The role of catecholamines in aneurysmal subarachnoid hemorrhage: a narrative review
- Author:
Samantha NALLIAH
1
;
Tariq JANJUA
;
Luis Rafael MOSCOTE-SALAZAR
;
Md YUNUS
;
Amit AGRAWAL
Author Information
- Publication Type:Review Article
- From: Acute and Critical Care 2025;40(4):513-520
- CountryRepublic of Korea
- Language:English
- Abstract: The marked release of catecholamines during subarachnoid hemorrhage is an important aspect of the pathobiology following aneurysmal rupture. This narrative review aims to identify how catecholamines influence aneurysmal subarachnoid hemorrhage (aSAH) outcomes. aSAH is a critical neurological condition characterized by hemorrhage into the subarachnoid space, leading to severe neurological deficits and mortality. Catecholamines, including epinephrine, norepinephrine, and dopamine, are the body's stress responses, which can lead to secondary injuries following aSAH. This review was conducted through a targeted literature search of relevant studies examining the relationship between aSAH, catecholamines, and clinical outcomes. Searches were performed in PubMed, Scopus, The Cochrane Library, Medline (Ovid), Embase (Ovid), and CINAHL, including publications up to July 2024. Search terms combined keywords and subject headings related to “subarachnoid hemorrhage” or “aSAH,” “catecholamines,” “epinephrine,” “norepinephrine,” “dopamine,” and outcome-related terms such as “prognosis,” “mortality,” and “neurological outcome.” Articles were selected based on relevance, and key findings were synthesized descriptively to provide a comprehensive overview of current knowledge in this area. Elevated levels of catecholamines are observed following aSAH and are associated with increased sympathetic nervous system activity. This catecholamine surge contributes to pathological processes, including vasospasm, blood-brain barrier disruption, cerebral edema, and neuronal damage. The review highlights the implications of catecholamine levels; where higher concentrations correlate with poorer outcomes and higher mortality rates. Understanding the mechanisms responsible for secondary injury due to catecholamines surge following aSAH shall facilitate the development of therapeutic approaches to prevent secondary brain injury and improve outcomes.
