PG Clinical Training in Pediatrics, KKCTH, 2013

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PG Clinical Training in Pediatrics, KKCTH, 2013

  1. 1. i
  2. 2. ii XIV KKCTH MILLENNIUM ENDOWMENT ORATION AND POST GRADUATE CLINICAL TRAINING IN PEDIATRICS 20-09- 2013 & 21-09-2013 Under the auspices of The CHILDS Trust Medical Research Foundation (CTMRF)
  3. 3. iii Kanchi Kamakoti CHILDS Trust Hospital & The CHILDS Trust Medical Research Foundation Post Graduate Clinical training in Pediatrics September 20, 2013 (Friday) 8 00 - 8.15 AM Registration 8.15 - 8.30 AM Overview of the program - Dr.S.Balasubramanian 8.30 - 9.30 AM Cyanotic heart disease - Dr.Nalini Bhaskaranand / Dr.Riyaz 9.30 - 10.30 AM Acyanotic heart disease - Dr Andal / Dr Srinivasan 10.30 - 10.45 AM Coffee break 10.45 – 12 noon Rheumatic heart disease -Dr.Srinivasan / Dr.Vasanthi 12.00 – 1.00 PM Neurodegenerative disorders —Dr.Rana /Dr.V.Viswanathan 1.00 - 2.00 PM Lunch 2.00 - 3.00 PM Hepatosplenomegaly (Hemato-oncology) - Dr.Riyaz / Dr.Janani 3.00 - 4.00 PM Chronic liver disease - Dr.V.S.Sankaranarayanan/Dr.R.Ganesh 4.00 - 5.00 PM Bronchiectasis - Dr.Subbarao/ Dr N.Suresh 5.00 - 6.00 PM Hemiplegia - Dr.Kumaresan / Dr.LalithaJanakiraman 6.00 - 7.00 PM Cerebral palsy- Dr Rana /Dr T.Ravikumar
  4. 4. iv Post Graduate Clinical training in Pediatrics September 21, 2013 (Saturday) 8.00 - 9.00 AM Differential diagnosis in Pediatric Neurology: Dr Rana 9.00 - 10.00 AM Nutrition& Anthropometry- Must know areas: Dr Nalini Bhaskaranand 10.00 -11.00 AM Differential diagnosis of Hepatosplenomegaly: Dr John Matthai 11.00 - 11.15 AM Coffee break 11.15 - 12 Noon Inauguration function 12.00 – 1.00 PM Millennium oration—“Pneumococcal disease- Past, Present & Future” by Prof Adam Finn Consultant in Pediatric Infectious Disease Royal Bristol children’s Hospital, UK 1.00 -2.00 PM Lunch 2.00 - 3.00 PM Case analysis in Respiratory system: Dr Subbarao 3.00 - 4.00 PM Approach to congenital heart disease: Dr Srinivasan 4.00 - 5.30 PM OSCE--Dr BalaRamachandran, Dr K.G.Ravikumar, Dr.Radhika, Dr.Rahul Yadav 5.30 - 6.00 PM Feedback & wrap up
  5. 5. v Organizing Committee Organizing Committee: Dr Jayanthi Ramesh Dr.Kalpana Gowrishankar Dr Lalitha Janakiraman Dr.LakshmiSundararajan Dr.Major K.Nagaraju Dr.S.Muralinath Dr.S.Namasivayam Dr.PriyaRamachandran Dr.RahulYadav Dr K.G.Ravikumar Dr.T.Ravikumar Dr T.Vasanthi Dr.V.Viswanathan Dr.Arathi Srinivasan Dr.AmrutaKanjani Dr.Eswararaja Dr.R.Ganesh Dr.M.Lakshmi Dr.Padma Balaji Dr.SenthilGanesh Dr S. Srinivas Dr.N.Suresh Patrons Mr.Karthik Narayanan, Chairman,KKCTH Dr.K.MathangiRamakrishnan, Chairman, CTMRF Dr A.Andal, Medical Director, KKCTH Academic coordinators Dr.V.S.Sankaranarayanan Dr.S.Balasubramanian Dr BalaRamachandran Organizing secretaries: Dr.Janani Sankar Dr.R.Radhika Finance & Administration Mr.Sivakumar Mr.Ananthanarayanan
  6. 6. vi Disclaimer This book contains the academic materials covering the common clinical exam topics in Pediatric Medicine. This material is prepared based on the information from the standard Textbooks. However there is absolutely no assurance that any statement contained in this material is precise, or up-to-date. Neither the individual contributors, nor anyone else involved in the preparation of this material take responsibility for any errors in the text on this material. We strongly recommend the readers to refer standard Textbooks in Pediatrics
  7. 7. vii
  8. 8. viii FOREWORD On behalf of the CHILDS Trust Medical Research Foundation (CTMRF), I wish to extend my hearty felicitation and best wishes to the organizing committee and the participants of the “Millennium oration - Pneumococcal disease - Past, Present & Future” to be held on 21st August 2013. I hope that this programme will help the delegates to update and enrich their knowledge on Pneumococcal disease, a common and serious infection of childhood and it is of utmost important for all pediatricians and pediatric postgraduates to keep up with recent updates about this infection. I also hope that the informative material in this sourvenir will be of immense help to pediatric postgraduates in particular. I wish the CME a grand success. Prof.Dr.K.Mathangi Ramakrishnan Chairperson-CTMRF
  9. 9. ix List of Millennium Orations First Commemoration Oration & Seminar in Pediatric Neurology 02.10.2000 Newer Perspectives in Pediatric Neurology Guest Oration given by Dr. Prem Puri Our Lady’s Hospital for Sick Children, Dublin, Ireland Venue Hotel Chola Sheraton Second KKCTH Commemoration Oration 02.10.2001 CME on Pediatric Gastroenterology Guest Oration given by Prof V.I.Mathan, Gastroenterologist & Senior Consultant, UNAIDS / NACO, Bangladesh Venue Hotel Savera Third KKCTH Commemoration Oration 02.10.2002 CME & Refresher Update of Laboratory Medicine in Pediatric Practice Guest Oration given by Dr Kusum Verma, Prof & Head, Dept of Pathology, AIIMS, New Delhi Venue Hotel Savera Fourth Millennium Guest Oration 02.10.2003 Advances in Pediatric Surgery Guest Oration given by Prof. Arnold G.Coran, Prof. of Surgery & Head of Section of Ped. Surgery University of Michigan Medical School, USA Venue Hotel Taj Connemara
  10. 10. x Fifth Millennium Guest Oration 02.10.2004 National CME on Pediatric Critical Care Guest Oration given by Dr. Brain Anderson, Associate Prof. of Anaesthesia Hospital, Auckland, New Zealand Venue Hotel GRT Grand Sixth Millennium Guest Oration 11.05.2005 Advances in Pediatric Surgery Guest Oration given by Prof Klass N.Bax, Prof of Pediatric Surgery Dept. of Ped. Surg., Wilhelmina Children’s Hospital, University Medical Center Utrecht, Netherlands Venue Hotel Taj Coromandel Seventh Millennium Oration & National CME on Pediatric Cardiiology 12.11.2006 Cardiac Surgery in Developing Countries Guest Oration given by Dr.K.M.Cherian, Cardio Thoracic Surgeon, Frontier Lifeline Ltd, Chennai Venue Hotel GRT Grand Days Eighth Millennium Oration 03.12.2007 Cardiac Surgery in Developing Countries Guest Oration given by Prof.Boix Ochoa Professor in Pediatric Surgery, University Barcelona, Spain Venue Hotel Taj Coromandel
  11. 11. xi Nineth Millennium Oration & National CME 05.10.2008 National CME on Metabolic and Growth disorders in Children Guest Oration given by Dr.A.V.Ramanan Consultant Pediatric Rheumatologist and Hony. Senior Lecturer, University of Bristol, United Kingdom Venue Hotel GRT Grand Tenth Millennium Oration & National CME 04.10.2009 Clinical Approach to difficult problems Guest Oration given by Prof.Y.K.Amdekar, Mumbai Venue Hotel GRT Convention Centre Eleventh Millennium Oration 03.10.2010 Bone Marrow Transplant – Past, Present and Future Guest Oration given by Prof.Anupam Sachdeva Hemato Oncologist, Delhi Venue Hotel GRT Convention Centre Twelveth Millennium Oration 05.10.2011 State of the World’s Children Guest Oration given by Prof Frank Shann Prof. of Critical Care Medicine Royal Children’s Hospital University of Melbourne, Australia Venue Hotel GRT Convention Centre Thirteenth Millennium Oration 07.10.2012 Tuberculosis in Children – Past, Present & Future Guest Oration given by Prof. S.Mahadevan JIPMER, Pondicherry Venue Hotel GRT Convention Centre
  12. 12. xii Contents Sl.No. Topic Page No. 01 Developmental Assessment 1 02 Cerebral Palsy 3 03 Acute flaccid paralysis 7 04 Aucte infantile Hemiplegia 11 05 Floppy Infant 16 06 Hydrocephalus 19 07 Neurodegenerative Disease 22 08 Tuberculous Meningitis 25 09 Rheumatic Heart Disease 28 10 Cyanotic Congenital Disease 31 11 Protein Energy Malnutrition (PEM) 33 12 Neonatal Cholestatsis 38 13 Hepatosplenomegaly with Anemia 44 14 Thalassemia 49 15 Approach to Short Stature 51 16 Approach to a child with rickets 58 17 Bronchiectasis 60 18 Tips to Post Graduates 62
  13. 13. Post Graduate Clinical Training in Pediatrics [2013] Page 1 Developmental Assessment Dr. Ganesh, Dr.Suresh Consulting Paediatrician KKCTH Item/Age Gross motor Fine motor & vision Social Hearing & language 6 weeks • Grasp reflex • Social smile • Cooing 3 months • Head control • Recognises mother • Turns head to sound 4 months • Reaches for objects 7 months • Rolls over • Crawling • Sits with hands forward for support • Palmar grasp • Transfers objects from hand-hand • Smiles at mirror • Babbling (ba,da,ka) 10 months • Sits without support • Pivoting-turns round to pick up a toy without overbalancing • Creeping • Pincer grasp • Waves bye-bye • Plays pat-a cake • Uses amma, appa 1 year • Can rise to Standing • Walks alone • Walks holding on to furniture (cruising) • Bottom shuffling • Holds two cubes and bangs • Casting • Pincer grip • Waves bye-bye • Plays pat a cake • Asks for objects by pointing • Drinks from cup • Turns to name • Tells 2 words with meaning 1 ½ years • Goes upstairs & down stairs using hand held/rails • Carries toys while walking • Walks backwards • Kneels without support • Makes tower of 3 cubes • Turns 2-3 pages in a book at a time • Scribbles • Dry by day • Holds spoon-takes food to mouth • Solitary play( plays alone) • Obeys simple command: Close the door • Points to parts of the body when asked • Echolalia 2 year • Goes upstairs & down stairs-both foot/step. • Runs • Kicks the ball • Makes tower of 6 cubes • Copies vertical line • Turns page in a book singly • Turns door knob • Unscrews lids • Feeds with spoon safely • Wears shoe and socks • Gives name • Obeys two step commands(pick the toy and put in the basket)
  14. 14. Post Graduate Clinical Training in Pediatrics [2013] Page 2 Item/Age Gross motor Fine motor & vision Social Hearing & language 2 ½ year • Tip toe walking • Jumps • Copies horizontal line • Makes tower of 7 cubes • Makes train • Recognize themselves in photos • Pretends play • Names one color 3 year • Goes upstairs -1 foot/step & down stairs-two foot/step. • Pedals tricycle • Stands on one foot for one second • Can copy a circle • Constructs a bridge • Begins to draw a man • Can construct a block tower of ten cubes • Can thread large beads on to a string • Cuts paper with scissors • Eats with fork and spoon • Dry by night • Dresses and undresses if helped with buttons • Knows own name, age, and gender (boy/girl) • Knows some nursery rhymes • Names 3 colors 4 year • Stands on one foot for five second • Walks heel-toe • Hops • Goes upstairs & down stairs-one foot/step. • Copies cross and square • Draws a man with three parts • Copies gate(6 cube steps) • Threads small beads • Right-left discrimination • Dresses without supervision • Knows own name, age, gender (boy/girl) and address • Names 4 colors 5 year • Skips • Copies triangle • Makes 10 cube steps • Uses knife and fork • Knows own name, age, gender (boy/girl) address and birthday
  15. 15. Post Graduate Clinical Training in Pediatrics [2013] Page 3 CEREBRAL PALSY Name : Age : Sex : Complaints : Not attained age appropriate mile stones since early infancy Convulsions. Description of compliants. Describe all 4 developmental domine important mile stones achieved by the child o Gross motor o Fine motor o Language o Social and adaptive mile stones. Stiffness or floppiness of limbs Convulsions - Generalised tonic clonic / myoclonic / focal /Infantile spasms. Detailed birth history. o Antenatal period - maternal drugs, Xrays, illnesses-like rash , PIH ,DM , fall Milestone History Gross motor, fine adaptive, social, language (with rough DQ to each category). Involuntary movement - Dystonia, tremors, chorea, dyskinesia. - Limb dyskinesia , oromotor dyskinesia, jark in the box tongue. Cranial nerve history: Blindness (cortical/optic atrophy) / Squint / facial deviation / pseudobulbar palsy (regurgitation, nasal twaning,) / tongue atrophy Sensory symptoms: pain while vaccination/hot and cold water differentiation Mannerisms, stereotypies. Bladder, bowel involvement.
  16. 16. Post Graduate Clinical Training in Pediatrics [2013] Page 4 For etiology :- Birth details :Antenatal Infections, twins , trauma, drugs Neonatal sepsis, kernicterus Meconium, asphyxia, hypoglycemia.,NICU stay Post meningitis / trauma. Family history :- Any neurological illness / convulsion in any sibling / family any sibling deaths, any CPs in family. H/O Complication :- Convulsions Feeding difficulty /constipation Recurrent LRTI Contractures, bed sores behavioral problems, injuries, falls. H/O Treatment :- Immunization:- ?? DPT Diet History Detailed dietary history type of food, swallowing difficulties, regurgitation, spitting, weight gain. Examination : Vitals Anthropometry with interpretation General- pallor o Cataract, strabismus, o Skull - Overriding of sutures. o Shape of skull o Anterior Fontanelle o Dysmorphism o Neurocutaneous markers o Eyes - cataract Dentition Evidence of. malnutrition , bed sores, contractures - static/ dynamic
  17. 17. Post Graduate Clinical Training in Pediatrics [2013] Page 5 CNS :- • Higher Functions • Cranial nerves • Tone power reflexes • Exaggeration of reflexes:- afferent spread. (Knee Jerk on tapping thigh) efferent spill over (crossed adductor on knee jerk) • Development :- supine, prone, pull to sit, ventral suspension, axillary suspension • Neonatal reflexes • Hearing • Vision • Fundus examination – choreoretinitis / optic atrophy / retinitis pigmentosa • Primitive reflexes Other systems (organomegaly/ murmurs) Diagnosis Name-------------, aged---------- has static encephalopathy/ Spastic or dyskinetic or atonic CP /hemiplegia or quadriplegia/microcephaly /seizures/Cranial nerve dysfunction – squint, cortical visual blindness, hearing deficit, pseudo-bulbar palsy,/with Gross motor functional classification of ---------/ with learning disability/recurrent LRTI/ PEM / Contractures (dynamic or fixed) with probable etiology being-----------------
  18. 18. Post Graduate Clinical Training in Pediatrics [2013] Page 6 Commonly asked questions :- 1) Early markers of CP 2) Functional grades of CP 3) Neonatal reflexes 4) Audiometry 5) MRI correlates in CP 6) Development - gross motor, fine motor, speech ,social 7) Drugs & Surgical procedure to reduce spasticity 8) Associated problems 9) What do you mean by perinatal depression 10) What is birth asphyxia 11) What are significance of primitive reflexes 12) What are differences between primitive reflexes and postural reflexes 13) What are poor prognostic indicators 14) Stages of kernictirus 15) Causes for feeding difficulties
  19. 19. Post Graduate Clinical Training in Pediatrics [2013] Page 7 Acute flaccid paralysis/Guillian Barre Syndrome Name : Age : Sex : Complaint: History of weakness in limbs : • Unilateral /Bilateral weakness of limbs • Bilaterally symmetrical or asymmetrical weakness • Where does it start: From lower limbs and progresses upwards or vice versa • Sudden or insidious onset • Proximal or distal weakness • Involvement of upper or lower limb • Involvement of respiratory muscles: anxious expression, difficulty in breathing, inability to speak without frequent pauses • Involvement of bulbar muscles-pooling of secretions in mouth, nasal regurgitation/nasal twang, dysphagia,dysarthria Associated history/-ve history: • Higher function abnormalities (sensorium, speech) • Cranial nerve deficit: o facial asymmetry,drooling saliva from angle of mouth(VII N); o nasal twang,regurgitation (IX,X N) o diplopia,eye movements (III,IV,VI N) • Sensory disturbances-tingling, numbness, pain. • Abnormal gait / posture( tripod sign) • Bladder/bowel disturbance • Autonomic disturbances : flushing, sweating, palpitations, postural hypotension • Ataxia, involuntary movements • Wasting of muscles • History suggestive of increased intracranial pressure
  20. 20. Post Graduate Clinical Training in Pediatrics [2013] Page 8 Etiological history: • Diarrhoeal /upper respiratory illness weeks prior to paralysis----GBS • Immunisation -OPV, IM injection & fever prior to paralysis –(-Polio ) • Previous history or familial history of Paralysis - Periodic paralysis • Throat pain, dysphagia,neck swelling(bull neck)---Diptheria • Consumption of honey/tinned food ( botulism) • H/O drug intake – vincristine, vinblastine • H/O pica (heavy metal intoxication (lead)) • H/O trauma to spine • H/O polyuria / polydipsia / weight loss (DM) • H/O fever with exanthem(herpes, mumps, rubella, entero/ EBV)H/O pain swelling Birth, Immunisation history (especially OPV), Developmental, dietary history Examination: Decubitus especially of lower limbs—Demonstrate flaccidity Vital parameters: Heart rate, Blood pressure for autonomic dysfunction Throat---patch for diphtheria Anthropometry with interpretation Blue line on gums, NC markers Spine CNS • Drooping of shoulder s/o diaphragmatic paralysis • Fasciculations • Thickened nerves • Reflexes Superficial – important as in case of transverse myelitis for level of the lesion • Signs of meningeal irritation
  21. 21. Post Graduate Clinical Training in Pediatrics [2013] Page 9 Features suggestive of GBS are • Ascending weakness, symmetrical involvement • Lower limbs involved before upper limbs • Proximal involvement earlier than distal • Weakness progressing over days to weeks with peak maximally at 4 weeks • Deep tendon reflexes absent even before paralysis. • Cranial nerves: common VII nerve • If abnormal gait(ataxia) with eye movements impaired (opthalmoplegia)--- Miller Fischer variant • Bladder distension Respiratory system • Involvement of respiratory muscles: increased respiratory rate , movements of alae nasi and other accessory muscles of respiration, inability to cough or sniff with full depth, Single breath count .Paradoxical abdominal movements due to diaphragmatic immobility. Deltoid paralysis suggests impending respiratory paralysis • Observation of patient’s capacity for thoracic breathing while abdominal muscles are splinted manually • Light manual splinting of thoracic cage helps assessment of diaphragmatic movts. • PA see for phantom hernia on abdominal wall ( polio) • CVS muffled heart sounds (viral myocarditis, diphtheria)
  22. 22. Post Graduate Clinical Training in Pediatrics [2013] Page 10 Diagnosis : Differential diagnosis of GBS - shown in the table below Polio Guillain-Barré syndrome Traumatic neuritis Transverse myelitis Installation of paralysis 24 to 48 hours onset to full paralysis From hours to 10 days From hours to 4 days From hours to 4 days Fever at onset High, always present at onset of flaccid paralysis, gone the following day Not common Commonly present before, during and after flaccid paralysis Rarely present Flaccid paralysis Acute, usually asymmetrical, principally proximal Generally acute, symmetrical and distal Asymmetrical, acute and affecting only one limb Acute, lower limbs, symmetrical Muscle tone Reduced or absent in affected limb Global hypotonia Reduced or absent in affected limb Acute, lower limbs, symmetrical Sensation Decreased to absent Globally absent Decreased to absent Absent in lower limbs early hyperreflexia late Deep-tendon reflexes Severe myalgia, backache, no sensory changes Cramps, tingling, hypoanaesthesia of palms and soles Pain in gluteus, hypothermia Anesthesia of lower limbs with sensory level Cranial nerve involvement Only when bulbar involvement is present Often present, affecting nerves VII, IX, X, XI, XII Absent Absent Respiratory insufficiency Only when bulbar involvement is present In severe cases, enhanced by bacterial pneumonia Absent Sometimes Autonomic signs & symptoms Rare Frequent blood pressure alterations, sweating, blushing and body temperature fluctuations Hypothermia in affected limb Present Cerebrospinal fluid Inflammatory Albumin-cytologic dissociation Normal Normal or mild in cells Bladder dysfunction Absent Transient Never Present Nerve conduction velocity: third week Abnormal: anterior horn cell disease (normal during the first 2 weeks) Abnormal: slowed conduction, decreased motor amplitudes Abnormal: axonal damage Normal or abnormal, no diagnostic value EMG at three weeks Abnormal Normal Normal Normal Sequelae at three months and up to a year Severe, asymmetrical atrophy, skeletal deformities developing later Symmetrical atrophy of distal muscles Moderate atrophy, only in affected lower limb Flaccid diplegia atrophy after years
  23. 23. Post Graduate Clinical Training in Pediatrics [2013] Page 11 ACUTE INFANTILE HEMIPLEGIA Name : Age : Sex : Address : Consanguinity : Handedness : CHIEF COMPLAINTS Paucity of movements of right/left side of the body. Convulsions Onset-Catastrophic/acute/sub acute/chronic/static/episodic Progressive/ static/ improving Involving the upper limb preferentially/equally Detailed H/O CNS involvement – H/O weakness, proximal/distal H/O sensory involvement H/O Cranial nerve involvement H/O involuntary movements H/O bladder / Bowel involvement H/O speech abnormality H/O gait abnormality H/O Complications Bed sores/shortening of limbs/contractures /trophic ulcers ETIOLOGICAL HISTORY H/o Trauma - Head injury/Oral cavity injury - Fracture (Fat embolism) Hematological causes H/O pallor H/O pain in hand/foot/ abdomen (sickle cell crisis) H/O bleeding from any site/petechae/purpura/ hematemesis / malena H/O Fever/ bone pain /weight loss (leukemia) H/O diarrhea/ vomiting oliguria/ hematuria (HUS) or, history of nephrotic syndrome
  24. 24. Post Graduate Clinical Training in Pediatrics [2013] Page 12 Cardiac causes H/o fever with chills/ petechiae/hematuria (Infective Endocarditis) H/o cyanosis /cyanotic spell (Cyanotic heart disease) (abscess/ Thrombosis ) H/o fever with joint pain/sore throat (Rheumatic) H/o Cardiac surgery (Prosthetic heart valve) H/o Hypertension-Headache/ Vomiting/Visual Disturbance Collagen Vascular Disease H/o fever with rash with joint pain (SLE) H/O Claudication (Takayasus) Infectious Causes H/O sore throat (Pharyngeal abscess) H/O Koch’s/Koch’s contact H/O Viral exanthems (HSV Encephalitis/ mumps/chicken pox) H/O Otorrhoea (brain abscess) H/O Vaccination/ sera (Demyelination) Dehydration H/O Acute Gastroenteritis followed by seizures/ coma (sagittal sinus thrombosis ) H/O recurrent attacks of TIA /hemi paresis (Migraine/Moya-Moya/alternating hemiplegia) H/O post seizure transient paralysis (Todd’s paralysis) FAMILY HISTORY H/O similar attacks in the family (Sickle cell/ homocystinurea/Hyperlipidaemia) BIRTH HISTORY Preterm-Subependymal Hemorrhage-Intraventricular hemorrhage Full-term- Breech/ Traumatic delivery/Birth Asphyxia H/O Umbilical sepsis / Catheterization (Embolism) H/o Rash/ fever/ petechae/jaundice (IU infection)
  25. 25. Post Graduate Clinical Training in Pediatrics [2013] Page 13 EXAMINATION: General Examination-Routine examination plus look for dysmorphic features Carotid pulses should be palpated as well as auscultated(Moya Moya,Takayasu) Anterior Fontanelle Head Circumference US/LS & Length (homocystinurea) Pallor/Cyanosis/Clubbing Xanthomas Petechiae/Purpura/ Joint bleed/ Rash Eyes-Ectopia lentis Neurocutaneous Stigmata Skull-Trauma/Crack pot/Bruit over the skull. CNS Higher Functions- Speech (dysphasia seen in involvement of dominant hemisphere) Intellectual impairment (Meningitis, Encephalitis, Homocystinurea) Gait (older child)/Gross motor assessment (infant) Cranial nerve examination (3,4,6 ,7th & gag reflex) Motor examination -Tone/Power/Reflexes Abdominal Reflexes & Plantars Visual fields for field defects& partial visual neglect (A field defect infers a lesion at or above the internal capsule) Higher Centers-Test for dysphasia/ Agraphia/ astereognosis/ two point discrimination, tactile localisation (these occur when the dominant side is involved) CVS Examination 1. Higher mental function 2. Cranial nerves 3. Motor system a. Tone b. Power c. Bulk/Nutrition
  26. 26. Post Graduate Clinical Training in Pediatrics [2013] Page 14 d. Involuntary movements e. DTR 4. Sensory system 5. Meningeal signs 6. Spine and cranium 7. Primitive reflexes LOCALIZATION OF THE LESION IN CASE OF ACUTE INFANTILE HEMIPLEGIA A) If the cranial nerve palsy is on the same side as that of hemiplegia then the lesion is above the level of brain stem-Ipsilateral hemiplegia B) If the cranial nerve palsy is on the side opposite to that of hemiplegia then the lesion is at or below the brain stem.-Contralateral hemiplegia IPSILATERAL HEMIPLEGIA The lesion is either in the cortex , internal capsule or sub cortical region A) Cortical lesion- Hemi paresis-Mild involvement & not dense hemiplegia Differential involvement (Upper limbs more than lower or lower limbs more than upper) Altered sensorium may be present Convulsions may be present Cortical sensory loss may be present Astereognosis Aphasia (if the dominant cortex is affected) Involvement of the frontal lobe o Altered behavior/personality o Upper limb affected more than lower limb o Motor aphasia o Convulsions o Bladder/ bowel involvement o Persistent neonatal reflexes on the opposite side
  27. 27. Post Graduate Clinical Training in Pediatrics [2013] Page 15 Involvement of the parietal lobe o Cortical sensory loss o Astereognosis Involvement of the Temporal lobe o Temporal lobe epilepsy o Sensory aphasia o Memory loss Involvement of occipital lobe o Homonymous hemianopia B) Internal capsule lesion Dense Hemiplegia Hemianaesthesia Homonymous hemianopia Dysarthria C) Subcortical lesion(Corona Radiata) Same as cortical lesion but features such as convulsions & loss of cortical sensation are absent CONTRALATERAL HEMIPLEGIA- Lesion at or below the level of brain stem A) Lesion in Midbrain WEBER SYNDROME- 3rd nerve palsy plus crossed Hemiplegia BENEDICTS SYNDROME-3rd nerve palsy + crossed hemiplegia + Red nucleus affected (Tremor, rigidity, ataxia on the opposite side) B) Lesion in Pons MILLARD GUBLER SYNDROME-7th nerve palsy +Crossed hemiplegia FOVILLE SYNDROME-6th nerve palsy + 7th nerve palsy + contra lateral Hemiplegia C) Lesion in Medulla JACKSON SYNDROME-12th nerve palsy + crossed hemiplegia.
  28. 28. Post Graduate Clinical Training in Pediatrics [2013] Page 16 FLOPPY INFANT Complaints : • Delayed motor and/ or mental milestones. • Weakness of all 4 limbs and limpness noticed since birth. • Abnormal posturing / contractures / arthrogyphosis. ELABORATION OF C/C. • H/O unilateral/ bilateral weakness of limbs, symmetrical or asymmetrical, sudden onset /insidious,starting from lower limb and progressing upwards or vice versa. . • Head holding achieved/ partial. • H/O frog like posture • H/O weak cry, h/o feeding difficulties • H/O repeated cough/ cold/fever/ breathlessness • H/O facial asymmetry, pooling of secretions,nasal regurgitation/nasal twang,dysphagia(involvement of bulbar muscles) • H/O sensory disturbances. • H/O wasting of muscles, H/O fasciculations / fibrillations. • H/O bladder/ bowel disturbances • H/O exaggerated startle (Taysach’s) ETIOLOGY • H/O Icterus, phototherapy, exchange transfusion (kernicterus) • H/O constipation, prolonged neonatal jaundice (if MR, coarse facies for hypothyroidism) • H/O cyanosis/ altered sensorium(respiratory muscle involvement) • H/O mental development(hypotonic CP) • H/O viral infection/ascending weakness(GBS) • H/O recent vaccination /ring/ pulse polio
  29. 29. Post Graduate Clinical Training in Pediatrics [2013] Page 17 • H/O flushing/sweating/ palpitation/ postural hypotension/ arrhythmias (dysautonomia) • H/O maternal myasthenia like illness • H/O diurnal variation (mysthenia gravis) • H/O lump in abdomen,early morning hypoglycaemic convulsions with breathlessness(GSD – Pompe’s) • H/O prelacteal feeds like honey followed by bulbar weakness (botulism) • H/O nonprogressive proximal muscle weakness-----congenital myopathies • H/O involuntary movements------congenital cerebellar ataxia • H/O obesity - Prader Willi • H/O cataract/ MR- Lowes ANTENATAL HISTORY H/o decreased fetal movements, fever with rash, irradiation, drug exposure (lithium/ phenytoin/ carbamazepine). ,polyhydramnios / prolonged labour / LSCS. PERINATAL HISTORY - breech presentation, h/o birth asphyxia, h/o limpness, feeding difficulties, breathlessness, convulsions in neonatal period, neonatal hyperbilirubinemia. FAMILY HISTORY - h/o deaths in infancy in sibling MILESTONES - motor +mental DIET & IMMUNIZATION- last vaccine given (for GBS/ polio) EXAMINATION Decubitus - pithed frog position. HR----/RR------/ regular, abdominothoracic, no e/o resp. distress/BP-------- ANTHROPOMETRY with interpretation Obesity,dysmorphic facies (Prader- Willi) Downy facies – Trisomy 21/ Zellweger’s syndrome Doll like faces – GSD (Pompe) V shaped face- myotonic dystrophy Pallor, clubbing, cyanosis, icterus, lymphadenopathy, oedema feet Anterior fontanelle Cataract’s(Lowe syndrome)
  30. 30. Post Graduate Clinical Training in Pediatrics [2013] Page 18 ENT Skull/ spine/ genitalia(hypogonadism in prader willi) Conntractures ,CTEV, CDH CNS EXAMINATION Higher functions---conscious, alert looking,recognizes others. Cranial nerves Tongue fasciculations Ptosis with diurnal variation Fundus---(cherry red spot in GSD type II) Motor system- muscle wasting (SMA) muscle hypertrophy(pompe/ congenital muscular dystrophy) Hypotonia in all 4 limbs Involuntary movements- ataxia, fasciculation/ fibrillation Power--shoulder/ elbow/ distal/ hip/ knee/ distal o Diaphragm/ intercostals o Reflexes Superficial-------cremasteric/ gluteal/ paraspinal reflex Deep reflexes Sensory system P/A-----hepatomegaly----GSD CVS-----cardiomegaly,murmur, abnormal heart sounds(pompe) RS--------r/o LRTI Orthopedic examination DIAGNOSIS--------month old child M/F gradually progressive/ static quadriparesis since birth ,decreased fetal movements ,no MR, no significant pre/ perinatal events, generalized hypotonia, areflexia, fasciculations. Most probable diagnosis
  31. 31. Post Graduate Clinical Training in Pediatrics [2013] Page 19 HYDROCEPHALUS Name : Age : Sex : DOB : Complaints : • History of progressive enlargement of head/large head noticed since (or) • History s/o raised ICT (if the onset of hydrocephalus is more than 2 yrs (or) • H/O abnormal eye movements (sunsetting / roving eye movements) (or) • H/o developmental delay (or) History of presenting complaints: Abnormalities of higher functions - scholastic backwardness, altered sensorium, convulsions History s/o cranial nerve palsy –diplopia,sunsetting. History of blindness or hearing disturbance. History of focal neurologic deficit. H/S/O gait abnormalities (spastic gait with frequent falls) History of bladder/bowel complaints H/o involuntary movements History of nausea/vomiting/head banging/headache. History of occipital enlargement (Dandy Walker) History of poor feeding/failure to thrive / stridor (nasal encephalocele) Etiological History ANTENATAL HISTORY - Infection (CMV, toxoplasma, mumps), Drugs-(vitamin A toxicity-pseudo tumor), Irradiation , Antenatal detection, presentation BIRTH HISTORY - Prematurity /Dystocia / PROM / Instrumentation POST NATAL HISTORY – enquire - H /O trauma, H /O infection (meningitis), H/O Koch’s contact, H/o prolonged hospitalization after birth, H/O hypo pigmented macule with infantile Spasm ( Tuberous sclerosis), H/O swelling at the back & limb weakness
  32. 32. Post Graduate Clinical Training in Pediatrics [2013] Page 20 FAMILY HISTORY- In males Congenital aqueductal stenosis (XLR) , Any sibs having similar problem? TREATMENT HISTORY – H/o treatment taken/shunt surgery MILESTONES – delay OR regression? Motor and mental milestones delayed. Weak head holding due to large head. If there is neuroregression with large head then S/O ( Krabbe / Tay sachs, Alexander / Canavan , Post TBM ) Diet history & socioeconomic history. EXAMINATION Vitals - BP (hypertension because of raised ICT) Bradycardia Shallow respiration Anthropometry with interpretation. Skull- a) Head circumference & Shape of the skull noted- in terms of AP diameter, Biparietal diameter, Frontal bossing& Occipital prominence. b) Presence of dilated veins c) Anterior & posterior fontanelle-(note their size, shape, borders, pulsation,tension in sitting & supine position) d) Sutural separation e) Transillumination-more than 2 cm in frontal & more than 1 cm in Occipital (it is positive only if the cerebral mantle is less than 1cm). It is positive in massive dilatation of the ventricular system or in Dandy Walker syndrome. f) Bruit over the head-It is positive in many cases of vein of Galen AV malformation. g) Prominent occiput in Dandy Walker/post fossa tumor/arachnoid cyst h) Flat occiput in achondroplasia/Arnold Chiary Malformation i) Craniotabes Sunsetting (paralysis of upward gaze) Spine-Neural tube defects. Look for tuft of hair
  33. 33. Post Graduate Clinical Training in Pediatrics [2013] Page 21 Others - Neurocutaneous markers-Hypo pigmented patches in Tuberous Sclerosis Dysmorphic features/ coarse features. Rhizomelic shortening (achondroplasia) IU infection (Rash/lymphadenopathy/Hepatosplenomegaly/Cataracts) Crackpot sign. CNS Examination- Higher functions – sensorium, speech Cranial nerves-Sixth nerve palsy, false localizing sign. Vision & hearing Motor -Spasticity is generally more in the lower limb than the upper limb. Brisk jerks in the lower limb. Gait-Truncal ataxia is seen in Dandy Walker. Fundus- Papilledema , Optic atrophy, Chorioretinitis, Cherry red spot Neonatal reflexes. Examination of spine Shunt side, patency , Reservoir present or absent? DIAGNOSIS
  34. 34. Post Graduate Clinical Training in Pediatrics [2013] Page 22 NEURODEGENERATIVE DISEASE Name : Age : Sex : DOB : Informant : Chief complaints:- - loss of achieved mile stones - convulsions - progressive increase in size of head - vision / hearing / speech regression Narrative History :- 1. Convulsions :- • Generalised tonic, clonic, myoclonic, tonic spasms, focal (convulsions suggest that the disease involves grey matter degeneration) • In certain epilepsy syndromes, convulsions are the hallmark which precede the onset of regression. o e.g. West Syndrome - Infantile spasms - Lennaux Gestaut syndrome - tonic spasms . o Certain aminoacidopathies & organic acidurias patients / urea cycle defects convulsions may be due to metabolic disturbances like hypoglycemia, hyperammonemia etc ) o SSPE - Myoclonic jerks 2. Progressive dementia / personality changes- o Scholastic backwardness - SSPE, HIV, encephalopathy Wilson’s disease. o Behavioural changes - hyperactivity - sanfillipo, X linked ALD, o Autistic behavioural - Autism, Rett's Syndrome 3. Loss of motor milestones o eg. loss of head control, turning over. o Period over which these milestones are lost in important. o Progressive - Neuro degenerative disorders o Sudden - Post encephalitis o Mitochondrial disorders like MELAS
  35. 35. Post Graduate Clinical Training in Pediatrics [2013] Page 23 White matter degeneration is characterised by focal neurological deficits / spasticity / blindness or hypotonia (looseness of body). 4. Progressive disturbance of gait and co-ordination - X linked Adrenoleuko dystrophy - Progressive hydrocephalus Focal neurological deficits - mitochondrial disorders 5. Vision problems : 1] Progressive loss of vision hydrocephalus, Tay sachs disease Neuronal ceroid lipofuschinosis, Wilson's disease ( Cataract) 2] Visual inattention - autistic spectrum disorders, Rett's syndrome 6. Speech abnormalities - Aphasia - Expressive aphasia - Rett / autism Dysarthria - cerebellar disorders ( Juvenile MLD) 7. Ataxia - MLD, ALD, Spasms mutan - pelizeus merchbacker 8. Involuntary Movements - o Chorea, athetosis - Huntington , Wilson, pelizeus merchbacker o Dystonia / Dyskinesis - o Hand wringing, washing, tapping movement o Sterotypy - Rett's syndrome 9. Increasing head size - progressive hydrocephalus, Alexander / Canavan 10. Sensory disturbances - trophic ulcers o associated with peripharal neuropathy - MLD, INAD, krabbes 11. Progressive bulbar symptoms - feeding difficulties 12. H/o. Repeated vomiting, failure to thrive - neurometabolic disturbances aminoacidopathies / organic acidemias 13. H/o. fever,, altered sensorium / convulsions Encephalitis H/o. lethargy, constipation, neck swelling hypothyroidism. 14. H/o. Jaundice - Wilson's 15. H/o. Measles - SSPE 16. H/o. Self mutilation Lesch nyhan syndrome
  36. 36. Post Graduate Clinical Training in Pediatrics [2013] Page 24 17. Family history of similor illness in other sib / sib death 18. Birth history 19. H/o. typical body / urine odor 20. H/o. complication - contractures / bedsore Repeated infections 21. Developmental history - Details of milestones - normal / delayed prior to onset of regression. 22. Diet history 23. Immunisation history EXAMINATION General examination Decubitus Temp. Pulse respiration BP Anthropometry with interpretation - size & shape of skull - overriding of sutures - Anterior fontanelle - Dysmorphic features - Grotesque features, Hypothyroid / MPS - NC markers - Tuberous sclerosis, ataxia telengiectasia, café au lait spots Chediac Higashi - Skin changes - Hypothyroidism - Xerodema pigmentosa - Hair - menke's kinky hair - Trophic ulcers - (peripharal neuropathy) - Self mutilation - Lesch nyhan Fundus - optic atrophy - Cherry red spot - Retinitis pigmentosa - Central nervous system Examination - PA - organomegaly Diagnosis:
  37. 37. Post Graduate Clinical Training in Pediatrics [2013] Page 25 TUBERCULOUS MENINGITIS Name Age Sex Address Handedness Complains: 1. Fever – 2. Convulsions :- focal / generalised seizures 3. Altered sensorium :- onset - sudden / insiduous. 4. Vomiting 5. Focal neurological deficit - Hemiplegia / monoplegia / cranial neuropathies. Origin/Duration/Progress Complains in details. H/o. Abnormality of higher functions - Lethargy, altered sensorium Convulsions Cranial nerve palsies - deviation of angle of mouth, drooling of saliva, squinting, diplopia. Focal neurological deficits ( hemiplegia /monoplegia). Abnormal / involuntary movements tremors / chorea / hemiballismus H/s/o increased intracranial pressure i.e. vomiting / headache / blurring of vision. H/s/o meningeal inflammation i.e.neck pain, photophobia, restriction of neck movement. H/o bowel, bladder complaints. History for etiology :- H/o. head injury ( may precipitate TBM) H/o. otorrhoea - (pyogenic meningitis ) H/o. any treatment taken outside in f/o intramuscular / intravenous injections (Partially treated pyogenic meningitis) H/o. vaccines / drugs / sera ( Acute disseminated encephalomyelitis) H/o. rash, fever, altered sensorium, convulsions ( Viral encephalitis) H/o. fever with rash (measles) H/o. whooping cough.
  38. 38. Post Graduate Clinical Training in Pediatrics [2013] Page 26 H/o. contact with tuberculosis. H/o. diarrhoea, fever, chronic cough (HIV) H/o. immunosuppressive drug intake. Immunisation history – BCG , Measles. History for complications :- H/o bed sores, contractures, skin changes, bladder, bowel complications. (constipation/ urinary infection ) H/o. seizures. H/o. decorticate / decerebrate posturing. Drug history, procedure history. H/o. any surgery, VP shunt / reservoir Family history - of koch’s Nutritional history - malnutrition may precipitate Tuberculous meningitis. Birth History :- Developmental history. Socio economic history - Overcrowding , sanitation. Examination :- General examination :- 1] Decubitus 2] Vitals - Temperature ,Pulse , Respiration , Blood pressure. 3] Anthropometry with interpretation. 4] Pallor, cyanosis, clubbing, icterus, lymphadenopathy, edema feet, 5] Stigmata of tubercolosis – Phlycten ,Scrofuloderma ,Sinuses, erythema nodosum 6] Anterior fontanelle 7] Size & heaviness of head 8] Crack pot sign 9] BCG scar - present / absent. 10] Neurocutaneous markers 11] Dysmorphic features 12] Presence or absence of IV line, Ryles tube 13] Skull, spine, scars
  39. 39. Post Graduate Clinical Training in Pediatrics [2013] Page 27 14] Skin - bedsores 15] Contractures 16] Signs of malnutrition & vitamin deficiency 17] Presence / absence & patency of VP shunt CNS :- Higher functions - state of conciousness Gag reflex Eye movements Pupillary reflexes Corneal / conjunctival reflexes Motor system examination Sensory system Cerebellar signs Meningeal signs Hydrocephalus : Heavy head, crackpot or sutural seperation - Signs of increased intracranial pressure. Involuntary movements Fundus - papilloedema / choroid tubercules / optic atrophy. Diagnosis :- ---years old M/F child with chronic meningoencephalitis with / without hemi / monoparesis with / without cranial nerve palsy with / without involuntary movement with / without signs of increased intracranial pressure. Probable etiology being TBM.
  40. 40. Post Graduate Clinical Training in Pediatrics [2013] Page 28 RHEUMATIC HEART DISEASES Four types of clinical scenarios usually present : 1. Acute rheumatic fever 2. Relapse /recurrence of acute rheumatic fever with chronic valvular heart disease. 3. Isolated Rheumatic valvular disease with H/o infective endocarditis 4. Combined chronic valvular disease History: • H/o streptococcal pharyngitis –Fever , sorethroat - in the recent past (2-3 weeks back) • H/o pallor, epistaxis , abdominal pain . • H/o Joint pain, swelling, duration, joints involved,characteristics of pain and relief with medications (arthritis),migratory or not • H/o dyspnoea,palpitations easy fatigability ,exercise intolerance, chest pain, syncope ( s/o Carditis) • H/o skin rash, or nodes ( erythema marginatum , sub cutaneous nodes) • H/o neurological symptoms- purposeless movements, emotional lability, ( Chorea) • H/o complications ( PND, orthopnoea, hemoptysis, palpitations, syncope , edema ). • S/o infective endocarditis (fever with chills,petechie, subcutaneous painful nodes , hemoptysis,hematuria ,skin lesions) • H/o medications taken for fever and other symptoms . • H/o previous similar such episodes, • If RHD – h/o penidura injection – compliance & frequency . • Family history of rheumatic fever / rheumatic heart disease. • Immunization, dietary , development & socioeconomic status enquired . Examination : General –Vitals, Growth parameters, Scars, Chest asymmetry, icterus, teeth- caries , lymph nodes. Skin - erythematous rash & subcutaneous nodes over extensor surface of head, back & limbs. Nails - pallor, clubbing, cyanosis. Joints - pain, swelling, tenderness & restriction of movements.
  41. 41. Post Graduate Clinical Training in Pediatrics [2013] Page 29 Cardiovascular examination – Peripheral - Venous, major arterial pulses & Blood pressure (upper & lower limbs). Precordium – o Inspection – Scars, symmetry, apical pulsation o Palpation – Apex position, point of maximal impulse (PMI), heaves, (parasternal, substernal, apical) Thrills (Suprasternal, supraclavicular and over precordium) Palpable S2- (pulmonary hypertension) o Auscultation- (use diaphragm initially, then the bell) Areas- Apex, parasternal border,pulmonary , aortic areas ( roll patient to left to accentuate mitral murmurs). o Heart sounds – intensity, splitting . Added sounds & Murmurs- systolic/ iastolic/ continuous – define intensity, character, grade , radiation of murmurs & Variation of murmurs on sitting , inspiration and expiration. Other Systems - Abdomen Liver – measure span, note pulsation and tenderness Spleen – infective endocarditis CNS Fundus and other signs of infective endocarditis. Choreiform movements Diagnosis - Investigations: Sleeping pulse rate ( tachycardia - myocarditis/ CHF) Complete blood count with ESR and CRP (Lab. Criteria) Throat culture, ASLO – (second antibody titre/ rising titres if initial is normal) Blood culture (if IE is suspected) X ray chest for cardiomegaly, pericardial effusion and pulmonary oedema ECG - PR interval and chamber enlargement 2 D Echo /CD– Status of cardiac –myocardial, valvular & pericardial involvement. Differential Diagnosis for rheumatic fever- Arthritis - Juvenile Rheumatoid arthritis , Collagen vascular diseases, virus associated arthritis, Hematological disorders causing arthritis.
  42. 42. Post Graduate Clinical Training in Pediatrics [2013] Page 30 Commonly asked questions: 1. Jones criteria- original, modified, update and limitations of Jones criteria. 2. Conditions causing similar cardiac lesions: 3. Differentiation between rheumatic arthritis and rheumatoid arthritis . 4. Nonspecific criteria for rheumatic fever (abdominal Pain, anorexia, wt. loss, epistaxis, pallor, chest pain,pneumonia , tachycardia) 5. Causes of diastolic murmur - Carey comb’s (active carditis) ,Flow murmur-severe MR , Mid diastolic murmur of MS and AR murmur. 6. Differentiation between ARF and RHD.Signs of rheumatic activity . 7. Prognosis and sequelae of carditis, arthritis and chorea. 8. Causes of chorea and description of rheumatic chorea. 9. Surgical indications in various Rheumatic valvular heart disease. 10. Peripheral signs of Infective endocarditis and Aortic regurgitation. 11. Drugs for primary and secondary prevention of rheumatic fever if patient is allergic to Penicillin. 12. Other tests to prove streptococcal infection.
  43. 43. Post Graduate Clinical Training in Pediatrics [2013] Page 31 CYANOTIC HEART DISEASE Checklist: 1. Complaints: a. Cyanosis age of onset,Distribution,precipitating and reliving factors. b. Cyanotic spell frequency of episode, improving or worsening, drugs c. Growth retardation/FTT d. Dysmorphis facies conotruncal facies e. History of vaccination due to association with Digeorge syndrome (T cell def) f. History of complication fever with altered sensorium (abscess) g. Prolonged fever with chills and rigors IE h. Older child syncope/chest pain/arthritis(gout) i. Any iron supplementation 2. Antenatal history: a. Mothers age Downs b. Maternal drug intake 3. Development history 4. Dietary history 5. Immunization history: stress on T cell dependent vaccine (ass. With Digeorge syndrome) 6. Family and socio economic history 7. Examination findings: a. Cyanosis,clubbing,Polycythemia b. Anthropometry c. Inspection: i. Precordial bulge ii. Apical impulse will be normal in position d. Palpation: i. Parasternal heave ii. Palpable murmurs
  44. 44. Post Graduate Clinical Training in Pediatrics [2013] Page 32 e. Auscultation: i. P2 is delayed & soft ,it is inaudible ii. S2 is single which is aortic component iii. ESM at left 3rd & 4th ICS iv. Continuous murmur if collaterals / after shunt surgery Diagnosis : case of cyanotic congenital heart disease/with decresed pulmonary blood flow/single s2/no s/o CCF or IE/sinus rhythm/
  45. 45. Post Graduate Clinical Training in Pediatrics [2013] Page 33 PROTEIN ENERGY MALNUTRITION (PEM) Name: Age: Sex: Religion: Care taker: Address: Presenting complaints - Poor gain in weight / height Associated complaints - Vomiting, loose motion - Cough, breathlessness, cyanosis - Difficulty in feeding, suck-rest-suck cycle - Polyuria, Polydypsia - Recurrent infections - Questions should be asked pertaining to each system Birth History - Age of expectant mother - Maternal nutritional status - Birth order, Birth weight - Prematurity - IUGR - Perinatal complications Dietary history - Calorie intake / day - Protein gms / day - Accurate assessment is difficult and good rapport with mother - Assessment is done by a 24 hr recall method or a food frequency table, diet during illnesses - Calculate calories and protein and calculate the calorie gap and protein gap as compared to ICMR recommendation H/O Breastfeeding ( to be taken in detail in infants ) - Time of initiation, duration, adequacy of breast milk. - Breastfeeding to be continued till two years of life.
  46. 46. Post Graduate Clinical Training in Pediatrics [2013] Page 34 - Breast milk is more advantageous as it is physiological, convenient, economical, with optimum fluidity and warmth, besides being bio-chemically superior, microbiologically sterile, immunologically safe, with psychological benefits of ensuring mother-infant bonding. - Epidemiologically breastfeeding decreases morbidity and mortality. H/O Artificial / Top feeding - Considered when either the mother is unavailable, critically ill or no more. - Formula feeding / cow’s milk -Dilution , bottle feeding. Over dilution and infection due to contamination are common causes of malnutrition H/O Weaning. - Weaning (meaning “to accustom to” ) / Complimentary feeding is started between 4 – 6 months of age. Breastfeeding must be continued during weaning. - Preparation and storage of weaning foods should be done under hygienic conditions. SOCIO-ECONOMIC HISTORY - Education of parents, occupation - Monthly income, Housing, Sanitary facility - Family size - Toilet habits - Safe drinking water - Availability of electricity, recreation facility - Kuppuswami scale – class I to V - Closely spaced families, - Working mother. Psychosocial history Cultural practices
  47. 47. Post Graduate Clinical Training in Pediatrics [2013] Page 35 On Examination – Anthropometry 1. Weight - Beam balance, electronic scale - simplest, most widely used, most reliable. 2. Height – Infantometer, stadiometer 3. US : LS ratio 4. MAC – between 1 –5 yrs of age, done on left arm midway between acromion & olecranon. (<12.5 cms – severe PEM, 12.5 –13.5 – moderate PEM, >13.5 normal ) Not a good parameter for growth monitoring during 1 – 5 yrs of age. 5. Head circumference – maximum occipito frontal circumference 6. Chest circumference 7. Skin fold thickness 8. Somatic quotient – average of Wt, Ht head circumference, MAC expressed as % age of expected Age independent anthropometric indicators 1. The Bangle test – inner diameter of bangle of 4 cms crosses above elbow 2. The Shakir’s tape – green (13.5 cms), yellow ( 13.5 – 12.5 cms), red ( < 12.5 cms) 3. The Quac stick – Quacker’s arm circumference stick 4. Modified Quac stick 5. The Nabarrow’s thinness chart 6. The head circumference to chest circumference ratio ( > 1 - normal) 7. MAC to height ratio ( < 0.29 severe PEM , 0.32 to 0.33 - normal ) 8. MAC to head circumference ratio 0.28 – 0.31 - mild PEM 0.25 – 0.279 - moderate PEM < 0.249 - severe PEM 9. Ponderal index ( Wt / Ht3 ) > 2.5 - normal 2.0 – 2.5 - borderline PEM < 2.0 - sever PEM 10. Dughdale’s ratio ( Wt / Ht1.6 ) > 0.79 - normal < 0.79 - malnutrition
  48. 48. Post Graduate Clinical Training in Pediatrics [2013] Page 36 11. Quatelet index ( Wt kg / Ht2 cm) X 100 > 0.15 - normal 12. BMI (Wt kg / Ht2 m) 13. Mid arm muscle circumference - MAC – ( 3.14 X SFT) cm Classification of PEM (I) IAP classification (1972) N - > 80 % (Wt for age – expected) I - 71 – 80 II - 61 – 70 III - 51 – 60 IV - < 50 % (II) Welcome Trust classification ( Boston Standard) Wt for age ( % of Exp.) Oedema Type of PEM 60 - 80 + Kwashiorkor 60 - 80 - Under weight < 60 - Marasmus < 60 + Marasmic Kwashiorkor (III) Gomez classification Normal - > 90 % 1st deg PEM - 75 – 90 2nd deg PEM - 60 – 75 3rd deg PEM - < 60 % (IV) Classification as per height for Age and Weight for age Ht for age - Waterloo’s classification Wt for age McLarein’s classification
  49. 49. Post Graduate Clinical Training in Pediatrics [2013] Page 37 Ht for age Waterloo’s McLarein’s Normal > 95 > 93 1st deg Stunting 90 - 95 80 - 93 2nd deg Stunting 85 - 90 - 3rd deg Stunting < 85 < 80 Wt for age Waterloo’s McLarein’s Normal > 90 > 90 1st deg Wasting 80 - 90 85 - 90 2nd deg Wasting 70 - 80 75 - 85 3rd deg Wasting < 70 < 75 (V) WHO classification Ht for age Wt for age HA & WH > - 2 SD Normal Normal Normal < - 2 SD Stunted Wasted Stunted & Wasted Spectrum of PEM - Kwashiorkor / Marasmus / Marasmic Kwashiorkor / Pre-Kwashiorkor/ - Nutritional dwarfing / Underweight /Invisible PEM Clinical Signs - Growth retardation - Hair changes – Lack luster, thin , sparse ,Flag sign - Hypochromotricia , Easily pluckable - Skin changes-Hypo-pigmented, Hyper-pigmented, erythematous, jet black - “Flaky paint dermatosis” , “Crazy pavement dermatosis” Xerosis, hyperkeratosis - Eye Signs.- Pallor, xerosis, bitot's spot ,angular palpebreitis.
  50. 50. Post Graduate Clinical Training in Pediatrics [2013] Page 38 - Mucosal changes- Glossitis, Stomatitis, chelosis - Glands. -Parotid, thyroid gland enlargement - Hepatomegaly - Purpura or Bleeding - Oedema – mooning of face - Mental changes – Irritability, apathy - Tremors – appear during treatment Investigations - Hb, CBC, Platlet count, Priferal serum, RBS, BUN, S electrolytes, S protein, Alb, CXR, MT, Urine – R & CS, LFT, RFT, CSF Management …4 STEPS - Resuscitation, Hospital care - Restoration, - Rehabilitation - Prevention care Resuscitation.. Treat medical emergencies o What emergencies? Hypothermia, hypoglycemia, electrolyte disturbance, sepsis , shock, dehydration, cardiac failure, Anemia Restoration. Achieve weight for height - How? 150-200Cal/actual weight , 3-4gm protein/actual weight , 150-165 ml fluid/ actual weight and Multivitamins and minerals Given as 2hrly feeds with a feed late night and early morning -Oral or gavage feeds What type of feed? Breast feeds, High energy milk Isodense formulas ,Hyderabad mix, amylase rich food, Cereal pulse mix Rehabilitation Allow RDA as per ICMR recommendations Supplementary through various national nutrition programmes…ICDS Growth monitoring Developmental stimulation
  51. 51. Post Graduate Clinical Training in Pediatrics [2013] Page 39 Prevention Prevent LBW babies….Antenatal care & Care of adolescent girls NIMFES .. Nutrition, Immunization, Medical care, Family planning, Education, Stimulation NUTRITIONAL RECOVERY SYNDROMES Gynecomastia, Parotid swelling, Hypertrichosis, Hepatomegaly, Ascites, Spleenomegaly, Eosinophilia, "Kwashi shake" All are self limited but keep the baby under observation. Commonly asked questions Complications of PEM / Poor prognostic signs National programmes in nutrition Classifications of PEM Nutritional recovery syndromes Difference between marasmus / Kwashiorkor Diet chart for PEM To prevent malnutrition the “Three plank protein bridge” by Jelliffe to prevent PEM - Continue breastfeeding - Introduce veg proteins - Introduce animal proteins Besides supplementary feeding, group eating and small frequent feeds.
  52. 52. Post Graduate Clinical Training in Pediatrics [2013] Page 40 NEONATAL CHOLESTASIS Name : Age : Sex : DOB : Consanguinity : C/O Jaundice Onset of Jaundice Associated with high colored urine +/- clay colored stools (Obstructive jaundice) Abdominal distension Progressively increasing (organomegaly, Ascites) Upper or lower abdomen Urine output Stool history History of etiology Maternal history of drug ingestion, jaundice / infection in pregnancy, Neonatal umbilical catheterization Associated skin rash, petechie, fever, cardiac disease Full term or preterm Dysmorphic features Family history of hemolytic anemia History of complications Bleeding from any site Altered sensorium Ascites Examination General examination Jaundice, Fundus for chorioretinitis Signs for Vitamin Deficiencies
  53. 53. Post Graduate Clinical Training in Pediatrics [2013] Page 41 Edema, anasarca Anemia Dysmorphic features (Chromosomal, Alagille) Cataracts Abdominal examination: Inspection : Localized bulge, distension (which quadrant is more affected) Palpation : Superficial palpation: Guarding, tenderness, rigidity Deep Palpation o Hepatomegaly - Tender/Nontender - Surface: Smooth/Nodular - Span and Size - Border: well felt/ sharp/diffuse - Consistency: Soft/firm/hard o Splenomegaly - Size (Grades of splenomegaly) - Consistency: Soft/firm - Splenic notch Kidneys Divarication of recti Hernial sites Percussion: Shifting dullness/horseshoe dullness/fluid thrill. Puddle’s sign Auscultation: Renal Bruit, Venous hum Other systems: Cardiac murmur, hydrocephalus, Meningitis Diagnosis Neonatal jaundice With/without hepatosplenomegaly, With/without ascitis With/without dysmorphic features With/without anemia With/without associated anomalies Most likely etiology being : Neonatal Hepatitis / Biliary atresia / Inborn error of Metabolism / Galactosemia/ Chromosomal disorder
  54. 54. Post Graduate Clinical Training in Pediatrics [2013] Page 42 Investigation: Biochemical/ Routine tests Special Etiological Tests Morphological Tests Other tests Histopathology LFT including Bilirubin SGOT/SGPT/GTP/ Alk.PO4 PT/PTT Total proteins RFT Hemogram S.electrolytes S.Ammonia VBG RBS Blood culture Urine culture Stool culture CRP VDRL TORCH titres (Both of child and mother) HbsAg, HIV Test for Galactosemia Antitrypsin levels UAA/PAA Thyroid function tests USG abdomen Hepatobiliary Scan Cholangiogram (Peroperative/ Laproscopic) X-ray spine: (Alagille) X-ray chest: (Cardiomegaly) Fundoscopy: (Chorioretinitis) Staining with HE and PAS. Jaundice in newborn Conjugated jaundice Unconjugated jaundice Infective: Viral :CMV, Rubella, Reovirus III, Hep B Bacterial: E. Coli, Listeria, Protozoal: Toxoplasma Inherited : Niemann-Pick Type C, Galactosemia, Alpa-1 antitrypsin deficiency, Biliary Hypoplasia (Syndromic), Progressive intrahepatic cholestasis Chromosomal Anomalies: Trisomy 13/18/21 Idiopathic Biliary atresia – Neonatal Hepatitis Choledochal cyst Miscellaneous: TPN, Hypothyroidism, Maternal alcohol Ingestion, Erythromycin estolate, Frusemide
  55. 55. Post Graduate Clinical Training in Pediatrics [2013] Page 43 Treatment: General measures: Proper nutrition and multivitamin supplementation in cholestatic doses Vitamin K supplementation Phenobarbitone Cholestyramine/Urodeoxycholic acid Specific measures Toxoplasmosis: Sulphamethaxazole, pyrimethamine Galactosemia: Galactose free diet Biliary Atresia: surgical intervention Choledochal cyst: Surgical intervention
  56. 56. Post Graduate Clinical Training in Pediatrics [2013] Page 44 HEPATOSPLENOMEGALY WITH ANEMIA Name: Age : Sex : Religion: Address: HISTORY: Complaints : Abdominal distension Abdominal lump Associated with lump elsewhere • H/o Icterus, pallor, petechie, purpura. • H/o anorexia, nausea, vomiting, dysphagia, diarrhea, constipation, clay colored stools, worms, mucus in stools. Etiological history: • No h/o Koch’s/ Koch’s contact or swelling of PPD given in hospital. • No h/o chronic fever with rigors (Chronic malaria/ Kala Azar) • No h/o jaundice in the past, hematemesis / malena / hematochezia / dilated veins on abdominal wall (portal hypertension) • No h/o umbilical catheterization/ History /s/o umbilical sepsis in neonatal period (Extrahepatic portal hypertension) • No h/o altered sensorium/ unconsciousness/ coma/ convulsions (hepatic encephalopathy) • No h/o blood transfusions, other sibs affected (Hepatitis B/ Hepatitis C / Chronic hemolytic anemia) • No h/o petechie, purpura/ ecchymosed (leukemia/ hypersplenism) • No h/o breathlessness/ edema feet/ increased precordial activity/refusal to feed (CCF) • No h/o delayed milestones/myoclonic convulsions/incoordination (storage disorder- Niemann-Pick disease, Gauchers) • No h/o defective vision/ hearing (Mucopolysacchridosis, Osteopetrosis)
  57. 57. Post Graduate Clinical Training in Pediatrics [2013] Page 45 • No h/o fever / rash in mother during pregnancy (intrauterine infection) • No h/o fractures (Osteopetrosis) EXAMINATION: • Acutely ill or chronically ill • Patient is conscious, irritable. • PRESENCE/ABSENCE: pallor, icterus, cyanosis, clubbing, significant lymphadenopathy, edema feet, increased JVP (CONSTRICTIVE PERICARDITIS) • Vital signs. • Anthropometry measurements – with percentiles. • Abdominal girth (in c/o ascites) • Look for platynychia / koilonychia, petechie, purpura / ecchymosis, xanthomas, pruritus marks, hemolytic facies, and phylecten. • Signs of liver cell failure • Genitals • BCG mark, abdominal tap mark, liver biopsy mark. • Skull/ spine • Dental cavity- dentition, fetor hepaticus SYSTEMIC EXAMINATION Abdominal system: INSPECTION: Abdomen: • Distended/not if so upper or Lower or both; more on right or left • Distended with everted stretched umbilicus with fullness in flanks. • There are scars, abdominal tap marks, liver biopsy, sinuses or dilated veins. • Hernial orifices and genitalia are normal.
  58. 58. Post Graduate Clinical Training in Pediatrics [2013] Page 46 PALPATION: There is edema of abdominal wall/ doughy abdomen. Superficial palpation: tenderness/guarding/ rigidity. Deep palpation : Liver : Enlarged ------- cms in Right midclavicular line and --------- cms in midline below the xiphisternum; upper border of liver dullness is in --------- Right Intercostal space; span ------- cm. The edge is sharp/ round/ leafy. The surface is smooth/nodular/ tender/nontender. Consistency----soft/firm/hard. Moves with respiration. Pulsations-Rub/bruit over the liver. SPLEEN is--------cm from the left subcostal margin; is non tender; smooth in consistency; soft/firm or hard; anterior notch is felt; there is/ is no bruit. PERCUSSION : S/o free fluid in the form of puddle sign (120cc)/ Shifting dullness (>1 litre)/ Fluid thrill (>2 litres). AUSCULTATION : Bowel sounds, Bruits Per rectal examination Diagnosis -------Yr old M/F born of a-------marriage with hepatosplenomegaly with pallor/ icterus/ hematemesis/ malena/ IU infection/ umbilical vein catheterization with, failure to thrive, with vitamin deficiency A/D/E/K. with s/s of liver cell failure, with s/s of Portal hypertension with s/s of hypersplenism with dysmorphic features, or s/s of congenital infection/ cataracts or s/s of storage disorder. Differential diagnosis: Hepatosplenomegaly: • Infection - Disseminated Koch’s, malaria, kala azar, SBE, IU infection, Neonatal Hepatitis syndrome. • Hematological - Chronic hemolytic anemia, leukemia, Hodgkin’s lymphoma. • Congestive - CCF, constrictive pericarditis, Budd-Chiari, Portal hypertension. • Storage - Niemann pick disease, Gaucher, GSD, MPS. Splenohepatomegaly: • Gaucher’s disease type 1 to 4
  59. 59. Post Graduate Clinical Training in Pediatrics [2013] Page 47 Hepatosplenomegaly with lymph nodes: • Disseminated Koch’s, leukemia, lymphoma, infectious mononucleosis. Splenomegaly with pallor/ icterus: • Hemolytic anemia, cirrhosis, Portal hypertension, hypersplenism. Splenomegaly with petechie / ecchymosis: • Acute leukemia, SBE, ITP, hypersplenism. Hepatomegaly: • TB, kwashiorkor, CCF, leukemia, lymphoma, congenital hepatic fibrosis, Storage disorders (glycogenosis, MPS, Gauchers disease, Niemann-pick disease), tumors (hepatoblastoma, wilms, neuroblastoma). Splenomegaly: • Infections- malaria, kala-azar, TB, SBE, CMV, EBV, Toxoplasmosis. • Hematological -hemolytic anemia, hemoglobinopathies. • Congestive - PHT, cirrhosis, chronic CCF, constrictive pericarditis. • Infiltrative- Niemann-pick disease, Gaucher’s disease. • Neoplastic -leukemia, lymphoma. • Miscellaneous-Rheumatoid arthritis, SLE. • Massive splenomegaly-disseminated Koch’s, malaria, kala-azar, Extrahepatic portal hypertension, tropical splenomegaly, spherocytosis, osteopetrosis. • Moderate splenomegaly- above+ leukemia, Hodgkin’s lymphoma, hemolytic anemia. • Mild splenomegaly -above+ typhoid, SBE, septicemia. Hepatosplenomegaly with anemia: • Neonatal-Isoimmune hemolytic anemia, congenital spherocytosis, alpha thalassemia, TORCH, TB, congenital malaria, congenital leukemia, histiocytosis, neuroblastoma, osteopetrosis. • Infancy- Thalassemia, sickle cell anemia, Malignancy, Malaria, Kala-azar, TB, Gauchers, Niemann-Pick disease, GSD.
  60. 60. Post Graduate Clinical Training in Pediatrics [2013] Page 48 Childhood – spherocytosis, Infection, JRA, SLE, Cirrhosis with portal hypertension, Malignancy Hepatosplenomegaly with ascites: • Disseminated Koch’s • Cirrhosis of liver- post hepatitis, Indian childhood cirrhosis, Wilson’s Disease, portal hypertension • Congestive- Constrictive pericarditis, Budd-Chiari, pericardial effusion. • Malignancy-rarely ascites.
  61. 61. Post Graduate Clinical Training in Pediatrics [2013] Page 49 THALASSEMIA Name: Age : Sex : Religion: Address: Complaints: • Presented with c/c of increasing pallor • Abdominal distension • Failure to thrive Elaboration of complaints: Increasing pallor: easy fatigability, palpitation, fast breathing, edema. Only symptoms pertaining to RBC or combined RBC+WBC(repeated infection)+Platelet(bleeding manifestations) H/o repeated transfusions—transfusions started at what age, regularity and frequency of transfusions. H/o receiving any regular injections/ medications. H/o discoloration of skin H/o not achieving adequate weight and height. Older child-----h/o having achieved puberty. H/o repeated chest infections/ breathlessness H/o deafness (sensorineural deafness due to Desferrioxamine toxicity or bony expansion and compression of the eight cranial nerve.) H/o complications of blood transfusion------ blood transmitted disease, iron overload FAMILY HISTORY - OF Sibling/ relatives receiving transfusions DIET HISTORY - to check the iron consumption in food Rest of the history as usual. ON EXAMINATION GENERAL INSPECTION • Position patient,Vital parameters, Growth Parameters –Height, Weight with Percentiles, Tanner staging for puberty , • Skin Colour , Pigmentation, Pallor, Jaundice
  62. 62. Post Graduate Clinical Training in Pediatrics [2013] Page 50 • Facial features-Frontal bossing/Parietal bossing/Chipmunk facies / Maxillary Overgrowth/ Dental malocclusion /Prominent malar eminence/ Broadened nasal bridge • Hands- Finger tip pricks / Pallor, pigmentation • Peripheral stigmata of chronic liver disease • Pulse – Slow (hypothyroid) ,Irregular (cardiomyopathy) , Alternans (CCF), Hyperdynamic(anaemia) • Head & neck- Conjuctival pallor ,Scleral icterus ,Cataracts(desferrioxamine) Retinopathy(desferrioxamine) , Teeth:dental malocclusion, Neck/goiter • Heart-Full precordial examination to detect cardiomyopathy, CCF, haemic murmurs • Abdomen - Distension, Splenectomy scar Injection sites –Desferrioxamine/ Insulin Hepatosplenomegaly • Lower limbs and gait- Leg ulcers , Ankle odema (CCF), Bony tenderness • Gait examination for long tract signs-----due to vertebral bony expansion and cord compression • Delayed ankle jerk relaxation • Back examination for lordosis, tenderness • Others-Urinanalysis for glucose • Chvostek’s and Trousseau’s signs(hypoparathyroidism) • Hearing(sensorineural deafness) Commonly asked questions: Differential Diagnosis of Hemolytic anemias. Ideal transfusion regime. Complications of Thal major and Blood transfusions. Penatal diagnosis. Diagnosis of hypersplenism. Chelation therapy Recent advances in management of Thal major.
  63. 63. Post Graduate Clinical Training in Pediatrics [2013] Page 51 APPROACH TO SHORT STATURE Chief complaint :- Child is not gaining in height. • To ascertain that the child is indeed short, measure height/ length with infantometer till 2 years of age and with stadiometer later on by appropriate technique. This parameter is plotted on growth charts. Different growth charts are available like NCHS, Tanners, ICMR , K.N.Agrawal . A child is said to have short stature if his/her height is below the 3rd percentile or more than 2SD below the mean for the reference population. A child is said to have growth retardation if his growth ( height) velocity is below 25th centile of reference population. History : • Age of onset …since when is the child not growing. • School, home or physician records of previous heights and weights must be sought and charted on growth charts. • Associated complaints …(suggestive of systemic cause), Polyuria----- Chronic renal failure, renal tubular acidosis(RTA) Polyuria, Polydypsia ---- RTA , Diabetes insipidus Shortness of breath, cyanosis, cough, fever----Congenital heart disease, asthma, cystic fibrosis, other chronic respiratory illness,TB Headache, vomiting, visual problems------pituitary /hypothalamic mass Diarrhoea, steatorrhea, abdominal pain-------malabsorption Constipation ,weight gain, inadequate growth-------Hypothyroidism Psychosocial disturbances-------psycosocial dwarf • Past history of illnesses.
  64. 64. Post Graduate Clinical Training in Pediatrics [2013] Page 52 • Antenatal history … maternal medical illnesses during pregnancy , maternal exposure to teratogens, irradiation, maternal infections • Birth history … Type of delivery (breech), Mode of delivery, Full term / preterm/ post term . Birth weight Neonatal period.. Seizures , prolonged hyperbilirubinemia, feeding difficulties, hypoglycemic episodes, delayed cry. • Family history .. Pedigree, Consanguinity , height of parents, Age at onset of puberty in parents, Presence of similar complaints in other family members. • Developmental milestones • Dietary history Calories and proteins intake. • Psycosocial history. A well taken history can give clues to aetiology of short stature like: • H/o antenatal substance abuse, medication, birth weight-------IUGR • Edema hands and feet at birth---------Turners syndrome • Breech delivery, neonatal hypoglycemia, jaundice, micropenis----Growth hormone deficiency • Dietary intake (caloric and protein intake) ,sunlight exposure-------malnutriiton, rickets • Family h/o short stature, delayed puberty in parents----familial short stature, constitutional delay in growth • Prolonged intake of steroids, amphetamine derivatives----drugs as cause of short stature
  65. 65. Post Graduate Clinical Training in Pediatrics [2013] Page 53 On Examination : Anthropometric measurements like weight, standing and sitting height, upper to lower segment ratio, arm span, rhizo, meso and acromelic lengths , head circumference, must be taken. • Growth points should be charted and growth velocity should be recorded. Normal growth velocity: In the first year of life a child grows by 25cm, 12.5 cm in 2nd year, 6-7cm in 3rd & 4th year, 5cm per year from 5-9 years with a nadir of 3.5 cm per year in pre pubertal age group. During pubertal growth spurt 10-30 cm height is gained , with peak height velocity of 9-11 cm per year in boys and 7-9 cm per year in girls. Upper to lower segment ratio helps to differentiate between proportionate and disproportionate causes of short stature. Body proportions (upper segment: lower segment) change from 1.7 at birth to 0.98-1 by 13- 14 years of age and to 1 in adult hood. • Plot the height against mid parental height range .Mid parental height (MPH) is calculated by adding 6.5cm to the average of mothers and fathers height in boys and by subtracting 6.5cm in case of girls. This should be plotted on growth chart with a range of about 8.5 cm below or above MPH. If a child lies within this range he has a genetic cause of short stature. • Thorough general and systemic examination needs to be performed to look for dysmorphism, skeletal and non-skeletal anomalies, signs suggestive of malnutriiton and vitamin deficiencies and chronic infections. Signs of chronic systemic disease and endocrine abnormality is to be sought for. Pubertal development to be assessed by Tanners sexual maturity rating. Clinical examination can give certain clues to the aetiology like: • Dysproportionate short stature------skeletal dysplasia, rickets, congenital hypothyroidism • Dysmorphism------congenital syndromes • Midline defects-------hypopituitarism
  66. 66. Post Graduate Clinical Training in Pediatrics [2013] Page 54 • Pallor ---------Chronic anemia ,chronic renal failure, hypothyroidism • Vitamin deficiency signs----PEM ,malabsorption • Hypertension-----chronic renal failure • Cherubic facies ,frontal bossing, depressed nasal bridge--------growth hormone deficiency • Jaundice, clubbing------chronic liver disease • Goitre ,impalpablethyroid, coarse skin------hypothyroidism • Central obesity ,striae ,proximal muscle weakness------Cushing’s • Round face ,short 4th metacarpal, mental subnormality---pseudohypoparathyroidism • Frontal bossing ,beading ,wrist widening------rickets • Visual field defect, optic atrophy, optic nerve hypoplasia, papilledema----- pituitary/hypothalamic tumour ,septooptic dysplasia Bone age is done to study the skeletal maturity IT IS DONE BY TAKING HAND AND WRIST X-RAY OF LEFT HAND. Two systems for reading bone ages are available-Greulich and Pyle’s Atlas method and Tanner and Whitehouse scoring method. Normal ranges of bone age range: Range + 2SD Chronological age Male Female +/- 3-6 mo 0-1yr 0-1yr +/- 1-1.5 yr 3-4 yr 2-3yr +/- 2yr 7-11yr 6-10yr +/- 2yr plus 13-14yr 12-13yr Familial short stature: H.A< B.A=C.A; Constitutional growth delay: H.A=B.A.<C.A If height is normal for national standards and midparenteral height and growth velocity is normal on follow up then reassurance is needed without any further investigations.Normal bone age at outset usually rules out pathological cause of short stature.
  67. 67. Post Graduate Clinical Training in Pediatrics [2013] Page 55 Investigations Laboratory tests can be requested if clinical findings are suggestive of a disease. Chest x-ray ,2-D Echo for cardiac defect, Thyroid functions for hypothyroidism, skeletal survey for skeletal dysplasias etc. However where there is no clue on history and examination and with delayed bone age and low growth velocity screening investigations are needed. Weight for height gives an important clue for investigations i.e. poor weight for height can suggest malabsorption or other systemic illnesses while good weight for height may mean growth hormone deficiency. Screening investigations for finding cause of short stature are: • Complete blood count, ESR----Anemia ,chronic infection • Sr.Creatinine------CRF • Sr.calcium, phosphorus, alkaline phosphotase ---- Rickets, pseudohypoparathyroidism • Sr.proteins, SGPT-------Chronic liver disease • Venou blood gas, S.Electrolytess------------RTA • Urine routine ,microscopy, pH-----RT , chronic pyelonephritis, glomerulonephritis • Stool routine microscopy--------malabsorption , giardiasis • X-ray hands --------bone age ,rickets If screening tests are normal suspect Turner syndrome, GHD, malabsorption .Other investigations like karyotyping, provocative assays for growth hormone and special tests for malabsorption need to be done.
  68. 68. Post Graduate Clinical Training in Pediatrics [2013] Page 56 APPROACH TO EVALUATION OF SHORT STATURE Is the child short ? ( Ht less than 3rd centile) No Yes *Reassurance 1) Is the height within midparental height (MPH) range *Assess growth velocity No Yes 2) Assess bone age (BA) Elicit history to rule out Systemic diseases, malnutrition, IUGR, Dysmorphic / chromosomal syndromes BA= CA >HA BA =HA <CA Hormone deficiency Familial short stature CDGP Assess growth velocity (over 6/12 mon) Screening tests CBC, Hb, ESR ( anemia ,infection), Bone age Renal, Liver function test (CRF, CLD) Total proteins, albumin (Nutrition) S.Ca, P, AlkPo4ase ( rickets, pseudohypoparathyroidism) Blood gas , serum electrolytes ( metabolic acidosis, RTA) Coeliac screen , malabsorption workup IGF1 Genetic studies (Turner,Russel Silver, Trisomy ) (BA- Bone age , CA – Chronological age , HA- Height age , CDGP- Constitutional Delay in Growth and Puberty, RTA- Renal Tubular Acidosis, CRF- Chronic renal failure, CLD- Chronic Liver Disease)
  69. 69. Post Graduate Clinical Training in Pediatrics [2013] Page 57 Note- • Measurement of height should be done on a well calibrated stadiometer / infantometer • Height velocity is measured over a period of 6 to 12 months. • KN Agarwal charts are used as the reference curve . • Mid Parental Height (MPH) ( All heights measured in cms. ) = (( Mother’s height +13) + Father’s height )/ 2 ( BOYS) = ((Mother’s height +( Father’s height-13) )/ 2 ( GIRLS) MPH Range = MPH +/- 8.5cm • Upper segment, lower segment ratio should be calculated in all short children to check for disproportionate short stature. Causes of disproportionate short stature- • Skeletal dysplasia, Rickets, Congenital hypothyroidism , Mucopolysaccaridosis • Calculation of weight for height is helpful in differentiating wasting (malnutrition, systemic illnesses), obesity (cushing’s syndrome) and stunting ( GHD). Commonly asked questions : 1] Discussion of differential diagnosis 2] Stages of coma 3] Stages of TBM & prognosis in each stage. 4] Signs of meningeal irritation. 5] Signs of increased intracranial pressure 6] Types of herniation 7] Management of TBM - supportive + definitive 8] Types of shunt & complications of shunt 9] Complication of TBM 10] Pathology in TBM & lesion localization 11] CT correlates in TBM 12] Precipitating factors in TBM 13] Poor prognostic factors in TBM 14] Role of steroids 15] Newer modalities of diagnosis of TBM
  70. 70. Post Graduate Clinical Training in Pediatrics [2013] Page 58 APPROACH TO A CHILD WITH RICKETS Complaints: Progressive bony deformity Bone pains, Fractures Seizures in young infants, Carpopedal spasm in older children Delayed dentition, dental deformities Proximal muscle weakness Delayed motor development Associated symptoms…(etiology) Polyuria, polydypsia (Renal rickets, RTA) Recurrent diarrhoea, steatorrhoea ( Malabsorption..fat) Jaundice, distension abdomen (Chronic liver disease, Cholestatic jaundice) Pallor (Nutritional, Wilson’s disease, Chronic renal failure) Visual problems (Lowe’s syndrome, Cystinosis) Alopecia - Patchy, totalis (Vit. D Dependent Rickets Type II) Hearing affection ( RTA) Recurrent respiratory infection Mental retardation Drugs ingestion- Anticonvulsants,anti tubercular drugs Antenatal history… Calcium supplement in expectant mother Consanguinity (Autosomal recessive disorder) Preterm /Full term (Osteopenia of prematurity) IUGR (may manifest with rickets during catch up growth) Dietary history… Breast feed/ top fed Vit D or Calcium supplement Weaning Balanced diet Exposure to sunlight Family history of similar complaints (X linked hypophosphatemic rickets)
  71. 71. Post Graduate Clinical Training in Pediatrics [2013] Page 59 Examination Anthropometry - Short stature, Disproportionate short stature Bony features of rickets Craniotabes (young infants) Wide open / persistent open anterior fontanelle Fronto parietal bossing giving a hot cross bun appearance Rachitic rosary Harrison sulcus Pectus excavatum Widening of wrists Double malleolus Bowing of long bones Genuvarus / genu valgus Coxa vera/ coxa valga deformity. Dental feature: - Delayed eruption of teeth, dental abcess, pulp defects, dental problem usually affect the secondary detention. Muscle and ligament: - Proximal muscle weakness causing waddling gait, difficulty in climbing stairs, difficulty in getting up squatting position. Visceroptosis, laxity of ligaments. Associated problems: - Pallor, Icterus, other vitamin deficiencies, hypertension, alopecia, hepatosplenomegaly, cataracts, glaucoma, sensorineural hearing loss. Diagnosis:
  72. 72. Post Graduate Clinical Training in Pediatrics [2013] Page 60 BRONCHIECTASIS Name : Age : Sex : Address : HISTORY: PRESENTING COMPLAINT: Patients typically present with fever, chronic cough, purulent sputum, weight loss and loss of appetite. A) RESPIRATORY SYSTEM SYMPTOMS o Impaired exercise tolerance o Cough-frequency/severity/nocturnal/exercise induced/change in pattern. o Sputum-volume/color/blood tinged/recent change o Fatigue/Dyspnea/Chest pain o Chronic sinusitis o Wheezing might point towards allergic bronchopulmonar aspergillosis o Bronchodilators required and response to their use PAST COMPLICATIONS : pneumothorax/hemoptysis INVESTIGATIONS DONE : Sputum culture, chest x-ray, pulmonary function tests, pulse oximetry. THERAPY RECEIVED - exercise, physiotherapy, nebulised saline, bronchodilators or antibiotics. B) GASTRO INTESTINAL SYSTEM : Generally GI symptoms are present in cystic fibrosis or in IgA deficiency. Liver is affected in alpha 1 antitrypsin deficiency. History of weight loss/pain abdomen/vomiting/loss of appetite History of oily, bulky or offensive stools. History of meconium ileus or rectal prolapse C) Recurrent pyogenic infections are suggestive of immunodeficiency. Recurrent middle ear infections are suggestive of ciliary dyskinesia or immunodeficiency. FAMILY HISTORY: History of tuberculosis or cystic fibrosis in the family.
  73. 73. Post Graduate Clinical Training in Pediatrics [2013] Page 61 IMMUNIZATION: History of receiving BCG or measles or pertussis vaccine. EXAMINATION: A) General Examination a) Pubertal status (Tanner staging) - A delay in puberty may be seen. b) Nutritional status parameters –Weight, height, head circumference, percentiles. c) Vitals- Pulsus paradoxus (severity of airway obstruction) Pulses Alternans (congestive cardiac failure) Bounding pulse (hypercarbia) d) Look for clubbing/ cyanosis e) Ears –Secretory otitis media f) Nose – Nasal polyps g) Mouth- cyanosis/thrush B) Affected system RESPIRATORY SYSTEM Inspection - Note the increase in AP diameter. Cough-Moist/productive/ foul smelling Perform peak flow measurement if possible. Palpation - Measure the AP diameter (hyperinflation), Tracheal position, position of apex, palpable pulmonary valve closure Percussion - Hyperinflation /consolidation Auscultation - Coarse leathery crepts over the affected region (First heard in the upper lobes in cystic fibrosis) Wheeze may be present Loud second heart sound in pulmonary hypertension Gallop rhythm in cor pulmonale Dextrocardia in Kartagener syndrome DIAGNOSIS:
  74. 74. Post Graduate Clinical Training in Pediatrics [2013] Page 62 TIPS FOR STUDENTS Dr. Ranjitha Registrar, KKCTH Firstly, exams are just a phase in life. It too will pass. So, do not make it a do-or-die experience. Be systematic. Plan ahead. Set realistic goals. Work towards your goals. Keep motivating yourself. Remember, it is just an examination. The real test, is your daily routine--- saving lives of kids. So don’t lose focus on that. If you are sincere and hard working at taking care of kids under your care, you will know what to do in the exams. Look at the exams as stepping stones. Do what you need to do to reach the top. Don’t think of the difficult nature of the stones. People have cleared the exams. So it is not impossible. Start with a positive attitude. Preparing for theory examination: Make a schedule that is realistic and covers every chapter in Nelson.
  75. 75. Post Graduate Clinical Training in Pediatrics [2013] Page 63 You may jumble up systems or sit with a single system till that is over, that is a personal choice. But do not omit any system. Prepare notes in your own style and revise them whenever possible. You must know the salient points in each topic, not necessarily every point. Work out previous question papers. You will get an idea of the pattern of questions and will be a good guide to your progress. Do not forget community medicine, vaccination, recent advances. If possible, formulate your own questions in each topic. Think about how you would answer that. Prepare algorithms and flowcharts for questions like –approach to a disease or a condition, line of treatment. Make a list of questions you want to revise the day before. On the night before the exam, stop reading by dinner time, have a good dinner, relax and give your body time to ease out the tension. Try to get a good night sleep. Do not worry about the questions, it is not in our hands. Do not think about all the “what if” questions the fill our heads with fear. It is just another day of your life. Face it with courage, determination and a will to win. Writing the theory paper: Answer in the given order. During presentation of an answer, highlight the salient points either by using a different colour or by underlining.
  76. 76. Post Graduate Clinical Training in Pediatrics [2013] Page 64 Use different colour / capitals/ underlining , to show the different parts of the same question. Marks are being allotted in parts. Ensure they know what is where. Space out neatly and write, let it not go on for pages. Make the answers neat, precise and legible. There is a high probability that you may not know the answer to a question or you are not sure of it completely. Do not panic. Face questions one at a time. Focus on the answer you are writing. Do not think and worry about a question you do not know. If you do not know the answer, leave out a few pages, write the remaining, come back to that question at the end when you will be able to think and write. For clinical questions, you can imagine what you would do, how you would approach a child with the given condition in the ER / OP. Do not think about the paper you have written and submitted. It is done. You cannot change. Focus on the next paper. That is the best thing to do. Practical examination: Relax for a few days / weeks after theory exams and then start preparing for practicals. Prepare a list of systems and diseases that are commonly kept in the clinicals. Write a fake case sheet for each disease ,so that you know what all needs to be covered in history, clinical examination. Present the entire history to your colleagues and teachers, don’t worry about making errors, it is better to make them now than in the exam. Learn from your mistakes and others’ too. Try to finish taking history and clinical exam within 45 minutes.
  77. 77. Post Graduate Clinical Training in Pediatrics [2013] Page 65 Request your teachers and friends to correct you / show you how to elicit signs and do the examination. Do not make errors in the basics. Be sure of the order of presentation. Be thorough in anthropometry, nutrition and immunization. These are what separate the kids from adults, pediatrics from general medicine. There is no excuse if you falter in these areas. Prepare for osce (objective structured clinical examination) parallelly. There are certain topics that need to be covered compulsorily for osce preparation. Dress neatly. Wear a coat with long sleeves. Take some toys / chocolates / biscuits to befriend the kid who is helping you in the exam (by being your patient) Do not panic if they ask you a question to which you do not know the answer. Try to think and answer or else respectfully say you do not know. But don’t make it a habit. Be loud and clear while you talk. Be confident. They are only making you do what you have been doing daily in the hospital—take history, do clinical examination, derive at a differential diagnosis, plan the line of management. You need to talk, converse and not keep quiet because by not doing that you are making it hard for them to help you. Do not worry about the reputation of the teachers / examiners. At the end of the day, you have to perform. Be at your best.
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