Pediatrics Remarks

Newborn Physical Examination

 Before sending baby to home within first week of [Link] the baby is
calm
 Term baby weight 3.2 kg, height 50 cm (lied down), head circumference 35 cm
average. All determined with percentiles: AGA-SGA-LGA (Approperiate-Small-
Large for Gestational Age)
 Vitals;
-Respiratory Rate:40-60
-Heart rate:100-180
-Blood Pressure; 65-90/45-60 mm Hg(Systolic/diastolic)

-Temperature; 36.3C-37.5C

 Head: Front fontanelle;9-12 months, Posteriror Fontanelle;4-6 wk maybe 2-3

months closure.

 Eyes: Absent Red reflex may indicate lens pathologies(cataract,glaucom etc.)

 Ears;Periauricular skint tag may assoc w renal anomalies

 Umblical cord late dissociation later than 2wk; hypothyroidism, Factor 8

deficiency, leukocyte adhesion defects.

 Undescended testes; normal in preterms youunger than 32 wks normally

descend in 32-34 wk.

 Meconium in first 48 hrs

 Take the pulse from femoral artery strong pulse may indicate PDA, if absent
pulse think about aorta coarctation.
 Posture: normal neonate -- lies predominantly in a flexed position

 The presentation at birth can influence posture for several days

 Spontaneous motor activity
 Muscle tone and strength: test by; Assessing resistance to passive movements,
Pull-to-sit maneuver, Ventral suspension
  Crying: note if it is either-high pitched or very weak
 Feeding and sucking patterns
 Root reflex; Touch the corner of the babies mouth, baby should open his mouth
and turn his head to the same direction.

 Suck Reflex; Touching the roof of baby’s mouth should elicit suckig movement.

 Moro Reflex; A sudden movement of baby into a backwards falling position,

should elicit outstrech movement of arms.

 Tonic Neck Reflex; Turning the head of the baby to a side same side arm
outstreches and contralateral elbow bends inwards.

 Grasp Reflex; Stroking the palm of the baby should result with grasping
movement of the fingers.

 Babinski Reflex; Firm stroke to sole of the baby result in drosiflexion of toes,
which is normal upto 1 yrs of age.

 Step Reflex; Also called walk or dance reflex. When babies feet touch to a solid
surface when held upright baby starts to move legs like dancing or walking.

Respiratory System Examination

 Clubbing nedenleri,pulmonary:bronchiectasis,CF,Pulmonary abcess.

CVS;cyanotic heart disease,bacterial [Link];celiac,IBD,GIS
lymphoma. Hepatic;chronic hepatitis,cirrhosis
 Cyanosis;if central: decreased o2 saturation(o2 responsive-pulmonary non
responsive -cardiac problem), if pripheral:cold respoonse, shock, sepsis.
 Overinflated chest in severe acute asthma
 Dyspnea; flared nostrils, intercostal retractions, acessory muscle use,
moaning indicates severe dypnea
 Kussmaul in diabetic ketoacidosis,acetone scent.
 Auscultation pathologic voices similar to adults.
 Wet cough more than 2 mo:TB,CF,bronchiectasis. Dry cough; viral
infection,FB aspiration,drugs(enalopril),asthma.

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  Hoarseness and stridor; croup,bronchitis,FB asp.,laryngomalacia
 Nocturnal cough;Asthma,sinusitis
 Moaning;Severe sepsis,RDS,Severe pneumonia

Abdominal Examination
 Inspection,auscultation Palpation
 Murmurs may indicate renal arter stenosis and hypertension
 Patient lies still in acute peritonitis
 Absent bowel sounds in ileus
 Ascites abdomen distended
 Cullen sign in pancreatitis
 Rebound and defence in acute abdomen
 Determine liver borders with percussion hepatomgaly? (upper border normal
4 in young 5 in older children) Down shift; emphysema,pneumothorax-
upward shift;hepatomegal,subphrenic abcess,right lowerlobe
pneumonia,right lung atelectesia
 Dullness in traube area left 6 th rib;full
stomach,hepatomegaly,splenomegaly,left inferior pleural effusion
 Tumors may identified w deep palpation
 Acites downward dulness, bladder-over cyst:upward looking dullness

CVS Examination

 First we make inspection for cyanosis, pallor, edema, rashes, shortness of

breath, xanthoma, spider fingers, absent thumbs for genetic disorders
associated with hear, finger clubbing, splinter hemorrhages, janeway lesions
and osler’s nodules associated with [Link] make palpation to
assess temperature by checking if hands are symmetrically warm, measure
capillary refill time by applying five seconds pressure to distal phalanx of one
of child’s fingers and release. Pallor area should return to its normal color
less than two [Link] check radial pulse rate and rhythm, in babies
femoral pulse instead. Also we check radio-radial delay by palpating both
radial pulses simultaneously. Measurement of jugular venous pressure is
performed children older than 8 years. We make auscultation with bell for
murmurs;
• Mitral valve: 5th intercostal space in the midclavicular line.
• Tricuspid valve: 4th or 5th intercostal space at the lower left sternal edge.
• Pulmonary valve: 2nd intercostal space at the left sternal edge.
• Aortic valve: 2nd intercostal space at the right sternal edge.

 We should assess for thrills across each of the heart valves ,which are
palpable vibrations caused by turbulent blood flow.

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  Pulsus paradoxus in cardiac tamponade and other pericardial problems

 S1 splitting;ebstein anomaly,right bb block,pulmonary hypertension

 S2 splitting both in inspirium and expirium indicates atrial septal defect

 S4 is always pathologic except newborns

 S3 pathologic voice heard in poor cardiac function and large L-R shunts

 Innocent murmurs may be present in young children, characteristics of

innocent murmurs are:soft in character/usually grade1-2/well localized don’t
radiate/intensity change with position/first heard in 6months to 6 yrs/usually
first heard ata time of physical stress/confined to systole/short duration

 Still murmur is the most common innocent murmur of early childhood

 Rheumatic Fever cause PR prolongation

 Macrolides cause QT prolongation

Newborn Jaundice
 Physiologic jaundice of the newborn depends on 2main mechanisms;
1-increased erythrocte breakdown(HbF to normal Hb)
2-increased enterohepatic circulation of the newborn
Other contributing mechanisms are;
3-Dereased hepatic bilirubin uptake due to low ligandin levels
4-Decreased conjugation due to low activity of glucronyl transferase

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  Physiologic Jaundice start from 24hrs and ends max in 14 days and never
exceeds 15g/dl,usually starts in 2-3rd days and peaks at 5th day, doesn’t
require treatment. Mainly indirect bilirubin is increased.

 Pathologic jauindice(indirect)
1-hemolytic disorders;blood group incompatibilities,hemoglobinopathies
RBC membrane or enzyme defects(G6PD deficiency most common
enzyme defect)
2-Increased production;sepsis,DIC,polycthemia(maternal dm)
3- Low calorie intake(emzirme sarılığı) and delay of meconium passage
may contribute and lengthen jaundice.
4-Criegler najar(give phenobarbital) ,hypothyroidsm,pyloric stenosis

 Pathological Jaundice(Direct) DB over 2 mg/dl

Direct hyperbilirubinemia is always pathologic
Idiopathic hepatitis,TORCH,Hep B, biliary atresia,biliary
stenosis,metabolic disorders,total parenteral nutrition

 Bilirubin Encephalopathy(Kernicterus)
In acute period mild stupor, low sucking,hypotonic
In chronic permanent sequele(Bilirubin harms basal ganglia due to lack of
BBB)
Classic Sequele Tetrad(present fully at 6thweek)
-Extrapyramidal anomalies-atethosis
-Upward gaze
-Hearing problems
-Dental enamel hypoplasia
To avoid:
-All newborns should breastfed
-jaundice in first 24 hrs pathologic consider
-Treatment:Phototherapy,blood excahnge,medical(phenobarbital in
crigler najar,ursodeoxicolic acid,IVIG)

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 Constipation in Children

 Major components of defacation control:External anal

sphincter,puborectalmuscle,internal analsphincter.

 Infant and toddler min 1 month,4-18yrs min 2 months

2 or less defecation per week,1 incontinence episode after toilet
education,painful hard defaecation,retensive posture,large fecalith in
rectum
Risky Periods to develop constipation
1-supportive nutrition transition
2-toilet education
3-school start

 5%organic reason 95% functional constipation

 Treatment: Education,Emptying,Maintanance,End

 Toilet sit after meals for gastrocolic reflex,osmotics(lactulose,PEG,Mg

Hydroxide,Rectal(gliserol,saline,mineral oils,Phosphate)

 Treartment should continue for 6 months following the clinical response.

GIS Bleeding

 Upper GIS bleeding

-Necrotizing enterocolitis:ischemia+bacterial colonization mostly
prematue
-Esophageal Varices: search for peripheric manifestations of cirrhosis.
-Osler Rendau Weber Synd:hereditary hemorragic telangectesia, eyes,
ears,stomach affected. Recurrent epistaxis,AVM in viscera and
mucocutaneous telangectesia
-GI duplications
-Acute gastric mucosal lesions Ulcer: most common

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 -Mallory weiss tears: esophageal linear lacerations due to high pressure
vomitting treated and diagnosed w esophageal endoscopy

 Lower GIS Bleeding

-Necrotizing Enterocolitis,Anal fissure,Polyp,Volvulus, Hirschprung
Disease,Henosch Schonlein Purpura, AVM and Angiodysplasias
-if diarrhea+mucus present think about bacterial dysentery and IBD
-IBD:chron and UC
-Diverticulosis Coli: Most common cause mostly left colon.
-Meckel’s Diverticulum:Rule of 2’s 2%incidence, 2 feet proximal of
ileocecal valve, 2 inches size,2 types of heterotopic mucosa(gastric-
pancreatic),symptomatic in younger than 2 yrs. Associated with massive
hemmorage without pain.

 Upper and lower GIS Bleeding:GIS tumors,angiodysplasia,AVM,Osler

Weber Synd,Vasculitis,Amiloidosis,Trauma-FB,Fistula,Hematologic
Disorders, elastic tissue disorders

 Upper GIS bleeding may present w hypovolemia or shock

 Lab; CBC,Coagulation panel,thrombocthopenia(Kasabach-Merrit

Sign:Trappment of Throbocytes in hemangioma)

 If Endoscopy, Colonoscopy inconclusive Enteroscopy is indicated.

Prematurity and Postmaturity

 Preterm:<37 weeks Term;37-41 weeks Postterm:>42 weeks

 SGA: 2 SD below of mean or below 10% percentile

 LGA:2 SD above of mean or above 90% percentile

 Problems in Premature Babies:

-Lung developement problems(RDS due to surfactant deficiency)
-Patent ductus arteriosus and other cardiac problems
-Anemia,DIC,vitK def,hyperbilirubinemia
-Necrotizing enterocolitis

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 -Hypocalcemia,hypoglycemia,hypothermia
-Late metabolic acidosis
-CNS problems hipoxic or developemental
-Renal function problems

 Postmaturity Problems:
-Placenta wears off and loses it’s function
-Baby may develope hypoglycemia inside the uterus(infuse glucose after
delivery)
-Meconium aspiration
-Term baby delays 2 week indication for induced labor or c section

Rheumatic Fever

 GABHS infection M protein (mostly 5th serotype) antibody recognizes

certain tissues in the body and causes autoimmunity

2 major or 2 min+2 major/ sydenham chorea sufficient on it’s own

 Treatment of acute attack;

-penicillin G single IM shot or 10 days oral AB therapy
-Salicylates for arthrits
-Steroids for carditis
-For Chorea:Phenobarbital,chlorpromazine,BDZ,haloperidol

 Primary prevention; treatment of GBHAS with Ab

 Secondary prevention;Antibiotic prophylaxis

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 Infective Endocarditis

 Infection of endocardium, presence of congenital heart defects and

prosthetic valves are a risk factor.

 Poor dental hygeine(viridans strep) and illicit drug use ([Link] usually
acute).

 Treatment
-Empirical therapy:ivpenicllin/oxacillin+gentamycin or IM streptomycin
-[Link]: 4wk iv penicillin
-Enterococcus: iv penicillin 4wk+gentamycin or streptomycin 2wk
-[Link]: oxacillin/methicillin/cloxacillin 4-6 wks

Atopic Dermatitis

 Mixed type allergic disease: both IgG and non IgG

 Chronic inflammatory,pruritic(worse at night) ,relapsing, exaggerated cutaneous

response to enviromental triggers

 Activated dermal langerhans cells expressing surface bound IgE stimulates T cells-Th2
cells in active lesiond maintain local inflammation w IL-4 and 13-Those promeote IgE
production IL-5 promotes eosinophils

 In chronic form IL-12 and 18 takes place and Th-2 to Th1/Th0 response also external
bacterial toxins conttirbute the inflammation in chronic period([Link]/epidermidis)

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  Most patients develope allergic rhinits or asthma

 Diagnosis: History, typical skin lesions,increased IgE and immedeate skin response test.

 Dif diag:Histiocytois X(particularly feedind disorder),Wiscot Aldrich Synd,Hyper IgE

syndrome

 Atopic dermatitis does not affect diaper area!

 Treatment:
-Shower followed by oil based moisturizers for body and water based moisturizers for
face.
-Oral Antihistamines
-Steroid creams on active lesions,nonsteroid creams(tacrolimus) short term
iintermittent treatment can be applied everywhere

Allergic Rhinits

 IgE driven inflammation of nasal mucosa+eosinophilic inflammation

 Risk factor for asthma

 Nasal congestion,nasal itching,teary eyes,postnasal dripping,cough,ear

fullness,itching,allergic shiners(infraorbital darkening)

 Nasal polyps are important comorbidity

 Treatement:2nd generation oral antihistamines and nasal corticosteroids, removal of

allergens from patients enviroment.

Respiratory Distress Syndrome

 Acute lung disease of newborn due to surfactant deficiency

 Starts after 6 th hour and resolves in day 2-7

 Surfactant is produced by typeII pneumocytes after 20th week of gestation, reaches to

sufficient amounts at 34-36 wks, detecteble in amniotic fluid at 28-32 th wks of
gestation

 Lecithin/sphingomyelin ratio shold be above 2 to decide fetal lung maturity

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  Disease cause low lung compliance and atelectasis which result with
Ventilation/Perfusion V-Q mismatch.

 Constriciton of pulmonary vessels result in increased right ventricle pressure may lead
to R-L shunting and more severe hypoxemia.

 LBW,prematurity,cold stress,fetal aspyhxia, maternal DM(hyper insulinemia supress

surfactant production) are risk factors

 Use of antenatal steroids and intrauterine stress is beneficial(cortisol promotes

surfactant)

 Dx made by PE(dyspnea,nasal flaring,cyanosis,moaning,intercostal retractions)chest x

ray, blood gases, auscultation(crepitations),hemogram,CRP(exlude sepsis-
pneumonia),procalcitonin(ex seps-p) and blood culture.(ex seps-p)

 Treatment; if mild to moderate:nasal CPAP(Pressurized air), if severe:mechanical

ventilation and surfactant [Link] aim: PO2:60-70 SaO2:>90%
RESPIRATORY FAILURE

 Type I RF
-only hypoxemia, normal CO2
-impaired oxygenation
-low ambient O2,alvolar hypoventilation,pneumonia,ARDS,R-Lshunt

 Type II RF
-hypoxemia+hypercarbia
-Diseases which increase airway resistance:COPD,asthma,Chronic bronchitis,morbid
obesity,brainstem lesions,paralysis etc.)

 Dx;ABG,CBC,alveolar-arteriao O2 difference

 Treatment: supplemental O2 if fails proceed to mechanical ventilation

Immunization

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 ,

 Serious side effects

-OPV:vaccine assoc. Paralytic poliomyelitis

-tetanus:brachial neuritis,anaphylaxis

-DTP:persistent inconsoluble screaming,seizures,anaphylaxis,hypotonc hyporesponsive state

_Allergic reactions due to egg related antigens:yellow fever,influenza,MMR

 Other side effects

-BCG_supurrative BCG lymphadenopathy

-Measles:fever,anaphylaxis,temporary morbiliform rash

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 -Rubella:Acute arthritis,polneuroptahy

-:Mumps:sensorineural deafness

-MMR:Thrombocytopenia

-Tetanus:peripheric neuropathy

-HepB:injection site reaction,fever,anaphylaxis

-Varicella:Maculopapular/papullovesicular rash

 BCG vaccine do not elicit Ig production, T cell mediated immunity provided via type 4
hypersensitivity induction.

Fever

 38(fever) 40(hyperpyrexia) rectal

 Thermosensitive neurons in preoptic nucleus and anterior hypothalamus

 Thermoreceptors in capillary venous vessels

 Pyrogenic cytokines:IL-1,TNF, IFN(beta-gamma),IL-6 they increase circulating PGE2 levels and

PGE2 increase set point for thermoregulation in hypothalamus

 Pathogens and drugs(vancoycin,amphoterecinB,allopurinol) are exogenous pyrogens.

 Heat production>heat loss:salicylate tox,malignant hyperthermia

 Heat loss<heat production:ectodermal dysplasia,severe heat exposure

 Self limited viral infection and uncomplicated bacterial infection are most common cause of
acute fecer and hyperpyrexia

 >41.7 degrees is lethal

 Fever drops slowly and graually in a week after viralinfection

 Fever may drop abruptly to it’s normal range in response to antibiotics during a bacterial
infection.

 Fever +respiratory symptoms(RSV or nfluenza screen rapid Antigen and chest x ray),+meningel
irritation signs(CSF study for meningitis),+pharyngitis(GABHS swab test).

 If relapsing fever suspect malaria

 Do not drop the fever unless>39 degrees or except patient with confirmed heart disease

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  Fever+relative bradycardia:typhoid fever,brucellosis,leptospirorsis,drug fever.

 Management of fever: Acetaminophen and Ibuprofen

 Any febrile neonate should be assesed via CSF test

 Any febrile neonate needs urinalaysis

 Toxic appearence with fever or hypotheria should be hospitalized

 Drug fever drops after 72 hrs of discontinuation

 Underlying condition should be treated

 Polymorphonuclears<5000 rule out bacterial inf except typhoid fever.

 In case of FUO consider testing for rheumatologic disorders, malignancy, TB or abcess

Peptic Disease,[Link],Abdominal Pain

 Gastritis:suuperficial mucosa inflammation

 Ulcer:Deep tissue loss extending to muscularis mucosa

 Bicarbonates,phospholipids,prostoglandins are protective

 Ciggaretes,alcohol , 0 blood, familiy histoy,stress,[Link],gastrin,pepsinI-II ulcerogenic factors

 Gastric ulcers low acid secretion, duodenal ulcers high acid secretion

 NSAIDs cause ulcer via inhibition of Prostoglandin production

 H pylori increase gastric pH via prodtion of ammonium w urease and hinder gastrin negative
feedback,urease test,fecal antigen,serology,antral nodularity at biopsy

 Acute gastritis proceed chronic gastriris which may end up w: multifocal atrophic gastritis,Antral
gastritis,Gastric Ca,ulceration,MALT lymphoma,duodenal ulcer.

 Stress ulcers:Cushing(head trauma,surgery),Curling(burn victims)

 Endoscopy for chronic abdominal pain or acute bleeding(Ulcer,gastritis,h pylori,hiatus

hernia,esophagus polyps)

 Barium graphy:hiatus hernia,ulcer,malrotation of intestines

 Functional abdominal pain:Do not wake up, no loss of appetite or vomitting(Ususally do not
have an apperant reason)

 Biliary system diseases:increase with eating, right upper quadrant sensitive

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  Esophagitis,GER;night and early morning epigastric pain do not respond eating

 Pancreatic pain;epigastricregion with radiation to back

 Giardia inf: foul smelling stool, gas,mild abd pain

 Treatment:

-Antacids decrease pH and promote healing-give distant from other meds

-Sucralfate binds to proteins and covers the ulcer as a physical barrier thus blocks acid contact.

-Group E Prostaglandins decrease acid secretion and increase mucosal

perfusion(misoprostol,enoprostol)Xind in pregnancy valla bebek fıçık diye doğar tutamazsın

-H2 receptor antagonistsdirect inhition of acid secretion(fomotidin,cimetidin,ranalidin)

-PPI:strongly suppress acid secretion(may slightly elevate liver enzymes)

-[Link];metranidazol+clarithromycin+PPI+probiotic, Bismuth also beneficial but amoxicillin

resistant in Turkey

IBD

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  Extraintestinal manifestations are more common in Chron.

Growth and Developement

 Important factors for postnatal growth:nutrition,genetics,insülin,IGF-I,GH,thyroid

hormone,sex steroids

 Height:measured lied down until 2yrs,/25cm(0-1yrs)10-12cm(1-2 yrs),8-10cm(2-3yrs),5-

6cm 4-pubert and at puberty 20-29 cm

 Weight;at first 10 days physiologic weight loss 5-6% of body weight and regained in
following7-10 days. First 6 mo +20-30 g per day,6-12 mo15-20 g per day,1-2 yrs 2-2.5kg
per yr. 5months x2 of birth weight, approximately in 5yrs baby reaches 20 kg

 Head circumference; 35cm at birth (+1cm each month),47cm in 1 yr old. >97percentile

macro-<3 percentile microcephaly.

 BMI;>85percentile overweight,>95%obesity

 Skeletal maturity determined vi akne x ray in newborn and w x ray of wrist in child.

Growth Disorders
 Short Stature:-2SD below the mean or below the 3rd percentile fort he age

 Search the kids below 1.5SD of mean

 parental height or fialure to grow 7 cm per year at puberty

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  Non pathological SS;famillial SS,Constitutional delay of growth and puberty,combination of frist
two.

 Pathological SS

-Proportionate (Endocrine): GH deficiency,GH insensitivity,IGF defects,hypothyroidsm or other

hormone deficiencies.

-Proporionate(Non Endocrine):Chronc systemic disease,nutrition deficiency,growth supressing

drugs.

-Disproportionate:Rickets, Skeletal dysplasias((Spondyloepiphyseal

dysp.,Mucopolysaccharidoses,Scoliosis,Achondroplasias).

 Thyroid hormone,a adrenergic stimulation,hypoglycemia,stress,sleep and exercise stimulates

GH. B adrenergic stimulation and hyperglycemia inhibits GH secretion

 Constitutional delay is together with underdeveloped secondary sex characteristics

 Prader Willi Syndrome: Fetal and infant hypotonia,almond eyes,small hands and feet,insatiabile
apetite obesity,developemental delay

 Lawrence Moon Bardet Biedl Syndrome;Obesity,Polydactyly,hypogonadism,retinitis pigmentosa,

[Link].

 In constitutional delay HA=BA<CA. They Eventually catch up.

 Percentile loss after age 2-3 send to endocrinology

 Silver Russel Synd; riangle face,clindodactyly at 5 th finger,skeletal asymmetry,precocic puberty

 Noonan:Mitral regurg,pulmonary stenosis,sensorineural deafness,small

penis,cryptorchidism,chromosom anomaly,turner like stigmatas.

 Steroids,amphetamins,methylphenidate,chematheurapeutics cause short stature.

 Intrauterine growth retardation: teratogens,radiation,trauma,materanl systemic

diseases,TORCH infections,placental diseases.

 Turner syndrome cause ss,Shield chest,metacarpals hortness.

 SS and obese think Hypothyroidsm,Cushing,Albright’s hereditary osteodystrophy

 Cafe au lait spots: Neurofibromatosis type I,Mccune albright,tuberous sclerosis,fanconi

anemia,Silver russel,ataxia telangectesia,Gaucher syndrome

 Diagnostic tests include:Xray,CBC,urinalaysis,ESR,IGF I,GH stimulation test,Prolactin,FSH-

LH,T/E2,TFT,tTGA,IgA/ıgG,Karyotype,cranial imaging.

Pediatric Stroke

 Sudden onset focal neurologic deficit due to ischemia or hemorrhage

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  Ischemic strokes are more often in children

 Cardiac causes:Aortic stenosis,MS,VSD,PDS,shunts,endocarditis,RF etc.

 Hematologic causes:Sickle Cell Disease,polycthemia,leukemia,lymphoma,thrombocytosis or

thrombocythemia, cogulation disorders(ProteinC,S def,Factor V def,PNH etc)

 Maya Maya Disease: Type of AVM,poorest prognosis,cause arterial ischemic stroke,carotid

arteries inside skullbecomes blocked or narrowed

 Sturge Weber Synd:Angiomas involving leptomeningens,skin and [Link] cutaneous venous

dilation-Port wine stain.

 Metabolic causes:Homocysteinuria,pseudoxhantoma elasticum,Fabry disease,mitochondrial

encephalopathies(MELAS,Leigh’s synd)

 Make the diagnosis via MRI and angiography stabilize the paitent and search fort he cause later.
If hypercoagulation diagnosed do antithrombotic therapy w antithplatellet and anticoagulants.
Thrombolytic therapy w urokinase or streptokinase

Pediatric Coma

 Lethargy:awake but tend to sleep

 Stupor:only painful stimulation reponse

 Obduntation:wakes when poked

 Coma:No response

 İnfection,trauma,hypoxia-ischemia,epilepsy,stroke or metabolic

 Check ABC,general examination,trauma exam

 Lab: glucose,CBC,electrolytes BUN,Cr,urinalysis,urine drug screen,blood culture,liver blood

tests,carboxy hemoglobin for CO poisoning

 Head CT,EEG

 Pinpoint pupils;Damage to pons or opiate overdose

 One pupil dilated or unreactive:Damage to CNS or vascular pathology

 Both pupils dilated or unresponsice:Hypothermia ,severe anoxia, drug overdose

 Decorticated:Hyperflexion

 Decerebrated:Extension

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  If GCS<8 or resp failure intubate the patient
 Stabilize the patient, Supply O2, gain IV Access and start dextrose
 Infection:Ceftriaxone and vancomycin or acyclovir if viral
 Opioid intox give naloxone
 Treat definitive seizures with lorezapam
 Increased ICP more than 20 mm hg or decreased cerebral perfusion pressure<70mm hg
give mannitol (decrease blood viscosity and expands circulating volume by retaining the
water from cells thus increase cerebral perfusion.
Asthma
 Is an episodic airway obstruction due to inflammation of hyperresponsive airways.
 Mostly first attack <6yrs
 All type of allergy and hypersensitivity, past pneumonia or bronchiolitis(rhinovirus in
first 6 months of birth), LBW,enviromental tobacco or air pollution means increased risk
for asthma
 Chronic inflammation may lead airway remodelling and cause permanent loss of
pulmonary function
 Dry cough,expiratory wheezing,dyspnea,tachypnea,silent chest in severe bronchospasm.
Symptoms more common at night.
 Prolonged expiratory phase and decreased breath sounds at auscultation

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  Differential diagnosis include the diseases that cause obstruction in upper and lower
repiratory airways
 Diagnosis;spirometry(decreased FEV1/FVC <0.8) in children>5 yrs. Allergy skin test.
Chest Xray indicated in every chronic cough case. Responsiveness of the
symptoms(reversibility) with bronchodilators (SABA) is essential for definitive diagnosis
 Treatment: Short acting(Salbutamol)-Long acting B2 agonists,inhaled
corticosteroids(pulmicort-budesonide),leukotriene antagonists(montelukast),in severe
cases oral corticosteroids,LABA,high dose inhaled cs used.
 Do not send a patient to home until SaO2 reaches>90
 In severe asthma exacerbation give inhaled beta agonist every 20 min for 1 hr and give
systemic c sif needed(Effect after 6hrs)
 Salbutamol nebulizer continious nebulization or ipratropium bromide nebulizer can be
used.

URTI
 Nasopharyngitis-common cold
-Rhinovirus(most common),parainfluenza,RSV,coronavirus
-Rhinits,scratchy throat,myalgia,headache,low grade fever.
-2nd and 3rd day nasal discharge becomes purulent
-Systemic symptoms subsidin5-7 days,rhinitis and nonproductive cough may remain for
a week more
-Sinusitis,otitis media and pneumonia are complications
-Treatment:acetaminophen or iburofen,hydration and saline nose drops

 Sinusitis

-Maxillary sinus 5yrs,frontal sinus 7 yrs.

-Most common agents;[Link],[Link],[Link] same as otitis media
-Headache facial pain,cough worse at bed time,nasal discharge and malodor,fever.
-symptoms+visible post nasal dripping enough for dx
-In Xray infected sinus look opaque.
-Trt:Amoxicillin or amox+clavor macrolide or 2-3rd cephalosporins and decongestants
and nasal irrigation w [Link] not use antihistamines.

 Acute Pharygitis
-Uncommon in children<1yrs, peak at 4-7
-Bacteria,viruses,mycoplasma
-If viral: fever,malaise,throat pain,conjunctivitis,cough,rhinitis,LAP entire ilness do not
persist>5 days
-If streptococcal:Headache,abd pain,vomiting,fever 40 degrees resistant to
antipyretics,sore throat,tonsillar enlargement,white lesions(crypts) on tonsils.

20
 -Streptococcal disease should be trated w antibiotics to avoid osteomyelitis,sinusitis and
abcess and in long term to avoid acute rheumatic fever and acute glomerulonephritis.
-Perform throat culture for GBAHS if positive treat with penicillinor amoxicillin or
cephalosporins or macrolide.

 Croup:Most common mid airway infection. Parainfluenza type B (most

common)/RSV/adenovirus. Bark-like cough,subepiglottic narrowing, inspiratory stridor,
laryngotracheobronchitis of children<5 yrs old is called croup.
 Laryngitis: viral etiology mostly,inflammation of larynx, mild fever,hoarsnes,inspiratory
stridor,retractions,dyspnea.
 Laryngotracheobronchitis:mostly viral, cause high fever,decreased bilateral breath
sounds,ronchi and scattered rales,symptoms worsen at night.
 Acute spasmodic laryngitis: viral etiology,laryngeal form of asthma,narrowing of the
passage due to inflammation,tend to recur 1-2 in a month,occurs spontaneously and
responds anti-inflammatory drugs [Link] 2 doses of adrenalin half an hour appart.
 Bacterial tracheitis:[Link](most
common),parainfluenza,[Link],[Link],high fever,antimicrobial
therpy necessary. Intubation/tracheostomy may be recquired.
 Epiglottitis:Very severe condition. Rapid respiratory [Link]
stridor,hyperxtended neck,shiny cherry red epiglottis(look without abeslang).Thumb like
epiglottis on [Link] parenteral antibiotics and secure the airway, consider
intubation.

LRTI

 Acute Bronchitis:Usually preceded by a viral URTI, secondary bacterial infection with

[Link] or [Link] is uncommon,frequent dry cough,burning and
anterior chest pain,dry cough is followed by prulent sputum in days. Sterorous
[Link] specific treatment, do not use antihistamines.
 Acute Bronchiolitis:RSV,parainfluenza and adenovirus. Mild URTI followed by 38-39
degree [Link] obstruction,edema,and mucus cause decreased ventilation
and lead [Link] inflated lungs and scattered consolidation in [Link]
and air hunger.
-Treatment: Ribavirin(best administered early),bronchodilators(ventolin),cold
humidified O2,Respiratory monitoring,fever control,hydration

21
Community Acquired Pneumonia

 

 Pneumococcal Pneumonia:Most common bacterial etiology of childhood

[Link] lobe consolidates [Link] fever(39-40)
-suppressed breath sound on affected area
-crepitan rales
-initally dry proceed to productive cogh
-meningismus with upper lobe pneumonia
-abdominal pain with lower lobe pneumonia

22
 -leukocytosis with left shift
-hypoxemia without hypercapnia
-Culture the organism from sputum,blood,pleural fluid
-Penicilin,ceftriaxone,vancomycin can be used
 Staphylococcal Pneumonia:[Link] progressive!.Started via viral
[Link] [Link] areas of hemorrhagic necrosis and
[Link] abcesses and several lobes involved,[Link]
Xray,patchy involvement of entire hemithorax with [Link] with tracheal
aspiration or pleural tap culture. Treated with meticillin or vancomycin if resistant,1st
gen cephalosporins also approperiate.
 Klebsiella Pneumoniae:Consider CF!,in debilitated [Link] fulminant
course cause pulmonary abcess and cavitation 50%[Link] with 3r gen
cephalosporin+aminoglycoside
 Pseudomonas Pneumonia:CF(late stage),severe and ocasionally fatal necrotizing
bronchopneumonia.
 Single lobe involved think pneumococcus,multiple lobes involved bacterial pneumonia
think about [Link],Klebsiella,Pseudomonas
 Diffuse salt like appearance on X ray means viral disease or miliary Tb.
 Xray indicated in a coughing child who is having a varicella infection.
 Atypical Pneumonia:>[Link],Clamydia Pneumophilia,legionella. Children
usually have the infection without serious manifestationfüs with a good general
condition. Long term coughing with mild sputum,crackles present and butterfly sign
[Link]:Erythromycin or clarithromycin 10days or azithromycin 5 days.
 Factors for Hospitalization: <6mo,Sickle cell anemia w acute chest syndrome,multiple
lobe involvement,complicated pneumonia,supplemental O2 need,severe vomiting and
inability to tolerate oral intake,toxic appearance

Tuberculosis
 Tuberculosis bacilli acid fast,usually airborne by mucus droplet.
 Stay latent in inactivated macrophages and may reactivate.
 Primary infection in lungs,cavitary lesion ghon focus,connects to hilar lymph node via
lymphatic which forms a gohn complex. Primary infection resolves within a week
 PPD test to determine immunity and active disease.

23
  Low grade fever,malaise,mild cough.
 Extrapulmonary manifestations of sever Tb:
-disseminated and meningeal Tb;2-6 months after primary infection
-Bones and joins;in several yrs
-Renal lesions in decades
-Tuberculous pleural effusion w primary lung disease
-Tb pericarditis
-Lymphadenopathy
-Tb meningitis common in<5yrs
-Skeletal Tb /in spine called Pott’s disease
-Abdominal and urogenital Tb
 Cell mediated immune responses prevent from advanced progression in most
individiuals.
 Treatment
-Standard therapy for active disease:Isoniazid and Rifampin for 6mo also Pyrazinamide
added for the first 2 months. If extrapulmonary diease present treat for 9-12
[Link] may also added in extrapulmonary disease
-Children w positive PPD test but no symptoms and <6 yrs who had a contact with
infected adult are treated with isoniazid for 6 month.
-In exposed kids, PPD repeated after 3month of contact, if>5mm continue full dose to 6
months if>5 mm discontinue INH.
 Congenital Tb commonly appear as miliary Tb in 2nd and 3 rd wks of life,generlized LAP
and meningitis.
 Treatment of infectd pregnants is delayed until delivery.
 BCG vaccination 1 st dose at 2nd month and 2nd dose at infancy.

Urticaria(Hives)
 Acute or chronic itchy,red colored,raised,different shaped skin reactions.
 Affects epidermis but occasionally involve dermiş and result in angioedema(on
palpebrae,lips,hand-feet.
 Acute<6wk<chronic
 Etiology include;food or drug reactions,insect stings,infections,collagen vascular
diseases,malignancy w angioedema,cold/solar urticaria,pressure-aquagenic urt.,famillial
cold urticaria,dermatographism,cholinergic urt(psychological stress related)

 URTI is most common cause of urticaria in children

 Lesions associated with intradermal bleeding(purpura) means urticarial [Link]

lesion persists more than 24 hrs, has purpuric components or heal with hyperpigmented
residue biopsy is indicated for urticarial vasculitis diagnosis.

24
  Urticaria pigmentosa: Diagnosed with biopsy,increased number of dermal mast cells
[Link] common manifestation of mastocytosis but may ocur as an isolated
finding. Small yellow to reddish-brown macules(raised papules taht urticate on
scratching_Daner’s Sign-)

 Appearant skin urticaria should be investigated together with other systems to eliminate
anaphylaxis risk. Associated dyspnea,abdominal pain,hypotension should be considered
as anaphylaxis and treated accordingly.

 Treatment of isolated mild acuteskin reactions made with antihistamines(Avil,atarax 1 in

6 hrs). Acute severe angiedema relieved by epinephrin administration. For very severe
cases (joints involved) short burst of oral corticosteroid therapy may be applied.

Anaphylaxis
 Occurs when there is sudden release of biologically active metabolites from mast cells
and basophils. Type I hypersensitivity reaction created via IgE. Responsible mediators of
the clinic are: Histamine,TNF,PAF,leukotriens,PGs,cytokines,tryptase.
 Invlolvements:
-Cutaneous:urticaria,angioedema,flushing
-Respiratory:bronchospasm,laryngeal edema
-[Link],dizziness,tunnel vision,headache
-CVS:hypotension,dyryhmias,MI
-GI:nausea,colicky abdominal pain,vomit,diarrhea
2 system involvment enough for diagnosis, only hypotension alone is sufficient for
diagnosis.
 Most commonly skin>CVS>CNS>Upper airways
 Common causes in children:
nuts,milk,egg,shellfish,sesame,cephalosporins,penicillins,NSAIDs(paracetamol less
allergic then ibuprofen),honeybee,yellow jacket,latex(most common case in hospital
rxns),vaccinations,radiocontrast agents,food+specific exercise.
 Another cause of anaphlyaxis clinic is anaphlactoid reactions.
-Non immune mechanisms, activated mast cells and basophils.
-Reaction to cold,drugs and other agents
-Complement activation(C3a,C5a) (in serum sickness)
 Lab test for histamine and tyrptase. Tryptase is more useful it peaks in 1-1.5 hrs but
histamine is relesed rapidly and has a short halflife. Normal levels do not rule out
anphylaxis.
 Anaphlaxis realted hypotension and syncope always present with tachycardia.
 Arecurrent laryngeal edema with abdominal pain suggests hereditary
angioedema(evaluate accordingly)
 Treatment: ABC control.

25
 -Lay down the patient and elewate the feet.
-Open the airway(İntubation or tracheostomy may be recquired) and give high flow O2
-Open an IV line
-Fluid resuscitation if hypotensive
-Stridor present give epi
-Wheezing give B2 agonists
-If present urticaria give antihistamines
-Lastly apply corticosteroids(late effect in 6 hrs)
-IM epi is indicated in upper,lower airway obstructions and CVS symptoms with
anaphylaxis.

Newborn Resuscitation

 Term baby?,breathing/crying?,Muscle tonus sufficient?(if yes probbably no need

resuscitation) if no start resuscitation
 Warm the baby!
 Clean the airway, and position the baby with open airway
 Connect to pulseoxymeter trom the raight hand(ductuses are open)
-1 min 60-65%
-2min 65-70%
-3min70-75%
-4min 75-80% If below these levels start supplemental O2
-5min 80-85%
-10 min 85-90%
 If baby is apneutic or shallow breathing CPAP application.
 After 30 seconds of ventilaiton if heart rate<100 continue the ventilation
 If HR<60 Start chest compressions 3/1 with ventilation and consider intubation
 Despite 100% active O2 therapy or despite 100% at least 45-60 seconds active
compressions HR below 60 start diluted adrenalin administration 0.1-0.3 ml/kg
 Volume expander also can be considered.
 Despite 10 minutes of proper ventilation and compression if absent heart beats, end the
resuscitation
 Do not start resuscitation if:
-<23 week
-<400g
-Anencephalic
-trisomy 13-18 incompatible with life
 If>25 weeks certainly resuscitate!
 Try to provide early materna skin contact.

Hpoxic/Ischemic Encephalopathy
 Cardiopulmonary depression due to dimpaired placental or pulmonary gas exchange
 Hypoxia,hypercrbia,metabolic acidosis

26
  Decreased perfusion in brain and other organs
 Dep acidosis in cord blood gas,APGAR score between 0-3 longer than 5 min
 Seizure,coma,hypotonia presence,MODS.
 Etiology:
-distorted umblical flow; shoulder dystosis, chorda prolapsus related comprssion.
-Maternal placental perfusion insufficiency;maternal hypo/hypertension,maternal DM.
-Fetal problems:lung [Link] anemia,Cardiopulmonary adaptation
problems during delivery.
 Hyperalert/coma/lethargic/seizures
 Hypoxemia,arrythmia met/resp acidosis.
 Failure to suck
 Acute tubular necrosis oliguria -polyuria
 Hypo/hyperglycemia,Hyponatremia(SIADH),hpocalcemia,lactic acidosis.
 Thromboytopenia,bleeding,thrombosis
 EEG,cranial USG,MRG.
 Treatment ,supportive and within first 6 hrs start therapeutic hyptermia(33-34 degrees)
shown to provide neuroprotection.

Neonatal Transport
 Prevent Hypoglycemia,hypothermia,hypotension,
hypoxia/hyperoxia,hypocarbia/hypercarbia

Cerebral Palsy

 Persistence of primitive reflexes,abnormal tone or posture,excessice irritabilty,failure to

achive motor milstones, hyperreflexia,extensr plantar responses,clonus,impaired fine
motor skills,slow effortful voluntary movements, intellecyual disability,seizures,visual
impairment,speech disorders,orthopedid and pulmonary problems,hip dysplasia.
 EEG and metabolic evaluation(differential diagnosis for storage diseases),screening for
thrombophilia

27
  Management:
-spasticity:botilunum toxin,oral antispstic drugs
-hip dysplasia treatment
-Physical therapy

Poisonings in Children
 114 poison center:Call and give exct history amount of exposure and patient details and ask if
that specific dose is toxic for your patient

 Methanol metabolized to formic acid(toxic) conversion blocked by fomepizole(antidote and

ethanol.

 Make sure patient is breathing,treat shock if present.

 Treat hypotension with isotonic saline.

 Decontaminate chemical burns via istonic or water.

 Prevention of absorbtion with emesis or gastric lacage,characoal,whole gut irrigation

 Follow for hypokalemia, ECG changes?

 Hemodialysis

 Enhancement of excretion via urine alkalinization(salicylate poisoning) control hydration

 Immedeate dilysis in treatment resistant salicylate and methanol or ethylene glycol poisoning

 Acetaminophen overdose cause glutathione depletion in liver treated with N acetyl cystein
(NAC)ith loading dose IV alsogastric lavage,active carbon beneficial,monitör liver function tests
closely

 CO posioning,cherry red skin,carboxy hemoglobin levels [Link] syptoms

headache,vertigo,confusion,[Link] acute phase proteinuria,glycosuria,AST,ALT increase ECG
[Link] with high flow O2,hyperbaric O2 therapy decamethsone if cerebral edema
present.

 Caustics (corrosive acids):large dermal exposure or ingestion may cause severe hypocalcemia.

Emesis and lavage is contraindicated,give water and milk,treat electrolytes and hydrate,if
needed use TPN,endotracheal tube to alleviate laryngeal edema is [Link] gluconate
used in HF acid burns

 Cyclic antidepressants; may cause,dysrtyhmias,coma ,hallucinations,HT followed by

hypotension,treat with active characoal,ECG check for dyrythmia(widened QRS>100ms)
lidocaine helps dyrythmia,BDZ for convulsions.

 Naloxone for opiod overdose

 Alkalalinize urine with bicarbonate for salicylate poisoning, tinnitus is a very typical finding in
salicylate overdose also cause hyperthermia.

28
  Don’t give bases for neutralization in caustic ingestion

 Hydrocarbon ingestion contraindication for charcoal and cause high fever,giveO2 consider
ECMO.

 Drugs:

 -Oral hypoglycemics are fatal for children hypoglycemic convulsions leave sequele in
children(low IQ) Give dextrose immedeatly.

-Calcium channel blockers cause lethal arrythmias, intoxicated children should be observed in
ICU for 72 hours.

29
 Contraindications of charcoal and whole bowel irrigation are expected as Exam
Questions!!!!

Metabolic Bone Disease

 Hypocalcemia Ca<8.7mg/dL
-In case of hipoalbuminemia corrected Ca=CA+0.8(4-Albumin),in case of alkalosis Ca
seems falsely normal,ionized calcium levels are low in alkalosis
-Paresthesia around mouth and at finger,weakness,muscle cramps,Chevostek(cheek)
and Trousseau(arm)signs,tetany and convulsions.
-Etiology:Hypo/hypermagnesemia,Renal infections(due to increased PO4)
-Vit D deficiency or resistence
-Aspyhxia,sepsis
-Hypoparathyroidism:primary,secondary,DiGeorges Syndrome(congenital parthy
hypoplasia),in genetically acquired form together with(cardiac disease,deafness,short
stature,renal dysplasia,medullar stenosis and other autuiimmune diseases)
-Increased phosphate due to renal insuf,diet or tumor lysis syndrome
-Pseudohypoparathyroidism(patrhormon receptor or signalling abnormalities)
-Exchange and transfusion
-Nutrients and [Link] dietary phosphate ,HCO3,citrated blood,anticonvulsants.
-Treatment:
Treat the underlying cause like PTH for hypoparathyroidsm or vit d supplement
Convulsion/tetany;Calcium gluconate

30
 No convulsion or tetany;oral elementary Ca

Hypercalcemia:

 Ca>10.5 if >12 hospitalize

 Nausea,vomit
constipation,ileus,pancreatitis,polyuria,polydipsia,calcinosis,nephrolithiasis,osteoporosis
, convulsion,coma,shortQT,bradycardia and other arryhmias

 Etiology;excess vit d or ca in diet, famillial hypercalciuric hypercalcemia,

hyperparathroidsm(sporadic,famillial:neonatal severe hypoparathy.,MEN
syndromes,Jansens metaphseal dysplasia, PTHrP ectopic production. Etc,)Bartler
syndrome:excess PGE production, immobilization,hypophsophatemia related causes.

 Mccune Albright:GNAS1,polyostotic fibrous dyplasia,cafe au lait,precoc

puberty,hypophosphatic rickets

 Osteogenesis imperfecta:aCOL1A,COL2A mutation blue sclera

 Osteopetrosis: osteoslerosis,erlenmeyer flask deformity,sandvich/Rugger Jersey

vertebra

 Picnodysostosis:cathepsink,dense defective bones,lysosomal storage disease,short

stature,underdeveloped finger tips and nails,small face and chin.

 Treatment with biphosphonates,furosemide,calcitonin

Congenital Heart Disease

 VSD is most common CHD followed by ASD(secundum),PDA and coarctation of aorta.

 Etiology is consist of maternal rubella,viral diseases,radiation,hypoxia,drugs,

alcohol(septal defects), vitamin imbalances all impact in first trimester.

 Maternal DM:Truncus arteriosus,TOF

 Lithium users:Ebstein anomaly,tricuspid atresia,ASD

 Famillial:Hypoplastic left heart syn.,coarctation of aorta.

 Trisomy 18, Turner,Trisomy 21 all associated with high risk for CHD

31
  DiGeorge; heart defects,abnormal facies,thymic aplasia,cleft palate,hypocalcemia

 Maternal PKU:TOF

 Maternal SLE:Complete heart block

 Child with CHD may appear normal but O2 saturation is low in measurement

Acyonotic CHD
 ASD: Stable S2 splitting both in inspirium and expirium,mostly secundum type [Link]
asymptomatic,right ventricular hypertrophy and systolic murmur around pulonary valve,may
improve on it’s own at 4-6 yrs,heart failure progression uncommon

 VSD: Mostly membraneous type. In large defects may lead to pulmonary HT and eventually
eisenmenger syndrome wil cause cyanotic heart [Link] murmur on mesocardiac
area,may progress to failure. Mid diastolic murmur in ASD and VSD. VSD severity interferes with
cardiac changes, small defected hearts are normal, if moderate LV hypertrophy and LA dilation
if severe biventricular hypertrophy and LA dilation [Link] tele cardiomegaly ,increased pulm
vascılature and prominent pulmonary conus. Large defect is initially asymptomatic due to high

32
 pulmonary vascular resistance but symptoms start to occur as the PVR drops and shunt
becomes more apperant. PHTN developes afer 6th 12th month. If proceeds to congestive failure
treat with diqoxin and diuretics. VSD patients should recieve prophlaxis for endocarditis and
have a good oral hygiene.

 Patent ductus arteriosus:Machine-like murmur at infraclavicular area,Bounding pulse and high

pulse [Link] ductus close functionally in 6-48 hrs and antomically close 2-3weeks
due to increased O2. In ECG LV hypertrophy if mild or biventricular hypertrophy if [Link]
telecardiography cardiomegaly and increased pulmonary vascularity [Link] Prostaglandins
make the ductus remain opened. Within first week indomethacin treatment to block
prostaglandins thus close the ductus, if fails catheterzation or surgery may needed.

 AVSD(endocardial cushion defect):Cause AV valve abnormalities,recurrent lung infections and

CHF findings(1-2mo).Lelf lower sternal thrill and holosystolic [Link] hypertrophy observed
in ECG occasionally with LV [Link] and increased pulmonary vasculature in
tele.

 Pulmonary Stenosis:mostly valvular but supravalvular in rubella and Williams syndrome,systolic

ejection click(most important),S2 splitting and P2 [Link] in mild,dyspnea and and
effort intolerance in moderate,CHF and sudden death if [Link] dilatation in
tele,prominent main pulm artery in chest xray.

 Aort stenosis:Valvular stenosis is most common mostly together with bicuspid

[Link] stenosis with Williams syndrome. LV hypertrophy in [Link] thrill on
carotis and aortic focus. Systolic ejection murmur. Need IE prophylaxis and good oral hygiene.

 Coarctation of aorta(Narrowing).Most common HTN cause in [Link] in Turner and

usually associated with bicuspid [Link] symptomatic failure to feed and [Link] asymp, arm vs
leg great BP [Link] ejection Murmur [Link] esophagus graphy ‘E’ sign and 3
signin high penetration [Link] may require PDA to maintain lower aorta perfusion,PGE
infusion made. Diuretics O2 and CHF tratment together w IE prophlaxis, baloon angioplasty if
upper lower extremity pressure dif >20 mm Hg.

Cyanotic Heart Disease

 Tetralogy of Fallot(TOF):most common cyanotic CHD.

-pulmonary stenosis

-large VSD

-RV hypertrophy

-Overriding aorta

Cyanosis increase w cold, cry, exercise,. Recurrent syanotic spells and dyspnea,clubbing f
[Link] O2 drops due to decreased pulmonary circulation. Child tend to crouch down to
block low extremity deoxygenated blood return to heart thus increases Sa [Link] to grow
.Systolic ejection [Link] hypertrophy in ECG. Do not progress to heart [Link]
pulmonary vasculature in [Link]=LV pressure in catheterization for certain dx.
Treat w O2 during cyanotic spells.NAHCO3 to treat met acidosis,propranolol.,

33
  Transposition of Great arteries: Aort from RV,Pulm Art from LV. Single prominent
S2..Cardiomegaly in [Link] relation between right and left heart so septal defcts are required to
be alive,VSD40%[Link] shunt is not sufficient patient dies. CHF starts from 1 st week of life.
Give PGE1 to keep ductus open.

 Total Abnormal Pulmonary venous Return:No relation of pulmonary vein with LA. Patient needs
a patent foramen ovale or ASD to live,Snowman or 8 sign in tele.

 Tricuspid Atresia:Tricuspid flow completely closed no relation between RA and RV, ASD or PFO is
a must for life.

 Truncus Aretriosus: Mostly w di george. Prominent large VSD always present and a single large
artery arise from the ventricles. If Pulmonary stenosis initially no cyanosis is not present high
pulmonary flow cause eisenmenger and patient dies within 1 yr. If PS present cyanosis is present
and worsen progressively.

 Ebstein anomaly: Tricuspid valve is burried in RV ,RA dilation. Tricuspid valve problem. Exercise
intolerance may be dx [Link] dilation,Right bundle branch block,Wolf Parkinson White
syndrome. Treat CHF and arrythmias.

 Single Ventricle: w transposition of GA,Both Av valve open to a single ventricle

-If PS present clinc like TOF

-If no PS clinic like large VSD+CHF

 Hypoplastic Left Heart Syndrome:In fetal life with presence of ASD or PFO, PDA drived systemic
circulation maintained. After delivery PDA closure cause rapid cyanosis,acidosis and shock
developes must be treated immedeatly. Start PGEI,O2,HCO3 and surgery is required.

 Pulmonary Atresia:No developement of Pulmonary valve , fibrous membrane blocks RA pulm art
connection. PDA is insufficient for after delivery life, if not treated with urgent invasion patient
dies in days from hypoxemia and respiratory failure.

Acute Gastroenteritis
 Diarrhea increased defecation and liquid consistecy. Mostl 0-5 [Link] dehydratation risk in
neonates and [Link] to increased secretion or impaired [Link] children >3
defecation per day in liquid consistecy.

 Secratory Diarrhea(small intestine):Increased fluid and electrolyte secretion due tolaxatives

PGs,bactrial toxins etc. Fecal sodium >90 mmol/L,don’t contain leukocytes,do not respond to
fasting. Cholera,ETEC.

 Osmotic Diarrhea(Small intestine): Watery [Link] to mucosal surface loss or increased

osmotic load(carbohydrates lactulose PEG etc.).Seen in short intestine syndrome or mucosal

34
 [Link] responds to [Link]’t contain [Link],Giardia Lamblia,laxative
use.

 Inflammatory Diarrhea(Colon):Seen with mucosal invasion,inflammation,ulceration Exuda in

lü[Link] consist of clood and mucus(dysenteria feces).Feces contain [Link]
Shigella,Yersinia,campylobacter,entamobea histolytica,[Link].

 Peristalsism problems

-Hypomotility:upper small intestine flora proliferation may occur

-Hypermotility:Decreased liquid pass time in small intestine cause decreased absorbtion.

(thyrotoxicosis,dumping syndrome (after gastric surgery),some infections,irritable bowel)

 Fever is usually associated with inflammatory diarrhea but may be due to dehydration or
concurrent infetions.

 Rotavirus :Most common cause of acute diarrhea<2 [Link] vaccination [Link] and
vomit 1-2 day in prodromal period followed by 5-7 days diarrhea,risk of [Link]
secondary disaccharidase insufficiency,cause osmotic [Link] intolerance may prolong

 Norovirus:>4yrs,vomitting prominent,no leukocytes 2 days diarrhea,abundant watery light color

diarrhea

 Adenovirus:8-10 day incubation,5-12 days diarrhea clinically mimic rotavirus.

 In isolated secratory diarrhea promoted by enterotoxins(food poisoning) systemic symptoms are

uncommon. However systemic symptoms like fever, myalgia and tenesmus is usually present
with mucosal invasion of infections.

 Salmonella:chiken,egg,[Link] [Link],<6mo and sickle cell anemia patients

tend to develope more severe complicated [Link] and leukocyte [Link]
findings with [Link] [Link] diarrhea hard to differentiate from bacille
[Link] for septicemia(hyperpyrexia,bradycardia,splenomegaly,petechial
rash,meningismus)

 Shigella([Link]):Shigatoxin [Link] protein synthesis is cytotoxic. Shigatoxin is

neurotoxic it may cause [Link](bacilli dysenteria).High fever and toxic
[Link] diarrhea intial then proceeds mucus and blood [Link] with 5 day
ampicillin or trimethoprim-sulfamethoxazole.

 [Link] EHEC and EPEC has low minor infective [Link] water or food.

-ETEC: (secratory diarrhea),travellers diarrhea,common in infant in developing cuntries,water

and electrolyte loss,risk for dehydration

-EHEC: Shiga-like toxin,hemorragic toxin,starts with watery diarrhea proceeds to hemmorhagic

colitis with abdomina [Link] is [Link] cause hemolytic uremic
syndrome(microangipathic hemolytic anemia,thromboctoenia,acure renal failure triad)

-EPEC:Fist 2 [Link] blood mucus containing diarrhea,no fever. Epidemics in neonatal services.

35
  Campylobacter Jejuni: Fecal [Link]>7 days,Crampy abdomianl pain.
Mucus,blood,[Link] [Link] with Guillan Barre syndrome
dvelopement(acute inflammatory demyalinaztion neuropathy,weakness start from lower
extremitiees and escalates)

 Yersinia Enterocolitica:Dysenteryform,watery or malabsorbtion [Link]

firt 3 yrs.7-10 day [Link] symptoms and diarrhea. Abdomen is hyprsensitive maybe
mistaken as [Link] in colonoscopy may resemble chron. Diarrhea may prolong to
[Link],arthritis,erythema nodosum may [Link] arthritis with HLAB27 type.

 [Link]<1 yrs asymp [Link] related

dairrhea(penicilin,cephalosporin,vancomycin,clindamycin).Pseudomembrane at colon
[Link] signs [Link] with metronidazole.

 Vibrio cholerae:Osmotic diarrhea,rice water stools,muscle [Link] progress to shock due to

severe [Link] <8yrs TMP-SMX,>8yrs with tetracyclines.

 Giardia:Chronic Diarrhea,bloating,weight loss,fatty foul smelling persistent diarrhea. No blood or

leukocyte. Treat with metronidazole

 [Link]:Amobean Dysenteria,colon infection,acute bloody diarrhea wih mucus,fever

uncommon,occasionally leukocytes.

 Treat dehdration with oral rehydration Liquid with NG if severe IV

 Supplement with zinc

 Provide dietary modification,probiotics.

 Morphine and codein contraind in children for diarrhea trx

 Antibiotic for indicated organisms.

Mumps Diptheria Tetanus Pertussis

 Mumps:Paramyxovirus,5-9yrs befor vaccine but now adolescent and young [Link] and
saliva spread route through respiratory [Link] gland is most commonly affected but other
tissues can involved too.14-24days incubation. Parotids are painful and increased by salivaitng
events like seeing [Link] of mandible no longer [Link] in acute disease,increased
serum amylase and [Link] are:sensorineural deafness(most
common),meningoencephalomyelitis,orchitis-epididymitis,oophoritis,pancreatitis,thyroiditis,
optic neuritis,[Link] specific treatment just supportive,vaccine at 12th month and 4-5 yrs.

 Tetanus([Link]):Neonatal-Non neonatal(traumatic injury).Tatanus toxin inside motor neuron

block neurotransmitter relaese and cause paralytic ilness by preventing the inhibition of
antagonistic muscles so the involved muscle stays at full contraction.

36
 1) Localized:rare form near the trauma region,commony transform to generalized

2) Generalized:more common,trismus,headache,irritability,stiffnes,dysphagia,sardonic
smile,opistotonos,laryngeal and respiratory muscle spasm cause airway
[Link] is concious,slightest touch trigger tetanic spasm,defecation and
urination affected,sensory nerves are [Link] followed by
hypotension,arrythmias,tachycardia,resp [Link] severe in 1st week and start to
resolve at 2 nd week,trismus lastly [Link] die till day 10

3)Cephalic:Most severe form,poorest prognosis, Retracted eyelids + trismus +  risus

sardonicus + spastic paralysis of tongue and pharyngeal [Link] to generalized
form 

4)Neonatal:3-12 days,difficult feeding,excessive cry,paralysis or diminished

movement,stiff to touch.

Diagnosis made clinically,CSF normal.

Treatment:Penicillin G,metronidazole (for [Link] erad.),TIG(tetanus IG for toxin

neutr),IVIG,TAT,Diazepam(seizure and spasm control),muscle relaxants,neuromuscular
blockers,baclofen in ICU.

Favorable prognosis w long incubation period,absent fever,Poor prognosis early trismus

and generalized tatany.

37
  Diptheria:Acute toxoinfetion,respiratory transmission,2-5yrs,2-4 days incubation, Toxin
A →initiating protein synthesis in the cell,Toxin B → to cell receptor → tissue necrosis →
patchy exudate initially be removed As the toxin production increases → the area of
infection widens and deepens  and a fibrinous exudate develops → tough adherent
pseudo-membrane is formed that varies from gray to black → attemps to remove it are
followed by bleeding.

Types:nasal,tonsillar/pharyngeal(most common form),cervical lymphadenitis(bulls

neck),laryngeal,cutaneous,conjuctival,aural.

Toxin spread through lyphatics and hematogenous and can cause,myocarditis(10-14

days),peripehral neuritis(3-7 weeks)

Dx made clinically and with culture. Anemia seen due to rapid hemolysis.

Trx:IV diptheria antitoxin,Penicillin or Erythromycin,end is with three consecutive

negative [Link] diptheria require [Link] adn 2-3 wk bed rest.

Myocarditis,renal failure,thrombocytopenia,leukocytosis>25000 indicate poor prognosis.

Td,DT vaccination for immunization and booster for close contacts.

 Pertussis(Whooping Cough):Bordatella Pertussis,stubborn,spasmodic cough

[Link] antigens not protective neonates under risk. Pertussis toxin
Peribronchial lymphoid hyperplasia → necrotizing process Bronchiolar obstruction and
atelectasis ← accumulation of mucus secretions and also liver is fatty infiltrated. May be
complicated by bronchiectasis,cerebral hemorrages,cortical atrophy.

Cough more than 2 weeks,10-15 consequitive repetetive cough pattern,posttussive

emesis are typical for diagnosis.

IV hydration and O2 support and macrolides are the mainstay of therapy.

38
 <3months,prematures and complicated illness should be [Link] and CNS
complications are the most [Link] vaccine is for immunization.

 Rickets:Disease of defective growing bone due to impaired vitD,Ca and P

metabloism. D2(storage form seasonal var),D3 (active form no seas. Var.)

39
40
 Treatment:

-Give Vit D replacement if Vit D deficient,don’t give stss therapy <3 yrs

-If calcium Deficient Rickets ensure calcium intake 1000mg per day.

-Type I vit D dep Rickets: calcitriol+ca

-Type II high dose calcitriol and calcium

-Phospophenic rickets:give elementary phosphorus

Cushing
Iatrogenic or exogeneous is most common.
Most common endogeneous one is Cushing
Syndrome in>7 yrs but in <7 yrs adrenal causes
predominate

41
 -If spot test for ACTH is high,
confirmed ACTH dependent Cushing sella
MRI is indicated.

42
Adrenal Insufficiency

Diabetes Insipidus

43
 Celiac
Type of humoral and cellular
immunity mediated enteropathy
which is triggered by gluten in
genetically sensitive (HLA-DQ2
and HLA-B8)individuals.

Cerebral salt wasting due Villous atrophy related

to trauma or surgery malabsorption is the
consequence of disease.

Diagnostic Tools

44
-Villous atrophy,hyperplastic crypts and lymphocytic infiltration in intestinal
biopsy Histological eamination according to Marsh Score(gold standard)
-Serology

45
 Symptoms

Treatment

-Only treatment is lifelong gluten free diet, even one gluten containing diet
can bring the symptoms back.

Approach to Immune Defficiencies

46
 

47
48
 -marked decrease of IgG and marked decrease of IgA with or without low IgM levels
(measured at least twice;<2SD of the normal levels for their age)

 Hyper Ig M syndrome:Low IgG,IgA,IgE, high IgM. Defective CD40 ligand. Increased

susceptibility to bacterial infection particularly in lungs (Pneumocystis carnii)
 X-linked Agammaglobulinemia: Congenital defect (Btk mutation), absent B cells,
IgA,IgM,IgE absent small amount of IgG due to maternal antibodies, require large
amounts of Ig replacemnt to remain healthy. Recurrent pyogenic infections.
 Severe Combined Immunodeficiencies(SCIDs):Heterogenic group of monogenic
disorders.

X linked most common

type-absent Tcells

SCID- Adenosine
Deaminase
Deficiency:Defect in salvage nuclotide [Link] dATP,d-GTP
accumulation result in imparied developemnt and reduced lifespan of T and
B cells.

49
50
51
 Wheezing Infant

52
  Most common causes of wheezing in ifants are asthma and viral respiratory infections.

 Atophy and Lower respiratoy viral infections(RSV,rhinovirus) <3 yrs increase the risk of allergic
sensitization mediated asthma in following yrs.

 The location of wheezing (unilateral, suggestive of a foreign body or bronchomalacia, or

bilateral, suggestive of a more generalized process) 
 Wheezing and crackles (suggestive of an interstitial lung component including infection,
bronchopulmonary dysplasia [BPD], or pulmonary edema with congestive heart disease)
 Majority of childhood wheezing attacks disappear,minority transform to asthma 15%.

 Children with recurrent wheezing attacks should be assed with Asthma Predictive Index API.

 Differential Diagnosis of astma include followings:

53
  Body box pletismograph for respiratory examination of infants instead of pulmonary function
test.

 FB aspiration usually located at right main bronchus due to it’s anatomical course.

Cystic Fibrosis

 CFTR genes are mutated in both alleles.

 Deranged transport of chloride and/or other CFTR-affected ions, such as sodium and

bicarbonate, leads to thick, viscous secretions in the lungs, pancreas, liver, intestine, and
reproductive tract, and to increased salt content in sweat gland secretions 

54
  In neonatal presentation, hyperechogenic fetal bowel in USG, evidence of meconium
peritonitis(scattered calcifications in peritoneum).

 Respiratory function tests are consistent with obstructive lung disease

 Sweat is very salty due to high chloride content

 Patient is hyponatremic,hypochloremic and has metabolic alkalosis.

 Sweat test for neonatal screening at least 2 occasional sweat chloride>60mmol/L. Other
suggestive test are CFTR gene test and abnormal nasal potential difference. Together with these
tests there should be at least one organ or system showing symptoms consistent with CF.

 Pancreatic exocrine function can be evaluated with fecal elastase level, low levels are suggestive
for pancreatic insufficiency.

Treatment

 Antibiotics: 
 oral, intravenous, aerosolized (aminoglycosides, carbenicillin, ticarcillin, colistin.

 bronchodilators

 anti-inflammatory agents (corticosteroids, NSAIDs)

 mucolytics: recombinant human DNase (Pulmozyme) hypertonic saline 

 chest physiotherapy 

 transplantation 

 high-calorie diet (35-40% fat) 

 Pancreatic enzymes: Creon 

 Vitamins A, D, E, K 

 salt 

 ursadeoksikolik acid 
 liver transplantation

 future therapies: gene therapy

Viral Paralytic Diseases

55
  POLIOVIRUS (ENTEROVIRUS TYPE)

-Fecal oral route from intestinal tract to CNS

cause aseptic mengitis and poliomyelitis,
extremely resistant to enviorement in room
temp.

56
57
58
 No specific treatment, only
supportive care. (analgesics,
respiratory support) every IM shot
and surgical procedure is
contraindicated during the illness.

 Affected muscle do not Show progression after 6 months, any residual weakness or paalysis
means permanent. Disease do not affect sensory nerves.

59
RABIES
 Zoonosis from rhabdoviridae family

 Infected saliva inoculation,distrupted skin integrity, from rabid animal

 1-3 months incubation, virus disseminates to brain via axonal routes(retrograde fashion)

 Proximity to head determines the symptom onset time.

 No specific diagnostic tool,PCR Works from saliva but slow. Late brain MR lesions.

 No treatment available once the symptoms appear.

Guillan Barre Syndrome

60
(Albuminocytologic dissociation)

61