Recommended
More Related Content
Similar to 9. RDS _ using CPAP - April 2021(2).pptx
Similar to 9. RDS _ using CPAP - April 2021(2).pptx (20)
Recently uploaded
Recently uploaded (20)
9. RDS _ using CPAP - April 2021(2).pptx
- 1. Respiratory Distress Syndrome (RDS) and Using CPAP
- 2. Objectives Introduction • Define Respiratory Distress Syndrome (RDS) and its clinical course • Briefly outline lung growth and development • Discuss the prevention of RDS • Outline the specific management of RDS – using CPAP • Illustrate the complications of CPAP and their prevention • List strategies to improve CPAP success rates
- 3. Introduction
- 4. Definition of Respiratory Distress Syndrome (RDS) Disease caused by absence/inadequate production of pulmonary surfactant & related lung underdevelopment The disease is found mainly in preterm newborns (before 37 weeks' gestation) Characterized by a progressive increase in respiratory effort and a decrease in the amount of air entering the lungs favoring hypoxia. Sweet LR, Keech C, Klein NP, et al. Respiratory distress in the neonate: Case definition & guidelines for data collection, analysis, and presentation of maternal immunization safety data. Vaccine. 2017;35(48 Pt A):6506‐6517. doi:10.1016/j.vaccine.2017.01.046; Bahadue FL, Soll R. Early versus delayed selective surfactant treatment for neonatal respiratory distress syndrome. Cochrane Database Syst Rev. 2012;11(11):CD001456. Published 2012 Nov 14. doi:10.1002/14651858.CD001456.pub2 Introduction
- 5. RDS increases with decreasing gestational age • The risk of RDS is inversely proportional to gestational age; occurs in approximately: • RDS is seen soon after birth, worsens during the first few hours of life • In contrast to Transient Tachypnea of the Newborn (TTN), worse at birth but improves within hours of birth 5% 30% 60% Sweet LR, Keech C, Klein NP, et al. Respiratory distress in the neonate: Case definition & guidelines for data collection, analysis, and presentation of maternal immunization safety data. Vaccine. 2017;35(48 Pt A):6506‐6517. doi:10.1016/j.vaccine.2017.01.046 Near-term infants Infants <30 weeks Infants<28 weeks Introduction
- 6. How is diagnosis of RDS made? Diagnosis is based on: No laboratory test to diagnose RDS Kamath BD, Macguire ER, McClure EM, Goldenberg RL, Jobe AH. Neonatal mortality from respiratory distress syndrome: lessons for low-resource countries. Pediatrics. 2011;127(6):1139‐1146. doi:10.1542/peds.2010-3212 Initial clinical symptoms A chest radiograph The clinical course Response to surfactant treatment. Introduction
- 7. Clinical Course of RDS Neonates present within the first several hours of life • Hours after birth If untreated the disease worsens • 24 - 48 hours The course of RDS is self-limited • 5 - 7 days Very preterm infants will not be able to make it without support. Sweet D, G, Carnielli V, Greisen G, Hallman M, Ozek E, te Pas A, Plavka R, Roehr C, C, Saugstad O, D, Simeoni U, Speer C, P, Vento M, Visser G, H, A, Halliday H, L: European Consensus Guidelines on the Management of Respiratory Distress Syndrome – 2019 Update. Neonatology 2019;115:432-450. doi: 10.1159/000499361 Introduction
- 8. Periods of Treatment for RDS Beena D. Kamath, Emily R. MacGuire, Elizabeth M. McClure, Robert L. Goldenberg and Alan H. Jobe,Neonatal Mortality From Respiratory Distress Syndrome: Lessons for Low-Resource Countries,Pediatrics June 2011, 127 (6) 1139-1146 RDS was first described by Hochheim 14 in 1903, who noted unusual membranes in the lungs of 2 infants who died shortly after birth Period 1 - Before 1950s: No widely used treatment Period 2 – 1950 – 1969: Oxygen therapy was the specific intervention Period 4 – After 1990: Antenatal corticosteroids, surfactant, advanced care technologies e.g. ECMO, high frequency oscillation Period 3 – 1970 – 1989: CPAP therapy was the specific intervention. Later on use of mechanical ventilation was attempted Introduction
- 9. Increased % in RDS survivors with introduction of specific treatments Beena D. Kamath, Emily R. MacGuire, Elizabeth M. McClure, Robert L. Goldenberg and Alan H. Jobe,Neonatal Mortality From Respiratory Distress Syndrome: Lessons for Low-Resource Countries,Pediatrics June 2011, 127 (6) 1139-1146 Introduction
- 10. Lung Growth and Development
- 11. Lung growth and Development Schittny, Johannes C. “Development of the lung.” Cell and tissue research vol. 367,3 (2017) Surfactant Gestation Cortisol peaks 4 wks Birth 24 wks 20 wks 32 wks Alveolar type II cells Lung bud Surfactant Lung growth and development
- 12. Transition to extrauterine life Source - Neonatal Asphyxia, Resuscitation and Beyond. Dipak, Rashmi, Padmapriya. Chapter 1 – intrauterine and Natal Cardiopulmonary physiology Hillman, Noah H et al. “Physiology of transition from intrauterine to extrauterine life.” Clinics in perinatology vol. 39,4 (2012) Fluid replaced by air (labour & delivery, first breath and cry) Reduced secretion; increased absorption (regulated by hormones) Surfactant coats alveoli Fetal fluid secreted into lungs Promotes development Maintains distension Pressure = 2 - 4cmH20 Mechanical stretch stimulates surfactant production Fetal lungs Birth Neonatal lungs Cortisol Levels increase at 30 - 36 wks, prior to term labor & peak at labour Regulates thyroid hormones and catecholamine release Lung growth and development
- 13. Surfactant Nkadi, Paul O et al. “An overview of pulmonary surfactant in the neonate: genetics, metabolism, and the role of surfactant in health and disease.” Molecular genetics and metabolism vol. 97,2 (2009): Surfactant production can be hindered by inflammation, genetic defects, infection • A complex mixture of phospholipids and proteins • Reduces surface tension at the air-liquid interface of the alveoli • Prevents collapse of alveoli during end exhalation • Secretion is stimulated by hormones such as thyroxine and glucocorticoids • Mechanical stretch (distension and hyperventilation) can stimulate secretion from Alveolar type II cells Lung growth and development
- 14. What can go wrong during transition? Premature delivery – insufficient surfactant Premature delivery – lung absorptive capacity not optimum Meconium aspiration inactivates surfactant Cold stress inactivates surfactant Caesarian section – no benefit from catecholamine surge Caesarian section – no benefit from mechanical force of labour Hillman, Noah H et al. “Physiology of transition from intrauterine to extrauterine life.” Clinics in perinatology vol. 39,4 (2012) Morton, Sarah U, and Dara Brodsky. “Fetal Physiology and the Transition to Extrauterine Life.” Clinics in perinatology vol. 43,3 (2016): Lung growth and development
- 16. Antenatal steroids and the fetal lung 24 - 34 weeks Administration of antenatal corticosteroids (ACS) Fetal lung maturation Glucocorticoids and Lung Development in the Fetus and Preterm Infant R J Bolt , M M van Weissenbruch, H N Lafeber, H A Delemarre-van de Waal 2001 Antenatal Corticosteroids for Accelerating Fetal Lung Maturation for Women at Risk of Preterm Birth Devender Roberts, Julie Brown, Nancy Medley , Stuart R Dalziel, 2015 Prevention of RDS How is lung maturation induced? Enhance Surfactant Production Antioxidant Enzyme Production Stimulates lung fluid absorption Enhance alveolar development
- 17. 1. Association Between Antenatal Corticosteroid Administration-to-Birth Interval and Outcomes of Preterm Neonates Melamed N, Shah J, Soraisham A, Yoon EW, Lee SK, Shah PS, Murphy KE Obstet Gynecol. 2015;125(6):137; 2. WHO recommendations on interventions to improve preterm birth outcomes 2015 3.Brownfoot FC, Gagliardi DI, Bain E, Middleton P, Crowther CA. Different corticosteroids and regimens for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2013;8:CD006764. Administration of ACS • 1-7 days before anticipated delivery- Betamethasone vs dexamethasone - none superior over the other. • Betamethasone 12 mg IM every 24 hours for 2 doses • Total dose (24mg) • Dexamethasone 6mg IM 12 hours apart for 4 doses • Total dose (24mg) 24 - 34 weeks gestation 2 Prevention of RDS
- 18. WHO recommendations on use of ACS Prevention of RDS • Administer within 1-7 days before imminent preterm birth (24 - 34 weeks) • Use IM Dexamethasome or beclomethasone (total 24mg) • Use for both single and multiple gestation pregnancies • Recommended for women with PROM and no signs of infection, hypertensive disorders, at risk of delivering IUGR baby, Maternal DM • A single repeat course of ACS recommended if preterm birth does not occur within 7 days after the initial dose and the risk of preterm birth is still there • Not recommended for those with chorioamnionitis and those undergoing c/s for late preterms.
- 19. Benefits of ACS Intraventricular hemorrhage (RR- 0.69, 95% CI-(0.59-0.81)) Necrotizing enterocolitis (RR-0.50, 95% CI-(0.32-078)) Neonatal sepsis (RR-0.60, 95% CI- (0.41-0.88)) Respiratory distress syndrome RR- (0.66, 95% CI- (0.56-0.77)) Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) Roberts D, Brown J, Medley N, Dalziel SR 2017 Mechanical ventilation (RR-0.68, 95% CI-(0.56-0.84)) Prevention of RDS
- 21. Approach to management Keep warm and Maintain neutral thermal environment - Reduce oxygen consumption Circulation- feeds and fluids; Initiation of early feeds & Maintenance fluids D - Close monitoring of vitals; Blood sugars, Hypotension common in early RDS, Antibiotics, Caffeine Breathing - Specific management; Surfactant use and Respiratory Support (CPAP) Airway patency should be ensured Management of RDS
- 23. Continuous Positive Airway Pressure (CPAP) •Non invasive method of oxygen delivery Provides continuous distending pressure that’s keeps alveoli open during expiration Reduces work of breathing therefore improves oxygenation Decreases atelectasis and respiratory fatigue Management of RDS
- 24. Why use CPAP? CPAP In-utero • Fetal lungs in utero remain distended due to the pressure of 3-4 cm/H20 maintained by the fluid in the fetal lungs • CPAP mimics normal physiology. • Constant distending pressure at 2-3cm/H20. Nasal Continuous Positive Airway Pressure (CPAP)for the Respiratory Care of the Newborn Infant Robert M DiBlasi RRT-NPS 2009 Image borrowed from https://consultqd.clevelandclinic.org/bubble-cpap-for-prevention-of-chronic-lung-disease-in-premature-infants/ Management of RDS
- 25. Benefits of using CPAP Image borrowed from https://newbornsbaby.blogspot.com/2019/01/premature-baby-lung-complications.html CPAP 1. Improves oxygenation 2. Continuous distending pressure keeps alveoli open which maintains FRC 3. Promotes Lung growth and development. 4. Promote surfactant production Management of RDS
- 26. • 28 - 30 weeks (1-1.3kgs) • Initiated as soon as possible within the delivery room • For the newly born with good cardiac activity and breathing spontaneously • Not in respiratory distress • Intended to avoid mechanical ventilation • Above 30 weeks (>1.3kgs) • Initiated after trial of oxygen therapy • Neonate with increased work of breathing and SpO2< 90% on nasal prongs at 1L/min Prophylactic versus Rescue CPAP 5-10 mins After 10 mins Prophylactic CPAP Rescue CPAP Nasal Continuous Positive Airway Pressure (CPAP)for the Respiratory Care of the Newborn Infant Robert M DiBlasi RRT-NPS 2009 Management of RDS
- 27. How CPAP delivers varying Fraction of Inspired Oxygen (FIO2) Oxygen sources provide > 90% Oxygen Ambient air provides 21% oxygen • Varying FiO2 delivered to the baby depending on the oxygen saturations. • Pulse oximetry is important • Titrate to achieve targets of SPO2 90-95% Blend ambient air with the oxygen from the source • Titrate the flow rate from the oxygen source by increasing or decreasing 1L/min to achieve varying levels of FiO2 (30-100%) • Need for a ***blender Management of RDS
- 28. Using CPAP
- 30. bCPAP Initiation Criteria Using CPAP Oxygen 1L/min via nasal prongs & Consult Team Initiate Prophylactic CPAP in the delivery room Give oxygen 1L/min Reassess SpO2 and Work of breathing after 15 min If still in Distress, initiate Rescue CPAP Adapted from the TRY algorithm
- 31. The Pumani bCPAP Using CPAP
- 32. The Pumani bCPAP Using CPAP
- 33. Back View Front View The Pumani bCPAP Using CPAP
- 34. The Pumani bCPAP – Blending table Using CPAP
- 35. The Pumani bCPAP - Interface Assorted hats Assorted nasal prongs Hat Clips Connection Elbows Using CPAP
- 36. Preparing the Pumani bCPAP 1. Perform Hand Hygiene 2. Position CPAP machine 30cm from wall on a firm surface 3. Fill Pressure generating bottle with 6cm water Using CPAP
- 37. Preparing the Pumani CPAP 4. Connect the patient tubing to the patient port and bottle tubing to bottle port. Must hear a click! 5. Connect the correct size of nasal prongs to the bottle and patient tubings using right and left elbows Using CPAP
- 38. Preparing the Pumani CPAP 6. Connect an oxygen source to the CPAP machine and turn the machine on. Determine the oxygen flowrate to use; • Set the total flow at 6L/min • Start at 50% FIO2. • Using the blending table, read value where the total flow rate of 6L/min meets 50% FIO2 • Set value read (3L/min) on the oxygen flowmeter on the oxygen source Using CPAP 3L/min
- 39. Preparing the Pumani CPAP 7. Test for functioning (bubbling) • Pinch the nasal prongs with your fingers. • Water in the pressure generator bottle should bubble • Machine is ready for use Using CPAP
- 40. Preparing the Baby for CPAP 1. Determining correct size of the hat and its placement 2. Insert an orogastric tube (OGT) 3. Suction the nostrils if necessary 4. Instill a drop of normal saline in each nostril 5. Size, insert and secure nasal prongs Using CPAP
- 41. Preparing the Baby for CPAP 6. Check for effective functioning (water bubbling) 7. Attach pulse oximeter 8. Check baby’s response to bCPAP (assess WoB, HR and SpO2) 9. Increase flow rate of oxygen by 1liter/min every 60 seconds to achieve SpO2 of 90-95%. 10.Institute supportive care Using CPAP
- 42. Before increasing bCPAP Treatment; • Is the water bubbling? • Is the connection circuit complete and well secured? • Does the baby need suctioning? When increasing bCPAP Treatment • Base need to increase on SPO2 and work of breathing • Use Oxygen blending table to determine oxygen flow rate to use After changing bCPAP Treatment • Reassess the baby’s immediate response and then at 15 min, 1 hour then 3-4hourly Increasing bCPAP Treatment Using CPAP
- 44. Weaning & Stopping bCPAP Criteria for weaning CPAP Treatment 1. Baby has been on CPAP for at least 24hours 2. RR less than 60/min for at least 6 hours 3. Oxygen saturation consistently greater than 90% for at least 6 hours 4. No significant grunting, indrawing, nasal flaring, apnoea or bradycardia for at least 6 hours Using CPAP Decrease oxygen using Oxygen blending table Decrease pressure by removing water (1cm/H2O = 40mls of water)
- 47. Monitoring • Vital signs • Work of breathing • Nasal blockage • Abdominal distension • Position of the prongs • Nasal septum intact • Tubing not kinked • Hat snuggly fit • Correct water level • There is bubbling • Correct total Flow rate • Correct oxygen flow rate Monitoring on CPAP
- 48. Monitoring the Baby Monitoring on CPAP
- 49. CPAP - Infection Prevention & Control Non-critical patient care items o Items which come in to contact with patient’s intact skin o Non metallic items e.g. hat, hat clips, pressure generating bottle, the tube hanger to be cleaned o Metallic items – outer part of CPAP machine for disinfection with 70% alcohol Semi-critical patient care items o Items which come in to contact with patient’s mucosa and non intact skin (non sterile body parts) o Elbow connectors & tubings for high level disinfection o Silicon Nasal Prongs for Autoclaving Trevor Duke (2014) CPAP: a guide for clinicians in developing countries, Paediatrics and International Child Health, 34:1, 3-11, DOI: 10.1179/2046905513Y.0000000102 Anna M. Bonner & Petra Davidson (2020) Infection Prevention: 2020 Review and Update for Neurodiagnostic Technologists, The Neurodiagnostic Journal, 60:1, 11-35, DOI:10.1080/21646821.2020.1701341 CPAP- IPC
- 52. Skin Complications • Constant pressure on nares, ears, head and forehead can lead to reduced skin integrity and injury causing pressure ulcers. Fischer C, Bertelle V, Hohlfeld J, et alNasal trauma due to continuous positive airway pressure in neonates Archives of Disease in Childhood - Fetal and Neonatal Edition 2010;95:F447-F451.newborn care protocols. Queensland Clinical Guidelines. Respiratory distress and CPAP Guideline No. MN20.3-V7-R25. Queensland Health. 2020. Prevention • Frequent observation • Minimize points of contact • Keep skin dry and clean • Avoid tight fitting hat over forehead, ears and bony prominences First sign of skin breakdown is nasal erythema. Complications of CPAP
- 53. Nasal Complications Nasal flaring Nasal septal injury Source: Respir Care 2009; 54(9):1209 1235 –Comprehensive newborn care protocols, connect.springerpub.com, Queensland Clinical Guidelines. Respiratory distress and CPAP Guideline No. MN20.3-V7-R25. Queensland Health. 2020. Prevention a) Maintain 2mm distance between columella and nasal prongs b) The prongs should fill the entire nare without blanching the external nare c) Ensure appropriate size of the nasal prongs and positioning of the whole interface Nasal snubbing a Complications of CPAP b c c
- 54. Lung Complications Pneumothorax CPAP increases risk of air leaks. PRIYADARSHI, A., HINDER, M., BADAWI, N., LUIG, M., TRACY, M.. Continuous Positive Airway Pressure Belly Syndrome: Challenges of a Changing Paradigm. International Journal of Clinical Pediatrics, North America, 9, Feb. 2020, Queensland Clinical Guidelines. Respiratory distress and CPAP Guideline No. MN20.3-V7-R25. Queensland Health. 2020. Abdominal distension Image borrowed from https://ep.bmj.com/content/102/3/166 Complications of CPAP Prevention a) Always check CPAP pressure b) Do not exceed pressures of 8cm H20. c) Check for any air leaks in circuit
- 55. Lung Complications Hyperinflation of lungs • Occurs due to high CPAP pressures. • Results in reduced cardiac output secondary to reduced venous return. PRIYADARSHI, A., HINDER, M., BADAWI, N., LUIG, M., TRACY, M.. Continuous Positive Airway Pressure Belly Syndrome: Challenges of a Changing Paradigm. International Journal of Clinical Pediatrics, North America, 9, Feb. 2020, Queensland Clinical Guidelines. Respiratory distress and CPAP Guideline No. MN20.3-V7-R25. Queensland Health. 2020. Abdominal distension Image borrowed from https://ep.bmj.com/content/102/3/166 Complications of CPAP Prevention a) Always check CPAP pressure b) Do not exceed pressures of 8cm H20.
- 56. Abdominal Complications Abdominal distention • Excessive swallowed air • Feeding intolerance and desaturation episodes. PRIYADARSHI, A., HINDER, M., BADAWI, N., LUIG, M., TRACY, M.. Continuous Positive Airway Pressure Belly Syndrome: Challenges of a Changing Paradigm. International Journal of Clinical Pediatrics, North America, 9, Feb. 2020, Queensland Clinical Guidelines. Respiratory distress and CPAP Guideline No. MN20.3-V7-R25. Queensland Health. 2020. Abdominal distension Image borrowed from https://ep.bmj.com/content/102/3/166 Complications of CPAP Prevention a) Insert an OGT b) Leave OGT open c) If OGT is used for feeding, close for 30mins after feeding the baby then open OGT
- 57. Oxygen Therapy Complications Hypoxia SPO2 - 85 - 89% • Increases mortality • Does not alter rates of developing; a) Chronic lung disease- BPD b) Blindness c) Neurodevelopmental impairment. Walsh BK, Smallwood CD. Pediatric Oxygen Therapy: A Review and Update. Respir Care. 2017;62(6):645‐661. doi:10.4187/respcare.05245 Complications of CPAP Hyperoxia SPO2 - > 95% • Free radicals that cannot be metabolized by immature antioxidant systems. • Chronic lung disease - BPD • Eye Injury - RoP Prevention a) Monitor SpO2 b) Aim for O2 saturation of 90-95% c) Titrate the FiO2 based on SpO2
- 58. CPAP Failure CPAP leads to a 35% reduction in death and use of assisted ventilation1. It however can fail Ho JJ, Subramaniam P, Davis PG. Continuous distending pressure for respiratory distress in preterm infants. Cochrane Database of Systematic Reviews 2015, Issue 7. Art. No.: CD002271. DOI: 10.1002/14651858.CD002271.pub2Wright CJ, Sherlock LG, Sahni R, Polin RA. Preventing Continuous Positive Airway Pressure Failure: Evidence-Based and Physiologically Sound Practices from Delivery Room to the Neonatal Intensive Care Unit. Clin Perinatol. 2018;45(2):257‐271. doi:10.1016/j.clp.2018.01.011 A diagnosis of CPAP failure is made on any baby who has been on correctly applied CPAP for 72 hours and who continues to have; 1. Moderate to severe recessions and grunting 2. SpO2 < 90% 3. Recurrent apneas even on a maximum CPAP pressure of 8cm H20 Complications of CPAP
- 59. Risk factors for CPAP failure Newborn Characteristics • Weight <1000g • Gestation <28 weeks • Sex - Male Ho JJ, Subramaniam P, Davis PG. Continuous distending pressure for respiratory distress in preterm infants. Cochrane Database of Systematic Reviews 2015, Issue 7. Art. No.: CD002271. DOI: 10.1002/14651858.CD002271.pub2Wright CJ, Sherlock LG, Sahni R, Polin RA. Preventing Continuous Positive Airway Pressure Failure: Evidence-Based and Physiologically Sound Practices from Delivery Room to the Neonatal Intensive Care Unit. Clin Perinatol. 2018;45(2):257‐271. doi:10.1016/j.clp.2018.01.011 Complications of CPAP Maternal Factors • Poor antenatal steroid coverage • PPROM Severity of the Disease • Moderate or Severe RDS • Delayed onset of treatment
- 61. Increasing CPAP success rates Implementing CPAP Policy Change Required 1. Improved ANC care to ensure antenatal steroid coverage in management of preterm labor. 2. The NBU care of patients on CPAP is one level below NICU, this means staffing is key as poor supervision increases mortality. 3. Nursing care takes priority - proper application of CPAP interface, monitoring, providing supportive care and above all a gentle and human care.
- 63. Summary Summary 1. CPAP promotes lung growth/development and protects lung – all babies deserves the best care. 2. CPAP should be initiated at an FiO2 of 50%, which then is titrated upwards or downwards to achieve oxygen saturation targets of 90-95% 3. Regularly monitor patient to optimize CPAP benefits and reduce risk of complications
Editor's Notes
- Respiratory distress syndrome (RDS) is a disease caused by a deficiency or dysfunction of pulmonary surfactant. Pulmonary surfactant is an active agent that keeps the pulmonary alveoli open and facilitates the entry of air to the lungs, thus improving the oxygenation of the newborn. The disease is found mainly in preterm newborns (before 37 weeks' gestation) and is characterised by a progressive increase in respiratory effort and a decrease in the amount of air entering the lungs favouring hypoxia (a condition in which the body is deprived of an adequate oxygen supply). RDS affects up to 60% of newborns before 37 weeks of gestation and weight below 2500 g (Roberts 2006) and is the main cause of hospitalisation in the neonatal intensive care (up to 12.7%) (Sarasqueta 1996). These infants may develop several complications including: pulmonary hypertension, persistent ductus arteriosus (Appendix 1), periventricular and intraventricular haemorrhage (bleeding in the brain), asphyxia (Appendix 1) and death (up to 33% of cases) (Carbajal 1998; Udaeta 2004).
- Growth is followed by maturation 1st trimester – Foregut => Lung bud => Bronchopulmonary segments Fetal breathing starts at 10 weeks gestation and is associated with REM sleep – inhibited by hypoxemia and stimulated by hyperoxemia. Without these fetal breathing movements (FBM), there is lung hypoplasia 2nd trimester – Gas exchanging portions of the airway are formed during Canalicular phase 24 weeks – Alveolar ductal development 36 weeks – Septation of the air sacs WHAT IS THE TAKE HOME MESSAGE? – Surfactant production begins around 24 weeks gestation and gradually increases with a surge at term. Lung growth and development Embryonic period 4 weeks – lung appears as a protrusion of the foregut 33 days – initial branching forming main bronchi which begin to extend into mesenchyme; segmental bronchi soon form Pseudoglandular stage 5 weeks to 16 weeks – 15 to 20 generations of airway branching occur from main segmental bronchi to terminal bronchioles Loosely packed mesenchyme surrounds the airways (contains blood vessels; lined by glycogen-rich, undifferentiated epithelial cells which are columnar to cuboidal); proximal airways lined with the most differentiated cells Breathing movement (chest wall and diaphragm) starts at 11 weeks and is controlled by aorta and carotid chemoreceptors Canalicular stage 16 weeks to 25 weeks – transition from previable lungs to viable lungs Respiratory bronchioles and alveolar ducts of the gas exchange region are formed Vascularity increases in mesenchyme around the airways – capillary and epithelial basement membranes fuse 20 weeks – cuboidal epithelial cells differentiate into alveolar type II cells (AT2) with formation of cytoplasmic lamellar bodies. These indicate production of surfactant. Produced from glycogen and stored in lamellar bodies Saccular stage 24 weeks – potential for viability; gas exchange is possible in large, primitive forms of the future alveoli Surfactant is produced Alveolarization occurs by outgrowth of septae that subdivide terminal saccules into anatomic alveoli where air exchange occurs 32 weeks – alveoli are zero Term infant – 50 to 150 million alveoli; alveolar growth continues for two years after term birth Adults – 300 million alveoli Surfactant production is developmentally regulated It reduces alveolar surface tension, facilitating alveolar expansion and reducing chances of alveolar collapse Surfactant production is expressed in the lung around 20 weeks Surfactant is detectable in amniotic fluid from around 26 weeks gestation
- Cortisol is the major regulatory hormone for terminal fetal maturation & neonatal adaptation at birth Initiation of breathing involves interaction of biochemical, neural and mechanical factors The yolk sac and the placenta carry out gas exchange initially with the placenta becoming dominant at 10 weeks gestation Transition from intrauterine to extrauterine life requires the baby to adjust to achieve conversion from placental gas exchange to pulmonary respiration. In utero the lungs secret a fluid in the bronchial tree resulting in accumulation of fluid within the foetal airways, thus the foetal lungs are in hyperexpanded The presence of this airway fluid is critical for stimulating lung development Foetal lung fluid contains components that change over the course of gestation with increased surfactant being produced prior to birth Surfactant secretion into the foetal lungs is stimulated by labour. During spontaneous labour and immediately after birth, the respiratory epithelium changes from active fluid secretion (with active chloride transport into the intraluminal space) to active fluid absorption (with active sodium transport into the interstitium) Increased oxygenation after birth helps to maintain the expression of these sodium-mediated channels Recent imaging studies have demonstrated that after birth, airway liquid clearance and lung aeration are intrinsically linked and regulated primarily by transpulmonary pressures generated during inspiration. This indicates that airway liquid clearance is not solely dependent on sodium reabsorption and that a variety of mechanisms that may act before, during, and after birth are involved. The level of contribution of each mechanism likely depends on the timing and mode of delivery During spontaneous labour and immediately after birth, the respiratory epithelium changes from active fluid secretion (with active chloride transport into the intraluminal space) to active fluid absorption (with active sodium transport into the interstitium) Increased oxygenation after birth helps to maintain the expression of these sodium-mediated channels Cortisol levels begin to rise at 30 weeks’ gestation and peak just following delivery. The combined action of cortisol and thyroid hormone activates sodium channel activity that drives resorption of lung fluid. Cortisol production increases from 30 to 36 weeks’ gestation, and a second peak occurs before spontaneous labour at term gestational age The fluid in the lungs is about 25ml/kg prior to onset of labour – decrease to 18ml/kg at onset of labour and to 10ml/kg at delivery Intrauterine relatively hypoxemic environment The placenta is a free flowing space so poorly oxygenated blood mixes with well oxygenated blood, leading to fetal blood oxygen saturation that is lower than the maternal uterine arterial blood The highest oxygen saturation in fetal circulation is in umbilical venous blood which is 70% to 80% Surfactant is secreted into the lung fluid with labor. It coats the alveoli and lowers the pressure required to maintain it open and thus establish FRC During both lung growth & maturation, distal pulmonary epithelial cells actively secrete a chloride-rich fluid into the bronchial tree. 1 Fetal lung fluid components change with time – contains more surfactant by end of 3rd trimester Lung volume is maintained by liquid secretion into pulmonary lumen Vascular bed remains constricted due to the fluid and low oxygen levels Blood reaching intrauterine pulmonary circulation has 55% O2. hypoxemia decreases pulmonary blood flow which in turn suppresses production of nitric oxide and PG12 This results in elevated PVR at baseline Lungs produce fluid through several mechanisms Lungs need to be mature enough to get inflated PVR needs to decrease to allow increase in pulmonary blood flow to accommodate entire cardiac output Fluid must be removed from alveolar spaces Alveolar spaces must be maintained open Neurologic drive to generate and maintain spontaneous continuous breathing After birth what needs to happen Fluid must be replaced by air in the alveoli – from fluid secretion to fluid absorption Blood vessels in lungs must relax to increase flow to alveoli for oxygen to be transported Initiation of first breath after labor and delivery – cord clamping, tactile and cold stimuli, hypoxia and acidosis Fetal hypoxia and acidosis Acid level – respiratory center in medulla is activated to initiate respiration; how? Clamping umbilical cord decreases oxygen concentration, increases CO2 concentration and decreases blood pH which stimulates fetal aortic and carotid chemoreceptors Mechanical Intermittent compression of chest during vaginal birth forces 1/3 of fluid out of fetal lungs; Thoracic squeeze during labor and deliver removes 25% to 33# of lung fluid Expansion after delivery generates a negative pressure, drawing air into the lungs; Passive inspiration of air replaces fluid The first breath and crying establishes a positive intrathoracic pressure which keeps the alveoli open to establish 75% of FRC (functional residual capacity), forcing remaining fluid into the lymphatic circulation; Exhalation with a cry in the first breath against a closed glottis generates more force than normal breaths (this intrathoracic pressure) Surfactant stabilizes expanded alveoli (Askin, 2008) Fluid absorption Reduced secretion from pulmonary epithelium in late gestation Active sodium transport across pulmonary epithelium drives fluid from lung lumen into interstitium Catecholamine surge occurs just before onset of labor. Facilitates drop in fetal lung fluid levels. (Catecholamines, vasopressin, prolactin, glucocorticoids, thyroxine, prolactin enhance fluid absorption and trigger change in lung epithelia from chloride secretion to sodium resorption by activating expression of apical sodium channels – this induces a parallel movement of chloride and water Immature epithelial sodium channel expression is part of pathogenesis in RDS) C/S results in lower serum catecholamine levels Surfactant is secreted into the lung fluid with labor. It coats the alveoli and lowers the pressure required to maintain it open and thus establish FRC Pulmonary blood flow Clamping the cord also doubles systemic vascular resistance as placenta with its low resistance is lost. There is a five-fold increase in pulmonary vascular resistance during expansion of lungs after the first inspiration. Reduction in pulmonary arterial, RV and RA pressures Results in increased pulmonary blood flow and thus oxygenation of blood Surfactant is secreted into the lung fluid with labor. It coats the alveoli and lowers the pressure required to maintain it open and thus establish FRC Cortisol levels are lower in the setting of preterm delivery or CS without labor Cortisol levels are increased with chorioamnionitis Lungs produce fluid through several mechanisms Lungs need to be mature enough to get inflated PVR needs to decrease to allow increase in pulmonary blood flow to accommodate entire cardiac output Fluid must be removed from alveolar spaces Alveolar spaces must be maintained open Neurologic drive to generate and maintain spontaneous continuous breathing Lung volume is maintained by liquid secretion into pulmonary lumen Vascular bed remains constricted due to the fluid and low oxygen levels After birth what needs to happen Fluid must be replaced by air in the alveoli – from fluid secretion to fluid absorption Blood vessels in lungs must relax to increase flow to alveoli for oxygen to be transported
- Preterm infants have lower lung volumes relative to body weight compared to term infants, and have delayed clearance of foetal lung fluid because of decreased sodium resorption. Infants with transient tachypnoea of the newborn or surfactant deficiency also have decreased sodium resorption. This is further affected by transpulmonary pressures generated during inspiration.
- Antenatal corticosteroid therapy is recommended for women at risk of preterm birth from 24 weeks to 34 weeks of gestation when the following conditions are met:n gestational age assessment can be accurately undertaken;n preterm birth is considered imminent;n there is no clinical evidence of maternal infection;n adequate childbirth care is available (including the capacity to recognize and safely manage preterm labour and birth);n the preterm newborn can receive adequate care if needed (including resuscitation, thermal care, feeding support, infection treatment and safe oxygen use). No significant difference when beclomethasone compared to dexamethasone- neonatal death, perinatal death, RDS and NICU admission
- Multiple benefits of use of ACS- respiratory distress- benefits seen in overall respiratory distress RR as well as moderate to severe RDS
- Infants should be maintained in a thermal neutral environment to minimize heat loss and maintain the core body temperature in a normal range, thereby reducing oxygen consumption and caloric needs. The ambient temperature should be selected to maintain an anterior abdominal skin temperature in the 36.5 to 37ºC range. Rectal temperatures should be avoided in infants with RDS because of the greater risk of trauma or perforation associated with their use. As a result, abdominal temperatures are used to set the servo-controlling temperatures in incubators and in radiant warmers The administration of early nutrition is important in the overall care of preterm infants. Energy needs must cover both metabolic expenditure (eg, resting metabolic rate and thermoregulation), and growth. The nutritional needs of preterm infants, especially very low birth weight (VLBW) infants (BW <1500 g), are often dependent upon parenteral nutrition (PN) during early postnatal life.
- By avoiding endotracheal intubation and mechanical ventilation, the constant distending pressure maintained in the lung by CPAP may also provide some physiologic benefits regarding lung protection and development. In utero the transpulmonary pressure of the fluid-filled developing lung is approximately 3–4 cm H2O.51 Coincidently, CPAP at 5 cm H2O results in nasal pharyngeal distending pressure of approximately 2–3 cm H2O.52 In theory, spontaneous breathing, at a constant “low” distending pressure, as provided by CPAP, would seem to be more likely to provide some mechanical similarities to the lungs in the intrauterine environment, promoting lung growth/development and protection, than would mechanical ventilation, which uses relatively high inflation pressure. Much of the experimental evidence used to evaluate these physiologic effects has been limited to a few studies using animal models of prematurity
- An important aspect of understanding FRC (and the respiratory cycle in general) is knowledge of the forces involved. There are 2 main mechanical forces throughout the breathing cycle: the force of the chest wall and the force of the lungs. Without the necessary physiological pressures, the chest wall would expand outward, and the lungs would collapse. This is what occurs when the vacuum is disrupted such as with a stab wound leading to a pneumothorax. FRC is the point at which these forces are at equilibrium; that is, the difference between the inner recoil forces of the lungs and the outer recoil forces of the chest wall are balanced
- For those we fix early at birth with no weight, so we use gestation
- Power switch Patient tubing (usually narrow). Also called the inspiratory limp Patient port Hook to hold long expiratory tubing in place 100% oxygen port Oxygen flow meter – this is usually controlled at the oxygen source. Do not change oxygen flowrate using this flowmeter. Change at the oxygen source and it will adjust as changed. Flow rate determined by fraction of inspired oxygen (FIO2) chosen by clinician Total Flow rate flow meter – this represents the sum of pure oxygen plus oxygen coming from room air which enters the machines through the back vent. Ranges from 5 – 10L/min Pressure generator – bottle filled with clean distilled water. Water level should be 5-8cm/water. The lid on the bottle contains perforations which are used to add or remove water from the bottle using an NG tube. Bottle strap – this is used to hold the bottle in place so it doesn’t fall off Bottle tubing – (wider tubing). Also called the expiratory limb. This tubing carries the pressure generated by the water in the bottle to the patient Oxygen blending table – this is useful to determine the correct oxygen flowrate to use
- It is important to understand the connections inside the Pumani CPAP because these explain its use The Pumani has a vent at the back that allows room air containing 21% oxygen to enter the machine as shown on the yellow highlights. There is a pump which helps to suck up room air 100% oxygen coming from the oxygen port also gets into the machine using the red highlights The 2 gases both flow into the total flow as shown with the blue highlight This blended air is what goes to the patient port where the patient tubing is attached as shown with the purple highlight This means; At all times the total flow rate flowmeter should never be closed as it is the main source of blended oxygen to the patient. That the oxygen concentration in the total flow rate can be increased or decreased by increasing the 100% oxygen flow rate (FIO2) The oxygen blending table should be used to determine the amount of oxygen to set on the oxygen source The pressure generator is not connected in any way to the total flow rate. The PEEP generated is purely associate d with the amount of water put in the pressure generating bottle.
- This table is used to determine the amount of oxygen to set on the 100% oxygen source flowmeter The steps are as described on the table; Choose a favourable flow rate to begin with. During the Malawi Trial on the use of the Pumani, they found beginning at 6L/min therapeutic. Choose the FIO2 to deliver to the baby. This is a clinical decision based on the babies SPO2 and work of breathing. During the Malawi trial, they found starting at 50% FIO2 therapeutic. Set the oxygen source flowmeter at the value where the total flow rate meets the FIO2 chosen Once set, the flowrate should be increased or decreased using the total flow rate flowmeter based on the baby’s response to the CPAP. Increase the flow rate to the next column when you have reached the maximum FIO2 limit of 90% in one column before moving to the next column Once set, the FIO2 should be increased or decreased based on the baby’s response to the CPAP. This is a decision best made by the clinician based on the baby’s condition
- The Pumani accessories help connect the baby to the machine as shown on the top left picture Assorted hats based on weight to ensure a snuggly fit Assorted nasal prongs also based on weight to ensure a good seal is applied on the nasal interface without being too tight to cause complications Hat clips to hold the nasal prongs in place Elbow connectors to connect the patient tubing with the bottle tubing using the nasal prongs
- Communicate with the mother (parents) about CPAP and why their baby needs it Observe hand hygiene Prepare items required as per check list Position the bCPAP device Fill bottle with water to 6cm level
- Connect the bottle tubing (wide tube) to the pressure generating bottle Connect the patient tubing (narrow tube) to the patient port Size the CPAP nasal prong to use Connect the correct size of nasal prongs to the bottle and patient tubings using right and left elbows
- Connect an oxygen source to the CPAP machine Set 3L/min of oxygen on the oxygen flowmeter on the oxygen source (This will give and FIO2 of 50%) Set the total flow at 6L/min Test for bubbling by pinching the nasal prongs opening The bCPAP device is ready for use.
- Functioning test must be performed before use. A positive test (presence of bubbling) indicates the circuit is complete
- All newborns on CPAP must have an Oral gastric tube inserted. The tube will be kept open to release air and prevent abdominal distention. Close the OGT for 30 minutes after using it to feed
- After
- 24 hours mechanical distention which allow better
- Monitor patient; Vital signs (respiratory rate, heart rate, SPO2 and temperature) Work of breathing Nasal blockages - Provide a few drops of saline to each nostril Abdominal distension – ensure oral gastric tube is in situ and open. Check Attachment Check position of the prongs - Prongs should not be against the nose Check nasal septum for skin compromise Check tubing - Tubing should not be kinked or misplaced Check that the hat is not loose; if it is loose, replace with new hat Check Equipment Function Check water level: If water level is below or above the decided treatment level, add or remove the water from bottle cap holes using a syringe and an NG tube. Decrease or increase by 1cm of H2O. For Pumani CPAP 1cm of H2O = 40mls of water Check that the CPAP is bubbling. If not may be due to the patient’s mouth being open or nasal prongs not fully fitting the patient’s nostrils. Check that the seal at the patient port is not cracked Check that oxygen and total flow settings are correct
- Monitor patient; Vital signs (respiratory rate, heart rate, SPO2 and temperature) Work of breathing Nasal blockages - Provide a few drops of saline to each nostril Abdominal distension – ensure oral gastric tube is in situ and open.
- Classification of nasal trauma. (A) stage I (non-blanching erythema), (B) stage II (superficial erosion), (C) stage III (necrosis of full thickness) Frequency and severity of nasal trauma increased with lower gestational age (>90% in neonates <28weeks,lower birth weights and longer duration Constant pressure on the nares, nasal septum and forehead can lead to reduced skin integrity and injury causing pressure injury (ulcers) and friction shear from respiratory tubing of ncpap ) .The majority of nasal trauma appeared during the first days of nCPAP. Nasal trauma occurred rarely after several weeks of treatment. The immaturity of the skin could be implicated in the pathogenesis of such trauma. Watch for color, perfusion, areas of pressure points and areas of skin excoriations
- Snub nose- a short nose that looks rather flat The columella is the bridge of tissue that separates the nostrils at the nasal base. Ensure nasal prongs are not in contact with septa columella – leave 2mm, ensure the 2 lines are visible! Size of prongs is dependent on weight of infant, <1000g-0 1000-1250-1 1250-2000-2 2000-3000g-3 3000-4000g-4 >4000g- 5 Ensure the prongs are fit snuggly into the nares. Watch for symmetry of nose, blanching of ·the skin and any skin break down. Ensure distance between columella and nasal prongs. Overall nasal and nasal septal injury is preventable by careful observation, using correct ·prong size, appropriate prong fixation and attachment of prongs to cap and CPAP tubings. Most common nasal injuries–necrosis, scab formation, excoriation of the septum, nasal hyperaemia and disfigurement of the size and shape, nasal erosion, functional airway obstruction
- Resp-Pleural air with no or decreased lung markings (hyperlucent) Collapsed lung Shift of Mediastinum to opposite side Transillumination <32wks-increased illuminationExcessive swallowed air. Distension of stomach and intestines. Increased intra-abdominal pressure. Need to increase CPAP to overcome the abdominal pressure effects. Resulting vicious cycle.
- Resp-Pleural air with no or decreased lung markings (hyperlucent) Collapsed lung Shift of Mediastinum to opposite side Transillumination <32wks-increased illuminationExcessive swallowed air. Distension of stomach and intestines. Increased intra-abdominal pressure. Need to increase CPAP to overcome the abdominal pressure effects. Resulting vicious cycle.
- Resp-Pleural air with no or decreased lung markings (hyperlucent) Collapsed lung Shift of Mediastinum to opposite side Transillumination <32wks-increased illuminationExcessive swallowed air. Distension of stomach and intestines. Increased intra-abdominal pressure. Need to increase CPAP to overcome the abdominal pressure effects. Resulting vicious cycle.
- Premature infants are at particular risk from oxidative stress because both endogenous and passively acquired exogenous antioxidant defense systems do not accelerate in maturation until late in the third trimester. Saugstad- has suggested the term oxygen radical disease of neonatology to encompass a variety of newborn diseases whose pathogenesis involves oxidative stress and injury, which include retinopathy of prematurity, bronchopulmonary dysplasia (BPD), necrotizing enterocolitis, and intraventricular hemorrhage. BPD- bronchopulmonary dysplasia ROP-retinopathy of prematurity
- PPROM- Preterm prelabor rupture of membranes SAS- Silverman Anderson Score Continuous distending pressure (CDP) is associated with lower risk of treatment failure (death or use of assisted ventilation) (typical risk ratio (RR) 0.65, 95% confidence interval (CI) 0.52 to 0.81; typical risk difference (RD) ‐0.20, 95% CI ‐0.29 to ‐0.10; number needed to treat for an additional beneficial outcome (NNTB) 5, 95% CI 4 to 10; six studies; 355 infants),
- PPROM- Preterm prelabor rupture of membranes SAS- Silverman Anderson Score Continuous distending pressure (CDP) is associated with lower risk of treatment failure (death or use of assisted ventilation) (typical risk ratio (RR) 0.65, 95% confidence interval (CI) 0.52 to 0.81; typical risk difference (RD) ‐0.20, 95% CI ‐0.29 to ‐0.10; number needed to treat for an additional beneficial outcome (NNTB) 5, 95% CI 4 to 10; six studies; 355 infants),
- Monitoring for complications, providing temperature regulation, feeding and fluid balance and overall developmental supportive care. Right infant- hemodynamically stable, has good respiratory effort(spontaneous breathing), know your contraindications eg, can’t put infants with cleft palate, choanal atresia or those with congenital diaphragmatic hernia.