Asian Journal of Medical Principles and Clinical Practice

Background: Critically ill trauma patients in Nigerian intensive care units (ICUs) face a disproportionate burden of healthcare-associated infections (HAIs). While trauma-induced immune dysregulation is well documented, the additional immunomodulatory contribution of routine ICU pharmacotherapy remains insufficiently characterised in this setting.

Objective: To synthesise available evidence on whether commonly administered drugs in Nigerian trauma ICUs may amplify infection vulnerability, and to propose a context-specific research and implementation agenda.

Methods: We conducted a transparent narrative review of the literature published between January 2000 and 31 May 2025. Searches were performed in PubMed/MEDLINE, African Journals Online (AJOL), Embase, and the WHO Institutional Repository for Information Sharing. Grey literature was sourced from the Nigeria Centre for Disease Control (NCDC) and WHO. We operationalised a PICO framework, used dual-independent screening, and graded mechanistic evidence by source (preclinical, observational, systematic review). We did not perform quantitative meta-analysis. Claims were restricted to the strength of available data.

Results: Pooled HAI prevalence in Nigerian healthcare facilities is approximately 15.8% (95% CI 14.4–17.1), with ICU-specific rates of 30.9–45%. Predominant pathogens include Staphylococcus aureus (41.7%), Klebsiella pneumoniae (21.4%), and Escherichia coli (15.5%), with high resistance to first-line antibiotics. Trauma triggers a biphasic immune response (SIRS followed by CARS/immunoparalysis). Corticosteroids, opioids, propofol, catecholamines, and allogeneic blood products possess immunomodulatory properties that may compound trauma-induced immune dysfunction, though direct clinical quantification in Nigerian trauma populations is absent. Nigeria’s severe ICU infrastructure deficit (<0.1 beds per 100,000 population) amplifies these risks through overcrowding and inadequate infection prevention.

Conclusions: The convergence of trauma-induced immunosuppression and drug-mediated immune modulation represents a plausible, biologically grounded, but clinically unquantified vulnerability window for nosocomial infection in Nigerian trauma ICUs. Evidence-based mitigation requires antimicrobial stewardship, rational drug selection guided by immunological risk, care bundle implementation, and targeted investment in infection prevention infrastructure. Prospective studies quantifying the independent contribution of specific drugs to HAI risk in this population are urgently needed.