Using the headings of history, examination, biochemical findings, haematological findings, imaging and biopsy, compare and contrast the clinical features and investigation findings of Acute Fulminant Hepatic Failure with Decompensated Chronic Liver Disease


 


 

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College answer

Acute Fulminant

Decompensated Chronic

History

Acute, toxic ingestion (examples) Viral Infections, Ischaemia

Post-surgery

Chronic  Liver disease

Encephalopathy GI Bleeding

Examination

Jaundice

Jaundice

Coma

Coma

Intracranial hypertension common

Intracranial hypertension rare

No signs chronic liver disease

Signs chronic liver disease

No ascites

Ascites/oedema

No portal hypertension

Signs of Portal hypertension

Biochemistry

Hypoglycaemia common

Hypoglycaemia rare

Hyponatraemia rare

Hyponatraemia common

Severe acidosis

Mild acidosis

High Bilirubin

High Bilirubin

LFT’s severely deranged

LFT’s mildly deranged

Renal failure common

Renal failure less common

Haematology

Platelets usually normal

Platelets usually low

INR very high

INR mildly raised

Fibrinogen low

Fibrinogen normal

Imaging

Head

Cerebral oedema

No cerebral oedema

Abdomen

Normal – may show swollen liver or vascular cause of fulminant failure

Small fibrotic/cirrhotic liver, splenomegaly, varices.

Biopsy

Necrosis

Fibrosis

Discussion

This question is well-formed and gives an accurate impression of exactly what the college wanted to from this comparison of Inappropriately Capitalised Conditions. 

Differences between Acute and Chronic Liver Failure
Domain Acute fulminant hepatic failure Decompensated chronic liver disease
History
  • Abrupt onset
  • Clear antecedent cause, eg. toxin ingestion like paracetamol, or trauma, or ischaemia
  • Gradual onset
  • Associated virus (eg. Hep C)
  • Associated toxin exposure (eg. alcohol)
Examination
  • Acute lung injury
  • Systemic inflammatory response, vasodilated state
  • SvO2 is high because of hyperdynamic circulation
  • Decreased level of consciousness due to cerebral oedema
  • Euvolaemic and without ascites
  • Well-nourished
  • No evidence of portosystemic shunting (thus, no varices)
  • SvO2 is an unreliable marker of tissue perfusion, because of all the shunts.
  • Confusion and delirium due to hepatic encephalopathy
  • Fluid-overloaded, with ascites
  • Portal hypertension is present (thus, varices)
  • Malnourished
  • Spider naevi
Biochemistry
  • High ammonia level
  • Normal urea
  • Extremely high LFTs
  • Acute renal failure
  • Ammonia may be normal 
  • Low urea (unless bleeding)
  • Normal-ish LFTs
Haematology
  • Initially, normal coags
  • INR may be elevated
  • Chronically low levels of clotting factors
Imaging
  • US/CT: enlarged liver, hypodense, heterogenous echogenicity
  • US/CT: small liver, irregular contours, increased density, hyperechoic. Dilated portal vein, evidence of portal hypertension
Biopsy
  • "Acute necrosis" is what it usually says (i.e. it is often uninformative)
  • Discriminates between different causes
  • Diagnostic for cirrhosis
  • Useful for prognosis
CT brain
  • Cerebral oedema
  • No cerebral oedema

Credit was given to any additional correct answers under the relevant headings.

References

Oh's Manual: Chapter 44   (pp. 501) Liver  failure by Christopher  Willars  and  Julia  Wendon

Kim, Tae Yeob, and Dong Joon Kim. "Acute-on-chronic liver failure." Clinical and molecular hepatology 19.4 (2013): 349.

Bernal, William, et al. "Acute liver failure." The Lancet 376.9736 (2010): 190-201.