Ards rahul
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This document discusses acute respiratory distress syndrome (ARDS). Key points include: - ARDS occurs in 1-4% of PICU admissions and has a mortality rate varying between 20-75%. - It is defined by acute onset pulmonary edema, hypoxemia, and absence of heart failure. Severity is classified by PaO2/FiO2 ratio. - Causes include direct lung injury from pneumonia/aspiration or indirect injury from sepsis/trauma. - Management focuses on mechanical ventilation with low tidal volumes, permissive hypercapnia and optimal PEEP to reduce lung injury while improving oxygenation. Prognosis depends on severity of hypoxemia and underlying cause.
Ards rahul
- 1. Acute Respiratory Distress Syndrome Rahul Illaparambath
- 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 ¨C 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 ¨C The PaO2/FiO2 is >200 mmHg, but ¡Ü300 mmHg, -Moderate ARDS ¨C The PaO2/FiO2 is >100 mmHg, but ¡Ü200 mmHg -Severe ARDS ¨C The PaO2/FiO2 is ¡Ü100 all accompanied by ventilator setting that include PEEP ¡Ý5 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 ¡ýpulmonary compliance, arterial hypoxemia, tachypnea, hypocarbia. ,x ray (pulmonary edema) Fibroproliferative phase ¡ü 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 .
- 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
- 16. Full blown ARDS picture
- 17. CT scan picture
- 18. 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)
- 19. Management ? MECHANICAL VENTILATION ? FLUID MANAGEMENT ? SEDATION AND ANALGESIA ? POSITIONING ? HFOV ? DRUGS
- 20. Ventilation-Goals ? Maintain adequate gas exchange ? Minimal VILI -Keep FiO2 less than 60% -Avoid volutrauma and barotrauma -Avoid repetitive disconnection
- 21. ? 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
- 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
- 25. Adjuvant Therapies in ARDS ? HFOV ? NITRIC OXIDE ¨C pulmonary vasodilatation ? STEROIDS ? SURFACTANT ? ECMO ? Inhaled &systemic beta agonists
- 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, ¡Ý12 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.