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© 2002 American Society for Clinical Oncology
Some Unusual Complications of MalignanciesCase 1. Spontaneous Rupture of Hepatocellular Carcinoma Demonstrated by Contrast-Enhanced SonographyVeterans General Hospital–Taipei and School of Medicine and Institute of Biomedical Engineering, National Yang Ming University, Taipei, Taiwan A 69-year-old man was brought to the emergency room because of the sudden onset of severe upper abdominal pain and abdominal distension. He had a known history of hepatitis B-related chronic hepatitis and liver cirrhosis for 10 years, and had been regularly checked sonographically at 3- to 12-month intervals. Occasional minimal ascites had been documented. He had been lost to clinical follow-up for 2 years. Physical examination revealed increased abdominal girth and shifting dullness on percussion. Minimal rebound pain was noted in the right upper abdomen. His temperature was 37.5°C, with a pulse rate of 84 beats/min, and his blood pressure was 80/58 mmHg. Laboratory findings showed only mild abnormalities in the serum transaminase levels (ALT, 52 U/L; AST, 45 U/L; normal, < 35 U/L for both). The alpha-fetoprotein level was 71 ng/mL (normal: 8 ng/mL), and his hemoglobin level was 10.2 g/dL. The clinical impression was liver cirrhosis with ascites, with the possibility of ruptured hepatocellular carcinoma (HCC) or perforated peptic ulcer with peritonitis or sepsis. Due to his critical condition, an urgent ultrasound (US) study of the abdomen was performed and revealed massive ascites (Fig 1, arrowheads) and an area of hypoechogenicity approximately 3 cm in size in the right hepatic lobe (Fig 1, arrows). Color Doppler US (CDU) showed color flow signals, suggesting a hypervascular tumor, especially HCC. The background of the liver showed a coarsened echo pattern with small liver size, indicative of liver cirrhosis. Spectral Doppler US of the vessels in the focal pathologic lesion showed high flow velocity (peak velocity, 33.6 cm/sec; resistive index, 0.83), suggesting that the tumor vessels were chiefly arteries (Fig 1). Because a ruptured HCC was the major concern, an echo-enhancing agent (Levovist; Schering, Berlin, Germany) was administered intravenously at a dose of 300 mg/mL (x 7.5 mL). Eighteen seconds after bolus injection of Levovist, the tumor vessels could be better observed (Fig 2A, small arrows; Fig 2B, arrows), and the focal liver pathologic lesion was optimally enhanced with profuse color flow signals (Fig 2A, large arrows; Fig 2C, arrows). Dramatic, extrahepatic color flow signals projecting from the liver capsule covering the mass lesion were seen (Figs 2B and 2C, arrowheads). The diagnosis of a spontaneously ruptured HCC was confidently made according to the echo-enhancing US findings. The patient refused angiography and transarterial embolization. A triphase computed tomography (CT) scan showed a hypodense tumor (Fig 3A, small arrowheads) and ascites (Fig 3A, arrows). A hyperdense area covering the liver surface, representing blood clots, was visible on the noncontrast CT scan (Fig 3A, large arrowheads). A small well-enhanced area (Fig 3B, small arrows) was seen embedded in the unenhanced blood clots (Figs 3A and 3B, large arrowheads) anterior to the HCC during the arterial phase on CT scans. These CT findings were compatible with perihepatic hematoma and contrast extravasation from a ruptured HCC. The patient refused therapy, so only supportive care was given. He died of hepatic failure 6 months later.
In the endemic areas of HCC, a sudden onset of upper abdominal catastrophe should lead one to suspect a ruptured HCC.1 If a patient has HCC and is undergoing either treatment or investigation, the sudden onset of pain accompanied by shock and/or pallor should also prompt the diagnosis. Primary peritonitis, gall bladder empyema with rupture of gall bladder, rupture of liver abscess, acute hemorrhagic pancreatitis, acute appendicitis, and perforated duodenal ulcer could all be confused with ruptured HCC.2 When intraperitoneal free fluid is present, paracentesis should be performed. Peritoneal fluid with pure blood suggests the rupture of a solid organ.2 Regardless of the nature of the bleeding, the clinical recognition of internal bleeding with unstable cardiovascular hemodynamics may lead to an exploration of the abdomen.2 However, bloody ascites has been noted in 5% of cirrhotic patients with ascites.3 Both US and CT scans accurately depict hepatic tumors and hemoperitoneum, as well as bleeding from other solid abdominal organs.4,5 On the basis of knowledge of splenic injury and ruptured hepatic tumor, active hemorrhage is recognized as a focal high-attenuation collection surrounded by lower-attenuation hematoma or damaged parenchyma. The appearance will vary depending on the rate of the hemorrhage and the CT technique used.5,6 When contrast material is mechanically injected intravenously, the area of active extravasation will have a similar attenuation as that of adjacent major arteries or the aorta, with an attenuation range of 80 to 370 Hounsfield units (mean, 132 Hounsfield units) for active extravasation.4,7 Generally, US shows the presence of a subcapsular hepatic tumor and ascites. The rupture site appears as a hyperechoic area located around the tumor in 66% of patients.8 However, in cirrhotic patients with ascites, blood clots may not form near the bleeding site. Jet flow from active bleeding invisible on real-time US can be displayed with CDU, which enables an operator to confirm rapidly the location of a tumor rupture.9 The active blood leaking from the liver surface may not be well demonstrated by using conventional CDU because of its location and its low hemorrhage rate. In our patient, active bleeding was represented by the profuse color flow signals projecting from the liver surface covering the well-enhanced hypervascular hepatic tumor. The leaked microbubble contrast agents strongly reflected the transmitted sound beams and dramatically enhanced the Doppler signals. Since contrast-enhanced US is becoming one of the important adjuncts in the evaluation of hepatic tumors,10 application of US contrast agents may be of significant help in the confirmation of tumor rupture with low hemorrhage rate, and may lead to prompt treatment. If contrast-enhanced CDU cannot demonstrate active bleeding, one-stage partial hepatectomy is not indicated and nonsurgical management is suggested.5
NOTES Copyright © 2002 American Society of Clinical Oncology REFERENCES 1. Chen CY, Lin XZ, Shin JS, et al: Spontaneous rupture of hepatocellular carcinoma: A review of 141 Taiwanese cases and comparison with nonrupture cases. J Clin Gastroenterol 21: 238-242, 1995[CrossRef][Medline]
2. Ong GB, Taw JL: Spontaneous rupture of hepatocellular carcinoma. BMJ 4: 146-149, 1972 3. DeSitter L, Rector WG: The significance of bloody ascites in patients with cirrhosis. Am J Gastroenterol 79: 136-138, 1984[Medline]
4. Jeffrey RB Jr, Cardoza JD, Olcott EW: Detection of active intra-abdominal arterial hemorrhage: Value of dynamic contrast-enhanced CT. AJR Am J Roentgenol 156: 725-729, 1991 5. Zhu LX, Wang GS, Fan ST: Spontaneous rupture of hepatocellular carcinoma. Br J Surg 83: 602-607, 1996[Medline] 6. The Liver Cancer Study Group of Japan: Primary liver cancer in Japan. Ann Surg 211: 277-287, 1990[Medline]
7. Shanmuganathan K, Mirvis SE, Sover ER: Value of contrast-enhanced CT in detecting active hemorrhage in patients with blunt abdominal or pelvic trauma. AJR Am J Roentgenol 161: 65-69, 1993 8. Corr P, Chan M, Lau WY, et al: The role of hepatic arterial embolization in the management of ruptured hepatocellular carcinoma. Clin Radiol 48: 163-165, 1993[CrossRef][Medline] 9. Ishida H, Konno K, Hamashima Y, et al: Sonography and color Doppler findings of rupture of liver tumors. Abdom Imaging 23: 587-591, 1998[CrossRef][Medline] 10. Chou YH, Lui WY, Chiou HJ, et al: Contrast-enhanced US in assessment of hepatocellular carcinoma following percutaneous ethanol injection. J Med Ultrasound 7: 29-37, 1999
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Copyright © 2002 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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