THE ACUTE RESPIRATORY DISTRESS SYNDROME. Daniel Brockman, DO

Transcription

1 THE ACUTE RESPIRATORY DISTRESS SYNDROME Daniel Brockman, DO

2 Objectives Describe the history and evolution of the diagnosis of ARDS Review the diagnostic criteria for ARDS Discuss the primary interventions in ARDS Address salvage therapies for severe hypoxia in ARDS.

3 Case Presentations A 23 year old male college student 18 year old female 60 year old male SNF resident 40 year old female with an SBO

4 Case presentations...is found down after ODing on Heroin. comes to the ICU after DCS for abdominal trauma from an MVC. is sent to the ED with a fever and cough. vomits on the wards and collapses.

5 Next they develop severe hypoxia.

6 And a CXR reveals

7 Or this

8 Or this

9 Or maybe it was a CT to r/o PE

10 Epidemiology Approximately 190, ,000 cases annually reported. Incidence estimated to be 86 case per 100,000 Increased incidence in the elderly 306 case per 100,000 Estimated mortality between 30-40%.

11 Historical Perspective During the Vietnam War a clinical syndrome of severe hypoxia was identified soldiers who suffered serious injuries.

12 The Adult Respiratory Distress Syndrome In 1967 a case series reported 12 cases of sudden onset severe hypoxia associated with diffuse patchy infiltrates on chest X-ray. The condition was termed the Adult Respiratory Distress Syndrome. The X-ray appeared very similar to the Infant Respiratory Distress Syndrome.

13 Pediatricians are for babies As the condition was diagnosed more it became apparent that ARDS occurred in all ages. Pediatricians REALLY don t like writing the word adult and were quite vocal about it. Therefore the name was changed to ACUTE Respiratory Distress Syndrome

14 Shortly there after Tom Petty, MD had a new ABG machine Discovered in a patient with what was later identified as ARDS after trauma that retarding expiratory flow resulted in an increase in PaO2(40->130). This maneuver was repeated in 12 additional patients with similar clinical picture with consistent improvements in oxygenation.

15 So what is ARDS? Diffuse pulmonary edema due to fluid leaking in to alveolar spaces and damage to lung tissues from inflammation and loss of oncotic forces.

16 So all of these: Neurogenic Pulmonary Edema Fat Embolism Shock Lung TRALI Pump Lung Capillary Leak Syndrome Are just ARDS

17 Clinical Diagnosis AECC Definition: Due to the disparate causes and unclear definition a diagnostic criteria was composed in 1994 to standardize the definition of ARDS Main diagnostic points were Acute Onset Hypoxia Bilateral Infiltrates Absence of Heart Failure

18 Refining the Diagnosis The Berlin Criteria was devised by a panel of experts in 2011 and released in Provided more concrete criteria for some of the diagnostic requirements. Added a severity scale to diagnosis. Not very different from AECC in actuality.

19 AECC vs. Berlin Acute Onset. Diffuse patchy infiltrates on CXR. Absence of LV dysfunction on Echo or PAWP<18. PaO2/FiO2 <200. Onset within 7 days. Diffuse patchy infiltrates on CXR or CT scan. No clinical suspicion of heart failure or absence of LV dysfunction on Echo. PaO2/FiO2<300 on at least 5 of PEEP or EPAP.

20 Berlin Criteria Severity Scale Based on PaO2/FiO2 ratio. Mild Moderate Severe <101 Correlates with mortality Mild: 27% Moderate: 32% Severe: 45%

21 So if you want to be technical Patient s with cardiomyopathies can t have ARDS. Patient s with a pneumonectomy can t have ARDS

22 Pathophysiology Inciting event causes release of inflammatory markers causing damage to capillaries and alveoli resulting in fluid exiting the vascular space into the lung parenchyma resulting in filling of or collapse of alveoli.

23 Pathophysiology Results in patches of alveoli that receive no ventilation causing shunting of deoxygenated venous blood through portions of the lung without oxygenation.

24 Phases of ARDS Acute(or exudative) Phase Edema and diffuse alveolar damage. Generally Days 1-6

25 Phases of ARDS Healthy Lung Acute ARDS

26 Phases of ARDS Proliferative Phase Edema begins to improve, overgrowth of Type 2 Aveolar Cells, myofibroblasts invade into interstitium and collagen deposition occurs.

27 Thank you Pediatricians Chronic Acute Respiratory Distress Syndrome Also called Fibrotic Phase of ARDS Fibrosis of lung parenchyma, formation of cysts in damaged parts of the Lung.

28 Inciting Events Pulmonary Pneumonia Aspiration Pulmonary Contusion Near Drowning Smoke Inhalation Extrapulmonary Sepsis Severe Trauma Burns Pancreatitis Blood Transfusions Drug Overdose/Reaction Head Injury Cardiac Bypass Bone Marrow Transplant

29 Complications Pneumothorax Pneumomediastinum Decreased venous return-hypotension Worsening of pulmonary edema and worsening oxygenation Organ dysfunctiomn Many are actually are complications of mechanical ventilation in ARDS

30 Barotrauma Injury to lung due to High Ventilatory pressures. Pneumothorax Pneumomediatinum

31 Volutrauma Increase in inflammatory markers caused by distension of alveola. Leads to further lung injury from inflammation and extrapulmonary organ injury.

32 Atelectrauma Increase in both inflammatory cytokines and alveolar injury due to shearing caused by the repeated opening and closing of alveolar units.

33 Optimizing Treatment in ARDS Low Tidal Volume Ventilation Controlling Plateau Pressures Permissive Hypercapnia Providing adequate Oxygentaion Early Neuromuscular Blockade

34 The ARMA Trial Randomized control trial 861 patients meeting AECC definition of Acute Lung Injury (PaO2/FiO2<300) Randomized to: 6 ml/kg(pbw) and Plateau pressure <30 12 ml/kg(pbw) and Plateau pressure <50 Stopped early due to significantly higher mortality in 12 ml/kg group

35 Demographics

36 Results 12 ml/kg 6 ml/kg P-value Mortality 39.8% 31.0% Ventilator free days Days without other organ failure Barotrauma Events

37 PEEP strategies Best PEEP using flow volume loops Super PEEP Optimum PEEP for compliance Minimum PEEP for oxygenation No good evidence to support one strategy over another for determining PEEP.

38 Some points about PEEP It takes time to recruit alveoli with PEEP, don t expect rapid changes in oxygenation. A lung opening procedure or recruitment maneuver can be used to more rapidly open the lung and improve oxygenation. Increase PEEP to for seconds.

39 Early Neuromuscular Blockade Randomized Double Blind Placebo Controllede Trial 340 patients with AECC definition of ARDS and PaO2/FiO2<150 on at least 5 of PEEP Randomized to Deep Sedation for 24 hours Deep Sedation plus Neuromuscular Blockade with cisatricurium for 48 hours.

40 Demographics

41 Results

42 Results Adjust 90 day Hazard Ratio for Death: 0.68 (p-value: 0.04)

43 Neuromuscular Blockade Subgroup analysis based on severity of ARDS defined by PaO2/FiO2 ratio demonstrated that mortality benefit occurred in patients with PaO2/FiO2 ratio <120.

44 Fluid Management(The FACCT Trial) Randomized Controlled Trial Two major questions: Do PAC s help management of ARDS Keep this short: NO Liberal(give fluid) vs restrictive(diurese) management

45 The FACCT Trial 1000 patient meeting AECC definition of Acute Lung Injury (PaO2/FiO2<300) Randomized to:

46 Demographics

47 Results

48 Salvage/Rescue Therapies Proning Inhaled Vasodilators APRV HFOV ECMO

49 Proning

50 Proning Reverses dependant areas of lung leading to decreased V/Q mismatch. Creates increase in extrathoracic pressure. Recent NEJM study showed improved mortality in patients with severe ARDS (PaO2/FiO2<100 after 36 hours of treatment) kept prone for 14 hrs a day.

51 Inhaled Nitric Oxide Vasodilator Enters opened areas of lung and dilates capillaries increasing blood flow to open areas of lung. Improves V/Q matching. Expensive. Improves oxygenation but no proven mortality benefit. Increased incidence of renal failure.

52 Epoprostenol Same mechanism of action as INO. Administered as continuous 50 ng/kg/min Again improves oxygenation but no proven mortality benefit Significantly cheaper than INO. No evidence of increased renal failure.

53 Iloprost Another inhaled vasodilator Administered Ever 2 to 4 hours Has the least evidence supporting its effectiveness. Cheapest option of Inhaled Vasodilators

54 APRV

55 APRV Alternate mode of ventilation high steady airway pressure that drops to a lower pressure for a brief period of time. Allows higher airway pressures. Some small studies show decreased rates of developing ARDS, but no other evidence of outcomes differences in patients with ARDS.

56 HFOV

57 HFOV Continuous high airway pressures, a piston rapidly pushes tiny amounts of air into and out of the lungs. Allows higher mean airway pressures without large tidal volumes or shearing improving recruitment and oxygenation. In 2 large studies no benefit or worsened outcomes if used in early ARDS.

58 ECMO

59 ECMO By running Venous blood through a membrane oxygenator the patient can have effective CO2 removal and oxygenation without relying on the lungs. Allows for minimal vent settings to rest the lungs. Evidence is limited but shows some potential benefit in severe ARDS.

60 Key Points ARDS is a clinical diagnosis with specific criteria. Acute Onset <7 days PaO2/FiO2 <300 Bilateral patchy infiltrates Not cardiac related

61 Key Points Low tidal volume ventilation improves mortality. 6 ml/kg PBW(based on Height) Diuresis decreases ventilator days and organ failure in hemodynamically stable patients. Early Neuromuscular Blockade of benefit in moderately severe cases Variety of salvage therapies Proning, Inhaled Vasodilators, APRV, HFOV, ECMO Only proning has shown any mortality benefit.

62 Key Points Variety of salvage therapies Proning, Inhaled Vasodilators, APRV, HFOV, ECMO Only proning has shown any mortality benefit.