Accepted Manuscript Conservative Management of a Cervical Vertebral Fracture in a Gelding Heather L. Murphy, BS, Nathan C. Nelson, DVM, MS, DACVR, Harold C. Schott, II, DVM, PhD, DACVIM PII:
S0737-0806(16)30461-0
DOI:
10.1016/j.jevs.2016.10.014
Reference:
YJEVS 2206
To appear in:
Journal of Equine Veterinary Science
Received Date: 29 July 2016 Revised Date:
27 October 2016
Accepted Date: 31 October 2016
Please cite this article as: Murphy HL, Nelson NC, Schott HC II, Conservative Management of a Cervical Vertebral Fracture in a Gelding, Journal of Equine Veterinary Science (2016), doi: 10.1016/ j.jevs.2016.10.014. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Case Report
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Conservative Management of a Cervical Vertebral Fracture in a Gelding
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Heather L. Murphy, BS; Nathan C. Nelson, DVM, MS, DACVR; Harold C. Schott II, DVM,
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PhD, DACVIM
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From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine,
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Michigan State University, East Lansing, MI 48824-1314.
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Address correspondence to Dr. Schott at
[email protected]
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The authors have no conflict of interest.
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Keywords: Horse; neck pain; computed tomography; physical therapy; vertebra
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Abstract
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The presentation, diagnostic evaluation, treatment, and 5 year follow-up of a 12-year-old Arabian-
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Saddlebred cross gelding with neck pain and stiffness, attributable to a fracture of the third
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cervical vertebrae (C3), is described. Initial cervical spinal radiographs revealed a concave defect
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in the ventral aspect of the cranial endplate of C3. However, both this finding and
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ultrasonographic imaging of the area were inconclusive for a fracture. Nuclear scintigraphy
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revealed that the lesion was metabolically active, prompting computed tomographic imaging that
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revealed a fracture of C3. Sequential radiographs documented progressive fusion of C2-C3 and
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no neurological deficits developed over the 5 years following the injury. Cervical vertebral
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injuries in horses can lead to various clinical signs including ataxia, weakness, and neck stiffness
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or pain. Diagnosis with cervical radiographs alone can be challenging and, in some cases as the
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horse in this report, multiple imaging modalities may be required to establish a definitive
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diagnosis. Horses without neurological signs may recover successfully with conservative
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medical management, which was performed in this case.
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1. Introduction
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Cervical injuries and vertebral fractures in horses often lead to ataxia and weakness that sometimes can be catastrophic, due to damage to the spinal cord [1,2]. In a retrospective study of
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450 horses with neurological disease, 60 were reported to have spinal cord injury and vertebral
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fractures were found in 38 cases, with the majority in the cervical region. Further, case fatality
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rate for spinal cord injury was high with the diagnosis established by necropsy examination in 46
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horses [3]. However, cervical vertebral fractures are not always accompanied by neurologic
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deficits and several cases, notably younger horses, have been successfully managed
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conservatively with rest and analgesic medications [4-6]. Thus, presenting signs for cervical
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vertebral fractures can vary from neck stiffness and pain to severe neurological deficits resulting
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in recumbency or sudden death. Although bone abnormalities may be apparent on routine
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cervical radiographs, detailed documentation of fracture lines and bone fragments can be
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challenging [1,2]. Thus, in many cases additional imaging modalities, including scintigraphy,
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ultrasonography, and computed tomography may need to be pursued in order to establish a
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definitive and accurate diagnosis [7].
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2.1 Case History
A 12-year-old Arabian-Saddlebred cross gelding was presented for evaluation of neck
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pain and stiffness. Two weeks previously the horse, noted to be normal in the morning, was
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acting quiet and did not greet the manager as was usual later that day. No evidence of external
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trauma was detected but over the next couple of days, the gelding was repeatedly observed to
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hold the head in a mildly extended position and the neck appeared stiff. Examination by the
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referring veterinarian revealed an alert horse with normal vital parameters but neck movement
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was restricted and the gelding appeared painful on manipulation of the neck. No neurological
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deficits were apparent at rest or while walking. Treatment included flunixin meglumine (1.0
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mg/kg, IV) and dexamethasone (0.1 mg/kg, IV) and the horse was started on phenylbutazone
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(4.4 mg/kg, PO, q 12 h) for 7 days. The horse continued to eat and drink, although it was
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reluctant to eat from the ground, but minimal improvement in neck stiffness was noted over the
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next few days. Consequently, a blood sample was collected for serum western blot testing for
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antibodies against Sarcocystis neurona and yielded negative results. Because no significant
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improvement had been observed over the week of treatment, the horse was referred for further
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evaluation. The only other previous problems were several sarcoids on the inner thighs and a few
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small melanomas on the tail that had responded well to surgical removal. Up until the time of
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suspected injury, the gelding had been used for light trail riding several times a week.
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2.1 Clinical Findings and Diagnostic Evaluation
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At admission, the gelding was bright, alert, and responsive and all vital parameters were within normal ranges. No asymmetry was noted in the neck musculature although a small (5 mm
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diameter) non-painful crusted lesion was found on the upper right side. The horse was reluctant
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and appeared painful when encouraged to bend the head and neck in either direction to follow a
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handful of grain toward the elbow; however, it could eat grain from the floor without signs of
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pain. A localized site of pain could not be ascertained. No gait deficits were apparent when
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walking or turning in tight circles. However, when circling, the gelding exhibited clear
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reluctance to flex the neck to either side and head and neck position was maintained in extension.
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All other physical and neurological examination findings were normal. A complete blood count
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(CBC) and serum biochemistry profile, performed to assess potential adverse effects of previous
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treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), yielded normal results.
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Standing lateral radiographs of the cervical spine revealed mild arthritis in the articular
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facet joints of the lower neck (C5-C6 and C6-C7) but a more notable finding was a concave
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lucency in the ventral aspect of the cranial endplate of C3 with a thin adjacent mineral fragment
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(Figure 1A). No fracture lines or larger displaced bone fragments were apparent. In addition to
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trauma, infectious, or neoplastic destruction of bone was considered but a lack of periosteal
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reaction and proliferation of adjacent bone made these differentials less likely. Avascular
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necrosis or osteochondrosis with bone resorption were other possible causes. Further diagnostic
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evaluation, including ultrasonography, nuclear scintigraphy, and computed tomography were
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discussed, but the owner elected ongoing conservative management. The horse was discharged
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with instructions for stall rest for 1 month that included daytime turnout in a small paddock.
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Further NSAID treatment consisted of phenylbutazone (2.2 mg/kg, PO, q 12 h for 3 d followed
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by 2.2 mg/kg, PO, q 24 h for 10 d).
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1 week after initial examination (3 weeks after onset of clinical signs) the gelding was
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presented for re-evaluation of neck pain and stiffness that had worsened after reduction of the
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phenylbutazone dosage. Again, vital parameters were within normal ranges and lateral neck
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movement remained guarded. Pain (manifested as muscle spasm and neck tensing) was elicited
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on deep palpation of the lower aspect of the right brachiocephalicus muscle. No neurological
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deficits were noted at rest or while walking, although minimal lateral neck movement was
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observed during circling and head carriage remained mildly extended. Due to a lack of
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improvement, the horse was hospitalized for further diagnostic imaging. On the following day,
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scintigraphic examination was performed 2 hours following IV administration of 150 mCi of
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technetium 99m MDP. A substantial amount of homogenous radiopharmaceutical uptake was
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focused at the C2-C3 ventral intervertebral space (Figure 2), supporting active bone remodeling
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consistent with a fracture, osteomyelitis, or neoplasia.
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To further investigate an infectious or neoplastic disease process, bilateral transverse ultrasonographic imaging of the C2-C3 articulation and surrounding soft tissues was performed.
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The margins of the dorsal articular facets were mildly irregular and imaging of the ventral
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cervical joint also revealed irregular margins; however, a fracture could not be documented.
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Next, a right-sided ultrasonographically guided needle aspirate was collected from the soft tissue
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adjacent to the C3 osseous lesion. Microscopic examination revealed iatrogenic hemorrhage,
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with well-differentiated osteoblasts and rare osteoclasts. There was no cytological evidence of
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inflammation, sepsis, or neoplasia and culture of the aspirate yielded no bacterial growth. A CBC
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collected on that date had a normal white blood cell count with a mildly increased estimated
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fibrinogen concentration (500 mg/dL; reference range 200-400 mg/dL). Because a definitive diagnosis could not be established despite imaging with radiographs,
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ultrasonography, and nuclear scintigraphy, computed tomography (CT) of the cervical spine was
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subsequently performed with the horse under general anesthesia. CT images revealed a
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transversely oriented, curvilinear lucency in the cranial endplate of C3 (Figure 3), with a thin
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adjacent mineral fragment. The rostral margin of C3 was irregular with a stippled lucency
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throughout and there was loss of cortical bone. Sclerosis was evident caudal to the endplate,
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within the body of C3. The cranioventral margin of C3 exhibited irregular periosteal reaction and
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a hypoattenuating semicircular defect in the adjacent soft tissue. While under anesthesia,
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cerebrospinal fluid (CSF) was collected from the atlanto-occipital space and cytological analysis
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revealed rare red blood cells (2/µL) with no nucleated cells or infectious organisms, consistent
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with normal CSF. Taken together, these findings were most consistent with a fracture of the
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cranial aspect of C3.
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Unfortunately, after recovery from anesthesia the horse was considerably more painful.
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The neck was quite stiff and the gelding had minimal voluntary movement of the head and neck
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(Videos 1-4). When approached in the stall, noticeable tensing of the neck and spasms of the
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ventral neck musculature were intermittently observed. Treatment included phenylbutazone (2.2
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mg/kg, PO, q 12 h) and gabapentin (4 mg/kg, PO, q 8 h) for possible neuropathic pain, and
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chloramphenicol (40 mg/kg, PO, q 8 h) for possible sepsis and the horse remained hospitalized
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for a total of 8 days until the level of pain had decreased to that apparent at admission. The horse
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was discharged with instructions to continue phenylbutazone (2.2 mg/kg, PO, q 12 h for 3 d
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followed by 2.2 mg/kg, PO, q 24 h for an additional 30 d) and chloramphenicol was continued
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for a total of 30 days. Stall rest was also recommended for 30 days, with turn out in a small
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paddock when footing was good.
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2.3 Case Progression and Outcome
Reassessment 12 weeks after initial onset of clinical signs revealed persistence of mild head extension. Neck stiffness was still apparent but had improved considerably, although
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movement to the right remained limited as compared to the left. The horse had been off
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medication for the past 4 weeks and no neurological gait deficits were apparent. Cervical
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radiographs revealed progression of the defect in the cranial endplate of C3; the majority of the
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endplate had become lucent and the ventral aspect had a thin layer of bone, with the previously
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identified fragment less distinct. Sclerosis was apparent at the caudal aspect of the lucency.
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Additionally, the space between C2-C3 had collapsed with overriding of the articular process and
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mild kyphosis had developed. The only abnormality on a CBC and biochemistry profile was
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mild hypoalbuminemia (2.8 g/dL; reference range 3.6-4.8 g/dL), possibly associated with prior
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phenylbutazone treatment. Continued rest with no riding was advised for the next 60 days, but
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turn out on pasture was permitted. Neck exercises consisting of carrot stretches (side-to-side and
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up and down) several times a day were recommended at this time.
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Re-examination 24 weeks after initial onset of clinical signs revealed further
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improvement. Although the horse continued to hold the head mildly extended, this abnormality
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was less apparent than at previous visits. The gelding still exhibited stiffness bending the neck to
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the right but pain was not apparent. On palpation of the neck, bony prominences could be felt on
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both sides at the level of C2-C3, consequent to atrophy of neck muscles below this area. Cervical
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radiographs revealed that the lucent defect of the cranial endplate of C3 remained similar in size,
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but sclerosis surrounding this defect had increased (Figure 1B). The space between C2-C3 was
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more collapsed with further overriding of the articular processes and kyphosis. Based on
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improvement in clinical signs, it was deemed reasonable to allow the horse to return to light
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riding but the owner was cautioned that neurological deficits could develop at any time and that
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minimal rein tension should be used. Continuation of physical therapy (carrot stretches) was
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encouraged.
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Further re-evaluation was performed 46, 101, 151, and 234 weeks (Figure 1C) after initial onset of clinical signs. The gelding continued to have minimal evidence of pain and was
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being ridden twice weekly. The owner had been performing carrot stretches prior to riding and
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no gait deficits were reported or observed at these re-examinations. Bony proliferation over the
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C2-C3 region remained palpable, largely attributed to muscle atrophy. Cervical radiographs were
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performed on all four occasions and revealed progressive remodeling and further collapse of the
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space between C2-C3, although kyphosis had lessened. All in all, progression of the radiographic
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changes supported resolution of a cervical vertebral fracture.
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3. Discussion
Cervical vertebral injuries should be suspected in horses that develop neck stiffness after
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a kick, a fall during work or turn out, or other traumatic episodes such as getting the head stuck
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or rearing and falling. Commonly, affected horses will also have moderate to severe neurological
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gait deficits that may warrant immediate euthanasia [1-3]. However, a traumatic event may not
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always be observed and horses with cervical injuries may also present for evaluation of neck
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pain or abnormal head and neck carriage in the absence of neurological deficits [1,2,7]. For the
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gelding described in this report, no trauma was observed and neurological deficits were not
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apparent at initial examination. Lateral radiographs are the standard “screening tool” for detecting osseous lesions of the
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cervical vertebral column in horses and are the initial imaging modality used in evaluation of
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horses with neck injuries. Radiographs may reveal fractures, developmental abnormalities,
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osteoarthritis, and narrowing and/or angulation of the spinal canal supportive of spinal cord
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compression [1,2,8]. Unfortunately, the two dorsal articular facet joints are superimposed on
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lateral radiographs, making detection of facet fractures and osteoarthritis difficult. Consequently,
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oblique radiographic projections may need to be pursued to more completely evaluate the
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articular facets and to determine which side of the cervical spine may be affected [9]. C-Arm
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fluoroscopy is another imaging technique that has also been used to improve imaging of a
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fracture and callus formation in a horse with a neck injury [10]. Ultrasonography can also be
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used to image osseous lesions of the cervical spine and this imaging modality has the additional
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benefit of allowing assessment of synovial effusion and soft tissues surrounding the vertebrae
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[11].
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Radiographic imaging of the gelding in this report was initially limited to lateral
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radiographs that revealed the lucency in the cranial endplate of C3, but did not provide
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conclusive evidence of a fracture. Further, the extent of apparent bone loss and lack of bone
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proliferation was considered atypical for a recent fracture. Oblique radiographs were not
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considered necessary in this case because the lesion was in the ventral aspect of the vertebra.
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Because a definitive explanation for the cause of the C3 lucency remained elusive, nuclear
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scintigraphy was the next imaging procedure performed and once the “hot spot” was detected,
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the C3 lesion was considered the likely cause of neck stiffness and pain. Ultrasonographic
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imaging was also pursued in order to assess the margins of the articular facets, synovial effusion,
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as well as surrounding soft tissues. Although articular margins were irregular, a fracture could
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not be definitively diagnosed. Ultrasonography was also used to guide needle aspiration of the
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ventral C2-C3 intervertebral region. Cytological evaluation of the sample collected failed to
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provide supportive evidence of either sepsis or neoplasia.
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Computed tomographic imaging provides the greatest detail of osseous lesions of the cervical vertebral column and also allows image reconstruction in multiple planes [8]. Although
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CT imaging can be costly and limited to use at referral centers, this imaging modality was
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essential to ultimately diagnosis the C3 fracture in the horse in this report. CT imaging also
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provided detailed information to determine whether surgery should have been recommended.
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Detection of multiple fracture lines would have made any attempt at surgical stabilization
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challenging. Further, because CT imaging revealed that there was minimal displacement of the
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C2-C3 alignment and that the cortex of the dorsal aspect of the C3 vertebral body, and by
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inference, the intervertebral ligament at that site appeared to be intact, the fracture was likely
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stable and further surgical stabilization was not deemed necessary. At the time that this gelding
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was initially examined, a further limitation of CT imaging was the requirement for general
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anesthesia. Caution should be exercised when considering general anesthesia in a horse with a
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suspected cervical vertebral fracture as manipulation of the neck under anesthesia could lead to
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increased pain, as observed in the horse in this report, and possible damage to the spinal cord
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with an unstable fracture [2]. Recent development of robotic CT scanners that can be used on
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standing, sedated horses may allow clinicians to avoid these potential complications of general
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anesthesia with future cases [12].
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Initial management of horses with cervical vertebral injuries, with or without neurological deficits, is usually conservative and includes stall confinement and judicious use of
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analgesic medications [1,2]. Pain and cervical muscle spasm can initially help stabilize the
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cervical vertebral column and limit spinal cord injury [1]. Anecdotally, there have been
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descriptions of many forms of external coaptation support to limit neck mobility; however, these
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attempts have rarely been tolerated by horses. However, when imaging reveals an unstable
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fracture or when neurological signs worsen, surgical repair and stabilization (or euthanasia) must
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be considered. Either lag screw fixation or dynamic compression plates, to fuse C2-C3 or
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stabilize fractures of the body of the axis, have been successfully performed with horses
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returning to full activity [13-15]. Surgical stabilization and/or intervertebral fusion may also be
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worthy of consideration in horses that continue to have neck pain after several weeks to months
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of conservative treatment. As with CT imaging, however, general anesthesia for fracture repair is
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not without risk of worsening both pain and neurological status. Thus, for minimally displaced
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fractures in horses without neurological deficits, conservative management is the preferred
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treatment and has been documented to yield favorable outcomes [4-6]. Regardless of whether a
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fracture is managed by surgical stabilization or conservatively, there is a risk of subsequent
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spinal cord compression at the adjacent intervertebral joints, the so-called domino effect, if the
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vertebral column becomes misaligned during the months to years following recovery [2].
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Because neurological deficits were not present, the horse in this report was managed
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conservatively and successfully returned to the desired use of trail riding. In addition to stall rest
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and analgesic medications, physical therapy was also used for rehabilitation as part of
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conservative management of this gelding. Specifically, stretching exercises using a carrot were
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performed to encourage the horse to move its head and neck to each side, to raise the head, and
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to lower the head both to the sternum and to the ground between the front legs. The goals of
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these exercises included increased flexibility (maintenance and/or improvement of range of
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motion), muscle strengthening, and decreased stiffness and pain [16]. Physical therapy was
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recommended at least twice daily and required a dedicated owner.
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4. Conclusion
Establishing a definitive diagnosis for the initial C3 lucency in this gelding was
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challenging. Although clinical signs developed acutely, there was no observed trauma and initial
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radiographic imaging failed to document a fracture. Consequently, an infectious or neoplastic
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disease process was also considered, although these problems appear to be rare in the cervical
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spine of adult horses [3,17]. Computed tomography clearly provided the best detail of the
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osseous lesions, but this imaging modality was still unable to document trauma as the inciting
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cause. Over time, as the lesion remodeled and progressive fusion of C2-C3 developed, a healing
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traumatic compression fracture was considered the most probable inciting cause. Although neck
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pain and stiffness were clearly evident at the onset, these problems improved over time and the
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patient never developed neurological deficits over the 5 years of follow-up. Further, the cervical
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vertebral column was maintained in a normal alignment as the fracture healed; consequently, the
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long-term prognosis for this gelding should remain favorable.
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Figure 1. Standing lateral radiographs taken 2 (A), 24 (B) and 234 (C) weeks after onset of
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clinical signs. (A) concave defect in the ventral aspect of the cranial endplate of C3 with a small
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adjacent fragment (white arrow); (B) remodeling of the lesion with collapse of the C2-C3 disc
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space, surrounding sclerosis and kyphosis of the spine in this region; (C) apparently healed
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lesion with static kyphosis.
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Figure 2. Lateral scintigraphic bone phase images of the cranial cervical vertebrae taken 3 weeks
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after onset of clinical signs revealed a large amount of homogenous radiopharmaceutical uptake
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centered at C2-C3 (white arrow).
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Figure 3. Sagittal computed tomography view 3 weeks after onset of clinical signs detailing a
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curvilinear region of lucency within the cranial endplate of C3 and small adjacent fragment
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(black arrowheads); osteolysis and periosteal proliferation are present along the ventral margin of
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the body of C3.
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Case Report
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Conservative Management of a Cervical Vertebral Fracture in a Gelding
Highlights •
Cervical vertebral fractures in horses can lead to various clinical signs including ataxia,
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weakness, and neck stiffness or pain.
Diagnosis of a cervical vertebral fracture may require multiple imaging modalities, including
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radiography, ultrasonography, nuclear scintigraphy, and computed tomography. Computed tomography provides the greatest detail of all imaging procedures but general anesthesia is not without risk in horses with a suspected cervical vertebral fracture. In horses with stable fractures and no neurological deficits, conservative management of cervical
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vertebral fractures can be successful with horses returning to prior use.
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