An 8-year-old 37.1-kg (81.6-lb) sexually intact male pit bull-type dog was referred to the University of Georgia because of a 3-month history of left pelvic limb lameness. Three months prior to the referral evaluation, the dog was chasing water from a hose when it suddenly cried out and was immediately lame on the left pelvic limb. The referring veterinarian treated the dog with tramadol (4 mg/kg [1.82 mg/lb], PO, q 8 to 12 h) and carprofen (2.2 mg/kg [1.0 mg/lb], PO, q 12 h). Despite medical treatment, the dog remained lame and would intermittently hold the left pelvic limb off the ground. Over the subsequent 3 months, the dog's activity level decreased. Three days prior to the referral evaluation, radiography of the pelvis revealed an enlarged prostate and a round, mineralized mass extending from the left ventrolateral aspect of the body of the L7 vertebra causing ventral deviation of the descending colon. Pronounced osteolysis of the L7 vertebra was not present. On the basis of the radiographic findings, the dog was referred for further evaluation. At that evaluation, results of physical and orthopedic examinations were considered normal.
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Assessment
Anatomic diagnosis
Problem | Rule out location |
---|---|
Left pelvic limb lameness | Lower motor neuron (LMN) units of the left pelvic limb (ie, L6-S1 spinal cord segments, spinal nerve roots, spinal nerves, lumbar plexus, the sciatic nerve, or neuromuscular junctions of the muscles or the muscles themselves that are innervated by the sciatic nerve) or an orthopedic disease involving the bones, tendons, ligaments, or joints of the left pelvic limb |
Decreased hock flexion during the protraction (swing) phase of the gait in the left pelvic limb | Lower motor neuron units of the left pelvic limb (ie, L6-S1 spinal cord segments, spinal nerve roots, spinal nerves, lumbar plexus or the fibular [peroneal] branch of the sciatic nerve, neuromuscular junctions of the muscles that are innervated by the sciatic nerve, or the cranial tibial muscle) |
Weight off-loading from the left pelvic limb when standing | Pain in the left limb attributable to compression or inflammation of a nerve, musculoskeletal disease, tendon or ligament disease, arthropathy, or disease involving the weight–bearing surface of the foot such as the footpads |
Delayed postural reactions in the left pelvic limb | Nerves of the left pelvic limb (LMN units or the sensory nerves) or a lesion involving the general proprioceptive and upper motor neuron pathways (ie, the ipsilateral side of the spinal cord and brain from the midbrain to the medulla or the contralateral prosencephalon [cerebrum or thalamus]) |
Reduced withdrawal (flexor) reflex with normal patellar (quadriceps) reflex in the left pelvic limb | Lower motor neuron units from L6 through S1 spinal cord segments, spinal nerve roots, spinal nerves, lumbar plexus, the sciatic nerve, or neuromuscular junctions of the muscles or the muscles themselves that are innervated by the sciatic nerve |
Atrophy of the muscles of the left pelvic limb | Neurogenic or disuse atrophy |
Likely location of 1 lesion
Left-sided lesion involving the LMN units from L6 through S1 spinal cord segments, spinal nerve roots, spinal nerves, lumbar plexus, the sciatic nerve, or neuromuscular junctions of the muscles or the muscles themselves that are innervated by the sciatic nerve, specifically the fibular (peroneal) branch. |
Etiologic diagnosis—Given the progression of the clinical signs and the radiographic findings, the primary differential diagnoses included vertebral neoplasia (primary vertebral neoplasms [ie, osteosarcoma, chondrosarcoma, fibrosarcoma, or hemangiosarcoma], metastatic neoplasia [ie, prostatic neoplasia or transitional cell carcinoma of the urinary bladder or urethra], or hematopoietic neoplasia [lymphoma, histiocytic sarcoma complex, or plasma cell neoplasia]). Because of the absence of notable osteolysis, osteomyelitis was unlikely. The diagnostic plan included a CBC and serum biochemical profile (to evaluate for evidence of systemic involvement other than the L7 vertebra), 3-view thoracic radiography (to evaluate for evidence of primary or metastatic neoplasia), abdominal radiography and ultrasonography (to evaluate for evidence of primary or metastatic neoplasia and to further evaluate the prostatomegaly), and cross-sectional imaging of the caudal lumbar vertebral column, sacrum, and pelvis with CT (to define the extent of the bony involvement of the L7 vertebra, adjacent vertebrae, and the paravertebral soft tissues) and MRI (to define the extent of involvement of the L6 through S1 spinal cord segments, spinal nerve roots, spinal nerves, lumbar plexus, or sciatic nerve on the left side). Additional diagnostic testing including fine-needle aspiration and biopsy of the mineralized mass; CSF fluid sample collection and analysis was to be considered depending on initial diagnostic findings.
Diagnostic test findings—Results of the CBC, serum biochemical profile, and 3-view thoracic radiography were considered normal. Abdominal ultrasonography revealed an approximately round (3.5-cm-diameter) mass with a thin (0.2-cm-wide) rim of echogenic tissue and complete distal acoustic shadowing that resulted in ventral and rightward deviation of the descending colon. The prostate was symmetrically enlarged (2 × 3 × 4 cm) and hyperechoic with anechoic cysts. Ultrasound-guided fine-needle aspiration of the prostate and mineralized mass was performed. Cytologic evaluation of the mineralized mass specimen revealed mesenchymal cells with features suggestive of osteosarcoma; definitive diagnosis necessitated histologic examination of tissue sections. Results of cytologic evaluation of the prostate specimen were consistent with benign prostatic hypertrophy.
By use of a 3.0-T MRI unit, sagittal and transverse T1-weighted and T2-weighted images without and with fat saturation (Dixon technique) of the caudal lumbar vertebral column, sacrum, and pelvis were obtained. Following IV administration of a gadolinium-based contrast medium, T1-weighted images without and with fat saturation (Dixon technique) also were obtained. The MRI examination revealed a well-delineated mass (4.8 × 5.9 × 5.4 cm) extending from the left ventrolateral aspect of the body of the L7 vertebra. The mass extended cranially over the ventral surface of the body of the L6 vertebra and caudally over the cranioventral aspect of the sacrum (Figure 1). Laterally, the mass extended to the medial surface of the left ilium from the cranial aspect of the iliac wing to the cranial aspect of the sacroiliac articulation. The mass extended dorsally into the left L6–7 and lumbosacral intervertebral foramina and obscured visualization of the left L6 and L7 spinal nerves and lumbar plexus. The mass caused ventral deviation of the adjacent vasculature and colon. The mass had a heterogeneous signal intensity on T1-weighted and T2-weighted sequences with areas that were hypo-, iso-, and hyperintense compared with the cancellous bone of unaffected vertebral bodies. There were areas of lysis of the ventrolateral cortex of the body of the L7 vertebra. Compared with the unaffected vertebrae, the cancellous bone of the L7 vertebral body appeared similar on T2-weighted images and hypointense on T1-weighted images. The mass and the cancellous bone in the body of the L7 vertebra had strong heterogeneous contrast enhancement.
On the CT images, the mass was lobular, heterogeneously and densely mineralized with a thin soft tissue periphery. The extent of lysis of the cortical bone of the body of the L7 vertebra was more conspicuous than it appeared on MRI images. There was marked heterogeneity and sclerosis of the cancellous bone of the body of the L7 vertebra. A CT-guided core tissue biopsy of the vertebral body mass was obtained with 14-gauge soft tissue biopsy needle. Microscopically, the biopsy specimen was composed of irregular sheets of chondrocytes with mild anisocytosis and anisokaryosis consistent with chondrosarcoma.
After discussion with the owner, gross cytoreductive surgery was performed with palliative intent (to alleviate compression of the L6 and L7 spinal nerves, thereby relieving pain as well as potentially delaying future impairment of urination and defecation from compression of the urethra and colon, respectively). A caudal ventral midline celiotomy was performed, the left and right internal and external iliac arteries and veins were isolated and retracted to their respective sides, and gross cytoreduction of the mass was accomplished with a periosteal elevator (Figure 2). Portions of the mass were submitted for histologic examination.
Histologically, sections of the mass were composed of a well-structured lattice of mature, bony spicules that were interdigitated by neoplastic cells surrounded by osteoid material with multifocal areas of transition into disorganized cartilage supported by various amounts of chondroid matrix. The neoplastic cells were elongated and spindloid with indistinct cell borders. Nuclei were large, oval, and hyperchromatic with 1 to 3 small nucleoli. Anisocytosis and anisokaryosis were mild. The mitotic rate was 9 mitotic figures/10 hpfs (400X). There were large, multifocal areas of organized endochondral and intramembranous ossification with periosteal proliferation within the woven bone. Findings were consistent with osteosarcoma (likely periosteal with chondroid differentiation).
Comments
The anatomic diagnosis of LMN dysfunction includes the LMN cell body located within the CNS (brainstem or spinal cord), its axons that form the roots and named nerves (cranial nerves or nerves of the limbs), neuromuscular junctions, and effector muscles. Lower motor neuron dysfunction and orthopedic disease have several clinical features in common, which make differentiation challenging. Both LMN dysfunction and orthopedic disease can result in lameness, inability or reluctance to bear weight, signs of pain, and muscular atrophy. In the case described in the present report, the observation of abnormal postural reactions and reduced spinal reflexes supported the diagnosis of LMN dysfunction. As often occurs, orthopedic disease can coexist with LMN dysfunction, creating difficulty in determining the principal cause of the clinical signs. Ultimately, radiography defined the presumptive etiologic diagnosis of a vertebral neoplasm in this case.
Vertebral neoplasms are the most common neoplasms to affect the spinal cord, spinal nerve roots, or spinal nerves in dogs. Vertebral neoplasms are categorized as primary or metastatic. The most common primary vertebral neoplasm is osteosarcoma.1–3 Other primary vertebral neoplasms include fibrosarcoma, hemangiosarcoma, and chondrosarcoma.1–3 Hematopoietic neoplasms can also affect vertebrae but typically are multicentric.
In dogs, osteosarcomas account for approximately 85% of malignant neoplasms that affect the skeleton.4,5 Osteosarcoma most often affects the appendicular skeleton, whereas vertebral osteosarcoma accounts for only 6.5% of cases.2 Osteosarcoma tends to affect large-breed dogs at a median age that ranges from 8 to 10 years.2,3,6,7 Commonly affected breeds include Great Dane, Saint Bernard, Doberman Pinscher, German Shepherd Dog, Rottweiler, Golden Retriever, and Irish Setter.4
Neurologic signs secondary to vertebral osteosarcoma may include signs of pain, paresis, or paralysis. The specific vertebra affected dictates the anatomic diagnosis. Signs are secondary to extradural compression of the spinal cord or compression of spinal roots or spinal nerves. A presumptive diagnosis is based on imaging findings. Radiography reveals a vertebral mass with a mixed pattern of osteolysis and proliferation3; however, similar radiographic changes may be observed with other primary vertebral neoplasms.3 Computed tomography and MRI better characterize the extent of involvement of the affected vertebra.8,9 Furthermore, MRI allows for identification of compression of nervous tissues. With MRI, affected vertebrae are often hypointense on T1-weighted images, hyperintense on T2-weighted images, and variably contrast enhanced.8,9 A definitive diagnosis requires histologic examination of sections of the neoplasm.
The case described in the present report highlighted the importance of obtaining a representative specimen of the neoplasm for histologic examination. The histologic appearance of osteosarcoma is diverse; osteosarcoma is comprised of malignant neoplastic mesenchymal cells and variable types and amounts of extracellular matrices such as collagen, cartilage, and osteoid.5 For the dog of the present report, the initial histologic diagnosis was based on examination of a tissue core specimen that was devoid of osteoid but contained cartilage, suggesting a diagnosis of chondrosarcoma. As a consequence of the small size of needle core specimens, the sample collected was composed mostly of cartilaginous matrix. The small size of a needle core biopsy specimen is a limitation that can lead to a misdiagnosis. To overcome this issue, multiple samples of a lesion should be collected when possible.
Treatment for vertebral osteosarcoma includes surgery, radiation therapy, or chemotherapy; often multimodal treatment is used. Median survival times for dogs with vertebral osteosarcomas that receive definitive treatment range from 55 to 155 days.6,7,10 Alternatively, palliative treatment can be given to improve neurologic function and pain control by means of cytoreductive surgery; administration of corticosteroids, analgesics, and bisphosphonates; and palliative radiation protocols.
The prognosis for dogs with vertebral osteosarcoma is guarded to poor. Approximately 55% of affected dogs die of local disease, whereas approximately 45% die of metastatic disease.6,7 In the case described in the present report, cytoreductive surgery alone was undertaken. Following surgery, the dog had difficulty walking and urinary incontinence, both of which resolved over 7 days. Two months after surgery, the dog appeared comfortable and continued to have improvement in neurologic function of the left pelvic limb. Approximately 6 months after surgery, the dog was euthanized via IV injection of a barbiturate solution because of recurrence of lameness and an inability to defecate.
References
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