Patent ductus arteriosus

thumb|200px|Otevřená Botallova dučej 200px|thumb|Ductus arteriosus Botalli thumb|200px|right|CT perzistující Botallova dučej Patent Ductus Arteriosus (persistent ductus arteriosus, PDA) is an acyanotic congenital heart defect which the ductus arteriosus (ductus Botalli) has not been closed. Ductus arteriosus is a vessel that connects pulmonary artery and aorta. It is important in the fetal circulation, for it allows to bypass the lung by directing the deoxygenated blood from pulmonary artery to aorta.

In healthy full-term neonates, a functional closure of the duct occurs shortly after the birth. Complete closure occurs within 24 hours in almost 50% of cases, within 48 hours the 90% of cases, and within 96 hours after birth, the duct should be closed in all full-term newborns. The failure to close this duct is called patent ductus arteriosus or persistent ductus arteriosus (PDA).

PDA is more common in preterm infants. Widths and lengths of the persistent duct can vary among individuals, therefore the severity of the symptoms of the PDA is dependent on individual cases–it can manifest from an accidental murmurs to a severe acute heart failure–.

Risk Factors
Higher incidence of PDA is associated with the following factors:
 * Preterm birth (80% of incidence rate in neonates with a birth weight below 1000g),
 * Respiratory Distress Syndrome (RDS) and its surfactant treatment,
 * High intravenous fluid administration in the first days of life,
 * Asphyxia,
 * Congenital rubella, trisomy 13, trisomy 18, …,
 * high altitude,
 * Congenital heart defects (aortic coarctation, pulmonary atresia, transposition of the great vessels, …).

Lower incidence of PDA is associated with the following factors :
 * Use of antenatal corticosteroids (induction of pulmonary development in premature neonates),
 * IUGR,
 * Premature amniotic fluid outflow(PROM).

Pathophysiology
The ductus arteriosus shunts the blood from pulmonary artery to descending aorta, bypassing the pulmonary circulation which is with high vascular resistance. Various factors influence whether the duct closes or persists. Closure of the duct is stimulated by the presence of oxygen in the blood flow, and the duct is kept open by prostaglandin E2. Sensitivity to these opposing factors differs with gestational age. The younger the fetus is, the more sensitive it is to prostaglandin E2 and indometacin, while the effect of oxygen is small. Indometacin is a medication used to stimulate the closure of the ductus arteriosus.

Clinical Manifestation
It is often asymptomatic in mild cases. In severe cases, its consequences can be growth retardation, failure to thrive, collapsing pulse (Watson's water hammer pulse), hypotension (this can be an initial symptom in ELBW), ventilation problems, heart failure (with pulmonary edema and hepatomegaly) Peripheral pulses are bounding and forceful and hyperdynamic precordium is often seen. Resting tachycardia and tachypnea are also apparent.

Wide and short ductus arteriosus result in heart failure, pulmonary hypertension, and differential cyanosis (refers to cyanosis in both lower extremities but with acyanotic upper extremities). A moderate size of ducts may result in recurrent respiratory infections and failure to thrive. A narrow ductus arteriosus is asymptomatic. All patients are at risk of infectious endocarditis.

In premature infants with RDS (respiratory distress syndrome), PDA may lead to dependence on artificial ventilation. In infants, it causes circulatory failure, manifested as dyspnea from pulmonary edema


 * continuous "machine-like" heart murmur (or three-period rhythm) can be heard in left subclavicular region. maximum murmur is heard at second heart sound (it can be described as a low frequency sound of "pouring coke").

Diagnosis
Diagnosis of PDA is based on:
 * Finding in physical examination,
 * Echocardiogram, including doppler echocardiography,
 * X-ray of the heart-cardiomegaly, blood flow to the lung.

Patients with aortopulmonary septal defect (direct communication of the ascending aorta and pulmonary trunk, aortopulmonary window) have a similar clinical manifestation.
 * Differential diagnosis

Treatment

 * Asymptomatic PDA – monitoring. In most cases, the duct close spontaneously (especially in premature infants)
 * symptomatic PDA;
 * Limited fluid intake,
 * maintenance of sufficient oxygen saturation in the blood,
 * Treatment of heart failure: furosemide,
 * Possible pharmacological closure of the duct: indometacin, ibuprofen,
 * absolute contraindication: concurrent heart defects which requires PDA is necessary for survival (e.g., aortic coarctation),
 * side effects: oliguria, fluid retention and hyponatremia due to decreased renal blood flow, decreased blood flow to the brain, gastrointestinal complications (bleeding, ulceration), bleeding (impaired platelet function), jaundice,
 * Surgical treatment (ligation, excision).
 * Cardiac catheterization (Amplatzer duct ocluders)

Related Pages

 * Congenital heart defects
 * Acquired heart defects