Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.



Published on

a complete brief of ARDS

Published in: Health & Medicine
  • Be the first to comment


  1. 1. Acute Respiratory Distress Syndrome (ARDS) Dr. Md. Monirul Islam MS Resident (Phase –B) Orthopaedic Surgery , BSMMU
  2. 2. Outline • Introduction • Definition • Etiology / Risk Factors • Pathology & Pathogenesis • Clinical presentation • Workup • Management of ALI/ARDS • Prognosis • Conclusion
  3. 3. Introduction  ARDS is a clinical devastating syndrome that affects both medical and surgical patients.  Despite great advances in understanding the pathogenesis of disease mortality rate is still high.  Even survivors of ARDS usually experience long ICU stay, hospital stay and several co- morbidities.  Moreover survivors require prolonged rehabilitation time till full recovery.
  4. 4. ARDS: What Is It? Term Acute respiratory distress syndrome was first described in 1967 by Ashbaugh and colleagues. Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid resulting in severe dyspnea, hypoxemia and diffuse pulmonary infiltrates In brief - Acute respiratory failure with non- cardiogenic pulmonary edema, capillary leak after diverse insult
  5. 5. ARDS is also referred with variety of terms like • Stiff Lung • Shock lung • Wet lung • Post traumatic lung • Adult respiratory distress syndrome • Adult hyaline membrane disease • Capillary leak syndrome & • Congestive atelectasis.
  6. 6. Diagnostic Criteria  Acute onset  Bilateral CXR infiltrates  PA pressure < 18 mm Hg  PaO2 : FiO2 < 200 - 1994 American - European Consensus Conference
  7. 7. Clinical Disorders Associated with ARDS Direct Lung Injury Indirect Lung Injury Common causes Common Causes Pneumonia Sepsis Aspiration of gastric contents Severe trauma with shock , multiple transfusions Less common causes Less common causes Pulmonary contusion Cardiopulmonary bypass Fat emboli Drug overdose Near-Drowning Acute pancreatitis Inhalational injury Transfusions of blood products Reperfusion pulmonary edema
  8. 8. Factors Influencing Risk of ARDS • Chronic alcohol abuse, • Hypoproteinemia, • Advanced age, • Increased severity, and extent of injury or illness as measured by injury severity score (ISS) or APACHE score, • Hypertransfusion of blood products, • Cigarette smoking
  9. 9. Pathology and Pathophysiology • In normal, healthy lungs there is a small amount of fluid that leaks into the interstitium.  The lymphatic system removes this fluid and returns it into the circulation keeping the alveoli dry.
  10. 10. • ARDS is a consequence of an alveolar injury which produces diffuse alveolar damage.   The injury causes the release of pro-inflammatory “cytokines”. • Cytokines recruit neutrophils to the lungs, where they become activated and release toxic mediators (eg, reactive oxygen species and proteases) that damage the capillary endothelium and alveolar epithelium.
  11. 11. • Damage to the capillary endothelium and alveolar epithelium allows protein to escape from the vascular space.
  12. 12. The oncotic gradient that favors resorption of fluid is lost and fluid pours into the interstitium, overwhelming the lymphatic system.
  13. 13. Breakdown of the alveolar epithelial barrier allows the air spaces to fill with bloody, proteinaceous edema fluid and debris from degenerating cells. In addition, functional surfactant is lost, resulting in alveolar collapse.
  14. 14. • Healthy lungs regulate the movement of fluid to maintain a small amount of interstitial fluid and dry alveoli. • Lung injury interrupts this balance causing excess fluid in both the interstitium and alveoli.
  15. 15. Results of the excess fluid include impaired gas exchange, decreased compliance, and increased pulmonary arterial pressure.
  16. 16. NORMAL ALVEOLUS Type I cell Endothelial Cell RBC’s Capillary Alveolar macrophage Type II cell
  17. 17. ACUTE PHASE OF ARDS Type I cell Endothelial Cell RBC’s Capillary Alveolar macrophage Type II cell Neutrophils
  18. 18. SCHEMATIC REPRESENTATION OF PATHOPHYSIOLOGY OF ARDS Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli 18 Lung injury Release of Vasoactive substances (serotonin, histamine, bradykinin) Damaged Type II alveolar cell Surfactant production Alveolocapillary membrane permeability Vascular narrowing & obstruction Alveolar Compliance and recoil Bronchoconstriction Outward migration of blood cells & fluids from capillaries Atelectasis Pulmonary Edema Hyaline membrane formation Lung compliance Impairment in gas exchange ARDS Pulmonary hypertension
  19. 19. Abnormalities in Gas Exchange Hypoxemia : HALLMARK of ARDS • Increased capillary permeability • Interstitial and alveolar exudate • Surfactant damage • Decreased FRC • Diffusion defect and right to left shunt
  20. 20. Stages : • Three distinct stages (or phases) of the syndrome including:   Exudative Stage   Proliferative (or fibroproliferative) stage   Fibrotic stage
  21. 21. Exudative Stage (0-6 Days)  Characterized by:  • Accumulation of excessive fluid in the lungs due to exudation (leaking of fluids) and acute injury.  • Hypoxemia is usually most severe during this phase of acute injury, as is injury to the endothelium (lining membrane) and epithelium (surface layer of cells). • Some individuals quickly recover from this first stage; many others progress after about a week into the second stage.
  22. 22. Proliferative Stage (7-10 Days)  • Connective tissue and other structural elements in the lungs proliferate in response to the initial injury, including development of fibroblasts • The terms "stiff lung" and "shock lung" frequently used to characterize this stage. • Abnormally enlarged air spaces and fibrotic tissue (scarring) are increasingly apparent.
  23. 23. Fibrotic Stage ( >10-14 Days)  • Inflammation resolves.  • Oxygenation improves and extubation becomes possible. • Lung function may continue to improve for as long as 6 to 12 months after onset of respiratory failure, depending on the precipitating condition and severity of the initial injury. • Varying levels of pulmonary fibrotic changes are possible.
  24. 24. CLINICAL PRESENTATION • Development of acute dyspnea and hypoxemia within hours to days of an inciting event • Tachypnea, tachycardia, and the need for a high fraction of inspired oxygen (FiO2) to maintain oxygen saturation. • Confusion • Extreme tiredness
  25. 25. CLINICAL PRESENTATION • Change in patient’s behavior :Mood swing,Disorientation .. • Think frothy sputum • Febrile or hypothermic. • Sepsis-hypotension and peripheral vasoconstriction with cold extremities  • Manifestations of the underlying cause
  26. 26. • WORK UP
  27. 27. Approach to Clinical Diagnosis • Chest Radiograph -diffuse, bilateral alveolar infiltrates consistent with pulmonary edema • cardiogenic edema: increased heart size, increased width of the vascular pedicle, vascular redistribution toward upper lobes, the presence of septal lines, or a perihilar (“bat’s wing”) distribution of the edema • Lack of these findings, in conjunction with patchy peripheral infiltrates that extend to the lateral lung margins, suggests ARDS
  28. 28. Cardiogenic Non-Cardiogenic Bilateral infiltrates predominately in lung bases. Kerley B’s. Cardiomegaly. Diffuse Bilateral patchy infiltrates homogenously distributed throughout the lungs. No Kerley B’s.
  29. 29. Cardiogenic v/s non cardiogenic edema • Patchy infiltrates in bases • Effusions + • Kerley B lines + • Cardiomegaly + • Pulmonary vascular redistribuition • Excess fluid in alveoli • Homogenous pluffy shadows • Effusions – • Kerley B lines – • Cardiomegaly – • No pulm.vascular redistribuition • Protein,inflammatory cells,fluid cardiogenic Non-cardiogenic
  30. 30. ARDS early late
  31. 31. Cardiogenic Non-Cardiogenic No septal thickening. Diffuse alveola infiltrates. Atelectasis of dependent lobes usually seen . Septal thickening. More severe in lung bases.
  32. 32. Arterial blood gas analysis • PaO2/FiO2 Ratio  ARDS Severity   PaO2/FiO2  •  Mild 200 – 300 • Moderate 100 – 200 • Severe < 100 • respiratory alkalosis. • However, in ARDS occurring in the context of sepsis, a metabolic acidosis with or without respiratory compensation may be present. • As the condition progresses and the work of breathing increases, the partial pressure of carbon dioxide (PCO2) begins to rise and respiratory alkalosis gives way to respiratory acidosis
  33. 33. To exclude cardiogenic pulmonary edema • Echocardiogram -left ventricular ejection fraction, wall motion, and valvular abnormalities • plasma B-type natriuretic peptide (BNP) value. • CT scan of the Chest
  34. 34. Hematologic • Septic patients -leukopenia or leukocytosis. Thrombocytopenia (DIC). • Renal function Test - Acute tubular necrosis • Liver function Test - hepatocellular injury or cholestasis. • Von Willebrand factor (VWF) may be elevated in patients at risk for ARDS and may be a marker of endothelial injury • Cytokines - (IL)–1, IL-6, and IL-8, are elevated 
  35. 35. • Invasive HemodynamicMonitoring- pulmonary artery wedge pressure (PCWP • Bronchoalveolar Lavage- to rule in or rule out acute processes that may have specific therapies.(eg: acute eosinophilic pneumonia, diffuse alveolar hemorrhage,
  36. 36. Histologic Findings • Typical histological findings in ARDS  alveolar inflammation, thickened septal from protein leak (pink), congestion and decreased alveolar volume ←←Normal LungNormal Lung Histology—largeHistology—large alveolar volumes, septal spacesalveolar volumes, septal spaces very thin, no cellular congestion.very thin, no cellular congestion. Hyaline Protein in air spaces Cellular Congestion
  37. 37. MANAGEMENT
  38. 38. ARDS - Principles of Therapy • Provide adequate gas exchange • Avoid secondary injury
  39. 39. Goals of Management of Patients with ARDS • Treatment of respiratory system abnormalities • Diagnose and treat the precipitating cause of ARDS • Maintain oxygenation • Prevent ventilator-induced lung injury (VILI) by using a low tidal volume ventilatory strategy • Keep pH in normal range without compromising goal to prevent VILI
  40. 40. • Enhance patient-ventilator synchrony and patient comfort by use of sedation, amnesia, opioid analgesia, and pharmacological paralysis, if necessary • Liberate or wean from mechanical ventilation when patient can breathe without assisted ventilation • Treatment of non-respiratory system abnormalities • Support or treat other organ system dysfunction or failure • General critical care • Adequate early nutritional support • Prophylaxis against deep vein thrombosis (DVT) and gastrointestinal (GI) bleeding
  41. 41. MEDICAL MANAGEMENT • Persons with ARDS are hospitalized and require treatment in an intensive care unit. • No specific therapy for ARDS exists. • Supportive measures :  Supplemental oxygen  Mechanical respirator  Positioning strategies Turn the patient from supine to prone. Another position is lateral rotation therapy • Fluid therapy Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli
  42. 42. MEDICAL MANAGEMENT contd……. • Medications :  Antibiotics  Anti-inflammatory drugs; such as corticosteroids  Diuretics  Drugs to raise blood pressure  Anti-anxiety  Muscle relaxers  Inhaled drugs (Bronchodilators) Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli
  43. 43. Steroid in ARDS • The patient should have evidence of ARDS and require an FiO2 >/= 50% • The steroid regimen:  Loading dose 2mg/kg  Then 2mg/kg/day from day 1 to 14  Then 1mg/kg/day from day 15 to 21  Then 0.5mg/kg/day from day 22 to 28  Then 0.25mg/kg/day on days 29 and 30  Finally 0.125mg/kg on days 31 and 32.
  45. 45. What does surfactant do?What does surfactant do? Alveoli without surfactant Alveoli with surfactant
  46. 46. ARDS - Outcomes • Most studies - mortality 40% to 60%; similar for children/adults • Death is usually due to sepsis/MODS rather than primary respiratory • Risk factors- - advanced age - CKD,CLD - Chronic immunosuppression - chronic alcohol abuse • ARDS from direct lung injury has double mortality
  47. 47. Conclusion • ARDS is a multisystem syndrome – not a “disease” • Characterized by accumulation of excessive fluid in the lungs with resulting hypoxemia and ultimately some degree of fibrotic changes. • The most frequent causes of ARDS include sepsis,  aspiration, pneumonia and severe trauma • Treatment is primarily supportive and can non- traditional types of ventilation and oxygenation strategies. • Many theoretical therapies • The best proven strategy to improve survival is low tidal volume ventilation
  48. 48. thank u….