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Cyanosis in term neonates


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The presentation discusses two case scenarios of cyanosis in a term neonate and a general approach to management

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Cyanosis in term neonates

  1. 1. Cyanosis in term neonates – Aproblem oriented approach Dr.Gopakumar.H Assistant Professor Dept of Neonatology AIMS , Kochi
  2. 2. Aims• To provide a 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
  3. 3. 03/14/12
  4. 4. Fetal circulation03/14/12 Placenta – gas exchange
  5. 5. Changes with onset ofrespiration• 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 ovale03/14/12
  6. 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 therapy03/14/12
  7. 7. Diagnostic dilemma in hypoxemiain a full term neonate• Cyanotic congenital heart disease• Persistent pulmonary hypertension03/14/12
  8. 8. Identifying right to leftshunt• 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 shunting03/14/12
  9. 9. 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 out03/14/12
  10. 10. 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 hyperventilation03/14/12
  11. 11. 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 PPHN03/14/12
  12. 12. 03/14/12
  13. 13. 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 tachypnea03/14/12
  14. 14. 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 management03/14/12
  15. 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 Bronchopneumonia03/14/12
  16. 16. • 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 negative03/14/12
  17. 17. 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
  18. 18. Review echo Infra-diaphragmatic -Total anomalous pulmonary venous connection . Emergency corrective surgery done03/14/12
  19. 19. TAPVC Entry of pulmonary veins into systemic venous pathwaysSupracardiac Cardiac InfracardiacRight SVC Right atrium Portal veinBrachiocepha Coronary IVClic vein sinusAzygous vein Obstruction to venous return – venous hypertension Worsening cyanosis , increasing respiratory distress, No significant cardiomegaly03/14/12 Corrective surgery
  20. 20. 03/14/12
  21. 21. 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 CCHD03/14/12
  22. 22. On admission inAIMS• 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. 23. Possibilities• Cyanotic heart disease• Persistent pulmonary hypertension Uncontrolled GDM Elective LSCS without induction of labour Polycythemia Presumed Chronic hypoxia03/14/12
  24. 24. Cardiac evaluation• Emergency Echo– No structural heart disease• Mild PPHN – oxygenate well, Treat the precipitating cause –? Polycythemia,03/14/12
  25. 25. 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%03/14/12
  26. 26. ManagementVentilatory adjustements were changed based on CXR and ABG results . Standard management for PPHN was institutedpartial exchangeBaby improved with management03/14/12 Chest –x-ray after 6hrs .
  27. 27. Highlights – Multiple risk factors forPPHN• Infant of poorly controlled diabetic mother• Born without labour pains – delayed clearance of lung fluid• Delayed administeration of CPAP• Polycythemia03/14/12
  28. 28. Differentiating PPHN from CCHD PPHN CCHDHistory Risk factors( NSAID ) May have positive family historyDelivery Fetal distress / birth Uneventful asphyxiaExamination Respiratory and / or May have cardiac neurological signs signsChest X ray F/0 resp path Often non specificECG Non specific May have clear abnormality ( Usually non specific )Hyperoxia test Variable response . Often low fixed PaO2 Fluctuating oxygen tensionUpper limb / lower Lower limb Sometimeslimb saturations saturation often discrepent lowerEcho Rules out structural Diagnosis heart disease
  29. 29. 03/14/12
  30. 30. 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 AIMS03/14/12
  31. 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. 32. Problems • Cyanosis • Normal PaO2 • Low SpO2 • Sepsis screen negative • Peripheral perfusion problem • Dark arterial bloodDiscordance between clinical suspicion and investigations Normal PaO2 and low SpO2 ? Impairment in tissue release 03/14/12
  33. 33. 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 problem03/14/12 Methemoglobin levels sent
  34. 34. Methhemoglobin - revealed 21% total Hb%.Hematology consultation done – supportive measures , correction of metabolic acidosis and Blood transfusion / ET advisedImproved with transfusion ( deferred exchange transfusion )Methylene blue not availabeBaby gradually improved over the next 2 days and was off ventilatorTo repeat Methemoglobin levels at a later date Methemoglobinemia – probably transient03/14/12
  35. 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. 36. Causes of acquired methemoglobinemia• Metabolic acidosis• Exposure to certain drugs• Nitrites• Nitrate containing compounds Definitive treatment – Methylene blue03/14/12
  37. 37. Neonatal cyanosis Category Details CommentsRespiratory Any respiratory diseaseCardiac Common mixing Especially if TAPVC obstructed Truncus arteriosus Cardiac failure Right to left shunts Pulmonary atresia ( IVS ) Pulmonary atresia ( VSD ) Tricuspid atresia , TGAPPHN ( includes CNSinsult )Hematologic Methemoglobinemia Grey / blackish blood . Arterial oxygen tension normal 03/14/12
  38. 38. 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 decisions03/14/12
  39. 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 babies03/14/12
  40. 40. 03/14/12