Introduction Lidocaine is a common local anesthetic used during minor procedures performed on pediatric patients. A rare but toxic and life-threatening side effect of lidocaine is methemoglobinemia. It should be considered in children who are hypoxic after exposure to an oxidizing agent. Methods We developed this simulation case for pediatric emergency medicine (PEM) fellows, but it can be adapted for interprofessional simulation. The case involved a 1-month-old male with hypoxia and resulting central cyanosis after exposure to lidocaine. The team performed an initial evaluation and intervention, collected a history, and developed a differential diagnosis for hypoxia and central cyanosis in an infant. Methemoglobinemia was confirmed by CO-oximetry. Preparatory materials, a debriefing guide, and scenario evaluation forms assisted with facilitation. Results Fifty-six participants (including 18 PEM fellows) completed this simulation across four institutions. Participants rated the scenario on a 5-point Likert scale (1 = strongly disagree, 5 = strongly agree ), finding it to be relevant to their work (median = 5) and realistic (median = 5). After participation in the simulation, learners felt confident in their ability to recognize methemoglobinemia (median = 4) and implement a plan to stabilize an infant with hypoxia (median = 4). Discussion This simulation represents a resource for learners in the pediatric emergency department. It teaches the recognition and management of an infant with lidocaine toxicity and resultant methemoglobinemia. It uses experiential learning to teach and reinforce a systematic approach to the evaluation and management of a critically ill infant with acquired methemoglobinemia.

Herpetic stromal keratitis (HSK) is the leading cause of infectious blindness in developed nations and occurs following infection with herpes simplex virus. The mechanism underlying this disease is immune-mediated, involving neutrophils, macrophages, cytokines, and chemokines. We hypothesized that neutralizing the proinflammatory cytokine IL-6 or the chemokine KC (murine CXCL1) would significantly reduce disease in an animal model of HSK. Latently infected mice were reactivated 6 weeks following infection with UV-B light to stimulate recurrent disease. At that time, we administered mAbs against IL-6, KC and control IgG via intraperitoneal injection. We monitored recurrent infection by daily testing tear film for virus for 7 days following reactivation. Corneal disease was evaluated weekly for five weeks. Data shows that neutralizing KC resulted in lower opacity and neovascularization scores for all time points measured when compared to controls. Surprisingly, unlike what is seen in acute HSK, neutralizing IL-6 did not decrease disease. Futhermore, treatment with anti-KC results in significantly less neutrophilic infiltrate of infected corneas. We conclude that CXCL1 and not IL-6 is important in developing recurrent HSK. Furthermore, these results further demonstrate that recurrent and acute HSK share some but not all aspects of disease, and that one common thread is the crucial role that neutrophils play in this potentially blinding disease.