Ards

Question 1

Def

Answer 1

Ards is an acute diffuse inflammatory lung injury , leading to increased lung weight and loss of aerated lung tissue

Question 2

Etiology

Answer 2

Direct cause
Pneumonia
Aspiration
Pulmonary contusion
Pulmonary embolism
Perfusion injury
Reperfusion injury
Inhalation injury

Question 3

Etiology indirect

Answer 3

Sepsis
Acute pancreatitis
Burns
Trauma with multiple fracture
Blood transfusion with tralt

Question 4

Anatomical alterations

Answer 4

:

1. Diffuse Alveolar Damage (DAD)

Hallmark pathological finding in ARDS.

Damage to the alveolar-capillary barrier, comprising:

Endothelial damage: Increased vascular permeability.

Epithelial damage: Loss of type I and type II alveolar cells (responsible for gas exchange and surfactant production).

2. Interstitial and Alveolar Edema

Due to increased permeability of the alveolar-capillary barrier.

Protein-rich fluid leaks into the interstitial and alveolar spaces, causing non-cardiogenic pulmonary edema.

3. Hyaline Membrane Formation

Composed of fibrin and cellular debris from necrotic epithelial cells.

Lines the alveoli, impairing gas exchange.

4. Reduced Surfactant Production

Loss of type II alveolar cells decreases surfactant synthesis.

Leads to alveolar collapse (atelectasis) and reduced lung compliance.

5. Alveolar Collapse (Atelectasis)

Caused by surfactant deficiency and alveolar flooding.

Contributes to severe hypoxemia and impaired ventilation.

6. Fibrosis and Scarring (Chronic Phase)

Prolonged inflammation leads to fibroblast activation and deposition of collagen.

Causes thickening of the alveolar walls and impaired lung elasticity (fibrotic phase).

7. Pulmonary Vascular Changes

Pulmonary capillary damage and microthrombi formation.

Leads to pulmonary hypertension and further impairs oxygenation.

Question 5

Pathogenesis

Answer 5

Exudative phase
★First few hours or days
★Interstitial and alveolar edema
★Cappilary congestion
★Intra alveolar hemorrhage
★Later the inflammatory cells becomes numerous within interstitium
★extensive necrosis of type 1 alveolar epithelial cells
★alveolar edema inactivated surfactant leads to atelectasis

Question 6

Proliferative phase

Answer 6

1.7-10 days after initial injury
2.Type 2 alveolar fibroblast and miofibroblast prol
3.High MV requirement
4Pulmonary htn
5.reduction in lung compliance

Question 7

Fibrotic phase

Answer 7

1.Extensive alveolar duct and intestinal fibrosis
2.Emphysema like changes and bundle formation
3.Fibrosis may result progressive vascular occlusion and pulmonary hypertension

Question 8

Diagonosis

Answer 8

1.Onset of ards must be acute as defined within 7 days

2.bilateral opacities consistent with pulmonary edema may be present but maybe detected on ct and chest xray

3.categories-ventilation with peep >5cm h2
Ards severity
Mild 200-300
Moderate 100-200
Severe<100

4.exclusion criteria
Pleural effusion
Lung collapse
Lobar collapse
Pulmonary nodules

5.ards characteristics
V/Q mismatch
Shunting
Refractory hypoxemia
Peep doesn’t allow lung to get descruited

Question 9

Pressure volume graph

Answer 9

Area btw vip and lip is known as safe window

If tv goes beyond the graph causes
Alveolar distension
Ventilator lung injury>barotrauma
>Volume trauma
Smaller tidal volume.echmo(vv type
Steroids

Question 10

Management

Answer 10

Definitive management
Lung protective ventilation
Tv-4.6ml/kg×ideal body weght
Increased tv result barotrauma
Optimal peep

Adjunctive management
Prone position

Supportive management
Oxygenation
Niv

Question 11

Indication of tht management

Answer 11

Moderate ards
<48 hrs
Pa02fi02<200
Duration 12-16 hrs

Question 12

Contraindications

Answer 12

Spinal cord injury
Increased icp
Facial trauma
Anterior burns.increased abdominal pressure
Pelvic fracture