Acute Respiratory Distress Syndrome: A Lung Inflammation
The Acute Respiratory Distress Syndrome or ARDS is a major lung injury characterized by modifications in both lungs and comprises dispersion of epithelial cell injury with increased permeability of the alveolar-capillary membrane (Porth 715). It is often mistaken as an infection due to the accretion of edema fluids but it is actually a lung inflammatory injury. Twelve persons were reported in the first clinical account of this disease and seven or 60% percent of them died during that time. Records now show that 150,000 to 200, 000 people are affected by ARDS every year and 50%-60% of them die (Porth 715). Currently, it is the leading cause of acute respiratory failure in the United States. (Marino 419)
ARDS, through the years, gained different calls or names, all trying to identify the roots and results of the disease. It had been named shock lung, non-cardiogenic pulmonary edema, and adult respiratory distress syndrome (Marino 419). However, since the reports of children having the same symptoms and effects of the disease, the name was again changed, permanently, to acute respiratory distress syndrome.
Varied factors may cause the origin of ARDS in a patient. The disease may result from aspiration of gastric contents, major trauma (with or without emboil), sepsis secondary to pulmonary or non-pulmonary infections, acute pancreatitis, hematologic disorders, metabolic events, and reactions to drugs and toxins. (Porth 715)
Through the progress of ARDS, breathing gradually becomes a struggle for the patient for the reason that the lungs begins to become stiff and thus limits inflation. Different organs began to be affected as well, resulting to some predisposed clinical conditions. Eventually, ARDS is accompanied by one or more, or sometimes all, of the following: intracranial hypertension, blood products catheter sepsis drugs, pneumonia pulmonary contusion, cardio pulmonary bypass, pancreatitis, translocation endotoxemia, urosepsis amniotic fluid embolism, long bone fracture (Marino 421).
It was also observed that there comes an increased pulmonary shunting of blood, impaired gas exchange, and profound hypoxia in the development of the disease (Marino 715). In due course, if the injury is not treated, disordered epithelial repair may effect into fibrosis. The pathology or pathogenesis of ARDS came to be as vague and unclear to most people at first. However, Paul Marino said that the process undergone by the disease is actually a diffused inflammation:
The lung consolidation in ARDS is believed to originate from a systematic activation of circulating neutrophils. The activated neutrophils become sticky and adhere to the vascular endothelium in the pulmonary capillaries. The neutrophils then release the contents of their cytoplasmic granules, and this damages the endothelium and leads to a leaky-capillary type of exudation into the lung parenchyma. Neutrophils and proteinaceous material gain access to the lung parenchyma and fill the alveolar air spaces. (420-421)
Cure for ARDS had been difficult to find due to multiple organ failure that joins it. However, after approximately 40 years of study, a solution for a more significant survival rate from the disease was found; low tidal volume mechanical ventilation. Although mechanical ventilation is the key process in treating ARDS, it is later found out to be harmful to the lungs. That is where low tidal volume mechanical ventilation comes in. Inflation volumes are delivered into the patient’s lungs that have a marked reduction in functional volume (Marino 426). However, in delivering oxygen, certain ideas standing as objectives are considered. Porth clearly states it in her book, “The treatment goals in ARDS are to supply oxygen to vital organs and provide supportive care until the condition causing the pathologic process has been reversed and the lungs have had a chance to heal” (716).
Low tidal volume mechanical ventilation procedure for ARDS patients are secured and tested by different organizations. The most successful of these tests being the trial conducted by the ARDS Clinical Network which is joined by a total of 800 patients.
Recently, some similar patterns of ARDS are found in a volume-related injury caused by overdistention and rupture of the distal airspaces. It is identified by the name ventilation-induced lung injury (VILI). As its name implies, VILI is brought upon by the use of normal mechanical ventilation in the lungs. Excessive inflation volumes producing stress fractures in the alveolar capillary interface leading to infiltration of the distal airspaces with inflammatory cells and proteinacous material causes this injury (Marino 427). It is to note that VILI is observed from ARDS patients who utilize a common method of mechanical ventilation for their treatment.
Marino, Paul L. The ICU Book Third Edition. Lippincott Williams & Wilkins, 2006.
Porth, Carol Mattson. Pathophysiology: Concepts of Altered Health States 7th Edition. Lippincott Williams & Wilkins, 2004.