Patent Ductus 2
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Transcript of Patent Ductus 2
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Patent Ductus Arteriousus
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History
In 1593 Giambattista Carcano described ductusarteriosus in book great cardiac vessels of the fetus
Leo bottani falsely associated with ductus
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Anatomy
Normal fetal vascular channel between aorta andpulmonary artery.
The pulmonary end is located to left of bifurcation of
pulmonary trunk Aortic end is just beyond the origin of left subclavian
artery
With a right aortic arch, the ductus arteriosus may be
on the right, joining the right pulmonary artery andthe right aortic arch just distal to the right subclavianartery
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Introduction
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microscopic structure of the ductus arteriosus differs
the media of the ductus arteriosus consist largely oflayers of smooth muscle arranged spirally in both
leftward and rightward directions The intimal layer of the ductus arteriosus is thicker
than that of the adjoining arteries and contains anincreased amount of mucoid substance
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Embryology
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Physiology
Role in the Fetus
6 weeks of gestation, the ductus arteriosus isdeveloped sufficiently to carry most of the right
ventricular output The right ventricle ejects about two thirds of
combined ventricular output
ductus arteriosus permits flow to be diverted away
from the high-resistance pulmonary circulation
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Normal Postnatal Closure
closure of the ductus arteriosus is effected in twophases
Immediately after birth, contraction and cellular
migration of the medial smooth muscle in the wall ofthe ductus
resulting in functional closure
commonly occurs within 12 hours after birth
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Normal Postnatal Closure
The second stage usually is completed by 2 to 3weeks
produced by infolding of the endothelium, disruption
and fragmentation of the internal elastic lamina replacement of muscle fibers with fibrosis
permanent sealing of the lumen to produce theligamentum arteriosum
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mechanisms responsible for the initial postnatalclosure of the ductus arteriosus are not fullyunderstood
increase in pO2, as occurs with ventilation after birth,constricts the ductus arteriosus
prostaglandins play an active role in maintaining theductus arteriosus in a dilated state
PGE1, PGE2, and PGI2 dilate isolated ductusarteriosus strips or rings from term fetal lambs
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At birth, the placental source is removed, and themarked increase in pulmonary blood flow allowseffective removal of circulating PGE2
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INCIDENCE OF PDA
increased dramatically over the last two decades
improved survival rate of premature infants
incidence is approximately 0.02 to 0.04 percent
among term infants born at sea level slight female predominance
incidence is as high as 60 percent in infants bornbefore 28 weeks gestation
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Clinical History
The diagnosis of PDA canot be made at birth
The murmur emerges after few days as thepulmonary vascular resistance falls
History of prematurity is very important. Premature babies with respiratory distress tend to
have large shunts
PDA is moe common in females with a ratio of 2:1
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Family history is important , as it tends to recur insiblings
Rubella infection to mother during the first trimester
is a common cause maternal coxsackie virus infection is another cause
Low birth weight is common, even in small shunts
More common in children born in October toJanuary
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Another interesting point is the relation to thealtitude the patient was born
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Small Ductus Arteriosus
the resistance to flow across the ductus arteriosus ishigh
only a small left-to-right shunt develops
Pulmonary blood flow is increased only minimally left ventricular failure does not occur
Most of the infants are asymptomatic
Murmur is detected on routine physical examination.
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Moderate Ductus Arteriosus
In infants a moderate shunt produces symptoms ofheart failure
Poor feeding, irritability, and tachypnea are present
symptoms ordinarily increase until about the secondto third month
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Large Ductus Arteriosus
Infants with a large PDA are invariably symptomatic
They are irritable, feed poorly, fail to gain weight andsweat excessively
They have increased respiratory effort andrespiratory rates
prone to develop recurrent upper respiratoryinfections and pneumonia
symptoms indicative of severe left ventricular failurewith pulmonary edema may occur early in infancy
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Patients with reversed shunt
Small number of cases
High pulmonary vascular resistance, from infancy
Effort dyspnea is the most common symptom
Symptoms of left ventricular failure are absent Hoaseness of voice may be present.
Cyanosis may be overlooked.
There is marked leg fatigue and absence of dyspnea Rarely patients may have swelling and pain in lower
limbs.
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Physical apperance
Physical underdevelopment due to a large shunt
Maternal rubella syndrome: cataract, deafness andmental retardation
Rocker bottom feet and loose skin is present intrisomy 13
In this syndrome assosiated VSD is usually present
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Examination
Differential cyanosis and clubbing is pesent in shuntreversal
It can be brought out by exersise or a warm water
bath Useful to have patient sit with hands and feet
together.
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Arterial pulse
A wide pulse pressure is present
Pulse has a brisk rise, single peak and rapid collapse
Diastolic pressure is low, systolic is high
The peripheral pulses are bounding If the shunt is small or if there is pulmonary
hypertension the bounding pulse is absent
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JVP
JVP is normal in small shunts
In patients of cardiac failure the jvp is elevated andprominent A and V waves are present
Prominent A waves are present in high pulmonaryresistance
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Auscultation
The classic murmur of uncomplicated PDA rises topeak in latter systole
Continues without interruption through the second
heart sound Declines in intensity in diastole
a silent interval may be present towards the end ofdiastole
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Continious murmur
A small duct results in a soft , high frequencycontinuous murmur
A larger duct causes a loud noisy machinery murmur
Loud murmur becomes soft if there is narrowing ofthe duct.
The murmur is dependent on the pressure differencebetween aorta and pulmonary artery
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Progression of murmur
As the diastolic pressure of pulmonary arteryincreases the patient is left with a holosystolicmurmur
As pulmonary hypertension progresses further thesystolic component also disappears
Right to left flow across PDA does not have amurmur
With increasing PH Gibson murmur is abolished Findings of pulmonary hypertension are present
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Newborn
In newborns the classic murmur is absent
Only a soft systolic murmur may be present
this is due to high pulmoary pressures
However the signs of cardiac failure are present
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Second heart sound
Paradoxical spitting is present in patients of large leftto right shunts
due to Prolonged LV ejection and short RV ejection
Difficult to detect on auscultation With shunt reversal the second heart sound is closely
split with loud pulmonary component
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ECG
Small ductus ECG may be normal
Variation in ecg depend on the volume overload ofLV and pressure overload of RV
Usually have sinus rhythm P waves are notched, bifid and prolonged
s/o left atrial enlargement
With development of pulmonary hypertension signsof biatrial enlargement are present
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PR interval is prolonged in 10 to 20 percent ofpatients
QRS axis is normal
Volume overload of left ventricle results in deep swaves in v1, tall r waves I v5 to v6, deep q waves andtall t waves
A large shunt with pulmonary hypertension results
in features of biventricular hypertrophy Large equidiphasic complexes are present from v1 to
v6
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ECG in right to left shunt
In PDA with right to left shunt peaked narrow rightatrial P waves appear in 2,3,and v1
QRS axis shows right axis deviation
Right ventricular hypertrophy R waves in v5, v6 remain tall bur the q waves and the
tall t waves disappear
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X ray chest
Variation in XRAY depend on size, duration anddirection and pulmonary pressures
The ductus may be seen as a convexity between aorta
and pulmonary artery In older patients calcium may be depoisted
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Left to right shunt causes increase in pulmoaryplethora
Pulmonary trunk and main branches are dilated
Ascending aorta is enlarged in adults LA and LV are enlarged
RA and RV dilatation occurs when pulmonaryhypertension is present
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Right to left shunt
RV is hypertrophied
Pulmonary trunk and main branches are dilated
Peripheral vasculature is reduced
Ascending aorta is normal sized Patients who have shunt reversal have larger hearts
Both RV and LV enlargement is seen
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Echocardiography
A complete echocardiographic evaluation of the PDAincludes
two-dimensional imaging of the ductus,
evaluation of the degree of shunting at the ductus,and
evaluation of pulmonary artery pressure usingDoppler echocardiography
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Anatomic assessment
Most commonly, the ductus is imaged in theparasternal and suprasternal notch views
In the high parasternal short axis view, with the
transducer oriented leftward toward the pulmonaryartery bifurcation, the ductus can be imagedcoursing between the pulmonary artery and thedescending aorta
Absolute quantification of its diameter is the bestway to determine its presence or absence
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In the suprasternal notch window, the ductus arisesfrom the descending aorta at the level of the leftsubclavian artery, and courses anteriorly to join thepulmonary artery
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Color flow mapping is particularly helpful in thesetting of a small PDA,
Determination of the origin of the retrograde flowinto the pulmonary artery using two-dimensionalimaging as well as color flow mapping is crucial toavoid confusion of the patent ductus with otheraortopulmonary shunts
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The Size of the Left Atrium Left atrial (LA) enlargement signifies increased
pulmonary venous return because of left-to-rightductal shunting
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Left Ventricular Size
This will enlarge as cardiac output increases withboth increased pulmonary venous return and with
increased diastolic run-off Descending Aortic Flow in Diastole
The presence of a significant ductal shunt resultsin diastolic run-off to the pulmonary circulation
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Left Pulmonary Artery Diastolic FlowVelocity
This is higher with large left-to-right
shunts. Values less than 15cm/sec are seen whenthe duct is closed
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Hemodynamic assessment
The pulmonary to systemic flow ratio (Qp:Qs) can bedetermined echocardiographically
When the pulmonary artery pressure is lower thansystemic arterial pressure, there is continuous left-to-right shunting demonstrated.
The velocity of flow across the ductus, measured byeither pulsed or continuous wave Doppler,
can be translated into the gradient between theaorta and the pulmonary artery
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When the pulmonary artery pressure is equal tosystemic pressure, pulsed Doppler within the ductusdemonstrates systolic right-to-left shunting, withdiastolic left-to-right flow within the vessel
Cardiac Catheterization
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Cardiac Catheterization
Color Doppler flow mapping is generally as sensitiveas cardiac catheterization for detecting even a smallPDA
In children with pulmonary hypertension,determining the exact location of the shunt can bedifficult
Right heart catheterization alone usually suffices to
confirm the diagnosis an additional lesion such as ventricular septal defect
is suspected
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An increase of pulmonary arterial blood oxygencontent of >0.5 mL/dL or a saturation increase of>4% to 5% from that in right ventricular bloodindicates a significant left-to-right shunt at the
pulmonary arterial level
An increase in oxygen saturation in pulmonaryarterial blood is not diagnostic of a PDA, but may be
present in lesions such as aortopulmonary windowor a high ventricular septal defect
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a small communication, pulmonary arterial bloodpressures are normal, but systemic arterial pulsepressure may be slightly widened
a moderate-sized defect,
1. pulmonary arterial systolic, diastolic, and meanblood pressures may be slightly elevated.
2. Systemic arterial diastolic blood pressure falls,
3. whereas systemic arterial pulse pressure increases
l h h d
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large shunt hemodynamics
pulmonary and systemic arterial pressures are equal, left atrial mean pressure may be increased substantially,
and a prominent V wave is seen.
Left ventricular end-diastolic pressure may be elevated,
a diastolic pressure gradient between the left atrium andleft ventricle is demonstrated.
A small systolic pressure difference between the left
ventricle and aorta is also encountered
Angiography
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Angiography
it is the most effective test for defining the anatomyof the PDA
Contrast medium is injected into a catheter passedthrough the PDA into the aorta from the pulmonaryartery or into the aorta retrogradely from thefemoral artery
PDA usually is widely dilated, and the ductus
narrows down at the pulmonary arterial end
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the lateral projection, or occasionally the left anterioroblique projection, demonstrates the anatomy mostclearly
The AP camera can be positioned in the rightanterior oblique caudal position to demonstrate thePDA
selective descending aortography is essential in
patients of VSD or ASD to demonstrate PDA
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M i R I i
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Magnetic Resonance Imaging
simpler techniques such as two-dimensionalechocardiography Doppler evaluation accuratelydefine the anatomy
These studies can be of use in adolescents or adultswith poor echo windows
Velocity-encoded cine MRI imaging for estimation ofleft-to-right shunting may have additional clinical
utility
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P t l
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Percutaneous closure
A variety of devices have been used for percutaneousclosure of a PDA
It is the standard of care in most patients
Exception in premature and small infants with largeshunts
Have been available for last 20 years
C il
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Coils
Stainless steel Gianturco coils Earlier used for AV malformations
For duct closure the PDA should be less than 2 mm
in diameter, long to accommodate loops and shouldhave sufficient aortic ductal diverticulum
The coils are deployed in a retrograde fashion fromthe aorta
Coil embolisation is a dangerous complication Modified coils with release mechanism are available
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Multiple coils are used for large PDA PDA closure rate are around 95 to 100% at 2 years
Residual shunt causes haemolysis
Modifications available areGiantruco-grifika vascular occlusion device
Nit occlud PDA occluder
D t l d d i
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Duct occluder device
AMPLATZ duct occluder is only device which is FDAapproved
Cone shaped device
Antegrade venous approach Delivery cable- release notch
98% closure at 6 months in large PDA
Complications are left pulmonary artery stenosis,
aortic coarctation
Small ducts are avoided
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Follow up
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Follow up
Anticoagulation for 6 months Endocarditis prophylaxsis
Follow up 2d echo after 6 months
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Thank you