Initial Management of Acute Spinal Cord Injury

Primary Assessment and Management

Stabilise the patient (airway, breathing, circulation) as for any other emergency. Routine blood work and urinalysis should be obtained where possible. A coagulation panel and buccal mucosal bleeding time may be appropriate for some cases. FIV and FeLV testing should be performed in feline patients (a positive result would markedly increase the likelihood of lymphoma as a cause for neurological deficits).

A thorough (but gentle) physical, orthopaedic and neurological examination should be performed (reluctance to walk because of acute bilateral cranial cruciate ligament rupture is sometimes confused with paraparesis) provided the patient is not placed at risk; be mindful that moving or manipulating a patient with a spinal fracture may cause significant additional spinal cord injury.

Early consideration should be given to systemic blood pressure and oxygenation. Hypotension will result in a further decrease in the already compromised perfusion of the injured spinal cord segment. Hypoxaemia will exacerbate the local energy failure. Hypotension should be treated by the administration of appropriate fluids, and oxygen supplementation provided as necessary (face mask, nasopharyngeal catheter, transtracheal catheter). Oxygen supplementation can be particularly important for animals with cervical spinal cord injury, where hypoventilation is not uncommon. Patients that are severely tetraparetic on initial presentation should be evaluated for hypoventilation using blood gas analysis or a capnometer. ECG should be performed if there is any suspicion of cardiac dysfunction.

Restrict Movement

Some degree of immobilisation of patients following spinal cord trauma is important. Immediate cage confinement should be instituted as a minimum for a patient suspected to have suffered a Hansen type I disc extrusion. If vertebral fracture or subluxation is suspected, strapping the patient to a board is recommended.

Analgesia

Analgesia should be instigated, as appropriate. NSAIDs are useful, although they should be avoided in hypotensive animals. I would strongly advise against the use of any glucocorticoids (see the following discussion).

Opioids may be used where additional analgesia is required, although these will influence the neurological examination. Ideally, a thorough neurological examination should be performed before the administration of opioids, but at the very least evaluate the presence/absence of deep pain sensation; an animal with weak deep pain sensation may appear to have completely lost perception of pain under the influence of opioids. This is particularly significant as the single most important indicator of prognosis is deep pain sensation.

Prognosis

Prognosis; disc extrusion: For paraplegic patients retaining deep pain sensation following Hansen Type 1 disc extrusions, the prognosis is excellent, with functional recovery expected in approximately 90 to 95% of cases following surgical decompression. For patients that lose deep pain sensation, functional recovery is anticipated in approximately 50 to 60% of cases.

Prognosis; spinal fracture: For paraplegic patients retaining deep pain sensation following spinal fracture/subluxation, the prognosis is actually very good, with functional recovery expected in approximately 80 to 90% of cases following surgical stabilisation. For patients that lose deep pain sensation, the prognosis is extremely poor.

Remember when assessing pain sensation to look for a conscious response e.g. vocalising, looking around (sudden dilation of the pupils at the time of the stimulus may also indicate sensation of pain). Limb retraction i.e. a withdrawal reflex is not an indication of pain sensation. Deep pain should be assessed in the medial and lateral digits of the affected limbs and also the tail; use finger pressure first, and if no response progressively increase the level of noxious stimulus e.g. small haemostats with light pressure, then heavier pressure, then large haemostats with sufficient pressure to compress the periosteum.

Additionally, the (careful) use of pliers across the calcaneus may be considered in patients that show no evidence of deep pain sensation with the previously described techniques. This may sound brutal, however, the presence or indeed absence of deep pain perception is often a significant factor in an owner's decision to proceed with treatment (or to consider euthanasia). Furthermore, in cases of spinal fracture confirmed absence of deep pain sensation essentially precludes any chance of functional recovery. It is vitally important to be sure.

Should you Refer?

Animals exhibiting apparent back pain may have marked spinal cord compression, even in the absence of neurological deficits. For this reason, these cases should always be considered candidates for further investigation, including myelography and/or advanced imaging (+ surgery if indicated by imaging). Investigation (and possible surgery) should ideally be discussed and offered to the clients on initial presentation.

Furthermore, acute onset back pain and particularly ambulatory paraparesis should always be regarded as serious (particularly in chondrodystrophoid breeds), and the owner warned of potential consequences if investigation is delayed e.g. in the case of a partially extruded intervertebral disc, nuclear disc material may continue to extrude, with potentially catastrophic consequences; consider a patient that presents with back pain +/- mild neurological deficits, is sent home on anti-inflammatories only to be re-presented two days later, paraplegic with absent deep pain sensation. Remember; acute onset non-ambulatory paraparesis or paraplegia should always be considered a potential surgical emergency.

Should you undertake a Radiographic Investigation before considering Referral?

For the reasons presented in the ensuing discussion, probably not; however if you do, my advice would be to instigate appropriate analgesia (including opioids once the neurological examination has been performed), allowing sufficient time for the patient to relax. Next, gently immobilise the patient by strapping to a board and taking radiographs whilst conscious or very lightly sedated (Do not use benzodiazepines e.g. diazepam or alpha-2-agonists e.g. medetomidine).

• When spinal cord injuries occur, the paraspinal muscles typically spasm resulting in a splinting effect; this phenomenon contributes substantially to the stability of the spinal column. Heavy sedation or anaesthesia results in the loss of paraspinal muscle "splinting"; unstable vertebral segments are more likely to displace. Similarly increased movement at disc spaces may increase the likelihood of further disc extrusion in an already herniated disc. For these reasons, it is quite common for patients to show neurological deterioration following sedation/anaesthesia. The example below, although extreme, illustrates the potential consequences of anaesthetising an animal and then waking it up again before definitive treatment is undertaken.
• Survey radiographs may be useful to screen for fractures, although in some cases of vertebral luxation forceful contraction of the paraspinal musculature may return the vertebrae to a relatively normal position despite significant displacement occurring acutely at the time of injury. Well-positioned, high-quality radiographs (and typically myelography or advanced imaging) are essential for diagnosis in these cases. Sedation or anesthesia is necessary to achieve accurate positioning for radiography in most animals. However, like opioid administration, this must not be given before a thorough neurological examination, as sedation will influence the results of neurological examination performed thereafter. Once sedation and particularly anaesthesia are administered, surgery should ideally be performed immediately after imaging has been completed (assuming a compressive lesion, fracture or intervertebral instability is identified) to minimise the potential for ongoing injury.
• It is rare that plain radiographs will yield sufficient information to make a diagnosis AND plan appropriate management in a spinal case. Myelography, MRI or CT are necessary for the majority of cases, followed by (immediate) surgical decompression, stabilisation or further investigation as appropriate. For animals that are acutely paraparetic or paraplegic, it is obviously ideal to minimize unnecessary time delays between initial presentation and definitive therapy. In these instances, sedating or anaesthetizing an animal to perform plain radiographs prior to referral will at the very least cause a significant delay before a diagnosis +/- decompression can be achieved, and at worst, may seriously compromise the prognosis for recovery.

Glucocorticoids in the management of Neurological Emergencies

Glucocorticoids are widely used in veterinary practice for the management (mismanagement!!) of spinal cord trauma. Glucocorticoids may reduce inflammation, however, they can also prejudice the survival of any injured neurons by interfering with their glucose metabolism (Sapolsky, 1994; Smith-Swintosky et al, 1996). In particular, the use of dexamethasone has been associated with a poorer prognosis in patients with spinal injury. In addition, there is almost certainly no neuroprotective benefit provided by any corticosteroid, with the possible exception of methylprednisolone sodium succinate.

The use of methylprednisolone sodium succinate in veterinary medicine is based on human data (Bracken MB et al, 1990), although many studies have now raised serious questions about the value of methylprednisolone sodium succinate in humans, reporting extensive complications with minimal neurological gain. There are NO veterinary studies to demonstrate benefits following the use of methylprednisolone sodium succinate. The benefits reported originally in man were relatively small improvements mainly associated with upper-body function, e.g. improved dexterity of digits. Whilst these relatively small changes may be important in people, they are of little value in animals. It is worth noting that the use of methylprednisolone in humans more than 8 hours following spinal cord injury actually worsens the prognosis, presumably due to interference with neuronal glucose metabolism, as previously described. There is no reason to believe this may not be the case in animals, and possibly in a relatively shorter time.

Corticosteroids can precipitate clinically significant gastrointestinal bleeding in as many as 15% of neurosurgical patients, with mortality rates up to 2%. Dexamethasone is most likely to cause problems and has no role in the management of spinal trauma. Furthermore, dexamethasone may actually exacerbate spinal cord injury. With the current body of knowledge, the use of dexamethasone in the management of spinal cord trauma would not only be unwise; it may well be considered negligent.

Duodenal or colonic perforations are the most serious potential gastrointestinal complications following corticosteroid use. (Toombs et al., 1986; Hinton et al., 2002). It is important to note that standard gastrointestinal protectant agents may not be effective in preventing corticosteroid-induced side effects (Hansen et al, 1997). In one study endoscopy revealed severe, subclinical gastrointestinal hemorrhage in 90% of dogs after methylprednisolone sodium succinate treatment (Rohrer et al.,1999). For all of the above reasons, routine glucocorticoid therapy in spinal patients is strongly discouraged (LeCouteur and Sturgess, 2003).