Electrocardiography (ECG), in which electrodes are used to record the electrical activity of the heart, is not particularly helpful as no specific rhythms or ECG patterns can be used to detect PDA.A chest X-ray may be taken, which reveals overall heart size (as a reflection of the combined mass of the cardiac chambers) and the appearance of blood flow to the lungs. A small PDA most often accompanies a normal-sized heart and normal blood flow to the lungs. A large PDA generally accompanies an enlarged cardiac silhouette and increased blood flow to the lungs. Prevention
Some evidence suggests that intravenous NSAIDs, such as indomethacin, administration on the first day of life to all preterm infants reduces the risk of developing a PDA and the complications associated with PDA. Intravenous Indomethacin treatment in premature infants also may reduce the need for surgical intervention. Administering ibuprofen probably helps to prevent PDA and reduce the need for surgery but it also likely increases the risk of kidney complications. Treatment
Symptomatic PDA can be treated with both surgical and non-surgical methods. Conservative
Neonates without adverse symptoms may simply be monitored as outpatients. Surgery
Surgically, the DA may be closed by ligation (though support in premature infants is mixed). This can either be performed manually and be tied shut, or with intravascular coils or plugs that leads to formation of a thrombus in the DA.Devices developed by Franz Freudenthal block the blood vessel with woven structures of nitinol wire.Newer procedures performed effectively in older, bigger children include catheter PDA occlusion and video-assisted thoracoscopic PDA clipping.
Tissue culture studies have shown that arsenic compounds block both IKr and Iks channels and, at the same time, activate IK-ATP channels. Arsenic compounds also disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. These metabolic interferences lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. A post mortem reveals brick red colored mucosa, due to severe hemorrhage. Although arsenic causes toxicity, it can also play a protective role. Mechanism
Arsenite inhibits not only the formation of acetyl-CoA but also the enzyme succinic dehydrogenase. Arsenate can replace phosphate in many reactions. It is able to form Glc-6-arsenate in vitro; therefore it has been argued that hexokinase could be inhibited. (Eventually this may be a mechanism leading to muscle weakness in chronic arsenic poisoning.) In the glyceraldehyde 3-phosphate dehydrogenase reaction arsenate attacks the enzyme-bound thioester. The formed 1-arseno-3-phosphoglycerate is unstable and hydrolyzes spontaneously. Thus, ATP formation in glycolysis is inhibited while bypassing the phosphoglycerate kinase reaction. (Moreover, the formation of 2,3-bisphosphoglycerate in erythrocytes might be affected, followed by a higher oxygen affinity of hemoglobin and subsequently enhanced cyanosis.) As shown by Gresser (1981), submitochondrial particles synthesize adenosine-5-diphosphate-arsenate from ADP and arsenate in presence of succinate.