Ards level 3 lecture
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Transcript of Ards level 3 lecture
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Acute Respiratory Distress Syndrome
Dr. Eric Mugambi
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Historical perspective
1821 – Laennec in ‘A treatise on
diseases of the chest’
Idiopathic anasarca of the lungs
Trauma associated
World war 1 & 2
Vietnam war
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Historical perspective
1950s - Advances in critical care
Respirators
Airway access
Hence the term ‘respirator lung’
Other terms related to inciting agent
Post-traumatic, shock lung, wet lung,
DaNang lung)
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Historical perspective
1967 – Case series of 12 patients
acute onset
tachypnœa
hypoxæmia
loss of compliance
Ashbaugh D, Boyd Bigelow D, Petty T, Levine B. ACUTE RESPIRATORY DISTRESS IN ADULTS. The Lancet. 1967;290(7511):319-23.
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Defining features
Hypoxemia
Low Pa02
Stiff lungs
Reduced compliance
Hyaline membranes
Early fibrosis in patients who died
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Epidemiology
Not well characterized due to lack of uniform diagnosis
Before ICUs – most patients died No opportunity for organized
investigations US data
50,000 to 200,000 cases per year (2003) 79/100,000 – ALI 59/100,000 – ARDS 4-9% in ICU settings
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Epidemiology
Substantial recovery in lung function occurs within 6-12 months In few cases muscle weakness and neuropsychiatric
problems may persist
Mortality has improved significantly from 54% in 1983 to as low as 25% in 2004 but has plateaued since then Better prognosis with younger age
Leading cause of death is multiple organ failure
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Definitions
1967 – Ashbaugh et al
1988 – Murray and colleagues
1992 – American European Consensus Conference (AECC)
2012 – Berlin definition
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AECC (1994)
1. Acute onset of respiratory failure
2. Bilateral infiltrates resembling pulmonary
edema
3. No evidence of left atrial pressure elevation -
PCWP <18mmhg
4. Ratio of PaO2 to FiO2 is <200mmhg –
ALI – 200<PaO2/FiO2 < 300mmHg (Desaturation)
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“Acute lung injury” no longer exists
Onset of ARDS (diagnosis) must be acute, as defined as within 7 days of some defined event, which may be sepsis, pneumonia, or simply a patient’s recognition of worsening respiratory symptoms.
The Berlin definition
The ARDS Definition Task Force: JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669.
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Berlin definition
Bilateral opacities consistent with pulmonary edema must be present but may be detected on CT or chest X-ray.
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There is no need to exclude heart failure in the new ARDS definition An “objective assessment“– meaning
an echocardiogram in most cases — should be performed if there is no clear risk factor present like trauma or sepsis.
Berlin definition
The ARDS Definition Task Force: JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669.
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Hypoxemia
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Cause of hypoxemia
Hypoventilation
Ventilation perfusion mismatch
Right to left shunt
Diffusion impairment
Reduced inspired oxygen tension
(Pio2)
Very low cardiac output
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Etiology
Common causes (mnemonic PAST) Pneumonia Aspiration Shock Sepsis Trauma *Transfusion (multiple)
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Other causes
Lung Contusion Near drowning Inhalational injury Reperfusion pulmonary edema
Other Cardio-pulmonary bypass Drug overdose Acute pancreatitis (alcohol increases risk!) Transfusion of blood products
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Pathophysiology
Endothelial injury Increased vascular permeability – hallmark
Epithelial disruption Alveolar flooding Disorganized repair leads to fibrosis Septic shock in patients with bacterial
pneumonia Loss of type 2 cells
Impaired fluid transit – no fluid removal Loss of surfactant Loss of type 1 progenitor cells
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Consequences
Impaired gas exchange leading to severe hypoxemia - 2/2 ventilation-perfusion mismatch, increase in physiologic dead space
Decreased lung compliance – due to the stiffness of poorly or non-aerated lung
Pulm HTN – 25% of pts, due to hypoxic vasoconstriction, Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction
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Normal BGB
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Small bronchiole and alveolae
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Alveoli and capillaries
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Clinical Presentation
Acute onset within 12-36 hrs of inciting event, upto 5-7days
Dyspnoea, tachypnoea, hypoxemia, dry cough chest pain
O/E: tachycardia, cyanosis, tachypnoea, diffuse rales,
BGAs: resp alkalosis, hypoxemia
CXR: bilateral alveolar infiltrates over 75% of lung fields
No pulm venous congestion, no kerley b lines, no cardiomegaly, pleural effusions
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Differential diagnoses
1. Pneumonia
2. Diffuse alveolar hemorrhage
3. Idiopathic acute eosinophilic pneumonia
4. Cryptogenic organising pneumonia
5. Acute interstitial pneumonia
6. Rapidly progressive cancer
7. Cardiogenic pulmonary edema
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Management
Investigations Guided by clinical suspicion of
underlying illness (ddx) For monitoring progress in patients with
critical illness▪ Routine e.g. ABGs▪ Tests of Organ function
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Management
Treat underlying illness
Minimize procedures
Prevent complications
Barotrauma
DVT
Stress ulcers
Promptly recognize nosocomial infections
Provide adequate nutrition
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Therapies in ARDS
THERAPY RECOMMENDATION
Low tidal volume A (strong evidence from RCTs)
Minimize left atrial filling pressures
B (limited clinical data)
High PEEP C (recommended only as alternative)
Prone positioning C
Recruitment maneuvers C
ECMO C
High frequency ventilation D (Not recommended)
Glucocorticoids D
Surfactant, Inhaled NO, other anti-inflammatory
D
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The future
Gene therapy Mesenchymal stem cells
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Consequences
Impaired gas exhange leading to severe hypoxemia - 2/2 ventilation-perfusion mismatch, increase in physiologic deadspace
Decreased lung compliance – due to the stiffness of poorly or nonaerated lung
Pulm HTN – 25% of pts, due to hypoxic vasoconstriction, Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction