ACUTE RESPIRATORY DISTRESS SYNDROME
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1 ACUTE RESPIRATORY DISTRESS SYNDROME Angel Coz MD, FCCP, DCE Assistant Professor of Medicine UCSF Fresno November 4, 2017
2 No disclosures
3 OBJECTIVES Identify current trends and risk factors of ARDS Describe the pathophysiology Define phases during development List clinical manifestations List criteria that must be present for diagnosis Describe treatment for patients with ARDS
4 HISTORY 1821 Laennec Idiopathic lung anasarca 1925 Sir William Osler Uncontrolled septicemia leads to frothy pulmonary edema
5 INTRODUCTION Acute respiratory distress syndrome (ARDS) was described 50 years ago Alveolar spaces filled with hyaline membranes Substantial outcome improvement over time Common and lethal / disabling
6 DEFINITION CRITERIA 1994 Acute onset Bilateral Infiltrates on Chest-X-ray PCWP 18 mm Hg or no clinical evidence of volume overload Oxygenation: PaO 2 / FiO à Acute Lung Injury (ALI) PaO 2 / FiO à ARDS
7 Berlin Definition Timing within one week Imaging bilateral opacities on CXR or Chest CT Edema not fully explained by cardiac failure or volume overload Oxygenation - Mild - Moderate - Severe On PEEP 5 cmh < PaO 2 / FiO mmhg 100 < PaO 2 / FiO mmhg PaO 2 / FiO mmhg JAMA. 2012;307(23):
8 1994 Definition Berlin 2012 ALI ARDS Mild Moderate Severe Mortality 26 % 37 % 27 % 32 % 45 % Progression from mild 29 % 4 % Progression from moderate 13 % Ventilator free days (d) Duration of MV survivors (d) JAMA. 2012;307(23):
9 EPIDEMIOLOGY
10 EPIDEMIOLOGY Population-based estimates range from 10 to 86 cases per 100,000 person years About 200,000 cases per year Likely underreported in developing countries Causes can be direct or indirect N Engl J Med 2005;353:
11 N Engl J Med 2005; 353: EPIDEMIOLOGY
12 RISK FACTORS DIRECT INDIRECT Pneumonia Sepsis (non pulmonary) Aspiration of gastric contents Non thoracic trauma Pulmonary contusion Hemorrhagic shock Inhalation injury Pancreatitis Near drowning Major burn injury Transfusion Cardiopulmonary bypass Reperfusion edema after transplant or embolectomy
13 Am J Respir Crit Care Med 1995;151: ONSET TIME
14 PATHOPHYSIOLOGY
15 PATHOPHYSIOLOGY Direct Injury Regional consolidation from destruction of alveolar architecture Indirect Injury Pulmonar vascular congestion, interstitial edema and less severe alveolar involvement
16 PHASES
17
18
19 PATHOPHYSIOLOGY Systemic inflammation Activation of complement and coagulation systems Stimulation of inflammatory cells Release of proinflammatory mediators Sequestration of neutrophils in microvasculature Endothelial and epithelial disruption
20 PATHOPHYSIOLOGY Exudation of protein rich fluid from microvasculature into alveolar and interstitial space Disruption of surfactant Fibrotic repair Failure of hypoxic vasoconstriction resulting in severe hypoxemia
21 PHASES
22 PHASES
23 CLINICAL PRESENTATION
24 HYPOXEMIA Pulmonary Edema Diffuse Alveolar hemorrhage Pulmonary embolism Interstitial lung disease Pneumonia Pneumonitis Neoplasm Pulmonary contusion Atelectasis Emphysema Asthma Chronic Bronchitis Bronchiolitis
25 RADIOGRAPHIC FEATURES Diffuse bilateral infiltrates Patchy, confluent Alveolar, ground glass In contrast to heart failure, no prominence of Cardiomegaly Pleural effusion
26 CHEST CT
27 CHEST CT
28 HALLMARKS OF DISEASE Hypoxia Tachypnea Decreased compliance C = Δ Volume Δ Pressure
29 SUMMARY Common and deadly disease New classification excludes ALI Causes can be extrinsic or intrinsic Phases: exudative, proliferative and fibrotic Hypoxemia, dyspnea and poor lung compliance
30 TREATMENT
31 TREATMENT Treat underlying condition Support oxygenation and ventilation Supportive non ventilatory therapy Rescue for refractory hypoxemia
32 VENTILATOR SUPPORT
33 VENTILATOR ASSOCIATED LUNG INJURY Volutrauma Atelectotrauma Biotrauma
34 LUNG PROTECTIVE VENTILATION N Engl J Med 2007;357:
35 LUNG PROTECTIVE VENTILATION Lung injury is heterogeneous Br J Anaesth 2004; 92: 261±70
36 LUNG PROTECTIVE VENTILATION N Engl J Med 2007;357:
37 Parameter Conventional Protective BAL % PMN BAL TNF α BAL IL 1β BAL IL 6 BAL IL 8 No Δ Plasma TNF α No Δ Plasma IL 6 Plasma IL 8 No Δ No Δ JAMA 1999;282:54-61
38 LOW TIDAL VOLUME
39 N Engl J Med 1998;338:347-54
40 Tidal volume 6 ml/kg (Ideal body weight) P plat < 30 cmh 2 0 Aim for ph > 7.2 by increasing RR Add bicarbonate if ph < 7.15 N Engl J Med 2000;342:1301-8
41 Ppeak = Pplat + Pres P High Pressure Peak P 30 V t Plat P 26 t Vti = 402 Vte = 400
42 N Engl J Med 2000;342:1301-8
43 N Engl J Med 2000;342:1301-8
44 Crit Care Med 2004; 32:
45 Journal of Critical Care 44 (2018) 72 76
46 RECRUITMENT MANEUVER
47 RECRUITMENT MANEUVER World J Crit Care Med 2015 November 4; 4(4):
48 N Engl J Med 2006;354:
49 Cochrane Database of Systematic Reviews 2016, Issue 11. Art. No.: CD006667
50 JAMA. 2017;318(14):
51 PEEP
52 N Engl J Med 2004;351:327-36
53 N Engl J Med 2004;351:327-36
54 VENTILATORY SUPPORT Protective lung strategy: improves mortality, organ failure and ventilator days Low TV (< 6 ml/kg IBW) Plateau pressure < 30 cm H 2 0 PEEP improves oxygenation but not mortality Recruitment maneuvers can worsen outcomes
55 NON VENTILATORY SUPPORT
56 VOLUME STATUS
57 N Engl J Med 2006;354:
58 N Engl J Med 2006;354:
59 N Engl J Med 2006;354:
60 STEROIDS
61 N Engl J Med 2006;354:
62 PARAMETER Methylprednisolone Placebo P value 60 day mortality day mortality Ventilator free days (through day 28) < N Engl J Med 2006;354:
63 PARALYTICS
64 340 patients Within 48 hours of onset PaO 2 /FiO 2 < 150 Cisatracurium vs placebo N Engl J Med 2010;363:
65 N Engl J Med 2010;363:
66 PRONE POSITIONING
67
68 N Engl J Med 2001;345:568-73
69 466 patients PaO 2 /FiO 2 < 150 Prone position within first hour of randomization Prone for 16h /day N Engl J Med 2013;368:
70 N Engl J Med 2013;368:
71 NON - VENTILATORY SUPPORT Fluid management: decreases days on ventilator Corticosteroids: decreases days on ventilator Can worsen mortality if initiated after 14 days Paralytics in PaO 2 /FiO 2 < 150 improve mortality Prone positioning in PaO 2 /FiO 2 < 150 improve mortality
72 RESCUE STRATEGIES
73 OSCILLATORY VENTILATION
74 N Engl J Med 2013;368:806-13
75 Planned for 1200 patients PaO 2 /FiO 2 < 200 Stopped at 548 patients N Engl J Med 2013;368:
76 N Engl J Med 2013;368:
77 INHALED NITRIC OXIDE
78 N Engl J Med 2005;353:
79 BMJ Apr 14;334(7597):779
80 Crit Care Med 2014; 42:
81 Crit Care Med 2014; 42:
82 ECMO
83
84 180 patients PaO 2 /FiO 2 < 80 Conventional management vs referral for ECMO consideration Lancet 2009; 374:
85 PROTECTIVE LUNG STRATEGY 93 % 70 % Lancet 2009; 374:
86 RESCUE THERAPIES HFOV can worsen mortality. Increases use of sedatives and paralytics ino: Improves oxygenation. No evidence of mortality benefit ECMO: Consider in PaO 2 /FiO 2 < 80
87 FINAL SUMMARY Hypoxemia, opacities and low lung compliance Three phases: exudative, proliferative and fibrotic Low tidal volume: improves survival PEEP: Improves oxygenation Recruitment and HFOV: Could be harmful Keep them dry and steroids but not past 14 days Paralytics and prone position for PaO 2 /FiO 2 < 150 ino: improves oxigenation but not mortality ECMO: Consider in severe.more data needed
88 THANK YOU
89
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