Kuliah Tk Iugr

8/9/2019 Kuliah Tk Iugr

1/41

Growth & Development

Perinatology Division, Child Health Department,

Medical Faculty of Hasanuddin University


2/41

Defnitions

IUGR: Failure of a pregnancy to reachexpected fetal growth and manifest as adeviation of fetal growth from normalpattern.

SGA: birth weight < 10th percentile forGA or ! " #$s below mean for GA.

LowLow birth weight (LBW)birth weight (LBW)

birth weight < "%00 g which could bebirth weight < "%00 g which could bedue to &'G( or )rematuritydue to &'G( or )rematurity


3/41


4/41

!

&'G( suggests diminished intrauterinegrowth velocity

&'G( indicates the presence of apathologic process in*utero that inhibitsfetal growth

#GA and &'G( are not synonymous

#GA refers to the si+e of the infant atbirth and not fetal growth

IUGR vs SGA


5/41

"

A child who is born #GA is not always&'G(

&nfants born after a short period of&'G( are not always #GA

#GA:

&'G( ,onstitutionally small infant

IUGR vs SGA


6/41

&ntrauterine Growth pattern -

)atophysiology of &'G( Stage I (Hyperplasia)

* to "0 wee/s

* (apid mitosis * &ncrease of $A content

Growth inhibition in stage I

* 'ndersi+ed fetus with fewer cells. * ormal cell si+e.

(esult in sy!!etri" IUGR#


7/41

Growth inhibition in stage I #ymmetric &'G(

Associated conditions:

* Genetic

* ,ongenital anomalies

* &ntrauterine infections

* #ubstance abuse

* ,igarette smo/ing * herapeutic irradiation


8/41

Intra$terine Growth pattern %

&atophysiology o'IUGR Stage II (Hyperplasia % Hypertrophy) * "0 to "2 wee/s

* $eclining mitosis.

* &ncrease in cell si+e.


9/41

Stage III ( Hypertrophy)

* "2 to 0 wee/s

* (apid increase in cell si+e. * (apid accumulation of fat muscle

and connective tissue.

3%4 of fetal weight gain occursduring last "0 wee/s of gestations.

Intra$terine Growth pattern %

&atophysiology o' IUGR


10/41

Growth Inhibition in Stage IIIII

*$ecrease in cell si+e and fetal weight

* 5ess e6ect on total cell numeric fetallength head circumferance.

(esult in asymmetric &'G(.

Associated ,onditions:

* 'teroplacental insu7ciency.

8 ,ombination above associated mixed type&'G(.

&atophysiology "ont*


11/41

+ypes o' IUGR

Sy!!etri" IUGR 9 4 of &'G( &nfants;: weightlength and head circumferenceare all below the 10th percentile.

Asymmetric &'G( 9%% 4 of &'G(; :

weight is below the 10th percentileand head circumference and length arepreserved

,ombined type &'G( 91" 4 of &'G(; : &nfant may have s/eletal shorteningsome reduction o soft tissue mass.


12/41#$

SymmetricaSymmetricall AAsymmetricalsymmetrical

In a normal infant, the brain weighs about three times more than the liver. InIn a normal infant, the brain weighs about three times more than the liver. In

asymmetrical IUGR, the brain can weigh five or six times more than the liver.asymmetrical IUGR, the brain can weigh five or six times more than the liver.

Types of

IUGR

Baby's head and body are

proportionately small

ay occur when the fetus

experiences a problemduring early development

Baby's head and length are

preserved

!ccur when the fetus

experiences a problem laterin pregnancy


13/41#

Symmetric IUGR

Type I

arly onset growthrestriction

'niform growthrestriction 5ong*term growth

failure Associated with

decreased cellnumber

Associated with lesscatch*up growth inthe =rst year of life

Asymmetric IUGR

Type II

5ate onset growthrestriction

>ead #paring )otentially reversible

Associated withdecreased cell si+e

&nfants demonstratemore catch*upgrowth thansymmetric &'G( in=rst year of life

Types of

IUGR


14/41

,tiology

-) .etal 'a"tors Genetic Factors:

* (ace ethnicity nationality

* sex 9 male weigh 1%0 *"00 gm more thanfemale ;

* parity 9 primiparous weigh less than

subse?uent siblings;

*genetic disorders 9 Achondroplasia (ussell *

silver syn.; ,hromosomal anomalies:

* ,hromosomal deletions

* trisomies 112 - "1


15/41

,ongenital malformations:examples:Anencephaly G& atresiapotter@s syndrome andpancreatic agenesis.

Fetal ,ardiovascular anomalies ,ongenital &nfections:

mainly (,> infections. &nborn error of metabolism:

* ransient neonatal diabetes* Galactosemia* )B'

,tiology"ont*


16/41

/) 0aternal .a"tors

$ecrease 'teroplacental blood Cow:* )re eclampsia D eclampsia* chronic renovascular disease* ,hronic hypertension

Eaternal malnutrition Eultiple pregnancy $rugs

* ,igarettes alcohol heroin cocaine* eratogens antimetabolites and

therapeutic agents such astrimethadione warfarin phenytoin


17/41

Eaternal hypoxemia* >emoglobinopathies* >igh altitudes

8 thers

* #hort stature* ounger or older age 9


18/41


19/41

#%

Diagnosis

&'G( can be di7cult to diagnose.

)resence of ris/ factors.

&nade?uate growth detected by serialmeasurement of Ht. abdominal girthand fundal

'ltrasound to evaluate the foetal

growth. &nade?uate fetal growth. )lacental calci=cation.

&ntrauterine *


20/41

Diagnosis,cont...

$

eonatal )ostnatal assessment

Growth parameters: weight height>,

Assess GA with Iallard score.

)lotted growth parameters in growthchart

Ponderal inde'


21/41

Ponderal Index

Hay of characteri+ing the relationshipof height to mass for an individual.

)& J 1000 x

ypical values are "0 to "%.

)& is normal in symmetric &'G(.

)& is low in asymmetric &'G(.

Mass ()gs*

Height (cms*


22/41


23/41


24/41

Neonate and Placenta inIUGR

ormal - &'G(ewborn babies

ormal - &'G()lacentas

$!


25/41

Physical appearance:

8 >eads are disproportionately large for theirtrun/s and extremities

8 Facial appearance has been li/ened to that

of a Kwi+ened old manL.8 5ong nails.

8 #caphoid abdomen


26/41

PhysicalPhysical

AppearanceAppearance


27/41

8 #igns of recent wasting

* soft tissue wasting * diminished s/in fold thic/ness * decrease breast tissue

* reduced thigh circumference

8 #igns of long term growth failure

* Hidened s/ull sutures large fontanelles * shortened crown M heel length

* delayed development of epiphyses

8 ,omparison to premature infants&'G( has

brain and heart larger in proportion to thebody weight in contrast the liver spleenadrenals and thymus are smaller.


28/41

Complications

0etaboli"

* >ypoglycemia

* result from inade?uate glycogen stores.

* diminished gluconeogenesis.

* increased IE(

* >ypocalcemia* due to high serum glucagon level which

stimulate calcitonin excretion


29/41

,omplication

Hypo2ia

* )erinatal asphyxia

* )ersistent pulmonary hypertension

* meconium aspiration +her!oreg$lation

* >ypothermia due to diminished

subcutaneous fat and elevatedsurfaceDvolume ratio


30/41

,omplications

He!atologi"

* hyperviscosity and polycythemia due toincrease erythropoietin level sec. to

hypoxia

I!!$nologi"

* &'G( have increased protein catabolismand decreased in protein prealbumin andimmunoglobulins which decreasedhumoral and cellular immunity.


31/41

Management

Antenatal diagnosis and management isthe /ey to proper management of &'G(

$elivery and (esuscitation

* appropriate timing of delivery* s/illed resuscitation should be available

* prevention of heat loss

>ypoglycemia* close monitoring of blood glucose

* early treatment 9 & dextrose earlyfeeding ;


32/41

Management

>ypothermia : &ncubator Bangaroo Eother ,are >ematological $isorder

* central >ct to detect polycythemia* ,I, with di6 to rDo leu/openia or thrombocytopenia

,ongenital infection

* infant should be examined for signs of congenital

infection 9eg.rash microcephaly hepatosplenomegalylymphadenopathy cardiac anomalies etcN.;

* (,> titer screening

* iral cx of urine nasopharynx

* >ead , to rDo calci=cation


33/41

Management

Genetic anomalies* screening as indicated by physicalexam

* chromosomal analysis 9infant with

dysmorphic features; thers

* serum calcium to rDo hypocalcemia

* fractionated bilirubin sec topolycythmia congenital infection

* urine meconium tox for substanceabuse


34/41

Management

arly feeding and caloric inta/eshould be 100*1"0 /calD/gDd

$evelopmental and growth follow upin all &'G( infants


35/41

Outcome

#ymmetric vs. Asymmetric &'G(

* symmetric has poor outcome compare toasymmetric

)reterm &'G( has high incidence ofabnormalities

&'G( with chromosomal disease has1004 incidence of handicap

,ongenital infection has poor outcome *handicap rate ! %04

&'G( has higher rate of learning disability.


36/41

Short Term Risks of IUGR

&ncreased perinatal morbidity andmortality. &ntra uterine D &ntrapartum death.

&ntrapartuum foetal acidosis

characteri+ed by*.5ate deceleration.

#evere variable deceleration.

Ieat to beat variability.pisodes of bradicardia.

+


37/41

Short Term Risks of IUGR

&ntrapartum foetal acidosis may occur inas many as 0 4 of &'G( leading to ahigh incidence of 5#,#.

&'G( infants are at greater ris/ of dying

because of neonatal complications*asphyxia acidosis meconium aspirationsyndrome infection hypoglycemiahypothermia sudden infant death

syndrome. &'G( infants are li/ely to be susceptible

to infections because of impairedimmunity


38/41

ong term Prognosis

.

&nfants with asymmetrical &'G( are more li/ely tocatch up in growth after birth than are infants whosu6er from prolonged symmetrical &'G(.

&f &'G( is related to a disease or a genetic defect

the future of the infant is related to the severityand the nature of that disorder.

-


39/41

ong term Prognosis

&'G( infants are more li/ely to remain

small than those of normal birth weight. hey will need the special attention ofprimary health nutrition and social

services during infancy and earlychildhood.

&mplication of &'G( can be life longa6ecting:

Iody si+e growth composition andphysical performance.

&mmunocompetence.

%


40/41

ong term Prognosis

ach case is uni?ue. ,an not reliablypredict an infantOs future progress.

!


41/41

Kuliah Tk Iugr

Documents

Transcript of Kuliah Tk Iugr