Congenital Condition Of Congenital Heart Defects

Congenital heart disease is a cardiovascular condition resulting from an abnormality in the structure of the heart. The exact time this defect forms is unknown but it is during the fetal development in the womb. Researchers think the defect could be case partially by genetics and medical conditions of the fetus and the parents. If the baby’s mother had rubella, while pregnant or other conditions such as diabetes could have caused the defect. Some medications that were taken by a pregnant mother could also have caused birth defects. An error on chromosome 22 could also have caused the heart defect. Some symptoms that a person may have a congenital heart may not show up until later in life but many children also have the symptoms. Symptoms of a congenital heart defect are abnormal heartbeat, bluish tint to skin, shortness of breath, dizziness or fainting, and swelling of body tissues and organs.

Syndrome. Approximately half of all infants born with Down’s syndrome have a heart defect. Many of these defects have serious implications”

For both Atrial and Ventricular septal defect the size of the opening or hole affects how severe the child’s

Critical Congenital Heart Defect (CCHD) is a subgroup of congenital heart defects that normally necessitates surgical intervention or catheterization procedure during the neonatal period (Good, Canale, Goodman, & Yeager, 2015). According to Mahle et al. (2009), although there are measures taken to detect CCHD like prenatal ultrasound and comprehensive newborn physical examination during newborn’s birth hospitalization, there is still a significant percentage of newborns with CCHD that is left undetected and discharged home without being diagnosed. Delay in diagnosis of CCHD increases morbidity and mortality (Mahle et al., 2009). In response to this, Riede et al. (2010) mentioned that the diagnostic gap in CCHD could be bridged by screening newborns using pulse oximetry

In general, with every pregnancy there is a 3-5% chance of having a baby with a birth defect. If a woman takes Thalidomide during her first trimester of pregnancy, the chance of her giving birth to a child with a birth defect increased to a 20%+ chance and the fetal and infant death rate is estimated to be 40% or more due to severe birth defects. (Thalidomide Side Effects on Babies). A portion of the children who suffer from birth defects caused by Thalidomide also suffer from developmental disabilities such as autism. Thalidomide victim survivors still suffer from these symptoms today. How does Thalidomide create all of these issues? The answer is science. The placenta is a very important organ that develops in the womb during pregnancy. The placenta nourishes the baby through through the umbilical cord and gets rid of all waste. The placenta is the first line of defense for the baby. It is a barrier that many harmful substances do not have the ability to cross. Before a pharmaceutical is offered to

In December 2014, a study was published in Reproductive Toxicology that indicated a doubled risk of septal heart defects in infants whose mothers took Zofran during early pregnancy from

Lamotrigine is categorized as class C drug according to the pregnancy safety category (42)With overall risk for major congenital malformation estimated to be 2-3% based on registry based studies of pregnant women with epilepsy (30,44,69). Data obtained from the international lamotrigine pregnancy registry have shown that combination of lamotrigine with valproate has much higher rates for congenital malformations (10.7%) compared with lamotrigine monotherapy

From 1958 through 1961 a mild barbiturate wreaked havoc for expectant mothers and their fetuses. The drug was originally marketed in Europe, by a pharmaceutical company named Grunenthal. The, unknown at the time teratogen or placenta passing, drug is called Thalidomide. Its popularity grew quickly because it is nonlethal, even in overdose, and a deadly quantity has yet to be found. Thalidomide is still used today, despite the extraordinary suffering, it has caused. Alas, Thalidomide was prescribed to pregnant women to help them through pregnancy symptoms, caused thousands of infants to be born with terrible deformities and deficient in countless areas, and has made a life of struggles for the children of Thalidomide.

Having a diagnosis of Tetralogy of Fallot should mean having a death sentence. With an occurrence rate of 3 in every 10,000, it is the most common cause of cyanotic cardiac disease. [Wynbrandt, 366] There are four defects that commonly occur together; ventricular septal defect, hypertrophied right ventricle, malposition of the aorta, and pulmonary stenosis. For one to be diagnosed as a Tetralogy of Fallot baby, the patient must present with at least two of the four defects. Any one of these defects can cause serious catastrophe to the cardiac system. Combining these defects together makes it that much more complicated for the cardiologist to correct. Without the advancements made in cardiology, this diagnosis would mean certain death to the postnatal child.

Tetrology of Fallot(TOF) is the most common prenatal congenital cyanotic heart disease accounts for about 1/3600 live births and about 7% to 10% of of all congenital heart disease and is the most common cause of cyanosis in the neonatal period1 , 2. Typical Tetralogy of Fallot (TOF) may be missed in Four chamber view. An abnormal Four chamber view is rarely seen in typical TOF cases . In the typical form of TOF the fetal echocardiography is often characterized by a normal four-chamber view, a subaortic Ventricular septal defect (VSD), Dilated over riding of aorta seen in a LVOT view, Pulmonary stenosis and an increased Aorta/Pulmonary artery ratio, minimal antegrade flow in the main pulmonary artery and the aortic flow originated from right and left ventricle. All pregnant women with low risk factors , suspected fetal cardiac anomalies and with increased risk factors should be analyzed by extended fetal echo during the level 2 scan (18 – 22 weeks scan ). It is also important to identify the side of the aortic arch, which is quite easier in the prenatal period in three vessel view . This will be useful if surgery is planned postnatally. Extracardiac abnormalities, such as midline defects, central nervous system and renal abnormalities may be found in fetuses with TOF. These extracardiac defects are associated with chromosomal abnormalities. When TOF is diagnosed, serial follow up scans at 5 – 6 weeks intervals are adviced to know about the growth of the

Due to great progress in genetic testing during the last decade, there is an increasing awareness of congenital heart diseases that give a higher risk of sudden cardiac death (SCD). A good example of such heart disease is the congenital Long QT Syndrome (LQTS). This disorder is a leading cause of SCD in the non-adult population.1 Ion channels responsible for the ventricular repolarization are mutated, causing a prolongation of the QT-interval on ECG.2 This aberrant repolarization of the heart gives a risk of the occurrence of ventricular arrhythmias, called torsades de pointes. These arrhythmias are mainly precipitated by emotional or physical stress2 and cause symptoms such as syncope or cardiac arrest.

Exposure to the maternal SSA/Ro (Anti-Sjögren’s-syndrome-related antigen A, also called anti-Ro) antibody has been recently associated with complications of the atrioventricular node, or the node in the heart that electrically connects the atrial and ventricular chambers, during the fourth and fifth month of in utero life, often resulting in fetal congenital heart block (Satoh, 2012). This complication is fatal in approximately one in five infants, and the surviving infants will face life-long heart complications including, but not limited to, the necessity of pacemaker use and further surgery. It is estimated that 1 in 50 women who are anti-Ro positive will have a fetus that develops congenital heart block.

Several chronic maternal medical conditions, including diabetes mellitus, hypertension, connective tissue disorders, and congenital heart disease confer an increased risk of CHD in the offspring. (3)

ithdrawal symptoms from Zolpidem are thought to occur as the newborn baby’s body has to adapt to no longer getting certain types of medicines through the placenta. Since Zolpidem has not been studied separately, there is no scientific information as to whether taking zolpidem in pregnancy could cause a baby to experience withdrawal symptoms. However, because zolpidem is similar to other medicines that are known to cause neonatal withdrawal, close monitoring of babies for a few days after birth may be advised if Zolpidem has been taken regularly in the weeks before delivery. With breastfeeding, Zolpidem does pass to the baby through breast milk (CITE). However, little known is known in terms of contraindications. There have been no reports of

The drugs that are used to treat neonates can be used multipurposely and often innovation drives creative uses of drugs to treat uncommon multifactorial complications (Allegaert & van den Anker, 2015). Knowledge of the drugs and their adverse effects is increasingly important when dosing a neonate. Due to their undeveloped body systems, in an event of an undesired reaction or drug error, the neonate would not be able to compensate and recover like the other patient groups may (Skene, Gupta, Flaherty, & Sherwood, 2012). Furthermore, this stresses the importance of being competent in drug calculations and being aware of the effect of medicines on this particularly vulnerable patient group (Stavroudis, Shore, Morlock, Hicks, Bundy, & Miller,