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Samira Saadoun - One of the best experts on this subject based on the ideXlab platform.
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Targeted Perfusion Therapy in Spinal Cord Trauma
Neurotherapeutics, 2020Co-Authors: Samira Saadoun, Marios C. PapadopoulosAbstract: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.
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Markedly Deranged Injury Site Metabolism and Impaired Functional Recovery in Acute Spinal Cord Injury Patients With Fever.
Critical care medicine, 2018Co-Authors: Mathew J Gallagher, Marios C. Papadopoulos, Argyro Zoumprouli, Isaac Phang, Jan M. Schwab, Marcel A. Kopp, Thomas Liebscher, Samira SaadounAbstract:Objectives:To characterize the effect of fever after acute, traumatic spinal cord Injury on Injury Site metabolism and patient outcome.Design:Longitudinal cohort study. In 44 patients (London cohort), we determined the effect of fever on intrathecal Injury Site metabolism by analyzing 1,767 hours of
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Spinal cord Injury: is monitoring from the Injury Site the future?
Critical Care, 2016Co-Authors: Samira Saadoun, Marios C. PapadopoulosAbstract: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.
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Microdialysis to Optimize Cord Perfusion and Drug Delivery in Spinal Cord Injury.
Annals of neurology, 2016Co-Authors: Isaac Phang, Argyro Zoumprouli, Marios C. Papadopoulos, Samira SaadounAbstract:OBJECTIVE: There is lack of monitoring from the Injury Site to guide management of patients with acute traumatic spinal cord Injury. Here we describe a bedside microdialysis monitoring technique for optimizing spinal cord perfusion and drug delivery at the Injury Site. METHODS: 14 patients were recruited within 72 hours of severe spinal cord Injury. We inserted intradurally at the Injury Site a pressure probe, to monitor continuously spinal cord perfusion pressure, and a microdialysis catheter, to monitor hourly glycerol, glutamate, glucose, lactate and pyruvate. The pressure probe and microdialysis catheter were placed on the surface of the injured cord. RESULTS: Microdialysis monitoring did not cause serious complications. Spinal cord perfusion pressure 90 - 100 mmHg and tissue glucose >4.5 mM minimized metabolic derangement at the Injury Site. Increasing spinal cord perfusion pressure by ∼10 mmHg, increased the entry of intravenously administered dexamethasone at the Injury Site three-fold. INTERPRETATION: This study determined the optimum spinal cord perfusion pressure and optimum tissue glucose concentration at the Injury Site. We also identified spinal cord perfusion pressure as a key determinant of drug entry into the injured spinal cord. Our findings challenge current guidelines, which recommend maintaining mean arterial pressure at 85 - 90 mmHg for a week after spinal cord Injury. We propose that future drug trials for spinal cord Injury include pressure and microdialysis monitoring to optimize spinal cord perfusion and maximize drug delivery at the Injury Site. This article is protected by copyright. All rights reserved.
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monitoring of spinal cord perfusion pressure in acute spinal cord Injury initial findings of the injured spinal cord pressure evaluation study
Critical Care Medicine, 2014Co-Authors: Melissa C Werndle, Samira Saadoun, Isaac Phang, Marek Czosnyka, Georgios V Varsos, Zofia Czosnyka, Peter Smielewski, A Jamous, B A Bell, Argyro ZoumprouliAbstract:Objectives:To develop a technique for continuously monitoring intraspinal pressure at the Injury Site (intraspinal pressure) after traumatic spinal cord Injury.Design:A pressure probe was placed subdurally at the Injury Site in 18 patients who had isolated severe traumatic spinal cord Injury (Americ
Marios C. Papadopoulos - One of the best experts on this subject based on the ideXlab platform.
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Targeted Perfusion Therapy in Spinal Cord Trauma
Neurotherapeutics, 2020Co-Authors: Samira Saadoun, Marios C. PapadopoulosAbstract: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.
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Markedly Deranged Injury Site Metabolism and Impaired Functional Recovery in Acute Spinal Cord Injury Patients With Fever.
Critical care medicine, 2018Co-Authors: Mathew J Gallagher, Marios C. Papadopoulos, Argyro Zoumprouli, Isaac Phang, Jan M. Schwab, Marcel A. Kopp, Thomas Liebscher, Samira SaadounAbstract:Objectives:To characterize the effect of fever after acute, traumatic spinal cord Injury on Injury Site metabolism and patient outcome.Design:Longitudinal cohort study. In 44 patients (London cohort), we determined the effect of fever on intrathecal Injury Site metabolism by analyzing 1,767 hours of
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Spinal cord Injury: is monitoring from the Injury Site the future?
Critical Care, 2016Co-Authors: Samira Saadoun, Marios C. PapadopoulosAbstract: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.
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Microdialysis to Optimize Cord Perfusion and Drug Delivery in Spinal Cord Injury.
Annals of neurology, 2016Co-Authors: Isaac Phang, Argyro Zoumprouli, Marios C. Papadopoulos, Samira SaadounAbstract:OBJECTIVE: There is lack of monitoring from the Injury Site to guide management of patients with acute traumatic spinal cord Injury. Here we describe a bedside microdialysis monitoring technique for optimizing spinal cord perfusion and drug delivery at the Injury Site. METHODS: 14 patients were recruited within 72 hours of severe spinal cord Injury. We inserted intradurally at the Injury Site a pressure probe, to monitor continuously spinal cord perfusion pressure, and a microdialysis catheter, to monitor hourly glycerol, glutamate, glucose, lactate and pyruvate. The pressure probe and microdialysis catheter were placed on the surface of the injured cord. RESULTS: Microdialysis monitoring did not cause serious complications. Spinal cord perfusion pressure 90 - 100 mmHg and tissue glucose >4.5 mM minimized metabolic derangement at the Injury Site. Increasing spinal cord perfusion pressure by ∼10 mmHg, increased the entry of intravenously administered dexamethasone at the Injury Site three-fold. INTERPRETATION: This study determined the optimum spinal cord perfusion pressure and optimum tissue glucose concentration at the Injury Site. We also identified spinal cord perfusion pressure as a key determinant of drug entry into the injured spinal cord. Our findings challenge current guidelines, which recommend maintaining mean arterial pressure at 85 - 90 mmHg for a week after spinal cord Injury. We propose that future drug trials for spinal cord Injury include pressure and microdialysis monitoring to optimize spinal cord perfusion and maximize drug delivery at the Injury Site. This article is protected by copyright. All rights reserved.
Argyro Zoumprouli - One of the best experts on this subject based on the ideXlab platform.
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Markedly Deranged Injury Site Metabolism and Impaired Functional Recovery in Acute Spinal Cord Injury Patients With Fever.
Critical care medicine, 2018Co-Authors: Mathew J Gallagher, Marios C. Papadopoulos, Argyro Zoumprouli, Isaac Phang, Jan M. Schwab, Marcel A. Kopp, Thomas Liebscher, Samira SaadounAbstract:Objectives:To characterize the effect of fever after acute, traumatic spinal cord Injury on Injury Site metabolism and patient outcome.Design:Longitudinal cohort study. In 44 patients (London cohort), we determined the effect of fever on intrathecal Injury Site metabolism by analyzing 1,767 hours of
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Microdialysis to Optimize Cord Perfusion and Drug Delivery in Spinal Cord Injury.
Annals of neurology, 2016Co-Authors: Isaac Phang, Argyro Zoumprouli, Marios C. Papadopoulos, Samira SaadounAbstract:OBJECTIVE: There is lack of monitoring from the Injury Site to guide management of patients with acute traumatic spinal cord Injury. Here we describe a bedside microdialysis monitoring technique for optimizing spinal cord perfusion and drug delivery at the Injury Site. METHODS: 14 patients were recruited within 72 hours of severe spinal cord Injury. We inserted intradurally at the Injury Site a pressure probe, to monitor continuously spinal cord perfusion pressure, and a microdialysis catheter, to monitor hourly glycerol, glutamate, glucose, lactate and pyruvate. The pressure probe and microdialysis catheter were placed on the surface of the injured cord. RESULTS: Microdialysis monitoring did not cause serious complications. Spinal cord perfusion pressure 90 - 100 mmHg and tissue glucose >4.5 mM minimized metabolic derangement at the Injury Site. Increasing spinal cord perfusion pressure by ∼10 mmHg, increased the entry of intravenously administered dexamethasone at the Injury Site three-fold. INTERPRETATION: This study determined the optimum spinal cord perfusion pressure and optimum tissue glucose concentration at the Injury Site. We also identified spinal cord perfusion pressure as a key determinant of drug entry into the injured spinal cord. Our findings challenge current guidelines, which recommend maintaining mean arterial pressure at 85 - 90 mmHg for a week after spinal cord Injury. We propose that future drug trials for spinal cord Injury include pressure and microdialysis monitoring to optimize spinal cord perfusion and maximize drug delivery at the Injury Site. This article is protected by copyright. All rights reserved.
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monitoring of spinal cord perfusion pressure in acute spinal cord Injury initial findings of the injured spinal cord pressure evaluation study
Critical Care Medicine, 2014Co-Authors: Melissa C Werndle, Samira Saadoun, Isaac Phang, Marek Czosnyka, Georgios V Varsos, Zofia Czosnyka, Peter Smielewski, A Jamous, B A Bell, Argyro ZoumprouliAbstract:Objectives:To develop a technique for continuously monitoring intraspinal pressure at the Injury Site (intraspinal pressure) after traumatic spinal cord Injury.Design:A pressure probe was placed subdurally at the Injury Site in 18 patients who had isolated severe traumatic spinal cord Injury (Americ
Isaac Phang - One of the best experts on this subject based on the ideXlab platform.
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Markedly Deranged Injury Site Metabolism and Impaired Functional Recovery in Acute Spinal Cord Injury Patients With Fever.
Critical care medicine, 2018Co-Authors: Mathew J Gallagher, Marios C. Papadopoulos, Argyro Zoumprouli, Isaac Phang, Jan M. Schwab, Marcel A. Kopp, Thomas Liebscher, Samira SaadounAbstract:Objectives:To characterize the effect of fever after acute, traumatic spinal cord Injury on Injury Site metabolism and patient outcome.Design:Longitudinal cohort study. In 44 patients (London cohort), we determined the effect of fever on intrathecal Injury Site metabolism by analyzing 1,767 hours of
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Microdialysis to Optimize Cord Perfusion and Drug Delivery in Spinal Cord Injury.
Annals of neurology, 2016Co-Authors: Isaac Phang, Argyro Zoumprouli, Marios C. Papadopoulos, Samira SaadounAbstract:OBJECTIVE: There is lack of monitoring from the Injury Site to guide management of patients with acute traumatic spinal cord Injury. Here we describe a bedside microdialysis monitoring technique for optimizing spinal cord perfusion and drug delivery at the Injury Site. METHODS: 14 patients were recruited within 72 hours of severe spinal cord Injury. We inserted intradurally at the Injury Site a pressure probe, to monitor continuously spinal cord perfusion pressure, and a microdialysis catheter, to monitor hourly glycerol, glutamate, glucose, lactate and pyruvate. The pressure probe and microdialysis catheter were placed on the surface of the injured cord. RESULTS: Microdialysis monitoring did not cause serious complications. Spinal cord perfusion pressure 90 - 100 mmHg and tissue glucose >4.5 mM minimized metabolic derangement at the Injury Site. Increasing spinal cord perfusion pressure by ∼10 mmHg, increased the entry of intravenously administered dexamethasone at the Injury Site three-fold. INTERPRETATION: This study determined the optimum spinal cord perfusion pressure and optimum tissue glucose concentration at the Injury Site. We also identified spinal cord perfusion pressure as a key determinant of drug entry into the injured spinal cord. Our findings challenge current guidelines, which recommend maintaining mean arterial pressure at 85 - 90 mmHg for a week after spinal cord Injury. We propose that future drug trials for spinal cord Injury include pressure and microdialysis monitoring to optimize spinal cord perfusion and maximize drug delivery at the Injury Site. This article is protected by copyright. All rights reserved.
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monitoring of spinal cord perfusion pressure in acute spinal cord Injury initial findings of the injured spinal cord pressure evaluation study
Critical Care Medicine, 2014Co-Authors: Melissa C Werndle, Samira Saadoun, Isaac Phang, Marek Czosnyka, Georgios V Varsos, Zofia Czosnyka, Peter Smielewski, A Jamous, B A Bell, Argyro ZoumprouliAbstract:Objectives:To develop a technique for continuously monitoring intraspinal pressure at the Injury Site (intraspinal pressure) after traumatic spinal cord Injury.Design:A pressure probe was placed subdurally at the Injury Site in 18 patients who had isolated severe traumatic spinal cord Injury (Americ
Stephen Tomlinson - One of the best experts on this subject based on the ideXlab platform.
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Injury Site-specific targeting of complement inhibitors for treating stroke
Immunological Reviews, 2016Co-Authors: Ali Alawieh, Stephen TomlinsonAbstract:Summary Cumulative evidence indicates a role for the complement system in both pathology and recovery after ischemic stroke. Here, we review the current understanding of the dual role of complement in poststroke Injury and recovery, and discuss the challenges of anti-complement therapies. Most complement directed therapeutics currently under investigation or development systemically inhibit the complement system, but since complement is important for immune surveillance and is involved in various homeostatic activities, there are potential risks associated with systemic inhibition. Depending on the target within the complement pathway, other concerns are high concentrations of inhibitor required, low efficacy and poor bioavailability. To overcome these limitations, approaches to target complement inhibitors to specific Sites have been investigated. Here, we discuss targeting strategies, with a focus on strategies developed in our lab, to specifically localize complement inhibition to Sites of tissue Injury and complement activation, and in particular to the postischemic brain. We discuss various Injury Site-specific targeted complement inhibitors as potential therapeutic agents for the treatment of ischemic stroke treatment, as well as their use as investigative tools for probing complement-dependent pathophysiological processes.
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Injury Site‐specific targeting of complement inhibitors for treating stroke
Immunological reviews, 2016Co-Authors: Ali Alawieh, Stephen TomlinsonAbstract:Cumulative evidence indicates a role for the complement system in both pathology and recovery after ischemic stroke. Here, we review the current understanding of the dual role of complement in poststroke Injury and recovery, and discuss the challenges of anti-complement therapies. Most complement directed therapeutics currently under investigation or development systemically inhibit the complement system, but since complement is important for immune surveillance and is involved in various homeostatic activities, there are potential risks associated with systemic inhibition. Depending on the target within the complement pathway, other concerns are high concentrations of inhibitor required, low efficacy and poor bioavailability. To overcome these limitations, approaches to target complement inhibitors to specific Sites have been investigated. Here, we discuss targeting strategies, with a focus on strategies developed in our lab, to specifically localize complement inhibition to Sites of tissue Injury and complement activation, and in particular to the postischemic brain. We discuss various Injury Site-specific targeted complement inhibitors as potential therapeutic agents for the treatment of ischemic stroke treatment, as well as their use as investigative tools for probing complement-dependent pathophysiological processes.