Dementia, Delirium & Altered Mental Status

Delirium versus dementia

Delirium is an acute, fluctuating disturbance of attention and awareness with disorganized thinking, developing over hours to days. Inattention is the cardinal feature. It may be hyperactive (agitated) or hypoactive (quiet, withdrawn); the hypoactive form is the most commonly missed and carries a worse prognosis. The Confusion Assessment Method captures it: acute onset and fluctuating course plus inattention, with either disorganized thinking or an altered level of consciousness.

Dementia is an insidious, progressive decline in memory and other cognitive domains with clear consciousness and attention preserved early. The two often coexist: dementia is a major risk factor for delirium, and delirium can be superimposed on dementia.

Finding and treating the cause of delirium

Delirium is a symptom, so hunt the trigger. Elderly hospitalized and postoperative patients are at highest risk. Common causes:

• Drugs: anticholinergics, benzodiazepines, opioids.
• Infection: UTI, pneumonia.
• Metabolic derangements: glucose, sodium, uremia, hepatic failure; also hypoxia.
• Withdrawal: alcohol or benzodiazepines.

DELIRIUM: Drugs, Electrolytes, Lack of drugs (withdrawal), Infection, Reduced sensory input, Intracranial, Urinary or fecal (retention, impaction), Myocardial or metabolic.

Initial workup. Review the medication list first, then check vital signs, oxygen saturation, glucose, electrolytes, renal and liver function, a CBC, and a urinalysis. Neuroimaging is reserved for focal deficits, head trauma, or an unrevealing initial evaluation.

Management. Treat the cause and use nonpharmacologic measures first: reorient, restore the sleep-wake cycle, mobilize, remove unnecessary lines and catheters, and provide glasses and hearing aids. AVOID benzodiazepines (they worsen delirium) except in alcohol or benzodiazepine withdrawal, avoid anticholinergics such as diphenhydramine, and avoid physical restraints. Reserve low-dose haloperidol for dangerous agitation.

The major dementias

Alzheimer disease is the most common dementia: memory goes first, then language and visuospatial function, with cortical as well as hippocampal atrophy. APOE ε4 raises the risk of late-onset disease; APP and presenilin mutations and Down syndrome cause early onset.

Alzheimer treatment is symptomatic. Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) are used for mild-to-moderate disease and memantine (an NMDA-receptor antagonist) for moderate-to-severe disease; neither halts progression. Cholinesterase inhibitors can cause GI upset and bradycardia. Anti-amyloid antibodies (lecanemab, donanemab) modestly slow decline in early disease with confirmed amyloid, with MRI monitoring for amyloid-related edema and microhemorrhage.

Vascular dementia declines in steps with focal neurologic deficits and vascular risk factors, unlike the smooth slope of Alzheimer disease. Risk-factor control prevents further ischemic steps.

Dementia with Lewy bodies shows severe neuroleptic sensitivity: haloperidol can precipitate marked rigidity and decline. Dementia precedes or accompanies parkinsonism within about a year; parkinsonism preceding dementia by more than a year indicates Parkinson disease dementia.

Frontotemporal dementia (Pick disease) begins with disinhibition, apathy, or progressive aphasia at a younger age; Pick bodies are the classic inclusions.

Reversible causes and normal pressure hydrocephalus

Screen every new dementia for reversible causes: vitamin B12, TSH (hypothyroidism), RPR or HIV if indicated, a metabolic panel, and neuroimaging (CT or MRI) for NPH, subdural hematoma, tumor, or hydrocephalus.

Pseudodementia: depressed elders often answer "I don't know" and improve cognitively once the depression is treated.

Normal pressure hydrocephalus (NPH) presents with urinary incontinence, dementia, and a magnetic or apraxic gait: wet, wacky, and wobbly. Gait disturbance usually appears first and is the feature most likely to improve. MRI shows ventriculomegaly out of proportion to atrophy.

Coma and brain death

Coma exam. Quantify with the Glasgow Coma Scale, then test brainstem reflexes: pupillary, corneal, oculocephalic (doll's eyes), oculovestibular (cold caloric), and gag. Structural causes give focal, asymmetric findings; metabolic or toxic causes give symmetric findings with reflexes, especially pupillary responses, often preserved.

• Cold calorics: with an intact brainstem the eyes deviate toward the irrigated ear; no movement means brainstem dysfunction.
• Pupils: pinpoint with opioids or pontine lesions; a unilateral fixed, dilated pupil signals CN III compression from uncal herniation.
• Coma mimics: locked-in syndrome (ventral pons; awake, with vertical eye movements and blinking preserved) and the persistent vegetative state (sleep-wake cycles without awareness).

Brain death is irreversible loss of all cerebral and brainstem function: coma, absent brainstem reflexes, and a positive apnea test.

Spinal reflexes may persist; spinal-mediated movements (the Lazarus sign) do not indicate brain function.