Respirtory distress in neonates up dated

Respirtory distress in neonates

1. Neonatal Respiratory Distress Prepared by: Dr. Mohammed Moqaibel Supervisor : Dr. Abdullah Al- Tayar

2. Neonatal Respiratory Distress: It is common immediately after birth, and is typically caused by abnormal respiratory function during the transition from fetal to neonatal life. Neonatal respiratory distress may be transient; however, persistent distress requires a rational diagnostic and therapeutic approach to optimize outcome and minimize morbidity. INTRODUCTION

3. TRANSITION FROM FETAL LIFE: The successful transition from intrauterine to extrauterine life is dependent upon significant physiologic changes that occur at birth. In almost all infants, these changes are successfully completed at delivery without requiring any special assistance. However, about 10 percent of infants will need some intervention, and less than 1 percent will require extensive resuscitative measures at birth  

4. Fetal oxygenation  — The intrauterine oxygen tension is low compared with that seen in extrauterine life. FETUS  : Prior to delivery, the human fetus depends upon the placenta for gas and nutrient exchange with the maternal circulation 

5. Despite the low oxygen tension in the fetus, there is adequate tissue oxygenation because of the following factors : - Fetal hemoglobin - Decreased fetal oxygen consumption - Differential blood flow in the fetus, the blood flow is structured so that vital organs ( eg , liver, heart, and brain) receive blood with a relatively high degree of oxygen saturation

6. TRANSITION AT DELIVERY  :  To successfully make the transition from intrauterine to extrauterine life when the umbilical cord is clamped at birth, the neonate must rapidly make physiologic changes in cardiopulmonary function.

7. A successful transition is characterized by the following features: ●Alveolar fluid clearance ●Lung expansion ●Circulatory changes with increases in pulmonary perfusion and systemic pressure, and closure of the right-to-left shunts of the fetal circulation

8. DIFFICULTIES IN TRANSITION   The following risk factors are associated with a greater likelihood of having difficulty making a successful transition and of requiring resuscitation : Advanced maternal age , maternal diabetes mellitus Hypertension , maternal substance abuse, or previous history of stillbirth, fetal loss, or early neonatal death Maternal conditions Prematurity, postmaturity , congenital anomalies, or multiple gestation Fetal conditions Placental anomalies (eg, placenta previa), or either oligohydramnios or polyhydramnios Antepartum complications Transverse lie or breech presentation, chorioamnionitis , foul-smelling or meconium -stained amniotic fluid, antenatal asphyxia with abnormal fetal heart rate pattern, maternal administration of a narcotic within four hours of birth, delivery that requires instrumentation ( eg , forceps, vacuum, or cesarean delivery) Delivery complications

9. Neonatal difficulties at birth include the following ●Lack of respiratory effort ●Blockage of the airways ●Impaired lung function (External causes , Pulmonary hypoplasia , Intrinsic lung disease) ●Persistent increased pulmonary vascular resistance (also referred to as persistent pulmonary hypertension or persistent fetal circulation) ●Abnormal cardiac structure and/or function ● Preterm infants

10. Evaluation of neonatal respiratory distress

11. Evaluation of respiratory distress using Down’s score

12. Evaluation of respiratory distress using The Silverman Andersen

13. Assessing and Monitoring Respiratory Status Physical examination : The presence of the following signs may be useful in recognizing respiratory distress and evaluating the response to treatment 1. Nasal flaring. One of the earliest signs of respiratory distress, nasal flaring may be present in incubated, ventilated patients as well. 2. Grunting. Commonly seen early in respiratory distress syndrome (RDS) and transient tachypnea , grunting is a physiologic response (partial closure of the glottis during expiration) to prevent end-expiratory alveolar collapse. Grunting helps maintain functional residual capacity (FRC) and therefore oxygenation.

14. Assessing and Monitoring Respiratory Status 3. Retractions. Intercostal , subcostal , and sternal retractions are present in conditions of decreased lung compliance or increased airway resistance and may persist during mechanical ventilation if support is inadequate. 4. Tachypnea . A respiratory rate >60 breaths/min implies the inability to generate an adequate tidal volume and may persist during mechanical ventilation. 5. Abnormal breath sounds. Inspiratory stridor , expiratory wheezing, and rales should be appreciable. Unfortunately, unilateral pneumothorax may escape detection on auscultation.

15. Assessing and Monitoring Respiratory Status 6. Cyanosis. Central cyanosis indicates hypoxemia. Cyanosis is difficult to appreciate in the presence of anemia. Acrocyanosis is common shortly after birth and is not a reflection of hypoxemia. The degree of visible cyanosis on physical examination depends on both oxygen saturation and hemoglobin concentration. The appearance of cyanosis depends upon the absolute amount of reduced hemoglobin. Normally cyanosis is perceptible at 85% saturation when the hemoglobin concentration is 15 g/ dL and the reduced hemoglobin is >3 g/ dL . In a polycythemic infant one will detect cyanosis at a higher level of oxygen saturation ( Hbg 20 g/ dL detects cyanosis at 87% saturation) and in anemic infant cyanosis may not be apparent since one will only detect cyanosis at a lower level of oxygen saturation ( Hgb of 6 g/ dL detects cyanosis at 62.5% saturation).

16. Assessing and Monitoring Respiratory Status 6. Cyanosis. If the infant has increased respiratory effort with increased rate, retractions, and nasal flaring, respiratory disease should be high on the list of differential diagnoses of Cyanosis . Cyanotic heart disease usually presents without respiratory symptoms (“happy blue baby”) but can have effortless tachypnea (rapid respiratory rate without retractions).

17. Differentiation of Cyanotic Heart Disease from Pulmonary Disease in Respiratory Distress: Assessing and Monitoring Respiratory Status

18. Assessing and Monitoring Respiratory Status MEASUREMENT OF OXYGENATION   Blood gases: Management of ventilation, oxygenation, and changes of acid-base status is most accurately determined by arterial blood gas studies.

19. MEASUREMENT OF OXYGENATION Pulse oximetry  — Pulse oximetry measures hemoglobin saturation (SpO 2 ) and reflects the 98 percent of arterial oxygen content that is carried normally by hemoglobin. This monitoring technique provides data that are continuous and noninvasive, and, therefore, avoids some limitations of intermittent arterial blood sampling. As a result, in most neonatal intensive care units (NICUs), pulse oximetry is the accepted standard for routine monitoring, and SpO 2  has been called the "fifth vital sign"  Assessing and Monitoring Respiratory Status

20. Distinguishing Features of TTN, RDS, and MAS

21. Respiratory Distress Syndrome (RDS) (RDS) was previously called hyaline membrane disease (HMD). The Vermont Oxford Network definition for RDS requires that babies have: A. An arterial oxygen tension (PaO2) <50 mm Hg and central cyanosis in room air,a requirement for supplemental oxygen to maintain PaO2 >50 mm Hg, or a requirement for supplemental oxygen to maintain a pulse oximeter saturation >85%. B. A characteristic chest radiographic appearance (uniform reticulogranular pattern to lung fields and air bronchogram ) within the first 24 hours of life. The clinical course of the disease has been changed because of advances in treatment practices, including the use of early continuous positive airway pressure (CPAP).

22. Respiratory Distress Syndrome (RDS) surfactant is present in high concentrations in fetal lung by 20 weeks of gestation, it does not reach the surface of the lungs until later. It appears in amniotic fluid between 28 and 32 weeks. Mature levels of pulmonary surfactant are present usually after 35 weeks of gestation. The major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol , apoproteins (surfactant proteins SP-A,SP-B,SP- C,and SP-D),and cholesterol. With advancing GA, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells.

23. Respiratory Distress Syndrome (RDS) Incidence Respiratory distress syndrome (RDS) occurs primarily in premature infants; its incidence is inversely related to gestational age (GA) and birthweight . It occurs in 60–80% of infants <28 weeks’ GA, in 15–30% of those between 32 and 36 weeks’ GA, and rarely in those >37 weeks’ GA.

24. These surface-active agents are released into the alveoli, where they reduce surface tension and help maintain alveolar stability at end-expiration.

25. Surfactant deficiency (decreased production and secretion) is the primary cause of RDS. In the absence of pulmonary surfactant, significantly increased alveolar surface tension leads to atelectasis , and the ability to attain an adequate functional residual capacity (FRC) is impaired.

26. Respiratory Distress Syndrome (RDS) Risk factors associated with RDS include: maternal diabetes, multiple births, cesarean delivery, precipitous (abrupt) delivery, birth asphyxia, cold stress, and maternal hx of previously affected infant as well as male & white race infants. Risk of RDS is reduced in; pregnancies with chronic or pregnancy- induced hypertension, prolonged rupture of membranes, antenatal corticosteroid Px , and maternal heroin addiction Risk factors

27. Respiratory Distress Syndrome (RDS) Risk factors

28. Respiratory Distress Syndrome (RDS) CLINICAL FEATURES History: The infant is often preterm or has a history of perinatal asphyxia. Infants have at birth some respiratory difficulty, which becomes progressively more severe. The classic worsening of the atelectasis seen on chest radiograph and increasing oxygen requirement for these infants have been greatly modified by exogenous surfactant therapy and effective ventilatory support.

29. Respiratory Distress Syndrome (RDS) CLINICAL FEATURES Physical examination. The infant with RDS exhibits tachypnea , grunting, nasal flaring, and retractions of the chest wall, and may have cyanosis in room air. Grunting occurs when the infant partially closes the vocal cords to prolong expiration and develop or maintain some FRC. This actually improves alveolar ventilation. The retractions occur and increase as the infant is forced to develop high transpulmonary pressure to reinflate atelectatic air spaces. Clinical course  — Prior to surfactant use, uncomplicated RDS typically progressed for 48 to 72 hours. This was associated with an improvement in respiratory function as endogenous surfactant production increased. RDS typically resolves by one week of age.

30. Respiratory Distress Syndrome (RDS) CLINICAL FEATURES Respiratory severity score. Some facilities in low-resource settings use the respiratory severity score (RSS) designed by Silverman and Andersen to quantify respiratory distress among neonates. The RSS is objective, easy to learn, quick to perform,and requires no expensive equipment. It is rated by giving scores from 0 to 2 from upper chest movement, lower chest retractions, xiphoid retractions, nares dilatation, and expiratory grunting The RSS can be used for predicting the need for escalation of respiratory support and can help facilitate transfer decision making to higher resourced facilities. Scores ≥5 have been the most useful cutoff point for transfer, although the sensitivity of the score is decreased in patients with a higher score.

31. Respiratory Distress Syndrome (RDS) DIAGNOSIS   Blood gas sampling is essential in the management of RDS. Although there is no consensus, most neonatologists agree that arterial oxygen tensions of 50 to 70 mm Hg and arterial carbon dioxide tensions of 45 to 60 mm Hg are acceptable. Most would maintain the pH at or above 7.22 and the arterial oxygen saturation at 90% to 94%. Continuous transcutaneous oxygen and carbon dioxide monitoring and/or oxygen saturation monitoring are valuable in the treatment of these infants. Sepsis workup. A partial sepsis workup, including complete blood cell count and blood culture Serum glucose: Hypoglycemia alone can lead to tachypnea and respiratory distress. Serum electrolyte Hypocalcemia can contribute to more respiratory symptoms

32. Respiratory Distress Syndrome (RDS) DIAGNOSIS   Echocardiography is used to confirm the diagnosis of PDA and in the evaluation of an infant with hypoxemia and respiratory distress. A significant congenital heart disease can also be excluded. Chest radiograph . An anteroposterior chest radiograph should be obtained for all infants with respiratory distress of any duration. The typical radiographic finding of RDS is a uniform reticulogranular pattern, referred to as a ground-glass appearance, accompanied by peripheral air bronchograms Point-of-care lung ultrasonography showing lung consolidation, pleural line abnormalities, and A-line disappearance provides a sensitivity and specificity of 100% for the diagnosis of neonatal RDS. However, some acute complications secondary to air leak syndrome ( eg , pneumomediastinum , interstitial emphysema, pneumopericardium ) cannot easily be discovered by using ultrasound

33. Chest radiograph showing diffuse granular opacification of the lungs with air bronchograms . In the premature neonate, this would almost always represent respiratory distress syndrome.

34. Respiratory distress syndrome (RDS) of the newborn (hyaline membrane disease [HMD]). There is a diffuse ground-glass or finely granular appearance (circle) in a bilateral and symmetric distribution. Hypoaeration is seen in nonventilated lungs (double arrow).

35. Respiratory Distress Syndrome (RDS) Differential diagnosis Diagnosis Key Points Transient Tachypnea of the NB Mature infants Milder respiratory distress with quick improvement Rarely will require mechanical ventilation Bacterial Pneumonia and Sepsis Signs and symptoms overlap with RDS Infants with respiratory distress will need blood cultures Air Leak Syndromes May result from RDS and treatment of RDS Congenital Heart Disease If lung function does not improve after support and surfactant therapy, obtain an ECHO.

36. Preventive - Antenatal corticosteroids: administration to the mother of 2 doses of betamethasone 12 mg given intramuscularly 24 hours apart. Dexamethasone is not recommended because of increased risk for cystic periventricular leukomalacia among very premature infants exposed to the drug prenatally. Corticosteroid should be given weekly for all women with preterm labor (between 24 and 34 wk of gestation). Respiratory Distress Syndrome (RDS) Management

37. Delivery room management. In spontaneously breathing babies, stabilize with CPAP via mask or nasal prongs. Gentle positive-pressure lung inflations should be used for persistently apneic or bradycardic infants. Intubation should be reserved for babies who have not responded to positive-pressure ventilation via face mask. Babies who require intubation for stabilization should be given surfactant Respiratory Distress Syndrome (RDS) Management

38. Respiratory support: 1. Continuous positive airway pressure and nasal synchronized intermittent mandatory ventilation. Nasal CPAP ( nCPAP ) or nasopharyngeal CPAP (NPCPAP) providing a pressure of 5 to 6 cm H2O can be used early to delay or prevent the need for endotracheal intubation and mechanical ventilation. CPAP treatment is recommended to be started from birth in all infants at risk of RDS, such as those born at <30 weeks’ gestation. 2. Humidified high-flow nasal cannula system. Respiratory Distress Syndrome (RDS) Management

39. 3. Endotracheal intubation and mechanical ventilation are mainstays of therapy for infants with RDS in whom apnea or hypoxemia with respiratory acidosis develops. Weaning from mechanical ventilation should be started as soon as satisfactory gas exchange is achieved. Respiratory Distress Syndrome (RDS) Management

40. Management Surfactant replacement. Dosage and administration • Dose: Should be guided according to the type of surfactant used. • Timing: Usually within 1-2 hours of age, but without delaying resuscitation measures. • Administration: Check ET tube position. Insert 5F feeding tube with end-hole into the ET tube – with its tip above the carina and below the ET tube end. Give each dose of surfactant with baby’s head turned 45°. Between each dose baby is ventilated by bag and tube for at least 30 seconds

41. Management Surfactant replacement. During dosing monitor for: - Transient bradycardia. - Hypoxia. - Hypotension. ET blockage. After dosing: - Do not suction ET tube for at least 1 hour. - Monitor ABGs and adjust ventilator setting.

42. Management Surfactant replacement. Surfactant therapy for diseases other than RDS. Encouraging preliminary reports of surfactant therapy have been noted in cases of pneumonia, meconium aspiration syndrome, persistent pulmonary hypertension, pulmonary hemorrhage, and acute respiratory distress syndrome (ARDS), but no protocols for treatment are available at this time.

43. -Inhaled nitric oxide It should not be used in preterm infants with RDS unless there is pulmonary hypertension or hypoplasia . - Fluid and nutritional support - Antibiotic therapy. Antibiotics that cover the most common neonatal infections are usually begun initially. - Caffeine. Should be initiated for all premature infants at high risk of MV, such as those with birthweight of 1250 g who are on CPAP treatment. It should also be used in order to facilitate weaning from MV. Respiratory Distress Syndrome (RDS) Management

44. Sedation. Commonly used to control ventilation in these sick infants. Morphine and fentanyl may be used for analgesia as well as sedation, The basic defect requiring treatment in RDS is inadequate pulmonary O2-CO2 exchange . Basic supportive care (thermoregulatory, circulatory, fluid, electrolyte, and respiratory) is essential while FRC is established and maintained. Because most cases of RDS are self-limited, the goal of treatment is to minimize abnormal physiologic variations and superimposed iatrogenic problems. Treatment of infants with RDS is best carried out in the NICU. Respiratory Distress Syndrome (RDS) Management

45. Major morbidities such as IVH, BPD and NEC remain high in smaller infants Endotracheal tube complications. Air leak syndromes – rupture of over distended alveoli BPD Death can be due to severe impairment of gas exchange, alveolar air leaks (interstitial emphysema, pneumothorax ), pulmonary hemorrhage, or IVH. Death may be delayed by weeks or months if BPD develops Respiratory Distress Syndrome (RDS) Complications

46. Although the survival of infants with RDS has improved greatly, the survival with or without respiratory and neurologic sequelae is highly dependent on birth weight and gestational age. Major morbidity (BPD/CLD, NEC, and severe IVH) and poor postnatal growth remain high for the smallest infants. Respiratory Distress Syndrome (RDS) Prognosis.

47. REFERENCES UpToDate : Noninvasive oxygen delivery and oxygen monitoring in the newborn Overview of neonatal respiratory distress: Disorders of transition Transient tachypnea of the newborn MANUAL OF NEONATOLOGY ( YEMEN MOHP)