Neonates with certain congenital heart diseases are at risk of hemodynamic compromise after birth as ductus arteriosus and other fetal shunts begin to close. Common conditions presenting in the newborn period include obstructive left-sided lesions like coarctation of the aorta and hypoplastic left heart syndrome which rely on ductal patency. Symptoms include heart failure, shock, and death if not recognized and treated promptly with prostaglandin infusion or palliative surgery. Screening programs aim to detect critical congenital heart diseases to prevent newborn collapse.

1. Neonatal
presentation
of congenital
heart diseases
DR. SANKHA JAYASINGHE
07/12/2018

2. Outline
▪ Introduction and epidemiology
▪ Classification
▪ Overview of common cardiac problems presenting in newborn
period
▪ Case discussion
▪ Screening for critical congenital heart diseases in newborns

3. Introduction
▪ Birth is a great event from fetal to the postnatal circulation
▪ The most important changes are from an aquatic amniotic environment
and placental gas exchange to breathing and pulmonary ventilation
▪ Air breathing means sudden drop of pulmonary vascular resistance and
marked increase in pulmonary blood flow
▪ Fetal structures such as foramen ovale, ductus venosus and ductus
arteriosus, which were vital for fetal circulation is no longer needed for
survival and begin to close
▪ Neonate with CHD associated with ductus-dependent pulmonary or
systemic blood flow or with mixing physiology such as TGA is at a great
risk of compromise and collapse as they fail to make an adequate
transition

4. Epidemiology
▪ The incidence of CHD has been estimated to be 6‒8/1,000 live
births in the general population with duct dependent CCHD being
present in 2-3/1000 live births
▪ Infant’s death from CHD accounts for around 6-10%
▪ With early intervention, neonatal mortality from the heart diseases
can fall from 2‒3/1000 to 0.6‒0.8/1000 live births
▪ However, other associated important factors such as combined
congenital anomalies, low birth weight, prematurity, lung
problems, persistent pulmonary hypertension and sepsis also
influence the overall outcome of newborn with CHD

5. Classification
Congenital
heart
diseases
Acyanotic
L to R
shunts
Valvar
Cyanotic
Next slide

6. Atrial level
(cardiomegaly)
Ebstein anomaly,
Tricuspid atresia
Ventricular level
(no cardiomegaly)
(TOF)
Venous
TAPVD
Atrial
Single atrium
Ventricular
Single ventricle
Great vessels
Truncus arteriosus
D-TGA
Right to left
shunts
Admixtures TGA
physiology

7. Ductus dependent circulations
Left sided obstructive lesions (ductus dependent
systemic circulation)
Right sided obstructive lesions (ductus
dependent pulmonary circulation)
Hypoplastic left heart syndrome (HLHS) TOF with pulmonary atresia (PA)
Critical aortic stenosis (AS) Pulmonary atresia (PA)
"shone” complex variants Pulmonary atresia with intact ventricular
septum (PA /IVS)
Coarctation of the aorta (COA) Critical pulmonary stenosis (PS)
Interrupted aortic arch (IAA) Tricuspid atresia, with PS/PA (with/without VSD)
Univentricular heart with PA /PS
Severe Ebsteins anomaly
Complete transposition of the great arteries
with intact ventricular septum (TGA/ IVS)

8. Left sided obstructive lesions (ductus dependent
systemic circulation)
▪ These require ductal patency to maintain perfusion to the whole or
even just the lower sides of the body, or the child develops
progressive acidosis as the duct constricts.
▪ Consequently, perfusion falls and leg pulses become weak,
impalpable and oliguria develop due to renal impairment and
become progressively compromised.

9. Right sided obstructive lesions (ductus dependent
pulmonary circulation)
▪ Most of these CHDs present with progressive cyanosis without
response in proper oxygen supply
▪ Because their fetal physiology is chronically adapted to the hypoxia
in the uterine life, newborn infants are able to tolerate some
degree of cyanosis than older infants or children

10. Specific CHDs

11. Aortic valve
stenosis (AS)
▪ 6% of CHD
▪ Restriction of blood flow through the aortic
valve
▪ Stenotic aortic valve looks small and
dysplastic and often bicuspid
▪ Left ventricle may be markedly dilated with
poor contraction or be hypertrophied when
the systolic function is preserved
▪ Clinical symptoms depend entirely on the
severity of the obstruction and associated
abnormalities
▪ Severe or critical (i.e. PDA dependent) aortic
stenosis may present in a very similar fashion
to isolated CoA as described below, except all
pulses will be reduced
▪ Severe heart failure or other symptoms all
require palliation by valvotomy through
surgery or transcatheter methods

12. Coarctation of the
aorta (COA)
▪ 4 per 10,000 live births, 4% to 6% of CHD
▪ 10% of patients with Turner’s syndrome are
affected, and the risk is thought to be higher
in patients with abnormalities of the X
chromosome
▪ 30% of patients with CoA presenting in
childhood have other associated congenital
heart defects, including PDA, VSD, mitral
valve abnormalities and AS. A bicuspid aortic
valve is present in nearly two thirds of infants
with CoA
▪ Major malformation is narrowing of distal part
of the aortic arch commonly near the ductus
arteriosus, and it is often accompanied by
hypoplasia or diffuse narrowing of the aortic
arch.
▪ In this case usually the lower half of the body
is a ductus dependent and the symptoms will
develop as it starts to close

14. ▪ Initially, while the PDA is open and the
sling of ductal tissue is relaxed, there is
ample forward flow from the aortic arch
to the descending aorta
▪ The baby is clinically well, there is no
difference in saturations between the
arms and feet (PDA flow will be
bidirectional or predominantly left-to-
right), and femoral pulses are likely to be
either normal or slightly weak

15. ▪ At some stage, there may be a transition where
the coarctation tissue starts to constrict while the
PDA remains open
▪ The right ventricle will then be able to provide
adequate perfusion to the body distal to the
coarctation
▪ It will be shunting deoxygenated blood into the
descending aorta, leading to differential
saturations between the arms and legs
▪ Haemodynamically stable at this point with
possibly normal or weak femoral pulses
▪ The kidneys will remain perfused, so there is also
likely to be good urine output
▪ At this point, the left ventricle is exposed to a very
large afterload which will eventually compromise
function, and the upper limb blood pressure (BP)
will climb
▪ This phase may occur very transiently or not at all,
meaning that routine oxygen saturation screening
can often miss these patients

16. ▪ Once the PDA restricts or closes, there is
inadequate perfusion of the organs distal to the
coarctation
▪ This results in severe acidosis from lower body
ischaemia, oliguria due to poor renal perfusion
and electrolyte imbalance
▪ The acidosis will compromise ventricular function
in the already pressure overloaded left ventricle
and circulatory collapse can occur
▪ This can present initially with tachypnoea due to
acidosis and pulmonary oedema, often with rapid
progression to hypotension, clinical signs of low
cardiac output (grey colour, mottling, prolonged
capillary refill time), worsening acidosis, coma and
cardiac arrest
▪ Due to impaired left ventricular function and
reduced cardiac output, upper limb blood pressure
may be low making four-limb blood pressure
measurement an unreliable clinical sign
▪ In any neonate (especially less than 1 week old)
presenting this way, there must be a high index of
suspicion of coarctation

17. Typical CXR of a child
with CoA showing
cardiomegaly and
pulmonary venous
congestion due to
high LA pressure

18. Medical management of COA
What to avoid……..
▪ It is helpful to maintain ductal patency whenever possible
▪ Therefore try to avoid hyperventilation and high FiO2
▪ Vasodilators should also be avoided
▪ If CoA is suspected then fluid boluses should be given with considerable
caution
▪ If required, they should be used in aliquots of 5 ml/kg instead of 10
ml/kg and signs of congestive cardiac failure monitored closely before
giving further boluses
▪ Once established heart failure is difficult to treat and diuretics may
worsen the child’s clinical status

19. Morphological
spectrum of
obstruction in the
aortic arch

20. Interruption of the
aortic arch (IAA)
▪ Failure of development in a portion of the
aortic arch is the major pathology, so there is
no direct connection between ascending and
descending aorta
▪ Lower half of the body has an entirely ductus
dependent circulation.
▪ IAA is always associated with other anomalies
such as VSD, truncus arteriosus,
aortopulmonary window, or other complex
anomalies
▪ Infants with IAA deteriorate very quickly once
their duct begins to close, with initial
breathlessness, congestive heart failure,
acidosis, cardiovascular collapse, and death
within few days
▪ Early recognition and intervention will
inevitably lead to a better outcome

21. Hypoplastic left
heart syndrome
(HLHS)
▪ 1 per 5000 live births , 2‒3% of all CHD
▪ Some genetic syndromes are associated with
HLHS and chromosomal anomalies are seen in 4-
10% of cases (Turner Xn, trisomy 13 and 18)
▪ HLHS includes aortic valve atresia and some forms
of mitral atresia
▪ Absent forward flow through the left ventricular
outlet is characteristic
▪ Left ventricle is markedly underdeveloped and
often rudiment
▪ Aortic arch is also hypoplastic and ascending aorta
is very small, acting simply as a passage into the
coronary arteries
▪ Pulmonary venous return can only reach systemic
circulation by traversing the patent foramen ovale
to reach the right atrium
▪ This implies mixing of pulmonary venous and
systemic venous flow, creating a mild cyanotic
condition

22. ▪ A plain chest radiograph can reveal
cardiomegaly with pulmonary plethora
and oedema, but is not diagnostic.

23. Hypoplastic left heart syndrome (HLHS)
▪ All systemic circulation is absolutely dependent on the ductus arteriosus
▪ After birth, systemic vascular resistance is higher than pulmonary, with the ductal closure,
nonfunctioning left ventricle cannot take charge of the cardiac output
▪ This leads to circulatory deterioration, metabolic acidosis, and shock
▪ Increased pulmonary flow leads to increase in the left atrial pressure and subsequent
pulmonary edema
▪ Clinical presentations are early heart failure, listlessness, duskiness, tachypnea or even death
due to circulatory collapse
▪ The median age at diagnosis is about two days of life
▪ The natural history is early death with almost no prospect of prolonged natural survival
▪ PGE1 infusion is necessary to survive
▪ The increased incidence of NEC in neonates with CHD and duct dependent systemic
circulations may justify a ‘nil by mouth’ strategy to minimize the risk of NEC in babies born
with HLHS

24. ▪ Congestive cardiac failure is treated initially with diuretics but inotropic
support (often dobutamine 5-10 mcg/kg/min) may be needed to
support the volume loaded right ventricle
▪ Positive-pressure ventilation reduces pulmonary oedema, and permissive
hypercapnia can raise pulmonary vascular resistance and so reduce
pulmonary overcirculation, although this is rarely necessary
▪ Those who remain profoundly cyanosed despite ventilatory support need
urgent decompression of the left atrium (pulmonary venous congestion)
with either balloon atrial septostomy or early surgery
▪ The ‘Norwood strategy’ is undertaken through three stages: (i) the
Norwood operation on neonates; (ii) superior cavopulmonary
anastomosis at 6-8 months of age; and (iii) total cavopulmonary
connection between 18 months and 5 years of age (most commonly
around 4 years)

25. Characteristics of
pulses in obstructive
left heart lesions

26. Pulmonary atresia
(PA)
▪ Main pathology in PA is the absence of a
direct connection between the right
ventricle and the lungs
▪ Two main types
▪ PA/VSD
▪ PA/IVS
▪ PA/VSD
▪ also known as tetralogy of Fallot type pulmonary
atresia
▪ favorable sized two ventricles with large
subaortic VSD and variable source of pulmonary
arterial supply
▪ PA/IVS
▪ tricuspid valve and right ventricle are usually
severely underdeveloped
▪ pulmonary arteries are relatively well developed
and supplied by PDA

27. PA/IVS- a typical form of ductus-dependent
pulmonary circulation
▪ Become more cyanosed and aggravated as the ductus closes
▪ Without prostaglandin infusion, eventually will collapse and
perhaps die within a first few day of life
▪ Functionally single ventricular physiology, and the eventual surgical
goal may usually be ‘Fontan’ type operation, more often a
cavopulmonary shunt achieving a right heart bypass
▪ Early palliation involves shunt such as Blalock-Taussig (BT) shunt to
replace the ductus

28. Total anomalous
pulmonary venous
return (TAPVR)
▪ 1% of CHD
▪ All four pulmonary venous directly connect to
the right atrium instead of the left atrium
▪ There are four main types
▪ Supracardiac type (50%) to the innominate vein
▪ Cardiac type (20%) to the coronary sinus
▪ Infradiaphragmatic type (20%) to the hepatic or
portal vein
▪ Mixed type (10%)
▪ The timing and mode of presentation depend
on the type and degree of obstruction
▪ Infracardiac type is the most commonly
obstructed and may have serious
manifestations
▪ Survival rate is reported 50% at 1-month and
0% at 12-month without treatment

29. ▪ Common pulmonary venous channels are delivered to the right atrium,
and there the mixing of the pulmonary and systemic circulations occurs
▪ Systemic desaturation occurs as the result of mixing of two circulations.
▪ In patients with TAPVR with obstruction, progressive cyanosis and
respiratory distress dominate the presentation
▪ Infants with obstructed TAPVR often have unremarkable clinical findings
except progressive cyanosis and dyspnea, they frequently masquerade
as parenchymal lung disease with pulmonary hypertension such as
congenital pneumonia, meconium aspiration pneumonitis, respiratory
distress syndrome and pulmonary lymphangiectasia
▪ Unless definite evidence for parenchymal lung lesions is present, or there
is no appropriate response to conventional therapeutic measures, early
echocardiography should be considered to make these distinctions

30. Supracardiac
TAPVD

31. ▪ Infants may not present immediately after birth, but most affected
babies present with the combination of cyanosis and heart failure
▪ The only option is early primary repair as soon as possible
▪ Prostaglandin infusion is not helpful in this case, can even be
harmful
▪ It leads to increased pulmonary blood flow and reduces the
pulmonary vascular resistance and may exacerbate the pulmonary
venous congestion when obstruction is combined

32. Transposition of the
great arteries with
intact ventricular
septum (TGA/IVS)
▪ 5‒8% of CHD
▪ Characterized by atrioventricular
concordance and ventriculoarterial
discordance
▪ If the ventricular septum is intact or ASD
is restrictive, limited intercirculatory
mixing leads to progressive and profound
cyanosis within the first few hours of life
▪ Its severity and onset depend on the
degree of mixing between the two
circulations
▪ Complete separation of two circulatory
systems will lead to death
▪ After birth some cross-flow between two
separated circulations such as ductus or
foramen ovale are necessary to survive

33. ▪ There will be a loud, single S2, but no specific murmur is notable
▪ On the chest X-ray, cardiomegaly with increased pulmonary vascular
markings and so called” egg-shaped heart” with a narrow mediastinum
is the characteristic findings on chest x-ray, but not always
▪ Congestive heart failure with dyspnea in addition to intractable cyanosis
which does not respond to the oxygen is the common presentation
▪ Acidosis as well as hypocalcemia and hypoglycemia are also frequent
▪ If large VSD or PDA coexists, congestive heart failure with dyspnea and
feeding difficulties in addition to the cyanosis is a common
manifestation in the first week of life, and eventually progress into
obstructive pulmonary vascular disease

34. d-TGA

35. ▪ Babies with TGA should be started on PGE1 infusion to maintain
ductal patency which increases the pulmonary flow, and leads to
pulmonary venous return and left atrial pressure, thus promoting
left to right shunt at the atrial level
▪ If the foramen ovale is restricted, PGE1 alone could not achieve
clinical improvement and emergency balloon atrial septostomy
(Rashkind balloon septostomy) is the only way to rescue these
infants

36. Management

37. Ductus dependent pulmonary circulatory lesions
▪ These infants require to start on PGE1 infusion to keep the ductus open until Blalock Taussig
(BT) shunt is created
▪ PGE1 decreases pulmonary vascular resistance and enhances the left to right shunting and
eventually increases pulmonary blood flow
▪ The initial intravenous dose of PGE1 is 0.05 μg/kg/min. If no improvement, increment to 0.1
μg/kg/min.
▪ After stabilization, the usual maintenance dose of PGE1 is 0.025 μg/kg/min
▪ Apnea, bradycardia, hypotension, fluid-electrolyte imbalances, irritablilty, fever and cutaneous
flushing are potential complicating side effects of PGE1
▪ Apnea secondary to prostaglandin is not a rare indication for tracheal intubation, but do not
reduce the dose and never stop
▪ Long-term use is associated with cortical hyperostosis, an effect that does not seem to be
dose related
▪ Although there is no CHD for which PGE1 is contraindicated, obstructed TAPVR and TGA with a
restrictive atrial septum may exacerbate with PGE1

38. Ductus dependent systemic circulation lesions
▪ Oxygen supplementation can exacerbate the closure of the ductus arteriosus and
worsen the infant’s condition by cardiogenic shock
▪ Therefore, do not increase oxygen supply until after PGE1 has been Started
▪ In these patients treatment should aim to optimize systemic oxygenation and
prevent metabolic acidosis, which can be harmful to perioperative condition
▪ Two fundamental principles underlie the management of these patients
▪ Firstly, maintain ductal patency
▪ The starting dose is usually 5.0-15.0 nanogram/kg/minute and this can be increased up to
100 nanogram/kg/minute if needed. It should be administered as soon as possible and it
can take between 15 minutes and 4 hours to re-establish forward circulation
▪ Secondly, when ductal patency has been prepared, attention should be directed to
the flow balance between the pulmonary and systemic circulation.
▪ Ventilatorory strategies must aim to increase pulmonary vascular resistance to avoid
pulmonary over circulation

39. ▪ Maintaining the balance between two competitive circulations allows
adequate perfusion to the systemic and myocardium and the ideal
pulmonary to systemic flow ratio are of about 1:1.
▪ This goal can be achieved by adjusting PEEP (4‒6 cm H2O), modulating
inspiratory rate, pressures or tidal volumes to keep an arterial CO2
tension of 5‒6 kPa. Avoid too much oxygen supply, maintain systemic
arterial saturation around 80% and avoid respiratory alkalosis
▪ The risk of high FiO2 or low partial pressure of CO2 (paCO2) is that these
might lower pulmonary vascular resistance, may lead to volume loading
to the pulmonary circulation, and lead to cardiac failure
▪ Sedation with morphine is usually necessary; muscle relaxants should be
considered for infants in shock who sustains tachypnea

40. ▪ Recent focus has been given to lowering systemic vascular
resistance to secure better systemic perfusion, using vasodilators
such as phenoxybenzamine and the phosphodiesterase inhibitor,
milrinone
▪ Functionally univentricular palliative treatment consists of three
stages: (1) Neonate: Norwood operation, (2) 6‒8 months of age:
stage II, (3) 18 months and 5 years of age: stage III

41. Left to right shunts
INCREASED PULMONARY BLOOD FLOW

42. Post-tricuspid
shunts
VSD, PDA
Shunt directions is
governed by relative
resistances (or
pressures if the
defect is small)
Pre-tricuspid
shunts
ASD, AVSD
Shunt direction is
governed by relative
ventricular
compliances

43. Case presentation
▪ 30 year old primi mother, on Thyroxine for hypothyroidism
▪ POA 39+6, forceps delivery (delayed 2nd stage), Bwt 2.5kg
▪ Thick meconium at birth, not cried, Apgar 2/6/7, resuscitated and
intubated (extubated after admission to PBU)
▪ Treated as for MAS+PPHN
▪ D1 to D3 on HFNPO2
▪ D4 NIPPV, intubated and ventilated from D5 due to increased RD and
weaned to CPAP on D10
▪ D10 R/S lung collapse, put on NIPPV till D12
▪ Reintubated on D12 developed pulmonary haemorrhage on D17

44. Ctd
▪ Baby had a systolic murmur from D1 with a loud P2, off colour
▪ Was on inotropes
▪ D3 started on sildenafil 1mg/kg 6H
▪ From D6 on, long systolic murmur, P2 normal, pulse pressure
normal
▪ Inotropes discontinued by D8
▪ D12 increasing RD, hepatomegaly intubated, fluid restricted
▪ D13 started on frusemide and sildenafil tailed off
▪ D14 Paracetomol started and continued for 2 days

45. Ctd
▪ D18 Ibuprofen started and continued for 3 days
▪ 2D Echo showed large PDA with heart failure
▪ D21 Captopril started
▪ D22 Indomethacin started for 5 days
▪ D23 transferred to LRH for ductal closure
Other problems
▪ D4 neonatal convulsions (normal USS brain, S/E and Ca)
▪ Neonatal jaundice+ anaemia (blood picture- mild haemolysis, both mother and
baby were O positive, maternal AB negative, blood transfusion done, folic acid)
▪ Oedema (albumin transfusion)
▪ Sepsis (blood culture positive for Acenatobactor, I.V. antibiotics)

46. PATENT DUCTUS
ARTERIOSUS

47. ▪ Persistence of the fetal communication between the aorta and the pulmonary trunk
▪ In most term babies, functional closure occurs by 24 hours of age
▪ Rising oxygen tension and withdrawal of endogenous prostaglandins
▪ Following birth, if the ductus arteriosus remains patent, the shunt as pulmonary
resistance falls changes from the aorta to the pulmonary artery
▪ As pulmonary vascular resistance falls following birth, the volume of pulmonary
blood flow increases
▪ If ductal shunting has a negative relationship of systemic blood flow, it does so very
early after birth. After that time, in most cases, the heart seems to compensate well
by increasing left ventricular output to maintain systemic blood flow
▪ This early low systemic blood flow is associated with the development of
intraventricular haemorrhage and later necrotising enterocolitis
▪ If the volume of pulmonary blood flow is large, congestive cardiac failure occurs
because of the excessive volume load placed upon the left ventricle

48. ▪ While the heart can compensate for effective loss of blood from
the systemic circulation, the overload of the pulmonary circulation
is passive, inevitable and only limited by the resistance of the
vasculature
▪ The immediate clinical risk of this seems to be pulmonary
haemorrhage (a misnomer because it’s not blood but
haemorrhagic pulmonary oedema)
▪ PDA features consistently as a risk factor for chronic lung disease
but treatment of the PDA, including prophylactic treatment, makes
no difference to incidence of chronic lung disease

49. ▪ Patent ductus arteriosus occurs more frequently in females and in
prematurely born infants
▪ Also common in children with Down syndrome
▪ Children whose mothers had rubella during the first trimester of
pregnancy, patent ductus arteriosus is the most commonly
observed cardiac anomaly
▪ The classical physical finding is a continuous, often machinery-
sounding murmur best heard over the upper left chest below the
clavicle
▪ The murmur may not continue through the entire cardiac cycle, but
generally it does extend well into diastole except in the first few
months of life. At this age, the murmur may be confined to systole

50. Wide pulse pressure
▪ The aortic systolic pressure is elevated because of an increased
stroke volume into the aorta (normal cardiac output + the volume
of blood through the shunt) and the diastolic pressure is lowered
because of the flow into the pulmonary circuit
▪ Peripheral arterial pulses are prominent
▪ In patients with a small patent ductus arteriosus, the blood
pressure readings are normal
▪ However, those patients with a larger flow show wide pulse
pressure
▪ P2 is loud due to increased pulmonary blood flow

51. Medical management
▪ Ibuprofen is usually given as three doses, 24 hours apart, of 10 mg/kg, 5
mg/kg and 5 mg/kg
▪ Consider the higher dose if treating after day 5 (double doses)
▪ There is now consistent evidence from several trials that oral ibuprofen
(cheap) achieves better closure rates than IV ibuprofen (expensive)
▪ Indomethacin three doses, 24 hours apart, of 0.2 mg/kg, 0.1 mg/kg and
0.1 mg/ kg seems as effective as longer courses and may have less side
effects
▪ The studies in the Cochrane review suggest that about 75% of PDAs will
close with these drugs
▪ Those that fail to close with one course are unlikely to respond to a
second, but occasionally they do, particularly if they closed and then
reopened, so it’s probably worth repeating at least once

52. ▪ Paracetamol is emerging as a possible alternative to indomethacin
and ibuprofen following a chance observation made by
Hammerman et al. in a baby with a PDA who was given
paracetamol for pain relief
▪ Failing medical management, surgical ligation or Transcatheter
closure must be tried.

53. EVALUATION OF SUSPECTED
CONGENITAL HEART DISEASE

55. The clinical presentation of CHD
conditions can be broadly
divided into three categories:
Cyanotic CHD
presenting as
blue baby
CHD
presenting
with neonatal
collapse or
even sudden
death in
infancy
CHD
presenting as
heart
murmur or
heart failure

56. Newborn screening to detect critical CHD
▪ The CCHD that are of concern include HLHS, PA/IVS, TOF, TAPVD, TGA,
tricuspid atresia and truncus arteriosus
▪ Even after anomaly scan and neonatal examination, upto 1/3 of babies
with CCHD are missed
▪ In conjunction with pre-existing screening tools, Pulse oximetry screening
can detect up to 78-92% of critical CHDs
▪ It has high specificity (more than 99-99.6%) and moderate sensitivity
(75-80%) in detecting critical CHD in asymptomatic neonates
▪ Should be performed 24 hrs after birth to reduce the false positive rates
▪ Oxygen saturations of less than 95% in air or a difference over 2-3%
between pre- and post-ductal saturations, is considered significant

57. Our practice
▪ If SPO2 in RH or any foot <90%, test is positive and do not
discharge till 2D echo is done (exclude respiratory and septic
conditions)
▪ If SPO2 95% or more and difference is <3%, the screen is negative
▪ If SPO2 between 90-94% (in RH or foot) or difference is more than
3%, can repeat screen 2 more times with hourly intervals and
results are considered as above

59. Thank you!

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