3. ARDS
• Acute respiratory distress syndrome is sudden and progressive
form of acute respiratory failure characterized by severe dyspnea,
hypoxemia & defuse pulmonary infiltrates.
• The syndrome was first described in 1967, and has been referred
to by several terms, including shock lung, traumatic capillary leak
syndrome, and adult hyaline membrane disease.
4. Berlin definition of ARDS
• Onset within 1 week
• Bilateral opacities on chest X-ray
• Respiratory failure not fully explained by cardiac failure or fluid
overload
• Impaired oxygenation
5.
6. Pathophysiology
• Inflammation occurs throughout the lungs, affecting both endothelial
and epithelial surfaces.
• Activated neutrophils are sequestered into the lungs and capillary
permeability is increased, with damage to type I and II alveolar cells.
• This results in exudation and accumulation of proteinrich cellular fluid
within alveoli and the formation of characteristic ‘hyaline membranes’.
• Local release of cytokines and chemokines by activated macrophages
and neutrophils results in progressive recruitment of inflammatory cells.
• Secondary effects include loss of surfactant and impaired surfactant
production.
9. Exudative Stage (0-6 Days)
• Accumulation of excessive fluid in the lungs due to exudation
(leaking of fluids) and acute injury.
• Hypoxemia is usually most severe during this phase of acute
injury, as is injury to the endothelium (lining membrane) and
epithelium (surface layer of cells).
Some individuals quickly recover from this first stage; many others
progress after about a week into the second stage.
10. Proliferative Stage (7-10 Days)
• Connective tissue and other structural elements in the lungs
proliferate in response to the initial injury, including development
of fibroblasts.
• The terms "stiff lung" and "shock lung" frequently used to
characterize this stage.
• Abnormally enlarged air spaces and fibrotic tissue (scarring) are
increasingly apparent.
11. Fibrotic Stage (>10-14 Days)
• Inflammation resolves.
• Oxygenation improves and extubation becomes possible.
• Lung function may continue to improve for as long as 6 to 12
months after onset of respiratory failure, depending on the
precipitating condition and severity of the initial injury.
• Varying levels of pulmonary fibrotic changes are possible.
13. Early Signs & Symptoms
• Dyspnea
• Restlessness
• Confusion
• Drowsiness
• Extreme tiredness
• Low blood pressure
• If pneumonia causing ARDS: Cough, Fever etc.
14. Late Signs & Symptoms
• Severe difficulty in breathing (i.e. labored, rapid breathing.)
Shortness of breath
Tachycardia
Thick frothy sputum
Metabolic acidosis
Cyanosis
Abnormal breath sounds (i.e. crackle, wheeze.)
Decreased PaCo2 with respiratory alkalosis
15. Diagnosis
• History
• Examination: cyanosis, wheeze, crackles, tachycardia etc.
• Investigation:
• ABG
• CBC
• Chest X-ray
• Sputum for C/S
• Chest CT scan
• All other routine investigations
16.
17. Management
• No specific therapy for ARDS
• Patients should be hospitalized and may require ICU support
• Supportive measure includes O2 supplementation & mechanical
ventilation
• Position strategy includes porne & lateral rotation
• Adequate fluid management
18. Oxygen Therapy
• Goal of O2 therapy is to correct hypoxemia (SpO2= ≥92-94%)
• Oxygen can be administered by-
• Nasal cannula: upto 6L/min
• Simple facemask: upto 10L/min
• Venturi facemask: upto 15L/min
• Partial rebreathing facemask: upto 15L/min
• Non-rebreather facemask: upto 15L/min
• High flow nasal cannula: upto 70L/min
• Mechanical ventilation
21. Prone Positioning
• About 2/3rd of patients with ARDS improve their oxygenation after
being placed in a prone position
• The mechanism includes:
• Increased FRC
• Change in regional diaphragmatic motion
• Perfusion redistribution
• Improved clearance of secretions
23. VAP
• Ventilator Associated Pneumonia (VAP) is a type of hospital
acquired pneumonia that develop more than 48 to 72 hours after
endotracheal intubation.
24. Know The Enemy
• Endotracheal intubation increases risk of developing pneumonia by
6 to 21 fold
• Accounts fot 90% of infections in mechanically ventilated patients
25. Why in ICU patients?
• Sickest patients (multiple diseases, immunocompromised,
multi-organ failure, septic and trauma)
• Less movements
• Malnourished
• Diabetic & heart failure
26. Types
• Early onset VAP:
• Less than 4 days after intubation
• Responsible pathogens are usually susceptible to antibiotics
• Late onset VAP:
• Greater than 4 days after intubation
• Responsible pathogens are usually resistant to antibiotics
27. Pathophysiology
• Bacteria enter the lower respiratory tract via following pathways-
• Inspiration of organisms from the oropharynx & GIT (most common cause)
• Direct inoculation
• Inhalation of bacteria
• Haematogenous spread
29. Diagnosis
• Clinical:
• Fever
• Leukocytosis
• Purulent secretions, Bronchial breath sound
• Cough, Dyspnea,Tachypnea, reduced SpO2 etc.
• Microbiological: Culture & sensitivity
• Radiological:
• New and progressive pulmonary infiltrates
• Consolidation, opacity or cavitation
30. Treatment
• Treatment of VAP still remains a difficult and complex
undertaking.
• Clinical evidence suggests that early use of appropriate empiric
antibiotic therapy improves patient outcome in-
• Reduced mortality
• Reduced morbidity
• Reduced hospital stay
31. Prevention
• Hand washing before & after suctioning or touching
• Restriction of visitors
• Continuous removal of subglottic secretions
• HOB elevation (if not contraindicated)
• HME prevents bacterial colonization
