Lecture 62: Dr.

Cohen, Clinical Correlations

Respiratory Distress in a Newborn

• Respiratory Distress Case #1:

– 30 wk gestation newborn in respiratory distress
– Exam reveals premature baby with no abnormalities except lung distress
• Prematurity:
– < 37 weeks gestational age (however 37-38 wks still have higher morbity rate
than if allowed to go to full term of 42 wks)
– Risk factors include low socioeconomic status, inadequate prenatal care, poor
nutrition, poor education and intercurrent or untreated illness or infection
– Complications include RDS (respiratory distress syndrome), apnea (typically
central and obstructive), IVH (interventricular hemorrhage), infections,
hypothermia, metabolic (hypercalcemic, low blood glucose, etc), GI, renal, and
hyperbilirubinemia
• RDS:
– Common cause of morbidity
– Male predominance
– Low gestational age (almost 100% at 25 wks, doesn't reach 0% until over 38
weeks)
– Maternal diabetes
– Perinatal asphyxia
– Caused by a decreased production and secretion of surfactant
– Failure to develop FRC and alveoli tend to collapse
– Surfactant synthesis depends on pH, temp and perfusion
– Hypoxia, asphyxia, hypovolemia and cold may worsen condition
– Atelectasis (collapse of alveoli) makes lungs less compliant
– Increased work of breathing
– Ventilation/Perfusion mismatches - hypoxia
• 2 Causes of RDS:
– Fetal Lung Development
 Pseudoglandular Stage (7-17 wk gestation): branching that yields fetal
lung
 Canalicular Stage (16-25 wk): pre-viable lung becomes potentially
viable, development of air-blood barrier, development of Type II cells
and beginning of surfactant production
 Saccular and Alveolar Stages (25 wks): final branching, potential
increase in lung volume for gas exchange *POTENTIAL FOR VIABLE
BABY
 Surface area and lung volume increase exponentially after 25 wks
– Surfactant
 Made by type II alveolar cells
 Made of phosphatidylcholine and SP-A, B, C and D
 SP-B is required for life
 Has polar and non-polar end
 Alveolus wants to collapse due to water surface tension however
 surfactant acts by reducing surface tension of water
 Laplace’s Law (decrease T thereby decreasing P)
 Saline lungs would eliminate air-water interface and therefore less
pressure is required
• Vicious circle
– Clinical manifestations:
 Signs occur within minutes of birth
 Tachypnea respiratory rate
• mechanical pulmonary dysfunction, acid-base imbalance, blood
gas abnormalities
• minimize work of breathing by adjusting resp. rate
• Pts w/ stiff lungs breath fast and shallow
• Pts w/ increased resistance breath slower and deeper
 Grunting
• Expiration through a partially closed vocal cord
• Produces an elevated transpulmonary pressure in the absence
of airflow
 V/Q ration is enhances b/c of increased airway pressure and lung
volume
 Intercostal and subcostal retractions
• Retractions are caused by use of accessory muscles of
respiration
• Due to decreased compliance
 Nasal flaring
• Enlargement of nostrils during inspiration to reduce resistance
(by power of 4)
• Nasal resistance contributes to airway resistance
• Poiseuille’s Law
 Cyanosis
• Fick's Law of Diffusion
• Increased membrane thickness decreases the rate of diffusion
• What do you see?
– Breath sounds may be diminished or normal; they may havea harsh quality or
fine rales or crackles
• Natural Course
– Progressive worsening or cyanosis and distress
– BP falls
– Fatigue, cyanosis and pallor increase
– Apnea and irregular resp appear
– Acidosis
– Peaks at 3 days w/ gradual improvement if infant survives
• Diagnosis
– CXR (Chest X-Ray)
 Fine reticular granularity ("ground glass appearance")
– Air bronchograms
– Lab
  Hypoxemia
 Hypercarbia (increased pCO2)
– Metabolic acidosis
• Differential Dx
– Group B strep Pneumonia
– Cyanotic Heart Disease
– Persistent Pulmonary Hypertension
– Pneumothorax
– Aspiration Pneumonia
• Treatment
– *Treat the basic defect = Prematurity
 Gentle handling and minimal disturbance
 Isolette to maintain neutral core temp and reduce O2 consumption
 IV fluids, glucose, electrolytes and nutrition
– RDS
 Warm humidified O2 should be administered to keep pO2 between 55-
70mmHg (>90% Saturation)
 Continuous positive airway pressure by nasal prongs
 Mechanical ventilation
 Antibiotics
 Exogenous surfactant administration
• Has improved survival, increased compliance and reduced vent
pressures
• Has not reduced incidence of chronic lung disease and has
complications
– Complication includes pneumothorax
– Inadequate exchange of O2 and CO2
– Treat secondary manifestations such as circulatory insufficiency and metabolic
acidosis
– Careful monitoring of heart rate, respiratory rate, BP, fluids and electrolytes
• Prognosis
– Mortality from RDS has decreased to about 10%