Acute respiratory distress syndrome is a type of noncardiogenic pulmonary edema caused by diffuse alveolar injury. This diffuse alveolar injury is secondary to an inflammatory process. Inflammation can occur as a direct injury to the lungs or as an indirect injury from systemic causes.
According to the Berlin criteria: ARDS defined by time (within 1 week of the onset of clinical injury or respiratory symptoms); imaging changes (bilateral cloudiness not fully explained by effusion, solidity or pulmonary atelectasis); origin of edema (not fully explained by heart failure or fluid overload); and severity based on the PaO2/FiO2 ratio of 5 cm continuous positive airway pressure ventilation (CPAP). 3 categories are mild (PaO2/FiO2 200-300), moderate (PaO2/FiO2 100-200), and severe (PaO2/FiO2 ≤100).
Acute respiratory distress syndrome: definition (Berlin)
Etiology
Most cases are attributed to pneumonia and sepsis (40-60%).
The clinical conditions usually associated with ARDS can be divided into two types:
Direct lung injury
Pneumonia
aspiration of gastric contents by mistake
Pulmonary contusion
Drowning
Toxic inhalation injury
Indirect lung injury
Sepsis
Long bone fracture (fat embolism)
Amniotic fluid embolism
Multiple blood transfusions
Drug overdose
Pancreatitis
Acute respiratory distress syndrome: etiology
Pathogenesis
ARDS is divided into three phases: the exudative, proliferative and fibrotic phases. They all have characteristic clinical and pathological features
Exudative phase
During this phase, alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells) are damaged and the tight alveolar barrier is compromised, preventing the entry of fluid and macromolecules. Protein-rich edema fluid accumulates in the interstitial and alveolar spaces. Pro-inflammatory cytokines increase during this acute phase, leading to the recruitment of leukocytes (especially neutrophils) into the interstitial and alveolar spaces of the lungs. Plasma proteins aggregate in the airspace with cellular debris and dysfunctional pulmonary surfactants to form intra-alveolar hyaline membranes. Alveolar edema primarily involves the ventilation-dependent portion of the lung that is reduced. Collapse of large pieces of accessory lung leads to reduced lung compliance. It leads to intrapulmonary shunts and hypoxemia, and increased respiratory work done, resulting in dyspnea.
The exudative phase includes the first 7 days of illness after exposure to risk factors that trigger ARDS. The shortness of breath and increased respiratory effort often lead to respiratory fatigue and eventually to respiratory failure.
Proliferative phase
This phase of ARDS usually lasts from day 7 to day 21. Most patients recover rapidly during this phase and are taken off mechanical ventilation. Despite this improvement, many patients continue to experience dyspnea, shortness of breath, and hypoxemia. Histologically, the initial signs of regression are usually evident during this phase as pulmonary repair begins, alveolar exudate becomes organized, and the transition from a neutrophil-dominated to a lymphocyte-dominated pulmonary infiltrate occurs.
As part of the repair process, type II pneumocytes proliferate along the alveolar basement membrane. These specialized epithelial cells synthesize new lung surface active substances and differentiate into type I pneumocytes.
Fibrotic phase
Most patients with ARDS regain lung function within 3-4 weeks, with a very small number of patients progressing to the fibrotic stage, which may require long-term support with mechanical ventilators and/or supplemental oxygen. Extensive alveolar ductal and interstitial fibrosis is present. Significant disruption of alveolar structures results in emphysema-like changes with large alveoli.
Intimal fibroproliferation in the pulmonary microcirculation leads to progressive vascular occlusion and pulmonary hypertension. Physiological consequences include increased risk of pneumothorax, decreased pulmonary compliance, and increased pulmonary dead space.
According to the Berlin criteria: ARDS defined by time (within 1 week of the onset of clinical injury or respiratory symptoms); imaging changes (bilateral cloudiness not fully explained by effusion, solidity or pulmonary atelectasis); origin of edema (not fully explained by heart failure or fluid overload); and severity based on the PaO2/FiO2 ratio of 5 cm continuous positive airway pressure ventilation (CPAP). 3 categories are mild (PaO2/FiO2 200-300), moderate (PaO2/FiO2 100-200), and severe (PaO2/FiO2 ≤100).
Acute respiratory distress syndrome: definition (Berlin)
Etiology
Most cases are attributed to pneumonia and sepsis (40-60%).
The clinical conditions usually associated with ARDS can be divided into two types:
Direct lung injury
Pneumonia
aspiration of gastric contents by mistake
Pulmonary contusion
Drowning
Toxic inhalation injury
Indirect lung injury
Sepsis
Long bone fracture (fat embolism)
Amniotic fluid embolism
Multiple blood transfusions
Drug overdose
Pancreatitis
Acute respiratory distress syndrome: etiology
Pathogenesis
ARDS is divided into three phases: the exudative, proliferative and fibrotic phases. They all have characteristic clinical and pathological features
Exudative phase
During this phase, alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells) are damaged and the tight alveolar barrier is compromised, preventing the entry of fluid and macromolecules. Protein-rich edema fluid accumulates in the interstitial and alveolar spaces. Pro-inflammatory cytokines increase during this acute phase, leading to the recruitment of leukocytes (especially neutrophils) into the interstitial and alveolar spaces of the lungs. Plasma proteins aggregate in the airspace with cellular debris and dysfunctional pulmonary surfactants to form intra-alveolar hyaline membranes. Alveolar edema primarily involves the ventilation-dependent portion of the lung that is reduced. Collapse of large pieces of accessory lung leads to reduced lung compliance. It leads to intrapulmonary shunts and hypoxemia, and increased respiratory work done, resulting in dyspnea.
The exudative phase includes the first 7 days of illness after exposure to risk factors that trigger ARDS. The shortness of breath and increased respiratory effort often lead to respiratory fatigue and eventually to respiratory failure.
Proliferative phase
This phase of ARDS usually lasts from day 7 to day 21. Most patients recover rapidly during this phase and are taken off mechanical ventilation. Despite this improvement, many patients continue to experience dyspnea, shortness of breath, and hypoxemia. Histologically, the initial signs of regression are usually evident during this phase as pulmonary repair begins, alveolar exudate becomes organized, and the transition from a neutrophil-dominated to a lymphocyte-dominated pulmonary infiltrate occurs.
As part of the repair process, type II pneumocytes proliferate along the alveolar basement membrane. These specialized epithelial cells synthesize new lung surface active substances and differentiate into type I pneumocytes.
Fibrotic phase
Most patients with ARDS regain lung function within 3-4 weeks, with a very small number of patients progressing to the fibrotic stage, which may require long-term support with mechanical ventilators and/or supplemental oxygen. Extensive alveolar ductal and interstitial fibrosis is present. Significant disruption of alveolar structures results in emphysema-like changes with large alveoli.
Intimal fibroproliferation in the pulmonary microcirculation leads to progressive vascular occlusion and pulmonary hypertension. Physiological consequences include increased risk of pneumothorax, decreased pulmonary compliance, and increased pulmonary dead space.
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