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Acute and chronic acalculous cholecystitis associated with aortic dissection.

Inagaki FF, Hara Y, Kamei M, Tanaka M, Yasuno M - J Surg Case Rep (2015)

Bottom Line: 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.History of aortic dissection could be a risk factor of acute and CAC due to relatively decreased splanchnic blood flow.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department 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.

No MeSH data available.


Related in: MedlinePlus

(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).
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RJV101F1: (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).

Mentions: A 69-year-old male who had an 8-year history of Stanford type B aortic dissection presented with vomiting and abdominal pain. Physical examination revealed right upper abdominal tenderness, but no muscular defense. Blood tests revealed leukocytosis and elevated levels of amylase, but other laboratory data were within normal range. Abdominal sonography showed the inflammatory thickened gallbladder wall without any gallstones and biliary sludge. Contrast-enhanced computed tomography (CT) also showed the enlargement of the false lumen compared with a study 5 years earlier. The gallbladder and pancreatic body and tail were swollen, indicating acute pancreatitis and AAC (Fig. 1A). A highly enhancing lesion was detected in the gallbladder, which appeared to be the gallbladder hemorrhage. Laparotomy revealed necrotized cholecystitis with dominant histopathologic changes at the fundus of the gallbladder (Fig. 1B). Pathological exams showed partial mucosal defect and submucosal bleeding in the whole gallbladder wall (Fig. 1C). In addition, fresh thrombi formation was found in the arterioles at the fundus and less frequently in the body/neck of the gallbladder (Fig. 1D).Figure 1:


Acute and chronic acalculous cholecystitis associated with aortic dissection.

Inagaki FF, Hara Y, Kamei M, Tanaka M, Yasuno M - J Surg Case Rep (2015)

(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).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4522049&req=5

RJV101F1: (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).
Mentions: A 69-year-old male who had an 8-year history of Stanford type B aortic dissection presented with vomiting and abdominal pain. Physical examination revealed right upper abdominal tenderness, but no muscular defense. Blood tests revealed leukocytosis and elevated levels of amylase, but other laboratory data were within normal range. Abdominal sonography showed the inflammatory thickened gallbladder wall without any gallstones and biliary sludge. Contrast-enhanced computed tomography (CT) also showed the enlargement of the false lumen compared with a study 5 years earlier. The gallbladder and pancreatic body and tail were swollen, indicating acute pancreatitis and AAC (Fig. 1A). A highly enhancing lesion was detected in the gallbladder, which appeared to be the gallbladder hemorrhage. Laparotomy revealed necrotized cholecystitis with dominant histopathologic changes at the fundus of the gallbladder (Fig. 1B). Pathological exams showed partial mucosal defect and submucosal bleeding in the whole gallbladder wall (Fig. 1C). In addition, fresh thrombi formation was found in the arterioles at the fundus and less frequently in the body/neck of the gallbladder (Fig. 1D).Figure 1:

Bottom Line: 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.History of aortic dissection could be a risk factor of acute and CAC due to relatively decreased splanchnic blood flow.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department 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.

No MeSH data available.


Related in: MedlinePlus