History
A 6-month-old Quarter Horse filly was brought in a trailer to a veterinary teaching hospital for evaluation because of acute-onset recumbency and paraparesis. The filly was housed on pasture with 4 other weanlings and was last observed standing the evening prior to hospital admission. The filly was bright and alert, with appropriate mentation; it was in left lateral recumbency in the trailer. The filly could masticate normally and was able to hold its head up; it would attempt to rise with its thoracic limbs when assisted into sternal recumbency. The filly was tachycardic (heart rate, 90 beats/min), afebrile (38.0°C [100.4°F]), and clinically dehydrated (tacky mucous membranes and slow jugular fill), although Hct, total protein concentration, and plasma lactate concentration were within reference ranges. Abnormalities on CBC included mild neutrophilic leukocytosis (total WBC count, 13,700 WBCs/μL; reference range, 4,700 to 10,600 WBCs/μL) and segmented neutrophilia (11,100 segmented neutrophils/μL; reference range, 2,400 to 6,400 segmented neutrophils/μL). On the serum biochemical profile, mild electrolyte and enzyme activity derangements included hyperphosphatemia (5.2 mg/dL; reference range, 1.2 to 4.8 mg/dL), hypochloremia (95.5 mg/dL; reference range, 97 to 105 mg/dL), high creatine kinase activity (4,360 U/L; reference range, 150 to 360 U/L), high alkaline phosphatase activity (290 U/L; reference range, 80 to 187 U/L), and high aspartate aminotransferase activity (553 U/L; reference range, 170 to 370 U/L). A neurologic examination was performed but was limited because of the filly's inability to stand; nociception with withdrawal reflex was intact in all limbs, motor function was delayed in response to nociception in the pelvic limbs, bilateral thoracic extensor rigidity was noted, and the filly was paraplegic with mildly decreased tail tone. No cranial nerve deficits were noted. Radiographic images of the cervical (not shown; no abnormalities noted) and thoracic vertebrae were obtained (Figure 1).
Radiographic Findings and Interpretation
The T9 vertebra is cranioventrally luxated, with T9-T11 vertebral bodies ventrally displaced and T9 overriding T8 (Figure 2). A smoothly marginated, oblong mineral opacity (a fracture fragment of the T8 vertebral body) is noted cranial to the cranial aspect of the T9 vertebral end plate. There are fractures of the spinous processes of T10-T13, with slight ventral and cranial displacement of the dorsal fracture fragments. The articular joint space of T9-T10 is widened. There is a fracture through the T10-T11 articular process, and a rectangular fracture fragment is evident ventral to the T11 spinous process. The remaining soft tissue and osseous structures are unremarkable. The radiographic interpretation was traumatic fracture and luxation of T8-T9 with spinous process fractures.
Radiographic findings were consistent with severe, acute trauma that likely resulted from ventrally directed blunt force over the T9-T13 thoracic vertebrae (as might occur if the filly flipped over backward or collided with a herd mate). In addition to the survey radiographs, a view was made to focus on and highlight the vertebral fracture (Figure 1). Other differential diagnoses considered for this filly included bone fragility syndrome, nutritional osteodystrophy, or congenital vertebral malformation that might predispose an animal to this type of catastrophic injury. These conditions were deemed unlikely because of the filly's normal radiographic bone opacity, the acute appearance of the fractures, lack of evidence of underlying pathological fractures, and absence of other congenital or developmental abnormalities.
Treatment and Outcome
The filly was given IV fluid therapy, treated with single doses of flunixin meglumine (0.5 mg/kg [0.23 mg/lb], IV) and morphine (0.1 mg/kg [0.045 mg/lb], IM), and sedated with acepromazine (0.2 mg/kg [0.09 mg/lb], IM), xylazine hydrochloride (0.2 mg/kg, IV), and detomidine hydrochloride (0.01 mg/kg [0.0045 mg/lb], IV). After consultation with the owner and discussion of treatment options, euthanasia was elected in consideration of the grave prognosis for recovery. At postmortem examination, multiple fractures of the midthoracic vertebrae with complete luxation of T9 at the intervertebral space of T8-T9 were noted. Fractures included the caudoventral aspect of the vertebral body of T8, lateral pedicles of T10, and caudodorsal aspect of T11. The vertebral column was deviated ventrally and cranially at the area of luxation. There were multiple fractures of the thoracic spinous processes spanning T10-T13, with cranioventral displacement of the dorsal fracture segments. Sections of spinal cord from the affected area were examined histologically, in which segmental axonal sheath dilation and swelling were noted. The meninges were intact and surrounded all sites of the affected spinal cord.
Comments
Trauma is one of the most common causes of neurologic disease in horses1; however, vertebral fractures and complete vertebral column luxations are rare in horses. A study2 of 450 horses with neurologic disease found that of 60 horses with spinal cord injury that underwent postmortem examinations, 35 (76%) of the documented injuries were the result of vertebral fractures; only 4 (9%) were vertebral subluxations or luxations. The most common causes of vertebral trauma in horses are collisions with immovable objects or falls. Injury can occur at any site along the vertebral column at any age. Foals tend to be more susceptible to fractures than adults, with the cranial aspect of the cervical vertebral column (C1-C3) and caudal aspect of the thoracic vertebral column (T15-T18) most commonly affected. The caudal aspect of the cervical vertebral column (C5-T1) and caudal aspect of the thoracic vertebral column are more often affected in adult horses.3 Luxations and subluxations of the vertebral column are more common in younger horses and result in damage to the surrounding musculature, ligamentous structures, and spinal cord. Horses with spinal cord trauma involving the caudal aspect of the cervical vertebral column and thoracic vertebrae are more commonly recumbent.4 In the case described in the present report, radiographic and gross pathological findings were consistent with acute, severe trauma resulting in multiple fractures and complete luxation of the thoracic vertebral column. Interestingly, despite this severe injury, all meningeal layers remained intact, consistent with the preservation of deep pain perception and some motor function of the pelvic limbs noted clinically.
Damage to the middle portion of the thoracic vertebral column in the filly of the present report resulted in paraplegia and extensor rigidity in the thoracic limbs. Observation of the Schiff-Sherrington syndrome (extensor hypertonia in the thoracic limbs) in this filly assisted in neuroanatomic localization to a region of spinal cord caudal to the cervicothoracic intumescence. This syndrome is rarely observed in horses, has a short duration, and can be confused with loss of upper motor neuron control of the thoracic limbs. Because deep pain perception was preserved in this filly, spinal cord injury was likely restricted to the more superficial, myelinated motor and proprioceptive fibers at the level of the vertebral injury.3
Radiography remains one of the most important diagnostic tools in identifying fractures and subluxations of the axial skeleton associated with neurologic disease in large animals.4 Myelography and other diagnostic tests, including evaluation of CSF and electromyography, can be useful for both confirmation of the location and extent of injury and prognostic purposes. Although it was confirmed that the meninges were intact despite luxation of the vertebral column, prognosis would have remained guarded to grave because of instability of the vertebral column and inaccessibility of the affected segments for surgical stabilization. The degree of injury on the radiographs underestimated the amount of damage that was found on necropsy. This has been reported for small animals, where there is not always a direct relationship between radiographic displacement and the degree of spinal cord trauma.5 The lateral radiographic view of the middle portion of the thoracic vertebral column (T5-T14) is a good example of the importance of centering the x-ray beam over the area of interest when obtaining radiographs of the vertebral column. X-ray beam divergence can geometrically distort structures at the edge of the field of view, leading to potentially inaccurate interpretations of findings. Vertebral column radiographs should therefore be made in sequential sections of fewer vertebrae to avoid x-ray beam divergence.
1. Nout YS, Reed SM. Management and treatment of the recumbent horse. Equine Vet Educ 2005; 17: 324–336.
2. Tyler CM, Davis RE, Begg AP, et al. A survey of neurological diseases in horses. Aust Vet J 1993; 70: 445–449.
3. Furr M, Reed S. Equine neurology. Ames, Iowa: Blackwell Publishing, 2008.
4. Feige K, Fürst A, Kaser-Hotz B, et al. Traumatic injury to the central nervous system in horses: occurrence, diagnosis and outcome. Equine Vet Educ 2000; 12: 220–224.
5. Bali MS, Lang J, Jaggy A, et al. Comparative study of vertebral fractures and luxations in dogs and cats. Vet Comp Orthop Traumatol 2009; 22: 47–53.