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Monitoring Bone Healing

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Most derangements in fracture healing require surgery or further surgery and a change in fixation technique. Exogenous therapies may also be of benefit (Section Exogenous Factors That Influence Fracture Healing). The point at which revision must be considered is difficult to determine objectively, but persistent or progressive pain and/or instability are pivotal in decision‐making.

Fractures with impaired healing are usually described as delayed or non‐unions. A delayed union requires increased time, but healing will occur without surgical (or further surgical) intervention [6]. In adult horses, normal cortical bone healing is thought to occur within four months, and in foals within three months [16]. In contrast, a non‐union cannot heal without surgical intervention [6]. Mechanical factors, principally lack of stability, are the most common causes of non‐union; however, biological factors including impaired vascularity (usually due to severe soft tissue damage) and infection can play a role. Non‐unions have been defined by their radiographic appearance and clinical symptoms divided into biological reactive and biological non‐reactive, non‐viable unions [6]. Biological reactive non‐unions are further classified according to radiographic appearance: hypertrophic non‐unions (elephant foot non‐unions) have exuberant callus formation due to instability, while oligotrophic non‐unions lack callus. Horses with non‐unions generally have less callus formation and are a milder form of hypertrophic non‐union compared to humans. Biological non‐reactive, non‐viable non‐unions are defined by lack of activity on nuclear scintigraphic examination. This is typically caused by lack of vascularity at the fracture site. Torsion wedge non‐unions fail to heal due to lack of fragment vitality. Comminuted fracture non‐unions are characterized by a devitalized intermediate fragment; the fracture ends are vascular, but the intervening fragment is avascular. Defect non‐unions occur at sites of bone loss or an intervening infected area. Non‐unions when fibrous tissue alone develops within the defect are described as atrophic [6]. In appropriate cases in humans, vascular grafts and stabilizing techniques can be used to overcome non‐union healing. However, the need for immediate weight‐bearing and cost often restrict use of these techniques in horses.

In clinical practice, objective assessment of fracture healing is difficult. Clinicians generally rely on pain and planar imaging (radiographs) to dictate management. Pain is constantly monitored. In cortical bone, the periosteum contains many nerve endings, and in fractures these are activated creating painful stimuli. The associated inflammatory response also increases nociception, and there is evidence that even with fracture repair, there is an ingrowth of nerve endings into the site [34]. Chronic pain frequently reflects instability, and one of the primary goals of repair is to produce a rapid decrease in pain in order to prevent contralateral limb overload (Chapter 14). In most cases, this can be achieved with rigid internal fixation, giving the clinician a good subjective baseline from which to monitor progress. If repair is compromised there is usually instability, and resultant pain is probably the most sensitive indicator of bone healing and construct integrity. Additionally, in humans, although not well characterized in horses, persistent pain leads to a central upregulation of pain sensitivity which can, in turn, lead to chronic dysfunction [35].

Diagnostic imaging is important in monitoring fracture healing in horses. Ultrasound has been used to monitor the soft tissue environment around implants in order to identify potentially infected sites at an early stage (Chapter 14) [36]. Radiography is the most commonly used modality (Chapter 5). Changes in bone density and architecture are monitored. It is common, especially in conservatively treated fatigue fractures, for the fracture gap to appear wider after two to three weeks due to normal osteoclastic function [37] (Figure 6.3). Soft and hard calluses can be monitored and their activity characterized over time. This allows correlation with clinical progress and can help direct rehabilitation (Chapter 15). In delayed unions, the radiographic fracture line is persistent and there is minimal callus; intramedullary opacification may also be evident [16]. Non‐unions lack osseous bridging or callus, the bone ends or margins become diffusely opaque (sclerotic) and blunt, and the fracture line persists [6].

Figure 6.3 Conservatively managed long oblique fracture of the radius (yellow arrows). (a) Presentation. (b) Five weeks post fracture demonstrating osteolysis and widening of the fracture gap and initial periosteal (white arrow heads) and endosteal (black arrow heads) callus formation. (c) Eight weeks post fracture demonstrating continued periosteal and endosteal (trabecular) callus formation resulting in medullary opacification and partial loss of demarcation of the fracture line.

Although it can present practical difficulties, nuclear scintigraphy has been advocated as the most sensitive indicator of vascular integrity at fracture sites [38]. In human medicine, nuclear scintigraphy can also be used to identify and characterize fracture‐related infection. Gallium scans, white blood cell scans and 18FDG‐PET appear to be most sensitive and specific, particularly when combined with computed tomography [36].

Volumetric imaging techniques can also be used to monitor fracture healing. In most cases, this is accomplished through computed tomography that can be used to monitor the fractured gap and the surrounding tissues. This provides more objective information than two‐dimensional radiographs and does not suffer from superimposition of normal and abnormal tissues. Implants create difficulties in interpretation, but metal reduction algorithms aid interpretation/visualization and sequences are being improved [36]. Internal sensors on implants have been developed on an experimental basis and in the future may be of clinical benefit [39].

Fractures in the Horse

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