ObjectiveTo study the mechanisms of spontaneous rupture of hepatocellular carcinoma and the treatments in the acute phase and the second phase after hemostasis. MethodsRelated domestic and foreign literatures were reviewed. ResultsThe mechanism of spontaneous rupture of hepatocellular carcinoma was still not quite clear. In China, spontaneous rupture of hepatocellular carcinoma was closely related with hepatitis B virus infection. Immune complex deposition in vessel wall led to the injuries of small arteries and bleeding. Treatments included conservative therapy, surgical intervention （lobectomy of liver, hepatic artery ligation, packing, and suturing), transarteial embolization, other medications (percutaneous ethanol injection, radiofrequency ablation, bio-immunotherapy). ConclusionTransarterial embolization has been shown to be highly effective in achieving immediate hemostasis, and can be used as the basis of phase two comprehensive treatment.
OBJECTIVE To evaluate the effect of various covering tissues for improving the cure rate of spontaneous rupture of esophagus. METHODS From 1970 to 1994, 13 cases with spontaneous rupture of esophagus were performed primary repair, among them, 10 cases were covered by pedicled greater omentum after impair, and the other 3 cases were covered by pedicled pleural flap. RESULTS: Satisfactory result and complete recovery were obtained in all 10 cases by using pedicled greater omentum. Two cases among 3 cases using pedicled pleural flap suffered re-rupture of esophagus at 5 days and 8 days after operation, and died because of whole body exhaustion. CONCLUSION Pedicled greater omentum is a good covering tissue for repair of spontaneous rupture of esophagus.
Objective To study the relationship of hepatitis B virus （HBV） to spontaneous rupture of hepatocellular carcinoma （HCC-SR） and its mechanism. Method The related literatures about theory of HCC-SR were consulted and reviewed. Results The injury of small arteries was usually followed in patients with HCC-SR， which was related to vascular autoimmune injury caused by the HBV infection. The small arteries in which immune complex deposited were readily injured， as a result HCC-SR happened while vascular load increased. Conclusion The HBV infection resulted in vascular autoimmune injury maybe a important factor in the pathogenesis of HCC-SR.
【Abstract】ObjectiveTo study the mechanism of spontaneous rupture of hepatocellular carcinoma (HCC). MethodsArticles have been reviewed to find out the theory of spontaneous rupture of HCC. ResultsResearchful results suggested that the injury of small arteries was usually followed in patients of spontaneous rupture of HCC. In this review, the immune complex, which composed of hepatitis B virus e antigen, complement C1q and immunoglobulins, was found deposited in the elastic membrane of arteries. Likely as a result of immune complex deposition, vascular injury occurs mainly in the small arteries where the deposition of immune complex was present. The small arteries in which immune complex deposited are readily injuried and cause hemorrhage and rupture of HCC during vascular load increase. ConclusionWe would conclude that immune complex deposition in vessel wall led to the small arteries injury may be the factor involved in the pathogenesis of spontaneous ruptured HCC.