Acute respiratory distress syndrome

Brief and informative discussion on ARDS

1. Acute Respiratory Distress Syndrome Presenter: Dr. Priyam Dalmia MBBS Intern, 14 th batch Department of medicine

2. Content Introduction Epidemiology Causes Clinical course and pathophysiology Clinical features Diagnostic criteria Differential diagnosis Investigations Management Prognosis and recovery

3. Introduction ARDS is a clinical syndrome of dyspnea of rapid onset,hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. ARDS is also referred with variety of terms like Stiff Lung Non cardiogenic pulmonary edema Shock lung Wet lung Post traumatic lung Adult respiratory distress syndrome Adult hyaline membrane disease Capillary leak syndrome & Congestive atelectasis.

4. Epidemiology Annual incidence : 60 cases/ 1,00,000 population Approximately 10% of all intensive care unit (ICU) admissions involve patients with ARDS The mortality rate was traditionally very high (50–70%), Changes in patient care have led to mortality decline to 30%

5. Causes Clinical disorder associated with development of ARDS Direct Lung Injury: Pneumonia Aspiration of gastric contents Pulmonary contusion Near drowning Inhalation injury

6. Indirect lung injury Sepsis Severe trauma Multiple bone fracture Flail chest Burns Acute pancreatitis Multiple transfusion (TRALI)

7. Clinical course and pathophysiology Natural history of ARDS is marked by 3 distinct phases: Exudative (0-7 days) Proliferative ( 7-21 days) Fibrotic ( > 21 days)

8. Exudative (0-7 day) Capillary endothelial cells and alveolar epithelial cells are injured, Exudation and protein rich edema fluid accumulates in the interstitial and alveolar spaces. Increased pro-inflammatory cytokines Recruitment of leukocytes (especially neutrophils) into the interstitium and alveoli. Formation of hyaline membrane Alveolar edema in dependent portions of the lung Intrapulmonary shunting Hypoxemia Work of breathing increases, leading to dyspnea.

9. Proliferative phase This phase of ARDS usually lasts from day 7 to day 21 Marked, with the initiation of lung repair Exudates cleared and a shift from neutrophil- to lymphocyte-predominant pulmonary infiltrates. Type II pneumocytes regenerate along alveolar basement membranes. These specialized epithelial cells synthesize new pulmonary surfactant And differentiate into type I pneumocytes.

10. Fibrotic ( > 21 days) Most patients with ARDS recover Very few progresses into fibrotic phase There is extensive alveolar-duct and interstitial fibrosis. Marked disruption of acinar architecture leads to emphysema-like changes, with large bullae. Intimal fibro proliferation in the pulmonary microcirculation causes progressive vascular occlusion and pulmonary hypertension. The physiologic consequences include an increased risk of pneumothorax, reductions in lung compliance, and increased pulmonary dead space.

11. Clinical features Precipitating insult is usually evident Fever Cough Dyspnea Tachypnea Tachycardia Restlessness Due to worsening hypoxemia Agitation, anxiety, confusion Cyanosis even with supplemental oxygen ( refractory hypoxemia)

12. Berlin Diagnostic criteria Acute onset (within 7 days of a known clinical insult ) Chest x-ray: Bilateral opacities not fully explained by lobar collapse, mass or effusion 3. Absence of left atrial hypertension (no hydrostatic edema) 4. Severity: Pao 2 /fio 2  ≤ 300 mm of Hg , with a positive end-expiratory pressure (PEEP) of at least 5 cm H 2 o Mild ARDS ( pao 2 /fio 2  ≤ 300  mm of Hg ) Moderate ARDS (pao 2 /fio 2  ≤ 200  mm of Hg) Severe ARDS (pao 2 /fio 2  ≤ 100  mm of Hg )

13. Differential Diagnosis Cardiogenic pulmonary edema Diffuse alveolar hemorrhage Acute pulmonary embolism TACO

14. Investigation CBC Chest x-ray ABG analysis CT chest Echo Pro-NBP level( less than 100 pg /mL ) Na+, K+ Blood urea S. creatinine Blood culture/sensitivity Procalcitonin LFT Anti nuclear, Anti mpo ,Anti cytoplasmic, anti ds- dna

15. X-ray of ARDS -Bilateral diffuse opacity over lung field -No Cardiomegaly -No Pleural effusion

16. CT chest Hyperdense shadow at dependent part of lung Dependent pulmonary edema in ARDS

17. Cardiogenic pulmonary edema

18. Diffuse alveolar hemorrhage

19. Pulmonary Embolism

20. TRALI Vs TACO Fever No Fever Hypotension Hypertension JVP Unchanged JVP Raised EF- Normal Decreased Pulmonary Edema Fluid- Exudate Transudate Response To Diuretic- Minimal Significant

21. Management 1. TREATMENT of the cause e.g. antibiotics for pneumonia, sepsis 2.Supportive therapy Protective lung ventilation, Fluid management Prone positioning 3.Pharmacological treatment Steroids, vasodilators, DVT prophylaxis & sedation.

22. Lung protective ventilation Patients meeting clinical criteria for ARDS frequently become fatigued from increased work of breathing and progressive hypoxemia, requiring mechanical ventilation for support. Mechanical ventilation with low tidal volume (4-6 mL/kg ideal body weight) PEEP of atleast 5cm of H2O P plateau <30 cm of H2O Alveolar over distension and cyclic atelectasis are the principal causes of ventilator- associated lung injury(VALI)

23. Low tidal volumes Prevents from volutrauma and barotrauma by alveolar overdistention Because of the mortality benefit, the pCO2 of the patient is allowed to rise. (known as permissive hypercapnia) For patients in ARDS, the pH is allowed to drift down to 7.30 When pH< 7.2 then it needs to be buffered.

24. Advantages of PEEP: Minimize cyclic atelectasis It opens collapsed alveoli / Reverse atelectasis - known as lung Recruitment, and it increases the available surface area in the lungs for gas exchange  Increases arterial oxygenation at lower fio2 by decreasing intrapulmoary shunting

25. Neuromuscular blockade In severe ARDS sedation alone is not beneficial for lung protective ventilation but also adequate for ventilator patient synchrony. Early NMB is the preferred in severe ARDS for initial 48 hrs. This increase rate of survival and ventilator free days without increasing ICU acquired paresis

26. Prone position A recent trial demonstrated a significant reduction in 28-day mortality with prone positioning (32.8 to 16%) for patients with severe ARDS Possible mechanisms : Recruitment of dependent lung zones, Improved ventilation-perfusion matching Relief of compression of the lung by the heart and mediastinal structures  This maneuver requires a critical-care team that is experienced in “ proning ,” as repositioning critically ill patients can be hazardous, leading to accidental endotracheal extubation , loss of central venous catheters, and orthopedic injury

27. Fluid management Primary cause is leakage of fluid and pulmonary edema, so negative fluid balance should be done Fluid restriction and diuretics is an important aspect of ARDS management, not causing hypotension or hypoperfusion of vital organs(MAP>65 mm hg) Maintaining a low left atrial pressure minimizes pulmonary edema and improves oxygenation and lung compliance.

28. Inhaled Nitric Oxide It is very short acting pulmonary vasodilator When delivered (5-10ppm) improves blood flows to well ventilated areas, thus improving V/Q matching Effect lasts only for 48 hour and rebound effect can occur if withdrawn No mortality benefit is shown in clinical trials Used as Rescue therapy , when other modality has failed Also in patients with PAH

29. Glucocorticoids use Many attempts have been made to treat both early and late ARDS with glucocorticoids, with the goal of reducing potentially deleterious pulmonary inflammation. Current evidence does not support the routine use of glucocorticoids in the care of ARDS patients.

30. Extracorporeal membrane oxygenation (ECMO) There use is restricted to specialized centres . Controlled trials indicate improved survival in severe ards pts Veno -venous ECMO is designed to provide gas exchange ARDS associated with pneumonia (viral or bacterial) is the most common cause of refractory hypoxemia that requires ECMO 

31. Bundled Care For ICU Patients Venous thrombosis should be prevented with the use of sc low-molecular-weight heparin To help prevent decubitus ulcers, frequent changes in body position and the use of soft mattress overlays and air mattresses are employed. To prevent gi mucosal injury h2 –receptor antagonists, antacids, and sucralfate have all been used Nutritional support by enteral feeding through either a nasogastric or an orogastric tube should be initiated and maintained whenever possible. Delayed gastric emptying is common in critically ill patients taking sedative medications but often responds to promotility agents such as metoclopramide.

32. Decision To Wean From Mechanical Ventilation Conditions as indicating amenability to weaning: Lung injury is stable or resolving; Gas exchange is adequate, with low PEEP<8 cm of H2O and FiO2<0.5 Hemodynamically stable , not on vasopressors Able to initiate spontaneous breaths If the patient passes the wean screen then can be tried for spontaneous breathing trials (SBT)consist of breathing through the ET tube without ventilator support or minimal pressure support (T-piece using 1–5 cmH2O CPAP or PSV from the ventilator to offset resistance from the endotracheal tube) for period of 30-120 min.

33. The spontaneous breathing trial is declared a failure and stopped if any of the following occur: respiratory rate >35/min for >5 min, O2 saturation <90% Pulse :20% increase or decrease from baseline systolic blood pressure >180 mmHg or <90 mm Hg increased anxiety or diaphoresis. If, at the end of the spontaneous breathing trial, none of the above events has occurred and the ratio of the respiratory rate and tidal volume in liters (f/VT) is <105 , patient can be extubated

34. Prognosis Mortality declined from 50% to ~30% in past decade In the recent report from LUNG SAFE trial, hospital mortality estimates for ARDS range from 34.9% for mild ARDS, 40.3% for moderate ARDS, and 46.1% with severe ARDS. Risk factors having higher mortality rates: Advanced age>70yr Non pulmonary cause of ards (sepsis) Chronic medical illness >60 yr and sepsis Severe ARDS

35. Functional Recovery in ARDS Survivors It is a testament to the resolving powers of the lung that the majority of patients who survive regain nearly normal lung function. Patients usually recover maximal lung function within 6 months. A year later, more than one-third of ARDS survivors have normal spirometry values and diffusion capacity. Most of the remaining patients have only mild abnormalities in pulmonary function.

36. Reference Harrison’s Principle Of Internal Medicine,20 th Edition Davidson’s Principal And Practice Of Medicine,22 nd Edition

37. Thank you …