Heterotopic Ossification Encountered During a Complex Ventral Hernia Repair

Case Report and Literature Review

Takintope Akinbiyi, MD; Sanjeev Kaul, MD

Disclosures

ePlasty. 2017;17(e29) 

In This Article

Discussion

Heterotopic ossification involves the formation of extraskeletal trabecular bone between muscle planes and is a known sequela of orthopedic surgery,[6,7,17] severe neurological injury,[7,8,18,19] traumatic injury,[19–22] and less frequently of surgical intervention[4,5,9–15] and burns.[23–25] It can be distinguished from truly malignant neoplasms such as osteosarcoma or osteochondroma on the basis of its radiographic and histological properties. Histologically, HO initially appears as a focus of inflammatory infiltration and progresses to areas of osteoid or cartilaginous tissue formation. On occasion, mature HO can resemble lamellar bone.[1] Radiographically, it can appear as a radiopaque rim surrounding a radiolucent center, an appearance dissimilar to that of malignant lesions, although there is a high degree of overlap.[2,26,27]

Some reports suggest that patients may have a genetic predisposition to HO with a higher expression of the HLA-B27, HLA-B18, and HLA-DRW7antigens in neurogenic HO.[1,8] In patients with neurogenic impairment, traumatic brain injury or spinal injury, superimposed trauma has also been found to increase the rate of HO both in animal models and in clinical observational studies.[6,8] Other observed risk factors include male sex, young age (20–30 years), completeness of any associated spinal lesions, and prolonged coma.[8,10]

While the etiology Would it be better to change "etiology" to "cause" throughout the text? Please advise. of HO is unknown, it is assumed to be multifactorial. It is speculated that the calcified tissue found in HO may be the result of the transformation of mesenchymal cells in the connective tissue septa of muscle into osteogenic cells.[9,28] The role of mesenchymal cells is supported by the finding that bone morphogenetic proteins (BMP), which are known to induce mesenchymal stem cells toward ostoblastic differentiation, have been speculated to exist in supraphysiologic concentrations around areas of trauma or surgical incisions.[2,24,29] In addition, a mutation in a BMP-type I receptor has been associated with inherited and sporadic fibrodysplasia ossificans progressiva, a rare condition predisposing to HO.[30] The role of inflammation has been suggested by many authors and studied in experimental models and has been found to play a strong role.[24] Baird and Kang[6] proposed that HO could also be mediated by systemic factors, local inflammation, cell death, upregulation of mineralization growth factors, or ischemia-induced free radical production leading to tissue injury. The development of HO may also partially be due to venous stasis or damage to bone and its surrounding connective tissue.[9]

While HO has been anecdotally observed in abdominal incisions, little is known about its true incidence or characteristics.[12] Kim et al[11] retrospectively looked at CT scans from 152 postoperative patients with abdominal incisions, approximately 50% involving upper midline incisions, and found radiographic evidence of HO in 25%. The mean time to follow-up was 378 days.[11] Jacobs et al[12] retrospectively reviewed 11 patients with HO and found that they all had undergone upper midline incisions and developed HO between the anterior abdominal fascia and the peritoneum, originating in close proximity to the xiphoid. Mean follow-up was 6.7 months.[12] Another retrospective review over 9 years found 7 cases of HO, all between the fascia and the peritoneum in upper midline incisions.[14] In a review of reported cases of HO published between 1920 and 1998, Gaffey and Winston[5] found 130 cases of HO described in surgical incisions. Of the cases with available clinical information, 72% had palpable lesions of which 62% were located in upper midline incisions.[5] While the majority of suspected lesions in the aforementioned case series were not sampled for pathology, a diagnosis of HO over calcinosis was made by the authors on the basis of radiographic appearance or clinical examinations.

Prophylaxis and Treatment

Multiple groups have studied prophylaxis of HO in high-risk populations. Nonsteroidal anti-inflammatory drugs have been shown to reduce HO formation by inhibiting prostaglandin-mediated bone remodeling, especially PGE-2.[6,17,31] Free radical scavengers, allopurinol and N-acetylcysteine, have been shown in experimental models to reduce HO formation.[32] Bisphosphonates are known to limit the mineralization of organic osteoid and have also been shown to inhibit or limit the formation of HO in the spinal cord injury population.[18,33] Radiation therapy is another treatment modality known to inhibit HO formation. Studies in the orthopedic literature have shown that radiation therapy can reduce HO formation and has been used as prophylaxis against its formation.[34,35] However, radiation therapy has been associated with posttreatment complications including seroma formation.[36] Finally, warfarin has been studied as a prophylactic agent, as osteocalcin, an osteoblast-specific noncollagenous protein important in bone development, is vitamin K dependent.[37]

While prophylactic measures have shown benefit in the neurogenic injury and orthopedic literature, abdominal incisions are too common to justify the expense of routine HO prophylaxis. Furthermore, exposing patients to the risks of the side effects of abdominal radiation or systemic anticoagulation is not appropriate. In ventral hernia repair with mesh, seroma formation after radiation is also undesirable. Therefore, surgical resection currently appears to represent the sole viable treatment option.

There is limited information available to guide timing and technique of resection. Some authors have suggested that only mature, symptomatic HO be excised,[13,15,33] as immature lesions may have a higher rate of recurrence.[38,39] Koolen et al[10] attempted a systematic review of the literature pertaining to the treatment of HO in abdominal incisions but were unable to find any randomized control trials, only case reports. This dearth of knowledge has contributed to the uncertainty in managing symptomatic HO in burned patients and ventral abdominal incisions. Some authors have advocated a 12- to 18-month delay before surgical excision to reduce the likelihood of recurrence,[40,41] but this is in regard to HO in neurogenic patients and may not be necessary in HO identified in burn injuries and abdominal incisions.

Objective evidence supporting delaying resection is lacking.[42–45] Trending the levels of creatine phosphokinase[2] and serum alkaline phosphatase or using bone scans as markers of maturation has been suggested, but the accuracy and clinical utility of these are controversial.[46] In a study of 37 joints, 25 had postoperative radiographic studies available and 14 of these (55%) had evidence of recurrence. However, neither the extent of recurrences nor the follow-up duration was fully documented.[41] Conversely, Tsionos et al[43] evaluated 28 consecutive patients with burn injury involving 35 elbows and hypothesized that in this patient population, early excision would be beneficial. They observed only 4 recurrences (radiographic and/or clinical) after resection, with a mean delay of 12 months from formation. No recurrences were observed in HO originating away from bone, which may be more applicable to HO in abdominal incisions. In addition, another study of 9 elbow joints postoperative resection of HO found no recurrences over a follow-up period of 10 months to 8.7 years.[40] Therefore, there is some evidence that early excision is appropriate.

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