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DEPARTMENT OF MEDICINE
SEMINOR PRESENTATION ON:
MANAGEMENT OF MEDICAL DISORDERS IN PREGNANCY
PREPARED BY: 1. AWOKE W.
2. AYANO T.
MODULATOR : DR.TESHOME
NOV 18,2016
AMBO,ETHIOPIA
 Introduction
 Hypertensive disorders in pregnancy and their managment
 Gestational DM and its management
 Cardiac disease in pregnancy and treatment approaches
 References
 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.
 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
Definition
 Systolic B.P. >=140 mmHg
 and/or
 Diastolic B.P. >= 90 mmHg
◦ Documented on two occasions at least 6 hours apart
 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
Medical disorders in pregnancy
There are five types of hypertensive diseases:
◦ Gestational hypertension (pregnancy-induced
hypertension or transient hypertension).
◦ Preeclampsia.
◦ Eclampsia.
◦ Preeclampsia superimposed on chronic
hypertension.
◦ Chronic hypertension.
1. Gestational hypertension
o
BP >140/90 mmHg after 20wks during pregnancy or after
delivery and resolves by 12wks post-partum.
o
No proteinuria
o
Final diagnosis made only postpartum
 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
 Generalized tonic-clonic seizure in a
patient with Preeclampsia not
attributed to any other cause.
Eclampsia Preeclampsia
Seizure/
Convulsion/
Coma
 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
 New onset proteinuria in hypertensive
women but no proteinuria before 20
weeks' gestation
 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.

Age < 20 years or > 35 years

Nulliparity

obesity

Multiple gestation

Hydatidiform mole

Diabetes mellitus

Chronic hypertension

Renal disease

Family/personal history of preeclampsia
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
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.
Medical disorders in pregnancy
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.
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.
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
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
 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
 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.
 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.
 Blood Pressure
 Proteinurea
 Retinal vasospasm or Retinal edema
 Right upper quadrant (RUQ) abdominal
tenderness stems from liver swelling and
capsular stretch
◦ Brisk, or hyperactive, reflexes are common during
pregnancy, but clonus is a sign of neuromuscular
irritability that raises concern.
 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)
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
●HELLP Syndrome
●Cerebral hemorrhage
●ARDS
● Eclampsia
● Postpartum
hemorrhage
●Eclampsia(
in < 48hrs
of delivery)
●Shock
●Sepsis
●Recurrent pre-
eclampsia
●Chronic Renal Disease
• Abruptio placentae
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
HEMOLYSI
S
(due to
passage of
RBCs
through
partially
obstructed
vessel)
s)
HEPATIC
DYSFUNCTIO
N (due to
intravascular
fibrin
deposition &
sinosoidal
obst.)
Decreased
Liver blood
flow
HELLP
Syndrome
THROMBO-
CYTOPENIA
(due to
platelet
aggregation
& diposition
in the sites
of
endothhelia
l damage)
 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
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 ANC visit
 NST and serial fetal growth and amniotic fluid evaluation
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
 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
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.
 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.
Principles of mgt of sever preeclampsia
1. Blood pressure control
2. Prevent convulsions
3. Delivery as a definitive mgt
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.
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.
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.
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
 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.
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 SBP is at least 160mmHg or if DBP is at
least 110mmHg
 Antihypertensive medications are
discontinued if the BP remains below the
hypertensive levels for at least 48 hours.
 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.
MATERNAL FETAL
●Asphyxia
●Prematurity
●Hypoxia & IUD
Injuries Systemic
●Tongue bite
●Injuries due
to fall
●Bed sore
●CARDIAC: acute left
ventricular failure
●RENAL: renal failure
●HEPATIC: necrosis,
subcapsular hematoma
●CNS: cerebral
hemorrhage, edema
Hematology
●Low platelet
count
●Disseminated
Intravascular
Coagulation
Postpartum
●Shock
●Sepsis
●Psychosis
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.
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 BP to a safe range
-maintaining SBP b/n 140 and 160mmHg and
DBP b/n 90 and 110 mmHg is a reasonable
goal.
4. Delivery
 Vaginal delivery & Cesarean delivery for
obstetric indication
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
Withhold MgSO4 if:
 RR falls below 16/min
 Patellar reflexes are absent
 Urinary out put falls below 30ml/hr over the
preceding 4 hrs
50
 Stop MgSO4
 Iv 1g 10% of calcium gluconate
 Administer oxygen
 secure airway
 Ventilation
 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.
Medical disorders in pregnancy
 most common medical complication of
pregnancy.
 complicates 2-3% of pregnancies and 90% of
the cases represent women with GDM.
1.Pre gestational : diagnosed before pregnancy.
 Accounts for 20% of DM in pregnancy
Could be:
type 1 or
type 2
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.
 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
 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
 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.
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
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.
 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.
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%
 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
 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
 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
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
Three hour OGTT test
 100 gm after 8-14 hours fasting
 This will identify 80% of women with GDM
Time Plasma
mg/dl
 Fasting 95
 1hour 180
 2hour 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.
 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
 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
 Maternal
◦ preeclampsia
◦  infections -UTI
-Chorioamnionitis
-Endomyometritis
-moniliasis
-PPH
-Polyhydraminos
- C/S rates
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
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
 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, Polycystic kidney
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
Target
 To keep the maternal fasting capillary
glucose level <95mg/dl
 Can be achieved by non-medical means if it
fails by medical means
 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
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
 Initiated when the above fails
 Insulin – widely used
 Oral hypoglycemic agents – rarely used
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
First trimester
 Date the pregnancy (LNMP and US)
 Renal fuction test, ophthalmic and cardiac
evaluation
 HbA1C
 Weight and baseline tests
Second trimester
 Check BP
 Careful FH measurement
 Maternal serum Αfp at 16-18wks
 US for detection of fetal anomaly
Third trimester
 Assess BP values frequently
 Serial US to assess fetal growth and fetal
surveillance
 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
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
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
 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
 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
 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
 maternal diabetes
 childhood glucose intolerance/diabetes
 childhood obesity
 neurological development
 cardiovascular disease
 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
 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.
 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.
 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
Medical disorders in pregnancy
Medical disorders in pregnancy
 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
 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
Medical disorders in pregnancy
 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
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 septal defects 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.
Medical disorders in pregnancy
Diagnostic Studies:
 electrocardiography, chest radiography, and
echocardiography
 Transesophageal echocardiography
 cardiac catheterization with limited
fluoroscopy time to minimize radiation
exposure
Medical disorders in pregnancy
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
 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
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.
 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
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
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,
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.
Medical disorders in pregnancy
 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
Hypertrophic Cardiomyopathy
 In pregnancy it causes:
 dyspnea
 chest pain, and palpitations
 a pregnant woman can present with
preeclampsia and an acute myocardial
infarction.
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
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,
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.
Medical disorders in pregnancy
 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
 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
Medical disorders in pregnancy
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
Medical disorders in pregnancy

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Medical disorders in pregnancy

  • 1. DEPARTMENT OF MEDICINE SEMINOR PRESENTATION ON: MANAGEMENT OF MEDICAL DISORDERS IN PREGNANCY PREPARED BY: 1. AWOKE W. 2. AYANO T. MODULATOR : DR.TESHOME NOV 18,2016 AMBO,ETHIOPIA
  • 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 BP >140/90 mmHg after 20wks during pregnancy or after delivery and resolves by 12wks post-partum. o No proteinuria o 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 ●HELLP Syndrome ●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) s) HEPATIC DYSFUNCTIO N (due to intravascular fibrin deposition & sinosoidal obst.) Decreased Liver blood flow HELLP Syndrome 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 ANC visit  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 SBP is at least 160mmHg or if DBP is at least 110mmHg  Antihypertensive medications are discontinued if the BP remains 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: renal failure ●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 BP to a safe range -maintaining SBP b/n 140 and 160mmHg and DBP b/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:  RR falls 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 95  1hour 180  2hour 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, Polycystic kidney
  • 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  US for detection of fetal anomaly
  • 83. Third trimester  Assess BP values frequently  Serial US to 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 septal defects 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