Patent Ductus Arteriosus

Patent ductus arteriosus with small caliber may present with minimal signs or no signs at all. However, large caliber PDA may present with the following system wise symptomatology:

• General appearance: Patients will appear fatigued due to tissue hypoxia. Infants will have difficulty in eating because of breathlessness during swallowing.
• Integumentary system: Patients will appear cyanotic due to poor oxygen perfusion of the skin.
• Head and Neck: Dark discoloration around the eyes due to chronic cyanosis.
• Chest and heart: Machinery like murmur on auscultation due to volume overload through the PDA. Infants will exhibit tachypnea due pulmonary congestion.
• Abdomen: Ascites may occur with late stage heart failure.
• Extremities: Fingernail clubbing may be due to nail bed chronic hypoxic state. 

The diagnosis of PDA in infants is initially done by clinical examination by the attending pediatrician. However, additional tests may be recommended to confirm the diagnosis of PDA. The following diagnostic modalities are used in the examination of PDA patients:

• Electrocardiography (ECG): A left ventricular hypertrophy may be demonstrated by voltage in ECG.
• Chest X-ray: This radiograph will show a prominent left atria, left ventricle and ascending aorta. There is an increased pulmonary markings in a significant shunt.
• Echocardiography: A two dimensional imaging of the heart with colored Doppler studies can identify the patent ductus radiographically [3]. A suprasternal view of the aortic side of the PDA in echocardiogram can accurately reveal its diameter [4].

In premature babies, the PDA may close spontaneously within the first two years of life. This may no longer need any treatment especially when the PDA is small with minimal symptoms. In full term babies, the non-closure after a few weeks from birth may suggest that it may never will. The first line treatment for the closure of PDA in newborns is the use of indomethacin and ibuprofen. Both cyclooxygenase inhibitors are equipotent in PDA closure capabilities [5].

However, excess indomethacin may cause renal toxicity; thus, dose reduction is imperative if warranted [6]. Ibuprofen may be given orally or intravenously with no significant advantage over the other [7]. These regimens are noted to have fewer side effects and may significantly help in the closure if given at an early stage.

An invasive procedure known as trans-catheter device closure may be implored by blocking the PDA with a small metal coil to block the blood flow, this device is introduced through a small cardiac catheter [8]. When conservative medical management fails, a surgical repair of the PDA by ligation may be indicated by doing a chest incision in through the baby’s ribs [9]. Cardiac surgery in infants post no greater risk and threats than those given ibuprofen and indomethacin [10].

Prognosis in patent ductus arteriosus is dependent on ductal size. Smaller sized PDA may convey cardiac symptoms but infants may thrive with some difficulty. Small PDA that occurs even prematurity that appears as a solitary lesion caries a good prognosis.

The patent ductus in premature infants may close spontaneously within the first 3 months of life in 72-75% of cases. The use of prophylactic ibuprofen may lead to a 92% closure rate. However, larger PDA may lead to heart failure, pulmonary hypertension and recurrent infection of the lungs.

Complications

Patients with small PDA may not lead to any complications but larger PDA may complicate into either of these clinical disorders if left untreated:

• Pulmonary hypertension: The increased blood flow the patent ductus may cause permanent damage to the lungs.
• Eisenmenger’s syndrome: An irreversible type of pulmonary hypertension that causes a reversal of blood flow.
• Bacterial endocarditis: The PDA increases the risk of patients to any infection of the myocardial endothelium (inner lining).
• Heart failure: This is a chronic outcome if the heart muscles over works due to volume overload 
• Cardiac dysrhythmias: Arrhythmias usually develop with the enlargement of the heart.

The congenital heart defect in patent ductus arteriosus is believed to have developed early in the embryology of the heart muscle. The exact mechanism is still unknown to medical science and is continually being researched up to this day. Research scientists believes in the major role of genetics and environmental factors in the development of PDA.

Infants that suffer congenital rubella syndrome whereby the mother had rubella in the first trimester of pregnancy are most prone to PDA. Maternal intake of amphetamine, alcohol and phenytoin may be a causative factor in its development. Premature infants has a very high likelihood of a persistent ductus.

In the United States, the general incidence of patent ductus arteriosus is 6 to 20 per 100,000 live births. Premature infants less than 28 weeks old has a PDA incidence of 60% while those born more than 32 weeks gestation has an incidence rating of 20% for PDA.

Patent ductus arteriosus as an isolated case represents 5 to 10% of all congenital heart diseases. Females are more prone with a 2:1 ratio as compared with male infants. A great deal of children are usually left undiagnosed until they get older.

The failure of the ductus closure among premature neonates are primarily due to poor prostaglandin metabolism from an immature lung. The failure in prostaglandin metabolism is usually brought about by perinatal asphyxia, hypoxemia, increased pulmonary blood flow, renal failure, and respiratory disorders. It was also postulated that cyclooxygenase-2 (COX-2) induction, an isoform of the COX producing prostaglandin can prevent the duct from closing.

There is no definitive cause for PDA; thus, preventive measures in ensuring that PDA doesn’t occur in your baby are hard to determine. This precludes that one must do everything to have a healthy pregnancy to prevent PDA and other congenital diseases of the infant. The following tips are most helpful in having a healthy pregnancy:

• Regular prenatal care with your doctor
• Exercise regularly
• Balanced diet
• Avoid infections
• Avoid smoking, alcohol, X-ray and illegal drugs
• Diabetic mothers should have their glucose controlled

Patent ductus ateriosus or PDA is a clinically characterized as the persistent fetal connection (ductus arteriosus) between the two major vessels from the heart, pulmonary artery and aorta after birth that usually results into the shunting of blood from left-to-right. The ductus arteriosus is a vestigial vessel that shunts the blood from the heart directly to the aorta, this vessel physiologically closes when the lung expands after birth which usually happens within 3 months from birth [1].

The persistence of the vessel is clinically referred to as patent ductus arteriosus that transmits poorly oxygenated blood to the body manifested as failure to thrive, poor feeding, tachycardia, and tachypnea in infants. The symptomatic persistence of the ductus arteriosus may need cardiac surgery or catheter-based correction to achieve normalcy [2].

Definition

Patent ductus arteriosus is a clinical disease characterized by the persistent fetal connection between the pulmonary artery and the aorta.

Cause

Genetics, rubella infection, amphetamine, phenytoin, and alcohol may cause the disorder.

Symptoms

Failure to thrive, tachypnea, easy fatigability, tachycardia, and cyanosis may occur. 

Diagnosis

Clinical examination, ECG, echocardiogram and chest X-ray are used to diagnose PDA.

Treatment and follow-up

Indomethacin and ibuprofen, trans-catheter closure device and surgical repair are the common treatment options.

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9. Kang SL, Samsudin S, Kuruvilla M, Dhelaria A, Kent S, Kelsall WA. Outcome of patent ductus arteriosus ligation in premature infants in the East of England: a prospective cohort study. Cardiol Young. 2013; 23(5):711-6 (ISSN: 1467-1107)
10. Malviya M, Ohlsson A, Shah S. Surgical versus medical treatment with cyclooxygenase inhibitors for symptomatic patent ductus arteriosus in preterm infants. Cochrane Database Syst Rev. Jan 23 2008; CD003951.