(Acute Confusional State)
A clinical state characterized by fluctuating disturbances in cognition, mood, attention, arousal, and self-awareness, which arises acutely, either without prior intellectual impairment or superimposed on chronic intellectual impairment.
Some practitioners use the terms delirium and acute confusional state synonymously; others use delirium to refer to a subset of confused people with hyperactivity. Still others use delirium to refer to full-blown confusion and confusional state to refer to mild disorientation.
A person who is less alert (with clouding of consciousness) and has difficulty paying attention also has difficulty accurately perceiving and interpreting data from the environment and acquiring or remembering new information; he may misinterpret factual information or have illusions. As a result, the person does not reason logically, has difficulty manipulating symbolic data (eg, performing arithmetic or explaining proverbs), becomes anxious and agitated or withdraws from the environment, and may think in paranoid and delusional ways.
Delirium may occur in persons with a normal brain but is more common in those with underlying brain disease, such as dementia. It is more common in the elderly, probably due to changes in neurotransmitters, geriatric cerebral cell loss, and concomitant disease. Delirium may be due to primary brain diseases or diseases elsewhere in the body that affect the brain; causes are usually metabolic, toxic, structural, or infectious. Regardless of cause, the cerebral hemispheres or the arousal mechanisms of the thalamus and reticular activating system of the brain stem become physiologically impaired. Disruption of sleep and extreme stress superimposed on acute disease may worsen symptoms of delirium (as in intensive care psychosis).
Metabolic or toxic causes: Virtually any metabolic disorder can cause delirium. Some important metabolic and toxic causes of delirium are listed in Table 171-2. In elderly persons, drug side effects are the most common cause.
Structural causes: Structural lesions that can precipitate delirium include vascular occlusion and cerebral infarction, subarachnoid hemorrhage, cerebral hemorrhage, primary or metastatic brain tumors, subdural hematomas, and brain abscesses. Most structural lesions can be detected by CT or MRI, and many produce focal neurologic signs observable during physical examination.
Infectious causes: Delirium may be caused by acute meningitis or encephalitis or by infections outside the brain, perhaps through the elaboration of toxins or production of fever. Pneumonia (even without impaired oxygenation), urinary tract infections, sepsis, or fever from viral infections can produce confusion in the vulnerable brain. Slower-developing embolic abscesses or opportunistic infections are difficult to diagnose clinically and, in some cases, require brain biopsies for proper evaluation.
The symptoms of delirium often fluctuate rapidly, even within a matter of minutes, and tend to be worse late in the day (sundowning). The most prominent is a clouding of consciousness accompanied by disorientation to time, place, or person. The ability to pay attention is poor. Confusion regarding day-to-day events and daily routines is common. Changes in personality and affect are common. Symptoms include irritability, inappropriate behavior, fearfulness, excessive energy, or even frankly psychotic features, such as delusions, hallucinations (commonly visual), or paranoia. Some persons become quiet, withdrawn, or apathetic, whereas others become agitated or hyperactive; physical restlessness is often expressed by pacing. A person may display contradictory emotions within a short time span. Thinking becomes disorganized, and speech is often disordered, with prominent slurring, rapidity, neologisms, aphasic errors, or chaotic patterns. Normal patterns of sleeping and eating are usually grossly distorted. Some persons experience dizziness.
A rapid medical evaluation is imperative because delirium can have a grave prognosis and the underlying condition is often treatable. According to some estimates, 18% of hospitalized elderly persons with delirium die, and hospitalization is twice as long for those who develop confusion as for those who do not.
The diagnosis rests almost entirely on clinical grounds. Diagnostic criteria are listed in Table 171-3. Laboratory tests should include full chemistries, CBC with differential, a test for syphilis such as the Venereal Disease Research Laboratories (VDRL) test, urinalysis with culture, blood cultures, thyroid function tests, vitamin B12 levels, and a toxicology screening. Unless status epilepticus (an extremely rare finding in the elderly) or encephalitis is suspected, EEGs, lumbar punctures, single photon emission computed tomography, and positron emission tomography are not useful. A single CT scan with contrast can detect old or recent infarctions or subdural hematomas.
Delirium with apathy must be differentiated from depression, especially in the elderly, although the two often occur together. Similarly, agitation and hallucinations associated with delirium must be distinguished from those of a functional psychosis--a psychiatric disorder that almost always lacks the disorientation, memory loss, and cognitive impairment found in delirious (or intoxicated) patients. A history of manic illness or schizophreniform disorders suggests a diagnosis of psychiatric disease.
Systemic medical diseases may precipitate delirium and should be sought to guide treatment; an example is the Wernicke-Korsakoff syndrome, which is marked by confusion, disorientation, and memory loss. Hypothermia, tachycardia, hypotension, tremor, and ophthalmoplegia strongly suggest alcohol-related disease. Status epilepticus consisting of absence or complex partial seizures can produce a confused state that is hard to distinguish from delirium. The seizure states, however, produce a steadier but less intense pattern of bewilderment and less drowsiness than does delirium. Despite a confused appearance, affected epileptic patients usually have a surprisingly good sense of direction compared with most delirious patients. Nonconvulsive status epilepticus can be readily detected by EEG. EEG recordings with spike and wave or sharp wave discharges are diagnostic. Delirium alone seldom precipitates convulsive status epilepticus, but a generalized tonic-clonic seizure often results in a state of delirium for up to a day or more. In encephalopathy, the EEG shows a rhythm slower than alpha from both hemispheres. Triphasic waves may appear in hepatic or renal encephalopathy.
Symptoms are usually reversible when the underlying cause is identified quickly and managed properly, particularly if the cause is hypoglycemia, an infection, an iatrogenic factor, drug toxicity, or an electrolyte imbalance. However, recovery may be slow (days to even weeks or months), especially in the elderly.
All unnecessary drugs should be stopped. Identifiable disease should be treated, and fluids and nutrients should be given. A patient suspected of alcohol abuse or withdrawal should be given thiamine 100 mg IM daily for at least 5 days, to ensure absorption. During hospitalization, such patients should be monitored for signs of withdrawal, which can be manifested by autonomic disturbances and worsening confusion.
The environment should be as quiet and calm as possible, preferably with low lighting but not total darkness. Staff and family members should reassure the patient, reinforce orientation, and explain proceedings at every opportunity. Additional drugs should be avoided unless needed to reverse the underlying condition. However, sometimes agitation must be treated symptomatically, particularly when it threatens the well-being of the patient, a caregiver, or a staff member. Restraints used judiciously can help prevent the patient from pulling out IV and other lines. Restraints should be applied by someone trained in their use, released at least every 2 h to prevent injury, and discontinued as soon as possible.
Few scientific data are available to guide the choice of drugs
to treat delirium. Low doses of haloperidol (as little as 0.25
mg po, IM, or IV) or thioridazine (5 mg po) can help in managing
the delirious patient. Larger doses (haloperidol 2 to 5 mg or thioridazine
10 to 20 mg) are sometimes needed. Newer drugs, such as risperidone,
can be used instead of haloperidol for oral therapy but are not
available IM or IV. Short- or intermediate-acting benzodiazepines
(eg, alprazolam, triazolam) can control agitation over the short
term; benzodiazepines may worsen confusion, but if required, the
smallest effective dose should be used. All psychoactive drugs
should be reduced and then eliminated as soon as possible so that
recovery can be assessed.