| Japanese Journal of Clinical Oncology | Pages |
Introduction
Case Report
Pathologic Examination
Discussion
Acknowledgment
References
Hepatocellular Carcinoma with Gastrointestional Hemorrhage Caused by Direct Tumor Invasion to the Duodenum
INTRODUCTION
Upper gastrointestinal (GI) bleeding is one of the most common complications in patients with hepatocellular carcinoma (HCC). The bleeding is usually caused by variceal rupture, hemorrhagic ulcer or oozing of gastrointestinal mucosa. We report here a patient who showed massive hematemesis and melena caused by direct HCC invasion to the duodenum.
CASE REPORT
A 60-year-old man with multiple HCC was admitted to our hospital in December 1995 because of massive melena and hematemesis. He had received various treatments for HCC during the last ten years, i.e. hepatectomy once, transcatheter arterial embolization (TAE) eight times and percutaneus ethanol injection (PEI) once. He had a history of heavy alcohol intake. Hepatitis B surface antigen and hepatitis C antibody were not detected. Computed tomography and angiography were performed prior to this admission and they revealed multiple liver masses with tumor stains which were compatible with the finding of HCC. Ultrasound examination demonstrated hypoechoic, isoechoic and hyperechoic masses in the liver. Several tumors had marginal hypoechoic zones typical of HCC.
Laboratory examination at the time of admission revealed a moderate normocytic and normochromic anemia (red blood cell count 245 * 104/[mu]l, hemoglobin 8.6 g/dl, hematocrit 25.4%). His hepatic reserve was poor (serum albumin 2.6 g/dl, total bilirubin 1.3 mg/dl, cholinesterase 56 IU/l, prothrombin activity 82%). Emergent upper gastrointestinal fiberscopy revealed multiple nodular venous dilatation in the lower esophagus. We could not find an obvious bleeding point or red-color sign in the esophagus. Hemorrhagic gastritis with clot was present. The duodenum could not be observed due to extramural compression to the stomach from the liver tumor. After receiving blood transfusion, he recovered rapidly without any other evidence of bleeding and left the hospital five days after admission.
Two weeks later, he was admitted again due to vomiting and hepatic encephalopathy. A mass of about 8 cm in size in the upper abdomen was palpable through the abdominal wall. After the admission, he felt severe epigastric pain and presented with massive melena and hematemesis. We found the bleeding from esophageal varices at endoscopy and succeeded in hemostasis by endoscopic varicial ligation (EVL). The stomach was not examined owing to massive hemorrhage from esophageal varices.
One week after the EVL, he suddenly felt severe pain in the upper abdomen and the palpable liver tumor decreased in size. We performed abdominal ultrasound because we speculated that tumor rupture into the peritoneal cavity might be the cause of the pain. Although peritoneal fluid was detected, there was too little to perform paracentesis so we could not clarify the cause of his pain at that time. Massive GI hemorrhage continued to occur and the patient developed progressive hepatic failure. He died two days after this attack of abdominal pain.
At autopsy, the liver weighed 2111 grams and had multiple neoplastic nodules. Some tumors showed central necrosis. A nodule in the right lobe was the largest (11 * 10 cm). This nodule invaded the second portion of the duodenum and perforated into the lumen (Fig. 1 ). Coagulate and necrotic tissues adhered to the surface of the protrudent HCC tumor with massive hematic contents seen in the duodenum. Most of the other tumors were 1-3 cm in diameter. Liver cirrhosis and 400 ml of straw-colored ascites were found. Varices and an ulcer scar caused by EVL were seen in the lower part of the esophagus, but there was no evidence of recent esophageal bleeding. The stomach and large intestine had hemorrhagic mucosa.
DISCUSSION
Upper gastrointestinal (GI) bleeding is often seen in patients with HCC. Many patients with HCC have portal hypertension due to associated liver cirrhosis or tumor thrombus in the portal vein. Therefore, GI bleeding in patients with HCC is often caused by variceal rupture. Hemorrhage from HCC invading the GI tract directly is extremely rare.
Duodenal bleeding caused by direct invasion of HCC had not been diagnosed before his death. The HCC invading the duodenum may have ruptured when the size of the liver tumor decreased on palpation, although we speculated that variceal rupture was the main cause of his GI bleeding. The duodenum could not be observed by endoscopy due to extramural compression. Angiography and gastro-duodenography were not performed because of his poor condition. Although CT scanning was not performed, it might have revealed the direct tumor invasion to the duodenum.
Acknowledgment
This work was supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Health and Welfare of Japan.
References
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Copyright© Japanese Journal of Clinical Oncology, 1997.
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