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DDX
1. Hydrorrhea gravidarum
2. Vaginitis /cervicitis foul smelling vaginal discharge, no loss of fluid, itching of
vagina/vulva, lower abdominal pains, dysuria
3. Increased vaginal secretions
4. Urinary incontinence
Amnionitis
Increases risk of fetal mortality due to RDS, IVH and Neonatal sepsis.
Its safer to deliver than keep the fetus in utero.
(Organism: streptococcus B/D; anaerobes
The following S/S are suggestive of amnionitis:
1. Fever temperature chart 4 hourly.
2. Maternal leukocytosis of >16,000/ml considered alarming.
3. Uterine tenderness checked 4 hourly
4. Tachycardia maternal pulse of >100/min
5. Fetal heart rate >160/min
6. Foul smelling amniotic fluid is a proof of infection. Deliver actively regardless of gestational
age.
Start broad spectrum antibiotics. NB: -Frequent fundal examination may cause uterine
tenderness.
Use of steroids may cause mild leucocytosis.
Also in labour there is a leucocytosis (20 25% increase)
Amniotic fluid if numerous leucocytes bacteria on gram stain or aerobic or anaerobic culture,
amnionitis is present deliver irrespective of gestation and cover with broad spectrum
antibiotics.
Continuous fetal monitoring if possible.
Term pregnancy without amnionitis (>37 wks)- observe for the next 6-12 hours and if not yet in
labour induce labour if no contraindication. If term with indication for caesarian deliver
immediately.
Preterm pregnancy
without amnionitis
2.PRETERM LABOUR
Predisposing factors:
1. Unknown 50%
2. Maternal infections
Bacterial-
U.T.I
Severe Cervicitis
Pneumonia
Meningitis
Pyelonephritis
Chorioamnionitis
Viral,
HIV/Aids
Rubella
Cytomegalovirus
Herpes Simplex
Protozoa,
Toxoplasmosis
Malaria
Fungal- CryptococcalNeoformans
3. Maternal diseases.
a) Hypertensive diseases in pregnancy
b) Diabetes Mellitus
c) Hypothyroidism
d) Renal diseases, ARF, CRF
e) S.L.E
f) Cardiac diseases
g) Severe anaemia.
4. Fetal factors
a) Severe congenital malformation eg hydrocephalus, omphalocoele, anencephaly etc.
b) Multiple gestation eg twins, triplets etc.
c) Macrosomia, of any cause.
d) I U F D any cause.
5. Liquor factors
a) Severe oligohydramnious
b) Severe polyhydramnious
6. Placental factors
10. Drugs.
Prostagladins
Quinine
Oxytocics
Diagnosis: History Complete history with emphasis on the aetiological factors and gestation.
Physical Examination complete physical examination general and systemic emphasis on vital
signs, abdominal examination, vaginal examination.
Active Management:
1. Involve neonatologist
2. IV syntocion
3. Caesarean section due to obstetric indications
4. Manage the aetiological condition
5. Cervical cerclage
6. Myomectomy before next pregnancy
7. Metroplasty before next pregnancy.
DDX:
1. False labour
2. Braxton Hicks contractions
3. U.T.I
4. Concealed Abruption
5. Uterine fibroids, undergoing red degeneration
Prevention
Preconception Counselling
Primary Care: - aims at reducing the high risk factors eg infections, malaria, anaemia etc.
Secondary Care; - early screening tests and detection for prophylaxis eg tocolytics
Teritiary Care; - aims to reduce the perinatal morbility and mortality after diagnosis eg use of
corticosteroids/in utero-transfer.
Prognosis
Good after 34 weeks
Below 34 weeks out come depends on personel availability, neonatal ICU and use of surfactant
which has greatly improved the out come of preterm infants.
3.MULTIPLE PREGNANCY
.
Plan
1. Epidemiology
2. Physiology
3. Complications
4. Diagnosis
5. Management ANC, intrapartum ,post partum .
Epidemiology
Universal prevalence = 3% , in ART prevalence = 25-30%
Predisposing factors black race, familial (maternal), increasing age, increasing parity and
ovulation induction.
Physiology
Twin gestation is commonest multi-fetal type of pregnancy.
Two types of twins uniovular and binovular.
75% of twins
Genotype different
Familial
Variable phenotype
25% of twins
Non- familial
Division into two fetuses occurring in less than 72 hrs (before morula stage) 2Placentae /
dichorionic and diamniotic
Division into two fetuses occuring on 4th 5th day (inner cell mass ready) diamniotic
monochorionic.
Conjoined (Siamese) twins occur due to incomplete division of germinal plate at sternum
(thoracopagus), skull (craniopagus) , pelvis (ischiopagus) or posterior fusion (pyopagus).
Follows division after 14 days.
Complications
Maternal Event
1. Hyperemesis gravidarum- due to increased HCG
2. Anemia- Due to increased demand.
3. Pre-eclampsia (x3)-due to increased HCG
4. Polyhydramnios (10%) due to large placenta and membranes.
5. Placenta praevia- due to large placenta and membranes.
6. U.T.I- due to stasis
7. Varicose veins, haemorrhoids, oedema- due to venous return
8. P.R.O.M due to overdistension, malpresentation
8. Malpresentations (45%=C/C, 35%=C/B 20% others - due to limited space
Fetal complications
1. Congenital malformation (x2)
2. Low birth weights- due to prematurity or dicondant transformation
3. I.U.F.D due to pre-eclampsia , cord accidents, congenital malformation
4. Locked twins due to malpresentations.
5. Retained 2nd twin due to undiagnosed twin gestation
6. Cord prolapsed due to malpresentation, polyhydramnios, overdistension
7. Compound presentation.
NB: 2 Twin has high mortality rate if not delivered in 30 minutes of 2nd stage
ND
Diagnosis
High index of suspicion if:
Hyperemesis gravidarum
Pre-eclampsia
Excessive fetal movements
Rapid abdominal growth
Discomfort &dyspnoea
Massive oedema
Signs
1. FH greater than dates
2. Multiple fetal parts
3. Fetal heart heard in 2 places 10cm apart
DDX
1. Hydramnios
2. Wrong dates
3. Molar pregnancy
4. Fetal macrosomia
Investigations
U/S scan
Management
Antenatal
1. Haematinics , multivitamins , balanced diet
2. Adequate rest to increase weight gain and prevent preterm labour / pre-eclampsia
3. Prevent prematurity- tocolytics for triplets and quadruplets.
4. Post-datism is not allowed
5. Treat asymptomatic bacteuria to prevent preterm labour
1st Stage
1ST twin must be in cephalic presentation.
5% dextrose drip necessary
Oxytocin may be used if uterus is hypotonic.
ARM should be done with assistant applying fundal pressure to prevent cord prolapsed
3rd STAGE
1. I.V oxytocin 40 I.U in a drip at 40 drops/min
2. I.M ergometrine 0.5mg stat
Diagnosis
INVESTIGATIONS
Clinical concept:
MANAGEMENT
Uncomplicated-Routine induction when 6 days past EDD,or if oligohydramnios present.
-Selective induction,awaits spontenous onset of labor, not preferred.
Cervical assessment is preferred ,unfavorable cervix use PGE2
Complicated group-Elective caeserian section for postmaturity with CPD,prevscar,
malpresentation ,elderly primi.
CARE DURING LABOR- Labor expected to prolong due to big baby,poor moulding of
head ,possibility of shoulder dystocia is high.
COMPLICATIONS
During pregnancy -Reduced placental function, oligohydramnios, may cause fetal hypoxia,
fetal distress.
Definition:
Any vaginal bleeding that occurs in the third trimester of pregnancy (at or after 28 weeks of
gestation)new definition bleeding at 24wks.
Incidence:
3-4%
Differential diagnosis
1. Placental site bleeding
Placenta praevia
Abruptio placentae
2. Local causes
Infections
Neoplasms
Benign e.g. polyps
Malignant e.g. ca cervix
Vulval varicosities
Heavy show
3. Ruptured uterus.
Prognosis of APH
Is an obstetrical emergency
Can very easily lead to maternal mortality
Perinatal mortality is always high
Easily progresses into a state of collapse (shock)
Principles of Mx
Objective in management must therefore be to prevent the possibility of the adverse outcomes
mentioned above
Hence, the first step is to fix an intravenous line & draw blood for grouping and cross matching
(GXM) before shock sets in. Then, and only then, should other aspects of management be
considered!
PLACENTA PRAEVIA
Definition
The placenta is wholly or partially placed in the lower uterine segment (LUS)
Clinical significance
The mother is likely to bleed as a result of premature placental separation
Mechanisms of placenta separation
The shearing effect on the placenta is as a result of the formation of the LUS or the taking up
(effacement) of cervix due to uterine contractions
Types of placenta praevia
1. Minor - if it can allow vaginal delivery
2. Major -if it cannot allow vaginal delivery
Definitive diagnosis:
Made at examination under anesthesia (EUA); 4 types of placenta praevia are recognized:
Type I Placenta reaches the LUS but does not encroach on the internal cervical os
Type II Placenta encroaches on the internal os but does not cover it:
Type II anterior if the placenta is anterior
Type II posterior if the placenta is posterior
Type III the placenta covers the internal os but not completely
Type IV- the placenta covers the internal os completely, even if it was to reach full dilatation
Pathogenesis
Several theories:
1. Rapid embryo development reaches the uterine cavity before the endometrium is
receptive
2. Previous endometrial damage, or poor vascularization
Multiple uterine scars
Previous D&C
Fibroids
3. Multiple pregnancy the large placenta encroaches on to the LUS
4. Rising maternal age
Clinical features
Painless vaginal bleeding, often before 36 weeks
First haemorrhage often less severe termed as warning haemorrhages
Blood is often fresh & bright red
Pain is not a feature
The general condition of the patient is commensurate with the amount of blood loss
Abdominal examination:
Non-tender
Uterine size corresponds with the gestational age
Presenting part is high
Malpresentation is common
Oblique lie is especially common
Pelvic examination:
NB: No room for digital examination
Speculum examination is permissible
The fetus is often in good condition
Definitive diagnosis:
Placental localization (placentography)is key to the determination of the mode of delivery
Ultrasound is very accurate
EUA with a double set-up
Management
Basic principles:
If at or near term, delivery is always indicated; mode of delivery depends on amount of
bleeding and type of the placenta
If hemorrhage is life threatening at any gestation, emergency cesarean delivery is indicated
If not at or near term and hemorrhage is not life threatening, conservative management is
preferred
Conservative management
Objective:To achieve fetal maturity without compromising on maternal safety
1. Bed rest
2. Sedatives to enhance bed rest
3. GXM 2-3 units of blood & keep ready in case it is required
4. Lung maturing steroids in event delivery becomes necessary
Delivery is indicated:
1. If there is torrential hemorrhage at any time (by emergency cesarean)
2. If significant bleeding after 34 weeks of gestation
3. Once at 37 weeks of gestation
Mode of elective delivery at term
Caesarean delivery if placenta praevia is obviously major type by ultrasound
EUA in a double set-up situation outcome of which is:
a) Caesarean if placenta praevia is major type
b) Artificial rupture of membranes &labour induction if placenta praevia is minor type
Complications
As a result of poor ability of the LUS to retract:
1. Increased blood loss at caesarean section
2. Postpartum hemorrhage
ABRUPTIO PLACENTA
Definition
Premature separation of a normally situated placenta
Types
1. Concealed abruptio placenta bleeding is confined in the retroplacental space
2. Revealed abruptio placenta blood trickles from the retroplacental space, through the
placental margin
Etiological factors
1. Trauma external blow; fall; external cephalic version
2. Hypertensive disease in pregnancy
3. Nutritional deficiency, especially folic acid
4. Grand multi parity
5. Previous abortion, preterm labour, intrauterine growth restriction or fetal malformation
6. Previous history of abruptio placenta
Clinical features
Severity of symptoms depends the amount of retro placental bleeding
Only 50% present with the classic clinical features e.g.
1. Hemorrhage:
Dark blood because of retention
Amount of bleeding not commensurate with degree of anaemia
2. Abdominal findings:
Pain related to the degree of intravasation& to peritoneal irritation
Tense abdomen woody hard
Fetal parts difficult to define
Uterine size > dates
Fetal heart tones difficult to auscultate (ultrasound may be necessary to confirm fetal
viability)
3.General condition: Degree of anemia & shock not commensurate with the apparent blood loss
Differential diagnosis
1. Placenta praevia
2. Local conditions
3. Uterine rupture
4. Acute polyhydramnios
Complications
1. Coagulation disorders:Due to;
Release of thromboplastin from damaged tissues
Consumption of the clotting factors by the retroplacental clot
2. Pituitary necrosis:Due to shock
3. Renal failure:Due to shock & DIC
4. Postpartum bleeding:Due to uterine damage, atony& coagulation failure
5. Fetal complications influenced by the degree of placenta separation & the degree of
shock/anaemia;
Intrauterine hypoxia
Intrauterine fetal death
Preterm delivery
Management
Once the diagnosis is established, the following should be done:
1. Resuscitative measures shock, hypoxia, DIC, etc.
2. Delivery should be effected:
a.Fetus alive cesarean delivery preferable
b. Fetus not alive vaginal delivery preferred unless hemorrhage is life-threatening
3. Determine coagulation status
4. Monitor urine output
6.HYPERTENSIVE DISORDERS IN PREGNANCY
OBJECTIVES
1. Be able to define Hypertensive disease in pregnancy
2. Be able to make diagnosis based on the history and physical examination and request
appropriate investigations
3. Should be able to manage hypertensive disease in pregnancy, an impending
eclampsia/eclampsia and prevent complications
4. Know when to deliver and the mode of delivery
.Introduction.
There are four major hypertensive disorders in pregnancy :
1. Preeclampsia-eclampsia (also called pregnancy-induced hypertension)
2. Chronic hypertension
3. Preeclampsia superimposed upon underlying hypertension
4. Gestational hypertension (also called transient hypertension)
Definitions.
Preeclampsia refers to the new onset of hypertension and proteinuria after 20 weeks of
gestation in a previously normotensive woman .
Chronic hypertension is defined as systolic pressure 140 mmHg and/or diastolic pressure 90
mmHg that antedates pregnancy, is present before the 20th week of pregnancy, or persists longer
than 12 weeks postpartum .
Gestational or transient hypertension refers to elevated blood pressure first detected after 20
weeks of gestation without proteinuria
Pathophysiology of preeclampsia.
Vasospasm accompanied by intravascular volume depletion.
Spiral arteries fail to dilate maximally
Placental underperfusion results into release of free radicals that cause endothelial
dysfunction
Microangiopathy associated with the disease affects multiple organ systems, sometimes with
life-threatening results; as a result, it is far more complicated than simple hypertension
Risk Factors.
1. Nulliparity
2. Extremity of age<20,>35
3. African race
4. Family history
5. Chronic hypertension
6. Chronic renal disease
7. Antiphospholipid syndrome
8. Diabetes mellitus
9. Multiple gestation
Other contributors
Health service factors: failure to monitor BP during ANC visits, delayed referral, lack of
guidelines in management, lack of equipments
Community factors;lack of awareness of symptoms of preeclampsia and importance of
ANC,low socio economic factors, community distrust of health care personnel ,religious
factors
Symptoms.
1. Visual Complaints
2. Headache
3. Abdominal pain
4. Rapid weight gain
5. Swelling of face or hands
6. Confusion and apprehension
7. Nausea and vomiting
Physical findings.
1. BP>140/90 mmhg
2. Generalized oedema
3. Fundoscopic exam(A-V) nicking
4. Small fundal height for gestation
5. Hyper reflexia of deep tendons
6. Liver tenderness
Lab evaluation.
1. CBC may reveal anemia, thrombocytopenia
2. Electrolytes and Serum creatinine may be elevated
3. Urinalysis may reveal proteinuria
4. 24 Hour Urine for protein
5. LFT may reveal elevated aspartate aminotransferase, ALT bilirubin, and LDH
Monitoring- imaging.
1.Assessment of fetal well-being Components of fetal evaluation in preeclamptic pregnancy
include daily fetal movement counts and nonstress testing and/or biophysical profiles at
periodic intervals, depending upon clinical status.
2.Assessment of fetal growth -Early fetal growth restriction may be the first
manifestation of preeclampsia or a sign of
severe preeclampsia. A sonographic
estimation of fetal weight should be
performed to look for growth restriction and
oligohydramnios upon diagnosis of
preeclampsiaand repeated serially . Doppler
velocimetry is useful if fetal growth
restriction is present.
3. CT scan of the brain
Medication
Blood pressure goal - A reasonable goal is a systolic pressure of not more than140 mmHg
and diastolic pressure of 90
Recommendation - Methyldopa and labetalol are considered first line oral drugs. Long-acting
nifedipine is also acceptable.
Hydralazine and Labetalol are the preferred therapy for treatment of severe hypertension in
pregnancy. Oral short-acting nifedipine has been used safely in the setting of preeclamptic
hypertension; however sublingual use has been associated with excessive falls in maternal
blood pressure .
Antihypertensive drugs that are contraindicated in the later stages of pregnancy are
nitroprusside (due to possible fetal cyanide poisoning if used for more than four hours) and the
angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs),
which can aggravate uterine ischemia and cause renal dysfunction in the fetus.
Management of Eclampsia
General principles - If the seizure is witnessed, maintenance of airway patency and
prevention of aspiration should be the first responsibilities of management.
The gravida should be rolled onto her left side. A bed with raised, padded side rails also
provides protection. Supplemental oxygen (8 to 10 L/min) via a face mask has been
recommended to treat hypoxemia due to hypoventilation during the convulsive episode.
Maintenance of maternal vital functions to prevent hypoxia
Control of convulsions and blood pressure
Prevention of recurrent seizures
Evaluation for prompt delivery.
The definitive treatment of eclampsia is delivery, irrespective of gestational age, to reduce
the risk of maternal morbidity and mortality from complications of the disease.
Initial control of convulsions - The drug of choice is intravenous magnesium sulfate. A
benzodiazepine is another option. Phenytoin can also be used, but is less effective in preventing
recurrent seizures. It is generally more important to prevent recurrent convulsions than to try to
stop the initial convulsion because it is usually of short duration and intravenous access and
drugs are often not readily available.
Magnesium sulfate -Magnesium sulfate (6 g intravenously over 15 minutes) is administered
to achieve resolution of an ongoing convulsion. An alternative dose/route is magnesium sulfate
5g intramuscularly into each buttock; however, the onset of a therapeutic effect will be slower.
A diazepam gel for rectal administration is also available (0.2 mg/kg).
These doses may be given safely even in the presence of renal insufficiency;
However, magnesium sulfate is contraindicated in women with myasthenia gravis since it can
precipitate a severe myasthenic crisis.
Concurrent use of magnesium sulfate with calcium channel blockers may result in
hypotension.
Magnesium toxicity is related to serum concentration: loss of deep tendon reflexes occurs at
8 to 10 mEq/L, respiratory paralysis at 10 to 15 mEq/L, and cardiac arrest at 20 to 25 mEq/L.
Magnesium freely crosses the placenta; the cord blood concentration approximates the
maternal serum concentration.
Maternal therapy causes a slight decrease in baseline fetal heart rate and fetal heart rate
variability, which is not clinically significant.
Magnesium therapy also results in:
Transient reduction of total and ionized serum calcium concentration due to inhibition of
parathyroid hormone and increased calcium excretion.
Over time, parathyroid hormone levels rise but calcium concentration continues to fall.
Rarely, the hypocalcemia becomes symptomatic (myoclonus, delirium, ECG abnormalities)
Cessation of magnesium therapy will restore normal calcium levels; calcium may be
administered if symptoms are present (calcium gluconate 1 g intravenously over 5 to 10
minutes).
Postpartum course.
1. Maternal vital signs, input, and output should be monitored closely to detect large changes in
blood pressure and fluid imbalance.
2. Seizures due to eclampsia always resolve postpartum, generally within a few hours to days.
3. Diuresis (greater than 4 L/day) is believed to be the most accurate clinical indicator of
resolution of preeclampsia/eclampsia, but is not a guarantee against the development of
seizures.
4. Anticonvulsant drugs are generally continued for 24 to 48 hours postpartum, when the risk
of recurrent seizures is low. The optimal duration of therapy has not been studied.
Maternal morbidity/mortality
Maternal complications occur in up to 70 percent of women with eclampsia and include;
1. Abruption placentae
2. Disseminated intravascular coagulopathy
3. Acute renal failure
4. Hepatocellular injury
5. Liver rupture
6. Maternal morbidity/mortality cont.
7. Intracerebral hemorrhage
8. Transient blindness
9. Cardiorespiratory arrest
10. Aspiration pneumonitis
11. Acute pulmonary edema
12. Postpartum hemorrhage
Hepatocellular damage, renal dysfunction, coagulopathy, hypertension, and neurologic
abnormalities typically resolve following delivery.
However, cerebrovascular damage from hemorrhage or ischemia may result in permanent
neurologic sequelae and is the most common cause of death in eclamptic women
Wigglesworth Classification
4. Immaturity
5. Infection
9. Unclassifiable
A. Fetus
2. Infection
2.1. Chronic (e.g., TORCH)
2.2. Acute
3. Nonimmunehydrops
4. Isoimmunization
5. FMH
6. Twin-twin transfusion
7. Intrapartum asphyxia
9. Other
B. Umbilical Cord
1. Prolapse
3. Velamentous insertion
4. Other
C. Placenta
1. Abruptio
2. Previa
3. Vasa previa
4. Placental infarction
6. Other
D. Amniotic fluid
1. Chorioamnionitis
2. Oligohydramnios
3. Polyhydramnios
4. Other
E. Uterus
1. Rupture
2. Uterine anomalies
3. Other
F. Mother
1. Diabetes
2. Thyroid diseases
3. Essential hypertension
5. Lupus/APS
6. Cholestasis
7. Drug abuse
8. Other
G. Trauma
1. External
2. Iatrogenic
H. Unclassified
2. No information available
DIAGNOSIS
Initially present
INVESTIGATIONS
COMPLICATIONS
Psychological upset
PREVENTION
Preconceptional counseling
MANAGEMENT
Expectant management-In 80% spontenous expulsion occurs in
2weeks,fibrinogen levels must be checked weekly
-Uterine infection
BEREAVEMENT MANAGEMENT
The medical team should provide psychological support and empathy to the
breavedcouple,should explain in simple terms cause of death.Counselling for
future pregnancy is also done and fears allayed.
8.PUERPERAL SEPSIS
There is marked decline of puerperal sepsis in past few decades Better obstetric
care,increased resistance to infection ,availability of wide range of antibiotics sensitive to
organisms responsible.
Anaerobic Streptococcus,bacteroides,clostridia
Most genital tract infections are polymicrobial with both aerobic and anaerobic organisms.
Pueperal sepsis is a wound infection i.e placental site a raw surface,genital lacerations
,caeserian wounds maybe endogenous organisms from genitals e.g anaerobic
streptococcus,autogenous from the skin,throat migrate by blood or direct contact by patient
herself.Exogenous from outside the patient,streptococcus is important.
PATHOLOGY
Vagina- Lacerations get infected by direct extension from the perineum.Retained cotton plugs
forgotten inside vagina results in offensive discharge.
CLINICAL FEATURES
Local infection-Slight fever,wound red and swollen,pus formation with disruption of the wound.
Pelvic peritonitis-Pyrexia with increased pulse rate,low abdominal pains tenderness,ve- tender
fornix with positive cervical excitation test. Pus in POD evidenced by ,swinging
temps,diarrhoea,flactuant bulging mass in the POD.
Septicaemia-Very high temps,rapid pulse even after temp has settled,blood cultures are positive
TREATMENT
Definition-Babies whose weight is below the tenth percentile of the average for the
gestational age
TYPES OF IUGR
Symmetrical IUGR
Result in early pregnancy (hyperplasia), affecting all cells somatic and cerebral growth are
affected small proportionate fetus
Etiology
1. Genetic anomaly
2. Congenital anomaly.
3. Congenital infection(TORCHES)
4. Maternal medical illness-
Anaemia,HPT,Heartdisease,renaldisease,alcohol,smoking,cocaine
5. Placental pathology-previa,abruption,infarction.
Asymmetrical IUFGR
Results later in pregnancy (hypertrophy)
Affects hepatic glycogen deposit and fat deposition reduced liver size hence lower AC
Redirection of blood to vital organs spares brain (Normal BPD) but affects somatic growth
(AC) increased head-to-liver ratio.
DIAGNOSIS
Clinical palpation is less sensitive
Symphysis Fundal Height-Measured in cm closely correlate with gest ageafter 24wks,a lag of
4cms or more suggests growth restriction.
Amniotic fluid index- Reduction associated with asymmetric IUGR.Vertical pockets <2cm is
associated with oligohydramnios.
COMPLICATIONS
Immediate-
Asphyxia,,RDS,hypoglycaemia,meconiumaspirationsyndrome,hypothermia,necrotizingenteroc
olitis.,IVH.
Late symmetrical growth retarded babies grow slowly,asymmetricals tend to have catch up
growth..Retarded intellectual development is noted if retardation occurs before
3rdtrimester.Worstprognosis for IUGR caused by congenital infection,congenital
abnormalities,chromosomal defects.
MANAGEMENT
Antepartum evaluation-Serial evaluation of fetal growth is done,U/S at 3-4wk interval
Fetal Well Being-NST,BPP,