1/74. Rib metastasis revealing hepatocellular carcinoma. Bone metastasis infrequently appears as the first manifestation of hepatocellular calcinoma (HCC), and in any case in most patients the primary tumour is detected a few months after its development. We report the case of a patient with alcoholic liver disease, increased levels of alpha-fetoprotein, and no evidence of hepatic lesion in the different imaging modalities, in whom metastasis of HCC was detected in the ribs, whereas the primary tumour was not diagnosed until 15 months later. We believe that all patients with increased levels of alpha-fetoprotein should be tested in an intensified search for HCC and possible metastases, given that hepatic lesions may not be detected until many months alter the diagnosis of metastatic disease. ( info) |
2/74. Fulminant hepatitis A in patients with chronic liver disease. Fulminant hepatitis is a rare complication of acute hepatitis a virus (HAV) infection. We report three cases of fulminant hepatic failure with death due to HAV infection in patients with pre-existing chronic liver disease. Data from the literature also indicate a high case fatality rate during HAV superinfection in patients with chronic hepatitis b, particularly those with cirrhosis, and in patients with alcoholic cirrhosis. In patients with chronic hepatitis c, results are conflicting with some reports indicating a high fatality rate of HAV superinfection and others not, irrespective of the presence or absence of cirrhosis. Based on our observations and this review of the literature, we suggest that patients with chronic liver disease should be vaccinated against hepatitis A. ( info) |
3/74. Novel approach to bleeding in patients undergoing cardiac surgery with liver dysfunction. We describe two patients with significant liver dysfunction (child--Pugh class B) who underwent cardiac surgery at our institution facilitated by the use of a prothrombin complex concentrate for the management of postoperative bleeding. ( info) |
4/74. Pseudo-budd-chiari syndrome: decompensated alcoholic liver disease mimicking hepatic venous outflow obstruction. Three patients with rapid onset decompensated liver disease who were referred to our hospital with presumed budd-chiari syndrome are described. This diagnosis was based on marked hepatomegaly, caudate lobe hypertrophy and failure to visualize hepatic veins by Doppler-ultrasound examination. Detailed history, biochemistry, and histology were, however, highly suggestive of alcoholic liver cirrhosis with steatohepatitis-induced hepatomegaly. On angiographic examination narrowed but patent hepatic veins were demonstrated in 2 patients. A third patient died before further work-up could be performed; autopsy showed patent hepatic veins. These cases show that the radiological diagnosis of budd-chiari syndrome due to hepatic vein obstruction can be false positive and that suspected hepatic vein occlusion on Doppler-ultrasound should be confirmed by angiographic studies and on liver histology. ( info) |
5/74. Kayser-Fleischer like rings in alcoholic liver disease: a case report. Kayser-Fleischer rings are brown pigmented rings that run along the periphery of the cornea. Situated in Descemet's membrane and being comprised of granules of deposited copper they have traditionally been thought of as pathognomic of Wilson's disease. However, they can also be seen in other forms of liver disease. We document a case of Kayser-Fleischer like rings occurring in alcoholic liver disease--a previously unreported association. ( info) |
6/74. Decompensation of chronic stable alcoholic liver disease by severe exfoliative dermatitis. Of the numerous precipitants of hepatic decompensation in chronic liver disease, there are no reports in the literature documenting an acute decompensation following an acute episode of severe dermatitis. This case highlights the haemodynamic consequences of a severe flare up of exfoliative dermatitis in a patient with stable chronic alcoholic liver disease, speculates on the mechanism by which this may provoke clinical decompensation and the impact this may have upon liver failure. ( info) |
| corneal perforation is one of the most vision-threatening consequences of vitamin a deficiency. Amniotic membrane transplantation was performed in a 36-year-old man who presented with bilateral corneal ulcers. There was a small, sharply demarcated superficial ulcer with crevices of surrounding keratinized epithelium converging on the ulcer and minimal infiltration at the inferior periphery of the right cornea. A 3-mm perforation on a 9 x 7-mm area of stromal melting was noticed in the left cornea. The serum vitamin A level was 14.0 microg/dL (normal, 24.57 to 105.71 microg/dL) at presentation. A biopsy of the right corneal epithelium was performed to confirm the diagnosis. Multilayered amniotic membrane transplantation with debridement of the necrotic corneal stroma was performed on the left cornea. In addition to systemic vitamin A replacement, topical antibiotics and lubricants were also administered. The cornea ulcers healed in 10 days along with the restoration of the serum vitamin A level. The visual acuity improved from 20/250 to 20/20 in the right eye and from light perception to hand movement in the left eye at 3 months. Amniotic membrane transplantation could save eyes with corneal perforation related to vitamin a deficiency before reconstructive surgeries, such as penetrating keratoplasty, are necessary. ( info) |
8/74. Rapid development of esophageal squamous cell carcinoma after liver transplantation for alcohol-induced cirrhosis. Liver transplant recipients have an increased risk of developing de novo malignancies. It is generally accepted that chronic alcohol abuse is a contributive factor in the pathogenesis of several malignancies, in particular, of oropharyngeal squamous cell carcinoma (SCC). Thus, patients with end-stage alcohol-induced cirrhosis could be at risk of esophageal SCC following orthotopic liver transplantation (OLT). From January 1986 to December 1997 a total of 313 patients underwent OLT for various indications. Of these patients, 72 had alcohol-related cirrhosis. Oropharyngeal and esophageal malignancies after OLT were not observed in non-alcoholic patients. In contrast, these malignancies were diagnosed in three male patients who underwent transplantation for alcohol-induced cirrhosis (incidence 4.2%). Furthermore, all patients had a history of tobacco abuse. The tumors were located in the tongue of one patient and in the esophagus of two patients. While SCC of the tongue became apparent 5 years after OLT, esophageal SCC was detected 8 and 16 months after transplantation. Shortly before transplantation, endoscopy of the esophagus had not revealed evidence of pre-malignant dysplastic lesions in any of these patients. Thus, esophageal SCC may develop rapidly in patients undergoing transplantation for alcohol-related cirrhosis with a history of tobacco abuse before liver transplantation, which warrants careful post-transplant screening of these patients. ( info) |
9/74. Lymphatic cardiac tamponade after open-heart surgery with liver dysfunction. A 46-year-old female with alcoholic liver dysfunction was admitted for mitral regurgitation due to infective endocarditis. She underwent mitral valvuloplasty and resection of the vegetation without complication. After removal of the chest tube, late cardiac tamponade occurred and subsequently recurred. On the 64th day after mitral valvuloplasty, we performed redo median sternotomy with small laparotomy trying to reveal and repair injured lymphatic vessels in the pericardial space and successfully cured the leakage of lymph. The post reoperative course was uneventful and the patient was discharged 20 days after reoperation. We review a rare complication of recurrent cardiac tamponade of lymphatic leakage associated with liver dysfunction. ( info) |
10/74. Severe steatosis as the initial histologic manifestation of recurrent hepatitis c genotype 3. Steatosis is a common finding that is seen in patients with both chronic hepatitis c and alcoholic liver disease; however, the extent of involvement in the former is generally minimal to mild. We present 2 patients who underwent live donor liver transplantation for end-stage liver disease that was caused by chronic hepatitis c (genotype 3) and alcohol abuse. Both patients presented with liver allograft dysfunction, with liver biopsy findings of moderate to marked steatosis. Exclusion of a relapse of alcohol use required intense questioning of both the patients and their families. A definitive diagnosis of recurrent hepatitis c was established by viral markers with institution of the proper therapy and resolution of graft dysfunction. We conclude that recurrent hepatitis c, particularly genotype 3, may present with severe steatosis. Recognition of this phenomenon is important, and confirmation with viral markers is necessary to provide optimal patient care. ( info) |