Gems Pediatrics

Short Cases
PEDIATRICS-CASE FORMAT
Name: sexr address:
Age (precisely in months for small children), DOB (date of birth)
Informant (reliable or not)
Presenting Complaints
Mention in chronological ord.er (e.g. fever-S days, cough-a a1y+ breathlessness-1 day)
History of Present Illness

Onset, duration, progression, associated symptoms, aggrevating or relieving factors, present status
(you should be able 6 say the relevant negative history in respect to case, try to make negative history into positive)
History of Past Illness

. Any history of similar ilbress in past
. Any history of vaccine preventable illness in past-measles, mumps,TB, pertusis
. History of asthma, jaundice, seizure, previous hospitalization
Antenatal History
. 1st trimester l
. 2ndtrimester I Look obstetrics case format-tell relevant history only
. 3rd trimester )
(If no relevant history, we can write as 2nd child of non consanguineous marriage without any previous history of
abortion)
At least this should be asked-regular antenatal checkup folic acid, TT complication (any)
Natal History 'Postnatal History

o Whether term/preterm . Baby cried soon after birth
. Home/hospital o Put to breast immediately after delivery/within how many
. Normal labor /CS,if CS-indication hours
. Birth weight . Any resuscitation
o Jaundice, seizure
. When was urine passed - normally within 48 hours
. When was meconium passed - normally within 24 hours
GEMS-A Golden Endeavor for Medical Students
Developmental History
. Day of dischaige
. Read chapters of development (milestones) (do not forget to ask hearing and vision)
Dietetic History
o \zVhether prelacteal food given/not
o When put to breast
. Exclusivelybreastfed/not
o Complementary feeding started at with-
o Started sharing family diet at-
-month
. Any history of food allergy
. The child has getting ... calories (expected is ... calories, and there is a gap of ... calories)
. The child has getting ... gm protiens (expected is ... g, and there is a gap of ... g) as per ICMR
o Diet rich in fruits and green leafy vegetables
. Any diet modification advised
Item Kcal Protein

'Cooked rice L cup . 175 4
Uncooked rice 6 tsp 100 2
Dosa 1 70 2
Iddty 1 50 2
Chappathi 1 70 2
Puri 1 35' 1
Uppuma l cup 250 6

.-- \
Bread 1 slice 70 2
Pathiri 1 50 1
Porotta 1 100 J
Biscuit 1 20 0.5
Puttu 50 2
Vadai 1 50 1
Banana 1 100 1
Plantain 1 50 1
Fqo
--bt 1, 80 6
Mutton Loz 50 6
Beef Loz 30 6
Fish 1, 80 6
Sardine (mathi) 1 30 3
246 Cows milk 100 mL 70 3.5

Human milk 100 mL' 70 1.5
Volume at 6 months 600-700 mL
Volume at L year 400-500 mL
Pappad 1 tsp 20 0.5
Cooked dhal 1 tsp 8 0.5
Smash, 50 40 0
Short Cases
Item Kcal Protein

GLV .
t help 50 0
Upperi L cup 10 0.5
Sambar 100 g ,50 2.5
Fruits 100 g 60 0.5
Coconut 1 tsp 4M 4.5
Stgar/ jiggery 1 tsp 20 0
Oils/ghee 1 tsp 36 0
Lactogen 100 g (6 tsp) 100 kcal 2g
Ragi 100 g (6 tsp) 100 kcal 3g
Amritham 100 g (6 tsp) 130 kcal 3.5 g
Lactogen: L:r 100 mL (1/z glass) boiled and cooled water add 3 spoon of lactogen (for 30 mL water 1 tsp)
Working formula for calories (bedside calculation)
At 1 year 1000 calories, after that add 100 calories for ev
iup of tea/ coffee containing Yz glass milk and 1 tsp sugar will give 90 kcal 3.5 g protein.
cup tea containing t/e, glass milk and 1 tsp sugar will give 55 kcal and 1.75 g protein.
Holliday and Segar formula for calculation of calories and fluid o lteaspoon-5mL
. RDA-> for expected weight of child Fluid-> for present o 1 tablespoon - 15 mL
weight . lcup-200mL
. Up to 10 kg - 100 kcal or mlleach kg . 1 tumbler - 250 mL
o 10-20 kg - 1000 + 50 kcal or mllkg for each kg >10 kg
. >20 kg - 1500 + 20 kcal or mllkg for each kg,>20
NEW ICMR
0-6 months 1,.76g/kg 92kcal/kg
6 months to 1 year L.65 g/kg 79kcal/kg
L,2,3 years 15.7 g 1036 kcal
4,5, 6 years 20.3 1350
7,8,9 years 29.3 1690
10,11.,12 male 39.3 2189
Femal 40.4
__ 2008
OLD
0-6 months 2.05 g/kg 108 callkg
6 months to L year 1.6s g/kg 98 cal/kg
1-3 years ))q
--b 1240 cal
4-6 years 3og 1.690 cal
7-9 yearc 419 L950 cal
10-12 years male 549 57 g (Female) Female -1970 cal
Male -2190 cal
Immunization History
. Fully immunized to date according to National Immunization Schedule
r Look for BCG scar
o Last vaccine taken
'r Any optional vaccine
If not taking vaccine, why?, pulse polio?
Family History
o Draw pedigree chart
.' 49" of parents, consanguinity

Similar illness in family
. Chronic illness in famiiy
SES
. Occupation of parents
o Income
. Housing
r Education of parents
o Sanitatiory environment, ApL or BpL
r Financial supports (RSBY, thaloalm)
GENERAL EXAMINATION TCODE-GVHAD]

I. General suryey
cooperative, bedridden, playful and active
__ -Con-scious,
I{. Vitals
a' Pulse: rate, rhythm, volume, character, other peripheral pulses,
femoral pulse palpab
delay
le / not,radiofemoral
Ag" Pulse rate

Newborn 120-1.60
Up to l year 120/mn For practical purpose tachycardia is
Up to 5 years 100/min 1. NewbOm >200/mtn
Up to 10 years go/mn 2. Infants >150/min
>10 years 80/min 3.r Older child >120lmin
b. Blood pressure: refer AGN
c. Temperafure:
d. Respiratory rate:
Age Normal RR Tach54rnea

Newbom 40/min ' Age group RR
Up to l year 30/min
Up to 5 years
>2 months 60 or more
20/min 2-12 months 50 or more
Up to 10 years 18/min 12 months to 5 years 40 or more
>10 years 18lmin >5 years > 30
p-n t9 0 years in female and all males , Gurin females 7- thoruiJEtlj
III. - Abdominothoracic, rrrvr.(
Head to foot examination
Head: Size
Shape
Anterior fontanelle- size, closed /not, bulging/ depressed
(measured
ly$:lryqjoining the midpoiits"or u,,i, opplrit" ria"r;
try to include PICCLE in head to foot examination
248 -Hair: Hyperpigmentatiory sParseness, alopecia (PEM features-refer
chapter nutrition), low hair line,
pyoderma
Face: Any dysmorphism
Pallor, jaundice, signs of vit A deficiency, cataract,
-El"tt Any hypertelorism, slant
Ears: anomaly, low set ears
DNS, polyp, depressed nasal bridge
fos.e
oral cavity: Hygiene,
{u$,r.o", cheritis, g'iossitis,. stomatitis, tonsils, caries, lips, palate
Neck Lymphnodes,fVp, shortneck, ilebbing
Chest: Shape, wide nipple
ll1b* U /L-pallor, clubbing, flat nail L/t _edema, (look for BCG scar)
Abdomen: Distended, dilated vein
Genitalia:
Skin: PEM, neurocutaneous markers, pyoderma, rash
Spine: Any deformities
Notes:
1. Macrocephaly - causes (> 2 SD)
Hydrocephalus, hydrencephaly, rickets, achandroplasia, hemolytic anemia, familial
2. Microcephaly - (> 3 SD)
Primary:Present since birth and causes ar'e inherited - For example, Down's slmdrome, cranioslmostosis
- Secondary: Due to an insult to growing brain - For example, TORCH infections, malnutrition, IU toxin
- Drugs: Phenytoin, steroid
3. Anterioi fontanelle: time of closure of anterior fontanelle is7-19 months
- Early closure: Craniostenosis or craniosynostosis, primary microcephaly
Delayed closureolAF: Rickets, hypothyroidism, hydrocephalus, mucopolysaccharidoses
- Bulging AF: Ne#born on crying, hydiocephalus, increased intracranial Pressure, pseudotumor cerebri
4. Posteriorfontanelle:
- Closes completelY bY 2 months
It may be open in Down's slmdrome
-5. MacE{ven's sign - make sure that fontanelle is closed
Cracked pot sound on percussion of the skull. Present in hydrocephalus, increased intracranial Pressure or
suture separation
6. Canthal index Ratio of the distances between the inner and outer canthi of both eyes multiplied by 100.
Normal is 33-38.
Interpupillary distance: Distance between centres of the pupils of both eyes measured with child looking
upward
Hypotelorism: spacing between eyes is less than normal, canthal index <33
Hypertelorism: Abnoimally wide spacing of the eyes with broadened bridge of nose, usually due to
maldevelopment of the sphenoid bone. Canthal index >38
Slanting oI uyest Difference in levels between inner and outer canthi of the eyes
fUangoioid slant: Slanting downward from lateral to medial canthus/upward slanting of eyes, for
example, Down's slmdrome
7. Low set iars: With patient standing straight, an imaginary line is drawn from the inner canthus, parallel to
floor. Normally thisline crosses the ear in such a way that superior attachment of pinna should be at or above
that line.
8. High arched palate: Ask child to stand straight,look forward and open mouth. Normally the posterior part of
the palate is easily visualized. In high arched palate one cannot visualize the posterior part of the palate. For
example, Marfan's slmdrome, Down's slmdrome.
9. Hess test: To assess the capillary fragility. The sphygmomanometer cuff is tied on the arm and the pressure
is elevated to.a point in between the systolic and diastolic BP for 5 min. The appearance of purPura on the
forearm should 6e noted. The test is said to be positive if >20 petechiae apPear in a 2.5 cm2 area. Test is positive
in - poor platelet function, thrombocytopenia, scurvy.
10. Lymphadenopathy:
r Significant LNE - if any of the following factors are present
- Size-inguinal nodes >1.5 cm diameter, cervical and axillary nodes >1 cm diameter, epitrochlear 249
nodes-any size
Site - multiple sites
Matted nodes
Nodes which are red/tender/ulcerated
Associated with focus of infection
- Associated with systemic signs and symptoms
r Generalized LNE-involvement of >2 non-contiguous ly-ph node areas due to systemic disease
fV. Anthropometry
1. Weight (most reliable criterion of assessmnt of the health and nutritional status of children)
f"r* tyla weighing scale, electronic weighing.scale for infants' bathroom fire
In fieldconditi5ns, Salter spring scales are used
Birthweight-3kg Quadraples-2Year
o .. 5times -3year
Newborns loses 10% ofweight during 1st 7 days
. By 7-10th day regains birth weight
e 6times-5Year
'. 7 ti*", -7 year
. Weight doubles--4 months
.' 10 times - 10
Weight gain Formulas

. 1.,2,3months 309/daY . 3 months to 1 year: (x in month +9)/2
. 4,5,6 months 209/daY . 1.-6 years: 2x in Year +8
. 7,8,9 months 159/ day . 7-liyears: (Txtnyeat-S) /2
. 1.0, 11, 12 months 129/ day (Weech's formula)
L SD = L2,5"/" of valuq
IAP classification:
Weight for age Wellcome trust classification:
Normal >80% Weight for age Nutritional status
Grqde 1 71-80% 60-8-0 % + noedema Undernutrition
60-80%+ edema Kwashiorkor
Grade II 6L-70%
<60"/" + no edema Marasmus
Grade III 5L-60%
<60"/"+ edema Marasmic
Grade IV <50"/"
+ k = edema
kwashiorkor
2. Height:
(1en[th-below 2years-Infantometer) {
(H"ryht - above 2years - Stadiometer)

Makethechildstandbarefeetonalevelfloor,feetslightlyseparated
in contact with the\^/all
- Heels, buttocks and back arebrought rootr airectly forwgd with the Frankfurt plane (line joining floor
of
the
- Head is so positior,ua ,o that*h" "lilaof the orbit) and the biauricular planehorizontal'
external auditory;;;t i; floo.
the point using pencil
- A firm cardllong scale is kept firmly over vertex to compress the haiiand
- Remove the child fixed drawn point'
- The 0 of the tape is fixed at the floor and is measured upward to the
Birth 50 cm
6 months 62cm Rate of height VelocitY
1 years 75 cm L,2,3 month 3.5 cm/month
2years 87.5 cm 4,5,6 month 2 cm/month
3 years 94cm 7,8,9 month 1.5 cm/month
4 vears 100 cm 10,11.,L2 month 1.2 cmlmonth
1 SD = 4% of value Weech's formula

Short stature---red.uction inheightby >2 SD ftom notmal r{t(2-L2)
Waterlow grading of wasting based on weight for height
=Aqex6+77
Waterlow grading of stunting based on height for age

>95% Normal
>90% No wasting
90-95% Grade I stunt
80-90% Mild wasting
85-gO% Grade II stunt
< 85% Grade III stunt
7 0-80% Moderate wasting
WHO classification
Moderate malnutrition Severe malnutrition
Symmetrical edema NO YES (edematous malnutrition)
Weight for height SD score between SD score <-3 (<70%)
-2 to -3 (70-79%) (severe wasting)
Height for age SD score between SD score < -3 (<85%)
-2to -3 (85-89%) (severe stunting)
Observed value - median reference value Weight Height

SD score(Z) = Double- 4 m Ayear
SD of reference population
Triole- 12 m 12year
3. Head circumference:
Ideally use a fiber glass type
Tape should encircle the most prominent part of the occiput and the supraorbital frontal area
- The occipitofrontal HC is measured by the overlapping technique
Birth 35 cm 0-3 month 2 cm/month
,3 months 40 cm
6 months 43 cm 4-6 month 1cm/month
1 year 45 cm
3 years 4549 cm 6-12 month 0.5 cmlmonth
4years 4849 cm 1,-2year 2 crn/year
5 years 49-5L cm
l2years 52 cm 2year 0.5 cm/year
Dines formula-for estimating HC in first year of life
(length in cm + 9.5) +/ - 2.5
2\
> adult size reached between 5-6 years
Microcephaly: Reduction in HC by >3 SD from normal
1 SD = 2.5/" of value (approx 1 SD = 1.25 cm)
Macrocephaly: Increase in HC by >2 SD from normal
Chest circumference:
- Keep the child in recumbent position
- Measure at the level of the nipple, midway between expiration and inspiration
Atbirth 31cm
HC=CC 1 year
After l year CC >HC
In malnourished case CC is < HC even beyond 1 year.
Mid-arm circumference:
Measure using fiber glass or steel typ9, use the overlapping type. While the child sitting, semiflex his
Left upper limb at the elbow and mark the midpoint betweenlcromion and olecranon process.
Then take measurement in extended position
Age independent criteriabetween 7-S year
Arnoldis classification:
>13.5 cm - Normal
At birth 11-12 cm 12.5 - 13.5 cm - Moderate PEM
At 1 year 15-16 cm <11.5 -sAM
Shakir tape: Plastic tape with colored zones - greery yellow and red
Green - 13.5 cm
Yellow -125 - 13.5 cm
Red-<12.5cm
with an inner diameter 4 cm up the rom iI

?tTilg;t*l;:f,;H{ffi:;g a bangre
malnourished
' t#;?"Ki::;i,
HfflilH",rl"'lffi"nt
betory 6 m-
*"-elllepresentativ: "{'1",::-'1:*::f::'^"i-t*:}',i?ffffiffi*
ir""" il;;;;;;;Jerely malnourished it mav rall
Mid-arm circumference/head circumtrerence

a. Kanawati and Mclaren's index 2 (incrt)Ixlffi
b. Rao and Singh's index i*"ign, (in kg)/height increase 1'6 (in cm)
weift t (in tcg)/treigttt increase
C. Dugdale's index
d.
4.Quacksfick:Quackerarmcircumferencestick'Itisarodwith2setsofmarkings,
other MAC for the corresponding h"'ght'
iil
u'*.lit*tt:::^:t-:"iXt:*,T*
AC, child is *1;]fr
marno*lffi
;i:"JXf;J:;,,4:;T.EfflT"t:;iH".p*i"Jn"ight ror,,'"u,,,"d
Upper,"gm",t'Low.e1sesm.en|T"1io-,.^-.r^.+^^+al-|l_
:t'Sh;e; iaken if the fatient is too short or too tail
- f.d - from pubic symphasis to sole of foot 6 month IJB
- US = Height-LS stature-USlS ratio is normal for age l year ryI
- f-p*,iJnate short Zyears r-firr::"ii
3years Ifl
. Cau"es-fami1ial, constitutional 4 years I >t
IUG& nutritional defi ciencY 5 vears Lffl'
- Endocrine disorders - GH deficiency' zJ:loy"urc rfl
. Cushing's slmdrome Adult l:l il
Misc - McCune \
'-,
not normal for age
Disproportionate dwarfism-S:LS ratio is
Types:
imperfecta,
1. Short limbs _ Achondroplasia, rickets, osteogenesis
chondrodYsPlasia
2. Short trunk - fvfu"ofofytuc"ttutidotit' *"oliPidot
tips of middle fingers of both arms when the
arms are outstretched atrt|I
7. Arm span: It is the distance between
a.rgtes to the body facing away from wall'
Bqlow 5 years 2cm<height
5-10 yeais L cm < height
Atl0years arm sPan = l"igl'
Above 10 vears arm > heightby2cm
Armspan>height_Marfan,sslmdrome,klinefelter,sslmdrome,Homocystinuria
Arm span < trei[trt-Achondroplasia' cretinism
V. DeveloPmental assessment
252 systemic examination: Refer medicine caseformat...
NUTRITION
food'
It is the Process by which organism utilizes
1. Macronutrients
2. Micronutrients Food
Macronutrients (Proximate principle or major nutrients) 1. Energy Yielding - CHO
Main components are: 1' Carbohydrate 2. BodY building - Protein
2. Protein 3. Protlctive - vitamins and minerals
3. Fat
Short Cases
CHO and protein will provide 4kcat/ s

Fat will provide 9 kcal/g
Protein
Nitrogen intake --> Nitrogen absorbeil -+ Nitrogen retained
Kilocalorie- amount of heahrecessary
N"btotb"d temperature of 1 kg of water by
Digestability coefficient = , 100 t9 1q"
1oC from 14.5 to 15.S.C
N, intake
N, retained
BV= x 100
N, absorbed
NPU =
TDx BV Retained N x 100
or
100 \ intake
_ No. of mg of particular aminoacid per gram of protein

Amino acid score
. No. of mg of that AA per gram of egg protein
Energy from protein
ProtJin energy r.atio -- x 100
Energy (total) derived from food
Essential Amino Acids

TT HALLIM VP Fats
o f - Threonine r Essential fatty acids
o f-Tryptophan 1. Linoleic acid (ror)
o f[ - Histidine only in infancy 2. Linolenic acid (rrlu)
o { -Arginine 3. Arachidonic acid
r | - Lysine o Functions
o | - Leucine - 1. Antithrombotic
o I - Isoleucine 2. Antivasorestrictive
o \z[ - Methionine - 3. Antihypertensive
o ! - Valine 4. Antiarrhythmic
r P-Phenylalanine 5. Anti-inflammatory
Fiber
r Fiber includes polysaccharides such as cellulose, hemicellulose,
t Eunctions:
pectin and lignin.
1.
Maintains growth of normal intestinal flora
2.
Elimination of waste
3.
Essential for normal functioning of gut
' [RDA: Range of acceptable or saie iniake levels has been formulated based on the current knowledge
of
._ nutritional requirement of different age and sex]
[Balanced dieft one which contains a viriety of al.o such quantities and proportion that the need for
amino acid' vitamins, minerals, carbohydrate, fat and I energy,
other nutr'ients adequateiy;Jf.l
and general well-being and also makes a smallprovisio.r qrrintaining health vitality
ror extrunutrienti to #ithstand short duration 2s3
of leannessl
COMPLEMENTARY FEEDING (WEANING)
lo breast milk (excrusive breastreeding up to 6 months). rdear weaning
F'Jffi[tTi*;l^n:X'#i:lt"'If
1. Culturally acceptable
2. Physiologicallysuitable
3- Eagily prepared at home with the existing facilities
. to provide all nutritional requlrements of the infant with
respect to energy, proteins, vitamins and
*ff"t;ite
B enefit s o f br e a stf e e iling :
o Benefit to baby:
1. Nutritional superiority
2. Immune superigrity
3. Higher IQ
4. Protection from allergy
' i:Tlil:il:TJ,. presnancy (lactational amenorrhea)
2. Reduced severity of PPH
3. Helps in uterine involution
4. Prevents cancer (ovarian and breast cacncers)
5. Helps in shedding of extra weight of mother
. True contraindication for breastfeeding is when mother is on anticancer drugs, galactosemia and phen
Protein Energy Malnutrition (PEM)
Definition: Range of pathological condition arising from coincidental lack in varying proportions of .proteins
calories occurring most frequently in infants and young children and commonly associated with infection
Clipical Findings of Marasmus and Kwashiorkor
Occurrence More common Less common
Edema +
Activity Active Apathetic
Appetite Good Poor
Liver enlargement +
Mortality Less than kwashiorkor High in early stage
Recovery Recover early Long to recover
Infection Less prone More prone
,\
Marasmus - Monkey facies, BagW pants appearance
Grading of marasmus
- wasting axilla and groin
Grade I
II - I+ thighs and buttocks
Grade Grading of kwashiorker
III - II+ chest and abdomen
Grade
I. Pedal edema
IV - III+ buccal pad of fat
Grade
2. 1,+ facial edema
Kwasiorkor-Hairchanges: Hypopigmentation (lightcoloredhair) 3. 2+paraspinaland

Sparse hair (alopecia)
edema
Easily pluckable hair 4. 3 + ascitis
FIag sign
Straight/Brittle /Coarse/ Lusterless /Dry
Nail changes: Brittle nails, paronychia/platynychia/koilonychias
Skinchanges: Pigmentation,desquamation, dyspigmentation
Marbling/Mosaic pattern
Crazy pavement sign
Flaky paint dermatoses
Enamel paint dermatoses (buttock, perineum, upper thigh)
Edema
254 Shiny skin
Infection (like scabies, pyoderma)
Ulceration
MANAGEMENT
Mild and Moderate Severe
Treatment-giving adequate amount of: L0 step management
Protein and energy
150 kcal/kglday
Protein-3 g/kg/day
Usage of oil and fat rich foods
Give milk (if the child drinks tea without milk, add milk to it)
Short Cases
10 step management
Steps Stabilization Rehabilitation
Daysl-2to days3-7 Weeks 2-6
1. Hypoglycemia
2. Hypothermia
3. Dehydration
4. Electrolytes
5. l:rfection
6. Micronutrients No iron With iron
7. Initiate feeding
8. Catch up growth
9. Sensory stimulation
10. Prepare for follow
1st 6 steps can be easily studied by the mnemonic: "SHIELDED-
S - Suger deficiency, i.e. hypoglycemia
H - Hypothermia
I - Infection
EL - Electrolyte imbalance
' PE -
Dehydration
D - Deficiency of micronutrients
CEREALS
o Deficient in lysine, threonine and tryptophan
I Rice-100 g gives 350 kcal, 7 g proteins. It is deficient in lysine. Polished rice causes beriberi
r Wheat-100 g gives 350 kcal, 11 g proteins. It is deficient in lysine and threonine
' Ragi-100 g gives 350 kcal, 7 g proteins ,3.1.4 mg Ca,3.9 mg Fe and Iodine. It is a weaning food. Maize-it has
high leucine content. It interferes with the absorption of niacin, vitBr: causes pellagra.
PULSES
o Deficient in methionine, vit C (but germinated pulses contain vit C)
o Combined in the ratio of 1:4 with cereals (compiementary action of food)
o Green gram (cherupayar) 350 kcal, 24 g protein
r Red gram (unakkapayar) 350 kcal, 20 g protein
. Black gram (uzhunnu) 350 kcal,24 g protein
r Bengal gram (kadala) 350 kcal, 17 g protein
o Soyabean 350 kcal,43 g protein
EGG
o Reference protein (BV = 100)
. 60 g egg contains 80 kcal energy 6 gfat 30 mg calcium
ECG deficient in:
6g protein L.5 mg iron 250 mg cholesterol
. CHO
o (Duck egg has increased amount of avidin which decreases the availability of biotin) . VitC
MILK
r Deficient in Vit. C and Fe 255
r Rich in Ca
VITAMINS
Fat soluble vitamins: (A, D, E, K)
VTTAMIN A Source
RDA Infant 350 pg (300-400)
. Animal - liver, egg, fish, liver oil
Children 550 pg (400-600)
o Plants - sp madi, amarnath carrot
Adolescent 750 pg
r Fortified vanaspati
B enef it s of b re astfe e ilin g :

. Benefit to baby:
1. Nutritional superiority
2. Immune superiority
3. Higher IQ
4. Protection from allergy
' i:TiX,l:il:ffi presnancy (ractational amenorrhea)
2. Reduced severity of PPH-
3. Helps in uterine involution
4. Prevents cancer (ovarian and breast cacncers)
5. Helps in shedding of extra weight of mother
r True contraindication for breastfeeding is when mother is on anticancer drugs, galactosemia and phenylketonuria-
Protein Energy Malnutrition (PEM)
Definition: Range of pathological condition arising from coincidental lack in varying proportions of proteins and
calories occurring most frequently in infants and young children and commonly associated with infection
Clinical Findings of Marasmus and Kwashiorkor
Occurrence More common Less common
. Edema +
Activity Active Apathetic
Appetite Good Poor
Liver enlargement +
Mortality tess than k-ashiorkor , High in early stage
Recovery Recover early Long to recover
Infection Less prone More prone
..'\
Marasmus - Monkey facies, Buggy pants appearance r-
Grading of marasmus Grade I - wasting axilla and groin
Grade II - I+ thighs and buttocks Grading of kwashiorker
Grade III - II+ chest and abdomen I. Pedal edema
Grade IV - III+ buccal pad of fat 2. 1+ facial edema
Kwasiorkor-Hair changes: Hypopigmentation (light colored hair) 3. 2 + paraspinal and chest
Sparse hair (alopecia) edema
Easily pluckable hair 4. 3 + ascitis
Flag sign
Straight/Brittle/Coarse / Lusterless/ Dry
Nail changes: Brittle nails, parony c}na/ platynychia/koilonychias
Skin changes: Pigmentation, desquamation, dyspigmentation
Marbling/Mosaic pattern
Crazy pavement sign
Flaky paint dermatoses
Enamel paint dermatoses (buttock, perineum, upper thigh)
Edema
254 Shiny skin
Lrfection(like scabies, pyoderma)
Ulceration
MANAGEMENT
Mild and Moderate Severe
Treatment-giving adequate amount of: 10 step management
Protein and energy
1,50kcal/kg/day
Protein-3 g/kg/day
Usage of oil and fat rich foods
Give milk (if the child drinks tea without milk, add milk to it)
Short Cases
1.0 step management

Steps Stabilization Rehabilitation
Daysl-2to days 3-7 Weeks 2-6
1. Hypoglycemia
2. Hypothermia
3. Dehydration
4. Electrolytes
5. Infection
6. Micronutrients No iron With iron
7. Initiate feeding
8. Catch up growth
9. Sensory stimulation
10. Prepare for follow
1st 6 steps can be easily studied by the mnemonic: -SHIELDED-
S- Suger deficiencp i.e. hypoglycemia
H - Hypothermia
I - Infection
EL - Electrolyte imbalance
DE - Dehydration
D - Deficiency of micronutrients
CEREALS
o Deficient in lysine, threonine and tryptophan
' Rice-100g gives 350_kcal, 7 g proteins. it i" d"fi.i"nt in lysine. polished rice causes beriberi
' Ifr:u'-100 g gives_350 kcal, 11 g proteins. It is deficient "in lysine and threonine
' Ragi-100 g gives 350 kcal, z g proteins ,,3.14mgCa,3.9 mgie und Iodine. It is a weaning food. Maize-it has
high leucine content. It interferes with the absoiption of niXcin,
vit Br: causes pellagra.
PULSES
o Deficient in methionine, vit C (but germinated pulses contain vit c)
o Combined in the ratio of 1:4 with (compiementary action of food)
r Green gram (cherupayar) ceieals 350 kcal,)4 g prot"'lr,
r Red gram (unakkapayar) 350 kcal,20 [ protein
. Black gram (uzhunnu) 350 kcal,2a I protein
o gram (kadala) 350 kcal, 17 ! protein
leng_al
r Soyabean 350 kcal, a3 [ protein
EGG
o Reference protein (BV 100)
=
. 60 g egg containr kcal energy 6 g fat 30 mg calcium ECG deficient in:
90
protein 1.5 mg iron
6g 250 mg cholesterol
. CHO
o (Duck egg has increased amount of avidin *rri"n decreases
ihe availability of biotin)
. VitC
MILK
r Deficient in Vit. C and Fe 2s5
r Rich in Ca
VITAMINS
Fat soluble vitamins: (A, D, E, K)
VITAMIN A Source
RDA Infant 350 pg (300-400) . Animal - liver, egg, fish, liver oil
Children 550 pg (400-600) o Plants - sp madi, amarnath carrot
Adolescent 750 pg r Fortified vanaspati
Deficiency 1. Defective dark adaptation

2. Nightblindness
3. Coniunctival xerosis
4. Bitot sPcit
5' Comeal xerosis
6. Keratomalacia Iinfection (respiratory, intestinal[
manifestations: Forlicular keratosis, anorexia, growth retardation,
Extraocurar
Treatment
Oral vit A: 0, 1 daY,l month (3 doses)
<6 month-50,000IU
6 month to 1 Year - L lakh IU
>1 Year - 2 lakh IU
Prevention
Vitamin A ProPhYlaxis Program
iTHJ;iJ:ii,ffi 'Jffi
;;'.,*i"tr,'o'"r:,?dl:Ti:?*l',i'#)
z rar.r, iiven with Dpr booster
(at 15 mon&s)l
J i:tr1i":#Tffil,?il:J',1ffiI,,f;ii"#;1;Jtli;;;thsy,
SecondarY signs
Primary signs
XN Nightblindness
X1A Conjunctival xerosis
XF Fundalchanges
X1B Bitot's sPots
XS Comeal scarring
X2 Corneal xerosis
ige Co*"al ulceration (<1/3 of cornea)
X3B Comeal ulceration (>L/3 of comea)
VITAMIN D
Source a. Sunlight .. , cheese)
-1 ^^^^ Metabolism
b. Food - animal origin (liver' egg yolk' butter' 7 dehydrocholesterol
RDA Infant - 5 Pg (200IU) J
Children - 10 Pg (400 ru) Cholecalciferol
DeficiencY: Rickets in children J
Osteomalacia in adults 25 hydroxY cholecalciferol
J
Clinical Features 1, 25 dihYdroxY cholecalciferol
1. Soft skull
2. DelaYed closure of AF
3. Rickets rosary
4. Harison's groove
5. Widened wrist
6. Genu valgum/genu varum
7. Double malleoli
8. Spinal and Pelvic abnormaltY
9. Growth disturbance
10. Splaying
the lower end of ulna and radius)
Radiological features (findings mainlr s9e1in
t. Loss"of normal ,one of prJvisionaf calcification-earliest sign
2. Widened ePiPhYsis
3. CupPing
. Frying metaPhYseal end
5. Sptaying
followed by 400 ll-J / day and oral Ca supplements'
Treatment - Oral vitamin D 6 lakh IU given
Short Cases
VITAMIN E (Tocopherol)
Deficiency leads to:
1. Hemolytic anemia
2. Spinocerebelar cells
VITAMIN K
o Vitamin K, is called phylloquine.
o Function - cofactor in the post transalational carboxylation of glutamic acid to form glutamate (takes place in
liver)
. Vit K dependant factors in coagulation system - II, VII, D; X
o RDA: 5 pg (newborns)
10 pg (children)
. Deficiency causes hemorrhagic disease of newborn.
WATER.SOLUBLE VITAMINS (VIT B AND C)

VITAMIN B
Vit 81- Thiamine
Vit B, - Riboflavin
Vit 83 - Niacin
Vit Bs - Pantothenic acid
Vit 86 - Pyridoxine
Vit Be - Folic acid
Vit B12 -Cobalamine
WTAMIN 81
o Polished rice deficient in 81 and leads to beriberi \
o Biological action: Active form is TPP (Thiamine pyrophosphate) and is involved in:
a. Oxidative decarboxylation of pymvate to form acetyl CoA (pymvic acid + acetyl CoA)
b. Pentose pathway (transketolase)
Deficiency: Beriberi
1. D.y beriberi - nerve involvement like peripheral neuritis (no edema, cascliomegaly)
b. Wet beriberi - involvement of heart
c. Infantile beriberi and Wernicke's encephalopathy
Diagnosis is made by 24lv thiamine urinary excretion (increase in beriberi).
Treatment
o Mild disease - 5 *g vitBr/day
o Severe disease - 10 mg IV bd
WTAMIN B,
r Function: It is the constituent of two coenzymes (FAD and FMN)
. RDA
- lnfants:0.4 mgl1000 kcal
- Children:0.8 mgl1000 kcal 257
Deficiency
Photophobia, glossitis, angular stomatitis, seborrheic dermatitis, cataract.
Treatment
l mg vit Brtid for few weeks.
yTTAMIN 83
o Function: Constituent of two coenzymes, i.e. NAD and NADP
o RDA: 6.4-8 NE/kcal [NE= Niacin equivalent]
Deficiency: Seen in children who take maize
. Pellagra
. Diarrhea, dermatitis, dementia (3 Ds)
Treatment: 10 times the.RDA
wTAMtN BDAND Bs
. Deficiency causes megaloblastic anemia
. Refer Pediatrics
o RDA of vit Bp
lnfants;0.3 pg/ day
- Children:0.5-1.5 tg/ day
WTAMIN C (ASCORBIC ACID)

. Rich in citrus fruits
o Functions:
1. Strong reducing agent
2. .Required for normal functioning of leukocytes, fibroblasts and mlcrosomes.
O I(DA
lnfants:3040 rng/ day
- Children: 40-70 mg/ day
Deficiency: Scurvy
In infancy clinical features of scurvy (Bailoztt's disease) are:.
1. Pallor
2. Anorexia
3. Diarrhea
4. Irritability
"','\
5. Pseudoparalysis
6. Infections
7. Subperiostealhemorrhage
8. Tenderness ofbone
In older childrery hemorrhagic signs usually predominate with bleeding gums, conjunctivae and intestinal tracL
is diagnosed by X-ray of long bones.
SOME IMPORTANT MINERATS

Zinc
' Zn' dependant enz)..rnes: 1. Thymidine kinase Macro minerals-conc > 0.01% body weight
2. DNA polyrnerase Ca,K, Na, Mg
3. RNA polymerase Micro minerals (trace elements)
4. Carbonic anhydrase Fe, I, Cu, Cr,Zrt, Se, Mn, Ni, Si
RDA
3.5-5mg/day
2s8 Deficiency
l..Hypogonadism
.
Typical syndrome of Zn deficiency includet <-\
2. Anemia
3. Growth retardation
Other manifestations include diarrhea, dermatitis, hair loss and anorexia.
Acrodermatitis enteropathica 1. AR condition of Zn deficiency
2. due to defective Zn absorption
3. Anorexia is a prominent feature
Treatment 0.5-1 mglkg/ day for several months.
Short Cases
Selenium (Se)
Function:Component of glutathione peroxidase (an antioxidant which scavenges free radicals)
Deficiency: Severedeficiency-Keshan disease (presentsascardiomyoPathy)
Mild deficiency of Se presents as macrocytosis and loss of hair pigment.
Iodine (I)
RDA 90 pg (0-5 year)
120 1tg (6-12year)
150 pg (>l2year)
200-250 pg (pregnant and lactating women)
The term iodine deficiency disorders (IDD) refers to all the ill-effects of iodine deficiency in a population that can
be prevented by ensuring an adequate intake of iodine.
Setus Abortions, stillbirths, congenital anomalies, increased perinatal mortality, endemic
cretinism
Neonate Neonatal goiter, neonatal hypothyroidism, endemic mental retardation
Child and adolescent hlpothyroidism, impaired mental function, retarded physichl
f$:i:rtr"t"jJinical
N)DITIONAL POINTS
BFHI (Baby Friendly Hospital Initiative)
Ten steps to succesful breastfeeding:
L. Have a written breastfeeding policy that is routinely communicated to all health staff.
2. Train all health care staff in skills necessary to implement this policy.
3. In{orm all pregnant women about the benefits and management of breastfeeding.
4. Help mothers initiate breastfeeding within half an hour of birth.
5. Show mothers how to breastfeed, how to maintain lactation even if tirey should be separated from their infants.
6. Give newborn in-fants no food or drink other than breast milk, unless medically indicated.
7. Practise rooming in - allow mothers and infants to remain together 24 hours a day.
8. Encourage breastfeeding on demand.
9. Give no artificial teats or pacifiers (also called dummies or soothers) to breastfeeding infants
10. Foster the establishment of breastfeeding support groups and refer mothers to them on discharge from the
hospital or clinic.
T MIX
It is a combination of roasted and powdered rice, wheat, blackgramand powdered sugar in the ratio 1:1,:1,:2.
L00 g mix give 380 kcal energy and 8 g protein.
gy of Kwashiorkor and Marasmus

Classical theory of deficiency
Gopalan's theory of dysadaptation
Golden theory of free radicals
Program
for supplementary nutrition in ICDS 259
Beneficiaries CaloriesJkcal) Protein (g)
Children 3 year 300 8-10
Ctrildren 3-6 year 300 8-10
Severely malnourished children Double ofabove
Pregnant and lactating women 500 2o-zs
Day Mea[ Program

The meal should be a supplement and not a substitute to the home diet.
The meal should supply at least one third of the total energy requirement, and half of the protein needed.
i
c. The cost of the meal should be necessarily low.
d. The meal should be such that it canbe prepared in schools; no complicated cooking process should be involved-
e. As far as possible, locally available foods ihould be used; this will reduce the .o"t-of meal, and
f. The menu should be frequently changed to avoid monotony.
National Nutrition Anemia Prophylaxis Program

Forexpecting/nursing mothers, give 100 mg elemental 'Fe'and 0.1 mg folic acid for a period of 100 days.
Children (1-5 year) are given one tablet containing 20 mg elemental'Fe' and 0.1 mg folic acid daily foia period of
100 days.
Amruthum powder
o Protien
. CHO Breast milk vs Cow's milk
. Sodium, potassium, calcium Protien 1.1 3.3
o Iron, vit C Lactose 7g 45g
o Cholestrol Fat 3.8 3.7.
r Moisture EFA '1370 2%
r Ash Ca:P >2 <2
e Calorie 395.06 VitK 15Fg 60V
GROWTH AND DEVELOPMENT

Growth: Increase in size or mass of tissue.
Deaelopment; Maturation of function and related to mafuration and myelination of nervous system and indicats
acquisition of various skill for the functioning of individual.
LAWS OF GROWTH "- \
o Its continuous and orderly process

o Growth pattern of every individual is unique (cephalocaudal and distal to proximal)
. Different tissue of body grow at different rates
PERIODS OF GROWTH
Prenatal Period
Ovum 0-14 days
Embryo 14 days to 9 weeks
Fetus 9 weeks to birth
Perinatal period 22 weeks of gestation to 7 days afterbirth
Postnatal Period
Newborn 1st 4 week afterbirth
Infancy First year
Toddler 1-3 years
260 Preschool child 3-6 years
School age child 6-72years
adolesence Early:7V13 years
Middle:14-16 years
Late:17-20 years
Principles of Development
. Developement is a continous process from coneption to mafurity.
o Sequence of development is same in all children but rate of development varies from child to child.
o Development is intimately related to mafuration of nervous system.
o Generalized mass activity is replaced by individual response.
Short Cases
o Development is in cephalocaudal direction.

o Certain primitive reflexes have to be lossed before the corresponding volentary movement is acquired.
Functional developmental estimation

Main domains Extended neurological examination
o Gross motor . Vision
o Fine motor . Hearing
e Social, adaptive o Muscle tone
r Language . Primitive reflexes
DEVELOPMENTAL MILESTONES
Gross motor
Main domains Extended neurological examination
3 months Neck holding
5 months Sit with support
6 months Prone to supine and tripod posture
7 months Supine to prone
8 months Sitting without support
9 months Standing with support and crawling
10 months Walk with support and ereeping
12 months Standing without support
i3 months Walking with out support
1.5 years Run
2years 2 feet per step
3 years 1 feet per step upstairs
4 years 1 feet down
Fine motor
Up to 3 months Grasp reflex
5 months Bidexstrous approach
5-6 months Ulnar grasp
6-7 months Transfer objects
8-9 months Radial grasp
9 months Pincer grasp (immature)
1 year Mature grasp and pull out cap
1.5 years 3 blocks tower and scribbles and turn 21page
2 years 6 block and circular scribbling and turns one page at time
3 years Draw circle
4 years Draw squares
5 years Draw triangle
6 Draw hexagon
Social and adaptive 26t

2 months Social smile
3 months Recognition smile
6 months Mirror smiie
9 months Bye bye
10 months Peek a boo
1.5 years Domestic mimicry and follow orders
2years Ask for toilet, food and drink
years \
3 Know sex and age and handedness
4 years Imaginative play and go to toilet himself
5 years Bladder control
Language milestone
2 months Social smile
l months Turn head to sounds
2 months. Cooing
6 months Monosyllables - ma, ba
9 months Bisyllables - mama, baba
15 months |argon speech
1.5 years 10 words with meaning
2years 100 words with meaning (23word sentence)
3 years Ask questions, knows full name and gender
4years Tell story and poems
5 vears Ask meaninss of words
Vision
Atbirth Fixation follow 45'
l month Fixation follow 90o
3 months Fixation follw 180'
4 months Binocular vision
6 months fix only on interest
7 Fix rapid movi
Hearing
At birth Respond to sound by cry, blink
5-6 months Child turn head to o.re iide then downward if the sound is
made below the level of ears
7 months Is able to localize sound by turning head to oneside then
upward if sound mad.d above the level of ears
L0 months Child directly looks at source of sound directl
Global development delay-delay in 3 or more spheres of milestone
Dissociated development delay-in one sphere only
Development regression---<ross of previously attained milestone. It is seen in dejenerative disorder (Lr Cp, there
is no development regression).
Deaelopment quotient DQ = A/O*100

A-Average age of attainment
O-observed age of attainment
If <70% evaluation should be needed
DISORDERS OF GROWTH
SHORT STATURE
Height below 3rd percentile or more than 2 SD below the median height for the age and sex according to standard
population.
CAUSES
Physiological or normal variant short stature
a. Familial
b. Constitutional
Pathological Short Stature
a. Undernutrition
Short Cases
Chronic systemic illness

- Renal: renal tubular acidosis, chronic renal failure, steroid dependent nephrotic syndrome
Cardiopulmonary: conginital heart disease, cystic fibrosis, asthma
Gastrointestinal and hep atic: malabsorption
Chronic sea er e infections
Endocrine causes
Growth hormone deficiency
- Hypothyroidism
Cushing syndrome
- Pseudoltypoparathyrodism
- Precious or delayed puberty
Psychosial dwarfism
Children born small for gestaional age
oSkeletal dysplasias,
e. g. achondraplasia, rickets
Genetic syndromes, e.g. Turner slmdrome, Down's slmdrome
to Thrive
Term used in children below 5 years of age.
It refers to wei,ght below 3rd or Sth percentile, or failure to gain weight over a period of time, or change in rate
of growth that has crossed two major centiles.
Organic causes:
Gastrointestinal - gastroesophageal reflex, malabsorption, inflammatory bowel disease, pyloric stenosis
Neurological - mental retardatiory cerebral palsy
Renal -renal tubular acidosis, chronic renal failure
Cardiopulmonary - congenital heart disease, cystic fibrosis, asthma " ' \
Endociine-hypothyroi-dir*, DM, adrenal inslfficiency
Infections - chronic parasitic or bacterial infections of GI tract, tuberculosis, infection with HIV virus
Gsnetic - inborn errors of metabolism, chromosomal anomaly
Miscellaneous - lead poisoning, malignancy, collagen vascular disease
Non organic causes
Poverty
Misperception or lack of knowledge about diet and feeding practices
lack of breastfeeding, feeding diluted formulae
Dysfunctional parent child relationship with child abuse and neglect
t
the cause and nutritional rehabilitation
L DEVETOPMENT
Flag Sign in Child Development
Milestone Age
No visual fixation or following by 2 months 263
No vocalization by 6 months
Not sitting without support by 9-10 months
Not standing alone by 16 months
Not walking alone by L8 months
No single words by 18 months
Loss of imaginative play 3 years
Ioss of comprehension, single words or phrases At any age
Pondral index
Weisht in srams
" " -100
Length in cm
>2.5- normal
if <2- asymetric (malnourished)
if 2-2.5 - symmetric (hypoplasia)
IMMUNIZATION
o Vaccination-process of administration of a vaccine
o Immunization-induction of immune response
o Vaccine failure-if disease occurs despite immunization
Vaccine Failure
. Primary-when admistration of recommended dose of vaccine does not result in adeque
disease
r ,Secondary-disease occurs despite of immunization
. Adiuaant----substance given along with antigens in order to enhance immunological efficiprlr
example, aluminum salt used in DPT vaccine
TYPES OF VACCINE (live, killed, toxoid., subunit)
Live vaccine Killed vaccine
Adzsantages Aduantages
Single dose enough No danger of spread
Stability and safety
Produce local immunity _r
Induce cell mediated immunity
Given as combined vaccine of virus from vaccine
More convenient for mass immunization Disadoantages
Multiple injection may be required
Disadoantages
Reversion to virulence May be contaminated with
dangerous infectious agent
Difficu1ty in storage
- Toxoid-modified toxin, and are nontoxic to recipient
subunit vaccine-capsular polysaccharide and viral or bacterial subunit
Description Example
Live attenuated vaccine
Bacterial BCG, oral typhoid
Viral OPV, rneasles, MMR varicella
Killed or inactivated organism
264 Bacteria DTPw, whole killed vaccine, typhoid,
Viral inactivated polio vaccine, rabies, H"p A
Modified bacterial toxins or toxoids D,T
Subunit
Bacterial capsular polysaccharide S. typhi, Hemophilus influenzae type b
menigiococcal, pneumococcal
Viral Hepatitis B
(surface antigen)
Short Cases
Category of Vaccines by IAP Now, two categories are there

Category L: Vaccines in EP1' 1. IAP recommended vaccines for
BCG, OPV, DTP measles, TT routine use
New additions-hepatitis, Hib, MMR, typhoid, Td BCG, OPV,IPV, MMR, Rotavirus,
Category2: IAP recommended vaccines (in additions to EP1 vaccines) chicken pox. HepA, B, MM&
hep B, Hib, MM& typhoid, Td measles, etc.
.New additions-Tdap, IPV, HPV 2. Vaccine under special circum-
Category 3: Vaccines to be given after one to one discussion with parents stances
hepatitis, varicella, PCV7, DTPa Rabies, infl u enza,JE, meningocccal,
New addition-rotavirus cholera, yellow fever
Category 4: Vaccines under special circumstances
influenza, PPY23, menigiococcal vaccine, IE vaccine
Immunization schedule
Age National immunization program IAP recommendations
At birth BCG, OPV BCG, OPV0, Hep 81
6 weeks DTPw1, OPV1, and BCG if not givenbirth DTPwI/DPTaL, OPVL, HepB2, Hibl
10 weeks DTPwZ, OPV2 DTPw2, DPTa2, OPV2, Hib2
14 weeks' DTPw3, OPV3 DTPw/DPTa3, OPV3, Hep 83, Hib3
9 months Measles Measles
15-18 months DTPwBI/DPTa 81, OPY4, Hib 81, MMR1
18-24 months DTPwBl, QPV 81
2years Tlphoid
5 years DTB2 DTPwB2, OPV5, MMR2
10 years TT Td/Tdap/TTTd/TT
16 years TT 2 doses of TdlTT
t woman 2 doses of TT 1 month
COLD CHAIN
It is the system of transporting, storage and distributing vaccine at recommended temperature from manufacture
site to which it administered:
. OPV stored in freezed compartment (0-4"C)
o Lr the main compartment (4-10"C)
. Top rack (below freezer) - BCG, measles, MMR
o Middle rack-DPT, Hep A, typhoid
r Lower Rack - Hep B, varicella
BCG VACCINE
It should contain at least fype of vaccine, dose, schedule, route, contraindication
o live attenuated vaccine administered intradermally in the left hand on insertion of deltoid (site is selected for
universal equality)
r Dose: 0.05 mL in neonate and 0.1 mL in all others
r Protect against military Tb and Tb meningitis (efficacy 50-80%)
e Contraindicated in immunocompromised 265
o Complication-ulceration lympadenitis, osteomyelitis
r Strain used: Copenhagen and Pasteur
r Vaccine reconstituted with normal saline
BOLIO VACCINE
Two type of vaccine:
o Live-Sabin
. Killed-salk
GEMS-A Golden Endeavor for Medical Studem
Oral Polio Vaccine

r Contain 10s-106 median cell culture infectious dose of type I, II, Itr viruses
o Dose: 2 diops in L:rdia (look NIp)
r i?,
o Contraindication-in immunocompromised, diarrhea, infectious fever ..t1";l 6
. MgCl, is the stablizing agent
. Mopping up
' ;f{r
. Pulse polio immunization - giving 2 doses 1 month apart
,'fi
o Vaccine vial monitors - to know potency of vaccine

i;J&
o Reverse cold chaim

o Complication: vaccine associated paralytic polio-vApp (due to type 2)
Injectable Vaccine
. Formaldehyde killed and purified poilio virus :
r Contain 40D,8D,32Dunitsof types l,,2,3polioviruses,respectively(40-g=32)
. 6,10,L4weeks according to IAP
DTPw Vaccine
o .D,T-toxoid, pertussis -killed, whole cell D -20 - 30lf Qeve{d
o, Give IM in the anterolateral aspect of thigh (0.5 mL) TT - 5 -25A
o Complications P- >4IU
- Prolonged screaming episodes
- Progressive neurological diseases/encephalopathy
- Complication is due to pertussis component in these situation give DT or TT
- Absolute contraindication-immediate anaphylaxis, encephilitis lasting >24 hours wilh
L
vaccination
DTPaVaccine
o Here perfussis vaccine is acellular pertussis vaccine ._,1
o It contains inactivated pertussis toxin and one or more additional pertussis antigen
like
(FHA), fimbrial protein, nonfimbrial protein
. Adoantage: Fever systemic and local side effect less
c Disadoanfage: High cost
MEASLES
. Live attenuated vaccine (Edmonston-Zagreb strain)
. Given IM or SC
o civen at 9 months (because at that time maternal antibody wean off)
o Contraindications
- Malignancy
- Therapy with alkylating agent/corticosteroid
- Immune deficiency
o side effect - TSS (toxic shock slmdrome) due to bacterial contamination
MMR
o Measles-Edmonston-Zagreb strain
266 . Mumps-Jeryl Lynn straii
. Rubella-RA 27 /3 strarn
o Dose is 0.5 ml (2 dose one at 15 month and another g weeks later) (s/C)
'. Each dose contain 1000, 5000, 1000 TCID 50 of measles, mumps, rubella, respectively
Contraindication-pregnancy, immunosuppression
HEPATITIS B VACCINE
o Recombinant DNA vaccine (in yeast)
. 0.5 mL IM in <1 year and 1 mL > 1 year
r 3 doses at0,L,6 months
'o IPI! gives passive immunity) dose-0.5 mL in newborns and 0.6 mllkg for all other ages
HBIG should be given preferably within 48 hours of exposure
Short Cases
i
TYPHOID VACCINE
o 2 doses
. 0.5 mL SC 1 month interval (killed vaccine)
. Typhoral - oral live vaccine (stable mutant S. typhi strain type 2 Ia)
. Typhim - give SC or IM s'ingle dose
Hib VACCINE Pentavalent vaccine (trail in Kerala, Tamil Nadu)

. Capsular polysaccharide used as antigen Contains D,P,T, Hib, Hep B
. Given particularly prior to splenectomy Schedule-6, 10, 14 weeks
. 3 dose below six months
. 2 dose between 6-12 months
. 1 dose between 12-15 months
. And a booster dose should be administered in this children at 18 months.
. >15 months-only one dose
HPV Vaccine
o 0.5 mL IM deltoid
. Recommended age for initiation of vaccine is 10-12 years-3 doses at 0, 2.6 months
Pneumotoccal Vaccine
. High-risk group (children<2 years, congenital immunodeficiency, HfV, immunosuppressive therapy, asplenia,
hyposplenia, nephrotic syndrome)
o Corrently two types:'
Polysachride vaccine
Conjugate vaccine
. Unconugited polysacchride vaccine (PPv 23)---0.5 mL IM
- S/E-poor$ immunogenic in < 2 year, immunological memory is low.
o Pneumococcal lonjugate iaccine -rc'iz z
. Dose-O.S mL IM 3 doses 6,1.0,1.4, with a booster at 15-18 months
Japanees Encephalitis Vaccine

o Dose 0.5 mL S/C
. S/C-anaphylaxis
Chickenpox
Dose--{.S mL S/C or IM 2 doses 4-8 weeks apart in children >13 years
IMMUNIZATION OF AN UNIMMUNIZED CHILD

Visit
1st visit -_ Measles (MMR if >1 year)
DTP1
- OPV1/IPV1 (only if <5 years)
Hibl (only if <5 years)
Hep 81
2nd visit - (1 month after 1st visit) BCG((on1y if <5 years)) 267
DTP2
OPV2
Hep 82
Hib2 (on1y if <15 months)
3rd visit - (1 month after 2nd visit) oPvs/rPYz
MMR (if more than 12 months)
Typhoid (if more than 2 years)
4th visit - (6 months after visit) DTP3
OPV4/IPVB1
Hep B3
Congenital Heart
Diseases
Diagnosis
1. Congenital heart disease
2. Cyanotic/Acyanotic
L:> Right shunt NADA's criteria (1 major or 2 minor indicates heart disease)
3. + Feafures of cardiac failure Major Minor
4. + Features of infective endocarditis 1. Systolicmurmergroup 1. Systolicmurmer
5. + Features of pulmonary hypertension 3or> <group3
6. In sinus rhythm ?, t Diastolic murmer 2. Abnormal 52
7. PEM, developmental delay 3. Cyanosis 3. Abnormal ECG
4. CCF 4. Abnormal X-ray
Presenting Complaints 5. Abnormal BP
a. Cough and breathlessness:
Dffirentiate CCF and Respiratory infection
- CCF:
- Poor feeding (suck-rest-suck cycle), interrupted feeding
- Breathes better when held against shoulder (equivalent to orthopnea)
- Excessive iread sweating. Due to increased sympathetic activity and large surface area of head to maintain
tissue perfusion
-Respiratoryinfection:
Fever, cough, sputum production.
b. History of increased precordial activity
c. History of failure to thrive
d. Cyanosis:
Bluish discoloration of skiry mucous membrane due to increased amount of reduced hemoglobin >5 g7o, met
FIb >1.5 g/ dL or sulf FIb > 0.5 g/ dL.
1. Look at tongue, nail bed, eEr lobule, tip of nose, cyanosis/pigmentation.
Diascopy: Blanch with a slide, cyanosis will blanch
2. Central Peripheral
Due to hypoxic hypoxia Stagnant hypoxia
Tongue and periphery cyanosed Not on tongue
Limb warm Limb cold
On warming cyanosis remains Cyanosis disappears
On breathingl}}% O, cyanosis disappears Cyanosis persists
3. Cardiac vs respiratory
Associated symptoms
During crying cyanosis will improve in respiratory causes and worsens in cardiac causes.
Congenital Heart Diseases
I
4. If due to cardiac disease:
tt
Cyanotic Acydnotic
I
Cyanotic (Eisenmenger)
Cyanotic heart disease:

A. With increased pulmonaryblood flow:
. STs of cyanotic heart disease
TGA (Transposition of great arteries)
. 1.. Truncus arteriosus
TAPVC (Total anomalous pulmonary venous circulation)
' . Truncus arteriosus
2. Two vessel parallel-TGA
. Tricuspid atresia without pulmonary stenosis
3. Tricuspid atresia
. Double outlet right ventricle without PS.
4. Tetralogy of Fallot
C/F: Mild cyanosis.
5. TAPVC
Recurrent RTI
CCF--develop early
Do not survive long (80% die in 3 months due to CCF/pulmonaqz infection.
B. With decreased pulmonary blood flow:
1. TOF (commonest cyanotic heart disease above 2 years)
2. TGA with VSD and PS
3. Corrected TGA, VSD and PS
4. Double outlet right ventricle RV with PS.
5. Tricuspid atresia with decreased pulmonaryblood flow
Fallot's physiology
C/F:
- More cyanosis, cyanotic spells, squatting episode, less dyspnea
- CCF late
L
- Survive more ,.-
- In decreased PBF
- Time of cyanosis:
- At birth - severe TOF (Unlikely to survive without associated PDA)
- Tricuspid atresia with decreased PBF
- 1 year-Double outlet right ventricle
- Teenage-Ebstein's anomaly (Lithium cause it)
Acyanotic heart disease:

(ASD/VSD/PDA) Recurrent RTI, CCF
J
Pulmonary hypertension
J
Period of quiescence
T
Cyanosis
Infective endocarditis (Not seen if < 2 years)
History of high-grade fever with chilIs. 269
Petechial hemorrhage
Dental procedures / surgery.
History of complications:
Fever, vomiting, seizure, focal neurological deficit (cerebral abcess in congenital cyanotic heart disease,
thromoembolism)
PEM
Recurrent respiratory tract infections->6 / y ear
of Loss of Weight in CHD

Increased respiratory rate, poor feeding
2. Respiratory infection
3. Increased metabolism Normal feeding:
4. Decreased metabolism o Continous up to 15-20 min
5. Gastric congestion - poor absorption . In first 5-7min -90% feeding completed
5. Tissue anoxia e Rest - for satiety
Brain (pituitary) blood flow. Suck-rest-suck cycle-after 1-2 min -+
breathlessness -+ stop feeding
Past History
o Historl of LRTI
. Any treatment (Digoxin, Lasix)
. Prophylaxis (rheumatic fever)
' Cyanosis
Antenatal History
r IU infection
Fever with rash
Rubella-> PDA, PS
o Diabetes mellitus - Asymmetrical septal hypertrophy, VSD, TGA
r Drug:
Phenytoin or Valproate (septal defect) (Safe drug - phenobarbitone)
Lithium: Ebstein anomaly
Thalidomide
Alcohol (Fetal alcoholic syndrome)
Natal history Postnatal history
Prematurity - PDA Cyanosis in newbom period
(Delivery at high altitude - PDA, ASD) Birth asphyxia - PDA
Gross motor delay - Congenital heart disease
. Global delay - In systemic anomalies
GENERAL EXAMINATION
. pallor I
'. Cyanosis L Congenital
----o------ cyanotic
-, heart disease
Clubbing
. Polycythemia -JI
Pedal edema, presacral edema
Infective endocarditis feautures like:
. Splinter haemorrhage
I . \Jslersnooes
I ' ranewav lesrurl
-I . xorhsspor
I
-JJ o Down's slmdrome - Endocardial cushion defects
270 r ASD,VSD AofIE
.
Turner's slmdrome: o Splenomegaly
.
Bicuspid aortic valve, coarctation of aorta, aortic stenosis, pulmonary stenosis. . Tender
o
Slmdactyly, polydactyly, VSD . Pollar
Holt-Oram s5mdrome - Familial atrial septal defect + Limb anomaly
. Marfan syndrome - AR" P& MVP
Head to Foot
r Microcephaly, cataract - congenital rubella
. Signs of infective endocarditis
. Signs of vitamin deficiency
Congenital Heart Diseases
Pulse
. PDA, AR: water hammer pulse
. Pulses bigeminus: Digitalis toxicity
. All peripheral pulses: to rule out emboli in IE
Blood Pressure
Apex beat:
Outer most and lower most part of precordium (part of anterior chest wall overlying the heart) where definite
cardiac impulse is felt.
Position of apex:
<4 yrs 4th intercostal space 1 cm lateral to midclavicular line
4-7 yrs 5th intercostals space On MCL
, >7 yrs 5th intercostal space 1 cm medial to MCL
Types:
r Tapping:MS Investigations:
e Forceful: VSD, PDA, M& VR 1. CBC
. Heaving: AS 2. ESR
3. Chest X-ray
Gastrointestinal System 4. ECG
r Hepatomegaly: CCF 5. Echocardiogram
. Splenomegaly: IE
Respiratory System
Features of infecton
Extracardiac anomalies Likely congenital cardiac lesion

1.. Down'slmdrome ASD (endocardial cushion type), VSD
2. Turners syndrome Coactation of aorta
3. Rubella sundrome PDA,PS
4. Marfan's syndrome Aortic or pilmonary artery dilatation
5. Holt-Oram syndrome Familial ASD
6. Hurler slmdrome MR or AR
VENTRICULAR SEPTAL DEFECT (VSD)

Differential Diagnosis of PSM
llpes-of V$O:'a@qdingtssile
271
i lhlBt,
Endscardbl
cu**iiiin defoct
less chance
r .. .to closur8 l
. According to size-small(<.5 cm2 /rt:2 of body SA)

- Mbdeiate (0.5-1 crrf / rfr of body SA)
- Large (>7 cm2 /mz of bodY SA) and nonrestrictive VSD
. AccordLg to flow_restrictive vsD
Spontaneous closure:
-80% chance in muscular VSD
-35% chance in Perimembranous VSD
. Vast majority of defeCt that close do so below age of 4years.
Commonest cardiac lesion complicated by IE - VSD
-
- VSD reversal - Eisenmenger complex
Roger's VSD - small VSD
Gazul VSD - Right ventricular infundibular hypertrophy- leading to,reversal' .
of ventricular aneurysm'
Benjamin vso:"night ventricular outflow obsiruction = due to development
GerLodes VSD - Left ventricle to right atrial shunt'
Why L to R shunt manifest at 8 weeks?
- frefore birth pulmonary vasculature is closed. RV pressure > LV pressure. decreases'
After cryint prf"o"uJy vasculature opens and pulmonary vascular resistance
Gradually nV pi"ttrr." < LV pressure by 6 weeks'
- Then L to R shunt become apparent' -+ pulmonary HTN _>
Gradually pulmonary blood flow increases -+ Pulmonary vascular resistance
ventricuiaipressure increases -+ Reversal of shunt -+ Eisenmenger.
Indications of Surgery in VSD

o Large vsD with CCF + FTT not responding to medical treatment
r Pulmonaryhypertension
. Supracrystaf VSO any size because high risk of AR
.*..t
PATENT DUCTUS ARTERIOSUS (PDA)

Functional closure: 3 hours to 3 days
Anatornical closure: 3 weeks to 3 months
Ductus arteriosus:
. m f",ut tife, mostblood from right ventricle flows into descending aorta via ductus - as lungs are
(less blood flows to pulmonary circulation)
. At birth: After clamping cord ihere is sudien increase in the systemic vascular resistance d"" t: th:-'",t:-:l
resistance placental cirJuhtion. \rly'hen the baby breathes lung expand + pulmonary
artery Pressure ctecrl
-+ flow reverse from aorta to pulmonary truhk'
Differential Diagnosis of Continuous Murmur

1. AV fistula-coronary, pulmonary, systemic
2. RSOV (Ruptured sinus of Valsalva)
J. AorticopulmonarY sePtal defect
4. Venous hum (TAPVC)
5. MR/TR+ AR
272
6. VSD + AR
Diferential Cyanosis
Differential cyanosis - PDA reversal + coarctation of aorta'
TETRALOGY OF FALLOT (TOF)

Components
1. Valvular/infundibular pulmonary stenosis-most important
2. large VSD
3. Overriding of aortic root over the ventricular septum
{. Right ventricular hypertrophy
Cyanotic'spells: During crying (in infundibular PS) there is muscle spasm leading to more right to left
shunt
ysyally seen from 2nd monthto 2nfl year. IJncommon after 2years due io fibrosis ofluscle unde"rgoing spasm.
Why spells in early morning?
sleep respiratory center is suppressed. After waking and crying the center becomes active, tissue hypoxia
Tti"g
to brain so respiratory center becomes unstable leading to hyperventilation.
Squatting Episodes
During squatting:
1' Femoral artery kinks - systemic pressure increases - pressure of LV increases L-R shunt increases and pulmonary
flow incrases----cyanosis decreases.
2* Decreased venousretum of high unsaturated blood to right side of heart by trapping blood in lower
extrimities
-+ decreased R to L shunt at ventricular level.
3. Increased intrathoracic pressure, thereby helping in decreased venous return
Why cyanosis around first 5rear:
1. Infundibular stenosis is proglessive
2. ccHD with decreased pulmonary blood flow ductus arteriosus close late.
3' Amount of fdtal Hb is more in eariy life. So more oxygen carrying capacity and cyanosis at later age (pink Fallot)
Management of Cyanotic spells (Tet spells or Hypercyanotic spells)
1. Knee chest position-decreased venous retum
2. Humidified oxygen Investigation:
3. Morphine: 1. Hb - increased
Suppresses respiratory center z. ?CV - increased
Decreases infundibular spasm 3. TC - decreased
Pharmacological venesection ..- 1
4. Platelet decreased
- Decreases anxiety and activity of child 5. CXR
4. Propranalol0.l mglkg tV 6. ECC
- Decreases infundibular spasm 7. Echo
Decreases heart rate
- Vasoconsfriction
- Shift of oxygen dissociation curve to left
5. IV sodium bicarbonate if cyanosis persists
6. Administer general anesthesia if spell not subsides by 30 minutes.
7. If spell not responding to above measures, corrective surgery/emergency shunt surgery.
PINKFALLOT
In ToF, if PS is less severe, it
r Fallot's monology - VSD
acts like vsD. so there is little cynosis and o
hence name. Triology - single ventricle + pS
o Pentology-+ASD
CONGESTIVE CARDIAC FAILURE

Inability of heart to maintain an output at rest or during stress, necessary for the metabolic
needs of body (systolic
failure) and inability to receive blood into ventricular civities at low pr"rrr." during
diastole (diastolic fril"r;;:"'
-f
X
Symptoms
o Poor weight gain
o Difficulty in feeding
. Baby is more comfortable on shoulder (orthopnea)
o Persistant cough
r Suck-rest-suck cycle
o Edema
Signs of CCF
RHF LHF Failure of either side
Elevated fVP Tachypnea CardiomegalY
Tender hepatomegalY Tachycardia 53
Edema Basal crepts Small pulse volume
Wheezing
Gallop rh},tirm Sa
Treatment
1. Reduce cardiac work
2. Augumenting myocardial contractility
3. Improving cardiac Performance
4. Correcting underlYing cause
7 Steps of Management of CCF
i. Frusemide + digoxin + ACE inhibitor
ii. Add isosorbide nitrate (if there is pulmonary congestion) or carvedilol (if HR is fast)
iii. lnvolves addition of nitrate or carvedilol which not used in previous step
iv. Intermittent use of dobutamine or dopamine with dobutamine if BP is low
.v. Make sure that patient get all medications mentioned above'
- If the patientis not af,equately controlled either have medical/surgical correction of cause of CCF
- If the patient is not controlled and do not have a correctable cause would be patient with myocarditis'
- For them,
vi. Take myocardial biopsy and treat with corticosterol if there is myocarditis
- In the absence u.tirr" myocarditis therapy with p-blocker should be increased maximuin.
vii. Ventricular assist device or cardiac transplantation
'
*whywidefixedsplitinAsD? '- \
since the right ventricle is fully loaded, further increase in right ventricular volume during aspiration cannot occu
*commoneJt congenital cyanotic heart disease in newborn period is TGA.
*if one sibling afLcted o, if f parent affected, then24% ihance of CHD. If 2 primary relative affected-20-30!
chance
*hyperoxia test
RHEUMATIC FEVER
. Immunologic disorder caused by Group A beta-hemolytic streptococci
o AntibodieJproduced against streptocolcal antigen cross react with connective tissue of body and heart.
r Most corunon age grouP is 5-15 years
o Poor socioeconomic status is a predisposing factor.
Criteria to Diagnose RF
Duckett Jones criteria Minor criteria
Clinical
274 Major critria 1. Fever
L. Carditis 2. Arthralgia
2. Arthritis - migratory fleeting polyarthritis early Iaboratory
3. Erethyma marginatum * serPegenous form 1. IncreasedESR
4. Subcutaneous nodule - on bony prominence 2. CRP
5. Chorea 3. Prolongrd PR interval
Essential Criteria (Evidence of Recent Streptococcal Infection)

1. Increased ASO titer
,)
+ve throat culture
Recent scarlet fever
[(2 major ) or (1 major +:2 minor)] along with one essential criteria
+ Suppressive therapy
Bed rest - for 2l weeks

Patient with carditis can be rested for 1-3 months
Diet - if there is carditis then salt should be restricted, otherr.rrise no need of salt restriction
Pencillin - oral penicillin or single IM benzathine penicillin (12 lakh)
ve Therapy
B the patient has carditis with CCF, corticosteroid is mandatory (prednisolone)
Carditis without CCF, either steroid or aspirin is used. Steroids aie preferred.
Without carditis, use aspirin (100 mglkg / day (100 mg/kg/ day in 4 aivided doses for 4 days)
tion Management of chorea

Primary prevention(antibiotic for sorethroat) .
Phenobarbitone 30 mg thrice daily
Secondary prevention
Givebenzathine pencillin 1.2 million units every 21 days or 0.6 million units every 15 days or daily oral penicillin
RF without carditis - 5lears or until 24years whichever is longer
RF with carditits without residual features - 10 years or well into adulthood whichever is longer
RF with carditis with residual features - at least 10 years since last episode pr at least 40 years,-sometime life
long
Usually large joints (knee joint), lasts for 3-.7 daysand migratoiy. Younger the patient, lesser is arthritis.
tis: Commonest manifestation-5G-60%, pancarditis
carditis: Pericardial pain and rub
Cardiomegally, soft 51, 53 gallop, Carqz{oomb's murmer, CCF
Regurgitation murmers
rma marginafum: Rare in Indians, red rash with pale center (serpiginous outline)
taneous nodule: 6 weeks after the onset of acute renal failure, occupies bony prominences like elbow, shin,
Almost always have carditis.
sydenham's chorea-late feature (3 months after onset of acute renal failure)

Teacher scolds due to handwriting
llother scolds dropping object
Grandmother scolds grimace
streptococcal skin infection do not produce RF?
lipase content in skin
275
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Respiratory System
APPROACH TO A CASE OF RESPIRATORY SYSTEM (PNEUMONIA)

NG COMPLAINTS
Fever
Cough
Breathlessness in the form of fast breathing
Chest pain
Feeding difficulty, fits, cyanosis, head nodding - features of severe pneumonia
RY OF PRESENT ILLNESS
Cough
Productive/nonproductive
Color, amount, smell
- Nature of cough (brassy, barking, etc.)
- Diurnal variatiory foreign body aspiration
Complications of cough
a. Post-tussive vomiting
b. Affects feeding
c. Disturbs sleep
d. \A/hoop
e. Complications - subconjunctival hemorrhage, ulceration of frenulum, appearance of umbilical /femoral
hernia, cough syncope, rib fracture
Fever
Onset/gradual/sudden
Type / continued/intermittent
Fever with rashes, arthritis
Relieved by medication
Diumal variation
Breathlessness
"Mother noticed breathlessness in the form of fast breathing"
Severity - unable to speak
- Words
- Phrases
- Sentences
Not able to drink
Not able to eat
4. Chest pain
5. Reppiratory sound
Rattling
- Grunt
Wheezb
6. Running nose, nasal obstruction
7. Poor feedingrflts, cyanosis, head nodding - severe pneumonia
8. Predisposing factors
Pyoderma - staphylococcal pneumonia
Rash - predisposing measles
Conjunctivitis, arthralgia, myalgia - viral pneumonia
PAST HISTORY
If recurrent respiratory tract infection
. Bronchial aithma - history of nebulization which relieved symptoms
. Cardiac symptom
. Foreign body aspiration
. GERD - symPtom following food intake followed by vomiting
o History of seizure (aspiration)
Antenatal
Natal
Postnatal
DIETETIC HISTORY Predisposing conditions

o Histoy of mesles
GLV - Vit A o History of skin lesions
Chickenpox, abscess in axilla or anywhere in
IMMUNIZATION , q
the body - staphylococcal pneumonia
. BCG
. DPT
. Measles Respiratory sounds
. Hib 1". Snoring - oropharyngeal obstruction
. Pneumococcal 2. Grunting - ejection of air through partially
closed glottis
FAMILY HISTORY 3. Rattling - secretion in trachea/bronchi
o Historl of bronchial asthma/TB 4. Stridor - obstruction of larynx/trachea
o Overcrowding 5. Wheeze - lower airway obstruction
. Passive smoking (Inspiratory-ISSR)
SOCIOECONOMIC STATUS
. House nearby roads
r Pets in the house
. Sleeping on the floor
. Cooking with firewood
O/E general assesment - tachypneic, position of conforf conscious, alertness
280 In a case of bronchial asthma:
o Presenting complaint - cotigh, breathlessness - for which he was undernrent nebulization from home/hospit
- symptoms relieved
. In past history - first episode of symptom at the age of
. Number of episodes per month
. Whether he was on inhaler
. Famrly history of bronchial asthma, allergy, atopy
. Socioeconomic status in detail
Recurrent Respiratory Tract Infection
r Lower respiratory tract infection >6/yt
Causes
Surgical Medical
- CHD: L to R shunt - Bronchial asthma
- Foreign body aspiration - Immunodeficiency-congenital/acquired
- Cleft palate - Celiary dysfunction (Kartagener slmdrome)
- Tracheoesophagealfistula (cystic fibrosis)
- Congenital lobar emphysema
- Congenital cystic malformation
NITIONS
Reccurrent pneumonia-2 or > episodes/1, year or >3 episode at any time with radiological clearance between
2 episodes
'Persistent pneumonia-persistance of s;rmptoms and X-ray abnormalities >4 weeks
BRONCHIOLITIS
episode of expiratory wheeze of acute onset in a child less than 2 years of age, which has signs of viral
illness,like coryza, otitis media or fever with or without indication of respiratory distresses, pneumonia
atopy.
Bronchial asthma Bronchiolitis
Age greater than 6 months
- Recurrentepisodes First episode
- Positive family history Negative
- Responds to bronchodilators No much response
AGEMENT OF BRONCHIOLITIS
Admit in ICU
a. Humidified oxygen *
b. Tepid sponging - using lukewarm water
c. IV fluid
Then do investigation
_FIb I
- Tc,Dc L Types of pneumonia
Anatomical
- CXR- over inflation I
1. Lobar or lobular
- Homogenous opacity_J 2. Bronchopneumonia
If not improving, superadded infection - start antibiotic
- Nebulization with racemic epinephrine 3. Interstitial pneumonia
- Ribavirin - indication - 4. Multilobarpneumonia
f . impending respiratory failure Duration
2. congenital heart disease 1. Persistent
2. Recurrent
Etiological
PNEUMONIA 1. Infective-bacterial, viral, atypical
tions 2. Noninfective-chemical
Source 281
X-ray 1. CAP
- Consolidation - opacity with air bronchogram 2. HAP
- Bilateral patcy opacity - bronchopneumonia lmmunity
- Pneumatocele - Staph. aureus, Klebsiella 1. Primary-high virulent organism in
Microbiological examination good immunity
- Gram and Ziel-Nielson staining 2. Seconadary-low virulent organisms
- Culture and sensitivity in immunodeficient
- Blood culfure - positive in pneumococcal pneumonia
Serology - Mycoplasma, Chlamydia, Legionella and viral infection
Throat and nasopharyngeal swab-influenza
Blood test
- Neutrophil leukocytosis - bacterial pneumonia
- WBC count marginally raised - atypical pneumonia
Bacterial pneumonia vs Viral pneumonia
Onset Abrupt Gradual
Epidemic Not seeen Common
Associated coditions Infn at other sites, septicemia Associated with URI, coryza
Fever High grade May be present
Toxemia Common Absent
Respiratory distress Common Common in infants
Lung signs Crackle Wheeze
X-ray Confluent infiltrate Diffuse in peripheral areas
Prognosis Complication - emPyma/ Self-limiting
Pneumatocele
Typical vs Atypical (walking Pneumonia)

Causative organisms S. pneumoniae M. pneumoniae
H. influenzae Chlamydia
Staph. aureus Legionalla
Onset Sudden , Gradual
Agu Any age >5 years
Fever Common , t Maybe present
Cough Productive Dry
X-ray Localized Diffuse
DEFINE ARI
o Acute infection of respiratory tract including ear, nose/ throat, paranasal sinus, and pleura of less than 30 days
and in case of ear in{ection, less than 14 days.
o Acute URl-common cold, otitis media, pharlmgitis
. Acute LRl-croup (epiglititis,laryngitis,laqmgotracheitis), bronchitis, bronchiolitis, pneumonia
ARI CONTROL PROGRAM

Clinical category Essential featutes
1. Very severe pneumonia - Central ryanosis or feeding difficulty or convulsion or lethargy or unconsciousness or
severe respiratory distress (e'g. head nodding)
2. Severe pneumonia - Lower chest indrawing or nasal flaring and no signs of very severe Pneumonia
3. Pneumonia - Fast breathing - age-newbom >60/min

282 2-i2 months-> 50/mh, 12 months to 5 years >40/rrttn
- No signs of severe or very severe pneumonia
4. Cough or cold - No fast breathing and no indicators of severe or very severe Pneumorua
Why co-trimoxazole DOC
o Active against cornmon organism
o Cheap and better compliance
gns indicating admission in hospital (Danger signs)
o Oniy BD dose
1. Central cyanosis
2. Inability to drink or take food
3. Convulsions
4. Lethargy or inconciousness
5. Severe respiratory distress (head nodding) or grunting
6. Lower chest indrawing
7. Nasal flaring 283
8. Stridor in a calm child
9. Severe dehydration or shock
10. Severe malnutrition or severe anemia
: lM:oag( clilti iieal''',,,:.,,'

.ii .a.:.::,- .i.:t,:rt Cfa,r., tr.:ii:
lM or lV benzyl pencillin + gentambin
lf no improvernent,winr*in *S houi lf improves

io gentamicin, gi eloxiacilli$ir4dtan dlild continue orally for total 10 days
. inrprol&q 666661ue,clmalillin lrElty.
for total 3 weeks
Causes of recurrent pneumonia

Samelobe Dffirent lobe
o Congenital anomaly ' . Aspiration
o Tumor o Asthma
o Foriegn body . Immune deficiency
' TB o Cystic fibrosis
e L->R shunt
* Indicators of good response to antibiotics in severe and very severe pneumonia

a. Subsiding fever if initially present
b. Less severe chest indrawing, it should disappear by 4g hours
c. Decreasing respiratory rate
d. Child begins to drink and eatbetter.
* Discharge from the hospital i
- The clinical condition has improved markedly
- No lower chest indrawing or fast breathing
- Afebrile
- Alert
- Eating and sleeping normally
- Oral antibiotic treatment has been started
- In case the patient is a malnourished infant or child or is a non breastfed
infant weight gain on 2 cons
days has been observed.
Infant <2 months

Symptoms and signs of pneumonia, septicemia or meningitis
are offen indistinguishable during firsi 2 months of life-and
it is necessary for certain nor,specific signs that indicate that
young infant may have possible seriouJbacterial infection
Treatment: Ampicillin IM or IV, or benzyl penicillin +
gentamicin (BAG)
284
*Lower chest indrawing-tlefinite
inward movement of lower chest wall
Additional Discussion
. Lobar pneumonia
. Bronchopneumonia
o Intestinal pneumonia
o Pneumonia - Etiology
- <2months -+ gram -ve
- Staph. aureus
Respiratory System
3months-3years
- H. influenzae
- Staph. aureus
>3 years
- Pneumococci
- Staph. aureus
Gram -ve organism cause pneumonia in early infancy, severe malnutrition and immunocompromised children.
Pneumococcal pneumonia Complicatio ns of St aph. pneumoniae
Associated herpes labialis
Can diagnose by blood culture
- Empyema
Treatment - fV or IM penicillin G
- Pericarditis
Staph pneumoniae
- Arthritis
Osteomyelitis
- Rapidly progressive Mastoiditis
- Associated pyoderma
- Pneumatocele - on X-ray
Treatment
Penicillin G, cloxacillin, vtu:rcomyciry ticoplan, cephalosporin
Usually longer duration (6 weeks) of therapy bacteria persist in the necrotic area
Specific treadment
- Intercostals drainage - empyema
- Intercostals decompression - for large pneumatocele causing respiratory distress
3. H. influenzae pneamonia
- Treatment - Ampicillin + Chloramphenicol
Or
Cef otaxime / Ceftriaxon
4. Streptococcalpneumonia
- Secondary to measles, chicken pox, influenza or whooping cough o
5. Primary atypical pneumonia

- Constifutional symptoms fever, sore *uoat, myalgia, cough
o/E
X-ray poorly defined hazy or fluffy exudates which radiate from the hilar region
5. Viral pneumonia
Constitutional symptoms fever, myalgia, arthralgia, conjunctivitis, rash
Always B/L
Signs minimal, symptorns more
Complication less
Precipitating factors: Otitis media, pyoderma
Leukopenia
- X-ray: Interstitial pneumonia
Pseudomonas may colo.rire airways of patients with cystic fibrosis and cause recurrent pulmonary exacerbation
'.'
'.' Pneumatocele
1. Staphylococcal pneumonia
2. Klebsiella
'3. Causes for delayed resolution 285
1. Underlying immunosuppression
2. Resistance to antibiotics
3. Inadequate dose and duration of treatment
4. Noncorrect predisposing LR shunt
5. Underlying TB
6. Underlying congenital anomalies, TOF
7. Underlying osteomyelitis of rib
{. Nocturnal cough
_ LVF
_ GERD
GEMS-A Golden Endeavbr for Medical Students
- Bronchial asthma
- fostnasal driP
*\A/hyampicillin is preferred over CP in smaller children? Ans: H. influenzae coverage is for ampicillin
*When can child expectorate sputum? Ans:4 years
*Most conunon congenital anomaly of lung-congenital lobar emphysema
*Normal amount fluid in pleural cavity - <1 mL
*MC cause of community acquired pneumonia - Pneumococci
*Why asthma is common in children ? Ans: refer
*MOA of co-trimoxazole? Ans: refer
BRONCHIAL ASTHMA
Bronchial asthma is characteri zedby an increased responsiveness of the airway to various stimuli; it manifests
by
widespread narrowing of the airways causing paroxysmal dyspnea, wheezing or cough (Mucosal hypertrophy,
edema, secretions, bronchospasm).
Pathophysiology
. Trigger of an attack of asthma
Early reaction
o a. Allergens in the environment
Late reaction
b. Viral infections
5 P's in Asthma c. Exercise
r d. Weather change
Pest e. Emotional factor
o Pets f. Food
. Pollen g. Endocrine factor
. Perfumes
. Passive smoking
ln case of bronchial asthma your diagnosis will h,u*4g. acute exacerbation of mild persistent asthma.
Classification Day symptoms Night symptoms PEFR
Severe persistent Continual Frequent < 50% predicated variability > 30%
Moderate persistent Darly >ltimesaweek > 60"/o < 80% predicated; variability > 30%
Mild persistent > 1./wk, but < 1 time/day >2timesamonth < 80% predicated; variability >2010"/"
Intermittent < 1/wk < 2 times amonth < 80% predicated; variabili$ > 20%
"Classification of asthma severity (Nelson)
What is Life-threatening Asthma?

Presence of any of the following indicates a life-threatening asthma
'o Cyanosis
Silent chest
. Poor respiratory effort
. Exhaustion
. Fatigue
. Altered sensorium
286 . PEFR <30% of predicted
. Oxygen saturation of <90%
Treatment of Mild Acute Asthma

Beta-2agonist nebulizer (0.5 mL salbutamol respiratory solution in 3 mL saline water)
. MDI + spacer + or - Mask (every minute - 1 puff for 10 puff)
. Then discharge;
. Repeat MDI or oral beta-2 agonist every 8 hours;
. Follow-up after 2 weeks.
Hoderate and Severe Asthma
Q inhalation (full O, sdturation >95%)
+
Inhalation ofbeta-2agonist (repeat every 20 minutes - for t hour)
+
Oral prednisolone (1'-2 mg /kg - 7 days)
a- lf improoement after t hour
Repeat inhalatiln ofbeta-Zagonist every 30 minutes then every 4-8 hours
Patient discharged when,
Patient need for bronchodilator is every rt-6 hourly
- Able to speak well and feed
- Maintains O, saturation of >95% in room air need of regular follow-up, avoidance of triggers
Discharged patients are educated about the disease,
b- lf no imprortement after t hour
Inhalation ofbetal}agonist is continued and ipratropium 250 pg is also added every 20 minutes
+
Injection hydrocortisone 10 mg/kg
If no respopse
Injection theophYlline
+
Inj MgSO, (50 mglkg in dextrose over 30 min)
Treatment of Life-threatening Asthma

Qinhalation
+
Inhalation of salbutamol + ipratropium bromide
+
Subcutaneous injection of adrenaline/terbutaline
+
Hydrocortisone 10 mg /kg
(Shift to ICU with accompanying physician)
ffimprotsed
Repeat inhaled salbutamol + ipratropium every 30 minutes
Injlction hydrocortisone 5 nigTkg every 8 hours, till patient can take orally
ffno improoement
Ioading dose of theophylline
OR
Injection MgSq - 50 mglkg every 30 minutes
If there is no improvement with this management, patient is prepared for mechanical ventilation
In case of poor response/ susPect: 287

o Acidosis
o Pneumothorax
. Electrolyteimbalance
. Infection
Effective Long-term Management of Asthma
1- Identification and elimination of exacerbating factors
2 PharmacologicaltheraPY
3- Education oipatient and parents about the nature of disease and the steps required to avoid acute exacerbation
Pharmacotherapy
Goals of therapy
1. Bronchodilators o Maintain (near) normal pulmonary function
2. Corticosteroid . Minimal use of short-acting inhaled B2
3. Mast cell stabilizers o Minimal or no adverse effects from
Cromblyin sodium o Preventionofexacerbations
- Nedocromil
Ketotifen
4. Leukotrienemodifiers
Zileuton - decreasing synthesis of leukotriene
- Montelukast and Zafirlukast - antagonizing receptors
5. Theophylline
6. Immunotherapy
This_consists of giving gratlually increasing quantities of air allergen exkact to a clinically sensitive subject
so asi
ameliorate the symptoms associated with subsequent exposure to causative allergen. 1
r Pharmacological Mx Selection of appropriate initiation dei,ice

o Assessment of sensitivity . MDl->12years
. Stepwise treatment of asthma . MDI + Spacer-4 to 12 years
. MDI + Spacer + Mask-< 4 years
Monitoring and Modification of Treatment . Dry powder inhaler - Rota haler, Disk haler, Spin haler,
(Step up, Step down) Turbo haler, accuhaler
After starting appropriate treatment patient . Nebulizers
should be seen every 4-l2weeks (How to use these..? study in detail from Op Ghai)
On each visit detailed history is taken regarding
. Frequency of symptoms
o Sleep disturbance Four components of optimal asthma management
. Physical activity t. Rggular assessment and monitoring
o School absenteeism - Asthma checkups
o Visit to a doctor - L*gfunctionmonitoring
. Need for bronchodilator 2. Control of factors contributing to asthma
If a child examine,look for: Eliminate or reduce problematic environmental exposures
o Adverse effect of drugs Treat comorbid conditions : rhinitis, sinusitis, gastroesophageat
o Records height, weight, pEFR reflux
*Assessment
of control of asthma? 3. Asthma phnrmacotherapy
*Step up and step
down of treatment? Long-term control vs quick-relief medications
refer OP Ghai Step-up, step-down approach
4. Patient education
288
Practical Approach to a Child with ]aundice
laundice
Definition (refer Medicine)
1. Is it true jaundice?
2. If jaundiced, is it conjugated/unconjugated jaundice?
3. Assess severity of functional statb
4. Identifycomplication
5. Establish etiology
1. Is it true jaundice?
To rule out pseudo-jaundice - drugs, carotinemia
Ask history of ingestion of drugs (Am, NSAID)
Sclera would not be discolored in carotenemia
2. Coniugated - staining of clothes Unconjugated - clear urine
If unconjugated - bilirubin more, enz).mes normal
Enzyme absent, bilirubin normal
- Increased bilirubin - hemolytic anemia - hemolytic facies, pallor, splenomegaly
- If no splenomegaly
a. Sickle cell anemia - autosplenectomy
b. Postsplenectomy - look for scar
- If no pallor - compensated synthesis
- Enzyme problem
- Gilbert
- Criggler-Najjarslmdrome
In a case of conjugated hyperbilirubinemia
- Sructural problem - like a block
- Bilirubin transport from cell to canaliculi affected - Dubin-|ohnson slmdrome.
- In a structural probl"*; clinical features due to:
a. Accumulation of bile - itching, xanthelasma
b. Deficiency of nutrients carried via bile
- Vit ADEK deficiency, steatorrhea,
- Rickets, bleeding - take longer time to appear
In Dubin-johnson s5mdrome - only bilirubin transport from cell to canaliculi affected, no other deficiency
manifestations
3. Assess severity of functional stale
i
4. Complications
5. Any signs"of liver failure
- Edema (abdominal, pedal, facial puffiness) - chronic liver failure
Bleeding manifestations - acute liver failure
- Altered sensorium, sleep rhythm - fulminant hepatic failure
}AUNDICE-CASE TAKING
o Yellowish discolorartion of urine
o Yellowish discoloration of eye
r Itching
o Pale stools

o ]aundice-onsetprogress, duration
o Color of stool
. Color of urine
. ' Itching
. Lr hemolytic jaundice - urine and stool - normal
o Lr hepatocellular jaundice - high colored urine and normal stools
o Lr obstructive jaundice - high colored urine and pale stools
If hemolytic jaundice (acholuric jaundice)
o History of exertional dyspnea, fatigue, palpitatioru pallor - anemia
o Histoy of blood transfusion - transfusion dependant anemia
o Abdominal distensiory abdominal pain - splenomegaly
o Antimalarial drug intake - G6PD deficiency .-,\
o Foot ulcer, chest, bone pain - sickle cell anemia
. Oliguria, hematuria, diarrhea, dysentery - HUS
In hepatocellular iaundice
o Infection
. Drugs
. Malignancy
. Collagen vascular diseasea
. Metabolic disease
Infection
Viral
1. Hepatitis A - prodromal symptoms - anorexia, fatigue
- Fever - subsides - jaundice
- History of contact, clustering of cases
2. Hepatitis B, C - history of blood transfusion
3. Others - CMV, IMN, mumps, measles, rubella
Bacterial
1. Leptospirosis - high-grade fever, rigor
- Conjunctival injection, myalgia
- Bleeding tendencies
2. Enteric fever - mild icterus
- 1st week - constipatioin
- 2ndweek- diarrhea
- 3rd/ 4+hweek- complication
3. Disseminated TB - historv of contact
4. Malaria
Gastrointestinal SYstem
Malignancy
r Loss of appetite
. Weight loss
o Hematological
Leukefr ia-bleeding manif estation
- LymPhorna
-Joint Pain
-Petechial rash
-Progressive Pallor
e Other malignancies
- Hepatoblastoma
- Neuroblastoma
Wilms tumor
Collagen vascular disease (PAN, Kawasaki disease)
. Rash
. Arthralgia
Drugs
o Paracetamol
o Anti-TB drugs
If we suspect obstructive jaundice -
. Fever.with rigor, colicky Pain - cholangitis
HEPATIC FAILURE
rEdema-edema(abdominal,pedal,facialpuffiness)_chronicliverflure
. Bleeding manifestations - acute liver failure
. Altered ,urrrorl*rr, si""p - fulminant hepatic failure
'ftyttt*
o History of similar complaint (Hepatitis B)
. History of transfusion
o Drugs
. Travel to endemic area - malaria
oHistorYoftreatmentforTB-historyofcontactwithopencaseofTB
Antenatal History
o Fever with rashes - toxoplasmosis, CMV
r Natal-LBW (Iow birth *"igttg in IU infection' In biliary atresia weight is normal
o Postnatal
Developmental History of Delaying in IU Infection

Dietetic HistorY
Immunization history
. HePA
. HepB
. BCG scar
Family History
. History of similar illness
. Metabolic diseases - Wilson disease
. Alpha-1 antitrypsin deficiencY
GENERAL EXAMINATION
. Irritable, less active - hepatic encephalopathy
o Sick Uilta - malignancy
. Pallor - hemolytic jaundice
. ]aundice
. generahzed lymphadenopathy - TB, malignancy
. |B.in"unt/
Pedal edema -C/C liver failure
SES - income, boiled water usage, sanitations, etc.
Head to Foot Examination

o Hemolytic facies
. Head
Microcephaly - intrauterine infection
Open A-F - hypothyroidism
o Eyes
- Cataract - galactosemia
KF ring - Wilson disease
. Features of hepatic failure
- Bleedingmanifestation
Spider naevi
Palmar erythema
- Abdomen - ascites, dilated veins
Investigations
. FIb - anemia
r Tc - increased (leukemia)
. DC - lymphocytosis - TB ., q
o Blood indices
r RDW
o Peripheral smear
Type of anemia
- Malaria
- Malignancy - lymphoblast/myloblast
. LFT
Conjugated bilirubin SGPT = ALT
SGOT = AST
- Unconjugatedbilirubin
- SGPT/
ALP
Total protein/albumin
PTINR
. Modified Fouchet's test - bile pigment
Urine
. Ehrlich's test - urobilinogen
.
- Bilirubin S.-ollqutedhyper bilirubinemia - if conjugated
Urobilinogen bilirubin >1510o/" of total
. Hay's test - bile salt
292 ' USG abdomen
- Hepatomegaly
- . Focal mass
Lymphnode
Other organomegaly
- Ascites
- CxR
Lymph node Bx
Bone marrow aspiration
Gastric aspirate for AFB
Bilirubin Metabolism Bilirubin (unconjugated)
Reticuloendothelial system
.f Urobilinogen
Hemoglobin {4 mg/day)
J
I
Heme
.t Heme oxygenase I
Biliverdin Urobilin
.1, Biliverdinreductase
Bilirubin
.t UDP-glucuronyl transferase
Bilirubin diglucuronide
I Reaches gut
J Deconjugation by gut bacteria
Bilirubin
J
Urgbilinogen + urobilin -+ urine
Stool
J,
Stercobilinogen
J
Stercobilin -> faeces
Urine
Hemolytic Hepatocellular Obstructive
Urobilinogen - 3+ Urobilinogen-2+ Urobilinogen - 0
Bilirubin - 0 Bilirubin - 2+ Bilirubin - 3+
*Pale stools due to absence of stercobilin
-
Hepatitis A
. Hepatitis A in water is sterilized by:
1. Boiling<5min
2. Autoclaving
3. Chlorination - (1.5 -2.5 mg/L for 15 min)
o Feces are infective one week before and two weeks after onset of jaundice
Clinical Features
Four phases
1. hrcubation or preclinical period
30 days
- Asymptomatic in spite of active multiplication of virus
2 Prodromal or preicteric period
- Loss of appetite, fatigue, abdominal pain nausea and vomiting
Fever, diarrhea, dark urine and pale stools
3. Icteric period
Fever subsides and jaundice develogs
4. Convalescent period
Laboratory Investigation
r ALT,AST,ALP,GGT
'. IgM, anti HAV
PCR_HAV,RNA
Treatment
Supportive treatment maintain adequate nutrition (monitor liver spary signs of liver failure)
-
(Antivirals have no role because hepatic injury is immunopathologically mediated)
. '
Prevention
a. Passive immunization - pooled immunoglobtnl,6o/" - 0.02mL/ke given within 2 weeks of contact (efficmlr
- 6months)
b. Active immunization:
1. Killed formalin inactivated vaccine from 9 R326, HM 175)
(efficacy - 10 years)
2.
Live attenuated vaccine from CR 326
o Avoid hepatotoxic drugs (p mol)
Hepatitis B
. DNA virus (all hepatitis virus except Hep B virus are
Extrahepatic manifestation of hepatitis B
RNA viruses) 1. Serum sickness like syndrome
. Spread through serum, saliva, semen 2. Essential mixed
o In case of FIbs Ag +ve mother only 5-10% is infected ln Cryoglobulinemia
utero and the rest is infected at the time of delivery 3. Polyarthritisnodosa
4. Aplastic anemia
Clinical Features 5. Pleural effusioru myocarditis, pericarditis
1. Acute hepatitis
2. Chronic acute hepatitis
3. Chronic persistent hepatitis
4. Fulminent hepatitis
Chronic persistent hepatitis
Laboratory Investigation
. HbsAg
o Anti FIbs
o Anti Hbc
. FIbeAg
o Anti-Flbe
. Anti-Flbs- after immunizatiory previous infection
o Anti-Hbs + Anti-Hbc - previous infection
Treatment
r Acute hepatitis - bedrest
(prolonged bedrest should be avoided and early ambulation is prefferd)
r Chronic active hepatitis
a. IFN-alpha - 5-10 million/nf; 3 times a week for 4-6 months
b. Lamivudine - 3 mg/kg/day for 1 year
o Fulminant hepatitis
- Antibiotic - neomycin, ampicillin
- Carbohydrate rich diet/protein elimination
- Lactulose - 10-15 mL/ day x 3 doses
Exchange transfusion/plasma pheresis
ACUTE DIARRHEAL DISEASE (ADD)
Name: Age: Sex: Address: hrformation:
ksenting Complaints
Ioose watery stool (duration)

Imse stools:
o Onset
o Duration
. Number of episodes
. Whether blood stained/not
r Consistency - watery /solid
. Whether frothy/not, smell
Associated symptoms
r Abdominal pain
. Vomiting'
r Fever (in parenteral diarrhea), seizures or other foci of infection
Srgns of Severe Dehydration

o Thirst
o Urine output
r Seizures {
e Tears, appearance of eye (sunken)

o Altered sensorium r
. Malnourishment (J weight)
Also ask about (to know the cause)
l. History of weaning, artificial feeding
2 History of similar illness in family
3. Any travel to outside/food from outside
{. A.y history of previous infections like UTI, pneumonia, otitis externa (parenteral diarrhea)
5. A^y drug intake (antibiotics-cause loss of normal intestinal flora and cause diarrhea)
Erom the history toe should get answers for 4 questions:
l. Is the child dehydrated ?
L Is the child malnourished?
3- Is the child have other disease than loose motion?
.L Dysentry or not?
Past History
o Similar illness in the past (if plesent child is malnourished)
. Ask about food from outside )
- Travel outside I *" are already asked in presenting complaint 295
- Any history of infection )
Antenatal
Natal
floetnatal
I)evelopmental history
Dietetic history
r Any history of prelacteal food, breastfeeding adequate or not
. Any history of bottle feeding
. Any weaning problems
Immunization
Any special vaccine taken like typhoid vaccine, rotavirus vaccine
Family History.
Similar illness in the family or neighborhood
SES ' ..
Hygiene of food, water should be asked like source of water, whether boiled/cooled water, catrines, whether
material washed before cooking (Clean hand, clean container, clean environment)
GENERAL EXAMINATION
Playful /aler t / letharyic/unconscious (to know severity of dehydration)
Vitals
Look for sign of nutritional deficiency and sign of dehydration, also about perianal excoriation ii any comment
anterior fontenelle in infants.
Anthropometry
If the child has recurrent ilL:ress, then there is malnourishment, so anthropometry is important
Systemic Examination
. GIT
. Respirat ory - r / o any infection (pneumonia)
. CVS
. CNS -tor/o meningitis ..-.i
DISCUSSIONS
Diarrhea - it is the passage of watery stools at least three times a day, with recent change in consistency
change in consistency is more important).
e Acute diarrhea-<2 weeks
o Persistent diarrhea-Iasts >2 weeks
Dysentery - presence of gross blood and mucous in stool, usually associated with tenesmus
Etiology
Bacterial infections
. Salmonella
. Shigella
. E. coli
. Vibrio cholerae
Viral
o Rotavirus
. Corona virus
. Norwalk virus
o Astrovirus
Protozoa
o Cryptosporidium
. Amoebiasis
. Giardia, lsospora belli
Organism causing dysentery - EHEC, Shigella, Campylobacter, arnoeba
Danger Signs
1. Drowsiness
2. Not able to drink
3. Not able to feed
4. Urine output nil for last 6 hours
5. Blood in stools
6. Fever
7. >3 episodes of/hr of stools.
Assessment of Dehydration Status
Clinical signs (key signs)
General conditions Well alert Restless, irritable Lethargic or unconscious
Eyes Normal Sunken Sunken
Thirst Drinks normally Drinks eagerly Drinks poorly or not
not thirsty thirsty able todrink
Skin pinch Goes back quickly Goes back slowly Goes back'very slowly'
,Mouth and tongue Moist Dry Very dry
Tears Present Absent Absent
Decide No signs of dehydration Some dehydration* Severe dehydration*
Treatment plan Plan-A Plan-B Plan-C
*If child has 2 or more signs
Causes of convulsions in ADD
Star Signs iri ADD HyPo- and hypernatremia
r '.
General condition Febrile seizures
. Skin pinch-lot reliable in child with malnutrition thirst . Nalidixic acid
. Vertebral venous/sagittal sinus thrombus
e Vomiting in ADD . Shigellaencephalopathy
o Gastritis/Gastroenteritis o Meningrtis
. ORS . Reye's slmdrome
. DruB induced
Abdominal Distension in ADD

HyPokalemia
Content LO ORS (new) WHO ORS
'o Na 75 90
Necrotizing enterocolitis
K2020
' Septicemia
cl 65 80
MANAGEMENT Citrate 10 10
Glucose 75 111
Plan A Total 245 3ll
Giae ORT (Oral Rehydration Therapy)
a. ORS solution
WHO ORS
b. Solution made from sugar (40 g) + salt (4 g)
NaCl-90,80
c. Food-based solution-rice water + salt
K citrate-2O, 10
d. In the presence of continued feeding, a variety of commonly available, structurally
fluid irrespective of presence of sugar and salt (Coconut water, rice kanji) Low osmolar ORS
a It is given in sips (10 mllkg)
a If large gulps giverg it stimulates gastric colic reflex and results in quick Passage
NaCl-7S,65
K citrate-20, 10
of stools.
a In addition to this, Continue breastfeeding
a Give 1 teaspoon of ORS every l-2minute (<z'ir)
a Give frequent sips (older child)
a If the child vomits, then stop for 10 minutes and continue feeding
a ORS solution is prepared by taking boiled, cooled water (1" L or 5 cup) then add one packet ORS into it and use
within one day
If the child is not better in 3 days or develops danger sign then take to hospital.
Plan B
If IV route not getting, we can infuse fluids through interosseous
Rehydration Therapy
route (upper end of tibia).
75 mL/kg ORS given within 4 hours
Maintenance Therapy
'. orys should be given in volume equal to diarrhea (10-20 mllkg) for each stool
Breastfeedingcontinue
Plan C
Start IV fluid (RL or NS) 100 mglkg
Age Initially give Then girie'
<1 year 30 ml/kg in t hour 70mL/kgin 5 hours
1-5 year . 30 mllkg in 30 minutes 70 mllkg in 2% hours
Look for radial pulse, if it is still very weak repeat it
If there is improvement, change to Plan B and then to Plan A, respectively.
Indication of Antibiotics
o Dysentery
- Co-trimoxazole
- Nalidixic acid
Ciprafloxacin
r Cholera
Tetracycline (adult)
Furazolidone (child)
. Systemic infection
o Probiotics - Lactobacillus
Contents Amou
- not preferred Glucose
c Zn- <6monthsoldchild -t0mg/day 1?5
>6 months old child -20 mg/day

Na 45
It decreases the severity and helps in iaster recovery, improves immune function
K40
' cl 7A
RESOMAL (Rehydration Solution for Malnofirished Child) Citrate 7

o It is different from ORS by increased K* concentration and decreased Na, Mg3
concentration
Zn 0.3
o It is prepared by:
Ca 0.05
Standard ORS + 4 g potassium + 50 g sucrose in 2 L water
APPROACH TO HEPATOSPLENOMEGALY
Liver Examination
Conaentional Method
Place the palm of the hand over the abdomen with fingers parallel to the right subcostal region. Start from the
iliac fossa. The radial border of index finger is used to palpate liver. Ask the child to take d-eep breath, the enli
_willle feltby the fingers. If not felt, keep moving the hand upward till it becomes palpible. The lower bc
liver
is defined by palpation. The upper border is defined by tidal percuision. The size is *"uir.ud in midclavicular
Preferred Method Age Liver span

298 Sit on the couch beside the patient. place both hands side by (cm)
! side flat on the abdomen in the right subcostal region lateril Birth s.GS9
to rectus, with fingers pointing toward the ribs. If resistance 2 months 5
is encountered, move the hands further down the until the 1 year 6
resistance disappears, exert gentle pressure and ask the patient 2yearc 6.5
to breath in deeply.Concentrate on whether the edge of the 3 years 7
liver can be felt moving downward and under the examining 4 years 7.5
hand 5 years 8
Normally in infants liver palpable 3 cm below coastal margin 6-1,2years 9
(It is normal). Adolescents 8-10 (girls)
So liver span is important. 10-12 (boys)
Gastrointestinal System
SPLEEN
1. Start from the righi iliac fossa and move toward left hypochondriun, with palm of right hand with fingers
pointing toward"the left costal margin. The left hand is kept posterolaterally over the left lower rib cage to
support it from below.
2. Patient in right lateral position and fingers should be insinuated below the left subcostal margin
3. Hooking The examinar should stand on the left side facing the foot end of the child, palpate with
^ithod,
hooked fir,gers of the left hand
4. Dipping m"ethod: In the presence of ascites, sudden pressure is exerted by their palpating fingers to displace the
fluid and palpate any enlarged organ
5. Percuss the Traube's sPace
Features SPleen KidneY

Site 9th,
Located anteriorly behind Located posteriorly in the L1
10th, 11thrib vertebral region
Plane Intra-abdominal Retroperitoneal
Notch Present Absent
Finger insinuation Fingers cannot be insinuated Can be insinuated
between spleen costal margin
Bimanual palpation possible
Not Possible Ballotable
Movement with respiration Moves freely Restricted mobility
Direction of enlargement Toward right iliac fossa Toward lumbar fossa
Band ofcolonic resonance Absent Present
Loin Free and resonant FuIl and dull
Grading of splenomegaly (cm) Palpable spleen below left costal margin

. Mild <3
o Moderate 3-7
r Massive >7
HSM with Pallor

1. Infections
- Bacterial
- Infective endocarditis
- Disseminated TB
- Protozoal
- Chronic malaria
- Kala-azar
2. Hematological
- Hemolytic anemia
3. Malignancy
L0ukemia
- Lymphoma
4. Collagen vascular diseases
- SLE
JRA
5. Metabolic
Wilson's disease
- Gaucher's disease
6. Other causes
Extreme PEM
HSM with iaundice

1. Infections
- Viral
- Hepatitis
- IMN
- Neonatal hepatitis
Bacteridl'
- Leptospirosis
- Septicemia
Protozoal
- Malaria
- Kala-azar
2. Hemolytic anemia
3. CCF leading to cardiac cirrhosis
4. Metabolic
Galactosemia
Cystic fibrosis
5. Malignancy
- Metastasis liver
6. disorders leadine to cirrhosis
HSM with fever

1. Infection
TB, kala-azar, chronic malaria, IMN
2. Malignanry
Leuken+ia
Lymphoma
3. Collagen disorder
- SLE,JRA
NEONATAL IAUNDICE
Neonatal jaundice is the visible manifestation in skin and sclera of elevated serum concentration of bilirubin
neonate.
Physiological )aundice
Causes
2. Loss of effective binding and transportation

3. Inefficient conjugation
4. Decreased efficiency of excretion
5. Enhanced enterohepatic circulation
300
Criteria to Rule Out Physiotogical )aundice
1. ]aundice in first 24 hours of life
2. |aundice extending beyond 1 week in term baby and 2 weeks in preterm
3. Total serum bilirubin increasing more than 5 rl::.g/ dL/ day
4. Total serum bilirubin more than 12.9 mg/ dL in teim and more than 15 mg/ dL in preterm
Pathological |aundice
Caus es of Unconj ugated Hyp erbilirubinemia
1. Excessbilirubin production
ABO and Rh incompatibility
RBC enzyme abnormality (G6PD, pyruvate kinase deficiency)

RBC membrane defect (hereditary spherocytosis)
Extravasated blood (cephalohematoma)
Polycythemia
L Impaired conjugation or excretion
Hormone deficiency-hypothyroidism, hypopituitarism
3. Disorders of bilirubin metabolism
Criggler-Najiar sy"ndrome
Gilbert's syndrome
{ Enhanced enterohepatic circulation
Intestinal obstruction
Meconeum plugs
Cystic fibrosis
C-auses of Conjugated Hyperbilirubinemia

1- Obstruction to bile flow
- Biliary atresia-extra and intrahepatic
- Choledochal cyst
- Inspissated bile slmdrome
Hepatocellular injury
a. Infection
Bacterial - TB
Viral - rubella, CMV
- Parasitic
toxoplasmosis
-
b. Idiopathic
- neonatal hepatitis
c.Toxic - bacterial sepsis
Metabolic - galactosemia, Rotor slmdrome, Dubin-|ohnson syndromp
APPROACH TO NEONATAL IAUNDICE

o Mother and baby's blood group
o Antenatal
- Fever with rash - TORCH
- GDM hyperbilirubinemia
r Natal -
Instrumental delivery (cephal hematoma-extravasated blood)
Delayed cord clamping-polycythemia
o Postnatal
Preterm
Birth trauma
- Asphp<ia
r Family history
Anemia
Gallstone
Splenectomy
301
MENT OF NEONATAL IAUNDICE .
. Physiological or pathological
Age of onset-< 24hour or not
Duration of jaundice
. Severity
Krammer's rule
1. 4to6mg/dl
2.6to8mg/dl,
3. 8 to l2rng/dL
4. 12to14mg/dL
5. > 15 rr.g/dL
Dermal zones for estimation of serum total bilirubin evels
Danger signs present Etiology of jaundice

- Vomiting ? premature/ScA
- Lethargy Evidence of infection - microcephaly,
Poor feeding microphthalmia, chorioretinitis
Fever Evidence of birth tr,auma - cephalhematoma, bruising
Highpitched cry ? pallor, polycythemia - evidence of hypothyroidism
Dark urine evidence of. neonatal infection/sepsis
.-, \
Light stool
HSM
INVESTIGATION
1. Cord blood
Blood group and Coomb's test in Rh negative mother
Serum bilirubin, FIb
2. Ser,um bilirubin (Total and direct)
3. Other hemolytic conditions other than Rh, ABO incompatibility
PS
G6PD assay
4. Evaluation for sepsis
5. L:r cholestatic jaundice
Bacterial culture
USG
Radionuclide scan - HIDA scan
Liver biopsy
- Biliary atresia-ductular perforation and fibrosis
- Neonatal hepatitis-alteration in lobular architecture, focal hepatocellular necrosis and
- Giant cell with ballooning of their cytoplasm
TREATMENT
L. Hydration
Correct dehydration
- Increase intestinal motility
- Enhanced removal of photoproducts in urine and stool
Phototherapy
Procedure
Undress the baby comPletelY .
Cover the eyes and genitalia to prevent damage by bright light
Keep baby at a distance 6f 30-45 cm from light source
Tum the Laby after each feed to express maximum surface area of baby to light
- Ensure adequatebreastfeeding
Record body weight daily and ensure that baby passes adequate amount of urine (6-8 times per day)
Phototherapy acts by seaeral w aY:
Configurational isomerization
- Structural isomerization
Photo-oxidation
Side effects
Rash, over heating
Complications
- Dehydration,diarrhea
1. Bacterial sepsis, thrombocytopenia
Exchange transfusion
2. Portal vein thrombosis
Procedure
J. Arrhythmias, cardiac arrest
Push - ball technique via umbilical vein 4. Hypocalcemia, hypoglycemia, hypomagnesemia
- Blood drawn <72 hours preferred
5. Hep B and Hep C inJection
Features Neonatal hepatitis EHBA

Onset Any time in neonatal period Usually end of first week
Sex More in males More in females
Gestation Preterm, ruGR Term
Familyhistory +ve in 15% Absent
Cataract May be present Absent
Stools Pale/normal ' ttuy colored
General condition at birth Looks sick Healthy initially
HSM (hepatosplenomegaly) Early Late
Urine urobilinogen Increased Absent
Transaminases Veryhigh High
ALP (alkaline phosphatase) High Very high
TORCH screen May be +ve Negative
Serum lipoprotien X High High
AFP High Normal
USG GB imaged GB usually not imaged
Liver biopsy Giant cells predominate; Very few giant cells
No bile ductular proliferation Marked proliferation
No bile lakes Bile lakes +++
Biliary scintigraphy Radioactivity in gut + No radioactivity in gut
Operative cholangiogram Normal Block may be visualized
Prognosis Better Poor
303
Nervous System
CEREBRAL PALSY
CASE FORMAT
C/o - Delayed milestones
- Fever and cough
- Seizures
- Say as not attaining age appropriate milestones\

1st child of a nonconsanginous marriage with normal/abnormal
antenatal
attaining age aPPropriate milestones from 4th month onward, now lristoflt detected to have difficufty
presented with fever and cough for 6 days.
Explain history of fever and cough (briefly).

Since the child as having problem from early infancy,I
am starting from antenatal history.
Antenatal History
a C_onceived 2years after marriage
a No historyof abortions or treatment for infertility (more chance for.genetic
abnormality)
a No historyof any drug intake other than Fe and iolic acid .
a No historyof UTI or radiation exposure
a No historysuggestive of rubella like fever with rash and associated
a
swelling behind neck
She has taken regular antenatal checkups
a USG taken at 4th,6th and 8th months urd r,o abnormalities
detected
a
Quickening felt at 4th.month (absent in congenital anomalies), decreased fetal movements
(hypotonia)
a No history of GDM, PIH, IUGR detected or ApH
a No history of polyhydramnios (open NTD)
a No history of trauma during pregnancy, prolonged 2nd stage
Natal History
o Hospital/homedelivery
. Term/preterm
. CS (indication)/FTND, birth weight
. trduction (indication)
Nervous System
r History of passage of forrt smelling liquor

. Maternal pyrexia
r History of chorioamniontUr/PROU
r History of instrumentalisation/infrapartum convulsions
Postnatal History
. CSAB
r Birth weight was ...
. Ifasphyxiaask
o When child handed over, when does child discharged
o When BF started
o Mechanicalventilation
. \rVhether taken to NICU
n
o If neonatal jaundice ask
Detected at
Color of urine/stool to know whether it is unconjugated and severity of jaundice
Sites of jaundice
Phototherapy/ET done
o No history suggestive of bilirubin encephalopathy like shrill cry, hypotonia, poor suck, seizures and opisthotonic
posture during these days.
r Neonatal meningitis (21. day IV drugs)
r Neonatal seizures
o No history of detection of any congenital malformations (hydrocephalus)
. Started hand preference at
o History of drooling of saliva or pooling of secretion (pseudobulbar palsy)
r Abnormal arching of body detected at
r Mother detected stiffening oIUL/LL
o Detected hand preference at
L
I
o History of cortical thumb/constant fisting > 2 months
o Had history of difficulty in changing diapers
I History of commando crawl detected
r History of chewing movements/lip masking
r History of inconsolable cry
r Increased sensitivity to light and noise
o Bowel and bladder control attained at
. Say the development of child as a story touching all spheres
. Ask whether on regular physiotherapy
a Gross motor
a Fine motor a Developmental age in each sphere
a Language a Global or dissociative developmental delay
a Social a Whether child is attaining mile stone (suggestive of Cp)
a Vision a Any regression in milestones (suggestive of netrrodegenerative disorder)
a Hearing 30s
a There is no history of regression of any attained milestones.
lmmunization History
o Which ever vaccines given
. DPT how many?
. DPT can be given/if not advice
r Optional vaccines/(Hep B and Hib are must due to rehospitalization)
I Dietetic Historv
t' PrelactealteedsnotSlven
5 . pri ,o breast within--hours of birth
. EBF uo to months
l-il
I
fil. Weaned at months by
]J,.f
E ' BF uP to -
-vears
H:y,i,','"?;1"';;'::fi ifl1"#ffiJ;ff :["#'T:tion'nasarresurgitation)
o"
: ;f, ::ff l?ff
f, :,? ril:,?1""1"fr-"*o,t"J
f
El .
:'*:.T#:?il.^,
Maternal age atgestation was 30 years
EI . No historv oi abortrons
I :. N:il:Hl:f ilIx}#i1ilil.ma,ies
No history of any developmental delay
' . No history of any neonatal death in family
. Younger brotheis development is normal and he is fully immunized to age and healthy.
SES
o Economic status
. Who is looking after child
. Impact of illness in the family
Head to Foot Examination ,. r

. Head size appears to be decreased
. Facial dysmorphism +
'AF
. Hair line
. Brownish hair, bushy
. occipital flattening
'. Ridging of sutures
No receding of forehead
. Single circular parietal whorl/microcephaly
o Vit deficiency
'. EYebrows
Eves Mouth
I - No cataract (crs) Open mouth with drooling of saliva
II I\o mrcropntnaunra (crs, - A^gur,r ltr.u,r.dlrtrD
I - bqumt, t)?e Cheilitis
-Nystagmus -Teeth
-
306 Hypertelorism - Dysplastic teeth/kernicterus
- Ey" lashes Poor oral hygiene
- Eye slants Glossitis
Epicanthal folds High arched palate
. Ear
No low set ears
- Pinna
. Webbing or short neck
. Flexion contracture of elbow
. Cortical thumb or constant disting
. Simian crease
Nervous System
a Scissoring (Delagae sign)

a Plantar flexion
a Achilles tendon cont?actures
a Nail not trimmed (muddy)
a Cotractures
a Chest
- No pectus excavatum or carinatum
- Kyphosis or scoliosis
a Spinal deformities
a Tuft of hair at low back (spinabifida)
a Evidence of dehydration
a Evidence of malnutrition on skin
a Callus/bed sores
a Perineal excoriation
a IV cannulated at r
a NGTput
a External genitalia N
a 180" deviation assessment (only after consent) - 180" flip method in small infant
a Supine t
- ATNR (Asyrnmetrical Tonic Neck Reflex)

- Hand open
- Reaching out
- Mouthing
Pull to sit
Reflex Appearance Disappearance
- Grasp
Moro Birth 2-3 months
Head lag +/Back
ATNR l month 3-5 months
- Roundornot
STNR
Vertical suspension ',2 months 6 months
Sucking Birth 4 months-awake il
- Scissoring
and rooting 7 months-sleep
- Slipping through
Parachute 9 months Persists for life
- Bearing weight
Ventral suspension
- Head lag
- Head same plane/Head
- Raise abovebody/Parachute+
- Landau
Prone
- Head off the couch
- Crawling/
H
- Sitting up
- Forearm support
a Motor system
a Bulk
- Wasting+
- Measurements
o Tone
- Explain posture
- Palpate muscle-flabby or firm
- Hypertonia of UL/LL all joints
o Power
- Bed movements
r Reflexes
Superficial Deep
- Conjunctival faw jerk
- Corneal Biceps jerk
- Gag/palatal Triceps jerk

- Abdominal+in CP - Supinator
- Cfemasteric - Knee jerk
- Plantar - extensor bilateral - Ankle jerk
. Clonus
NEONATAL REFLEXES
o Glabellar tap
. Rooting/sucking
o Palmar grasp
o Plantar grasp
. ATNR
. Moro
Coordination
Abnormal movements
Gait
Sensory
Spine and skull
Diagnosis (should include physiologic, topographic, etiology, +mental retardation, seizures,
hearing visio4
squint, etc, + complication)
Itis a case of spastic quadriperesisCPwithpseudobulbarpalsydue toperinatal asphyxia andhavingMR,
seizurreq
speech, visual and hearing impairment, miciocephaly, gradelli PEM rrra rrly immunizea
+ broncfropneumonia-
It is a case of spastic diplegia due to prematurity and having microcephily, grade II pEM, no MR, seizrueq,
speech, visual or hearing impairment and is fully immunized.
CEREBRAL PALSY_DISCUSSION
It is a dynamic disorder of posture and mobility being motor manifestation of a nonprogressive
brain damage
occurring during the period of brain growth.
.-.\
Classification
Topographical Neurologi.g classification

1. Paraplegia 1. Spastic
2. Diplegia (quadriplegia with more 2. Hypotonic
involvement of LL) 3. Choreoathetoid
3. Hemiplegia
Funtional classifi cation (grade) Pathological

1. Mild 1. Infective-intrauterine infection, meningitis
2. Moderate 2. Genetic
3. Severe 3. Vascular problem-thrombophilia
4. Periventricularleukomalacia (pVL)
308 5. Metabolic
Causes of Cerebral Palsy
o Antenatal cause (80%)
o Birth asphp<ia
Treatment
Participation of parents- they should be explained about the prognosis of disease
Multidisciplinary team approach (pediatrician, pediatric neurologist, occupational therapist,
physiotherapis!
child psychologis! counselor, orthopedic rrrg"on,tphthalmologist,-ENT surgLon)
Nervous System
Methods to decrease spasticity

1. Nonpharmacological-physiothetapyt occupational therapy, electrical stimulation, use of orthoses,
manipulative methods
2. Pharmacological
Oral - Diazepam or nitrazepam
Dandrolene sodium
- Tizanidine, baclofen, levo dopa
Parenteral - Alcohol or Phenol injections
- Bohrlinum toxin injection
- hrtrathecal Baclofen
3. Surgical
- Tenotomy .
Osteotomy, tendon lengthening, arthrodesis, etc.

Selective posterior rhizotomy-selective sectioning of 2040% of dorsal nerve roots
Treatment of aisociated features--epilepsy, visual disturbances, hearing, speech, behavioral problems special
education
Nursing care and nutritional management
Spastic Type
PVL
r Ventricle is very vascular and controls, motion of lower limb (mainly) in addition to upper limb, so it produce
diplegic type of cerebral palsy
. PVL clinicaly seen in preterm babies with asphyxia
Clinical Features
o Here LL involvement is more (PVL)
o Increased stiffness of LL
. Limb position - scissoring position due to adductor
o Spasm (difficulty in changing diapers)
o Paucitl of movement
r Commando crawling
o Abnormal posturing
(Sometimes, we think developmental milestones are early attained, it is due to false impression)
Hemiplegia
. Paucity of movement on one side of body
. Early hand preference
r Cortical thumb
. Limb length deformity (sometime, affected limb is small)
Choreoathetoid
o Cause
Birth asphyfa
Kemicterus 309
o There is abnormal deposition of myelin in place of gray matter of basal ganglia (status marmoratus)
Complications
1. Neurological
- Mental retardation
- Visual loss
Hearing problem
Communication disorder
2. GIT- GERD
- Constipation
Orthopedic
Contracfu res (Achille's contracture)
Scbliosis, kyphosis
- Equinus deformity
Miscellaneous
Respiratory problem
Learning problem
Earlv markers of CP?

Differential diagnosis
r Neurodegenerative disorders
o Ataxic telangiectasia
.' Subdural effusion
o Hydrocephalus
FEBRILE SEIZURES
APPROACH
o Fever
o Seizures

. Detailed history of fever
o Seizures - onset: within 24 hours of fever
r Duration
- <10 minutes (typical febrile seizures)
>15 minutes (atypical febrile seizures)
' TyPe
Focal/ganeralized
- Associated history of 1. Fever
2. Head trauma (SAH)
3. Aura
. \umber of episodes: single/repeated episode (atypical FB)
o Similar history of among siblings
. To r / o other causes of febrile seizures
- Frontalheadache
310 Projectile vomiting meningitis
- Photophobia
o Motor system - history of any weakness
r sensory system - history of any pins and needle sensations, numbness
r Autonomic system - bladder and bowel disturbance
o Cranial nerves - mention as negative history
Past History
o Previous episode in the past
o History of any seizure drug intake
Nervous System
Any delay in attaining milestones (atlpical seizures)
Examination of a CNS case
1. Attitude-active ln FS
Irritable /aPathetic in menigitis
2. Posture
3. Head to foot examination
4. Cranial nerves system examination
Il-btinks to light
Menace reflex
3,4,6 No Ptosis, squint, nYstagmus
Refl ex-direct / indirect
5 No deviation on opening mouth for food
Jaw jerk
Corneal/ conjunctival reflex
7 No facial dYsmorPhism
No historY of drooling
' No facial deviation
8 Startle resPonse +/
9 and 10 Whether babY feeds normal
HistorY of anY regurgitation
Position of uvula
Palatal reflex, gag reflex
11 Shrugging of shoulders +/
12 Position of tongue
Strength of movements \
Any f-asiculation/tremor
MOTOR SYSTEM PROPER
. Bulk-wasting +/
o Tone
o Power
For babies mention Power as
Child move his limb actively and appears to be normal
r Reflexes
Superficial
Deep
Primitive
. Any involuntary movements
' Any signs of meningial irritation
Kerning sign
Brudzinki sign
- Neck stiffness 311
o Mention other systems within normal limits (CVS, GIT, RESP)
DIAGNOSIS
First/reccurent episod,e of seizure probably FS probably typical/ atypical FS
DISCUSSION
Indication of LP in FS
Management: investigation to r/o other causes of seizures
1. <1y,
1. FIb, Tc, Dc, ESR 2. Suspectingmeningitis
2. Blood glucose 3. Atypical FS
3. Blood calcium 4. 1 episode ofFS
4. Serum electrolYtes
9. study-lumbar punture-meningitis
6. !-SF
Blood culture
Ql. Why you said it is a c/o FS
-Seizure started within 24 hours of onset of fever
Duration < 10 minutes
Single episode, generalized
Positive family history
No developmental delay in milestones
O/E : child is active
no signs of meningial irritation
Q2. what is FS
it is provocative seizure, occurring in a neurologicaly active child
of age between 6 months and 5 years
the absence of CNS infection.
QS. Typical FS Arypical FS
No of febrile episode ingle Recurrent
Onset Within 24 hours Any time
Duration <10 minutes > 15 minutes
TYP" Generalized Focal
Postictal phase No postictal confusion Focal neurological deficit in
Postictal period
Chance of epilepsy in
Fufure No yes
Q4. Treatment
1. Supportive measures- nurse in semi prone position
ABC
2. Fever-paracetamol - 15 mglkg tid
Tepid sponge ._ x
Hydrotherapy
3. Seizure-IM diazepam - 0.3 mglkgldose
(maximum of S mglkg)
FS prophylaxis
o Intermittentprophylaxis
Indicated During the episode of fever
Given within 3 days
o Continuous prophylaxis
Indicated Atypicalseizure
Failure of intermittent prophylaxis
+ve family history of epilepsy
Drugs Sodium rratproutJ, \USOig'/kg/day or
phenobarbitone: 3_5 rng
/ kg / aiy
Until 5 years of age or 1._Zyears,whichever comes earlier
ACUTE FLACCID PARALYSIS

o Acute onset of (<4 weeks) flaccid paralysis
. hr.r. acute onset of flaccid paralysis for which
*,::T^:,*1lll,I^,Tt-:I,1:1?-t:ur.old,*.h:
found or paralytic iliness of any age in which polio is ,"G;,"d. no obvious cause is
Causes
. Poliomyelitis
. GBS
o Transverse myelitis
o Traumatic neuritis
!"
Nervous System
Polio Spectrum of Polio

. Fever present alongwith the paralysis . Inapparent (90-95%)
. As)rmmetrical paralysis, proximal muscle weakness more . Abortive
. Bladder dysfunction absent. . Nonparalytic
. Paralytic
Guillain-Barr6 syndrome (GBS)
o History of fever, diarrhea prior to the onset of weakness (Campylobacter jejuni)
. S)rmmltric, ascending parilysis with involvement of distal muscle is more
o ComPlication is respiratory failure' aCytoalbummino dissociation
. Affecting eranial nerves 7,9,10, LL, t2 I )1. GBS
o Bladder dysfunction transient
. CSF show cytoalbumino dissociation 2. Froin's slmdrome
r Asbury criteria used
o Treatment-fvlc, plasmapheresis, supportive care
AFP Surveillance
A11 cases of AFP should be reported regardless of final diagnosis.
Step 1 - caqe identification
St"p2- informnodalofficer ..1 __.,:_-1^-.^t^-^ ^. se>'; address) is taken'
Step 3 - line listing - detailed history includlng iTmynization along with particulars !age,-1ame,
stool samples are collected'(2 specimln) at least 24 hour apart, collected
within 14 days of paralysis onset, each
step 4 - it sent to lAtrHO accredited lab in reverse cold drain'
having adequate volume (8-10 g or thumb size) and is
Step 5 - active search of similar illness.
Stui, O - Outbreak resPonse immunization (ORI)
the cases (5 km radius)
Single dose oi OpV is given to 500 children below 5 years residing around
Step 7 - manage the cases
stef s - th" cale should be followed up for 60 days, look for residud paralysis
Laboratories
o Pasteur institute of India, Conoor
. National Lrstitute of Communicable Disease, New Delhi
. King Lrstitute of Preventive Medicine, Chennai
HYDROCEPHALUS
. of flow or decreased
The accumulation of CSF within ventricle either due to increased production, obstruction
absorption.
. CSF production
3t3
Classification and Causes

1. Communicating hydrocephalus (nonobstructive/external)
2. Noncommunlciting hydrocephalus (obstructive/internal)
Or due to excess CSF production in papilloma choroid plexus
Congenital hydrocephalus Acquired hydrocephalus

1,. Intrauterine infections 1.. Pyogenic meningitis
2. Congenital malformations - Aqueductal stenosis, 2. Posterior fossa fumor
Arnold-Chiari slmdrome 3. Intraventricularhemorrhage
3. Midline tumor bbstructing CSF flow 4. Intracranialhemorrhage
CLINICAL FEATURES
1. Enlarging head size, suture separation
2. Delayed closure of fontanelle
3. Headache, nausea, vomiting, irritability, head banging, diplopia
4. Forehead prominent
5. Scalp vein become prominent
e. Cracked pot soundon skull percussion (only if fontanelle closed), transillumination (+ve)
7. Sclera above the cornea visible (sunset sign)
8. Difficult in delivery of head during labor
9. Spasticity of lower limb
Look for
Investigations . Neurofibroma
'1. Serial recording of head circumJerence o Cataract, CHD, deafness - Klebsiella
2. USG . Spina bifida, meningocele, mylomeningocele
3. CTIMRI (periventricular ooze) (Arnold-Chiari malformation)
Treatment
1. Medical 2. Surgical
- Acetozolamide - Ventriculoatrial/ventriculoperitoneal shunt - Upudhyaya shunt, Chopra shunt
- Glycerol - Thfud ventriculotomy
.-- I
Hematology
APPROACH TO BLEEDING DISORDERS

CLOTTING FACTORS
Petechiae: <2 mm
I. Fibrinogen Purpura:2-5 mm
II. Prothrombin Ecchy,rnosis: > 5 mm
III. Thromboplastin
iV. Ca
V. Proaccelerin
VI. No factor
VII. Stable factor
VIII. Hemophilia A
IX. X-mas factor
X. Stuart-Prower
XI. Plasma thromboplastin
XII. Hageman
XIII. Fibrin stabilizing factor
Extrinsic paihway
lntrinsic pathway tissue factor pathway
contact activation pathway
lul
l.
l
l
TXll
\Xlla
Activated
Partial (xl
thromboplastin \Xla
time
(,lX I
I
Va
ch"
Phospholipid
Bleeding disorder Coagulation disorder

Site Skin, mucous membrane Deep (soft tissue, joint, muscle)
(epistaxis, oral, GIT)
Petechiae Yes No
Ecchymoses Small, siperficial larse Deep
Hemarthrosis Extremly rare Common
Bleedine after minor trauma Yes No
Bleeding after surgery Immediate Delayed
Example vWD,ITP Hemophilia
Bleeding Disorders: Causes

I. Vessel wall abnormality
a. L:rfection: Meningococcemia
IE, Rickettsiae
b. Drug
r c. Scurvy
d. Henoch-Schonleinpurpura
e. Hereditary hemorrhagic telangeictasia
II. Platelet abnormality
a. Decreased number
1.. Decreased production
i. Diseases of bone marrow
- Aplastic anemia
- Leukemia, disseminated cancer
ii. Selective destruction of platelets .- &
- Drug: Alcohol, thiazide

- infection: HIV, measles
iii. Ineffectivemegakaryopoiesis
- Megaloblastic anemia
-
Myelodysplastic slmdrome
2. Increased destruction
ITP, SLE
Quinidine, sulpha
DIC, TTP, MAHA
b. Qualitative defects
1. Inherited
Glanzmann thrombocytopenia (IIb - IIIa defect)
Bemard-Soulier syrdrome (Ib)
2. Acquired
NSAID, Uremia
III. Coagulation disorders
3r6 lnherited Acquired
. Hemophilia A o Liver disease
. Hemophilia B r Vit K deficiency
o Von Willebrand disease (vWD) o Warfarin overdose
o DIC
HISTORY
1. Sex (heriditary)
2. Onset, mucosal bleed
Like epistaxis, gum bleed
Hematology
Joint swelling, muscle hematoma

- History of transfusion Steps of coagulation
4. History of trauma i. Vasoconstriction
5. Drug intake ii. Io hemostasis
6. HSP Arthralgia, abdirminal Pdffi, purPura/ Platelet adhesion, activation (release of ADp,
oliguria, edema, hematuria TXAr), aggregation
7. HUS - Oliguria, diarrhea iii. II" hemostasis
8. Anemia Thrombin formation fibrinogen clot
9. Recurrent infection
10. Bone pain, loss of weight, loss of appetite-malignancy
11. Complications: IC Bleed
- ICT - vomiting, siezures, focal neurological deficit, malena, hematuria
Past History
o First episode and each episode
r History of blood transfusion
r History of prior viral infection (usually 1 month in ITp)
o History of bleeding
- From trmbilicus at birth
-Duringvaccination,circumcision,toothextraction
r History of drugs
_ NSAID
- Anticoagulants
- Cephalosporin
- Anticonvulsive
o Jaundice - in liver disease
. SLE -rash, arthralgia
Antenatal
o Matemal drug
r History of infection CMV, rubella, neonatal thromborytopenia
Natal
Bleeding from cord - factor XIII deficiency
Postnatal
Blood in stool - hemorrhagic disease of newborn
Developmental Delay
If IC bleeds
Immunization
r Bleeding during vaccination
o HepB Decrease number of injections
. IM injections into S/C 317
Family History: . lJse smallest diameter needle
Ifuee generation o LJse ice packs after vaccination
. X-linkedrecessive-hemophilia
. AD-vWD
o Family history of menorrhagia
SEC
r Literacy
o Income
Endothelium
GENERAL EXAMINATION
o Pallor (proportionate or disproportionate)
o .Jaundice - liver disease, HUS, hepatitis B
. 'Lymph nod.e enlargement - malig-nancy
- Edema - HUS, HSP
Respiratory Rate
o Tachypnea-CCF
o Fever - malignanry (due to infection)
. Anybleedingmanifestation .- \
o Facies - due to hemolytic anemia
o Mouth
- Blebs in lips and oral cavity, ITp \
Gum hypertrophy (Leukemia)
- Oral thrush
o Malar rash - SLE
o Purpura: Nontender, nonblanching (Diascopy) purpura
r Bone tenderness, eczerna
. Abdominal distension
' Limbs - absent radii, thumb (TAR), thumb hypoplasia with anemia (Fanconi's), hyperextensibility
of joints
(Hur1er Danlos)
o External genitalia (testis)
Examination of ]oint (refer Ortho)

A. Inspection
- Attitude
318 - Deformity
- A.y wasting, shortening of limby
Any swelling (site, size, shape, surface, skin over swelling)
- Redness
B. Palpation
- Local rise of temperature, tenderness
- Swelling
C. Movement flexiory extension, etc.
D. Measurements:
Linear
- Circumferential
Hematology
o HSM
CNS: Rule out intracranial bleed.
CVS: CCF
Respiratory: Respiratory infections
Fundoscopy: not done - retinal bleed, papilledema.
Investigations
Hb: Decreased in aplastic anemia, leukemia
TC, DC: To rule out infections, leukemia
Platelet count
>50,000 - Easy bruisability
20,000-50,000 - Petechiae
<20,000 - Spontaneous bleeding
<10,000 - Intracranial bleed
Bleeding time: Normal:Z-3 minutes
Increased in any platelet function defect, decrease in number, vWD
Clotting tirhe: Normal: 8 minutes
Elevated in coagulation disorders
Then,
i. aPTT (Normal:35-45 sec)
- Elevated in intrinsic pathway
ii. PT (Prothrombin time: 12-14 sec)
- Elevated in extrinsic pathway
Peripheral Smear r
r Anemia *
. Leukemia - blast cells
o Low platelet count
Bone marrow:
Indications
o Before starting steroid therapy
. If suspecting malignancy, aplastic anemia
. In ITP bone marrow shows increased megakaryocytes
X-ray ioint - in hemophilia
o Factor assay VIII, IX - in hemophilia
r Ristosectin co-factor assay - vWD disease
Hess test Positive in:
. HSP, ITP, dengue
o Elevated BP between systolic-diastolic pressure
t If >20 petechiae/inch in forearm after 5 min
IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP)

Acute ITP
. Sudden onset
o Duration 4-6 weeks
o 1-7 years old
o Spontaneous remission in 807o cases
Chronic ITP: >6 months duration

Relapsing ITP: Relapses and remission during disease course
Course of ITP
i. 60-80%- spontaneous remission
ii. 20%'-becomes chronic ITP
iii. <1% - produce complications
The presence of lymphadenopathy or splenomegaly suggests other causes of thrombocytopenia.
LABORATORY DIAGNOSIS
. ITP is a diagnosis of exclusion
o Platelet count <1 lakh
. BT - prolonged
. CT, PT, aPTT normal
Peripheral smear
o Varying no of large platelets
Bone marrow aspirate
o Lrcreased number of megakaryocytes
Indications for BM examination in ITP
a. Chronic ITP
b. Abnormal TCIDC
c. Moderate,severe anemia (disproportionate)
d. Atypical history
e. Before steroid treatment
f. Failure to respond to steroids
MANAGEMENT
Supportive care
o Bedrest
o Avoid IM injections
o Avoid trauma
Treatment
a. Steroids
_ MOA
- Reduced antibody production
- Antigen-antibodyreactiondelayed
- Delayed platelet destruction
- Capillary stability increased
- CI - malignancy
- Prednisolone 4 mg/kg/day x7 days
b. IVIG
MOA
-
Block Fc receptor
-
Protect platelet from Abs induced phagocytosis
1g/kg/day x 1-2 days
320 c. Anti-Rh D therapy----only in Rh+ve patients
- Block fc receptors by antibody coated RBC in place for platelets
- 50-75rng/kg
d. Platelet transfusion
- If significant IC bleed
For surgical procedures
Management of Chronic ITP
o Altemate day low dose steroids
r Cyclophosphamide, vincristine, azathioprine, danazole
Hematology
o Splenectomy
- Reduced antibody production
- Increased platelet destruction
. Anti CD20 - Rituximab
HEMOPHILIA
o Most common clotting disorder
o X-linked recessive
- Hemophilia A - Factor VIII deficiency Mild hemophilia 540% factor
- Hemophilia B - Factor IX deficiency Moderate hemophilia 1-5oh factor
Severe hemophilia <1"h f.actor
- Hemophilia C - Factor XI deficiency-AR
i - Parahemophilia-FactorVdeficiency
Treatment
1. Factor replacement
- Cryoprecipitate - contains all factors except IX
- Fresh frozen plasma - contains all factors including IX
1 unit bf factor VIII/kg rises factor level by 2%
- To prevent hemarthrosis target level = 30%
- Needs = 15 U/kg factor VIII
- TopreventICbleed30-100%
1unit of factor X rise factor level by 1%
- Adjuvant therapy
- Epsilon aminocaproic acid
- Tranexamic acid
2. Physiotherapy for joint diseases .\
3. Advise for injury prevention i I
4. Supportive care ----/
Prevention
o Genetic counseling and prenatal diagnosis Most common muscle involved in bleeding
o Most corunon cause of death are: . Flexors ofarm
- AIDS o Gastrocnemius
- IC bleed o Iliopsoas
HEMORRHAGIC DISEASE OF NEWBORN

of vit K and hence vit K dependent coagulation factors II, vr, x, X leadin-
fi?il"H*,tili[ffi:Tdeficiencies
. Types
a. Early onset I
- Etiology: malarial drugs, phenobarbitone, phenytoiry warfarin
Sites of hemorrhage
Cephalohematoma
Subgalleal
- Intracranial
Gastrointestinal
- Intra-abdorninal
b. Classic diseases
- Age:2-7 days
- Etiology: Vit K deficiency, breastfeeding
c. tate onset
- Age: 1-6 months
- Etiology: Cholestasis - malabsorption of vit K
Investigations
L. Prothrombin time, aPTT
2. PIVKA (Protein induced vit K absence) - tends to be positive for longer period and even after blood transfusion
Treatment
. Injection vit K 2-5 mg tV
Prevention
o Injvit K
. 1 mg IM (if >1 kg)
0.5 mg IM (if <1 kg)
LEUKEMIAS
ALL (ACUTE LYMPHOCYTIC LEUKEMIA)
T cell - Adolescence (boys)
B cell - 2-Syears (Common ALL)
French-American-British Classification
L1(85%) L2(10%) r3 (s%)
Small homogenous cells Large homogenous Large homogenous
(Burkit lymphoma)
Clinical Features .-,\
o Short duration PUO, Pallor, LNE, HSM, bleeding manifestations
o ]oint pain
Myeloblast vs Lymphoblast
Investigations . Abundant cytoplasm . Scanty cytoplasm
1. CBC-increased total count o Auer rods presenf o No Auer rods
2. Decresed lymphoblast o Fine chromatin o More condensed chromatin
3. Bone marrow . 3-5 nucleoli, distint . Nucleoli 1-3, indistinct
- >20% blasts
4. Stained by Periodic acid Schiff and terminal deoxy peroxidase
5. Flow cytometry: look for specific CD (in blood)
6. Immunochemistry: to see CD in solid tissue like liver and spleen
B cell precursor - CD14,CD20,CDL\CDZT
B cell precursor - Ig on surface
T cell - CD2,CD3,CDs,CD7
7. Cytogenetics
322 Management
1. tnduction phase: For remission Prognosis
(vAPA) Adverse effects
1. Age at diagnosis (1-9 years)
2. Initial leukocyte <50,000/mm3
Vincristine - Neuropathy
3. Female sex
- Adriamycin Cardiotoxicity
4. B cell type (4)
- Prednisolone - Pancreatitis
5. Hyperploidy
- Asparaginase
6. Trisomy 4, 10 (Translocations 8:1.4, 4:1.7,9:22 -bad
2. Consolidation phase: Intensification
prognosis features)
- (MECA)
7. Response to treatment with prednisolone
Methotrexate
B. No LNE, HSM, CNS involvement
- Etopside
Cytarabine
- Adriamycin ..
3. Maintenance phase:
- 6 mercaptopurine
- Methotrexate
- Prednisolone
- Vincristine
4. CNS preventive therapy
- Intrathecal methotrexate and cranial radiation
AML (ACUTE MYELOID LEUKEMIA)

C/F
o Short duration, fever, pallor, bleeding tendency, sternal tenderness
o Gum hypertrophy (AML - M4 M5)
o Chluroma (AML - M2)
r Oral petechiae
. Fundal hemorrhage
. Diffuse bone pain
FAB Classification
1. AML M0 - Undifferentiated
2. AML M1 - Acute myeloblastic leukemia with minimal maturation
3. AML M2 - AML with maturation
- most conunon, t(8:21)
4. AML M3 - Acute promyelocytic leukemia
- t(15:17)
- Increased risk of DIC .. 11
- PML - RARcr translocation \r/

5. AML M4 - Acute myelocytic leukemia )
6. AML M5 - Acute monocytic leukemia I G* hypertrophy
- t(9:11) )
7. AML M6 - Acute erythrocytic leukemia (Di Guglielmo's slmdrome)
8. AML M7 - Acute megakaryocytic leukemia - Associated with Down's slmdrome
Investigations
1. CBC _TC
2. PS - Myeloblast
3. BM -Blast >20'h
4. Stained by - Sudan black, myeloperoxidase and nonspecific cytometry
Treatment
o Cytosine arabinoside + Doxorubicin .
. AML M3 - All trans-retinoic acid (ATRA) and AsrQ
323
TRANSFUSION DEPENDENT ANEMIAS
CLASSIFICATION OF ANEMIA
Due to Blood Loss
Increased destruction (hemolytic anemia)
o Intrinsic (intra-corpuscular)
- Acquired
- Hereditary
. RBC membrane defect, e.g. hereditary spherocytosis, hereditary elliptocytosis
. RBC enzyme defect, e.g. G6PD deficiency
. Disorder in FIb slmthesis

Decreased globin
- Abnormal globin
o Extrinsic (extra-corpuscular)
o Autoimmtrne heinolytic anemia, micro AHA, DIC
Impaired Production
. Proliferation and differentiation of stem cell
- Aplastic anemia, Aplasia, pure red cell
. Proliferation and mafuration of RBC
- Decreased DNA slmthesis, e.B. B, deficiency, folate deficiency
- Decreased FIb
- Heme, e.g. Fe deficient anemia
- Globin, e.g. thalassemia . Pallor
- BM infiltration o Jaundice
. R/o SCA, Fe deficient anemia, G6PD
HISTORY . R/o leukemia, aplastic anemia
a. Pallor and its severity
- Easy fatigability, tiredness, decreased concentration, breathlessness/ progressive/not
PND, pedal edema, PICA, hookworm
b. Jaundice
- Time of appearance
c. Abdominal distension
- AD - H.S <4 months
- AR - Thalassemia 6 months-2 years
SCA 1-5 years hemolytic anemia
- XR_G6PD drug . Pallor
d. Leg ulcer (Sickle cell anemia) o ]aundice
- Chest pain (Acute chest syndrome) . Splenomegaly
- Extremity pain (Dactylitis)
- Repeated left sided abdominal pain (Acute splenectomy) .
Sudden increase in depth of pallor and jaundice (Hemolytic crisis)

'shock (sequestration
- Features of crisis)
e. History of drug intake, e.g. G6PD deficiency
f. History of bleeding tendancies
- (Ap1astic anemia, leukemia, aplastic crisis, sequestration crisis)
- Bleeding from orifices
- Nasal bleed
- Gumbleed
APPROACH TO HEMOLYTIC ANEMIA

Urine Stool
Hemolytic Normal Normal
Obstructive Cola colored Pale
Hepatocellular High colored " Normal
Associated Symptdms
o History of recurrent infection-leukemia
o History of bone pain
PAST HISTORY
Blood transfusion and its complications
' Age of onset
r Frequencyofbloodtransfusion
Hematology
o Pretransfusion andpost-transfusionchanges
o Transfusionreactions
r Drug intake - folic acid
o Chelation therapy (History of chemotherapy/RT (aplastic anemia)
. Surgery- splenectomy,'cholecystectomy
(Gallstone risk: HS > SCA > Thalassemia)
Complications of Transfusion
1. Hep B-Fever + ]aundice
2. Malaria
3. Cardiomyopathy - CCF (arrhythmias is the most common cause of death around 10-20 years)
4. Hypothyroidism - constipation, somnolence
5. Hypoparathyroidism - tetani
6. Diabetes mellitus/diabetes insipidus - polyuria, polydipsia
7. Hypogonadism - delayed 2" sexual character, 1" amenorrhea
8. Growth retardation
9. Recurrent bacterial infection
Complication of Disease
r Sequestration crisis
. Hemolytic crisis
o Vaso occlusive crisis
Antenatal History
Anemia in pregnancy
Natal
o Neonatal jaundice
. Sepsis
. Exchange transfusions
Developmental Delay
Diet
r Intake ofFe rich food
. Cooking in steel container
o Tea, chocolate decreased Fe intake
. Milk cause Fe deficiency and poor in folate
x
Immunization
. HBV
r Pneumococcal (4 weeks prior to splenectomy)
. Meningococcal
Family History
o Consanguinity
o Similar illness
r History of splenectomy
Socioeconomic status
GENERAL EXAMINATION
o Hemolytic facies (Chipmunk facies)
- Prominent frontal and parietal eminences
- Flattened vault
- ftyp"rt.ophied muscles
- Prominent maxillae
- Prominent malar eminence
- Depressed nasal bridge
. Pallor, jaundice (Hepatitis B, hemolysis, Fe overload)
. Clubbing (CLD),
. Edema (CCF)
. LNE (Malignancy) '
o Oral cavity (gum hypertrophy in leukemia)

. Eye (subconjunctival hemorrhage, proptosis in leukemia)
. Skin (Hyperpigmentation in Fe overload)
o Mucocutaneous bleed
. Thyroid swelling
r Skeletal deformity
- Absent thumb - Fanconi's anemia
- TAR- thrombocytopenia with absent radius (Diamond-Blackfan slmdrome)
- Abdominal distension
External genitalia (size of penis, scrotum, pubic hair)
, External genitalia
- Signs of liver failure
Pulse
o Tachycardia - CCF, anemia
. High volume - anemia
. Low volume CCF
. Peripheral pulsations embolism (sickle)
ANTHROPOMETRY
o Head circumference increases (frontal bossing)
o Height decreased (short stature)
. HSM
. CVS-{CF
o CNS-{ompressionmyopathy
Examine parents for HSM
Respiratory System (any hereditary disease)
Chest syndrome
Diagnosis
1. Transfusion dependent anemia
2. Prob ably thalassemia
3. With/without features of Fe overload
4. With/without complications
5. Protein-energy malnutrition o Elevated
326 reticulocyte count o Feature of a post-splenectomy
Hemolysis - Howel-Jolly bodies
= Recovery from vitlFe
o - Basophilic stippling
Deficiency Anisopoikilocytosis
- Hemorrhage Heinz bodies
- Sepsis, splenic sequestration - Normoblast
RHS o Immediate
r Low reticulocyte count . Thrombocytosisandleukocytosis
Fe deficiency anemia
Pure red cell aplasia
- BM infiltration
Hematology
INVESTIGATIONS
L. Hemoglobin and red cell indices
Low MCV and MCH
- RDW - elevated:
- Fe deficiency anemia
- Normal-thalassemia
2. Total count
- Leukocytosis - shift to left
Low platelet and WBC - hypersplenism
3. ESR - elevated in all anemias except sickle cell anemia
4. Reticulocyte count - elevated
- Using supravital staining - crystal blue
- .Corrected reticulocyte count - patient's reticulocyte count X patient hematocrit
Normal hematocrit
5. Peripheral smear
- Microcytic hypochromic anemia (Thalassemia, Fe deficiency anemia, sideroblastic anemia)
- Anisopoikilocytes (Different size and shape of RBC)
Polychromasia
- Normoblast
- Sickle cell (drepanocytes) in SCA \
- Spherocytes (HS, autoimmune hemolytic anemia)
6. Definitive diagnosis I
In thalassemia, SCA - High performanceliqy{d chromatography (HPLC)
Thalassemia major - FIb A absent, FIbF elevated
- Thalassemia trait - I-Ib A2 elevated, HbF normal/increased
7. Sickling test: Using 2% Na metabisulfite
8. Osmotic fragility ',' \
Using Kahn tube
Normally starts at 0.45% and ends at 0.35.
- Increased in hereditary spherocytosis
- Decreased in thalassemia
NESTROF (Naked Eye Single Tube Rapid Osmotic Fragility Test) - used for mass screening
9. G6PD estimation - in G6PD deficiency
10. Coomb's test - AIHA
11.. PNH (Paroxysmal Nocturnal Hemoglobinuria)
CD55/C59 assay
Ham's test
Sucrose hemolysis
12. Serum bilirubin
Elevated unconjugated bilirubin Hemolytic anemia
Elevated LDH
13. Urine
Urobilinogen - elevated
- Bile salt and bile pigment - absent
14. CT, BT: If bleeding tendencies.
15. Indication for marrow examination
Bone tendemess
Bleeding manifestations
15. X-ray
Hair on end appearance on skull - thalassemia
Earlier X-ray change - metacarpal tuberculations
AGEMENT
Blood transfusion
Fe chelators
3. Splenectomy
4. Diet
5. Drugs :
6. BM transplants
7. Prenatal diagnosis and genetic counseling
Aims of Management
a. Limit size of spleen by suppressing extramedullary erythropoiesis
b. Limit facial change by suppressing medullary erythropoiesis
c. Promote normal growth and development
d. Limit Fe overload
If the FIb low - body absorb more Fe
lf transfused - decreased Fe absoYption
1. Blood transfusion
OP Ghai - Pre transfusion level 9-70 g/ dL
Types:
a. Low transfusion
' Pretransfusion level is maintained (6;10 g%)
' b. Hypertransfusion i
Keep pre transfusion level >10 g"(
Transfuse blood to raise Hb to fZ-\3 g% when Hb<10 g%
Check FIb every 2-3 week \
Advantages:
a. Maintain normal growth
b. Limit size of spleen
c. Super transfusion
Keep pre transfusion llb> 12mg"h ._ h
Give blood to keep llb 1.4-1.5 g%
- Transfusion reaction can be minimized by the saline wash (deplete leukocyte and plasma protein) using
leukocyte filters
- Allergic reaction can be prevented by giving hydrocortisone and antihistamines
- Fe overload occurs after 10-20 transfusions due to
a. Increased GI absorption
b. Transfusional siderosis
Diagnosis: Serum ferritin > 1000 yrg/L (ng/mL)
Monitoring of Patient
1. Hb
2. Size of spleen (for Fe overload)
3. Serum ferritin (normal - 300 nglml.)
4. TFT
5. Serum calcium
6. FBS/PPBS
7. LFT,liverbiopsy, USG abdomery MRI liver
328 8. Chest X-ray, ECG, Echo, Cardiac T2 MRI
9. Evaluate height, hypogonadism
10. HBV, HIV
2. Fe chelation
After ll years of transfusion
a. Deferoxamine
- Dose: 40-60 mg/kg/ day S / C / over 8-12 hours. Daily night over 56 days/week by mechanical pumps
- tV ifcardiac failure occurs
- Chelate Fe frorn ferritin and hemosiderin (not from transferrin)
Adverse effect
- Hypersensitivity, red discoloration of urine.
Hematology
Contraindication: Renal failure, Sensorineural hearing loss, Visual toxicity

- Monitoring: Slii lamp, RFT, Audiometry
b. Deferiprone c. Deferasirox
71mg/day orul Oral20 rng/kg/day
- Mobilize Fe from trandferrin, hemosiderin and ferritin - Tridentate ligand finds Fe from
Adverse effect: intracellular and extracellular Fe
- Arthritis throughout the body including
- Agranulocytosis liver, heart, reticuloendothelial
- Monitoring: system and circulation
- ]oint examination Adverse effect:
- Total count - Rashes
- GI toxicity
- Renal and hepatic toxicity
Monitoring: RFT, LFT
Shuttle Hypothesis
Combination of oral and parenteral drugs is more effective
tcl-670
-New synthetic oral chelator
It chelates Fe from parenchymal organs and RES
Remove Fe directly from myocardial cell
Role of vitamin C i
Vitamin C converts hemosiderin to ferultti,ftom which Fe can be easily chelated 100 mgldaily
Splenectomy --/
Indications:
a. Hypersplenism
b. >12 whole blood transfusions/year
c. >24 packed cell transfusion/year,>200-250 mL/kg/yr i
d. Splenic sequestration crisis in sickle cell anemia
e. Hereditary spherocytosis (After 5 years is curative)
Hypersplenism criteria Causes of cytopenia in hypersplenism

a. Splenomegaly a. Sequestration'-
b. Pan/bicytopenia b. Increased splenic function
c. Corrected by splenectomy c. Splenic phagocytosis
d. BM normal/ hypercellular d. Increased antibodies
Before splenectomy
- Pneumococcal vaccine
- Meningococcalcaccine
- lnfluenza
-
Ml
Anti-malarial prophylaxis in endemic areas
After splenectomy
- Penicillin prophylaxis <5 years - 125 mgbd po
>5 years - 250 mg bd po
OPSI: opportunistic post splenectomy infection
- Fever in splenectomized patients should bdconsidered as sepsis.
Diet
- Supplements of folic acid, ascorbic acid and vitamin E
Fe preparation should not be given
Drinking tea with meals decrease Fe absorption
Avoid cooking in steel vessel
Drugs
Folic acid - 5 mg/ day
Hydroxyl urea (15-20 mg/kg/day)
-
Increased production and reduce need for transfusion
-
It is leukemogenic
5. Hematopoietic stem cell transplantation
It is the only known curative treatment of thalassemia.
Poor outcome:
- If hepatomegaly, fibrosis
- Inadequate chelation prior to treatment
Types of stem cell transplantation
a. Autologous - from patient
b. Allogeneic - HLA matched sibling
7. Prenatal diagnosis
Genetic counseling
To create awareness and prevent thalassemia major in offspring
8. Others
Bone problem: Chipmunk facies
- Osteoporosis
- Bisphosphonate
- Calcium
i - Vitamin D
Compression fractures of spine
Psychological counseling ./
t--:--/
THALASSEMIA
AR
. o(, - Decreased u gtobin synthesis
o B - Decreased B globin synthesis ._.\
B-thalassemia Major
. B. /9 or 0'l0' p* Decreased synthesis of p chain
. TDA p'- Absence of B
B-thalassemia Intermedia
. B*/0'
o Monitor patient
o Blood transfusion not needed.
B-thalassemia minor (Thalassemia trait)

. g*/gorg./p' HbA-orp, 95%
. Mild anemia HbAr-crr6, 21%
. FIbA, increases HbF - ory, traces
s-thalassemia
330 .o Absent/decreased clt chain
Newborn Adult
o yu (Hb Bart) p.
(Hydrops fetalis) I-Ib H
cr-thalassemia Trait
o u/a,-/- or a/-,a/-
Silent Carriers
o -fu,a/a
Hematology
pthalassemia
,r--$"\ Reduced p-globin synthesis, ,,--3\ a-gtobin aggregate
HbA_6gffi with retative excess of cr-stobin.
6g@h,rsotubte
,."..HffiJ
(-z.z)
ffi)fl
Normal erythroblast
\sefnun
#m
ry Few abnormal
red cell leave
*
o,-globin
aggregate
Normal red blood cells Normal HbA
Hypoch romic red cell

1
Dietary iron Extravascular hemolysis

Destruction of
aggregate containing
rrBd,rqell$ it!, spl*en
Systemic iron overload
Skeletal deformities
HEREDITARY SPHEROCYTOSI S
.AD
. Ankyrin /Band 3/Spectrin molecules
o Decrease membrane stability -+ loss of membrane fragment -+ spherocytes -+ less deformable -+ distruction in
spleen.
.WVN
tffin Spherocyte
* ff rc $
tr*
Iffi.W
w'::'_J
:V !
6ffi \./lffi
Diagnosis
. Family history
o Increase osmotic fragility
. Decrease MCV
o Increase MCHC (very important)
Treatment
o Folic acid 1-5 mg/ d,ay
. Splenectomy
o Cholecystectomy
THALASSEMIA VS HS
Thalassemia HS
After first 6 month (6 month to 2 year) Neonatal penod (or at any time)
Jaundice - very minimal Mild jaundice
Reticulocytes-1-8"/" 5-15%
Site of RBC destruction - bone marrow spleen
Osmotic fragility - decreased Increased
SICKLE CELL ANEMIA

,AR
6th position in beta chain, valine for glutamic acid
(glutamic acid go)
Point
mutation
CF
Pain, icterus, pallor, mild splenomegally, tachypnea,
infections, etc.
Crisis
V - Vaso-occlusive '-'!
A - Aplastic
Deoxyglenation
S -Sequestration lrreversibly - -l
I - Infiltration
A - Acute chest syndrome
?ff
sickled ceUr'
*iM |
K,H2o
Hemorysis ffi*1
Management of Crisis
a. Analgesics nacrotics
Y r##:" {,rnjn.,.n I
b. Hydration I Rooitionat
c. Oxygen
d. Blood transfusion-aplastic crisis/sequestration crisis
L. | ,*ilil??,31,";
oeoxysenation,
e. Ventilation in CVA Microvascurar*k .,::"li'1ffi:. &___l
occtusion
f. Exchange transfusion in CVA, chest slmdrome
Preaentioe Care
=q
\ W
,"t"1:nfg:*:;"
a. Penicillin prophylaxis at least until5 year
332
b. Pneumococcal, meningococcal, influenza vaccine
c. Folate supplementation
d. Hydroxy urea
FE DEFICIENCY ANEMIA
CLINICAL FEATURES Investigations
a Pica o Low FIb
a Koilonychia o Decreased MCV
a Angular stomatitis o Decreased MCH
Glossitis o Increased RDW
Hematology
Management . Peripheral smear

a. Ferrous sulfate
- Microcytic hypochromic anemia
3-6mg/kg/dayFe' - Anisopoikilocytosis
After correction of anemia o Serum Fe decreased,
Continue oral Fe for 44 mcinths to replenish Fe stores r Serum ferritin decreased,
b. ParenteralFe r Increased total iron binding capacity
IV Fe sucrose preparation
Dose:
Fe required = wt (in kg) x 2.3 x (15-patient's FIb) + 500 to 1000 mg
- Given as divided doses
lndications
1. lrtolerance to oral iron
2. Malabsorption states
3. Rate of ingoing blood loss is more so that cannot be replenished by oral Fe.
c. Blood trasnfusion
lndication
1. Urgent surgery
2. Hemorihage
3. Severe anemic with CCF
MEGALOBLASTIC ANEMIA
CF
o Glossitis M - malaise, memory loss
o Stomatitis E - easy fatiguability
o Oral ulcer G - grey hair, a glossitis
r Hyperpigmentation of skin, knuckle A -anorexia
. HSM (40%) L - loss of weight\
o Petechiae (25%) O - optic atrophy
o Neurological: memory loss, confusion, loss of B - bleeding manifestations, breathlesness, beafy tongue
position and vibration sense. L - liver and spleen enlargement .
A - angular stomatitis
Peripheral Smear S - skin pigmentatiom SCD
Macrocyte, cytopenia, hypersegmented neutrophil T - thrombocytopenia
> 5lobe I - impotence
C - change in personality, confusioru CCF
Bone Marrow
Cellular increased precursors
Treatment
o Folate L-5 mg/kg
. BrrlmglM
Renol, Arthritis and
Pediatric Surgery
RENAL SYSTEM
APPROACH
1. Renal edema
First on face, then lower limbs-t ascites -+ hydrocele -> scrotal edema
More in early morning
2. History of acute glomerulonephritis
- Hematuria (if present r/o drug history (rifampicin), colored food (Beetroot), bleeding manifestations,
muscle iniury: as myoglobinuria) "-
x
Oliguria Edema causes

Pyoderma, sore throat Cardiac
3. History of nephrotic syndrome Hepatic
Frothy urine Endocrine
Generalized edema Renal
4. History of HSP Inflammatory
- Abdominal pain, fever, rash, arthritis Angioedema
History of HUS Nutritional
aLaominat pain, diarrhea
Rule out other causes of edema
Localized - insect bite reaction, lymphedema, angioedema
Generalized
a. Cardiac cause
First on dependant parts (LL, presacral edema)
More in the evening
Cardiac symptoms
b. Hepatic cause
Early abdomilral distension (ascites)
]aundice
c.Nutritional causes
Associated growth retardation
Recurrent infections
History of nutritional deprivation
d. Endocrine - hypothyroidism
Complications
Nephrotic syndrome
a. Spontaneous bacterial peritonitis - abdominal pain, fever
b. Pleural effusion - breathlessness
Renal, Arthritis and Pediatric Surgery
\
c. Pericarllial effusion - pain on leaning forward
d. Thrombosis - Pulm embolism - dyspnea, chest pain
esteroid*.,.,,r1i1;t:T":THJil;ffi ['#:#;ffi :iXrdation

f. infection
AGN
a. Acute renal failure (ARF) - oliguria, anuria
b. Hypertensive encephalopathy - headache, vomiting, seizures, altered sensorium
Left ventricular function (LVF) - exertional dyspnea
IgA nephropathy - recurrent hematuria, 2-5 days after respiratory illness.
Alport's syndrome - family history of deafness
PAST HISTORY
1. History of similar episodes in the past
Number of episodes, treatment taken, monitoring in case of relapse, precipitating factors like urinary tract
infection (UTI), respiratory tract infections.
Response to drug
2. Sore throat L - 2 weeks prior - strain4,l2
Pyoderma 2 - 4 weeks prior - strain 49
3. )aundibe (hep B, C), malaria - 2o nephrotic slmdrome
4. TB - Steroid Rx + Flaring up of TB
Development History
Gross motor delay, hearing - Alport's slmdrome
Diet
Any diet modification
Immunization
Hep B, pneumococcal vaccine
Family History
Hearing loss-Alport's s5mdrome
GENERAL EXAMINATION
. Pallor due to hemodilution (AGN)
Hemolytic uremic syndrome (filJs)
Severe hematuria
Chronic renal failure (CRF)
o jaundice - Hep B, Hep C, hemolysis 95th percentile BP _ 100 + (age in year x 3)
. Edema (>1 year of age) - ?0 . ("g" 111 ygrr)( 15)
Vitals
. Respiratory rate - effusion 33s
oBP
. IVP - right heart failure

. Cushingoid facies
o Oral candidiasis - steroid treatment - immunosuppression
. Malar rash - SLE
o Features ofliver disease(s)
. Skin - pyoderma scars
Anthiopometry
Height decreased in:
1. Steroid.Rx
2. Recurrent infections
3. Hypothyroidism
Examination of gastrointe stinal sy stem
o Abdorriinal wall edema - hold for 30 seconds i '
o Scrotal edema - very important finding

o Renal mass
. HSM
. Ascites
Examination of respiratory system
. Effusion
. Basal creps
r Pneumonia
Examination of cardiooascular system (CVS)
Congestive cardiac failure
Diagnosis
o Generalized edema
o Due to renal disease (s)
. Probably nephrotic (relapse, which episode, treatment failure, etc.)
r Withoutcomplications
ti
ACUTE GLOMERULONEPHRITIS
1. HTN
2. Hematuria .'..\
Causes of AGN
3. Oliguria 1. Post-infectious - streptococcal,
4. Edema staphylococcal, hep B and C
(code HrQ) 2. Systemic vasculitis-HSP, SLE, PAN
Type 3 immune reaction 3. Membranoproliferative GN
Intravascular fl uid overload 4. IgAnephropathy
5. Familial-Al
INVESTIGATIONS
1. CBC - Hb low due to hemodilution
2. Urine
Protein 1+/2+
RBC
- WBC due to glomerular inflammation (not UTI)
- RBC cast, granular cast
3. RFT-in acute renal failure increased blood urea and serum creatinine
4. Serum electrolytes-low Na, elevated K
336 5. Low C}-singlemost imp investigation (post-skeptococcal)
I 6. ASO titer increased in >80% pharyngitis cases
DNAase B >50% pyoderma cases
7. Chest X-ray-hypervolemia
8. Renal biopsy-indications
- Impaired renal functionbeyond 1 week (7-10 days)
Hypertension or gross hematuria beyond 2-3 weeks Confirmatory test for NS
Low serum C3 beyond 6 weeks o High cholestrol level
- Those with features of systemic illness. e Low albumin level
MANAGEMENT
1. Diet :
- Limit sodium, potassium, proteins

- Avoid pickles, bakery items, pappads, salted fish, fruits rich in potassium, muringa leaves, tender coconut
water
- Carbohydrates and fats are allowed
Calories = RDA + 10% extra
2. Fluid intake - renal output + insensible water loss (400mL/mz/day)
J. Weight (monitor daily), should lose 0.5% daily.
Gain indicates fluid overload
In severe oliguria, there is 0.5% loss of weight due to endogenous catabolism.
4. BP-frequent monitoring (labile HTN)
Mild-salt and water restriction, nifedipine, atenolol
(Spironolactone, ACE inhibitors contraindicated)
Hyp6rtensive emergency - IV nitroprusside or labetalol
5. Diuretics-oral frusemide
IV frusemide in pulm edema
6. Leftventricular failure
Propped up position
IV frusemide {j
- Respiratory support with positive end expiratory pressure I
7. Prolonged oliguria
Dialysis if severe renal failure Course of AGN
- Fluid overload
- Life-threatening electrolyte concentration
o Urinary protein excretion and HTN becomes normal
by 4- 6 weeks
t
,t
Management of hyperkalemia (>5.5 mEq) o Persistent microscopic hematuria may persist for 1-2 ;1,
Stop intake of potassium and offending drugs years aftet' the initdl presentation T
h$
- Glucose insulin infusion ;l
NaHCQ infusion II
1[
IV calcium gluconate
- ry salbutamol or nebulization itii
Dialysis It
Potassium binding ion exchange resin 'l
8. Pyodrema lesions - even if healing, penicillin for 10 days (prophylaxis) ;l
il
MONITORING
1. Intake output chart daily i
t
2. Monitoring pulse, frequent BP measurement, respiratory rate (labile HTN)
3. Daily temperature chart
4. Dailyweightmonitoring.
Hematuria-presence of more than 5 RBC/HPF, causes?
LOCALIZATION OF BLEEDING SITES IN HEMATURIA

Glomerular
Cola colored
- Proteinuria
RBC cast
- Deformed RBCs
DCT and collecting duct
WBC and epithelial casts Complications
Lower urinary tract r Acute ranal failure
Gross hematuria
. LVF
Terminal hematuria o Hypertensive encephalopathy
- Normal RBCs
Blood pressure at least 80% of arm circumference

-Length 40-50% of arm circumference
: -Width
FLUSH METHOD IN INFANTS
Mean BP = diastolic + l/3rdpulse pressure
Doppler method is accurate. i
Hypertension-average systolic/diastolic BP-gsth percentile for that age and sex in at least 3 occasions 50th
percentile of SBP in children more than Zyears = 90 + 2 x age in years
On dischnrge:
. BP should be normal
. Renalouput should be normal
o No complications.
l
NEPHROTIC SYNDROME
INVESTIGATIONS
1. Flb-elevated if there is contracted plasma volume due to hypoalbuminemia
, TC, DC increased even in absence of infections
Etiology
ESR to rule out TB.
1. Idiopathic-90%
'2. Urine:
24 hour urine protein more than 40 mg/r* /hor 1 g/rfi / day
minimal change-8S%
mesangial proliferative-S%
Protein creatinin ratio more than 2
FSGS-10%
Pus cells > S/HPF-UTI in males
2. Secondary (10%)-membranous
> 1O/hpf-UTI in females\
membrano-prolif erative
RBC > 5/hpf-hematuria.
glomerulonephritis (MPGN)
3. RFT-if abnormal indicates different histology or. accute renal
failure '- \
4. LFT - serum albumin < 2.5 g/ dL
Serum globulin normal or elevated
5. Lipid profile - HDL decreased
LDL, VLDL, total cholesterol increased
6. Serum C3low in afypical presentation
7. Chest X-ray-r/o TB, effusion
B. USG abdomen-kidney size, ascites
9. Mantoux-TB
10. Indication for renal biopsy
- Age <1.yr,>9yr AGN Nephrotic syndrome
- Hemafuria 1. Age group Older 2-6years
- LowC3 2. Preceding ilness Present Not
(skin, throat infection)
- Hypertension 3. Pathogenesis immune
- Impaired renal function
- Frequentrelapses complex Minimal-T cell dysfunction
- steroid resistance. 4. Onset Acute Insidious
338 *eNAGEMENT 5. Hematuria, HTN Present Absent
6. Edema + +++
1. Diet 7. Reccurence Rare Present
No added salt 8. Urine RBC cast, Fat laden cells
granular cast
- Highnormalgoodquality
9.Albuminuria Moderate Massive
protein diet
10. Serum cholestrol Normal Increased
- High CHO,low fat
11. FIb Hemodilution Hemoconcentration
No water restriction
2. Treatanyassociatedinfection
3. Diuretics:
If significant edema
- Frusemide 1-4 mg/kg/day in 2 divided doses

- Spironolactone 21 mg/kg/ day
- Should be cautiotis since plasma volume contraction may already be present and may lead to hypovolemic
shock.
Specific management
,dn
rspal
Remission-urine albumin nil/trace for 3 consecutive days

Relapse-3+ /4+ and edema for > 3 days in a patient who was in remission
Frequent relapse-patient who respond well to predinisolone therapy but relaps > or = 4fimes/yr
Steroid dependence-if relapse occurs while on altemate day steroid therapy or within 28 days of stopping
d*g
Steroid resistance-failure to respond steroid therapy within 8 weeks.
5. Human albumin:
If-serum albumin <1.5 gm%
Symptomatic ascites
Symptomatic hypovolemia
Dose - 1,g/kgover 30---60 mts followed by frusemide.
MONITORING
o BP, temp
. Input output chart
. Daily weight
. Urine albumin 339
Nephrotic syndrome is defined as a clinical stateeharacteizedby:
L. Edema
2. Proteinuria > 40 rr.g/m2 per hr
3. Hypoalbuminemia <2.5 gm/dL
4. Hypercholesterolemia.
1, Edema-causes
Proteinuria + hypoalbuminemia -+ decreased oncotic pressure -) extravasation of fluid in interstitial spaces
Increased secretion of renin angiotensin system -+ sodium and water retention
Increased secretion of ADH -> water retention
- Blunted responsiveness to atrial natriuretic peptide.
- Normal prgtein excreted in urine < 150 mglday, Normal protein excretion < 4 mg/r*/hr, Abnormal
4-40 mg/m2lhr, Nephrotic range > 40 mg/r*/lv
Transient proteinuria-after fever, exercise, etc. doesnt reach 2+, no evaluation or Rx needed
Orthostatic proteinuria-if child with persistent asymptomatic proteinuia r / o orthostatic proteinuria,
- Supine-normal/slight proteinuri
- Upright position-up to 10 fold
- Dx-absence of protinuria (p:c <.2) in first morning urine sample for 3 consecutive days.
Causes of proteinuria:
Loss of fixed negative charges from glomerular basement membrane
Abnormality of epithelial foot processes (podocytes)
Heat and acetic acid test:
Fill2/3rd of test tube with urine and heat upper part of test tube. A coagulum is formed at the top. Add few
drops of 3% acetic acid and compare with the lower part.
Other method useful-sulphosalicylic acid test.
Proteinuria While reading newspaper across test tube
Trace clear (0.1gldl.)
1+ can read bold and small letter (0.3 g/dl.)
2+ can read bold letters, not small ones (1 g/ dL)
3+ can read bold letters, not small ones can (3 g/ dL)
4+ see something is written nothing is seen (10 g/dl.)
3. Hypoalbuminemia
Due to selective proteinuria
<2.5 gm/dL
Edema appears when serum albumin' <2 gm/ dL
Pleural and pericardial effusion may appear when s. albumin <1.5 gm/dl
4. Hypercholesterolemia
- Due to hepatic synthesis of lipoproteins 2o to heplUc slmthesis of albumin (due to closely related pathways)
- Increased loss of lipoprotein lipase in urine.
Lipid profile-VlDl and LDL increased
HDL normal or increased in MCNS.
Causes of 2'Nephrotic Syndrome

1. Collagen vascular disease-rheumatoid arthritis, SLE, pAN
2. Infections-hepatitis B, P. malariae
3. Malignancies-leukemia, lymphoma
4. Endocrine-diabetes
5. Drugs-captopril, NSAID, penicillamine
*MCNS vs significant lesions?
Complications of nephrotic s5mdrome

1. Edema
2. Infections-SBP
o Pneumonia
340 3. Thrombotic complications
o Due to hemoconcentration
o Loss of antithrombin, protein C, S
. Increased fibrinogen
. Immobilizatton.
4. Steroid toxicity
5. Acute renal failure
6. Abnormal srowth and nutrition
Henoch-Schonlein Purpura
Palpable purpura in the presence of at least one of the following four features:
1. Diffuse abdominal pain
2. Any biopsy showing predominant IgA deposition
3. Arthritis or arthralgia
4. Renal involvement (any hematuria + / - proteinuria)
Treatment-supportive with maintenance of hydration and pain rglief
Prednisolone
Hemolytic Uremic Syndrome

Characterized by microangiopathic hemolytic anemia, thrombocytopenia and acute (a/c) renal insufficiency
D+ HUS in 2*3 yr old follows Shigella dysentriae
D- HUS *y ug" lacks history of diarrhea/dysentery
NOTES
il
341
APPROACH TO ARTHRITIS
Arthrit is Swelling/effusion in joint or,
Two out of the followirs 4-
o |oint pain (arthralgia)
o Tendemess Swelling is not a must to dx arhtritis
o Warmth
r Limitation of range of movements.
HISTORY
I. Onset
1. Acute<2weeks
a, Acute rheumatic fever
b. Transient synovitis
C; Kawasaki disease
d. Septic arthritis
e. Henoch-Schonlein purpura. :
2.. Subacute 2-6 weeks

a. Reactive arthritis
b. SLE,PAN
c. Dermatomyositis
d. Lyme disease, brucellosis.
3. Chronic>6weeks
a. Juvenile rheumatoid arthritis $RA)
b. Ankylosing spondylitis
c. TB
d. Psoriasis
e. Legg calve Perthe's disease .--\
II..Site
joints-SlE, vasculitis
Peripheral
Axial-fRA
III. Number of joints
o Monoarthritis
Post-traumatic
Septic arthritis
- Hemarthrosis
TB arthritis
- Oligoarticular---4 joints or less
- polyarticular-S joints or more-For example: A/c RF, reactive arthritis, rheumatoid arthritis, SLE,
PAN, for example; viral, ARF, poncet, lyme d/s, Kawasaki disease
\t . Aililitiae-]RA, Migratory-ARF, gonococcal
r Distal interphalangeal joints - psoriatic arthritis
Knee, ankle, elbow - Acute rheumatic fever
Pauciarticular
342 - Typ" 1 - knee, elbow, ankle
- Typ" 2 - large jointsof lower limb
-_ Polyarticular RF +ve - MCP joint, proximal Ip joint, cervical spine, TM|
-ve - knee, hip, wrist.
V. Time-Night pain disturbing sleep-malignancy
During activity-mechanical pain
Mornig stiffness-JRA
VI. Fever - quotidian fever with twice daily peak - SOIIA
VII. Rash
' Salmon transient evanescent with spike of fever with central clearing, more common in trunk (SOJIA)
. Erythemamarginatum-ARF
. Erythema chronicum migrans-lyme disease.

. Derrnatomyositis-Heliotropic rash + Gottron papules.
VIII. Recurrent ulcer-Bechet's disease.
IX. Disability-
Daily activities limitation
School days lost
Deformities
Arthritis mimickers:
. Growing pain (rt-8 yr)-localized to calf muscle, occurs in night
o Benign hypermobility of joint
. Chondromalaciapatella.
HEAD TO FOOT EXAMINATION
1. Eye
Non-purulent conjunctivitis-KD
Uveitis-]RA
2. Oral cavity-ulcer in Behcet's disease
Strawberry tongue in KD.
3. Skin-
Psoriatic patches
Malar rash
- Erythemamarginatum,subcutaneous nodules-AM
Subcutaneous nodules-over occipital protuberance, spine of scapula, medial and inferior'borders of
scapula, spinous process of vertebra, extensors of forearm, dorsum of hand, iliac crest, shin, foot.
4. Nail pitting, onycholysis-psoriasis
5. Malignancy features - petechiae, pallor, LN enlargement
EXAMTNATION OF IOINTS
. Inspection
. Palpation
. Range of movements
. Measurements.
1. cervical spine-whether able to touch the ear on either shoulders
2. TM joint-opening of mouth (able to pass 3 fingers in mouth)
3. Shoulder-whether able to touch opposite shoulder with hand
4. Elbow-refer ortho
Grades of joint tenderness
5. Wrist I-patient says
6. Hip
7. Knee Il-patient winces
T
8. Ankle-inversion and eversion Ill-patient winces and withdraws the affected part
9. Ankylosing spondylitis IV-will not allow to touch
Mark a vertical line (10 cm) on the skin overlying lumbar spinous process and sacral dimples, and measuring
the increase in line length on flexiory normally this should be 5 cm or more (Modified shober's test)
Draw a line L0 cm above and parallel to iliac crest and 5 cm below
Ask the patient to flex
Normally the distance between these two I 21 cm
L:r AS, it is < 21 cm
Other Systems
. GIT-HSM (R/o malignancy, SOJIA)
. CVS-R/o ARF
. Resp-dyspnea
o Renal-HSP
. Nervous system--chorea, fits, psychosis.
IUVENILE RHEUMATOID ARTHRITIS

Investigations
1. CBC-Hb - anemia
Dc-increased PMN in SOJIA
Thrombocytosis
2. ESR-elevated
3. CRP-for follow-up (note RF is for prognosis)
4. Antinuclear antibodies-to r/o collagen vascular disease
5. Slit lamp examination:
ANA +ve-3 month follow-up
ANA -ve-6 month follow-up
6. ]oint X-ray--early soft tissue swelling, cortical erosion
7. Synovial aspiration-in monoarthritis to r/o septic arthritis
8. Bone marrow-to r/o leukemia, before steroid treatment
9. ECHO-to r/o ARF
10. USG abdomen.
Management
1. NSAIDs-Naproxen
- Ibuprofen
- Indomethacin
- Diclofenac
2. DMARDs (Disease Modifying Anti-Rheumatoid Drugs)
- Methotrexate 15 -25m9/m2lwk + folic acid
- Gold
- D- pencillamine
- Hydroxychloroquine '-'\
3. Steroids
brtra-articular-triamcinolone
Topical-in uveitis
Syitemic-in unremitting arthritis, systemic manifestations (Predniiolone)
4. Biological
Etanercept-TNF receptor fusion protein
hrfliximab-TNF alpha MAB
jRA definition according to ACR:
o Criteria of ]RA
. Age < 1.6 yr
r Arthritis in morethan or equal to l jont
. Duration>or=6weeks
e Onset type defined by articular involvement in 1st, 6 months of age-poly, oligo, SOJIA
o Exclusion of other causes of iuvenile arthritis
344 ACR Classification

1. Pauciarticular onset }RA (< or =4 joints)-hip never involved
'Typ"
- 1-young girls, uveitis
1970-ACR-EA3types
- Type 2-4oys, may develop AS
1977-EULAR-JCA6types
2. Polyarticular onset IRA (> or = 5 joints)
Rheumatoid factor +ve-similar to rheumatoid arthritis
1997-ILAR -IrA6
Rheumatoid factor -ve
3. Systemic onset |RA
ILAR (International League of Association for Rheumatology)

Use term-fuvenile idiopathic arthritis
i
ILAR_JIA soIrA
Onset < 16 yr Arthritis
Duartion > 6 weeks Daily fever-for 2 weeks
Types 1. Systemic onset Quotidian for atleast 3 days
- 2. Oligoarticulat-< or = 4 joint 1 or more of following:
3. Poly articular > or = 5 joint - Evanesent erythematous rash
4. Psoriatic - Generalized lymphadenopathy
5. Enthesitic arthritis _ HSM
- Serositis
DOWN SYNDROME
o Trisoml of chromosome 21
o Incidence increases with maternal age (Exposure of maternal oocyte to harmful environmental influences for
longer period , since graffian follicles are present in the fetal life,
Causes:
o Miotic non-disjunction of chromosome 21 (94%)
. Translocation-4"/o
o Mosaicism-1.'/"
HISTORY
. Delayed milestones
o Recurrent RTI
o Motor clumpsiness
r Complaints related to other system abnormality like CVS, GIT, etc.
Anenatal
Age of mother at conception, polyhydramnios
Natal
Flailness at birth
Postnatal
Prolonged jaundice (hlpothyroidism), poor activivty
Developmental
Delay in milestone, decreased scholastic performance
Family
History of downs in siblings.
HEAD TO FOOT EXAMINATION

Skull appears small, brachycephalic with flat occiput 345
. Epicanthic eyefold, upward slant eye, catdract, nystagmus
o Flat facies
o Small nose with flat nasal bridge
r Furrowed and protruding tongue, small teeth, narrow short palate (mouth)
o Ears are small, conductive hearing loss and prone to otitis media
o Clinodactyli (hypoplasia of middle phalanx with single flexion crease of 5th finger), simian crease, sandle gap
(wide gap between 1st and second toe)
- Thorax-small sternum
- Genitals-smallexternal genitals
- CVS-congenital heart disease (endocardial cushion defects, VSD, MVP)
RESP-RTI, obsteuctive sleep apnea, hypoplastic lung

GIT malformation-duodenal atresia, Hirschsprung'J disease, GERD, TEF
- hypotonia, weak reflexes, spinal L.d Jo*pression (atlantoaxial dislocation), Alzheimer's like
-CNS-MI!
dementia
Musculoskeletal-DDH, lax j oints
- Endocrine-thyroid-dysfunction - hypothyroidism, DM, short stature, obesity
-
Immune--decieased T cell immunity
- Hematological-leukemia, transientmyloproliferative disorder
MANAGEMENT
. Early stimulation
. Physiotherapy
. Speech therapy-visual and hearing
o Nutritionalsupport,immunization
o Treat complicitions
. Prenatal diagnosis (karyotyping of cell done by):
1. CVS (10-lzweeks)
2. Amniocentesis (16 - 18 weeks)
3. Cordocentesis (after 18 weeks)
4. Triple test-AFP (decreased), BHCG (increased), oestriol (decreased)
Quadraple test-tripple + inhibin A (increases)
5. USG
- lsttrimester-nuchal transluscency
- 2nd trimester-nuchal fold thickness
Short femur length l
- Short humerus length
Duodenal atresia !
PYREXIA OF UNKNOWN ORIGIN (PUO)

Fever > 38.3"C for which no cause is identifiable after 1 week of IP investigation and duration
>3 weeks
CAUSES
1. Infection
_TB
- Brucellosis
- Enteric fever
_ IMN
-IE
- Malaria
_ UTI
2. Collagen vascular diseases
3. Malignanacy-lymphoma, leukemia
346
4. Abcess-subdiaphragmatic abcess, hepatic abscess
5. Factitious-drug intake
6. Munchausen by proxy syndrori-re
7. Familial dysautonomia (anhidrotic ectodermal dysplasia)
History
r Travel history
- Enteric fever
- Malaria
o Sorethroat-IMN
o History of contact with TB
. Evening rise of temperature-TB

o History of heart disease-IE
o Arthritis-collagen'vascular disease
r Anemia, bleeding manifestation - malignancy-lymphoma, leukemia
General Examination
. Pallor-malaria, malignancy, IE
r Jaundice
'o LymPh node
Rash
. Petechiae
o Features of IE
. Malar rash
. Oral ulcer
. Coated tongue
. CVS-murmurs-IE
o Abdomen-HSM
INVESTIGATION
O CBC,Hb,TC,DC . CXR, MANTAUX
. ESR . ECHO
. WIDAL . ANA
o Peripheral smear-cells, malaria . Paul Bunnel/Monospot test
. LFT
PEDIATRIC SURGERY
RESPIRATORY DISTRESS IN NEWBORN

Medical Causes
o Respiratory distress syndrome
o Meconium aspiration syndrome
o Pneumonia
. Transient tachypnea of newborn
o Persistentpulmonaryhypertension
Surgical Causes
o Tracheoesophageal fistula
r Lobar emphysema
o ConB diaphragmatic hernia
Congenital Diaphragmatic Hernia

Types 347
1. Esophageal hiatal hemia
2. Through foramen of Morgagni
3. Posterolateral - most common (Bochdalek hernia)
4. Para-esophagealhernia
Pathology
o LunB hypoplasia
o Surfactant deficiency
o Failure of fusion of pleuroperitoneal canal
Clinical Features
o Respiratory distress
. Scaphoid abdomen
o Mediastinal shift
. Bowel sounds in chest
-It is a medical emergency
Pulmonary hypoplasia -+ persistent pulmonary hypertension + cyanosis -+ hypoxia
Prenatal diagnosis-USG at16-24weeks t-Contraindication for bag and
- Investigations-Chest X-ray neck to knee and abdomen with mask ventillation
nasogastric tube
1. Diaphragmatic hernia
Management 2. Meconium stained liquor
. Ventilation (no bag and mask ventilation)
o Nitricoxide-pulmonaryvasodilator
o Surgery-transabdominal approach
Reduction of contents
- Repair of sac
- Increase the volume of abdominal cavity by stretching
Tracheoesophageal Fistula
Types
ffi&,
ffi W
o
ffi? A
Clinical features-respiratory distress
B (Common)
ffi C
o Complications
Pneumonia
- Gastroesophageal reflux disease (GERD)
- Atelectasis
o Prenatal diagnosis
- Pglyhydramnios in mother
Single umbilical artery
o Investigations
- Orogastric tube cannot be passed to stomach
348 Plain X-ray shows coiled feeding tube
Management
o Prone head down position
o Chest physiotherapy
o Frequent suction
. IV fluid
. Surgery-Right thoracotomy
- Via 4th space
Identify and disconnect
- Anastomosis of upper and lower pouch
o Associations
V-vertebral anomalies
A-atresia
C-cardiac anomalies
T-trachea
E-esophageal fistula
R-renal anomalies
L-limb anomalies
NON.BILIOUS VOMITING
' Hypothyroidism
'e SePticemia
Maternal drugs
. Congenital adrenal hyperplasia
. IHPS
. Gastric volvulus
o Gastroesophageal reflux
IHPS (Infantile Hypertrophic Pyloric Stenosis)

Rule of 4
a. Incidence 4 in 1000
b. Male: female 4:1 't,l
c. Presentation 4 days- months
d. Symptoms rl
1. Non-bilious vomiting-progressive, projectile, persisting
2. Visible gastric peristalsis
3. Palpable pyloric mass in right hypochondrium
4. Voracious appetite
e. Metabolic derangement
- Hyponatremia
- Hypokalemia
Hypochloremic metabolic alkalosis
f. Signs
- USG-muscle thickness > 40 mm (Doughnut sign)
Canal length > 14 mm
- Barium meal
1. String sign
2. Shoulder sign
3. Beaking
m
4. Double track sign
g. Surgery- Ramstedt'spyloromyotomy
Four approaches
1. Via linea alba
2. Laterul to rectus
3. Supraumbilical
4. Rectus splitting
h. Recurrence 47o
i. Mortality 0.4%
BILIOUS VOMITING
Causes
. Duodenal atresia-6 hours after food
r Jejuno ileal atresia-24 hours sfter food
o Meconium ileus--48 hours after food
GEMS-A Golden Endeavor for Medical
Students
o $rJecrotizingenterocolitis
o Malrotation
. Volvulus
. Intussusception
INTUSSUSCEPTION
Rule of 6
o Most common -idiopathicgl%
Secondary causes 67o
. Age 6 month
. Six symptoms
1. Abdominal distension
2. Lump
3. Abdominal pain
4. Vomiting
5. Bleeding per rectum (red currant jelly stool)
6. Rectal prolapse.
r Six signs
1. Sausage shaped mass with concavity
towards umbilicus
?. SiS" de dance - empfy right iliac foJsa
3. Target sign in USG
4. Pseudokidney sign in USG
5. Claw sign in barium meal
6. Coiled spring in Barium meal
. Management
1. Conserv allrve (6.o/oresolves)_[VF, nasogastric
2. Hydrostatic saline tube, antibibtics
3. Barium
4. Pneumatic reduction .- \
5. Squeezing
6. Resection and anastomosis
. Double bubble sign
. Duodenal atresia
o Malrotation of intestine
DELAYED PASSAGE OF MECONIUM

lll dilated proximal colon_normal ganglia
Causes
r Prematurity
. Sepsis
. Hypothyroidism
. Birth asphyxia
. Hirschsprung,sdisease
o Anorectalmalformation
3s0 . Meconium ileus
r Atresia ll cone-scanty
ganglia
HIRSCHSPRUNG'S DISEASE I spasm segment
o Congenital megacolon no nerye ganglia
o Absence of Auerbach,s and Meissner,s plexus

o Arrest of descend of neural crest cell
r
o Mutation in RET nroto_oncogene
o Male: female 4: 1 ' in chromosome 10
o Associated diseases_Down,s syndromg
VSD
Rqnal, Arthritis and Pediatric Surgery
Three zones
I. Distal immobile spastic segment (aganglionic zone)
II. Middle transitional zone - with sparse ganglion
III. Normal hypertrophied dilated segment (normal ganglionic area)
Types
. Ultrashort segment-anal canal and terminal rectum
r Short segment-anal canal + rectum
o Long segment-anal canal + rectum + part of colon
r Total colonic-anal canal + rectum + whole colon
Clinical Features
r Delayed passage of meconium
Bilious vomiting, abdominal distension, constipation
o Introduce rectal thermometer and withdraw gradually, there wll be a spurt of meconium
Investigations
1. X-ray abdornen-absence of rectal gas shadow
2. Barium enema-transition zone, abnormal rectosigmoid ratio
3. Biopsy-gold standard-shows hypertrophy of nerve terminals
4. Anorectal manometry
Management
. After diagnosis
Antibiotics
Decompression
- Temporary colostomy
. Definite management
1. Swenson's procedure-removal of aganglionic segment and coloanal anastomosis
2. Duhamel operation-remove distal part, bring pioximal colon behind rectum, crush wall between rectum
and colon
3. Soave operation-mucosectomy and endorectal pull through
Complications-enterocolitis and sepsis
Perforation
Constipation
ANORECTAL MALFORMATIONS
Imperfect fusion of allantoic gut with proctodeum
Types
. High
+ fistula
1. Anorectal agenesis
2. Rectal atresia 35t
3. Rectovaginal fistula
o Intermediate
1. Anal agenesis
2. Males-rectovesical, rectourethral fistula
3. Females-rectovaginal, rectovestibular fistula
o Low
1. Anal stenosis
2.Anocutaneous fisfula
Two line in invertogram
Above I line
Pubococcygeal line
Below PC line
Most common
- In males-rettobulbar fistula
In females-rectovestibular fisfula
Clinical Features
.' High-flat perineum, absence of dimple
e l6y7-peconium in perineum, anal membrane through which meconium is visible.
Associations
VACTERL (or VATER syndrome)
Investigations
r hrvertoglam
r Prone cross table lateral radiograph (PCTLR)
Management
Low Anoplasty
- Incision of anal membrane
High Initial colostbmy
- Followed by posterior sagittal anorectoplasty (PSARP)
POSTERIOR URETHRAL VALVE

o Congenital symmekical valve in posterior urethra just below verumontanum
. It allows passage of catheter .--\
r But obstruct urine outflow *
o Proximal urethra enormously dilated with obstructive pathology in bladder
'. HyPertroPhied
Sacculation and diverticula
r Cricket ball bladder (palpable in suprapubic area)
Clinical Features
. Poor urinary stream
o History of infections
. Hydronephrosis
Investigations
r Micturatingcystourethrography(MCU)
r Intravenous urogram (rVU)
. USG abdomen
. Blood urea, serum creatinine-renal failure
3s2 . Antenatal USG
Treatment
o l-nitialsuprapubiccatheterization
. After several weaks, resection of posterior valve
. Endoscopic ablation fulguration
VESICOURETERIC RELUX (VUR)

Causes
o Congenital-associated with posterior urethral valve
. Acquired-trauma, after surgery
Grading
L Ureters seen
II. Ureters and pelvis seen
III. Ureters, pelvis, calyces seen
IV. With grossly distended calyces
V. Tortuous elongated serpentine ureters
Investigations
r Urine microscopp culfure and sensitivity
. Blood urea and serum creatinine
o hrtravenous urogram (IVU)
o Micturatingcystourethrogram(MCU)
CASE CHARTS
1. A 10-year-old boy presented with high fever, jaundice, severe myalgia, headache, conjuctival congestion, CBC:
There is increase in WBC count (which predominantly neutrophil)
a. What is most probable diagnosis?
b. \A/hat is etiological agent?
c. Give complication?
2-year-old child is unimmunized. He has fever,.c@ugh, coryza since 5 days. O / e, he has maculopapular rash.
a. Mention most probable diagnosis.
b. What other pathognomic sign will you look for?
c. Mentioncomplication?.
lYzyears old child is admitted with cough and fever of 2 days duration. She is lethargic and not feeding. O/E
her RR is70/rrtin, cyanosis, lower chest retraction present.
a. What is your probable diagnosis?
b. \A/hat is Rx?
c. Name 3 investigations?
4. Five year old Unni fully immunized is admitted with weakness of both lower timbs. No sensory nerual
symptoms or urinary involvement. No history of trauma.
a. What is most probable diagnosis?
b. To whom you report?
c. Write specification of stool sample collection
d. What other investigation you will do?
5. Cerebrospinal fluid study in a S-year-old child with high grade fever with generalized seizures.
Pressure-increased, protein-10 8 mg"h, sugar-Z4 mgo/"
Microscopy-cells polymo rphs-9l/", Lyrnphocyte-2%
a. Diagnosis?
b. Most probable organism?t
c. DOC?
d. \A/hat bedside examination you like to perform before LP?
6. A 4-year-old child admitted with fever, headache, vomiting, CSF, findings are-color clear, tension increase4
protein 40 mg"/", sugar - 30 mg"/", microscopic examination : 15 lymphocytes/HPF
a. What is diagnosis?
b. \tVhat precaution you will take before LP?
7. Eight month old girl admitted with one day h/ o vomiting, loose watery stools w/o blood. The mother says
baby is thirsty, crFng always, urine output decreased.
a. Discuss the plan of management?
b. A.y 5 relevant clinical sign you look for?
c. Advice on discharge?
d. \Atrhat advise to prevent further episodes?
Eight years old child is brought to casualty with hematuria.
Urine findings:
Urine microscopy-plenty of pus cells/hpf
Urine albumin-++
a. Write down 5 question to be asked in history?
b. What is the most probable diagnosis?
c. Three common complication?
9. Eight years old fully immunized boy is admitted with 2 day history of progressive weakness of both LL and
difficulty in walking. He gives history of fever and running nose 10 days back. O/e tones of both his LL were
reduced with grade 2power, absent knee and ankle jerks and down going plantars. No sensory impairement
or muscle tenderness or signs of meningeal irritation.
a. , Most likely diagnosis?
b. Three differential diagnosis?
c. Most dangerous complication?
d. Specifications of sample to be sent.
e. Two investigations to confirm the diagnosis?
10. Baby of Mini, born of full-term normal delivery (FTND) weighing 3 kg brought to you with c/o jaundice.
a. Give 3 question you will ask mother first?
b. Name 3 clinical sign you look for?
11. A 4-year-old child brought with multiple ecchymotic patcfm and purpuric spots.
a.
Write 4 important points you will ask in history?
b.
Name 2 relevant investigations?
c. Two DDs?
t2. A 3'year-old child gives history of poor vision after sunset. O/e of bulbar conjur'rctiva shows dry greyish area.
a. \zVhat is nutritional deficiency and eye lesion?
b. Name 2 other eye signs?
c. How will you treat the condition?
13. Al2-year-old child was brought with history of difficulty in opening mouth, pain of back and neck muscles.
H/o wound in left index finger 1 week back.
a. Most probable diagnosis?
b. Four essential steps in management?
c. How will you prevent?
d. Two complications?
14. A 2 years unimmunized child admitted with weakness and areflexia of 1 week duration.
a. Define AFP?
b. Step you will take after acute management done?
15. Define kwashiorkor. 35s
a. Mention 3 complication?
b. Give the therapeutic diet to be given in initial phase of treatment.
1,6. A 9-year-old child is admitted with fever, vomiting. She is disoriented and her deep tend.on reflexes are brisk.
FIb - 12.8 & TC - 6500, P - 45y",E - 5o/o, ESR - 15 mm/ 1st hour.
Serum bilrubin - 9.6 rrrg, Direct - 3.6 mg,SGPT - 117 6 IIJ
a. What is diagnosis?
b. Write any 2 relevant questions in history?
c. List 2 investigations.
d. Management?
17. A 3-year-old child has come with history of poor apetite, poor activity for past few
weeks. O/e child is pale,
no jaundice, no HSM laboratory investigation given below:
LIb-? goh, TC-1 0500/mm3. MCV-60, Wt(t+ZO
a. What is the first investigation you will do?
b. Two important points you will ask in history.
c. Treatment.
t8' A7-year-old child was admitted with fever, cough, not responding to injection Cp from outside hospital.
RR
20/ rnin, auscultation revealed occassional cr"pr, chest X-ray revealed bilateral dispropotionately
large non-
homogenous opacities.
a. What is the likely organism?
b. Other organism causing this?
c. DOC
19. A 3-week-old child on presented with non-bilious vomiting, since 4 days
a. Most likely diagnosis?
b. Clinical features of child?
c. \tVhich is theIV fluid of choice?
d. Defenitive management?
20' A 2-month-old infant presented with yellowish discolaration of sclera with normal
colored urine, pallor
b. Peripheral smear findings?
c. Confirmatory test?
d. Pattern of inheritance.
21' A 11-month-old child presented with epistaxis and gum bleeding. o/e multiple
- ecchyrnotic patches are seen.
Abdomen within the normal limit (I /NL)
BT-12 minutes, CT-16 minutes, APTT-1 minutes, pTT_12 sec
platelet-3 lakh/mm3
a. What is the likely diagnosis? '- t
b.
Confirmatory test?
c.
Drugs used?
22' A 1'4-day-old baby of sangeetha presents with prolonged jaundice delayed
passage of meconium, poor cry,
floppiness and poor sucking
b. Radiological investigation you will do?
c. Important screening test?
d. Drug used?
23. A 32-week-o1d preterm of diabetic mother presented
with respiratory discom fort. o / e RR-62/mt, grunting,
cyanosis.
b. \tVhat is the bedside test?
c. Treatment
d. How will you prevent this?
24. How will you differentiate term and preterm infant?
356
Viva
ANSWERS
1. a. Leptospirosis
b. Leptospira
c. Liver failure, renal failure, myocarditis, ARDS, thrombocytopenia.
2. a. Measles
b. Koplik's spot
c. otitis media, pneumonia, glant-cell pneumonia, croup, meningoencephalitis, sspE.
d. Vit A,2lakh IU (because 2-year-old child).
3. a. Very severe pneumonia
b. Chloramphenicol, gentamicin (Dose)
c. Chest X-ray, CBC, sputum microscopy
4. a. GBS
b. District immunization officer.
c. Two specimen, at least 24 hour apart, collected within 14 days of paralysis onset, each having adequate
volume (8-10 g) and sent to \AtrHo accredited laboratory in reverse cold chains
d. CSF study, EMG.
5. a. Bacterial meningitis
b. Neisseria
c. Pdnicillin 4lakh ItJ /kg/Day for 7-10 days
d. Fundoscopy to r/o papilledema.
CSF Normal Value
Total protein-2G40 mgldl
Glucose-4040mg/dL
Pyogenic Tuberculous. Viral
Appearance Turbid Clear Clear
On standing Cobr,yeb coagulation
Protein Increased
Sugar Decreased Decreased Normal
Cells Predominantly neutrophil Lymphocyte Lymphocyte
6. a. TB meningitis
b. R/o infection
R/o bleeding abnormality
R/ o increased intracranial pressure (fundoscopy).
7. a. Some dehydration
b.
c. Refer book
d.
8. a. Hi9tory of drug intake, food intake, oliguria, edema, pyoderma, sorethroat.
xl
b. AGN
c. LVF
Renal failure
Hypertensive encephalopathy
9. a. GBS
b. Polio, traumatic neuritis, transverse myelitis
c. Respiratory muscle paralysis
d. Read Q No.4
e. CSF study, EMG
10. a. Whether jaundice appeared within 24 hours, it stains nappy.
Clay colored stool.
Blood group of baby and mother.
b. Pallor
HSM
Hypothyroidism
a. Infection, growth retardation, hypoglycemia

b. F-75
Breastfeeding.
ti 16. a. Viral hepatitis with encephalopathy
r,. b. Similar ilbress in surrounding
,l Food from outside
History of vaccination
c. EEG, USG abdomen
i{ d. Supportive measurement-nutrition, 't bedrest
. T - -r,,1---
Lactulose
Treatment the precipitating factor.
t, 17. a. Peripheralsmear
i
t,
b. History of pica
; History of worm infestation
c. FeSQ @-6rng/kg/day) and continue oral Fe 4-6 months after correction of anemia.
18. a. Mycoplasma pneumoniae
,, b. Chlamydia, Legionella
,,' c. Macrolide.
19. a. IHPS
b. Abdominal mass, visible gastric peristalisis, succusion splash
c. Here there is loss of hyponatremia, hypokalemia, hypochloremia with alkalosis (Loss of Na, K, Cl, H)
Treatment: 5% Dextrose, % NS, KCI
d. Ramstedt's pyloromyotomy.
20. a. HS
b. Microcytes, spherocytes
c. Osmotic fragility
r 358 d. Autosomal dominant.
21. a. VWD
b. Ristocetin induced aggregation
c. Tranexamic acid, EACA.
22. a. Congenital hypothyroidism
b. X-ray knee-absence of ossification center in upper tibia and lower femur
c. TSH > 100 pglml.
d. L thyroxine- 10-15 Vg/kg/ day (ideally life-long).
23. a. RDS
b. Shaketest
c. Continuous positive airway Pressure/ intratracheal surfactant
d. Injection betamethasone 1"2 mg IM, 2 dose,24 hour apart.
24. Clinical assessment of term and preterm
Tenrr Preterm
Hait Silky hair-individual strands can Fuzzyhair
be made out
Ear Well-curved pinna, cartilage Flat, soft pinna,
reaching uPto PeriPherY cartilage not reaching upto periphery
Breast Well-formed breast Poorly formed breast bud
bud (>5 mm)
Genitalia Well pigmented, pendulous scrotal Light pigmentation, not yet descencied
sac with fully descended testes testes
OI or
labia majora covering clitoris and labia minora Prominent labia minora and clitoris
Soles Deep transverse creases No deep creases
angle
Popliteal Acute Obtuce
Scarfsign Absent Present
Arm recoil Recoil No
ADVICE AND HISTORY TAKING

1. Assessment.of a case of diarrhea: Remember the following things
- Rapport and consent o Stand on right side
General appearance of patient o Always ask name, age, make rapport
- Anterior fontanelle o Ask consent and explain procedure
Eyes: sunken/no! tears . Redress the child
Tongue, buccal mucosa: dry / not Anylnarking (with chalk) that you made should
- Skin pinch be erased before leaving the child
edema
Pulse, BP
- Capillary filling time
Ask for urine ouput frequency
- If time persists, ask for a glass of water and bring it near the child and assess the thirst.
2. Advice on the discharge of a child with diarrhea:
Rapport and consent
- Explain the condition of disease to the mother
Explain to her about preparation of oral rehydration solution (ORS) and the frequency of administration
Boil and cool 1L of water (5 glasses)
- 1 packet of ORS is dissolved in 1L of water
2-3 spoons every 5-10 minutes after every episode of diarrhea
Continue breast feeding and all other home available solutions (kanji, lassi, solution made of sugar and
salt)
Discourage bottle feeding
Next day, new ORS should be used
If there is any complication, take the child to a hospital: blood in stools, repeated watery stools, marked
thirst, drinking poorly, altered sensorium
Preventive measures:
- Drinkboiled and cooled water
- Clean utensils
- Breastfeeding
- Immunization
- Handwashing
- Discourage bottle feeding
- Environmentalsanitation
- Do not eat food from outside

- At last, ask for any doubts.
3. Advice on immunization:
- Rapport and consent
Ask the hge of the child
- Explain the importance of immunization
\tVhy it was not taken
Look for BCG scar
Tell the mother that all are available free of cost
Whether other children in the family have been immunized
Mention about an optional vaccine
- It will not cause any harm to the child
Not contraindicated in mild illness (fever)
- Explain the importance of ppl
Ask if she has any doubts.
4. Advice on prophylaxis of febrile seizutes:
Explain the condition to the mother
During febrile episodes, explain to the mother to decrease the temperature by using:
light clothing, a
ventilated room, tepid sponging, tablet paracetamol
Diazepam (if on intermittent prophylaxis)
- Rush to the doctor if temperature does not subside
In case of seizures:
- Keep the child away from danger
- Do not put anything into the mouth
- Keep the head tilted to one side
- Explain about immunization \
- Side effects of diazepam "-
- Ask if she has any doubts.
5' A7'yeat-old child admitted with seizures, started on antiepileptics (sodium valproate). Advice
the mother
on discharge.
Rapport and consent
Explain the condition to the mother
Tell her about the drug administration
- Never discontinue or miss any drug
Lrform the doctor if some other drugs are taken
- Explain the side effects
Precautions during an episode of seizures
Ask her if she has any doubts.
6. Advice on discharge of a child with nephrotic syndrome:
Explain the condition to the mother and reassure her
Tell her that there are chances for relapse
360
- Tell her about the drug administration
S/E of drugs: Moon-face
Dietary advice: Avoid yolli fatty food, excess salt
- Manage infection early
- Weekly BP monitoring
Educate the mother on heat and acetic acid test:
FillS/4th of a test tube with urine and heat the upper part by tilting it over
a flame. Then add g drops of
vinegar (acetic acid). Hold the test tube in front of a.,"*rpupu, and"try
to read through it.
Can read small letters clearly : Nil
- Canreadbutunclear : 1+
- Can read only headlines : 2+
- Cannot read headlines but can see them as a Dark area : 3+
Cannot see the papff at all: 4+
If reading comes as 3+ or 4+ for 3 consecutive days, then as her to consult
a doctor and report it
- Ask her if she has any doubts.
7. Advice regarding breastfeeding:
Rapport and consent
- Position: tummy to tummy; chest to chesf chin to breas! baby to mother and not mother to baby
Burping
Exclusive breastfeeding up to 5 months
Discourage bottle feeds
Continue breastfeeding during the disease
Breastfeeding up to 2 years
Advantage to mother:
- Reducing chance of ppH
- Protectionagainstpregnancy
- Reduces risk of cancer of breast and ovary
- Emotionalbonding
Advantage to baby:
- Nutritionalsuperiority
Immunologic iuperiority
- Mental$o*ttt ligy
- Immunization and advice on weaning
8. Advice on discharge of a child on ATT:
Rapport and consent t;
Explain the condition to the mother and reassure
Isolation of the child is not needed
Tell her about the drug administration
- 3drugs-2 months ... \
- 2drugs-4months
Rifampicin---on an empty stomach
- Never discontinue the drug during any other illness
Qrange discoloration of urine is not a problem
Explain about DOTS
Srreening of other family members
9. Advice on weaning:
Continue breastfeeding
Start weaning at 6 months
Weaning food-ragi
Start one weaning food at one time
Hygiene is very important---dean utensils and hand washing
Initially there may be diarrhea and vomiting; if severe, consult a
doctor
-. Immunization
- Doubts.
10. History taking of a child with febrile seizures:
361
- Rapportandconsent
- Whether it is the fust episode or a recurrence
Onset (within 24 hours after fever), duration, no: of attacks
Whether moving all his limbs or local (focal/generalized)
- Any loss of consciousness
- Any abnormal behavior in the post ictal period
- Any associated headache,vo-iti.g (increased ICT)
- Whether seizures in the absen"" olferre,
- Whether seizures present before 6 months
- Any stoppage of antiepileptics
,i
Any developmental delay Causes for hypothyroidism:
Any family history of seizures. o Goitrogens
11. Take a case history of diarrhea: . Endemic
Rapport and consent . Thyroid agenesis
When t\e episode began o Autoimmune
Number of stools passed, frequency, color, consistency, smell, frothy o Iatrogenic
Is itbloody . Dyshormogenesis
- Is there any associated fever, vomiting, abdorninal pain r' Secondary to pitituary or
- Urine output ic disease
- Are eyes sunken or normal
- Do tears come while crying
- Thirst of the child
History of feeding-bottle feeding, breastfeeding, any history of weaning, food from outside
Sensorium, seizures, abdominal distension
Contact with similar illness
- Fully immunized or not
- Any drugs
- Source of drinking water, environmental sanitation.
12. Assessment of jaundice in a neonate:
Age of child (pathological/physiological jaundice)
Never look in the eyes
1st apply pressure over the tip of the nose and look for yellowish discoloration in the blanched skin
Apply pressure over the face, chest, abdomen below umbilicus, overskin, overfoot palms, soles in that
order (Kramer's dermal zone)
- Urine and stool culfure
- Umbilical sepsis
- Activity of child
Anybleeding .- \
Comment on the level of jaundice.
DRUGS-PEDIATRICS
1. Hydrocortisone
Short acting glucocorticoid
Uses
1. Status asthmaticus (25-50 mg/kg/dose tV 6 hourly)
2. Endotoxic shock
3. Adrenal insufficiency
2. Aspirin
NSAID (acetylsalicylic acid)
Uses:
1. Anti-inflammatory dose-9G-120 mg/kg/ day orally 4 hourly in acute rheumatic disease
2. Antipyretic dose-3G-60 mg/kg/ day orally 4{ hourly should be avoided in empty stomach
S/E-peptic ulceratiory hypersensitivity (Rye's syndrome).
362 3. Paracetamol
Uses
- Analgesic
- Antipyretic
- Dose--40-60 mglkg / day QID
Or
5mg/kglM (injection).
4. KCI
Used in hypokalemia (diarrhea)
11 mEq/ kg / day 8th hourly
Max dose-20 mEq/h.
Ketoconazole
Imidazole group of antifungals
Effective in dermatophytes, candidiasis
Dose-3-6 mg/kg/day orally single dose
S/ E-gynecomastia, thrombocytopenia, photophobia.
Ceftriaxone
A 3rd generation cephalosporin
Widely used in meningitis (high concenkation CSF)
Dose-100-150 mglkg IV 12th hourly.
Phenytoin
Hydantoin class of antiepileptic drug
Dose-5-10 mg/kg/day
Uses:
Epilepsy
1-2 dose given slow [V
Cardiac arrhythmia
S/E
Hirsutism
Osteomalacia
- Fetal hydatoin slmdrome
- Megaloblastic anemia
- Gum hyperplasia
- Toxicity, if blood level > 20 ng/dL.
Antiretroviral drug
NRTl-zidovudine, stavudine, lamivudine
NNRTl-nevirapine, ef avirenz
Protease inhibitor-indinavir, ritonavir.
Atropinesulphate
Anticholinergic drug
0.01 mglkgldose SC or IV
Indicated in supravenkicular tachycardia
S/E-dry mouth, blurred vision, tachycardia, constipation.
10. Chloramphenicol
11. Cotrimoxazole
12. Albendazole refer medicine refer medicine
L3. Metoclopramide
1,4. Chlorpheniramine maleate
0.5 ng/kg/ day per orally 8th hourly
Antihistaminics
S/E-hypotension, sedation, urinary retention.
15. Salbutamol-bronchodialator
Short acting beta agonist
Bronchodialator and antiasthmatic agent
Dose{).1-0 .4 ng / kg / dose orally 8th hourly.
363
INSTRUMENTS
1. Bone malrow needle
- Salah and Klima
Salah-with guard
lndications:
Diagnostic-hematological malignancies, ITP, storage disorder, infection like Kala azar
Therapeutic-intraosseous infu sion.
Contraindication:
lrfection, bleeding disorder.
Sifes: Iliac crest/posterosuperior iliac spine

- Tibia (infants)
- Sternum.
Lumbar puncfure needle
Site:Between L3 and UorIA and L5
lndications:
Therapeutic-to give drugs, spinal anesthetics.
Diagnostic-meningitis, GBS, Convulsions, subarachnoid hemorrhage.
Complication:
- In-fections
Contraindications:
Bleeding disorder, infection, raised ICT.
Before doing this procedure fundus is examined to r / o papilledema.
J. Liver biopsy needle
Vim Silverman needle, Menghini needle.
lndications:
- Cirrhosis, storage disorder, Wilson's disease, hemochromatosis, malignancies.
Contraindications:
- Prolonged PT, infection at site, thrombocytopenia, biliary obstruction.
Complications:
Infectioru bleeding, injury to liver.
Site:
10th ICS in MAL in the supine position.
4. Nasogastric Tube (Ryle's Tube)
Stomach wash, aspiration of fluid
There is metal beads at the end.
5. Infant feeding tube
No metal beeds. .. !
Uses:
- Gastric lavage
To diagnose esophageal atresia, tracheoesophageal fistula
To feed a child not taking orally
Catheterization
Intrarectal diazepam.
6. Intravenous cannula-venipuncture for infusion of IV fluids, drugs, etc.
7. Scalp vein set
- Butterfly shaped
Uses:
To withdraw blood
To give medication,IV fluids.
A 3 way connector
T shaped device containing 2 inlets and 1 outlets
Uses:
364
- Pleural or ascitic fluid
Exchange transfusion
Hemodialysis.
9. Endotrachial tube
Curved tube used for intubation
Distal end has Murphy's eye (opening in the lateral wall)
It can be cuffed or uncuffed
- Administration of anesthesia
- Used in unconscious patient with respiratory difficulty
- To carry out artificial respiration.
10. Tongue depressor
- Examination of throat/oral cavity
Oral surgery
Lrdirect laryngoscopy
Spatula test in tetanus.
Elicitation of gagreflex.
11. MDI
Contains medicine along with propellent
Adaantage:
- Rapid onset
- V"ry small quantity of drug required
- V"ry little medicine reach the systemic circulation so S/E is minimum.
Disadoantage:
- Skill is required to coordinate hand mouth movements.
lnfection like candidiasis.
12. Spacer:
Adoantage:
Incidence of infection like candidiasis is minimum
No need of hand mouth coordination.
13. Ambulatory mobile breathing unit (AMBU Bag)
In resuscitation for grving intermittent positive pressure ventilation size of bag varies from 25V750 mL for
pediatric use
It has outlet to which mask is attached, at the other end there are 2 openings (oxygen inlet, air inlet)
14. Biopsy gun
To take liver biopsy.
15. Infusion set (IV set)
Uses-administration of [V fluids, drugs, total parenteral nutrition, etc.
15. Laryngoscope
It consists of handle and blade
Uses
-Prior to endotracheal intubation
-Cord palsy, to detect foreign body.
17. Thermometer
- Used to record body temperature
- Range-35-420
- Two type-axillary, rectal.
18. Tuberculin syringe
It is a 1 cc syringe with white or metal pistol.
Uses:
To administer PPD for mantoux
To administef BCG
Insulin injection in DM.
t9. DPI-dry powder inhaler (rota haler)
- Upper half consists-of mouth piece and a slot for capsule, lower half is a kind of reservoir to which upper
half can be attached.
Advantage-small and portable, no need of hand mouth coordination
- It cannot be used in children below 5 years. 36s
20. Hypodermic needle
21. Face mask
To deliver intermittent positive pressure ventilation by means of AMBU bag.
22. Fluids
Normal saline (0.9%)
- Na-154 (mEq/L)
Cl-154 mEq/L
Osmolarity-3O8 mosm/L
5% DNS
- Na-154 (mEq/L)
I
Cl-1s4 (mEq/L)
- Glucose-S (g/100 mL)
Ringer lactate
Na-130 (mEq/L)
- C1-10e(mEq/L)
K--a (mEq/L)
HCO3-28 (mEq/L)
Osmolarity-3 10 (mosm/ L)
Isolyte P (pediatric maintanance solution)
Na-25 (mEq/L)
Cl-variable
K-20 (mEq/L)
Glucose-S (g/100 mL).
X.RAYS
STEPS
1. Positioning
Distance between medial ends of clavicle from vertebral border must be equal on both sides.
Problems:
- Apparentcardiacdisplacement,cardiomegaly
l
- Hilar prominence.
l
2. Soft tissues i
l
l
Soft tissue swelling-neurofibroma l
- Air-surgical emphysema
l
Muscle shadow
Breast shadow-adolescents.
3. Bony cages '-.1
Exposure
Normal-intervertebral spaces of first 2-3 vertebrae
Over exposed-all vertebrae are clearly seen
Horizontal----emphysema
Crowding---<ollapse.
4. Trachea
Air column in the trachea casts a black shadow through which vertebral spines are seen in the mid point.
-Tracheal shift
Same side-collapse
Opposite-effu siory pneumothorax.
5. Cardiac border
6. Lung fields
- Lungzones
Upper zone-above anterior ends of 2nd rib.
Mid zone-between anterior ends of 2nd to 4th rib.
366 - Lower zone-below 4th rib.
Lrspiratory film-6th rib cut diaphgram anteriorly.
7. Diaphragm
8. Costophrenic and cardiophrenic angles.
1. Right upper lobe consolidation
- Upper border not clear

Lower margin is formed by horizontal fissure
No shift of trachea or heart
- "Silhouette sign" +ve
- Air bronchogram.
Lower lobe consolidation
- Dense opacity in right lower and mid zone
- Air bronchograni
Costophrenic and cardiophrenic angles spared
- No mediastinal shift
- Upper border not clear.
Air bronchogram
- Intrapulmonary airways have thin walls, contain air and surrounded by air in alveoli
- In consolidatioru air in the alveoli is replaced by fluid-air within the bronchi stands out
4. Bronchopneumonia
Breast Image Reporting and Data
- More patchy alveolar, nodular shadows
System (BIRADS)
- Not limited by interlobar fissures.
0 - Incomplete assesment
5. Lobar pneumonia
L- Negative
- Dense opacity 2 - Benign
- Limited by fissures. 3 - Probably benign
6. Collapse
4 - Probably malignant
- Dense opacity right upper zone 5-
- Volume loss-trachea shifted to right
- Crowding of ribs
- Inter-lobar fissure pulled up
- Hyperlucency on other areas.
Pleural effusion
- Tracheal shift to opposite side
- Cardiac shift to opposite side
- Homogenous opacity, no air bronchogram
- Obliteration of costophrenic and cardiophrenic angle e
- Ellis's'shapedcnrve.
Bilateral effusion
Dffirential Diagnosis of Dense Shndow
Consolidation Pleural effusion
Air bronchogram Homogenous opacity, no air bronchogram
Angles not obliterated Angles obliterated
Trachea and heart not shifted Mediastinal shift to opposite side DD of hyperlucency
Upper border indistinct. Diaphragm not seen clearly Lung markings attenuated, but seen
Highest level in axilla. o Emphysema
Pneumothorax o Unilateral or bilateral
- Increased volume of right hemisphere Lung markings absent
- Hyperlucency on right side o Lrtrapulmonarycavity,i.e. bullae
- Absent lung markings r Extrapulmonary
Margin of collapsed lung markings at hilum (collapsed lung markings seen)
- Mediastinal shift to opposite side. o Pneumothorax
94'. Hydropneumothorax
+ fluid leoel
- Pleural o Hydropneumothorax
- Elliptical
- No wall Hollow parenchymal lesions
- Compressed lung margin. . Lung cavity (abscess)
10. Lung cavity
o Lungcyst
- Large circular opacity o Pneumatocele
- Thickwall o Bleb/bullae
- Fluid level o Hydatid cyst
- No tracheal/heart shift o Bronchiectasis
- Due to necrosis of lung parenchirma with evacuation of o Cystic adenomatoid lung malformation
necrotic tissue, destruction of alveoli, entry of air.
11. Air/fluid level

Cayity (lung abscess)
Intiapulmonary
- Roundshape
- Thickwall'
- No compressed lung margin
12. Pneumatocele
Seen in staphylococcal pneumonia DD of fluid level above the hemi
Breaking down lesion-partial obstruction of small diaphragm
bronchus or bronchiole lnside the lung
Thin-ill-defined wall. Lung abscess
13. Mediastinal mass Outside the lung
- Mediastinum-extrapleural space within the thorax hydropneumothorax
lyingbetween the lungs
The most common mediastinal mass-thymus
RING SHADOWS AND CAVITY
Sail sign
Thickwalled (wall thicknbss > 3 mm)
- Lymphoma. Lung abscess
14. Bronchiectasis
Honeycomb lung-coarse reticular interstitial densities
Thin walled
Bulla
with intervening lucencies that appear as cystic spaces
Pneumatocele
Miliary mottling
Bronchectasis
Fine, well-defined, pinpoint (1--2 mm) shadows
cYst
uniformly distributed throughout both lung fields
Seen in miliary tuberculosis.
15. Miliarymottling
,,
Fine, well defined, pin point (1-2 mm) shadows uniformly distributed throughout both lung fields
,, .Jfi;&il1;TH:::"#:l':*"
ratio- SO-cardiomegaly
Cardiothoracic >
.\
- Pericardial effusion
- Myocarditis
- Cardiomyopathy
- CCHD-Ebsteins
- L-R shunts
- Multivalvulardefects.
- LVH-angle formed between apex and diaphragm is obtuse
RVH-angle is acute.
16,4.. Cardiac border
17. Eventeration of diaphragm
18. Rickets
Cupping
Fraying
Splaying
Thinning
368 hrcreased width
Green stick fracfure.
19. Hair on end appearance.
SUGGESTED READING
1. Ghai Essential Pediatrics.
2. Nelson Textbook of Pediatrics.
3. Clinical Pediatricsj-Aruchamy Lakshmanaswamy.
4. Practical Aspects of Pediatrics-Dr Mayoor K Chheda.

Gems Pediatrics

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Gems Pediatrics

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Short Cases

History of Present Illness

History of Past Illness

Natal History 'Postnatal History

Item Kcal Protein

Uppuma l cup 250 6

246 Cows milk 100 mL 70 3.5

Item Kcal Protein

.' 49" of parents, consanguinity

GENERAL EXAMINATION TCODE-GVHAD]

Ag" Pulse rate

Age Normal RR Tach54rnea

Weight gain Formulas

(H"ryht - above 2years - Stadiometer)

1 SD = 4% of value Weech's formula

Waterlow grading of stunting based on height for age

Observed value - median reference value Weight Height

with an inner diameter 4 cm up the rom iI

Mid-arm circumference/head circumtrerence

CHO and protein will provide 4kcat/ s

_ No. of mg of particular aminoacid per gram of protein

Essential Amino Acids

Kwasiorkor-Hairchanges: Hypopigmentation (lightcoloredhair) 3. 2+paraspinaland

B enef it s of b re astfe e ilin g :

1.0 step management

Deficiency 1. Defective dark adaptation

WATER.SOLUBLE VITAMINS (VIT B AND C)

WTAMIN C (ASCORBIC ACID)

SOME IMPORTANT MINERATS

gy of Kwashiorkor and Marasmus

Day Mea[ Program

National Nutrition Anemia Prophylaxis Program

GROWTH AND DEVELOPMENT

LAWS OF GROWTH "- \

o Its continuous and orderly process

o Development is in cephalocaudal direction.

Functional developmental estimation

Social and adaptive 26t

Deaelopment quotient DQ = A/O*100

Chronic systemic illness

Genetic syndromes, e.g. Turner slmdrome, Down's slmdrome

Category of Vaccines by IAP Now, two categories are there

Oral Polio Vaccine

o Vaccine vial monitors - to know potency of vaccine

o Reverse cold chaim

Hib VACCINE Pentavalent vaccine (trail in Kerala, Tamil Nadu)

Japanees Encephalitis Vaccine

IMMUNIZATION OF AN UNIMMUNIZED CHILD

Cyanotic heart disease:

Acyanotic heart disease:

of Loss of Weight in CHD

Extracardiac anomalies Likely congenital cardiac lesion

VENTRICULAR SEPTAL DEFECT (VSD)

. According to size-small(<.5 cm2 /rt:2 of body SA)

Indications of Surgery in VSD

PATENT DUCTUS ARTERIOSUS (PDA)

Differential Diagnosis of Continuous Murmur

TETRALOGY OF FALLOT (TOF)

CONGESTIVE CARDIAC FAILURE

Essential Criteria (Evidence of Recent Streptococcal Infection)

Bed rest - for 2l weeks

tion Management of chorea

sydenham's chorea-late feature (3 months after onset of acute renal failure)

APPROACH TO A CASE OF RESPIRATORY SYSTEM (PNEUMONIA)

lf no improvernent,winrin S houi lf improves