Delirium Barbara Kamholz

INTRODUCTION

Delirium is prevalent, dangerous and costly. It is caused by medical or surgical problems and medication burdens that are beyond the physiological tolerance of the patient. Delirium costs between $38 and $152 bn per year¹. In ICUs, episodes of delirium average 39% higher ICU costs and 31% higher hospital costs². Long considered a reversible epiphenomenon of hospital care, delirium is an independent risk factor for death and dementia³ and it contributes heavily to lengths of stay, in-hospital complications, and new institutionalization. Deliriums that are more severe or persistent have even more dire outcomes²: 22-76% of hospitalized inpatients with delirium die⁴. Delirium occurs in 15-60% of nursing home patients, 14-56% of inpatients and up to 60-80% of ICU patients⁵. Yet delirium can be prevented or mitigated in health care settings that understand it, diagnose it and implement interdisciplinary programmes across the health care spectrum to address it, and there is considerable economic potential in doing so. Progress in the field has been seriously hampered by difficulties with diagnosis; up to 95% of cases are missed⁶.

PRESENTATIONS, PHENOMENOLOGY AND IDENTIFICATION OF DELIRIUM

Delirium is misdiagnosed in all settings, including emergency rooms, hospitals, and long term and palliative care settings. The clinical presentation of delirium remains a ‘black box’; as of this time we have no explanations for the variations in behavioural, affective, sensory and motor signs of delirium. These signs can change within seconds or hours, and most likely reflect the complex underlying pathophysiologies. The DSM IV-TR diagnostic criteria are shown in Table 36.1⁷.

Many rating scales have been developed to assist with the diagnosis, the most widely used including the CAM⁸ and CAM-ICU⁹. Inattention and the broad fluctuations of symptoms are characteristics not found in other psychiatric illnesses. At the same time, they are the most difficult to measure and identify. Attention is a complex phenomenon that involves distractibility, vigilance and concentration, and is our most basic interface with the environment. Unless patients are grossly agitated and irrational, the clinical expression of inattention can be very subtle. It is easily mistaken for the withdrawal and lack of environmental engagement found in depression. Fluctuations, unless they are marked, are often written off as fatigue, uncooperativeness, withdrawal, differing responses to different health practitioners, or reactions to procedures. Given changeovers of physicians and nurses in busy hospitals, such indefinite characteristics go largely unrecognized unless staff nursing notes are carefully mined for evidence of these subtle changes. Nurses are the first to recognize early symptoms of delirium, although they do not reliably diagnose it as such, and are a rich source of descriptive information that can greatly assist with diagnosis¹⁰.

Broadly accepted subcategories include ‘active’, ‘mixed’, and ‘quiet’ delirium. These subcategories may have implications for prognosis or pathophysiology. Significant investigation of these subtypes has been done, although these have not yet provided clear implications for causality, prognosis or intervention. Active delirium is defined as a state marked by agitation, physically aggressive and often violent activity, hyperattentiveness (the inability to suppress responses to the environment or to internal states) and emotional lability. In this condition, deficits in focused attention and fluctuations of presentation are easily identified. Quiet delirium is defined as a state marked by withdrawal, lack of involvement in or communication with the environment, bland or flat affect, and a depressed level of consciousness short of frank stupor. These symptoms reflect an inability to attend appropriately and in sequential fashion to the demands of the environment. Mixed deliriums are considered to be a combination of the two. The prevalence of these subtypes is variably reported but averages 25% for quiet delirium, 45% for mixed delirium, and 30% for active delirium. All subtypes of delirium can present with motor symptoms (dysarthria, difficulty swallowing, gait disturbances), affective symptoms (dysphoria, lability, anxiety), sensory difficulties that are associated with incorrect cerebral processing of sensory data (clinically expressed as difficulties with hearing, appreciation of pain), and illusory phenomena, aphasia (partial or global) and impaired cognitive function (dysexecutive function, disorientation, nonsensical speech). Any of these symptoms may fluctuate, even within seconds. The appreciation and reporting of pain by the delirious patient is particularly problematic, as untreated pain can worsen delirium, yet overtreatment with narcotic agents can have the same result. Psychotic-like symptoms such as disorganized speech and visual hallucinations may also be associated, although the hallucinations in delirium are more illusory than hallucinatory. They commonly involve nonsensical images such as ‘clowns on bicycles’ or ‘tires in the ceiling’. The differentiation of delirium from prominent psychotic illnesses, including schizophrenia, schizoaffective disorder and bipolar disorder, can be problematic. Pre-existing psychiatric diagnoses are a principal cause of poor identification of

Table 36.1 DSM-IV-TR diagnostic criteria for delirium

A. Disturbance of consciousness (i.e. reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention.

B. A change in cognition (e.g. memory deficit, disorientation, language disturbance) or

C. Development of a perceptual disturbance that is not better accounted for by a pre-existing, established, or evolving dementia.

D. Disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day.

E. There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by the direct physiological consequences of a general medical condition.

delirium, as the patients’ symptoms are often attributed to them¹¹. In these cases, reliance on clues from the patient’s clinical history is critical. Quietly delirious patients are frequently misidentified as depressed. Farrell and Ganzini¹² found that 42% of patients referred to psychiatry consultation services for depression were actually delirious. However, an additional finding was that 60% of patients with delirium have symptoms of dysphoria, and 52% have passive or active thoughts of suicide. Acutely ‘suicidal’ patients suffering with prolonged hospitalizations and multiple medical problems are prototypically confusing. In such cases, the burden of risk and need for immediate medical intervention rest with delirium rather than depression.

A further consideration is that symptoms of delirium present along a spectrum. Evidence for the existence of subsyndromal delirium has been presented by Levkoff et al., among others¹³. Marcantonio et al. found that patients with subsyndromal delirium had worse outcomes than patients with diagnosable mild delirium¹⁴.

The recognition of delirium remains one of the most prominent problems in the field. The term ‘recognition’ includes not just diagnosis of the medical condition of delirium, but also the recognition that it is a severe illness that cannot be assumed to resolve on its own with few sequelae. Recent appreciation of this has led to skyrocketing numbers of publications in the field in recent years¹⁵.

THE ETIOLOGY OF DELIRIUM

Population at Risk

A multitude of risk factors have been identified in treatment studies of delirium, often with little overlap. However, most would agree that age, cognitive impairment, medication and medical burden define the characteristics of the population at highest risk². Efforts to advance the field by seeking universal ‘causes’ of delirium have therefore been very frustrating. It is easiest to conceptualize the aetiology of delirium from the perspective of the syndrome of frailty. Frailty has many definitions, but on a physiological level its most commonly accepted conceptualization is sarcopaenia, or progressive deterioration of skeletal muscle¹⁶. It is usually found in patients who are older, cognitively impaired and medically ill, and in fact the majority of patients who develop delirium are frail. Some investigators provide a broader view of the components of frailty by including socioeconomic stressors, psychiatric disorders, medication and home environment as well as medical vulnerabilities, which reference the broad network of resources that frail geriatric patients require to avoid catastrophic illness¹⁷. The increased vulnerability of frail patients to the catastrophic decline represented by delirium is related to their limited physiological reserve. With ageing, there is diminution of redundant systems such as neurons and neuronal circuits in the brain and excess metabolic capacity in the liver and kidney. Patients with the least reserve are more susceptible to any stressor, however small, than healthier individuals, in a striking resemblance to chemical equations far from equilibrium. The implication is that the patient’s underlying vulnerability and disequilibrated status (as opposed to any specific ‘last minute’ precipitating causes), are the most important predictors of delirium in an individual person. It is then easy to conclude that the prominent precipitating causes of delirium are the most common complications, including iatrogenic ones, found in hospitalized patients. A short list includes hyponatraemia, acute blood loss, pain, acute renal failure, fractures, acute infections (urinary tract or pulmonary), the use of longer term indwelling bladder catheters, dehydration, decubiti, malnutrition and the use of psychotropic medications².

Pathophysiology of Delirium

Historically, multiple interacting theories have been proposed to explain the pathophysiology of delirium. Any given delirium may have an unknown number of associated clinical conditions (baseline and precipitating factors), and they do not necessarily occur in the same combinations. It is only when the patient has recovered that there is any clinical certainty that the basic physiological process(es) have been fully addressed. However, many deliriums do not fully resolve. It is also not necessarily the case that two patients who appear to have equal degrees of baseline and precipitating stressors will both become delirious. This lack of reproducibility has wreaked havoc with our investigations of pathophysiology. We are left with broad-based geriatric clinical intervention methods that are helpful but quite non-specific, and this may account for some of our difficulty in making progress in the field.

At a cellular or molecular level, the most compelling evidence indicates that excess dopamine and/or insufficient acetylcholine in the brain could best explain the cascade of metabolic and behavioural complications of delirium. Each has complex and interactive impacts on cellular function within the CNS¹⁸

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