Chapter 2

Neonate
Part 1

Index

Neonatal jaundice 1-16

Breastfeeding 17 - 20

Infant of diabetic mother 21-23

M.khalil
 Neonatal Jaundice: ‫فدوي الدغيلي‬.‫د‬
Definition :
•Yellowish discoloration of skin and mucous membrane due to increase amount of
bilirubin

•The main source of bilirubin is breakdown of RBC (hemolysis)

•Is the most common problem in neonatal period ,it is app 60% of term, and ,80%
of preterm infant during the 1st wk of life

•3-5 mg/dl is Called subclinical hyperbilirubinemia (Not appears clinically)

•90% of total normal bilirubin Presents as indiret Unconjugated bilirubin becuase

it’s a powerful antioxidant Against the oxidative stress Post delivery and its a fat
soluble

•Abnormal amount of indirect bilirubin >>>> Cross BBB (neurotoxic) >>> Kernicterus
(irreversible)

•Most Unconjugated bilirubin formed by the fetus is cleared by the placenta so the
fetus is completely protected (imp) .The main soure of bilirubin is From RBC
breakdown  

•Normal albumin level is 4mg / dl >>> Every gram binds to 6mg of bilirubin >>> So
albumin ables to Protect the Body against the raising of indiret bilirubin up to 24 mg
>>> HyPoalbuminemia >>> increase risk of kernicterus, also the Use of ceftriaxone
increase the risk of kernicterus
•After 120 days >>> RBC normally destructed by spleen >>> HB :

1) Globin >>> destructed into A.A

>
2) heme >>> iron + protophyrin. Heme oxygenase Biliverdin >>> indirect bilirubin

Note:
•life span of RBC in neonate is 80 days , in IDM is 40-50 days due to
glycosylated HB called early hemolysis, in adult 120 days

2
•Bilirubin >>> 85-90% indirect and 10-15 % direct
•neonatal jaundice ( total bilirubin is above 5 )

•physiological jaundice is the commonest cause of NN jaundice in general, so it’s the

commonest cause of unconjugating hyperbilirubinaemia

•direct conjugated hyperbilirubinemia (always pathological) so look for the

underlying cause

Jaundice is classified as:

1) early neonatal jaundice (less than 2weeks)
2) prolonged (late) neonatal jaundice (persists more than 2 weeks in term , more than
3weeks in preterm)

1) prolonged neonatal jaundice >>> A) prolonged direct b) prolonged indirect

causes of prolonged direct hyperbilirubinemia :-

3
1) intrahepatic:

A) hepatocyte injury:
•infection (TORCH >>> sepsis) (hepatitis) (most common) ,
•toxic (TPN) like in necrotizing enterocholitis ,
•idiopathic (common in SGA and preterm) ,metabolic (eg: galactosemia , alpha1
antitrypsin deficiency and cystic fibrosis)

B)intrahepatic biliary duct injury >>> intrahrpatic biliary duct atresia

2) extra hepatic >>> biliary atresia , choledochal cyst

•Hepatitis is the Commonest cause of direct Hyperbilirubinemia

C/P
•Green olive skin (direct bilirubin under skin) >>> Itching And irritability (bile Salt
under skin) >>> No cross BBB >>> no kernicterus
•Dark colored or tea colored Urine (less important)
•clay colored Pale stool (watery stool) (colorless) (most important) >>> if always
colorless >>> biliary atresia
•If colorless but sometimes baby passes normal colored stool >>> hepatitis

•galacosemia : discuss later

•Alpha 1– antitrypsin deficiency :

•AR >>> predisposing pt to Chronic liver disease and early onset pulmonary
emphysema
•common in SGA
•direct hyperbilirubinemia
•hepatospleenomegally and recurrent pulmonary disease

Cystic fibrosis:
•AR >>> defect in long arm of chromosome 7
•recurrent chest infection, FTT
•liver disease U
•steatorrhea (frothy stool)
•diagnosis >>> sweat test

Biliary atresia:
•newly named as progressive obliterative cholangiopathy
•by surgical exploration >>> 2 types

1) distal segment bile duct obliteration >>> uncommon, correctable

2) obliteration of entire extrahepatic biliary tree >>> common and uncorrectable
>>> managed by Kassai operation (hepatoporto enterostomy)

Note :
•Dubin –johnson sydrome and Rotor syndrome are inherited causes of prolonged
direct hyperbilirubinemia

Causes of prolonged indirect hyperbilirubinemia:

1) Infection e.g UTI                  
2)Congenital hypothyrodism .            
3) Breast milk /feeding (commonest)          
4) hemolytic jaundice (Hemolysis) >>> Inspissated bile syndrome
5) Crigler najjar’s syndrome
6) gilbert syndrome
7) GIT obstruction  

UTI:
•most common causes are E.coli ,Klebsiela .
•The mechanism for the liver impairment is the toxic action of bacterial products
(endo toxins) and inflammatory cytokines

Clinical presentation: 

1) well thriving baby 2) fever +\- 3) crying 4) normal liver enzymes 5) usually
asymptomatic S
investigation : suprapubic aspiration
mx: iv antibiotic

Congenital hypothyroidism:
•Decrease in T3 and T4 >>> inhibition of glucuronyl transferase activity

Clinical presentation:
1) LGA 2) large fontanel 3) hypothermia 4) cyanosis 5) lethargic 6) poor feeding
7) delayed passage of meconium 8) umbilical hernia 9) macroglossia
10) lower limb edema

Management:
•Thyroxin 10 microgram per kg (neonatal dose which is double the dose after 2
years) (double the dose of aquired hypothyroidism which is 5 microgram per kg) >>>>
because thyroxin is very important in brain development

•although throxin is excreted with breast milk but it doesn’t alter TFT and not
protect against hypothyroidism

Breast milk jaundice:

•usually jaundice starts at day 7 (after one week) , peak level at day 12-14 ( at two
weeks) >>>> may reach 30 >>> no case reported to have kernicterus even with these
high levels, decline by 3 to 4 weeks

Clinical presentation:

1) patient is thriving well 2) positive family history 3) normal liver function test
4) no evidence of hemolysis (no pallor)

•The most common cause of prolonged indirect hyperbilirubinemia

•Diagnosed by exlusion >>> you have to exclude UTI and congenital hypothyroidism
first
6
Note:
UTI , congenital hypothyroidism and breast milk jaundice are the most important
causes of indirect prolonged hyperbilirubinemia

Mechanism: factors associated with breast milk jaundice :

1) pregnandiol >>> inhibits glucuronyl transferase enzyme >>> decrease in conjugation

2) high lipoprotein lipase enzyme >>> releases free fatty acids from TAG and then
these free fatty acids interfere with hepatic uptake or conjugation
3) stimulation of B.glucuronidase enzyme >>> increase in enterohepatic circulation

Breast feeding jaundice:

•Inadequate breast feeding >>> dehydration >>> affect the conjugation

Note:
•breast feeding should not be stopped to reduce the Severity

Hemolytic jaundice:

a-immune hemolysis occur in Rh .incompatibility and ABo incompatibility.

b- non .immune hemolysis occur in G6PD and Congenital spherocytosis.
•gives very high bilirubin level in early neonatal jaundice
•Associated with pallor (anaemia)
•mixed direct and indirect but mainly indirect
•managed by double volume exchange transfusion
•after 14 days >>> mild mixed jaundice with little high level of bilirubin and mainly
pale >>> Inspissated bile syndrome (The cause is unclear but jaundice clear
spontaneously with few wks)

Crigglar Najjar syndrome :

1) type 1 ( AR ) >>> Absent glucuronyl transferase >>> very high risk for neurological
complications ( kernicterus) I
2) type 2 (AD) >>> decrease in glucuronyl transferase without risk of neurological
complications ( kernicterus)

Gilbert syndrome (AD):

•more common than crigglar najjar syndrome
•Decrease in activity (expression) of glucuronyl transferase
•level of bilirubin increases with fast
•excellent prognosis

GiT obstruction:
.Increase in Enterohepatic circulation

Investigations:

Investigations of prolonged direct :

1)the main investigation to distinguish is liver biobsy >>> liver architecture is lost or
destructed in hepatitis , intact in biliary atresia

•Hepatobilliary scientigraphy can be used to distinguish Billiary atresia from neonatal

hepatitis but it is not the main

•its important to differentiate between hepatitis and biliary atresia because the
management of biliary atresia is surgical and must be done as early as possible

2) Liver function test >>> liver enzymes (baby aged more than 2 weeks) (if they are
very high 5 to 6 times normal) (normally is up to 40) >>> hepatitis but if they are
mildly high >>> biliary atresia

3) blood sugar >>> hypoglycemia >>> galactosemia

4) blood culture >>> sepsis

5) uss >>> choledochal cyst , biliary atresia
8
6) enzyme assay >>> metabolic >>> galactosemia and alpha 1 antitrypsin deficiency
7) sweat test >>> cystic fibrosis

Investigations of prolonged indirect :

8) urine >>> UTI
9) thyroid function test >>> congenital hypothyroidism
10) cBc , peripheral blood smear, reticulocyte count >>> (will discuss later) >>>
hemolytic jaundice >>> Inspissated bile syndrome

Management:
.treat the underlying cause

Causes of early neonatal jaundice (mainly indirect) :

1) physiological jaundice (always indirect)

2) pathological
A) hemolytic jaundice (hemolysis)
B) polycythemia >>> IDM ( due to high insulin and early RBC hemolysis), SGA (IUGR)
C) birth trauma >>> cephalohematoma
D) drugs eg: vitamin K
E) Down syndrome >>> due to immaturity of the liver and polycythemia

Physiological Jaundice:

Etiology:
1) Hb exchanging >>> increase in bilirubin Production
2) decrease level of z and Y Proteins (Decrease uptake)
3) decrease activity of glucuronyl transferase ( decrease in conjugation) (normal
activity after 3-4 weeks)
4) increase in Enterohepatic circulation.
•occurs in 60% of terms , 80% of preterms ( preterm is more prone to jaundice more
than term because they have :
1) short RBc life span 2) immature liver 3) hypoxia >>> polycythemia 4) NPO >>> less
bilirubin excretion (DR. Saeda zarrog) I
Criteria of Physiolgical Jaundice:
1) Never in the 1st day (starts at day 2 >>> peak at 4th to 5th days)
2) Never direct >>> always indirect
3) Level of bilirubin is not More than 15 mg in preterm and not more than 12 in full
term

•In Physialogical jaundice the brain is Protected by the Normal albumin level

4) Rate of increasing bilirubin day by day is not more than 5 mg/dl

5) Spontanous recovery >>> no need for treatment
6) No Pathological features >>> no hemolysis …etc
7)Never Persist 2 wks (Usually clears off or declined by 7th-10th day) (usually
umbilical stump still present) (if not declined >>> pathological)

Hemolytic jaundice:

•1st day jaundice is due to hemolysis until proven otherwise

a-immune hemolysis occur in Rh .incompatibility and ABo incompatibility (most
important)
b- non .immune hemolysis occur in G6PD and Congenital spherocytosis (less important)

•gives very high bilirubin level in early neonatal jaundice

•Associated with pallor (anaemia)
•mixed direct and indirect but mainly indirect

Rh incombatibility:

•hemolysis in the 2nd Pregnancy due to escaping phenomena >>> (+ve) mother’s
memory cells >>> IgG >>> crossing placenta
•Gets more sever with Successive Pregnancy
Invx >>> Blood group

Note: if there is history of abortion the current pregnancy is high risk because it is
the second pregnancy 18
ABO incombatibility

Eg : mother O and fetus A >>> 85% IgM (not crossing placenta) & 15% IgG (crossing
Placenta) >>> Mild hemolysis (Mild jaundice and Mild anemia) that's why direct combs
test is usually Negative but in Some cases may be Positive and often doesn’t need
exchange transfusion

•Can affect babies of the first Pregnancy

•The mother is Usually group O
•Investigation >>> Blood group

•In case of AB0 and RH together >>> ABO Protect from Rh >>> Fetus blood in mother’s
circulation will be destructed Quickly before synthesis of memory cells

Investigations of early neonatal jaundice:

1) CBC
•normal HB in neonate is 16-20 g/dl
•normal hematocrit in neonate is 35-55
•HB if high (more than 20) >>> polycythemia >>> next step look for hematocrit if more
than 60 >>> polycythemia
•HB if low (less than 13) >>> anaemia

2) peripheral blood smear

•for signs of hemolysis :

A) fragmented RBC B) destructed RBC c) nucleated RBC (immature RBC) indicates

active Bone marrow trying to compensate the hemolysis

3) mother blood group and baby blood group >>> if mother O and baby A or B >>>
significant. Also if mother is RH (-) and baby is RH (+) >>>> significant
(Don’t say husband blood group)

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4) DCT (direct combs test):
•Detects antibodies coating the RBC of the baby in cases of RH

5) reticulocyte count (normal reticulocyte count in neonate is up to 5) >>>> if more

than 5 >>> reticulocytosis >>> hemolysis eg: RH

Mx of NN jaundice
•Phototherapy , double volume Exchange transfusion and drugs

1) Phototherapy
blue light with wave length (425-475 nm) acts on bilirubin precipitated under the skin
that’s why the body must be exposed (420-470 nm >>> DR. Fadwa)

•Converts indirect to bilirubin isomere (water soluble) by Photo isomerization >>>

bilirubin isomere by circulation >>> liver no need to conjugated in the liver >>>
intestine >>> irritant to intestine

•Reduce indirect bilirubin 5 mg/daily so it's not used in Sever Case

(2mg /daily >>> DR.fadwa)
Eg:- RH

•White light doesn’t work on bilirubin

but it is used with the blue to decrease
irritation of the doctor’s eyes by the blue
light so doctor can be able to examine the baby

Indications:

1) If the serum bilirubin is equal to or above the result of (wt * 10) / 2

For example if the weight is 1.6 kg >>>> wt * 10 >>> 16 >>> if the bilirubin level is 16
or more >>> needs double volume exchange transfusion.
16/2 = 8 >>>> but if bilirubin level is 8 to 15 >>> phototherapy

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2) Complementary step after or while waiting for exchange transfusion
3) Prophylactic for low birth WT baby (IUGR) (SGA) >>> stress >>> polycythemia

Note :
•in general Phototherapy is not required in the Physiological jaundice And not used in
Rh incompatibility

•Bilirubin when reaches 1.5 - 3 >>> stop the photo therapy and Follow up with serial
bilirubin

Precuations of photo therapy:

1) Cover the eye (Retinal damage) and erythema

Note:
A) the cover may cause eye infection
B)if baby trying to open his eyes frequently behind the cover >>> corneal abrasion
and permanent scar may occur
2) cover the genetalia (proved in animals that the phototherapy may cause DNA
changes)
3) Distance between light and infant >>> 45-50 cm to avoid heat trauma which cause
dehydration and renal impairment (35-40 cm >>> DR . Fadwa)

S/E:

A)Dermatitis, skin rash And erythema

B) increase in insensible & Sensible water loss >>> increase in breathing, Sweating and
diarrhea (Bilirubin increases gut motility) >>> Dehydration and electrolyte disturbance
and hypocalcemia

That's why babies on Photatherapy need an increase In fluid intake

C) Bronze baby syndrome if used in direct hyperbilirubinaemia >>> so photo therapy is
C.I in direct

note: Gray baby syndrome occurs as a side effect of chloramphenicol 13

D) Pyrexia (hyperthermia)
E) DNA breaks

2 types of phototherapy
A) the old or usual phototherapy >>> need to change the position of the baby
continuously (prone to supine , supine to prone)

B) slender or intensive phototherapy:

•no need to change the position of the baby because the rays are coming from all
directions
•more side effects specially dehydration and electrolytes disturbance
that’s why it is used only if the bilirubin level near the indication of double volume
exchange transfusion

Notes :
1)simple blood transfusion >>> packet cell transfusion >>> to treat anaemia
2) partial exchange transfusion >>> used to treat polycythemia by normal saline
3) Double volume exchange transfusion: >>>> used to treat jaundice

Double volume exchange transfusion:

•reduce bilirubin level by 50% by the end of session

indication depends on the weight , age and cause:

1)25mg /dl or more if normal birth weight (2.5-4kg)
but if the weight is below 2.5kg >>> To know if this baby needs double volume
exchange transfusion or not >>> wt * 10

Eg : if the weight is 1.6 kg >>> 1.6 * 10 = 16 >>>> so if the bilirubin level is 16 or

more this is an indication for double volume exchange transfusion
•So double volume exchange transfusion depends on the weight

Iw
2) dependent also on the age:

Eg: two babies both babies have weight of 3 kg , age of the first baby is 2 days and
the second is 8 days both have serum bilirubin 18 which one needs double volume
exchange transfusion?

Answer is 2 days old baby >>> because the bilirubin will increase by 5 mg on day 3 ,
another 5 mg at day 4 and another 5 mg at day 5 >>>> (5 + 5 + 5 = 15) + 18 >>>
Total will be 33 on day 5 which is very high
While the bilirubin of the second baby who aged 8 days will not be increased >>> no
need for double volume exchange transfusion >>> phototherapy

2) Rapid rise bilirubin ( > 1 mg /dl/hour) despite phototherapy

3) If antibodies are the cause eg: RH (positive peripheral blood smear ,

reticulocytosis in reticulocyte count and positive DCT) >>> we use double volume
exchange transfusion to remove the antibodies (depends on the cause)

4) decrease in level of Hb >>> less than 10 >>> in case of RH

5) if you suspect kernicterus clinically

Note: if there is an indication for double volume exchange transfusion >>>>

phototherapy doesn’t replace double volume exchange transfusion

•Umbilical catheter inserted through Umbilical Vein >>> WTx85 >>> result * 2 (Double
Volume) (WTx80 *2 >>>> DR.fadwa)

Example:-

Wt =3 >>>3x85= 255 >>> 255*2=510mL

•So the volume of blood needed is 510 ml
•At 50ml>>> Give dextrose, Calcium and mg+
IS
•Give O- Fresh blood (washed) (leukocyte depleted)

Cx:
1) Embolism 2)heart failure 3)Thrombosis 4)infection and Sepsis (most common
complication) 5)Portal HTN (Portal Vein thrombosis) 6) hypoglycemia 7) HyPo calcemia
>>> patient receives blood containing citrate >>> chelates calcium >>> hypocalcemia >>>
convulsion 8) Hyperkalemia 9) Volume overload 10) Necrotizing enterocolitis 11) if you
put the catheter by mistake in umbilical artery >>> spasm and expired 12)
incompatibile blood >>> reaction and expired

•In case of criggler najjar syndrome tyPe 2 and gilbert syndrome we use
phenobarbitone (luminal) as enzyme inducer (stimulates glucuronyl transferase
enzyme)

•the main goal of treatment is to avoid kernicterus

•Kernicturs is aneourologic syndrome result from the deposition of unconjugated

bilirubin in the brain cells (in basal ganglion)

•The precise blood level above which indirect-reacting bilirubin or free bilirubin will
be toxic for an individual infant is unpredictable

•kernicterus >>> H/O poor feeding , lethargic, inactive , convulsion , later on >>>>
Bilateral choreoathetosis

Other complications of jaundice:

•Seizure ,Mental deficiency ,High-frequency hearing loss >>> that’s why hearing test is
indicated in jaundice

16
 Breast feeding ‫ناديه الجروشي‬.‫د‬

Types of breast milk:

1) Colostrum ( first 5 days)
2)Transitional milk (5-20 day)
3)Mature milk
•Breast milk >>> 1) fore milk  2)Hind milk
•Premature milk – term milk

Colostrum
•Thick yellow contains:
•high calories – high protein and mineral’s
•Low in fat and carbohydrate
•Contain IgA »»»»» provide immunity
•Leukocyte »»»»» prevent infection
•Laxative effect initiate stool »»»»» prevent jaundice
•Interferon like substance >>>> antiviral activity.
•B12 binding protein >>>> inhibits growth of E-Coli & other bacteria.
•It also contain antibodies against viral disease (polio, measles &influenza).
•enhance the development & maturation of gut.

Transitional breast milk

•It’s whiter and thinner than colostrum
•Immunoglobulin and protein content decrease while fat and sugar increase
•Exclusive breast feeding colostrum and transitional milk minimizing infection related
to neonatal death
•Composition of milk changes even during the length of a single feed to exactly suit
the need of a particular baby

Mature milk
•less protein , minerals and calories
•higher fat and carbohydrates

↓
 Breast milk in general:
•Protein - whey , casein ratio  80-20%  
•Whey (lacalbumine – lactglobuline) ( soluble protein ) more than casein (insoluble
protein) that’s why it’s easily broken-down and digested
•Fat >>> small size globule easily digested
•Contain small amount volatile fatty acid (not irritant gut)
•Carbohydrate-- (beta lactase) facilitate growth of lactobacillus that prevent growth
of pathogenic organism
•Minerals breast milk contain small amount of phosphorus – calcium
•Iron = content less than that in formula milk but bioavailability is high
•Adequate amounts of vit A&B complex.

Cow milk protein formula

•more protein (whey—casein >>> 20%-80%)
•more Carbohydrate –mainly lactose
•more Fat
•same calorie

Disease protected by breast feeding

Acute disorder :-
•Diarrhea ,otitis media, urinary tract infection,
•Necrotizing enterocolis
•Septicemia &infant botulism
•Allergy &eczema
•Sudden infant death syndrome
 
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Chronic disorder :-
•Insulin-dependent diabetes mellitus type 1
•Celiac disease
•Crohn’s disease
•lymphoma ,Leukemia
•Less likely to suffer from depression &other psychological problem

Contraindication of breast milk

1)Mother with HIV
2)Mother on chemotherapy or radiotherapy
3)Herpes simplex active lesion on breast
4)Mother with active T.B start feeding after 2wks of treatment
5)Psychic mother.
6)CMV can be transmitted through breast feeding
7)If the infant has in born error of metabolism such as galactosemia or
phenylketonuria are contraindication

Notes:
•Mother with HBV give immunoglobulin and HBV vaccine breast feeding not
contraindication.
•HCV ,cleft lip and cleft palate Covid-19 are not contraindication of breastfeeding

Soy formula
•Soy protein–based formulas on the market are all free of cow's milk protein and
lactose and provide same calories as mature breast milk
Used in:
1)Galactosemia
2)hereditary lactose intolerance
3)Secondary lactose intolerance

Protein hydrolyzed formula

•It contains medium chain triglyceride &its free of lactose
Used in:
1)Cow milk allergy &soy milk allergy
2)GIT malabsorption due to cystic fibrosis &prolonged diarrhea 19
 Amino formula
•It contains essential &non essential amino acid
Used in:
1)cow milk allergy
2)Failure to thrive on hydrolyzed formula

Risk of artificial feeding

1)Interfere with bonding
2)More diarrhea and respiratory infection
3)More allergy and milk intolerance
4)Risk of chronic disease
5)Low score on intelligence tests  
6)Over weight

Note:
1)weaning = supplement

2)Low iron, Low protein, low wit.D & low Uit.K

3) contains phenyLalanine, Branched chain A.A, Galactose lactose so it is c.I in

phenylkenuria, Maple syrup, Galactosemia & primary lactose intolerance

4) Contains lactoferrin, IgA & free from organisms

5) mature milk contains more lactose than colostrum

20
 IDM (infant of diabetic mother). ‫سعيده الزروق‬.‫د‬

Maternal hyperglycemia:
•Gestational diabetes is the most common cause :
1) vascular changes in placenta >>> placental insufficiency >>> chronic fetal hypoxia
which leads to:

A)positive feedback on bone marrow >>> polycythemia (IDM is never anaemic)

•polycythemia >>> increase in RBC destruction >>> jaundice , stroke and renal vein
thrombosis

Note: definition of polycythemia >>> hematocrit more than 60

B) minority (20 %) will have impaired fetal growth >>> IUGR (SGA) occurs when the
DM is tightly controlled leads to maternal hypoglycemia >>> thats why not all IDM
are macrosomic

C) hypoxia to parathyroid glands >>> transient hypoparathyroidism >>> hypocalcemia

>>> Convulsion

2) Glucose transport across the placenta passively to the fetus >>> Fetal
hyperglycemia >>> in the 1st trimester >>> teratogenic (Congenital anomalies) occurs
only in Pre conceptual diabetes :

•The CNS and cardiac anomalies make up to 2/3 of the malformations

1)Heart anamolies
2)Renal agenesis
3)Neural tube defect
4)sacral agenasis (pathognomonic) called Caudal Regression Syndrome or Mermaid
syndrome and Hypoplastic femur
5)neurogenic bladder
6)Git >>> most commonly doudenal atresia , 2nd common is imperforated anus , 3rd
common is Small left colon 2)
Notes:
A) congenital Anomalies constitutes 30 to 50% of Perinatal death of IDM
B) Higher level of maternal HBA1C are predictive of High risk of Congenital anomalies

3) transient Hypomagnesemia (Mg < 1.5 mg/dl) >>> Thought to be from increased
renal losses in diabetic mom

Fetal hyperglycemia:
1) inceases in fetal osmotic diuresis >>> polyhydramnios >>> risk to PROM >>> preterm
>>> RD and jaundice

Note: prematurity occurs also when the diabetes is poorly controlled , associated
preeclampsia and maternal UTI

2) (+ve) feedback on fetal Pancreatic beta cells >>> increase in insulin

(hyperinsulinemia) :

1) Anabolic

A) increase in oxygen consumption of the fetus

B) increase in fat synthesis and deposition

C) increase in hepatic glucose uptake >>>> glycogen synthesis >>> visceromegally >>>
enlargement in any body tissue except the brain and kidneys (macrosomia which is
defined as birth weight is greater than 90th percentile on growth chart or above
4000 g)

•30% of IDMs >>>> glycogen precipitation and stored in the heart >>> transient HOCM
(Cardiomyopathies) (More Common than congenital heart anomalies) :

22
•asymptomatic but may presents with acute heart failure
•it takes 6 weeks >>> improved spontaneously
Mx : treats acute heart failure if present >>> D.O.c is propranolol

Note: digoxin is contraindicated if develops acute HF >>> enhance contractility against

obstruction >>> worse the condition

Note : good control of diabetes during pregnancy affect the Severity of

cardiomyopathy (decrease the Severity)

•most of or majority of IDM (80%) are overweight Relative to gestational age

(plumpy or macrosomic baby)

•Macrosomia >>> if normal vaginal delivery >>> birth trauma ex: erbs Palsy, shoulder
dystocia , facial palsy , subdural hge , cephalohematoma , clavicle # , humerus #

•More prone to C/S >>> TTN

2) increase in insulin >>> decrease in corticosteroid >>> decrease in surfactant >>>

more prone to ARDS >>> So taccypnea is frequently occur in IDM

•After delivery >>> hypoglycemia which is usualy manifested at the

First hour (develops soon after birth) >>> May be Asymptomatic and may cause
lethargy and jitterness Called NN hypoglycemia

Investigations:
1) Glaucose ,ca 2) Echo and xray for congenital heart disease & for HOCM and DCM
(cardiomyopathy) are mandatory for all cases of IDM
Other investigations : 3) mg , bilirubin level 4) CBC for Polycythemia

MX : treat the Complication

Note: 1) K+ is normal in IDM
2) 50% of IDM have risk to be diabetic

23