Kaylee A. Brown1*+; Martha A. Delaney2; Kathleen M. Colegrove2; Sophie Dennison-Gibby3; Christine M. Fontaine1; Alissa C. Deming1
Abstract
An estimated 5-month-old male Northern elephant seal (Mirounga angustirostris) weanling presented to the Pacific Marine Mammal Center for evaluation of malnutrition and abnormal external spinal conformation. Examination and radiographs revealed thoracic spinal kyphosis and lordosis without instability or visible fractures. Neurological assessment showed no abnormalities. During rehabilitation, the patient displayed normal behaviors and appeared comfortable while swimming and ambulating.
Approximately eight weeks later, the patient developed acute discomfort and paraplegia (hindlimb paralysis and fecal incontinence). Activity restriction and anti-inflammatory therapy was initiated, including dexamethasone (0.2 mg/kg PO SID), transitioned to prednisone (0.2 mg/kg PO BID). After 13 days of treatment without improvement, computed tomography (CT) and magnetic resonance imaging (MRI) were performed at a specialty veterinary clinic. Tiletamine/Zolazepam (1.5 mg/kg IM once) was administered; adequate sedation was achieved within 10 minutes. An intravenous catheter (18-gauge, 2.5-inch needle) was placed in the extradural intravertebral venous sinus. The patient was induced with propofol titrated to effect (1 mg/kg IV slowly; 10 mL total), intubated via laryngeal palpation with an 11 French endotracheal tube, and maintained on inhalant anesthesia (Isoflurane 1–1.5%). Intravenous contrast (Optiray® 300 (300 mgI/mL), 820 mgI/kg IV over 4 minutes; 276 mL total) was delivered without signs of acute negative reactions. The patient remained stable throughout the 3.5-hour anesthetic procedure.
Diagnostic imaging showed thoracic spinal kyphosis with dorsal displacement of an abnormal thoracic vertebra (T4), intervertebral disc space narrowing, endplate sclerosis with bony proliferation, and severe neural canal stenosis. These results suggested a chronic thoracic vertebral injury with subluxation causing severe spinal cord compression. Based on these findings and grave prognosis, humane euthanasia was elected.
Post-mortem examination supported findings of an abnormal spinal conformation with the kyphotic region caudal to C6 vertebra, and apex at T4, followed by a region of lordosis, and diffuse atelectasis of the ventrally displaced lungs. The abnormal spine segment was dissected intact, formalin fixed, and submitted to the Zoological Pathology Program of University of Illinois where it was sectioned longitudinally with a bandsaw. On cut section, the T4–T5 intervertebral disc space was collapsed, T4 dorsally displaced, and T5 positioned at a roughly 45-degree angle ventrally. Histologic evaluation of the affected intervertebral space and associated vertebrae revealed loss and degeneration of disc material and replacement by fibrous tissue. Vertebral end plates had regional sclerosis though otherwise exhibited normal cortical bone and growth plates without evidence of congenital malformation, abnormal physes, or defective endochondral ossification.
Based on clinical history, diagnostic images, and gross and histologic findings, this weanling likely sustained a traumatic vertebral injury in early life stages causing severe disc damage. Without the intervertebral disc as scaffolding, the spine grew abnormally, resulting in dorsoventral curvature and instability, followed by an acute destabilization event and spinal cord compression. This case demonstrates the importance of a complete clinical, imaging, and post-mortem evaluation to determine the cause of skeletal anomalies in elephant seals given their predisposition for congenital malformations.
Acknowledgements
The authors would like to thank the Pacific Marine Mammal Center Animal Care Staff and Volunteers for their continuous care of the rehabilitation patients. The authors would like to also thank Dr. Ali Gorgi of Brightcare Veterinary Group Animal Neurology and their Imaging Staff for their contributions to this study.