NEONATOLOGY V.pptx

NEONATOLOGY V RESPIRATORY PROBLEMS IN THE NEWBORN DR UGOLEE JERRY INTRODUCTION • Respiratory distress is among the most common symptom complexes seen in new-borns whom have immature pulmonary function and compliance following the abrupt cardiopulmonary changes that occur at birth • Causes of respi...

NEONATOLOGY V RESPIRATORY PROBLEMS IN THE NEWBORN DR UGOLEE JERRY INTRODUCTION • Respiratory distress is among the most common symptom complexes seen in new-borns whom have immature pulmonary function and compliance following the abrupt cardiopulmonary changes that occur at birth • Causes of respiratory distress in new-borns maybe noncardiopulmonary or maybe of cardiac or pulmonary origin • Chest x-ray, arterial blood gases and pulse oximetry are useful in assessing both the aetiology and severity of the respiratory problem INTRODUCTION • Non-cardiopulmonary causes of respiratory distress in newborn’s include hypo/hyperthermia, hypoglycaemia, polycythaemia, anaemia, metabolic acidosis, asphyxia, intraventricular haemorrhage, phrenic nerve injury • Cardiac causes include hypoplastic left heart syndrome, coarctation of the aorta, TGA, TAVPVR, tricuspid atresia • Pulmonary causes include choanal atresia, vocal cord paralysis, meconium aspiration, Transient tachypnea of the newborn, congenital pneumonia, Respiratory distress syndrome, Pneumothorax (air leaks) TRANSIENT TACHYPNEA OF THE NEW BORN •TTN (wet lung): usually follows an uneventful normal preterm or term vaginal delivery but its incidence is higher in term deliveries following CS due to the absence of the thoracic squeeze accompanying SVD •It is characterized by respiratory distress typically present from birth manifesting as fast breathing with retraction and expiratory grunting, occasionally the child may be cyanosed but the cyanosis is easily relieved by minimal O₂ TRANSIENT TACHYPNEA OF THE NEW BORN • Chest x-ray shows prominent pulmonary vascular markings with perihilar streaking and interlobular fissures and a flat diaphragm • Pathophysiology is thought to be secondary to the slow absorption of fluids from the fetal lungs resulting in reduced pulmonary compliance and tidal volume but increased physiologic dead space • It is usually self-limiting and should resolve in 2-3days • Treatment is supportive. There is no evidence that IV fursemide helps MECONIUM ASPIRATION SYNDROME • MAS: meconium stained amniotic fluid is found in 10-15% of birth especially term and post-date babies. Only about 5% of them aspirate and suffer MA pneumonitis • Commoner in term new-borns who have experienced some form of fetal distress in utero or is depressed at birth with hypotonia, bradycardia, apnoea and depressed reflexes • MAS may occur in utero but commonly follows the first breath taken to initiate respiration. Thick, particulate meconium is aspirated into the lungs causing small airway obstruction MECONIUM ASPIRATION SYNDROME •Respiratory distress ensues within 1hour of birth, clinical manifestations include fast breathing, difficulty in breathing, ICR,SCR, grunting and an overextension of the chest wall(barrel shape) and cyanosis in severe cases •There are widespread coarse breath sounds heard on auscultation. Mild cases improve within 72hrs,in severe cases respiratory distress persists for days to weeks and may require intubation and ventilation with a high risk of mortality MECONIUM ASPIRATION SYNDROME • Chest x-ray shows irregular patchy infiltrates with a hyperextension of the chest wall and a flattening of the diaphragm • Treatment involves the suctioning of the mouth first then the nostrils of the newborn at the delivery of the head before the chest is delivered to prevent of secretions in the airway especially in the presence of meconium stained liquor • If the newborn is vigorous at birth, suction the trachea under direct vision or through an ET tube before IPPV. Treatment should also include antibiotics& steroids CONGENITAL PNEUMONIA • Inflammation of the lung parenchyma of the newborn following infection with microbes, rarely viruses but more of bacteria • Transmission maybe transplacental, via an ascending infection following colonization of the maternal birth canal or by aspiration of infected amniotic fluid, in utero or during delivery • Common bacterial culprits include GBS, Strep pneumoniae, Kebseilia spp, E. coli, syphilis, viral causes include CMV, adenoviruses, influenza, varicella CONGENITAL PNEUMONIA • Risk factors include maternal colonization with infections on VDRL panel, premature labour, premature/preterm PROM, chorioamonitis, meconium stained liquor, multiple VE and APH • Clinical manifestations are usually nonspecific signs and symptoms of respiratory distress(tachypnea, flaring, grunting ,ICR). There may be fever after 24hrs, poor feeding, lethargy and apnoea • A good history, detailed physical examination and radiological findings aid in diagnosis CONGENITAL PNEUMONIA •Chest x-ray findings show bilateral diffuse infiltration. •Confirmatory testing is a positive respiratory culture of lung aspirate obtained from intubated babies but should not be routinely done •Ancillary investigations include blood culture, FBC, Creactive protein and pulse oximetry readings •Supportive treatment should include O ₂ support (face mask, CPAP or ECMO depending on severity) and broad spectrum Abiotics(ceftrixione/genticin ) APNOEA IN THE PRETERM NEW BORN • Apnoea is defined as a temporary cessation in breathing or a respiratory pause lasting less than 20seconds,often accompanied by cyanosis and bradycardia • It is a common recurrent finding in preterms • It must be differentiated from periodic breathing in them which is regular, recurring ventilatory cycles interrupted by short pauses not associated with colour changes or bradycardia APNOEA IN THE PRETERM NEW BORN • Precipitating factors include temperature instability, as a response to the passage of a feeding tube, hypoxemia, anaemia, sepsis, hypoglycaemia, intracranial haemorrhage, drugs(morphine) • Apnoea of prematurity refers to the temporary cessation of breathing resulting from an immaturity of both the central respiratory regulatory centre and the protective mechanism that protect and maintain airway APNOEA IN THE PRETERM NEW BORN •It is rare on the 1st day of life but may occur in severe preterms not requiring mechanical ventilation or in term newborns with neuromuscular disorders from birth trauma, asphyxia or congenital hypotonia •All newborns with apnoea should be evaluated at least minimally for general well-being, feeding tolerance, temperature stability, RBS, PCV, SPO₂ •Treatment should be directed at the underlying cause •When due to prematurity alone, its not usually severe or so frequent as to affect feeding or require frequent bag &mask ventilation. Apnea monitor or intermittent tactile stimulation APNOEA IN THE PRETERM NEW BORN •Drug treatment includes caffeine citrate and theophylline. •Supportive management may include CPAP or intubation and mechanical ventilation if severe •Prognosis depends of severity of maturity and underlying co-morbidities. Majority of preterms with apnoeic and bradycardia spells cease by 34-37weeks post conception HYALINE MEMBRANE DISEASE(RDS) •Common cause of respiratory distress occurring primarily in preterm newborns •It may occur in term newborns but its incidence of occurrence is inversely related to the gestational age. It occurs in 60-80% of infants≤ 28weeks GA,15-30% of infants born b/w 32-36weeks GA and in less than 5% of those born after 37weeks GA. •The risk of developing RDS is increased in the face of maternal DM, multiple gestation, CS delivery and precipitate delivery HYALINE MEMBRANE DISEASE(RDS) •Surfactant is present in the lungs at 20weeks GA but does not reach the lung surface till about 35weeks GA •Signs of RDS appear within minutes of birth but become more recognizable as respiratory distress worsen over time. •Clinical manifestations include tachypnea, grunting, ICR, SCR, a dusky appearance, and cyanosis often responsive to O₂ therapy. Breath sounds are diminished and rales may be heard at the lung bases HYALINE MEMBRANE DISEASE(RDS) • Its incidence is decreased in the face of maternal hypertension, PROM, and antepartum maternal corticosteroid administration • Pathophysiology follows surfactant deficiency. • Surfactant is produced and stored in type II alveolar cells and is a surface active agent that reduce surface tension thus preventing alveolar collapse during expiration and preventing small air space collapse • This maintains functional residual capacity, increases lung compliance and reduces the work of breathing HYALINE MEMBRANE DISEASE(RDS) • If untreated, cyanosis worsens, pallor appears, grunting disappears and apnoea ensues. Respiratory failure and death may follow • Death is rare on the 1st day of life, commonly occurs b/w 2-7days and is often associated with air leak syndromes(interstitial emphysema/ pneumothorax) • Chest x-ray show ground glass appearance and air bronchograms that occur as a result of major airway atelectatic air sacs HYALINE MEMBRANE DISEASE(RDS) •Prevention would include avoiding unnecessary poor timed CS •Giving antepartum betamethasone/ dexamethasone 48hrs prior to delivery •Prenatal glucocorticoid therapy •Treatment is best done in NICU, close monitoring of vital signs and O₂ saturation •Endotracheal instillation of exogenous surfactant •Rescue therapy 2-4doses given 6-12hours apart •Humified oxygen therapy via CPAP, or mech ventilation HYALINE MEMBRANE DISEASE(RDS) • • • • • • Differential Diagnosis: Congenital Pneumonia Total Anomalous Pulmonary Venous Return Meconium Aspiration Syndrome Transient tachypnea of the Newborn Pulmonary Lymphagiectasia