Abstract

Background/ObjectiveWe have recently developed monitoring from the injury site in patients with acute, severe traumatic spinal cord injuries to facilitate their management in the intensive care unit. This is analogous to monitoring from the brain in patients with traumatic brain injuries. This study aims to determine whether, after traumatic spinal cord injury, fluctuations in the monitored physiological, and metabolic parameters at the injury site are causally linked to changes in limb power.MethodsThis is an observational study of a cohort of adult patients with motor-incomplete spinal cord injuries, i.e., grade C American spinal injuries association Impairment Scale. A pressure probe and a microdialysis catheter were placed intradurally at the injury site. For up to a week after surgery, we monitored limb power, intraspinal pressure, spinal cord perfusion pressure, and tissue lactate-to-pyruvate ratio. We established correlations between these variables and performed Granger causality analysis.ResultsNineteen patients, aged 22–70 years, were recruited. Motor score versus intraspinal pressure had exponential decay relation (intraspinal pressure rise to 20 mmHg was associated with drop of 11 motor points, but little drop in motor points as intraspinal pressure rose further, R2 = 0.98). Motor score versus spinal cord perfusion pressure (up to 110 mmHg) had linear relation (1.4 motor point rise/10 mmHg rise in spinal cord perfusion pressure, R2 = 0.96). Motor score versus lactate-to-pyruvate ratio (greater than 20) also had linear relation (0.8 motor score drop/10-point rise in lactate-to-pyruvate ratio, R2 = 0.92). Increased intraspinal pressure Granger-caused increase in lactate-to-pyruvate ratio, decrease in spinal cord perfusion, and decrease in motor score. Increased spinal cord perfusion Granger-caused decrease in lactate-to-pyruvate ratio and increase in motor score. Increased lactate-to-pyruvate ratio Granger-caused increase in intraspinal pressure, decrease in spinal cord perfusion, and decrease in motor score. Causality analysis also revealed multiple vicious cycles that amplify insults to the cord thus exacerbating cord damage.ConclusionMonitoring intraspinal pressure, spinal cord perfusion pressure, lactate-to-pyruvate ratio, and intervening to normalize these parameters are likely to improve limb power.

Highlights

  • Traumatic spinal cord injury (TSCI) affects about 180,000 people globally each year [1]

  • Intraspinal pressure (ISP) and spinal cord perfusion pressure (SCPP) correlate with injury site metabolism [25], neurological status [26], and longterm neurological outcome [20], and patients with neurologically complete TSCIs have more deranged cord metabolism than those with neurologically incomplete injuries [22]

  • The objective of our study is to address the question whether changes in ISP, SCPP, and injury site metabolism cause changes in limb power

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Summary

Introduction

Traumatic spinal cord injury (TSCI) affects about 180,000 people globally each year [1]. Intraspinal pressure (ISP) and spinal cord perfusion pressure (SCPP) [19,20,21] are monitored with a pressure probe, as well as injury site metabolism with a microdialysis (MD) catheter [22, 23]. These techniques are safe and analogous to multi-modality monitoring for brain injury [24]. ISP and SCPP correlate with injury site metabolism [25], neurological status [26], and longterm neurological outcome [20], and patients with neurologically complete TSCIs have more deranged cord metabolism than those with neurologically incomplete injuries [22]. These relations between ISP, SCPP, and injury site metabolism versus neurological outcome are associations that do not imply causation

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