Patent Ductus Arteriosus and Prematurity
David Stein
Fun-Sun F. Yao
A 2-week-old male infant weighing 900 g was scheduled for ligation of patent ductus arteriosus (PDA). He was born at 27 weeks’ gestation as part of a triplet pregnancy complicated by preterm labor. Immediately after delivery, he was intubated because of respiratory distress. He was given indomethacin prophylactically because of his prematurity and presumed PDA. A transthoracic echocardiogram (TTE) confirmed the patency of the ductus arteriosus and demonstrated its closure after one course of indomethacin. His respiratory function was gradually improving with ventilatory support until 2 weeks later when his oxygenation and ventilation suddenly worsened. A murmur was heard over his chest. A repeat TTE demonstrated left-to-right shunting through the ductus arteriosus. Another course of indomethacin was administered, but the ductus remained patent. His blood pressure was 50/20 mm Hg; heart rate, 165 beats per minute. The laboratory data were as follows: white blood cell (WBC) count, 17,000 per µL; hemoglobin, 11 g per dL; hematocrit, 34%; urine specific gravity, 1.005; protein, 1+; sugar, 1+; serum calcium, 6.0 mg per dL; blood glucose, 60 mg per dL; arterial blood gases: pH, 7.30; PaCO2, 60 mm Hg; PaO2, 49 mm Hg on FIO2 50%, inspiratory pressure, 19/6 cm H2O; and ventilation rate, 40 breaths per minute.
A. Medical Disease and Differential Diagnosis
How would you classify prematurity? What are the common problems associated with prematurity?
What are the survival rates of preterm infants?
What are the incidence and survival rates of respiratory distress syndrome (RDS)? Discuss its pathophysiology.
What is bronchopulmonary dysplasia (BPD)? How would you treat it?
What are apnea spells? What are the possible causes of apneic spells?
Discuss the incidence and pathophysiology of PDA in preterm infants.
How would you make a diagnosis of PDA? Describe its treatment.
Would you give digitalis to treat congestive heart failure in preterm infants? Why?
How does indomethacin close the ductus? What are the adverse effects of indomethacin?
What is retinopathy of prematurity (ROP) (retrolental fibroplasia [RLF])? Discuss its etiology, pathophysiology, prognosis, and prevention.
Define neutral and critical temperatures. What are these values in the preterm neonate, in the term neonate, and in the adult? Discuss temperature regulation in the neonate.
B. Preoperative Evaluation and Preparation
How would you evaluate this patient preoperatively?
What are the normal values of arterial blood gases and pH in preterm and term pediatric patients?
Interpret the arterial blood gases: pH, 7.30; PaCO2, 60 mm Hg; PaO2, 49 mm Hg;
, 20 mEq per L on 50% oxygen; and 6 cm H2O of positive end-expiratory pressure (PEEP). How would you improve them?
What are the normal values of arterial blood pressure, heart rate, and respiratory rate for preterm infants?
What are the normal values of WBC, red blood cells (RBCs), hemoglobin, glucose, electrolytes, calcium, blood urea nitrogen, and creatinine for preterm infants?
Would you transfuse blood to this patient preoperatively?
How would you interpret the urinalysis: specific gravity, 1.005; sugar, 1+; and protein, 1+?
Would you correct a serum calcium level of 6.0 mg per dL? What other information would you like to have? Which contains more calcium, 10 mL of 10% calcium chloride or 10 mL of 10% calcium gluconate? Could you hyperventilate this child safely?
How would you premedicate this patient?
C. Intraoperative Management
What monitors would you use for this child during surgery?
How does the oxygen analyzer work?
What is the Doppler effect? How does the Doppler transducer measure blood pressure?
What is the mechanism of pulse oximetry? Why is it important to monitor arterial oxygen saturation? What levels of arterial oxygen saturation would you like to keep during surgery?
How would you maintain the patient’s body temperature?
How do the anesthetic requirements of the preterm infant differ from those of the adult?
What size endotracheal tube would you have used if the patient had not been intubated?
How would you have induced anesthesia if the patient had not been intubated?
How would you maintain anesthesia?
How would you ventilate the patient? What tidal volume, respiratory rates, and FIO2 would you set for the infant?
Discuss blood and fluid therapy in this preterm infant.
During dissection of the ductus arteriosus, the arterial oxygen saturation dropped from 92% to 80% and the heart rate decreased from 140 beats per minute to 80 beats per minute. What were the causes? How would you correct this situation?
D. Postoperative Management
Would you reverse the muscle relaxants and extubate the patient at the end of surgery?
How can one minimize the risk of transporting the patient to the neonatal intensive care unit (ICU) after surgery?
The patient’s condition deteriorated postoperatively in the ICU. Physical examination revealed persistent cardiac murmur. What was the possible diagnosis?
A. Medical Disease and Differential Diagnosis
A.1. How would you classify prematurity? What are the common problems associated with prematurity?
Live born infants delivered before 37 weeks from the first day of the last menstrual period are termed premature by the World Health Organization. Preterm infants can be classified into three groups, as shown in Table 44.1. Infants of borderline prematurity usually require no special care, but, because of their susceptibility to RDS, they should be observed closely
for 24 to 48 hours in the newborn nursery. Further, those with a poor suck reflex may require gavage feedings. Infants classified as moderately premature require intense neonatal care, and neonatal mortality correlates inversely with gestational age. Neonates of extreme prematurity constitute only 1% of all preterm infants; however, mortality in this group is extremely high, accounting for greater than 70% of all neonatal deaths. Furthermore, morbidity in surviving infants is substantial, often secondary to irreversible neurologic or respiratory insult.
for 24 to 48 hours in the newborn nursery. Further, those with a poor suck reflex may require gavage feedings. Infants classified as moderately premature require intense neonatal care, and neonatal mortality correlates inversely with gestational age. Neonates of extreme prematurity constitute only 1% of all preterm infants; however, mortality in this group is extremely high, accounting for greater than 70% of all neonatal deaths. Furthermore, morbidity in surviving infants is substantial, often secondary to irreversible neurologic or respiratory insult.
TABLE 44.1 Classification of Prematurity | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Coté C, Lerman J, Anderson B. Coté and Lerman’s A Practice of Anesthesia in Infants and Children. 5th ed. Philadelphia, PA: Saunders/Elsevier; 2013:733.
Gregory GA, Andropoulos DB, eds. Gregory’s Pediatric Anesthesia. 5th ed. West Sussex, United Kingdom: Wiley-Blackwell; 2012:475-476.
Kliegman RM, Stanton BF, St Geme JW, et al, eds. Nelson Textbook of Pediatrics. 20th ed. Philadelphia, PA: WB Saunders; 2015:818.e1-831.e1.
A.2. What are the survival rates of preterm infants?
The survival rates of preterm infants depend mainly on their maturity or birth weights. Because of the advancement in neonatal care, survival rates have increased twofold in the last two decades. Recently, the survival rates for infants with birth weights 500 to 750 g, 750 to 1,000 g, 1,000 to 1,250 g, 1,250 to 1,500 g, and 1,500 to 2,000 g have been approximately 53.9%, 86.3%, 94%, 96.8%, and 97%, respectively. Recent reports showed the survival rates for premature infants born at 24, 25, and 26 weeks’ gestation to be 43%, 74%, and 83%, respectively.
Kliegman RM, Stanton BF, St Geme JW, et al, eds. Nelson Textbook of Pediatrics. 20th ed. Philadelphia, PA: WB Saunders; 2015:819.
Lemons JA, Bauer CR, Oh W, et al; for the NICHD Neonatal Research Network. Very low birth weight outcomes of the National Institute of Child Health and Human Development Neonatal Research Network, January 1995 through December 1996. Pediatrics. 2001;107:E1.
A.3. What are the incidence and survival rates of respiratory distress syndrome (RDS)? Discuss its pathophysiology.
RDS, formerly called hyaline membrane disease, is common in preterm infants. RDS is a life-threatening condition associated with 50% to 75% of all deaths of premature infants. It occurs three times more often in those born by cesarean section than in those born vaginally. The incidence of RDS depends on the birth weight. It happens in 86% of preterm infants
weighing 501 to 750 g; 79% of preterm infants weighing 751 to 1,000 g; 48% of preterm infants weighing 1,001 to 1,250 g; and 27% of preterm infants weighing 1,251 to 1,500 g.
weighing 501 to 750 g; 79% of preterm infants weighing 751 to 1,000 g; 48% of preterm infants weighing 1,001 to 1,250 g; and 27% of preterm infants weighing 1,251 to 1,500 g.
The survival rate has increased dramatically over the last 50 years. Survival depends on the infant’s size. Ninety percent of those weighing 900 to 1,000 g survive, whereas approximately 70% of those weighing 500 to 700 g survive. Recently, an increase in survival and a decrease in severity of RDS have been associated with maternal steroid administration and routine administration of exogenous surfactant into the lungs of neonates of less than 28 weeks’ gestation at birth. This may pose a problem for the anesthesiologist if these patients require surgery. Ventilation with high positive pressures and large volumes increases the likelihood of pulmonary gas leaks, pneumothorax, and lung injury.
Physical examination of the infant with RDS will likely reveal cyanosis, tachypnea, intercostal retractions, and bilateral rales that fail to clear with suctioning. An arterial blood gas sample will demonstrate hypoxemia, metabolic acidosis, and respiratory alkalosis; a chest radiograph will show diffuse, hazy (“ground glass”) infiltrates.
Deficiency of the alveolar phospholipid surfactant is thought to be the cause of RDS. The surfactant is produced by the type II alveolar cells and is necessary for the maintenance of alveolar stability. Surfactant production is usually inadequate before 35 weeks of gestational age. In its absence, alveolar collapse and a decrease in functional residual capacity (FRC) occur, with consequent right-to-left shunting, arterial hypoxemia, and metabolic acidosis. Administration of betamethasone to women 48 hours before the delivery of fetuses less than 34-week gestation significantly reduces the incidence, mortality, and morbidity of RDS.
Andropoulos D, Stayer S, Russell I, et al, eds. Anesthesia for Congenital Heart Disease. 2nd ed. West Sussex, United Kingdom: Wiley-Blackwell; 2010:374.
Gregory GA, Andropoulos DB, eds. Gregory’s Pediatric Anesthesia. 5th ed. West Sussex, United Kingdom: Wiley-Blackwell; 2012:477-478.
Hines RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-existing Disease. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:589-590.
Kliegman RM, Stanton BF, St Geme JW, et al, eds. Nelson Textbook of Pediatrics. 20th ed. Philadelphia, PA: WB Saunders; 2015:848.e2-867.e2.
A.4. What is bronchopulmonary dysplasia (BPD)? How would you treat it?
BPD is defined as oxygen dependence at 36 weeks’ postconceptual age with oxygen requirements to maintain PaO2 >50 mm Hg beyond 28 days of life in infants with birth weight less than 1,500 g. BPD is a chronic lung disease as a result of mechanical ventilation, oxygen toxicity, infection, or a combination of these factors. It includes interstitial fibrosis, lobar emphysema, and components of reactive airway disease, and may render the baby oxygen, steroid, or ventilator dependent. With progressive disease, it may lead to pulmonary hypertension and right heart failure. It usually progresses through four stages:
Stage I: At 2 to 3 days of age, the chest radiograph shows classic RDS. There are atelectasis, hyaline membrane, hyperemia, lymphatic dilation, metaplasia, and necrosis of bronchiolar mucosa.
Stage II: At 4 to 10 days of age, the chest radiograph shows obscure cardiac borders and nearly complete opacification of lung fields. The pathology reveals necrosis and repair of epithelium, persisting hyaline membrane, emphysematous coalescence of alveoli, and thickening of alveolar and capillary membranes.
Stage III: At 10 to 20 days of age, the chest radiograph shows small rounded areas of spongelike radiolucency. There are few hyaline membranes, regeneration of clear cells, bronchiolar metaplasia, mucus secretion, emphysematous alveoli, and focal thickening of basement membrane.
Stage IV: After 30 days of age, the radiolucent areas seen in stage III enlarge and alternate with thin strands of radiodensity. The pathology reveals emphysematous alveoli and marked hypertrophy of epithelium.
BPD causes maldistribution of ventilation and perfusion, resulting in hypoxemia and hypercarbia. The treatment is supportive. The goals of treatment are to minimize the FIO2 and
mean airway pressure, reduce the amount of lung water with diuretics (furosemide 5 to 10 mg per kg every 6 hours), and support cardiac contractility with inotropes.
mean airway pressure, reduce the amount of lung water with diuretics (furosemide 5 to 10 mg per kg every 6 hours), and support cardiac contractility with inotropes.
Andropoulos D, Stayer S, Russell I, et al, eds. Anesthesia for Congenital Heart Disease. 2nd ed. West Sussex, United Kingdom: Wiley-Blackwell; 2010:253.
Gregory GA, Andropoulos DB, eds. Gregory’s Pediatric Anesthesia. 5th ed. West Sussex, United Kingdom: Wiley-Blackwell; 2012:478.
Hines RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-existing Disease. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:590-591.
Kliegman RM, Stanton BF, St Geme JW, et al, eds. Nelson Textbook of Pediatrics. 20th ed. Philadelphia, PA: WB Saunders; 2015:848.e2-867.e2.
A.5. What are apnea spells? What are the possible causes of apneic spells?
Apnea spells are defined as cessation of breathing lasting more than 20 seconds or more than 10 seconds and produces oxygen desaturation and bradycardia. Apneic spells are common in preterm infants, especially after the first week of life and almost universal in infants who are less than 1,000 g at birth. The causes are multiple and include the following:
Hypothermia or hyperthermia
Hypoglycemia or hyperglycemia
Hypocalcemia or hypercalcemia
Hypovolemia or hypervolemia
Anemia
Decreased FRC
PDA
Constipation
Hypothyroidism
Immature brainstem function
Lack of type I muscle fibers in diaphragm
Excessive handling
Sepsis
Gastroesophageal reflux disease
Repeated apnea increases the likelihood of central nervous system damage because of repeated episodes of hypoxemia. Infants who have apneic spells do not breathe during anesthesia; therefore, they should be ventilated throughout anesthesia, including the induction phase. Inhaled and intravenous anesthetics affect the control of breathing and contribute to upper airway obstruction, thereby increasing the likelihood of apnea during the postoperative period, especially in preterm infants less than 60 weeks postconception age.
Coté C, Lerman J, Anderson B. Coté and Lerman’s A Practice of Anesthesia in Infants and Children. 5th ed. Philadelphia, PA: Saunders/Elsevier; 2013:734-735.
Finer NN, Higgins R, Kattwinkel, et al. Summary proceedings from the apnea-of-prematurity group. Pediatrics. 2006;117:47-51.
Gregory GA, Andropoulos DB, eds. Gregory’s Pediatric Anesthesia. 5th ed. West Sussex, United Kingdom: Wiley-Blackwell; 2012:478-479.
A.6. Discuss the incidence and pathophysiology of PDA in preterm infants.
Fifty percent of infants weighing less than 1,000 g and 20.2% of infants under 1,750 g have hemodynamically significant PDA. In term infants, the ductus arteriosus closes soon after birth in response to the increased arterial oxygen tension. However, in preterm infants, it has a thinner, poorly contractile muscular layer with diminished responsiveness to the increasing oxygen levels after birth. In addition, preterm infants often suffer from hypoxemia because of RDS, so that there are both a reduced stimulus to and a reduced response to physiologic closure. As many as 20% of neonates with RDS have a PDA. However, on the third to fifth day of life, some resolution of the RDS usually occurs, with a concurrent decrease in pulmonary
resistance. This allows blood shunting from the systemic to the pulmonary circulation by way of the PDA, resulting in pulmonary vascular overload and ultimately left heart failure. The pulmonary congestion worsens respiratory failure, resulting in further hypoxemia and CO2 retention.
resistance. This allows blood shunting from the systemic to the pulmonary circulation by way of the PDA, resulting in pulmonary vascular overload and ultimately left heart failure. The pulmonary congestion worsens respiratory failure, resulting in further hypoxemia and CO2 retention.
Andropoulos DN, Stayer SA, Russell IA, et al, eds. Anesthesia for Congenital Heart Disease. 2nd ed. West Sussex, United Kingdom: Wiley-Blackwell; 2010:253.
Coté C, Lerman J, Anderson B. Coté and Lerman’s A Practice of Anesthesia in Infants and Children. 5th ed. Philadelphia, PA: Saunders/Elsevier; 2013:742-743.
A.7. How would you make a diagnosis of PDA? Describe its treatment.
The diagnosis of PDA in preterm infants may be suspected when there is sudden increase in respiratory failure, tachycardia, tachypnea, and a widened pulse pressure. The typical continuous or machinery murmur of PDA is usually not present in this population, but a systolic murmur, sometimes extending into diastole, and a hyperdynamic precordium are nearly always present. The diagnosis is confirmed by echocardiography that demonstrates left atrial enlargement. Two-dimensional echocardiography can identify the aortic end of the ductus. Continuous-wave Doppler can detect abnormal flow in the pulmonary artery. Color Doppler can visualize the jet of abnormal flow.
The initial treatment of PDA is medical. It includes fluid restriction and administration of diuretics and indomethacin. Indomethacin, 0.1 to 0.2 mg per kg, three doses for every 12 hours, usually closes the ductus within 24 hours. If the ductus fails to close with medical treatment, surgical ligation is indicated. There is now the option of percutaneous closure of PDA with an AMPLATZER Duct Occluder.
Andropoulos D, Stayer S, Russell I, et al, eds. Anesthesia for Congenital Heart Disease. 2nd ed. West Sussex, United Kingdom: Wiley-Blackwell; 2010:374.
Coté C, Lerman J, Anderson B. Coté and Lerman’s A Practice of Anesthesia in Infants and Children. 5th ed. Philadelphia, PA: Saunders/Elsevier; 2013:742-743.
Gregory GA, Andropoulos DB, eds. Gregory’s Pediatric Anesthesia. 5th ed. West Sussex, United Kingdom: Wiley-Blackwell; 2012:479.
Pass RH, Hijazi Z, Hsu DT, et al. Multicenter USA Amplatzer patent ductus arteriosus occlusion device trial: initial and one-year results. J Am Coll Cardiol. 2004;44:513-519.
A.8. Would you give digitalis to treat congestive heart failure in preterm infants? Why?
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