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TTN vs RDS.pptx
- 1. TTN vs RDS byTowfik Sebai
- 2. TTN Introduction • Parenchymallung disorder • Edema • Delayed resorption and clearance • Most common
- 3. TTN Pathophysiology • Airspaces • Interstitium • Decreased compliance • Tachypnea • Collapse of bronchioles
- 4. TTN Pathophysiology • Hypoxemia •Hypercapnia • Drainage and absorption • Decreased surfactant • Reduced NO
- 5. TTN Epidemiology • 5/1,000term births • C-Section • Antenatal corticosteroids • Maternal diabetes and obesity • Maternal asthma
- 6. TTN Clinical Features •Birth – 2 hours • Tachypnea > 60 • Cyanosis and work • Clear breath sounds • Symptomatic for 12-72 hours
- 7.
- 8. TTN Diagnosis • Respiratorydistress • Radiograph • 12-24 hour resolution • Ultrasound
- 9. TTN Differential Diagnosis •Pneumonia • Congenital cardiac disease • Respiratory distress syndrome • Sepsis
- 10. RDS Introduction • Commonin preterm infants • Deficiency of surfactant • Major cause of morbidity and mortality
- 11. RDS Pathophysiology • Highsurface tension • Instability, decreased volume, and compliance • Hypoxemia (atelectasis) • Inflammation and injury • Edema
- 12. RDS Pulmonary Edema •Inflammation and injury • Reduced absorption • Low urine output
- 13. RDS Epidemiology • MaleAOR = 1.7 • White > Hispanic > Black > Asian • Young GA Risk of RDS (%) GA (weeks) 93.0 ≤ 28 10.5 34 6.0 35 2.8 36 1.0 37 0.3 ≥ 38
- 14. RDS Clinical Features •Birth – first few minutes to hours • Respiratory distress and cyanosis • Tachypnea and work • Cyanosis/pale • Decreased breath sounds, pulses, and urine output
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- 17. RDS Diagnosis • Preterminfant with respiratory failure • Radiograph • 1 week resolution • Marked diuresis
- 18. Difference s TTN RSD Radiograph Flatdiaphragm; cardiomegaly; sunburst pattern Low volume; ground glass appearance Resolution 12-24 hours 1 week (after marked diuresis) Severity Generally benign and self-limited Major cause of morbidity and mortality in preterm Risk factors C-Section; maternal diabetes, obesity and asthma White; male baby Severity Can lead to respiratory distress Can lead to respiratory failure Features Edema and increased lung volume Edema, decreased lung volume, and atelectasis
Editor's Notes
- #3 Transient tachypnea of the newborn (TTN) is a parenchymal lung disorder characterized by pulmonary edema resulting from delayed resorption and clearance of fetal alveolar fluid. It is the most common cause of respiratory distress in late preterm and term infants and is generally a benign, self-limited condition.
- #4 In TTN, delayed resorption of fetal lung fluid fills the air spaces and moves into the interstitium, where it pools in perivascular tissues and interlobar fissures. The excess lung water in TTN results in decreased pulmonary compliance. Tachypnea develops to compensate for the increased work of breathing associated with reduced compliance. In addition, accumulation of fluid in the peribronchiolar lymphatics and interstitium promotes partial collapse of the bronchioles with subsequent air trapping.
- #5 Continued perfusion of poorly ventilated alveoli leads to hypoxemia, and alveolar edema reduces ventilation, sometimes resulting in hypercapnia. Eventually fluid is cleared by lymphatic drainage or absorbed into small blood vessels. The underlying mechanism leading to delayed absorption of alveolar fluid in neonates with TTN is unknown. ●Decreased surfactant function has been proposed as contributing to the pathophysiology of TTN. In one small study of term infants delivered via elective cesarean delivery, patients with TTN compared with age-matched controls were more likely to have lower surfactant function as determined by gastric aspirate measurement of lamellar body count and stable microbubble test [5]. However, further studies are needed to confirm these findings. ●Reduced nitric oxide (NO) has also been proposed as a contributing cause. Asymmetric dimethylarginine (ADMA) is an endogenous NO synthase inhibitor. Increased ADMA concentration may reduce NO synthesis, leading to increased pulmonary vascular resistance associated with fetal lung fluid retention and resulting in prolonged duration of tachypnea. In one small study, ADMA levels were elevated in newborns with TTN compared with healthy newborns [6].
- #6 TTN is the most common cause of respiratory distress in term and late-preterm infants, with an estimated incidence of 4.0 to 5.7 per 1000 term births. Additional reported risk factors for TTN besides prematurity include: ●Cesarean delivery – Cesarean delivery is associated with a higher risk of TTN than vaginal delivery, thought to be due to reduced alveolar fluid clearance. (See "Physiologic transition from intrauterine to extrauterine life", section on 'Alveolar fluid clearance'.) •In a single center review of 29,669 consecutive deliveries from 1992 to 1999, TTN occurred in more infants after cesarean deliveries (n = 4301) than after vaginal delivery (n = 21,017, 3.5 versus 1.1 percent, odds ratio [OR] 3.3, 95% CI 2.6-3.9) [10]. •In a population-based German study of almost 240,000 term deliveries from 2001 to 2005, the incidence of TTN was 5.9 cases per 1000 singleton births [11]. Elective cesarean section without labor was the most significant risk factor and the risk increased with each additional week of gestation between 37 and 40 weeks. For the newborns with TTN in this cohort, 42 percent were delivered by elective cesarean delivery compared with the 9.2 percent of TTN reported in the German perinatal registry. ●Antenatal corticosteroids – The administration of antenatal corticosteroid therapy appears to reduce the rate of TTN in late preterm and term infants. However, it remains uncertain whether the benefit of reducing TTN outweighs the potential adverse effects of corticosteroid therapy. (See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery", section on '34+0 or more weeks'.) ●Other reported risk factors: •Maternal diabetes and obesity – TTN occurs two to three times more often in infants of mothers with diabetes mellitus. The mechanism may be related to decreased fluid clearance in the fetal lung, although cesarean delivery, which is more frequently performed in pregnancies of diabetic mothers, is likely a contributing factor. (See "Infants of women with diabetes", section on 'Other causes of respiratory distress'.) Maternal obesity without chronic disease has been associated with TTN [12,13]. •Maternal asthma – Maternal asthma has been reported to be a risk factor for TTN. In one study, 493 infants of asthmatic mothers appear to be more likely to have TTN than a control sample of infants with mothers without asthma (OR 1.8, 95% CI 1.4-2.4) [14].
- #7 The onset of TTN is usually between the time of birth and two hours after delivery. Tachypnea (respiratory rate greater than 60 breaths per minute) is the most prominent feature. Infants with more serious disease will have cyanosis and increased work of breathing, manifested by nasal flaring, mild intercostal and subcostal retractions, and expiratory grunting. The anterior-posterior diameter of the chest may be increased. Breath sounds in affected infants typically are clear, without rales or rhonchi. Infants with mild to moderate TTN are symptomatic for 12 to 24 hours, but signs may persist as long as 72 hours in severe cases.
- #8 The characteristic findings on chest radiograph include increased lung volumes with flat diaphragms, mild cardiomegaly, and prominent vascular markings in a sunburst pattern originating at the hilum. Fluid often is seen in the interlobar fissures, and pleural effusions may be present. Alveolar edema may appear as fluffy densities. There are no areas of alveolar densities or consolidations
- #9 TTN is a clinical diagnosis (typically made in late preterm and term infants) based on respiratory distress presenting shortly after delivery with characteristic findings on chest radiograph. The diagnosis is confirmed with resolution of symptoms within 12 to 24 hours. (See 'Radiographic features' above.) It has been suggested that lung ultrasonography is an accurate and reliable tool for diagnosing TTN and is used in our center [15]. Findings suggestive of TTN include evidence of pulmonary edema, compact B lines, double lung point, and pulmonary interstitial syndrome. However, additional studies are needed to confirm the accuracy of these findings in predicting TTN before recommending ultrasound as a routine diagnostic imaging procedure [16,17].
- #11 Respiratory distress syndrome (RDS), formerly known as hyaline membrane disease, is a common problem in preterm infants. This disorder is caused primarily by deficiency of pulmonary surfactant in an immature lung. RDS is a major cause of morbidity and mortality in preterm infants.
- #12 Overview — The primary abnormality in RDS is surfactant deficiency. In the premature lung, inadequate surfactant activity results in high surface tension leading to instability of the lung at end-expiration, low lung volume, and decreased compliance. These changes in lung function cause hypoxemia due to a mismatch between ventilation and perfusion primarily due to collapse of large portions of the lung (atelectasis), with additional contributions of ventilation/perfusion mismatch from intrapulmonary and extrapulmonary right-to-left shunts. Surfactant deficiency also leads to lung inflammation and respiratory epithelial injury, which may result in pulmonary edema and increased airway resistance. These factors further exacerbate lung injury and worsen lung function. At the same time, abnormal fluid absorption results in inefficient clearing of liquid in the injured lung, leading to edema lung that also impedes gas exchange.
- #13 ●Inflammation and lung injury. (See 'Inflammation and lung injury' above.) ●Reduced pulmonary fluid absorption − In the fetus, lung fluid is actively transported into the potential airspaces in a process mediated by chloride channels. In preparation for birth and air-breathing, the lung shifts from a secretory to an absorptive mode. Fluid absorption is mediated by sodium channels expressed on epithelial cells (ENaC). However, ENaC expression increases with gestational age in parallel with the surge in surfactant production. In preterm infants, an inadequate number of ENaC may result in fluid retention, similar to what is seen in infants with transient tachypnea of the newborn [25,26]. ●Low urine output − Infants with RDS typically have low urine output contributing to fluid retention in the first few days, which may exacerbate pulmonary edema. Some infants have hyponatremia due to increased free water. Infants recovering from RDS typically have a spontaneous diuresis on the second to fourth day, followed by improved pulmonary function.
- #14 The incidence of RDS increases with decreasing gestational age (GA). The risk is highest in extremely preterm infants, as illustrated by a study from the National Institute of Child Health and Human Development Neonatal Research Network that found a 93 percent incidence of RDS in a cohort of 9575 extremely preterm infants (GA 28 weeks or below) born between 2003 and 2007 [32]. Although the incidence is lower, RDS still occurs in a significant number of late preterm infants (GA between 34 weeks and 36 weeks and 6 days). In a report from the Safe Labor Consortium of 233,844 deliveries from 2002 and 2008, RDS was diagnosed in 10.5, 6, 2.8, 1, and 0.3 percent for infants born at 34, 35, 36, 37, and ≥38 weeks gestation, respectively [33]. In late preterm and term infants, male sex is associated with an increased risk of RDS (adjusted odds ratio [AOR] 1.7, 95% CI 1.45-1.93), and being White is also associated with increased risk, as opposed to being of Asian (AOR 0.57, 95% CI 0.47-0.7), Black (AOR 0.66, 95% CI 0.5-0.87), or Hispanic race/ethnicity (AOR 0.76, 95% CI 0.64-0.9) [34].
- #15 The clinical manifestations of RDS result primarily from abnormal pulmonary function and hypoxemia. Because RDS is primarily a developmental disorder of deficient surfactant production, it presents within the first minutes or hours after birth. If untreated, RDS progressively worsens over the first 48 hours of life. In some cases, infants may not appear ill immediately after delivery, but develop respiratory distress and cyanosis within the first few hours of age. These infants may have a borderline amount of surfactant that is consumed or becomes inactivated. The affected infant is almost always preterm and exhibits signs of respiratory distress that include: ●Tachypnea. ●Nasal flaring, which reflects the use of accessory respiratory muscles and lowers total respiratory system resistance. ●Expiratory grunting, which results from exhalation through a partially closed glottis and slows the decrease in end-expiratory lung volume. ●Intercostal, subxiphoid, and subcostal retractions, which occur because the highly compliant rib cage is drawn in during inspiration by the high intrathoracic pressures required to expand the poorly compliant lungs. ●Cyanosis due to right-to-left intra- and extra-pulmonary shunting. (See 'Hypoxemia' above.) On physical examination, auscultated breath sounds are decreased, and infants may be pale with diminished peripheral pulses. The urine output often is low in the first 24 to 48 hours and peripheral edema is common.
- #16 Chest radiography is generally obtained for all neonates with respiratory distress. The radiographic features of neonatal RDS (low lung volume and the classic diffuse reticulogranular ground glass appearance with air bronchograms) in a preterm infant with respiratory distress fulfill the clinical diagnosis criteria for RDS (image 1). (See 'Diagnosis' below.) Classic respiratory distress syndrome (RDS). Bell-shaped thorax is due to generalized underaeration. Lung volume is reduced, the lung parenchyma has a fine granular pattern, and peripherally extending air bronchograms are present.
- #18 The diagnosis of RDS is based on a clinical picture of a preterm infant with the onset of progressive respiratory failure shortly after birth (manifested by an increase in the work of breathing and an increase in the oxygen requirement), in conjunction with a characteristic chest radiograph. The chest radiographic features of RDS include a low lung volume and the classic diffuse reticulogranular ground glass appearance with air bronchograms (image 1). This radiographic pattern results from alveolar atelectasis contrasting with aerated airways. Pulmonary edema may contribute to the diffuse appearance. Pneumothorax and air leaks are uncommon findings in the initial chest radiography, and are more frequently observed when lung compliance improves. (See 'Clinical manifestations' above and "Pulmonary air leak in the newborn".) RDS typically resolves by one week of age. A marked diuresis typically preceded the improvement in lung function.