A patent ductus arteriosus (PDA) is common in preterm infants, occurring in 15-65% of very low birth weight infants. The ductus arteriosus normally closes after birth to direct blood flow to the lungs, but in preterm infants closure may be delayed. A PDA can cause left-to-right shunting, increasing cardiac output but reducing blood flow and oxygenation to vital organs. Echocardiography is the gold standard for diagnosing and assessing the severity of a PDA, but treatment should not be based on echocardiographic criteria alone and requires consideration of clinical symptoms. While PDA closure interventions are effective, evidence for long term benefits is inconclusive, so
This document discusses the patent ductus arteriosus (PDA), including its anatomy, physiology, diagnosis, and management. It begins with an overview of fetal circulation and the normal transition to circulation after birth. It then covers the anatomy of the PDA, associated anomalies, diagnosis using physical exam findings and imaging tests, complications of an untreated PDA, and approaches to medical and surgical treatment. Key points include that a PDA allows blood to shunt from the pulmonary artery to the aorta in the fetus but normally closes after birth, and preterm infants are more likely to have a PDA that remains open, sometimes requiring treatment.
Patent ductus arteriosus (PDA) is a congenital disorder in the heart wherein a neonate's ductus arteriosus fails to close after birth. Early symptoms are uncommon, but in the first year of life include increased work of breathing and poor weight gain. With age, the PDA may lead to congestive heart failure if left uncorrected. The ductus arteriosus is a normal fetal blood vessel that closes soon after birth. In a patent ductus arteriosus (PDA) the vessel does not close and remains "patent" (open) resulting in irregular transmission of blood between two of the most important arteries close to the heart, the aorta and the pulmonary artery. PDA is common in neonates with persistent respiratory problems such as hypoxia, and has a high occurrence in premature children. In hypoxic newborns, too little oxygen reaches the lungs to produce sufficient levels of bradykinin and subsequent closing of the DA. Premature children are more likely to be hypoxic and thus have PDA because of their underdeveloped heart and lungs.
A patent ductus arteriosus allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs. This uses more calories than normal and often interferes with feeding in infancy. This condition, as a constellation of findings, is called congestive heart failure.
In some cases, such as in transposition of the great vessels (the pulmonary artery and the aorta), a PDA may need to remain open. In this cardiovascular condition, the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the patent ductus arteriosus open
International conference «Actual approaches to the extremely preterm babies: International experience and Ukrainian realities» (Kyiv, Ukraine, March 5-6, 2013)
Patent ductus arteriosus (PDA) is the persistent opening of the ductus arteriosus after birth, allowing blood to flow from the aorta to the pulmonary artery. It is common in preterm infants under 1.5kg. Untreated PDA can lead to pulmonary overload and congestive heart failure. Symptoms include tachypnea, bounding pulse, and frequent respiratory infections. Diagnosis involves physical exam, chest x-ray, echocardiogram, and cardiac catheterization. Treatment options include medications to close the ductus like indomethacin or surgery to ligate the ductus if medications fail or for symptomatic patients. Complications can include congestive heart failure, infective end
Patent Ductus Arteroisus, PDA, Cardiology, Paediatrics, Pedicatrics, Critical Care, Emergency medicine, Medicine, Internal Medicine, MBBD, MD, India, CMC Vellore, Christian Medical College
The document discusses the management of patent ductus arteriosus (PDA) in preterm infants. PDA occurs in 31% of very low birth weight infants and can be left untreated in some cases. Treatment may include conservative management, pharmacological closure with drugs like indomethacin or ibuprofen, or surgical ligation if drugs fail. Prophylactic drug treatment may help prevent complications in very preterm infants under 25 weeks gestation. The optimal management of PDA in infants under 800g is still debated, as untreated PDA carries risks but interventions also pose dangers.
THIS SLIDE IS PREPARED BY SURESH KUMAR FOR MY STUDENT SUPPORT SYSTEM TO WATCH THIS VIDEO VISIT YOUTUBE CHANNEL- https://www.youtube.com/channel/UC3tfqlf__moHj8s4W7w6HQQ
YOU CAN JOIN FACEBOOK GROUP FOR MORE SUCH VIDEOS BY THIS LINK- https://www.facebook.com/groups/241390897133057/
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,#patentductusarteriosus,#PDA,#birthdefects,#childhealthnursing#anm,#gnm,#bscnursing
PDA closure
G Agnoletti
Citta’ della Salute
gagnoletti@cittadellasalute.to.it
Torino, Italy
IPC 9th Milan, March 2013
The document discusses various methods for percutaneously closing a patent ductus arteriosus (PDA), including using coils, occlusive devices like the Amplatzer Duct Occluder (ADO) systems, and the Nit-Occlud PDA-R device. It summarizes the advantages and disadvantages of different approaches for closing PDAs in various patient populations, from preterm infants to children and adults. The document concludes that while percutaneous closure of
This document discusses the patent ductus arteriosus (PDA), including its anatomy, physiology, diagnosis, and management. It begins with an overview of fetal circulation and the normal transition to circulation after birth. It then covers the anatomy of the PDA, associated anomalies, diagnosis using physical exam findings and imaging tests, complications of an untreated PDA, and approaches to medical and surgical treatment. Key points include that a PDA allows blood to shunt from the pulmonary artery to the aorta in the fetus but normally closes after birth, and preterm infants are more likely to have a PDA that remains open, sometimes requiring treatment.
Patent ductus arteriosus (PDA) is a congenital disorder in the heart wherein a neonate's ductus arteriosus fails to close after birth. Early symptoms are uncommon, but in the first year of life include increased work of breathing and poor weight gain. With age, the PDA may lead to congestive heart failure if left uncorrected. The ductus arteriosus is a normal fetal blood vessel that closes soon after birth. In a patent ductus arteriosus (PDA) the vessel does not close and remains "patent" (open) resulting in irregular transmission of blood between two of the most important arteries close to the heart, the aorta and the pulmonary artery. PDA is common in neonates with persistent respiratory problems such as hypoxia, and has a high occurrence in premature children. In hypoxic newborns, too little oxygen reaches the lungs to produce sufficient levels of bradykinin and subsequent closing of the DA. Premature children are more likely to be hypoxic and thus have PDA because of their underdeveloped heart and lungs.
A patent ductus arteriosus allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs. This uses more calories than normal and often interferes with feeding in infancy. This condition, as a constellation of findings, is called congestive heart failure.
In some cases, such as in transposition of the great vessels (the pulmonary artery and the aorta), a PDA may need to remain open. In this cardiovascular condition, the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the patent ductus arteriosus open
International conference «Actual approaches to the extremely preterm babies: International experience and Ukrainian realities» (Kyiv, Ukraine, March 5-6, 2013)
Patent ductus arteriosus (PDA) is the persistent opening of the ductus arteriosus after birth, allowing blood to flow from the aorta to the pulmonary artery. It is common in preterm infants under 1.5kg. Untreated PDA can lead to pulmonary overload and congestive heart failure. Symptoms include tachypnea, bounding pulse, and frequent respiratory infections. Diagnosis involves physical exam, chest x-ray, echocardiogram, and cardiac catheterization. Treatment options include medications to close the ductus like indomethacin or surgery to ligate the ductus if medications fail or for symptomatic patients. Complications can include congestive heart failure, infective end
Patent Ductus Arteroisus, PDA, Cardiology, Paediatrics, Pedicatrics, Critical Care, Emergency medicine, Medicine, Internal Medicine, MBBD, MD, India, CMC Vellore, Christian Medical College
The document discusses the management of patent ductus arteriosus (PDA) in preterm infants. PDA occurs in 31% of very low birth weight infants and can be left untreated in some cases. Treatment may include conservative management, pharmacological closure with drugs like indomethacin or ibuprofen, or surgical ligation if drugs fail. Prophylactic drug treatment may help prevent complications in very preterm infants under 25 weeks gestation. The optimal management of PDA in infants under 800g is still debated, as untreated PDA carries risks but interventions also pose dangers.
THIS SLIDE IS PREPARED BY SURESH KUMAR FOR MY STUDENT SUPPORT SYSTEM TO WATCH THIS VIDEO VISIT YOUTUBE CHANNEL- https://www.youtube.com/channel/UC3tfqlf__moHj8s4W7w6HQQ
YOU CAN JOIN FACEBOOK GROUP FOR MORE SUCH VIDEOS BY THIS LINK- https://www.facebook.com/groups/241390897133057/
FOR MAKING EASY NOTES YOU CAN ALSO VISIT MY BLOG - https://mynursingstudents.blogspot.com/
Instagram- https://www.instagram.com/mystudentsupportsystem_nursing/
Twitter-https://twitter.com/student_system?s=08
,#patentductusarteriosus,#PDA,#birthdefects,#childhealthnursing#anm,#gnm,#bscnursing
PDA closure
G Agnoletti
Citta’ della Salute
gagnoletti@cittadellasalute.to.it
Torino, Italy
IPC 9th Milan, March 2013
The document discusses various methods for percutaneously closing a patent ductus arteriosus (PDA), including using coils, occlusive devices like the Amplatzer Duct Occluder (ADO) systems, and the Nit-Occlud PDA-R device. It summarizes the advantages and disadvantages of different approaches for closing PDAs in various patient populations, from preterm infants to children and adults. The document concludes that while percutaneous closure of
Patent ductus arteriosis types evaluation and management (2)Aswin Rm
1) Patent ductus arteriosus (PDA) is a persistent opening between the aorta and pulmonary artery that normally closes shortly after birth. It can be classified based on its shape and the location of any narrowing.
2) A PDA causes excess blood to flow from the aorta to the pulmonary artery, putting strain on the left side of the heart and potentially causing heart failure. The murmur produced by a PDA is continuous.
3) Diagnosis involves a physical exam finding a machinery murmur and confirming with an echocardiogram. Treatment depends on severity and may involve medications to close the ductus or interventional catheterization procedures.
Patent ductus arteriosus A long case presentationNizam Uddin
The document discusses the history, diagnosis, and management of patent ductus arteriosus (PDA), including the timeline of surgical and transcatheter closure techniques. PDA is a persistent opening between the aorta and pulmonary artery that normally closes shortly after birth; if it remains open, closure may be recommended depending on the size of the shunt. Transcatheter closure has largely replaced surgery as the treatment of choice, with high success rates using devices designed to occlude the opening in the PDA.
Patent Ductus Arteriosus: Clinical manifestation and DiagnosisNinia Kabir
Descriptive and informative facts about Patent Ductus Arteriosus focusing on its clinical features, physical findings, natural course and diagnostic work up. The diagnostic work up does not include Echocardiography in this presentation.
The patent ductus arteriosus (PDA) is a fetal blood vessel that normally closes after birth. It connects the pulmonary artery to the aorta. During fetal life, it allows most blood to bypass the high-resistance lungs and go to the systemic circulation. After birth, factors like decreased prostaglandins and increased oxygen cause the PDA to contract and close within 3 weeks. A PDA that remains open is called a patent ductus arteriosus. This allows oxygenated blood to shunt from the aorta back to the pulmonary artery, overloading the left heart and lungs. If left untreated, it can cause the pulmonary vascular resistance to rise over time and reverse the shunt to become right-
This document summarizes information presented by Dr. Stefan Johansson on the patent ductus arteriosus (PDA). It discusses the definition, diagnosis, treatment, and management of PDA in preterm infants. Specifically, it notes that echocardiography is important for visualizing and defining a hemodynamically significant PDA. It also reviews different treatment approaches for PDA including medical treatment with ibuprofen or indomethacin and the need for more research on optimal dosing schedules and timing of treatment.
A 30-minute talk, presented as part of the weekly teaching activities in Alder Hey Children's Hospital (Liverpool, UK). It addresses PDA evaluation in children - starting with embryology & anatomy with the basis behind physiological closure versus patency after birth. What is the role of echo study in diagnosing/evaluating PDA? Modes used with some clear movies? Its limitations?
This document discusses anaesthetic considerations for closed heart procedures including those correcting lesions like patent ductus arteriosus and coarctation of the aorta, as well as palliative procedures like banding of the pulmonary artery. It covers the relevant anatomy, pathophysiology, clinical presentation, diagnosis and management of these conditions. Specifically, it emphasizes the importance of invasive hemodynamic monitoring during surgery due to risks of hypotension and paraplegia from spinal cord ischemia. Careful blood pressure control is needed during and after the procedures.
This document discusses atrial septal defect (ASD), an acyanotic congenital heart disease where there is an abnormal opening in the septum between the two upper chambers of the heart. It describes the different types of ASD, symptoms like breathlessness and frequent infections, physical exam findings like widened heart sounds, investigations like chest X-ray and echocardiogram, and management including medical treatment and surgical closure of the defect. Complications, natural history, associated conditions and differences between ostium secundum and primum defects are also summarized.
This document provides information about critical congenital heart diseases (CCHD). It discusses the importance of CCHD as heart defects are a leading cause of birth defect deaths. Approximately 1 in 4 babies born with a heart defect has a CCHD, which often requires surgery or procedures in the first year of life. The document outlines the primary and secondary targets for CCHD screening, including conditions like hypoplastic left heart syndrome and transposition of the great arteries. Risk factors for CCHD can include genetic conditions and environmental exposures. Timely screening and treatment of CCHDs is important to prevent disability and death in newborns.
The document provides an overview of patent ductus arteriosus (PDA). Some key points:
1. PDA is more common in preterm infants, occurring in up to 80% of infants weighing less than 1000g. It refers to the failure of the ductus arteriosus to close after birth.
2. Diagnosis is typically made using echocardiography. Symptoms can include respiratory issues, apnea, heart murmur, and increased work of breathing.
3. Treatment involves supportive care initially and drug therapy with indomethacin or ibuprofen to close the ductus. Surgery may be needed for larger PDAs or those that do not close with medication
The ductus arteriosus is a normal fetal connection that allows blood to bypass the lungs and flow directly to the systemic circulation. After birth, it usually closes within 48 hours, but sometimes remains patent (open), resulting in a condition called patent ductus arteriosus (PDA). A PDA allows blood from the aorta to flow back into the pulmonary artery, overloading the lungs. Symptoms range from none with small PDAs to congestive heart failure with large ones. Diagnosis involves listening for a heart murmur and using echocardiography. Treatment options include medications to close the ductus, catheter procedures, or surgery.
This document discusses the perinatal management of a newborn with congenital heart disease. Key details include:
- The newborn was delivered via c-section, needed intubation, and had low oxygen saturation levels. Echocardiogram revealed a congenital heart defect.
- Risk factors and causes of congenital heart defects are discussed, including maternal conditions, genetics, infections, and drugs.
- Screening methods like pulse oximetry can help identify defects, though timing and factors can impact results. Criteria for positive screens are outlined.
- Initial management may include supportive care, antibiotics, prostaglandin E1, and referral for cardiac procedures or surgery depending on the defect.
The document discusses the Patent Ductus Arteriosus (PDA), which is a persistent opening between the pulmonary artery and the aorta that usually closes shortly after birth. It provides details on the epidemiology, pathophysiology, clinical features, diagnostic measures, and management of PDA. PDA is more common in preterm infants and left untreated can cause complications like pulmonary hypertension, congestive heart failure, and infections. Treatment involves the use of medications like indomethacin or ibuprofen to close the opening or surgical ligation if medications fail. Nursing care focuses on relieving respiratory distress, improving cardiac output and oxygenation, adequate nutrition, and preventing infections.
The document discusses treatment options for patent ductus arteriosus (PDA) in infants. There are three main options: medical management using drugs like indomethacin or ibuprofen, catheter-based procedures to close the PDA, or surgical intervention. Medical management is usually the first approach using anti-inflammatory drugs and involves balancing treatment against potential renal or gastrointestinal side effects. If medical management fails, catheter or surgical closure may be considered, with catheter procedures preferred if the PDA is suitable due to lower risks. Surgical ligation is an option when other approaches are not viable or have failed.
This document discusses several congenital heart diseases including patent ductus arteriosus (PDA) and coarctation of the aorta. For PDA, the ductus arteriosus fails to close after birth which allows excess blood to flow to the lungs. Left untreated it can cause pulmonary hypertension and heart failure. Coarctation of the aorta is a narrowing of the aorta near the ductus arteriosus which restricts blood flow and can lead to high blood pressure if not corrected. Both conditions are typically diagnosed via echocardiogram and may require drug treatment or surgery to repair the abnormalities.
The document discusses acyanotic heart disease, which refers to congenital heart defects present at birth that do not cause cyanosis. Common types include atrial septal defect, ventricular septal defect, and patent ductus arteriosus. These defects cause diminished pulmonary blood flow due to left-to-right shunting. Symptoms may not be present initially but can develop over months or years and include dyspnea, fatigue, and heart failure. Diagnosis involves physical exam, chest x-ray, ECG, and echocardiogram. Treatment depends on the severity but may involve surgery to correct the structural abnormality, with earlier intervention reducing long-term risks from conditions like pulmonary hypertension.
Ventricular Septal Defect (VSD) is a developmental defect allowing shunting of blood between the left and right ventricles. It is the most common congenital heart defect, accounting for 25% of cases. VSDs occur when the interventricular septum fails to fuse properly during embryonic development of the heart. Small VSDs often close spontaneously, while large VSDs can cause heart failure if not surgically repaired before irreversible pulmonary damage. Surgical repair has excellent outcomes, restoring a normal heart size and function while preventing complications like Eisenmenger's syndrome.
1. The document discusses various types of acyanotic congenital heart disease including ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), and coarctation of aorta.
2. It provides details on the classification, symptoms, diagnosis, and treatment options for each condition.
3. The conditions are characterized by shunting of blood between the left and right sides of the heart without cyanosis, and can cause heart failure if left untreated.
This study aimed to evaluate myocardial injury in children with unoperated congenital heart diseases using cardiac troponin I levels. The study found an 80% incidence of elevated cTnI levels in children with CHDs, indicating a high prevalence of myocardial injury. Univariate analysis revealed significant correlations between higher cTnI levels and hemodynamic factors like higher pulmonary to systemic blood flow and pressure ratios. The study concludes that cTnI is a useful marker for detecting myocardial injury in children with unoperated CHDs.
This document summarizes a seminar on cardiac arrhythmia and its treatment. It discusses the epidemiology of cardiac arrhythmia, noting it affects between 180,000-450,000 people annually in the US. It also discusses the genetics involved, noting mutations in ion channel genes can cause long QT syndrome, short QT syndrome, and Brugada syndrome. The document also provides a detailed classification and discussion of drug treatments for cardiac arrhythmia, separating drugs into Classes I-III.
Patent ductus arteriosis types evaluation and management (2)Aswin Rm
1) Patent ductus arteriosus (PDA) is a persistent opening between the aorta and pulmonary artery that normally closes shortly after birth. It can be classified based on its shape and the location of any narrowing.
2) A PDA causes excess blood to flow from the aorta to the pulmonary artery, putting strain on the left side of the heart and potentially causing heart failure. The murmur produced by a PDA is continuous.
3) Diagnosis involves a physical exam finding a machinery murmur and confirming with an echocardiogram. Treatment depends on severity and may involve medications to close the ductus or interventional catheterization procedures.
Patent ductus arteriosus A long case presentationNizam Uddin
The document discusses the history, diagnosis, and management of patent ductus arteriosus (PDA), including the timeline of surgical and transcatheter closure techniques. PDA is a persistent opening between the aorta and pulmonary artery that normally closes shortly after birth; if it remains open, closure may be recommended depending on the size of the shunt. Transcatheter closure has largely replaced surgery as the treatment of choice, with high success rates using devices designed to occlude the opening in the PDA.
Patent Ductus Arteriosus: Clinical manifestation and DiagnosisNinia Kabir
Descriptive and informative facts about Patent Ductus Arteriosus focusing on its clinical features, physical findings, natural course and diagnostic work up. The diagnostic work up does not include Echocardiography in this presentation.
The patent ductus arteriosus (PDA) is a fetal blood vessel that normally closes after birth. It connects the pulmonary artery to the aorta. During fetal life, it allows most blood to bypass the high-resistance lungs and go to the systemic circulation. After birth, factors like decreased prostaglandins and increased oxygen cause the PDA to contract and close within 3 weeks. A PDA that remains open is called a patent ductus arteriosus. This allows oxygenated blood to shunt from the aorta back to the pulmonary artery, overloading the left heart and lungs. If left untreated, it can cause the pulmonary vascular resistance to rise over time and reverse the shunt to become right-
This document summarizes information presented by Dr. Stefan Johansson on the patent ductus arteriosus (PDA). It discusses the definition, diagnosis, treatment, and management of PDA in preterm infants. Specifically, it notes that echocardiography is important for visualizing and defining a hemodynamically significant PDA. It also reviews different treatment approaches for PDA including medical treatment with ibuprofen or indomethacin and the need for more research on optimal dosing schedules and timing of treatment.
A 30-minute talk, presented as part of the weekly teaching activities in Alder Hey Children's Hospital (Liverpool, UK). It addresses PDA evaluation in children - starting with embryology & anatomy with the basis behind physiological closure versus patency after birth. What is the role of echo study in diagnosing/evaluating PDA? Modes used with some clear movies? Its limitations?
This document discusses anaesthetic considerations for closed heart procedures including those correcting lesions like patent ductus arteriosus and coarctation of the aorta, as well as palliative procedures like banding of the pulmonary artery. It covers the relevant anatomy, pathophysiology, clinical presentation, diagnosis and management of these conditions. Specifically, it emphasizes the importance of invasive hemodynamic monitoring during surgery due to risks of hypotension and paraplegia from spinal cord ischemia. Careful blood pressure control is needed during and after the procedures.
This document discusses atrial septal defect (ASD), an acyanotic congenital heart disease where there is an abnormal opening in the septum between the two upper chambers of the heart. It describes the different types of ASD, symptoms like breathlessness and frequent infections, physical exam findings like widened heart sounds, investigations like chest X-ray and echocardiogram, and management including medical treatment and surgical closure of the defect. Complications, natural history, associated conditions and differences between ostium secundum and primum defects are also summarized.
This document provides information about critical congenital heart diseases (CCHD). It discusses the importance of CCHD as heart defects are a leading cause of birth defect deaths. Approximately 1 in 4 babies born with a heart defect has a CCHD, which often requires surgery or procedures in the first year of life. The document outlines the primary and secondary targets for CCHD screening, including conditions like hypoplastic left heart syndrome and transposition of the great arteries. Risk factors for CCHD can include genetic conditions and environmental exposures. Timely screening and treatment of CCHDs is important to prevent disability and death in newborns.
The document provides an overview of patent ductus arteriosus (PDA). Some key points:
1. PDA is more common in preterm infants, occurring in up to 80% of infants weighing less than 1000g. It refers to the failure of the ductus arteriosus to close after birth.
2. Diagnosis is typically made using echocardiography. Symptoms can include respiratory issues, apnea, heart murmur, and increased work of breathing.
3. Treatment involves supportive care initially and drug therapy with indomethacin or ibuprofen to close the ductus. Surgery may be needed for larger PDAs or those that do not close with medication
The ductus arteriosus is a normal fetal connection that allows blood to bypass the lungs and flow directly to the systemic circulation. After birth, it usually closes within 48 hours, but sometimes remains patent (open), resulting in a condition called patent ductus arteriosus (PDA). A PDA allows blood from the aorta to flow back into the pulmonary artery, overloading the lungs. Symptoms range from none with small PDAs to congestive heart failure with large ones. Diagnosis involves listening for a heart murmur and using echocardiography. Treatment options include medications to close the ductus, catheter procedures, or surgery.
This document discusses the perinatal management of a newborn with congenital heart disease. Key details include:
- The newborn was delivered via c-section, needed intubation, and had low oxygen saturation levels. Echocardiogram revealed a congenital heart defect.
- Risk factors and causes of congenital heart defects are discussed, including maternal conditions, genetics, infections, and drugs.
- Screening methods like pulse oximetry can help identify defects, though timing and factors can impact results. Criteria for positive screens are outlined.
- Initial management may include supportive care, antibiotics, prostaglandin E1, and referral for cardiac procedures or surgery depending on the defect.
The document discusses the Patent Ductus Arteriosus (PDA), which is a persistent opening between the pulmonary artery and the aorta that usually closes shortly after birth. It provides details on the epidemiology, pathophysiology, clinical features, diagnostic measures, and management of PDA. PDA is more common in preterm infants and left untreated can cause complications like pulmonary hypertension, congestive heart failure, and infections. Treatment involves the use of medications like indomethacin or ibuprofen to close the opening or surgical ligation if medications fail. Nursing care focuses on relieving respiratory distress, improving cardiac output and oxygenation, adequate nutrition, and preventing infections.
The document discusses treatment options for patent ductus arteriosus (PDA) in infants. There are three main options: medical management using drugs like indomethacin or ibuprofen, catheter-based procedures to close the PDA, or surgical intervention. Medical management is usually the first approach using anti-inflammatory drugs and involves balancing treatment against potential renal or gastrointestinal side effects. If medical management fails, catheter or surgical closure may be considered, with catheter procedures preferred if the PDA is suitable due to lower risks. Surgical ligation is an option when other approaches are not viable or have failed.
This document discusses several congenital heart diseases including patent ductus arteriosus (PDA) and coarctation of the aorta. For PDA, the ductus arteriosus fails to close after birth which allows excess blood to flow to the lungs. Left untreated it can cause pulmonary hypertension and heart failure. Coarctation of the aorta is a narrowing of the aorta near the ductus arteriosus which restricts blood flow and can lead to high blood pressure if not corrected. Both conditions are typically diagnosed via echocardiogram and may require drug treatment or surgery to repair the abnormalities.
The document discusses acyanotic heart disease, which refers to congenital heart defects present at birth that do not cause cyanosis. Common types include atrial septal defect, ventricular septal defect, and patent ductus arteriosus. These defects cause diminished pulmonary blood flow due to left-to-right shunting. Symptoms may not be present initially but can develop over months or years and include dyspnea, fatigue, and heart failure. Diagnosis involves physical exam, chest x-ray, ECG, and echocardiogram. Treatment depends on the severity but may involve surgery to correct the structural abnormality, with earlier intervention reducing long-term risks from conditions like pulmonary hypertension.
Ventricular Septal Defect (VSD) is a developmental defect allowing shunting of blood between the left and right ventricles. It is the most common congenital heart defect, accounting for 25% of cases. VSDs occur when the interventricular septum fails to fuse properly during embryonic development of the heart. Small VSDs often close spontaneously, while large VSDs can cause heart failure if not surgically repaired before irreversible pulmonary damage. Surgical repair has excellent outcomes, restoring a normal heart size and function while preventing complications like Eisenmenger's syndrome.
1. The document discusses various types of acyanotic congenital heart disease including ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), and coarctation of aorta.
2. It provides details on the classification, symptoms, diagnosis, and treatment options for each condition.
3. The conditions are characterized by shunting of blood between the left and right sides of the heart without cyanosis, and can cause heart failure if left untreated.
This study aimed to evaluate myocardial injury in children with unoperated congenital heart diseases using cardiac troponin I levels. The study found an 80% incidence of elevated cTnI levels in children with CHDs, indicating a high prevalence of myocardial injury. Univariate analysis revealed significant correlations between higher cTnI levels and hemodynamic factors like higher pulmonary to systemic blood flow and pressure ratios. The study concludes that cTnI is a useful marker for detecting myocardial injury in children with unoperated CHDs.
This document summarizes a seminar on cardiac arrhythmia and its treatment. It discusses the epidemiology of cardiac arrhythmia, noting it affects between 180,000-450,000 people annually in the US. It also discusses the genetics involved, noting mutations in ion channel genes can cause long QT syndrome, short QT syndrome, and Brugada syndrome. The document also provides a detailed classification and discussion of drug treatments for cardiac arrhythmia, separating drugs into Classes I-III.
Low dose dopamine increases GFR and RBF. The DAD-HF trial investigated 60 patients randomized to low dose furosemide (continuous infusion 0.5 mg/kg/day) with or without low dose dopamine (2 μg/kg/min). Dopamine preserved renal function compared to furosemide alone in patients with acute decompensated heart failure. There were no significant differences found in a trial comparing high vs low dose furosemide or bolus vs continuous infusion on renal function or symptoms. Novel agents targeting fluid overload, renal function, contractility, and vasomotion may provide new therapeutic options for acute heart failure.
Prof. U. C. SAMAL provides an overview of acute decompensated heart failure and what is new in the field. He discusses similarities and differences between acute myocardial infarction and acute heart failure syndromes. Mortality rates are high for both conditions, though clinical benefits of interventions are greater for acute MI based on published clinical trials. The document then discusses definitions and classifications of acute heart failure syndromes, as well as guidelines for diagnosis and treatment from ESC and ACC/AHA. Biomarkers that can help with diagnosis, prognosis, and guiding therapy are also summarized.
The document discusses the goals and performance of radionuclide imaging for diagnosis and prognosis of coronary artery disease (CAD). It notes that radionuclide imaging has high sensitivity but moderate specificity for detecting CAD based on angiography. A normal stress myocardial perfusion imaging (MPI) study is associated with a low cardiac event risk over 2 years, but risk factors can increase risk. Abnormal MPI can occur with preserved coronary arteries due to endothelial dysfunction.
Critical congenital heart disease (CCHD) can cause cyanosis in newborns. Cyanosis is a bluish discoloration of the skin due to low oxygen levels in the blood. It is an important sign of CCHD that requires prompt evaluation and treatment. Diagnostic tests for newborns with cyanosis include a hyperoxia test, hyperventilation test, physical exam, electrocardiogram, and chest x-ray. These tests help differentiate between cardiac and pulmonary causes of cyanosis and identify those newborns with CCHD who require urgent cardiac intervention. Early diagnosis of CCHD is important because delays can lead to significant morbidity and mortality.
CARDIAC COMPLICATIONS & ITS MANAGEMENT OF CKDMohd Tariq Ali
Uremic cardiomyopathy is the primary manifestation of cardiac complications in patients with chronic kidney disease. It results from the combined effects of pressure and volume overload on the heart from conditions like hypertension as well as the uremic state itself. This leads to left ventricular hypertrophy initially as an adaptive response but later maladaptive changes like cardiomyocyte death, fibrosis, and dilated cardiomyopathy if left unmanaged. Early initiation of hemodialysis, preferably non-conventional daily or nocturnal dialysis, can help halt progression of uremic cardiomyopathy while kidney transplantation has been shown to reverse it.
The document discusses several factors related to arrhythmias and their potential to cause symptoms. The type and origin of the arrhythmia can influence whether it is symptomatic. Short, isolated episodes are less likely to cause symptoms than sustained episodes of the same rhythm abnormality. Faster heart rates, lower ejection fractions, and the presence of comorbidities make arrhythmias more likely to be symptomatic.
Linking HFpEF and Chronic kidney disease magdy elmasry
Cardio-renal interactions
Introducing nephro-cardiology
{ or cardio-nephrology }
Where are we in 2022 with HFpEF ?CKD in HFpEF { or HFpEF in CKD } Cardiorenal
Syndrome .Four-step
HFA-PEFF diagnostic algorithm
heterogeneity in patients with HFpEF.Phenotyping HFpEF :
Beyond EF.Management of HFpEF .patients with HF on dialysis
Catheterisation study and operability assessmentIndia CTVS
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1. Patent Ductus Arteriosus
in Preterm Neonates
Introduction
Patent ductus arteriosus (PDA) is a major morbidity seen in premature infants, with its incidence being
inversely related to gestational age and birth weight. Studies report incidence of 15-40% in very low
birth weight infants (<1500g) where as in premature extremely low birth weight infants (<28weeks; <
1000g) it’s as high as 50-65%.1,2
The closure of ductus arteriosus (DA) following birth is an important component of transitional
circulation, thereby directing the entire right ventricular output to the lungs to facilitate its oxygenation.
Contrary to this the ductus arteriosus acts as conduit for diverting the partially oxygenated blood to
support systemic circulation in fetus. The closure of DA is mediated by a shift in balance of
vasoconstricting (endothelin) and dilating (PGE2) mediators, which in turn is mediated by increased
oxygenation and reduced flow through the DA. Premature infants are at increased risk of PDA due to
elevated levels of PGE2, increased PGE2 receptor levels and reduced intrinsic vascular tone as a result of
weak actin myosin complex formation. Generally the ductus arteriosus functionally close in term infants
by 12-24 hrs, whereas the closure may be delayed by 3-5 days in preterm neonates.3
Hemodynamic consequences of PDA
The presence of PDA has significant effects on myocardial functions as well as systemic and pulmonary
blood flow. Preterm newborns adapts, by increasing the left ventricular contractility, and thereby
maintaining the effective systemic blood flow even when the left to right shunts equals 50% of the left
ventricular output∙4
This is mainly accomplished by increase in stroke volume (SV) rather than heart rate.
Despite the increased left ventricular output, there is significant redistribution of blood flow to major
organ systems, with the presence of ductal steal due to left to right shunt. There is flow across the
ductus all throughout the cardiac cycle, the direction of which depends on the difference between
systemic and pulmonary pressures. Usually there is shunting from systemic to pulmonary circulation
called ductal steal, the maximum of which occurs at the beginning of the cardiac systole when the
pressure gradient is maximum. Contrary to the belief that ductal run off occurs only in diastole, it is
present all throughout the cardiac cycle. However, its effect on systemic circulation is best
demonstrated on echocardiogram during diastole, as a retrograde flow in the descending aorta, or other
systemic vessels on Doppler, instead of the normal low velocity forward flow. This steal phenomenon
may lead to systemic hypo perfusion, despite increased cardiac output. Hence hemodynamically
significant PDA has negative effect on cerebral circulation and oxygenation, which may lead to injury of
the immature brain.
2. Diagnosis of PDA
Clinical diagnosis of PDA and its pitfalls
The clinical features of a PDA are mainly because of the hyperdynamic circulatory effects caused by the
shunt, resulting in bounding peripheral pulses (diagnosed clinically by easily palpable dorsalis pedis),
wide pulse pressure (>25 mm of Hg), hyperactive precordium (visible precordial pulsations in more than
2 rib spaces), systolic murmur (usually ejection systolic; rarely pansystolic or continous), persistant
tachycardia etc.
In a ventilated infant, fluctuating FiO2, increasing pressure requirements, unexplained CO2 retention or
metabolic acidosis, recurrent apnea etc suggests a symptomatic ductus. However diagnosis of PDA
based on clinical features alone has mainly two pitfalls i.e. low sensitivity and delay in detection. In
studies comparing clinical examination vs echocardiography, there was a delay of 1-4 days in diagnosis
of PDA based on clinical findings alone.5
More over these signs were insensitive (sensitivity of 30-40%)
and had poor predictive value (60%).
Role of echocardiography
Echocardiography is the gold standard, for diagnosis as well as for assessing severity of PDA.6
The
features suggestive of patent ductus arteriosus include
(a) 2-D and color Doppler- short axis view: Direct visualization of the ductus. In 2-D short axis view,
in the presence of a patent ductus, the appearance is classically described as ‘three-legged stool’
appearance. In color Doppler, there is continuous flare in the MPA.
(b) Short axis view, Pulsed Doppler: Turbulence in main pulmonary artery (MPA) due to left to right
shunt jet flowing into MPA.
(c) Four chamber view: Bowing of interatrial septum to right with enlarged left atrium and left
ventricle
(d) Long axis view: LA/Ao ratio > 1.5:1
(e) Raised left ventricular stroke volume
However these signs only establish the presence of a patent ductus and do not reflect the
hemodynamic significance of the ductus. The echocardiographic markers indicating the
hemodynamic significance and degree of shunting have been well described in a recent review by
Sehgal, et al (Table 1).7
3. Table 1: Echocardiographic markers of hemodynamically significant PDA
Echocardiography parameter* No PDA Mild Moderate Large
Features of ductus arteriosus
Trans ductal diameter (mm) 0 <1.5 1.5-3.0 >3.0
Ductal velocity Vmax (cm/sec) 0 >2 1.5-2.0 < 1.5
Antegrade PA diastolic flow (cm/sec) 0 >30 30-50 >50
Pulmonary overcirculation
Left atrial /aortic root width ratio 1.1 ± 0.2 <1.4:1 1.4-1.6 >1.6:1
Left ventricular/ aortic root width ratio 1.9 ± 0.3 - 2.2 ± 0.4 2.27± 0.27
E wave/ A wave ratio <1 <1 1-1.5 >1.5
IVRT(ms) <55 46-54 36-45 <35
LVSTI 0.34 ± 0.09 - 0.26 ± 0.03 0.24 ± 0.07
Systemic hypoperfusion
Retrograde diastolic flow (as % of forward
flow)
10 < 30 30-50 > 50
Aortic stroke volume (ml/kg) ≤2.25 ≥2.34
Left ventricular output (ml/kg/min) 190-310 - - >314
LVO/SVC flow ratio 2.4 ± 0.3 - - 4.5 ± 0.6
* LVO = left ventricular output, SVC = superior vena cava, LVSTI = left ventricular stroke volume index, IVRT = isovolumic relaxation time, PWD = pulse wave Doppler,
CWD = continuous wave Doppler, PA =pulmonary artery. (Empty boxes implies data not available)
Echocardiography also helps in ruling out other structural heart diseases and facility for in-house
echocardiography enables serial monitoring as well as determines treatment responses.
Limitations of echocardiography
Even though echocardiography is the gold standard for diagnosis of PDA, it has its own limitations
especially with regard to decisions on treatment.8
a) There is limited data prove that functional echocardiography alters the neonatal outcomes.
b) Though the criteria for assessment of degree of shunting are established, there is lack of
universal consensus regarding the best criteria for initiating treatment of PDA. No data till date
supports decision to treat PDA based of echocardiography criteria alone.
c) Many neonatal units lack ready access to echocardiography and it is still a consultative tool,
making serial assessments practically difficult.
d) Last but not least, the echocardiography is highly operator dependent and hence it needs to be
always used in conjunction with clinical findings.
4. Recommendations on use of echocardiography in PDA
a) Though early screening echocardiography could predict possible significant PDA, there is no data
to support routine screening in all preterm infants, as it does not seem to change the long term
outcomes.
b) Echocardiography establishes presence of ducts and its hemodynamic significance, but it cannot
be used in isolation to decide on treatment. Treatment decision should be in conjunction with
clinical symptoms.
c) In all infants in whom treatment of PDA is considered, echocardiography before treatment is
essential to establish the diagnosis as well as to rule out other structural heart disease (e.g. duct
dependent condition in which closure of PDA is contraindicated)
d) Post treatment echocardiography is required to document the response to treatment and assess
the ductus.
e) Early targeted treatment based on echocardiographic criteria alone cannot be recommended at
this point of time even though some large RCT (DETECT Trial , Australia) is currently evaluating
the same
Other diagnostic tests
The other diagnostic tests have very limited role, especially in preterm babies with PDA. Chest
radiograph findings are non-specific and features like cardiomegaly and pulmonary plethora occurs late
when significant PDA leads to congestive heart failure.
An emerging newer diagnostic modality is biomarkers like brain natriuretic peptide (BNP) and N-
terminal-pro- BNP which has shown good sensitivity and specificity. Though these markers are
promising, there widespread clinical use is yet to emerge.9
Management of PDA
The management of PDA could be broadly divided into three aspects- pharmacological closure of
ductus, general supportive measures and surgical ligation of the PDA.
To treat or not to treat a PDA
Despite three decades of intense research enrolling thousands of preterm infants, yet evidence for the
long term benefits of pharmacological closure of PDA is inconclusive and debatable.9
The decision to
treat PDA depends on the 3 factors- the spontaneous closure rate, adverse effect of ductal patency and
risk benefit of treatment.
In a recent systematic review, Benitz et al evaluated the effect of medical and surgical treatment- either
prophylactic or therapeutic on various outcomes.10
Although all modes of interventions effectively
closed the ductus, there was little beneficial effect on the outcomes. Hence the therapeutic decision to
5. treat ductus arteriosus is complex and there is a hot debate for conservative approach especially in
preterm infants more than 1000g in whom the spontaneous closure rate is high.
Pharmacological closure of PDA
Indications for treatment*
Treatment should be considered in preterm infants with echocardiographically proven hemodynamically
significant ductus arteriosus with one of the following conditions
1. Features of congestive heart failure
2. Requiring prolonged respiratory support ( invasive or non invasive) unlikely to be due to other
reasons
3. Unexplained oxygen requirement(FiO2 ≥ 30%) or rising O2 requirement on respiratory support
4. Recurrent apnea requiring respiratory support (CPAP/Nasal IMV/invasive ventilation) attributed
to PDA
* These indications are based on pragmatic clinical decision and not based on high quality evidence
* Treatment of all infants otherwise clinically asymptomatic, based on echocardiography findings of hs-
PDA alone is not warranted
*Definition of hs-PDA: Presence of PDA >1.5mm with one of the following LA/Ao ratio >1.5:1, LV/Ao ratio
>2.2:1, retrograde flow diastolic flow in descending aorta, celiac or cerebral arteries > 30% of ante grade
flow; Left ventricular output >320mL/kg/min.
Mechanism and agents of pharmacological closure
The pharmacological basis for medical therapy is the use of non selective cyclo-oxygenase (COX)
inhibitors, which inhibits prostaglandin synthesis and causes ductal constriction.11
The two most widely
studied and used non selective COX inhibitors are
Indomethacin
Ibuprofen
Indomethacin versus Ibuprofen
The Cochrane meta-analysis comparing ibuprofen with indomethacin in preterm <37 weeks gestation or
low birth weight (<2500 gm), involving 20 trials enrolling 1092 infants, there was no difference in the
failure of duct closure (RR=0.94; 95% CI 0.76, 1.17).12
Oral ibuprofen was used in 3 trials, while
intravenous preparation was used in the rest. The ibuprofen group had significantly lower serum
creatinine levels and decreased incidence of oliguria. There was 32% reduction in NEC in ibuprofen
group (RR=0.68; 95% CI 0.47, 0.99). There was no difference in other outcomes like mortality, reopening
rate of PDA, need for surgical ligation of PDA, duration of ventilator support, chronic lung disease (CLD),
IVH or ROP. Studies have shown a closure rate of 70-80% with either indomethacin or ibuprofen in
preterm babies’ ≤ 32 weeks.
6. Oral Iboprufen
Considering the fact that intravenous ibuprofen is not available in Indian market and the high cost for
imported indomethacin injections, oral ibuprofen is a promising alternative. In randomized controlled
trial of oral vs. intravenous ibuprofen for VLBW infants with PDA, the rate of ductal closure was higher
(oral=84.3% vs. IV=62.5%; P=0.04) and renal side effects were lesser in the oral ibuprofen group. Hence
oral ibuprofen may be a safe and easily available cheap option for treatment of PDA.13
The though
concerns of pulmonary hypertension, increased risk of unconjugated hyperbilirubinemia, lack of short
term neuroprotective effect were reported with iboprufen, it seems to be of little clinical significance.
There is very limited data on use of oral indomethacin and it’s not generally recommended especially
with oral iboprufen being easily available.
Recommendation
1. Both Indomethacin and Iboprufen are equally effective in closing PDA with closure arte of 70-
80%.
2. Iboprufen currently appears to be the superior option with its better safety profile, especially
reduced NEC rates.
3. Infants
a. On full enteral feeds (atleast 120ml/kg/day) – Oral Iboprufen
b. On parentral fluids, partial feeds – IV Indomethacin*
4. The question of which drug confers better long term intact survival is yet unanswered
*IV iboprufen is not available in Indian market
Dosage and Duration of treatment
Indomethacin
Short versus Long course
The two most commonly followed dosing schedules for indomethacin are the short course (3
intravenous doses at 12 hourly intervals with starting dose of 0.2 mg/kg followed by 0.1 mg/kg for
babies less than 2 days of age, 0.2 mg/kg for 2-7 days and 0.25 mg/kg for > 7 days old infants) and the
long course (0.1 mg/kg per day for 6 doses) therapy.
The basis for the long course therapy is that, indomethacin induced prostaglandin inhibition is a
transient phenomenon and the prostaglandin levels normalizes within 6-7 days after the short course
therapy, which increases the chance for reopening of the duct.
A Cochrane meta-analysis, comparing short course (0.3 to 0.6 mg/kg, 3 doses) vs. the long course (0.6 to
1.6 mg/kg, 6 to 8 doses) indomethacin therapy for PDA included 431 preterm infants from 5 randomized
controlled trials, failed to reveal significant difference between the two groups as regards to PDA closure
7. rate, need for surgical ligation or re-opening rates. The prolonged course group had nearly two times
more risk of necrotizing enterocolitis (NEC) compared to the conventional dose group (RR=1.87, 95% CI
1.07, 3.27). Hence prolonged long course treatment cannot be recommended for routine treatment of
PDA.14
Continuous vs intermittent bolus administration of Indomethacin
There have been concerns of effect of continuous versus bolus administration of indomethacin on the
efficacy of therapy as well as side effect profile, especially reduced blood flow to various organ systems
particularly reduced cerebral circulation when bolus administration was given. The recent Cochrane
meta-analysis involving 2 trials comparing the continuous i.e. indomethacin given after 24 hours of life
as slow intravenous infusion over 36 hours vs. bolus dose i.e. indomethacin given after 24 hours of life
as intravenous infusion over 20 min concluded that the evidence was insufficient to draw conclusion
regarding the efficacy for the treatment of PDA. There is an insignificant trend towards increased rates
of PDA closure rate on day 2 and day 5 in the bolus administration group. There was no significant
difference in secondary outcomes like reopening of PDA, neonatal mortality, IVH or NEC. The review
demonstrated that there was a decrease in cerebral blood flow velocity, after bolus injections which
persisted even at 12-24 hours compared to the continuous infusion group. However the clinical impact
of this reduced blood flow to organ systems, especially brain is unclear.15
Recommendation on dosage
Dosage of Indomethacin and Iboprufen for pharmacological treatment of a PDA16
Indomethacin IV
Infusion
over 30
min
Loading dose: 0.2 mg/kg/dose
Subsequent doses ( adjusted as per postnatal age)
<2 days: 0.1 mg/kg/dose 12 hourly x 2 doses
2-7 days: 0.2 mg/kg/dose 12 hourly x 2 doses
>7 days: 0.25 mg/kg/dose 12 hourly x 2 doses
Iboprufen IV or oral Loading dose: 10 mg/kg/dose
Subsequent dose: 5mg/kg/dose 24 hourly x 2 doses
Following the first course, a second course with same dosage could be used in case of persistent
PDA needing treatment or re-opening of the ductus with symptoms.
Failure of medical treatment: Persistence of hemodynamically significant ductus or reopening
despite two courses of treatment defines failure of medical treatment.
Side effects and monitoring
Adverse effects of treatment with NSAIDS include
Renal compromise due to its effect on COX 1,
Bleeding tendency due to its effect on platelet function and
Increased risk of necrotizing enterocolitis.
8. Monitoring during therapy
Baseline Urine output, RFT, platelet count
Daily Urine output
Alternate day
RFT,
Platelet counts (daily if baseline counts are <150,000/mm3
Contraindications
Renal: Urine output< 0.6 ml/kg/h, blood urea > 40 mg/dL, creatinine >1.8 mg/dL
Bleeding: Bleeding from IV sites, skin bleeds, gastrointestinal bleeding, enlarging or evolving
intraventricular hemorrhage (IVH), platelet count < 60,000/mm3
Gastrointestinal: necrotizing enterocolitis; blood in stool
General measures
1. Fluid restriction
In Cochrane metaanalysis, restriction of fluid intake to mean of 120 ml/kg/day as compared to 160
ml/kg/day in the initial few weeks of life is found to be beneficial with lower incidence of PDA, CLD and
mortality.17
Similarly Vanhaesebruock et alin a prospective observational study, in 30 preterm infants
≤30 weeks gestation with RDS requiring surfactant replacement therapy and mechanical ventilation,
showed 100% ductal closure rate with conservative treatment i.e. restricted fluid (130 ml/kg/day) with
low inspiratory time (Ti=0.35) and high positive end expiratory pressure (PEEP=4.5mbar), with no
increase in complication rates.18
2. Role of furosemide and dopamine in medical management of PDA
There has been concern of furosemide adversely affecting the efficacy of indomethacin therapy, by
increasing the clearance of indomethacin, resulting in failure of therapy.19
However, the latest Cochrane
meta-analysis involving 70 patients enrolled in 3 trials, fails to show any increase in treatment failure
(RR=1.25; 95% CI 0.62, 2.52) or reduction in toxicity of indomethacin therapy in PDA.20
Hence routine
use of furosemide in indomethacin treated symptomatic PDA is not recommended and is
contraindicated in presence of dehydration.
Low dose dopamine is considered to be beneficial in reversing indomethacin induced oliguria in preterm
babies with PDA. However, there is no evidence to support this notion. In the Cochrane meta-analysis by
Barrington, et al21
use of dopamine in indomethacin treated symptomatic PDA showed improvement in
urine output but there was no effect on serum creatinine or incidence of oliguria. The use of dopamine
had no effect on the rate of failure for ductal closure. The evidence for effect of dopamine on cerebral
circulation, IVH or death before discharge is insufficient. Hence use of dopamine for prevention of renal
dysfunction induced by COX inhibitors cannot be recommended
3. Mechanical ventilation strategy
In infants on ventilator support with hs-PDA, using slightly higher PEEP and lower Ti might be helpful,
though data is very limited.18
9. Recommendations
1. In clinically symptomatic or echocardiographically diagnosed PDA, it is recommended to restrict
parenteral fluid intake to 120 mL/kg/day, provided other parameters like urine output, serum
Na, urine specific gravity etc are within normal limits
2. Infants on full enteral feeds with hs-PDA a fluid intake of up to 150 ml/kg/day may be used and
calorie density may be increased in case of inadequate weight gain
3. No role for routine use of dopamine in treating NSAID induced oliguria
4. No role for routine use of frusomide in treatment of PDA except in case of established
congestive heart failure
Surgical ligation
It is reserved for infants with symptomatic hs-PDA with
1. Failure of medical therapy
2. Contraindications to medical therapy
Studies have also shown in preterm <28 weeks gestation that need for surgical ligation of PDA is an
independent risk factor for increased rates of CLD, ROP and adverse neurodevelopmental outcome.22
PDA and Neonatal Outcomes
The presence of PDA has been associated with adverse neonatal outcomes like CLD and NEC. 23,24
However none of the studies have shown cause-effect relationship, and studies have failed to
consistently show association between symptomatic PDA and adverse outcomes like cerebral palsy,
cognitive delay, ROP, NEC or CLD once adjusted for prematurity and perinatal factors.22
References
1) Van Overmeire B, Van de Broek H, Van Laer P, Weyler J, Vanhaesebrouck P. Early versus late
indomethacin treatment for patent ductus arteriosus inpremature infants with respiratory distress
syndrome. J Pediatr 2001; 138:205-11.
2) Fanaroff AA, Stoll BJ, Wright LL, et al. Trends in neonatal morbidity and mortality for very low birth
weight infants. Am J Obstet Gynecol. 2007; 196:147e1–e8.
3) Clyman R I. Mechanisms regulating the ductus arteriosus. Biol Neonate 2006; 89: 330–335.
4) Shimada S, Kasai T, Konishi M, Fujiwara T. Effects of patent ductus arteriosus on left ventricular
output and organ blood flows in preterm infants with respiratory distress syndrome treated with
surfactant. J Pediatr 1994; 125: 270-277.
5) Skelton R, Evans N, Smythe J. A blinded comparison of clinical and echocardiographic evaluation of
the preterm infant for patent ductus arteriosus. J Paediatr Child Health. 1994;30:406–411.
6) Evans N, Malcolm G, Osborn D, Kluckow M∙ Diagnosis of patent ductus arteriosus in preterm infants.
NeoReviews 2004; 5: 86-97.
7) Sehgal A, McNamara PJ. Does echocardiography facilitate determination of hemodynamic significance
attributable to the ductus arteriosus. Eur J Pediatr 2009; 168: 907–914.
10. 8) Kluckow M, Seri I, Evans N∙ Functional Echocardiography: An emerging clinical tool for the
Neonatologist∙ J Pediatr. 2007 Feb;150(2):125-30.
9 ) Sasi A, Deorari AK. Patent ductus arteriosus in preterm infants. Indian Peditr 2011; 48: 301-308.
10) Benitz WE. Treatment of persistent patent ductus arteriosus in preterm infants: time to accept the
null hypothesis. Journal of Perinatology 2010; 30: 241–252.
11) Narayanan-Sankar M, Clyman RI. Pharmacologic closure of patent ductus arteriosus in the neonate.
NeoReviews 2003; 4: 215-221.
12) Ohlsson A, Walia R, Shah SS. Ibuprofen for the treatment of patent ductus arteriosus in preterm
and/or low birth weight infants. Cochrane Database Syst Revs. 2010; 4: CD003481.
13) Cherif A, Khrouf N, Jabnoun S, Mokrani C, Amara MB, Guellouze N ,et al. Randomized pilot study
comparing oral ibuprofen with intravenous ibuprofen in very low birth weight infants with patent ductus
arteriosus. Pediatrics 2008; 122: e1256-e1261.
14) Herrera C, Holberton J, Davis PG. Prolonged versus short course of indomethacin for the treatment
of patent ductus arteriosus in preterm infants. Cochrane Database Syst Rev. 2007; 2: CD003480.
15) Gork AS, Ehrenkranz RA, Bracken MB. Continuous versus intermittent bolus doses of indomethacin
for patent ductus arteriosus closure in symptomatic preterm infants. Cochrane Database Syst Rev. 2008;
1: CD006071.
16) Clyman RI. Patent ductus arteriosus in preterm neonates. In Avery’s diseases of the new born. Eds:
Taeush HW, Ballard RA. 7th edn WB Saunders pp 699-710.
17) Bell EF, Acarregui MJ. Restricted versus liberal water intake for preventing morbidity and mortality in
preterm infants. Cochrane Database Syst Rev 2000;(2):CD000503.
18) Vanhaesebrouck S, Zonnenberg I, Vandervoort P, Bruneel E, Van Hoestenberghe M, Theyskens C.
Conservative treatment for patent ductus arteriosus in the preterm Arch. Dis. Child Fetal Neonatal Ed
2007; 92:F244–F247.
19) Green TP, Thompson TR, Johnson De, Lock JE. Furosemide promotes patent ductus arteriosus in
premature infants with respiratory distress syndrome. N Engl J Med 1983; 308: 743-8.
20) Brion LP, Campbell DE. Furosemide for prevention of morbidity in indomethacin treated infants with
patent ductus arteriosus. Cochrane Database Syst Rev. 2001; 3: CD001148.
21) Barrington KJ, Brion LP. Dopamine versus no treatment to prevent renal dysfunction in indomethacin
treated preterm newborn infants. Cochrane Database Syst Rev. 2002; 3: CD003213.
22) Chrone N, Leonard C, Piecuch R, Clyman R I. Patent ductus arteriosus and its treatment as risk
factors for neonatal and neurodevelopmental morbidity Pediatrics 2007; 119:1165-1174.
23) Rojas MA, Gonzalez A, Bancalari E, Claure N, Poole C, Silva-Neto G: Changing trends in the
epidemiology and pathogenesis of neonatal chronic lung disease. J Pediatr 1995; 126: 605– 610.
24) Dollberg S, Lusky A, Reichman B. Patent ductus arteriosus, indomethacin and necrotizing
enterocolitis in very low birth weight infants: a population-based study. J Pediatr Gastroenterol Nutr
2005; 40:184–8.