Fractures in the Horse. Группа авторов
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reconstruction of a complex fracture should not be attempted unless there is at least 180° of the cortex available to support axial weight bearing and load sharing with any implants [180]. Cortical discontinuity or comminution results in a gap at the fracture site such that there is no fracture compression with applied axial loads. A fracture gap promotes cyclic bending or torsion of the implant with the fulcrum at the level of the fracture and results in eventual failure of the implants [180]. Many complex long bone fractures that are not considered repairable in the adult horse are repairable in the foal because of lower body weight and propensity for rapid healing [172,181–184] (Chapter 37).
Displacement
The distinction between non‐displaced, minimally displaced and displaced fractures is often arbitrary and can be difficult to define radiographically. Complete oblique and spiral fractures of the proximal long bones (humerus, radius, femur and tibia) can displace markedly due to the forces placed on the fragments by associated large muscles [180]. Non‐displaced or minimally displaced fracture lines may not be obvious on radiographs obtained in the acute stage [185]. Taking multiple radiographic projections (for example, as recommended in the diagnosis of third tarsal bone slab fractures) or repeating radiographs in 5–10 days may help to confirm clinical suspicion of a non‐displaced or minimally displaced fracture. The use of additional imaging modalities such as ultrasound (particularly for pelvic and scapular fractures), nuclear scintigraphy (for incomplete fractures of the proximal portions of the limbs and axial skeleton), computed tomography and magnetic resonance imaging (standing systems likely to be preferred in most cases) if available and applicable may help to identify and better characterize displacement [147].
Contamination
A closed fracture is one in which the skin is intact over the fracture site, and an open fracture is one in which the skin is disrupted. However, intact skin that has been extensively bruised or stretched becomes less of a barrier to bacterial invasion. Open fractures carry a significantly poorer prognosis than those that are closed [172, 182, 186]. In one study, closed fractures were 4.2 times more likely to remain uninfected and horses were 4.6 times more likely to leave the hospital following internal fixation than open fractures [187]. A follow‐up retrospective study from the same institution did not find an association between open fractures and surgical site infection; however, the authors postulate that a relationship may have been missed due to the inclusion of fewer open fracture cases in the more recent study [188]. In human traumatology, open fractures are subdivided into types I–III based on the length of skin opening and soft tissue damage [171]. Most equine open fractures are type I (skin laceration <1 cm) or type II (larger skin laceration, but little tissue loss). Type III is defined as an open fracture with extensive lacerations, massive skin defects and gross contamination [180]. The majority of horses that sustain type III open fractures are euthanized without an attempt at repair [180].
Articular Involvement
Articular involvement often influences treatment decisions and can affect prognosis depending on the location of the fracture. Disrupted articular congruity can predispose to development of osteoarthritis and reduce the prognosis for return to athletic activity. For example, conservative management of all but the smallest supraglenoid tubercle fractures typically results in residual lameness secondary to osteoarthritis of the shoulder joint [189]. In other anatomic locations, articular involvement does not appear to be as detrimental. For example, 98% of horses that sustain an incomplete fracture of the proximal aspect of the third metacarpal bone return to athletic function, even though these fractures typically involve the carpometacarpal joint [190].
Figure 3.20 Salter–Harris physeal injury classification. Type I injuries are confined to the physis. Type II injuries traverse along the physis and then exit into the metaphysis. Type III and IV injuries involve the epiphysis and adjacent articulation. Type III injuries are restricted to the epiphysis and physis, while type IV injuries cross into the metaphysis. Type V injuries are compression fractures of the physis with little or no displacement.
Source: Modified from Richardson et al. [177].
Other Factors
Involvement of additional bones can substantially impact prognosis. For example, an axial proximal sesamoid fracture occurring concurrently with a displaced lateral condylar fracture is associated with a poor prognosis for return to athletic function [177]. Disruption of vasculature supplying the fracture site can slow or prevent healing or lead to avascular necrosis precluding the possibility of salvage. Examples include transection of the popliteal artery in femoral fractures [191] and thrombosis of palmar/plantar digital arteries in acute fetlock breakdown injuries [192].
Pathologic fractures occur through abnormal or diseased bones at lower loads than those that would cause fracture in healthy bones. Among the more common examples of conditions that predispose to complete fracture are neoplasia (e.g. osteosarcoma, lymphosarcoma and chondrosarcoma) and osteomyelitis [193–196]. Regionally, in California, a silicate‐associated systemic osteoporosis syndrome known as ‘bone fragility’ manifests with pathologic fractures [197]. Most affected horses have concurrent pulmonary silicosis and a history of exposure to soil containing cytotoxic silica dioxide crystals [198, 199]. Horses with pituitary pars intermedia dysfunction (PPID) or chronic hyperglucocorticoidism are also susceptible to pathologic fractures [200]. Fractures associated with a pre‐existing stress fracture or subchondral stress remodelling are also considered pathologic fractures.
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