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The etiologic subtype of intracerebral hemorrhage may influence the risk of significant hematoma expansion.

Abstract：

BACKGROUND:Intracerebral hemorrhage (ICH) growth is an important independent predictor of clinical deterioration and outcome. Little is known about the association between etiology of ICH and occurrence of hematoma expansion (HE). The aim of the present study was to assess whether ICH etiologic subtype may influence the risk of significant HE. METHODS:We conducted an analysis on retrospectively collected data of 424 consecutive patients with ICH, who were admitted to the Verona General Hospital, from March 2011 to December 2014. Using the SMASH-U (Structural vascular lesions, Medication, Amyloid angiopathy, Systemic disease, Hypertension, or Undetermined) classification, we identified the ICH etiologic subtypes. Outcome measure was significant HE (an absolute increase in ICH volume>12.5 mL or >50%) within 48 h. RESULTS:Significant HE occurred in 11/57 (19.3%) Amyloid, 7/14 (50%) Structural, 31/57 (54.4%) Medication, 25/44 (56.8%) in Systemic, 62/139 (44.6%) Hypertensive, and 21/68 (30.9%) Undetermined ICH. Baseline ICH volume (OR 1.011 per mL, 95% CI 1.006-1.017, p<0.001) and onset-to-baseline CT time (OR 0.919 per hour, 95% CI 0.852-0.990, p=0.027) were predictors of significant HE. Compared with Amyloid ICH, ORs for significant HE were higher in patients with Structural ICH (OR 1.430, 95% CI 1.060-1.948, p=0.023), Medication ICH (OR 4.344, 95% CI 1.382-13.653, p=0.012), Systemic ICH (OR 1.796, 95% CI 1.070-3.015, p=0.027), and Hypertensive ICH (OR 3.081, 95% CI 1.426-6.655, p=0.004). CONCLUSION:Our study shows that Structural, Medication, Systemic, and Hypertensive ICH were the etiologic subtypes associated with a higher risk of significant HE, compared with Amyloid ICH patients.

journal_name

J Neurol Sci

journal_title

Journal of the neurological sciences

authors

Cappellari M,Zivelonghi C,Moretto G,Micheletti N,Carletti M,Tomelleri G,Bovi P

doi

10.1016/j.jns.2015.11.024

subject

Has Abstract

pub_date

2015-12-15 00:00:00

pages

293-7

issue

1-2

eissn

0022-510X

issn

1878-5883

pii

S0022-510X(15)30032-0

journal_volume

359

pub_type

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