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COMMON COMPLICATIONS OF PREGNANCY

Compiled by Dr Francis Were-Consultant


Obstetrician/Gynaecologist,Laparoscopy specialist,Cosmetic Gynaecologist
2016.

1.PREMATURE RUPTURE OF MEMBRANES (PROM)

PROM Rupture of membranes before onset of labour


Preterm PROM - Rupture of fetal membrane before term (37 completed weeks)
Prolonged PROM if 24 hrs elapse between rupture of the membrane and onset of labour in a
term pregnancy.

Risk factors/conditions associated with PROM


1. Family history of PROM
2. Decrease tensile strength of the membranes
3. UTI/STIs
4. Preterm labour
5. Occult amniotic fluid infection
6. Multiple pregnancy
7. Breech presentation
8. Polyhydramnios
9. Trauma
10.Cervical incompetence

PROM can result to;


1. Preterm labour premature birth
2. Prolapse of the cord
3. Placental abruptio
4. Chorioamnionitis
5. Intrapartum fetal distress due to oligohydramnios /infection

Maternal effects of PROM: It can lead to amnionitis which is an important cause of


endomyometritis and puerperal sepsis)
Effects of Preterm PROM on the infant; when prolonged it leads to potters syndrome like
features extra ordinary flexions and wrinkling of the skins.
There is also risk of pulmonary hypoplasia and limbs positioning defect in the newborn due to
Oligohydramnios
PROM can also result to prematurity
Symptoms/signs
1. Report of sudden gush of fluid or continued leakage
Color and consistency of the fluid.
2. Presence of flecks of vernix or meconium
3. Decrease in size of the uterus.
4. Increase prominence of the fetal parts to palpation

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

Sterile speculum examination


1. Pooling the collection of amniotic fluid in the posterior fornix.
2. Nitrazine test sterile cotton tipped swab used to collect fluid from the posterior fornix and
apply it to nitrazine paper. In presence of amniotic fluid the paper turn blue (Alkaline PH 7.0
7.25)
3. Ferning a drop of fluid from the posterior fornix should be placed on a slide and allowed to
air dry. Amniotic fluid will form a fern like pattern of crystallization.
The above three confirm ROM. Absence of one of the above is an indication for further testing
because other factors can produce false positive results eg Alkaline PH on nitrazine test can be
due to other reasons other than PROM. These include;
- vaginal infections
- Presence of blood or semen in post.fornix
- Ferning can be due to cervical mucus.

During speculum examination;


Inspect cervix to determine degree of dilation, effacement and for cord prolapse.
Patient can cough or perform a valsalva maneuver and check loss of fluid through os.
If there is a significant vaginal pool;
Collect for fetal lung maturation.
Collect for gram stain and culture and sensitivity and wet mount preparation.
NB: If no fluids take cervical secretion for gram stain and culture and sensitivity. Do NG
culture/fetal lung maturity testing. If infection present aerobes/anaerobes, leukocytes, bacteria
on gram stain.
If no free fluid is found, a dry pad should be placed under the patients perineum and observed
for leakage.
Ultrasound dating/oligohydramnios if still no confirmation and patients history is highly
suspicion for PROM, perform an amniocentesis and insert a dilute solution of Evans blue or
indigo carmine dye. Remove some amniotic fluid first for physiologic maturity testing; analysis
for white blood cells or bacteria and possible culture and sensitivity testing. After 15-20
minutes, insertion of a sterile vaginal speculum will reveal blue dye in the vagina if the
membranes are ruptured.
Laboratory tests
1. Complete blood count with differential count.
2. Urinalysis and culture and sensitivity
3. Amniocentesis Determine fetal lung maturity and check presence of infection.

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

34 37 weeks manage as term pregnancy because there is no evidence that antibiotics,


corticosteroids or tocolytics improve outcome hence deliver.
(NB: Must be sure of dates, if not, do carry lung maturity testing before delivery)
If lungs not mature give steroids and antibiotics cover -48hrs - then deliver. There are no
benefits of prolonging pregnancy if lung maturity is present.
<24 weeks there are very low rates of fetal salvage with considerable maternal risk.
Use of steroids/tocolytics/antibiotics to prolong the pregnancy have no proven benefit. Hence
expectant management or actively terminate pregnancy. Discuss with patient
24 34 wks interventions to prolong pregnancy and improve outcome.
Rule out amnionitis by collecting a sample of amniotic fluid from pool in the vaginal fornix or
amniocentesis culture and sensitivity, Gram stain, check for lung maturity.
Antibiotic (choice depend on local drugs sensitivity pattern).MgSo4 stat-Neuroprotective.
Effective in prolonging the pregnancy or interval to delivery period and also
decreases infection rate.
Steroids - dexamethasone 6mg 1M 4 dose 12hly or Betamethasone 12mg 1M 2 doses 24 hrs
apart for 48 hrs.12mg dose is just as good in urgent situations.
Betamethasone advantages
1. Preferable dosing schedule
2. Stronger potency
3. Favorable side effect profile
Betamethasone is known to reduce fetal movement (not dexamethasone). The steroids have been
shown to have global effect on major development transitions (multi system effects) - Fetal
lungs, liver, intestine, skin, adrenal gland, kidneys and heart.
Overall benefits RDS/IVH/Necrotizing enterocolitis are remarkably reduced
Tocolytics limited for 48 hrs to permit administration of steroids and antibiotics.
If lung maturity or any signs of infection deliver.

Role of Outpatient management


If leakage of fluid stops or cease, pt stable, afebrile, BPS normal, no evidence of infection, no
uterine irritability (no pain/no contractions) Monitor patient closely, must be reliable and
compliant with follow-up appointment, frequent BPS. Must report to hospital immediately if any
signs/symptoms of infection.

2.PRETERM LABOUR

Definition:This is defined as labour that occurs before 37 completed weeks of pregnancy,


starting from the first day of the last menstrual period.
The lower margin of gestation is 20 weeks (WHO) but 28 weeks locally.
Incidence prevalence, varies widely but its generally 5-10%.
Clinical importance:
Preterm labour leads to preterm deliveries, and hence is a major contributor to Perinatal
morbidity and mortality.
Clinical features:
Confirmed gestation between 28-37 competed weeks.
Uterine contractions increasing in frequency/duration/intensity(at least one contraction/10
minutes)
Progressive Cervical effacement and dilation.
Clinical features are attributed to the predisposing (aetiological factor/s)

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

Placental insufficiency of any cause .


7. Uterine factors
Uterine fibroids
Bicornuate uterus
8. Cervical incompentenceeg congenital or acquired.
9. PROM - Preterm PROM

10. Drugs.

Prostagladins
Quinine

Oxytocics

11. Severe Emotional Disturbance:

Death of a spouse/close relative


12.Trauma
Direct on abdomen
Head injury etc.
13. Radiation,egCaCx in pregnancy
14. Iatrogeniceg after amniocentesis
15. History of previous preterm labour.

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.

Investigations. Relevant ones are:-


1. FBC
2. Urinalysis
3. VDRL
4. BS MPs
1. B/Group + RhSevere congenital malformations
2. Abruptio placenta
3. PROM after 34 weeks

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%

Prevalence in blacks 1:70, Caucasians 1:90 , Asians 1:150

Predisposing factors black race, familial (maternal), increasing age, increasing parity and
ovulation induction.

Perinatal mortality and morbidity increase with increasing number of fetuses.

Physiology
Twin gestation is commonest multi-fetal type of pregnancy.
Two types of twins uniovular and binovular.

Binovular / Dizygotic / Fraternal


2 ova fertilized

75% of twins

Genotype different
Familial

Variable phenotype

Separate Placentae ,Chorion& amnion.

Variable blood group.

May be caused by ovulation induction .

Uniovular / Monozygotic / Identical


Single ovum fertilized

25% of twins

Similar genotype % phenotype

Non- familial

One placenta with anastomoses

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.

Division into two fetuses after 8 days (amnion formed)monoamniotic monochorionic

Discordant transfusion discordant growth IUFD Fetus papyraceous.

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

9. Uterine hypotonia- due to overdistension


10.P.P.H- due to uterine atony, largeplacenta
11. Abruptio placenta- due to overdistention
12.High C/S rate- due to many complications

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

2nd Stage intra partum


1. First twin in cephalic presentation delivered as singleton
2. Clamp cord x2 ,don't deliver placenta, don't give ergometrine
3. Palpate abdomen to align 2nd fetus longitudinally.
4. Pelvic exam to check for cord prolapse or presentation.
5. Transverse lie with intact membranes do external cephalic version (ECV) or internal
podalic version.
6. Transverse lie with ruptured membranes C/S
7. Breech presentation with cord prolapse breech extraction Breech presentation with
intact membranes ECV
8. Cephalic presentation with cord prolapse vacuum extraction
9. Cephalic presentation, intact membranes, no cord presentation , do ARM with assisted
fundal pressure.

3rd STAGE
1. I.V oxytocin 40 I.U in a drip at 40 drops/min
2. I.M ergometrine 0.5mg stat

Indications for C/S


1. 1ST twin malpresentation
2. Multi fetal pregnancies other than twins.
3. Any other obstetric complications.

4.POST TERM PREGNANCY


Definition-Pregnancy beyond 42weeks
Aetiology
1. Wrong dates-due to inaccurate LMP
2. Biological variability seen in families
3. Maternal factors; Primiparity,previous prolonged pregnancy,elderly multipara.
4. Fetal factors-anencephaly-abnormal fetal HPA axis ,adrenal hypoplasia-diminished fetal
cortisol response.

Diagnosis

Maybe difficult to diagnose but using menstrual history-regularity,pdt,use of


contraceptives,quickening.

INVESTIGATIONS

Sonography-asses crown rump length(CRL),biparietal diameter (BPD),femoral length(FL)

Amniocentesis- This invasive method has been replaced by sonography

Straight Xray abdomenThickness and density of skull bones shadow,appearance of


ossification centres on the upper end of tibia(38-40wks),lower end of femur (36-37)-no
longer used

Clinical concept:

1. Baby-General appearance looks thin and old,wrinkled skin,absence of vernix caseosa,


body and cord stained greenish yellow,head hard without evidence of moulding
2. Liquor Scanty stained with meconium.
3. Placenta-Evidence of ageing with calcification and infarction
4. Cord- Diminished whartons jelly May precipitate cord compression.

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.

Associated complications likely to produce placental insufficiency-PET,APH,DM,RH-VE,


should not go beyond the the EDD

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.

During labor- Meconium aspiration ,fetal hypoxia and acidosis,labor dysfunction,cord


compression due to oligohydramnios, shoulder dystocia, birthtrauma ,increased incidence of
operative delivery.

5.LATE PREGNANCY BLEEDING (LPB):


ANTEPARTUM HEMORRHAGE (APH)

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!

Assessment of the patients condition


1. General condition
2. Vital signs
3. History
4. General examination
5. Abdominal examination
6. State of the fetus
7. Speculum examination

Supportive treatment if & when required


1. Treatment of shock
Raise foot of the bed
Plasma expanders e.g. crystalloids,dextran
Blood transfusion
Oxygen
2. Treatment of anemia
Transfusion
Hematinics
3. Make a prognostic diagnosis of APH
Mild, moderate or severe
Placenta praevia, placenta abruption or other
4. Make a decision on the projected management plan
Conservative
Immediate intervention

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

Clinical significance of typing


Types I & II anterior: Are non-obstructive & vaginal birth can be allowed if not bleeding
Type II posterior: Directly impedes descent along the sacral curve
Types III & IV: Obstruct the cervical os and delivery by cesarean section is mandatory in order
to avoid bleeding

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

Differential diagnosis include


1. Abruptio placenta
2. Local genital causes of bleeding

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

Nb:Abruptio placenta is often recurrent in the subsequent pregnancies.


Pathogenesis of abruptio placenta
Faults at implantation may result in an area of weakness
Decidual infarcts
Extravasation of blood into the myometriun responsible for woody hardness of the uterus
Excessive extravasation with resultant myometrial damage leads to couvelaire uterus

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

Hypertensive disorders of pregnancy.


Defined as BP> 140/90 or DBP >90 on more than one occasion.

Occurs in about 10% of the pregnancies.

Its a major cause of maternal and fetal morbidity and mortality

.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

Classification based on severity.


1. MILD-BP elevated but 160/110 mmhg
2. SEVERE-
BP 160/110 mmhg
Eclampsia
Pulmonary edema
Oliguria
HELLP syndrome
Proteinuria > 5g/24hrs
Symptoms suggesting end organ failure
Treatment.
Bed rest in the lateral decubitus position augments uteroplacental blood flow, which can be of
value if there is uteroplacental insufficiency.
The definitive treatment is delivery, which is always beneficial for the mother. As long as the
gravida remains undelivered, she is at increased risk of complications such as seizures,
abruption, thrombocytopenia, cerebral hemorrhage, pulmonary edema, liver hemorrhage, and
renal failure. The risk of these complications subsides with delivery since preeclampsia is a
completely reversible disease process.
However, delivery may not be beneficial for the fetus if it is born preterm. Although the fetus is
at increased risk of intrauterine growth restriction and stillbirth in the preeclamptic
environment, conservative management may be entertained in selected cases to gain fetal
maturity.

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's mechanism of action as an anticonvulsant in preeclampsia/eclampsia is not


clearly understood.

Some possibilities include vasodilatation of the cerebral vasculature, inhibition of platelet


aggregation, protection of endothelial cells from damage by free radicals, prevention of
calcium ion entry into ischemic cells, decreasing the release of acetylcholine at motor end
plates within the neuromuscular junction, and as a competitive antagonist to the glutamate N-
methyl-D-aspartate receptor (which is epileptogenic)

Side-effects and complications of magnesium therapy - Rapid infusion of magnesium


sulfate causes diaphoresis, flushing, and warmth, probably related to peripheral vasodilation
and a drop in blood pressure. Nausea, vomiting, headache, visual disturbances, and palpitations
can also occur. Dyspnea or chest pain may be symptoms of pulmonary edema, a rare side effect
of magnesium sulfate administration.

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

7.INTRA UTERINE FETAL DEATH


Definition: Fetal death after 20weeks gestation.The threshold of 20 weeks is somewhat arbitrary,
pregnancy losses could be classified as pre-embryonic or anembryonic (conception to 5 weeks gestation),
embryonic (6 to 9 weeks gestation), and fetal (after 10 weeks gestation) losses. In the past, anembryonic losses
were termed blighted ova. This term is best avoided. Another approach would be to describe losses prior to 20 weeks
gestation as early losses and those after 20 weeks gestation as late losses.
Stillbirth often is defined as the death of a fetus after 20 completed weeks of gestation. In cases of uncertain
gestational age, losses weighing >500 g are considered.

Wigglesworth Classification

1. Congenital defect/malformation (lethal or severe)

2. Unexplained antepartum fetal death

3. Death from intrapartum asphyxia,anoxia

4. Immaturity

5. Infection

6. Death due to other specific causes

7. Death due to accident or nonintrapartum trauma

8. Sudden infant death, cause unknown

9. Unclassifiable

Relevant Condition of Death (ReCoDe) Classification

A. Fetus

1. Lethal congenital anomaly

2. Infection
2.1. Chronic (e.g., TORCH)
2.2. Acute

3. Nonimmunehydrops

4. Isoimmunization

5. FMH
6. Twin-twin transfusion

7. Intrapartum asphyxia

8. Fetal growth restriction

9. Other

B. Umbilical Cord

1. Prolapse

2. Constricting loop or knot

3. Velamentous insertion

4. Other

C. Placenta

1. Abruptio

2. Previa

3. Vasa previa

4. Placental infarction

5. Other placental insufficiency

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

4. Hypertensive diseases in pregnancy

5. Lupus/APS

6. Cholestasis

7. Drug abuse

8. Other

G. Trauma

1. External

2. Iatrogenic

H. Unclassified

1. No relevant condition identified

2. No information available

DIAGNOSIS

Symptoms: Absence of fetal movements which were

Initially present

P/A- Retrogression of fundal height


Uterine tone diminished

Fetal movements absent

Fetal heart sounds absent

INVESTIGATIONS

Sonography-Lack of fetal movements over 10mins

-Oligohydramnios,collapsed cranial bones.

Straight X-ray abdomen-Overlapping cranial bones

-Hyperflexion of the spine

-Crowding of ribs shadow,loss of parallelism

-Roberts sign,gas in the heart chambers.

Lab tests-coagulation profile,ABO-RH,VDRL,TORCHES,RBS

COMPLICATIONS

Psychological upset

Infection-Once membranes rupture,Cl.welchi which is gas producing

Blood coagulation disorders-consumption of coagulation factors=DIC,if dead fetus is


retained for 4weeks

During labor- Uterine inertia,retainedplacenta,PPH.

PREVENTION

Preconceptional counseling

Regular antenatal care-to prevent,detect at earliest,institute effective therapy

MANAGEMENT
Expectant management-In 80% spontenous expulsion occurs in
2weeks,fibrinogen levels must be checked weekly

Interference- Psychlogical upset of patient

-Uterine infection

-Falling fibrinogen levels-raise to above threshold

Tendancy to prolong preg beyond 2wks.

Use prostaglandins depending on gestation 50ug vaginally 3hrly max 6doses.

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

Definition: Infection of the genital tracts which occurs as a complication of delivery .

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.

Vaginal flora in late pregnancy-Dorderleins bacillus 70%,Candida


albicans,Streptococcus,Ecoli,Bacteroides,Cl.welchi occasionally.

PREDISPOSING FACTORS :1)Conditions lowering immunity2)Multiplication of organisms in


devitalized tissues,usually two days postpartum.3)Introduction of organisms from
outside.4)Increased resistance to antibiotics.

Antepartum factors-Malnutrition and anaemia,Pretermlabor,PROM,Chronicillness,Prolonged


rupture of membranes.

Intrapartumfactors-Repeated vaginal exams,Prolonged rupture of


membranes>18hrs,Dehydration and ketoacidosis during labor,Traumatic
delivery,Haemorrhage ,Retained placental tissues,Placentaprevia,Caeserian section.

Organisms gain foothold in traumatized tissues or in placental bed.

Microorganism responsible-Aerobic-Group A Strep Haemolyticus(GAS)-can cause Toxic Shock


Syndrome,necrotizing faciatis in episiotomy,caeserian section wound.GBS responsible for
neonatal deaths.

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

Primary sites include:1.Perineum2.Vagina3.Cervix4.Uterus.Lacerations on the


perineum,vagina,cervix often infected due to presence of blood clots and dead space.Wound
disruption occurs if infection is not controlled.Risk factor responsible for infection
,DM,Obesity,Low nutritional status

Perinuem-Lacerations repaired or not can be infected by


staph.aureus,anaerobicstreptococcus.There is sangopurulent discharge or pus which results in
wound disruption.

Vagina- Lacerations get infected by direct extension from the perineum.Retained cotton plugs
forgotten inside vagina results in offensive discharge.

Cervix-Infections are common due to lacerations

Uterus-Endometritis,a commonly polymicrobial(GpAor B streptococci,clostridia.Thedeciduas


over placental site are commonly affected.The risk factors for endometritis : retained
pocs,c/s,chorioamnionitis,prolongedprom,pretermlabor,repeated vaginal exams.Discharge is very
offensive.
Spread of infection

Pelvic cellulitis(parameritis) due to spread to the pelvic cellular tissues.

Salphigitis-Pelvic abscess following pelvic peritonitismaybe due to spread of infection directly


through tubes,lymphatic spread, or bursting through parametrium.

Septic pelvic thrombophlebitis-may involve ovarian vein,uterineveins,pelvicveins,raely inferior


vena cava.Infected thrombus may resolve or undergo suppuration.

Septiciemiaand septic shock-maybe due to haemolytic streptococci or anaerobic


streptococci,may cause lung abscess,meningitis,pericarditis,multipleorgarnfailure.Death occurs
in about 30% of the cases.

CLINICAL FEATURES

Local infection-Slight fever,wound red and swollen,pus formation with disruption of the wound.

Uterine infection-1)mild infection-Temp rises,lochia discharge copious and offensive,uterus


subinvoluted and tender.

Spreading infection-Evident by pelvic tenderness, parametritis or tender fornix,bulging pelvic


mass or pelvic abscess.

Parametritis- Onset on the 7- 10thday inpeuperium.,constant pelvic pains,tenderness on the


hypogastrium,vaginal exam reveals a mass pushing the uterus to one side.

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.

Generalized peritonitis-High fever ,rapid pulse ,vomiting,dehydration ,patient looks ill,abdomen


distended and tender rebound tenderness is present.

Septicaemia-Very high temps,rapid pulse even after temp has settled,blood cultures are positive

Bacteraemia,Endotxic shock or Septic shock-Due to release of bacterial endotoxins causing


circulatory inadequacy,tissue hypoperfusion,manifested by-hypotension,olguria,ARDS.

INVESTIGATIONS OF PUEPERAL SEPSIS

History-Antenatal history of anaemia,APH,septicfoci in


teeth,gums,tonsils,heartdisease,DM,UTI,malaria.

Intra natal history-Preterm labor,Duration of PROM,number of vaginal exams done outside


and inside the hospital,duration of labor, method of delivery,Nature of intra uterine
manipulation.

Postnatal details- on nature of fever, associated symptoms.

Clinical exam-General exam, abdominal exam-note involution of uterus,tenderness or peritonitis


or pelvic abscess

Vaginal exam-note lochia character,condition of wound,,pelvic abscess,

Limbs- Check for thrombophlebitis or thrombosis.

Investigations- HVS,URINALYSIS,FULL BLOOD COUNTS-low platelate think DIC.,BLOOD


CULTURES,PELVIC U/S- detect abscess,pocs,color Doppler flow for DVT,U/E/C incase renal
failure.

PREVENTION OF PUEPERAL SEPSIS

Antenatal-Improve nutritional status,eradicate any septic foci eg throat,skin,tonsils.

Intranatal- prophylactic antibiotics during C/S.

Postpartum prophylaxis-aseptic precautions like saline sitz,restricting number of visitors,use of


sanitary pads.

TREATMENT

IV fluids for adequate hydration.

Correct anaemia,transfusion if necessary.

Pain- adequate analgesia

Indwelling catheter- relieve discomfort,monitor output.

Antibiotics- Depending on culture give IV antibiotics for 7-10days.

Perineal wounds-remove stitches to facilitate healing,secondary suturing at later date.

Retained POCS->3CM give antibiotic cover for 24hrs then evacuate

Pelvic abscess- do colpotomyunder U/S guide.


Laparotomy limited indications except peritonitis unresponsive to antibiotics,TAH if uterus is
gangrenous.

Septic shock-Fluid and electrolyte balance,respsupport,,circulatory support with


dopamine,infection control with antibiotics.

9.INTRAUTERINE GROWTH RESTRICTION

Definition-Babies whose weight is below the tenth percentile of the average for the
gestational age

Phases of Fetal Growth


3 consecutive phases;
1. Hyperplasia during the first 16 weeks
2. Hyperplasia and hypertrophy between 16 and 32 weeks
3. Hypertrophy after 32 weeks

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.

Pathopysiology-Reduced transfer of nutrients,reduced availability of nutrients,reduced


utilization of nutrients.Brain cells are reduced as well as cell numbers.Oligohydramnios due
to reduced renal and pulmonary blood flow.SGA fetuses are at risk of intrauterine hypoxia
and if severe leads to fetal death.

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.

Maternal weight gain remains static or falls


Biophysical exam-Sonography HC and abdominal circumference AC,the HC/ACratio is 1 @
32 -34 wks,falls below 1 after 34wks.In fetuses with asymmetrical IUGR the HC is larger.In
symmetrical IUGR the ratio is normal though

Femur length not affected in IUGR

Amniotic fluid index- Reduction associated with asymmetric IUGR.Vertical pockets <2cm is
associated with oligohydramnios.

PHYSICAL FEATURES AT BIRTH


-WT 600gms below minimum percentile standard.

Head circumference relatively larger than the body.

Physical features-Dry ,wrinkled skin giving baby an old mans look.

Baby alert with normal cry.

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,

Pregnancy should be terminated at 37 wks


Before 37wks-Uncomplicated IUGR improve if measures are taken to improve placental
functions if factors causing it are avoided.
In severe IUGR before 36wks give steroids and deliver,if cervix is unfavorable then consider
C/S.
NB- Paediatrician should be at hand to receive the baby,centres should be eqiupped with
neonatal ICU.
Quote:Continous effort,not strength or intelligence is the key to unlocking our potential.
Sir Winston Churchhill