2. EPIDEMIOLOGY
• ARDS occurs in 1-4% of PICU admissions
• 10% of PICU patients who receive mechanical ventilation
meet diagnostic criteria for ARDS
• Mortality varies between 20 – 75%
3. • Multicentered, prospective cohort study - Flori et al.
-overall hospital mortality was 22% among children
with a PaO2:FIO2 ratio <300
-ARDS (PaO2: FIO2 <200) had a mortality of 26%
-MC diagnosis associated with ALI and ARDS among
the entire study cohort pneumonia (35%)
4. American-European Consensus Criteria
ALI and ARDS
• Acute onset
• Bilateral pulmonary infiltrates on chest radiography
• Pulmonary artery occlusion pressure >18 mm Hg or
no clinical evidence of left atrial hypertension
• PaO2:FIO2 ratio <300 = ALI
• PaO2:FIO2 ratio <200 = ARDS
• Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on
ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J
Respir Crit Care Med 1994;149:818–24.
5. The Berlin Definition of ARDS
• Respiratory symptoms must have begun within
one week of a known clinical insult, or the patient
must have new or worsening symptoms during
the past week
• Bilateral opacities consistent with pulmonary
edema must be present on a chest radiograph or
computed tomographic (CT) scan
• The patient’s respiratory failure must not be fully
explained by cardiac failure or fluid overload
6. • A moderate to severe impairment of
oxygenation must be present(PaO2/FiO2)
-Mild ARDS – The PaO2/FiO2 is >200 mmHg,
but ≤300 mmHg,
-Moderate ARDS – The PaO2/FiO2 is >100
mmHg, but ≤200 mmHg
-Severe ARDS – The PaO2/FiO2 is ≤100
all accompanied by ventilator setting that
include PEEP ≥5 cm H2O.
7. ETIOLOGY
DIRECT INJURY INDIRECT INJURY
Common Common
-Pneumonia , -Sepsis
-Aspiration of gastric content -Severe trauma
Less common Less common
-Pulmonary concussion -Cardiopulmonary bypass
-Fat embolism -Drug overdose
-Near drowning -Acute pancreatitis
-Inhalational injury, -Blood transfusion
8. Mechanisms preventing alveolar
edema
• Retained intravascular protein
• The interstitial lymphatics
• Tight junctions btw alveolar epithelial cells
9. Injury
• Injury causes release of pro-inflammatory
cytokines
• Damage to the capillary endothelium and
alveolar epithelium
• Functional surfactant is lost
• Ability to upregulate alveolar fluid clearance
may also be lost
10. Consequences
• Impaired gas exchange
- ventilation-perfusion mismatching
-while increased physiologic dead space
impairs carbon dioxide elimination
• Decreased lung compliance
-stiffness of poorly or non-aerated lung
• Pulmonary hypertension
-hypoxic vasoconstriction,
-vascular compression by positive airway pressure,
-parenchymal destruction, airway collapse,
11. Phases of ARDS
Exudative phase
↓pulmonary compliance, arterial hypoxemia, tachypnea, hypocarbia.
,x ray (pulmonary edema)
Fibroproliferative phase
↑ alveolar dead space / refractory pulmonary hypertension due to
chronic inflammation and scarring of the alveolar-capillary unit.
Recovery phase
restoration of alveolar epithelial barrier/ gradual improvement in
pulmonary compliance resolution of arterial hypoxemia/ return to
premorbid pulmonary function in many patients .
12.
13. Clinical features
• Fluid accumulation
• Lung compliance declines and tachypnea ensues
• Regional atelectasis and small-airways closure
• Hypoxia / breathing labored
• Hypocarbia followed by hypercarbia
• Rales over areas of atelectasis or alveolar congestion
and decreased air entry over areas that are largely
consolidated. Occasionally rhonchi
14. Investigations
Chest Xray
• Small volume lungs
• Diffuse infiltrates
• Airbronchograms , atelectasis
• Fibrosis with reticular opacities
CT scan
• Heterogenous opacification in dependent
regions
22. • PEEP
-augment anatomical dead space by distending large
airways
-cardiovascular compromise in high PEEP
• Optimal PEEP
-Improves oxygenation
-Displacement of fluid from alveoli
-Recruitment and opening up of collapsed alveoli
-Improved FRC
• Permissive hypercapnia
-Accept high CO2 till pH 7.2
23. • Most children have concomitant shock
• Aggressive fluid resuscitation till stable
• Excess lung water will decrease saturation
• Adequate sedation and analgesia
• Antibiotic therapy for primary cause
• Early enteral nutrition
24. Prone positioning
• Prone position improves V/Q mismatch
• Recruitment of dependent portions
• Decreases chest wall compliance (transmitting
airway pressure to the alveoli more efficiently
and stabilizing alveolar volume over a larger
portion of previously nonaerated lung units)
• If no deterioration with prone position,
continue for 18-20 hours
26. Predictors of outcome
• Disease-related
-Oxygenation-PaO2/FiO2( mild, moderate, and
severe ARDS had mortality rates of 27, 32, and 45
percent, respectively)
-Pulmonary vascular dysfunction(elevated
transpulmonary gradient (ie, ≥12 mmHg)
-Underlying cause of the ARDS
• Patient related
27. • Treatment related
-Fluid balance-positive fluid balance may be
associated with higher mortality (1)
-Treatment with glucocorticoids
-Packed red blood cell transfusion-increased
likelihood of death (odds ratio 1.10 per unit
transfused, 95% CI 1.04-1.17) (2)
1.Rosenberg AL, Dechert RE, Park PK, et al. Review of a large clinical series: association of cumulative
fluid balance on outcome in acute lung injury: a retrospective review of the ARDSnet tidal volume
study cohort. J Intensive Care Med 2009; 24:35.
2.Gong MN, Thompson BT, Williams P, et al. Clinical predictors of and mortality in acute
respiratory distress syndrome: potential role of red cell transfusion. Crit Care Med 2005;
33:1191.
