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    • On arrival her vital signs were stable Laboratory

    2018-11-06

    On arrival, her vital signs were stable. Laboratory data showed normal hemoglobin levels, low platelet counts (66,000/μL), elevated international normalized ratio (1.29), and elevated total bilirubin (1.9 mg/dL). A triphase abdominal CT was applied. In the arterial phase (Figure 3A), a single 16-cm tumor over the right lobe with hemoperitoneum was noted but no nebivolol hcl extravasation was identified. In the portal vein phase (Figure 3B), some contrast extravasations were observed in the tumor. Bleeding from the portal vein was highly suspected. Additionally, multiple smaller nodules were observed in the right lobe of the liver. After the examination, her vital signs stabilized with resuscitation and the use of hemostatic medication; hence, no angiography was performed. The preoperative indocyanine green (ICGR-15) test administered after admission was>30%. The patient was informed of the high risk involved in liver resection, and hepatectomy including Segments 6–8 was performed 1 week after initial presentation to prevent recurrent tumor bleeding. During the operation, we observed a single huge, pulsating tumor occupying the right lobe of the liver and presenting with high vascularity. After the Pringle maneuver was applied to the main portal vein, the tumor underwent shrinkage and bleeding decreased. The resected specimen consisted of a 16 cm×8.5 cm×7.2 cm mass. The morphological image revealed a ruptured hepatic angiosarcoma. The resection margin was tumor free. Elevations of total bilirubin (≤ 15 mg/dL) and massive ascites of>1 L/d were identified 3 days postoperation. Liver decompensation was noted. After conservative treatment, bilirubin levels and the amount of ascites gradually decreased. The patient was discharged 33 days postoperation. However, newly developed intrahepatic lesions and lung lesions were noted 1 month after discharge. No further salvage treatments were applied and the patient chose hospice care. The patient died 3 months later as a result of cancer progression. During the 4-month follow-up period, no further internal bleeding episodes were noted.
    Discussion Hepatic angiosarcoma remains the third most common primary liver malignancy and the most common malignant mesenchymal liver tumor. Its reported annual incidence is 0.26 per million population and mortality is ∼0.075 cases per million population, with a strong male predominance. It often occurs in elderly patients, particularly those in their 60s and 70s. Previous reports have associated this malignancy with environmental carcinogens, yet most cases currently reported are unrelated to these reported factors or have unknown etiology. Hepatic angiosarcoma originates in masses of endothelial cells. Over 70% of hepatic angiosarcoma patients have multifocal lesions. When the normal liver parenchyma is replaced by a tumor, it may cause liver decompensation, including ascites and jaundice, and even fulminant hepatic failure. Poor prognosis has been reported for hepatic angiosarcoma. Earlier data have shown that the median survival of patients is only 6 months without treatment; even after treatment, only 3% of them live longer than 2 years. Surgical resection is the standard treatment for hepatic angiosarcoma. Currently, there are no effective adjuvant therapies after surgery including radiation therapy or chemotherapy. Hepatic angiosarcomas spontaneously rupture in ∼27% of patients. This may induce severe intra-abdominal bleeding, and is associated with high morbidity and mortality. Spontaneous rupture leads to tumor cell spillage and peritoneal seeding, which may compromise prognosis. TAE has been the primary procedure used to control hemoperitoneum resulting from tumor rupture. However, this is not effective for all hepatic angiosarcoma patients; possibly because the condition can involve different blood supplies. Some reports have shown that angiosarcoma might be supplied both by the portal vein and by the hepatic artery. The tumor may originate near cells that form in abnormal vascular spaces that continuously infiltrate the dilated sinusoids and, in certain cases, connect with the portal vein. In our case, the hepatic artery was thrombosed by TAE when bleeding first occurred. However, repeated bleeding episodes were noted, and no active bleeding was observed in the angiograph. This indicates portal venous bleeding via abnormal spaces and dilated sinusoids. The only method of preventing such a condition is surgical resection of the tumor.