Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are clinical syndromes characterized by rapid onset hypoxemia due to diffuse pulmonary infiltrates. ARDS is a more severe form with a PaO2/FiO2 ratio below 200. The natural history involves an initial exudative phase followed by a proliferative phase and potential fibrotic phase. Treatment focuses on supportive care including low tidal volume ventilation, conservative fluid management, and use of PEEP to open lung volumes. Other potential therapies include prone positioning, neuromuscular blockade, inhaled nitric oxide, and extracorporeal membrane oxygenation. The Berlin definition updated diagnostic criteria in 2011 to categorize ARDS as mild, moderate,

1. ACUTE LUNG INJURY & ARDS
Presenter - Dr. Chandan kumar

2. Definition
• Clinical syndrome of severe dyspnea of rapid onset,
hypoxemia and diffuse pulmonary infiltrates leading to
respiratory failure without increased left atrial pressure.
• Acute lung injury is a less severe disorder potential to
evolve in ARDS
• Po2 (in mm Hg ) / FIO2 (Inspiratory O2 fraction)< 200- ARDS
• Between 200-300 - ALI

3. ARDS Diagnostic Criteria
Acute Onset
Predisposing Condition
Bilateral Infiltrates
PaO2/FiO2 ≤ 200 mm Hg
Pulmonary capillary Wedge Pressure ≤ 18 mm Hg or
no clinical evidence of increased LA pressure.

4. • 10% of ICU admission suffer from acute
respiratory failure- 20 % meeting criteria of ALI
or ARDS
• Most cases (>80%) caused by small number of
clinical disorders (severe sepsis , bacterial
pneumonia, multiple transfusions)
• Risk increases in patient suffering for more than
one predisposing factors

5. ARDS causes
• Direct Lung Injury:
a) Pneumonia
b) Pulmonary contusion
c) Near drowning
d) Inhalation injury
f) Aspiration of gastric contents

6. • ARDS causes
• Indirect lung injury
a) sepsis
b) severe trauma
Multiple bone fractures
Flail chest
Head trauma
Burns
c) acute pancreatitis
d) Multiple blood transfusion
e) Post cardiopulmonary bypass
f) Drug overdose

7. • Natural history of ARDS
• 3 phases
- Exudative (0-7 days)
- Proliferative ( 7-21 days)
- Fibrotic ( > 21 days)

8. • Exudative phase
• Alveolar capillary endothelium and type one
pneumocyctes are injured
• Edema fluid rich in protein accumulate in
interstitial and alveolar space
• Cytokines (IL 1,IL 8,TNF) ,LTB4 present in acute
phase neutrophil migrate in alveoli
• Alveolar edema predominantly involve
dependent portion of lung

9. • Vascular obliteration by microthrombi and
fibrocellular proliferation increased dead
space and pulmonary hypertension
• CXR : alveolar and interstitial opacity involving at
least 3/4 of lung field.
• Rarely : cardiomegaly, pleural effusions and
pulmonary vascular redistribution.

10. Histologic Findings
←Normal Lung Histology—large alveolar
volumes, septal space very thin, no cellular
congestion.
Hyaline Protein in air
spaces
Cellular Congestion

11. • Proliferative phase
• Usually last day 7 to 21
• Many still experience dyspnea , tachypnea and
hypoxemia.
• Shift from neutrophil to lymphocyte predominant
pulmonary infiltrate.
• Proliferation of type 2 pneumocytes along alveolar
basement membranes- synthesize new pulmonary
surfactant and differentiate in type 1 pneumocytes

12. • Fibrotic phase
• After 3-4 wk : some patient fibrotic phase -
require long term mechanical ventilators or
supplemental oxygen.
• Acinar architecture markedly disrupted
emphysematous changes , pulmonary
hypertension

14. • Therapy- goals
• Treatment of underlying cause
• Cardio-pulmonary support
• Specific therapy targeted at lung injury
• Supportive therapy.

15. • Low tidal volume mechanical ventilation (A)
• In large scale RCTs low VT (6 ml/kg) ventilation
compared to conventional VT (12ml/kg)
ventilation reduced mortality .
• Ventilator induced lung injury require two
processes-repeated alveolar overdistention and
recurrent alveolar collapse.
• High tidal volume ventilation resulting in
additional alveolar damage.

16. • NEUROMUSCULAR BLOCKADE (A)
• In severe ARDS Cisatracurium besylate increases
rate of survival and ventilator free days.
• No increase in incidence of ICU acquired paresis
(CINM).
• Sedation alone can be inadequate for patient
ventilator synchrony required for lung
protective ventilation.

17. • FLUID management (B)
• Low left atrial filling pressure minimize
pulmonary oedema.
• Fluid restriction and diurectics beneficial in
management
• Monitor for hypotension and hypoperfusion of
critical organs.

18. • High PEEP or Open lung (C)
• Presence of alveolar and interstitial fluid and loss
of surfactant lead to marked reduction in lung
compliance in ARDS.
• Optimal PEEP (12-15 mm Hg) in ARDS required
for alveolar recruitment.
• PEEP empirically set to minimize FIO2 and
maximize Pao2

19. Prone Positioning (C)
• Makes regional ventilation/perfusion ratios more
uniform.
• Facilitates drainage of secretions
• Potentiates beneficial effect of recruitment
maneuvers
• Can lead to accidental endotracheal tube
extubation , loss of central venous catheter

21. • Inverse ratio ventilation-
• Inspiration time longer than expiration
(I:E>1:1)
• Increased end expiratory pressure
• High frequency ventilation- (D)
• Ventilating at extremely high RR (5-20
cycles/s) and low tidal volume (1-2 ml/kg).

22. • Partial liquid ventilation (PLV) with
Perfluorocarbon, an inert high density liquid.
Easily solubilizes oxygen and carbon dioxide (D)
• Lung replacement therapy with ECMO : utility in
ARDS patient. (C)
• Glucocorticoids (D)

23. • Inhaled Nitric Oxide (D)
• Selective pulmonary vasodilatation (decreases arterial
and venous resistances)
• Bronchodilator action
• Inhibition of neutrophil adhesion
• Protects against neutrophil oxidants

24. • Other Drug Therapy (D)
• Prostaglandin E1 (PGE1) (pulmonary vasodilatation and anti-
inflammatory effects on neutrophils /macrophages)
• Aerosolized Prostacyclin (PGI2) (selective pulmonary
vasodilatation of ventilated lung areas)
• Surfactant (prevents alveolar collapse and infection)
• Antioxidants

25. • EVIDENCE BASED RECOMMENDATIONS For ARDS
Therapies
Treatment Recommendation
Mechanical ventilation:
Low tidal volume A
Minimize left atrial filling pressures B
High PEEP C
Prone position,ECMO C
Recruitment maneuvers C
Early neuromuscular blockade A
HFV, Glucocoticoids D
Surfactant replacement & inhaled NO , D
Other anti inflammatory therapy

26. • ARDS… ‘Berlin definition’
Adopted in 2011; initiated by European Society Of
Intensive Care Medicine
3 mutually exclusive categories.. based on PaO2/FIO2
(at CPAP or PEEP> 5 cm of H20)
• Mild- 300 - 200 mmHg.
• Moderate- 200 - 100 mmHg.
• Severe- < 100 mmHg.

27. • Acute Lung Injury… No longer exists . Replaced by
mild ARDS.
• Onset within 7 days of some defined event or
worsening of respiratory symptoms.
• Bilateral opacities consistent with pulmonary
edema; may be detected on CT scan.
• No need to exclude heart failure. Patients with
high PCWP can still have ARDS.

28. • Prognosis
• mortality estimates for ARDS range from 26 to
44%
• largely attributable to nonpulmonary causes
• recover their maximum lung function within 6
months.

29. THANK YOU