TRANSIENT TACHYPNOEA OF THE NEWBORN By: Nicole Stevens

Objectives Discuss the pathophysiology of TTN Identify the risk factors for TTN Describe the clinical signs of TTN Discuss the medical and nursing management of TTN

Introduction TTN is a parenchymal lung disorder It is characterised by pulmonary oedema This results from delayed resorption and clearance of fetal alveolar fluid TTN is a common cause of respiratory distress in newborns It is generally a benign and self-limiting condition 3

Introduction Also known as wet lung Interfers with gas exchange Increased risk with caesarean birth (without labour) Usually effects near or full term infants Usually presents within the first few hours of life and often resolves within the first day

Introduction If clinical deterioration occurs, or if symptoms persist, an alternate diagnosis should be considered Differential diagnosis could include: RDS, MAS, neonatal pneumonia, congenital heart disease or polycythaemia Respiratory fatigue may result if symptoms persist

Introduction Differentiation from other conditions may take time So in the meantime, evaluation, monitoring and basic supportive care should continue with management of symptoms

Pathophysiology The main issue with TTN is that fetal alveolar fluid is not sufficiently cleared before birth or shortly afterwards The process of clearing fetal alveolar fluid begins before term birth, continues through labour and after birth In response to hormones released by the woman during labour the fetus’ adrenal glands release higher levels of catecholamines

Pathophysiology These catecholamines are the same as those produced in the fight flight response. This fetal stress response is designed to help the baby transition to life outside the uterus The catecholamines also help with increasing the amounts of surfactant that are secreted Also responsible for increasing HR, BGL’s and BP – explains fetal tachycardia and then initial high BGL’s in the stressed fetus/infant.

Pathophysiology Within the lung the catecholamines, and other hormones, cause the mature lung epithelium to switch from secreting chloride and liquid into the air spaces to actively reabsorbing sodium and liquid. Failure of fluid clearance to occur results in excess lung liquid

Pathophysiology Liquid fills the air spaces and moves into the interstitium It pools in perivascular tissues and interlobar fissues Eventually, it is cleared by the lymphatics or absorbed into small blood vessels The excess lung water results in decreased lung compliance

Pathophysiology Tachypnoea develops to compensate for the increased WOB associated with reduced compliance In addition, fluid can also accumulate in the peribronchiolar lymphatics and interstitium causing partial collapse of the bronchioles with subsequent air trapping Continued perfusion of poorly ventilated alveoli leads to hypoxaemia, alveolar oedema, reduced ventilation and sometimes hypercapnia (↑CO2 levels)

Risk Factors History of maternal analgesia or aneasthetic Intrauterine asphyxia Antepartum haemorrhage Maternal diabetes Caesarian section Precipitate labour Second twin Prolapsed umbilical cord

Risk Factors Maternal analgesics or anaesthetic The effect of opioids may be directly through placental transfer to the fetus Or the effect may be secondary to maternal respiratory depression or decreased uterine tone Effects are usually dose dependent, not drug dependent The effects from GA’s on the fetus are proportional to the length of time between induction of GA and clamping of the cord (time of exposure to the drug)

Risk Factors Intrauterine Asphyxia Depressed state at birth results in accumulation of mucous and secretions Swallow and cough mechanisms may be diminished Pulmonary and capillary congestion may occur Increased PVR can occur secondary to hypoxaemia and acidosis

Risk Factors Maternal Diabetes Respiratory distress requiring admission to SCN is 6 times more likely in the infant of a mother with diabetes Delayed maturation of surfactant synthesis has been observed in these infants, but it is unclear if the cause is hyperglycaemia or hyperinsulinaemia inutero Glycogen is normally depleted from the lungs as part of the maturation process and this coincides with an increase in surfactant synthesis Insulin inhibits glycogen breakdown

Risk Factors Caesarean Section (without labour) There is a higher incidence of TTN in infants born via caesarean than those born vaginally. A fetus who does not endure a trial of labour may not receive the benefits of the endogenous steroid and catecholamine surge that occurs during labour to assist in clearing fetal lung fluid at birth.

Clinical Signs Usually good apgar scores Manifests soon after birth Tachypnoea (RR >60) Nasal flaring Grunting or ‘moaning’ sounds on expiration Retractions Cyanosis

Clinical Signs Tachypnoea An ↑RR will ↓expiratory time With less expiratory time there is an ↑FRC ↑RR will ↑MV which acutely reduces PCO2 and raises pH In infants with persistent tachypnoea and cyanosis (but no other signs laboured breathing) consider other diagnosis, such as, cyanotic heart diseases, PPHN, or sepsis without pneumonia

Clinical Signs Nasal flaring ↓air resistence allows ↑flow through upper airways Retractions Active contractions of intercostal, subcostal & supra sternal chest wall muscles which function to stabilise the relatively compliant chest wall of the neonate Aids in ↑ the negative pleural pressure

Clinical Signs Grunting Exhaling against a partially closed glottis Increases the FRC Loudness of the grunt is proportional to the severity of the lung disease ALL SIGNS TOGETHER DESCRIBED AS INCREASED WORK OF BREATHING

Diagnosis Non specific features One of exclusion Time will tell Chest X-ray can reveal diffuse haziness, streakiness in lung fields and mild hyper-inflation Blood Gas can show mild hypoxia and acidaemia

Diagnosis Increased central vascular markings ("star-burst" appearance) Hyperaeration Evidence of interstitial and pleural fluid Prominent interlobar fissures Cardiomegaly 22

Day of birth Day 3 Transient Tachypnea of the Newborn (TTN). CXR of a term newborn (left) shows streaky, perhilar linear densities (white circles), indistinctness of the blood vessels and fluid in the minor fissure (black arrow), all signs of increased fluid in the lungs. Three days later (right), a CXR of the same baby shows complete clearing of the fluid and a normal CXR.

Management On arrival to SCN: Weigh Place in incubator & apply monitoring equipment for SaO2, HR & RR(if available) Record weight, time & observations Position prone & leave alone!

Management Monitor temperature 1/2hrly until stabilised, may initially be cold, but big, term babies will quickly warm up in incubators and become too hot (which will cause tachypnoea!) Give supplemental oxygen if low SaO2 (remember to change upper alarm limits so you are prompted to wean oxygen if SaO2 are high). Refer to NETS handbook for target SaO2 (depends on gestation).

Management Monitor BGL’s/TBG, first level preferably at about 1 hour of age, discuss with paediatrician ongoing frequency of monitoring after that – will depend on initial result, ongoing symptoms and whether or not symptoms permit feeding Consider IV therapy if low BGL’s, or if symptoms persist and feeding is not desirable (increased risk of aspiration in the tachypnoeic infant who is fed)

Management If symptoms persist consider: Antibiotics (need to site cannula, take blood cultures, CRP and FBE for baseline) Benzylpenicillin & Gentamycin Chest Xray Respiratory support (such as CPAP or high flow) – if not in a tertiary centre, consult with NETS. Managed well infants with TTN have an excellent prognosis.