09. Altered Mental Status (AMS)

If the patient has HIV/AIDS, see Infectious diseases: HIV and neurologic deficits

Differential Diagnosis

MOVE STUPID mnemonic

  • Metabolic: vitamin B12 or thiamine deficiency, hepatic encephalopathy (hyperammonemia; even if LFTs are normal), Wilson’s disease (rare), niacin deficiency (rare)
  • Oxygen: hypoxemia, hypercarbia, anemia, decreased cerebral blood flow (e.g., from low cardiac output), hypovolemia, and carbon monoxide poisoning
  • Vascular: stroke (especially large hemispheric, brainstem), hemorrhage (intra-parenchymal, subarachnoid, subdural, epidural), hypertensive encephalopathy, hyperviscosity syndromes, vasculitis, TTP/HUS, DIC
  • Endocrine: hyper/hypoglycemia (can cause focal neurologic deficits), hyper/hypothyroidism, high/low cortisol. Electrolytes: hyper/hyponatremia, hyper/hypocalcemia, hypophosphatemia, hypermagnesemia
  • Seizures: post-ictal confusion, non-convulsive status epilepticus, complex partial seizures. Structural: lesions with mass effect, hydrocephalus, cerebral edema
  • Tumor, trauma, or temperature (either fever or hypothermia)
  • Uremia: also dialysis disequilibrium syndrome
  • Psychiatric: diagnosis of exclusion, although ICU psychosis and “sundowning” are common. Consider catatonia, conversion disorder, personality disorder. Rarely, porphyria
  • Infection: of any sort, commonly UTI or pneumonia, sepsis, less commonly meningitis/encephalitis. A simple UTI in an elderly patient can bring out signs of an old, focal stroke (recrudescence)
  • Drugs: intoxication or withdrawal from alcohol or illicit, prescribed, or over-the-counter drugs; other (anticholinergics, etc.). Degenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s cause a slower decline in cognitive function, but patients with dementia with Lewy bodies (DLB) can have prominent fluctuations in mental status, especially when hospitalized

Initial Evaluation of AMS

  • A standard approach: use the “DON’T” mnemonic
  • Dextrose, 1 amp of D50 after thiamine. Check finger stick glucose first if possible
  • Oxygen by nasal cannula or mask, with oropharyngeal airway if necessary
  • Naloxone (Narcan®), usually 0.4-2 mg (IV preferred, can give IM, SC, or intra-tracheal), repeat q 20-30 minutes. Especially useful as diagnostic tool or treatment if respiratory compromise. Severe symptoms may require Narcan gtt. Be careful because can precipitate withdrawal symptoms
  • Thiamine, 100 mg IV (before glucose to prevent precipitation of Wernicke's encephalopathy)
  • Neuro exam:  See Neurology: Examination of the Comatose Patient.
  • Key signs to focus on: presence of focal neurologic deficits, fever, tachycardia, O2 saturation, meningismus, myoclonus (uremia, cerebral hypoxia, hyperosmolar non-ketotic coma), tremor/autonomic symptoms/hyperactivity (withdrawal), asterixis (liver/renal failure, pulmonary encephalopathy, drug intoxication). All suggest metabolic rather than structural disease as the etiology

Work-up

  • Labs: CBC, chemistries, LFTs, TSH, Ca/Mg/Phos, ammonia, Utox, U/A, ABG, ECG, blood and urine cultures, CXR, HIV. The diagnosis of hepatic encephalopathy is made clinically; serum ammonia levels do not rule in or rule out HE. Check serum levels of any drugs a patient is taking for which serum level available (e.g. lithium, valproic acid, phenytoin, phenobarbital, digoxin)
  • Imaging: low threshold for getting a CT stroke protocol in any patient who has focal neurologic signs or who is at risk for stroke. Normal non-contrast head CT does not rule out acute stroke, mass lesions, or posterior fossa abnormalities. If your suspicion of these scenarios is high, follow up with an MRI brain without contrast
  • Lumbar puncture: important in patients with fever/meningeal signs or those who are immunosuppressed
  • EEG: consult neurology and consider in any patient who is fluctuating

Management of Delirium

See Night Calls and Geriatrics sections