Marios Papadopoulos and Samira Saadoun write in Spinal News International about the ISCoPE trial, which aimed to develop techniques to continuously monitor the pressure of the spinal cord at the injury site in the intensive care unit (ICU). They conclude that monitoring from the injury site provides clinically important information, and note that they are now in the process of setting up a randomised controlled trial to test whether, compared with bony decompression, expansion duroplasty improves functional outcome after severe spinal cord injury.
Many spinal surgeons manage patients in the first few days after a severe spinal cord injury. In general, surgeons fix the fracture using metalwork to eliminate instability and the risk of further cord damage. Nothing much can be done in the first few days to improve long-term neurological recovery.
About seven years ago, we set up a study termed ISCoPE (Injured Spinal COrd Pressure Evaluation) aiming to develop techniques to continuously monitor the pressure of the spinal cord at the injury site in the ICU. We call this pressure intraspinal pressure or ISP by analogy to intracranial pressure or ICP that we routinely measure in patients with severe brain injuries. The pressure probe is inserted intradurally during surgery and the ISP is monitored for up to a week and used to compute the spinal cord perfusion pressure (SCPP=mean arterial pressure minus ISP) by analogy to cerebral perfusion pressure for injured brain.1 More recently, we also started monitoring hourly the metabolism of the injured spinal cord (glucose, lactate, pyruvate, glutamate, glycerol) by placing a microdialysis catheter intradurally at the injury site next to the pressure probe.2 These measurements are displayed on the ICU monitors to help the intensivists optimise management to reduce secondary cord damage.
Inserting the two monitoring probes (pressure, microdialysis) intradurally, next to the injured cord and leaving them there for up to a week is safe.3 The ISP signal that is measured from the injured cord is pulsatile and is similar to the ICP signal that is measured from the injured brain. In most patients with a spinal cord injury, the ISP is high and the SCPP is low. ISP and SCPP are important physiological parameters; the chance of functional improvement at one year correlates with SCPP and inversely correlates with ISP (each averaged over the first week after injury).4 Too low SCPP appears to be detrimental and thus intervening to increase the SCPP improves spinal cord metabolism at the injury site and, in some patients, sensory and motor function below the injury. Interestingly, increasing the SCPP too much also appears to be detrimental and worsens injury site metabolism. The observations that too low and too high SCPP are both detrimental, suggest that there must be an intermediate optimum SCPP. We developed a technique to compute the optimum SCPP in real-time and display this on the ICU monitor. A key finding is that the optimum SCPP varies between patients and with time in each patient, thus supporting the concept of individualised management, i.e. not applying the same MAP guidelines to each patient.5 Intervening to increase the SCPP allows more intravenously administered drugs to enter the injury site, which has important implications for the design of drug trials for spinal cord injury.2
In most patients with severe injuries (AIS grades A–C), the cord swells soon after the injury and becomes compressed against the surrounding dura. Such compression is evident on MRI as well as persistently high ISP despite the bony decompression. The concept that the dura is responsible for spinal cord compression after injury is not unappreciated, but has two important clinical implications. First, dural compression causes three compartments to form intrathecally, each with a different pressure: the cerebrospinal fluid compartment above the injury, the cerebrospinal fluid compartment below the injury and the injury site where the cord is compressed against the dura. Because of this compartmentalisation, draining cerebrospinal fluid by placing a lumbar catheter does not effectively reduce the ISP in most patients. Second, the dural cord compression raises the intriguing possibility of expansion duroplasty as a novel treatment to reduce the ISP after acute, severe spinal cord injury. The idea of performing expansion duroplasty to treat uncontrolled cord swelling is analogous to performing a decompressive craniectomy to treat uncontrolled brain swelling after a brain injury. We thus explored expansion duroplasty in patients with acute, severe spinal cord injuries in a phase II trial; our key findings are that the technique is not only safe, but also effectively reduces the ISP and increases the SCPP.6 Based on these observations, we are now in the process of setting up a randomised controlled trial to test whether, compared with bony decompression, expansion duroplasty improves functional outcome after severe spinal cord injury.
Many patients with spinal cord injuries have fever in the first two weeks after injury. We noticed that during these periods of fever, the spinal cord metabolism at the injury site becomes very deranged.7 In patients with severe spinal cord injuries, fever burden appears to be an adverse prognostic factor independent of age and AIS grade on admission. These findings suggest that fever should be treated to reduce further spinal cord damage.
Our recent work focuses on monitoring spinal cord blood flow during surgery.8 We observed several novel phenomena including three different spinal cord blood flow patterns, which we term necrosis-penumbra (a core of low blood flow with regions of intermediate blood flow on either side), hyper-perfusion (very high blood flow throughout the injury site) and patchy-perfusion (irregular regions of low, intermediate and high blood flow), blood pressure-induced local steal (with increased blood pressure, blood flow increases in some regions but, decreases in other regions) and diastolic ischaemia (parts of the injury site only perfused in systole, but not diastole).
Based on our experience with ISCoPE over the last few years, we conclude that monitoring from the injury site provides clinically important information. We thus propose that injury site monitoring be employed in ICUs as standard of care to provide the basis to guide management aiming to improve neurological outcome.
1. Werndle MC, Saadoun S, Phang I, et al. Monitoring of spinal cord perfusion pressure in acute spinal cord injury. Crit Care Med 2014;42:646–55.
2. Phang I, Zoumprouli A, Papadopoulos MC, et al. Microdialysis to optimise cord perfusion and drug delivery in spinal cord injury. Ann Neurol 2016;80:522–31.
3. Phang I, Zoumprouli A, Saadoun S, et al. Safety profile and probe placement accuracy of intraspinal pressure monitoring for traumatic spinal cord injury. J Neurosurg Spine 2016;25:398–405.
4. Saadoun S, Chen S, Papadopoulos MC. Intraspinal pressure and spinal cord perfusion pressure predict neurological outcome after traumatic spinal cord injury. J Neurol Neurosurg Psychiatry 2017;88:452–453.
5. Chen S, Smielewski P, Czosnyka M, et al. Continuous monitoring and visualisation of optimum spinal cord perfusion pressure in patients with acute cord injury. J Neurotrauma 2017;34:2941–2949.
6. Phang I, Werndle MC, Saadoun S, et al. Expansion duroplasty reduces intraspinal pressure and increases spinal cord perfusion pressure after traumatic spinal cord injury. J Neurotrauma 2015;32:865–74.
7. Gallagher MJ, Zoumprouli A, Phang I, et al. Markedly deranged injury site metabolism and impaired functional recovery in acute spinal cord injury patients with fever. Crit Care Med 2018;46:1150–7.
8. Gallagher MJ, Hogg FRA, Zoumprouli A, et al. Spinal cord blood flow in patients with acute spinal cord injuries. J Neurotrauma 2018 [EPub]
Marios C Papadopoulos is a professor of neurosurgery at St George’s, University of London (London, UK) and a neurosurgeon at St George’s University Hospitals NHS Foundation Trust (London, UK). He has a specialist interest in complex spinal surgery and vascular neurosurgery.
Samira Saadoun is a senior lecturer in neuroscience at St George’s and has published a number of papers on spinal cord injury.