Acute hepatic failure

(Redirected from Hepatic failure)

Background

Liver vascular anatomy.

Definitions

  • Hyperacute liver failure: encephalopathy occurs within 7 days of the onset of jaundice; this subset is likely to survive with medical management despite the high incidence of cerebral edema[1]
  • Acute liver failure: interval of 8-28 days from jaundice to encephalopathy; this subset has a high incidence of cerebral edema and a poorer prognosis without liver transplant[2]
  • Subacute liver failure: interval of 5-12 weeks from the onset of jaundice to the onset of encephalopathy; this subset has a lower incidence of cerebral edema, but a poor prognosis[3]

Causes of acute hepatitis

Drug or Toxin Related Liver Disease

Other Rare Causes of Acute Liver Failure

  • Wilson's disease: unexplained elevations in LFTs, neuro-psychiatric symptoms, Kayser-Fleischer rings on eye exam
  • Autoimmune hepatitis: more common in women, liver disease without explanation, may have family history of other autoimmune disorders
  • Hemochromatosis: family history of liver disease and cardiac disease
  • Budd-Chiari: history of hypercoagulable disorder, abdominal pain, and ascites

Clinical Features

Jaundice of the skin
Spider angioma
Ascites secondary to cirrhosis.
Pediatric jaundice with icterus of sclera.

Differential Diagnosis

Encephalopathy (altered mental status)

Jaundice

Hepatic Dysfunction

Infectious

Neoplastic

Metabolic

Biliary

  • Biliary cirrhosis

Drugs

Miscellaneous

Evaluation

Labs

  • LFTs
    • AST and ALT
      • Enzymes found mainly in hepatic cells, though ALT is more specific to the liver than AST
      • Extreme elevation in AST (>3000U/L, or >40x upper limit of normal) is consistent with acetaminophen toxicity or ischemic injury
      • Moderate elevations (10-40x upper limit of normal) is consistent with viral hepatitis
      • Mild elevations (<10x upper limit of normal) is consistent with alcoholic hepatitis
    • Alkaline Phosphatase
      • Found in bile canaliculi (but also in placenta, ileal mucosa, bone, and kidney)
      • Elevated in diseases of cholestasis
      • Rare for levels to be >3x normal limit in acute liver failure
    • Bilirubin
      • Elevated in diseases of cholestasis
      • In obstructive diseases, the direct bilirubin will usually be about 50% of the total bilirubin; if indirect bilirubin is higher, more suggestive of hemolysis or problem with conjugation
  • Coagulation Studies
    • Reflects the liver’s ability to synthesize clotting factors
    • INR >6.5 or PT >20 seconds indicates patients at high risk for death
  • Albumin
    • Reflects synthetic function of the liver
    • Has a long half-life (20 days) and may not be decreased early in disease
  • Ammonia
    • Elevated as a result of impaired clearance
    • Poor correlation between degree of elevation and severity of encephalopathy symptoms
  • Chemistry Panel
    • Electrolyte abnormalities may indicate malnutrition or dehydration
    • Creatinine is used as a prognostic indicator
    • Need to check a glucose because patients with liver failure are prone to hypoglycemia
  • CBC
  • Viral hepatitis Serologies
    • Consider for all patients with undifferentiated liver failure
    • IgM anti-HBc may be the only positive marker in acute Hepatitis B infection
    • Anti-HCV and HCV RNA are present in both chronic and acute Hepatitis C infections, so it is difficult to differentiate based on serologies, but presence of HCV RNA in the absence of anti-HCV is more suggestive of acute infection[7]
    • Only need to test for IgM anti-HEV in patients who are symptomatic and have just travelled from areas where Hepatitis E is endemic

Imaging

  • Consider RUQ US or CT in patients with jaundice to evaluate for a mechanical obstruction
  • Otherwise, tailor imaging towards specific complaints

Ascites Diagnosis

The differential diagnosis of ascites is often clarified by the calculation of the serum albumin to ascites gradient (SAAG).^

^SAAG = (serum albumin in g/dL) − (ascitic albumin in g/dL)

Management

  • Treatment is mostly supportive and tailored towards the specific etiology
  • Early consideration regarding transporting patient to a transplant center given potential for rapid deterioration
  • Symptom specific supportive treatment options

Disposition

  • Admission to ICU with early consideration for transportation to transplant center

See Also

References

  1. ↑ O’Grady, JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes. Lancet. July 1993, Volume 342, Issue 8866, Page 273-275
  2. ↑ O’Grady, JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes. Lancet. July 1993, Volume 342, Issue 8866, Page 273-275
  3. ↑ O’Grady, JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes. Lancet. July 1993, Volume 342, Issue 8866, Page 273-275
  4. ↑ Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002 Dec 17; 137(12): 947-54.
  5. ↑ Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204
  6. ↑ Tintanelli's
  7. ↑ Bailey, C, Hern HG. Hepatic Failure: An Evidence-Based Approach In The Emergency Department. Emergency Medicine Practice. Vol. 12, No. 4, 2014.
  8. ↑ Runyon BA. Management of adult patients with ascites due to cirrhosis: update 2012. Amer Assoc Study Liv Dis. 2012; 1-96.
  9. ↑ Runyon BA. Cardiac ascites: a characterization. J Clin Gastro. 1998; 10(4): 410-412.
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