ICU Clinical Summary

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Upon entering my second clinical rotation I was given a tour, along with my fellow nursing students, of St. Francis where I would be completing a rotation on a medical and surgical unit. As being our first day at the site we were taken on a tour of the entire facility. While doing the tour our group was allowed to enter the medical and surgical intensive care unit. In doing so, we were allowed to observe a client that was undergoing treatment for acute respiratory distress syndrome (ARDS). I was intrigued by the case, as the client was in a prone position and intubated. I had no prior experience with a client who has suffered from ARDS and wanted to learn what more this diagnosis meant for the client needing oxygenation in an acute …show more content…
In this particular article, the objective was to determine the effects of fever (temperatures above 38.3 degrees C) and nursing interventions to reduce its effects on client hemodynamics and oxygenation in surgical intensive care unit clients presenting febrile. Çelik et al.’s study (2011) took a retrospective and descriptive approach to a sample of 53 febrile clients from one hospital facility. ICU clientele are more likely to be in a febrile state when compared to their counterparts of hospitalized clients. Although fever is more likely due to infection, ICU clients may become febrile from numerous noninfectious …show more content…
near drowning, vasculitis, gastric aspiration) or nonpulmonary (e.g. sepsis, major trauma with shock, obstetric events) insults, with sepsis the leading cause. Associated risk factors for ARDS are: Afro-Caribbean ethnicity, age, chronic alcohol abuse, liver disease, pregnancy, obesity, immunosuppression, and genetic predisposition (Liew and Martin, 2014). ARDS is believed to be a direct or indirect injury to the lungs that triggers an inflammatory response, releasing numerous cytokines and activating neutrophils and alveolar macrophages (Liew and Martin, 2014). This increases capillary permeability and damages the alveolar epithelium, resulting in vast alveolar edema and surfactant production compromise (Liew and Martin, 2014). Clinical symptomatology includes acutely progressive dyspnea, tachypnea, and hypoxemia (Liew and Martin,
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