Highlights
1. Patient background
Eileen Walker is an81-year-old woman who lives alone following her husband’s passing. She recently saw her general practitioner (GP)for treatment of a urinary tract infection (UTI),where she was prescribed oral cephalexin 250mg QID for ten days. For the last two days, Eileen states she has been experiencing shortness of breath,a productive cough, chills and hot flushes, nausea and, vomiting and muscle weakness. Eileen’s daughter, Nora, decided to bring her mother into the emergency department (ED) at Royal Perth Hospital (RPH) due to worsening symptoms and the onset of mental confusion and difficulty breathing. Nora disclosed to the triage nurse that Eileen has been forgetful with her medications and was therefore not compliant with taking her antibiotics when required, and has frequently missed doses.
2. Reason for admission
Due to the information gathered from the initial triage assessment, Eileen was promptlyadmitted to the ED for further investigation (Department of Health and Ageing, n.d.). Her vital signs were as follows: Respiratory rate (RR)of 26 (tachypnea), with labored breathingand the use of accessory muscles noted, peripheral capillary oxygen saturation (SP02)84% on room air (RA), blood pressure (BP) 94/60 (hypotension), heart rate (HR) 120 (tachycardia), tympanic temperature 38.9 degrees Celsius (°C). Due to Eileen’s ongoing and inadequately treated UTI, her high-grade fever is a significant concern as the infection has the potential to spread systemically (Doenges & Moorhouse, 2012; Warrell, 2012). Eileen also presented with an apparent decline in her functional and cognitive state. Based on this information, an urgent medical review was required (University of Technology Sydney, 2017).
3. Past medical/surgical history
Eileen’s medical history indicates she is likely to be more susceptible to disorders such as ARDS. There are several risk factors for the development of ARDS, including cigarette use and being of mature age and female gendered that relate to Eileen’s case (Zayed & Askari, 2019). She was a smoker for the majority of her adult life, significantly increasing her susceptibility for ARDS(Zayed & Askari, 2019). This is due to the alveolar damage prolonged smoking causes in the lungs (Yan et al., 2015).
Elieen is also classified as obese with a BMI of 41 (Tollefson & Hillman, 2018). This also increases the risk of ARDS development due to pathological changes in obese people (Hibbert, Rice & Malhotra, 2012). These changes include increased pleural pressures, decreased total, residual and vital capacity of the lungs as well as increased upper and lower resistance in the airway (Hibbert, Rice & Malhotra, 2012).
The previous medical history of ongoing UTIs also indicates that she is susceptible to infection (LeMone et al., 2017). Considering sepsis is the most common cause for ARDS onset, this is another significant risk factor for Eileen (LeMone et al., 2017).
4. Aetiology and Pathophysiology
The exact aetiology of ARDS in unclear, but it is known that it develops as a consequence of various conditions that adversely affect the lungs (LeMone et al., 2017). Theaetiology can be divided into direct and non-direct mechanisms (Zayed & Askari, 2019). Direct lung injury is associated with conditions such as near-drowning, aspiration, pneumonia, pulmonary contusion and inhalation injury (Saguil & Fargo, 2012; Zayed & Askari, 2019). Non-direct lung injury can result from trauma, burns, massive blood transfusion and non-pulmonary sepsis (Saguil & Fargo, 2012; Zayed & Askari, 2019). Sepsis is the most common cause for the onset of ARDS and accounts for approximately 79% of cases in adults (Saguil & Fargo, 2012).Sepsis is defined as a potentially fatal dysfunction of the organs secondary to an unregulated systemic response to infection, such as in Eileen’s case (Angus, 2016).
The pathophysiology of ARDS relates toan uncontrolledinflammatory response due to lung injury/inflammation (LeMone et al., 2017).ARDS is characterised by three distinct phases: the exudative, proliferative and fibrotic phase (Zayed & Askari, 2019).The exudative phase occurs within the first 24 hours of injury. In response to lung injury, inflammatory cellular responses and biochemical mediators are activated, causing damage to the capillary-alveolar membrane (LeMone et al., 2017). Thisincreased permeability leads to hemorrhage and the accumulation of fluid containing high concentrations of protein in the interstitial space, resulting in oedema (LeMone et al., 2017; Zayed & Askari, 2019). In stage two (proliferative phase), fluid enters the alveoli due to the comprised alveolar membrane and high interstitial pressure (LeMone et al., 2017). Once inside the alveoli, fluid dilation results in surfactant inactivation.This is due to the inflammatory response causing damage to the cells that produce surfactant in the epithelium. The surfactant deficiency results in the reduced compliancy of the lungs and gas exchange becomes impaired.(LeMone et al., 2017). Not all cases of ARDS progress to the fibroticphase. In this phase, fibrous tissue forms within the lungs which causes symptoms such as refractory hypoxemia (Zayed & Askari, 2019).
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