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Acute Respiratory Distress Syndrome Dr. Eric Mugambi

Ards level 3 lecture

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Page 1: Ards level 3 lecture

Acute Respiratory Distress Syndrome

Dr. Eric Mugambi

Page 2: Ards level 3 lecture

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

Page 32: Ards level 3 lecture

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