Human factors-based risk analysis to improve the safety of doffing enhanced personal protective equipment.

OBJECTIVE: To systematically assess enhanced personal protective equipment (PPE) doffing safety risks. DESIGN: We employed a 3-part approach to this study: (1) hierarchical task analysis (HTA) of the PPE doffing process; (2) human factors-informed failure modes and effects analysis (FMEA); and (3) focus group sessions with a convenience sample of infection prevention (IP) subject matter experts. SETTING: A large academic US hospital with a regional Special Pathogens Treatment Center and enhanced PPE doffing protocol experience.ParticipantsEight IP experts. METHODS: The HTA was conducted jointly by 2 human-factors experts based on the Centers for Disease Control and Prevention PPE guidelines. The findings were used as a guide in 7 focus group sessions with IP experts to assess PPE doffing safety risks. For each HTA task step, IP experts identified failure mode(s), assigned priority risk scores, identified contributing factors and potential consequences, and identified potential risk mitigation strategies. Data were recorded in a tabular format during the sessions. RESULTS: Of 103 identified failure modes, the highest priority scores were associated with team members moving between clean and contaminated areas, glove removal, apron removal, and self-inspection while preparing to doff. Contributing factors related to the individual (eg, technical/ teamwork competency), task (eg, undetected PPE contamination), tools/technology (eg, PPE design characteristics), environment (eg, inadequate space), and organizational aspects (eg, training) were identified. Participants identified 86 types of risk mitigation strategies targeting the failure modes. CONCLUSIONS: Despite detailed guidelines, our study revealed 103 enhanced PPE doffing failure modes. Analysis of the failure modes suggests potential mitigation strategies to decrease self-contamination risk during enhanced PPE doffing.

Increased lethality and defective pulmonary clearance of Streptococcus pneumoniae in microsomal prostaglandin E synthase-1-knockout mice.

The production of prostaglandin E2 (PGE2) increases dramatically during pneumococcal pneumonia, and this lipid mediator impairs alveolar macrophage (AM)-mediated innate immune responses. Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme involved in the synthesis of PGE2, and its expression is enhanced during bacterial infections. Genetic deletion of mPGES-1 in mice results in diminished PGE2 production and elevated levels of other prostaglandins after infection. Since PGE2 plays an important immunoregulatory role during bacterial pneumonia we assessed the impact of mPGES-1 deletion in the host defense against pneumococcal pneumonia in vivo and in AMs in vitro. Wild-type (WT) and mPGES-1 knockout (KO) mice were challenged with Streptococcus pneumoniae via the intratracheal route. Compared with WT animals, we observed reduced survival and increased lung and spleen bacterial burdens in mPGES-1 KO mice 24 and 48 h after S. pneumoniae infection. While we found modest differences between WT and mPGES-1 KO mice in pulmonary cytokines, AMs from mPGES-1 KO mice exhibited defective killing of ingested bacteria in vitro that was associated with diminished inducible nitric oxide synthase expression and reduced nitric oxide (NO) synthesis. Treatment of AMs from mPGES-1 KO mice with an NO donor restored bacterial killing in vitro. These results suggest that mPGES-1 plays a critical role in bacterial pneumonia and that genetic ablation of this enzyme results in diminished pulmonary host defense in vivo and in vitro. These results suggest that specific inhibition of PGE2 synthesis by targeting mPGES-1 may weaken host defense against bacterial infections.