mastering the art of ards

8/3/2019 Mastering the Art of Ards

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4/23/12

Critical Case Conference

Presented by:

Reinalyn S. Cartago MDFellow in Training

Gelza Mae Zabat and Joanna Marie BalbuenaResident Rotators

ART of ARDS


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Objectives

Clinical Scenario

ARDS Definition and Background

Criteria for the Diagnosis of ARDS

Causes and Risk Factors Associated withARDS

Mechanism of Injury

Stages of ARDS

MANAGEMENT

O U T L I N E


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To be able to discuss a case of Acute

Respiratory Distress Syndrome

To review and discuss the definition, criteria

for diagnosis, and pathophysiology of ARDS

To enumerate risk factors and causes of ARDS

To discuss the management and critiquecurrent literature on ARDS

OBJECTIVES


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The Case

MC

23/M

Call Center Agent


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The CaseM. C.

23/M, single, Filipino

Call Center Agent

Chief Complaint:

Dyspnea

PROFILE:

Previously well, withgood functionalcapacity

January 2011

On and offundocumented fever

Generalized bodymalaise

Anorexia, weight lossof about 10 15 %

February 2011

Consulted at ourinstitution due topersistence of above

symptoms


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The CaseFebruary 2011

Abdominal CT scandone

Retroperitoneallymph nodes

Biopsy donerevealed:Tuberculosis

Quadruple anti-

kochs therapy wasstarted

ICC screen was doneand was noted to be

(+) for ELISA andWestern blot

1 week PTA

Cough productive ofwhitish sputum

Pleuritic chest pain;easy fatigability

Worsening dyspnea

Generalized bodymalaise

Fever with T max: 38

No additionalmedications taken


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The CaseDiagnosed to have

TB pneumoniaSputum AFB

allegedly waspositive

MEDS:

Ceftriaxone 1 g IV q8

Clarithromycin

500mg/tab, 1 tab BIDPO

HRZE, 4 tabs ODprebreakfast

Paracetamol,

PGH (04/12/11)

Initial PE:

Conscious, oriented,conversant, ambulatory,speaks in sentences

On O2 via Nasal Cannula at6lpm

BP: 120/70 CR: 130s RR: 40T: 36.9

AS, PPC, (-) CLAD/ NVE/ TPC

ECE, clear breath sounds,(-) crackles/rales

AP, tachycardic, regularrhythm, no murmurs


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The CaseCXR


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ADULT PULMONARY SVC(04/16/11)

Conscious, followscommands , speaks in

words supraclavicular retractions

noted

BP: 140/70 CR: 150s RR:40 T: 37.4O2 sats 80s despite Face

Mask at 10 LPM

AS, PPC, (+) CLAD, right/NVE/ TPC

ECE, (+) rhonchi bilateral

AC MODEVT 300

FiO2 100

PEEP 15IFR 60BUR 18

Meropenem 1 g IV q8hCombivent q6h

Azithromycin 500mg/tab ODCo-trimoxazole 800/160/tab, 2

tabs BIDHRZE 3 tabs OD pre breakfast

Fluconazole 100mg OD


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The Case

ETA CS

No growth after 2days

Blood CSNo growth after 5

days

Ortho-Toluidine Bluestain

Positive for

Pneumocystis


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Acute Respiratory DistressSyndrome

(ARDS)DefinitionBackground


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A syndrome often progressive and

characterized by distinct clinical, pathologicaland radiographic stages

Characterized by non-cardiogenic pulmonaryedema, lung inflammation, hypoxemia, anddecreased lung compliance

Murray et al., 5th Edition

Acute onset of severe respiratory distress andcyanosis that was refractory to oxygentherapy and associated with diffuse CXRabnormality and decreased lung compliance

Ashbaugh, Bigelow, Petty Lancet 1967

DEFINITION


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DEFINITION


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First described in 1967Annual incidence 75/100,000 in the US High mortality- 40%-60% Decreased mortality in the late 1990s: 30 40%


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Diagnosing ARDS

Criteria

Differential Diagnosis


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The 1994 North American-European Consensus

Conference

(NAECC) criteria:

Onset - Acute and persistent

Radiographic criteria:

Bilateral pulmonary infiltrates consistent

with the presence of edema

Oxygenation criteria: Impaired oxygenation

regardless of the PEEP concentration

CRITERIA


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Descriptive definition

Does not address the cause of lung injury

Does not provide guidelines on how to defineacute

Radiological criteria are not sufficientlyspecific

Does not account for the level of PEEP used,

Limitations of the Current

Criteria

Th 1998 NAECC U d t d


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1. The collection of epidemiologic data should

be based on the 1994 NAECC definitions.

2. The severity of ALI/ARDS should be assessedby the Lung Injury Score (LIS) or by the APACHE

III or SAPS II scoring systems.

3. The factors that affect prognosis should be

taken into account.

The most important of these are incorporatedinto the GOCA stratification system

The 1998 NAECC UpdatedRecommendations

Th 1998 NAECC U d t d


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4. It will be also useful to record:

Information relating to etiology (at aminimum,

direct or indirect cause)

Mortality, including cause of death, andwhether

death was associated with withdrawal of

care Presence of failure of other organs and other

time

dependent covariates

The 1998 NAECC UpdatedRecommendations


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Lung Injury Score


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GOCA


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Similar CXR findings:

Acute Lung Injury

Diffuse Pneumonia

Cardiogenic Pulmonary Edema

Diffuse Alveolar Hemorrhage

Acute Interstitial Pneumonia

Acute Eosinophilic Pneumonia

DIFFERENTIALS


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Causes of ARDS

Pulmonary (direct)

Non-Pulmonary (indirect)


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PULMONARY

CAUSESNON-PULMONARY


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Risk Factors for ARDS

Risk Factors Predictive of Poor Outcome


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RISK FACTORS


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Mechanism of Injury

Pathophysiology

Stages of ARDS


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Severe injury to thealveolocapillary unit:alveolocapillary leak

Permeabilitypulmonary edema

(protein rich edemafluid)

Surfactant disruption Hyaline membrane

formation Alveolar collapse,

consolidation

Cellular necrosis,epithelial hyperplasia,

inflammation

Fibrosis


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DIFFERENCE IN PATHOLOGIES THRU TIME


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DIFFERENCE IN PATHOLOGIES THRU TIME

5 days

post-injury

12 dayspost-injury

17 dayspost-injury

PROLIFERATIVE PHASE (day 7-21)

EXUDATIVE PHASE (day0- 7)

Gattinoni et al. AJRCCMWare, Matthay. NEJM2000.


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DE- Stressing ARDistressS

Principles of Mechanical Ventilation

Medical/ Non-Ventilatory Management

Other Treatment Modalities


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Characteristics of ARDS / ALI

V/Q < 1

Exudative stage: heterogeneous lung injury

poorlyAerated

(recruitable)

normallyaerated

nonaerated


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VENTILATORY STRATEGIES FOR ACUTE LUNG INJURYAND THE ACUTE RESPIRATORY DISTRESS SYNDROME


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Previous Ventilator Settings in ARDS

Selective barotrauma = Volutrauma

high Vt (10-14 ml/kg), high Pplat

Alveolaroverdistention

Alveolaroverdistention

RecruitedLung segments

Hyperaeratedpart Non-aerated segmentscore disease


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Ventilatory Strategies in

ARDS: Standard of Care

Principle: Lung Protection

Avoid alveolar overdistention: Vt < 6 ml/PBWEnsure Pplat < 30 cm H20

Maintain FiO2 < 0.6

Use sufficient PEEP to prevent cyclicatelectasis

Consider that the mode of ventilation is lessimportant than attending to the above goals

May tolerate hypercapnia, if necessary


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ARDS network studypatients with ALI/ARDS at 10 centers, 861

patients

Patients randomized to tidal volumes of 12mL /kg or 6 ml/kg(volumecontrol, assist

control, plat Press =30 cm H2O)

22% reduction in mortality in patientsreceiving smaller tidal volume

Number-needed to treat: 12 atients


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PERMISSIVE

HYPERCAPNIA Consequence of low VTs but current lung protectivestrategies do not cause clinically significant

hypercapnia

Safety of a very high PaCo2 is not proven

Still unclear how low a value of arterial pH can be

considered safe

PHC usually well-tolerated, the ARDSNet usedNaHCO3 when pH < 7.3 aside from increasing

respiratory rate


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Effect of PEEP in ARDS

PEEP PEEP

Pneumatic splint or prevents derecruitment;Keeps the opened or recruited alveoli open, prevents

re-collapse (PEEP does NOT recruit but maintains recruitment)

On end of expiration,


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L Hi h PEEP T i l (ALVEOLI t i l)


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Lower vs. High PEEP Trial (ALVEOLI trial)

ARDSNet. NEJM 2004,351:327-34.


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PRONE POSITION VENTILATION

Improves oxygenation but not survival MOA:

Limits expansion of cephalic &parasternal lung regions

Relieves cardiac & abdominal

compression on dorsal lung Makes uniform the regional V/Q ratios Facilitates drainage of secretions

Associated w/ adverse events NO sufficient evidence to support routine

use of prone position in patients withARDS

Girard & Bernard. ChestDernaika et al. Amer J > 6 hrs x 10


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PRONE POSITION VENTILATIONon Mortality

Sud et al. CMAJ April 22,-

decreased VAP increased

pressure ulcers

Prone Positioning: Maneuver related


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Prone Positioning: Maneuver-relatedComplications

Complication Events Percentage

Airway obstruction (secretion) 102 / 772 13

Transient oxygen desaturation 97 / 764 13

Arrhythmias 16 / 773 2

Hypotension 15 / 773 1.9Vomiting 12 / 773 1.6

Accidental loss of central

venous catheter

5 / 775 0.6

Accidental extubation 3 / 772 0.4

Accidental loss of thoracic

or abdominal drains

2 / 671 0.2

Pelosi et al Eur

NIV as first-line intervention in ARDS


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4/23/12Antonelli M. et al. Crit Care Med2007;35:18-25

NIV as first-line intervention in ARDS

54% ofpatients

46% ofpatients


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Other Modes ofVentilation


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Airway Pressure ReleaseVentilation

Inverse ratio ventilation

High frequency ventilation

Liquid Ventilation

Extracorporeal Life Support

Airway Pressure Release


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Airway Pressure ReleaseVentilation

pressure-targeted, time-cycled modesimilar to conventional pressure-controlled

ventilation (PCV)

allows spontaneous breathing during inflationby pressure release mechanism leading tomore comfortable ventilation

high airway pressure maintains adequate

alveolar recruitment

Outcome on survival not yet proven

Dernaika et al. Amer J

Esan et al. Chest 2010;137;1203-

1216


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Inverse Ratio Ventilation

Prolong inspiratory time (I:E > 1)

Exact MOA unclear but may be due to alveolar

recruitment with inc in mean airway P

lower peak inspiratory & end expiratory airway P andbetter distribution of ventilation

Patient usually paralyzed

auto-PEEP & hemodynamic compromise risk

Dernaika et al. Am J Med Sci

High Frequency Oscillatory


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High Frequency OscillatoryVentilation

HFOV allows small tidal volumes using high respiratoryrates.

Vt at 1-2 ml/kg with rates of up to 20 cycles/sec or 60-300/minto allow pCO2 to hover to near-normal levels

HFOV oscillates the lung around a constant mean airwaypressure that is higher than usual conventional MV

- Alveolar recruitment is maintained

- Low end-expiratory pressures areavoided

- High peak pressures are avoided

Outcomes same

Chan et al. CHEST 2007; 131:

Li id V til ti


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Partial or total

Perfluorocarbon - dissolves 17 x more O2than saline & 4 x CO2. Non-toxic, not

absorbed thru resp epith

Improved lung recruitment with lower

surface tension, dependent areas reached

Liquid Ventilation

Diaz et al. Crit Care Med 2010; 38:1644



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patient's blood is circulated to external machine (veno-

venous circuit) that provides oxygenation or CO2

removal

used routinely in neonates with severe ARF

? Survival benefit; in experienced centers only

High risk of bleeding; BT 1.7 li/day


Peek et al. Lancet 2009;


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Non Ventilatory Management

Ph l i M t


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Pharmacologic Management

Glucocorticoids

Methylprednisolone 1 mkd

Improved oxygenation & LIS in some studies;ARDSnet inc mort if given > 14 d

Vasodilators (vasodilatation in aerated lung portionsV/Q improvement)

Inhaled Nitric Oxide

Prostaglandin E1

Neb Prostacyclin (Prostaglandin I2)

-Esan et al. Chest

Fluid Management


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Fluid Management


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Fluid Management


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Fluid Management


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Complications

Ventilator Induced Lung Injury


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Alveolar over distension with high tidal

volumes

SIRS/ sepsis

Increased levels of inflammatory mediators in

BAL

Multiple organ dysfunction

Hypercapnia/Acidosis

BAROTRAUMA, VOLUTRAUMA, BIOTRAUMA

VAP

Ventilator Induced Lung Injury


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Long Term Outcomes

Mortality

Outcomes

MORTALITY


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MORTALITY

ONE YEAR OUTCOMES IN SURVIVORS


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ONE YEAR OUTCOMES IN SURVIVORS


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120pts randomized to low Vt or high Vt

25%mortality w/ low tidal volume

45% mortality w/ high tidal volume

20% had restrictive defect and 20%had obstructive defect 1 yr afterrecovery

About 80% had DLCO reduction 1 yrafter recovery


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Looking Back(Clinical Correlation and

Summary)MGH

mastering the art of ards

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