Stroke-associated pneumonia: from immunodepression to bedside management and future research directions.
4 affiliations
- 1Department of Neurology with Experimental Neurology, Charité - University Medical Center Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Charitéplatz 1, Berlin, 10117, Germany. [email protected].
- 2Center for Stroke Research Berlin, Charité - University Medical Center Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Charitéplatz 1, Berlin, 10117, Germany. [email protected].
- 3Department of Neurology with Experimental Neurology, Charité - University Medical Center Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Charitéplatz 1, Berlin, 10117, Germany. [email protected].
- 4Center for Stroke Research Berlin, Charité - University Medical Center Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Charitéplatz 1, Berlin, 10117, Germany. [email protected].
Abstract
Stroke-associated pneumonia (SAP) is one of the most frequent complications after acute stroke, affecting approximately one in eight stroke patients. Besides prolonged hospitalisation and increased healthcare costs, it is also a major risk factor for mortality and poor functional recovery. The pathophysiology of SAP is driven by two converging processes: impaired local airway defence due to dysphagia as well as reduced airway clearance reflexes, and systemic stroke-induced immunodepression driven by dysfunction of the autonomic nervous system. While post-stroke immunodepression is a major risk factor for SAP, it might limit unwanted autoimmune responses within the brain. Conversely, SAP itself may drive neuroinflammation and contribute to post-stroke cognitive impairment. Despite its clinical importance, high-quality evidence to guide practice on prevention, diagnosis, and treatment of SAP remains scarce and guideline recommendations are mostly based on expert consensus. Diagnosis of SAP is suggested to be based on standardised clinical criteria supported by chest radiography and C-reactive protein as an adjunct where uncertainty persists. After diagnosis, guidelines suggest prompt empirical antibiotic therapy according to local protocols. In contrast, preventive antibiotics, even for high-risk patients, neither improve clinical outcome nor reduce SAP frequency. Currently recommended preventive strategies for SAP therefore mostly focus on dysphagia management and early mobilisation. This review integrates the pathophysiology, long-term consequences of SAP and further research directions based on the current knowledge on post-stroke immunology with prevention, diagnosis and treatment of SAP as set out in the recent European Stroke Organisation guideline and related guidelines.
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BibTeX
@article{benkendorff2026strokeassociated,
title = {{Stroke-associated pneumonia: from immunodepression to bedside management and future research directions.}},
author = {Alexander Benkendorff and Andreas Meisel},
journal = {Neurological research and practice},
year = {2026},
month = oct,
doi = {10.1186/s42466-026-00546-9},
url = {https://europepmc.org/article/MED/42902359},
note = {CC BY},
}
RIS
TY - JOUR
TI - Stroke-associated pneumonia: from immunodepression to bedside management and future research directions.
AU - Alexander Benkendorff
AU - Andreas Meisel
PY - 2026
DA - 2026/10/20
JO - Neurological research and practice
DO - 10.1186/s42466-026-00546-9
UR - https://europepmc.org/article/MED/42902359
AB - Stroke-associated pneumonia (SAP) is one of the most frequent complications after acute stroke, affecting approximately one in eight stroke patients. Besides prolonged hospitalisation and increased healthcare costs, it is also a major risk factor for mortality and poor functional recovery. The pathophysiology of SAP is driven by two converging processes: impaired local airway defence due to dysphagia as well as reduced airway clearance reflexes, and systemic stroke-induced immunodepression driven by dysfunction of the autonomic nervous system. While post-stroke immunodepression is a major risk factor for SAP, it might limit unwanted autoimmune responses within the brain. Conversely, SAP itself may drive neuroinflammation and contribute to post-stroke cognitive impairment. Despite its clinical importance, high-quality evidence to guide practice on prevention, diagnosis, and treatment of SAP remains scarce and guideline recommendations are mostly based on expert consensus. Diagnosis of SAP is suggested to be based on standardised clinical criteria supported by chest radiography and C-reactive protein as an adjunct where uncertainty persists. After diagnosis, guidelines suggest prompt empirical antibiotic therapy according to local protocols. In contrast, preventive antibiotics, even for high-risk patients, neither improve clinical outcome nor reduce SAP frequency. Currently recommended preventive strategies for SAP therefore mostly focus on dysphagia management and early mobilisation. This review integrates the pathophysiology, long-term consequences of SAP and further research directions based on the current knowledge on post-stroke immunology with prevention, diagnosis and treatment of SAP as set out in the recent European Stroke Organisation guideline and related guidelines.
SN - 2524-3489
ER -