Cerebral Perfusion Pressure Thresholds for Brain Tissue Hypoxia and Metabolic Crisis After Poor-Grade Subarachnoid Hemorrhage

Schmidt, J. Michael; Ko, Sang‐Bae; Helbok, Raimund; Kurtz, Pedro; Stuart, R. Morgan; Presciutti, Mary; Fernandez, Luis; Lee, Ki-Won; Badjatia, Neeraj; Connolly, E. Sander; Claassen, Jan; Mayer, Stephan A.

doi:10.1161/strokeaha.110.596874

Cited by 137 publications

(107 citation statements)

References 39 publications

(42 reference statements)

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“…In another study, CPP Ͻ70 mm Hg was associated with metabolic crisis (lactate:pyruvate ratio Ͼ40), suggesting that cerebral microdialysis may be used to determine a safe lower limit of CPP on a patient-specific basis. 54 Furthermore, the duration of metabolic crisis during monitoring correlated with a poorer outcome at 3 months. However, not all authors have found that ischemic patterns precede clinical deterioration.…”

Section: Cerebral Microdialysismentioning

confidence: 97%

Multimodal Monitoring in Subarachnoid Hemorrhage

Sandsmark

Kumar

Park

et al. 2012

Stroke

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In severely injured patients, the immediate goal of resuscitation is restoration and maintenance of adequate tissue metabolism by ensuring sufficient delivery of fuel, typically oxygen and glucose, to meet cellular metabolic demands. In neurocritical care, traditional goals of resuscitation-intracranial pressure (ICP), cerebral perfusion pressure (CPP), and the clinical examination-have been extrapolated from those of general critical care. These variables are analogous to central venous pressure, mean arterial pressure, and urine output and are similarly crude. These distant surrogates for cerebral perfusion do not account for dynamic changes in cerebral autoregulation, tissue metabolic rate, cellular fuel use, and microcirculatory dysfunction, all of which impact tissue metabolic health. Although standard, it seems intuitively obvious that a uniform approach of maintaining ICP Ͻ20 mm Hg and CPP Ͼ60 mm Hg is overly simplistic. This approach does not address either significant baseline differences in patient physiology nor the complex, dynamic, and variable pathophysiological changes that ensue after severe brain injury. A more tailored therapeutic strategy that responds to multiple simultaneously measured and more relevant physiological variables is logically appealing. Until recently, however, the requisite individual patient physiology was inaccessible at the bedside.The emergence of technology that allows for continuous real-time bedside monitoring of cerebral physiology marks a new era in neurocritical care. These monitors facilitate assessment of therapeutic efficacy and may provide more relevant physiological end points for resuscitation. Combining these monitors in a multimodal approach allows for the practice of goal-directed cerebral resuscitation that emphasizes the individual patient's unique neurological and systemic physiology.

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Section: Cerebral Microdialysismentioning

confidence: 97%

Multimodal Monitoring in Subarachnoid Hemorrhage

Sandsmark

Kumar

Park

et al. 2012

Stroke

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“…The pathogenesis of cerebral injury due to SAH is multifactorial and complex. Cerebral vasospasm, 18,31,42 hydrocephalus, 40 cortical spreading ischemia, 39 elevated intracranial pressure, 40 and cerebral metabolic dysfunction 34 have all been implicated in cerebral injury following aneurysm rupture. Our results suggest that in select patients, particularly younger patients with no radiographic evidence of large or eloquent stroke, the potential for delayed improvement is greatest.…”

Section: Figmentioning

confidence: 99%

Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design

Wilson¹,

Nakaji²,

Albuquerque³

et al. 2013

JNS

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Object Data regarding the time course of recovery after poor-grade subarachnoid hemorrhage (SAH) is lacking. Most SAH studies assess outcome at a single time point, often as early as 3 or 6 months following SAH. The authors hypothesized that recovery following poor-grade SAH is a dynamic process and that early outcomes may not always approximate long-term outcomes. To test this hypothesis, they analyzed long-term outcome data from a cohort of patients with poor-grade aneurysmal SAH to determine the incidence and predictors of early and delayed neurological improvement. Methods The authors reviewed outcome data from 88 poor-grade SAH patients enrolled in a prospective SAH treatment trial (the Barrow Ruptured Aneurysm Trial). They assessed modified Rankin Scale (mRS) scores at discharge, 6 months, 12 months, and 36 months after treatment to determine the incidence and predictors of neurological improvement during each interval. Results The mean aggregate mRS scores at 6 months (3.31 ± 2.1), 12 months (3.28 ± 2.2), and 36 months (3.17 ± 2.3) improved significantly compared with the mean score at hospital discharge (4.33 ± 1.3, p < 0.001), but they did not differ significantly among themselves. Between discharge and 6 months, 61% of patients improved on the mRS. The incidence of improvement between 6–12 months and 12–36 months was 18% and 19%, respectively. Hunt and Hess Grade IV versus V (OR 6.20, 95% CI 2.11–18.25, p < 0.001) and the absence of large (> 4 cm) (OR 2.76, 95% CI 1.02–7.55, p = 0.05) or eloquent (OR 5.17, 95% CI 1.89–14.10, p < 0.01) stroke were associated with improvement up to 6 months. Age ≤ 65 years (OR 5.56, 95% CI 1.17–26.42, p = 0.02), Hunt and Hess Grade IV versus V (OR 4.17, 95% CI 1.10–15.85, p = 0.03), and absence of a large (OR 8.97, 95% CI 2.65–30.40, p < 0.001) or eloquent (OR 4.54, 95% CI 1.46–14.08, p = 0.01) stroke were associated with improvement beyond 6 months. Improvement beyond 1 year was most strongly predicted by the absence of a large stroke (OR 7.62, 95% CI 1.55–37.30, p < 0.01). Conclusions A substantial minority of poor-grade SAH patients will experience delayed recovery beyond the point at which most studies assess outcome. Younger patients, those presenting in better clinical condition, and those without CT evidence of large or eloquent stroke demonstrated the highest capacity for delayed recovery.

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“…These biochemical signatures of metabolic distress both predict poor outcome. They can occur both in response to decreases in cerebral perfusion 9,24,26,52,54,60,61 and when CBF is normal. 56,64,70 "Nonischemic" metabolic crises are probably due to injury-associated mitochondrial dysfunction, which reduces the brain's ability to use oxygen and triggers compensatory hyperglycolysis.…”

Section: Cerebral Biochemistrymentioning

confidence: 99%

Unraveling the complexities of invasive multimodality neuromonitoring

Sinha¹,

Hudgins²,

Schuster³

et al. 2017

Neurosurgical Focus

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Acute brain injuries are a major cause of death and disability worldwide. Survivors of life-threatening brain injury often face a lifetime of dependent care, and novel approaches that improve outcome are sorely needed. A delayed cascade of brain damage, termed secondary injury, occurs hours to days and even weeks after the initial insult. This delayed phase of injury provides a crucial window for therapeutic interventions that could limit brain damage and improve outcome.A major barrier in the ability to prevent and treat secondary injury is that physicians are often unable to target therapies to patients’ unique cerebral physiological disruptions. Invasive neuromonitoring with multiple complementary physiological monitors can provide useful information to enable this tailored, precision approach to care. However, integrating the multiple streams of time-varying data is challenging and often not possible during routine bedside assessment.The authors review and discuss the principles and evidence underlying several widely used invasive neuromonitors. They also provide a framework for integrating data for clinical decision making and discuss future developments in informatics that may allow new treatment paradigms to be developed.

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Cerebral Perfusion Pressure Thresholds for Brain Tissue Hypoxia and Metabolic Crisis After Poor-Grade Subarachnoid Hemorrhage

Cited by 137 publications

References 39 publications

Multimodal Monitoring in Subarachnoid Hemorrhage

Multimodal Monitoring in Subarachnoid Hemorrhage

Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design

Unraveling the complexities of invasive multimodality neuromonitoring

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