Abstract

Vascular anomalies of the spinal cord are rare in mammals, with humans being the most frequently recognized species with such lesions. In man, they account for 3–11% of spinal space-occupying lesions. Traditionally, these abnormalities in the spinal vasculature have been classified as cavernous angiomas (cavernomas), arteriovenous malformations, capillary telangiectasias, metameric angiomatosis (Cobb syndrome), disseminated angiomatosis (Osler-Weber-Rendu syndrome) and venous angiomas.^1-4

An 8.5-year-old female African warthog (Phacochoerus africanus) presented in the late afternoon with an acute onset of tetraparesis while on exhibit. This warthog resided in the exhibit with two other warthogs: her 11-month-old female offspring and a male conspecific. She was able to partially lift her head but was lying on her right side, unable to rise. Although movement was present in all four limbs, the forelimbs were most severely affected by the paretic state, with withdrawal reflexes present in the hindlimbs. A tail flick was still present, and anal tone was preserved. There was no external evidence of trauma, and there was no salivation or oral frothing to suggest seizure activity. Both pupils were equally dilated but reactive. A cursory examination of cranial nerve function was normal.

The warthog was immobilized with medetomidine (49 µg/kg IM; Zalopine, Orion Corporation, Espoo, Finland), butorphanol tartrate (0.20 mg/kg IM; Torbugesic, Ayerst Veterinary Laboratories, Guelph, ON, Canada), and midazolam (33 µg/kg IM; Versed, Hoffman-La Roche, Mississauga, ON, Canada) and was transported to the zoo’s animal health centre for further diagnostics. Initial therapy consisted of 100% oxygen via facemask and placement of an intravenous catheter for blood collection and fluid therapy (PLASMA-LYTE, Baxter Corporation, Mississauga, ON, Canada). A complete blood count revealed a mild increase in hematocrit, likely due to excitatory splenic contraction. Abnormalities on the biochemical profile were a moderate stress hyperglycemia, mild hypoalbuminemia, and mild hyperglobulinemia.

Due to the tetraparetic state, with lower motor neuron dysfunction of the forelimbs and upper motor neuron dysfunction of the hindlimbs, a cervicothoracic (C7–T2) spinal cord lesion was suspected. The lack of a Horner’s sign suggested that the lesion could further be isolated to the cervical spine.

With the acute onset of clinical signs, differentials included trauma (including intervertebral disc disease), ischemia (vascular lesion, fibrocartilaginous emboli), and infectious (spinal abscess) and inflammatory disease. Neoplasia, such as lymphosarcoma, was also considered, while metabolic, nutritional, and toxic etiologies were considered less likely. Survey radiographs of the cervical, thoracic and lumbar spine did not reveal any significant abnormalities except for mild bridging spondylosis in the mid-lumbar spine.

The warthog was treated with dexamethasone sodium phosphate (0.25 mg/kg IV; Dexamethasone 5, Vétoquinol, Lavaltrie, QC, Canada), vitamin E/selenium (0.025 ml/kg IM; Dystosel DS, Pfizer Animal Health, London, ON, Canada), vitamin B complex (0.07 ml/kg IM; Vétoquinol, Lavaltrie, QC, Canada), and florfenicol (20 mg/kg IM; Nu-Flor, Schering Plough Animal Health, Pointe Claire, QC, Canada). After being transferred to an indoor hospital holding enclosure, anesthesia was reversed using atipamezole (0.25 mg/kg; Antisedan, Novartis Animal Health Canada, Mississauga, ON, Canada) and naltrexone (1 mg/kg; Trexonil, Wildlife Laboratories Inc., Fort Collins, CO, USA) administered intramuscularly and subcutaneously in equal proportions. Straw bales were used to further confine movement. Over the next 12 hours, there was further decline in neurologic status with increasing mental depression and development of profound hypothermia (33°C). Hyperreflexia was present in the hindlimbs, while there was hyporeflexia in the forelimbs, with extensor rigidity in the right foreleg. Pain perception was still preserved in all four limbs. The warthog had urinated overnight; however, no feces were passed. There was no interest in food or water.

Response to warming efforts was sluggish with a rise in rectal temperature to only 34.7°C. Meloxicam was administered (Metacam, Boehringer-Ingelheim Ltd., Burlington, ON, Canada) at a dosage of 0.1 mg/kg subcutaneously. The warthog was then immobilized using the same anesthetic protocol as before, an intravenous catheter was placed for intravenous fluid administration (PLASMA-LYTE with 5% dextrose), and the warthog was transported to Foothills Hospital for magnetic resonance imaging (MRI), where findings confirmed suspicions of the spinal lesion. At the level of approximately the C7 vertebral body, there was an increase in T1 and T2 signal strength consistent with a focus of intramedullary spinal cord hemorrhage with surrounding edema. Over 50% of the cord was affected on the sagittal view, with approximately 30–40% affected centrally on the transverse view. Blood vessels in the arachnoid space also appeared abnormal. The MRI findings were suggestive of an arteriovenous malformation or a cavernous angioma.

The warthog was transported back to the zoo hospital and recovered from anesthesia through administration of flumazenil (4 µg/kg IV; Anexate, Hoffmann-La Roche, Mississauga, ON, Canada) and atipamezole (0.25 mg/kg IM). The butorphanol was not reversed in order to provide additional analgesia. Mannitol (0.15 mg/kg) was administered intravenously over 40 minutes. Intravenous fluids were continued at 2 ml/kg/hour. By 2 hours post anesthesia, mentation had improved, the rectal temperature had increased to 35.1°C, and the warthog consumed a few pieces of chopped vegetables and fruit. No further changes in neurologic status were observed. The warthog spent the next several hours resting comfortably. Approximately 6–7 hours post anesthesia, the warthog expired in a resting position, with a body temperature that had increased to 41°C.

On necropsy, the entire spinal canal contained a sanguinous fluid, most prominent in the cervical and cranial thoracic segments. Extending from the C6–C7 intervertebral space caudally was a 15x10-mm area of bruising and hemorrhage of the spinal cord visible beneath the dura. The dorsal aspect of the cord was most prominently affected. On transverse sectioning, the hemorrhage obliterated the central third to half of the spinal cord, affecting most of the dorsal, intermediolateral and ventral grey columns, as well as the dorsal and ventral funiculi. Cavitation of the dorsal funiculus of the cervical cord, due to hemorrhagic myelomalacia, was apparent. A small, 6–8-mm focus of hemorrhage also was present in the left cerebral cortex at the level of the callosomarginal branch of the anterior cerebral artery. Culture of the cerebrospinal fluid yielded scant growth of Corynebacterium sp. Other gross findings included moderate to marked pulmonary, hepatic and splenic congestion, patchy white streaking in the myocardium suggestive of mild myocardial fibrosis, multifocal endometriosis of the uterine serosa, and historic vulvar herniation of retroperitoneal fat. Histologic consultation is still pending to further characterize the nature of the spinal cord lesion; however, preliminary findings are most suggestive of a cavernous angioma.

Vascular malformations of the spinal cord have not been described in porcine species and are a rare finding in companion animals.^4,5 In humans, these malformations represent a major cause of spinal cord myelopathy.³ Magnetic resonance imaging is the screening modality of choice. Prognosis is dependent on the duration and severity of the hemorrhage. Surgical options exist in people, but even with surgery, a return of normal neurologic function is often not possible, even with small lesions.^1,3 Even if a surgical option were possible in this case, the acute onset of clinical signs, with rapid deterioration of neurologic function due to the severe intraparenchymal hemorrhage, would have precluded successful surgical intervention.

Acknowledgments

The authors would like to thank the veterinary technologists (Lori Rogers and Wanda Angermyer) and animal keepers (Glenda Misurelli and Kathy Twamley) of the veterinary services department, as well as the Calgary Zoo’s animal care staff, for their invaluable assistance with this case. Our gratitude is also extended to Dr. Rob Sevick, Dr. Richard Frayne, and the support staff of the Foothill’s Hospital Magnetic Resonance Imaging Unit.

Literature Cited

1.  Annand, S., V. Puri, S. Sinha, and V. Malhotra. 2001. Intramedullary cavernous hemangioma. Neurol India. 49:401–403.

2.  Braund, K.G. (ed). 2003. Clinical Neurology in Small Animals—Localization, Diagnosis and Treatment. International Veterinary Information Service (www.ivis.org), Ithaca, NY.

3.  Caragine, L.P., V.V. Halbach, P.P. Ng, and C.F. Dowd. 2002. Vascular myelopathies—vascular malformations of the spinal cord: presentation and endovascular surgical management. Semin. Neurol. 22(2):123–131.

4.  Hayashida, E., K. Ochiai, T. Kadosawa, T. Kimura, and T. Umemura. 1999. Arteriovenous malformation of the cervical spinal cord in a dog. J. Comp. Pathol. 121(1):71–76.

5.  Olivier, J.E. and Lorenz, M.D. (ed). 1993. Handbook of Veterinary Neurology. 2nd ed. W.B. Saunders Company, Philadelphia, PA. 415 pp.