Extensive type B aortic dissection with Michels type IX hepatic arterial anatomy causing acalculous gangrenous cholecystitis

A 36-year-old man with hypertension presented with a 3-day history of abrupt-onset back and chest pain, followed by abdominal pain. Computed tomography angiography demonstrated an acute Stanford type B aortic dissection (Panel A, arrowheads) extending from the proximal descending thoracic aorta to both common iliac arteries, with multiple re-entry tears and severe ostial compromise of the superior mesenteric artery (SMA) (Panel A, red arrow). Three-dimensional reconstruction showed a replaced common hepatic artery arising from the SMA (Michels type IX anatomy1; Panel B, blue arrows), rendering the entire hepatobiliary arterial inflow SMA-dependent. The gallbladder was markedly distended without visible calculi (Panel C, asterisk). Angiography confirmed non-opacification of the SMA origin and poor distal perfusion. Endovascular aortic repair involved three overlapping stent grafts and supra-aortic branch reconstruction. Subsequent SMA stenting restored visceral flow (see Supplementary data online, Figure S1). Persistent abdominal pain and gastrointestinal bleeding prompted immediate laparoscopy. Moderate bile-stained ascites was present. The small bowel and colon were viable, but the gallbladder was gangrenous, measuring 10 × 8 × 6 cm, with focal bile leakage (Panel D). Laparoscopic cholecystectomy was performed. The opened specimen showed haemorrhagic mucosal necrosis without gallstones (Panel E), and haematoxylin and eosin staining confirmed haemorrhagic necrosis with acute inflammation (Panel F). Michels type IX anatomy is rare, occurring in 2.96% of 5002 patients.2 Here, the variant rendered cystic arterial perfusion SMA-dependent; SMA malperfusion from the type B dissection therefore caused acalculous gangrenous cholecystitis despite viable bowel. Clinicians should consider gallbladder ischaemia in this setting.