Presentation

1. Abnormal pregnancy
By Alemnesh Mosisa (BSc, MSc)
1

2. Hypertensive Disorders in
Pregnancy
2

3. Hypertensive Disorders in Pregnancy
The hypertensive disorders of pregnancy (HDP) refer to a
broad list of diseases affecting pregnancy and presenting
with HTN and/or proteinuria and/or significant edema.
Most common medical complications of pregnancy
Increased maternal and perinatal morbidity and mortality
Affect 5-10% of all px’s and is responsible for
approximately 15% of Maternal Mortality (worldwide
50,000 death/year)
3

4. Hypertensive Disorders ……….cont.
Etiologies
1. Placental implantation with abnormal trophoblastic
invasion of uterine vessels. The magnitude of invasion
correlates with the severity of the hypertensive disorder
2. Immunological maladaptive tolerance between
maternal, placental and fetal tissues
3. Maternal maladaptation to cardiovascular changes of
normal pregnancy
4. Genetic – inherited genes
4

5. Hypertensive Disorders ……….con’t
Diagnosis
Two appropriately taken BP measurements exceeding
140/90 mm Hg, taken at least six hours apart
 A single measurement of BP > 160/110 is sufficient to
diagnose hypertension during pregnancy
 Proteinuria of ≥300mg/24hrs OR 2+ dipstick or more on
at least two occasions at least 6 hrs apart but not > 1 week
5

6. Hypertensive Disorders ……….con’t
NB- Edema has been no longer a diagnostic criteria unless
the edema
Persists after night rest
Edema that involves the face, the hands or the whole body
Abnormal weight gain of more than 2 pounds per week.
6

7. Hypertensive Disorders ……….con’t
 Hypertensive disorders of pregnancy are classified as
1, Gestational HTN
2, Preeclampsia pregnancy induced HTN
3, Eclampsia
4, Superimposed preeclampsia on chronic hypertension -
Pregnancy aggravated hypertension
5, Chronic hypertension
7

8. 1.Gestational hypertension
• Most frequent cause of hypertension during pregnancy
• BP≥ 140/90mmHg for first time after 20wks of pregnancy
or with in 24 hrs postpartum, without proteinuria
• BP returns to normal < 12 weeks’ postpartum
• 50% of patients progress to preeclampsia tend to develop
essential hypertension later in life
• Called transient hypertension if preeclampsia does not
develop and BP returned to normal by 12 wks postpartum
8

9. Gestational HTN…………..Cont’d
Risk factors
• Kidney disease
• Diabetes
• Hypertension with a previous pregnancy
• Mother's age younger than 20 or older than 40
• Multiple fetuses (twins, triplets)
9

10. 2.Preeclampsia
 BP ≥140/90mmHg after 20weeks‘ of gestation Plus
proteinuria of ≥0.3g per 24-hour urine collection or urine
dipstick reading ≥1+ and/edema after 20 wks of gestation
which resolves within 6 weeks postpartum.
 Incidence is 2-7%
 Differentiation between mild & severe preeclampsia can be
misleading because apparently mild disease may progress
rapidly to severe disease
10

11. Preeclampsia……… cont’d
￭Signs of severe preeclampsia
• BP ≥160/110mmHg (severe hypertension)
• Proteinuria ˃5g/24hrs or dipstick ≥+3
• Elevated indirect bilirubin levels
• Increased serum transaminase levels /AST and ALT
• Thrombocytopenia (Platelets <100,000/mm3)
• Serum creatinine >1.1mg/dl
• Oliguria ≤400 milliliters in 24 hours
• Persistent headache and Persistent epigastric pain 11

12. Preeclampsia……… cont’d
• A particularly severe form of preeclampsia is the HELLP
syndrome (Hemolysis, Elevated Liver enzymes, and Low
Platelet count)
• Characterized by reduced organ perfusion secondary to
vasospasm and endothelial activation
12

13. Risk factors for preeclampsia
 Nulliparity
 Extremes of reproductive ages(<20 and˃35 )
 BMI ˃30
 Multifetal
 Gestational trophoblastic disease
 Diabetus mellitus
 Prior preeclampsia
 Genetic
 Low socio-economic status 13

14. Preeclampsia………Cont’d
Complications of Preeclampsia
 Eclampsia
 Abruptio placenta
 Acute renal, heart failure and hepatic failure
 HELLP syndrome
 DIC, cerebral hemorrhage and pulmonary edema
 Intrauterine growth restriction and death are fetal
complications.
14

15. 3. Preeclampsia superimposed on
Chronic Hypertension
Chronic underlying hypertension is hypertension
diagnosed in women before pregnancy or before 20 wks’
gestation
New-onset proteinuria ≥ 300mg/24 hrs in hypertensive
women but no proteinuria before 20 weeks’ gestation
A sudden increase in proteinuria or blood pressure or
recorded platelet count <100,000/mm3.
15

16. Preeclampsia………Cont’d
Risk factors for superimposed Preeclampsia
Strong family history of hypertension
Chronic renal disease
Diabetes mellitus
16

17. Preeclampsia……… cont’d
Management objective
• Control of Hypertension.
• Prevention of convulsions
• Expectant Treatment or Termination of pregnancy with
the least possible trauma to mother and fetus.
• NB- The “cure” for preeclampsia is delivery
17

18. Preeclampsia………Cont’d
Management – there are two management options
1, Aggressive management /delivery
 GA ≥37wks
 Severe preeclampsia or Eclampsia
 Worsening preeclampsia despite conservative management
 HELLP syndrome and
 Fetal compromise
18

19. Preeclampsia………Cont’d
Management –
Objectives of aggressive management
- to forestall convulsions and save a life of a mother
- to prevent maternal complication
- to deliver a healthy infant and prevent neonatal
complication
19

20. Preeclampsia………Cont’d
2, Conservative management
Indications
 Controlled hypertension
 No fetal compromise
 No HELLP syndrome
20

21. Expectant management
Admission
 Observe for symptoms such as headache, visual
disturbances, epi-gastric pain and rapid weight gain.
 Weight on admittance and every day thereafter.
 Analysis for proteinuria on admittance and at least every 2
days thereafter.
 BP recording every 4 hours and monitoring urine output
 Frequent evaluation of fetal size and amnionic fluid
volume either clinically or with sonography
 Necessary laboratory investigations the severity
21

22. Expectant management
Control of hypertension
 Parenteral drugs
-Hydralazine, Labetalol, Diaz oxide
 Oral drugs
-Nifedipine, α-methyl DOPA, Monohydralazine
22

23. 23

24. Prevention of convulsion
• Magnesium sulfate is highly effective to prevent
convulsions in women with preeclampsia and to stop
them in those with eclampsia.
• Seizure prophylaxis should be instituted in all pre
eclamptic women during labor and delivery using
magnesium sulphate
NB- Magnesium sulfate is not given to treat hypertension.
24

25. Prevention of convulsion
Administration
• Loading dose - 4gm MgSO4 as20% soln IV given over 5
minute(mix 8ml of 50% with 12 ml of DW or NS to make
20% soln)
• 10gm of 50% MgSo4 soln, 5gm in each buttock as deep
Im injection with 1ml 2% lidocaine in same syringe
• If convulsion recur, give 2gm MgSo4(20%) IV over
2.5minute
25

26. Prevention…….cont’d
Maintenance dose
• 5gm of 50% MgSo4 +1 ml of 2%lidocaine every 4hr into
alternatives buttock
• Continue the treatment with MgSo4 for 24 hr after
delivery or last convulsion.
NB:- Before repeating the administration of the drug ensure
that:-
• Respiratory rate >= 16b/m
• Urine out put >=30ml/hr
• Patellar reflex must be positive
26

27. Prevention…….cont’d
Side effects of Mgso4 are
 Facial flushing, feeling warm
 Irritation at the site of injection
 Nasal stuffiness
 GI- upset (diarrhea, nausea and vomiting)
 Urinary retention
 Tissue necrosis at injection site
27

28. Prevention…….cont’d
 Signs of Mgso4 toxicities
 Respiratory rate falls below 16 per minute
 Patellar reflexes are absent
 Urinary output falls below 30 mL per hour over
preceding 4 hours
 With the above signs with hold magnesium
 Anti dot : calcium gluconate 1 g IV
28

29. 4. Eclampsia
• The occurrence of generalized tonic-clonic convulsions
and/or coma that cannot be attributed to other causes in a
woman with pre eclampsia => Preeclampsia + convulsion
• Eclampsia is derived from the Greek word “eclampien”
meaning “lightening” indicating the sudden seizure in a
woman who was apparently healthy with no significant
symptoms of illness and was expecting a normal delivery.
• The incidence of eclampsia is 1–3/1000 pre-eclamptic
patients.
29

30. • It is one of the most serious and often fatal complications
of preeclampsia
• Seizures are generalized and may appear before (50%),
during(25%), or after(25%) labor
• Eclampsia is a result neglected preeclampsia
• Eclampsia is a preventable complication of preeclampsia
and has almost disappeared in countries with universal
antenatal, intra-partum and post partum care provision
• Risk of death is 1%
30

31. Diagnosis of Eclampsia
• Preeclampsia plus Generalized tonic-clonic seizures with four
phases:
• Aura (pre-ictal phase)- severe global headache, blurred vision,
scotomas, epigastric pain etc
• Tonic phase (stiffening)- arms and legs will go rigid, she can bite
her tongue, and the face and hand muscles that where twitching
will now be clenching.
• Clonic phase - (rhythmical jerking)- muscles will begin to jerk
violently, while frothy and slightly bloody saliva will appear
• Post ictal coma- a deep unconscious state. This can persist for
hours, or pass quickly. 31

32. Eclampsia……… Cont’d
Status epilepticus is a rare condition in which convulsions
continue to persistent.
 Thiopentone sodium 0.5 g dissolved in 20 mL of 5%
dextrose is given intravenously very slowly.
 The procedure should be supervised by an expert
anesthetist.
 If the procedure fails, use of complete anesthesia, muscle
relaxant and assisted ventilation may be employed.
 In unresponsive cases, cesarean section in ideal
surroundings may be a lifesaving attempt
32

33. 33

34. Management of Eclampsia
Management Description
General •Airway and oxygenation- put in left lateral position; suction airway,
insert airway to depress tongue and prevent injury, administer oxygen
via face mask or endotracheal tube if in respiratory failure
•Prevent trauma – tongue depressor ; fall accident etc
Control
convulsions
Administer anticonvulsants – Magnesium sulphate (first line drug);
diazepam ( if magnesium is not available); phenobarbitone
Control
severe HTN
If BP >160/110 mmHg, use fast acting antihypertensives (hydralazine;
labetalol; diazoxide; sodium nitroprusside) to maintain BP between
140/90-160/110.
Fluid Mx Restrict fluid administration to 125ml/hr and monitor input-output
including urine output
Organ
support
If any evidence of organ failure; requires critical care and organ support
to maintain homeostasis
Delivery After the above measures are taken and patient is stabilized; pregnancy
should be terminated by the most appropriate route. No conservative
Mx ! 34

35. 5. Chronic hypertension
Hypertension present before 20th week of gestation or
before pregnancy and persists after the 6th post partum
week
35

36. Antepartum hemorrhage
(APH)
36

37. ANTE PARTUM
HEMORRHAGE
APH is the occurrence of vaginal bleeding after 28th wks
of gestation and before delivery of the fetus.
During pregnancy and labor but before childbirth
It occurs in 2-4% of all pregnancies
Obstetrics hemorrhage (APH +PPH) is one of the five
leading cause of MMR
37

38. APH in early pregnancy
• Implantation bleeding/spotting - harmless light
bleeding, when the developing embryo plants itself in the
wall of uterus.
• Miscarriage - If a pregnancy ends before the 28th week
• Ectopic pregnancy - is when a fertilized egg implants
outside the womb
38

40. APH in late pregnancy
1. Placenta previa - is implantation of the placenta in the
lower uterine segment, with the placenta either overlying
or reaching the cervical os.
 A placenta that is implanted somewhere in the lower
uterine segment, either over or very near the internal
cervical os
Incidence:- 1 in 200 births
40

41. APH…….Cont’d
41

42. Classifications of PP
• Type I (Low-lying placenta previa)
The placental edge does not reach the internal os, but is in
close proximity to it (within 6cm)
• Type II (Marginal placenta previa)
The edge of placenta is at the margin of the internal os
• Type III (Partial placenta previa)
The internal os is partially covered by placenta
• Type IV(Total placenta previa)
The internal os is covered completely by placenta
11/4/2023 42

43. Types of placenta previa
43

44. Placenta previa…….Cont’d
• On repeated ultrasonography about 90% of low lying
placentas will resolve around term (placenta moves away
from the internal os).
• This is because as pregnancy progresses with greater
blood flow in the upper uterus, placental growth is more
likely directed toward the fundus, and this is known as
"placental migration"
44

45. Risk factors for PP
Increasing parity
Increasing maternal age
Cigarette smoking
Multiple gestations
Previous placenta previa
Prior curettage
Prior cesarean delivery
45

46. Clinical features of PP
 Painless hemorrhage - is the cardinal sign of PP
• The bleeding is bright red, sudden, painless and recurrent.
It may follow sexual intercourse or vaginal examination.
• The closer to term, the greater is the amount of bleeding
 The uterus usually is soft, relaxed, and non-tender.
 Asymptomatic (incidental finding in less than 10% of low-
lying placentas)
46

47. Clinical features of PP
 Floating head despite gestational age
 Signs of anemia may be presented
 Ultrasonography is needed to justify diagnosis.
47

48. Management of PP
• Admit all patients to hospital & NEVER do PVE
1, Conservative ( for pre-term and uncomplicated)
Bed rest, avoid PV exam and coitus
Investigations— like Hg estimation and blood grouping
Steroid therapy if pregnancy is less than 34 weeks.
Use of tocolysis can be done if vaginal bleeding is
associated with uterine contractions.
Rh immunoglobin should be given to all Rh negative
(unsensitized) women.
48

49. Management of PP
2, Termination of pregnancy/ delivery
Indications
Term pregnancy
Fetal death, distress or malformation incompatible with life
Bleeding continued after admission or labor starts.
Mode of termination
1, Vaginal delivery - type 1 and type 2 anterior
2, Cesarean delivery- type 2 posterior, type 3 and 4
49

50. APH…….Cont’d
2, Abruptio placenta/ accidental hemorrhage/ placental
abruption
• Premature separation of the normally implanted placenta
from uterus before fetus is delivered
• Incidence - 0.4 – 1.3% of all births OR 1/3rd of all APH
• Have two major types
• 1. revealed / external 2. concealed 3, mixed
50

51. APH…….Cont’d
1, Revealed- Following separation, blood flows downward
between membranes and decidua.
Ultimately, the blood comes out of the cervical canal to be
visible externally. This is the most common type.
2, Concealed- The blood collects behind the separated
placenta and collected in between the membranes and
decidua. The collected blood is prevented from coming out
of the cervix by the presenting part which presses on the
lower segment.
3, Mixed 51

52. Revealed VS Concealed Abruption
52
REVEALED
ABRUPTIO
CONCEALED
ABRUPTION

53. 53

54. Risk factors
 Prior abruption = 4-5%
 Advanced age and parity = 2.5%
 Preeclampsia and Chronic hypertension - 5 fold
 Trauma
 Polyhydramnios with rapid uterine decompression
 PPROM
 Multi-fetal pregnancy = twin B, 3 fold
 Cigarette smoking
 Folate deficiency 54

55. Clinical manifestation
Vaginal bleeding = dark red, painful (80%)
Uterine tenderness & back pain & abd. Pain (50%)
Uterine hyper tonus (focal or generalized)
Preterm labor
Fetal distress / NRFHRP
Coagulopathy
Diagnosis- clinical manifestation and Ultrasonography
55

56. Management
 Admission or Referring all patients to a hospital
• NEVER do PV- EXAM unless PP is ruled out
• Take Resuscitative measures
• Plan further management depending on GA & Severity
 Expectant management for mild abruption & pre-terms
• Secure IV-line, follow feto-maternal condition, steroid
therapy
 Termination of pregnancy – vaginally or by CS
 If any deterioration in mother or fetus despite the
gestational age (GA)
• If term, IUFD
56

57. Complications
 Maternal mortality(1%) and perinatal mortality (4.5 -60%)
 Couvelaire uterus – pathologic condition caused by severe
form of concealed abruptio placentae, resulting in massive
intravasation of blood into
the uterine musculature
 Hypovolemic shock, PPH,
 DIC, RH sensitization
 IUGR, Neonatal anemia
57

58. APH…….Cont’d
3, Vasa previa - When fetal blood vessels cross or run in
close proximity to the internal opening of the cervix
• Incidence -1 in 5000 singletons
• Causes – cord abnormality (velamentous insertion)
• Multiple gestation
• Low-lying placenta
• Previous cesarean delivery
• Uterine surgery
• Artificial fertilization 58

59. APH…………Cont’d
Diagnosis: Painless, dark vaginal bleeding
• Fetal bradycardia in connection with rupture of
membranes
• Identifying maternal blood from fetal respectively
59

60. APT TEST
 To determine whether bleeding is from the fetus or mother.
 4-6 drops of the antepartum hemorrhage blood is added to
10 ml of water then 2 ml of sodium hydroxide is added.
 After 2 minutes – if it remains red/ pink it is fetal blood,
and if it turns to yellow/dark it is maternal in origin.
Management:
 Emergency Caesarean section
60

61. APH…….Cont’d
4, Other causes
• Local lesions of the cervix and vagina such as vaginitis,
cervicitis, cervical cancer or polyps, foreign bodies,
ruptured uterus, leech infestation or placental
hemangiomas may cause vaginal bleeding in the
antepartum period.
• Bloody show- vaginal discharge that occurs at the end of
pregnancy. It's a sign that mucus plug has loosened or
already has been dislodged and labor is about to start.
61

62. APH…….Cont’d
5, Unknown causes
 These account for a significant proportion of cases of APH.
 Some of these are thought to be due to abruption placenta
that are so small to be diagnosed by clinical evaluation or
special investigations.
NB: The cause of any APH should be taken to be placenta
previa unless ruled out
62

63. APH…….Cont’d
 Start resuscitation immediately
 Admit all patients with APH to a hospital.
 No vaginal examination should be performed until a
placenta previa has been ruled out
 Specific management depending on cause.
 Women with APH are at increased risk for postpartum
hemorrhage (PPH). Thus universal active 3rd stage
management has to be implemented
63

64. QUIZ ???
64

65. Activity
Scenario for discussion
1, Mrs ‘X’ is a gravida 6, para 5, 30 wks pregnant women who
comes to your health center with a complaint of sudden bright
red bleeding which is painless. She doesn’t have any ANC
follow-up. What would be your management plan and your
possible diagnosis with possible risk factor.
2, Mrs X is a 38 weeks gravida women who came to your
hospital with a complaint of painful, dark red bleeding after
falling down. Her last medical record shows a normal pregnancy
with normally implanted placenta. What would be your possible
diagnosis and further management plan.
65

66. RH and ABO ISOIMMUNIZATION
66

67. RH (D) isoimmunization
Definition
Isoimmunization - process of becoming isoimmune
(developing the relevant antibodies) for the first time.
Isoimmunity - immune response to non-self antigen
 D - a cell protein or an antigen found on RBC.
 RH (rhesus)- mostly used name for antigen D
RH isoimmunization -hemolytic disease of the fetus and
newborn which happens when a D-ve mother who is
pregnant with a fetus with +ve fetus develops antibodies
against it. 67

68. RH (D) isoimmunization
Definition
Every individual either has or does not have the “Rh
factor” on the surface their red blood cells and this is
described as being RH +ve or RH -ve
68

69. RH (D) isoimmunization
Etiology
1. An RH (D) negative pregnant mother is exposed to RH-
positive fetal red blood cells secondary to feto-maternal
hemorrhage
2. An RH negative female receives an RH positive blood
transfusion.
69

70. 70

71. RH (D) isoimmunization
INCIDENCE
 Rate of sensitization before delivery is 1-2%
 If not given anti-D, about 16% of Rh-ve mothers will
develop Rh incompatibility by their 1st incompatible Px
 The risk of sensitization approaches 50% after several
incompatible pregnancies.
 D alloimmunization complicating pregnancy ranges from
0.5 to 0.9 percent
71

72. Pathogenesis

73. 73

74. Risk Factors
 Loss of pregnancy- Abortion, ectopic px, fetal death
 Procedures – Amniocentesis, Chorionic villus sampling,
fetal blood sampling, evacuation of molar pregnancy
 Others – delivery, abdominal trauma, external cephalic
version, placental abruption, unexplained vaginal
bleeding, manual removal of placenta.
74

75. Examination
 Rh blood type of the mother
 During ANC follow-up if the pregnant women is found to
be D-ve, her partner should be checked for presence of
antigen D.
 If her partner is D+ve and she had no risk factors provide
anti-D immune globulin
 Anti-D - is an immune globulin derived from human
plasma
75

76. Examination
If the women had risk factors of sensitization like
 History of prior blood transfusion
 Previous pregnancies, including spontaneous and elective
abortions
 Presence of vaginal bleeding, injury and/or amniotic
discharge then maternal antibody titer should be done
to test whether the mothers is sensitized or not.
76

77. Complications of D-isoimmunization
 Hemolytic anemia due RBC destruction and release of
free Hg into circulation
 Hydrops fetalis - massive RBC destruction and death
 Jaundice – free Hg is converted into billirubin resulting in
yellowish discoloration of the new born
 Fetal neurological impairment, respiratory distress and
circulatory collapse after born.
77

78. Prevention
Timing of anti-D Ig
 At 28 weeks’ gestation - to reduce the third-trimester
isoimmunization rate
 After delivery - anti-D immune globulin should be given
within 72hrs only after the newborn is confirmed to be D
positive
Dosage
 300 μg
78

79. ABO incompatibility
• ABO incompatibility occurs when the mother has group O
blood (with anti-A and anti-B antibodies in her serum) and
fetus is group A, B or AB.
• The mother's immune system react and make antibodies
against her baby's red blood cells.
• 20% pregnancies are ABO incompatible but only 5%
clinically affected
• ABO incompatibility is one of the diseases which can cause
jaundice.
79

80. ABO incompatibility
Clinical manifestations
 The infant becomes jaundiced within the first 24 hours
with a variable amount of anemia and hyperbilirubinemia
Diagnosis
 Maternal and fetal blood type
 Variable amount of anemia
 Hyperbilirubinemia which is usually mild
Management - provision of phototherapy to the newborn.
80

81. Common Medical problems
during pregnancy
81

82. Contents
Anemia
Cardiac disease
Diabetes mellitus
Malaria
82

83. Anemia in pregnancy
Definition
Anemia in pregnancy is defined as hemoglobin (Hg) level of
11 g/dL in the first and third trimesters and 10.5 g/dL in
the second trimester
 Commonest medical disorder of pregnancy.
 Incidence is higher in developing countries.
 Increased Maternal morbidity & mortality
83

84. Anemia in pregnancy
Depending on severity anemia can be classified as
Mild anemia -------- 9 -10.9 gm /dl
Moderate anemia---- 7-8.9 gm /dl
Severe anemia-------- < 7gm /dl
Very severe anemia--- <4gm/dl
84

85. Anemia in pregnancy
 Etiology - The two most common causes of anemia during
pregnancy and are iron deficiency anemia (80-95%) and
anemia secondary to acute blood loss
 In a singleton gestation, the maternal need for iron
averages nearly 1000mg
 In multi-fetal gestational requirements are considerably
higher
85

86. IRON DEFICIENCY ANAEMIA
ETIOLOGY
 Dietary habits: Consumption of low-bio availability diet
 Defective iron absorption due to intestinal infections, hook
worm infestation, amoebiasis, giardiasis, chronic malaria
 Increased iron loss: Frequent pregnancies, menorrhagia.
 Repeated and closely spaced pregnancies, and prolonged
period of lactation.
 Multiple pregnancies
86

87. IRON DEFICIENCY ANAEMIA
CLINICAL MANIFESTATION
• Fatigue
• Dizziness / light headedness
• Breathlessness
• Chest pain
• Cold hands and feet
87

88. MANAGEMENT
 Objectives:
1- To treat the underlying cause
2- To achieve a normal Hg
3- To replenish iron stores
 Two ways to correct anemia:
I- Iron supplementation . Oral Fe
. Parenteral Fe
II- Blood transfusion
 Choice of method:
It depends on three main factors:
 Severity of the anemia
 Gestational Age.
 Presence of additional risk factor
88

89. MANAGEMENT
Treatment
For mild and moderate
 200mg elemental iron daily till Hg level becomes normal
 Continue therapy for about 3 months after corrected
For severe
 Transfuse slowly with packed red cell blood and continue
with oral supplemantion.
89

90. MANAGEMENT
Prevention
1. Family spacing
2. Dietary precautions - Iron salts
3. Treatment of underlying infections and infestations
4. Iron supplement- daily 60mg Fe +Folic Acid 250μg.
• Preferable time to start supplementing is at 20 wks(to
decrease nausea and vomiting) and continue for 3 months
NB- Vitamin C may enhance absorption of Iron
– Do not take iron with milk or antacid or Calcium
90

91. CARDIAC DISEASE IN
PREGNANCY
• Major cause of non-obstetric maternal morbidity in US
• Cardiac diseases complicate 1-4% of pregnancies in
women without pre-existing cardiac abnormalities.
• The marked pregnancy-induced hemodynamic alterations
can have a profound effect on underlying heart disease.
91

92. CARDIAC DISEASE……….Cont’d
• During normal pregnancy blood volume increases by
40% to 50% and Cardiac output rises by 30% to 50%
above baseline
• The physiological adaptations of normal pregnancy can
induce symptoms and alter clinical findings that may
confound the diagnosis of heart disease.
92

93. CARDIAC DISEASE……….Cont’d
Critical times for cardiac disease in pregnancy
 Max changes around –30 weeks
 Intra partum period
 Just after delivery
 Second week of puerperium
93

94. Indicators of Heart Disease during Px
Symptoms
 Dyspnea / orthopnea
 Nocturnal cough
 Hemoptysis
 Syncope
 Chest pain
Clinical findings
 Cyanosis
 Clubbing of finger
 Persistent neck vein distention
 Systolic and diastolic murmur
 Cardiomegaly
 Persistent arrhythmia
 Criteria for pulmonary
hypertension
94

95. Risk factors for cardiac disease in Px
 Anemia
 Infections
 Hypertension
 Weight gain
 Multiple pregnancy
 Caffeine, alcohol intake
 Drugs – tocolytic
95

96. CARDIAC DISEASE……….Cont’d
Diagnosis
• Electrocardiography
• Chest Radiography
• Echocardiography
96

97. NYHA (New York Heart Association)
Functional grading of heart disease
• Grade I: No limitation of physical activity-
- asymptomatic with normal activity
• Grade II: Mild limitation of physical activity
-Symptoms with normal physical activity
• Grade III: Marked limitation of physical activity
-Symptoms with less than normal activity, comfortable at rest
• Grade IV: Severe limitation of physical activity
-symptoms at rest

98. CARDIAC DISEASE……….Cont’d
Management objective
 Women in NYHA class I and most in class II proceed
through pregnancy without morbidity. Special attention
should be directed toward both prevention and early
recognition of heart failure
 Fortunately, NYHA class III and IV are uncommon today, if
presented close follow-up and admission should be
considered.
 Termination of pregnancy should be considered if
complications develop
98

99. CARDIAC DISEASE……….Cont’d
During ANC
• Clear counseling of risk and prognosis
• ANC every 2 weeks up to 30 weeks then weekly
• On each visit note - pulse rate, BP, cough dyspnea,
weight, anemia, auscultate lung bases, re-evaluate
functional grade
• Fetal monitoring
99

100. CARDIAC DISEASE……….Cont’d
• If symptoms of pulmonary congestion develop:
Activity is further reduced
Dietary sodium is restriction
Diuretic therapy
• Additional advice
 Rest, Avoid undue excitement/strain
 Hygiene, dental care to prevent any infection
 Diet/ Iron and vitamins
 Avoid smoking and drugs 100

101. CARDIAC DISEASE……….Cont’d
• Management during labor and delivery
During labor, mother with significant heart disease
should be in semi-recumbent position with lateral tilt.
Vital signs are taken frequently between contractions.
Relief from pain and apprehension is important
When induction is indicated - Oxytocin is preferred
with higher concentration and restricted fluid
Diuretics in pulmonary congestion
101

102. CARDIAC DISEASE……….Cont’d
• Management during labor and delivery
Avoid forceful bearing down
Cut short second stage of labor - apply episiotomy,
vacuum or forceps when indicated
AMTSL - use oxytocin and avoid bolus Ergometrine
After delivery - Propped up/sitting position
Watch for signs of pulmonary edema
Sedation and use of antibiotics
102

103. CARDIAC DISEASE……….Cont’d
Management during Puerperium - high risk time
• Women who have shown little or no evidence of cardiac
distress during Px & labor may still decompensate
postpartum.
Auto transfusion from the contracting uterus to
maternal ciculation
• Cardiological consultation for definitive management of
heart disease
103

104. CARDIAC DISEASE……….Cont’d
Advice at discharge – on contraception
 Progesterone – good option, Norplant
 IUCD - Less preferred
 COC (Combined oral contraceptive)– b/c estrogen increases
risk for venous thrombus they are contraindicated
 Sterilization – tubal ligation/ vasectomy is best option
Prevention – Pre-conceptional counseling helps women with
severe heart disease before deciding to become pregnant
104

105. DIABETUS IN PREGNANCY
Definition
• Diabetes mellitus is a chronic metabolic disorder
characterized by either absolute or relative insulin deficiency,
resulting in increased glucose concentrations.
• About 1–14% of all pregnancies are complicated by
diabetes mellitus .
• 90% of them are gestational diabetes mellitus (GDM).
105

106. DIABETUS IN PREGNANCY
Classification of DM in Pregnancy
1.Gestational Diabetes(GDM) – is defined as carbohydrate
intolerance of variable severity with onset or first recognition
during the present pregnancy two types: Type A1 & A2
Nearly 50% of women with GDM would develop overt diabetes
over a follow-up period of 5–20 years.
2. Pre-gestational Diabetes / Overt DM
106
CLASS ONSET FBS 2-HR PP GY THERAPY
A1 Gestational <105 mg/dl <120 mg/dl Diet
A2 Gestational >105 mg/dl >120 mg/dl Insulin

107. Metabolic changes in pregnancy
• Late 2nd and 3rd trimester are characterized by increased
insulin resistance because of
1. “Diabeto-genic” hormones secreted by placenta
• Growth hormone
• Human placental lactogen
• Progesterone
• Corticotropin releasing hormone
2. Insulin inactivation by placental insulinase
107

108. DIABETUS……. Cont’d
Risk factors
Age >35 yrs
Obesity (BMI>30kg/m2 )
 Previous history of GDM
Persistent glucos-uria
Strong family history of DM (1st degree relative)
Previous baby with > 4kg birth weight
108

109. Effect of DM in Px
 Abortion
 Preterm labor due to infection or polyhydramnios
 Preeclampsia
 Macrosomic baby ˃ 4000g
 Prolongation of labor due to big baby.
 Shoulder dystocia
 Perineal injuries.
 Postpartum hemorrhage.
 Operative interference.
109

110. Management of DM in Px
 Maintenance of mean plasma glucose level between 105
mg/dL and 110 mg/dL for good fetal outcome
 The control of high blood glucose is done by restriction
of diet, exercise with or without insulin.
 Human insulin should be started if fasting plasma glucose
level exceeds 90 mg/dL or 2hrs postprandial plasma
glucose level of more than 140 mg
 Exercise (aerobic, brisk walking) programs are safe in
pregnancy and may obviate the need of insulin therapy.
110

111. Management of DM in Px
 Oral hypoglycemic drugs are effective and safe.
 Commonly used drugs are glibenclamide and metformin
 The drugs do cross the placenta but no teratogenic effect
has been observed yet.
 Women with good glycemic control and who do not
require insulin may wait for spontaneous onset of labor.
 Elective delivery (induction or cesarean section) is
considered in patients requiring insulin or with
complications at 38 wks
111

112. Management of DM in Px
 Cesarean delivery accounts for 50% of diabetic deliveries,
indications are fetal macrosomia, complicated diabetes,
fetal compromise, elderly primi-gravida and multi-gravida
with a bad obstetric history
 After delivery antibiotics should be given prophylactically
 Encourage breastfeeding
 Insulin requirement falls dramatically following delivery,
therefore revert to the insulin regime as was prior to
pregnancy.
112

113. Management of DM in Px
• A neonatologist should be present at the time of delivery
and the baby should be kept in NICU
• Assess for congenital malformation and respiratory distress
• Check fetal blood glucose within 2 hours of birth to avoid
problems of hypoglycemia (blood glucose < 35 mg/dL).
• Initiate early breast feeding and educate the mother about
appropriate breast feeding to prevent hypoglycemia
113

114. Malaria and Pregnancy
 Pregnant women have increased susceptibility to malarial
infections
 Antibodies to the parasite surface antigen mediate placental
accumulation of infected erythrocytes (placental malaria)
and lead to the harmful effects of malaria
 Some immunity is accrued with parity and is called
pregnancy-specific antimalarial immunity.
114

115. Malaria ………Cont’d
Clinical findings
 Fever, chills, headaches, myalgia, and malaise
 Pregnant women are although often asymptomatic
 Anemia and jaundice may be presented
 Falciparum infections may cause kidney failure, coma, and
death
 NB- Malarial infections during Px whether symptomatic or
asymptomatic are associated with higher rates of perinatal
morbidity and mortality
115

116. Malaria ………Cont’d
Diagnosis of malaria
 The diagnosis is confirmed by the detection of malarial
parasites in peripheral thick blood smear.
Pathophysiology
 The infected erythrocytes become rigid, irregular and sticky
 The infected red cells are broken down (hemolysis).
 Congenital malaria (< 5%) only when placenta is damaged.
116

117. Malaria ………Cont’d
Adverse outcomes -
 Stillbirth
 Preterm birth
 Low birth-weight
 Maternal anemia
 Early infection of P. falciparum raises the risk for abortion
 In <5% congenital malaria is reported, the risk increases if
infection happens in 1st trimester
117

118. Malaria ………Cont’d
Management
 For uncomplicated - artemisinin-based regimen is
preferable. If not artemetherlumefantrine can be used
 For malaria caused by P vivax, malariae and ovale-
chloroquine or hydroxychloroquine
 Primaquine is contraindicated in Px
 For uncomplicated Artesunate or Quinine IV followed by
oral therapy can be used
118

119. Malaria ………Cont’d
Management
 Patients with severe anemia may need blood transfusion.
 Folic acid 10 mg should be given daily to prevent
megaloblastic anemia.
Prevention
Prevention from mosquito bites is done using permethrin and
pyrethroids-spray kill mosquitoes inaddition to bed nets
Electrically heated mats will kill mosquitoes in the room.
Prophylaxis - Chloroquine
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