Surveillance neuroimaging and neurologic examinations affect care for intracerebral hemorrhage.
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ABSTRACT: Objective
We tested the hypothesis that surveillance neuroimaging and neurologic examinations identified changes requiring emergent surgical interventions in patients with intracerebral hemorrhage (ICH).Methods
Patients with primary ICH were enrolled into a prospective registry between December 2006 and July 2012. Patients were managed in a neuroscience intensive care unit with a protocol that included serial neuroimaging at 6, 24, and 48 hours, and hourly neurologic examinations using the Glasgow Coma Scale and NIH Stroke Scale. We evaluated all cases of craniotomy and ventriculostomy to determine whether the procedure was part of the initial management plan or occurred subsequently. For those that occurred subsequently, we determined whether worsening on neurologic examination or worsened neuroimaging findings initiated the process leading to intervention.Results
There were 88 surgical interventions in 84 (35%) of the 239 patients studied, including ventriculostomy in 52 (59%), craniotomy in 21 (24%), and both in 11 (13%). Of the 88 interventions, 24 (27%) occurred subsequently and distinctly from initial management, a median of 15.9 hours (8.9-27.0 hours) after symptom onset. Thirteen (54%) were instigated by findings on neurologic examination and 11 (46%) by neuroimaging. Demographics, severity of hemorrhage, and hemorrhage location were not associated with delayed intervention.Conclusions
More than 25% of surgical interventions performed after ICH were prompted by delayed imaging or clinical findings. Serial neurologic examinations and neuroimaging are important and effective surveillance techniques for monitoring patients with ICH.
SUBMITTER: Maas MB
PROVIDER: S-EPMC3770177 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Although intracerebral hemorrhage (ICH) volume and location are important predictors of outcome in adults, few data exist in children.A consecutive cohort of children, including full-term newborns to those younger than 18 years of age with nontraumatic, acute ICH and head CT available for analysis were studied. Clinical information was abstracted via chart review. Hemorrhage volume was expressed as percentage of total brain volume (TBV) with large hemorrhage defined as >or=4% of TBV. Hemorrhages were manually traced on each head CT slice and volumes were calculated by multiplying by slice thickness. Location was classified as supratentorial or infratentorial. Logistic regression was used to identify predictors of poor neurological outcome, defined as a Glasgow outcome scale <or=2 (death or persistent vegetative state).Thirty children were included, median age 6 years. Median ICH volume was 20.4 cm(3) and median ICH size as a percentage of TBV was 1.9%. Only 4 of 22 children with ICH <4% of TBV had poor outcomes, vs 5 of 8 children with ICH >or=4% of TBV (P=0.03). In multivariate analysis, hemorrhage >or=4% of TBV (OR, 22.5; 95% CI, 1.4-354; P=0.03) independently predicted poor outcome 30 days after ICH. In this small sample, infratentorial hemorrhage location and the presence of intraventricular hemorrhage did not predict poor outcome.ICH volume predicts neurological outcome at 30 days in children, with worst outcome when hemorrhage is >or=4% of TBV. Location and ICH etiology may also be important. These findings identify children with ICH who are candidates for aggressive management and may influence counseling regarding prognosis.
| S-EPMC2830068 | biostudies-other
Project description:BACKGROUND AND PURPOSE:Intracerebral hemorrhage is a considerable source of morbidity and mortality. This 3-center study describes outcomes of pediatric intracerebral hemorrhage and identifies 2-year neurological outcome predictors. METHODS:Children 29 days to 18 years of age presenting with intracerebral hemorrhage from March 2007 to May 2015 were enrolled prospectively. Exclusion criteria included trauma; intracranial tumor; hemorrhagic transformation of arterial ischemic stroke or cerebral sinovenous thrombosis; isolated subdural, epidural, or subarachnoid hemorrhage; and abnormal baseline neurological function. Intracerebral hemorrhage and total brain volumes were measured on neuroimaging. The Pediatric Stroke Outcome Measure assessed outcomes. RESULTS:Sixty-nine children were included (median age: 9.7 years; interquartile range: 2.2-14). Six children (9%) died during hospitalization. Outcomes in survivors were assessed at early follow-up in 98% (median 3.1 months; interquartile range: 3.1-3.8) and at later follow-up in 94% (median: 2.1 years; interquartile range: 1.3-2.8). Over a third had a significant disability at 2 years (Pediatric Stroke Outcome Measure >2). Total Pediatric Stroke Outcome Measure score improved over time (P=0.0003), paralleling improvements in the sensorimotor subscore (P=0.0004). Altered mental status (odds ratio, 13; 95% confidence interval, 3.9-46; P<0.001), hemorrhage volume ≥4% of total brain volume (odds ratio, 17; 95% confidence interval, 1.9-156; P=0.01), and intensive care unit length of stay (odds ratio, 1.1; 95% confidence interval, 1.0-1.2; P=0.002) were significantly associated with poor 2-year outcome. CONCLUSIONS:Over one third of children experienced significant disability at 2 years. Improvements in outcomes were driven by recovery of sensorimotor function. Altered mental status, hemorrhage volume ≥4% of total brain volume, and intensive care unit length of stay were independent predictors of significant disability at 2 years.
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Project description:Opinion statementIntracerebral hemorrhage is a medical emergency. It is the most deadly and disabling form of stroke, and no individual therapy has been demonstrated to improve outcome. However, it appears that aggressive medical care in general, and management by neuroscience specialists in particular, offers substantial benefit. Therefore, providing the best supportive care based on currently available evidence may well improve outcomes. Airway management and management of blood pressure aimed at maximizing cerebral perfusion while minimizing ongoing bleeding, as well as rapid reversal of anticoagulation, are likely to be important in the early phase. Additionally, efforts should be undertaken to provide careful glucose management and temperature management and to maximize cerebral perfusion pressure. Selected patients are likely to benefit from external ventricular drainage or even hematoma evacuation. Except in rare circumstances, most patients should be managed in a neuroscience intensive care unit during the acute phase. Some patients appear to have no reasonable likelihood of recovery and can be considered for limitations of care such as Do Not Resuscitate orders or Comfort Measures Only orders. However, it can be difficult to accurately predict long-term outcome in the acute phase; formal prognostic tools should be used to offer information to patients and their families. After the hemorrhage has stabilized, efforts to minimize complications include thromboembolism prophylaxis, physical therapy, and acute rehabilitation.
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Project description:Background and Purpose- The aim of this study was to prospectively validate our prior findings of smaller hematoma volume and lesser neurological deficit in nonvitamin K oral anticoagulant (NOAC) compared with Vitamin K antagonist (VKA)-related intracerebral hemorrhage (ICH). Methods- Prospective 12-month observational study in 15 tertiary stroke centers in the United States, Europe, and Asia. Consecutive patients with premorbid modified Rankin Scale score of <2 with acute nontraumatic anticoagulant-related ICH divided into 2 groups according to the type of anticoagulant: NOAC versus VKA. We recorded baseline ICH volume, significant hematoma expansion (absolute [12.5 mL] or relative [>33%] increase), neurological severity measured by National Institutes of Health Stroke Scale score, 90-day mortality, and functional status (modified Rankin Scale score). Results- Our cohort comprised 196 patients, 62 NOAC related (mean age, 75.0±11.4 years; 54.8% men) and 134 VKA related (mean age, 72.3±10.5; 73.1% men). There were no differences in vascular comorbidities, antiplatelet, and statin use; NOAC-related ICH patients had lower median baseline hematoma volume (13.8 [2.5-37.6] versus 19.5 [6.6-52.0] mL; P=0.026) and were less likely to have severe neurological deficits (National Institutes of Health Stroke Scale score of >10 points) on admission (37% versus 55.3%, P=0.025). VKA-ICH were more likely to have significant hematoma expansion (37.4% versus 17%, P=0.008). NOAC pretreatment was independently associated with smaller baseline hematoma volume (standardized linear regression coefficient:-0.415 [95% CI, -0.780 to -0.051]) resulting in lower likelihood of severe neurological deficit (odds ratio, 0.44; 95% CI, 0.22-0.85) in multivariable-adjusted models. Conclusions- Patients with NOAC-related ICH have smaller baseline hematoma volumes and lower odds of severe neurological deficit compared with VKA-related ICH. These findings are important for practicing clinicians making anticoagulation choices.
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Project description:Intracerebral hemorrhage (ICH) is a life-threatening condition associated with significant morbidity and mortality. Understanding the molecular mechanisms underlying ICH and its severe form is crucial for developing effective therapeutic strategies. This study investigates transcriptomic alterations in rodent models of ICH and severe intracerebral hemorrhage to shed light on the genetic pathways involved in hemorrhagic brain injury. We performed principal component analysis, revealing distinct principal component segments of normal rats compared to intracerebral hemorrhage and severe intracerebral hemorrhage rats. We further employed heatmaps and volcano plots to identify differentially expressed genes and utilized bar plots and KEGG pathway analysis to elucidate the different molecular pathways involved. Using comprehensive RNA sequencing and bioinformatics analyses, we identified a multitude of differentially expressed genes in both the ICH and severe ICH models. Our results revealed 5679 common genes among the normal, intracerebral hemorrhage, and severe intracerebral hemorrhage groups in the upregulated genes group, and 1196 common genes in the downregulated genes. A volcano plot comparing the groups further highlighted common genes, including PDPN, TIMP1, SERPINE1, TUBB6, and CD44. These findings underscore the complex interplay of genes involved in inflammation, oxidative stress, and neuronal damage. Furthermore, pathway enrichment analysis uncovered key signaling pathways, including the TNF signaling pathway, protein processing in the endoplasmic reticulum, MAPK signaling pathway, and Fc gamma R-mediated phagocytosis, implicated in the pathogenesis of ICH.
2024-06-11 | GSE264394 | GEO
Project description:ObjectiveGenetic variants ε2/ε4 within the APOE gene are established risk factors for lobar intracerebral hemorrhage (ICH). Published preliminary data suggest a potential role for APOE ε4 in risk of nonlobar ICH. We therefore investigated the role of APOE in recurrent nonlobar ICH, and sought to clarify whether effects of APOE on circulating lipids mediate this association.MethodsThree hundred sixty-three survivors of nonlobar ICH were followed prospectively for ICH recurrence, with APOE genotype determined at enrollment. All participants had clinical, demographic, and laboratory data captured at time of index ICH and during follow-up. Using a multivariate model, we performed association and interaction analyses of the relationships among APOE genotype, lipid levels, and recurrent nonlobar ICH.ResultsWe observed 29 nonlobar ICH recurrences among 363 survivors. APOE ε4 was associated with recurrent nonlobar ICH (hazard ratio = 1.31; 95% confidence interval = 1.02-2.69; p = 0.038) after adjustment for age/sex/ethnicity and cardiovascular risk factors. Increasing low-density lipoprotein (LDL) levels were associated with decreased risk of recurrent nonlobar ICH (p = 0.027), as were decreasing HDL levels (p = 0.046). LDL levels modified the association of APOE ε4 with recurrent nonlobar ICH (mediation p < 0.05). No associations were identified between APOE ε2 and recurrent nonlobar ICH.ConclusionAPOE ε4 is associated with recurrent ICH in nonlobar brain regions, providing further evidence for its causal role in ICH unrelated to cerebral amyloid angiopathy. LDL levels modulated this effect, suggesting that circulating lipid levels may mediate a portion of the role of APOE ε4 in nonlobar ICH.
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Project description:OBJECTIVE:Clinicians caring for patients with intracerebral hemorrhage must often discuss prognosis and goals of care with their patients' surrogate decision makers, and may make numeric estimates of likelihood of survival and functional independence, informed by validated prediction models. Surrogates' prognostic estimates are often discordant with physicians', suggesting that physicians' numeric statements may not be accurately interpreted. We sought to assess the relationship between numeracy and interpretation of prognostic estimates in intracerebral hemorrhage among surrogate decision makers. We also assessed surrogates' application of prognostic estimates to decisions regarding goals of care. DESIGN:Single-center, survey-based, cross-sectional study. SETTING:Twenty-two-bed neurologic ICU at an urban, academic hospital. SUBJECTS:Surrogate decision makers for patients admitted to the neurologic ICU. INTERVENTIONS:Participants completed a survey containing five clinical vignettes describing patients with nontraumatic intracerebral hemorrhage. For each patient, numerical estimates of survival and functional independence were explicitly provided, based on the validated outcome risk stratification scale (intracerebral hemorrhage score) and the Prediction of Functional Outcome in Patients with Primary Intracerebral Hemorrhage score. MEASUREMENTS AND MAIN RESULTS:Participants were asked to make their own prognostic estimates, as well as to describe their preferred goals of care for each hypothetical patient. Respondent demographics were collected, and numeracy was assessed using a modified Lipkus 11-item scale. Poor numeracy was common (42 of 96 total subjects) in this relatively highly educated population. Most prognostic estimates (55%) made by surrogates were discordant with the provided estimates. High numeracy correlated with better concordance (odds ratio, 23.9 [5.57-97.64]; p < 0.001), independent of several factors, including level of education and religion. Numeracy also affected goals-of-care decisions made by surrogates. CONCLUSIONS:Poor numeracy is common among surrogate decision makers in an intensive care setting and poses a barrier to communication between surrogates and clinicians regarding prognosis and goals of care.
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Project description:In this study, we examined the effect of progesterone on histopathologic and functional outcomes of intracerebral hemorrhage (ICH) in 10- to 12-month-old mice. Progesterone or vehicle was administered by intraperitoneal injection 1 hour after collagenase-induced ICH and then by subcutaneous injections at 6, 24, and 48 hours. Oxidative and nitrosative stress were assayed at 12 hours post-ICH. Injury markers were examined on day 1, and lesion was examined on day 3. Neurologic deficits were examined for 28 days. Progesterone posttreatment reduced lesion volume, brain swelling, edema, and cell degeneration and improved long-term neurologic function. These protective effects were associated with reductions in protein carbonyl formation, protein nitrosylation, and matrix metalloproteinase-9 activity and attenuated cellular and molecular inflammatory responses. Progesterone also reduced vascular endothelial growth factor expression, increased neuronal-specific Na(+)/K(+) ATPase ɑ3 subunit expression, and reduced protein kinase C-dependent Na(+)/K(+) ATPase phosphorylation. Furthermore, progesterone reduced glial scar thickness, myelin loss, brain atrophy, and residual injury volume on day 28 after ICH. With multiple brain targets, progesterone warrants further investigation for its potential use in ICH therapy.
| S-EPMC4857017 | biostudies-literature
Project description:ObjectiveTo compare comorbidities and use of surgery and palliative care between men and women with intracerebral hemorrhage (ICH).MethodsThe Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study is a prospective, multicenter, case-control study of ICH risk factors and outcomes. We compared comorbidities, treatments, and use of do-not-resuscitate (DNR) orders in men vs women. Multivariate analysis was used to assess the likelihood of ICH surgery and palliative care after adjustment for variables that were p < 0.1 in univariate analyses and backward elimination to retain those that were significant (p < 0.05).ResultsWomen were older on average (65.0 vs 59.9, p < 0.0001), and higher proportions of women had previous stroke (24.1% vs 19.3%, p = 0.002), had dementia (6.1% vs 3.4%, p = 0.0007), lived alone (23.1% vs 18.0%, p = 0.0005), and took anticoagulants (12.8% vs 10.1% p = 0.02), compared with men. Men had higher rates of alcohol and cocaine use. After adjusting for age, hematoma volume, and ICH location, there was no difference in rates of surgical treatment by sex (odds ratio [OR] 0.93 for men vs women, 95% confidence interval [CI] 0.68-1.28, p = 0.67), and there was no difference in DNR/comfort care decisions after adjustment for ICH score, prior stroke, and dementia (OR 0.96, CI 0.77-1.22, p = 0.76).ConclusionsAfter ICH, women do not receive less aggressive care than men after controlling for the substantial comorbidity differences. Future studies on sex bias should include the presence of comorbidities, prestroke disability, and other factors that may influence management.
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Project description:Intracerebral hemorrhage (ICH) is a devastating type of stroke, frequently resulting in unfavorable functional outcomes. Up to 15% of stroke patients experience ICH and approximately half of those have a lethal outcome within a year. Considering the huge burden of ICH, timely prevention and optimized treatment strategies are particularly relevant. Nevertheless, ICH management options are quite limited, despite thorough research. More and more trials highlight the importance of the genetic component in the pathogenesis of ICH. Apart from distinct monogenic disorders of familial character, mostly occurring in younger subjects, there are numerous polygenic risk factors, such as hypertension, neurovascular inflammation, disorders of lipid metabolism and coagulation cascade, and small vessel disease. In this paper we describe gene-related ICH types and underlying mechanisms. We also briefly discuss the emerging treatment options and possible clinical relevance of the genetic findings in ICH management. Although existing data seems of more theoretical and scientific value so far, a growing body of evidence, combined with rapidly evolving experimental research, will probably serve clinicians in the future.
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