3. INTRODUCTION
Patent ductus arteriosus (PDA) is the most common
type of extra cardiac shunt seen in clinical practice. It
is also the commonest cardiac defect in the neonatal
period.
4.
5. EPIDEMIOLOGY
PDA accounts for 5-10% of all congenital heart
defects (CHDs) with much higher incidence in
preterm infants, due to immaturity of ducal smooth
muscles and less responsiveness to oxygen.
Female- male ratio is 2:1
6. RISK FACTORS
1. Prematurity (very low birth weight infants)
2. Children born at high altitude
3. Maternal Rubella infection during early
pregnancy.
4. Full term infants asphyxiated at birth.
7. PATHOPHYSIOLOGY
The ducts arteriosus (DA) is derived emvryologically from the
6th aortic arch, and plays a significant role in intrauterine life.
During fetal life, most of the pulmonary arterial blood is
shunted through the DA into the aorta to maintain circulation.
However, soon after birth, functional closure occurs.
Ducal closure is dependent on vasoconstriction. After birth,
oxygen concentration increases resulting in vasoconstriction.
In preterm infants, the ducts is less sensitive to high oxygen,
hence the increased incidence among them. If the DA remains
patent after birth, aortic blood is then shunted into the
pulmonary artery.
The volume of shunting depends on the length and size of the
ductus, and on pulmonary vascular resistance. There is
persistence between the pulmonary artery and the DA after
birth.
8. CLINICAL FEATURES
HISTORY;
• Asymptotic for small size ductus arteriosus.
• Preterm newborn may present with respiratory
distress.
• Intermittent apneic spells and bradycardia.
• Congestive heart failure for large defects.
PHYSICAL EXAMINATION;
• Hyperdynamic precordium.
• Bounding peripheral pulses, wide pulse pressure.
• Continuous (machinery) murmur in the infraclavicular
area.
9. LABORATORY INVESTIGATIONS
1) Chest x-ray
• Normal with small shunt.
• Cardiomegaly with evidence of plethora.
2) Electrocardiogram (ECG)
• Normal or left ventricular hypertrophy in small to
moderate sized PDA.
• Combined ventricular hypertrophy in large PDA.
• Right ventricular hypertrophy develops in reversal of
shunt.
3) Echocardiography (2D-Echo) "confirms diagnosis"
• Provides dimensions of the left atrium and ventricle.
• Continuous flow pattern of left to right shunt.
11. MANAGEMENT
SUPPORTIVE;
1) Maintenance of adequate haemoglobin levels.
2) Nutritional support; glucose and electrolytes.
3) Manage complications
• Antibiotics for recurrent chest infections.
• Appropriate anti congestive drugs for patients that develop congestive heart failure.
• Infective endocarditis prophylaxis should be given when indicated.
DEFINITIVE;
1) Non-surgical closure
• Indomethacin therapy
• Catheter closure
2) Surgical ligation
• Early
• Delayed: may be delayed in congenital heart defects that are not compatible with life
except some mixing occurs via intrauterine communication like PDA. Prostaglandin
E2 is used to maintain its patency in this case.
12.
13. CONCLUSION
For infants with just an isolated PDA, the prognosis is
good. In premature infants, the prognosis is
dependent on other comorbidities. After closure of
the PDA, most children have a normal life
expectancy. Spontaneous closure of the PDA is rare.
With the use of indomethacin, close to 80-90% of
infants will have successful closure of the PDA. In
adults, a surgical closure is always required provided
the patient has not developed fixed pulmonary
hypertension.