Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) occurs within a critically ill individual who demonstrates failures within breathing due to essential illnesses. Though, acute respiratory distress syndrome is not defined as a precise disease and/or illness, “it is a life-threatening condition that occurs when there is a severe fluid buildup in both lungs. The fluid buildup prevents the lungs from working properly – that is, allowing the transfer of oxygen from air into the body and carbon dioxide out of the body into the air (“ARDS Acute Respiratory Distress Syndrome 2011).” The irritation found within the lungs and buildup of several fluids in the alveoli leads to low blood oxygen levels. Acute respiratory distress syndrome usually occurs in young individuals who are affected by major insults such as multiple trauma, sepsis and aspiration of gastric contents. Acute respiratory distress syndrome generally begins to expand within 24 to 48 hours of the injury or illness of the patient, and the period and/or intensity of ARDS varies within the patient. Also, the current mortality of acute respiratory distress syndrome remains moderately high at 35% to 50%. Outcome in acute respiratory distress syndrome (ARDS) is influenced by a number of factors, including the nature of the precipitating condition and the extent to which multiorgan failure ensues. Most studies of potential therapeutic interventions have been unsuccessful due to the enrollment of limited numbers of patients with a wide variety of pathologies of varying severity. Moreover, the value of initiating single-agent interventions at varying time points in what is an evolving and complex inflammatory process must be questioned (Evans 1999). Though there have been several “improvements in drug therapy, mechanical ventilation, hemodynamic management, more potent antibiotics, better prevention of complications (e.g., stress ulceration), better supportive care (e.g., nutrition), and more effective methods of weaning from ventilation (Russell and Walley 1999),” the mortality rate remains the same. However, there are a number of indications that the mortality rate of ARDS may be decreasing. “Despite these uncertainties, survival appears to be improving, possibly due to the application of-supportive techniques in a protocol driven fashion to patients in whom the underlying condition has been rigorously treated (Evans 1999).” Nevertheless, on a positive note, “the quality of life for survivors of ARDS is good with generally very good to excellent return of pulmonary function, good return to quality of life in many, and even preliminary reports of excellent return of quality of life in most (Russell and Walley 1999).”
Common symptoms of Acute Respiratory Distress Syndrome (ARDS): A number of early reports of Acute Respiratory Distress Symptom indicated that the majority of ARDS survivors were symptom free. “ARDS can occur in people with or without a previous lung disease. People who have a serious accident with a large blood loss are more likely to develop ARDS. However, only a small portion of people who have problems that can lead to ARDS actually develop it (“ARDS Acute Respiratory Distress Syndrome 2011).” In several cases, a patient who is already being treated for another major illness may obtain acute respiratory distress syndrome. As a result, doctors and other health care providers must focus on the symptoms of ARDS because, in some cases, the patient may be too weak and/or ill to complain or notice the symptoms identified. The key symptoms of acute respiratory distress syndrome are shortness of breath, fast and labored breathing, a bluish skin color – due to a low level of oxygen in the blood – and/or a lower amount of oxygen in the blood. If a patient shows signs of developing ARDS, doctors will do tests to confirm that ARDS is the problem (Villar, 2011).
ARDS is associated with diffuse alveolar damage (DAD) and lung capillary endothelial injury. The early phase is described as being exudative, whereas the later phase is fibroproliferative in character (Emedicine.medscape.com, 2018). Early ARDS is characterized by an increase in the permeability of the alveolar-capillary barrier, leading to an influx of fluid into the alveoli. The alveolar-capillary barrier is formed by the microvascular endothelium and the epithelial lining of the alveoli. Hence, a variety of insults resulting in damage either to the vascular endothelium or to the alveolar epithelium could result in ARDS. ARDS expresses itself as an inhomogeneous process. Relatively normal alveoli, which are more compliant than affected alveoli, may become overdistended by the delivered tidal volume, resulting in barotrauma. Alveoli already damaged by ARDS may experience further injury from the shear forces exerted by the cycle of collapse at end-expiration and expansion by positive pressure at the next inspiration (Emedicine.medscape.com, 2018). The acute phase of ARDS usually resolves completely. Less commonly, residual pulmonary fibrosis occurs, in which the alveolar spaces are filled with mesenchymal cells and new blood vessels. This process seems to be facilitated by interleukin (IL)-1. Progression to fibrosis may be predicted early in the course by the finding of increased levels of procollagen peptide III (PCP-III) in the fluid obtained by BAL. This and the finding of fibrosis on biopsy correlate with an increased mortality rate.
Upon diagnosis of ARDS, a person is hospitalized and given a treatment plan in an intensive care unit. Treatment for ARDS requires a mechanical ventilator and supplemental oxygen. As we learned in class, oxygen is generally the first thing given to any patient in the hospital with any sort of respiratory problem. IV fluids are given to the patient to provide nutrition and prevent dehydration, they are carefully monitored to prevent fluid from accumulating in the lungs (pulmonary edema). Inhaled drugs administered by a Respiratory Therapist will be given to open up the airways. These drugs are known as bronchodilators. Because infection has been found to often to be the underlying cause of ARDS, appropriate antibiotic therapy is administered. Corticosteroids may also sometimes be administered if the patient is in shock, but their use is controversial. An ABG will commonly be given to reveal hypoxemia (reduced levels of oxygen in the blood). A chest x-ray would be helpful in showing the presence of fluid in the lungs. Lastly, a bronchoscopy may be considered to evaluate the possibility of a lung infection.
The outlook for a person with ARDS has improved over the last twenty years and a majority of ARDS patients survive. People with a poorer outlook include those older than sixty five years old and those with sepsis as the underlying cause. The adverse effect of age may be related to the underlying health status of the patient. Survivors of ARDS may recover with normal lung function. However, some of them may have residual lung impairments or persistent muscle weakness. Typically, the lung dysfunction is mild, but ARDS can lead to severe lung damage and a reduced health-related quality of life. Severe disease and prolonged duration of mechanical ventilation are both predictors of persistent abnormalities in lung function (Emedicine.medscape.com, 2018).
Currently, in spite of the remarkable advancements in the understanding of its pathogenesis, the only effective therapeutic measure to decrease mortality is low-tidal volume mechanical ventilation and prone ventilation for severe ARDS cases. In extreme, life-threatening cases, ECMO seems to serve as a bridge to recovery and enables lung-protective ventilation. Most ARDS patients die of multi-organ failure rather than irreversible respiratory failure, indicating that ARDS is closely associated with other organs by neurological, biochemical, metabolic, and inflammatory reactions. Moreover, the lungs may play an important role in the development of non-pulmonary organ failure in ARDS. Thus, early recognition of ARDS modified risk factors and the avoidance of aggravating factors during the patient’s hospital stay (e.g., non-protective mechanical ventilation, multiple blood product transfusions, positive fluid balance, ventilator-associated pneumonia, and gastric aspiration) can help decrease its incidence. In addition, efficient antifibrotic strategies are still lacking for patients with late-stage ARDS. Therefore, new therapies that address the underlying pathophysiology are needed to reduce the mortality of patients with ARDS. (younsuck, 2014).
Emedicine.medscape.com. (2018). Acute Respiratory Distress Syndrome: Background, Pathophysiology, Etiology. online Available at: https://emedicine.medscape.com/article/165139-overview#a3 Accessed 29 Oct. 2018.
Kacmarek, R., Stoller, J. and Heuer, A. (2017). Egan’s fundamentals of respiratory care. St. Louis (Mo.): Elsevier.
Villar, J. (2011). What is the acute respiratory distress syndrome?. online pubmed.gov. Available at: https://www.ncbi.nlm.nih.gov/pubmed/22008395 Accessed 29 Oct. 2018.
younsuck, k. (2014). Update in acute respiratory distress syndrome. online Journal of Intensive Care. Available at: https://jintensivecare.biomedcentral.com/articles/10.1186/2052-0492-2-2#Sec2 Accessed 29 Oct. 2018.