ArticleMedical science monitor : international medical journal of experimental and clinical research2017
No Awakening in Supratentorial Intracerebral Hemorrhage Is Potentially Caused by Sepsis-Associated Encephalopathy.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- The Biphasic Effect of Lipopolysaccharide on Membrane Potential.Membranes · 2025Article
- The molecular basis of brain injury in preterm infants with sepsis - associated encephalopathy.BMC pediatrics · 2022Article
- The effects of bacterial endotoxin LPS on synaptic transmission at the neuromuscular junction.Heliyon · 2019Article
- Angiopoietin-Like 4 Attenuates Brain Edema and Neurological Deficits in a Mouse Model of Experimental Intracerebral Hemorrhage.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Natural killer cell deficiency experiences higher risk of sepsis after critical intracerebral hemorrhage.International journal of immunopathology and pharmacologyArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Acute supratentorial intracerebral hemorrhage (sICH) with secondary sepsis is increasing in frequency. We investigated whether no awakening (NA) after sICH with coma is potentially caused by sepsis-associated encephalopathy (SAE). MATERIAL AND METHODS A case-control study of 147 recruited sICH cases with NA and 198 sICH controls with subsequent awakening (SA) was performed at 2 centers in China. All patients underwent brain computed tomography (CT) scans on admission. The odds ratio (OR) of NA was calculated using logistic regression. RESULTS During the study period, 56.5% (83/147) of the patients with sICH with coma and NA had SAE, and 10% (20/198) with sICH with coma and SA had SAE; this difference between the 2 groups was significant (p<0.000). The sICH patients with coma and NA exhibited a longer median time from onset to coma (2.0 days vs. 0.5 days), more frequent confirmed infection (98.0% vs. 24.2%), and a higher Sequential Organ Failure Assessment (SOFA) score (6.3±1.5 vs. 3.4±0.8). These patients also exhibited lower hematoma volume (28.0±18.8 vs. 38.3±24), a lower initial National Institutes of Health Stroke Scale score (19.5±6.6 vs. 30.3±6.8), more frequent brain midline shift (59.2% vs. 27.8%), more frequent diffuse cerebral swelling (64.6% vs. 16.0%), and higher 30-day mortality (54.4% vs. 0.0%) than the patients who did awaken. Logistic multivariable regression analyses revealed that only a higher SOFA score (OR, 1.4; 95% CI, 1.079-1.767; p=0.010) and SAE (OR, 4.0; 95% CI, 1.359-6.775; p=0.001) were associated with NA events in patients with sICH. CONCLUSIONS NA in sICH patients with coma is potentially caused by secondary SAE.
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