A 4-year-old sexually intact male mixed-breed dog (weight, 26 kg [57.2 lb]) was referred to the Department of Medicine and Clinical Biology of Small Animals, Ghent University, for the investigation of rapidly progressive general malaise and paraplegia. The day before the initial examination, the dog started to display signs of lethargy and anorexia. Results of a general physical examination, performed by the referring veterinarian, demonstrated an increased body temperature of 39.9°C (104°F). A CBC, biochemical panel, and abdominal radiographs were unremarkable at this time. The dog started to show neurologic signs of spinal hyperesthesia and pelvic limb ataxia, rapidly progressing to paraparesis and finally paraplegia. At this time, the dog was referred.
General physical examination revealed a body temperature of 39°C (102°F), a pulse rate of 140 beats/min, and a respiratory rate of 44 breaths/min. The dog was reluctant to move.
Neurologic examination revealed paraplegia with absent proprioception, urinary incontinence, bilaterally absent cutanei trunci reflexes, increased patellar reflexes, and decreased nociception in both pelvic limbs. Palpation of the thoracolumbar region elicited signs of extreme pain. A CBC revealed a mild leukocytosis (17.109/L; reference range, 6 to 12.109/L) with a neutrophilia (14.4 109/L; reference range, 3 to 10.109/L), and the results of a biochemical profile were within the reference range. The dog was premedicated for low-field MRIa with acepromazine maleate (0.01 mg/kg [0.0045 mg/lb], IV) and methadone (0.02 mg/kg [0.009 mg/dL], IV). Anesthesia was induced with alfaxalone (2 mg/kg [0.91 mg/dL], IV)b and maintained with isoflurane in oxygen.
Magnetic resonance imaging of the thoracolumbar region demonstrated a marked hyperintense, heterogeneous, ill-defined lesion bilaterally in the longissimus thoracic, semispinosus, and multifidus thoracic muscles from the caudal aspect of T10 through the cranial aspect of L2 on the sagittal (Figure 1), dorsal, and transverse (Figure 2) T2-weighted and short tau inversion recovery sequences. This lesion appeared isointense to mildly hyperintense on T1-weighted images and demonstrated prominent enhancement with gadolinium contrast (0.3 mg/kg [0.14 mg/lb], IV).c No obvious involvement of the surrounding vertebral structures was seen. This lesion extended into the vertebral canal and was determined to be hyperintense on T1- and T2-weighted images, causing marked dorsal to dorsolateral extradural spinal cord compression at the level of T12–13 and showing mild contrast enhancement. Immediately following the MRI procedure, CSF was collected by a lumbar puncture and was within reference limits.
Spinal epidural empyema with inflammation of the epaxial muscles was considered the most likely differential diagnosis. Urine and blood samples were obtained under sterile conditions for further bacteriologic culture. A urinary catheter was placed. Because of the rapidly progressive neurologic deterioration and the presence of extradural spinal cord compression, the dog was immediately admitted for decompressive surgery. Intraoperative analgesia was provided with a continuous rate infusion of fentanyl (7 μg/kg/h [3.2 μg/lb/h], IV) and lidocaine (30 μg/kg/min [13.64 μg/lb/min], IV). The patient was positioned in sternal recumbency and prepped and draped for aseptic surgery in standard fashion. During a standard dorsal approach1 to the thoracolumbar vertebral column, abnormalities of the epaxial musculature were noticed. The muscles had a swollen, pale, and friable appearance. A standard dorsal laminectomy with preservation of the articular facet joints was performed at the level of T12–13. During inspection of the vertebral canal, the spinal cord was swollen, and the epidural fat had a granular and dark red appearance. Several biopsy samples were collected from the epaxial musculature, epidural fat, and spinous processes. Thereafter, broad-spectrum antimicrobials were administered (amoxicillin-clavulanic acid, 20 mg/kg [9.09 mg/lb], IV, q 2 h). The laminectomy defect was extended cranially and caudally until normal-appearing epidural fat was encountered. This resulted in a continuous dorsal laminectomy from T10 through L2. Finally, the abnormal, granular epidural fat was removed as much as possible by means of curettage, and the vertebral canal was copiously lavaged with sterile physiologic saline (0.9% NaCl) solution. A synthetic cellulose patchd was placed in the laminectomy defect, and the surgery site was closed via a routine 3-layer closure by means of polydioxanone and polyglecaprone. The biopsy samples were submitted for aerobic bacteriologic culture and histologic examination.
The dog was hospitalized after surgery with an indwelling urinary catheter and was administered IV fluids, a broad-spectrum antimicrobial (amoxicillin-clavulanic acid, 20 mg/kg, IV, q 8 h), enrofloxacin, (5 mg/kg [2.27 mg/lb], IV, q 24 h), a gastroprotective agent (ranitidine, 2 mg/kg [0.907 mg/lb], IV, q 12 h), and an NSAID (carprofen, 2 mg/kg, IV, q 24 h). The postoperative analgesia consisted of a constant rate infusion of lidocaine (30 μg/kg/min, IV), morphine (0.4 mg/kg [0.18 mg/lb], IV, q 4 h) for the first 24 hours, and paracetamol (10 mg/kg [4.55 mg/lb], IV, q 12 h)e for 4 consecutive days. On postoperative day 4 a fentanyl patch (100 μg/h) was applied, and was removed one day before discharge from the hospital, when the dog commenced oral pain medication.
During hospitalization, a complete neurologic examination was performed daily. Two days after surgery, nociception had returned to normal. After 5 days of inappetence, a nasoesophageal tube was placed and enteral feeding was initiated. On the seventh day after surgery, the dog was able to support its weight and started eating on its own. At this time, the urinary catheter and the nasoesophageal tube were removed, and the dog started urinating. The dog was discharged 8 days after surgery. Pending the results of bacteriologic cultures and histologic examinations, the owners were advised to administer enrofloxacin (5 mg/kg, PO, q 24 h), amoxicillin-clavulanic acid (12.5 mg/kg [5.67 mg/lb], PO, q 12 h), carprofen (4 mg/kg [1.81 mg/lb], PO, q 24 h), and ranitidine (2 mg/kg, PO, q 12 h). No physical therapy was initiated at this time.
Cultures of blood and urine samples as well as aerobic bacterial cultures of muscle and epidural fat specimens were negative. Histologic examination of the muscle biopsy specimen revealed diffuse intercellular edema with infiltration of neutrophils between the mostly swollen myocytes, which showed a hyaline eosinophilic or fragmented sarcoplasm. The epidural fat specimen revealed well-differentiated adipose tissue with infiltrated neutrophils and macrophages and scattered bleedings. Histologic examination of the spinous process revealed a normal bony structure. These findings confirmed a diagnosis of suppurative myositis and suppurative epidural steatitis. In light of the negative bacteriological cultures, antimicrobial treatment was discontinued.
Twenty-nine days, 30 days, 62 days, and 2 years after surgery, the dog was re-evaluated at Ghent University. Twenty-nine days after surgery, the dog was able to ambulate with support, although still severely ataxic. At this time, proprioceptive deficits were still present. The owners were advised to initiate hydrotherapy, which they started the same day. The next day, the dog had a clinical relapse, consisting of recurrence of spinal hyperesthesia. On admission, physical and neurologic examinations were unchanged, and a CBC and biochemical panel were unremarkable. A tapering oral prednisolone treatment was initiated for 3 weeks (1 mg/kg [0.45 mg/lb], PO, q 24 h for 1 week; 0.5 mg/kg [0.23 mg/lb], PO, q 24 h for 1 week; and 0.5 mg/kg, PO, q 48 h for 1 week). Sixty-two days after surgery, the dog was able to ambulate independently. Neurologic examination revealed only moderate pelvic limb ataxia. No more clinical relapses were noticed by the owners. Two years after surgery, only mild pelvic limb ataxia was present, and further neurologic examination was unremarkable. Three years after surgery, the owners confirmed an unchanged neurologic status.
Airis Mate, Hitachi Ltd, Tokyo, Japan.
Alfaxan, Vétoquinol, London, England.
Dotarem, Guerbet, Brussels, Belgium.
Gelfoam, Pfizer Manufacturing, Puurs, Belgium.
Perfusalgan, Bristol-Meyers Squibb, Braine-l'Alleud, Belgium.
1. Coates JR, Hoffman AG, Dewey CW, Surgical approaches to the central nervous system. Slatter D, Textbook of small animal surgery. 3rd ed. Philadelphia: Saunders, 2003; 1157–1159.
2. Scott DW, Miller WH, Griffin CE, Miscellaneous skin diseases. Scott DW, Miller WH, Griffin CE, Muller and Kirk's small animal dermatology. 6th ed. Philadelphia: WB Saunders Co, 2000; 1156–1162.
3. Gross TL, Ihrke PJ, Walder EJet al., Diseases of the panniculus. Gross TL, Ihrke PJ, Walder EJet al., Skin diseases of the dog and cat: clinical and histopathologic diagnosis. 2nd ed. Ames, Iowa: Blackwell Science Ltd, 2005; 538–551.
4. O'Kell AL, Inteeworn N, Diaz SFet al., Canine sterile nodular panniculitis: a retrospective study of 14 cases. J Vet Intern Med. 2009; 23:1–7.
5. Yamagishi C, Momoi Y, Kobayashi Tet al., A retrospective study and gene analysis of canine sterile panniculitis. J Vet Med Sci. 2007; 69:915–924.
6. Aikawa T, Yoshigae Y, Kanazono S, Epidural idiopathic sterile pyogranulomatous inflammation causing spinal cord compressive injury in five miniature Dachshunds. Vet Surg. 2008; 37:594–601.
8. Cherrone KL, Eich CS, Bonzynski JJ, Suspected paraspinal abscess and spinal epidural empyema in a dog. J Am Anim Hosp Assoc. 2002; 38:149–151.
10. De Stefani A, Garosi LS, McConell FJet al., Magnetic resonance imaging features of spinal epidural empyema in five dogs. Vet Radiol Ultrasound. 2008; 49:135–140.
12. Sutton A, May C, Coughlan A, Spinal osteomyelitis and epidural empyema in a dog due to migrating conifer material. Vet Rec. 2010; 166:693–694.
13. Darouiche RO, Hamill RJ, Greenberg SBet al., Bacterial spinal epidural abscess. Review of 43 cases and literature survey. Medicine. 1992; 71:369–385.