Browsing by Author "Kramer, Andreas H."
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Item Open Access Anemia and red blood cell transfusion in neurocritical care(BioMed Central, 2009-06-11) Kramer, Andreas H.; Zygun, David AItem Open Access Cerebrovascular pressure reactivity and brain tissue oxygen monitoring provide complementary information regarding the lower and upper limits of cerebral blood flow control in traumatic brain injury: a CAnadian High Resolution-TBI (CAHR-TBI) cohort study(2022-12-23) Gomez, Alwyn; Sekhon, Mypinder; Griesdale, Donald; Froese, Logan; Yang, Eleen; Thelin, Eric P.; Raj, Rahul; Aries, Marcel; Gallagher, Clare; Bernard, Francis; Kramer, Andreas H.; Zeiler, Frederick A.Abstract Background Brain tissue oxygen tension (PbtO2) and cerebrovascular pressure reactivity monitoring have emerged as potential modalities to individualize care in moderate and severe traumatic brain injury (TBI). The relationship between these modalities has had limited exploration. The aim of this study was to examine the relationship between PbtO2 and cerebral perfusion pressure (CPP) and how this relationship is modified by the state of cerebrovascular pressure reactivity. Methods A retrospective multi-institution cohort study utilizing prospectively collected high-resolution physiologic data from the CAnadian High Resolution-TBI (CAHR-TBI) Research Collaborative database collected between 2011 and 2021 was performed. Included in the study were critically ill TBI patients with intracranial pressure (ICP), arterial blood pressure (ABP), and PbtO2 monitoring treated in any one of three CAHR-TBI affiliated adult intensive care units (ICU). The outcome of interest was how PbtO2 and CPP are related over a cohort of TBI patients and how this relationship is modified by the state of cerebrovascular reactivity, as determined using the pressure reactivity index (PRx). Results A total of 77 patients met the study inclusion criteria with a total of 377,744 min of physiologic data available for the analysis. PbtO2 produced a triphasic curve when plotted against CPP like previous population-based plots of cerebral blood flow (CBF) versus CPP. The triphasic curve included a plateau region flanked by regions of relative ischemia (hypoxia) and hyperemia (hyperoxia). The plateau region shortened when cerebrovascular pressure reactivity was disrupted compared to when it was intact. Conclusions In this exploratory analysis of a multi-institution high-resolution physiology TBI database, PbtO2 seems to have a triphasic relationship with CPP, over the entire cohort. The CPP range over which the plateau exists is modified by the state of cerebrovascular reactivity. This indicates that in critically ill TBI patients admitted to ICU, PbtO2 may be reflective of CBF.Item Open Access Prognostic value of near-infrared spectroscopy regional oxygen saturation and cerebrovascular reactivity index in acute traumatic neural injury: a CAnadian High-Resolution Traumatic Brain Injury (CAHR-TBI) Cohort Study(2024-03-14) Gomez, Alwyn; Froese, Logan; Griesdale, Donald; Thelin, Eric P.; Raj, Rahul; van Iperenburg, Levi; Tas, Jeanette; Aries, Marcel; Stein, Kevin Y.; Gallagher, Clare; Bernard, Francis; Kramer, Andreas H.; Zeiler, Frederick A.Abstract Background Near-infrared spectroscopy regional cerebral oxygen saturation (rSO2) has gained interest as a raw parameter and as a basis for measuring cerebrovascular reactivity (CVR) due to its noninvasive nature and high spatial resolution. However, the prognostic utility of these parameters has not yet been determined. This study aimed to identify threshold values of rSO2 and rSO2-based CVR at which outcomes worsened following traumatic brain injury (TBI). Methods A retrospective multi-institutional cohort study was performed. The cohort included TBI patients treated in four adult intensive care units (ICU). The cerebral oxygen indices, COx (using rSO2 and cerebral perfusion pressure) as well as COx_a (using rSO2 and arterial blood pressure) were calculated for each patient. Grand mean thresholds along with exposure-based thresholds were determined utilizing sequential chi-squared analysis and univariate logistic regression, respectively. Results In the cohort of 129 patients, there was no identifiable threshold for raw rSO2 at which outcomes were found to worsen. For both COx and COx_a, an optimal grand mean threshold value of 0.2 was identified for both survival and favorable outcomes, while percent time above − 0.05 was uniformly found to have the best discriminative value. Conclusions In this multi-institutional cohort study, raw rSO2was found to contain no significant prognostic information. However, rSO2-based indices of CVR, COx and COx_a, were found to have a uniform grand mean threshold of 0.2 and exposure-based threshold of − 0.05, above which clinical outcomes markedly worsened. This study lays the groundwork to transition to less invasive means of continuously measuring CVR.Item Open Access Red blood cell transfusion in patients with subarachnoid hemorrhage: a multidisciplinary North American survey(BioMed Central, 2011-01-18) Kramer, Andreas H.; Diringer, Michael N.; Suarez, Jose I; Naidech, Andrew M.; Macdonald, Loch R.; Le Roux, Peter D.Item Open Access Understanding Brain Injury-Induced Immunosuppression and the Relationship to the Development of Infection(2018-06-05) Scott, Brittney Noelle Vivian; Kubes, Paul; Zygun, David A.; Kramer, Andreas H.; Ousman, Shalina S.; Schryvers, Anthony B.; Fox-Robichaud, Alison E.Infection is a leading cause of morbidity and mortality among hospitalized patients. It has become increasingly apparent that patients with neurological injury have an increased risk for infection due to secondary immunodeficiency. Previous work from our research group found a novel role for invariant natural killer (iNKT) cells in stroke-induced immune suppression, characterized by a shift from a Th1- to Th2-dominant systemic cytokine profile and an increased risk for infection. This work better defined the crosstalk that occurs between the brain and systemic immune system after ischemic stroke, however, many questions remained and whether similar mechanisms were involved in other types of brain injury was unclear. Thus, we evaluated the relationship between iNKT cells, Th1 and Th2 systemic cytokine profiles, and the development of infection among critically ill patients with traumatic brain injury and haemorrhagic stroke. We found that these patients had significantly subnormal levels of many immune mediators, including IFN-γ and TNF-α, indicative of systemic immune suppression. Moreover, iNKT cells were activated among these patients and positively associated with plasma Th2/Th1 cytokine ratios. Infection was common and occurred among forty-six percent of the patients. Additionally, we used animal models to investigate traumatic brain injury-induced immune modulation and its relationship to infection. We observed rapid activation of iNKT cells in the circulation and a >2-fold increase in plasma Th2/Th1 cytokine ratios, which peaked at 8 hours after injury. Remarkably, we also observed rapid changes in the lung microenvironment induced by traumatic brain injury, which influenced the outcome after infection. Moreover, in an attempt to better understand the epidemiology of infection among patients with traumatic brain injury, we conducted a systematic review of the world’s literature on this topic. We summarize and discuss the reported occurrence rates of infection, and the microbiology and risk factors associated with different types of infection, among patients hospitalized after traumatic brain injury. This thesis provides new insights into the relationship between brain injury and the development of infection. Understanding the unique risk for infection after acute brain injury will ultimately translate to better prevention and treatment regimens for these patients.