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You are here: Home / Podcasts / Episode 129: Encephalopathic Disorders

Episode 129: Encephalopathic Disorders

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Wernicke’s Encephalopathy

  • Acutely reversible neurologic syndrome due to thiamine (B1) deficiency.
  • Commonly seen in alcoholics, malnourished patients, and those with a history of bariatric surgery.

Clinical Presentation

  • Classic triad:
    • Ataxia – impaired coordination and gait instability.
    • Ophthalmoplegia – weakness or paralysis of the eye muscles.
    • Confusion – disorientation and cognitive impairment.
  • May progress to Korsakoff syndrome (irreversible amnesia, confabulation).

Labs, Studies & Imaging

  • MRI: Mammillary body atrophy (late finding).
  • Clinical diagnosis; thiamine levels may be low but are not required for diagnosis.

Treatment & Management

  • IV thiamine BEFORE glucose
    • Prevents lactic acidosis due to poor glucose metabolism without thiamine.
  • Nutritional rehabilitation.

High-Yield Facts

  • Always suspect in altered mental status in alcoholics or malnourished patients.
  • Giving glucose before thiamine can worsen symptoms.

Hepatic Encephalopathy

  • Brain dysfunction due to accumulated ammonia and neurotoxins in liver failure.
  • Triggers: GI bleeding, infection, dehydration, sedatives.

Clinical Presentation

  • Altered mental status
  • Asterixis – flapping tremor of the hands.
  • Hyperreflexia – exaggerated deep tendon reflexes.

Labs, Studies & Imaging

  • Serum ammonia: Often elevated but does not correlate with severity.
  • Liver function tests (LFTs): May show elevated AST/ALT, bilirubin, and INR.
  • Electrolytes: Hypokalemia and metabolic alkalosis can worsen symptoms.
  • CT/MRI brain: Used to rule out structural causes if diagnosis is unclear.

Treatment & Management

  • Lactulose (first-line, reduces ammonia absorption).
  • Rifaximin (second-line, reduces ammonia-producing gut bacteria).
  • Correct underlying cause (e.g., treat infection, stop sedatives).

High-Yield Facts

  • Asterixis is a hallmark finding and strongly suggests hepatic encephalopathy.
  • Ammonia level alone does not diagnose hepatic encephalopathy—clinical correlation is key.

Toxic & Metabolic Encephalopathy

  • Encephalopathy secondary to systemic illness, metabolic derangements, or toxins.
  • Common causes: Hypoglycemia, hyperglycemia, hypoxia, uremia, drug overdose (opioids, benzodiazepines), sepsis.

Clinical Presentation

  • Fluctuating altered mental status
  • Hyperreflexia – exaggerated deep tendon reflexes.
  • Myoclonus – sudden, brief involuntary muscle jerks.

Labs, Studies & Imaging

  • EEG: Generalized background slowing is the classic finding for metabolic encephalopathy. Triphasic waves may be seen in hepatic or uremic encephalopathy.
  • CMP: Check for glucose, sodium, potassium, calcium, and renal/liver function abnormalities.
  • ABG: May show acidosis, hypoxia, or hypercapnia depending on etiology.
  • Toxicology screen: Identify potential drug or toxin exposure.
  • Blood cultures: Consider if sepsis is suspected as a cause.
  • CT/MRI brain: Rule out structural pathology if presentation is unclear.

Treatment & Management

  • Address underlying cause (e.g., correct glucose, oxygen, electrolytes).
  • Supportive care.

High-Yield Facts

  • EEG background slowing is the classic finding in metabolic encephalopathy.
  • Always correct reversible causes first (oxygen, glucose, electrolytes).

Uremic Encephalopathy

  • Occurs in advanced renal failure due to accumulation of uremic toxins.
  • Common in patients with end-stage renal disease (ESRD) who are not receiving adequate dialysis.

Clinical Presentation

  • Altered mental status
  • Asterixis – flapping tremor of the hands.
  • Myoclonus – sudden, brief involuntary muscle jerks.
  • Seizures – may occur in severe cases.

Labs, Studies & Imaging

  • Elevated BUN and creatinine – hallmark of renal failure (typically BUN > 100 mg/dL, creatinine > 10 mg/dL in severe cases).
  • Electrolyte abnormalities – hyperkalemia, metabolic acidosis, hypocalcemia.
  • EEG – May show generalized slowing or triphasic waves.

Treatment & Management

  • Urgent dialysis – definitive treatment.
  • Electrolyte correction – address hyperkalemia, acidosis, and calcium imbalance.
  • Seizure management – if present, treat with antiepileptic drugs.

High-Yield Facts

  • Uremic encephalopathy resolves with dialysis.
  • Triphasic waves on EEG may be seen but are not specific.

Hypertensive Encephalopathy

  • Severe hypertension leading to cerebral edema and dysfunction.
  • Part of hypertensive emergency spectrum.

Clinical Presentation

  • Severe headache
  • Altered mental status
  • Vomiting
  • Seizures
  • Papilledema – optic disc swelling due to increased intracranial pressure.

Labs, Studies & Imaging

  • CT head: Rule out stroke, hemorrhage.

Treatment & Management

  • Lower BP gradually with IV medications (nicardipine, labetalol, clevidipine). Nitroprusside is generally avoided due to risk of rapid BP drop and cyanide toxicity.
  • Avoid rapid BP drops to prevent ischemia.

High-Yield Facts

  • BP must be severely elevated (typically >180/120 mmHg) to cause symptoms.

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