Approach to a Neonate with Cyanosis

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comprehansive review of approach to neonatal cyanosis

Text of Approach to a Neonate with Cyanosis

  • 1.Dr.Afnan Shamraiz

2. Contents Introduction Central, Peripheral and Differential cyanosis Mechanism Etiology Approach Principles of Treatment Conclusion 3. Introduction Cyanosis is derived from the colour cyan, which comes from kyanous, the Greek word for blue It is defined as the bluish discoloration of the skin and the mucous membranes, resulting from an increase in the reduced Haemoglobin or of haemoglobin derivatives in the small vessels of those areas. Bluish discoloration of the tissues that results when the absolute level of reduced hemoglobin in the capillary bed exceeds 3- 4 g/dL Depends upon the total amount of reduced hemoglobin rather than the ratio of reduced to oxygenated hemoglobin. 4. Sites to detect cyanosis Lips Nail beds Ears Malar Prominences Palms and Soles Tongue Mucous membranes of gum,soft palate,cheeks 5. Types of Cyanosis Central Cyanosis Peripheral Cyanosis Mixed Cyanosis Other Types Enterogenous/Pigment Cyanosis Differential Cyanosis Acrocyanosis Orthocyanosis 6. Central cyanosis Pathologic condition caused by reduced arterial oxygen saturation. Involves highly vascularized tissues, such as the lips and mucous membranes, through which blood flow is brisk and the arteriovenous difference is minimal. Cardiac output typically is normal, and patients have warm extremities. 7. Mechanism Decreased arterial oxygen saturation due to marked decrease in oxygen tension in the arterial blood(arterial PaO2 is reduced)Sites-Tongue (margins & undersurface) Inner aspect of lips Mucous membranes of gums,soft palate,cheeks 8. Peripheral cyanosis Causes vasomotor instability,vasoconstriction caused by exposure to cold, venous obstruction, elevated venous pressure, polycythemia, and low cardiac output,Affects the distal extremities and circumoral or periorbital areas . 9. Mechanism Normal systemic arterial oxygen saturation and increased oxygen extraction, resulting in a wide systemic arteriovenous oxygen differenceThe increased extraction of oxygen results from sluggish movement of blood through the capillary circulationSites Tip of nose Ear lobules Outer aspect of lips,chin,cheek Tips and nailbeds of fingers,toes Palms,soles 10. Mixed Cyanosis Cardiogenic shock+ pulmonary oedema CCF due to lt.sided heart failure Polycthemia (rare)Orthocyanosis Present in upright position due to hypoxia occuring in erect posture in Pulmonary Arteriovenous Malformation 11. Enterogenous/pigment cyanosis Due to presence of excessive sulphaemoglobin(>0.5g/dl),methaemoglobin( >1.5g/dl Causes Hereditary haemoglobin M disease Poisoning by aniline dyes Drugsnitratres,nitrites,phenacetin,sulphonamides Carboxyhaemoglobinaemia 12. Differential Cyanosis Hands red (less blue) and feet blue seen in PDA with reversal of shunt (Differential Cyanosis) Requires pulmonary vascular resistance elevated to a systemic level and a patent ductus arteriosus LR shuntPulmonary hypertensionReversal of shuntR to L Desaturated blood from the ductus enters the aorta distal to the left subclavian artery, sparing the brachiocephalic circulation. 13. Reverse Differential Cyanosis Hands blue and feet red seen in Coarctation of Aorta with TGA(Reverse Differential CyanosisIntermittent Cyanosis seen in Ebsteins Anomaly 14. Central Vs Peripheral Cyanosis SITESTONGUE,ORAL CAVITYTONGUE UNAFFECTEDHANDSHAKEFEELS WARMFEELS COLDAPPLICATION OF WARMTH,COLDNO CHANGEWARMTH-CYANOSIS INCR,COLDDECREASESAPPLICATION PURE O2MAY IMPROVENO RESPONSECLUBBING,POLYCYTHA EMIAUSUALLY PRESENTABSENTPULSE VOLUMEMAYBE HIGHLOW VOLDYSPNOEAPT BREATHLESSNO RESPIRATORY PROBLEM 15. Acrocyanosis Condition in which there is arterial vasoconstriction,and secondary dilation of capillaries and venules with resulting persistant cyanosis of the hands and less fequently the feet. part of normal transition may last 72hr beware APGAR of 10 hypoperfused severe anemia 16. Psuedocyanosis Bluish tinge to the skin and or mucous membranes that is not associated with either Hyoxemia or Peripheral VasoconstrictionMetals Drugs 17. Factors altering cyanosis Colour of the cutaneous pigment Thickness of the skin State of cutaneous capillaries Cyanosis becomes apparent when the concenteration of the reduced haemoglobin in capillary blood vessels exceeds 40 g/l or 4g/dl 18. Factors affecting the detection of cyanosis in the newborn Hemoglobin concentration Detected at higher levels of saturation inpolycythemic than in anemic patients.Significant oxygen desaturation can be presentin an anemic patient without clinically detectable cyanosis. As an example, 3 g/dL of reduced hemoglobin is associated with an oxygen saturation of 67 percent when the total hemoglobin concentration is 9 g/dL, and 85 percent when the hemoglobin concentration is 20 g/dL. 19. 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. 20. Factors affecting the detection of cyanosis in the newborn Fetal hemoglobin Binds oxygen more avidly than adult hemoglobin. The oxygen dissociation curve is shifted to the left, sothat for a given level of oxygen tension (PO2), the oxygen saturation (SO2) is higher in the newborn than older infants or adults It also follows that for a given level of oxygen saturation, the PO2 is lower in newborns. As a result, cyanosis is detected at a lower PO2 in newborns compared with older patients. Thus, in evaluating a cyanotic newborn, PO2 should be measured in addition to SO2 to provide more complete data. 21. Factors affecting the detection of cyanosis in the newborn Other physiologic factors common in sick newborns affect the oxygen dissociation curve. Those that increase the affinity of hemoglobin for oxygen (shifting the oxygen dissociation curve to the left), decrease the concentration of reduced hemoglobin at a given arterial P02, and lower the PO2 at which cyanosis first appears. 22. These factors include alkalosis, hyperventilation (low PC02), cold temperature, and low levels of 2,3 diphosphoglycerateFor fetal hemoglobin, the normal curve (a) is shifted to the left (b) 23. CyanosisCyanosis is dependent on HCT and % Sat Florescent light makes cyanosis hard to see. Except in the extreme, cyanosis is not obvious Any question, check a pulse ox100 90 80 70 % SaturationCyanosis60 50 40 30 20 10 0 02040 HCT6080 24. In contrast, acidosis, fever, or increased adult hemoglobin shift the curve to the right. As a result, at a given arterial PO2, there is increased oxygen delivery to the tissues resulting in a greater concentration of reduced hemoglobin, and cyanosis appears more readily.For fetal hemoglobin, the normal curve (a) is shifted to the left (b) 25. Factors affecting the detection of cyanosis in the newborn Skin pigmentation Less apparent in the skin of patients withdarker pigmentation. Examination should include the nail beds, tongue, and mucous membranes, which are less affected by pigmentation. 26. Etiology Can be divided in to,, Site of cynosisCentral causes Peripheral causesMecanism of cynosisAlveolar hypoventilation Diffusion impairment Ventilation-perfusion mismatch Right-to-left shunting at the intracardiac, great vessel, or intrapulmonary level Hemoglobinopathy (including methemoglobinemia) that limits oxygen transport 27. Central Cyanosis: Decreased arterial oxygen saturation Decreased atmospheric pressure-High altitude Impaired pulmonary function Alveolar hypoventilation Pulmonary ventilation perfusion imbalance Impaired oxygen diffusion Anatomic Shunts ASD,VSD,PDA Congenital Heart Diseases-Fallots Tetrology,TGA Pulmonary AV fistulas Mutiple small intrapulmonary shunts Haemoglobin Abnormalities 28. Peripheral Cyanosis Decreased Cardiac Output Cold Exposure Redistribution Of blood from extremities Arterial Obstruction-embolus,raynauds phenomenon Venous Obstruction-thrombophlebitis,SVC syndrome Frost bite CCF,shock,Peripheral Circulatory Failure Hyperviscosity -Multiple myeloma,Polycythemia Peripheral Vascular Diseasesatherosclerosis,buergers Mitral Stenosis Cryoglobulinemia 29. Non- cardiac causes Alveolar hypoventilation Central nervous system depression:asphyxia, maternal sedation, intraventricular hemorrhage, seizure, meningitis, encephalitis Neuromuscular disease: Werdnig-Hoffman disease, neonatal myasthenia gravis, phrenic nerve injury Airway obstruction: choanal atresia, laryngotracheomalacia, macroglossia, Pierre Robin syndrome 30. Non- cardiac causes Ventilation/perfusion mismatch Airway disease: pneumonia, aspiration, cysticadenomatoid malformation, diaphragmatic hernia, pulmonary hypoplasia, labor emphysema, atelectasis, pulmonary hemorrhage, hyaline membrane disease, transient tachypnea of the newborn Extrinsic compression of lungs: pneumothorax,pleural effusion, chylothorax, hemothorax, thoracic dystrophy 31. Non-cardiac causes Hemoglobinopathy Methemoglobinemia: congenital or secondary totoxic exposure Other hemoglobinopathies Diffusion impairment Pulmonary edema: left-sided obstructive cardiacdisease, cardiomyopathy Pulmonary fibrosis Congenital lymphangiectasia 32. Cardiac causes Decreased pulmonary blood flowTetralogy of Fallot Tricuspid valve anomaly Pulmonary valve atresia Critical valvular pulmonary steanosisIncreased pulmonary blood flowTransposition of great arteries Truncus arteriosus Total anomalous pulmonary venous connection 33. Cardiac causes Severe heart failureHypoplastic left heart syndrome Coarctation of the aorta Interrupted aortic arch Critical valvular aortic steanosis 34. The 6 Ts Total Anomalous Pulmonary Veins Tetrology of Fallot Tricuspid Atresia Transposition Truncus ArteriosusTotal Acardia 35. Mnemonic A 7T" 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 connect