ACUTE RESPIRATORY DISTRESS SYNDROME.pptx

ARDS

1. ACUTE RESPIRATORY DISTRESS SYNDROME

2. BERLIN DEFINITION A/c diffuse ,inflammatory lung injury leading to increased pulmonary vascular permeability,increased lung weight and loss of aerated lung tissue with hypoxia and bilateral radiogenic opacities,associated with increased venous admixture,increased dead space and decreased lung compliance.

3. ESICM DEFINITION Spectrum of condition with different etiologies which share common clinical pathological charecteristics including 1.Increased permeability of alveolo -capillary membrane,resulting in inflammatory edema 2.Increased non aerated lung tissue resulting in higher lung elastance . 3.Increased venous admixture and deadspace,which results in hypoxia and hypercapnia .

4. PREDISPOSING CONDITIONS INFECTION RELATED SOURCES Pneumonia Sepsis syndromes

5. NON INFECTIOUS SOURCES Gastric aspiration Blood transfusion Multisystem trauma Pancreatitis drug overdose.

6. DIRECT LUNG INJURY Pneumonia Aspiration of gastric contents Pulmonary contusion Fat,amniotic fluid or air emboli Near drowning Inhalational injury Reperfusion pulmonary edema

7. INDIRECT LUNG INJURY Sepsis Multiple trauma Cardiopulmonary bypass Drug overdose Acute pancreatitis Transfusion of blood products.

8. PATHOGENESIS Activation of circulating neutrophils Neutrophil sequestration into pulmonary microcirculation. Neutrophils degranulate and release toxic metabolites Damages endothelial cells and pneumocytes Exudation of RBC ,platelets and protein rich fluid.

9. Cellular and proteinaceous exudation fills and obliterates distal airspaces. Progressive inflammation causes fibrin accumulation

10. PATHOLOGICAL STAGES EXUDATIVE STAGE Diffuse alveolar edema within first week.

11. PROLIFERATIVE STAGE Resolution of pulmonary edema Proliferation of type 2 alveolar cells Squamous metaplasia Early deposition of collagen

12. FIBROTIC STAGE Obliteration of normal lung architecture. Diffuse fibrosis

13. CLINICAL PRESENTATION Acute onset dyspnoea tachypnoea Persistent hypoxemia

14. DIAGNOSIS CLINICAL CRITERIA Several definitions since 1967 Before 1994-murray lung injury score 1994- AECC –published new definition for ALI and ARDS Berlin definition –recent modification.

15. DIFFERENCE BETWEEN AECC AND BERLIN DEFINITION Term ALI –no longer used. ARDS- classified as mild,moderate and severe based on degree of hypoxemia. Berlin definition requires a minimum positive end expiratory pressure of 5 cm of H2O for consideration of Pa02/Fi02 ratio.

16. It specifies onset occurs within 1 week of a known precipitant. Definition recognises that elevated vascular pressures and ARDS can coexist. No absolute requirement to rule out cardiac cause.

17. Potential limitation: Need for ABG to calculate PaO2. Uses only clinical criteria. Presence or absence of multiorgan dysfunction not included.

18. RADIOLOGICAL APPEARANCE Granular or ground glass infiltrates. Evenly distributed in all lung fields without pleural effusion.

19. INVASIVE METHODS 1.BRONCHOSCOPY Indicated in early ARDS No identifiable risk factors And immunocompromised .

20. 2.BRONCHOALVEOLAR LAVAGE To identify cause of pneumonia. Diagnosis of opportunistic infections. Usually neutrophil predominant –diffuse alveolar hemorrhage .

21. 3.Open biopsy/ thoracoscopic biopsy. Rare Uncertain/unknown cause. Unsuspected diagnosis requiring specific therapy- miliary TB,Pulmonary blastomycosis,aspergillosis .

22. TREATMENT Standard supportive therapy Treatment of predisposing factors Fluid and hemodynamic management Nutrition.

23. TREATMENT OF PREDISPOSING FACTORS Treat underlying cause Appropriate treatment for any precipitating infection In the immunocompromised host, look for evidence of opportunistic infections.

24. Sepsis and ARDS of unknown source, an intraabdominal process should be considered. Timely surgical management of intraabdominal sepsis is associated with better outcomes. In some patients, the cause of lung injury will not be specifically treatable (such as aspiration of gastric contents) or will not be readily identifiable

25. FLUID AND HEMODYNAMIC MANAGEMENT A large, randomized European trial of PAC use compared to no PAC use in all patients admitted with ARDS No difference in clinical outcomes Routine PAC use in ARDS without specified PAC-guided interventions is not beneficial.

26. The ARDS Clinical Trials Network tested the value of pulmonary artery catheterization in the context of specific fluid management protocols unable to demonstrate the superiority of PAC over the central venous catheter PAC use did not improve outcomes in these patients.

27. For decades there was disagreement as to the best fluid management strategy in patients with ARDS. Proponents of a liberal fluid strategy reasoned that increased circulating volume would preserve end organ perfusion and protect patients from the development of nonpulmonary organ failures

28. Reductions in intravascular volume can have adverse effects on cardiac output and tissue perfusion. This concern is legitimate, since mortality in ARDS is usually from nonpulmonary causes including other organ failures.

29. conservative fluid strategy Reduction in circulating volume, thereby reducing the driving force for pulmonary edema formation. In experimental lung injury, lower left atrial pressures are associated with less formation of pulmonary edema .

30. ARDS Network conducted a large, multicenter , RCT of catheter (central venous catheter vs. pulmonary artery catheter)—driven fluid management in patients with ARDS Once patients were out of shock they were randomized Into 2 groups

31. 1.liberal fluid treatment strategy average of 1L of fluid accumulation per day 2. conservative fluid treatment strategy aggressive use of diuretics to achieve a goal CVP <4 or a goal PAOP <8 resulting in average of zero net fluid accumulation by day 7.

32. No difference in mortality at 60 days (the primary outcome of the study) patients in the conservative group had improved oxygenation and significantly more ventilator-free days without the development of additional organ failures.

33. Currently, the recommended strategy is to aim to achieve the lowest intravascular volume that maintains adequate tissue perfusion as measured by urine output, other organ perfusion, and metabolic acid-base status using central venous pressure monitoring to direct therapy

34. NUTRITION Standard supportive care for the patient with ARDS includes the provision of adequate nutrition. The enteral route is preferred to the parenteral route and is associated with less infectious complications. Enteral feeding may also have other beneficial effects.

35. Experimentally, lack of enteral feeding promoted translocation of bacteria from the intestine. In normal volunteers, administration of parenteral nutrition with bowel rest increased circulating levels of TNF-α, glucagon and epinephrine, and increased febrile responses compared to volunteers who received enteral nutrition.

36. The goals of nutritional support include 1.provision of adequate nutrients for the patient’s level of metabolism and 2. treatment and prevention of any deficiencies in micro- or macronutrients Whether a particular dietary composition could be beneficial in patients with ARDS is unclear.

37. Immunomodulation via dietary manipulation has been attempted by a number of investigators in critically ill patients using various combinations of omega-3 fatty acids, ribonucleotides , arginine, and glutamine. A meta-analysis of these trials suggested a beneficial effect on infection rate but not overall mortality.

38. . Using a different approach, a high-fat, low-carbohydrate diet reduced the duration of mechanical ventilation in patients with acute respiratory failure. due to reduction of the respiratory quotient and a resultant fall in carbon dioxide production

39. Overall, there is still no compelling evidence to support the use of anything other than standard (enteral) nutritional support, with avoidance of overfeeding, in patients with ARDS