Al-Howasi Manual of Clinical Pediatrics PDF

Manual of Clinical PAEDIATRICS For Medical Students & Postgraduate Doctors Mansour N. Al Howasi / 8th -:.. Edition  MANUAL OF CLINICAL PAEDIATRICS (For Medical Student & Postgraduate Doctors) MANSOUR NASER ALHOWASI M.B.B.ch, DCH, MRCP (U...

Manual of Clinical PAEDIATRICS For Medical Students & Postgraduate Doctors Mansour N. Al Howasi / 8th -:.. Edition  MANUAL OF CLINICAL PAEDIATRICS (For Medical Student & Postgraduate Doctors) MANSOUR NASER ALHOWASI M.B.B.ch, DCH, MRCP (UK), FRCP (E) Consultant Paediatrician Former (Consultant Paediatrician, King Fahad medical city, Paediatrric Hospital Clinical Assistant Professor of Paediatrics King Saud University Teaching Professor at the Department of child life and Health University of Edinburgh [part time] Vice Minister of Health for Health Affairs) Riyadh,KSA  Distributed by www.jarir.com For More Details [email protected] © Mansour Naser Affiowasi, 1996 King Fahad National Library Cataloging-In-Publication Data Manual of Clinical Paediatrics for Medical Student & Postgraduate Doctors/ Edited by Mansour Naser AlHowasi-Riyadh.. p.,.. cm ISBN: 9960-31-345-X 1- Paediatrics 2- Children - Diseases - Diagnosis I - AlHowasi, Mansour N. (ed.) 618.92 de 3619/16 First Edition 1996 Reprinted 1997 Second Edition 2000 Third Edition 2004 Reprinted 2005 Fourth Edition 2006 Fifth Edition 2008 Reprinted 2009 Sixth edition 2011 Reprinted 2012 Reprinted 2013 Seventh edition 2015 Eighth Edition 2019 All rights reserved. No part of this publication may be reproduced in any form or by any means electronic or mechanical including photocopying without written permission from the editor.  Ill TABLE OF CONTENTS Chaoter Subiect Pa!!e No. IDSTORY AND CLINICAL EXAMINATION I Hjstory 1 Clinical exantlnation 6 Golden rules 9 NEONATOWGY 11 Delivery Room Management 11 Care of the normal newborn 13 Physical examination 14 The premature neonate 18 Neonatal problems of interest 21 Evaluation of neonatal jaundice 23 Infants of diabetic mother 25 Metabolic disorders in newborn 25 Newborn metabolic screening 26 NUTRITION 29 Nutritional reqmrements 30 Estimating energy needs 31 Enteral nutrition 33 Parenteral nutrition 34 Nutritional support 36 Infant Feeding 37 Infant formulas 39 Weaning 40 Common nutritional disorders 41 IMMUNIZATON IDSTORY 43 Basic Vaccination schedule 44 Vaccination in special circumstances 45 Active irnmuni:zation after exposure 46 BCG vaccine 46 DTP, DTaP vaccine 47 (HIB) vaccine 49 Hepatitis A Vaccine 49 Hepatitis B Vaccine so Influen:za virus vaccine SI MMR Vaccine 52 Meningococcal Vaccine 53 Pneumococcal Vaccine 54 Poliomyelitis Vaccines 55 Rota Virus Vaccine 56 Varicella Vaccine 57 Typhoid Vaccine 58 Summary Of Commonly Used Vaccines 59 INFECTIOUS DISEASES 60 Meningitis 60 Brucellosis 62 Enteric Fever 63 Tuberculosis 64 Malaria 65 Pertussis (whoopinh cough) 66 Septic Shock Algorithm 67  IV Approach To Pediatric Septic Shock 68 Measles 69 Rubella 70 Mumps 70 Infectious Mononucleosis 71 Chicken Pox 72 Viral Hepatitis 73 PEADIATRIC EMERGENCIES & INTENSfVE CARE 75 Norma l Vital Signs in infants and Children 75 Basic Life Support 75 Advanced Life Support 79 Respiratory Failure 80 Acute Respiratory Distress Syndrome 83 Diabetic Ketoacidosis 85 Status Epilepticus 87 Causes of Status Epilepticus 88 Traumatic Brain Injury and Increased lntracranial Pressure 89 Causes of Brain injury and increased ICP 90 Shock 92 Differential Diagnosis of septic shock 96 Acute Upper Airway Obstruction 98 Comatose Child 99 CARDIOVASCULAR SYSTEM 102 History 102 Examination l02 Innocent Murmur 104 Finger Clubbing l08 Chest Scar 108 Cyanosis 109 Presentation and Management of Heart Disease in the Neonatal Period 111 Ductus Dependent Lesion 112 Electrocardiogram (ECG) 113 Congenital Malformation syndromes associated with congenital heart disease 117 Acyanotic lesion with left to right shunt 118 Cyanotic Heart Disease 119 Obstructive Lesion 120 Valvular Lesions 121 Hypertentioa 122 RESPIRATORY SYSTEM 124 History 124 Clinical Examination 125 Examination Of The Young And Uncooperative Patients 130 Respiratory Failure 132 Clinical Anatomy of The Lungs 133 Causes of Some Important Respiratory Signs 134 Apnea 137 Bronchial Asthma 138 GASTROINTESTINAL SYSTEM 144 History 144 Examination 144 Causes of Ascitis ISO Abnomial abdominal masses 151  V Causes of hepatomegal y 152 Causes of Splenomegaly 153 Portal Hypertension 154 Causes of Hepatosplenomega ly 154 Causes of Bleeding Per Rectu m 154 Di ffi rential Dianosis Of The Recurrent Abdominal Pain In Children 155 Etiology of Chronic Dian-hea In Children 156 The Major Causes OfCholestasis In Infa ncy 157 Dehydration 158 Oral Reydration solution (ORS) 159 RENAL SYSTEM 160 History 160 Examination 162 Urine Analysis 164 Urinary Tract Infection (UTI) 164 Hematuria 166 Proteinuria 169 Renal Tubular Acidosis (RTA) 170 Acute Renal Failure (ARF) 173 Chronic Renal Failure 176 ENDOCRINOLOGY & DIABETES 178 Growth 178 Short Stature 178 Obesity 180 Tall Stature 181 Calcium Disorders 181 Thyroid Disorders 184 Ambigious Genitalia 185 Hypoglycemia 188 Puberty 189 Precocious Puberty 190 Diabetes Mellitus 191 Di abetes lnsipidus (DI) 194 Adrenal ~1sufficiency 195 Cushing Disease / Syndrome 195 NERVOUS SYSTEM & DEVELOPMENT 198 Genera l Examination 199 Mental status examination 201 Cranial Nerves 203 Golden Rule 213 Refl exes 215 Golden Rule 222 Abnormal Head Shape 224 Abnormal Head Size 224 Clinical approach to abnormal head size 225 Sudden Onset of Unsteady Gait (ATAX IA) 226 Causes of Ataxia 227 Acute Paralysis 227 Acute Hemi plegia 229 Floppy In fa nt Syndrome 231 Cerebral Palsy (CP) 234 Neurodegenerati ve Disorders (N OD) 237  VI Developmental Examination 243 Essential Milestones 245 MUSCUOSKETLETAL SYSTEM 251 History 251 Examination 252 Knee joint examination 253 Genu Varum (Bow Legs) 255 Genu Valgum (Knock Knees) 255 HIP Joint Examination 256 Congenital Hip Dislocation (CDH) 257 Ankle Joint and Foot Examination 258 Flat foot (PES PLANUS) 259 PesCavus 259 II;permobility of the Joints 260 Talipes Equinovarus 260 Torti coll is 260 Toe Walking 261 Examination of the Spine for Scoliosis 261 Pain Amplification Syndromes in Children 262 Assessment of child with juvenile chronic arthritis 264 DEVELOPMENTAL AND BEHAVJORAL PEDIATRICS 267 Autism Spectrum Disorder (ASD) 267 Attention deficit Hyperactivity Disorder (ADHD) 269 Conduct disorder 274 BREAKING BAD NEWS 277  VII PREFACE Previous edition of Manual of Clinical Pediatrics proved to be very successful as a practical manual, both here and overseas; providing the opportunity for this eighth edition. Many chapters in the eighth edition of this manual have been extensively updated and revised. The new chapters on Emergency and Intensive Care and Breaking Bad News have been added. The format of the manual has remained essentially the same. The management principles and protocols in the update of this manual are not based on practices at only one institution. Contributors are from different institutions in the Kingdom of Saudi Arabia. I feel this has enabled us to produce a manual that is not institution-specific but reflects a cross section of contemporary approaches to pediatric management. My sincerest thanks to the contributors of the first, second, third, fourth, fifth, sixth and seventh edition, and my family for their continued support, which has been indispensable to the completion of this edition. I would like to extend my SPECIAL THANKS TO DR. SAMEEH GHAZAL who had worked very hard, in spite of his tight schedule on reviewing all the manuscripts, in addition to his contribution to the manual by two chapters, several drawing, and figures. Also I would like to thank Dr. MARAM SAMEER for her great effort to prepare and design this edition. I welcome any suggestions and comments regarding the manual; letters should be addressed to: Dr. Mansour AI-Howasi P.O. Box 62300 Riyadh, 11585 KS.A. [email protected]  VIII CONTRIBUTORS (Alphabetic order) PROFESSOR ABDULLAH AL HERBISH MBBS, FRCPC, FAAP Consultant, Professor of Pediatrics and Endocrinology College of Medicine & King Saud University, Riyadh (Endocrinology) Dr. ALIA AL IBRAHIM MBBS, DCH, CABP, Fellowship in Paediatric Nephrology Consultant in Paediatrics & Paediatric Nephrologist KKUH Hospital Riyadh, KSA (Renal System) 9 PROFESSOR ASAAD ABDULLAH ASSIRJ MBBCh, MRCP (UK), FRCP Consultant, Professor of Paediatrics and Gastroenterology King Saud University, Riyadh, KSA (Gastrointestinal System) Dr. DHIMAN CHOW1JHURY MBBS, DCH, MRCP (UK), FRCP (Edin.) Consultant and Assistant Professor of Paediatrics !WK Grave Health Center, Department of pediatrics, Dalhousie University. Canada (Gastrointestinal System) Dr. IBRAHIM S. ALHIFZI MBBS, DCH, CABP, FRCPCH, FRCP Consultant Neonatologist Clinical Professor of Paediatrics Armed Forces Hospital, Southern Region (Examination of Neonate) Dr. MAHER AHMED KHALIFA MBBCh, DCH, MRCP (UK) Consultant Paediatrician & Paediatric Neurologist Insurance Hospital (Riyadh), Riyadh, KSA (Neurology & Development) Dr. MANSOUR M. ALQURASHI MBBS, DCII, MRCP (UK), ABP, Fellowship in Cardiology Consultant PaediatTician & Paediatric Cardiologist AlYammamah hospital, Clinical Assistant Professor of Paediatrics King Saud University Riyadh, KSA (Cardiovascular System)  IX Dr. MANSOUR NASER ALHOWASI MBBCh, DCH, MRCP (UK), FRCP (Edin.) Consultant Paediatrician. KSA Former, (consultant paediatrician King Fahad Medical City K.S.A Clinical Assistant Professor of Pediatrics King Saud University Teaching Professor at the Department of child life and Health University of Edinburgh [part time] Deputy Minister for Executive Affairs, MOH) Riyadh, KSA (History and Clinical Examination, Neonatology, Immunization, Nutrition and infant feeding, Cardiovascular system, Gastrointestinal system, Urinary system, Neurology and development, [nfectious Diseases) Dr. MOHAMMED F. FAROUQ MBB.ch, F AAP Consultant in Paediatrics and Infectious Disease Assistant Professor in Paediatrics and Haed of paeditrics department King Abdu laziz University, Jeddah, K.S.A. (Immunization) PROFESSOR MOHAMMED MOHAMMED JAN MBBCh, FRCPC Consultant Paediatric neurology Professor of Paediatrics & Neurology King Abdu laziz University Hospital & ' King Faisal Specialist Hospital and Research Center, Jeddah, K.S.A. (Neurology) Dr. SALEH MOHAMMED ALSALEHI MD, DBP Consultant Developmental and Behavioral Pediatrics, KFMC Assistant Professor KSU, Riyadh, K.S.A. (Developmental and Behavioral Pediatrics) Dr. SAMEEH S. GHAZAL MBBCh, DCH, MRCP (UK), ABP, MRCPCH (UK), CIC (USA), Epidemiology fellowship (USA) Consultant Paediatrician, Infectious Diseases and infection Control Prince Mohammad bin Abdulaziz Hospital (Medical Director) Assistant Professor of Paediatrics King Saud Bin AbdulAziz University- Health Science, Riyadh, KSA (Infectious Diseases & Respiratory System and Bronchial asthma) Dr. SMRJTI CHOWDHURY MBBS, DCH, MRCP (UK) Consultant Paediatrician Department ofneonatology, Dalhousie University. Canada (Gastrointestinal System) Dr. WAFAA AL SUWAIRJ MBBS, DCH, MRCP (UK), ABPP. Consultant Paediatric Rheumatologist King Abdulazez Medical City, National Guard, Riyadh, KS.A. (Musculoskeletal System)  X Dr. WALEED HAMED ALBUALI Consultant pediatric lntensivist, Assistant professor Pediatric ICU director, Department of Pediatrics King Fahd Hospital of the University AI-khobar, Saudi Arabia (Emergency & Intensive Care) Dr. YOUSEF K. GHAZAL MBBCh, MRCP (UK), CABP, SBP, MRCPCH (UK) Consultant Paediatrician, lntensivist King Fahad Medical City, Children 's Hospital, Riyadh, KSA (Nutrition & Infectious Diseases) 1 History & Clinical Examination History Demographic data: Name Age (date of birth) Sex Nationality Address Source of history: (mother, father & others) Presenting complaints: Use their words. (The parents may actually tell you the diagnosis). Symptoms with duration. History of presenting complaints: Obtain a complete chronological sequence of events. Deeper inquiry about important symptoms must be made regarding: Onset Course Duration Site Frequency Severity Relieving factors Exacerbating factors Diurnal or seasonal variation Relation to food Relation to exercise e.g. cough School missing related to the complaint Any associated symptoms 1  System Inquiry: System inquiry is important when there is complain not specific to one system. E.g. fever or when there is there multisystem disease. There are few questions, which provide useful "screening" General e.g.: Feeding and appetite ( very important) Irritability Weight loss Cardiovascular e.g.: Breathlessness Sweaty on feeding Cyanosis Respiratory e.g.: Breathlessness Runny nose Cough Noisy breathing (wheeze or strider) Sore throat or earache Hemoptysis Gastrointestinal e.g.: Vomiting Abdominal pain Constipation or diarrhea (frequency and appearance of stool) Jaundice Genitourinary e.g.: Frequency Dysuria Nocturia or enuresis Hematuria Incontinence Age of menarche 2  Neurological e.g.: Irritability Drowsiness Fits or abnormal movements Headache Numbness or unpleasant sensation Weakness Hematological & oncological e.g.: Pallor Jaundice Bone pain Bruises Bleeding from the nose Infections e.g.: Skin rash Contact with infectious patients Recent travel Musculoskeletal& skin e.g.: Joint swelling Joint pain Skin rash N.B. If any symptom during the system review is positive, deeper inquiry must be made e.g.: Cough-Nocturnal or related to exercise points towards bronchial asthma. Purulent sputum points towards suppurative lung disease. Past medical history: This includes: Previous diseases Previous medications taken by patient: -Frequency 3  -Does Previous hospitalization Previous surgery Previous transfusion Any known drug or food allergies? Pregnancy and neonatal history: Follow up during pregnancy Mother's illness during pregnancy (nature of the illness-which trimester) e.g.-flue like illness or skin rash during early pregnancy may point towards congenital infections. Mother's medication: e.g.- Valproate taken by the mother during pregnancy increase risk of fetal neural tube defect. Anabolic steroids taken by the mother during pregnancy may cause virilization of female fetus. Phenytoin taken by the mother during pregnancy may cause increase risk of fetal congenital anomaly especially cardiac anomaly. Exposure of mother to radiation during pregnancy. Fetal movement: weak fetal movement may point towards intrauterine hypotonia. e.g. dystrophia myotonica, spinal muscular atrophy. Polyhydramnios- may point towards fetal GIT obstruction. e.g. esophageal atresia or intrauterine hypotonia. Oligohydramnios:- may point towards fetal urinary system abnormality. e.g. bilateral renal agenesis. Length of gestation. Mode of delivery. Birth weight, height and head circumference. Apgar score. Any neonatal disease or admission and why? Nutritional history: Breast-fed or bottle-fed and for how long? If bottle-fed: -Which formula did he receive? -How is it prepared? 4 -What volume did he take at each feed? -And how long did he take it? -Frequency offeeds -Total daily intake Time of weaning- timing of introduction of solids and cereals. N. B. Normally, breast-fed baby might pass up 6 motions daily. Immunization history: The recommended vaccination program in Saudi Arabia will be described later on: Check immunization card. If there is fai lure in taking any vaccine ask for the reasons in details. Developmental history: This includes: Gross motor. Fine motor. Speech and hearing. Social and play. Schooling (level and performance). N.B. -If the mother has other children, compare his or her development with his or her other siblings. -some important development milestones will be described later on. Family and social history: Ages of parents. Consanguinity Number of siblings and age range (any sibling from previous or another marriage) Family history of similar condition. 5  Which region the parents originally came from (e.g. sickle cell anemia common in south- west and eastern region of Saudi Arabia) Neonatal deaths (e.g. metabolic disease) Previous abortions. Housing - type of accommodation (rented or owned, house or flat, number of bedrooms, washing and toilet facilities, air conditions and heaters) Parents' occupation and income of the family. Parents' education Parents' smoking habit (especially in bronchial asthma cases) Contact with animals Recent travels (e.g. malaria in southwest of Saudi Arabia) N.B. Pay more attention to detailed family history, if hereditary, allergy or infectious disease is involved e.g. sickle cell anemia, bronchial asthma, and tuberculosis. Transportation: Make sure there is available transportation for the child and his or her attendance to be able to attend any follow-up. Try to make the appointment of any follow-up suitable for the condition of the father's work. If the patient came from poor family, contact the social worker to arrange for the family financial support and airplane tickets between the regions if the family came from far area... etc. Golden role: at the end of your history, ask the historian if she or he likes to inform you anything else or if she or he expects you to ask her or him any other question about her or his child that was not asked yet. Clinical examination General advice on examining children: I. Introduce yourself to the child and or his attendant. 2. Ask the child's name. 3. Wash your hands especially if the child is an infant. 4. Warm your hands and remove watch or ring, which might scratch the child. 5. Inform the child that you are going to examine him e.g. I am going to percuss your chest. 6. Avoid standing over a small child by getting down to his level. 6  7. Distract the child with a toy or any other thing if this will help you to continue your examination. 8. Talk to the child as you examine and smile to him or her. 9. Remember to thank him at the end of the examination. 10. During examination some of the examiners like to hear running commentary while you examine the child. Never & Do not Never handle the child roughly. Never refer to a child as dysmorphic without first seeing the parents (except the common known syndromes e.g. trisomy2 l) Do not get the sex of the child wrong. Do not use potentially worrying tenns in front of parents without explaining them e.g. tumor or mental retardation. Do not use abbreviations in your clinical notes except if it is internationally known and accepted. Do not discuss the case with your colleague in front of parents using foreign language without explaining to the parents what you are doing and reassuring them. General examination: General condition: Looking sick Looking well Vital signs: (very important) Temperature Respiratory rate Pulse Blood pressure Growth parameter: (plot them in standard centile chart) very important Weight Height Head circumference Color: Pallor Jaundice Cyanosis 7 Dysmorphic features: Upward slanting eyes Depressed nasal bridge Obvious abnormality: Club foot Legs censoring Pectus deformities Skin condition: Hyperpigmentation Skin rashes Supportive measures: Oxygen Intravenous fluid Splint Wheelchair Systemic examination: Inspection: A great deal of information can often be elicited without even touching the child. In addition some children will cry as soon as you touch them. You should expose the relevant area, (the whole chest, the whole abdomen or the legs). If the parents are present ask them to undress the child, otherwise you will miss an operation scar, hydrocele, muscle wasting or some other important signs. Do comment in the general condition of the patient (well or ill), and on intravenous drips, nasogastric tubes, urinary catheter, or obvious dysmorphic features if present... etc. Palpation: If there is any possibility of the part you are palpating being painful, you should ask the patient if it hurts and being particularly gentle. e.g. abdomen, joints and lumps. Percussion: Do not forget the percussion is an important method to detect organomegaly especially in young children. 8  Technique of Percussion: Auscultation: Do not forget to auscultate the abdomen , for intestinal sound and bruits. Do not forget to auscultate the anterior fontanel for bruits when you examine a newborn with heart failure. (A-V malformation) N.B. - Try to start from the periphery then go central. Sequence of examination might be difficult to apply in young children. ~Golden Rules: ✓ If there is one congenital anomalies, look for other congenital anomalies. e.g. examine the heart and urinary system in any child with dysmorphic features. ✓ If there is one endocrine disease, look for other endocrine diseases. e.g. look for signs of hypothyroidism in any diabetic patients. ✓ If there is one nutritional disease, look for other nutritional disease. e.g. look for iron deficiency anemia in any patient with rickets. 9 ✓ If there is one "atopic" disease look for other atopic diseases. e.g. look for atopic eczema in any patient with bronchial asthma. ✓ If there is one autoimmune disease, look for other autoimmune diseases. e.g. look for signs of Addison's disease in any patient who has alopecia area or vitiligo. Do not forget in clinical examination the principles: Growa paramt tr 10 2 Neonatology The success of the health care system in countries is commonly judged by infant mortality rate (death occurring from birth to 12 months / 1000 live births). The neonatal period ( I s1 four weeks of life) is a highly vulnerable time for the infant and neonatal mortality where it accounts for about 65% of infant mortality; hence proper care of the neonate contributes significantly to reduction in infant mortality. I. Delivery Room Management 1. Anticipation Proper information obtained from the obstetrician or the midwife about maternal condition should identify neonates at risk of developing problems in the delivery room. This includes mothers with certain diseases or problems such as premature labor, IUGR, prolonged rupture of membranes (18 hours before delivery), oligohydramnios, polyhydramnios, diabetes, pregnancy induced hypertension, infections, fetal distress, etc. 2. Preparation Check the resuscitation equipment and the medications needed for resuscitation. 1. Radiant warmer switched on, warm towels 2. Arnbu bag connected to air-oxygen blinder 3. Laryngoscope and blades (Size: 00, 0, 2) 4. Endotracheal tubes (size 2.5, 3, 3.5) 5. Stethoscope 6. Stop clock 7. Catheters, cannulas, syringes and needles 8. Medications 11  3. Ressuscitation : Place Wider" raiianl heater (SUclion trachea if mecomm-siained Iliad) Dry thorougHy Remove wet Lenin :I Evauate response Position SUclion mouth then nose Non or gasping Spontaneous Provide tactile stimulation respiration breathing l Provide positive I Evaluate heart rate preSSure ventilation for 30 Secs ~ < 100/min >100/min Evaluate heart rate I l J. --..L ! Below60 HR fi0-100 HR 60-100 Above 100 --l Evaluate. Continue not increasing Increasing Watch for color veritilatioo. Continue spontaneous. Chest ~ ventilation. Continue respiration compression. Chest ventilation then DIC compression ventilation I Initiate medication if HR < 60 after 30 Secs. I Pink or peripheral cyanosis Provide ,I, oxygen PPV and chest compression I Observe and mocitor - Resuscitation with room air is safe and effective - lntrapartum suctioning of oro and nasopharynx is not recommended for infant born with meconium stained liquor and suction of trachea is not recommended if baby is vigorous. During this process Apgar score should be estimated as fo llows: SCORE 0 2 A = Appearance Blue/ Pale Blue extremities Pink P = Pulse (HR)/min. 0 < 100 > 100 G = Grimace None Grimace Cry (Reflex Irritability) A= Activity Flat Some limbflexion Active movements (Muscle Tone) R = Respiration Absent Slow, irregular Strong cry Leuthner et al Ped Clinic of NA Vol 41 No 5 Oct 1994 12 Chest compressjon techniques Ccardjac massage} a) Two Thumbs Method (Preferred} Place both thumbs on the middle third of the sternum just below an imaginary line drawn between the nipples, with the fingers encircling the chest and supporting the back. The xiphoid or lower portion of sternum should not be compressed to avoid abdominal trauma. :W Two Finger Method The index and middle finger are placed over the middle third of the sternum. Medications The medications that are currently recommended during resuscitation of the newborn infant are: Adrenaljne ffipjnephrine}: 0.01 - 0.03 mg / kg of 1: 10000 solution using high dose Epinephrine may lead to hypertension, decreased myocardial function and poor neurological outcome. ET dose is 0.1 mg/kg/dose. Naloxone: Used to reverse respiratory depression caused by narcotic administration to the mother. Dose: 0.1 mg I kg Route: IV only. Volume Expander: 10 mls / kg as Normal Saline, or O-Negative blood if blood loss is suspected. The routine use of Sodium Bicarbonate is discouraged, except in prolonged arrest. Atropine and calcium is not recommended in resuscitation of the newborn. A brief examination should be done in delivery room to look for major congenital malformations. The baby will then be sent to Nursery or Neonatal ICU according to his/her condition. II. CARE OF THE NORMAL NEWBORN Normal newborns should be given to mothers as soon as they are stable enough to be breast-fed and should always be nursed with their mothers. A detailed examination must be performed within 24 hours of birth. It should be done in the presence of the mother or both parents to answer their questions and to give advice about feeding and care of their baby. Vaccinations should be given, routinely BCG and hepatitis B vaccine, but hepatitis B irnmunoglobulin is added to babies of mothers with hepatitis B positive screening. 13 1,..............---. -: : -.'I -·.. _ _._ _... -----:-~- - - -~~ Physical examination of the newborn infant This requires patience, gentleness, & flexibility, so auscultation of the heart and palpation of the abdomen can be done while the infant is quiet and relaxed. Adequate light, warm hands and environment are prerequisite. Proper hand washing before examination is essential. Vital signs should be recorded: Pulse (normal 120 - 160 / minute), Respiratory Rate (30 - 60 I minute), and temperature. Weight, length, and head circumference should be plotted on centile GENERAL APPERANCE Alertness Movements Color (cyanosis of cold periphery is normal) Dysmorphism SKIN Pallor (circulatory failure or anemia) Mottling Plethora (polycythemia) Jaundice Birth marks, hemangiomas, mongolian blue spots Rash (erythema toxicum, septic spots, herpes, transient pustular melanosis) Edema (generalized: hydrops) (localized: hands and feet in Turner's syndrome) HEAD Size - Microcephaly: familial, congenital infection - Macrocephaly: hydrocephalus, familial, achondroplasia,hydranencephaly, etc. Shape Fontanelles & sutures Masses - cephalohematoma (collection of blood w1der the periosteum which does not cross sutures) - Caput succedaneum (edematous scalp of the presenting part) FACE Dysmorphic features EYES Microphthalmia as in congenital rubella syndrome Buphthalmos (corneal diameter > I cm) Slant of palpebral fissures (upward or downward) Conjunctiva! hemorrhage Coloboma of the lids or the iris (syndromes) Aniridia (association with Wilms tumor and other urogenital anomalies) Red reflex suggests absence of cataract and major intraocular pathologies Leukokoria (white pupillary reflex) seen with cataract, ROP, and retinoblastoma 14  Hypertelorism (widely spread eyes), or hypotelorism EARS Low set ears (classically seen in Down' s Syndrome) Malformations and periauricular tags Ear drums appear normally dull gray MOUTH Natal teeth (remove only if loose or interfere with feeding) Large tongue is seen in congenital hypothyroidism, Beckwith-Wiedemann syndrome and others but glossoptosis is seen with Pierre Robin syndrome Cleft lip and palate High arched palate Lingual thyroid NECK Normally short Swellings: goiter, cystic hygroma, thyroglossal cyst, sternomastoid mass. Redundant skin at the back of the neck is seen with Down's Syndrome and is assoc iated with webbing in Turner's Syndrome RESPIRATORY Chest Shape: pectus, nipples, space Sounds: (grunting, stridor, crying), air entry, breath sounds, added sounds Movements CARDIOVASCULAR Pulse: rate, rhythm, volume, etc. Weak femoral pulse and higher BP in upper limbs than lower limbs (Coarctation of the Aorta) Dextrocardia Heart sounds Murmur ABDOMEN Distended or scaphoid Organomegaly Hernias Bowel sounds GENITALIA Sex Ambiguity Testis 15 -- - - - -- -- - -- --~ -~.~- --=--~ - '. Labial fusion Hypospadias Check anal patency NEUROLOGY Alertness Movement and posture Tone Reflexes Primitive reflexes: (Leave them to the end of examination) Reflex Stimulus Response Appearance Disappearance (Gestational (Corrected age) age) Moro Lift the head slightly Rapid extension & 28 - 32 weeks 3 - 5 months and then drop it gently abduction of arms with on your palm hand opening followed by slow return to mid line Sucking Nipple or teat Strong & synchronized 32 weeks 4- 7 months sucking Rooting Gently stroke the cheek Baby searches with his 32 weeks 4 - 7months with finger tip mouth Palmar Touch the baby's open Baby grasps the finger 32 weeks 3-4 months palm with your finger Plantar Firmly press the ball of Toes flex 32 weeks 8 months infant's sole with your thumb Stepping Hold the infant Alternating stepping 34 weeks 2 months upright with the sole movement touching a flat surface Placing Touch the dorsum of a Baby climbs over the 34 weeks 5 months foot with the edge of the edge of the table table EXTREMITIES Size and shape (e.g. hernihypertrophy) Digits (count, syndactyly, etc.) Club feet BACK Mongo lian blue spots Hair tuft 16  Dimples Sinus Scoliosis HIPS Asymmetry of groin creases Barlow's & Ortolani's Test - (to assess hip dislocation) Lay the infant supine on a flat hard surface and remove the nappy. Stand in the mid line at the foot end of the infant, flex infant's knees fully and hips to 90°. Hold the lower limbs with your thumbs on the medial condyles and tips of the middle finger on the greater trochanters of each femur. Bring the knees together and attempt to push the hips posteriorly. If you feel a 'click ', it means the head of the femur has dislocated (Barlow's sign). Keeping the grip unchanged, now abduct the infant's thighs with the thumbs and lift the femoral heads forward with the middle fingers. If you feel a definite 'clunk', it means the previously dislocated head of the femur has slipped back into the acetabu lum (Orto lani's sign). e.rtowtt ~ t>ac art111 to vy to P.i., -,.~ --- diskx:sie hlo Ort.olanl Utt Ali,iil,cting ther-,, tc U}' to n:locak hlr F~..-'1i pu!,I, mur forw rd rtca~l,ui.;rr. Examine newborn requires: Patience, gentleness & flexibility 17  THE PREMATURE NEONATE The New Ballard Score New Ballard Score Sheet Use this score sheet to assess the gestational maturity of your baby. At the end of the examination the total score determines the gestational maturity in weeks. NEUROMUSCULAR MATURITY - SIGN SCORE SIGN SCORE -1 0 1 2 3 4 5 Posture a:i=: ~ « ~ ~ Square Window r~. [ r,~ ~ 45 ~w r~ ~, ~ tr~ Arm Recoil 1 1 ~.1w 110- 140" ttllO" CD''°" c6 cb d) ~ Popliteal Angle CI:) ,w a:) ,t 8 ears ol 1st drug: Doxycycline/Tetracycline 1st drug : (6 weeks) Bactrim 6 weeks Simple infections 2nd drug 2nd drug: Bactrim (3 weeks) or Rifampicin 6 weeks Rifampicin (6 weeks) -Use Streptomycin (2 weeks) or Gentamicin (1-2 weeks) in place of the 2nd drug. *Serious infection or -N.B. Rifampicin can be used as well as adjunctive therapy to complications: reduce the rate of relapse. - Endocarditis -For life threatening complication such as meningitis or - Osteomyelitis endocarditis, the duration of therapy is often extended for - Meningitis several months. -For osteomyelitis, earty surgical intervention should be considered. DRUG DOSE/DAY Divided to --=-~--___;;==;;;;;:;;=;;;; Bactrim Trim. 10mg/kg/day + Sulph.-50mg/kg/day 2 doses Rifampicin 20 mg/kg/day 1 or 2 doses ~--~--- ~------====;;;; Doxycycline 2-4 mg/kg/day 2 doses ------------ Tetracycline 30-40 mg/kg/day -----====="'"". 4 doses ------- Streptomycine Gentamicin 20 5 mg/kg/day {IM) --=2_...dc,018S 3 doses _---====::::: NB. Ist drug should be given to all patients Inform infection control department in all positive cases ENTERIC FEVER Clinical manifestation: Fever Constitutional symptoms: e.g. Headache, malaise, anorexia and lethargy Abdominal pain, tenderness, splenomegaly and hepatomegaly 63  Rose spot (maculopapular rash) Change in mental status Diagnosis: 1) Cultures: Blood culture Urine and stool culture after the first week Bone marrow culture (the most sensitive method) 2) Serology: Wida! test Treatment: Empirical therapy with Ceftriaxone or Cefotaxirne until antibiotic susceptibility is available In case ofresistance to Ceftriaxone, Ciprofloxacillin can be used as alternative. TUBERCULOSIS Clinical manifestation: General: Fever, night sweat, anorexia, decreased activity, weight loss... Local: According to site involved Diagnosis: High index of suspicion High ESR Positive PPD test (Mantoux test) Quantiferone golden test Chest x ray Positive smear for acid-fast bacilli and/or culture for mycobacterium tuberculosis fromsputum, gastric aspirate, lymph node or other involved site. Mantoux test: is intradermal injection of 0.1 ml containing 2 tuberculin units (TU) of purified protein derivative (PPD) Interpretation of PPD skin test: PPD considered positive if the amount of indurations after 48-72 hours is either: History of contact with open Personal risk factors No personal or case or. < 4 years environmental risk Suspected tuberculosis. Lymphoma factors (symptoms, signs or chest. D.M. radiograph) or. Renal failure lmmunocompromised patient. Malnutrition or - Environmental risk factors (environmental exposure to TB) 64  Treatment: Short course of treatment gives better compliance and drugs combination decreases the risk of resistance, so the following protocol is recommended: A- Positive PPD in otherwise normal child (clinically and after investigation) Start INH alone for 3 months (as prophylaxis) then re-evaluate the patient: I. No disease continue INH for 6 months 2. Sign of disease: treat as in B 8- Diseased patient: Full treatment: 1. INH: 6 months and 2. Rifampicin: 6 months and 3. Pyrazinamide: 2 months 4. In severe infections: (meningitis, rniliary) give in addition Streptomycin (in patients < 8 years of age) or Ethambutol in patients> 8 years of age for 2-3 weeks N.B. In Renal, Bone and CNS infection, treatment should continue for up to 12-18 months. Before starting therapy and during follow up CBCs, liver functions tests should be monitored. Tuberculosis is a reportable disease, report to the health authority. MALARIA Clinical manifestation: - History of travel to endemic area - Fever, chills, rigors, sweat, headache, pallor, jaundice, hepatosplenomegaly. Diagnostic test: Stained blood film: - Thick blood film: for parasite identification - Thin blood film: for species identification Parasitic index: % of infected RBCs < 1%: mild Parasitemia 1-5%: moderate Parasiternia > 5%: severe Parasiternia Treatment: I. Supportive therapy: for fever, fluid and electrolytes 2. Specific therapy: A. Oral therapy: all types of malaria provided that P. Falciparum is susceptible. 65  - Chloroquine phosphate: l Omg/kg stat, then 5 mg/kg 6 hours later, then 5 mg/kg/day for 2 consecutive days. - lf no response (no decrease in the parasitemic index in 24 hours) after consultation of infectious disease department give Fansidar (Pyrimethamine and sulphadoxine) as single dose. If no response - Mefloquine hydrochloride as single dose (not in children < 15 kg weight). B. Parenteral therapy: For those who have persistent vomiting or who are in coma. - Quinine dihydrochloride, if not available - Quinidine gluconate, if not available - Chloroquine hydrochloride - Parenteral therapy should be replaced by oral therapy as soon as possible. C. Prevention of relapses (plasmodium vivax or p. ovale): - Primaquine phosphate for 14 days starting in the 3rd day of chloroquine phosphate. Chemoprophylaxis: Starting day: 1 week before traveling to endemic area End day: 8 weeks after leaving the endemic area Drugs: Chloroquine is generally preferred: 5 mg/kg/once per week For chloroquine resistant area other drugs can be used like: proguanil or fansidar. PERTUSSIS (WHOOPING COUGH) Etiology: Bordetella pertussis (Gram-negative bacilli). [ncubation period: 6 - 21 days Clinical features: Catarrhal phase ( 1-2 wk): rhinorrhea. Paroxysmal phase (2-4 weeks or longer): Bouts of coughing in runs of IO or more followed by whoop and ends by vomiting. Convalescent phase (1-2 weeks): coughing slowly subsides over period which can last up to 3 months (hundred days cough as used to be said). Complications: Respiratory: Pneumonia (more commonly by secondary bacterial infection), apnea, atelectasis, otitis media, sinusitis, pneumomediastinum, pneumothorax, interstitial or subcutaneous emphysema. Later on: Bronchiectasis. Hemorrhage: Epistaxis, retinal, subconjunctival, intraventricular. Hernia: Inguinal, umbilical, rectal prolapse, rupture of diaphragm. 66  Cerebral anoxia: following apnea manifests as fits - 2.5%, encephalopathy 0.5%, apnea and sudden death may occur during very severe paroxysm. Treatment: Erythromycin, when given within 14 days ofonset of the disease, may eliminate the organism from nasopharynx, improve symptoms and reduce communicability. In severe paroxysmal attacks salbutamol nebulization and steroid might be helpful. Treat complications. Isolation & infectivity: The patient should be placed in droplets precautions for at least 5 days Treat with erythromycin for a total of 14 days. Close contacts of less than 7 year of age who are unimmunized or who have received fewer than 4 doses of DTP should have pertussis vaccine according to the recommended DTP schedule and erythromycin for 14 days. SEPTIC SHOCK ALGORITHM Definitions Systemic inflammatory response syndrome - SIRS is the presence of two or more of the following criteria (one of which must be abnormal temperature or leukocyte count): o Core temperature of >38.5°C or 2 standard deviations above normal for age o Mean respiratory rate >2 standard deviations above normal for age o Leukocyte count elevated or depressed for age, or > 10 percent immature neutrophils Infection - Infection is defined as a suspected or proven infection caused by any pathogen. Sepsis - SIRS in the presence of or as a result of suspected or proven infection. Severe sepsis - Sepsis associated with cardiovascular organ dysfunction, or acute respiratory distress syndrome, or with two or more other organ dysfunctions. Septic shock - Sepsis with cardiovascular dysfunction despite the administration of 2:40 mL/kg of isotonic fluid in one hour. Do not discuss the case with your colleague in front of parents using foreign language without explaining to the parents what you are doing and reassuring them. 67  Approach to Pediatric Septic Shock 0 min ' Recognize decreased mental status and perfusion. 5 min Maintain airway and establish access according to PALS guidelines. Push 20cc/kg isotonic saline or colloid boluses up and over 60cc/kg. Correct hypoglycemia and hypocalcemia. Administer antibiotics. J 15 Fluid refractory shock min + i--- Fluid responsive 1 Establish central venous access, begin dopamine or dobutamine therapy and establish arterial monitoring. Fluid refractory - dopamine/dobutamine resistant L Obs~rve in] PICU Titrate epmephrine for cold shock, norepinephrine for warm shock to normal clinical endpoints and ScvO2 saturation ~70% 7 Catecholamine - resistant shock t l 60 min r L__ Begin hydrocortisone if at r'.sk for absolute adrenai msuffic1ency __J 7 __ i= Normal Blood Low Blood Pressure Pressure Pressure Cold Shock Cold Shock Warm Shock ScvO2t at 1 year - Start chest compression at lower half sternum or one finger below nipple line in infants. a) < 1 year give 100 compressions/min: depth 2 cm b) 1 year give 100 compressions/min: depth 3 cm c) Old child: depth 4-5 cm or 1h- ½ depth of chest. d) Give I breath/ 5 compressions in general e) For neonate give 120 compressions/min & l breathe for every 3 compressions. Old child (>8yrs) may also be given 2 breaths/IS compressions as adult. f) For compression use 2 fingers (index and middle finger) or both thumbs encircling the chest for neonates & small babies, and use heel of one hand for younger children, and heel of 2 hands for older children. Continue BLS until advanced life support can be offered or ifno response after 30 minutes. Activate advanced life supp01t team after 1 minute & continue resuscitation. 8: For breathing: - Open airway: Head tilt and chin lift or jaw- thrust (in case of suspected neck trauma) - Check breathing: Look to respiratory movement, Listen breathing sound, and feel flow of air by your -- - - + I Aclivale emergency l8SpOllS9 and monitor until Is pulse definitely felt syslem [If not ahady dona) emargancy withi, 10 seconds? after 2 mirutas. l9SJlOll(lels a'l'MI. Conln,e 1811Q18braalhing; check pulse about_, No breathing 2 mi-ua If no pulse, begin or only gasping, IOGll itll Mlllllle. AED analyzes rhythm. Shodcable rhythm? Yes, No, shockable nonshockable Give 1 shock. R8Slm8 CPR Resume CPR inmediately for immediately for about 2 mrutes about 2 minutes (until prompted ('-"llil prompted by AED to allow by AED to allow rhythm check). rhythm check). Conlnle w1lil Al.S pnwiclers take ConlnJe until AI..S p,oviders take av« or victim ats to move. IMl'Of vic:llm.... loimN. 0 2015 American Heart - l i o n 78  2.ADV ANCED LIFE SUPPORT(ALS):Remember by letters A & B, C, D, E, F. : Invasive procedures aimed at restoration of ventilation and circulation. These include bag- valve-mask venti lation, endotracheal intubation, intravenous, introsseous and /or endotracheal drug administration A & B: Airway & Breathing: - Intubate and ventilate with 100% 02, alternatively use Ambubag and mask for ventilation. C: Circulation: - Continue cardiac massage same as in BLS. D: Drugs: - Intravenous or Intraosseous line for drugs Drugs used most commonly for ALS. a) Adrenaline: (0.1 ml/kg of I in 10,000) IV or via ET tube (10 times of IV dose via ET tube). Dose of adrenaline may be increased ifthere are recurrent subsequent arrests. b) Bicarbonate 1 mmol/kg of 8.4% IV (dilute in 5% dextrose 1: 1), Should not be given until ventilation is established. c) Atropine 0.02 mg/kg (maximum 0.6 mg) IV or via ET tube (used mainly for vagal induced bradycardia) d) Other ionotropic agents, antiarrhythmic drugs, DC shock, colloids and crystalloids are used in special circumstances subsequently. E: Evaluation: - Evaluate the success of CPR by clinical examination: When there is spontaneous cardiac output feel for pulse if pulse& BP good, stop cardiac massage & monitor ECG. Evaluate the success of CPR further by some essential laboratory investigations. - Investigations: - Arterial blood gas, complete blood count, urea, creatinine, glucose, - Electrolytes, liver functions, chest x-ray, ECG. F: Further steps & follow up: Inform family about cardiac arrest & resuscitation. Proceed for further history, examination and management. Decide about fluid therapy. Look for urine output. Consider ionotropic support by dopamine and/ or dobutamine 2-20 µgm/ kg/min. Consider need for further ventilatory management. Maintain body temperature. Find and treat underlying cause of cardiac arrest. Follow up for neurological impairment. 79  RESPIRATORY FAILURE Definition: Respiratory failure is said to occur when the respiratory system is unable to deliver oxygen to and/or remove carbon dioxide from pulmonary circulation, there by leading to hypoxemia and/or hypercapnia. Classifications: a) Acute & chronic b) Type l & type II Type I: Low arterial PaO2 (hypoxemia) & normal or low PaCO2 Type II: Low arterial PaO2 (hypoxemia) & elevated PaCO2 (hypercapnia) Clinical Features: Features due to hypoxemia: Cyanosis, pallor, restlessness, irritability, tachycardia, increased respiratory efforts evident by: active alae-nasi; intercostals; subcostal; suprasternal retractions; grunting, etc. Features due to hypercapnia: Sweating, tremor, warm extremities, bounding pulses, hypertension, bradycardia, headache, mental confusion, seizure, coma etc. Other features: may be related to the underlying cause of respiratory failure. Diagnosis of respiratory failure is to be confirmed by arterial blood gas estimation. Etiology of Respiratory Failure: Respiratory failure may result from- a) Obstructive respiratory diseases: - Neonates and young infants: Choanal atresia, meconium aspiration, bronchiolitis etc. - Older infants & children: bronchial asthma, adenotonsillar hypertrophy Bronchopneumonia, foreign body inhalation, epiglottitis etc. b) Restrictive respiratory diseases: - Neonates & young infants: hyaline membrane disease, Pulmonary hypoplasia, diaphragmatic hernia, congenital lobar emphysema etc. - Older infants & children: o Pulmonary: pneumonia, pneumothorax, plural effusion etc. o Neurological: Depression of respiratory centre from poisoning, injury or raised intracranial pressure, or weakness of respiratory muscles (poliomyelitis, Guillain- Barre syndrome, myasthenia gravis, myopathies etc.). o Mechanical: severe obesity, kyphoscoliosis, chest wall injury etc. c) Inefficient gas transfer: - Pulmonary edema, carbon monoxide poisoning, embolism, severe anemia, Right to left shunt.. 80 Approach to Management: Severest from of respiratory failure may present with cardiopulmonary arrest. Management in such cases should be according to the guidelines of cardiopulmonary resuscitation. Most of the respiratory illnesses which presents with respiratory failure come to the hospital before arrested. Following is a general guideline for their management. l. Oxygen therapy: Oxygen may be given by; nasal cannulas, nasal prongs, face mask, or by head box. Many patient's with Type I respiratory failure will improve with oxygen therapy while proper treatment for the underlying cause is provided. Oxygen therapy may be guided by pulse oxyrnetric monitoring. Give enough oxygen to keep SpO2 (02 saturation) around 95%. SpO2 of less than 90% while patient on high inspired oxygen may indicate the need for more aggressive steps. 2. Further respiratory support: If despite of oxygen therapy and adequate treatment of underlying cause the patient continues to deteriorate, following respiratory supports should be considered: a) Continuous positive airway pressure (CP AP) b) Artificiel ventilatory support (traditional artificiel ventilation) c) High frequency ventilation d) Extra corporeal membrane oxygenation (ECMO) 3. Investigational therapy: Liquid ventilation, Nitric oxide inhalation. Artificial ventilatory support: Present day most of the artificial ventilators deliver air and oxygen to the patients by positive pressure. Institution of intermittent positive pressure ventilation (IPPV) requires endotracheal intubation. Size of the endotracheal (ET) tube varies with age of the child. At birth: 1 kg. birth weight 3.0 mm. 1 - 6 months 3.5 mm. 6 - 12 months 4.0 mm. 12 - 18 months 4.5 mm. After 2 years use the following formula or select a size comparing the little finger of the patient. Age in years ETT Size=-------------------+ 4mm (3mm for cuffed tube)± 0.5mm. 4 Changes ofventilator settings Suggested in Hypoxemia and Hypercapnea: If the patient is hypoxemic: I. Increase FiO2 ( Fractional Inspiratory Oxygen or 02% 2. Increase PEEP (Positive End Expiratory Pressure) 81 3. Increase PIP (Peak Inspiratory Pressure), MAP(Mean Airway Pressure), I:E (Inspiratory Expiratory ratio ) 4. Increase Rate of Respiration or Frequency If patient is hypercapnic: I. Increase Rate 2. Increase PIP 3. Reduce PEEP and I:E Every change in ventilator settings is to be followed by blood gases to see the desired effect. One or two changes should be made at a time. Consider the possible complications of changes of ventilator setting to the patient. Complications of artificial ventilation: A) Respiratory: - Complications related to intubation: Cardiac arrest during the procedure from vagal stimulation, injury to nose and mouth, sinusitis, otitis media, subglottic stenosis. - Barotrauma - pneumothorax, pulmonary interstitial emphysema, pneumomediastinum - Complications of oxygen therapy: Retinopathy of prematurity, adult respiratory distress syndrome, bronchopulmonary dysplasia etc. 8) Circulatory: - Reduced venous return, reduced cardiac output, systemic hypotension. - Impaired venous return from high PEEP and high mean airway pressure may increase venous congestion in the brain causing raise of intracranial pressure and chance of intracranial hemorrhage. C) Complications from medications which are used for assisted ventilation Checklists for a patient who suddenly deteriorates on artificial ventilation: Remember by the abbreviation DOPED: I. The tube may be displaced from trachea to the pharynx and esophagus. During bagging air will go to the stomach which may be heard over epigastrium by the stethoscope, abdomen will be distended. Remove and replace the tube to the trachea. 2. The tube may be obstructed by thick mucous secretions. You will feel high resistance during Ambu bagging. Chest wall will not move. Absent breathe sounds on both sides. The endotracheal tube is to be removed and replaced by another new tube. You can see the mucus plug in the previous ET tube. 3. Patient may have developed pneumothorax. Breath sounds will be absent or reduced on the side ofpneumothorax. Percussion note will be hyper-resonant. Bed side transillumination will be positive in neonates. Patient needs intercostal drainage. 4. l'..quipment failure: Check the ventilatory circuit, a tube might have been accidentally disconnected. Disconnect the patient from ventilator and ventilate by Ambu-bag and oxygen, patient will improve. Connect again the disconnected tube 5. The pathological process might have been seriously deteriorated. 82  Acute Respiratory Distress Syndrome Definition: Acute respiratory distress characterized by acute lung injury, noncardiogenic pulmonary edema and severe hypoxia. Diagnostic Criteria I. Identifiable associated condition 2. Acute onset 3. Pulmonary artery wedge pressure < or = to 18mm or absence of evidence of left atrial hypertension 4. Bilateral infiltrates on chest radiography 5. Pao2/Fio2 ratio < or= to 200 *[Pao2/Fio2 ratio < or = to 300 is defined as Acute Lung Injury] -American-European Consensus Connference Statement, 1994 Risk Factors~ Pulmonary Extra-pu !woo ao: Bacterial pneumonia Sepsis Viral pneumonia Trauma Aspiration Multiple transfusion Near Drowning Peritonitis Inhalation injury Cardiopulmonary bypass Pathophysiology: 1. Direct lung injury or systemic insult occurs 2. Release of pro-inflammatory agents i.e. TNFa, interleukins 3. Migration of neutrophils producing oxygen radicals and proteases 4. Endothelial and epithelial cell damage leads to increased permeability and the influx offluid into the alveolar space. (pulmonary ARDS-epithelial damage, extra-pulmonary ARDS-endothelial damage initially) 5. Surfactant is abnormal 6. Impaired fibrinolysis leads to capillary thrombosis/microinfarction. To test for severity of Respiratory Distress ask the patient to speak or count. 83  Pathology of ARDS Exudative Phase Proliferative Phase Fibrotic Phase (Day 1-7) (Day 7-21) (>Day v21) Interstitial and intra- Interstitial Collageneous fibrosis alveolar edema myofibroblast reaction Hemorrhage Lumenal organizing Microcystic honeycombing Fibrosis Leukoagglutination Chronic inflammation Traction bronchiectasis Necrosis-Type I Parenchymal necrosis Arterial tortuosity Hyaline membranes Type TI pneumocyte Mural fibrosis hyperplasia Platelet-fibrin Obilterative endartitis Medial hypertrophy thrombi Macrothrombi Tomoashefski, J. Acute Respiratory Distress Syndrome. Clinics in Chest medicine: 21 (3) Sept. 2000 Evaluation : physical exam: tachypnea, tachycardia, altered mental status blood gas montoring: initial respiratory alkalosis may precede infiltrates, later: alveolar edema ➔ VQ mismatch/shunt ➔ severe hypoxia lma2io~: CXR progression from diffuse interstitial infiltrates to diffuse, fluffy alveolar spaces; later reticular pattern suggests interstitial fibrosis. CT demonstrates dependent (posterior if supine) infiltrates and atelectasis, with anterior hyperinflation. *most patients with ARDS develop diffuse alveolar infiltrates and progress to respiratory failure within 48 hours of the onset of symptoms Treatment: I. Treatment of underlying cause or associated condition 2. Yentilatory support- ensure "adequate" oxygenation/ventilation while minimizing ventilator induced lung injury. Avoid over or under-inflation: Usually this requires PEEP of 6-12, depending on severity. Remember things tend to get worse before they get better-it is not unusual for patients to require increasing PEEP as their disease worsens. Use low tidal volumes, 5-7 cc/kg. Monitor peak pressure (PIP or plateau pressure). It should be less than 30-35. Use longer inspiratory times than usual for age. Tolerate hypercapnia, monitor pH, try to keep >7.2 Tolerate hypoxemia if necessary to keep FiO2 21 mm under 1 year). Sin V1 greater than 30 mm(> 20 mm under I year). An increase in the R/S ratio in Vs, V6- S in VI greater than twice R in Vs. Left axis deviation for the patient's age (LAD). Right Ventricular Hypertrophy: R in Y1 greater than 20 mm (after 1 month). S in V6 greater than 6 mm (after 1 month). An increase in the R/S ratio in Y1, Y2. Upright.T wave in V3R or Y1 after 3 days. QR pattern in V1, V3 R. Right axis deviation for the patient's age (RAD). Combined ventricular hypertrophy: Large equi phasic QRS complexes in mid - precordial leads V3- V4 greater than 70 mm. RVH and S in VI or R in V6 greater than mean for age. LVH and R in VI or S in V6 greater than mean for age. RVH in Newborn: I. Pure R wave in VI greater than IO mm. 2. R in VI greater than 25 mm or R in AYR greater than 8 mm 3. QR pattern in V1 (can occur in 10% of normal newborn). 4. Upright Tin V1 after 3 days ofage. 5. RAD greater than + 180 degree. 115  OBSTRUCTIVE LESION CARDIAC LESION HEART SOUND MURMURS Ejection systolic murmur in Wide splitting of second sound, the pulmonary area, following Pulmonary stenosis single second sound in severe ejection systolic click. stenosis. Ejection systolic murmur in 1. Narrow splitting of second aortic area. It radiates to the sound (mild}. neck, may be heard also at 2. Single second sound Aortic stenosis apex and lower left sternal (moderate). edge. It may be preceded by 3. Paradoxical splitting of second ejection systolic click. sound (severe stenosis). Short systolic murmur at left sternal edge and between Normal scapulae, occasionally Coarctation of aorta murmur of collaterals over the scapula (continuous). Occasionally systolic murmur Hypoplastic left heart Normal or single second sound. at left sternal edge. syndrome Ejection systolic murmur in Loud second sound (pulmonary the pulmonary area. Early Pulmonary component). diastolic murmur in the hypertension pulmonary area. 120  VALVULAR LESIONS CARDIAC LESION HEART SOUND MURMUR Late systolic murmur at apex. It is often preceded by a mid systolic Normal Mitral valve prolapse click, more prominent with standing and the Valsalva maneuver. Wide splitting of the second Blowing pansystolic murmur at heart sound occasionally 3rd Mitral regurg itation apex radiates to left axilla. heart sound. Low-pitched mild diastolic rumbling murmur at apex proceeded by Mitral stenosis Loud 1st heart sound opening snap. High pitched early diastolic, blowing murmur over left sternal Aortic regurgitation Normal edge. It is best heard with expiration. Normal or wide splitting of the second sound. Narrow splitting Pansystolic murmur at lower part Tricuspid in the presence of the of left sternal edge. regurgitation pulmonary hypertension. Pulmonary Normal or narrowly splitting Early diastolic murmur in the regurgitation second sound. pulmonary area. 121  HYPERTENSION Hypertension is defined as an average diastolic or systolic blood pressure exceeding the 95th percentile for age and sex measured on at least three occasions. Classification of hypertension by age group Significant Severe Age Group Hypertension (mmHg) Newborn IHypertension( mmH g) 7 Days SBPc:96 SBPc:106 8-30 Days SBPc:104 SBPc:110 Infant (< 2 yr) SBPc:112 SBPc:118 DBPc:74 DBPc:82 Children 3 - 5 yr SBPc:116 SBPc:124 DBPc:76 DBPc:84 6 - 9 yr SBPc:122 SBPc:130 DBPc:78 DBPc:86 10-12yr SBPc:126 SBPc:134 DBPc:82 DBPc:90 Adolescent 13-15yr SBPc:136 SBPc:144 -- DBPc:86 DBPc:92 16-18yr SBPc:142 SBPc:150 DBPc:92 DBPc:98 (SBP= Systolic blood pressure -DBP= Diastolic blood pressure) Causes of hypertension in children and adolescents Renal Disease Renal artery stenosis Cardiovascular Coarctation of the aorta Endocrine Mineralocorticoid excess Primary hyperaldosteronism 11 B - Hydroxy lase deficiency 17a - Hydroxylase deficiency Dexamethasone - suppressible hyperaldosteronism Apparent mineralocorticoid excess Hyperthyroidism Pheochromocytoma Hypercalcemia 122  Tumors Neurofibromatosis Neurogenic tumors Others Immobilization - induced Essential hypertension REFERENCES: AlbertW. Pruitt, M.D., Welton M. Gersony, MD.Nelson test book of Pediatrics 14th ed. Philadelphia, W.B. Saunders Co, 1992. Anderson RH , Macartney FJ , Shirebourne EA: Pediatric Cardiology. Vol.1 and 2 Edinburgh , Churchill Livingstone 1987. John Vann Jones, Roger Black Wood: Outline of cardiology 2nd ed. 1992. Butterwonth Heinemann Ltd. Jordan SC, Scott 0 : Heart disease in Pediatric, London Butterworths 1989 Kathleen M. Finta, MD; Stuart Berger, M.D.: Pediatric clinics of North America.Vol. 46 No. 2, Apr. 1999 Michael D. Freed , M.D.: Nada s Pediatric Cardiology Philadelphia. Hanley and Belfus INC 1992 M.L. Rigby: Current Paediatrics 1994 (4) Long Man Group Ltd. 1994 Mohamed Ali Khan , Saad Al Yousef: Saudi Medical Journal 1988 9 (3) Mohamed Ali Khan : Saudi Medical Journal 1988, 9 (2) Myung K. Park, Warren G. Gunthorath: How to Read Pediatric ECG. Second ed. Mosby year Book Inc. 1987 N. Wilson : Current Paediatrics 1994, 4 Long man Group Ltd. 1994 Park MK: Pediatric Cardiology of practitioners 2nd Chicago, year book medical. Publishers, 1988 Pediatric Physical diagnosis: 1985 Appleton - Century - Crofts S.C. Jordan : Current Paediatrics 1994, 4 Long Man Group Ltd. 1994 Moss and Adams; Heart Disease in infants, children and adolescents. 5th Edition, 1995 Neonatal Clinical Pharmacology and Therapeutics; Rylance, Harvey and Avanda Freed MD. Heymann MA. Lewis AB. Roelh SL. Kensey RC. Prostaglandin El in infants with ductus arteriosus-dependent congenital heart disease. Circulation 1981; 64:899-905 Silove ED. Medical manipulation of the ductus arteriosus. In : Macartney FJ ed. Congenital heart disease. Current status of clinical cardiology Series. Lancaster, UK: MTP, 1986: 133 -143. 123 8 Respiratory System HISTORY Please refer to the chapter dealing with the history taking. In addition give particular emphasis to the following points: Cough : Character: barking, croupy. Duration: acute or chronic (more than 3 weeks) Severity: interfers with sleeping, feeding, and speaking. Painful cough: lesion related to the pleura or ribs (pleurisy, rib fracture) Timing: more at night, seasonal (asthma) Dry or productive: dry in pleurisy, productive in pneumonia. Notice character of sputum: - Nature: purulent, mucoid, frothy. - Quantity: scanty or copious. - Color: blood stained (pneumonia, mitral stenosis), greenish (cystic fibrosis), yellowish (pneumonia). - Smell: fetid (lung abscess, cystic fibrosis, bronchiectasis) Difficulty in breathing At rest or on exertion (during feeding in infant) Choking during feed or inability to complete feeds. Bluish discoloration of the lips (cyanosis) Presence of abnormal sounds during breathing Wheezing: may be heard without stethoscope. Stridor: "Harsh high pitched sound, heard during or at the end of inspiration" Snoring: "Stridor that occurs at sleep" Grunting: ''Noise produced at the beginning of expiration by a forceful expiration against a partially closed glottis" Rattling: "Rapid succession of short, sharp sounds due to passage of air in pooled saliva in the throat" Other important symptoms: Fever: mention character Loss of weight: acute or chronic Presence of loose foul smelling stools. Chronic diarrhea Known chronic diseases: neuromuscular, cardiopulmonary, immunodeficiency. 124  Gestational age History of mechanical ventilation Family history of atopic disorders. CLINICAL EXAMINATION General evaluation : Look for: General appearance: well or ill looking. State ofalertness Color (pallor, cyanosis) Speech ability (reading Qura'an, counting 1-10 in one breath) Tachypnea (respiratory rate > expected for age) Gnmting Active ala-Nazi Audible wheezes Stridor Snoring Built and nutrition Note the presence of: Oxygen supply and delivery systems (nebulizer apparatus, spacer devices, and inhaler devices) sputum pot. Examination of upper limbs: Check for: Clubbing: increased rounded appearance of the nails with obliteration of the angle between the nail and its soft tissue base, or a positive Scrarnroth's sign (obliteration of the diamond shaped space when the nail beds of two corresponding fingers of both hands meet together). Peripheral cyanosis. Pulse: count and note the character (bounding pulse - CO2 retention) "count apex beat in children below the age of 3 years". Blood pressure: Pulsus paradoxus (> 10 mm Hg fall of systolic blood pressure during inspiration) e.g. severe asthma, constrictive pericarditis. Examination of the face: Check for: Lips: peripheral cyanosis Tongue: central cyanosis Ala-Nazi: active or not Examination of the Ear, Nose and Throat: Keep it for the last, but remember to do it. Explain to the patient or use proper restrain as indicated. 125  Throat: - Use a good source of light and a strong wooden spatula. - Don't miss a spontaneous gag to have a clear view of the throat. - Don't over-interpret tonsillar enlargement in a gagging child. Ears: - Use proper size speculum. - Gently pull the auricle upward, backward and laterally to make the external auditory canal straight to have a better view of the tympanic membrane. Note: presence of wax or foreign body. - Examine the tympanic membrane for: light reflex, color (remember the ear drum may appear reddish in a crying child), bulging or retracted. perforation, discharge and mobility (by a pneumatic device in the otoscope) Nose: - Use large size speculum and the usual otoscope (if indicated) - Look for: Foreign body Foul smell Bleed Color of the nasal mucosa. - Presence of discharge and its character - Turbinate hypertrophy - Polyps - Edema of the nasal mucosa (allergy) Examination of the chest: Examine both front and back of the chest. Proceed to the back after completion of the examination of the front. Inspection: - Respiratory rate (minimum 30 seconds) - Expose the chest fully and look for: Type of breathing: o Abdominal in infants. o Thoracic after 4 - 5 years of age o Flat abdomen with reduced movements indicates diaphragmatic hernia Use of accessory muscles: suprastemal, intercostal and subcostal retractions. Apex pulsation Scars, describe its type Shape of the chest: o Pectus Excavatum (funnel shaped chest) o Pectus Carinatum (pigeon shaped) o Barrel shaped (increased antero-posterior diameter) 126 o Harrison Sulcus (indrowing of the lower chest with rib flaring) o Chest wall asymmetry and unequal chest movement (should be observed from the foot end of the bed, with keeping your eye in the same level of chest wall) o Shield-shaped chest: Turner's syndrome o Flattening of the hemi-chest, absence ofpectoralis muscle i.e., Poland anomaly o Others: Rachitic rosary Absent clavicle in cleidocranial dysplasia Supernumerary nipple in renal anomaly Palpation: Proceed gently with warm hands. Note: o Obvious swelling and tenderness o Position of trachea: by comparing the gap between the sternal head of the stemomastoid and tracheal margin by your index finger. Normally trachea is slightly deviated to the right. In young children this is not a reliable sign to detect mediastinal shift o Position of the apex beat. Remember dextrocardia o Tactile vocal fremitus: (in older children) place the palm of the hand on either side of the upper chest and ask the child to say ninety-nine. Feel the difference between sides rather than absolute increase or decrease. o Chest expansion: (in older children) hook little fingers of both hands in the axillae with thumbs meeting in the mid-line. Ask the child to take a deep breath and observe which thumb moves the least. Percussion: - Perform very gently - Explain to the older patients and the attendants - Use: 1. Pleximeter finger: placed in an intercostal space flush with the chest wall, other fingers kept away from touching the chest wall. ii. Percussing finger (plexor): middle finger of the dominant hand. Finger should pivot at wrist and not at the elbow, with a gentle blow hitting perpendicularly to pleximeter finger. Percuss at: (corresponding points) from up to down. Mid-clavicular lines, and mid-axillary lines Note: o apices: percuss on the clavicle directly o Area of the liver dullness o Area of cardiac dullness o Character of resonance: (normal, increased, reduced, absent, stony dullness) 127  - - ·-..!I. Auscultation. Use a child size stethoscope Be sure that the chest piece is adequately warm Use either the bell or the diaphragm (practice the use of any one). Apply the chest piece firmly to the chest wall to avoid rubbing noises and escape ofbreath sounds Auscultate the corresponding points in both sides: Front 1. Character of air entry: - Normal - Reduced - Equality on both sides 2. Character of breath sounds: I Vesicular with prolonged expiration + rhonchi Character of inspiratory and expiratory phase note whether: - Inspiration prolonged. - Expiration prolonged. 3. Presence of added sounds: - Wheezes: continuous, uninterrupted, musical sound Inspiratory: example: croup Expiratory: example: asthma - Crackle: discontinuous, interrupted sounds like popping of bubble which may be: Course: i.e., friction rub (rubbing leathery sound) Medium Fine crepitations may also be: - Early inspiratory i.e., in obstructive airway disease - Late inspiratory i.e., in restrictive airway disease 4. Vo