“Rwandan National Neonatal Protocol_Cardiology” by Emmanuel Rusingiza for OPENPediatrics
11
October

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , /


Rwandan National Neonatal Protocol: Cardiology by Dr. Emmanuel Rusingiza. Introduction. Hello. My name is Emmanuel Rusingiza. I am a pediatric cardiologist
at Kigali University Teaching Hospital, called also CHUK. Today I’m going to
talk on a chapter on cardiovascular
diseases in newborns. Overview. By the end of this
chapter, participants should be able to identify two
presenting symptoms of patent ductus arteriosus,
identify methods for non-pharmacological
support of an infant with PDA, identify methods for
pharmacological treatment of an infant with a PDA. Understanding Patent Ductus Arteriosus. Patent ductus
arteriosus, or PDA, is the major cardiovascular
risk for newborns. PDA is postnatal persistence
of the normal fetal vessel that joins the pulmonary
artery to the aorta. The ductus arteriosis
is a blood vessel that shunts blood away
from the infant’s lungs to the systemic circulation. After the infant is born
and the lungs fill with air, it’s no longer
needed, and it usually closes in the first
several days after birth. If the ductus arteriosis
does not close after birth, it results in
abnormal blood flow between the aorta and pulmonary
artery, two major blood vessels that carry
blood from the heart. PDA is most common in
premature patients. There is also an increased risk
for PDA in settings of hypoxia. PDA can also occur as a congenital defect in newborns of any gestational age. In these cases, PDA
is often associated with the more complex
congenital heart disease. In preterm infants,
blood is typically shunted through the
PDA from left to right. This increases blood
flow to the lungs, resulting in
tachypnea, crackles, and respiratory distress due
to pulmonary overcirculation. Consequently, blood flow
to the body decreases and the patient’s systemic
blood pressure decreases. Some signs and
symptoms of PDA can be identified by physical exam. Flow through the ductus creates
a systolic or continuous murmur at the left sternal border. The pulmonary
overcirculation manifests as tachypnea, increased
work of breathing, and pulmonary hemorrhage. The systemic hypotension
with diastolic runoff through the ductus
can be identified by wide pulse pressure, bounding
pulses, and palmar pulses, often accompanied by a
hyperactive pericardium. To confirm a diagnosis of PDA, a
chest X-ray or echocardiography can be obtained if available. Look for pulmonary
edema or cardiomegaly on the chest X-ray. There are two types
of PDA management– non-pharmacological
and pharmacological. Non-pharmacological
management involves supporting increased
respiratory needs and restricting fluid to about
80% of maintenance fluids. If there is evidence of
significantly decreased perfusion– for example,
decreased urine output or low blood pressure– hold enteral feeds due to
decreased intestinal perfusion and risk of necrotizing
enterocolitis. Necrotizing
enterocolitis is caused by decreased blood flow
to the intestines, which leads to localized
necrosis, bacterial entry into the bloodstream,
and subsequent sepsis. Pharmacological
management of PDA involves giving
a medication that is directed at closing the PDA. This is typically
given to infants who have a PDA in the
setting of prematurity. One pharmacological option
is enteral ibuprofen. The first dose should
be 10 mg per kg, followed by a dose of 5
mg per kg 24 hours later. Then another 5 mg per kg dose
24 hours after the second for a total of three doses. If the ductus remains open, the
course can be repeated once. If not, this approach
is less likely to be effective in babies
older than one month. There is a real risk of
intestinal perforation associated with
ibuprofen treatment. Ibuprofen is
contraindicated in setting of marked thrombocytopenia,
less than 50,000, bleeding disorders,
impaired renal function, and hyperbilirubinemia
approaching exchange transfusion levels. Pharmacological
management of PDA– that is part of a broader
congenital heart defect. It’s different from
the treatment of PDA in the setting of prematurity. When managing PDA is
a congenital defect, consider the risks and
benefits of diuretics, specifically
Furosemide at a dose of 1 milligram per kilogram
per day, IV or enteral. If medical treatment is
contraindicated or has failed, the PDA may need to be
repaired surgically. Case Studies. To review the content
from this chapter, we will look at the case of
a newborn named Jean Claude. He is five days old, 29
weeks of gestation age. He had been steadily weaning
in nasal cannula oxygen. Today, his oxygen saturation has
fallen from 95% to 87%. He is also tachypneic and
has retractions and mild nasal flaring. In addition to the
potential pulmonary cause of his respiratory dcompensation,
what cardiac condition should you consider? These symptoms suggest
that Jean Claude has PDA. His respiratory symptoms are
due to left to right shunting with pulmonary over-circulation,
causing tachypnea, increased work of breathing, and hypoxia. What else would you look
for during a physical exam to support this
cardiac diagnosis? On cardiac exam, he may also
have a systolic or continuous murmur at the upper
left sternal border due to the turbulent blood
flowing through the PDA. He could also have hyperactive
precordium, bounding peripheral pulses, and
palpable palmar pulses. You complete your exam and
decide that Jean Claude has likely a PDA. What are some
non-pharmacological treatments you could try first
to support him hoping his ductus closes on its own? Support his
increased respiratory needs with nasal cannula
oxygen or CPAP if available. Restrict fluids to around
80% of maintenance fluids. If you see evidence of
significantly decreased systemic perfusion,
such as decreased urine output or low blood
pressure, hold enteral feeds due to the decreased
intestinal perfusion. After three days of
non-pharmacological support, his ductus does not seem to
have closed by physical exam, and his respiratory
condition is worsening. What pharmacological
treatment can you offer? Since Jean Claude
is a preterm newborn of less than 14
days of age, attempt to close the PDA with
enteral ibuprofen. Provide a first dose of 10 mg
per kg, then 5 mg per kg doses every 24 hours, times two doses. This course of three doses
may be repeated once. When giving ibuprofen, what
are the contraindications and the risks? Contradictions include
thrombocytopenia, less than 50,000, bleeding
disorders, impaired renal function, and
hyperbilirubinemia approaching exchange transfusion levels. Rare intestinal perforation
is one risk of this treatment. Summary. You have now
completed this chapter and you should be
able to identify two presenting symptoms of
patent ductus arteriosus, identify methods for
non-pharmacological support of an infant with patent
ductus arteriosus, identify methods for
pharmacological treatment of an infant with PDA. Keep in mind the
following key points from this
cardiovascular chapter. Patent ductus arteriosus
is postnatal persistence of the normal fetal vessel
that joins the pulmonary artery to the aorta. PDA is most common
in premature infants. It can be diagnosed
using a physical exam and by looking for signs of
pulmonary over-circulation and systemic hypotension. PDA can be managed with
both pharmacological and non-pharmacological
treatments. Pharmacological
management of PDA differs from premature
infants and infants with congenital cardiac defects. Thank you for watching. Please help us improve the
content by providing us with some feedback.


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