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Minimally Invasive Endoscopic Intracerebral Hemorrhage Evacuation
Published on: October 15, 2021
Assessing etiological classification systems and their relationship with neurological deterioration in patients with
Daniel Vázquez-Justes1,2, Gerard Mauri-Capdevila1,2, Yhovany Gallego1,2
1Stroke Unit. Neurology Department. Hospital Universitari Arnau Vilanova, IRBLleida. Universitat de Lleida, Av, Rovira Roure 80, Lleida, Spain.
Insights
Intracerebral hemorrhage (ICH) etiology impacts neurological deterioration (ND). Anticoagulation-related ICH, especially with hypertension, significantly increases ND risk. Understanding these links aids patient care.
Area of Science:
- Neurology
- Clinical Medicine
- Stroke Research
Background:
- Intracerebral hemorrhage (ICH) lacks a standardized etiological classification, unlike ischemic stroke.
- The relationship between ICH etiological classifications and neurological deterioration (ND) is not well understood.
Purpose of the Study:
- To investigate the association between etiological classifications (SMASH-U, H-ATOMIC) and ND in intracerebral hemorrhage patients.
- To identify specific etiological subtypes linked to increased risk of neurological deterioration during hospitalization.
Main Methods:
- Prospective cohort study of 301 consecutive ICH patients (2015-2022).
- Systematic recording of demographic, radiological, and clinical data.
- Multivariate logistic regression analysis to identify variables and etiological groups associated with ND.
Main Results:
- 41.2% of patients experienced neurological deterioration (ND).
- Anticoagulation (AC)-related ICH was associated with a higher risk of ND.
- SMASH-U: medication-related ICH (OR 6.02) linked to ND. H-ATOMIC: HT+AC combination (OR 9.91) and combined groups (OR 17.49) related to ND.
Conclusions:
- ICH etiology is associated with the risk of neurological deterioration.
- Anticoagulation-related ICH, particularly when combined with hypertension, presents the highest risk for ND.
- Factors like intraventricular extension and initial hematoma volume also correlate with ND.
Abstract:
Unlike ischemic stroke, there is no consensus on the etiological classification of intracerebral hemorrhage (ICH). Our study focuses on two commonly used classification systems: SMASH-U and H-ATOMIC. The association between these classifications and neurological deterioration (ND) as well as clinical outcomes remains largely unexplored. We aimed to determine whether the etiological groups defined by these classifications are related to ND during hospitalization. We prospectively recruited consecutive ICH patients from 2015 to 2022. Demographic, radiological and clinical characteristics were systematically recorded. Etiology was determined at discharge. Variables and etiological groups associated with ND were included in a multivariate logistic regression analysis. A total of 301 patients were recruited, of whom 124 patients (41.2%) experienced ND. The hypertensive subtype was the most frequent etiology with both classifications systems. In 149 (49.5%) more than one possible etiology for ICH was identified, with the most common combination being hypertension and either probable or possible amyloid angiopathy, in 64 patients (21.3%). ICH related to anticoagulation (AC) was associated with a greater risk of ND. In the multivariate analysis, certain etiological subtypes were independently associated with ND. In the SMASH-U classification, medication-related ICH was linked to a higher risk of ND (OR 6.02 95% CI 1.87-19.34). while in H-ATOMIC, the combination of HT and AC (OR 9.91 CI: 2.54-38.69), and combined groups (OR 17.49, CI: 3.86-79.30), were related to ND. Intraventricular extension, blood pressure control and initial volume were also related to ND. In addition, intraventricular extension, blood pressure control, and initial hematoma volume were also found to be related to ND. The etiology of the ICH could be related to the risk of ND during hospitalization. AC-related etiologies appear to confer the highest risk, particularly when combined with HT-related mechanisms.
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