Spinal Cord Perfusion Research Articles

Complications and outcomes of vasopressor usage in acute traumatic central cord syndrome

OBJECT The optimal mean arterial pressure (MAP) for spinal cord perfusion after trauma remains unclear. Although there are published data on MAP goals after spinal cord injury (SCI), the specific blood pressure management for acute traumatic central cord syndrome (ATCCS) and the implications of these interventions have yet to be elucidated. Additionally, the complications of specific vasopressors have not been fully explored in this injury condition. METHODS The present study is a retrospective cohort analysis of 34 patients with ATCCS who received any vasopressor to maintain blood pressure above predetermined MAP goals at a single Level 1 trauma center. The collected variables were American Spinal Injury Association (ASIA) grades at admission and discharge, administered vasopressor and associated complications, other interventions and complications, and timing of surgery. The relationship between the 2 most common vasopressors-dopamine and phenylephrine-and complications within the cohort as a whole were explored, and again after stratification by age. RESULTS The mean age of the ATCCS patients was 62 years. Dopamine was the most commonly used primary vasopressor (91% of patients), followed by phenylephrine (65%). Vasopressors were administered to maintain MAP goals fora mean of 101 hours. Neurological status improved by a median of 1 ASIA grade in all patients, regardless of the choice of vasopressor. Sixty-four percent of surgical patients underwent decompression within 24 hours. There was no observed relationship between the timing of surgical intervention and the complication rate. Cardiogenic complications associated with vasopressor usage were notable in 68% of patients who received dopamine and 46% of patients who received phenylephrine. These differences were not statistically significant (OR with dopamine 2.50 [95% CI 0.82-7.78], p = 0.105). However, in the subgroup of patients > 55 years, dopamine produced statistically significant increases in the complication rates when compared with phenylephrine (83% vs 50% for dopamine and phenylephrine, respectively; OR with dopamine 5.0 [95% CI 0.99-25.34], p = 0.044). CONCLUSIONS Vasopressor usage in ATCCS patients is associated with complication rates that are similar to the reported literature for SCI. Dopamine was associated with a higher risk of complications in patients > 55 years. Given the increased incidence of ATCCS in older populations, determination of MAP goals and vasopressor administration should be carefully considered in these patients. While a randomized control trial on this topic may not be practical, a multiinstitutional prospective study for SCI that includes ATCCS patients as a subpopulation would be useful for examining MAP goals in this population.

Pre-hospital and acute management of traumatic spinal cord injury in the Netherlands: survey results urge the need for standardisation.

Questionnaire survey. Although a range of novel therapeutic approaches for traumatic spinal cord injury (tSCI) are being trialled in highly standardised, pre-clinical research models, little has been published about the extent of standardisation in health service delivery for newly injured tSCI patients. All Emergency Medical Services (EMSs) and 11 level-1 trauma centres (L1TCs) in the Netherlands. A survey assessing the organisation of pre-hospital and acute tSCI management was developed and distributed across all 23 pre-hospital EMSs and 11 L1TCs based in the Netherlands. Response rates for EMSs and L1TCs were 82 and 100%, respectively. Thirteen EMSs (68%) transported all patients who are suspected of having tSCI to L1TCs. The decision to transfer tSCI patients to L1TCs was primarily made by paramedics at the scene of accident (79%). Nonetheless, no EMS reported the use of validated neurological assessments for determining the likelihood of tSCI. The International Standards for Neurological Classification of SCI were used to determine the level and severity of tSCI in four centres, and three centres performed magnetic resonance imaging in all tSCI patients. Three L1TCs had spinal cord perfusion support protocols in place, and two centres administered methylprednisolon to acute tSCI patients. We found a large variance in the delivery of pre-hospital and acute tSCI management in a well-defined geographical catchment area. This survey urges the need for implementing standardised assessments and developing best-practice guidelines, which should be endorsed by all pre-hospital and acute tSCI health-care providers.

Cerebrospinal fluid drainage and induced hypertension improve spinal cord perfusion after acute spinal cord injury in pigs.

Acute spinal cord injury (SCI) is commonly treated by elevating the mean arterial pressure (MAP). Other potential interventions include cerebrospinal fluid drainage (CSFD). To determine the efficacy of aggressive MAP elevation combined with intrathecal pressure (ITP) reduction; our primary objective was to improve spinal cord blood flow (SCBF) after SCI. All 15 pigs underwent laminectomy. Study groups included control (n = 3); SCI only (n = 3); SCI combined with MAP elevation (SCI + MAP) (n = 3); SCI combined with CSFD (SCI + CSFD) (n = 3); and SCI combined with both MAP elevation and CSFD (SCI + MAP + CSFD) (n = 3). SCBF was measured with laser Doppler flowmetry. In the SCI group, SCBF decreased by 56% after SCI. MAP elevation after SCI resulted in a 34% decrease in SCBF, whereas CSFD resulted in a 59% decrease in SCBF. The combination of CSFD and MAP elevation resulted in a 24% increase in SCBF. The SCI + MAP group had an average ITP increase of 5.45 mm Hg after MAP elevation 1 hour after SCI and remained at that level throughout the experiment. Both MAP elevation alone and CSFD alone led to only short-term improvement of SCBF. The combination of MAP elevation and CSFD significantly and sustainably improved SCBF and spinal cord perfusion pressure. Although laser Doppler flowmetry can provide flow measurements to a tissue depth of only 1.5 mm, these results may represent pattern of blood flow changes in the entire spinal cord after injury.

Spinal Cord Ischemia After Selective Cerebral Perfusion in a Porcine “Frozen Elephant Trunk” Simulation Model

The "frozen elephant trunk" procedure (FET) represents the therapy of choice for extended aortic diseases. The aim of our study was to analyze whether 90 minutes of selective cerebral perfusion (SCP) at 28 °C followed by permanent occlusion of the thoracic segmental arteries (TSA) would cause spinal cord ischemia in a porcine model. 14 pigs (41 ± 3 kg) were cooled on CPB to 28 °C. After aortic clamping, SCP was established for 90 minutes. Randomly, in 7 animals the TSA were clipped (T4-T13); the TSA of 7 animals remained untouched. After the animals were weaned from CPB, hemodynamic data were registered for 120 minutes. Regional spinal cord blood flow (SCBF) was calculated, and motor-evoked potentials (MEP) were assessed at 6 time points. After sacrifice of the animals, the spinal cord was analyzed histologically by use of a schematic grading system (0 = normal; 8 = total necrosis). During SCP the SCBF was maintained at baseline (5.9 ± 2.4 mL/min/100 g) in the T4-T13 region but showed a decrease (from 8.4 ± 4.3 to 1.3 ± 1.5 mL/min/100 g) in the L1-L5 region. During reperfusion it increased, with two to three times higher values in the nonclipped animals. After 90 minutes of SCP, the MEP reached lower levels in the L1-L5 region of the TSA-clipped animals: 59% ± 7% vs 84 ± 15% (vastus medialis muscle) and 48% ± 6% vs 82% ± 26% (tibialis anterior muscle). The MEP recovered only in the nonclipped group. Higher ischemia rates were seen in the L1-L5 region of the TSA-clipped animals (score: 6.0 ± 0.6 vs 2.5 ± 2.3). 90 minutes of SCP provided sufficient spinal cord protection during arch replacement at 28 °C. In combination with permanent TSA occlusion, the lumbar spinal cord perfusion may be altered, which causes functional and structural damage.

Porcine aortic surgical model to study isolated intraspinal collateralization

The function of the intraspinal collateral system, which includes repetitive epidural arcades and anterior radiculomedullary arteries, is not well understood in the setting of segmental artery ligation during aortic surgery. The animal model presented here can be used to characterize the function of the intraspinal collateral backup system in detail. BACKGROUND The incidence of spinal cord ischemia during extensive aortic surgery is still reported to be as high as 15% to 20%. Preoperative risk prediction according to individual collateral anatomy is not currently possible. The porcine model has been established as a valuable opportunity to study spinal collateral physiology in an aortic surgical setting. 1 The intraspinal compartment of the spinal collateral network includes a serial pattern of circular arcades and anterior radiculomedullary arteries (ARMAs) 1 and has not yet been functionally characterized. We postulate an important contribution of this system to immediate recovery of a sufficient spinal cord perfusion pressure directly after serial occlusion of segmental vessels. We sought to createalargeanimalmodelwithspinalcollateralflowbeing exclusively delivered through the intraspinal system. In a proof-of-concept study, a shutdown of thoracic and lumbar paraspinous inflow was achieved through percutaneous ethanol ablation of dorsal segmental arteries. The goal was to create a model suitable for investigation of the intraspinal collateral system in isolation, to understand more clearly its role in maintaining adequate spinal cord perfusion during aortic surgery.

A prospective, open-label trial of clevidipine for controlled hypotension during posterior spinal fusion.

Controlled hypotension is one means to limit or avoid the need for allogeneic blood products. Clevidipine is a short-acting, intravenous calcium channel antagonist with a half-life of 1 to 3 minutes due to rapid metabolism by non-specific blood and tissue esterases. To date, there are no prospective evaluations with clevidipine in the pediatric population. We prospectively evaluated the dosing requirements, efficacy, and safety of clevidipine for ontrolled hypotension during spinal surgery for neuromuscular scoliosis in the pediatric population. Patients undergoing posterior spinal fusion for neuromuscular scoliosis were eligible for inclusion. The study was an open label, observational study. Maintenance anesthesia included desflurane titrated to maintain a bispectral index at 40 to 60 and a remifentanil infusion. Motor and somatosensory evoked potentials were monitored intraoperatively. When the mean arterial pressure (MAP) was ≥ 65 mmHg despite remifentanil at 0.3 mcg/kg/min, clevidipine was added to maintain the MAP at 55 to 65 mmHg. Clevidipine was initiated at 0.25 to 1 mcg/kg/min and titrated up in increments of 0.25 to 1 mcg/kg/min every 3 to 5 minutes to achieve the desired MAP. The study cohort included 45 patients. Fifteen patients (33.3%) did not require a clevidipine infusion to maintain the desired MAP range, leaving 30 patients including 13 males and 17 females for analysis. These patients ranged in age from 7.9 to 17.4 years (mean ± SD: 13.7 ± 2.2 years) and in weight from 18.9 to 78.1 kg (mean ± SD: 43.4 ± 14.2 kg). Intraoperatively, the clevidipine infusion was stopped in 6 patients as the surgeon expressed concerns regarding spinal cord perfusion and requested a higher MAP than the study protocol allowed. The data until that point were included for analysis. The target MAP was initially achieved at a mean time of 8.9 minutes. Sixteen of the 30 patients (53.3%) achieved the target MAP within 5 minutes. Heart rate (HR) increased from a baseline of 83 ± 16 to 86 ± 15 beats per minute (mean ± SD) (p=0.04) with the administration of clevidipine. No patient had a HR increase ≥ 20 beats per minute or required the administration of a β-adrenergic antagonist. The duration of the clevidipine administration varied from 8 to 527 minutes (mean ± SD: 160 ± 123 minutes). The maintenance infusion rate of clevidipine varied from 0.25 to 5.0 mcg/kg/min (mean ± SD: 1.4 ± 1.1 mcg/kg/min). Clevidipine was paused a total of 43 times in the 30 cases. In 18 of the 30 patients (60%), the clevidipine infusion was temporarily paused more than once due to a MAP < 55 mmHg. A fluid bolus was administered to only 1 patient to treat the low MAP. No patient required the administration of a vasoactive agent for hypotension. When the clevidipine infusion was discontinued as controlled hypotension was no longer required, the MAP returned to baseline or ≥ 65 mmHg within 10 minutes in 12 of the 30 patients (40%). Clevidipine can be used to provide controlled hypotension during posterior spinal fusion. The response of the MAP, both the onset and duration of action, were rapid. Although titration of the infusion with occasional pauses of administration may be needed, excessive hypotension was not noted.

Increased mean arterial pressure goals after spinal cord injury and functional outcome

Introduction:Acute spinal cord injury (SCI) is often treated with induced hypertension to enhance spinal cord perfusion. The optimal mean arterial pressure (MAP) likely varies between patients. Arbitrary goals are often set, frequently requiring vasopressors to achieve, with no clear evidence supporting this practice. We hypothesize that increased MAP goals and episodes of relative hypotension do not affect hospital outcome.Materials and Methods:All cervical and thoracic SCI patients treated at a level one trauma and regional SCI center over at 2.5-year period were retrospectively reviewed. Lowest and average hourly MAP was recorded for the first 72 h of hospitalization, allowing for quantification of mean MAP and the total number of episodic relative hypotensive events. These data were further compared to daily American spinal injury association motor score (AMS), which was used to determine the severity of SCI and improvement/decline during hospitalization. Patient's data were finally analyzed at theoretic MAP set points.Results:One hundred and five patients had complete data during the study period. At higher theoretic MAP set points (85 and 90), increased number of relative hypotensive episodes correlated with lower admission AMS (85 mmHg: <10 episodes, AMS 66.2; >50 episodes, 22.0; P < 0.001) and the need for vasopressors (P < 0.03) but showed no statistical change in AMS by hospital discharge. The need for vasopressors correlated with the number of hypotensive episodes and inversely related to admission AMS at all theoretic MAP goal set points but was not correlated with the change in AMS during the hospitalization.Conclusions:The frequency of relative hypotension and the need for vasopressors are progressively related to more severe SCI, as denoted by lower admission AMS. However, episodes of hypotension and the need for vasopressors did not affect the change in AMS during the acute hospitalization, regardless of theoretic MAP goal set-point. Arbitrarily elevated MAP goals may not be efficacious.

Directly measuring spinal cord blood flow and spinal cord perfusion pressure via the collateral network: Correlations with changes in systemic blood pressure

During thoracoabdominal surgery in which segmental arteries are sacrificed over a large area, blood supply routes from collateral networks have received attention as a means of avoiding spinal cord injury. The aim of this study was to investigate spinal cord blood supply through a collateral network by directly measuring spinal cord blood flow and spinal cord perfusion pressure experimentally. In beagle dogs (n=8), the thoracoabdominal aorta and segmental arteries L1-L7 were exposed, and a temporary bypass was created for distal perfusion. Next, a laser blood flow meter was placed on the spinal dura mater in the L5 region to measure the spinal cord blood flow. The following were measured simultaneously when the direct blood supply from segmental arteries L2-L7 to the spinal cord was stopped: mean systemic blood pressure, spinal cord perfusion pressure (blood pressure within the aortic clamp site), and spinal cord blood flow supplied via the collateral network. These variables were then investigated for evidence of correlations. Positive correlations were observed between mean systemic blood pressure and spinal cord blood flow during interruption of segmental artery flow both with (r=0.844, P<.01) and without (r=0.834, P<.01) distal aortic perfusion. In addition, we observed significant correlations between spinal cord perfusion pressure and spinal cord blood flow with and without distal perfusion (r=0.803, P<.001 and r=0.832, P<.01, respectively), and between mean systemic blood pressure and spinal cord perfusion pressure with and without distal perfusion (r=0.898, P<.001 and r=0.837, P<.001, respectively). The spinal cord was perfused from the collateral network from outside the interrupted segmental arteries, and high systemic blood pressure (∼1.33-fold higher) was needed to obtain the preclamping spinal cord blood flow, whereas 1.68-fold higher systemic blood pressure was needed when distal perfusion was halted. Spinal cord blood flow is positively correlated with mean systemic blood pressure and spinal cord perfusion pressure under spinal cord ischemia caused by clamping a wide range of segmental arteries. In open and endovascular thoracic and thoracoabdominal surgery, elevating mean systemic blood pressure is a simple and effective means of increasing spinal cord blood flow, and measuring spinal cord perfusion pressure seems to be useful for monitoring perioperative spinal cord blood flow.

Periconal arterial anastomotic circle and posterior lumbosacral watershed zone of the spinal cord

BackgroundThe existence of spinal cord watershed territories was suggested in the 1950s. Segmental infarcts within the junctional territories of adjacent radiculomedullary contributors and isolated spinal gray matter ischemia constitute two...

Post anaesthetic myelopathy in the horse: a case report

The first case of post anaesthetic myelopathy in a horse is described. A two year old 530 kg Shire stallion underwent surgical removal of a granuloma in the ventral sternal region under general inhalation anaesthesia in dorsal recumbency. Total duration of the operation was 85 min. The anaesthesia was uneventful except for profuse sweating and arterial hypertension observed during the whole period. During recovery the horse was not able to stand, and flaccid paralysis of hind limbs, absence of reaction to an induced pain stimulus on the hind limbs and no patellar or anal reflex was recorded; in addition, tail tonus was weak. Panniculus reflex was absent distally from the 17&lt;sup&gt;th&lt;/sup&gt; intercostal space. Head, neck and front limb movement was not affected. The horse did not respond to treatment by intravenous administration of dexamethasone, hypertonic or isotonic saline. The status deteriorated and the horse was euthanised 4 h after the end of anaesthesia. The main pathological findings were haemorrhage, oedema and malacia of L5&amp;ndash;L6 spinal cord segments and cauda equina. Histological examination of the spinal cord revealed haemorrhage and areas of necrosis predominantly in the grey matter of L5 and L6 segments. Impairment of spinal cord perfusion due to haemodynamic changes associated with dorsal recumbency and general anaesthesia is presumed. Predisposition factors could include young age, dorsal recumbency and high weight. &amp;nbsp;

Spinal cord injury following thoracic and thoracoabdominal aortic repairs.

To discuss the currently available approaches to prevent spinal cord injury during thoracic and thoracoabdominal aortic repairs. We carried out a PubMed search up to 2013 using the Medical Subject Headings: "aortic aneurysm/surgery" and "spinal cord ischemia"; "aortic aneurysm, thoracic/surgery" and "spinal cord ischemia"; "aneurysm/surgery" and "spinal cord ischemia/cerebrospinal fluid"; "aortic aneurysm/surgery" and "paraplegia". All 190 original articles satisfying our inclusion criteria were analyzed for incidence, predictors, and other pertinent variables related to spinal cord injury, and we compared the results in recent publications with those in earlier reports. The mean age of the 38,491 patients was 65.3 ± 4.9 years. The overall incidence of paraplegia and/or paraparesis was 7.1% ± 6.1% (range 0%-32%). The incidence of spinal cord injury before 2000, from 2001 to 2007, and 2008-2013 was 9.0% ± 6.7%, 7.0% ± 6.1%, and 5.9% ± 5.2%, respectively (p = 0.019). Various predictors of spinal cord injury were identified, extent of disease being the most common. Modification of surgical techniques, use of adjuncts, and better understanding of spinal cord perfusion physiology were attributed to the decrease in postoperative spinal cord injury in recent years. Spinal cord injury after thoracic and thoracoabdominal aortic repair poses a real challenge to cardiovascular surgeons. However, with evolving surgical strategies, identification of predictors, and use of various adjuncts over the years, the incidence of spinal cord injury after thoracic/thoracoabdominal aortic repair has declined. Embracing a multimodality approach offers a good insight into combating this grave complication.

Spinal dural arteriovenous fistula with intramedullary cord hemorrhage

Spinal dural arteriovenous fistula (SDAVF) consists of an acquired arteriovenous shunt between a dural artery and perimedullary veins.1 This results in arterialization of radicular veins, venous hypertension, and decreased spinal cord perfusion.1 The condition has a male predominance and presents as a myelopathy in the fifth or sixth decade. Initial misdiagnosis is common.1–3 We present a man with a SDAVF and associated intramedullary cord hemorrhage.

The microanatomy of spinal cord injury: a review.

Spinal cord injury is a highly prevalent condition associated with significant morbidity and mortality. The pathophysiology underlying it is extraordinarily complex and still not completely understood. We performed a comprehensive literature review of the pathophysiologic processes underlying spinal cord injury. The mechanisms underlying primary and secondary spinal cord injury are distinguished based on a number of factors and include the initial mechanical injury force, the vascular supply of the spinal cord which is associated with spinal cord perfusion, spinal cord autoregulation, and post-traumatic ischemia, and a complex inflammatory cascade involving local and infiltrating immunomodulating cells. This review illustrates the current literature regarding the pathophysiology behind spinal cord injury and outlines potential therapeutic options for reversing these mechanisms.

Commentary on “Temporary Aneurysm Sac Perfusion as an Adjunct for Prevention of Spinal Cord Ischaemia After Branched Endovascular Repair of Thoracoabdominal Aneurysms”

The pathogenesis of spinal cord ischaemia following open surgical repair of thoracoabdominal aortic aneurysms (TAAAs) has been established over many years and includes spinal cord ischaemia during aortic clamping, haemodynamic instability, ischaemiaereperfusion injury, and reduced intercostal and lumbar perfusion. To reduce the incidence of spinal cord ischaemia, surgical techniques have evolved to combat each of these pathological mechanisms. Open repair of TAAA is now commonly performed on left heart bypass with distal aortic perfusion, sequential aortic clamping, intercostal reimplantation, visceral perfusion, cerebrospinal fluid (CSF) drainage, and the utilisation of evoked potential monitoring to guide surgical strategies. 1 However, the advent of endovascular repair of TAAA has posed a different set of challenges. While spinal cord injury remains a significant complication, 2 the pathogenesis has not been so extensively studied, and strategies to reduce the incidence of neurological complications are still being formulated. Fundamentally, spinal cord ischaemia after endovascular repair of TAAA appears to be primarily caused by coverage of the thoracoabdominal aorta with an endograft that reduces or abolishes flow through the intercostal and lumbar arteries. Therefore, the causative mechanism would appear to be primarily ischaemic, although embolisation has been implicated in some cases of immediate postoperative paraplegia. As a consequence, endovascular strategies have evolved in an attempt to reduce spinal cord injury, although there is no absolute consensus around a “gold standard” set of procedural and adjunctive preventive measures. The primary management strategy for preventing and treating spinal cord ischaemia is achieving an effective spinal cord perfusion pressure. The principle determinants of spinal cord perfusion pressure are the mean arterial pressure (MAP) and CSF pressure. Most experts would agree than an effective MAP is essential to prevent spinal cord ischaemia. The place of CSF drainage (whether routine or selective) is more controversial, although it appears to be of benefit in symptomatic patients, and has become extensively utilised. In light of the ischaemic aetiology of spinal cord injury, maintenance of existing collateral perfusion to the spinal cord would appear to be important in preventing neurological complications. The spinal cord vascular plexus receives important contributions from the vertebral and hypogastric arteries, and maintaining perfusion through these vascular beds is likely to influence favourably spinal cord perfusion. 3 Recently, several authors have suggested that staging endovascular TAAA procedures may deliver benefits regarding the prevention of spinal cord ischaemia. Staging these procedures maintains a degree of aneurysm sac perfusion through not attempting to obtain complete aneurysm exclusion during the primary procedure. Staging may be achieved in one of several ways, including staging the thoracic and abdominal components; leaving an anatomical branch unstented (e.g., coeliac or iliac); or incorporating a dedicated perfusion branch. In between the procedural stages, the spinal cord is theoretically exposed to a relative degree of ischaemia, which may then stimulate collateral formation. 4 The endovascular reconstruction may then be completed at a later date. The second procedure is usually of a smaller magnitude than the primary procedure and may be performed under local anaesthesia with evoked potential monitoring. In the preceding article, Kasprczak et al. 5 describe their

Electrophysiologic deterioration in surgery for thoracic disc herniation: impact of mean arterial pressures on surgical outcome.

Severe thoracic disc herniation leads to increased pressure in adjacent neural structures, which in turn can require an increase in mean arterial pressure (MAP) to maintain adequate spinal cord perfusion. We report a case series of three patients with severe thoracic disc herniation that experienced deteriorations in motor-evoked potentials (MEPs) and somatosensory evoked potentials (SSEPs) following induction of general anesthesia, but prior to decompression of the neural elements. In-depth chart reviews were completed for each patient from their initial presentation to long-term post-operative course. Careful attention was taken with regards to MAP at induction of each operative case. The origin of the decreased signals in all patients was thought to relate to inadequate cord perfusion pressures. Two of the patients recovered pre-operative neurologic function while the third was left with mild post-operative paraparesis. Mean arterial pressures at time of deterioration were noted to be 58, 80, and 60 mmHg. These measurements represented MAPs approximately 65, 92, and 60 % those of baseline values, respectively. Based on these experiences, the authors' institution has adopted new guidelines in the setting of thoracic disc herniations that includes pre-operative optimization of volume status, placement of an awake arterial line prior to induction of anesthesia, use of MEP and SSEP electrophysiologic monitoring, careful selection of anesthetic, and aggressive maintenance of MAPs >110 % of preoperative values at all times prior to decompression of the spinal cord.

Real-time monitoring of spinal cord blood flow with a novel sensor mounted on a cerebrospinal fluid drainage catheter in an animal model

The aim of our study was to develop a novel monitoring system for spinal cord blood flow (SCBF) to test the efficacy of the SCBF sensor in an animal model. The sensor system consisted of 2 optical fibers, a pedestal for fiber fixation, and a mirror for the laser reflection and was incorporated into a cerebrospinal fluid drainage catheter. In vivo studies were performed in a swine model (n=10) to measure SCBF during spinal cord ischemia induced by clamping the descending thoracic aorta and supra-aortic neck vessels, when necessary. A temporary low cardiac output model was also created by inflow clamping of the inferior vena cava to analyze the quantitative changes in SCBF during this maneuver. The developed SCBF monitoring catheter placed intrathecally could detect SCBF in all the swine. The SCBF after aortic crossclamping at the fourth intercostal level exhibited diverse changes reproducibly among the swine, with a >25% reduction in SCBF in 5 pigs, an increase in 3, and no significant changes in 2. Consistent reductions were recorded during inferior vena cava occlusion. The mean SCBF decreased by 32% after inferior vena cava occlusion when the cardiac output had decreased by 27%. We have developed a novel SCBF sensor that could detect real-time changes in spinal cord perfusion in a swine model. The device holds promise to detect imminent ischemia or ensure acceptable blood perfusion in the spinal cord and could further enhance our understanding of spinal cord circulation.

Monitoring of Spinal Cord Perfusion Pressure in Acute Spinal Cord Injury

To develop a technique for continuously monitoring intraspinal pressure at the injury site (intraspinal pressure) after traumatic spinal cord injury. A pressure probe was placed subdurally at the injury site in 18 patients who had isolated severe traumatic spinal cord injury (American Spinal Injuries Association grades A-C). Intraspinal pressure monitoring started within 72 hours of the injury and continued for up to a week. In four patients, additional probes were inserted to simultaneously monitor subdural pressure below the injury and extradural pressure. Blood pressure was recorded from a radial artery catheter kept at the same horizontal level as the injured segment of the spinal cord. We determined the effect of various maneuvers on spinal cord perfusion pressure and spinal cord function and assessed using a limb motor score and motor-evoked potentials. Neurosurgery and neuro-ICU covering a 3 million population in London. Patients with severe traumatic spinal cord injury. Control subjects without spinal cord injury (to monitor spinal cerebrospinal fluid signal and motor evoked potentials). Insertion of subdural spinal pressure probe. There were no procedure-related complications. Intraspinal pressure at the injury site was higher than subdural pressure below the injury or extradural pressure. Average intraspinal pressure from the 18 patients with traumatic spinal cord injury was significantly higher than average intraspinal pressure from 12 subjects without traumatic spinal cord injury. Change in arterial PCO2, change in sevoflurane dose, and mannitol administration had no significant effect on intraspinal pressure or spinal cord perfusion pressure. Increase in inotrope dose significantly increased spinal cord perfusion pressure. Bony realignment and laminectomy did not effectively lower intraspinal pressure. Laminectomy was potentially detrimental by exposing the swollen spinal cord to compression forces applied to the skin. By intervening to increase spinal cord perfusion pressure, we could increase the amplitude of motor-evoked potentials recorded from below or just above the injury level in nine of nine patients with traumatic spinal cord injury. In two of two patients with American Spinal Injuries Association grade C traumatic spinal cord injury, higher spinal cord perfusion pressure correlated with increased limb motor score. Our findings provide proof-of-principle that subdural intraspinal pressure at the injury site can be measured safely after traumatic spinal cord injury.

Re-thinking spinal blood supply of descending aortic aneurysms: intraoperative monitoring of spinal cord perfusion is essential to avoid paraplegia

Re-thinking spinal blood supply of descending aortic aneurysms: intraoperative monitoring of spinal cord perfusion is essential to avoid paraplegia

Surgical and anesthetic considerations for the endovascular treatment of ruptured descending thoracic aortic aneurysms

Ruptured descending thoracic aortic aneurysm (rDTAA) is a life-threatening disease. In the last decade, thoracic endovascular aortic repair (TEVAR) has evolved as a viable option and is now considered the preferred treatment for rDTAAs. New opportunities as well as new challenges are faced by both the surgeon and the anesthesiologist. This review describes the impact of current developments and new modalities for the surgical and anesthetic management of rDTAAs. A collaborative approach between the anesthesiologist and surgeon during critical moments such as induction, moment of aortic occlusion and placement of the aortic stent-graft is mandatory. Important issues to consider on preoperative imaging evaluation are correct sizing of the aortic stent-graft and localization of the artery of Adamkiewicz. Emergency TEVAR should preferentially be started under local anesthesia and could be switched to general anesthesia after stent placement. Patients should be kept in permissive hypotension preoperatively and during the intervention before stent-graft deployment and relative hypertension after deployment. The use of a proactive spinal cord protection protocol could decrease the risk of spinal cord ischemia and/or paraplegia and consists of permissive hypertension after stent deployment, cerebrospinal fluid drainage to maintain adequate spinal cord perfusion, relative hypothermia and possibly use of mannitol. In order to improve outcomes of TEVAR for rDTAA, a close communication between the anesthesiologist and the surgeon and a thorough understanding of the events during the procedure is mandatory. The use of a proactive spinal cord protection protocol may decrease the rates of devastating spinal cord ischemia.

Monitoring Brain and Spinal Cord Metabolism and Function

Monitoring the metabolism and function of the central nervous system not only is an old idea but also is a topic that is of increasing interest to the technological evolution. Beside the optimization of cerebral and spinal cord perfusion and the preservation of vasoreactivity to ensure the viability of cerebral tissues and structures, we want to know more and more about the real intimate situation of these organs in real time at the patient’s bedside. To this end, several tracks have been explored during the two last decades, leading to the development of numerous concepts and the conception of various monitoring systems. One of the main problems is to characterize the respective strong points and weaknesses of those ones and to conclude regarding their individual relevance and value in current clinical practice. It is more and more clear that the combination of different categories of monitoring is a way to try to find the most valuable technological compromise, to increase the chance of prediction or of early detection of intercurrent deleterious events corresponding to the concept of multimodality. The intraoperative period and the intensive care goals and targets are appreciably different. This is the reason for the attempt to define different and distinct sets of goals and targets for the intraoperative anesthetic setting and for the intensive care unit.