Optimizing infection management after cardiac arrest: addressing diagnostic uncertainty and therapeutic dilemmas—a narrative review

TL;DR

This review discusses challenges in diagnosing and treating infections after cardiac arrest and suggests strategies to improve outcomes.

Contribution

The paper provides practical guidance for managing infections in post-cardiac arrest patients, emphasizing multimodal approaches and research priorities.

Findings

Infections are common after cardiac arrest and are complicated by post-cardiac arrest syndrome and treatment interventions.

Conventional biomarkers are unreliable early on, and serial assessments are preferred for accurate diagnosis.

Prevention strategies and antimicrobial stewardship are critical for reducing complications and improving outcomes.

Abstract

Infections are frequent after cardiac arrest and materially affect post-ICU care and outcomes. Diagnostic uncertainty is heightened by post-cardiac arrest syndrome (PCAS)—hypoxic–ischemic brain injury, myocardial dysfunction, systemic ischemia–reperfusion injury, and immune dysregulation—and by sedation and targeted temperature management (TTM), which can mask clinical signs and modulate host defenses. Pneumonia predominates; bloodstream infection and intra-abdominal or hepatobiliary infections are under-recognized, especially in device-dependent or extracorporeal membrane oxygenation (ECMO)-treated patients. Conventional biomarkers such as C-reactive protein and procalcitonin show reduced infection specificity early after return of spontaneous circulation; therefore, single timepoint cutoffs are unreliable, and serial trajectories interpreted with clinical examination, microbiology, and imaging are preferred. Risk scores (e.g., Sequential Organ Failure Assessment [SOFA], Clinical Pulmonary Infection Score [CPIS]) may support stratification but are insufficient for definitive diagnosis. Observational cohorts report higher pneumonia rates with TTM, and temperature control can blunt fever and leukocytosis and alter cytokine and biomarker kinetics, complicating timely recognition. Prevention should emphasize protocolized bundles, including hand hygiene and asepsis, head-of-bed elevation, structured oral care per local policy, minimization of sedation with spontaneous breathing trials, and early removal of unnecessary devices, within an antimicrobial stewardship framework that supports early de-escalation once cultures and trajectories clarify etiology. Procalcitonin-guided early discontinuation reduces antibiotic exposure in general critical-care populations; in PCAS, use should prioritize serial trends integrated with clinical context rather than single thresholds. No fixed algorithm is prescribed; instead, practical considerations are presented to guide diagnostic practice, emphasizing early microbiological sampling and imaging, integration of serial biomarker trajectories with clinical assessment, and timely de-escalation as the clinical picture clarifies, without endorsing single-test cutoffs. Priorities include quantifying infection-attributable morbidity and mortality; developing and validating PCAS-specific biomarkers and composite decision tools, including electronic health record-based early warning models; evaluating short post-intubation prophylaxis in selected high-risk patients; optimizing TTM parameters (target temperature, duration, rewarming rate); and systematically characterizing under-recognized infections. A protocol-driven, multimodal program that integrates prevention, standardized diagnostics, and stewardship is required to deliver timely, appropriate therapy and improve outcomes after cardiac arrest.

Figures