Targeted Perfusion Therapy in Spinal Cord Trauma.

We review state-of-the-art monitoring techniques for acute, severe traumatic spinal cord injury (TSCI) to facilitate targeted perfusion of the injured cord rather than applying universal mean arterial pressure targets. Key concepts are discussed such as intraspinal pressure and spinal cord perfusion pressure (SCPP) at the injury site, respectively, analogous to intracranial pressure and cerebral perfusion pressure for traumatic brain injury. The concept of spinal cord autoregulation is introduced and quantified using spinal pressure reactivity index (sPRx), which is analogous to pressure reactivity index for traumatic brain injury. The U-shaped relationship between sPRx and SCPP defines the optimum SCPP as the SCPP that minimizes sPRx (i.e., maximizes autoregulation), and suggests that not only ischemia but also hyperemia at the injury site may be detrimental. The observation that optimum SCPP varies between patients and temporally in each patient supports individualized management. We discuss multimodality monitoring, which revealed strong correlations between SCPP and injury site metabolism (tissue glucose, lactate, pyruvate, glutamate, glycerol), monitored by surface microdialysis. Evidence is presented that the dura is a major, but unappreciated, cause of spinal cord compression after TSCI; we thus propose expansion duroplasty as a novel treatment. Monitoring spinal cord blood flow at the injury site has revealed novel phenomena, e.g., 3 distinct blood flow patterns, local steal, and diastolic ischemia. We conclude that monitoring from the injured spinal cord in the intensive care unit is a safe technique that appears to enable optimized and individualized spinal cord perfusion

Acute Spinal Cord Injury: Correlations and Causal Relations Between Intraspinal Pressure, Spinal Cord Perfusion Pressure, Lactate-to-Pyruvate Ratio, and Limb Power.

BACKGROUND/OBJECTIVE: We 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. METHODS: This 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. RESULTS: Nineteen 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. CONCLUSION: Monitoring intraspinal pressure, spinal cord perfusion pressure, lactate-to-pyruvate ratio, and intervening to normalize these parameters are likely to improve limb power

Spinal cord injury: is monitoring from the injury site the future?

This paper challenges the current management of acute traumatic spinal cord injury based on our experience with monitoring from the injury site in the neurointensive care unit. We argue that the concept of bony decompression is inadequate. The concept of optimum spinal cord perfusion pressure, which differs between patients, is introduced. Such variability suggests individualized patient treatment. Failing to optimize spinal cord perfusion limits the entry of systemically administered drugs into the injured cord. We conclude that monitoring from the injury site helps optimize management and should be subjected to a trial to determine whether it improves outcome

Giant central lumbar disc herniations: a case for the transdural approach.

Giant central lumbar disc protrusions can pose a significant operative challenge. Clinically, these patients are at risk of permanent disability, due not only to preoperative neural compromise caused by the protrusion itself but also to the potential iatrogenic risks associated with the standard extradural microdiscectomy technique. This is the first report to date of a giant central L3/4 disc protrusion being successfully treated through a transdural microdiscectomy approach. Prior to this report, there have been just two cases describing its application in the lumbar spine. However, neither of these reports has described its use below the level of L2/3. We compare our surgical technique with these authors and discuss the pros and cons of this surgical approach relative to the standard extradural microdiscectomy technique. Overall, we have observed encouraging results from this approach and this report would support a role for further investigation into this rarely used technique

Measurement of Intraspinal Pressure After Spinal Cord Injury: Technical Note from the Injured Spinal Cord Pressure Evaluation Study.

Intracranial pressure (ICP) is routinely measured in patients with severe traumatic brain injury (TBI). We describe a novel technique that allowed us to monitor intraspinal pressure (ISP) at the injury site in 14 patients who had severe acute traumatic spinal cord injury (TSCI), analogous to monitoring ICP after brain injury. A Codman probe was inserted subdurally to measure the pressure of the injured spinal cord compressed against the surrounding dura. Our key finding is that it is feasible and safe to monitor ISP for up to a week in patients after TSCI, starting within 72 h of the injury. With practice, probe insertion and calibration take less than 10 min. The ISP signal characteristics after TSCI were similar to the ICP signal characteristics recorded after TBI. Importantly, there were no associated complications. Future studies are required to determine whether reducing ISP improves neurological outcome after severe TSCI

Safety profile and probe placement accuracy of intraspinal pressure monitoring for traumatic spinal cord injury: Injured Spinal Cord Pressure Evaluation study.

OBJECTIVE A novel technique for monitoring intraspinal pressure and spinal cord perfusion pressure in patients with traumatic spinal cord injury was recently described. This is analogous to monitoring intracranial pressure and cerebral perfusion pressure in patients with traumatic brain injury. Because intraspinal pressure monitoring is a new technique, its safety profile and impact on early patient care and long-term outcome after traumatic spinal cord injury are unknown. The object of this study is to review all patients who had intraspinal pressure monitoring to date at the authors' institution in order to define the accuracy of intraspinal pressure probe placement and the safety of the technique. METHODS At the end of surgery to fix spinal fractures, a pressure probe was inserted intradurally to monitor intraspinal pressure at the injury site. Postoperatively, CT scanning was performed within 48 hours and MRI at 2 weeks and 6 months. Neurointensive care management and complications were reviewed. The American Spinal Injury Association Impairment Scale (AIS) grade was determined on admission and at 2 to 4 weeks and 12 to 18 months postoperation. RESULTS To date, 42 patients with severe traumatic spinal cord injuries (AIS Grades A-C) had undergone intraspinal pressure monitoring. Monitoring started within 72 hours of injury and continued for up to a week. Based on postoperative CT and MRI, the probe position was acceptable in all patients, i.e., the probe was located at the site of maximum spinal cord swelling. Complications were probe displacement in 1 of 42 patients (2.4%), CSF leakage that required wound resuturing in 3 of 42 patients (7.1%), and asymptomatic pseudomeningocele that was diagnosed in 8 of 42 patients (19.0%). Pseudomeningocele was diagnosed on MRI and resolved within 6 months in all patients. Based on the MRI and neurological examination results, there were no serious probe-related complications such as meningitis, wound infection, hematoma, wound breakdown, or neurological deterioration. Within 2 weeks postoperatively, 75% of patients were extubated and 25% underwent tracheostomy. Norepinephrine was used to support blood pressure without complications. Overall, the mean intraspinal pressure was around 20 mm Hg, and the mean spinal cord perfusion pressure was around 70 mm Hg. In laminectomized patients, the intraspinal pressure was significantly higher in the supine than lateral position by up to 18 mm Hg after thoracic laminectomy and 8 mm Hg after cervical laminectomy. At 12 to 18 months, 11.4% of patients had improved by 1 AIS grade and 14.3% by at least 2 AIS grades. CONCLUSIONS These data suggest that after traumatic spinal cord injury intradural placement of the pressure probe is accurate and intraspinal pressure monitoring is safe for up to a week. In patients with spinal cord injury who had laminectomy, the supine position should be avoided in order to prevent rises in intraspinal pressure

Expansion duroplasty improves intraspinal pressure, spinal cord perfusion pressure, and vascular pressure reactivity index in patients with traumatic spinal cord injury: injured spinal cord pressure evaluation study.

We recently showed that, after traumatic spinal cord injury (TSCI), laminectomy does not improve intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), or the vascular pressure reactivity index (sPRx) at the injury site sufficiently because of dural compression. This is an open label, prospective trial comparing combined bony and dural decompression versus laminectomy. Twenty-one patients with acute severe TSCI had re-alignment of the fracture and surgical fixation; 11 had laminectomy alone (laminectomy group) and 10 had laminectomy and duroplasty (laminectomy+duroplasty group). Primary outcomes were magnetic resonance imaging evidence of spinal cord decompression (increase in intradural space, cerebrospinal fluid around the injured cord) and spinal cord physiology (ISP, SCPP, sPRx). The laminectomy and laminectomy+duroplasty groups were well matched. Compared with the laminectomy group, the laminectomy+duroplasty group had greater increase in intradural space at the injury site and more effective decompression of the injured cord. In the laminectomy+duroplasty group, ISP was lower, SCPP higher, and sPRx lower, (i.e., improved vascular pressure reactivity), compared with the laminectomy group. Laminectomy+duroplasty caused cerebrospinal fluid leak that settled with lumbar drain in one patient and pseudomeningocele that resolved completely in five patients. We conclude that, after TSCI, laminectomy+duroplasty improves spinal cord radiological and physiological parameters more effectively than laminectomy alone

Aquaporin-4 and brain edema.

Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid (CSF) and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. Experiments using AQP4-null mice provide strong evidence for AQP4 involvement in cerebral water balance. AQP4-null mice are protected from cellular (cytotoxic) brain edema produced by water intoxication, brain ischemia, or meningitis. However, AQP4 deletion aggravates vasogenic (fluid leak) brain edema produced by tumor, cortical freeze, intraparenchymal fluid infusion, or brain abscess. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 deletion also worsens obstructive hydrocephalus. Recently, AQP4 was also found to play a major role in processes unrelated to brain edema, including astrocyte migration and neuronal excitability. These findings suggest that modulation of AQP4 expression or function may be beneficial in several cerebral disorders, including hyponatremic brain edema, hydrocephalus, stroke, tumor, infection, epilepsy, and traumatic brain injury