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The term delirium is synonymous with the term acute confusional state . Delirium is common in hospitalized patients, particularly in the elderly, and refers to an acute, global disorder of thinking and perception, characterized by impaired consciousness and inattention. Restlessness, agitation, and combativeness may be seen, as well as bizarre behavior and delusions. A call to evaluate delirium may therefore be one for “agitation” or “confusion.” Delirium may be distinguished from dementia by the fact that with dementia alone, the sensorium remains clear, despite the occurrence of confusion and disorientation. Furthermore, it should be emphasized that although delirium is often defined as a transient condition, it may take days to weeks to clear, and if delirium is left untreated, the mortality rate may be as high as 25% in elderly inpatients. As with other mental status alterations discussed in this book, delirium is a symptom, not a disease. Successful management depends on accurate diagnosis of the underlying condition.
Amnesia is defined as a pure loss of memory without other cognitive dysfunction. Although memory is affected by delirium, amnesia may occur in isolation, with a clear sensorium. Retrograde amnesia refers to loss of memory for events before a specific point in time. Anterograde amnesia is the inability to lay down new memory. Memory is often categorized into immediate recall (seconds), short-term memory (minutes to hours), and long-term memory (days to years), with short-term memory being the most vulnerable to pathologic processes, both in acute amnestic states and in dementia syndromes.
The hippocampi and parahippocampal structures, dorsomedial thalamus, and the dorsolateral prefrontal cortex mediate short-term memory function. Long-term, verbal memory is mediated predominantly by the dominant (typically left) hemisphere, and visuospatial memory is mediated by the nondominant (typically right) hemisphere.
Most of this chapter will focus on diagnosis and management of acute confusional state. Two acute amnestic disorders will be discussed in brief here. Dementia as a disorder of memory along with broader cognitive decline will be discussed in depth is Chapter 28 .
Is the patient fully awake and alert? In what way is the patient confused? When did the change occur?
Clarify the acuteness and nature of the mental status change. It is important to distinguish between acute and chronic changes and also to distinguish delirium from dementia (see Chapter 28 ) and stupor (see Chapter 5 ).
What are the vital signs?
Fever suggests infection; tachypnea may suggest hypoxia, metabolic acidosis, or hyperglycemia (Kussmaul respiration); and irregular heart rhythm may suggest cardioembolic stroke.
Was there any head injury?
What is the patient’s underlying medical condition?
Diseases that are likely to cause metabolic disarray, such as renal or liver disease, endocrinopathies, diarrheal illnesses, or malignancy, may alter electrolytes. HIV infection or AIDS opens a wider array of differential diagnoses.
Is the patient diabetic?
Both hypoglycemia and hyperglycemia can cause altered mental status.
Is the patient known to be a user of alcohol, nicotine, or other nonprescription drugs?
Order a finger stick glucose level.
If the patient is tachypneic or drowsy, obtain arterial blood gas measurements. A pulse oximeter may be useful for monitoring oxygen saturation.
Provide orientation and reassurance to the patient. Make sure the room is well lit. The treatment of the behavioral and emotional manifestations of delirium, to the extent possible, will make the subsequent etiologic evaluation easier.
Restrain the patient with a Posey chest restraint if necessary. Significant agitation or combativeness may put the patient or those nearby at risk for physical injury.
If possible, do not medicate. Perform the evaluation first. If sedation is given before a good neurologic examination can be obtained, the opportunity for making a diagnosis may be lost.
“Will arrive at the bedside in…minutes.”
What are the causes of delirium?
V (vascular): stroke (infarct or hemorrhage causing a sensory aphasia), subarachnoid hemorrhage, hypertensive encephalopathy, cholesterol emboli syndrome
I (infectious): herpes simplex encephalitis or other viral encephalitis; bacterial, fungal, or rickettsial meningoencephalitis; neurosyphilis; Lyme disease; parasitic abscess (e.g., toxoplasmosis, cysticercosis), bacterial abscess; HIV encephalitis; systemic infection such as urosepsis or pneumonia
T (traumatic): open or closed head trauma, acute or chronic subdural hematoma
A (autoimmune): systemic lupus erythematosus (SLE), multiple sclerosis
M (metabolic/toxic): hypoglycemia or hyperglycemia, hyponatremia, hypercalcemia, hepatic encephalopathy, uremia, porphyria; drug or alcohol ingestion or withdrawal
I (iatrogenic): drug toxicity (particularly in the elderly) such as psychotropic drugs, steroids, digoxin, cimetidine, anticonvulsants, anticholinergics, dopaminergics (see Table 8.1 for common medications with central nervous system [CNS] side effects; Table 8.2 lists medications associated with memory impairment), rare-heavy metal poisoning, pellagra, vitamin B 12 or folate deficiency, Wilson disease
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N (neoplastic): primary brain tumor, metastatic brain disease, paraneoplastic syndrome (limbic encephalitis with small-cell lung cancer)
S (seizure): postictal state, nonconvulsive status epilepticus (rare)
Other (psychiatric): bipolar disorder/mania, psychosis
Expanding mass lesion with impending herniation
Although it is rare for a mass lesion to progress to impending herniation without focal neurologic signs, the first changes may be confusion or altered state of consciousness. Progression can be rapid if there is an expanding subdural hematoma or edema from subarachnoid hemorrhage.
Bacterial meningitis or encephalitis
Bacterial meningitis is a major treatable illness that can be fatal if missed. Other meningitides are likely to be less fulminant yet also can be fatal if left untreated. Herpes simplex encephalitis is the most common sporadic encephalitis. Aside from direct brain damage from infection, encephalitides can produce edema and subsequent herniation.
Delirium tremens
Usually occurring more than 48 hours after cessation of alcohol consumption, the autonomic instability of delirium tremens may produce high fevers, tachycardia, and severe fluctuations in blood pressure ( Fig. 8.1 ). The mortality rate is approximately 15%.
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