27 Jan 2014
Andy Fiske-Jackson
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ANDY FISKE-JACKSON describes the different stages of superficial digital flexor tendon injury in horses, as well as some of the therapies available and when to best use them
Tendon injuries – particularly those involving the superficial digital flexor tendon – are common in sports horses and the attending veterinarian is faced with a myriad of different treatment options. A full understanding of the healing process allows timely interventions with appropriate therapies. Over the years, a number of therapies have risen to prominence, but evidence behind their efficacy has often been lacking. This article describes some of the treatments available and where they fit into the rehabilitation process.
TENDON injuries are common in equine veterinary practice – especially within the sports horse population. They can be caused by overstrain or percutaneous injury.
Overstrain injuries result from either a sudden overwhelming stress through the tendon or following a process of clinically silent molecular degeneration, which weakens it. The latter is important with superficial digital flexor tendon (SDFT) injuries, as often, the contralateral “uninjured” leg requires treatment and monitoring as well.
The SDFT functions close to failure with a low safety margin, which may explain the high incidence of partial rupture of this specific tendon. Following injury, the repair process is slow, with fibrous scar tissue formation. This scar tissue is similar to that forming in skin wounds and does not have the same matrix composition as the normal tendon.
Over time, the repair tissue becomes mechanically strong, but there is an increase in elastic modulus (Figure 1) compromising its functional efficiency. The stiffer scar tissue puts increased strain on adjacent areas of the same tendon, increasing the risk of reinjury.
The diagnosis of tendon injury is not usually challenging, with the classic signs of inflammation being heat, pain and swelling over the affected structure. Lameness is often severe in the acute phase, but rapidly reduces over the ensuing one to two weeks. With more severe SDFT injuries, a hyperextended metacarpophalangeal (MCP) joint will be seen, with more subtle injuries requiring careful palpation to establish the site of injury.
In the acute stage, cold therapy is required to cause vasoconstriction, reduce proteolytic enzymatic activity, decrease influx of inflammatory mediators and provide pain relief.
The author recommends 20 minutes of cold hosing three to four times a day.
While labour-intensive, the author considers cold hydrotherapy to be superior to ice packs, providing increased contact and evaporation. Nevertheless, cold boots that provide a genuine reduction in temperature are useful in busy yards, while the use of hypertonic cold water (5°C to 9°C) spa bath hydrotherapy may provide the gold standard treatment (Hunt, 2001). The author also recommends the continued use of cold therapy after each exercise session during the ensuing controlled exercise programme.
Pressure applied in the form of a padded bandage reduces oedema by increasing hydrostatic pressure. The combination of repeated hosing and bandaging presents a conundrum, with repeated drying of the limb required prior to bandaging. The use of thick, reusable Gamgee is more cost-effective than repeat modified Robert-Jones bandages.
If the injury is severe, with concurrent hyperextension of the MCP joint, a splint may be applied to the palmar aspect of the limb. Layered casting tape modelled on the contralateral (uninjured) limb can be used to create a customised splint extending from the carpus to the bulbs of the heel on the palmar aspect of the limb. This should be applied over a thick, padded bandage.
Alternatively, a distal limb cast applied over a thick bandage (“bandage cast”) can be used and the author has applied these successfully to standing (sedated) horses. If a splint or cast is required, cold therapy becomes largely infeasible. The horse should undergo a minimum period of two weeks’ box rest, regardless of the severity of the injury.
Systemic corticosteroids (dexamethasone 0.1mg/kg IV) are beneficial if administered during the first 24 to 48 hours after injury. After this, they should be avoided as they inhibit fibroplasia and tendon repair. Phenylbutazone has greater analgesic than anti-inflammatory properties, thus its dose and duration of treatment should be dictated by the horse’s comfort.
Ultrasonographic examination of the lesion should be performed one to two weeks following injury as the lesion can expand during the first few days with the action of proteolytic enzymes. Ultrasound evaluation is important, both as a reference point and as a prognostic indicator; the greater the severity of the initial lesion, the worse the prognosis for return to work (Marr et al, 1993).
Serial ultrasound scans should be performed every two to three months (Table 1) and before any change in the exercise level. At the initial ultrasound scan, the suitability of the tear for intralesional medication (for example, mesenchymal stem cells) can be assessed. The ideal lesion would be a first time injury appearing as a distinct hypoechoic region within the tendon (Figure 2).
After one to two weeks, a reduction or absence of lameness will be seen alongside resolution of the signs of inflammation, but the tendon will remain palpably enlarged and soft. Angiogenesis and fibroplasia will be occurring and our goal is to optimise the organisation of the scar tissue. At this stage, the repair contains a higher proportion of collagen type-three than normal tendon.
Early progressive mobilisation helps maintain gliding function and optimises collagen remodelling. A suggested controlled exercise programme is shown in Table 1, but this must be adapted on the basis of serial ultrasonographic monitoring and clinical signs, such as lameness, heat and swelling.
The reparative phase merges with the remodelling phase and involves the transformation of collagen typethree to a higher proportion of collagen type-one fibres, which are thicker and have increased cross-linking.
Clinically, this will manifest as a reduction in the tendon size and increased stiffness; this may display as reduced fetlock extension.
During this phase, the goal is to promote remodelling, but prevent reinjury through the controlled exercise programme.
Intralesional therapies are primarily aimed at “educating” the reparative tissue to be more functional. They are used in conjunction with a controlled exercise programme, which aims to provide the functional stimulus to modulate the repair process in terms of both the structural morphology of the repair tissue and the molecular composition of the matrix.
Mesenchymal stem cells
Smith et al (2003) first described the reimplantation of autologous mesenchymal stem cells (MSCs), which had been expanded in numbers in vitro into the damaged tendon of the same horse. SDF tendinitis lesions usually occur in the central core of the tendon, providing a natural enclosure for implantation (Richardson et al, 2007). At the time of implantation, the core lesion is partly filled with granulation tissue, providing a highly vascularised scaffold capable of nutritionally supporting the cells.
National hunt racehorses with SDF tendinitis treated with intralesional MSCs have been shown to have a reinjury rate of just 27 per cent after three years (Godwin et al, 2012). This compares favourably to other studies assessing the reinjury rate following conservative therapy. It is crucial owners appreciate this treatment does not reduce the length of the convalescence period, but improves the quality of the repair.
The optimum time to implant MSCs is after the initial inflammatory phase and before fibrous tissue has formed. This requires aspiration of bone marrow from the sternum or tuber coxae (Figure 3) at, or soon after, the first ultrasound scan, allowing implantation (following expansion in culture for approximately three weeks) one month after injury.
Too long a delay before aspiration of bone marrow and subsequent treatment can result in infilling of the defect with granulation tissue and an inability to inject the cells. Implantation of MSCs within one month of injury also appears to be associated with a reduction in reinjury rate in sports horses compared to later implantation (VetCell data). The 10 million to 40 million MSCs are suspended in 2 x 1ml aliquots of autologous bone marrow supernatant, providing a convenient volume for injection.
The horse is sedated and a repeat ultrasonographic examination is performed. A high four-point nerve block is placed with an additional subcutaneous block superficial to the fascia. Following aseptic preparation of the limb, the cells are implanted under ultrasound guidance at two to four sites proximodistally within the lesion (Figure 4). A thick distal limb bandage is placed before the horse is discharged.
Despite the suggested reduction in reinjury rate, the exact mechanism of action remains unclear. MSCs have been shown to inhibit two of the most important proinflammatory cytokines – tumour necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ) and increase expression of the suppressive cytokines, thus they appear to exert an immunomodulatory effect on the healing process (Aggarwal and Pittenger, 2005). It is, therefore, doubtful that MSCs differentiate into tenocytes and synthesise a tendon-like matrix; more likely, they exert a trophic or paracrine effect on the resident cells, thus modulating the repair.
Platelet-rich plasma
An advantage of platelet-rich plasma (PRP) is cost and that it is a “stall side” treatment; it is produced and implanted into the lesion during the same sedation period. PRP is blood plasma with a concentrated platelet count, usually two to four times the normal levels. It is generated through a simple centrifugation or filtration process from venous blood. As with MSCs, the PRP is injected into the lesion under ultrasound guidance. Platelets are a natural reservoir of growth factors, including platelet-derived growth factor (PDGF), transforming growth factor β (TGF-β) and vascular endothelial growth factor (VEGF).
Following injection, PRP clots through exposure of the platelets to the basement membrane of cells in damaged tissue. The resulting fibrin scaffold facilitates cell migration into the lesion and provides a mechanism to retain growth factors at the site of the injury.
A study compared the biochemical, biomechanical and histological tissue properties of SDF tendons following treatment of surgically created lesions with either PRP or saline (Bosch et al, 2010).
The lesions were injected seven days post-surgery and the six horses in the study were euthanised after 24 weeks. Subsequent analysis found the PRP-treated tendons had a higher strength at failure, but a higher elastic modulus (Figure 1).
Although the lesions produced had ultrasonographic and clinical similarities to naturally occurring lesions, the pathophysiology is different. Also, the timing of PRP injection may be important in terms of the phase of repair. Tendon injuries in practice are frequently treated many weeks after injury; PRP may not be as beneficial if administered later in the healing process.
Consequently, the use of PRP in acute and chronic tendon injuries needs to be assessed in double-blinded, placebo-controlled clinical trials. PRP is generated by drawing whole blood aseptically from the horse into a syringe containing anticoagulant. The blood is collected as atraumatically as possible, using an 18 gauge or larger needle, to avoid activating the platelets prematurely by exposing them to excessive shear forces. The PRP is subsequently produced either by filtration – for example, equine platelet enhancement therapy (E-PET; Figure 5) – or centrifugation. Approximately 8ml of PRP is generated, which can be immediately injected into the lesion under ultrasound guidance in a similar way to that described for MSC implantation.
Hyaluronic acid and polysulphated glycosaminoglycans
A study by Dyson (2004) compared the outcomes following intralesional injection of hyaluronic acid (HA) or polysulphated glycosaminoglycans (PSGAG) into SDFT core lesions with conservative therapy. It was found that the incidence of reinjury in treated limbs was 43 per cent to 44 per cent, with no apparent benefit of treatment with either HA or PSGAG compared with controlled exercise alone.
Desmotomy of the accessory ligament of the SDFT
The rationale for transection of the accessory ligament of the superficial digital flexor tendon (ALSDFT) is to lengthen the ALSDFT-SDFT complex, thereby reducing the peak loads on the SDFT at full weight bearing during the chronic phase when the horse returns to work (Hogan and Bramlage, 1995).
There is some controversy of the efficacy of the procedure as the criteria for success in different studies assessing it has varied. One prospective study found not only was there no benefit in performing the procedure with respect to the SDFT, but the treated horses were 5.5 times more likely to develop suspensory ligament desmitis (Gibson et al, 1997).
The combination of desmotomy of the ALSDFT with intralesional injections of insulin-like growth factor-1 has demonstrated a return to racing of 61 per cent to 80 per cent with a reinjury rate of 53 per cent to 70 per cent (O’Meara et al, 2010; Witte et al, 2011).
Tendon splitting
Tendon splitting was initially advocated for the treatment of chronic SDF tendinitis to improve blood flow, but subsequent research demonstrated excess granulation tissue formation, trauma to the tendon tissue and persistent lameness following treatment (Stromberg et al, 1974).
It was subsequently suggested to be beneficial in acute cases by decompressing the core lesion through removal of serum or haemorrhage and enhancing vascular ingrowth. It can be performed standing or under general anaesthesia, usually under ultrasonographic guidance.
A No 11 blade can be used, or to reduce damage to adjacent tissue, a 23 gauge needle in multiple locations; the latter can be combined with intralesional treatments.
While a multitude of treatments are available for tendon injuries, the evidence behind them is often lacking. In the author’s opinion, the most important treatment is initial cold therapy and rest, followed by a controlled exercise programme with regular ultrasonographic monitoring. The author uses intralesional MSCs where appropriate in an attempt to reduce the reinjury rate.
Figure 1. The functional properties of the healing tendon.
Figure 2. Transverse (2a) and longitudinal (2b) ultrasonographic images of a superficial digital flexor tendon (SDFT) core lesion, two weeks post-injury.
Figure 2. Transverse (2a) and longitudinal (2b) ultrasonographic images of a superficial digital flexor tendon (SDFT) core lesion, two weeks post-injury.
Figure 3. Aspiration of bone marrow from the sternum.
Andy Fiske-Jackson
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