Which symptoms would alert the nurse to the potential for delirium tremens in a client who has been admitted for alcohol intoxication?

Acute General Rx

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Admission to a detoxification unit where patient can be observed closely.

Vital signs q30min initially (neurologic signs, if necessary).

Use of lateral decubitus or prone position if restraints are necessary.

Nothing by mouth: Nasogastric tube for abdominal distention may be necessary but should not be routinely used.

Vigorous hydration (4-6 L/day): IV with glucose (Na+, K+, PO4−3, and Mg2+ replacement). May be necessary in some patients but commonly there is little support for routine administration of magnesium. Use vigorous hydration with caution in patients with CHF.

Vitamins: Thiamine 500 mg infused IV over the course of 30 minutes daily for 3 days. The initial dose of thiamine should precede the administration of IV dextrose; multivitamins (may be added to the hydrating solution).

Sedation (sedation can be achieved using fixed-dose regimen or individualized benzodiazepine administration [see CIWA-Ar score] in Chapter):

Initially: Lorazepam 8 mg IM/IV every 15 minutes as needed, after the patient has received 16 mg. If delirium is still severe, administer an 8 mg bolus IV, then administer 10 to 30 mg/hr.1

Maintenance (individualized dosage): Chlordiazepoxide, 50 to 100 mg PO q4 to 6h, lorazepam 2 mg PO q4h, or diazepam 5 to 10 mg PO tid; withhold doses or decrease subsequent doses if signs of oversedation are apparent.

Midazolam is also effective for managing DTs. Its rapid onset (sedation within 2 to 4 min of IV injection) and short duration of action (approximately 30 min) make it an ideal agent for titration in continuous infusion.

In addition to benzodiazepines, administer medications such as the antipsychotic agent haloperidol for uncontrolled agitation or hallucinations (0.5-5 mg IV/IM every 30-60 minutes as needed for severe agitation or hallucinations, not to exceed 20 mg).

Treatment of seizures: Diazepam 2.5 mg/min IV until seizure is controlled (check for respiratory depression or hypotension) may be beneficial for prolonged seizure activity; IV lorazepam 1 to 2 mg q2h can be used in place of diazepam. In general, withdrawal seizures are self-limited and treatment is not required; the use of phenytoin or other anticonvulsants for short-term treatment of alcohol withdrawal seizures is not recommended.

Diagnosis and treatment of concomitant medical, surgical, or psychiatric conditions.1

Delirium tremens

Delirium tremens is the most severe manifestation of the alcohol withdrawal syndrome. It is characterized by severe disorientation, exaggerated sympathetic activity, psychomotor agitation, and marked hallucinations. Risk factors include concurrent acute medical illness, daily heavy alcohol consumption, history of delirium tremens or withdrawal seizures, old age, abnormal liver function, and severe withdrawal symptoms (Bayard et al., 2004; Corfee, 2011). Although many symptoms of alcohol withdrawal syndrome begin early following cessation of the drug, the manifestations of delirium tremens can develop abruptly several days following alcohol cessation. Delirium tremens can mimic alternate critical illnesses such as sepsis or head injury, may precipitate respiratory and cardiovascular collapse, and, if left untreated, death may occur from respiratory or cardiovascular collapse (Hall and Zador, 1997; Corfee, 2011). In one study, 24% of 200 consecutive alcohol-dependent patients admitted to an inner-city US hospital developed delirium tremens and 8% of those individuals died from complications of delirium tremens (Ferguson et al., 1996). Among other factors, those who developed delirium tremens were more likely to be unemployed, homeless, and to show signs of more severe alcohol-related end-organ disease (Ferguson et al., 1996; Eyer et al., 2011). While high mortality rates (30–50%) from delirium tremens were reported in earlier clinical studies, mortality today has generally been reduced to less than 3–5% (Lukan et al., 2002) and is usually associated with other alcohol-related diseases such as hepatitis, aspiration, and fatal cardiac arrhythmias (Eastes, 2010; Carlson et al., 2012).

Medical Management of Alcohol Withdrawal and Delirium Tremens

Patients admitted to a general medical hospital who have a history of heavy alcohol use have an approximately 2% to 7% chance of developing severe alcohol withdrawal syndrome (SAWS). Appropriate identification, prophylaxis, and treatment of withdrawal are essential in reducing morbidity and mortality associated with this disorder. Unfortunately, individual symptoms or signs do not effectively predict or exclude SAWS. The most effective method for predicting SAWS in acute care settings is use of a risk assessment tool that combines findings from a patient’s history and clinical examination. The Prediction of Alcohol Withdrawal Severity Scale (Table 128.5) performs best for predicting the development of SAWS and requires an interview, examination (heart rate), and testing (blood alcohol).

For the patient with probable alcohol withdrawal, comorbid conditions that may coexist or mimic the symptoms of withdrawal (e.g., infection, trauma, hepatic encephalopathy, drug overdose, gastrointestinal bleeding, and metabolic derangements) should be excluded. Once this has been accomplished, the patient should be placed in a quiet and protective environment and should receive parenteral thiamine and multivitamins to decrease the risk of Wernicke encephalopathy or Korsakoff amnestic syndrome.

The Revised Clinical Institute for Withdrawal Assessment for Alcohol (CIWA-Ar) scale (available athttps://umem.org/files/uploads/1104212257_CIWA-Ar.pdf), a measure of withdrawal severity, is useful in guiding symptom-triggered therapy in medically stable (i.e., non-ICU or postoperative) patients. Benzodiazepines are the only medications proved to ameliorate symptoms and to decrease the risk ofseizures and DTs in patients with alcohol withdrawal. Typically, diazepam (5 to 20 mg), chlordiazepoxide (50 to 100 mg), or lorazepam (1 to 4 mg) is administered intravenously every 5 to 10 minutes until symptoms subside, with the last of these medications preferred in patients with advanced cirrhosis, considering that the liver minimally metabolizes it. All benzodiazepines appear to be similarly efficacious in treating alcohol withdrawal, but long-acting agents may be more effective in preventing withdrawal seizures and are associated with fewer rebound symptoms. Conversely, short-acting agents may offer a lower risk of oversedation. For the patient who is resistant to benzodiazepines, intravenous phenobarbital (130 to 260 mg administered intravenously every 15 minutes until symptoms are controlled) may be given. If the agitation is not controlled by phenobarbital, propofol (0.3 to 1.25 mcg/kg/hr for maximum 48-hour infusion) can be tried, with intubation strongly recommended.

Delirium tremens

Delirium tremens (DTs) is a short-lived toxic, confusional state with somatic disturbance, usually arising as a consequence of absolute or relative withdrawal of alcohol in severely dependent individuals. Disorientation and confusion are the hallmarks of the syndrome accompanied by vivid (usually visual) hallucinations, the risk of seizures and evidence of autonomic overactivity. Occurring in less than 5% of withdrawals, delirium tremens remains potentially fatal, with a mortality rate possibly as high as 10%. Historically known as ‘the horrors’, the DTs peak on day 3–4 (though may occur up to a week after stopping drinking) of withdrawal and are characterized by a dramatic and rapidly changing picture, with a characteristic triad of clouding of consciousness, sensory distortion and tremor. It frequently has its onset at night, heralded by a prodrome of agitation, insomnia and fear (Box 28.9).

Past withdrawal complicated by seizures or DTs is the best predictor of future alcohol withdrawal complications. Management includes aggressive reduction in autonomic arousal and a reduction in seizure risk with benzodiazepines, which, in the highly agitated patient, may be more effectively administered intravenously.

Patients should be nursed in a single room, with low but adequate levels of stimulation and frequent review. Neuroleptics may be required if hallucinations are not controlled with high dose benzodiazepines. Drugs such as haloperidol should be used cautiously in low doses (2.5–5 mg), since they may lower an already compromised seizure threshold. Predisposing factors include medical illness and older age, with a physical examination and routine bloods being mandatory to exclude precipitating factors such as dehydration, metabolic disturbance and intercurrent infection, all of which must be treated aggressively if present.

Acute General Rx

Alcohol withdrawal syndrome (AWS) occurs when a person stops ingesting alcohol after prolonged consumption. It can result in four possible clinical patterns depending on the severity of the patient’s alcohol use and the time from the patient’s previous alcohol ingestion. Blood ethanol level decreases by ∼20 mg/dl/hr in a normal person. Although discussed separately, these withdrawal states blend together in real life.Table 3 summarizes medications for the treatment of alcohol dependence. The cornerstone of treatment for alcohol withdrawal syndrome is the use of benzodiazepines.

Tremulous state (early alcohol withdrawal, “impending DTs,” “shakes,” “jitters”)

Time interval: Usually occurs 6 to 8 hr after the last drink or 12 to 48 hr after reduction of alcohol intake; becomes most pronounced at 24 to 36 hr

Manifestation: Tremors, mild agitation, insomnia, tachycardia; symptoms are relieved by alcohol

Detoxification can be in the outpatient (ambulatory) or inpatient setting. Candidates for outpatient detoxification should have a reasonable support system (e.g., reliable contact person) who can monitor progress and lack of any significant comorbid conditions (e.g., suicide risk, seizure disorder, coexisting benzodiazepine dependence, prior unsuccessful outpatient detoxification, pregnancy, cirrhosis) or risk factors for severe withdrawal (age >40 yr, drinking >100 g of ethanol daily [e.g., 1 pint of liquor or eight 12-oz cans of beer, random blood alcohol concentration >200 mg/dl])

Inpatient treatment:

The management of alcohol withdrawal is facilitated by the use of ethanol withdrawal charts. An example of such a chart is shown inFig. E1

Admit to medical floor (private room); monitor vital signs q4h; institute seizure precautions; maintain adequate sedation

Administer lorazepam as follows:

Day 1: 2 mg PO q4h while awake and not lethargic

Day 2: 1 mg PO q4h while awake and not lethargic

Day 3: 0.5 mg PO q4h while awake and not lethargic

NOTE: Hold sedation for lethargy or abnormal vital or neurologic signs. The preceding doses are only guidelines; it is best to titrate the dose case by case

In patients with mild to moderate withdrawal and without history of seizures, individualized benzodiazepine administration (rather than a fixed-dose regimen) results in lower benzodiazepine administration and avoids unnecessary sedation. The Clinical Institute Withdrawal Assessment Scale for Alcohol, Revised (CIWA-Ar) scale (Box 1) can be used to measure the severity of alcohol withdrawal. It consists of 10 items: Nausea; tremor; autonomic hyperactivity; anxiety; agitation; tactile, visual, and auditorydisturbances; headache; and disorientation. Each item is assigned a score from 0 to 7. For example, in the “agitation” category 0 indicates normal activity, and 7 indicates that the patient constantly thrashes about. For the category of “tremor,” 0 indicates that tremor is not present and 7 that tremor is severe, even with arms not extended. The maximum total score is 67. Patients with mild AWS symptoms (CIWA-Ar score <8) can be monitored on an outpatient basis. Benzodiazepines are beneficial for most patients with a CIWA-AR score ≥8 and are strongly recommended in patients with substantial withdrawal symptoms (CIWA-Ar score >12). Patients with CIWA-Ar score of ≥15 should be admitted to detox unit. In-patient treatment is also recommended for patients with history of withdrawal seizures and for those with suicidal ideation and significant comorbidities

Beta-adrenergic blockers: Beta-blockers are useful for controlling blood pressure and tachyarrhythmias. However, they do not prevent progression to more serious symptoms of withdrawal and, if used, should not be administered alone but in conjunction with benzodiazepines. Beta-blockers should be avoided in patients with contraindications to their use (e.g., bronchospasm, bradycardia, or severe congestive heart failure). Centrally acting alpha-adrenergic agonists such as clonidine ameliorate symptoms in patients with mild to moderate withdrawal but do not reduce delirium or seizures

Vitamin replacement: Thiamine 100 mg IV or IM for at least 5 days plus oral multivitamins. The IV administration of glucose can precipitate Wernicke encephalopathy in alcoholics with thiamine deficiency; therefore thiamine administration should precede IV dextrose

Hydration PO or IV (high-caloric solution): If IV, glucose with Na+, K+, Mg2+, and phosphate replacement prn

Laboratory studies:

CBC, platelet count, INR

Electrolytes, glucose, blood urea nitrogen, creatinine

GGTP, ALT, AST

Phosphorus and magnesium

Serum vitamin B12 and folic acid (if megaloblastic features in blood smear)

Diagnostic imaging: Generally not necessary; if subdural hematoma is suspected (evidence of trauma, persistent lethargy), a CT scan should be ordered

Social rehabilitation: Group therapy such as Alcoholics Anonymous; identification and treatment of social and family problems should be initiated during the patient’s hospital stay

Delirium tremens

Delirium tremens is the most severe manifestation of the alcohol withdrawal syndrome and constitutes a medical emergency. It is characterized by acute or subacute confusional state with anxiety, insomnia, and tremor; vivid visual, auditory, or tactile hallucinations; and fluctuating levels of psychomotor activity. These manifestations are accompanied by sympathetic hyperactivity with tachycardia, fever, diaphoresis, flushing, and hypertension. In general, delirium appears after 2–3 days of cessation of drinking and usually lasts 48–72 h, but occasionally lasts much longer. A similar clinical picture may occur after sudden withdrawal of barbiturates or benzodiazepines. The main treatment is benzodiazepines, such as chlordiazepoxide or lorazepam. Clonidine and propranolol can reduce hypertension and tachycardia in selected patients but should only be given together with benzodiazepines.

Delirium tremens

The DTs is a potentially life-threatening condition and psychiatrists may be involved in its diagnosis and further management. Patients should be assessed physically and mentally, with daily checks of electrolytes and for signs of associated infection, such as pneumonia. It should be treated with reducing doses of benzodiazepines (usually chlordiazepoxide) over a period of approximately 7 days. Withdrawal convulsions may require the use of intravenous lorazepam and prolonged psychotic symptoms may be treated with haloperidol. Patients should be nursed in a well-lit room and assessed for the level of supervision required. Most hospitals have protocols for how to implement a reducing sedative regime and good practice guidelines are available (see Royal College of Physicians 2001).

Other management considerations

Brains of patients with liver failure are hypersensitive to any sedative, and coma persisting as sedatives are tapered may be hepatic in origin.

Most patients with DTs are dehydrated, some severely so, and many require up to 10 liters of intravenous saline daily. Patients with liver disease, however, retain salt and water. Hyponatremia must be treated cautiously to avoid central pontine myelinolysis. Hypokalemia can cause cardiac arrhythmia. Fever, with or without infection, is often marked, requiring cooling. Coexisting disorders, including hypoglycemia, liver failure, pancreatitis, sepsis, meningitis, and intracranial hemorrhage, may go unrecognized.

Hypomagnesemia occurs early during alcohol withdrawal and returns to normal before the appearance of DTs. Probably both intracellular shift and body loss contribute to hypomagnesemia, which should be corrected (Flink, 1986). Hypokalemia and hypocalcemia also require correction, and hypocalcemia sometimes responds to treatment only after hypomagnesemia is corrected.

Glucose can precipitate Wernicke–Korsakoff syndrome, and because there is often impaired gastrointestinal absorption, thiamine and multivitamins are given parenterally.

Discussion

Alcohol withdrawal syndrome and delirium tremens characterize the spectrum of symptoms observed after a relative or absolute withdrawal from alcohol, especially with chronic use. Delirium primarily involves alterations of attention and is characterized by a fluctuating course, difficulty with concentration, and altered mental status. Tremens refers to the tremors seen in patients with delirium tremens. Most patients who stop alcohol use acutely do not develop withdrawal symptoms, or they simply experience minor symptoms that do not require medical attention. Clinically significant alcohol withdrawal symptoms occur in up to 20% of patients. If the symptoms go untreated, 10% to 15% of these patients progress to withdrawal seizures. Delirium tremens is the last stage of alcohol withdrawal; it occurs in 5% to 10% of alcohol-dependent individuals, with a mortality rate of 5% to 15% when left untreated.

The physiologic mechanism of alcohol withdrawal is based on the inhibitory and excitatory neurotransmitters of the brain. Alcohol increases the effects of the GABAA receptor by increasing its inhibitory effects. In contrast, glutamate (excitatory neurotransmitter that acts on the NMDA receptor) is inhibited, thereby decreasing neuronal excitability. The presence of alcohol has an inhibitory effect by enhancing GABAA and depressing the NMDA receptor. On withdrawal of alcohol, there is an abrupt cessation of the neuronal inhibition and a subsequent state of hyperexcitability.

There are multiple stages of withdrawal based on the chronology of symptoms occurring after the cessation of alcohol use. These stages, from least to most severe, include acute intoxication, alcohol withdrawal, withdrawal seizures, and delirium tremens. Withdrawal may be apparent as early as 6 hours after the last drink but may last up to 12 to 24 hours; symptoms include depression, anxiety, tremulousness, and insomnia. Withdrawal seizures, which have a 2% to 5% incidence in alcohol withdrawal syndrome and delirium tremens, typically occur approximately 48 hours after cessation of alcohol use and present as generalized tonic-clonic seizures. Delirium tremens peaks at 48 to 72 hours after the last drink. The patient may present with delirium, hallucinations (visual, auditory, or tactile, with awareness that he or she is hallucinating), diaphoresis, or fever, but the key feature of delirium tremens is autonomic instability. Scales such as the Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) may help determine the severity of alcohol withdrawal symptoms.

Wernicke-Korsakoff syndrome encompasses two different syndromes associated with chronic alcohol use and severe malnutrition. Wernicke's encephalopathy is primarily a clinical diagnosis involving the classic triad of encephalopathy, ophthalmoplegia, and ataxia. Confusion is usually of a subacute to chronic nature and is characterized by inattention, memory loss, and apathy. Ophthalmoplegia (weakness or paralysis of one or more of the extraocular muscles) mostly involves the lateral recti but may also involve any of the extraocular muscles. Nystagmus (rhythmic oscillation of the eyes) is commonly present in the lateral and/or vertical gaze. Ataxia is the unsteady, clumsy motion of the extremities and, more commonly, the trunk. Left untreated, Wernicke's encephalopathy has a mortality rate of 10% to 20%. It is treated with the administration of thiamine 50 to 100 mg IV once a day (this should be given before glucose, because glucose further depletes thiamine and accelerates the development of Wernicke's encephalopathy). Korsakoff syndrome primarily involves memory impairment without significant deficits of other cognitive functions, such as attention or social behavior. It is also characterized by both anterograde and retrograde amnesia, along with confabulation, in which the patient's recall is distorted in relation to reality (a prominent feature). This condition also is treated with thiamine, but the prognosis is less favorable.

Withdrawal states with delirium (ICD-10 F10.4)

The condition commonly known as delirium tremens (DTs) is often taken as a hallmark of alcoholism but it is relatively rare, being reported by only about 5% of patients attending specialist clinics. It occurs when an individual who is severely dependent on alcohol stops or reduces drinking.

The full syndrome is characterised by marked tremor of the limbs, body and tongue, restlessness, loss of contact with reality, clouding of consciousness, disorientation and illusions progressing to hallucinations, sometimes frightening, which are most commonly visual, but may be auditory or tactile. Delusions often of a paranoid kind may also occur, often associated with the hallucinations. Sweating and tachycardia are pronounced. The disturbance usually develops out of milder withdrawal symptoms 1 day after cessation of drinking and rarely persists for more than 4 days. Symptoms are often worse at night. There is a significant mortality (approximately 10%), partly because it often complicates other medical emergencies such as infections or injuries. The development of fever, dehydration and signs of shock are ominous prognostic signs. Concomitant infection, Wernicke's encephalopathy, metabolic disturbance, hypoglycaemia or head injury may complicate the clinical features and prognosis. Withdrawal fits may occur at any time from the first to the 14th day (Isbell et al 1955). The development of DTs and seizures can often be aborted by prompt and adequate sedation with a benzodiazepine.

Admission to hospital will usually be necessary. The patient's environment should be safe, uncluttered and uniformly lit to avoid ambiguities. Parenteral multivitamin preparations are given and haloperidol reduces the intensity of delusions and hallucinations. Electrolytes and plasma glucose should be checked. An oral benzodiazepine, such as chlordiazepoxide, commencing at 100–150 mg/day or diazepam 50–80 mg/day and reducing after the second or third day, will usually be sufficient to contain the patient's agitation and can be progressively reduced and stopped by the end of 1, or at most, 2 weeks.