Respiratory Distress Syndromes:
Hyaline membrane dz (Neonatal Resp distress syndrome)
If something has a lot of pink in it, what is it? Hyaline
Key to understanding this dz is massive atelectasis
1. What is atelectasis? Collapse of airways. Why did these airway collapse? No surfactant (aka
lecithin/phosphotidyl choline/phosphotidyl glycerol – they are all surfactant). So, deficient of
surfactant causes atelectasis b/c:
Collapsing pressure in the airways = surface tension/radius of airway. So, on expiration,
normally the airway will be smaller b/c there is a pos intrathoracic pressure. If you decrease the
radius, you will increase the collapsing pressure in the airways. Therefore, on expiration (in all
of us), we have to decrease surface tension (which is what surfactant does) – by doing this, it
keeps the airways open on expiration, preventing atelectasis.
Three causes of RDS:
a. Prematurity: surfactant begins syn early, but it peaks at 32-35 week, so if you are born
prematurely, you will not have enough surfactant, and baby will develop increased risk
of developing RDS. Sometimes mother has no choice and must deliver baby, or else it
will die, and there is something you can do to the mom so the baby has more surfactant:
give mother glucocorticoids b/c they stimulate surfactant synthesis. Example: what can
you do to increase surfactant (but glucocorticoids wasn’t one of the answer choices) –
thyroxine (thyroid hormone) (as does prolactin); does that mean you give thyroxine b4
delivering the baby? No, will give mom and baby hyperthyroidism.
b. Diabetes: gestational diabetes = woman who wasn’t pregnant, becomes pregnant, and
then obtains glucose intolerance after delivery – so if a diabetic gets pregnant, this is not
called gestational diabetes, but a diabetic that got pregnant. Its imp that a woman in
pregnancy has good glucose control b/c if she is hyperglycemic, baby will be, too. B/c
baby is hyperglycemic, it will stimulate insulin synthesis, and insulin has a negative
effect on surfactant syn and will decrease its synthesis.
c. C section – b/c the baby is not delivered vaginally, there is no stress. B/c the baby has
not been stressed, the ACTH and cortisol are not released, and surfactant is not made.
Whereas a child that is delivered vaginally has a lot of stress and therefore a lot of ACTH
and cortisol is being released, which stimulates surfactant release. So, C section
predisposes to RDS.
So, these are the three main causes (prematurity, diabetes, and C section).
Complications and associated conditions:
a. Example: why are the babies of poor glycemic control big (macrosomial)? The baby’s
insulin is increased to keep the glucose down. Insulin will increase storage of triglyceride in
adipose (it increases fat storage). Where is most of the adipose located? Centrally. So, one
of the reasons why they have macrosomia is b/c insulin stimulates synthesis of TG and
deposition of fat. Also, insulin increases uptake of aa’s in muscle (like growth hormone). So,
it will increase muscle mass. So, the reason for macrosomia is increased adipose and muscle mass, both due to insulin. This also explains why they get hypoglycemia when they
are born. The mother’s hyperglycemia is coming into the baby, causing the baby to release
insulin; the moment insulin is made and the cord is cut, and no more increase in glucose,
glucose goes down, and leads to hypoglycemia.
b. Superoxide free radical damage seen in retinopathy of prematurity and blindness and
c. Why do babies with RDS commonly have PDA? B/c they have hypoxemia. When a normal
baby takes a breath, it starts the process of functional closure of the ductus. However, with
hypoxemia after they are born, it remains open, and they have a machinery murmur.
d. Hyaline membranes are due to degeneration of type II pneumocytes and leakage of
fibrinogen, and it congeals to form the membrane. So, they will give a classic history for
RDS, and then will ask for the pathogenesis of hypoxemia in the baby. This is a massive
ventilation defect b/c everything is collapsing. This is a SHUNT problem, which leads to a
massive interpulmonary shunt. Rx=PEEP therapy – positive end exp pressure b/c these
airways are collapsed and you need to get O2 into them and surfactant. So, give O2 and at
the end of exp