This note is prepared by Wogene Morka (Lecturer)

1. Arsi University
Midwifery department
Obstetrics ii notes for 3rd year midwifery
students
By wogene M.(Msc. in Maternity &
Reproductive Health)
2021/22
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2. Chapter 1.
MINOR DISORDERS AND
HYPEREMESIS
GRAVIDARUM IN
PREGNANCY
W.M(Msc.) DBU
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3. Minor disorders of pregnancy
 Learning objectives
 Outline the minor disorders of pregnancy
 Define the minor complaints of pregnancy
 Discuss the reasons for the occurrence of minor
complaints of pregnancy
 Discuss the mgt of minor disorders of pregnancy
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4. Introduction
 Most pregnant women do suffer from minor
disorders during pregnancy.
 Their severity and occurrence differs from mother
to mother and on other factors including maternal
age and parity
 It should be solved by offering minor treatment and
proper explanation for the reduction of these
problems and anxiety.
 caused by pregnancy and subside after delivery and
the end of the puerperium.
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5. Intro…
 The minor complaints of pregnancy occur due to
 hormonal, e.g. hcG, progesterone…
 anatomical, e.g. organ displacement b/c of growing
Ux
 physiological e.g. vasodilatations b/c of progesterone
 biochemical alterations of pregnancy. E.g. reduced
glucose utilization by mom b/c of placental lactogen
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6. Intro…
 The exact cause of minor disorders are still unknown but it
could be due to increasing level of hormone especially
progesterone in the blood
 Most of these symptoms signify significant disease states
when they occur in a non-pregnant woman
 As long as further history, physical exam and diagnostic
work up do not indicate the presence of serious illness, the
minor complaints of pregnancy can be managed
symptomatically.
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7. Some of the minor complaints of pregnancies are:
 Urinary system
 Frequency; hcG- sensitive
bladder
 leg edema (80%); generalized,
edema(30%), blood volume &
growing Ux.
 Musculoskeletal system (rh)
 Back pain;
 leg pain;
 pelvic pain;
 Integumentary system
 Chloasma
 Glandular system
 Breast tenderness;
 feeling of fullness
 Cardiovascular system
 Palpitation;
 headache;
 sweating;
 feeling of heat; fainting;
fatigue; varicosities
 Respiratory system
 Dyspnoea; (air hunger)
 Gastrointestinal tract
 Nausea; vomiting;
 heartburn;
 constipation; bloat
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8. Nausea and vomiting
 the most common medical conditions in pregnancy
 Occur in 50% of px and most marked at GA of 2-
12 wks
 Usually most severe in the morning – morning
sickness - but can occur at any time.
 Precipitated by cooking odors and strong sharp
smells.
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9. NAV…
 Occurs especially in the morning, soon after getting
out of bed,
 are usually common in primigravida.
 It may due to
emotional factors,
fatigue, and
 May worsen to hyperemesis gravidarum.
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10. Management of NAV
 Identify the particular odor of foods that are most upsetting and avoid the
odor of certain foods, because of its smell.
 Eat dry foods 15 minutes before getting up from the bed in the morning.
 Advice to consume small frequent meal (every 2 hours if possible).
 Avoiding spicy and greasy food and consuming protein snack at night
 Advice to take light and dry snacks instead of heavy meal.
 Avoid brushing after eating.
 Keep room well ventilated for fresh air
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11. Varicose veins
 Varicose veins are enlarged
superficial veins on the legs,
vulva and anus
 varicose veins are disorder of the
second and third trimesters.
 It is due to increased maternal
age, excessive weight gain, large
foetus and multiple pregnancies
etc.
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12. Management
 Exercise regularly and avoid tight clothes.
 Avoid standing for long time and sitting with feet
hanging down.
 Lift the legs up with extra pillows while sitting, resting
or sleeping.
 Avoid crossing legs at the knees because it provides the
pressure on the veins
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13. Backache
 This is common problem during pregnancy
especially in the third trimesters.
 Slight backache may be due to faulty posture and is
more common in multigravida.
 It may be due to fatigue, by lifting heavy objectives
and poor postures,
 Relaxin hormones
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14. Management
 Take adequate rest in proper position and posture.
 Wear supportive shoes with low heels, avoid high
heels shoes.
 Do prenatal exercise and do not gain more weight.
 Avoid excessive twisting, bending, stretching and
also excessive standing or walking.
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15. Fainting / syncope
 It is common in second and third trimester.
 Many pregnant women occasionally fall to faint,
especially in warm and crowed areas.
 It is due to anemia, sudden changes of position,
standing for long periods in warm and crowd areas.
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16. Management
 Avoid prolonged standing.
 Rest in side lying position in left lateral to prevent
supine hypotension.
 Eat regularly iron containing food and plenty of
liquid.
 Advice to be alert for safety
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17. Heartburn
 Heartburn is a burning sensation in the mediastinal
region due to back flow(regurgitation) of acid contents
into the oesophagus often accompanied by bad test in the
mouth.
 Pregnancy hormones can cause the lower esophageal
sphincter (the muscular valve between the stomach and
esophagus) to relax, allowing stomach acids to splash
back up into the esophagus.
 Enlarged uterus can crowd the abdomen, pushing
stomach acids upward.
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18. Management
 Avoids foods known to cause gastric upset.
 Avoid greasy, fried foods, coffee, alcohol and cigarettes.
 Advice to take small frequent meal, but eat slowly.
 Take adequate rest in sleeping with more pillows on
propped position.
 Explain that this is related to pregnancy and the problem
disappears after pregnancy.
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19. Constipations
 Constipation is a condition of infrequent, irregular and
difficulty in passing stool or the passing of hard stool.
 It is common during pregnancy.
 It is due to lack of physical activity or
exercise,
decrease fluids,
oral iron supplement,
 pressure of enlarging uterus on intestine
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20. Management
 Encourage to maintain bowel habit, going to toilet at
same time everyday and toilet when having the urge.
 Encourage to drinking adequate liquid ( of least 200ml
per day)
 Advice to eat in regular schedule.
 Encourage eating fruits, vegetables, gains and
roughage in the diet.
 Advice to do regular daily exercise
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21. Medical management of constipation
 Glycerin suppository
 Sorbitol
 Bisacodyl
 laxative
 Tap-water enema
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22. Leg cramps
 Leg cramps are painful muscle spasm ( b/c of placental parathyroid
hormones)
 They occur most frequently at night but may occur at other times.
 Leg cramps are more common in the third trimester.
Management
 Advice to take enough calcium ( milk, green leafy vegetables)
 Advice to take warm bath to improve the circulation.
 Advice to do exercise regularly.
 Strengthen the legs, point or pull toes upward towards the knees.
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23. Group discussion
 Do you think nausea and vomiting may be
helpful?
 protective mechanism—it may protect the
pregnant woman and her embryo from harmful
substances in food.
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24. Hyper emesis gravid arum
 HEG is Vomiting not confined to morning but repeated throughout
the day until it affect the general condition of the patient.
 Excessive vomiting in pregnancy is approximately 1 in 500
pregnancies.
 More common in westernized industrialized societies and urban
areas than rural areas.
 Existence of dehydration and keto-acidosis escalate with the result
that the serum electrolyte balance is disrupted.
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25. HEG…
 Risk factors
 Previous pregnancies with HEG
 Multiple gestations
 Trophoblastic disease
 Nulliparity
 The risk of HEG appears to decrease with advanced
maternal age.
 Cigarette smoking is associated with a decreased risk for
HEG.
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26. Etiology of HEG
 It is unclear but it is known to be associated with:
 Multiple pregnancy
 Hydatidiform mole
 A history of unsuccessful pregnancies
 Psychological.
 Other (H.pylori infection)
 A proportion of women who experience HEG will have a recurrence
in subsequent pregnancies.
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27. Etiology …
 Women with hyperemesis gravidarum often have high hCG levels
that cause transient hyperthyroidism.
 High human chorionic gonado trophin (hCG) stimulate the chemo
receptor trigger zone in the brain stem including vomiting center.
 Evidence by High hCG in :
 Early pregnancy,
 Vesicular mole,
 Multiple pregnancy.
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28. Diagnosis
 Clinical picture (symptoms) Vomiting through day and
night
 ptyalism
 Sleep disturbance
 Hyperolfaction
 Dyspepsia
 Depression, Anxiety, Irritability, Mood changes ,Decreased
concentration
 Clinical picture (sign)
 Dehydration.
 Weight loss,
 Sunken eye,
 Dry mouth, Mild fever, Hypotension, Electrolyte abnormalities
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29. Differential Diagnosis
 Gastrointestinal disorders
 Hepatitis
 Intestinal obstruction
 Peptic ulcer disease
 Pancreatitis
 Appendicitis
 Pyelonephritis
 Degenerating uterine leiomyoma, Metabolic disorders
Diabetic keto-acidosis, Hyperthyroidism, Neurologic
disorders, Migraine headaches, Central nervous system
tumors, Nausea and vomiting of pregnancy
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30. Investigations
 Urinalysis:
 for ketones and specific gravity .
 Serum electrolytes : -
 low Na or K.
 LFT:
 Elevated transaminase levels .
 TSH free thyroxine :HEG is associated with
hyperthyroidism.
 Hematocrit; is elevated
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31. Investigation….
 Imaging Studies:
 Obstetric ultrasonography :
 evaluate for multiple gestations or trophoblastic
disease.
 upper abdominal ultrasonography;
 evaluate the pancreas and/or biliary tree
 In rare cases, abdominal CT scan may be indicated if
appendicitis is under consideration.
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32. Management
 Dietary and lifestyle changes
 Separating solids and liquids.
 Eating small, frequent meals consisting of bland
foods.
 Avoiding fatty foods such as potato chips. Avoiding
drinking cold or sweet beverages.
 High protein snacks are helpful.
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33. Managemnt…
 Admission:
 Intravenous Fluids: The pulse rate will be weak and
rapid and the blood pressure will be low.
 Normal saline or lactated Ringer’s solution is the
mainstay of intravenous fluid therapy.
 It should be given by infusion over 2-3 hours.
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34. Managemnt…
 Pharmacological
 Thiamine (vitaminB1) or pyridoxine (B6)
 Essential for normal DNA synthesis and play a role in
various metabolic processes
 A - Safe in pregnancy at a dose of 10-12.5 mg PO
qid/bid.
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35. Mgt …
 Anti-emetics :
 dopamine antagonists:
 Useful in the treatment of symptomatic nausea
 ( chlorpromazine)
 blocking postsynaptic dopamine receptors through anti-
cholinergic effects and depressing reticular activating system
 C -Safety for use during pregnancy has not been established.
 Once vomiting has ceased for a period of 24 hours oral fluid may
be commenced and if these are tolerated a light diet may follow.
 Normal food is gradually introduced and intravenous therapy
discontinued.
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36. Group discussion
 What are our goals when treating hyperemesis?
 control vomiting,
 correct dehydration,
 restore electrolyte imbalance,
 maintain adequate nutrition
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37. Amniotic fluid Disorders
 Learning objectives;
 Discuss amniotic fluid function
 List Clinical importance of AF
 Identify Volume and composition of AF
 Discuss Amniotic fluid abnormalities
 Diagnose abnormalities of AF
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38. Intro…
 Fetal membranes
 Are all structures that
develop from zygote but
not from embryo
 These are;
 Chorion
 Amnion
 Yolk sac
 The umbilical cord
including allantois and
body stalk
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39. Intro…
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40. Definitions
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41. Defn…
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42.  The factors involved in regulating AF volume are
still not completely understood.
 The 6 proposed pathways for fluid movement into and
out of the amniotic cavity include:
 Fetal swallowing
 Oral secretion
 Secretion from the respiratory tract
 Fetal urination
 Intramembranous flow across the placenta, umbilical cord
 Transmembranous flow from the amniotic cavity into the
uterine circulation
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43. 44
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44. AF…
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45. Amniotic fluid function:
 Allow room for fetal growth, movement and
development.
 Ingestion into GIT→ growth and maturation.
 Fetal pulmonary development (20 weeks).
 Protects the fetus from trauma.
 Maintains temperature.
 Contains antibacterial activity.
 Aids dilatation of the cervix during labour.
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46. Fun…
 Amniotic fluid helps protect and cushion the fetus and
plays an important role in the development of many of
the fetal organs
lungs,
kidneys, and
gastrointestinal tract.
It is taken up with fetal swallowing and sent across
the placenta to the mother's circulation
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47. Clinical importance of AF:
 Screening for fetal malformation
 (serum α-fetoprotien). E.g. Neural tube defect
 Assessment of fetal well-being
 (amniotic fluid index).
 Assessment of fetal lung maturity
 (L/S ratio).
 Diagnosis and follow up of labour.
 Diagnosis of PROM
 (ferning test).
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48. Amniotic fluid formation & composition
 First & early second trimester :
Amount is 5-50 ml & arises from:
- ultra filtrate of Maternal plasma through the
vascularized uterine decidua (in early pregnancy).
- Transudation of fetal plasma through the fetal skin &
umbilical cord (up to 20 weeks' gestation).
* It is iso-osmolar with fetal & maternal plasma, though it
is devoid of proteins.
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49. Volume and composition
 From 20 weeks up to term (mainly fetal urine):
- At 18th week, the fetus voids 7-14ml/day;
- At term fetal kidneys secretes 600-700ml of urine/day into AF.
- Fetal respiratory tract secretes 250ml/day into AF.
- Fluid transfers across the placenta.
- Fetal oro-nasal secretions.
 Secretion is controlled by:
- Fetal swallowing at term removes 500ml/day.
- Reabsorption into maternal plasma (osmotic gradient).
 AF constituents:
- Urea, creatinine, uric acid, desquamated fetal cells, vernix,
lanugo & others
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50. Amniotic fluid volume
 About 500 ml enter and leave the amniotic sac each
hour.
 gradual ↑ up to 36 weeks to around 600 to 1000 ml
then↓ after that.
 The normal range is wide but the approximate
volumes are:
- 500 ml at 18 weeks
- 800 ml at 34 weeks.
- 600 ml at term
- < 500 ml at 42 weeks
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51. Amniotic fluid volume
assessment
 Objective assessment depends on U/S to measure:
- Amniotic fluid index (AFI).
 An AFI between 8-18cm is considered normal
 An AFI < 5-6cm is considered as Oligohydramnios
 An AFI > 20-25cm is considered as Polyhydramnios
 It is a total of the DVPs in each four quadrants of the
uterus.
 It is a more sensitive indicator of AFV throughout
pregnancy.
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52. Amniotic fluid abnormalities
 Oligohydramnios:
 Defined as reduced amniotic fluid
 Amniotic fluid index of 5 cm or less or
 The deepest vertical pool < 2 cm.
 Polyhydramnios:
 Defined as excessive amount of amniotic fluid of
1500 ml or more.
 AFI of > 25 cm or
 The deepest vertical pool of > 8 cm) .
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53. Causes of oligohydramnios:
Fetal causes:
* Renal cause
 birth defects,
especially kidney and
urinary tract
malformations
 Chromosomal
abnormalities
Fetal growth restriction.
* Fetal death.
* Post term pregnancy.
* Premature rupture of
membranes
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54. Causes…
Maternal causes:
• Uteroplacental
insufficiency.
• Heypertensions
• Preeclampsia.
• diabetes
Placental causes:
• twin-twin transfusion.
• abruption
Drug causes:
Prostaglandin synthase
inhibitor as NSAID.
Idiopathic
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55. signs/symptoms
 Fundal height < gestational age
 Decreased fetal movement
 Fetal Heart Rate tracing abnormality
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56. Diagnosis:
- Fundal < date.
- AF I < 5cm , DVP < 2.
- IUGR
- Ultrasound.
 Management:
- Treat the cause (PPROM, preeclampsia).
- Assess fatal wellbeing (U/S//Doppler/BPP).
- Vesicoamniotic shunting (urethral obstruction).
- Amnioinfusion (no↓ in fetal death).
- Delivery
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57. Management flow chart
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58. Why is oligohydramnios a concern?
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59. Complication of oligohydraminous
 Too little fluid for long periods may cause abnormal
or incomplete development of the lungs called
pulmonary hypoplasia.
 Intrauterine growth restriction (poor fetal growth) is
also associated with decreased amounts of amniotic
fluid
 Extremely poor fetal prognosis, especially in early
pregnancy
 Adhesions between amnion and fetal parts ---
malformations and amputations
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60. Cxn…
 Musculoskeletal deformities
 Pulmonary hypoplasia
 Cord Compression -- >fetal hypoxia
 Passage of meconium into low AF volume: thick
particulate suspension -->respiratory compromise
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61. Complication of oligohydraminous
 IUGR
 Fetal distress
 Operative delivery
 Congenital anomalies
 Meconium aspiration
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62. Cxn…
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63. Cxn…
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64. Polyhydraminous
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65. Why is polyhydramnios a
concern?
 Too much amniotic fluid can cause the mother's uterus to
become over distended and may lead to preterm labor or
premature rupture of membranes.
 Polyhydramnios is also associated with birth defects in
the fetus.
 When the amniotic sac ruptures, large amounts of fluid
leaving the uterus may increase the risk of placental
abruption (early detachment of the placenta) or umbilical
cord prolapse (when the cord falls down through the
cervical opening) where it may be compressed.
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66. Etiology
 Increased production or decreased consumption of amniotic fluid
will result in polyhydramnous.
 Fetal causes
 Congenital anomalis
 Uniovular twins
 Increased placental mass
 Maternal causes
 DM
 PIH
 Severe generalized edama
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67. Congenital anomalies
 Anacephaly
 Transudation of CSF from the exposed meninges
 Atresia of the esophagus , diffcculty of swallowing liquor
 Fetal polyuria resulting from absence of ADH
 Uniovular twins
 b/c there area interconnected vascular in the placenta, one fetus
obtains more circulation so that its heart & kidneys
hypertrophy leading to increased urinations
 So one amniotic sac only affected
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68. Etiology …
 Increased placental mass
 Hydrops fetalis resulting from Rh incompatibility
 Severe anemia
 Cytomegalovirus infections
 True knot of the cord causes obstruction of venous return with
placental congestions
 Fetal liver cirrhosis as in syphilis
 Maternal causes
 DM due to increased osmotic pressure of the liquor amnii b/c of
high sugar content.
 Fetal polyuria resulting from hyperglycemia
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69. Etiology…
 Pregnancy induced hypertensions
 This will leads to edema of placenta
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70. Clinical varieties
 Acute polyhydramnous
 Rare
 Rapid accumulations of liquor
 Occurs before 20 weeks
 The commonest causes is uniovular twins but fetal
anomalies
 Chronic polyhydramnous
 More common
 Accumulations of liquor is rapid
 It occurs in late pregnancy
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71. Clinical pictures
 Abdominal discomfort and pain in acute polyhydramnous
 Pressure symptoms; dyspnea, palpitation, indigestion,
haemorrhoids, edema, & varicosities of lower llimbs
 Examinations of polyhydramnous
 General examinations-
 Abdominal examinations
 Inspection- over distended abdomen
 Palpations-
 The ux is tense
 Fundal level is higher than GA
 Difficult of feeling fetal parts
 Fluid thrill
 Malpresentation & non-egagement are common
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72. Differential diagnosis
 Causes of oversized pregnant Ux
 Ovarian cyst with pregnancy
 Ascites
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73. Management – acute polyhydramnous
 Termination of pregnancy by high artificial rupture
of membranes.
 This allows gradual escape of liquor thus shock and
separation of placenta are avoided
 Drew smythe catheter is used for rupture of hind
water
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74. Mgt … chronic polyhydramnous
 During labour
 Mal-presentation, cord presentation, cord prolapse
should be detected and managed
 Do ARM if the Cx is half dilated
 AMTSL – to guard against PPH
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75. Complications
 Maternal
 During pregnancy
 Abortion
 Preterm labour
 PIH
 Pressure symptoms
 Malpresentation
 During labour
 PROM
 Cord prolapse
 Abrutio placenta
 Shock
 PPH
 Fetal
 Prematurity
 Asphyxia due to cord
prolapse or placental
separation
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76. 77
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77. IUGR
 A comparison between normal and IUGR
babies.
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78.  Normal and IUGR placenta
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79. Intra Uterine Growth Restriction
 Learning objectives
 Define IUGR
 State risk factors contributing to IUGR
 Identify characteristic features of neonate with IUGR
 Recognize potential neonatal complications
associated with IUGR
 Identify how IUGR is diagnosed
 State the general principles of management of IUGR
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80. Defintion
 Foetuses of birth weight less than 10th percentile of those born at
same gestational age or two standard deviations below the
population mean are considered growth restricted.
 Small for gestational age (SGA) fetuses, all of which may not
necessarily growth restricted as many of these may be just
constitutionally small and not at risk of any adverse outcome.)

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81. Defn…
 Fetus who is below the tenth percentile in weight for
its gestational age.
 It refers to a condition in which a fetus is unable to achieve its
genetically determined potential size.
 The term IUGR should more strictly refer to foetuses that are
small for gestational age and display other signs of chronic
hypoxia or failure to thrive.
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82. Normal Fœtal Growth
 depends on two components:
 Genetic Potential
 Substrate supply
 The genetic potential is derived from both parents and is
mediated through growth factors such as insulin-like growth
factor.
 Adequate substrate supply is essential to achieve genetic
potential.
 This is derived from placenta which is dependent upon the
uterine and placental vascularity
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83. Normal…
 Normal fetal growth is characterized by
cellular hyperplasia followed by
hyperplasia and hypertrophy and lastly by
hypertrophy alone.
 Weight gain
 Foetal growth accelerates from about 5g per day
at 14 -15 wks of gestation to 10g per day at 20
wks Peaks at 30 -35g per day at 32-34wks after
which growth rate decreases.
84
W.M(Msc.) DBU

84. Classifications of IUGR
1. Type 1 or symmetrical or intrinsic IUGR
2. Type 2 or assymetric or extrinsic IUGR
3. Intermediate IUGR
85
W.M(Msc.) DBU

85. Classification…
 Type 1 or symmetrical IUGR- (20-30%)
 Occurs as a result of growth inhibition early in
pregnancy i.e. the hyperplastic stage.
 Any pathological insult at this phase leads to reduced no.
of cells in fetus and overall decreased growth potential.
 Causes include-
 Intrauterine infections (TORCH )
 Chromosomal disorders
 Congenital malformations
86
W.M(Msc.) DBU

86. Classification…
Type 2 or asymmetric IUGR (70-80%)
Occurs as a result of restriction of nutrient supply in utero
i.e. uteroplacental insufficiency.
 It is usually associated with maternal diseases like:-
 Chronic hypertension
 Renal disease
 Vasculopathies
The onset of growth restriction occurs usually after 28 wks of
gestation i.e. in the stage of hypertrophy.
87
W.M(Msc.) DBU

87. Characteristics of asymmetric
IUGR
 Normal total no. of cells, but reduced cell sizes
 Has brain sparing effect, hence
 Normal head growth
 Abdominal girth slows down
 Ponderal index is low
 Increased blood flow to the brain
 Decreased blood flow to splanchnic
 Organs affected b/c of reduced blood flow;
 Liver size
 Placental insufficiency
 Head also affected
 Decreased amniotic fluid
 Chronic hypoxia
 Fetal death
88
W.M(Msc.) DBU

88. Intermediate IUGR (5-10%)
 It is a combination of type 1 and type 2.
 Fetal growth restriction occurs during intermediate
phase of growth affecting both hyperplasia and
hypertrophy, resulting in decrease in cell no. as well
as size.
 Causes include
 Chronic HT
 Lupus nephritis
 Maternal vascular diseases that are severe and have
onset in early 2nd trimester
89
W.M(Msc.) DBU

89. Aetiology
 IUGR is a manifestation of fetal, maternal and
placental disorders that affect fetal growth.
A. Fetal Causes
1. Chromosomal Disorders-
usually result in early onset IUGR.
 Trisomies 13, 18, 21 contribute to 5% of IUGR cases
 Autosomal deletions
 Ring chromosomes
 Sex chromosome disorders are frequently lethal,
fetuses that survive may have growth restriction
(Turner Syndrome)
90
W.M(Msc.) DBU

90. Fetal causes..
2. Congenital Infections:
• The growth potential of fetus may be severely impaired
by intrauterine infections.
• The timing of infection is crucial as the resultant
effects depends on the phase of organogenesis.
• Viruses- rubella, CMV, varicella and HIV
 rubella is the most embryotoxic virus, it cause capillary
endothelial damage during organogenesis and impairs fetal
growth.
 CMV causes cytolysis and localized necrosis in fetus.
• Protozoa- like malaria, toxoplasma, trypanosoma have
also been associated with growth restriction.
91
W.M(Msc.) DBU

91. Fetal causes…
3. Structural Anomalies-
 All major structural defects involving CNS,CVS,GIT, Genitourinary and
musculoskeletal system are associated with increased risk of fetal growth
restriction.
 If growth restriction is associated with polyhydramnios, the incidence of
structural anomaly is substantially increased.
4. Genetic Causes-
 Maternal genes have greater influence on fetal growth.
Inborn errors of metabolism like agenesis of pancreas, congenital
lipodystrophy, galactosemia, phenylketonuria also result in growth
restriction of fetus.
92
W.M(Msc.) DBU

92. Placental causes
 Placenta is the sole channel for nutrition and
oxygen supply to the fetus.
 Disorders associated with placental abnormalities
include:
 Single umblical artery
 abnormal placental implantation
 velamentous umblical cord insertion
 bilobed placenta
 placental haemangiomas have all been associated with
fetal growth restriction
W.M(Msc.) DBU
93

93. Maternal causes
1. Maternal Characteristics that contributing to IUGR
are-
 Extremes of maternal age
 Grandmultiparity
 History of IUGR in previous pregnancy
 Low maternal weight gain in pregnancy
 Maternal drug ingestion e.g. alcohol, cigarettes
94
W.M(Msc.) DBU

94. Maternal causes…
2. Maternal diseases:
Uteroplacental insufficiency resulting from medical
complications like
 Hypertension
 Renal disease
 Autoimmune disease
 Hyperthyroidism
 Long term insulin dependent diabetes
95
W.M(Msc.) DBU

95. Summary of causes of IUGR
 Maternal causes
 hypertensive disorders of pregnancy,
 diabetic vasculopathy
 chronic renal disease
 collagen vascular disease
 certain hemoglobinopathies and anemias
 Poor maternal weight gain
 maternal hypoglycemia
 Maternal drug ingestion e.g. alcohol, cigarettes
96
W.M(Msc.) DBU

96.  Fetoplacental causes
 Chromosomal abnormalities,
 congenital malformations
 genetic syndromes, Twin gestation
 (TORCH) intrauterine infection, e.g. cytomegalovirus, rubella, and
toxoplasma gondii
 Abnormal placental development ….. placental insufficiency
 circumvallate placenta,
 partial placental abruption,
 placenta accreta,
 placental infarction, or
 hemangioma
97
W.M(Msc.) DBU

97. Complications of IUGR
Perinatal mortality and morbidity of IUGR infants is 3-20 times
greater than normal infants.
 Antepartum period- increased incidence of-
-still births
-oligohydramnios
 IUGR is found in 52% of unexplained stillbirths.
 During labour- higher incidence of-
 meconium aspiration
 fetal distress
 intrapartum fetal death
98
W.M(Msc.) DBU

98. Complication…
 Neonatal period- increased incidence of-
-Hypoxic ischemic encephalopathy
-Persistent fetal circulation insufficiency
 Hypothermia- They have difficulty in temperature regulation
because of absent brown fat and small body mass relative to
surface area.
 Hypoglycemia - Lack of glycogen stores may predispose to
hypoglycemia
 Chronic intrauterine hypoxia may lead to polycythemia,
necrotizing enterocolitis, and other metabolic abnormalities.
W.M(Msc.) DBU
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99. Complications…
 Childhood mortality increases from;
 Infectious diseases
 Congenital anomalies
 Incidence of cerebral palsy are 4-6 times higher.
 Subtle impairment of cognitive performance and
educational underachievement.
 Long term complications-
 Increased risk of coronary heart disease,
 Hypertension, type II diabetes mellitus,
 Dyslipidaemia and stroke.
W.M(Msc.) DBU
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100. Diagnosis of IUGR
Identifying mothers at risk of:
 Poor maternal nutrition
 Poor BMI at conception
 Pre-eclampsia
 Renal disorders
 Diseases causes vascular insufficiency
 Infections (TORCH)
 Poor maternal wt. gain during pregnancy
W.M(Msc.) DBU
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101. Dx…
 Determination of gestational age is of utmost
importance-
 Can be calculated from the date of LMP- not reliable
 Ultrasound dating before 21 wks of pregnancy
provides more accurate estimate.
1. Clinically- Serial measurement of fundal height
and abdominal girth.
 Symphysio-fundal height normally increases by 1cm
per wk b/w 14 and 32 wks.
 A lag in fundal ht. of 4wks is suggestive of
moderate IUGR.
 A lag of >6 wks is suggestive of severe IUGR.
W.M(Msc.) DBU
102

102. Dx…
2. Sonographic evaluation-
 most useful tool for diagnosis of IUGR
 To differentiate between symmetrical and
asymmetrical IUGR
 To monitor the fetal condition.
Fetal biometry:
i. BPD(Biparietal Diameter)- determines
gestational age and type of IUGR.
When growth rate of BPD is below 5th
percentile, 82% of births are below 10th
percentile(i.e. IUGR).
W.M(Msc.) DBU
103

103. Dx…
ii. Head circumference- better than BPD in
predicting IUGR.
iii. Abdominal circumference(AC)- AC and fetal
wt are most accurate ultrasound parameters
for diagnosis of IUGR.
AC has highest sensitivity and greatest
negative predictive value for sonographic
diagnosis of IUGR
W.M(Msc.) DBU
104

104. Dx...
 An increase in fetal AC of less than 10 mm in 14 days
has sensitivity of 85% and specificity of 74% for
identification of IUGR.
iv. Measurement ratios- there are some age
independent ratios to detect IUGR.
 HC/AC: decreases linearly from 16 to 20 wks of
gestation.
HC/AC >2 SD above mean is predictive of IUGR.
 FL/AC: normal value ranges from 22 + 2% in the
second half of pregnancy. Ratio above 23.5% is
considered abnormal.
W.M(Msc.) DBU
105

105. Dx…
 Placental Morphology:
 Acceleration of placental maturation may occur
with IUGR and PIH.
(Placenta is graded from grade 0 to grade III)
 Amniotic fluid volume:
 Type 2 IUGR is usually associated with
oligohydramnios.
W.M(Msc.) DBU
106

106. MANAGEMENT of IUGR
 Principles:
1. Identify the cause of growth restriction.
2. Treat the cause if found.
3. General management
W.M(Msc.) DBU
107

107. Mgt…
 First step is to identify the etiology of IUGR:-
 Maternal history pertaining to the risk factors of IUGR.
 Clinical examination- maternal habitus, height, weight, BP etc.
 Laboratory investigations- Hb, blood sugar, renal function
tests, serology for TORCH
Specific investigations for thrombophilias in pts with history
suggestive of early onset growth restriction.
 Fetal evaluation: thorough ultrasound for growth restriction,
amniotic fluid, congenital anomalies and doppler evaluation
W.M(Msc.) DBU
108

108. Mgt…
 Treatment of underlying cause:
 such as hypertension, cessation of smoking, protein energy
supplementation in poorly nourished and underweight
women.
 General Management:
 Bed rest in left lateral position to increase uteroplacental
blood flow
 Maternal nutritional supplementation with high caloric and
protein diets, antioxidents, haematinics and omega 3 fatty
acids, arginine .
W.M(Msc.) DBU
109

109. Judge Optimum Time Of
Delivery
RISK OF
PREMATURITY
 DIFFICULT EXTRA
UTERINE
EXISTENCE
110
W.M(Msc.) DBU
RISK OF IUD
• HOSTILE INTRA
UTERINE
ENVIRONMENT

110. Mgt…
 The optimum timing of delivery is determined by gestational
age, underlying aetiology, possibility of extrauterine survival
and fetal condition.
 Strict fetal surveillance is needed to monitor fetal well being
and to detect signs of fetal compromise
W.M(Msc.) DBU
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111. Fetal Surveillance
1. Daily fetal movement score
2. Non stress test(NST)
3. Biophysical profile(BPP)
4. Amniotic fluid index(AFI)
5. Growth parameters
6. Doppler studies
Sonography is usually repeated every 2 wks.
W.M(Msc.) DBU
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112. Mode of Delivery
 Fetuses with significant IUGR should be preferably
delivered in well equiped centres which can provide
intrapartum continuous fetal heart monitoring ,
fetal blood sampling and expert neonatal care.
 Vaginal delivery: can be allowed as long as there
is no obstetric indication for caesarian section and
fetal heart rate is normal.
 Fetuses with major anomaly incompatible with life
should also be delivered vaginally.
W.M(Msc.) DBU
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113.  Caesarian section:
 In all cases of IUGR with features of acidosis caesarian
section should be done without trial of labour.
 These include:
 Repetitive late decelerations
 poor biophysical profile
 reversal of end diastolic flow in umblical artery
 abnormal venous doppler
 blood gas analysis showing acidic pH on cordocentesis.
W.M(Msc.) DBU
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114. Group discussion
 What are the causes of IUGR?
 What are the characteristic features of neonate
with IUGR?
 State types of IUGR with their causes
W.M(Msc.) DBU
115

115. Intra uterine fetal death
 Learning objectives;
 Introduction
 Definition of intrauterine death
 Epidemiology of IUFD
 Etiology or causes of IUFD
 Risk factors and clinical features
 Diagnosis of IUFD
 Treatment & management
 Nursing care of IUFD
116
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116. Introduction
 Fetus die b/c of
 Asphyxia
 Difficult of labour
 Death in utero before labour
 Fetal death refers to the spontaneous death of a
fetus at any time during pregnancy, although the
term is often used interchangeably with ‘stillbirth’.
 A stillbirth is a death that occurs after 20 weeks of
gestation.
W.M(Msc.) DBU
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117. Definition
 Intrauterine fetal death:
 IUFD is usually pregnancy loss that happen after
20th weeks of gestation.
 Its the clinical term for the death of a baby in the
uterus, during pregnancy and before birth.
W.M(Msc.) DBU
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118. Etiology
Pregnancy complications:
- Pre-eclamptic toxemia
- Antepartum haemorrhage; placenta previa, abruptio
placentae
Pre- existing medical disease and acute illness:
- Chronic hypertension
- Chronic nephritis
- Diabetes
- Severe anemia
- Hyperpyrexia
- Syphilis, Hepatitis, toxoplasmosis etc.
W.M(Msc.) DBU
119

119. Etiology…
 Fetal
- Congenital malformation
- Rh-incompatibility
- Post maturity
 External version
 Idiopathic
W.M(Msc.) DBU
120

120. Risk factors
 Multiple pregnancy
 Advanced maternal age
 History of fetal demise (IUFD)
 Maternal colonization with certain pathogens
 Small for gestational age infant
 Obesity
 African American race
W.M(Msc.) DBU
121

121. Clinical features
 Absence of fetal movement
 Vaginal bleeding
 Abdominal pain
W.M(Msc.) DBU
122

122. Diagnosis of IUFD
 An inability to obtain fetal heart tones upon
examination suggests fetal demise; however, this is
not diagnostic and death must be confirmed by
diagnostic tests.
 Labor should be induced as soon as possible after
diagnosis.
W.M(Msc.) DBU
123

123. Diagnostic tests
 Ultrasound: Caregivers can see if there is a heartbeat and
movement of the fetus.
 Non-stress testing:. Two belts placed across abdomen record
changes in the heart rate of the fetus when uterus contracts.
 Biophysical profile: This test uses ultrasound to check the
heart rate, breathing, and body movements of the fetus. It also
checks amount of amniotic fluid.
 Umbilical artery Doppler velocimetry: This test uses
ultrasound to check the blood flow inside the umbilical artery.
This artery carries blood from the fetus to the placenta.
W.M(Msc.) DBU
124

124. Treatment & management
 Explain the problem to the woman and her family.
Discuss with them the options of expectant or active
management.
 If expectant management is planned:
 Await spontaneous onset of labour during the next four
weeks
 Reassure the woman that in 90% of cases the fetus is
spontaneously expelled during the waiting period with no
complicatons.
 If platelets are decreasing, four weeks have passed
without spontaneous labour, fibrinogen levels are low
or the woman request it,consider active management
(induction of labour) W.M(Msc.) DBU
125

125. Cont…
 Medical induction of labor, medicine is used to start labor and
fetus delivered naturally.
 Dilation and evacuation (D and E):
 The cervix is dilated, or made larger.
 The fetus is then removed through the vagina
 Dilation and curettage (D and C)
 The cervix is dilated, and caregivers use tools to remove the
fetus through the vagina.
W.M(Msc.) DBU
126

126. Multiple pregnancies
127
W.M(Msc.) DBU

127. W.M(Msc.) DBU
128
THORACOPAG
US ISCHIOPAGUS
CRANIOPAGU
S
RACHYPAGUS
PYOPAGUS
OMPHALOPAGU
S

128. Multiple pregnancies
 Learning objectives
 Define multiple pregnancies
 Identify types of multiple pregnancies
 State complications associated with multiple
pregnancies
W.M(Msc.) DBU
129

129.  Presence of fetuses in uterus or birth of more than one fetuses
 According to their number, they could be categorized into:
 twins (most common),
 triplet,
 quadriplet, …etc
 The gestational age at delivery decreases as fetal number
increases.
 The average gestational age was 35.3, 32, 30.7, and 28.5
weeks for twins, triplets, quadruplets, and quintuplets and
higher order multiples, respectively
W.M(Msc.) DBU
130

130. W.M(Msc.) DBU
131
Types of twin pregnancy
 Monozygotic
 Fertilization of a single ovum,
 Similar sex.
 Identical in every way including the
HLA genes
 Not genetically determined
 Constant in all races; its prevalence:
1/250.
 Dizygotic
 Fertilization of 2 separate ova
 Its etiology and prevalence
varies, with racial / hereditary
difference,
 Its actual prevalence is
increasing due to:
 Early diagnosis by U/S.
 Induction of ovulation
 Change of the ages of women
experiencing their first
pregnancy and delivery ( > 35
years age).

131. W.M(Msc.) DBU
132
CLASSIFICATION:-
 zygosity (number of ovum) :- Monozygotic:- 30%. Dizygotic:- 70%.
 chorionicity (Number of placenta):- Monochorionic(shared placenta),
Dichorionic(Two placentae) it could be either Mono or Dizygotic,
Placenta fused or separate, and septum has four layers.
 amniocity:- Number of amniotic sacs.
One sac- Monoamnionic(Monozygotic) and increase chances of TTT
Syndrome.
Two Sacs- Diamnionic, these could be mono or dichorionic, if
dichorionic then either mono or dizygotic.

132. TWIN GESTATION TYPE :-
 D C – D A, M C – DA, M C - M A, CONJOINED
Plac No. 2 1 1 1
Amni No. 2 2 1 1
Incidence. 1:300 1:400 1:3000 1:50,000
Time of Cleav. 0- 72 hrs 4 to 8days 9–12 days > 12 days.
DC (Dichorionic), DA(Diamnionic),
MC(Monochorionic),MA(Monoamnionic), DC- DA :- may be Dizygo if
diff gender; Same gender Di or Monozygo
W.M(Msc.) DBU
133

133. Ctd…
 MZ twins (30%) a single fertilized ovum splits into two distinct
individual after a variable number of division
 Timing of egg division Determines placentation in twins
 DC DA placentation occurs with division prior to the morula
stage (within 3 days post fertilization)
MC DA placentation occur with division b/n days 4 and 8 post
fertilization
 MC MA placentation occurs with division b/n days 8 and 12 post
fertilization
 Division at or after day 13 results in conjoined twins
W.M(Msc.) DBU
134

134. W.M(Msc.) DBU
135
Monozygotic Twins…
Different Scenarios of Cleavage
If the separation takes place just after the first cellular division [1st 3 days ]
both of the twins will have their own placenta and an amniotic sac each.
Scenario 1
Monozygotic twin pregnancy
Bi-chorial and bi-amniotic

135. W.M(Msc.) DBU
136
Scenario 2
Monozygotic twin pregnancy
Mono-chorial and bi-amniotic.
Separation can also take place a little later in the development [4-8 days]
of the embryonic cells but before the blastocyte has defined the roles of each cell.
Twins will be in the same placenta, but they will have 2 amniotic sacs.

136. W.M(Msc.) DBU
137
Scenario 3
Monozygotic twin pregnancy
Mono-chorial & mono-amniotic
Separation takes place at the stage when the amniotic bag is already being
formed[day 8-14]
Twins will be in the same placenta, and in the same amniotic sac.

137. W.M(Msc.) DBU
138
Conjoined Twins
 If the division occurred just
after embryonic disc
formation, incomplete or
conjoined twins will occur.
They may be joined at;
 anteriorly [thoracopagus-
commonest],
 posteriorly [pyopagus]
 cephalad [craniopagus] or
 caudal [ischiopagus].

138. W.M(Msc.) DBU
139
Maternal Complications
 Increased maternal mortality.
 Increased pregnancy risks:
 Anemia (15%): due to iron deficiency or folic acid
deficiency
 Preeclampsia- eclampsia: 3x
 Glucose intolerance.
 Threatened or actual abortion.
 Polyhydramnios (12%): acute: more in monozygotic
than dizygotic twins. OR Chronic: not related to type.

139. Ctd..
 Mechanical effects: with the uterus larger than
period of amenorrhea; it may be associated with
dyspnea, dyspepsia, pressure on ureter with
increased UTI, supine hypotension syndrome,
increased varicosities and lower limb edema.
 Premature rupture of membranes
 Antepartum hemorrhage: both abruption (due to
PIH and folic acid deficiency) and placenta previa
(due to large placenta).
 Psychological: problem of caring, prolonged rest
and hospitalization.
 Malprentation and malposition
W.M(Msc.) DBU
140

140. Ctd…
 Increased labor risks:
 Preterm labor (50%): which may be spontaneous
or induced Uterine dystocia.
 Abnormal fetal presentation.
 Twins entanglement and locked twins
 Cord accident
• Cord prolapse.
• Vasa Praevia (vilamentous insertion of the cord).
• Two Vessel cord (7% especially monozygotic)
 Postpartum Hemorrhage
 Puerperal Sepsis
W.M(Msc.) DBU
141

141. W.M(Msc.) DBU
142
Fetal/Neonatal Complications
 Increased abortion rate:
 Increased intra-uterine fetal death (IUFD):
 More in MZ > DZ.
 Vanishing twin syndrome: (incidence rate 21%)
 Early death - (papyraceous fetus).
 Later death - macerated fetus.
 Death during delivery:
 first fetus: prolapsed cord,
 second fetus: [ due to excess sedation, premature seperation of
placenta, constriction ring ,dystocia, operative manipulation,
hypoxia].

142. Ctd…
 Increased perinatal mortality (10-20%):
 More in monozygotic twins.
 It is mainly related to low birth weight.
 It may be due to
 preterm delivery
 IUGR with PIH
 hypoxia (placental or cord accident)
 operative manipulation: Birth trauma and CP
 congenital malformation.
 Increased low body weight:
 Neonates are lighter [due to preterm or IUGR],
 More in monozygotic and with increased fetal number
W.M(Msc.) DBU
143

143. W.M(Msc.) DBU
144
Twin to Twin transfusion
 Vascular communication between 2
fetuses, mainly in monochorionic
 Twins are often of different sizes:
 Donor twin = small, pallied, dehydrated
(IUGR), oligohydramnios (due to
oliguria), die from anemic heart failure.
 Recipient twin = plethoric, edematous,
hypertensive, ascites, kernicterus (need
amniocentesis for bilirubin), enlarged
liver, polyhydramnios (due to polyuria),
die from congestive heart failure, and
jaundice. Hemoglobin concentrations
differ by >5g/dL.

144. W.M(Msc.) DBU
145
Diagnosis
 25% of antenatal diagnosis of twin is missed .
 Twin should be suspected by history and
examination
 It should be confirmed by U/S (as early as 10 wks).
 To decrease PNM, it should be early diagnosed,
properly assessed antenatally and properly managed
intranatally.

145. W.M(Msc.) DBU
146
History…
 Patient profile:
 Etiological factors; with positive past history and family
history specially maternal.
 Early pregnancy: Hyperemesis, bleeding.
 Mid-pregnancy:
 Greater weight gain than expected,
 abdominal size > period of amenorrhea,
 early PIH symptoms, persistent fetal activity.
 Late pregnancy:
 Pressure symptoms (dyspnea, dyspepsia, UTI, edema and
varicose veins in LL).

146. W.M(Msc.) DBU
147
Examination
 General:
 An early increase of weight
 Pallor
 Early PIH
 Early edema, and varicose veins in LL.
 Abdominal:
 Fundal level > amenorrhea especially in mid-pregnancy
 exclude other causes.
 Palpation: Multiple fetal parts – 3 poles, 2 heads, small head in relation to
uterine size, fetal movement all over abdomen.
 identify presentations.
 Auscultation of FHS:
 2 different recordings by 2 observers and a difference > 10 bpm a Gallop
between 2 points
 Pelvic: Specially during the course of labor
 small presenting part compared to abdominal size

147. W.M(Msc.) DBU
148
Ultrasonography
 Confirm fetal number
 Two gestation sacs
 Two fetus with heart beats ( >=6 weeks)
 Diagnosis of vanishing twin syndrome.
 Diagnose any liquor abnormality
 Diagnose their presentation and position and
relation to each other
 Assess fetal well-being and growth
 Diagnose type of twin:
 Mono- vs. dizygotic twins.

148. Management
 Antepartum :- Care as high risk pregnancy.
- Nutritional counseling.
- Iron &Folic acid supplementation.
- More ANC Visits.
- Extra rest & Early work leave.
- Counsel on danger signs of high risk pregnancy.
- Monitor for PIH / PE. Glucose intolerance
W.M(Msc.) DBU
149

149. Mgt…
- Counsel about headache, vision disturbance and
epigastric pain.
- Clinical US for Fetal monitoring for wellbeing.
- More frequent BPP/NST when indicated.
- Fetal mov counts. Not reliable
- Preterm labor: tocholytic agents & steroid inj.
<34wks indicated.
W.M(Msc.) DBU
150

150. Mgt…
W.M(Msc.) DBU
151
 Intrapartum
 Induction & augmentation are contraindicated.
 Route of Delivery :
- If both Twins are by Vertex: Vaginal delivery.
- If first twin not cephalic and twins are viable :Cesarean
section.
- If both twins are about 2000gm or more:-
first twin cephalic – vaginal delivery & second twin
external version & vaginal delivery or assisted breech
vaginal delivery

151. Mgt…
Twin A-Vertex / Twin B Non vertex :-
Twin A vaginal & for Twin B Options are :
 External Cephalic Version,
 Assisted breech extraction,
 Total breech extraction,
 Internal Podalic version & breech extraction.
Routine cesarean delivery for :
 Conjoint twin, triplets and so on,
 Placenta previa ,
 Monoamniotic twins .
W.M(Msc.) DBU
152

152. RH incompatibility
 One of the first tests performed during pregnancy
is blood-type test.
 Incompatibility with respect to D-antigen is the
most common causes of hemolytic disease and
newborn.
 85% of the population is believed to be RH-+ve.
 About 60% of individuals with Rh- positivity are
heterozygous while 40% are homozygous.
153
W.M(Msc.) DBU

153.  Rh incompatibility occurs when a woman is Rh
negative, but her fetus has inherited Rh-
positive blood from the father.
 She only becomes sensitized to the fetus's Rh-
positive blood once she comes in contact with
it.
W.M(Msc.) DBU
154

154. Fetomaternal hemorrhage
c/s delivery
Placenta praevia/ abruptio placenta
Manual removal of placenta
Miscarriage/abortion
induced abortion,
ectopic pregnancy
Amniocentesis
W.M(Msc.) DBU
155

155. Symptoms of the fetus
 Anemia
 Swelling of the body ( hydrops fetalis), which may be
associated with:
 Heart failure
 Respiratory problems
 Kernicterus (a neurological syndrome), which can
occurs
 Early:
 High bilirubin level (greater than 18 mg/cc)
 Extreme jaundice
 Poor suck
 Lethargy
W.M(Msc.) DBU
156

156.  Intermediate:
 Arched back with
neck
hyperextended
backwards
(opisthotonos)
 Bulging fontanel
(soft spot)
 Seizures
 Late:
 Intellectual disability
 Muscle rigidity
 Speech difficulties
 Seizures
 Movement disorder
157
W.M(Msc.) DBU

157. Management of un sensitized
Rh-ve
 For pregnant mother, it is standard procedure to
order blood test
 If Indirect Coomb’s test at initial visit is negative,
1. Father Rh +ve or unknown status
2. Repeat indirect coomb’s test at 28 wks of GA
and give 300µg of Rh immune globulin if test
result is negative
3. Check Rh status of newborn after delivery
4. If Rh+ve give 300µg immune globulin for mother
5. If father is Rh-ve , no prophylaxis for mother
W.M(Msc.) DBU
158

158. Treatment to Newborn
 Treatment of a pregnancy or newborn depends on
the severity of the condition.
 Mild:
 Aggressive hydration
 Phototherapyusing bilirubin lights
 Hydrops fetalis:
 Amniocentesis to determine severity
 Intrauterine fetal transfusion
 Early induction of labor
 Kernicterus:
 Exchange transfusion (may require multiple exchanges)
 Phototherapy
W.M(Msc.) DBU
159

159. Late Pregnancy Bleeding
 APH-
160
W.M(Msc.) DBU
Bleeding
In
Pregnancy
Bleeding in
early
Pregnancy
Antepartum
haemorrhage
(APH)
Post partum
Haemorrhage
(PPH)

160. ANTEPARTUM
HAEMORHAGE
 Bleeding from the vagina during pregnancy after
28 weeks of gestational age
 APH is bleeding from the genital tract after the
28th wks of gestations up to delivery.
 Avoid vaginal/rectal examination in any px women
with APH.
 Mothers with APH should be managed at a site with
operative and blood transfusion
W.M(Msc.) DBU
161

161. W.M(Msc.) DBU
162
CAUSES of APH
PLACENTAL
 Placenta Praevia
 Placenta Abruption
 Vasa Praevia
NON PLACENTAL
 Labour (Heavy show )
 Uterine rupture
 Local / Non obstetrical
Cervicitis
Polyp
Lacerations
 Bleeding Disorders
Conginital
acquired

162. W.M(Msc.) DBU
163
Placenta praevia
 Definition
Insertion of the placenta, partially or fully, in
the lower segment of the uterus

163. W.M(Msc.) DBU
164
Etiology
 No definitive cause
 Endometrial factors:
 A scarred endometrium
 Curettage for several times
 Abnormal uterus
 Placental factors
 Large placenta
 Abnormal formation of the placenta

164. W.M(Msc.) DBU
165
Risk factors for Placenta praevia
• Multiparity
• Advanced maternal age
• Prior LSCS or other uterine surgery
• Prior placenta praevia
• Uterine structural anomaly

165. W.M(Msc.) DBU
166
Degrees of Placenta praevia

166. W.M(Msc.) DBU
167
Classification of Placenta praevia
 Four grades:
 Type I ( Low lying): Placenta encroaches lower
segment but does not reach the internal os
 Type II (Marginal placenta previa): Reaches
internal os but does not cover it
 Type III (Partial Placenta previa): Covers part of
the internal os
 Type IV (Complete): Completely covers the os,
even when the cervix is dilated

167. W.M(Msc.) DBU
168
Placenta praevia- Clinical Features
 Recurrent painless vaginal bleeding (not always)
 Abdominal findings
Uterus is soft, relaxed and non tender
Contraction may be palpated
Presenting part is usually high
Abnormal presentations
 Maternal cardiovascular compromise
 Vaginal examination- should not be done

168. W.M(Msc.) DBU
169
Investigation
1: For Localization of placenta:
 Ultrasound:
 Abdominal ultrasound can easily diagnose
placenta previa with an accuracy of 93-97%.
 Transvaginal ultrasound is safe and is more
accurate than transabdominal ultrasound in
locating the placenta
2: Haematological Investigations:
 A. Complete blood picture.
 B. Blood grouping. C:Renal profile

169. W.M(Msc.) DBU
170
Placenta praevia-Complications
Maternal
• Major hemorrhage, shock, and death
 Renal tubular necrosis and acute renal failure
 Post partum haemorrhage
 Morbid adherence of Placenta : placenta accreta
complicates placenta praevia cases
 Anaemia in chronic haemorrhage
 Disseminated intravascular coagulopathy (DIC)

170. W.M(Msc.) DBU
171
Placenta praevia-
Complications cont….
Foetal
 IUFD
 Hypoxic ischemic encephalopathy
 Cerebral paulsy
 Placental abruption
 Premature labour

171. W.M(Msc.) DBU
172
Placental abruption
 Definition
Premature separation of a normally
situated placenta in a viable foetus
 Placental abruption should be considered in
any pregnant woman with abdominal pain
with or without PV bleeding, as mild cases
may not be clinically obvious

172. W.M(Msc.) DBU
173
Etiology
Risk factors
1. Increased age and parity
2. Vascular diseases: preeclampsia, maternal
hypertension, renal disease,SLE
3. Mechanical factors: Trauma, intercourse
Sudden decompression
of uterus
Polyhydroamnios
Multiple pregnancy
4. Smoking, cocaine use,
5.Premature rupture of membranes

173. W.M(Msc.) DBU
174
Pathology
 Main changes
Hemorrhage into the decidua basalis → decidua
splits → decidural hematoma → separation,
compression, destruction of the placenta
adjacent to it
 Types of abruption
1. Revealed abruption
2. Concealed abruption
3. Mixed type

174. W.M(Msc.) DBU
175
Revealed abruption Concealed abruption

175. W.M(Msc.) DBU
176
Diagnosis-Clinical Features
Vaginal bleeding associated with
persistent abdominal pain
 Tenderness on the uterus
 “Woody” hard uterus
 Change of foetal heart rate
 Features of hypovolemic shock

176. W.M(Msc.) DBU
177
Complication of Placental
abruption
Maternal
 Disseminated intravascular coagulopathy
 Hypovolemic shock
 Amniotic fluid embolism
 Renal tubular necrosis and acute renal failure
 Post partum haemorrhage
 Maternal death

177. W.M(Msc.) DBU
178
Complication of Placental
abruption
Feotal
 Premature labour
 IUGR in chronic abruption
 Hypoxic ischemic encepalopathy and cerebral
paulsy
 Foetal death

178. W.M(Msc.) DBU
179
Investigations
 1: Diagnostic investigations:
 Ultrasonography
Mainly to exclude placenta praevia
Can detect
Retroplacental hematoma
Feotal viability
 2: Laboratory investigations
1. Investigation for Consumptive coagulopathy – Platelet count
2. Liver and Renal function tests

179. W.M(Msc.) DBU
180
Vasa praevia
 Foetal blood vessels from the placenta or umbilical
cord cross the internal os beneath the baby
 Rupture of membranes leads to damage of the
foetal vesseles leading to exsanguinations and
death
 High foetal mortality

180. W.M(Msc.) DBU
181
Vasa praevia

181. W.M(Msc.) DBU
182
Diagnosis - Vasa praevia
1.Moderate vaginal bleeding + feotal
distress
2.Vessels may be palpable through dilated
cervix
3.Vessels may be visible on ultrasound
(Transvaginal colour Doppler ultrasound)
 Difficult to distinguish from abruption
 Can look for feotal Hb (Kleihauer-Betke test) or
nucleated RBC’s in shed blood

182. W.M(Msc.) DBU
183
Management of APH

183. W.M(Msc.) DBU
184
Management of APH
 Admit to hospital for assessment & management
 May need resuscitation measures if shocked or
severe bleeding
Airway, breathing and circulation
Senior staff must be involved –Consultant
obstetrician and consultant anaesthetist,
neonatalogist
Two wide bore canula
Take blood for Grouping, coagulation
profile,Liver & renal function

184. W.M(Msc.) DBU
185
Management of APH cont…
History
 Obtain a history if patient’s condition allow
including:
• Colour and consistency of bleeding
• Quantity and rate of blood loss
• Precipitating factors i.e. Sexual intercourse,
Vaginal examination
• Degree of pain, site and type
• Placental location-review ultrasound report
if available
• Ascertain foetal movements

185. W.M(Msc.) DBU
186
Management of APH cont…
Examination
 Assess maternal and foetal well-being
Pallor, record temperature, pulse and BP
 Perform abdominal examination
Note areas of tenderness and hypertonicity
Determine gestational age of foetus,
presentation
and position, auscultate foetal heart
 No vaginal examination should be attempted at least
until a placenta praevia is excluded

186. W.M(Msc.) DBU
187
Placenta praevia - Management
1.Near term / Term
 Delivery is considered
Types I and II - May be able to deliver
vaginally
Types III and IV - Will require caesarean
section by senior obstetrician

187. W.M(Msc.) DBU
188
Placenta praevia – Management
cont…
2.Early in pregnancy
 Continuation of pregnancy is better if possible
• Need bed rest
• Educate patient regarding condition and risk
• 3 pint of crossed matched blood should be
available till delivery
• Foetal well being and growth should be
monitored
• Medications may be given to prevent premature
labour- Nifidipine,

188. W.M(Msc.) DBU
189
Placental abruption - mgt
 Moderate or severe placental abruption:
• Restore blood loss
• Ideally measure central venous pressure (CVP) and
adjust transfusion accordingly
• Prevent coagulopathy
• Monitor urinary output
• Delivery
1.Caesarean section
2.Vaginal
If coagulopathy present
If feotus is not compromised
If feotus is dead

189. W.M(Msc.) DBU
190
Vasa Previa management
 Urgent delivery
Most of the time urgent LSCS
 Neonatologist involvement
 Aggressive resuscitation of the baby with
blood transfusion following delivery

190. Chapter 2.
MEDICAL DISEASES
ASSOCIATED WITH
PREGNANCY
191
W.M(Msc.) DBU

191. Hypertensive disease in
pregnancy
W.M(Msc.) DBU
192
 Its one of the most leading maternal morbidity &
mortality
 Hypertension during pregnancy can be defined as
Bp greater than 140/90 mmHg, measured on two
consecutive occasions 6 hrs or more apart or
 Single Bp measurement of 160/110mmHg.

192. Classification
 Pre-existing (chronic) hypertension:
Hypertension that is present before pregnancy,
detected in early pregnancy ( before 20 weeks
in absence of vesicular mole ) and persists
postpartum.
Examples:
essential hypertension ,
Hpn secondary to chronic renal disorders e.g.
pyelonephritis and renal artery stenosis,
systemic lupus erythematosus and
pheochromocytoma. W.M(Msc.) DBU
193

193. Classification…
 Pregnancy-induced hypertension (PIH):
Gestational Hypertension:
Hypertension without proteinuria
Pre-eclampsia:
Hypertension with proteinuria and oedema
after 20 weeks of pregnancy, but may be
earlier in vesicular mole.
Eclampsia:
Pre-eclampsia + convulsions.
W.M(Msc.) DBU
194

194. Classification…
 Superimposed pre-eclampsia or eclampsia:
Development of pre-eclampsia or
eclampsia in pre-existing hypertension
detected by a further increase of 30
mmHg or more in systolic blood
pressure or 15 mmHg or more in
diastolic blood pressure.
W.M(Msc.) DBU
195

195. PRE-ECLAMPSIA…
 Refers to new onset of HTN and
proteinuria after 20 weeks of GA in
previously normotensive woman
 HTN=SBP greater or equal to 140 and
DBP greater or equal to 90 mmHg
 Proteinuria=urine protein of greater or
equal to 300 mg per 24 hour
 Random urine protein of 30 mg/dl or +1
on dipstick is suggestive but not
diagnostic of proteinuria
W.M(Msc.) DBU
196

196.  BP elevation should be sustained
 Generally two measures at least 6 hours apart
 DBP is determined by 5th
kortkoffsound(disappearance) with patient sitting
 Pre-eclmpsia can be mild or severe
 No moderate pre-eclampsia
W.M(Msc.) DBU
197

197. Severe preeclampsia features
1. Symptoms of CNS dysfunction
1. Blurred vision, scotomata, altered mental status,
sever headache
2. Symptoms of liver capsule distension
1. RUQ or epigastric pain
3. Hepatocellular injury
1. Serum transaminase conc.at least 2x(elevated or
rising)
4. Thrombocytopenia(less than 100,000 /mm3)
W.M(Msc.) DBU
198

198. Severe pre-eclampsia
5.Severe BP elevation
 SBP greater or equal to 160 and DBP greater or
equal to 110 at least 2x 6 hours apart
6.Proteinuria of 5 gm or more in 24 hours or 3+ or
greater
7.Oligouria or deranged RFT(elevated or rising
creatinine)
8.Sever IUGR
9.Pulmonary edema or cyanosis
11.Eclampsia W.M(Msc.) DBU
199

199. Pre-eclampsia
 Predisposing factors:
 Primigravidae
 Pre-existing hypertension.
 Previous pre-eclampsia.
 Family history of pre-eclampsia.
 Hyperplacentosis i.e. excessive chorionic
tissue as in hydatidiform mole ,multiple
pregnancy, uncontrolled diabetes mellitus and
foetal haemolytic diseases.
 Obesity.
W.M(Msc.) DBU
200

200. Complications
 Maternal :
 Convulsions and coma (eclampsia).
 Cerebral haemorrhage.
 Renal failure.
 Heart failure.
 Liver failure.
 Disseminated intravascular coagulation.
 Abruptio placentae.
 Recurrent pre-eclampsia in next pregnancies.
W.M(Msc.) DBU
201

201. Complication…
 Foetal :
 Intrauterine growth retardation (IUGR).
 Intrauterine foetal death.
 Prematurity and its complications.
W.M(Msc.) DBU
202

202. Eclampsia
Development of grandmal seizure in a
woman with preeclampsia
Seizure should not be attributable to
another cause. E.g. epilepsy
W.M(Msc.) DBU
203

203. Chronic/Pre-existing
hypertension
 Refers to SBP greater or equal to 140 or
DBP greater or equal to 90 mmHg or both
that antecedents pregnancy
Present before 20 wks of GA
Persist after 12 wks postpartum
 Can be
Primary/essential
Secondary(of medical disorders)
W.M(Msc.) DBU
204

204. Preeclampsia Superimposed on Chronic
hypertension
If new onset of proteinuria after 20 wks GA
If exacerbation of BP to the severe
range(SBP greater or equal to 160 or DBP
greater or equal to 110 mmHg) especial
If accompanied by symptoms or increased
LFT or thrombocytopenia
W.M(Msc.) DBU
205

205. GESTATIONAL HTN
 Refers to HTN (usually mild) w/o proteinuria
or other signs of preeclmasia
 Should resolve by 12 wks postpartum
 If not, diagnosis=chronic HTN(was masked in
early pregnancy by physiologic changes of
pregnancy)
 Some progress to preeclampsia
 Mostly when gestational HTN develop before 30
W.M(Msc.) DBU
206

206. Management of Pre-eclampsia
 Termination of pregnancy is the definitive & curative
treatment
 It is the most important treatment for the mother.
 Factors that determine whether to follow aggressive
(delivery) or conservative management are
- The gestational age
- The severity of the disease
- The fetal maturity & fetal condition
W.M(Msc.) DBU
207

207. Mgt…
Ambulatory management in patient with;
 DBP b/n 90-100 mmHg or SBP 140-160 mmHg.
 Proteinuria 1+ or less dipstick or
 24 hrs urine protein less than 500mg.
 Compliant patient
 No fetal jeopardy
Follow up
 Random urine protein twice/ week
 Bp measurement twice/ week
 Daily fetal movement counting
 Weekly ANC follow up W.M(Msc.) DBU
208

208. Mgt…
 The patient should report immediately if:
 Sudden increase in wt
 Generalized edema including the upper limb &
face
 Decrease in urine out put
 Persistent headache
 Blurring of vision
 Right upper quadrant or epigastric pain
 Decreased fetal movement
 Vaginal bleeding
 Convulsion or loss of consciousness
W.M(Msc.) DBU
209

209. Mgt…
Hospital management
 Indication for admission: Patient deserves admission if the
criteria for ambulatory patient is not fulfilled.
Maternal Follow up:
 Close follow up of mother in search of imminent sign &
symptom.
 Daily weight measure.
 Bp every 6 hrs
 Urine protein every 48 hrs
 Hgb( hct), platelet, RFT, LFT, coagulation profile on weekly
bases.
W.M(Msc.) DBU
210

210. Mgt…
Fetal follow up
 Growth by ultrasound
 Fetal well being (biophysical profile 2x (week)
 Daily FHR auscultation
 Daily fetal movement counting (kick chart)
W.M(Msc.) DBU
211

211. Mgt…
Anticonvulsant:
Indications to use
All women with severe pre eclampsia admitted for
the 1st time.
 For the 1st 24 -48 hrs parentral route should be
used to administer medication.
 Discontinue anti-couvulsant if Bp is controlled &
expectant management is planned
All women with PIH going into labor & delivery
The 1st 48 hrs post partum period.
W.M(Msc.) DBU
212

212. Management of Eclampsia
 Shout for help - mobilize personnel
 Rapidly evaluate breathing and state of consciousness
 If not breathing, assist ventilation using Ambu bag and mask
 Check airway, blood pressure and pulse
 Give oxygen at 4–6 L per minute via nasal cathetor;
 Position on left side
 Protect from injury but do not restrain
 Start IV infusion with large bore needle (16-gauge)
 If eclampsia is diagnosed, initiate magnesium sulfate
 If the cause of convulsions has not been determined, manage as
eclampsia and continue to investigate other causes.
W.M(Msc.) DBU
213

213. W.M(Msc.) DBU
214
Drugs
 Antihypertensive
Drugs
Hydralazine
Labetolol
Nifedipine
 Anticonvulsive Drugs
 Magnesium sulfate
 Diazepam
 Phenytoin
Principles:
 Initiate
antihypertensive if
diastolic blood
pressure > 110 mm
Hg
 Maintain diastolic
blood pressure 90-
100 mm Hg to
prevent cerebral
hemorrhage 214

214. W.M(Msc.) DBU
215
1. Hydralizine (vasodilator)
 Dose - 5mg Iv stat, repeat every 20min until diastolic
Bp is 110 mmHg.
2. Nifedipine (Ca++ channel blocker)
 Dose - 10mg sublingual, repeat same dose in 30 min
until DBP is 100mm Hg.
3. Labatalol (B- Blocker)
 Dose - 5-15 mg IV push, every 10-20 min
- Double the dose (maximum, 300mg) & then
600 mg po six hourly, if conservative management
is planned.
Antihypertensive Drugs

215. W.M(Msc.) DBU
216
 Use magnesium sulfate in
 Women with eclampsia
 Women with severe pre-eclampsia necessitating
delivery
 Start magnesium sulfate when decision for delivery
is made
 Continue therapy until 24 hours after delivery or the
last convulsion, whichever occurs last
Magnesium Sulfate

216. W.M(Msc.) DBU
217
 Loading dose
 Magnesium sulfate 10 g of 50% magnesium
sulfate solution, 5 g in each buttock as deep IM
injection with 1 mL of 2% lignocaine in the same
syringe. Ensure that aseptic technique is
practiced when giving magnesium sulfate deep
IM injection. Warn the woman that a feeling of
warmth will be felt when magnesium sulfate is
given.
 If convulsions recur after 15 minutes, give 2 g
magnesium sulfate (50% solution) IV over 5
minutes.
Magnesium Sulfate protocol:

217. Magnesium …..
 Maintenance dose
 5 g magnesium sulfate (50% solution) + 1 mL
lignocaine 2% IM every 4 hours into alternate
buttocks.
 Continue treatment with magnesium sulfate
for 24 hours after delivery or the last
convulsion, whichever occurs last.
W.M(Msc.) DBU
218

218. Magnesium sulfate…
 Before repeat administration, ensure that:
 Respiratory rate is at least 16 per minute.
 Patellar reflexes are present.
 Urinary output is at least 30 mL per hour over 4 hours.
 Withhold or delay drug if:
 respiratory rate falls below 16 per minute.
 patellar reflexes are absent.
 urinary output falls below 30 ml/hour over preceding 4
hours.
 Keep antidote ready
 In case of respiratory arrest:
 Assist ventilation (mask and bag, anaesthesia apparatus, intubation).
 Give calcium gluconate 1 g (10 mL of 10% solution) IV slowly until
respiration begins to antagonize the effects of magnesium sulfate.
W.M(Msc.) DBU
219

219.  Diazepam
10mg IV bolus over 2 minutes
30mg/1000ml 5% D/w 30 drop/min
Repeat 10mg IV bolus, if convulsion recur.
 Phenytoin
 Used for prevention of convulsion /recurrent
convulsion
 Loading dose 1grm IV over 20min &
maintenance 200mg every 6 hrs after 12hrs of
initial dose.
W.M(Msc.) DBU
220

220. Delivery
 All patient with sever pre eclampsia & GA 34 week
termination of pregnancy should be considered; mode
of delivery can be:
 Cesarean section - for obstetric indications
 Induction if
 Term
 Favorable Cx,
 No contra indication for vaginal delivery
 Mature fetus,
 Controlled maternal - fetal condition
W.M(Msc.) DBU
221

221. Intra partum care
 FHB monitoring every 15 min
 Maternal vital sign every 30 min-1 hr
 Urine out put every 4 hrs
 Shorten the second stage of labor
 Prevent PPH (mange third stage actively using
oxytocin)
N.B - Ergometrine use is contraindicated
W.M(Msc.) DBU
222

222. Post partum care
 Continue anti - convulsant for 24-48 hrs post
partum
 Closely monitor Bp
 If hypertension persists beyond 6 weeks
post partum the patient needs further follow
up.
W.M(Msc.) DBU
223