Treatment Strategy for Nonunion
Fracture nonunion has been described as the “cessation of all healing processes and union has not occurred.”1 It has also been defined as no progression of healing on sequential radiographs performed at a defined interval, usually 6 to 8 weeks. Radiographic nonunion has been defined as a lack of bridging callus across the fracture site on orthogonal views. From a biomechanical perspective cortical continuity is the best predictor of torsional strength in the fracture zone, and the amount of callus is the least important indication of union.2
There is general agreement that a nonunion has occurred when the fracture has not united in the expected period of time for that fracture (usually 3 to 6 months). This range is a reflection of the variable healing of fractures because of diversity in patient characteristics and the risk factors for nonunion. Such risk factors include injury-related issues such as a high-energy mechanism,3 fracture and soft tissue characteristics (location, degree of displacement, bone comminution, segmental bone loss, soft tissue and vascular compromise),3–8 as well as patient factors such as age, nutritional status, presence of an endocrinopathy (such as hypothyroidism), nicotine ingestion,9,10 diabetes,9,11 alcohol consumption,9 vasculopathy12 and certain medication (steroids, nonsteroidal anti-inflammatories, anticonvulsants, antibiotics, and anticoagulants).13–19 Finally, infection is a significant factor in recalcitrant nonunions.
Classification
Nonunions are usually classified as either hypertrophic or atrophic (avascular) (Fig. 6.1).20 Hypertrophic nonunions are those that have not healed despite significant callus formation. Hypertrophic nonunions generally have adequate vascularity but lack sufficient stability to achieve union, and are considered to be mostly a biomechanical problem. In contrast, atrophic nonunions are those that show no callus formation. The primary cause of an atrophic nonunion is inadequate vascularity, but there also may not be sufficient stability at the fracture site. Although hyper-trophic and atrophic nonunions have been further subclassified, the consistent characteristics are presence of callus in hypertrophic nonunions, and lack of callus and bone vascularity (or even presence of necrotic fragments) in atrophic nonunions.21
Evaluation
The initial assessment of a patient with a nonunion must be detailed in order to determine the etiology. This includes an evaluation of the patient, including physical examination, imaging, as well as bloodwork. The local environment of the nonunion should be carefully examined regarding the condition of the soft tissues, as well as an assessment of the vascularity to both the local area and the entire limb. Baseline bloodwork includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). One caution is that these test results can normalize in chronic conditions, and therefore cannot be reliably used to rule out associated infection. Finally, malnutrition may contribute to impaired fracture healing, so the patient′s nutritional status should be assessed, including calcium, vitamin D, thyroid levels, and even testosterone levels in males.
Radiographic evaluation of a nonunion requires multiple views including anteroposterior (AP), lateral, and oblique images. Although radiographic union has been defined as bridging callus with cortical continuity across the fracture site, this method has poor reliability.22 A scoring system developed for tibia fractures, the radiographic union score for tibia fractures (RUST), assesses the presence of bridging callus and that of a fracture line on each of the four cortices seen on two orthogonal radiographic views.23 The RUST has been shown to have greater inter-rater reliability when compared with the surgeons’ general impression or the number of cortices bridged by callus. Computed tomography (CT) can also be useful to evaluate the degree of union, as well as to assess subtle bone changes, including the presence of sequestra and devitalized bone fragments. Magnetic resonance imaging (MRI) is highly accurate for evaluating pathological processes in bone and soft tissue, especially when enhanced with intravenous gadolinium. However, it has limitations in the presence of metallic implants, as well as difficulty in differentiating among edema, infection or inflammation, and postoperative changes.
Diagnosing associated infection can be difficult. The clinical signs of an acute infection, such as erythema, pain, fever, and swelling, are often absent in patients with chronic infection. Swabbing open wounds or sinus tracts is not very useful in identifying pathogens that might be at the nonunion site. “Sterile” aspirations have variable success. The optimal method of determination of the presence of infection is bone biopsy (with multiple samples) of the site of the nonunion. Nuclear medicine studies are frequently ordered to determine the presence of an acute or chronic infection at the site of a nonunion. There are several radionucleotide studies available, each with different characteristics and advocates. Indium (111In)-labeled leuko cyte (white blood cell) scintigraphy, technetium (99mTc)-immunoscintigraphy, and 99mTc-labeled nanocolloids have all been used to diagnose infection. Some authors suggest that suspected chronic, low-grade infections are best evaluated by 111In-labeled leukocyte (white blood cell) scintigraphy, as it tracks cell migration over a 48-hour period. Recently, Stucken et al24 evaluated the contribution of laboratory values and scintigraphy in the diagnosis of infection in patients with nonunions. In a series of 95 non-unions that were all evaluated with a standardized protocol, both the ESR and CRP were independently accurate predictors of infection. Furthermore, the likelihood of infection was greater with the number of positive tests. The additional use of a sulfur-colloid scan was not beneficial or cost-effective.
Indications for Surgical Treatment
Surgery is warranted for management of a nonunion when it is infected, or when it causes pain or decreased function. Asymptomatic nonunions, most often seen in the upper extremity, do not require treatment.
Surgical Treatment
The principles of nonunion treatment are based on the same concept as initial fracture management—namely, establishing an environment that facilitates successful bone union. Thus, treatment is based on the availability of mesenchymal cells found in the periosteum of living bone, bone growth factors that enhance cell function, adequate vascularity of the local environment, and finally, appropriate stability of the nonunion. The preoperative evaluation should determine which of these factors is lacking and therefore needs to be addressed, and whether other patient-related factors require correction. Strategies to eradicate infection are employed prior to, during, and after surgical treatment of the nonunion.
Hypertrophic nonunions are the result of inadequate biomechanical stability. Stable fixation with compression of the fragments with minimal vascular disruption of the nonunion site has a high rate of success (Fig. 6.1).
Atrophic nonunions are generally the result of inadequate vascularity to the fracture site, and can be caused by one or more of the following: severe displacement of the fragments, bone loss following open injuries, soft tissue compromise due to a high-energy mechanism, infection, and excessive soft tissue dissection at the time of fracture repair leading to avascular bone fragments. Treatment includes resection of nonviable bone to create bleeding surfaces, stable fixation of the fragments, and the addition of osteoinductive material (usually autogenous bone graft). When the surrounding soft tissues are inadequate to provide local vascularity (as in most tibia nonunions), soft tissue transfer may be required. The method of stabilization is chosen depending on multiple factors, including the soft tissue environment, the location of the nonunion, as well as surgeon preference. Whenever possible, compression should be imparted to the nonunion because of the enhanced stability.
Bone loss that causes a defect, either due to the injury or its treatment, can result in an atrophic nonunion. Multiple strategies are available, including bone grafting (with autogenous, allograft, substitute, or combination grafts), bone transport (with almost universal need to bone graft the docking site) (Fig. 6.2), or free vascularized fibula autograft. In the following subsections, the approaches to specific nonunion sites are reviewed.
Clavicle Nonunion
Clavicle nonunions occur most often following nonoperative treatment of fractures with significant displacement of the fracture fragments. The nonunion can be hyper-trophic, due to excessive motion at the fracture site, or atrophic, due to patient factors such as nutrition and advanced age. Atrophic nonunions seen following operative repair are associated with fixation failure and with excessive soft tissue stripping at the fracture site.
In cases treated initially nonoperatively, an incision is made parallel to the course of the clavicle (similar to acute fixation). Some experts advocate protecting the supraclavicular sensory nerves during dissection, but others do not. However, it is agreed that an extraperiosteal approach is ideal except at the nonunion site. Exposure of the non-union surfaces is undertaken, and the surfaces are drilled if they are required to stimulate bleeding surfaces. There is often an oblique plane to the nonunion, allowing the insertion of one or two lag screws; either 2.7- or 3.5-mm cortical screws are used, depending on the size of the bone. There is often shortening of the clavicle with the nonunion, and a small external fixator (or distractor) can facilitate length restoration. The selection of the plate to be used for stabilization is based on surgeon preference, The possibilities include locking or nonlocking, anatomic or surgeon-contoured, 2.7 or 3.5 mm, and dynamic compression type or reconstruction type. The goals are to obtain stable fixation and to enable early range of motion of the upper extremity. In atrophic nonunions, autograft is often utilized, and typically applied inferior to the clavicle. In hypertrophic nonunions, the abundant callus often needs to be partially resected, and it can be used for bone graft if required.25
Humeral Shaft Nonunions
For atrophic nonunions of the humeral shaft, plate fixation leads to a better outcome than an intramedullary device.26 The choice of surgical approach depends on many factors, including the location of the nonunion, the location of any existing hardware, and the condition of the soft tissues. An anterior incision (usually an extended deltopectoral) is typically chosen for proximal nonunions, a posterior approach (triceps-sparing if possible) for distal nonunions, and either an anterior or posterior approach for nonunions in the middle third of the humerus.
An important principle of management is to achieve compression across the site of the nonunion. Maintenance of the biological viability of the nonunion site is important, and an extraperiosteal approach should be utilized outside the area of the nonunion. At the nonunion site, the bone ends are debrided until vascularized surfaces are created. On occasion this may require shortening of the bone, which is well tolerated in the upper extremity. The length of the plate is usually 10 to 12 holes with balanced, spaced fixation utilizing three or four screws (six to eight cortices) on each side of the nonunion (Fig. 6.3). Bone graft may or may not be utilized depending on the vascularity of the nonunion area, patient-related factors, and surgeon preference.