scholarly journals Detection and Analysis of Perfusion Pressure through Measuring Oxygen Saturation and Requirement of Dural Incision Decompression after Laminectomy

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Jamal Alshorman ◽  
Yulong Wang ◽  
Guixiong Huang ◽  
Tracy Boakye Serebour ◽  
Xiaodong Guo
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Oxygen Saturation ◽  
Spine Injury ◽  
Secondary Injury ◽  
Traumatic Spinal Cord Injury ◽  
Trauma Patients ◽  
Injury Site ◽  
Cord Injury

Background. Traumatic spinal cord injury (SCI) can continue and transform long after the time of initial injury. Preventing secondary injury after SCI is one of the most significant challenges, and early intervention to return the blood flow at the injury site can minimize the likelihood of secondary injury. Objective. The purpose of this study is to investigate whether laminectomy can achieve the spinal cord blood flow by measuring the spinal blood oxygen saturation intraoperatively without the presence of light. Methods. Between June and August 2021, eight patients were admitted after traumatic spinal cord injury for surgical treatment. We explored the effectiveness of laminectomy and whether the patients required further procedures or not. We used a brain oxygen saturation monitor at the spine injury site under dark conditions. Results. Eight cervical trauma patients, six males and two females, underwent laminectomy decompression. Three patients’ ASIA grade improved by one level, and one patient showed slight motor-sensory improvement. Oxygen saturation was in the normal range. Conclusion. Performing bony decompression can show good results. Therefore, finding an examination method to confirm the improvement of blood perfusion by measuring oxygen saturation at the injury site after laminectomy is essential to avoid other complications.

scholarly journals Revascularization After Traumatic Spinal Cord Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Chun Yao ◽  
Xuemin Cao ◽  
Bin Yu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Vessel ◽  
Vascular System ◽  
Mechanical Damage ◽  
Pathological Process ◽  
Secondary Injury ◽  
Traumatic Spinal Cord Injury ◽  
Physical Stimulation ◽  
Cord Injury

Traumatic spinal cord injury (SCI) is a complex pathological process. The initial mechanical damage is followed by a progressive secondary injury cascade. The injury ruptures the local microvasculature and disturbs blood-spinal cord barriers, exacerbating inflammation and tissue damage. Although endogenous angiogenesis is triggered, the new vessels are insufficient and often fail to function normally. Numerous blood vessel interventions, such as proangiogenic factor administration, gene modulation, cell transplantation, biomaterial implantation, and physical stimulation, have been applied as SCI treatments. Here, we briefly describe alterations and effects of the vascular system on local microenvironments after SCI. Therapies targeted at revascularization for SCI are also summarized.

Acute, severe traumatic spinal cord injury: improving urinary bladder function by optimizing spinal cord perfusion

2021 ◽  
pp. 1-8
Author(s):  
Florence R. A. Hogg ◽  
Siobhan Kearney ◽  
Eskinder Solomon ◽  
Mathew J. Gallagher ◽  
Argyro Zoumprouli ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Urinary Bladder ◽  
Perfusion Pressure ◽  
Bladder Function ◽  
Traumatic Spinal Cord Injury ◽  
Injury Site ◽  
Bladder Compliance ◽  
Cord Injury

OBJECTIVE The authors sought to investigate the effect of acute, severe traumatic spinal cord injury on the urinary bladder and the hypothesis that increasing the spinal cord perfusion pressure improves bladder function. METHODS In 13 adults with traumatic spinal cord injury (American Spinal Injury Association Impairment Scale grades A–C), a pressure probe and a microdialysis catheter were placed intradurally at the injury site. We varied the spinal cord perfusion pressure and performed filling cystometry. Patients were followed up for 12 months on average. RESULTS The 13 patients had 63 fill cycles; 38 cycles had unfavorable urodynamics, i.e., dangerously low compliance (< 20 mL/cmH2O), detrusor overactivity, or dangerously high end-fill pressure (> 40 cmH2O). Unfavorable urodynamics correlated with periods of injury site hypoperfusion (spinal cord perfusion pressure < 60 mm Hg), hyperperfusion (spinal cord perfusion pressure > 100 mm Hg), tissue glucose < 3 mM, and tissue lactate to pyruvate ratio > 30. Increasing spinal cord perfusion pressure from 67.0 ± 2.3 mm Hg (average ± SE) to 92.1 ± 3.0 mm Hg significantly reduced, from 534 to 365 mL, the median bladder volume at which the desire to void was first experienced. All patients with dangerously low average initial bladder compliance (< 20 mL/cmH2O) maintained low compliance at follow-up, whereas all patients with high average initial bladder compliance (> 100 mL/cmH2O) maintained high compliance at follow-up. CONCLUSIONS We conclude that unfavorable urodynamics develop within days of traumatic spinal cord injury, thus challenging the prevailing notion that the detrusor is initially acontractile. Urodynamic studies performed acutely identify patients with dangerously low bladder compliance likely to benefit from early intervention. At this early stage, bladder function is dynamic and is influenced by fluctuations in the physiology and metabolism at the injury site; therefore, optimizing spinal cord perfusion is likely to improve urological outcome in patients with acute severe traumatic spinal cord injury.

scholarly journals SCING—Spinal Cord Injury Neuroprotection with Glyburide: a pilot, open-label, multicentre, prospective evaluation of oral glyburide in patients with acute traumatic spinal cord injury in the USA

BMJ Open ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. e031329 ◽  
Author(s):  
Amy Janelle Minnema ◽  
A Mehta ◽  
Warren W Boling ◽  
Jan Schwab ◽  
J Marc Simard ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Drug Administration ◽  
Transient Receptor Potential ◽  
Secondary Injury ◽  
Traumatic Spinal Cord Injury ◽  
Open Label ◽  
Transient Receptor Potential Melastatin ◽  
Cord Injury ◽  
Neuroprotective Strategy

IntroductionAcute traumatic spinal cord injury (tSCI) is a devastating neurological disorder with no pharmacological neuroprotective strategy proven effective to date. Progressive haemorrhagic necrosis (PHN) represents an increasingly well-characterised mechanism of secondary injury after tSCI that negatively impacts neurological outcomes following acute tSCI. Preclinical studies evaluating the use of the Food and Drug Administration-approved sulfonylurea receptor 1-transient receptor potential melastatin 4 channel blocker glyburide in rodent models have shown reduced secondary microhaemorrhage formation and the absence of capillary fragmentation, the pathological hallmark of PHN.Methods and analysisIn this initial phase multicentre open-label pilot study, we propose to enrol 10 patients with acute cervical tSCI to primarily assess the feasibility, and safety of receiving oral glyburide within 8 hours of injury. Secondary objectives include pharmacokinetics and preliminary evaluations on neurological recovery as well as blood and MRI-based injury biomarkers. Analysis will be performed using the descriptive and non-parametric statistics.Ethics and disseminationGlyburide has been shown as an effective neuroprotective agent in preclinical tSCI models and in the treatment of ischaemic stroke with the additional risk of a hypoglycaemic response. Given the ongoing secondary injury and the traumatic hyperglycaemic stress response seen in patients with tSCI, glyburide; thus, offers an appealing neuroprotective strategy to supplement standard of care treatment. The study protocol was approved by the Ohio State University Biomedical Institutional Review Board. The protocol was amended in February 2017 with changes related to study feasibility and patient recruitment. Specifically, the route of administration was changed to the oral form to allow for streamlined and rapid drug administration, and the injury-to-drug time window was extended to 8 hours in an effort to further enhance enrolment. Participants or legally authorised representatives are informed about the trial and its anticipated risks orally and in written form using an approved informed consent form prior to inclusion. The findings of this study will be disseminated to the participants and to academic peers through scientific conferences and peer-reviewed journal publications.Trial registration numbersNCT02524379and 2014H0335.

scholarly journals Spinal Cord Perfusion Pressure Correlates with Anal Sphincter Function in a Cohort of Patients with Acute, Severe Traumatic Spinal Cord Injuries

2021 ◽  
Author(s):  
Florence R. A. Hogg ◽  
Siobhan Kearney ◽  
Mathew J. Gallagher ◽  
Argyro Zoumprouli ◽  
Marios C. Papadopoulos ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Anal Sphincter ◽  
Spinal Cord Injuries ◽  
Perfusion Pressure ◽  
Traumatic Spinal Cord Injury ◽  
Anal Pressure ◽  
Injury Site ◽  
Cord Injury ◽  
Resting Anal Pressure

Abstract Background Acute, severe traumatic spinal cord injury often causes fecal incontinence. Currently, there are no treatments to improve anal function after traumatic spinal cord injury. Our study aims to determine whether, after traumatic spinal cord injury, anal function can be improved by interventions in the neuro-intensive care unit to alter the spinal cord perfusion pressure at the injury site. Methods We recruited a cohort of patients with acute, severe traumatic spinal cord injuries (American Spinal Injury Association Impairment Scale grades A–C). They underwent surgical fixation within 72 h of the injury and insertion of an intrathecal pressure probe at the injury site to monitor intraspinal pressure and compute spinal cord perfusion pressure as mean arterial pressure minus intraspinal pressure. Injury-site monitoring was performed at the neuro-intensive care unit for up to a week after injury. During monitoring, anorectal manometry was also conducted over a range of spinal cord perfusion pressures. Results Data were collected from 14 patients with consecutive traumatic spinal cord injury aged 22–67 years. The mean resting anal pressure was 44 cmH2O, which is considerably lower than the average for healthy patients, previously reported at 99 cmH2O. Mean resting anal pressure versus spinal cord perfusion pressure had an inverted U-shaped relation (Ȓ2 = 0.82), with the highest resting anal pressures being at a spinal cord perfusion pressure of approximately 100 mmHg. The recto-anal inhibitory reflex (transient relaxation of the internal anal sphincter during rectal distension), which is important for maintaining fecal continence, was present in 90% of attempts at high (90 mmHg) spinal cord perfusion pressure versus 70% of attempts at low (60 mmHg) spinal cord perfusion pressure (P < 0.05). During cough, the rise in anal pressure from baseline was 51 cmH2O at high (86 mmHg) spinal cord perfusion pressure versus 37 cmH2O at low (62 mmHg) spinal cord perfusion pressure (P < 0.0001). During anal squeeze, higher spinal cord perfusion pressure was associated with longer endurance time and spinal cord perfusion pressure of 70–90 mmHg was associated with stronger squeeze. There were no complications associated with anorectal manometry. Conclusions Our data indicate that spinal cord injury causes severe disruption of anal sphincter function. Several key components of anal continence (resting anal pressure, recto-anal inhibitory reflex, and anal pressure during cough and squeeze) markedly improve at higher spinal cord perfusion pressure. Maintaining too high of spinal cord perfusion pressure may worsen anal continence.

Survival Analysis in Patients with Chronic Traumatic Spinal Cord Injury

2020 ◽  
Author(s):  
Mahsa GHAJARZADEH ◽  
Abbas RAHIMI FOROUSHANI ◽  
Saharnaz NEDJAT ◽  
Abdolreza SHEIKHREZAEI ◽  
Hooshang SABERI
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cox Regression ◽  
Spine Injury ◽  
Rank Test ◽  
Traumatic Spinal Cord Injury ◽  
Probability Of Survival ◽  
Kaplan Meier ◽  
Cord Injury

Background: The goal of this study was to determine hazard rate of death rate and the causes of death in Iranian patients with Traumatic spinal cord injury (TSCI). Methods: Overall, 1024 patients with chronic traumatic spinal cord injury referred to Brain and Spinal Injury Research Center, Tehran University of Medical Sciences, Tehran, Iran from Jan 2013-2017 were enrolled. Epidemiological and neurological data, along with secondary complications were recorded for all participants. In the case of death, the cause, and the date of death were recorded. The Kaplan–Meier method was used for survival analysis. A log-rank test was carried out to compare survival due to different risk factors. Risk factors and relative risk estimates associated with death were assessed by means of a Cox regression model. Results: Nineteen percent were lost to follow up. During the follow-up period, 22 out of 830 remaining cases (2.6%) died. Deaths were only observed in patients with cervical injuries (59% in C1-C4 level and 41% in C5- C7 level). Kaplan–Meier Log-rank test showed that probability of survival was significantly less in females, complete injury cases, patients with cervical spine injury, depression, and ADR (Autonomic dysreflexia). Controlling for age, sex and education level, Cox regression model showed that hazard rate of death was significantly affected by the categorical variables such as level of injury (HR=0.2, 95% CI=0.12-0.39), severe ADR. Conclusion: Probability of survival is lower in female individuals, cases with complete injuries, patients with cervical spine injury, individuals wi-th depression (BDI>10), and clients who experience ADR.

Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms

1991 ◽  
Vol 75 (1) ◽  
pp. 15-26 ◽  
Author(s):  
Charles H. Tator ◽  
Michael G. Fehlings
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Cord Blood ◽  
Volume Expansion ◽  
Acute Spinal Cord Injury ◽  
Secondary Injury ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Cord Injury

✓ In patients with spinal cord injury, the primary or mechanical trauma seldom causes total transection, even though the functional loss may be complete. In addition, biochemical and pathological changes in the cord may worsen after injury. To explain these phenomena, the concept of the secondary injury has evolved for which numerous pathophysiological mechanisms have been postulated. This paper reviews the concept of secondary injury with special emphasis on vascular mechanisms. Evidence is presented to support the theory of secondary injury and the hypothesis that a key mechanism is posttraumatic ischemia with resultant infarction of the spinal cord. Evidence for the role of vascular mechanisms has been obtained from a variety of models of acute spinal cord injury in several species. Many different angiographic methods have been used for assessing microcirculation of the cord and for measuring spinal cord blood flow after trauma. With these techniques, the major systemic and local vascular effects of acute spinal cord injury have been identified and implicated in the etiology of secondary injury. The systemic effects of acute spinal cord injury include hypotension and reduced cardiac output. The local effects include loss of autoregulation in the injured segment of the spinal cord and a marked reduction of the microcirculation in both gray and white matter, especially in hemorrhagic regions and in adjacent zones. The microcirculatory loss extends for a considerable distance proximal and distal to the site of injury. Many studies have shown a dose-dependent reduction of spinal cord blood flow varying with the severity of injury, and a reduction of spinal cord blood flow which worsens with time after injury. The functional deficits due to acute spinal cord injury have been measured electrophysiologically with techniques such as motor and somatosensory evoked potentials and have been found proportional to the degree of posttraumatic ischemia. The histological effects include early hemorrhagic necrosis leading to major infarction at the injury site. These posttraumatic vascular effects can be treated. Systemic normotension can be restored with volume expansion or vasopressors, and spinal cord blood flow can be improved with dopamine, steroids, nimodipine, or volume expansion. The combination of nimodipine and volume expansion improves posttraumatic spinal cord blood flow and spinal cord function measured by evoked potentials. These results provide strong evidence that posttraumatic ischemia is an important secondary mechanism of injury, and that it can be counteracted.

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