Preeclampsia pdf - دكتوره ايناس

Lec-1-2-3-4-5 Gynecology د.إيناس



Affects 80% of women



Several theories

o  Exact cause remains unclear
o  Elevated progesterone levels?
o  HCG and estrogen?
o  Some studies have indicated H. pylori involvement…
o  Vit deficiency

At least 80% of women experience nausea &vomiting. The term morning sickness is often
used to describe this condition when symptoms usually disappear after the first trimester.
This mild form affects he quality of life of women &her family where the sever form
hyperemesis gravidarum results in dehydration, electrolyte imbalance and the need for
hospitalization

Pathophysiology

Decrease fluid intake& prolonged vomiting cause dehydration which increase serum
concentration of hCG;



Endocrine theory :high levels of hCG & estrogen during pregnancy



Metabolic theory :vitamin B6 deficiency



Psychological theory : Psychological stress increase the symptoms

Laboratory & Diagnostic test



Liver enzyme: elevation of (AST) & (ALT) are usually present.



CBC: elevated level of RBC & hematocrit indicating dehydration.



Urine ketones: positive when the body breaks down fat to provide energy in the absence
IIT



BUN :increase in the presence of salt &water depletion



Urine specific gravity: greater than 1.025 indicating concentrated urine linked to
inadequate fluid intake



Serum electrolyte decrease levels of k, Na, Cl



Ultrasound :evaluation for molar or multi pregnancy

Lec-1  Nausea and Vomiting of Pregnancy

Benefits?

Women with uncomplicated “morning sickness” have been noted to have improved
pregnancy outcomes



Fewer miscarriages



Fewer preterm deliveries



Fewer stillbirths



Fewer instances of low birth weight, growth retardation and mortality

Possible Complications?



Hyperemesis gravidarum is linked to increased maternal adverse effects

o  Splenic avulsion
o  Esophageal rupture
o  Mallory-Weiss tears
o  Pneumothorax
o  Neuropathy
o  Preeclampsia



Fetal Complications

o Increased fetal growth restriction
o Increased mortality



Weight loss



Dehydration



Metabolic acidosis from starvation



Alkalosis from loss of HCL



Hypokalemia (electrolyte imbalance)

Management



Dietary measures



Emotional support



Acupressure



Ginger



Chiropractic

Dietary Measures



Frequent small meals



Bland foods, high in CHO, low in fat

o salty foods (eg. crackers) are usually well tolerated in the morning
o sour & tart (eg. lemonade) are often better tolerated than water



Avoid smells and food textures that cause nausea

Emotional Support



She may become depressed or exhibit other mood changes

o Family support is critical!



Psych consult may be indicated if

o  she’s depressed
o  domestic violence is suspected
o  evidence of substance abuse



Maintain NPO status to allow GI tract to rest



Administer antiemetic drugs like: promethazine, prchlorperazine, odanse-tron.



Administer IV fluid like 5% dextrose in lactated ringer



Administer electrolyte replacement therapy



In severe cases total parenteral protein



Vit. B complex



A tapering course of steroid is used sometimes



Termination of pregnancy may needed in severe cases



Avoid tight waistband



Eat small frequent meals (6 meals)



Separate fluid from solid by consuming fluid In between meals



Use high protein supplement



Avoid lying down for at least 2 hours after eating



Avoid food high in fat drink herbal tea



Eat food that settle the stomach such as toast or soda

Non-”Morning Sickness” Causes of Vomiting



Gastrointestinal disorders



Genitourinary tract disorders



Metabolic disorders



Neurologic disorders



Pregnancy-related conditions



Drug toxicity or intolerance

But what if...?

Non-resolving or worsening symptoms or nausea began after 9 weeks of gestation



consider other causes.

Cholestasis: What does it mean?



Pathology: Histological demonstration of bile in liver tissue



Physiology: Measurable reduction in hepatic secretion of solutes and water



Biochemical: Demonstrable accumulation in blood of substances normally excreted in
bile (bilirubin, cholesterol, bile acids)

Liver Diseases in Pregnancy



High estrogen state:

– Intrahepatic cholestasis of pregnancy

– Gallstones and sludge occur more frequently



Altered fatty acid metabolism:

– Acute fatty liver of pregnancy



Vascular diseases affect the liver:

– Pre-eclampsia

– HELLP Syndrome



Viral hepatitis:

– Vertical transmission of hepatitis B and C

Pathophysiology



Liver is an estrogen sensitive organ

o Estrogen affects organic anion transport (bilirubin, bile acids)



Bilirubin excretion very mildly impaired during normal pregnancy



Biliary phospholipids secretion may be impaired (gene mutation, estrogen effect)



Pregnancy is associated w/ decreases in GI motility, including gall bladder motility

Lec-2  Intrahepatic Cholestasis of Pregnancy

Physiological Consequences: The Liver in Pregnancy



Pregnant women more likely to become jaundiced if cholestatic or hepatocellular injury
occur



Spider angiomata and palmar erythema develop in up to 2/3 pregnancies due to effects
of estrogen and progesterone



Cholecystectomy generally safe



3rd Trimester see increased alk phos 2/2 developing placenta (not liver)

Intrahepatic Cholestasis of Pregnancy (IHCP)



Incidence 0.5% - 1% of pregnancies



Recurrence in subsequent pregnancies



Pruritis develops in late 2nd and 3rd trimester in palm and soles



High transaminases - 40% > 10 x (Hay)



Bilirubin < 5mg/dL



Total bile acids increase 100 fold

Pathogenesis: genetic, hormonal



Women who develop clinical cholestasis during pregnancy or with oral contraceptives
likely have genetic polymorphisms in the genes responsible for bile formation and flow



Familial - 10% occurrence in 1st degree relatives



Hormonal – timing in pregnancy, twins

ICHP Clinical Features



Pruritis is the defining characteristic



jaundice is unusual



Anorexia, pale stool , dark urine and steatorrhoea



Fetal death (unknown cause) ,preterm L., meconium stained Liq,intrauterine fetal
distress



Disappears rapidly after delivery



Severity is variable



No effect on mother but complications such as bleeding,PTL,steatorrhoea



Rarely see a familial, progressive course to cirrhosis



Elevated transaminases ,bile acids ,



Full blood count, clotting profile, renal function test, hepatitis serology, autoimmune
antibodies, liver ultrasound, fetal U/S,CTG

IHCP Therapy



Ursodeoxycholic acid 10mg- 10mg/Kg/day



Emolliants and antihistamines



Vitamin K antenatally.



Reassurance and support



Consider early delivery in severe cases

o Unbearable maternal pruritis or risk of fetal distress/death
o Deliver at 38 weeks if mild, at 36 weeks for severe cases – if jaundice

Summary



Normal pregnancy is associated w/ characteristic, benign changes in liver physiology



Several unique diseases occur during pregnancy and all resolve following delivery



Implications are disorder specific

Acute fatty liver



1/10000 pregnancies. rare



At the end of pregnancy



Abdominal pain, headach, nausea,



Jaundice,encephalopathy,hypoglycemia,coagulopathy,renal failure



Etiology unknown



Fatty infiltration of liver



maternal & Fetal death due to metabolic disturbances



HT,DIC



No role to liver biopsy,Ix.by liver and renal function test.



Treatment is by delivery of baby ,usually by C/S under GA



FFP,B.transfusion,vit.k,50% glucose,acetyl cysteine,and dialysis may needed

- O, A, B, AB

- C, D, E Ag Rh system  on chromosome 1  2 genes (C/c , E/e) and (D)

- Anti D more common (d/d or depled Ag)

- Anti C less common

- Fetus Rh +ve  large blood volume of fetus pass to maternal blood

- Maternal AB pass to fetus

- 1

baby not affected because acute reaction is by IgM

- Frequent pregnancy  hemolysis by IgG  severe anemia

Potential sensitizing events for Rhesus disease

1.  Miscarriage
2.  Termination of pregnancy
3.  Antepartum hemorrhage
4.  Invasive prenatal testing (chorion villus sampling, amniocentesis and cordocentesis)
5.  Delivery

Prevalence of Rhesus disease

The prevalence of D Rhesus negativity is 15 per cent in the Caucasian population, but lower
in all other ethnic groups. It is very uncommon in Orientals.

Give Anti-D after each procedures within 72 hours "intramuscular administration of anti-D
immunoglobulins to a mother, preferably within 72 hours of exposure to fetal red cells"

A Kleihauer is a test of maternal blood to determine the proportion of fetal cells present
(relying on their ability to resist denaturation by alcohol or acid); it will allow calculation of
the amount of extra anti-D immunoglobulin required

Prophylaxis  give Anti-D

Lec-3  Rh iso-immunization

Signs of fetal anemia

Note: Clinical and ultrasound features of fetal anemia do not usually become evident unless
fetal hemoglobin is more than 5 g/dL less than the mean for gestation. Usually, features are
not obvious unless the fetal hemoglobin is less than 6 g/dL.

• Polyhydramnious.

• Enlarged fetal heart.

• Ascites and pericardial effusions.

• Hyper-dynamic fetal circulation (can be detected by Doppler ultrasound by measuring
increased velocities in the middle cerebral artery or aorta).

• Reduced fetal movements.

• Abnormal CTG with reduced variability, eventually a ‘sinusoidal’ trace.

Management of Rh disease

1- Not sensitized + father Rh +ve  blood group of father (heterozygous or homozygous)

2- Sensitized mother

Booking visit (2-4 weeks)

Monitoring the antibody level by standard quantification method

4 IU/mL HDFN unlikely

4–15 IU/mL    Moderate risk of HDFN
> 15 IU/mL     High risk of hydrops fetalis

If level raise  anemia

Do Doppler of middle cerebral artery

Delivery > 36 weeks        Fetal blood transfusion <36 weeks

3- Help restore hemoglobin levels, reversing or preventing hydrops or death

Routs:



Umbilical vein



Intrahepatic vein



Into the peritoneal cavity



Into the fetal heart

* First take a sample to confirm the anemia and then infuse the blood during a single
puncture.
Transfused blood is:
• RhD negative
• Cross-matched with a maternal sample
• Densely packed (Hb usually around 30 g/L) so that small volumes are used
• White cell depleted and irradiated
• Screened for infection including CMV

At delivery  blood count, blood group and indirect Coomb's test.

ABO

Mother is blood group O and Baby is blood group A or B Ag (Not fully developed Ag  IgM
not cross and A or B pass  fetal circulation  hemolysis, anemia mild + jaundice



Placenta is a fetomaternal organ



Functional part of placenta is fetal cotyledon = 120 cotyledons = Hollow structure
contain terminal villi, tertiary villi, fetal blood inside it



Spiral arteries give blood in to intercotyledon space, 2 exchange of blood occur



narrow venous cannels



material decidual plate



Ma to veins



maternal circulation



The transferee of O2, CO2, nutrition, waste products occur through three layers
trophoblastic tissue, connective tissue, endothelium of fetal capillaries



Blood flow in the placenta from 50 in 1

trimester to 500 -750 ml/min in 3

trimester



Trophoblastic invasion of spiral arterioles at 12 weeks of pregnancy and replace the
smooth muscles of wall of blood vessels  wide pore, low resistance, large capacitance
vessels  20 weeks complete

Abnormal placentation
If no invasion  narrow blood vessels, high resistance, low capacitance, impaired perfusion
of fetoplacental  infarcts + basal hematoma  ischemic necrosis and spiral artery
occlusion  thrombosis, multiple infracts, damaged of spiral artery  Intrauterine death
(IUD) and intrauterine growth retardation (IUGR)

PE (Pre-eclampsia)

-  Blood pressure > 140/90   4 hours apart
-  300 mg protein/2a                                                   > 20 weeks of pregnancy and resolve
                                                                                             spontaneously
-  Incidence: 2-3 % of pregnancies

- Risk factors:

1. First pregnancy
2. Multiparous with:

o pre-eclampsia in any previous pregnancy
o ten years or more since last baby

3.  Age 40 years or more
4.  Body mass index of 35 or more
5.  Family history of pre-eclampsia (in mother or sister)
6.  Booking diastolic blood pressure of 80 mmHg or more
7.  Booking proteinuria (of _1_ on more than one occasion or quantified at _0.3

g/24 hour)

8. Multiple pregnancy
9. Certain underlying medical conditions:

o  pre-existing hypertension
o  pre-existing renal disease
o  pre-existing diabetes
o  antiphospholipid antibodies

Lec-4  PET (Pre-eclamptic Toxemia)

Etiology and pathophysiology

- In pregnancy
- Molar pregnancy
- Abdominal ectopic pregnancy

Placental bed biopsies  patchy in preeclampsia  retain their muscular walls   high
flow, low impedance uteroplacental circulation under perfusion at the placenta 
releases a factors  endothelial tissue (cytokines, growth factors, oxidative stress) 
multisystem disease, multiple organ system

CVS
- Peripheral vasoconstriction
- Endothelial injury  increase vascular permeability  generalized edema

Renal system
- Glomeruloendotheliosis  impaired GFR  loss of intermediate weight proteins
(albumin, transferrin)  proteinuria  reduction in plasma oncotic pressure  edema

Hematological system
- Damaged endothelium  platelets adhesion  laying down of fibrin  decrease platelet
count

The liver
- Subendotheilal fibrin deposition
- Increased liver enzymes
- Hemolysis
- Low platelets  HELLP syndrome 2-4% of women  high fetal loss rate

Neurological system
- Brain edema
- Headache
- Papilledema
- Retinal hemorrhage

Clinical features



Frontal headache



Visual disturbance



Epigastric pain + tenderness



Flu like illness



Rapid progressive edema of face



Hyperreflexia and clonus hand in severe cases

Testing for proteinuria

1- Dipstick urinalysis



Instant result but quantitatively inaccurate



Results: trace: seldom significant; 1_: possible significant proteinuria, warrants
quantifying; _2_: probable significant proteinuria, warrants quantifying

2- Protein:creatinine ratio



Fast (within an hour)



Results semi-quantitative: _30 mg/mol – probable significant proteinuria

3- 24 hour collection



Slow



Results: _0.3 g/24 hour represents confirmed significant proteinuria

Investigations for pre-eclampsia

To monitor maternal complications:



Full blood count (with particular emphasis on falling platelet count and rising
haematocrit)



If platelet values are normal, additional clotting studies are not indicated



Serum renal profile (including serum uric acid levels)



Serum liver profile



Frequent repeat proteinuria quantification is probably unhelpful once a diagnosis of pre-
eclampsia has been made

To monitor fetal complications



Ultrasound assessment of:

o  fetal size
o  amniotic fluid volume
o  maternal and fetal Dopplers



Antenatal cardiotocography used in conjunction with ultrasound surveillance, provides a
useful but by no means infallible indication of fetal well-being. A loss of baseline
variability or decelerations may indicate fetal hypoxia

Management



There is no cure for pre-eclampsia other than to end the pregnancy by delivering the
baby



Decease blood pressure



Oral Methyldopa centrally acting till 2000 mg/day



Oral labetalol (alpha-blocking and beta blocking agent)



Oral nifedipne 10-40 mg (calcium-channel blocker)



IV hydralazine, IV labetalol, IV Mg sulphate (in severe cases to decrease blood pressure
and control convulsion)

Additional points in management

1- Delivery at 34 weeks after steroids were given I.M usually by C/S

2-  Given thromboembolism prophylactic subcutaneous heparin
3-  Epidural anesthesia
4-  Ergometrine is contraindicated

Screening and prevention

1- Doppler U/S of uterine artery waveform analysis to identify female with future

preeclampsia in previously having preeclampsia (high risk patient)

2- Aspirin 75 mg/ day (in high risk women)
3- Calcium supplement, Vit C, Vit E no benefit

Imminent eclampsia

Fulminating preeclampsia

Eclampsia



1/2000

40% antepartum
20% intrapartum
40% postpartum

Diagnosis:  >160/110, proteinuria on dipsticks, decreased fetal size and movement,
oligohydroamnious, hypoxia, eclampsia grand mal conus

Symptoms: Frontal headache, Visual disturbance (blurred vision and flashing lights),
Epigastric pain, General malaise and nausea, Restlessness

Signs:

Agitation, Hyper-reflexia and clonus, Facial (especially periorbital) edema, Right

upper quadrant tenderness, Poor urine output, Papilledema

Management:
o  Air way maintenance
o  Side positive O2
o  Large bore intravenous cannula
o  Clotting studies
o  renal and liver function tests
o  cross-matching
o  blood pressure control
o  Intravenous magnesium sulphate (initial dose 4 gm maintenance 1 gm/hr)
o  Labetalol
o  Nifedipine
o  Hydralazine

o  Maintenance of fluid balance
o  Stabilize the patient 
o  34 weeks  steroids  C/S to deliver
o  Monitoring every 5–15 minutes depending on condition)

Before pregnancy:

1-  Dental management.
2-  Heart echocardiography.
3-  Medical treatment and be optimize.
4-  Surgical heart treatment if need.

Antenatal management:

1-  Cardiac examination.
2-  Obstetric – cardiac clinic.
3-  Decrease activity.
4-  Echocardiography at the start of pregnancy and 28 weeks.
5-  Table 12-1 , 12-2 (p 152)
6-  Admission for bed rest.
7-  Prosthetic heart disease 10% risk of thrombosis :

a-  Use anticoagulant 6 -12 weeks (heparin).
b-  Congenital heart diseases (warfarin).
c-  Pulmonary hypertension (warfarin).

8- High risk heart conditions (p 153).
9- Fetal risk of maternal heart disease (p 153).

Management of labor:

1-  Normal vaginal delivery is better.
2-  Avoid induction.
3-  Use antibiotic in structural heart defects.
4-  Ensure fluid balance.
5-  Avoid supine position.
6-  Anesthesia – epidural with benefit to decrease pain and cause hypotension.
7-  Shortened 2

stage of labor by using oxytocin – slow administration.

8- Ensure good oxygenation.
9- Cesarean section (infection , hemorrhage , thrombosis ) unless its indicated.

Treatment of heart failure:

1-  The same as non-pregnant.
2-  Oxygen.
3-  Digoxin, morphine, diuretics.
4-  Selective adrenergic blocker (arrhythmias).
5-  Fetal well-being by using cardiotocography CTG.

Lec-5  Heart disease in pregnancy

)

6- If severe, preterm labor of termination of pregnancy.

Risk factors of heart failure:

1- Obesity.
2- Renal and urinary tracts infection.
3- Corticosteroids.
4- Tocolytics.
5- Anemia.
6- Multiple gestation.
7- Hypertension.
8- Arrhythmias.
9- Pain-related stress.
10- Fluid overload.

Ischemic heart disease:

The risk of MI during pregnancy is estimated as 1 in 10 000, and the peak incidence is in the
third trimester, in parous women older than 35.

Percutaneous transluminal coronary angioplasty (PTCA) is now considered acceptable but
should still be only used when absolutely necessary, avoiding the time when the fetus is
most susceptible to radiation (8–15 weeks).

Mitral and aortic stenosis:

1- Obstructive lesions of the left heart is increase morbidity and mortality of fetus and

mother.

2- Mitral heart disease (rheumatic).

Aortic heart disease (congenital).

3- Mitral stenosis: 40% experience pulmonary hypertension usually at 30 weeks.
4- The aim of treatment of mitral stenosis is to reduce the heart rate by bed rest, oxygen,

beta-blockade and diuretic therapy.

5-  2% maternal mortality.
6-  Balloon valvotomy is the treatment of choice after delivery.
7-  The risk of maternal death in those with severe aortic stenosis is reported as 17%, with

fetal mortality of 30%.

8- Treatment of aortic stenosis:

- Bed rest and medical treatment.
- Valvotomy in needed in several cases.

Marfan syndrome:

1- Autosomal dominant.
2- Connective tissue abnormality that may lead to mitral valve prolapse and aortic

regurgitation, aortic root dilatation and aortic rupture or dissection.

3- 50% maternal mortality rate according to echocardiography.
4- Associated with obstetric complications:

-  Early pregnancy loss.
-  Preterm labor.
-  Cervical weakness.
-  Uterine inversion
-  Postpartum hemorrhage.

Pulmonary hypertension:

1- is characterized by an increase in the pulmonary vascular resistance resulting in an

increased workload placed on the right side of the heart.

2- The main symptoms are fatigue, breathlessness and syncope, and clinical signs are

those of right heart failure.

3- Diagnosis by exercise test (echocardiography).
4- Treatment include:

-  Endothelin blockers, such as bosentan.
-  Phosphodiesterase inhibitors, such as sildenafil.
-  More complex therapies include nebulized SC and IV prostaglandins.

5-  Women may deteriorate early (second trimester).
6-  30% - 50% mortality rate.
7-  It is currently recommended that women with pulmonary hypertension should be

strongly advised against pregnancy and given clear contraceptive advice, with early
termination advised in the event of pregnancy.

Hypertensive disorders:

1- Complicates 5% - 7%.
2- Classification of hypertension in pregnancy:

a-   Gestational hypertension:
• Gestational hypertension (no proteinuria).
• Gestational proteinuria (no hypertension).
• Pre-eclampsia (proteinuria and hypertension).
b-  Pre-existing hypertension and/or renal disease:
• Chronic hypertension (no proteinuria).
• Chronic renal disease (hypertension and/or proteinuria).
• Chronic hypertension with superimposed pre-eclampsia.
c-   Unclassified hypertension and proteinuria.

3- Defined as diastolic BP more than 90 mmHg and systolic BP more than 140 mmHg.

Chronic hypertension:

1- 90% of them is essential hypertension.
2- Causes of chronic hypertension

a- Idiopathic

• Essential hypertension

b- Renal disease

        • Polycystic disease
        • Diabetic nephropathy
        • Chronic glomerulonephritis
        • Nephrotic and nephritic syndrome

c- Vascular disorders

• Renal artery stenosis
• Coarctation of the aorta

d- Collagen vascular disease

        • Systemic sclerosis
        • Systemic lupus erythematosus
        • Rheumatoid disease

e- Endocrine disease

        • Phaeochromocytoma
        • Conn’s syndrome
        • Cushing’s syndrome
        • Diabetes mellitus

3- Investigations include:

-  Serum creatinine.
-  Serum electrolytes.
-  Serum urea.
-  Liver functions test.
-  Urine analysis (blood, protein, glucose).
-  24 hrs. urinary protein – creatinine clearance.
-  Renal ultrasound.
-  Autoantibody screen.
-  ECG.
-  Echocardiography.

4- Complications are:

-  Pre-eclampsia.
-  Heart failure.
-  Intracerebral hemorrhage.

5- Pre-eclampsia may develop in around one-third of women with severe hypertension

and chronic renal diseases.

6- Management of chronic HT:

- In mild cases (>150/100 mmHg) there is no treatment and only monitoring of

baby and blood pressure.

- If BP <150/100 mmHg start treatment and stop pregnancy.
- Preferred antihypertensive agents include methyldopa (centrally acting agent),

labetalol (alpha and beta-blocker), and nifedipine (calcium-channel blocker).

- Obstetric management include :

a- Dose monitoring to ante-partum hemorrhage, detect pre-eclampsia and fetal

growth restriction (FGR).

b-  Cesarean section if indicated.
c-  Wait for normal vaginal delivery if there is no risk.
d-    Breast feeding encouraged.
e-  Monitoring in 24 hrs. post-partum.

7- Risk factors for developing superimposed pre-eclampsia:

• Renal disease.
• Maternal age < 40 years.
• Pre-existing diabetes.
• Multiple pregnancy.
• Connective tissue disease, e.g. antiphospholipid syndrome.
• Coarctation of the aorta.
• Blood pressure < or = 160/100 mmHg in early pregnancy.
• Pre-pregnancy BMI < 35.
• Previous pre-eclampsia.
• Antiphospholipid syndrome.

Notes:



Cholecystectomy done in the second trimester (any operation done in 2

Trimester)



Transaminase level  MCQ



Cholestasis  due to estrogen and contraceptive drugs



Classification of pre-eclampsia  important



Glomeruloendotheliosis  MCQ



GUE (albumin)and blood pressure must be done in every visit during antenatal care



Diastolic notch in Doppler U/S of uterus artery  diagnostic for preeclampsia



Methargin is contraindicated in hypertensive women post.op due to cardiac effects



Termination of pregnancy is the definitive treatment of preeclampsia  MCQ

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