Acute Respiratory Distress Syndrome

ACUTE RESPIRATORY DISTRESS SYNDROME

Angel Coz MD, FCCP, DCEAssistant Professor of Medicine

UCSF – FresnoNovember 4, 2017

• No disclosures

OBJECTIVES

• IdentifycurrenttrendsandriskfactorsofARDS

• Describethepathophysiology

• Definephasesduringdevelopment

• Listclinicalmanifestations

• Listcriteriathatmustbepresentfordiagnosis

• DescribetreatmentforpatientswithARDS

• 1821 – Laennec Idiopathic lung anasarca

• 1925 – Sir William OslerUncontrolled septicemia leads to frothy pulmonary edema

HISTORY

INTRODUCTION

• Acuterespiratorydistresssyndrome(ARDS)

wasdescribed50yearsago

• Alveolarspacesfilledwithhyalinemembranes

• Substantialoutcomeimprovementovertime

• Commonandlethal/disabling

DEFINITION

CRITERIA – 1994

• Acuteonset

• Bilateral InfiltratesonChest-X-ray

• PCWP≤18mmHgornoclinicalevidenceofvolumeoverload

• Oxygenation:• PaO2 /FiO2 ≤300à Acute LungInjury(ALI)

• PaO2 /FiO2 ≤200à ARDS

JAMA.2012;307(23):2526-2533

BerlinDefinition- 2012

• Timing within oneweek

• Imaging bilateralopacitiesonCXRorChestCT

• Edema not fullyexplainedbycardiacfailureorvolumeoverload

• Oxygenation- Mild- Moderate- Severe

OnPEEP≥5cmH20200<PaO2/FiO2 ≤300mmHg100<PaO2/FiO2 ≤200mmHg

PaO2/FiO2 ≤100mmHg

1994Definition Berlin– 2012

ALI ARDS Mild Moderate Severe

Mortality 26 % 37% 27% 32% 45%

Progressionfrommild 29% 4%

Progression frommoderate 13%

Ventilatorfreedays(d) 20 12 20 16 1

Duration ofMVsurvivors(d) 5 7 5 7 9

JAMA.2012;307(23):2526-2533

EPIDEMIOLOGY

EPIDEMIOLOGY

• Population-basedestimatesrangefrom10to86casesper100,000person– years

• About200,000casesperyear

• Likelyunderreportedindevelopingcountries

• Causescanbedirectorindirect

NEngl JMed2005;353:1685-93

EPIDEMIOLOGY

NEngl JMed2005;353:1685-1693

DIRECT INDIRECT

• Pneumonia • Sepsis(nonpulmonary)

• Aspirationofgastriccontents • Nonthoracictrauma

• Pulmonarycontusion • Hemorrhagic shock

• Inhalationinjury • Pancreatitis

• Neardrowning • Major burninjury

• Transfusion

• Cardiopulmonarybypass

• Reperfusionedema aftertransplantorembolectomy

RISK FACTORS

ONSET TIME

AmJRespir Crit CareMed1995;151:293-301

PATHOPHYSIOLOGY

• DirectInjuryRegionalconsolidationfromdestructionofalveolararchitecture

• IndirectInjuryPulmonar vascularcongestion,interstitialedemaandlessseverealveolarinvolvement

PATHOPHYSIOLOGY

PHASES

• Systemicinflammation– Activationofcomplementandcoagulationsystems

– Stimulationofinflammatorycells– Releaseofproinflammatorymediators

• Sequestrationofneutrophilsinmicrovasculature

• Endothelialandepithelialdisruption

PATHOPHYSIOLOGY

• Exudationofproteinrichfluidfrommicrovasculatureintoalveolarandinterstitialspace

• Disruptionofsurfactant• Fibroticrepair• Failureofhypoxicvasoconstrictionresultinginseverehypoxemia

PATHOPHYSIOLOGY

PHASES

CLINICAL PRESENTATION

• Pulmonary Edema

• Diffuse Alveolar

hemorrhage

• Pulmonary embolism

• Interstitial lung disease

• Pneumonia

• Pneumonitis

• Neoplasm

• Pulmonary contusion

• Atelectasis

• Emphysema

• Asthma

• Chronic Bronchitis

• Bronchiolitis

HYPOXEMIA

RADIOGRAPHIC FEATURES

• Diffuse bilateral infiltrates– Patchy, confluent– Alveolar, ground glass

• In contrast to heart failure, no prominence of – Cardiomegaly– Pleural effusion

CHEST CT

• Hypoxia

• Tachypnea

• Decreasedcompliance

Δ VolumeC=

Δ Pressure

HALLMARKS OF DISEASE

SUMMARY

• Commonanddeadlydisease

• NewclassificationexcludesALI

• Causescanbeextrinsicorintrinsic

• Phases:exudative,proliferativeandfibrotic

• Hypoxemia,dyspneaandpoorlung

compliance

TREATMENT

• Treatunderlyingcondition

• Supportoxygenationandventilation

• Supportivenonventilatory therapy

• Rescueforrefractoryhypoxemia

TREATMENT

VENTILATOR SUPPORT

VENTILATOR ASSOCIATED LUNG INJURY

• Volutrauma

• Atelectotrauma

• Biotrauma

LUNG PROTECTIVE VENTILATION

NEngl JMed 2007;357:1113-20.


• Lunginjuryisheterogeneous

BrJAnaesth2004;92:261±70


NEngl JMed 2007;357:1113-20.

Parameter Conventional Protective

BAL%PMN ↑ ↓

BALTNF– α ↑ ↓

BALIL– 1β ↑ ↓

BALIL– 6 ↑ ↓

BALIL– 8 NoΔ ↓

PlasmaTNF– α ↑ NoΔ

PlasmaIL– 6 ↑ ↓

PlasmaIL– 8 NoΔ NoΔ

JAMA1999;282:54-61

LOW TIDAL VOLUME

NEngl JMed 1998;338:347-54

NEngl JMed 2000;342:1301-8

• Tidalvolume6ml/Kg(Idealbodyweight)

• Pplat<30cmH20

• AimforpH>7.2byincreasingRR

• AddbicarbonateifpH<7.15

P

t

V

t

PeakP

30

Vti =402Vte =400

HighPressure

PlatP

26

Ppeak =Pplat +Pres

NEngl JMed 2000;342:1301-8

Crit Care Med 2004;32:1260–1265

JournalofCriticalCare44(2018)72–76

RECRUITMENT MANEUVER

RECRUITMENT MANEUVER

WorldJCrit CareMed2015November4;4(4):278-286

NEngl JMed 2006;354:1775-86

CochraneDatabaseofSystematicReviews2016,Issue11.Art.No.:CD006667

JAMA.2017;318(14):1335-1345

NEngl JMed2004;351:327-36

VENTILATORYSUPPORT

• Protectivelungstrategy:improvesmortality,organfailureandventilatordays– LowTV(<6ml/KgIBW)– Plateaupressure<30cmH20

• PEEPimprovesoxygenationbutnotmortality

• Recruitmentmaneuverscanworsenoutcomes

NON VENTILATORY SUPPORT

VOLUME STATUS

NEngl JMed2006;354:2564-75.

STEROIDS

NEngl JMed2006;354:1671-84.

NEngl JMed2006;354:1671-84.

PARAMETER Methylprednisolone Placebo Pvalue

60day mortality 29.2 28.6 1

180daymortality 31.5 31.9 1

Ventilatorfreedays(throughday28) 11.2 6.8 <0.001

PARALYTICS

• 340patients• Within48hoursofonset

• PaO2/FiO2 <150• Cisatracurium vsplacebo

NEngl JMed2010;363:1107-16

NEngl JMed2010;363:1107-16

PRONE POSITIONING

NEngl JMed2001;345:568-73

• 466patients

• PaO2/FiO2 <150

• Pronepositionwithin

firsthourof

randomization

• Pronefor≥16h/day

NEngl JMed2013;368:2159-68

NEngl JMed2013;368:2159-68

NON- VENTILATORYSUPPORT

• Fluidmanagement:decreasesdaysonventilator

• Corticosteroids:decreasesdaysonventilatorCanworsenmortalityifinitiatedafter14days

• ParalyticsinPaO2/FiO2 <150improvemortality

• PronepositioninginPaO2/FiO2 <150improvemortality

RESCUE STRATEGIES

OSCILLATORY VENTILATION

NEngl JMed 2013;368:806-13

NEngl JMed2013;368:795-805.

• Plannedfor1200

patients

• PaO2/FiO2 <200

• Stoppedat548patients

NEngl JMed2013;368:795-805.

INHALED NITRIC OXIDE

NEngl JMed2005;353:2683-95.

BMJ.2007Apr14;334(7597):779

Crit CareMed2014;42:404–412

• 180 patients PaO2/FiO2 <80• Conventional management vs referral for ECMO consideration

Lancet2009;374:1351–63

Lancet2009;374:1351–63

93% 70%PROTECTIVELUNGSTRATEGY

RESCUETHERAPIES

• HFOVcanworsenmortality.Increasesuseofsedativesandparalytics

• iNO:Improvesoxygenation.Noevidenceofmortalitybenefit

• ECMO:ConsiderinPaO2/FiO2 <80

FINALSUMMARY

• Hypoxemia,opacitiesandlowlungcompliance• Threephases:exudative,proliferativeandfibrotic• Lowtidalvolume:improvessurvival• PEEP:Improvesoxygenation• RecruitmentandHFOV:Couldbeharmful• Keepthemdryandsteroidsbutnotpast14days• ParalyticsandpronepositionforPaO2/FiO2 <150• iNO:improvesoxigenation butnotmortality• ECMO:Considerinsevere….moredataneeded

THANK [email protected]

Acute Respiratory Distress Syndrome

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