Diferencia entre revisiones de «Acute hepatic failure»

(Text replacement - "IV drug use " to "IV drug use")
Sin resumen de edición
Línea 86: Línea 86:
**[[Verapamil]]
**[[Verapamil]]
===Other Rare Causes of Acute Liver Failure===
===Other Rare Causes of Acute Liver Failure===
*'''Wilson’s disease''': unexplained elevations in LFTs, neuro-psychiatric symptoms, Kayser-Fleischer rings on eye exam
*'''[[Wilson's disease]]''': unexplained elevations in LFTs, neuro-psychiatric symptoms, Kayser-Fleischer rings on eye exam
*'''Auto-immune hepatitis''': more common in women, liver disease without explanation, may have family history of other autoimmune disorders
*'''[[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
*'''[[Hemochromatosis]]''': family history of liver disease and cardiac disease
*'''Budd-Chiari''': history of hypercoagulable disorder, abdominal pain, and ascites
*'''Budd-Chiari''': history of hypercoagulable disorder, abdominal pain, and ascites
*'''Infections''': [[HSV]], [[Epstein-Barr virus]], [[varicella zoster virus]], [[toxoplasmosis]]
*'''Infections''': [[HSV]], [[Epstein-Barr virus]], [[varicella zoster virus]], [[toxoplasmosis]]
==Clinical Features==
==Clinical Features==
*Common findings in acute liver failure
*Common findings in acute liver failure
**Tender hepatomegaly
**Tender [[hepatomegaly]]
**[[Jaundice]]
**[[Jaundice]]
**Encephalopathy
**[[Hepatic encephalopathy]]
**Asterixis
**Asterixis
*Common findings in chronic liver failure
*Common findings in chronic liver failure
Línea 111: Línea 111:
*[[Hypoglycemia]]
*[[Hypoglycemia]]
*[[Hypoxia]]
*[[Hypoxia]]
*Intracerebral hemorrhage or mass
*[[Intracerebral hemorrhage]] or mass
*[[Meningitis]]/[[encephalitis]]
*[[Meningitis]]/[[encephalitis]]
*[[CVA]]
*[[CVA]]
Línea 125: Línea 125:
*[[Hepatitis]]
*[[Hepatitis]]
*Hemolysis
*Hemolysis
*Biliary pathology (CBD obstruction)
*[[Biliary disease]] (e.g. [[Choledocholithiasis|CBD obstruction]])
*[[Pregnancy]]
*[[Pregnancy]]
*[[Congenital diseases]] (more likely to present in early childhood)
*Congenital diseases (e.g. [[inborn errors of metabolism]]; (more likely to present in early childhood)


{{Ascites DDX}}
{{Ascites DDX}}
Línea 133: Línea 133:
==Evaluation==
==Evaluation==
===Labs===
===Labs===
*AST and ALT
*[[LFTs]]
**Enzymes found mainly in hepatic cells, though ALT is more specific to the liver than AST
**AST and ALT
**Extreme elevation in AST (>3000U/L, or >40x upper limit of normal) is consistent with acetaminophen toxicity or ischemic injury
***Enzymes found mainly in hepatic cells, though ALT is more specific to the liver than AST
**Moderate elevations (10-40x upper limit of normal) is consistent with viral hepatitis
***Extreme elevation in AST (>3000U/L, or >40x upper limit of normal) is consistent with acetaminophen toxicity or ischemic injury
**Mild elevations (<10x upper limit of normal) is consistent with alcoholic hepatitis
***Moderate elevations (10-40x upper limit of normal) is consistent with viral hepatitis
*Alkaline Phosphatase
***Mild elevations (<10x upper limit of normal) is consistent with alcoholic hepatitis
**Found in bile canaliculi (but also in placenta, ileal mucosa, bone, and kidney)
**Alkaline Phosphatase
**Elevated in diseases of cholestasis
***Found in bile canaliculi (but also in placenta, ileal mucosa, bone, and kidney)
**Rare for levels to be >3x normal limit in acute liver failure
***Elevated in diseases of cholestasis
*Bilirubin
***Rare for levels to be >3x normal limit in acute liver failure
**Elevated in diseases of cholestasis
**Bilirubin
**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
***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
*Coagulation Studies
**Reflects the liver’s ability to synthesize clotting factors
**Reflects the liver’s ability to synthesize clotting factors
Línea 166: Línea 167:
**Only need to test for IgM anti-HEV in patients who are symptomatic and have just travelled from areas where Hepatitis E is endemic
**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===
===Imaging===
*Consider US or CT in patients with jaundice to evaluate for a mechanical obstruction
*Consider [[RUQ US]] or CT in patients with jaundice to evaluate for a mechanical obstruction
*Otherwise, tailor imaging towards specific complaints
*Otherwise, tailor imaging towards specific complaints
==Management==
==Management==
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*Early consideration regarding transporting patient to a transplant center given potential for rapid deterioration
*Early consideration regarding transporting patient to a transplant center given potential for rapid deterioration
*Symptom specific supportive treatment options
*Symptom specific supportive treatment options
**Encephalopathy: consider [[lactulose]] of [[neomycin]]
**[[Hepatic encephalopathy|Encephalopathy]]: consider [[lactulose]] of [[neomycin]]
**[[Seizures]]: consider [[phenytoin]] over [[benzodiazepines]] (prevent benzodiazepine oversedation secondary to decreased hepatic clearance)
**[[Seizures]]: consider [[phenytoin]] over [[benzodiazepines]] (prevent benzodiazepine oversedation secondary to decreased hepatic clearance)
**[[Increased ICP|Intracranial Hypertension]]: elevated head of bed, [[mannitol]], short-term hyperventilation; hypothermia may be a bridge to transplant; no benefit from steroids
**[[Increased ICP|Intracranial Hypertension]]: elevated head of bed, [[mannitol]], short-term hyperventilation; hypothermia may be a bridge to transplant; no benefit from steroids
**Coagulopathy
**Coagulopathy
***Prophylactic normalization of the INR is not necessary unless procedure (such as paracentesis) is planned; then can give [[Vitamin K]]
***Prophylactic normalization of the INR is not necessary unless procedure (such as paracentesis) is planned; then can give [[Vitamin K]]
***Recommend platelet transfusion to 10K for asymptomatic patients, and to 50-70K for patients undergoing invasive procedures
***Recommend [[platelet transfusion]] to 10K for asymptomatic patients, and to 50-70K for patients undergoing invasive procedures
**See [[Acetaminophen toxicity]] for specifics regarding treatment of acetaminophen toxicity
**See [[Acetaminophen toxicity]] for specifics regarding treatment of acetaminophen toxicity
**See [[Spontaneous Bacterial Peritonitis]] for specifics regarding diagnosis and treatment of SBP
**See [[Spontaneous Bacterial Peritonitis]] for specifics regarding diagnosis and treatment of SBP

Revisión del 18:50 27 ene 2019

Definitions[1]

  • 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
  • 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
  • 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

Causes

Acetaminophen Toxicity

  • Now the most common cause of acute liver failure in the US[2]
  • Small amount of acetaminophen is metabolized by CytochromeP450 into NAPQI, which is a toxic metabolite
  • In therapeutic doses, NAPQI combines rapidly with glutathione to form nontoxic metabolites that are excreted in the urine
  • In overdose, glutathione stores are used up and NAPQI binds to cell proteins in the liver which leads to cell death
  • See Acetaminophen toxicity

Viral Hepatitis

  • Hepatocellular pattern of injury, where AST and ALT are higher than Tbili and Alk Phos; likely to have significantly elevated ALT and AST (20x normal or higher)
  • Of note, transmission of Hepatitis B and Hepatitis C through donated blood, blood products, and organs is rare in the US since blood screening became available in 1992
  • Hepatitis A
    • Fecal-oral transmission
    • Associated with epidemics linked to a common source (water)
    • Most common risk factor is travel outside of the US [3]
    • Not associated with chronic carrier state; incubation period is approximately 30 days, and infectivity usually resolved prior to symptom onset
  • Hepatitis B
    • Transmitted parenterally, blood contact, and unprotected sex
    • 90% of exposed infants progress to chronic hepatitis; 10% of exposed adults progress to chronic hepatitis
    • Serology[4]
Clinical Scenario HBsAg anti-HBc anti-HBs
Susceptible to infection negative negative negative
Immune due to natural infection negative positive positive
Immune due to Hep B infection negative negative positive
Acutely infected positive anti-HBc- positive; IgM anti-HBc- positive negative
Chronically infected positive anti-HBc- positive; IgM anti-HBc- negative negative
  • Hepatitis C
    • Transmitted through IV drug use(most common) and infrequently through sexual contact
    • 90% of HCV infections progress to chronic hepatitis[5]
  • Hepatitis D
    • Transmission similar to Hepatitis B
    • Can only co-infect patients with Hepatitis B (actively producing HBsAg)
    • Presentation can range from acute self-limited disease to fulminant hepatitis or chronic infection
  • Hepatitis E
    • Fecal-oral transmission
    • Usually results in mild illness, but can cause fulminant hepatitis in pregnant women[6]

Alcohol-related Liver Disease and Alcoholic hepatitis

  • Presentation can range from mild abdominal pain, nausea and vomiting to acute liver failure
  • May have large palpable liver from fatty infiltration, or may have small nonpalpable liver secondary to cirrhosis from chronic disease
  • Will have moderate elevations in AST and ALT (levels >10x normal are unusual)
    • AST:ALT ration >2 is typical
  • May also have electrolyte abnormalities from malnutrition or alcoholic ketoacidosis

Drug or Toxin Related Liver Disease

Other Rare Causes of Acute Liver Failure

Clinical Features

  • Common findings in acute liver failure
  • Common findings in chronic liver failure
    • Ascites
    • Caput medusae
    • Palmar erythema
    • Spider angiomata
    • Gynecomastia
    • Testicular atrophy
    • Parotid gland enlargement
    • Muscular atrophy
    • May also have jaundice, encephalopathy, and asterixis as in acute liver failure

Differential Diagnosis

Encephalopathy (altered mental status)

Jaundice

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)

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
    • Not useful in diagnosing the cause of liver failure, but helpful in determining coexisting infection, anemia, thrombocytopenia
  • Hepatic Viral 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[10]
    • 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

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. ↑ 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.
  3. ↑ 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.
  4. ↑ www.cdc.gov/hepatitis
  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. ↑ Rein DB, Stevens GA, Theaker J, Wittenborn JS, Wiersma ST. The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005. Hepatology, Vol. 55, No. 4, 2012: 988-997
  7. ↑ 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
  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.
  10. ↑ Bailey, C, Hern HG. Hepatic Failure: An Evidence-Based Approach In The Emergency Department. Emergency Medicine Practice. Vol. 12, No. 4, 2014.
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