Acute Respiratory Distress Syndrome and its managment

ARDS

1. ARDS

2. ARDS DEFINATION ARDS is characterized by the acute onset of hypoxemia and bilateral pulmonary infiltrates consistent with pulmonary edema but without evidence of left heart failure C haracterized by: - diffuse alveolar - capillary wall injury - increased alveolar- capillary permeability - noncardiogenic pulmonary edema - hyaline membrane formation, and atelectasis

3. PATHOPHYSIOLOGY The physiologic reaction of all body tissues sometimes results in pathologic changes in the lung A systemic insults causes low tissue perfusion and cellular hypoxia Consequently, peripheral tissues are deprived of essential nutrients, and intracellular metabolic derangements result Certain chemical factors such as prostaglandins, clotting factors, lysosomal enzymes, activated complement, or histamine are released into the systemic circulation Prostaglandin contribute to vasodilation, capillary permeability, pain and fever, which accompany cell injury Changes in the vessel walls and disturbances in blood flow increase platelet function, causing adhesiveness and aggregation

4. PATHOPHYSIOLOGY CONTINU.. Lysosomal enzymes from neutrophils increase vascular permeability and cause tissue damage Histamine is released from platelets, mast cell, and basophils and cause arterial vasodilation and enhanced permeability of capillaries and venules Neutrophils and other inflammatory mediators can thus gain access to the lung parenchyma and carry on the inflammatory process The inflammation then produces the lung injury, Severe ventilation-perfusion mismatching occurs Alveolar collapse of the inflammatory infiltrate, blood fluid and surfactant dysfunction

5. PATHOPHYSIOLOGY CONTI.. The lung compliance becomes markedly decreased (stiff lung) The blood returning to the lung for gas exchange is pumped through the nonventilated, nonfunctioning areas of the lung, causing a shunt to develop The blood interfacing with nonfunctioning alveoli and gas exchange is markedly impaired, resulting in severe refractory hypoxemia

6. REVISION OF DEFINITION 1988 Four-Point L ung I njury Score: Level of PEEP PaO2 / FiO2 ratio Static lung compliance Degree of chest infiltrates

7. INICIATING/PREDOSPOSING FACTORS Aspiration of (Gastric Secretion, drowning, hydrocarbons) Hematologic disorders (disseminated intravascular coagulopathy (DIC) , Massive transfusion of blood products, cardiopulmonary bypass Prolonged inhalation of high concentration of oxygen, smoke, or corrosive substances, Toxic Gases and Fumes Systemic Sepsis Drugs and poisons Shock (any cause)

8. INICIATING/PREDOSPOSING FACTORS Localized infection (Bacterial, F ungal, V iral Pneumonias), Trauma (Pulmonary contusion, Multiple F racture, Head injury) Major surgery Metabolic disorders (Pancreatitis, Uremia) Urosepsis, A mniotic fluid embolism Long bone fracture Fat or air embolism

9. ETIOLOGY Examples of common causes of ARDS include: Breathing vomit into the lungs (aspiration) Inhaling toxic chemicals Pneumonia Septic shock or sepsis Trauma

10. PHASES OF ARDS   1. Acute, Exudative P hase R apid onset of respiratory failure after trigger Diffuse alveolar damage with inflammatory cell infiltration hyaline membrane formation C apillary injury P rotein-rich edema fluid in alveoli D isruption of alveolar epithelium

11. PHASES OF ARDS CONT.. 2. Subacute, Proliferative P hase: P ersistent hypoxemia D evelopment of hypercarbia F ibrosing alveolitis F urther decrease in pulmonary compliance P ulmonary hypertension

12. PHASES OF ARDS CONTI… 3. RESOLUTION OR RECOVERY PHASE Recovery phase Gradual resolution of hypoxemia I mproved lung compliance R esolution of radiographic abnormalities

13. CLINICAL FEATURES OF ARDS The Earliest C linical signs of ARDS include: T achypnea and progressive hypoxemia Within 24 hours, the chest x-ray begins to Reveal B ilateral P ulmonary infiltrates Progression to mechanical ventilation often occurs in the first 48 hours of the illness

14. MANAGEMENT OF ARDS Treat the underlying Cause Maintaining Tissue Oxygenation Drug Therapy Lung Protective Strategies Reducing Lung Water Specific Therapies

15. Maintaining Tissue Oxygenation Safest FiO2 Optimal PEEP Inverse Ratio Ventilation Early Prone Position ECMO

16. Drug Therapy Antibiothetics Steroids Gastrokinetics Thromboprophylaxis Sedatives Analgesics Neuromuscular block Agent Nutrition

17. Lung Protective Strategies Lung protective Ventilation Low Tidal volume and High RR (Baby Lung Ventilation) Lung Mechanics Monitoring (Peak Pressure, Plateau Pressure, Driving Pressure,) Lung Compliance Permissive Hypercapnia

18. Reducing Lung Water The two measures that are advocated for reducing lung water are diuretics and PEEP Unfortunately , neither measure is likely to be effective in ARDS ( F ew Studies) The application of PEEP does not reduce extra vascular lung water in ARDS The use of diuretics to minimize or reduce fluid overload seems a more reasonable measure, but only when renal water excretion is impaired (otherwise the best way to prevent fluid overload is to maintain an adequate cardiac output) Positive End-Expiratory Pressure In fact, high levels of PEEP can actually increase lung water (Right Heart failure) This latter effect may be the result of alveolar overdistension, or may be the result of PEEP-induced impairment of lymphatic drainage from the lungs

19. Specific Therapies Surfactant: Aerosolized surfactant has proven effective in improving outcomes in the neonatal form of respiratory distress syndrome, but it has not met with similar success in adults with ARDS (Anzueto 1996). Antioxidant: Neutrophil-mediated tissue injury may play an important role in the pathogenesis of ARDS, it is no surprise that there is conciderable interest in the possible role of antioxidants as a specific therapy for ARDS Nitric oxide: Nitric Oxide can improve oxygenation and reduce pulmonary artery pressures in ARDS, mortality is unchanged (Lunn 1995) Nitric oxide is a pulmonary vasodilator, which inhaled crosses the alveolar membrane and acts locally on the pulmonary vasculature, dilating vessels and increasing blood flow

20. Specific Therapies 4. P rone Position: Study shows that prone positioning significantly improves oxygenation in about 65 of patients. This help in reduce the percentage of inspired oxygen and positive end-expiratory pressure. Prone therapy assists pts with ARDS by reducing the ventilation\perfusion mismatch 5. ECMO

21. SUMMARY ARDS Definition SIGN AND SYMPTOMS AIM OF MANAGEMENT OPTIMAL TISSUE OXYGENATION (At lowest possible FiO2 and Optimal Peep, Inverse Ration Ventilation and Prone Position) LUNG PROTECTIVE VENTILATION (ARDs.net) Low Tidal and High RR Optimal PEEP Peak Pressure <45 Plateau Pressure <30 Driving Pressure < 15 Permissive hypercapnia Ph >7.15 PO2 > 55mmhg ECMO

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