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Clinical Specialties · Internal Medicine

Approach to Altered Mental Status

A board-focused framework for altered mental status: stabilize ABCs, check a fingerstick glucose, and give universal reversibles while working the AEIOU-TIPS differential — then anchor on the classic next-best-step vignettes (hepatic encephalopathy, Wernicke, opioid toxicity, and delirium management).

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AMS is a presentation, not a diagnosis

Altered mental status (AMS) is a spectrum — from delirium (acute confusion) to stupor and coma — that signals an underlying organic derangement until proven otherwise. On the boards, the winning sequence never changes: stabilize ABCs, reflexively check a fingerstick glucose, and give universal reversibles while a broad differential is worked in parallel.

Delirium is the most testable form: an acute, fluctuating disturbance of attention and cognition that is a medical emergency — never dismissed as "sundowning" or baseline dementia without a workup.

Three questions organize every vignette:

  • How depressed is consciousness?GCS / AVPU
  • Is there a focal deficit or meningismus? → drives CT / LP
  • What single reversible cause fits the clues? → glucose, opioids, thiamine, sodium, ammonia
Initial approach and the coma cocktail
  • ABCs first, then an immediate fingerstick glucose — the fastest reversible cause.
  • Coma cocktail for undifferentiated AMS: Thiamine, Dextrose (D50 only if hypoglycemic), Naloxone (if opioid suspected), +/- O2.
  • Give thiamine before/with glucose in alcoholics or malnourished patients — a glucose load alone can precipitate Wernicke encephalopathy.
  • Naloxone treats respiratory depression (RR <12); miosis (pinpoint pupils) supports opioid toxicity but is not itself the reason to give it.
  • Sodium is reversible, but correct hyponatremia slowly — raising Na >8 mEq/L/24h risks osmotic demyelination (central pontine myelinolysis).
  • Vitals drive the DDx: fever → infection/meningitis; hypertension + bradycardia + irregular breathing (Cushing triad) → raised ICP; hyperthermia + rigidity → NMS/serotonin syndrome; both hypo- and hyperthermia cause AMS.
  • Inattention is the clinical hallmark of delirium (can't recite the months backward / poor digit span).
  • Common precipitants in a hospitalized elder: infection (UTI, pneumonia), deliriogenic drugs (anticholinergics, benzodiazepines, opioids), and metabolic upset.
AEIOU-TIPS and "DON'T"

AEIOU-TIPS — the differential for AMS/coma:

  • A — Alcohol, Acidosis
  • E — Electrolytes, Endocrine, Encephalopathy (hepatic/uremic)
  • I — Insulin (hypo-/hyperglycemia)
  • O — Oxygen (hypoxia/hypercapnia), Opiates
  • U — Uremia
  • T — Trauma, Temperature (hypo-/hyperthermia)
  • I — Infection (sepsis, meningitis, encephalitis)
  • P — Poisoning, Psychiatric
  • S — Stroke, Seizure (postictal), SAH, Shock

"DON'T" — reflex empiric therapies in undifferentiated coma: Dextrose, Oxygen, Naloxone, Thiamine (give thiamine first in the malnourished, before dextrose).

Delirium vs. dementia

FeatureDeliriumDementia
OnsetAcute (hours–days)Insidious (months–years)
CourseFluctuating, worse at nightSlowly progressive, stable day-to-day
AttentionImpaired (hallmark)Preserved until late
ConsciousnessClouded / alteredNormal until late
HallucinationsCommon (visual)Uncommon early
ReversibilityUsually reversibleUsually irreversible
ApproachFind + treat underlying causeRule out reversible mimics
Vignette — the flapping cirrhotic

Vignette: A 58-year-old man with cirrhosis is brought in confused and lethargic. Exam shows scleral icterus, ascites, and a flapping tremor when the wrists are extended. He has been constipated for several days.

Buzzword: asterixis + cirrhosis. Diagnosis: Hepatic encephalopathy, likely precipitated by constipation (other triggers: GI bleed, infection/SBP, hypokalemia/alkalosis, dehydration, sedatives, TIPS). Next best step: Identify and treat the precipitant and start lactulose, titrated to 2–3 soft stools/day; add rifaximin for recurrent/refractory disease.

Board traps:

  • Ammonia supports the diagnosis but you do not treat to a number or trend it.
  • Do not restrict dietary protein.
  • Always hunt for a trigger — paracentesis to exclude SBP, and look for a GI bleed.
Vignette — confusion, ophthalmoplegia, ataxia

Vignette: A disheveled man with heavy alcohol use is found confused. Exam: ophthalmoplegia (lateral gaze palsy / nystagmus), a wide-based ataxic gait, and global confusion. An intern hangs D5W and he worsens.

Buzzword triad: confusion + ophthalmoplegia + ataxia = Wernicke encephalopathy (thiamine/B1 deficiency). Next best step: IV thiamine — given before or with any glucose, because a carbohydrate load in a thiamine-deficient patient can precipitate or worsen Wernicke.

Key points:

  • The full triad appears in only a minority (~10–30%) — treat empirically when any single feature occurs in an at-risk patient; don't wait for all three.
  • It is a clinical diagnosis — treat empirically, don't wait for a level.
  • Untreated it progresses to Korsakoff syndrome: irreversible anterograde amnesia + confabulation.
  • MRI (not required to treat) may show mammillary body, medial thalamic, or periaqueductal changes.
Axial FLAIR brain MRI showing symmetric hyperintense signal in the periaqueductal grey matter, a classic finding in Wernicke encephalopathy.
Wernicke encephalopathy: FLAIR hyperintensity in the periaqueductal grey matter (also seen in mammillary bodies and medial thalami). MRI supports but is not required for the diagnosis — treat empirically with IV thiamine. · Wikimedia Commons — Jto410 — CC BY-SA 3.0, via Wikimedia Commons
Workup — labs, when to CT vs. LP
  • First-tier labs: fingerstick glucose, CBC, BMP (Na, Ca, BUN/Cr, glucose), LFTs + ammonia, TSH, ABG, UA, tox screen, blood cultures if febrile.
  • Non-contrast head CT when there is head trauma, a focal neurologic deficit, anticoagulation, papilledema, or no metabolic cause identified.
  • Lumbar puncture for suspected meningitis/encephalitis (fever + AMS ± headache/neck stiffness). Do CT first only if focal deficit, papilledema, or immunocompromise — but do not delay empiric antibiotics ± acyclovir.
  • EEG when the exam is "off" with no cause — think nonconvulsive status epilepticus (persistent AMS after a seizure, or unexplained coma).
  • Avoid empiric flumazenil — it can precipitate seizures in chronic benzodiazepine users.
Managing delirium — nonpharmacologic first

Nonpharmacologic measures are first-line:

  • Treat the underlying cause — this is the actual therapy.
  • Reorient frequently; restore the sleep–wake cycle; provide glasses/hearing aids; mobilize early; remove tethers (Foley, lines, restraints) — restraints worsen agitation and delirium.
  • Ensure hydration/nutrition, treat pain, and stop deliriogenic drugs (anticholinergics, benzodiazepines, opioids, sedative-hypnotics).

Pharmacologic — only for severe agitation endangering the patient or staff:

  • Low-dose antipsychotic (e.g., haloperidol or an atypical), shortest duration; check the QTc.
  • Avoid antipsychotics in Parkinson disease / Lewy body dementia (severe neuroleptic sensitivity) — use low-dose quetiapine if one is unavoidable.
  • Avoid benzodiazepines — they worsen delirium — except when the cause is alcohol or benzodiazepine withdrawal (or seizures), where benzos are first-line.
  • Prevention bundles (sleep, mobility, orientation, hydration) beat treatment and lower incidence.

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