Pathology in Practice

Brent E. Walling Department of Pathobiology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Matthew C. Stewart Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Victor E. Valli Department of Veterinary Diagnostic Laboratory, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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 DVM, PhD, DACVP

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History

An 11-year-old 632.7-kg (1,392-lb) Quarter Horse gelding was evaluated at the University of Illinois Veterinary Teaching Hospital 3 days after acute onset of lateral recumbency without subsequent signs of clinical improvement. The owners reported no premonitory signs or evidence of trauma.

Clinical and Gross Findings

Results of an initial neurologic examination indicated that all cranial nerve functions were intact, peripheral nerve reflexes were considered normal, and deep pain sensation was present in all 4 limbs. While positioned in a sling, the gelding was able to support most of its weight on the fore-limbs but had bilateral hind limb ataxia with a compensatory base-wide stance. During the first few days of hospitalization, the gelding developed right forelimb weakness and tremors during the periods of sling use. Physical examination and radiographic evaluation of the right forelimb's skeletal and articular structures did not identify a cause for this limb weakness. Furthermore, radiographic views of the cervical vertebrae revealed no evidence of a vertebral fracture, vertebral canal stenosis, or articular facet alterations that might contribute to spinal cord compression. At the time of the initial evaluation, analysis of a blood sample revealed a stress leukogram (8.93 × 103 neutrophils/μL [reference range, 3.00 × 103 neutrophils/μL to 7.00 × 103 neutrophils/μL] and 1.37 × 103 lymphocytes/μL [reference range, 1.50 × 103 lymphocytes/μL to 5.00 × 103 lymphocytes/μL]); fibrinogen concentration was within the reference range. The most notable serum biochemical abnormalities included high activities of aspartate aminotransferase (727 U/L; reference range, 160 to 300 U/L) and creatine kinase (5,598 U/L; reference range, 120 to 350 U/L), which were attributed to prolonged recumbency and muscular trauma during transportation. High activities of alkaline phosphatase (296 U/L; reference range, 45 to 239 U/L) and sorbitol dehydrogenase (17.2 U/L; reference range, 0.0 to 8.0 U/L) and high concentration of total bilirubin (4.1 mg/dL; reference range, 0.60 to 2.60 mg/dL) were attributed to a combination of subclinical dehydration and decreased food intake prior to hospitalization. The concentration of BUN was also mildly high (27.2 mg/dL; reference range, 14.0 to 26.0 mg/dL), which was thought to also be secondary to dehydration. Glucose concentration was mildly high (176 mg/dL; reference range, 71 to 100 mg/dL), which was presumed to be a stress-induced effect. Electrolyte abnormalities included low bicarbonate concentration (27.2 mmol/L; reference range, 28.0 to 38.0 mmol/L) attributed to lactic acidosis from muscle trauma and slightly low concentrations of chloride (97 mEq/L; reference range, 98 to 110 mEq/L) and magnesium (1.6 mg/dL; reference range, 1.7 to 2.6 mg/dL), both of which were likely secondary to decreased food intake. Despite medical treatment and sling support, there was no improvement in the gelding's neurologic status. Following the development of pressure sores, inappetence, and signs of depression, the gelding was euthanatized 11 days after the initial evaluation and submitted for necropsy.

At necropsy, there was mild narrowing of the C7–T1 intervertebral disk space relative to the adjacent spaces. However, no evidence of trauma was present in the vertebral canal and the intervertebral disks appeared grossly unremarkable. A 3-cm segment of the spinal cord at the C7–T1 junction contained a locally extensive area of cavitation and malacia, consisting of a tan-gray, semiopaque material mixed with hemorrhage (Figure 1), which exuded from the cut surface. The degree and distribution of the malacia varied with the level of the spinal cord, involving the white matter in both the left and right ventral funiculi and the gray matter of the left ventral horn. The cord lesion diminished rostrally and caudally, blending into normal parenchyma.

Figure 1—
Figure 1—

Photograph of cut sections of the cervical portion of the spinal cord (region of the C7 through T1 vertebral bodies) in a horse that was evaluated 3 days after acute onset of lateral recumbency without signs of clinical improvement. The horse was hospitalized but subsequently euthanatized 11 days after the initial evaluation. Serial sections illustrate unilateral necrosis of the gray matter progressing to bilateral involvement of the gray and white matter in the ventral aspect of the spinal cord.

Citation: Journal of the American Veterinary Medical Association 239, 2; 10.2460/javma.239.2.199

Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page

Histopathological Findings

Sections of the spinal cord from C1 through S1 underwent routine processing for histologic examination. Histopathologic lesions were limited to the C7 through T1 segment, corresponding with what was observed grossly. Multiple coalescing foci of necrosis with loss of parenchyma and infiltration by macrophages and gitter cells were detected bilaterally in the ventral portions of the gray matter (Figure 2). Adjacent intact gray matter was edematous and contained a few degenerate neurons with swollen, pale eosinophilic neuronal cell bodies and peripherally located Nissl substance. Large areas of degeneration and necrosis were found in the medial and ventral funiculi with numerous gitter cells, swollen eosinophilic axons (spheroids), and digestion chambers along with edema and mild hemorrhage (Figure 3). Multiple vessels in the gray matter, the ventral median fissure, and the meninges were partially to completely occluded by amphophilic, granular emboli (Figures 2 and 4). Emboli were often intimately associated with the vessel wall, and those which partially occluded vessels were occasionally covered by a layer of endothelium. Rarely, cartilage with lacunae was present in the thrombi. The embolic material stained strongly with toluidine blue and Alcian blue stains and stained light to dark red with phosphotungstic acid hematoxylin stain. Immunohistochemical staining for Sarcocystis neurona failed to reveal organisms, and results of bacterial culture of a swab sample from the meninges were negative.

Figure 2—
Figure 2—

Photomicrographs of a section of the spinal cord obtained from the horse in Figure 1. In the main image, notice the loss of definition of the ventral horn (secondary to ischemic necrosis), compared with the appearance of the unaffected dorsal horn. In the inset, the boxed area delineated in the main image is magnified to illustrate an artery that has been occluded by fibrocartilaginous material. H&E stain; in the main and inset images, bar = 2 mm and 50 μm, respectively.

Citation: Journal of the American Veterinary Medical Association 239, 2; 10.2460/javma.239.2.199

Figure 3—
Figure 3—

Photomicrograph of a section through the gray matter-white matter interface of the spinal cord in the horse in Figure 1. Many macrophages and gitter cells have infiltrated the parenchyma. Evidence of Wallerian-type degeneration is present with dilated axons (arrows) and swollen myelin sheaths. H&E stain; bar = 50 μm.

Citation: Journal of the American Veterinary Medical Association 239, 2; 10.2460/javma.239.2.199

Figure 4—
Figure 4—

Photomicrographs of a cross section of a large artery in the meninges of the horse in Figure 1 that is almost completely occluded by fibrocartilaginous material (A) and higher magnification views of cartilaginous lacunae that are embedded within the embolus (B and C). In panel A, the lower half of the cross-sectioned artery is stained with H&E stain and the upper half is stained with toluidine blue stain; bar = 100 μm. In the 2 stained portions of the cross-sectioned arterial embolus, cartilaginous lacunae are evident; although visible following H&E staining (B), application of toluidine blue stain enhances the appearance of the cartilaginous lacunae (C). In panels B and C, bar = 20 μm.

Citation: Journal of the American Veterinary Medical Association 239, 2; 10.2460/javma.239.2.199

Morphologic Diagnosis

Severe, multifocal to coalescing spinal cord necrosis with multiple fibrocartilaginous emboli and Wallerian-type degeneration.

Comments

Ischemic necrosis secondary to fibrocartilaginous embolism in domestic species has most often been diagnosed in dogs and pigs,1–4 but there are a few reports5–11 involving several other species. For the horse of this report, a diagnosis of ischemic necrosis secondary to fibrocartilaginous embolism was established on the basis of identification of vascular obstruction in the gray matter and meninges by cartilage with lacunae and intervertebral disk material; the disk material stained strongly with toluidine blue and Alcian blue stains, which was indicative of proteoglycans. Because fibrocartilaginous embolism is rare in horses, its occurrence poses a diagnostic challenge for equine practitioners. Clinically, the effects of fibrocartilaginous embolism can resemble other conditions that result in peripheral neuropathy including focal compression of the cervical spinal cord (ie, wobbler syndrome), trauma, inflammation (as a result of viral, protozoal, or bacterial infection), toxicosis (ie, as a result of ryegrass ingestion), congenital malformations, cerebellar hypoplasia, and degenerative lesions.9,12 Mixed upper motor neuron and lower motor neuron signs with lateralization, the absence of radiologic evidence of compression or trauma, nonspecific diagnostic test results, and failure to respond to treatment are suggestive of fibrocartilaginous embolism in a horse, but a definitive diagnosis requires histologic examination of spinal cord sections and identification of intravascular fibrocartilaginous tissue.

Reports8–11 of fibrocartilaginous embolism in horses have described asymmetric lesions that were limited to the cervical intumescence (ie, C6 through T1) as was detected in the horse of this report; this localization of asymmetric lesions associated with fibrocartilaginous embolism has been described in other species.3 In dogs, asymmetric lesions, which are more common in the cranial portion of the spinal cord, are in part attributable to the distribution of unilateral and bilateral branches of the central arteries that arise from the ventral spinal artery.2,13 This anatomic feature may also explain the lesion asymmetry observed in horses. In dogs, herniated intervertebral disks have been implicated as a cause of fibrocartilaginous embolism1 and the intercapital ligament may provide protection from the development of fibrocartilaginous embolism in the thoracic portion of the spinal cord.2 More case reports of fibrocartilaginous embolism in horses would be necessary before drawing a similar conclusion in that species.

The source of embolic material in fibrocartilaginous embolism is generally accepted to be the nucleus pulposus of the intervertebral disks. The cause of fibrocartilaginous embolism in the horse of this report was not determined. Histologic examination of the C7–T1 intervertebral disk did not reveal any evidence of degeneration. Reported associated conditions and predisposing factors for the development of fibrocartilaginous embolism in humans and other animals include trauma or exercise,13,14 heavy musculature and rapid growth,3 diskospondylitis,4 and degenerative intervertebral disk disease.14 Individual case reports of horses with fibrocartilaginous embolism have linked the emboli to intervertebral disk disease8,9 or trauma.11 In 1 report10 of spinal cord ischemic necrosis due to fibrocartilaginous embolism in a horse, it was suggested that stress and physical exertion of the animal following entrapment in a cattle chute resulted in development of fibrocartilaginous embolism; necropsy of that horse revealed no gross lesions other than spinal cord malacia. All horses in the aforementioned reports8–11 were 8 to 11 years old. The horse of this report was similar to the previously recorded cases in that it was a relatively older horse and had a sudden onset of asymmetric clinical signs. Additionally, the lack of evidence to support trauma or intervertebral disk disease would suggest physical exertion as a cause. Clinicians should consider fibro cartilaginous embolism as a cause of acute spinal cord disease in middle-aged horses, particularly in horses with asymmetric neurologic signs that are localized to the cervical intumescence and involve both upper and lower motor neuronal deficits and for which there is no history of trauma and no overt radiographic evidence of pathological changes in the cervical portion of the vertebral column.

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