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Acute Acalculous Cholecystitis
Editorial l*
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Acute Acalculous Cholecystitis Frazee, Nagorney, and Mucha, in their discus sion of acute acalculous cholecystitis in this issue of the Proceedings (pages 163 to 167), review the salient features of this potentially lethal disease. When the high frequency of severe underlying or associated illness is considered, it is surprising that the mortality in their series of patients was limited to 30%. They appropriately ascribe the relatively favorable outcome to their use of biliary scintigraphy in conjunction with ultrasonography and computed tomographic scanning. Even with an aggressive diagnostic approach, more than half of the patients who underwent cholecystec tomy had either gangrene or perforation of the gallbladder. That the use of percutaneous transhepatic cholecystostomy in suspected cases of acute acalculous cholecystitis may delay a lifesaving cholecystectomy is an appropriate concern. Frazee and his colleagues comment only briefly on possible pathogenetic factors. Progressive en largement of the gallbladder and biliary sludge detected by ultrasonography are common find ings in patients at risk for acute acalculous chole cystitis. I favor their speculation that biliary debris likely plays a role in the process. Another possible sequence of events is that prostanoid synthesis in the gallbladder epithelium may lead to secretion of mucus that occludes the cystic duct and prevents secretion of water; thus, the gall bladder may become further distended, and vas cular perfusion of the gallbladder wall may be impaired. On the basis of my experience, hydrops, or extensive edema of the wall of the gallbladder in association with white bile within its lumen such as is seen in calculous cholecystitis, is un common. Clearly, the process is a bland ischemia, which accounts for the lack of localized clinical signs in many cases and a delay in diagnosis. No substitute exists for clinical diligence and a high level of suspicion for the possibility of acute acalculous cholecystitis. Early percutaneous chole-
cystostomy possibly will become an essential step in the diagnosis, inasmuch as mucosal ulcération and bleeding into the gallbladder lumen are fre quent findings. Decompression of the gallbladder, even in the presence of local ischemia or gan grene, might lead to resolution of the problem and thereby obviate cholecystectomy and its attendant risks and complications. This update on the contemporary approach to acalculous cholecystitis is timely and authoritative. It should remind all physicians of the complexi ties of this uncommon but ominous clinical entity. Frank G. Moody, M.D. Department of Surgery University of Texas Health Science Center Houston, Texas
Address reprint requests to Dr. F. G. Moody, Department of Surgery, Texas Medical Center, 6431 Fannin, Suite 4.020, Houston, TX 77030. Mayo Clin Proc 64:255,1989
255
A
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Acute Acalculous Cholecystitis Frazee, Nagorney, and Mucha, in their discus sion of acute acalculous cholecystitis in this issue of the Proceedings (pages 163 to 167), review the salient features of this potentially lethal disease. When the high frequency of severe underlying or associated illness is considered, it is surprising that the mortality in their series of patients was limited to 30%. They appropriately ascribe the relatively favorable outcome to their use of biliary scintigraphy in conjunction with ultrasonography and computed tomographic scanning. Even with an aggressive diagnostic approach, more than half of the patients who underwent cholecystec tomy had either gangrene or perforation of the gallbladder. That the use of percutaneous transhepatic cholecystostomy in suspected cases of acute acalculous cholecystitis may delay a lifesaving cholecystectomy is an appropriate concern. Frazee and his colleagues comment only briefly on possible pathogenetic factors. Progressive en largement of the gallbladder and biliary sludge detected by ultrasonography are common find ings in patients at risk for acute acalculous chole cystitis. I favor their speculation that biliary debris likely plays a role in the process. Another possible sequence of events is that prostanoid synthesis in the gallbladder epithelium may lead to secretion of mucus that occludes the cystic duct and prevents secretion of water; thus, the gall bladder may become further distended, and vas cular perfusion of the gallbladder wall may be impaired. On the basis of my experience, hydrops, or extensive edema of the wall of the gallbladder in association with white bile within its lumen such as is seen in calculous cholecystitis, is un common. Clearly, the process is a bland ischemia, which accounts for the lack of localized clinical signs in many cases and a delay in diagnosis. No substitute exists for clinical diligence and a high level of suspicion for the possibility of acute acalculous cholecystitis. Early percutaneous chole-
cystostomy possibly will become an essential step in the diagnosis, inasmuch as mucosal ulcération and bleeding into the gallbladder lumen are fre quent findings. Decompression of the gallbladder, even in the presence of local ischemia or gan grene, might lead to resolution of the problem and thereby obviate cholecystectomy and its attendant risks and complications. This update on the contemporary approach to acalculous cholecystitis is timely and authoritative. It should remind all physicians of the complexi ties of this uncommon but ominous clinical entity. Frank G. Moody, M.D. Department of Surgery University of Texas Health Science Center Houston, Texas
Address reprint requests to Dr. F. G. Moody, Department of Surgery, Texas Medical Center, 6431 Fannin, Suite 4.020, Houston, TX 77030. Mayo Clin Proc 64:255,1989
255