Recovery after inadvertent intramedullary microchip implantation at C1–C2 in a kitten

Abstract

Case summary

A 15-week-old male British Shorthair cat was presented for peracute paralysis immediately after microchip implantation. Neurological examination revealed a non-ambulatory tetraparesis and left thoracic limb plegia localised to C1–C5 spinal cord segments. CT of the cervical spine showed a diagonally orientated metallic foreign body (microchip transponder, 10 mm in length) within the vertebral canal at the level of C1–C2, resulting in a penetrating spinal cord injury. Based on concerns about further iatrogenic spinal cord injury through surgery, medical management was chosen. Despite the severe clinical signs, the kitten returned to ambulation within 6 days of the injury, with controlled urination and defecation. Continuous neurological improvement was seen for up to 6 weeks after the injury at which point a mild-to-moderate ambulatory tetraparesis and ataxia remained, with an overall good quality of life. Follow-up CT at the age of 13 months revealed a relative cranial displacement and rotation of the microchip towards the foramen magnum, while the cat’s neurological status was unchanged.

Relevance and novel information

This case demonstrated a cervical penetrating spinal cord injury in a growing cat caused by a microchip, which was successfully managed with medical treatment, suggesting that this might be an option for patients at risk of severe surgery-related complications or where owners reject surgery.

Introduction

Penetrating spinal cord injuries (PSCIs) in humans are often associated with severe myelopathies, and the prognosis for neurological improvement is guarded to poor in the majority of affected patients.^1,2 There are still ongoing discussions about whether medical or surgical therapy is the treatment of choice, as recent studies have not demonstrated a difference in outcome in humans with PSCI.^2–4 In veterinary medicine, PSCIs appear to be rare and only a small number of cases in companion animals have been reported, which were all treated surgically.^5–9

Here, we report on a 15-week-old male British Shorthair (BSH) cat with a PSCI due to inappropriate microchip placement that was successfully managed with medical treatment.

Case description

A 15-week-old intact male BSH cat weighing 1.3 kg was referred to the Neurology Service of the Small Animal Clinic Oberhaching 1 day after peracute onset of paralysis immediately following microchip implantation (Figure 1). According to the owner, clinical signs had already mildly improved at the time of presentation. A radiograph of the cervical spine provided by the referring veterinarian showed a diagonally orientated microchip transponder within the vertebral canal at the level of C1–C2 (Figure 1a,b). The patient was pretreated with corticosteroids and vitamin B complex injections.

Figure 1

(a) Microchip of the same construction type and size as implanted in the presented case. The microchip transponder was lodged diagonally within the vertebral canal at the level of C1–C2 as shown in a lateral radiograph (b); (c) sagittal and (d) dorsal CT image reconstruction

On presentation, the physical examination was unremarkable and neurological examination revealed the kitten to be alert and responsive with mild ventroflexion, a non-ambulatory tetraparesis with plegia in the left thoracic limb (Figure 2a), preserved nociception and a normal cranial nerve examination. Paw positioning was absent in the left thoracic and left pelvic limb, mildly reduced in the right thoracic limb and normal in the right pelvic limb. Withdrawal and patellar reflexes were normal apart from a crossed flexor–extensor reflex in the right pelvic limb. A markedly increased muscle tone was present in the left thoracic and left pelvic limb and the patient showed no signs of discomfort on spinal palpation. The neuroanatomical localisation was consistent with a slightly lateralising C1–C5 myelopathy (see Video 1 in the supplementary material) with a traumatic or vascular cause (haematoma secondary to trauma) as the most likely differential diagnosis.

Figure 2

Clinical signs (a) 1 day post-injury and (b) at the 5-week follow-up. The cat’s signs improved from (a) non-ambulatory tetraparesis with plegia in the left thoracic limb to (b) ambulatory mild-to-moderate tetraparesis and ataxia

Complete blood count, serum biochemistry and electrolytes were within normal limits, except for a mildly decreased haematocrit of 28.4% (reference interval 30.3–52.3), which was most likely age related. The cat was sedated with an intravenous bolus of propofol (Narcofol; CP-Pharma) and positioned in dorsal recumbency for CT of the cervical spine. Scans were performed using a 16-multislice helical CT scanner (Supria; Hitachi) with a slice thickness of 1.25 mm and 0.63 mm for soft tissue and bone window, respectively. Transverse planes and additional multiplanar reconstruction were obtained. On CT, the microchip could be identified as a linear, well-defined, strongly hyperattenuating structure, which was 10 mm in length and 2 mm in transverse diameter, and was diagonally lodged within the vertebral canal (diameter 6 × 7 mm) at C1–C2 and surrounded by streak artefacts (Figure 1c,d). No obvious deviation of the spinal cord was noted, and all bony structures appeared to be intact. Based on the CT findings, the diagnosis was PSCI at the level of C1–C2 by an intramedullary placed microchip.

As the kitten’s neurological status had already slightly improved and further iatrogenic spinal cord injury through surgery was a concern, continued medical management was chosen. Treatment included continuous rate infusion of lactated Ringer’s solution (B Braun) and dexamethasone (Hexadreson; MSD Animal Health) 0.1 mg/kg q24h IV for two consecutive days, followed by physiotherapy after discharge. During hospitalisation normal urination was observed and the cat demonstrated no signs of pain, with a Glasgow composite measure pain scale (CMPS-Feline) score of 1/20, indicating that no additional analgesia was required.^10,11

As the long-term prognosis and possible future complications were uncertain, the breeder transferred the kitten to one of the authors, who was willing to take care of it. The kitten was discharged 3 days after the first presentation with non-ambulatory tetraparesis; however, there was markedly improved motor function in all but the left thoracic limb, which was still plegic. The cat returned to ambulation within 6 days of the injury with resolution of the ventroflexion, and controlled urination and defecation. In the following 6 weeks the kitten continuously improved to an ambulatory mild-to-moderate tetraparesis and ataxia with the ability to climb, run and jump (Figure 2b). Hyperthermia of the left ear was repeatedly noticed after exercise. No further neurological improvement was seen 6 weeks after the PSCI.

The patient was anaesthetised for routine neutering at the age of 13 months at which point follow-up radiographs and CT were performed. General anaesthesia was performed using medetomidine hydrochloride (2  μg/kg IV [Dorbene; Zoetis]) and ketamine (0.2 mg/kg IV [Ketamin; CP-pharma]) and the cat was intubated. Meloxicam (0.2 mg/kg SC [Metacam; Boehringer Ingelheim]) was applied in terms of standard analgesic management for castration.

Compared with the initial CT, both imaging modalities demonstrated a more cranial displacement and rotation of the microchip relative to the surrounding vertebral bone, which was now straight in orientation and reaching from the dens axis to the foramen magnum (Figure 3). The hyperattenuating microchip was surrounded by a hypoattenuating rim, consistent with beam hardening.

Figure 3

(a) Follow-up lateral radiograph, (b) sagittal CT, (c) dorsal CT and (d) sagittal CT three-dimensional reconstruction of the cervical spine of the cat at 13 months of age. Note the more cranial displacement and rotation of the microchip (arrow) vs the CT images at the time of first presentation. The microchip is located ventrally and left-sided within the vertebral canal, reaching from the base of the left side of the dens axis to the foramen magnum

At the time of writing, the patient was 20 months old with a stable neurological status and overall good quality of life (see Video 2 in the supplementary material).

Discussion

Spinal cord injuries (SCIs) caused by inappropriate placement of a microchip are rare in animals, but have been reported in three dogs and one cat, most commonly presenting as an acute-onset ambulatory or non-ambulatory tetraparesis.^8,9,12,13 All of these animals underwent surgical treatment with a good outcome, although small residual deficits remained in some patients.^9,12,13 The patient with the most similarities compared with our cat was a 6-week-old, 1.6 kg, Tibet Terrier with the microchip located within the vertebral canal at C2, which was removed during hemilaminectomy. ⁹ In the other two dogs the microchip could be removed without hemilaminectomy because a part of it still protruded into the paraspinal soft tissue, while the other part protruded into the vertebral canal, causing the SCI.^8,13 The cat was 2 years old at the time of the SCI; the microchip was located within the vertebral canal at C5–C6 and was removed during dorsal laminectomy. ¹²

In our cat an intramedullary location of the microchip seemed most likely, owing to its position across the midline of the vertebral canal and no obvious signs of deviation of the spinal cord on CT. An intramedullary location was also compatible with the lack of pain on cervical palpation due to the lack of sensory innervation of the spinal cord parenchyma; ¹⁴ and also with the ventroflexion in our cat, which has frequently been reported in intramedullary lesions caused by feline cervical ischaemic myelopathy and is thought to arise from an involvement of spinal grey matter, which leads to paralysis of the cervical dorsal epaxial musculature. ¹⁵ Interestingly, the cat showed repeated hyperthermia of the left ear after exercise, which could have arisen from a left-sided sympathetic lesion attributed to an impairment of the left lateral tectotegmentospinal tract of the cervical spinal cord. ¹⁶

To the best of our knowledge, this is the first report of the successful medical management of a cervical PSCI in a kitten caused by a microchip with an outcome comparable to surgically treated animals.^9,12,13 The treatment of choice for PSCIs in humans is still a matter of debate. While some authors recommend the surgical removal of all foreign bodies within the vertebral canal as they are at risk for migration, recent studies in humans with PSCIs could not demonstrate a difference in outcome between surgically and medically treated patients.^2–4,17 PSCIs in humans are normally caused by stab wounds or, more commonly, as a consequence of gunshot injuries.^1,18 Affected patients often present with severe neurological grades with a rate of 50–61% for complete SCIs (total loss of motor and sensory function).^1,2 In more than 50% of patients with incomplete PSCIs, no improvement or a worsening of their initial neurological grade has been reported at the 1-year follow-up. ² This seems to be in contrast to PSCIs in cats and dogs, which have shown good recovery after surgery and after medical management, although large controlled studies in animals are lacking.^5,6,8,9,12

There are a number of complications of PSCIs in humans, including neurological deterioration, spinal instability and cerebrospinal fluid (CSF) fistulas, which prompt the decision for surgical removal of the foreign body; otherwise, no guidelines exist on indications for either surgical or medical management of PSCIs in humans.^1,4,17 Medical management in humans with acute SCIs involves fluid therapy, the administration of vasopressors like norepinephrine for maintaining spinal cord perfusion in the case of hypotension, analgesic therapy (eg, opioids or ketamine) and antithrombotic therapy.^19,20 Airway and ventilator support might be necessary in severely affected patients. ¹⁹ Broad-spectrum antibiotics are recommended for 7–14 days after PSCI injury in humans. ²¹ In our cat, no antibiotics were administered as identification microchips are generally placed as an aseptic technique. As our cat was pretreated with prednisolone, we administered dexamethasone instead of non-steroidal anti-inflammatory drugs, to avoid gastrointestinal adverse events. ²² In humans, there is no evidence for a beneficial effect of corticosteroids on functional neurological recovery in SCI.^19,23

Although our cat demonstrated a favourable outcome with medical management, the clinician should be aware of late-onset complications in patients with central nervous system (CNS) foreign body diseases. Migration of foreign bodies,^13,24,25 inflammatory reactions like granuloma^26–30 and abscess formation,^31–33 myelitis, ³⁴ arachnoiditis with and without subsequent subarachnoid diverticula or syrinx formation^35,36 and CSF leakage ³⁷ have been reported in veterinary and human medicine. In our cat, some degree of migration of the microchip was identified on follow-up CT that might have occurred in the context of maturing of the spine. However, migration was not associated with neurological deterioration. Abscess formation within the CNS is mostly described with foreign bodies of plant origin.^31,32,38 Sterile CNS foreign bodies like suture material, ³⁰ cotton pledget^28,29 and bone wax ³⁹ have been reported to cause late-onset clinical signs in humans due to granulomatous reactions that could potentially lead to complications in our cat in the future.

Conclusions

Our findings suggest that medical management may be an alternative treatment option for kittens and perhaps also other patients with PSCIs caused by a microchip inadvertently placed within the cervical spine, if severe surgery-related complications are anticipated or surgery is rejected by the owner. The clinician should be aware of late-onset complications that might occur weeks to years after the primary insult.