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Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by injury to the lungs. It is characterized by inflammation and fluid in the lungs, preventing enough oxygen from entering the bloodstream. The Berlin Definition provides criteria for diagnosing ARDS based on timing of symptoms, chest imaging findings, origin of edema, and level of hypoxemia. Treatment involves supportive care in an intensive care unit, including mechanical ventilation, maintaining fluid balance, antibiotics, and sometimes corticosteroids. The goal is to keep oxygen levels in an adequate range using the lowest possible pressures and oxygen levels.
Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by injury to the lungs. It is characterized by inflammation and fluid in the lungs, preventing enough oxygen from entering the bloodstream. The Berlin Definition provides criteria for diagnosing ARDS based on timing of symptoms, chest imaging findings, origin of edema, and level of hypoxemia. Treatment involves supportive care in an intensive care unit, including mechanical ventilation, maintaining fluid balance, antibiotics, and sometimes corticosteroids. The goal is to keep oxygen levels in an adequate range using the lowest possible pressures and oxygen levels.
Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by injury to the lungs. It is characterized by inflammation and fluid in the lungs, preventing enough oxygen from entering the bloodstream. The Berlin Definition provides criteria for diagnosing ARDS based on timing of symptoms, chest imaging findings, origin of edema, and level of hypoxemia. Treatment involves supportive care in an intensive care unit, including mechanical ventilation, maintaining fluid balance, antibiotics, and sometimes corticosteroids. The goal is to keep oxygen levels in an adequate range using the lowest possible pressures and oxygen levels.
Description • Acute respiratory distress syndrome (ARDS) is a systemic process that is considered to be the pulmonary manifestation of multiple organ dysfunction syndrome. • It is characterized by noncardiac pulmonary edema and disruption of the alveolarcapillary membrane as a result of injury to either the pulmonary vasculature or the airways The Berlin Definition of ARDS is as follows • Timing—within 1 week of known clinical insult or new or worsening respiratory symptoms • Chest imaging—bilateral opacities not fully explained by effusions, lobar/lung collapse or nodules • Origin of edema—respiratory failure not fully explained by heart failure or fluid overload; need objective assessment to exclude hydrostatic edema if no risk factor present • Oxygenation—mild (200 mg Hg less than Pao2/Fio2 less than or equal to 300 mm Hg with positive end-respiratory airway pressure [PEEP] or constant positive airway pressure [CPAP] greater than or equal to 5 cm H2O); Moderate (100 mg Hg less than Pao2/Fio2 less than or equal to 200 mm Hg with PEEP greater than or equal to 5 cm H2O); or Severe (Pao2/Fio2 less than or equal to 100 mm Hg with PEEP greater than or equal to 5 cm H2O) Etiology • These are categorized as direct or indirect, depending on the primary site of injury (Box 20-5). • Direct injuries are those in which the lung epithelium sustains a direct insult. Indirect injuries are those in which the insult occurs elsewhere in the body and mediators are transmitted via the bloodstream to the lungs. • Sepsis, aspiration of gastric contents, diffuse pneumonia, and trauma were found to be major risk factors for the development of ARDS Pathophysiology • Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells • Increased permeability of alveolar capillary membrane • Influx of protein rich edema fluid,blood cells, inflammatory cells into alveoli • Dysfunction of surfactant • Alveoli collapse(atelektasis) fibrotic • Lungs become stiff, less compliant, very hard to inspire • Decrease in gas exchange /shunted Hypoxia STAGES 1. Exudative (acute) phase - 0- 4 days 2. Proliferative phase - 4- 8 days 3. Fibrotic phase - >8 days 4. Recovery Clinical Manifestation • Rapid onset of severe dyspnea • ABG’s • with in 12-48 hours PaO2 < 70mmHg • Intercostal and suprasternal PaCO2 > 45 retractions HCO3 • Increased resp rate • Normal • Hypoxemia that does not respond to • < 22 O2 pH • Confusion anxiety • low • Restlessness Analysis • Cyanosis • Resp. and met. Acidosis • Fever Complication • Lung damage (such as pneumothorax) due to use of high settings on the breathing machine needed to treat the disease • Multiple organ system failure • Pulmonary fibrosis • Ventilator-associated pneumonia Diagnostic Test • Arterial blood gas analysis reveals hypoxemia (reduced levels of oxygen in the blood) • A complete blood count may be taken. The number of white blood cells is increased in sepsis • Chest x-ray will show the presence of fluid in the lungs • CT scan of the chest may be required only in some situations (routine chest x-ray is sufficient in most cases) • Echocardiogram (an ultrasound of the heart) may help exclude any heart problems that can cause fluid build-up in the lung Diagnostic Test • Monitoring with a pulmonary artery catheter may be done to exclude a cardiac cause for the difficulty in breathing. • Bronchoscopy (a procedure used to look large airways of the lung) may be considered to evaluate the possibility of lung infection • Sputum cultures and analysis MANAGEMENT INTENSIVE CARE UNIT • O2 Intubation and mechanical vent • Give lowest possible level of O2 to prevent toxicity • Higher airway pressures usually necessary • PEEP may be indicated • Maintain PaO2 at > 60mm Hg • Potitioning and chest fisioterapi • Increase cardiac output and maintain blood pressure • Fluid therapy • Dobutrex, dobutamine • Maintenance of fluid balance • Diuretics may be indicated Diuretics may be indicated MANAGEMENT • Surfactant replacement • Corticosteroids • Antibiotis • Sedatives • Diuretics SELECT PEEP • PEEP/FiO2 relationship to maintain adequate PaO2/SpO2 • PaO2 goal: 55-80mmHg or SpO2 88-95% use FiO2/PEEP combination to achieve oxygenation goal