Patent ductus arteriosus

Presented bySandeep kaur

Ductus arteriosus
The ductus arteriosus is a blood vessel that allows fetal blood to bypass the lungs. This vessel usually partially closes 10 to 15 hours after birth and completely seals closed by 10 to 21 days after birth. The closure of the ductus arteriosus after birth allows blood flow to reach the lungs only through the pulmonary artery.

Introduction
It is the failure of fetal ductus arteriosus (artery connecting aorta and pulmonary artery) to close within first weeks of life. The continued patency of this vessel allows blood to flow from higher pressure aorta to lower pressure pulmonary artery, causing a left-to-right shunt.

 A PDA allows blood to flow directly from the aorta into the pulmonary artery and to the lungs. This extra amount of blood flowing into the lungs strains the heart and increases blood pressure in the lung's arteries.

Definition
It is a condition in which a blood vessel called the ductus arteriosus fails to close normally in an infant soon after birth. (The word "patent" means open.)

The condition leads to abnormal blood flow between the aorta and pulmonary artery, two major blood vessels surrounding the heart.

Incidence
The incidence is inversely related to gestational age & birth weight. A hemodynamically significant shunt due to PDA has been reported in 40% of infants <1000 gm & 20% of infants between 1000-1500 gm.

CAUSE/ETIOLOGY
Cause is unknown Genetics may play a role. A defect in one or more genes could prevent the ductus arteriosus from

closing
after birth.

normally

RISK FACTORS
Infants with genetic disorders, such as Down syndrome Infants whose mothers had German measles (rubella) during pregnancy, babies with congenital heart problems, such as hypoplastic left heart syndrome, transposition of the great vessels, and pulmonary stenosis Occurs more often in premature infants (on average,

occurring in about 8 of every 1,000 births).

 Respiratory distress syndrome in preterm infants needing ventilation & surfactant

Prophylactic use of synthetic surfactant increases risk for PDA

Pathophysiology and hemodynamics

During fetal life, ductus arteriosus connects to pulmonary artery at its bifurcation to aorta It remains patent through vasodilatory action of prostaglandins within its tissue

Postnatally, increase in oxygen tension has constricting effect on ductus It may reopen in preterms in response to lowered oxygen tension a/w respiratory impairement

At birth, pulmonary & systemic resistance are equal

As systemic resistance inc, blood shunts from aorta across ductus to pulmonary artery (left to right shunt) The additional blood is recirculated through lungs & returned to left atrium & ventricle It causes increased workload on left side of heart, inc pulmonary vascular congestion & resistance Increased right ventricular pressure & hypertrophy

Clinical manifestations
Infants may be asymptomatic or shows signs of CHF Common sign of PDA is HEART MURMUR

extra or unusual sound heard during the heartbeat (pan systolic & continous murmur) heard at 2nd left parasternal area

may develop signs or symptoms of volume overload on the heart and excess blood flow in the lungs including: Dyspnea on exertion Easy fatigability Physical underdevelopment Increased respiratory infections Heart rate>150/min

Assessment
Heart rate >150/min Gallop rhythm due to rapid filling of ventricle Bounding pulses due to increased systolic pressure Widened pulse pressure (>25 mm Hg) High systolic pressure due to increased left ventricular stroke volume and rapid rise in aortic pressure Low diastolic pressure due to continous shunting of blood through ductus and reduced peripheral resistance

DIAGNOSTIC TESTS
Radiological examination reveals left atrial and left ventricular enlargement, dilated ascending aorta and pulmonary artery with increased pulmonary vascularity

 ECG shows left ventricular hypertrophy and possible right ventricular hypertrophy

 Echocardiogram is normal if ductus is small. Echo criteria includes Left atrial dilatation Diastolic turbulence (backflow) in pulmonary artery

 Doppler ECHO is more specific & sensitive for diagnosing PDA Cardiac catheterization, if necessary revels normal or increased pressure in right ventricle and pulmonary artery and oxygenated blood in pulmonary artery

Management
Prophylactic treatment is started before appearance of PDA within first 24 hrs of birth with indomethacin, especially in neonates <1000 gm. It was found to dec symptomatic PDA but not cause any change in long term morbidity. It dec renal & cerebral blood flow, hence not recommended.

 Early symptomatic weight<1000gm- treatment is started early even if PDA is not hemodynamically significant.
weight>1000gm- treatment is usually not recommended as progression to symptomatic PDA is less common & spontaneous closure occurs. Late symptomatic- only significant PDA is treated hemodynamiclaly

General measures Fluid restriction <60% maintenance fluid Avoid hypoxia & acidosis High PEEP & lower inspiratory time

Medical management
Pharmacological closure of ductus in low birth weight babies is done with indomethacin, which inhibits prostaglandin synthesis. Improvement can be seen within 12-18 hrs after medication. It also reduces albumin bound serum bilirubin and therefore contribute to hyperbilirubenemia & a risk of renal dysfunction & hyponatremia.

IndicationsEarly symptomatic treatment of PDA in <1000gm Late symptomatic treatment of PDA in >1000gm Re-treatment after failure of first course of indomethacin Reccurance of PDA after first course of indomethacin

 Ibuprofen is also inhibitor of prostaglandin & is effective in closing ductus. It has equal efficiency as indomethacin with fewer side effects.

Dosage of indomethacin and ibuprofen

Indomethacin 0.2mg/kg stat followed by<2 day- 0.1mg/kg/dose 12 hourly for 2 doses 2-7day- 0.2mg/kg/dose 12 hourly for 2 doses >7 day- 0.25mg/kg/dose 12 hourly for 2 doses

Ibuprofen 10mg/kg stat followed by5mg/kg/dose 24 hourly for 2 doses

Surgical management
Surgical treatment is by transaction or ligation of ductus of patent vessel via thoracotomy. A newer technique, VATS (visual assisted thoracoscope surgery), uses a thoracoscope & instruments placed through 3 small incisions on left side of chest to place clip (titanium clip) on ductus.

 It can be done at any time, preferably done at 6 months of age. It can be done early to prevent risk of infective endocarditis. After repair, symptoms of cardiac failure disappear, heart becomes normal in size, murmurs disappear & generalised improvement in childs condition & development.

Non-surgical treatment Use of coils to occlude PDA in catheterization laboratory. A catheter is placed in a large blood vessel in the upper thigh (groin) and guide it to child's heart. A small metal coil or other blocking device is then passed up through the catheter and placed in the PDA to block blood flow through the vessel.

Presence of PDA
birth weight <1000gm Contraindicated to Indomethacin yes no indomethacin >1000gm hemodynamically significant PDA yes no follow up

closure
No yes

Repeat indomethacin closure surgery No yes

Research input
Treatment of patent ductus arteriosus: indomethacin or ibuprofen? K C Sekar and K E Corff Several clinical studies comparing indomethacin to placebo showed significant PDA closure rates. Schmidt et al (trial of indomethacin prophylaxis in preterms trial) looked at the neurodeveplomental outcome at 18 months of age when indomethacin was given as a prophylaxis compared to placebo. This study showed no differences in neurodevelopmetal outcome between both groups. Ibuprofen lysine when given as prophylaxis compared to placebo showed significant PDA closure rates but did not have an effect on the incidence of IVH. Studies comparing indomethacin and ibuprofen lysine showed equal efficacy rates in ductal closure. In these comparative trials, the indomethacin group had statistically significant higher incidence of oliguria and elevated creatinine levels.

 Recent analysis of children at 4 and 8 years of age who were treated with indomethacin prophylaxis at birth showed favorable neurodevelopmental outcome vs those treated with placebo. Long-term neurological outcome in infants who received ibuprofen lysine is not yet available since it has only been approved for use since 2006.

Prognosis
The outcome is variable when medical management is used. The fatality rate with elective surgery is <1% but may be higher in sick neonates. The outcome with pharmacological closure is favorable if complications do not intervene.

Aortopulmonary window
Aortopulmonary window is a rare heart defect in which there is a hole connecting the major artery taking blood from the heart to the body (the aorta) and the one taking blood from the heart to the lungs (pulmonary artery). The condition is congenital, which means it is present from birth. It can occur on its own or with other heart defects such as patent ductus arteriosus, tetralogy of Fallot, or pulmonary atresia.

Causes
Aortopulmonary window is very rare. It accounts for only 0.1% of all congenital heart defects. It occurs when the aorta and pulmonary artery do not divide normally as the baby develops in the womb.

Sign & symptoms

If the defect is small, it may not cause any symptoms. However, most defects are large. Symptoms can include: Delayed growth Heart failure Irritability Poor eating and lack of weight gain Rapid breathing Rapid heartbeat Respiratory infections

Diagnostic test
The pediatrician will usually hear an abnormal heart sound (murmur) when listening to the child's heart with a stethoscope. Cardiac catheterization - a thin tube inserted into the arteries around the heart to view the heart and blood vessels and directly measure pressure in the heart and lungs Chest x-ray Echocardiogram MRI of the heart

Treatment
The condition usually requires open heart surgery to repair the defect. Surgery should be done as soon as possible after the diagnosis is made, usually when the child is still a newborn. During the procedure, a heart-lung machine takes over for the child's heart. The surgeon opens the aorta and closes the defect with a patch made either from a piece of the sac that encloses the heart (the pericardium) or a man-made material.

Complications
Delaying treatment can lead to complications such as: Congestive heart failure Pulmonary hypertension Death

T H A N K S