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Cyanosis in term neonates

May 26, 2015



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

  • 1. Cyanosis in term neonates Aproblem oriented approach Dr.Gopakumar.H Assistant Professor Dept of NeonatologyAIMS , Kochi

2. Aims To provide a brief approach tocyanosis in term neonates Representative case scenarios anddiscussion Common presentation of common condition Uncommon presentation of common condition Uncommon presentation of uncommon condition Fetal circulation and basicphysiology 3. 03/14/12 4. Fetal circulation03/14/12Placenta gas exchange 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. Pathology of PPHN Any condition thatinterferes with normalperinatal transition Hypoxia and acidosis pulmonaryvasoconstriction( impaired perinataltransition as in birthasphyxia , MAS etc ) Pulmonary hypoplasia Premature closure ofductus arteriosus as inmaternal NSAIDtherapy03/14/12 7. Diagnostic dilemma in hypoxemiain a full term neonate Cyanotic congenital heartdisease Persistent pulmonaryhypertension03/14/12 8. Identifying right to leftshunt Obtain ABG from right radial artery( preductal ) and posterior tibialartery ( postductal ) simultaneously A higher PaO2 in right radial arterysample by 20 mm of Hg indicatespresence of right to left shunting An SpO2 difference may alsosuggest right to left shunting03/14/12 9. Hyperoxia test Place infant in 100% oxygenconcentration for 5 to 10 minutes Sample arterial blood Persistent hypoxia after 5 to 10minutes of 100% oxygen exposuresuggest presence of right to leftshunting If PaO2 > 100 mm of Hg , CCHD moreor less ruled out03/14/12 10. Hyperoxia hyperventilation test Hypoxia and acidosis causes pulmonaryvasoconstriction Alkalosis and increased blood oxygen can decreasepulmonary vascular resistance By increasing minute ventilation PaCO2 falls andpH rises . This markedly increase pH and mayresult in dramatic increase in PaO2 A dramatic increase along with extreme lability ofPaO2 is more suggestive of PPHN Differentiates PPHN from CCHD CCHD fixed right to left shunting ( PaO2 between40 to 50 mm Hg ) even with inhalation of 100%oxygen and hyperventilation03/14/12 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 highFiO2 Echo to rule out congenitalcyanotic heart disease and todiagnose PPHN03/14/12 12. 03/14/12 13. Case scenario Term male baby with birth weight of3.7kg Born to IDM mother by Elective LSCS at anoutside hospital ANP uneventful Baby cried immediately after birth Tachypneoic - 70/min - shifted to NICU . Managed in hood oxygen along with othersupportive measures On Day 2 Baby had increasing tachypnea03/14/12 14. On examination Spo2 on 5ltrs O2-90-92%, not muchdifference b/n upperand lower limb. Other systems withinnormal limits Chest x-ray Bronchopneumonia Echo done at referringhospital PPHN Referred for furthermanagement03/14/12 15. Admission in AIMS Baby tachypnic Spo2 on 5ltrs O2 85-88%, Nosignificant upper and lowerlimb difference Blood pressure WNL CVS - S2 appeared loud Systolic murmur at tricuspidarea ABG( preductal) - On 100%Fio2 pH 7.23, PO2 45mmHg, PCO2 55mmHG, HCO3-15mmol Chest X-ray suggestiveof Bronchopneumonia03/14/12 16. Baby had increasing tachypneaand frequent desaturation upto80% and electively ventilated Hyperoxia hyperventilation - pH 7.5,PO2 50mmHg, PCO2 32mmHg , HCO3 21mmol,Lactate- 3mmol Sepsis screen negative03/14/12 17. Problems Tachypnea in a term neonatesince birth Differentiation between PPHNand CHD Discordance between clinicalsuspicion of sepsis / pneumoniaand lab investigation ( No riskfactors of sepsis ) Low PaO2 in Hyperoxia hyperventilation testDetailed cardiac evaluation 18. Review echo Infra-diaphragmatic -Total anomalous pulmonary venous connection . Emergency corrective surgery done03/14/12 19. TAPVC Entry of pulmonary veins into systemic venous pathwaysSupracardiac Cardiac InfracardiacRight SVC Right atrium Portal veinBrachiocepha CoronaryIVClic vein sinusAzygous vein Obstruction to venous return venous hypertension Worsening cyanosis , increasing respiratory distress, No significant cardiomegaly03/14/12 Corrective surgery 20. 03/14/12 21. Case scenario A Term male baby ( birth weight of 3.5 kg ) Mother with uncontrolled gestationaldiabetes mellitus Elective LSCS at 38wks gestational age atoutside hospital Cried soon after birth Developed tachypnea soon after birth Initially managed with O2 hood At 4hrs after birth - Tachypneaworsened.Had desaturation to around 85%in hood oxygen and hence referred to AIMSwith suspected CCHD03/14/12 22. On admission inAIMS Baby had tachypnea . No chest retractionsor grunt Cyanotic with an Oxygen saturation about75% Had tachycardia with low pulse volume Hyperoxia test saturation improved to82% Chest X-ray from outside mildcardiomegaly, Lung fields clear(adequatelung volume ) ABG - pH 7.2, PCO2 60mmHg, PO2 34mmHG, HCO3 14mmol PCV 71 %03/14/12 23. Possibilities Cyanotic heart disease Persistent pulmonaryhypertensionUncontrolled GDMElective LSCS withoutinduction of labourPolycythemiaPresumed Chronic hypoxia03/14/12 24. Cardiac evaluation Emergency Echo Nostructural heart disease Mild PPHN oxygenate well,Treat the precipitatingcause ? Polycythemia,03/14/12 25. Management Baby was ventilatedafter 2hrs in view ofsevere hypoxia andfeatures of respiratoryfailure Hb 24gm%, PCV 71% Chest X-ray- lungsfields normal , Mildcardiomegaly Preductal- 88%,Postductal- 82% onFio2- 100%03/14/12 26. ManagementVentilatoryadjustements werechanged based on CXRand ABG results .Standard managementfor PPHN wasinstitutedpartial exchangeBaby improved withmanagement03/14/12 Chest x-ray after 6hrs . 27. Highlights Multiple risk factors forPPHN Infant of poorly controlleddiabetic mother Born without labour pains delayed clearance of lung fluid Delayed administeration ofCPAP Polycythemia03/14/12 28. Differentiating PPHN from CCHDPPHN CCHDHistoryRisk factors( NSAID )May have positivefamily historyDelivery Fetal distress / birth Uneventful asphyxiaExaminationRespiratory and / or May have cardiac neurological signs signsChest X rayF/0 resp pathOften non specificECGNon specific May have clearabnormality ( Usuallynon 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. 03/14/12 30. Case scenario Term AGA male baby Elective LSCS ( persistent breech) inoutside hospital,. Baby had mild tachypnea initially , whichsettled with 2lts of free flow O2 for 2hrs. At 18hrs of birth , baby had bluishdiscoloration of extremities and lips Shifted the baby to NICU in view obviouscyanosis, tachypnea and SPO2 of 80%.SPO2 did not improve with hood oxygen Systemic examination was within normallimits exept for tachypnea and low SPO2 Baby shifted to AIMS03/14/12 31. Admission in AIMS Supportive measuresgiven Sepsis screen done Negative Chest X-ray done Normal PH- 7.26, PO2 300mmHg , PCO2 40 ,Lactate 8 mmol, HCO3 17mmol, BE- 15 mmol.-suggestive of Acidosiswith lactate build up ( peripheral perfusionproblem ) Echo reported normal Arterial blood was darkbrownish 03/14/12 32. Problems Cyanosis Normal PaO2 Low SpO2 Sepsis screen negative Peripheral perfusion problem Dark arterial bloodDiscordance between clinical suspicion and investigationsNormal PaO2 and low SpO2? Impairment in tissue release 03/14/12 33. Clinical progress Baby worsened over 1hr , Babyirritablilty increased Spo2 dropped to 75% on 6ltrsd O2 ,cyanosis worsened electivelyintubated Echo no structural heart disease /PPHN ABG pH 7.48, PCO2- 35 mm,PO2-300 mmHG , But correspondingovernight Spo2 persisted around85-88%.Baby still looked cyanotic. Dark colour of blood with normal PaO2 ?Hematologic problem03/14/12 Methemoglobin levels sent 34. Methhemoglobin - revealed 21% total Hb%.Hematology consultation done supportivemeasures , correction of metabolicacidosis and Blood transfusion / ET advisedImproved with transfusion ( deferredexchange transfusion )Methylene blue not availabeBaby gradually improved over the next 2days and was off ventilatorTo repeat Methemoglobin levels at a laterdate Methemoglobinemia probably transient03/14/12 35. Causes of cyanosis Relatively high levels ofdeoxyhemoglobin generallymore than 5 gm / dL When nonphysiologic hemoglobin( eg Methemoglobin is presentmore than 1.5 gm / dL )03/14/12 36. Causes of acquired methemoglobinemia Metabolic acidosis Exposure to certain drugs Nitrites Nitrate containing compounds Definitive treatment Methylene blue03/14/12 37. Neonatal cyanosisCategoryDetailsCommentsRespiratory Any respiratory diseaseCardiac Common mixing Especially ifTAPVC obstructedTruncus arteriosusCardiac failureRight to left shuntsPulmonary atresia ( IVS )Pulmonary atresia ( VSD )Tricuspid atresia , TGAPPHN ( includes CNSinsult )Hematologic Methemoglobinemia Grey / blackish blood .Arterial oxygentension normal03/14/12 38. Summary Respect respiratory distress in a termNeonate Consider early CPAP to recruit lung volume Differentiate PPHN and CCHD .Role of earlypediatric cardiology evaluation Discordance between clinical suspicionand labortary result think of analternative diagnosis as well Involve experienced specialists at theearliest to guide management decisions03/14/12 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 andHematology ) and Nursing staff involved inthe