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CONTENTS

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) 1. Normal Growth and Disorder of Growth & Development'.................. ........................-...011

Ir
NMR}V{AL GROWTH
ANP DISORDER
OF GROWTH 6
PEVELOPMEI\TT

o Growth follows a qig44-shaped curve. The fetus grows_@l1in the EIJ half ,qf-ggstation, thereafter the rate of growth
is slowed down till the baby is born.
o lntheeailypostnatallteriodvelocityofgrowthishighduringthefirstfewmonths@Psc'u).Asecondphaseofaccelerated
growth is during puberty.
o The brain enlarges rapidly during the latter m-onJlrs oJfetal life and early months of pqstqptallife. At birth, thehead
size_is about 65 to 70 percent ofthe expected head size in adults. It reaches g0percent ofthe adult head size by the
07' IGnta 07).
age of 2 y-qqr-q(comed

o Maximumgrowthof lymphoidtissueoccursbetweentheage of 4-Syeans0io-oss).


Weight !.
o The average birth weight ofneonates is about 3 Kg.
o During first few days aftg: birt-h, the newbor4 loses extracell.!'ar fluid equivalent tg about 10% of the body weight.
Most full term infants regain their birth weight by the age of 10 days. l
o Subsequently, they gain weight at a rate of approfmatelyls t9 3O gm per day for the 41qt : months of life.
Thereafter they gain about 400 gm of weight every month for the remaining part of first year@rs).

Birth 3Kg

)
t year 9 Kg {3 x birth weight)6't$s

3 years 15 kg {5xbirth welghlSt**ttt

7 year' 21kg(7 x birth weight)


cl,i,@i:p@:Nat Wlhand oisorder of Growth & Development

e A child gains about 2 kg every year between the age of 3 and 7 years and 3 kg per
year after that till the pupertal
groMh spurt begins.

Height
r Theaveragebirthheightis50cm(ArMsse).Theheightgaininfirstyearisaround25cm@NB13t(so%ofbirthheight@
ot)).

e The height of a child becomes double the birth height at around 4Yz years(NEEr, uPsces) and becomes triple by 12
years of age.
c After the age of 4 years, a child grows at rate of 6 cmlyear4t ez)
.

Birth 50 cm
,':,:.3,mohths "., 60cni .:.

9 months /u cm
.,. /eal..
1 ,:.: 75.im'.::
2years 90 cm
' 4r4 y,ears too
'ma"rtr
For clinical significance upper segment and lower segment should be measured separately. The lower segment extends
from the symphysis pubis to the heels. The lower segment grows rapidly after birth as compared to upper segment
giving rise to the gradual reduction in the upper segment/lower segment ratio with the progression of age.

At birth 1.7 :1.0


: 3 yeai5j:::,...,:i,:.1 i..3ir1;ifi,errl:'.'r..;, :,:::.'..'

At 7 years 1.0 : 1.0


TheieafGr,,. 1.O:1.1. ,.':": '
Note : Height before 2 years of age is measured as length on an infantometer. After 2 years ofage, height (standing
height) is measured.

trdeniifr the inrtrumenf given in the image:

a) Beamscale
b) Infantometer
c) Dynamometer
d) Osteometric board

Ans. is'b' i.e., Infantometer


r It is an infantometer for measuring the length of an infant.
Head cincunrference
o Head circumference is measured from the occipital protuberance to the supraorbital ridge of forehead(pcr04)
which
is the maximum occipito frontal diameter of skull. The head circumference in utero grows by
0.5 cm in first 2 weeks,
0.75 cmin 3'd week and after that 1 cm/week till birth.
o The average head circumference at birth is 35 cm, which becomes 40 cm at 3 months, 43 cm at 6 months(ups c ss),
46
cm at 1 year,48 cmat2 years and 52 cmat12years.
o Headcircumferenceisimportanttoaddtothediagnosisofreurologicaldysfunctionandmicrocephaly.Microcephaly
is defined as a head circumference that measures more than three standard deviation below the mean for age(DNB
rr . llacrocephaly
is defined as head circumference that measure more than two standared deviation greater than
mean tbr age.
CHAp r s a r Nor,mal Grawth and DisorderatG.rg;wth.$,Dqelgpment

Chest circumfenence
o The circumference of chest is about 3 cm less than head circumference at birth.
o The circumference of head and chest are almost same by the age of 9 months to 7 yea/K"'" 06).
Thereafter the chest
circumference exceeds the head circumference.
o The chest circumference is usually measured at the level of nipples.

lVlid-Arm circumference (MAC)


o Mid-arm circumference is measured between acromian and olecranon,i.e. in the middle of upper arm.It is measured
e6' Ar 13).
bY Shakir's taPe@PG

o The shakir's tape is divide lnto three coloured zones, the green zone is above 1-3.5 cm is normal; yellow-orange zone
is between 12.5 - 13.5 cm and represents border line malnutrition; and red zone is below 12.5 cm which represents
severe malnutrition.
o During
l-,!years of age, mid-upper arm circumference remains reasonably static(Pcre6) between15-17 cm among
health children because fat of early infancy is gradually replaced by muscles.
o Kanawati index(ar ra) is calculated by multiplying MAC and head circumference(Ar "). It is used to diagnose
malnutrition. Normal value is > 0-32. Value less than 0.32 indicates malnutrition.

DEVE!.OPIVI ENTAL MI LESTON E5

o Children accomplish maturation of different biological functions (level of development or milestone) at an anticipated
age, with a margin of few months on either sides. Thus, a childt growth (normal or abnormal) can be assessed by
evaluation of these milestones. Important milestones are :-

* 1 month r ln ventral suspension, starts lifting his head.


r In prone position lifts the chinup momentarily in midline.
r Turns head to soundrPc'o',.
r Regards a lighted torch or the face of mother.
r On pulling the child to sit, head lags behind and back is rounded before 4 weeks of age.

a j months r In ventral suspension Iifts his head above horizontal plance {Neck holding)rA' tsPc'or.
r ln prone position lifts his head and upper part of forearms.
r Head Cc,nttillAtoa, Pcto3,ol).

r Starts cooing
r Recognizes mother
r Can follow an object upto l$Oo?Gto3'ot)
r On pulling the child to sit, head lags partially (between 2-3 months). After 3 months head control develops.

* 5 months r Gains control of head in supine position.


r Sits with stltpport(Atls,Pctos)
r Reaches out to an object and holds it with both hands (bidextrous grasp).
r Turns from back to side (Rolls over(Dlv8 '5))
r Transfer the objects from one hand to another (between 5-7 months){rcto&os,04,AtozAttnsut)
':i:aa!rr:.:1,i:r.:i:@r::1-;#5si-

7 months s Hofdsthe obJects with crude grasp from palm (palmar grasp)(Pclos)
* Pivots
* Shows strangers anxietyrPc'07')
* Resista if a toy is pulled frorn his hand.
* gabbleiPc! sl, 02, AuMs 00)
^!

9months * Stand with supportrA/ 66,


T Makes early stepping rnovCrnentswhea feet are placed on the surface of the table.
f, Develops Fincer gtasp6,t3,07,A'ilrse1PctaToo withthe index finger and thumb apposition;
t Develops finer and more Cooridinated hand skills -+ Can scoop on a pellet crudely with his palm.
I Waves bye-bye
I Produces bisyllable sound like baba, mama. :

I Standswithoutsupport@6l8",,:. :

; Tries to feed hirnself with a spoon but spills the contents.


s Tries to remove his eoat and attempts to wear his socks or shoes without suecess.
* Does rnimicry. :

l; Plays a simple ball gamswo'icaoet.


)
T
s Tries to scribble spontaneously (between 12-24 months).

* 15 fionths : Can take several,steps sideways arnd,takes r! steps


::Ie'r'u'rv rqI\!J ua few backward.
illuJ vs!^rYor u' '
f Creeping upstairs
: Can'walk to the,toilet (b€tween 1 5-1 6 months),
u Learns',to feed hiriself With spoon without spllling ltsaontents(Ntusos,DPGoe,PGto4.
) Makesi towei'of 3 cubes. '

* Vocabulary of 4 to 6 words
; Enjoy polysyllabic jargoning

k
Cnap rn rt Normal Grotdlr ondDisordbr of Grulxil,

o 2 yeors walking up and downstairsfiEEr'AilMse4'e3'PGto3), one step at a time i.e., brings both his fuet up on one step
before climbing to the next step (but not by alternate feet).
I Can turn pages of book one at a time?G'o3).
n Draws a vertical or horizontal line.
rt ls able to wear socks or shoes.
r Kicks ball on request
Jumps of the floor with both feet.
n Builds tower of 7 cubes.
I Makes simple r"ni"na", and uses pronounsrD'v8' 2'PGtto'AilMsss,s4).
T ls trainable for toilet and verbalizes toilet needs.
I Can unscrew lids and turn door knobs(Pcr 'o.,.
t Points 3-4 body parts.
't SofionthE '* €Jimbistairs:*ItErnatirig.feelafEs0e.estoa;,,,,,..,
:.a, * MakEStOWerof9ttlb€s{fft{5oel., "'
.a Refers ta self ai,!l'qnd kistiltsfull *amdAillloe-): : ':

a 3yeors I Rides tricy(le{Pcr04'


n Stands momentarily on one foot(aEEr'AilMss8).
Draws a rirrlat*"', o''-*t "tt.
r Can dress or undress himself completely ond succesfully buckles his shoeslAn$sos,DPGos).
I Builds tower of 10 cubes.
& KnowS his gender an d age4rmsos'orcos'PGt04).
r Repeats a sentence of 6 syllables.
x Has a vocabulary of 250 words.
I Counts 3 objects correctly.
n Can withhold and postpone bowel movement.
I Handedness is established(At 1s,rN01t.

*, .'4'yeqr| r. Hopi on oEC foqt{aruie8l;


x Goes down stairs with'alternating fe€t|,rtMieej,
a Draws a cross (plus sign)
,.,. ,' Draws a rectanglerP6"or
,.. *. ldentifi es colots tPGt o)
t

':r':'.r.1* Co,nts4.:B.ennies aic.urately, :ii' :,:,:.. .i r.,,.: :,:,'::. . ::

t Can identi$ Ieft and,right {left.rightrdis{rim.iiritiot)rryJ!4,: , r. .:':i ' .:,,


*, (an use sentence of sii'iriordi(NEtvt' , , ," : ':

11tr'
can tell astory/Petoa).: ''-
s 5 years I Draws a tilted corss (multiplication sign)
t Draws a trianglelAt 't DNB t3' NEEI)
-
5 SkiP5{nrrusrar
a Name 4 colors
t Counts 10 pennies correctly
T Can use sentence of 1 0 words.

I MPORTANT MI LEsTCIN E TUAGES I

A. S'TTINIG

The age of the given child is:

a) 4 weeks
b) 3 months
c) 5 months
d) 9 months

Ano" is ? i.e.,4 weeks


* )
The child in question showing head lag when pulling to sit Age is less than 4 weeks. In newborn, the head
completely lags behing and back is rounded when pull to sit.
C rr.q. p r n n r Narmal Growth and Disorder of Growth & Development

The milestone in t&e given figure develops at:

a) 6 weeks
b) 3 months
c) 6 months
d) 9 months

Ans. is'b' i.e., 3 months


. is showing partial head lag on pulling to sit t occurs at 2-3 months. After 3 months head control devel-
llt-"r"
ops.

The age ofthe given chind:

a) 2 months
b) 3 months
c) 4 months
d) None

"&-xrs. is k'i.e.,4 months


r There is no head lag while pulling to sit ) Age is 4 months.

The given milestone develops at which age:

a) 2 months
b) 3 months
c) 5 months
d) 9 months

Als. is'c' i.e., 5 months


* Child in given figure lifting the head up when pulled up to sit ) Head control in supine position develops at 5

months.

Tlrc age of t&e giveu cleild is:

a) 2 months
b) 3 months
c) 4 months
d) 6 months

i? Kg,:
i€'

Ans. is t'i.e.,6 months


*l Sitting with support develops at 5-6 months.
irowthrrOr,r:

Ttree given milestone develops at which age:

a) 3 months 4'1:
rvC.
%-
b) 4 months '\e,'-
c) 6 months
d) 8 months .J"'
', i.

3€
'El
. ,,% Wiz
-t"\*ei
.*-^
i. qffi+; _>

Ans. is'd' i.e., 8 months


* Sitting without support develops at 8 monihs'
B" VETUTRAI- 5t"' 5p&ru51&I\!

Age of the giveer cldld is:

a) 4 weeks
b) 2 months
c) 3 months
d) 4 months

Ans. is'a' i.e.,4 weeks


e The child is not lifting his head in ventral suspension > Age is less than 4 weeks.

Given rnile stone develops at which age:

a) 2 months
b) 4 months
c) 6 months
d) None

Ans. is'a'i.e,, 2 months


* Child lifts the head in the horizontal plane (in the plane of the body) at 2 months (8-10 weeks).

i{ilestone in t}ee given figure suggest the age:

a) 2 months
b) 3 months
c) I months
d) None

Ans. is'-o" i.e., 3 rxlonths


o child raises his head above the horizontal plane at 3 months ( l2 weeks).
Cueprpn r Normar Grawth and Disorderof Growth & Deveropment
ry
e" p&&&'€ pas,Tt&ru

The age of given child is:

a) 2 weeks
b) 4 weeks
c) 6 weeks
d) 8 weeks

Ans, is'a'i"e., 2 wceks


* The image shows child in prone position with high pelvis and knees drawn under
upto 2 weeks.
the abdomen ) It occurs

?ke given rnilest*ne elevelopes at:

a) 2 weeks
b) 4 weeks
c) 6 weeks
d) 8 weeks

Ans" is'e'i.e., 6 weeks


r The child rs in prone position wirh flat pervis and extended hips + Age is 6 weeks.

?he age clf the ekild in frg.ure is:

a) 2 weeks
b) 4 weeks
c) 6 weeks
d) 8 weeks

Ans. is'd'i.e., 8 weeks


* In prone position face is lifted to 45. by 2 months (g weeks).

Est.i.xrxate t&e age *f given ekild:


a) I month
b) 2 months
c) 3 months
d) None

Ans. is t'i,e., 3 monlhs


a A child iifts his head and upper part of chest by 3 months.

&" STAru mtruG,S{ WeLKt pi,6

Age of the giv*n cXeild is:

a) 2 months
b7 5 months
c) , months
d.1 9 months

Ans" is ?'i,e., 9 rnonths


* A child can stand with support by 9 months.
CHlPrsn r Normal Growth and Disorder of Growth

The given milestone develops at which age:

a) 5 months
b) 9 months
c) 1 year
d) None

Ans. is t' i.e., I year


r Standing without suPpoft develops by 1 year.

The age of given child is:

a) 4 months
b) 6 months
c) 8 months
d) 10 months

Ans. is t'i.e., 10 months


o A child can crawl by the age of 10 months.

Child can do the given rmilcstone atr

a) 5 months
b) 6 months
c) 8 months
d) l0 months

Ans. is'd'i.e", 10 months


* A child walks with support by 10 months.

The given milestone develoPs at:

a) 5 months
b) 8 months
c) 10 months
d) 13 months

Ans. is'd'i.e., 13 months


r A child can walk without supPort by 13 months.
CEApTE n r' Normal Growth and Disorder of Growth & Development

T&e mitrestone ira figure devetrops at:

a) 5 months
b) 15 months
c) 30 months
d) 4 years

Ans. is'c' i.e.,30 months


r Climbing stairs with alternating leel develops at 30 months.

T&e meilestone in &gure rlevelops at:

a) 5 months
b) 15 months
c) 30 months
d) 4 years

Ams, is K'i.e.,4, years


e A child goes down stairs with alternating feet by the age of 4 years.

E. OTHER MILESTONES

?hc given rmilestone develops at:

a) 2 months
b) 5 months
c) 8 months
d) l0 months

Ans. is'b'i.e,, 3 months


o Bidextrous grasp (holding of object with both hands) after reaching to it develops at 4-5 months.

&{i}estone in figurc deve}ops at:

a) 2 months
b) 5 months
c) 9 months
d) I year

Ans. is t' i.e., 9 months


r Grasping object between thumb and index finger (Pincer grasp) develops by 9 months.
Cnep rrn t Normal Growth and Disorderof,Grdwth,&

The milestone in figure develoPs at:

a) 2 months
b) 5 months
c) 9 months
d) 1 year

Ans. is'*d i.e",2 months


o Social smile develops at 2 months.

The age ofthe given infant is:

a) 2 months
;; 3;;;;h;
c) 4 months
d) 6 months

Ans. is W i.e.,6 months


r A child enjoys watching his own image in the mirror bv 6 months.

PETUT'T!CITU ,4NB EMUPTIOIU OF TEET'H

o There are two sets of teeth : temporary and permant.


* Temporary teeth, (milk teeth or deciduous teeth) start appearing at about 6 months, are 20 in number(NnEr): being 4

incisors, 2 canines and 4 molars in each jaw. They start shedding at about 6 years, when permanent teeth start appearing.
o permanent teeth are 32 in number : being 4 incisors, 2 canines (cuspids), 4 premolars (bicuspids), and 6 molars
(tricuspids), in each jaw. 6 perm4nent molars which erupt extra in each jaw without replacing any teeth are called
superadded permanent teeth, while all other permanent teeth are successional permanent teeth.
o Eruption of temporary teeth is called primary dentition and eruption of permanent teeth is called secondary dentition.
rs)
c Temporary teeth start erupting at 6 months age@t .
r:'i. Therefore, between 6-12
o Temporary teeth start falling at,6 years when permanent teeth start appearing(oNr
e8l.
years, there is mixed dentition(o""o
o First temporary tooth to appear (in primary dentition) is lower central incisors and last temporary tooth
to

eruptis-2nd 11.olareclls,titnPetl2).Thesequenceof eruptionislowercentralincisor>uppercentralincisor>upperlateral


eGI0s,linper 02) > 2d molar. Therefore eurption of temporary teeth
incisor > lower lateral incisor > i,t molar > Canine
e0' limpet e7)
is completed by eruption of 2"d molar at 25 months (2 yeats){x*a" '

a First permanent tooth to erupt (in secondary dentition) is 1" molar(NE


Er' ArIMS e7' Iinper 02' PGI 0s) and last to erupt is 3'd

rnolarlrerutael).Lhe sequence of eruption is 1'r molar > central incisor > lateral incisor > 7't premolar > 2d premolar >
17 -25years'
canine > 2,d molar > 3,d molar.Eruption of permanent teeth is completed by eruption of 3'd molar between
a EruptionofteethmaybedelayedinhypothyroidismNEE.'PGI0s'AIIM'eT),hlpopituitarism(ArrMseT),Rickets(xrrr),Down's
AilMS s7),malnutrition and cleidocranial dysplasia.
syndrome(NEEr'
e Permanent teeth appear first in lower jaw.
e Permanent teeth appear a few month earlier in females'
o Third molar appears first in lefi side of lowet jaw and then on right side.
r t Normal Grawth and Disorder of Growth & Development

SHOMT STATIJRE

* If the height of the child is below the 3rd percentile or less than 2 S.D. from
the mean, he or she is considered to be
short stature.

a Causes ofshort stature:

A) Proportionate short stature


Normal variant l) Familial
2) Constitutional delay in growth
Prenatal causes 'I
) lntrauterine growth retardation (l UGp;rccrozl

2) lntrauterine infections
3) Genetic disroders (chromosomal and metabolic)
Posnatal causes 1) Nutritional dwarfism (due to malnutrition)
2) Chronic visceral disease

;; ;;;;;;0",o",, *ro"pituitrism, Juven ire DM)


4) Psychosocial (emotional deprivation, nrafe rnal deprivatislleetuty
$| Dlip-roBorttoiiite,*ortstatuie,' :.:'' -:: :::':: .. l
I

t , ,Wlh.shnrt lirr&s:,.Achon:dronlasia;,hypoehondro;litas;a; chonaioe.itoa l dyjplaiia,.defoiirtiiies


:' due'tolic&ets,,+'nd,.osteogeaesis impti64til. hypot.IittioldJimipn,orl. ...,-'
; ..Wlth:ihort,itrutk i Spondylo:epithyseal dystiasia,,.mucopfy-s rrid*is; muc,olipjdosis;.caries
:'.. spinei hemiv€r:tebrae.

A ehild is with dwarfisrn has following picture what can be the


cause of dwarlism:

a) Hypothyroidism
b) Achandroplasia :-
c) Mucopolysaccharidosis
d) CFI deficiency

Ans. is'd'i.e., GH deficiency


e The givr" pi.tu,. i, ,io*irrg proportionate short stature. Among the given
options, only GH deficiency (hypo-
pituitarism) causes proportionate short stature.

Constitutiomal delay in growth


o It is the most comrnon cause of short oz)
s[nfu1s(aro& in mid childhood period but the ultimate height is normal.
o Their birth weight and height are normal. Strong family
history of parents having short stature in childhood
with
delay in onset ofpuberty is usually present.
e The average growth velocity@Nn n' AI 11' 06)
is normal and ultimate growth
Ttotential is adequate.
The bone age is less than chronological age@NB 13,A1 11,06),
".b.
.-,* Upper segment and lower segement ratio
is normal.
a IGF-[ levels tend to be low for chronological age but within the normal range
for bone age@Ns t3). Growth hormone
and gonadotropin level after puberty are within normal range.
Cnaprun t Narmal Gra$rth.arrd
Differentia I d ia g n os is

Short stature

Normal groMh velocity Altered growth velocity


t
Normal variant short stature
+
Short stature other than normal variant
(see above table)

Bone age < chronological age Bone = chronological age


J +
Constitutional delay Familial short stature

Other important educational facts about short stature


A) Features of short stature due to growth hormone deficiency
1. Ratio of upper to lower segment is normal@EEr).
2. Bone age or epiphyseal developmgnt in less than chronological age by about 2 years@EEr).
3. Children\ are normal inheight and weight at birth@EEr).
4. Delay in growth is usually observed after the age of one year@EEr).

B) Bone age is less than chronological age


c Constitution delay in puberty.
c Marked delayed in hypothyroidism and Ltypopituitarism.
c Moderate delay in malnutrition and chronic illnesses.

C) Bone age is advanced than height age


, ; Down's syndrome t Intrauterine infections o Turner syndrome

D) Infantile type body porportion


r Achandroplasia(Pcl0r) r |uvenile myxedema (hypothyroidism(Pcr0') o Cretinism

E) Reverse infantile body proportion


o Eunuchoidism c Homocystinuria t Frolich's syndrome
o Marfan\syndrome t Klinefelter\ syndrome

BTHAVIORAL AND PSYCHOLOGICAL PROBLEMS

Enuresis
o Enuresis is defined as the voluntary or involuntary repeated discharge of urine into clothes or bed after a

developmental age when bladder control should be established (mostly mental age of 5 years).
r Diagosis of enuresis requires voiding of urine twice a week for 3 consecutive months or clinically significant distress
in child's life as a result of wetting.
r Enuresis is more common in males than females.

o Enuresis in classified into :-


1) Primary (persistent) enuresis
r It is the most common type (90%), in which child has never been dry at night. It is further divided into :-
l) Nocturnal enuresis: It is the most common type of eil)resis and is more common in boys.
ii) Diurnal: This is more common in girls.
2) Secondary(regressive) enuresis
r It is less common (10%). Child has been continent for at least 6 months and then wetting.
C,Ar:'p,ia*,l":',Niirmal Orowth and Dlsorder of Growth & Development

Tneatmemt
a No treatment is given to children below 6 years because of high spontaneous cure rate(Arr3). After 6 years, treatment
include :-
i) Behavioral therapy
x It is the treatment of choice, Most ffictive treatment is bed alarm and motivational therapy with least
chances of recurrence(Ar08). Motivational therapy includes _

a) Keep diary of wet & dry night. d) Restrict fluid at bed time.
b) Void urine before going to bed. e) Avoid punishment.
c) Change wet cloth & bedding. f) Positive reinforcement(ArI5).
x Consistent dry bed training with positive reinforcement has a success rate of B5o/o and bed and pad alarm
systems have a success rate of approximately 75o7o\r ts;
with relapse rate that are lower than those with
pharmacotherapy.

ii) Pharmacologicaltreatment
x It is used when non-pharmacological (behavioral) therapy fails. DesmopressinKarnee) is the drug of choice.
Other drugs used are impramine(uPor) and oxybutinin.
Thumb srickimg
o Thumb sucking is normal in infancy and toddlerhood, i.e. upto 4-5 years@e oz, 0s' ripmer el) .It is a
behavioral problem,
which may be self soothing, i.e. a source of pleasure(uP 07' 0s' lipnet e1).
o Presistent thumb sucking in adolescence is more common in girls and may be sign of insec rtrityop 07,0s, ripnet sl)
.
o Presistent thumb sucking in older children can cause dental malali gnment(up07,0s,lipnerei). For lessening the
effect on
dentition, thumb sucking should be discontinued before 8 years of age(ez.ussr, 7s,PGI7e).
s Treatment is not required till the age of 4-5 years. After that behavioral therapy in the form of
Ttositive reinforcement
(giving reward for not sucking the thumb) is treatment of choice. Negative reinforcemenf (application
of noxious
agents to thumb) is second line of treatment.
Breath ho!ding spells
* Breath holding spell is a paroxysmal event occuring in 0.1% - 57o of healthy children from the age of 6 months
to 6
szl
featS1IIMs .
* The name for this behaviour maybe misnomer in that it connotes prolonged inspiration. Infact, breath-holding
occurs
during expiration and is reflexive (not volitional) in nature.
e There are two major types of breath holding spells :-
A) Cyanotic form (cyanotic spells)
x This is more common and is provoked in response to frustration and anger precipitated by upsetting or scolding
infant/child.
x Cyanotic spells are dre to central sympathetic overactivity.
x Clinical features include generalized cyanosis(A[Ms e7), apnea, forced expiration, opisthotonus, shrill cry and
bradycardia. Seizures may occur due to cerebral hlpoxia, but antiepileptics are not required 6IIMI s7).

x The only treatment is support and reassurance to parents.


B) Pallid form (Pallid spells)
x These are initiated bypainfut experience, e.g falling and striking the head.
x Pallid spells are due to excessive central parasympethetic activity.
x Clinical features include pallor, apnea, loss ofconsciousness, hypotonia, seizures and bradycarda.
x Treatment includes support and reassurance of parents. AtropinerA IIMS s7) may be used in refractory cases.
e Iron supplementation may be useful in some children with breath holding spell5(oxr r:;.
Learnimg disability
a Learning disability (LD) is defined as a disorder in one or more of the basic psychological processes involved in
understanding or in using language, spoken or written, which may manifest itself in an imperfect ability to listen,
speak, read, write, spell or to do mathematical calculations. Learning disability is suspected when there is unexpected
underachievement in adequate educational settings.
Cnapr,rt r Normal

o The DSM-IV defines three academic skill specific learning disorders:-


t Readingdisorder
t Mathematic disorder
t Disorder in written exPression
o Another subtlping is language-based LD commonly known as dyslexia (problem in reading, spelling and written
expression) and nonyerbal LD (deficrts in arthmetic and spacial cognition). Dyslexia is the most common type of
os). fhs
learning disability. Children with dyslexia have problem in reailing, spelling and written expression\lrMs
important clues to dyslexia in school age children include delayed language, trouble rhymic words, mispronunciation,
hesitation, work-finding difficulties and poor spellings with presence of letter reversal. Reading is slow, inaccurated
and labored.
Attention deficit hyperactivity disorder (ADHD)
o ADHD is one of the most common psychiatric problem in school age population. It is three times more common in
boys than girls.
13'04'AttMs08'oz)
r ADHD is characterized by an age inappropriate hyperactivitytdtts'04'ArrMs08'0'), impulsiveness\l and
01' AIIMS 08' 02).
inattentionat 1s'
Hyperactivity is usually the first symptom to be noticed.
o The disorder is divided into three classes :-
r Class I (most common) -+ AII three symptoms are present i.e., hyperactivity, impulsiveness and inattention.
r Class II + First two symptoms are present, i.e., hyperactivity and impulsiveness.
r Class III (Least common) -+ Only inattention is present.
ts' oe' ilIMs 0s' 02)
impulsivenes sal 13' 04' AIIMS 08' 02)
inattentivenessar
o Child with ADHD presents with hyperac tivity,at , arrd
08),
)3,04, AilMs 08,02), restlessness 6IIM; 0s)
, decreased self control, distractability{t't
ss)
, desira to play outsiile(ArrMs difficulty
os)
in concentration, difficulty in playing(AzMs 0s),
dimculty in sitting, inability to wait for his turn while playing(efl'us
and frequently interferes others.

r Treatment options are :-


1) Non-pharmacological : Psychosocial and behaviorol therapyarnrs o<).

2) Pharmacological treatment: Psychostimulant ilrugs are most efiective treatmenf. Methylphenidate(Pcro8) is the
drug of choice. Amphetamines(Pcro8) and atomoxetine(Pcr08) are alternatives.

Pervasive development disorders


r Pervasive development disorders include several clinically similar conditions which are characterized by three s)'mptom
clustors: -
1) Impairment of social interaction : - e.g., Lack of social smile or eye contact.
2) Impairment of communication (language and non-verbal) : - Language problems, delayed or absent speech.
3) Restricted repititiye and styerotyped behavior interests and. activities: - e.g., Sterotlpy.

Autism
r Autism is a pervasive development disorder (PDD) which is characterized by: -
i) Marked impairment in social interaction@Gror'00)
r There is no social smile(MP06) or eye contact. These children prefer to play alone with inanimate objects and do
not like to mingle with others(ArrMs0r) (do not make friends). There is lack of attachement to parents and absence
ofseparation anxiety.
ii) Impairment in communication?Gr0l'0o'Attus06'01) (language well as non-verbal communication) as

r Delayed or absence speecharMs06), lack of verbal or facial response to sounds or voices, abnormal speech
patterns, echolalia, perseveration and prominent reversal (referring to selfas 'you' and to others as'I').

iii) Sterotyped and restricted repetitive behavior, interests and activities


r Mannerism, Sterotype behavior (head banging, body-spinning, rocking, clapping, watching own handarMs0').
iv) Other features
r Mental retardation(MP 06) (it 50 -7 5o/o patient)
r Epilepsy (in 25-35o/o)
Ap r E R I Normal Growth dnd Disorder of Growth & Development
r Hyperkinesis
r Inability to concentrate 6trMs06).

o Onset of symptoms of infantile autism (usual form of autims) is before 2.5 - 3years@P06). If onset of symptoms
are
afier 3 years, it is referred to as childhood autism.
r Autism is more common in boys and among low socio-economic groups(pcr04).
I Presently, the cause of infantile autism seems to be predominantly biologi calecl0l).

Other pervasive development disorders


c Two other pervasive development disorders are : -

Rett's syndrome
r Age of onset is around 5 months.
: Development may proceed normally until 1 yr of age, when regression of language and motor milestones become
apparent.
r This is the characteristic features, that they begin to loose their acquired skills, e.g., cognitive and head growth
is normal during early period after which there is an arrest of growl6rez,uso,rl.
I Acquired microcephaly (Decleration of head growth due to significantly reduced brain weight(-Arus0i,).
r Most children develop peculiar sighing respirations with intermittent periods of apnea that may be associated
with cyanosis -+ Breath holding spells(ar'uso'rt.
s Austistic behaviour is a typical finding in all patienfs -+ Impaired social interaction, language and
o3).
communicationazM's
r Generalized tonic-clonic convulsions occur in the majority.
r Feeding disorder and poor weight gain are common.
r Death occurs in adolescence or in the 3.d decade.
: Cardiac arrhythmias may result in sudden, unexpected death.
Asperger syndrome
r Qualitative impairment in the development of reciprocal social interaction after the age of 3 years.
r More common in males
r Normal intelligence, The only pervasive development disorder in which intelligence is normal.
r Eccentric interests.
s No language impairments that characterize autism.
r Children with Asperger syndrome appear to be at high risk for other psychiatric disorder.

ADOLESCENCE
Adolescence
r Adolescence is defined as the period from the onset of puberty to the termination of physical growth and attainment
offina1 adult hight, i.e. adolescence is considered as a period oftransition from childhood to adulthood. Adolescence
is usually the period 10 to 20 yr@NB 13' AI0s)
.

Puberty
r Puberty is the biological process in which a child become adult, i.e. biological process which occurs during transition
from childhood to adulthood. Changes include appearance of secondary sex characteristics and development of
reproductive capacity.

Adolescent -) 1 0-1 9 years


x Eariy adolescent ) 1 0-1 3 years
a Middle adolescent -+ i 4-1 5 years
t Late adolescent -+ 1 6-1 9 years
t \iouth, ', , :+ t5-24yeats
t Young people -) 10-24 years
Culprpn t Narmal Growth and

In Girls
o In girls, puberty starts with onset of breast development (appearance of breast buds), called thelar che(Al 13. DNB 12,
13' AI 08' PGt ee),
between 8 and 13 years (corresponds to Tanner SMR stage - 2at 1s)) . This is followed by appearance of
pubic hair (pubarche) and axillary hair (adrenarche)Atset. Pubarche is followed by peak growth velocity, immediately
after which menarche (onset of mensturation) occurs.

Theldrche _+ Pubarche & adrenorcheote6) _.> peak growth velocity'nrn, ete6sa ) menarcheNEEr, At oo, s8)

Preadolescent Preadolescent
Sparse, lightly pigmented, straight, Breast and papilla elevated as small
medial border of labia mound; diameter of areola increased
Darker, beginning to curl, increased Breast and areola enlarged, no contour
amount separation
Coarse, curly, abundant, but less than in Areola and papilla form secondary mound
adult
Adult feminine triangle, spread to Mature, nipple projects, areola part of
medial surface of thighs general breast contour

ln Boys
o In boys,frst sign of puberty is enlargement of testis\I se),
at around 9/z years. This is followed by penis enlargement
after which pubarche (pubic hair growth) starts. Then occur peak growth velocity, adrenarche (axillary hair growth)
andfacialhair growth (beard){ectsat, in that sequence.

Testicular enlargement -+ Penis enlargement -+ Pubic hair growth -+ Peak growth velocity + Axillary hair --> facial hair.

1 None Preadolescent
2 Scanty, Iong, slightly pigmentedrntrsr Minimal change/enlarge- Enlarged scrotum(A"'), pink, tex-
ment ture altered
3 Darker, starting to curl, small amount Lengthens Lar;1er
4 Resembles adult type, but less quantity; Larger; glans and breadth Larger, scrotum dark
coarse, curly increase in size
Adult distribution, spread to medial surface Adult size Adult size
of thighs

. Avlrage birth helght in lndia :50 cm.


:li;.,..A.iightirtachildfi.diibliinaArtineighi'o:4Vzyearsof,ag€.:"',".,...,,.,,.:,"''
o Gain of height in 1't year of life: 25 cm (500/o).

ffi;*m :aiiwia*41z
y9or:,:,.6-,,,ecm per year:-r,,,,: :,,,., :,,::: i,
; Body weight is tripted (3 times of birth weight) at : 1 yea r of age.
y ;.;.; y.w*tgfii iiuiaru$les 14t e;of b;ii{Ew;ight} iit : 2 yea,i.':of age,','
* Body weight is 5 times the birth weight at:3 years of age.
. Weight gain during 2'd year of life:3 kg.
. Head circumference is measured from: Occipital protuberance to supraorbital ridge of forehead.
Curprrn r Normal Growth ond Disorder of Growth& Development
I
o Maximum growth of lymphoid tissue occurs : Between 4-B years.
. lmportant causes of proportionate short stafure : Familial, constitutional delay, IUGR, malnutrition. hypopituitrism (GH deficiency).
c lmportant causes of disproportionate short stature : Hypothyroidism, achondroplasia, mucopolysaccha ridosis.
o Features of constitutional delay in growth:Normal birth height, bone age < chronological age, normal growth velocity, positive family
history, IGF-1 is low for chronological age but normal for bone age.
o Features of familial short stature i low birth weight, bone age is normal for chronological age, positive family history, normal growth
velocity.
& Short ststare due to GH deficiency: Normal body porportion, bone age < chronological age, normal birth height and weight, altered
growth velocity.
@ Most common cause of short stature: Constitutional delay in growth.
* lnfantile body proportion is seen in: Achondroplasia juvenile myxedema (hypothyroidism), cretinism.
* Reverse infantile body proportion is seen in: Marfan's syndrome, Homocystinuria, Klinefelter syndrome, Frolich's syndrome, Eunuchoidism.
w Difficutty in expressing in writting, reoding problems, mathematic mistakes, problem in spelling: Specific learning disability.
w Characteristic triad of ADHD : Hyperactivity (first symptom), impulsiveness, inattention.
a Other features of ADHD: Disturbing others, difficulty in playing, does not listen to teaching, restlessness, uncontrolled desire to play
outside.
a Not a feature of ADHD : Mental retardation.

o Drugs used for ADHD: Methylphenidate (DOC), amphetamines, atomoxetine.


e lmportant features of autism: Impaired communication/social interaction, stereotype repetitive behavior, impaired imagination,
delayed speech, low socio-econom.ic aroup, onset before 3 years.
* Not o feature of autism :Vision problem.
w Features of Rett's syndrome: Repetitive hand wringing movement with autistic behavior, breath holding spells, microcephaly.
w Lower recunence of nocturnal enuresis is seen when treated by : Behavioral therapy (bed alarm & motivational therapy).
& Treatment of choice for nocturnal enuresis in a 5 years old child: No treatment (no treatment is required up to 6 years).
w Drugs to treat nocturnal enuresis: Nasal desmopressine (drug of choice), imipramine, oxybutynin.
* True about breath holding spells: May be cyanotic or pallid, treatment is reassurance, atropine and iron may be used, antiepileptics

. i;::;::r:r"Uiioor*u,*: A source of pleasure. may be a sisn of insecurity, may cause matocctusion, no treatment is required upto
4-5 years.
@ To avoid malocclusion of teeth, thumb sucking should be terminated by:7-B years.
& Pica referes to: lngestion of non-nutritive substances.
@ Cretinism (hypothyroidism) is characterized by: Disproportionate short stature (short stature with short limbs).
w Chitdhood disorder which improves with age: Temper tantrum.
& Adolescence period extends from : 10 20 years (starts ,,.10 ,".t:,
, .
& First sign of puberty in girls:'lhelarche (development of breast buds).

@ Sequence of events at puberty in girls:fhehrche + pubarche/adrenarche -+ peak growth velocity -+ Menarche.


@ Peak growth velocity in girls is seen just after: Appearance of pubic hair (pubarche) and axillary hair (adrenarche).
w Peak growth velocity in girls is seen iust before/at the time of : Menarche.
& First siqn of puberty in boys : Enlargement of testis.
w Sequence of events at puberty in boys :Testicular enlargement -+ penis enlargement + pubic hair growth -+ peak growth velocity
-+ axillary hair -+ facial hair.

* Thelarche is: Hormone induced breast enlargement in girls.

'TI
I Disorder of Growth & Development

QUESTIONS

| ^L, Child rolls over by: (CET luly 15 pattern)


a) 3monthsb) 5 months
c) 7 months d) 8 months
NORMAT GROWTH Which about development is not
13. true: (ATIMS May 9s)
a) Pincer grasp at 3 months
l. The height of a child is doubie the birth height at the b) Sitting at 6 months
age of: (All India Dec.1t Pattern) c) Social smile at 3 months
a) 1 year b) 2 years d) 2year old can use pleurals
c) 4 years d) 6 years t^ Pincer grasp is attained at rnonths:
Z. Average gain nfheight in first year is ? (All India Dec.13 Pattern)
(CET Nov.13 Pattern) a)4 b) 10
a) 25 cm b) 50 cm c) 12 d) 18
c) /5 cm d) 100 cm 15. A 3 year old child can do all, except: (ArrMS May e3)
3" Height of child aequire 100 crn in: a) Eat with a spoon
(All India Decj5 pattern) b) climb stairs running
a) 2.5 year b) 3.5 year c) Walk properly
c) 4'5 year d) 5'5 year d) Vocabulary of20-100 words
4. Height ofchildren in 2,10 years ofage is increased t()" Child knows his/her sex by age of:
byt (Ai e7) (All India Dec15 pattern)
a) 2 cmlyear b) 4 cmlyear a) 2year b) 3 year
c) 6 cmlyear d) l0cm/year c) 4year d) 5 year
5" From 6 weeks to 12 weeks.". trnfant weight increases 17. A child speaks sentences at the age of ?
@ aft (All India DecI5 pattern) (CET Aug. 12 pattern)
il 3bild b) a0 g/d a) 6 months b) 1 year
c) s0 g/d d) 60 g/d c) 18 months d) 2 years
6. Infant bodyweight istripled byageof: 6ilMSe6) 18. A female child has recently learned to eat with
a) 5 months b) 11 months spoon without splling, to dress and undress herself
c) 2 years d) 18 months with supervion and to understand that she is a girl.
7. I{eightofnewbornquadruplesbyr These skills are first mastered between the ages of:
(All India Dec.t3 pattern) (AIIMS Nov 05, DpG 09)
a) 6 months b) 1 year
a) 2and3years b) 3and4years
c) 2 years d) 3 years
c) 4and5years d) 5and6years
lo
8. Anthropometric assessment, which does not show Purposeful movement is st*rted as:
much change in 1-4 years: (PGI Dec 96) (All India Dec15 pattern)
a) Mid arm circumference a) 6 month b) Infant
b) Skin fold thickress c) 8 month d) 9 month
c) chest circumference- Head circumference ratio z{',t. Child draws triangle at what age?
d) Height (CET Aug. 13, All India Dec.13 pattern)
a) 3 years b) 5 years
DEVELOPMENTAL MILESTON E
c) 6 years d) 7 years
21. A boy can grasp a rattle & recently he become able to
9. Sitting without support appear$ at whiclr rnonth: transfer objects, hand to hand. He can do: @Gl Nov 14)
(All India Decl5 pattern) a) Babble
a) 5months b) 6 months b) Say'mama'or'dada
c) 10 months d) 12 months c) Sit without support
10. Neck hotrding comes at lvhat a.gei (Alt hrlia Decl5 pattertr) d) Stand with support
a) 2 months b) 3 months
e) Able to walk
c) 4 months d) 5 months 22. A child climbs with alternate steps, builds a towerg:
11. Sitting in Tripod position at which month 9 cubes, tells '[' but not his name and can not say his
?
(All India Dec15 pattern)
age and sex, the probable age is: (AtrMS May 0t)
a) 5 months b) 6 months
a) 36 months b) 24 months
c) 8 months d) 9 months
c) 30 months d) 48 months
Cnlprr.n r

23. A child makes tower of 4 cubes at: b) Read a sentence


(All India Dec.lj Pattern) c) Ride a bicycle
a) lyear b) lr/z years d) Copy a triangle
c) 3 years d) 4 years 34. A child has a vocabulary of4-6 words however the
24. Which of the following cannot be done by 3 years main mode of communication and social interaction
old child: (NEET Dec.12 Pattern) continues to be non-verbal what is the most likely
a) Draw a triangle b) Draw a circle developmental age of the child: (Ar 12)
c) can arrange 9 cubes d) cango up and a) 12 months b) 15 months
down c) 18 months d) 24 months
e) Stands on one foot for 5 second 35. Object permanence milestone develop at:
25. Handedness develops by age of: (AlllndiaDecl| Pattern) (CET Nov 15 Pattern)
a) 2years b) 3 years a) 6months b) 9 months
c) 4 years d) 5 years c) 12 months d) 15 months
26. Which of the milestone develops first: (Ar 07)
a) Mirror play b)crawling ERUPTION OFTEETH
c) creeping d) Pincer grasp
27. A baby has recently developed mouthing but has not 36. The primary dentition begins to show teeth eruption
developed stranger anxiety. Likes and dislikes for byt (All India Dec.13 Pattern)

food. What is the most appropriate age of this baby: a) 6 weeks b) 12 weeks
(At 07) c) 6 months d) l2months
a) 3 months b) 5 months 37. At what age do first permanent teeth appear ?
c) 7 months d) 9 months (CET Nov. 13 Pattern)

28. A normally developing l0 months old child should a) 5 years b) 6 years


be able to do all of the following except: (Ar 06) c) 7 years d) 8 years
a) Stand alone 38. Ist permanent teeth to appear: (NEET Dec.13 Pauen)
b) Play peak to boo a) Molor b) Premolor
c) Pick up a pellet with thumb and index finger c) Incisor d)cannine
d) Build a tower of 3-4 cubes 39. Milk teeth-Total no. in hurnan being:
29. An 8 week infant can do all the following except: (All India Dec.14 Pattern)
(PGI May ru) a) 20 b) 28
a) Head control c) 32 d) 24
b) Lift its head up to horizontal line in ventral 40. Delayed dentition is seen in alllexcept:
suspension (NEET Dec.12 Pattern)
c) Follows red object upto 180 a) Down syndrome
d) Social smile b) congenital hypothyroidism
e) Turns head towards sound c) Rickets
30. A two month old child is able to: (At 04) d) All of above
a) Show a positive parachute protective reflex
b) Hold head steady in seated position MISCELLANEOUS
c) Lfft head and chest of a flat surface with extended
elbow 41. When tCF and ECF of child becomes equal to adult
d) Sustain head level with the body when placed in person: (NEET Dec.12 Pattern)
ventral a) 1 year b) 2year
suspension c) 3year d) 4year
31. A child is able to say short sentences of6 words: 42. Upper segment to lower segment ratio in 3 yr age
(NEET Dec.12 Pattern)
child is: (CET June 14 Pattern)
a) 2years b) 3 years
a) 1.2 b) 1.3
c) 4 years d) 5 years
c) 1.4 d) 1.6
32. A neonate is able to: (AlllndiaDec.ilPattern)
43. Bilabial consonants are: GEf luly 15 Pattern)
a) Fix his gaze at a object 8 to 12 inches apart a) PBSL b) PBMW
b) Focus on bright object
c) MNLO d) TLMW
c) Left his heaJ& chest on elbow '
d) Roll from side to side
33. A year 6 old child with IQ of 50. Which of the
following can the child do: @:.:uS May 07, Nov 06, At 07)
a) Identify colours
C r*e.s.i"x&?': ilormal Growth and Disorder of Growth & Developrnent

51" A 9 year old child is restless. [Ie is hlperactive and


his teacher cornplaints that he does not listen to the
DE\lELOPMENT teachings. Disturbs other students, he also shows
less interest in playing. The likely diagnosis is:
(AIIMS May 02)
SHORT STATURE
a) cerebral palsy
M. b) Attention deficit hyperactive child
A child is below the third percentile for height. His
growth velocity is normal, but chronologic age is
c) Deliruium
d) Mania
more than skeletal age. The most likely diagnosis is:
(Ar 11,06)
52. A 10 year old child is always restless, inattentive to
a) constitutional delay in growth study and always wants to play outsite. Farents are
b) Genetic short stature extremely distressed. What would you adivise:
c) Primordial dwarfism (AIIMS Nov 08)
d) Hlpopituitarism a) It is a normal behaviour
45" A ehild's growth variation io normal but trone devel-
b) Behaviour therapy
opment is not acc to the chronological age. What ls
c) It is a serious illness requires medical treatment
d) Needs change in environmenl
diagnosis ? (CET Nov. 13 Pattern)
a) Genetic
5.3" True about autisrn; (All India Dec.1j Pattern)
b) Dwarfism a) Occurs in high economic striata
c) constitutionaldelay b) Normal communication
d), Familial short stature c) Starts before2-3 years ofage
d) More common in girls
46_ The most €ommon cause of short stafure is (AI 07,08)
a) constitutional 54. A 3 year old tloy with norrnal developrnental mile-
b) Systemic diseases stones with delayed speech and diificulty in com-
c) Hypothyroidism munication and concentration. lle is not rnaking
d) Growth hormone deficiency friends. Most probable diagnosis is:
47. Which of the following is true about constitutional
a) Autism
@I.MS MaY 07' AI 07)

delay in growth? (CET Nov. 14 Pattern)


a) b) ADHD
Neonates with constitutional delay show anomalies
at birth
c) Mental retardation
d) Specific learning disability
b) IGF-1 Ievels are low for chronological age
c) Bone age is normal 55. Which of the following is not true atraut the autistic
d) IGF-I levels are low for bone age specific disorder: (All tndia Dec.14 pattern)

48. Short stature, secondary to growth hormone defi-


a) Impairedcommunication
ciency is associated withl
b) Impaired imagination
(NEET Dec.12 pattern)
a) Normal body proportion.
c) Language developmental delay
d) Vision problems
b) Low birth weighr
c) Normal epiphyseal development The following are characteristic of autism except:
d) Height age equal to skeletal age (All lndia Dec. 15 Pattern)
a) Onset after 6 years ofage
b) Repetitive behaviour
PSYCHOLOGICAL PROBLEM5 c) Delayed language development
d) Severe deficit in social interaction
49_ A 14 year old boy has dtffhculty in expressing himself
in writing and rnakes frequent spelling mistakes, 57. A two year old girl child is brocght to the out patient
does not follow instruction and cannot wait for his with features of hand wringing stereotype move-
turn while playing a garne" t{e is likely to tre sufering rtents, impaired language and communication de-
fiom: velopment, breath holding spells, poor social skills
(AIIMS Nov o5)
a) Mental retardation and deceleration of head growth after 6 mont&s of
b) Lack ofinterest in studies age. The most likely fiagnosis is: (AIIMS Nov 03)
c) Specific learning disability a) Aspergert syndrome
d) Examination anxiety b) Rettt syndrome
c) Fragile x-syndrome
50. Attention de{icit hyperactivity disorder is character-
d)colarad syndrome -
ized by: (All India Dec.13 Pattern)
a) Hyperactivity Sg, A boy does not speak at school but has normatr
speech at other placeo. IQ assessment is normal. The
b) Impulse activity
c) Poor attention diagnosis is: (All India Dec15 Pattern)

d) All of the above a) Selective mutism b) ADHD


CHAPTER:':'I

c) -{utism d) Dyslexia MISCELLANEOUS

ENURES!S 68. Arm span and height become same at what age (year):
(All India Dec15 Pattern)
59. 5 vear old child bed wetting Rx of choice: a)9 b) 11
(All lndia Dec.1j Pattern) c) 13 d) 1s
a) No treatment b) Imipramin 69. Pica refers to: (NEET Dec.12 Pattern)
c) Desmopressin d) Motivational therapy a) IU sucking
60. Lowest recurrence in nocturnal enuresis is seen b) Thumb sucking
with: 61 0B) c) Foreign object being put in the mouth
a) Bed alarms b) Desmopressin d) None ofabove
c) Imipramine d) Oxybutynin
61. Treatment ofnocturnal enuresis in a 14 year old ADOLESCENT
child is: (All India Dec15 Pattern)
a) Positive reinforcement
70. WHO defines adoleseent age between;
b) Punishment
(All India Dec.14 Pattern)
c) Bed alarm
d) Desmopressin a) 10-19years b) 10-14years
c) 10-25years d) 9-14years
62. Which of the following nasal spray is very effective
in eontrol of enuresis: (All India Dec.14 Pattern)
7r. Adolescent starts at the age of ? (CET Aug lj pattern)

a) Pitressin b) Desmopressin a) 7 years b) 10 years

c) Lipressin d) None ofthe above c) l4years d) lTyears

63. The behaviour therapeutic falls in management of


72. Peak growth velocity in adolescent girls is seen just
enuresis, The pharmacological drug of choice for
after: (AIs6)
this case is: (uP 07)
a) Appearance ofpubic & axillary hair
a) Phenltoin b) Diazepalm b) Breast enlargement

c) Imipramine d) Alprax c) Onset of menstruation


d) Enlargement of external genitalia
73- First sign ofpuberty in girlsr
BREATH HOLDING SPELLS
(CET Aug. 1i, 12 Pattern, PGI Dec 99, AI 08)

64. True regarding breath holding spells is all except:


a) Puberchy

(AIIMS Iune 97)


b) Thelarchy

a) Antiepileptic treatment is necessary


c) Growth spurt
b) Atropine is sometimes used
d) Menarche

c) Attacks ofcyanosis can occur 74. First sign of pubertal development in female isr
d) Occurs between 6 months to 5 years (All India Dec.13 Pattern)

65. T?eatment of breatlr holding spells is?


a) Breast enlargement

(CET Nov.1j Pattern)


b) Onset of mesturation

a) Pyridoxine c) Enlargement of pubic hair

b) Zinc d) Maximum growth velocity


c) Iron /5. What is the order of puberty: (Ar 2K)

d) Molybdenum a) Telarchy-pubarchy-menarchy
b) Puberchy-telarchy-menarchy
c) Puberchy-menarchy-telarchy
THUMB SUCKING d) Adrenarchy-telarchy-pubarchy

66. Which is incorrect about Thumb sucking: 1rMpERsi) 76, Order of development of secondary sexual charac-
a) can lead to malocclusion teristic in male: (PGr e6)

b) Is a source ofpleasure a) Testicular development--pubic hair--axillary hair--


c) Is a sign ofinsecurity beard
d) Must be treated vigorously in the first year b) Pubic hair--testicular development--axillary hair--
beard
67. To avoid displacement of permanent teeth, finger
c) Testicular development--beard--pubic hair-,
sucking should be terminatedbyt 1ru zo, AilMS 78, sl)
axillarlhair
a) 8 years b) 5 years d) Axillary hair--beard--pubic hair--testicular
c) 3 years d) 2 years development
Cueprrnl Normal,Grawth
c) Autism d) Dyslexia MISCELLANEOUS

ENURESIS 68. Arm span and height become same at whatage (year)t
(All lndia Dec15 Pattern)
59. 5 year old child bed wetting Rx of choice; a)9 b) 11
(All India Dec.13 Pattern) c) 13 d) 15
a) No treatment b) Imipramin 69. Pica refers to: (NEET Dec.12 pattern)
c) Desmopressin d) Motivationaltherapy a) IU sucking
60. Lowest recurrence in nocturnal enuresis is seen b) Thumb sucking
with: (Ar 08) c) Foreign object being put in the mouth
a) Bed alarms b) Desmopressin d) None ofabove
c) Imipramine d) Oxybutynin
61. Treatment ofnocturnal enuresis in a 14 year old ADOLESCENT
child is: (All lndia Dec15 Pattern)
a) Positive reinforcement
74, WHO defines adolescent age between:
b) Punishment
c) Bed alarm (All India Dec.14 Pattern)

d) Desmopressin a) 10-19years b) 10-14years

62. c) 10-25years d) 9-14years


Which of the following nasal spray is very effeetive
in control ofenuresis: (All India Dec.14 Pattern)
7L, Adolescent start$ at the age of ? (CET Aug 1j pattern)

a) Pitressin b) Desmopressin a) 7 years b) 10 years


c) Lipressin d) None ofthe above c) 14 years d) 17 years

63, The behaviour therapeutic falls in management of


72. Peak growth velocity in adolescent girls is seen iust
enuresis, The pharmacological drug ofchoice for afterl (At s6)

this case is: (uP 07)


a) Appearance ofpubic & axillary hair
a) Phenytoin b) Diazepalm b) Breast enlargement
c) Imipramine d) Alprax c) Onset of menstruation
d) Enlargement of external genitalia
73, First sign ofpuberty in girlo:
BREATH HOLDING SPELLS
(CET Aug. 13, 12 Pattern, PGI Dec 99, At 08)

64. True regarding breath holding spells is all except:


a) Puberchy

(AIIMS Iune 97)


b) Thelarchy
a) Antiepileptic treatment is necessary
c) Growth spurt
b) Atropine is sometimes used
d) Menarche
c) Attacks ofcyanosis can occur First sign of pubertal development in female isr
d) Occurs between 6 months to 5 years (All lndia Dec.13 Pattern)

55. Tleatment of breath holding spells is? a) Breast enlargement

(CET Nov.1j Pattern)


b) Onset of mesturation
a) Pyridoxine c) Enlargement of pubic hair
b) Zinc d) Maximum growth velocity
c) Iron. 75. What is the order of pubertyr (Ar 2K)
d) Molybdenum a) Telarchy-pubarchy-menarchy
b) Puberchy-telarchy-menarchy
c) Puberchy-menarchy-telarchy
THUMB SUCKING
d) Adrenarchy-telarchy-pubarchy
66. Which is incorrect about Thumb sucking: (ilMpERsl) 76, Orderofdevelopment ofsecondary sexualcharac-
a) can lead to malocclusion teristic in male: (PGr e6)

b) Is a source ofpleasure a) Testicular development--pubic hair--axillary hair--


c) Is a sign ofinsecurity beard
d) Must be treated vigorously in the first year b) Pubic hair--testicular development--axillary hair--
beard
67 . To avoid displacement of permanent teeth, finger
c) Testicular development--beard--pubic hair--
sucking should be terminated by; 1tct zs, AtMS 78,8i)
axillary'hair
a) 8 years b) 5 years
d) Axillary hair--beard--pubic hair--testicular
c) 3 years d) 2 years
development
77. fuakgowth r,elocifyin adolescentgirt is indicated 87- A newborn baby has a head circumference of 35
bp (CET Nov. 14 Pattern) cms. at birth, His optimal head circumference will
a) Breast enlargment be43 cms at: (UPSC 9e)
b) Axillary hair a) 4 months of age b) 6 months of age
\ c) Public hair c) 8 months of age d) 12 months of age
\
d) Iust before commensement of menarche 88. Ia
l healthy chil4 the head and chest circumference
a
78" I ltlhat is thelarche (NEET Dec.12 Pattern) equal each other arouad the age of: (Karnat 06)
a) Pubertal breast enlargement in boys a) 3-6months b) 6-9 months
b) Breast enlargement in pregnancy c) 9-l2months d) l2-l5months
c) Hormone related breast enlargement in girls
d) Post hormonal therapy breast enlargement in
V/eight gain in the second year of life is: (cMC 0s)
a) lkg b) 2kg
postmenopausal females
c) 3kg d) akg
pkst sign of pub€rty in feaaalel (AlI India Dec15 pattern) e) 5kg
a) Thnner stage I
A normal healthy child has a height of t{X) cm and
b) Tanner stage II
c) Pubic hair
we:ghs f 6 kg. What is his most Lkely age? (upsc 06)
a) 3 years b) 4 years
d) Axillary hair
c) 5 years d) 6 years
88" Characteristics of SMR-2 in boysdAil rn dia Dect5 pattern)
91. Shakir tape is used for: (Delhi 96)
a) Appearance ofpubic hair a) Measurement of height
b) Appearance of axillary hair b) lvleasurement of length of infant
c) Enlargement of scrotum c) Measurement of midarm circumferance
d) All of above d) Measurement of the learning ability of child
A child plays a simple ball game at: (Manipal 08)
QUESTIONS OF VARIOUS OTHER a) 52 weeks b) 36 weeks
EXAMINATIONS c) 12 weeks d) 48 weeks
W'hea achild is not able to perform the following
motor functions such as skippinS walking on heels,
GROWTH & DEYELOPMENT hoppingin place orgoing forwards in tandem gati,
his motor deyelopment is considered to be below:
81. Postnatallywheaisthe grewthvelocityma-imrrm ?
a) 3 years b) 4 years
(UPSC 06)
c) 6 years d) 8 years
a) In the firstyear oflife Child changes a rattle from one hand to another at
b) In the secondyear oflife the age of: (Comed 07)
c) In the seventhyear oflife a) 3 months b) 6 months
d) In adolescence c) 9 months d) 1 year
82. 90% ofbrain growth is achieved by the: 95. A normal infant sits brieflyleaning forward on her
(Comed 02, Kerala 04) hands, reaches for and grasps a cube aad transfer it
a) 2d year b) 3'd year from hand to hand. She babbles but cannot wave
c) 5th year d) l5ftyear bye-bye nor can she grasp objects with the finger and
83. Ihe maxirnum age for growth of lymphoid tissue: thumb. Her age is: (U\SC 2K)
a) 4 months b) 7 months
ULPMER es)
a) 3-4 years b) 5-7 years
c) 10 months d) 10 months
c) 7-11 years d) 11-i4years 96. Vocabulary of 1.5 year old child is: (AMU es)
84. Increase ia height in frst year is by: (DNB 2001)
a) 1-10 words b) 10-20 words
a) 4oo/o b) 507o c) 20-30 words d) 30-40 words
c) 600/o d) 75o/o 97. A normal child develops the abilityto use 10 words
85. Birth weight of a cbild doubles at five months of age with meaning at the age oi (Karn 11)

while the birthlength doubles at the age of: a) 12 months b) 15months


c) 18 months d) 24 months
(UPSC 98,07)
a) 1 year b) 2years 98. An infant can sit with leaning forward on his
c) 3 years d) 4 years hands. He bounces actively when made to stand.
86. The weight of the child at 3 years is usually_times He laughs aloud and becomes conoerned when the
thebirthweight (Karn
mother moyes away. What is his most likely age:
11)
a)3 b)4 (UPSC 07)

c)s d)7 a) 12 weeks b) 16 weeks


c) 22 weeks d) 28 weeks
I
'C.rrepit*.

99. A normal infant sits briefly leaning forward on her DISORDER OF GROWTH & DEVELOPMENT
hands, reaches for and grasps a cube and transfer it
from hand to hand. She babbles but canot wave bye- 103. \faking up at night, screamingwit] fear, at2.Syexrr*
bye nor can she grasp objects with the finger and ag9 is generallya manifestation of: (PGt 01,79)
thumb. Her age is: (UPSC 2K) a) Organic illness
a) 4 months b) 7 months b) Normal development pattern
c) 10 months d) 14 months c) castration anxiety
f 00. At which one of the follo-rving age period a child can d) Separation anxiety
remove front opening garment ? (coMED 06) l(}4. Cretinism is: (uP 08)
a) 24 months b) 36 months a) Disproportionatedwarfism
c) 48 months d) 60 months b) Short stature with long trunk
f 0f . Which ef the following are the first incisors to c) Short stature with short trunk
erupt in an infant: (UPSC 07) d) Long stature with long trunk
central
a) Lower b) Lower lateral tO5. Which of the following childhood disorder improves
central
c) Upper d) Upper lateral with increase in age: (MP 2K)

lA2. By-years allmillcteethareerapted: (AMC 2K) a) conduct disorder b) Emotional problems


a) 1.5 b)2 c) Temper tantrum d) Sleep disorder
c) 2.5 d):

III
af,, G rowih', & D eveI o p m e n t

ANSWERS

NORMAL GROWTH

t. Ans. is 'd' i.e., 4 years fRef: A.P. Ghai Bth/e p. 13 dr Vh/e p" 6)
r An infant usually doubles his birth height by the age of 4r/2 year s
) Ans. is 'a' i.e., 25 cm [Ref O.P. Gkai Bth/e p. 6]
o At birth, height is around 50 cm.
r At one year, height is around 75 crlrr.
r Thus gain in height in first year is 25 cm.
3. Ans. is t'
i.e.,4.5 year [Ref O.P. Ghai t"Bth/e p. d]
o A child acquire height of 100 cm by age of 4% year.

4. Ans. is t' i.e., 6 cmlye* fRef: O.P. Ghai \th/e p. 13 6 Vh/e p. 6; Nelson lyth/e p. 54, 551
'After 4 years, the child gains about 5 cm in height eyery year, until the age of 10 years" --
O.p Ghai.
'An average child gains approximately 7-8 cm in height between the age of 2-6 years and 6-7 cm
in height between
6-12 years". __ Nelson
Amongst given option, 6 cmlyear is the best answer.

5. Ans. is'a'i.e., 30 g/d lRef: Gbai Vhle p. 6l


o Average weight of New born baby is 3 kg.
o Newborn loses extracellular fluid about 10% of body weight and start gaining weight and become equal to birth weight
at day l0 oflife.
o Subsequently, they gain weight at a rate of approximately 25 to 30 gm per day for the first 3 month of life.
r Thereafter they gain about 400 gm weight every month, for remaining part of first year.
6. Ans. is 'b' i.e., 1l Months {Ref: O.P. Ghai Bth/e p. 13 b Vh/e p. 6)

3Kg

I year 9 Kg (l x birth weight)


i'Y-eil
3 years 15 kg (5 x birth weight)

7 years 21 kg (7 x birth weight)

7. Ans. is t'i.e., 2 years tRel O. p. Ghai Sthle p. 6]

8. Ans. is 'd i.e., Mid arm circumference lRef Meharbqn Singh 3d/e p. 53)
r During 1-5 years of age, the mid-upper arm circumference (MUAC) remains reasonably static between 15-17 cm
among healthy chidren because fat of early infancy is gradually replaced by muscles.

DEVELOPMENTAL M I LESTON E

9. Ans. is'b'i.e., 6 month [Rel Nelson l}thle ch. S (Table. S.l)]


'A child sits alone without support at 6-8 months"
Clinical pediatrics
'A 7-8 month old baby can sit without support"
Textbook of child care
CHeprsn'r
10. Ans. is'b'i.e., 3 month -1
lRef: Ghai 7h/e p /l
o Neck holding comes at 3 months.

ll. Ans. is'b'i.e., 6 month lRel Ghai Vh/e p 271

3 month Neck holding

12. Ans. is'b' i.e., 5 months [Rel Ghai 7h/e p.7]


o A child rolls over (turn from back to side) by 5 months of age.

13. Ans. is 'a'i.e., Pincer grasp at 3 months lRef: O.P. Ghai 8th/e p. 45,46, 49 6 7h/e p. 27; CPDT 18th/e p. 751
o Pincer grasp develops by 9 months 1 1 months)(9-
r Child can sit with support by 5 months
o Social smile will be present at 3 months (social smile develops by 2 months).
e 2 year old child makes simple sentences and can use pleurals.

t4. Ans. is 'b' i.e., l0 IRel O.P. Ghai 8th/e p. 49 & Vh/e p. 28)
15. Ans. is 'b' i.e., Climb stairs runninglRef: O.P. Ghai 9th/e p. 49, 5A, 51 /2 Vh/e p. 28, 3A; Nelson 18th/e p. 441
lmportant milestones of a 3 years child
o Rides tricycle o Knows his age and sex.
o Stands momentarily on one foot. r Repeat a sentence of6 syllables
o Draws acircle e Has a vocabulary of 250 words.
o Can dress or undress himself completely o Counts 3 objects correctly.
r Builds tower of 10 cubes o Can withhold and postpone bowel movement.

16. Ans. is 'b' i.e., 3 year lRef: O.P. Ghai 7h/e p. j}l
17. Ans. is'd'i.e., 2 years fRef: Nelson 18'h/e table 32-1, table 591-11
e At2years, a child can make simple sentences and uses pronouns.

t8. Ans. is 'd i.e., 2 and3 yeffs lRef: O.P. Ghai 8'h/e p. 50-52 6 Vh/e p. 28; Nelson 18th/e p. 49f
r A child learns to feed herself with spoon without spilling its contents by the age of 15 months.
o A child can dress or undress herselfcompletelyby the age of3 years.
r A child knows his gender by the age of 3 years.
So, the given milestones develop between the age of 15 months and 3 years.
Amongst the given options best answer is 'a' i.e., 2 and 3 years.

19. Ans. is 'a' i.e., 6 month fRef: Clinical pediatrics 2il/e p. 17)
o Purposeful movement through space starts at 6-8 months.
r During this period, children begin to move towards and away from objects or people independently.
20. Ans. is 'b' i.e., 5 years lRef Nelson 18th/e p. 49; O.P. Ghai 6th/e p. 44-461

12-24 months Tries to scribble spontaneously

A:€
3 years Draws a circle

al_gg-e.! rT::=
5 years Draws a triangle
of Growth & Development

21. Ans. is h'i.e., Babble {Ref: Nelson 18th/ep.49)


o A child is able to grasp an object (palmar grasp) at the age of 7 months.
o A child can transfer the object form one hand to another by the age of 5-7 months.
o So, the age of this child is 7 months.
r A 7 months old child can do :-
1) Holds the objects with crude grasp from palm (palmar grasp)
2) Pivots
3) Shows stranger anxiety
4) Resists if a toy is pulled from his hand
5) Babbles
About other options
o A child produces bisyllable sound (mama, dada) and stands with support by 9 months.
o A child sits without support by 8 months.

)', Ans. is t'


i.e., 30 months lRef. Nelson 18'h/e p. 49 & O.P. Ghai 8'h/e p. 50-52 6 7h/e p. 28, 301
o A child climbs stairs with alternating feet, refers to self as 'I' and builds a tower of 9 cubes by the age of 30 months.
o A child knows his gender and age by 3 years.

11 Aae . is'H i.e., l'k years {Ref: O. n Ghai */e p. 30; Nelson 18e/e p. 49)

I 12 months

18 months

. 36 months 10

24. Ano. io '{ i.e., Draws a triangle t&ef: O.p. Ghai */e p. 50, 51 6 fr/e p, 28; Nelson l}*/e p. 491
o A child can draw a triangle by 5 years.
o A child can draw a circle by 3 years.
o A child can make a tower of 9 cubes by 30 months.
o A child can go up and downstairs with one step at a time by 2 years.
r A child can stand momentarily on one foot by 3 years
ob'
L). Ans. is i.e., 3 year {Ref. Nelson 1*/e p. 50)
o Handedness develops by the age of 3 years (36 months).

26. Ans. is 'a' i.e., Mirror play fRef: O.P. Ghai 8th/e p. 49-51; Nelson 18th/e p. 491
o A child enjoys watching his own image in the mirror (mirror play) by 6 months.
o A child crawls in the bed by 8 months.
o Full creeping and crawling develop by 10 months.
o Pincer grasps develops by 9 months.
27. Ans. is 'b' i.e., 5 months {Ref: O.P. Ghai 8th/e p. 52 6 Vh/e p. 30; Nelson 18th/e p. 491
I
o Mouthing develops by 4 months, while stranger anxiety develops by 7 months.
o So, the age of this child is between 4 to 7 months.
o Amongst the given options best answer is 5 months.

28. Ans. is t' i.e., Build a tower of 3-4cubes [Rel O.P. Ghai 8th/e p. 49 dt Vh/e p. 28; Nelson 18'h/e p. 45, 49; CPDT 18th/e
p. 7s1
o A child starts trying to build a tower of cubes (2 cubes) by the age of 1 year.
About other options
o Child can stand with support by 9 months.
e Chiid can play peak-a-boo game by 10 months.
CrraPft.ri.:r
o Child can pick up a pellet with thumb and index finger (pincer grasp) by 9 months.

29. Ans. is 'l i.e., Head control fRef: Nekon 18h/ep.49l


r Head control develops by 3 months.
o In ventral suspension a child can lift his head in the horizontal plane by 2 months (8 weeks)
o A child follows object with steady movementby 2 months (8 weeks).
r Social smile develops by 2 months ( 8 weeks).
o A child turns head to sound by 1 month.

30. Ans. is'd'i.e., Sustain head level with the body when placed in ventral suipension lRef: Nekon 18e/e p.
4ej
Important rnile stones of a 2 months child.
o In ventral suspension, lifts his head in the horizontal plane (in the plane ofthe body).
e Social smile develops
o Follow object with steady movement of eye.
About other options
r Parachute reflex develops during 9th month of life --- CPDT 18'h/e p. 709
e Control of head develops by 3 months
c A child can Iift head and chest off a flat surface with extended elborv by 6 months.

31. Ans. is 'c' i.e., 4 years lR$: Nelson lSthle Ch*p. 8-9\
r word sentences = 19 month
2
o 6 word sentences = 48 month
o 10 word sentences = 60 month

32. Ans. is'lf


i.e., Focus on bright obiect [Ref Nelsoa l&h/ep. 49)
o Neonatal age is up to 1 month.
oA month old child regards a lighted torch at a distance of 20 cm.
1
o The infant fixes gaze by 8 weeks -- Meharban Singh 3'd/e p. 67
e Infant lifts his head and greater part of his chest on extended arms by 6 months.
r Rolls from back to side by 5 months.
-r-r. Ans. is 'a' i.e. Identify colours j0; Nelson l*/e p. 491
fRef. a.P. Ghai 8th/e p. 5a, 54 & Vh/e p.

o IQ is defined by as the mental age divided by the chronological age multiplied by f 00.
M0ntal Age '.,
I.Q.=---------x100
Chronological age 1

r child 6 years of age with an IQ of 50%, means that his mental age is that of
So a a3 year old child.
e Thus we have to look for the developmental milestones of a 3 year old child.
t At 3 years of age, a child can identifu two colours.
: A 3 year old child can speak a small sentence but he cannot read a sentence.
t At 3 years, a child can ride a tricycle (not a bicycle).
t A child copies a triangle at 5 years of age.
34. Ans. is'H i.e., 15 months lRef. Nelson l8thle p. 48,49)
o Vocabulary of 4-6 words in adilition to jargon is achieved by 15 months of age. However <20o/o of speech is
understood and hence main mode of communication continnues to be non-verbal,

35. Ans. is'H i.e.,9 month [Ref Nelson 18'h/e eh.81

"Object permanence, a major milestone, develops around 9 months when the infant understands that objects continue to
exist even ifthey are not seen". Smith's Anaesthesia for infants and children
--
'A major milestone is the achiyement by 9 months of object permanency (constancy), the understanding that object continue
to exist, even when not seen". Nelson
--
Note : Child fully understands object performance at 18-24 months.
htiia,b- ilaiaer of Growth & Devetopment

ERT"'PTION OF TEETH

36. Ans. is t' i.e ., 6 months lRef: Netson l9tt /e p" 4Z-Z3l
o Rule of six :-
r Primary (temporary) dentition begins --> 6 months.
r Secondary (permanent) dentition begins -+ 6 years.

2.-l Ans. is 'b' i,e., 6 years [Ref: Nelson lSth/e Chapter S)


o First primary (milk) tooth erupts at 6 months.
e First secondary (permanent) tooth appear at 6 year of age.
38" Ans. is'a'i"e., Molor
o 1't primary (temporary) teeth to erupt is mandibular (lower) central incisor.
o l't seconilary (permanent) teeth to erupt is 1.t molor.

39. Ans. is'a'i.e., 2O [Rel Nelsom tfl,/c Chap. 504)


c Primary teeth/temporary teeth/milk teeth -+ 20
o Secondary teeth/Permanent teeth -+ 32
40. Ans. is ?' i.e., All of above lRel CPDT tgth/e p. 452; Nelson tBtt/e p.42,73)
Causes of Delayed eruption
r Idiopathic (most common) r Hypopituitarism -- CPDT r Cleidocranial dysplasia
r Hlpothyroidism r Trisomy2l (Downsyndrome) --CPDT
r Hypoparathyroidism r Rickets

MISCELLANEOUS

41. Ans. is 'a'i.e., I year [Rel Nelson Chapter 52)

r By the age of 1 year, ratio of ICF to the ECF volume approaches adult level.

42. Ans" is'b'i.e., 1.3 tRdl Chhedda jd/e p. 22)

At birth 1.7 :1.A

1.3 _ 1.0

1.0 : 1.0

43. Ans. is'H i.e., pBl,Iw[Rel NCxRr sanskrit-Textbook r class lt; Nelson 18il'/e chap. 322]
t Bilabial words are pronounced or articulated with both lips, as the consonants b, p, m, and w.
: Baby starts producing bilabial words by 4th month of age.

DISORDER OF GROWTH & DEVELOPMENT

SHORT STATURE

44. Ans. is'a' i.e., Constitutional delay in growth lRe! A.p. Ghai Bth/e p. j7 b 7,/e p. 19)
r The child in this question has :

1. Height below 3rd percentile, i.e., short stature.


2. Normal growth velocity, i.e., normal variant of short stature.
3. Skeletal age is less than chronological age.

r There are two types of normal variant of short stature:


l. Constituional delay in growth
2. Familial genetic short stature
CItapTan,'r

c In constitutional delay the bone age is less than chronological age, while in familial short stature bone age is normal
for the chronological age.
o So, the most likely diagnois of this child is constitutional delay in growth.

Short stature
I

YV
Normal growth velocity Altered growth velocity
+ +
Normal variant short stature Short stature other than normal variant
'1,

+ v
Bone age < chronological age Bone = chropological age
v v
Constitutional delay Familial short stature

45. Ans. is t'i.e., Constitutional delay fRef: See above explanation)


In constitutional delay the bone age is less than chronological age, while in familial short stature bone age is normal
lor the chronological age.
So, the most likely diagnois of this child is constitutional delay in growth.

Short stature
I

Y-_}
Normal growth velocity Altered g rowth velocity
+ +
Normal variant short stature Short stature other than normal variant
'J,

v v
Bone age < chrlonological age
+ +"
Bone = ch ronolooical aoe

Constitutional delay Familial short stature

-15. Ans. is *e'i.e", Constitutional delay lRef: See above explawation)


+6. Ans. is'd i.e., Constitutional [Rel: O.P. Ghai yth/e p. 35-36 6 Vh/e p. 19-20; CPDT 18th/e p. 938]
o Constitution delay in growth is significant cause of short stature in mid childhood period but the ultimate height is
normal, \
+7. Ans. is 'tr' i.e., IGF-I levels are low for ehronologieal age lttef: Nelson {?tt'le Chopter 14, 7, Sl8;Pedistrics for
medicsl students dqniel bernstein PG 3$3, bedside clinias in paediatrics by Sibarjwn Ghaskl" p. 357)
o In constitutional growth delay, IGF-I levels tenil to be low for chronological age but within the normal range for
bone age.
r Birth weight and height are normal.
r Bone age is less than chronological age.

18. Ans. is'a'1.e",lu{orma} body proportion [ftef A.F. Ghai 8't'le p. 35-36 6 7h/e p. 474-475]

Short stature due to Human Growth hormone deficiency in characterized by -


l. Ratio of upper to lower segment is normal.
2.Bone age or epiphyseal development in less than chronological age by about 2 years.
3. Children! are normal in height and weight at birth.
4. Delay in growth is usually observed afier the age of one year.

PSYCHOLOGICAL PROBLEMS

49. Ans. is t' i.e., Specific learning disability [Ref: O.P. Ghai 8th/e p. 59-60 6 Vh/e p. j9; Nelson 1"6th/e p. 150, 151

r This child has -


i) Difficulty in expressing himself in written (problem in written expression)
ii) Makes spelling mistakes (problem in spelling).
o Both these are manifestations of dyslexia, a specific learning disability.

50. Ans" is 'd' i.e., All of the ahove fR"ef: O.P. Ghai Sthle p' 38'4A; Nelsan ISoh/e p. 148)

o ADHD is characterized by an age inappropriale hyperactivitia. impulsiveness and inattenton.


o Hyperactivity is usually the first symptom ta be noticed,

51. Ans. is 'H i.e., Attention deficit hyperactive child iRe/ 0.F. Ghai Sthle p. 59 6 Vh/e p. 381

r The child in question has following problems.


1.Child is hlperactive 3. Difficulty in playing
2. He does not listen to teachings 4. Disturbs other students

r All these are features of attention deficit hlperactivity disorder (ADHD).

52. Ans. is 'b' i.e., Behaviour therapy lRef: A.P. Gkai 9'h/e p. 59 dt(h/e p. 38; Nelson 18th/e p. 1481

o This child has -+ i) Restlessness ii) Inattentivenessiii) Uncontrolled desire to play outside
o Al1 are features of attention deficit hyperkinetic disorder.
1)Psychosocial treatment

' ff:l:'*ill1Tl'.[1f be educated with regard to the ways in


which ADHD can affect tearning, behaviour,

r Goals should be set for the family to improve the


childt interpersonal relationships, develop study
decrease disruptive behaviors. skills, and

2. Behavior therapy
r The goal of behavior therapy is to identift targeted behaviors
that cause impairment in childs life so that child
can work on progressively improving his or her
skill in these area.
3. Medications
r The drugs used for ADHD are -+ i) Methylphenidate (Doc) ii) Amphetamines iii) Atomoxetine
53. Ane ts xi i-e.,,stants before 2{ years of age{Ref GteaiStulc p-,az r{tgt? yieild py&iatry zdlo p. zzl
Autism
r Autism is aneurologic disroder characterized by _
1. Qualitative impairment in social interaction
2. Qualitative impairment in communication.
3' Restricted repetitive and streotyped patterns
ofbehaviour, interests, and activities.
o Onset of syfiI,toms is usually before 3 years of age.
o 3-5 times more common in boys, but more
severe when occurs in girls.
o More common among low socio-economic
groups.
54. An* is h' i.e.' Autism tRef. o.p. Ghai Be/e p. 61 & fl/e p. 40; High yielit
psychiatry p/e p. 22)
r Delayed speech' difficulty in communication and concentration
in a 3 year old child suggests the diagnosis of autism.
55- Am" is W i-e- Vision pr*a&lems LR€f:$_e Ghai #/e p- dt; CFU{ t#/a p_ 95, tti6 r

' by Impaired social intera ction, impaired communication,


and.restricted repetitive & stereotyped
frffi ffffi]f,t:fed
r Restricted repetitive stereotlpes pattern of behavior
is due to impaired imagination.
w- Ams" is b' i-a-, Ormet aftar 6 y*ars at rye tW O-p, Ghai #/* p-
ffi e p{e p. A{fi
57. Ans. is'b'i.e., Rett's syndrome [Ref Nelson t*/e p.
2504, 25051
r This 2 years child has following problems:_
1. Hand wringing movements.
4. Poor social skills.
2. Impaired language and communication
development. 5. Decleration of hand growth after 6 months.
3. Breath holding spells.
r All are the clinical features
of Rett syndrome.
58" Aeaa" ns?ile,Scilortivermre{iurm {eaf: M*ax n#/c p 24" SZ 31, m!
t selective mutism is defined as a
failure to speyk in specific social s_ituations, despite speaking in other situations;
typically a symptom of an undeilying anxiety d*order. it
ciildren with selective *itir* can speak normally in
certain
with their parents, but do not ,p,ik in other sociat
::::rf:;:::r:;T:"y,""',1:;'iX::;:l:Tr:::irr;:^ne settings,

ENURESIS

59-
o No treatment is given to. children below
6 years of age because ofhigh spontaneous
o After 6 years treatment include. cure rate.
i) Behaviorat therapy: This is the treatment of choice.
ii) Pharmacological treatmenf : It is used when non-pharmacological (behavioral)
therapy) fails . Desmopressin is
the drug of choice. other drugs used are impramii" '
o*yiiiinir.
""a
60. Ans. is h' i.e., Bed alarms {Ref t*/e p.
Nelson 113, I lal
o First line treatment for enuresis is behavioral
therapy. It consisls of rewarding the child for
being dry at night, child
oefore retiring and the use of conditionlrg d.',ric.s
f".g. u.a ahrm-that ring. *rr." rrr. child wets a special
:*JJr1*to
o Consistent dry bed training with positive reinforcement has a success rate of 85% and bed and pad alarm systems have
a success rate of approximately 75o/o with relapse rate that are lower than those with pharmacotherapy.
61. Ans. is'a'i.e., Positive reinforcement fRef: Ghai Vhle p. 35]
o Consistent dry bed training with positive reinforcement has a success rate of 85% and bed and pad alarm systems have
a success rate of approximately 75o/o with relapse rate that are lower than those with pharmacotherapy.

62. Ans. is 'b' i.e., Desmopressin [RS A.P. Ghqi 8e/e p. 6 Thle p. 36; Nelson l9*le p. 113, 114]
505

63. Ans. is t' i.e., Imipramine lRef: A.P Ghai Sthle p. 5a5 d* flle p. j6j
r Desmopressin is best answer.
o But it is not given in options.
r Amongst the given options only imipramine is used in enuresis.

BREATH HOLDING SPELLS

64. Ans. is 'a'i.e., Antiepileptic treatment is necessary lRef. Nelson l8.*/e p. 2476, 2477; CPDT 18th/e p" 911
o Antiepileptics are never required (please refer to text of the chapter).
e Other options are correct.
65. Ans. is t' i.e., tron [Ref Pediatrics by Lucy M. Osbom p. 758; Netsan l9hle Chapter 594f
"A subgroup of infants with breath holding spells have iron deficiency anemia. Iron therapy may treat not only the
anemia, but also th6 breath-holding spells. Pallid infantile syncope may respond to atropine sulfate, which is used on
an ongoing basis if spells are frequent, or intermittently if spells are situationally predictable (such as with venepuncture)'i

THUMB SUCKING

66. Ans.is1d'i.e.,Mustbetreatedvigorouslyinthefirstyear lRef:O.P"GhaiYe/ep.SSbZ"rcp.38;NekonlP*le


p. 1lsl
Intervention to reduce thumb sucking should not be considered until at least 4-5 yr and then only if it is causing
impairment for the child. Nelson
67. Ans. is'a'i.e., 8 years lRef : O.P. Ghai 9ft/e p. 59 6 7/e p" 38; Nekon l*le p. 15321
o The earlier the habit of digit sucking is discontinued after the eruption of the permanent maxillary incisors (7 -8 yr),
the greater the likehood that there will be lessening effect on the dentition.

MISCELLANEOUS

68. Ans. is'b'i.e., ll tRef: Textbaakaf anthraparnetry\

Arm span r
o It is the distance between the tips of middle fingers of both arms outstretched at right angles to the body, measured
across the back ofthe child.
r In under-5 children , arm span is 1 to 2 cm smaller than body length.
r During 10-12 years ofage , arm span = height.
r In adults arm span is more in adults by 2 cm.
r Abnormally large arm span is seen in patients with : (1) Arachnodactyly (Marfan syndrome) (2) Eunuchoidism
(3) Klinefelter's Syndrome (4) Coarctation of aorta.
r Armspanisshortcomparedtoheightinpatientswith:(1)Shortlimbeddwarfism(2) Cretinism(3)Achondroplasia
69. Ans. is t'i.e., Foreign object being put in the mouth lRef: Nelson lThle Chap. 22.2; AP Ghai Sele p. 58\
o Pica involves repealed or chronic ingestion of non-nutritive substances, which includes plaster, charwal, clay, wool,
ashes, patent & earth. :
o More common associated with autism :
r Family disorganisation
r Poor supervision
r Psychologic Neglect
o Geophagia (eating of earth) is associated with pregnancy and some culture.
ADOLESCENT
70. Ans. is 'a'i.e., 10-19 years lRef : O.P. Ghai 8th/e p. 63 6 Vh/e p. 42]
o Adolescence is usually the period l0 to 20 yr.
71. Ans. is'H i.e., l0 years lRef: See above explanation)

72. Ans. is'd i.e., Appearance of pubic hair and Axillary hair lRef: Nelson l},h/e p. 61]
e Thelarche -+ Pubarche -+ Peak growth velocity -+ Menarche
r Thelarche (development of breast buds) is first visible sign of puberty.
o Pubarche / Adrenarche (development of axillary and pubic hair) is the second sign. Itoccurs about 6-12 months
after thelarche
73. Ans. is'b' i.e., Thelarchy fRef: O.P. Ghai 8,h/e p. 6j dt 7/e p. ag|l
r In girls, the first visible sign of puberty is the appearance of breast buds (Thelarche), between 8-12 years of
age.
o In boys the first visible sign of puberty is testicular enlargement, beginning as early as 9lz yr.

74. Ans. is 'a' i.e., Breast enlargement lRef: Has been explainedl

75. Ans. is 'd i.e., Thelarchy-Pubarchy-Menarchy fRef: O.P. Ghai 8th/e p. 6j 6 7h/e p. 498; Nelson lSth/e p. 611

76. Ans. is'd i.e., Testicular development - pubic hair - axillaryhair - beard fRef: O.P. Ghai 8th/e p. 63 b Vh/e p.
498; Nelson 18th/e p. 51, 621
o In boys, the first visible sign of puberty and the hallmark of SMR 2 is testicular enlargement.
o The sequence of development of secondary sexual characteristic in boys is -
Testicular-enlargement -> Penis enlargement -+ Pubic hair growth -+ Peak growth velocity -+ Axillary hair -+ facial
hair.

77. Ans. is 'd' i.e., |ust before commincement of menarche [Rel Nelson lgth/e p. 60-621
Mensus typically appears around the peak in height velocity -Nelson
Menarche usually occurs afier peak velocity has been attained and as the growthrate begins to decline.
78. Ans. is t'i.e., Hormone related breast enlargement in girls
Thelarche
o Definition :- Begining of secondary (Post natal) breast development at onset of puberty in girls.
r Tanner stage2 breast development
r Usually after 8 years of age
r Because ofrising level ofestradiol
o Breast development during puberty in male termed as gynaecomastia not thelarche.
79. Ans. is 'b' i.e., Tanner stage II fRef: Ghai 7h/e p. 4971

r Thelarche- first sign of puberty in Girl around age of 10 year in Girl


r Definition :- Begining of secondary (Post natal) breast development at onset of puberty in girls.
r Tanner stage2 breast development.
r Because ofrising level ofestradiol
80. Ans. is'a' i.e., Appearance of pubic hair & t' i.e., Enlargement of scrotum lRef: Nelson lSth/e ch. 12)
o Scanty & long pubic hair appear at SMR-2. Enlargement of scrotum is there at SMR-2.
GROWTH & DEVELOPMENT

81. Ans. is'd i.e., In the first year of life lRef: O.P, Ghai 8th/e p. 9, 10 6 7h/e p. 7)
o ln the early postnatal period velocity of growth is high duringthefirstfew months,
82. Ans. is'd i.e., Zndyear fRef: O,P, Ghai 8th/e p. 10 lt 7h/e p. 4l
o The brain enlarges rapidly during the latter months of fetal life and early months of postnatal life.
o At birth, the head size is about 65 to 70 percent of the expected head size in adults.
o It reaches 90 percent ofthe adult head size bythe age of2 years.

83. Ans. is'b'i.e., 5-7 years fRef: O.P. Ghai 8th/e p, 10-11 b Vh/e p. 4)
r The growth of lymphoid tissue is most notable during mid-childhood.
o Children between 4 and 8 years of age often have hlpertrophied tonsils and large lymph nodes, which is infact a sign
of lymphoid hyperplasia.

84. Ans. is'b'i.e., 50Yo lRef: O.P. Ghai |th/e p. 13 b Vh/e p. 6l


o At birth, the average height of a child is 50 cm.
r During first year height increases about 50% of birth height (25 cm).
85. Ans. is'd' i.e., 4yet lRef: O,P, Ghai 9th/e p. 13 6 Vh/e p. 6)
Cg,Aprsn,,rt

ANSWERS OF VARIOUS OTHER EXAMINATIONS

GROWTH & DEVELOPMENT

81. Ans. is'd i.e., In the first year of life lRef: O.P, Ghai 8th/e p. 9, 10 & Vh/e p. fl
o In the early postnatal period velocity of growth is high duringthefirstfew months,
82. Ans. is '{ i.e.,Zndyear- fRef: O.P. Ghai 8th/e p. 10 dr 7tu/e p. a)
o The brain enlarges rapidly during the latter months of fetal life and early months of postnatal life.
o At birth, the head size is about 65 to 70 percent of the expected head size in adults.
o It reaches 90 percent of the adult head size by the age of 2 years.

83. Ans. is'b'i.e., 5-7 years fRef: O,P, Ghai 9th/e p. 10-11 dt 7h/e p. 4l
r The growth of lymphoid tissue is most notable during mid-childhood.
o Children between 4 and 8 years of age often have hypertrophied tonsils and large lymph nodes, which is infact a sign
of lymphoid hlperplasia.

84. Ans. is'b'i.e., 50Yo lRef: O.P. Ghai 8th/e p. lj 6 Vhle p. 6)


r At birth, the average height of a child is 50 cm.
e During flrst year height increases about 50% of birth height (25 cm).

85. Ans. is ? i.e., 4year lRef: O.P. Ghai $th/e p. 13 & Vh/e p. 6)

86. Ans. is t' i.e., 5 lRef: Child ilevelopment: Birth to adolesence, Dr Rajesh Dixit, 2006 ed. p. 38; Health, Safety
andNutritionfor the young child, Lynn R Marotz, p. 261
87. Ans. is 'b"i.e., 6 months of age lRef: O.P. Ghai $th/e p. 13 b 7h/e p. 6; Meharban Singfi 3d/e p. 521
r At 6 month of age head circumference is between 40.0-43.5cm.

88. Ans. is t' i.e., 9-12 months [Rel O.P. Ghai 8th/e p. 1j 6 7h/e p. 6; Meharban Singh 3d/e p. 52]
o The circumference of chest is about 3 cm less than head circumference at birth.
o The circumference of head and chest are almost same by the age of 9 months to I year.
r Thereafter the chest circumference exceeds the head circumference.

89. Ans. is'c'i.e., SKglRef: O.P. Ghai 9th/e p. lj 6 Vh/e p. 6l


90. Ans. is'H i.e., 4 years lRef O.P. Ghai 8th/e p. 13 & Vh/e p. 6l

91. Ans. is t'


i.e., Measurement of midarm circumferance [Ref O,P, Ghai \th/e p. 97 dt Vh/e p. 64;Nutrition &
Child d.evelapment K.E, Elizabeth IIh/e p,tual
92, Ans. is'a' i.e., 52 weeks lRef: O,P. Ghai 8th/e p. 49-50 (! Vh/e p. 301
r A child plays a simple ball game at I year (52 weeks).

93, Ans. is 'H i.e., 4years lRef: Nelson 18th/e p. 49; O,P, Ghai 9th/e p, 49)
r A child hops on one foot by 4 years and skips by 5 years.
o As this child can not hop, the age of this child is less than 4 years.

94, Ans. is 'b' i.e., 6 months lRef: O,P. Ghai 9th/e p, 49 dr Vh/e p, 27; Nelson 18th/e p, 46, 47)
o A child can transfer objects from one hand to the other by 5-7 months.

95. Ans. is'b' i.e., 7 months IRe{Nelson 18th/e p. 49; O.P. Ghai lth/e p. 49-501
96. Ans. is'b' i.e., 10-20 words lRef: O.P. Ghai 8th/e p. 53 6 Vh/e p. 301

97. Ans. is t' i.e., 18 months fRef: O.P. Ghai 8th/e p, 53 & Vh/e p. 28)
98. Ans. is'd' i.e., 28 weeks fRef: Nelson 18th/e p, 45; O,P, Ghai 8th/e p. 521
o A child bounces actively, leans forward on hands in sitting position and prefers mother by the age of 7 months (28
weeks).
:t:tr:.:,:,.:.:t.

99. Ans. is'-o" i.e., 7 months fRef: Nelson 18n/e p. 45; O.P. Ghai Sn/e p. SA, 527
r A normal infant sits leaning forward on his hands and babbles by 7 months.
o An infant transfer the object from one hand to other by 5-7 months.

100. Ans. is'H i.e.,36 months fRef: Nelson 18*/e p.491


o A child can dress or undress himself completely by 3 years.

101. Ans. is'l i.e., Lower central {Ref: Nelson 18e/e p. 47, 731
,O2. Ans. is "c' i.e.,2.5 {Ref: Nelson 18n/e p. 47, 737
r Between 20-30 months all milk (primary) teeth are erupted.

DISORDER OF GROWTH & DEVELOPMENT

103. Ans. is't i"e., Separation anxiety {Ref : Nelson 1*/e p. 1171
o Separation anxiety disorder is characterized by unrealistic and persistent worries of possible harm befalling the
affected child or his or her primary caregivers, reluctance to go to school or sleep without being hear the parents
persistent avoidance of being alone, nightmares involving themes of separation numerous somatic symptoms and
complaints of subjective distress.

104. Ans. is't i.e., Disproportionate dwarfisrn [Rel o.P. Ghai Bth/e p. 519 & Th/e p. 1g]
Note - Patient has short stature with short limbs.

105. Ans" is'C i.e., Temper tantrum lRef : O.P. Ghai 9e/e p. 5S & 7/e p. 371
o Temper tantrum reaches its peak point durin$ second and third year of life and gradually subsides in between 3 to 6
years as the child learns to control his negativism and complies to the requests ofothers.

rrr
b{&JY'KXYXON

N UTRITIONAL STATUS I N DICATORS

o Surveillance of growth and development is an important component of the routine anticipatory care of children'
o The main purpose of growth surrveillance is to identifu those children who are not growing normally.

o Nutritional status indicators for surveillance of physical growth are l-


1) Weight for age
s MeasurementofweightandrateofgaininweightarethebestsingleparametesforassessingphysicalgrowthurlMs
10,06)
.

r 8070 of the median weight for age of the reference is cut-off point below which children should b,e<6isideted
malnourished. I
/
r Low weight for age (underweight) is a combined indicator to reflect both acute and chronic mhlnutrition(ArMs
07).
B:ut it cannot diferentiate acute from chronic malnutrition. \
2) Height for age
r Height for age is a stable measuremeni of growth as opposed to body weight.
r Low height for age (stunting or dwarfism) reflects chronic (past) malnutrltionat,zArrMs,7).
r The cut-offpoint commonly taken for the diagnosis of stunting is 90% of the united states NCHS height for age.

3) Weight for height


t Weight in relation to higbt_is now considered more imltortant than weight alor'te(AllMst0'06).
s Low weight for height (wasting) indicates acute malnutritionQct 0s' ArtMS 0s) .

4) Head and chest circumference


r Chest circumference t
At birth -+ Less than 2 cm from head circumference
6-9 months -+ Two measurements become equal
> 6-9 months -+ Overtakes head circumference
I In severely malnourished children this overtaking may be delayed by 3 to 4 years.
Weight heig ht SD score - 2 to -3
(wasting) (70 - 79o/o of expected) (<7070 of expected)
.
r:.]r,,:,i
,:, .; ,5,Q,sctite -2 tq.-3- ''': aD:;i{;e.<,.ti,'',::r,
:,r..li..ijng)t.'',.:,r,, ::.,.,,:r.::.. .,
{85 .89%,oflexpectqd) (< 85olo of expected)

Reference (standard) values of growth


o For national and international comparisons and for monitoring, "reference
or standard values" of growth are essential.
r The well known reference standards are -
1) Harvard (or Boston) standards
r These are not in common use and have been replaced by WHO refrence values.
2) WHO reference values (NCHS standards)
r These are most commonly used and best availableallMss, reference values
for international use.
r These values are based on the data assembled by United States National
Centre for Health Statistics (NCHS).
t Classification of pEM is based on these standards.
3) Indian standards (ICMR)
t These are used for Indian children and based on data assembled by rndian Council of Medical Research
(lCMPStu"'oo1'

* The normal expected value is 50th percentile of the reference value.


o When weight for age is <807o of expected (expected 50th percentile
= of refrence) -+ wasting.
e When height for age is <9oo/o of expected (expected = 5oth percentii" oi ,"rr"n.")
-+ stuntin!.

CLASSIFICATION OF MALNUTRITION

lndian acaderny of pediatrics (!Ap) classification


o Indian academy of pediatrics (IAP) classification of malnutrition is
based on weight for age. IAp designates a weight of
more than 80o/o of expected for age as normal. Grades of malnutrition are :-
t Grade 1(Mild) -) 71-80o/o
t Grade 1I (Moderate) -+ 61-700/o
t Gradelll (Severe) ) 57-6lo/o(PGI ee)

s Grade IV Sery Severe) -+ ! 50o/o

Gomez classification
o It is based on weight retardation (not on height retardation)Gr ost,
o The child on the basis of his/her weight is compared with a'normal'child
of the same age.
o The'normal'reference child is the 50th centile of the Boston slsnflqyflsLroa).

Weight of child
Weight for age (o/o) :
x 100
Weight of normol child of same

9O-1100/o Normal Nutritional status


75-89o/o Mild Malnutrition (1 st degreeyAt oo)

6O-74o/o Moderate malnutrition (2nd degree)


Under 60%o Severe malnutrition (3rd degree)

r classification is easy to compute as weight is widely recorded parameter.


r classification has prognostic value for hospitalized patients (This is because
the Cut off values were set during
a study of risk of death based on weight for age at admission to a hospital
unit).
Waterlow's classifi cation
r It is based on stunting (height for age) and wasting (weight for height)roNr rsr

>m-2SD Normal Wasted


< m - 2 SD Stunted Wasted and stunted

m = mean, SD = standard deviation

Interpretation of indicators

'i/eight of the child


Weight/Height (%) = x 100
Weight of a normal child at same height

Height of the child


Height/Age (%) = x 100
Height of a normal child at same age

Itola] >95
" tfrilily:iniiraitiid:'il:".-:.:
Moderately impaired 80 - 87.5
<80

PROTEIN ENERGY MALNUTRITION (PEM)

o Protein energy malnutrition (PEM) is a spectrum of conditions ranging from mild undernutrition ot extreme forms of
malnutrition, i.e. Marasmus and Kwashiorkor.
r Most of the child suffer from mild to moderate nutritional deficit and extreme forms (marasmus and kwashiorkor)
account only for a small proportion of cases of malnutrition.

Mild to Moderate malnutrition


r If the dietry intake is deficient for a short period, the body adapts its metabolism to compensate for the deficit to some
extent. Moderately malnourished children appear more slow and less energetic.
o Growth lag is more pronounced in weight than the length. Head circumference is not reduced significantly.

Marasmus
rs).
o It is due to prolong deficiency of calories and proteins(Ar Thus there is exessive catabolism of adipose tissue and

muscle proteinarrs).
o It is characterized by gross wasting of muscle and subcutaneous tissues resulting in emaciation and marked
stunting:NEBr). There is no edema. Body weight is less then 6070 of expected.
o Fat in adipose tissues is severely depleted. However the buccal pad of fat is preserved till the malnutrition becomes
extreme because a higher proportion of saturated fatty acids is stored there and the saturated fat is the last to be
depleted.
o Skin is dry, scaly and inelastic with wrinkles. The hair is hlpopigmented. Abdomen is distended due to wasting and
hypotonia of abdominal wall muscles. i
o The child is alert but irritable.
o Child may show voracious appetite(NEEl /'pmer 11)
. .

o Marasmus represents the compensated phase of PEM.


Kwashiorkar
r Kwashiorkar represents the uncompensated phase of pEM.
r Itischaracterizedbyclassical'triad'ofedema(NEEr'AIee) (Duetohypoalbuminetniaar..,riptue,rr)),markedlyretarded
gr owth( AI 8e ), and psychomotor (mental) changs5ovrrr).

r Associated features are :-


1) Hepatomegaly(NBEr,AnMs0s'DPG0e) (due to fattyinfiltratior{Aree,tipne,1l)).
2) skin changes : Er1'thema, hlperpigmentation, fl aky paint dermatosis(,,r Nnnr). 13,

3) Hair changes: Thin, dry and brittle hair; hypopigmented, flag sign{rcrre) (alternate bands of hypo-and hyper-
Pigmentaion{errr);.
4) Infections: Diarrhoea, respiratory and skin infections.
5) Impaired (decreased) appetiteal 13).

Itffif,hi(,r*or

Sar€frl1us

Pmmiflent
bore*
&6ffsasa
lt $ub.ule,r6o&6
fat

Fo$t w{ufld

Complications of pEM
A) Changes in body composition: Increased total body water,
Reduced BMR, decreased insulin levels(Alrlfs 0s, DpG 0e),
increased cortisol and growth hormone, decreased activity
of sodium pump, reduced Bp and stroke volume/cardiac
output, decreased renal blood flow and GFR, poikilothermia,
and reduced IgA levsls{aroa.).
B) Acute complications (Mnemonic-sHIELDED) : sugar deficiency (hypoglycem
iao,cr 06,0s)); Hypothe rmiaecr 06, os).
Infection & septic shock; Electrolyte imbalance (hypokale miao,G'06,05),hlpomagnes
, iurror ou, orl; DEhydration;
and Deficiency of iron, vitamins and other micronutrients. There
may be megaloblastic anemia, which responds
well to folic acid and vitamin B,, supplemelf4fl61arer).

r Poor prognostic factors in pEM, which can lead to early


death _
1. HYPothermidxqn'ea) 4. Diarrhea 7. Cardigc falluretDPc 0, rN 8s)
2. Hypoglycemia 5, Severe anemia 8. Dehydration or overhydration
3. Systemic infections 6. Liver failure 9. Fluid & electrolyte imbalantetoPcos,rNse)

PEM and infection


r The resistance of the human organism to infections is adversely
affected in malnutrition.
r Following changes are seen :
1) The skin and mucosa do not offer effective physicql barriers against infection@pscoe).
2) Impaired chemotaxis, defective candidacidol and bactericidol capacitytuos, ort.
3) cell mediated immunity (ilelayed hypersensitivity) is impairsfl@tscoe;.
4) Circulating antibodies are usually normal or elevated. \
c The number and proportion of B lymphocytes are not altered@psc 0e)
.
o Humorql antibody response to a variety of immunizing
agents (TT 6 DT) is adequate.
I But secretory IgA is generally reduced(Are1).
Evaluation of Malnutrition
o Mid-Arm circumference (MAC): Normal value in children (1-5 years) is 16-17 cm. Value 12.5-13.5 cm represents
borderline malnutrition, whereas value < 12.5 cm represents severe malnutrition.
o Bangletest:Abangle of 4cmdiameterpassesaboveelbowinacaseof malnutrition.
o Skinfold thickness: Skin fold thickness over tricepts is evaluated. Normal value is 10 mm and value less than 6 mm
represents malnutrition.
c Various ratios: Kanawati index (MAC/head circumference6"')), Dugdale's index, Quaker arm circumference, leliffe's
ratio.

Treatment
r Treatment is done in three stages :-
A) First stage: Dehydration and infections are dealt dtringfirst 24-4Shoursby rehydration and antibiotic therapies.
B) Second stage : Dnring next 7- 10 days patient is given a diet of 75 callkglday along with antibiotics, to maintain
protein and energy need.
C) Third stage : This is aimed at restoring patient's protein and fat contents by providing diet of 175-2OO kcalikg/
day4nrvts
ss' 'u se)
in severe malnutrition and 1 50 kcal/kg/day in moderate malnutrition.
r Iron should be started when child is gaining weight once stabilization phase is over("").

'1ha.p,atii*i l*.figure ii'6ir&riag 661p:1 ' : ' , ', ,

a) Scuny
b) Rickets
c) Kwashiorkor
:.1. ,.
'

:Au*iri*&1leii.&ranhiorkor. . ., ::

':a'':Thiaiifi ag'sigron.heirr-eharaeterislicof kwashio:ko:.

The fi agtostu,'o{ the given chlldril i:

' d nickets,' ,t,',':. ,

. b) 'MarasrRus ',:
' 6) ,l(6i6sliiorkor.
r d):' Iv[3lfln syqdrome ']: ,I ' 'l

r This flaky paint dermatosis is characteristic of kwashiorkor.

BREA5T FETDING AND BBEAST MIt.K

o Breast feeding should be initiated within 30 minutes of a normal vaginal delivery and within 4 hours of delivery by
04' PGI ee).
caesarian sectionAl
r WHO recommends 'exclusivebreastfeeding'for the first six months of life(NEEr AilMs06), i.e. during first 6 months only
breast milk is given and nothing else (even water). Wealring should start by 6 months of age when complementary
food should be started in addition to breast milkarq4).
r Breast feeding should be continued with semisolid and solid foods upto two yearsatoa).
t Human breast milk is the best source of nutrition for infant with following benefits :-
1) Superiornutrition(Pcr08)
A) Carbohydrate
r Lactose is in a high concentration in breast milk which helps
in the absorption of calcium and enhances
the growth of Iactobacilli in the intestine.
B) Protein
r The protein content of breast milk is low which causes lower
solute load on the kidney. Most of the protein
is whey proteins (lactalbumin and lactoglobulin), which can
be digested easily (In contrast cow milk
contains more casein).
r Breast milk contains the ideal ratio of the amino acids cystine,
taurine and methionine to support
development of central and peripheral nervous system.
C) Fats
r Breast milk is rich in polyunsaturated fatty acids, necessary for the myelination of the nervous system
and brain growth.
r Active lipase in the breast milk promotes digestion of fats and provides
FFA. The pattern of fats facilitates
absorption of calcium.
D) Minerals
r Breast milk protects against neonatal hlpocalcemia and tetany
due to ideal calcium phosphorus ratio (2: 1)
and better calcium absorption.
r Iron of breast milk is very well absorbed -> breast feeding prevents against iron deficiency
anemia.
r Breast milk also prevents deflciencies of vitamin A, c, D, E and zinc.
r Breast milk has a water content of 88% and hence a breaslfed baby does not require
additional water in
thefirst 6 months of lift even in summer months.
r Breast milk has a low mineral and sodium content -> low osmolality presents
a low solute load to the kidney.
,\ Lower risk of infection(Pcros)
r The breast milk is clean and uncontaminated with several anti-infective factors -+
protect the baby from infection
and diarrhea.
3) Protection from allergy (atopy) {lctoa;
: Low protein contents of breast milk along with a higher concentration of secretory IgA decreases the absorption
of protein macromolecules -+ less chances of allergy and asthma.
4) Emotional bonding
r Breast feeding promotes close physical and emotional bonds
between the mother and the babv.
5) Others
r Breast feeding lowers the risk of ovarian and breast cancer
in mother.
r Breastfed babies have a higher IQ and have less chances ofdeveloping
hypertension, obesity, coronary artery
disease and diabetes in their adulthood.
I The other diseases which are less common in breastfed babies include
inflammatory bowel disease, Hodgkins
lymphoma, necrotizing enterocoritis and sudden infant death syndrome.
r Breast feeding protects against evening colical e8, AIIMIe6).
r Breast milk contains docosahexaenoic acid(ArMsrI'06), required
for the growth of nervous system(izMsir,06).
Anti-infective effect of breast milk
o Breast milk provides protection against infection because
of the following facts -
.
I The breast milk is clean and uncontaminated@cr 0s).

2. Breast milk contains several antiinfective


factors
i) Antibodies -+ secretory IgA, Igl4@eros)
ii) Lysozyme
iii) Antktaphylo co ccal factor
iv) Specific inhibitory substances against viral infections.
v) Lactoferrin -+ Inhibits growth of E. coli.
vi) Bile stimulated lipase -+ kills entamoeba histolltica and Giardia
1amblia.
vi1) Bifidusfactor ) Inhibits growth of E. coli
v1lt) Para-amino-benzoic acid (PABA) -+ Provides protection against malaria
ix) Phagocytic macrophages and lymphoid cells

3. Lower pH of the stool of breastfed infants contributes to the favorable intestinal Jlora -+ more bifidobacteria
and lactobacilli, fewer E. coli(Pcr 08) .

Some disadvantages of exclusive breast feeding


o Exclusive breast feeding may cause deficiency of vitaminBrr4uussz) (if mother is pure vegetarian), vitamin K, vitamin
D and fluoride.
r Vitamin K deficiency can cause hemorrhagic disease of newbornar es' AttMS e6)
.

e6) e6).
o There may be neonatal jaundice('{[Ms and golden colour stool(Ar e&
'{[Ms

Differing composition of breast milk


o The composition of breastmilk varies at different stages after birth to suit the needs of the baby.
o According to the postnatal period the breast milk is divided into -
1. Clostrum
r Is the milk secreted during the first three days after delivery.
r It is yellow and thick.
r It contains more antibodies andcells and high amounts of vitamins A,D,E and K.
r It contains less fat atnd stgar6o'n'st) .

2. Transitional milk
r Is secreted during the following two weelcs (after clostrum).
r The immunoglobulin and protein content decreases while the fat and sugar content increases.
3.Mature milk
r Follows transitional milk.
r It is thin and watery but contains all the nutrients essential for optimal growth of the body.
o According to feed the breast milk is divided into -
1. Fore milk
t lt is watery and is rich in protein, suga6 vitamins, minerals and water that satisfy the baby's thirst.
2.Hindmilk
r Comes towards the end of feed
: Rich in fat content(comed 07)
and provides more energy, and satisfies the baby's hunger.
r The milk of mother who delivers prematurely differs from the milk of a mother who delivers at term -
Preterm milk
r Contains more protein S, sodium, iron, immunoglobins and calories as they are needed by the preterm baby.

Storage of breast milk


o Breast milk can be stored at room temperature for 8- 70 hours@EEr) , in a refrigerator for 24 hours(up 0& PGI e8) and in a

freezer (-20" C) for 3 months.

Breast milkVs Cow milk


e7' AI 07),
o In cprnparison to cow milk, human milk contains more : Lactose (7 gllOO ml or 7o/r)(ArrMs
10' 07'
antibodies,
lactoferrin and other antiinfective factors.
o In comparison to cow milk, human milk contains less amount of : ProteinsailMs 10' 07' Ar07'PGI11) (1 gm/100 ml), salts
(sodium, chloride, potassium), fatrPct 11' At07) (3.4 gm/100 ml), and minerals(Ar07) (calcium, phosphate).
o Though, the amount of mineral and salts is less in human milk, they are in correct amount,lvhereas they are in excess
in cow milk. The coeficeint of uptake of iron in breast milk is 7|o/oqrrMs 11' 08' At 04) .
o Human milk protein constitute mainly whey protein, where as casein is the main protein in cow's milk(A[Ms r0' 07).
o Different constituents of human breast milk provides evergy in following percentage. Carbohydrate 30-40o/o, protein
oe).
7 - 1 0% and fat 4 5 - 60o/o@Gr
, Fqt content of milk: Baffalo > Gaat > Cow > Humon@NB H)
t Protein content of milk: Buffolo > Goat > Cow > Human;DNs tat
. Loctose content of milk: Humon > Buffalo > Goat > Cowt.DNB t4l
. Energy content of milk: Buffalo > Goot > Cow > HumantDNBt4)

Contraindications of breast feeding


o These are:
1) Galactosemia
2) Active untreated tuberculosis - only in initial periofltoxn tt.
3) HIV positive mother - especially in developed country.
4) Some medication

RICKETS

o Rickets is a metabolic disorder of growing children in which


there is defective minerali zation(Ar 13,pGre8)
of normally
formed osteoid (protein matrix) (Pcres).
o Most common area affected is growth plate (physis or epiphyseal
plate) of long bon-estAr ss).
o Rickets is a disease of growing skeleton.It is character izedby
following pathological changes in skeleton :-
i) Thickening of growth plate (physis).
ii) widening of growth plate (physk); clinically it presents as palpable enlargement at wrist, elbow, ankle, and also
at costochondral junction (cailed rachitic rosary).
iii) Cupping or tlaring of metaphysis@Gl s8).
iv) Fraying of metaphysis.
v) Widening of epiphysb@ct se, sst
.

vi) Softening and deformity of long bones -+ Bowing of bones@cr es)


.

Clinical features of rickets


o clinical manifestations of rickets are usually manifested
by 6 months of age. Rickets is unusual below the age of 3
months.
r Clinical features ofrickets are :-
A) Regionalmanifestations
o These are :-
i) Skull CraniotabesallMs0T'03'PGI 03) (eailiest manifestation(Alee)),
frontal and parietal bossing; widened
"
sutures; delayed closure of anteriorfontanelLrrMsoT); Caput quadratum
or hot cross_bun skull:soft skull
with ping-pong ball like feel.

I craniotabes is the softening of skull bones, which may be present in normal newborn,
in pre-
especially
mature'ItismostlyseeninJccipital andparietal bonl;.rt'*uyuisobeseen
inricketspcteT),osteogenesis
imperfecta,Pcrez', congenital syphiti5recrc;; and hydrocephflus.

ii) Chest; Rachitic rosaryallMs rr),(prominent costochondral junction);


pectus craniatum (pigeon breast);
Harrison's groove (horizontal depression along lower border
of chest corresponding to insertion of
diaphragm).
iii)Teeth : Delayed eruption; enamel hlpoplasia; dental caries.
iv) Limbs and joints : Bone pain & tenderness (most common
manifestation); coxavara; genu valg1rs,Gerss))
or genu varus ; bowing of legs (tibisltorr*s or' 03), femur, radus
& tlna; widening of wris{W ost, elbow, knee &
anue; windswept deformityNEEr); string-of-pearls deformifT (Saucage-like
enlargement of ends of phalanges
and metacarpals with constrictions at joints); double malleoli
sign(two medial malleoli are palpable instead
ofone).
v) spine Thoracic klphosis (rachitic cat back); increased lumbar lordosis;
" scoliosis (uncommon).
vi) Abdomen: Pot-belly{'trrus '3) (protruded abdomen) due to hypotonia
of abdominal muscles.

rl
B) Systemicmanifestations
o These are growth retardationect 03) ' apathy, listlessness, irritability; hlpotonia; ligament laxity; and tetany,
convulsions and laryngeal stridor when there is hypocalcemia.

The follor+ing type of skull can be seen,in -

a)."'RiCkets:, ,' ,

b) Osteogenesis imperfecta
, 1
16) ,Congenital syphilis ::
d) All of,lhe above

Ans, is'?! i.e., AII of the above


,, .. Softening of skull (craniotabe$) can be seen il rickels, osteogenesis imperfecta; hydrocephalui
and con.
genital shyphilis.

Followingdeformityis seen ln -

a)Scurly ' . ,

c) Keratomalacia
d) None

Ans. is'H i.e., Rickets


i ,,,r'Itiq,$rhdsweptldeforrni*(gerxr'val$usinonekneeandgemtvarusinotherkiiee). Itisseeninrickets.

Rachitic (RickeU) rosary


o The prominent knobs of bone at costochondral junctions of rickets patient is known as rachitic rosary or beading
of ribs. The knobs create the appearance of large beads under the skin of the rib cage, hence the name by analogy with
the beads ofa rosary.
o Differentialdiagnosisof enlargementof costochondral junction (Rosary) -+ Rickets(Pcls7'Iipner87),Scvr\y(eettz'tip^"'
s7), ez Jipner 87)
Chondrodystrophy(Pcr ,

Types and (auses of rickets


o Rickets is of 3 types:-
1) TypeI -+ Due to calcium deficiency
2) Tlpe II -+ Due to phosphate deficiency
3) Tlpe III -+ End organs are resistant to active form of VitD i.e., L,25 (OH), D3.

Serum calcium
Causes : i) Deficiency of vitamin Dro^/8,5/ i) Primaryhypophosphatemia Vitamin D dependent
r Dietary(rNe4 uPe5) rickets (x-linked), type llro,v8,5)
r Lack of sunlight ii) Fanconi syndromes(D,va?5,
r Congenital r Cystinosis
ii) Malabsorption of vitamin D r Tyrosinosis
iii) Liver disease r Lowe syndrome
iv) Anticonvulsant therapy iii) Proximal renal tubular
v) Renal osteodystrophy@nars1 aciGlOSiSrDrvsr5,
vi) Vitamin D dependent rickets type I
iv) Deficiency ofphosphate or
malabsorption

Serum markers of rickets


r Depending on the tlpe of rickets following changes are seen in serum
markers _

1. Vit D deficiency or calcium deficiency

r vit D enhances absorption of Ca*2 from gut, So its deficiency results in decreased absorption.
r Initially serum calcium level is maintained because of increased activity of parathyroid
gland in response to
calcium deficit' After sometimes' even the compensatory increase
in parathormone cannot sustain normal
calcium level --> J calcium.
r Parathormone also enhances renal excretion of phosphat e + phosphaturia@cr -+ J 06)
serum phosphate.
r Because of unavailability of calcium and phosphate, bone mineralization is decrease -+
compensatory increase
in osteoblastic activity -) Increase alkaline phosphatase.
r So, there is :-
i) Normal to decreased calcium
ii) Decreased phosphass(euoe'ee) (except in renal osteodystrophy,
where phosphate level is increased because
kidney is not able to excrete calcium).
iil) Increased parathormone
iv) Increased alkaline phosphatase@Gl 06, ee)

2. Hlpophosphatemic Rickets
r This is due to deficiency of phosph ate -) Decreased Tthosphate,
t Calcium level is normal.
r As there is no calcium deficiency, there is no compensatory hyperparathyroidism
-+ Normal parathormone.
: Due to unavailabilityof phosphate, mineralization of bone is decreased
and there is increase in compensatory
osteoblastic activity + I Alkaline phosphatase.
r
Serum alkaline phosphatase is a consistent marker and is raised in
all types of rickets(.ares).
Radiological signs of rickets
o Earliest radiological changes are seen around the wrist, i.e,
at lower end ofradius dt ulna,
o Later on, similar changes may also be seen around knee, elbow
& ankle.
o X,ray findings are - ./

I Cupping &Jlaring of metaphysis@ero*os) ' '


t Large gap between epiphysis and metaphysis because of widening of physis (growth plate).
t Fraying of metaphysis due to irregurar calcification at metaphysear margins.
t Generalized osteopenia
s Cortical thinning
t Coarse (tfuzzy trabeculation
t White line of calcification (frenkel's line) at physeal region -+ It is the first radiological sign of healing and
appears after administration of Vit D.
Diagnosis of .the given X:iay-,.

b) Bone dysplasia
c) Rickets
d) None

o Widening, cupping and fraying of metaphysis is characteristic of rickets.

Treatment of rickets
r There are two startgies for administration of vitamin D -
A) Startgy 1 (stoss regimen)
r 6 lac IU (15,000 pg or 15 mg) Vit D3 is administered every 2 weekly.
r At every follow up monitoring is done by X-rays and blood investigations.
r Once healing is started, children are further put on 400 IU br 10 pg of vitamin D, per daI.
B) Startgy 2
r 2,000 - 5,000 IU (50 - 125 pg) of vit D, is given every day for 4-6 weeks.

SCURVY

o Scurr,yis due to deficiency of vitamin C. Vitamin C is required for normal collagen synthesis. Thereforemanifestations
of scurvy are mainly due to defective collagen synthesis :-
I) Defective osteoid productional 10' NrMs eB) .
ii) Deranged capillary function predisposingfor bleeding e.g. subperiosteal bleeding@cl00), gingival bleeding{rcroor.
111) Defective endochondral ossification causing epiphyseal separation@Gr 0o) and brittleness of bone.
iv) Defective dentition and poor wound healing.

a Collagen is a component of osteoid (protein matrix).


a Collagen synthesis is deficient in scurvy; therefore, osteoid formation is defective(A,1o,NIMSsa).
a On the other hand, in rickets osteoid formation is normal, but mineralization (Calcification) of osteoid is defective.

Clinical manifestations of scurvy ,


o The usual age of manifestations of scurr,y is 6-i8 months.
o The manifestions are
1. General symptoms -) Low grade fever, irritabiliry tachlpnea, digestive disturbances, Ioss of appetite.
2. Bleedingluess) + Subperiosteal@Gt00), gingival(rcroo) and conjunctival hemorrhage, purpura & ecchymoses,
petechiae, perifollicular hemorrhage, epistaxis.
3. Defective dentition -+ Bluish purple, spongy swellings of mucous membrane (due to hemorrhage), especially
over the upper incisors.
4. Generalized tenderness(Pcle6) and pseudoparalysi5@et oe t
-+ child is dilficult to handle due to pain and generalized
tenderness. The pain results in pseudoparalysis with the hips and knees in semi-flexed position and the feet
rotated externally.

Pseudoparalysis is also seen in osteomyelitis, septic arthritis, nd congenital syphitis


5' scorbutic rosary(uPe8)-) Due to epiphyseal separation,
costochondral junctionrK,,.00) is disrupted and
sternum
is displaced backward with attached costal cartiiages.
The end of ribs becomes prominentr, rn00) -)rosary.

e, D y...............e
to m elaph ys ea I w i d e n i n g Due to epiphyseal separation
o Non-tender
r Rounded

6' !ns1ni6(ut ss)


-+ Due to defect in utilization of iron & folic acid.
7. Bones arebrittle and easilyfractured.
8. Irritability and other psychologic symptoms.
9' others -+ Arthralgia, muscle weakness, degeneration of
skeletal muscres, cardiac hlpertrophy, adrenal
and bone marrow atrophy
depletion.

Following deformity is seen in -

a) Scurvy'
b) Rickets
c) Keratomalacia
d) None

Ans. is'b' i.e., Rickets


r This is rounded beading ofribs + rachitic rosary (In scur\7, rosary is pointed
or angulated).

Following deformity is seen in

a) Sgurvy
b) Rickets
c) Keratomalacia
d) None

Ans. is'a'i.e., Scurvy


r Pointed rosary is seen in scurly, i.e. scorbutic rosary,
Radiological features of scurvy
o The tlpical radiological features occur at the ends
of long bones, partic tlarly around knee, i.e. lower
end of femur
and upper end of tibia. other commo n site is
Ttroximal end of humerus.
r Features are :-
t Ground glass appearace ofbone
t Pencil thin cortex
t white line offraenkel 6arn -+ represents well calcified cartilage in
00)
(riptner s7)
metaphysi s
t wimburger sign(ter oo) -+ white ring surrounding the epiphyseal centres ,

of ossification . winburgersign is also


called ting sign@IMHANS es)
as there is white ring surrounding the
epiphyseal centers of ossificatign.
t Zone of rarefoction under the *7i1' 1lns1i,nere7) ) represents
u lin"u. break in the bone, proximal and
parallel to
white line and epiphyseal separation may occur along this 00).
line@Gr
: Lateral part ofthis rarefaction is seen as a triangular clefect.
t Palkan spur or lateral spur -+ lateral prolongation ofwhite line.
r During healing phase, subperiosteal hemorrhages become calcified
and the affected bone assume s a dumbbell
or club shaPe(ter oo).
White line of fraenkel is seen in:
i) ScurvY iii) Plumbism v) severe protein energy malnutrition
iv) Acute leukemia vi) Congenital sYPhilis
ii) Healing rickets

Given,X.rg is.diagnoetiiof'-,

a),.RickBts,'r. . '.,' ''


b) Osteomalacia
.'C)t Scuryy.., ,:.:.:.' .....::
r,'''d),:]r{ofl€,,.,,, .,:1. ..

Ans. is'c'i.e., ScurvY


. ,,.,i ,,,_GiteiiX,ray is,showiir$,1wifr:baicq's r ris" tteiis*hite,line,of ialcifidation'eociicllng.&c .qlleoporot-
ic epiPhYsis).

Circn '&raf is diagrrostic, o-f'.

a) Rickets
b) Osteomalacia
c) Scurrry
d) None

: l.r. ,,Giten X,ray il ihowi1g$Iittdbr$Flienkel and wimburger'sign 9 Diagnosis is scu(YYl

Laboratory diagnosis
Leukocyte vitamine C
o Leukocyte concentration of vitamin 'C' is a better indicator of body store,
it may be deficient even in the absence
of clinical signs of deficiency' It is estimated by buffy coat PreParation@Gles).
Plasmavitamin C
early vitamin C deficiency'
o plasmi dscorbic and levels vary widely and cannot be relied upon to detect
Urinaryvitamin C
excretion of the vitamin after a test dose
o Saturation of the tissues with vitamin c can be estimated frorir the urinary
of ascorbic acid. Excretion of 80% of the test dose in the urine
within 3-5 hr after parenteral administration is
80% of test dose is excreted'
considered to be normal. In vitamin c deficiency, less than

VITAMIN'A'

o Important functions of vitamin A in the body are :-


t) Normat vision (regeneration of rhodopsin in dark light)
pGI 88' e7)
ii) Anti-infective activity(Arse'
lil) Anti-cancet effect
iv) Anti-oxidant PtoPertY@EEr)
v) Skeletal growth.
cod-liver oil (2d richest) and liver ox (3'd richest)'
o rhe richest sotnce of vitamin-A is halibut liver oilfollowed by
Among vegetables carrot is the richest source'
Clinical rnanifestations of vitamin A deficiency
o The most obvious symptoms of vitamin A deficiency are associated with
requirement of this vitamin for
maintenance of epithelial functions -
i) Intestine -) Pathogenic attack causes diarrhea
ii) tract -)
Respiratory Infections{Pcte6) & bronchial obstruction
iii)Urinary tract -+ UTI and caliculi
iv) Skin -) Dry, scaly, hlperkeratotic patches
v) Squamous metaplasia of renal pelves, ureter, vaginal epithelium, and pancreatic & saiivary d.ucts.
c Poor grawth(Pc1e6) because of :-
i) Above health problems in children
ii) Vitamin A helps in bone growth + deficiency may retard growth
o Other features are :-
i) Skin becomes toad like (phrynoderma). But it is due to associated deficiency of essential fatty
acids.
it) Vitamin A deficiency may rarely lead to hydrocephalus@Gl e6).
o The most characteristic and specific sign of vitamin-A deficiency are eye lesios. The term
xerophthalmia(pclo4) (dry
eye) comprises ail ocular manifestations of vitamin-A deficiencv.
r It has following stages :-
1) Nightblindness (earliest symptom)@eroo
2) Conjunctival xerosis (eailiest sign)
3) Bitot's sPot@Grol)
4) Corneal xerosis
5) Corneal ulcer (t keratomalacia.
Requirement and doses
o The daily requirement of vitamin A for infant is 300-400 s7),
children is 400-600
VgGIrMs prg and adolescents is 750
trc.
o For treatment of vitamin A deficiency, oral vitamin A is given at a dose of 50000 IU, 100000
IU and 200000 IU in
children <6 months, 6-12 months and > I yea6 respectively4r ts;, The same dose is repeated next day and 4
weeks
later.
o For prevention (vitamin-A prophylaxis programme) a total of 9 doses of vitamin-A
are given between the age of 9
months to 5 years. The first dose (1 lakh units(AzMs,s'AI0e)) is given at 9 months of age along with
measles vaccination.
The second dose (2 lakh units) is given along with DPT/OPV booster doses (at 18 months).
Subsequent doses (2 lakh
units each) are given at six months interval upto 5 years age.

MISCELLANEOUS

Hypervitaminosis-D
o The sign and symptoms of vitamin D intoxications are secondry to hypercalcemia which
is caused by -
i) Excessive bone resorption (major cause) -+ Vit D causes bone resoryfiion@Gl06) .
ii) Increased calcium absorption
r Manifestations are i-
1' GIT -+ NauseaattMss6'PGI 7e),
vomiting, onsvsxciqLrtuss6'PGr7e),poor feeding, constipation, abdomifal pain
and pancreatitis.
2. CVS -+ Hlpertension, arrhyhmias and decreased eT interval.
3. CNS -+ Lethargy, hypotonia, confusion, psychosis, disorientation, depression, hallucinations & coma.
4. Kidney -+ PolyuriaatrMss6'PGr7e),hypernatremia, dehydration, nephrolithiasis and nephrocalcinosis.
5. Metastatic calcificationAltMss6'PGI7e).
Hypervitaminosis-A
o Excess of vitamin A can lead to ruptute of lysosomal membrane.
o Acute manifestations -+ Signs and symptoms are due to raised intracranial tension (pseudotumor cerebri or benign
intracranialhypertension6"t)) + headache, nausea, vomiting, dror,r,siness, bulging fontanelles, diplopia, papilledema
and cranial nerve palsies.
o Chronic intoxication -) Anorexia, weight loss, painful extremities, dry itchy desquamating skin, alopecia, coarsening
bone abnormalities and bony swellinglPct
1s), 06)
of hair, hepatospleno megaly4l .

Zinc deficiency
e Important clinical features of zinc deficiency are :-
L. Dwarfism (growth retardation)(Pct 0s)
7. Decreased immunocomPetance

2. Diarrhea 8. Poor woundhealingleero:"uest


3. Dermatitisares) g. Hyperpigmentation(Pcr03)
03' Ar e8)
4. Hepatosplenomegaly 10. Hypogonadism@Gt
5. Iron defciency anemia 71. Perioralrash
6. Acrodermatitis enteroposlliss@t ts)
o Loss of hair and taste alterations may also be seen.

r Dose for treatment of zinc deficiency is 10 mg/d.ay for 14 days for infant 2-6 months of age and 20 mg/day for 14

days for older than 6 months@EBr).

Acrodermatitis enteroPathica
o AcrodermatitisenteropathicaisarareautosomalrecessivearMsir)disordercausedbyaninabilitytoabsorbsufficient
Zincfromthe diet.
o Initial signs and symptoms occur during the first few months of life often after weaningfrom breast to Cow's milk.

The manifestations are:-


i) Skin :- Vesciobullous, eczematous, dry, scaly or psoriasiform skin lesions, symmetrically distributed in the peri-
oral6lt), acral and perineal areas and on the cheeks, knees and elbows.
ii) Hair :- Hair often has a peculiar reddish tint and alopecia of some degree is characteristic.
iii) Ocular :- Photophobia, conjunctivitis, blepharitis, Corneal dystroply.
iv) Associated manifestations :- Chronic diarrhoea(A[Ms11), stomatitis, glossitis, Paronychia, Nail dystrophy, Growth
retardation, irritability, delayed wound healing, Bacterial & candidal infection.
rr'e3).
r Diagnosis is made by tlpical clinical findings and detection of low plasma zinc concentration(AzMs
o Oral therapy with zinc compound is the treatment of choice. Zinc therapy rapidly abolishes the manifestation of
the disease6zMs ").

..:,:,:r.: r..::;r:ii.:, .i:r::;i,i::,:


jj
.. :::".r;i,i'. :Iti:

': r::.:. ':::t:. i::;:: ----_ r. :.::: i:

| ::i::r:r;:,1ij .:r:: ji
r !--.r,,;.::. -:r:t
.r:r;!.
r.i:.r;r:r:-:j:.
,1,e.Hap,.:rpn,1 z Nitrition

* Other important features of Kwashiorkor: Hepatomegaly (fatty infiltration), flag sign on hair, flaky paint dermatosis, hypoalbumine-
mia, apathy, poor appetite, low insulin.
o Flaky pain dermatosis is characteristic of : Kwashiorkor.
o Not seen in Kwashiorkor :Vocarious appetite (it is a feature of marasmus), altertness (there is lethargy).
* I lmportant features of Marasmus : No edema, vocarious appetlte, no skin or hair,changes, no hepatomegaly;'active child,
nolmal
.a[buminandinsu[in,musclewastingandweakness.
. Most affected antibody in
PEtVt : lgAl

*Cal.bric.suppIementationrequiredinseverePEM:175.200.kcal/kg/day
,. ...:.
r Exclusive breast feeding is till : 6 months.
* Breastfeeding shoutd be initiated: Within 30 minutes,of normal vaginal delivery and'within 4 hours of delivery.by iae*rianiaitionr
o Most important protective component of breast milk against infection : lgA.
* Fatty acid in breast milk which is required for normaf g;owth of brain ; Docosahexaenoeic acid. :. :]:. ' 1
r' . I :., . :

':
* PABA in breast milk provides protection against : plasmodium.
* -, Exctusive breast fee:d:ing may.cause deficiency,of : Vitamin.Bl2, Vitami.n (, Vitamin D and fluoride ,.:.: ,.
..

c Exclusive breast feed ing can cause : Hemorrhagic d isease of newborn (d ue to deficiency of vita min K), prolongation of physiologica I
jaundice, golden colour stool.
o Not seen in exclusive breast feeding : Evening colic (breast feeding protects against evening colic). :.

o Main protein in human milk :Whey protein.


:

.x.Main.protein.inCowtmilk:Casein..,...]
o Human milk contains more (than Cow's milk) : Lactbse, antibodies, lactoferrin.
* Cowtmilkcontains'moie(thanhumanmil'ki:iProtein;saks(sodium;chloride,potassium),fat,minerals(calcium,phosphate). .i,,
o Percentage of lactose in human milk:7.0o/o(7 gm/100 ml).
a Fore-milk is rich- in : Protein, sugar. vitamins, minerals,water. :

o Hind milk is rich ," ,tr;,.;";


r clostrum contains : More vitamins but less fat and sugar (than mature milk).
o Premature milk contains : Less lactose (in comparison to term milk).
* Breast milk can be stored for : 8-10 hrs at rosm ternp€rature, 24 hours in'refriger:ato5 3 months
in freezer at -20oC.
o Breast milk is known to transmit:CMV HlV.

. Most prominently affected in Rickets : Growth plate (physis), i.e. defective mineralization of growth plate.
*,. lmportantfeaturesofrickets:Thickening&wideningof..physi5,cupping/flarlng&ftayingofmetaphysis,wideningofepiphysis.
* Earliest manifestation of Rickets : Craniotabes.
. lmportant features of rickets : Craniotabes, delayed closure of anterior fontanel, caput quadratum (hot cross-bunn skull), rachitic
' rosa$ genu valgus, bowing of tibia, double malfeoli
sign, windswept deformity, widening of wrlst, gror44h.retardation, pai*fry.
* Windswept deformiiy in children is seen in : Rickets (most common cause), physeal osteochondromatosis, herediatary epiphyseal
dysplasia.

* Most common cause of genu valgum in childlen : Rickets,


*: ', Not afeature of Riekets.:Gun5tockdefOrmity (it is seen in ma!united supracondy[arfracturgl' '' ''''' .

o craniotabes is seen in : Rickets, hydrocephalus, syphilis, osteogenesis imperfecta.

..::.,:' I
* lmportant lab findings in vitamin D dependent rickets : Normal or slightly decreased serum calcium and phosphate, raised serum
alkaline phosphatase, increase PTH,irlcreased serum bicarbonate.
lmportant labfindings in hypophosphatimic Rickets. ormalselum calcium, decreased run:l
ahosphate;jn$eased,seru.m atkaline'

a Primary defect in scurvy : Decreased osteoid (protein matrix) formation due to defect in collagen synthesis.
rl lmportant features of scurvy : Subperiosteal & gingival bleeding, generalized tendeinesi. pseudoparalysis, scorbutic rosary.
& Pseudoparalysis in an infant suggests : Scurvy.
c r'seuoopaiatysis is also seen in r septic arthritis, osteomyelitis,:congenital syphilis. , , '
a

e
a

a
a

a
a

a
a

a
a

a
a

a
a

III
QUESTIOT{S

N UTRITIONAL STATUS INDICATORS 10" Frotein requirement for 2 year otd child @er dayl
(CET luly 15 Pauern)
I. Deficit in weight for height in a 3 years old child a) 10 gm b) 15 gm
indicates- eET luly 15 pattern) c) 20 gm d) 25gm
a) Acute malnutrition 11. The amount ofcalories required at I year ofage are-
b) Chronic malnutrition (Ar e6)
c) Concomittant acute and chronic a) 900 K callday b) 1000 K call
d) Under weight duy
2. Best indicator for nutritional status for a child is - c) 1200 K callday d) 1400 Kcallday
(AIIMS May 10, Nov 06) 12. The normal calorie requirement for a 5 year old
a) Mid arm circumference child is- (PGt e3)
b) Head circumference a) 800 calories b) 1000 calories
c) Rate ofincrease ofheight and weight c) 1500 calories d) 2000 calories
d) Chest circumference
3. Acute malnutrition is manifested by - @Gr Nov t4) PROTEIN ENERGY MALNUTRITION
a) Weight for age
b) Weight for height
c) Age for height
13. In marasmus wasting is due to - (All Inriia Dec15 pattern)
a) Prolong dietery deficiency ofcalories
d) Brocas index b) Prolong dietery deficiency ofprotein
c) Ponderal index c) Excess catabolism of fat & muscle mass to provide
4. Which of the following is the besr indicator of long energy
tenn nutritional status - (CET Nov. 15 pattern) d) All of above
a) Mid arm circumference t4. Kwashiorkar is diagnosed in growth retarded chil-
b) Height for age dren along with- (NEET Dec.12 pattern)
c) Weight for age a) Edema and mental changes
d) Weight for height b) Hypopigmentation and anemia
5" Common to both acute and chronic malnutrition c) Edema and hypopigmentation
is- (AIIMS May 07) d) hepatomegaly and anemia
a) Weight for age b) Weight for height 15. Which of the following is seen in Marasrnus and not
c) Height for age d) BMr in Kwashiorkor - (All India Dec. 15 pattern)
6. Weight of child is 70% of normal - according to IAp a) Vocarious appetite
classification, categorised in - (AlltrutiaDec15 pauern) b) Fatty change in liver
a) Mild b) Moderate c) Hlpoalbuminemia
c) Severe d) Normal d) Edema
7. A 2 year old child has a weight of 6.4 kg. and has L6. Kwashiorkar is characterised by all of the following
vitamin A deficiency,What is the grade of malnutri- features except - (AI s9)
tion in this child - (AIIMS 87) a) Edema
a) First degree b) Second degree b) Patchy depigmentation of hair
c) Third degree d) Fourth degree c) Fatty liver
R The following statement about Gomez classification d) Fatty infiltration ofpancreas
is false - (Ar 08) t/. All are seen in lVlarasmus except -
a) Based on height retardation (All India Dec.14 Pattern)
b) Based on 50tl'centile Boston standards a) Hepatomegaly b) Muscle wasting
c) Between 75 a:nd 89% implies mild malnutrition c) Voracious appetite d) Weight loss
d) This classification has prognostic value for
hospitalization of children
18. Not Seen in Iftuaqhiorkar - (All rndia Dec15 pattern)
a) Apathy
9. \{aterlow elassifieation of malnutrition in ehild b) Flaky paint dermatosis
takes into account ? (CET lune 14 Pattern) c) Baggy paint appearance
a) Weight for height (wasting) d) Increased tra4saminase
b) Height for age (stunting) 19. Not seen in kwashiorkor- (Alt India Dec.t3 pauern)
c) Weight for height (wasting) and height for age a) Apathy
(stunting)
b) Flaky paint dermatosis
c) Poor appetite d) Increased albumin
d) Percent ofreference weight for age
20. All of the following conditions are obseryed inMt- d) 24
rasmus, except - (AllMS May 0s, DPG 09)
31. The current recommendation for breast feeding is
a) Hepatomegaly b) Muscle wasting that - (Ar 04)
c) Low insulin levels d) Extreme weakness a) Exclusive breast feeding should be continued till
21. l5 months old child feeding on cow milk with water 6 month of age followed by supplementation with
wih severe wasting and bipedal edema with poor additional foods
appetite - (CET luly 15 Pattern) b) Exclusive breast feeding should be continued till
a) Kwashiorkar b) Marasmus 4 month of age followed by supplementation with
c) Both d) None additional foods
22. In Kwashiorkor, which immunoglobulin is most c) Colostorum is the most suitable food for a new
afiected- (At 94) born baby but it is best avoided in first two days
a) IgD b) IgA d) The baby should be allowed to breast feed till one
c) IgE d) IgM year of age
23, A child is sufiering from severe PEM. Calories to be 32. The protective efiects of breast milk are known to be
given per kg of body weight to regain weight- associated with - (Ar 0s, DPG 09)
(AIIMS lune 99) a) IgM antibodies b) Lysozyme
a) 200 Kcal b) 150 Kcal c) Mast cells d) IgA antibodies
c) 400 Kcal d) 100 Kcal JJ. The important fatty acid present in trreast milk
24. Caloric supplementation required for a severeh which is important for gronth is - (AIIMS Nor, 1 1, Nov 06)
malnourished child @erkg-body weight) is - (Ar ee) a) Docosahexaenoeicacid
a) 100 callkg b) 125 callkg b) Palmitic acid
c) 150 callkg d) t75 callkg c) Linoleic acid
25. Ideal time to start Iron theapy in a marasmic child d) Linolenic acid
with fever and hemoglobin 7 gm%o is - 34. What is deficient in exclusively breast fed baby -
(All India Dec15 Pattern) (AIIMS Feb 97)
a) Immedietly a) Vitamin B b) Vitamin A
b) At discharge c) Vitamin C d) Proteins
c) When fever goes down 35. Exclusive milk ingestion can manifest as- (ArrMS s7)
d) At any time a) Scurr,y b) Beri-Beri
25, Flaky paint appearance of skin is seen in- c) Phryenoderma d) Night blindness
(NEET Dec.12 Pattern) 36. Which of the following will occur in an exclusively
a) Dermatitis b) Pellagra breast fed baby - (AIIMS Sep e6)
c) Marasmus d) Kwashiorkor a) Jaundice b) Scurry
27 . All of the following are characteristic features of c) Tetany d) Eczema
Kwashiorkar, except - (AIIMS May 0j) 37. Exclusive breast feeding may be associated with all
a) High blood osmolarity of the following except - (Ar e8, ArrMS 96)
b) Hypoalbuminemia a) Hemolysis due to Vit-K deficiency
c) Edema b) Evening colic
d) Fatty liver c) Golden colour stool
28. Severe acute malnutrition (Sav), true in manage- d) Prolongation ofphysiological jaundice
ment - (CET Nov 15 Pattern) 38. Breast feeding contraindication - (CET luty 15 pattern)
a) SAM with severe edema should be hospitalised a) Hep A
b) SAM wifh good appetite should be hospitalised b) Hep B
c) SAM with poor appetite should be treated in OPD c) CMV
d) Decision of transfer from in patient to out patient d) Active untreated T.B.
care depends upon specific mid-Upper arm
39. True about cow's milk are all except-
circumference value
(AIIMS May 10, May 07)
a) Cow's milk contains 80% whey protein not casein
BREAST FEEDING & BREAST MILK b) Cow milk has less carbohydrate than mothers
milk
29. Exclusive breast feeding is at least till- c) Has mo(e K* and Na* than infant formula feeds
(CET Nov.14 Pattern) d) milk
Has more protein than breast
a) 4 month b) 6 month 40. Percentage of lactose in human milk is -
c) 8 month d) 10 month (All India Dec.14 Pattern)
30. Breast feeding should begin ... hours after delivery- a) 7.2 gm b) 4.s gm
a)2 b)4 c) 8.0 gm d) 6.7 gm
ti

41. Compared with Cow's milk, mothers milkhas more- 50. True about nutritional rickets - (PGI May u)
(Ar 07) a) Craniotabes
a) Lactose b) vit D b) Multiple #
c) Proteins d) Fats c) Widening of wrist
42. Hind milk is richer in - (Comed 07) d) J Phosphate in serum
a) Carbohydrate b) protein e) GroMh retardation
c) Fat d) Minerals 51. Rickets in infant present as all except- (AtrMS May07)
43, Breast milk rtorage in a refrigeratcr io upto - a) Cranitabes
(CET Nol',.14 Pattern) b) Widened Fontanel
a) 4 hrs b) 8 hrs c) Rachitic Rosary
c) 12 hours d) 24 hrs d) Bow legs
44. Breast milk at room temperature stored for- 52- All of the following are seen in Rickets except-
(NEET Dec.12 Pattern) (AIIMS May 0j)
a) 4 hrs b) 8 hrs a) Bow legs b) Gunstock deformity
c) 12 hrs d) 24 hrs c) Pot belly d) Craniotabes
53. Most common cause of genu valgum in children is -
RICKETS a) Osteoarthritis b) Rickets
c) Paget disease d) Rheumatoidarthritis
45. Basic pathology in rickets - (AIl rndia Dec.t3 pauern) 54. Windsweptdeformityis,seen ilo,- 1Nz,ar oec.12 pattern)
a) Defective bone matrix formation a) Scurly b) Rickets
b) Defect in mineralization c) Achondroplasia d) Osteoporosis
c) Defect in osteoid formation
55. Causes of hypophosphatearic rickets - Nn -
d) All of the above
(CET luly 15 Pattern)
46. Deficient mineralisation in epiphysical growth carti- a) Vit D deficiency
lage is seen in - (Ar ee) b) CRF
a) Rickets b) Osteomalacia c) X-linkedhypophosphatemicrickets
c) Scurly d) Hyperparathyroidism d) Fanconi syndrome
47- A 2-year-old troy has vltamia D reeistant rickets. His 56. Vit-D deficiency Rickets is Characterised by -
investigations renealcd s€rum Calcium- 9 n $ dl"
@GI Nov 14)
Phosphate- 2.4 rugJ dl, alkaline phosphataoe- I 04 1
a) t ed forehead sweating
IU, nornral intact parathyroid horraone aad tricar- b) Characteristically Jed Car*
bonate 22 mfi.q/L.1&'hich of the fo0owiag is the rnost
c) Anterior fontanel widened
probable diagnosis - NEET Dec.l2 Pattern, AIIA.{S
d) ted alk. phosphatase
May{M,02)
57. il,arlier manif€statioa of Riekets is -
a) Distal renal tubular acidosis
(All lndia Dec.14 Pattern)
b) Hlpophosphatemic rickets
c) Vitamin D dependent rickets a) Craniotabes b) Rachitic rosary
d) Hypoparathyroidism c) Harrison groove d) Pigeon chest
58. Craniotabes is seen in following except- (pGt Dec 97)
48. A old boy has vitamin D refractory rickets.
2 year
Investigations show serum calcium 9 mg/dl. phos-
a) Rickets
phate2.4mg dl, alkaline phosphate 1040 tU. para-
b) Syphilis
thyroid hormone and bicarbonate levels are normal.
c) Osteogenesis imperfecta
the most probable fiagnosis is -
d) Thalassemia
(ArrMS Nov 02, 00)
a) Distal renal tubular acidosis 59" Splayiag aud Cupping of the metaphysis is seea
b) Hlpophosphatemic rickets. in - (CETNov.l4pattern)
c) Vitamin D dependent rickets a) tuckets b) Scurry
d) Proximal renal tubular acidosiS-.. c) Paget's disease d) Lead poisoning
49- A l0 year old boyhas a fracture of femur. Biochem- Rickety rosary seen in all except - (PGI Dec 97)
ical evaluation revealed Hb lf .5 gm/dl and ESR lS a) Rickets b) Scuny
mm lst hr. Serum calcium 12.8 mg/dl, serun phos, \ c) Chondrodystrophy d) Slphilis
phorus 2.3 mg/dl,, alkaline phosphate 28 KA units 61. Costochondral junction swelling are seen in-
and blood urea 32 mC/dI. Which of the following is (JIPMER 87)
the most probable fiagnosis in his case- (At 04) a) Scurvy b) Rickets
a) Nutritional rickets c) Chondrodystrophy d) Alloftheabove
b) Renal rickets 62" How to acsess Vit" D tfuerapyin Rickete is -
c) Hyperparathyroidism (All India Dec15 Pattern)
d) Skeletal dysplasia a) Sr calcium b) Sr. alkaline phosphatase

I
: \-rav wrist d) Sr. phosphatase 73. The vitamin A eupplement administered in 'Pre-
vention $. nurtntiana;l blindness in children pro-
SCURVY gra;mmc" contain - (Al0s, AIIMS Nov 0s)
a) 25,000IU/ml b) I Lakh ILr/ml
!f Primary metabolic bonc disorder in sflrrvy i$ - (AI 10) c) 3 Lakh IU/ml d) IU/ml
5 Lakh
a r Decreased mineralization 74. 2 year old boy of weight 12 kg with vitamin A defi-
b r Decreased osteoid matrix formation ciency what is oral dose of vitamin A -
. ) Increased bone resorption (All India Decl5 Pattern)
d) Decreased bone mass with normal mineralization a) 50,000 I.U. b) 1 lakh LU.
and osteoid formation c) l.5lakh I.U. d) 2lakh I.U.
b4. A six month old infant fedtatilly on cow's milk has
been brought with bl€€ding spots, anaeffiia,fcver MISCEttANEOUS
and generalised tenderness. On examinetian, there
were swelling in both the lower extremities and the 75. Allare features afYit. D intoxicatiofl,except-
blood count was normal. The most likely diagnosis (PGr 79, AilMS 86)
ts- (PGt e6)
a) Nausea and vomiting
a) Arthritis b) Poliomyelities b) Muscular weakness
c) Osteomyelities d) Scurr,y c) Anorexia
65. Pseudoparalysis in an infantis suggeetive of.- (Pqoa) d) Oliguria
a) Acute Rheumatic fever e) Metastaticcalcification
b) Vitamin 86 deflciency 76. Hypewit*minosis of which of the followingwill
c) Vitamin E deficiency cause bony abnormalities - (PGI Dec 06)
d) Vitamin C deficiency a) VitA b) VitD
6. l{inberger sign is present in - (PGt 2K) c) Vit C d) Vit E
a) Rickets b) Scurly e) Vit K
c) Secondary syphilis d) Tubercuiosis 77. Hypervitaminosis A causes - (All tndia Dects Pauern)
67. Deficiency of vit. C in infant is best estimated by Vit a) Benign cranial hlpertension
C level in - (CET lune 14 Pattern) b) Craniotabes
a) Plasma c) Liver damage
b) Urinary excretion d) All of above
c) Buffy coat estimation 78. A child with alopecia, hyperpigmentation psoriatic
d) Adrenal cortical Vit. C estimation dermatitis in genitals & mouth and hypogonadism is
68. Boy who refuses to eat fruit cornes with knee swell- likely to be sufiering from - (AI e8)
ing and hematoma, deficiency of which vitamin is a) Cu defeciency b) Iron deficiency
suspected ? (CET Nov. 12 Pattern)
c) Zn deficiency d) Mg deficiency
a) Vitamin C b) Vitamin D
79. Zincdeficiencycauses - (PGlDeclj)
c) Vitamin E d) Vitamin B,
a) Sexual infant ilism b) Loss of libido

VITAMIN A c) Poor weight gain d) Poor wound healing


80. In a child having diarrhoea with perianal moist
69. Anti infective vitamin is - (CET lune 11 Pattern) crust. The diagnosis is - (All India Dect5 Pattern)
a) Vitamin Bu b) Vitamin A a) Acrodermatitis enteropathica
c) Vitamin D d) Vitamin C b) Riboflavin dificiency
70. All of the following statement$ are true regarding c) Pellagra
Vitamin Adefrciency except - (PGte6) d) None ofabove
a) Growth retardation is common 81. Selenium defi.ciency is seen in - (NEET Dec. 12 Pattern)
b) Frequent infections can occur a) Keshan disease
c) Hydrocephalus is infrequent b) Wilson disease
d) Anterior segment of the eye is initia\ty involved c) Acrodermatitis enteropathica
71. Vitamin A deficiency is charactetizedby- (PGI May tt) d) None ofabove
a) Bitot spot b) Xerophthalmia 82. Diarrhoea in a child of 12 month, dose of Zinc is -
c) Night blindness d) Tranta's spot (CET July 15 Pattern)

72. Dailydoseofvitamin Aina6-l2months oldchild a) lmgll0-l4day


ts- (AIIMS lune 97) b) 10mglr0-t4day
a) 500 microgram b) 200 microgram c) 15mgl10-14day
c) 300 microgram d) 700 microgram d) 20mg 110-t4day
83. Elemental iron and folie acid content ofpediatric iron gZ. One year old baby exclusively breast fed ha$ a lcm.
folic acid tablet supplied under RCH programme hepatomegaly severe pallor and no spleen.The most
are- 6t 03) important investigation is - (rN s0)
a) 20 mgiron & 100 microgram folic acid a) B,, estimation
b) a0 mg iron & 100 microgram folic acid b) Serum iron estimation
c) 40 mg iron & 50 microgram folic acid c) Folic and estimation
d) 60 mg iron & 100 microgram folic acid d) Fetal hemoglobin estimation
&4, Requirement of potas*ium in child is - 93. Iron supplementation in a healthy term breast fed
(All India Dec15 pattern) -baby should be started at the age af - lcouro ool
a) 1-2 mEq/kg b) 4-7 mEq/kg a) 2 weeks b) 4 weeks
c) 10-12 mEq/kg d) 13-14 mEq/kg c) 8 weeks d) 6 weeks
94" Breast milk is maximum at - (APPGE 04)
a) l-2months b) 3-4months
c) 5-6 months d) 7-Smonths
85, The most important factar ta overcome protein gS,
Breast milk is known fo transmit -
energy malnutrition in ehildren less than 3 years is- (MAHE 07)
a) Tirberculosis b) CMV
(ArrMS 83)
a) Supply of subsidised food from ration shoo c) Varicella d) Rubella
b) Early supplementation of solids in infants 96, After premature delivery, mother,s milk is low in -
c) Immunisation to the child a) Lactose b) Fat (MH
d) Treatment of anaemia and pneumonia in infant 10)
and toddlers c) Protein d) Sodium
86, Kwashirokar in Ghanian Ga language means- 97. Lactose content of breast milk per 100 ml is - (MH t1)
(Kerala 2K)
a) 3.5 gm b) 4.5 gm
a) Condition seen in 2"d child c) 6gm d) 7gm
b) Condition seen in the displaced child 98. Which of the following is not a sign of active rick-
c) Condition seen in cousin ets?
d) Condition seen in the stepchild a) Prominent fontanelle (COMED 09)
e) Condition seen in the 3.d child b) Hot cross bun sign
87, In Kwashiorkor, the letter ,K, is post-fi.xed to de- c) Saddle nose
note- (Mh 10)
d) Caries teeth
a) Weight for height b) Skin changes 99. Definitive sign of scurvy in X-ray - jipmer u)
c) Edema d) Muscle wasting a) Ringed epiphysis
88. When can a severely malnourished child be safely b) Ground glass appearance
discharged from the hospital ? fupsc_t 0B)
c) White line in metaphysis
a) The child attains his height for age d) Thin cortex
b) The child reaches his ideal weight for height f 00. The recommended oral dose of vitamin A to be
c) The child loses edema and starts gaining weight given in a 10 month child with deficiency on each of
d) The child attains weight for his age day 1,2 and 28 is - (Karn 11)
89, The skin changes seen in proteinenergy malnutrition a) 50,000 IU b) t,oo,ooo ru
can be due to deficiency all of the following nutrients c) 2,00,000 IU d) 6,00,000 ru
except - (DELHI pG Mar.09) l0l. Phrynoderma is due to ...deficiency-
a) Zinc (Kerala 90, Karn pgi 90)
b) Trlptophan a) Vitamin D b)
89,

Niacin
c) Essential fatty acids c) Vitamin A d)Essential fatty acid
d) Pyridoxine
t02. Toad skin is seen in deficiency of vitamin -
90. Para amino benzoic acid of breast milk prevent the a)A b) B,
infection of - (up 07) c)D d) Biotin
a) Plasmodium vivax b) Kleibsella_pneumonia 103. Growth retardation, taste alteration, hepato_spleno_
c) Giardia d) E.coli megly, hypochromic microcytic anemia, loss of hain
91. The substance that has anti infective property direct- hypogonadism in aboyindicate deficiency
ly or indirectly in milk is all except-
of- (Ka,n
]TPMER es) es)
a) Lactoferin b) Lactalbumin a) Selenium b) Copper
c) Lysozyme d) Nucleotides c) Zinc d) Iron
xS4. Deficiency of which element can lead to syndrome of
gro*th failure, anaemia and hlpogonadism - 107, Child ruith frog like position and resietanc€ to move
a Calcium b) Copper (COMED 09) the Imbs - (cMC 01)
; Zinc d) Magnesium a) Scurly
tr,15. -{,bnormalities of copper metabolism are imphcated b) Rickets
in the pathogenesis of all the following except - c) Trauma
(UPSC-t o9) d) Congenital dislocations
a) Wilson's disease 108. Pseudoparalyeis is seen in - (cMC o1)
b) Monkes' Kinky-hair syndrome a) Scurr,y b) Rickets
c) Indian childhood cirrhosis c) Polio d) Osteomalacia
d) Keshan disease 109. Calorie requirement per day of.a childweighing 15
106. Dosage ofYitamin-A forchildrenbetw€en l-3 yeus- kgwouldbe - (MH 1o)
a) 1250 IU b) 1333lU (Manipal0S) a) 1150 kcal b) 1250 kcal
c) 7667 IU d) 2333 rU c) 1450 kcal d) 1550 kcal

I-I
ANSWERS
N UTBITIONAL STATUS I}I DICATOBS

1. Ans. is 'a' i.e., Acute malnutrition [Ref : O.p" Ghai Be/e p. 97 & Zh/e p. 62)
r Wasting (deficit in weight for height) -+ Acute malnutrition.
r Stunting (deficit in height for age) -+ Chronic malnutrition.
o Wasting and stunting -) Acute on chronic malnutrition.
r Underweight (low weight for age) -+ combined indicator to reflect both acute and chronic malnutrition.
) Ans, is 'c' i.e., Rate of increase of height and weight {Ref: o.p. Ghai B&/e p. 13 {t 7n/e p. 6, 6j)
a

t Weight in relation to height is now considered more important than weight alone. Ithelps to determine
whether a
child is within range of normal weight for his height.

3. Ans. is 'V i"e.,Weight for height {Ref : O.p. Ghai *h/e p. 97 & p/e p. 621

o Wasting (deficit in weight for height) usually signifies acute onset malnutrition.
. Stunting (deficit in height for age) usually signinei a chronic.orrr" of rutrrrariai""
o Wasting and stunting --> Acute on chronic malnutrition.
r Underweight {low weight for age) -+ Combined indicator to reflect both acute and chronic malnutrition.

4. Ans. is 'b' i.e., Height for age {Ref : o.p. Ghai d'/e p. 101 6 Th/e p. 62; park lgh/e p. aja)
r
Stunting (deficit in height for age) generally points towards a chronic course of malnutrition. O.p. Ghai
5. Ans. is 'i i,e., Weight tot age{Ref : hdian academy of
-
3d/e p. 12n
Ttediatui{s
r Weight for height is decreased in both acute as well as chronic malnutrition. However, it cannot
distinguish between
acute and chronic malnutrition.
r Therefore, weight for age is a common indicator to reflect both acute and chronic malnutrition.
However, it is not the
best indicator for this (as weight for age cannot differentiate acute from chronic malnutrition).
r Best indicator for this purpose( to differentiate acute from chronic malnutrition) is the
simuitaneous measurement of
'weight for height (wasting)' and 'height for age' (stunting)'which is
useful to understand the dynamics of malnurrition,
distinguishing between current ( acute) malnutrition and long term (chronic)malnutrition.

5o, for both acute and chronic malnutrition:


i) Single common indicator --+ weight for age
ii) Best indicator is simultaneous measurement for stunting (deficit in height
for age) and wasting (deficit in weight for height)

6. Ans. is 'b' i.e., Moderate fRef: Ghai Th/e p. 641

_l
Normal > BOa/o Normal
t: ,,-J=::,,
II
, 6] 70. Moderate
51 -60 Severe
-'..:..,'tlt.it;
IV < 50 V"ry r"u"r""

7" Ans. is 'c' i.e", Third degree {Ref : O.p. Ghai Be/e p. 97 6 7"/e p- 64}
r Normal expected weight at 2 years Df age is 12 kg.
r This child has a weight of 6.4 kg, i.e.53.30/o of the expected.
e So, this child is having grade III (51-610/o of expected weight) malnutrition.
8. Ans. is 'a' i.e., Based on height retardation fRef.: Park lSth/e p. 463; Op Ghai 8tu/e p. 991
o It is based on weight retardation (not on height retardation,)
9. Ans. is'c'ie.,\Seightfarheight(wastinglandheightf*r*ge(stunting)lRef:A.P,Ghai*thlep.62-64;Nelsan
1*/e p. s9!
o Waterlow's classification is based on stunting (height for age) and wasting (weight for height).
10. Ans. is 'c' i,e,,2fr WlRef: Gbai 7h/e p. 5&|

lnfant 0-6 month


?:ol/kg
6-12 month 1.r,,,,,,lrl,:6.5=/.!g.,,;,..'
Children 1-3 year z29m
4-6year : r:iri: . .30:gm:::,:r'-

7-9 year 41 9m

'l::,:,::rJ O.'l 2ty.Saf,,;


- ',..,=.-1*19.m,,,..
13-15 gm 65-70 gm

ll. Ans. is t'i.e., 1200 K cal/day lRef : PSM Park lgth/ep. 502)

lnfancy
0-6 months 118
7-12 months 108 ] K.Cal/kg/day
,:ehilirr.elL:tit..t..

1 :3,aars:::,: :t2.03 1Z4A 5,t


.1690 7.O
1950 :: : ::
'::,::::: 8.1

t2. Ans. is t'i.e., 1500 calories [Ry'; See above explanationl


o It is 1690 KCal.

PROTEIN ENERGY MALNUTRITION

t3. Ans. is id' i.e., All of above lRef: Ghai 7h/e p. 67|
o Marasmus is due to prolong deficiency of calories and protein. There is excessive catabolism of fat and muscle pro{in.

14. Ans. is '* i.e., Ederna and mental changes lRef : A. P. Ghai *th/e p- 99-]AA & Thle p. 671
r Classical triad of kwashiorkor is markedly retarded growth, psychomotor (mental) changes and edema.
15. Ans. is '{ i,e., Vocarious appetite lRef: O.P. Ghai *e/e p. gg-$0 d, 7h/e p. 6d; IAp p. }251

lncidence More common


lTid:n:" .. . Less common
Uncompensated phase
Active. Apathic
-
.:,;'O'b*-ioUS,1r,:,:f:,.. .i.' Sornetimai $dd*11,.ny,,g6;r.t qnd far.
Severe loss of subcutaneous fat Fat often retained but not firm
Pi€Sent..l. :r.:- ,. , i. :"

Low but may be masked by edema


Vocarious (good) appetite .Poor :
Diffuse pigmentations, flaky paint dermatosis

:Rd..eover.*r , '.
Mortality

16. Ans. is 't i.e., Fatty Infiltration of Pan creas {Re! O. P. Ghai 8th/e p. 99-100 & Vh/e p. 67)
17, Ans. is 'a' i.e., *trepatomegaily lRef: A. p" Ghai 8th/e p. 99 & Vhle p. 6Zl
r Hepatomegaly is seen in kwashiorkor (not in marasmus).

18. Ans. is'c' i.e., Baggy paint appearanee fRef: Gh*i Vh/e p. 6Z)
r Baggy Paint appearamce -- refer to loose skin of buttock hanging down.
t Seen in Marasmus
r Flaky paint appearance :- Refer to hyperpigmentation, depigmentation, desquemation which may be confluent seen
in kwashiorkar.
r Apathy, increase liver enzyme is also seen in kwashiorkar.

19. Ans. is 'd' i.e., Increased albumin lRef: previous explanationsl


r Albumin level is low in kwashiorkor, which results in generalized edema.
r Other options are true regarding kwashiorkor.

20- Ans. is 'a & c'i.e", Hepatornegaly & Low insulin levels {Ref : O.P. Ghai */e p. 99 & 6n/e p. 104, 105, t06l
r Hepatomegaly is not seen in marasmus and insulin level is normal.
21. Ans. is 'a' i.e., Klvashiorkar {Ref Ghai Bth/e p. 99-100; Th/e p. 6\
r Odema with muscle wasting is seen in Kwashiorkor.
22. Ans. is 'H i.e., lgL[Ref: O. P. Ghai 6,h/e p. 1071
In malnourished subiects, secretory IgA is generally reduced, Therefore infections tend to be severe and recovery
delayed. - Ghai 6th/e p. 107
23. Aas. is '* i.e.,200 Kcal {Rel API Medicine 6th/e p. 1145, O.p. Ghai Btu/e p. 103-104 & 7n/e p. 7jl
Energy requirements for -
l. Severe protein energy malnutrition -) 175 - 200 Kcal/kg/day
2. Moderate protein energy malnutrition -) 150 Kcal/kg/day.
t About 8-10o/o of total calories should be obtained from proteins ofhigher biological ualue.

24. Ans. is'd'i.e., 175 CallKg{Ref: O.P. Ghai te/e p. 103-104 6 Vh/e p. 731
?< Ans. is'c' i.e., When fever goes down [Rel Ghai Vh/e p. 68] '\
r Iron at 3 mg/kg per day should be started when child gaining weight once stabilisationlhasejsiyer.
zo. Ans. is 'd' i.e., Ift,vashiorkor {Ref : A.P. Ghai S,h/e p" 100 dr Vh/e p. 6ZJ

27. Ans. is 'f i.e., High blood osmolarity tRef O. p. Ghai Bn/e p. gg-100 {z fl/e p. 671
*d
28" Ans" is i.e", SAM with $ey€re Adema should be hospitalised leef TJpdates on the management a! savere acute
malnutrition infants nnd children, WHA protocol p. 361
c Children who are identified as having severe acute malnutrition shouldfirst be assessed with afull clinical examination to
confirm whether they have medical complications and whether they haye an appetite. Children who have appetite (pass the
appetite test) and are clinically well and alert should be treated as outpatients. Children who haye medical complications,
severe oedema (+++), or poor appetite (fail the oppetite test), or present with one or more Integrated Management of
Childhood Illness (IMCI) danger signs should, be treated as inpatients.
t Children with severe acute malnutrition who are admitted to hospital can be transferred to outpatient care when their medical
complications, including oedema, are resolving and they have a good appetite, and are clinically well and alert. The decision
to transfer children from inpatient to outpatient care should be determined by their clinical condition and not on the basis
of specific anthropometric outcomes such as a specific mid-upper arm circumference or weight-for-height/length.

BREAST FEEDING & BREAST MILK

29. Ans. is'b'i.e., 6 months fRef. O. P. Ghai 8th/e p. 150 b Vh/e p. 60)
c The WHO recommends exclusive breast feeding for the first six months of life and then breast feeding up to two
years or more.
30. Ans. is 'd i.e., 2 hours lRef, O, P, Ghai 9'h/e p. 150)
o Breast feeding should be initiated within i0 min. of a normal vaginal delivery.
o Breast feeding should be initiated within 4 hrs of delivery by caesarian section.

31. Ans. is 'a' i.e., Exclusive breast Feeding should be continued till 6 month of age followed by supplementation
with additional foods lRel O.P. Ghai 9th/e p. $a & Vh/e p, 601
o The baby should be given exclusive breast feeding not even water for first six months of life.
o Breast feeding should be given, whenever baby feels hungry (DEMAND FEEDING).
r Complementary foods (other foods in addition to breast milk) should be started after six months of age.
o Breast feeding should be continued with semisolid and solid foods upto two years of age and beyond.

32. Ans. is'd'i.e., IgA antibodies [Rel Nelson 18th/e p. 215; O,P. Ghai 8th/e p" 151 6 6th/e p. 971
Although antibodies and Lysozyme, both are important for protective effects of breast milk, antibodies play the
major role. Out of IgM and IgA antibodies, breast milk is especially rich in secretory IgA which is the single best
answer here.
33. Ans. is 'a' i.e. Docosahexaenoeis acid lRef: C.P.D.T. 18th/e p. 286; Park 20th/e p. 4631
o Up to 5-l0o/o of fatty acids in human milk are poly'unsaturated. Most of these are linoleic acid wrth smaller amounts
of linolenic acid.
o Linoleic acid -+ gives rise to Arachdonic acid
o Linolenic acid -+ gives rise to Docosahexaenoeic acid
o Docosahexaenoeic acid is found in human milk and brain lipids and is required for the development of our nervous
system and visual abilitie.s during the first six months of life.
o Lack of sufEcient Docosahexaenoeic acid may be associated wlth impaired mental and visual functioning as well as
attention defi cit hlperactivity disorder.

34. Ans. is'a' i.e., Vitamin B lRef: A. P. Ghai 6th/e p. 149, 158; Nelson 18th/e p. 215; Cloherty 4th/e p. 1131
o Deficiency of VitaminBnrtaf occur in exclusive breastfed infants of mother who is on strictvegetarian diet.
Remember following important facts -
o Milks from the mother whose diet is sufficient and properly balanced will supply all the necessary nutrients except

o The iron content of human milk is low but most normal term infants have sufficient iron stores for the first 4-6
months. Human milk iron is well absorbed. Nonetheless, by 6 months the breast-fed infant's diet should be
supplemented with iron fortifled complementary foods.
o The Vitamin K content of human milk is low and may cause hemorrhigic disease qf newborn.

35. Ans. is'None' explanationl\


\.. ____,..'
fRef: See above
o Exclusive breasfed infants may have folloWing deficiencies -
i) Vit Brz (if mother is strict vegetarian) iii) Fluoride
ii) vitD iv) VitK
r For one option, you can go ahead with option 'a', i.e. scurvy -
"Breastfed infants are protected as the breastmilk contains adequate amounts of vitamin C, except when the
mother is deficient in Vitamin C". O. P. Ghai 127
-
So, if mother has deficiency of vitamin C, exclusive breastfed infant may develop Vit C deficiency.
36. Ans. is h'i.e., faundice {Ref. Ghai 6e/e p. 97, 121)
o "tr3o/o of breast fed infants develop unconjugated hyperlbilirubinemia in the Ist week of life. The breast
fed infants
have higher, bilirubin levels than formula fed infants."
r It is due to inhibitory substances (Pregananediol and free fatty acids) in breast milk that interfere with bilirubin
conjugation.

37. Ans. is'-o" i.e., Evening colic [Ref Nekon 18h/e p. 215)
c Breast feeding protects against evening colic.
c Evening colic may be seen as a manifestation of allergy to cow's milk, but not with - Nelson 18th/e 215
breast milk.
o Haemorrhage due to vit K ileficiency may be seen. Breast milk contains very little Vit K - Dutta 4th/e p. 515
Hypoprothrombinemia, may therefore occur along with defeciency of other vit K dependent coagulation factors.
(VII, IX, X). this predisposes to haemorrhagic disease in new borns.
r There is strong association between exclusive breast feeding and neonatal jaundice. It is presumed to be due to
inhibitory substance in the breast milk, that intefere with bilirubin conjugation e.g. pregananediol and free fatty acids.
t Golden colour stool may be seen.
38. Ans, is *,* i,e,, Active untreat€d auberculosi$ {Ref: ctoherty - manual of Newatot-ogyJ
Contraindication of Breast feeding
1) Galactosemia
2) Active untreated tuberculosis - only in initial period
3) HIV positive mother - especially in developed country.
4) Some medication
39. Ans. is 'd i.e., Cow's milk contaia 80% whey protein not casein fRef: Nutrition and child develolrment, Fliz
beth F/e p. 18; Park 2ff/e p. $l
r Whey protein constitutes 80% of the protein in human milk, while the main protein in cow's milk is casein.
Comparison of human milk and cow's milk

Bacterial contamination

Protein 47o (too much)


Total 3%'(too much)
Casein

'40/o' .'::
Saturation oJ fatty acids Too much saturated
Linoleic acid (essential) Enough for qoryi"g Uraifr$ Notenough. , '

Cholesterol l
Notenough '":

Minerals {mg)
Calcium 350 (coirect amount) 1;400 (too fiuch)
Phosphate 150{correct amount) 900 (too inuch) :
tf,iiil': .:-::":,., 5in6X,,irrrounr b,ut well-absortred Smali aryouht pborly' absorbed
(enough) (not enough)

Vitamin tnouqh Extra needed

About option'C'
o Cow's milk has more K* and Na* than infant formula' CPDT 18th/e 302
-
10. Ans. is 'a' i.e., 7.2Vo lReJ. O. P. Ghai 6tt'le p. 97, 147, 149; Park 2$'t'le p. 46i, 5451
o It is 7.0 o/o.
41. Ans. is 'a' i.e., Lactose lRef. Park 20th/e p. 4631

12. Ans. is t' i.e., Fat [Rel O. P. Ghai 9n/e p. 15j 6 Vh/e p. 1251
Hind milk
r Comes towards the end of feed
t infat content and provides more energy, and satisfies the baby's hunger.
Rich
-13. Ans. is U'i.e., 24 hrs [R{: O. P. Ghai }'h/e p. 155 d" Thle p. }27)
Breast milk
o Canbestoredatroomtemperature -+ ForS-l0hours
e In a refrigerator -+ For 24hours
c In a freezer :) -200' for 3 months

44. Ans. is 'H i.e., I hrs [R{: O.P" Ghai }tt'le p. }55 d'Vhle p. 12fi

RICKETS

45. Ans. is'bn i"e., Defect in mineralization lRsf A' P" Ghai 7h/e p. 82i
r Inricketsosteoid(proteinmatrix)isformednormallybutmineralizationofthisosteoiddoesnotoccuri'e.thereis
defective mineralization.
o Rickets is a syndrome of diverse etiology characterizedby defective mineralization of bone and epiphyseal cartilage
(growth plate) of growing bones.

46. Ans. is 'a' i.e., Rickets lRef : O.P. Ghai 9'h/e p. 113 (t 7h/e p. 821

47" Ans. is'b'i.e., Hyphosphaternic rickets [Ref 0. P. Ghai 8'hle p. 11j, ]15 & 7h/e p.83; Nelsor 17'/e p. 2342]

o Clues in this question are -


1. Normal calcium 3. Low phosphate
2. Normal paratharmone 4. Elevated alkaline phosphatase

o All these suggest the diagnosis of hlpophosphatemic rickets.


r D/D of Rickets -

Normal 9-10.5 mg/dl 3-a-5mg/dl 30-120 IU 1O-55 units 21-30 rneqil

tAilSQpfresphii*ifgi;fq1lv''..:']::r:
1::r.Ni":,-'l-i','"' ]' '1:- ; f. .:; ,:':' N, :
..::, N: :ir

Vit D dependent Rickets iN/J


i(7.s-8)
N/..1 t t 1

\+
\i vI r'' ''.r+. :l
,:r,. t,.i: ',,
N
r' 'i'\ r.

Nutrit!onal rickets
Nutritional rickets -
c\r
J J
I
I t N

::d;tritbniai:ta {dtLq11t','r,.,.,':,,,,f.:,-:':"':'
: ::. j.:l::'1,.:l:':: ,.r:: . t., .,t,
-,:1

48. Ans. is 'b, i.e., Hypophosphatemic rickets lRel O.P. Ghai 8'h/e p. 113, 115 dt Vh/e p. 831

r In the patient :-
r Serum Ca2* -) Normal (Normal value -> 9-10 mg/dl)
r Serum POr2* -+ Decrease (N -+ 3-4.5 mgidl)
r Alkaline phosphatase -) increase (N + 30-120 IU or 5-15 KA
r Serum parathormone + Normal (X _+ to_ss units)
)
r Serum bicarbonate leyel _+ Normal (N _+ ZZ_ZS units)
o it is clear that it is a case of Hypophospheternic rickets.
So
c Proximal Renal tubular acidosis ulto .u,.r..,
hlpophosphetemic Rickets but the bicarbonate
in a case of proximal renal iubular acidosis. level will be reduced
r Distal renal tubular acidosis causes vit D. dependent rickets
so it is easily ruled out.
49. Ans. is t'i.e., Hyperparathyroidism
[Ref: Nelson lVh/e p. 2345]
'ff:lr#];.ji:tJi;ttt"" just looking at calciurn value. Amongst
the given options onry hyperparathyroidism

e The patient in question has an increased serum


ca**, decreased serum phosphorus and increased
phosphatase, all of which characterize hyperparathyroidism. values of alkaline

50. Ans. is 'a' i.e., Craniotabes, t, i.e., Widening of wrist, .d, i.e., JpOA, ,e, i.e.,
Ghai 9th/e p' 113 & vh/e
Growth retardation [Ref : O, p,
p' 82; welson lvh/e p. 186; Forfar and Arniel's peiatrics
r craniotabes, widening of wrist and growth retardation
6th/e p, d2 sstl
occur in rickeis.
o Serum phosphate is low
5t. Ans. is 'd' i.e., Bow legs laey o. p. Ghai Bth/e p. 113 & vh/e p. 82)
' otT:.T:;::i'ff.t;:::"formed when the chil{ starts bearing weight. rherefore
deformities of tegs are unusuat

q,)
Ans. is 'b'i.e., Gustock deformity {Ael O. p. Ghai gth/e
p. it3 6 Th/e p. 821
c Gunstock deformity is seen in malunited supraconrlylar
fracture of humerus.
Note -
r Dont get confuse between option'a'and answer.ofprevious
question. In this question the age of the chilcl
been mentioned. Bow legs can occur, once has not
the child starts ;"'il;;
53. Ans. is 'b'i.e., Rickets [ne! O.e Ghai 7/e p. 82; Maheshwari
3d/e p. 275)
r Genu valgum (also known as knock knee) is
a condition where knees are abnormally
abnormaliy divergent. approximated and ankles are
c It is caused due to softening of bones or damage
to laterar Femorar epiphysis
Out of given options -
o Most common cause in children is Rickets.
o Other diseases given in option are seen in eiderly.

54. Ans. is'b'i,e., Rickets lRef: Internetl


Windswept deformity
r A valgus deformity of one in association of varus
deformity of other ftnee is known as windswept deformity.
Causes of windswept deformity
o Rickets r physeal osteochondromatosis
o Hereditary dysplasia (epiphyseal dysplasia)
ofbone.
55. Ans. is 'a'i.e., vit D deficiency &'b, i.e., cRF
IR4 Netsqru 18th/e ch.48 (Table a)l
r vitamin D deficiency and cRF (renalosteodystrophy) cause calcium deficient (tlpe-r) rickets.
e Primary hypophosphatemic rickets (x-linkei) p*.orri .frrd.o*.
urrd cause hlpophosphatemic rickets.
56. Ans. is t'i.e., Anterior fontanel widened & d, i.e.,
ted line phosphatase [Ref : O. p. Ghai
7h/e p. 821 Sth/e p. il3 d,

5/. Ans. is 'a'i.e., Craniotabes [Rel p Ghai gth/e p. 113 ("


O. 7h/e p.\g2f_,
Craniotobes is the earliest manifestation of Rickets.
58. Ans. is ld' i.e., Thalassemia lRef : Nelson lgth/e p. 2531
Craniotabes is seen in *) r Rickets o Hldrocephalus r eslsogenesis imperfecta o Syphilis
59. Ans. is 'a' i.e., Rickets {Ref: O. p. Ghai 8*/e p. 113 6 Th/e p. 82)
60. Ans. is'd' i.e., Syphilis fRef: www.fpnotebook. coml
Rachitic (Rickety) rosary
o The prominent knobs of bone at costochondral junctions of rickets patient is known as rachitic rosary or beading
of ribs.
o The knobs create the appearance oflarge beads under the skin ofthe rib cage, hence the narne by analogy with the
beads of a rosary.
Differential diagnosis ofenlargement ofcostochondral junction (Rosary) -+ Rickets, Scurvy, Chondrodystrophy

61. Ans, is 'd' i.e., All of the above lRef : See above explanationf
62. Ans. is t' i.e., X-ray wrist lRef: Ghai 7/e p. 83)
r In nutritional rickets either single dose Vit. D. 6 iakh l/m or 60,000 IV daily for 10 days.
r It shows evidence of radiological healing within 4 weeks of therapy.
r Reduction in serum alkaline phosphatase and resolution of clinical sign occur slowly.
o Ifno healing - repeat dose.
o If no healing can be demonstrated with 2 mega dose of Vitamin-D, then labelled as refractory rickets.

SCURVY

63. Ans. is 'b' i.e., Decreased osteoid matrix fRef: O.P. Ghai 8th/e p. 120 6 Vh/e p. 82-911
o Coliagen is a component of osteoid (protein matrix).
o Collagen synthesis is deficient in scur\T; therefore, osteoid formation is defective.
e On the other hand, in rickets osteoid formation is normal, but mineralization (Calcification) of osteoid is defective.

64. Ans. is 'd' i.e., Scurvy lRef : O. P. Ghai 8th/e p. 120 6 Vh/e p. 911

o Exclusive feeding on Cow's milk in a 6 months infant with anemia, bleeding, fever and generalized tenderness suggest
the diagnosis of scurr,y.
r Cow's milk does not contain sufficient amount of Vitamin C. On the other hand breast milk contains suffrcient
Vitamin C.
65. Ans. is t'i.e., Vit C deficiency lRef : O. P. Ghai 8th/e p. 120 6 Vh/e p. 91]
Pseudoparalysis
o A voluntary restriction of motion because of pain, incordination or other cause, but not due to actual muscular
paralysis.
Causes of pseudoparalysis
o Scurry (vitamin C def,ciency) o Osteomyelitis
o Septic (arthritis) o Congenital syphilis

66. Ans. is 'b' i.e., Scurvy [Ref : See above explanation)

67. Ans. is 'c' i.e., Bufly coat estimation l&ef : Nelson lse/e p. 252)
o Leukocyte concentration of vitamin 'C' is a better indicator of body store, it may be deficient even in the absence of
clinical signs of defi ciency.
. It is estimatedby buffy coat prqvaal
68. Ans. is 'l i.e., Yitamin C [Ref: Nelson 18*/e p. 252)
o The history is suggestive of bleeding disorder and the vitamin most likely associated is Vit. C and disease is scurry.
The other hint in questions is that the boy doesrt't eat fruits. Fruits are rich sources of Vitamin C.
o Vitamin C deficiency causes scur\y.

VITAMIN A

69. Ans. is 'b' i.e., Yitamind. {Ref : O. P. Ghai {/e p. uq & 7/e p. 79; Park 1*/e p. 48sl
o Vitamin A is necessary for integrity of epithbiQ!$ides that resist invasion by pathogens.
o Vitamin A has some role in immune response.
70. Ans. is t' i.e., Anterior segment of eye is initially involved lRef : O. P. Ghai 8'h/e p. 111 6 Vh/e p. 791
o Night-biindness is the earliest symptom, which is due to inability to regenerate rhodopsin. Thvl pasterior segment is
involvecl initialiy (rhodopsin is present in ret,inaand retina
is a part of posterior segment of eye).
o Infections, poor growth and rarery hydrocephrus
occur in vitamin A deficiency.
71. Ans' is 'a' i'e" Bitot spot; 'H i.e., Xerophthalmia & 'c' i.e.,
Night blindness {Ref : o, p. Ghai gth/e p. 1 I I 6 Vh /e
p.7e1
Xerophthalmia (Dry eye)
o It is a syndrome due to def,ciency of vitamin A.
o it has foilowing stages :
l. Night blindness : Eailiest acular symptom 4. Corneql xerasis
2. Caniuctival xerasis : Eailiest ocular sign 5. Keratomalacia & corneal ulcers
3. Bitot's spot
72. Ans. is t'i.e., 300 microgram lRef O. p Ghai Bth/e p. 111 6 Vh/e p. Z9)
Daily dose of vitamin in
o Infants 300-400 microgram
o Children 400-600 microgram
o Adolescen[s 750 microgram

73. Ans' is 'H i'e" I Lakh IUlmt fRef. IAP ln/e p. 417; Nutrition & child Development KE Elezabeth
3d/e p. 941
o According to vitamin A prophyiaxis programme
children between 9 rnonths and 5 years are given 9
megadoses of
vitamin a concentrate at 6 month interval.
o The first tlvo doses are integrated with measles vaccination
and DpT Ist Booster.
o For infant the dose is I ml equivalent to I lakh IU and
in chjldren it is 2 ml i.e. 2lakh IU.
74. Ans. is 'd'i.e., 2 lakh I.IJ. [Re! Ghai Tt/e p.SA]
o For treatment of vitamin A deficiency, oral vitamin
A is given at a dose of 50000 IU, 100000 lu and 200000 IU in
children <6 months, 6-12 months and > 1 year, respectivell'.
The same dose is repeated next day and 4 weeks later.

MISCETLANEOUS

75. Ans. is t'i.e., Oliguria lRef O.p. Ghai Bth/e p. & p.


113 Zh/e 81; Nelson l1th/e p. 2621
o There is pol1'uria (not oligtiria)
76. Ans' is 'a'i.e., vit A; 'b'i.e., vit D IRel O. P. Ghai Yth/e p. 111, 113 6 7h/e p. 80; Nelson 18th/e p. 2451
o In chronic vitamin-A intoxication there are bone abnormalities
ancl bony swelling.
o In hypervitarninosis D, there is excessive bone resorption.
77. Ans' is 'a' i'e', Benign cranial hypertension &'e'i.e", Liver
darnage {Ref: Nelsatt lgil,/e ch. 45 (table-1)}
o vitamin A intoxication can cause benign intracranial
hypertension and hepatomegaly. It is not a cause of craniotabes.
78. Ans. is t'i.e., Zinc deficiency fRef: Nelson 18,h/e p. 266; O. p.
Ghai gth/e p. 122 6 Vh/e p. 921
e The patient in question ltresents with hyperpigmentation,
hypogonadism, dermatitis and alopecia, all of which
may be seen with Zinc deficiency.
79. Ans. is All tR$ Nelson 18th/e p. 266; O. p. Ghai 8th/e p. 122 6 Th/e p. 92)
o Hlpogonadism (sexual infantilism, loss of libido), p.oor
weight gain (growth retardation) and poor wound healing
are
seen in zinc deficiency.

80. Ans. is '* i.e., Acroderrnatitis enter*pathica


{Re;!: Netsan rg,h/e ch. 6z$, 46.21
81" Ans" is 'a'i.e., Keshan disease {Re_f: Netsan lVh/e Chap. 5 j; Ap Ghai gt,/e p. 122}
r Keshan disease -+ Disorder of Se metabolism
r Wilson'.s disease -+ Disorder of Cu metabolism
o Acrodermatitis enteropathica -+-Disorder of Zn metabolism
82. Ans. is'd'i.e., Z0 llrg/10-14 days
According to WHO guidlines
\.,
\i
-\
\l
t-..
'--/
./
Dose of Zinc
2 month - 6 month = 10 mg I day x 14 days
> 6 months = 20 mgl day x 14 days

i.e.,20 mg of iron and 100 microgram folic acid Nutrition & chitd development by K.E. Elizabeth
83. Ans. is 'l fRef:
3'd\ep.111,1121
o National nutritional anemia prophylaxis programme is based on daily administration of Iron & folic acid tablets to
maintain rural child health.
r For anemia prophylaxis FOLIFER tablets with 20 mg elemental iron and 100 microgram folic acid are given to children
for 3 months.
o For treatment upto 6 mg/kg elemental iron should be given for 3 months.

84" Ans. is 'd i.e.,I-2 rmEqItr{g $te}: Nets*n t9'h/e ch. 52.7}

o Recommended dietary requirement is 1-2 mEq/kg

ANSWERS OF VARIOUS OTHER EXAMINATIONS

g5. i.e., Early supplementation of solids in infants & t' i.e., Immunisation to the chil dlRef : O.P-
Ans. is
.b, Ghai
8'hle P. 108-109 dr 7h/e P. 76-771
PEM can be prevented in children by -
i) Exclusive breast feeding for first 6 months.
ii) Supplementary food after the age of 6 months'
iii) Sup;lementary food should be-complementary, so that the deficiency of a limiting amino acid is compensated bv'
a amino acid in other food.
iv) Immunization of vaccine preventable diseases'
v) Restriction of feeding in fever & diarrhea should be discouraged. \
vi) Adequate time between two pregnancies.
\)
g6. Ans. is'b'i.e., condition seen in the displaced child lRef : www.popline.orgl
r The name kwashiorkof comes from the Ga language of Accra, Ghana, and is used to describe the disease of the
displaced baby when the next one is born.

87. Ans. is t' i.e., Edema fRef: A.P. Ghai 6th/e p.I01l
gg. Ans. is t' i.e., The child loses edema and starts gaining weight [Rel: OP Ghai 9'h/e p. ru7 d" 7h/e p. 751

Criteria for discharge in PEM


i) The appetite should have retured and oral intake is adequate'
ii) Gain in body weight with loss edema.
iii) All infections, mineral and vitamin deficiencies should have been treated.
iv) Mother should have been educated regarding domiciliary care.

89. Ans. is 1f i.e., Pyridoxine fRef: Ghai 6tule p. 105, 12j, 1251

90. Ans. is'a'i.e., Plasmodium vivax [Ref O.P. Ghai 6'h/e p' 9fl
91. Ans. is 'b' i.e., Lactalbumin & t'i.e., Nucleotides lRef A.P. Ghai 8'h/e p. 151 & 6'h/e p. 147-148; SPM Park
17*le P. 373 dr 2ffh/e P. 462, 4637

92. Ans. is'H i.e., Serum iron estimation [Ref: O.P. Ghai 6h/e p. 3A] dr Thle p. 3aAl
o By the age of 6 months the breast-fed infant's diet should be supplemented with iron fortified complementary foods
because iron in breast milk is sufficient upto the age of 6 months'
o The baby in question has been exclusively breast fed upto I year, so he has developed iron deficiency anemia.

93. Ans. isNone [Rel: O.P. GhaiTh/e p. 30Al


o Correct answer is 6 months.

94. Ans. is t' i.e., 5-6 months lRef : Park 19h/e p. 4221
o Breast milk is maximum at 5-6 months of lactation --> 730 ml/day'
e It is minimum at 37-38 rnpnths of lactation ) 345 mllday'

)
\ _--,
95. Ans. is'b'i.e., CMV
[Ref Nelson lgth/e p. 215]
o Breast milk transmits (with
definitive_evidence) : (l)
o Breast milk can rarery transmit HIV (2) CMV
: (1) HTLV - tFpe 1 (2) Rubelra virus (3) HBV (4) HSV
96, Ans.is 'i i,e,,Lactose [Ref O.p, Ghai
r premature mirk
Vh/e p. t2S d" 6th/e
15g] p,
contains ress ractose in comparison
to term miik.
97. Ans is t' i.e., 7 gm [Ref Ghai 6th/e p.
97, 142, 149; park 20th/e p. 463, S4S]
98. Ans. is t'i.e., Saddle nose
[Ref Nelson t4h/e p. 186; Op Ghai
o Saddle nose
gtu/e p. 113)
is not seen in rickets_

99' Ans' is 'd i'e"Ringed epiphysis


{Ref o.p. Ghai *tu/e p. 120 6 7h/e p. 911
' :;:::rl,r'i:i?::;{'*'"rger sign):It is white ring surrounding the #;r.:, centres of ossicification.
rt is relatively
' H}t::lmlft*Tnrt" (Freaenkel) can be seen in scur\y, hearing rickets, plumbism, severe pEM,
congenitar slphilis
r Option b & d are not specific for
scurly.
100. Ans' is 'b'i'e" 1,00,000 ru
[Ref: o.p. Ghai gth/e p. 112 6 vh/e p. g0;KE Elezabeth
3th/e p. g4]
l0t. Ans. is 'd'i.e., Essential fatty acid
[Ref O.p Ghai 6h/e p. 121)
r In vitamin A deficiency there is toud iik
skin arso known as phrynoderma.
r But this is due to associated a.n.i.".foi".r.rrtiut fatty acids.
102. Ans. is 't
i.e., A fRef: O.p Ghai 6th/e p. 121
6 7tu/e p. 79]
o Here, essential fatty-acid
has not been provided as an option.
e So, amongst the given options
vitamin K is ihe best answer.
r03. Ans. is t'i.e., Zinc [Ref O.p. Ghai 8th/e p. 122 6 p.
Vh/e 92]
104. Ans. is t' i.e., Zinc [Ref Harrison lVh/e
p. 443; Op Ghai gth/e p. 122)
105. Ans. is 'd'i.e., Keshan disease
lRef : O.p. Gha_i gtu/e p. 122 6 Vh/e p. 93;
r Keshan disease is a disorder of selenium
Harrisons lVh/e p. 4491
metabolism.
o Following diseases are related
to copper metabolism :_
i)Wilson's disease
ii) Menkes kinkyhair syndrome
iii)
indian childhood cirrhosis (increased
hepatic, urinary and serum copper
concentration are characteristic
ofICC).
f 06. Ans. is'H i.e., 1333IU
[Ref O.p. Ghai 6th/e p. 120)
107. Ans. is '* i.e,,Scurvy
tRef O.p, Ghai gth/e p. 1201
r It is a case ofpseudoparalysis.

r08. Ans" is'a'i.e., Scurry


IRd O.p, Ghai gth/e p. 120 & Vh/e p. 911
109. Ans. is .b, i.e., 1250 kcal
fRef: O.p. Ghai Vh/e p. zz O On/e p. SO]

rrr
Q',, t[ A P':T'r.,,,E:r':'rR

NEWffi#Rh$ TNFANY

NORMAL NEWBORN

o From birth to under four weeks of age (< 28 days), the infant is called newborn (neonate) and that petiod.is called
neonatal period@EBr).

o Neonatal period is divided into :-


i) Early neonatal period (first'week of life, i.e. < 7 days)
ii) Late neonatal period (7h day to < 28 days).
t Term neonate (term baby)
r Any neonate born between3T and < 42 weeks (259 - 293 days) of pregnancy irrespective of the birth weight'
t Preterm baby
o Any neonate born before 37 weeks (<259 days) ofpregnancy irrespective ofthe birth weight.
t Post-termbaby
o Any neonate born at or after 42 weeks (294 days or more) of pregnancy irrespective of the birth weight"

r Features of normal'terni newborn infant are :-


t Length -+ 50 cmalt3)
r Head circumference -) 34 cm
r Chest circumference + 31 cm (3 cm less than head circumference)
r Upper segment lowet'segment ratio -) 1.7 to 1.9

t Heart rate + 120 - 140 per minute(Iipnere3)


r Respiratory rate -+a35 - 40 per minute
t ,4ttitue -) Flexion(Ar13)
t Peripheral cyanosis (acrocyanosis) may be presen{Al 13' Iipmer e3)

r Urine is passed by 24 hours after birth


r Meconium (first stool) is passed within 24hoars6"'). After that meconium stools (black tarry) can be passed
upto 3 days(/rrs). On 4th-5th days transitional stools (greenish) are passed. After 5 days regular milk stools (golden
yellow) are passed.
r The skull shows moulding with parietal bones slightly overriding the occipital and frontal bones.
r There maybe pulmonary Jlow (systolic) TnvvTnvv1itnere3), especially in low birth weight neonates.
s Liver, spleen andkidney may be palpable{x,-.sst
o There are some minor clinical problems which can occur in normal newborn
and require no treatment (NEET,DNB 12,
AI 05, pGI 08,02, 98)
.

o The problems are -

1. Milia@cro& e8)

r White dots on nose and face due to distended sebaceous glands. These diseappear spontaneously.
2. Erytherna toxi6sln(rcroa' o2' e5)
r Erythematous papules on trunk & face. They appear on 2"d & 3'd day and disappear
spontaneously.

Mongolian sPots(ecr oa ra)

r There ate 'bluish spots' most commonly


found in pre-sacral area@crh8) (mainly in lower back & butto*),bfi
may also be found over pastefior thighs{eeroat,legs@.orot), and shoulders.
r They disappear spontaneously before first birthday.

Stork bites
r Pinkish gray capillary hemangiomas on the nape of neck, upper eyelids, forehead
& nose. These disappear
spontaneously.
5. Peeling of skin
r More frequent in post-teim infonts, but can also occur in term infants.
6. Subconjuctival hemorrhages @Gr 02' s8)

r Disappear spontaneously.
7. Breast engorgment
r Due to transplacentally acquired maternal hormones. It is seen on 3d or 4s day.
r*-'
EPstein pearl@Gro8'02)
r Epithelial inclusion cysts, which appear as whitish spots. These are of two t,?es -
i) Palatal + On hard p{rte or on either side of median raphe.
ii) Prepucial --> At the rip of prepuce at 6'O'clock position.
Cnl:P.r:E,(

!{hat are these white $pots in a term newborn:


a) Lipoma
b) Vesicles
c) Epstein pearls
d) Stroke bite

Ans. is t'i.e., Epstein pearls


. Whitish ipotr on hard palate on either side of median raphe suggest the diagnosis o[Epstein pearl.

9. Pre-deciduous (natal) teeth


r Supernumerary teeth in the lower incisor position. These are shed before the primary dentition.
rz ar osl
10. Vaginal bleedilg(owr
r On 3'd to 7'h day. it is due to withdrawl of maternal hormones after birth.
11. Vaginal mucoid discharge
r Because oftransplacentally acquired estrogen on vaginal mucosa.

12. Hymenal tags(rvrrrt


r Around margins of hymen
13 Physiological phymosis

Skin changes in newborn that disapper spontaneously :MiliafctoB), erythema tox'cum(P6r08), mongolian spots(P6i '8'), stroke
bite, pustular melanosis, peeling of skin, and Harlequin color change(Pci "r.
o A new born loses upto 1 0o/o of his body weight in first few days and regiins his birth weight by age of 10 days.
a " The number, colour and consistency of stools may vary greatly in the same infant and between infants of similar age. The
color of the stoot has little signifrcance except for the presence of blood or absence of bilirubin products;'
Larynx of a neonate is at higher position (thon adults) which allows infdnt to use nasal airway to breath while suck-
ingqttMslO,

PRIMITIVE REFLEXES
o A number of primitive neonatal reflexes can be elicited in healthy term neonate.
o These disappear as the child grows -+ These reflexes are inhibited by frontal lobes as child grows.
o Absence of reflex responses indicates d),sfunction of central or peripheral motor function.
pcl D).
c Abnormal persistence of neoruatal reflexes is pathognomonic of central motor lesions@Pc 0e'

i) Rooting, sucking'and swallowing reflexes i) Symmetric tonic neck reflexutM'NtMs07)

ii) fiossed.extensior \gfleltiYsff' 4!on ;'' : ii)'Parachutereflex , " :


"
iii) M or o\ r efl elAt t tils 07' A1 07 )
iii) Landau reflex.

ivl Falmar.qraip {grasp reflex) ." ," : ,'

AtMsaT)
v) Assymetrictonic neck reflelAtaT

:ii?: ''&qtifappiiii€nee't Ag-g' ol,$appe-qra6ee{:iftef:birth) :

, Less prominent after 1 32 wks of gestation


:fotl6.vg. ' :: :: 2&32 wks of gestation 3-G fl'onthsttlfis04.
.,'0
a Palmar grasp 28 wks of gestation 2-3 months
,Aisynm*lctoaie-neik 35 wks of gestation 6:7 monthstP6'e't.
o Symmetric tonic neck ,
4-6 months 8-12 months

* ,.LaRdau , .-il 10 rnonths 24 months


. PArAChUteUtt3) 819 mgnths rem a in throug hout I ifeat t 3)
r.:iic!.o5irE .e)itenjOi;,l :: .:28r$r.k afrge-jt tio.ri 1-2 months

o Earliest reflex to disappear -+ Rooting reflex.


t Swallowing reflex is earliest to appeor _+ I 2_ I
3 weeks of gestationtAl 1,

I Moro',sreflexdevelopsby28thrveekofgestationanddisappearsat6mottthsofags{dnus'7,e5Ar07),andneverrea\rytssr.r(1'ct
e8)
' Persistence of Moro's reJlex beyond 6 manths is ahnormararrMs 07)
.

t Unilateral Moro's reJlex is seen in :


i) Erb\ palsyrtersz) (Cr-Cu lesiofl(4llrlsee))
ii) Spastic hemiplegia
lii) Shoulder dislocation@ct s7)
iv) Fracture proximal hwmerus or clayicle@cr e?).

t Exaggerated Moro',s reJlex or persistence of Moro's


reflex is seen in : brqin (cerebral) d.amage@tc as, ecroz)
"

The following figureis showing which reflex:

: a) Parachute reflex.
b) Sucking,re{lex
c) Tonicneikreflex
d) Moro's,reflex

o This'is a figure of Moro's reflex' sudden dropping of


head in relatisnito trunk causes'opening of
abduction and extension of arm; forlorved by-fleion -' hands.with
of apper . extremities.
Morgan's Neonatal Neurobehavioral assessrnent scale
r This consists of three parts : (i) Tone and motor pattern, (ii) primitive
reflexes, and (iii) Behavioral responses.

Stage I : Deep sleep, eye closed, no eye movement, regular


breathing
Stage 2: Light sleep, eye closed, rapid eye movement.
Stage 3: Drowsy or semidrowsy, eye opening and closing (eyclids fluflering).
Stage 4:Awake and alerl, eye op"r, ,,ini*ni*"r", ,.,,Jr*i;;;;";;;. "'
Stage 5: Wi<ie awake, considerable (vigrous) movement.
Stage 6 : Cryingletws tot
intense and lortd, High.motor acti\_iry

HYPOTHERMIA

r A newborn is more prone to deveiop hlpothermia


because of large surface area per unit ofbody
weight. The protective
mechanism for heat generation (thermogenesis)
in response to cold environment are :-
i) Peripheral vasoconstrictionullMs 11,06).
ii) 'Non-shiveringthermogenesis'inbrownfatbyadrenaline^rrMsit,06).Brownfatislocatedaroundo
8e), drenalglan4{eor
kidney, nape of neck(pcr ss),
and. intersca?turar and axi,ary regions.
iii) Increased heart rate to meet more O, demand.
o Newborn daes not haue shivering mechanism
for thermogenesisGr^s 11, Li6,Ar es).

o Clinicai features of hypothermia in a neonate are :_


1) Peripheral vasaconstriction : Acrocyanosis, cooi extremities, decreased peripherai perfusi.n.
ii) CNS depression : Lethargy(Pct 0, , bradycardia@Gr 06, Ar es)
, flpnea{pcr 06, a2), poo, f..airrg.
iii) Increased metabolism : Hypoglycemia@Gt 06' 02)
, hypoxiq@"' out
, metabolic acidosis(At ee)
.

iv) Incre pulrnonary artery pressure : thchlpnea, respiratory distress.


ased
v) Other:Depressed immunity, increased chances of septicemia, sclerornaule'qr, DIC (due to infection), hemorrhagic
manifestation.

LOW BIRTH WEIGHT AND PREMATURITY

o Birthweightisthesinglemastimportantdeterminantafchancesofsurvival,growthanddevelopmentafaninfant{tt
'3). Birth weight should ideally be measured within lst haur of birth. Average birth weight in lndia is 2.7- 2.9 kg (2.8
kg){Nntrt.
s Most common causes of low birth weight (LBW) in India is maternal malnutrition. Maternal nutrition has linear relation
with birth weight.
o Following terms are reiated to birth weight and maturity of a neonate at birth :-
1) Lowbirthweight
r Anyneonatelveighing/essthan2500gm(2.5kg1r*uu':'GMCETq7']'G103)atbirthirrespectiveofgestationalage(WHO
definition). But some lndian scientists consider LBW as < 2ftyleouctrozl.
2) Very low birth weight
r Any neonate weighing less than 1500 gm (1.5 kg) at birth irrespective ofgestational age.
3) Extremely low birth weight
rAny neonate weighing less than 1000 gm (1 kgy*uu't at birth irrespective of gestational age.
4) Appropriate for gestational age (appropriate for date)
r Neonate with birth weight between 10th to 90th percentile.
5) Small for gestational age (small for date)
r Neonate with birth weight less than 10th percentile(Pct00). These are the baby cailed as intrauterine growth
retardation (IUGR).
6) Largefor gestational age (largefor date)
r Neonate with birth weight more than 90th percentile.
7) Tertn neonate (termbaby)
r Neonate born between 37 and < 42 weeks (259-293 days), irrespective of birth weight.
8) Preterm baby
r Neonate born before 37 weeksql 01) (< 259 days), irrespective of birth weight.
9) Post-termbaby
r Neonate born at or after 42 weeks (> 294 days), irrespective of birth weight.
Causes of intrauterine growth retardation (smal! for date)
r Important causes of IUGR are :-
1) Maternal malnutrition: Most important cause.
2) Substance/drug intake: Smoking and tabacco(NEEr' AttMS 87), alcohol$EEr' AIIMS 87), propranolol\IlMs 87) "

3) Maternalfacfors: Short stature mother, primi or grand multipara, yound mother (< 20 years),lowpre-pregnancy
weight.
4) Maternal illness/diseases : Anemia, CRF$'rr), heart disease, malaria, pre-eclampsia, hlpertension.
5) Placentalfacfors: Abruptio placenta, excessive infarct, single umblical artery.
6) Fetal factors : First born babies, genetic/chromosomal aberrations, twin/multiple pregnancies, intrauterine
infection@at) .

Types of IUGR (smallfor date neonate)


r IUGR is classified as :-
1) SymmetricIUGR
I Reduced growth is symmetric. Head circumference, length and weight are equally affected.
2) AsymmetricIUGR.
r Reduced growth is asymmetri c with relativ e sp aring af head@EEr ) .
-t Newborn lnfanit
Predisposing factors for neonatal sepsis
1) Forearlyonsetsepsis
o Low birth weight or prematurityaleB)
t Prolonged rupture of membrans(erse)
r Foul smelling liquor
o Multiple per vaginum examination
o Maternal fever
r Di{ficult or prolonged labor
r Meconium aspiration
2) Forlate onset sepsis
r Low birth weight
o Superficial infections (pyoderma, umblical sepsis)
r Disruption of skin integrity with needle pricks and use of iv fluids.
o Lack of breast feedingler wt
o Aspiration of feeds
Clinical features of neonatal sepsis
o Early onset sepsis manifests frequently as pneumonia and less commonly as septicemia or meningitis"
e Late onset sepsis manifests as septicemia or pneumonia or meningitis.
o The most common and characteristic manifustations is an alteration in the estabilished feeding behavior -+ baby
refuses to suck arud becomes lethargic, inactive or unresponsive.

r Important laboratory finding are :-


1) Neutropenia is common (rarely neutrophilia may occur in severe neonatal infection{ttsa)1.
ii) Increased number of immature neutrophils1l e6).
111) Increased ESR and CRPute6).

Treatment of neonatal sepsis


r Antibiotic treatment for neonatal infection is :-
1) Neonatal pneumonia : Ampicillin plus gentamicinurlMseT).
2) Neonatal meningitis: (i) Ampicillin plus gentamicin pius chloramphenicol or (ii) Cefotaxime plus gentamicin, or
(iii) Ampicillin plus cefotaxime.

RESPIRATORY DISTRESS
o The principle features ofrespiratory distress in a neonate are :-
1) Taclrypnea (fast breathing): Fast breathing is defined as :-
l) Child less than 2 months of age + > 60 breaths per miflute?Gto4)
ii) Child aged 2 months upto 12 months -+ > 50 breaths per minute
iil) Child aged 12 months upto 5 years ) > 40 breaths per minute

2) Use of accessory muscles for respiratio n@NB


12' PGI 04)
r Features include use of sternocleidomastoid muscles, nasal
alar flare and tracheal tug.
3) Use of intercostal or subcostal mural"rtnN'.'' rcr 0a)
for respiration resulting in intercostal or subcostal recession-
lower chest wall indrawing.
4) Audible grunting(DNr 12'PGI01)

5) CYanosis(DNB12'PGI04)

Apnea
o Apnea malr !s defined as -
i) Cessation of respiration for 20 seconds with or without bradycardia and cyanosis(Ar 13' NEEI' DNB 12)
.

or
ii) Cessation of respiration for less than 20 seconds if it is associated with bradycardia or cyanosisGr 13' Nnnr' DNB 12)
.

i.

h
ti

I
. Apnea is more common in preterm infants.
c Apnea of prematurity ocatrs in preterm neonates in 2nd to 5th day of life and is because of immaturity of
developing brain.
o Important causes of neonatal apnea are : Hypoglycemia@Grqg),metabolic acidosis ,hypothermia@G108) andpretnaturity@er
oB)
.

Pulmonary causes of neonatal respiratory distress


o Respiratory distress syndrome (hyaline membrane disease){dtsst.
o Meconium aspiration syndrorngqt ss),

r Pneumonia.
t Transient tachypnea of newboyn(etess.
r Persistent pulmonary hypertension
o Congenital malformation -+ TER Diaphragmatic hernia(Pclo3' 0r), lobar emphysema, pulmonary hlpoplasia.
r Upper airway obustruction -+ choanal atresia, vocal cord palasy, lingual thyroid.
r Pulmonary hemorrhage
Causes of respiratory distress with mediastinal shift in neonates
r Diaphragmatic hernia
r Congenital lobar emphysema
o Congenital mediastinal mass
o Pneumothorax
o Congenital cystic adenomatoid malformation

Meconium Aspiration Syndrome


t Meconium is the first stool of an infant, composed of materials ingested during the time the infant spends in
uterus, i.e. intestinal epithelial cells, lanugo, mucus, amniotic Jluid, bile and water.
o Meconium aspiration syndrome (MAS) occurs when infants take meconium into their lungs during or before delivery.
o lt ts more common in post-term neonates@Gl0a) but may also occur in term neonates.
Consequences of meconium aspiration
o Three main problems occur due to meconium aspiration -
i) Obstructive emphysema or atelectasis(NEEr) ) when aspirated material blocks the airways.
ii) Pneumonitis and chemical pneumonia -> because of irritant property of meconium.
iii) Defective gas exchange.

Clinical maiifestations
r Respiratory distress within lst hour with tachlpnea, retraction, grunting and cyanosis.
r Overdistention of the chest.
Complications
r Respiratory distress sl,ndrome r Pneumothorax r Persistent pulmonary hlpertension

Radiographic pictures of MAS


o Hlperventilated lungs with patchy infiltration. r Flattening of diaphragm.
r Increased anteroposterior diameter of chest.

The following chest X-ray of a post-term neonat€ is seen in:

b) Transient tachypnea
'trc)l,.+keola;1protf.;i,*dsis'.',1:,,,,1.' "'',, ',',, .,r,

irrr.l:d},:rMbeqniirin.as?iratiOn.;,1r .' ,::,::1.. 'r,..:,: ., ..: :


:i.:

Ans. is'd' i.e, Meconirrrn asprration


p,11.Ttit$venehgst X-iii4,li, lho,wrry
'''1":' hff erinflation with p'iofitirution (inpost;teim nionate)+.diagnosis
:i,,.:,
'. ,- i* *6aodrt* asoitation sfiidrornsi' ' r:'" ,
' r There is herniation of abdominal contents, i.e. stomach (most of the time),
intestine, liver; into thorax through a defect
in the diaphragm.
r Females are affected more than males.
o More common on left sidearrus e7) and is poster sl4Llalanus sz)
.
o Components of CDH are :-
i) Herniation of abdominal contents into thorax
ii) Pulmonaryhypoplasia
iil) Malrotation of intestine
o Associated anomalies may be seen 30% of cases -+
cNS lesions, esophageal atresia, omphalocele and CVS lesions.
Most cases are sporadic.
r cDH is a reconized part of several chromosomal syndromes -+ Trisomy 21, 1g, 13, turner syndrome, pallister-Killian,
Fryn.

Clinical features
o CDH may present as
l. Soon (within 6 hrs) after birth (most of the cases)
or
2. After neonaral period (small group)
l) Soonafterbirth
t Respiratory distress is a cardinal sign@Nn o -> presents as tachypnea, grunting@rva re, chest
retraction,
cyanosis.
t Scaphoid abdomen@NB ls)
r Increased chest wall diameter
r Bowel sounds may be heard in the chest with decreased breath sound.
r Cardiac impulse is displaced away from the side of hernia.
2) Afterneonatalperiod
: Vomiting as a result of intestinal obstruction
r Mild respiratory symptoms
r
occasionally, incarceration of the intestine will proceed to ischemia
with sepsis and shock.
o Most common cause of death in CDH is pulmonary
complications(ArrnseL) (pulmonary hypoplasia{ArruseB)
and pul-
monary hypertension).
Diagnosis
o Prenatal ultrasound can diagnose CDH between 16 and
14 wk.
o After delivery chest X-ray and nasal gastric tube is all that
is usually required to confirm the diagnosis.
Prognosis
o Two most important prognostic
facto.rs are pulmonary hypertension(AilMs il, 0s,At oe) and pulmonary hypoplasiailrrMs
"). Other prognostic factors are : Gestational age at detectionailMs 11Ar lt),associated
anomalies, size of 11,
d.efect{ArrMs
AI11)
aldside of defect (right side has poor prognosis). Timing of surgery is not Ar
a prognostic factor*nus 11, 11).

Management
e cDH is no longer considered as surgical emergency child
is first resuscitated and stabilized before surgery.

,,,*
't
Dlttercnlial diagnosir
r Pulmonary sequestration.
o Pleuropericardial cysf |tt Ms s7 ).
r Cystoid adenomatoid malformation.

The follorring che*t )Lrayis showing:

a) Hyaline mernbrane disease


b)'Transient tachlpnea
c) Congenital di4phragmatic hernla

Aas, ts t' i.e., Congeaikl diaphragmatic hcrnia


o This chest X-ray is drowing herniation of boryel loops into left hemithorax with shift of heart and mediasti-
num to opposiie side + diJgnosis is CDH.

Hyaline membrane disease (HMD) or respiratory distres; tyndrome {RDSI


r HMD always occurs ln preterm babies often less than 34 weeks of gestation. It is the commonest cause of respiratory
distress in a preterm neonate.Incidence is highest in preterm male and white infant.
o HMD disease is due to deficiency of surfactant@Gl ee). Surfoctant start appearing in fetal lung by 20th week of
gestationAllMs e8). But mature levels appear only afier 35 weeks of gestation; therefore HMD is more common in
ee)
premature newborns. In amniotic fluiils, surfactant appears between 28-32 weelcs of gestation@Gt .

Risk factors for HMD


t Prematurity (most important)at ts' ozt r Cesarean section
r Asphyxia r Cold stress
o Acidosis o A history ofpreviously affected infants
o Maternal diabetesGt 02, PGI Be)
o Multiple bifthAl 02, PGr se)

Protective factors for HMD


r Hypertension r Maternal heroin use
r Prolonged rupture of membrane r Antenatal corticosteroid prophylaxis
Morphological changes in HMD
o Diffuse alveolar damage is the characteristic histological
manifestatio of HMD.
I In the acute stage, the lungs are heal7, firm, red and boggy with congestion, interstitial
and intra-alveolar edema.
r The alveolar walls become lined with waxy hyaline membrane. Hyaline membrane
consist of fibrin rich edema fluid
mixed with the cytoplasmic and lipid remnants of necrotic epithelial
cells(NrE").
Clinical features of HMD
o Respiratory distress occurs within the first 6 hours of life.rcr 08, AMU 88)

r Clinical features include -


t Tctchypnst@etot) r Decreased air entry r BP mav fall \
r Retraction(Pcl01) r Fatigue . oliguria I lf untreuted
r Grunting r Pollor r Ileus )
r Cyanosis r Mixed respiratory & metabolic acidosis,:Pcrol)
o FRC is smaller than closing volumeallMs 10).

X-ray appearance in HMD


r The initial roentgenogrom is occasionally normalK"oros't),withtypical
pattern developing at 6-12 hours.
i) Reticulogranulat patternullMs 12, 10, PGI e7, Kerata s4)

ii) Ground glass opacities\lrMs 12, 10' PGI e7, Keralae4)

iii) Air broncho gramArrMs 12, PGI s7' Kerata e4)


10,

iv) In severe case whiteout lunglenus n' t0, PGr e7, Keruta e4)
Prenatal diagnosis of HIUID
r Prenatal diagnosis of HMD can be made by -
1) Lecithin / sphingomyelin (L/S) ratio in amnioticfluid @EEr)

r L/S ratio > 2 indicates adequate lung maturity.

2) Shake test
r Amniotic fluid or gastric aspirate is mixed with absolute alcohol and shaken for 15 seconds and
allowed to settle' copious bubbles are formed in the presence
of adequate surfactant indicating extent of lung
maturity.

Treatmentof HMD
r Neonate should be managed in NICU (neonatal intensive care
unit).
o Oxygen should be given ,
Mild distress _+ Without ventilator
Moderate distressqllMs 10' 0e) -) Continuous positive airway pressure (CpApltenus n, os1

Severe distress -) Intermittent mandatory ventilation (IMV)


Oxygen tension is kept at 90o/o (100% oxygen is not given{AI02)
' because ofrisk ofretrolental fibroplasia).
t Intratracheal surfoctant therapy is the specific therapy. Its indications
are : -
i) All neonates less than 2g weeks irrespective of presence or absence of HMD (RDs).
ii) Neonates with > 28 week with severe respiratory distress.
Prevention of HMD
r Administration of prenatal glucocorticoids to mother at least 24 hrs prior to delivery pregnancies of less than
34 weeks gestation, reduces the risk of HMD'

olnjectionbetamethasone (l2mglmevery24hours(Nnnr)JFor2doses)ispreferred.Dexamethasone(6mglmevery
12 hours for 4 doses) i.s an alternative. Beside reducing HMD risk, corticosteroids also reduces mortalfiy(AlrMsee) and
v entri cular h emorrhage(
ut us sa) .
incidence of int er

fire followlag lLray of a pretergr newbornsuggest the diagnosis ofi


a) Meconium aspiration
b) Transient tachypnea
c) Hyaline membrane disease
d) None '.r . .,....

'Ans. i* lcii,e., Hyalinemernbrane disease


'
i.' . Il_re chestix,ray is showin$ reticulogranular pattern with increased aiibronChogram > hyaline membrane
disease.

Bronchopulmonary dysplasia {BPD}


o Bronchopulmonary dysplasia is usually defined as a need for supplemental oxygen at 36 weeks afier conception.
BPD is usually defined as a needfor supplementel oxygen at 36 wk afier conception.
e Respiratory distress persists or worsen and is characterized by hlpoxia, hlpercapnia, oxygen dependence and in severe
cases right sided heart failure.
o BPD is a result of lunginjury in infants requiring mechanical ventilation and supplemental oxygen.
o Most of the children with BPD are [,remature and have hyaline membrane disease. But, BPD can also occur in full
term newborns with meconium aspiration or persistent pulmonary hlpertension.
r The premature lung makes insufficient functional surfantant and the antioxidant defence mechanisms are not sufficiently
mature to protect the lung from the toxic oxygen metabolites generated from oxygen therapy.
r The major underlying pathogenic mechanisms causing BPD are :-
1) Oxidant damage by toxic oxygen metabolites$In&'u).
ii) Mechanical trauma\le6) z Atelecto trauma (alveolar collapse and volutrauma/barotrauma(Ale8) due to
overdistension by mechanical ventilation).
lll) Pulmonary edema due to capillar! damage@Ies'se)

Moderate Sev€re{A' 73)

Supplement 28 days) and Supplement O, (for 28 days) and Supplement O, {for 28 days) and

' . Breathing > O, and/or


3Ao/o

> 32 weeks
r Breathingroomairby56days r <300/oQrby56dayspostnatal positive pressure (PPV) by
psstnatalageoratdischarge ageoratdischarge(whichev- 56 days postnatal age or at
GA at birth
(whichevercomesfirst). ercomesfirst). whichever comes
l::i,:"tn"
=qR. tp,u,a."=q{gffi::;SlFiiiiti;i: ::.:iii:.j'r:, .::::i:...::i::.,j.,,,...rr,..ii#L't?i,t;.i:i,il:;,.::.-:iii': :ir!

Transient tachypnea of Newborn


r Transient tachlpnea of the newborn is a benign self-limiting disease occuring usually in term neonates and is due to
delayed clearance oflung fluid. It is also called respiratory distress syndrome type II.
o TTN follows -
cxapren 3,.New.,bornrr&
FI
i) Uneventful normal preterm or term vaginal
delivery
ii) Cesarean deliveryLauusoz)
I TTN is believed to be secondary to slow absorption
of fetal lung fluid resurting in decreased
and tidal volume and increased dead space pulmonary compriance
therefore arso knowi as wet rung.
o Clinical manifestations
r Early onset of tachlpnea
r Sometimes retraction or expiratory grunting
I Occasionally cyanosis
: Patients usually recover rapidly within 3 days,
t Hypoxemia, hypercapnia and acirJosis are uncommon.
r The lungs are generally clear without rales
or rhonchi and chest roentgenogram shows
-
s Prominent pulmonary vascular markings s overaeration(ArrMs5s)
t Fluid lines in the fissure t Fbt diaphragms
r Prominent inter-labarfissureLrrMs05,pcree)
t occasionally pleuralfluid.
r Distinguishig this disease from hyaline membrane
disease is difficult. The distinctive
feature of transient tachyapnea
are -
: Mild symptomology
s Sudden recovery ofthe infant
: Absence of roentgenogralthic reticulogranular
pattern or air bronchogram(pcr e8).
Pulmonar), alveolar proteinosis
o Pulmonary alveolar proteinosis disorder characte rized by the intraarveolar
is a
accumulation ofpulmonary surfactant.
' ":7^:!::r*'n-B component or swractant, which results
in imparied spread and absorption ormajor
;H.ffi:Jfl?
r Thus there is functionar deficiency
of surfactant and.failure of expansion
c usually newborn is full term and may have positive
of arveori.
famiry histovrr*,*s,, 08.07).
r chiid usually present with respiratory distress immediately
after birth which does not respond to
08,07). surfactant(Arr*s 11.

o fhere may be ground-glass appearanceon


chest x-ray.
t Histopathological examination of lung biopsy
specimen is the gold standard for diagnosis.on histopathological
examination distal air spaces are filled with a granular, eosinophillic material that stains
schiff reagent and is diastase resistant- positiv ery withperiodic - acid

RESUSCIT4T|ON OF NEWBORN

r The goal of pediatric resuscitation is to


maintain adequate oxygenation and perfusion
of blood throughout the body
while steps are taken to stabirize the chird and
estabrish rong term hemostasis.
o The most common indication for neonatal
resuscitation is asphlxia. Second most
prematurity. common indication is extreme
r The components of neonatal resuscitation
are TABC _
t T - Maintenance of tempetAture@G107): By radient heat source,
and by drying the baby with removal
t A - Airway(Pcl,7) : Establishment of open airwayby placing of wet linen.
the neonate on his back with stight
extension of neck by
':::':"f.::shoulder 3/4 or 1 inch of the mattress with the help of rolled blanket o, to*J Suction of mourh and
s B - Initiate breathinglpcr07) : Tactile stimulationis
given and when necessary,bagand
ET tube can be used. mask ventilation is given or

t C - Maintain circulation@G|07) : This is done


by chest compression@Gr o7)and/or medications.
Resuscitation protocol
r As soon as the babyis delivered, five signs
are assessed _

1. Clearance of meconium
2. Active breathing or crying
3. Good muscle tone (flexed posture and active movement of baby).
4. Pink color (look at tougue and lips)
5. Term gestation (deliverybetween3T-42 weeks of pregnancy).
r Ifall signs are positive no active resuscitation is required.
r Ifany ofthe 5 signs is absent, baby requires resuscitation.
r The baby should be placed under the heat source (radiant warmer) and subjected to a set ofintervention known as

initial steps.

lnitial steps of resustitation


1. Positioning
r The neonate should be placed on her back or side with the neck slightly extended. This can be achieved by
putting a rolled blanket or towel under the shoulders, elevating them 3/t or 1 inch off the mattress.
2. Suctioning
r The mouth and nose should be suctioned. The mouth is suctioned first{Pcl
10)
to ensure that there is nothing for
the infant to aspirate when the nose is suctioned.
r One should not insert the catheter very deep in mouth or nose for suction -+ Stimulation of posterior pharynx
during the first few minutes after birth can produce a vagal responce, causing severe bradycardia or apnea.
r Therefore, during oral suctioning, a suction tube is gently introduced into the babys mouth until the 5 cla
10)
markGGI 10) is at the babyt lip. During nasal suctioning, a suction tube is introduced upto 3 cm mark@Gl into
each nostril.

3. Dry, stimulate and reposition


r After suctioning, the baby should be dried by using pre-warmed linen to prevent heat loss.
1 A brief tactile stimulation in the form of flicking the soles or rubbing the back may be provided in case of
non-establishment of good respiratory efforts(Are7).

4. Freeflowofoxygen
r Ifthe baby continues to be depressed, provide free flow of oxygen using a facemask.

o After providing initial steps, the baby should be evaluated for three signs -
1. Respiration
2. Heart rate (HR)
3. Color
r If baby has good breathing, HR >100 and pink color, he should be given supportive care.
o If the baby is not breathing well or HR <100 then bag and maskventilation is needed.
o After the infant has received 30 seconds of ventilation with 100% oxygen by bag and mask, evaluation of heart rate
should be done -
HR >100 -+ Discontinue ventilation if spontaneous respiration is presenl(ersz).

HR 60 to 100 -+ Continue ventilation


Below 60 -+ Continue ventilation + chest compressions
o After 30 seconds of chest compressions, the heart rate is checked.
HR < 60+ Continue chest compression and bag & mask ventilation + initiate medications.
HR > 60+ Discontinue chest compression but continue bag & mask ventilation until the heart rate is above 100'

Resuscitation in newborn through meconium stained liquor


r When baby passes meconium in utero, there is a chance that the mecomium will be aspirated into infant's mouth and
potentially into the trachea and lungs.
o Appropriate steps must be taken imrii'ed irtely after delivery to reduce the risk of serious consequences resulting from
aspiration of meconium.
t Intrapartuffi nasopharyngeal suctioning just afier the delivery of head is no longer recommended ss it does not
reduce the risk of meconium aspiration syndrome and, on rare occasions, may cause nasopharyngeal trauma or a
cariliac arrhythmia.
r The first step after delivery is to identify whether
the newborn is vigrous or non-vigrous :
A) Vigrous newborn
r A newborn is classified as vigrous, if he has all the three signs are present :
1) Strong respiratory effoyl\rrus os)
2) Good muscle lon"6rlMsoe)
3) Heart rate greater than 717GIIMI0e)
r The vigrous child does not require any tracheal suctioning
and the usual
initial steps of resuscitation are provided,
i'e'' provide warmith, positioning, suctioning of mouth and
nose (not tracheal suctioning), Dry, stimulate and
02 if necessary.
B) Non-vigrous newborn
: If any of the above three signs is present, the newborn is classified
as non_vigrous.
r For non-vigrous child, the initial steps are modified: _
r) Place the baby under racliant warmer and postpone
suctioning to prevent stimulation of posterior
pharyngeal wall that can cause bradycardia.
ii) Residual meconium in the mouth and posterior pharynx
should be removed by suctioning under direct
vision using a laryngoscope.
iil) The trachea
should then be intubated and mechonium suctionecl
from the lower airway. Tracheal
suctioning is best done by apprying suction directry to
the endotrachear tube.
I After providing initial steps, the further management is
same as with resucitation for other conditions-

a Forchildren,uncuffedandstroightblade(,4//M599]endotra.n;;l*b"
a
";rt* ;;;l,lli;on,o,
ofpremature
a l:::::"j:1,::l
birth l"j_,1"_1l.,l"sutation
In cases of asphyxia, corticosteroidsr,renotuseclhtos).
,,,,6,pcles,
warmed
vvqlrrreu rrtLuu..u'5'
incubators.
a Bagandmaskventilationiscontraindicatedin:Diophragmtatichernia(AtMsoa,ss),Tracheo-esophagealfistulorucscoz),and
meco nium aspi roti on sy n d rom e4il.vs 8s).
Important druqs used for neonatal resuscitation are epinephrine
(adrenaling){A/75,, normal saline or
naloxone/4i,5) and sodabicarbonate#i rir. ringer lactate,
Dose of adrenaline inneonatal resuscitation : 0.1
to 0.3 mg/kg diluted l n. :l o,oggurrr

APGAR Scoring
o APGAR Score is a quantitative method for assessing infants respiratory,
circulatory and neurological status

. Respiratory efforl

:l*i
o Color ofthe bodytAttMseT) (Ap-
pearance) Blue or pale Body pink extremities blue pink

Flaiiid
o Reflex stimulation (Grimace)
or putting catheter in nose No response GrimaCerrr,5l Cries, coughs or sneezes

r Scoring for APGAR Score


r Total score l0
r No depression 7-t0
r Mild depression 4-6
r Severe depression 0-3
o The test is generally done at one and
five minutes after birth, and may be repeated later if the score is and remains
low' Scores 3 and below are generally regarded as critically
lo w, 4 to 6fairly low, and 7 to 10 generally
normal.
o A low scote on the one-minute test may show that
the neonate requires medical attention (e.g. resuscitation@nMs 11))
x3 Newborn lnfant

The first step after delivery is to identify whether the newborn is


vigrous or non-vigrous : -
A) Vigrous newborn
r A newborn is classified as vigrous, ifhe has a[ the three signs are present: _

l) Strongrespiratory effortGIIMSoe)
2) Good muscle toneGIIMSos)
3) Heart rate greater than 700aIIMS0s)
r The vigrous child does not require any tracheal suctioning and the
initial steps of resuscitation are provided,
usual
i'e', provide warmith, positioning, suctioning of mouth and nose (not tracheal
suctioning), Dry, stimulate and
02 if necessary.

B) Non-vigrous newborn
r If any of the above three signs is present, the newborn is classified as non-vigrous.
: For non-vigrous child, the initial steps are modified: -
i) Place the baby under radiant warmer and postpone suctioning to prevent stimulation of posterior
pharyngeal wall that can cause bradycardia.
ii) Residual meconium in the mouth and posterior pharynx should be removed
by suctioning under direct
vision using a laryngoscope.
iil) The trachea should then be intubated and mechonium suctioned
from the lower airway. Tracheal
suctioning is best done by applying suction directly to the endotracheal
tube.
r After providing initial steps, the further management is same as with resucitation for other conditions.

a For chi ld ren, u n cuffed a nd stra ight blade^rMs ss) enclotr achea l tu be is used.
a lncubators used for thermal regulation of premature neonates are convectio
nut13.06,pctsa) warmed incubators.
a ln cases ofbirth asph;n<ia, corticosteroidsare not asedal0s).
f Bagandmaskveniilaiioniscontraindicatedi; riiopnrng^oticherniaulMsM,se),Trocheo-esophagealfistutatuescoz),and
mecon i u m aspi rotion sy n d rome(At tns 8st.
lmportant drugs used for neonataf resuscitation are epinephrine
{adrenaline)(,4r,5.r, normal saline or ringer lactate,
6616;qpgFr rs,r and sodabicaylgn31g(er ;s).
Dose of adrenaline inneonatal resuscitation : 0.1 to 0.3 mg/kg
diluted l :l o,ooo(Ntr).

APGAR Scoring
r APGAR Score is a quantitative method for assessing infants respiratory,
circulatory and neurological status :

. Respiratory
iii.;:#;*irefforttil"*ai j\rr,.r.;
None

;,,,*,,,,;4,;
Slow irregular
i:,=,'r1?itf.ii-,.1-'r...;1"
Good, crying
> 100
t Color ofthe boayroiisin lg;-
pearance) Blue or pale Body pink extremities blue Pink
.-,rt*:i:t:::.j -:rr*r::=i:.: a.: -.... ..
o ii.:::r.:1::::1-1

Mrislcle tone(Affi er, (A(tivity)


Some flexion .t
Aatival, moving extremity
r Reflex stimulation (Grimace)
or putting catheter in nose No response Grimacer'ari5., Cries, coughs or sneezes

Scoring for APGAR Score


r Total score 10
r No depression = 7-10
r Mild depretsion = 4-6
r Severe depression = 0-3
The test is generally done at one and
five minutes after birth, and may be repeated later if the score is and remains
low' Scores 3 and below are generally regarded as critically low, 4 to 6 fatlylow,
and 7 to l1generally normal.
A low score on the one-minute test may show that the neonate requires medical
attention (e.g. resuscitation(ArrMs11))
but is not necessarily an indication that there will be long-term problems, particularly if there is an improvement by
the stage of the five-minute test.

c lf the Apgar scote remains below 3 at later times such as 10, 15 or 30 mintues, there is a risk that the child will suffer
longer-term neurological damage. There is also a small but significant increase of the risk of cerebral palsy.

r However, the purpose of the Apgar test is to determine quickly whether a newborn needs immediate medical care; it
was not designed to make long-term predicitions on a child's healthallMs 11) .

Assessment of respiratory depression


c The severity of respiratory distress is assessed by Silverman- Anderson score and Downes' score.
r While the Silverman Anderson Retraction Score is more suited for preterms with HMD, the Downes' score is more
comprehensive and can be applied to any gestational age and condition.

Lort.thest .,,,
Xiphoid:retraction .,. Na!-l'flaring G'i*nt. ,:.
retra(tion.
Nong None None None
,:t :.:1 , Lag oqin$pirqliqh :': Jnii'tti.bte .r.:.,i. Just visible Minimal :Stetho5c0peonly
2 See- saw Marked Marked Marked Naked ear

e A score of >6 is indicative of impending respiratory failure

Nil
0 < 60/min Nil Normal None
' \.\
:',,. .:r';;;',,,11.,14
Au,sc with',,.'
:,,r.-1 ,,.1'l :60.80/m.in ',.[n'rgorn air :Mild:?::',: ,.
stethoslo:pe
Mild,. .1.: :,::.':.

Audible with
2 >80/ min ln >4Oo/o O, Marked? Moderate
naked ear

e A score of >6 is indicative of impending respiratory failure

NEONATAL HYPERBILIRUBINEMIA AND JAUNDICE


a Bilirubin is the end product of catabolism of hemoglobit 1 gm of hemoglobin yields 35 mg of bilirubin(NEEr).
a A bilirubin level of more than 5 mg/dl manifests as clinical jaundice or icterus in neonate (in adults jaundice occurs at
2-2.5 mg/dl).
As the bilirubin levels increase, jaundice involves more distal parts of body:-

Head & Neck 5 mg/dl


Lower trun k. &, thigh. ..,,
:',
:..10mgldl
Legs 15 mg/dl
PaIm {hands) & sole {fedt} 5 1,5 mgldr*/'sr
e Hyperbilirubinemia may be of two types : (i) Unconjugated; and (ii) Conjugated.

A) UnC,onjugated hyperbilirubinemia
* Conjugated hyperbilirubinemia is seen when -
1) lncreasedproductionofbilirubinfromhemoglobin,Sothatthecapacityoflivertoconjugatebilirubinisoverwhelmed
by increased production, e.g. -
t Hemotytic on"^iotn"''tto7t -+ Hereditory spherocytosis, G6PD deficiencyulittsaT).
o lneffective erythropoiesis - + Thalassemia, Pernicious anemia.
2) Reduced hepatic uptake of bilirubin from bilirubin - albumin complex + Drugs,
3) lmpaired hepatic conjugation, e.g.
i) -) Liver of a neonate is functionally immature (, UDPG transferase)
Physiologicol joundice4ilMs0T)
ii) Breastmilkiqundiceottusair-+ Pregananedial in breast milk interferes with bilirubin conjugation.
iii) Geneticdeficiencyof UDPGtransferase-+ Crigter-Nojjatsyndrome\'ls,NEETDNBl3,Pctosa6Aufsot),Gilbertsyndrome(At
I 3, NEEI DN| | 3, pct 0g. 06, AIIMS O I )

iv) Hepatocellular disease --+ Virol or drug induced hepatitistatBs),cirrhosis.


v) Hypothyroidism(At;t'l\ 07),
cepholohematomo
B) Conjugatedhyperbilirubinemia
r Conjugated hyperbilirubinemia is seen when -
i) lmpaired secretion of conjugated bilirubin into bile -+ Dubin-johnson syndrome(At 13, NEEI. DNB 13 PGtas M AilMs o1),
Rotor
Sffidrom2tAt : 1 Nrfi' DNB t3 PLt as 06' AttMS a4.

ii) lmpaired bile flow --> Obstructive jaundice(AttMsol), primary biliary cirrhosis, Neonotal cholestosis, e.g. Extrahepotic
biliaryatresia(At13)/neonateidiopathichepatitis,Choledocolgyst(PctM,sclerosingcholangitis, Carolidiseose,Metobolic
(Tyrosinemia, Wolman disease, Nieman pick disease, Galactosemia, Fructosemia).

Tirne of appearance of jaundice


Jaundice pres€nt at birth or within 24 hours of life
a Erythroblastosis fetalis (Rh incompatibility;wanr eGI 04' 02' AI es)
-) most common cause
r ABO incompatibility
r Concealed hemorrhage
r Congenital infections -+ Rubella, slphilis, CMV, toxoplasmosis
r Red cell enzyrne defects (G6PD deficiency)
r Red cell membrane defect (Hereditary spherocytosis)
. SePsis(At e5)

Jaundice appearing on 2nd or 3rd days of life


t Physiologicalqtes) r Crigler - Najjar syndrome
\ r Early onset breast milk jaundice

Jaundice appearing frorn 3rd to 7th days of life


r Bacterial sepsis r Urinary tract infection
r Other infections _> syphilis, CMY enterovirus, toxoplasmosis r Polyclthemia
Jaundice appearing after 1st rveek of life
r AII other causes ofjaundice.

Physiological jaundice
r Most neonates develop visible jaundice due to elevation of unconjugated bilirubin concentration during their
first week. This common condition is called physiological jaundice.
r This pattern of hyperbilirubinemia has been classified into two functionally distinct periods -
1. Phase one
r Last for 5 days in term infant with peak bilirubin levels to 12 mg/dl.
r Last for 7 days in preterm infrnt with peak bilirubin levels to 15 mg/dl.

2. Phase two
r 'Ihere is decline to about 2 mgldl, which iasts for 2 weeks after rvhich adult values are attained.
Criteria for physiological jaundke
. Clinicaljaundice appears after 24hours ofage'PCI03'.
'.'. Total bilirubin rises by less than Smg/dl per day (no sudden rise)@etos).
;llt Peak bilirubin occurs at i-5 days of age, with a total bilirubin of no more than 15 mg/dl
it t Clinical jaundice is resolyed by I weeks in term infants and 2 weeks in preterm infants(eet ost,

Breast milk jaundice


o There is strong association between exclusive breastfeeding and neonatal jaundice.
o ^\ fery babies who remain on exclusive breast feed develop jaundice rn the second week of life and continue well
into the thirdmonth. This is called breastmilkiaundice.
o -\ bilirubin level of over 20 mg/dl may be attained. (It is presumed to be due to inhibitory substances in the
breastmilk that interfere with bilirubin conjugation e.g. pregananediol and free fatty acids).
. Teffiporary interruption of breastmilk feeds will dramatically reduce the serum levels of bilirubin and there may
be slight increase in bilirubin when breast feeding is resumed, but it never reaches the previous levels.

ABO hernolytic disease


o ABO hemolytic incompatibiliry It causes unconjugated neonatal hlperbilirubinemia.
disease is less common then Rh
r It occurs it neonates havingblood group A or B with mother of blood group O. |aundice appears within 72-24hosrs
of life.
o Direct agglutination test (DAT) test is positive.
to)
o Reticulocy.tosis and the presence of microspherocytesunus on smear help to confirm the diagnosis.

Congenital hyperbilirubinemias
r Important congential hlperbilirubinemias are :-
1) IJnconjugatedhyperbilirubinemia (ilefective conjugation): Gilbert syndromeql 13'NEETDNa n'PGIoe'06'AIIM\01'%),
Crigler Najiar Synilrome (type I dt II)(u t:' Nrnr'
DNB ls' PGr 0e' 06' AIIMS 01' e3)
,

2) Conjugated hyperbilirubinemia z Rotor syndromeut


13' NEEI' DNB 13' PGr 0e' 06' AttMS 01' %)
, Dubin lohnson syndrome.

Gilbertsyndrome
e7) 13' NEEI' DNB 13' PGI
e Gilbert syndrome rs an autosomal dominantattMs congeflital unconjugated hyperbilirubinemiaat
09, 06, 02, 4ttMs 0 L 97, 93).

c Allhepaticbiochemicaltestsandliverhistologyarenormal\ttMseT),butinsomepatientsincreasedlipofuscinpigment
may occur.
ls' AttMS e7),
e There is mild increase in unconjugate bilirubin(/r thus kernicterus does not occur.
e Basic defects are: - \
l) Decreased hepatic uptake of bilirubin.
ii) Decreased activity of UDPG transferaseql
ls).

e Usually no treatment is requiredarrs).


e Phenobarbitone induces the enzyme UDPG transferase; thus it can reduces the level of unconjugated bilirubin by
increasing its conjugation. Hemolysis may also occur.
e The disposition of most xenobiotics metabolizedby glucronidation appears to be normal exceptfor antitumor
0')
drug irinotecan. Thts, irinotecan toxicity can occur@G' .
o There is no association with cirrhosis\I 13).

Criggler-Najjar Syndrome (CN)


o CNsyndromeisacongenitalunconjugatedhyperbilirubinemia(Al)3'DNBI3'NEEI).Basicdefectiseitherreducedorabsent
UDPG transferase.
r There are two types of CN syndrome :-
L) Typel
r It is an autosomal recessiye disorder in which UDPG transferase is absent. Thus phenobarbitone has no effect
(as enzlT ne is absent).
s It is more severehyperbilirubinemia than type II. There may be kernicterus.
Criteria for physiological jaundice
i) Clinicaljaundice appears after 24hours ofage@Glos).

ii) Total bilirubin rises by less than Smg/dl per day (no sudden rise)(ecr 03)
.

ili) Peak bilirubin occurs at i-5 days of age, with a total bilirubin of no more than 15 mg/dl
iv) Clinical jaundice is resolved by 1 weeks in term infants and 2 weeks in preterm infants@ct ost
.

Breast milkiaundice
o There is strong association between exclusive breastfeeding and neonatal jaundice.
o A few babies who remain on exclusive breast feed develop jaundice in the seconil week of life and continue well
into the third month. This is called breastmilkiaundice.
o A bilirubin level of over 20 mg/dl may be attained. (It is presumed to be due to inhibitory substances in the
breastmilk that interfere with bilirubin conjugation e.g. pregananediol and free fatty acids).
o Temporary interruption of breastmilk feeds will ilramatically reduce the serum levels of bilirubin and there may
be slight increase in bilirubin when breast feeding is resumed, but it never reaches the previous levels.

ABO hemolytic disease


r ABO hemolltic disease is less common then Rh incompatibility. It causes unconjugated neonatal hyperbilirubinemia.
r Itoccurs inneonateshavingbloodgroupAorBwithmotherofbloodgroup O. |aundice appearswithin l2-24hotrs
of life.
e Direct agglutination test (DAT) test is positive.
to)
o Reticulocltosis and the presence of microspherocytesGltus on smear help to confirm the diagnosis.

Congenital hyperbilirubinemias
o Important congential hyperbilirubinemias are :-
l) (Jnconjugated hyperbilirubinemia (defective conjugation) t Gilbert syndrome6"i'NEEI'DNB 13'PGt0e'06'AilMS01'e3),
ts' Nnnr' DNB 13' PGI 0e' 06' AIIMI 0t' e3)
Crigler Najiar Syndrome (type I dt IISGT .

2) Conjugated hyperbilirubinemia : Rotor syndrotneat 13' NEEr' DNB 13' PGt 0e' 06' AIIMS 01' e3)
, Dubin f ohnson syndrome-

Gilhert syndrome
e7) 13' NEET' DNB 13' PGI
e Gilbert syndrome is atr autosomal dominan{or/Ms congenital unconjugated lryperbilirubinemiaAl
09,06,02, ArlMS 01,97,93)
.

e Allhepaticbiochemicaltestsandliverhistologyarenor*o1{utusez),butinsomepatientsincreasedlipofuscinpigment
may occur.
1s' ArrMseT),
o There is mild increase in unconjugate bilirubin(Ar thus kernicterus does not occur.
t Basic defects are: -
l) Decreased hepatic uptake of bilirubin.
ii) Decreased activity of UDPG transferaseql
ts).

r Usually no treatment is required'Als).


e Phenobarbitone induces the enzl,rne UDPG transferase; thus it can reduces the level of unconjugated bilirubin by
increasing its conjugation. Hemolysis may also occur.
e The disposition of most xenobiotics metabolizedby glucronidation appears to be normal exceptfor antitumor
drug irinotecan. Thus, irinotecan toxicity can occur@G'0') .
e there is no association with cirrhosis^I 13).

€ri ggler-ftlajjar Syndrome (CN)


DNB 13' NEET).
e CN syndrome is a congenital unconjugated hyperbilirubinemiaarr3' Basic defect is either reduced or absent
UDPG transferase. I
o There are two tlpes of CN syndrome :-
A) Typel
r It is an autosomal recessive disorder in which UDPG transferase is absent. Thus phenobarbitone has no effect
(as enzyme is absent).
s lt is more severehlryerbilirubinemia than tlpe mav be kernicterus.
Cnaprrn 3 llewbornlnfant ,: " .':,

I LFTs and liver histology are normal,Pcl02).


B) TypeII
r It is an autosomal dominantQcleT) disorder in which
UDPG transferase is ysflusgrrnersz;.
t Phenobarbitone can reduce unconjugated bilirubinrpprsT)
by inducing uDpG transferase.
r LFTs and liver histology are normal?Gl02) and. there
is no kernicterus@Gre7).
Dubin Jhonson syndrome (DJS)
o DfSisatypeofcongenitalconjugatedhyperbiliruginsnxirrer13,NLLI',ArrMs07).
o It is autosomal recessive.
r coniugated bilirubin is increased because of defective biliary excretion of
bilirubin glucuronides due to mutation in
canalicular multidrug resistance protein 2 (MRP 2). Liver function
tests are normal
o A cardinal feature of DIS is the accumuiation in
the lysosome of centrilobular hepatocltes of dark, coarsely
granular pigment' As a result, the liver is black in appearance.
This pigment is thought to be derived from epinephrine
metabolites that are not excreted normally.
o There is increased urinary excretion ofcoproporphyrine (normal
I coproporphyrine III is more excreted), but total
coproporphyrine level is normal.
o Gall bladder is not visualized on oral cholecystography.
After iv administration, there is reflux of conju gated.sulfubro-
mophthalein (Bromsulphalein, BSp) from liver to circulation.

Rotor syndrome
o Rotor syndrome is a type of congenital conjugated hyperbilirubinemiaut n, NEEI, AnMs 07).

o It is autosomal recessiye.
r It is due to decreasedbiliary excretion ofconjugatedbilirubinand
also due to decrease hepatic uptake & storage of
bilirubin.
o Differentiating features of rotor syndrome (from DIS) -
i) Liver is not pigmented and liver histology is normal(pcr02).
ii) coproporphlrine I is increased in urine but total coproporphyrine level
is also increased.
iii) Gall bladder is visualized
iv) There is no reflux ofconjugated BSp.
Kernicterus
r Kernicterus or bilirubin encephalopathy, is a condition caused
by bilirubin toxicity to the basal ganglion(Aree) and
various brainstem nuclei.
e It is mainly caused by unconjugated bilirubinal 12) as unconjugated bilirubin
can cross blood brain barrier.
Unconjugated bilirubin level of more than 20 mgl dltl't tst increases
the risk of kernicterus.
o Clinicaily, kernicterus is described in 3 phases, which may
progress over 24 hours to 7 days :-
l. Phase I -s poor suck, lethargy, hypotonia{o, ,i), depressed sensorium.
2. Phase II -) Fever, hypertonia progressing to opisthotonus(,Arrs).
3. Phase III -+ High pitched cry, conulsions, death.
o Long term survivors demonstrate choreoathetoid cerebral
palsyLl 13),
upward gaze palsyar 13),
sensorineural
hearing lo ss( AI 3) andmental retariation.
1

o The toxic effects ofunconjugated bilirubin (and therefor


e chances ofkernicterus) are increased by:-
1) Hypoproteinemia (t albwminl{,'ost -+ Normally unconjugated bilirubin binds to albumin
in circulation. If the
Ievel of albumin decreases, concentration of free unconjugated
bilirubin will increase.
2) Drugs (sulfunamides)Gt ut .

3) Acidosis, 4r ,o','"""-"o' l
4) Increased FFA (secondary to hypoglycemia, Oisllace bilirubin from its binding
starvation or hypothermia)Gr t'tt /I site on albumin
5) Asphyxiqal ta)
6) Hyperosmolarity\tt4 )t
Make neurones more susceptible lo
7) Prematurity{At u) I
toxic effec1 ofunconjugate bilirubin
8) Infection J
IREATM ENT OF HYPERBILIRUBINEMIA

. Treatment options of hyperbilirubinemia are :-

A) Drugs (Pharmacological therapy)


r Drugs used for hlperbilirubinemia are :-
1) Barbiturates?Gt06'02) (Phenobarbitone):Indtce UDPG transferase and enhance conjugation of bilirubin.
2) Metalloporphyrins (Tin : Sn and Zinc : Zn) ': Decrease bilirubin formation by inhibiting heme oxygenase.
3) Miscellaneous: Frequent milkfeeding charcol and agar prevent reabsorption of bilirubin from gut.
B) Phototherapy
o Phototherapy has emerged as the most widely used form of treatment for unconiugated hwerbilirubinemia.
c Phototherapy converts unconjugated bilirubin into isomers that are able to bypass the conjugating system of
liver and are excreted in the bile or urine.
o Three types of photochemical reactions occtr; in decreasing order of importance :-
1 . Structural isomerization@IlMs 0s)
r Bilirubin is converted into lumirubin, which is excreted in the bile and urine.
2. Photoisomerization
r Less toxic, polar isomers are formed which are excreted in bile. But, the photoisomer can revert back to
unconjugated bilirubin and get reabsorbed from the gut ifthe baby is not having stools.
3. Photo-oxidation
r It converts bilirubin into small polar products that are excreted in urine.
t "The most effective lights for phototherapy are those with high energy output near the maximum absorption
peak of bilirubin (450 to 460 nm). Special blue lamps with a peak output of 425 to 475 nm are the most eficient
for phototherapy."
r Complications of phototherapy are :-
1) Bronze baby syndrome@Gle8). 4) Purpuric rabh with transient porphyrinemia.
2) Loose stool. 5) lncrease environmental and body temperatureql es).

3) Retinal damage(retss). 6) Erythematous macular rash.


C) Exchange transfusion
o Exchange transfusion is indicated when bilirubin level is high and chances of brain damage are significant.

lndications to start phototherapy and exchange transfusion


1) Accordingto gestational age
o It is usually used for premature newborn.

11-14

30-31 8-1 0 t 3-'t6

34 12-14 17-19

2) According to gestational weight (at birth)


o It is used when age is not available.
1 00i-1 500 g 7-10

2001-2so0 g
10-12

3) According to age after birth


o It is used for full term (mature) neonates

,F.hii,fe&rii1y.
24 - 48hrs >15 >20
48,-72hrs:,. ,)18 >25
> 72 hrs{AEMs ee)
> 20@aM3se)
>25

NEONATAT HYPOGLYCEMIA

o Hlpoglycemia in a neonate is defined as blood sugar less


than < 40 mg/dl{cutofiot;.
o According to serum level h}polycemia is
defined as serum glucose level < 35 mg/dl between
1-3 hours of life; < a0
mg/dl between 3-24 hours of life antt < 45 mg/cll
thereafter. After neoratal period (especialy
afier 2 months@NB t2))
hypoglycemia is defined as serum glucose < 54 mg/dl{oNn u;.
t is the most common metabolic problem in
newborns. Important causes of neonatal hypoglycemia
]ruoslrcemia
A) Due to inadequate substrate enzyme
function : prematurity(euusoz),small for gestational age (SGA), smaller of
twrns, respiratory distress syndromeallMs 021 and infant
of toxeinic mother.
B) Due to hyperinsulinism : Infant of diabetic motherLllMso')
(large for dateurrMse2)),erythroblastosis
fetalis (Rft
incompatibilityqnus szt',, and perinatal asphyxis(.arus oz, sz))
.

Treatment of neonatal hypoglycemia


1) Asymptomatic with blood glucose between 2O_40 mg/dl
r Direct breast feeding is started' If neonate is unable
to suck, expressed breast milk is given. Expressed
milk should be fortified by 59 sugar per 100 ml of milk. breast

2) Symptomatic or asymptomatic with blood glucose


< 20 mg/dl
r Bolus l0% dextroseul l'))
2 mllkgis given IV Followed by continuous infusion
of 6 mg/kg/minute. If normogly,
cemia is not achieved within 24 hours, glucocorticoids
(prednisone or hydrocortisone) should
be administered.
For intractable hlpogrycemia, glucqgon, epinephrine
or diazoxide can be given.
r In hypoglycemic seizures, dose of l}o/odextrose is
4 ml/ftgrarrst

Dertrose in concentration > l2.So/o is never used


through peripheral linestiElt) as il
can cause thrombophresnis. centrar Iine is
prererre d for > r2.50/odextrose.

I
n;;;;';;i,*;*i
Neonate of diabetic rnother
r Neonates of diabetic mother have following probiems :-
1) Hyp o gly cemi aGI
t[s 06' I'Gr 07 ) (non-ketotic) (ArrMs e8' Ar e5r.
6) Polyclthemia.

2) Macrosomia(vcto:) (large for date6"Mser) )' 7) Transienttachypneaofnewborn.

3) Hyperbilirubinemia\iltts06'PGt07)' 8) CardiomegalY.

4) HYPocalcemiaGIIMS06'|'jGI07)' 9) Asymmetric septal hypertrophy.

5) HyPomagnesemia. 10) Increased risk of RDS'


07 )
r Neonates of diabetic mother are at increased risk for fetal malformatiofl(Pct
!: i:!:: :::::nl:;: li;::+::J+:,:r i+i:.:i : jiai.

:*E-.i.ri:
Cardiac malformations
c Ventricular or atrial septal defect
a Double-outlet right ventricle
o TransPosition of great vessels
* Coarctation ofthe Aorta.
c Truncus arteriosus
Congenital anomolies other than <ardiovascular system
* Neurat tubl fl2fg6l5tearazt
o Situs inversus
e HydronePhrosis
c Double ureter
s Renal agenesis and.DYsPlasia
r HoloprosencePhalY

a Caudal r,egressian syndrame {specifico'a6)}


rr'ArrMs0e)) and
(most common cause@I
Two most common causes of seizures in these neonates are hypogtycemia
t1' AtIMs0e))'
hypocalcemia (2d most common causeal
DMtAltuses.
A"s) in futrtre.
o These infants are at increased risk ofdeveloping obesity(tttuset'A1e5r and

MISCELLANEOUS

Ferinatal asPhYxia
(hlpoxia) and/or a lack of perfusion
o perinatal asphlxia is an insult to the fetus or newborn due to lack of oxygen
(ischemia). Effects of perinatal asphyxia are :-
l) CNS : Hlpoxic ischmeic encephaiopathy, infarction, cerbral edema, seizures\"Mso'), hypotonia ot hypertonia
(generalized, involving all muscles simultaneouslyallMs03)), altereil sensorium(^"Mso')'
2) CVS : Myocardial ischemia, tricuspid insufficiency' hypotension'
3) Pulmonary : Pulmonary hypertension, pulmonary hemorrhage' RDS'
4) Renal: Acute tubular or cortical necrosis '
5) Adrenal : Adrenal hemorrhage'
6) Metabolic: SIADH, Hyponatremia, Hypoglycemia, Hypocalcemia, Myoglobinuria'
7) Integument : Subcutaneous fat necrosis'
8) HematologY: DIC.
g) Gastrointestinal : Perforation, ulceration with hemorrhage, Necrosis.
CneprsR. 3 Hewbornlnfant. .-..r. 1,,. .,,,.. ;: .. '

Hypoxic ischemic encephalopathy


e Encephalopathy progress over time _
1) Birth to 12 hours -) Decreased level of conciousness, poor tone,
decreased spontaneous movement, periodic
breathing or apnea, seizuresarlMs 10).
2) 12-24 hours -) More seizuers, Apneic spells, jitteriness, weakness.
3) --) Hvpotonia, J conciousness' poor feeding, brainstem
signs (oculomotor) and pupiuary
{:r:r::^:::rs
o Hypotonia is generalized, involves both limbs
and trunk and all muscles simultaneou
sly,trusto).
Causes of respiratory depression in neonates
r Intrapartum asphixia (most common cause).
c Drugs :- Norcotic analgesics (morphine or other opioids(ArrMs10.Aro7)), anaesthetics.
o Sepsis
o Prematurity:- CNS immaturity, surfactant deficiency.
r Respiratory problems :- Diaphragmatic hernia, obstructive lesions.
r CNS abnormalities :- Malformation, trauma.
r Muscle disorders :- Myopathy, prematurity.
Erythroblastosis fetalis
r Erlthroblastosis fetalis is caused by the transplacental passage
of maternal antibody active against paternal RBC
antigens ofthe infant and is characterizedby an increased
rate ofRBC destruction.
o Although more than 60 different RBC antigens
are capable of eliciting an antibody response,
significant disease is
associated primarily D antigen of Rh group{AIIMSeT)
andwith ABo incompatibil ilyL+ilusez).
r Other rare antigens involved are _
z C or E antigen of Rh grosp{.,,nusszt
r RBC antigens - Cw, Cx, Cu, K (kell), M, Duffy, S, p, MNS, Xg, Lutheran,
Diego and Kidd.
r Anti_Lewis antibodies do not cause diseaseUrrMseT).

Hydrops fetalis
r Hydrops fetalis (fetal hydrops) is a serious fetal condition
characterized by abnormal accumulation of
more fetal compartments, including ascites, pleural effusion,
fluid in 2 or
pericardial effusion and skin edema.
o Important causes of hydrops are :_
1) Immune: Rh incompatability.
2) Non-immune: Twin-Twin transfusion, chorangioma ofplacenta, congenitalheartblockrcone(t0e),
0e)' cystichygroln4@omert
mediastinal teratoma, congenital infections (TORCH)
and. congenital ,ephrosi5ao-"aos).
Microcephaly
e Microcephaly is defined as a head circumference (occipitofrontal
circumference) that meastnes more than three
standard deviation below the meAn@NB 12) for age and sex.
r Important causes of microcephaly are :_
A) Primary (genetic)
i) Isolated: Autosomal recessive, autosomar dominant,
x-rinkbd.
ii) syndrome: Down syndrome (trisomy 21), Edward
syndrome (trisomy lg), patau syndrome (trisomy
cri-du-chat syndrome.
l3),

B) Secondary
i) Structurar defects: Neurar tube defects (anencephary,
encephalocele).
ii) Metabolic disorders: RhenylketonuriaarMse4),citrullinemia,
methylmalonic aciduria.
iii) congenital infections i RubeilqLrrMss4), cMy,HS{ toxoplasmosis, syphiris, varicelra.
iv) Teratogens: Alcohol, tobacco, cocaine, heroin.
v) others: Maternal diabetes, maternal phenylketonuria,
hypothy,oidism, hlpopituitrism, adrenal insufficiency.
C ria p t,g R :,s.:' N€nt.Or

Congenital infections causing microcephaly with intracerebral calcification


o Following congenitai infections can cause microcephaly, intracerebral calcification and hydrocephalus :

(i) Commonlyby toxoplasmosis and CMV and (ii) Less commoniy by HSV and rubella.

Hydrocephalus ++ ++ +/- (Rare)

Micibcephaly,. ':'. ++r.'l +++ r:+i

lntracranial ++ +++ +\-


edeifeatioh.. {C6rnmon) {eomman)',..:.,'(Unc0mmon} : (Rare)

o Hydrocephalus with intracerebral calcificationin a neonate with history of 'spiramycin' treatment of mother in
pregnancy suggest the diagnosis of congenital toxoplasmosis(AlrMs 11' At 0e) .

Diagnosis in the figure below is:

a) Macrocaphaly
b) Microcephaly
c) Dolchocaphaly
d) Plagiocephaly

Ans. is'H i.e., Microcephatry


r Head circumference in the given figure is 13- l4 cm (normal overage head circumference at birth is about
35 cm) + Diagnosis is microcephaly.
Hidrocephalus is the most important cause. Macrocephaly is associated with frontal bossing dolicocephalic
r shape, narrowing of biparetal diamete and a square shaped face.

Macrocephaly
o Macrocephaly is defined as an occitrtito frontal circumference greater than two standard (SD) above the mean@I
is) for age and sex (Note : Microcephaly is three standard deviation below the mean).
r Important causes are :-
l) Syndromes : Fragile-X syndrome, and neurocutaneous syndromes (Neurofibromatosis), tuberous scierosis, Sturge-
Weber.
ii) Increased CSF : Hydrocephalus, choroid plexus papillom6l{Atss).
111) Bone disease: Achondropiasia, osteogenesis imperfecta, osteopetrosis.
iv) Others: AV malformation, intracranial hemorrhage (subdural, epidural, subarachnoid), Thalassemia major,
, hlpervitaminosis-A, lead poisoning, pseudotumor cerebri, galactosemia, Canavan's leukodystrophy(AflMs08).

The diagnosis in the given figure isr

a) Microcephaly
b) Macrocephaly
c) Plagiocephaly
d) Dolichocephaly

Ans, is'H i"e., Maerocephaly


r The figure in question is showing large head with frontal bossing and square shaped face + features of
macrocephaly.

Fetalalcohol syndrome \
r High level of alcohol ingestion in pregnancy can cause damage to fetus, known a s fetal alcohol syndrome. The harmful
effects may be due to alcohol itself or due to one of its breakdown products.
r Some evidence suggests that alcclhol may impair placental transfer of essential amino acids and zinc, both necessary
for protein synthesis, which may account for IUGR.
r Characterististics of fetal alcohol syndrome include : -
1) I(JGRarIMsoe) 5) Facial abnormalities
Cnaptrn' 3''Newborn Infant
2) MicrocePhalyGrrMsoe) 6) Minor joint anomalies
3) Congenital heart defects (ASD, V51l/utus ont
7) Hlperkinetic movements
4) MentalretardationattMsoe)

l"larNeqr.rin eoNon chanEe


o This rare but dramatic vascular evenf occurs in immediate newborn period and is most common in low birth weight
infants. If reJlects an imbalance in the autonomic yascular regulatory mssl,rsni5fll1il,netss).
o When the infant is placed on the side, the body is bisected longitudinally into pale upper half and a deep red dependent
half.

Note: Ihe fefus in ichthyosis appears grostesque and the appearance is called horleguin fefus. But, it is different from Harlequin color change.

Cephalohennatoma
o Cepholhematoma is a subperiosteal hemorrhage usually involving parietal and temporal bones. It appears within
12-24 hours. It is more common in forceps delivery, vaccum extraction and prolonged labor. It is soft and fluctuant
swelling with well defined margins.
o A cepholhematoma crossing the midline indicates underlying fracture of the skuli -+
fracture is linear not clepressed.
a It disappears between 2 week to 3 months(uPsceT).

The diagnosis in the given figure is:

a) Macrocephaly
b) Microcephaly
c) Cephalohematoma
d) None rr

Ans. is ?' i.e., Cephalolleruatorna


o Swelling not crossing suture line with distinct margins suggests the diagnosis of cephalohematoma.

& Neonatal period extends upto : First 28 days of life.

murmur.
o Not a finding in a normal newborn : Central cyanosis (there is peripheral cyanosis).

* Treotmmt'ofvaginal bleedinqina4daysoldneoncte:Notreatment(it.isminorclinical'problembetween3-Tneonatal daysl


* Common sites of mongolian spots: Presacral area (lower back & buttocks), legs, shoulder, posterior thighs.
a, Tteatment of hymen tog in'a neondfe: No treatment (it is a normal finding), .

s Newborn babies are able to breath and suck at the same time because of : High position of larynx.
x Reflexes pre*enf qf &rth :rRootinglsucking/swallowing reflexes, crossed extensor, moro! reflex, Assymelrlc tonic neckrefiex, graspreflex.
a Reflexes appear after birth: Symmetric tonic neck reflex, parachute reflex, landau reflex.
x' Parachute reflex disappsars af : Never iit remains throughout:life). . ,

* Persistence of moro's reflex is abnormal beyond the age of :6 month (morot reflex disappears at 6 months).
*',Refle*wltichfieve.r.recppears:Morosreflex .' , , ', ' .,

& Persistence of moro's reflex beyond 6 months indicates: Dysfunction of CNS (e.g. brain damage).
* unilatera! morob re{lex is seen in Erb's patly {Cu-Cu damage}, spastic hemiplegia,tracture of humerus or'clavicle, shoulderdislocation.
r

* Not a mechanism of heat production in a neonote:shivering (neonates respond bytnon-shivering thermogenesis).


*.Smal|fardotebobyis:Birthweightlessthan10thpercentile'..
a Low birth weight baby :Birth weight < Z-.1=OO Om irrespective of gestational age at birth.
& txtremely law birth weighitbcby: Birth wEigftt <t OOOgm (< 1kg) irrespective of gestational age at birth. l

e Not a cause of IUGR: Maternal diabetes.


6 Treatmentfor birth asphyxia includes:Glucose, calcium gluconate, normal saline, oxygen, anticonvulsants (but-not corticosteroids).
& Bag and maskventilation is contraindicated in: Diaphragmatic hernia,TE fistula, meconium aspiration syndrome
@ Dose of adrenaline in neonatal resuscitation:0.1-0.3mg/kg diluted 1:10,000.
w APGAR score components are: Respiratory effort, heart rate, color of the body, muscle tone, reflex stimulation (grimace).
b Not a component of APGAR score : Respiratory rate
Cur prrn 3 Newborn lnfant

& One gram of hemoglobin liberates: 35 mg of bilirubin.


& lmportant congenital causes of conjugated hyperbilirubinemia: Rotor syndrome, Dubin-lohnson
syndrome.
& lmpartant cangenitol causes of unconjugated hyperbitiribinemia:Crigler-Najjar syndrome,
Rotor syndrome. :

& Jaundice appearing within 24 hours of birth: Erythroblastosis fetalis (most common cause), infections, G6pD deficiency, hereditary
spherocytosis.
& PeripheralsmeqrofneonatewithABahemolyticdiseaseshows:Microspherocyte5.
& Drug which inqeases the risk of kernicterus in a child with hyperbitirubinemia : Sulfonamide.
* Not a late feature of kernicterus: Hypotonia (it is an early feature).
@ lmportant late features of kernikterus: Choreoathetosis, sensorineural deafness, upward gaze palsy,
mental retardation.
& Kernicterus is due to:High unconjugated bilirubin (not conjugated bilirubin).
@ Drugs used in treatment of hyperbilirubinemia/kernicterus: Barbiturates, metalloporphyrins (tin, zinc).
* Mechonism mainly resposnsible for reduction of bilirubin by phototherapy:5tructural isomerization.
@ Bronz-baby syndrome is due to: Phototherapy
* A child with hyperbilirubinemia, parameters measured should be:Total bilirubin and direct (conjugated) bilirubin.
& Not a cause of neonatal hypoglycemia: post-terminfant
@ lmportant causes of neonatal hypoglycemia: Prematurity,
RDS, maternal diabetes, asphp<ia, erythroblastosis (Rh incompatibility).
& Symptomatic neonatal hypoglycema should be managed by: IOyo dextrose.
& lmportant complications of neonate of diabetic mother: Hyperbilirubinemia, hypocalcemia, hypomagnesemia, polycythemia,
HMD,
TTN, CHD.
@ Not a complication of neonate of diabetic mother:Hyperglycamia (there is hypoglycemia).
@ Most specific fetal malformation in neonate of diabetic mother:Caudal regression syndrome.
& Type of hypoglycemia in neonate of diabetic mother: Nonketotic hypoglycemia.
& Most common cause of seizures in neonates of diabetic mother : Hypog lycemia (most common) followed by hypocalcemia.
& Maximum concentration of dextrose that can be given to neonate through periphera! lines:12.5o/o.
& Neonatal hyperglycemia is defined as: Blood glucose > 1 25mg/dl orlplasma glucose > 1 5gmg/dl.
& Neonatal hypogtycemia is defined as:Blood glocose < 4omgld l; or seru m g lucose < 35 mgldl between -3
1 hou rs of life, serum glucose
< 40 mg/dl between 3-24 hours of life, serum g*ucose < 45 mg/dl after 24 hours of life.
& Hypogtycemia in infant> 2 month o/d: Serum glucose < 54 mg/dl.
& Resolution of physiological umbilical hernia occurs at:1Oth week of gestation.
& lmportant drug causing neonatal respiratory depression: Opioids (morphine).
& Tests used to differentiate maternal from fetal btood : Alkali denaturation {Apt. test), and acid denaturation (kleihouer
betke) test.
& Causesofvomitinganfirstdayoflife:Aerophagy;esophagealatresia,faultyfeedingtechnique, amnioticfluidgastritts.
@ Best way to monitor neanate's breathing and apnea in incubator for preterm nonventilated baby : lmpedence technique.
a lnflation pressure required for first'inflation in a neonate : 25-40 cm H for > 1 .5 seconds.
,o
Organs palpable in a normal neonate: Liver, kidney and spleen.
& Common rashes in a newborn: Erythema toxicum (most common), acne neonatorum, transient pustular melanosis.
& M.C cause of respiratory distress in preterm neonate: Hyaline membrane disease.
& MC cause of respiratory distress in term or post-term neonate: Meconium aspiration syndrome.
& Heart rate in a normal neonate: l ZO-l40 per minute.
I Respiratory rate in a normal neonate:35-4ber miiute.
& Best method for transport of newborn with maintainance of temperature: Kangaroo Mother Care (KMC).

xxx
QUESTIONS

NORMAL NEWBORN a) 3 months b) 6 months


c) 9 months d) Never
Neonatal period extends upto- (NEET Dec.12 Pattern) 12. Child of 9 months, which reflex is most abnormal -
a) 21 days oflife b) 30 days of life (PGI lune 98)
c) 28 days oflife d) 35 days oflife a) Asymmetric neck reflex
Normal finding in a newborn - (All India Dec.1j Pattern) b) Parachute reflex
a) Length 30 cm c) Righting reflex
b) Peripheral cyanosis d) None
c) Central cyanosis 13. A baby on examination shows unilateral moro's
d) Extension ofbody reflex with positive palmar grasp reflex. The site of
3. Meeonium can passed upto ----- days in healthy lesion is - (AIIMS Nov 99)
bady- (Atl India DeclS Pattern) a) Cr- Cn b) C-C
a)l b)3 c) Cr- T, d) C,- C,
c) s d)7 L4. Atypical moro's reflex is seen in A/E - (PGI Dec e7)

The apropriate approach to a neonate presenting a) # clavicle


with vaginal bleeding on day 4 of life is - b) Sternomastoid tumor
(CET Aug.12 Pattern, Al 05) c) Shoulderdislocation
a) Administration of vitamin K d) Brachial plexus injury
b) Investigation for bleeding disorderl2 15. Persistence of Moro's reflex is abnormal beyond the
c) No specific therapy age af - (All lndia Dec. 15 Pattern)
d) Administration of i0 ml/kg of fresh frozen plasma a) 3rd month b) 4th month
over 4 hours c) 5th month d) 6th month
5. Common sites for mongolian spot are- (PGI Nov 15) 16. Reflex which never reappears is - (PGl lune 98)
a) Face b) Neck a) Moro's b) Grasp
c) Lumbosacral'area d) Leg c) Snout d) Glabellar
e) Thigh
6. A hymenal tag in a newborn is best treated by - HYPOTHERMIA
(All lndia Dec.14 Pattern)
a) Steroids b) Surgery 17. All the following can occur in a neonate for heat
c) Leaving it alone d) None ofthe above production except - (AIIMS Nov 11, Nov 06)

7. New born babies are able to breathe and suck at the a) Shivering
same time due to - (AIIMS Nov 10) b) Breakdown of brownfat with adrenaline secretion
a) Wide short tongue b) Short soft palate c) Universal flexion like a fetus
c) High larynx d) Short pharynx d) Cutaneous vasoconstriction
18. Following features may be seen in cold injury of
PRIMITIVE RELFEXES neonates except - (Ar ee)
a) Bradycardia
8. Which of the following reflexes is not present at b) Uncontrolled shivering
birth- (AilMS May 07, At 07) c) Scleroma
a) Asymmetric Tonic Neck Reflex d) Metabolic acidosis
b) Morot Reflex
c) Symmetric tonic neck reflex LOW BIRTH WEIGHT
d) Crossed extensor reflex
9. Swallowing breathing reflex - not seen in fetus for - 19. Small for date baby is - (All India Dec. 11 Pattern)
(All lndia Dec15 Pattern) a) < 10 percentile for the gestational age
a) 14 weeks b) < 50 percentile for gestational age
b) 12 weeks c) < 2000 gm
c) 16 weeks d) < 2500 gm
d) Appear in all above period '
20" Extremely low birth weight baby-
10. Persistant Moro's reflex at 6-7 months indicates - t' (All India Dec.lj Pattern)
(PGI 02, DPG oe) a) < 2.5 kg b) <2kg
a) Normal child b) Brain damage c) < 1.5 kg d) <lkg
c) Hungry child d) Irritable child ,1 IUGR is caused by all except - (NEET Dec.12 Pattern)

1I. Parachute reflex disappear at- (All lndia Dec.13 Pattern) a) Diabetes b) Alcohol
.r;.,;. .,t ::.:
''
:iii{dit
smokrng
c) Smoking
cJ d)
Chronic renal failure c) 36
22. d) 72
For a term small for date baby, true is _ (ArrMS May 9s)
31. Most commoa cause of sepsis in Indiawithin 2
a) No nipple nodule
b) No palmar/plantar crease
months- (AIIMS Nov 09)
a) H influenza
c) Weight less than lOth percentile b) E.coli
d) Hperbilirubinemia
c) Coaguiase positive staph aureus
23. All of the fr:Ilnwing are features of prernaturity in a d) Group B streptococcus
neonate, except - (All India Dec. 15 Pattern) 32.
A 7 day old iafant develops syrnptoms of neoaatal
a) No creases on sole
septicemia. Most likely cause is _ (Ar
b) Abundantlanugo s8)
a) Local nursery environment
c) Thick ear cartilage
d) Empty scrotum
b) Infection through umblical cord
c) Exclusivelybreast fed baby
24. A premature infant is more likelythan a full term d) Infection by GIT bacteria
infant to - (AilMS 80, pG Bs) JJ. Most corn:aon caus€ of Ne{rnatal sepsis in hospital
a) Suffer fromjaundice ofhepatic origin
in India is ^
b) Maintain in normal body temperature in a cold @rrMS May 07)
environment
a) Escherichia coli

c) Excrete urine with a uniform specific gravity b) Klebsiella

d) Suffer from anaemia


c) Staph aureus
d) Listeria monoc)togen
25. Full 1erm, Srnsll for Date Babies are at high risk of_
34. In neonate with meningitis, grarn positiye cocci,
(Ar 2000)
CAMP test positive most comm{rn source of
a) Hypoglycemia
infection is -
b) Intraventricularhaemorrhage (All India Decl5 Pattern)

c) Bronchopulomonarydysplasia a) Genital tract


d) Hyperthermia b) Respiratorytract
c) Hematogenous
25. True staternent about IUGR is _ (Ar ee) d) May be any
a) Hepatomegaly is due to fatty infiltration
35. Least obseryed laboratory finding in Neonatal Sepsis
b) Head circumference is 3 cm more than chest
circumference
is- (ai 96)
c) Hyaline membrane disease is
a) t C-reactive proteln
a common cause of b) Neutrophilia
death
d) Hypothermia does not occur due to good
c) Increased ESR
d) Increased Immature Neutrophils
shivering mechanisms
35. Neonatal septicemia is most commonly caused by
27 " In asymmetrical IUGR which organ is not _

affected - (NEET Dec.12 Pattern)


(CET Nov. lt pattern)

a) Subcutaneous fat a) Group B Streptococci


b) E.coli
b) Muscle
c) Liver c) Streptococcusviridans
d) Staphyloceccus aureus
d) Brain
37. Neonatal sepsis and meaingitis most common
28. What is the ponderal index of a child with werght cause-
2000 g and he:ght 50 crn - (ArrMS Nov 10) a) Streptococcuspyogenes
@G198)
a) 1.6 b) 3.6
c) 2.2 b) Streptococcus agalactacea
d) z.e c) Enterococcusfecalis
29, A aeonate weighing 1500 grams is delivered at 33 d) Staphylococcus aureus
weelrs. Which of the following would tre most appro_
38. Most common cause of neonatal meningitis
priate method of nutrition for the baby? _
fi ul (All India Dec.14 pattern)
a) IV fluids and oral feeding
b) Orogastric feeding/alternate oral feeding a) Staphylococcus

c) Total parenteral b) E. coli


nutrition
d) IV fluids and assessment/follow_up c) H. influenze
d
d) Pneumococcus
39. Eommunity acquired Neonatal pneumonia treat_
I{EONATAL 5EP5IS ment of choice - @IIMS Feb 97)
a) Cefotaxime + Amikacin
30. Early neonatatr sepsis occurs within &ours) _
b) Ampicillin + Chloramphenicol
(CET luly t5 pattern) c) Ampicillin + Gentamicin
a)8 b) rz d) Metronidazole + Amikacin
c) Smoking d) Chronic renal failure c) 36 d) 72
22. For a tean emall for date babS true is - (ArrMS May s3) 31" Most common cause of sepsis ia India rryithin 2
a) No nipple nodule moaths- (AIIMS Nov 09)
b) No palmar/plantar crease a) H influenza
c) Weight less than 1Oth percentile b) E.coli
d) Hyperbilirubinemia c) Coaguiase positive staph aureus
23. All of the following are features of prematurityin a d) Group B streptococcus
neo'I1ate, exc€pt - (All India Dec. 15 pattern) 32" A 7 day old iafant develnps symptoms of neonatal
a) No creases on sole eepticemia" Most likely cause is - (Ar e8)
b) Abundantlanugo a) Local nursery environment
c) Thick ear cartilage b) Infection through umblical cord
d) Empty scrotum c) Exclusivelybreast fed baby
24. A premature infant is more likely than a full term d) Infection by GIT bacteria
infani to - (ArrMS 80, PG 8s) 33. lVlost common cause of Neoaatal sepsis in hospital
a) Suffer fromjaundice ofhepatic origin in India is - (AilMS May 07)
b) Maintain in normal body temperature in a cold a) Escherichia coli
environment b) Klebsiella
c) Excrete urine with a uniform specific gravity c) Staph aureus
d) Suffer from anaemia d) Listeriamonoc)togen
25. Full terrn, Small f,or Date Babies are at high risk of- 34- IR neonate with meningitis, grarn positive cocci,
(Ar 2000) CAMP test positive mo$t common source of
a) Hypoglycemia infection is - (All India Dec15 Pattern)
b) Intraventricularhaemorrhage a) Geniial tract
c) Bronchopulomonarydysplasia b) Respiratory tract
d) Hlperthermia c) Hematogenous
26, True statemeat about IUGR is - (Ar 9s) d) May be any
a) Hepatomegaly is due to fatty infiltration 35. Least obseryed laboratory finfing in Neonatal Sepsis
b) Head circumference is 3 cm more than chest is- (ai s6)
circumference a) t C-reactive protein
c) Hyaline membrane disease is a common cause of b) Neutrophilia
death c) Increased ESR
d) Hlpoihermia does not occur due to good d) Increased Immature Neutrophils
shivering mechanisms 36. Neonatal septicemia is most commonly caused by -
27. In asymmetrical IUGR which organ is not (CET Nov. 14 Pattern)
afiected - (NEET Dec.12 Pattern) a) Group B Streptococci
a) Subcutaneous fat b) E.coli
b) Muscle c) Streptococcus viridans
c) Liver d) Staphyloceccus aureus
d) Brain
5/- Neonatal sepsis and meningitis most common
28. lflhat is the ponderal index of a child with weighl cause- (PGI?B)
2000 g and height 50 cm - (AIIMS Nov 10) a) Streptococcus pyogenes
a) 1.6 b) 3.6 b) Streptococcus agalactacea
c) 2.2 d) 2.6 c) Enterococcusfecalis
29. A aeonate weighins 1500 grams is delivered at 33 d) Staphylococcusaureus
weeliis. Which of the followiag would be most appro- 38. Mnst cornmon cause of neonatal meningitis -
priate method of nutrition for the baby? (Ar 11) (All India Dec.14 Pattern)
a) IV fluids and oral feeding a) Staphylococcus
b) Orogastric feeding/alternate oral feeding b) E. coli
c) Totai parenteral nutrition c) H. influenze
d) IV fluids and assessment/follow-up d) Pneumococcus
?
39- pommunity acquired Neonatal Pneumonia treat-
NEONATAL SEPSIS ment of choice - (AtrMS Feb s7)
a) Celotaxime + Amikacin
30. [arly neonatal sepsis occurs within (hour) - b) Ampicillin + Chloramphenicol
(CET luLy 15 Pattern) c) Ampicillin + Gentamicin
a)8 b) 12 d) Metronidazole + Amikacin
RESPIRATORY DISTRESS
Most probahle diagnosis is - (CET luly 15 Pattern)

a) HMD
40. \{hich of the following d*es not indicates respirato* b) Diphragmatic hernia
neonate? (CETNou' 12Pattern) c) Pneumothorax
ry distress in
a) Wheeze d) Meconium aspiration syndrome

b) Grunt 48. A new born baby has been referred to the casualty as
c) Retraction a case of congenital diaphragmatic hernia. The first
d) Tachypnea clinical intervention is to - @IIMS May 03)

With a) Insert a central venous pressure line.


41. [n a child cessation of breathing for 2O sec'
b) Bag and mask ventilation
bradycardia is - (NEET Dec'12 Pattern)

a) Apnea c) Insert a nasogastric tube


b) Dyspnea d) Ventilate with high frequency ventilator
c) Cheyne stokes resPiration 49. A child presented with respiratory distress was
d) None brought to emergencywith bag and maskventi-
lation. Now child is intubated. Chest X-ray shows
42. Apnea of prernafurity of lasts fot ? Tcnr eug' 12 Pattern)
right- sided deviation of mediastinum with scaphoid
a) 10 sec b) 15 sec
atrdomen. His Pulse rate is increased. What is the
c) 20 sec d) 30 sec
(AltMSNov 07)
next step ?
a) Endotrachealintubation
MECONIUM ASPIRATION SYNDROME b) Put a nasogastric tube
c) Surgery
43. Meconium passage in utero leads to which of the d) Endtidal CO, to confirm intubation
following - (NEET Dec.12 Patern)
50. 2 days after birth, child developed respiratory
a) Listeriosis
distress and had scaphoid abdomen. Breath sounds
b) Obstructive emPhYsema
were decreased on the left side. After bag and mask
c) Pathological jaundice
ventilation, ET tube was put and the maximal car&-
d) Meconium ileus
ac impulse shifted to the right side. What should be
44. A 3 kg term baby delivered by caesarian section the next step in management ? (AIIMS Nov 07)
develops respiratory distress soon after birth. The a) Confirm the position of endotracheal tube
liquor was meconium stained. Breathing rate is 90/ b) Emergency surgery
min. correct statements - @GI Dec 04)
c) Naso gastric tube insertion
a) Transient tachlpnoea ofnewborn d) Chestx-ray
b) Meconium asPiration sYndrome
c) Reticulonodular shadows in X-ray chest 51. A neonate having congenital fiaphragmatic hernia
developed respiratory distress. Breath sounds were
d) I Surfactant Production
decreased on the left side. After bag and mask ven-
e) Oral feeding started earlY
tilation, ET tube was put and the maximal cardiac
45. Post term baby with tachypnea - commonest cause- impulse shifted to the right side. What should be the
(All India Dec15 Pattern) (Ar 08)
next step in management -
a) Transient tachlPnea of newborn a) Confirm the position of endotracheal tube by x-ray
b) Meconium asPiration sYndrome chlst
c) Hyaline membrane disease b) Remove tube & reattempt intubation
d) Infection c) Naso gastric tube insertion
d) Chest x-ray
CONGENITAL DIAPHRAGMATIC H ERNIA 52. A neonate having congenital diaphragmatic hernia
developed respiratory distress. Breath sounds were
46. The cause of death in congenital diaphragmatic decreased on the left side. After bag and maskven-
hernia is - (CET lune 14 Pattern)
tilation, ET tube was put and the maximal cardiac
a) SePticaemia impulse shifted to the right side. What should be the
b) Hemorrhage next step in management - (Ar 08)
c) PuimonaryhypoPlasia a) Confirm the position of endotracheal tube by x-ray
d) Intestinalobstruction chest
47. New born term baby born by vaginal delivery had' p Emergency surgery
respiratory distress, glY"L1lt! .caphoid abdomen- c) Naso gastric tube insertion
d) Chest x-ray
53. Which of the following is the least important prog-
nostic factor in congenital diaphragmatic hernia?
(AllMSNov 11' Al 11)
a) PulmonaryHypertension
c) Ultra sound
b) Delay in emergent surgery
d) Amniocentesis
c) Size ofdefect
62. Which one of the following is true of hyaline
d) Gestational age at diagnosis
membrane disease of the newborn _
54. Most irnportant prognostic factor in congenital @psc ss)
a) Prematurity provides relative protection of the
diaphragmatic hernia - (Al 11, AIIMS Nov 09) occurrence
a) Pulmonaryhlpertension b) Maternal steroid exposure increase severity of the
b) Size ofhernia disease
c) Timing of surgery c) Phosphatidyl glycerol estimation is a reliable
d) Gestational age
method of
diagnosis
HYALINE MEMBRANE DISEASE d)
Surfactant increases the surface tension ofa lveoli
53. With reference to RDS, all of the following state_
55. Most important risk factor for neonatal respiratory ments are true, except - (Ar 02)
distress syndrome- (All India Dec. lj pattern) a) Usually occurs in infants born before 34 weeks of
a) Diabetic mother gestation
b) Asphyxia b) Is more common in babies born to diabetic
c) Prematurity mothers
d) Twin pregnancy c) Leads to cyanosis
56. Deficiency of surfactant is seen in - (pGI Dec 99) d) Is treated by administering 100% oxygen
a) BPD 64. A 1.5 kg child born at 32 weeks by LSCS presents
b) Neonatal asphlxia with moderate respiratory difficulty @R70/ minutes).
c) HMD Which of the following is the appropriate manage_
d) Anencephaly ment- (AIIMS Nov 10, 09)
57" The clinical sign ofhyaline rnernbrane disease
Sener_
A) CPAP
ally first appears - (All India Dec.14 pattern) b) Mechanicalventilation
a) In the first 6 hours of life c) Warm oxygen
b) Between 12 and24 hours of life d) Surfactant and ventilation
c) Between 36 and 48 hours of life 65. Allare true regarding administration of beta-meth_
d) After 48 hours of lilfe asone to a mother with premature delivery except_
58. A 3l week pregnant lady delivers a child. In 4 hrs (AilMS ee)
haby develops dyspnoea and cyanosis. X-ray chest a) Neonatal morbidity better
shows ground glass appearance. The diagnosis _ b) Helps lung maturity
(AITMS Nov 99) c) Prevents hyperbilirubinemia
a) Meconium Aspiration d) Decreases intraventricuiar hemorrhage
b) Hyaline membrane disease 66. The dose of betamethasone in prenatal to prevent
c) Tracheo esophageal atresia respiratory distress syndrome is - (NEET Dec.t2 pauern)
d) Esophageal atresia a) 6mg
59. A 3 hour old preterm baby develop respiratory b) 12 mg every 24 hours
grunt and X-ray shows reticulonodular pattern. c) 6 mg every 12 hours
Diagnosis is- (All India Dec15 Pattern) d) 4 mg start
a) Hyaline membrane disease 67. Hyaline membrane disease of lungs is characterized
b) Transient tachlpnea of newborn bY-
c) Meconium aspiration syndrome @rrMS Nov jo)
a) FRC is smaller than closing volume
d) All of above b) FRC is greatefthan closinivolume
60. A term gestation newborn developed respiratory c) FRC is equal to closing volume
distress. Which of the following would f*oo. Respi- d) FRC is independent of closing volume
ratory distress syndrome (HMD)?
(AIIMS May 12, Nov 10) BRONCHOPULMONARY DYSPLASIA
a) Historyofreceiving antenatal corticosteroids
b) Air bronchogram on chest x-ray 68. All of following are causes of bronchopulmonary
c) Onset of distress after 6 hrs of birth dysplasia except
d) Term birth
a) Oxygen toxicity
@r s6)

61. Foetal lung maturity is assessed by - b) Theophyline use


(NEET Dec.12 Pattern) ,6) Traumatic damage to lungs
a) L/S ratio 'd) Pulmonary odema due to capillary damage
b) Billirubin content of amniotic fluid 69. "d baby is bo'rn at 2Z weeksof gestation required me*
chanical ventilation for next 4 weeks & O2 for next a) Discontinue ventilation
1 week. He maintained at room air subsequently. As b) Continue ventilation
per new Bronchopulmonary dysplasia definition, he c) Give chest compression
has which of the following- (All India Dec.13 pauern) d) ET intubation
a) Miid BPD b) Moderate BPD 76. True regarding neonatal resuscitation- (pGtNov. t4)
c) Severe BPD d) NoBPD a) Ist nasal suctioning done
b) Ist mouth suctioning done
TRANSIENT TACHYPN EA OF N EWBORN c) Max. length of nasal suctioning is upto 3 cm and
mouth suctioning is upto 5 cm
70. Transient tachypnea of new born (TTN) is commonly d) Max. length of nasal suctioning is upto 5 cm and
seen in which of the following situations - mouth Suctioning upto 3 cm.
(AIIMS May 02) 77. A baby is born with rneconium stained liquor which
a) Term delivery requiring forceps of the following is taken account of in terming a
b) Term requiringventouse
baby vigorous except - (AIIMS Not 09)
c) Elective caesarean section a) Tone b) Colour
d) Normal vaginal delivery
c) HR d) Respiration
71. Characteristics radiological feature oftransient 78. A 5 year old child is rushed to casualty reportedly
tachypnoea of newborn is - (AIIMS May 0s) electrocuted while playing in a park. The child is
a) Reticulogranular appearance apneic and is ventilated with bag and a mask. Which
b) Low volume lungs of the following will be the next step in the manage-
c) Prominent horizontal fissure ment - (AIIMS Nov 01, Nov 05)
d) Air bronchogram a) Checkpulses
72. True about transient tachlpnoea ofnewborn is - b) Start chest compressions
(PGI Dec 99) c) Intubate
a) Air bronchogram seen d) Check oxygen saturation
b) Common in preterm infants 79. Bag and maskventilation is contraindicated in -
c) Interlobar fissure effusion
(AilMS Mav o4' lune ee)
d) Respiratory distress resolves in 6-10 days a) cleft lip
b) Choanal atresia
PULMONARY ALVEOLAR PROTEINOSIS c) Diaphragmatichernia
d) Multicentric bronchogenic cyst
73. 3.5 kg term male baby, born of uncomplicated
80. Which of the following is the principal mode of heat
pregnancy, developed, respiratory distress at birth,
exchange in an infant incubator ?
not responded to surfactant, ECHO finding revealed (All India Dec.13 Pattern, AI 06, PGI 98)
nothing abnormal, X-ray showed ground glass a) Radiation b) Evaporation
appearance and culture negative. Apgars 4 and 5 at
c) Convection d) Conduction
1 and 5 minutes. History of one month female sib-
ling died before. What is the diagnosis?
81. All of the following therapies may be required in a 1
(AIIMS May
hour-old infant with severe birth asphpia except-
11, May 08, Nov 11, Nov 08, Nov 07)
a) TAPVC (At 0s)

b) Meconium aspiration
a) Glucose
c) Neonatal pulmonary alveolar prciteinosis
b) Dexamethasone
d) Diffuse herpes simplex infection
c) Calcium gluconate
d) Normal saiine

RESUSCITATION
82. Grimace with APGAR score - (All rndia Dec15 pattern)
a)0 b)1
74. Meconium aspiration is done for
c)2 d)3
3 times but no
breathing occurs. Next step in resuscitation would 83. Which is not a component of APGAR Score -
be- (At e7) (All India Dec.14 Pattern)
a) Chest compression a) Colour ofthe body
b) Orinhalation $
b) Muscle tone
c) Bag & mask intubation c) Heart ratelminutes
d) Trikling of sole d) Respiratory rate per minute

75. A 3 hours old neonate with apnea is on bag and 84. Which of the following is not true about newborn
mask ventilation for last 30 seconds, now showing assessment - (AIIMSNov 11)

spontaneous breathing with heart rate 110/min. The a) APGAR at7 minindicates neonatal mortality
next step should be - (Ar e2)
depression
b) APGAR at 1 min, indicators for neonatal
Cnaprnn 3 Newborn lnfant

resuscitation c) Biliary atresia


c) Fetus can rapidly washout CO, through placenta d) Physiological
d) Anaerobic metabolism causes acidemia
93. Neonatal |aundice first time appe&r$ in the 2nd week
85. A newborn with respiratory distress with RR 86/ not a cause iS - (NEET Dec.12 pattern)
min, nasal flaring, auditlle gruntinS abdomen a) Galactossemia
lagged behind chest respiratory movement, no lower b) Rh Incompatibility
chest or xiphoid retraction. What is silvermans c) Hlpothyroidism
score - (AIIMSNov 10) d) Breast milk |aundice
a) I b)3 94. A term neonate with unconjugated hyperbili-ru-
c) s d)6 binemia of 18 mg/dl on 20th day. All are common
86. Drugused in neonatal resuscitation- causes except - (AIIMS May 07)
(All lndia Dec15 Pattern) a) Breast milk jaundice
a) Adrenaline b) Soda bi carbonate b) Congenital cholangiopathy
c) Naloxone d) Allofabove c) G 6PD deficiency
87" Dose of i.v. adrenaline in term infant is during d) Hlpothyroidism
neonatal resuscitation - (NEET Dec.12 pattern)
a) 0.1 - 0.3 ml/kgin l:1000 CONGENITAL HYPERBILIRUBINEMIA
b) 0.3 - 0.5 ml/kg in 1:1000
c) 0.1-0.3 ml/kg in 1:10,000 95. Defective hepatic conjugation is seen in all the
d) 0.3 - 0.5 ml/kg in 1:10,000 following except - ki s6)
a) Neonatal jaundice
HYPERBILIRUBINEM!A & NEONATAL JAUN. b) Gilbert syndrome
DICE
c) Crigler-Najjar syndrome
d) Novobiocin therapy
88. Hyperbilirubinemia in newborn involving palm & 96. All are true about Gilbert's syndrorne except -
sole- (All Irulia Dec15 pattern) (AILMS Dec 97)

a) 8 mg/dl a) Mild conjugated hlperbilirubinemia


b) 10mg/dl b) Autosomal dominant
c) 14mg/dl c) Normal liver histology
d) >15 mg/dl d) Almost normal liver function tests
89. Conjugated bilirubin is increased in 97 " Gilbert syndrome- True is - (All India Decl; pattern)
?
(CET Nov.13 Pattern)
a) Reduced activity ofglucuronyl transferase
a) Rotor syndrome
b) Causes indirect hlperbilirubinemia

b) Gilbert's syndrome
c) Not required any treatment
c) Criggler Najjar syndrome I d) All oTabove
d) Criggler Najjar syndrome 2
98. True about criggler najjar type-Il syndrome is -
(All India Dec. t4 Pattern)
90. A child has bilirubin of 4 mg. Conjugated bilirutrin
a) Diglucuronide deficiency
and alkaline phosphatase are normal, trile salts and
b) Dominant trait
trile in urine are atlsent. However urobilinogen in
urine is raised. What is the likely diagnosis -
c) Kernicterus is seen
d) Phenobarbitone not useful
@IIMSNov0l)
a) obstructivejaundice 99. A case of jaundince with 50% direct bilirubin, other
b) Rotor's syndrome LFTs normal. Diagnosis is - (ArrMS Nov 0e)
c) Biliary cholestasis a) Rotor syndrome
d) Hemolytic jaundice b) Gilbert syndrome
91. A 5-years old male child presentgwith episodic
c) Glucuronyl transferase deficiency
d) Primary biliary cirrhosis
anaemia and jaundice since birth. He is least likely
to have which of the following - (AIIMS Nov 11) 100. Unconjugated hyperbilirubinemia is seen in -
a) Hereditary spherocltosis (All India Dec.13 pattern)
b) Sickle cell anemia a) Rotor syndrome
c) PNH b) Dubin-fohnson syndrome
d) G-6-PD deficiency c) Biliary atresia
d) Crigler-Najjar syndrome
92. |aundice at birth or within 24 hours of birth is com-
monly due to - (Ar e5)
101. Causes of conjugated hyperbilirubinemia is -
a) Erythroblastosis (NEET Dec.12 pattern)

b) Congenital hlperbilirubinemia a) Rotor syndrome


b) Breast milk jaundice
; i Crigler najjar
d) Gilbert syndrome UjtiyUin to start phototherapy - (AIIMS June 99)
I0l. a) 20 mgo/o
-\Iildly elevated bilirubin, aormal liver enzymes b)
are 12.5 mgoTo
Seen in- (All India Dec15 pattern) c) I8 mgTo
a) Maiaria d) t5 mgo/o
b) Thalassemia
c) G-6 pD deficiency 1l l. A 30_weeks premature infants, 900gm
weight on
the third days. The serum bilirubin"is
d) All of above 13 mgyo.
The treatment of choice is_ (Ail India Dec. js pattern)
a) Exchangetransfusion
KERNICTERUS b) Phototherapy
c) Wait and watch therapy
I 03. False about kernicteres is (All India Decl| pattern) d) Pharmacologictherapy
a) No long term effect I12. What should be measured in a newborn
b) Occurs with bilirubin more than 25 who pres-
mg% ents with hyperbilirubinemia -
c) deposition in basal ganglion a) Total & Direct bilirubin @I 2000)
d) Opisthotonus b) Total bilirubin onlv
104. fu unconjugated hyperbilirubinemia, c) Direct bilirubin only
the risk of
kernicterus increases with the os. of - d) Conjugated bilirubin only
@I 0s)
a) Ceftriaxone
b) phenobarbitone
NEONATAT HYPOGLYCEMIA
c) Ampicillin
d) Sulphonamide f13. Serum glucose levels in children >
105. The late features
2 rnonths with
ofkernicterus include all except - hlpoglycaemia is ? (CET Aug. 12 pattern)
(All India Dec.13 pattern) a) <4}mgldL b) < 4s mgtdL
a) Hlpotonia c) < 50 mg/dL
b) Sensorineural d) < s+ mg/dl
hearing loss l14. All of the following groups of newborns
c) Choreoathetosis increased risk of hypoglycemia
are at an
d) Upward gaze palsy except _

f 06. All of the following statemeats regardiag jaundice


in a) Birth asphlxia
(AIIMS Nov 02)

a newtrorn are true, except - b) Respiratory distress syndrome


@112)
a) Physiological /aundice usually peaks after 4g hours c) Maternal diabetes
b]
!*1.1 milk jaundice usually peaks after day 7 d) Post term infant
c) High levels of conjugated biliiubin may
cause 115. Alargefor gestationalagebabydelivered
Kernincterus at40
weeks was otrserved to be lethargic.
d) All of the above are true The blood sugar
was measured to be 35 mg/dl.
The management is _
(Ar 12)
TREATMTNT OF HYPERBILIRUBINEMIA a) Fortified Breast Milk
b) 10% IV Dextrose
1O7. Drugs that can be used in kernicteru s_ (pGI c) Oral Glucose Solution
06, Dec 02)
a) Barbiturates , b) Benzodiazepines d) Normal Saline
c) Phenl.toin d) lChlorpromazine 116. Child comes with blood suger 32 mg/dl
e) Carbamazepine with conyul_
sioas Treatment is-
108. Which mechanism in phototherapy ltii naia Decjs pattern)
is chiefly re_ a) 5o/o dextrose 2mllkg
sponsible for reduction in serumLillirubin _ b) t\%o dextrose 2 ml/ig bolus
(AIIMS May 0s) c) l0o/o dextrose a mVkg
a) Photo-oxidation d) 5o/o dextrose 4mllkg
b) Photo-isomerization ll7. Maximum concentration of dextrose that can be
c) Structural isomerization given through peripheral yascular
d) Conjugation line in neonate
* _

(NEET Dec.12 partern)


f09. Bronze trabysyndrome is due to _
(PGI Dec 98) a) 5 b) 10
a) Phototherapy c) 12.5 d) 2s
b) Wilson disease 118. Administration of glucose solution is prescribed for
c) Chloramphenicoltoxicity all of the following situations except J ptums
d) Hemochromatosis a) Neonates
uay ool
f 10. A full term, g0 hrs old new born baby
develops jaun_ b) Child of a diabetic mother
dice what should tre the minimum level
of serum c) History of unconsciousness
d) History of hypoglycemia
NEONATE OF MOTHER d) Trunkinvolved
128. Asphyxial injury in a term baby is characterized by
I 19. All of the following are the complications in the new all except - (AilMS Nov 03)
born of a diabetic mother except - (ArrMS May 06) a) Seizures
a) Hyperbilirubinemia b) Hlperglycemia b) Differential hypotonia (lower limbs > upper limbs)
c) Hlpocalcemia d) Hlpomagnesemia c) Altered sensorium
l2A. Which of the following malformation in a newborn d) Difficulty in clearing oral secretions
is specific for maternal insulin dependent diabetes
129. A newborn with eyes closed 6 hrs after birth lustily
mellitus? @r 06) crying, no chest retraction and movements of all
a) Transposition ofgreat arteries
four limbs. Neonatal behavioral response grading -
b) Caudal regression
(AIIMS Nov 10)
c) Holoprosencephaly a) State I
d) Meningmyelocele b) State 3
121. Infant of diabetic mother with weight 3.8 Kg c) State 5
presented with seizures after 16 hours ofbirth. d) State 6
What is the cause - (AI 11, AIIMS Noy 09)
a) Hlpoglycemia
130. A neonate requires how much pressure for first
b) Hypocalcemia inflation ? ICET Nov. t2 pattern)

c) Birth asphyxia a) 25 mm of Hg

d) Intraventricularhemorrhage b) 25 cm of HrO
c) 25 cm of Hg
d) 25 mm of HrO
MISCELLANEOUS
131. Vomiting on the first day of baby's life may be
122, Kangaroo mother care-True is - (All India Dec15 pattern)
causedbyallofthefollowingexcept - (Ate7)

a) Can also be given by fathar a) Pyloric stenosis


b) Especially for low birth weight body b) Oesophageal atersia
c) Effective thermal control c) Aerophagy
d) AII of above d) Amniotic gastritis
123. Resolution of physiological umbilical hernia occurs
132. A non ventilated preterm baby in incubator is under
observation. Which is the best way to monitor the
at which week of gestation ? (CET Aug 12 Pattern)
baby's breathing and detect apnaea ?
a) 6 weeks b) 8 weeks (Ar 07)

c) weeks a) Infrared throraric movement study


10 d) 12 weeks b) Capnography
124. Hyperglycemia in Neonate if blood sugar is above - c) Nasal digital temperature monitoring
(NEET Dec.12 Pattern)
d) Impedence technique
a) mg/dl
150
b) mg/dl
125
133. Which of the following agents is likely to cause cere-
bral calcification and hydrocephalus in a newborn
c) 180 mg/dl
whose mother has history of taking spiramycin but
d) 100 mg/dl
was not complaint with therapy - (Ar oe)
I25. A newborn was given a drug in neonatal ICU, but a) Rubella
then was found in respilatory distress. The likely b) Toxoplasmosis
drug is? (Ar 07)
c) CMV
a) Morphine
d) Herpes
b) Naloxone \
c) Salbutamol
134. A pregnant lady had no complaints but mild cervical
\
lymphadenopathy in first trimester. She was pre- \
d) Soda-bicarb
\
scribed spiramycin but she was noncompliant. Baby
L26. A new born child developed respiratory depression was born with hydrocephalous and intracerebral
in neonatal ward. Which of the following drug is the calcification. Which of these is likely cause?
cause - , (AllMS Nov 10)
(AllMS May 11)
a) Opioids a) Rubella b) Toxoplasmosis
b) Barbiturates
c) CMV d) Herpes
c) Diazepam
d) Propofol
135. Microcephaly is defined as head circumference?
(CET Aug. 12 Pattern)
127. Hypoxic Ischemic encephalopathy true is - a) < lSD for age and sex
(AIIMS Nov 10)
b) < 2SD for age and sex
a) Lower limbs affected more than upper frrnbs c) < 3SD for age and sex
b) Prox. Muscles > distal muscles d) < 4SD for age and sex
c) Seizure
136. Hydrops fetalis rnay be caused by the following, 146. Most common newborn rash which presents at 24-
except- (All India Dec.14 Patrern) 48 hours of life is - (UPSC - il oe)
a) Congenital heart block a) Erythematous papular pustular lesions
b) Cystic hygroma b) Milia
c) Congenital varicella syndrome c) Transient neonatal pustular melanosis
d) Congenitalnephrosis d) Haemangioma
137. Fetal alcohol syndrome is characterized by all ex- 147. Which one of the following medical disorders
cept- (AIIMS Nov 09) leads to delayed foetal lung maturity - (UPSC 07)
a) Microcephaly a) Heart disease b) Diabetes
b) Low intelligence c) Thalassemia minor d) Epilepsy
c) Large proportionate body 148. Most common cause of respiratory distress after
d) Septal defects ofheart birth in frrst24 hours is - (JIPMER 95)
138. Test used to differentiate maternal from fetal a) Neonatal sepsis
blood? \uMSNov to) b) Meconium aspiration
a) Osmotic fragility test c) Bacterial pneumonia
b) Water bulb test d) Air embolism
c) Apt test 149, Cephalhematomausuallydisappearswithin
d) Kleihauer Betke test
ULPMER 80, UPSC 82)
139. Macrosomia is - (All lndia DecL5 Pattern) a) 3-5 months b) 2-5 weeks
a) Large size baby c) 3-5 weeks d) 5-7 weeks
b) Big mouth 150. Which one of the following is true of Transient
c) Large head Tachlpnea of Newborn (TTNB) - (UPSC 97)
d) Large tongue a) It is the commonest respiratory disorder caused
by absence of surfactant
QUESTIONS OF VARIOUS OTHER EXAMINA. b) In premature babies, it is often fatal
TIONS c) Onset of respiratory distress is immediately after
birth and it rarely lasts beyond 48 hrs
l4O, Grasp reflex develops by - (lipmer t1)
d) It often leads to chronic lung disease
a) 20 weeks b) 24 weeks 151. 8 days old neonate with extensor posture- (rN s9)
c) 28 weeks d) 32 weeks a) Cerebral palsy
I4l. The following is of serious pathological significance b) Hlpoxic ischemic encephalopathy
in infants - (Karnotaka 89) c) Malnutrition
a) Loss of weight d) Infection
b) Palpable left kidney 152. A26year old third*gravida mother delivered a male
c) Palpable spleen baby weighing4-Zkgat 37 weeks of gestation
d) Deviation of trachea from midline through an emergency caesarean section, for
L42. Harlequins Skin change in the newborn is seen obstructed labour. The child developed respiratory
in - (lipmer 93) distress one hour after birth. He was kept nil per
a) Autonomicdysfunction orally (NPo) and given intravenous fluids. He
b) Icthyosis maintained oxygen saturation on room air. No
c) Septicemia antibiotics were given. Chest radiograph revealed
d) Polyclthemia fluid in interlobar fissure. Respiratory distress
seffled by 24 hours of life. What is the most likely
143. In a new born, what is the normal respiratory rate ?
diagnosis ? (UPSC 06)
(UPSC-II o8)
a) Transient tachlpnea of the newborn
a) 10-20 breaths/minute b) Meconium aspiration syndrome
b) 30-40breaths/minute c) Persistent fetal circulation
I
c) 40-60 breaths/minute ,
d) Hyaline membrane disease
d) 60-80 breaths/minute
- 153. The foetal length is affected if the mother has
K The newborn heart rate is about
a) 120 - 160 /min b) 160 - 180 /min
(TN 04)
undernutrition during the -
a) First trimester
(UPSC e8)

E) 180 - 200 lmin d) 200 - 220 llrlin


b) Second trimester
145. "Mkrosomid'is defined as - (MAHE0s)
c) Third trimester
a) Blrth weight below 90'h percentile d) Any time during the pregnancy
b) Sl|th weight below 10'h percentile
L54. Meconium contains all except - (PGr 88)
c) Birth weight below 20'h percentile
a) Lanugo b) Bacterial flora
d) Birth weight below 50'h percentile
c) Epithelial debris d) Bilirubin
155. Which of the following is best fur transport of t&e b) Bile salt
*ewborn with rnaintainance of warm ternperature _
c) Haemoglobin
(MH 11) d) Melanin
a) Kangaroo Mother Care (KMC)
162,. A S0-hour old fuIl-term breast-fed newborn boy
b) Transport incubator
weighi*g 3l&Ig preser*s with ctinieatrtry evident
c) Thermacol box
jaundice. Fhysical examination is qthen€i$e
d) Hot bottle
nomal. The totatr bilinrbin is l t"CI mgldl with a
156. In Rh lso Imunisation, exchaage transfusion is direct bilirubin of 0.4 mgldtr. What woutrd be &e
indicated if - (AilMS 8e) €orrect treatment - (UPSC 07)
a) Cord blood hemoglobin is less than 10 g % a) Continue breast feeds and review after 4g hours
b) Cord bilirubin is more than 5 mg. b) Stop breast feeds and review after 24 hours
c) History of previous sibling afected c) Continue breast feeds and start blue-light
d) Hydrops fetalis phototherapy
157" Indications for exchange transfusion are all except_ d) Arrange for a double,volume exchange transfusion
(lipmer 03) 163. Fetallungm*turityasses.sedbyallexcept - (Up0B)
a) Unconjugated bilirubin > 18 mg/100 ml a) Measurement of cr-feto protein
b) Cord hemoglobin < 10 mg/100 ml b) Lecithin:sphingomyelin ratio
c) Cord bilirubin < 5 mg/100 ml c) Measurements of amnotic fluid creatinine
d) Bilirubin protein ratio > 3.5 d) Phosphatidyl choline concentration in amniotic
158. |auudice in the new-b,orn is physiological when _ fluid
(UPSC e8) Itr. Respiratory rate in * 2 montt et{ to }abe} it tachy-
a) The infant is visibly jaundiced in the first 24 hours pnea is - (DPGEE 08)
ofbirth a) 40 b) so
b) The total bilirubin concentration in the serum c) 60 d) zo
increases by 1 mg/dl per day
165" The blood sugar in a neqnate shortly after hirth
c) The total bilirubin concentration is above l5 mg/dl
reaches t&e lcweet Ievel of 3* mgldl at t&e age af -
d) ]aundice persists for more than one week in a
term infant @PGEE oB)
a) t hour
159" In a neonate, jaundice appears for tle first time in b) 3 hours
the 2nd week The following is not a cause _ @pG 10) c) 6 hours
a) Galactosemia d) 8 hours
b) Rh Incompatibility
c) Hypothyroidism 166. Whi€h of r&e fullowing is NCT the correct sign cf
good attachment cf;ababyto t&e breast _ (upsc_r
d) Breast milk jaundice 0e)
a) Baby's mouth wide open
160. Which of the following is not true about late onset
b) Lower areola more visible
Hemorrhagic disea,se of newborr (IIDN)? @H j0)
a) Begins between 2-7 days of life
c) Baby's lower lip everted
b) Intracranial hemorrhage is common d) Babyt chin touching the breast
c) Biliary atresia can predispose 167. \ffhictrl is an abnorrnal finding in * nesnate ?
d) Warfarin therapy is associated (Delhi PG Feb. 09)

l6f . Whi€h of the following subtance


a) Glycosuria
is toxic to neurons_
b) Bacteriuria
iipmER es)
a) unconjugated bilirubin c) WBCs in urine
d) Hlperbiiirubinemia

IIN

T
ANSWERS
NORMAL NEWBORN

L Ans. is 'c' i,e,,28 days of life fRef: O.P, Gkai }th/e p. 124 6 7h/e p. 96]
o From birth to under four weeks ofage (< 28 days), the infant is called neonate.
2. Ans, is 'c' i.e., Central cyanosis lRef : O.P. Ghai 6th/e p. 145 & Vhle p. 11jl
r There is peripheral cyanosis (not central cyanosis).
o Length is approximately 50 cm and the attitude of body is in flexion (not extension).

J. Ans. is'H i.e., 3 days fRef: Textboak af maternal dt wamenhealth carel


r The baby may pass meconium in utero or soon after birth, but all healthy babies must eyacuate within 24 hours.
After that, in normal breastfed baby meconium stools can be passed upto 3 days and on 4th and 5th days transitional
stools are passed. After 5 days regular milk stools are passed.

s Meconium is passed within -+ 24 hours ofbirth.


t Meconium stools are passed -+ upto 3 days.
t Transition stools are passed -+ 4s &5d days.
t Regilar milk stools are passed -+ After 5 days.

4. Ans. is 'c' i.e., No specific therapy fRef: O.P. Ghai 6thle p. 1471

r Menstural-like bleeding (vaginal bleeding) may occur from the third to seventh day of life.
o This is attributed withdrawl of maternal hormones after birth.
o The bleeding would subside after 2-3 days and no therapy is required.

5. Ans. is t' i.e., Lumbosacral area; 'd' i.e., Leg & t' i.e., Thigh lRef: Netson l8'k/e p. 26621
o Mongolian spots are blue or slate - gray macular lesions which occur most commonly in pre-sacral area (mainly in
lower back dt buttoclcs) but may be found over the posterior thighs, legs, and shoulders.

6. Ans. is'c'i.e., Leaving it alone [Ref: O.P. Ghai 6'h/e p. 146, 147]
o Hymenal tags around margins of hymen is normal finding.

7. Ans. is t' i.e., High larynx lRef : Gray's 40th/e p. 584; Andrew Gr*yson p. 821
o The infant larynx differs markedly from its adult counterpart. Although it is about one - third adult size, it is
proportionately larger. Its lumen is short and funnel - shaped and disproportionately narrower than that of adult. It
lies higher in the neck than the adult larynx. At rest, the upper border ofthe infant epiglottis is at the level ofthe
second or third cervical vertebra; when the larynx is elevated, it reaches the level ofthe first cervical vertebra. This
high position enables an infant to use its nasal airway to breath while sucking.

PRIMITIVE REFLEXES

8. Ans. is t' i"e., Symmetric Tonic neck reflexes lRef : Nelson 18'h/e p. 2$9; A.P. Ghai 8'h/e p. 142 {z
7h/e p. 114; Meharban singh 3'd/e p. 71; Chedda 3'd/e p. 31)
A. Reflexes present at birth
1. Rooting, sucking & swallowing reflexes 4. Crossed extensor
2. Moro reflex 5. Assymmetric tonic neck reflex
3rfalmar grasp (grasp reflex)
B. Reflexesappearafterbirth
1. Symmetric tonic neck -+ appears at 4-6 months
2. Parachute reflex -) appears at 8-9 months
3. Landau reflex -> appears at 10 months

9. Ans. is'b' i.e., 12 weeks fRef: Nelson 18'h/e ch. 6.1)


r Swallowing reflex appears at 1.2-13 weeks of intrauterine life.
I

"rhe suck-swattow reftex,:: to appear. rt typicauy begins


to appear by 12_13 week of pregnancy,,
{,1;l;:;:!,:;::
c By 13-14 wk' breathing and swallowing
motions appear and tactile stimulation
elicits graceful movements.
t0. Ans. is 'b' i"e., Brain dama ge
[Ref : A.F. Ghai trh/e p. 145, 146 6 Th/e p. 114]

Absent
Abnormal persistence
'l +
Dysfunction of CNS or pNS
Dysfunction of CI\S

u. Ans. is ?'i.e., Never [Ref l{elson l}th/e p. 2439; Meharban Singh


3d/e p. 7l}
r Parachute reflex appears at 8-9 months
of life and remains thtroughout tifeafter
that.
12. Ans. is 'd i.e., Asfm1elfl1 neck reflex
{Ref: A.F. Ghai tth/e p. 142 dr Th/e p. 114;Nelsan tSth/e p. ZqSg;
singfi 3'd/e p. 71; Chedda 3d/e p. 31) Meharban
o Asymmetric tonic neck reflex
is prominant between 2nd and
4th months.
' ,1T,'::t:1.o.u:iliffiffirTvond
the age of 6 - e months o. u .o,r.iu,r,
tonic neck posture are abnormar and
usuary

13. ,dns" is'b'i,e., Cr-Cu[Ref: o,p. Ghai 6thle p. 146; Nelson lg,h/e p. 2439, z2l)
o Unilateral Moro,s reflex is seen
in :_
t E-rbspalsy (Cs-Cu) damage
t Fracture of humerus or clavicle.
I Spastic hemiplegia
t Shoulder dislocation
o Exaggerated Moro,s reflex is
seen in _ cerebral damage.

14. Ans' is 'b'i.e., sternomastoid tumour


[Ref : o.p. Ghai ,th/e p. 142 6 6th/e p. 146)
15. Ans" is t'i.e., 6th rnonth
lLef : Tachdjian p. 371; O,p. Ghai gth/e p. t42
"In normal infant the Moro's 6 Zhle p. t14]
reJlex begins to at rhree
when persii, t ryona 6 months it fade months o and gradually disappears at 4-6
irailotrr'iday in cNS arr,op*rn{,age months.
"Moros.it reflex disappears
by six months in normal'infant.,,
r "-'""
____l__T:llr#",
t6. Ans. is 'a'i.e., Moro,s lRef : 0,p, Gkai 6th/e
p. 146 6 Vh/e p. l l4l
r Moros reflex disappe ar at 3_6 months
and never reappears.
a GrasP reflex' snout reflex' palmomental
reflex and *.rurrg reflex are n_ormally
inhibited by frontal lobe as the child
i.l,Ilii"t'J}Iffi::
reieased from inhibition in frontar
rJo. So, ;;;;;;.
these reflexes .ui, b. ,..r, in persons
with

Newborn infant Grasp reflex, sucking reflex, snout


&
palmomental refl ex present

lnhibition by frontal lobe +


Child grows
Disappearance of these refl exes

Frontal lobe lesions


Loss of lnhibition *
Reappeara nce of these refl exes

HYPOTHERMIA

t7. Ans. is 'a'i.e., ShiveringfRef: O.p. @tai gth/e p. l4j 6 Vh/e p. t t5]
"Always remember that newborn
cannot produce heat by shivering),
xs' Ans. is'b'i.e., Uncontrolled shivering fRef: o.p. Ghai B,h/e p. 143 6 vh/e p. 118]
"N e o n at e s Re sp o n d b y N on- shiv er ing thr mo gene sis',.

LOW BIRTH WEIGHT

19. Ans. is 'd i.e., < tr 0 percentile for gestational age lRef o.p. Ghai 6th/e p, 136 d, Th/e p. 1291
o Appropriate for gestational age (appropriate for date)
Babies with birth weight ranging between 10th to 90th percentile on such a chart are considered
appropriate for date.
o Small for gestational age (small for date)
Babies with birth weight less than 10th percentile are categorized as small for dates.
r Large for gestational age (large for date)
Babies with birth weight more than 90th percentile are categorized as large for date.

20. Ans. is kg [Ref Ghai 7h/e p. 128]


1d' i.e., < 1
o Low birth weight newborn
Any neonate weighing less than 2500 gm at birth irrespective of the gestational age.
r Verylowbirth weight newborn
Any neonate weighing less than 1500 gm at birth irrespective ofthe gestational age.
r Extremely low birth weight newborn
Any neonate weighing less than 1000 gm at birth irrespective ofthe gestational age.

21, Ans. is 'a'i.e., Diabetes [Ref O.p" Ghai B,h/e p. 155 6 f,/e p. 1281
o In DM, there is large for date baby (not small for date : IUGR). Other three are causes
of IUGR.
)) Ans. is t' i.e., weight less than l0th percentile [Ref o.p. Ghai 8'h/e p. 138-140 6 Thle p. 109]
o First let me differentiate the following three terms
i) Low birth weight neonates
ii) Preterm infant (Premature infant)
iii) Small for gestational age (small for date)
i) Lowbirth weight
r
Any neonate weighing less than 2500 gms at birth irrespective of the gestational age.
ii) Preterm infant (premature infant)
r Any neonate born before 37 weeks of gestation irrespective of the birth weight.
r Because birth weight is a function of gestation, a preterm baby is expected to have less weight.
iii) Small for date (IUGR)
r Babies with a birth weight less than 10 percentile for that gestational age. These may be preterm (born before
37th week) or term (born between 37 to 42 weeks).
o So, both preterm infant and small for date neonate have low birth weight.

Low birth vyeight baby

Pre term Small for gestational age (IUGR)


+
Fullterm

r Low birth weight neonates will have following problems -


i) Problems of small for date babies
ii) Problems of preterm babies
23. Ans. is t' i.e., Thick ear cartilage lRef : O.p. Ghai Bth/e p. 138-140 6 Vh/e p. 109)
c The ears in a premature neonate are sofi and flat with ear cartilage being deficient and pliant (and not thick).
24, Ans, is 'a'i.e., Suffer from jaundice of hepatic origin fRef: O.P. Ghai 8th/e p. 156 6 Vh/e p. 129-tj0)
c The liver of premature (preterm) neonate is functionally immature that leads to hlpoglycemia, hyperbilirubinemia
(jaundice) and poor detoxification ofdrugs.
25. Ans. is'd i.e., HypoglycemialRef O.p. Ghai tth/e p. 156 6 Vh/e p. t2g_130)
o Small for date babies are prone to hlpoglycemia.
o Intraventricular hemorrhage occurs in preterm infants (not
in full term, small for date babies).
26. Ans' is'b'i'e" Head circumference is 3 cm more than chest circumference
p. 1561
fRef: o.p. Ghai gth/e p. 156 6 6th/e

IUGR is synonymous with smallfor gestationalage


infants -
Malnourished small for dates (commonest variety of IUGR
infants) some important features are -
r The difference in the head and chest circumferences is more than 3 cm.
r Internal organs like Liver, thymus and lungs are shrunken,
although pulmonary alveoli appear mature. (i.e. No
Hepatomegaly)
o Pulmonary alveoli are mature; patient is not premature
but only LBW or SFD -+ No ARDS
27. Ans. is t'
i.e., Brain I Ref : O.p Ghai Bth/e p. 156 6 Vh/e p_ 129; Nelson trth/e p.
202, 7031
IUGR is classified as
1) Symmetric IUGR
e Reduced growth is symmetric + head circumference,
length and weight equally affected.
o Has earlier onset.
o Is associated with diseases that seriousiy affect fetal
cell number, such as conditions with chromosomal,
genetic malformation, teratogenic, infectious or severe '
maternal hypertensive .tiofogi...
2) Asymmetric IUGR
o Reduced groMh is asymmetri cwrth relative sparing
of head growth.
o Has late onset.
r Is associated with poor maternal nutrition or with late onset / exacerbation
(preeclampsia, chronic hypertension).
of maternal vascular disease

28. Ans. is 'a'i.e., 1,6 fRef: O.p. Ghai Zh/e p. 109)

Weight (gm)x roO


Ponderal index
Length (cm)'

r The PI of the baby in question is -

pI='ooo*too=r.o
(s0)'

o That means the baby is having assymeric IUGR (pI <


2).
29. Ans is 'b' i.e., Orogastric [Re! Handbook of pediatric nutrition p.
50_60)
Feeding ofa preterm neonate
o The aim of nutritionai management of a preterm infant is to achieve full enteral feeding as soon as possible.
o For preterm infants of more than 34 weeks of gestation,
it is possible that breast or bottle feeding can be adopted
as
they should be able to coordinate sucking, swalowing and
bieathing.
o But for those younger infants who may have compromised
respiration or be neurologically less well developed, this
may not be advisable and nutrients may need to be passed
lnto the stomach through a fine tube either through the
mouth (oro-gastric tube) or the nose (naso-gastric tube). Naso-gastric
tube increases the airway impedance and
work ofbreathing, therefore, orogastric tube is preferred
orr". rlrogurtric tube.
o Breast milk is food of choice as it is best tolerated and includes other benefits
the
as well as nutrition.
r TPN is given to vLBW infants who cannot tolerate gastric
tube feeds, have gastric disease, enteral feeding (by tube)
is not possibie or just while enteral nutrition is being established.
other important indication for TpN is sick pre-
mature/LBW infants which include Infants with:
(i) Significant respiratory distress required assisted ventilation.
(ii) Shock requiring inotropic support.
(iii) Seizures, renal/cardiac failure
(iv) Symptomatic hlpoglycemia/hypocalcemia, electroly.te abnormalities.
(v) Surgical condition of GIT, NEC, hydrops
o Even in these sick infants, enteral feed should be started as early as possible.

<28 weeks No proper sucking efforts lntravenous fluids


No propulsive motility in the gut
9:;
*!;:jit;n
ri'.:r:r;\iiin

32-34 weeks

Alogrithm for feeding of a preterm infant

tr4week;l
J
I nititate b r eas t fe edin g
I
V
Observe iJ
1. Positioning and attachment are good.
2. Able to suck effectively and long enough
(about 10-15 min)

I Breast feeding I ---- Startfeed I


by spoon/paladai
I I

J
Observe i/
l. Accepting well without
spilling/coughing

H
2. Able to accept adequate amount
I
+
Start feed by OG/NG tube
spoon/paladai feeding I
Y
Observe if
1. Vomiting / abdominal
distension occurs
l7&-..k.1
2. The prefeed aspirate exceed
>25%o of feed volume

I
Gastric tube feeding

Coming to question
o Best answer of this question is feeding by spoon or paladia. However these are not provided in options.
o Amongst the given options orogastric tube is the answer of choice.
30. Ans. is 'd' i.e., 72 hours 7/e p. t36l
fRef: Ghai
o Early onset neonalal sepsis occurs within 72 hours of life.

31. Ans. is 'b' i.e., E.coli [Rel A.F. Ghai |th/e p. 163 6 7h/e p. 136; Care of the new born 6th/e, Meharban Singhl
New born sepsis can be classified into early onset sepsis-occurring within 72 hours and late onset sepsis occuring after
,/2 hours-
Early onset sepsis -
r It is caused by organisms prevalent in the genital tract or in the labor room and maternity operation theatre.
o In the west it is mostly caused by group B streptococcus and E.coli.
o In our country it is mostly due to gram negative organisms-E.coli, klebsiella and enterobactor sp.
r
Majority of the neonates with early onset sepsis manifest as respiratory distress due to intrauterine pneumonia.
Late onset Septicemia :
o Late onset septicemia is acquired as nosocomial infection from the nursery or lying in ward.
o The onset is delayed for 48-72 hours after birth.
r In most cases symptoms appear by the end of first week or during second week of life.
o About two third cases of late onset septicemia are caused by gram negative bacilli, Klebsiella pneumonea, entero
bacteria, E.Coli, pseudomonas aeruginosa, alkaligenese fecalis, salmonella tyhimurium, proteus, citrobacter and
serratia.
32. Ans. is 'a' i.e., Local nursery environment [R4 O.p, Ghai gth/e p. 163 & Th/e p. 1361
. Late onset sepsis is caused by organisms of the external environment of home or hospital and the infection is
transmitted most frequently by the hands of the care-provider.
33. Ans" is 'b' i.e., Klebsiella lR ef : OP Ghai 8th/e p. 163 dz Vh/e p. 1i6; Meherbsan Singfi 6th/e p. 209 and lournal of past-
graduate medicine (IPGM)I
t Most common cause of neonatal sepsis in hospitals in India is -+ Klebsiella
t Most common cause of neonatal sepsis in hospitals across the world is -+ E. coli
o Most common cause of overall neonatal sepsis -+ Group B streptococci
34. Ans. is 'a' i.e., Genital tract lR.ef: Nelson lBth/e ch. lB3l
. Gram positive CAMP positive coccus is group B streptococcus (Str. agalactiae), the most common cause of neonatal
r mepingitis.
------...:tt"habitat in human hosts is female genital tract and rectum.
35. Ans. is 'H i.e., Neutrophilia lRef: O.P. Ghai 8th/e p. 164 & Thle p. 137; Nelson t6h/e p. 54Bl

Laboratory finding in Neonatal Sepsis :

Neutropenio is more (ommon than Neutrophilia


in severe neonotal infections

An lmmature Neutrophils /Total Neutrophils ratio


neutrophils
of 0.1 6 or greater suggests bacterial infection
,ii' i::i:li+::l::::::i:l:lr: :i,iil :-:i:t:l

:1!=eti:tr:ie$as.slra[s-ai1
inflammatory response ERS is lncreased

36. Ans. is 'a' i.e., Group B streptoco ccifRef: O,p. Ghai 8th/e p. 163 6 Vh/e p. 1j6)
J/. Ans. is '-o" i.e., Streptococcus agalactiae [Rel O.P. Ghnl Sth/e p. 16j 6 Vh/e p. 136; Nelsan lrth/e p. Z4\
38. Ans. is 'b' i"e., E. coli [Rel Nelson l|th/e p. 747]
r E. coli & streptococcus agalactie (group B streptococci) are the two most common cause of neonatal sepsis and
meningitis.
39' Ans. is'c'i.e., Ampicilrin and Gentamicin
[Rl o.p. Ghai Bth/e p. 171 6 p/e p. r38;]
r Antibiotic therapy for neonatar pneumonia incrudes ampicillin prus gentamycin.

RESPIRATORY DISTRESS

40. Ans. is 'l i.e.,Wheeze {Ref: Nekon ltth/e Chapter 101.4)


o The principre features of the respiratory
distress in a neonate :-
1' Thchypnoea : Rates of > 60 breaths/min, > 50 breaths/-i,
urra > 40 breaths/min for young infants (0-59
infants (60-365 days) and childhood (1-5 years). days),
2' use of accessory muscles for respiration : Features include
use of sternocleidomastoid muscles, nasal alar flare
and tracheal tug.
3' Use ofintercostal or subcostal muscles for respiration
resulting in intercostal or subcostal recession
wall indrawing. - lower chest

4. Audible grunting
5. Cyanosis

41. Ans. is 'd i.e.,Apnea [Re! O.p. Ghai dth/e p. 169 6 Zh/e p. 116]
e Apnea may be defined as _
i) cessation of respiration for 20 seconds with or without bradycardia
and cyanosis.

ii)cessation of respiration ro. t..o.ttrrur, 20 seconds


if it is associated with bradycardia or cyanosis.
42. Ans, is 'c' i.e.,20 sec fRef: See above explanation]

MECONIUM ASPIRATION SYNDROME

43. Ans. is'b'i.e., Obstructive emphysema


{Ref: Dtttta 4th/e p.
p. 20, 2t)
511; O"p, Ghai Bth/e p. 170 6 Vh/e p. 144_145; CryDT lyth/e

Consequences of meconium aspiration


o Three main problems occur due to meconium
aspiration _
i) obstructive emphysema or atelectasis- *h.r, aspirated material
blocks the airways.
ii) Pneumonitis qnd chemical pneumonia-+ because of irritant property
of meconium.
iii) Defective gas exchange.
44. Ans. is'b'i.e., Meconium aspiration syndrome
[Ref Nelson lgth/e p. 742; O.p. Ghai gth/e p. j1y d2 Th/e p. 144_
14s)
o Meconium stained liquor (amniotic fluid)
with respiratory distress soon after birth suggests
the diagnosis ofmeconium
aspiration syndrome.
r The important clues in this question are :_
i) Baby is full term +
MAS occurs in term or post term neonates.
ii) Respiratory distress soon after birth -+ MAS presents
like this
iii) Liquor is meconium stained -) supports the diagnosis
of MAS
o In transient tachypnea of newborn and hyaline
membrane disease (Jsurfactant production)
stained with meconium. amniotic fluid will not be

45' Ans' is'b' i.e., Meconium aspiration syndrorne


Ghai vh/e p.
rRef: 142)
o Tachypnea (or respiratory distres) in post term -->
Meconium aspiration syndrome.
r Transient tachypnea occurs in preterm or term
baby and HMD occurs in preterm baby.

CONGENITAL DIAPHROGMATIC HERNIA

46. Ans. is t' i.e., Pulmonary hypoplasia


fRef: Nelson tSth/e p. 748]
o Most common cause of death in congenitar
diaphragmatic hernia is -+ Pulmonary complications
c 2d most common cause of death in congenitar
di.ph.ng-utic hernia in -+ Intestinal obstruction
47. Ans. is'o" i.e., Diaphragmatic hemia lRef; Xttetsan lghle eh.Ml.9l
o Term newborn with respiratory distress and scaphoid abdomen
suggests congenital diaphragmatic hernia.
48. Ans. is t' i.e., Insert a nasogastric tube fRef. Schwartz Vhle p. lZ20]
Management of congenital diaphragmatic hernia
o Earlier congenital diaphragmatic hernia was considered to be a surgical
emergency. It was believed that the mass
efect of herniated viscera is the major factor in cardiorespiratory compromise.
r Nowitisrecognizedthatmajorcauseofcardiorespiratorycompromiseispzlmonaryhypertensionandpulmonary
hypoplasia.
o So now the patient is initially resuscitated before surgery is performed.
This resuscitation consists of
a) Stabilization by mechanical ventilation with 100o/o O,
b) I'{asograstric suction
o ventilation prevents the development of pulmonary hypertension
and provide adequate oxygen delivery. Now
days infants are ventilated by high frequency oscillation.
e Nasogastric tube is used for suction to aspirate swallowed air and to prevent
distension of the herniated bowel
which would further compress the lung.
o So both option t' & A' are preoperative procedures in congenital diaphragmatic
hernia. The question is which
should be performed fist.
r Remember that nasogastric suction is performed first in a case of CDH unless the patient presents with
following
symptoms -+ a) Cyanosis, b) Apnea, c) Respiratory disease
o Here in the question the patient does not complain of any of the above
symptoms so nasogastric suction should
be the first priority.

49. Ans. is 'H i.e., Put a nasogastric tube {Ref. see previous expranatian}
r Mediastnal deviation, scaphoid abdomen with respirator-y distress suggest the
diagnosis of congenital diaphragmatic
hernia (CDH).
o The resuscitation of CDH patient consist of :
a) Stabilization by mechanical ventilation with 100% 02.
b) Nasogastric suction
r This child has already been intubated.
r Now nasogastric suction should be done to aspirate swallowed air and to prevent
distension of the herniated bowel
which would further compress the lung.

50. Ans. is'a'i.e., Confirm the position of endotracheal tube


[Ref Nelson lgele p" 246-z4sl
This is a case of congenital diaphragmatic hernia
The clinical features suggesting this arer
r Respiratory distress after birth with decreased air entry on the left side
r Scaphoid abdomen
r Mediastinal shift
o In the above question, mediastinal shift occurred after bag and mask
ventilation and endotracheal intubation.
o So there is a possibility of wrong endotracheal intubaiion (i.e., endotracheal
tube entered esophagus instead of
trachea).
I This caused distension of stomach with gas which resulted in mediastinal
shift. So the confirmation of the
position ofthe endotracheal tube should be done.
r If the endotracheal tube is in proper position the next immediate treatment modality in this patient would be
decompression of the gastric distension by nasogastric tube insertion.

51. Ans. is 'b'i.e., Remove tube & reattempt intubation


[Ref Read.beraw]
o Dont get confuse with answer of previous question.
o There is difference between option a ofprevious question and option'a'ofthis
question :-
Previous question - confirm the position ofendotracheal tube.
This question - confirm the position ofET tube by chest x_ray.
r Best answer would have been, confirm the position of endotracheal
tube.
o But, chest x-ray cannot distinguish between tracheal and esophageal
intubation and cannot confirm the position
ofthe ET tube in trachea. Chest x-ray is done to confirm the corrJct length oftube (not
the position).

I
Method to confirm tracheal intubation
l. Tests which suggest tracheal placement (not confirmatory)
r Symmetrical Bilateral chest movements when reservoir bag is squeezed.
r Equal breath sounds over lung fields when reservoir bag is squeezed-
r Absence of gurgle over lung fields when reservoir bag is squeezed.
r Misting of the tube (water vapour deposition) during expiration.
: Feeling of correct lung compliance and refilling of bag during expiration.
2. ConfirmatorY tests
r Capnography -+ Measures end tidal CO2 in expired gas.
r Esophageal detector device.
o None of these method has been mentioned in the options of this question.
r Amongst the given options, best course of action is to remove the tube and reattempt intubation : -
"If there is any doubt about tube placement the tube should be removed" --- Lee'

Neonatal respiratory distress


v
Signs of CDH
(Scaphoid abdomen, mediastinal shift)
v
lmmediate ET lntubation

Signs of improper positioning of tube Proper positioning of tube


+
Dysfunction gf CNS or PNS
*
Confirm the position of tube
v
Remove the tube & reattempt intubation Nasogastric tube insertion
to decompress bowel
t
Chest x-ray to confirm the Diagnosis of CDH
v
urgery as required

52. Ans. is t'i.e., Nasogastric tube insertion[Ref See above explanation)

r Here "removal of tube and reattempting intubatiori' is not provided amongst the option.
o The next best stept is to decompress the distended stomach by nasogastric tube insertion.
So, the same question has three different answers depending on the options provided :-
1) Confirm the position of ET tube (not by chest x-ray) -+ Best answer
ii) Removal of the tube and reattempting intubation -+ If previous one is not provided as an option.
111) Nasogastric tube insertion -+ lf previous two are not provided in option.

Note : In previous three explanations I have explained the management protocol of CDH in which intubation has
already been used. But you should keep in mind that nasogastric suction should be the flrst procedure except
in
Apnea, cyanosis and respiratory desease, where intubation is preferred initially.

53. Ans is'-o- i.e., Delay in emergent surgery fRef: Nelson 18th/e p. 748; Fundamentals of pediatric Surgery p.
535,5361
r Timing of surgical repair has gradually shifted from an emergency repair, to a policy of stabilization using a variety
ofventilatory strategies prior to operation.
o Current recommenJation is to adopt a conservative approach and delay surgical repair of the CDH until the infant
stablizes from a hemodynamic and respiratory point of view'

Prognostic factors in CDH


r Prognostic factors can be divided into:-
A) Primary prognostic factors (Pathophysiological)
I These are the most important prognostic factor which affect morbidity and mortility.
Method to confirm tracheal intubation
l. Tests which suggest tracheal placement (not confirmatory)
r Symmetrical Bilateral chest movements when reservoir bag is squeezed.
r Equal breath sounds over lung fields when reservoir bag is squeezed.
r Absence of gurgle over lung fields when reservoir bag is squeezed.
r Misting of the tube (water vapour deposition) during expiration.
r Feeling of correct lung compliance and refilling of bag during expiration.
2. Confirmatory tests
r Capnography -+ Measures end tidal CO2 in expired gas.
r Esophageal detector device.
. None of these method has been mentioned in the options of this question.
o Amongst the given options, best course of action is to remove the tube and reattempt intubation :

"If there is any doubt about tube placement the tube should be removed" --- Lee.

Neonatal respiatory distress

Signs of CDH
(Scaphoid abdomen, mediastinal shift)

lmmediate ET lntubation

Signs of improper positioning of tube Proper positioning of tube


+
Dysfunction of CNS or PNS
v
Confirm the position of tube
+
Remove the tube & reattempt intubation Nasogastric tube insertion
to decompress bowel

Chest x-ray to confirm the Diagnosis of CDH

Surgery as required

52. Ans. is t'i.e., Nasogastric fube inserti onfRef: See above explanation)
r Here "removal of tube and reattempting intubation" is not provided amongst the option.
o The next best stept is to decompress the distended stomach by nasogastric tube insertion.
So, the same question has three diferent answers depending on the options provided :-
1) Confirm the position of ET tube (not by chest x-ray) -+ Best answer
ii) Remoyal of the tube and reattempting intubation -+ lf previous one is not provided as an option.
111) Nasogastric tube insertion -+ If previous two are not provided in option.
Note : In previous three explanations I have explained the management protocol of CDH in which intubation has
already been used. But you should keep in mind that nasogastric suction should be the first procedure except in
Apnea, cyanosis and respiratory desease, where intubation is preferred initially.

53. Ans is '-o- i.e., Delay in emergent surgery lRef: Nelson 18th/e p. 748; Fundnmentals of pediatric Surgery p.
535, 5361
r Timing of surgical repair has gradually shifted from an emergency repair, to a policy of stabilization using a variety
ofventilatory strategies prior to operation.
r Current recommendation is to adopt a conservative approach and delay surgical repair of the CDH until the infant
stablizes from a hemodynamic and respiratory point of view.

Prognostic factors in CDH


e Prognostic factors can be divided into:-
A) Primaryprognostic factors (Pathophysiological)
r These are the most important prognostic factor which affect morbidity and mortility.
:.:'..t'.:.a.:'.::..'...,
a:':.,:.,: : :,,.1: ::::::,. :a::.,.- a . : :.). :

.1!$*aa*,!itq',
r These factors are :-
i) Pulmonary hypoplasia (most important)
ii) Pulmonary hlpertension (2nd most important)
B) Secondary or relative predictors (diagnostic/clinicai)
a These poor prognostic factors are:
a) Antinatal
i) Detection at an early gestational age (< 24 wks)
ii) Associatedextradiaphragmatic congenital anomalies
iii) Liver herniation into thorax (Liver above diaphragm)
v) Stomach herniationinto thorax (Stomach above diaphragm)
vi) Presence of poiyhydraminios
vii) Small lung to head circumference ratio (LHR ratio)
viii) Small fetal abdominal circumference (< than 5th percentile)
b) Postnatal
i) Early age (< 6 hours) ofpresentation
ii) PO, and PCO, unresponsive to ventilation
iii) Need for extracorporeal membrane oxJgenation (ECMO)
c) Side ofdefect
i) Right sided defect
54. Ans. is'a'i.e. Pulmonary hlryertension IRel Sabistan 18th/e p. 20731
"Compression of the lung results in pulmonary hypoplasia involving both lungs, with the ipsilateral lung being the
most affected. In addition to the abnormal airway development, the pulmonary yasculature is distinctly abnormal in
that the medial muscular thickness of the arterioles is excessive and extremely sensitive to the multiple local and
systemic factors known to trigger vasospasm. Thus, the two main factors that affect morbidity and mortality are
p ulm o n ar y hy p opla si a and p ulmon ar y hy p er ten si on, " - S ab i st o n 1 8th / e p 2 0 7 3

HYALI NE NIEMBRAI\IE DISEASE

55. Ans. is t' i.e., Prematurity lReJ: Nelson !.9't'/o p. 731, 7321
o HMD always occurs in preterm babies often less than 34 weeks of gestation.

55. Ans. is t' i.e., }IMD lRef : O.P. Ghai 9th/e p. 169 & 7h/e p. 143; Nelsan tVth/e p. 7jtr)
o Surfactant deficiency (decreased production and secretion) is the primary cause o/RDS.

57. Ans. is'a' i.e., In ttre flrst 6 hours of life lRef : A,P. Ghai 9th/e p. 169 6 Vh/e p. 1.43; Nelson IBth/e p. 7321
c Respiratory distress occurs within the first 6 hours of life.
58" Ans. is 'b' i"e., Hyaline membrane disease [Ref: A.P. Ghai ?th/e p. 169 6 Vh/e p. ]43; Nelson lYthle p. Z3l, Zj2l
Respiratory distress in a preterm infant and X-rays showing ground glass appearance with air bronchogram suggest
the diagnosis of neonatal respiratory distress syndrome (RDS) also called hyaline membrane disease.
"Hyaline membrane disease is the commonest couse of respiratory distress in a preterm neonate". Ghai
-
About other options
o Meconium aspiration sl, rdrome usually occurs in full-term or post-term newborn.
o ARDS is adult respiratory distress syndrome.

59. Ans. is 'a' i.e", Flyaline membrane disease {Ref: Ghai Vh/e p. l4jl
60. Ans. is 'b' i.e., Air bronchogram on chest x-ray {Ref : Nelson 18th/e p, 7fi; aP Ghai Bth/e p. 169 6 Vh/e p. 143)
The chest x-ray of an infant with RDS is characterized by atelectasis, air bronchograms, and a diffuse reticular-
granular pattern commonly referred to as 'ground glass'i The chest x-ray may progress to a complete "white out"
with severe disease.
About other options
r Antenatal corticosteroids are given in pre-term (pre-mature) pregnancies not in term pregnancies. Further, antenatal
corticosteroids are given to prevent RDS (HMD) -> after antenatal corticosteroids administration, risk of HMD is
reduced.
. Respiratory distress occurs within first 6 hours.
r HMD occurs in pre-term neonate.
a1. Ams, ic i,*., LIS uafi*r {Ref : {},ff" {itr*i Vtt'lt. y, l{t* ,*. Vt'le p, t4,ll
"d
Prenatal diagnosis o[ HMD can be made bv -
1) Lecithin / sphingomyelin (L/S) ratio in amniotic Jluid -+ LIS ratio > 2 indicates adequate lung maturity.
2) Shake test -+ Amniotic fluid or gastric aspirate is mixed with absolute alcohol and shaken for 15 seconds and
allowed to settle. Copious bubbles are formed in the presence of adequate surfactant indicating extent of lung
maturity.

62, Ans. is t' i.e., Phosphatidyl glycerol estimation is a reliable method of diagnosis [Ref : O"F. Ghai 8th/e p. 169
dz Vh/ep. 143-144)
o In HMD surfactant is reduced and its measurement can be used for diagnosis e.g. in shake test.
r Constituent of surfactant are - dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins
(surfactant proteins -+ SPA, SPB, SPC, SPD) and cholesterol.

63. Ans. is 'd' i.e., Is treated by administrating 100% orygen [Ref : A.P. Ghai 9th/e p. 169 6 Vh/e p. 143-144]
o Premature infants receiving high concentrations ofoxygen may deveiop retrolental fibroplasias. So generally oxygen
tension is kept approximately 90o/o and not 100%.
ff. Ans. is 'd i.e., CPAP lRef: Neonatology by Eval4th/e p. 591
r Specific treatment for HMD is intratracheal surfactant therapy. This therapy requires endbtracheal intubation, which
also may be necessary to achieye adequate ventilation and oxygenation.
o Less premature infants (those > 1kg or > 28-30 weeks gestation) and those with lower O.requirements (FiO2 <
40 - 50%) may respond well to supplemental A, alone or to treatment with nasal continuous positive airway
pressure (CPAP).

65. Ans. is t' i.e., Prevents hlperbilirubinernia lRef : O.P Ghai ?'h/e p. 170 & 7h/e p. 144)
Prevention of HMD
r Prenatal steroids are effective in preventing HMD.
o Steroids acts by enhancing lung maturity.

Benefits
r 50 percent reduction in the incidence of respiratory distress syndrome (RDS)
c 5O percent reduction in the incidence of intraventricular hemorrhage (lVH)
e 40 percent reduction in mortality.
lndications
r All mother at risk of preteim delivery between 24 and 34 weeks of gestation.
r Cases of preterm premature rupture of membrane at less than 32 weeks of gestation
in the absence of overt clinical chorioamnionitis

Contraindicotion
a Clinical chrioamnionitis. (Maternal hypertension and diabetes mellitus are no
contiaindications. Careful monitoring and management of hypertension and hy-
perglycemia should be ensured).

Treatment schedule
r Inj. Betamethasone 12 mg lM evety 24 hours, 2 doses (preferred).
* Inj. Dexamethasone 6 mg tM every '12 hours,4 doses (only if betamethasone can
not be arranged).
Timing of effect
r Optimal effect occurs after 24h of initiating treatment.
c The effect ofone course lasts for 7 days.

uh'
6&,
'&ns.
l$ i,e,, tr? mg eveyy 24 h*qrg {fl,ef : See oLtove cxplanation)
o/. Ans. is 'd i,e,, FRC is snialler than closing yolume lRef : Handbook of pediatric intensive care l"t/e p. 1j8|
"Hyaline membrane disease reduces compliance and causes a fall in FRC (to levels below the normal closing yolume
of the lung)". -- Handbook of pediatric intensive care
o Respiratory distress occurs within.first 6 hours.
o HMD occurs in pre-term neonate.

6t. &l*s. 1s "lt i.*,, X,15 r*tiey {t4.{"{ : t}"t!. ti&a*i ttt,/r p. I {i9 ,$, 7tt'/* yt, I 4 4}

Prenatal diagnosis of HMD can be made by -


1) Lecithin / sphingomyelin (L/S) ratio in amniotic Jluiil -+ LIS ratio > 2 indicates adequate lung maturity.
2) Shake test -+ Amniotic fluid or gastric aspirate is mixed with absolute alcohol and shaken for 15 seconds and
allowed to settle. Copious bubbles are formed in the presence of adequate surfactant indicating extent of lung
maturity.

62. Ans. is'c'i.e., Phosphatidyl glycerol estimation is a reliable method of diagnosis [Ref : O.P. Ghai *thle p. 169
dr 7h/e p. 143-1441
r In HMD surfactant is reduced and its measurement can be used for diagnosis e.g. in shake test.
o Constituent of surfactant are - dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins
(surfactant proteins -+ SPA, SPB, SPC, SPD) and cholesterol.

63. Ans. is 'd' i.e., Is treated by administrating 100% oxygen lRef : O.P. Ghai 8th/e p. 169 6 7h/e p. 14i-1441
o Premature infants receiving high concentrations of oxygen may develop retrolental fibroplasias. So generally oxygen
tension is kept approximately 90o/o and not 100%.
64. Ans. is 'a' i.e., CPAP lRef: Neonatology by Eval4th/e p. 591
r Specific treatment for HMD is intratracheal surfactant therapy. This therapy requireq endotracheal intubation, which
also may be necessary to achieve adequate ventilation and oxygenation.
o Less prcmature infants (those > 1 kg or > 28-3A weeks gestation) and those with lower O, requirements (FiO2 <
40 - 50o/o) may respond well to supplemental O, alone or to treatment with nasal continuous positive airway
pressure (CPAP).

65. Ans. is 'c' i.e., Prevents hyperbilirubinemia [Ref : O.P. Ghai 8th/e p. 170 6 Vh/e p. Ma)
Prevention of HMD
r Prenatal steroids are effective in preventing HMD.
r Steroids acts by enhancing lung maturity.

Benefits
e 50 percent reduction in the incidence of respiratory distress syndrome (RDS)
f 50 percent reduction in the incidence of intraventricular hemorrhage (lVH)
I 40 percent reduction in mortality.
lndications
o All mother at risk of preterm delivery between 24 and 34 weeks of gestation.
c Cases of preterm premature rupture of membrane at less than 32 weeks of gestation
in the absence of overt clinical chorioamnionitis

Controindicatio
q Clinical chrioamnionitis. (Maternal hypertension and diabetes mellitus are no
contraindications. Careful monitoring and management of hypertension and hy-
perglycemia should be ensured).

Treatment schedule
e lnj. Betamethasone 12 mg lM every 24 hours, 2 doses (preferred).
. lnj. Dexamethasone 6 mg lM every 12 hours, 4 doses (only if betamethasone can
not be arranged).
Timing of effect
a Optimal effect occurs aftet 24 h of initiating treatment.
a The effectofone course lasts for 7 days.

{:t{x, A&s, ,s
rt:u'
i,*,, n } lug *veyy A4, k*urs lii,.cf' ; See ll;i:,vr tt:flttuttlianl
67. Ans. is 'd i.e., FRC is smaller than closing yolume [Ref : Hand book of pediatric intensiye care l't/e p. 138f
"Hyaline membrane disease reduces compliance and causes a fall in FRC (to leyels below the normal closing yolume
of the lung)" Handbook of pediatric intensive care
--
Ans. is 'b' i.e., Theophylline use [Rel: A.P. Ghai Sthle p. 171 6 Vh/e p. 146; Nelson l1,t,/e p. 737, 73g1
Bronchopulmonary dysptasia {BPD}
o BPD is a resuit of lwng iniury in infants requiring mechanical ventilation and suppiemental crxygen.
e Nlost of the children with BPD are premflture and have hyaline membrane disease. But, BPD can also occur in fultr
term newborns with meconium aspiration or persistent pulmonary hlpertension.
Pathogenesis
o The premature lung makes insufficient ftrnctional surfantant and the antioxidant defence mechanisms are not
sufiiciently mature to protect the lung from the toxic oxygen metabolites generated from oxygen therapy.

Premature newborn
J
lmmature lung (.f surfactant)
.t
Hyaline membrane disease
Jr
Oxygen therapy to newborn

Alveolar collapse T
Generation of toxic oxygen metabolites
(atelectotraiuma)
j J
Oxidant damage to lung because in prernature
Ventiiator induceci
newborn the antioxidant defence mechanisms
overdisiension
(volutrauma) are not sufficiently mature
J
Pulmonary edema, lnflammation & hypercellularity
followed by fibrosis and repair
J
Bronchopulmonary dysplasia

tLl ,1.-:"r-*. ir 'a' i.e", 3{itr{3Y,P'* i.?.':i: \e{s*rt l#'i':* {.-i;,:::ttr ii}i.i1:

SevereG,,3,
Supplement Or(for 28 days) Supplement O, (for 28 days) Supplement O, (for 28 days)
and and and
< 32'wereks GA:at birth, r, 'Br,eatlinE room airat36weeks Breathing with < 307o O, at Breathing > 3oo/o O, and/or
36 week corected',GA of at positive pressure ventilotion
, . . ,
-,:,, ,,,,. ., iwhichever.comes first). ,
discharge (whichever come (PPvltn'r) at 36 weeks
first). corrected GA or at discharge
(whichever come first).
:.
,
..1,'

: 32 weeks GA at birth Breathing room air by 56 days < 30olo O, by 56 days postnatal Breathing > 30o/o O, and/or
postnatal age or at discharge age or at discharge (whichever positive pressure ventilation
(whichever comes fi rst). comes first). (PPV) by 56 days postnatal
age or at discharge (whichever
comes first).
GA : gestational age

r The baby in question falls in category < 32 weeks gestation age at birth.
r Sirryly looking at question, answer seems to be sever BPD as mechnnical ventilation (ptositive pressure ventilatian)
orrX:., in diagnostic criteria of sever BPD.
l::rs iar:luded
e But, this question is not as simpie as it is looking. It is tricky one.
o In baby with > 32 gestation age at birth, we will have to see the respiration at 36 weeks corrected gestational age -
r This ba\ born at 27 weeks of gestati6n and required mechanical ventilation for 4 more weeks, i.e. upto 31 weeks
was
corrected gestational age. After that he maintained at room air. Thus, at 36 weeks corrected gestaional age, baby is
breathing at room air + diagnostic criteria of mild BPD.

TRANSIENT TACHYPNEA OF NEWBORN

:0. Ans is t' i.e., Elective caesarean section lkef. O.P. Ghai */e p. 171 & 7e/e p. 145; Variaus artides af Abs & Gynaej
o In text books, both elective caesarian section and normal preterm or term vaginal delivery have been mentioned as
risk factors for transient tachypnea of newborn.
e But the best answer is caesarian section -
"Delivery by caesarian section and gestational age are the risk factors for TTN". Articles Obs & Gvnae
-
7 L. Ans. is 'c' i.e., Prominent horizontal fissures lRef : A.P. Ghai */e p. l7I & 7/e p. 146; Nek*n 18*le p" 741]
r The lungs are generally clear withoui rales or rhonchi and chest roentgenogram shows
t Prominent pulmonary vascular markings - Overaeration
t Fluid lines in the fissure : Flat diaphragms
- Prominent inter lobar fissure s Occasionally pleural Jluid.

72. Ans" is t' i"e., Interlobar fissure effusion lRef : O"F" Gk*i */e p. 171 {z Tele p. 146; Nekar' 1*/e p. 741}

PU LMONARY ALVEOLAR PROTEINOSIS

73. Ans. is t' i"e., Neonatal pulrnonary alveolar proteinosis f&ef : Nekon 18"1e p" 1821!
"Respriratory distress in an infant along with a positive family history of similaily affected newborn infants
strongly suggests, pulmonary alveolar proteinosis".

RESUSCTTATION _ _ __
74. Ans. is 'd' i.e., Trikling of sole lRef: A.P. Gb*i */e p. 128 & flle p. 98-99]
r After suctioning, the baby should be dried by using pre-warmed linen to prevent heat loss.
r A brief tactile stimulation in the form of flicking the soles or rubbing the back may be provided in case of non-
establishment of good respiratory efforts.
75. Ans. is "d i.e., Discontinue ventilation [Re, O.P" Ghai 8*/e p. 127 {r */e p- 99
}{.A"TEB

c But, this question is not as simple as it is looking' It is tricky one'


have to see the respiration at 36 weeks corrected
gestational age:'
r In baby with > 32 gestati.o., ug. at birth, we will
i'e' upto 31 weeks
r and required mechanical ventilation for 4 more weeks,
This baby was born at 27 weeks of gestation
gestaional age' baby is
that he maintalned at room air' Thus' at 36 weeks corrected
corrected gestational age. After
breathing at room air + diagnostic criteria
of mild BPD'

TRANSIENT TACHYPNEA OF NEWBORN


.c i.e., Elective caesarean section l*ef- a.P. Ghei *le p. varia*s articles af *bs & Gynce]
171 6'7ele p' 146;
T&. Ans is
preterm or term vaginal delivery have been mentioned
as
c In text books, both elective caesarian section and normal
risk factors for transient tachlpnea of newborn'
I But the best answer is caesarian section
-
& Gynae
for TTN" '
,,Delivery by caesarian section and gestational age are the riskfactors - Articles obs
.c i.e", Prorninent horizontal fissures lRef : o"P' Gkai */e p' 171 dr */e p' 3'46; Nels*zt lythle p' 741\
71" Ans. is
c The lungs are generally clear withoui rales
or rhonchi and chest roentgenogram shows
s Prominentpit*o'oiy vascular markings t
O-vera.eration
* Flat diaphragms
: Fluid linesin the fissure
z occasionally pleural fluid'
t Prominent inter lobar fissute "
72. Ans.ist'i.e.,traterlob'arfissrreeffirsion lkef :o"P"GkaiSelep'171&Velep'146;Nek*se1*lep'7a1]

Pu LMoHARY ALvEoL4ElBqIFf q09I q


: Nekon lg*le p' 1821\
73. Ans. is t' i.e., Irleonatal pulmonarY alve*lar prcteinosis f&ef
,,Respiratory distress in an infant along with a..positive family history of similarly affected
newbarn infants

stroigly suggests, pulmonary alveolar proteinosis" '

er5{"tsctTATION
i.e., Triklicg of sole lkef: A"p' *hai p' & Ple p' 9s-991
74. Ans. is ? Sele 12s

usjng pre-warmtd
r After suctioning, tnJbaUy shoul<i be dried-bJ
"i:-1-1"- Y;t^t:::,t]::l:i:

0'P" Ghai sele p" 127 {z Ple p' 99


75" Ans" is 'd i.e., Discontinse ventilatioa IReJ!
'

e But, this question is not as simple as it is looking' It is tricky one'


at 36 weeks corrected gestational age:-
o In baby with > 32 gestation age at birth, we will have to see the respiration
mechanical ventilation for 4 more weeks, i'e' upto 31 weeks
r This baby was born at 27 weeks of gestation'and required
Thus, at 36 weeks corrected gestaional age, baby is
corrected gestational age. After that he maintained at room air.
breathing at room air --> diagnostic criteria of mild
BPD'

TRANSIENT TACHYPNEA OF NEWBORN


Ghai */e p. 171 & Tele p' 146; variaus articles af cbs {t cyxae}
78. Ans is t, i.e., Elective caesarem section lRef. o.P.
term vaginal delivery have been mentioned as
o In text books, both elective caesarian section and normal preterm or
risk factors for transient tachlpnea of newborn'
r But the best answer is caesarian section -
,,Delivery by caesarian section and gestational age are the riskfactorsfor TTN"' Articles Obs & GYnae
-
i.e., Prominent horizontal fissures lR$: o'P' Ghai 8*/c
p' 171 & 7/e p" 146; Nekon 1*/e p 741"1
7L. Ans. is'c
and ches|.rolntEenogram shows
r The lungs are generally clear withoui rales or rhonchi
: Prominent pulmonary vascular markings
t Overaeration
t Fluid lines in the fissure
: Flat diaphragms
t Prominent inter lobar fissure
t Occasionally Pleural Jluid.

Yele p. {r Ple p. 145; Nels*x x&*/e p' 741}


Ans. is i.e., Interlobar fissure effirsion lRef : a.P. Ghai
.c, 171
zz.
i
PU LMO NARY ALVEO LAEIROTEI N Oqq
: Nekon 18"1e p' 1821]
73. Ans. is.c i.e., Neonatal pulmonary alvealar proteinosis lRef
,,Respiratory distress in an infant along with a.positive family history of similaily affected newborn infants
stroigly suggests, pulmonary alveolar proteinosis"'

RTSUSCITATION

74. Ans. is lf i.e-, Trikling of sote [Ref A'P' Ghai */e p" 12s e f
p' 9s-991
le

r dried-bf using pre-warmed linento


After suctioning, the baby should be ftl:1'l::-9::
establishment of good respiratory efiorts'
Ts"Ans.is.di"e.,Discontinueventilationl&efa.P.Ghai*/ep.127&fr4ep"99
Birth

o Clearance of meconium
o Active breathing or crying
o Good muscle tone Routine care
o Color -+ Pink
o Term gestation

lnitial steps
o Provide warmth
o Positioning
o Good muscle tone
o Clear airways + suctioning
o Dry stimulate -+ flicking sole or rubbing back
r Orif necessary

I
Supportive care
HR>100&Pink

Apnea or
HR < 100

Ongoing care
HR>100&Pink

76- Ans is'b' i.e., Ist mouth suctioning done & 'c' i.e.,Max. length of nasal suctioning is upto 3 cm and mouth
suctioning is upto 5 cmlRef: A.P. Ghai 8th/e p. 128 6 Vh/e p. 98-994ganual of neonatatiare p" 68, 3S5l
Suctioning during resuscitation "

r The mouth and nose should be suctioned


r The mouth is suctioned first to ensure that there is nothing for the infant to aspirate when the nose is
suctioned.
r one should not insert the catheter very deep in mouth or nose for suction -+ Stimulation of posterior
pharynx during the first few minutes after birth can produce a vagal resp once, causing severe bradycardia
or al,nea.
o Therefore, during oral suctioning, a suction tube is gently introduced into the babyt mouth
until the 5 cm mark rs
at the babyt lip.
I During nasal suctioning, a suction tube is introduced upto 3 cm mark into each nostril.
77. Ans. is 'H i.e., Colour lRef: O.P. Ghai Bth/e p. 126 & Th/e p, 100)
r A newborn is classified as vigrous, ifhe has all the three signs are present :-
1) Strongrespiratary effart
2) Good muscle tone
3) Heart rate greater than 100

L
j] ]. ]: i,:,]i,..,,ji....-:11:..,i i,i. '',: ]v

-8. Ans. is '* i.e., Check pulses lRef: O.P. Ghai 8'h/e p. 126 & Vh/e p. 1001

o After airway has been opened and two rescue breath! provided, determine the need for chest compression. For
this check the pulse in carotid (in children) or branchial artery (in infants).
r If the pulse is not palpable or heart rate is <60/min, begin chest compression.
-9. Ans. is 'c' i.e., Diaphragmatic hernia lRet O.P. Ghai 9th/e p. 129 (t Vh/e p. 100, 1537
r In diaphragmatic hernia, the abdominal contents herniating into thoracic cavity have already comprornised venti-
lation.
r Giving bag and mask ventilation to this patient will worsen the condition of the patient as air will also enter in the
stomach and further compress the lungs.
o Indications of Bag and Maskventilation.
t Bag and mask ventilation is indicated if even after tactile stimulation.
a) Theinfantis apneic or gasPing
b) Respiration is spontaneous but heart rate is below 100 beats/minute.

Remember
Bag and mask ventilation causes abdominal distention as air or oxygen not only enters the lung, but also escapes
into the stomach via esophagus. Distended stomach presses on the diaphragm and compromises ventilation. Therefore
if ventilation continues for more than two minutes, an orogastric tube should be inserted and left open to decompress
the abdomen.

80. Ans. is t' i.e., Convcetion [Ref : 0.P. Gksi $tt'le p. 128 & 7h/e p. 117)

"Conyection warmed incubators are being routinely used for thermal regulation of the premature neonate's ambient
air" - Ghai 6'h/e 154

81. Ans. is 'b- i.e., Dexamethasone ["&e/ This is an extraet of the book PAEDIATRICS pOR DACTORS; Frank Shann
and John Vince; http://www.develapmentgateway.com.au/health/paed,iatrics/PaediatricsFarDoctors-pg236-2 2"pdfl
'Corticosteroids should not be used' - Paediatrics for doctors - Frankshann 6 /ohn Vince

Management Protocol
The management protocol of babies with asphlxia:
1. Oxygen. In the absence of continuous oxygen saturation monitoring, it is reasonable to give nasopharyngeal
oxygen (0.5 litre/min) untii the baby recovers. If monitoring is available, oxygen is given as appropriate.
2. Thermal control. Baby's body temperature should be kept in the normal range of 36.5-37.20C (sometimes the babies
become hlperpyrexic).
3. Correction of shock, If peripheral perfusion is poor, it is reasonable to give 20 ml/kg of normal saline initially. If
perfusion remains poor, the use of dopamine should be considered.
4. Fluid balance. Give IV fluids at 213 maintenance. Use 107o dextrose"
5. Monitor blood glucose with dextrostix and do not let it fall below 2.2 r4mol (explains gJucose administration)
6. Prevent/control convulsions. In less severely affected babies, phenobarbitone should be given when there is
anyrspicion of actual or impending convulsions (phenobarbitone loadid! dose 20 mg/kg IM or 10mg/kg slowly
IV then 5 mg/kg daily orally).
T.Treath)tpocalcaemiaif it occurs (or more practically, if the babyhas uncontrollable fitting with anormal dextrostix).
(explains calcium gluconate administration )

Notes
l.Corticosteroids should not be used, and although many paediatricians use mannitol, there is no evidence for its
effectiveness.
2. Babies with severe asphlxia may appear to settie relatively quickly after the resuscitation - but there is likely to be
a deterioratiorr after 6-12 hours or so as cerebral oedema develops.

82, Ans. is'b' i.e., I [i?ef NeJsor l\il'le ch. 9 .31

r Grimace is given score-1 in APGA.R score.

r Respiratory effort None Slow irregular Good, crying

i,t:i.Heairrnle{p4,IsEJ1 .:,: :'.Ab;er'tt':'1 r..r,,r:. :!a. I'eO ..r:.::. 1


>:11]O:::' i::1.::
* Colorofthebody Blue or pale Body pink extremities pink
(Appearance)
blue
*, Muscle tone,{ArtiVi_ty- 1..,' ',.,., .r,:,,Flaccid .' .
Some fleiionr: Actively mwing extremity
* Reflex stimulation (Grimace) No response Grimace Cries, coughs or sneezes
or putting catheter in nose

Ans" as'W i-e.,&*",ytxxttarv rat*lr,*txtate


?1"1.
iR.e:i" *.p. Gfuai,qtie *. )2* * 7$le ;t. i. li]
: Breathing ffirt (not respiratory rTte) is used in A.pGAR score.

84. Acs is ?' i-e., APGAR at 7 rnia iadicates neonatal mortality depression
[Re! Avery,s pediatrics]
I Later times APGAR score (after 5 minutes) indicates about long term
neurological damage (not neonatal mortality)
lnterpretation of APGAR Score
t The test is generally done at one andfive minutes afier birth, and
may be repeated later if the score is and remains
low. Scores 3 and below are generally regarded as critically low, 4 to
6 fairly low; and 7 to 10 generally normal.
a A low score on the one-minute test may show that the nei,onate
requires medical attention (e.g. resuscitation)but
is not necessarily an indication that there wiil be long-term problems, particulariy
if there is an improvement by the
stage of the five-minute test- lf the Apgar score remains below
3 at liter times such as 10, 15 or 30 mintues, there
is a risk that the child will suffer longer-term neurological damage.
There is also a small but significant increase of
the risk of cerebral palsy. However, the purpose of the Apgar test i
to determine quickly whether a newborn needs
immediate medical care; it was not designed to make long-term predicitions
on a childl health.
CO2 transport across placenta
r
Coz is cleared by placenta by simple diffusion. Co, is produced abundantly
in the fetus, and the pCo2 of fetal blood
is higher than maternal blood. co, therefore diffuses from fetal blood,
through the placenta, into the maternal
circulation, and is disposed by expiration from mother,s iung.
Anaerobic metabolism causes acidemia due to lactate (lactic acid) production
o Anoxic perfusion causes an increase in glucose consumption
which is more than two fold higher than that seen in
the oxygenated perfusion, resulting finally in placental uptake of glucose
not only from the maternal but also from
the fetal circulation.
t
Lactate production i-s increased during the anoxic peifusion,whiie
the final tissue energy value lies between the
values observed for fresh tissue and for the oxygenated perfusion.
The shift to anerobic ietabolism shown by pla-
cental tissue in anoxic conditions enables continued functioning ofthe
tissue over the 2-h perfusion period but it
appear that under anoxic conditions the tissue may incur u, .rr".gy
debt not observed in oxygenated perfusions.
85. Ans. is 'c' i.e.,5 {Ref : Meharban Singh 6a/e p. 2621

0 Synchronized None None None None


1,' Lag.on'inspiration lust visible Just visible Minimal.,. S.lethosco,ire only
2 See- saw Marked Marked Marked Naked ear
r A score of >6 is indicative of impending respiratory failure. -
o Now analyzing our question data :-
l) Upper chest - Lag on inspiration present u score -_) 1
ii) Lowerchest retraction
- No score 0
iii) Xiphoid retraction
- No _) score 0
iv) Nasal flaring - present _+ score 2
v) Grunting - present _+ score 2
o So, total score is 5.

Qri Ans, is 'rj' i.e., &Yl qlt *kl*v* {Re t Netsc}y, xgtr/e p. l{}{}}
o Drug used during neonatal resuscitation : (l) Epinephrine/Adrenalin, (2)
l/S or RL, (3) Naloxoneand (a) Sodium-by-
carbonate. Dose of Adrenaiin 0.1 - 0.3 ml/kg of l: 10,000.
Ans" is k't"c", *"1-*"3 rcL/kgira l:3*,{}*Xl [fr# {,}.p"

Dose or adrenlaine -
0.1 ml/kg to 0.3 ml/kg diluted (1:10,000)
:
Routs (1) Intravenous (umbilical vein) or
(2) Endotracheal
lndication -
HR < 60/min after 30 sec. of positive pressure ventilation & chest compression

HYPERBILIRUBINEMIA

SS. A*s" is'# i"e.n >15 xxlgld{ {1}-e! &leai Tkle 1t. }'a7}

Head & Neck 5 mg/dl

s9. Ams, is 'a' i-e", K*€err c3xdreme* {R.ef: X$**isrtee's 17r'le Ck 7*b!* a3- 11

o Conjugated hyperbilirubinemia is seen when -


i) Impaired secretion of conjugated bilirubin into bile -+ Dubin-johnson synilrome, Rotor syndrome"
ii) Impaired bile flow -+ Obstructive jaundice, primary biliary cirrhosis, Neonatal cholestasis, e.g. ExtratLet:a'ric
biliary atresia / neonate idiopathic hepatitis, Choledocal cyst, Sclerosing cholangitis, Caroli disettse,
Metabolic (Tposinemia, Wolman disease, Nieman pick disease, Galactosemia, Fructosemia).

90. Ans. is 'd' i.e., Hemolytic jaundice fRef: Chatterjee Shinde 4th/e p. 593; Chanilrasoma 3th/e p. 6j5l
o-Important clues provided in question are'-
1) lncreased total bili.rubin lj
2) Normal."r;,rg"*i btlorut" so' t unconjugated bilirubin

o Amongst the given options, only hemolytic jaundice causes increased unconjugated bilirubin.
o Remaining three cause conjugated hlperbilirubinemia'
91. Ans is t' i.e., PNH tRel Readbelowl
o Causes of )aundice since birth are:-
i) Rhincompatibility(erythroblastosisfetalis)
ii) ABOincompatibility
iii) Congenital infections (TORCH)
iv) Sepsis
v) Concealedhemorrhage
vi) Red cell membrane defect (hereditary sphero-cytosis)
vii) Red cell enzyme defect (G6PD deficiency)
o So, option a & d can cause jaundice si*ce birth. ,
o In sickle cell anemia, affected infants do not develop symptoms in the first few months of life because the hemoglobin
produced by the developing fetus (fetal hemoglobin) protects the red blood celis frcrn sickling. This fetal hernogiobin
disappears after 5 month of age so that by 5 months of age, the sickling of the red blood cells is prominent and symp-
toms begin.
o PNH is manfested in adults.
o So, both PNH and sickle cell anemia does not cause jaundice since birth.
o But among these two I would prefer PNH as the answer because it is manifested in adulthood while the patient in
question is a 5-years old child.
o Sickle cell anemia slrnptoms develop at the age of 5 months and it is one of the cause of jaundice (en.wikipedia.org).
Ans. is 'l i.e., Erythroblastosis [Ref, Nelson l9th/e p. 258)
c Er1'throblastosis fetalis (due to Rh incompatibility) is the most common cause ofjaundice
presenting at birth or within
24 hours oflife.
&ytt;. i:r't3' i,r;,,b?"fu r.taxe*xrzy*aZltzigit,z,{iLr:l: :r,rt trbLt..,, 1..,-!t,tt,rt..,:,}
o laundice of Rh incompatibility appears at birth or within 24 hours.
94. Ans. is nb' i.e., congenital cholangiopathy lRef : o.p. Ghai Bth/e p. 122 6 vh/e p. 1491
This child has unconjugated hyperbilirubinemia, while congenital cholanglopathy causes
conjugated
hlperbilirubinemia.

€OI\N6ENITA!. HYPEREILIRU B!NEMIA

95" Ans. is 'd'i.e., Novobiocin therapy [Ref: Robbins Vh/e p. 887, 888]

ttr,'',i;,tl jr;;*:=;tnt $ffi - - i:i:'ij;r'i:'!B:€


''
Physiological joundice of newborn Decreased UGT activity
Breast milk jaundice @ tnhibition of UGT activity
Crigler Najjar synd rome Genetic deficiency of bilirubin UGT activity
Type I m Autosomal recessive / Absent UGT activity
Type ll w Autosomal dominant / Decreased UGT activity
Gilbert syndrome Decreased UGT,activity due to mixed,etiologies .

D iffuse he patace! lula d i seose

96" Ans. is'a' i.e., lVtrild conjugated hyperbilirubinemialRef. Robbin's vh/e p. BB8; Harrisan lVh/e p. 19291
e Gilbert syndrome is a type of congenital unconjugated hlperbilirubinemia.
x lt is autosomal dominant.
o Hepatic biochemical tests are normal
a There is normal hepatic histology, but in some patients increased lipofuscin pigment may occur.
o There is mild increase in unconjugated bilirubin.
{}'7" |z*y.. tt'ttr'i.t:., l,1l *{ atzazv*. 1}tttl: {,{*lsa.rz t8,t'le t:/t. .1.:i,11 \
o In Gilbert syndrome there is unconjugated (indirect) hyperbilirubinemia due to decreased activity of UDPG
transferase,
o usually no treatment is required. But phenobarbitone can be used to reduce the level ofunconjugated bilirubin.
{}{i. *,y'r*. it't:' s.*",13**s'tt$.**t t *ratt {llLl: {.{*ryisez* tythl*, y l,}:tr|

a lnheritance Autosomal recessive Autosomal dominant


e LFT 'Normal .' :' :, : .. Normal : '. 1

* Liver Histology Normal Normal


q Kernicterus Yes Rare...,., . ..i
s UDPG transferase Absent' Reduced
+ Response to phenobarbitone No responsaas thereis absenceof :',Deciease,bilirubin' r.,.
.'
UDPG transferase
{.
* Hemolysis Absent Absent

99. Ans. is "d i.e., Rotor sydrome


* 50% direct bilirubin means conjugated hyperbilirubinemia.
o Normally the direct (conjugated) bilirubin is iess than L5-20o/o of total bilirubin.

Total bilirubin 0.2 - 1.9 mg/dl


Direct bilirubin 0 - 0.3 mg/dt,
o So, this child has : -
0 Conjugatedhlperbilirubinemia
ii) Other LFTs normal
o Amongst the given options, Rotor slT rdrome and Primary biliary cirrhosis cause conjugated hlperbilirubinemia.
o In Primary biliary cirrhosis, other LFTs are also abnormal, e.g., SGOT and SGPT are raised.
. Now we are left with Rotor syndrome which causes conjugated hlperbilirubinemia. Other LFTs are normal.
10S" ,Ans. is 'd' i.e", Crigler-Najjar syndrorn* {Ref: Nelson trVth/e p. 20E4; Ghai 7h/e p. 32a}

101" Ans. is od i.e., &,otor syndrome {l?.ef: Nelson lVt'/e Chap" 3521

102" ,4"ns. is 'd' i.e., ,{ltr of atrove [Ref: Gkai 7h/e p. ja4]
o Mildly elevated bilirubin especially indirect and normal liver enzyme seen in hemolytic anemia.
o In above question all causes hemolytic anemia.

KERNICTERUS

103. Ams. is 'd i.e,, No nong term effect &'H i.e., Occurs with bilirubin rnore than 25 mga/o {R.ef: Read belaw}
r Long term survivors demonstrat e choreoathetoid cerebral palsy, upwaril gaze palsy, sensorineural hearirug loss and
mental retardation.
o Kernicterus occurs when bilirubin level is > 20 mg/dl or > 20 mgo/o.
"It is generally believed that unconjugated bilirubin lewl of more than 20 mg/dl may lead to kernicterus"
pediatrics
--Clinical
"Risk of kernicterus increases with bilirubin levels more than 20 mg/dl and this became the conyentional cut-of pointfor
therapeutic intervention in term neonates" Pediatric essentials
--
o Unconjugated bilirubin causes toxicity to basal ganglion and various brainstem nuclei.
o Opisthotonus is seen in phase II of kernicterus.

f 04. Ans. is'd' i.e., Sulfonamides [Rel KDT Sn/e p. 644; Goad.man Gilman 10th/e p. 117fl
The administration of sulfonamides to newborn infants, especially if premature, may lead to the displacement of
Bilirubin from plasma albumin. In newborn infants, free Bilirubin can become deposited in the basal ganglia and
subthalamic nuclei of the brain. causing an encephalopathy called kernicterus. Sulfonamides should not be given
to pregnant women near term because these drugs pass through the placenta and are secreted in milk.
Kernicterus is due to unconjugated hyperbilirubinemia.

105" Ans. is'a'i.c,, Hypotoni* ltlef: Gkai $'h/e p, 172)


o Hypotonia is an early feature (in Phase I).
f 06. Ans. is t' i.e., High levels of conjugated bilirubin may cause Kernincterus [Ref O.P. Ghai vth/e p. 173-174 6
Vhle p. 14fl
o Kerruincterus is caused by high lev els of un- conjugated bilirubin.

TREATMENT OF HYPERBILIRUBINEMIA

lO7. Ans. is 'd i.e., Barbiturate lRef O.P. Ghai 6th/e p. 172, 173 6 Vh/e p. 1501
Barbiturates (Phenobarbitone)
o It is effective only if given to mother before delivery.
o It acts by inducing the conjugation of bilirubin -+ Phenobarbitone is an enzyme inducer.

108. Ans. is t'i.e., Structural isomerization [Ry'; Manual of Neonatal Care Sthle p. 2A8l
o "Structural isomerization is the intramolecular. cyclization of bilirubin to lumirubin. It is the most important
pathway for the lowering of serum bilirubin levek! - Manual of Neonatal Care 5/e, p 208

109. Ans. is 'a' i.e., Phototherapy I Ref : O.P. Ghai thle p:-175 dz 6hle p. 17j)
Bronze baby syndrome -
r It refers to dark grayish brown discoloration of the skin in infants undergoing phototherapy. Almost all infants ob-
served with this slmdrome have had a rnixed type of hlperbilirubinemia with significant elevation of direct reacting
bilirubin and often with other evidence of obstructive liver disease.
o So, this child has : -
i) Conjugatedhlperbilirubinemia
ii) Other LFTs normal
o Amongst the given options, Rotor syndrome and Primary biliary cirrhosis cause conjugated hyperbilirubinemia,
o In Primary biliary cirrhosis, other LFTs are also abnormal, e.g., SGOT and SGPT are raised.
o Now we are left with Rotor syndrome which causes conjugated hlperbilirubinemia. Other LFTs are normal.

na'
XSl" Ams, is i"c., Rotqlr syndreir*e {{lef: Nelsaw 1.7t'/e Chap^ 3521

L&2. Ans" is 'd' i"e", AII mf above {Ref: Gkai Thle p" 3a4)
o Mildly elevated bilirubin especially indirect and normal liver enzyme seen in hemolytic anemia.
o In above question all causes hemolytic anemia.

KERNICTERUS

XS3, Ams. is 'd 2.e., N*r lmng term effect &'b' i.e., Occurs with bilirutrin more tban25 wegak {R.ef: &eadbelaw}
o Long term survivors demonstrat e choreoathetoid cerebral palsy, upward gaze palsy, sensorineural hearing loss and
mental retardation.
r Kernicterus occurs when bilirubin level is > 20 mg/dl or > 20 mgo/o.
"It is generally believed that unconjugated bilirubin level of more than 20 mg/dl may lead to kernicterus"
pediatrics
--Clinical
"Risk of kernicterus increases with bilirubin leuels more than 20 mg/dl and this became the conyentional cut-of point for
therapeutic intervention in term neonates" P ediatr ic es senti als
--
o Unconjugated bilirubin causes toxicity to basal ganglion and various brainstem nuclei.
o Opisthotonus is seen in phase II ofkernicterus.

104. Ans. is 'd' i.e., Sulfonamides [Rel KDT 5'h/e p. 644; Goodman Gilman 10th/e p. 1176]
The administration of sulfonamides to newborn infants, especially if premature, may lead to the displacement of
Bilirubin from plasma albumin. In newborn infants, free Bilirubin can become deposited in the basal ganglia anil
alo be ven
, . .: t.j.l::i::::,rri:'::l:;..:
:,, ::.r,.
i ... : .rl:ii::ii.:i .r ii:ir,i
.,' :.:ii-;. r'r,'ii..:nl,:
. ...t,::t.,:....: ):.-;;r.a.)

r So, this child has : -


i) Conjugatedhlperbilirubinemia
ii) Other LFTs normal
r Amongst the given options, Rotor syndrome and Primary biliary cirrhosis cause conjugated hyperbilirubinemia.
o In Primary biliary cirrhosis, other LFTs are also abnormal, e.g., SGOT and SGPT are raised.
o Now we are left with Rotor syndrome which causes conjugated hlperbilirubinemia. Other LFTs are normal.

nCI0, ,&ns. is 'd' i"e", Crigler-Najjar symdrorne lRef: Nelsow tr9th/e p. 20E4; Ghai 7h/e p. 32Al

101" "&ns. is 'd 1.e., Kotor syndrome {flef: Nelsow tr7t'/e Chap. 3521

1CI2" Ans. is 'd' i"e., ,&ll of above l&ef: Glaai Th/e p. N_<1)
o Mildly elevated bilirubin especially indirect and normal liver enzyme seen in hemolytic anemia.
o In above question all causes hemolytic anemia.

KERNICTERUS

1&3, Ans" is 'd i,e.,lnlo long term effect &'tr' i.e., Occurs with bilirut in more tbax 25 mgYa lRef: Read belawl
o Long term survivors demonstrat e choreoathetoid cerebral palsy, upward gaze palsy, sensorineural hearing loss and
mental retardation.
o Kernicterus occurs when bilirubin level is > 20 mgldl or > 20 mgo/o.
"It is generally believed that unconjugated bilirubin level of more than 20 mg/dl may lead to kernicterus"
pediatrics
--Clinical
"Risk of kernicterus increases with bilirubin levels more than 20 mg/dl and this became the conventional cut-of point for
therapeutic intervention in term neonates" Pediatric essentials
--
o Unconjugated bilirubin causes toxicity to basal ganglion and various brainstem nuclei.
r Opisthotonus is seen in phase II of kernicterus.
104. Ans. is 8' i.e., Sulfonamides [Rel KDT Sth/e p. 644; Goodman Gilman 10th/e p. 11761
The ailministration of sulfonamiiles to newborn infants, especially if premature, may lead to the displacement of
Bilirubin from plasma albumin. In newborn infants, free Bilirubin can become deposited in the basal ganglia and.
subthalamic nuclei of the brain. causing an encephalopathy called kerhicterus. Sulfonamides should not be given
to pregnant women near term because these drugs pass through the placenta and are secreted in milk.
Kernicterus is due to unconjugated hyperbilirubinemia.

X05. Ans. ie *d i.e., Hypotonia fllef: Ghai 6't'/e p, 172)


r Hypotonia is an early feature (in Phase I).
f 06. Ans. is t' i.e., High levels of conjugated bilirubin may cause Kernincterus [Rd O.,R Ghai \th/e p. 17j-174 d,
7h/e p. 147)
o Kernincterus is caused by high lev els of un- conjugated bilirubin.

TREATMENT OF HYPERBILIRU BINEMIA

lO7. Ans. is'a' i.e., Barbiturate lRef: O.P. Ghai 6h/e p. 172, 173 6 Vhle p. 1501
Barbiturates (Phenobarbitone)
o It is effective only if given to mother before delivery.
o It acts by inducing the conjugation of bilirubin -> Phenobarbitone is an enzyme inducer.

f 08. Ans. is t' i.e., Structural isomerization [Relr Manual of Neonatal Care Sth/e p. 2081
o "structural isomerization is the intramoleculary cyclization of bilirubin to lumirubin. It is the most important
pathway for the lowering of serum bilirubin levekl - Manual of Neonatal Care 5/e, p 208

f 09. Ans. is 'd i.e., Phototherap y I Ref : O.P. Ghai t;nt, p. vs 6 dhle p. 17j)
Bronze baby syndrome -
o It refers to dark grayish brown discoloration of the skin in infants undergoing phototherapy. A1most all infants ob-
served with this syndrome have had a mixed type of hyperbilirubinemia with significant elevation of direct reacting
bilirubin and often with other evidence of obstructive liver disease.
r l0'
Ans' is 'a' i'e', 2omg% [Ref cpDT r*/e Figure(I-3]
Nerson r8h/e p. 7641
o in full term newborn phototherapy is
indicated when total serum bilirubin
birth; (ii) > 18 mg/dl in 48_72hrs. after birth; level is : (i) > l5 mg/dl in24-4ghrs.
and (tii);_';; ;g/dl more than 72 after
hrs. after birth.
111' Ans'isk'i'e.,Exc&amg*tr&lxsfu*ic:aa
isrri e"r; Gia*i8rr*p.:"rs-:z*";;;p ,r'--ri*
' ff:::1ifffl:[1t;ii['fi];Jl,ffi1Tf to weight (< rooo gm) birirubin rever
orthis newborn (13 mgo/o or 13 ms/
rl2' Ans' is h'i.e., Totar and direct bilirubin
[Ref Nelsoa lPh p. 75sl
o Measurement of total and direct bilirubin
will make us available with all the three parameters
bilirubin levels' These will help to classify jau"ai." i.e. direct, indirect, total
into-rtr..lp..ti". type and aid in diagnosis.

ilTEoNATAL HYPOG LYCEM tA

r13' Netson textbook of pediatrics


#$:;id2;"'lfrf*f,ffjief tule p. 816, lele p. slz; hup//www.unicef.org/india/

Agre

Between 1-3 hours of life


,eetwein irza h6ris;*ife
After 24 hours
Older infant and children >2 months

ll4. Ans. is t'i.e., post term infant


[Ref Nelson 1*/e p zl5l
t Neonatal hypoglycemia is seen in preterm infants (not
post term)

l15' Ans' is'b'i'e., r0% IV Dextrose [Ref, Essence of peditrics (Elsevier, rndia)
4e/e p.44,451
t
symtomatic (Lethargy) Hypoglycemia (<4hmg/dl)
should be managed i,tith 10o/o IV Dextrose,
116" A:rs. is t' i"e." 1$% dextrqls x 4 xallk g,
iRri Nefs*zr iS&le y, l)31
o In seizures, dose of l07o dextrose is 4
ml/kg.
l1?. Ans. is'c'i.e., 12"S A,{IMSi{e*w$taansgr iwl}t **{ - *€9,7ttzg$r*rxziqe{l.Ne*qg$x.nl
{fie_f
r
Dont give > l2'5o/o dextrose infusion through peripheral
line because of risk of thrombophlebitis. (prefer
18. central line)
I Ans. is t' i.e. History of Unconsciousness
r Neonates are susceptible for developing hypoglycemia
during the first 2-4 hours of life.
' is not started wi{r,in ulnhour of brrih about
r0% of normal ,,eor,"t"s are likely to develop
dffi:t"?tfeding
o This hypoglycemia is corrected either
by starting breast-feeding or by administering
glucose.
' ,l#1,i,[:ff:etic
mother is prone ror hipoglv;mia -+ gt,r.o-r.
solution is given #iire child deverops symptoms
of
o In a child with history of hlpoglycemia,
glucose administration is indicated if the
spnptoms of hypoglycemia recur.

NEONATES DIABETIC MOTHER

I19. Ans. is 'H i.e. Hyperglycemia


[Ref O.p. Ghai 86/e p. t8t & fl/e p. 156; Nekon pediatrics lple p.
t At birth the separation of placenta suddenly interrupts 613_6141
glucose infusion into the neonate without
a proportional
t Hyaglycemia -+ which is nonketotic
t Decreased lipolysk
o In addition these infants have following
abnormalities:
r Hyperbilirubinemia r Transient tachyapnea of the newborn
r Polycythemia . incidence.i..rpi*a.y disrress sl,ndrome
r Hypocalcemia Tigl:.
r Caidiomegaly
r Hypomagnesemia r As)rmmetric septal hlpertrophy
120. Ans. is'V i.e.,Caudal Regreseion lRqf : Readbelowl
'The fetal malformations seefl in Caudal regression syndrome are the most typical seen in cases of maternal
diabetes'.- Early detection of caudal regression syndrome, D. Subtil et al.

Caredal regr€siion:
o Caudal regression syndrome (CRS) is a rare malformative syndrome seen mainly in cases of maternal diabetes with
poor metabolic control.
r This syndrome associates vertebral agenesis of variable level with genito-urinary and digestive malformations.
These abnormalities are related to the impaired development of the mid-posterior axis mesoderm

l2l. Ans. is'l i.e.,Hypa$y*wia


o Electrolyte disturbances, includinghypoglycemia andhypocalcemia, are commonly seen in association with infants
of diabetic mother and may result in early-onset seizures.
o Sorry friends, I could not find any reference which hasdirectly mentioned that hlpoglycemia is a more common cause
of seizure than hypocalcernia in infants of diabetic mother.
c I was just able to find following two statements :-
"Infants of diabetic mother are most at risk for hypoglycemia which can result in seizure". - Clinical Pediatrics
"Infant of diabetic mothers with seizures, that does not respond to glucose should have their serum calcium
measured" - Cloherty
o From these two statements, it seems to me that hlpoglycemia is a more common cause of seizures in infants of diabetic
mother.

MISCETTAHEOUS

122" Ans. is'ff i.e., .&71erf abovc lR$: Nl{F manual}


l(argaroo mother care (KMC)
r Special way for LBW body
t Benefit
1) Eftective Temperature control 5) Weight gain
2) Breast feeding 6) Apnea decreases
3) Infection control 7) Mother satisfaction
4) Parentalbonding
s Component
1) Skin to skin contact
2) Exclusivebreastfeeding
TheKtrilCprocedure /
c The baby should be placed between the mother\ breasts in an upright position.
s The head should be turned to one side and in a tlrChtly upturned position. This position helps in breathing af and
allows eye-to-eye contact between the mother and her baby.
s The legs and arms should be folded.
t Baby\ abdomen should be at the level of the mother\ upper abdomen"
: Support the baby bottorn with a sling/binder.

123. Ans.isnc'i.c.*lOweeksfR.ef:AbdaminolW,altHernias:'Principlesandmanagcm:entbyRabertBmdavip.5g4l
c During development the intestinal loops lie outside the abdominal cavity in the umbilical cord called the physiological
umbilical hernia.
r The loops go back into the abdominal cavity by 10uh week of gestation"

124. ,4ns. is "H i.e., 125 mgldl lRej': Indian Pediatrics 20{t8;45:29-38},
o No established definition of neonatai hlperglycemia and upper safe limit of blood glucose has been determined
o Various researches has suggested
Whole blood glucose > L25 mgldl
Plasma glucose > 150 mg/dl

125" Ans. is
ol i.e.,Morphi*e *
{Ref : Avery's d**ase af newborrc /e p. 442}
e Morphine and other opioids can cause neonatal respiratory depression.
126. Ans is 'a' i.e., Opioids fRef: Cloherty 6h/e p. 220, 237; Auery,s disease of the newborn gth/e p. 4421
127. Ans. is t' i.e., Seizure lRef : o.P. Ghai 8th/e p. 167 6 Vh/e p. l4t; Nelson lgth/e p. 718; CpDT lSth/e p. ill
Clinical features of hypoxic ischemic encephalopathy
r Encephalopathy progress over time -
1) Birth to 12 hours -+ Decreased level of conciousness, poor tone, decreased spontaneous movement, periodic
breathing or apnea, seizures.
2) 12-24 hours ) More seizuers, Apneic spells, jitteriness, weakness.
3) After 24 houts -+ Hypotonia, J conciousness, poor feeding, brainstem signs (oculomotor) and pupillary
disturbances.

128. Ans. is'b' i.e., Differential hypotonia (lower limbs > upper limbs) fRef. a.p. Gbai 8th/e p. 166, 167 6 vh/e p.
139-MA; Nelson 18'h/e p. ZISI
o During asphyxia the infant may remain hypotonic or change
from hypotonia to extreme hypertonia or their tone
may appear normal. These changes are seen simultaneousty and the change in muscle tone
is also of the same degree in
both the limbs.

129 ' Ans' is 'd' i.e., State 6 [Ref : Brazelton TB' The Neonatal intensive care unit network neurobehaviaral scales procedures.
Pediatrics 20a4; I 1 3:641 -67)
r Crying lustily n'ith all limbs moving (child in question), straight away goes in state 6.
."ry-
r 3&" 'A"ns' is i.e., 25 crn of F{r0 fRef: Texthoak af paediatric errxergerxcy nzedicine - peter catner*n, George
felirzek, Ia*
Everitt p. 49; obstetrics: Narmal and prabtew Ttregruarocies by Steven G.Gsbbe, R. Nieb),t p. 4g6llennifer
r Higher inflation pressure of about '25 to 40 cms of Hro and higher inflation time > 1.5 sec. may be required for first
several breaths (=5).
r The volume of first breath is between 30-67 rnl.
o Residual volume after first breath : 4-30 ml (average : 16,20 ml).
o By around 30 minutes most neonate achieve normal FRC.

l3l. Ans is 'a' i.e., Pyloric stenosis fRef: Neanatology by Meharban singh p. loSl
c A large number of normal babies vomit on first day due to irritation of stomach by swallowed
amniotic fluid
o The regurgitation / vomiting in a neonate is due to -+ faulty feeding techniques
or, aerophagy
o Eosophageal atresia may present with vomiting on the first day.
r In hypertrophic pyloric stenosis vomiting characteristically occurs after 2 weeks of age. (2-3weeks).
132. Ans. is H' i.e., Impedence technique lRef : Care of the newbarnby Meharban singh 6h/e p. 30, 2801
r The respiratory monitor based on impednace technique measures changes in the electrical
resistance during breathing.
The electrode is fixed on the chest wall to pick up signals which are displayed as respiratory
rate.
o capnography - It is a simple non invasive method to assess arterial cor.
r It is used to assess the placement of ET tube in esophagus or trachea.

133. Ans. is 'b'i.e., Toxoplasmosis [Rel Moffets 4th/e p. 46jl


r This question is straight forward; spiramycin is in pregnancy is given for toxoplasm osis. prenatally acquired
T'gondii may infect the brain and retina of the fetus and can cause chorioretinitis, intracerebral
calcifications,
and hydrocephalus,
o Cerebral calcification and hydrocephalus may also occur with congenital CMV
and HSV infection, but spiramycin is
not given for these infections.

134, Ans is'H i.e., Toxoplasmosis [Rel Williams 27dle p, SB]

135, Ans. is'c'i.e., < 3SD for age and sex {Ref: Nelsan lgth/e p. 2aA\
I Microcephaly is defined as a head circumference that measures more than three standard deviation
below the mean
for age.
.Cllap.t:Eirii

136. Ans" is t'i"e., Congenital variceltra syndrorne {Ref Nelsan tr811'/e p. 77$7

Causes of Hydrops fetalis


lmmune
e Rh incompatability
Non-immune
c Anemia o-thalassemia, G-6PD defi ciency
r Cardiacdysarrhythmias Supraventricular tachycardia , AF, congenital heart block
o Structual cardiac de- Tricuspid insufficiency, ednocardial cushion defect, cardiomyopathy, hypoplastic left heart,
fects premature closure of foramen ovale
* Vascular Chorangioma of placenta, Twin-Twin transfusion, umblical artery aneurysm, thrombosis
of renal or umblical vein or IVC
* Lymphatic Lympha n giect asia, cysti c hygroma, Noona n synd rome
r CNS Encephalocele, intracranial hemorrhage
e Thorasic Mediastinal teratoma, diaphragmatic hernia
& Teratomas Choriocarcinoma, sacrococcygeal teratoma
o Tumor & storage dis- Neuroblastoma, hepatoblastoma, Gaucher disease,
eases

Niemann-Pick disease, Mucopolysaccharidosis


e Chromosomal Trisomy 13, 1 5, 1 6, 18, 21
* Bone diseases Osteogenesis imperfecta, skeletal dysplasias
o Congenitalinfections CMV rubella,Toxoplasmosis, Syphilis, Parvovirus, Leptospirosis, chaga's disease
* Others Congenitol nephrosis, Myotonic dystrophy, lnfant of diabetic mother, Maternal therapy
with indomethacin, Hepatic fi brosis

137, Ans. is t' i.e., Large proportionate body fRef: Nelson 18th/e p. 7811
r Characterististics of fetai alcohol syndrome inciude : -
1) IUGR (not large proportionate body) 4) Mental retardation
2) Microcephaly 5) Minor joint anomalies
3) Congenitalheart defects (ASD, VSD) 6) Hlperkinetic movements
7) Facial abnormalities -+ Short palpebral fissures, epicanthal folds, maxillary hlpoplasia, micrognathia, low set
ears, smooth philthrum, thin smooth upper lip.
138. Ans. is t > d' i.e., Apt test > Kleihauer Betke test [Relr Perinatal transfusion ?ned.icine 2d/e p. 218]
j.*.*=.r*..,
i*g[t4'S-;'
sourc::J::mry. M,ut"lul or neonatll . .
Mut9rnlt
.
How jt,Wolkl :: r : '.,,. fiil6[i6g'1'%-NaOfJ,destigysiduk.llbAibut. Addingnciddestroys adult HbA but noi fetalHbF ,:,.

..:,"i, ,r:::.t '


..,:.'11,.,,,, ..ngletai:t+bf r::',:,.:r: ::,: .i::i:' .- ',
.:"'
Assessment type Qualitative Quantitative

o Both Apt test and KB test are used to differentiate maternal blood from fetal blood. So, trvo options are correct.
r However, we have to choose one option and according to me Apt test is best here because Apt test is used
specifically for differentiating maternal and fetal blood while KB test is used to quantifli fetomaternal hemorrhage.

139. Ans, is'a'i.e", Large size baby


o Macrosomia refers to newborn with excessive weight, i.e. large for date. Causes are maternal diabetes and maternal
obesity.

ANSWERS OF VARIOUS OTHER EXAMINATIONS

140. Ans. is t' i.e., 28 weeks lRef: Meharban Singh S'd/e p. 71)
136" -&ns' isne'i.e,,C<ragemitatrvaricellasy&dr${TelRef:Nels**{*il'lep'77a}
Causes of HYdroPs fetalis

lmmune
c Rh incomPatability
Non-immune
q-thalassemia, G-6PD defi ciencY
o Anemia
, congenitol heort block
c CardiacdYsarrhYthmias Supraventricular tachycardia AF,
hypoplastic left heart'
ednocardial cushion defect, cardiomyopathy,
o Structual cardiac de- Tricuspid insufficiency,
fects premature closure of foramen ovale

* Vascular Chorangiomaofplacenta,Twin.Twintransfusion,umblicalarteryaneurysm,thrombosis
of renal or umblical vein or IVC
syndrome
* Lymphatic Lymphangiect asia, cystic hygroma, Noonan

o CNS Encephalocele, intracranial hemorrhage

* Thorasic Mediastinal teratoma, diaphragmatic hernia

a Teratomas Choriocarcinoma, sacrococcygeal teratoma

* Tumor & storage dis- Neuroblastoma, hepatoblastoma' Gaucherdisease'


eases
Niemann-Pick disease, Mucopolysaccharidosis

* Chromosomal TrisomY 13, 1 5, 1 6, 18, 21

c Bone diseases Osteogenesis imperfecta, skeletal dysplasias


Leptospirosis' chaga's.disease
* Congenitalinfections CMV rubella, Toxoplasmosis, Syphilis, Parvovirus'
therapy
Congenitol nephrosis, Myotonic dystrophy' lnfant of diabetic mother' Maternal
6 Others
\ivith indomethacin, Hepatic fi brosis

lRef: Nelson 18'h/e p. 7811


137. Ans. is t' i.e., Large proportionate body
include : -
r Characterististics of fetal alcohol syndrome
4) Mental retardation
1) IUGR (notlarge proportionatebody) 5) Minor joint anomalies
2) MicrocePhalY ySD) 6) HlPerkinetic movements
3) Congenitalheart defects (ASA epicanthal foids, ma*illary hlpoplasia' micrognathia'
low set
7) Facial ab"ormalities + Short palpebral fissures'
lip'
upper
ears, smooth philthrum' thin smooth
Perinatal transfusion medieine 2d/e p' 2181
138. Ans. is'c > d i.e., Apt test > Kleihauer Betke test [Re/r

lvlolcl I lol
Source of samPle Maternal or neonatal
Adding acid destroy!'aduti HbA but'no!fetal'HbF
How it'works.., :' Adding loloNaOH destloys adult HbA but
notfetal HbF
Ouantitative
Assessment tYPe Qualitatlve
Positive neais blood ls af fetal o tigln :'' Reboited'in estimated''ml3of futal,blood..''
Results: .: .:: i:
are correct'
maternal blood from fetal blood' So, two options
r Both Apt test and KB test are used to differentiate
rHowever,wehavetochooseoneoptionandaccordinqtomeApttestisbestherebecauseApttestisused
to quantifli fetomaternal hemorrhage'
and fetal blood while KB test is o..d
specifically for differentiating maternal

139. Ares. ie 'a'i.e., I-arge slz"ebaby i diabetes


,. r- a^^ and
^-r mater..'-
"-^1
newborn with excessive weight, i.e. large for date. causes are maternal
o Macrosomia refers to
obesitY.

ANSWERS OF V
Mehatban Singh S'd/e p' 711
140. Ans. is t'i.e., 28 weeks lRef:
Aas, is'd i.e.,Loes ofweight [Ref: Netson l.*/e p. 220" 22107
r An infant should gain weight progressively, except for the first few days of lifb.
r Liver, spleen and kidney may be palpable ia normal newborn.
Nelson
o Sometimes trachea may be deviated from midline without any significance. --
142. Ans, is'l i.e",Autonomic dysfunction {Ref: Nelson t*/e p. 2262}
o If reflects an imbalance in the autonomic vascular regulatory mechanism.

143" Ans. is '8 i.e",30-40 breathc/minute {Ref : op Ghai &/e p. 145 d? p/e p. 10sl
o Heart rate in neonate -) l2O-l4O per minute.
I Respiratoryrate -+ 35 to 40 per minute.

lM. Anc, is'd i.e,,120-tfilm,-{Ref: O.p, Ghai tr/e p. 145 {r p/e p. 105)
145, Ane" ic 'V Le,,Birthweight below t0* percentile {Ref: Internetl
c lVlicrosomia means small for date baby, i.e. newborn baby with a birth weight less than 10e percentile.
l#. Ans, ie 'd i"e.,Erythcrnatouc papular pustular leeion * {Ref : Dutta #/e p. 446; Gupte S. */e p. 522)
Common neubom raches
r Erlthema toxicurn -> Most common
r Acne neonatorum
r Transient neonatal pustural melanosis.

147. Ans, ic '8 i,a., Diabetec {Ref: Has been explained)


r Maternal diabetes predisposes to HMD.

148" Ans. ic *A i.e,tvleconium aepiration


o Most common cause of respiratory distress in a term or post-term neonate -+ Meconium aspiration.
c Most common cause of respiratory distress in a preterm infant -+ hyaline membrane disease.

149, Ane. io'il i,e,,5-7 weeks{Ref A.P" Ghai *le p" 141 6 Zh/e p. fi2; Nelson 18tu/e p. 214)
r It disappears between 2 week to 3 months.

150. Anc. ie 'C i.e., Olset of reepiratory distresc is immediately after birth and it rarely laste beyond 4g hrs
{Ref O"P, Ghai */e p" tz1 & Zh/e p" t46l
151, Ano, ic 'd i.e., cerebral palsy &'U i,e.,rlypoxic lcchemic encephalop *hy {Ref: Internetl
r Normal posture of a full term neonate is flexor posture.
o Extensor postlrre may be seen when there is brain damage as in hlpoxia --> hlpoxic
ischemic encephalopathy and
cerebral palsy.

,52, Anr, ic'* i,e,,Transient tachypnea of newborn fRef: o,p, Ghai gth/e p, l7l & ztu/e p. rufl
I Respiratory distress, which resolves within 24 hours without any respiratory support and fluid in interlobar
fissure
on chest X-ray suggest the diagnosis of TTN.

153. Ane" is 'il i,e,, Any time during pregn fRef: Read below]
^cy
r Fetal growth is affected by maternal nutrition during any trimester in pregnancy.
r Fetal growth is affected even by nutritional status of mother prior to pregnancy.

154. Anc, ie 'H i,e., Bacterial flora fRef: Has been explained]
r Meconium contains -
i) Intestinal epitheliai cells iii) Mucus v) Bile
ii)Lanugo iv) Amniotic fluid vi) Water

155, Ans is '* i.e., Kangarooo Mother Care (KMC) lRef, O.P. Ghai Bth/e p. 14s, 148 6 Vhle p, 121,153; K.N.
Agrawal l,t/e p, 1A4l
"Preferably mother should accompany and baby can be transported in KMC position.
Even father can provide KMC during
transport if mother can not acompany. _ K.N. Agrawal
i.e., cord bilirubin is more than 5 mg;
156. Ans. is .d i.e., cord blood hemoglobin is less than l0 g %;'H
.c,
i.e., History of previous sibling affected [Ref lVelsolr
l*/e p- 77ll

lndications of Exchange transfusion


o Bilirubin Protein ratio > 3.5 o PrematuritY
o Cord hemoglobin < 10g/dl
e Reticuloclte count > 1570
o Cord bilirubin > 5mgld
o Previous kernicterus or severe erythroblastosis in a sibling

p'
157. Ans. is t'i.e., Cord bilirubin < 5 mll00 ml [Rel: Nelson
18e/e 7711

I Cord bilirubin 5 or more is an indication'


.H i.e., The total bilirubin concentration in the serum increases by r mgldl per day lRef': o'P' Ghai
r5g. Ans. is
8*le p. 172 & Ple p. 147; Nelson lf le p. 594\
o Rate of rise is less than Smgo/o
l*le p' V58l
159. Ans. is'b'i.e., Rh Incompatibility [Re/: O.P. Ghai 8*/e p' 174 6 ffle
p' 172; Nelson

of Newborn by Maherbarcingb 6h le p' 336; Nelsott


r 60. Ans. is ? i.e., Begins between 2-7 days of Me fRef: cate
lSele P.7731
Hemorrhagic disease of the newborn
o Early onset -) 0-24hr
r disease ->
Classical 2-7 days
r Late onset -) 1-6 months

f 61. Ans. is'd bilirubin tRef Has been explainedf


i.e., Unconjugated
hours lRef Clohetty 5*/e p' 187)
162. Ans. is'b' i.e., Stop breast feeding and review after 24
r This is a case of breast milkiaundice' may be
r Temporary interruption of breast milk feeds will dramatically reduce the serum levels of bilirubin and there
but it never reaches the previous levels'
slight increase in bilirubin when breast feeding is resumed,

f 63. Ans. is 1d i.e., Measurment of ct - fetoprotein [Ref : Nelsorc l*le p' 6951

164. Ans. is'C i.e., 60 [Ref: O.P. Ghai }e/e p' 381 & *le p' i52l

Tachypnea
o < 2 months -+ 60 or more RR/min
o 2-12 months ) 50 or more RR/min
o 12-60 months -+ 40 or more RR/min

165. Ans. is'H i.e., 3 hours [Ref Netson 18th/e p' 655]
o Blood glucose reaches its nadir in initial 2-3 hrs' of life'
; A'P' Ghai Sele p' 154 & 7e/e p' 126i
166" Ans. is'b' i.e., Lower areola more visible [Ref

Signs of good attachement of baby's mouth to nipple


1. The babY's mouth is wide oPen one'
2. Most oithe nipple and areola in the mouth, only upper areola visible, not the lower
3. The baby's chin touches the breast'
4. The ba\t lower liP is elevated'

167. Ans.is.b,i.e.,BacteriuriatRef o.P. Ghai8th1ep.468&6h/ep.443;SmithGeneralurologylvhlep'491

III
P T E'R

CAKffiXffi\{&SCq"-fX"r&K
SYSTEM

FETAL CIRCULATION

o Fetal circulation differs from adult circulation in several ways. Almost all differences are attributable to the fundamental
difference in the site of gas exchange. In the adult gas exchange occurs in the lungs, while in the
fetus placenta

provides the exchange of gases and nutrients.


Course of fetal circulation
A) Blood returing to heart
o Bloodoxygenatedintheliacentareturnsbywayoftheumblicalvein?Gt|T),whichenterthefetusattheumblicus
and course through to join the portal vein'
o tine iluctus venotts is a blpass shunt between portal vein and IVC'
o Most of the umblical venous blood shunts through the ductus venosus to the IVC.
o Blood frorr,lVC (which carries the blood drained from lower extremities, umblical veins, hepatic veins and renal
return of
veins) enters the right atrium. On reaching the right atrium, about 1/3rd of total inferior vena caval
blood enters the left atrium through formen oval. The rest two third mixes with the venous return from SVC
(which carries the blood drained from head, neck and upper limbs) to enter the right ventricles.

B) Blood coming out of the heart


1. Right side
o The right ventricle pumps out the blood into pulmonary trunk -+ very small amount of this blood enters the
pulmonary circulation because the lungs are collapsed and pulmonaryvascular resistance is high. Most of this
blood passes to desending aorta through ductus arteriosus, a shunt between pulmonary trunk and desending
aorta
Aorta. Descending aorta carries blood to umblicus through umblical artery, for oxygenation. Descending
also supplies the blood to lower lumbs, kidney and abdominal viscera.

2. Left side
o The left ventricle pumps blood into the ascending aorta for distribution in coronary circulation, head and upper limbs.

llmblical cord contains one umblical vein and two umblical arterieswEEr)
CAKMKffire$CULAK
$YSYKivg

FETAL CIRCULATION

o Fetal circulation differs ffom adult circulation in several ways. Almost all differences are attributable to the fundamental
difference in the site of gas exchange. In the adult gas exchange occurs in the lungs, while in the fetus placenta
provides the exchange ofgases and nutrients.
Course of fetal circulation
A) Blood returing to heart
o Blood oxygenated in the placenta returns by way of the umblical vein@Groz), whichenter the fetus at the umblicus
and course through to join the portal vein.
o The ductus yenous is a bypass shunt between portal vein and IVC.
o Most of the umblical venous blood shunts through the ductus venosus to the IVC.
o Blood from fVC (which carries the blood drained from lower extremities, umblical veins, hepatic veins and renal
veins) enters the right atrium. On reaching the right atrium, about 1/3rd of total inferior vena caval return of
blood enters the left atrium through formen oval. The rest two third mixes with the venous return from SVC
(which carries the blood drained from head, neck and upper limbs) to enter the right ventricles.

B) Blood coming out of the heart


1. Right side
o The right ventricle Pumps out the blood into pulmonary trunk -+ very small amount of this blood enters the
pulmonary circulation because the lungs are collapsed and pulmonaryvascular resistance is high. Most of this
blood passes to.desending aorta through ductus arteriosus, a shunt between pulmonary trunk and desending
Aorta. Descending aorta carries blood to umblicus through umblical artery, for oxygenation. Descending aorta
also supplies the blood to lower lumbs, kidney and abdominal viscera.

2. Left side
' e fhe left ventricle pumps blood into the ascending aorta for distribution in coronary circulation, head and upper limbs.

Umblical cord contains one umblicol vein and two umblical arterieswEEt)
$i a : ; a:)ir: ;.:.:::t a:i:,:..
t::,,:::::::::t: : a::::,.::,
$:P:ff,-f,:.{::

Fetal circulation

I uPPer"-""**l
timus
I I

+-Er*
syc

Pulmonary vein

RA
+LA
T
1t3
2t3

RV*+ * r-v
A

I Heart
i --------+-
I

V
P u I m o n a ry tru n k -------------**
I

I Major
---.-------}Ductus arferrosus----> Descending aorta

Lower limb, Kidney

r Blood in IVC has more oxygen saturation than blood in SVC as IVC carries the oxygenated blood of
umblical vein.
The left ventricular blood has more oxygen saturation that right ventricular blood because it
carries the blood of IVC,
while blood in right ventricle is a mixture of blood from IVC and SVC. Sq thebrain and coronary circulation
receiye
blood with higher oxygen saturation (through ascending aorta) than the lower half of boflyrtr tst.
r The left ventricular output is approximately half of right ventricular output because volume of
blood reaching in left
atrium is considerably lower than volume of blood reaching in right atrium. Infact right atrium is the major
source of
blood to left atrium.
r Aorta and pulmonary trunk are connected by ductus arteriosis, and pulmonary trunk has pressure slightly
higher or
equal to that of arota + So, blood flows from pulmonary trunk to aorta.
. The pressure in right and left ventricles are equal@r ts).

Circulatory adjustments at hirth


r These are brought about because of a shift from placental dependance for gas exchange in the fetus to pulmonary
gas exchange in neonate.
1) Pulmonarycirculation
r Immediatly after birth lungs expand due to first few breaths of neonate. This causes a fall in pulmonary
vascu-
lar resistance (O, causes pulmonary vasodilatation). This results in increased flow into pulmonary
trunk and
arteries-
: The pulmonary artery pressure falls due to lowering of pulmonary vascular resistance. The pressure
relations
between aorta and pulmonary trunk are reversed so that the blood flow through the ductus arteriosus
is reversed
-+ Instead of blood flowing frorn the pulmonary artery to aorta, the direction of flow through ductus, is from
aorta to pulmonary trunk.
r Functional closure of ductus occurs within 15 hours after birth(Arse). Increasing oxygen saturation causes
the muscle of ductus to constrict ) In full term neonates the ductus arteriosus closes within l0 to 25
days
(Anatomic closure)6t oo' DPG es).
2) System circulation and circulation through heart
Cn,eplEx 4
r Loss of placental circulation and clamping of the cord after birth results in increase in systemic vascular resist-
ance. This tends to increase the aortic blood pressure and the left ventricular systolic pressure.
r Thelossofplacentalcirculationresultsinsuddenreductionofflowthroughductusvenosuswhichclosesoff->
Flow through ductus venosus disappears by the 7th day of posnatal life(Alse).
r The loss of placental flow results in a decrease in the volume of blood returning to right atrium -+ Right atrial
pressure decreases.
: T1ae lefi atrial pressure becomes higher than right atrial pressureK"tutaoa) and the septum primum which ats as
a valve of fossa ovalis, approximates with the septum secundum to close offformen ovale.
r Functional closure of foramen ovale occurs very quickly(pcr8e).
r Over a period of months, the septum primum and septum secundum become firmly adherent resulting in
anatomical closure of the foramen ovale.
r After closure of ductus arteriosus, there is establishment of postnatal circulation: -
I The blood reaching the right atrium through IVC and SVC is emptied into the right ventricle from where it
pumped into pulmonary trunk.
r After coursing through lungs for gas exchange, it reaches the left atrium and ventricle.
r The Ieft ventricle pumps it out for distribution in the body for oxygenation of the tissues. The venous return again
comes back to right atrium through IVC and SVC.
r AII of the blood leaving the right ventricle, after coursing through lungs, reaches the left ventricle -+ The two ventricles
are connected in series and therefore, the output ofright and left ventricles are same (in contrast to fetal circulation,
where right ventricular output is more).

CONGEN ITAL HEART DISEASES


r Congenital heart disease (CHDs) are abnormalities caused by faulty development during 3 - 8 weeks of intrauterine
Iife.
r Both hereditary and environmental t'actors play a role in etiology of CHDs.
A) Hereditary factors
r A higher incidence of CHD in siblings suggests heredity as an important factor.
t The strongest familial tendency is known in ASD associated with bony abnormalities (Holt oram syndrome)
(ArrMs os)
,

i*.*:ir€;l::;r:ii# |.=i:j ',:ep.s .-. .. .:.;.,.. ..."-. ..,.Fr::#:t$ir'.:3ir#


..Syndrome, ., ,' ' . :,'::: Arsociatedcongenitalcardiovas(ulardisease ,. ',
Holt-oram syndrome ASD (most common), 1't degree heart block

Down'ssyndrome{trisomy2l} Enidocardlatcushiondefect{Atse){atypeofASD),VSDIOF
Turner syndrome Bicuspidaorticvolve (mostcommon)@NB13),asarctotionof aortq(2d MC)6,tMs08), AS, MVP

ttlaonan syndrome

William syndrome Suprava lv ular AS(il ee, Bra nch P5, hypercalcem ia

Marfan syndrame Aortic root dilatation

Edward syndrome VSD (most common), PDA

Apeftqtndrome ' VSD

Cri-du chat syndrome VSD

Osteogenesis imperfecta AR

B) Environmentalfactors
I Those who have an inherited tendency, develop CHD due to unfavorable environmental factors.
I of these the most well known is high altitude -> There is higher incidence
of pDA and ASD in children born
at a high altitude.

Phenytoin Pulmonary stenosis, Aortic stenosis, Aortic .our.t..Uon, pOn


Alcohal .
VSD, PDA, ASD, TOF
Rubello PDA (most common)NlEn, PS (2d 6s/nerr), VSD (3td
mcyNEEr)
Valproate : '. ASOVSqAS.PA,COA . -,,,
tnfant of diabetic mother TGA, VSD, COA, PpHN, Cardiomyopathy
Lithium Ebstein anoma$AilMl e),Tricuspidatiesia :
I

NADA's criteria
o The Assessment of a chird
for the presence or absence of heart disease can be done with the help of some guidelines
suggested by NADA. These guidelines are called NADAs
criteria(At )3, Arrfts e7)

* Systolic murmur, grade lll or more, * Systolic murmur < grade lll
especially with thrill
a Diastolic murmur o Abnormal 2ndheart sound
o Abnormal ECG
& Cyanosis * Abnormal X Ray
& Congestive cardiac failure o Abnormal Bp

Presence of one maior or two minor criteria are


essential for indicating the presence of heart disease,

cLASStF|CAT|ON qESOryCENtTAL HEART DTSEASES

o Congenital heart diseases are divided into two main


groups :_
1) Cyanotic
2) Acyanotic
o Each group is further subdivided accroding to :_
i) Pulmonary blood Jlow : Decreaserl (origemia), increased (prethora) or normal.
ii) Dominated (hypertrophied) ventricle: Right, or left.
A) Cvanotic CHD's
o These are characterized by presense of cyanosis.
cyanotic cHDs are :-
1) Increased pulmonary blood flow (pulmonary pletfi61a(arr:1
i) Left venh'icular or both ventricular hypertrophy: Persistant
truncus arteriosus; single ventricle;
TGA+VSD.
ii) Right ventricularhypertrophy:TGA;TAPVR (total
anomalous pulmonaryvenous return); hwoplastic
1eft heart.
2) Decreased pulmonary blood flow (pulmonary oligemia)
i) Both ventricle hypertrophy: TGA + PS; Persistent truncus
arteriosus with hlpoplastic pulmonary
artery; single ventricie with pS.
ii) Left ventriclehypertrophy : Tricuspid atresia(Al13, pcrse, Reraro r%
pulmonary atresia with hypoplastic right
ventricle.
iii) Right ventricle hypertrophy :ToF;Eisenmenger's syndrome;
Ebsteins urro..ruty.
r Of these the most well known k high altitude -+
There is higher incidence of pDA and
ASD in children bor,
at a high altitude.

Phenytoin Pulmonary stenosis, Aortic


Alcahol VSD PDA, AsD,TOF
Rubella PDA (most com6gn)tNEEr), pS (2nd mc1{nee\, VSD (3td
111syxrcrt
Valproate ASD, VSD, AS, PA, COA
lnfant of diabetic mother TGA, VSD COA, ppHN, Cardiomyopathy
Lithium Ebstein onomal/An[s s7),
Tricuspid atresia

NADA's criteria
t The Assessment of a child
for the Ttresence or absence of heart disease can be done with the herp
suggested by NADA, These guidelines are of some guidelines
called NADAs criteria,r 13,AnMse7)

Abnormal 2nd heart sound


& Abnormal ECG
& Cyanosis
Abnormal X Ray
& Congestive cardiac failure
Abnormal Bp

Presence of one maior or two minor criteria


are essential for indicating thepresence
of heart disease.

CLASSIFICATION OF CONGENITAL HEART


DISEASES
r Congenital heart diseases are divideci into two
main groups :_
1) Cyanotic
2) Acyanotic
r Each group is further subdivided accroding
to :_
i) Puimonary blood Jraw : Decreased (oligemia),
increased (plethora) or normal.
ii) Dominated (hypertrophiecl) ventricle: Right, or
left.
A) Cyanotic CHD,s
o These are characterized by presense of
cyanosis. cyanotic cHDs are
1) Increased pulmonary blood flow (pulmonary plslfrslarerr:.); :-
i) Left ventricular or both ventricular hypertrophy: persistant
truncus arteriosus; single ventricle;
TGA+VSD.
ii) (total anomalous pulmonaryvenous
rerurn);hypoplastic
*,'iT"'::.""ularhypertrophy:TGA;TAPVR
2) Decreased pulmonary blood flow (pulmonary
oligemia)
i) Both ventricle hypertrophy: TGA + PS; Persistent
truncus arteriosus with hlpoplastic pulmonary
afiery; single ventricle with pS.
ii) Lefi ventriclehypertrophy z Tricuspid atresia$I 13,pcree.Ke,,roe%
pulmonary atresia with hypoplastic right
ventricle_
iii) Right ventricle lrypertrophy : ToF; Eisenmenger,s
syndrome; Ebsteins anomaly.
B) Acyanotic CHDS

o These CHDs are characterizedby absence of cyanosis. Acyanotic CHDs are :-


1) Increased pulmonary blood flow (pulmonary plethora(.arI3))
i) Le[t ventricle or both ventricle hypertrophy. ySD(,41r3); pDA.
ii) Rightwntriclehypertrophy i ASD6IIMS03) (often RBBB); PAPVR (Partial anomalous pulmonaryvenous
return).
2) Normal pulmonary blood flow
i) Left ventricle hypertrophy: AS or AR; coarctation of aorta (COA); Mitral regurgitation (MR).
ii) Rightventriclehypertrophy: Pulmonic stenosis (PS);COA (in infants); mitral stenosis (MS).
Axis deviation on ECG
o CHDs maybe associated withleft axis deviation (LAD) or right axis deviation (RAD),depending upon the compartment
hypertrophied.
r Left ventricular hlpertrophy causes LAD, and CHDs causing LVH are : _
i) YsDrez'Mssal |-:l) Endocardial cushion ASD v) Tiuncus arteriosus vIl) Pulmonary a1resia@nMses)
ii) PDA iv) COA (in older children) vi) Tricuspi d atr e s i aaII Ms e 8)

o Right ventricular hlpertrophy causes RAD, and CHDt causing RVH are : -
i) TGA iii) ToF v) Eisenmenger\ syndrome
ti) TAPVR iv) AgPtdttusstl vi) COA (in infants)

. Most common congenital heort disease. VSD(atee)


t Mo,s;t common irforoti, ,*genital heart disease : VSD
e Most common cyanotic congenital heort diseose i TOFfl,EEII

PATHOPHYSIOLOGY OF CHDs

Acyanotic congenital heart disease


e These are divided into two types :-
A) Left to right shunts
r These are atrial septal defect (ASD), ventricular septal defect (VSD) and patent ductus arteriosus (pDA).
o Patients with Ieft to right shunts have following features : -
1. Frequent respiratory tract infection(AllMs0S) -> Because pulmonary circulation is overloaded which may
result in pulmonary edema, CHF and infection.
2. No cyanosis _) Most of the blood is in pulmonary circulation. So there is no impairment in oxygenation of
blood.
3. Precardial buldge -> Frequent chest infections with tachypnea causes the soft rib cage being drawn inward
at the diaphragmetic attachments of the ribs. This combined with cardioamegaly gives them a precordial
buldge.
4. Hyperkineticprecordium
5. Delayed diastolic murmur in tricuspid or mitral area -+ Due to increased flow through these areas depending
on the type of CHDs.
6. Cardiomegaly with plethoric pulmonary vasculature on chest X-ray -+ Due to increased flow through pul-
monary circulation (plethoric iung) there is increased volume overload to left side of heart -+ Cardiomegaly.
Left atrium is enlarged in these CHDs, except in ASD in which lefi atrium is not enlargediAr oe).
B) Obstructive lesions
o These are pulmonic stenosis (PS), aortic stenosis (AS), and coarctation of aorta (COA).
r Obstructive congenital diseases have following features :-
1' Absence offrequent chest infection{A'Ms0s)
-)purmonary circulation is not overroaded.
2' Absence of cyanosis -) No defect in pulmonary
oxygenation and there is no shunt where
blood can mix. arterial and venous

3' Absence of precardiar buldge -+ There is no chest infection or cardiomegaly.


4' Heaving (forcible) cardiac impulse -+ obstructive
lesions cause concentric hypertrophy
produce forcibie contraction. of ventricles that

5. systolic thrill due to systolic ejection murmur


-> \Arhen hl.pertrophied ventricles forcibly pump the blood
through stenotic pulmonary or aortic valve,
systolic thrill and.yr,olr. ejection murmur
are produced.
6. Absence of delayed diastolic murmur in
mitral or tricuspid area -)Blood flow through
increased. these area is not
7. Presence of delayed corresponding second
sound (A, in AS and p2 in ps) -+Because prolonged
these area results in delayed closure ofthat flow through
valve.
8. Normal sized heart and pulmonary vasculature
in chest x-ray-> There is concentric hlpertrophy,
pertrophy without dilatation. So, heart size is i.e., hy-
normal on x_ray.
Cyanotic Congenitial heart diseases
o Cyanotic CHDs are Right to Left shunts.
o These are further divided into : _
1) Cyanotic CHD with decreased pulmonary
blood flow.
rThis group includes -+ ToF, Pulmonary
atresia with intact se|ttutn, tricuspid
atresia, total anomalous pul-
monary venous return with obstruction.
r These lesions have following components
: _

a) obstruction to puimonary blood flow at tricuspid


right ventricular or pulmonary valve level.
b) A pathway by which systemic venous blood enters
the systemic circulation via a patent foramen
ASD or VSD. ovale or
r Degree of cyanosis depends on the
degree of obstruction to pulmonary
brood flow :
i) Mild obstruction -) cyanosis is precipitaed by
stress, but may be absent at rest.
ii) olood flow is dependent on patency
::,X ",Y::l':: :, 1",,i:"*,
ductus closes (10-21 days), the neonate experience
of the ductus arteriosus. when the
profound hypoxemia, cyanosis and
r These diseases do not have frequent chest infectionas pulmonary shock.
circulation is not overloaded.
2) Cyanotic CHD with increased pulrnonary
blood flow.
r This group of lesions is not associated with obstruction
to pulmonary blood flow.
: Cyanosis caused by anv of the following mechanisms.
u connection (e.g
, Transposition of great vessels6rr^sos))-+ rn
ti:'::j"1'.lll,'!Y' .,'rterial brood.retir.ni"; ff;-';il;;;;;*,.;;::H:ffffiT,:
this, aorta arises

[:Ti:J::'::'::.-""-':i:y,']li"'.*":"
the body, and oxygenated brood returning from
rung is pumped
I ruur ro Pu

back into the rungs.


ii) btoad (e.g., totat anomatous
i#,I::X,,r,::t:,:':-::,'^:.' ':o !"'*onctry.venous Ttutmonary yenous

:.::,:,:^::::'::"?: :'::,:ilo i*'a -Ir putmonarv btood rtow ,' ",;,;:;;;;;,";;:r,;;":;:il:::


cyanosi nlon,
cyanosis alone.
e
;;;;;;;;;;,";;,;,:"ff;:';:;
t Tftese diseases are chatacterized by frequent chest infections(ArrMs Bs)as
pulmonary circulation is overloaded.

ATRIAT SEPTAL DEFECT (ASD}

o ASD is an abnormal communication


between the trvo atria. There are two
types of ASD:-
1) Ostium secundum (most comm ontArls,AilMS81))
rIt is generally located at fossa avalis, but may
aiso be superior or posterior to
fossa ovalis.
2) Ostium primum (endocardial cushion defect)
r It is situated inferior to fossa ovalis. It associated with cleft in the anterior leaflet of mitral valve, with or without
a

a cleft in the septal tricuspid leaflet. It is the most common CHD in Down syndrolrrreulls).
r ASD is more common in females than males.
o lmportant syndromes associated with ASD are :-
t Holt - oram syndrome@t1s'PGI0L) t Thrombocytopenia absent radius (TAR) slfldrome(Pctot)
t Down slndromsedot) t Pierre Robin syndrome
t Ellis-van crevald syndromeecl 01 ) s Ehler Danlos syndrome
t Rubinstein - Taybi syndrome t Fetal alcohol syndrome
Hemodynamics of ASD
o There is abnormal connection between left and right atrium, which is due to defect in atrial septum.
r Blood flows from left atrium to right atrium because left atrium has slightly higher pressure than r@t atrium@I e7)

+ Left to right shunt6arMs8l).


o Because the pressure difference between two atria is small, blood passes at a narrow pressure difference -+ No shunt
e& PGr oe).
murmurar
r There is volume overload to right atrium because ofleft to right shunt-+Right atrial dilatation and hypertrophy(or00).
o During diastole large amount of blood passes from right atrium to right ventricle through tricuspid valve -+ delayed
diastolic murmur and accentuation of first heart sound.
r Volume overload to right ventricle -+ Right ventricular hlpertrophy that produces parasternal heeve('{ror, e8).
o Large blood volume passes through pulmonary valve *> Pulmonary ejection systolic murmur.
o Prolonged blood passage along pulmonary valve causes delayed closure of pulmonary valve -+ P, is delayed and
accentuated, wide split anilfixed S2are8),

o Increased blood flow through pulmonary circulation -+ Pulmonary plethora that may cause pulmonary
otr.
hYPertensisnrar
o The left atrium is not enlargedal 11' 06)
because it decompresses itself by shunting blood to right atrium at a minor
difference in pressure. The left atrium may enlarge once Eisenmanger's syndrome develops and a reversal of shunt is seen
across the defect.
Clinical manifestations of ASD
r Patients with ASD are generally asymptomatic.
o Mild effort intolerance and respiratory tract infection may occur.
: CHF is rare.
o Infective endocarditis is very rare in ASDNEID.
r Complications usually develop in 4'h decade and include pulmonary hypertension, strokeNEEr), right sided HF and
Eisemmenger's syndrome.
Physical examination
o Parasternal impulse
r Systolic thrill at 2dleft interspace.
o Accentuation of S, due to loud tricuspid component.
o Wide split andfixed S2euoe'AltMsa3).

o Ejection systolic murmur at the second anil thirdleft interspacesallMs0s).


o Delayed diastolic murmur at the lower left sternal border.
r ASD with mitral stenosis -+ Lutembacher syndrom e@NB ls' AIIMS06).
t There is riglrt axis deviation on ECG in usual osteum secundum type of ASD(PGI 0e)
. Ostium primum type of is associated
PGI0e)
with lefr axis deviation4lMso3' due to maldevelopment of anterosuperior division of left bundle branch (LBB).

Chestx-ray in ASD
o Mild to moderate cardiomegaly o Prominent pulmonary artery segement.
c Right atrial and right ventricular enlargement c Relatively small aortic shadow{NBgr)
t Plethoric lungfields. o Normal left atrium@IlMs t' 06, 01)
1
r It is situated inferior to fossa ovalis. It associated with a cleft in the anterior leaflet of mitral valve, with or without
a cleft in the septal tricuspid leaflet. It is the most common CHD in Down syndrome(Arls).
r ASD is more common in females than males.
o Important syndromes associated with ASD are :-
t Holt - otam sYndrome4l 1s'PGIol) t Thrombocytopenia absent radius (TAR) sffld.rome@cl ot)

: Down sfndrotns@etot) t Pierre Robin syndrome


t Ellis-van crevald syndromeecl 01)
s Ehler Danlos syndrome
t Rubinstein - Taybi syndrome t Fetal alcohol syndrome
Hemodynamics of ASD
o There is abnormal connection between left and right atrium, which is due to defect in atrial septum.
r Blood flows from left atrium to right atrium because lefi atriumhas slightly higher pressure than right atrium(Ale7)
-+ Left to right shunta[Ms8r).
o Because the pressure difference between two atria is small, blood passes at a narrow pressure diference -> No shunt
murmurare& PGroe).
o There is volume overload to right atrium because of left to right shunt-+Right atrial dilatation and hypertrophy(Arm).
o During diastole large amount of blood passes from right atrium to right ventricle through tricuspid valve -+ delayed
diastolic murmur and accentuation of first heart sound.
o Volume overload to right ventricle -+ Right ventricular hypertrophy that produces parasternal heeve@r01'e8).
o Large blood volume passes through pulmonary valve -> Pulmonary ejection systolic murmur.
o Prolonged blood passage along pulmonary valve causes delayed closure of pulmonary valve -> P, is delayed and
accentuated, wiile split andfixeil S2aIeB).

r Increased blood flow through pulmonary circulation -+ Pulmonary plethora that may cause pulmonary
hYPertension6ror).
o The lefi atrium is not enlarged@I 11' 06)
because it decompresses itself by shunting blood to right atrium at a minor
difference in pressure. The lefi atrium may enlarge once Eisenmanger\ syndrome develops and a reversal of shunt is seen
across the defect.

Clinical manifestations of ASD


o Patients with ASD are generally asymptomatic.
o Mild effort intolerance and respiratory tract infection may occur.
c CHF is rare.
c Infective endocarditis is very rare in ASD@Exr).
r Complications usually develop in 4s decade and include pulmonary hypertension, stroke@EEr), right sided HF and
Eisemmenger's syndrome.
Physical cxamination
o Parasternal impulse
o Systolic thrill at 2d left interspace.
r Accentuation of S, due to loud tricuspid component.
o Wide split and fixed S
r{PGr
0e' AIrMs 03)
.

o Ejection systolic murfiiur at the second and thirdleft interspacesalrMs03).


r Delayed diastolic murmur at the lower left sternal border.
r ASD with mitral stenosis -+ Lutembacher syndrom e@NB ts' AIIMS06).
t There is rigfut axk ileviation on ECG in usual osteum secundum type of Aspteet ot . Ostium primum type of is associated
withlefi axis deviationqltMso3'PGI0e) due to maldevelopment of anterosuperior division of left bundle branch (LBB).

Chest x-ray in ASD


c Mild to moderate cardiomegaly c Prominent pulmonary artery segement.
. Right atrial and right ventricular enlargement c Relatively small aortic shadow(NBBr)
o Plethoric lungfields. t Normal lefr atrium@IlMs 11' 06' ot )
r It is situated inferior to fossa ovalis. It associated with a cleft in the anterior leaflet of mitral valve, with or without
a cleft in the septaltricuspid leaflet. It is the most common CHD in Down slndromsrdrs).
o ASD is more cotwnon infemales than males.
o Important syndromes associated with ASD are :-
t Holt - oram syndrome@Ils'PGIo1) s Thrombocytopenia absent radius (TAR) syndromeecl0l)
t Down Slndromseetot) s Pierre Robin syndrome
t Ellis-van crevald syndrome@Gl 01 ) t Ehler Danlos syndrome
t Rubinstein - Taybi syndrome t Felal alcohol syndrome
Hemodynamics of ASD
o There is abnormal connection between left and right atrium, which is due to defect in atrial septum.
e7)
o Blood flows from left atrium to right atrium because lefi atrium has slightly higher pressure than right atrium@I
+ Left to right shunt6rMs8r).
o Because the pressure difference between two atria is small, blood passes at a narrow pressure difference -) No shunt
98, PCI oe).
murmur(Ar
o There is volume overload to right atrium because of left to right shunt+Right atrial dilatation and hlpertrophy{eroo).
o During diastole large amount of blood passes from right atrium to right ventricle through tricuspid valve -+ delayed
diastolic murmur and accentuation of first heart sound.
o Volume overload to right ventricle -+ Right ventricular hypertrophy that produces parasternal heeve(Aror' e8).
o Large blood volume passes through pulmonary valve -+ Pulmonary ejection systolic murmur.
o Prolonged blood passage along pulmonary valve causes delayed closure of pulmonary valve --> P, is delayed and
andfueil S2('ue8).
accentuated, wide split
o Increased blood flow through pulmonary circulation --> Pulmonary plethora that may cause pulmonary
oI).
hypertension(Ar
o The lefi atriuffi is not enlarged(At 11' 06)
because it decompresses itself by shunting blood to right atrium at a minor
difference in pressure. The lefi atrium may enlarge once Eisenmanger's syndrome develops and a reversal of shunt is seen

across the defect.


Clinical manifestations of ASD
o Patients with ASD are generally asymptornatic.
o Mild effort intolerance and respiratory tract infection may occur.
t CHF is rare.
t Infective endocarditis is very rare in ASD(dEET).

r Complications usually develop in 4th decade and include pulmonary hypertension, strokeNnnr), right sided HF and
Eisemmengert syndrome.
Physical examination
o Parasternal impulse
r Systolic thrill at 2"d left interspace.
o Accentuation of S, due to loud tricuspid component.
o Wide split andfixed Sr{PeIqe'AIIMSo3).

t Ejection systolic murmur at the second and third left intetspacesqllMs


os)
.

o Delayed diastolic murmur at the lower left sternal border.


o ASD with mitral stenosis -+ Lutembacher syndrome@NB1s'AllMs06).
t TherekrightaxisdeviationonECGinusualosteumsecundumtypeofASDecroe).Ostiumprimumtypeofisassociated
with lefi axis deviation@IlMs 03, PGI 0e) due to maldevelopment of anterosuperior division of left bundle branch (LBB).

Chestx-ray in ASD
t Mild to moderate cardiomegaly o Prominent pulmonary artery segement.
t Right atrial and right ventricular enlargement c Relatively small aortic shadow$EB?')
t Plethoriclungfields. o Normal left atrium4ilMs 1' 06' ot )
1
Fluoroscopic examination shows vigorous pulmonary pulsations due to increased pulmonary
blood flow called as ,Hilar dance slgn(et tst or Great Hilar Dance sign,.
Note r Hilar dance sign may be seen in other left-to-right shunts, but it is typically described in
relation to ASD.

VENTRICT.|LAR sEPTAL DEFECT (VSD)

o vsD is the most common congenital heart diseaseal se). 'fhere is a communication between two ventricies. VSD mav
be located at :-
i) Membraruous part of interventricular septum (called membranous VSD) : Most commot 6t t3,ArrMssz).

ii) Muscular septum (muscular VSD).


o VSD is more commofl infemales.

Hemodynamics of VSD
o A vsD results in shunting ofoxygenated blood from left to right because
left ventricle has more pressure than right
-+ Left to right shunt(Arr3).
I Blood flow from Ieft to right ventricle due to high pressure gradient -+ Pansystolic
murmur and systolic thrill(Arr3).
r Because Ieft ventricle starts contracting before Right ventricle, pansystolic murmur starts early -+ Masking
of S,.
o This pressure gradient is maintained throughout the systole pansystolic
murmur lasts long -+ Masking of Sr.
e Towards the end of systole, the declining left ventricular pressure
becomes lower than aortic --> Early closure of Ar.
o Left to right shunt occurs during systole at a time when the right ventricle
is also contracting, therefore left to right
shunt streams to pulmonatY artery more or less directly -+ No volume overload
-+ Rightventricle size remains
normal.
o Increased blood flow through pulmonary valve -+ Pulmonary ej ection
systolic murmur and delay & accentuated pr.
o Early closure of A, and delayed closure of P, cause -+ Widely split s2(Ar,3) (But
this is usually masked by pansvstolic
murmur).
o Larger volume reaches the ieft atrium + Left atrial hypertrophy(eii:r.
c Increased blood flow through mitral valve Accentuated S, (But it is masked
-) by pansystolic murmur) and delayed
diastolic murmur.

o Ejection systolic murmur of pulmonary valve can not be separated from pansystolic
murmur.
a The effect of ejection systolic murmur is a selective transmission of pansystolic
murmur to the upper left
sternal border (pulmonary valve area) --> ln this area ejection characteristic of
this murmur can be recognized
since it does not mask the aortic component of Sr. For the same reason second
heart sound (Sr) can be heard
in the pulmonary area where it is not masked by pansystoric murmur.

Clinical manifestation of VSD


r The patients become symptomatic around 6 to 10 weeks of age.
t At this time CHF may d.eyelop\ilMs01),
o Frequent symptoms -+ Palpitation, dysnea on exertion and chest infections.
o Symptoms of CHF improve and cyanosis develops once pulmonary vascular
resistance increases above systemic
. vascular resistance (Eisenmeneger physiology){Peteo.
Si$ns
o Hyperkinetic precordium with a thrill at the left sternai border.
r Pansystolic murmur at left sternal border.
Sr & S, are masked by pansystolic murmur maximum intensity of murmur is at
' 3.d, 4,h or 5th left interspace.
t S, can be make out at pulmonary area (upper left sternal border) where it is not masked by pansystolic murmur -+
S, is widely spliy'Al )3) with accentuation of pr.
r S. may be audible at apex.
r A delayed diastolic murmur in mitrai area.
r Pulmonary systolic ejection murmur in pulmonary area.
Clllprnq 4
Course and complications
o 70 to 80% of all vsDs become smaller in size rtr disappear
si*tultaneously, i.e. spontaneous crosure of vSp1o,*ssz;
Large VSD may have some complication :
i) Infective endocarditis@Glss)
ii) Pulmonaryhypertension
iii) cHF
iv) Aorticregurgitation.
o vSD is the mast cafitmofi crtngenital heart defect complicated
by infective endoc(trditis6rrMsez).
Chest x-ray in VSD
o Increased pwlmorcarl, v ast ulature (pulmonary plethorq)Grrus sz:.
o Left atrial enlargement1l lt).
o Cardiomegaly if defect is large"
o Normal to smali aorta.
e Normal size heart it. ciefect is small.

This chest X,ray is suggeeting tle diagno$is of -


a) ASD b) VSD
C) TOF d) PDA
Ans, is'b'i,e., YSD
r '',The X-rayis showing cardiornegaly involving left ventricre with increased pul_
monary vasculature (pulmonary plethora) as suggested by
the size nrra m.r"u..a
number of end on vessels in lung fields + Diagnosis is ViO.

PATENT DUCTUS ARTERIOSUS

c Patent ductus arteriosus is a communication between the pwlmonary


@rtery and aorta(N}Er).
o The ductus arteriosus is present in fetal life which connects
p,rlmonary trunk to aorta. It closes functio.gaily
and
anatomically soon after birth.
t 'Functional closure' takes place within 15 hours of birth.
Anatomic clasure' of ductus qrteriosus acctffs N-21
days
sfter birthataat.
c Prostaglandins maintain the patency of ductss{.rt oot.

a Thepersistenceaffunctionofductttsarteriosus beyond24hoursafterbirthisconsidere|aspDAinterm,eanate,i.e.if
functional closure does not take place in 24 hours afier birth, it is considerecl as pDA.
r The aortic attachment of ductus arteriosus is just distal
to subclavian artery.
o PDA is more cammon infemales than in males(Aros).

Hemodyrramics of pDA
I In PDA blood flows from aorta to pulmonary artery because
aortic pressure is higher than pulmonary artery pressure
-+ Left to right shunt.
e Pressure gradient between aorta and puhnonary artery
is maintained throughout the cardiac cycte (cluring
systole and
diastole) -> continous murmur, i.e., murmur starts in systole
after s, and reaches a peak at s2. It then dimi'ishes
and audible only a part ofdiastole.
r Larger biood volume passes through pulmonary circulation (blood
from right side of heart plus some blood from
aorta) -+ Fulmonary plethora which may cause pulmonary
h1p ertensionKetuta 00 ).
o Increased flow after passing through lung reaches the left
atrium and causes volume overload + Left atrial
dilatation
and hypertrophy.
c Increased blood volume passes from ieIl atrium to left ventricle
through mitral vaive, i.e., increasecl flow through mitral
valve -+ Accentuation of Sl and delayed diastolic
murmur.
System
r Left ventricle recieves larger amount
of blood that results in vorume
overroad -+ Left ventricre enrargement.
'"T:,;'".ff;:il:iffii*".t:#::r;.Tffs;:H":*rticvarvewhichmavcroseevenafterpurmonary
ur r* varves,' -> raradoxical spliting
A, occurs before pr). of Sr, i.e.,
{ occurs after p, (Normally
t left ventricular volume ejected
into the aorta resulrs in diratation
:fli: of the ascending aorta + Aortic ejection
" passes through normal aortic valve -+
Aortic ejecrion systoric murmur (bur
:;:il:JrTr:.Tl;o it is masked by
Clinical manifestations of pDA
c Patient may be asymptomatic
r Symptoms develop early and CHF
may develop at 6 to gth weeks of
e Common symptoms -+ Dysnea age,
on exertion, palpitation and.frequent
chest inf,ections@erataq|).
Signs
o Tachypnea & Thchycardia
o Bounding pulse with wide
pulse pressure (with elevated
systolic and lower diastolic
o Hyperkinetic cardiac impulse pressure).
o Systolic or continuous thrill.
o Accentuated S,
t split of s' (But it may be masked
by continuous murmur since
X;H:.T:, maximum intensity of conrinous
"",U1
o Continous (machinery) murmur -> Murmur starts after
S, and reaches the peak at
audible only during a part of the sr. It then diminishes and is
diastole' Murmur is best heard at second reft
below left clavicle. irntercostal space and is arso
heard
o S, may occur at apex followed
by a delayed diastolic murmur.
Differential diagnosis
o 'Small'Aor topulmonary window
defec{AIIMSll) has symptoms
similaT fs pl)1{.aaus0r). Aortopurmonary
is an abnormar communication window defect
between ascending aort) ana
mati:in, purmonary artery.
Course and comptications of pDA
c spontaneous closure of PDA does
not usually occur infull infants
because pDA in term infonts
abnormality of ductal smooth muscles resultsfo,rm structural
(In premature infants spontaneous
infants results from unresponsiveness crosure may occur because pDA in these
to oxlgen){euus t0, 06, es,Kerata 00).
o Pulmonary vascular pressure
regress slower than normal and
maximum decrease occurs around
at 1-3 weeks). 6-g weeks (normary
o Common complications are _
:
i) ctlp -> MC complication and MC cause of
deathar 13,NEE)).
ii) Infective end.ocayfllslsrNrnr) --y 2nay6 cause
of death.
iii) Aneurysm of pDA _+ Rare and possible rupture in adult life.
iv) Pulmonary hypertension.
v) Pneumonia (6
frequent chest infections)(Kerata00).
vi) Eisenmenger syndromeNEED.

Management of pDA
r NSATDs (most commonly indomethacin)^'ttusoalare
used to induce crosure of pDA,
of prostaglandins,llMs 06) (Prostaglanding as these drugsinhibit synthesis
oot).
are involved in maintainance of patency of
ductus arteriosus@rrMs 04, ss,Ar
o If indomethacin is not successful
and the duc hemodynamically significant,
without division of ductus should surgical ligation{Aros.) yri16 o,
u. p.rro.-'JJ.remains
r Left ventricle recieves larger amount of blood that results
in volume overload -+ Left ventricle enlargement.
o Extra volume passes through aortic area
cause delayed closure of aortic
valve which may close even after pulmonary
valve (normal pulmonaryvalves close
after aortic valves). -+ paradoxical spliting
of Sr, i.e. A, occurs after p, (Normally
A, occurs before pr).
t left ventricular volume ejected into the aorta
results in dilatation of the ascending
Hi: aorta + Aortic ejection

' through normal aortic valve -+ Aortic ejection


systolic murmur (but it is masked by
*|,.J:J.T;#|..]'passes
Clinical manifestations of pDA
o Patient may be asymptomatic
o Symptoms develop early and CHF may develop
at 6 to gth weeks of age.
r Common symptoms -+ Dysnea on exertion, palpitation andfrequent
chest infectior.ts(Keratao0),
Signs
r Tachypnea & Thchycardia
r Bounding pulse with wide pulse pressure (with
elevated systolic and lower diastolic
pressure).
o Hyperkinetic cardiac impulse
r Systolic or continuous thrill.
e Accentuated S,
o Narrow or paradoxical sPlit of s, (But it
may be masked by continuous murmur
since maximum intensity of continous
murmur occurs at S,).
o continous (machinery) tnurmur -+ Murmur
starts after S, and reaches the peak
at Sr. It then diminishes and is
audible only during a part of the diastole.
Murmur is best heard qt second lefi intercostal
space and is also heard
below left clavicle.
c S, may occur at apex followed by a delayed diastolic murmur.
Differential diagnosis
o 'Small' Aor topulmonary window defect(AllMs 0t)
has symptoms similay fs ppn{lrmsoi). Aortopulmonary
is an abnormar communication between ascending window defect
aori and main purmonary artery.
Course and complications of pDA
o spontaneous closure of PDA does not usually
occur infull infants because pDA in term
infants resultsfotrm structural
abnormality of ductal smooth muscles (In premature
infants spontaneous closure may occur
infants results from unresponsiveness to oxygen)@rrMs 10, 06, es, Ke;h 00). because pDA in these

t pressure regress slower than normal and


maximum decrease occurs around 6-8 weeks (normally
:Ji:T..lJascular
o Common complications are: _
i) CHF -'> MC complication and MC cause of death(Ar13,NEEI).
ii) Infective endocarditis@EED __s 2naylgcause of
death_
iii) Aneurysm of pDA -+ Rare and possible rupture
in adult life.
iv) Pulmonary hypertension.
v) Pneumonia (6 frequent chest infections)(Kerota00).
vi) Eisenmenger syndrom4NElt ).

Management of pDA
r NSATDs (most commonly indomethacin)^ilMs06)
are used to induce closure of pDA,
as these d^tgs inhibit synthesis
of prostaglandiflsallMs 06) (Prostaglanding
are involved in maintainance of patency
oo)). of ductus arteriosus'rrMs 04, es, Ar

o If indomethacin is not successful and


the ductus remains hemodynamically significant,
surgical ligation(Ar's) with or
without division of ductus should be performed.

h.

I
&, fl
fhe X-ray isrsuge*tive- of irhi{h CI{D , .
a) ' ppA,:"' 1.

b)',, :,.,, T1{PVC,,', t .

c) .''TOF ''r .

d) 'TGA,'''
Ans. is,lql i,e;;,PDi!l

r This,chest'X"r:rv is $owing enlargement of aofta with,prominent aortic knuck-


le,withrlarge main pulmonaryrartery,and increased pufmonaryvasculature -+
DiagnosisisPDA.l . -

TETRALOGY OF FALLOT
r TOF is the commonest cyanotic congenital heart disease@EEr).
o It has four components :-
06' NEEI' PGt 04)
i) VSDaI 13'

ii) Pulmonic stenosisal 13,06)


1i1) Overriding or dextroposed aorta4l 13' 06' NEEI' AITMS 07)

iv) Right ttentricular hypertrophy@I 13' 06' AIIMI 07).


o Pulmonicstenosis(rightventricularoutflowobstruction)ismainlyduetoinfundibularstenosis@Ecr,AltMsoT).Obstruction
at pulmonary valve level (vah'ular stenosis) is very uncommon (only 10%o).

'Pentology of fallot'consists of components of TOF plus atriol septal defect4t tl,07,AttMslo).

Hemodynamics of tetrology of fallot


o ThedirectionofflowisdeterminedbyseyerityofobstructiontorightventricularoutJlow(infundibularpulmonicstenosis).
o Most of the time there is significant obstruction, resulting in :-
i) Enjection systolic mufmur at pulmonary area and delay in P
26IIM|
0s)
: due to flow of blood against tesistance
during systolic.
ii) Right to left shun/AIIMS 'sl : As there is resistance at pulmonary level, blood is shunted to Ieft ventricle through
VSD.
11i) There no shunt murmur: As pressure difference across the shunt is low.
iv) CHF does not occur(NEET PGro' r As right ventricle is effectively decompressed by large VSD.
Clinical features
. DysPnea on exertion and exercise intolerance are the most common symptoms.
c Cyanosis and clubbinglPct0e"AIIMSes), Cyanosis usually develops after neonatal period and patients are rarely (if ever)
cyanotic at birth.
c Hypoxic or cyanotic spells (Tet spells),
cSquattinglPcr0e): TOF is the commonest CHD in which squatting is used.
o Normal jugular venous pulse(AIIMS 0s' e8) or slight prominence of 'a' wave
o Normal first heart sound
o Single second soundalrMs 0s' e8) (P is soft and delayed, hence generally inaudible. S, is therefore single and the audible
2
sound is Ar. Since the aorta is anteriorly displaced, A, is quite loud).
o Ej ection systolic murmur@IlMs 0s' e8),
t Parasternal impulse.

There is concentric right ventriculor hypertrophy$'Inses) without ca rdiomegolytAttMsss).


There is no CHFAfiMSes, no rect rrent chest infectionsedoe) and no cardiomegolytAttMssB).

o Chest x-ray shows normal heart sizewith oligaemic lungfields. The heart is boot shaped@NB ts) (coeur an sabot)@Elr,
Al0a).'Ihere may be right aortic
arch in 25o/o patients.
o ECG shows right axis deviation, inverted T waye and'P' pulmonale.
i;:9,r,x1gt* :A. ca r di$ 5 cu Ia r sy st e m

Management of TOF
o Management consists of :
A) Medical management : It is mainiy concerned about management of anoxic/cyanotic spells (tat spells)
correction of anemia :-
r Knee chest position r Propranoiol : 0.1 mg/kg/IV
r Humidified oxygen r Vasopressors : Methoxamine IM or IV
r MorphinerPclat) A.l to 0.2 mg/kg subcutaneous inj r Correction of Anaemia.
r Correction of acidosis with sodium bicarbonate TV
w lsoprenaline should be ovoided asitcausesperiphera! pooling of blood@nMsA).

E) Snrrgicalmanagernent:Itconsistsofanastomosingasl,stemicartervwithpuimonaryarterytoincreaseoulmonarr.
biood florv. These shunt are :,
i) Blalock - Taussig shunt -> Subclavian artery - Pulmonary Artery anastomosisur06).
ii) Modifieil Blalock-Taussig shunt: Subclavian-pulmonary artery shunt by Gore-'fer
interposition graft. It is
the most popular procedure at any age@NB 1s).

iii) Pott's shunt -+ Descending Aorta to Pulmonary Artery@rot) (no longer performed).
iv) Waterston's shunl -+ Ascending Aorta to right pulmonary Artery (no longer performed).

The X-ray is suggestive of which CHD -


a) PDA
b) TAPVC
c) TOF
dl rGA

Ans. is t'i.e., TOF


c The given chest X-ray is showing'boot shaped'heart (coeren sabot) -+
charac.
teristic of TOF.

Fallot's physiology
c Group of condition presenting with similar feature of TOF.
e These includes -
1) TOFGIi5) 4) Single ventricle with pS
2) TGA with VSD &Psrerisr 5) Corrected TGA with VSD & pS
3) TA(AI ls) 6) Double outlet right ventricle with pS

TRICUSPIS ATRESIA

c Congenital absence of tricuspid valve is called tricuspid atresia. TA has following


featgres : -
i\ Absence oftricuspid valve.
ii)Hypoplastic right ventricre@Il,s eB) witfu absence of inftow portion of RV.
o So' blood can not flow direciiy from right atrium to right ventricle and following
associatecl defect a-re neccessary fbr
survival : -
x For flow of blood from RA to LA -+ patent foramen ovale or ASD.
r
For flow of blood frorn LV to PJ -+ VSD (VSD is always muscuiar in tricuspid
atresia)
o Therefore blood flow in following direction.
Right atrium

I ThroughASD
Left atrium

I Through nomal mitral valve

Left ventricle
Pulmonary circulation rhroush *rZ\ hroush aortic vatve

Right ventricle Aorta Systemic circulation


Through pulmonary valve
-+
r Tricuspid atresia is classified according to : -
1) Presence or absence of pulmonic stenosis (PS)
2) Presence or absence of TGA (Trasnposition of great vessels).
o In 70 of cases, great arteries are normally related, i.e., pulmonary artery is connected to right ventricle and aorta is
%o

connected to left ventricle.


o In 30 % of cases TGA is present, i.e., Aorta is connected to right ventricle and pulmonary artery is connected to left
ventricle.
r In patients with normally related great arteries, VSD is small and PS is present -+ J Pulmonary blood flow and
pulmonary oligemia.
r When TGA is present, following two defect may be seen : -
i) Normal pulmonary valve (2l3rd of cases) -+ Increased pulmonary blood flow (PBF).
ii) Pulmonic stenosis (1/3rd cases) -+ Decreased PBF.
Tricuspid atresia

Normally related great vessels Transposition of great vessels


(70 o/o) (30 vo)

t +- I

Pulmonic stenosis (PS) present


Normal pulmonary valve PS Present
in all cases
+ +
+ tPrlronury blood flow Jper
JPulmonary blood flow

Haemodynamics
o The inflow portion of R.V. is hlpoplastic
r The systemic venous blood coming to R.A. exits by way of a patent foramen ovale@EBr) or an ASD.
o A VSD provides communication between L.V and outflow portion of R.V
r The L.V. thus maintains both the systemic and pulmonary circulation.
o The saturation of blood in the pulmonary artery and aorta is identical --> Because unoxygenated blood from right
atrium mixes with oxygenated blood into left atrium.
o The pulmonary blood flow is dependent on size of VSD -+ Smaller the VSD, less the pulmoanry bloodJlow@IlMsss).

Clinical features
o Child is cyanotic from birth@101' AIIMS 00)
.

o Anoxic spells and squatting may be present.


I Normal Srand single S26nMSe8'NEEr).
o Murmur (Grade II to grade IV)
Features suggestii'e of tricuspid atreria i .
a) L.V. Qpe of apical impulse
b) Prominent large'a waves
c) Enlarged liver with presystolic pulsations (a waves)
d) ECG characterised by Left axis deviation and Lefi ventricular hypertrophy\EEr. N 01. AI.MS 00, e8)
.

e) There is pulmonary oligemia on chest x-rayNEEr).


EBSTEIN ANOMALY

o Ebstein anomaly consists of downward displacement of an abnormal tricuspid valve into the right ventri-
el, 80)
cle@NB .

c Normally tricuspid valve has three leaflets -+ Anterior, posterior and septal.
r Fixed end ofthese leaflets is attached to valve ring in tricuspid area.
r In Ebstein anomaly, anterior leaflet is attached to valve ring as normal, but the other two leaflets (posterior and septal
are displaced downward and are attached to the wall of left ventricle.
c The portion of right ventricle above he tricuspid valve becomes a part of right atrium -+ atrialized right ventricle.
Hemodynamics
* The tricuspid valve anomaly results in obstruction of blood flow as well as regurgitation of blood from the righ;
ventricle into the right atrium -+ Dilatation and hypertrophy of right atrium@r 15 DNB 12) due to volume overload.
e Blood flows right atrium to left atrium through patent foramen ovale or ASD + Right to left shunt and cyanosis.
Clinical manifestations
o Cyanosis o Fatigue
o Dysnea on exertion o Paroxysmal attacks of tachycardia

Signs
o Cyanosis and clubbing
o Dominant V wave on JVP.
e Systolic thrill at the left sternal border
e S, normal
o S, wides split but variable
c Rightventricular S.
0 Right.atrial 54.
e Systolic murmur due to regurgitation at tricuspid valve.
e Delayed diastolic murmur due to obustruction at tricuspid valve like tricuspid stenosis.
c Both systolic and diastolic murmur produced at the tricuspid valve have scratchy character like pericardial
friction rib.
e Patients with Ebstein anamoly may have accessory conduction pathway causing WPW syndromerA,rs).

The chest X-ray suggests the diagnosis of-


a) PDA
b) VSD
c) Ebstein anomaly
d) ToF

Ane, !rt'i-e'r E_-bf,lianotnali '


o X-ray is showing almost 'box-shaped' heart due to enlargement of right atrium
-+ seen in Ebstein anomaly.

Tffi&&'SPOSITION OF GREAT VESSELS {TGA}

c It is the most common conot-runcal defect(Arls).


o Transposition ofgreat vessels is defined as : -
\\ Notto orismgJ,rom ,right ^'rentric\e.
ii) Pulmonary artery arisingfrom the left ventricle.
c Anatomically TGA is divided into : -
A) Complete variety
r Right atrium is connected to right ventricle and right ventricle is connected to aorta.
r Left atrium is connected to left ventricle and left ventricle is connected to pulmonary artery.
This results in complete separation of systemic and pulmonary circulation : -
i) Blood from pulmonary circulation flow in following direction

Pulmonary artery --------+ Pulmonary circulation -------) Pulmonary veln


(oxygenated blood)

Left atrium <- Left ventricle

ii) Blood from systemic circulation flow in following direction

Systemic circulation -------) SVC & IVC


| (Deoxygenated blood)
Aorta j
I

Right ventricle <- Right atrium

r As oxygenated blood is not available for systemic distribution, survival of the patient depends on the
presence of atrial, ventricular or aortopulmonary communication.

B) Physiologically correctedtype
r Right atrium is connected to an inverted morphologically left ventricle and Ieft ventricle is connected to
pulmonary arterY.
r Left atrium is connected to an inverted morphologically right ventricle and right ventricle is connected to
Aorta.
r So, these patients have normal route ofblood flow except for that, the functions ofright and left ventricles
are interchanged due to Position.
r This type of TGA is associated with other anomalies.
: The hemodynamics and clinical features depend on other anomalies because corrected TGA itself has normal
route of blood flow.

Hemodynamicsof TGA
13' PGI ee).
o ln TGA aorta lies anterior and to the right of pulmonary 4rtery6r
o In patients with TGA the oxygenated pulmonary venous blood recirculates in the lungs whereas deoxygenated
systemic venous blood recirculates in the systemic circulation -> Pulmonary artery saturation is always higher than
aortic saturation (opposite to normal person).
o Because oxygenated blood is not available for systemic circulation, survival depends on the mixing available between
the two circulation.
r So, patientswith TGA can be divided into : -
i) TGA with intact ventricular septum.
ii) TGA with VSD.

i) TGA with intact sePtum


r The mixing of blood depends on atrial communication.
r As patent foramen ovale is very small communication, mixing of oxygenated blood with deoxygenated blood is
ArrMsol'Ato4), and CHF may develop during
inadequate +
Patients are symptomatic and cyanotic at birth(Pcroz
first week.

ii)TGAwithVSD
t Presence of VSp/rctoz'se) of adequate size results in good mixing of blood.
r patients become symptomatic, at 4-8 weeks when fetal pulmonary vasculature regresses maximally -+ CHF
develops at this time.
r The failing left ventricle and large pulmonary blood flow cause increase in Ieft atrial pressure + t back
pressure -> Pulmonary venous hlpertension and pulmonary plethora'
r The presence of a large VSD equalizes the pressure in the two ventricles as well as in two great vessels.
r pulmonary artery carries large flow -+ patients with TGA and large VSD develop pulmonaryvascular obstructive
disease (Eisenmenger physiology) early in life.
eardlouasculsr System

Clinical features of TGA


r Time of presentation depends whether the ventricular septum is intact
or VSD is present.
o Patients of TGA with intact septum are cyanotic at birth, with CHF?GI a7)
occuring in first week -) because adequate
mixing does not occur.
I Patients of TGA with VSD presents :,vith mild cyanosis {tfid Ctrtrf:ecl0r)
occurs in 6-g weeks.
lmportant signs are :-
r Cyanosis o CHF o Eiection systoiic murmur
o Single S, c Normal S,

X-rays
e Cardiomegaly
o Plethoric lungfields
o "Egg on Side'(NEEr) appearance -+ right upper fields appear more plethoric
than other areas.
o Absent thymic shadow.

Management of TGA
o when TGA is suspected, an infusion of prostaglanding E,6t tst (Misopro{Alts),
riaprostil) should be iwitiated to
maintain potency af dwctus arteriosus\t 04, Arr/rs 04) to allow mixing of biood.
a Infants who remain severely hypoxic or acidotic clespite PGE infusion I .r:
should undergo atrial septostomy(lr i.e.
artilrcial ASD to allow mixing of blood. Septostomy is successful only upto
the age c;f 6 -12 weeks.
r Arterial Switch Procedure is the definitive swrgico.l
ltrocedure.In this, aorta and pulm,nary artery are divided and
reanastomosed in correct position. Two arterial switch procedures are
:-
i) Iantene arterial switch procedure (surgical treatment of choice)
ii) Mustard and senning procedure.

The X-ray is suggestive of which CHD -


a) PDA
b) TAPVC
C) TOF
d) TGA

Ans. is'd'i.e., TGA

r The chest X-ray is showing Eg3' on side appearancewhichis characteristic


of
Transposition of great artertes ffG,4).

TOTA L A NO MA LO U S PU LM O NA RY VlN q UIC9 N N ECTI O N (TA PVS)


o Total anomalous pulmonary venous connection (TAPVC) is characterized
by abnormai d.rainage of pulmonary
veins into the right heart either by direct connection into the right atrium
or into its tributaries.
r According to the site or level of connection of the pulmonary veins to the systemic venous system
TApVC has been
classified into four types :-
e Type I (mosf s6tn ','tsn(uos) :45o/o): Anomalous connection at supracardi46lsysl(eros)
(pV drains into left innominate
vein or SVC).
t Type II (25%o) : Anomalous connection at cardiac level (PV joins the coronary sinus or enter right
atrium directly).
I Type III (25%): Anomalous connection at infracardiac level (pV
drain into portal vein).
t Type IV (5o/o) :
Anomalous connection at multiple levels,
e In supracardiac TAPVC the pulmonary ueins join to
form a single trunk (common pulmonary vein) which than
drain through anomalous cannection@I e7),

Hemodynamics of TAPVC
c TAPVC results in the pulmonary venous blood reaching the right atrium which
also receives the systerrtic venous
blood(Ate7).
o This results in volume overload to right atrium -+ Right atrial enlargement.
r I-arger volume of blood reaches the right ventricle + Right ventricle enlargement.
o bloodJlow to the lefi atrium is through patentforamen ovale or ASD(AIe7).
The
o Because there is mixing of unoxygenated blood from systemic circulation and oxygenated blood from pulmonary
circulation in the right atrium -+ The oxygen saturation of blood in pulmonary artery is higher or identical to that
in AortaGIeT).

r TAPVC can be divided into : -


i) TAPVC with pulmonaryvenous obstruction
r Pulmonary venous obstruction results in pulmonary arterial hypertension.
r Because ofpulmonary venous obstruction oxygenated blood cannot reach heart -+ Cyanosis and CHF during
first week of life.
ii) TAPVC without obstruction (more common)
r In TAPVC without obstruction, pulmonary blood flow is high.
r Patients develops CHF at around 6-8 weeks when the fetal pulmonary resistance falls maximally and pulmonary
circulation reaches the maximum.
o Infracardiac type of TAPVC is always obstructive whereas cardiac and supracardiac type may be obstructive or
nonobstructiYeal e7).

X-ray findings of TAPVC


r Cardiomegaly
r Plethoric lung fields
o Snowma.n or figure of '8' configurationNEEr'
AI ee)
-+ In supracardiac TAPVC.
r Ground glass appearance of lung -+ In obstructive TAPVC.

Clinical manifestations of TAPVC


1) Nonobstructive TAPVC -+ Patients presents with mild cyanosis and CHF at 6-8 weeks.
2) Obstructive TAPVC -+ Paients presents with severe cyanosis and CHF within first week.
ECG
o Right axis deviation with right ventricular hypertrophy.
o In obstructive TAPVC'P' pulmonale.

The X-ray is suggestive of which CHD -


a) PDA
b) TAPVC
c) TOF
d) TGA

Ans. is't)'i.e., TAPVC

: ", t'
a l Figqre tof S,appearance (Snowman,sign) is characteristic of TAPVC.

EISENMENGER SYNDROME

o There are two diflerent terms : -


1) Eisenmengersyndrome
r It refers to patients with a ventricular septal defect in which blood is shunted from right to left as a result o'f the
development of pulmonary vascular resistance.
r This physiologic abnormality can also occur with ASD, atrioventricular septal defect, PDA or any other
communication between aorta and pulmonary artery.
ii) Eisenmenger complex
r It consists of pulmonary hypertension with a VSD(Pcroo.) providing the right to left shunt.
o Eisenmenger physiology is defined by an absolute elevation in pulmonary arterial resistance to greater than 12 wood
units or by a ratio of puln'lonary to systemic vascular resistance of > 1.0.
r The pulmonary hr,Dertension is the result of : -
r Early in the course it is due to markdely increased pulmonary biood flow --> Hyperkinetic pulmonary hypertension.
This form of pulmonary hypertension decreases with the administration of pulmonary vasodilators or oxygen.
t With the develapment of Eisenmenger syndrome pulmonary hypertension is due to pulmonary vascular ohstructive
disease, i.e., obstructive chunges in the pwlmonary vessels. This tlpe of pulmonary hlpertension only minimally
responsive to prilmonary vasodilators or oxygen.

Hernodynarni<s of Eisenmenger syndrome


i) If right to left shunt is VSD or PDA
r Rigtrt ventricular pressure cannot go beyond the systemic pressure because, before reaching to that high level,
Right ventricle decompresses into Ieft ventricle.
r So, there is novolume overload to right ventricle.
r But due to pulmonary hypertension there is pressrlre overload + Right ventricular concentric hypertrophy
*'ithout enlargement -+ Only a mild parasternal heave.
ii) If fight to left shwnt is ASD
. . to right to left shunt more blood flows to systemic circulation -+ More venous return to rt atrium -+ Iarger
Dure
amount of blood enters the right ventricle.
r So, there is voiume overload -+ Hlpertrophy with dilatation of right ventricle + Parasternal heave.

Cyanosis in Eisenmenger syndrome


r ln ASD and VSD, the deoxygenated blood reaches the ascending aorta and is thus distributed to the whoie systemic
cii'culation -+ Equal cyanosis of finger and toes.
r trn PDA deoxygenated blood reaches the aorta distal to left subclavian artery. So, upper extrimities receive mixed
'n1ood -+ flifferential cyanosis (Fingers remain pink whereas toes show cyanosis
and clubbing).
t Di-fferential cyanasis is diagnostic of pulmonary arterial hypertnsion with a pDA.

lmpending signs of Eisenmenger syndrome


o tlne should keep in mind that term Eisenmenger syndrome is used most frequently in relation to VSD (Eisenmenger
complex), though it can also occur in other defects also (see above).
r Eisenmenger syndrome refers to patients with a VSD in which blood is shunted from right to left as a result of
l
l

development of pulmonary vascular resistance. Initially shunt is from left to right as the systemic vascular pressure
l

is greater than pulmonary vascular pressure. With time pulmonary vascular resistance increases due to change in
pulmonary vessel wail as a result of increased flow in pulmonary vessels. When pulmonary vascular pressure exceeds
the systemic vascular resistance, reversal of shunt into right to left shunt occurs.
t Tltus, development of pulmonary hypertensian can be assurmed to be a sign of impending Eisenmenger's syndrome.
Signs of pulmonary hypertension are : -
1) Loud' P2ttrrrurs 'ot

ii) Single S2(AIrnIs


10)

11i) Parasternalheaye

iv) Pulmonary ejection click


v) Graham steel murmur (a high pitched decrescent diastolic murmur due ta pulmonary regurgitation)@ntts ro).

Clinical manifestations of Eisenmenger syndrome


. Syrnptoms -+ Cyanosis (Dillerential cynosis in PDA), fatigue, effort intolerance and dyspnea.
o Physical examination
r Cyanosis and clubbing r Parasternal impulse (more in ASD)
: Palpable P, r Wide and fi,xed splitting of S, in ASD
r Pulmonary regurgitation murmur.
r Ejection systolic murmur (pulmonic).

Chest X-ray in Eisenmenger syndrome


1a' AI as)
e Dilateil and Trominent central arteries@IlMs '
10' AI0s).
o Rapid tapering (pruning) of the petipheral pulmonary vasculature(AllMs

o The hilar (central) area suggests pulmonary plethora whereas the peripheral lung fields suggest pulmonary oligemia'

ECG
o tught ventricular hlpertrophy with right axis deviation'

e 'P'pulmonale.

COARCTAtrION OF AORTA
andposterior
r Coarctation of aorta (coA) is a constriction of aorta due to sharp indentationinvofuinganterior,lateral
wall of aorta. The medial wall is spared in the narrowing'
arteriasus
o of coarctation@t se) occur just below the origin of left subclavian occur at the arigin of ductus
9go/o

(luxtaductal coarctation).It may occur just proximal to subclavian artery also.


Mosl
o CoA is the 2nd most common congenital heart disease in Turner syndrome(AIrMses) (after bicuspid aortic valve)"
11' 08' AIIMi eB)
. other associated defects
common associated heart anomaly in coA is bicuspid aortic valve (50-7ao7o1ro' "'
VSD, ASD, TGA, hypoplastic Ieft heart, PDA, and berry aneurysm' When CoA is associated with
are aortic stenosis,
mitral valve abnormality and subaortic stenosis, it is called as shone complex'
a coarctation'
e Malesare afecter3 twice often asfemales although females withTurner syndrome frequentlyhave
e Two classic forms of coarctation of Aorta have been described :-
1) An infantileform with tubular hypoplasia of the Aortic arch\l
ee)
proximal to a PDA that is often asynaptomatic
in chiidhod. (.This is known as coarctation syndrome)'

Z) An,,adult'forru in which there is discrete ridge like in{biding of the Aorta just opposite to ciosed ductus arteriosus'

Hemodynamicsof COA during fetal life


o In fetal life, blood from right ventricle passes to puimonary artery and then to descending aorta through ductus
and left subclavian artery.
arteriosus. Blood from left ventricle passes to Aorta and then to innominate, left carotid
is no
e If constriction (coarctation) is proximal to ductus arteriosus (preductal or infantile coarctation), there
obstruction to flow because constriction is not obstructing the florv of upper limb and lower
limb.+ Collaterals are

not formed.
o Ifthe constriction is distal to tluctus arteriosus (post ductal or adult type coarctation ofaorta), it causes obstruction
circuiation + This
offlow ofdesending aorta, and parts ofbody that are suppiied by descending aorta, have impaired
stimulates formation of collaterals in fetal life'
This collateral circulation
r Collateral circulation connects the proximai and the distal aspects of the vessels over time.
will develop mainlY from the : -
r Subclavian
r Axiliary
07)
s Internal thoracic@rttts
t Superior and infetior epigastric@uMs 07)

r Intercostal arteries
Hemodynamics after birth
r After birth, ductus arteriosus closes, so that blood flow to descending aorta from right ventricle does not occur and
descending aorta must receive its total supply from left ventricle via ascending aorta.
r But there is obstruction due tc coarctation'
-+ Hypertension
r In preductal coarctation, there are no collaterals -+ Neonates become symptomatic imrnediatly
results in CHF.
r In postductal coarctation, due to Presence ofcollaterals neonates are spared
from developing hypertension & cHF.
r Due to obstruction, there is pressure overioad to ieft ventricle -+ Left ventricular
hypertrophy.
Clinical manifestations of CoA
o Symptoms of coarctation of aorta occurs due to decrease
in blood suppty distai to aortic obstru