ACUTE RESPIRATORY DISTRESS SYNDROME

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ARDS for the ED Physician
Rafi Israeli, MD
Assistant Professor of Medicine
Emergency services Institute
Cleveland Clinic Foundation
Cleveland, Oh
Conflicts of Interest
None
ARDS for the ED Physician
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History
Clinical Course
Pathophysiology
Causes
Incidence
Therapy
1967: Ashbaugh, et al. described Adult Respiratory
Distress Syndrome
 Respiratory Distress
 Cyanosis
 Hypoxemia despite oxygen
 Diffuse infiltrates on Chest Xray
Drawback: No specific Criteria
1988: Murray, et al. expanded the definition of
ARDS using a 4- point scale, based on:
 Extent of Chest Xray abnormalities
 Severity of Hypoxia : PaO2/FiO2
 Amount of PEEP
 Search for cause of ARDS
Drawback: Does not predict Outcome
Does not exclude Cardiogenic Pulm Edema
1994:Ameican- European Consensus
Conference Committee
 Renamed Acute Resp Distress Syndrome
 Described ARDS as “syndrome of
inflammation and permeability”
 Coined the term ALI as a precursor to
ARDS
1994:Ameican- European Consensus Conference
Committee Criteria:
 Acute Onset
 Bilateral infiltrates
 PAWP≤ 18
 ALI: PaO2/FiO2 ≤ 300
 ARDS: PaO2/FiO2 ≤ 200
Drawback: Does not specify cause
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Rapid Onset
Exudates
Consolidations
Respiratory failure
Hypoxemia refractory to O2
Inflammation (even in non-edematous lung)
IL-1,6,8,10, Cytokines
Diminished Lung compliance
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Patchy infiltrates Coalesce
Air Bronchograms
Pulmonary Hypertension
Intrapulmonary Shunting
Endogenous Vasoconstrictors
Hyperadrenergic State
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Persistent Hypoxia
Pulmonary Fibrosis
Worsening Compliance
Neovascularization
Pulmonary Hypertension
Macrophages clear neutrophils
Chronic Inflammation
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Active transport of Na into interstitium
Endocytosis of Protein
Transcytosis of Protein
Alveolar Epithelial type II cells proliferate
Apoptosis of remaining neutrophils?
The Normal Alveolus (Left-Hand Side) and the Injured Alveolus in the Acute Phase of Acute Lung
Injury and the Acute Respiratory Distress Syndrome (Right-Hand Side)
Ware L and Matthay M. N Engl J Med 2000;342:1334-1349
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Alveolar Epithelial Basement Membrane
Breakdown
Damage to Vascular Endothelium
Third Spacing of Protein-Rich fluid
Flooding of Alveoli
Shock
Type II cells damaged:
Less Surfactant
Diminished fluid removal
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Platelet Aggregation
Microthrombi → Shunting
Fibrosis from disorganized repair of intersitium
DIRECT LUNG INJURY
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Aspiration
Pneumonia
Pulmonary Contusion
Toxic Inhalation
Near-Drowning
INDIRECT LUNG INJURY
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Sepsis
Shock
Extrathoracic Trauma
Multiple Fractures
Burns
Eclampsia
Pancreatitis
DIC
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20-75 per 100,000
30% mortality
Recovery may take 6-12 months
Residual: Restriction
Obstruction
Gas- Exchange Abnormalities
Reduced Quality of Life
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Treat Underlying Cause
Antibiotics
 Surgery
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Enteral Feedings
Peyer’s Patches
 Less Catheter Sepsis
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Supportive: ARDS Network (ARDSNet)
The Problem: Ventilator- Induced Lung Injury
 High volumes and pressures: Stress
 Overdistension & Alveolar Cracking
 Cyclic Opening and closing of atelectatic alveoli
Cause increased permeability and alveolar damage
The Problem: Oxygen Toxicity
 Free Radicals
 Oxygen Washout and De-Recruitment
High FiO2 can lead to further alveolar damage
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Intubation almost always necessary
In past, goal was to normalize pH, PaCO2,
PaO2
High volumes and pressures were used
Worse outcomes
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Amato et al. 1998, Effects of a protective- ventilation strategy
on mortality in the acute respiratory distress syndrome. N. Engl.
J. Med. 338:347-54
53 pts with early ARDS
Compared “conventional” ventilation of 12ml/kg to
“protective” 6ml/kg
Low PEEP. PaCO2 35-38
Improved survival at 28 days
Higher percentage of ventilator weaning
Less barotrauma
The Acute Respiratory Distress Network. 2000. Ventilation
with lower tidal volumes as compared with traditional tidal
volumes for acute lung injury and the acute respiratory distress
syndrome. N. Engl. J. Med. 342:1301-8
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Larger Trial. 861 patients
Compared 12 ml/kg vs. 6ml/kg ventilation.
Plateau pressures 50 cm H2O vs. 30 cm H2O.
Trial ended early:
 39.8% mortality vs. 31% mortality
THIS HAS CHANGED CLINICAL PRACTICE
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PEEP
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http://content.nejm.org/content/vol354/issue1
7/images/data/1839/DC1/NEJM_Slutsky_183
9v1.swf
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Minute Ventilation=RR x Tidal Volume
High PEEP Levels (12-15cm H2O)
Low Tidal Volumes and Peak and Plateau Pressures result in
Hypercapnea
Carvalho et al.(1997) found the following
 Increased HR
 Increased PA pressures
 Increased Cardiac Output
 Respiratory Acidosis
 But no adverse Outcomes
Gattinoni et al. 2006.Lung Recruitment in Patients with ARDS.
N. Engl. J. Med. 354:1775-86.
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What is optimal PEEP in individual Patient?
PEEP in non-recruitable lung causes
overdistension: barotrauma and alveolar stress
Study measured %age of recruitable lung using
CT
Gattinoni et al. 2006.Lung Recruitment in Patients
with ARDS. N. Engl. J. Med. 354:1775-86
Inclusion Criteria
 PaO2:FiO2 < 300
 Bilateral pulmonary infiltrates
 PACWP < 18
PEEP Trial Prior to CT, high airway pressures and
PEEP were applied.
Lung weight measured by CT
Frequency Distribution of Patients According to the Percentage of Potentially Recruitable Lung
(Panel A) and CT Images at Airway Pressures of 5 and 45 cm of Water from Patients with a Lower
Percentage of Potentially Recruitable Lung (Panel B) and Those with a Higher Percentage of
Potentially Recruitable Lung (Panel C)
Gattinoni L et al. N Engl J Med 2006;354:1775-1786
Gattinoni et al. 2006.Lung Recruitment in Patients
with ARDS. N. Engl. J. Med. 354:1775-86
Results
 In patients where higher %age of recruitable
lung, mortality higher, worse gas exchange.
 Use of PEEP in patients with lower %age of
recruitable lung was harmful.
Results were variable
Bedside Peep Adjustment
Increase the Peep and Plateau pressure
constant= recruitment.
If increase in plateau pressure is proportional to
PEEP increase= overdistension
Pros
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Inflammatory nature of
disease
Treatment of Fibrosing
alveolitis
Cons
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Historically, no benefit
shown with high dose
steroids
Increased infection
Tang, et al.2009. Use of corticosteroids in acute lung injury and
acute respiratory distress syndrome: A systematic review and
meta-analysis. Crit Care Med 37;5:1594-1602
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Systematic review of studies with low-dose
steroids
Primary outcome: Hospital mortality
Secondary outcomes: length of ventilation, ICU
LOS, Lung injury score, PaO2:FiO2.
Tang, et al.2009. Use of corticosteroids in acute lung injury and
acute respiratory distress syndrome: A systematic review and
meta-analysis. Crit Care Med 37;5:1594-1602
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Results
9 studies reviewed (4 RCT, 5 cohort)
648 total subjects, mean age 51
40-250mg/d Methylprednisolone
7-32 days
Tang, et al.2009. Use of corticosteroids in acute lung injury and
acute respiratory distress syndrome: A systematic review and
meta-analysis. Crit Care Med 37;5:1594-1602
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Mortality: Trend toward reduction.
RTC: P=0.08. Cohort: P=0.06.
Combined: P=0.01
Morbidity: Reduced ventilation: 4 days Reduced
ICU stay: 4 days
Improved Disease Severity Scores
Improved PaO2:FiO2
Tang, et al.2009. Use of corticosteroids in acute lung injury and
acute respiratory distress syndrome: A systematic review and
meta-analysis. Crit Care Med 37;5:1594-1602
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Adverse Effects: No difference in infection,
musculoskeletal complications, GI bleeding,
major organ failure.
Can diuresis or fluid restriction minimize alveolar
edema?
ARDSNet 2006. Comparison of Two-Fluid Management Strategies
in Acute Lung Injury. N. Engl. J. Med. 354;24 2564-75
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Prospective, RCT comparing liberal fluid use vs.
conservative (more Lasix, less boluses).
More positive fluid balances in liberal vs. conservative .
Subjects were intubated, PaO2:FiO2< 300
Protocol initiated ~ 43 h post ICU admission.
ARDSNet 2006. Comparison of Two-Fluid Management
Strategies in Acute Lung Injury. N. Engl. J. Med. 354;24 2564-75
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Hemodynamics: Lower intravascular pressures in
conservative group
Lung Function: Lower PEEP, plateau pressures,
shortened ventilation time in conservative group
Metabolic: Higher creatinine values in conservative.
Mortality: No difference in 60 day mortality
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1994 American- European criteria require the
absence of LA hypertension
PAC information often ambiguous
Practitioners often misinterpret PAC info
Associated Risks
The Acute Respiratory Distress Network. 2006. PAC versus
CVC to Guide Treatment of Acute Lung Injury. N. Engl. J. Med.
354;21. 2213-24
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Included: intubated pts with PaO2:FiO2<300.
Bilateral infiltrates
Excluded: ALI > 48 Hours, dialysis, irreversible
conditions
All pts were ventilated with low tidal volumes
The Acute Respiratory Distress Network. 2006.PAC versus
CVC to Guide Treatment of Acute Lung Injury. N. Engl. J. Med.
354;21. 2213-24
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Death within 60 days was similar
Ventilator- Free days similar
No difference if patients were in shock
More Arrhythmias in PAC group
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Bajwa et al. 2008. Crit. Care. Med. Found that
BNP Levels are elevated in ARDS.
Levitt et al 2008. Crit Care found that BNP levels
do not distinguish CHF from ARDS.
Reasons
Myocardial Dysfunction in sepsis
 Direct inflammation on myocytes
 RA and RV stretch in ARDS
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Diagnosis
Procalcitonin
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Marker that indicates likelihood of having a
systemic response to a bacterial infection
One study found it to be a Marker for mortality
in ARDS
Diagnosis
Ultrasound
Copetti et al. Cardiovascular Ultrasound 2008, 6:16
NIVPPV
Zhan, et al. 2011. Early use of noninvasive positive pressure
ventilation for acute lung injury: A multicenter randomized
controlled trial. Crit Care Med
RTC
40 patients randomized to high flow oxygen vs. NIVPPV
Less intubations in NIVPPV (P <0.04)
Total organ system failure less in NIVPPV group (P<0.001)
NIVPPV
No good studies assesing NIVPPV as a means to
prevent intubation in ARDS.
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Prognosis primarily depends on underlying
cause of lung injury
Sepsis has worst prognosis
Pneumonia has intermediate prognosis
Trauma has best prognosis
Surviving Sepsis Guidelines
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6 cc/ kg Tidal Volume
End- inspiratory plateau pressures < 30
Hypercapnea is acceptable
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