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Cyanosis in newborn
- 2. Contents Introduction Factors affecting detection of cyanosis Etiology Types Cardiac vs pulmonary Approach Conclusion
- 3. Introduction Cyanosis is the bluish discoloration of the skin and mucous membranes due to increased concentration of reduced hemoglobin to about >5g/100 mL in the cutaneous veins Desaturation of arterial blood Increased extraction of oxygen by peripheral tissue in the presence of normal arterial saturation Detected –lips,fingernails,oral mucous membranes,conjuctiva and tip of tongue
- 4. Factors affecting detection of cyanosis in newborn Hemoglobin concentration Fetal hemoglobin Skin pigmentation
- 5. Hemoglobin concentration The arterial oxygen saturation level at which cyanosis is detectable at different total hemoglobin concentrations is illustrated above. The solid red portion of each bar represents 3 gm/dL reduced hemoglobin.
- 6. Fetal hemoglobin The oxygen-dissociation curve of human blood and the effects of changes in the H+ ion concentration, Pco2 temperature and level of 2, 3-diposphoglycerate (2,3-DPG) are depicted above. For fetal hemoglobin, the normal curve (a) is shifted to the left (b).
- 7. Skin pigmentation Less apparent in the skin of babies with darker pigmentation. Examination should include the nail beds, tongue, and mucous membranes, which are less affected by pigmentation.
- 9. Ventilation/perfusion mismatch Airway disease: transient tachypnea of the newborn (TTN), respiratory distress syndrome (RDS), pneumonia, aspiration (meconium, blood, amniotic fluid), atelectasis, diaphragmatic hernia, pulmonary hypoplasia, pulmonary hemorrhage, CCAM Extrinsic compression of the lungs: pneumothorax, pleural effusion, hemothorax,
- 10. Alveolar hypoventilation CNS depression: asphyxia, maternal sedation, intraventricular hemorrhage, seizure, meningitis, encephalitis Airway obstruction: choanal atresia, laryngomalacia, Pierre Robin syndrome Neuromuscular disease: phrenic nerve inury, neonatal myasthenia gravis
- 11. Diffusion impairment Pulmonary edema: left-sided obstructive cardiac disease, cardiomyopathy Pulmonary fibrosis Congenital lymphangiectasia
- 12. Cardiac causes Decreased pulmonary blood flow- Tetralogy of Fallot Tricuspid valve anomaly Pulmonary valve atresia Critical valvular pulmonary steanosis Increased pulmonary blood flow- Transposition of great arteries Truncus arteriosus Total anomalous pulmonary venous connection
- 13. Cardiac causes- "five Ts" of cyanotic CHD: Transposition of the great arteries Tetralogy of Fallot Truncus arteriosus Total anomalous pulmonary venous connection Tricuspid valve abnormalities. A sixth "T" is often added for "tons" of other diseases, such as double outlet right ventricle, pulmonary atresia, multiple variations of single ventricle, hypoplastic left heart syndrome, or anomalous systemic venous connection (left superior vena cava connected to the left atrium).
- 14. Hemoglobinopathies Hereditary < exposure to toxic substances >15%- cyanosis >70% -lethal Remain chocolate brown-even with full oxygenation or long exposure to room air
- 15. Central cyanosis Inadequate alveolar ventilation CNS depression Inadequate ventilatory drive Obstruction Structural changes Muscle weakness Desaturated blood bypassing alveolar units Intracardiac R-L Intrapulmonary shunt Pulmonary hypertension with R-L shunt
- 16. Peripheral cyanosis Peripheral cyanosis, involves a bluish discoloration of the skin but sparing of the mucus membranes & tongue. In this type, a normal PaO2 value is detected Increased oxygen extraction due to sluggish movement through the capillaries leads to increased deoxygenated blood on the venous side Vasomotor instability,vasoconstriction caused by cold, low cardiac output, venous obstruction, elevated venous pressure and polycythemia
- 18. Acrocyanosis Bluish discoloration of fingers seen in neonates and infants due to vasoconstriction as a result of transient hypothermia No clinical significance unless associated with circulatory shock Circum-oral cyanosis Healthy child with fair skin due to sluggish blood flow with vasoconstriction No clinical significance unless associated with low cardiac output
- 19. Cardiac vs Pulmonary Hyperoxiatest- Response of arterial PaO2 to 100%oxygen inhalation Result in PaO2 Disease >100mm Hg Lung disease Large pulmonary blood flow (TAPVR) <100mm Hg Massive intra-pulmonary shunt with normal heart <10-30mm Hg increase (<100) Intra-cardiac right to left shunt
- 21. Approach to cyanotic neonate
- 22. Antenatal history Fetal ultrasound scans- congenital heart disease, diaphragmatic hernia and congenital cystic adenomatoid malformation (CCAM). Family history of CHD
- 24. Physical examination Vitals R/o choanal atresia Respiratory system Cardiovascular system Abdomen Neurological disorders
- 25. Vitals Vital signs- signs of respiratory distress such as tachypnea, retractions, nasal flaring & grunting usually indicate a respiratory problem congenital heart disease is often accompanied by absent or effortless tachypnea. Sepsis often has the following findings: peripheral cyanosis, HR, RR, BP, / temp
- 26. R/o choanal atresia Cyanosis decreases during crying Confirmed by failure to pass a soft No. 5F to 8F catheter through each nostril
- 27. Respiratory system Inspiratory stridor- upper airway obstruction Chest- Asymmetric chest movement combined with severe distress- alarming sign for tension pneumothorax, diaphragmatic hernia Transillumination of the chest- Pneumothorax
- 28. Cardiovascular system A systolic murmur audible in most forms of cyanotic CHD (exception: d-TGA with intact ventricular septum & no pulmonary stenosis). Respirations often are unlabored unless there is pulmonary congestion or complicated by the development of heart failure or acidosis, which will affect the respiratory pattern
- 29. Per abdomen Scaphoid abdomen-congenital diaphragmatic hernia
- 30. Neurological disorders Observe for apnea and periodic breathing, which may be related to immaturity of the nervous system. Seizures can cause cyanosis if the infant fails to breathe during the episodes.
- 31. Investigations • CBC • Serum glucose • ABG Chest X-ray films,ECG Arterial PaO2 in preductal and postductal arteries Hyperoxitest
- 32. CBC & diff : or WBC sepsis hematocrit > 65% polycythemia Serum glucose: to detect hypoglycemia Arterial Blood Gases (ABGs): Arterial PO2: to confirm central cyanosis SaO2 not as good an indicator due to fetal Hb affinity for O2 (left-shift) PaCO2: may indicate pulmonary or CNS disorders, heart failure pH: sepsis, circulatory shock, severe hypoxemia Methemoglobinemia: SaO2, normal PaO2, chocolate-brown blood
- 33. X-ray -Increased pulmonary vascularity RVH on ECG D-TGA TAPVR with obstruction DORV with subpulmonary VSD PPHN LVH/BVH on ECG Persistent truncus arteriosus Single ventricle TGA and VSD Polysplenia syndrome
- 34. X-ray -Decreased pulmonary vascularity RVH on ECG TOF DORV with PS Asplenia syndrome RBBB on ECG Ebstein’s anomaly LVH on ECG Pulmonary atresia Tricuspid atresia BVH on ECG TGA and PS Persistent truncus arteriosus Single ventricle and PS
- 35. Total Anomalous Pulmonary Venous Return Snowman
- 36. Tetralogy of Fallot Boot shape
- 37. Transposition of Great Arteries Egg on a string
- 38. Arterial PaO2 in preductal and postductal arteries Right upper body-radial,brachial,temporal Umbilical artery line PaO2 should be compared Right radial-umbilical artery=>10-15 mm Hg
- 39. Differential cyanosis In severe R-L ductal shunt Pink-upper and cyanosed-lower Causes PPHN Severe AS Interrupted aortic arch Coarctation of aorta
- 40. Initial management Monitor Airway, breathing, circulation (ABCs) with respiratory compromise, establish an airway & provide supportive therapy (e.g., oxygen, mechanical ventilation) Monitor Vital signs Establish vascular access for sampling blood & administering medicatons(if needed) umbilical vessels convenient for placement of intravenous & intra-arterial catheters
- 41. If sepsis is suspected or another specific cause is not identified, start on broad spectrum antibiotics (e.g., ampicillin and gentamycin) after obtaining a CBC, urinalysis, blood & urine cultures (if possible). Left untreated, sepsis may lead to pulmonary disease & left ventricular dysfunction. Secure a separate intravenous catheter to provide fluids for resuscitation and ensure accessibility of intubation equipment should they be required.
- 42. Prostaglandin E1 infusion Prostaglandin E1 For cyanotic CHD/duct dependent cardiac defect Infusion of prostaglandin E1 at a dose of 0.05- 0.1mcg/kg/min intravenously Increase PaO2,increase systemic blood pressure,improved pH-tapered 0.01mcg/kg/min No effect-increased upto 0.4mcg/kg/min Side effects-apnea(12%),fever(14%),flushing(10%) Less common side effects- tachy/bradycardia,hypotension,cardiac arrest
- 44. System Causes Clinical findings CNS depression Perinatal asphyxia Heavy maternal sedation Intra uterine fetal distress • Shallow irregular respiration • Poor muscle tone • Cyanosis disappears when patient is stimulated or O2 given Pulmonary disease Parenchyma Pneumothorax or pleural effusion Diaphragmatic hernia PPHN • Tachypnea, respiratory distress with retraction and expiratory grunt • Crackles or decreased breath sounds • X-ray findings • Improve/abolish with oxygen inhalation Cardiac disease Cyanotic CHD with R-L shunt • Tachypnea without retractions • lack of crackles/abnormal breath sounds • Continuous murmur(PDA) • X-ray findings • Little/no increase with O2
- 45. Conclusion Central cyanosis in a newborn is an abnormal finding and one must consider all of the possible etiologies with a complete history, physical examination and relevant investigations. Remember to think about the various mechanisms causing cyanosis and go through each systematically until you have your diagnosis. Prompt management should be undertaken while you are trying to figure out your diagnosis. For ductal dependent lesion, start prostaglandin E1 and early referral
- 46. Thank You