A 7-year-old 55.6-kg (122.3-lb) castrated male Great Dane was evaluated at the North Carolina State University's Veterinary Teaching Hospital because of a 2-month history of fecal incontinence. The owner speculated that the incontinence was associated with the trauma of being mounted by another Great Dane in the household; these traumatic events occurred regularly during play. The fecal incontinence appeared to wax and wane because the dog was fecally continent for periods of 1 to 2 weeks.
The owner had noticed 2 different types of incontinence. First, although the dog could defecate voluntarily when taken outside, at times it appeared unaware that it was defecating as it walked. In addition, formed stools were found on its bedding and were frequently eliminated as the dog rose from a lying position. However, the owner also reported that the dog occasionally became acutely aware of the need to defecate, but was unable to prevent defecation as it tried to get outside of the house. On these occasions, the owner thought that the dog was aware that it was defecating, but could not control the reflex. The owner was able to minimize episodes of fecal incontinence by taking the dog outside frequently. The owner had not noticed any urinary incontinence and reported that the dog postured normally to urinate and defecate, producing normal streams of urine as well as feces that were formed and normal in appearance.
Additional historical information included a long-term history of intermittent scuffing of the left hind limb. The owner had noted that the nails of the left hind foot were more worn on the dorsal aspect than those of the other feet. The dog also had a long-term history of hip dysplasia, for which it received medical treatment. One and a half months prior to the initial evaluation, treatment with glucosamine (9 mg/kg [4.1 mg/lb], PO, q 12 h) and chondroitin (7.2 mg/kg [3.3 mg/lb], PO, q 12 h) provided in a supplementa had been initiated for chronic hip dysplasia and presumed arthritis. The owner noticed mild improvement in the dog's scuffing during treatment with this medication, particularly at night. No other problems were reported. The vaccination status of the dog was current, and it was treated monthly with selamectinb (6.5 mg/kg [3 mg/lb], PO) as a flea, tick, and heartworm preventative medication. Results of analyses of blood samples performed by the referring veterinarian 6 months previously were within reference limits.
On physical examination, the dog was alert but apprehensive and panting; rectal temperature was 38.8°C (101.8°F) and heart rate was 132 beats/min. Mild muscle atrophy was evident in both hind limbs. Findings of the physical examination were otherwise unremarkable, and no orthopedic abnormalities were detected. Results of a digital examination per rectum were also considered within normal limits. On neurologic examination, the dog had an abnormal posture at rest with a wide-based hind limb stance. When walking, the dog was mildly paraparetic with moderate hind limb ataxia; the left hind limb was more severely affected than the right. Postural reactions including conscious proprioception were decreased in the left hind limb, but were considered normal in all other limbs. Mild hyperesthesia was detected via palpation of the lumbosacral junction of the vertebral column. Mentation, cranial nerve, and spinal reflexes (including the perineal reflex) were within normal limits. No further abnormalities were detected during the neurologic examination. While in the hospital, feces were found in the cage where the dog had been lying, although normal defecation was also witnessed. On the basis of the presence of paraparesis with normal spinal reflexes, the neurologic signs were localized from the third thoracic to the third lumbar spinal cord segments.
Routine blood analyses were performed. A CBC revealed mild thrombocytopenia (183 × 103 platelets/μL; reference range, 206 to 378 × 103 platelets/μL), and results of serum biochemical analyses were unremarkable. Because of the age of the dog, 3 orthogonal radiographic views of the thorax were obtained to assess for metastatic neoplasia. Radiography revealed spondylosis deformans of the thoracic portion of the vertebral column, but no other abnormalities. Abdominal ultrasonography did not reveal any notable abnormalities.
Magnetic resonance imaging of the thoracolumbar portion of the vertebral column was performed by use of a 1.5-Tesla MRI unit.c Multiple imaging sequences of the vertebral column from the third thoracic to the third sacral vertebrae were obtained, before and after IV administration of contrast mediumd; these included T2-weighted sagittal and transverse sequences, a sagittal STIR sequence, a T2-weighted sagittal myelographic sequence, and sagittal and transverse T1-weighted sequences obtained before and after administration of contrast medium. The sagittal T2-weighted and STIR images revealed subtle narrowing of the T13-L1 intervertebral space, and hypointensity of the corresponding intervertebral disk (compared with surrounding disks) that was consistent with desiccation of the nucleus pulposus at this site (Figure 1). On sagittal and transverse T2-weighted images, an area of signal void that was overlaid dorsally by an epidural mass (which was isointense, compared with the surrounding musculature) was detected in the vertebral canal above the T13-L1 intervertebral disk space (Figures 1 and 2). On transverse images, the epidural mass was located on the right side of the vertebral canal, causing displacement and compression of the spinal cord over the disk space, and extended caudally over the body of the first lumbar vertebra for approximately 1 cm. The intensity varied along the length of the mass. Compared with the spinal cord, the mass was both isointense to mildly hypointense and moderately hyperintense on T2-weighted images; on T1-weighted images, the epidural mass appeared variably hyperintense and isointense. Additionally, contrast enhancement of the periphery of the epidural material was detected on comparison of the T1-weighted images obtained before and after contrast medium administration. A small area of increased signal was evident within the spinal cord on transverse T2-weighted images; this area surrounded the central canal at the level of compression. Multiple desiccated intervertebral disks were also present in the thoracic portion of the vertebral column.
On the basis of findings of MRI, a presumptive diagnosis of a compressive intervertebral disk extrusion with secondary hemorrhage and epidural hematoma formation was made. It was speculated that extruded disk material was a component of the mass because of the region of signal void overlying the disk space at that site and because of the hypointensity of the nucleus pulposus of the intervertebral disk, which was indicative of desiccation. However, the variable appearance of the epidural compressive mass and, specifically, the increased signal on the T1-weighted images was not consistent with herniated disk material, but rather more consistent with a vascular event. The compressive lesion was therefore attributed to an organizing chronic hematoma containing primarily methemoglobin, with associated extruded disk material and spinal cord compression. Because of the contrast enhancement of the lesion in images obtained after administration of contrast medium, an epidural hemorrhagic neoplasm could not be excluded, but was considered unlikely. The area of hyperintensity within the spinal cord was presumed to be intraparenchymal edema at that site.
A right-sided hemilaminectomy was performed (centered at the T13-L1 intervertebral space) to further characterize the lesion and decompress the spinal cord. The dog was premedicated with hydromorphonee (0.05 mg/kg [0.023 mg/lb], IM) and acepromazinef (0.01 mg/kg [0.005 mg/lb], IM). Anesthesia was induced with propofolg (2.6 mg/kg [1.18 mg/lb], IV) and midazolamh (0.2 mg/kg [0.09 mg/lb], IV) and maintained via inhalation of isoflurane and oxygen. A continuous rate infusion of lidocainei (0.03 to 0.07 mg/kg/min [0.01 to 0.03 mg/lb/min], IV) was also administered during the surgery; cefazolinj (22 mg/kg [10 mg/lb], IV) was administered perioperatively. A routine surgical technique was used to perform the right-sided hemilaminectomy. A small amount of extruded disk material was found overlying the T13-L1 intervertebral space along with moderate amounts of what appeared to be an organized hematoma. The hematoma and disk material were removed and submitted for histologic analysis. The spinal cord was fully decompressed and appeared normal at the time of surgical closure. The dog tolerated anesthesia well and recovered without complications. Postoperative care included pain management with a fentanyl patchk (100 μg/h), hydromorphonee (0.05 mg/kg, IV, q 4 to 6 h as needed), and carprofenb (2.2 mg/kg [1 mg/lb], PO, q 12 h), and controlled exercise.
Histologic examination of the material obtained at surgery revealed multiple areas of pale, amphophilic matrix with scattered chondrocytes and areas of mineralization, consistent with disk material. Most of the sections analyzed contained a moderate amount of hemorrhage along with clusters of organizing proliferative fibroblasts and infiltrates of macrophages containing hemosiderin pigment. The histopathologic diagnosis was extruded intervertebral disk material with chronic hemorrhage and inflammation.
One day after surgery, the dog was able to ambulate independently, although the hind limb ataxia was slightly more pronounced than it had been previously. The dog was discharged to its owner the following day. At home, the owner had been instructed to restrict the dog's activity (ie, running, jumping, and traversing stairs) and to provide controlled exercise and supportive and incision care. The owner reported that the dog's paraparesis and hind limb ataxia had improved and had returned to the preoperative level within 1 week after discharge. Three weeks after surgery, there was complete resolution of the dog's incontinence and moderate improvements in its hind limb function. On neurologic examination, the dog retained a wide-based stance of the hind limbs as well as mild hind limb ataxia, predominantly on the left side. Postural reactions were improved, compared with findings before surgery, although the dog still had mild proprioceptive deficits in the left hind limb. Mild hind limb muscle atrophy remained. All other aspects of the neurologic and physical examinations were within normal limits. During a follow-up conversation with the owner 43 days after surgery, it was reported that the dog retained complete fecal and urinary continence, and the hind limb ataxia was unchanged.
Magnetic resonance imaging
Short T1 inversion recovery
External anal sphincter
Internal anal sphincter
Nutramax Laboratories, Edgewood, Md.
Pfizer Animal Health, LaJolla, Calif.
MAGNETOM Symphony MRI unit, Siemens Medical Solutions USA Inc, Malvern, Pa.
Gadoversetamide, OptiMARK injection, Mallinckrodt Imaging, St Louis, Mo.
Baxter Health Care Co, Deerfield, Ill.
Vetus Animal Health, Rockville Centre, NY.
Scherring-Plough Corp, Irvine, Calif.
American Pharmaceutical Partners Inc, Schaumburg, Ill.
Butler Co, Dublin, Ohio.
Watson Laboratories Inc, Corona, Calif.
Janssen Pharmaceuticals, Titusville, NJ.
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