We report an unusual case of Müllerian duct cyst in an 8-month-old infant who presented with frequent vomiting and recurrent urinary tract infections. Computed tomography showed a midline giant cyst in the pelvic floor. Delayed enhanced computed tomography demonstrated contrast filling of the cyst, indicating a communication with the urotract. Subsequent cystourethrogram and surgery confirmed a giant Müllerian duct cyst.

A 71-year-old woman presented with vomiting, abdominal pain and vague right gluteal discomfort. Abdominal ultrasound showed ascites and dilated small bowel loops with peristaltic movement, while transgluteal ultrasound revealed entrapped ascites beneath gluteal muscles and an oedematous, immobile bowel loop trapped between the sacrum and iliac bone with barely visible colour Doppler flow suggestive of an incarcerated sciatic hernia. CT demonstrated similar findings and subsequent surgery confirmed the diagnosis. To our knowledge, this is the first report of a pre-operative diagnosis of incarcerated sciatic hernia on ultrasound.

MECHANISM AND STIMULUS FOR FAT DEPOSITION Assessment of the fat content in a donor liver for transplantation remains one of the least scientific aspects in the practice of liver transplantation. Despite the efforts of many groups over 30 years to develop a reliable means of predicting the function of a liver after transplantation, the most universal and reliable remains the assessment of the surgeon at the time the liver is retrieved. This is based on the combination of appearance and texture. Thus an important and highly subjective assessment is routinely carried out by the retrieving surgeon, who is often the least experienced. Biochemical liver function tests frequently fail to identify a liver with even a considerable degree of steatosis. However, such a liver is at substantial risk of primary nonfunction or, at least, a period of very poor function after reperfusion. In either case the patient is placed at considerable risk. With the shortage of donor organs, steatotic livers are increasingly now used for transplantation and there is a clear need for a reliable and objective means of assessing a potential donor liver before transplantation. It is also important to understand the mechanisms by which fat deposition occurs and has such a deleterious effect on the outcome of transplantation. Cheng et al. have developed a noninvasive method for the quantification of the hepatic fat content in vivo by using calibrated computer tomography density. They have shown that this correlates well both with survival and serum markers of liver injury after transplantation (glutamic oxaloacetic transaminase and glutamic pyruvate transaminase). The data also suggest that microvesicular fatty change has less deleterious impact on transplant outcome than macrovesicular change. Fatty change refers to any abnormal accumulation of fat within parenchymal cells. At the outset, lipid accumulates in a microvesicular form within the cytoplasm of liver cells, predominantly in the perivenular (centrilobular) zone. With further accumulation the small vacuoles coalesce, creating large clear microvesicles. Excess accumulation of triglycerides within the liver may result from defects in any one of the events in the sequence from fatty acid entry to lipoprotein exit. These include: Excessive entry of free fatty acids into the liver (as seen in starvation) Enhanced fatty acid synthesis and decreased fatty acid oxidation Increased esterification of fatty acids to triglycerides, due to an increase in alpha-glycerophosphate (thought to be one effect of alcohol poisoning) Decreased apoprotein synthesis (associated with carbon tetrachloride poisoning) Impaired lipoprotein secretion MECHANISM OF LIVER INJURY An etiological agent that causes liver injury may induce fatty change acting at more than one location within the complex process of fat metabolism. Alcohol, the most common cause of fatty change within industrialized countries, increases free fatty acid synthesis, diminishes triglyceride utilization, decreases fatty acid oxidation, blocks lipoprotein excretion, and enhances lipolysis. Other important causes include protein malnutrition, diabetes mellitus, obesity, hepatotoxins, and brain death. Although hepatic steatosis may develop without biochemical evidence of liver disease, after cold preservation these organs demonstrate an increased susceptibility to ischemia/reperfusion injury. The mechanisms behind this are not completely understood. Some postulate that the critical injury is to the sinusoidal lining cell, with an alteration in plasma membrane fluidity (1) and subsequent blood cell adhesion and Kupffer cell activation. Others suggest that fat-laden hepatocytes undergo changes including solidification during cold injury and are responsible for the increased sensitivity to reperfusion injury (2), releasing fatty globules that can disrupt the sinusoid microcirculation. The combination of steatosis and cold preservation is associated with a high risk of nonfunction. ASSESSMENT OF DONOR LIVERS It is widely assumed that an experienced transplant surgeon is able to estimate the degree of fatty change within a liver at the donor retrieval. Certainly severe steatosis can be identified by yellow discoloration after flushing and a greasy firm texture. However this is obviously a highly subjective test, which becomes less sensitive with lesser degrees of steatosis. It is suggested, but not universally agreed, that donor liver biopsies are useful in determining preexisting hepatic pathology that is associated with poor graft function after transplantation (3). A strong association of severe macrovesicular steatosis (greater than 60%) to primary nonfunction has been confirmed by most authors. However, liver biopsy can be misleading, with apparently “normal” livers going on to display poor function. Two other methods that have shown some promise are measurement of monoethylglycinexylidide (4) (MEGX), a metabolite of lignocaine, and lecithin:cholesterol acyltransferase (LCAT) activity. The latter was shown by Shimada et al. (5) to correlate well with early allograft function. POTENTIAL FOR NOVEL PRESERVATION One theoretical method for the successful preservation of steatotic organs is normothermic machine perfusion. If the liver could be perfused with warm oxygenated blood while ex vivo, this would prevent cold injury associated with fatty change and preservation/reperfusion injury. It might also allow organ function and viability to be assessed accurately by biochemical analysis of the perfusate.In this way it would be safe to retrieve more marginal donor organs because those displaying substan-dard function would be identified and discarded before transplantation.

On computed tomography (CT), neurilemomas have generically been described as well-defined, round masses with heterogeneous contrast enhancement. The CT scans of 38 surgically proven thoracic neurilemomas in 36 patients were reviewed to characterize further the CT features of this tumor, with an emphasis on different enhancement patterns. Unenhanced CT was available in 32 patients; 10 tumors appeared isodense, and 22 tumors appeared slightly hypodense compared with chest wall muscle. Except for an intraosseous neurilemoma of the T8 vertebral body, which mimicked bone metastasis, the tumors could be categorized into five different patterns on CT after contrast enhancement. Twenty tumors (54.1%) revealed diffuse, but amorphous and inhomogeneous enhancement. Seventeen (45.9%) tumors appeared as masses with multiple hypodense or cystic areas. Of these 17, the pattern was somewhat radial enhancement (n = 6, 16.2%), peripheral enhancement with a large central hypodense area (n = 5, 13.5%), homogeneous hypodensity (n = 5, 13.5%), and central enhancement with peripheral hypodensity (n = l, 2.7%). Appreciation of various CT manifestations is important in the diagnosis of this tumor.

We report two cases of small bowel obstruction (SBO) due to phytobezoar impaction. In both cases, computed tomography (CT) demonstrated a well-defined, ovoid intraluminal mass with mottled gas pattern within the dilated small bowel at the site of obstruction and an abruptly collapsed lumen beyond the lesion. Recognition of these CT findings allows specific preoperative diagnosis of SBO owing to this uncommon lesion.

CASE 1. A twenty-four-year-old man had an episode of hypotension after a motorcycle accident. At a local general hospital, the right subclavian vein was catheterized through an infraclavicular route, to allow for the rapid administration of fluid and the measurement of central venous pressure. The catheter was removed twelve hours later. The patient went home the next day. at which time he had some

Journal of Ultrasound in MedicineVolume 7, Issue 9 p. 511-513 Case Reports Wall defect as a sign of urinary bladder rupture in sonography. Y L Wan, Y L WanSearch for more papers by this authorH Hsieh, H Hsieh Department of Diagnostic Radiology, Chang Gung Memorial Hospital, Kao-Hsuing, Taiwan.Search for more papers by this authorT Y Lee, T Y LeeSearch for more papers by this authorC C Tsai, C C TsaiSearch for more papers by this author Y L Wan, Y L WanSearch for more papers by this authorH Hsieh, H Hsieh Department of Diagnostic Radiology, Chang Gung Memorial Hospital, Kao-Hsuing, Taiwan.Search for more papers by this authorT Y Lee, T Y LeeSearch for more papers by this authorC C Tsai, C C TsaiSearch for more papers by this author First published: 01 September 1988 https://doi.org/10.7863/jum.1988.7.9.511Citations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume7, Issue9Sep 1988Pages 511-513 RelatedInformation