ACUTE RESPIRATORY DISTRESS SYNDROME Angel Coz MD, FCCP, DCE Assistant Professor of Medicine UCSF Fresno November 4, 2017
No disclosures
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
HISTORY 1821 Laennec Idiopathic lung anasarca 1925 Sir William Osler Uncontrolled septicemia leads to frothy pulmonary edema
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
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 2 300 à Acute Lung Injury (ALI) PaO 2 / FiO 2 200 à ARDS
Berlin Definition - 2012 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 2 0 200 < PaO 2 / FiO 2 300 mmhg 100 < PaO 2 / FiO 2 200 mmhg PaO 2 / FiO 2 100 mmhg JAMA. 2012;307(23):2526-2533
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) 20 12 20 16 1 Duration of MV survivors (d) 5 7 5 7 9 JAMA. 2012;307(23):2526-2533
EPIDEMIOLOGY
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;353:1685-93
N Engl J Med 2005; 353:1685-1693 EPIDEMIOLOGY
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
Am J Respir Crit Care Med 1995;151:293-301 ONSET TIME
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY Direct Injury Regional consolidation from destruction of alveolar architecture Indirect Injury Pulmonar vascular congestion, interstitial edema and less severe alveolar involvement
PHASES
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
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
PHASES
PHASES
CLINICAL PRESENTATION
HYPOXEMIA Pulmonary Edema Diffuse Alveolar hemorrhage Pulmonary embolism Interstitial lung disease Pneumonia Pneumonitis Neoplasm Pulmonary contusion Atelectasis Emphysema Asthma Chronic Bronchitis Bronchiolitis
RADIOGRAPHIC FEATURES Diffuse bilateral infiltrates Patchy, confluent Alveolar, ground glass In contrast to heart failure, no prominence of Cardiomegaly Pleural effusion
CHEST CT
CHEST CT
HALLMARKS OF DISEASE Hypoxia Tachypnea Decreased compliance C = Δ Volume Δ Pressure
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
TREATMENT
TREATMENT Treat underlying condition Support oxygenation and ventilation Supportive non ventilatory therapy Rescue for refractory hypoxemia
VENTILATOR SUPPORT
VENTILATOR ASSOCIATED LUNG INJURY Volutrauma Atelectotrauma Biotrauma
LUNG PROTECTIVE VENTILATION N Engl J Med 2007;357:1113-20.
LUNG PROTECTIVE VENTILATION Lung injury is heterogeneous Br J Anaesth 2004; 92: 261±70
LUNG PROTECTIVE VENTILATION N Engl J Med 2007;357:1113-20.
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
LOW TIDAL VOLUME
N Engl J Med 1998;338:347-54
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
Ppeak = Pplat + Pres P High Pressure Peak P 30 V t Plat P 26 t Vti = 402 Vte = 400
N Engl J Med 2000;342:1301-8
N Engl J Med 2000;342:1301-8
Crit Care Med 2004; 32:1260 1265
Journal of Critical Care 44 (2018) 72 76
RECRUITMENT MANEUVER
RECRUITMENT MANEUVER World J Crit Care Med 2015 November 4; 4(4): 278-286
N Engl J Med 2006;354:1775-86
Cochrane Database of Systematic Reviews 2016, Issue 11. Art. No.: CD006667
JAMA. 2017;318(14):1335-1345
PEEP
N Engl J Med 2004;351:327-36
N Engl J Med 2004;351:327-36
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
NON VENTILATORY SUPPORT
VOLUME STATUS
N Engl J Med 2006;354:2564-75.
N Engl J Med 2006;354:2564-75.
N Engl J Med 2006;354:2564-75.
STEROIDS
N Engl J Med 2006;354:1671-84.
PARAMETER Methylprednisolone Placebo P value 60 day mortality 29.2 28.6 1 180 day mortality 31.5 31.9 1 Ventilator free days (through day 28) 11.2 6.8 < 0.001 N Engl J Med 2006;354:1671-84.
PARALYTICS
340 patients Within 48 hours of onset PaO 2 /FiO 2 < 150 Cisatracurium vs placebo N Engl J Med 2010;363:1107-16
N Engl J Med 2010;363:1107-16
PRONE POSITIONING
N Engl J Med 2001;345:568-73
466 patients PaO 2 /FiO 2 < 150 Prone position within first hour of randomization Prone for 16h /day N Engl J Med 2013;368:2159-68
N Engl J Med 2013;368:2159-68
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
RESCUE STRATEGIES
OSCILLATORY VENTILATION
N Engl J Med 2013;368:806-13
Planned for 1200 patients PaO 2 /FiO 2 < 200 Stopped at 548 patients N Engl J Med 2013;368:795-805.
N Engl J Med 2013;368:795-805.
INHALED NITRIC OXIDE
N Engl J Med 2005;353:2683-95.
BMJ. 2007 Apr 14;334(7597):779
Crit Care Med 2014; 42:404 412
Crit Care Med 2014; 42:404 412
ECMO
180 patients PaO 2 /FiO 2 < 80 Conventional management vs referral for ECMO consideration Lancet 2009; 374: 1351 63
PROTECTIVE LUNG STRATEGY 93 % 70 % Lancet 2009; 374: 1351 63
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
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
THANK YOU acoz@fresno.ucsf.edu