Intraspinal pressure monitoring improves management of patients with spinal cord injury

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By Marios Papadopoulos

There is a lack of monitoring techniques in the neurointensive care unit to guide management of patients with acute severe traumatic spinal cord injury. As a result, the optimum mean arterial pressure is unknown as is the role of laminectomy.1 The ability to monitor fundamental physiological variables, such as intraspinal pressure and spinal cord perfusion pressure, from the site of injury would be a major advance as it would allow doctors to limit secondary spinal cord damage that arises from hypoperfusion.


I recently established a novel method to monitor intraspinal pressure and spinal cord perfusion pressure at the injury site in patients with traumatic spinal cord injury in the neurointensive care unit.2 The procedure involves inserting a pressure sensor intradurally between the swollen spinal cord and the dura. Our data show that, after severe traumatic spinal cord injury, intraspinal pressure is high (typically 20–40mmHg) and spinal cord perfusion pressure is low (typically 40–60mmHg). By intervening to increase spinal cord perfusion pressure, outcome in some patients was improved, as assessed using motor evoked potentials and a limb motor score. Mannitol administration, reduction in paCO2, and increase in sevoflurane dose had little effect on intraspinal pressure after traumatic spinal cord injury, even though these manoeuvres have a major effect on intracranial pressure in traumatic brain injury. Increasing the dose of inotropes caused an increase in intraspinal pressure and mean arterial pressure but with a net increase in spinal cord perfusion pressure.


My group proposed a novel way to optimise spinal cord perfusion pressure in patients with traumatic spinal cord injury.2 We defined the parameter sPRx, which stands for spinal pressure reactivity index, and is the running correlation coefficient between intraspinal pressure and mean arterial pressure. sPRx ≤0 denotes intact pressure reactivity, whereas PRx >0 indicates impaired reactivity. A plot of PRx vs. spinal cord perfusion pressure yields a U-shaped relationship. The optimum spinal cord perfusion pressure corresponds to the minimum sPRx. Reducing the spinal cord perfusion pressure below optimum level causes hypoperfusion of the cord and is detrimental. Hyperperfusing the injured cord is also detrimental. An interesting observation is that the optimum spinal cord perfusion pressure varies widely between patients. This suggests that general guidelines (eg. aiming for mean arterial pressure between 85mmHg and 90mmHg) may be meaningless.


There are other interesting findings with important clinical implications. One finding is that laminectomy does not adequately decompress the injured cord, which remains compressed against the surrounding dura. This may explain why studies of laminectomy without dural opening have not convincingly shown a beneficial effect on outcome. I suggest that a laminectomy without expansion duraplasty in traumatic spinal cord injury is analogous to a decompressive craniectomy without durotomy for traumatic brain injury, which is largely ineffective at reducing intracranial pressure. Another interesting finding is that laminectomy allows compression forces applied to wound to be transmitted to the spinal cord, thus reducing spinal cord perfusion pressure and potentially causing further damage. This observation has important implications for nursing care. It raises the possibility that a patient with a traumatic spinal cord injury who is nursed supine with a pillow under the wound may develop spinal cord ischaemia from wound compression.


Though intracranial pressure monitoring to guide management of patients with traumatic brain injury is the standard of care, intraspinal pressure monitoring to guide management of patients with traumatic spinal cord injury is not used. Intraspinal pressure monitoring is a novel idea based on basic physiological principles and may be applied to any spinal cord pathology that causes spinal cord swelling (eg. oedematous transverse myelitis).


References

1. Werndle et al. J Neurotrauma 2012; 29: 880–88

2. Werndle et al. Crit Care Med 2014; 42: 646–55 (editorial: Crit Care Med 2014; 42: 749–50)


Marios Papadopoulos is a professor of Neurosurgery at St George’s, University of London, UK. He spoke about intraspinal pressure monitoring in his keynote talk at the Annual London Spine Course (25–27 June, London, UK).

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