Transcript Patent Ductus Ateriosis PDA Muhammad Syed MD

Patent Ductus Ateriosis
PDA
Muhammad Syed MD
Heart
High vascular resistance
of the fluid-filled fetal lung
Low vascular resistance
of the placenta
Right-to-left shunts
Two right-to-left shunts occur in the fetus
• Foramen ovale — Blood shunted from the right
to left atrium
• Ductus arteriosus — Blood shunted from the
pulmonary artery to the aorta
Ductus
Arteriosus
Foramen
Ovale
Two right-to-left shunts occur in the
fetus
• Foramen ovale — Blood shunted from the
right to left atrium
• Ductus arteriosus — Blood shunted from
the pulmonary artery to the aorta
TRANSITION AT DELIVERY
• Alveolar fluid clearance
• Lung expansion
• Circulatory changes
Circulatory changes
• clamping of the umbilical cord,
• rise in neonatal systemic blood pressure.
• lung expansion reduces both pulmonary vascular
resistance and the pulmonary artery pressure.
• increased pulmonary arterial blood flow
• raises pulmonary venous return to the left atrium and left
atrial pressure.
• As the left atrial pressure increases and the right atrial
pressure falls, right-to-left shunting across the foramen
ovale decreases.
Patent Foramen Ovale
If the flap forms incompletely or
does not completely seal close,
then deoxygenated blood can
pass from the right atrium to the
left atrium. A patient with an
open or patent foramen ovale
will have a heart murmur.
Unfortunately, this heart
murmur maybe undetectable and
the patient will exhibit no other
obvious symptoms.
Patent Ductus Arteriosus
If the ductus arteriosus remains open after birth and fails
to close it is referred to as a patent ductus arteriosus.
• PDA occurs commonly in premature
infants, especially in those with respiratory
distress syndrome
• Among very low birth weight (VLBW)
infants (birth weight below 1500 g) PDA
occurred in 30 percent
Because of the large volume of blood flow, the ductus becomes a
large vessel with a diameter similar to that of the descending aorta
Patency of the ductus
Mainly on Low arterial oxygen content
Also is influenced by dilators,
• prostaglandins
• nitric oxide
HYDROCORTISONE
Facilitates ductal constriction
Hydrocortisone treatment decreases the
sensitivity of the ductus to the dilating action
of PGE2
CLOSURE
PGE2, a vasodilator
Constrictors (Increased O2)
Anatomic closure usually is complete within one to three months.
Gestational age
In term infants, functional closure after birth
24 hours 50 %
48 hours in 90 %
72 hours in virtually all
In preterm infants, ductal closure can be
delayed and the ductus can reopen following
constriction.
Delayed closure
Occurs especially when accompanying respiratory disease is present.
Severe respiratory distress syndrome; in ill infants less than 30 W
gestation, PDA persists on the fourth day in approximately 65 %
Two other factors may be important:
• Contractile capacity in ductal tissue is less in immature
• Ductus in preterm infants continues to dilate in response to
PGE2 and NO, in contrast to term infants whose ductus
loses responsiveness shortly after birth
Reopening
•
The histological changes following constriction of the
ductus occur rapidly in term infants and prevent
subsequent reopening.
• Reopening may occur because the effects of ductal
constriction on events that lead to anatomic closure are
influenced by immaturity.
• In one study, for example, constriction resulted in
hypoxia, cell death, VEGF expression, endothelial
proliferation, and intimal mound formation in the ductus
of term but not preterm baboons
Shunting of blood flow through a PDA in prematures is essentially all left-to-right
Excessive flow through the
pulmonary circulation
Pulmonary edema
Pulmonary hemorrhage
Bronchopulmonary dysplasia
Systemic and cerebral blood
flow effects
Preterm animals and infants with a PDA
increase their cardiac output. However,
postductal blood flow is reduced, which may
lead to organ dysfunction.
NEC
IVH
CLINICAL FEATURES
• Machinery Murmur ( infraclavicular region
and upper left sternal border)
• Prominent left ventricular impulse
• Bounding pulses,
• and widened pulse pressure (greater than
25 mmHg)
• "silent," especially in the first three days
(deterioration of respiratory status )
Diagnosis
• ECHO
• A transductal diameter that exceeds 1.5
mm is the most commonly used definition
of a significant PDA
PDA closure indications
• Significant left-to-right shunt + symptomatic
• Evidence of left-sided volume overload (ie,
left atrial or ventricular enlargement),
• reversible pulmonary arterial hypertension
• PDA closure is not recommended in patients
with severe and irreversible PAH
Small PDA
Recommend closure of a small audible PDA
even in the absence of a significant L-to-R
right shunt
Silent PDA
Never have hemodynamic consequences
Risk Of endocarditis
Infants with a persistent PDA had a four-fold increased risk of
death compared to infants who never had a significant PDA
Management
• Supportive therapy — During evaluation and treatment,
supportive measures are applied.
• A neutral thermal environment and adequate
oxygenation minimize demands on left ventricular output.
• Positive end-expiratory pressure (PEEP) may improve
gas exchange in infants with respiratory compromise.
• Maintaining the hematocrit at 35 to 40 percent may
increase pulmonary vascular resistance and reduce the
left-to-right shunt
• Not recommend routine use of furosemide or any other
loop diuretic, which stimulates renal synthesis of PGE2.
THERAPEUTIC
INTERVENTIONS
Interventions for PDA closure include:
• Pharmacologic therapy, which is used
exclusively in premature infants
• Surgical ligation
• Percutaneous catheter occlusion
Pharmacologic therapy
Inhibitors of prostaglandin synthesis, such
as indomethacin and ibuprofen, are used as
the initial interventions for PDA closure in
preterm infants.
Indomethacin has proven to be ineffective in
term infants and older patients with a PDA.
Thank you