Læknablaðið

Volume

Læknablaðið - 15.10.1986, Page 39

Læknablaðið - 15.10.1986, Page 39
LÆKNABLAÐIÐ 265 hættu og hafa sjúkdóminn ávallt i huga ef þeir hafa einkenni frá kviðarholi, brengluð lifrarpróf eða hita. í ljósi þess hversu algeng alvarleg slys eru hér á landi miðað við nágrannalöndin, má búast við vaxandi fjölda þessara tilfella á næstu árum ef sú þróun heldur áfram, sem átt hefur sér siað hins síðari ár. SUMMARY Acute acalculous cholecystitis. Six case histories. This article reviews acute acalculous cholecystitis (AAC) which has been an increasing entity the last decades. This is a hazardous disease which usually developes in critically ill patients, suffering from massive trauma, burns, major operations etc. The best diagnostic procedures are believed to be ultrasonography and cholescintigraphy and the only effective treatment is surgical (cholecystectomy and cholecystostomy). Six cases, which were diagnosed at the Reykjavik City Hospital during a six year period (1980-1986) are presented here. The first case was a 70 years old male who developed AAC 30 days after beginning cytostatic therapy for histiocytic lymphoma. At operation he was found to have perforation of the gallbladder and was septic. No gallstones were found. He never made full recovery and died a month later. The second case was a 44 years old male who developed AAC 23 days after an operation of a stab wound of the abdomen. The diagnosis was confirmed at operation and he made a good recovery after cholecystostomy (and cholecystectomy 6 weeks later). No gallstones were found. The third case was a 72 years old male who developed AAC after an operation for ileus and made good recovery after cholecystectomy. The fourth case was a 25 years old male who was admitted in shock, suffering from a massive shotgun wound of the abdomen. The patient’s conditions stabilized after multiple blood transfusions and surgical repair of the wound, but a few days Iater he developed acute renal failure which was treated by hemodialysis. He was also treated by hyperalimentation. A month later he developed signs of acute cholecystitis and diagnosis of AAC was confirmed at operation. He made good recovery after cholecystectomy. The fifth case was a 43 years old male admitted 10 days after a coronary bypass operation. At the beginning of the operation he had an attack of ventricular fibrillation and was suspected afterwards of having developed a myocardial infarction during or after the operation. The following days he had low grade fever and was suspected to have Dressler’s syndrome. His condition did not get any better and 20 days after the operation he had developed signs of cholecystitis. The diagnosis of AAC was conftrmed at operation and the patient recovered. The sixth case was a 64 years old male admitted after being run down by a car. He was found to have a fracture of the pelvis and fractures of both knees. He was confused but his conditions was otherwise stable. No abnormalities were found in the abdomen or in the thorax. His mental conditions got worse and he developed acute renal failure. In the third week he became septic and developed signs of acute abdomen. The diagnosis of AAC was confirmed at operation. The patient recovered. The causes of this disease are unknown but it is believed that the fundamental change is vascular damage in the gallbladder wall through a factor XII dependent pathway. Why the gallbladder is affected is unknown, but this vascular damage in conjunction with dehydration, fasting and narcotic analgesics could be detrimental to the gallbladder. Narcotic analgesics cause spasms of the sphinter of Oddi and prolonged fasting and dehydration cause thickening of the gallbladder contents, both delaying emtying of the gallbladder. Today no preventible factors are known. It is therefore necessary to follow critically ill patients closely and always have this disease in mind if fever or signs from the abdomen arise.

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