Hepatectomy for spontaneous rupture of hepatocellular carcinoma without portal triad clamping

Abstract

Hepatectomy without portal triad clamping may decrease the incidence of liver injury; however, the effects of hepatectomy without portal triad clamping in the treatment of spontaneous rupture of hepatocellular carcinoma (SRHCC) remain unclear. The aims of the present study were to evaluate the therapeutic value of hepatectomy without portal triad clamping in the treatment of patients with SRHCC. The present study retrospectively reviewed patients with SRHCC who received hepatectomy without portal triad clamping (non-clamping group) and the therapeutic efficacy was compared with that of 20 patients with SRHCC undergoing the same surgery in the presence of portal triad clamping (clamping group). Following hepatectomy, the non-clamping group exhibited a significantly lower incidence of acute liver failure compared with the clamping group (P<0.05). No significant differences in operative time, intra-operative blood loss, disease-free or overall survival times between the two groups were identified (all P>0.05). At 1 week and 2 weeks after surgery, the non-clamping group exhibited significantly lower alanine aminotransferase, aspartate aminotransferase and total bilirubin serum levels compared with the clamping group (all P<0.05). Hepatectomy without portal triad clamping may decrease the incidence of liver injury and liver failure in patients with SRHCC, suggesting that it may be a safe and effective therapeutic strategy.

Keywords: hepatectomy; portal triad clamping; spontaneous rupture.

Figure 1.

Levels of (A) Hb, (B) PLT, (C) ALT, (D) AST, (E) TBil, (F) PT, (G) KPTT, (H) FBI and (I) AFP prior to, and 7 and 14 days after, clamping or non-clamping hepatectomy (mean ± standard deviation). At 1 week and 2 weeks after surgery, the non-clamping group exhibited significantly lower serum levels of ALT, AST and TBil compared with the clamping group (all P<0.05). Hb, hemoglobin; PLT, platelets; ALT, alanine aminotransferase; AST, aspartate aminotransferase; TBil, total bilirubin; PT, prothrombin time; KPTT, kaolin partial thromboplastin time; FBI, fibrinogen; AFP, α-fetoprotein.

Figure 2.

(A) Prior to surgery, computed tomography scans of the liver identified discontinuity of the liver tumor capsule, cancer rupture and a crescent hematoma at the site of rupture (arrowhead) and necrotic foci in cancer (arrow). (B) At 2 weeks after surgery, computed tomography scans revealed no space-occupying lesions in the liver, and surrounding hematomas and hemoperitoneum were not observed.

Figure 3.

Pathological examination of liver specimens from clamping and non-clamping groups demonstrated: (A) Disordered hepatic cords, dark, multipolar and heteromorphic nuclei and mitose atypique identifying moderate differentiation hepatocellular carcinoma (arrow), (hematoxylin and eosin; magnification, ×100); (B) discontinuity of small venous wall, venous rupture and thrombi at the site of rupture (hematoxylin and eosin; magnification, ×400).

Figure 4.

(A) Cumulative and (B) recurrence-free survival rates of patients with spontaneous rupture of hepatocellular carcinoma following hepatectomy with or without portal triad clamping. No significant difference in survival rate between these two groups was identified.