PEDIATRIC CARDIOLOGY FOR THE BUSY PEDIATRICIAN

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PEDIATRIC CARDIOLOGY FOR THE BUSY PEDIATRICIAN

  1. 1. PEDIATRIC CARDIOLOGY FOR THE BUSY PRACTITIONER 2012 VIKAS KOHLI MD FAAP FACCDIPLOMATE AMERICAN BOARD PEDIATRICS & PEDIATRIC CARDIOLOGYPEDIATRIC CARDIOLOGY & CARDIAC SURGERY INDRAPRASTHA APOLLO DELHI CHILD HEART CENTER
  2. 2. WHATS NEW INPEDS CARDIOVIKAS KOHLI AMERICANBOARD CERTIFIEDSR CONSULTANTPEDS CARDIOLOGY
  3. 3. Single Ventricle:Fetal
  4. 4. FACTS ABOUTFETAL HEART DS
  5. 5. Facts about Fetal Heart 1. THE HEART IS FULLY FORMED BY THE 6TH WEEK..THE LAST STRUCTURE TO BE FORMED IS THE AV VALVES
  6. 6. HEART FACT 2 HEART DEFECTS ARE THE MOST COMMON BIRTH DEFECTS INCIDENCE IS 1 IN 100
  7. 7. HEART FACT 3 HEART DEFECTS ARE NOT PICKED UP ON ULTRASOUND WE DID A STUDY: 100 CONSECUTIVE NEWBORNS WITH DIAGNOSED HEART DEFECTS PRESENTING TO OUR INSTITUTION AVG NO OF ANTENATAL USGS: 4 NO OF PATIENTS OF SUSPECTED HEART DEFECTS ANTENATALLY: 1/100
  8. 8. HEART FACT IFDIAGNOSED ANTENATALLY, THERE ARE SEVERAL ADVANTAGES BY CLOSING EYES THE PROBLEM DOES NOT GO AWAY PREPARATION AND MORE INFORMATION MANY TIMES ONLY REASSURES PARENTS AFTER INITIAL SURPRISE
  9. 9. FETAL CARDIOLOGY In US 80% cardiac diagnosis made in utero In India almost 100% diagnosis made post natal Devastating diagnosis usually They are not preprared Childs life lost in 30% cases For critical illness: no preparation
  10. 10. INCIDENCE OFHEART DISEASEWHY NOT FETAL ECHO ALLPREGNANCIES ?
  11. 11.  1,75,000 CHILDREN BORN WITH HEART DISEASE IN INDIA EVERY YEAR SO IN 2011 THESE MANY CHILDREN HAVE BEEN BORN AND ADDED TO THE POOL OF KIDS WITH HEART DS IN INDIA OF THESE 30,000 NEED SURGERY IN THE FIRST YEAR BEFORE THEY ARE 1 YR OLD IN INDIA TOTAL PEDIATRIC HEART SURGERIES ARE 10-12,000 PER YEAR AGE 0-18 YR
  12. 12. RECENT LITERATUREA recent review of articles in USA: 30% of antenatal cardiac diagnosis were being picked upon by sonologists Rest by fetal cardiologist The review of this articles asks for more screening for CHD by sonologists
  13. 13. Twin to TwinTransfusion
  14. 14. FETAL CARDIOLOGY: ACONTEMPORARY PERSPECTIVE Vikas Kohli MD FAAP FACC Delhi Child Heart Center & Indraprastha Apollo Hospital DELHI CHILD HEART CENTER
  15. 15. FETAL DIAGNOSIS ANDNEONATAL MANAGEMENT DELHI CHILD HEART CENTER
  16. 16. FETAL PULM STENOSIS 36WKS PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  17. 17. FETAL PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  18. 18. Counseling• Urgent CS• Immediate Cardiac Intervention• Excellent longterm Prognosis• Mother underwent CS that night• Neonatal Diagnosis confirmed• Prostaglandin started• Intervention planned PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  19. 19. Critical PSFetal diagnosis PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  20. 20. Critical PSPostnatal Confirmation PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  21. 21. Critical PS17 Hours of Life on PGE PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  22. 22. Post- Balloon Pulmonary ValvotomyPEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  23. 23. Critical Pulmonary Stenosis PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  24. 24. SINCE THEN FETAL CARDIOLOGY AS AN INDEPENDENT FEILD DELHI CHILD HEART CENTER
  25. 25. FETAL CARDIOLOGY• In US 80% cardiac diagnosis made in utero• In India almost 100% diagnosis made post natal• Devastating diagnosis usually• They are not preprared• Childs life lost in 30% cases• For critical illness: no preparation PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  26. 26. Abnormal Fetal Echo• 37% Abnormal Fetal Echo• Abnormalities classified as: – STRUCTURAL HEART DS – FUNCTIONAL HEART DS – ELECTRICAL PROBLEMS PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  27. 27. Structural Heart Ds : 214• VSD = 52• ICEF= 74• Single ventricle 22• A-V septal defect 12• CoA/arch interruption 6• DORV 9• TGA 6• PA with VSD 12• absent ductus venosus(3), pulmonary stenosis (5), Ebstein’s anomaly (3), , LV cardiomyopathy (9), LV aneurysm(1) PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  28. 28. FUNCTIONAL ABNORMALITY 81cases• Valvar dysfunction – TR 42 • 12/42 Severe TR : RV failure : 3 • 14 had Moderate TR • 16 had Mild TR – Fetal hydrops (n=10) – Ventricular Dysfunction 9 – decreased biventricular function (n=11) – High output failure (n=2) – Twin to twin transfusion (TTT) (4) – Twin-Reversed Arterial Perfusion Sequence (TRAP) (3) PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  29. 29. Fetal Therapy: Cardiac• Fetal SVT = 6• Fetal bradycardia 14 Ascites 2• Fetal Complete Heart Block 22 PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  30. 30. Neonatal Interventions & Surgery• INTERVENTIONS – Balloon Pulmonary Valve Dil 5 – PDA Closure 3 – Aortic Valve Ballooning 2 – Septostomy 3• SURGERY – Coa Repair 2 – Arterial Switch 1 – Arch Repair 1 – ToF repair 4 PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  31. 31. HEART FACT• HEART DEFECTS ARE THE MOST COMMON BIRTH DEFECTS• INCIDENCE IS 1 IN 100
  32. 32. Heart Fact• 1,75,000 children born with CHD each year• 30,000 require surgery before their first birthday otherwise they will not live• Total Pediatric surgeries being done in India not more than 12,000 for 0 to 18 years !!
  33. 33. FETAL CARDIOLOGY• In US 80% cardiac diagnosis made in utero• In India almost 100% diagnosis made post natal• Devastating diagnosis usually• They are not preprared• Childs life lost in 30% cases• For critical illness: no preparation
  34. 34. Clinical Presentation of CHD in theNeonate
  35. 35. Well Baby Exam• A normal neonatal exam definitely does not mean the baby is normal• Infact it does not rule out life threatening CHD’s even those not compatible with life• So, when to suspect CHD in a new born ?
  36. 36. Why Cyanotic CHD is missed at Birth• Cyanosis esp peripheral is not an uncommon finding in newborns• Cyanosis is not always visible to naked eye• Cyanosis on crying is not uncommon in normal newborns• Cyanosis does not become apparent till the duct begins to close
  37. 37. Presentations• Prenatal Diagnosis• Asymptomatic Newborn• Postnatal Cardiac Murmur• Postnatal Critical Illness Presentation: – The Cyanotic Newborn – The Newborn with Respiratory Distress – The Newborn presenting with Shock
  38. 38. SCREENING FOR CHD IN WELLNEWBORNS
  39. 39. Detection of CHD Predischarge• Prior to discharge can we evaluate clinically to detect more pts ?• Can we introduce some screening tools ?• Lets look at how we can detect CHD before their presentation-screening.
  40. 40. The Baltimore-Washington StudyIt was observed that, of all infants with cardiovascular malformations whodied in the first week of life, one infour did not have the cardiovascularmalformation identified before death.Kuehl KS et al. Failure to diagnose congenital heart disease in infancy. Pediatrics 1999;103:743-747
  41. 41. Neonatal Cardiac Mortality• In the best centers, the in-hospital mortality for the arterial switch operation for TGA now approaches 1%.• Death before surgery is becoming proportionally greater: 4% of neonates with TGA died before surgeryArch Dis Child Fetal Neonatal Ed 2001;84:F141-F145
  42. 42. What are the consequences of late missed diagnosis ?• Mortality• Brain Damage• Multiorgan failure• Perioperative mortality
  43. 43. Can we screen for CHD ?• 1990’s: – 4 extremity BP – Palpation of pulses in lower extremity• This was anticipated to help• But still diagnosis was missed• 2000’s – Pulse Oximeter Saturation
  44. 44. Which Cy CHDs will be picked up• If a screening program is started: – IAA – Pulm Atresia – HLHS• Will not be missed• Will get detected before dramatic crash
  45. 45. Screening for duct-dependant congenital heart disease with pulse oximetry: a critical evaluation of strategies to maximize sensitivity• Acta Paediatr. 2005 Nov;94(11):1590-1596.• CTO2 Vs NGO2• 200 normals compared with 66 with critical CHD• IF ONLY ONE MEASUREMENT WAS MADE 7/66 PTS HAD A FALSE NEGATIVE• BUT WHEN CRITERIA WERE CHANGED TO: – > 3% DIFFERENCE BET UL & LL – BOTH UL AND LL SATS < 95%• Then sensitivity of 98.5%, specificity of 96.0%, positive predictive value of 89.0% and negative predictive value of 99.5%
  46. 46. The reliability of a single pulse oximetry readingas a screening test for congenital heart disease in otherwise asymptomatic newborn infants. • Pediatr Cardiol. 2008 Sep;29(5):885-9. • Routine pulse oximetry was neither reliable nor an important diagnostic tool in our cohort.
  47. 47. Strategies for implementing screening for critical congenital heart disease• .• The work-group members found sufficient evidence to begin screening for low blood oxygen saturation through the use of pulse- oximetry monitoring to detect CCHD in well- infant and intermediate care nurseries.• Pediatrics. 2011 Nov;128(5):e1259-67. Epub 2011 Oct 10
  48. 48. NEONATAL PRESENTATIONS• THE BLUE BABY• THE PINK BABY IN DISTRESS• THE SHOCKY BABY
  49. 49. INDICATORS OF CARDIAC PROBLEM PRIMARY SECONDARY • Desaturation • Murmur • Shock • Cardiac Enlargement • Resp Distress • Peripheral Pulse Abn
  50. 50. DESATURATION• PPHN is presumed to be the cause• Surprisingly: CHD can have exactly same presentation• Low saturation without resp cause: r/o cardiac
  51. 51. DIFFERENTIAL DIAGNOSIS• Cyanosis all over – Intracardiac Mixing: Single Ventricle – Intrapulmonary mixing: PPHN• Differential Cyanosis – Upper Limb Blue: TGA+PDA – Lower Limb Blue: Duct Shunting R to L with normally related GA’s• Combination: PPHN – Intrapulmonary + PDA + PFO shunting
  52. 52. THINK CARDIAC WHENTHINKING PULMONARY ESPECIALLY IF ANY OF THE SECONDARY FACTORS PRESENT
  53. 53. INDICATORS OF CARDIAC PROBLEM SECONDARY PRIMARY • Murmur • Desaturation • Cardiac Enlargement • Shock • Peripheral Pulse • Resp Distress Abn
  54. 54. CHD (Obstructive) Vs SEPSIS(HLHS)Coarctation, Aortic Stenosis, Hypopl LV• Most NB’s transferred to tertiary centers are already on ABx• Differentiating Sepsis is very difficult !• Most markers dont have reliable sensitivity• 22/47 such cardiac newborns did not have murmur• Majority with fulminant sepsis had weak pulses due to low cardiac outputDifferentiation of systemic infection and congenital obstructive left heart disease in the very young infant. Pediatr Emerg Care 1998;14:263-267
  55. 55. IN SHOCKY PATIENTS :ALWAYS R/O CARDIAC ESPECIALLY IFSECONDARY SIGNS PRESENT
  56. 56. WITH RESP DISTRESS IN NEONATES: HAVE A LOW THRESHOLD TO SUSPECT CARDIAC LESIONS
  57. 57. HOW TO REACH A DIAGNOSIS ?• SUSPECT: KNOWLEDGE BASE REQUIRED• DIAGNOSTIC MODALITY: ECHOCARDIOGRAM: Ready availability of reliable Bedside Pediatric/Neonatal Echo remains the single most important hurdle in the diagnosis of neonatal CHD
  58. 58. An era is approaching when the time of greatest hazard to the infant is not while under the surgeons knife or in the intensive care unit after surgery, but before actually being admitted to the specialist centerPaediatric intensive care: a framework for the future. London: National Health Service Executive, 1997.
  59. 59. BRIDGE TO TRANSPORT ACRITICALLY ILL CHILD PROSTAGLANDIN
  60. 60. WHO SHOULD BE GIVEN PROSTAGLANDIN • The threshold for starting prostaglandin is directly proportional to severity of the childs illness • In the critically ill child: start Prostin without wasting time • Go by clinical findings
  61. 61. Physical Exam helps in deciding • THE CLINICALLY USEFUL FINDING IS CYANOSIS IN A CRITICALLY ILL NEWBORN: – IF MURMUR+CYANOSIS IS PRESENT START PROSTIN
  62. 62. Physical Exam helps in deciding• The clinically useful finding IN A NON- CYANOSED CRITICALLY ILL NEWBORN IS:• PRESENCE OF ABNORMAL PULES: IF PRESENT START PROSTIN Danford DA et al. Application of information theory to decision analysis in potentially prostaglandin-responsive neonates. JACC 1986;8:1125-1130
  63. 63. STARTING PROSTIN• USUALLY THE DECISION TO START IS EASY IN CRITICALLY ILL “DYING” NEWBORN• RESPONSE IS DRAMATIC
  64. 64. TIPS• EARLY INSTITUTION OF PROSTIN• CY NB’s WITH MURMUR• ACY NB’s WITH ABNORMAL PULSES• EVEN WITHOUT ECHO• EARLY TRANSPORT• SUSPECT CHD WHEN: – PPHN TYPE PRESENTATION – SEPSIS
  65. 65. STARTING PROSTIN• Prior to starting, one needs to have Prostin available• This also remains a critical step outside the NCR• Since cost issues involved Pediatricians may not want to use it without a confirmation
  66. 66. STARTING PROSTIN• Ease of use of Prostin is directly proportional to: – Severity of Illness – Ease of availability• Confounding Factor: Echo should be done or not ?
  67. 67. DOSAGE• START WITH 0.05 mcg/Kg/Min• 500 mcg/ml• Put 1 ml in 25 ml• Infuse at 0.5ml/hr = 0.05mcg/Kg/Min• To allow 0.1 mcg/kg/min increase drip rate to 1ml/hr
  68. 68. SIDE EFFECTS• APNEA – DOSE RELATED – OVERCOME WITH AMINOPHYLLINE – NO NEED TO INTUBATE• Aminophylline: Bolus dose of 6 mg/kg before or during initiation of PGE1, and continued at 2 mg/kg dose every 8 hours for 72 hours.• PEDIATRICS Vol. 112 No. 1 July 2003, pp. e27-e29
  69. 69. • PROSTIN VR Rs 7-8000 (Pfizer)• ALPROSTADIL Rs 5000 (Samarth)• BIOGLANDIN Rs 4000 (United)
  70. 70. EARLY INFANCY ANDDETECTION OF CHD
  71. 71. CLASSIFICATION OF CHD• ACYANOTIC • CYANOTIC• Increased Flow • Decreased Flow – ATRIAL: ASD – TOF – VENTR: VSD – Pulm Atresia – ARTERIAL: • Increased Flow PDA – TAPVD – COMBINED: – TGA VSD+PDA – Truncus• No Shunts – Tricuspid Atresia – Pulm or Aortic Stenosis
  72. 72. STEPS IN CLINICAL DIAGNOSIS• CYANOTIC Vs ACYANOTIC• INCREASED FLOW Vs DECREASED FLOW
  73. 73. CLINICAL DIAGNOSIS• HISTORY: Increased flow or not• Pulse oximeter: Acyanotic vs Cyanotic• Chest Xray: increased Flow or not
  74. 74. HISTORY • Sweating while feeding • Shortness of breath • Failure to thrive • Recc infections (Lower) chestINCREASED PULMONARY BLOOD FLOW ACYANOTIC OR CYANOTIC
  75. 75. HISTORY• Cyanosis• Spells• Squatting• Syncope, Chest Pain
  76. 76. ACYANOTIC Vs CYANOTIC• Normal Saturations are >94%• Between 93 and 85% human eye cannot detect desaturation• Below 85% we can visually diagnose Cyanosis
  77. 77. ACYANOTIC Vs Cyanotic• ACYANOTIC • CYANOTIC• Pulse Oximeter • Sats less than 93%• Sats >94%
  78. 78. CHEST XRAY• LUNG FIELDS: – INCREASED : INCRD PULM BLOOD FLOW – OR OLIGEMIC: NORMAL OR DECRSD PBF
  79. 79. ECHO / ECHO REPORT• Should fit in with findings: – Should explain the symptoms – Should explain the sats – Should explain the murmur
  80. 80. CHEST X-RAYS IN CHD PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  81. 81. VSD
  82. 82. ASD
  83. 83. MODERATE VSD
  84. 84. LARGE VSD LARGE SHUNT
  85. 85. AV CANAL
  86. 86. TGA
  87. 87. TRUNCUS
  88. 88. EISENMANGERS
  89. 89. KAWASAKI DISEASE
  90. 90. Epidemiological case definition (Classic Def) • Fever persisting at least 5 days • PRESENCE OF AT LEAST 4 PRINCIPAL FEATURES: 1. Changes in extremities – Acute: Erythema of palms, soles; edema of hands, feet – Subacute: Periungual peeling of fingers, toes in weeks 2 and 3 2. Polymorphous exanthem 3. Bilateral bulbar conjunctival injection without exudate 4. Changes in lips and oral cavity: Erythema, lips cracking, strawberry tongue, diffuse injection of oral and pharyngeal mucosae 5. Cervical lymphadenopathy (1.5-cm diameter), usually unilateral Exclusion of other diseases with similar findings
  91. 91. DIFFERENTIAL DIAGNOSIS• Viral infections (eg, measles, adenovirus, enterovirus, Epstein-Barr virus)• Scarlet fever/TSS• Staphylococcal scalded skin syndrome• Bacterial cervical lymphadenitis• Drug hypersensitivity reactions• Stevens-Johnson syndrome• Juvenile rheumatoid arthritis• Rocky Mountain spotted fever• Leptospirosis• Mercury hypersensitivity reaction (acrodynia)
  92. 92. Other clinical and laboratory findings CARDIOVASCULAR FINDINGS • Congestive heart failure, myocarditis, pericarditis, valvular regurgitation • Coronary artery abnormalities • Aneurysms of medium-size noncoronary arteries • Raynaud’s phenomenon • Peripheral gangrene MUSCULOSKELETAL SYSTEM • Arthritis, arthralgia GASTROINTESTINAL TRACT • Diarrhea, vomiting, abdominal pain • Hepatic dysfunction, Hydrops of gallbladder
  93. 93. CENTRAL NERVOUS SYSTEM• Extreme irritability, Aseptic meningitis• SN hearing loss,GENITOURINARY SYSTEM• Urethritis/meatitisOTHER FINDINGS• Erythema, induration at BCG inoculation site• Anterior uveitis (mild)• Desquamating rash in groin
  94. 94. Laboratory findings in acute Kawasaki disease • Leukocytosis with neutrophilia and immature forms • Elevated ESR, CRP • Anemia • Abnormal plasma lipids • Hypoalbuminemia • Hyponatremia • Thrombocytosis after week 1 • Sterile pyuria • Elevated serum transaminases & GGT • Pleocytosis of cerebrospinal fluid • Leukocytosis in synovial fluid
  95. 95. FEVER• The fever typically is high-spiking and remittent, with peak temperatures generally 39°C (102°F) and in many cases 40°C (104°F).
  96. 96. HANDS AND FEET• Erythema of the palms and soles or firm, sometimes painful induration of the hands or feet• Desquamation of the fingers and toes usually begins in the periungual region within 2 to 3 weeks after the onset of fever and may extend to include the palms and soles• Approximately 1 to 2 months after the onset of fever, deep transverse grooves across the nails (Beau’s lines)
  97. 97. SKIN RASH• Erythematous rash usually appears within 5 days of the onset of fever most common is a nonspecific, diffuse maculopapular eruption.• Urticarial exanthem, a scarlatiniform rash, an erythroderma, an erythema-multiforme- like rash, or,rarely, a fine micropustular eruption• Bullous and vesicular eruptions have not been described
  98. 98. EYES• Bilateral conjunctival injection bulbar conjunctivae (sparing the limbus, an avascular zone around the iris)• Exudate, conjunctival edema or corneal ulceration usually is painless• Mild acute iridocyclitis• Anterior uveitis
  99. 99. ORAL CAVITY• Erythema, dryness, fissuring, peeling, cracking, and bleeding of the lips• A “strawberry tongue” that is indistinguishable from that associated with streptococcal scarlet fever, with erythema and• Prominent fungiform papillae• Diffuse erythema of the oropharyngeal mucosae.
  100. 100. LYMPH NODES• Cervical lymphadenopathy is the least common of the principal clinical features• It is usually unilateral and confined to the anterior cervical triangle• Classic criteria include 1 lymph node that is 1.5 cm in diameter.
  101. 101. JOINT INVOLVEMENT• Arthritis or arthralgia can occur in the first week of the illness• Tends to involve multiple joints, including the small interphalangeal joints as well as large weightbearing joints• Arthritis or arthralgia developing after the 10th day of illness favors large weight- bearing joints, especially the knees and ankles.
  102. 102. RARE PRESENTATIONS• Transient unilateral peripheral facial nerve palsy occurs rarely• Transient high-frequency sensorineural hearing loss (20–35 dB) can occur during acute Kawasaki disease
  103. 103. DIAGNOSIS OF KD• Supplemental laboratory criteria include • albumin <3.0 g/dL, • anemia for age • elevation of alanine aminotransferase,• Platelets after 7 days >450 000/mm3• White blood cell count >15 000/mm3• Urine >10 white blood cells/high-power field.
  104. 104. ENZYME ELEVATION• Mild to moderate elevations in serum transaminases occur in 40% of patients and mild hyperbilirubinemia in 10%• Plasma GGT is elevated in 67% of patients• Hypoalbuminemia is common and is associated with more severe and more prolonged acute disease
  105. 105. URINE ANALYSIS• Urinalysis reveals intermittent mild to moderate sterile pyuria in 33% of patients, although• Suprapubic urine generally does not show pyuria, which suggests urethritis
  106. 106. LUMBAR PUNCTURE• Lumbar puncture, 50% demonstrate evidence of aseptic meningitis with a predominance of mononuclear cells, as well as normal glucose and protein levels.
  107. 107. DIAGNOSIS• The classic diagnosis of Kawasaki disease has been based on the presence of 5 days of fever and 4 of the 5 principal clinical features• All of the clinical features are not present at a single point in time, and watchful waiting is sometimes necessary before a diagnosis can be made
  108. 108. DELHI CHILD HEART CENTERPEDIATRIC CARDIOLOGY OPD AND ECHO CENTER
  109. 109. CUTTING EDGE PEDIATRICCARDIAC INTERVENTIONS PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  110. 110. PA VSD MAPCA’s
  111. 111. PA VSD MAPCA’s
  112. 112. Post op hemoptysis
  113. 113. TOF ABNORMAL ORIGIN OF LPA-NEWBORN PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  114. 114. NEAR FATAL PULM AV MALFORMATIONSSATURATIONS 30% PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  115. 115. Migrated PIC line
  116. 116. WILLIAMS SYNDROME MULTIPLE STENOSES SUPRA-AORTIC SURGERY CAROTIDS, COARCTATION PREVIOUSLY INVOLVED NOW RESTENOSIS PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  117. 117. RCCA LCCA COA STENT IN STENT RE STENOSIS
  118. 118. PRE RE STENTPOST RE STENT
  119. 119. LIFE SAVINGINTERVENTION SEPTOSTOMY BLADE BALLOON PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  120. 120. TGA INTACT IAS,IVS
  121. 121. TGA INTACT IAS,IVS
  122. 122. TGA INTACT IAS,IVS
  123. 123. OUTCOMES:EMERGENCY PALLIATION• IMMEDIATE OUTCOMES EXCELLENT• RARELY MORTALITY FROM PALLIATIVE INTERVENTION• IN INDIA: LATE PRESENTATION MAY PREDISPOSE TO POOR OUTCOME OF PROCEDURE
  124. 124. OUTCOMES• FINAL OUTCOME DEPENDS ON THE SURGICAL OUTCOME• THAT IS WHY A TEAM IS IMPORTANT
  125. 125. NEONATAL AORTICVALVULOPLASTY CRITICAL AORTIC STENOSIS LV FAILURE PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  126. 126. AORTIC VALVEBALLOONING
  127. 127. NEONATAL AORTIC VALVULOPLASTY• 90% survival at 8 yrs• Re-intervention: 50% by 8 yrs• 10% : Surgery by 8 years• PALLIATIVE PROCEDURE
  128. 128. CRITICAL NEONATAL BALLOON PULM VALVPLSTY FETAL DIAGNOSISBALLOON AT 4 HOURS AGE PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  129. 129. FETAL DIAGNOSIS ANDNEONATALMANAGEMENT PEDIATRIC CARDIOLOGY & CONG CARDIAC SURGERY UNIT PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  130. 130. Critical PSFetal diagnosis
  131. 131. Critical PSPostnatal Confirmation
  132. 132. Critical PS17 Hours of Life on PGE
  133. 133. Post- Balloon Pulmonary Valvotomy
  134. 134. Critical Pulmonary Stenosis
  135. 135. OUTCOMES• NEONATAL BALLOON PULM – RE INTERVENTION: ONLY 10% – LONG TERM OUTCOMES EXCELLENT – CURATIVE INTERVENTION – NOT PALLIATIVE – 90% DONOT REQUIRE ANY INTERVENTION/SURGERY
  136. 136. NEONATAL COARCTATION OLDER CHILDRENWITH COARCTATION PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  137. 137. NEONATALCOARCTATION
  138. 138. NEONATALCOARCTATION
  139. 139. NEONATALCOARCTATION
  140. 140. COA BALLOON OLDER CHILD
  141. 141. COARCTATION
  142. 142. COA STENTING
  143. 143. ATRIAL SEPTAL DEFECT DEVICE CLOSURE PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  144. 144. Muscular VSD’s • Single or Multiple • Suturing difficult • Apical defects LV approach • 54% of LV ventriculotomies had: • Residual shunt • Dyskinesia • AneurysmJ Interv Cardiol. 2003 Oct;16(5):399-407
  145. 145. PDA DEVICE CLOSURE >2000 DEVICE IMPLANTED 5 IN <2.5 kG PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  146. 146. POST OP HYPOPLASTIC REPAIR
  147. 147. HYPOPLASTIC ARCH REPAIR
  148. 148. POST OP HYPOPLASTIC ARCH
  149. 149. POSTOP HYPOPLASTIC ARCH REPAIR
  150. 150. FOREIGN BODY RETRIEVAL PEDIATRIC CARDIOLOGY & CARDIAC SURGERY UNIT
  151. 151. PRETERM WITH TOF SPELLS
  152. 152. KAWASAKI ANEURYSMS
  153. 153. FLOW RESTRICTOR IMPLANTATION• 2 CASES PERFORMED IN INDIA BY YOUR SPEAKER• PART OF US TRIAL• > 6 MO FOLLOW UP• NON-NEONATAL PTS• REFUSED SURGERY BY ALL CENTERS• FINAL GRADIENT AT END OF PROCEDURE 75 mmHg
  154. 154. TAKE HOME MESSAGE• INTERVENTIONS REQUIRE TEAM MANAGEMENT• OUTCOMES ARE EXCELLENT• MAY BE THERAPUETIC or• THE MOST IMPORTANT COMPONENT RE OUTCOME IS THE EARLY REFERRAL: AN ESSENTIAL PART OF THE TEAM !
  155. 155. Stent Implantation  Stent implantation of the arterial duct in newborns with duct- dependent circulation.• Eur Heart J. 1998 Sep;19(9):1401- 9  21 neonates  mean 8.7 months increased growth of the pulmonary arteries was seen in all the patients
  156. 156. TOF ? PNEUMONIA
  157. 157. WHEN TO OPERATE WHAT
  158. 158. ATRIAL SEPTAL DEFECT: SECUNDUM• CLOSE >2 YRS OR WHEN DIAGNOSED• ELECTIVE• DEVICE vs SURGERY• BOTH HAVE EXCELLENT OUTCOME• DECISION RE MODE OF CLOSURE BY INTERVENTIONALIST:SHLD ECHO HIMSELF
  159. 159. ATRIAL SEPTAL DEFECT• AFTER FIRST YR: ANNUAL CARDIAC EVALUATION• PT F/U CLOSELY BY PEDIATRICAN• NL Q OF LIFE; NL LIFE SPAN• DEVICE: NO MRI LIMITATION
  160. 160. ATRIAL SEPTALPRIMUM DEFECT SINUS VENOSUS
  161. 161. ATRIAL SEPTAL DEFECT• SINUS VENOSUS: SURGICAL CLOSURE• MAKE SURE NO PULM VENOUS DRAINAGE ABN• PRIMUM ASD: LIKE AV CANAL DEFECT• MAKE SURE NO MITRAL VALVE ABN
  162. 162. ATRIAL SEPTAL DEFECT• PRIMUM & SINUS VENOSUS: INDICATION SAME AS FOR SECUNDUM• OCCASIONALY EARLY CLOSURE DEPENDS ON PRESENTATION• LONG TERM PROGNOSIS: – S/VENOSUS: rhythm problems – PRIMUM: F/U FOR MITRAL VALVE ISSUES
  163. 163. ATRIAL SEPTAL DEFECT-II
  164. 164. ATRIAL SEPTAL DEFECT-II
  165. 165. ASD-DEVICE
  166. 166. TRANSCATHETER ASD CLOSURE • RAPID RECOVERY • NO SCAR • SUCCESS > 98% OF SELECTED CASES • SELECTION IS THE KEY • NO BLOOD TRANSFUSION • PTS WITH SURGERY HAD LOWER IQ SCORES
  167. 167. MINISTERNOTOMY
  168. 168. VENTRICULAR SEPTAL DEFECT
  169. 169. Well Baby Check: Murmur• Commonest murmur is VSD murmur• Next step routinely taken is an Echo• Should pediatric echocardiography be performed in adult laboratories? Pediatrics. 1998 Aug;102(2):e15• Diagnostic accuracy of pediatric echocardiograms performed in adult laboratories. Am J Cardiol. 1999 Mar 15;83(6):908-14.
  170. 170. Well Baby Check: VSD• Echocardiogram shows a VSD• This is obviously not an emergency:• Except: if an assoc lesion is not picked up• Especially if Coarctation is missed
  171. 171. Well Baby Check: VSD• From echo report determine if the VSD is –LARGE: Most likely to require surgery –MODERATE: Needs f/u –SMALL: Reassurance
  172. 172. LARGE VSD• Today the surgical mortality of VSD closure is 1-2%.• It is a curable lesion• No long term implications• Beyond 1 yr post-op only once a year f/u required• Normal life-span and quality of life• ONLY TIMING OF SURGERY AND MEDS IN MEAN TIME NEED BE DECIDED
  173. 173. LARGE VSD: MEDICAL• Mx NEED MAX A/LOAD REDUCTN – Tab. Envas(2.5mg) start w 1/4th OD->BD – Then increase to ½ later• PRELOAD REDUCTN HELPS – T. Frusemene (20mg) 1/8th in newborns – & 1/4th in infants ~ 5 Kg weight• DIGOXIN IN EARLY STAGE WHEN IN CHF – Elixir Dixin 0.3 ml BD for a 3 Kg child
  174. 174. VSD WHEN TO OPERATE ?• LARGE VSD’s: 3 MONTHS; By 6 MONTHS – IF WEIGHT GAIN NOT APPR – AND/OR IF PULM HTN DEVELOPING• MODERATE VSD’S INDIVIDUALIZED• SMALL VSDS – • AORTIC INSUFFICIENCY • INFECTIVE ENDOCARDITIS
  175. 175. Interventional PM VSD CLOSURE• AN EXPERIMENTAL METHOD• LONGTERM EFFECTS NOT KNOWN• HEART BLOCK: NEED OF PACEMAKER• AORTIC INSUFFICIENCY NOT KNOW• WOULD NOT RECOMMEND
  176. 176. VENTRICULAR SEPTAL DEFECTS
  177. 177. MUSCULAR VSD CLOSURE• AN ESTAB METHOD• PREFERRED METHOD• LONGTERM EFFECTS: NONE• FAR FROM CONDUCTION SYSYTEM• AORTIC INSUFFICIENCY UNKNOW
  178. 178. VSD: MX ISSUES• IMMUNIZATN: NO CONTRA-INDICATION• TRAVELLING: NO C/I (INCL AIR)• AVOID INFECTIONS (HOW EASY ?) – AVOID CROWDED PLACES – USE OF BRONCHODIL• PLOT HT & WT ALL VISITS• FEEDING ISSUES/ WEANING-VERY IMPORTANT
  179. 179. MX ISSUES• SPORTS: – ALL SPORTS ACTIVITIES CAN BE UNDERTAKEN – WEIGHT LIFTING IS NOT REC IN CHILDREN• PROFESSIONAL LIFE – SMALL VSD PTS CAN UNDERTAKE ALL PROFESSIONS EXCEPT: MILITARY, AEROSPACE AND OLYMPIAN• FINANCES – ONE TIME SURGERY MAY BE LESS EXPENSIVE THAN THE LIFETIME MX OF AN ASTHMA PT
  180. 180. PATENT DUCTUS ARTERIOSUS
  181. 181. NEONATAL PRESENTATION• THE BLUE BABY• THE PINK BABY IN DISTRESS• THE SHOCKY BABY
  182. 182. PINK BABY W/RESP DISTRESS• PREMATURE – THIS IS THE BABY WITH PDA-HAS BEEN DOING WELL NOW W INC O2 REQUIREMNTS; OR WITH APNEA; NEC; POOR PERFUSION ! – DIAGNOSIS IS BY ECHO ONLY !• START THERAPY AFTER ECHO ONLY*
  183. 183. PREMATURE-PDA• THERAPY – INDOMETHACIN: IV OR ORAL• ORAL OR RECTAL BRUFEN SYRUP – ADVANTAGES Vs DISADVANTAGES
  184. 184. PREMATURE-PDA• THERAPY – ONLY RECORDED DIFFERENCE IN THE PDA CLOSURE BETWEEN BRUFEN AND INDOMETHACIN IS THE RECURRENCE RATE – BENEFIT: RENAL
  185. 185. BRUFEN/INDOMT-COCHRANE ANALYSIS-2003 • BRUFEN AND INDOMETHACIN: equally potent in closing PDA; trials to evaluate long-term neuro issues needed • PROPHYLACTIC INDOMTH: no longterm benefit in survival or outcome; only short term decrease in IVH • PROLONGED Vs SHORT COURSE INDOMTH: dec rate of PDA re- opening; prolonged course-assoc w/dec IVH & renal imapirment
  186. 186. PDA BEYOND NEONATAL PERIOD
  187. 187. PDA-WHEN TO CLOSE• ANY PDA THAT CAN BE AUSCULTATED NEEDS TO BE CLOSED• ANY SYMPTOMAYTIC PDA NEEDS TO BE CLOSED• SILENT PDA’S MAY/MAYNOT BE CLOSED IN POST NEONATAL PERIOD
  188. 188. PDA-WHEN TO CLOSE• POST 3 KGS ANY PDA CAN BE CLOSED• VERY LARGE PDAS: BABY DOES NOT GAIN WEIGHT-SO NO POINT WAITING• SMALL PDAS MX MEDICXALLY TILL ABOUT 5-
  189. 189. PATENT DUCUTS ARTERIOSUS
  190. 190. THORACOSCOPIC PDA CLOSURE
  191. 191. THORACOSCOPIC PDA CLOSURE
  192. 192. Veneous CatheterArterial Catheter
  193. 193. RASHKIND DOUBLE UMBRELLA DEVICE Double stainless 2 polyurethane discs mounted steel skeleton on the skeleton
  194. 194. TRANSCATHETER CLOSURE PDA• SUCCESS RATE >99 % FOR COMPLETE CLOSURE• NO SCAR• FAST RECOVERY• NO BLOOD TRANSFUSION• COILS OR DEVICES• SIZE NO LIMITATION• WEIGHT: SMALLEST 2.2 Kg in IPAH-NO COA• >1000 cases by Speaker• J Interv Cardiol. 2001 Apr;14(2):247-54.
  195. 195. TETRALOGY OF FALLOT
  196. 196. Embryology
  197. 197. HYPERCYANOTIC SPELL• MANAGEMENT:• DONOT MAKE THE CHILD CRY• SEDATE MORPHINE/PHENERGAN• HEPLOCK: IV FLUIDS BOLUS• BICARB• IV METOPROLOL 0.05 MG/KG VERY SLOW IV OVER ½ HR
  198. 198. SURGERY-WHEN ?• HYPERCYANOTIC SPELL- EVEN ONE IS ENOUGH TO INDICATE SURGERY• IF AN INFANT < 6 MO…DO A BT SHUNT
  199. 199. Treatment-TOF• Surgical – Palliative to improve the pulmonary blood flow- Systemic to Pulmonary shunt
  200. 200. NO SPELLS:SURGERY- WHEN ?• IF SATS APPROACHING 75% PLAN FOR SURGERY• SURGERY DECIDED ON BASIS OF – AGE/WT AND PULM A SIZE – IF ANATOMY FAVOURABLE: WT> 7.5 KG REPAIR• IF WT> 8 KG & ANATOMY FAVOURABLE – COMPLETE REPAIR OR ELSE BT SHUNT
  201. 201. TOF- Interventional Cardiology • Balloon Dilatation of pulmonary valve in cyanotic children with indication of shunt – In a randomised study evaluating for postponement of palliative surgery and growth of pulmonary arteries. • Coil closure of collaterals
  202. 202. CYANOTIC CHD OTHERS
  203. 203. BLUE BABY..CARDIAC• DUCTAL DEPENDING LESIONS:RT HEART – PULM ATRESIA – TOF SEVERE – PULMONARY STENOSIS, SEVERE• MIXING LESIONS – TRANSPOSITION• START PROSTIN IN ANY OF THESE
  204. 204. CYANOTIC CHD• FURTHER OPTIONS – SEPTOSTOMY: MIXING LESION – STENTING THE DUCT: DUCT DEPENDENT – BT SHUNT• MOST IMP OUTCOME FACTOR – ACCURATE ECHO – EARLY TRANSPORT – AVOID INFECTIONS
  205. 205. TGA:WHEN & WHAT SURGERY• ALL TGA’s DIAGNOSED IN NEWBORN PERIOD: ARTERIAL SWITCH OPERATION• IDEALLY IN SECOND WEEK• CAN BE PERFORMED UPTO 4 WEEKS
  206. 206. ARTERIAL SWITCH
  207. 207. OTHER LESIONS• TAPVD: OPERATE AT DIAGNOSIS; DON’T DELAY• TRUNCUS; OPERATE AT DIAGNOSIS: NO ADVANTAGE IN DELAYING
  208. 208. COARCTATION• TO BE TREATED WHEN DETECTED• BALLOON AS PRIMARY MANAGEMENT GOOD OPTION EVEN IN THE NEWBORN:• RECURRENCE 30%; IF NO ASSOC PROBLEMS• POST-6 MO BALLOON IS PREFERRED
  209. 209. THANK YOU
  210. 210. THANK YOU

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