The Association Between Spontaneous Hyperventilation, Delayed Cerebral Ischemia, and Poor Neurological Outcome in Patients with Subarachnoid Hemorrhage

Williamson, Craig A.; Sheehan, Kyle M.; Tipirneni, Renuka; Roark, Christopher; Pandey, Aditya S.; Thompson, B. Gregory; Rajajee, Venkatakrishna

doi:10.1007/s12028-015-0138-5

Cited by 43 publications

(45 citation statements)

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“…Williamson et al reported that severe hypocapnia, which was defined as PaCO 2 ≤ 30 mmHg, was significantly associated with poor neurological outcomes (OR, 4.52; p < 0.01) [15], and this finding is consistent with our result. However, they reported that moderate hypocapnia, which was defined as PaCO 2 < 35 mmHg, was not independently associated with poor neurological outcomes (OR, 1.30; p = 0.58) [15]. Hypocapnia was previously shown to be associated with brain tissue hypoxia and poor outcomes in patients with TBI [26, 27].…”

Section: Discussionsupporting

confidence: 92%

“…Several previous studies reported that hypocapnia was associated with poor neurological outcomes or DCI [14, 15]. Williamson et al reported that severe hypocapnia, which was defined as PaCO 2 ≤ 30 mmHg, was significantly associated with poor neurological outcomes (OR, 4.52; p < 0.01) [15], and this finding is consistent with our result. However, they reported that moderate hypocapnia, which was defined as PaCO 2 < 35 mmHg, was not independently associated with poor neurological outcomes (OR, 1.30; p = 0.58) [15].…”

Section: Discussionsupporting

confidence: 92%

“…In addition to general intensive care, all the patients were monitored for clinical deterioration or for the development of cerebral infarction owing to DCI. Using previously published criteria, DCI was defined as either (1) the development of new focal neurological signs or deterioration of the consciousness level thought to be caused by the presence of ischemia after the exclusion of other possible causes or (2) the appearance of new infarcts caused by vasospasm on CT or MRI [15, 20]. Fluid management was targeted to maintain euvolemia.…”

Section: Methodsmentioning

confidence: 99%

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Association of abnormal carbon dioxide levels with poor neurological outcomes in aneurysmal subarachnoid hemorrhage: a retrospective observational study

et al. 2018

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BackgroundIn patients with aneurysmal subarachnoid hemorrhage (SAH), an association between hypocapnia and poor clinical outcomes has been reported. However, the optimal arterial carbon dioxide tension (PaCO2) remains unknown. The present retrospective study aimed to examine the association of abnormal PaCO2 levels with neurological outcomes and investigate the optimal target PaCO2 level in patients with SAH.MethodsWe retrospectively selected consecutive adult patients hospitalized in the intensive care unit (ICU) for SAH between January 2009 and April 2017. Univariate and multivariate analyses were performed to identify the independent predictors of unfavorable neurological outcomes (i.e., modified Rankin scale score of 3–6 on hospital discharge).ResultsAmong 158 patients with SAH, 73 had unfavorable neurological outcomes. During the first 2 weeks in the ICU, the median number of PaCO2 measurements per patient was 43. The factors significantly associated with unfavorable neurological outcomes were age, Hunt and Kosnik grade, maximum lactate levels during the first 24 h, and maximum (odds ratio [OR], 1.12; 95% confidence interval [CI], 1.03–1.21; p < 0.01) and minimum PaCO2 levels (OR, 0.81; 95% CI, 0.72–0.92; p < 0.01). Receiver operating characteristic curve analysis revealed that the cutoff range of PaCO2 was 30.2–48.3 mmHg. Unfavorable neurological outcomes were noted in 78.8% of patients with PaCO2 levels outside this range and in 22.8% of patients with PaCO2 levels within this range.ConclusionsBoth the maximum and minimum PaCO2 levels during ICU management in patients with SAH were significantly associated with unfavorable neurological outcomes. Further prospective studies are required to validate our findings and explore their clinical implications. Our findings may provide a scientific rationale for these future prospective studies.Electronic supplementary materialThe online version of this article (10.1186/s40560-018-0353-1) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

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Association of abnormal carbon dioxide levels with poor neurological outcomes in aneurysmal subarachnoid hemorrhage: a retrospective observational study

et al. 2018

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“…A few very interesting randomized trials are currently investigating neurocritical care measures beyond neurosurgery in or including SAH: EARLYDRAIN on early lumbar drainage combined with EVD [9], SETPOINT2 on early tracheostomy [10], NEWTON on slow-release nimodipine via EVD [11], ULTRA on early tranexamic acid [12], and HIMALAIA on induced hypertension [13]. However, there are so many other NCCU aspects to be addressed prospectively: level of sedation, modes of ventilation [14,15], cardiopulmonary stability [16,17], monitoring-based circulatory strategies [18], temperature control [19][20][21], delirium management, the nursing factor and mobilization, policies of do-not-resuscitate orders and withdrawal of care [22,23], and many other day-to-day care decisions that may substantially impact outcome. Particularly, the poor-grade SAH patient, prone to so many cerebral and systemic complications, may benefit from aggressive surveillance, superb nursing care, and close clinical monitoring.…”

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confidence: 99%

What Do We Mean by Poor-Grade Aneurysmal Subarachnoid Hemorrhage and What Can We Do?

Bösel

2016

Neurocrit Care

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“…Such factors will need to be considered in future studies exploring pathophysiologic pathways, understanding that the impact of a pathway may be exacerbated or attenuated over time post insult based on such endogenous responses. For example cerebral ischemia/acidosis begets spontaneous hyperventilation ( 77 – 80 ) and systemic hypertension is a typical concomitant of brainstem ischemia ( 81 ). Other examples include ischemia-mediated adjustments in protein transcription and ischemic preconditioning ( 82 – 90 ) and issues in resilience or plasticity of pathophysiological networks, e.g., apoptosis networks ( 91 , 92 ).…”

Section: Discussionmentioning

confidence: 99%

Reframing the Biological Basis of Neuroprotection Using Functional Genomics: Differentially Weighted, Time-Dependent Multifactor Pathogenesis of Human Ischemic Brain Damage

et al. 2018

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Background: Neuroprotection studies are generally unable to demonstrate efficacy in humans. Our specific hypothesis is that multiple pathophysiologic pathways, of variable importance, contribute to ischemic brain damage. As a corollary to this, we discuss the broad hypothesis that a multifaceted approach will improve the probability of efficacious neuroprotection. But to properly test this hypothesis the nature and importance of the multiple contributing pathways needs elucidation. Our aim is to demonstrate, using functional genomics, in human cardiac surgery procedures associated with cerebral ischemia, that the pathogenesis of perioperative human ischemic brain damage involves the function of multiple variably weighted proteins involving several pathways. We then use these data and literature to develop a proposal for rational design of human neuroprotection protocols.Methods: Ninety-four patients undergoing deep hypothermic circulatory arrest (DHCA) and/or aortic valve replacement surgery had brain damage biomarkers, S100β and neurofilament H (NFH), assessed at baseline, 1 and 24 h post-cardiopulmonary bypass (CPB) with analysis for association with 92 single nucleotide polymorphisms (SNPs) (selected by co-author WAK) related to important proteins involved in pathogenesis of cerebral ischemia.Results: At the nominal significance level of 0.05, changes in S100β and in NFH at 1 and 24 h post-CPB were associated with multiple SNPs involving several prospectively determined pathophysiologic pathways, but were not individually significant after multiple comparison adjustments. Variable weights for the several evaluated SNPs are apparent on regression analysis and, notably, are dissimilar related to the two biomarkers and over time post CPB. Based on our step-wise regression model, at 1 h post-CPB, SOD2, SUMO4, and GP6 are related to relative change of NFH while TNF, CAPN10, NPPB, and SERPINE1 are related to the relative change of S100B. At 24 h post-CPB, ADRA2A, SELE, and BAX are related to the relative change of NFH while SLC4A7, HSPA1B, and FGA are related to S100B.Conclusions: In support of the proposed hypothesis, association SNP data suggest function of specific disparate proteins, as reflected by genetic variation, may be more important than others with variation at different post-insult times after human brain ischemia. Such information may support rational design of post-insult time-sensitive multifaceted neuroprotective therapies.

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The Association Between Spontaneous Hyperventilation, Delayed Cerebral Ischemia, and Poor Neurological Outcome in Patients with Subarachnoid Hemorrhage

Abstract: Spontaneous hyperventilation is common in SAH and is associated with DCI and poor neurological outcome.

Cited by 43 publications

References 44 publications

Association of abnormal carbon dioxide levels with poor neurological outcomes in aneurysmal subarachnoid hemorrhage: a retrospective observational study

Association of abnormal carbon dioxide levels with poor neurological outcomes in aneurysmal subarachnoid hemorrhage: a retrospective observational study

What Do We Mean by Poor-Grade Aneurysmal Subarachnoid Hemorrhage and What Can We Do?

Reframing the Biological Basis of Neuroprotection Using Functional Genomics: Differentially Weighted, Time-Dependent Multifactor Pathogenesis of Human Ischemic Brain Damage

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