A 6-day-old boy in the neonatal intensive care unit has a heart murmur. The patient was born at 27 weeks gestation and intubated due to surfactant deficiency. Birth weight was 1.14 kg (2 lb 8 oz). Temperature is 37 C (98.6 F), blood pressure is 66/12 mm Hg, and pulse is 182/min. A continuous murmur with systolic accentuation is best heard at the left heart border. There are bounding femoral and palmar pulses. Abdominal examination is unremarkable. Blood culture is sterile. Elevated levels of which of the following substances is most likely contributing to this patient's condition?

Question

A 6-day-old boy in the neonatal intensive care unit has a heart murmur.  The patient was born at 27 weeks gestation and intubated due to surfactant deficiency.  Birth weight was 1.14 kg (2 lb 8 oz).  Temperature is 37 C (98.6 F), blood pressure is 66/12 mm Hg, and pulse is 182/min.  A continuous murmur with systolic accentuation is best heard at the left heart border.  There are bounding femoral and palmar pulses.  Abdominal examination is unremarkable.  Blood culture is sterile.  Elevated levels of which of the following substances is most likely contributing to this patient's condition?

Quizplus · Accepted Answer

11ec160b_3b99_822e_9249_5f40f0b3d0bf_MD0001_00 This preterm infant has a continuous murmur, bounding pulses, and a wide pulse pressure; findings consistent with a patent ductus arteriosus (PDA). The ductus arteriosus is a fetal vascular connection that connects the trunk of the pulmonary artery to the proximal descending aorta; it shunts right ventricular output directly into the systemic circulation, bypassing the lungs. Patency of the ductus arteriosus is maintained in utero due to smooth muscle dilation induced by placental prostaglandin E2 (PGE2) and the relative hypoxemia of the fetal circulation. After birth, closure of the ductus arteriosus is normally initiated by loss of placental PGE2 and the vasoconstrictive effects of increased systemic oxygen levels (eg, increased endothelin-1 production) (Choice A). Persistence of the ductus arteriosus after birth occurs most commonly in preterm infants and is associated with elevated postnatal PGE2 and/or increased sensitivity to prostaglandins. The decrease in pulmonary vascular resistance caused by lung inflation results in reversal of flow across the ductus arteriosus, with blood flowing from the aorta into the pulmonary circulation (ie, left-to-right shunt); this results in a continuous machinelike murmur and lower diastolic pressures (responsible for pulse findings). Although individuals with small shunts may be asymptomatic, increased blood flow across the PDA can eventually lead to heart failure or progressive pulmonary hypertension (causing Eisenmenger syndrome in older patients). Nonsteroidal anti-inflammatory drugs (eg, indomethacin, ibuprofen) are sometimes used to help initiate PDA closure by inhibiting the synthesis of PGE2. (Choice B) Treatment with nonsteroidal anti-inflammatory drugs can increase leukotriene synthesis; elevated leukotriene D4 levels cause vasoconstriction and would, therefore, facilitate closure of a PDA. (Choice D) Thromboxane A2 increases platelet production and aggregation. Much of the antithrombotic effect of aspirin is through its inhibition of cyclooxygenase enzymes, resulting in decreased thromboxane A2 synthesis. (Choice E) Vasopressin (ie, antidiuretic hormone) promotes water reabsorption in the kidney and causes arteriolar constriction. Elevated levels cause water retention and hyponatremia, but would not contribute to the pathogenesis of PDA. Educational objective: Patency of the ductus arteriosus is maintained in utero due to placental production of prostaglandin E2 (PGE2) and low oxygen levels in the fetal circulation. Persistence after birth (ie, patent ductus arteriosus) is associated with elevated postnatal PGE2 and typically presents with a continuous murmur, widened pulse pressure, and bounding pulses in a preterm infant. __________ References: Current perspectives on pathobiology of patent ductus arteriosus. (http://www.ncbi.nlm.nih.gov/pubmed/23519783) Managing the patent ductus arteriosus: current treatment options. (http://www.ncbi.nlm.nih.gov/pubmed/24903455) Understanding the pathobiology in patent ductus arteriosus in prematurity-beyond prostaglandins and oxygen. (http://www.ncbi.nlm.nih.gov/pubmed/30965358)

A 6-Day-Old Boy in the Neonatal Intensive Care Unit Has