Overview

Delirium is a dangerous diagnosis. It is common; it is commonly missed; and it is associated with several adverse outcomes. Although most clinicians label patients with delirium as having an ‘acute change in mental status’, the formal diagnostic criteria according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-Text Revision) paints a more complete and descriptive picture of these patients if put into sentence form: ‘A sudden onset of impaired attention, disorganized thinking or incoherent speech. The patient usually has a clouded consciousness, perceptual disturbances, sleep–wake cycle problems, psychomotor agitation or lethargy and is disoriented’.1

History and Pathophysiology

Although the term ‘delirium’ was not used, references to patients with delirium date as far back as the time of Hippocrates. Delirium has only attracted attention as a syndrome or a diagnosis in the past three decades, with the first textbook dedicated solely to delirium being published in 1980.2 The reasons for this long misunderstanding of what to call this constellation of symptoms are related to the various ways in which delirium can present (hypoactive, hyperactive or a combination of the two) and the complex pathophysiology that causes such a variety of presentations. Although research into the pathophysiology of delirium is in its infancy in clearly defining the contribution each neurotransmitter system and biochemical mechanism has on the clinical picture of delirium, one proposed pathoaetiological model of delirium (Figure 71.1) is important in helping clinicians understand the complexity of a patient with delirium.3 By keeping the complex systems and mechanisms in mind when trying to diagnose or manage a patient with delirium, clinicians will better be able to understand the challenges in making an accurate diagnosis (especially in the face of dementia) and the significant limitations that medications have in the ‘treatment’ of delirium.

Figure 71.1 The pathoetiological model of delirium. Reprinted from Maldonado JR (2008).3 Copyright (2008), with permission from Elsevier. A high-resolution version of this figure is available at Wiley Book Support homepage, http://booksupport.wiley.com.

Prevalence and Incidence for Various Sites and Situations

Associated Adverse Outcomes

The Comprehensive Approach to Delirium

Delirium is not dementia. There is no difference in the core features of delirium in the DSM-IV-TR version compared with the previous version, DSM-IV, except that the DSM-IV-TR version recognizes that delirium can arise during the course of dementia.1 Although this appears to be a minor detail, the message that this gives to healthcare professionals is a critically important one: ‘delirium is not dementia’. Most types of dementia have a progressive downhill course. Delirium should be considered reversible. A mislabelling or lack of differentiation between these two diagnoses is thought to be the reason why delirium is missed by physicians and by nurses. Misdiagnosis or late diagnosis may also partly explain why delirium is associated with adverse outcomes. Table 71.1 details some of the differentiating characteristics between delirium and dementia, based on DSM criteria, keeping in mind that one of the criteria not in Table 71.1 is that delirium must occur in the context of a medical illness, metabolic derangement, drug toxicity or withdrawal.

Table 71.1 Differentiating delirium from dementia.

Altered level of consciousness (LOC) is an excellent clue in differentiating delirium and dementia because it is not always possible to know the patient’s baseline mental status. Without ever having seen the patient before, one can determine whether the patient’s LOC lies towards the agitated or vigilant side of the spectrum of LOC or towards the lethargic, drowsy or stuporous side of the spectrum.

One can ask orientation questions, but since disorientation and problems with memory are present in both delirium and dementia, the key in determining delirium from dementia is how the patient answers. The delirious patient will often give disorganized answers, which can be described as rambling or even incoherent.

The classic identifiers of delirium are acute onset and fluctuating course, both of which are usually obtained by close caregivers (family or nurses). Although acute implies 24 h, the term subacute is used to emphasize that subtle mental status changes can be overlooked by caregivers. Over a period of many days, the patient may appear to be slowly declining mentally due to the underlying dementia. If left unchecked, the initial delirium may impair other necessary functions, leading to further medical problems, such as dehydration and malnutrition, further complicating the delirium. This snowball effect explains in part why the aetiology of delirium is typically multifactorial. Therefore, if it is unclear how long the change has been occurring, patients should be put in the category of delirium and an evaluation should be made.

Attention is also one of the classic identifiers of delirium, which may often be helpful if the patient’s baseline mental status is not known. It can be tested by having a conversation. Patients may have difficulty maintaining or following the conversation, perseverate on the previous question or become easily distracted. Attention can also be tested with cognitive tasks such as days of the week backwards, spelling backwards or digit span.

Psychomotor agitation or lethargy, hallucinations, sleep–wake cycle abnormalities and slow or incoherent speech can all be seen in patients with delirium, but these features are not necessary for the diagnosis.

Evaluation

General guidelines for the medical evaluation of patients are to consider all possible causes, proceed cautiously with appropriate testing and keep in mind that delirium is usually caused by a combination of underlying causes.

After a physical check and ascertaining the history, which includes obtaining details from anyone considered a caregiver (e.g. family, nurse’s aide) and a thorough medication list, the mnemonic D-E-L-I-R-I-U-M-S can be used as a checklist to cover most causes of delirium (Table 71.2). Drugs are notorious for causing delirium. According to most authors in this area, ‘virtually any’ and ‘practically every’ drug can be considered deliriogenic. Several drugs have been found in vitro to have varying amounts of anticholinergic properties. However, since the pathophysiological and neurotransmitter mechanisms of delirium go beyond anticholinergic mechanisms, a more practical approach is to remember certain categories of medications that have been reported to cause delirium, some more common than others. The mnemonic A-C-U-T-E C-H-A-N-G-E I-N M-S is long, as would be expected, but highlights why drugs are such a common cause of delirium (Table 71.3). In order to be as inclusive as possible and because many older reports did not discuss strict delirium criteria or such criteria were not commonly used, the following paragraphs describe not just delirium as a side effect, but also psychiatric side effects that might indicate presence of delirium, such as hallucinosis, paranoia, delusions, psychosis, general confusion, aggressiveness, restlessness and drowsiness.17

Table 71.2 Causes of delirium.

Table 71.3 Medications that can cause (have been reported to cause) an A-C-U-T-E C-H-A-N-G-E I-N M-S (mental status).

Levodopa (an antiparkinson drug) has been reported to cause mental status changes at a rate of 10–60% and include hallucinosis on a background of a clear sensorium, delusional disorders and paranoia. Abnormal dreams and sleep disruption may precede the more frank delirium symptoms and may be an early clue to their onset. Selegiline has been reported to cause mental status changes described as psychosis, aggressiveness and even mania.

Corticosteroids have been reported to cause ‘psychiatric complications’ in up to 18% of patients with doses above 80 mg per day. The mental status changes seen have been described as depressive/manic, an organic affective disorder with associated paranoid-hallucinating features and general ‘confusion’.

Although short-acting urinary incontinence drugs have a greater potential to cause delirium, newer sustained release agents have also been reported.

Theophylline ‘madness’ probably meets delirium criteria. One of the first case reports described a patient with a toxic blood level that correlated with hyperactive periods marked by flailing of limbs, intense emotional lability, incessant crying and ripping out of intravenous lines and nasogastric tubes.

‘Emptying’ drugs is a reminder that drugs such as metoclopramide and droperidol that are often used for nausea and vomiting have potential for mental status changes. Reported mental status side effects include restlessness, drowsiness, depression and confusion. The mechanism is likely because of their antidopaminergic properties.

Cardiovascular drugs rarely cause mental status problems, but because they are so commonly prescribed for older persons, it is worthwhile to remember that some are more likely to cause problems, and also a few that have been reported in case reports. One of the first reports of confusion due to digoxin toxicity was over 100 years ago. Since then, reports of confusion even at therapeutic levels have been published. Antihypertensive agents that may cause mental status changes have primarily been reported in the literature through case reports. However, since they are so commonly used, it is worthwhile being suspicious about a few of them. These include beta-blockers (including in the form of eye drops), angiotensin-converting enzyme inhibitors and calcium channel antagonists.

H2 blockers, because they are primarily renally excreted and may have some H1 activity (antihistamine receptor subtype-1), may cause delirium, especially if patients have underlying risk factors such as renal insufficiency and dementia.

Antimicrobials, like cardiovascular drugs, rarely cause mental status changes, but are very commonly used; some examples worth being aware of are penicillin, erythromycin, clarithromycin, gentamycin, tobramycin, streptomycin, trimethoprim-sulfamethoxazole, ciprofloxacin, some cephalosporins and the antiviral acyclovir, particularly at high doses. Most reports propose that the mechanisms by which antimicrobials cause mental status changes are related to impaired renal function, drug–drug interaction and occasionally idiosyncratic behaviour. Several types of non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to cause delirium, even the selective cyclooxygenase-2 inhibitors.

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