This document discusses acute respiratory distress syndrome (ARDS), including its definition, causes, pathogenesis, management challenges, and treatment strategies. ARDS is characterized by acute lung injury leading to hypoxemia. Common causes include pneumonia, sepsis, and trauma. The lung injury progresses through exudative, proliferative, and fibrotic phases. Conservative fluid management, low tidal volume ventilation, and positive end-expiratory pressure are the primary treatment approaches.

1. ARDS
Atef Kamel

2. Outline
 Define ARDS and describe the pathological
process
 Know causes of ARDS, and differential diagnosis
 Understand specific challenges in mechanical
ventilation of patients with ARDS
 Understand treatment strategies and evidence
behind

3. ARDS
Severe lung injury characterized by non-
cardiogenic pulmonary
edema, decreased lung
compliance, refractory hypoxemia
Definition
 Acute onset (<2 weeks)
 Bilateral infiltrates on chest x ray
 PCWP ≤18mmHg
 Acute lung injury if PaO2/FiO2 ≤300
 ARDS if PaO2/FiO2 ≤200

4. Most common causes ARDS
Pneumonia (34%)
Sepsis (27%)
Aspiration (15%)
Trauma (11%)
 Pulmonary contusion
 Multiple fractures

5. Causes cont.

6. Risk factors for ARDS
 Preexisting lung disease
 Chronic alcohol use
 Low serum pH
 Sepsis
40% of patients with sepsis
develop ARDS

7. Differential diagnosis
Pulmonary edema from left heart failure
Diffuse alveolar hemorrhage
Lupus pneumonitis
Drug-induced pulmonary edema and
pneumonitis
Acute major pulmonary embolus
Sarcoidosis
Interstitial pulmonary fibrosis

8. Excluding other diagnoses
 Echo
 Central venous catheter
 Bronchoscopy with bronchoalveolar
lavage (to evaluate for
hemorrhage, etc)
 Chest CT

9. Pathogenesis

10. Pathophysiology
 Diffuse alveolar damage
 Lung capillary damage
 Inflammation/pulm edema
 Resulting severe hypoxemia and decreased
lung compliance

11. Phases of ARDS
 Acute - exudative, inflammatory
(0 - 3 days)
 Subacute - proliferative
(4 - 10 days)
 Chronic - fibrosing alveolitis
( > 10 days)

12. Phases of ARDS

13. Exudative phase (Acute Phase)
 Alveolar-capillary barrier is formed by
microvascular endothelium and alveolar
epithelium
 Under normal conditions epithelial barrier is
much less permeable than endothelium
 Epithelium is made up of type I and II cells
 Type I cells are injured easily and Type II cells
are more resistant

14. Exudative Phase
In ALI/ARDS – damage to either one
occurs resulting in increased permeability
of the barrier
influx of protein-rich edema fluid into the
alveolar space
Injury of Type I cells results loss of
epithelial integrity and fluid extravasation
(edema)
Injury of Type II cells then impairs the
removal of the edema fluid (loss of
surfactant)

15. Exudative Phase

16. Proliferative Phase
 With intervention (mechanical ventilation)
there is clearance of alveolar fluid
 Soluble proteins are removed by diffusion
between alveolar epithelial cells
 Insoluble proteins are removed by
endocytosis and transcytosis through
epithelial cells and phagocytosis through
macrophages

17. Proliferative Phase
 Type II cells begin to differentiate into Type I
cells and reepithelialize denuded alveolar
epithelium
 Further epithelialization leads to increased
alveolar clearance

18. Proliferative phase

19. ARDS - Outcomes
Most studies - mortality 40% to 60%;
similar for children/adults
Death is usually due to sepsis/MODS
rather than primary respiratory

20. Management of ARDS
Treat underlying illness
 Sepsis, etc
Nutrition
Supportive care
DVT prophylaxis
GI prophylaxis
Medications

21. Fluid management
“Dry lungs are happy lungs”
Conservative fluids:
 Improved oxygenation
 More ventilator-free days
 More days outside ICU
 No increase in shock or dialysis
 No mortality effects

22. Pulmonary support
KEYS
 Low tidal volumes – 6-8mL/kg ideal
body weight
 Maintain plateau (end-inspiratory)
pressures <30cm H20
 Permissive hypercapnia and
acidosis
Decreased mortality by 22%

23. Positive End-Expiratory Pressure
(PEEP)
Titrate PEEP to decrease FiO2
 Goal sat 88% with FiO2 <60%
Minimize oxygen toxicity
 PEEP can improve lung recruitment and
decrease end-expiratory alveolar
collapse (and therefore right-to-left
shunt)
 Can also decrease venous return, cause
hemodynamic compromise, worsen
pulmonary edema

24. Other Ideas in Ventilator
Management
 Prone positioning
 May be beneficial in certain subgroup, but
complications including pressure sores
 RCT of 304 patients showed no mortality benefit
 High-frequency oscillatory ventilation
 In RCT, improved oxygenation initially, but
results not sustained after 24 hours, no
mortality benefit
 ECMO
 RCT of 40 adults showed no benefit

25. Complications of mechanical
ventilation
Mechanical ventilation causes:
 Overdistention of lungs (volutrauma)
 Further damaging epithelium
 Increased fluid leak, indistinguishable from
ARDS damage
 Barotrauma
 Rupture alveolar membranes
 Pneuomothorax, pneumomediastinum
 Sheer stress
 Opening/closing alveoli
 Inflammatory reaction, cytokine release
Oxygen toxicity
 Free radical formation

26. Drug therapy
 Agents studied:
 Corticosteroids
 Ketoconazole
 Inhaled nitric oxide
 Surfactant
 No benefit demonstrated