Heterotopic Mesenteric Ossification (HMO): A Rare Complication of Tertiary Peritonitis Following Penetrating Trauma

Author(s):
Philip Barie; Mayur Narayan; Caitlin Egan

Background:

HO, the reactive formation of bone in soft tissue, was described in an abdominal scar by the Swiss-German pathologist Max Askanazy in 1901. It is associated with trauma/burn injuries, usually orthopedic, specifically hip/pelvis injury. We describe a rare case of HMO after post-traumatic tertiary peritonitis.

Hypothesis:

NA

Methods:

A 40-year-old man presented with penetrating right flank trauma due to impalement by industrial shears after a fall from height. Massive hemoperitoneum from lacerated mesocolon and near-transection of the right renal vein required damage control laparotomy and right nephrectomy/colectomy. 2 d later, ileocolostomy was performed. Abdominal wall closure on postoperative day (POD) 4 included bilateral rectus abdominis flaps, and synthetic mesh in the retro-rectus space. On POD 10 after the index case, a CT scan for tachycardia/leukocytosis showed mesenteric enhancement and peri-anastomotic fluid. After unsuccessful percutaneous drainage (PD), he underwent washout/drain placement via a right flank incision, and parenteral nutrition.  After PD again, one month later, after which he stabilized for 3 mos. 5 mos after injury, CT showed extensive mesenteric calcification (Fig. 1)  Loop ileostomy through the prior midline incision/mesh. Multiple firm, sharp , calcified deposits in the abdomen and mesentery represented HMO (Fig. 1.)  There was no incisional HO. Adhesiolysis and subtotal resection of HMO was performed. (Fig. 2). After protracted recovery, the ileostomy was closed.

Results:

NA

Conclusions:

The pathogenesis of HMO is not well delineated. Serum alkaline phosphatase (sALP), a marker of osteogenesis, is elevated early during HO formation, Here, a normal admission sALP of 62 IU/L (normal, 41-133 U/L), peaked at 414 IU/L 3 wks after initial injury (Fig. 2). The molecular pathway leading to ectopic bone deposition in the abdomen is unknown, but may be a synchronous polymorphism in the causative gene (ACVR1/ALK2) for fibrodysplasia ossificans progressiva (a known genetic cause of HO). To our knowledge, this is only the second case reported of HO associated with tertiary peritonitis.