What is our goal in managing spinal cord injuries?
Most complications occur within 24 hours of the injury. Avoiding secondary injury by appropriate early management is crucial.
Understanding the primary injury is easy. Force x spinal cord = primary spinal cord injury. In the ED, in PICU and on the wards, we follow spinal precautions to avoid worsening the initial damage (primary injury). But, aside from supporting public health campaigns, wearing seatbelts, not exceeding the speed limit and not going headfirst down a water slide, there’s very little that we, as clinicians, can do to reverse the primary spinal injury.
It’s the next bit that we can influence. Disruption of the supply of oxygen and nutrients to the cord causes an acute pathophysiological response. This cascade includes ischaemic stress, secondary haemorrhage and inflammation, and resultant glial and nerve cell necrosis. As these cells undergo apoptosis, further inflammatory proteins are released, activating neighbouring cells so that they enter an inflammatory state. This promotes further damage in a cascade that can last months after the primary injury.
This secondary insult can cause more damage than the original primary injury. And this is where we come in.
Our goal is to prevent secondary injury to the spinal cord. As soon as a spinal cord injury is suspected, we should optimize conditions for the cord to curtail the inflammatory cascade. This is neuroprotection.
It’s worth an early discussion about the role of steroids. The use of steroids in spinal cord injuries is contentious. A 2012 Cochrane review of the role of high-dose methylprednisolone in patients in spinal cord injury concluded that steroids are the only pharmacologic agents to show efficacy when given within 8 hours of injury. However, complications such as hyperglycaemia, infection, GI haemorrhage and impaired wound healing, are seen in children with spinal cord injuries treated with high dose steroids. Many spinal teams have moved away from using steroids in spinal trauma in children. My favourite quote from a local paediatric spinal specialist underpins this exactly: “Ask 100 spinal specialists whether they’ll use steroids in spinal trauma and you’ll get 100 different answers”. The bottom line is that no clinical evidence exists to definitively recommend the use of steroids as a neuroprotective agent in the treatment of acute spinal cord injury in children. Involve your spinal specialists early and be guided by their recommendations, which are likely to be based on the severity of injury and indicators of early oedema.
Discussions about steroids aren’t the only reason to involve your multidisciplinary team early. Early decompression of subdural or epidural blood around the cord may be considered in time-critical cases to prevent further injury.
Spinal cord syndromes
Spinal cord syndromes are also worth a mention. This fabulous post by CanadiEM explains how compromise to different sections of the spinal cord can lead to the different spinal syndromes: central cord, anterior cord and hemicord, aka Brown-Sequard. The title’s great: A boring guide to spinal cord syndromes – it’s really not boring and explains the syndromes incredibly well. It’s worth remembering, though, that aside for Brown-Sequard in penetrating injuries, the typical spinal cord syndromes are much less common in paediatrics than in adults.
How does this fit into our approach to managing a child with major trauma?
A full spinal assessment is conducted as part of our trauma secondary survey. If you find any neurological deficits, a careful neurological exam and documentation are crucial.
In older children, or if you have interdisciplinary team support to help you acutely, you should reach for an ASIA chart. This is most useful for neuroprognostication and determining the potential for recovery and should be done within 72 hours of injury. The American Spinal Injury Association chart is a detailed, two-page sheet, enables you to document the complete spinal cord assessment. This baseline neurological assessment should be performed by two experienced team members, as experience is required especially in young children. In suspected spinal cord injuries, the most important thing to document is perianal sensation, as sparing of S3/4/5 gives the best prognosis. Of course, any assessment of dermatomes should be done with a carefully coordinated log roll. (It can be argued that leaving log rolls for the secondary survey is valid, unless you are looking for a penetrating injury). As well as mapping the distribution of sensory loss, log rolls are used to examine the spine for wounds and bruises and to palpate the spinal column for any tenderness, steps or gaps. More on the careful approach to log rolls later.
Serious spinal cord injury following blunt trauma is rare, but crucial to recognise. It occurs in approximately 1% of all paediatric blunt trauma cases (0.4% in the preschool age, 2.5% in the adolescent age) and most are injuries are stable. Suspect a spinal cord injury when:-
A good neurological assessment is important to identify the signs, but cervical spine precautions should be followed in appropriate cases with distracting injuries.
To prevent secondary injury, the “moment of risk” approach has been suggested. Use soft neck collars, thoracic elevation devices (TEDs) in children less than 8 years of age, lateral sandbags in unconscious patients and careful attention to neutral handling and positioning at moments of risk. These include a change in position during intubation, imaging, transfers, and logrolls
Before the secondary survey comes the primary survey
We need to understand and anticipate the effect spinal cord injuries might have on other body systems, as they impact our ability to manage the trauma patient. Let’s work through a case…
A 13-year-old boy jumps into a lake, trying to execute the perfect tumble mid-air. He strikes the water head-first and immediately feels neck pain and a burning sensation in his right arm. Frightened, he tells his friend that his arm feels like it’s on fire. Whilst waiting for the rescue services his GCS drops. On initial assessment by paramedics, his oxygen saturations are 96% on room air, his respiratory rate is 28, his heart rate is 55 with a blood pressure of 80/40. His GCS is 6 made up of E1, V1, M4. He’s brought to the hospital on a spinal board with 3-point cervical spine immobilisation and an oropharyngeal airway in situ. The paramedics point out the history of neck pain and altered sensation of the arm when they hand over to the receiving ED team.
As we work through the different systems, think about corresponding injuries to body parts at each level of spinal cord injury.
A is for Airway
In trauma Airway really means Airway + Cervical Spine. Hard collars are no longer advocated for paediatric c-spine immobilisation (or in fact in any patient). Blocks and tape can be used in cooperative children. During intubation, an extra person will be needed to maintain manual in-line stabilisation (MILS) to reduce excessive neck movement.
Suxamethonium should be avoided in patients with a spinal cord injury due to the risk of hyperkalaemia, which can last many months. This comes from studies from the 1970s that demonstrated hyperkalaemia after suxamethonium in patients with spinal cord injuries, though other studies have failed to corroborate it. A clearer consideration, however, is that suxamethonium can lead to muscle contractions and potentially increase the risk of moving the spine. Given the availability of rocuronium, for paediatric rapid sequence induction, it seems a bit of a moot point, but worth bearing in mind if the anaesthetic assistant reaches for the sux.
As well as the need to maintain spinal alignment, the process of intubation is also risky. In patients requiring c-spine immobilisation the airway, by definition, is difficult and the most experienced operator should perform the intubation. To optimise their view, we use suctioning to clear secretions away. Stimulation of the vagus during tracheal manipulation and toileting activates cardiac branches which convey parasympathetic innervation to the sino-atrial and atrioventricular nodes of the heart. In a spinal cord lesion, these parasympathetic fibres are unopposed, meaning there’s a high risk of profound bradycardia and hypotension during suctioning and introduction of the endotracheal tube. This bradycardia may be so profound that the child develops an asystolic arrest. The vagus nerve, the 10th cranial nerve, is known as the “wandering nerve” from the Latin ‘vagary’ (meaning wandering). It’s functionally diverse, with sensory, motor and parasympathetic functions, arising from the brainstem and extending down to the abdomen.
The emergency treatment of bradycardia is atropine at 20 mcg/kg (minimum 100 mcg, maximum 600 mcg), repeated after 5 minutes if required,. Inotropes (adrenaline and noradrenaline) may be needed to manage hypotension.
On assessment, his GCS remains low and the decision is made to secure his airway as part of his neuroprotective measures. Manual inline stabilisation is applied, rocuronium is used with ketamine and fentanyl. Atropine is drawn up and attached via a 3-way tap in case of bradycardia with adrenaline boluses ready in case of hypotension. The child is intubated using videolaryngoscopy.
B is for Breathing
In cervical and thoracic injuries below C3, 4, 5 (which keeps the diaphragm alive – a medical school rhyme that has stood the test of time), the diaphragm may function normally, but intercostal muscle function can be impaired. This results in the paradoxical chest and abdominal movement of diaphragmatic (seesaw) breathing. In the unconscious patient, this may be one of the first clues of a spinal cord injury.
This impaired intercostal muscle function leads to a decreased vital capacity. V/Q mismatch due to immobility follows. In a spontaneously breathing child with a spinal cord injury, keep a close eye out for signs of respiratory fatigue and hypoventilation.
Sympathetic nervous dysfunction can cause hypersecretion within the lungs which, when coupled with an impaired cough impulse, may trigger bronchospasm. Bronchodilators may be helpful and, in the conscious child with no other indication for intubation, CPAP may help to reduce the work of breathing.
All the while, it’s important not to forget that other traumatic chest injuries will also cause respiratory distress. A proper primary survey is important. Respiratory distress due to pneumothorax or haemothorax is far more common than distress due to a spinal cord injury.
The boy has no bruising to his thorax, his trachea is central and his chest has a normal resonance. He becomes wheezy, however, and is given nebulised salbutamol through his anaesthetic circuit. The wheeze improves.
C is for Circulation
It’s time to think about neurogenic shock (which is different to spinal shock. Spinal shock is like a concussion of the spinal cord – a motor paralysis and sensory loss which can recover). Children with lesions above T5 develop neurogenic shock.
It’s worth a quick recap of the autonomic nervous system, made up of sympathetic and parasympathetic nerves; the sympathetic nervous system stimulates the ‘fight or flight’ response, while its parasympathetic counterpart controls the impulse to ‘feed and breed and rest and digest’.
Injuries above T5, cause a loss of sympathetic tone, with unopposed parasympathetic action resulting in reduced vascular tone. This vasodilation causes pooling of blood in the extremities and resultant hypotension. The higher the spinal cord injury, the greater the loss of vasomotor tone.
Neurogenic shock occurs in lesions above T5 = hypotension due to loss of vascular tone.
The challenge is identifying the cause of hypotension in the trauma setting. Is it because of neurogenic shock? Haemorrhagic shock? Or a combination of the two? Haemorrhagic shock is far more common than neurogenic shock: examine the abdomen, chest, pelvis and long bones for clues to bleeding. Hypotension WITH bradycardia and NOT RESPONDING to fluid resuscitation should lead to a suspicion of neurogenic shock, a triad of hypotension, bradycardia and peripheral vasodilation.
If spinal cord injury is suspected, hypotension should be treated aggressively – it can lead to secondary neurological injury.
Lesions above T3 may lead to a loss of sympathetic innervation to the heart, resulting in bradycardia and decreased stroke volume. The end result is a combination of hypotension with bradycardia. Making the situation even more challenging is the fact that blood pressure and heart rate cannot be used to quantify the degree of shock. Fluid resuscitation may be helpful but it’s important not to chase the blood pressure – it will be lower than expected. To reduce the risk of secondary neurological injury vasopressors like noradrenaline are useful to maintain the MAP (the mean arterial pressure) but the optimal target pressure isn’t known. Expert advice is to aim for a high normal MAP 70th to 95th centile for age and length. Fluid resuscitation must be careful; too little fluid can cause tissue ischaemia while too much can cause pulmonary oedema. Judicious fluid use is key, tailored to urinary output.
The heart rate and blood pressure remain low. There’s no bruising to his abdomen and it’s not distended. He’s in a pelvic binder. His long bones appear undamaged. His heart rate does not respond to two 10ml/kg bolus of O negative blood. Perhaps a spinal cord injury has led to neurogenic shock? You start noradrenaline while waiting for CT to rule out a surgical cause for the hypotension. Once back from CT, he will be examined for signs of a possible urethral injury.
Sometimes hypotension is not the problem, hypertension is. Hypertension can be seen in autonomic dysreflexia, a spinal cord emergency, that may occur later in patients with spinal cord injuries. Typically this occurs weeks to months following the acute injury and can continue to be a problem for months to years. You might see a patient with a high c-spine injury present to ED from home. Many patients have an autonomic dysreflexia management plan to follow from their home team.
Imagine a situation where someone has a spinal cord injury above T6 with sensory loss below the level of the injury. They don’t feel pain. Or do they just feel it differently? Intact lower sensory neurons can still sense painful stimuli below the level of injury and transmit the message up the cord. When the pain signal reaches the level of the cord injury, it’s interrupted and prevented from being transmitted to the cerebral cortex. No pain is perceived.
But this painful signal does reach the major splanchnic sympathetic nerves at the level of T5-T6, stimulating a sympathetic ‘fight or flight response’. Vasomotor tone increases leading to vasoconstriction. This then leads to hypertension, a pounding headache, anxiety and visual changes.
Hypertension stimulates baroreceptors in the carotid sinuses and aortic arch, triggering a parasympathetic signal to travel down the vagus nerve. When the signal reaches the level of injury, it is disrupted and cannot travel any further – the counterbalancing parasympathetic response only occurs above the level of the injury. These parasympathetic changes include vagal nerve stimulation that slows down the heart rate, leading to bradycardia and vasodilatation. Because this vasodilatation can only occur above the level of the spinal cord injury, the end result is flushing, sweating and warmth above the level of the spinal cord injury (due to parasympathetic activity which cannot pass down the cord beyond the lesion) with pallor and coolness below (because of the sympathetic overdrive from the distal painful stimulus), with hypertension and bradycardia. The feedback loop between the two branches of the autonomic nervous system function independently. Older patients often report a “sense of impending doom”.
Autonomic dysreflexia occurs with lesions above T6 = flushing, sweating and warmth above the level of the SCI and pallor and coolness below with hypertension and bradycardia
Treatment of the hypertensive crisis associated with autonomic dysreflexia is a medical emergency.
- Sit the patient upright, remove the binder (if safe to do so), compression stockings and loosen tight clothes – this will help reduce blood pressure and headache whilst you search for a cause.
- Remove the noxious stimulus. Any distal painful stimulus can trigger autonomic dysreflexia: blocked urinary catheters, impacted bowel, urinary tract infections and pressure sores. Check whether the patient’s position has been changed recently.
- Use nifedipine, a calcium channel blocker, to treat hypertension.
- Monitor cardiovascular signs continuously until the hypertensive crisis has resolved, keeping a heightened awareness of the possibility of a repeat attack.
D is for Disability
The boy has blood from his right ear, suspicious for a base of skull fracture. CT are now ready and given the extent of his physiological derangement, he’ll have a trauma scan to include the head, neck, chest, abdomen and pelvis.
In the context of a possible spinal cord injury, D for disability doesn’t only mean potential traumatic brain injury but also means traumatic spinal cord injury. Every patient should be removed from a spinal board within 20 minutes of arriving because the risk of a pressure sore is high (thankfully spinal boards are going out of fashion but the name is terrible – much better to call them “extrication devices” so no one thinks they’re good for the spine). An extrication device can be used to transfer between surfaces, such as from the ED trolley to the CT table, but a scoop with head blocks is just as good. Spinal alignment should be maintained at all times, supporting the body to keep the neck neutral, and should be rechecked every time the child is moved. If they are kept in spinal precautions, they should be turned every 2 hours, (starting in the ED), to prevent pressure sores. Log roll guidance and guidelines on how to turn are on the MASCIP (Multidisciplinary Association for Spinal Cord Injury Professionals) website at www.mascip.co.uk
Pain management needs to be optimised to prevent dysautonomia.
The CT confirms a base of skull fracture with subdural haematoma. There are also burst fractures of T1 and T6. He is taken to theatre by the neurosurgeons for evacuation of the subdural haematoma before going on to have an MRI to assess the extent of the spinal cord injury.
E is for Everything Else
There are a couple of important “everything elses”.
Minimise heat loss – children with spinal cord injuries cannot control or maintain their body temperature so blankets and Bair huggers should be used and the thermostat cranked up in the Resus Room. Hypothermia should be avoided as it is linked to an increased risk of neurological injury.
Spinal cord injuries also lead to bowel and bladder impairment. If there’s no evidence of urethral injury a urinary catheter can be placed and left on free drainage. Urine output can then be used to titrate fluids, aiming for 0.5 ml/kg/hr. And don’t forget, a full bladder can trigger an episode of autonomic dysreflexia.
Children with spinal cord injuries should be kept nil by mouth initially, but once bowel sounds are heard, it’s important that feeds are started. That one’s outside of the remit of the PEM team and something to be considered once on a trauma ward.
Not every child with a traumatic spinal cord injury will be able to tell you about altered neurology. So, here is the final take-home – clues to a spinal cord injury in an unconscious or non-verbal patient:
Clues to a spinal cord injury
Hypotension and bradycardia
Flaccid areflexia / absent reflexes below a level
Loss of response to pain below a level
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