Pediatric Acute Respiratory Distress Syndrome.pptx

Pediatric Acute Respiratory Distress Syndrome.pptx

1. Pediatric Acute Respiratory Distress Syndrome (PARDS ) Moderator: Dr. Arpitha Presenter: Dr. Kunal

2. Section 1. Definition and Terminologies

3. ARDS i s defined as a syndrome with non-cardiogenic pulmonary oedema. It is characterized by Hypoxemia. Radiologically visible infiltrate. Decrease in functional residual capacity. Decrease in lung compliance.

4. Terminologies P/F ratio, stands for PaO2/FiO2, is a hypoxemia indicator is associated with ARDS. S/F ratio , stands for SPO2/FiO2 , is used if P/F ratio is unavailable . It shows the accurate value if the SPO2 is between 80-97%.

5. O xygenation index (OI)- used to access the degree of ventilatory support needed to maintain oxygenation . Illustrate the need for MAP and FiO2 needed during ventilation. The formula for oxygenation index ( OI) = MAP X FiO2 / PaO2 . ( OI) is = MAP X FIO2 / PaO2 .   Oxygen saturation index (OSI): when SpO2 is used instead of PaO2.

6. Berlin Defnitio n Pertained to both Adults and children While evaluating of edema , it needed objective evidence like 2D-Echo to exclude hydrostatic edema Chest imaging needed bilateral opacities not fully explained by effusions, collapse or nodules Oxygenation was defined based on PF ratio Mild - PF 200 to <300 Moderate – PF 100 to <200 Severe – PF <100

7. Section 2. Pathophysiology

8. Etiology & Types Of Injuries Direct injury (Alveolar-Epithelial) Pneumonia- MCC in Children Aspiration Drowning Inhalational injury Pulmonary Contusion Near drowning Indirect Lung Injury ( Alveolar-Capillary ) Sepsis/SIRS- MCC in Adults Major trauma Acute pancreatitis Major Burns Shock TRALI/Massive Transfusion Head injury Cardio-pulmonary bypass  Drug Overdose

9. Pathophysiology Normal alveolar's microscopic structure prevents fluid accumulation in the alveolus. A single layer of epithelial cells lines the inside of the alveolus. 2 types of epithelial cells (I) Flattened epithelial cells or type 1 alveolar epithelial cells and ( II) Cuboidal epithelial cells or type 2 alveolar epithelial cells.

10. Direct or indirect injury to the alveolus causes alveolar macrophages to release proinflammatory cytokines

11. Cytokines attract neutrophils into alveolus & interstitium , where they damage the alveolar-capillary membrane (ACM)

12. ACM integrity is lost, interstitial and alveolus fills with proteinaceous fluids and surfactant no longer support alveolus

13. Injury to the alveolar epithelial-vascular endothelial interface . Damage to alveolar epithelium Type 1 damage leads to V/Q mismatch – decreased gas exchange – Hypoxemia Type 2 damage leads to decreased Fluid/Na+ - flooding of interstitium and alveoli with edema fluid & surfactant deficiency leads to increased surface tension

14. 2. Damage to vascular endothelium Migration of neutrophils into alveoli - release cytokines - Activate macrophages - Alveolar epithelial injuries Interstitial and alveolar edema Clot formation

15. 12:2 Proliferative / organizing ( subacute ) phase: 1 - 3 weeks -Proliferation of type II pneumocytes and differentiation into type I pneumocytes . -Proliferation of myofibroblasts . -Drainage of alveolar edema by restored type II pneumocytes . Fibrotic (chronic) phase: after 3 weeks -Collagenous fibrosis in alveolar spaces and - interstitium -Refractory rigidity of alveoli due to architectural remodeling

16. Clot formation leads to fibrin degradation, and plasmin will be formed. Plasmin again will cause multiple injuries to the alveolar epithelium . Healing by fibrosis- Produces stiff lungs (reduced lung compliance) and reduced lung volumes (decreased FRC). There will be marked regional differences and varying amounts of inflammation. Therefore, ARDS is a Heterogenous disease.

17. Consequences of lung injury include: Impaired gas exchange Decreased compliance Increased pulmonary arterial pressure

18. Decreased Compliance Hallmark of ARDS Consequence of the stiffness of lung & fluid filled lung becomes stiff/boggy Requires increased pressure to deliver Vt

19. Increased Pulmonary Arterial Pressure In 25 % of ARDS patients Results from hypoxic vasoconstriction Positive airway pressure causing vascular compression Can result in right ventricular failure

20. Section 3. Stages

21. Phase 1: Early Changes Radiology Symptoms Lab findings Pathophysiology Normal Dyspnea Tachypnea Normal Examination Hypoxemia – Absent/Mild Hypercapnia Mild pulm . HTn Neutrophil sequestration

22. Phase 2: Onset of parenchymal changes Radiology Symptoms Lab findings Pathophysiology Patchy alveolar infiltrates Dyspnea Tachypnea Cyanosis Tachycardia Coarse rales Hypoxemia – Mod/Severe Hypercapnia Pulmonary Hypertension Decreased compliance Neutrophil sequestration Vascular congestion Pulmonary edema Platelet clumps Type 1 AEC damage

23. Phase 3: Acute Respiratory Failure with Progression; 2-10 days Radiology Symptoms Lab findings Pathophysiology Diffuse alveolar infiltrates Air bronchogram Reduced lung volume No cardiomegaly Tachypnea Tachycardia Signs of pneumonia Consolidation Diffuse rales Sepsis signs Worsened Hypoxemia Low compliance Impaired O2 extraction Alveolar and interstitial inflammation Exudate with macrophages Type 2 AEC and fibroblasts proliferate Thromboemboli

24. Phase 4: Pulmonary fibrosis, pneumonia with progression; >10 days Radiology Symptoms Lab findings Pathophysiology Persistant d iffuse alveolar infiltrates Air leak Cor pumonale & cardiomegaly Phase 3 + MODS features Phase 3 + progressive lung failure, MODS features Type 2 AEC hyperplasia Interstitial thickening Fibrosis Thickening of arterioles Lymphocytes infiltration

25. Other blood tests Increased C reactive protein Increased procalcitonin in septic ARDS Increased ferritin Brain natriuretic peptide (BNP) test may helpful to distinguish ARDS and cardiogenic pulmonary edema BNP ≤ 200 pg /mL is suggestive for ARDS (sensitivity: 40%, specificity: 91 %) BNP ≥ 1,200 pg /mL is suggestive for cardiogenic pulmonary edema (sensitivity: 52%, specificity: 92 %)

26. Chest Xray Exudative phase Ground glass opacity and consolidation with air bronchogram Proliferative phases Reticular shadow and volume reduction Chest CT Exudative phase Patchy to diffuse ground glass opacity, with or without interlobular septal thickening Dorsal consolidation due to infiltrate Ground glass opacity with bronchiolectasis and bronchiectasis Volume reduction Fibrotic phase Septal thickening and reticular shadow in ground glass opacity Peripheral cystic and honeycomb-like lesions due to fibrosis

27. not showing any pathological findings. some pulmonary consolidations at the lower lobes. Over the next 2–3 days, a rapid deterioration progressing to diffuse alveolar involvement, with “white lung” appearance (d). The normal-sized heart and vascular structures help in the differential diagnosis of pulmonary oedema due to heart failure.

28. Long-term evolution of acute respiratory distress syndrome. a , b) multiple and bilateral ground-glass opacities, homogeneous in distribution. c , d) advanced stage of pulmonary fibrosis, with honeycombing and bronchiectasis, which are more evident in the anterior lung regions

29. Section 3. Management With PALICC-2 Guidelines

30. Non-invasive Support Invasive Support Ancillary pulmonary treatments Non-pulmonary therapies General monitoring

31. NIV NIV Success Reduction in RR to Normal for Age Absence of Retractions Absence of Paradoxical breathing Improvement in Gas Exchange Improved pH Improved P/F Ratio Reduction in PaCo2 NIV Failure Signs of Work of Breathing Poor Gas exchange Hemodynamic instability Signs of Respiratory Fatigue Change in mental status Increased Agitation The high-flow nasal cannula, CPAP or BiPAP role is limited and not recommended in pediatric ARDS.

32. Clinical Indication For Escalating To Invasive Ventilation 1 . Increasing Respiratory Rate 2 . Increased Work of Breathing 3 . Worsening Gas exchange 4 . Altered Level of Consciousness

33. Invasive mechanical ventilation in PARDS Aim is to balance the management of hypoxemia with preventing ventilator-associated lung injury . Lung-protective ventilation is used . Baby lung concept (Low TV 4-6ml/Kg) Open lung concept (Optimal PEEP) Permissive Hypercapnia Permissive Hypoxemia

34. Tidal Volume Tidal volume-3-6ml/kg (low) (predicted/ideal body weight) in poor compliance. Tidal volume-5-8ml/kg (predicted/ideal body weight) in better compliance .

35. High PEEP Leaky capillaries due to Inflammatory mediators - Pulmonary edema secondary to fluid leak out - causes diffusion barrier and collapse of alveoli - resulting in derecruitment PEEP Keeps or Prevents Decruitment Of Good Lung Ideal PEEP Should recruit and prevent derecruitment Least effect on cardiac output Minimise VILI Low levels may not open alveoli PEEP must be kept between 10-15 cm H2O and titrated. In severe PARDS, >15 cm H2O PEEP can be used.

36. Permissive Hypercapnia & Hypoxemia Permissive Hypercapnia To achieve low airway pressures & volume, to reduce burden of gas exchange, at last to minimize VALI PaCO2 <90 as long as pH>7.15 Permissive Hypoxemia At Optimal PEEP- PaO2 50-88mm Hg, Sp02 88-95% High Fio2 (>60%) - absorption atelectasis, lung toxicity

37. Endotracheal Tubes Cuffed endotracheal tubes should be used when ventilating a patient with PARDS.

38. Gas exchange goals Mild PARDS with PEEP<10 cm H2O: target SpO2 is 92- 97 %. More severe PARDS with PEEP ≥10cm H20: target SpO2 88-92%.

39. HFOV in PARDS An alternative ventilatory mode in those with elevated plateau pressure>28cm H2O despite the absence of reduced compliance. No recommendation Adults studies like the OSCILLATE and the OSCAR trials showed no significant difference between the use of HFOV and conventional ventilation . Use in pediatric ARDS is institution/clinician-dependent

40. Ancillary Therapies - iNO Acts as a pulmonary vasodilator and can improve V/Q mismatch and reduce dead space ventilation. PALICC does not recommend the routine use of iNO in PARDS, But recommend use in severe cases or cases complicated by pulmonary hypertension. It shown transient benefits in oxygenation but no overall improvement in survival.

41. Prone positioning Improve oxygenation in ARDS, through a combination of improved V/Q matching, recruitment of lower-lobe atelectasis, reduced ventilator-induced lung injury, improved secretion clearance, and improved right ventricular dysfunction. PALICC doesn’t recommend Consideration in only severe cases of PARDS.

42. Improvement is immediate Blood is redistributed to areas that are better ventilated. Redistribution improve alveolar recruitment in previously closed areas of the lung . Redistribution of fluid and gas results in an improved relation between ventilation and perfusion. Changes the position of the heart so it no longer puts weight on underlying lung tissue.

43. Absolute Contraindication • Spinal cord instability Strong Relative Contraindications • Hemodynamic abnormalities • Cardiac rhythm disturbances Relative Contraindications • Thoracic and abdominal surgeries

44. Prone Positioning Preparation for prone positioning includes the following: Adequate sedation of the patient Moving the patient to one side of the bed Checking all lines for length Checking the security of the endotracheal tube ( ET) Endotracheal suctioning prior to turning . Hyperoxygenation with 100% Checking all vital signs The procedure includes the following: Tilting the patient to the side Unhooking ECG leads Turning the patient prone Turning the patient's head toward the ventilator Reattaching ECG leads Checking all lines Checking ventilator pressure and volume Monitoring vital signs Pillow supports should be placed on each side of the patient's chest and forehead

45. Corticosteroids PALICC do not recommend corticosteroids as routine therapy for PARDS. May benefit PARDS in children with co-morbidities like reactive airway disease, BPD. No standard recommendations exist.

46. Recruitment maneuvers RM are transient, sustained increases in transpulmonary pressure designed to open up collapsed airless alveoli In Severe Acute Respiratory Distress Syndrome (ARDS) PALICC doesn’t recommend and should not be considered part of routine Sustained high pressure inflation- 30-40mmHg for 30s Intermittent sigh- 3 sighs/min of 40mmHg Intermittent PEEP increase practice- 2-3cmH2O every 30s till no increase in Vt

47. Surfactant Exogenous surfactant with no benefits and not recommended now.

48. Fluids management in PARDS A fter initial fluid resuscitation goal-directed fluid management is used to maintain adequate volume, aiming to prevent a positive fluid balance. C onservative fluid strategy targeting lower cardiac filling pressures, with CVP <4mm Hg, is associated with better oxygenation and a short duration of mechanical ventilation

49. Nutrition in PARDS PALICC stresses the importance of nutrition, preferably enteral, Helps in maintaining growth, meeting metabolic needs, and facilitating recovery. In general, critically ill children have reduced mortality when enteral nutrition is started within 48 hours of admission. Research on the potential benefits of Omega -3 FA-enriched lipid emulsion but not recommended.

50. Blood transfusion With Hb of 7 g/ dL in absence of severe hypoxemia or hemodynamic instability, PRBC transfusion is indicated.

51. Sedation . S edation (minimal yet effective) should be titrated to achieve the targeted MV strategy.

52. ECLS-extracorporeal life support in PARDS PALICC recommends consideration of ECLS in severe PARDS, where the cause is likely reversible, or the child is suitable for lung transplantation. Veno -venous ECMO is most commonly applied strategy of ECLS. Survival rates of>70% have been reported when venovenous ECMO is used in viral infection-associated severe ARDS. Beneficial if used within the 1st 7 days of mechanical ventilation

53. Section 4. Long-Term Outcomes

54. Long-Term Pulmonary Function in Patients Who Survive PARDS . Advised to screen for pulmonary function abnormalities within 3 months of discharge from the hospital. A follow-up assessment within the first year should be added if spirometry is abnormal .

55. Outcomes The mortality rate of ARDS in children (0-18 years) is 40 -60 %. Outcomes similar for adults and children Majority of deaths sepsis or MODS rather than primary respiratory illness

56. Thank you.