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ARDS for the ED Physician

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Title: ARDS for the ED Physician


1
  • ARDS for the ED Physician
  • Rafi Israeli, MD
  • Assistant Professor of Medicine
  • Emergency services Institute
  • Cleveland Clinic Foundation
  • Cleveland, Oh

2
Conflicts of Interest
  • None

3
ARDS for the ED Physician
  • History
  • Clinical Course
  • Pathophysiology
  • Causes
  • Incidence
  • Therapy

4
History
  • 1967 Ashbaugh, et al. described Adult
    Respiratory Distress Syndrome
  • Respiratory Distress
  • Cyanosis
  • Hypoxemia despite oxygen
  • Diffuse infiltrates on Chest Xray
  • Drawback No specific Criteria

5
History
  • 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

6
History
  • 1994Ameican- 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

7
History
  • 1994Ameican- European Consensus Conference
    Committee Criteria
  • Acute Onset
  • Bilateral infiltrates
  • PAWP 18
  • ALI PaO2/FiO2 300
  • ARDS PaO2/FiO2 200
  • Drawback Does not specify cause

8
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9
Clinical CourseAcute Phase
  • 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

10
Clinical CourseAcute Phase
  • Patchy infiltrates Coalesce
  • Air Bronchograms
  • Pulmonary Hypertension
  • Intrapulmonary Shunting
  • Endogenous Vasoconstrictors
  • Hyperadrenergic State

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12
Clinical CourseFibrosing Alveolitis
  • Persistent Hypoxia
  • Pulmonary Fibrosis
  • Worsening Compliance
  • Neovascularization
  • Pulmonary Hypertension
  • Macrophages clear neutrophils
  • Chronic Inflammation

13
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14
Clinical CourseRecovery
  • Active transport of Na into interstitium
  • Endocytosis of Protein
  • Transcytosis of Protein
  • Alveolar Epithelial type II cells proliferate
  • Apoptosis of remaining neutrophils?

15
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
20003421334-1349
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17
Pathophysiology
  • 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

18
Pathophysiology
  • Platelet Aggregation
  • Microthrombi ? Shunting
  • Fibrosis from disorganized repair of intersitium

19
Causes
  • DIRECT LUNG INJURY
  • INDIRECT LUNG INJURY
  • Aspiration
  • Pneumonia
  • Pulmonary Contusion
  • Toxic Inhalation
  • Near-Drowning
  • Sepsis
  • Shock
  • Extrathoracic Trauma
  • Multiple Fractures
  • Burns
  • Eclampsia
  • Pancreatitis
  • DIC

20
Incidence Outcome
  • 20-75 per 100,000
  • 30 mortality
  • Recovery may take 6-12 months
  • Residual Restriction
  • Obstruction
  • Gas- Exchange Abnormalities
  • Reduced Quality of Life

21
Therapy
  • Treat Underlying Cause
  • Antibiotics
  • Surgery
  • Enteral Feedings
  • Peyers Patches
  • Less Catheter Sepsis
  • Supportive ARDS Network (ARDSNet)

22
TherapyMechanical Ventilation
  • 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

23
TherapyMechanical Ventilation
  • The Problem Oxygen Toxicity
  • Free Radicals
  • Oxygen Washout and De-Recruitment
  • High FiO2 can lead to further alveolar damage

24
  • Intubation almost always necessary
  • In past, goal was to normalize pH, PaCO2, PaO2
  • High volumes and pressures were used
  • Worse outcomes

25
TherapyLung-Protective Mechanical Ventilation
  • Amato et al. 1998, Effects of a protective-
    ventilation strategy on mortality in the acute
    respiratory distress syndrome. N. Engl. J. Med.
    338347-54
  • 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

26
TherapyLung-Protective Mechanical Ventilation
  • 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. 3421301-8
  • 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

27
Therapy
  • PEEP

28
TherapyPEEP
  • http//content.nejm.org/content/vol354/issue17/ima
    ges/data/1839/DC1/NEJM_Slutsky_1839v1.swf

29
TherapyPermissive Hypercapnea
  • Minute VentilationRR 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

30
TherapyOptimal PEEP
  • Gattinoni et al. 2006.Lung Recruitment in
    Patients with ARDS. N. Engl. J. Med. 3541775-86.
  • 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

31
TherapyOptimal PEEP
  • Gattinoni et al. 2006.Lung Recruitment in
    Patients with ARDS. N. Engl. J. Med. 3541775-86
  • Inclusion Criteria
  • PaO2FiO2 lt 300
  • Bilateral pulmonary infiltrates
  • PACWP lt 18
  • PEEP Trial Prior to CT, high airway pressures and
    PEEP were applied.
  • Lung weight measured by CT

32
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 20063541775-1786
33
TherapyOptimal PEEP
  • Gattinoni et al. 2006.Lung Recruitment in
    Patients with ARDS. N. Engl. J. Med. 3541775-86
  • 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

34
Bedside Peep Adjustment
  • Increase the Peep and Plateau pressure
    constant recruitment.
  • If increase in plateau pressure is proportional
    to PEEP increase overdistension

35
TherapySteroids
  • Pros
  • Inflammatory nature of disease
  • Treatment of Fibrosing alveolitis
  • Cons
  • Historically, no benefit shown with high dose
    steroids
  • Increased infection

36
TherapySteroids
  • 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 3751594-1602
  • Systematic review of studies with low-dose
    steroids
  • Primary outcome Hospital mortality
  • Secondary outcomes length of ventilation, ICU
    LOS, Lung injury score, PaO2FiO2.

37
TherapySteroids
  • 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 3751594-1602
  • Results
  • 9 studies reviewed (4 RCT, 5 cohort)
  • 648 total subjects, mean age 51
  • 40-250mg/d Methylprednisolone
  • 7-32 days

38
TherapySteroids
  • 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 3751594-1602
  • Mortality Trend toward reduction.
  • RTC P0.08. Cohort P0.06.
  • Combined P0.01
  • Morbidity Reduced ventilation 4 days Reduced
    ICU stay 4 days
  • Improved Disease Severity Scores
  • Improved PaO2FiO2

39
TherapySteroids
  • 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 3751594-1602
  • Adverse Effects No difference in infection,
    musculoskeletal complications, GI bleeding, major
    organ failure.

40
TherapyFluids
  • Can diuresis or fluid restriction minimize
    alveolar edema?
  • ARDSNet 2006. Comparison of Two-Fluid Management
    Strategies in Acute Lung Injury. N. Engl. J. Med.
    35424 2564-75
  • Prospective, RCT comparing liberal fluid use vs.
    conservative (more Lasix, less boluses).
  • More positive fluid balances in liberal vs.
    conservative .
  • Subjects were intubated, PaO2FiO2lt 300
  • Protocol initiated 43 h post ICU admission.

41
TherapyFluids
  • ARDSNet 2006. Comparison of Two-Fluid Management
    Strategies in Acute Lung Injury. N. Engl. J.
    Med. 35424 2564-75
  • 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

42
TherapyPA Catheter
  • 1994 American- European criteria require the
    absence of LA hypertension
  • PAC information often ambiguous
  • Practitioners often misinterpret PAC info
  • Associated Risks

43
TherapyPA Catheter
  • The Acute Respiratory Distress Network. 2006. PAC
    versus CVC to Guide Treatment of Acute Lung
    Injury. N. Engl. J. Med. 35421. 2213-24
  • Included intubated pts with PaO2FiO2lt300.
  • Bilateral infiltrates
  • Excluded ALI gt 48 Hours, dialysis, irreversible
    conditions
  • All pts were ventilated with low tidal volumes

44
TherapyPA Catheter
  • The Acute Respiratory Distress Network. 2006.PAC
    versus CVC to Guide Treatment of Acute Lung
    Injury. N. Engl. J. Med. 35421. 2213-24
  • Death within 60 days was similar
  • Ventilator- Free days similar
  • No difference if patients were in shock
  • More Arrhythmias in PAC group

45
DiagnosisBNP
  • 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

46
DiagnosisProcalcitonin
  • 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

47
DiagnosisUltrasound
  • Copetti et al. Cardiovascular Ultrasound 2008,
    616 

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49
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 lt0.04)
  • Total organ system failure less in NIVPPV group
    (Plt0.001)

50
NIVPPV
  • No good studies assesing NIVPPV as a means to
    prevent intubation in ARDS.

51
Prognosis
  • Prognosis primarily depends on underlying cause
    of lung injury
  • Sepsis has worst prognosis
  • Pneumonia has intermediate prognosis
  • Trauma has best prognosis

52
Surviving Sepsis Guidelines
  • 6 cc/ kg Tidal Volume
  • End- inspiratory plateau pressures lt 30
  • Hypercapnea is acceptable
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