ards rahul
TRANSCRIPT
Acute Respiratory Distress Syndrome
Rahul Illaparambath
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%
• 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%)
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.
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
• 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.
ETIOLOGYDIRECT INJURY INDIRECT INJURY
Common-Pneumonia , -Aspiration of gastric content
Common-Sepsis-Severe trauma
Less common-Pulmonary concussion-Fat embolism-Near drowning-Inhalational injury,
Less common-Cardiopulmonary bypass-Drug overdose-Acute pancreatitis-Blood transfusion
Mechanisms preventing alveolar edema
• Retained intravascular protein• The interstitial lymphatics• Tight junctions btw alveolar epithelial cells
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
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,
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 .
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
Investigations
Chest Xray • Small volume lungs• Diffuse infiltrates• Airbronchograms , atelectasis• Fibrosis with reticular opacitiesCT scan• Heterogenous opacification in dependent
regions
Early ARDS picture
Full blown ARDS picture
CT scan picture
Differentials….
• Cardiogenic pulmonary edema • An acute exacerbation of IPF - previous chest radiographs - subpleural reticulocytic
changes -surgical lung biopsy• Diffuse alveolar hemorrhage• Idiopathic acute eosinophilic pneumonia(IAEP)• Malignancy • Acute interstitial pneumonia (Hamman-Rich syndrome)
Management
• MECHANICAL VENTILATION• FLUID MANAGEMENT• SEDATION AND ANALGESIA• POSITIONING• HFOV• DRUGS
Ventilation-Goals
• Maintain adequate gas exchange• Minimal VILI -Keep FiO2 less than 60% -Avoid volutrauma and barotrauma -Avoid repetitive disconnection
• Controlled oxygen exposure -Direct cellular injury -Absorption atelectasis -Accept saturation of 86-90%• Low tidal volume ventilation -To limit harmful airway pressures -TV of 6 ml/kg
• 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
• 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
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
Adjuvant Therapies in ARDS
• HFOV• NITRIC OXIDE – pulmonary vasodilatation• STEROIDS• SURFACTANT• ECMO• Inhaled &systemic beta agonists
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
• 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.