Abstract
A 2-year-old, male neutered domestic shorthair cat was presented for investigation of an acute onset of tetraparesis immediately following the implantation of a pet identification microchip. A left-sided C6–T2 spinal segment localisation was suspected from the neurological examination, with spinal cord trauma being the primary differential diagnosis. Myelography demonstrated obliteration of the contrast columns by the microchip at the C5–C6 intervertebral disc space. A dorsal laminectomy was undertaken and the microchip was successfully removed. Eleven months after the surgery, the cat was able to weight bear in all limbs but with mild residual paresis in the left thoracic limb.
Over the past decade, microchip implantation has been increasingly used as a sensitive and specific identification method for pets (Sorensen et al 1995). The microchips are passive transponders, ranging in size from 11 to 29 mm by 0.82 to 3.6 mm, that are implanted subcutaneously or intramuscularly and contain a memory and a transmitter enclosed in a biocompatible microencapsulated quartz glass (Sorensen et al 1995). Implantation in dogs and cats does not require sedation or local anaesthesia, but the needle used to implant a microchip (12 gauge) is larger than that used for vaccines (Sorensen et al 1995). The microchip should lodge in the subcutaneous fat between the scapulae, making migration unlikely, although not impossible. This report describes a cat that experienced spinal cord trauma following inappropriate, forceful implantation of a microchip.
A 2-year-old, male neutered domestic shorthair cat was presented for investigation of an acute onset of tetraparesis immediately following the implantation of a pet identification microchip (Pet-iD UK Ltd; Hurstpierpoint, West Sussex). The owners had implanted the device themselves and admitted to using some force when restraining the cat for its injection, following which it became immediately recumbent and urinated. Excessive respiration and panting followed as the owners attempted to get the cat to stand. The cat was taken to their veterinarian and was subsequently referred as an emergency to the neurology unit at the Animal Health Trust.
On general examination the cat was noted to be alert and recumbent with an increased respiratory rate of approximately 20 breaths per minute. There was no evidence of swelling or haemorrhage at the site of the implantation and pain could not be elicited on gentle manipulation of the surrounding soft tissues.
Gait analysis revealed that some voluntary movement existed in the right thoracic limb, but the remaining limbs were plegic. Proprioception was reduced in the right thoracic limb and absent in all others. Extensor (cranial tibial and triceps tendon) and flexor withdrawal reflexes were reduced in both thoracic limbs, most markedly on the left side. Nociception was present in all limbs. Cranial nerve examination was considered to be normal apart from an anisocoria with a left-sided miosis (partial Horner's syndrome). The cutaneous trunci reflex was bilaterally present. Vertebral palpation and manipulation did not elicit any hyperpathia. A C6–T2 spinal segment localisation was suspected from this examination, with spinal cord trauma being the primary differential diagnosis.
Initial diagnostic evaluations, including a complete blood count, serum biochemistry and urinalysis were all within normal limits.
Survey cervical spinal radiographs taken with the cat under general anaesthesia revealed a small, rectangular metallic opacity, compatible with a microchip, within the vertebral canal, dorsal to the C5–C6 intervertebral space and on the left side. There was no evidence of vertebral malalignment or fracture. Based on the history of a trauma and the cat's increased respiratory rate, thoracic imaging was performed. A ventro-dorsal view of the thorax using manual inflation revealed cranial displacement of the left diaphragmatic crus compatible with hemi-diaphragmatic paresis. No other thoracic or abdominal abnormalities were noted. MRI of the spine was inappropriate as microchips produce a large surrounding signal void and so lumbar myelography was performed while the cat was still anaesthetised using 0.3 ml/kg of contrast medium (Omnipaque 300; Nycomed) injected into the subarachnoid space at the level of L6–L7. Lateral radiographs demonstrated obliteration of the contrast columns by the microchip at the C5–C6 intervertebral disc space, and absence of subarachnoid opacification more cranially, confirming its location within the vertebral canal (Fig 1a). On the ventro-dorsal radiographs, there was a slight lateral shift of the right contrast column and attenuation of the left side by the microchip (Fig 1b).
(a) Lateral radiograph of the cervical spine following a lumbar myelogram. The microchip can be seen orientated vertically at the level of the vertebral canal and the intervertebral disc space C5–C6. Attenuation of the dorsal and ventral contrast columns associated with the location of the microchip confirms its vertebral canal location. (b) Ventro-dorsal radiograph of the cervical spine following a lumbar myelogram showing a slight lateral shift of the right contrast column and attenuation of the left side by the microchip.
A standard dorsal surgical approach was undertaken to remove the microchip via a dorsal laminectomy. Once the dorsal laminae of both the fifth and sixth cervical vertebrae were exposed, a defect could be identified in the associated inter-arcuate ligament. Dissection of the ligament and its removal, revealed the microchip inside the vertebral canal, orientated vertically. The microchip was removed and a pedicle-free fat graft was placed over the cord following inspection for dural pathology and extradural haemorrhage, neither of which were present. A standard four-layer closure was performed.
Following the surgery, the cat was medicated with methadone (0.2 mg/kg IM q 4–6 h), clavulanated amoxycillin (20 mg/kg IV q 6 h) and metronidazole (10 mg/kg IV q 12 h) for the first 24 h. Oral clavulanated amoxycillin (20 mg/kg q 12 h) and metronidazole (10 mg/kg q 12 h) were then prescribed for a 3-week period, along with oral meloxicam (0.1 mg/kg q 24 h) for 4 days. The cat remained unable to stand but recovered voluntary movement in all limbs over the next 10 days, at which time it was discharged and referred to a chartered veterinary physiotherapist. The partial Horner's syndrome had resolved during the hospitalisation period. Two months later, a report by the physiotherapist noted that the cat had residual motor dysfunction in the left thoracic limb, with weak extensor function. A telephone conversation with the referral veterinarian 11 months after the surgery following a recheck examination, confirmed that the cat had regained weight-bearing ability in the left thoracic limb, but had mild residual paresis of this limb. Extensor reflexes in both thoracic limbs were considered intact and the left thoracic limb flexor withdrawal reflex was present but reduced. The proximal musculature of the left thoracic limb was slightly reduced in mass on comparison to the right side. The left-sided Horner's syndrome had completely resolved.
Many companies now market an implantable transponder (microchip), which has a unique number programmed into its memory for pet identification purposes. The microchip is implanted into an animal, usually under the skin between the shoulder blades or in the mid left side of the neck, and can usually be read by any scanner worldwide. The microchips come in a pre-packed sterile format and simply push onto the specially-designed implant guns or needles. The applicator is designed to assist with implanting the chip quickly, safely and with control into the respective implant site. Following implantation, a foreign body reaction is initially observed surrounding the microchips in the form of infiltration of cells such as neutrophils, macrophages and plasma cells (Murasugi et al 2003). This is followed by granulation tissue formation and encapsulation of the microchip by collagen fibres (Murasugi et al 2003).
Based upon voluntary reporting of adverse reactions in the UK to the Microchip Advisory Group, the number of reports received until the end of 2004 totalled 287, with 36 being in cats. The types of adverse reaction reported include local swelling, infection, migration, failure and loss and are documented on the British Small Animal Veterinary Association website (www.BSAVA.com). Tumour formation has been associated with one implanted microchip in a dog (Vascellari et al 2004). To the authors' knowledge this report is the first to document spinal cord injury following the incorrect implantation of a microchip.
The cat in this report displayed neurological signs compatible with a cervicothoracic myelopathy caused by a lesion affecting spinal cord segments C6–T2. The grey matter of these segments gives rise to various nerves (eg, suprascapular, musculocutaneous, axillary, radial, median, and ulnar nerves) supplying thoracic limb muscles (Braund 2003). A lesion in this location can cause weakness or paralysis in all four limbs, with the ipsilateral limbs often being most severely affected. Depression or absence of thoracic limb segmental spinal reflexes can accompany the reduced motor function (Braund 2003). Animals with lesions in cord segments T1–T3 may have one or all signs of a Horner's syndrome, including miosis, ptosis, enophthalmos and prolapse of the third eyelid (Braund 2003). The cat in this report demonstrated an ipsilateral partial Horner's syndrome with the only abnormality noted being miosis. This resolved in the early postoperative period.
Prognosis of animals with acute spinal trauma due to any cause is always guarded and is influenced by several factors, including the degree and location of spinal cord damage (Braund et al 1990). Spinal cord dysfunction reflects varying degrees of damage to the grey matter, white matter, or both. Severe grey matter lesions in caudal cervical segments may result in death from respiratory failure due to damage to neurons giving rise to the phrenic nerves; the cat in this report may have experienced ipsilateral phrenic nerve damage based upon radiographic evidence of hemi-diaphragmatic paralysis. Repeat radiographs were not performed to evaluate the diaphragm postoperatively.
In summary, reports of adverse reactions following identification microchip implantation are infrequent and are mostly benign. However, severe spinal cord injury may result from incorrect implantation technique and may require decompressive surgery to allow maximal potential recovery.