Neonatal RDS

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Slide 1: 

RESPIRATORY DISTRESS SYNDROME

Definition : 

Definition aka Hyaline Membrane Disease (HMD) This clinical diagnosis is warranted in a preterm newborn with respiratory difficulty, including tachypnea (>60 breaths/min) chest retractions cyanosis in room air that persists or progresses over the first 48-96 h of life characteristic chest x-ray appearance (uniform reticulogranular pattern and peripheral air bronchograms)

Incidence : 

Incidence RDS occurs primarily in premature infants incidence is inversely related to gestational age and birthweight 60–80% of infants less than 28 wk of gestational age 15–30% of those between 32 and 36 wk 5% beyond 37 wk rarely at term

Incidence : 

Incidence The incidence is highest in preterm male or white infants. Survival has improved significantly, especially after the introduction of exogenous surfactant and is now at >90%. Currently, RDS accounts for <6% of all neonatal deaths.

Incidence : 

Incidence Risk factors that increase or decrease the risk of RDS

Incidence : 

Incidence Prognosis and outcomes in patients with hyaline membrane disease based on birth weight.

Pathology : 

Pathology Surfactant deficiency (decreased production and secretion) is the primary cause of HMD, often complicated by an overly compliant chest wall. Both factors lead to progressive atelectasis and failure to develop an effective functional residual capacity (FRC). Surfactant is a surface-active material produced by airway epithelial cells called type II pneumocytes. This cell line differentiates, and surfactant synthesis begins at 24-28 weeks' gestation. Type II cells are sensitive to and decreased by asphyxial insults in the perinatal period.

Pathology : 

Pathology The maturation of this cell line is delayed in the presence of fetal hyperinsulinemia. The maturity of type II cells is enhanced by the administration of antenatal corticosteroids and by chronic intrauterine stress such as pregnancy-induced hypertension, intrauterine growth retardation, and twin gestation.

Pathology : 

Pathology The major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin) Phosphatidylglycerol apoproteins (surfactant proteins SP-A, -B, -C, -D) cholesterol

Pathology : 

Pathology With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells. These surface-active agents are released into the alveoli, where they reduce surface tension and help maintain alveolar stability by preventing the collapse of small air spaces at end-expiration.

Pathology : 

Pathology Surfactant is present in high concentrations in fetal lung by 20 wk of gestation, but it does not reach the surface of the lungs until later. It appears in amniotic fluid between 28 and 32 wk. Mature levels of pulmonary surfactant are usually present after 35 wk.

Pathology : 

Pathology In the absence of surfactant, the small air spaces collapse; each expiration results in progressive atelectasis. Exudative proteinaceous material and epithelial debris resulting from progressive cellular damage, collect in the airway and directly decrease total lung capacity.

Pathology : 

Pathology Alveolar atelectasis, hyaline membrane formation, and interstitial edema make the lungs less compliant, so greater pressure is required to expand the alveoli and small airways. In affected infants, the lower part of the chest wall is pulled in as the diaphragm descends, and intrathoracic pressure becomes negative, thus limiting the amount of intrathoracic pressure that can be produced; the result is the development of atelectasis.

Pathology : 

Pathology The highly compliant chest wall of preterm infants offers less resistance than that of mature infants to the natural tendency of the lungs to collapse. Thus, at end-expiration, the volume of the thorax and lungs tends to approach residual volume, and atelectasis may develop.

Pathology : 

Pathology Contributing factors in the pathogenesis of hyaline membrane disease. The potential “vicious circle” perpetuated hypoxia and pulmonary insufficiency.   (From Farrell P, Zachman R: In Quilligan EJ, Kretchmer N [eds]: Fetal and Maternal Medicine. New York, John Wiley, 1980. Reprinted by permission of John Wiley and Sons, Inc.)

Clinical Manifestations : 

Clinical Manifestations Signs of RDS usually appear within minutes of birth The infant with HMD exhibits tachypnea, grunting, nasal flaring, and retractions of the chest wall. The infant 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.

Clinical Manifestations : 

Clinical Manifestations Some patients require resuscitation at birth because of intrapartum asphyxia or initial severe respiratory distress (especially with a birthweight <1,000 g). Cyanosis increases and is often relatively unresponsive to oxygen administration. Breath sounds may be normal or diminished with a harsh tubular quality and, on deep inspiration, fine rales may be heard, especially posteriorly over the lung bases.

Clinical Manifestations : 

Clinical Manifestations The natural course of untreated RDS is characterized by progressive worsening of cyanosis and dyspnea. If the condition is inadequately treated, blood pressure may fall; fatigue, cyanosis, and pallor increase, and grunting decreases or disappears as the condition worsens. Respiratory failure may occur in infants with rapid progression of the disease.

Clinical Manifestations : 

Clinical Manifestations Improvement is often heralded by spontaneous diuresis and the ability to oxygenate the infant at lower inspired oxygen levels or lower ventilator pressures. Death is rare on the 1st day of illness, usually occurs between days 2 and 7, and is associated with alveolar air leaks (interstitial emphysema, pneumothorax), pulmonary hemorrhage, or IVH. Mortality may be delayed weeks or months if BPD develops in mechanically ventilated infants with severe RDS.

Diagnosis : 

Diagnosis Chest X-ray Study An AP chest x-ray film should be obtained for all infants with respiratory distress of any duration. The typical radiographic finding of HMD is a uniform reticulogranular pattern, referred to as a “ground-glass” appearance, accompanied by peripheral air bronchograms.

Diagnosis : 

Diagnosis Chest X-ray Study

Diagnosis : 

Diagnosis Chest X-ray Study The initial roentgenogram is occasionally normal, with the typical pattern developing at 6–12 hr. During the clinical course, sequential x-ray films may reveal air leaks secondary to mechanical ventilatory intervention as well as the onset of changes compatible with BPD.

Laboratory Studies : 

Laboratory Studies Blood Gas Sampling Most neonatologists agree that arterial oxygen tensions of 50-70 mm Hg and arterial carbon dioxide tensions of 45-60 mm Hg are acceptable. Most would maintain the pH at or above 7.25 and the arterial oxygen saturation at 88-95%.

Laboratory Studies : 

Laboratory Studies Sepsis Work-up A partial sepsis workup, including complete blood cell count and blood culture, should be considered, because early-onset sepsis (eg, infection with group B streptococcus or Haemophilus influenzae) can be indistinguishable from HMD on clinical grounds alone.

Laboratory Studies : 

Laboratory Studies Serum Glucose Levels Hypoglycemia alone can lead to tachypnea and respiratory distress. Serum Electrolyte Levels Should be monitored every 12-24 hrs for management of parenteral fluids. Hypocalcemia can contribute to more respiratory symptoms and is common in sick, nonfed, preterm, or asphyxiated infants.

Differential Diagnosis : 

Differential Diagnosis Early-onset sepsis may be indistinguishable from RDS. In pneumonia manifested at birth, the chest roentgenogram may be identical to that for RDS. Cyanotic heart disease (total anomalous pulmonary venous return) can also mimic RDS both clinically and radiographically (Echocardiography with color flow imaging should be performed)

Differential Diagnosis : 

Differential Diagnosis Persistent pulmonary hypertension, aspiration (meconium, amniotic fluid) syndromes, spontaneous pneumothorax, pleural effusions, and congenital anomalies such as cystic adenomatoid malformation, pulmonary lymphangiectasia, diaphragmatic hernia, and lobar emphysema must be considered, but can generally be differentiated from RDS by roentgenographic evaluation.

Differential Diagnosis : 

Differential Diagnosis Transient tachypnea may be distinguished by its short and mild clinical course. Congenital alveolar proteinosis (congenital surfactant protein B deficiency) is a rare familial disease that manifests as severe and lethal RDS in predominantly term and near-term infants In atypical cases of RDS, a lung profile (lecithin:sphingomyelin ratio and phosphatidylglycerol level) performed on a tracheal aspirate can be helpful in establishing a diagnosis of surfactant deficiency.

Prevention : 

Prevention Avoidance of unnecessary or poorly timed cesarean section, appropriate management of high-risk pregnancy and labor, and prediction and possible in utero acceleration of pulmonary immaturity are important preventive strategies. Antenatal and intrapartum fetal monitoring may similarly decrease the risk of fetal asphyxia; asphyxia is associated with an increased incidence and severity of RDS.

Prevention : 

Prevention Antenatal Corticosteroids The 1994 National Institutes of Health Consensus Development Conference on the effect of corticosteroids for fetal maturation on perinatal outcomes concluded that antenatal corticosteroids reduce the risk of death, RDS, and IVH.

Prevention : 

Prevention Antenatal Corticosteroids Administration of Betamethasone to women 48 hr before the delivery of fetuses between 24 and 34 wk of gestation significantly reduces the incidence, mortality, and morbidity of RDS. Corticosteroid administration is recommended for all women in preterm labor (24–34 wk gestation) who are likely to deliver a fetus within 1 wk.

Prevention : 

Prevention Antenatal Corticosteroids Repeated weekly doses of Betamethasone until 32 wk may reduce neonatal morbidities and the duration of mechanical ventilation. The recommended glucocorticoid regimen consists of the administration to the mother of two 12-mg doses of betamethasone given intramuscularly 24 h apart.

Prevention : 

Prevention Antenatal Corticosteroids Dexamethasone is no longer recommended because of increased risk for cystic periventricular leukomalacia among very premature infants exposed to the drug prenatally

Prevention : 

Prevention Early Surfactant Administration of a 1st dose of surfactant into the trachea of symptomatic premature infants immediately after birth (prophylactic) or during the 1st few hours of life (early rescue) reduces air leak and mortality from RDS, but does not alter the incidence of BPD.

Prevention : 

Prevention Other measures antenatal ultrasonography continuous fetal monitoring tocolytic agents that prevent and treat preterm labor assessment of fetal lung maturity before delivery (lecithin-sphingomyelin [L-S] ratio and Phosphatidylglycerol) to prevent iatrogenic prematurity.

Management : 

Management Surfactant Replacement is now considered a standard of care in the treatment of intubated infants with HMD. Since the late 1980s, more than 30 randomized clinical surfactant, whether used prophylactically in the delivery room to prevent HMD or in the treatment of the established disease, leads to a significant decrease in the risk of pneumothorax and the risk of death.

Management : 

Management Surfactant Replacement Rescue treatment is initiated as soon as possible in the 1st 24 hr of life. Repeated dosing is given via the endotracheal tube every 6–12 hr for a total of 2 to 4 doses, depending on the preparation. Complications of surfactant therapy include transient hypoxia, bradycardia and hypotension, blockage of the endotracheal tube, and pulmonary hemorrhage

Management : 

Management Surfactant Replacement Although proved to be immediately effective in reducing the severity of HMD, surfactant replacement has not clearly been shown to decrease the long-term oxygen requirements or the development of chronic lung changes. Evidence exists that the length of stay on mechanical ventilation and total ventilator days have been reduced with the use of surfactant at all gestational age levels, even with the increase of extremely low birth weight infants.

Management : 

Management Surfactant Replacement A dramatic fall in deaths from HMD began in 1991. In long-term follow-up studies, no adverse effects attributable to surfactant therapy have been identified.

Management : 

Management Surfactant Replacement Preparations Synthetic Exosurf Surfaxin (KL4) Natural Survanta (bovine) Infasurf (calf) Curosurf (porcine)

Management : 

Management Respiratory Support 1. Endotracheal Intubation and Mechanical Ventilation The goals is to improve oxygenation and elimination of carbon dioxide without causing pulmonary barotrauma or oxygen toxicity usually begins with rates of 30-60 breaths/min and I:E ratio of 1:2 An initial PIP of 18-30 cm H2O is used, depending on the size of the infant and the severity of the disease.

Management : 

Management Respiratory Support 1. Endotracheal Intubation and Mechanical Ventilation A PEEP of 4-5 cm H2O results in improved oxygenation, presumably because it assists in the maintenance of an effective FRC. The lowest possible pressures and inspired oxygen concentrations are maintained in an attempt to minimize damage to parenchymal tissue.

Management : 

Management Respiratory Support 2. CPAP and Nasal SIMV Nasal CPAP (NCPAP) or nasopharyngeal CPAP (NPCPAP) may be used early to delay or prevent the need for endotracheal intubation. To minimize lung injury associated with intubation and mechanical ventilation even in very low and extremely low birth weight infants.

Management : 

Management Respiratory Support 3. Complications Pulmonary air leaks, such as pneumothorax, pneumomediastinum, pneumopericardium, and PIE, may occur. Chronic complications include respiratory problems such as BPD and tracheal stenosis.

Management : 

Management Weaning Strategies Once extubated, many infants transition to nasal CPAP to avoid postextubation atelectasis and hypoxia. Nasal SIMV has been shown to decrease the need for reintubation in VLBW infants. High flow (1–2 L/min) or warmed, humidified high flow (2–8 LPM) nasal cannula oxygen is commonly used to support term and near-term infants following extubation and to wean premature infants off nasal CPAP. Preloading with caffeine may enhance the success of extubation.

Management : 

Management Metabolic Acidosis in RDS, may be a result of perinatal asphyxia and hypotension and is often encountered when an infant has required resuscitation Sodium bicarbonate, 1–2 mEq/kg, may be administered over a 15–20 min period through a peripheral or umbilical vein, with the acid-base determination repeated within 30 min, or it may be administered over a period of several hours. Often, sodium bicarbonate is administered on an emergency basis through an umbilical venous catheter.

Management : 

Management Antibiotic Therapy Antibiotics that cover the most common neonatal infections are usually begun initially. Aminoglycoside dosing intervals are increased for the premature infant.

Management : 

Management Sedation might be indicated for infants who "fight" the ventilator Phenobarbital is often used to decrease the infant's activity level. Morphine, fentanyl, or lorazepam may be used for analgesia as well as sedation. Muscle paralysis with pancuronium for infants with HMD remains controversial.

Management : 

Management Sedation Midazolam is approved for use in neonates, and has demonstrated sedative effects. Diazepam is not recommended due to its long half-life, its long-acting metabolites, and concern about the benzyl alcohol content.

Thank you… : 

Thank you…