Acute non-ambulatory tetraparesis attributable to cranial cervical intervertebral disc disease in a cat

Abstract

A 10-year-old domestic longhair cat was presented for acute non-ambulatory tetraparesis. Clinicopathologic diagnostics revealed no abnormalities. Cervical myelogram revealed an extradural compressive lesion consistent with intervertebral disc disease of the C2–C3 intervertebral disc space. Ventral slot decompression confirmed the presence of extruded intervertebral disc material into the vertebral canal of the C2–C3 intervertebral space. The patient succumbed to cardiorespiratory arrest 3 days postoperatively.

A 10-year-old, 8.4 kg, neutered male, domestic longhair cat presented with acute non-ambulatory tetraparesis. The cat was a strictly indoor pet and no exposure to toxins, ticks or trauma could be identified by the owner. Previous medical history included steroid-responsive polyarthritis in July 2005 and the cat had been hit by a car several years earlier. The cat was current on vaccinations and was feline leukemia virus/feline immunodeficiency virus negative.

At the time of presentation, the cat was non-ambulatory tetraparetic. Conscious proprioception deficits were noted in all four limbs. Segmental spinal reflexes were hyper-reflexic on all four limbs. The panniculus reflex was intact. Anisocoria was noted; however, the owner reported the anisocoria had been present since the hit-by-car incident. No spinal hyperpathia could be appreciated in the neck or back. The neurological examination was consistent with a C1–C5 spinal cord segment anatomic diagnosis. Differentials for this presentation include neoplasia, inflammatory central nervous system disease, intervertebral disc disease, fibrocartilaginous embolism, luxation and/or fracture of vertebrae, hematoma, cysts and abscesses.

Complete blood count revealed a hematocrit of 26.1% (normal range 29–48%). Biochemical profile showed no abnormalities. Cerebrospinal fluid was obtained from the lumbosacral cistern. Cerebrospinal fluid protein was 17.1 mg/dl (normal range 15–45 mg/dl); no nucleated cells and 14 red blood cells were present. Feline infectious peritonitis immunofluorescence assay performed on the cerebrospinal fluid was negative. Serology based latex agglutination for Cryptococcus neoformans was negative. IgM and IgG titers against Toxoplasma gondii were both negative.

Cervical myelogram under general anesthesia was pursued as he was progressively becoming tachypneic and cyanosis of the tongue and gingiva could be appreciated. Iohexol (Omnipaque; Amerisham Health) 4 cc was injected into the subarachnoid space of the cerebellomedullary cistern. A ventral extradural compressive lesion could be noted between the second and third cervical vertebrae (C2–C3) on the lateral myelographic view (Fig 1). Mild column splitting on the lateral view indicated a degree of lateralization of disc material. This could be further determined using oblique views, which were not performed in this case as lateralization was deemed mild and would not change the surgical approach. Widening of the contrast column at the level of the C2–C3 intervertebral space was evident on the ventrodorsal myelographic view consistent with the ventral compression evident on the lateral myelographic view (Fig 2). Differential diagnoses for this type of lesion included intervertebral disc disease, neoplasia, hematoma and ligamentous hypertrophy. The patient was immediately taken to surgery given his respiratory status noted during hospitalization.

Fig 1.

Lateral cervical myelogram focused on the extradural compressive lesion at the level of the C2–C3 intervertebral space (white arrow). Mild column splitting indicated a degree of lateralization of disc material (black arrowhead).

Fig 2.

Ventrodorsal cervical myelogram indicating widening of the contrast medium over the C2–C3 intervertebral disc space consistent with the ventral compression evident in the lateral myelographic view (white brackets).

The ventral cervical region was clipped and prepared for aseptic surgery. A standard midline approach to the ventral vertebral column was performed. Standard ventral slot decompression was performed between the second and third cervical vertebrae. Upon entry to the vertebral canal, a large amount of extruded intervertebral disc material was noted in the vertebral canal compressing the spinal cord. A moderate amount of bruising could be noted in the spinal cord in that region. The disc material was removed, followed by gentle lavage of the surgical site. Closure of the surgical site was routine.

Postoperatively an indwelling urethral catheter was placed. The cat was experiencing ongoing respiratory depression postoperatively. He was unable to maintain end-tidal carbon dioxide (ETCO₂) below 50 mmHg based on capnography. The cat was placed on positive-pressure ventilation until he was able to maintain ETCO₂ between 35 and 45 mmHg at which time he was placed in an oxygen cage. The cat was given dexamethasone sodium phosphate (Butler) (0.2 mg/kg) intravenously twice daily to reduce the inflammation associated with the surgery. Intravenous fluids consisted of 0.45% sodium chloride plus 2.5% dextrose plus 80 mg/l doxapram (Dopram; Fort Dodge) at maintenance rate. The patient's temperature despite warming with a Bair Hugger (Augustine Medical) device and heated oxygen cage remained between 34.9°C (95°F) and 37.2°C (99°F) postoperatively.

Day 2 postoperatively, enrofloxacin (Baytril; Bayer) (5 mg/kg) once daily intravenously was initiated. The patient was maintained in the oxygen cage with continued corticosteroid injections and intravenous fluids as stated above. The patient's temperature remained suboptimal and respiratory effort appeared exaggerated.

Day 3 postoperatively the patient showed dyspneic respirations and was intubated. The cat received 100% oxygen via the anesthesia machine. Electrocardiogram leads, pulse oximeter and a capnograph were placed on the patient for monitoring. The cat's ability to ventilate proved to be impaired as he was unable to maintain ETCO₂ below 55 mmHg. Within minutes, cardiac arrest occurred with electrocardiogram showing the isoelectric line and no evidence of cardiac electrical flow. Chest compressions were initiated followed by administration of epinephrine (Butler) (0.2 mg/kg) intravenously. After three administrations of epinephrine with no successful response, cardiopulmonary cerebral resuscitation was discontinued. Post-mortem necropsy was denied by the owner.

Intervertebral disc disease is a disease commonly overlooked when presented with a cat with neurologic signs of the limbs. The incidence of intervertebral disc disease in cats is reported to be 0.12% (Munana et al 2001). This is much lower than the 2% reported in dogs (Oliver et al 1997). King and Smith (1958, 1960a, 1960b, 1964) showed that intervertebral disc protrusion is more common than extrusion, and that protrusions occur more commonly in the cervical vertebrae but seldom cause clinical signs. King and Smith (1960b) also showed that protrusions more commonly occur in cats older than 15 years of age. Littlewood et al (1984), however, reported a 4½-year-old cat with the presence of a protruded disc at C5–C6 classified as Hansen type II and Heavner (1971) reported an 18-month-old cat with protrusion at C5–C6.

Clinical signs associated with intervertebral disc disease in cats appear to occur more frequently with extrusions (Hansen type I) than with protrusions (Hansen type II). A series of studies have shown clinical signs in cats to be a consequence of dorsal extrusion of disc material (Hansen type 1) (Hoerlein 1978, Seim and Nafe 1981, Gilmore 1983, Sparkes and Skerry 1990, Bagley et al 1995, Kathmann et al 2000, Lu et al 2002). Eight out of 10 cases (80%) reported in one study were considered to be Hansen type 1 (Munana et al 2001). The same paper also reported the mean age of these cats to be 9.8 years, which is younger than the reported age for disc protrusions (King and Smith 1960b). This is also supported by another study of six cats (Knipe et al 2001) where the ages ranged from 3 years to 9 years, as well as two other case studies in which a 6-year-old cat (Smith and Jeffery 2006) and a 5-year-old cat (McConnell and Garosi 2004) were both diagnosed with dorsal extrusion, the latter extruding into the spinal cord proper. The cat reported here was 10 years old.

In most of the published literature, cats with clinical signs of disc disease presented with acute onset, and the majority of the lesions occurred in the thoracic and/or lumbar segments of the spinal cord. In contrast to dogs, where cervical disc disease has been shown to be 14–16% of intervertebral disc disease seen in that species (Toombs and Waters 2003), few case reports were noted describing cervical lesions in cats (Heavner 1971, Littlewood et al 1984, Lu et al 2002). However, on necropsy of older cats protruding discs occurred more commonly in the cervical vertebral canal with no resultant clinical signs (King and Smith 1958). This can potentially be explained by the fact that chronic protruding discs in the cervical canal can be better tolerated given the larger canal diameter compared to spinal cord diameter within the cervical vertebrae (Toombs and Waters 2003). The thoracolumbar vertebral canal is much smaller in comparison, and explosive Hansen type 1 disc extrusions have greater potential to result in clinical signs. The presence of the intercapital ligaments and the rib cage gives added stability to the thoracic spine cranial to T10, resulting in a low incidence of disc extrusion in that area (Toombs and Waters 2003). In one report, the authors noted that the weight of cats with lumbar lesions was greater than those with thoracic lesions and postulated this could be due to the nature of jumping in the daily routine of cats, placing excessive strain on the lumbar region (Munana et al 2001).

The cat presented in this case had labored breathing secondary to paralysis of the intercostal nerves and diaphragmatic paresis. Interruption of the descending motor function pathways within the spinal cord secondary to inflammation and ischemia from injury, as well as surgery, can result in respiratory paralysis and death (LeCourteur and Grandy 2000, Beal et al 2001). The intercostal nerves are the ventral branches of the thoracic nerves which exit from the corresponding vertebral foramen. These nerves supply both sensory and motor to the intercostal musculature (Evans and Christensen 1979). The phrenic nerves are reported to originate from cervical spinal cord segments five and six in the cat (Crouch 1969). These nerves supply motor and sensory fibers to the diaphragm (Evans and Christensen 1979). Upper motor neuron and lower motor neuron disease of the spinal cord segments supplying the phrenic nerve could result in paresis or paralysis of the diaphragm (LeCourteur and Grandy 2000). Spinal cord injury cranial to the origin of the motor neurons to the muscles of respiration can lead to respiratory compromise (Beal et al 2001). In cats, the afferent tracts to the respiratory center of the brain can be damaged by cranial cervical spinal surgery (Beal et al 2001). Weight may also play a role in the effectiveness of thoracic expansion. This cat weighed 8.4 kg. Excessive weight certainly increased the amount of work involved in each breath taken.

An additional possibility for respiratory failure in this cat is that glucocorticoid use could have led to the formation of a pulmonary thromboembolism on day 3 postoperatively. This is supported by the fact that mechanical ventilation did not improve the cat's ventilatory function, which should have improved if the hypoventilation was solely caused by respiratory muscle paresis or paralysis. In a recent study of cats on positive-pressure ventilation, 14% of cats that required ventilatory support due to respiratory failure survived (Lee et al 2005). The cats that survived were on the ventilator significantly longer than non-survivors (Lee et al 2005). Another recent study of dogs undergoing surgery because of cervical spinal disorders showed that 4.9% of the dogs developed hypoventilation and the site of injury was most commonly between C2 and C4 (Beal et al 2001). Most of the dogs had minimal pulmonary parenchymal disease. Exogenous or endogenous corticosteroids can block activation of plasmin and increase factors V, VIII, IX and X resulting in a hypofibrinolytic state (Norris et al 1999). The cat in this report was receiving glucocorticoids for 5 days, which is of sufficient duration to result in a thromboembolus (personal communication, Guillermo Couto 2006). The majority of cases of feline thromboembolism reported in the literature indicated the cats suffered from severe underlying diseases (Norris et al 1999, Schermerhorn et al 2004, Davidson et al 2006).

Previous reports cited in this paper have shown surgical decompression of the intervertebral disc as the treatment of choice for cats with severe clinical signs as a result of the disc extrusion (Seim and Nafe 1981, Gilmore 1983, Sparkes and Skerry 1990, Bagley et al 1995, Kathmann et al 2000, Munana et al 2001, Knipe et al 2001, Smith and Jeffery 2006). They also reported a good outcome resulting from surgical decompression. The cat presented here did not survive more than 3 days postoperatively. One very notable difference between this cat and the others reported previously was the location of the disc. To the author's knowledge, the most cranial disc lesion reported in cats is the C3–C4 intervertebral disc (Lu et al 2002). No report could be found presenting a cat with disc disease of C2–C3, which as stated above, can lead to respiratory paralysis.