MATERNAL NEWBORN HEALTH 2 (MNH2)

COMPLICATIONS IN PREGNANCY
1
 OBJECTIVES
This unit deals with complications that may arise during pregnancy, labour and
puerperium affecting either the mother, the unborn foetus, the newborn or both.

By the end of the module the learner should be able to:

1. Provide care to women with complications in pregnancy

2. Provide care to women with complications of labour
3. Provide care to women with complications of puerperium
4. Provide care to newborns with complications
5. Apply the concept of community midwifery in maternal and
newborn care. 2
 INTRODUCTION
Focused Ante-natal Care(FANC) aims at ensuring safety of the mother, and the unborn child
during pregnancy, delivery and Peurperium.
In this section, we shall look at the high risk factors (pre-existing and during
pregnancy) including the medical conditions that may affect pregnancy.
The types of women in this group are those who are at higher risk of having
complications either during pregnancy or labour.
This may be because in their past deliveries they had problems like postpartum
haemorrhage, which are likely to recur, or they have chronic diseases such as diabetes
which are likely to get worse with pregnancy.
Note that:
1. These are the major causes of both maternal and foetal morbidity and
mortality.
2. Thus, early diagnosis and proper management is essential for a
successful pregnancy and delivery 3
 INTRODUCTION
The complications may broadly be;
a) Pre-existing medical conditions
b) Pregnancy related/ induced complications
For each of the condition, we shall look at:
 Definition,

 Incidence,

 Pathophysiology,
 Risk Factors,

 Screening,

 Clinical Presentation,

 Diagnosis,

 Management,

 Prevention And Control 4

 Possible Complications
CONT
 MATERNAL CAUSES  FOETAL RELATED CAUSES
1. Anaemia in pregancy
2. Hypertension in pregnancy, i. Intra-uterine growth
3. Diabetes in pregnancy, retardation/restriction
4. Cardiac disease in pregnancy, (IUGR),
Pyelonephritis in pregnancy
5.
ii. Rhesus and ABO
6. Malaria in pregnancy
incompatibility,
7. Tuberculosis in pregnancy,
8. Syphilis in pregnancy. iii. Multiple pregnancy
9. Malnutrition in pregnancy, iv. Post datism
10. Deep venous thrombosis (DVT) in
pregnancy, v. Intrauterine foetal death
11. Opportunistic infections of STI/HIV/AIDS,
12. Sickle cell disease in pregnancy,
6
13. Thyrotoxicosis in pregnancy
 1. HYPEREMESIS GRAVIDARUM
Def: This is a condition in pregnancy where vomiting is severe and continuous
throughout the day.
Its common before 20 weeks of gestation.
The nausea and vomiting persists and the woman vomits everything she has eaten.
OR It is a severe type of vomiting of pregnancy which has got deleterious effect on
the health of the mother and /or incapacitates her day-to-day activities.

7
EFFECTS OF HYPEREMESIS GRAVIDARUM

 Usually leads to severe dehydration due to loss of fluid(extracellular

initially)
 Shock from dehydration

 Metabolic acidosis (from starvation),

 Alkalosis (from loss of hydrochloric acid),through vomiting

 Weight loss, wasting

 Ketoacidosis ( from gluconeogenesis)

 Malnutrition.

If treatment is not timely initiated, liver and kidney damage may

result( intracelular dehydration). Anaemia may develop as a result of lack of
vitamin B, folic acid and iron. 8
 PATHOPHYSIOLOGY
Incidence: less than 1 in 1000 pregnancies.

The exact cause of hyperemesis gravidarum remains unclear. However, there are several theories
for what may contribute to the development of this disease process;
1. Hormonal theory:
 Excess Human Chorionic Gonadotropin Hormone (HCG) Peak during
the 1st trimester corresponding with the typical onset of hyperemesis
symptoms and association with hydatidiform mole and multiple pregnancy
when HCG titre is very much raised.
 Oestrogen is also thought to contribute to nausea and vomiting in pregnancy.

 Estradiol levels increase early in pregnancy and decrease later, mirroring the

typical cause of nausea and vomiting in pregnancy. As the level of oestrogen

9
increases so does the incidence of vomiting.
CONT..
2. Changes in the gastrointestinal system theory
 It is well known that the lower oesophageal sphincter relaxes during
pregnancy due to the elevations in oestrogen and progesterone which relaxes
the sphyncter muscles. There is decreased gut mortality. This leads to an
increased incidence of Gastro-Esophageal Reflux Disease (GERD).
 Due to regurgitation, hyperacidity, hyper salivation becomes common
leading to nausea, and vomiting.
3. Psychological theory : psychological stress increases the symptoms
4. Multiple pregnancy-high levels of HCG Hormone
5. Hydatidiform mole-high levels of HCG Hormone
6. Allergic or immunological basis 10
 RISK FACTORS /CAUSES OF HYPEREMESIS
GRAVIDARUM
Hyperemesis gravidarum occurs in very few women.Common risk factors are;

 Multiple pregnancies,
 1st pregnancy
 hydatidiform mole and/or a
 history of habitual abortions.
 Obesity
 Family history of hyperemesis gravidarum

11
 CLINICAL PRESENTATION
 Early sign:
 The main symptom is persistent nausea and vomiting through out the day,
normal day-to-day activity are curtailed, no sign of dehydration or starvation,
ptyalism (excessive salivation).
 Late signs ; if no intervention vomiting continue leading to:
 Signs of Dehydration, low BP, rapid pulse rate and loss of skin elasticity,
sunken eyes, oliguria, dry coated tongue, ketosis
 Fatigue

 Weakness

 Dizziness

 Weight loss (>5% of weight)

 Breath smell of acetone

 Electrolyte imbalance hyponatremia, hypokalemia, hypocalcemia 12

 DIAGNOSIS
 From signs and symptoms persistent nausea and vomiting
 Complete blood count: haemoconcentration leads to rise in Hb, RBC count and
haematocrit and slight increase in WBC count
 Electrolyte: Na+, K+, Cl- decrease due to loss in vomitus
 Random Blood Glucose: hypoglycemia
 Urinalysis: oliguria, dark colour (due to concentration), high specific gravity due with
acid reaction, presence of acetone, occasion presence of protein and bowel pigment,
diminished or even absence of chloride
 LFTs (liver function test): albumin, prothrombin time, ALT, AST, ALP, Bilirubin levels
 Renal function test: urea and creatinine levels elevated
 Opthalmoscopic examination: Retinal haemorrhage, detachment of retina
 ECG ( electrocardiogram) : abnormal potassium levels can cause arrthmias
 USG (Ultra sonography OR ultrasound): confirm pregnancy, exclude molar or twin
pregnancy, exclude other gynaecological, surgical and medical causes for the hyperemesis13
 MANAGEMENT OF HYPEREMESIS GRAVIDARUM

 The principles of management

1. To stop the nausea and vomiting
2. Prevent fluid/electrolyte imbalance
3. To correct the fluid and electrolyte imbalance if present
4. To prevent and correct metabolic disturbances ( acidosis and
alkalosis) if present.
5. To prevent the serious complication of severe
vomiting( organ failure)
6. Care of pregnancy 14
 MANAGEMENT
Nursing roles:
Assessment:
 Ask the client about onset, duration and cause of her nausea and vomiting,

 Ask her about any medication or treatment she uses and how effective they were
in relieving symptoms
 Obtain a diet history from the client include a diet for the past one week

 Ask about any complaints of ptyalism

 Ask if she has noticed blood in stool

 Note the client’s knowledge on nutritional and need for appropriate nutritional in
take.
 Weigh the client

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NURSING ASSESSMENT
 Inspect mucus membrane for dryness
 Assess the skin turgor
 Assess vital signs TPR/BP, notedeviation from normal
 Note any complaints of weakness, fatigue, activity intolerance, dizziness or
sleep disturbance

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 MANAGEMENT

 If in a health center, refer and accompany the mother to a hospital immediately a diagnosis is
made.
1. Hospitalization :
AIM of hospitalization; Fluid and drug administration, diet, close observation and nursing care.
 Admit the patient for complete bed rest

 Reassure the patient and restrict visitors

 NPO: Oral feeds are withheld for at least 24 hours after the cessation of vomiting.

 Take and send samples for relevant investigations

 Commence IV fluids administration to prevent or correct electrolyte imbalance

 Maintain an input and output chart

 Monitor urine out put, catheterize the patient PRN

 Monitor the vitals at least twice daily ( TPR/BP) and general state of patient

 Monitor foetal hear rate BD, Keep foetal kick charts

 Test urine periodically for ketone bodies. 17

 Record amount of vomitus, note content, frequency of vomiting

MANAGEMENT CONT..
2. Fluids :
 The amount of fluids to be infused in 24 hours is calculated as total amount
approx. 3litres of 5% dextrose to alternate with ringer’s solution.
 Extra amount of dextrose equal to amount of vomitus and urine in 24 hours,
is to be added.
These measure help to correct dehydration, electrolyte imbalance and keto-
acidosis.

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MANAGEMENT CONT..
3. Drugs
 Vitamin B6 (Pyridoxine) Plus doxylamine

 Anti emetics like promethazine hydrochloride (phenergan) or metoclopromide

hydrochloride (plasil) are given usually parenterally to control the vomiting.
 Multivitamin supplements are given. Vitamin B6, B1 plus doxylamine

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 MANAGEMENT CONT
4. Promoting comfort
 The mother should made as comfortable as possible through out her stay in
the ward, maintain warm environment
 Regular general and oral hygiene should be carried out. E.g. changing linen,
Pay special attention to the environment making sure to keep the area free
from pungent odor. Vomitus must be removed from the vicinity of the
mother as the odor may precipitate further vomiting
5. nutrition:
 Once vomiting has ceased for a period of 24 hours , oral fluids can be
commenced and if tolerated a light diet may follow.
 Normal food is gradually introduced and intravenous therapy discontinued.
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MANAGEMENT CONT
6. Providing support and education:
 offer reassurance that all interventions are geared promoting good
pregnancy outcome for both mother and baby.
 Provide information on expected plan of care.

 Listen to her concerns and feelings by answering all her questions.

 Teach the client therapeutic life style changes like avoiding stresses and

fatigue.
 Avoid noxious stimuli

 Avoid tight waist band

 Patient to eat small frequent meals

 Use high protein supplement

 Avoid lying down at least for two hours after eating

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 Avoid food high in fat

 Eat food that settle the stomach such soda and toast
MANAGEMENT CONT
7. Discharge:
The patient should be discharged at least two to three days after
vomiting has ceased. The case should be followed up in the antenatal
clinic.

Nursing diagnosis
1. Imbalanced nutrition less than the body requirement related to nausea and
vomiting as evidenced by poor skin turgor/ dry lips
2. Fluid volume deficit related to excessive fluid loss, excessive vomiting……
3. Anxiety related to ineffective coping, physiological changes in pregnancy……
4. Activity intolerance related to weakness….

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 MORNING SICKNESS VS HYPEREMESIS GRAVIDARUM
SYMPTOMS MORNING SICKNESS HYPEREMESIS GRAVIDARUM
Occurrence rate 75% of all women 1- 1.5% of all women
Typical onset and duration of nausea and Begin around 4-6 weeks, generally ease May begin before pregnancy is confirmed,
vomiting between 12-20 weeks typically peak at 9-13 weeks, but often last
throughout pregnancy.
Severity of nausea and vomiting Varies, however typicall short periods of Nausea often constant, with multiple
nausea and infrequent vomiting episodes episodes of vomiting per day. Affects ability to
eat, drink and care for self and others

Weight loss Minimal if any Weight loss is often severe and rapid. >5% of
pre-pregnant weight is common
Clinical signs none Dehydration, weight loss, ketosis, electrolyte
imbalance. If left untreated can lead to other
complication
Effects on quality of life Minimal if any QOL affected completely patient cannot eat,
drink, speak, read, watch TV, cope with bright
light or look after self.
Treatment options Change in lifestyle should be enough , rest, Medical treatment is crucial , anti-emetics, IV
eating “eating little and often” hydration, multivitamins and mineral
supliments
Other considerations none Antenatal depression ,postnatal depression
and post- traumatic stress disorders 23
 POSSIBLE COMPLICATIONS
1. Dehydration and electrolyte imbalance
2. Metabolic acidosis due to starvation
3. Alkalosis due to loss of Hcl
4. Premature labour
5. Preeclampsia in prolong cases of hyperemesis gravidarum
6. Other Less common but severe complications of HG include: Ruptured
oesophagus from forceful vomiting, collapsed lung , liver disease,
blindness, brain swelling from malnutrition, kidney failure, blood clots,
seizures.
7. To the foetus ;preterm birth and low birth weight baby
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PREVENTION
 Although there are no known ways of preventing hyperemesis gravidarum
the following measures might help:
1. Eat small, frequent meals
2. Eat bland foods
3. Waiting until nausea has improved before taking iron supplement

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 2. MULTIPLE GESTATION/MULTIPLE PREGNANCY
The term multiple pregnancy is used to describe the development more than
one foetus in utero at the same time.
 Twin pregnancy is the most common form of multiple pregnancy

 Others are development of 3 fetuses (triplets), (four) quadruplets and six

(sixtuplets) which are rare.

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TYPES OF TWIN PREGNANCY

1. Monozygotic/ uniovular/identical- one vum, one

spermatozoo,commonly same sex, identical twins

2. Dizygotic/binovular/fraternal-two ova, two spermatozoo,

not identical twins, commonly different sexes

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 1. MONOZYGOTIC OR UNIOVULAR OR IDENTICAL TWINS
( 20%)
 The twining may occur at different periods after fertilization and this markedly
influences the process of implantation and formation of foetal membranes.
 The following possibility may occur:
1. If the division takes place within 72 hours after fertilization
( prior to morula stage) the resulting embryos will have two
separate placentae, chorion, amnions 33% (DCDA placenta)
2. If the division takes place between the fourth and eighth day
after the formation of the inner cell mass when chorion has
already developed there will be two amnion, one chorion 66%
(MCDA)
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MULTIPLE GESTATION

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 CONT..
3. If the division occurs after eighth day of fertilization
when the amniotic cavity has already formed a one
amnion/one chorion monoamniotic-monochorionic twin
develop 1-2% (MCMA)
4. In Extremely rare occasion division occur after 12-13
days of development of the embryonic disc resulting in
conjoined twins when division is incomplete(<1%) called
Siamese twins
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 MONOZYGOTIC TWINS
 Monozygotic twins develop from one ova and one spermatozoon
 They have two amniotic sack

 One placenta

 Usually one chorionic, although occasionally two chorion are found.

 There is a connection between the foetal circulation

 The twins are always of the same sex and have similar palm and

finger prints.

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CONT...
 There is high incidence of errors in development and
malformation
 Conjoined or Siamese twins are mainly monozygotic.

 Perinatal mortality are higher than in dizygotic and single

foetuses

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 DIZYGOTIC OR BINOVULAR OR FRATERNAL TWIN
(80%)
 Dizygotic twins develop from two ova and two distinct grafian follicles usually
of the same or one from each ovary and two spermatozoa.
 The genetic factor which causes double ovulation is carried by the mother and
passed on by the females in the family
 There is a well known familial tendency.
 dizygotic twining is a sign of fertility
 They are more common than the monozygotic twins
 They have two placenta which may be fused to form one
 They have two amniotic sacs
 They have two chorion
 There is no connection between foetal circulation
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 These twins may be of same sex but are often of different sexes
 MONOZYGOTIC VS DIZYGOTIC MULTIPLE
PREGNANCY
Monozygotic or uniovular or identicle Dizygotic or binovular or fraternal

1. One ovum 1. Two ova

2. One spermatozoon 2. Two spermatozoa
3. One placenta 3. Two placentae (may be fuse)
4. One chorion 4. Two chorions
5. two amnion (rarely one) 5. Two amnion
6. Mostly Same sex 6. Different sex or same sex

34
 MULTIPLE PREGNANCY…….
 If diagnosis is made at 6 weeks the woman should be told about the risk of
vanishing twin syndrome
 One foetus may die in utero and become a foetus papyraceous which may be
expelled with the placenta at delivery
 The baby may be very small and are often preterm but bigger babies may be
delivered.
 On examination of the placenta the presence of two chorions and two amnion
should make a diagnosis of dizygotic twins obvious even if they are of the same
sex.
 One twin may be considerably larger than the other and there may be a marked
discrepancy in weight.
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 DIAGNOSIS OF MULTIPLE PREGNANCY
 Diagnosis may be difficult , although a family history of twins may alert the
midwife to the possibility
Abdominal examination:
1. On inspection:
 Uterus looks bigger than expected period of gestation
 Foetal movement are seen over a wide area of the abdomen

36
 CONT..
2. On palpation;
 Fundal height may be greater than expected for the period of gestation.
 Abdominal girth will be 105.5 or more centimeters

 There is presence of two foetal poles (head or breech at the fundus)

 Multiple foetal limbs may be palpated

 The size of the head in relation to the size of the uterus may lead one to

suspect there could be more than one foetus in utero

 Lateral palpation may reveal more than one foetal back or limbs on

both sides.
 Pelvic palpation may give findings similar to those at the fundus

although one foetus may lie behind the other making palpation difficult;37
 Location of three poles in total is diagnostic of at least two fetuses.
 CONT..
3. On auscultation:
 Hearing two distinct and separate foetal hearts with a variation of at
least 10 beats per minute may be assumed that two hearts are being
heard.
4. Confirmatory:
 Ultrasound can demonstrate the presence of two foetal sac as early as 8
weeks gestation but the presence of two fetuses may not be detected
until 15 weeks when the outline of the head will be noted.
 X-ray may be used after 30 weeks of gestation due to the risks

involved.
5. At birth: If multiple gestation was missed antenatally
 After the birth of the first baby the uterus still feels heard 38
 Uterine fundal height remains above the umbilicus
 DIFFERENTIAL DIAGNOSIS

1. Large single foetus

2. Wrong dates
3. Polyhydramnios
4. Obesity of the mother
5. Hydrocephalus
6. Uterine / ovarian mass

39
 EFFECTS OF MULTIPLE PREGNANCY
a) To mother:
These are:
1. Exacerbation of minor disorders of pregnancy,
2. Anaemia,
3. Pre-eclampsia,
4. Polyhydramnios,
5. Increased pressure symptoms,
6. APH (antepartum haemorrhage) due to placenta praevia
7. Premature labour
8. Congenital malformations e.g. co-joined twins
40
 EFFECTS ON PREGNANCY
1. Exacerbation of minor disorders in pregnancy this is due to higher
levels of circulation hormones. Morning sickness, nausea and heartburn
may be more persistent and more troublesome than in single uterine
pregnancy.
2. Anaemia iron deficiency and folic acid deficiency are more common.
Early growth and development of the uterus and its content make greater
demands on maternal iron stores and in later pregnancy ( after the 28 th
week ) foetal demand for iron deplete those stores further.

41
 CONT..
3. Pre-eclampsia ( pregnancy induced hypertension)
 More common in twin pregnancy and may be associated with large
placental site or the increased hormonal output.
 Incidence of pre-eclampsia is higher is higher in monozygotic twins
4. Polyhydramnios
 This is also common and is a associated with monozygotic twins and
foetal abnormalities.

42
 EFFECTS ON PREGNANCY
5. Pressure symptoms
 The increase in weight and size of uterus and its content leads to
impaired venous return from the lower limbs increasing the
tendency to varicose veins and oedema of the lower limbs.
Backache , dyspnea and indigestion is also common
6. APH due to placenta praevia as a result of large placental area
7. Premature labour due to bulky uterus pressing on the cervix
8. PPH post delivery due to poor uterine contraction

43
EFFECTS TO THE FOETUS

1. Prematurity-preterm labour due to overstretching of the

uterus.
2. Congenital malformations e.g. co-joined twins

44
 EFFECTS ON LABOUR
1. Labor often occurs spontaneously before term due to the overstretching of the
uterus or it may be induced early if complications arise.
2. Malpresentation, malpositions
3. Unstable lie
4. Premature labour
5. Cord prolapse
6. Postpartum haemorrhage
7. Low birth weight baby
8. Premature Rupture Of Membranes(PROM
9. Retained second twin.

45
 MANAGEMENT OF MULTIPLE PREGNANCY

Management and Nursing Interventions

a)Antenatally:
 Early diagnosis of twin pregnancy is important in order to anticipate or prevent
problems.
 Prevention of anaemia is essential and haemoglobin estimations should be
carried out at regular intervals. prescription of iron, folic and vitamins should help
keep her haemoglobin at an acceptable level
 Avoid heavy work to prevent pressure symptoms
 Rest She may be admitted to ensure rest and close monitoring

46
 ANTENATAL MANAGEMENT………
 Nutrition counseling: stress increased caloric and protein intake as well
as vitamin supplements to meet the demands of multiple gestation.
 Fetal evaluation encourage follow-up for serial sonograms during the

pregnancy to evaluate growth and development and to detect IUGR.

 Explain non stress test (NST), biophysical profile (BPP), and

amniocentesis for detection of fetal lung maturity. Percutaneous

umbilical cord sampling may be used to establish fetal well-being if
twin-to-twin transfusion is suspected.
 Evaluate the woman for signs and symptoms of obstetrical

complications as noted above, which are more common in multiple

gestation.
47
 CONT..
 Evaluate the woman for signs and symptoms of obstetrical
complications as noted above, which are more common in
multiple gestation.
 Preterm Labor (PTL) prevention; explain that
hospitalization may be necessary for signs and symptoms
of PTL.
 Encourage bed rest and hydration.
 Institute fetal monitoring and assist with tocolytic therapy

48
 CONT..
 Labor often occurs spontaneously before term due to the overstretching of the uterus
or it may be induced early if complications arise.
 Explain to the woman that mode for delivery depends on:
 The presentation of the twins,
 Maternal and fetal status, and gestational age.

 Cesarean delivery is commonly used for multiples other than twins;

 However, vaginal birth of triplets may be indicated in the presence

of non-contracted pelvis, vertical lie of first triplet, unscarred uterus,

and onset of labor at more than 32 completed weeks of gestation.
 Labour can be induced at 38 weeks due to copmlications like IUGR

(Intra uterine growth retardation), hypertention, foetal-foetal

transfusion syndrome. 49
INTRAPARTUM (DURING LABOUR AND DELIVERY)
 Allow spontaneous labour only if the first twin is presenting
cephalic.
 start patient on IV fluids on admission.

 Set up an IV line and take blood for grouping and cross matching

and full blood count. (GXM & FBC)

 If the first baby is a malpresentation, C/S should be performed.

 Obtain informed consent incase of C/S and inform theater in

advance;
 Prepare to receive a premature or an asphyxiated babies

 Ensure preparedness of neonatal/paediatric unit teams

50
 INTRAPARTUM………..
 Nurse the woman in sitting up position to relieve dyspnea or she
may adopt a position she finds comfortable
 If uterine activity is poor labour may be augmented with oxytocin

once the membranes have ruptured.

 ARM May be sufficient in its self to stimulate good uterine

activity.
 Monitor both foetal heart closely

 If foetal distress occurs during labour delivery should be

expedited , often by caesarean section.

 Physical and psychological support of the mother is key in having

a successful outcome
51
 INTRAPARTUM………..
During second stage of labour:
 An obstetrician, paediatrician and anaesthetist should be present for delivery
because of the risk of complications
 Monitoring of both foetal hearts should continue

 An elective episiotomy may be performed to shorten second stage if it is

premature labour or the second twin is breech to prevent intracranial injury
 After delivery of the first twin , note the time of delivery, sex, APGAR score, and
label the baby ‘twin one’ immediately confirm with the mother before applying
on the infants ankle or wrist, place the baby on skin to skin and initiate breast
feeding if the baby is stable .if unstable resuscitation hand over to the
paediatrician

52
 SECOND STAGE…………
 perform abdominal examination to ascertain lie, presentation and
position of the second foetus and to auscultate the foetal heart rate.
 Iflie is not longitudinal an attempt is made to correct it by external
cephalic version(ECE)
 If longitudinal VE is done to confirm the presentation
 Ifit is not engaged it is pushed to the pelvis by fundal pressure before
the second sac of membranes is ruptured, check the FHR

53
 SECOND STAGE………
 Assess uterine contractions if absent in ten minutes start oxytocin drip to
stimulate contractions.
 Give oxygen by mask to prevent foetal hypoxia of 2nd twin due to reduced
placental site after delivery of the 1st twin
 Deliver will proceed as normal in vertex presentation but if it is breech the
midwife may need to hand over the delivery to the doctor or most senior or expert
in breech delivery.
 Delivery should be complete in 15-20 minutes
 After delivery note time , sex, APGAR score, lable ‘twin two’

54
 SECOND STAGE……………………
 In case of retained subsequent baby (>30 minutes after delivery
of first twin), consider C/section
 After delivery of the 2nd twin, Palpate uterus and ensure that there

is no baby before giving oxytocin

 Conduct active management of third stage of labour

 Examine placenta(s)

 Continue with IV oxytocin for one hour after delivery of placenta

to ensure uterus is well contracted and prevent PPH due to uterine

atony
 Double setup is recommended for delivery.

55
GUIDELINES FOR VAGINAL BIRTH OF TWINS

1. Availability of two units of cross matched whole blood.

2. I.V. access with large bore catheter.
3. Surgical suite immediately available.
4. An obstetrician and assistant experienced in vaginal births of
twins.
5. Best choice of anesthesia: epidural.
6. Anesthesia provider capable of administering general
anesthesia.
7. Neonatal team for each neonate present at birth for neonatal
resuscitation. 56
 POSSIBLECOMPLICATIONS OF LABOUR AND
INTERVENTIONS
1. Delayed second twin more than 20 minutes due to absence of contractions. If
cervix is open, instruct the mother to bear down.
2. Malpresentation especially transverse lie, do internal cephalic version and turn
into cephalic or breech.
3. Locked twins one being cephalic and the other breech take mother for C/S
4. Premature expulsion of the placenta before the birth of the second twin
5. Co-joined twins e.g. at the abdomen they may share intestines
6. Cord prolapse especially if 2nd twin presents transversely manage appropriately
7. Postpartum haemorrhage due to uterine atony manage appropriately.

57
 CONT..
8. Prolonged labour: Malpresentation and overdistended uterus may cause to
poor uterine contraction leading to prolonged labour
9. Twin to twin transfusion syndrome

58
 3. POLYHYRAMNIOS/HYDRAMNIOS
Polyhydramnios is a condition in which the quantity of amniotic fluid exceeds
1500mls ( normal at term is 800-1000). It may not become apparent until it reaches
3000mls.
It is a fairly rare condition.
Polyhydramnios is associated with the following conditions:
 Foetal oesophageal atresia
 Open neural tube defect
 Multiple pregnancy, especially in monozygotic twins
 Maternal diabetes mellitus
 Rarely in rhesus isoimmunisation
 Severe foetal abnormalities
 In many cases the cause is unknown
59
 TYPES OF POLYHYDRAMNIOS
There are two types of polyhydramnios:
1. Chronic
2. Acute.
1. Chronic Polyhydramnios
 This occurs gradually, usually from about the 30th week
of pregnancy.
 It is the most common type.
2. Acute Polyhydramnios
 This is a rare type,
 It occurs at between 16 to 20 weeks of gestation and comes on very
suddenly.
 The uterus reaches the xiphisternum in about three to four days.60
 It is associated with monozygotic twins or severe foetal abnormality.
 PATHOPHYSIOLOGY

Pathophysiology and Etiology

 The etiology is usually unclear.
 Normal amniotic fluid volume at term is 500 to 1,000 mL.
The volume in polyhydramnios exceeds 2,000 mL
between 32 and 36 weeks.
 Anomalies causing impaired fetal swallowing or
excessive micturition may contribute to the condition.

61
 POSSIBLE CAUSES

 Causes may be foetal or maternal conditions that increase formation of amniotic

fluid or reduce its absorption.
1. Foetal conditions:
 Oesophageal atresia- foetus can not swallow amniotic fluid
 Anecephally and spinabifida – there is transudation of CSF

through exposed meninges.

 Hydrofoetalis due to rhesus iso-immunization- there is excessive

breakdown of RBCs leading to oedema and more water is

secreted.

62
 CONT…
2. Maternal conditions:
 Diabetes mellitus: the foetus takes a lot of sugar from the
maternal blood which leads to foetal polyuria that increases
amniotic fluid.
 Multiple pregnancy: two or more fetuses are excreting urine.

It is more in monozygotic twins.

 Tumours of the placenta e.g chorioangiomas with excess

fluid production

63
 CLINICAL PRESENTATION

 The mother may complain of breathlessness and discomfort.

 The abdomen is tense and shiny
 If the condition is acute in onset,
She may complain of severe abdominal pain,
Nausea and vomiting,
Palpitation due to effects on the respiratory and cardiac
pressure.
The condition may aggravate other symptoms associated with
pregnancy such as…. 64
 S&S IN CHRONIC POLYHYDRAMNIOS
1. Pressure symptoms are less since the enlargement is gradual
2. Indigestion,
3. Heartburn,
4. Constipation,
5. Varicose veins of the vulva and lower limbs.
6. Oedema of the abdomen, vulva and legs
7. Haemorrhoids due to poor venous return
8. Abdomen is larger than dates
9. Superficial blood vessels on the abdomen
10. On auscultation, No FHR or mild due to the accumulated fluid between
65
the foetus and abdominal wall.
 CONT…
 On abdominal inspection,
 The uterus is larger than expected for the period of
gestation and is globular in shape.
 The abdominal skin appears stretched and tight with marked
striae gravidarum and marked superficial blood vessels
 On palpation: foetal parts are difficult to be palpated
 Fluid thrill may be elicited by placing a hand on one side of the abdomen
and tapping the other side with the fingers
 On auscultation: FHNH or mild due to the accumulated fluid between the
66
foetus and abdominal wall
 DIAGNOSIS

 A diagnosis is made based on the present symptoms and

ultrasound evaluation revealing AFI (amniotic fluid index)
greater than 25 cm.
 Ultrasound evaluation will show large pockets of fluid

between the fetus and uterine wall or placenta.

 Difficult to palpate fetus or hear FHR; non-reassuring FHR

tracing.
 Fundal height (FH) greater than gestation

67
 MANAGEMENT OF POLYHYDRAMNIOS
 Management depends on the severity and the cause; hospitalization is indicated
for maternal distress or for interventions regarding foetal prognosis.
 Indication to allow pregnancy to continue
1. Pregnancy that is less than 35 weeks gestation
2. No major pressure symptoms
3. Absence of congenital abnormalities
 Indications for termination of pregnancy
1. Pregnancy that is near term or at term
2. When major congenital malformation are diagnosed
3. If the mother presents in labour
68
 MANAGEMENT OF POLYHYDRAMNIOS
 The mother is admitted to hospital
 The cause of the condition is determined.
 The subsequent care will be determined by the condition of the mother, the cause
and the period of gestation.
 If there is foetal abnormality, the method and timing of delivery will depend on
the severity.
 If there is gross abnormality, Counsel the mother/couple then induction should be
started.
 The nursing care should include rest in bed in sitting position to relieve
dyspnoea.
 Administer oxygen PRN
 Antiacids to relieve heartburn
 Assist the patient with personal hygiene and routine prenatal observations.
FHR, TPR/BP, Foetal kick chart, weighing 69
 CONT..
 Ifimpairment of maternal respiratory status occurs, amniocentesis for
removal of fluid may be performed.
 If abdominal discomfort is severe, abdominal amniocentesis may be
considered to relieve pressure.
 If it is done, infection prevention measures must be observed and
only 500ml should be withdrawn at a time.
 The amniocentesis is performed under ultrasound for location of the
placenta and fetal parts.
 The fluid is then slowly removed.

 Rapid removal of the fluid can result in a premature separation of

the placenta. 70
 Usually 500 to 1,000 mL of fluid is removed.
 CONT..
 Nurse the woman in bed until there is engagement to reduce chances of cord
prolapse.
 Incase of cord prolapse, prepare for emergency C/S.

 Hypotonic uterine action is likely so give oxytocin.

 Prepare for possible PPH.

 Nurse the baby in an incubator with the head tilted to enhance drainage of
aspirated liquor.
 Pass an NG tube into the stomach of the baby to rule out oesophageal atresia.

 Aspirate stomach to empty any fluid to prevent regurgitation

71
 POSSIBLE COMPLICATION OF POLYHYDRAMNIOS
There are several complications associated with polyhydramnios. These include:
 Increased foetal mobility leading to unstable lie
and malpresentation
 Cord presentation and cord prolapse
 Premature rupture of the membranes
 Spontaneous abortion.
 Placenta abruption (APH) when the membranes rupture
 Premature labour
 Postpartum haemorrhage (PPH) due to uterine atony

72
 3. OLIGOHYDRAMNIOS
Oligohydramnios is condition when there is an abnormally small
amount of amniotic fluid. It may be 300 to 500ml at term but
amounts vary and it may be much less.
Occures in 3-5% of all pregnancies
When diagnosed in the first half of pregnancy it is associated with
absence of kidneys or Potter's syndrome in which the foetus has
pulmonary hypoplasia.

73
CONT...
Diagnosis before 37 weeks is associated with PROM or foetal
malformation.
The lack of amniotic fluid reduces intrauterine space and
causes:
 Deformities of the foetus such as talipes, flat nose or a

squashed-looking face due to compression.

 The newborn’s skin may be dry and leathery in appearance

74
 CLINICAL PRESENTATION
The following characteristics will help you recognise the presence
of oligohydramnios:
History- The mother notices reduced foetal movements if she
has had a previous normal pregnancy.
 On inspection,the uterus is smaller than expected for the

gestation period with visible foetal parts and movement.

 On palpation the foetal parts are easily felt and the uterus is
small and compact.

75
 MANAGEMENT OF OLIGOHYDRAMNIOS
 Manegement depends on gestation age , severity and cause of the
oligohydramnios
 The woman should be admitted for investigations, usually in the form
of an ultrasound scan.
 If there are no foetal abnormalities, the pregnancy will be allowed to
continue.
 Labour may be induced early to avoid placental insufficiency.
 Analgesics are given during labour because the contractions are
usually very painful.
 Monitor foetal heart very closely
 However, be aware that impaired circulation may cause foetal
hypoxia. 76

 After delivery the baby is examined carefully for abnormalities.

 POSSIBLE COMPLICATIONS

 Umbilical cord compression

 Passage of meconium

 Fetal/neonatal death

77
 4. BLEEDING IN LATE PREGNANCY; ANTEPARTUM
HAEMORRHAGE (APH)
• APH is bleeding from the genital tract from the 28th week of
gestation and before the onset of labour.
• Antepartum Hemorrhage is one of the leading causes of
antepartum hospitalization, maternal morbidity, and operative
intervention
• Bleeding can be due to:
1. Bleeding from local lesions of the genital tract (incidental
causes)
2. Bleeding from placenta separation due to placenta praevia
or placenta abruption 78
APH
Most common causes of bleeding in pregnancy:
1. Placenta Previa, 31%
2. Placental Abruption, 22%
3. ‘Unclassified bleeding’ 47% of which
Marginal 60%
Bloody Show 20%
Cervicitis 8%
Trauma 5%
Vulvovaginal varicosity 2 %
Genital tumours 0.5%
Genital infections 0.5%
Haematuria 0.5%
Vasa praevia 0.5%
Others 0.5% 79
TYPES OF APH (ANTEPARTUM HAEMORRHAGE)
1. Placenta praevia
2. Placenta abruption

80
 1) PLACENTA PREVIA
Placenta Previa is bleeding from a partially separated placenta, which is wholly or
partially situated in the lower uterine segment.
It might be covering either part or the entire internal cervical OS.
Pathophysiology:
• Lower uterine segment stretch and grow after 12 weeks,
• Later weeks ,placenta separate and cause severe bleeding

Risk factors
1. It is more likely to occur with increasing maternal age.
2. It is more common in women aged 35 and above.
3. It is also associated with increasing parity, and is twice
as common in multigravida as in primigravida.
81
TYPES/DEGREES OF PLACENTA PRAEVIA
TYPE 1(1ST DEGREE)
 The placenta is mainly in the upper uterine segment with only a tip of it in
the lower segment.
TYPE 2 (2ND DEGREE)
 The placenta is mainly in the lower segment with its margin on the inner
internal cervical OS
TYPE 3(3RD DEGREE)
 The placenta is mainly in the lower segment with its margin partially
covering the internal OS
TYPE 4(4TH DEGREE)
 The placenta is centrally located over the internal cervical OS 82
TYPES/DEGREES OF PLACENTA PRAEVIA

83
DEGREE/TYPES OF PLACENTA PREVIA

84
85
TYPES OF PLACENTA PREVIA

86
EFFECTS OF THE DEGREES ON DELIVERY

TYPE 1(1ST DEGREE)

• Majority of placenta in upper uterine segment.

• Vaginal birth is possible.

• There will be mild bleeding/blood loss .

• Mother and fetus in good condition

87
TYPE 2 (2ND DEGREE)
 This is also called placenta praevia marginalis
 The placenta is mainly in lower uterine segment.

 Only a tip of it is the upper segment

 The margin is near the internal cervical os.

 Vaginal birth is possible if the placenta is implanted

anteriorly " placenta anterior"

 There would be moderate bleeding/ moderate blood loss.

 Maternal shock is possible.

 Fetal hypoxia may be common

88
TYPE 3(3RD DEGREE)
 The placenta is located entirely in the lower segment
 It partially covers the internal cervical OS

 Severe bleeding is inevitable

 C.S delivery is preferable.

89
TYPE 4(4TH DEGREE)

• The placenta is located centrally over the internal cervical os

 Torrential Hemorrhage is inevitable

 C .S delivery is the only option

90
SIGNS AND SYMPTOMS OF PLACENTA PRAEVIA
 Painless vaginal bleeding which starts when at rest or sleeping.
 It starts suddenly,
 Usually from the 32nd week of gestation because of Braxton Hicks
contractions.
 The foetal head remains high, which results in malpresentation and unstable
lie.
 If bleeding is severe, the blood pressure is low, the pulse and respirations are
high,
 There is shock corresponding with the amount of bleeding.

91
 ASSESSMENT OF MOTHERS CONDITION
Assessing of mother condition:
 History of small repeated blood loss (intervals) after 20 th weeks
gestation, but common after 34th weeks.
 Assess the amount of vaginal bleeding.

 Bleeding occur when doing activity, or even on bed rest.

 Bright red color bleeding (fresh).

 Degree of the Hemorrhage : mild, moderate, severe.

 Retro placental blood clot not formed "So no pain”

 DO NOT perform vaginal or rectal examination nor perform

an enema or suppositories to a woman with APH as this could

92
result in torrential haemorrhage
 MANAGEMENT OF PLACENTA PRAEVIA
 If in a health centre or dispensary:
1. Refer all pregnant women with vaginal bleeding to hospital.
2. Establish IV line ,take blood for grouping and cross matching
3. Ensure there is a running intravenous drip of saline or ringers lactate
solution before transferring the patient to the hospital.
4. A nurse should always accompany the patient to
the hospital.
In the hospital
The type of management will depend on:

1. The amount of blood loss,

2. The condition of the mother
3. The condition of the foetus,
4. The location of the placenta
5. The gestation period. 93
 MANAGEMENT OF APH (PLACENTA PRAEVIA)
The aim of management is to:
 Control haemorrhage and to try to conserve the pregnancy up to
38 weeks gestation when the foetus is viable/mature.

 Where there is slight vaginal bleeding, conservative treatment is started if the

pregnancy has not reached 38 weeks of gestation.
 The patient is admitted for complete bed rest and total care

94
CONSERVATIVE MANAGEMENT OF PLACENTA
PRAEVIA
 Admit the mother, and Put her on total bedrest.
 Take blood for HB, grouping and cross matching

 She is put on mild sedation like phenobarbitone BD

 No abdominal palpation is done as it may trigger severe bleeding.

NO V.E
 Take two hourly vital signs, FHR with a sonicaide,

 Assess blood loss PV, Save all pads

 On the third day speculum examination is done to exclude

incidental haemorrhage
95
 CONT…

 At 34 weeks, scanning is carried out to confirm diagnosis, assess progress and

foetal viability.
 The patient should be retained in hospital until the 37th week.

 Ensure hygiene, reassure, Give high protein diet

96
FURTHER MNX...DELIVERY
 At 37th week gestation, Examination Under Anaesthesia (EUA) is done in
theatre ready for caesarean section in case of severe bleeding.
 In placenta praevia type one and two and if placenta is anterior, the
membranes are ruptured and spontaneous delivery awaited.
 Labour is induced with oxytocin drug.

 In placenta praevia type two with placenta posteriorly situated and in type
three and four, caesarean section is performed.

97
ACTIVE MANAGEMENT OF PLACENTA PRAEVIA
 Moderate to Severe bleeding in Placenta praevia is an obstetric
emergency.
 Shout for help- call obstetrician, theater team, paediatrician,

laboratory team and prepare for C/S regardless of the degree of

the placenta praevia, gestation or foetal viability.
 The aim is to prevent maternal death.

 Collect blood for HB, GXM and clotting time.

 Give IV fluids; Plasma expanders , normal saline or ringers lactate

rapidly to correct hypovolemia,.

 Give analgesics for pain e.g. pethidine 100mgs or morphine 10 mgs

 Transfuse when blood is ready.

98
 Call new born unit to prepare for an asphyxiated baby.
 CONT…
 Prepare the patient physically and psychologically for emergency
caesarean section
 Patient or partner( if patient is not stable) to give informed

consent.
 Take observations TPR/BP and FHR assess general state of

mother.
 Emergency blood group o –ve

 Monitor intake & output,

 Comforting mother & support partner by sharing information

 Placenta Praevia type 2 posterior, types 3, or 4 require C/S even

99
if the baby is dead to stop hemorrhage & prevent maternal death
 POSSIBLE COMPLICATIONS
1. Maternal shock- resulting from blood loss and
hypovolaemia
2. Maternal death, a very rare outcome
3. Fetal hypoxia and its sequelae due to placental separation
4. Fetal death, depending on gestation and amount of blood
loss
5. Anesthetic and surgical complications, which are more
common in women with major degrees of placenta praevia.
6. Placenta accreta, in up to 15% of women with placenta
praevia
100
 CONT…
7. Air embolism, an occasional occurrence when the sinuses
in the placental bed have been broken
8. Postpartum hemorrhage: occasionally uncontrolled
hemorrhage will continue, despite the administration of
uterotonic drugs at delivery even following the best efforts
to control it, and a ligation of the internal iliac artery, a
caesarean hysterectomy may be required to save the
woman's life
9. Maternal death, a very rare outcome
101
 2) PLACENTA ABRUPTION
( ACCIDENTAL HAEMORRHGE)
 Abruptio Placentae is bleeding from premature separation of a normally situated
placenta occurring after the 28th week of gestation.

• Pathophysiology
 Placental abruption is initiated by hemorrhage into the decidua basalis.
 The decidua then splits, leaving a thin layer adherent to the
myometrium.
 Development of a decidual hematoma leads to separation, compression,
and the ultimate destruction of the placenta adjacent to it.
102
 PREDISPOSING FACTORS TO PLACENTA ABRUPTION
 Placenta abruption is associated with the following conditions:

1. Trauma e.g accidental fall, blow onto the uterus. RTA

2. Fright or sudden shock, for example, bad news
3. Hypertensive conditions and pre-eclampsia
4. High parity due to laxed uterine muscles
5. Sudden reduction in uterine size as in rupture of membrane in
polyhydramnious or after birth of a 1st twin
6. Traction of abnormally short cord during labour
7. Traction of abnormally short umbilical cord during labour
8. External cephalic version(ECV)
9. High fever 103

10. Cigarette smoking

 PLACENTA ABRUPTION
Incidence : occurs in0.49-1.08% of all pregnancies with 30% of cases being concealed and
70% being revealed although there is a probability of both in many situations (mixed
haemorrhage)

Types of Abruptio Placenta

There are three clinical presentations.

1. External or revealed:There is free (visible) vaginal haemorrhage.(
all the blood lost is seen dripping from the cervix to the vaginal
canal
2. Concealed; The blood is trapped between the placenta, membranes
and the uterine wall forming a clot. There is no visible bleeding.
3. Mixed or combined, where bleeding is partly revealed and partly
104
concealed.
PLACENTAL ABRUPTIO

 The hallmark symptom of placental abruption is pain which can

vary from mild cramping to severe pain.
 A firm, tender uterus and a possible sudden increase in fundal
height on exam.
 The amount of external bleeding may not accurately reflect the
amount of blood loss.
 Importantly, negative findings with ultrasound examination do not
exclude placental abruption.
 Ultrasound only shows 25% of abruptions.

105
SIGNS AND SYMPTOMS OF ABRUPTION PLACENTA
Revealed Abruption type,

 There is slight to severe vaginal bleeding.

 On abdominal palpation there may or may not be
pain and tenderness.
 The pulse is raised and there is low blood pressure
or hypertension.

106
CONT…
Concealed Abruption type
 There is severe abdominal pain and the patient is in shock.
 There is no vaginal bleeding and the uterus is very tender
and is board like.
 The foetal parts cannot be palpated and there are no foetal
heart sounds.
 The pulse is raised and there may be oliguria and
proteinuria.

107
CONT...
Combined type,
 The patient has both features of revealed and concealed
bleeding.
 The degree of shock is higher than the visible blood loss.
 The uterus is tender and rigid and pain is constant.

108
 DIAGNOSIS

Diagnosis is from history and physical examination

1. History:
1. History of trauma or recent surgery
2. History of ROM or labour pains
3. Present obstetric history
4. Symptoms of hypovolemia
5. Symptoms of pre-eclampsia
6. Lower abdominal pain or colic
7. The presence or absence of fetal movements
8. Previous uterine operations 109
 2. PHYSICAL EXAMINATION
 Inspect the external genitalia and vagina for:
 Amount of blood loss
 Signs of trauma or infection.
 General examination:
 Tachycardia, hypotenstion
 Signs of shock
 Lower limb edema.
 Abdominal examination:
 Abdominal tenderness, or rigidity
 Pelvic examination:

DON NOT perform a digital vaginal examination at this stage.

110
INVESTIGATIONS

 Laboratory investigations:
 ABO blood group and Rh type
 Crossmatch at least 2 units of blood

 CBC

 Fibrinogen, PTT, PT,CT

 Serum creatinine or BUN

 Urine analysis for protein and RBCs

111
ULTRASOUND

Confirm the fetal viability

Localize the site of placenta, and its relation to the cervix

Estimate the gestational age

Detecting the presence of retroplacental hematoma

In case of severe bleeding, do not wait for an US

examination .Begin first aid management and the quickly start

active management .
Even if the amount of bleeding is mild NEVER perform PV

examination until placenta previa has been excluded by US

112
MANAGEMENT
 General rules:
 This is an obstetric emergency
 Call for help

 Keep the mother on Nil Per Oral(NPO)

 Remember that the mother and the neonate require

evaluation and intervention if needed

113
 FIRST AID MANAGEMENT
 Insert 2 wide bore cannulae
 Blood for CBC, Grouping & crossmatching

 Immediately start iv crystalloid solutions

 Provide 100% oxygen via mask

 Warm the mother

 Insert Foley catheter

 Monitor blood pressure and pulse/ 5 min

 Monitor urine output /hour

114
WHEN TO USE CONSERVATIVE MANAGEMENT
 Bleeding is light or has stopped AND
 The fetus is alive

 The fetus is premature.

 Cases of abruptio placentae which are diagnosed only on US

examination, with no clinical finding (no bleeding, no shock,

no tender or tonically contracted uterus)

115
INDICATIONS OF WHEN TO TERMINATE
PREGNANCY
 A mother in labour
 Heavy bleeding (evident or hidden) manifested by shock

 Gestational age equals or more 37 weeks

 There is fetal distress

 There is IUFD and /or fatal congenital anomalities by U/S

 When the clinical diagnosis is clear

 Or in the presence of acute fetal distress:…. Do not waste your time for U/S
examination.
 U/S is neither sensitive nor specific diagnosis modality in abruptio placentae


116
 POSSIBLE COMPLICATIONS OF
ABRUPTION PLACENTAE
1. Maternal shock
2. Fetal death
3. Uterine atony
4. Amniotic fluid embolism
5. Caogulopathy( 30%)
6. Renal failure
 The principal cause of maternal death is renal failure due to
prolonged hypotension
 Don not underestimate the amount of the hemorrhage

117
DIFFERENCE BETWEEN PLACENTA PRAEVIA AND
ABRUPTION PLACENTAE

118
 VASA PRAEVIA
Definition: vasa previa is a condition in which the fetal vessels from the
placenta cross the entrance to the birth canal.
 Vasa previa refers to vessels that traverse the membranes in the
lower uterine segment in advance of the fetal presenting
part(head /breech).
 Rupture of these vessels can occur with or without rupture of the
membranes and result in fetal exsanguination.

119
CONT…
• Associated with velamentous insertion of the umbilical cord
(1% of deliveries)
• Bleeding occurs with rupture of the amniotic membranes (the
umbilical vessels are only supported by amnion.
• Bleeding is FETAL (not maternal as with placenta praevia)
• Fetal death may occur with trivial symptoms

120
RISK FACTORS OF VASA PRAEVIA
 Risk Factors:
 Bilobed and succenturiate placentas
 Velamentous insertion of the cord
 Low-lying placenta
 Multiple gestation
 Pregnancies resulting from in vitro fertilization
 Palpable vessel on vaginal exam
121
DIAGNOSIS
 The diagnosis of vasa previa is considered if vaginal bleeding occurs upon
rupture of the membranes.
 Ideally, vasa previa is diagnosed antenatally by UltraSound with color flow
Doppler.

122
 ANTENATAL MANAGEMENT
 Consider hospitalization in the third trimester to provide
proximity to facilities for emergency cesarean delivery.
 Fetal surveillance to detect compression of vessels.

 Antenatal corticosteroids to promote lung maturity.

 Elective cesarean delivery at 35 to 36 weeks of gestation.

123
ANTEPARTUM MANAGEMENT
 Immediate C/S.

 Avoid amniotomy as the risk of fetal mortality is 60-70% with rupture of the
membranes.

124
 MANAGEMENT:
 When vasa previa is detected prior to labor, the baby has a
much greater chance of surviving.
 It can be detected during pregnancy with use of transvaginal
sonography.
 When vasa previa is diagnosed prior to labor, elective
caesarian is the delivery method of choice.

125
 6. PRE-ECLAMPSIA
Definition: Pre-eclampsia is an elevated blood pressure specific to pregnancy that occurs
after 20 weeks of gestation in a woman who previously had a normal blood pressure.

Incidence; It occurs in 3% of all pregnancies.

It can occur during pregnancy, Labour, or during puerperium.
 It is characterised by:
1. Hypertension,
2. Oedema
3. Proteinuria
4. Or any two of the three.

 Preeclampsia is the third leading pregnancy-related cause of death, after hemorrhage 126
and sepsis.
 PRE ECLAMPSIA ( RISK FACTORS)
 It is more common in the following conditions:
1. Primigravida,
2. Extreme maternal age the too young <20 or >35 years
3. Primiparternity (first pregnancy with a new partner)
4. Multiple pregnancy
5. Diabetes mellitus
6. Hydatidiform mole
7. Essential hypertension
8. Polyhydramnios
9. Mothers with past history of pre-eclampsia
10. Family history of pre-eclampsia
11. Obese mothers
It is important to take a good history as it will enable you to detect this condition early.127
 PATHOPHYSIOLOGY
 Pre-eclampsia is commonly known as a disease of theories and the
pathophysiology is not fully understood. The cause is unknown.
 It is thought that the condition arises from the influence of placenta tissue and it
can arise in molar pregnancy (gestational trophoblastic disease). Theories of the
etiology include the exposure to chorionic villi for the first time, or in large
amounts, along with immunologic, genetic, and endocrine factors.
 Multisystem disease with widespread vasospasms occur and result in increased
resistance in vascular flow, increasing the arterial BP and causing endothelial
damage. Stimulates platelet and fibrinogen use, causing hypoxic damage to
vulnerable organ systems.

128
 DIAGNOSIS OF PRE-ECLAMPSIA

 The diagnosis of pre-eclampsia is not easy since the mother has no

obvious complaints.
 There are three cardinal signs.
1. Hypertension
2. Oedema
3. Proteinuria

129
 DIAGNOSIS

1. Hypertension
 There is a rise in diastolic pressure of 15 to 20mm/hg above the
mother's normal diastolic pressure, or an increase above 80 to
90mm/hg on two occasions.
 A marked increase in systolic pressure above that expected for
the mother's age is important to note, for example, 140 to170
where the mother's normal pressure is between 90/60 and
130
120/70mm/hg.
 CONT…
2. Proteinuria
 This is important in the absence of urinary tract infection. It
may be detected in testing a midstream specimen of urine,
which should be followed by laboratory investigation.
 The amount of protein in the urine indicates the severity of
pre-eclampsia.

131
 CONT..
3. Oedema
 Oedema of ankles is common in late pregnancy but it
disappears overnight. This is known as physiological oedema.
 Any generalised oedema is significant and what is expected
for the gestation. Clinical oedema may be mild or severe.
 The oedema pits on pressure and is found in the following
areas:
• Feet, ankles, and pretibial region; lower
abdomen; vulva, which is uncomfortable and
distressing to the mother; sacral area in a mother
confined to bed; facial puffiness of the face and eye
lids, fingers.
132
 CLASSIFICATION OF PRE-ECLAMPSIA
1. Mild Pre-eclampsia
 This is detected when, after resting, the diastolic pressure is 15 to 20mm/hg
above the basal blood pressure recorded in early pregnancy or a diastolic
above 80 to 90mm/hg, for example, BP 130/80 to 140/90. Oedema of feet,
ankles and pretibial region may also be present.
2. Moderate Pre-eclampsia
 This is diagnosed when there is marked rise in both systolic and diastolic

pressure - 140/100 to 160/100mm/hg, proteinuria of 0.5gm/litre with no

evidence of urinary tract infection and generalized oedema.
3. Severe Pre-eclampsia
 Symptoms include the blood pressure exceeding 160/110mm/hg and an
133
increased proteinuria over 1gm/litre. There may be marked generalised
oedema, frontal headache and visual disturbances
 EFFECTS OF PRE-ECLAMPSIA TO MOTHER
The effects of severe pre-eclampsia on the mother include:
 Abruptio placenta
 Condition may worsen, leading to eclampsia
 The kidneys, lungs, heart and liver may be seriously
damaged due to haematological disturbance
 The capillaries within the fundus of the eye may be
irreparably damaged causing blindness

134
 EFFECTS OF PRE-ECLAMPSIA TO THE FOETUS
The effects on the foetus are:
1. Low birth weight due to reduced placental function
2. Increased incidence of hypoxia during prenatal and
intranatal periods
3. Prematurity if the baby is delivered early delivery due to
placenta abruptio or worsening of the condition
4. Placenta abruptio leading to hypoxia and later death

135
 MANAGEMENT OF PRE-ECLEMPSIA

 The midwife plays an important role in detecting pre-eclampsia.

 There should always be vigilant antenatal care to enable early
detection and management.
 You should also ensure a thorough history taking to detect the
mothers at risk early in pregnancy.
 Follow up should include monitoring of weight and blood
pressure and urine testing on every subsequent visit.
 Factors that may predispose the patient to pre-eclampsia, such
as multiple pregnancies and obesity should be noted early. 136
 MANAGEMENT OF PRE-ECLAMPSIA
 The method of management will depend on the severity of the condition.
The main principles of care are:

1. Provide adequate rest and monitoring of observations

to avoid eclampsia;
2. Prolong the pregnancy until the foetus is mature
enough to survive;
3. Safeguard the life of the mother;

137
 MANAGEMENT OF PRE- ECLAMPSIA
1. Mild Pre-eclampsia Management
The mother should be advised on bed rest at home and she
is seen weekly to assess her condition.
DRUGS;She should be given anti-hypertensive drugs such

as aldomet 500mg 8 hourly.Sedatives such as diazepum or

phenobarbitone should also be administered to help her
rest
She should be advised to report to the hospital in case of

any problem.
Danger signs in pregnancy eg…..need to be reported
138
 MANAGEMENT OF PRE-ECLAMPSIA
2. Moderate Pre-eclampsia Management
 The patient should be admitted to hospital for bed rest. Bed
rest will reduce oedema by improving the renal circulation,
facilitating kidney filtration and producing diuresis. It also
lowers the blood pressure.
 She should only be allowed to go to the toilet.
 She should be nursed in sitting position or lying on the side to
encourage uterine blood flow.
 The patient's diet should be rich in protein, fibre and vitamins
and low in carbohydrates and salt.
 Her weight should be recorded twice a week.
 Observe for oedema daily.
139
 Urine should be tested for protein and Ketones.
MANAGEMENT OF (MODERATE PRE-ECLAMPSIA)
 Esbach setting is done daily to assess level of protein loss.
Twenty four hour urine collection should be done to estimate
oestriol (oestrogen) level as an indication of placental
function.
 Fluid intake and output should be maintained strictly to
monitor renal function.
 Drugs;Sedatives, such as phenobarbitone, may be given to
ensure rest and sleep.Give antihypertensive drugs like aldomet
to lower blood pressure.
 Take vital signs: blood pressure, temperature, pulse and
respirations four hourly.
140
CONT…
 The foetal heart rate should be taken four hourly or two times
daily, depending on the condition.
 A foetal kick chart to monitor foetal movement should also
be kept.
 When the mother's condition improves, she can be discharged
to attend clinic weekly until she goes into spontaneous labour.
 Otherwise, she should be admitted at 38 weeks for induction
of labour.
 If, in spite of the above care, the condition does not improve,
caesarean section should be performed.
141
 MANAGEMENT DURING LABOUR

Remain with the mother throughout labour.

Maintain close vigilant observations of:

1. Presence of oedema
2. Urinary output
3. Urinalysis results
4. Blood pressure
Report any deviations to the doctor immediately.

142
 MANAGEMENT DURING LABOUR

 Take vital signs as follows: blood pressure and pulse rate half
hourly, temperature four hourly, unless otherwise indicated.
 Perform abdominal examination and observe for contractions and
foetal heart rate half hourly.
 At the same time, observe for signs of second stage of labour and
immediately alert both the obstetrician and paediatrician.
 After delivery, monitor blood pressure four hourly for 24 hours.
 Urinalysis should be done twice a day.
 You should maintain a urinary output chart and continue with
antihypertensive drugs and normal postnatal or caesarean section
care. 143
3. ACTIVE MANAGEMENT OF SEVERE PRE-ECLAMPSIA
 Admit the mother in a quiet, dimly lit room on complete bedrest.
 In the room there should be an emergency tray and an epileptic
tray in case of a fit.
 The aim of care is:
 To prevent convulsions and Control hypertension To prevent
death of the mother and foetus.
 Place the mother on lateral position to improve foetal circulation
and to prevent vena cava compression by the uterus.
 Remain with the mother and maintain vigilant observations.
 On admission you should take all observations and note them on
a chart and continue half hourly or as prescribed by the doctor.
(TPR/BP, FHR,) 144
ACTIVE MANAGEMENT OF SEVERE PRE-ECLAMPSIA
 The doctor will prescribe antihypertensive drugs like hydralazine
5-10mg which is administered slowly and blood pressure monitored
every five minutes until it stabilises.
 Magnesium sulphate as per regimen or Diazepam is also given 10mg
stat followed by 40mg in 5% dextrose.
 Antibiotics may be prescribed if necessary.
 Strict monitoring of blood pressure should be done.
 Maintain a strict intake and output chart and test all urine that is passed.
 In some cases an indwelling catheter may be passed.
 Fluid intake is restricted to one to two litres in 24 hours.
 Esbach should be set daily.
 The weight should also be measured daily or on alternative days. 145
ACTIVE MANAGEMENT OF SEVERE PRE-
ECLAMPSIA
 Administer medication as prescribed antihypertensive, sedatives and
anticonvulsive therapies.
 Observe for signs of onset of labour and signs of impending
eclampsia.
 If protenuria and high blood pressure persist, the doctor should induce
labour by artificial rupture of membranes followed by syntocinon drip.
 If there is some obstetric contra-indication a caesarean section will be
done.
Insummary: observe bed rest, diet, weight, urine, fluid in
take and out put, BP, abdominal examination, FHR, foetal
kick chart, hypotensive agents, sedatives, anticonvulsive,
monitor signs of labour and impending eclampsia. 146
 CARE DURING LABOUR
 Treatment for severe pre-eclampsia should be continued.
 Perform a vaginal examination to assess the progress of labour.
 During the second stage, episiotomy should be performed to shorten

the phase and the doctor will use vacuum extractor to prevent the
mother from pushing.
 Ergometrine is avoided because of its vaso-constrictive effect and

instead syntocinon 5 IV in a drip or intramuscularly is given.

 A Caesarean section may be performed if the condition does not

improve or there is obstetric contra-indication for vaginal delivery.

 Post Delivery Care for Pre-eclampsia Cases
 Sedate the mother and continue observations of vital signs.
Continue and adjust drugs as necessary. 147
 SIGNS OF IMPENDING ECLAMPSIA
 Mothers with severe pre-eclampsia can proceed to eclampsia.
 The following are warning signs of impending eclampsia:
1. A sharp rise in blood pressure >160/100 on two occasions 6hrs apart
2. Diminished urinary output ( less than 400mls in 24 hours)
3. Increased proteinuria +++ or 1gm/l in 24 hours
4. Severe persistent frontal or occipital headache
5. Drowsiness or confusion (due to cerebral oedema)
6. Blurring of vision or flashing lights (due to retinal oedema)
7. Nausea and vomiting
8. Epigastric pain which the mother may interpret as indigestion (due to oedema
of the liver)
 Should a mother present to your clinic with these signs, give her an anticonvulsant and refer to
hospital immediately for further management. 148

 In the hospital, the midwife should summon the doctor immediately.

 7. ECLAMPSIA
 Eclampsia is an acute condition characterised by convulsions and
coma.
 Eclampsia is a complication of severe pre-eclamsia and is
characterised by convulsions and coma.
 The incidence of eclampsia is 0.2 to 0.5% of all pregnancies.
 It can occur in the antenatal period at the rate of about 20%;
during the intrapartum period at the rate of about 25% and
during the postnatal period within the first few hours after
delivery (35%).
 A midwife should be able to preserve life of the mother until help
comes 149
 SIGNS AND SYMPTOMS OF ECLAMPSIA
The prodromal signs of eclampsia are those we have described as
serious signs of pre-eclampsia.
The more immediate precursors of eclampsia are vomiting,
intense headache and epigastric pain.
 There are four stages of an eclampsia fit.
1. Premonitory stage
2. Tonic stage
3. Clonic stage
4. Coma stage

150
STAGES OF ECLAMPTIC FIT
1. Premonitory stage, which lasts 10 to 20 seconds.
 The mother is restless with rapid eye movements
 The head may be drawn to one side, twitching of the facial

muscles may occur, and the mother is not aware of what is

happening.
 If talking, the mother may report sudden alteration in sense of

smell, taste

151
 CONT..
2. The tonic stage lasts 10 to 20 seconds.
 The muscles of the mother's body go into spasms and
become rigid.
 The back may become arched and her teeth become
tightly clenched.
 The eyes appear like they are staring and her diaphragm
goes into spasm.
 Respirations cease and cyanosis occurs.
152
 CONT…
3 The clonic stage lasts 60 to 90 seconds.
 There is violent contraction and intermitted relaxation of the mother's muscles
causing convulsive movements.
 There is increased salivation and foaming at the mouth.
 The mother's face becomes congested and bloated while her features become
distorted.
 The mother becomes unconscious and breathing is stertorous while the pulse full
and bounding.
 The convulsions subside gradually.

4. The coma stage

 stertorous breathing continues and the coma may persist for minutes or hours.
 Further convulsions may occur before the mother regains conciousness 153
 DIFFERENTIAL DIAGNOSIS
Eclampsia must be differentiated from other conditions that may be associated with convulsions and
coma, e.g.
 Epilepsy,
 Cerebral Malaria,
 Meningitis,
 Head Injury,
 Cerebrovascular Accident,
 Intoxication (Alcohol, Drugs, And Poisons),
 Drug Withdrawal,
 Metabolic Disorders,
 Water Intoxication,
 Encephalitis,
 Hypertensive Encephalopathy,
154
 Hysteria.
 INVESTIGATIONS
 Significant proteinuria defining preeclampsia is 300 mg or more of
protein in a 24-hour urine sample.
 Proteinuria suggestive of preeclampsia is greater than or equal to
1+ protein on urine dipstick or 300 mg/L or more on urine dipstick.
 Abnormal coagulation profile: Prothrombin Time and a Partial
Thromboplastin Time are elevated.
 Disseminated intravascular coagulopathy testing will show fibrin
split products and decreased fibrinogen levels.
 Uric acid Hyperuricemia is one of the earliest laboratory
manifestations of preeclampsia. It has a low sensitivity, ranging
from 0-55%, but a relatively high specificity, ranging from 77-95%.155
 INVESTIGATIONS CONT,,,
Ultrasonography:
 This is used to assess the status of the fetus as well as to
evaluate for growth restriction (typically asymmetrical IUGR).
Aside from transabdominal ultrasonography, umbilical artery
Doppler ultrasonography should be performed to assess blood
flow.

156
 DIAGNOSIS
 From clinical feature and protein in urine (convulsions, coma ,protein in urine
and BP may be high or normal)
Investigations : Laboratory Studies
 CBC count and peripheral smear
 Liver function tests: Transaminase levels are elevated from
hepatocellular injury and in HELLP syndrome.
 Serum creatinine level: Levels are elevated due to decreased

intravascular volume and decreased glomerular filtration rate

(GFR).
 Urinalysis - Proteinuria is one of the diagnostic criteria for

preeclampsia. 157
DRUGS USED IN MANAGEMENT OF PRE-ECLAMPSIA AND
ECLAMPSIA
 Magnesium sulphate is the first-line treatment of prevention of
primary and recurrent eclamptic seizures.
 For eclamptic seizures: Diazepam and phenytoin may be used as

second-line agents.
 In the setting of severe hypertension (systolic BP, >160 mm Hg;

diastolic BP, >110 mm Hg), antihypertensive treatment is

recommended.
 Antihypertensive treatment decreases the incidence of
cerebrovascular problems but does not alter the progression of
preeclampsia.
158
 MAGNESIUM SULPHATE (MAGSO4)

Magnesium sulphate: first line treatment for seizure

 This works by antagonizing calcium channels of smooth muscle.
 Administer IV/IM for seizure prophylaxis in pre-eclampsia.
 Use IV for quicker onset of action in true eclampsia.


159
 MAGNESIUM SULPHATE (MGSO4)
Magnesium sulphate schedules for severe pre-eclampsia and eclampsia
Loading Dose
 Magnesium sulphate 20% Solution, 4g IV over 5 minutes

 Follow promptly with 10g of 50% magnesium sulphate solution, 5g in each

buttock as deep IM injection with 1mL of 2% lignocaine in the same syringe

 Ensure that aseptic technique is practiced when giving magnesium sulphate deep

IM injection.
 Warn the woman that a feeling of warmth will be felt when magnesium sulphate is

given.
 If convulsions occur after 15 minutes, give 2g magnesium sulphate (50% solution)

IV over 5 minutes
160
 MGSO4
Maintenance Dose
 Give 5g magnesium sulphate (50% solution) + 1 mL lignocaine
2% IM every 4 hours into alternate buttocks.
 Continue treatment with magnesium sulphate 4houry for 24 hours
after delivery or the last convulsion, whichever occurs last.
 If 50% solution is not available, give 1g of 20% magnesium
sulphate solution IV every hour by continuous infusion.

161
 NURSING RESPONSIBILITY ON A PATIENT WITH MGSO4
Before repeat administration, ensure that:
 Respiratory rate is at least 16/above per minute;
 MGSO4 depresses the respiratory cente. If respiratory rate is less than 16 breaths /
minute STOP magnesium and give calcium gluconate (10%)1 g IV over 10 minutes
 Monitor respirations closely and withhold or delay the administration of the drug if
respiratory rate falls below 16 per minute
 Patellar reflexes are present; MGSO4 toxicity can lead to reduced deep tendon
reflexes withhold or delay the administration of the drug if patellar reflexes are absent
 Urinary output is at least 30 ml per hour over preceding four hours; monitor urine
output and withhold or delay the administration of the drug if Urinary output falls
below 30ml per hour over the preceding 4 hours
162
 Keep antidote ready: calcium gluconate is the antidote for MGSO4
 MGSO4
Incase of respiratory arrest:
 Assist ventilation (mask and bag, anesthesia apparatus,
intubation)
 Give Calcium gluconate 1g (10mL of 10% solution) IV
slowly until calcium gluconate begins to antagonize the
effects of magnesium sulphate and respiration begins

163
 DIAZEPAM
 In the absence of MgSO4, diazepam is used following the regime below
 Diazepam schedules for severe pre-eclampsia and eclampsia
Intravenous administration:
Loading dose
 Diazepam 20mg IV slowly over 2 minutes
 If convulsions recur, repeat loading dose
Maintenance dose
 Diazepam 40mg in 500ml IV fluids (normal saline or Ringer's Lactate) titrated to
keep the woman sedated but can be aroused
 Maternal respiratory depression may occur when dose exceeds 30mgs in 1 hour
 Assist ventilation (mask and bag, anesthesia apparatus, intubation), if necessary
 Do not give more than 100mg in 24 hours.
164
 CONT…
Rectal Administration:
 Give Diazepam rectally when IV access is not possible.

 The loading dose is 20mg in 10ml syringe.

 Remove the needle, lubricate the barrel and insert the syringe into the

rectum to half its length.

 Discharge the contents and leave the syringe in place, holding the buttocks

together for 10 minutes to prevent expulsion of the drug.

 Alternatively, the drug may be instilled into the rectum through a catheter.

 If convulsions are not controlled within 10 minutes administer an additional

10mg per hour or more, depending on the size of the woman and her
clinical response
165
 PHENYTOIN
 Phenytoin has been used successfully in eclamptic seizures, but cardiac
monitoring is required due to associated bradycardia and hypotension.
 Central anticonvulsant effect of phenytoin is by stabilizing neuronal
activity by decreasing the ion flux across depolarizing membranes.
 Some benefits to using phenytoin are that:
 It can be continued orally for several days until the risk of eclamptic
seizures has subsided,
 It has established therapeutic levels that are easily tested,
 It has no known neonatal adverse effects are associated with short-term
usage.
Dosage:
 10 mg/kg loading dose infused IV no faster than 50 mg/min, followed by166
maintenance dose started 2 hrs later at 5 mg/kg
 ANTIHYPERTENSIVE
 These agents are used to decrease systemic resistance and help reverse
uteroplacental insufficiency.
1. Hydralazine (Apresoline)
 This is the first-line therapy against pre-eclamptic hypertension.
 It decreases systemic resistance through direct vasodilatation of arterioles,
resulting in reflex tachycardia.
 Reflex tachycardia and resultant increased cardiac output helps reverse
uteroplacental insufficiency, a key concern when treating hypertension in a patient
with preeclampsia. Adverse effects to the fetus are uncommon.
Dosage
 Give 5mg IV slowly over 10 mines if BP > or =160/110mm Hg; repeat 5 mg every
167
20min to maximum of 20 mg
 2. ALPHA –METHYLDOPA (ALDOMET)

 Safe and well tested;

 however, it has a delayed onset of 4 to 6 hours even with

I.V. administration, limiting its usefulness for hypertensive

emergencies.
 Can cause somnolence (sleepiness) in some patients.

168
 CONT…

2. Nifedipine
It relaxes coronary smooth muscle and produces coronary

vasodilatation, which, in turn, improves myocardial

oxygen delivery. Sublingual administration is generally
safe, despite theoretical concerns.
Dosage
Initial dosage is 10 mg orally of BP > or = 160/110 mm

hg. One may repeat after 30 minutes as needed

169
 CONT…

3. Labetalol
 This is the recommended second-line therapy that produces vasodilatation
and decreases in systemic vascular resistance.
 It has alpha-1 and beta-antagonist effects and beta2-agonist effects.
 The onset of action is more rapid than hydralazine and it results in less
overshoot hypotension.
 Dosage and duration of labetalol is more variable. Adverse effects to fetus
are uncommon.
Dosage
 Give 20mg bolus, subsequently give doses of 40mg followed by 80mg IV
at 10- 20 min intervals to achieve
 BP control to a maximum of 300 mg. Labetalol may also be administered170
by continuous IV infusion at 1mg /kg/hr.
 NURSING ASSESSMENT
 Evaluate BP using the correct size cuff and same arm for each measurement. The sitting
position is recommended with the (preferably right) arm supported in a horizontal
position at the level of the heart. In the side-lying position, the dependent arm should be
used, but the patient should not be lying on it.
 Check the protein level of a spot urine specimen and initiate a 24-hour urine specimen.
 Measure weight daily when the patient is stable.
 Evaluate DTRs and clonus.
 Evaluate fetal status, fetal movement (kick) counts, BPP, and contraction stress test (CST)
via nipple stimulation or oxytocin challenge test (OCT).
 Evaluate uterine activity for high-frequency, low-intensity uterine contractions.
 Observe for signs and symptoms of disease escalation.
 Monitor for signs of MgSO4 toxicity (absent knee-jerk reflex, respiratory depression,
oliguria). Discontinue MgSO4, and notify health care provider
 Serum magnesium level every 6 to 8 hours per your facility's policy.
171
 NURSING DIAGNOSIS
1. Excess Fluid Volume related to pathophysiologic changes of
gestational hypertension and increased risk of fluid overload as
evidenced by oedema
2. Ineffective Tissue Perfusion: Fetal Cardiac and Cerebral related to
altered placental blood flow caused by vasospasm and thrombosis
as evidenced ……
3. Risk for Injury related to seizures or to prolonged bed rest or other
therapeutic regimens
4. Anxiety related to diagnosis and concern for self and fetus
5. Knowledge deficit related to diagnosis and therapeutic regimen
6. Deficient Diversional Activity related to prolonged bed rest
172
7. Decreased Cardiac Output related to decreased preload or
antihypertensive therapy
 NURSING INTERVENTION
1. Maintaining Fluid Balance
1. Control I.V. fluid intake using a continuous infusion pump.
2. Monitor intake and output strictly; notify health care provider
if urine output is less than 30 mL/hour.
3. Monitor hematocrit levels to evaluate intravascular fluid
status.
4. Monitor vital signs every hourly.
5. Auscultate breath sounds every 2 hours, and report signs of
pulmonary edema (wheezing, crackles, shortness of breath,
increased pulse rate, increased respiratory rate).
173
 2. PROMOTING ADEQUATE TISSUE PERFUSION

1. Position on side to promote placental perfusion.

2. Monitor fetal activity.
3. Evaluate NST to determine fetal status.
4. Increase protein intake to replace protein lost through
kidneys

174
 3. PREVENT INJURY
 Instruct on the importance of reporting headaches, visual changes,
dizziness, and epigastric pain.
 Instruct to lie down on left side if symptoms are present.

 Keep the environment quiet and as calm as possible.

 If patient is hospitalized, side rails should be padded and remain

up to prevent injury if seizure occurs.

 If patient is hospitalized, have oxygen and suction setup, along

with a tongue blade and emergency medications, immediately

available for treatment of seizures.
 Assess DTRs and clonus every 2 hours. Increase frequency of

assessment as indicated by patient's condition 175

4. DECREASE ANXIETY AND INCREASE KNOWLEDGE
1. Explain the disease process and treatment plan including
signs and symptoms of the disease process.
2. Explain that preeclampsia does not lead to chronic
hypertension.
3. Discuss the effects of all medications on the mother and
fetus.
4. Allow time to ask questions and discuss feelings regarding
the diagnosis and treatment plan

176
 5. PROMOTING DIVERSIONAL ACTIVITIES
1. Explain the need for bed rest to the woman and her
support persons.
2. Explore woman's hobbies/diversional activities.
3. Instruct family to arrange for easy access to TV, phone,
computer, and stereo to limit woman getting out of bed.
4. Instruct family to arrange for community support (eg,
church, women's groups).

177
 6. MAINTAIN CARDIAC OUTPUT
1. Control I.V. fluid intake using a continuous infusion pump.
2. Monitor intake and output strictly; notify primary care provider if
urine output is less than 30 mL per hour.
3. Monitor maternal vital signs, especially mean BP and
respirations.
4. Assess edema status, and report pitting edema of ≥ +2 to
primary care provider.
5. Monitor oxygenation saturation levels with pulse oximetry.
Report oxygenation saturation rate of less than 90% to primary
care provider.
178
 EVALUATION: EXPECTED OUTCOMES
1. No evidence of pulmonary edema; urine output adequate
2. FHR within normal range; reactivity present
3. No seizure activity
4. Expresses concern for self and the fetus
5. Maintaining bed rest and pursuing diversional activities
6. BP and other vital parameters stable

179
 MANAGEMENT OF ECLAMPSIA
The aim of immediate care is to:
1. Clear and maintain mothers airway. This may be achieved by the
insertion of an airway as soon as premonitory stage is observed , by placing
mother in semi prone position in order to facilitate the drainage of saliva and
vomitus and by aspirating if suction facilities are present
2. Administer oxygen and prevent hypoxia
3. Prevent the mother from being injured during the chronic stage.
 The main principle of management is:
1. To stop convulsions
2. Deliver the pregnant woman by the quickest and safest method.
 The mother's welfare is of paramount importance and the foetus is the secondary
consideration as it is already in great danger.

180
 MANAGEMENT OF ECLAMPSIA
Steps in a health center:
Do not leave the woman alone.
Call for help.

Insert a mouth gag to prevent the mother from biting her

tongue.
Place the mother in semi-prone position to facilitate drainage

of saliva and vomitus.

Aspirate to remove mucus and to maintain clear airway and

administer oxygen as necessary. 181

 MANAGEMENT OF ECLAMPSIA IN A H/C
 Insert an IV canular and give fluids slowly
 Stop convulsions by giving intravenous magnesium sulphate

loading dose followed by maintenance dose (MGSO4) or

diazepam if no MGSO4
 Transfer the patient to hospital by quickest means and

accompany her.
 Take a delivery and emergency tray with drugs and mucus

extractor, the patient's notes and records.

 Inform the hospital before you leave. 182
 MANAGEMENT OF ECLAMPSIA IN HOSPITAL
 Call for help the patient should be managed by an obstetrician in form NBU, lab,
theater
 Maintain open airway Insert a mouth gag to prevent the mother from biting

her tongue.
 Place the mother in semi-prone position to facilitate drainage of saliva and

vomitus.
 Aspirate to remove mucus and to maintain clear airway and administer

oxygen as necessary to prevent hypoxia

 Control Convulsions by giving MGSO4 as per regimen or diazeperm

 Control the blood pressure with hydralazine and monitor quarter hourly

until diastolic BP is 90mmhg then maintain it at this level by titrating IV

infusion of hydrallazine 183
 MANAGEMENT OF ECLAMPSIA
 Start IV line but restrict fluid intake 2000mls in 24 hours avoid to
pulmonary and cerebral edema. Maximum of 30 drops per minute.
 Catheterize, to maintain continuous urine drainage

 Strictly monitor fluid intake and urine output

 The doctors will perform careful assessment to determine the method of

delivery. Vaginal delivery is preferred unless there is contra-indication.

 Once the blood pressure is under control, labour is induced by

artificial rupture of membranes and syntocinon drip commenced.

 If vaginal delivery is not possible she is delivered by caesarean

section.
 The patient should be nursed in a darkened, quiet room. 184
 MANAGEMENT OF ECLAMPSIA
 Take observations of vital signs and uterine contractions
half hourly.
 Protect from injury from the cot sides and nurse in semi-prone position to
encourage saliva and mucus drainage.
 Do not restrict convulsive movements.

 Ensure catheter care and keep the airway clear.

 Prepare for delivery or caesarean section as appropriate.

 After a fit continue oxygen therapy and, do not give oral fluids.

 Observe for signs of labour.

 Delivery is by vacuum extraction and sedation is continued.

 The baby should be nursed in the special care baby unit (nursery).

185
 MANAGING A PATIENT DURING A
CONVULSION/SEIZURE/FIT
 Patient should be put in semi prone position so that mucous and saliva
can drain out
 Tight fitting dresses around the neck should be loosened or removed
 No attempt should be made to insert any instrument into the mouth
 Administer magnesium sulphate (or diazepam) as per regime to control
fits
 Aspirate secretions from the mouth and nostrils as necessary
 Give Oxygen continuously during fit and for 5 minutes after each fit (if
available)
 Fitting should be allowed to complete its course without restraining the
patient 186

 Privacy and dignity of patient must be observed - pull screens around her
 DELIVERY
 Delivery should take place as soon as the woman’s condition has
been stabilized, preferably within 6-8 hours from first convulsion;
or within 12 hours of admission
 Delaying delivery to increase fetal maturity will risk the lives of
both the woman and the fetus.
 Delivery should occur regardless of the gestational age, but
Eclampsia alone is not an indication for C/section.
 Get skilled anaesthetic help early; this will also aid the
management of hypertensive crises and fits.
187
 MODE OF DELIVERY
 Vaginal delivery is recommended:
 If the cervix is favorable (soft, dilated, effaced), rupture the membranes and

induce labor using oxytocin

 If there is no absolute indication for Caesarean section

 If safe anesthesia is not available for C/section or if the fetus is dead

or too premature for survival:
 If the cervix is unfavorable (firm, thick, closed), ripen the cervix

using prostaglandins or a Foley catheter

 Caesarean section should be done:
 If vaginal delivery is not anticipated within 8 hours (for eclampsia) or 24 hours

(for severe preeclampsia), deliver by C/section

 If there are fetal heart rate abnormalities (< 100 or > 180 beats / minute)

 If the cervix is unfavorable (firm, thick, closed) and the fetus is alive, 188
 POSTNATAL CARE
 Continue anticonvulsive therapy for 24 hours after delivery or last
convulsion, whichever occurs last.
 Continue antihypertensive therapy as long as the diastolic pressure

is 110 mmHg or more.

 Continue to monitor urine output. If urine output is less than 500

ml in 24 hours, limit the amount of fluid intake to 500 mills per 24

hours + an amount equal to the amount of urine passed
 Watch carefully for the development of pulmonary edema, which

often occurs after delivery.

 Life threatening complications can still occur after delivery. Monitor

carefully until the patient is clearly recovering. 189

 POSTNATAL CARE
 Consider referral of women who have:
 Oliguria (less than 500 ml urine output in 24 hours) that persists
for 48 hours after delivery
 Coagulation failure (e.g. coagulopathy or hemolysis, elevated
liver enzymes and low platelets (HELLP) syndrome)
 Persistent coma lasting more than 24 hours after convulsion.
Prognosis:
 Early detection and frequent obstetric assessment and prompt
management markedly improves
 Delivery is the only cure for pre-eclampsia and eclampsia
190
 COMPLICATIONS OF PRE-ECAMPSIA AND ECLAMPSIA

1. Cerebral haemorrhage and oedema 10. Asphyxia neonatorum

2. Thrombosis 11. Still birth
3. Acute renal failure 12. Pulmonary oedema
4. Abruptio placentae 13. Bone fractures
5. Liver necrosis 14. Foetal distress
6. Confussion 15. IUGR
7. Myocardial failure 16. Neonatal death
8. Temporary blindness 17. Maternal death and foetal death
9. Prematurity 18. HELLP syndrome (haemolysis, elevated
liver enzymes, reduced platelet) 191
 8. PREMATURE RUPTURE OF MEMBRANES (PROM)
 Premature rupture of membranes (PROM) is defined as rupture of the
membranes before the onset of labor.
 PROM is independent of gestational age; when it occurs prior to term it is
referred to as preterm PROM (PPROM).
 Due to confusion of the terms PROM and PPROM, the term prelabor rupture of
membranes may be used in place of PROM.
 This condition occurs in 3% to 18.5% of pregnancies.

192
 PATHOPHYSIOLOGY
 The exact etiology of PROM is not clearly understood,
although nonpathologic causes such as the combination of
stretching of the membranes and biochemical changes are
suspected to contribute.
 PROM is manifested by a large gush of amniotic fluid or

leaking of fluid per vagina, which usually persists.

193
 PREDISPOSING FACTORS
 Multiple pregnancy
 Polyhydramnios

 Cervical incompetence

 Trauma e.g. Pelvic exam, abdominal amniocentesis, external

versions, sexual intercourse, blows.

 Maternal vaginal colonization with potentially pathogenic

infections
 Smokers and recreational drug users

194
 DIAGNOSIS
1. Sterile speculum examination for identification of pooling of fluid in the vagina.
2. Nitrazine test: positive test will change pH paper strip from yellow-green to blue
in the presence of amniotic fluid taken from the vaginal canal.
3. Fern test: positive test will reveal ferning on a slide viewed under a microscope.
A swab of the posterior vaginal fornix is taken to obtain amniotic fluid.
4. Ultrasound to assess amniotic fluid volume.
5. Amniocentesis to inject indigo carmine or Evans blue dye. Watch for vaginal
leakage of blue fluid to assess for ruptured membranes.

195
 RISK OF PROM
 Imminent labour resulting in premature birth
 Chorioamnionitis, which may be followed by foetal and maternal systemic infections
 Oligohydramnios if prolonged PPROM occurs
 Cord prolapse
 Malpresentation associated with prematurity
 Antepartum haemorrhage
 Neonatal sepsis
 Psychosocial problems resulting from uncertain foetal and neonatal outcome and long
term hospitalization; impaired mother and baby bonding after birth.

196
 CLINICAL FEATURES

 Early - intermittent vaginal drainage of amniotic fluid

 late – chorioamnionitis (inflammation of chorionic villi of theplacenta due to
ascending infection)
 May complicate if delivery is not done within 24 hours

197
 MANAGEMENT
 When PROM is confirmed, the woman is admitted to the hospital and usually
remains there until delivery
 May prolong pregnancy to reach almost term so as to ensure maturity of foetal lungs
and preferable birth weight
 This is indicated if:
 Gestation is less than 35 weeks
 Foetal weight is less than 1800gms
 Thereis no chorioamnionitis
 Take history to determine the period that has elapsed after membranes have ruptured
and rule out maternal conditions that may contraindicate mode of delivery.
 Do speculum examination to see if cervix is open
198
 CONT…
 Take cervical swab for c/s to rule out infections
 Admit the woman for bed rest and arrest labour

 Give sedatives to promote rest and allay anxiety

 give antibiotics prophylactically

 If prognosis is good , pregnancy is allowed to continue to term or near term

 Administer dexamethasone 4mg tds to promote maturation of the lungs

 May allow labour to continue or induce with syntocinon drip if

1. There signs of infection chorioamnionitis

2. Cervix is more than 3cm dilated or 50% effaced
3. Pregnancy is 36 weeks and above.

199
 POSSIBLE COMPLICATIONS
1. Preterm delivery
2. Cord prolapse when the cord is swept by gush of fluid
3. Malpresentation – the foetus is small and can assume varieties
of presentation
4. Chorioamnionitis due to infection if no intervention within 24
hours
5. Placenta abruptio

200
 NURSING ASSESSMENT
 Evaluate maternal BP, respirations, pulse, and temperature every 2 to 4 hours. If
temperature or pulse is elevated, continue monitoring every 1 to 2 hours as
indicated.
 Monitor the amount and type of amniotic fluid that is leaking, and observe for
purulent, foul-smelling discharge.
 Evaluate daily CBC with differentials, noting any shift to the left (ie, increase of
immature forms of neutrophils).
 Evaluate fetal status every 4 hours or as indicated, noting fetal activity and heart
rate and uterine activity.
 Determine if uterine tenderness occurs on abdominal palpation.
 Nursing Diagnosis

 Risk for Infection related to ascending bacteria

201
 NURSING INTERVENTION
Preventing Infection
 Evaluate amount and odour of amniotic fluid leakage.
 Do not perform vaginal examinations without consulting the health care provider.
 Place patient on disposable pads to collect leaking fluid, and change pads every 2
hours or more frequently as needed.
 Review the need for good hand-washing technique and hygiene after urination and
defecation.
 Monitor FHR and fetal activity every 4 hours or more frequently as indicated.
 Monitor maternal temperature, pulse respirations, BP, and uterine tenderness at least
every 4 hours or more frequently as indicated.

202
EVALUATION: EXPECTED OUTCOMES

 Evaluation: Expected Outcomes

 No signs of infection

203
PRETERM PREMATURE RUPTURE OF MEMBRANES
(PPROM)
 Preterm premature rupture of membranes (PPROM) is defined
as rupture of membranes before 37 completed weeks' gestation
with or without the onset of spontaneous labor.
 Recently, due to the confusion over the meaning of premature
rupture of membranes (ie, before labor versus preterm), the
term preterm prelabor rupture of membranes is used to
signify rupture of membranes in preterm gestations

204
 PATHOPHYSIOLOGY
Exact cause is unknown. However, PPROM is likely to be either
a pathologic intrinsic weakness or extrinsic factors causing the
membranes to rupture prematurely.
 In PPROM, risk factors include:
1. Infection (amnionitis; group B beta-hemolytic
Streptococcus)
2. Previous history of PROM or PTB
3. Hydramnios (polyhydramnios/oligohydramnios)
4. Incompetent cervix
205
 RISK FACTORS
5. Increased intrauterine volume (multiple gestation, fibroids,
polyhydramnios)
6. Abruptio placentae
7. Cigarette smoking
8. Fetal anomalies
9. Coitus (intercourse)
10. Vaginal colonization with group B beta-hemolytic
Streptococcus
11. Prenatal vaginal bleeding in more than one trimester
206
 DIAGNOSIS
1. Sterile speculum examination for identification of pooling of fluid in the vagina.
2. Nitrazine test: positive test will change pH paper strip from yellow-green to blue in the
presence of amniotic fluid taken from the vaginal canal.
3. Fern test: positive test will reveal ferning on a slide viewed under a microscope. A
swab of the posterior vaginal fornix is taken to obtain amniotic fluid.
4. Ultrasound to assess amniotic fluid volume.
5. Amniocentesis to inject indigo carmine or Evans blue dye. Watch for vaginal leakage of
blue fluid to assess for ruptured membranes.

207
 MANAGEMENT OF PPROM
 For PPROM, tocolytics, corticosteroids (to promote lung maturity
and decrease the severity of RDS in the premature neonate), and
prophylactic antibiotics are used.
 Management is influenced by gestational age.
Initial management:
 Confirm rupture of membranes.

 Determine if bacterial infection is present at time of rupture by

vaginal/cervical cultures.
 Document age of gestation.

 Determine fetal lung maturity by amniocentesis or vaginal

culture 208
MANAGEMENT OF PPROM
Conservative management:
 Bed rest.
 Vital signs per your facility's policy and patient condition.

 Monitor fetal well-being daily or more frequently as

dictated by your facility's policy and patient condition.

Active management:
 Tocolytic therapy.
 Antibiotic therapy.

 Corticosteroid administration.
209
 Amnioinfusion.
 COMPLICATION
 Same as PROM

Fetal infection
 Neonatal RDS,

Nursing assessment as for PROM

210
 8. PREMATURE LABOUR
 Pemature labour refers to onset of labour before 37 weeks of gestation
Predisposing factors
 Premature rupture of membranes

 Polyhydramnios

 Cervical incompetence

 Multiple pregnancy

 Preeclampsia

 Cardiac disease

 Pyelonephritis

 Diabetes mellitus

 Emotional stress 211

 Rhesus isoimunization
 Clinical Manifestations

 Uterine cramps (menstrual-like, intermittent or constant)

 Uterine contractions occurring at intervals of 10 minutes or

less
 Low abdominal pressure (pelvic pressure)

 Dull low backache (intermittent or constant)

 Increase or change in vaginal discharge

 Feeling that baby is pushing down or that something is in the

vagina
 Abdominal cramping with or without nausea, vomiting, or
212
diarrhea
 MANAGEMENT
 The focus of treatment is prevention of delivery of a preterm neonate starting with
preconception care and focusing on the many risks attributable to preterm labor and birth.
Preconception Care
 Baseline assessment of health and risks with advice to decrease the risks
attributable to PTL/PTB.
 Pregnancy planning and identification of barriers to care.

 Adjustment of prescribed and over-the-counter medications that may

pose a threat to the developing fetus.

 Advice to improve maternal nutrition.

 Screening for and treatment of diseases.

 Genetic counseling for those with a history of genetic disease or a

213
previously affected pregnancy
MANAGEMENT DURING ANTEPARTUM PERIOD
 Educate mother regarding signs/symptoms of PTL (noted above).
 Instruct mother and provide resources for lifestyle modifications:

 Ifmother smokes, encourage smoking cessation classes.

 Ensure mother has a healthy diet and adequate maternal weight gain during

pregnancy.
 Initial treatment for a patient who is at risk for PTL is the use of bed
rest in a left lateral position with continuous monitoring of fetal status
and uterine activity.
 Hydration with I.V. fluids, with careful assessment of intake and

output and auscultation of lungs to assess for the development of

pulmonary edema.
214
 If this stops the contractions, tocolytic therapy is not needed.
INDICATION FOR PROGRESS OF PREMATURE LABOUR
 Severe maternal conditions e.g. pe-eclampsia, APH, rhesus
isoimmunization
 Cervix more than 3cm dilated, and greater than 50% effacement
 Membranes are ruptured and large amount of liquor is draining out
 Acute fetal distress (not to include intrauterine resuscitation)
 Intra-amniotic infection
 Intra Uterine Fetal Death(IUFD)

215
 CONT…
 Fetal maturity
 Maternal hemodynamic instability
 Fetal abnormality incompatible with life
 Severe IUGR
 Premature labour without rupture of membranes
 No signs of foetal distress
 Satisfactory maternal condition
 Cervix is less than 3cm dilated and effacement is less than 50%

216
 MANAGEMENT DURING LABOUR
 The woman should be admitted early and given bed rest. Mild sedation may be
necessary
 Give corticosteroids to accelerate lung maturity e.g. dexamethasone or
betamethasone 12mgs 2 doses 24 hours apart
 Manage the febrile conditions

 If the contractions are mild, tocolytics e.g MagSO4, Nifedipine, give salbutamol
tabs 4mg tds to relax uterine contractions but if severe give IV buscopan
 Monitor FHR and rule out foetal distress

 If labour has to be augmented, low doses of syntocinon are used

 ARM is delayed until labour is advanced and the presenting part has engaged to
prevent cord prolapse and risk infections

217
 CONT..
In 2nd stage:
 Inform a paeditrician and have your resuscitation tray ready in anticipation for an
asphyxiated baby.
 Give a generous episiotomy to prevent intracranial injury

 Deliver baby in a warm delivery room to prevent hypothermia

 Clamp and cut the cord immediately to reduce blood flow to the foetus since
chances of physiological jaundice are high due to immature liver.
 Assist baby to establish respiration by clearing the air way and administer oxygen
to prevent respiratory distress.
 Nurse the baby in an incubator to prevent hypothermia

 If membrane had ruptured early, give prophylactic antibiotics

218
 POSSIBLE COMPLICATIONS
 Prematurity and associated neonatal complications such as,

 lung immaturity
 Intraventricular haemorrhage (IVH)
 Respiratory distress syndrome (RDS)
 Patent ductus arteriosus (PDA)
 Necrotising enterocolitis (NEC)

 Potential complications of tocolytic agents

 Financially,its costly keeping the patient and the baby in the Hospital

219
 PREVENTION OF PREMATURE LABOUR
1. All susceptible cases should be admitted early and given bed
rest and appropriate management
2. Febrile conditions should be treated well
3. Prevent anaemia with balanced diet and give haematinics if it
occurs.
4. Abdominal amniocentesis should be done to those with
polyhydrmnios
5. Treat pre-eclampsia if it occurs and control BP
6. Give health education to mothers on importance of antenatal
care, nutrition, bed rest 220
 NURSING DIAGNOSIS
1. Anxiety related to hospitalization, medication and fear of
outcome of pregnancy as evidenced by the mother being
inquisitive.
2. Deficient Diversional Activity related to prolonged bed
rest……
3. Risk for Injury to fetus secondary to prematurity
4. Risk for Injury secondary to tocolytic therapy
5. Compromised Family Coping secondary to hospitalization

221
 DRUGS GIVEN IN PREMATURE LABOUR
1. Acceleration of Fetal Lung Maturity
 Corticosteroid administration betamethasone or dexamethasone
 Pregnant women between 24 and 34 weeks' gestation with any
possibility of PTL are candidates for this therapy.
 Betamethasone is given I.M. in two doses of 12 mg each, 24 hours

apart.
 Decreases intraventricular hemorrhage (IVH), necrotizing

enterocolitis (NEC), and respiratory distress syndrome (RDS) that

may be a result of prematurity.
 Timely administration is essential; given before delivery to mother;

try to postpone delivery for 48 hours

222
 CONT…
2. Tocolytic Therapy
 If antepartum therapy is not successful, tocolytic therapy may be instituted. These
drugs should be used only when the potential benefit to the fetus outweighs the
potential risk.
a) MgSO4 interferes with smooth muscle contractility, although its exact
mechanism of action is unknown.
 Administration is I.V. on an infusion pump.

 During administration, the woman is monitored for pulmonary edema, loss

of deep tendon reflexes, decreased respirations, hypotension.

 Other maternal adverse effects include flushing, headache, nausea and

vomiting, shortness of breath, and chest pain.

 Serum magnesium levels are monitored.

 Calcium gluconate is the antidote for MgSO and should be at the bedside. 223
4
 If used, protocol is the same as for preeclampsia
 CONT
2. Prostaglandin inhibitors: indomethacin (Indocin) inhibits
contractions; however, after 34 weeks' gestation, indomethacin may
cause premature closure of the fetal ductus arteriosus, increasing the
risk of fetal pulmonary hypertension.
 Administration is oral or rectal; short-term use is recommended for only 48 to 72
hours.
 Suggested for use before 32 weeks' gestation, if fetus shows no evidence of IUGR

and AFI is normal.

3. Calcium channel blockers nifedipine (Procardia) relaxes smooth
muscle by inhibiting the transport of calcium.
 Administration is sublingual or oral.

 Maternal adverse effects include headache, nausea, hepatotoxicity,

224
and flushing from vasodilatation. Fetal adverse effects include
decreased uteroplacental blood flow, fetal hypoxia, and bradycardia.
 8. POSTDATISM/ PROLONGED PREGNANCY
 Pregancy is deemed prolonged if it goes beyond 42 weeks of
gestation (294 days) from the first day of the last menstrual period or
280days from the day of conception.
 This is based on the Naegele’s rule that the cycle is 28 days and that

ovulation occurs on the 14th day.

 The incidence is between 5-10%

 A true incidence is difficult to assess in because many cases women

are induced before reaching 42 weeks as defined due to specific

complications of pregnancy.
 Only a small proportion of pronged pregnancy result in babies that are

post mature 225

 CONT..
 The use of ultrasound in early pregnancy for precise date
significantly reduces the number of post term pregnancies
compared to dating based on LMP
 Around 20% of pregnant women will need induction of

labour –the majority for post-term pregnancy

 74% of women will have delivered by 40 weeks of gestation

and 82% by 42 weeks.

 Post term pregnancy is now one of the most common

indications for induction of labour

226
 EFFECTS TO THE MOTHER
 Large for gestation infant which may lead to:
1. Shoulder dystocia
2. Genital tract trauma
3. Operative birth C/S, vacuum, forceps de
4. Postpartum haemorrhage
5. Psychological

227
 EFFECTS TO THE FOETUS
Effects on the foetus due to placenta insufficiency
Oligohydramnios,
Restricted foetal growth
Meconium aspiration
Neonatal hypoglycaemia
Asphyxia
Still birth

228
 PREDISPOSING FACTORS
 Obesity
 Primigravida or Nulliparity

 Family history of prolonged pregnancy

 Male foetus

 Foetal anomaly such as anecephally

 Factors increasing the risk: elderly primigravida, poor obstetric history, pre-
eclampsia, diabetes mellitus
 Previous large baby

229
 INVESTIGATIONS

 Women with no other indication for induction, who do not wish labour to be
induced can be offered monitoring to assess placental function and foetal
health.
 If there is low risk monitor mother and foetal well being weekly at ANC
clinic,
 U/S, amniotic fluid index, assessment of foetal breathing, muscle tone and
gross body movement

230
 PRESENTATION (SIGNS AND SYMPTOMS)

 There may be reduced foetal movement before delivery

 A reduced volume of amniotic fluid may cause a reduction in the size of the
uterus.
 Meconium stained amniotic fluid may be seen when membranes have ruptured

 Lowered amount of sub cutaneous fat and reduced mass of soft tissue

 The skin is loose, flaky and dry

 There is presence of peeling of the epindermis

 Finger nails and toe nails may be longer than usual and stained yellow from
meconium
231
 MANAGEMENT
 Admit or refer any woman with a pregnancy that exceeds 41 weeks for review by
an obstetrician
 Induction of labour should be done after 41 weeks between 41+0- 42+0 to avoid
post term pregnancy and the compliaction
 Any prolonged pregnancy with obstetric complication induce labour artificially

 Assess mother for sudden weight gain, rising BP, proteinuria this would indicate
pre-eclampsia
 Assess psychological well being of the mother

 Perform a cervical membrane sweep, this attempts to initiate labour

physiologically
 Induction of labour should be done after 41 weeks

232
 INDICATIONS FOR INDUCTION
Foetal:
1. Intrauterine growth restriction (IUGR)- the foetus will be compromised if
pregnancy is around to continue.
2. Macrosomia- to reduce the risk associated with shoulder dystocia.
3. Foetal death
4. Foetal anomaly not compatible with life

233
 INDICATIONS FOR INDUCTION
Maternal:
1. prolonged pregnancy >42 weeks
2. Hypertension including pre-eclampsia
3. Diabetes the type and severity of diabetes influences the decision to induce.
Risk of macrosomia is increased.
4. Prelabour rupture of membranes (24 hours)

234
 9. ANAEMIA IN PREGNANCY

 Anaemia is a deficiency in the quality or quantity of red blood

cells with the result that the oxygen carrying capacity of the
blood is reduced.
 The normal haemoglobin level in a female is 12 to 14gm per
deciliter.
 Anaemia is diagnosed in pregnant women when the
haemoglobin level is below 10gm per deciliter
 50% of all pregnant women are considered to be anaemic.
 52% in the non industrialised countries and 23% in the
industrialized world.
235
 FEMALE HB BLOOD RANGES
 Non pregnant women Hb < 12gm%
 Pregnant women (WHO) Hb < 11 gm%
 Haematocrit < 33%
 Pregnant women (CDC) Hb <11 gm%
 1st&3rd Trimester
 2nd trimester Hb < 10.5 gm%

236
 WHO IS AT RISK OF ANAEMIA
1. Women from low social economic status
2. Young primigravida
3. Frequent or too many pregnancies
4. Heavy menses
5. Previous history of APH or PPH
6. Multiple pregnancy

237
 CLINICAL PRESENTATION OF ANAEMIA
 The onset of the symptoms is slow and the mother may disregard
them, believing them to be part of being pregnant.
 The following are some of the signs and symptoms of anaemia:
 Pallor of mucous membranes
 Breathlessness
 Palpitations (awareness of fast heart beats)
 Dizziness
 Fatigue and lethargy
 Fainting attacks
 Headaches due to lack of sufficient oxygen to brain cells
 Anorexia and vomiting

238
EFFECTS OF ANAEMIA IN PREGNANCY TO MOTHER
1. It reduces resistance to infection caused by impaired cell
mediated immunity
2. Predisposition to postpartum Haemorrhage
3. Potential threat to life
4. Problems caused by treatment and side effects
like constipation
5. It reduces enjoyment of pregnancy due to fatigue

239
EFFECTS OF ANAEMIA IN PREGNANCY TO THE
FOETUS/BABY
1. High perinatal morbidity and mortality if maternal
haemoglobin level is below 8gm/deciliter
2. Increased risk of intra uterine hypoxia and IUFD
3. Intrauterine growth retardation (IUGR)
4. Severe asphyxia in severe anaemia
5. Increased sudden infant death when maternal
haemoglobin is below 10gm/decilitre

240
 DEGREES OF ANAEMIA
These are classified according to the severity in pregnancy:
 Mild anaemia is when haemoglobin level is between
9gm/dl to 10.9gm/dl
 Moderate anaemia is when the haemoglobin level is between
7gm/dl to 10gm/dl
 Severe anaemia is when the haemoglobin is less than
7gm/dl
In severe anaemia there is:
 Renal hypoxia resulting in retention of sodium and
electrolytes.Myocardial hypoxia leading to heart failure
 Mental confusion
 Cough, especially with congestion in lungs 241
 TYPES OF ANAEMIA IN PREGNANCY
1. Physiological anaemia
2. Iron deficiency anaemia
3. Folic acid deficiency anaemia
4. Vitamin B12 deficiency anaemia
5. Haemolytic anaemia
6. Haemoglobinopathies e.g. thalassemia and sickcle cell and
glucose-6 phosphate dehydrogenase (G6PD)

242
 1. PHYSIOLOGICAL ANAEMIA
 During pregnancy the blood plasma volume increases by
15% by the 10th week of gestation and 50% by the 32nd to
the 35th week of pregnancy.
 The red cells mass increases by 30%.
 These result in HAEMODILLUTION with resultant
increased cardiac output from five to seven litres per minute.
 These changes result in apparent anaemia but as this
represents the normal pregnancy state, they should not be
regarded as pathological.
243
 2. IRON DEFICIENCY ANAEMIA

Iron deficiency anaemia is thought to be the leading cause of

anaemia globally.
During pregnancy approximately 1400gm of iron is needed

during the entire period.

This is necessary for:

 The increased number of red blood cells

 The foetus and the placenta
 Replacement of blood lost during delivery
 Lactation

244
 CAUSES OF IRON DEFICIENCY ANEMIA

1. Reduced intake of iron due to gastric malabsorption, gastric surgery or dietary

deficiency
2. Short intervals between pregnancies
3. Increased demand such as in multiple pregnancy
4. Chronic infections such as malaria and HIV
5. Chronic blood loss e.g. menorrhagia before conception or gastric ulcers,
Hookworm, UTI.
6. Haemorrhage e.g. APH, PPH
7. Secondary cause to medical condition
245
 2. FOLIC ACID ANAEMIA

 Folic acid is part of vitamin B complex.

 In pregnancy it is necessary for effective cell growth and

synthesis of ribonucleic acid (RNA) and deoxyribonucleic acid

(DNA) especially in the embryo.
 Deficiency is associated with neural tube defects in the foetus

resulting in spina bifida, anecephally.

 Folic acid is required for the increased cell growth of both the

mother and the foetus.

 Chronic maternal deficiency of folic acid and vitamin B12 can

lead to megaloblastic anaemia

246
 CAUSES OF FOLIC ACID ANAEMIA
 The main causes of folic acid deficiency anaemia are:
1. Low dietary intake
2. Reduced absorption
3. Interference with utilization like in substance abuse,
anti-convulsant drugs and sulphonamides which are
folate antagonists
4. Excessive demand like in multiple pregnancy
5. Blood loss like in haemolytic anaemia

247
 3. VITAMIN B12 ANAEMIA
 Deficiency vitamin B12 also causes pernicious anaemia.
 Vitamin B levels fall during pregnancy but anaemia is rare because the body
draws on its stores.
 Deficiency is most likely in vegans and in some asians

248
 DIAGNOSIS
 A comprehensive history and physical examination is imperative to rule out the underlying causes
of anemia, and to detect any complications that may have occurred.
 Basic laboratory work up should include the following:
1. Hemoglobin and hematocrit Estimation (to know degree of anemia)
2. Full blood count and peripheral blood film (to know the type of anemia)
3. tool examination for ova and cysts, Blood Slide or RDTs for malaria diagnosis,
urinalysis /
4. microscopy etc. (to know the cause of anemia)
5. Blood group and Rhesus factor determination
6. Other tests will be determined by the findings on history and physical
examination
249
 MANAGEMENT OF ANAEMIA IN PREGNANCY
 The approach to management of anaemia in pregnancy is
1. Prevention of anaemia
2. Early detection of anaemia
3. Early treatment/correction of anaemia
The management of a woman with anaemia depends on
 the type
 severity of anaemia, and
 the duration of pregnancy.

250
MILD ANAEMIA

This is characterised by haemoglobin between 9 to

10.9gm/decilitre.
At a gestation of 20 to 29 weeks, the woman is given

heamatinics and a diet rich in protein and iron

251
 1. MANAGEMENT OF MILD ANAEMIA
 At 30 to 36 weeks, the haemoglobin levels are checked,
 Diet is emphasised and haematinics continued.
 These include oral iron, for example, ferrous sulphate 200mg
three times daily folic acid 5mgs daily
 Investigations are carried out to establish the cause of the
anaemia, for example, malarial parasites, hookworms, sickle
cell disease.
 The mother is given health messages on nutrition, rest and
taking drugs as prescribed,
252
 MANAGEMENT OF MODERATE ANAEMIA
Moderate Anaemia
 This is characterised by haemoglobin levels of between 7.1
to 10 gm per decilitre.
 At gestation of 29 to 30 weeks investigations are carried out
to establish the cause and institute treatment.
 Haematinics are given and a total dose of parenteral inferon
50 mgs/mililitre is given in a slow intravenous infusion of
normal saline after a test dose to rule out sensitivity.

253
 MANAGEMENT OF MODERATE ANAEMIA
 Intramuscular iron in the form of sorbital 50mg/ml is also
administered.
 The dose is 1.5mg/kg body weight weekly.
 The injection should not be given in conjunction with oral iron as
this enhances toxic effects
 Haemoglobin levels are monitored regularly starting on the third
day after commencement of treatment and then monthly.
 At 30 to 36 weeks of gestation the woman is given total dose
inferon and transfused with no more than 500ml whole blood.
 The blood is given slowly under close supervision.
 After transfusion, the woman will be put on folic acid.
 At 37 weeks blood transfusion is given again as above. 254
 SEVERE ANAEMIA

Severe Anaemia
 This is characterised by haemoglobin below 7gm per decilitre.
 This is an emergency where the mother is admitted and put on
complete bed rest to reduce cardiac workload as she could go into
cardiac failure.
 Investigations are carried out to establish the cause.
 Meanwhile, she is nursed in left lateral position to prevent
compression of the vena cava by the gravid uterus.

255
 SEVERE ANAEMIA CONT
 Vital observations are taken quarter hourly and the foetal
heart rate is monitored.
 Transfuse three units of packed cells slowly.
 Monitoring is continued quarter hourly. Administration of
haematinics is continued.
 In case of malaria, hookworm or sickle cell disease, the root
cause of the anaemia is treated.
 Health messages are shared on diet and general prevention .

256
 MANAGEMENT DURING LABOUR
 Blood is cross-matched and the patient is started on transfusion
of packed cells only toavoid cardiac overload.
 Emergency drugs are kept ready.

 In the second stage of labour, oxygen is given and a vacuum

extraction is carried out, the mother should not strain

Active Management of Third Stage of Labour (AMTSL) must be
practice which involves-
 IM oxytocin within a minute of delivery,

 Controlled cord traction and

 Counter pressure of the uterus in delivery of the placenta

257
 Uterine massage to expel clots and enhance uterine contraction
 POSTNATAL CARE
 The mother is given antibiotics to prevent infection, and put
on haematinics for three months.
 The haemoglobin is checked on the third and sixth week.
 Family planning and good nutrition are encouraged.
 If a pregnant woman has folic acid deficiency, you should
give folic acid supplements and oral Iron.
 If she has vitamin B12 deficiency she should be given a
weekly dose of 100mg of vitamin B12 injections until the
condition is reversed.
258
 PREVENTION OF ANAEMIA IN PREGNANCY
 Health Education
1. You should advise mothers in the antenatal clinic about a balanced
diet.
2. Green vegetables should not be overcooked as this destroys the folic
acid.
3. Teach them about proper disposal of faeces to avoid hookworm
infestation.
4. Encourage the practice of child spacing to avoid frequent
pregnancies so as to give the woman's body time to replenish her
body stores.
259
 PREVENTION OF ANAEMIA IN PREGNANCY
5. In addition encourage her to continue coming to antenatal clinic.
6. Prophylactic Medication: Give the following supplements to the women
throughout pregnancy:
Ferrous sulphate 200mg three times a day
 Folic acid 5mg daily
 Prophylactic anti malarial medication in high malaria endemic
regions
 Membendazole in 2nd trimester
7. Ensure early detection and adequate treatment of malaria, anaemia,
antepartum and postpartum haemorrhage.
260
 10. HYPERTENSION IN PREGNANCY

 Blood pressure is the pressure exerted by the blood volume on the blood vessel
walls, known as peripheral resistance.
 Hypertension is a systolic or diastolic blood pressure that is raised from normal
value. Or blood pressure of >140/90mmhg
 Essential hypertension or chronic hypertension this is hypertension diagnosed
before pregnancy , before 20 weeks of gestation and its presence beyond the 12 th
week after delivery.
 Essential hypertension accounts for about 5% of cases of hypertension in
pregnancy

261
 CAUSES OF HYPERTENSION
The cause of hypertension is unknown but there contributing factors
It is associated in:
 Obesity
 Black race
 Family history
 Lifestyle factors such as lack of exercise, poor diet high in salt or fat intake,
 Age: the risk increase with age
 It can occur secondary to other medical conditions:
 Renal disease
 Systemic lupus erythromatosis
 Coarctation of the aorta and cushing syndrome which is rare
 Phaechromocytoma which is rare but a dangerous tumour of the adrenal medulla.

262
 COMPLICATIONS
 IUGR
 Pacenta abruption

 Superimposed pre-eclampsia

 Cerebral vascular accident and organ damage

 Management is the same as in pre eclampsia

263
 10. DIABETES IN PREGNANCY
Diabetes is a metabolic disorder due to partial or total lack of insulin,
characterised by hyperglycaemia. This may seriously complicate a pregnancy
as you will see later on.

264
 CLASSIFICATION OF DIABETES

1. Insulin Dependent Diabetes Mellitus is where the patient has abnormal blood
sugar and is on insulin therapy to control the blood sugar levels.

2. Non Insulin Dependent Diabetes Mellitus is where the patient has abnormal
blood sugar but it is controlled by diet alone.

3. Gestational Diabetes Mellitus is where the patient develops abnormal glucose

during pregnancy.

4. Potential Diabetic is where the individual has an increased tendency to

develop the disease during pregnancy, due to having delivered an unduly large
265
baby (4.5kg or more), family history of diabetes, chronic obesity or glycosuria.
 CARBOHYDRATE METABOLISM IN PREGNANCY
 Review normal carbohydrate metabolism
There are a lot of changes, which occur due to pregnancy these are
1. Fall in fasting blood sugar
 The foetus obtains glucose from its mother via the placenta by
the process of diffusion. From the 10th week of pregnancy there
is progressive fall in maternal fasting glucose from 4 to 3.6
mmol/l.
2. Ketoacidiosis
 During the third trimester the mother begins to utilise fat stores
laid down in the first and second trimester. This results in free
fatty acids and glycerol in the blood stream and the woman
becomes ketotic more easily.
266
 CARBOHYDRATE METABOLISM IN PREGNANCY
3. Hormonal Effect
 The foeto-placental unit alters the mother's carbohydrate
metabolism to make glucose more readily available.
 Human Placental Lactogen hormone (HPL), manufactured by
the placenta, causes resistance to insulin in the maternal
tissues. The blood glucose remains raised for a longer period
than in the non-pregnant state.
 The extra demands on the pancreatic beta cells can precipitate
glucose intolerance or overt diabetes in those whose capacity
for producing insulin was just adequate prior to pregnancy. If
the mother was diabetic before pregnancy her insulin demand 267

will be increases.
 THE EFFECTS OF PREGNANCY ON DIABETES
 When the mother who has diabetes and then becomes pregnant, there will be
further increase in insulin demand and even a mother who had only been on a
controlled diet, without need for medication, may now require insulin
supplements.
 This is due to low renal threshold to glucose and also low glucose intake by
mother due to nausea and vomiting.
 The mother easily gets ketoacidosis as the fat is broken down.
 In late pregnancy, insulin requirements are still high as there is reduced
sensitivity of the tissues due to the Human Placental Lactogen hormone.
 Those with juvenile diabetes may progress to nephropathy hence kidney failure
and retinopathy leading to blindness.
268
 EFFECTS OF DIABETES ON THE MOTHER
 Unrecognised or a badly treated diabetes leads to complications in
both the mother and the baby.
 If well controlled, then the effects to pregnancy may be minimal.
Maternal complications include:
1. Urinary tract infection
2. Candidiasis of vulva and vagina
3. Reduced fertility,
4. spontaneous abortion,
5. pregnancy induced hypertension
6. Hydramnios (polyhydramnios)
7. Pre-term labour
269
EFFECTS OF DIABETES ON THE MOTHER
8. Diabetic retinopathy
9. Chronic hypertension
10. Increased operative deliveries
11. Abruptio placentae
12. HELLP syndrome
13. Maternal mortality

270
 EFFECTS OF DIABETES TO THE FOETUS/NEONATE
 The foetal and neonatal complications occur when the blood sugar is not
controlled and are mainly due to glucose being attached to the haemoglobin
(glycosulated haemoglobin).
 This results into impaired oxygen carrying capacity resulting in the
following conditions.
 Congenital abnormalities or birth defects
 Macrosomia / very large babies
 Pramaturity
 Still births
 Newborn complication: hypoglycaemia, hypothermia,
hypocalcaemia, jaundice, RDS, perinatal mortality. 271
 Effect Of Diabetes On foetus
1. Birth defects: These include heart defects or neural tube defects
(NTDs), birth defects of the brain or spinal cord
2. Premature birth (before 37 completed weeks of pregnancy):
Premature babies are at increased risk of health problems in the
newborn period as well as lasting disabilities.
3. Macrosomia: Women with poorly controlled diabetes are at
increased risk of having a very large baby (10 pounds or more).
Macrosomia is the medical term for this. These babies grow so
large because some of the extra sugar in the mother's blood
crosses the placenta and goes to the foetus excess sugar
converted in to glycogen and is stored as fat by the foetus.
 CONT..
5. Stillbirth: Though stillbirth is rare, the risk is increased with
poorly controlled diabetes
6. Newborn complications: These include respiratory distress
syndrome, hypoglycaemia, polycythaemia, neonatal
hypocalcaemia and neonatal jaundice. These complications can
be treated, but it's better to prevent them by controlling blood
sugar levels during pregnancy.
7. Obesity and diabetes: Babies of women with poorly
controlled diabetes may be at increased risk of developing
metabolic syndrome (childhood obesity, glucose intolerance,
hypertension and diabetes as young adults)
Diagnosis Of Gestational Diabetes Mellitus

A fasting blood sugar > 7.8 mmol/l or random blood sugar

>11.1 mmol/l, meets the criteria for diabetes if confirmed
on a subsequent day.
Symptoms of diabetes (polyuria, polydypsia, and/or
unexplained weight loss) plus a fasting blood sugar > 7.8
mmol/l should raise suspicion of gestational diabetes.
 NB: Glycosuria is a common finding in pregnancy due to
increased glomerular filtration and is therefore unreliable as a
means of diagnosis.
 Antenatal Care

The following should be observed on top of the routine ANC care.

Note that diabetic patients will require more ANC visits.
The patient should be managed jointly by the diabetes and antenatal clinic
team. Maintain contact with the diabetes care team every 1–2 weeks to assess
glycaemic control
Stop oral hypoglycaemic agents, apart from metformin2, and commence insulin
Nutritional support
Exercises and lifestyle modification
Preterm labour is increased in patients with diabetes, and they should be
treated with magnesium sulphate as the initial tocolytic agent because the
beta mimetics markedly influence glucose control.
Induction of labour is recommended at 38 weeks in patients with poor
glucose control and macrosomia
 Management Of Labour
•Diabetic patients must be advised to deliver in hospital under skilled birth attendance.
•Insulin-dependent diabetics should be induced at 40 weeks’ gestation if spontaneous labor has
not occurred.
•Diabetes Mellitus alone is not an indication for C/section. Oxytocin is given for
labour induction similarly to normal pregnancies.
•Continuous foetal heart rate monitoring is required with careful attention to decelerations.
•Glucose infusion (D5W, lactated Ringer’s solution) is given to all patients in labor unless delivery
is immediate. During the 4-6 hours prior to delivery, there is increased risk of transient neonatal
hypoglycemia
•Glucose levels are monitored every 2-4 hours with the goal of maintaining levels at 3-7 mmol/L till
delivery.
 MANAGEMENT OF LABOUR
 In those requiring insulin, give half the dose of insulin with a light meal in the
morning on the day of delivery.
 Maintain with regular insulin (25 i.u. /250 mL normal saline, giving a dilution
of 0.1 i.u./mL) by continuous infusion at levels of 0.5-2 i.u. /h.
 monitor blood sugar hourly
 Shoulder dystocia should always be anticipated and prepared for.
 If repeat caesarean section or other indication for elective surgery occurs, the
patient should be directed to take the evening insulin dose prior to surgery, but
not her morning dose.
 Showering with a bacterial solution the night before delivery seems reasonable
due to the increase in wound infections in this group.
 The patient is at increased risk of thromboembolic events due to decreased
277
prostacyclin production by the platelets.
 Neonatal Care

Babies of women with diabetes should be kept with their

mothers unless there is a clinical complication or there are
abnormal clinical signs that warrant admission for intensive or
special care.
However they need to be observed carefully for
complications such as hypoglycemia,
Respiratory Distress Syndrome (RDS) and neonatal jaundice.
Breastfeeding is not affected by diabetes and is generally
encouraged.
 Postnatal Care

Women who were diagnosed with gestational diabetes should be

offered lifestyle advice (including weight control, diet and exercise)
and offered a fasting plasma glucose measurement at 6-week
postnatal check and annually thereafter.
Contraception should be offered.
 For gestational diabetes, all methods are MEC category 1.
However if the diabetes is persistent, hormonal methods are MEC
category 2, while IUCD is MEC category 1. Female sterilization needs
extra preparation and precaution (category C).
In case of vascular complications including kidney, ocular or
nerve damage, hormonal contraceptives are categories 3 /4
meaning they should generally not be used.
11. URINARY TRACT INFECTIONS IN PREGNANCY
 Urinary tract infection is a common problem among
pregnant women.
 In a pregnant woman, this infection presents in different
forms, some of which are serious, and others of mild
consequence.
 The common conditions of urinary tract infection in
pregnancy are:
1. Asymptomatic bacteriuria
2. Acute cystitis
3. Acute pyelonephritis
280
 UTI IN PREGNANCY
UTI is common in pregnancy
This is because:

1. The pregnant uterus causes pressure on the ureters and the

bladder which delays emptying.
2. The action of hormones on the smooth muscles of the ureters
and bladder also causes them to relax and dilate easily. This
causes urine to move more slowly down the dilated tubes and
infection lodges in them easily.
 Normally the urinary tract mucosa is highly sensitive to
invading organisms and the ureters go into spasmodic
contractions to get rid of such invaders.
281
 1. ASYMPTOMATIC INFECTIONS
 Asymptomatic bacteriuria is more common in pregnant women
than in non-pregnant women.
 The condition is also twice as common in pregnant women with
sickle cell trait and three times in those with diabetes as compared
to normal pregnant women.
 A woman with asymptomatic UTI may feel nothing except a slight
pain when passing urine.
 She may also have offensive smelling urine.
 If the condition remains untreated during pregnancy, about
25 to 35% of these women will develop acute pyelonephritis.
 Diagnosis is through laboratory investigations
 E-coli is the most common organism causing this condition and282
accounts for 80% of the cases.
 2. CYSTITIS
 Acute cystitis is less common in pregnancy than asymptomatic bacteriuria.
 However, it causes more concern because of its symptoms.
 Acute cystitis presents with:
1. Urinary frequency and urgency,
2. Dysuria,
3. Suprapubic discomfort,
4. Urine is cloudy with offensive smell if
5. Cultured, bacteria cells are identified.

283
 3. ACUTE PYELONEPHRITIS
DEFINITION: Bacterial pyelonephritis is an acute infection and inflammatory
disease of the kidney and renal pelvis involving one or both kidneys.
Etiology

 Enteric bacteria, such as E. coli, is most common pathogen;

 Other gram-negative pathogens include Proteus species,
Klebsiella, and Pseudomonas.
 Gram-positive bacteria are less common, but include
Enterococcus and Staphylococcus aureus.
284
 PATHOPHYSIOLOGY

Bacterial infection usually ascends from the lower

urinary tract;
Low-grade inflammation and abscess formation.

Chronic pyelonephritis may result in scarred,

atrophic, and nonfunctioning kidneys.

285
 CLINICAL PRESENTATION OF ACUTE
PYELONEPHRITIS
In acute pyelonephritis, the patient will present with the
following symptoms:
 Fever
 Nausea and vomiting
 Headache
 Urinary frequency
 Dysuria
 Shivering or chills
 Lower abdominal pain
 Dehydration if vomiting has been severe
286
 Renal angle tenderness on examination
 DIAGNOSIS
Diagnostic Evaluation
 Urinalysis (dipstick or microscopic) to identify leukocytes,
bacteria, and RBCs and WBCs in urine; white cell casts may also
be seen.
 Urine culture to identify causative bacteria.
 CBC shows elevated WBC count consisting of neutrophils and
bands.
 Intravenous urography (IVU) or renal ultrasound to evaluate
for urinary tract obstruction; other radiologic or urinary tests as 287

necessary.
 MANAGEMENT
 Treatment:

1. For severe infections (dehydrated, cannot tolerate oral

intake) or complicating factors (suspected obstruction,
pregnancy, advanced age), inpatient antibiotic therapy is
recommended.
2. Usually immediate treatment is started with a penicillin or
aminoglycoside I.V. to cover the prevalent gram-negative
pathogens; subsequently adjusted according to culture
results. 288
MNGX TREATMENT

3. An oral antibiotic may be started 24 hours after fever has

resolved and oral therapy continued for 3 weeks.
4. Oral therapy antibiotic therapy is acceptable for
outpatient treatment.
5. Repeat urine cultures should be performed after the
completion of therapy.
6. Supportive therapy is given for fever and pain control
and hydration. 289
 NURSING INTERVENTION
1. Reducing Body Temperature
 Administer or teach self-administration of antibiotics as prescribed, and monitor
for effectiveness and adverse effects.
 Assess vital signs frequently, and monitor intake and output; administer
antiemetic medications to control nausea and vomiting.
 Administer antipyretic medications as prescribed and according to temperature.
 Report fever that persists beyond 72 hours after initiating antibiotic therapy;
further testing for complicating factors will be ordered.
 Use measures to decrease body temperature if indicated; cooling blanket,
application of ice to armpits and groins, and so forth.
 Correct dehydration by replacing fluids, orally if possible, or I.V.
290
 Monitor CBC, blood cultures, and urine studies for resolving infection.
 NURSING INTERVENTIONS

2. Relieve pain:
 Administer or teach self-administration of analgesics, and
monitor their effectiveness.
 Use comfort measures, such as positioning, to locally
relieve flank pain.
 Assess patient's response to pain control measures .

291
 NURSING INTERVENTIONS
3. Patient Education and Health Maintenance
 Explain to patient possible causes of pyelonephritis and its
signs and symptoms; also, review signs and symptoms of
lower UTI.
 Review antibiotic therapy and importance of completing
prescribed course of treatment and having follow-up urine
cultures.
 Explain preventive measures, including good fluid intake,
personal hygiene measures, and healthy voiding habits.
292
 POSSIBLE COMPLICATIONS
 Bacteremia with sepsis
 Papillary necrosis leading to renal failure
 Renal abscess requiring treatment by percutaneous drainage
or prolonged antibiotic therapy
 Paralytic ileus

293
 12. MALARIA IN PREGNANCY
 Malaria is a life threatening disease caused by plasmodium parasite that are
transmitted to people through bites of infected female anopheles mosquitoes.
 It is preventable and curable

 Malaria in pregnancy is a major, preventable cause of maternal morbidity and

poor birth outcomes

294
 FACTS ABOUT MALARIA IN PREGNANCY
1. Pregnant women get malaria more easily than women who are not
pregnant.
2. Many pregnant women have malaria parasites but have no symptoms at
all.
3. When a women are pregnant she loses some of her ability to fight malaria
infections
4. Blood test for peripheral parasitaemia is often negative, despite malaria
parasites in the placenta.

295
 EFFECTS OF MALARIA ON PREGNANCY
TO THE MOTHER/UNBORN BABY
1. Haemolysis of red blood cells, causing anaemia and jaundice
2. Hyperpyrexia (very high fever), which may cause abortion or Preterm
labour
3. Malaria parasites have affinity for the placenta and this interferes with
nutrition of the unborn baby and may cause
 Premature labour/ premature delivery
 Spontaneous abortion

 30% of the preventable low birth weight (IUGR)

 IUFD

 3-5% of the neonatal deaths 296

 SIGNS AND SYMPTOMS OF UNCOMPLICATED
MALARIA
 Fever with or without shivering.
 Headaches

 Weakness

 Loss of appetite

 Nausea and vomiting

 Joint pains

 Backache and muscle pains.

 False labour pains (uterine contractions)

297
MANAGEMENT OF UNCOMPLICATED MALARIA

1. All trimester oral quinine 10mg/kg body weight 8hourly for

7days ( adult dosage 600mgs 8 hourly).
2. Coartem (Artimether 20mgs/lumefantrine tablets120mgs).
Dosage 4 tablets stat, 4 tablets after 8 hours and then 4 tablets
twice daily (12 hourly) for 2 days. ( total course of 24 hours).

298
 CONT
3. Give paracetamol 500mgs 8 hourly to relieve fever and pain.
4. Give plenty of oral fluids
5. Rule out anaemia
6. Supportive therapy and follow up

299
REMEMBER
 DO NOT withhold AL in first trimester if quinine is not
available.
 Give 1st dose of AL as Directly Observed Therapy (DOT)

 All drugs should be given with a meal to enhance

absorption but DO NOT withhold the first dose due to lack

of a meal.

300
 SEVERE/COMPLICATED MALARIA
 In addition to other symptoms of uncomplicated malaria , the patient will present
with at least one of the following:
1. Extreme tiredness.
2. Changes in behaviour: sleepiness/drowsiness, confusion,
convulsions, unconsciousness, inability to walk, sit, speak or
recognize relatives.
3. Fast breathing due to (pulmonary oedema or cardiac failure)
4. Passage of very dark coloured urine (coffee like or coca
cola)

301
 SIGNS OF SEVERE/ COMPLICATED MALARIA

1. Anaemia (Hb < 7g/dl,

2. High fever, breathing difficulties
3. Signs of cerebral malaria (convulsions, coma and other behavioural change)
4. Signs of low blood sugar (hypoglycaemia) sweating, weakness and cold skin.
5. Signs of severe dehydration, especially if she has been vomiting repeatedly
6. Spontaneous bleeding from the gums, skin and vein puncture site
7. Severe jaundice of conjunctiva, palms and skin

302
MANAGEMENT OF SEVERE/COMPLICATED MALARIA

 Malaria progresses fast, leading to severe illness and death

 Severe malaria is a medical emergency
 Patients with severe malaria should be managed promptly
 Admit all case of severe/ complicated malaria
 Weigh the patient.
 Treatment of severe complicated malaria in pregnancy
1. Quinine is safe to use in pregnancy
 Parenteral quinine IV route is preferred, however IM route
303
can be used as an alternative where IV route is not feasible.
TREATMENT OF SEVERE /COMPLICATED MALARIA
First dose (loading dose): 20mgs/kg in ½ litre of 5% dextrose or
normal saline given over 4 hours up to a max of 1200mg
 8 hours from commencement of the initial dose of quinine, give
10mg/kg (maximum 600mg) diluted in 10mls/kg (maximum 500ml)
of isotonic solution (5% dextrose or normal saline) to run over 4
hours.
 Repeat l0mg/kg quinine infusion every 8 hours until the patient can
take medication orally.
 Change to oral quinine to complete 7 days of therapy OR
304
 A Complete course of artemether-lumefantrine (AL) is given
MANAGEMENT OF SEVERE/COMPLICATED MALARIA
2. Artesunate IV 2.4 mg/kg at 0, 12, 24 hours, then daily there after until
the patient can take orally maximum of 7days. When patient is able to take
orally prescribe a 3 day dose of AL .

305
CONT…
 Manage fever with IV /IM/PO paracetamol 500mgs 8 hourly till fever
subsides
 Manage dehydration with parenteral IV fluids N/S alt 5% dextrose

 Monitor for hypoglycaemia and correct it with 50% dextrose at 1ml/kg

body weight
 Provide total nursing care physical and emotional support. Vital signs
TPR/BP, FHR and foetal kick chart, diet, hygiene, catheterization, input and
output, reassurance emotional support …………..

306
PRE-REFERAL MANAGEMENT OF SEVERE/COMPLICATED
MALARIA
 Take vital signs
 Give a loading dose of 20mg/kg of quinine IM Stat
 A maximum of 3mls should be injected into one site.
 Repeat dose at 10mgs/kg 8 hourly until IV treatment is initiated
 In absence of quinine artemether injection 3.2mgs/kg stat or
artesunate injection 2.4 mgs/kg stat may be used to initiate
treatment (in second and third trimester)
 Arrange for transport
 Give oral glucose( non-comatose)
 Accompany the patient.
307
 PRECAUTIONS QUININE
1. A loading dose of quinine should not be used if the patient has received any
quinine in the last 24 hours, or mefloquine in the last 7 days.
2. The maintenance dose of quinine should be halved in patients with renal
failure after 2 days
3. Look for signs of hypoglycaemia and correct it with 50%D 1ml/kg
4. Quinine should be used as soon as it is reconstituted
5. Protect quinine from direct sunlight.

308
 COMPLICATIONS OF SEVERE/ COMPLICATED
MALARIA
1. Coma and/or convulsions due to cerebral malaria
2. Severe anaemia with a Hb<7gm/dl
3. Renal failure
4. Hypoglycemia
5. Fluid and electrolyte imbalance
6. Pulmonary oedema
7. Hypovolemic shock
8. Haemogloinuria ( Coca cola coloured urine)
9. Intravascular coagulopathy 309
PREVENTION OF MALARIA IN PREGNANCY

 Pregnant women are more at risk of malaria infections

because pregnancy reduces the degree of partial immunity.
 Women in their first and second pregnancy are at a greater
risk (because of lack of exposure to placental infection
before)
 All pregnant women at risk should be advised on malaria
prevention measures 310
 CONT…
1. Intermittent preventive treatment in pregnancy (IPTp) with sulfadoxine-
pyrimethamine sp (fansidar)
2. Use of insecticide treated net (ITNs) they are available in ANC
3. Intermittent screening and treatment in pregnancy (ISTp) using rapid
diagnostic kit (RDTs) during antenatal care visits.
4. Case management of symptomatic women
5. Good antenatal care
6. Use of insect repellents

311
 CONT…
7. Wearing protective clothing that covers the body including arms and legs
this prevents mosquito bites.
8. Having mosquito screening in windows prevents mosquito from entering
our houses.
9. Environmental management including draining of stagnant water, where
feasible
10. Indoor residue spray in endemic areas.

312
 INTERMITTENT PREVENTIVE TREATMENT (IPTP)
1. Intermittent preventive therapy (IPTp) is an effective approach to preventing
malaria in pregnant women by giving antimalarial drugs in treatment doses at
defined intervals after quickening to clear a presumed burden of parasites.
2. The ministry of health quidelines on malaria directs us to give SP to pregnant
women in endemic malaria areas , at least twice during each pregnancy, even if
she has physical signs and haemoglobin is within normal range.
3. Administer IPTp with each scheduled visit after quickening (16 weeks) to
ensure women receive at least 2 doses at an interval of at least 4 weeks.
4. IPTp should be given on an empty stomach

313
 IPT
5. One tablet of SP contains sulfadoxine 500mg and pyrimethamine 25mgs
6. For now IPT means using of sulfadoxine/pyrimethamine (SP) trade names
(FANSIDAR, FALCIDIN etc.), but we will always have to keep abreast of
changes and treat our patients according to the latest MOH guidelines
7. A single dose consists of 3 tablets of SP taken once
8. SP is best to clear placenta parasites during period of maximum foetal
growth.
9. It also allows the mother to recover from anemia by clearing the peripheral
parasitaemia.

314
 IPT
9. SP should not be taken together with folic acid , delay folic acid for 2 weeks
after taking SP ( folic acid reduces the efficacy of SP)
10. Record on the ANC card the date SP is given
11. Explain to the woman the importance of coming back for the second dose
12. Always ask about side-effects from the first dose of SP before giving the second
dose
13. HIV positive women requires 3 doses of SP at monthly interval, until she
delivers
14. Pregnant HIV positive women on cotrimoxazole chemoprophylaxis should not
be given SP

315
 13. TUBERCULOSIS IN PREGNANCY (TB)
 Tuberculosis is a chronic infectious disease caused by a bacilli called
mycobacterium tuberculosis
 Over 90% of new TB cases and deaths occur in developing countries

 TB is one of the leading infectious causes of death among women of

reproductive age.
TB has increased by 10 over resent years in Kenya because of its association
with HIV/AIDS epidemic, poverty, overcrowding, poor nutrition and
limited access to health services,

316
 TYPES OF TUBERCULOSIS
1. Pulmonary tuberculosis (PTB) is the most common and infectious type of
TB. It affects the lung and causes 81% of all TB cases.
2. Extra pulmonary tuberculosis ( outside the lungs) any organ such as the
kidneys, bladder, ovaries, testis, eyes, bones or joints, intestines, skin and
glands etc. EXCEPT the nails and hair.
3. The most common extra pulmonary TB is TB of the glands also called
TB lymphadenitis

317
 CLINICAL MANIFESTATION OF PULMONARY TB
Clinical presentation of pulmonary tuberculosis in pregnancy may be
asymptomatic but typical symptoms include:
1. Persistent cough productive cough
2. Excessive Night sweats
3. Fever in the evenings
4. Shortness of breath secondary to pleural efussion and empyema
5. Weight loss
6. General weakness
7. Loss of appetite
8. Occasionally haemoptysis
9. In advance PTB the woman will present with anaemia and she may go
into premature labour.
10. The anaemia which will not respond to haematinics until the PTB has318
been brought under control.
SIGNS AND SYMPTOMS OF TB OF THE GLANDS
(TB LYMPHADENITIS)
 Slow and painless enlargement of the lymph nodes which
later become matted and eventually discharge pus.
 The most common lymph nodes are the cervical (neck) lymph

nodes
 Generalized lymph nodes enlargement is becoming common

in HIV related TB.

 This should be confirmed during head to toe examination.

319
 WHEN DOES TB PASS FROM MOTHER TO BABY
1. During pregnancy through the placenta barrier causing fetal death or
infection (congenital TB is rare)
2. At birth when baby inhales or ingests infected amniotic fluid or secretions
3. After delivery when the baby inhales droplet secretions if the mother is
coughing (commonest mode of transmission)

320
 INVESTIGATIONS/DIAGNOSIS
 History taking- history of exposure, unexplained weight loss
 Physical examination-extrapulmonary

 Sputum smear for AAFBS – pulmonary PTB

 Chest x-ray

 Mantoux test

 Histology

 Genexpert (Currently sputum is tested for presence of TB

bacteria as well as test resistant to the drug Rifampicin)

321
 MANAGEMENT
ANTENATAL CARE
1. All pregnant women should be screened for TB

2. All pregnant women suspected for TB should be

investigated sputum for AAFBs OR genexpert
3. Pregnant women found to have TB should be refered to
TB clinic for treatment
4. women with sputum smear positive TB and with children
under 5 years should be requested to get the children
screened for TB
NB: Negative Sputum does not exclude TB! 322
 COUNSELLING FOR TB DURING PREGNANCY

 If the pregnant woman has been confirmed to have TB;

 Explain that treatment for TB is free
 Explain that TB is treated over a six to eight-month period and
 The drugs are safe to use during pregnancy and breastfeeding
 Explain the importance of drug compliance and contact
invitation

323
CONT...
 Explain that after delivery, discussions on methods of family
planning are necessary as some TB drugs (rifampicin)
interfere with the absorption of hormonal contraceptives
 Explain the need for high nutritious diet obtained from
locally available sources

324
 MANAGEMENT
Treatment:
 Most countries have standard drug treatment regimens in their

national anti -TB programmers.

 Generally, treatment is in 2 phases. The following drug

regimens are used in Kenya :

For new TB case (previously untreated)
 Intensive phase (2 months): Ethambutol (E), Rifampicin
(R), Isoniazid (H), pyrazinamide (Z)
 Continuation phase (4 months): Rifampicin (R) and 325

Isoniazid (H)
CONT…
For retreatment TB cases
 Intensive phase (3 months): Ethambutol (E), Rifampicin
(R), Isoniazid (H), pyrazinamide (Z)

 Continuation phase (5 months):Rifampicin (R) and

Isoniazid (H) - Ethambutol (E),

326
 TREATMENT
DOT: Directly Observed Treatment
Initial phase:
 The first 2 months of TB treatment should be administered under direct observation
of either a health worker in the facility or a member of the household or community.
 If client is too sick or observed treatment is not possible, the client should be
admitted to hospital.
Continuation phase:
 The client collects supplies two weekly for daily DOT at home.
 For pregnant women who are HIV positive and also have TB, the treatment should
be continued and the client referred to comprehensive care clinic.
 All co-infected patients (HIV and TB) should be started on co-trimoxazole
327
prophylaxis as it reduces mortality.
 DURING PUERPERIUM
 The mother is encouraged to breastfeed but remember to protect
the baby from tuberculosis by giving prophylactic Isoniazid
(INAH, 25mg per kg per day).
 INAH resistant BCG should be given since ordinary BCG may
be inhibited by INAH.
 If INAH resistant BCG is not available, the baby should be
given ordinary BCG at birth and separated from its mother for
two weeks.
 If the baby still gives a negative reaction (mantoux test) to
tuberculosis at six to eight weeks, it should be re-vaccinated with
INAH resistant BCG and prophylaxis should be maintained with
INAH for a further six weeks until mantoux conversion occurs. 328
 PREVENTION OF TB
Patient Management
 Early recognition of patients with suspected or confirmed TB disease, through
 screening – may be done by registering officer/clerk
 Education of the above mentioned persons identified through screening in cough
etiquette and respiratory hygiene
 Triaging symptomatic patients to the front of the line for the services they are
 seeking
 TB suspects or TB cases identified by the screening questions, are separated from
other patients and requested to wait in a separate well-ventilated waiting area or
patient ward
 Provide identified TB suspects with a surgical mask or tissues to cover their mouths
329
and noses to ensure compliance with cough etiquette.
 PREVENTION AND CONTROL OF TB
Environmental control:
This is used to reduce the concentration of infectious droplet It includes:
 Maximizing natural ventilation through open windows and doors
 Early identification
 Treatment of contact and cases
 Defaulter tracing
Infection Prevention of Air Borne diseases
 Each facility should have a written airborne disease(TB/MDR-TB) infection
prevention control plan that outlines protocol for the immediate
Recognition, Separation, Investigation for TB; Provision of services and/or
Referral for services of patients with suspected or confirmed TB disease
 Administrative support for implementation of the plan, including quality
330
assurance should be available
 14. CARDIAC DISEASE IN PREGNANCY
 These are disorders that affect the heart muscles, valves or blood vessels in
pregnancy. The disease impairs the ability of the heart to supply tissue with
oxygen.
 Cardiovascular disorders complicate 1% of all pregnancies,
 They include:

 Pre-existing diseases,
Conditions developed during pregnancy
Conditions developing during the postpartum period,
Congenital or acquired structural abnormalities and
arrhythmias. 331
 PHYSIOLOGICAL CHANGES IN THE CARDIAC
SYSTEM

 There are changes that occur in the cardiac system during

pregnancy due to the increased demand in the foeto-placental unit.
 These changes increase the workload of the heart.
 The major changes are:
1. Blood volume increases by 35%
2. Cardiac output increases by 40%, that is from
4.5 to 6l/min 332
PHYSIOLOGICAL CHANGES IN THE CARDIAC SYSTEM
 The extra work that the heart has to do is reduced by:
1. The decreased blood viscosity and lowered
peripheral resistance due to vasodilation.
2. The pulse rate rises slightly in order to pump out the
extra blood around the body.
3. Oxygen consumption is raised.
 The heart is displaced upwards during the last trimester by the
gravid uterus.
 During the third stage of labour 300 to 400ml of blood is
added to the circulating volume by the contracting uterus.
These changes commence in early pregnancy and gradually reach
their maximum at the 30th week and are maintained until term . 333
 RISK FACTORS FOR HEART DISEASE
The following factors predispose patients to heart disease:
1. Anaemia, which should be avoided and if present, igorously treated.
2. Infections, the most common of which are upper respiratory infections. These should be
treated with antibiotics.
3. Obesity should be avoided. Controlled weight gain should be encouraged to avoid extra strain
on the heart.
4. Hypertension and pre-eclampsia should be admitted and controlled.
5. Smoking mothers should be advised to control their habits.
6. Multiple pregnancies should be well monitored.
7. Strain(Psycho-emotional) of any form should be avoided and mothers should be encouraged
to have enough rest and adequate sleep.
8. Exercises that induce breathlessness should be discouraged.
9. Fatigue of any kind should be avoided. 334
 CLASSIFICATION/GRADES OF CARDIAC DISEASE

Cardiac disease in pregnancy has been classified

in four grades. These are:
Cardiac Grade I
In this grade, there are no symptoms
but a heart murmur is discovered on general examination.
Cardiac Grade II
There are symptoms during ordinary physical activity
(breathlessness) but no symptoms when at rest. 335
CONT...

Cardiac Grade III

There are symptoms during mild physical activity.
The mother is unable to perform ordinary daily activity.
On slight exertion, she gets exhausted and severely
dyspnoeic.She has anginal pain.

Cardiac Grade IV
There are symptoms even at rest. There are signs of
cardiac disease and heart failure. 336
 EFFECTS OF CARDIAC DISEASE IN PREGNANCY

 The increase in blood volume and body weight causes strain

on the already impaired heart.
 The increased cardiac output reaches maximum at 30 weeks
when the output is 25% above normal and, therefore, there is
greater need for rest.
 The normal venous dilation, which accompanies pregnancy,
slows the venous return to the heart and, therefore, increases
the difficulty in maintaining adequate output.

337
 EFFECTS OF CARDIAC DISEASE IN PREGNANCY
This results in: effects to mother
1. an increased risk of thrombo-emboli
2. Bacterial endocarditis
3. Raised maternal mortality due to impaired blood flow

 There also risks to the foetus and these include:

1. Intrauterine growth retardation,
2. Raised incidence of congenital heart disease,
3. and raised risk of foetal loss.

338
 DIAGNOSIS OF CARDIAC DISEASE
1. Full cardiovascular examination to including personal history and
assessment of life style risk factors.
2. Blood tests: FBC, clotting studies, and cardiac enzymes.
3. 12 lead electrocardialgram (ECG)
4. Echocardiogram: an ultrasound examination to examine the
cardiac structures and functions.
5. Chest x-ray to assess cardiac size and outline, pulmonary
vasculature and lung fields (always undertaken when clinically
indicated e.g. women with chest pain)
6. Other imaging: computerized tomography (CT) scan or magnetic
resonance imaging (MRI) scan of the chest. 339
 MANAGEMENT OF HEART DISEASE

The mother is followed up by:

1. An obstetrician,
2. A cardiologist,
3. Haematologist
4. and anaesthetist for effective management.
The main aim of management is to; maintain and improve the physical
and psychological well being of both the mother and the foetus and to
340
prevent complications.
 PRENATAL MANAGEMENT FOR MILD
CARDIAC DISEASE (GRADES I & II)
Prenatal management for mild cardiac disease (Grades I & II) should include:

1. Careful history taking and examination of the mother should be done

on the first visit.
2. The mother is seen fortnightly until 32 weeks, then weekly until term.
3. Ideally, she should be admitted between 29 to 32 weeks for rest.
4. All infections should be prevented and, if present, treated promptly.
5. Anaemia should be treated effectively and prevented by extra iron
Therefore, check regularly for anaemia.
341
PRENATAL MANAGEMENT FOR MILD CARDIAC
DISEASE (GRADES I & II)
5. Health messages on the importance of a balanced diet,
avoiding excess weight, adequate rest and sleep, need
for house help, and the effects of smoking, should be
shared.
6. Tooth extraction is possible under antibiotic cover but
should be discouraged.
7. Drugs like digoxin, diuretics such as lasix to reduce
oedema, and sedatives may be taken as prescribed.
8. At 38 weeks gestation, the patient should be admitted for
complete bed rest. 342
 GRADE I&II DURING LABOUR
Infirst stage labour, follow normal admission procedure.
 You should:
 Inform the obstetrician and the cardiologist
 Vigilant observations quarter to half hourly, especially of
pulse, respirations, colour and foetal heart rate
 Administer prophylactic antibiotics
 Mild sedation

343
 GRADE I&II DURING LABOUR
 During second stage of labour
 The patient should avoid exhaustion
 Paediatrician to be around
 The mother should be placed in the dorsal position or the position in which she feels
most comfortable
 Episiotomy and vacuum extraction may
be performed
During third stage of labour
 Active management of third stage labour (AMTSL) with slow IV Oxytocin 2iu/min
 NO ERGOMETRINE it can cause vasoconstriction and hypertension.
 The placenta should be delivered by controlled
cord traction and counter pressure on the uterus.
344
 GRADE I&II DURING LABOUR
During the puerperium,
The following measures should be taken:

 The patient may need to rest and may require sedatives

 Keep her under strict observation half hourly until stable
then two to four hourly
 Treat any infections promptly
 If there are no complications, discharge on the tenth day
post delivery
 Breastfeeding should be encouraged as CO is not affected
by lactation.
 Provide appropriate FP Method 345
 MANAGEMENT OF HEART DISEASE
GRADE III&IV ANTENATALLY
When managing a patient with severe cardiac disease,
the following steps should be taken in the prenatal stage.
 The patient should be nursed as a cardiac failure patient.
 She should be admitted on first contact for complete bed rest
 Patient should be propped up in bed preferably on a cardiac bed.
 The strain is greatest between the 23rd and 32nd weeks and so total
nursing care should be given during that period.
 There should always be two nurses present to perform any346
procedure.
 MANAGEMENT OF HEART DISEASE
GRADE III&IV ANTENATALLY
 You should monitor foetal heart and foetal placental blood flow.
 Administer a diet low in salt
 Ensure adequate rest, through the use of sedatives if necessary.
 Maintain good hygiene.
 Administer drugs as prescribed by the doctor and treat anaemia.
 Ensure that there is social care and support by family members and social
workers.
 In terms of psychological care, it is very important to reassure the patient
about her condition.
 Attend to her emotional needs and give counselling on reproductive health.
347
MNX GRADE II&IV INTRAPARTUM PERIOD (LABOUR AND
DELIVERY)
Intrapartum management usually involves an easy delivery due to hypoxia.
Take the following measures:

1. Avoid exhaustion
2. Prop up in bed to prevent orthopnoea
3. Give oxygen continuously
4. Give analgesics but avoid inhalation
5. Observations should be taken quarter hourly
In the second stage:
Avoid pushing and give episiotomy and vacuum extraction.
No ergometrine should be administered.
If there is any post partum haemorrhage, give oxytocin.

348
 MNX GRADE III & IV IN PUERPERIUM
Puerperium management involves nursing in Intensive Care Unit (ICU) for 48 hours.
 You should take the following steps:

1. Ensure that the patient has complete bed rest and total nursing
care
2. Observations half hourly until stable, then four hourly
3. Withhold breast feeding if mother is in heart failure
4. Admit the baby in a special care unit
5. Remember: Carry out a thorough first examination to rule out
congenital heart condition.
6. Continue antibiotics and sedatives for two weeks.
7. Discharge when condition is satisfactory.
349
POSSIBLE COMPLICATIONS OF CARDIAC DISEASE IN
PREGNANCY
1. Congestive cardiac failure
2. Pulmonary oedema
3. Cardiac arrest
4. Puerperal sepsis as a result of lowered resistance
to infection
5. Deep venous thrombosis, pulmonary embolus, which may
lead to death
6. Postpartum haemorrhage due to anaemia
7. Bacterial endocarditis
350
8. Myocardial infarction
Reference :

1. THIRD EDITION MYLES TEXT BOOK FOR

MIDWIVES AFRICAN EDITION
2. DC DUTTA’S TEXT BOOK OF OBSTETRICS
Hilaral Konar

351