ARDS is a serious-onset and a progressive hypoxic illness that manifests through bilateral lung infiltration. The development of the condition increases rapidly following insults, traumas, or different illnesses. Diffuse alveolar damage is considered to be the main pathological result for ARDS (Han & Mallampalli, 2015).
The body’s immune reaction contributes significantly to ARDS pathophysiology. Tissue injury emerges due to different immunologic mechanisms that involve dendritic cells, macrophages, and neutrophils. Local or systemic inflammatory insults impair gas exchange and cause an edema fluid rich in protein to accumulate in the alveoli. In turn, this leads to hypoxemia due to the effect of the inflammation on the vascular endothelium, alveolar macrophages, and bronchial epithelium (Han & Mallampalli, 2015).
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The stimulation of alveolar macrophages leads to the recruitment of circulating macrophages and neutrophils to the injury’s pulmonary location. These cells propagate inflammatory reactions by influencing the elaboration of different bioactive mediators, such as cytokines, phospholipids, eicosanoids, reactive oxygen species, and proteases. These mediators harm or cause the alveolar type 2 epithelial cells to die. The inflammatory activities cause histological changes that significantly impair gas exchange and lung processes (Han & Mallampalli, 2015).
Alveolar macrophages coordinate during the early ARDS inflammatory stages to interact with mesenchymal stem cells, lymphocytes, and epithelial cells. In turn, this leads to tissue injury accentuation or inflammatory response intensification. Non-healing protracted ARDS emerges due to the proliferation of naturally triggered macrophage (M1) or alternatively triggered macrophage (M2) phenotypes (Han & Mallampalli, 2015).
ARDS occurs systematically and involves the lungs and other body organs. Both the circulating plasma and bronchoalveolar lavage fluid in patients increase due to inflammatory cytokines. For patients experiencing protracted and non-healing ARDS, both systemic immunosuppression and pulmonary inflammation occur concurrently. Autoantibodies also increase quickly during ARDS (Han & Mallampalli, 2015). Risk factors for ARDS, such as brain injury, sepsis, and traumatic brain injury, lead to systemic immunosuppression and robust inflammation in the lungs (Han & Mallampalli, 2015).
Aspiration Pneumonitis (AP) Pathophysiology
AP is a condition characterized by instant hypoxemia, tachycardia, fever, and chest radiograph abnormalities due to macroaspiration of noxious fluids. These liquids mainly entail sterile intestinal contents. The fluids may also include bile or other stomach substances (Son, Shin & Ryu, 2017).
Aspiration pneumonitis emerges due to macroaspiration of refluxed abdominal substances. Acid plays a vital role in the pathophysiology of AP. Acidic abdominal contents induce chronic pneumonitis in the lungs and lead to a distinctive biphasic reaction against an injury in the lung. Acid aspiration first corrodes the epithelium of the airway directly within 1 to 2 hours after aspiration due to the low pH. In turn, this leads to a neutrophilic inflammatory reaction 4 to 6 hours following aspiration. Following the acid aspiration, the lung processes are characterized by reactive oxygen species, interleukin-8 enzymes, tumor necrosis alpha, adhesion molecules, inflammatory cells, and inflammatory mediators due to neutrophils (Son, Shin & Ryu, 2017).
Intestinal substances include both food particles and acid. Food particles cause acute neutrophilic inflammation without causing a direct injury during the initial phases. The combined food substances and acid cause a more serious lung injury than injuries caused by acid alone (Son, Shin & Ryu, 2017).
Gastric substances are normally sterile. Fluctuations in intestinal pH, nevertheless, inhibit the growth of bacteria after the use of proton-pump inhibitors, H2-receptor antagonists, or antacids. In turn, this creates a suitable environment that can sustain potentially pathogenic bacteria. It can also lead to gastric colonization caused by gram-negative bacteria, particularly among patients using enteral feeding or among patients experiencing small-bowel obstruction or gastroparesis. In addition to the severe inflammation caused by food particles or acid, the occurrence of gastric aspiration in these situations can lead to lung infections due to bacterial load in intestinal substances (Son, Shin & Ryu, 2017).
References
Han, S., & Mallampalli, R. K. (2015). The acute respiratory distress syndrome: from mechanism to translation. The Journal of Immunology , 194 (3), 855-860.
Son, Y. G., Shin, J., & Ryu, H. G. (2017). Pneumonitis and pneumonia after aspiration. Journal of dental anesthesia and pain medicine , 17 (1), 1-12.
