Hepatic cavitation. A marker of transient hepatocellular injury during biliary lithotripsy.

Sonographically visible microbubbles attributable to cavitation effects have been observed in bile (within the gallbladder), in hepatic vessels, and within the liver of patients undergoing biliary lithotripsy. Cavitation effects are believed to contribute to stone fragmentation and possibly tissue injury during lithotripsy. To study the latter, the relationship between intraparenchymal hepatic cavitation and serum transaminase activity and clinical follow-up was analyzed in 81 patients undergoing 164 lithotripsy treatments. Seventy-one treatments (43%) resulted in sonographically evident microbubbles in the liver parenchyma during lithotripsy. A temporary, yet statistically significant (P < 0.01) rise in SGOT and SGPT was observed within 2 hr of completion of lithotripsy compared to those patients without hepatic microbubbles. All but one patient had a return to pretreatment baseline levels of SGOT and SGPT by two weeks after lithotripsy. In this patient, persistent elevation of transaminases was attributed to the delayed passage of fragments and not to any sequelae from hepatic cavitation effects. Ultrasound immediately after, two weeks after, and 3-12 months after lithotripsy showed no hepatic structural abnormalities. Ursodiol administration at the time of treatment did not predispose to hepatic cavitation or elevation of transaminase. Detection of hepatic microbubbles during lithotripsy is a marker of hepatocellular injury. Their correlation with transaminase elevation refutes the contention that transaminasemia results solely from fragment passage after lithotripsy. Although not associated with recognizable structural damage or long-term sequelae, cavitation effects and transaminasemia reiterate that shockwaves are not entirely benign as they traverse parenchymal organs.