Neonatal Respiratory Distress Syndrome

Neonatal Respiratory Distress SyndromeNeonatal respiratory distress syndrome (RDS, formerly termed as hyaline membrane disease, most often

occurs in preterm infants, infants of diabetic mothers, infants born by cesarean birth, or those for any reason have decreased perfusion of the lungs. The pathologic feature of RDS is a hyaline-like membrane formed from exudates of an infant’s blood that begins to line the terminal bronchioles, alveolar ducts and the alveoli. This membrane prevents exchange of oxygen and carbon dioxide at the alveolar- capillary membrane. The cause of RDS is a low level of absence of surfactant that normally lines the alveoli and reduces surface tension on expiration to keep the alveoli from collapsing on expiration. The condition makes it difficult to breathe.

CAUSES

Neonatal RDS occurs in infants whose lungs have not yet fully developed.

The disease is mainly caused by a lack of a slippery, protective substance called surfactant, which helps the lungs inflate with air and keeps the air sacs from collapsing. This substance normally appears in fully developed lungs.

Neonatal RDS can also be the result of genetic problems with lung development.

In addition to prematurity, the following increase the risk of neonatal RDS:

A brother or sister who had RDS Diabetes in the mother

Cesarean delivery

Delivery complications that reduce blood flow to the baby

Multiple pregnancy (twins or more)

Rapid labor

The risk of neonatal RDS may be decreased if the pregnant mother has chronic, pregnancy-related high blood pressure or prolonged rupture of membranes, because the stress of these situations can cause the infant's lungs to mature sooner.

PATHOPHYSIOLOGY

Risk factors

A brother or sister who had RDSDiabetes in the motherCesarean delivery

Reduced perfusion to the lungs Multiple pregnancy Rapid labor

Increased cardiac rate Venous vasoconstriction

Central blood redistribution

Acidosis

Increased cardiac work load

Increased respiratory rate

Increased in size of right ventricle

Blood regurgitates to systemic circulation

Edema

Decreased urine output

Decreased cardiac output

Aerobic respiration shifts to anaerobic

respiration

Lactic acid as a byproduct of anaerobic respiration

Hyaline membrane formation

Nasal flaring, expiratory grunting, chest retractions

Decreased cardiac filling time

Absence or decreased surfactant production

Decreased lung compliance

Shunting

Ductus areteriosus and foramen ovale

remains open

Pulmonary hypertension

Poor perfusion

Increased work of breathing

Alveolar dead space

Haziness seen in chest x-ray

Tissue hypoxia

Increase oxygen demand

Poor O2 and CO2 exchange

Tissue injury

Activation of the inflammatory

process

Carbon dioxide

accumulationCyanotic mucous membrane

Apnea

Increased surface tension in alveoli

Decreased functional residual capacity

Heart failure

High pressure is required to fill the lungs with air for the first time. Id alveoli collapse with each expiration, forceful inspirations are required to inflate them.

With deficient surfactant, areas of hypoinflation begin to occur and pulmonary resistance increases. Blood then shunts through the foramen ovale and the ductus arteriosus as it did during fetal life. The lungs are poorly perfused, affecting gas exchange. As a result, the production of surfactant decreases even further.

The poor exchange leads to tissue hypoxia which causes the release of lactic acid. This, combined with the increasing carbon dioxide level resulting from the formation of hyaline membrane on the alveolar surface, leads to severe acidosis. Acidosis causes venous vasoconstriction which leads to poor perfusion further compounding the ill surfactant production. In addition, vasoconstriction causes blood to shunt centrally increasing the workload of the heart.

EXAMS AND TESTS

Blood culture - may indicate bacteremia. Not helpful initially because results may take >48 hours

Blood gas - used to assess degree of hypoxemia if arterial sampling, or acid/base status if capillary

sampling

Chest radiography

Complete blood count with differential

Leukocytosis or bandemia indicates stress or infection

Neutropenia correlates with bacterial infection

Low hemoglobin level shows anemia

High hemoglobin level occurs in polycythemia

Low platelet level occurs in sepsis

Lumbar puncture - if meningitis is suspected

Pulse oximetry - used to detect hypoxia and need for oxygen supplementation

THERAPEUTIC MANAGEMENT

Surfactant Therapy

Surfactant can be given to help the air sacs in the lungs expand and take in more oxygen. There are two options, both of which are delivered directly into the baby's windpipe. One type of surfactant comes from cows and the other is synthetic. As the surfactant takes effect, use of the respirator can gradually be reduced.

Muscle Relaxants

Pancuronium (Pavulon) abolishes spontaneous respiratory action, therefore allowing mechanical ventilation to be accomplished at lower pressures because there is no normal muscle resistance to overcome.

Mechanical Respirator

A mechanical respirator is used to keep the air sacs from collapsing and to improve the exchange of oxygen and other gases in the lungs. This treatment helps the baby breathe better and is almost always required in severe RDS. High-frequency ventilation may be used to reduce lung injury.

A breathing machine can be lifesaving, especially for babies with the following:

High levels of carbon dioxide in the arteries Low blood oxygen in the arteries

Low blood pH

Extracorporeal Membrane Oxygenation

Blood is removed from the baby by gravity using a venous catheter advanced into the right atrium of the heart. The blood circulates from the catheter to the ECMO machine, where it is oxygenated and rewarmed. It is then returned to the baby’s aortic arch by a catheter advanced through the carotid artery.

Liquid Ventilation

Liquid ventilation involves the use of perfluorocarbons, substances used in industry to assess for leakage in pipes. This helps to distend the lungs and aid in oxygen exchange.

Nitric Oxide

Nitric oxide caused pulmonary vasodilatation which can be helpful to increase blood flow to the alveoli when persistent pulmonary hypertension is present.

Nutritional Support

Newborns with RDS may be given food and water by the following means:

Tube feeding—a tube is inserted through the baby's mouth and into the stomach

Parenteral feeding—nutrients are delivered directly into a vein

It is important that all babies with RDS receive excellent supportive care, including the following, which help reduce the infant's oxygen needs:

Few disturbances Gentle handling

Maintaining ideal body temperature

Infants with RDS also need careful fluid management and close attention to other situations, such as infections, if they develop.

OUTLOOK (PROGNOSIS)

The condition often worsens for 2 to 4 days after birth with slow improvement thereafter. Some infants with severe respiratory distress syndrome will die, although this is rare on the first day of life. If it occurs, it usually happens between days 2 and 7.

Long-term complications may develop as a result of too much oxygen, high pressures delivered to the lungs, the severity of the condition itself, or periods when the brain or other organs did not receive enough oxygen.

POSSIBLE COMPLICATIONS

Air or gas may build up in:

The space surrounding the lungs (pneumothorax) The space in the chest between two lungs (pneumomediastinum)

The area between the heart and the thin sac that surrounds the heart (pneumopericardium)

Other complications may include:

Bleeding into the brain (intraventricular hemorrhage of the newborn) Bleeding into the lung (sometimes associated with surfactant use)

Delayed mental development and mental retardation associated with brain damage or bleeding

Retinopathy of prematurity and blindness

PREVENTION

Good prenatal care beginning as early as possible in pregnancy. Eat a healthful diet and take vitamins suggested by thedoctor. Do not smoke or use alcohol or drugs.

If you are at high risk of giving birth to a premature baby: Steroids administration Amniocentesis Surfactant administration right after birth

FOCUS CHARTING

Date Focus Data, Action, Response

In from EINC cuddled by Nurse Roberto

010912/5am dyspnea D: pale; c nasal flaring; c subcostal retractions

A: placed under radiant warmer

5:01 am

A: oxygen administered at 10LPM via hood; placed on moderate high back rest

5:05 am A: attended by Dr. Fancubit c orders

Marie Paz P. Hementera, RN

5:10am Admission A: condition explained to mother and mother by Dr. Fancubit; consent for admission obtained c consent form signed

A: 25cc D10 Water placed in volumetric chamber and inserted aseptically by Dr. Fabcubit thru umbilical cannulation and regulated at 3mgtts

A: 99.4cc D5 Water + 0.6 Dopamine placed in volumetric chamber and hooked as side drip and regulated at 3mgtts/min

Marie Paz P. Hementera, RN

5:30am Diagnostic procedure D: CBC APC BT

A: request and specimen sent to laboratory

Marie Paz P. Hementera, RN

5:45am Diagnostic procedure D: CXR APL + Abd

A: sent to radiology department cuddled by Nurse Villanueva accompanied by father and came back after 20 minutes

Marie Paz P. Hementera, RN

6am Hypoglycemia D: jittery, skin cold to touch, diaphoretic

6:05 am A: capillary blood glucose taken and revealed 20mg/ dl

6:05 am A: referred to Dr. Fancubit c orders

A: 2.2 cc of D10 Water given as IV bolus as ordered

6:35am R: capillary blood glucose retaken and revealed 100mg/dl

7am Endorsed for continuity of care

Marie Paz P. Hementera, RN