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| CECIL |
| TEXT BOOK of MEDICINE |
Section IV Aging and Geriatric Medicine
| 26 DELIRIUM AND OTHER MENTAL STATUS PROBLEMS IN THE OLDER PATIENT Sharon K. Inouye • |
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Mental status change, one of the most common presenting symptoms in acutely ill elders, is estimated to account for 30% of emergency evaluations for older patients. Mental status often serves as a barometer of the underlying health of an elderly patient and is commonly the only symptom of serious underlying disease. A broad range of medical, neurologic, and psychiatric conditions can lead to mental status changes (Chapters 420 and 425). A systematic approach aids in the evaluation of suspected mental status change in an older patient (see Fig. 26-1).
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The first step in evaluating suspected altered mental status in an older patient is to obtain a detailed history from a reliable informant to establish the patient's baseline level of cognitive function and the clinical course of any cognitive changes. Chronic changes (i.e., changes occurring over months to years) most likely represent an underlying dementing illness, which should be evaluated accordingly (Chapter 425). Acute changes (i.e., changes occurring over days to weeks)—even if superimposed on an underlying dementia—should be evaluated further by detailed cognitive assessment to determine whether delirium is present. If features of delirium (e.g., inattention, disorganized thinking, altered level of consciousness, fluctuating symptoms) are not present, further evaluation for depression, acute nonorganic psychotic disorders, or other psychiatric conditions is indicated.
▪ DELIRIUM
Delirium, a clinical syndrome characterized as an acute disorder of attention and cognitive function, is the most frequent complication of hospitalization for elders and a potentially devastating problem. Delirium often is unrecognized despite sensitive methods for its detection, and its complications may be preventable.
Definition
The definition and diagnostic criteria for delirium are evolving. The Diagnostic and Statistical Manual of Mental Disorders, fourth edition, has been used widely (Table 26-1), but development of the criteria in this manual was based on expert consensus, and their diagnostic sensitivity and specificity have not been determined. The Confusion Assessment Method provides a simple, operationalized diagnostic algorithm with a sensitivity of 94 to 100%, a specificity of 90 to 95%, and a high interrater reliability.
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Epidemiology
In the elderly, the prevalence of delirium at hospital admission is 13 to 60%. Delirium develops anew in 6 to 56% of patients during hospitalization. Higher rates are found when frequent surveillance is performed in older, surgical, and intensive care populations. Delirium occurs in 15 to 74% of postoperative patients and 60 to 80% of patients in medical intensive care units.
The associated hospital mortality rates for delirium are 25 to 33%, rates as high as those associated with acute myocardial infarction and sepsis. The problem of delirium in hospitalized elderly patients has assumed particular prominence because patients aged 65 years and older currently account for about 50% of all inpatient days of hospital care. Based on U.S. vital health statistics, delirium complicates hospital stays for at least 20% of the 12.5 million older persons hospitalized each year and increases hospital costs by more than $2500 per patient, amounting to more than $6.9 billion (2004 U.S. dollars) of Medicare expenditures yearly. Substantial additional costs are incurred after hospital discharge because of the increased need for rehabilitation services, nursing home placement, and home care. These extrapolations highlight the extensive economic and health policy implications of delirium.
Pathogenesis
Similar to other common geriatric syndromes (Chapter 23), delirium usually has multifactorial causes. A search for the innumerable potential underlying contributors requires clinical astuteness and a thorough medical evaluation, especially because many of these factors are treatable but, if untreated, may result in substantial morbidity and mortality. The process is made more challenging by the frequently nonspecific, atypical, or muted features of the underlying illness in older persons. Delirium is commonly the only initial sign of underlying life-threatening illness, such as pneumonia (Chapter 97), urosepsis (Chapter 306), or myocardial infarction (Chapter 72), in the older population.
The development of delirium usually involves a complex interrelationship between a vulnerable patient with pertinent predisposing factors and exposure to noxious insults or precipitating factors. Delirium may develop in vulnerable patients, such as cognitively impaired or severely ill patients, after a relatively benign insult, such as a single dose of sleeping medication. Conversely, in patients who are not vulnerable, delirium would develop only after exposure to multiple noxious insults. Previous studies have shown that the effects of these risk factors may be cumulative. The importance of this multifactorial causation to the clinician is that removal or treatment of one factor in isolation usually is not sufficient to resolve the delirium. The full spectrum of vulnerability and precipitating factors should be addressed.
Predisposing, or vulnerability, factors include preexisting cognitive impairment or dementia, severe underlying illness, high levels of comorbidity, functional impairment, advanced age, chronic renal insufficiency, dehydration, malnutrition, and vision or hearing impairment. Dementia is an important and consistent risk factor for delirium; demented patients have a two-fold to five-fold increased risk for delirium. Of delirious patients, 30 to 50% have underlying dementia. Delirious patients commonly have evidence of underlying chronic brain disease, particularly conditions associated with cognitive impairment, such as Alzheimer's disease, Parkinson's disease, cerebrovascular disease, and space-occupying lesions.
Medications, the most common remediable cause of delirium, contribute to delirium in 40% of cases (Chapter 25). Insufficiency or failure of any major organ system, particularly renal or hepatic failure, can precipitate delirium. Hypoxemia and hypercarbia have been associated with delirium. Clinicians must be attuned to occult respiratory failure, which in the elderly often lacks the usual signs and symptoms of dyspnea and tachypnea and can be missed by measurement of oxygen saturation alone. Acute myocardial infarction or heart failure can be manifested as delirium in an elderly patient without the usual symptoms of chest pain or dyspnea. Occult infection is a particularly notable cause of delirium. Older patients frequently fail to mount the febrile or leukocytotic response to infection, and clinicians must assess carefully for signs of pneumonia, urinary tract infection, endocarditis, abdominal abscess, or infected joints. A variety of metabolic disorders may contribute to delirium, including hypernatremia or hyponatremia, hypercalcemia, acid-base disorders, hypoglycemia and hyperglycemia, and thyroid or adrenal disorders. Immobilization and immobilizing devices (e.g., indwelling bladder catheters, physical restraints) have been shown to be important factors in precipitating delirium. Dehydration and volume depletion and nutritional decline during hospitalization (e.g., decline in weight, fall in serum albumin concentration) are well-documented factors contributing to delirium. Drug and alcohol withdrawal are important and often unsuspected causes of delirium in the elderly. Environmental factors, such as unfamiliar surroundings, sleep deprivation, deranged schedule, frequent room changes, sensory overload, and sensory deprivation, may aggravate delirium in the hospital. Psychosocial factors, such as depression, psychological stress, pain, and lack of social supports, also may precipitate delirium.
The basic pathogenesis of delirium is unclear. Most investigators agree that delirium seems to be a functional rather than structural lesion. Electroencephalographic studies show global functional derangements in patients with delirium, characterized by generalized slowing of cortical background activity with appearance of delta and theta activity. Neuroimaging studies coupled with cognitive testing demonstrate generalized disruption in higher cortical function, with dysfunction in prefrontal cortex, frontal and temporoparietal cortex, fusiform cortex, lingual gyri, subcortical structures, thalamus, and basal ganglia. The leading hypotheses for the pathogenesis of delirium focus on the roles of neurotransmission and inflammation. The most widely postulated mechanism for delirium is the failure of cholinergic transmission. Evidence supporting this hypothesis includes the frequent association of anticholinergic drugs with delirium, the reversal of delirium with pro-cholinergic drugs such as physostigmine, the increased levels of serum anticholinergic activity in some delirious patients, and the benefit of cholinesterase inhibitors for some delirium cases. Other neurotransmitter systems, such as dopamine, serotonin, tryptophan, norepinephrine, and γ-aminobutyric acid, may also play a role in delirium, but the evidence is less well developed. In special circumstances, such as infections or cancer, delirium may be mediated through cytokines, such as interleukin-2 and tumor necrosis factor. Although delirium has long been considered a transient syndrome, several of these basic mechanisms may not be completely reversible, particularly mechanisms resulting in hypoxic damage. The dose and duration of the noxious insults, along with the degree of vulnerability of the patient, also may exert great influence on the ultimate reversibility of the delirium.
Clinical Manifestations
The cardinal features of delirium include acute onset and inattention. Establishing the acuity of onset requires accurate knowledge of the patient's baseline cognitive function. Patients are inattentive; that is, they have difficulty focusing, maintaining, and shifting attention. They appear easily distracted and have difficulty maintaining conversation and following commands. Objectively, patients may have difficulty with simple repetitive tasks, digit spans, and recitation of months backward. Other key features include disorganization of thought processes, which is usually a manifestation of underlying cognitive or perceptual disturbances; altered level of consciousness, which typically is lethargy with reduced clarity of awareness of the environment; and fluctuation of cognitive symptoms. Although not cardinal elements, other features frequently occurring during delirium include disorientation, cognitive deficits, psychomotor agitation or retardation, perceptual disturbances such as hallucinations and illusions, paranoid delusions, and sleep-wake cycle reversal.
Diagnosis
The cornerstone of evaluation of delirium is a comprehensive history and physical examination. The first step in evaluation (Table 26-2) is to establish the diagnosis of delirium through cognitive assessment and to determine whether the present condition represents an acute change from the patient's baseline cognitive function. Because cognitive impairment may not be apparent during conversation, brief cognitive screening tests, such as the Mini-Mental Status Examination and the Confusion Assessment Method (CAM), should be used. Attention should be assessed further with simple tests, such as a forward digit span (inattention indicated by an inability to repeat five digits forward) or recitation of the months backward. A delirium assessment for nonverbal (e.g., intubated) patients, called the CAM-ICU, has been developed. The history, which should be obtained from a reliable informant, is targeted to establish the patient's baseline cognitive function and the time course of any mental status change and to obtain clues about potential precipitating factors, such as recent medication changes, intercurrent infections, or medical illness. Physical examination should include a detailed neurologic examination for focal deficits and a careful search for signs of occult infection or an acute abdominal process.
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Review of the medication list, including over-the-counter medications, is crucial, and use of medications with psychoactive effects should be discontinued or minimized whenever possible. In the elderly, these medications may cause psychoactive effects even at doses and measured drug levels that are within the “therapeutic range.” Consideration should be given to the possibility that withdrawal from alcohol or other medications is a contributor to delirium.
Laboratory Findings
Laboratory evaluation must be tailored to the individual situation (see Table 26-2). In patients with preexisting cardiac or respiratory diseases or related symptoms, electrocardiography or arterial blood gas determination may be indicated. The need for cerebrospinal fluid examination is controversial except when it is clearly indicated, such as in a febrile delirious patient. Brain imaging should be reserved for patients with new focal neurologic signs, for patients with a history or signs of head trauma, and for patients without another identifiable cause of the delirium. Electroencephalography, with a false-negative rate of 17% and a false-positive rate of 22% for distinguishing delirious from nondelirious patients, has a limited role and is most useful for detection of an occult seizure disorder and in differentiation of delirium from psychiatric disorders.
Differential Diagnosis
A crucial difficulty in the differential diagnosis of delirium is distinguishing a long-standing confusional state (dementia) from delirium alone or delirium superimposed on dementia (Fig. 26-1). These two conditions are differentiated by the acute onset of symptoms in delirium (dementia is much more insidious) and the impaired attention and altered level of consciousness associated with delirium. The differential diagnosis also includes depression and nonorganic psychotic disorders. Although paranoia, hallucinations, and affective changes can occur with delirium, the key features of acute onset, inattention, altered level of consciousness, and global cognitive impairment assist in the recognition of delirium. At times, the differential diagnosis can be difficult, particularly with an uncooperative patient or when an accurate history is unavailable. Because of the potentially life-threatening nature of delirium, it is prudent to manage the patient as having delirium and to search for underlying precipitants (e.g., intercurrent illness, metabolic derangements, drug toxicity) until further information can be obtained.
Treatment
Prevention
The most effective strategy to reduce delirium and its associated complications is primary prevention of delirium before it occurs. Preventive strategies should address important delirium risk factors and target patients at a moderate to high risk for delirium at baseline (Table 26-3). Randomized trials have shown that a geriatrics consultation1 or a multidisciplinary intervention2,3 aimed at the risk factors for delirium can reduce the incidence of delirium by 40%. On a larger scale, preventive efforts for delirium require system-wide changes to educate physicians and nurses to improve recognition and heighten awareness of the clinical implications, to provide incentives to change practice patterns that lead to delirium (e.g., immobilization, use of sleep medications, bladder catheters, and physical restraints), and to create systems that enhance high-quality geriatric care (e.g., geriatric expertise, case management, clinical pathways, and quality monitoring).
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Medical Therapy
In general, nonpharmacologic approaches should be used in all delirious patients and usually are successful for symptom management. Pharmacologic approaches should be reserved for patients in whom the delirium symptoms may result in interruption of needed medical therapies (e.g., intubation, intravenous lines) or may endanger the safety of the patient or other persons. No drug is ideal for the treatment of delirium symptoms, however; any choice may cloud the patient's mental status further and obscure efforts to monitor the course of the mental status change. Any drug chosen should be given in the lowest dose for the shortest time possible. Neuroleptics are the preferred agents of treatment. Haloperidol, the most widely used agent, causes less orthostatic hypotension and fewer anticholinergic side effects than thioridazine does and is available in parenteral form; however, it has a higher rate of extrapyramidal side effects and acute dystonias. If parenteral administration is required, intravenous use results in rapid onset of action with a short duration of effect, whereas intramuscular use has a more optimal duration of action and is preferred. The recommended starting dose is 0.5 to 1 mg of haloperidol orally or parenterally, repeated every 30 minutes after the vital signs have been rechecked until sedation has been achieved. The end point should be an awake but manageable patient. The average elderly patient who has not been treated previously with neuroleptics should require a total loading dose of no more than 3 to 5 mg of haloperidol. Subsequently, a maintenance dose consisting of half of the loading dose should be administered in divided doses during the next 24 hours, with doses tapered in the next few days as the agitation resolves.
Benzodiazepines are not recommended for the first-line treatment of delirium because of their tendency to cause oversedation and exacerbate the confusional state. They remain the drugs of choice, however, for treatment of withdrawal syndromes from alcohol and sedative drugs (Chapters 31 and 32).
Nonpharmacologic management techniques recommended for every delirious patient include encouraging the presence of family members, use of “sitters” to be orienting influences, and transfer of a disruptive patient to a private room or closer to the nurse's station for increased supervision. Interpersonal contact and communication, including verbal reorientation strategies, simple instructions and explanations, and frequent eye contact, are vital. Patients should be involved in their own care and allowed to participate in decision making as much as possible. Eyeglasses and hearing aids may reduce sensory deficits. Mobility, self-care, and independence should be encouraged, and physical restraints should be avoided, if possible, because of their tendency to increase agitation, their questionable efficacy, and their potential to cause injury. Attention must be focused on minimizing the disruptive influences of the hospital environment. Clocks and calendars should be provided to assist with orientation. Room and staff changes should be kept to a minimum. A quiet environment with low-level lighting is optimal for delirious patients. Perhaps the most important intervention is to schedule checking of vital signs, administration of medications, and procedures to allow an uninterrupted period for sleep at night. Nonpharmacologic approaches to relaxation, including music, relaxation tapes, and massage, can be highly effective.
End-of-Life Care
Delirium occurs in at least 80% of patients at the end of life and is considered part of the dying process by many hospice care providers (Chapter 3). Establishing the goals for care in advance with the patient and family is critical to guide appropriate management. For example, some patients may prioritize preservation of alertness and ability to communicate with loved ones as long as possible; others may prioritize comfort above all else. Physicians must be aware that even in terminal care, many causes of delirium are potentially reversible with simple interventions (such as medication adjustment, providing oxygen, or treatment of dehydration); however, aggressive diagnostic evaluation is usually inappropriate in this population. Nonpharmacologic measures for treatment of agitation and delirium should be instituted in all patients (including massage, music, and relaxation therapies). Haloperidol remains the first-line therapy for delirium in terminally ill patients. If more sedation is indicated, a short-acting benzodiazepine, such as lorazepam (starting dose, 0.5 to 1.0 mg PO, IV, or SC), which is easily titrated, is recommended in this setting. Because sedation poses the risks of decreased interaction and communication, increased confusion, and respiratory depression, this choice should be made in conjunction with the family.
Prognosis
Delirium is an important independent determinant of prolonged hospital stay, increased mortality, increased rates of institutional placement, and functional and cognitive decline—even after controlling for age, gender, dementia, illness severity, and baseline functional status. Delirium previously had been considered to be a reversible, transient condition, but more recent studies on the duration and persistence of delirium symptoms document that delirium may be much more persistent than previously believed. Delirium typically persists for 30 days or more, and only 20% of patients may have complete resolution of all delirium symptoms at 6-month follow-up. Delirium seems to have greater deleterious effects in patients with underlying cognitive impairment. The long-term detrimental effects are most likely related to the duration, severity, and underlying cause of the delirium and the vulnerability of the patient.
Future Directions
It is hoped that future research will elucidate the pathophysiologic mechanisms of delirium by use of neuroimaging modalities, neuropsychological testing, and genetic and laboratory markers; clarify the contribution of delirium to irreversible cognitive impairment; and improve the evidence-based management of delirium.
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