CHAPTER 16 Kathryn A. Seabaugh, DVM, MS, Diplomate ACVS and ACVSMR and Gary M. Baxter, VMD, MS, Diplomate ACVS Wounds in the horse frequently involve synovial structures. Prompt recognition of synovial involvement, and treatment, are important to prevent or resolve synovial infection. The primary goals of treatment are to remove bacteria, foreign material, and inflammatory mediators from the synovial structure, through the use of high‐volume lavage and administration of broad‐spectrum antimicrobial drugs. Methods of diagnosis and treatment of contaminated or infected synovial structures are detailed in this chapter. Horses frequently sustain injury. Forty percent of horse owners responding to a survey in the United Kingdom reported that their horse had suffered an injury within the previous 12 months.1 Of those injuries, 54% were wounds. Wounds of the limb are especially at risk of involving a synovial structure (joint, tendon sheath, or bursa). Wounds that communicate with a synovial cavity can result in synovial infection, which may lead to permanent disability. Septic synovitis can result in irreversible cartilaginous damage, capsular fibrosis, and intrathecal adhesions if the infection is not eliminated rapidly (Figure 16.1).2 Early recognition of synovial involvement to prevent the development of infection, together with appropriate treatment, is the best protection against the negative consequences that often accompany these wounds. Figure 16.1 An adhesion is present between the superficial digital flexor tendon (SDFT) and the plantar surface of the digital flexor tendon sheath. Although any synovial structure of the horse might be breached by a laceration or a puncture, the synovial cavities of the distal aspect of the limb (i.e., distal to and including the carpus and tarsus) are most frequently wounded.3–5 Synovial structures most often penetrated include the following: the digital flexor tendon sheath, the metacarpo/metatarsophalangeal joint, and the tarsal joints.5–7 Although most injuries involve a single synovial structure, large wounds, particularly those of the foot, shoulder, and tarsal regions, may result in contamination of multiple synovial structures. Joints are closed, sterile spaces of variable size and shape located around opposing bony surfaces that enable the limb to flex and extend. The ends of bones within joints are covered with hyaline cartilage and are usually stabilized by a combination of collateral ligaments, a joint capsule, tendons, and muscle. The joint capsule is composed of an outer fibrous layer and an inner synovial membrane. The fibrous joint capsule is attached to bone and/or soft‐tissue structures on the perimeter of the joint and serves to protect the joint cavity from injury. The synovial membrane is composed of intimal and subintimal layers that line the synovial capsule. The cells within the intimal layer are responsible for producing components of the synovial fluid, for absorbing products from the joint cavity, and for exchange of ions and molecules between blood and synovial fluid.8 The subintimal layer contains the vascular supply and nerves to the joint.8 Proper function of the synovial membrane is especially important for joints because the synovial fluid is vital for maintaining the health of the articular cartilage. Synovial fluid contains lubricants (i.e., hyaluronan and lubricin) that ensure frictionless movement of opposing bone and/or soft tissue.8,9 The close proximity of the fibrous layer of the joint capsule of many synovial cavities to the skin results in damage to the joint when the overlying skin is lacerated. Although a wound can penetrate the fibrous capsule without penetrating the inner synovial membrane, this situation is observed uncommonly in horses. Complications of joint infection in horses include damage to articular cartilage, leading to osteoarthritis and lameness, fibrosis of the joint capsule, resulting in reduced range of motion, and chronic osteomyelitis.4 Tendon sheaths and bursae serve primarily to protect and promote the normal gliding motion of tendons. Bursae are located between a tendon and an adjacent bone in a high‐motion area; examples are the navicular and the bicipital bursae. In contrast to joints, bone surfaces associated with bursae are covered with fibrocartilage, rather than hyaline cartilage. Tendon sheaths are located in areas of high motion, such as the palmar/plantar regions of metacarpo/metatarsophalangeal joints, and serve a function similar to that of bursae. Bursae, unlike tendon sheaths, do not completely surround the tendinous structure, and are located on one side of the tendon only, between the tendon and the underlying bony prominence.10 Annular ligaments and retinaculi (adjacent to many sheaths and bursae) overlie the synovial cavity and form an inelastic canal through which the tendon glides.11 The inner synovial membrane and outer fibrous layer of tendon sheaths and bursae are anatomically similar to those of joint capsules. The primary anatomic difference is that most tendon sheaths and bursae have one or more annular ligaments and/or retinaculi that function to stabilize the tendon. Damage to these supporting structures can result in “subluxation” of the tendon from the synovial cavity, the most common subluxation being distraction of the superficial digital flexor tendon from the calcaneal bursa.4,12 The synovial fluid within a tendon sheath or bursa is similar to that within joints and possesses many of the same properties and functions. Lubrication within tendon sheaths and bursae is possibly even more critical to pain‐free movement than is lubrication within joints due to the high mobility of the tendon within the tendon sheath or against the bursa.11,13 Complications of infection of tendon sheaths and bursae include formation of adhesions within the sheath, septic and non‐septic tendonitis, and osteomyelitis of the adjacent bone, leading to restricted movement and chronic lameness (Figure 16.2). Figure 16.2 This skyline radiograph is from a horse that sustained a puncture wound to the foot approximately 6 weeks earlier. Severe lysis of the navicular bone is evident, consistent with chronic infection of the navicular bursa. A laceration or puncture into synovial structures often introduces bacteria and contaminants (e.g., hair, dander, dirt) directly into the synovial space (Figure 16.3). Provided that appropriate treatment is performed early, infectious arthritis, tenosynovitis, or bursitis can be avoided.3,4 Early diagnosis of and treatment for an open synovial structure is important to provide the best chance for the horse to return to pre‐injury‐level athletic performance. Figure 16.3 An arthroscopic view of the distal interphalangeal (coffin) joint that sustained a penetrating wound 24 hours earlier. Note the pieces of hair and debris within the joint. These foreign bodies could be identified only by endoscopic examination of the joint, and it is unlikely they could have been removed by lavage alone, without arthroscopic observation. Source: Baxter 2004.4 Reproduced with permission of Elsevier. The size of the bacterial inoculum required to produce a synovial infection varies according to: (1) the virulence of the bacteria; (2) the specific joint, tendon sheath, or bursa involved (i.e., size of the inoculum in relation to the size of the synovial cavity); (3) the severity of the concurrent soft‐tissue trauma; (4) the immune response of the horse; and (5) whether or not foreign material is present.14,15 Experimentally, 1.6 × 106 colony‐forming units (CFU) of Staphylococcus aureus injected into the tarsocrural joint of normal horses caused synovial infection.16 In another study, as few as 33 CFU of S. aureus, combined with polysulfated glycosaminoglycans (PSGAGs), inserted into the middle carpal joint of horses resulted in synovial infection.17 The results of these studies indicate that a very small bacterial inoculum, under the right conditions, is capable of causing synovial infection. Bacterial colonization of the synovial membrane incites an inflammatory response intended to re‐sterilize the synovial structure.18 The inflammatory cascade produces a multitude of cytokines, proteolytic enzymes, and other inflammatory mediators from a variety of cell types within the synovial cavity. These inflammatory mediators serve to increase vascular permeability within the synovium, attract neutrophils and monocytes to the synovial space, degrade hyaluronan within the synovial fluid, and promote the formation of fibrin.18 Reactive oxygen metabolites and proteolytic enzymes derived from infiltrating neutrophils, chondrocytes, synoviocytes, monocytes, macrophages, and the bacteria may contribute to the degradation of hyaluronan and depletion of proteoglycans in the articular cartilage.19,20 In one in vitro study, exposure of cartilage explants to Escherichia coli or S. aureus caused a 28% and 83% loss of glycosaminoglycan from cartilage, respectively, and induced death of chondrocytes within 48 hours of exposure.21 Synovial sepsis often results in the formation of a fibrinocellular clot, referred to as pannus, which is similar to the biofilm found on the surface of infected bone.15 Pannus impedes effective treatment of synovial sepsis by protecting foreign debris and devitalized tissue, by serving as a bacterial growth medium, and by inhibiting delivery of drugs to the site of infection.15 Although pannus is a term used primarily to describe what occurs within infected joints, a similar yet often more substantial deposition of fibrinous material often occurs within an infected tendon sheath or bursa. Fibrin is often abundant within an infected tendon sheath or bursa and should be removed because it may serve as a scaffold for the formation of fibrous tissue/adhesions within the structure. The longer the duration of the infection, the greater is the likelihood of permanent damage to the synovial structure. Alterations in synovial fluid usually occur early during infection, often before clinical signs of infection are present, and can impede function of the synovial membrane and interfere with nutrition of chondrocytes.22 Chronicity can lead to a prolonged inflammatory response by the synovium, which may contribute to synovial hyperplasia and hypertrophy, vascular proliferation, thrombosis of synovial vessels, pannus, and fibrosis of the joint capsule.15 Prolonged infection of a joint may lead to disease of the articular cartilage, resulting in the loss of proteoglycans and exposure of the cartilage to mechanical damage and enzymatic breakdown.20 Irreversible damage to cartilage is the end stage of infectious arthritis and contributes to impaired joint function and permanent lameness (Figure 16.4). Chronic infection within a tendon sheath or bursa can lead to fibrosis of the synovial lining, tendonitis with superficial fraying of the tendon, formation of adhesions, development of fibrotic masses within the sheath, and osteomyelitis of bone within the synovial cavity.4,11,13 Figure 16.4 This postmortem sagittal section of the phalanges demonstrates the damage that can occur with chronic infection of the proximal interphalangeal joint secondary to a wound. The articular cartilage was completely lost from all joint surfaces, and bone within the middle phalanx was lysed (arrow). Multiple retrospective studies have provided mixed reports regarding the effect of timeliness of treatment on the outcome of horses with infected synovial structures caused by a wound.23–28 A few older studies found that horses with an infected synovial structure had a more favorable response to treatment if treatment was initiated within 36 hours of injury.27,28 Fraser and Bladon (2004) found that horses with a laceration involving the digital flexor tendon sheath were more likely to return to athletic function if the sheath was lavaged and debrided endoscopically within 36 hours of injury.27 Gibson et al. (1989) reported a 65% incidence of survival when horses with an open joint were treated within 24 hours, whereas only 38.5% of horses survived when treatment was initiated more than 48 hours after injury.28 Wereszka et al. (2007) found that horses with septic tenosynovitis were significantly more likely to survive if treated during the first day after clinical signs of synovial infection were first observed than were horses that did not receive treatment within 10 days after clinical signs of infection first appeared.26 Promptness of treatment, however, did not seem to affect the incidence of survival of horses for which treatment was initiated between days 1 and 10 of observation of clinical signs of synovial infection. More recent reports have found no significant difference in the incidence of survival or the likelihood of return to function based on the time elapsed between the onset of clinical signs of synovial infection and initiation of treatment.7,23,24,29 Although early treatment of horses with synovial infection is obviously desirable, the outcome for horses with delayed treatment of synovial sepsis may still be favorable. In most cases, a wound is the reason why a horse with a septic synovial structure is presented to a veterinarian. If the wound is fresh, the horse may be fully weight‐bearing on the injured limb. A small wound may be missed until lameness or a swelling is observed (Figure 16.5). If the wound and synovial cavity continue to drain, lameness may be subtle, even when the wound is chronic. When infection becomes established within a closed synovial structure, however, lameness usually becomes severe.30 Figure 16.5 This horse was seen backing into a pitchfork 1 week prior. The small puncture wound was not identified until the area was clipped. The puncture communicated with the digital flexor tendon sheath. Any wound near a synovial structure should be assumed to communicate with that synovial structure until disproven. The anatomic location of joints and tendon sheaths is well known, but some clinicians may not appreciate the magnitude of the various synovial pouches (Figure 16.6). For example, the palmar pouch of the metacarpophalangeal joint extends further distally on the proximal phalanx than most clinicians realize. The location of many bursae can be elusive, thwarting recognition of their involvement in a wound. Table 16.1 gives a list of bursae that could be involved in a wound. Figure 16.6 Important synovial structures associated with the carpus (a), tarsus (b), and distal aspect of the limb (c) . Illustrations by Ray Wilhite. Table 16.1 Bursae to consider when evaluating wounds in the horse. Bursae are located between the listed tendon/ligament and bone. Wounds near synovial structures must be cleaned thoroughly after the hair from the wound’s edge has been clipped. After the wound is cleaned, it should be explored, once the clinician has donned sterile gloves, using caution to avoid carrying contamination deeper into the wound.30 Proteinaceous fluid flowing from the edge of a wound often appears similar to synovial fluid; consequently, the presence of such fluid within a wound is not confirmation that the wound communicates with a synovial structure. Palpation or visual identification of the surface of a joint or tendon confirms that the wound communicates with a synovial structure. Contrast radiographic and/or ultrasonographic examinations may be necessary to assess the integrity of a synovial structure. If communication between a wound and a synovial structure cannot be determined by physical examination, further diagnostic tests may be necessary. Imaging of the region and cytologic evaluation of fluid obtained by synoviocentesis from synovial structures adjacent to the wound may provide additional clues as to whether a synovial structure has been breached. When performing synoviocentesis, the needle should be placed at a site remote from the wound to minimize the risk of iatrogenic contamination. When cellulitis is present, the risks of synoviocentesis should be weighed against its benefits. Cleaning the wound, bandaging the limb, and administering an antimicrobial drug for 24 hours prior to synoviocentesis may be advisable in some cases to reduce the risk of iatrogenically contaminating a synovial structure. Synoviocentesis should be performed only after properly preparing the site and using aseptic technique. Synovial fluid can be aspirated from most synovial structures, but if the wound and synovial cavity are open and draining, collecting fluid may be difficult. The presence of fibrin within the synovial structure may also complicate the collection of fluid. When a sample cannot be obtained, sterile isotonic saline solution or a balanced electrolyte solution can be injected into the joint to facilitate aspiration of fluid.32 Although the collected sample is diluted, making cell counts inaccurate, cytologic examination of the sample may still be helpful in determining if the synovial structure is contaminated, and fluid obtained can be used for bacterial culture. The concentration of urea in synovial fluid mimics that in serum, so paired samples could be used to determine the degree of dilution.33 After aspirating synovial fluid for bacterial culture and cytologic examination, the synovial structure should be distended with isotonic saline solution or a balanced electrolyte solution to determine if it communicates with the nearby wound. Fluid is injected into the synovial structure while the wound is observed for presence of fluid flowing from it (Figure 16.7). Communication between the synovial structure and the wound should be considered unlikely if fluid fails to flow from the wound when the synovial structure is pressurized. If the wound is in a high‐motion area, the limb should be moved through an exaggerated range of motion to ascertain that fluid does not egress from the wound when the limb is placed in different positions. An antibiotic should be infused into the structure prior to withdrawing the needle. Figure 16.7 A needle was inserted into the proximal interphalangeal joint at a location distant from the wound. Isotonic saline solution instilled into the joint flowed from the wound. Elevation of total protein in synovial fluid can cause the sample of synovial fluid to clot if the collection vial does not contain an anticoagulant, therefore, synovial fluid should be collected into an ethylenediaminetetraacetic acid (EDTA) blood tube.32 Inflamed or infected synovial fluid often contains red blood cells, but normal synovial fluid should contain few, if any.32 Synoviocentesis may result in some hemorrhage into the synovial structure, which is another reason why fluid should be collected in an EDTA blood tube. Normal synovial fluid should contain less than 1000 nucleated cells/μL, of which most should be mononuclear cells (i.e., macrophages and lymphocytes).32 The concentration of total protein in the synovial fluid should normally be approximately 20–25% of the horse’s concentration of plasma protein.34 Generally, this concentration should be less than 2.0 g/dL. A differential cell count is also important for a complete assessment. Neutrophils should account for less than 10% of the cellular content.32 Nucleated cell counts associated with non‐septic osteoarthritis and traumatic synovitis are reported to be between 5000 and 10 000 cells/μL.34 Characteristics of synovial fluid consistent with synovial infection are reported to include a nucleated cell count greater than 30 000 cells/μL, of which more than 90% are neutrophils, and a concentration of total protein greater than 4.0 g/dL.34 With experimentally induced septic arthritis, nucleated cell counts in the synovial fluid increased significantly within 8 hours, in one study, after the joints were inoculated with bacteria (range 23 000–37 000 cells/μL); by 12 hours, 80% of the infected joints had a white blood cell count greater than 50 000 cells/μL.35 Substantial increases in nucleated cell counts were seen by 30 hours in another study, even after a corticosteroid had been administered into the joint.22 In both of these studies, the most consistent findings indicating that a joint was infected were a concentration of neutrophils greater than 90% and a pH less than 6.9.22,35 Total protein may be elevated in non‐infectious inflammatory conditions, but it generally remains less than 4.0 g/dL.32,34 The concentration of total protein in an infected synovial structure has been used as a prognostic indicator.23 A retrospective analysis found that the preoperative concentration of total protein in the synovial fluid could be used to predict survival after endoscopic treatment for synovial infection.23 The cut‐off value indicating that the horse was likely to survive was 5.5–6.0 g/dL.23 Bacteria are seen during cytologic examination of fluid obtained from an infected synovial structure in approximately 25% of cases.5,32 Consequently, the “gold standard” for definitive diagnosis of septic arthritis is a positive bacterial culture. If contamination or infection of a synovial structure is suspected, synovial fluid aspirated from that structure should be placed into a dry, sterile tube (i.e., red top, or clot tube) for bacterial culture. When possible, synovial fluid should be placed into a blood culture enrichment medium. Using a blood culture enrichment medium resulted in 79% positive culture whereas other methods of culture resulted in 23–28% positive culture.36 Although the primary benefit of a positive culture is to help direct antimicrobial therapy, a positive bacterial culture has also been reported to be a prognostic indicator. In one report, only 50% of horses with a positive culture from synovial fluid survived to discharge, whereas 71% of horses that did not have a positive culture survived.6 In that report, culture of S. aureus was associated with a poor prognosis for return to function.6 In another study, culture of S. aureus was associated with persistent infection.24
Diagnosis and Management of Wounds Involving Synovial Structures
Summary
Introduction
Location of Injuries
Synovial anatomy and physiology
Joints
Tendon sheaths and bursae
Pathogenesis of synovial infections
Time to treatment
Clinical findings
Wound assessment
Name
Tendon/ligament
Bony structure
Further information
Cranial nuchal bursa
Nuchal ligament (funiculus)
Atlas (first cervical vertebra)
Caudal nuchal bursa
Nuchal ligament (funiculus)
Axis (second cervical vertebra)
Supraspinous bursa
Supraspinous ligament
Spinous process of thoracic vertebrae (~T3–T6)
Subtendinous bursa of infraspinatous muscle
Infraspinatous muscle (tendon)
Greater tubercle of humerus
Bicipital bursa
Biceps tendon
Intermediate tubercle and intertubercular groove of humerus
Also called intertubercular bursa
Subtendinous bursa of subscapularis muscle
Subscapularis muscle (tendon)
Lesser tubercle of humerus
Subtendinous calcaneal bursa (SCB)
Superficial digital flexor tendon
Tuber calcaneus and gastrocnemius tendon
Also called intertendinous bursa
Communicates with gastrocnemius bursa 50–100% of the time and the subcutaneous calcaneal bursa 39% of the time31
Gastrocnemius bursa (GB)
Gastrocnemius tendon
Proximal tuber calcaneus
Navicular bursa
Deep digital flexor tendon
Navicular bone
Subtendinous bursa of the deltoid muscle
Deltoid muscle
Deltoid tuberosity of the humerus
Cunean bursa
Cunean tendon (from cranial tibial muscle)
Central and third tarsal bones, medial
Trochanteric bursa
Medial gluteal muscle
Greater trochanter of the femur
Synoviocentesis
Synovial distension
Synovial fluid analysis
Bacterial culture
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