UBP 3.3 (Short Form): Pediatrics – Ligation of Patent Ductus Arteriosus Flashcards
Secondary Subject -- Neonatal Circulation / Respiratory Distress of the Newborn / Neonatal Glucose Homeostasis / Retinopathy of Prematurity / Neonatal Temperature Regulation / Neonatal Seizure
Tell me about the normal closure of the ductus arteriosus.
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
- *Watch UBP “Pre-Op” online lecture**
- Narrow River – Explained well in Online UBP “Pre-op” 00:00 - 09:30*
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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.
- Clinical Notes:*
- Illustration of a patent ductus arteriosus: (see attached figure).
What is the most likely reason it didn’t close in this case?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
- Narrow River*
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In this case, this neonate’s ductus arteriosus has most 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, because their ductus arteriosus is comprised of a poorly contractile muscular layer, making it less responsive to increasing oxygen levels and other endogenous mediators (e.g. bradykinin).
“Pre-Op” 11:25 – What are predisposing factors?
Predisposing factors to PDA include –
- prematurity,
- respiratory distress syndrome (RDS),
- hypoxia,
- acidosis, and
- excessive fluid therapy.
“Pre-Op” 11:52 – How diagnose PDA?
What is respiratory distress syndrome of the newborn (RDS)?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
Neonatal respiratory distress syndrome is a condition that commonly occurs shortly after delivery in premature infants secondary to insufficient surfactant production
(production is usually inadequate prior to 35 weeks gestation).
Insufficient surfactant results in widespread atelectasis following delivery, which in turn leads to intrapulmonary shunting with subsequent hypoxemia and metabolic acidosis.
Xtra Q – 14:15: How do RDS patients present? Radiographic exam? ABG?
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.
Fortunately, survival in infants who develop RDS has been greatly increased with maternal steroid administration (to increase surfactant production in utero) and neonatal exogenous surfactant administration.
- Clinical Notes:*
- ACOG recommends a single course of antenatal corticosteroids be administered to any woman between 24-34 weeks gestation who is at risk for delivery before 34 weeks. Antenatal steroids are, therefore, administered between 24 and 34 weeks.
Xtra Q 14:47: Risk factors of RDS?
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Risk factors for RDS include:
- low gestational age,
- low birth weight, and
- surgical delivery without labor.
- (Some authors mention maternal diabetes)
- The long-term consequences of RDS is the potential development of bronchopulmonary dysplasia.
Xtra Q 15:30 (16:58): How prevent RDS?
Xtra Q 17:08: How treat RDS?
Xtra Q 19:00: Anesthetic considerations for Bronchopulmonary dysplasia?
Why is this infant taking indomethacin?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
Narrow River
Locally produced and circulating prostaglandins (primarily PGI2 and PGE2) play a major role in the patency of the ductus arteriosus through smooth muscle relaxation.
Therefore, prostaglandin synthetase inhibitors, like indomethacin and ibuprofen, are often used in the medical management of PDA to encourage closure.
Side effects associated with indomethacin include – thrombocytopenia, hyponatremia, and reduced renal (renal failure), mesenteric (intestinal perforation), and cerebral blood flow.
Ibuprofen is often utilized in low birth weight premature neonates, because its efficacy is equivalent to that of indomethacin, and it has less detrimental effects on end-organ perfusion.
Xtra Q (21:37): How tx PDA?
An echocardiogram shows left atrial enlargement.
Why would a PDA result in this finding?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
Narrow River 22:30
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).
The fact that this child is experiencing left atrial enlargement would suggest that blood is shunting from left-to-right despite his initial respiratory distress (which often leads to increased pulmonary vascular resistance).
Echocardiography with Doppler studies may prove helpful in confirming the direction of flow through the PDA.
- Clinical Note:*
- 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.
Xtra Q 24:21: Wouldn’t RDS result in a right-to-left shunt?
What would be included in your pre-operative evaluation of this infant?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
Wide River
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 torn) 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 affect 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).
Would you administer any premedication?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
Narrow River 28:00
I would probably not premedicate this sick neonate with narcotics or a benzodiazepine, as sedation is unnecessary in this age group.
(below… recognized that some other practitioners give this drug:)
Atropine (0.01-0.02 mg/kg) is sometimes administered to –
- decrease secretions,
- minimize vagal reflexes resulting from laryngoscopy and/or surgical manipulation (e.g. strabismus surgery), and
- prevent bradycardia secondary to succinylcholine and/or volatile agent administration (the latter results secondary to myocardial depression).
However, since modern 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.
The urinalysis reveals 1+ glucosuria.
Does this concern you?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
Narrow River 30:28
I am concerned, as glucose homeostasis is somewhat precarious in premature infants secondary to reduced glycogen stores and immature renal function.
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 >/= 34 weeks gestation, I would be more concerned that this finding represented hyperglycemia.
What are the potential complications that you are anticipating during this procedure?
(A 5-day-old infant weighing 980 grams and born at 28 weeks gestation is scheduled for ligation of a patent ductus arteriosus (PDA). After delivery, the infant was intubated while still in the operating room secondary to respiratory distress. On day four, his respiratory condition deteriorated further with worsening hypoxia and increased CO2 retention. Auscultation of the chest revealed a systolic murmur, and a PDA was confirmed with echocardiography. Medical management failed to resolve the condition and the decision was made to surgically ligate the PDA. He is currently receiving indomethacin and being mechanically ventilated with a Fio2 of 50%.)
Wide River 31:24
Potential surgical complications associated with this procedure include:
- recurrent laryngeal nerve injury (hoarseness),
- left phrenic nerve injury (left hemidiaphragm paralysis),
- thoracic duct injury (chylothorax),
- massive blood loss (secondary to inadvertent ligation or laceration of the ductus arteriosus, aorta or pulmonary artery),
- hypertension (often occurs post-operatively following the ligation of the ductus arteriosus), and
- 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 –
- hypothermia,
- retinopathy of prematurity,
- intraventricular hemorrhage,
- postoperative apnea, and
- hypoglycemia.
Given the neonate’s cardiopulmonary status and the nature of the surgery, I would also be concerned about –
- hypoxemia (secondary to retraction on the lung or pulmonary hypertension leading to intrapulmonary and/or extrapulmonary right-to-left shunting),
- heart failure (due to cardiac ischemia, increased afterload, and/or increased left-to-right shunting), and
- hypotension (secondary to massive blood loss, anesthetic overdose (36:58), 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).