- Acute Respiratory Distress Syndrome (ARDS) is characterized by severe respiratory failure caused by diffuse lung injury from medical or surgical disorders. It involves three phases - exudative, proliferative, and fibrotic. - The management of ARDS focuses on treating the underlying cause, lung-protective ventilation with low tidal volumes, use of PEEP to prevent alveolar collapse, and consideration of prone positioning. Adjunctive therapies like neuromuscular blockade and fluid restriction may help but other proposed therapies like steroids have not proven beneficial. Mortality remains high depending on severity of hypoxemia and presence of other organ failure.

1. ARDS
Diana May B. Laraya, MD
Acute
Respiratory
Distress
Syndrome

2. Definition:
Severe dyspnea of rapid onset
Hypoxemia
Diffuse pulmonary infiltrates
RESPIRATORY FAILURE

3. ARDS
• Caused by diffuse lung injury
• Medical or surgical disorders
• Direct or Indirect

5. 18th ed HPIM
• ALI: PaO2/FiO2 ≤ 300mmHg
• ARDS: PaO2/FiO2 ≤ 200mmHg

6. etiology
• >80% caused by sepsis and Pneumonia
• 40-50% : trauma, transfusion-related,
aspiration of gastric contents
• Trauma ~ pulmonary contusion, multiple rib
fracture, chest wall trauma/flail chest
• Rare causes: head trauma, near-drowning,
toxic inhalation, burns

7. ARDS
• Clinical course
1. Exudative
2. Proliferative
3. Fibrotic

8. ARDS: pathophysiology

9. ARDS: exudative

10. ARDS: exudative

11. • Early alveolar edema
• Neutrophil-rich leukocyte infiltration
• Hyaline membrane from diffuse alveolar
damage
• ~First 7 days
ARDS: exudative

12. • Prominent interstitial inflammation
• Early fibrotic changes
• ~Day 7-day21
 Neutrophillymphocyte
 ↑type II pneumocytedifferentiate into type I
pneumocyte
 Synthesis of new pulmonary surfactant
ARDS: proliferative

13. • Alveolar type III procollagen peptide
~↑ mortality from ARDS
• Extensive alveolar duct and interstitial fibrosis
• Emphysema-like changes with bullae
• Intimal fibroproliferation in the pulmonary
microcirculation vascular occlusion
pulmonary HPN
ARDS: fibrotic

14. • Long-term support on MV and supplemental O2
• INCREASED RISK pneumothorax
• REDUCTION in lung compliance
• Increased pulmonary dead space
↑↑↑ Morbidity and Mortality
ARDS: fibrotic

15. Time course for the development of
ARDS

16. ARDS: MANAGEMENT
• GENERAL PRINCIPLES
Recognition and treatment of the underlying medical and
surgical disorder
Minimizing procedures and their complications
Prophylaxis against VTE, GI bleeding, aspiration, excessive
sedation and central venous catheter infection
Prompt recognition of nosocomial infections
Provision of adequate nutrition

17. • Mechanical ventilation management
• VENTILATOR-induced lung injury:
• Repeated alveolar lung overdistention
• Recurrent alveolar collapse
ARDS: MANAGEMENT

18. • National Institute of Health:ARDS Network
– RCT comparing low VT (6mL/kg BW) ventilation
vs
conventional VT (12mL/kg BW)
- Significantly low mortality rate in the low VT pxs
(31%) compare to conventional VT (40%)
ARDS: MANAGEMENT
VT=6mL/kg BW

19. • Mechanical ventilation management
• VENTILATOR-induced lung injury:
Repeated alveolar lung overdistention
• Recurrent alveolar collapse
ARDS: MANAGEMENT

20. • Prevention of alveolar collapse
• ALVEOLAR COLLAPSE due to
– Presence of alveolar and interstitial fluid
– Loss of surfactant
– Decrease in lung compliance
ARDS: MANAGEMENT

21. • Positive end-expiratory pressure (PEEP)
– Minimize FiO2
– Maximize PaO2
• “Optimal PEEP” in ARDS: 12-15mmHg
ARDS: MANAGEMENT

22. • Inverse-ratio ventilation
– Increase mean airway pressure
– Longer inspiration time than expiration time
I:E >1:1
• ↓ time to exhale => dynamic hyperinflation =>
increased end-expiratory pressure => oxygenation
improved
No benefit in ARDS mortality
ARDS: MANAGEMENT

23. • PRONE position
– Improve arterial oxygenation
– Uncertain effect on survival and outcomes
Hazards:
Accidental endotracheal extubation
Loss of central venous catheters
Orthopedic injury
ARDS: MANAGEMENT

24. • Other mechanical ventilation strategies:
1. High-frequency ventilation (HFV)
• High respiratory rates (5-20 cycles per second) and
• Low VTS (1-2mLkg)
2. Partial liquid ventilation (PLV)
• Perfluorocarbon
 No survival benefit from ARDS
ARDS: MANAGEMENT

25. • Lung-replacement therapy with extracorporeal
membrane oxygenation (ECMO)
– Neonates
– With survival benefit
ARDS: MANAGEMENT

26. adjunctive ventilator therapy
(PEEP, HFV, PLV, ECMO, etc)
incomplete efficacy data
rescue therapy
ARDS: MANAGEMENT

27. ARDS: Fluid Management
• Fluid restriction
• Diuretics
  reduce left atrial filling pressure
↓
Minimizes pulmonary edema  prevents further
decrements in arterial oxygenation and lung compliance

28. NEUROMUSCULAR blockade
• EARLY Neuromuscular blockade for 48H
– Cisatracurium besylate
lung-protective ventilation
 px-ventilator synchrony

29. ARDS: Glucocorticoids
• Reduce pulmonary inflammation
• Benefit in some studies
• Current evidence does not support the use
of glucocorticoids

30. OTHER THERAPIES
1. SURFACTANT replacement
2. Inhaled nitric oxide
3. Inhaled epoprostenol
 improve oxygenation-transient
***do not improve survival or decrease
time on Mech Vent

33. ARDS: Prognosis
• Mortality ~ 26%-44%
Nonpulmonary causes >80%
 Sepsis
 Nonpulmonary organ failure

34. ARDS: Mortality Risk Factors
• Nonpulmonary cause – major
• Advanced age (>75yo)
• Preexisting organ failure
• Direct lung injury (2x)
• Severe hypoxemia (PF ratio <100)

35. Functional Recovery in ARDS survivors
• Maximal lung fxn – 6months
• 1yr after extubation ~ 1/3 have N spirometry
• Most have mild abnormalities in pulmo fxn
• 5yr assessment ~ exercise limitation and
decreased physical quality of life

36. ARDS
Thank you…