Reference & Reading: Czverinske Chapter 28 & 30 Respiratory Distress Syndrome (RDS): aka Hyaline Membrane Disease (HMD)
Etiology – underlying etiology is related to surfactant deficiency. Although immature surfactant is produced at approximately 22 weeks gestation, it is easily disrupted by hypoxemia, hypothermia, and acidosis. Mature surfactant is not affected by these stressors and lungs are considered mature.
Pathophysiology – although surfactant deficiency is the main problem with RDS, overall prematurity also contributes to the disease:
Poor gas exchange
With all these factors combined the vicious cycle of RDS presents
Decreased surfactant, lead to widespread atelectasis
Atelectasis contributes to FRC & worsening V/Q mismatch
Hypoxia & hypercapnia lead to respiratory acidosis. Metabolic acidosis is a result of O2 at the cellular level
Condition worsens and damages alveoli & capillaries = more surfactant deficiency
Combined acidosis also leads to pulmonary vasospasm, causing worsening hypoxemia
If left untreated, the conditions worsens until patient can’t compensate for the disease
Clinical signs & Diagnosis – involves manifestations of respiratory distress
Grunting – effort to FRC by partially closing glottis
CXR – ground glass appearance, air bronchograms with presence of atelectasis
Hypothermia may present
Flaccid muscle tone & general hypoactivity
Symptoms worsen at around 48 – 72 hours followed by stabilization & very slow recovery
Treatment – Ideally, prevent it before it starts
Intubation – if patient shows signs of respiratory distress
Satge IV (beyond 30 days): increase lung density, & formation of larger, irregular cysts
Prevention: reduce factors that lead to its development & perpetuation.
Mechanical Ventilation: Appropriate ETT size to prevent subglottic stenosis, tracheostomy may be recommended.
Pharmacologic agents: corticosteroids, caffine
Fluid Therapy: aim at maintaining adequate hydration & urination. Diuretics may be required.
Right Heart Failure: close PDA. May require used of digoxin and diuretics.
Nutrition: adequate nutrition required to meet increased metabolic needs. 120 – 150 cal/kg/day to achieve growth & needs of tissue repair. Watch for O2 consumption & CO2 retention
Prognosis –with changes in mechanical ventilation long-term effects are hard to examine. Some suggest that there risk for Asthma or COPD later in life.
Retinopathy of Prematurity (ROP) - literally means formation of scar behind the lens;
Etiology - there is a link between O2 use and ROP; but other factors such as retinovascular immaturity, circulatory & respiratory instability.
The developing eye: Capillaries in the eye begin to grow at 16 weeks. They grow from optic nerve towards the ora serrata – retina’s anterior end; they do not reach the entire ora serrata until 40 weeks. Premature neonate’s capillaries do not have the time to reach the ora serrata. In this population the capillaries can either develop normally or cease to grow and cause ROP
Presence of PaO2 retinal vessels constrict which leads to necrosis of vessels (vaso-obliteration).
In an attempt to reestablish blood supply to retinas, remaining vessels begin to proliferate may cause hemorrhage in liquid portion of eye.
Results in formation of scarring behind retina with traction, detachment and blindness.
Once stopped, no further damage occurs
Diagnosis – Use ophthalmologic exam of internal eye anatomy.
Placement of a reservoir is used until a peritoneal shunt is placed
Treatment – avoid factors that lead to this occurrence
Avoid wide fluctuations in oxygenation, blood pressure, and pH
Once it occurs care is more supportive
Meconium Aspiration Syndrome – predominately a disease of term/postterm neonate that experiences some form of asphyxia either before or after onset of labor
Actual aspiration of meconium occurs in about ½ of neonates born with meconium staining
Occurs with first breath, before or during delivery
Risk for postterm due to diminishing amniotic fluid levels dilute meconium; diminishes placental function, and asphyxia
Meconium is the contents of the fetal bowel – includes amniotic fluid, bile salts & acids, squamous cells, vernix, intestinal enzymes
During an asphyxia episode the fetsus’ bowel relaxes and the meconium enters the amniotic fluid
In response to asphyxia the fetus begins to gasp – meconium in the fluid may enter the oropharynx & tracheobronchial tree
Physical presence of meconium can lead to blockage of the airway
Results in a ball-valve effect; leading to air-trapping and a pneumothorax can result
Second response is an inflammatory response in the tracheobronchial tree – chemical pneumonitis; mucosal edema, lung compliance, impairment of gas exchange
Vasospasm in the pulmonary vasculature because of MAS can lead to Pesisitant Pulmonary Hypertension (PPHN) aka Persistant Fetal circulation (PFC)- blood flow follows fetal routs bypassing lungs and leading to shunt & worsening ABGs
Pulmonary infection is another problem with MAS
Diagnosis & treatment
Baby is considered meconium stained until meconium aspiration into trachea is verifies
Upon delivery of the head the OB must sxn out the mouth and oropharynx and clear meconium