Pediatric Critical Illness, Immunometabolism and Cardiovascular Risk: A Narrative Review

The management of critical illness has significantly advanced, enabling a greater number of patients to survive conditions that were once fatal. However, survival often comes at a cost, as many patients experience long-term sequelae, including chronic critical illness (CCI) and post-intensive care syndrome (PICS). These syndromes can also be subclinical, driven by a persistent imbalance between pro-inflammatory and anti-inflammatory processes, resulting in sustained immune dysfunction, metabolic disturbances, and organ-specific complications. Among the most affected systems are the immune and cardiovascular systems, which undergo acute metabolic shifts during critical illness to meet energy demands. However, if unresolved, these shifts can support chronic inflammation and dysfunction. Failed resolution of inflammation may contribute to long-term cardiovascular disease (CVD), including hypertension and atherosclerosis, through impaired vascular integrity and healing. Clinical and animal studies demonstrate that acute inflammatory insults, such as trauma or severe infections, can trigger sustained vascular inflammation, endothelial dysfunction, and maladaptive immune responses, leading to an elevated risk of early-onset CVD. This review explores the interplay between immune dysregulation and cardiovascular outcomes in survivors of critical illness, particularly in children and young adults. It highlights the role of metabolic reprogramming, immune-mediated inflammation, and specialized pro-resolving mediators (SPMs) in both the acute and chronic phases of recovery. Current evidence and studies that provide a link between acute critical illness and immune and cardiovascular sequelae are discussed.