New Therapies for Pediatric ARDS
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This document summarizes new developments in pediatric acute respiratory distress syndrome (ARDS). It discusses the definition and pathophysiology of ARDS, as well as associated clinical disorders and outcomes. Therapies covered include mechanical ventilation strategies like low tidal volumes, permissive hypercapnia, high frequency oscillation, and prone positioning. Pharmacological approaches discussed are surfactant, steroids, inhaled nitric oxide, and partial liquid ventilation. The use of extracorporeal membrane oxygenation for severe respiratory failure is also mentioned.
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New Therapies for Pediatric ARDS
- 1. Whatâs New In Pediatric ARDS Nancy G. Hoover, MD Medical Director, PICU Walter Reed AMC
- 2. New and Improved Acute Respiratory Distress Syndrome Ashbaugh, Lancet , 1967 Adult Respiratory Distress Syndrome To distinguish from neonatal HMD/RDS Acute Respiratory Distress Syndrome American-European Consensus conference, 1994
- 5. The Problem: Lung Injury Other 4% Hemorrhage 5% Trauma 5% Noninfectious Pneumonia 14% Cardiac Arrest 12% Septic Syndrome 32% Infectious Pneumonia 28% Davis et al., J Peds 1993;123:35
- 9. Â
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- 12. Phases of ARDS
- 15. It would seem ironic that the very existence of humans is fully dependent on a gas that, in excess quantities, is toxic and lethal Lynn D. Martin
- 16. Therapies for ARDS Innovations: iNO PLV Proning Surfactant Anti-Inflammatory Mechanical Ventilation Gentle ventilation: Permissive hypercapnia Low tidal volume Open-lung HFOV ARDS Extrapulmonary Gas Exchange
- 19. Lung Injury Zones Atelectasis â Sweet Spotâ Overdistention
- 22. Lower Tidal Volumes for ARDS * * * p < .001 ARDS Network, NEJM, 342: 2000 22% decrease
- 29. High Frequency Oscillation: A Whole Lotta Shakinâ Goinâ On
- 30. Itâs not absolute pressure, but volume or pressure swings that promote lung injury or atelectasis. Reese Clark
- 32. Differences Between CMV and HFOV
- 34. HFOV vs. CMV in Pediatric Respiratory Failure - Arnold et al, CCM , 1994 *
- 37. Is turning the ARDS patient âproneâ helpful?
- 39. Â
- 40. Â
- 49. Steroids in Unresolving ARDS * * p<.01 *
- 54. Â
- 55. Inhaled NO and HFOV In Pediatric ARDS Dobyns et al., J Peds , 2000
- 58. ARDS- âMechanicalâ Therapies Low tidal volumes Outcome benefit in large study Prone positioning Unproven outcome benefit Open-lung strategy Outcome benefit in small study HFOV Outcome benefit in small study ECMO Proven in neonates unproven in children
- 59. Pharmacologic Approaches to ARDS: Randomized Trials Steroids - acute no benefit - fibrosing alveolitis lowered mortality, small study Surfactant possible benefit in children Inhaled NO no benefit PLV no benefit
- 60. ââŠWe must discard the old approach and continue to search for ways to improve mechanical ventilation. In the meantime, there is no substitute for the clinician standing by the ventilatorâŠâ Martin J. Tobin, MD
- 61. If you think about ECMO, it is worth a call to consider ECMO
- 62. Â
- 65. Impact of ECMO on Survival in Pediatric Respiratory Failure % Mortality p<0.05 Green et al, CCM , 1996 mortality risk quartile
Editor's Notes
- Ashbaugh first described the syndrome of severe respiratory failure similar to infant hyline membrane disease
- PCWP higher than 18 mmHg are generally considered to be c/w left-heart failure and may be the cause of cargiogenic pulmonary edema.
- Gattinoni âConcept of Baby Lungâ, Intensive Care Medicine, 2005: The &quot; baby lung &quot; concept originated as an offspring of computed tomography examinations which showed in most patients with acute lung injury/acute respiratory distress syndrome that the normally aerated tissue has the dimensions of the lung of a 5- to 6-year-old child (300-500 g aerated tissue). DISCUSSION: The respiratory system compliance is linearly related to the &quot; baby lung &quot; dimensions, suggesting that the acute respiratory distress syndrome lung is not &quot;stiff&quot; but instead small, with nearly normal intrinsic elasticity. Initially we taught that the &quot; baby lung &quot; is a distinct anatomical structure, in the nondependent lung regions. However, the density redistribution in prone position shows that the &quot; baby lung &quot; is a functional and not an anatomical concept. This provides a rational for &quot;gentle lung treatment&quot; and a background to explain concepts such as baro- and volutrauma. CONCLUSIONS: From a physiological perspective the &quot; baby lung &quot; helps to understand ventilator-induced lung injury. In this context, what appears dangerous is not the V(T)/kg ratio but instead the V(T)/&quot; baby lung &quot; ratio. The practical message is straightforward: the smaller the &quot; baby lung ,&quot; the greater is the potential for unsafe mechanical ventilation.
- Axial CT of an experimental model of ARDS showing the heterogeneous distribution of lung disease. The gravitationally nondependent lung region (ventral) is relatively spared, whereas the dependent lung region (dorsal) exhibits greater involvement
- Extrapulmonary techniques ECMO IVOX IV gas exchange Total Implantable Artificial Lung
- 40% vs. 31% mortality Vent-free days in the first 28 days was significantly higher in the low tidal volume group (12 +/- 11 vs. 10 +/-11;p=0.007
- In Stewartâs study, If peak pressure is <30 and tidal volume is <8 mL/kg, then there was no difference in mortality.
- Hickling, Intensive Care Med 1990
- When hypercapnia is produced through the limitation of tidal volumes and inspiratory airway pressures without adequate PEEP, the Qs/Qt ratio increases secondary to progressive derecruitment of alveolar units. Under such conditions, oxygenation will be further impaired by the hypercapnia-induced increase in cardiac output. This increase in cardiac output induces a worsening Qs/Qt ratio as blood flow increases preferentially to the gravitationally dependent, poorly ventilated lung regions and results in additional intrapulmonary shunting The increase in Qs/Qt can frequently be counteracted through the optimization of lung volume by means of recruitment maneuvers and application of suitable levels of PEEP. Hypercapnic acidosis enhances hypoxic pulmonary vasoconstriction, thus improving ventilation-perfusion matching, decreasing Qs/Qt, and increasing the PaO2. Hypercapnic acidosis positively affects oxygen availability to tissues by promoting a right shift in the oxygenâhemoglobin dissociation curve. Net effect is improvement in oxygenation
- Hypercapnic acidosis has been shown to cause marked sympathetic stimulation with predictable increases in cardiac output due to the augmentation of heart rate and stroke volume secondary to decreased systemic vascular resistance
- Within hours of the onset of sustained hypercapnic acidemia, the kidneys initiate compensatory net reabsorption of sodium bicarbonate, generally returning blood pH to physiologic levels within 2 days.
- Effect of prone position on ventilation distribution. In the supine position, the distribution of ventilation is preferentially distributed to the ventral regions. When the patient is prone, the stiffness of the dorsal chest wall favors the distribution of ventilation to the dorsal regions, facilitating reinflation in this area.
- Post-hoc analysis showed an improvement in 10-day mortality in the prone group but overall ventilator-free days, ICU discharge and length of hospitalization was unchanged
- In the study by Curely et al, you probably wonât see a benefit because with all of the other therapies, the mortality was so low, it would take a huge number of patients to show a mortality difference.