Neonatal Respiratory Distress And Treatment Modalities
Dr Piyush Shah, Dr. R. Kishore Kumar
Dr Piyush Shah
MD, M.Sc. (Neonatology), MRCPCH (UK)
Consultant Neonatologist, Department of Neonatology,
Cloudnine Hospital, Malad, Mumbai, India.
Dr. R. Kishore Kumar
MD, FRCPCH (UK), FRACP
Consultant Neonatologist & Paediatrician,
Cloudnine Hospital, 1533, 9th Main,
3rd Block Jayanagar, Bangalore – 560011.

First Created: 09/05/2018  Last Updated: 09/05/2018

Introduction

Keywords: RD, newborn, TTN, RDS.

Respiratory distress (RD) is one of the commonest reasons for admission in the neonatal intensive care unit (NICU).1 It is characterized by tachypnea, retraction of the chest, nasal flaring, grunting, and cyanosis.2,3 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 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 to increase RR in response to hypercarbia, hypoxemia, or acidosis.

Pathogenesis:

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 the 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 a 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 collect 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 for keeping the alveoli inflated and preventing collapse, assisting effective gas exchange. The fetal lung starts synthesizing surfactant around 22 weeks of intrauterine life. The prematurely born baby has a 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 the persistent 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 the 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 the sudden closure of the glottis during expiration in an attempt to maintain functional residual capacity (FRC) and prevent alveolar atelectasis.

  • Cyanosis: bluish discoloration of the skin and mucous membranes. It is caused by an 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) < 60 mm of Hg) and or high partial pressure of carbon dioxide (PaCO2 >45 mm Hg) with respiratory acidosis (pH <7.2).

Investigations

  1. SPO2: with signs of RD, SPO2 reading taken on right arm (preductal) with good digital trace
    • persistent <93% in room air

    • Differential SPO2 between pre- & post-ductal SPO2 >10% suggestive of PPHN.7

  2. Chest radiograph:
    • TTN- The chest radiograph will show bilateral perihilar streaking with evidence of fissure fluids.

    • RDS - Low volume lung, reticular granular pattern to white out appearing lung.

    • PPHN- usually a normal appearing lung or findings of secondary pathology e.g. meconium aspiration syndrome, pneumonia, pulmonary hypoplasia, congenital diaphragmatic hernia etc.

  3. Arterial Blood gas: Respiratory acidosis pH <7.2, with pCO2 >45 mm of Hg
    • Worsening oxygenation, PaO2 <60 mm Hg on supplemental oxygen

Management

  • Use of continuous positive airway pressure (CPAP) and if need supplemental oxygenation (target SPO2 90-95%).

  • Use of assisted ventilation: CPAP/Intermittent Positive Pressure ventilation (IPPV) if in respiratory failure.

  • Avoid hypo- hyperthermia; maintain euglycemia

  • Achieve optimum organ perfusion with use of inotropes

  • Optimum nutrition; enteral feeds with parenteral nutrition to meet calories and protein needs.

  • Consider antibiotics after septic workup.

Specific:

  • Use of antenatal steroids in mother, early PEEP with nasal CPAP, and use of exogenous surfactant for RDS.8

  • Use of pulmonary vasodilators7 - inhaled Nitirc Oxide, intravenous Sildenafil for PPHN

CPAP:

The continuous distending pressure at end of expiration improves oxygenation. CPAP decreases atelectasis, helps in establishing FRC, and eliminating foetal lung fluid. The resultant PEEP improves V/Q matching(9,10). It also splints the upper airway, decreasing resistance to the airway. It is useful in infants with RD with good spontaneously breathing efforts. It is increasingly used in the early acute and late weaning/recovery phases of RD. Consider starting CPAP at PEEP 4-6 cm of H2O and inspired oxygen of 30%.

Intermittent Positive Pressure ventilation (IPPV):

IPPV delivered by constant flow, time-cycled, pressure limited ventilators is the most frequently used modality of neonatal ventilation. On a constant flow of gas through the circuit, the neonate breaths to set positive inspiratory pressures above PEEP. With newer modalities, the ventilator breaths can now be synchronized to those of the neonate. Also, now calculated preset TV can be given, as part of a lung-protective strategy.


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3. Warren JB, Anderson JM. Newborn respiratory disorders. Pediatr Rev. 2010;31(12):487–495, quiz 496.
4. Hooper SB, Te Pas AB, Kitchen MJ. Respiratory transition in the newborn: a three-phase process. Arch Dis Child Fetal Neonatal Ed. 2016 May;101(3):F266-71.
5. Jain L, Eaton DC. Physiology of fetal lung fluid clearance and the effect of labor.Semin Perinatol. 2006;30(1):34.
6. Avery ME. Surfactant deficiency in hyaline membrane disease: the story of discovery. Am J Respir Crit Care Med. 2000;161(4 Pt 1):1074.
7. Vinay Sharma, Sara Berkelhamer, Satyan Lakshminrusimha. Persistent pulmonary hypertension of the newborn Matern Health Neonatol Perinatol 2015; 1: 14.
8. Rashmi Jeenakeri, Mark Drayton. Management of respiratory distress syndrome. Paediatrics and Child Health 19:4, 158-164.
9. Sinha SK, Gupta S, Donn S. Immediate respiratory management of preterm infant. Semin Fetal Neonatal Med 2008; 13: 24–9.
10. Greenough A, Donn SM. Matching ventilatory support strategies to respiratory pathophysiology. Clin Perinatol 2007; 34: 35–53.


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