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Cyanosis in term neonates
- 1. Cyanosis in termneonates – A problem oriented approach Dr.Gopakumar.H Assistant Professor Dept of Neonatology AIMS , Kochi
- 2. Aims • To providea brief approach to cyanosis in term neonates • Representative case scenarios and discussion Common presentation of common condition Uncommon presentation of common condition Uncommon presentation of uncommon condition • Fetal circulation and basic physiology
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- 4. Fetal circulation 03/14/12 Placenta – gas exchange
- 5. Changes with onsetof 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 03/14/12
- 6. 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 03/14/12
- 7. Diagnostic dilemma inhypoxemia in a full term neonate • Cyanotic congenital heart disease • Persistent pulmonary hypertension 03/14/12
- 8. Identifying right toleft 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 03/14/12
- 9. Hyperoxia test • Placeinfant 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 03/14/12
- 10. Hyperoxia – hyperventilationtest • 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 03/14/12
- 11. Essential diagnosis ofPPHN • 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 03/14/12
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- 13. Case scenario • Termmale 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 03/14/12
- 14. On examination • Spo2on 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 03/14/12
- 15. 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 03/14/12
- 16. • Baby hadincreasing 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 03/14/12
- 17. Problems • Tachypnea ina 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
- 18. Review echo Infra-diaphragmatic -Total anomalous pulmonary venous connection . Emergency corrective surgery done 03/14/12
- 19. TAPVC Entry ofpulmonary veins into systemic venous pathways Supracardiac Cardiac Infracardiac Right SVC Right atrium Portal vein Brachiocepha Coronary IVC lic vein sinus Azygous vein Obstruction to venous return – venous hypertension Worsening cyanosis , increasing respiratory distress, No significant cardiomegaly 03/14/12 Corrective surgery
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- 21. Case scenario • ATerm 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 03/14/12
- 22. 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 % 03/14/12
- 23. Possibilities • Cyanotic heartdisease • Persistent pulmonary hypertension Uncontrolled GDM Elective LSCS without induction of labour Polycythemia Presumed Chronic hypoxia 03/14/12
- 24. Cardiac evaluation • EmergencyEcho– No structural heart disease • Mild PPHN – oxygenate well, Treat the precipitating cause –? Polycythemia, 03/14/12
- 25. Management • Baby wasventilated 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% 03/14/12
- 26. Management Ventilatory adjustementswere changed based on CXR and ABG results . Standard management for PPHN was instituted partial exchange Baby improved with management 03/14/12 Chest –x-ray after 6hrs .
- 27. Highlights – Multiplerisk factors for PPHN • Infant of poorly controlled diabetic mother • Born without labour pains – delayed clearance of lung fluid • Delayed administeration of CPAP • Polycythemia 03/14/12
- 28. Differentiating PPHN fromCCHD PPHN CCHD History Risk factors( NSAID ) May have positive family history Delivery Fetal distress / birth Uneventful asphyxia Examination Respiratory and / or May have cardiac neurological signs 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 . Often low fixed PaO2 Fluctuating oxygen tension Upper limb / lower Lower limb Sometimes limb saturations saturation often discrepent lower Echo Rules out structural Diagnosis heart disease
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- 30. Case scenario • TermAGA 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 03/14/12
- 31. 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 03/14/12
- 32. 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 03/14/12
- 33. Clinical progress • Babyworsened 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 03/14/12 Methemoglobin levels sent
- 34. Methhemoglobin - revealed21% 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 03/14/12
- 35. 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 ) 03/14/12
- 36. Causes of acquiredmethemoglobinemia • Metabolic acidosis • Exposure to certain drugs • Nitrites • Nitrate containing compounds Definitive treatment – Methylene blue 03/14/12
- 37. Neonatal cyanosis Category Details Comments Respiratory Any respiratory disease Cardiac Common mixing Especially if TAPVC 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 03/14/12
- 38. Summary • Respect respiratorydistress 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 03/14/12
- 39. 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 03/14/12
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