Severe Respiratory Compromise Secondary to Cervical Disk Herniation in Two Dogs

Case No. 1

A 9-year-old, 4.5-kg, male castrated Chihuahua presented to the VCA West Los Angeles Animal Hospital for acute collapse. On physical and neurological examination, he was obtunded, laterally recumbent, hypothermic, bradycardic, salivating, cyanotic, and exhibited an inspiratory dyspnea. An electrocardiogram (ECG) was performed, which showed that he had a heart rate of 42 beats per minute (bpm) with second-degree AV block. He was nonambulatory tetraparetic with no voluntary motor movements, and all postural reactions were absent. Assessment of his pelvic limbs revealed hyperreflexive patellar reflexes, normal gastrocnemius reflexes, normal withdrawals bilaterally, and normal anal tone. Thoracic limb reflexes demonstrated a slightly decreased biceps tendon reflex, decreased withdrawals bilaterally, and a normal triceps reflex. Deep pain was present in all limbs. Neck pain was not elicited with extension or flexion of his neck, and no spinal hyperesthesia was elicited elsewhere in the spine upon palpation. Cranial nerves were all within normal limits. The owners reported that the dog had exhibited seizure-like activity, which consisted of head tremors and salivation, while being transported. No head tremors or seizure-like activity were noted at this time.

An arterial blood gas was analyzed while the dog was on an oxygen face mask. The pH was 7.059, the partial pressure of carbon dioxide (PaCO₂) was 81.2 mm Hg, and the partial pressure of oxygen (PaO₂) was 306 mm Hg. His bicarbonate (HCO₃) was 23 mmol/L, and his base excess was −7 mmol/L. The dog was assessed as having respiratory acidosis without metabolic compensation, nonambulatory tetraparesis with no voluntary motor movements, second-degree AV block (Mobitz II), and a history of head tremors and salivation.

Differentials for the respiratory acidosis were hypoventilation due to brain-stem disease; muscular paralysis (intercostal muscles or diaphragm) due to damage to the phrenic nerves, nuclei, or neuromuscular junction; or pulmonary parenchymal disease.

The nonambulatory tetraparesis with no voluntary motor activity consisted of lower motor neuron disease to the thoracic limbs and upper motor neuron disease to the pelvic limbs, with a history of a head tilt being noted by the referring veterinarian. This indicated a lesion cranial to the second thoracic spinal cord segment, where a cranial cervical lesion may cause a head tilt associated with disruption of the vestibular system,^13–15 but a caudal cervical lesion will cause lower motor neuron signs to the thoracic limbs. This may be due to multifocal disease or a single focus and subsequent edema or hemorrhage. Differentials at this time included trauma (e.g., intervertebral disk disease), neoplasia, vascular, infectious, and inflammatory causes.

The second-degree AV block and bradycardia responded temporarily to atropine. Causes for this included enhanced vagal tone and cardiac disease.

Differentials for the seizure activity, which was noted to include salivation and head tremors, were primary cerebral disease, secondary cerebral disease (e.g., hypoxia), vestibular disease from a brain-stem or cranial cervical lesion, or cervical muscle spasms from nerve root involvement. An electroencephalogram (EEG) was not accessible at this time. The dog did not demonstrate any of these episodes during the examination.

Due to the profound hypoventilation, the patient was placed on a ventilator with a peak inspiratory pressure <20 mm Hg; the dog was initially hyperventilated (30 breaths per minute) to lower his PaCO₂, then his respiratory rate was about 15 to 20 breaths per minute. A myelogram was performed and demonstrated a third to fourth cervical (C₃–C₄) ventral extradural lesion centered above the disk space [Figure 1]; there was also a slight, ventral extradural lesion at the C₄ to fifth cervical (C₅) intervertebral space, the 12th to 13th thoracic (T₁₂–T₁₃) intervertebral space, and the T₁₃ to the first lumbar (L₁) intervertebral space. A ventral slot was performed at C₃ to C₄ to decompress the dog, and an abundant amount of gelatinous disk material was removed. Pain was managed with fentanyl (2 to 4 μg/kg body weight per hour intravenously [IV] as a constant-rate infusion [CRI]) to help minimize the amount of isoflurane and provide pain management while the dog was on the ventilator postoperatively. He was kept on the ventilator overnight and weaned off the next morning. Reevaluation of an arterial blood gas showed all parameters to be within reference ranges.

Postsurgical care consisted of pain management with oxymorphone (0.05 mg/kg body weight, subcutaneously [SC] q 6 hours for the first 24 hours, then as needed for pain control), sustenance, turning, bladder expression, and passive range of motion. He was discharged 5 days after surgery, following progressive neurological improvement. Upon discharge, he was able to stand and walk a few steps with support. Currently at 7 months postoperatively, the dog is doing very well according to the owner, and he has no residual pain or deficits.

Case No. 2

A 3-year-old, 22-kg, female spayed chow chow presented to the referring veterinarian for acute-onset tetraparesis that occurred when she jumped up suddenly. She began to jerk her head and neck to the right, and after about 10 spasms she fell down and, according to the owner, lost consciousness. The dog was taken to a local emergency clinic; diazepam was administered IV in response to tremors/focal seizures, and a 1-liter IV fluid bolus of saline was given. After the dog recovered from the diazepam, a neurological examination revealed that she was severely paretic and hypoventilating. The dog was referred to an internist.

On presentation to the internist, she was having mild head and neck tremors, but she was alert and responsive. She was weak, had limited ability to lift up her head, and had absent proprioceptive positioning in all four limbs. Her cranial nerves, panniculus, and perineal and pelvic limb reflexes were all within normal limits. She had bilateral entropion, bilateral mucoid ocular discharge, and bradycardia with fair pulse quality.

The ECG showed a second-degree AV block (Mobitz II, low grade 5:1 and 4:1). Her Schirmer tear test results were 2 mm per minute in the right eye and 3 mm per minute in the left. Three view chest radiographs were within normal limits. There were mild increases in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatine phosphokinase (CPK); a mild, nonregenerative anemia; and a markedly low total thyroxine (T₄), with a free T₄ by equilibrium dialysis of 0.2 ng/mL (reference range, 11 to 43 ng/mL). Resting bile acids, prothrombin time (PT), and activated partial thromboplastin time (PTT) were within reference ranges. Toxoplasma, Neospora, and Cryptococcus titers were negative. Arterial blood gases were analyzed, and the PaO₂ was 62 mm Hg on room air with a 91% saturation. With a face mask, the PaO₂ was 350 mm Hg. The PaCO₂ was 45 mm Hg.

The dog was managed in an oxygen cage set at 40% and given IV fluid therapy. Focal seizures, described as head and neck tremors, were treated with intermittent IV boluses of diazepam (0.5 mg/kg body weight), and the dog was loaded and maintained on phenobarbital (2 mg/kg body weight q 12 hours). Oral levothyroxine was instituted at 0.2 mg q 12 hours, and cyclosporine ointment was placed in both eyes twice a day. Glycopyrrolate (0.2 to 0.4 mg SC) was given repeatedly for the marked bradycardia when the dog was in second-degree AV block. She was then referred to a neurologist.

On presentation to the neurologist, the patient was alert, responsive, and nonambulatory tetraparetic with minimal voluntary movement. She had normal to exaggerated reflexes in all four limbs and normal cranial nerves. No seizures were noted upon presentation. At this time, the arterial blood gases on an oxygen mask showed a PaCO₂ of 79.4 mm Hg and a PaO₂ of 338 mm Hg; the pH was 7.287. The dog was monitored overnight. The owners declined mechanical ventilation.

The dog’s master problem list at this time included a first cervical to fifth cervical (C₁–C₅) myelopathy, possible seizure activity, hypoventilation and subsequent respiratory acidosis, second-degree AV block, bilateral keratoconjunctivitis sicca, bilateral entropion, and hypothyroidism.

Differential diagnoses for the possible seizure activity (which was noted as jerking movements of the neck) were primary cerebral disease, secondary cerebral disease from hypoxia, vestibular disease^13–15 from a cranial cervical lesion, exaggerated attempts to breathe, or muscle spasms from nerve root involvement.

Differentials for the respiratory acidosis were hypoventilation due to brain-stem disease, muscular paralysis (e.g., intercostal muscles or diaphragm) due to damage to the phrenic nerves or phrenic nuclei, neuromuscular disease, or pulmonary parenchymal disease.

Differentials for the second-degree AV block include increased vagal tone or cardiac disease.

The following day, arterial blood gas analysis showed a PaCO₂ range from 55.6 to 62.4 mm Hg and a PaO₂ from 59 to 74 mm Hg in a 40% oxygen cage. Magnetic resonance imaging was performed, and sagittal and axial T1- and T2-weighted images of the cervical spine were obtained. On the sagittal views, there was a signal void at the ventral aspect of the spinal cord at the level of the second cervical (C₂) to C₃ intervertebral space on T2-weighted images, and the C₂–C₃ intervertebral disk was hypointense with a dorsal extrusion [Figure 2]. On axial images, there was dorsal deviation of the spinal cord at C₂ to C₃ with focal cord swelling, as well as a mass effect in the left ventral spinal canal at the same level. The cord did not enhance on T1 sagittal or axial images after IV contrast (i.e., gadolinium) was administered. The patient was manually ventilated throughout the procedure. The diagnosis was a disk extrusion at C₂ to C₃. A ventral slot was performed, and the disk material was removed. Pain was managed with a fentanyl patch (5 mg) and oxymorphone (0.05 mg/kg body weight, SC q 6 hours for the first 24 hours, then as needed for additional pain management).

The dog recovered well from surgery and was placed on aminophylline to improve ventilatory effort,^6716–18 and she was kept in the oxygen cage for 1 day postoperatively. Her blood gases and neurological function continued to improve. She was monitored closely for additional respiratory depression while she was on opioids for pain management; no deterioration was seen. Pain management, supportive care, and passive range of motion were included in her postoperative care. At the time of discharge, she was ventilating adequately and had some postural reactions in her thoracic limbs, though they were decreased. No seizure activity or head and neck tremors were witnessed during hospitalization.

Currently, the dog is doing very well at 6 months postoperatively. She was reported to be walking within 2 weeks of discharge. She is being maintained on levothyroxine (0.2 mg per os [PO] q 12 hours).