Medical Disorders During Pregnancy

Front 1

Blood pressure during pregnancy ?

Hypertension definition ?

Classification of HTN during pregnancy ?

Incidence of HTN during Pregnancy ?

Back 1

* During Pregnancy :

There is a tendency towards a decrease in BP during 1st & 2nd TM with a return to pre-pregnancy levels at the begining of 3rd TM.

* HTN :

Eleavated BP > 140 /90 measured on two different occasions 6 hours apart

* Classification :

1- Gestational HTN :

HTN only + No proteinuria

Occuring 1st time in pregnancy usually 2nd half. "Formerly called PIH"

2- Pre-eclampsia :

Pregnancy specific syndrome of HTN + Proteinuria +/- edema

Mostly in 2nd half of pregnancy

3- Eclampsia :

Occurance of Siezures "fits or convulsions" in a patient with pre-eclampsia , which is not attributable to any other underlying cause / disease.

4- Chronic HTN :

HTN presenting before pregnancy or < 20 weeks or persistant after 12 weeks postpartum

* Incidence :

- Complicates 5-10 % of all pregnancies

- Serious effect on maternal & fetal mortality & morbidity

The 2nd MC cause for maternal mortality in Egypt.

Front 2

Pre-eclampsia ?

Defintion

Incidence

Risk Factors

Back 2

* Definition :

Acute Pregnancy specific syndrome of

1- HTN :

Eleavated BP > 140 /90 measured on two different occasions 6 hours apart

2- Proteinuria : "Non-selective"

Urinary PTN excreation > 300 mg/24 H

"Fluctuate widely over 24 H"

or persistant 30mg/dl "+1 Dipstick"

3- With or without edema :

Not a diagnostic criterion & usually present in many normal pregnancies.

- Occuring mostly in the 2nd half of pregnancy > 20 weeks

- It is a mlutisystem disorder characterized by reduced organ perfusion 2ry to vasospasm & endothelial activation

- If not treated it may induce fits "Eclampsia"

* Incidence :

- 3-7 % of all pregnancies

- More in PG especially extremes of age.

- Recurrence rate of 20%

* Risk factors :

1- Age / Parity / Race : black race

2- Chorionic villi :

- First time exposure in PG

- Superabundance CV in MFP / Vesicular mole

3- Abnormal placentation :

Hydrops fetalis / PHA

4- Pre-existing vascular disease :

DM / HTN / Autoimmune vasulitis

5- Genetic PDF for HTN :

PE in previous pregnancy / Chronic renal disease / Marked Obesity

6- Family Hx of PE or Eclampsia

Front 3

Aetiology of Pre-eclampsia ?

Back 3

- Exact Aetilogy is unknown but theories postulates the following :

A) Abnormal or Defective placentation (Zwefll theory) :

Result in placental ischemia or hypoperfusion

which result in release of unknown substance

(May be cytokine / Oxygen free radical or prostanoids or endothelin )

that passes into maternal circulation leading to vascular endothelial damage with all its sequlae.

B) Vascular endothelial damage & Generalized Vasospasm :

- Role of endothelium :

1- Control Vascular tone by balance between

VD = NO & Prostacycling

VC = Thromboxane & endothlin

2- Control vascular permeability

3- Control Hemostasis

- Effect of endothelial damage :

1- Inc. tone = VC

2- Inc. Permeability = edema & proteinuria

3- Platlet thrombosis & DIC in severe cases

- This Leads to :

Multisystem hypoperfusion state with ischemic effect on different organs especially in small capillaries & arterioles of :

Placenta / Kidney / Liver / CNS

But changes are non specific & evident only in severe cases.

Front 4

Pathophysiology if Pre-eclampsia ?

"Pathologic anatomy"

Back 4

1- CVS

- Increased vascular responsiveness to VCs leading to generalized VC whcih increases PVR & causes HTN

- Decreased plasma volume due to :

VC / Increased capillary permeability / decreased plasma proteins

2- Renal

- Glomerular endotheliosis :

Charecterestic lesion where glomeruli are enlarged swollen bloodless with hypertrophy of intercapillary cells.

- Decreased RBF & GFR : Oliguria

- Glomerular & Tubular Dysfunction :

Proteinuria : increased tubular permeability

Hyperuricemia : decreased clearance by renal tubules.

3- Placenta

A) Early = Failure of trophoblastic invasion of spiral arteries

- Normaly Invasion of of spiral arteries with its replacement by trophoblastic tissue converts narrow muscular vessels into wide flacid vessels not responsicve to vasoactive compounds with decreased resistance & increased placental blood flow.

- In PE : invasion is patchy & spiral arteries retain their muscular wall preventing increase in placnetal blood flow leading to placental ischemia.

B) Late = Acute atherosis of spiral arteries

Accumulation of fat -laden macrophages & perinuclear halo = narrowing of lumen = more placental ischemia

C) Placental Infarctions

Red infarcts is common in PE , maybe extensive leading to palcental insufficiency, IUGR & IUFD

4- Liver

Periportal / Subcapsular Hge & Necrosis

5- CNS

Vasospasm / Cerebral edema / Petechial Hge / Thrombosis

Front 5

Clinical Picture of Pre-eclampsia ?

A) Symptoms

B) Signs

C) Investigations

D) Criteria of severity

Back 5

Symptoms :

A) Asymptomatic : Early mild casses

B) Symptomatic : Non-specific,

late in severe complicated cases :

1- Persistant headache "not relieved by meds."

2- Visual disturbances : blurring / diplopia / scotoma / flashes / temporary blindness.

3- Persistant vomiting

4- Epigastric & Rt Upper abdominal pain

5- Diminished fetal movements

6- Oliguria "< 30 mg/hr"

7- Edema " LL - abdominal - generalized "

Signs :

- PE is a diseased of signs rather than symptoms ,Mainly HTN + Proteinuria +/- edema occuring in 2nd half of pregnancy

- Regular ANC allow early detection of PE before symptoms are evident.

1- HTN

- Earliest sign

- Elevated BP = 140/90 or more on two or more occasions either 6 hours apart

Or A rise of > 30 sytolic / > 15 Diastolic pressure "Only Close observation"

- Labile from time to time

- Resolves 6 weeks after delivery

2- Proteinuria

- Late sign but essential criterion

- Urinary PTN Excretion > 300 mg/24 H

OR Reagent urine strips > +1 in at least 2 random urine samples without collection of 24 H urine as proteinuria is variable over 24 H

3- Edema

- Common early feature but not a diagnostic criterion as it is a normal finding in pregnancy.

- Early : Occult edema

Abnormal rate of weight gain "> 1 kgm/Week"

Precedes clinical edema

- Late : Clinical edema

Significant in non dependant areas

+1 Ankle +2 Knee +3 Vulva +4 Lower abomen +5 Anasarca

Front 6

Speceial investigations for Preeclampisa ?

Back 6

A) Evaluation of Severity :

1- Complete urine analysis

1- Proteinuria :

- Dipstik random sample : rapid not accurate

- 24 H urine collection for total protein :

> 0.3 gm = Mild / > 5 gm = Severe

2- Others : Specific gravity / Epithelial casts / RBCs / Pus Cells

2- Serum Uric Acid

For Hyperuricemia "N 3.5 - 5"

it procede proteinuria but not specefic

3- KFT

Serum Creatinine + Blood Urea = Normal except in late severe

4- LFT

AST & ALT "N = 8-20 m.IU/ml"

for detection of HELLP syndrome

5- CBC

- Hb = low in anemia

- HCT = elevated due to hemoconcentration

- Platlets = low in help " N = 150000 - 250000"

6- Coagulation profile

For diagnosis of DIC :

PT "N = 11-12 S" & PTT "N = 24-36 S"

Serum fibrinogen "N = 300-600 mg/dl" & FDP

7- Fundus examination

For Retinal changes as :

Vasospasm / Hge / Exaudates

B) Evaluation of fetal well being :

1- DFMC

2- NST : if kick count is non reassuring

3- US : Detects IUGR / Oligohydramnios

Performs BPPS test

Doppler US : Umblical & Cerebral artery

Front 7

Criteria of Severity of PE ?

Back 7

A) Mild :

- BP < 160/110

- Mild Proteinuria 1+

- No or mild associated symptoms

B) Severe :

- Symptoms :

1- Persistant headache "not relieved by meds."

2- Visual disturbances : blurring / diplopia / scotoma / flashes / temporary blindness.

3- Persistant vomiting

4- Epigastric & Rt Upper abdominal pain

5- Diminished fetal movements

6- Oliguria "< 30 mg/hr"

7- Edema " LL - abdominal - generalized "

- Signs :

BP : 160/110 or more

- Investigations :

- Persistant Proteinuria :

+2 or more / 5gm or more per 24 hour urine

- Elevated liver enzyme :

ALT / AST / Billirubin / ALP = HELLP

- Thrombocytopenia : low platlets < 100000

- Complications :

1- Maternal : HELLP / DIC / HF or P.edema

2- Fetal : IUGR

Front 8

Complications of PE ?

Back 8

A) Maternal :

1- Eclampsia : 1-2% of cases

2- Abruptio placenta : Severe HTN = RP clot

3- Acute renal failure :

- Reversible : Acute tubular necrosis

- Irreversible : Bilateral cortical necrosis

4- HELLP : 2-4% High fetal+maternal mortality

- Hemolysis

- Elevated liver enzymes

- Low platlet count

5- DIC

6- Heart failure & Acute pulmonary edema

7- Intracranial Hge : ruptured vessels

8- Hepatic rupture : Subcapsular Hge = Internal bleeding & Shock

9- Retinal detachment & Cortical blindness

10- Remote : Residual HTN / Recurrence

11- Maternal Mortality : 2nd major cause

B) Fetal :

1- IUGR : placental insufficiency

2- IUFD : IUGR or Accidental Hge

3- Prematurity : spontaneous or induced PTL

Front 9

Differential Diagnosis of Pre-eclampsia ?

Back 9

A) Other Causes of HTN :

1- Gestational HTN : NO Albuminuria

2- Chronic HTN :

- Essential :

- Onset : before preg. or before 20 weeks or persistant > 6 weeks postpartum

- +ve Hx

- Ex : Cardiac enlargement + No edema

- Inv : No albuminuria + Normal KFT + Sclerotic fundal changes

- 2ry :

- Pheochromocytoma : Intermittent & urinaty VMAs

- Thyrotoxicosis : T3 & T4

- Coarctation of aorta : Differential HTN

B) Other Causes of Proteinuria :

1- Contamination by vaginal discharge

"Midstream sample or catheter specimen"

2- UTI : Complete urine analysis for Dx

3- Chronic kidney disease : Chronic nephritis, Dx by KFTs, Albuminuria precedes HTN

C) Other Causes of Edema :

1- Unilateral :

DVT / Cellulitis / Cancer ovary / Lymphedema / Varicose veins of LL

2- Bilateral :

- Physiological : pressure by gravid uterus especially oversized " MFP / PHA"

Improves with lifting feet

- Pathological : Cardiac / Renal / Hepatic

Front 10

Causes of Acute abdomen in PE ?

Back 10

1- Subcapsular Hge in liver

2- Accidental Hge

3- True labour pains

Front 11

Managment of Preeclampsa ?

Back 11

1- Prediction

Uterine artery doppler + Fibronectin

2- Prevention

Low dose aspirin + Antioxidants

3- Treatment :

Why ? Prevent complications esp. eclampsia

When ? Timing depend on GA & Severity of PE

How ? Only way is termination by delivery

1- Mild pre-eclampsia :

A) Full term : Termination

B) Preterm : Expectant

2- Severe Pre-eclampisa :

Front 12

Prediction & Prevention of PE ?

Back 12

* Prediction :

No Reliable tests but :

- Uterine artery Doppler studies :

At 18-24 Weeks revealing :

High resistance index + diastolic notching

may identify up to 80% of women who will subsequently develop PE.

- Fibronectin :

Elevated with endothelial damage

Precedes clinical course of PE

* Prevention :

1- Low Dose Aspirin

Infantile Aspirin 75-100 mg daily from 2nd TM

- Indications : High risk patients for PE :

Hx of severe PE before 30 weeks in a previous pregnancy or those with IUGR

- Action :

Inhibit thrombosis by inhibiting pl.aggregation

Promote VD by inhibiting release of TXA2 without impairing synthesis of VD prostacyclin prod. by endothelium

2- Antioxidants :

- Vitamin C & E

- High risk cases with uterine artery doppler showing high resistance index

- Act by inhibition of endothelial cell activation

Front 13

Treatment of Mild PE ?

Back 13

A) Mild PE :

- Full term = 37 Weeks or more

Delivery by induction of labour or CS

- Preterm < 37 Weeks

Expectant managment till fetal lung maturity is reassured

1- Rest Mental + Physical "Bed rest Lt lateral"

2- Diet PTN rich diet + Salt restriction

3- AntiHTN No documented benefit

alpha methyl dopa : 250 mg t.d.s

4- Close follow up :

Maternal

- Warning Symptoms

- Warning Signs : BP + Hyperreflexia at joints

- Labs. : Urinary protein & output + Serum uric acid + LFT + Daily maternal weight

Fetal

DFMC / NST / BPPS / Doppler US for umblical & cerebral arteries

5- Outpatient managment

For mild cases , twice weekly follow up visits till fetal lung maturity achieved or spontaneous labour pains start

6- Hospitalization

If rapid prog. deterioration or development of complications = immediate termination

7- Termination

VD : Whether spontaneous or induced

allowed with strict fetal surveillance with Continuous Electronic FHRM

CS : Is prefered

Front 14

Treatment of Severe PE ?

Back 14

A) Urgent adequate control by :

1- Hospitalization

2- Antihypertensive drugs :

Must be given by Parentral route to reduce maternal risk of cerebrovascular accident which is important cause of maternal mortality

- Hydralazine

- Direct VD

- 5 mg IV "Diluted by glucose 1:1" then 5 mg every 20 Mins till diastole is 100 mmHg.

- SE : tachycardia / flushing / headache

- Labetalol

- Combined alpha & beta adrenergic blocker = decreases BP by decreasing HR & contractility

- 10-20 mg IV repeated every 10 mins

- SE : Less than hydralazine

- Nifedipine

- Ca channel blocker

- 10 mg orally repeated in 4-8 hours

- SE : Better not used with Mg sulphate

3- Prophylactic anticonvulsants :

Magnesium Sulphate

to prevent developing convulsions in severe PE before termination

NB :

- Diuretics :

Contraindicated except in HF / Acute PE as they worsen hemoconcentration & predispose thrombosis

- Corticosteroids :

In cases of PTL to decrease risks of neonatal RDS or Tx of cases complicated with HELLP

B) Immediate delivery :

Mode of delivery depend on urgency of termination & ripeness of cervix.

1- Vaginal Delivery

- If favorable conditions for safe well monitored VD

- By INDUCTION OF LABOUR :

By : IV Oxytocin infusion

or Vaginal PGs "with or without amniotomy"

Prerequisites : Favourable conditions :

Cervix : Soft - Ripe - Effaced

Pelvis : adequate

Precautions :

- CEFHRM

- Adequate control of BP & Pain relief

- Avoid difficult prolonged labour & Shortening 2nd stage of labour

- Avoid PP ergometrin = inc. BP & VR

- Close Observation for PP eclampsia & PP Hge

2- Caesarean Section :

1- Unfavourable conditions

2- Extremely premature / LBW fetus

3- Non reassuring Ante/Intrapartum fetal surveillance tests

4- Other relative indications : PP / OHA / Prev.Scar / CP / IUGR

Front 15

Eclampsia ?

Definition

Incidence

Timing

Pathogenesis

Back 15

- Definition :

The Occurrence of Siezures / Convulsions / Fits in women with PE that cannot be attributed to any other underlying cause or pre-existing disease.

- Incidence :

1 in every 2000 deliveries

Complicate 1-2% of PE

- Timing :

A) Antepartum 65%

B) Interpartum 20%

C) Postpartum 15%

Most dangerous = denotes brain insult

- Pathogenesis :

Unknown exactly, but maybe 2ry to :

Cerebral edema & Vasospasm & Ischemia

Front 16

Clinical Picture of Eclampsia ?

Back 16

1- Premonitory stage = 0.5 Min

Twitches of face & hands + rolling up of eyes

2- Tonic stage = 0.5 Min

Genealized tonic spasm + Opisthotonus position

+ Respiratory arrest = Cyanosis

3- Dome stage = 0.5 - 1 Min

Bitten tongue + Stretous breathing

4- Coma stage

Variable according to degree of acidosis so patient may recover or fit again

NB : Death may occur due to :

Aspiration Pneumonia

Front 17

Differential Diagnosis of Eclampsia ?

Back 17

Epileptic Seizures :

1- Hx of previous fits antedating pregnancy

2- Hx of Tx with antiepileptic drugs

3- Preceded by aura of different stages

4- Not associated with HTN or Albuminuria

Front 18

Prevention of Eclampsia ?

Back 18

- Eclampsia is a preventable complication of PE through early diagnosis & proper Mx.

This can be achieved by :

- Proper antenatal care assessment & follow up

- Once PE develops it shoud be controlled & Managed

- If the disease is progressive = termination of pregnancy

- Post partum eclampsia is difficult to predict or prevent

Front 19

Treatment of Eclampsia ?

Back 19

A) Emergency 1st Aid Measures :

1- Room : Semi dark + minimal noise

2- Nursing : on side with head down

3- Airway :

Suction from mouth to avoid aspiration

Ensure free airway + Oxygen mask = Perfusion

Insert mouth gag = avoid tongue injury

4- IV line with good vein caliber & CVP monitor

5- Urinary catheter is inserted to record vol.

6- Initial IV dose of an anticonvulsant :

MgSO4 20% = 4-6 gm over 20 mins IV drip

Diazepam = 5-10 mg IV slowly

B) Control of Epileptic Fits :

1- MgSO4

Action :

- Inhibit Ms contractions by inhibition of NM transmission & decreasing Ca entry

- CNS depressant

Dose :

Loading : 4-6 gm IV infusion over 20 mins

Maintenance :

2 gm / hr by continuous IV infusion of 20% solution for 24 H

5 gm / 4 hrs by IM "buttocks" of 50% solution for 24 H " SE : convulsions or hematoma"

Theraputic serum lvl : 4-7 m.Eq/L

Precautions : before giving next dose :

- Urine output > 30 ml/hr : toxicity with oliguria

- RR > 16/min : Resp.center depression

- +ve Knee jerk : diminished if severe NMJ Inhibtion

Toxicity : Absent knee jerk / Respiratory distress / Cardiac arrest

Antidote : Ca gluconate 10% 10 ml IV slowly over 3-5 Mins

2- Diazepam :

Alternatice if MgSO4 is not available

Less effective but more safe with less toxicity

5-10 mg IV slowly

If quickly = sudden apnea + cardiac arrest

C) Control of Hypertention :

By IV Hydralazine or IV Labetalol

D) Immediate termination of pregnancy :

1- VD : by Induction of labour by IV oxytocin or Vaginal PGs in favourable conditions as :

Well controlled case + Cephalic pres. + engaged head + soft effaced cervix

2- CS : Rapid & Less traumatizing

So Safer & Better if safe anaethesia is available

E) Postpartum Care :

Continue MgSO4 for 24 hours after delivery to gaurd against postpartum fits

Front 20

Chronic HTN ?

Definition

Incidence

Types

Back 20

Definition :

Hypertension :

- Antedating pregnancy

- Detected before 20 weeks of gestation

- Persistent after 12 Weeks Postpartum

Incidence : 2-5% of all pregnancies

Types :

1- Essential = 90%

2- 2ry = 10% due to :

- Renal disease : Chronic nephritis / Renal artery stenosis

- Coarctation of aorta

- Hyperthyroidism

- Pheochromocytoma

Front 21

Chronic HTN ?

Diagnosis

Complications

Treatment

Back 21

Diagnosis :

A) Clinically = BP Measurment

- On two or more different occasions each is 6 hours apart

- in upper & lower limb

- Difficult to Diagnose in 2nd TM :

Physiological lowering of BP

B) Investigations :

For Cause :

KFTs - Thyorid FTs - Urinary VMA - Blood glucose levels

For Complications :

Fundus Examination - ECG & ECHO

* Complications :

Superimposed Pre-eclampisa :

aggregavation of HTN & appearance of proteinuria

* Treatment :

1- Rule out & Treat causes for 2ry HTN

2- Anti-hypertensive drugs :

If Diastole is 100 or more

to reduce risk of ICH & HF

3- Obstetric managment : as PE

Front 22

Diabetes Mellitus With Pregnancy ?

Definition

Incidence

Classification

Back 22

- Definition :

DM :

Chronic metabolic disorder caused by relative or absolute insulin deficiency which primarily disturbs CHO metabolism with 2ry affection of lipid & protein metabolism

Characterized by :

hyperglycemia / glucosuria / microangiopathy.

DM In pregnancy :

May cause many serious maternal & fetal complications

* Incidence : 1:350 pregnancies

* Classification :

A) Gestational DM :

DM with onset or first recognition during pregnancy

B) Established DM :

DM existing before onset of pregnancy

which may be :

Insulin Dependant = Type 1

Insulin independant = Type 2

Front 23

Effect of Pregnancy on DM ?

Back 23

A) Effect of pregnancy on DM :

- Pregnancy is diabetogenic :

Due to Increased production of insulin antagonists during pregnancy as (( hPL - Placental insulinase - Cortisone - Estrogen - Progesterone ))

- During Pregnancy the following occur :

1- Unmasking of latent DM : especially with repeated pregnancies & if the patient is predisposed

2- Established DM : becomes difficult to control due to increase in insulin requirements during pregnancy.

- After labour

Insulin Requirements decreases after delivery

The patient is at risk for hypoglycemia :

During labour : Utilization of glucose during uterine contractions

After Labour : Utilization of glucose by breasts

Front 24

Effect of DM on Pregnancy

( Complications of DM with pregnancy) ?

Back 24

A) Maternal : 8Ps

1- Pregnancy loss "Abortion"

2- Preterm labour

3- Pre-eclampsia

4- Polyhydramnios

5- Pruritis vulva "Monilial vulvovaginitis"

6- Pyelonephritis "UTI"

7- Peurperal sepsis

8- Breast infection & Deficient lactation

B) Fetal & Newborn :

1- Fetal Macrosomia :

- Oversized fetus 4.5 Kgm or more

- May occur even in prediabetic stage

- Due to :

1- Maternal & consequently fetal hyperglycemia which stimulates hyperinsulinism in fetus, Both fetal hyperglycemia & Hyperinsulinism enhance synthesis of glycogen & Fat & PTN in fetus.

2- Insulin has GH action

3- Salt & Water retention = High Cortisol

2- Fetal congenital anomalies :

- Higher incidence = 6-9%

- Risk Increases with poorly controlled DM during early pregnancy due to disturbance of 2ry yolk salk in 1st TM

- Anomalies :

Most common : VSD & Neural tube defect

Most specific : Caudal regression Syndrome "Sacral Agenesis"

3- Spontaneous abortion

Especially with poor control

4- Tendency to IUFD :

In last month, Unknown cause but maybe due to :

- Congenital anomalies

- Maternal hypoglycemia / ketosis

- PE or Placental insufficiency

5- Neonatal complications :

Infant of diabetic mother is at higher risk for neonatal morbidity & mortality due to :

- Birth trauma :

oversized with broad shoulder / premature

- Congenital anomalies

- RDS

- Neonatal Hypoglycemia :

Blood Glucose < 30 mg%

Due to increased insulin production by hypertrophied fetal pancreas

- Tendency to :

Hypocalcemia = birth hypoxia

Hyperviscosity

Hyperbillirubinemia = immature liver

NB : Uncontrolled DM :

Early Pregnancy = Congenital anomalies

Late Pregnancy = Fetal macrosomia

Front 25

Cases at high risk for DM during pregnancy ?

Back 25

1- Family history of DM

2- Age = 35 years or more

3- Gross obesity > 90 Kgm

4- Hypertension

5- Bad obstetric Hx :

- Previous unexplained intrauterine or neonatal deaths

- Previous 2 or more unexplained abortions

- Previous macrosomic babies

- Presence or history of major FCA

- Presence or history of polyhydramnios

6- Recurrent UTI / Moniliasis

Front 26

Diagnosis of DM in pregnancy ?

Back 26

1- History :

The patient is known diabetic or is at high risk for DM

2- Clinically : Symptoms suggesting DM ;

Polyuria - Polydepsia - Polyphagia - Loss of weight - Parathesia - Recurrent UTI / Pruritis vulvae

3- Investigations :

1- Fasting & 2 Hrs Postprandial blood glucose = Hyperglycemia

2- Abnormal Glucose tolerance test :

Raised FBG + Lagging GTT

A) Screening for DM during Pregnancy :

50 gm oral glucose followed by estimation of blood glucose after 1 hour :

IF < 140 mg% = Negative

> 140 mg% = Do 100 gm GTT

B) Dx of DM by GTT during Pregnancy :

- Fasting Blood glucose = 90 mg/100ml

- 100 gm oral glucose adminesteration test :

* Normal levels :

165 mg% at 1 hour / 145 mg% at 2 hours /

125 mg% at 3 hours

* If any 2 or more of these values are elevated = impaired glucose intolerance

3- Detection of complications

Front 27

Managment of DM during Pregnancy ?

Back 27

1- During Pregnancy :

A) Control DM :

1- More frequent ANC visits :

adequate follow up of maternal diabetic state & fetal wellbeing

2- Repeated blood sugar estimation :

For better control

3- Glycosylated Hemoglobin measurment: HbA1C = Glycosylayion of 1st carbon of alpha chain of hemoglobin during RBCs span

- Used as an indicator of blood glucose levels in the preceding 2-3 months

- Normally = 3-4 % of total Hb

If > 10% = poor control of DM in preceding 2-3 months

4- Diet control :

Total calories = 30-35 Kcal/kg/day

50% CHO - 30% PTN - 20% Fats

5- Insulin therapy :

* Indications :

1- All cases of established DM

2- Cases of GDMwhenever diet control aloneis not reassuring in the control of diabetes

* Dosage & Preparations :

- Insulin requirements < 50 units/day :

Single morning dose NPH/Regular insulin = 2:1

- Insulin requirement > 50 units/day :

In 2 doses :

2/3 in the morning "NPH/regular = 2:1"

1/3 in the evening "NPH/regular = 1:1"

NB : Oral Hypoglycemic

Poorly control DM during pregnancy & may have a teratogenic effect

B) Time & Mode of delivery :

- Indications of termination :

1- Evidence of placental insufficiency as

IUGR / Oligohydramnios / abnormal umblical doppler

2- Fetal lung maturity is achieved at 37 weeks

to avoid IUFD & Macrosomia

- Mode :

1- Induction of labour if favourable cervix + average fetal weight

2- CS is preferred if macrosomia or placental insufficiency

2- During labour :

40 grams of glucose "800 cc of glucose 5%"

+ 20 units of insulin to prevent ketosis

3- During Peurperium :

1- Reduction of insulin dose to prevent hypoglycemia

2- Proper antibiotic coverage to avoid peuroeral sepsis

3- If neonatal death, suppress lactation - control DM - avoid pregnancy for 1 year

4- Care of newly born infant :

- Mx of RDS : IDM is more liable to develop Hyaline membrane disease leading to RDS

- Hypoglycemia :

5% glucose IV solution given after delivery is needed to compact neonatal hypoglycemia due to overactive fetal pancreas

Front 28

Priscilla white classification of DM ?

Back 28

A = Chemical diabetes

B = Age > 20 years / Duration < 10 years

C = Age 10-19 years / Duration 10-19 years

D = Age < 10 years / Duration > 20 years / Benign retinopathy

E = Nephropathy

F = Cardiomyopathy

G = Proliferative Nephropathy

H = Diabetic after renal transplant

Front 29

Differential Dx of Jaundice in pregnancy ?

Back 29

1- Infective Hepatitis :

- Viral Hepatitis A / B / C

- May lead to : Abortion / PTL / IUFD in pregnancy

- > 50% of babies born to mothers with hepatitis B will have :

Hepatitis B surface antigens in their blood

and some will develop hepatic lesions

2- Hemolytic jaundice :

Hemolytic diseases as : Thalassemia

3- Surgical causes : Obstructive Jaundice

4- Hepatic Degeneration :

Severe HEG / Severe PIH "PE / Eclampsia"

5- Recurrent Cholestatic Jaundice of Pregnancy :

Oestrogen induced cholestasis in women unduely sensetive to estrogen or with oral contraceptive intake

6- Others :

1- Mismatched blood transfusion

2- Infection with hemolytic organisms

3- Acute fatty liver "Acute yellow atrophy"

4- Congenital Hyperbillirubinemia

Front 30

Vomiting

- Definition

- Physiology of vomiting

Back 30

Definition :

- Reflex emptying of stomach content through mouth.

- It may be preceded by sensation of nausea

- It may lead to dehydration / weight loss / electrolyte & acid base imbalance & finally organ failure that endangers life.

Physiology of Vomiting :

A) Vomiting Act :

- Reverse peristalsis empties small gut content into stomach

- Abdominal wall muscles contract to increase intra-abdominal pressure

- The gastric sphincter relaxes & gastric contents are ejected

- Breath is held at midrespiration & cricopharyngeus closes the glottis to prevent aspiration

B) Vomiting Center :

1- Vomiting Center

- In Medulla

- Acetyl choline transmitter

- Stimulated by : tickling the back of tongue / stomach distension / vesitibular stimulation

2- CTZ

- In 4th Ventricle

- Dopamine transmitter

- Stimulated by : emetics / uremia / hCG

Front 31

Emesis Gravidarum

"Simple Nausea & Vomiting of Pregnancy" ?

Incidence

Aetiology

Clinical picture

Managment

Back 31

* Incidence : 50% of PG but less in MP

* Aetiology :

Related to hCG levels but psychological conflicts & Avitaminosis "Thiamine deficiency" may worsen the condition & make it resistant.

* C/P :

Nausea & Vomiting

- Starting early in pregnancy with a peak at 7-9 weeks & ameliorate by 12 weeks of gestation

- Characters

- Mild to moderate severety

- Mostly confined to morning or related to food intake

- Doesn't affect general conditions

- Respond to treatment

* Managment :

A) Mild : No treatment , only reassurance as it is a sign of intact pregnancy

B) Moderate :

- Reassurance + Small frequent light meals

- Limited use of Antiemetics may be allowed

C) Severe :

Known as Hyperemesis gravidarum

Requires hospitalization + IV fluids + intense therapy

Front 32

Hyperemesis Gravidarum

"Pernicious Vomiting of Pregnancy " ?

Definition

Incidence

Pathogenesis "Causes"

Back 32

* Definition :

Severe nausea & vomiting in pregnancy that is :

- Not confined to morning

- Affects patient general condition

- Not responding to regular medical treatment

* Incidence :

- Affect about 1% of all pregnancies

- More common in PG

- Deaths from HEG is rare nowadays

* Pathogenesis "Causes" :

1- Neurosis theory :

Psychological conflicts play a role as evidenced by rapid improvement on isolation

2- Avitaminosis theory :

Therapy with vitamin B1 & B6 improvesmany cases of HEG

- Vitamin B1 "Thiamine"

Water soluble - Coenzyme for decarboxylases - Deficiency = HF "wet beriberi" neuritis "dry"

- Vitamin B6 "Pyridoxine"

Water soluble - NH2 carrier for De/transamination

3- Endocrine theory "Youssef Theory"

- Severity correlates with levels of hCG

- higher incidence of HEG in MFP & VM due to higher levels of hCG

- hCG have TSH action = gestational thyrotoxicosis

Front 33

Pathological changes in HEG ?

Back 33

A) Biochemical changes :

- Dehydration & Hemoconcentration

- Electrolytes imbalance :

Hyponatremia

Hypokalemia : renal loss

Hypochloremia : Depletion of chloride from urine indicates poor prognosis "Fantous test"

- Acid/Base imbalance : Metabolic alkalosis

B) Circulatory changes :

Hypovolemia & Circulatory collapse = lead to pre-renal failure

C) Metabolic changes :

- Starvation & Weight loss :

Depletion of liver glycogen = in late stages liver shows cental lobular necrosis

- Ketoacidosis : oxidation of fatty acids with production of ketone bodies

D) Wernicke's Encephalopathy :

- Degenerative changes in the brain due to thiamine deficiency

- Manifested as : Delirium / ataxia / nystagmus / Neuritis : optic nerve & 6th nerve

Late : Coma

- Dx : MRI shows petechial Hge in Wernicke's area of brain "Basal ganglia"

Front 34

Diagnosis of HEG ?

Clinical Picture

Criteria of diagnosis of HEG

Investigations

Differential Dx

Back 34

* Clinical Picture :

A) Early :

- As morning sickness but vomiting isn't confined to morning

- No signs of dehydration / Ketosis

B) Late :

Symptoms

1- Vomiting becomes :

- Frequent throuough the day

- Apart from food intake

- Bilious or nlood stained

2- Oliguria

3- Constipation

Signs

1- Weigh loss : Patient is emaciated & lethargic

2- Dehydration : dry tongue / sunken globe / loss of skin turguros

3- Hypovolemic shock : Low BP / Rapid weak pulse

4- Ketosis : Acetone odour in breath

C) End Stages :

Jaundice - Hepatorenal failure - neuritis - Delirium - Coma

* Diagnosis of HEG :

A diagnosis of exclusion as no single confirmatory test available.

Diagnosis should be based on he following :

- Vomiting starting early in pregnancy

"before 12 weeks" if after exclude other causes first.

- Rapid progressive course

- Not confined to morning

- Affects patient general condition

- Not responding to regular medical treatment

* Investigations :

A) US : Exclude VM & MFP

B) Assess General condition :

1- Blood electrolytes & ABG :

Fluids / Electrolytes / Acid-Base status

2- Urine analysis :

Oliguria / Keturia / Depleted chloride

3- Fundus examination

4- Liver & Kidney Function tests

* Differential Dx : Later

Front 35

Differential Dx of Hyperemesis Gravidarum ?

Back 35

1- MFP & VM : Excluded in every case

2- Other Pregnancy Related Causes of Vomiting :

- Severe Pre-eclampsia

- HELLP syndrome

- Acute fatty liver

- Pregnancy cholestasis

- Gestational Thyrotoxicosis

3- Other Associated Causes of Vomiting :

A) Medical :

Gastroenteritis / Pyelonephritis / Hepatitis / DKA / Uremia / Drug posioning

B) Surgical :

Appendicitis / Chloecystits / Perforated Peptic ulcer / IO

C) Gynecological :

Red degeneration of fibroid / Complicated ovarian cyst or tumor

4- Rare conditions : Brain tumors / Mismatched blood transfusion

Front 36

Management of HEG ?

Back 36

A) General :

- Hospitalization for early & aggressive treatment

- Psychological support

B) Fluid therapy :

- Normal Saline is best option

"Glucose worsens Wernicke's encephalopathy"

- Initial loading dose till urine flow exceeds 30 ml/hr then maintenance dose with observation by fluid balance chart

C) Feeding :

NPO & Total Parentral nutrition

- For severe cases at start of treatment till vomiting is controlled or ameliorated

- Method :

1- Calculate :

Daily caloric need = 30 Kcal/kgm/day &

Daily fluid needs 30ml/kgm/day

2- IV Hyperalimenation via catheter in subclavian vein

3- Fluid should contain : lipid emulsion / dextrose / aminoacids / electrolytes / Vitamins

& Should be kept in refrigerator

- Troubles of Prolonged TPN :

Line associated sepsis "Prolonged cathetrization - Circulatory troubles - Metabolic troubles

D) Medication :

1- Antiemetics :

IV / IM / Suppositories in severe cases

Oral in mild cases

- Metoclopramide "Primperan" - Class B :

Promethazine "Phenergan" - Class C :

Dopamine rec. blocker in CTZ -

SE : Extrapyramidal & Hyperprolactinemia

- Scopolamine "Hyosine" - Class B :

Acetyl choline rec. blocker in VC-

SE : Dry mouth

- Meclozine "Navidoxine" - Class B :

Histamine rec. blocker in Both VC & CTZ

SE : Sedation, Advantage : Rectally

- Ondansetron "Zofran" - Class C :

Serotonin rec. Blocker in both VC & CTZ

SE : Depression

2- Thiamine 100 mg IV diluted in saline

3- Prednisolone 40 mg/day

E) Termination of Pregnancy :

- Indication :

Last choice, rarely resorted to, only in :

Severe cases resistant to treatment with lifethreatening complications, including :

1- Drastic worsening of vital signs

2- Severe Dehydration / Anuria /Circulatory collapse with no response to IV Fluids.

3- Severly affected liver or kidney functions = Impending failure

4- Marked Fundus changes

5- Wernicke's Encephalopathy

- Method :

1- Medically indued abortion using PG E1

2- Surgical evacuation may be needed

Front 37

Significant Asymptomatic Bacturia ?

Definition

Incidince

Clinical Picture

Complications

Investigations

Treatment

Back 37

- Definition :

- Presence of 100,000 or more bacteria per ml in two freshly voided midstream specimen of urine without producing symptoms.

- The Presence of bacteria only without pus cells in the urine of pregnant women doesn't signify urinary tract infection.

NB : < 100,000 = Insignificant Asymptomatic bacturia

* Incidence :

2-10% of all pregnancies "Average = 6%"

* C/P : Asymptomatic

* Complications : Pyelonephritis

Risk increases to 25-30% of cases with untreated significant bacturia compared to 1% in patients without bacturia.

* Investigations :

1- Complete Urine analysis :

Presence of Pus Cells

2- Urine Culture & Sensetivity :

Identify Pathogenic organisms

* Treatment : The most common is E.Coli =

Ampicillin 500 mg every 8 hours for 10 days

If Recurrence in 1/3 of cases = Repeat course

If Resistant / Recurrence again give antibiotics according to culture & sensetivity

After Delivery : Resistant Recurrent cases should be offered full urological examination including Intravenous Pyelography

NB : Cause of recurrence : Stones + Anomalies

IVP in pregnancy : If indicated do 2 films only at 15 & 30 mins, each film is 0.1 rads

"Maximum is 5 rads during pregnancy"

Front 38

Acute Pyelonephritis in Pregnancy ?

Definition

Incindence

Aetiology

Back 38

* Definition :

Acute inflammation of renal pelvis & parynhema

* Incidence : 1-2% of all pregnancies

25-30% in women with Sign. Asymp.Bacturia

* Aetiology :

- PDF :

1- Significant Asymptomatic Bacturia

2- Urinary stasis by dilatation of ureter due to :

- Atony of ms by progesterone & relaxin

- Compression by enlarging gravid uterus

" It is more common in Rt Kidney due to more compression on Rt ureter due to dextro-roration of uterus in most of cases.

- Hypertrophy of wall of lower end of ureter

- Causative organism :

E.Coli is the most common

Others : Strept.fecalis / Staph / Klebsiella / Proteus

- Route :

1- Blood borne is the most common

2- Lympthatic spread : Ascending infection along periureteric lymphatics or from colon

Front 39

Diagnosis of Acute Pyelonephritis ?

Symptoms

Signs

Investifations

Differential Dx

Complications

Back 39

* Clinical Picture : ِUsually after 16 weeks

A) Symptoms :

1- High fevers & Rigors

2- Acute onset of loin pain :

Associated usually with nausea & Vomiting, Preceded by recurrent attacks of burning micturition

B) Signs :

- General : High temp + Tachycardia

- Local : Tenderness on one or both renal angle regions

* Investigations :

1- Complete Urine analysis :

- Diminished amount / acidic ph / fishy odour due to production of ammonia by E.Coli

- Contain Albumin

- Contain Pus cells > 10 per HPF

2- Urine Culture & Sensetivity

3- CBC : Leukocytosis with shift to the left in the ratio between staff/segmented RBCs

4- ESR Elevated / CRP +Ve

* Differential Dx :

1- Appendicitis :

Tender Rt Iliac fossa / Lower fever / Marked Leukocytisis / Free Urine

2- Twisted Ovarian Cyst

3- Other Causes of fever + Vomiting in pregnancy

* Complications :

1- Chronic Pyelonephritis & Renal failure : Recurrent inadequetly treated cases

2- Abortion / PTL / IUFD in severe neglected cases or IUGR / PTL in less severe cases

Front 40

Managment of Acute Pyelonephritis in Pregnancy ?

Back 40

A) General :

1- Rest / Light diet / Increase fluid intake

2- Alkalinzation of acidic urine

3- IV Fluids if there is excessive vomiting

B) Antibiotics :

Ampicillin 500 mg every 6 hours

Alternatives :

Augmentin = Amoxicillin + Clavulinic acid

Unacyn = Ampicillin + Sulbactam

then continue according to results of C&S

C) Theraputic Abortion if :

Solitary Kidney - Recurrent resistant infection

Front 41

Anemia During Pregnancy ?

Definition

Incidince

Classification

Back 41

* Definition :

- WHO : Anemia in pregnancy is

Hb concentration < 11 g/dl "7.45 m.mol/L"

Hematocrite < 33%

at any trimester of pregnancy

- CDC : Proposed a cut off point of 10.5 g/dl during 2nd TM

* Incidince :

- Commonest Medical disorder in pregnancy

- 50 % of pregnant women worldwide suffer from some degree of anemia

* Classification :

A) According to Cause :

1- Physiological Anemia of Pregnancy :

Increase in plasma volume > Increase in RBCs volume "Hemodilutional anemia"

2- Nutritional Anemia :

- Iron Deficiency Anemia :

Most common nutritional anemia in pregnancy, either due to increased iron loss or decreased absorption.

- Megaloblastic Anemia :

Vitamin B12 or Folate deficiency affects DNA replication leading to derangement of RBC's with production of abnormal RBCs precursors "Megaloblasts"

3- Hemorrhagic Anemia :

Severe recurrent blood loss as APH / GIT

4- Hemolytic Anemia :

1- Microangiopathic HA : In patients with severe PE / Eclampsia / ITTP

2- Acquired Immune HA : IgG Ab against red cell Ag found in collagen vascular diseases

3- Hemoglobinopathies : abnormal Hb as sickle cell anemia / Beta thalassemia

5- Aplastic Anemia : Rare with 30% mortality

B) According to severity :

Mild = 10 - 10.9

Moderate = 7 - 10

Severe = < 7

Decompensated = < 4

Front 42

Iron Requirements during pregnancy ?

Back 42

Basal iron requirements = 280 mg

RBCs = 570 mg

Placenta = 50 - 150 mg

Fetus = 200 - 350 mg

Blood loss at delivery = 100 - 250 mg

After deduction of Iron conserved by amenorrhea ( 240 - 480 mg )

An additional 500 - 600 mg is required during pregnancy which means

4-6 mg of absorped iron per day

Because absorped iron is only 10 % of ingested so 40-60 mg of iron should be available in diet which makes iron supplementation a necessity in all pregnancies

Front 43

Effect of Pregnancy on anemia ?

Effect of anemia on pregnancy ?

Back 43

Effect of Pregnancy on anemia :

Pregnancy will aggravate any already existing anemia

Effect of anemia on pregnancy :

A) Maternal :

Mild No effect on pregnancy or labour but mother show low iron stores

Moderate Weakness / Fatigue / Lack of energy / Poor work performance

Severe Poor pregnancy outcome as :

PE / PTL / Prolonged labour / Post partum Hge / Peurperal sepsis / Failure of lactation

B) Fetal :

- Decreased fetal iron stores

- PTL / SGA / Increased Perinatal morbidity & Mortality

Front 44

Diagnosis of Anemia in Pregnancy ?

Back 44

A) Symptoms :

1- Mild / Moderate : Asymptomatic

2- Severe :

Weakness / Exhaustion / loss of appetite

Dyspnea & Palpitations

CHF in severe cases

B) Signs :

1- Mild / Moderate : Asymptomatic

2- Severe :

Pallor

Hyperdynamic circulation + Systolic murmur

Glossitis & Stomatitis

Koilonychia

C) Investigations :

- CBC : Decreased Hb & Hct

-Serum iron : Decreased

& Serum Ferritin : < 30 ug/L "Diagnostic"

- Investigations for cause :

Hb electrophoresis / Peripheral blood smear

Front 45

Managment of Anemia with Pregnancy ?

Back 45

A) During Pregnancy :

- Prevention :

Proper ANC / Oral Iron Supplementation / Diet rich in iron & vitamin c

- Treatment :

1- Oral iron therapy : Iron gluconate
In Mid-TM or early 3rd TM = Induce vomiting

Hb rises about 0.3-1 g per week

2- Parentral iron therapy : Iron dextran

Severe anemia in late 3rd TM or Poor compliance for oral therapy

3- Packed RBCs :

Better than transfusion = avoid overload

Severe anemia beyond 36 weeks / associated infections / Compensation of APH

B) During Labour :

1st stage : Oxygen if dyspnea + Pro.Antibiotic

2nd stage : Shortened to avoid exhaustion

3rd stage : Active management except in very severe anemia for fear of cardiac failure + Prompt managment of PP Hge

C) During Peurperium :

1- Adequate rest

2- Continue iron & folate therapy for at least 3 months

3- Any infecion is promptly treated

Front 46

Cardiac disease with Pregnancy ?

Incidence

Aetiology

Classification

Back 46

- Incidence : 0.5 - 1% of pregnancies

- Aetiology :

Most Common in developping countries is Rheumatic heard disease mostly "MS"

In developped countries CHD is more common

- NYHA grading "Assessment of cardiac disease " :

Class 1 organic heart disease without limitation of house hold activities

Class 2 Limitation "dyspnea-chest pain" at ordinary house duties / at end of stairs

Class 3 Limitation of activity at less than ordinary house duties / during climbing stairs

Class 4 Dyspnea at rest

NB : Prgnancy worsen the condition by one grade

1&2 = compensated / 3&4 = Uncompensated

Front 47

Changes in

( COP - Heart rate & Pulse - Apex beat variation - ECG ) with pregnancy ?

Back 47

A) COP :

Increase gradually from 1st TM till reaching a peak of 40% increase above non-pregnant woman by 20 weeks & remain constant till full term, due to :

1- Increase SV by 40-50%

2- Incease pulse rate by 10-12 BPM

B) Heart rate & Pulse :

- Tachycardia

- Occasional extrasystole

- Water hammer pulse "Increased Sys - Dia"

- Obvious capillary pulsation "nail bed"

C) Apex beat variation :

- Shift of apex up to 4th IC + laterally one inch

- Soft systolic murmur

- Split of 1st sound = Mitral closes earlier

- Appearance of loud 3rd sound

D) ECG :

- Left axis deviation

- Deep Q in lead 3

- Flat T & Inverted ST in V2-V4

Front 48

Factors affecting maternal cardiac condition ?

Back 48

1- History of recent reactivation of rheumatic fever

2- Associated cardiomyopathy & tight mitral stenosis

3- Associated Anemia

4- Infections : UTI & Dental caries = SAIE

5- Hypertensive disorders / Thyrotoxicosis in pregnancy

Front 49

Management of cardiac diseases with pregnancy ?

Back 49

A) During Pregnancy :

1- ANC :

- More frequent

- Attended by both obstetrician & cardiologist

- Examination :

1- Obstetric : maternal & fetal condition

2- Cardiac assessment & early detection of HF

3- Detection of Risk factors
( Anemia / Infections / HTN )

- Advice :

1- Rest : 9H by night + 2 by day "Semi-setting"

2- Diet : Salt restriction

2- Gaurd against risk factors :

Weight gain / HTN / Anemia / Infections = SAIE

by dental care + Antibiotics before procedures

2- Indications for Digitalis :

- Already on it before pregnancy

- Class II or more or Impending HF

3- Indication for hospitalization :

- Class II : at 24-32 weeks & 1 week before EDD

- Class III & IV : earlier & longer periods

B) During Labour :

- Proper pain relief : minimize anxiety & tachycardia

NO Epidural in Rt-Lt shunt = Hypotension

- No straining : minimze tachycardia & Inc. VR

- Delivery :

VD in semisetting position + adequate O2

CS if obstetrically indicated

- Digitalis : if high risk for HF

- Antibiotics : gaurd from SBE

C) In Peurperium :

High risk for HF due to : Increased VR due to

reduced pressure on IVC + Mobilization of ECF

1- Monitoring : 2 weeks till COP normalization

2- Breast feeding : only CI if HF

3- Proper contraception : adequate spacing

D) Termination of pregnancy :

- Now : Only cases with pulmonary HTN or Rt to Lt shunt

- Past : Class III & IV / Hx of HF in prev.pregnancy / Reactivation of RF

But not encouraged now due to recent surgical treatments abailable & Proper medical control.

Front 50

Rhesus Factor ?

Back 50

- It is a complex antigent which is a lipoprotein component of RBCs membrane.

- Consists of 3 pairs of genes Cc / Dd / Ee

The most important is D = Common

C & E May cause incompitablity but are rare

- D gene is dominant over d so :

Rh +ve = DD & Dd = 85%

Rh -ve = dd = 15%

Front 51

Erythroblastosis Fetalis

"Hemolytic Disease of newborn " ?

Definition

Aetiology

Back 51

- Definition :

- Immunologic disorder charecterized by excessive hemolysis of fetal RBCs by antibodies that pass through the placenta from maternal blood.

- It occurs due to RH allo-immunization & is an important cause of neonatal morbidity & mortality.

- Aetiology :

Formation of anti-Rh antibodies in an RH-negative female following :

1- Blood transfusion with Rh-positive blood immune system responds by production of antibodies against the D antigen.

2- Pregnancy with an Rh-positive baby

Fetomaternal hge ( passage of fetal RBCs to maternal circulation ) may occur at :

Time of delivery "3rd stage" / Abortion / Disturbance of an ectopic / APH / Amniocentesis / ECV

The immune system produces antibodies against RH +ve antigens.

Front 52

Incidence of Erythroplastosis fetalis ?

Back 52

Rh +ve : 85% of caucasians

Rh -ve : 15% of caucasians

Erythroblastosis fetalis : Only less than 1% :

1- Rh -ve female married to Rh -ve male

2- Rh -ve female married to heterozygous Rh +ve male will have 50% chance of having RH -ve baby

3- ABO incompitability between mother & fetus : destruction of fetal RBCs in maternal circulation before they induce antibody response

4- Immunological variation in response to Rh +ve Ag : Some Rh -ve females are Non / Poor responders.

5- 1st baby is unaffected :

1st exposure = IgM immune response "Large doesn't cross the placenta"

But on following exposures = IgG immune response "Cross placenta affecting fetus"

1st baby maybe affected only if previous sensitization by blood transfusion or previous abortion,

Front 53

Clinical Picture of Erythroblastosis fetalis ?

Back 53

Passage of anti-Rh antibodies from maternal into fetal circulation leads to hemolysis of fetal Rh +ve RBCs, Clincal types depend on degree of hemolysis :

A) Congenital Hemolytic Anemia : Mildest

- Fetal Hemolytic anemia : develops after 2 weeks of birth

- Erythroblastosis : Increased production of immature nucluated RBCs "Erythroblasts" due to faster rate of erythropoiesis

B) Icterus Gravis Neonatorum : Commonest

- Fetal Hemoltic anemia : At birth

- Jaundice :

- Never at birth as placenta transfers unconjugated billirubin from fetal circulation to be conjugated by liver of mother.

- Develops within 48 H after birth due to inability of fetal liver to conjugate high amount of billirubin produced by RBCs hemolysis

- HSM : Inc. Extramedullary hematopoiesis

- Kernicterus :

When fetal billrubin exceeds 20 mg%

it crosses brain barrier & become deposited in basal ganglia of brain stem = serious condition causing neonatal death irreversible brain damage & Mental retardation

C) Hydrops Fetalis : Severest

- IUFD : Severe hemolysis = Anemic HF

- If born alive : death within few hours

The fetus : accumulated fluid in body cavities

Generalized edema / pleural effusion / ascites due heart failure + Hepatosplenomegaly

The Placenta : Large & edematous

US during pregnancy : Buddha attitude

Flexion of thigh / Abdominal distension / halo around skull = scalp edema

Diff.Dx : Parvo B19 / Organ failure : HF / RF / LF

Front 54

Diagnosis of Erythroblastosis fetalis ?

Back 54

A) During Pregnancy :

- 1st ANC visit :

All pregnant females should be checked for RH group, if -ve :

Ask about previous blood transfusion , previous fetal anemia / neonatal jaundice / IUFD

Test Husband for RH group , if +ve :

1- Indirect Coomb's test :

Detect presence & titre of Anti-D IgG in maternal blood :

> 1/16 : Amniocentesis is indicated

< 1/16 : Repeat every 4 weeks

2- Amniocentesis :

Detect amount of billirubin in amniotic fluid by spectrophotometry which reflects degree of hemolysis of fetal blood.

3- US : May show HSM / generalized edema / Buddha attitude

B) After Labour :

Cordocentesis : Cord is clamped at 20 cm & cord blood is obtained & tested for :

- Rh group : If +ve procede with the following

- Hb : Detect fetal anemia "N = 18 gm%"

- Serum billirubin : Detect jaundice "N = 2mg"

- Direct Coomb's test : Detect antibodies adsorbed to RBCs in fetal circulation.

Front 55

Managmenet of Erythroblastosis Fetalis ?

Back 55

A) Prophylaxis :

1- Never tranfuse Rh +ve blood to Rh -ve femal

2-Anti-D Immunoglobulins :

To all non-sensitized "Indirect Coombs -ve "

Rh -ve females married to Rh +ve males in the following conditions :

- After delivery of Rh +ve baby to destroy fetal RBCs before they induce maternal response

( 300 mcg Anti-D IM within 72 H of delivery )

- At time of Abortion / Disturbed ectopic / APH / Amniocentesis / Version : prevent sensitization during pregnancy

( 50-100 mcg Anti-D IM )

- If Rh +ve blood transfusion ( 300 mcg per 100 ml blood )

- Recently, Routinely at 28 weeks of pregnancy ( 300 mcg Anti D IM )

NB : Prophylaxis is contraindicated if :

Already sensitized ( Coombs +ve ) or have a previously affected baby

B) Managment during pregnancy :

1- IU Blood transfusion :

- Indications : severly affected fetus before 34 Weeks of gestation

- Method : Injection of RH -ve group O blood into the peritoneal cavity or umblical vein of fetus under LA & US guidance

2- Termination of pregnancy :

- Indications : Severly affected fetus after 34 weeks of gestation

- Method : Induction of labour or CS if indicated but only after lung maturity is demonstrated by L/S ratio

C) Neonatal managment :

Exchange Transfusion :

10-20 ml of blood are withdrawn from umblical vein & replaced with the same amount of Rh -ve group O antibodies & repeated till 80-90% of blood is replaced to Remove Ag & Ab + Corrcet anemia & jaundice

Front 56

Venousthrombosis in pregnancy ?

Incidence

Etiology

Back 56

- Incidence :

- 0.5-3 of every 1000 pregnancies are complicated by symptomatic DVT = 5 fold risk over the non-pregnant female.

- If untreated 25% may develop pulmonary embolism

- PE is fatal in 15% of cases

- Etiology :

Pregnancy is Hypercoaguable state due to the following changes of thrombotic & fibrinolytic activities :

1- Increased Coagulation factors 7 / 8 / 9 / 10

2- Increased fibrinogen levels

3- Increased platlet activation

4- Decreased PTN-S & Antithrombin III
5- Venous stasis in lower limb due to pressure by gravid uterus

Front 57

Thrombophilias ?

Back 57

Tendency to thrombosis due to acuired / inherited disorders of coagulation & fibrinolytic systems.
A) Acquired :

- Mostly Antiphospholipid syndrome :
Lupus anticoagulant +/- anticardiolipin Ab +/- other autoantibodies as SLE

- Causing thrombosis & recurrent abortion

B) Inherited : Protein S & C & Antithrombin III deficiency

Front 58

Risk factor for DVT & PE during pregnancy ?

Back 58

1- Age : above 35 = atherosclerosis

2- Weight : Prepregnancy > 80 kgm

3- Previous DVT : Hypercoaguability

4- Pre-existing Thrombophilia : Hyper

5- Severe PE : Hemoconcentration

6- Severe Varicose veins : Stasis + Phleboitis

7- MFP :

8- Prolonged bed rest

9- Pelvic surgery :

10- Sepsis esp. pelvic :

Front 59

Diagnosis of Deep Venous Thrombosis ?

Back 59

Symptoms :

Painful calf muscles with unilateral redness / hotness / swelling "Edema"

Signs :

- Unilateral tenderness / edema / redness / hotness

- Pressure on sole of the leg during extension = severe pain in calf muscles

Investigations :

1- Colour doppler US :

- Allow assessment of deep veins between knee & Iliac veins & dynamic assessment of femoral & illiac veins

- Prefered first line for a suspected DVT during pregnancy accurate & non-invasive

2- Venography :

- Allow excellent visualization of veins above & below the knee

- Invasive procedure requiring injection of a contrast medium & use of x-ray = not prefered

Front 60

Managment of Deep venous thrombosis ?

Back 60

A) Prophylactic anticoagulant :

1- History of DVT during or following a previous pregnancy :

Prophylactic LMW Heparin in subsequent pregnancies at least in the last trimester till the end of peurperium

2- History of DVT in non pregnant state :

- Screen for thrombophilias

- Anticoagulant prophylaxis starting from 2nd Trimester

3- History of Artificial valve / APS with recurrent DVT / previous Pul.Embolism :

Full anticoagulation throughout pregnancy

B) Managment :

1- Suspected Cases :

Anticoagulant therapy is started immediately with heparin / LMW heparin in treatment doses till Dx is confirmed

2- Established Cases :

- Complete rest & immobilization for the 1st 24 hours

- Avoid dehydration by oral fluid intake / IV fluid infusion

- Continuation of already started anticoagulant theapy with maintenance doses

NB : + Discuss Anticoagulants

Front 61

Anticoagulant therapy in pregnancy ?

Back 61

A) Heparin & LMW heparin derivatives

( Calcium Heparin ) :

Advantage :

1- Don't cross placent " Not Teratogenic"

2- Short action = stopped within hours

used safely before & after delivery without increaseing risk of hge

Action : Prolongs APTT+Decrease Factor X act.

Side effects :

1- Daily Repeated S.C injection

2- If prolonged > 6 months : Idiosyncrasy - Thrombocytopenia - Osteoporosis

B) Oral Anticoagulants :

Advantage : Drug of choice

1- Convenient for long term use : easily monitored & adjusted by INR

2- Safe during lactation

Action : Prolongs PT

Side effects :

Cross placenta "Teratogenic" Causing

- Limb & face defects in 1st TM

- Fetal ICH in 3rd TM

NB : Recently Some centers use

Heparin derivative in 1st trimester

Oral anticoagulants in 2nd trimester

Heparin derivativrs in 3rd trimester to be stopped only few hours during delivery / CS

Front 62

Pulmonary embolism ?

Cause

C/P

Managment

Back 62

* Cause :

Undiagnosed or improperly managed DVT :

already formed thrombus in LL or Pelvic vein fragments & small emboli will travel through venous circulation to be entrapped in lungs.

* C/P :

- Hx : Recent DVT or Prescence of clinical evidence of pelvic / lower limb DVT

- Symptoms :

Mild breathlessness

Inspiratory chest pain

- Signs :

Tachycardia / Hyopxia / Pleural rub / ECG changes

* Mx :

- Suspected Cases :

Full IV heparinization + Supportive O2 therapy

- Definitive Dx :

V/Q scan or pulmonary angiography

If +ve = longterm anticoagulation