Rosen & Barkin's 5-Minute Emergency Medicine Consult (334 page)

• Elicit history of liver disease and prior episodes of HE.
  
• Search for precipitating cause (particularly GI bleeding and infection).
  
• Check for electrolyte abnormalities:
  
  • Even minimal abnormalities may manifest as significant clinical changes.
    

• Blood NH
  ₃
  level:
  
  • Level correlates poorly with the degree of HE or the presence of cerebral edema.
    
  • Helpful in detecting HE in cases of altered mental status (AMS) of unknown cause
    
  • Normal NH
    ₃
    level with suspected HE warrants search for other causes of AMS.
    
  • Must be kept on ice and assayed within 30 min.
    
• Consider hemoccult testing and nasogastric (NG) lavage to rule out GI bleeding
  
• CBC to search for anemia
  
• Electrolytes, BUN, creatinine, glucose
  
• PT/INR with elevations suggesting significant liver failure
  
• Liver profile/liver enzymes
  
• Urinalysis for possible infection
  
• Culture urine and ascitic fluid to search for infectious cause
  
• Toxicology screen for alternate cause of altered level of consciousness:
  
  • Acetaminophen and alcohol level as necessary
    
• Additional labs as clinical scenario dictates:
  
  • TSH
    
  • Blood gases
    
  • Magnesium
    
  • Viral serology
    

• CXR for pneumonia and signs of CHF
  
• Head CT scan: For new-onset AMS, focal neurologic deficit, suspected cerebral edema, or trauma.
  
• MRI of the brain is especially helpful in diagnosing HE in patients with portosystemic shunts but no intrinsic liver disease.
  

• ECG for arrhythmia and electrolyte imbalance
  
• CSF exam:
  
  • For new-onset or unexplained worsening of HE
    
  • CSF glutamine level correlates with severity of HE.
    
• Paracentesis for SBP workup and culture of ascitic fluid
  
• EEG is usually abnormal, most commonly with generalized slowing and other nonspecific changes.
  

• Alcohol withdrawal syndromes including delirium tremens
  
• Cerebrovascular accident
  
• Congestive heart failure
  
• CO
  ₂
  narcosis
  
• Head trauma with concussion or intracranial hemorrhage
  
• Hypocalcemia and hypercalcemia
  
• Hypoglycemia
  
• Hypokalemia
  
• Meningitis or encephalitis
  
• Metabolic encephalopathy
  
• Neuropsychiatric disorders
  
• Toxic confusional states secondary to:
  
  • Sedative overdose
    
  • Alcohol intoxication
    
  • Illicit drugs
    
  • Medications
    
• Uremia
  

• Consider Reye syndrome early (most common cause of fulminate hepatic failure in children) even if PT is only mildly prolonged.
  
• Consider fatty acid β-oxidation disorder:
  
  • Freeze serum and urine sample for subsequent testing
    

TREATMENT

• Oxygen
  
• Airway protection:
  
  • Patients with grade 3 or 4 HE may require intubation for airway protection. Propofol is the preferred agent for sedation.
    
• Cardiac monitor
  
• Fluid resuscitation
  
• Initial AMS treatment:
  
  • Naloxone
    
  • D
    ₅₀
    W (or bedside glucose)
    
  • Thiamine
    

Identification and removal of precipitating factors is key and may improve clinical picture alone.

• Treatment of complicating conditions:
  
  • Acute GI bleeding
    
  • Sepsis
    
  • Electrolyte and pH abnormalities
    
  • Coagulopathy
    
  • Renal and electrolyte disturbances
    
• Avoid sedative/narcotics if possible:
  
  • If necessary, use agents not metabolized by the liver
    
• Increase NH
  ₃
  elimination:
  
  • Bowel cleansing with nonabsorbable sugars (i.e., lactulose is mainstay of treatment). Retention enema preferred in grade 3/4 HE
    
• Decrease NH
  ₃
  -producing intestinal flora (in combination with lactulose):
  
  • Neomycin (nephrotoxic and ototoxic)
    
  • Metronidazole (PO)
    
  • Vancomycin (PO)
    
  • Rifaximin: Recommended for lactulose-resistant HE. Current data suggests it is as effective as lactulose and neomycin and has a favorable safety and tolerability profile, although more expensive
    
• Treat associated cerebral edema if present
  
• Correct zinc deficiency
  
• Short-term restriction of protein intake in diet
  
• Flumazenil in patients who have received benzodiazepines may provide moderate, short-term improvement.
  
  • Avoid flumazenil unless you are sure that the patient is not a chronic alcoholic or benzodiazepine user as resultant seizures may occur.
    
• Precautions to prevent bodily harm to the confused patient with HE
  
• Liver transplantation provides cure for severe, spontaneous, or recurrent HE
  
• Possibly of benefit:
  
  • L-carnitine
    
  • Albumin dialysis
    
  • Broad-spectrum antibiotic coverage
    
  • N-acetylcysteine
    
  • Lactobacillus acidophilus
    supplementation
    
  • Ornithine aspartate
    
  • Benzoate or Bromocriptine
    
  • Branched-chain amino acids
    
  • Chelation of manganese with edetate calcium disodium
    

• Dextrose: 1–2 amps (25 g) of 50% dextrose (child: 2 mL/kg D
  ₂₅
  W) IV
  
• Lactulose: 30 mL (peds: 0.3 mL/kg) PO/NG tube q6h titrated to produce 2 or 3 soft stools per day and stool pH < 5 or retention enema at 300 mL + 700 mL saline/tap water q4–6h
  
• Metronidazole: 250 mg PO/NG (peds: 10–30 mg/kg/d) q8h for 2 wk
  
• Narcan: 2 mg (peds: 0.1 mg/kg) IV/IM initial dose
  
• Neomycin: 1–3 g (peds: 50–100 mg/kg/d) PO q6h
  
• Rifaximin: 550 mg PO/NG q12h. (safety not established for children <12 yr)
  
• Mannitol: 0.5 –1 g/kg IV
  
• Thiamine (vitamin B
  ₁
  ): 100 mg (peds: 50 mg) IV/IM
  
• Zinc acetate or sulfate: 220 mg PO/NG q8h
  

FOLLOW-UP

• HE grade 2, 3, or 4 or inadequate social support
  
• Type A HE (any grade) and type B or C (grade 2 or above) should be admitted to the ICU with urgent GI consult
  
• Associated complicating condition (GI bleeding and sepsis)
  
• Uncertainty about cause of AMS
  

• Known chronic or intermittent HE
  
• Grade 0 or 1 with remediable cause
  
• Adequate supervision with close follow-up
  
• Those appropriate for discharge should go home with:
  
  • Low-protein diet
    
  • Lactulose prescription
    

• Refer to primary physician or GI for consideration of medication or diet changes if recurrent early stage HE episodes
  
• For any grade of type A HE, consider transfer to a liver transplant facility
  

• Dietary consultation if possible cause of exacerbation
  
• Alcohol counseling if it is a concern
  

• Consider rifaximin for lactulose-resistant HE
  
• Hypoglycemia is common in HE patients.
  
• Avoid sedatives and narcotics if possible in HE patients. If necessary, use medications not metabolized by liver.
  

• Eroglu Y, Byrne WJ. Hepatic encephalopathy.
  Emerg Med Clin North Am
  . 2009;27(3):401–414.
  
• Khungar V, Poordad F.
  Hepatic Encephalopathy. Clin Liv Dis.
  2012;16:301–320.
  
• Riordan SM, Williams R. Treatment of hepatic encephalopathy.
  New Engl J Med
  . 1997;337(7):473–479.
  

See Also (Topic, Algorithm, Electronic Media Element)

Hypoglycemia

CODES

• 070.6 Unspecified viral hepatitis with hepatic coma
  
• 070.9 Unspecified viral hepatitis without mention of hepatic coma
  
• 572.2 Hepatic encephalopathy