Key result
Fatigue was present in 69.7% of patients 1 to 7 years after aneurysmal subarachnoid hemorrhage, with nicotine use, reduced consciousness at admission, and severe vasospasm independently doubling the risk of developing fatigue.
Why the study?
Prevalence estimates of post-aneurysmal subarachnoid hemorrhage fatigue in the chronic phase are scarce and vary greatly, and acute-phase predictors are barely established.
Observational (n=356)
No
Fatigue is highly prevalent (69.7%) up to 7 years after aneurysmal subarachnoid hemorrhage, with acute phase factors like nicotine use, reduced consciousness, and severe vasospasm serving as independent predictors.
High chronic fatigue prevalence post-aSAH supports screening in survivors; leaves open causal role of acute predictors.
BACKGROUND: Fatigue is a common and disabling sequel after aneurysmal subarachnoid hemorrhage (aSAH). At present, prevalence estimates of post-aSAH fatigue in the chronic phase are scarce and vary greatly. Factors from the acute phase of aSAH have hitherto barely been associated with post-aSAH fatigue in the chronic phase. METHODS: Prospective study assessing prevalence of fatigue using the Fatigue Severity Scale (FSS) in patients who were living independently 1 to 7 years after aSAH. We compared demographic, medical, and radiological variables from the acute phase of aSAH between patients with and without fatigue (FSS ≥ 4 versus < 4) and searched for predictors of fatigue among these variables applying univariable and multivariable regression analyses. RESULTS: Of 726 patients treated for aSAH in the period between January 2012 and December 2017, 356 patients completed the assessment. The mean FSS score was 4.7 ± 1.7, and fatigue was present in 69.7%. The frequency of patients with fatigue did not decline significantly over time. Univariable analysis identified nicotine use, loss of consciousness at ictus (LOCi), rebleed prior to aneurysm repair, reduced consciousness to Glasgow Coma Scale (GCS) < 14, large amounts of subarachnoid blood, the presence of acute hydrocephalus, and severe vasospasm as factors that were significantly associated with fatigue. In multivariable analysis, nicotine use, reduced GCS, and severe vasospasm were independent predictors that all more than doubled the risk to develop post-aSAH fatigue. CONCLUSIONS: Fatigue is a frequent sequel persisting several years after aSAH. Nicotine use, reduced consciousness at admission, and severe vasospasm are independent predictors of fatigue from the acute phase of aSAH. We propose inflammatory cytokines causing dopamine imbalance to be a common denominator for post-aSAH fatigue and the presently identified predictors.
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Western et al. (2020) conducted an observational in Aneurysmal subarachnoid hemorrhage (n=356). Nicotine use vs. Former and never nicotine use was evaluated on Post-aSAH fatigue (Fatigue Severity Scale ≥ 4) (OR 2.10, 95% CI 1.31-3.39, p=0.002). Fatigue was present in 69.7% of patients 1 to 7 years after aneurysmal subarachnoid hemorrhage, with nicotine use, reduced consciousness at admission, and severe vasospasm independently doubling the risk of developing fatigue.
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