Paediatric Emergency cardiology

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Gavin Burgess R5, PEM

description

Gavin Burgess R5, PEM. Paediatric Emergency cardiology. General. Review common presentations Uncommon Paediatric ECG Congenital heart disease Rhythm disturbances Long QT HOCM Rheumatic fever Carditis – myo, endo, peri. General. Innocent murmurs Kawasaki disease. Fetal circulation. - PowerPoint PPT Presentation

Transcript of Paediatric Emergency cardiology

Page 1: Paediatric Emergency cardiology

Gavin Burgess R5, PEM

Page 2: Paediatric Emergency cardiology

General

Review common presentations Uncommon Paediatric ECG Congenital heart disease Rhythm disturbances Long QT HOCM Rheumatic fever Carditis – myo, endo, peri

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General

Innocent murmurs Kawasaki disease

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Fetal circulation

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“Normal”

Age Respiratory rate

Pulse rate Systolic BP

O-1mo 30-60 120-160 50-701-12mo 20-40 80-140 70-1001-5y 20-30 80-130 80-1106-12y 20-30 70-110 80-120adolescents 12-20 60-100 110-120

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“Normal”

Ball-park BP? Neonate? Older?

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“Normal”

Gestational age should equal MAP Systolic BP = 70 + (2 x age)

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“Normal” ECG

Typically have shorter PR, QRS, QT RV dominance, RAD

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RVH

Causes Tetralogy of Fallot PS Coarct ASD TAPVD Large VSD with Pulm HT

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LVH

Causes AS VSD PDA Complete AV block Cardiomyopathy

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Diagnosis?

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Superior or “north west” axis Endocardial cushion defect

2% of congenital heart disease Down syndrome account for 70% Fatal due to pulm HT Banding in infancy

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Myocardial infarction

AT III Cardiomyopathy Congenital heart disease CAD (ALCAPA) Drugs (cocaine) Homocystinuria Hyperlipidaemia and cholesterolaemia Kawasaki Leukaemia Marfans Haemoglobinopathies Tumours (myxoma) Rheumatic fever SLE

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Diagnosis?

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Diagnosis?

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Diagnosis?

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Which lesions give cyanosis? Tetralogy of Fallot Tricuspid atresia Transposition of the great arteries (IDM) Truncus arteriosus Total anomalous pulmonary venous

drainage Hypoplastic left heart Ebstein’s anomaly (lithium) Pulmonary atresia/severe stenosis

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Pulmonary markings

Decreased: Pulmonary atresia/stenosis Tetralogy Tricuspid atresia Ebstein’s anomaly

Increased: TGA TAPVD Truncus

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What’s the hyperoxia test? ABG Give 100% O2 Repeat ABG after 10 min If rises by >10%, likely pulmonary

lesion

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When does the ductus close? 10-14 days after birth, it is

physiologically closed

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Neonatal and infant presentations to ED What are the 4 presentations in and

infants neonates? 1) shock 2) cyanosis 3) cardiac failure 4) murmur

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What are the ductal-dependent lesions? Systemic

Coarct/interrupted arch Aortic stenosis HLH

Pulmonary PS/atresia Tricuspid atresia

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Shock

L ventricular outflow obstruction Coarct AS HLH

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Shock

Management: ABC’s Start prostin CXR ECG

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What’s prostin?

Prostaglandin E1 Rate 0.05-0.2 mcg/kg/min Side effects?

Apnoea Fever Flushing Hypotension

Prostin has an “all or nothing” action Should work in 15min

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Time to presentation of cyanotic lesions

Age ECG X-ray0-1 week TGA RVH Increased1st week TAPVD RVH Increased1-4weeks Tricuspid

AtresiaLVH Decreased

Severe PS RVH Decreased1-12weeks TOF RVH DecreasedAnytime in infancy

Truncus arteriosus

BVH Increased

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Cyanosis

What is a tetralogy of Fallot? RVH Overriding aorta VSD RV outflow obstruction

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What’s a “tet spell”?

Change in the balance of pulmonary and systemic flow

Hypoxic and cyanotic event Decreased system vascular

resistance or increased RV outflow obstruction

Increasing hypoxia

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How do I treat it?

O2 Chest-knee (why?) Analgesia B-blocker (why?)

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Cardiac failure

History: Fussy Sweating FTT Short frequent meals

Physical: HSM Murmur FTT You will NOT see a JVP AVM – auscultate the head

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Murmurs

Features of an innocent murmur 80% of children will have a murmur at

some time in their lives All have normal ECG and X-rays Never diastolic

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Common innocent murmurs

Type Description AgeStill’s LLSB, 2/6, “twang” 3-6yPulmonary flow ULSB, blowing,

transmitsGone in 3-6mo

Venous hum Supra clavicular, rotate head, supine goes

3-6y

Carotid bruit Over carotid Any age

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Arrhythmia

SVT Very common Tolerated well, occasional LOC change Child is fussy Newborn >220 bpm <12y often accessory pathway

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Arrhythmia

SVT treatment In shock vs stable Vagal stim Adenosine Amiodarone ,verapamil use extreme

caution. Frequently develop profound hypotension and die

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Arrhythmia Long QT

History Deafness Single person MVC Swimming syncope Exercise syncope Family history of sudden death Seizure of unknown etiology Recurrent syncope/lightheadedness Sibling with SIDS

Physical Infant with bradycardia

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Arrhythmia

All first degree family members should be screened with ECG

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HOCM

2% under 2 y, 7% under 10y Variable history

CP Palpitations SOB Syncope Sudden death High risk if syncope Sudden death with strenuous exercise

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HOCM

Physical S4 gallop, mid systolic murmur Increased PVR decreases murmurs

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Rheumatic fever

Who was Jones? What where his criteria? What do you need to make a

diagnosis? Which valve? Then?

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Rheumatic fever

What about Sydenham’s chorea? And the rash?

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Rheumatic fever

Treatment ASA 75-100mg/kg Prednisone 1-2mg/kg Benzathine (Pen G) 600 000U (27kg), 1.2

million U (27kg) Prophylaxis Age questioned

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Myocarditis

Various causes, most notably viral Coxsackie A,B, ECHO, flu’ Non-specific viral prodrome Non-specifc fussiness, lethargy etc Heart failure IVIG may be indicated

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Infective endocarditis

Rheumatic fever, congenital heart defects, catheters, IVD

S. aureus, viridans are the usual suspects

Fungi in neonates, usually in the NICU

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Infective endocarditis

Major 2 + BC, (viridans, s. bovis, HACEK, S. aureus,

enterococci Persistently + BC (1 hr between multiple, or

12h or 3h +) + echo mass at typical sites Intracardiac abscess Prosthesis failure New regurgitant murmur

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Infective endocarditis

Minor Fever (38C) Predisposing condition/IVD Vascular phenomena Non-specific echo findings

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Prophylaxis -1997

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Prophylaxis

High risk Prosthesis Previous IE Transplants Complex CHD

Dropped from the list……. Moderate risk

(PDA,VSD,primumASD,coarct,bicuspidAV) Calcified AS,RF,HOCM,MVP

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Pericarditis

Classic chest pain worse when lying flat

Radiation to L shoulder Friction rub Most often viral causes Diffuse ST changes, “saddle”shaped CXR important Cefotaxime, ASA, prednisone,

colchicine

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Kawasaki disease

Etiology unkown, presumed infectious

More common in Asian and Pacific islanders

Peaks around 1-2years, 80% under 4y, 50% under 2y

Slight male preponderance 3mo-8y is typical range

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Kawasaki disease

3 phases Acute phase (10 days)

High fever for 5 days 4 of

rash (ANY rash, no bullae/vesicles), oedema of extremities/ peeling of extremities Non-exudative bulbar conjuctivitis Mucosal changes (cracked lips, strawberry

tongue – even on HISTORY) Cervical LN (1.5cm)

Carditis, other organs (arthritis, pyuria, gallbladder/liver, menigitis, irritable

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Kawasaki disease

Acute ESR, CRP WCC, plt Lipids, LFTs Echo coronary artery aneurysms unusual

before 10d Subacute phase

Desquamation Coronary disease Rash, fever, LN disappear plt

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Kawasaki disease

Convalescent phase ESR, plt normalise Beau’s lines

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Kawasaki disease

Rx IVIG ASA Vaccinations Steroid of no benefit Reduces CAD from 25% to 5% Untreated mortality 1-5%