History
A 3-year-old 473.0-kg (1,040.6-lb) British warmblood gelding intended for general riding was referred for severe left hind limb lameness (grade 4 on a scale1 of 1 to 5) of unknown duration and an acute decompensation over a 24- to 48-hour period. On examination, the horse was bright and alert, and all vital signs were within reference limits. The distal aspect of the left hind limb was diffusely swollen, with marked distention of the digital flexor tendon sheath (DFTS), and a small (0.5 × 0.5-cm) puncture wound was noted at the plantarolateral aspect of the heel bulb of that same limb. Results of ultrasonographic examination of the affected DFTS indicated marked tenosynovitis and effusion, with numerous, large floating, nonshadowing areas of increased echogenicity in the synovial fluid. Synoviocentesis of the affected DFTS yielded a turbid synovial fluid sample. Results of clinicopathologic analyses of the fluid indicated a WBC count of 21 × 109 WBCs/L (reference range, ≤ 1.0 × 109 WBCs/L), total protein concentration of 72 g/L (reference range, 18 to 30 g/L), and lactate concentration of 17.4 mmol/L (reference range, ≤ 3.9 mmol/L). Bacterial culture was performed on a sample of the synovial fluid, the gelding was admitted for tenoscopic lavage of the affected DFTS, and radiographic examination of the distal aspect of the left hind limb was performed (Figure 1).
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Diagnostic Imaging Findings and Interpretation
On the dorsoplantar and dorsolateral-plantaromedial oblique radiographic views, a well-defined radiolucent margin surrounded an elliptical sclerotic osteochondral fragment (approx 1 to 4 mm thick, by 18 mm wide, by 15 mm long) in the axial aspect of the proximal articular surface of the second phalanx (P2; Figure 2). Marked diffuse, extracapsular soft tissue swelling surrounded the proximal interphalangeal joint (PIJ), especially laterally. On the basis of radiographic findings, our differential diagnosis list included fracture, sequestrum, separate center of ossification, or osteochondrosis of the center of the proximal articular surface of P2.
Standing low-field (0.3-T) T1- and T2-weighted MRI was performed on the affected limb and revealed in the subchondral bone of the proximal articular surface of P2 a well-defined, ovoid (approx 2.0 × 1.5-cm) lesion with hypointense signal (but isointense to cortical bone) that was surrounded by a distinct, thin, halo of hyperintense signal (Figure 3). In addition, an irregularly shaped, poorly marginated area of hyperintense signal was evident in the lateral plantar eminence of P2. A thin, tubular lesion with hypointense signal was tracked from the plantarolateral aspect of the proximal surface of P2 toward the location of the puncture wound but could not be traced completely to the limb's surface. The lateral collateral ligament of the PIJ appeared markedly thickened and had increased T2-weighted signal intensity centrally. There was evidence of mild distention of the PIJ synovial cavity and marked effusion of the DFTS, characterized predominantly by T2-weighted, hyperintense signal. Diffuse T1-weighted hypointense and T2-weighted hyperintense signals were present in the subcutaneous soft tissues, especially along the lateral aspect of the limb.
On the basis of findings from diagnostic imaging, trauma involving a fracture of the proximal articular surface of P2 with subsequent sequestrum and involucrum formation was highly suspected. In addition, osteomyelitis or a relatively large, devitalized osteochondritis-like fragment was also considered. The small tract through nearby tissues may have been from a puncture wound or a small fistulous tract.
Treatment and Outcome
Arthrocentesis of the PIJ was performed. The synovial fluid sample was sero-sanguinous and had a WBC count of 11 × 109 WBCs/L, total protein concentration of 76 g/L, and lactate concentration of 11.3 mmol/L. Bacterial culture of the synovial fluid was performed. Neither the DFTS synovial sample nor the PIJ synovial sample yielded any growth on bacterial culture after 48 hours. A grave prognosis was communicated to the owner given the substantial articular and subchondral bone damage of P2, PIJ septic arthritis, and DFTS septic tenosynovitis. The owner elected euthanasia for the horse.
With owner consent, postmortem high-field (1.5-T) MRI (Figure 4) and CT (80 slice; Figure 5) were performed for academic reasons before necropsy, and results further supported the antemortem findings. Necropsy results indicated marked edema of the skin and subcutaneous tissue, with multifocal areas of fibrin deposition consistent with synovial sepsis present in the DFTS and PIJ. A focal, 0.5-cm-diameter dark-gray discoloration was evident at the plantar aspect of the PIJ, approximately 1.5 cm lateral to midline. The center of the proximal articular surface of P2 contained a 2.0 × 1.5-cm area of yellow discoloration with a thin, irregular dark bluish line of incongruity of the articular cartilage. When cut longitudinally, the lesion surface had a semilunar area of necrotic osseous tissue with a red rim, consistent with demarcation of necrotic bone. Necropsy findings were consistent with a bone sequestrum at the proximal articular surface of P2, and the lesion was presumed to have been caused by an unwitnessed traumatic concussive event and septic arthritis, with or without a penetrating injury.
Histologic examination confirmed severe diffuse lymphoplasmacytic and suppurative tenosynovitis of the DFTS and PIJ. The dark-gray area in the plantarolateral aspect of the PIJ capsule contained extensive infiltrates of degenerated and viable neutrophils arranged in a linear pattern, following the orientation of the collagen fibers. The lesion in the proximal articular surface of P2 was thickened cortical bone. The deep aspect of the semilunar lesion exhibited high numbers of osteoclasts in the Howship lacunae. At the margins of the lesion, the darkened rim observed grossly had focal discontinuity of subchondral cortical bone and several cyst-like lesions. The bone marrow was hypercellular in these areas, consistent with inflammatory infiltration.
Comments
Synovial sepsis is a serious condition in horses and can be life-threatening, especially in horses with delayed diagnosis. The distal interphalangeal joint, navicular bursa, and DFTS are most commonly affected by penetrating injuries.2 The diagnosis of septic arthritis and tenosynovitis is often made on the basis of patient history, physical examination findings, and results of synovial fluid analysis, including WBC count and total protein concentration.3 The involvement of multiple synovial structures is generally associated with a worse prognosis.4 Additionally, a lack of bony involvement and septic tenosynovitis are directly associated with a higher rate of survival in horses with infection of a synovial structure.5
Results of diagnostic imaging in the horse of the present report were consistent with a sequestration in the proximal articular aspect of P2, likely caused by trauma or a penetrating foreign body. Radiographic examination is essential in the assessment of a horse with severe lameness and suspected synovial sepsis, even though the bony structures frequently appear unremarkable radiographically, especially in the early stages of the disease.6
In people, MRI is the gold-standard diagnostic imaging used for detection of septic arthritis, osteomyelitis, and soft tissue infection.7 The advantages of MRI have also been described for horses (including foals) with synovial sepsis, and sequestration in the articular surface is a feature of chronic synovial sepsis.8 In addition, MRI is particularly useful for assessing pathological changes in bone and fluid accumulation in bone and soft tissue. The extent of osteochondral damage and concurrent soft tissue injury can have a major impact on prognosis. Given the increased availability of MRI for the diagnosis of orthopedic conditions that horses may have in their feet, MRI should be considered for horses with suspected synovial sepsis. Magnetic resonance imaging is the preferred imaging modality for the assessment of soft tissue abnormalities, including inflammation and hemorrhage in the limbs of horses, and provides for excellent assessment of abnormalities in bone,9 as was evident in the horse of the present report. In the absence of cross-sectional imaging (MRI and CT), additional radiographic procedures (eg, fistulography) could have provided additional means of assessment. Regardless, this report highlighted the importance of diagnostic imaging in diagnosing and treating synovial sepsis in horses.
Acknowledgments
Funded in part by the Institute of Veterinary Science, University of Liverpool, Liverpool, England.
The authors declare that there were no conflicts of interest.
References
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