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APPROACH TO CYANOSIS. Definition Bluish discolouration of skin or mucous membrane caused by excess amounts of reduced hemoglobin or abnormal hemoglobin.

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Presentation on theme: "APPROACH TO CYANOSIS. Definition Bluish discolouration of skin or mucous membrane caused by excess amounts of reduced hemoglobin or abnormal hemoglobin."— Presentation transcript:

1 APPROACH TO CYANOSIS

2 Definition Bluish discolouration of skin or mucous membrane caused by excess amounts of reduced hemoglobin or abnormal hemoglobin 4gm of reduced Hb in capillaries required for cyanosis to be apparent

3 Mechanism caused by absolute increase in reduced Hb,higher the Hb – greater tendancy towards cyanosis

4 In severe anemia, greater systemic arterial desaturation required for cyanosis to be evident In polycythemia even lesser systemic arterial oxygen saturation may result in clinical cyanosis If fetal Hb is high, tissue hypoxia may occur even if cyanosis is mild( arterial PaO2 low)

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6 centralperipheral CAUSEARTERIAL BLOOD DESATURATION OR ABNORMAL Hb CUTANEOUS VASOCONSTRICTION DUE TO LOWCO CONDITIONSSeen in R-L shunt, impaired pulmonary function, abnormal Hb exposure to cold air or water and abnormally greater extraction ofO2 from normally saturated blood SITESconjunctiva,palate,tongue,i nner side of lips& cheeks limited to ears,nose,cheeks outer side of lips hands feet&digits certainly central if associated with clubbing and polycythemia, clubbing is absent probably central if it deepens on effort

7 CARDIOVASCULAR DUCT-INDEPENDENT MIXING LESIONS TGA, TAPVC,TA DUCT-DEPENDANT PBF TOF,EBSTEINS,TricusidAtre DUCT-Dependant SBF HLHS,IAA,CoA,Critical AS L-RSHUNT &PUL EDEMA SV States PRIMARY LUNG DISEASE AIRWAY OBSTRUCTION EXTRINSIC LUNG COMPRESSION PULMONARY AV MALFORMATION PPHN CNS DYSFUNCTION HEMATOLOGIC MISCELLANEOUS HYPOGLYCEMIA, METABOLICACIDOSIS SEPSIS, HYPOTHERMIA, SHOCK

8 Diagnostic ladder Invasive cardiac evaluation Echo Simple lab investigation PO, CXray & ECG Hb conc &peripheral blood filim Clinical evaluation History Physical examination

9 MATERNAL HISTORY DIABETES- TTN,RDS,HYPOGLYCEMIA ASTHMA -TTN POLYHYDRAMNIOS - TEF PIH – IUGR,POLYCYTHEMIA,HYPOGLYCEMIA LABOUR& DELIVERY PROM –SEPSIS,PNEUMONIA CHORIOAMNIONITIS- SEPSIS C-SECTION- TTN,RDS,PPHN NEWBORN ONSET AT BIRTH- TTN,RDS,MAS,CDH, ONSET –HRS AFTER BIRTH- CCHD,aspiration,TEF

10 CLUES BASED ON ONSET 1st week > 1 week D TGA TOF TGA Pulmonary Atresia Admixture lesions Tricuspid atresia TAPVC Ebstein SV Critical PS DORV Truncus

11 Examined in neutral thermal enviornment Away from blue phototherapy lights Asses capillary refill time- <2 sec Barrel shaped chest –post term-MAS Bell shaped thorax – neurologic abnormalities Scaphoid abdomen-CDH Look for nasal flaring,grunting & retractions

12 Palpate brachial & femoral pulses BP- all four extrimities SBP-gradient quite specific for arch abnormality Not sensitive S2- split in 80% by 48 hours Differential cyanosis

13 CCHD in Newborns: Clues based on presentation Cyanosis No Resp Distress Cyanosis + Resp Distress Shock Differential cyanosis TGA DDPC TAPVC obstructed DDSC

14 CCHD in Newborns: Clues Based on S2 split S2 normal Excludes Cardiac cause single fixed DDPC TGA DDSC TAPVC

15 CCHD in newborns: Clues based on Murmurs Murmurs have poor sensitivity( < 50%) No Murmur TAPVC with obstruction DDPC( closed PDA) ESM TGA, DDPC, DDSC Continuous murmurs (are) DDPC with collaterals Diastolic murmur (to & fro) TOF- absent pulmonary valve

16 cardiacrespiratory HEART RATEFASTERFAST RESPIRATORY RATEFASTFASTER GRUNTABSENTPRESENT MURMURPROMINENTCAN BE PRESENT CHFPRESENTLESSLIKELY ABNORMAL PULSEYESNO RESPONSE TO O2NOT MUCHGOOD

17 Pulse oximetry Standard of care for all infants with respiratory distress & cyanosis Accurate& reliable method of monitoring o2 saturation in infants noninvasively Pulse oximeter probes on R hand & lower extremity Aim for 02 saturation of 90-95% by pulse oximetry PPHN- suspected –aim for higher o2 saturation

18 HYPEROXIA TEST ADMINISTER 100% O2 FOR 15 MINUTES ASSES O2 OF UPPER LIMB LOWER LIMB ABG - YES TCMO - YES PO - NO

19 HYPEROXIA TEST GIVE 100% O2 ASSES PO2 PO2>200 PO2<150 NO CCHD LIKELY CCHD PASS FAIL ?CCHD WITH PBF OR PPHN

20 PAO2 <50MM C X RAY CARDIOMEGALY NO CARDIOMEGALY PULMONARY VASCULARITY EBSTEINS PBF PUL EDEMA PBF TGA + IVS TAPVR With OBSTRN TA with PA orPS PA WITH IVS CRITICAL PS TOF & TOF + PA

21 Those with decreased PBF &normal or slightly increased heart size differentiated by there QRS axis on ECG & MURMUR + or – TA with PS or PA – SUPERIOR QRS AXIS ( 0 to-90) Critical PS & PA with IVS- 0 to 90 degree Differentiated by loud pul ejection murmur TOF & TOF with PA - QRS 90 to 180 Pulmonary continuous murmur Stenosis murmur

22 Prostaglandin (PGE1) Infusion Neonates –fail hyperoxia test High Signs& symptoms of CHD or likelihood Present in shock within 1 st 3 wk of life of CHD PGE1 administration –open ductus arteriosus Depending on lesion - PBF or SBF or improves Intercirculatory mixing- improves hypoxemia &metabolic acidosis Neonate with shock or CHF in 1 st few weeks of life - ductdependant SBF untilproven otherwise

23 PG sensitive lesions: Cyanosis + murmur or mild/no cyanosis + abnormal pulses Can be withheld in a relatively stable child ( SaO2 > 70%; no acidosis) Target SaO2 >80%; pO2 around 45-50, normal pH Once diagnosis is confirmed, it is ideal to start PGE1 before transport. WORSENING AFTER PGE1 – obstruction to blood flow out of pulmonary veins

24 Always given as continous IV infusion. Start at μg/kg/min, can be reduced to µg/kg/min once duct is opened( ^ SaO2) Available as 500 μg vial Trade name: Alpostin/Prostin Cost: Rs 5000/- per ampoule One vial will last 2-3 days for a 3Kg baby

25 Efficacy  with  age, less effective after 2 weeks of life, not effective after 4 weeks Adverse reactions more common in premature& LBW infants Apnea –typically in 1 st few hrs,tachycardia, bradycardia, fever, NEC, seizures, thrombocytopenia, Continous cardiorespiratory monitoring

26 PGE1 – peripheral vasodilation – hypotension& cutaneous flushing Separate IV line should be secured Hypotension treated by 10-20ml/kg bolus of NS,RL,5%albumin Remeasure ABG,reasses capillary refill& vitalsigns within 15 to 30 min of starting PGE1 infusion

27 Principles of managment Intial stabilisation – airway management reliable venous access – umblical vein Arterial line to monitor BP,acid-base,o2 Volume resucitation,inotropic support & correction of metabolic acidosis Blood glucose & sepsis workup-cyanosis+circ collpse

28 Non invasive delineation of anatomic defect- ECHO Evaluation & treatment of additional organ system-pulmonary,renal,hepatic&CNS Evaluation of additional congenital defects Genetic evaluation – if indicated Cardiac Cathetrisation Surgical managment

29 CCHD is an important differential diagnosis in neonate presenting with cyanosis after birth. Clinical evaluation with CXR and Hyperoxia test excludes CHD in most cases. Echocardiography recommended in all doubtful cases. Prior stabilization and a monitored transport to tertiary center ensures a optimal pre-operative state. Early intervention with very encouraging results is realistic for most forms of critical CHD in newborns

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31 r CCHD derived from heterogeneous group of conditions May have pulmonic stenosis,PAHor NL pulm pressure with out PS PBF may be NL,INCREASED or DECREASED Decreased PBF may be due to Pulmonic stenosis or PAH Anomalies where free mixing of systemic and venous blood occurs severity of cyanosis determined by pulmonary blood flow Thymus regresses very fast in cyanotic patients

32 CCHD With PS NO VSD With VSD With out PS PA pressu re NL PA pressure elevated PBF PULM VENOUS OBSTRN

33 This classification result in six sub group of cyanotic patients PS without VSD PS + large VSD Increased PBF with or without PAH(transposition physiology PAH withdecreased PBF(Eisenmengerphisiology) PAHdue to pul venous obstruction NL or MILD elevated pul pressure without PS

34 PS without VSD (cyanosis due to R toL shunt at atrial level& cardiomegaly) Triad-cyanosis,cardiomegaly,ischemic lung fields on Cxray Dominant a in JVP Cardiomegaly Parasternalimpulse Widely split 2 nd HS p2 late &soft 3 rd &4 th HS Pulm ejection systolic murmur,TR murmur Severe or critical pure PS with failing RV,Ebstein’s

35 PS with VSD (Fallot’s physiology) Prominent a wave in jvp NL heart size Mild parasternal impulse Systolic thrill uncommon Single 2 nd sound(widely split with inaudible pulmonic sound) ESM Clear diastolic period Ischemic lungs in xray without cardiomegaly

36 D/D of fallots physiology Fallot’stetrology(commonest >2yrs ) TGA TRICUSPID ATRESIA SV DORV correctedTGA AVCD If no rvh on ecg;posssibilities-rv hypoplastic &small,rv absent,PA not connected to RV Tricuspid atresia,hypoplasticRV with or without straddling TV, & single ventricle

37 Increased pulmonary blood flow with or without PAH(transposition physiology) Symptomatic in Neonate Cyanosis-mild to severe Failure to thrive& gain weight CCF Cardiomegaly –in2-3 wks of life 2 nd sound single,s3 gallop,insignificant systolic murmur Cardiomegaly with Incrs pulm vasculatureon xray& thymicshadow absent

38 Anomalies with cyanosis and increased PBF TGA DORV without PS TA with Incrs PBF (largeVSD+ NO PS) Persistent Truncus SV without PS TAPVC

39 Cyanosis with PAH and Diminished PBF (eisenmenger- defnd as nonreactive PAH resulting in a R to L shunt at atrial,ventricular or great artery level) Characteristics H/O frequent chest infections in infancy Cyanosis present from birth and appear late Jvp-prominent a wave No cardiomegaly or thrill(except when shunt at atrial level) No PSH Constant EC of PAH

40 2 nd sound is palpable,pulmonary component accentuated Systolic murmur in pulmonary area is insignificant or absent Pulmonary and/or TR murmurs may be present

41 EISENMENGER SYNDROME-DIFFERENTIATION ASDVSDPDA CYANOSISUNIFORM DIFFERENTIAL CARDIOMEGALYPRESENTABSENT PARASTERNAL IMPULSEHEAVINGMILD 2 nd SOUNDWIDE FIXED SPLIT SINGLENORMALLY SPLIT TRCOMMONRARE ASC AORTA IN C XrayNORMAL LARGE

42 PAH-DIFFERENTIATION HYPERKINETICOBSTRUCTIVE HEART SIZELARGENORMAL(except ASD) PARASTERNAL IMPULSEHYPERKINETICFORCIBLE &HEAVING-ASD, MILD IN VSD&PDA CLICK OF PAHABSENTPRESENT 2 nd SOUND(P2accentuated in both) ASD-WIDE&FIXED,VSD- WIDE&VARIABLE,PDA- PARADOXICALLY SPLIT ASD-WIDEFIXED VSD-SINGLE PDA-NORMAL Shunt murmurLOUDSHORT OR ABSENT Flow murmurPRESENTABSENT

43 Patients with PAH due to Pulmonary Venous hypertension(HLHS&TAPVC with obstruction) Generally present in neonatal period Severe cyanosis,CHF,S3 gallop,no cardiomegaly,absence of significant murmurs, Cxray –NL sized heart with severe PVH- causing GROUND GLASS appearance 2d echo- mitralatresia,aortic atresia,pulmonary venous obstruction, hypoplastic LV

44 Cyanosis without PS & PA pressure normal Heterogeneous group of anomalies TAPVC- features of 2 ASD but with cyanosis,figure of 8 Single atrium-mostly associated with polysplenia SVC entering LA Pulmonary AV fistula

45 Cyanosis +diagnos tic approac h Dex troc ardi a Levoc ardia With viscer al situsin versu s Dext roca rdia com plex Poor femoral pulse& Large brachio- poplipteal Systolic pressure gradient Booming p2 Cardiomegaly Prominent pulmonary conus Peripheral vascular pruning Large&r elativel y silent heart Huge RA oligemi c lung fields Giant p wave Prescence of Howell- jolly bodies Syndrome of Levocardi a with Visceral situs inversus Coarctation syndrome Eisenmein ger syndrome Ebstein’s anomaly Asplenia syndrome

46 Abnormal rhythm& CHD L- TGA - Heart Block ; SVT Ebstein - SVT

47 Cyanosis&RVH NL axis/RAD Plethora Oligemia TGA TAPVC DORV TOF PA PS+ASD&/OR VSD PS+TGA/DORV/ DOLV

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