Neonatal Respiratory Distress and treatment modalities

Dr Piyush Shah, Dr. R. Kishore Kumar
Keywords : RD, newborn, TTN, RDS.

Respiratory distress (RD) is one of the commonest reasons for admission in neonatal intensive care unit (NICU)1. It is characterized by tachypnea, retraction of chest, nasal flaring, grunting, and cyanosis2,3. Early recognition of RD is essential based on clinical signs and symptoms. If unrecognized, RD can progress to cardio-respiratory failure causing death. Thus RD in newborns is a major morbidity and a health burden.
Respiratory mechanics:
Respiratory function of lung is to maintain ventilation (PCO2) and oxygenation (PaO2)2.
Ventilation (Pco2) = Tidal Volume (TV) x Respiratory rate (RR).
Normal RR for newborn = 30-60 breaths/min
TV= 4-6 ml/kg body weight.
TV is decreased in pathologies involving decrease compliance e.g. surfactant deficiency, pneumonia, pulmonary hypoplasia. Thus, for compromised TV, the compensatory mechanism is increase RR in response to hypercarbia, hypoxemia, or acidosis
In normal lung alveoli, for effective gas exchange, requires an inflated air sac, and blood supply along pulmonary capillaries. Normally in utero, the foetal airspaces and air sacs are fluid filled, with high pulmonary vascular resistance (PVR). For effective gas exchange to occur after birth, the fluid gets cleared from the alveolar airspaces, with an effective fall of PVR. This clearance is enhanced by foetal thorax compression with uterine contractions and release of foetal adrenaline, whereas the fall in PVR enhanced by first cry of newborns(4,5,6).
Thus any cause affecting delayed clearance of amniotic fluid, inflation of alveoli or fall in PVR, would lead to ventilation- perfusion (V/Q) mismatch at alveoli. Thus resultant hypoxemia, hypercarbia will cause compensatory mechanism leading to signs of RD.
Transient tachypnea of Newborns (TTN): TTN is caused by failure clearance of alveolar fluid. TTN is common in late preterm (gestational age, GA 34-37 weeks) and infants born by elective C-section. The alveolar fluids collects in interstitial spaces and fissure, which later get cleared by lymphatics.
Respiratory distress of newborns (RDS): It is caused by alveolar surfactant deficiency(6). Endogenous surfactant at the alveoli is responsible in keeping the alveoli inflated and preventing collapse, assisting effective gas exchange. The fetal lung starts synthesizing surfactant around 22 weeks of intrauterine life. The premature born baby has relative deficiency of surfactant, with inverse relation to GA at birth. Thus the premature infant having RDS will have atelectatic lung leading to V/Q inequality, and hypoventilation with resultant hypoxemia and hypercarbia(6).
Persistent Pulmonary Hypertension of Newborns (PPHN): PPHN is caused by abnormal high PVR, which has not normalized at birth(7). This leads to persistent of right to left shunting of deoxygenated blood across foramen ovale and patent ductus arteriosus (PDA). The resultant hypoxemia causes tachypnea and cyanosis. It is common in term neonates.

Clinical signs & symptoms: RD in the newborn is recognized as one or more signs of increased work of breathing, such as tachypnea, nasal flaring, chest retractions, grunting or cyanosis(1,2,3).
• Tachypnea- RR > 60 breaths per minute.
• Nasal flaring: a compensatory symptom; increases upper airway diameter and reduces resistance and work of breathing.
• Retractions: evident by use of accessory muscles in the neck, rib cage, sternum, or abdomen; occurs when lung compliance is poor or airway resistance is high.
• Grunting: an expiratory sound caused by sudden closure of the glottis during expiration in an attempt to maintain functional residual capacity (FRC) and prevent alveolar atelectasis.
• Cyanosis: bluish discoloration of skin and mucous membranes. It is caused by increase in deoxygenated blood.
• Respiratory failure is defined as ineffective oxygenation or ventilation or both. It is characterised by increasing respiratory distress with low saturations on pulse oximetry (SPO2< 93%), low partial pressure of oxygen on arterial blood gas (PaO2) < 60mm of Hg) and or high partial pressure of carbon dioxide (PaCO2 > 45 mm Hg) with respiratory acidosis (pH < 7.2).

Neonatal Respiratory Distress and treatment modalities Neonatal Respiratory Distress and treatment modalities 09/05/2018
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