Thoracic Vertebral Subluxation in a Mixed Breed Dog
Jennifer Romano
Clinical Advisor: Ariane Jay, DVM
Basic Science Advisor: Marnie FitzMaurice, VMD, PhD
Senior Seminar Report
Cornell University College of Veterinary Medicine
February 12, 2014
Key words:
Spine, Trauma, Subluxation, Vertebrae, Myelopathy, Paraparesis
Abstract:
A five-year-old male castrated mixed breed dog presented to Cornell’s Emergency
Service for a 24 hour history of paraplegia. After being outside unsupervised, he ran back into
the house, up a staircase, and lay down beside his owner. He could not move from this position
for several hours, and was brought to the referring veterinarian. Radiographs revealed a probable
vertebral fracture and subluxation between thoracic vertebrae twelve and thirteen. He was
reportedly paraplegic without intact pain sensation. He was hospitalized overnight and referred
to Cornell.
On presentation, he was paraparetic with intact superficial pain sensation. Computed
tomography (CT) confirmed subluxation and fracture of the articular facets of the right twelfth
and thirteenth thoracic vertebrae. Surgical reduction and stabilization were achieved with String
of Pearl plates. Postoperative radiographs showed questionable placement of a screw, and CT
confirmed vertebral canal penetration. The screw was removed, and a mini-hemilaminectomy
revealed dural laceration. After weeks of hospitalization and aggressive physical therapy, he
currently ambulates well on textured surfaces.
Introduction:
This case report discusses many aspects of vertebral trauma including lesion localization,
use of advanced imaging, modalities in obtaining diagnoses, and medical or surgical
management options. Many of these principles can be used in other spinal cord injuries.
Case History:
A five-year-old, male castrated, mixed breed dog presented to the Cornell University
Hospital for Animals’ Emergency Service for a 24 hour history of hindlimb paraplegia of
unknown cause. The patient had been let outside unsupervised the previous morning, and ran
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around in the open yard for approximately ten minutes. When he returned, he ran up twenty
stairs in a hurry and lay down next to his owner. In the late afternoon, he was still laying in the
same position and the owner became concerned. Even with coaxing with food, he remained
down. He was brought to the local veterinarian where radiographs were taken of his thoracic and
lumbar vertebrae. He was given multiple doses of solu-delta cortef, ampicillin, and famotidine.
There were some superficial lacerations, which were stapled.
The neurologic examination
revealed no superficial or deep pain in the pelvic limbs and normal thoracic limb function. Due
to the presumptive diagnosis of vertebral subluxation, he was referred to a specialty veterinary
hospital the following day.
Clinical Findings:
On presentation to the Cornell Emergency Service, the dog was bright, alert and
responsive with a wagging tail. He was in sternal recumbency and could move his front legs
under him, but was not observed to voluntarily move his hindlimbs. He had minimal superficial
abrasions that had been cleaned and stapled by the referring veterinarian. He was tachycardic,
with a heart rate of 130, and euhydrated.
The neurologic examination was limited due concern about the potential of causing more
damage due to vertebral instability.10 The patient was brought inside on a guerney. Though the
best way to assess locomotion in our patient would have been to put him on the ground with a
sling under his abdomen to see if he had any hindlimb voluntary motor function, this was not
done in an effort to avoid additional spinal trauma. Though the patient appeared paraplegic, this
was not confirmed.
Reflexes and pain sensation were normal in all limbs. This is an important difference in
that deep pain sensation was not appreciated in the exam performed by the referring veterinarian.
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The cause of this disparity is unknown, however potential explanations include administration of
pain medications masking a pain response, differences in techniques of eliciting deep pain, and
improvement in pain sensation over the preceding 24 hours.
Although locomotion could not be properly assessed, the patient had normal motor
function to his tail, and good muscle tone of the hindlimbs, thus we were hopeful that he had
some motor function, but was unable to demonstrate it without support.5 No spinal palpation
was performed due to the possibility of exacerbating the injury. In a patient with a stable
vertebral column, this would have been good information to localize discomfort and rule out
non-painful differentials.4
Once the neurologic examination was performed, neurolocalization of the myelopathy
was necessary to create a differential list. Since the thoracic limbs had normal reflexes and
voluntary motor function, the lesion was believed to be caudal to the third thoracic vertebrae
(T3).4
Since the pelvic limbs were affected, the lesion was most likely in the T3-L3 or L4-S3
spinal cord segments. A lesion in the L4-S3 region may result in decreased to absent reflexes in
the pelvic limbs. However, a lesion in the T3-L3 region corresponds to upper motor neuron
signs in the pelvic limbs, with increased reflexes and tone in the pelvic limbs.4 A T3-L3
myelopathy is most consistent with the examination findings.
The cutaneous trunci reflex helped further localize the thoracolumbar myelopathy. A
normal reflex occurs when there is bilateral contraction of the cutaneous trunci muscles after
pinching the skin on either side of the spine with a hemostat. Since the afferent neurons are
segmental from T2 to L7, a lesion of the spinal cord may cause a cutoff point or absent
contraction on one side.4,6 Our patient had a cutoff near T13 and L1 bilaterally.
4
Since our patient had evidence of upper motor neuron dysfunction in the pelvic limbs
(intact reflexes with paraparesis), there was concern that the bladder was also affected.5 His
bladder palpated normally and was intact on flash ultrasound. Function was not known, so urine
output needed to be monitored.6,10
Problem List:
The most striking clinical sign was the bilateral pelvic limb paresis, which in light of
normal thoracic limb function and intact pelvic limb reflexes, indicates a thoracic vertebrae three
to lumbar vertebrae three (T3-L3) myelopathy. Tachycardia could easily be explained by his
excitement. The rest of the case study will focus on the T3-L3 myelopathy as the major problem
facing the dog.
Differential Diagnoses:
Differential diagnoses for an acute T3-L3 myelopathy can be divided into compressive
and non-compressive lesions. Compressive lesions include Intervertebral Disc Disease (IVDD),
vertebral fracture/luxation/subluxation, hemorrhage and neoplasia. Non-compressive lesions
include Fibrocartilagineous Embolic Myelopathy (FCEM), an ischemic event, spinal cord
bruising, infectious or inflammatory diseases.
An important differential in a dog with an acute T3-L3 myelopathy is IVDD. There are
two main classifications of IVDD, Hansen’s Type I and Type II. Hansen’s Type I is typically
seen in young to middle aged chondrodystrophoid breeds. The nucleus pulposus of the disc
dehydrates and mineralizes causing the annulus to weaken. Even normal activity may cause the
disc to extrude into the spinal canal and can have acute or chronic signs. Most disc protrusions
occur in the thoracolumbar vertebrae.
A decreased intervertebral space may be seen on
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radiographs as well as a mineralized disc, but usually advanced diagnostics such as magnetic
resonance imaging (MRI) or computed tomography (CT) are required for a definitive diagnosis.4
Hansen’s Type II IVDD is typically seen in middle aged to older large breed dogs. The
annulus becomes more fibrous as it degenerates and then protrudes into the vertebral canal.4
This is usually a chronic process and was therefore less likely to be the cause in this case.
Another cause of an acute T3-L3 myelopathy can be spinal cord trauma, including
vertebral fractures, subluxations and luxations. They occur in approximately 6% of cases that
present with neurologic defects indicative of spinal cord lesions. These cases tend to be quite
painful and are common in cases with a history of external trauma.6 Due to the probable
traumatic cause of the lesion in this case and the acute onset, this is an important differential and
can typically be seen on radiographs.6
Hemorrhage or spinal cord bruising can also cause a focal myopathy. Hemorrhage in the
spinal canal can cause compression of the spinal cord. Spinal cord bruising can also cause
damaged nerves. Hemorrhage, especially, may be seen on advanced imaging (MRI). Both may
heal well with crate rest and conservative management with anti-inflammatory and pain
medications, though in certain instances decompressive surgery may be indicated.10
Neoplastic diseases of the vertebral column or spinal cord can be extradural or intradural.
Extradural most commonly includes osteosarcoma and lymphosarcoma, while intradural often
includes meningiomas and malignant nerve sheath tumors. These are typically seen in dogs over
six years old and may have an acute or chronic presentation.4 Due to the acute presentation of
this case and the age of the dog, this diagnosis is possible, but less likely.
A fibrocartilaginous embolic myelopathy (FCEM) is also a likely differential in this case.
This is a vascular disease where a fibrocartilaginous embolus obstructs a blood vessel supplying
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the spinal cord causing a necrotizing myelopathy. It is usually seen in large breed dogs, and the
clinical signs are often lateralized and the vertebral column is non-painful. When the embolus
first lodges, there may be a shout of pain, but the condition is usually non-painful after the initial
event.
FCEM has traditionally been considered a diagnosis of exclusion, and therefore
radiographs and advanced diagnostics must be performed to rule out the other differentials first.4
In recent years, however, pathognomonic findings on MRI have been described.7
An inflammatory myelopathy can be a myelitis or meningomyelitis, steroid-responsive
meningitis or diskospondylitis. An inflammatory myelopathy such as myelitis or meningitis is
slightly less likely in this case since the myelopathy is localized to one small lesion of the spinal
cord. However, it cannot be ruled out and diagnostics such as a cerebrospinal fluid (CSF) tap
may be indicated if other diagnostics do not reveal a result and the clinical signs progress. 4
Diskospondylitis is an infection of the intervertebral disc and adjacent vertebral endplates
and is often caused by Staphylococcus intermedius or Brucella.
It can often be seen on
radiographs as bony lysis of the vertebral endplates and bony proliferation especially bridging of
the vertebrae ventrally. Diskospondylitis is most often seen at lumbar vertebrae seven and sacral
vertebrae one (L7-S1). Radiographs will help rule down this differential.4
Diagnosis:
A lateral radiograph obtained by the referring veterinarian revealed a step between
thoracic vertebrae twelve (T12) and thirteen (T13), with the thirteenth vertebra displaced
ventrally relative to the twelfth. There was also a collapsed intervertebral space between the
vertebrae. This is consistent with a vertebral subluxation. Only a lateral view was available so
the orthogonal plane displacement was unknown. To determine the extent of the damage of the
soft tissue structures and see exactly how much displacement had occurred between the
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vertebrae, advanced diagnostics were required.
Modalities considered included Computed
Tomography (CT) or Magnetic Resonance Imaging (MRI). Although MRI provides better
definition of soft tissue structures, it takes hours to perform and requires general anesthesia. CT
is excellent for bone imaging, good for soft tissues, and only takes a few minutes to perform
under sedation or anesthesia.10 Furthermore, MRI is associated with a greater expense than CT
at our institution. CT was performed to better characterize the subluxation.
The CT scan confirmed the subluxation with T13 to the left and ventral to T12 with some
minor rotation. The intervertebral disc was not observed to be protruding into the spinal canal.
The fractures of the right articular facets of T12 and T13 are commonly associated with
subluxations due to the movement of the vertebral column.6 The examination also included the
thorax to check for pathology as well as the pelvis to look for fractures, both of which were
within normal limits.
Prognosis:
The prognosis for acute spinal injuries is primarily based on clinical signs. Whether
animals receive surgical or conservative management, the prognosis seems to be most strongly
influenced by the presenting neurologic status. Those animals that still retain pain perception
generally have a fair to good prognosis. Those that have lost pain sensation have a poor to grave
prognosis, regardless of management strategy.3,10 Surgery is best used to stabilize and possibly
realign the vertebrae to prevent further spinal cord injury.
With injuries of the spinal cord, many animals do not improve until several weeks
following initiation of management strategies. Most of the recovery of function occurs in the
first three months.6
8
A study evaluating dogs and cats with spinal trauma undergoing either surgical or
conservative management1 found that percent dislocation of the vertebrae may affect the
prognosis of the patient. The degree of dislocation (0-100%) was calculated by the displacement
of the vertebral canal between the cranial and caudal segment. Our patient had less than twenty
percent dislocation and therefore had a good prognosis for return to normal or near normal
function. Although our patient may have improved with rest and medical management, surgical
stabilization was recommended in order to prevent further damage from occurring, and allow for
a faster recovery in a young, large breed, excitable dog.
Treatment:
As pelvic limb nociception was intact, he was a candidate for medical management.
However, the amount of instability of his spine was unknown, and the owner opted to proceed
with surgical stabilization.6
In animals that undergo medical management, strict crate rest for at least six to eight
weeks and vigilant monitoring for worsening sensation are essential.3,10 Anti-inflammatory
medications (non-steroidal anti-inflammatory drugs) as well as pain medications such as opioids,
are also mainstays of medical management6,10
Some veterinarians may splint or cast for
conservative management, but this has possible complications including loosening, abrasions,
sores, and slipping which can cause a fulcrum effect.3
Surgical management was deemed the best option for return to function.6 The purpose of
surgery was to reduce the subluxation and stabilize the spine in a position with the goal of
alleviating compression of the spinal cord.3,6 Pre-anesthetic blood work was unremarkable.
The dog was placed under general anesthesia, placed in sternal recumbency and prepped
for surgery in a sterile fashion. The skin was incised over the T10-L2 vertebrae and the
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subcutaneous tissues were undermined. The thoracolumbar fascia was exposed followed by the
epaxial muscles. Periosteal elevators and electrocautery separated the epaxial musculature from
the right surface of the dorsal spinous processes of T11-L1. An 11 hole 3.5 mm String of Pearls
plate was placed on the right side of the spinous processes from T11-L1 with 6 screws, and a 10
hole 3.5 mm String of Pearls plate was placed on the right side of the vertebral bodies and 7
screws. Screws were placed strategically as to contact only bone. The thoracolumbar and
subcutaneous tissues were each closed in a simple continuous pattern and the skin was closed
with stainless steel staples. Two large Tegaderm bandages were placed over the incision and it
was iced postoperatively. He woke from anesthesia without complications.
Due to the intense and expensive medical and surgical management of animals with acute
spinal injuries, euthanasia would have been a reasonable option.
The owner needs to be
counseled extensively prior to surgery on the realities of postoperative restriction, rehabilitation,
and nursing care.
Postoperative management of surgical patients is similar to medical
management with six to eight weeks of crate rest, sling walks, anti-inflammatory and pain
medications.
Outcome:
Postoperative radiographs of the thoracolumbar vertebrae revealed questionable
placement of the cranial screw of the vertebral body plate. It was difficult to tell whether the
screw had penetrated the spinal canal. Another CT scan was performed and demonstrated
penetration of the spinal canal, but the damage to the soft tissues was difficult to assess. As this
screw needed to be removed immediately, the patient went back to surgery.
The surgery was approached in a similar fashion as previously described with removal of
the staples and sutures to expose the thoracic vertebrae. A screwdriver was used to manually
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loosen the screw on the vertebral body plate. The first screw on the vertebral body plate was
removed as well as the cranial two pearls on the String of Pearls plate. A mini-hemilaminectomy
was performed and the spinal canal and cord were visualized were the screw had penetrated the
canal. There was damage to the dura and some bruising at the ventrolateral aspect of the spinal
cord, but the spinal cord had no hemorrhage, nor was a spinal cord puncture visualized. The site
was flushed and suctioned, and gelfoam was placed over the mini-hemilaminectomy site.
Closure of the site and postoperative care was similar to the previous surgery.
A neurologic examination postoperatively revealed no voluntary motor function in the
hindlimbs. Since locomotion could not be properly assessed before surgery, this finding may
have been the same or his neurological status may have deteriorated after surgery. Some animals
become slightly worse postoperatively due to manipulation of the spinal cord. Superficial pain
perception was still intact, and his prognosis was still good to regain locomotion.
Postoperatively, the patient was placed on intravenous pantoprazole, a proton pump
inhibitor, for gastrointestinal protection since he had a history of high corticosteroid
administration prior to his arrival. He was maintained on intravenous fluids, fentanyl, and
dexmedetomidine which were discontinued after a few days. His incision was iced every eight
hours. He was also given broad-spectrum antibiotics intravenously for one week and then
changed to oral antibiotics for an additional week. Pregabalin, which targets voltage-gated
calcium channels and decreases neuropathic pain, was added. He was unable to urinate on his
own for the first three days after surgery and became refractory to manual expression. An
indwelling Foley urinary catheter was placed. It was removed after one week, and the patient
exhibited voluntary urination two days after its removal.
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Five days post-operatively, his left pelvic limb strength was significantly improved as
compared to the right, as he was able to hold the left above the ground during walks. His
temperature was elevated at this time, and pneumonia was a concern. Chest radiographs showed
clear lung fields. On day seven postoperatively, he was able to flex his left stifle and hip
showing that he had motor in the left pelvic limb. Passive range of motion and massaging of the
pelvic limbs were performed every six hours. A cart was used to allow him to walk on his own
outside which he seemed to enjoy. He was flipped to the opposite side of recumbency every four
hours to prevent sores for the duration of his stay.
The cutaneous trunci reflex improved more quickly on the left side than the right. There
may have been more damage to the spinal cord on the right side that was unable to be seen in the
mini-hemilaminectomy site.
After the first couple of weeks, voluntary motor function slowly improved initially only
in the left hindlimb, though the right hindlimb demonstrated motor function in the third week.
The patient was discharged four weeks after his initial surgery with good motor function
bilaterally. He had good proprioception in the left limb, and improving proprioception of the
right limb. He was able to ambulate with minimal support of a sling.
Rehabilitation in the hospital included passive range of motion exercises and hindlimb
massage, as well as many other treatments. He received laser treatments which deliver energy
that is believed to quicken healing. Proprioceptive exercises included paw placements (flipping
the paw on its dorsal surface and have the patient correct it) and swaying his hind end side-toside to have him put weight on each limb separately. Sitting and standing exercises were
performed next to a wall for support, water treadmill exercises, and hill climbing with steady
inclines of twenty to thirty degrees helped strengthen his hindlimb muscles.6
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For home management, Purina Joint Mobility dry food and fish oil were recommended.
Both are joint protectants and the omega-3 fatty acids of fish oil have anti-inflammatory
properties. Caloric intake was monitored since weight gain can cause excess stress on joints.
Physical therapy exercises were taught to the owner to be continued at home. A sling was used
for slick surfaces as well as leash walks outdoors.
At the twelve-week recheck, radiographs revealed that the plates and screws remained in
the proper position and no other radiographic abnormalities were found.
The patient was
continuing to improve at home, and although he still had difficulty on slick surfaces, he was
comfortable on carpet and grass. He enjoyed playing and had begun using stairs with the support
of a sling.
Discussion:
Vertebral fractures and luxations occur in about 6% of cases that present with neurologic
deficits indicative of a myelopathy. The T10-L2 region is a very common site most likely due to
its location between the rigid thoracic spine and the more mobile lumbar spine.6
It is important to note that anti-inflammatory medication used in acute spinal injury is
controversial. It used to be thought that corticosteroids were important in treating these cases.
They are free-radical scavenging, anti-inflammatory, and preserve spinal cord blood flow.10 In
the 1990s, it was then found that they were beneficial if used in the first eight hours post-injury.10
It was reported that if given after eight hours, there is increased risk of complications, such as
pneumonia and sepsis. It seems that corticosteroids are currently being phased out and NSAIDs
are now more commonly used by small animal practitioners.10
A thorough neurologic examination is essential when evaluating animals with spinal
injuries, as it allows neurolocalization and prognostication.8 Without a thorough examination,
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there is a chance that a lesion may be missed and confused with an orthopedic lesion. Serial
examinations are equally as important to assess the patient over time.8
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References:
1) Bali, M. S. et al. "Comparative Study of Vertebral Fractures and Luxations in Dogs and Cats."
Veterinary and Comparative Orthopaedics and Traumatology (VCOT) 1 (2009): 47-53,
Print.
2) Burke RE. “Anatomy of the spinal cord.” The Encyclopedia of the Neurological Sciences 4
(2003): 339-348, Print.
3) Carberry, C., Flanders, J. et al. “Nonsurgical Management of Thoracic and Lumbar Spinal
Fractures and Fracture/Luxations in the Dog and Cat: A Review of 17 Cases.” Journal of
the Americal Animal Hospital Association 25 (1989): 43-54, Print.
4) Cerda-Gonzales, S. “Myelopathies I and II.” Animal Health and Disease Part II. Ithaca, NY.
13 Feb. 2014.
5) FitzMaurice, Marnie. "Neuroanatomy." Animal Health and Disease Part II. Ithaca, NY. 02
Feb. 2014.
6) Jeffery, Nick. “Vertebral Fracture and Luxation in Small Animals.” Veterinary Clinics of
North America: Small Animal Practice 5 (2010): 809-828, Print.
7) Johnson, P., Beltran, E., Dennis, R. and Taeymans, O. “Magnetic Resonance Imaging
Characteristics of Suspected Vertebral Instability Associated with Fracture or
Subluxation in Eleven Dogs.” Veterinary Radiology & Ultrasound 53 (2012): 552–559,
Print.
8) Kirby, B. “Spinal Fracture/Luxation.” Veterinary Clinics of North America: Small Animal
Practice, Management of Orthopedic Emergencies 25 (1995): 1149-1173, Print.
9) Olby, Natasha. “The Pathogenesis and Treatment of Acute Spinal Cord Injuries in Dogs.”
Veterinary Clinics of North America: Small Animal Practice 40 (2010): 791-807, Print.
10) Park, E., White, G., Tieber, L. “Mechanisms of Injury and Emergency Care of Acute Spinal
Cord Injury in Dogs and Cats.” Journal of Veterinary Emergency and Critical Care 22
(2012): 160–178, Print.
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