Case history
Case history #1
A 6 week-old infant girl is brought to her paediatrician with poor feeding. Since she was last seen at 2 weeks she has had poor weight gain. She sweats with feeds and seems to tire out easily. There is no significant family history. On physical examination she is noted to be tachypnoeic and uninterested in her bottle after a few minutes of feeding. She has increased work of breathing. On cardiac examination, she has a grade 4 continuous murmur that is heard in the left infraclavicular region and back. She also has an early diastolic rumble best heard at the apex. Her liver is 3 cm below her costal margin. Her pulses are bounding. Her chest x-ray (CXR) reveals an enlarged heart with a prominent main pulmonary artery segment and increased pulmonary markings.
Case history #2
A 28 week premature boy is treated with appropriate doses of surfactant. However, on his second day of life he has worsening symptoms of respiratory distress syndrome with increasing ventilatory requirements. He has also started demonstrating apnoeic episodes. He is noted to have a widened pulse pressure (30 mmHg) on his arterial line and he is starting to have some bloody stools. On physical examination, he is noted to have bounding pulses and a prominent precordial impulse. On auscultation a grade 3 systolic ejection murmur can be heard in the left infraclavicular area. His abdomen also appears distended. On CXR, his lung fields are almost completely opacified.
Other presentations
Clinical presentation depends on the age of the patient and the size of the shunt. Patients can be completely asymptomatic, have significant heart failure, or, if they present much later in life, may have signs and symptoms of pulmonary hypertension. Premature infants with a haemodynamically significant patent ductus arteriosus (PDA) usually develop clinical signs in the first week of life. Full-term infants with a PDA may present in early infancy with a murmur, or signs of heart failure if they have a large shunt across the ductus. Conversely, they may not present until late childhood with mild exercise intolerance if the shunt is smaller. Haemodynamically insignificant shunts will not be associated with symptoms but may be picked up by the presence of a murmur on examination. Atypically, if a haemodynamically significant PDA is missed in childhood, it may present in adulthood with heart failure, atrial arrhythmias, endarteritis, or, most seriously, with irreversible pulmonary vascular disease characterised by desaturation and evidence of right heart failure.
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