Neonatal Diseases

common causes of respiratory distress in the neonate are : -

1. Hyaline Membrane Disease (HMD)

2. Meconium Aspiration Syndrome (MAS)

3. Transient Tachypnoea of the Newborn (TTNB)

4. Congenital or acquired pneumonia

5. Persistent Pulmonary Hypertension of the Newborn

(PPHN)

6. Air leaks

Cont.. 7. Congenital anomalies of upper airway (choanal

atresia), gut (tracheoesophageal fistula, congenital

diaphragmatic hernia) or lungs (lobar emphysema,

cysts)

8. Cardiac shock or Congenital Heart Disease (CHD).

9. Haematological causes (severe anaemia,

polycythaemia)

10. Neurological ( seizures )

11. Metabolic causes- metabolic acidosis

Clinical Examination Clues to the likely aetiology on examination of the

neonate : 1. A preterm baby weighing <1500 gms with retractions and grunt is likely to have HMD.2. A term baby born through meconium stained amniotic fluid with an increase in the anteriorposterior diameter of the chest (full chest) is likely to be suffering from MAS.3. A depressed baby with poor circulation is likely to have neonatal sepsis with or without congenital pneumonia.4. A near term baby with no risk factors and mild distress may have TTNB.5. An asphyxiated baby may have PPHN.

Cont..

6. A growth retarded baby with a plethoric look may have polycythaemia.7. A baby with respiratory distress should be checked for an air leak by placing a cold light source over the chest wall in a darkened room.8. A baby presenting with tachypnoea and a cardiac murmur may have a congenital heart disease.9. Inability to pass catheter through the nostril of a term baby is suggestive of choanal atresia.

Cont..

For babies presenting later with distress ask for :

a) Is the distress associated with feed refusal and lethargy? (sepsis, pneumonia)

b) Is there a family history of early neonatal deaths?

(CHD).

Respiratory Distress Syndrome (RDS)Synonym: hyaline membrane disease

• Caused by the inadequate production of surfactant in the lungs. • produced by type II pneumocytes (reduce surface tension). • surfactant is produced after 30 weeks gestation.• Inadequate surfactant production causes air sacs to collapse

on expiration and greatly increases the energy required for breathing.

• The development of interstitial oedema makes the lung less compliant. This leads to hypoxia and retention of carbon dioxide.

• Right-to-left shunting occurs: - - in collapsed lung (intrapulmonary) or, - if pulmonary hypertension is severe, across the ductus arteries

and the foramen ovale (extrapulmonary).

Risk factors

• Premature delivery • Infants delivered via caesarian section

without maternal labour. • Hypothermia • Perinatal asphyxia • Multiple pregnancy • Family history of RD

Clinical features . Usually preterm delivery.

- tachypnoea,

- expiratory grunting,

- subcostal and intercostal retractions

- diminished breath sounds,

- cyanosis and

- nasal flaring.

• May rapidly progress to fatigue, apnoea and hypoxia

Investigations • Blood gases: respiratory and metabolic acidosis

along with hypoxia. • Pulse oximetry should be maintained at 90-95%. • Chest x-ray (ground glass opacity )• Monitor full blood count, electrolytes, renal and liver

function • Echocardiogram • diagnosing PDA• determine the direction and degree of shunting, • Cultures to rule out sepsis

Respiratory Distress Syndrome

(RDS)

Also known as Hyaline Membrane Disease

(HMD)

Occurrence

• 1-2% of all births

• 10% of all premature births– Greatest occurrence is in the premature and

low birth weight infant

Etiology & Predisposing Factors

• Prematurity– Immature lung architecture and surfactant

deficiency

• Fetal asphyxia & hypoxia• Maternal diabetes

– Increased chance of premature birth– Possible periods of reflex hypoglycemia in the

fetus causing impaired surfactant production

The cycle continues until surfactant levels are adequate

to stabilize the lung• Symptoms usually appear 2-6 hours

after birth– Why not immediately?

• Disease peaks at 48-72 hours

• Recovery usually occurs 5-7 days after birth

Clinical findings: Physical

• Tachypnea (60 BPM or >)

• Retractions• Nasal flaring• Expiratory grunting

– Helps generate autoPEEP

• Decreased breath sounds with crackles

• Cyanosis on room air• Hypothermia• Hypotension

Clinical Findings: Lab

• ABGs: initially respiratory alkalosis and hypoxemia that progresses to profound hypoxemia and combined acidosis

• Increased Bilirubin

• Hypoglycemia

• Possibly decreased hematocrit

CXR: Normal

RDS CXR: Ground Glass Effect

RDS CXR: Air Bronchograms & Hilar Densities

Time constant is decreased since elastic resistance is so

highIncreased elastic resistance

means decreased compliance!

RDS Treatment: Primarily supportive until lung stabilizes

• Maintain perfusion, maintain ventilation and oxygenation

• O2 therapy, CPAP or mechanical ventilation– May require inverse I:E ratios if oxygenation

can not be achieved with normal I:E ratio

• Surfactant instillation!!!– May cause a sudden drop in elastic

resistance!

Prognosis/Complications

Prognosis is good once infant makes it past the peak (48-72 hours)

Complications possible are:

• Intracranial Bleed

• BPD (Bronchopulmonary Dysplasia)

• PDA (Patent Ductus Arteriosus)

Meconium Aspiration Syndrome

-MAS-

Syndrome of respiratory distress that occurs when meconium is aspirated prior to or during birth

Occurrence

• 10-20% of ALL births show meconium staining– 10-50% of stained babies may be

symptomatic

• More common in term and post-term babies

Etiology & Predisposing Factors

• Intra-uterine hypoxic or asphyxic episode

• Post-term

• Cord compression

Pathophysiology: Check Valve Effect

Causes gas trapping (obstruction)

If complete obstruction, then eventually atelectasis occurs

Irritating to airways, so edema and bronchospasm

Good culture ground for bacteria, so pneumonia

possible

Pathophysiology (cont.)

• V/Q mismatch leads to hypoxia and acidosis which increases PVR

• TC increases because it increases airway resistance

• Meconium is usually absorbed in 24-48 hours; there are still many possible complications

Clinical Signs

• Respiratory depression or distress at birth

• Hyperinflation• Pallor• Meconium stained

body

• Possible cyanosis on room air

• Moist crackles• ABGs – hypoxemia with

combined acidosis• CXR – coarse, patchy

infiltrates with areas of atelectasis and areas of hyperinflation– May see flattened

diaphragms if obstruction is severe

Management• Surfactant replacement therapy (endotracheal

tube).

• Oxygen: infants with mild RDS.

• Continuous positive airway pressure (CPAP).

• CPAP may be administered via an endotracheal tube, nasal prongs, or nasopharyngeal tubes.

• Assisted ventilation at fast rates (more than 40 breaths per minute)

Supportive therapy includes the following : .

. Temperature regulation:

prevent hypothermia. • Fluids, metabolism, and nutrition:

monitor and maintain blood glucose, electrolytes, acid balance, renal function, and hydration.

• Once the infant is stable, intravenous nutrition with amino acids and lipid.

• After the respiratory status is stable, initiate small volume gastric feeds (preferably breast milk) via a tube to initially stimulate gut development.

Cont..

• Circulation and anaemia: monitor heart rate, peripheral perfusion, and blood

pressure. Blood or volume expanders may be required. • Antibiotics: start antibiotics in all infants who present with

respiratory distress at birth after obtaining blood cultures. Discontinue antibiotics after three to five days if blood cultures are negative.

• Support of parents and family: keep the parents well informed. Encourage parents to

frequently visit and stay with their baby.

Treatment schedule

• Inj. Betamethasone 12 mg IM every 24 hours , 2 doses

• Inj. Dexamethasone 6 mg IM every 12hours , 4 doses

Timing of effect :

• Opitimal effect occurs after 24 hours of initiating treatment

• Effect of one course lasts for 7 days.

Prevention

• Antenatal corticosteroids (dexamethasone) accelerate foetal surfactant production and lung maturation. They have been shown to reduce respiratory distress syndrome, intraventricular haemorrhage and mortality by 40%.

• Delaying premature birth. Tocolytics, e.g.nifedipine or ritodrine, may delay delivery by 48 hours and therefore enable time for antenatal corticosteroids to be given.

• Avoid hypothermia in the neonate.

M.A.S. Treatment

Amnioinfusion – artificial amniotic fluid infused into uterus to dilute meconium

Proper resuscitation at birth(clear meconium from trachea before stimulating respiration)

Oro-gastric tubeNTEO2

NaHCO3 if severe metabolic acidosis

Broad spectrum antibioticsBronchial hygieneMay need mechanical

ventilation– Slow rates and wide I:E

ratios because of increased TC

– Low level of PEEP may help prevent check valve effect

– May need HFO

Prognosis & Complications

Good prognosis if there are no complications

Complications:Pneumonia

Pulmonary baro/volutrauma

Persistent Pulmonary Hypertension (PPHN)

CXR: Pneumothorax