Acute liver failure: Difference between revisions

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==Diagnosis==
==Diagnosis==


===Physical Examination===
From history and clinical examination possibility of underlying chronic disease should be ruled out as it may have different management.
===Laboratory tests===
===Laboratory tests===
All patients with clinical or laboratory evidence of moderate to severe acute hepatitis should have immediate measurement of prothrombin time and careful evaluation of mental status. If the prothrombin time is prolonged by ≈ 4-6 seconds or more (INR ≥1.5)
All patients with clinical or laboratory evidence of moderate to severe acute hepatitis should have immediate measurement of prothrombin time and careful evaluation of mental status. If the prothrombin time is prolonged by ≈ 4-6 seconds or more (INR ≥1.5)

Revision as of 20:16, 28 August 2012

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Acute liver failure
ICD-10 K72.9
MeSH D017114

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2], Prashanth Saddala M.B.B.S

Diagnosis

Laboratory tests

All patients with clinical or laboratory evidence of moderate to severe acute hepatitis should have immediate measurement of prothrombin time and careful evaluation of mental status. If the prothrombin time is prolonged by ≈ 4-6 seconds or more (INR ≥1.5) and there is any evidence of altered sensorium, the diagnosis of ALF should be strongly suspected and hospital admission is mandatory[1]. Initial laboratory examination must be extensive in order to evaluate both the aetiology and severity.

Initial laboratory analysis[1]

Liver Biopsy

A liver biopsy done via the transjugular route because of coagulopathy is not usually necessary other than in occasional malignancies.

As the evaluation continues, several important decisions have to be made such as whether to admit the patient to an ICU, or whether to transfer the patient to a transplant facility. Consultation with the transplant centre as early as possible is critical due to possibility of rapid progression of ALF.

Treatment

King's College Hospital criteria

for liver transplantation in acute liver failure[2]

Patients with paracetamol toxicity

pH <7.3 or
Prothrombin time >100 seconds and
serum creatinine level >3.4 mg/dL (>300 μmol/l)
if in grade III or IV encephalopathy

Other patients

Prothrombin time >100 seconds or
Three of the following variables:

  • Age <10 yr or >40 yr
  • Cause:
    • non-A, non-B hepatitis
    • halothane hepatitis
    • idiosyncratic drug reaction
  • Duration of jaundice before encephalopathy >7 days
  • prothrombin time >50 seconds
  • Serum bilirubin level >17.6 mg/dL (>300 μmol/l)

Aim of therapy is to correct

  • Metabolic abnormalities
  • Coagulation defects
  • Electrolyte and acid-base disturbances
  • Advanced chronic kidney disease
  • Hypoglycemia
  • Encephalopathy

Treatment strategies

General measures

  • Treatment involves admission to hospital; often intensive care unit admission or very close observation are required.
  • Supportive treatment with adequate nutrition and, optimization of the fluid balance should be done
  • Mechanical ventilation, intubation is indicated for stage 3 or 4 encephalopathy
  • Sepsis and infections are common with fulminant liver failure. Though prophylactic antibiotic decreases the risk of infection, but is not routinely recommended as no survival benefits have been proved. Nevertheless, broad coverage with antibiotics is recommended for suspected cases of sepsis.
  • Routine administration of steroids for adrenal insufficiency is not recommended.
  • H2 receptor blocker and proton pump inhibitors are indicated to prevent and treat stress gastropathy.
  • Early transfer to a liver transplantation center should be decided based on patient's clinical status.

Management of increased intracranial pressure

  • Intracranial pressure monitoring in severe encephalopathy and impending cerebral edema should be done with extradural sensors
  • The goal should be to maintain the intracranial pressure below 20 mm Hg and the cerebral perfusion pressure above 70 mm Hg.
  • Lactulose is indicated in cases of encephalopathy.
  • Mannitol, 0.5 g/kg, or 100–200 mL of a 20% solution by intravenous infusion over 10 minutes for reducing cerebral edema
  • Mannitol should be avoided in patients with advanced chronic kidney diseases.
  • Hypernatremia (145-155 mEq/L) through intravenous hypertonic saline infusion to induce hypernatremia may be used to reduce intracranial hypertension.
  • Hypothermia (32–34 °C) may reduce intracranial pressure in refractory cases can be tried.
  • Other measures like elevation of head end to 30 degrees, hyperventilation and intravenous prostaglandin E1can also be used.
  • Short-acting barbiturate, propofol, or i/v indomethacin for refractory intracranial hypertension.

Treatment for specific underlying cause

Acetaminophen or Paracetamol poisoning

    • Acetylcysteine for paracetamol poisoning up to 72 hours after ingestion
    • It improves cerebral blood flow and increases transplant-free survival in patients with stage 1 or 2 encephalopathy due to hepatic failure of any cause.
    • Its treatment can increase prothrombin time giving a false alarm of worsening liver failure.
      • 140 mg/kg orally followed by 70 mg/kg orally every 4 hours for an additional 17 doses or
      • 150 mg/kg in 5% dextrose intravenously over 15 minutes followed by 50 mg/kg over 4 hours and then 100 mg/kg over 16 hours

Mushroom poisoning

  • Penicillin G - 300,000 to 1 million units/kg/day or
  • Silibinin/silymarin/milk thistle (not licensed in the United States)

Chronic viral hepatitis

  • Nucleoside analogs - Fulminant hepatitis B

Herpes simplex hepatitis

  • Intravenous acyclovir

Wilson disease

Other supportive measures

  • Drainage of ascites.
  • While many people who develop acute liver failure recover with supportive treatment, liver transplantation is often required in people who continue to deteriorate or have adverse prognostic factors.
  • "Liver dialysis" (various measures to replace normal liver function) is evolving as a treatment modality and is gradually being introduced in the care of patients with liver failure.

References

  1. 1.0 1.1 Polson J, Lee WM (2005). "AASLD position paper: the management of acute liver failure". Hepatology. 41 (5): 1179–97. doi:10.1002/hep.20703. PMID 15841455.
  2. O'Grady JG, Alexander GJ, Hayllar KM, Williams R (1989). "Early indicators of prognosis in fulminant hepatic failure". Gastroenterology. 97 (2): 439–45. PMID 2490426.

it:Insufficienza epatica fulminante ur:فشل جگری خاطف


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