Abstract

A 12-year-old 61.5-kg male Komodo dragon (Varanus komodoensis) was reported to have eaten a large rock. It was speculated that the rock was probably stained with rat blood or had a rodent odor after an outdoor feeding. A smaller rock had been ingested the week prior and had been regurgitated successfully by the animal. The size and weight of the larger ingested rock made regurgitation unlikely. The animal was sedated for manual gastric foreign body removal. It was removed successfully with careful external massage, combined with esophageal access to the region of the cardias. The rock measured 17 cm in length, 11 cm in width, and 5 cm in height and weighed 1.23 kg. A prolonged (24 hour) recovery from sedation ensued. Thereafter, the animal began to show reluctance to lower its head while eating. Ataxia was present and most severe while the animal attempted to feed, or when it ambulated rapidly. The monitor appeared to be otherwise normal and in relatively good health. The taxia was persistent, and lasted 12 months, until the animal was found acutely tetraparetic. During this period, the incoordination seemed exacerbated by posture changes (neck ventroflexion) or activity.

The onset of tetraparesis was sudden, and apparent in the early morning. The monitor was unresponsive and sedated for transport and examination. Radiographs were suggestive of cervical trauma and spinal cord compression. Following reversal, the animal was referred to a local hospital for advanced imaging. Computerized tomography (CT) and magnetic resonance imaging (MRI) revealed suspect lesions in the vertebral bodies. Images demonstrated degenerative changes between the first and second cervical vertebrae with osteophyte formation and mild bony vertebral canal narrowing. In addition, there was hyperdense extradural soft tissue ventrally, resulting in severe vertebral stenosis and cord compression. CT images were consistent with spinal cord compression in the region of the first three cervical vertebrae. Intermittent positive pressure ventilation, which was initiated following sedation, was maintained for 36 hours, while the animal was transported to the LSU School of Veterinary Medicine’s Exotic Animal department for surgical referral. Surgical decompression attempts were planned but discontinued when the animal’s general condition and blood pH appeared to be incompatible with survival. The animal was humanely euthanatized. Necropsy and histopathology confirmed vertebral instability with secondary spinal cord compression between C1 and C4. Acute cervical trauma, even in a slight form, may have caused the unstable vertebrae to compress the spinal cord.

Introduction

Komodo dragons have been observed to eat and regurgitate very large objects in the wild. Entire goat and boar skulls have been swallowed and eventually regurgitated with minimal visible effect on the monitor. Wild Komodo dragons eat almost their entire prey, including all bones. They regularly eat and cut the prey’s flesh with their teeth, ingesting large portions of the prey whole. As predators, they leave behind almost none of the carcass, ingesting as much as possible. The indigestible material, mostly hair, teeth, and feathers, are voluntarily disgorged as a gastric pellet a variable amount of time later.¹

Case Report

A pair (1.1) of Komodo dragons (Varanus komodoensis) was housed in adjoining and shared exhibits for over 10 years. The 12-year-old male reached close to 7 ft in total length and weighed 61.5 kg. One morning it was reported to have eaten a large rock. It was speculated that the rock was probably stained with rat blood or had rodent odor after an outdoor feeding. A smaller rock had been ingested the week prior and had been regurgitated successfully by the animal. The size and weight of the larger ingested rock made regurgitation unlikely. The animal was sedated with 300 mg total (5 mg/kg) IM ketamine and 3 mg total (0.05 mg/kg) IM of medetomidine for manual gastric foreign body removal, as described by Rasmussen et al.³ It was successfully removed with careful external massage, combined with esophageal access to the region of the cardia. Following removal, the rock measured 17 cm in length, 11 cm in width, and 5 cm in height and weighed 1.23 kg. The anesthetic combination was successfully reversed with 15 mg total of atipamezole IM.^4,5 Following a prolonged (24-hour mild ataxia) recovery from sedation, the animal began to show reluctance to lower its head while eating. Incoordination was present and most severe while the animal attempted to feed, or when it ambulated rapidly. The monitor appeared to be otherwise normal and in relatively good health. Ataxia was continuous, and lasted 12 months, until the animal was found acutely tetraparetic. During this period, the incoordination seemed exacerbated by posture changes or activity (e.g., neck ventroflexion).

Exactly 1 year following the procedure, the monitor was found unable or unwilling to move in its nocturnal enclosure. It appeared depressed, listless, and unresponsive. The monitor was breathing regularly, but otherwise was only mildly responsive to tactile and aural stimulation. Cursory evaluation on site revealed mild visible response to tactile or proprioceptive stimulation. All reflexes, including limb proprioception, appeared diminished or absent. Mild direct and consensual light responses were presumed to be extant but appeared subjectively diminished. Peracute tetraplegia secondary to trauma was suspected.

In spite of severe apparent neurologic compromise, the monitor was sedated with 300 mg total ketamine (5 mg/kg) and 3 mg total medetomidine (0.05 mg/kg) IM by hand syringe. It was then transported to the animal healthcare center for examination and radiographs. On arrival, the animal was intubated with a cuffed 8 mm endotracheal tube, and supplemental O₂ was administered at a rate of 5 L per minute. Spontaneous respiration at a rate of 12 rpm was observed during exam, blood sampling, and radiography. Dorsoventral radiographs of the head and neck revealed moderate scoliosis and narrowing of intervertebral space between C1–C2, C2–C3, and C3–C4. Attempts to position the cervical vertebrae by mechanical means were unsuccessful, so the deviation was not presumed to be positional. Severe apnea developed 85 minutes after induction. Sedation was reversed 90 minutes post-induction with 15 mg total atipamezole IM. Intermittent positive pressure ventilation every 15 seconds was initiated following reversal and was maintained for 36 hours. An intravenous port was secured in the coccygeal vein, and a solution of 50% lactated Ringer’s and 5% dextrose in water was given in a volume of 4 L over the following 36 hours. The animal was transported to a local hospital for advanced imaging.

Materials and Methods

Magnetic resonance imaging was performed on a GE signa 1.5T magnet (General Electric, Milwaukee, WI, USA). The study was performed in the neurovascular array coil. Sequences performed included FSE TI (TR 617, TE 11.0 Ef), FSE T2 (TR 3000-4450, TE 96.0 Ef), 3D FSE T2 (TR 4000, TE 150 Ef, 1.7-mm slice thickness/0.0 GAP, 1 NEX, 6:26), 3D SPGR/30 (TR 22/TE 6.0 1.2 mm).

Computerized tomography (CT) images were performed on a GE pro speed spinal CT scanner (General Electric, Milwaukee, WI, USA). The study was initially performed at 3 mm collimation, with 1 mm images obtained through the craniocervical junction with multiplanar reformations.

A website (http://digimorph.org/specimens/Varanus_gouldii/) with CT images of Varanus gouldii provided an approximation of expected “normal” images for the species.

Results

The MRI demonstrated severe vertebral stenosis at the C1/2 level, with narrowing of the effective diameter of the vertebral canal to a few millimeters, which caused severe cord compression. There was an abnormal increased T2 signal within the spinal cord at this level, consistent with edema/myelomalacia.

The CT images demonstrated degenerative changes at the C1/2 articulation with osteophyte formation resulting in mild bony vertebral canal narrowing. In addition, there was hyperdense extradural soft tissue ventrally, resulting in severe vertebral stenosis and cord compression. This tissue was markedly hypointense on the long TR/TE and was felt to represent epidural fibrosis.

CT and MRI revealed suspect degenerative articular lesions in the vertebral bodies with narrowing of the vertebral canal. CT images were consistent with spinal cord compression in the region of the first three cervical vertebrae.

The dragon presented to the LSU-SVM for additional diagnostics and possible surgery. At presentation, the animal was nonresponsive. An 18-gauge catheter was placed into the ventral tail vein for intravenous access, and fluids (Normasol: 2.5, 5% dextrose, 50:50) were initiated (25 ml/kg). Because the dragon was apneic, it was positive pressure ventilated 6–8 times per minute. The heart rate was determined using a stethoscope and ultrasonic Doppler. The animal was bradycardic (HR <25 bpm). Atropine (0.04 mg/kg IV) was administered to counteract the bradycardia. The dragon had no righting reflex, withdrawal reflex, deep pain reflex, corneal reflex, or any nociception. A blood sample was collected from the ventral tail vein for blood gas analysis. The venous pH was 6.1. A second sample was collected, and the venous pH was 5.8. Because of the absence of the reflexes and spontaneous breathing, in combination with the severe acidemia, euthanasia was elected. Following euthanasia, a full necropsy was performed.

Histologic examination of the spinal cord revealed moderate to severe axonal degeneration in all funiculi, but especially severe in the ventral lateral and ventral medial funiculi. The changes were attributed to compression related trauma; probably an impingement from within the ventral and/or lateral aspect of the vertebral canal. Additional histologic changes included a mild stress response in the adrenal and some thyroid follicular distention—considered a seasonal variation of normal thyroid morphology.

Necropsy and histopathology confirmed vertebral instability with secondary spinal cord compression between C1 and C4. The spinal cord was narrowed to 2 mm at the site of maximum compression between C2 and C3. Acute cervical trauma, even in a slight form, may have caused the unstable vertebrae to compress the spinal cord.

Discussion

Ataxia and paresis have been described in many domestic and wild animals. In kangaroos and some marsupials, unique cervical anatomy and late closure of epiphyseal plates make these animals prone to cervical injury and secondary compression of the spinal cord.² It is speculated that manipulation during the removal of the gastric foreign body may have led to vertebral subluxation and instability. Varanid cervical anatomy, with the presence of a single occipital condyle in the skull base, as well a single intervertebral articular surface in each cervical vertebra, may make the cervical vertebrae prone to instability.

Preliminary clinical signs for the 12 months prior to the presentation of tetraplegia were consistent with vertebral instability and ventral compression of the spinal cord. The fact that the signs were exacerbated with ventroflexion was suggestive of cervical vertebral displacement and dorsal compression of the cord. A C1–6 compression could cause a spastic tetraparesis and ataxia due to the loss of function of the upper motor neuron and the general proprioceptive tracts, respectively. The gait observed would be expected to have a delay in the onset of protraction of all the limbs and a tendency to take a longer stride that was inaccurate in its placement. The animal seemed to have an exaggerated gait when ambulating rapidly for the year prior to the sudden onset of tetraplegia. Limb tone and reflexes appeared to be normal or increased, which was also consistent with the expected clinical signs.

Acknowledgments

The authors are grateful to the Audubon Zoo’s Reptile Curator, Kevin Bowler, and to the reptile keeper staff, for their dedication and effort in working with large monitors.

Literature Cited

1.  Auffenberg, W. 1981. The Behavioral Ecology of the Komodo Monitor. Univ. Florida University Press. Gainesville, Florida. 202–221.

2.  Emerson, C. 1983. Kangaroos—unique cervical anatomy and its significance. In: Proc Assoc Zoo Vet Annu Meet. 8–9.

3.  Rasmussen, J.M, S.B. Love, and L.F. Graham. 2002. Retrieval of a gastric foreign body from an adult Komodo monitor (Varanus komodoensis). In: Proc Am Assoc Zoo Vet Annu Meet. 167–168.

4.  Spelman, L., R. Cambre, T. Walsh, and R. Rosscoe. 1996. Anesthetic techniques in Komodo dragons (Varanus komodoensis). In: Proc Am Assoc Zoo Vet Annu Meet. 247–250.

5.  Tabaka, C., and S. Reichling. 2002. Management immobilization techniques in the Komodo dragon (Varanus komodoensis). In: Proc Am Assoc Zoo Vet Annu Meet. 302–305.