Letter-to-the Editor: Approach to Tibial Shaft Nonunions: Diagnosis and Management

To the Editor: We feel commentary is warranted on the recent review1 “Approach to Tibial Shaft Nonunions: Diagnosis and Management on Tibial Non-unions.” Our response is directed toward the recalcitrant fracture (RCFx) group who have tibial nonunions, often infected, after one or more salvage attempts. A reported 27%2 incidence of RCFx was cited for this cohort. The authors discuss shock-induced hypoxia, poor local biology, and soft-tissue and/or sinus tract envelopes over sequestra as contributors to RCFxs and offer their approaches to management of these challenges. However, the following additional interventions and their potential benefits should not be overlooked. First, an “older” technique, that is, saucerization of the avascular bone segment with débridement of the infected sinus tract/fibrous tissue mantle followed by cancellous bone grafting (Papineau technique), has been effective in managing the RCFx. We recommend combining this with the delayed application of a microvascular free flap to expedite healing. External fixation provides stability while fracture healing ensues with the added benefit of avoiding internal fixation that often poses a risk of recurrent complications in RCFx. Second, in Gustilo type III B and C fractures, vascular injury3 is a concomitant feature. Evaluation for perfusion in the RCFx especially in patients with peripheral artery disease should be addressed. While the need for amputation due to ischemia may not be evident, it may be notable enough to interfere with healing and/or infection control. We are unaware of occlusion rates of vascularized Gustilo III C fractures. 50% complication rates3 are typical in these fracture types. Occlusion of the revascularization of the III C fracture may be a contributor to the RCFx. Third, hyperbaric oxygen (HBO) treatments are an adjunct for managing RCFx. Cicatrix formation (intrinsic mechanism to generate an interface between healthy and infected tissues) contributes to hypoxia of the RCFx site due to its avascularity. HBO increases plasma carried and tissue fluid oxygenation tenfold.4 This improves diffusion through hypoxia areas threefold to favor fibroblast-macrophage function, angiogenesis,5 and bone resorption. These factors are highly oxygen dependent for function; as an example, the metabolic activity6 of the osteoclast is 100-fold that of the osteoblast. In addition, HBO supports neutrophil and macrophage oxidative killing of bacteria, which is hampered in hypoxic environments. In the absence of intractable pain and/or loss of function secondary to deformity that negates functional ambulation to justify a lower limb amputation, we recommend the above considerations for management of RCFx.