Delirium Tremens in the Older Adult

Abstract

INTRODUCTION:

Caring for patients experiencing alcohol withdrawal syndrome can be challenging. Patients 65 and older are at increased risk for alcohol withdrawal syndrome related complications. The higher prevalence of co-morbidities, including cognitive impairment, longer drinking history and greater sensitivity to alcohol withdrawal syndrome treatment are the result of decreased ability of the brain to adapt to stressors such as illness, trauma, or surgery.

DELIRIUM TREMENS:

Symptoms may appear earlier from the last drink and present with a wide range of symptoms. The most effective interventions require high-quality nursing care delivery to prevent, decrease the severity and shorten the duration of delirium.

NURSING IMPLICATIONS:

Strategies that help minimize these challenges starts with obtaining the patient’s selfreport of their alcohol use history. Nurses should be diligent in their monitoring for signs of active alcohol withdrawal. Screening and assessment tools such as the Clinical Institute Withdrawal Assessment for Alcohol–Revised should guide pharmacological management. To support nurses in identifying delirium tremens, this manuscript seek to describe the underlying pathophysiology, key assessment components and nursing management of delirium tremens in the older adult.

There is a robust and growing body of literature discussing assessment and identification of delirium in the older adult.^1-3 Delirium is characterized by an acute onset of confusion that fluctuates throughout the day. Delirium tremens (DTs) is a unique form of delirium characterized by acute confusion in the setting of agitation, tachycardia, tremors, and hypertension occurring secondary to withdrawal from alcohol.^4,5 It is the most severe level of alcohol with-drawal, common in the acute and critical care environment, and may be particularly difficult to discern in the setting of traumatic brain injury and new-onset seizures.^4-6 Literature discussing alcohol-related DTs is well established.⁷ Despite age being a risk factor for both delirium and DTs, there is limited discussion of differentiating DTs, in the geriatric patient.

In hospitalized patients, DTs can be difficult to manage. Approximately 5% of patients with alcohol use disorder develop DTs.⁸ Although the underlying etiology is not well understood, there seems to be a relationship between duration of alcohol use and severity of withdrawal symptoms. Delirium tremens prolongs hospital length of stay, increases healthcare cost, and triples mortality risk.⁹ Effective management requires early recognition and aggressive treatment.^6,7 Because of their continuous presence and relationships with patients and families, nurses are in an ideal position to detect the signs and symptoms of alcohol withdrawal.⁴ Therefore, it is important for nurses to elicit information regarding alcohol use and critically assess for signs of withdrawal.⁵ This article seeks to describe the underlying pathophysiology, key assessment components, and nursing management of DTs in the older adult.

Alcohol depresses the central nervous system by increasing the activity of γ-aminobutyric acid (GABA), an inhibitory neurotransmitter responsible for downregulation of excitatory neurotransmitters (ie, glutamate). Downregulation is due to inhibition of N-methyl-D-aspartate (NMDA) receptors similar to a quickly progressing NMDA encephalitis.^4,10 Prolonged use further increases GABA production, function, and alteration in the associated receptors.^7,11 Because of the multifactorial complex nature, primary treatment is to alleviate the cause.

Stages of Alcohol Withdraw

Although all patients will not progress sequentially through the 3 stages of withdrawal, the stages describe how alcohol withdrawal symptoms evolve and de-fine the clinical features (Table 1). Most patients only progress to level 1. Stage 1 can occur within hours, if an individual stops or greatly reduces alcohol consumption, presenting with signs of a hangover including headache, nausea and vomiting, tremors, and anxiety. With resumed consumption, symptoms typically subside. If the individual does not consume enough alcohol, within 24 hours, he/she may progress on to stage 2. During the second stage, increased sympathetic system activity leads to tachycardia, hypertension, tremors, and diaphoresis. The individual’s demeanor may change as he/she becomes agitated but temporarily settles down when directed. Administering sedatives at this point may delay progression. Keeping these individuals in bed and preventing therapy interruption such as removing tubes, lines, and monitoring equipment may become increasingly challenging due to hyperactivity, restlessness, and frigidity. Advanced stage 2 becomes apparent when hallucinations, delusions, and nightmares develop. A distinguishing feature of these hallucinations is the ability to maintain lucidity and recognize altered perceptions that are related to alcohol withdrawal. Aggressive management with sedation and close monitoring for respiratory decline are needed at this point. Approximately one-third of patients require intensive care, especially older adults. Although more commonly seen in patients with a history of epilepsy, development of tonic-clonic seizures marks progression to stage 3. Although patients experiencing seizures may include DTs in the differential, DTs are not seizures.¹² Progression to stage 3 occurs in less than 10% of patients and usually takes more than 2 days.¹²

TABLE 1.

Stages of Alcohol Withdrawal

Stage	Onset	Duration	Physical Symptoms	Cognitive Symptoms
1	0-8 h	Up to 1 d	Headache, nausea and vomiting, and tremors	Anxiety
2	2-48 h	Up to 1 wk	Tachycardia, hypertension, tremors, and diaphoresis	Agitation Hyperactivity, restlessness, and frigidity Hallucinations, delusions, and nightmares Anhedonia, dysphoric behavior, and cravings
3	3-7 d	Up to 2 wk	Tonic-clonic seizures	Delirium tremens

Similar to onset and progression, recovery is also proportional to severity. Patients receiving interventions will typically recover within 24 hours of outpatient treatment. When patients progress beyond stage 1, the recovery is more complex and often requires hospitalization for a few days to several weeks. On-going symptoms including anhedonia, dysphoric behavior, and cravings are thought to be the result of alterations in dopamine within the central nervous system and can be more frequent in older adults.¹³

Patients 65 years and older are at an increased risk for AWS-relatedcomplications because of the higher prevalence of comorbidities, including cognitive impairment, longer drinking history, and greater sensitivity to AWS treatment. Older patients who have less physiologic reserve may become symptomatic sooner as a result of the brain’s limited ability to adapt to stressors such as illness, trauma, or surgery. However, these notions are not universally true, and a higher index of suspicion for AWS should be raised. Symptoms may appear earlier (6-12 hours) from the last drink and can present with a wide range of symptoms.¹⁴ When symptoms appear, severity of AWS scores may be higher and duration is likely to be longer than that of younger individuals.¹⁵

When an acutely ill older patient develops DTs, there is a greater hyperdynamic state and electrophysiological changes such as a prolonged QT interval, tendency for greater increases in cardiac enzymes, and the odds of dying increase by 1.56.¹⁶ Hypokalemia and hypomagnesemia secondary to renal and extrarenal losses increase the risk for arrhythmias including torsade de pointes, sustained ventricular tachycardia, atrial fibrillation, and supraventricular tachycardia, causing a supply-and-demand imbalance.¹⁶

Identifying and Determining the Severity

Like other forms of delirium, AWS-related delirium identification can be challenging. In addition, because of the increased risk for seizure with advanced age, AWS may be masked as a possible seizure disorder.¹² Monitoring older patients for complaints or signs of insomnia, depression, anxiety, memory loss, aches and pains, poor diet, and decreased libido may indicate the presence of an AUD but are often viewed as part of the aging process. Furthermore, the hallmark sign of becoming “nonfunctional” such as missing work or reporting intoxicated is not likely to occur in this age group because many are retired or live alone.¹³

Several bedside assessment tools are available to assist with early detection. When screening tools are part of the routine process, patient injury and risk of readmission are reduced.^17,18 In an effort to prevent DTs, screening tools are used to evaluate the frequency and quantity of alcohol consumption. Screening tool use is important and should be initiated at the point of hospital entry including emergency departments, preoperative surgical areas, and inpatient units. These screening tools are effective when used short-term or with acute drinkers. However, exercise caution with patients considered to be severely alcoholic because tool effectiveness in this population remains debatable.

Anytime a patient presents with an alcohol history, one should try to quantify the use.¹⁹ Additional assessments should include risk factors such as history of DTs, previous withdrawal or detoxification, fluid and electrolyte disturbances, nutritional status, advanced age, and coexisting illnesses. Patients experiencing DTs often present with severe dehydration (as much as 10-L deficits). Hypoglycemia, potassium, magnesium, and phosphorous levels may also be critically low. The untoward effects of alcohol on the various organ systems may also be more pronounced. For example, a reduction in gastric enzymes may allow for higher concentrations of alcohol to enter the blood stream, and tolerance may be reduced. Adding alcohol to regular diuretic use produces a synergistic effect in the presence cardiac disease and may, therefore, result in more significant hypovolemia and orthostatic hypotension.¹³ Falls associated with alcohol-induced gait impairment are more likely to result in fractures due to preexisting osteoporosis.

Nursing Management

During the admission process, nurses are in a perfect position to obtain a patient’s medical history, including alcohol consumption. Nurses are often the first clinicians to observe alterations and elicit information from the patient and family regarding alcohol use and abuse. When patients have a known or suspected drinking history, nurses should attempt to quantify alcohol use with a validated screening tool.²⁰ Exercise caution with family reports because only 1 study has found family reports to be equivalent to the patient’s self-report.²⁰

Nonpharmacological Interventions

In Memorandum of Nursing, Nightingale²¹ described the importance of direct sunlight. Through her belief in the environmental theory, she advocated for hospitalized patients to be moved within their room to follow the sun rather than being stationary in dim rooms. Using light, a patient’s circadian rhythm could be restored. Unfortunately, in current practice, rooms and beds are designed with the placement of medical equipment being the higher priority. The more serious the patient’s condition, the greater the reliance on artificial light.²¹

Interventions that target the patient’s specific risk factors through staff education, nonpharmacologic intervention protocolization, and improvement in the patient’s environment have been shown to be the most effective intervention. These interventions require high-quality nursing care delivery to prevent, decrease the severity, and shorten the duration of delirium.²² In addition, studies have shown that these interventions are cost-effective in acute care. Interventions should focus on cognitive and sensory impairment, hydration and nutrition, oxygenation, infection prevention, early mobility, sleep, and relief of pain. Routine nursing care should promote daily activity; a quiet, well-lit environment; and minimizing room and bed changes. Additional nursing interventions should include use of hearing and visual aids, care-giver continuity, and encouraging personal items. Because patients with delirium-associated withdrawal typically experience hyperactive delirium, interventions should focus on decreasing sensory overload. These interventions might include limiting visits, removing items associated with painful stimulus such as urinary catheters, limiting monitoring with medical devices, and testing such as routine daily laboratory tests and frequent vital signs.

An individualized plan of care must address signs and symptoms for patients experiencing AWS. This plan should include diligent monitoring, astute assessment, and use of clinical judgment to detect subtle changes in patient condition. Subtle changes include early identification of worsening withdrawal and differentiating these changes from a worsening medical condition and aggressive medication management. Use of a severity assessment scale such as the CIWA-Ar in conjunction with clinical assessment and critical thinking is recommended to guide the therapy. Although a specific delirium scale cannot be recommended, the Society of Critical Care Medicine recommends using the CAM-ICU or the ICDSC in critical care units. Delirium screening may help assess patients experiencing AWS requiring mechanical ventilation.²³ Early identification and preventative therapy are thought to reduce the risk of DTs and mortality.²⁴ Hypokalemia on admission may identify an increased risk for DTs, even after the potassium level is corrected. Kartasheva et al²⁴ found that CIWA-Ar scores of less than 10 indicate minimal alcohol with-drawal, whereas scores of 10 to 20 indicate moderate alcohol withdrawal, and scores greater than 20 indicate severe alcohol withdrawal; of those with a severe score, 24% developed DTs.

Pharmacological Management

Benzodiazepine administration remains the corner-stone for pharmacologic treatment of DTs. There are several common strategies for administering ben-zodiazepines: fixed, loading, and symptom-triggered. Fixed dosing means a predetermined dose is administered on a set and regular schedule. When using the loading strategy, a long-acting benzodiazepine is administered until the symptoms significantly improve, at which point the patient “self-tapers” as the benzodiazepine and associated metabolites slowly clear from his/her system.²⁴ This method is frequently used in emergency departments. Symptom-triggered therapy uses a scale like the CIWA-Ar to determine the dose of benzodiazepines. Most available US and European research has found symptom-triggered therapy superior to routine fixed dose when patients are not medically complicated, psychiatric, or multiple substance users and should be used cautiously in these populations.^8,17

Adjunct Therapies

Antipsychotics

Using antipsychotics such as haloperidol (phenothiazines and butyrophenones) in patients with AWS can be considered as an adjunct therapy.^25,26 When added to the treatment regimen, it is usually because symptoms such as agitation, hallucinations, or delirium are not adequately managed with benzodiazepines alone. Antipsychotics should be used with caution because they can prolong the cardiac QT interval, increasing the risk for cardiac arrhythmias and mortality.²⁷ In addition, they lower the seizure threshold, which may be problematic, especially in the first 48 hours when seizure risk is highest.

Antiepileptic Agents

Levetiracetam has a high affinity for GABAergic and glutamatergic receptors. It is thought that levetiracetam has a protective effect by reducing excessive neuronal activity.²⁸ However, its mechanism of action in the treatment of AWS remains unclear. Despite this lack of understanding, along with benzodiazipines, antiepileptics are widely used in the treatment of AWS. Because there are a limited number of quality studies to adequately evaluate the effects of antiepileptic agents, the Cochrane Review did not recommend their use in the treatment of AWS.²⁹ Although additional research is needed, available studies have shown levetiracetam shows the most promise by providing rapid stable clinical improvement. Significant study limitations and concerns with research design prevent recommendations related to carbamazepine, valproate, and gabapentin. Antiepileptic superiority to benzodiazepines remains unknown and, therefore, cannot be recommended for routine clinical practice and should be used with caution.²⁸

Sedatives and Barbiturates

Dexmedetomidine decreases sympathetic overdrive and norepinephrine release and therefore causes a “cooperative sedation.”^28,30 Because of its lack of GABAergic activity, it can only be used as an adjunct therapy to decrease autonomic hyperactivity not managed by benzodiapines alone. Dexmedetomidine use has been shown to reduce the amount of benzodiazepines needed to manage AWS. Propofol enhances the effects of GABA_A receptor and decreases NMDA activity. Although only a few case studies have evaluated propofol, these cases have shown a rebound withdrawal when the drug is discontinued. Although barbiturates have been shown to be as effective as benzodiazepines, because of their narrow therapeutic index and lack of toxicity antidote, they are rarely used to treat AWS. Conversely, baclofen interacts with GABA_B receptors. With limited research, its use cannot be recommended; however, the few available studies have indicated that baclofen may rapidly decrease severe AWS symptoms and cravings.^28,31

Additional Therapies to Consider

Magnesium plays an important role in inhibiting the release of neurotransmitters and may decrease the hyperexcitability associated with NMDA.²⁸ Chronic alcohol use has been associated with abnormal metabolism. Therefore, patients experiencing AWS are frequently given prophylactic doses of magnesium. However magnesium levels should be monitored to maintain normal levels. Like many of the other treatments, research is limited, leading to an inability of the Cochrane Review to recommend its routine use.³¹

Wernicke’s encephalopathy occurs as a result of lesions in the central nervous system. Thiamine depletion leads to lesions in the central nervous system.³¹ Thiamine deficiency causes the classic triad of symptoms including confusion, ataxia, and ophthalmoplegia seen with WE. The European Federation of Neurological Societies guidelines call for at least two of the following symptoms for a WE diagnosis: dietary deficiencies, eye signs, cerebellar dysfunction, and either an altered mental state or a mild memory impairment. Although WE rarely occurs, it has a high morbidity and mortality rate. According to the European Federation of Neurological Societies guidelines, patients experiencing AWS should receive parenteral thiamine supplementation regardless of the initial presentation. Thiamine has been found to prevent the development of WE and should be administered as early as possible to hasten recovery. In addition, thiamine should be administered parenterly before administering carbohydrate-containing fluids. This can only occur when clinicians obtain a thorough alcohol use history during the admission process.²⁴

Impact

Older adults with alcohol abuse are at an increased risk for developing withdrawal symptoms earlier. Because of age-related changes and the potential for a longer abuse history, nurses need to obtain a reliable drinking history. Nursing care should include diligent monitoring using a standardized assessment tool and tailored interventions. Multidisciplinary team collaboration and careful consideration regarding vitamin, mineral, and electrolyte deficit replacement as well as adequate nutrition are critical. The frequency of hypertension and hypokalemia has been seen more frequently in the older adult experiencing AWS and may require more aggressive management.¹⁵ Symptom duration and severity may likely be increased with younger adults typically reaching symptom resolution around day 7, whereas older adults may still be symptomatic at day 9.¹⁵ Appropriate medication management and good basic nursing care are the most effective interventions.²² Greater restraint use, often seen in older adults, may contribute to prolonged symptom duration.¹⁵ Unfortunately, this is contrary to research-based recommendations that suggest restraint use in older adults is inappropriate and should be rarely used.¹⁵

Conclusion

Caring for patients experiencing AWS can be challenging. Strategies that help minimize these challenges start with obtaining the patient’s self-report of their alcohol use history. Nurses should be diligent in their monitoring for signs of active alcohol with-drawal. For patients experiencing AWS, screening and assessment tools such as the CIWA-Ar should guide pharmacological management.⁴ Although nurses do not prescribe medical management, their knowledge, expertise, and collaboration with providers are important when treatment decisions are being made. Nurses’ constant presence at the bedside provides them with the unique ability to detect and report changes in the patient’s condition essential to determining the appropriate diagnosis and treatment.

TABLE 2.

DSM-5 Diagnostic Criteria (American Psychiatric Association, 2013)

Cessation of or reduction in alcohol use in patients with a history of heavy and prolonged use

Two (or more) of the following occur within a few days of reduced alcohol use and are clinically significant enough to cause distress or impairment in social, occupational, or other important areas of functioning Autonomic hyperactivity such as diaphoresis and tachycardia Increased hand tremor Insomnia Nausea or vomiting Hallucinations or illusions Agitation and/or anxiety Tonic-clonic seizures The symptoms are not due to a general medical condition and cannot be explained by another mental disorder.

Abbreviation: DSM-5, Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition).