Patent Ductus Arteriosus
By Jonas Wilson, Ing. Med.
Patent ductus arteriosus (PDA), one of the more common cardiac defects at birth, is the persistence of an opening between the pulmonary artery and the descending thoracic aorta. This opening is as a result of failure of the physiological fetus ductus arteriosus to close, which normally occurs soon after birth. This hole allows for oxygenated blood from the aorta to mix with oxygen-depleted blood from the pulmonary artery. As a consequence, significant strain is placed on the heart and pressure within the lungs’ arteries is dramatically increased.
Etiology and pathophysiology
Often, PDA has no clear-cut cause; however, it is believed that genetic and environmental factors may be involved. During fetal development, a connection between the two major arteries leaving the
…show more content…
The placenta is a major source of fetal prostaglandins and its removal after birth allows for the lungs to expand and become metabolically active, where most prostaglandins are degraded. This, in combination with increased pulmonary oxygen tension, in healthy full-term infants, normally causes functional closure of the ductus arteriosus within 15 hours after birth.
Several studies have suggested that PDA occurs in premature babies due to the lungs being underdeveloped and poor metabolizers of prostaglandins. Other risk factors that may be associated with an infant having a PDA is a positive family history of cardiac defects and genetically linked conditions like Down syndrome. Maternal infection with German measles during pregnancy can cause damaging effects to the fetal heart and circulatory system and put the infant at greater risk of acquiring a PDA. Studies have also shown that children born at higher altitudes have an increased susceptibility of having a PDA.
Bronchopulmonary dysplasia (BPD) develops as a result of an infant 's lungs becoming irritated or inflamed. It is considered a chronic lung disease. BPD progresses from respiratory distress syndrome (RDS), usually with atelectasis, consolidation, and massive fibrosis. Bronchopulmonary dysplasia is most common in premature infants who needed mechanical ventilation and oxygen therapy to survive. Although life-saving, these treatments can also cause lung damage. BPD has been a severe chronic lung disease in premature infants, going back to 1967. Northway et al described it a lung injury in premature infants and the classic BPD had four stages. Each of the stages has radiographically and pathologically differences.
Critical Congenital Heart Defects are abnormalities of the heart structure that are present at birth. These occur because of incomplete or abnormal development of the fetus’ heart. These defects can cause severe mortality within the newborn stage (Goldstein, 2013, p.1). Several are known to be linked to genetic disorders such as Down syndrome and others are thought to be linked to environmental factors that women can be exposed to while pregnant. The cause of most CCHD’s is unknown.
6 days old female with TOF, pulomanry atresia large VSD, right sided aortic arch with mirror image branching, left sided large PDA originating from the left innominate artery, confluent PA branches, and no significant AP collaterals.
There are two main types of PPIS which are defined as Arterial Presumed Perinatal Stroke (APPS) which “are due to an occlusion of a brain artery” (University of Calgary, 2017) and Periventricular Venous Infarction (PVI) that are strictly fetal strokes where “Bleeding of the germinal matrix is the primary problem” (University of Calgary, 2017). Presumed Perinatal Ischemic Strokes are so named because they occur between the middle of a mother’s second trimester into the first year of life of the child and are diagnosed after the stroke has occurred, usually later in the development of the patient. Several things can lead to perinatal ischemic strokes and each patient is different depending on surrounding circumstances as well as personal environments. However, one of the most common causes of a perinatal ischemic stroke is a blood clot forming in the heart and traveling to the brain which resulting in hypoxia. This can be a result of congenital heart problems like abnormal valves, infections, or diseases. One such disease is called sickle cell which is results in the red blood cells not carrying enough oxygen to the brain causing a stroke to occur. PPIS can also be caused by any trauma that injures the large arteries and results in a loss of
There is no definitive cause of PCa but age, race and family history are important risk factors.
The definition of TOF reads, a type of congenital heart defect. Congenital means that it is present at birth (UMMC, 2013). TOF occurs when there is 4 abnormalities all together. One of the 4 abnormalities is when a massive hole is in the wall of the muscle (septum) that separates the 2 bottom pumping cambers (ventricles) of the heart. The massive hole in the abnormality itself is a VSD. A VSD is known as a Ventricular Septal Defect. Due to the location of the VSD, two more abnormalities develop. One being that there is a vast blood vessel which take the blood to the body (aorta) is pulled toward, and “overrides” the ventricular septum so that it sits over both the left and right ventricles; this is called an overriding aorta (UMMC, 2013). The second abnormality that takes place is that the muscle produces obstruction to the blood flow going out the right across the pulmonary valve. The right ventricular outflow tract obstruction, can be due to obstruction below the valve, at the valve or in the pulmonary arteries as they deliver blood out to the lungs (UMMC, 2013). There is different severities of TOF. The most acute form is known as pulmonary atresia. In patients with pulmonary atresia there is no functional pulmonary valve. The right ventricular outflow obstruction leads to thickening of the
They did an ultrasound while I was still inside my mother when she was seven months pregnant. The doctors were able to tell that my heart had developed a single pumping chamber and my aorta was smaller than my lung arteries. They knew that I would need an operation called the Norwood procedure. Since the aorta was small as was the left ventricle, the right ventricle had to do all the work of pumping the blood to the lungs and through the ductus arteriosus to the rest of the body.
Congenital heart disease include many different types of defects. Some of these defects are simple, such as a hole in the septum. Others, are more complex and severe that include combinations of simple defects, problems with the location of blood vessels leading to and from the heart and other serious problems with the development of the heart. The different types of defects ranging from simple to complex are holes in the heart (septal defects or atrial septal defects-ASD), Patent Ductus Arteriosus (PDA-abnormal blood flow occurs between the aorta and pulmonary artery), Narrowed valves
The normal flow of blood through the heart consists of the entry of blood to the right atrium through to the right ventricle and then the blood passes through the tricuspid valve entering the lungs and then through to the left atrium and to the left ventricle via the mitral valve and finally into the body. During fetal development, however there are the risks for congenital anomalies. These congenital heart disorders consist of Atrial septal defect (ASD) and Ventricular septal defect (VSD). ASD is one of the common congenital heart defects that requires interventional measures or repair. The condition occurs when the foramen ovale the opening between the atria prior to birth does not close and there
Fetal echocardiography is indicated in high risk pregnancies where the chances of fetus having a congenital heart disease (CHD) are likely to be high - for exapmle, in a fetus with extracardiac anomalies picked up on obstetric ultrasound, those with a history of CHD in family, maternal diabetes and maternal connective tissue disorder (Srinivasan,2000). Congenital heart defects are abnormalities in the heart's structure that are present at birth. They are the most common congenital malformations with a reported incidence of 8 to 10 per 1000 live births, and about a third of these CHDs are severe (fatal or requiring an intervention in the first year of life) (Dolk and Loane, 2009; Hoffman and Kaplan, 2002; Vaartjes et al., 2007) . CHDs happen because of incomplete or abnormal development of the fetus' heart during the very early weeks of pregnancy.
Congenital heart disease (CHD) is a problem with the heart's structure and function that is present at birth (Weinrauch, 2015). Congenital heart disease is divided into two types, cyanotic (turns the skin blue due to a lack of oxygen) and non-cyanotic. Cyanotic heart diseases include Ebstein’s anomaly, tricuspid atresia, tetralogy of Fallot, Truncus arteriosus, transportation of the great vessels, pulmonary atresia, hypoplatstic left heart, and total anomalous pulmonary venous return. Non-cyanotic heart diseases include aortic stenosis, pulmonic stenosis, patent ductus arteriosus (PDA), arterial septic defect (ASD), coarctation of the aorta, ventricular septal defect (VSD), and atrioventricular canal (endocardial cushion defect).
Every isolated PDA needs closure beyond 3 months of age except for silent ducts, Eisenmenger ducts and ducts in premature infants. Percutaneously closure of PDA with device is an established modality of treatment worldwide and is regarded as safe and effective. Important information to have a successful duct occlude include age and weight of the patient, size and the experience of the center and operator. The PDA device closure is considered in infant with age beyond 6 months and weight of more than 6 kgs. If PDA is directly responsible for CHF, felling to increase duct closure is indicated as soon as possible. Early closure of PDA improve cardio-respiratory status and as a importance long-term follow-up
When peripheral arteries begin to narrow there is a reduction of blood flow through the body. The tissues that these arteries supply begin to compensate for the lack of oxygen through vasodilation of these vessels or collateral sprouting of new vessels1. Lack of fresh oxygenated blood leads to ischemia and the tissues supplied by the narrowed vessels begin to die. The main factor that causes this disease development is atherosclerosis, which is a build-up of plaque in these peripheral arterial beds cause by lipids in the blood steam narrowing the lumens of these vessels3. The most common peripheral arteries affected by this disease process are those of the lower extremity which present in 90% of those diagnosed with PAD1. When the plaque builds up on the walls of arteries it not only narrows the blood vessels but the plaque begins to harden the walls of the arteries. It is the narrowing and hardening of peripheral arteries that contributes to reduction of blood flow and a built up of cellular wastes in the
The pathophysiology of brochopulmonary dysplasia is not yet completely comprehended. (Hadjiliadis, 2013) There are indeed a variety of virulent causes that dower to the pattern of growth in BPD. BDP starts off by injuring the smaller airways, which eventually results in a reduction of the functional vital capacity in the lungs. Due to the premature nature in the lungs in preterm and low birth weight infants, the lungs most often than not, are under developed, making them easily irritated and susceptible to lung injury within hours or days after birth. (Hadjiliadis, 2013) As the injury progresses, gas exchange become compromised causing a decrease in oxygenated blood to the lungs therefore triggering irritation and
Proper embryological development of the heart is crucial to proper functioning of the heart as an adult. The developing heart of a fetus follows several steps to ensure that the heart that develops has two way flow from atrium to ventricles to pulmonary or systemic circulation. While the steps in heart development are normally well controlled in a developing fetus, defects can arise and cause substantial problems postnatally. Specifically, when the embryological origin of the portioning between the left and right atria fails to develop normally, atrial septal defects can arise. Fortunately, there are surgicial options to prevent this defect and prevent interatrial mixing of oxygenated blood from the left atria with deoxygenated blood in the