CT Evolution of Hematoma and Surrounding Hypodensity in a Cadaveric Model of Intracerebral Hemorrhage

Majidi, Shahram; Rahim, Basit; Gilani, Sarwat; Gilani, Waqas I; Adil, Malik M; Qureshi, Adnan I.

doi:10.1111/jon.12306

Cited by 14 publications

(9 citation statements)

References 25 publications

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“…Undoubtedly, many events of a large PHHD are associated with inflammatory mechanisms 26 and have been linked to the appearance of a cytotoxic edema in the first hours and with a vasogenic edema in later phases. 9,27,28 However, other mechanisms should not be ruled out, such as ischemic necrosis or neurotoxicity associated with coagulation mechanisms. 29,30 A novel and promising hypothesis associated the presence and progression of PHHD with the existence of spreading depressions and isoelectric spreading depolarizations, although its association with episodes of metabolic derangement and ischemic lesions remains speculative.…”

Section: Discussionmentioning

confidence: 99%

Antihyperthermic treatment decreases perihematomal hypodensity

et al. 2020

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ObjectiveTo investigate the effect on perihematomal hypodensity and outcome of a decrease in body temperature in the first 24 hours in patients with intracerebral hemorrhage (ICH). MethodsIn this retrospective study on a prospectively registered database, among the 1,100 patients, 795 met all the inclusion criteria. Temperature variations in the first 24 hours and perihematomal hypodensity (PHHD) were recorded. Patients ≥37.5°C were treated with antihyperthermic drugs for at least 48 hours. The main objective was to determine the association among temperature variation, PHHD, and outcome at 3 months. ResultsThe decrease in temperature in the first 24 hours increased the possibility of good outcome 11-fold. Temperature decrease, lower PHHD volume, and a good outcome were observed in 31.8% of the patients who received antihyperthermic treatment. ConclusionThe administration of early antihyperthermic treatment in patients with spontaneous ICH with a basal axillary temperature ≥37.5°C resulted in good outcome in a third of the treated patients.Glossary ANOVA = analysis of variance; CI = confidence interval; ICH = intracerebral hemorrhage; mRS = modified Rankin Scale; NIHSS = NIH Stroke Scale; OR = odds ratio; PHHD = perihematomal hypodensity.

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Section: Discussionmentioning

confidence: 99%

Antihyperthermic treatment decreases perihematomal hypodensity

et al. 2020

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“…The non-cytotoxic nature of PHE is further supported by the lack of effect of reductions in BP and cerebral blood flow (CBF) on the extent of PHE in a study of ICH patients (21). Furthermore, PHE occurs in cadaveric models of ICH in the absence of any blood flow (22). Surgical removal of ICH hematoma improves CBF on the ipsilateral side as shown in a single-photon-emission computed tomography (SPECT) study (23).…”

Section: Perihemorrhagic Edemamentioning

confidence: 99%

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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“…Early expansion of ICH occurs in approximately 50% of TBI cases ( 17 ), but most previous studies have measured the high density (blood) component only ( 18 – 21 ). ICHs are usually associated with a perihematomal low density component, which at least in part represents cytotoxic edema, and one recent study has demonstrated expansion of this perihematomal component in animal models ( 22 ). Hemostatic therapies aimed at preventing re-bleeding may increase the risk of perihematoma thrombosis and infarction, thereby increasing cytotoxic edema.…”

Section: Introductionmentioning

confidence: 99%

Evolution of Traumatic Parenchymal Intracranial Hematomas (ICHs): Comparison of Hematoma and Edema Components

et al. 2018

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This study seeks to quantitatively assess evolution of traumatic ICHs over the first 24 h and investigate its relationship with functional outcome. Early expansion of traumatic intracranial hematoma (ICH) is common, but previous studies have focused on the high density (blood) component. Hemostatic therapies may increase the risk of peri-hematoma infarction and associated increased cytotoxic edema. Assessing the magnitude and evolution of ICH and edema represented by high and low density components on computerized tomography (CT) may be informative for designing therapies targeted at traumatic ICH. CT scans from participants in the COBRIT (Citicoline Brain Injury Trial) study were analyzed using MIPAV software. CT scans from patients with non-surgical intraparenchymal ICHs at presentation and approximately 24 h later (±12 h) were selected. Regions of high density and low density were quantitatively measured. The relationship between volumes of high and low density were compared to several outcome measures, including Glasgow Outcome Score—Extended (GOSE) and Disability Rating Score (DRS). Paired scans from 84 patients were analyzed. The median time between the first and second scan was 22.79 h (25%ile 20.11 h; 75%ile 27.49 h). Over this time frame, hematoma and edema volumes increased >50% in 34 (40%) and 46 (55%) respectively. The correlation between the two components was low (r = 0.39, p = 0.002). There was a weak correlation between change in edema volume and GOSE at 6 months (r = 0.268, p = 0.037), change in edema volume and DRS at 3 and 6 months (r = −0.248, p = 0.037 and r = 0.358, p = 0.005, respectively), change in edema volume and COWA at 6 months (r = 0.272, p = 0.049), and between final edema volume and COWA at 6 months (r = 0.302, p = 0.028). To conclude, both high density and low density components of traumatic ICHs expand significantly in the first 2 days after TBI. In our study, there does not appear to be a relationship between hematoma volume or hematoma expansion and functional outcome, while there is a weak relationship between edema expansion and functional outcome.

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CT Evolution of Hematoma and Surrounding Hypodensity in a Cadaveric Model of Intracerebral Hemorrhage

Cited by 14 publications

References 25 publications

Antihyperthermic treatment decreases perihematomal hypodensity

Antihyperthermic treatment decreases perihematomal hypodensity

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

Evolution of Traumatic Parenchymal Intracranial Hematomas (ICHs): Comparison of Hematoma and Edema Components

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