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1/10. Fatal splenic arterial aneurysmal rupture associated with chronic pancreatitis.

    Splenic arterial aneurysms (SAA) are rare and are usually atherosclerotic and/or related to pregnancy. Because pregnancy is the most important predisposing factor, the strong predilection of SAA for women is not surprising. The authors report a case of SAA rupture in a man with chronic pancreatitis as the predisposing factor. A 56-year-old man with abdominal pain and hematemesis was resuscitated and underwent endoscopy, but he died 18 hours later of massive hematemesis before definitive surgery could be carried out. At autopsy, there was chronic pancreatitis with fibrous adhesions tethering the tail of the pancreas, spleen, and posterior wall of the stomach together. The SAA was indented into the posterior wall of the stomach, into which it had ruptured from without. He also had alcoholic cirrhosis but no esophageal varices or conventional gastric ulcers. Other important predisposing factors such as abdominal trauma, infective endocarditis, polyarteritis nodosa, and segmental medial arteriopathy were absent. Histologic examination confirmed the rupture of the SAA. The SAA had Monckeberg medial calcinosis but little evidence of atherosclerosis. The well-documented complications of acute and chronic pancreatitis include shock, abscess, pseudocyst formation, and duodenal obstruction. This report describes the rare complication of SAA rupture, which may be fatal.
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2/10. Loss of echogenic lesion of focal fatty infiltration in fibrotic liver.

    Five alcoholics with chronic liver disease showed focal low density areas of the liver that varied in distribution on computed tomography (CT) but no corresponding lesions on ultrasonography. The densities of these areas on CT were much lower than that of spleen. All the areas disappeared 2 days to 4 weeks after patients entered the hospital, suggesting that they were focal areas of fatty liver. Four patients had liver cirrhosis and one liver fibrosis. These observations may add further evidence to our previous finding that increased echogenecity of the liver produced by fatty infiltration is attenuated by complicating fibrosis.
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3/10. Spontaneous bacterial peritonitis.

    Spontaneous bacterial peritonitis is an infection of the ascitic fluid of patients who, in general, have severe chronic liver disease. Several variants of this disease exist including bacterascites, culture-negative neutrocytic ascites, and secondary bacterial peritonitis. Spontaneous bacterial peritonitis is frequently manifested by signs and symptoms of peritonitis although the findings may be subtle; however, occasionally it may be completely without clinical manifestation. The clinician must have a high index of suspicion in order to make this diagnosis at a relatively earlier stage of infection. An abdominal paracentesis is required to make the diagnosis of spontaneous bacterial peritonitis. This paracentesis should be performed on all patients who are admitted to the hospital for ascites and should be repeated if there is any manifestation of bacterial infection during the hospitalization. patients with severe intrahepatic shunting--as manifested by marked redistribution of activity from the liver to the spleen and to the bone marrow on liver-spleen scan as well as patients with an ascitic fluid total protein concentration of less than 1 g/dl--appear to be particularly susceptible to bacterial infection of their ascites. In order to optimize the yield of ascitic fluid culture, it is probably appropriate to inject blood culture bottles with ascites at the bedside immediately after the abdominal paracentesis. The mortality of spontaneous bacterial peritonitis continues to be very high. Perhaps routine admission paracentesis and prompt empiric antibiotic therapy with a third-generation cephalosporin will decrease the mortality of this infection if the Gram stain of the ascitic fluid demonstrates bacteria or the ascitic fluid neutrophil count is greater than 250 cells/cu mm. Repeating the paracentesis after 48 hours of treatment to reculture the fluid and reassess the ascitic fluid neutrophil count appears to be the best way to assess efficacy of treatment. After 48 hours of treatment the ascitic fluid neutrophil count should be less than 50% of the original value if the antimicrobial therapy is appropriate. The optimal duration of antibiotic treatment is unknown; however, until controlled trials provide data regarding duration of treatment it is appropriate to treat with parenteral antibiotics for 10 to 14 days. research is also needed to determine if there are measures which can be taken to prevent the development of spontaneous peritonitis.
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4/10. Simultaneous demonstration of pleural effusion and ascites by technetium-99m sulfur colloid liver-spleen scintigraphy.

    Scintigraphic evidence of ascites has been observed in Tc-99m sulfur colloid studies of the liver and spleen, in Tc-99m HIDA hepatobiliary scans, in Ga-67 citrate scans, and in Tc-99m phosphonate bone images. pleural effusion has been demonstrated in Tc-99m phosphonate bone scintigraphy. The case of a 48-year-old man whose Tc-99m sulfur colloid liver-spleen scintigram simultaneously demonstrated a right pleural effusion and ascites is presented.
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5/10. A low right-to-left hepatic lobe ratio. Is streamlining of ethanol to the right lobe of the liver the cause?

    The anterior view of a liver-spleen scintigram performed with Tc-99m sulfur colloid was used to calculate the right-to-left (R/L) hepatic lobe ratio in three patients (acute hepatitis, normal, alcoholic cirrhosis). Emission computed tomography (ECT) was also performed, and the images correlated with the data obtained from the planar images. A low R/L hepatic lobe ratio correctly identified the patient with alcoholic cirrhosis. Streamlining of ethanol to the right (R) lobe of the liver has been suggested as the principal reason why the R/L hepatic ratio is decreased in alcoholic cirrhosis. The evaluation of the ECT images, however, suggest that the count density in each lobe of the liver is similar in the patient with alcoholic cirrhosis. The latter and known information regarding the absorption of ethanol from the gastrointestinal tract are not in agreement with the alcohol streamlining theory.
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6/10. Renal gallium accumulation in the absence of renal pathology in patients with severe hepatocellular disease.

    Visualization of Ga-67 citrate in the kidneys at 48 hours and 72 hours post injection is usually interpreted as evidence of renal pathology. In reviewing approximately 200 consecutive patients referred for gallium scans, 40 patients who also underwent liver/spleen Tc-99m sulfur colloid (SC) studies within one month of the gallium study were identified. Fourteen of these patients showed advanced hepatocellular dysfunction on the Tc-99m SC liver/spleen images. Of these 14 patients, nine had persistent renal accumulation of gallium at 48 or 72 hours. Five of these nine patients had no evidence of primary renal disease by clinical or postmortem examination and subsequent clinical information indicated that two additional patients probably had no significant renal pathology. Therefore, bilateral symmetrically increased renal uptake of gallium in patients with advanced hepatocellular disease should not necessarily be interpreted as evidence of renal pathology.
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7/10. Delayed splenic rupture in a cirrhotic.

    We present the case of a young alcoholic with a history of mesocaval shunt for variceal bleeding who presented in hypovolemic shock three weeks following an auto accident. He was initially assumed to have recurrent gastrointestinal bleeding, but instead proved to have delayed rupture of the spleen.
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8/10. Spontaneous rupture of the spleen complicating portal hypertension.

    A 54-year-old male with alcoholic liver cirrhosis and hepatic coma grade IV is described, who succumbed as a result of spontaneous rupture of the spleen. A relationship to portal hypertension is suggested, although haemorrhagic diathesis and sepsis may have been contributing factors.
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9/10. Medical treatment of splenic abscess.

    I have described the first reported patient with a diagnosis of splenic abscess treated medically who survived. Another unusual aspect of this case was the establishment of the diagnosis of splenic abscess by ultrasonic examination. Some typical features of splenic abscess illustrated by this case were compromised patient, known abnormal spleen, febrile illness of uncertain cause, and a low index of suspicion causing delay in correct diagnosis. Despite this patient's survival, splenectomy with antibiotic coverage is the preferred treatment of splenic abscess.
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10/10. Disseminated cryptococcosis in an asymptomatic alcoholic man.

    Widely disseminated cryptococcosis was found on autopsy in a 50-year-old alcoholic man. The spleen, lungs, CNS, liver, kidney, and lymph nodes were all involved. In his clinical course, the patient showed no signs of immunologic anergy. His terminal hospital course resulted directly from end-stage liver disease and renal failure. The cryptococcal infection was of the nongranulomatous, diffuse type with little or no inflammatory response, which probably explains the lack of symptoms.
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