Pediatric - iranathero.ir · o Amphetamines are associated with VSD, PDA, ASD and TGA. o Phenytoin...

Pediatric

Cardiology

Second Edition

2015-2016

by

Dr Maged Zakaria IBRAHIM

Neonatologist and Pediatrician

MRCPCH, MSc. Pediatrics, IBCLC

Keynotes®

Keynotes “Pediatric Cardiology ”

Copyright © 2015 by Maged Zakaria Mahmoud.

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the author. Queries on how to seek permission, and arrangements can be sent to the author’s email: [email protected] Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, the author does not assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.

ISBN 978-977-94-1232-2 Printed in EGYPT

١٠٢٥ ©حلوق الطبع محفوظت

۲٠٢٥ - ٤۲٢٦٢زكم الايداع

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1

Keynotes Pediatric Cardiology

Index

Chapter 1 - Congenital Heart disease 3 Fetal Circulation 4 Introduction to CHD 5 Acyanotic Congenital Heart Disease - The Left-to-Right Shunt Lesions 8 Atrial Septal Defect (ASDs) 8 Ventricular Septal Defect (VSD) 11 Atrioventricular Septal Defect (AVSD) 14 Patent Ductus Arteriosus (PDA) 16 Acyanotic Congenital Heart Disease - The Obstructive Lesions 19 Pulmonary Stenosis 19 Aortic Stenosis 22 Coarctation of the Aorta 23 Complete Interruption of the Aortic Arch 26 Congenital Cyanotic Heart Disease with Pulmonary Blood Flow 27 Fallot Tetralogy 27 Tetralogy of Fallot with Pulmonary Atresia 31 Pulmonary Atresia with Intact Ventricular Septum 32 Double Outlet Right Ventricle (DORV) 33 Tricuspid Atresia 33 Ebstein Anomaly of the Tricuspid Valve 35 Congenital Cyanotic Heart Diseases with Pulmonary Blood Flow 37 D-Transposition of the Great Arteries (d-TGA) 37 Total Anomalous Pulmonary Venous Return (TAPVR) 39 Truncus Arteriosus 41 Single Ventricle (Double-Inlet Ventricle, Univentricular Heart) 42 Hypoplastic Left Heart Syndrome 43 Abnormal Positions of Heart and the Heterotaxy Syndromes 45 Scimitar Syndrome 46 Anomalies of the Aortic Arch 47 Anomalies of Coronary Arteries 48 Extracardiac Complications of Cyanotic CHD and Eisenmenger Physiology 49 Chapter 2 - Cardiac Arrhythmias 50 Electrical System of the Heart 51 ECG: The Basics 52 Extrasystoles 56 Tachyarrhythmias 57 Ventricular Tachyarrhythmias 64 Long QT Syndromes (LQTS) 66 The Holter monitor (Ambulatory ECG monitoring) 67 Bradyarrhythmias 68 Principles of Antiarrhythmic Therapy 72 Chapter 3 - Acquired Heart Diseases 75 Acute Rheumatic Fever 76 Auscultatory Sites 85 Rheumatic Heart Disease 86 Mitral Insufficiency 86 Mitral Stenosis (MS) 88 Aortic Insufficiency 91 Aortic Stenosis 93 Tricuspid Valve Disease 95 Infective Endocarditis (IE) 97 Chapter 4 - Diseases of Myocardium and Pericardium 102 Diseases of the Pericardium 103 Diseases of the Myocardium 106

2


Dilated Cardiomyopathy (DCM) 106 Hypertrophic Cardiomyopathy (HCM) 107 Restrictive Cardiomyopathy 108 Secondary Cardiomyopathy 109 Myocarditis 110 Endocardial Fibroelastosis (EFE) 111 Pediatric myocardial infarction 111 Tumors of the Heart 113 Chapter 5 - Cardiac Therapeutics 114 Congestive Heart Failure (CHF) 115 Cardiogenic Shock 120 Differential Diagnosis of Cardiomegaly without Heart Murmur 121 Systemic Hypertension 122 Hypertensive Crisis 132 Pulmonary Hypertension 134 Chapter 6 - Miscellaneous 138 Causes of Palpitation 139 Sudden Death 140 Innocent Cardiac Murmurs 141 Child with Chest Pain 142 Cyanosis 145 Syncope 147 Summary of Abnormal S2 153 Chest Radiography 154 Cardiac Manifestations of Systemic Diseases 158

3


Chapter 1

Congenital Heart Disease

5


Introduction to CHD - CHD occurs in ~ 0.8% of live births.

- Incidence is higher in stillborns (3-4%), spontaneous abortuses (10-25%) and premature

infants (2% excluding PDA).

- The most common CHD is VSD (35-50%).

Etiology

- The cause of most congenital heart defects is unknown.

- Most cases of CHD are multifactorial (combination of genetic predisposition and

environmental stimulus).

- Genetics Causes of Congenital Heart Disease:

Structural Heart Defects

o DiGeorge syndrome

o Familial ASD ± heart block

o Alagille syndrome (Peculiar facies, bile duct hypoplasia, right-sided cardiac lesions)

o Holt-Oram syndrome (limb defects, ASD)

o Trisomy 21 (AV septal defect)

o Isolated familial AV septal defect (without trisomy 21)

o Cri du chat syndrome (5p deletion) (Cat-like cry in infancy, microcephaly, downward

slant of palpebral fissures)

o Familial (total anomalous pulmonary venous return; TAPVR)

o Noonan syndrome (PS, ASD, hypertrophic cardiomyopathy)

o Ellis–van Creveld syndrome (polydactyly, ASD)

o CHARGE association (Coloboma, heart defects, choanal atresia, growth or mental

retardation, genitourinary anomalies, ear anomalies, genital hypoplasia)

o Williams syndrome (supravalvular AS, branch PS, hypercalcemia)

o Marfan syndrome (connective tissue weakness, aortic root dilatation)

o Familial laterality abnormalities (situs inversus, complex CHD)

6


Cardiomyopathies

o Hypertrophic cardiomyopathy

o Hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome

o Dilated cardiomyopathy (X-linked or AR)

Arrhythmias

o Complete heart block

o Long Q-T syndrome (AD, 6 types)

o Jervell and Lange-Nielsen syndrome (AR long QT syndrome, congenital deafness)

o Familial atrial fibrillation (autosomal dominant)

o Brugada syndrome (RBBB, ST segment elevation, unexpected sudden death)

- Environmental Factors:

Maternal infection e.g. TORCH

Maternal DM or SLE

Teratogenic drugs:

o Amphetamines are associated with VSD, PDA, ASD and TGA.

o Phenytoin and Valproic acid are associated with pulmonary stenosis (PS), aortic stenosis

(AS), coarctation of the aorta (COA), and PDA.

o ACE inhibitors and angiotensin II receptor antagonists cause congenital malformations of

multiple systems, including cardiac defects (e.g., ASD, VSD, PDA, and PS).

o Lithium is associated with Ebstein’s anomaly.

o Retinoic acid may cause conotruncal anomalies.

o Progesterone and estrogen.

o Excessive alcohol intake is associated with VSD, PDA, ASD, and TOF (fetal alcohol

syndrome).

Genetic Counseling

- Incidence of CHD is ≈0.8% of live births.

- If one parent has CHD or for the 2nd pregnancy after a previous child with CHD, the incidence

increases to 2-6%

- When 2 1st degree relatives have CHD, the risk for a subsequent child may reach 20-30%.

- Fetal echocardiography improves rate of detection of CHD in high-risk patients.

27


Congenital Cyanotic Heart Disease with Pulmonary Blood Flow

Fallot Tetralogy

- Infundibular pulmonary stenosis

- VSD (usually nonrestrictive and large)

- Dextro-position of aorta so that it overrides the ventricular septum

- RV hypertrophy

tetralogy of Fallot can be associated with DiGeorge syndrome

Pathophysiology

- Blood from RV is shunted across VSD into aorta (with marked PS) resulting in desaturation

and cyanosis (variable according to severity of pulmonary obstruction).

- Pulmonary blood flow may be compensated by a PDA.

The degree of RV outflow obstruction determines timing of onset of symptoms, severity of cyanosis and

degree of RV hypertrophy.

- With mild to moderate PS, patient may not be visibly cyanotic (acyanotic or “pink” tetralogy

of Fallot). With severe PS, cyanosis will be present from birth and worsen with ductal closure.

28


Clinical Picture

- Often, cyanosis is not present at birth; but with increasing RV hypertrophy over time,

cyanosis occurs later in the 1st yr of life (expect in neonates with severe PS; in whom

pulmonary flow is PDA dependent). A heart murmur is audible at birth.

- Dusky blue skin with marked clubbing of fingers and toes (extracardiac manifestations of

long-standing cyanotic CHD)

- Infants with mild PS may present with CHF (e.g. dyspnea on exertion and easy fatigability)

caused by ventricular left-to-right shunt.

- FTT and delayed puberty.

- Squatting (for relief of dyspnea caused by physical effort):

Kinking of femoral arteries causes intra-aortic pressure and thus systemic pressure to

overcome pulmonary pressure so blood is pushed through the stenosed RV outflow.

- Paroxysmal Hypercyanotic Attacks (hypoxic or “blue” Spells):

Mechanism of hypoxic spell

PaO2 stimulates respiratory center causing

hyperventilation. The hyperpnea systemic

venous return (SVR). In the presence of a fixed

right ventricular outflow tract (RVOT), the

SVR results in right-to-left (R-L) shunt,

worsening cyanosis (vicious circle)

Episodes of hyperpneic, restless, cyanosis, gasping and syncope; frequently in morning on

awakening or after vigorous crying and last from a few minutes to hours

Caused by infundibular spasm with reduction of an already compromised pulmonary blood

flow, which may result in severe hypoxia and metabolic acidosis

- Inspection and Palpation:

Left anterior hemithorax bulge because of long-standing RV hypertrophy

Systolic thrill along left sternal border in the 3rd and 4th parasternal spaces

29


- Auscultation:

S2 is single ( pulmonary component)

Ejection systolic murmur over left parasternal area ( in intensity with more severe PS)

Investigations

- Chest X-ray: pulmonary oligemia, RV hypertrophy with uplifted apex, large aorta (Cœur en

sabot, French for "clog-shaped heart").

- ECG: RV hypertrophy, right axis deviation with tall peaked P wave suggesting RA enlargement.

- Echocardiology establishes diagnosis, degree of RV outflow tract obstruction and PDA flow.

- Cardiac Catheterization with angiography (5-10% have coronary artery abnormalities).

Tetralogy of Fallot (Cœur en sabot)

Complications

- Cerebral thrombosis (due to polycythemia, dehydration, associated iron-deficiency anemia).

- Brain abscess with seizures, localized neurologic signs and ICT.

With a right-to-left shunt bypassing pulmonary circulation, bacteria in bloodstream are not filtered

through pulmonary macrophages. G+ve organisms are more common than G-ve

- Bacterial endocarditis.

- CHF is unusual except in young infants with “pink” or acyanotic tetralogy of Fallot

30


Treatment

- In neonates with critical PS, prostaglandin E1 (0.05-0.2 μg/kg/min IVI).

- For Hypercyanotic Attacks (Hypoxic Spells):

Knee-chest position (traps systemic venous blood in the legs, thereby

temporarily SVR and helping to calm the baby. The knee–chest position

may also SVR by arterial blood flow to the lower extremities).

Administration of O2

SQ morphine (max 0.2 mg/kg) (suppresses the respiratory center and

abolishes hyperpnea)

Correction of metabolic acidosis with IV NaHCO3 (in severe spells) ?!

Intubation and sedation (for resistant spells)

IV phenylephrine (to systemic vascular resistance)

β-Adrenergic blockade (IV propranolol; 0.1 mg/kg)

- Brain Abscess:

IV antibiotics with surgical drainage

- Cerebral Thromboses:

Adequate hydration, phlebotomy (for severe polycythemia)

- Surgical Correction:

Palliative Surgery (to bypass PS):

o Blalock-Taussig shunt (anastomosis between subclavian and pulmonary artery).

o Waterston shunt (anastomosis between ascending aorta and pulmonary artery).

o Potts shunt (anastomosis between descending aorta and pulmonary artery).

Total surgical correction

Blalock-Taussig Shunt Waterston Shunt Potts Shunt

50


Chapter 2

Cardiac Arrhythmias

75


Chapter 3

Acquired Heart Diseases

85


Auscultatory Sites

Mitral area is at the apex beat, as LV is closest to the thoracic cage.

The apical impulse is normally at the 5th intercostal space in the midclavicular line after age 7 years. Before this age, the apical impulse is in the 4th intercostal space just to the left of the midclavicular line.

Tricuspid area is at the inferior left sternal margin.

Pulmonary area is at the left 2nd intercostal space close to sternum.

Aortic area is at the right 2nd intercostal space close to sternum.

Erb's Area (mid-sternal area or the 2nd aortic area) corresponds to the inner end of the 3rd left

interspace. Soft early diastolic murmur of aortic insufficiency is best heard here.

96


Mitral Insufficiency Mitral Stenosis Aortic Insufficiency Aortic Stenosis

Chambers Enlarged

Symptoms PVC and Low COP PVC, hemoptysis and Low COP Palpitations, Dyspnea, angina Low COP, Syncope

General Examination Signs of Low COP and SVC Malar flush Signs of Low COP and SVC

de Musset's - Corrigan’s Water Hammer Pulse Quincke's pulse Wide Pulse pressure Durozier - Traube's - Hill’s

Low COP

Cardiac Examination – Inspection, Palpation and Percussion

Apex Localized Hyperdynamic Downward, Outward Shift

Diffuse Slapping Outward Shift

Localized Hyperdynamic Downward, Outward Shift

Localized Heaving Downward, Outward Shift

Left Parasternal Area (±) Heave Heave - -

Aortic Area - - - Systolic thrill

Pulmonary Area (±) Palpable S2 (±) Dull on percussion

(±) Palpable S2 (±) Dull on percussion

- -

Cardiac Examination – Auscultation

Apex

S1 Holosystolic; to axilla

S1 Diastolic; localized

Austin Flint Murmur -

Pulmonary Area (±) P2 (±) P2 (±) Garaham Steell Murmur

- -

Aortic Area

S1 Ejection Systolic; to neck

2nd Aortic Area Diastolic; to apex

http://www.google.com.eg/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&cad=rja&uact=8&ved=0CDIQFjAB&url=http%3A%2F%2Fmedical-dictionary.thefreedictionary.com%2FQuincke%27s%2Bpulse&ei=ErI1U9iPCcjMtQai0YG4CQ&usg=AFQjCNHi2OFVJq1rBle7QzVMHenUfqtT1w&bvm=bv.63808443,d.Yms

http://en.wikipedia.org/wiki/Traube%27s_sign

102


Chapter 4

Diseases of Myocardium and Pericardium

114


Chapter 5

Cardiac Therapeutics

138


Chapter 6

Miscellaneous

147


Syncope Syncope is a transient loss of consciousness and muscle tone that result from inadequate cerebral perfusion

1. Autonomic (non-cardiac) Disorders:

- Vasovagal syncope (simple syncope, neurocardiogenic syncope, or neutrally mediated syncope)

- Orthostatic (postural) hypotension (dysautonomia)

- Exercise-related syncope

- Situational syncope:

Breath holding

Cough, micturition, defecation, and so on

Carotid sinus hypersensitivity

- Excess vagal tone.

2. Cardiac Disorders:

- Arrhythmia:

Tachycardia: SVT, atrial flutter or fibrillation, VT (seen with long QT syndrome, arrhythmogenic

RV dysplasia, Brugada syndrome)

Bradycardia: sinus bradycardia, asystole, complete heart block, pacemaker malfunction

- Obstructive lesions:

Outflow obstruction: AS, PS, hypertrophic cardiomyopathy, pulmonary hypertension

Inflow obstruction: MS, tamponade, constrictive pericarditis, atrial myxoma

- Myocardial diseases:

Coronary artery anomalies

Hypertrophic cardiomyopathy, dilated cardiomyopathy, MVP, arrhythmogenic RV dysplasia.

3. Neuropsychiatric Disorders:

- Anxiety disorders: panic disorders, agoraphobia (fear of open space)

- Hyperventilation

- Seizure disorders

- Migraine

- Brain tumors

- Hysterical (conversion reaction)

4. Metabolic Disorders:

- Dehydration (or inadequate hydration)

- Hypoglycemia and Electrolyte disorders

- Drugs and toxins: anti-seizure drugs, sedatives and tranquilizers, antihypertensive drugs.

148


Proposed pathophysiology of neurocardiogenic (vasovagal) syncope.

Presumed points of action of various pharmacologic agents are also shown by open arrows.

Evaluation of a Child with Syncope

- Most children who present with presyncope (without loss of consciousness) or even syncope

have vasovagal phenomena or other benign causes of syncope.

- The goal of the evaluation is to identify high-risk patients with underlying heart disease.

- Evaluation may extend to other family members when a genetic condition is suspected.

History

- Because physical examinations are almost always normal long after the event, accurate history

taking is most important. Sometimes a complete history cannot be obtained owing to amnesia

about the event, but witness accounts are useful.

149


- Aspects of history taking:

About the syncopal event:

o The time of the day:

Syncope after rising in the morning or after morning shower suggests vasovagal syncope.

Hypoglycemia (a very rare cause), occurring in a fasting state in the morning

o Patient’s position (supine, standing, or sitting):

Syncope while sitting or recumbent suggests arrhythmias or seizures.

Syncope after standing for some time suggests vasovagal syncope.

o Relationship to exercise:

Syncope occurring during exercise suggests arrhythmias.

Syncope occurring immediately after cessation of physical activities suggests venous

pooling in the leg (with reduced venous return and cardiac output).

o Associated symptoms:

Palpitation or a racing heart rate suggests tachycardia or arrhythmias

Chest pain suggests possible myocardial ischemia

Shortness of breath or tingling or numbness of the extremities suggests hyperventilation

Nausea, epigastric discomfort, and diaphoresis suggest vasovagal syncope

Headache or visual changes suggest vasovagal syncope

o Duration of syncope:

Syncope < 1 min suggests vasovagal syncope, postural hypotension, or hyperventilation.

A longer duration of syncope suggests convulsive disorders, migraine, or arrhythmias.

o Patient’s appearance during and immediately after the episode:

Pallor indicates hypotension

Abnormal movement or posturing, confusion, focal neurologic signs, amnesia, or muscle

soreness suggests the possibility of seizure

History of a cardiac, endocrine, neurologic, or psychological disorders

Medication history

Family history:

o Coronary heart disease risk factors e.g. history of MI in family members < 30 years of age

o Cardiac arrhythmia, CHD, cardiomyopathies, long QT syndrome, seizures, metabolic and

psychological disorders

o A positive family history of fainting is common with vasovagal syncope.

150


Social history is important in assessing whether there is a possibility of substance

abuse, pregnancy, or a conversion reaction.

Physical Examination

- The results of the physical examination are usually normal:

If orthostatic intolerance group is suspected, the heart rate and BP should be measured

repeatedly while the patient is supine and after standing without moving for up to 10

minutes. In a well-hydrated state, positive test results for vasovagal syncope or postural

hypotension in the office setting are uncommon.

Careful auscultation to detect a heart murmur or an abnormally loud 2nd heart sound.

Neurologic examination should include a funduscopic examination, test for Romberg’s sign,

gait evaluation, test of deep tendon reflexes, and test of cerebellar function.

Differential Diagnosis

- Epilepsy:

Patients may have incontinence, marked confusion in the postictal state, and abnormal EEG.

Patients are rigid rather than limp and may have sustained injuries.

Patients do not experience the prodromal symptoms of syncope (e.g., dizziness, pallor,

palpitation, and diaphoresis).

Duration of unconsciousness is longer than that typically seen with syncope (<1 minute).

- Hypoglycemia:

Characteristics include pallor, perspiration, abdominal discomfort, lightheadedness,

confusion, unconsciousness, and possible subsequent occurrence of seizures.

Hypoglycemic attacks differ from syncope in that the onset and recovery occur more

gradually, they do not occur during or shortly after meals, and the presyncopal symptoms

do not improve in the supine position.

- Hyperventilation:

Hyperventilation is believed to produce hypocapnia, resulting in intense cerebral

vasoconstriction, and causes syncope (may also have a psychological component).

151


Patient often experiences air hunger, shortness of breath, chest tightness, abdominal

discomfort, palpitations, dizziness, numbness or tingling of face and extremities, and rarely

loss of consciousness. It often is associated with emotional disturbances.

- Conversion reaction:

Not associated with injury and occurs only in the presence of an audience.

Episodes are rare before 10 years of age.

Spells are not related to postural changes and are not improved by the supine position.

Diagnostic Studies

- A complete cardiac evaluation is indicated if there is a heart murmur, a family history of

sudden death or cardiomyopathy, or an abnormal ECG finding.

- Serum glucose and electrolytes is of limited value (patients seen after the episode).

- With suspected arrhythmia as the cause of syncope, the following may be indicated:

ECG for all patients presenting with syncope.

Ambulatory ECG monitoring e.g. Holter monitor.

Exercise stress test (if syncope is associated with exercise).

Echocardiographic studies.

Cardiac catheterization and electrophysiologic testing (rarely indicated).

Head-up tilt table test: If patients with syncope have

autonomic symptoms (e.g., pallor, diaphoresis, or

hyperventilation), tilt table testing is useful to provoke

symptoms exactly during orthostatic stress while being

closely monitored for cardiac rhythm and rate and BP

responses associated with symptoms.

Several distinct abnormal patterns have been

identified after head-up tilt table tests:

Vasovagal: An abrupt BP usually with bradycardia

Dysautonomia (or postural hypotension): A gradual BP leading to syncope.

Postural orthostatic tachycardia syndrome (POTS): excessive HR to maintain an

adequate BP to prevent syncope.

152


- Neurologic consultation and EEG are indicated with:

Prolonged loss of consciousness

Seizure activity

Postictal phase with lethargy or confusion

Treatment of Cardiac Causes

- Beginning empiric treatment without performing a head-up tilt table test may be reasonable.

- Most patients show spontaneous resolution of syncope in 6-12 months; therefore, long-term

medical prophylaxis is usually not necessary.

- Orthostatic Intolerance Syndromes (including vasovagal syndrome):

Adequate intravascular volume is the most important preventive element:

o Patient is recommended to drink 2-3 L of water a day.

o Physical activities, especially in a hot environment, require more fluid intake, preferably

electrolyte-containing fluids (e.g. sport drinks with additional sodium).

o Liberal use of salt with meals and non-fatty salted snacks.

o Caffeinated beverages should be avoided (because of their renal diuretic effect).

o Wearing elastic support hose (waist-high) may be useful in postural hypotension.

Medications:

o Fludrocortisone (Astonin-H®) intravascular volume and also produces both venous

and arterial vasoconstriction. It can be given in a low dosage (0.1 mg by mouth once or

twice a day) with salt intake or a salt tablet (1 g daily).

o α-Agonist (e.g. pseudoephedrine) stimulates heart rate and peripheral vascular tone,

preventing reflex bradycardia and vasodilation.

Cardiac Pacemaker is generally not indicated in pediatric patients.

- Cardiac Arrhythmias:

Antiarrhythmic medications as indicated.

Patients with long QT syndrome are treated with beta-blockers, pacemakers, or implantable

cardioverter defibrillators.

Propranolol may be indicated with symptomatic MVP syndrome.

Catheter ablation may be indicated in patients with WPW syndrome causing frequent SVT.

1. Pediatric Cardiology 2. Pediatric Gastroenterology 3. Pediatric Hepatology

4. Pediatric Genetics 5. Genetic Disorders of

Metabolism (IEM) 6. Immunology and Allergy

7. Pediatric Endocrinology 8. Pediatric Nephrology 9. Pediatric Nutrition

10. Pediatric Neurology 11. Pediatric Psychiatry, Growth & Development

12. Pediatric Rheumatology, Bone Disorders

13. Neonatology (Volume I) 14. Neonatology (Volume II) 15. Neonatologists’ Pocket

Drug Reference

16. Pediatric Hematology 17. Pediatric Oncology 18. Pediatric Infections

(coming soon)

Keynotes®

Pediatric Postgraduate Series

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Pediatric - iranathero.ir · o Amphetamines are associated with VSD, PDA, ASD and TGA. o Phenytoin...

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