Infant Respiratory Distress Syndrome (RDS) (also known as neonatal respiratory distress syndrome, respiratory distress syndrome of newborn, or surfactant deficiency disorder (SDD), and previously known hyaline membrane disease (HMD)). It commences shortly after birth (the baby may look well initially but develop respiratory difficulties within 2 to 4 hours of life) and increases in severity over the next two days.

Causes:

Prematurity (due to the infant not producing enough surfactant due to immaturity of the lungs -this leads to problems because if there is not enough surfactant in the lungs it increases the surface tension in the air liquid interface in the lungs. High surface tension leads to reduced expansion of the alveoli, resulting in collapse (atelectasis).) RDS occurs most frequently in infants which are up to 27 weeks gestation as production of surfactant is only starting in these infants.

Genetic (problems with production of surfactant associated proteins).

Risk Factors:

Sibling that had RDS.
Gestational diabetic mother.
Caesarean delivery.
Delivery complications which decrease blood flow to infant.
Multiple pregnancy.
Rapid labour.

Clinical presentation:

Tachypnoeic (RR greater than 60 breaths per minute).
Grunting (suggests a difficulty in aeration and oxygenation, it is an expiratory noise and suggests that there may be a partially obstructed glottis).
Nasal flaring (a compensatory mechanism in an attempt to take in more oxygen by increasing the size of the nares thus decreasing resistance of the airways).
Chest retraction (due to increased negative intrathoracic pressure which is necessary to ventilate the stiff, non-compliant lung).
Pallor or cyanosis (due to poor oxygenation).
Decreased breath sounds on auscultation.
Hypotension.
Prolonged capillary refill time.
Lethargy

Diagnosis:

Chest X-Ray will show reduced lung volume, absence of the thymus (after about 6 hours), uniform infiltrate (ground glass appearance), air-bronchograms (infiltrate that outlines the larger airway passages which remain air filled) and in severe cases the CXR can have a white out appearance in which cardiac borders become unapparent.

Labs -ABG (hypoxic, acidosis), septic screen (to rule out infection), glucose levels (to rule out hypoglycaemia which can cause tachypnoea and respiratory distress) and electrolytes (especially calcium as this can contribute to more respiratory symptoms).

Echocardiogram (used to confirm the diagnosis of PDA).

Treatment

Use of surfactants. Surfactant is normally produced in the lung and it helps to reduce the surface tension in the air liquid interface in the lung. It is made from a layer of phospholipids which have a hydrophilic head and hydrophobic tail which reduces the surface tension of the water at the air liquid interface of the lung. Premature infants (particularly those at 27 weeks gestation and below have only started their production of surfactant and thus have none of their own store built up. Term infants have produced surfactant and have a store built up for use at birth, to reduce the surface tension in their lungs. The larger the amount of surfactant available the greater the effect of the surface tension reducing properties. Surfactant is delivered intratracheally via an ETT. Curosurf is used within NICU, with either a rescue dose of 200mg/kg or 100mg/kg. Prior to use of surfactants, the babies condition should be stabilised (correction of acidosis, anaemia, hypoglycaemia and hypothermia if possible). The INSURE method is used sometimes for administration INtubate, SURfactant, Extubate. This is where an ET tube is inserted, surfactant given and infant extubated, this reduces the risks of using sedation and trauma caused by the use of the ETT.
Use of inhaled Nitric Oxide therapy. NO is a vasodilator which opens up blood vessels, this can help with oxygen uptake in the blood. iNO may increase the risk of haemorrhage, platelet aggregation (clumping) and methemoglobinemia (decreases the ability of oxygen binding).
Use of extracorporeal membrane oxygenation (ECMO), a type of cardiopulmonary bypass that allows gas exchange to occur outside of the lung by perfusion of the blood through a membrane oxygenator. This therapy can only be used for infants of GA greater than 34 weeks/2000g (vessels too small in infants younger/smaller than this). Risks of haemorrhage is increased in infants placed on ECMO due to the use of heparin to keep the circuit from clotting.
Steroids. To encourage maturation of lungs. (To be used with caution as steroid use can decrease mental function later in life in these infants.)
Ventilation -either invasive via ETT or non-invasive CPAP (which can prevent the need for ETT thus reducing the risks of barotrauma to the airways). This delivers pressure to help to keep the lungs from collapsing.
Supportive care to help reduce the infant's oxygen needs, such as gentle handling, lowering disturbances and maintaining body temperature (shivering uses up more oxygen).
Antibiotic therapy.
Fluid and nutritional support.
Sedation to decrease the infant's activity level thus decreasing their oxygen demands.
Infection control vigilance (preventative).

Prevention:

Try to avoid premature birth.
If premature birth expected mother should be given antenatal coricosteroids (Betamethasone).
Continuous foetal monitoring.

Complications:

Pneumothorax, pneumomediastinum or pneumopercardium which would require the insertion of a chest drain.
Intraventricular haemorrhage.
Bronchopulmonary dysplasia (BPD). Chronic lung disease which manifests hypercapnia/hypoxia, difficulty feeding and can possibly lead to heart failure, this is normally apparent within 7 to 10 days.
Delayed mental development and intellectual disability due to brain damage.
Retinopathy of prematurity.
Sepsis.
Periventricular leucomalacia (PVL) (a form of white matter brain injury).
Necrotising entercolitis (NEC).
Renal damage.
Death.

	Created by Elaine Henry over 10 years ago

RDS Note on Infant Respiratory Distress Syndrome, created by Elaine Henry on 08/13/2013.

Infant Respiratory Distress Syndrome