Download - Cyanosis in term neonates
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Cyanosis in term neonates – A problem oriented approach
Dr.Gopakumar.HAssistant Professor
Dept of Neonatology AIMS , Kochi
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Aims
• To provide a brief approach to cyanosis in term neonates
• Representative case scenarios and discussion
• Fetal circulation and basic physiology
Common presentation of common condition Uncommon presentation of common condition Uncommon presentation of uncommon condition
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Fetal circulation
Placenta – gas exchange
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Changes with onset of respiration • Breathing initiates abrupt fall
in pulmonary vascular resistance
• Gas exchange function transferred from placenta to lungs
• Concurrent increase in blood flow to the lungs . Pulmonary arterioles dilate in response to increased oxygen saturation
• Closure of 3 communicating channels - ductus arteriosus , ductus venosus and foramen ovale
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Pathology of PPHN
• Any condition that interferes with normal perinatal transition
• Hypoxia and acidosis – pulmonary vasoconstriction ( impaired perinatal transition as in birth asphyxia , MAS etc )
• Pulmonary hypoplasia • Premature closure of
ductus arteriosus as in maternal NSAID therapy
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Diagnostic dilemma in hypoxemia in a full term neonate
• Cyanotic congenital heart disease • Persistent pulmonary hypertension
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Identifying right to left shunt
• Obtain ABG from right radial artery ( preductal ) and posterior tibial artery ( postductal ) simultaneously
• A higher PaO2 in right radial artery sample by 20 mm of Hg indicates presence of right to left shunting
• An SpO2 difference may also suggest right to left shunting
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Hyperoxia test
• Place infant in 100% oxygen concentration for 5 to 10 minutes
• Sample arterial blood • Persistent hypoxia after 5 to 10 minutes
of 100% oxygen exposure suggest presence of right to left shunting
• If PaO2 > 100 mm of Hg , CCHD more or less ruled out
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Hyperoxia – hyperventilation test
• Hypoxia and acidosis causes pulmonary vasoconstriction
• Alkalosis and increased blood oxygen can decrease pulmonary vascular resistance
• By increasing minute ventilation – PaCO2 falls and pH rises . This markedly increase pH and may result in dramatic increase in PaO2
• A dramatic increase along with extreme lability of PaO2 is more suggestive of PPHN
• Differentiates PPHN from CCHD • CCHD – fixed right to left shunting ( PaO2 between 40 to
50 mm Hg ) even with inhalation of 100% oxygen and hyperventilation
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Essential diagnosis of PPHN
• Risk factors ( Birth asphyxia / MAS / Pneumonia etc )
• Chest Ray usually normal / underlying lung condition
• ABG – Low PaO2 in the face of high FiO2 • Echo – to rule out congenital cyanotic
heart disease and to diagnose PPHN
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Case scenario
• Term male baby with birth weight of 3.7kg • Born to IDM mother by Elective LSCS at an
outside hospital• ANP uneventful • Baby cried immediately after birth • Tachypneoic - 70/min - shifted to NICU .• Managed in hood oxygen along with other
supportive measures • On Day 2 Baby had increasing tachypnea
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On examination
• Spo2 on 5ltrs O2 -90-92%, not much difference b/n upper and lower limb.
• Other systems – within normal limits
• Chest x-ray –Bronchopneumonia
• Echo done at referring hospital – PPHN
• Referred for further management
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Admission in AIMS • Baby tachypnic • Spo2 on 5ltrs O2 85-88%, No
significant upper and lower limb difference
• Blood pressure – WNL • CVS - S2 appeared loud • Systolic murmur at tricuspid
area• ABG( preductal) - On 100%
Fio2 • pH – 7.23, PO2 –45mmHg,
PCO2 – 55mmHG, HCO3-15mmol
• Chest X-ray – suggestive of Bronchopneumonia
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• Baby had increasing tachypnea and frequent desaturation upto 80% and electively ventilated
• Hyperoxia – hyperventilation - pH – 7.5, PO2 – 50mmHg, PCO2 –32mmHg , HCO3 – 21mmol, Lactate- 3mmol
• Sepsis screen negative
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Problems • Tachypnea in a term neonate since
birth • Differentiation between PPHN and
CHD • Discordance between clinical
suspicion of sepsis / pneumonia and lab investigation ( No risk factors of sepsis )
• Low PaO2 in Hyperoxia – hyperventilation test
Detailed cardiac evaluation
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Review echo
Infra-diaphragmatic -Total anomalous pulmonary venous connection .
Emergency corrective surgery done
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TAPVC
Entry of pulmonary veins into systemic venous pathways
Supracardiac Cardiac Infracardiac
Right SVC Right atrium Portal vein
Brachiocephalic vein
Coronary sinus IVC
Azygous vein
Obstruction to venous return – venous hypertension Worsening cyanosis , increasing respiratory distress,No significant cardiomegaly Corrective surgery
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Case scenario
• A Term male baby ( birth weight of 3.5 kg )• Mother with uncontrolled gestational diabetes
mellitus• Elective LSCS at 38wks gestational age at
outside hospital • Cried soon after birth • Developed tachypnea soon after birth • Initially managed with O2 hood • At 4hrs after birth - Tachypnea worsened.Had
desaturation to around 85% in hood oxygen and hence referred to AIMS with suspected CCHD
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On admission in AIMS • Baby had tachypnea . No chest retractions or
grunt • Cyanotic with an Oxygen saturation about 75% • Had tachycardia with low pulse volume • Hyperoxia test –saturation improved to 82%• Chest X-ray from outside – mild cardiomegaly,
Lung fields clear(adequate lung volume )• ABG - pH 7.2, PCO2 – 60mmHg, PO2 –
34mmHG, HCO3 – 14mmol • PCV – 71 %
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Possibilities
• Cyanotic heart disease • Persistent pulmonary hypertension Uncontrolled GDM Elective LSCS without
induction of labour Polycythemia Presumed Chronic hypoxia
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Cardiac evaluation
• Emergency Echo– No structural heart disease
• Mild PPHN – oxygenate well, Treat the precipitating cause –? Polycythemia,
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Management • Baby was ventilated
after 2hrs in view of severe hypoxia and features of respiratory failure
• Hb – 24gm%, PCV – 71% • Chest X-ray- lungs
fields normal , Mild cardiomegaly
• Preductal- 88%, Postductal- 82% on Fio2- 100%
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Management
Ventilatory adjustements were changed based on CXR and ABG results . Standard management for PPHN was instituted
partial exchange
Baby improved with management
Chest –x-ray after 6hrs .
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Highlights – Multiple risk factors for PPHN
• Infant of poorly controlled diabetic mother
• Born without labour pains – delayed clearance of lung fluid
• Delayed administeration of CPAP • Polycythemia
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Differentiating PPHN from CCHD PPHN CCHD
History Risk factors( NSAID ) May have positive family history
Delivery Fetal distress / birth asphyxia
Uneventful
Examination Respiratory and / or neurological signs
May have cardiac signs
Chest X ray F/0 resp path Often non specific
ECG Non specific May have clear abnormality ( Usually non specific )
Hyperoxia test Variable response . Fluctuating oxygen tension
Often low fixed PaO2
Upper limb / lower limb saturations
Lower limb saturation often lower
Sometimes discrepent
Echo Rules out structural heart disease
Diagnosis
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Case scenario• Term AGA male baby • Elective LSCS ( persistent breech) in outside
hospital,. • Baby had mild tachypnea initially , which
settled with 2lts of free flow O2 for 2hrs.• At 18hrs of birth , baby had bluish
discoloration of extremities and lips • Shifted the baby to NICU in view obvious
cyanosis, tachypnea and SPO2 of 80%. SPO2 did not improve with hood oxygen
• Systemic examination was within normal limits exept for tachypnea and low SPO2
• Baby shifted to AIMS
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Admission in AIMS
• Supportive measures given • Sepsis screen done –
Negative • Chest X-ray done – Normal • PH- 7.26, PO2 – 300 mmHg ,
PCO2 40 , Lactate – 8 mmol, HCO3 – 17mmol, BE- 15 mmol.- suggestive of Acidosis with lactate build up –( peripheral perfusion problem )
• Echo – reported normal• Arterial blood was dark
brownish
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Problems • Cyanosis • Normal PaO2 • Low SpO2 • Sepsis screen negative • Peripheral perfusion problem• Dark arterial blood
Discordance between clinical suspicion and investigations Normal PaO2 and low SpO2
? Impairment in tissue release
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Clinical progress • Baby worsened over 1hr , Baby
irritablilty increased • Spo2 dropped to 75% on 6ltrsd O2 ,
cyanosis worsened – electively intubated
• Echo – no structural heart disease / PPHN
• ABG – pH – 7.48, PCO2- 35 mm, PO2-300 mmHG , But corresponding overnight Spo2 persisted around 85-88%.Baby still looked cyanotic.
Dark colour of blood – with normal PaO2 ?Hematologic problem
Methemoglobin levels sent
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Methhemoglobin - revealed 21% total Hb%.Hematology consultation done – supportive
measures , correction of metabolic acidosis and Blood transfusion / ET advised
Improved with transfusion ( deferred exchange transfusion )
Methylene blue not availabe Baby gradually improved over the next 2 days
and was off ventilator To repeat Methemoglobin levels at a later date
Methemoglobinemia – probably transient
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Causes of cyanosis
• Relatively high levels of deoxyhemoglobin – generally more than 5 gm / dL
• When nonphysiologic hemoglobin ( eg – Methemoglobin is present more than 1.5 gm / dL )
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Causes of acquired methemoglobinemia
• Metabolic acidosis • Exposure to certain drugs • Nitrites • Nitrate containing compounds
Definitive treatment – Methylene blue
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Neonatal cyanosis Category Details Comments
Respiratory Any respiratory disease
Cardiac Common mixing TAPVC
Especially if obstructed
Truncus arteriosus Cardiac failure
Right to left shunts Pulmonary atresia ( IVS ) Pulmonary atresia ( VSD ) Tricuspid atresia , TGA
PPHN ( includes CNS insult )
Hematologic Methemoglobinemia Grey / blackish blood . Arterial oxygen tension normal
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Summary
• Respect respiratory distress in a term Neonate • Consider early CPAP to recruit lung volume • Differentiate PPHN and CCHD .Role of early
pediatric cardiology evaluation • Discordance between clinical suspicion and
labortary result – think of an alternative diagnosis as well
• Involve experienced specialists at the earliest to guide management decisions
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Acknowledgement
• Dr.Rajiv . P.K• Dr.Mathew Kripail • Dr.Sudheer • Dr.Sivji• Dr.Sunil .B • Dr.Ashwin Prabhu • Dr.Prasanna • Dr.Laxmikanth• All specialists ( Pediatric cardiology and
Hematology ) and Nursing staff involved in the mangement of sick babies
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