Complications in pregnancy

1. Complication in
Pregnancy
Dr. Priyanka Sonam
Medical Officer, DPSRU

2. Introduction
Hypertensive disorders in pregnancy and their managment
Gestational DM and its management
Cardiac disease in pregnancy and treatment approaches
References

3. Hypertensive disorders in pregnancy form one of the deadly
triad, along with hemorrhage and infection, that contribute
greatly to maternal & perinatal morbidity and mortality.
Hypertensive disorders represent the most common medical
complications of pregnancy,
incidence of 5 -10%.
Black women are 3x as likely to die from preeclampsia than
white women.

4. Hypertensive disorders are among the most
significant & still now unresolving problem
complicating almost one in ten pregnancies
Responsible for 16%of Maternal Mortality in
developing countries

5. Definition
Systolic B.P. >=140 mmHg
and/or
Diastolic B.P. > = 90 mmHg
◦ Documented on two occasions at least 6 hours apart

6. Normal blood pressure in
pregnancy
Decreases in the first trimester
Reaching its lowest point at 20 weeks
Return to pre- pregnancy level during the
third trimester

8. There are five types of hypertensive diseases:
◦ Gestational hypertension (pregnancy-induced
hypertension or transient hypertension).
◦ Preeclampsia.
◦ Eclampsia.
◦ Preeclampsia superimposed on chronic
hypertension.
◦ Chronic hypertension.

9. 1. Gestational hypertension
o
o
o
BP>140/90 mmHg after 20wks during pregnancy or after
delivery and resolves by 12wks post-partum.
No proteinuria
Final diagnosis made only postpartum

10. New onset of hypertension after 20
weeks of gestation along with
properly documented proteinuria,
followed by return of B.P. to normal
within 12 weeks post-partum.
Preeclamsia
Gestational
Hypertension Proteinuria

11. Generalized tonic-clonic seizure in a
patient with Preeclampsia not
attributed to any other cause.
Eclampsia Preeclampsia
Seizure/
Convulsion/
Coma

12. Hypertension before pregnancy /
Diagnosed before 20 weeks of
pregnancy not due to gestational
trophoblastic disease.
Hypertension diagnosed after 20 weeks
but persistent after 12 weeks
postpartum

13. New onset proteinuria in hypertensive
women but no proteinuria before 20
weeks' gestation

14. Pregnancy-specific syndrome of reduced organ
perfusion secondary to vasospasm and endothelial
activation.
Proteinuria
 exceeding 300mg per 24hrs, or
 exceeding 30mg/dl or 1+ on dipstick in random urine
samples
 urine protein : creatinine ratio >0.2
all these are an important sign of preeclampsia.

15. Age < 20 years or > 35 years
Nulliparity
obesity
Multiple gestation
Hydatidiform mole
Diabetes mellitus
Chronic hypertension
Renal disease
Family/personal history of preeclampsia

16. Is a ds of theories with pathophysiology not well
understood,
Abnormal trophoblastic invasion of uterine vessels.
Immunological intolerance b/n maternal and
fetoplacental tissues.
Maternal maladaptation to cardiovascular/
inflammatory changes of normal pregnancy.
Dietary deficiencies
Genetic influences

17. Abnormal Trophoblastic Invasion
In normal implantation, the spiral arteries undergo
extensive invasion by endovascular trophoblasts.
In preeclampsia, however, there is incomplete
trophoblastic invasion - decidual vessels, but not
myometrial vessels.
This may result in placental ischemia & in turn to
the production of placental factors that enter the
maternal circulation resulting in endothelial cell
dysfunction & the clinical syndrome of
preeclampsia.

19. i) Renal blood flow and glomerular filtration rate
(GFR) in patients with preeclampsia are
significantly lower from constriction of the afferent
arteriolar system.
 The vasoconstriction eventually lead to damage to
the glomerular membranes, increasing their
permeability to proteins and leading to
proteinuria.

20. ii) Cerebral blood flow and oxygen
consumption are significantly less than in
normal pregnant subjects.
iii)Uteroplacental circulation - there is
decreased blood flow in preeclamptic
patients.
iV) Cardiovascular system
◦ Increased total peripheral vascular resistance.

21. For the purposes of management, preeclampsia
may be classified as no sever or severe.
1. Nonsever Preeclampsia
B/P >140/90mmHg but < 160/110mmHg on
two occasions at least 6hrs apart while the
patient is on bed rest
Proteinuria 3g/24h but < 5 g/24h
Asymptomatic

22. 2.Severe Preeclampsia
B/P >160mmHg systolic or 110mmHg diastolic on
two occasions at least 6hrs apart while the patient is
on bed rest
Proteinuria of 5g or higher in 24hr urine specimen or
3+ or greater on two random urine samples collected
at least 4 hours apart
Impaired renal function test
Evidence of HEELP syndrome

23. Oliguria < 500mL in 24hrs
Cerebral or visual disturbances
Pulmonary edema or cyanosis
Epigastric or right upper quadrant pain
Impaired liver function (elevated liver enzymes)
Thrombocytopenia
Fetal growth restriction, oligohydraminos

24. Visual disturbances: these disturbances are
presumed to be due to cerebral vasospasm.
Headache is of new onset and may be
described as frontal, throbbing, or similar to a
migraine headache.
Epigastric pain is due to hepatic swelling and
inflammation, with stretch of the liver capsule.
Pain may be of sudden onset, it may be
constant, and it may be moderate-to-severe in
intensity.

25. While mild lower extremity edema is
common in normal pregnancy, rapidly
increasing or nondependent edema may be a
signal of developing preeclampsia. However,
this signal theory remains controversial and
recently has been removed from most
criteria for the diagnosis of preeclampsia.

26. Blood Pressure
Proteinurea
Retinal vasospasm or Retinal edema
Right upper quadrant (RUQ) abdominal
tenderness stems from liver swelling and
capsular stretch

27. ◦ Brisk, or hyperactive, reflexes are common during
pregnancy, but clonus is a sign of neuromuscular
irritability that raises concern.

28.  Complete blood count
 Urine analysis
 Renal function tests
 Liver function tests
 Ultra sound ( fetal growth and BPP)
 Coagulation profile (if thrombocytopenia or elevated
liver enzymes)

29. IMMEDIATE REMOTe
MATERNAL
FETAL
● IUGR
● IUD
● Asphyxia
●Prematurity
During Pregnancy
During
Labour During
puerperium
●Eclampsia(2%) (more in acute cases)
●Accidental hemorrhage
●Oliguria
●Diminished vision
●HELLPSyndrome
●Cerebral hemorrhage
●ARDS
● Eclampsia
●Postpartum
hemorrhage
●Eclampsia(
in < 48hrs
of delivery)
●Shock
●Sepsis
●Recurrent pre-
eclampsia
●Chronic Renal Disease
• Abruptio placentae

30. HELLP Syndrome
Hemolysis, Elevated Liver enzyme and Low
platelet.
Criteria for dx HELLP syndrome
Hemolysis
◦ Abn peripheral. Blood smear
◦ Bilirubin > 1.2 mg /dl
◦LDH > 600IU/L
Elevated Liver enzymes
◦ AST or ALT > 72 Iu/L
◦ LDH > 600 Iu/L
Thrombocytopenia
P. Count < 100,000/mm3

31. HEMOLYSI
S
(due to
passage of
RBCs
through
partially
obstructed
vessel)
HEPATIC
DYSFUNCTIO
N (due to
intravascular
fibrin
deposition &
sinosoidal
obst.)
Decreased
Liver blood
flow
HELLP
s)
S
y
ndro
m
e
THROMBO-
CYTOPENIA
(due to
platelet
aggregation
& diposition
in the sites
of
endothhelia
l damage)

32.  Non sever Preeclampsia
Women with non sever preeclampsia at term
should be hospitalized for further evaluation
 At GA of 40wks all need to deliver
At gestational ages of >37wks, cervical status is
assessed and,
 If favorable, induction is initiated
 If unfavorable, preinduction cervical ripening agents are
used
 Need seizure prophylaxis in labor

33. Non sever preeclampsia <37 weeks
 OPD mgt is reasonable in carefully selected, reliable,
asymptomatic patients with minimal proteinuria and normal
lab. Results.
Follow up during opd mgt includes:
 ANC follow up twice weekly
 Urine protein on every visit
 BP measurement
 Weight measurement
 Fetal movement count daily
 CBC and liver enzymes during each ANCvisit
 NST and serial fetal growth and amniotic fluid evaluation

34. The patient should report the following :
Decreased urine output
Sudden increase in weight and generalized
edema
Persistent headache
Blurring of vision
Right upper quadrant or epigastric pain
Decreased fetal movement
Vaginal bleeding
Convulsion or loss of consciousness

35.  Severe preeclampsia
Always mandates hospitalization.
Delivery is indicated if:
 The gestational age is 34 wks or greater,
 Fetal pulmonary maturity is confirmed, or
 Severe IUGR (< 5th percentile)
 Suspected abruptio placentae
 Nonreassuring fetal testing

36. Expectant management is contraindicated in the
presence of:
Fetal compromise / IUFD
Uncontrollable HTN (considered after the use of
two anti hypertensive drugs with maximum dose)
Eclampsia
DIC
HELLP syndrome
Cerebral edema
Pulmonary edema, or
Evidence of cerebral or hepatic hemorrhage.

37.  Management of patients with severe preeclampsia b/n 28 -
34wks‘:
 when the maternal condition is stable and fetal condition is
reassuring - prolong pregnancy until dev`t of maternal or fetal
indications for delivery or until achievement of fetal lung maturity
or 34wks' gestation.
 Antenatal corticosteroids are recommended-dexamethasone 6mg
IM bid or bethamethasone 12mg bid for 48hrs.
 If gestational age is less than 28wks immediate delivery is
indicated.

38. Principles of mgt of sever preeclampsia
1. Blood pressure control
2. Prevent convulsions
3. Delivery as a definitive mgt

39. i) Acute blood pressure control achieved with
Hydralazine: 5–10mg IV, the dose can be
repeated in 20–30 min if necessary
(maximum of 60 mg IV).
Labetalol 5–10mg by slow IV push - dose can
be repeated in 10–20min.
Nifedipine 5–10mg orally - dose can be
repeated in 20–30min, as needed.

40. ii) Maintenance antihypertensive
Methyl dopa up to 4gm/day PO in divided
doses
Nifedipine 10-20mg PO every 6 hour
 The aim of antihypertensive therapy is to keep
systolic pressure b/n 140 and 150mmHg and
diastolic pressure b/n 90 and 100mm Hg.

41. Seizure prophylaxis
◦ Magnesium sulfate is superior to other antiepileptic
medications for preventing eclampsia-related
seizures and seizure-related morbidity and
mortality.
◦ Continuous Intravenous Infusion
An IV loading dose of 4-6 g is usually followed by a
maintenance infusion of 2g/hr.
Patients must be monitored for signs of
magnesium toxicity.

42. Intermittent Intramuscular Injections
10 g of 50% magnesium sulfate solution,
one-half (5g) injected deeply in the upper
buttocks.
Every 4hr thereafter give 5g of a 50% solution
of magnesium sulfate injected deeply in the
buttocks, but only after ensuring that:
i. the patellar reflex is present
ii. respirations are not depressed
iii. urine output the previous 4hr exceeded 100
ml

43. Magnesium sulfate is discontinued 24hr after
delivery.
Magnesium toxicity may be confirmed by
testing serum levels- It can be reversed with
1 g of calcium gluconate.
In instances in which magnesium sulfate
cannot be used (e.g., myasthenia gravis, end-
stage renal disease [because of impaired
magnesium clearance]), phenytoin/diazepam
is safe.

44. Postpartum Management
Close monitoring of BP, symptoms consistent
with severe disease.
Magnesium sulfate should be continued for at
least 24 hours.
Antihypertensive drug treatment continued if
the SBPis at least 160mmHg or if DBPis at
least 110mmHg
Antihypertensive medications are
discontinued if the BPremains below the
hypertensive levels for at least 48 hours.

45. The onset of convulsions or coma during
pregnancy or postpartum in a woman with
preeclampsia should be diagnosed as eclamptic
until otherwise proven.
Usually within the first 24 to 48 hours'
postpartum.
 25% develop the seizures before labor,
50% during labor, and
25% after delivery.

46. MATERNAL FETAL
●Asphyxia
●Prematurity
●Hypoxia & IUD
Injuries Systemic
●Tongue bite
●Injuries due
to fall
●Bed sore
●CARDIAC: acute left
ventricular failure
●RENAL:renalfailure
●HEPATIC: necrosis,
subcapsular hematoma
●CNS:cerebral
hemorrhage, edema
Hematology
●Low platelet
count
●Disseminated
Intravascular
Coagulation
Postpartum
●Shock
●Sepsis
●Psychosis

47. 1. Prevent maternal injury & resuscitation
Assess and establish ABC of life,
Prevent aspiration and ensure maternal
oxygenation by lying in the lateral decubitus
position,
Vomitus and oral secretions are suctioned.
Maintain adequate oxygenation during the
convulsive episode-supplemental oxygen
administration through a face mask.

48. 2. Prevention of Recurrent Convulsions
 Magnesium sulfate is the drug of choice to
treat and prevent subsequent convulsions
3. Control of Severe Hypertension
 Reduce the BPto a safe range
-maintaining SBPb/n 140 and 160mmHg and
DBPb/n 90 and 110 mmHg is a reasonable
goal.
4. Delivery
 Vaginal delivery & Cesarean delivery for
obstetric indication

49. 5. Postpartum Management
After delivery, patients with eclampsia should
receive close monitoring of vital signs, fluid
intake and output, and symptoms for at least
48 hours.
Parenteral magnesium sulfate should be
continued for at least 24hrs after delivery or
for at least 24hrs after the last convulsion.
Dangerous time

50. Withhold MgSO4 if:
RRfalls below 16/min
Patellar reflexes are absent
Urinary out put falls below 30ml/hr over the
preceding 4 hrs
50

51. Stop MgSO4
Iv 1g 10% of calcium gluconate
Administer oxygen
secure airway
Ventilation

52. Poor prognosis if one or more of the
following is present (Eden’s criteria):
1. Coma of 6 or more hours.
2. Temperature 39 degrees or more.
3. Pulse over 120/min.
4. Systolic blood pressure over 200 mmHg.
5. Respiratory rate over 40/min.
6. More than 10 convulsions.

54. most common medical complication of
pregnancy.
complicates 2-3% of pregnancies and 90% of
the cases represent women with GDM.

55. 1.Pre gestational : diagnosed before pregnancy.
 Accounts for 20% of DM in pregnancy
Could be:
type 1 or
type 2

56. 2. Gestational Diabetes Mellitus (GDM)
Diabetes diagnosed during pregnancy
80% of DM in pregnancy
During pregnancy, classification of women
with diabetes has often relied on the
WHITE’S classification.

57. Class A1- Diet controlled GDM
Class A2- GDM requiring insulin
Class B- Onset >20y, duration<10y
Class C- Onset 10-19y, duration 10-19y
Class D- Onset <10y, duration >20y or
Background retinopathy
Class F- Renal disease
Class H- Heart disease
Class R- Proliferative retinopathy
Class T - Renal transplantation

58. Pregnancy is characterized by insulin
resistance and hyper insulinemia.
The resistance stems from placental secretion
of diabetogenic hormones.
◦ HPL- most responsible
◦ Growth hormone
◦ Corticotropin-releasing hormone
◦ Progesterone
◦ Estrogen

59. Glucose is transported to the fetus via carrier
mediated active transport
Free fatty acids, triglycerides and ketones
increase resulting in accelerated starvation
Glucose is spared for fetal consumption.
Decreased fasting glucose level in early
pregnancy.
Fetal glucose level is 80% of maternal value.
Fetal amino acids are higher than maternal level.

60. GDM
Exagerated physiological response
Can be seen as unmasking marginal
glucose controlling potential by
pregnancy:
Leading to full blown glucose intolerance
during pregnancyOnly in some pregnant
women
Is associated with increased maternal &
fetal/neonatal morbidity
Can be early detected
Carries risk of future type 2 DM

61. Pre gestational
FBG > 126 mg/dL
2hr of a 75g OGTT > 200 mg/dL or
Classic signs and symptoms + RBS >200 mg/dl.
This must be confirmed on a subsequent day.

62.  Gestational diabetes
any degree of glucose intolerance of with
onset or first recognition during pregnancy
Fasting hyperglycemia early in pregnancy
almost invariably represents overt diabetes.

63. SCREENING
 Screening starts:as early as possible
:repeated at 24-28 wks
 selective screening Vs universal
screening
 Only half of patients with abnormal GTT
have risk factors
NB: Risk based screening detects only 50%

64.  Low Risk
Blood glucose testing not routinely required
if all of the following characteristics are
present:
◦ Member of an ethnic group with a low prevalence of
gestational diabetes
◦ No known diabetes in first-degree relatives
◦ Age less than 25 years
◦ Weight normal before pregnancy
◦ Weight normal at birth
◦ No history of abnormal glucose metabolism
◦ No history of poor obstetrical outcome
Selective screening

65.  Average risk
Perform blood glucose testing at 24-28 wks
using either
Two step procedure: 50g oral GCT followed
by 100g OGTT
One step procedure: 100g OGTT
 women of Hispanic
 African
 Native American
 South or East Asian origins

66.  High risk
Perform blood glucose testing as soon as
feasible if one or more of these are present
◦ Severe obesity
◦ Strong family history of type 2 DM
◦ Previous history of GDM
If GDM is not diagnosed repeat at 24-28wks
of gestation or at any time a patient has symptoms
or signs suggestive of hyperglycemia

67. 50gm oral glucose tolerance test
50gm oral glucose is given
After an hour without regard to the time of
the day or time of last meal determine blood
sugar
If RBG>140mg/dl - indicate a need for
diagnostic test
NB: some consider 130mg/dl as the threshold

68. Three hour OGTT test
 100 gm after 8-14 hours fasting
 This will identify 80% of women with GDM
Time Plasma
mg/dl
Fasting
1hour
2hour
95
180
155
3hour 140
Patient should remain seated and shouldn’t smoke
Dx when two values are abnormal
If only one value is met, the test be repeated in a month’s time.

69.  Insulin requirement : b/c of pregnancy
diabetogenic effect .
 Glucose control difficult: b/c of nausea &
vomiting in 1st TM.
 Risk of DKA & Hypoglycemia
 Progressive retinopathy
 Worsening nephropathy
If on Oral Agents: shift to insulin b/c
Teratogen?
Chronic cxn. Not worsened. But -Retinopathy

70. Insulin resistance
◦ HPL (Human Placental lactogen )
◦  production of cortisol, estriol & progesteron
◦  destruction of insulin by kidney & placenta
In normal pregnancy 44% decline in insulin
sensitivity compared to 56% in pregnancy
complicated by GDM

71. Maternal
◦ preeclampsia
◦  infections -UTI
-Chorioamnionitis
-Endomyometritis
-moniliasis
-PPH
-Polyhydraminos
- C/S rates

72. Fetal
1. In perinatal death
◦ Sudden unexplained stillborn occur in 10 -30% in
the pregnancies complicated by GDM
◦ Common after 36 weeks in patients with vascular
disease, poor glycemic control, hydraminos,
macrosomia or preeclampsia
◦ Cause - chronic intrauterine hypoxia

73. 2. Macrosomia
Birth weight in excess of 4000gm or above 90th
percentile
3. Congenital malformations
30-50% of PDA
2-6 fold increase in major malformations
Insult must act before 7th week
Sacral agenesis occur with 200-400 times
more often than other women

74. CVS-Transposition of great vessel, VSD,
ASD,Sinus invertus
CNS –Anencephly, meningomeyelocele,
microcephaly ,encephlocele
Skeletal – Caudal regression syndrome ,
spinabifida
GIT –Trcheoesophagial fistula
GUS–Absent kidney, Polycystickidney

75. 4.Hypoglycemia- BGL<35-40/dl during the
first 24 hours of life, common in macrosomic
infants up to 50%
5.Respiratory distress syndrome - Mechanism
unknown
6. Hypocalcaemia & hypomagnesium
7. Hyperbilirubinemia & polycythemia

76. Target
To keep the maternal fasting capillary
glucose level <95mg/dl
Can be achieved by non-medical means if it
fails by medical means

77. Diet -Caloric requirements during pregnancy
are increased by about 300 kcal above basal
daily needs in non-pregnant women.
◦ Daily caloric intake of 30kcal/Kg with 3 meals 3 snacks
◦ 10% breakfast, 30%lunch, 30%dinner & 30%snacks
◦ 40-50% CHO, 30% fat & 20-30% protein

78. Exercise
Glucose monitoring
Self testing recorded in a glucose diary,
along with dietary information
One hour postprandial monitoring is better
◦ Optimal values are FBS 70-95 mg/dl & 2hr post prandial <120
mg/dl
◦ Glycosylated hemoglobin (HbA1c) every 4 weeks to assess
control

79. Initiated when the above fails
Insulin – widely used
Oral hypoglycemic agents – rarely used

80. Insulin
◦ If FBG is > 105 mg/dl or 2hr BG is > 120 mg/dl
◦ Starting dose
0.6u/Kg, 0.7u/Kg & 0.8u/Kg in the 1st , 2nd & 3rd trimester
◦ 2/3 in the morning & 1/3 in the evening
◦ For the morning
2/3 intermediate acting & 1/3 short acting
◦ For the evening
1/2 intermediate acting & 1/2 short acting
◦ Oral hypoglycemic agent is not recommended
As it causes fetal & neonatal hypoglycemia

81. First trimester
Date the pregnancy (LNMP and US)
Renal fuction test, ophthalmic and cardiac
evaluation
HbA1C
Weight and baseline tests

82. Second trimester
Check BP
Careful FH measurement
Maternal serum Αfp at 16-18wks
USfor detection of fetal anomaly

83. Third trimester
Assess BPvalues frequently
Serial USto assess fetal growth and fetal
surveillance

84. Timing and route of delivery
Optimal time is 38-40wks, not later than
40WK
Induction of labor is recommended @
38wks in patients with poor Glycemic
control and macrosomia
If early delivery is indicated lung maturity
should be checked
C/S is done only for obstetric indications

85. Intrapartum glycemic management
Target to keep BGL 80-120
1. Insulin infusion method
Withhold the morning dose
Begin regular insulin infusion at 0.5u/hr
Monitor maternal glucose hourly and
adjust the drops acc. to the result

86. 2. Intermittent subcutaneous injection
method
Give ½ the usual insulin dose in AM
Begin and continue glucose infusion (D5W)
at 100ml/hr
Monitor maternal glucose hourly & and give
regular insulin as needed

87. GDM – no treatment required, if need be
use oral hypoglycemic agents
Need follow up as they may progress to overt
diabetes
Type 1 – 1/3 to ½ of antepartum daily dose
Type 2 – pre-pregnancy dose can be restarted

88. Barrier methods are safe and without
metabolic side effects
Women with pre-existing diabetes, who do
not have serious vascular disease, may be
prescribed either the lowest dose combination
or progestin only contraceptive under medical
supervision
Neither DMPA nor norplant is recommended
as 1st line methods of contraception in woman
with DM
Permanent methods of contraception are ideal
if family size is complete

89. One-third to two-thirds of women with
GDM will have GDM in a subsequent
pregnancy
As many as 20 percent of women with GDM
have impaired glucose tolerance during the
early postpartum period
At least 6wks after delivery, all women with
previous GDM should undergo an OGTT
using a 2hr 75 gm OGTT

90. maternal diabetes
childhood glucose intolerance/diabetes
childhood obesity
neurological development
cardiovascular disease

91. a life threatening metabolic complication of
absolute insulin deficiency
in approximately 1 percent of diabetic
pregnancies
Can occur with:
 Type I DM- most often
 Type IIDM and
 GDM

92. may develop with hyperemesis gravidarum, β-
mimetic drugs given for tocolysis, infection,
and corticosteroids given to induce fetal lung
maturation.
results from an insulin deficiency combined
with an excess in counter-regulatory
hormones such as glucagon.
characterised by the triad of:
o Hyperglycaemia
o Ketonaemia from fatty acid metabolism
o Metabolic acidosis.

93. The resulting hyperglycaemia results in loss
of water and electrolytes, hyperosmolality
and fluid depletion.
incidence of fetal loss can be as high as 20
percent with DKA.

94. History of polyuria, polydipsia, vomiting,
abdominal pain, weight loss, dehydration,
precipitating infection or event.
Hyperglycaemia, typically BGL>13mmol/L but
may be lower or normal in pregnancy
Metabolic acidosis (pH<7.30) with high anion
gap
Presence of ketones in urine or serum

97. Is the leading cause of indirect maternal
deaths accounting for 20 percent of all cases
a leading cause of obstetrical ICU admissions
The increasing prevalence in pregnancy is
likely due to a number of causes:
 obesity
 hypertension and
 diabetes

98. cardiac output increases approximately 40 %
Vascular resistance decreases
Resting pulse and stroke volume increase
Women with underlying cardiac disease may
not always accommodate these changes
98

100. A few women with severe cardiac dysfunction
may experience evidence of heart failure
before midpregnancy.
In others, heart failure may develop after 28
weeks when pregnancy-induced
hypervolemia and cardiac output reach their
maximum.
In most, however, heart failure develops
peripartum

101. 1. Rheumatic heart disease (80%):
- Mitral valve is the commonest followed by aortic
valve then both or others.
2. Congenital heart diseases (15%):
A. Acyanotic (left to right shunt):
- More common, includes septaldefects and
patent ductus arteriosus.
B. Cyanotic (right to left shunt):
E.g. Fallot‘s tetralogy and Eisenmenger‘s
syndrome which is more dangerous and carries a
maternal mortality rate exceeding 25%.
3. Others (5%): e.g. ischaemic heart disease,
arrhythmias and cardiomyopathy.

103. Diagnostic Studies:
 electrocardiography, chest radiography, and
echocardiography
 Transesophageal echocardiography
 cardiac catheterization with limited
fluoroscopy time to minimize radiation
exposure

105. Mitral Stenosis:
 Limited physical activity
 dietary sodium is restriction
 A β-blocker drug to slow the ventricular
response to activity
 If new-onset atrial fibrillation develops,
intravenous verapamil, 5 to 10 mg
 For chronic fibrillation, digoxin, a β-blocker,
or a
calcium-channel blocker

106.  Therapeutic anticoagulation with heparin is
indicated with persistent fibrillation.
 Labor and delivery
-vaginal delivery is preferable
-Elective induction so that labor and delivery
are attended by a scheduled, experienced
team.
-With severe stenosis and chronic heart failure,
insertion of a pulmonary artery catheter may
help guide management

107. Mitral Insufficiency
 β-blocking drugs are given to:
decrease sympathetic tone
relieve chest pain and palpitations and
reduce the risk of life-threatening
arrhythmias
Aortic Stenosis
If asymptomatic - no treatment except close
observation
If symptomatic- strict limitation of activity
and prompt treatment of infections.

108. If symptoms persist despite bed rest, valve
replacement or valvotomy
For women with critical aortic stenosis,
intensive monitoring during labor is important
During labor, narcotic epidural analgesia
Forceps or vacuum delivery is used for
standard obstetrical indications in
hemodynamically stable women

109. Aortic Insufficiency
 generally well tolerated during pregnancy
 If symptoms of heart failure develop,
diuretics are given and bed rest is
encouraged.
Pulmonic Stenosis
 Surgical correction ideally is done before
pregnancy
 if symptoms progress, a balloon angioplasty
may be necessary antepartum

110. Peripartum Cardiomyopathy
is very similar to other forms of nonischemic
dilated cardiomyopathy except for its unique
relationship with pregnancy
Currently, it is a diagnosis of exclusion
diagnostic criteria:
1. Development of cardiac failure in the last
month of pregnancy or within 5 months after
delivery,
2. Absence of an identifiable cause for the
cardiac failure,

111. 3.Absence of recognizable heart disease prior
to the last month of pregnancy, and
4.Left ventricular systolic dysfunction
demonstrated by classic echocardiographic
criteria, such as depressed ejection fraction
or fractional shortening along with a dilated
left ventricle
Management -Bed rest, sodium restriction,
digoxin & diuretic treatment. Anticoagulants
in pts with massively enlarged cardiac
chambers.

113. Absolute indications
◦ Primary pulmonary hypertension
◦ Eisenmenger’s Syndrome
◦ Pulmonary veno-occlusive disease
Relative indications
◦ NYHA Class 3 & 4
◦ NYHA Class 1 & 2 with previous history of heart
failure in early pregnancy or in between
pregnancies

114. Hypertrophic Cardiomyopathy
 In pregnancy it causes:
dyspnea
chest pain, and palpitations
a pregnant woman can present with
preeclampsia and an acute myocardial
infarction.

115. Management
Avoid Strenuous exercise
Avoid abrupt positional changes to prevent
reflex vasodilation and decreased preload.
β-adrenergic or calcium-channel blocking
drugs if symptoms develop,especially angina
The delivery route is determined by
obstetrical indications

116. Peripartum Cardiomyopathy
is very similar to other forms of nonischemic
dilated cardiomyopathy except for its unique
relationship with pregnancy
Currently, it is a diagnosis of exclusion
diagnostic criteria:
1. Development of cardiac failure in the last
month of pregnancy or within 5 months after
delivery,
2. Absence of an identifiable cause for the
cardiac failure,

117. 3.Absence of recognizable heart disease prior
to the last month of pregnancy, and
4.Left ventricular systolic dysfunction
demonstrated by classic echocardiographic
criteria, such as depressed ejection fraction
or fractional shortening along with a dilated
left ventricle
Management -Bed rest, sodium restriction,
digoxin & diuretic treatment. Anticoagulants
in pts with massively enlarged cardiac
chambers.

119. Uncommon in pregnancy: 1:10,000
pregnancies
28 – 50% mortality rate: worse rate in 3rd
trimester
Risk factors : hypercholesterolemia, smoking,
hypertension, diabetes, high BMI, systemic
lupus erythematosis, syphilis & cocaine
abuse.
Chest pain, SOB, nausea/vomiting
Labour and delivery: Standard cardiac care
Avoid elective delivery within two weeks of
infarction

120. Infective endocarditis is uncommon during
pregnancy and the puerperium.
Prophylaxis is recommended:
-for dental procedures in those with prosthetic
valves
-prior endocarditis
-unrepaired or incompletely repaired cyanotic
heart defects

122. 1. Williams obstetrics 24rd edition
2. Gabbe obstetrics normal and problem pregnancies
6th Edition.
3. Current diagnosis and treatment in obstetrics and
gynecology.
4. Uptodate 21.6