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Acute and chronic acalculous cholecystitis associated with aortic dissection
Fuyuki F Inagaki1, Yoshiaki Hara2, Masako Kamei2
1Department of Surgery, Tokyo Metropolitan Hiroo Hospital, Tokyo, Japan Hepato-Biliary-Pancreatic Surgery Division, Artificial Organ and Transplantation Division, Department of Surgery, Graduate School of Medicine, University of Tokyo, Tokyo, Japan inagaki-tky@umin.ac.jp.
Insights
Acalculous cholecystitis, a rare gallbladder disease, can be linked to aortic dissection. This study presents two cases, highlighting acute and chronic ischemic forms potentially caused by reduced blood flow.
Area of Science:
- Vascular Surgery
- Gastroenterology
- Pathology
Background:
- Acalculous cholecystitis (AC) is a severe condition with unclear pathogenesis.
- Aortic dissection is a critical cardiovascular emergency.
Observation:
- Two patients with aortic dissection developed acalculous cholecystitis.
- Case 1 presented with acute ischemic cholecystitis post-aortic dissection exacerbation.
- Case 2 showed chronic ischemic cholecystitis with gallbladder perforation after prolonged aortic dissection management.
Findings:
- Histological examination revealed distinct acute (necrotized cholecystitis, thrombi) and chronic (fibrosis, hemosiderosis) ischemic changes in the gallbladder.
- Chronic acalculous cholecystitis (CAC) is documented here for the first time in association with aortic dissection.
- Aortic dissection may be an underlying risk factor for both acute and chronic AC.
Implications:
- Reduced splanchnic blood flow secondary to aortic dissection is a potential mechanism for AC.
- This association broadens the understanding of AC etiology.
- Recognition of this link may improve diagnosis and management of AC in patients with aortic dissection.
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.
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