Increased Brain Volume Among Good Grade Patients with Intracerebral Hemorrhage. Results from the Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) Study

Qureshi, Adnan I.; Majidi, Shahram; Gilani, Waqas I; Palesch, Yuko Y.; Martin, Renée; Novitzke, Jill; Cruz‐Flores, Salvador; Ehtisham, As’ad; Goldstein, Joshua N.; Kirmani, Jawad F.; Hussein, Haitham M.; Suri, M. Fareed K.; Tariq, Nauman

doi:10.1007/s12028-013-9842-1

Cited by 14 publications

(10 citation statements)

References 24 publications

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“…Hence, it is quite prerequisite to analyze the possible risk factors that may lead to DHE so that physicians could take better treatment as early as possible in order to reduce the subsequent deterioration and improve patients' functional outcomes. Results from our patients in the DHE multifactor analysis study showed that initial hematoma volume and the effects of age are risk factors for DHE after sICH, concluding that the larger the initial hematoma volume, the more prone to DHE, which is in accordance with the results of previous studies . A recent review article detailed that a few days or weeks after sICH, the main cause of PHE is the release of hemoglobin degradation products after the red blood cells are dissolved; perhaps according to larger cerebral hemorrhage initial hematoma volume, the greater the toxicant secondary to the hemoglobin degradation more prone to cause the DHE .…”

Section: Discussionsupporting

confidence: 90%

“…It is generally recognized that the disruption of vessels will rapidly cause a hematoma and vasogenic edema in the super‐acute stage of ICH. Except the hematoma occupying effect, the production of thrombin and activation of blood coagulation cascade contributes to a slow progressive edema growth, approximately peaking on the seventh day after ICH . On the other hand, the breakdown of the blood brain barrier, inflammatory cascades, heme, and iron load secondary to red cell dissolution as well as hemoglobin degradation will give rise to or accelerate PHE, but PHE will ameliorate or disappear with the alleviation of hematoma .…”

Section: Introductionmentioning

confidence: 99%

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The risk factors and prognosis of delayed perihematomal edema in patients with spontaneous intracerebral hemorrhage

Peng

Tang

et al. 2019

CNS Neurosci Ther

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Purpose We hypothesize delayed perihematomal edema (DHE) leads to secondary injury after spontaneous intracerebral hemorrhage (sICH) with a poor prognosis. Hence, we need to investigate the risk factors of DHE and identify whether DHE will predict the poor outcome of sICH. Methods We retrospectively recruited 121 patients with sICH admitted to the Department of Neurology from January 2014 to August 2018. After dividing all these patients into DHE group and non‐DHE group, we analyzed the potential risk factors and outcome of DHE using a multivariate logistic regression model. Results We conclude DHE after sICH associates with age, hospitalization time, hematoma shape, blood pressure upon admission, alcohol consumption, blood sodium level, and baseline hematoma volume within 24 hours after symptom onset, among which differences were statistically significant (P < .05). Logistic regression analysis finally identified that age (OR = 0.958, 95% CI = 0.923‐0.995) and the baseline hematoma volume (OR = 1.161, 95% CI = 1.089‐1.238) were the most significant risk factors for DHE, and moreover, the DHE (OR = 3.062, 95% CI = 1.196‐7.839) was also a risk factor for poor prognosis in sICH patients. Conclusion We suggest DHE is a clinical predictor of secondary injury following sICH and poor prognosis. In addition, age and baseline hematoma volume are considered significant high‐risk factors for DHE in patients with sICH.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

The risk factors and prognosis of delayed perihematomal edema in patients with spontaneous intracerebral hemorrhage

Peng

Tang

et al. 2019

CNS Neurosci Ther

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“…Absolute, relative, and rate of increase in PHE are all related to death or dependency at 90 days (4, 7, 8). PHE-associated effect on clinical outcomes may be dependent on hematoma volume, as shown in three previous studies where PHE in setting of moderate size hematoma volume around 30 cc was associated with poor outcomes (9–11). Hematoma location in basal ganglion was also found to be associated with an increase in PHE-related adverse outcomes (10).…”

Section: Perihemorrhagic Edemamentioning

confidence: 78%

Intracerebral Hemorrhage: Perihemorrhagic Edema and Secondary Hematoma Expansion: From Bench Work to Ongoing Controversies

Mittal

LacKamp

2016

Front. Neurol.

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Intracerebral hemorrhage (ICH) is a medical emergency, which often leads to severe disability and death. ICH-related poor outcomes are due to primary injury causing structural damage and mass effect and secondary injury in the perihemorrhagic region over several days to weeks. Secondary injury after ICH can be due to hematoma expansion (HE) or a consequence of repair pathway along the continuum of neuroinflammation, neuronal death, and perihemorrhagic edema (PHE). This review article is focused on PHE and HE and will cover the animal studies, related human studies, and clinical trials relating to these mechanisms of secondary brain injury in ICH patients.

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“…We used a similar approach to determine the volume of the ventricular system for each scan. We determined brain tissue volume by measuring the volume of the entire intracranial space and subtracting the total intracranial CSF volume as previously been described by others (19, 20). Pixel thresholding has previously been used to measure intracranial CSF volumes (19–21) and accurately measures volumes with excellent inter-rater agreement (κ=0.97) (22).…”

Section: Methodsmentioning

confidence: 99%

23.4% Saline Decreases Brain Tissue Volume in Severe Hepatic Encephalopathy as Assessed by a Quantitative CT Marker

Liotta

Lizza

Romanova

et al. 2016

Critical Care Medicine

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Objective Cerebral edema is common in severe hepatic encephalopathy and may be life-threatening. Bolus 23.4% hypertonic saline (HTS) improves surveillance neuromonitoring scores, although its mechanism of action is not clearly established. We investigated the hypothesis that bolus HTS decreases cerebral edema in severe hepatic encephalopathy utilizing a quantitative technique to measure brain and CSF volume changes. Design Retrospective analysis of serial computed tomography (CT) scans and clinical data for a case-control series was performed. Setting Intensive care units of a tertiary care hospital. Patients Patients with severe hepatic encephalopathy treated with 23.4% HTS and control patients who did not receive 23.4% HTS. Methods We used clinically obtained CT scans to measure volumes of the ventricles, intracranial CSF, and brain using a previously validated semi-automated technique (Analyze Direct; Overland Park, KS). Volumes before and after 23.4% HTS were compared with Wilcoxon signed-rank test. Associations between total CSF volume, ventricular volume, serum sodium, and Glasgow Coma Scale Scores were assessed using Spearman correlation. Results Eleven patients with 18 administrations of 23.4% HTS met inclusion criteria. Total CSF (median 47.6 [35.1–69.4] to 61.9 [47.7–87.0] mL, p<0.001) and ventricular volumes (median 8.0 [6.9–9.5] to 9.2 [7.8–11.9] mL, p=0.002) increased and Glasgow Coma Scale Scores improved (median 4 [3–6] to 7 [6–9], p=0.008) after 23.4% HTS. In contrast, total CSF and ventricular volumes decreased in untreated control patients. Serum sodium increase was associated with increase in total CSF volume (r=0.83, p<0.001) and change in total CSF volume was associated with ventricular volume change (r=0.86, p<0.001). Conclusions Total CSF and ventricular volumes increased after 23.4% HTS, consistent with a reduction in brain tissue volume. Total CSF and ventricular volume change may be useful quantitative measures to assess cerebral edema in severe hepatic encephalopathy.

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Increased Brain Volume Among Good Grade Patients with Intracerebral Hemorrhage. Results from the Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) Study

Abstract: We found preliminary evidence of increased cerebral brain volume in subjects with good grade and small ICHs, which may be suggestive of global cerebral edema.

Cited by 14 publications

References 24 publications

The risk factors and prognosis of delayed perihematomal edema in patients with spontaneous intracerebral hemorrhage

The risk factors and prognosis of delayed perihematomal edema in patients with spontaneous intracerebral hemorrhage

Intracerebral Hemorrhage: Perihemorrhagic Edema and Secondary Hematoma Expansion: From Bench Work to Ongoing Controversies

23.4% Saline Decreases Brain Tissue Volume in Severe Hepatic Encephalopathy as Assessed by a Quantitative CT Marker

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