Book 3, Case 3-PDA Flashcards
Tell me about normal closure of ductus arteriosus:
What decreases to aid in its closure?
With the initiation of ventilation, arterial oxygen levels are increased
and pulmonary vascular resistance is reduced. The decrease in pulmonary vascular
resistance leads to a reversal of flow through the ductus arteriosus, thereby exposing
the ductus to systemic blood with a relatively higher oxygen concentration. This
exposure to increased oxygen levels in combination with the rapid decrease in
circulating prostaglandins (primarily prostaglandin E2) that occurs following placental
separation results in the functional closure of the ductus within 2-4 days of birth.
Permanent closure ( ductal fibrosis) occurs over several weeks, leaving a residual band
of tissue called the ligamentum arteriosum.
Baby is 28 weeks old and i didn’t close-why not? Baby born hypoxic
likely remained
patent due to a combination of hypoxia (baby was in respiratory distress) and the
thinner, less responsive muscular layer in the ductus of premature neonates. In the
setting of hypoxia, the normal increase in arterial oxygen concentration that occurs
following delivery is diminished or absent, thereby blunting one of the primary
stimulants of ductal closure. This is even more of a problem for premature neonates,
Pre-disposing factors to PDA
prematurity, respiratory distress syndrome (RDS), hypoxia, acidosis, and excessive fluid therapy.
What is RDS of the newborn? What does it lead to?
Respiratory distress syndrome.commonly
occurs shortly after delivery in premature infants secondary to insufficient surfactant
production (production is usually inadequate prior to 35 weeks gestation).
What does RDS lead to? How do these infants present? What would you see on imaging? CXR?
Insufficient surfactant results in widespread atelectasis following delivery, which in
turn leads to intrapulmonary shunting with subsequent hypoxemia and metabolic
acidosis. The infant with RDS typically exhibits tachypnea, tachycardia, nasal
flaring, intercostal and subcostal retractions, bilateral rales (that fail to clear with
suctioning), and cyanosis. Radiographic examination reveals diffuse, “ground glass”
bilateral infiltrates and reduced lung volumes (secondary to atelectasis ), while an
ABG shows hypoxemia, metabolic acidosis, and respiratory alkalosis.
What are risk factors for RDS?
(1) low gestational age, (2) low birth weight, and
(3) surgical delivery without labor.
Who does ACOG say should have corticosteroids as far as preggo goes?
Any woman after 24 weeks gestation who is at risk for delivery before 34 weeks.
Why do babies need indomethacin to help with PDA? Ibuprofen vs. indomethacin
prostaglandins keep it open. indomethacin (progstaglandin synthetase inhibitors) blockds that and ends the PDA. Ibuprofen used in low birth weight premie neonates due to less effects on end organ perfusion
An echocardiogram shows left atrial enlargement: Why would a PDA result in
this finding?
Neonates with a PDA may develop left atrial enlargement because the
PDA allows shunting of blood from the systemic to the pulmonary circulation. When
the shunt is large, the blood flow to the lungs can be 3-4 times normal, resulting in
volume overload of the left heart and pulmonary vasculature (potentially leading to
left heart and respiratory failure). Volume overloading may then lead to left atrial
dilation and left ventricular hypertrophy. If the condition is left untreated, pulmonary
vascular overload leads to irreversible pulmonary hypertension, right heart failure,
and a reversal of the left-to-right shunt to a right-to-left shunt (Eisenmenger’s
syndrome).
How is the direction of flow through PDA determined?
The direction of flow through the PDA is determined by the difference in pressure
between the pulmonary and systemic vasculature, and by the length and diameter
of the ductus arteriosus.
How would you evaluate the PDA pt pre-operatively?
why would you check serum electrolyte levels?
I would begin by reviewing the chart and having a discussion with the
neonatologist to determine the maternal drug history, the infant’s treatment course,
and the infant’s current respiratory, cardiovascular, and fluid status (e.g. blood
pressures, ABG results, ventilator settings, and oxygen requirements). Next, I would
perform a careful physical exam focusing on the airway, fluid status, and the
cardiopulmonary system. Finally, I would type and cross the patient (blood loss is
usually minimal, but could be massive if a major blood vessel, such as the aorta,
pulmonary artery, or ductus, is tom) and review or order a chest x-ray (to identify any
pulmonary edema or cardiac dilation), ABG (to identify any metabolic or respiratory
acidosis), urinalysis (indomethacin can effect renal function), H/H (potential for
major blood loss), and serum electrolyte levels (indomethacin can cause
hyponatremia, the neonate’s small intravascular volume places them at increased risk
for electrolyte disturbances)
Standard PdA: you giving any pre-meds?
Atropine (0.01-0.02
mg/kg) is sometimes administered to (1) decrease secretions, (2) minimize vagal
reflexes resulting from laryngoscopy and/or surgical manipulation (e.g. strabismus
surgery), and (3) prevent bradycardia secondary to succinylcholine and/or volatile
agent administration (the latter results secondary to myocardial depression).
However, since modem volatile agents are not associated with significant bradycardia
and because timing the anticholinergic effects with induction is often difficult, I
would not administer it as a premedication in this case. I would, instead, have this
drug available at induction and administer it if necessary.
UA in this PDA pt shows 1+ glucosuria-you concerned?
However, glucosuria is not uncommon in preterm infants less than 34 weeks gestation -
due to reduced renal tubular reabsorption of glucose. If the infant were 2: 34 weeks
gestation, I would be more concerned that this finding represented hyperglycemia.
Anticipated complications during PDA procedure?
(1) recurrent laryngeal nerve injury (hoarseness), (2) left phrenic nerve injury
(left hemidiaphragm paralysis), (3) thoracic duct injury ( chylothorax), ( 4) massive
blood loss (secondary to inadvertent ligation or laceration of the ductus arteriosus,
aorta or pulmonary artery), (5) hypertension (often occurs post-operatively following
the ligation of the ductus arteriosus ), and ( 6) reopening of the ductus (a rare event that
may occur when the ductus is ligated without division). The baby’s prematurity and
extremely low birth weight, place him at increased risk for (7) hypothermia, (8)
retinopathy of prematurity, (9) intraventricular hemorrhage, (10) postoperative apnea,
and (11) hypoglycemia. Given the neonate’s cardiopulmonary status and the nature
of the surgery, I would also be concerned about (12) hypoxemia (secondary to
retraction on the lung or pulmonary hypertension leading to intrapulmonary and/or
extrapulmonary right-to-left shunting), (13) heart failure (due to cardiac ischemia,
increased after load, and/or increased left-to-right shunting), and (14) hypotension
(secondary to massive blood loss, anesthetic overdose, vagal reflex in response to
surgical manipulation of the vagus nerve or lung tissue, heart failure, and/or
compression of the heart or great vessels).
Monitoring for PDA:
Which monitors are you placing? Where should BP be monitored and why? Where should O2 sat be monitored and why?
Standard monitors-TEMP too
precordial/adn or esophageal stethoscope to aid in monitoring of cardiopulmonary
status-dont think i would say thsi becasue i dont’ know how to use it
Blood pressure
should be monitored in the right arm (preductal) since clamping of the left subclavian
artery may become necessary should the ductus be tom causing massive bleeding.
Oxygen saturation should be monitored on the right hand and a lower limb to provide
pre-ductal and post-ductal readings respectively. While invasive blood pressure
monitoring and a CVP line would be helpful if already present, I would not routinely
require them for this procedure.
