Topic Progress:

Resus Priorities

Although these are ordered here, keep in mind you will be doing much of this concurrently.

In brief:

> Intubate, carefully, if airway or breathing necessitates, avoid hypoxia

> Do proper (ISNCSCI) neuro exam before sedating

> In cervical SCI, insert arterial and central venous lines

> In cervical SCI, have low threshold for vasopressors, don’t miss other causes of shock like haemorrhage

> Aim MAP > 85 for 5-7 days

> Get off hard board, roll every 2 hours

> Remove semi rigid collar ASAP, use MILS for intubation

> Actively warm

> Insert IDC

> Transfer to spinal centre as soon as feasible

WHY IS IT AN ISSUE?

With thoracic and lumbar SCI, respiration is NOT directly affected; other injuries from trauma may be relevant of course.
After cervical spinal cord injury, respiration is affected because:

> Paralysis of muscles of respiration below the neurological level of injury

> The diaphragm is the main muscle of respiration and is innervated by C3,4 and 5

> Injuries above C5 affect the diaphragm and impact the most on tidal volume and vital capacity

> Intercostal muscles and abdominal muscles are innervated at their corresponding spinal level and will be paralysed, affecting respiration, coughing and secretion clearance

> Sympathetic denervation to the lungs causes relative parasympathetic overstimulation, resulting in an increase in quantity of secretions and bronchial tone

> c.75% of patients with cervical SCI will require intubation and mechanical ventilation.

WHEN TO INTUBATE?

> Very high cervical SCI (complete injury at C1,2 or 3) will need ventilation immediately at the scene of injury

> If they can’t breathe – low tidal volumes, fatigue, increasing hypercapnia, oxygen desaturation, all more likely the higher the injury

> Reduced level of consciousness with threatened airway (e.g. concomitant brain injury, shock, medications given etc)

> High risk of vomiting and aspirating while flat and in a collar (e.g. full stomach, nausea)

> Threatened airway from airway trauma

> Also take into account imminent transport / imaging e.g. CT and MRI / surgery

TIPS FOR INTUBATION

The mission is to maintain oxygenation, avoid hypotension and avoid further damage to cervical spinal cord

Do a neurological assessment before giving sedation, and use only short acting sedative / analgesic agents

If time, awake fibreoptic intubation in OT with experienced staff

If urgent:

> Remove collar, cervical in-line stabilisation

> Rapid sequence induction and intubation by most experienced airway operator available

> Prepare glycopyrrolate / atropine / ketamine to offset potential bradycardia

> Prepare titratable vasopressor infusion (ideally noradrenaline via CVC with invasive arterial BP monitoring) to prevent hypotensive events

> Video laryngoscopy with use of Bougie or stylet to minimise cervical movement

If a cervical SCI is suspected, the neck must be immobilised.

Semi-rigid cervical collars carry significant risks and should be removed and exchanged for softer collars as soon as possible.

Hard spinal boards cause rapid development of pressure injury. This risk can be minimized by transferring the patient off a hard board as soon as feasible, and safely rolling the patient every two hours.

Of the hard collars available, the Miami J and Philadelphia collars restrict cervical range of movement more than Aspen or Miami J/Occian back.

The Miami J and Miami J/Occian back cause the lowest levels of mandibular and occipital pressure

Complications of prolonged immobilsiation and spinal precautions include cutaneous pressure ulceration, difficulties with the airway and intubation, potential venous obstruction affecting intracranial pressure, less options for central venous access, higher risk of VTE, and a higher risk of respiratory infections due to restricted physiotherapy, gastrostasis and an inability to provide optimal oral care.
REFERENCE

NEUROGENIC SHOCK

The heart receives its sympathetic innervation from the upper thoracic segments via the superior, middle and inferior cervical ganglions.

Vasomotor tone of the peripheral vasculature is also controlled by segmental sympathetic innervation.

The heart’s parasympathetic innervation comes from the vagus, and therefore is not affected by SCI.

Following SCI, loss of sympathetic supply, and unopposed vagal activity may cause profound vasoplegia combined with bradycardia, resulting in hypotension and neurogenic shock.

This occurs in 19% of patients with cervical and 7% of thoracic SCI REF

Other causes of hypotension, particularly hypovolemic shock must be excluded before a diagnosis of neurogenic shock is made.

Bradycardia and even asystole may occur during routine ICU procedures like endotracheal suction or repositioning in bed in patients with a cervical NLOI.

This phenomenon occurs most commonly in the first week and generally resolves within two to six weeks after injury  REF 

BLOOD PRESSURE TARGET

There are no high-quality data regarding optimal BP goals and duration in the management of acute SCI.
Based on the highest level of evidence available from the 2 prospective studies, MAP goals of 85–90 mm Hg for a duration of 5–7 days should be considered.

After judicious fluid resuscitation (i.e. not too much, carefully titrated) use noradrenaline as first choice vasopressor.
REF

NOTE: SPINAL SHOCK IS NOT NEUROGENIC SHOCK

SPINAL SHOCK

The period of flaccid paralysis, anaesthesia, loss of bowel and bladder function and areflexia following a spinal injury is called spinal shock.

It may last from 48 hours to weeks.

During emergence from spinal shock, deep plantar reflex and the cutaneous reflexes (e.g. bulbocavernosus, cremastric reflex) recovers first, with in 1-3 days, followed by reappearance of deep tendon reflexes and spasticity

Emergence from spinal shock evolves gradually.

Significantly, only once spinal shock has resolved may autonomic dysreflexia manifest.

Pressure ulceration is common after SCI due to immobility and loss of sensation

It starts to happen faster than you’d imagine

> Transfer off hard board immediately

> Change semi-rigid collar to properly fitted Miami J or equivalent ASAP

> Roll with full spinal precautions every 2 hours until pt can be on pressure relieving (alternating air cell) mattress

In high SCI there is initial flaccid paralysis of the detrusor (bladder) muscle and loss of spinal cord reflexes including bladder sphincter control.

There is also loss of bladder stretch sensation

> Insert an indwelling catheter in the emergency department even if priapism present

There is not a universal consensus to imaging in suspected SCI

Following trauma, if there is evidence of any new neurological deficit attributable to a spinal injury, an urgent MRI should be performed.

> MRI with T2 sequences is an acceptable method to rapidly screen patients with a cervical injury

If there is no neurological deficit but the other conditions of the Canadian C-Spine rules (CCCR) or National Emergency X-Radiography Utilization Study (NEXUS) criteria are not met, then high resolution multi-detector row CT (MDCT) of the entire spine is indicated.

For the obtunded blunt trauma patient who is likely to be un-assessable for a prolonged period, an MRI may follow the MDCT.

Policy for the use of MRI in this context should be discussed at your institutional level.

A policy with MDCT alone may miss a small percentage of injuries that would otherwise have required intervention BUT the false positive rate of MRI results in significant morbidity to patients with no injuries who are kept immobilised.

Short answer: don’t give steroids to acute traumatic SCI

Reality more complex

Several randomized controlled trials have investigated the potential efficacy and safety of methyl prednisolone in patients with acute SCI and comprise the largest therapeutic studies completed in the history of SCI research.

In the over 1500 patients enrolled in five RCTs, high-dose glucocorticoid treatment did not meaningfully improve the functional recovery of acute traumatic SCI patients when analyzed by the primary endpoint of the trial.

While it may be the case that glucocorticoid may be efficacious in a subset of traumatic SCI patients, e.g. those with incomplete SCI, this thesis has not been formally subjected to the scrutiny of a properly designed RCT and warrants future investigations.

Notably, all three National Acute Spinal Cord Injury Studies (NASCIS 1,2 & 3) studies demonstrated increased risk of adverse events in the steroid-treated populations.

There are still some advocates (e.g. this guideline) for using steroids for patients who present <8 hours of injury, despite the lack of evidence of benefit and evidence of harm.
REFERENCE

Urgent referral to a Spinal team is important. Depending on the situation, also referral to retrieval, anaesthetics and ICU may be needed.

Make sure you cover:

> Name

> Age

> Mechanism of injury

> Vital signs

> Basic neurologic examination including any sensory deficit, motor deficit, levelof deficit, and rectal tone and sensation

> Ideally ISNCSCI level and grade (see SCI Classification)

> Other trauma injuries

> Interventions and medications administered including IV fluids, blood products and vasopressors

> Imaging results

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