How To Choose The Correct Size Of Suction Catheter

 

Review/ Turk J Gastroenterol 2015; 26: 197-203

 

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How to interpret liver function tests in heart failure patients

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Liver damage secondary to cardiac failure may result from congestion or hypoperfusion of the organ.

 

There is no consensus on terminology, but the following has been used:

 

1. Cardiac Hepatopathy (CH)

2. Ischemic Hepatitis

3. Shock Liver

4. Hypoxic Hepatopathy

5. Acute Cardiogenic Liver Injury (ACLI)

 

We propose that ACLI provides more details about the underlying pathophysiological process.

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∎ Both the American College of Cardiology and European Society of Cardiology Heart Failure Guidelines recommend the inclusion of LFTs in the diagnostic workup of all patients presenting with HF.

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Acute cardiogenic liver injury is generally asymptomatic, but nausea, vomiting, weakness, right upper quadrant pain, and apathy may be present after a latent period of 2–24 h after the acute event.

 

In minority of cases, mental confusion, jaundice, flapping tremor or hepatic coma might develop; however, in a patient with acute cardiocirculatory failure, mental confusion and coma generally represent cerebral hypoxia rather than hepatic encephalopathy.

 

* CH generally occurs in the setting of chronic cardiac conditions that may increase systemic venous pressure such as chronic HF, constrictive pericarditis, mitral stenosis, tricuspid regurgitation, corpulmonale, severe pulmonary arterial hypertension, long-standing Fontan procedure, or right-sided HF of any cause.

 

* Acute cardiogenic liver injury, however, is most commonly associated with acute cardiocirculatory failure resulting from acute myocardial infarction, acute decompensated HF (ADHF), myocarditis, or massive pulmonary embolism.

 

Fulminant hepatic failure has also been reported in rare cases of HF.

Retrospective analysis of 1147 acute liver failure patients from the Acute Liver Failure Study Group revealed that 4.4% of patients had ischemic hepatitis. Only 31% of these patients had knowledge regarding their cardiac disease before presentation, but a cardiopulmonary precipitant of hepatic ischemia was identified in 69%.

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There is no specific pattern of derangement of liver function to denote ACLI, but the following facts were derived from various studies:

 

* Primary laboratory findings are elevated serum cholestasis markers including bilirubin, alkaline phosphatase (AP), and γ-glutamyl-transpeptidase (GGT).

 

* Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels generally show mild elevations up to 2-3 times the normal reference level.

 

* A mild decrease in albumin (approximately in 25% patients) levels and a slight increase in prothrombin time are also frequent in Cardiac Hepatopathy (CH) patients.

 

* Increase in liver function tests are more strongly correlated with decreased cardiac index, increased filling pressures, and severe tricuspid regurgitation.

 

* Both GGT and total bilirubin levels were found to be associated with disease severity, but only GGT level is independently associated with adverse outcomes in one study.

 

* After adjustment for other variables, only total bilirubin level was found to be independently associated with morbidity and mortality in the CHARM program.

 

* Another prospective study of 552 chronic HF patients suggested that all abnormal

LFTs are markedly associated with mortality, but AST and total bilirubin levels show the highest association.  

 

* Total bilirubin, AP, and GGT levels independently correlate with functional class and clinical signs of HF including jugular venous distention, tricuspid regurgitation, and peripheral edema.

 

* Hypoalbuminemia, mainly caused by HF-associated systemic inflammation, is also another prognostic marker in acute and chronic HF.

 

* The typical laboratory finding of ACLI is the presence of a striking elevation in transaminase and LDH levels (generally to 10-20 times the normal values, even up to 2000-fold).

 

* Transaminases and LDH levels reach their peak 1-3 days after the acute event and return to normal limits within 7-10 days if the patient’s hemodynamics recovers.

 

* In ACLI, an early and rapid increase of LDH levels in parallel with transaminase levels, a ratio of ALT to LDH <1.5, and a decrease in ALT levels by more than 50% within 72 h are characteristic findings that can be useful in the differential diagnosis of acute viral, alcoholic, or drug-induced hepatitis.

 

* Other laboratory findings are mild elevations of serum bilirubin and AP levels and prolongation of prothrombin time.

 

* Several trials evaluated the prognostic role of LFTs in ADHF patients. A post hoc analysis of 1134 inotropes-treated ADHF patients from the SURVIVE trial indicated that 46% of patients had abnormal LFTs, and among these tests, only abnormal transaminase level were associated with 180-day mortality.

 

* Another post hoc analysis of the placebo arm of the EVEREST trial that involved hospitalized ADHF patients showed that baseline LFTs abnormalities are common in ADHF patients but that only low albumin and elevated bilirubin levels have a prognostic value for mortality.

 

* Another acute HF study (Relaxin in Acute Heart Failure, RELAX-AHF study) reported that an increase of ≥20% at early days of acute event in serum ALT levels was associated with 180-day all-cause mortality.

 

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