Difference between revisions of "Patent Ductus Arteriosus"

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Also known as: '''''PDA'''''
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== Introduction  ==
|linkpage =Cardiology - WikiClinical
 
|linktext =Cardiology
 
|sublink1=Cardiovascular Conditions - WikiClinical
 
|subtext1=CARDIOVASCULAR CONDITIONS
 
|maplink1= Cardiovascular Conditions (Content Map) - WikiClinical
 
|pagetype=Clinical
 
}}
 
<br>
 
[[Image:patent_ductus_goat.jpg|right|thumb|125px|<small><center>'''Patent ductus arteriosus'''. Courtesy of A. Jefferies</center></small>]]
 
  
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This cardiac defect occurs in all animals, but is more likely to be diagnosed in the young.
  
Also known as PDA
+
The condition is the persistence of the ductus arteriosus after birth. During fetal life, the ductus arteriosus connects the pulmonary artery to the descending aorta. This fetal vessel allows most of the blood to bypass the developing lungs and go directly to the aorta and systemic circulation. In fetal life oxygen is provided by the placenta while the lungs are developing. At birth, the animal takes a breath of air and uses its lungs for the first time. High levels of oxygen from the pulmonary vasculature enter the circulation and the ductus arteriosus responds by contracting the smooth muscles lining its vessel wall. The functional closure of the ductus arteriosus occurs within 2-3 days after birth and with time it will become an anatomical closure. However, some animals have a ductus arteriosus that doesn't respond to the increased oxygen at birth and remains open (patent). After birth PDA causes a reversal of blood flow from the higher pressure of the descending aorta through the ductus arteriosus to the pulmonary artery and into the lungs. This is known as left-to-right shunting. The shunting of blood in this manner overwhelms the pulmonary vasculature and the left side of the heart. The increased volume of blood from the lungs travels to the left atrium and left ventricle which respond to the added pressure by dilation and hypertrophy. As a result, PDA can eventually lead to [[Pulmonary Oedema|pulmonary oedema]] and [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Normally the pulmonary circulation is equipped to handle increased volumes of blood without pulmonary arterial pressure changes. However, sometimes the increased blood volume in the lungs causes gross changes to the pulmonary arterioles causing [[Pulmonary Hypertension|pulmonary hypertension]] and raised pulmonary arterial pressures. If the pressure is high enough, it can cause a '''reverse PDA''' (right-to-left shunt) and unoxygenated blood will bypass the lungs heading straight for the descending aorta and the systemic circulation.
  
*Occurs in all animals
 
  
*Young animals have a greater risk
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==Signalment==
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It is a very common condition in dogs and is not very common in cats. Predisposed breeds include toy breeds (Yorkshire Terrier, Pomeranian, Maltese, Toy Poodles); Miniature Poodles, Shetland
 +
Sheepdogs, German Shepherds, Collies. There has been found to be a greater occurrence in females.
  
*Very common in dogs
 
  
*Not very common in cats
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== Clinical Signs ==
  
===Signalment===
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Clinical signs include left sided congestive heart failure, exercise intolerance, differential cyanosis (reverse PDA) and hindlimb weakness (reverse PDA). Sometimes, depending on severity of defect, there may be no clinical signs.
  
Genetics & Predisposed Breeds: Toy Breeds (Yorkshire Terrier, Pomeranian, Maltese, Toy Poodles); Miniature Poodles, Shetland Sheepdogs, German Shepherds, Collies
 
  
*Greater occurrence in females
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== Diagnosis==
  
===Description===
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Clinical signs and history may be indicative of the disease. Physical examination findings will include systolic and diastolic continuous machinery [[Heart Murmurs|murmur]] (left side of the heart is the loudest), a precordial thrill (palpable after a murmur) and the presence of waterhammer pulses (a forceful pulse that immediately collapses).
  
*Persistence of the ductus arteriosus after birth
+
In a reverse PDA, differential cyanosis (normal oral mucus membranes, cyanotic membranes everywhere else) and hyperviscosity (increased PCV from hypoxia-mediated polycythemia) may be seen.
  
 +
On radiographs of the thorax, you may see left atrial & ventricular enlargement, pulmonary overcirculation, dorsoventral view shows '''three bulges''': aorta (1 o’clock), pulmonary artery (2 o’clock), left auricle (3 o’clock) positions and signs of left-sided congestive heart failure (pulmonary congestion, edema). If there is a reverse PDA, you may see right ventricular enlargement, dilation of the pulmonary trunk and arteries and left ventricular enlargement.
  
*During fetal life, the ductus arteriosus connects the pulmonary artery to the descending aorta. This fetal vessel allows most of the blood to bypass the developing lungs and go directly to the aorta and systemic circulation. In fetal life oxygen is provided by the placenta while the lungs are developing.  
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On echocardiography you will see left atrial &amp; ventricular enlargement, dilation of pulmonary artery and a PDA might be visualized. Doppler can show abnormal flow. In a reverse PDA you will see right ventricular enlargement and left ventricular enlargement. Doppler can show abnormal flow.  
  
 +
On electrocardiographic (ECG) you may see classic signs for left atrial enlargement (wide P wave), classic signs for left ventricular enlargement (tall R wave, wide QRS) and atrial & ventricular arrhythmias may be present. In a reverse PDA you may see classic signs of right sided heart enlargement.
  
*At birth, the animal takes a breath of air and uses its lungs for the first time. High levels of oxygen from the pulmonary vasculature enter the circulation and the ductus arteriosus responds by contracting the smooth muscles lining its vessel wall. The functional closure of the ductus arteriosus occurs within 2-3 days after birth and with time it will become an anatomical closure. However, some animals have a ductus arteriosus that doesn't respond to the increased oxygen at birth and remains open (patent).
 
  
 +
== Treatment ==
  
*After birth PDA causes a reversal of blood flow from the higher pressure of the descending aorta through the ductus arteriosus to the pulmonary artery and into the lungs. This is known as left-to-right shunting. The shunting of blood in this manner overwhelms the pulmonary vasculature and the left side of the heart. The increased volume of blood from the lungs travels to the left atrium and left ventricle which respond to the added pressure by dilation and hypertrophy. As a result, PDA can eventually lead to pulmonary edema and left-sided congestive heart failure.  
+
For a PDA, surgical ligation of the ductus arteriosus (2-4 months of age) can be performed if refered. Animals with congestive heart failure need stabilization of [[:Category:Heart Failure|heart failure]] before surgery.
  
 +
For a reverse PDA surgery is contraindicated. Exercise restriction and palliative care may be all that can be done. Phlebotomy (bleeding to keep PCV at normal levels) can be performed on a regular basis to help treat the symptoms.
  
*Normally the pulmonary circulation is equipped to handle increased volumes of blood without pulmonary arterial pressure changes. However, sometimes the increased blood volume in the lungs causes gross changes to the pulmonary arterioles causing pulmonary hypertension and raised pulmonary arterial pressures. If the pressure is high enough, it can cause a reverse PDA (right-to-left shunt) and unoxygenated blood will bypass the lungs heading straight for the descending aorta and the systemic circulation.
 
  
===Diagnosis===
+
== Prognosis ==
====History & Clinical Signs====  
 
  
-Signs of left sided congestive heart failure
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'''PDA: '''Very good prognosis with surgical treatment.
  
-Exercise intolerance
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'''Reverse PDA: '''Poor prognosis.
  
-Differential cyanosis (Reverse PDA)
 
  
-Hindlimb weakness (Reverse PDA)
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{{Learning
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|flashcards = [[Cardiovascular Developmental Pathology Flashcards]]
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}}
  
-Asymptomatic
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== References ==
  
====Physical Exam====
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Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume''' 2 (Fifth Edition) ''W.B. Saunders Company''
  
'''PDA'''
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Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''
  
-Systolic & diastolic continuous machinery murmur (Left side of the heart is the loudest)
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Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition) ''Mosby Elsevier''
  
-Precordial thrill (Palpable after a murmur)
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Merck & Co (2008) '''The Merck Veterinary Manual '''(Eighth Edition)'' Merial''
  
-Waterhammer pulses (A forceful pulse that immediately collapses)
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Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine''' (Fourth Edition) ''Mosby Elsevier''
  
  
'''Reverse PDA'''
 
  
-Differential cyanosis (Normal oral mucus membranes, cyanotic membranes everywhere else)
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{{review}}
 
 
-Hyperviscosity (Increased PCV from hypoxia-mediated polycythemia)
 
 
 
====Radiographic Findings====
 
 
 
'''PDA'''
 
 
 
-Left atrial & ventricular enlargement
 
 
 
-Pulmonary overcirculation
 
 
 
-Dorsoventral view shows three bulges: aorta (1 o’clock), pulmonary artery (2 o’clock), left auricle (3 o’clock) positions
 
 
 
-Signs of left-sided congestive heart failure (pulmonary congestion, edema)
 
 
 
 
 
'''Reverse PDA'''
 
 
 
-Right ventricular enlargement
 
 
 
-Dilation of the pulmonary trunk and arteries
 
 
 
-Left ventricular enlargement
 
 
 
====Echocardiographic Findings====
 
 
 
'''PDA'''
 
 
 
-Left atrial & ventricular enlargement
 
 
 
-Dilation of pulmonary artery
 
 
 
-PDA might be visualized
 
 
 
 
 
Doppler can show abnormal flow
 
 
 
 
 
'''Reverse PDA'''
 
 
 
-Right ventricular enlargement
 
 
 
-Left ventricular enlargement
 
 
 
 
 
Doppler can show abnormal flow
 
 
 
====Electrocardiographic (ECG)====
 
 
 
'''PDA'''
 
 
 
-Classic signs for left atrial enlargement (wide P wave)
 
 
 
- Classic signs for left ventricular enlargement (tall R wave, wide QRS)
 
 
 
-Atrial & ventricular arrhythmias may be present
 
 
 
 
 
'''Reverse PDA'''
 
 
 
-Classic signs of right sided heart enlargement
 
 
 
===Treatment===
 
 
 
'''PDA'''
 
 
 
-Surgical ligation of the ductus arteriosus (2-4 months of age)
 
 
 
-Animals with congestive heart failure need stabilization of heart failure before surgery
 
 
 
 
 
'''Reverse PDA'''
 
 
 
-Surgery is contraindicated
 
 
 
-Exercise Restriction
 
 
 
-Phlebotomy (Bleeding to keep PCV at normal levels)
 
 
 
 
 
===Prognosis===
 
 
 
'''PDA'''
 
 
 
-Very good prognosis with surgical treatment
 
 
 
-Poor prognosis if large PDAs are left untreated
 
 
 
 
 
'''Reverse PDA'''
 
 
 
-Poor prognosis
 
 
 
==From Pathology==
 
 
 
 
 
Ductus Arteriosus shunts blood from the Pulmonary Artery to the Aorta in the foetus to bypass the lungs.  Usually closes shortly after birth due to smooth muscle contraction in repsonse to increased arterial oxygen tension.  When patent after birth, blood flows along the pressure gradient, left to right, leading to pulmonary hypertension.  If the hypertension is significant, as with larger defects, right sided pressure may increase enough to allow reversal of flow through the PDA and will result in cyanosis.  Reverse shunting is rare.
 
 
 
''Incidence:''
 
[[Image:patent_ductus_goat.jpg|right|thumb|200px|<small><center>'''Patent ductus arteriosus'''. Courtesy of A. Jefferies</center></small>]]
 
*Uncommon in cats.
 
*More common in dogs with distinct '''female predisposition'''.
 
*Predisposed breeds include; CKCS, Border Collie, GSD, Poodles.
 
*Research into PDAs in dogs has revealed a genetic component influencing the maturation of collagen.
 
*May be a normal finding in lambs and piglets up to 2 weeks of age.
 
 
 
''Clinical Signs:''
 
*Continuous '''machinery murmur''' at left heart base.
 
*'''Water-Hammer pulse''' (rapid diastolic decline).
 
*Variable other signs depending on size of defect E.g. syncope, cyanosis, exercise intolerance etc.
 
*May progress to left sided heart failure and so pulmonary oedema.
 
  
''Diagnosis:''
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{{OpenPages}}
*Left atrial and left ventricular enlargement radiologically and on ECG due to volume overload.
 
*Pulmonary overcirculation (enlargement of pulmonary arteries and veins) on radiology.
 
*DV radiographs show a '''three knuckled appearance'''; enlargement of:
 
**Aortic arch.
 
**Pulmonary artery.
 
**Left auricular appendage.
 
*PDA difficult to image on echocardiography but Doppler imaging may be useful.
 
  
''Treatment:''
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[[Category:Cardiovascular_System_-_Developmental_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Dog]] [[Category:Cardiac_Diseases_-_Horse]] [[Category:Cardiac_Diseases_-_Cattle]] [[Category:Cardiac_Diseases_-_Pig]]
*'''Surgical ligation''' for left to right shunts.  Needs stabilisation first.
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[[Category:Cardiology Section]]
*Right to left shunts are not operable.
 
*Untreated dogs face 60-70% mortality during their first year of life.
 
[[Category:Cardiovascular_System_-_Developmental_Pathology]]
 

Latest revision as of 17:01, 15 October 2013


Also known as: PDA

Introduction

This cardiac defect occurs in all animals, but is more likely to be diagnosed in the young.

The condition is the persistence of the ductus arteriosus after birth. During fetal life, the ductus arteriosus connects the pulmonary artery to the descending aorta. This fetal vessel allows most of the blood to bypass the developing lungs and go directly to the aorta and systemic circulation. In fetal life oxygen is provided by the placenta while the lungs are developing. At birth, the animal takes a breath of air and uses its lungs for the first time. High levels of oxygen from the pulmonary vasculature enter the circulation and the ductus arteriosus responds by contracting the smooth muscles lining its vessel wall. The functional closure of the ductus arteriosus occurs within 2-3 days after birth and with time it will become an anatomical closure. However, some animals have a ductus arteriosus that doesn't respond to the increased oxygen at birth and remains open (patent). After birth PDA causes a reversal of blood flow from the higher pressure of the descending aorta through the ductus arteriosus to the pulmonary artery and into the lungs. This is known as left-to-right shunting. The shunting of blood in this manner overwhelms the pulmonary vasculature and the left side of the heart. The increased volume of blood from the lungs travels to the left atrium and left ventricle which respond to the added pressure by dilation and hypertrophy. As a result, PDA can eventually lead to pulmonary oedema and left-sided congestive heart failure. Normally the pulmonary circulation is equipped to handle increased volumes of blood without pulmonary arterial pressure changes. However, sometimes the increased blood volume in the lungs causes gross changes to the pulmonary arterioles causing pulmonary hypertension and raised pulmonary arterial pressures. If the pressure is high enough, it can cause a reverse PDA (right-to-left shunt) and unoxygenated blood will bypass the lungs heading straight for the descending aorta and the systemic circulation.


Signalment

It is a very common condition in dogs and is not very common in cats. Predisposed breeds include toy breeds (Yorkshire Terrier, Pomeranian, Maltese, Toy Poodles); Miniature Poodles, Shetland Sheepdogs, German Shepherds, Collies. There has been found to be a greater occurrence in females.


Clinical Signs

Clinical signs include left sided congestive heart failure, exercise intolerance, differential cyanosis (reverse PDA) and hindlimb weakness (reverse PDA). Sometimes, depending on severity of defect, there may be no clinical signs.


Diagnosis

Clinical signs and history may be indicative of the disease. Physical examination findings will include systolic and diastolic continuous machinery murmur (left side of the heart is the loudest), a precordial thrill (palpable after a murmur) and the presence of waterhammer pulses (a forceful pulse that immediately collapses).

In a reverse PDA, differential cyanosis (normal oral mucus membranes, cyanotic membranes everywhere else) and hyperviscosity (increased PCV from hypoxia-mediated polycythemia) may be seen.

On radiographs of the thorax, you may see left atrial & ventricular enlargement, pulmonary overcirculation, dorsoventral view shows three bulges: aorta (1 o’clock), pulmonary artery (2 o’clock), left auricle (3 o’clock) positions and signs of left-sided congestive heart failure (pulmonary congestion, edema). If there is a reverse PDA, you may see right ventricular enlargement, dilation of the pulmonary trunk and arteries and left ventricular enlargement.

On echocardiography you will see left atrial & ventricular enlargement, dilation of pulmonary artery and a PDA might be visualized. Doppler can show abnormal flow. In a reverse PDA you will see right ventricular enlargement and left ventricular enlargement. Doppler can show abnormal flow.

On electrocardiographic (ECG) you may see classic signs for left atrial enlargement (wide P wave), classic signs for left ventricular enlargement (tall R wave, wide QRS) and atrial & ventricular arrhythmias may be present. In a reverse PDA you may see classic signs of right sided heart enlargement.


Treatment

For a PDA, surgical ligation of the ductus arteriosus (2-4 months of age) can be performed if refered. Animals with congestive heart failure need stabilization of heart failure before surgery.

For a reverse PDA surgery is contraindicated. Exercise restriction and palliative care may be all that can be done. Phlebotomy (bleeding to keep PCV at normal levels) can be performed on a regular basis to help treat the symptoms.


Prognosis

PDA: Very good prognosis with surgical treatment.

Reverse PDA: Poor prognosis.



Patent Ductus Arteriosus Learning Resources
FlashcardsFlashcards logo.png
Flashcards
Test your knowledge using flashcard type questions
Cardiovascular Developmental Pathology Flashcards


References

Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition) W.B. Saunders Company

Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2) W.B. Saunders Company

Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition) Mosby Elsevier

Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial

Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier




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