2_Acute_Respiratory_Distress_Syndrome.pptx

Presentation for a Lecture on Acute_Respiratory_Distress_Syndrome

1. Acute Respiratory Distress Syndrome Anesthesiology, Reanimatology & Intensive care Faculty with Ambulance/ Paramed course. TSMU of RF Health ministry

2. Introduction Acute respiratory distress syndrome (ARDS) is a clinically and biologically heterogeneous disorder associated with many disease processes that injure the lung, culminating in increased non-hydrostatic extravascular lung water, reduced compliance, and severe hypoxemia.

3. Introduction Since World War I, it has been recognized that some patients with nonthoracic injuries, severe pancreatitis, massive transfusion, sepsis, and other conditions develop respiratory distress, diffuse lung infiltrates, and respiratory failure, sometimes after a delay of hours to days. Ashbaugh et al described 12 such patients in 1967, using the term “adult respiratory distress syndrome” to describe this condition.   Dr Petty demonstrates the operation of an early volume controlled ventilator during a hands-on workshop. Courtesy Louise M Nett .

4. Bernard et al. AJRCCM 1994; 149:818 Rice et al. Chest 2007: 132: 410 AECC Definition Before research into the pathogenesis and treatment of this syndrome could proceed, it was necessary to formulate a clear definition of the syndrome. Such a definition was developed in 1994 by the American-European Consensus Conference (AECC) on acute respiratory distress syndrome (ARDS).

5. Berlin Definition

6. Kigali modification Riviello ED, Kiviri W, Twagirumugabe T, et al. Hospital incidence and outcomes of the acute respiratory distress syndrome using the Kigali modification of the Berlin Definition. Am J Respir Crit Care Med 2016; 193: 52–59.

7. Epidemiology Annual incidence: 60/100,000 20% ICU patients meet criteria for ARDS Morbidity / Mortality 26-44%, most (80%) deaths attributed to non-pulmonary organ failure or sepsis Risk Factors Advanced age, pre-existing organ dysfunction or chronic medical illness Patient with ARDS from direct lung injury has higher incidence of death than those from non-pulmonary injury Statistics A large international observational study (the LUNG SAFE trial [2017] ) evaluated the incidence of ARDS across 459 intensive care units (ICUs) in 50 countries [13]. To assess the clinical recognition of ARDS according to the latest definition, any patient inclusion into the trial was made through a computer algorithm following the Berlin criteria. Among 4499 patients who developed acute hypoxemic respiratory failure, ARDS occurred in 10.4% of total ICU admissions and in 23.4% of patients requiring mechanical ventilation. Overall, 30.0% of patients had mild ARDS, 46.6% moderate ARDS and the remaining 23.4% had severe ARDS according to the Berlin criteria. Levy BD, & Choi AM, Harrison’s Principles of Internal Medicine , 2012

8. ALI = acute lung injury; TRALI = acute lung injury ­associated with the transfusion of blood products; VALI = ventilator-­associated lung injury The evolution of acute respiratory distress syndrome

9. Direct lung injury: Bacterial pneumonia (e.g., Streptococcus pneumoniae) Viral pneumonia (e.g., influenza, COVID-19) Aspiration of gastric contents Pulmonary contusion Near-drowning incidents Toxic inhalation injury Lung transplant Indirect lung injury: Sepsis (most common cause) Severe trauma: Multiple bone fractures Flail chest Head trauma Burns Pancreatitis Multiple transfusions (transfusion-related acute lung injury (TRALI)) Drug overdose Postcardiopulmonary bypass Hematopoietic stem cell transplant Fat embolism and amniotic fluid embolism Etiology Acute respiratory distress syndrome results from clinical disorders that affect the lungs either directly or indirectly

10. Diagnostic Considerations Conditions to be considered include the following:

11. Pathophysiology Baseline Mechanisms that prevent alveolar edema Retained intravascular protein maintains an oncotic gradient favoring reabsorption The interstitial lymphatics can return large quantities of fluid to the circulation Tight junctions between alveolar epithelial cells prevent leakage into the air spaces

12. Pathophysiology Baseline High-power photomicrograph of alveoli containing capillaries within a narrow interstitium. The alveoli are lined with thin, elongated type I pneumocytes (arrow) and smaller numbers of cuboidal type II pneumocytes (dashed arrow). Protective mechanisms against pulmonary edema Arrows = lymphatic movement; small circles = protein .

13. Pathophysiology Injury Photomicrograph of early diffuse alveolar damage with minimal alveolar septal thickening, hyperplasia of pneumocytes, and eosinophilic hyaline membranes (arrow). Arrows = lymphatic movement; small circles = protein . Early development of interstitial pulmonary edema

14. Pathophysiology Injury Late development of interstitial pulmonary edema Arrows = lymphatic movement; small circles = protein . High-power photomicrograph showing edema-filled alveoli in the right portion of this section (arrows).

15. Development of alveolar edema Pathophysiology Injury Arrows = lymphatic movement; small circles = protein . High-power photomicrograph illustrates the edema fluid within the alveoli (1) and the congestion (RBCs) in the alveolar capillaries (arrows).

16. The development of ARDS is underpinned by disruption to the normal maintenance and repair of the AlveoloCapillarMembrane. Changes in alveolar fluid transport and clearance in addition to altered endothelial/epithelial permeability lead to alveolar proteinaceous oedema. Changes in the patterns of chemokine expression and cell, especially neutrophil, recruitment and activity, lead to augmentation of these injurious conditions. Alveolar epithelial cell apoptosis worsens physical barrier properties and function of the ACM in gas exchange. Pathophysiology

17. Pathophysiology

18. Impaired gas exchange Pathophysiology Consequences Decreased lung compliance Pulmonary hypertension

19. CLINICAL FEATURES History and physical — Patients typically present with dyspnea and a reduction in arterial oxygen saturation after 6 to 72 hours (or up to a week) following an inciting event. On examination patients may have tachycardia, tachypnea, and increased effort to breathe. When severe, acute confusion, respiratory distress, central or peripheral cyanosis resulting from hypoxemia, and diaphoresis may be evident. Despite 100% oxygen, patients have low oxygen saturation. Chest auscultation usually reveals rales, especially bibasilar, but are often auscultated throughout the chest. Cough, chest pain, wheeze, hemoptysis, and fever are inconsistent and mostly driven by the underlying etiology.

20. Laboratory tests. Workup Approach Considerations Complete blood count Routine chemistries Prothrombin time and activated partial thromboplastin time D-dimer Plasma B-type natriuretic peptide (BNP) value and echocardiogram.

21. Arterial blood gas (ABG) analysis Hypoxemia Acute hypercapnic respiratory acidosis Metabolic acidosis Workup Laboratory tests (cont.) Approach Considerations

22. Workup Hematologic Renal Hepatic Cytokines (interleukin (IL)–1, IL-6, and IL-8) Other abnormalities observed in ARDS

23. Workup Imaging Computed tomography (CT) of the chest may show widespread patchy and/or coalescent airspace opacities that are usually more apparent in the dependent lung zones ( image 2). The opacities can be subtle ( eg , patchy ground glass), particularly in early ARDS, but can become consolidative in appearance as severity worsens

24. As part of the workup, patients with ARDS should undergo two-dimensional echocardiography for the purpose of screening. If findings are suggestive of patent foramen ovale shunting, two-dimensional echocardiography should be followed up with transesophageal echocardiography Workup Echocardiography Invasive Hemodynamic Monitoring Although pulmonary artery catheters provide considerable information, their use is not without controversy. Bronchoscopy (bronchoalveolar lavage, brush) Bronchoscopy is most useful when the cause of ARDS is uncertain and concern is raised that the etiology may require specific treatment.

25. Clinical diagnosis (Berlin definition) Respiratory symptoms must have begun within one week of a known clinical insult, or the patient must have new or worsening symptoms during the past week. Bilateral opacities must be present on a chest radiograph or computed tomographic (CT) scan. These opacities must not be fully explained by pleural effusions, lobar collapse, lung collapse, or pulmonary nodules. The patient's respiratory failure must not be fully explained by cardiac failure or fluid overload. An objective assessment ( eg , echocardiography) to exclude hydrostatic pulmonary edema is required if no risk factors for ARDS are present. A moderate to severe impairment of oxygenation must be present, as defined by the ratio of arterial oxygen tension to fraction of inspired oxygen ( PaO /FiO ). The severity of the hypoxemia defines the severity of the ARDS:

26. Mild ARDS – The PaO /FiO is >200 mmHg, but ≤300 mmHg, on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H2O. Mortality, in cohort - 27 % Moderate ARDS – The PaO /FiO is >100 mmHg, but ≤200 mmHg, on ventilator settings that include PEEP ≥5 cm H2O. Mortality, in cohort - 32 % Severe ARDS – The PaO /FiO is ≤100 mmHg on ventilator settings that include PEEP ≥5 cm H O. Mortality, in cohort - 45 % Clinical diagnosis (Berlin definition) The severity of the ARDS Determining the PaO /FiO (oxygenation index) requires arterial blood gas (ABG) analysis. To calculate the PaO /FiO ratio, the PaO is measured in mmHg and the FiO is expressed as a decimal between 0.21 and 1. As an example, if a patient has a PaO of 60 mmHg while receiving 80 percent oxygen, then the PaO /FiO ratio is 75 mmHg ( ie , 60 mmHg/0.8).

27. Pathologic diagnosis and stages Patients with ARDS tend to progress through three pathologic stages

28. Early exudative stage (DAD) – The early exudative stage during the first 7 to 10 days is characterized by DAD. DAD is a nonspecific reaction to lung injury from a variety of causes. It is characterized by interstitial edema, acute and chronic inflammation, type II cell hyperplasia, and hyaline membrane formation Pathologic diagnosis and stages Courtesy of Jeffrey L Myers, MD. (A) High-resolution CT findings corresponding to exudative phase of acute respiratory distress syndrome (ARDS). HRCT scan at the level of right middle lobe shows dependent airspace consolidation without traction bronchiectasis and non-dependent areas of sparing . The patient was a 68-year-old man with ARDS due to Streptococcus pneumonia.

29. Fibroproliferative stage – After approximately 7 to 10 days, a proliferative stage develops, characterized by resolution of pulmonary edema, proliferation of type II alveolar cells, squamous metaplasia, interstitial infiltration by myofibroblasts, and early deposition of collagen. It is unknown how long this phase lasts but is probably in the realm of two to three weeks. Pathologic diagnosis and stages High power photomicrograph shows changes typical of the proliferative or late stage of diffuse alveolar damage. Although hyaline membranes are still identifiable, the histologic picture is now dominated by thickening and reorganization of interstitial structures due mainly to marked proliferation of mesenchymal spindle cells, including both fibroblasts and myofibroblasts. Courtesy of Jeffrey L Myers, MD. (B) High-resolution CT findings corresponding to fibroproliferative phase of ARDS. HRCT scan at the level of right lower lobe shows extensive airspace consolidation and ground-glass attenuation associated with traction bronchiectasis (arrows). The patient was an 84-year-old woman with ARDS due to sepsis.

30. Fibrotic stage – Some patients progress to a fibrotic stage, characterized by obliteration of normal lung architecture, fibrosis, and cyst formation. The degree of fibrosis ranges from minimal to severe. The proportion of patients that progress through the early phase to reach the later phases is unknown. Pathologic diagnosis and stages (C) High-resolution CT findings corresponding to fibrotic phase of ARDS. HRCT scan at the level of right inferior pulmonary vein shows extensive ground-glass attenuation associated with traction bronchiectasis (arrows), coarse reticulation and cystic changes (arrowheads). The patient was a 65-year-old woman with ARDS due to viral pneumonia.

31. CLINICAL COURSE Mechanisms of Repair

32. No drug has proved beneficial in the prevention or management of acute respiratory distress syndrome (ARDS). Early administration of corticosteroids to septic patients does not prevent the development of ARDS, adding an increased risk of superinfections. Numerous pharmacologic therapies, including the use of inhaled synthetic surfactant, intravenous antibody to endotoxin, interferon-beta-1a, IV prostaglandin E1 and some other have been tried and are not effective. Inhaled nitric oxide (NO) , a potent pulmonary vasodilator, seemed promising in early trials, but in larger controlled trials, it did not change mortality rates in adults with ARDS. It was found that inhaled NO results in only a transient improvement in oxygenation. Although no specific therapy exists for ARDS, treatment of the underlying condition is essential, along with supportive care, noninvasive ventilation or mechanical ventilation using low tidal volumes, and conservative fluid management. Because infection is often the underlying cause of ARDS, early administration of appropriate antibiotic therapy broad enough to cover suspected pathogens is essential, along with careful assessment of the patient to determine potential infection sources. Treatment Approach Considerations reducing shunt fraction increasing oxygen delivery decreasing oxygen consumption avoiding further injury. The chief treatment strategy is supportive care and focuses on

33. Treatment Fluid Management Goal and fluid choice The overall goal is to minimize or eliminate a positive fluid balance. It is reasonable to target a central venous pressure (CVP) of <4 mmHg or, if a pulmonary artery catheter is in place, a pulmonary artery occlusion pressure (PAOP) <8 mmHg. Diuretics, in addition to fluid restriction, may need to be administered to achieve this goal. However, in practice, these goals may be difficult to achieve. While fluid choice is dependent upon the type of support needed, generally favored a crystalloid solution, such as a balanced salt solution. This choice is based upon indirect data from critically ill patients with hypovolemic or septic shock.

34. Treatment Noninvasive Ventilation Patients who have a diminished level of consciousness, vomiting, upper GI bleeding, or other conditions that increase aspiration risk are not candidates for NIPPV. Other relative contraindications include hemodynamic instability, agitation, and inability to obtain good mask fit.

35. Importantly , when NIV is implemented, frequent evaluation is necessary and clinicians should have a low threshold for intubation. Treatment Ventilation Considerations SELECTING INVASIVE VERSUS NONINVASIVE VENTILATION

36. Treatment Invasive Ventilation

37. Treatment Invasive Ventilation Lung-protective ventilation

38. For patients with ARDS, recommended LTVV (also known as lung protective ventilation; 4 to 8 mL/kg predicted body weight [PBW]) LTVV is typically performed using a volume-limited assist control mode, targets a plateau pressure ( Pplat ) ≤30 cm H 2 O , and applies positive end-expiratory pressure (PEEP) using a strategy outlined in the table Treatment Invasive Ventilation LOW TIDAL VOLUME VENTILATION (LTVV)

39. Permissive hypercapnia Hypercapnic respiratory acidosis eg , pH <7.35 and PaCO >45 mmHg) is an expected and generally well tolerated consequence of LTVV The degree of hypercapnia can be minimized by using the highest respiratory rate that does not induce auto-PEEP. LTVV is generally well-tolerated but potential adverse effects include: Treatment Invasive Ventilation LOW TIDAL VOLUME VENTILATION (LTVV) Auto-PEEP Auto-PEEP is PEEP over and above the set-PEEP. Auto-PEEP is caused by insufficient expiratory time (e.g., high rates, short expiratory times, water in the ventilator circuit, inverse respiratory ratios, bronchospasm, and high minute ventilations

40. . Treatment Invasive Ventilation Volume- versus pressure-limited mode

41. Therapeutic algorithm regarding early ARDS management (EXPERT OPINION) Treatment Invasive Ventilation

42. FOLLOW-UP Treatment Invasive Ventilation

43. Recruitment maneuver is the brief application of a high level of continuous positive airway pressure (CPAP) or PEEP, with the goal of recruiting non-gas exchanging parts of the lung involved with ARDS to become involved in gas exchange. Recruitment maneuvers may be performed as an independent maneuver or as part of an open lung approach (when recruitment is followed by higher than usual titrated levels of PEEP). Adverse effects – The most common adverse effects of recruitment maneuvers are hypotension and oxygen desaturation. Recruitment maneuvers Treatment Invasive Ventilation

44. Prone ventilation involves ventilating patients with LTVV in the prone position (as opposed to the more commonly used supine position ) Treatment Invasive Ventilation Prone ventilation FRC – functional residual capacity VT – tidal volume

45. FOLLOW-UP Treatment Invasive Ventilation Patients who are improving Patients who are not improving or deteriorating Switching ventilatory mode

46. Treatment Extracorporeal membrane oxygenation There are few absolute contraindications other than a preexisting condition that is incompatible with recovery (severe neurologic injury, end-stage malignancy), and relative contraindications include uncontrollable bleeding and very poor prognosis from the primary condition. Importantly , early application ( eg , within seven days) is critical for the success of ECMO.

47. Patients with ARDS are at high risk for complications related to mechanical ventilation or critical illness. Complications related to mechanical ventilation include: Barotrauma – Among patients who are mechanically ventilated, ARDS is a risk factor for pulmonary barotrauma due to the physical stress of positive pressure mechanical ventilation on acutely damaged alveolar membranes. Barotrauma can be an early or late complication of ARDS. Nosocomial infection – Nosocomial infections ( eg , ventilator-associated pneumonia [VAP], or catheter-related infections, Clostridioides difficile ) are an important cause of morbidity and mortality in patients with ARDS. Other complications that frequently occur during the hospital course of patients with ARDS include the following: Delirium – ARDS is commonly complicated by delirium, the etiology of which is likely multifactorial Deep venous thrombosis Gastrointestinal bleeding due to stress ulceration Poor nutrition COMPLICATIONS

48. Treatment SUPPORTIVE CARE Sedation Hemodynamic monitoring Nutritional support Venous thromboembolism prophylaxis

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