Prostaglandins and Indomethacin treatments for PDA
Chemical treatment for the patent ductus arteriosis (PDA) are some of the most common reasons that an echocardiographer will be called to the NICU to do an echocardiogram. These neonates are often severely premature and may or may not have a complex congenital defect.
Very often, the echocardiographer will be imaging these patients that are simply premature without a significant congenital abnormality, and they will primarily be evaluating the PDA and the direction of the shunt. When patients are born prematurely and they have an open PDA, this causes an inordinate amount of blood flow to be directed to the pulmonary circuit via the open PDA (left-to-right shunt). This results in pulmonary overflow and will result in pulmonary distress and wildly fluctuating SaO2 levels.
Indomethacin (or Indomyacin) is used when there is pulmonary overflow and the neonatologist wishes to close the PDA. Prostaglandins are used when the neonatologist wishes to keep the PDA open, often in the presence of complex defects in which pulmonary flow is severely compromised and the PDA may be the only shunt keeping the neonate alive.
Keep in mind that the PDA is a normal shunting process, and the body is programmed to close this shunt at 40 weeks of gestation. Neonates born prematurely (say 30 weeks or so) often continue to have a patent ductus. Indomethacin treatments may be done in an effort to close this shunt. This therapy is not always successful and as a result, the echocardiographer may be called back several times to evaluate the patency of the duct.
If chemical treatment is not successful, then a PDA ligation may be necessary. An untreated patent ductus is highly associated with patient morbidity and the inability of the patient to compensate for this pulmonary overcirculation must usually be treated.
Prostaglandin treatments are done in many cases of complex congenital defects where it is imperative that the PDA kept open in order to provide adequate blood flow to (especially) the pulmonary circuit, while the patient is waiting for surgical intervention. This is especially true when there is significant obstruction is the pulmonary circuit, such as Ebstein’s malformation of the tricuspid valve, pulmonary atresia, tetralogy of fallot, D-transpositions or certain types of truncus arteriosis.
Echocardiography is a routine procedure in most institutions to evaluate the patency of an arterial duct (PDA) prior to intervention, and to rule out any other cardiac defects. Early detection of these types of defects contribute significantly to positive patient outcomes. Clinical outcomes are significantly impacted of the magnitude of the shunt, and include such secondary problems such as left ventricular failure, renal insufficiency, pulmonary edema, hemorrhage and myocardial ischemia.
First, rule-out other significant cardiac defects. If the PDA is what you are concentrating on, determine whether the shunt is left-to-right, right-to-left or bi-directional. If the shunt is right-to-left or bi-directional, then this indicates severely high pulmonary pressures and is a development that the neonatologist must be made aware of. PDA shunts are best evaluated in the parasternal short axis views or the suprasternal short axis views.
Measure the size of the PDA and the magnitude of the shunt (measure the gradient across the PDA). Determine the direction of the shunt. Rule out any other cardiac defects. Most importantly, measure right ventricular systolic pressure (pulmonary pressures) adequately. (see my post on “Measuring RVSP”). It is critically important that the neonatologist or pediatric cardiologist know accurately what the pulmonary pressures are.
Persistent pulmonary hypertension in the neonate is the failure of the neonate’s lungs to accomplish a reduction in pulmonary vascular resistance to incoming pulmonary blood flow that leads to the inability of the lungs to fully oxygenate pulmonary blood flow.
Pressures in the lungs must be substantially lower than that of the systemic circulation in order for proper flow and oxygenation of the systemic blood flow to occur. (see my posts on the “Normal Heart” and Morphology” sections).
To summarize, blood flow in the body is dependent upon pressure and volume differences between the pulmonary and systemic circulations. Venous and pulmonary circulations contain a large volume of blood, but low pressures (venous pressures average between 5 and 20 mmHg).
Arterial volumes are low, but the pressures are very high (systemic blood pressure as measured with a BP cuff e.g. 120 mmHg). It is this difference in pressure that allows blood to move form a high pressure environment to a low pressure environment and back again. This difference in pressure and volume also dictates how efficiently oxygen and CO2 is transferred back and forth between the two systems.
As pulmonary pressures increase, this decreases ability of the body to transfer oxygen and CO2 across the capillary beds of the lungs and the tissues of the body.
Pulmonary hypertension must be addressed by the neonatologist or pediatric cardiologist in order to prevent long term lung damage. If the cause is an open PDA, then it will be ligated or corrected chemically. If there are significant congenital defects, then palliative procedures will be used until the neonate is ready for surgery. The primary treatment is oxygen therapy in order to alleviate hyoxaemia (low SaO2 levels).
The goal of chemical treatments is to reduce pulmonary pressures while maintaining systemic pressures until the neonate is able to undergo surgical treatment. Surgical interventions are usually done when the neonate achieves appropriate maturity to undergo these interventions.
Ken Heiden RDCS