Respiratory distress syndrome and other causes of neonatal respiratory distress

Overview

Breathing difficulty is one of the commonest reasons for admission to a neonatal unit. The cause may be in the lungs, the airway, the heart, the brain or the body's metabolism, so the history (gestation, mode of delivery, liquor, infection risks) and a chest X-ray are essential.

Akbar notes that RDS accounts for about 20% of all neonatal deaths, so it is the condition examiners ask about most.

Recognising respiratory distress

• Tachypnoea: respiratory rate above 60/min.
• Recession: subcostal, intercostal and sternal.
• Expiratory grunting: breathing out against a partly closed glottis to keep the alveoli open.
• Nasal flaring, head bobbing.
• Cyanosis in room air; apnoea in severe cases.

Causes

Clues from the examination

Respiratory distress syndrome (hyaline membrane disease)

Definition

RDS is a clinical diagnosis in a preterm baby with respiratory distress (tachypnoea, recession, grunting, cyanosis) that persists or worsens over the first 48-96 hours, with a typical chest X-ray.

Pathophysiology

• Surfactant is a phospholipid-protein mixture made by type II alveolar cells. It lowers surface tension so that alveoli stay open at the end of expiration.
• Production starts at about 24-28 weeks and is enough only late in pregnancy, so preterm babies lack it.
• Without surfactant: alveolar collapse (atelectasis) at each breath out, stiff lungs, ventilation-perfusion mismatch, hypoxia, hypercapnia and acidosis.
• Hypoxia and acidosis further reduce surfactant production, a vicious circle.
• Protein leaks into the alveoli and forms the hyaline membranes seen on histology.

Risk factors

Antenatal corticosteroids given to the mother lower the risk.

Clinical course

• Signs start within minutes to hours of birth: tachypnoea, grunting, flaring, recession, cyanosis.
• The illness worsens over the first 24-48 hours, stays stable for about another 48 hours, then improves.
• Diuresis is often the first sign of recovery.

Investigations

• Chest X-ray: diffuse fine reticulogranular ("ground-glass") pattern with air bronchograms, low lung volumes; in severe disease a complete white-out.
• Blood gases: hypoxia, hypercapnia, respiratory and metabolic acidosis.
• Pulse oximetry.
• Septic screen and blood culture: congenital pneumonia (especially GBS) looks the same.
• Glucose and calcium.

Prevention

• Prevent preterm birth where possible.
• Antenatal corticosteroids (betamethasone or dexamethasone) to the mother at 24-34 weeks when preterm delivery is expected; most effective if given at least 48 hours before delivery. They also reduce IVH and neonatal death.
• Avoid elective caesarean section before term; delivery-room CPAP for at-risk babies.

Management

General care:

• Thermoneutral environment, minimal handling.
• IV fluids and glucose; withhold feeds until stable; monitor fluid balance.
• Keep BP normal; correct acidosis.

Oxygen and breathing support:

• Humidified oxygen to keep saturation about 91-95% (Akbar); avoid too much oxygen, which causes ROP and BPD.
• CPAP (nasal prongs, bubble CPAP) keeps alveoli open; start early, even in the delivery room.
• Heated humidified high-flow nasal cannula is an alternative for milder cases.
• Mechanical ventilation for respiratory failure, recurrent apnoea or failure of CPAP.

Surfactant replacement:

• An animal-derived surfactant given into the trachea (via endotracheal tube) reduces death and air leaks.
• Early rescue is standard; Akbar suggests giving it when the baby is worsening with FiO2 above 0.30 on CPAP of at least 6 cm H2O, or in the delivery room if intubation is needed.
• Poractant alfa (pig-derived) 200 mg/kg initially; a second or third dose if needed. Beractant is bovine-derived.
• Complications: tube blockage, pneumothorax, pulmonary haemorrhage.

Complications

• Air leak: pneumothorax, pulmonary interstitial emphysema.
• Patent ductus arteriosus.
• Intraventricular haemorrhage.
• Bronchopulmonary dysplasia (chronic lung disease: oxygen still needed at 28 days).
• Retinopathy of prematurity, infection, ventilator complications.

Transient tachypnoea of the newborn (TTN, "wet lung")

• Benign, self-limiting distress from delayed absorption of fetal lung fluid.
• Typical baby: term or near-term, born by elective caesarean section (no labour, so the chest is not squeezed in the birth canal to push fluid out); also male sex, macrosomia, infants of diabetic mothers (Nelson) and heavy maternal sedation.
• Tachypnoea soon after birth (above 60/min), mild recession and grunting; mild cyanosis that needs only low oxygen (under 40%); good air entry.
• Chest X-ray: hyperinflation, prominent vascular markings (streaky hilar shadows), fluid in the horizontal fissure and sometimes small effusions; mild cardiomegaly.
• Course: improves within hours; usually resolves in 1-3 days (12-24 hours in mild cases, up to 72 hours in severe).
• Treatment: supportive: oxygen, CPAP if marked distress, careful feeding; exclude sepsis.

Feeding a tachypnoeic baby (Akbar)

Meconium aspiration syndrome (MAS)

Who gets it

• Meconium-stained liquor is found in about 10-15% of births; about 5% of these babies develop MAS (Akbar).
• Typical baby: post-term or SGA with placental insufficiency and fetal hypoxia, which relaxes the anal sphincter and makes the fetus gasp.
• Other risks: pre-eclampsia, maternal hypertension or diabetes, abnormal fetal heart rate, heavy maternal smoking.

Pathophysiology

• Thick meconium blocks large airways: complete block causes atelectasis; partial block acts as a ball valve, causing air trapping, hyperinflation and air leak (pneumothorax).
• Chemical pneumonitis follows over hours.
• Meconium inactivates surfactant.
• Hypoxia and acidosis raise pulmonary vascular resistance, causing persistent pulmonary hypertension of the newborn (PPHN) with right-to-left shunting.

Clinical features

• Meconium-stained skin, nails and cord (yellow-green); features of post-maturity (long nails, peeling skin).
• Depressed at birth if asphyxiated; then severe distress, barrel chest, crackles and wheeze.
• Thick "pea-soup" meconium carries a worse outlook than thin meconium.

Investigations

• Chest X-ray: hyperinflation with flattened diaphragms, coarse patchy infiltrates, often pneumothorax or pneumomediastinum.
• Blood gases: hypoxaemia, acidosis.

Management

• At birth: a vigorous baby needs no tracheal suction; a non-vigorous baby gets PPV, with tracheal suction only if the airway is blocked (see the resuscitation chapter).
• Oxygen, CPAP or ventilation; watch for pneumothorax.
• Surfactant may improve oxygenation.
• Antibiotics after cultures, because MAS cannot be told from pneumonia on X-ray and meconium favours bacterial growth.
• PPHN: oxygen, ventilation, inhaled nitric oxide, sildenafil, ECMO in specialist centres.
• Prognosis depends mainly on the degree of brain injury from asphyxia.

Comparison of the three common conditions

Quick revision

• Distress = RR above 60 + recession, grunting, flaring or cyanosis.
• RDS: preterm, surfactant deficiency, ground glass + air bronchograms, worst at 24-48 h.
• RDS risks: prematurity, male, diabetic mother, caesarean without labour, asphyxia, cold.
• Prevent RDS: antenatal steroids at 24-34 weeks; treat: CPAP and surfactant, oxygen to 91-95%.
• Start antibiotics in RDS until GBS excluded.
• TTN: term, elective caesarean, fluid in fissure, settles in 1-3 days.
• MAS: post-term/SGA, hyperinflation, patchy infiltrates, pneumothorax, PPHN.
• Diaphragmatic hernia: scaphoid abdomen; intubate, do not bag.
• Feeds: oral below 60, NG 60-80, IV above 80 breaths/min.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).

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