Acute Kolesistitis Dan Acc
Acute Kolesistitis Dan Acc
Acute Kolesistitis Dan Acc
doi: 10.1093/jscr/rjv101
Case Report
CASE REPORT
Abstract
Acalculous cholecystitis is a rare but life-threatening disease, but its pathogenesis is not fully revealed yet. We experienced two
acalculous cholecystitis cases associated with aortic dissection. In Case 1, acalculous cholecystitis occurred just after the
exacerbation of the aortic dissection. Laparotomy showed necrotized cholecystitis with fresh thrombi formation. Case 2
developed acalculous cholecystitis on the 65th hospital day of aortic dissection. Laparotomy revealed the perforation of the
gallbladder. Histological study revealed fibrosis and hemosiderosis in the subserosal layer. The histological findings of these two
patients are quite different: Case 1 is acute ischemic and Case 2 is chronic ischemic. While a few cases of acute ischemic
cholecystitis have been reported previously, chronic acalculous cholecystitis (CAC) has not been documented. History of aortic
dissection could be a risk factor of acute and CAC due to relatively decreased splanchnic blood flow.
Received: July 5, 2015. Revised: July 13, 2015. Accepted: July 14, 2015
Published by Oxford University Press and JSCR Publishing Ltd. All rights reserved. © The Author 2015.
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2 | F.F. Inagaki et al.
Figure 1: (A) CT showed Stanford type B aortic dissection, gallbladder wall thickness without gallstones and swollen pancreas. (B) Macroscopic examination showed the
necrosis of the gallbladder fundus. (C) Histological examination revealed that partial mucosal defect, mucosal/submucosal arterial thrombi and submucosal bleeding in
the body of the gallbladder wall (H&E ×100). (D) Histological examination revealed the fresh thrombi formation in the arterioles at the fundus of the gallbladder (H&E ×400).
Figure 2: (A) CT showed Stanford type B aortic dissection, the wall defect of gallbladder fundus and the local fluid collection. (B) Laparotomy showed the perforation of the
gallbladder fundus. (C) Histological examination showed fibrosis and hemosiderosis in the subserosal layer (H&E ×100). (D) Fibrotic change of arterioles was dominant at
the peripheral part of the gallbladder (H&E ×100).
Table 1: Summary of the four reported cases of acalculous cholecystitis associated with aortic dissection
Roth et al. 57M de Bakey type III Soon after Open cholecystectomy Deep acellular necrosis with fresh thrombi in the small
vessels, slight polymorphonuclear infiltration,
gangrenous without perforation
Gokhan et al. 62M de Bakey type III Same day Open cholecystectomy Completely necrotic
Case 1 69M Stanford type B Same day Open cholecystectomy Partial mucosal defect, submucosal bleeding, fresh thrombi
in the arteriole
Case 2 74M Stanford type B 2 months Open cholecystectomy Perforation of fundus, fibrosis and hemosiderosis in the
later subserosal layer
Histological study of AAC showed that neutrophils margin- disease entity; acute and chronic. Further histological study
ation of blood vessels and lymphatic vessel dilatation were would be needed.
observed, indicating the existence of ischemic and reperfusion- The decrease in splanchnic blood flow due to aortic dissection
mediated injury [9]. On the other hand, Case 2 presented with could cause the acute and chronic ischemia in the peripheral part
perforation of the fundus of the gallbladder with relatively slight of the gallbladder. Therefore, the history of aortic dissection
acute inflammation and infiltration of lymphocytes. Long- could be a risk factor of both AAC and CAC. Immediate surgical
periods chronic ischemia leads to mucosal atrophy and wide approach is desirable to avoid poor prognosis.
range of fibrosis of lamina propria or deeper, including partial
hyalinization. Histological study of Case 2 also showed fibrosis
and hemosiderosis in the subserosal layer and chronic fibrotic CONFLICT OF INTEREST STATEMENT
change of arterioles, which was compatible with histological
None declared.
change of chronic ischemia. That is to say, Case 2 would be
more appropriately called ‘chronic acalculous cholecystitis
(CAC)’. Recent reports showed that the number of acalculous
cholecystitis in outpatients was increasing, and the outcome of
REFERENCES
these patients was much better than that of acalculous chole- 1. Kalliafas S, Ziegler DW, Flancbaum L, Choban PS. Acute acal-
cystitis in hospital inpatients [10]. The difference of the outcome culous cholecystitis: incidence, risk factors, diagnosis, and
was unknown, but might be explained by the difference of the outcome. Am Surg 1998;64:471–5.
4 | F.F. Inagaki et al.
2. Huffman JL, Schenker S. Acute acalculous cholecystitis: a 7. Roth T, Mainguene C, Boiselle JC. Acute acalculous cholecyst-
review. Clin Gastroenterol Hepatol 2010;8:15–22. itis associated with aortic dissection: report of a case. Surg
3. Orlando R 3rd, Gleason E, Drezner AD. Acute acalculous Today 2003;33:633–5.
cholecystitis in the critically ill patient. Am J Surg 1983; 8. Söğütlü G, Işik B, Yilmaz M, Karadağ N, Hoca O, Olmez A, et al.
145:472–6. Acute acalculous cholecystitis induced by aortic dissection:
4. Johnson EE, Hedley-Whyte J. Continuous positive-pressure report of a case. Ulus Travma Acil Cerrahi Derg 2010;
ventilation and choledochoduodenal flow resistance. J Appl 16:283–5.
Physiol 1975;39:937–42. 9. Laurila JJ, Ala-Kokko TI, Laurila PA, Saarnio J, Koivukangas V,
5. Warren BL. Small vessel occlusion in acute acalculous chole- Syrjälä H, et al. Histopathology of acute acalculous
cystitis. Surgery 1992;111:163–8. cholecystitis in critically ill patients. Histopathology 2005;47:
6. Hakala T, Nuutinen PJ, Ruokonen ET, Alhava E. Microangiopa- 485–92.
thy in acute acalculous cholecystitis. Br J Surg 1997;84: 10. Ryu JK, Ryu KH, Kim KH. Clinical features of acute acalculous
1249–52. cholecystitis. J Clin Gastroenterol 2003;36:166–9.