Beyond the bleed: complications after aneurysmal subarachnoid hemorrhage. Pathophysiology, clinical implications, and management strategies: a review.

Katharina M Busl, Elisa Gouvea Bogossian, Jan Claassen, Raimund Helbok, Jose Javier Provencio, Chiara Robba, Mervyn D I Vergouwen, Stefan Wolf, Eliza R Zanier, Giuseppe Citerio

Journal: Critical care (London, England) 2025;29(1):414

PMID: 41029753

Abstract

Aneurysmal subarachnoid hemorrhage is a critical condition with high case-fatality and lasting impacts on survivors. Acute events that are the direct result of aneurysm rupture, such as acute ischemia, elevated intracranial pressure, cerebral edema, seizures, and hydrocephalus, lead to early brain injury. A delayed cascade of processes, including a prominent systemic inflammatory response, may lead to secondary brain injury and delayed cerebral ischemia, which often further impairs recovery. Systemic complications, including cardiac and pulmonary dysfunction, fever, and electrolyte imbalances, arise in the interplay between early and secondary brain injury and challenge the clinical course. Early management focuses on the prevention of rebleeding mainly through aneurysm securement, amelioration of early brain injury through cerebrospinal fluid drainage, control of intracranial pressure, and organ support to avoid or attenuate secondary brain injury. Nimodipine remains the only pharmacological agent shown to reduce delayed cerebral ischemia, and lumbar drainage of cerebrospinal fluid to reduce subarachnoid blood may improve outcome. Management strategies for hemodynamic interventions, seizures, intracranial pressure control, large artery vasospasm, and electrolytes remain consensus-based and with large variation in practice. Several advances in understanding inflammation and delayed cerebral ischemia, as well as in monitoring and interventions hold promise, but robust trials are needed to refine protocols and improve patient recovery. Understanding and mitigating the cascade of damage from rupture to recovery is essential to reduce the burden of this devastating condition. In this review, we appraise the current understanding of the pathophysiology of post-rupture complications as well as scientific and management data, with a focus on recent advances.

© 2025. The Author(s).

Address: Department of Neurology, College of Medicine, University of Florida, McKnight Brain Institute, 1149 Newell Drive, Gainesville, FL, 32608, USA. [email protected].; Department of Intensive Care, Route de Lennik, Erasme Hospital, Université Libre de Bruxelles, 808, 1070, Brussels, Belgium.; Department of Neurology, Neurological Institute, Columbia University Medical Center, NewYork-Presbyterian Hospital, New York, NY, 10032, USA.; Department of Neurology, Kepler University Hospital, Johannes Kepler University Linz, Linz, Austria.; Clinical Research Institute of Neuroscience, Johannes Kepler University Linz, Kepler University Hospital, Linz, Austria.; Department of Neurology, University of Virginia, PO Box 800394, Charlottesville, VA, 22908, USA.; IRCCS Ospedale Policlinico San Martino, Genoa, Italy.; Dipartimento Di Scienze Chirurgiche Diagnostiche Ed Integrate, University of Genoa, Genoa, Italy.; Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.; Department of Neurosurgery, Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin and Berlin Institute of Health, Berlin, Germany.; Department of Acute Brain and Cardiovascular Injury, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.; School of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy. [email protected].; Department Neuroscience, NeuroIntensive Care Unit, IRCCS Fondazione San Gerardo Dei Tintori, Monza, Italy. [email protected].
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