iskemik hepatit

 ischemia should always be considered in the differential diagnosis of acute hepatitis, along with more common causes such as viral infection, drugs, toxins, autoimmunity, and metabolic disorders.

The typical pattern of liver biochemical tests consists of a rapid rise in serum aminotransferase levels associated with an early massive rise in lactate dehydrogenase (LDH) levels. Peak aminotransferase levels are typically 25 to 250 times the upper limit of normal and are reached within one to three days of the hemodynamic insult .

In the absence of ongoing hemodynamic instability, aminotransferase levels subsequently decline steadily, usually returning to normal within 7 to 10 days. The serum bilirubin level infrequently rises above four times the upper limit of normal, usually beginning its rise after aminotransferase levels have begun to decline. Serum ALP levels are rarely higher than twice the upper limit of normal.

Hepatic synthetic function usually remains normal or is only mildly impaired; the prothrombin time is infrequently prolonged by more than three seconds. Occasional patients develop changes in mental status, which generally reflect impaired cerebral perfusion rather than hepatic encephalopathy.

Hepatopulmonary syndrome develops in nearly one-half of patients but appears to be reversible following normalization of hepatic function . The pathogenesis is believed to involve intrapulmonary vasodilation.

Few causes of liver injury result in the striking increases in aminotransferase levels (exceeding 1000 international unit/L or 50 times the upper limit of normal) seen in ischemic hepatitis. Besides ischemic hepatitis, the most common are acute drug- or toxin-induced liver injury (eg, asetaminofen toxicity, toxicity caused by certain herbal and dietary supplements) and acute viral hepatitis. On occasion, similar values can be seen in a number of other settings :

●During an acute exacerbation of autoimmune hepatitis.

●Spontaneous reactivation of chronic type B hepatitis.

●Superimposition of hepatitis D in a chronic carrier of hepatitis B virus.

●Miscellaneous disorders such as acute Budd-Chiari syndrome (especially those with concomitant portal vein thrombosis), hepatic sinusoidal obstruction syndrome, HELLP syndrome, acute fatty liver of pregnancy, hepatic infarction, and acute biliary obstruction.

These disorders cannot be distinguished based upon the pattern of liver biochemical tests alone. However, some features may suggest an ischemic rather than a viral cause of liver injury:

●An early rapid rise in the serum LDH level is unusual in viral hepatitis.

●A ratio of serum ALT to LDH of less than 1.5 early in the course of acute hepatitis suggests ischemic hepatitis rather than viral hepatitis [19].

●A rapid fall in serum aminotransferase levels after the initial rise is characteristic of ischemic liver injury and atypical for other causes of hepatitis.

●Ischemic hepatitis is often accompanied by additional evidence of end-organ hypoperfusion, especially acute tubular necrosis of the kidney. Thus, a concomitant, early rise in the serum creatinine level favors a diagnosis of ischemic hepatitis

In addition to a careful medical history, reasonable evaluation might include serologic testing for acute viral hepatitis, a blood asetaminofen level, and right upper quadrant USG with Doppler studies of the portal and hepatic veins and hepatic artery in addition to evaluation for suspected underlying causes of ischemic injury such as cardiac or respiratory failure. 

Management — Management of ischemic hepatitis should be aimed at restoring cardiac output and reversing the underlying cause of hemodynamic instability. Overly aggressive diuresis should be avoided since it may worsen hepatic perfusion. Patients should be monitored closely for evidence of end-organ hypoperfusion, particularly decreased renal function and altered mental status.

As noted above, serum aminotransferase elevations typically resolve spontaneously over 7 to 10 days in the absence of ongoing hypotension. Normalization of serum bilirubin may be more protracted. A continually rising bilirubin and progressive prolongation of the prothrombin time should raise the suspicion of acute liver failure.