Acute Spinal Cord Injury

• Primary injury due to direct compression, haemorrhage or traction forces
• Secondary injury due to haemorrhage, oedema, neurogenic shock, hypoperfusion and cord ischaemia

• Motor vehicle accidents (40% ish)
• Falls (40% ish)
• Sports injury (10% ish)
• Assault and penetrating trauma (3%)

It won't surprise you that these are generally seen in an older cohort of patients, but are still very much possible in young people as well.

• Infection
• Tumour
• Cyst
• Inflammation
• Stroke
• Congenital
• Degenerative disease

• Age
• Degree of injury
• Level of injury
• Associated complications

• VTE prophylaxis
• Gastroprotection
• Early identification and treatment of infection
• High quality pressure area care (get them off the scoop asap)
• Psychological support

• The cord is physically damaged by compression and traction forces
• The usual culprit is subluxation of vertebral material
• Other injury patterns include hyperextension and retropulsion
• Don't forget direct penetrating injury as well

• After the initial insult, there is bleeding into the central grey matter
• Spinal cord oedema then impairs local blood supply leading to ischaemia
• This is made doubly bad by any hypotension and autonomic dysfunction seen in high thoracic lesions
• Then much like a stroke, this damage will spread in both directions along the cord and worsen if left untreated

A patient with a C4 injury will still have diaphragmatic function (C3-5) but if not treated appropriately in the acute setting, the injury can spread north to C3 and higher, leaving the patient requiring permanent ventilation.

• Neurogenic shock refers to the hypotension caused by loss of peripheral vascular resistance as a result of widespread loss of sympathetic tone, as seen after a high thoracic spinal cord injury
• Spinal shock is not 'shock' in the circulatory sense, it simply refers to the total loss of motor function and sensation distal to the spinal cord lesion

• Areflexia - 0-1 days
• Initial reflex return days - 1-2 days
• Early hyperreflexia - 4-28 days
• Late hyperreflexia - 1-12 months

If you're wondering why monosynaptic motor reflexes are absent even though the lesion is higher up, it's because even monosynaptic reflexes rely on tonic descending facilitation to work.

• The ligaments (flavum, interspinous, supraspinous)
• The processes (spinous, transverse)
• The complexes (anterior, middle, posterior)
• The joints (intervertebral, facets)

The posterior complex is the strongest, and if two complexes are disrupted then the column is deemed unstable.

The mid-thoracic spinal canal is narrowest, with highest risk of injury from retropulsion of vertebral bone or disc material.

The spinal cord extends from the brainstem to L1/2 in 90% of adults (some as low as L3) and L2/3 in the neonate.

Sensory pathways

• Posterior columns - ipsilateral vibration, fine touch, proprioception
• Spinothalamic tracts - contralateral pain, temperature and coarse touch

Motor pathways

• Corticospinal tracts - descending motor control

Arterial supply

• 1 anterior spinal artery, from the vertebral artery
• 2 posterior spinal arteries, from the posterior inferior cerebellar arteries
• Radicular arteries (artery of Adamkiewicz)

The anterior spinal artery is at risk from retropulsion of vertebral bone or discs, particularly around C7.

• First of all, don't get distracted by people talking about a spinal cord injury, and make sure you're happy with airway, breathing and circulation
• It is not uncommon for c-spine injury patients to also have max-fax injuries and blood in the mouth
• Manual inline stabilisation is key, especially in suspected cervical cord injury, and will make your intubation harder
• Trauma patients are more likely to aspirate for many reasons, so definitely RSI if intubating
• Using a hyperangulated videolaryngoscope blade may help reduce mechanical strain on the neck during intubation, as well as the concomitant haemodynamic effects of laryngoscopy*

*Flexion is thought to be more dangerous to a c-spine injury than extension, and remember to keep their head stable once they're paralysed and intubated.

• Huge initial catecholamine release with sudden hypertension and tachycardia
• Then paralysis of sympathetics causes hypotension - usually ending up with a systolic around 80mmHg
• Arrhythmia
• Vasodilatation
• Bradycardia - especially with bladder distension so catheterise early
• Hypotension may be fluid-resistant and require vasopressors
• Risk of ischaemic heart disease due to immobility
• Autonomic dysreflexia (more of a chronic issue but often gets a mark)

If you're intubating a patient with a high cord lesion, consider atropine to prevent profound bradycardia on laryngoscopy.

Oh, and definitely put in an arterial line.

• Intercostal failure leads to reduced tidal volume
• Vital capacity reduced to 30-80% of original
• Breathing worse in sitting position as abdomen pulls diaphragm down, reducing room for expansion
• Worse V/Q mismatch and atelectasis
• Poor cough and secretion clearance
• May require short or long term ventilation
• Oxygenation is key to prevent hypoxic secondary neuronal death

• Above C3 - diaphragmatic failure, needs immediate and ongoing ventilation
• C3-C5 - variable diaphragm function - 80% require ventilation
• C5-T8 - loss of intercostals - weak cough, may require short term ventilation, usually don't require longer term support
• Below T8 - weak cough due to loss of abdominal muscles so may need short term support

• Reduced gastric motility
• Delayed gastric emptying (increased risk of aspiration)
• Constipation
• Paralytic ileus
• Pseudo-obstruction
• Increased incidence of gallstones
• Stress ulceration*

*Unopposed vagal activity stimulates gastric acid production. Gastroprotection with a PPI for six weeks substantially reduces incidence of ulceration.

• Vasodilatation below the level of injury
• Anhidrosis below the injury
• Reflex hyperhidrosis above the injury
• Inability to shiver below the injury
• Loss of sensation to heat or cold below injury
• Reduced muscle mass and metabolic rate

• Unexplained hypotension
• Warm dry feet
• Priapism
• Inappropriate bradycardia
• Flaccidity in legs but not arms
• Areflexia in legs but not arms
• No response to pain in legs but response to pain higher up

• High cervical cord injury
• Rapid shallow breathing
• Vital capacity less than 15ml/kg
• Worsening vital capacity trend
• Hypercapnoea
• Poor cough
• Exhaustion

• Pounding headache
• Blurred vision
• Flushing above the level of the spinal cord injury
• Profuse sweating
• Goosebumps and chills (but no fever)
• Bradycardia*
• Severe hypertension

*This is a baroreceptor reflex due to the sudden hypertension - the same as is seen with metaraminol

• Bladder irritation - distension, UTI
• Bowel irritation - constipation, suppositories
• MSK - pressure sores, burns, ingrown toenail, ulcers
• Uterine contractions
• Fractures
• Acute intra-abdominal pathology

• Figure out what's causing it and treat that
• If systolic >170mmHg then start emergency medical management
• Glyceryl trinitrate NB: DO NOT use glyceryl trinitrate if sildenafil (Viagra) or vardenafil (Levitra) has been taken in the previous 24 hours or tadalafil (Cialis) in the previous 4 days. Give one spray of glyceryl trinitrate (Nitrolingual Pump spray) under the tongue. During administration the canister should be held uptight and the spray should not be inhaled. OR Apply 5 mg, transdermal patch to chest and upper arms according to manufacturer’s instructions. Remove patch once BP settles or if the BP drops too low.
• Blood pressure should start to drop within 2 minutes of GTN administration and last around half an hour
• Give another dose if inadequate response after 5 to 10 minutes

Note the contraindication to GTN:

• Sildenafil (or vardenafil/tadlafil) within last 24 hours
• If so then consider hydralazine, clonidine or something like captopril - check your local guidelines