mastering the art of ards
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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 ¶sternal 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
Extracorporeal Life Support
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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
Extracorporeal Life Support
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