Intraventricular hemorrhage and hydrocephalus after spontaneous intracerebral hemorrhage: results from the STICH trial

Bhattathiri, P. S.; Gregson, BA; Prasad, Kuskoor Seetharam Manjunath; Mendelow, A. D.

doi:10.1007/3-211-30714-1_16

Cited by 282 publications

(165 citation statements)

References 13 publications

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“…The specific biological phenomena associated with hematoma size and ventricular involvement remain only partially understood, and might include development of hydrocephalus, decreased consciousness, and intraventricular inflammation. 16 Our data do not allow us to further address these issues, which are of great relevance in devising effective therapeutic solutions. We do, however, present evidence suggesting that future research should focus on CT volumetric data as important markers of ICH severity, particularly for OAT-ICH.…”

Section: Results Cohort Characteristicsmentioning

confidence: 82%

Warfarin-related intraventricular hemorrhage

Biffi¹,

Battey²,

Ayres³

et al. 2011

Neurology

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Objective: Oral anticoagulation therapy (OAT) with warfarin increases mortality and disability after intracerebral hemorrhage (ICH), the result of increased ICH volume and risk of hematoma expansion. We investigated whether OAT also influences risk of development of intraventricular hemorrhage (IVH), the volume of IVH and IVH expansion, and whether IVH is a substantive mediator of the overall effect of OAT on ICH outcome. Methods:We performed a retrospective analysis of a prospectively collected single-center cohort of 1,879 consecutive ICH cases (796 lobar, 865 deep, 153 cerebellar, 15 multiple location, 50 primary IVH) from 1999 to 2009. ICH and IVH volumes at presentation, as well as hematoma expansion (Ͼ33% or Ͼ6 mL increase) and IVH expansion (Ͼ2 mL increase), were determined using established semiautomated methods. Outcome was assessed at 90 days using either the modified Rankin Scale or Glasgow Outcome Scale. Results:Warfarin use was associated with IVH risk, IVH volume at presentation, and IVH expansion in both lobar and deep ICH (all p Ͻ 0.05) in a dose-response relationship with international normalized ratio. Warfarin was associated with poor outcome in both lobar and deep ICH (p Ͻ 0.01), and Ͼ95% of this effect was accounted for by baseline ICH and IVH volumes, as well as ICH and IVH expansion. Conclusion: Warfarin increases IVH volume and risk of IVH expansion in lobar and deep ICH.These findings (along with effects on ICH volume and expansion) likely represent the mechanisms by which anticoagulation worsens ICH functional outcome. Neurology ® 2011;77:1840-1846 GLOSSARY AUC ϭ area under the curve; CI ϭ confidence interval; GCS ϭ Glasgow Coma Scale; GOS ϭ Glasgow Outcome Scale; ICH ϭ intracerebral hemorrhage; INR ϭ international normalized ratio; IVH ϭ intraventricular hemorrhage; MGH ϭ Massachusetts General Hospital; mRS ϭ modified Rankin Scale; OAT ϭ oral anticoagulation therapy; OR ϭ odds ratio; ROC ϭ receiver operator characteristic.Baseline hematoma volume and intraventricular hemorrhage (IVH) are potent predictors of outcome after spontaneous intracerebral hemorrhage (ICH).1-3 Hematoma enlargement and IVH expansion following presentation also worsen mortality and disability. 4,5 ICH in the setting of oral anticoagulation therapy (OAT) has almost twice the mortality compared to non-warfarin-related ICH. 6 The mechanisms underlying the effect of warfarin on ICH outcome are still not completely understood.7 While the underlying coagulopathy clearly plays a role in worsening the severity of OAT-ICH, patients on OAT often have higher rates of comorbidities, which may themselves influence ICH outcome. Hematoma expansion has been consistently found to be more frequent in OAT-ICH, and there is suggestive evidence that warfarin use is associated with larger ICH volume at presentation. 8 -10 We investigated whether OAT is associated with increased risk of developing IVH, as well as with increased IVH volume at presentation and rates of IVH expansion over time. Next, we

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Section: Results Cohort Characteristicsmentioning

confidence: 82%

Warfarin-related intraventricular hemorrhage

Biffi¹,

Battey²,

Ayres³

et al. 2011

Neurology

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“…First, rats received a 200-ml injection of saline (n ¼ 8), autologous blood (n ¼ 8), or heparinized blood (5 units heparin, n ¼ 6) into the right lateral ventricle over 15 minutes. Serial magnetic resonance imaging (MRI) scanning was performed at days 1,3,8,14, and 28. Rats were euthanized at day 28 after IVH.…”

Section: Experimental Groupsmentioning

confidence: 99%

Hydrocephalus after Intraventricular Hemorrhage: The Role of Thrombin

Gao

Liu

Chen

et al. 2013

J Cereb Blood Flow Metab

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Previous studies demonstrated that thrombin is an important factor in brain injury after intracerebral hemorrhage. This study investigated the effect of thrombin on hydrocephalus development in a rat intraventricular hemorrhage (IVH) model. There were three parts in this study. First, male Sprague-Dawley rats had an injection of 200 mL saline, autologous blood or heparinized blood, into the right lateral ventricle. Second, rats had an injection of 50 mL saline or 3U thrombin into the right lateral ventricle. Third, rats had an injection of thrombin (3U) with a protease-activated receptor-1 (PAR-1) antagonist, SCH79797 (0.15 nmol), or vehicle into the right lateral ventricle. Lateral ventricle volumes were measured by magnetic resonance imaging and the brains were used for immunohistochemistry and western blot analyses. Intraventricular injection of autologous blood induced hydrocephalus from day 1 to 28. Heparinized blood injection resulted in less hydrocephalus at all time points compared with blood injection alone (Po0.05). Intraventricular injection of thrombin caused significant hydrocephalus, ventricular wall damage, and periventricular blood-brain barrier disruption. Thrombin-induced hydrocephalus was reduced by co-injection of the PAR-1 antagonist SCH79797 (Po0.05). In conclusion, thrombin contributes to hydrocephalus development after IVH and thrombin-induced hydrocephalus is through PAR-1.

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“…[1][2][3] Hydrocephalus frequently occurs after IVH, developing in up to 55% of IVH patients. 1 Although it is well known that IVH is associated with hydrocephalus, the underlying mechanisms are still not clear. Evidence suggests a relationship between the incidence of posthemorrhagic hydrocephalus and the amount of intraventricular blood.…”

Section: Introductionmentioning

confidence: 99%

Role of Red Blood Cell Lysis and Iron in Hydrocephalus after Intraventricular Hemorrhage

Gao

Hua

et al. 2014

J Cereb Blood Flow Metab

126

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Thrombin and iron are two major players in intracerebral hemorrhage-induced brain injury and our recent study found that thrombin contributes to hydrocephalus development in a rat model of intraventricular hemorrhage (IVH). This study investigated the role of red blood cell (RBC) lysis and iron in hydrocephalus after IVH. There were three parts to this study. First, male SpragueDawley rats received an injection of saline, packed, or lysed RBCs into the right lateral ventricle. Second, rats had an intraventricular injection of iron or saline. Third, the rats received intraventricular injection of lysed RBCs mixed with deferoxamine (0.5 mg in 5 mL saline) or saline. All rats underwent magnetic resonance imaging at 24 hours and were then euthanized for brain edema measurement, western blot analysis, or brain histology. We found that intraventricular injection of lysed RBCs, but not packed RBCs, resulted in ventricular enlargement and marked increases in brain heme oxygenase-1 and ferritin at 24 hours. Intraventricular injection of iron also resulted in ventricular enlargement and ventricular wall damage 24 hours later. Coinjection of deferoxamine reduced lysed RBC-induced ventricular enlargement (Po0.01). These results suggest that iron, a degradation product of hemoglobin, has an important role in hydrocephalus development after IVH.

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Intraventricular hemorrhage and hydrocephalus after spontaneous intracerebral hemorrhage: results from the STICH trial

Cited by 282 publications

References 13 publications

Warfarin-related intraventricular hemorrhage

Warfarin-related intraventricular hemorrhage

Hydrocephalus after Intraventricular Hemorrhage: The Role of Thrombin

Role of Red Blood Cell Lysis and Iron in Hydrocephalus after Intraventricular Hemorrhage

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