Nonunion and Malunion

Nonunion and malunion are complications of fracture healing. Nonunion is defined as the permanent failure of a fracture to unite within the expected time frame for the specific bone and patient, with the absence of progressive healing on serial radiographs. It is characterized by a persistent fracture gap with sclerotic bone ends, often with a false joint (pseudoarthrosis) formation. Malunion is defined as the healing of a fracture in an abnormal anatomical position, resulting in angular, rotational, or shortening deformities. This can lead to limb dysfunction, joint incongruity, and altered biomechanics. Both conditions are significant clinical entities in veterinary orthopedics, requiring surgical intervention to restore limb function and alleviate pain.

Nonunion and malunion arise from a complex interplay of biological and mechanical factors. Primary causes include: 1) Inadequate fracture stability: insufficient immobilization, inappropriate implant selection, or premature weight-bearing can lead to excessive motion at the fracture site, disrupting the delicate vascular and cellular processes of healing. 2) Infection: osteomyelitis can cause bone necrosis, sequestrum formation, and impaired osteogenesis. 3) Poor blood supply: severe soft tissue trauma, open fractures, or surgical devascularization can compromise the local vascularity essential for healing. 4) Interposition of soft tissue: muscle, fascia, or periosteum may become entrapped between fracture fragments, preventing bony contact. 5) Metabolic and systemic diseases: hyperadrenocorticism, diabetes mellitus, malnutrition, and advanced age can impair bone healing. 6) Iatrogenic factors: excessive periosteal stripping, inadequate reduction, or overly rigid fixation leading to stress shielding. Malunion typically results from inadequate reduction or loss of reduction during healing, often due to premature implant failure or poor patient compliance with activity restriction.

Nonunion and malunion are more commonly reported in dogs than cats, with a higher incidence in large and giant breeds due to their greater body weight and associated biomechanical stresses. Certain breeds, such as Greyhounds and other sighthounds, may have a higher risk of nonunion due to their thin cortices and high-speed trauma. Age is a significant factor: young animals have a greater osteogenic potential and heal faster, while older animals are more prone to delayed healing and nonunion. There is no clear sex predilection. Fractures of the distal radius/ulna, tibia, and femur are particularly susceptible to nonunion due to limited soft tissue coverage and blood supply. Malunion is often seen in fractures managed conservatively or with inadequate surgical stabilization, especially in immature animals where remodeling can partially correct deformities but may also lead to progressive angular limb deformities.

Fracture healing involves a complex cascade of inflammation, repair, and remodeling. Nonunion occurs when this cascade is interrupted. The primary pathophysiological mechanisms include: 1) Excessive motion: leads to the formation of a hypertrophic nonunion, where abundant callus forms but fails to bridge the gap due to persistent instability. The fracture ends become rounded and sclerotic, with a fibrous or fibrocartilaginous tissue filling the gap. 2) Inadequate blood supply: results in an atrophic nonunion, characterized by minimal callus formation, osteopenia, and a gap filled with fibrous tissue. 3) Infection: causes a septic nonunion, with purulent discharge, sequestra, and a mixed picture of bone lysis and sclerosis. Malunion results from the healing of fragments in a non-anatomical position. This leads to altered joint angles, abnormal weight distribution, and secondary osteoarthritis. Angular deformities, such as valgus or varus, and rotational deformities can cause significant gait abnormalities and joint pain.

Intrinsic factors include: 1) Age: older animals have reduced osteogenic potential. 2) Breed: large and giant breeds have a higher risk due to increased biomechanical loads. 3) Nutritional status: deficiencies in calcium, phosphorus, vitamin D, and protein can impair healing. 4) Systemic diseases: hyperadrenocorticism, diabetes, and renal disease can delay bone healing. 5) Genetic factors: certain breeds may have inherent bone healing abnormalities. Extrinsic factors include: 1) Trauma severity: high-energy fractures with severe soft tissue damage are more prone to complications. 2) Open fractures: have a higher risk of infection and nonunion. 3) Surgical technique: excessive periosteal stripping, inadequate reduction, or improper implant selection can predispose to nonunion. 4) Postoperative management: premature weight-bearing, lack of activity restriction, or failure to address concurrent injuries can lead to implant failure and malunion.

Clinical signs of nonunion include persistent lameness, pain on palpation of the fracture site, and abnormal mobility at the fracture site. There may be swelling, muscle atrophy, and a palpable false joint. In cases of infected nonunion, there may be draining tracts and purulent discharge. Malunion presents with visible limb deformity, such as angular deviation, shortening, or rotation. Lameness may be present, especially after exercise, and there may be joint stiffness and crepitus. In severe cases, there may be neurological deficits due to nerve entrapment or compression. The gait may be abnormal, with a characteristic 'pawing' or 'circumduction' motion depending on the deformity.

Differential diagnoses for nonunion and malunion include: 1) Delayed union: a fracture that is healing slower than expected but still has the potential to heal with continued immobilization. 2) Osteomyelitis: a bone infection that can mimic nonunion on radiographs, but is differentiated by the presence of fever, draining tracts, and positive bacterial culture. 3) Bone neoplasia: primary bone tumors such as osteosarcoma can cause pathological fractures that fail to heal, but are distinguished by aggressive radiographic changes and histopathology. 4) Fibrous dysplasia: a benign bone lesion that can cause deformity and pathological fractures. 5) Osteogenesis imperfecta: a congenital collagen disorder leading to fragile bones and multiple fractures. 6) Nutritional secondary hyperparathyroidism: can cause bone weakening and pathological fractures. 7) Hypertrophic osteodystrophy: a developmental disease in young dogs that can cause lameness and radiographic changes. 8) Panosteitis: a self-limiting inflammatory condition of long bones in young dogs, causing pain and lameness but no fracture. 9) Craniomandibular osteopathy: a condition affecting the skull and mandible, but can be considered in cases of mandibular nonunion. 10) Rickets: a metabolic bone disease causing deformities and fractures.

The diagnostic algorithm for nonunion and malunion begins with a thorough history and physical examination, including orthopedic and neurological assessments. Palpation of the fracture site may reveal abnormal mobility, pain, or deformity. Radiography is the primary imaging modality: orthogonal views (craniocaudal and mediolateral) are essential to evaluate fracture alignment, callus formation, and the presence of a gap. Stress radiographs may be taken to assess instability. Advanced imaging such as CT is useful for detailed assessment of bone morphology, especially in complex deformities, and for surgical planning. MRI may be indicated if there is suspicion of soft tissue interposition or infection. Laboratory tests, including complete blood count, serum biochemistry, and urinalysis, are performed to rule out metabolic diseases. In cases of suspected infection, aerobic and anaerobic bacterial cultures and sensitivity testing should be obtained from deep tissue samples or joint fluid. Bone biopsy may be necessary to differentiate nonunion from neoplasia.

In uncomplicated nonunion, laboratory findings are often within normal limits. However, in cases of infected nonunion, there may be leukocytosis, elevated serum amyloid A (SAA), and increased C-reactive protein (CRP). Synovial fluid analysis, if a joint is involved, may show inflammatory changes with increased nucleated cell count and protein concentration. Cytology may reveal neutrophils and bacteria. Blood cultures may be positive in systemic infections. Coagulation panel (PT, aPTT, TEG) is recommended to assess surgical risk, especially if major reconstructive surgery is planned. Blood gas analysis may be indicated in patients with concurrent trauma or systemic disease.

Radiography is the cornerstone of imaging. In nonunion, radiographs typically show a persistent fracture gap with sclerotic, rounded bone ends. Hypertrophic nonunion is characterized by abundant, poorly organized callus, while atrophic nonunion shows minimal callus and osteopenia. Septic nonunion may show areas of bone lysis, periosteal reaction, and sequestra. Malunion is evident as angular, rotational, or shortening deformities. Stress radiographs can demonstrate instability. Ultrasonography may be used to assess soft tissue structures, but is of limited value for bone. CT with 3D reconstruction is invaluable for surgical planning, especially for complex deformities, allowing precise measurement of angles and rotation. MRI is useful for evaluating soft tissue interposition, infection, and the viability of bone fragments. Arthroscopy may be indicated if there is concurrent joint pathology. Fluoroscopy can be used intraoperatively to guide reduction and implant placement.

Cytology of joint fluid or fine-needle aspirates from the fracture site may be performed if infection or neoplasia is suspected. In septic nonunion, cytology may show degenerate neutrophils and intracellular bacteria. Histopathology of bone biopsies is the gold standard for differentiating nonunion from neoplasia. In nonunion, histology shows fibrous tissue, fibrocartilage, and islands of cartilage, with no evidence of neoplastic cells. In infected nonunion, there may be necrotic bone, inflammatory infiltrates, and sequestra. Special stains, such as Gram stain, can help identify bacteria. In cases of suspected neoplasia, histopathology can confirm the diagnosis and grade the tumor.

Treatment of nonunion and malunion is primarily surgical. The goals are to achieve bone union, correct deformity, and restore limb function. Preoperative stabilization may be necessary for severely unstable fractures. Surgical options include: 1) Bone grafting: autogenous cancellous bone graft is commonly used to stimulate osteogenesis. 2) Internal fixation: plates and screws are the most common implants. For nonunion, a compression plate may be used to provide rigid fixation. For malunion, an osteotomy may be performed to correct the deformity, followed by plate fixation. 3) External skeletal fixation: can be used for infected nonunions or when internal fixation is contraindicated. 4) Amputation: may be considered in cases of severe, non-reconstructable nonunion or malunion with intractable pain. The specific surgical approach depends on the bone involved. For example, for a nonunion of the radius, a craniomedial approach is used. The fracture site is exposed, fibrous tissue is debrided, and the bone ends are freshened. A cancellous bone graft is placed, and the fracture is stabilized with a bone plate. Postoperative pain management is crucial, using a multimodal approach with opioids, NSAIDs, and local anesthetics. Physical rehabilitation is essential to restore limb function.

The prognosis for nonunion and malunion is generally good with appropriate surgical intervention. Success rates for achieving union are reported to be 80-90% for nonunions treated with bone grafting and rigid fixation. The prognosis is worse for infected nonunions, with success rates dropping to 60-70%. Malunion correction has a good prognosis, especially if the deformity is corrected early. Negative prognostic indicators include severe infection, poor patient compliance, and concurrent systemic disease. Functional recovery may take several months, and some patients may have residual lameness or osteoarthritis.

Postoperative follow-up is critical. Sutures are typically removed 10-14 days after surgery. Serial radiographs are recommended at 4, 6, 8, and 12 weeks postoperatively to assess healing. Activity is restricted to leash walks for the first 6-8 weeks, with gradual increase in exercise. Physical therapy, including passive range of motion exercises and swimming, is initiated early. Long-term monitoring for osteoarthritis is recommended, especially in cases of malunion correction. In cases of infected nonunion, long-term antibiotic therapy and repeated cultures may be necessary.

Pearls: 1) Always obtain preoperative radiographs in two orthogonal views to fully assess the fracture. 2) Use autogenous cancellous bone graft for nonunions to stimulate healing. 3) For malunion, use CT for precise surgical planning. 4) Ensure rigid fixation to prevent motion at the fracture site. 5) In infected nonunions, obtain deep cultures and start appropriate antibiotics. Pitfalls: 1) Failure to debride all fibrous tissue and necrotic bone can lead to persistent nonunion. 2) Inadequate stabilization can result in implant failure and recurrence. 3) Overlooking concurrent joint disease can lead to persistent lameness. 4) In malunion correction, failure to address rotational deformities can lead to gait abnormalities. 5) Postoperative infection can be catastrophic, so strict aseptic technique is essential.

Perioperative antimicrobial prophylaxis: Cefazolin (22 mg/kg IV) administered 30 minutes before incision and repeated every 90 minutes during surgery. Postoperative antimicrobials: Amoxicillin-clavulanic acid (13.75-22 mg/kg PO q12h) for 7-10 days if infection is present. Analgesics: Opioids such as hydromorphone (0.05-0.1 mg/kg IV q4-6h) or fentanyl CRI (2-5 mcg/kg/hr) for the first 24 hours. NSAIDs: Carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) for 3-7 days. Local anesthetics: Bupivacaine (1-2 mg/kg) as a regional block. Muscle relaxants: Methocarbamol (20-40 mg/kg PO q8h) if muscle spasms are present. Chondroprotectants: Polysulfated glycosaminoglycan (4.4 mg/kg IM or SC twice weekly for 4 weeks) for joint health. Adjust dosages for renal or hepatic impairment.

Landmark studies have established the principles of fracture healing and the management of nonunion. The AO Principles of Fracture Management emphasize the importance of anatomical reduction, stable fixation, preservation of blood supply, and early mobilization. Studies by Fossum and others have demonstrated the efficacy of autogenous cancellous bone grafting in promoting union in nonunions. A study by Tobias and Johnston reported a success rate of 85% for nonunion repair using plate fixation and bone grafting. For malunion, corrective osteotomy and plate fixation have been shown to improve limb function in 90% of cases. The use of external skeletal fixation is recommended for infected nonunions, with success rates of 70-80%. Recent advances in biological fixation, such as locking plates, have improved outcomes. Consensus guidelines from the ACVS and ECVS recommend a multimodal approach to pain management and early rehabilitation to optimize outcomes.