, thus inhibiting ketogenesis.

      2. ii. Repletion of vitamins and electrolytes. Thiamine (100 mg) should be given before glucose-containing fluids. A multivitamin may be needed, and magnesium, potassium, or phosphorus repletion may be indicated.

      3. iii. Search for concurrent illness. The development of AKA may be associated with an underlying illness that led the patient to stop drinking. Pancreatitis, gastrointestinal bleeding, withdrawal, and infection should all be considered.

Suggested Further Readings

Allison MG, McCurdy MT. Alcoholic metabolic emergencies. Emerg Med Clin North Am 2014;32:293–301.Find this resource:

Mehta AJ. Alcoholism and critical illness: a review. World J Crit Care Med 2016;5:27–35.Find this resource:

Sachdeva A, Choudhary M, Chandra M. Alcohol withdrawal syndrome: benzodiazepines and beyond. J Clin Diagn Res 2015;9:VE01–VE7.Find this resource: