Article Contents ::
- 1 Details Descriptions About :: Acute Respiratory Distress Syndrome
- 2 Acute respiratory distress syndrome (ARDS) is a form of pulmonary edema that can quickly lead to acute respiratory failure. Also known as adult respiratory distress syndrome, shock lung, stiff lung, white lung, wet lung, or Da Nang lung, ARDS may follow direct or indirect injury to the lung. However, diagnosis is difficult; death can occur within 48 hours of onset if ARDS isn’t promptly diagnosed and treated.
- 3 Causes for Acute Respiratory Distress Syndrome
- 4 Pathophysiology Acute Respiratory Distress Syndrome
- 5 Signs and symptoms Acute Respiratory Distress Syndrome
- 6 Diagnostic Lab Test results
- 7 Treatment for Acute Respiratory Distress Syndrome
- 8 Disclaimer ::
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Details Descriptions About :: Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is a form of pulmonary edema that can quickly lead to acute respiratory failure. Also known as adult respiratory distress syndrome, shock lung, stiff lung, white lung, wet lung, or Da Nang lung, ARDS may follow direct or indirect injury to the lung. However, diagnosis is difficult; death can occur within 48 hours of onset if ARDS isn’t promptly diagnosed and treated.
Causes for Acute Respiratory Distress Syndrome
Causes Injury to the lung from trauma Sepsis Trauma-related factors, such as fat emboli, sepsis, shock, pulmonary contusions, and multiple transfusions Aspiration of gastric contents or diffuse pneumonia, especially viral pneumonia Anaphylaxis Drug overdose Idiosyncratic drug reaction to ampicillin or hydrochlorothiazide Inhalation of noxious gases, such as nitrous oxide, ammonia, or chlorine Near drowning Oxygen toxicity Coronary artery bypass grafting Hemodialysis Leukemia Acute miliary tuberculosis Pancreatitis Thrombotic thrombocytopenic purpura Uremia Venous air embolism
Pathophysiology Acute Respiratory Distress Syndrome
Pathophysiology Injury in ARDS involves both the alveolar epithelium and the pulmonary capillary epithelium. Damage can occur directly (by aspiration of gastric contents or inhalation of noxious gases) or indirectly (from chemical mediators released in response to systemic disease). The causative agent triggers a cascade of cellular and biochemical changes. After it’s initiated, this agent triggers neutrophils, macrophages, monocytes, and lymphocytes to produce various cytokines—which promote cellular activation, chemotaxis, and adhesion—and inflammatory mediators, including oxidants, proteases, kinins, growth factors, and neuropeptides, which initiate the complement cascade, intravascular coagulation, and fibrinolysis. These cellular events increase vascular permeability to proteins, increasing the hydrostatic pressure gradient of the capillary. Elevated capillary pressure, such as results from fluid overload or cardiac dysfunction, greatly increases interstitial and alveolar edema, which is evident on chest X-rays as whitened areas in the lower lung. Alveolar closing pressure then exceeds pulmonary pressures, and the alveoli begin to collapse. Exudative phase During the exudative phase, or phase 1, fluid accumulates in the lung interstitium, the alveolar spaces, and the small airways. This causes the lungs to stiffen, thus impairing ventilation and reducing oxygenation of the pulmonary capillary blood, which results in reduced blood flow to the lungs. Platelets begin to aggregate and release substances, such as serotonin, bradykinin, and histamine, which attract and activate neutrophils. Proliferative phase During the proliferative phase, or phase 2, the released substances inflame and damage the alveolar membrane and later increase capillary permeability. Additional chemotactic factors released include endotoxins, tumor necrosis factor, and interleukin-1. The activated neutrophils release several inflammatory mediators and platelet aggravating factors that damage the alveolar capillary membrane and increase capillary permeability, allowing fluids to move into the interstitial space. Next, as capillary permeability increases, proteins, blood cells, and more fluid leak out, increasing interstitial osmotic pressure and causing pulmonary edema. The resulting pulmonary edema and hemorrhage significantly reduce lung compliance and impair alveolar ventilation. Then, mediators released by neutrophils and macrophages also cause varying degrees of pulmonary vasoconstriction, resulting in pulmonary hypertension. The result of these changes is a mismatch in the ventilation-perfusion ratio. Although the patient responds with an increased respiratory rate, sufficient oxygen can’t cross the alveolar capillary membrane. Carbon dioxide continues to cross easily and is lost with every exhalation. Finally, pulmonary edema worsens and hyaline membranes form. Inflammation leads to fibrosis, which further impedes gas exchange. Fibrosis progressively obliterates alveoli, respiratory bronchioles, and the interstitium. Functional residual capacity decreases, and shunting becomes more serious. Hypoxemia leads to metabolic acidosis. At this final stage, the patient develops increasing partial pressure of arterial carbon dioxide (PaCO2), decreasing pH and partial pressure of arterial oxygen (PaO2), decreasing bicarbonate levels, and mental confusion. The end result is respiratory failure.
Signs and symptoms Acute Respiratory Distress Syndrome
Signs and symptoms Rapid, shallow breathing and dyspnea Increased rate of ventilation Intercostal and suprasternal retractions Crackles and rhonchi Restlessness, apprehension, and mental sluggishness Motor dysfunction Tachycardia Respiratory acidosis Metabolic acidosis
Diagnostic Lab Test results
Diagnostic test results Arterial blood gas (ABG) analysis with the patient breathing room air initially reveals a reduced PaO2 (less than 60 mm Hg) and a decreased PacO2 (less than 35 mm Hg). Hypoxemia, despite increased supplemental oxygen, is the hallmark of ARDS; the resulting blood pH reflects respiratory alkalosis. As ARDS worsens, ABG values show respiratory acidosis evident by an increasing PaCO2, (over 45 mm Hg), metabolic acidosis evident by a decreasing HCO3- (less than 22 mEq/L), and a declining PaO2, despite oxygen therapy. Clinical Tip It’s important to understand how ARDS differs from acute lung injury (ALI). Both have an acute onset, and patients have bilateral infiltrates on frontal chest radiograph and pulmonary artery wedge pressure (PAWP) less than or equal to 18 mm Hg or no clinical evidence of left atrial hypertension. The difference with ARDS is that the PaO2 is less than or equal to 200 mm Hg regardless of positive end-expiratory pressure (PEEP) level; with ALI, the PaO2 is less than or equal to 300 mm Hg regardless of PEEP level. Pulmonary artery catheterization may show a PAWP of 12 to 18 mm Hg, and pulmonary artery pressure may show decreased cardiac output. Serial chest X-rays in early stages show bilateral infiltrates; in later stages, long fields with a ground-glass appearance and “white outs” of both lung fields. Chest computed tomography reveals bilateral opacities, pleural effusions, and decreased lung volume. Sputum analysis, including Gram stain and culture and sensitivity, identifies causative organisms. Blood cultures identify infectious organisms. Toxicology testing reveals possible drug ingestion.
Treatment for Acute Respiratory Distress Syndrome
Treatment Therapy is focused on correcting the causes of ARDS and preventing progression of hypoxemia and respiratory acidosis. Treatment includes: intubation and mechanical ventilation humidified oxygen PEEP pressure-controlled inverse ratio ventilation high-frequency ventilation airway pressure release ventilation liquid ventilation inhaled nitric oxide permissive hypercapnia sedatives, opioids, and neuromuscular blockers high-dose corticosteroids sodium bicarbonate I.V. fluid administration or fluid restrictions vasopressors antimicrobial drugs diuretics correction of electrolyte and acid-base imbalances prone positioning extracorporeal membrane oxygenation surfactant administration.