Management of penetrating cardiac injury and tricuspid regurgitation with extracorporeal-membrane oxygenation (ECMO): a case report.

BACKGROUND: Gunshot wounds (GSW) to the heart are lethal, and most patients die before they arrive to the hospital. Survival decreases with number of cardiac chambers involved. We report a case of a 17-year-old male who survived a GSW injury involving two cardiac chambers with acute severe tricuspid regurgitation (TR) who subsequently developed cardiogenic shock requiring extracorporeal membrane oxygenation (ECMO) support. CASE PRESENTATION: A 17-year-old male sustained a single gunshot wound to the left chest, resulting in pericardial tamponade and right hemothorax. Emergency sternotomy revealed injury to the right ventricle and inferior cavoatrial junction with the adjacent pericardium contributing to a right hemothorax. The cardiac injuries were repaired primarily. Tricuspid regurgitation was confirmed immediately postoperatively. Five days after presentation, the patient developed cardiogenic shock secondary to TR requiring emergent stabilization with ECMO. He subsequently underwent successful tricuspid valve replacement. CONCLUSIONS: This is the first report to our knowledge of successful ECMO support of severe TR due to gunshot injury to the heart.

Alterations of pain pathways by experimental sleep disturbances in humans: central pain-inhibitory, cyclooxygenase, and endocannabinoid pathways.

STUDY OBJECTIVES: There is strong evidence that sleep disturbances are an independent risk factor for the development of chronic pain conditions. The mechanisms underlying this association, however, are still not well understood. We examined the effect of experimental sleep disturbances (ESDs) on three pathways involved in pain initiation/resolution: (1) the central pain-inhibitory pathway, (2) the cyclooxygenase (COX) pathway, and (3) the endocannabinoid (eCB) pathway. METHODS: Twenty-four healthy participants (50% females) underwent two 19-day long in-laboratory protocols in randomized order: (1) an ESD protocol consisting of repeated nights of short and disrupted sleep with intermittent recovery sleep; and (2) a sleep control protocol consisting of nights with an 8-hour sleep opportunity. Pain inhibition (conditioned pain modulation, habituation to repeated pain), COX-2 expression at monocyte level (lipopolysaccharide [LPS]-stimulated and spontaneous), and eCBs (arachidonoylethanolamine, 2-arachidonoylglycerol, docosahexaenoylethanolamide [DHEA], eicosapentaenoylethanolamide, docosatetraenoylethanolamide) were measured every other day throughout the protocol. RESULTS: The central pain-inhibitory pathway was compromised by sleep disturbances in females, but not in males (p < 0.05 condition × sex effect). The COX-2 pathway (LPS-stimulated) was activated by sleep disturbances (p < 0.05 condition effect), and this effect was exclusively driven by males (p < 0.05 condition × sex effect). With respect to the eCB pathway, DHEA was higher (p < 0.05 condition effect) in the sleep disturbance compared to the control condition, without sex-differential effects on any eCBs. CONCLUSIONS: These findings suggest that central pain-inhibitory and COX mechanisms through which sleep disturbances may contribute to chronic pain risk are sex specific, implicating the need for sex-differential therapeutic targets to effectively reduce chronic pain associated with sleep disturbances in both sexes. CLINICAL TRIALS REGISTRATION: NCT02484742: Pain Sensitization and Habituation in a Model of Experimentally-induced Insomnia Symptoms. https://clinicaltrials.gov/ct2/show/NCT02484742.