1.8.6 Hepatic Encephalopathy

Question 1

Describe hepatic encephalopathy classes A, B, and C

Answer 1

• Class A
  
  • Associated with acute liver failure
• Class B
  
  • Associated with portosystemic bypass without intrinsic liver dz
• Class C
  
  • Associated with chronic liver dz

Question 2

What are potential sources of ammonia (NH3)

Answer 2

• Intrahepatic deamination of amino acids
• Extrahepatic metabolism of nucleotides
• Gut metabolism of glutamine
• Bacterial breakdowns of proteins and urea in intestines
  
  • >50% of NH3

Question 3

Your patient has acute hepatic encephalopathy.

What is ammonia level usually?

When was the likely onset of their liver failure?

Their jaundice?

Answer 3

• Ammonia > 45
  
  • Neurotoxic
• Acute HE within 8 wks of onset/sx of liver failure
• Acute HE within 2 wks of onset of jaundice

Question 4

Your patient has acute HE. What is the clinical presentation?

Answer 4

• Abrupt onset
• Vague, flu-like prodrome
• Rapid progression (hours to days)
• A/w development of cerebral edema d/t astrocyte swelling
  
  • Can result in permanent ischemic damage or brain herniation
• Often fatal
  
  • < 20% survival without liver txp

Question 5

Your patient with liver disease may have the following clinical syndrome across these body systems:

• Brain
• Lungs
• Heart
• Liver
• Pancreas
• Adrenals
• Kidneys
• Bone marrow
• Immune

Answer 5

• Brain
  
  • HE, cerebral edema, elevated ICP
• Lungs
  
  • ALI
  • ARDS
• Heart
  
  • High CO state
  • Subclinical myocardial injury
• Liver
  
  • Metabolic function loss of:
    
    • Gluconeogenesis
    • Lactate clearance
    • Ammonia clearance
    • Synthetic capacity
• Pancreas
  
  • Pancreatitis, esp in liver fail d/t APAP od
• Adrenals
  
  • Inadequate glucocorticoid production leading to hypotension
• Kidneys
  
  • Frequent dysfunction/failure
• Bone marrow
  
  • Frequent suppression, esp in viral dz
• Immune
  
  • Systemic inflammatory response, high metabolic rate
  • Circulating leukocytes, impaired function
  • High risk of sepsis

Question 6

Describe lab findings associated with liver disease

Answer 6

• ALT > 24
• AST > 36
• Total bili > 1mg/dL
• PT/INR > 13s
• Ammonia > 45 mg/dL
• Metabolic acidosis (lactatemia)
• Hyperventilation, resp alkalosis
• Hypoglycemia

Question 7

Describe mgmt for acute HE.

How about chronic HE?

What causes HE to break through?

Answer 7

• Acute HE
  
  • Rehydrate and replete
    
    • Fix cause, correct lytes, induce BM
  • Avoid CNS depressant drugs
  • Decrease intestinal NH3 production through diet
  • Medicate:
    
    • Lactulose
    • Neomycin
    • Rifaxamin
    • Tx infxn
  • May need intubation for airway protection
  • May benefit from ICP monitoring and tx
  • Correction of acid/base & electrolyte abnormalities
  • Avoid over-txfn and over hydration
  • Start dialysis in renal failure
  • Liver txp
• Chronic HE
  
  • Sx can appear episodically vs persistent
  • Some have mild sx: common in 2/3 of cirrhosis
  • West Haven Criteria
    
    • 0: lack of changes
    • 1: Short atten span, mood changes
    • 2: Apathetic, disoriented, personality changes, asterixis
    • 3: Somnolent, arousable
    • 4: Coma
• Breakthrough
  
  • BZDs, psychoactive drugs
  • Increased protein loads
    
    • GI bleeds, increased dietary protein
  • Metabolic changes
    
    • Dehydration
    • Alkalosis
    • Hypokalemia
  • Infection
  • Constipation