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180 Cards in this Set

  • Front
  • Back
Umbilical vessels
2 Arteries
1 Vein

1/3 of babies with a single uterine artery will have another anomaly.
What is the placenta
Discoid mass composed of fetal (chorion frondosum) and maternal (decidua basalis) tissues divided by fissures into cotelydones (lobules) on the uterine side.
Pregnancy history of a woman (acronym)
GTPAL (GTPAV in french)

G : gravidity (twins = 1 pregnancy)
T : Term infants
A : Abortions
P : Premature infants
L : number of living infants
T1 : 0-12 weeks
T2 : 12-28 weeks
T3 : 28-40 weeks
Physical signs of pregnancy
Goodell's sign : softening of the cervix (4-6 weeks)

Chadwick's sign : bluish discoloration of the cervix and vagina due to pelvic vasculature engorgement (6 weeks)

Hegar's sign : softening of the cervical isthmus (6-8 weeks)

Uterine enlargment
Goodell's sign
softening of the cervix (4-6 weeks)
Chadwick's sign
bluish discoloration of the cervix and vagina due to pelvic vasculature engorgement (6 weeks)
Hegar's sign
softening of the cervical isthmus (6-8 weeks)
Investigations for pregnancy
- Peptide hormone composed of alpha and beta subunits produced by placental trophoblastic cells (maintains the corpus luteum during pregnancy)
- Positive in serum 9 days post-conception, positive in urine 28 days after last menstrual period
- Plasma levels double every 1-2 days, peak at 8-10 weeks, then fall to a plateau until delivery
+ Levels less than expected by dates suggest ectopic pregnancy, abortion or wrong date
+ Levels higher than expected suggest multiple gestation, mole, trisomy 21 or wrong dates

- Transvaginal
5 weeks : gestational sac visible (b-hcg >1200-1500)
6 weeks : fetal pole seen
7-8 weeks : fetal heart tones visible
- Transabdominal
6-8 weeks : intrauterine pregnancy visible (b-hcg > 6500)
B-Hcg rule of 10's
10 IU at time of misses menses
100 000 IU at 10 weeks
10 000 IU at term
Physiologic skin changes in pregnancy
- Increased pigmentation of perineum and areola
- Chloasma : pigmentation under eyes and on bridge of nose
- Linea nigra : midline abdominal pigmentation
- Hyperestrogenism : spider angioma, palmar erythema
- Striae gravidarum due to connective tissue changes
Physiologic cardiovascular changes in pregnancy
- Hyperdynamic circulation
- Increased CO, HR and blood volume
- Decreased BP due to decreased PVR
- Enlarging uterus compresses IVC and pelvic veins
- Decreased venous return leads to risk of hypotension
- Increased venous pressure leads to risk of varicose veins, hemorrhoids leg edema
Physiologic hematologic changes in pregnancy
- Hemodilution causes physiologic anemia and apparent decrease in Hb and Hte
- Increased leucocyte count but impaired function leads to improvement in autoimmune disease
- Gestational thrombocytopenia : mild and asymptomatic (platelets > 70 000), normalizes within 2-12 weeks following delivery
- Hypercoagulable state : increased risk of DVT and PE but also decreased bleeding at delivery
- Resetting of the osmostat under the influence of beta-hcg leads to non pathological hyponatremia in pregnancy
Physiologic respiratory changes in pregnancy
- Increased incidence of nasal congestion and epistaxis
- Increased O2 consumption to meet increased metabolic requirements
- Elevated diaphragm i.e. patient appears more "barrel-chested"
- Increased minute ventilation leads to decreased CO2 with a resulting mild respiratory alkalosis that helps CO2 diffuse across the placenta and be eliminated from the fetus
- No change in VC and FEV1
- Decreased TLC, FRC and RV
Physiologic GI changes in pregnancy
- GERD due to increased intra-abdominal pressure and progesterone (causing decreased sphincter tone and delayed gastric emptying)
- Increased gallstones due to progesterone causing inreased gallbladder stasis
- Constipation and hemorrhoids due to progesterone causing decreased GI motility
- Atypical appendicitis presentation due to displacement of appendix
Physiologic GU changes in pregnancy
- Increased urinary frequency due to increased total urinary output
- Increased incidence of UTI and pyelonephritis due to urinary stasis
- Glycosuria can be physiologic, must test for gestational diabetes mellitus
- Ureters and renal pelvis dilation due to progesterone induced smooth muscle relaxation and uterine enlargement
- Increased CO and thus increased GFR leads to decreased creatinine (normal in pregnancy : 35-44 mmol/L), uric acid and BUN.
Physiologic neurologic changes in pregnancy
Increased incidence of carpal tunnel syndrome and Bell's palsy
Physiologic endocrine changes in pregnancy
Thyroid : moderate enlargement and increased basal metabolism
- increased total thyroxine and TBG
- free thyroxine index and TSH levels are normal
Adrenal : maternal cortisol rises throughout pregnancy (total and free)
Calcium : decreased total maternal Ca due to decreased albumin
- free ionized calcium proportion remains the same due to PTH
- increased bone turnover but no loss of bone density because estrogen inhibits resorption
Foods rich in folic acid
Chick peas, asparagus, broccoli, peas, Brussels sprouts, corn and oranges
Folic acid supplementation
Encourage acid folic supplementation 8-12 weeks preconception to prevent neural tube defects
- 0.4 to 1 mg in all women
- 5 mg if past neural tube defect, anti-epileptic medication, diabetes mellitus or BMI > 35

Continue for first trimester of pregnancy
When to give 5 mg of folic acid supplementation
8-12 weeks preconception to women with :
- past NTD
- anti-epileptic medication
- diabetes mellitus
- BMI > 35
Neagle's Rule
1st day of LMP + 7 days - 3 months
Initial prenatal visit

- when
- what
Physical exam
- complete exam to obtain baseline
- BP and weight important for interpreting subsequent changes
- Pelvic exam

- bloodwork : CBC, blood group and type, Rh antibodies, infection screening as per preconception counselling
- Urine R&M, C&S : bacteriuria and proteinuria
- Pelvic exam
+ Pap smear, culture for N. gonorrhea and C. Trachomatis
+ Bacterial vaginosis swab

Verify in gynecology book or uptodate
Contraindications to exercise in pregnancy (absolute and relative)
Absolute contraindications
- ruptured membranes
- preterm labour
- hypertensive disorders of pregnancy
- incompetent cervix
- multiple gestation (>3)
- Placenta previa after 28th week
- Persistsent 2nd or 3rd trimester bleeding
- Unontrolled type I diabetes
- Thyroid disease
- Other serious disease

Relative contraindications
- previous spontaneous abortion
- previous preterm birth
- mild/moderate cardiovascular or respiratory disorder
- anemia <100
- malnutrition or eating disorders
Increase in caloric intake during each trimester
T1 : 100 cal/day
T2 : 300 cal/day
T4 : 450 cal/day
Nutritional advice during pregnancy
3-4 servings of milk products daily
daily caloric intake increase of 100 cal/d (T1) 300 cal/d (T2) 450 cal/d (T3)

Daily multivitamins should be continued in T2 for women who do not consume an adequate diet
- Iron is the only supplement for which requirements during pregnancy cannot be met by diet alone

Nutrients important during pregnancy
- Folate : 0.4-5mg per day
- Calcium : 1200-1500 mg per day
- Vitamin D : 200 IU per day
- Iron : 0.8 mg/d in T1 4-5 mg/d in T2 and > 6 mg/d in T3
- Essential fatty acids
Weight gain in pregnancy
Optimal gain depends on pre-pregnancy weight
- BMI < 19 : 13-18 kgs
- BMI 19-25 : 11-16 Kgs
- BMI > 25 : 7 to 11 Kgs

General rule :
- 1-3.5 kg in T1, then 0.45 KG/week until delivery
Sexual intercourse in pregnancy
May continue except in patients at risk for for abortion, preterm labour or placenta previa.

Breast stimulation may induce uterine activity and is discouraged in high risk patients near term.
Uterine heights in pregnancy
12 weeks : pubic symphysis
16 weeks : mid-way umbilicus
20 weeks : umbilicus
1 cm each week afterwards
Timing for prenatal visits
Q4-6 weeks until 28 weeks, Q2 weeks from 28 to 36 weeks and q weekly from 36 weeks until delivery
Leopold's maneuvers
First maneuver : to determine which fetal part is lying furthest away from the pelvic inlet
- palpate upper abdomen with both hands; the consistency, mobility and shape of the form palpated is noted
- head : moves independently of the trunk, is round and firm
- buttocks : moves with the trunk , is softer has bony processes

Second maneuver : to determine the location of the fetal back
- one hand remains steady on a side of the abdomen while the other hand palpates the other side
- the fetal back will feel smooth, while the limbs will feel like protrusions

Third maneuver (Pawlick's Grip) : to determine which fetal part is lying above the pelvic inlet
- palpate the lower abdomen with thumb and fingers
- should validate findings from the first maneuver

Fourth maneuver : to locate the fetal brow
- examiner faces patient's feet
- brow is located on the side when there is greatest resistance when fingers are moved down the side of the uterus towards the symphysis pubis
- fetal head flexed : brow and back on opposite side
- fetal head extended : brow and back on the same side
Differential diagnosis of decreased fetal movements
Death of fetus
Amniotic fluid decreased
Sleep cycle of fetus
Hunger / thirst

Decreased fetal movements = <6 movements / 2 hours
When are fetal movements first noticed?
18-20 weeks in primigravidas. Can occur 1-2 weeks earlier in multigravidas.
What is a non stress test?
Fetal heart rate tracing using an external Doppler to assess FHR and its relationship to fetal movement
Indication of non stress test
Any suggestion of uteroplacental insuffisiency or suspected fetal disease
Interpretation of non stress test
- Reassuring NST : at least 2 accelerations of FHR >15 BPM from the baseline lasting >15 s. in 20 min

- Non reassuring NST : < 2 accelerations in 40 min
+ If no observed accelerations or fetal movement in the first 20 minutes, stimulate fetus (fundal pressure, acoustic/vibratory stimulation) and continue monitoring for 30 minutes
+ if NST non reactive, then perform biophysical profile
What is a biophysical profile?

- Indications
- Interpretation
- Soring
It consists of a 30 minutes U/S assessment of the fetus +/- NST

BPP is the best choice for :
- non reassuring NST
- post-term pregnancy
- decreased fetal movement
- any other suggestion of fetal distress or uteroplacental insuffisiency

Scoring of BPP

1) Amniotic fluid volume
+ fluid pocket of 2 cm in 2 axes : 2 points
+ oligohydramnios : 0 points
2) Breathing
+ at least one episode of breathing lasting at least 30 seconds : 2 points
+ no breathing : 0 points
3) Limb movement
+ Three discrete movements : 2 points
+ two or less : 0 points
4) Fetal tone
+ At least one episode of limb extension followed by flexion : 2 points
+ no movement : 0 points

- 8 points : perinatal mortality rate 1:1000, repeat BPP as clinically indicated
- 6 points : perinatal mortality rate 31:1000, repeat BPP in 24 hours
- 0-4 points : perinatal mortality rate 200:1000; deliver fetus if benefits of delivery > risks
Differential diagnosis of increased maternal serum AFP
Incorrect GA
> 1 fetus
Fetal demise
Abdominal wall defects (e.g. omphalocele)
Differential diagnosis of decreased maternal serum AFP
Incorrect GA
Gestational trophoblastic neoplasia
Missed abortion
Chromosomal anomalies
Maternal DMI/DMII
First trimester screening (FTS)
11-14 weeks

- Nuchal translucency on U/S
- Beta-Hcg
- Pregnancy associated plasma protein A (PAPP-A)

Risk estimate for :
- Down syndrome : increased NT, increased AFP, decreased PAPP-A

Useful where patient wants results within the first trimester
More accurate estimate of Down syndrome risk than MSS, (Sn 85%)
5% false positive rate

Patients with positive screen should be offered CVS or amniocentesis
Maternal serum screening (MSS)
15-18 weeks

- Maternal serum AFP
- Beta-Hcg
- Unconjugated estrogen (estriol or uE3)

Risk estimate for :
- Open neural tube defect (oNTD) : increased MSAFP
- Trisomy 21 : decreased MSAFP, increased B-HCG, decreased uE3
- Trisomy 18 : decreased MSAFP, decreased B-HCG, decreased uE3

Only offered alone if patient missed the time window for IPS or FTS

8% of baseline false positive rate for t21, lower for oNTD and t18

Patients with positive screen should be offered U/S or amniocentesis.
Integrated Prenatal Screenin (IPS)
Nuchal translucency on 12 week U/S
FTS at 11-14 weeks
MSS + inhibin A at 15-18 weeks

Risk estimate for oNTD, T21, T18

Sn 85-90%
2% False positive rate

Patients with positive screen should be offered U/S and/or amniocentesis
Sensitization routes for Rh negative mothers
- Incompatible blood transfusions
- Previous fetal-maternal transplacental hemorrhage
- Invasive procedures in pregnancy
- Any type of abortion
- Labour and delivery
Overall risk of isoimmunization of an Rh negative mother
16% in total
- 2% antepartum
- 7% within 6 months of delivery
- 7% in the second pregnancy
Investigations for Rh isoimmunization
Routine screening at first visit for blood group, Rh status and antibodies are measured by the indirect Coombs test.

If Rh Positive with antibodies present, the severity of fetal anemia is determined primarily by antibody concentration
- Ab titres <1:16 considered benign
- Ab titres >1:16 necessitates amniocentesis to determine severity of fetal anemia (which correlates with the amount of biliary pigment in amniotic fluid from 27 weeks +)

** A positive titre means that the fetus is at risk of hemolytic anemia, not that it has occured or will developp

**** Kleihauer-Betke test used to determine extent of fetomaternal hemorrhage

Detailed U/S for hydrops fetalis
Rh negative mother prophylaxis
Exogenous Rh IgG (RhoGam or WinRho) binds to Rh Ag of fetal cells and prevents it from contacting maternal immune system.

RhoGam given to all Rh negative women in the following scenarios :
- routinely at 28 weeks GA (provides protection for 12 weeks)
- within 72 hours of the birth of an Rh positive fetus
- with a positive Kleihauer-Betke test
- with any invasive procedure in pregnancy
- in ectopic pregnancy
- with miscarriage or therapeutic abortion (only 50 ug requried)
- with an antepartum hemorrhage)

If mother Rh negative and Ab screen positive, follow mother monthly Ab titres throughout pregnancy +/- serial amniocentesis as needed (RhoGam has no benefits)
Risk factors for neural tube defects
- family history of NTD
- cosanguinity
- chromosomal (t13, t18, t21)

- Caucasians > africans

Insufficient vitamins : zinc and folate

Maternal chronic disease : diabetes

Maternal use of antiepileptic drugs
Hydrops fetalis definition and classification
Abnormal edema in 2 or more fetal compartments
- ascites
- pericardial effusion

Classified as immune (isoimmunization) or non immune (caused by many different end-stage fetal diseases)
Complications of isoimmunization
Hemolytic anemia
Erythroblastosis fetalis
Hydrops fetalis
Group B streptococcus screen
- risk factors
- clinical features
- investigations
- treatment
15-40% vaginal carrier state

Risk factors
- GBS bacteriuria during current pregnancy
- previous infant with invasive GBS infection ++++++++
- preterm labour < 37 weeks
- amniotic membrane rupture > 18 hours
- intrapartum maternal termperature > 38 ++++++++++
- positive GBS screen during current pregnancy

Clinical features
- not harmful to mother
- danger of vertical transmission (neonatal sepsis, meningitis or pneumonia)

- screening of all women at 35-37 weeks with vaginal and anorectal swabs for C&S

- Indications for ATB prophylaxis : positive GBS screen or GBS status unknown + 1 RF
- ATB for GBS prophylaxis (at least 4 hours pre delivery)
+ Penicillin G 5 million U IV then 2.5 million U IV Q4H until delivery
+ PCN allergic but not at risk of anaphylaxis - cefazolin 2 g IV then 1 g Q8H
+ PCN allergic and at risk of anaphylaxis - Clindamycine 900 mg IV Q8H or erythromycin 500 mg IV Q6H

- If fever, broad spectrum ATB indicated
Indications for chromosomal screening
Maternal age > 35

Risk factors in current pregnancy
- teratogen exposure
- abnormal U/S
- abnormal prenatal screen (FTS, MSS, IPS)

Past history / family history of :
- previous pregnancy with chromosomal anomaly or genetic disease
- either parent a know carrier of genetic disorder or balanced translocation
- family history of chromosomal anomaly, genetic disorder, birth defect or undiagnosed mental retardation
- cosanguinity
- three or more spontaneous abortions
Indications for amniocentesis
Identification of genetic anomalies (as per chromosomal screening indications)
Assessment of fetal lung maturity (T3) via the L/S ratio (Lecithin:sphingomyelin ratio)
+ if >2:1, respiratory distress syndrome is less likely to occur
Assessment of amniotic fluid bilirubin concentration in Rh isoimmunized pregnancies
Advantages and disadvantages of amniocentesis
- also screens for oNTD (acetylcholinesterase and amniotic AFP) 96% accurate
- in women > 35 years old, the risk of chromosomal anomaly (1:180) is greater than the increased risk of miscarriage from the procedure
- more accurate genetic testing than CVS

- 0.5% risk of spontaneous abortion and risk of fetal limb injury
- results take up to 14-28 days
Chorionic Villus Sampling

- Procedure
- Advantages
- Disadvantages
Biopsy of fetal derived chorion using a trans-abdominal needle or trans-cervical catheter at 10-12 weeks

- enables pregnancy to be terminated earlier than with amniocentesis
- rapid karyotyping and biochemical assay within 48 hours, including FISH analysis
- high sensitivity and specificity

- 1-2% risk of spontaneous abortion and risk of fetal limb injury
- does not screen for neural tube defects
- 1-2% incidence of genetic mosaicism (false negative rates)
How much iron is needed during pregnancy?
Mother needs 1 g of elemental iron per fetus, this amount exceeds normal stores + dietary intake
Etiology of iron deficient anemia in pregnancy
Inadequate iron intake
Decreased iron absorption (malabsorption syndrome, antacid use)
Increased losses (vaginal bleeding, other source of bleeding)
Increased requirement (fetal growth, multiple gestation)
Complications of iron deficient anemia in pregnancy
Mother : angina, CHF, infection, slower recuperation, preterm labour

Fetal : decreased oxygen carrying capacity leading to fetal distress, IUGR, low birth weight and hydrops fetalis
Management of iron deficient anemia in pregnancy
- 150 mg ferrous sulfate OD for all pregnant women in T2 and T3

If anemic
- 1 g ferrous sulfate OD
Complications of low folate during pregnancy
Neural tube defects
Epidemiology of folate deficiency anemia
Often associated with iron deficiency anemia.
Incidence varies with 0.5-2.5% depending on region, population, diet.
Prevention of folate deficiency anemia
- 0.4-1 mg folic acid PO daily for 1-3 months preconceptually and throughout T1
- 5 mg folic acid per day with past history of oNTD
Screening for gestational diabetes
28 weeks with O'Sullivan test
Risk factors for developing gestational diabetes
Age > 25
Family history of DM
Previous history of GDM
Previous child with birthweight >4.0 kg
Certain ethnicities (aboriginal, hispanic, asian, african)
Management of pre-existing diabetes in pregnancy
1. Pre-counselling
2. Pregnancy
3. Labour
4. Post-partum
1. Preconception
- Pre-plan and refer to high risk clinic
- Optimize glycemic control
- Counsel patient : potential risks and complications
- Evaluate for diabetic retinopathy, neuropathy, coronary artery disease

2. Pregnancy
- If already on medication, generally switch to insulin therapy; continuing glyburide or metformin controverial
+ Other oral hypoglycemiants are not studied
- Tight glycemic control
+ Diet management first line therapy
+ If blood glucose not well controlled, initiate insulin therapy
+ Insulin dosage may need to be adjusted in T2 due to increased demand and increased insulin resistance
- Monitor as for normal pregnancy plus initial 24 hour urine protein and creatinine clearance, retinal exam, HbA1C
+ if HbA1C > 140% of prepregnancy value associated with increased risk of spontaneous abortion and congenital malformations
- Increased fetal surveillance

3. Labour
- must consider size of baby for time of delivery
- can wait for spontaneous labour if glucose well controlled and BPP normal
- Induce by 40 weeks
- Type of delivery
+ increased risk of cephalopelvic disproportion (CPD) and shoulder dystocia with babies > 4000 g
+ elective C/S for predicted birth weight > 4500 g (controversial)
- Monitoring
+ during labour, monitor blood sugars Q1H with patient on insulin and dextrose drip
+ aim for blood sugar between 3.5 to 6.5 mmol/L to reduce the risk of neonatal hypoglycemia

4. Postpartum
- Insulin requirements dramatically drop with the expulsion of placenta
- No insulin is required for 48-72 hours postpartum in most type I DM
- Monitor glucose Q6H, restart insulin at 2/3 prepregnancy dosage when glucose > 8 mmol/L
Target blood values in pregnancy
Fasting blood glucose <5.3
1 hour post-prandial blood glucose <7.8
2 hour post-prandial blood glucose <6.7
Screening for gestational diabetes mellitus
- At 24-28 weeks
- Pregnant females age > 25 or age <25 with 1 risk factor
- 1 hour, 50 g OGTT

+ Plasma glucose < 7.8 mmol/L = no GDM
+ PG >7.8 and <10.3 = 2 hours OGTT
+ PG > 10.3 = GDM established

- Impaired glucose tolerance if
+ FPG >5.3 mmol/L
+ PG 1 hour, 75 g OGTT >10.6
+ PG 2 hour, 75 OGTT > 8.9
Management of gestational diabetes
- Treat both GDM and IGT
- Tight glycemic control optimal as in type 1 and type 2 DM
- Monitoring and timing for delivery as for type 1 and type 2 DM
- Stop insulin and diabetic diet postpartum
- Follow-up with 2 hour, 75 g OGTT 6 weeks-6months postpartum
Maternal complications of DM in pregnancy
- HTN/Pre-eclampsia (insulin resistance is implicated in etiology of HTN)
- Polyhydramnios (maternal hyperglycemia leads to fetal hyperglycemia which leads to fetal polyuria)

Diabetic emergencies
- Hypoglycemia
- Diabetic coma

End organ involvement (DM1&2 not GDM)
- Retinopathy
- Nephropathy

- Pyelonephritis/UTI (glycosuria provides a culture medium for E. Coli)
- Increased incidence of spontaneous abortions (in DM1, DM2 not GDM)
Fetal complications of DM in pregnancy
- Macrosomia (hyperinsulinism)
- IUGR (due to placental vascular insufficiency)

Delayed organ maturity
- Fetal lung immaturity (hyperglycemia interferes with surfactant synthesis RDS)

Congenital anomalies (DM1, DM2 not GDM)
- 2-7x increased risk of cardiac, NTD, GU(cystic kidneys), GI (anal atresia) and MSK
***** Pregnancies complicated by GDM do not manifest an increased risk of congenital anomalies because GDM develops after the critical period of organogenesis ******

Labour and delivery
- Preterm labour (mostly in patient associated with HTN/Pre-eclampsia)
- Birth trauma (due to macrosomia)
- Increased incidence of stillbirth

- Hypoglycemia (due to pancreatic hyperplasia and excess insulin secretion in the neonate)
- Hyperbilirubinemia and jaundice
- Hypocalcemia
- Polycythemia
Classification of hypertensive disorders of pregnancy

- Pre-existing hypertension
- Gestational hypertension
- Pre-existing hypertension + Pre-eclampsia
- Severe pre-eclmapisa
1. Pre-existing HTN
- diastolic hypertension that predates pregnancy or is diagnosed before 20 weelks gestation. In most cases HTN persists >42 d postpartum. It may be associated with proteinuria

2. Gestational hypertension
- Diastolic hypertension develops after 20 weeks gestation. In most cases it resolves < 42 days postpartum
A. Without pre-eclampsia : < 0.3g/d
B. With pre-eclampsia
i. with new onset proteinuria
ii. with one or more adverse conditions

3. Pre-existing HTN + pre-eclampsia : HTN associated with one of the following after 20 weeks:
- Resistant hypertension
- New or worsening proteinuria
- One or more adverse conditions

4. Severe Pre-Eclampsia
- Onset before 34 weeks gestation
- Heavy proteinuria (3-5 g/d in 24 hr urine) Or with one or more adverse conditions
Adverse conditions in pregnancy
1. Convlusions (eclampsia)
2. Very high diastolic pressure (>100 mm Hg)
3. Thrombocytopenia (<100 000) = bleeding, petechiae
4. Oliguria (<500 mL/d)
5. Pulmonary edema
6. Elefated liver function tests
7. Severe nausea and vomiting
8. Frontal headache
9. Visual disturbance (blurring, scotoma)
10. Persistent abdominal pain in RUQ
11. Chest pain or shortness of breath
12. Suspected placenta abruptio
13. HELLP syndrome
14. IUGR
15. Oligohydramnios
16. Absent or reversed umbilical artery end diastolic flow as determined by doppler velocitometer
17. CNS = hyperreflexia, somnolence, irritability, tremulousness
Definition of pre-existing HTN in pregnancy
HTN (>140/90) prior to 20 weeks GA (unless a gestational trophoblastic neoplasia), persisting postpartum
Management of pre-existing HTN in pregnant women
Alpha Methyldopa 250-500 mg PO tid/qid or labetalol 100-300 mg PO bid/tid


Monitor progress with serial U/S
Etiology and pathophysiology of gestational hypertension
- Imbalance of thromboxane (vasoconstrictor) and prostaglandin (vasodilator), arteriolar constriction, capillary damage, protein extravasation and hemorrhage.

- In patients with trophoblastic diseases (mole, hydrops, choriocarcinoma), occurs earlier than 20 GA, otherwise occurs after 20 weeks
Risk factors for gestational hypertension
Maternal factors
- Primigravida
- First conception with a new partner
- PMHx or FHx of gestational HTN
- DM, chronic HTN or renal insuffisiency
- Antiphospholipd antibody syndrome
- Extremes of maternal age (<18 and >35)

Fetal factors
- IUGR or oligohydramnios, GTN, multiple gestation, fetal hydrops
Pre-eclampsia investigations
Creatinine, Electrolytes, Urinalysis or urine dipstick
HELLP syndrome
Elevated liver enzymes
Low platelets
Management of gestational hypertension
Without Pre-eclampsia
- Bed rest + left lateral decubitus position, normal salt and protein intake
- Avoid diuretics and anti-hypertensives
- Monitor for progression
- If > 37 weeks

With Pre-eclampsia
- Verify if HELLP present
- Stabilize and deliver : only cure is delivery
- Increased maternal monitoring to hourly input and output, urine dip Q12H and neurological vitals Q1H
- Increased fetal evaluation
- Anticonvulsant therapy
+ Mg Sulfate : 4 g IV bolus over 20 minutes followed by 2-4 g/hour
+ Monitor for signs of Mg toxicity (give calcium gluconate = antagonist)

- Anti-hypertensive therapy
+ Hydralazine 5-10 mg IV bolus over 5 minutes Q15-30 minutes as necessary
+ Labetolol 20-50 mg IV Q10 minutes
2nd line : nifedipine 10-20 mg PO Q20-60 minutes

- Post-partum management
+ Risk of seizure highest in first 24 hours postpartum, thus continue Mg Sulfate for 12-24 hours
+ Vitals Q1H
+ Consider HELLP syndrome in toxic patients
+ Must return to a normotensive BP within 2 weeks
Signs of Mg toxicity
Depressed deep tendon reflexes
Decreased RR
CNS or cardiac depression
Complications of gestational hypertension
- Hemorrhagic stroke (50% of deaths)
- Left ventricular failure / pulmonary edema
- Liver and renal dysfunction
- Abruption
- Seizure
- DIC (release of placental thromboplastin = consumptive coagulopathy)
- HELLP syndrome
+ treat with FFP infusion or plasma exchange

- Fetal loss
- Prematurity
- Placenta abruptio
Definition of hyperemesis gravidarum
Intractable nausea and vomiting, severe enough to cause weight loss, dehydration, ketonuria, electrolyte imbalance, acid-base disturbances and if severe, hepatic and renal damage.

Usually presents in T1 then diminishes; persists throughout pregnancy in a minority

1% of pregnancies
Etiology of hyperemesus gravidarum
Rapidly rising B-HCG and estrogen levels
Investigations for hyperemesis gravidarum
Diagnosis of exclusion : r/o GI inflammation, pyelonephritis, thyrotoxicosis

Multiple gestation, GTN, HELLP syndrome

CBC, electrolytes, BUN, creatinine, LFTs, Urinalysis

Management of Hyperemesis gravidarum
- if severe, admit
- NPO initially, then small frequent meals of appealing foods
- Correct hypovolemia, electrolye imbalances and ketosis
- Thiamine supplementation may be indicated
- TPN if severe to reverse catabolic state

Pharmacological Options
- Diclectin (10 mg doxylamine succinate with vitamin B6) can be started at 2 tablets QHS + 1 tablet Qam + 1 tablet qPM; dosage can be increased up to 8 tablets per day
- Gravol can be safely used as an adjunct to Diclectin (1 suppository bid or 25 mg PO qid)

Non pharmacological options
- rest
- avoid triggers
- acupressure
- ginger
Complications of hyperemesis gravidarum
- dehydration, electrolyte and acid-base imbalance
- Mallory-Weiss tear
- Wernicke's encephalopathy
- Death

- usually none
- IUGR (15x more common in women losing >5% of pre-pregnancy weight)
Differential diagnosis of jaundice in pregnancy
- Viral hepatitis
- Unique to pregnancy
+ Cholestatic jaundice of pregnancy
+ Hepatic rupture, hematoma and infarct
+ Acute fatty liver of pregnancy (AFLP)
+ Hyperemesis gravidarum
- Pre-existing conditions
+ chronic hepatitis, cirrhosis, familial hyperbilirubinemia, Budd-Chiari syndrome, Wilson's disease, hepatic tumours, intrahepatic cholestasis, biliary obstruction, PBC, PSC.
Causes of jaundice unique to pregnancy
Cholestatic jaundice of pregnancy
Acute fatty liver of pregnancy
Acutre hepatic rupture, hematoma and infarct
Hyperemesis gravidarum
Presentation of HELLP syndrome
Epigastric, RUQ or chest pain, N/V, symptoms of pre-eclampsia (headahce, blurred vision, thirst) with or without jaundice

Atypical presentation : asymptomatic reduction in platelet count, "flu-like symptoms"
Laboratory findings and investigations for HELLP syndrome
High AST
Elevated LDH

Liver biopsy : rarely done = periportal hemorrhage and fibrin deposition with periportal necrosis

Management of HELLP
Supportive (ICU) and prompt delivery
Complications of HELLP
Multi-system organ failure
Hepatic failure
Definition of cholestatic jaundice of pregnancy
Clinical syndrome characterized by intense pruritus that precedes jaundice by 7-14 days
Risk associated with cholestatic jaundice of pregnancy
Risk of reduced vitamin K absorption = increased risk of newborn hemorrhagic disease
Epidemiology of cholestatic jaundice of pregnancy
17-29 weeks GA
High incidence in Chile and Scandinavia
Selenium may be preventive against cholestasis
Strong familial predisposition
Correlates with oral contraceptive sensitivity
Episode predisposes to cholestasis on subsequent gestation
Presentation of cholestatic jaundice of pregnancy
Intense pruritus (classically worst on palms and soles of feet) +/- icterus (1-2 weeks later)

ALT <500, ALP and GGT markedly elevated

Steatorrhea unusual
Management of cholestatic jaundice of pregnancy
- Ursodeoxycholic acid (20-25 mg/kg/day)
- Pruritus : cholestyramine
- Prophylactic vitamin K before delivery
- Consider induction of labour
Hepatic infarct, hematoma and rupture
- Presentation
- Diagnosis
- Management
- Complications
A rare consequence of pre-eclampsia typically occuring in T3
- Vasospasm induced hepatic infarction can lead to hematoma formation
- Hematoma can rupture

- Hepatic rupture : RUQ pain, abdominal distention, N/V and HTN followed by shock

- Hemoperitoneum (paracentesis, U/S, CT, MRI showing ruptured liver)

- Death if untreated
Etiology and epidemiology of UTI in pregnancy
- Increased urinary stasis from mechanical and hormonal (progesterone) factors
- Organisms include
+ Common organisms in UTI in non pregnant women

- Most common medical complication of pregnancy
- Asymptomatic bacteriuria in 2-7% of pregnant women depending on parity and socioeconomic factors

N.B. Asymptomatic bacteriuria to be treated in pregnancy because of increased risk of progression to cystitis, pyelonephritis and probable increase risk of preterm labour.
Features and investigations of UTI in pregnant women
- may be asymptomatic
- dysuria, urgency and frequency in cystitis
- fever, flank pain, CVA tenderness in pyelonephritis

- Urinalysis, Urine cultures
- VCUG, cystoscope and renal function tests in recurrent infections
Management of UTI in pregnancy
Uncomplicated UTI
- 1st line : Amoxicillin 250-500 mg PO Q8H x 7 days
- alternatives : TMP-SMX (Septra) or nitrofurantoin
- avoid sulfa drugs during last 6 weeks of pregnancy due to displacement of biliribun from albumin and increased kernicterus in newborn
- follow with monthly urine cultures

- hospitalization and IV antibiotics

- complications : acute cystitis, pyelonephritis and possible premature rupture of membranes
- recurrence common
Which antibiotic to avoid in last 6 weeks of pregnancy? and why?
Avoid sulfa drugs during last 6 weeks of pregnancy due to displacement of biliribun from albumin and increased kernicterus in newborn
Definition of acute fatty liver of pregnancy
A form of hepatic failure with coagulopathy and encephalopathy that is characterized by microvesicular fatty infiltrates in liver parenchyma

Usually in 3rd trimester
Risk factors for acute fatty liver of pregnancy
Male gestations (2.7x higher)
Long chain acyl-CoA dehydrogenase deficiency with at least one allele for the G1528 mutation in either mother or fetus
No recurrence with subsequent pregnancies
Clinical features of acute fatty liver of pregnancy
Acute N/V + severe upper abdominal pain preceding jaundice
Range in presentation
- mild
- fulminant : GI bleed, hepatic coma, renal failure and true hepatic failure
Diagnosis of acute fatty liver of pregnancy
- Elevated PTT and low serum fibrinogen
- Hypoglycemia
- Pre-Eclampsia and HELLP features frequently present
- Liver biopsy to establish diagnosis
+ microvesicular fatty infiltrates of the central zone hepatocytes
+ Oil Red O stain on frozen tissue
+ Electron microscopy
- U/S, MRI, CT : not useful, but try if liver biopsy is not possible (CT is most helpful)
Management and prognosis of acute fatty liver of pregnancy
- Early diagnosis with prompt delivery followed by maximal supportive care
+ ABC, mechanical ventilation, transfusion of blood products
+ Hepatic encephalopathy treatment - Lactulose, catharsis
+ Treat hypoglycemia

- recovery begins with delivery
- persistent or increasing hyperbilirubinemia and complications
Risk factors for venous thromboembolism in pregnancy
Previous VTE
Hypercoagulability (Antiphospholipid, Protein C/S deficiency, V leiden...)
Age >35
Shock / dehydration
Vascular damage at delivery
Stasis (compression by uterus)
Management of VTE in pregnancy
- Warfarin is contraindicated in pregnancy due to its potential teratogenic effects
- Unfractionned heparin
+ bolus of 5000 IU followed by an infusion of 30 000 IU/24 hrs
+ measure the aPTT six hours after the bolus
+ maintain the aPTT at a therapeutic level (1.5-2 times normal)
+ repeat Q24H once therapeutic
+ HIT uncommon (3%) but serious complications

- Compression stockings
- Prophylaxis
+ women on long term anticoagulation : full therapeutic anticoagulation throughout pregnancy and for 6-12 weeks postpartum
+ women with a non-active PMHx of VTE : unfractionned heparin regimens suggested

- Routine prophylaxis
+ insufficient evidence in pregnancy to recommend routine use of LMWH
+ current prophylaxis regimens for acquired thrombophilias, such as APLA syndrome, include the use of low dose ASA in conjunction with prophylactic heparin.
Etiology of recurrent pregnancy loss
Mechanical : uterine anatomy, cervical incompetence

Autoimmune : antiphospholipid antibody syndrome, lupus anticoagulant

Karyotype : both parents

Endocrine : hypothyroidism, diabetes mellitus

Maternal infection

Environment : smoking, alcohol, drugs, radiation
Differential diagnosis of first and second trimester bleeding
Physiological bleeding : spotting (due to implantation of placenta - reassure and check serial beta-hcg)
Spontaneous abortion
Abnormal pregnancy (ectopic, molar)
Genital lesion (cervical polyp, neoplasms)

- U/S
- Blood group and screen
Types of spontaneous abortions and characteristics
1) Threatened
- Vaginal bleeding with or without cramping
- Cervix closed and soft
- U/S shows viable fetus
- Tx : watch and wait, <5% go on to abort

2) Inevitable
- Increased bleeding and cramps with or without rupture of membranes
- Cervix closed until products start to expel, then external os opens
- Tx : watch and wait; misoprostol (PGE1); D&C with or without oxytocin

3) Incomplete
- Extremely heavy bleeding and cramps with or without passage of tissue
- Cervix open
- Tx : watch and wait; misoprostol; D&C +/- oxytocin

4) Complete
- Bleeding and complete passage of sac and plancenta
- Cervix open
- Tx : no D&C - expectant management

5) Missed
- No bleeding (fetal death in utero)
- Cervix closed
- U/S may show SGA
- Tx : watch and wait; misoprostol; D&C +/- oxytocin

6) Septic
- Contents of uterus infected (infrequent)
- Tx : D&C + IV broad spectrum antibiotics
Definition of recurrent abortions
3 or more consecutive spontaneous abortions
Definition of antepartum hemorrhage
Vaginal bleeding from 20 weeks to term
Differential diagnosis of antepartum hemorrhage
Bloody show (shedding of cervical mucous plug)
Placenta previa
Abruptio placenta (most common pathological etiology in T3)
Vasa previa
Marginal sinus bleeding
Cervical lesions (cervicitis, polyp, ectropion, cervical cancer)
Post coital
Uterine rupture
Bleeding from bowel or bladder
Placenta accreta
Abnormal coagulation
Definition of placenta previa
Abnormal location of the placenta near, partially or completely over the cervical os

Etiology : idiopathic
Presentation of placenta previa
- Painless bright red vaginal bleeding (recurrent), may be minimized and cease spontaneously, but can become catastrophic
- Mean onset of bleeding is 30 weeks, but onset depends on degrees of previa

- Uterus soft and non tender
- Presenting part high or displaced

Do NOT perform a vaginal exam until placenta previa has been ruled out by U/S
Risk factors for placenta previa
History of placenta previa
Increased maternal age
Multiple gestation
Uterine tumour
Uterine scar due to previous abortion, C/S, D&C, myomectomy
Classification of placenta previa
Total : placenta completely covers the internal os
Partial : placenta partially covers the internal os
Marginal : within 2 cm of os but does not cover any part of os (causes potential risk of hemorrhage during cervical effacement and dilatation)

Low lying placenta (not a previa) : placenta in lower segment but clear of os (can also bleed but usually in labour)
Complications of placenta previa (Fetal, maternal
- perinatal mortality low but still higher than with a normal pregnancy
- permaturity (bleeding often dictates early C/S)
- intra uterine hypoxia
- fetal malpresentation
- risk of fetal blood loss from placenta, especially if incised during C/S

- <1% maternal mortality
- Hemorrhage and hypovolemic shock, anemia, ARF, pituitary necrosis (Sheehan)
- Placenta Accreta
- Hysterectomy
Definition of placenta accreta
Placental tissue invades superficially into myometrium
Definition of placenta increta
Placental tissue invades deeply into myometrium
Definition of placenta pecreta
Placental tissue invades through the myometrium
Main diagnosis for placenta previa
REPEAT U/S throughout pregnancy
Management of placenta previa
Goal : keep pregnancy intrauterine until the risk of delivery < risk of not delivering

- Stabilize and monitor + blood work
- U/S assessment
- RhoGam if mother Rh negative
x Kleihauer-Betke test to determine extent of fetomaternal transfusion so that appropriate dose of rhogam can be given
- GA < 37 weeks and minimal bleeding (expectant management)
x admit to hospital
x limited physical activity, no douches, enemas or sexual intercourse
x consider corticosteroids for fetal lung maturity
x delivery when fetus is mature or hemorrhage dictates
- GA > 36 weeks, profuse bleeding or L/S ratio is >2:1 - deliver by C/S
Clinical features of Abruptio Placentae
PAINFUL vaginal bleeding (sudden onset, constant, localized to lower back and uterus)
Uterine tenderness and contractions
+/- fetal distress
+/- fetal demise
+/- bloody amniotic fluid
Definition of abruptio placentae
Premature separation of a normally implanted placenta after 20 weeks gestation
Risk factors for abruptio placentae
Previous abruption
Maternal hypertension
Cigarette smoking
Maternal age > 35
Rapid decompression of a distended uterus (polyhydramnios, multiple gestation)
Uterine anomaly
Complications of abruptio placenta
- Perinatal mortality 25-60%
- Prematurity
- Intrauterine hypoxia

- < 1% maternal mortality
- Anemia
- Hemorrhagic shock
- Sheehan syndrome
- Amniotic fluid embolus
Classification of abruptio placenta
Total vs partial
- external / revealed / apparent : blood dissects downward toward cervix
- internal / concealed : blood dissects upward toward fetus
- most are mixed
Grades of abruptio placenta
Graded according to :
- uterine irritability
- maternal hemodynamics
- maternal fibrinogen
- fetal heart rate
Investigations for placenta abruption
U/S not sensitive

Blood work and fetal heart rate
Management of placenta abruptio
- Maternal stabilization (hemodynamically...)
- Electronic fetal monitoring
- Maternal monitoring (vitals, urine output, blood loss, bloodwork (Hte, CB, PTT/PT, platelets, fibrinogen, FDP, type and cross match)
- Blood products on hand
- RhoGam if Rh negative
x Kleihauer-Betke test may confirm abruption

If GA > 36 weeks : stabilize and deliver
If GA < 36 weeks
- if mild, deliver when fetus is mature
- otherwise deliver by C/S for any beginning in complications
Definition of vasa previa
Unprotected fetal vessels pass over the cervical os; associated with velamentous insertion of cord into membranes of placenta or succenturiate lobe.
Presentation of VASA previa
PAINLESS vaginal bleeding and fetal distress (tachy and bradyarrhythmia)

50% perinatal mortality, increasing to 75% if membranes rupture (most infants die of exsanguination)
Investigations for vasa previa
Apt test : NaOH mixed with the blood, can be done immediately to detemine the source
- fetal : supernatant turns pink
- maternal : supernatant turns yellow

Wright stain on blood smear and look for nucleated RBC (in cord, not maternal blood)
Management of vasa previa
Emergency C/S
Definition of ectopic pregnancy
Embryo implants outside of the endometrial cavity
Common locations of ectopic pregnancies
Ampullary 78%
Isthmic 12%
Fimbrial 5%
Interstitial 2%
Abdominal 2%
Etiology of ectopic pregnancy
50% due to damage of fallopian tube cilia from PID
Intrinsic abnormality of the fertilized ovum
Conception late in cycle
Transmigration of fertilized ovum to contralateral tube
Risk factors of ectopic pregnancy
50% idiopathic

Older women of african descent
IUD use (although decreased pregnancy rate, if pregnancy occurs there is increased risk of ectopic)
History of PID (especially with C. Trachomatis)
Clomiphene citrate use (for induction of ovulation)
Previous procedures
- any surgery on fallopian tube
- abdominal surgery for ruptured appendix
- IVF pregnancies following ovulation induction

- uterine leiomyomas
- adhesions
- abnormal uterine anatomy (T-shaped uterus)
Presentation of ectopic pregnancy
Temperature > 38 degrees
Abdominal tenderness (90%) +/- rebound
Bimanual examination
- cervical motion and adnexal tenderness
- palpable adnexal mass
Other signs of pregnancy : Chadwick, Hegar, Goodell
If ectopic pregnancy ruptures
- acute abdomen with increasing pain
- abdominal distention
- symptoms of shock
Investigations for ectopic pregnancy
Treatment of ectopic pregnancy
Goals of treatment : be conservative (preserve tube if possible)

- Linear salpingostomy if tube salvageable
- Salpingectomy if tube damaged or ectopic is ipsilateral recurrence
- 15% risk od persistent trophoblast
- is patient is Rh negative give WinRho
- may require laparotomy

Medical (MTX)
- use 50 mg/m2 body surface area; given in single IM dose
- this is 1/6 chemotherapy dose, therefore minimal side effects
- follow B-HCG levels weekly until B-HCG is non detectable
- success 67%, as many as 25% will require a 2nd dose
- tubal patency following MTX treatment approaches 80%
Prognosis of ectopic pregnancy
9% of maternal deaths
40-60% of patients will become pregnant again after surgery
10-20% will have subsequent ectopic gestation
Treatment algorithm of ectopic pregnancy
Complications associated with maternal gestation
- Hyperemesis gravidarum
- Gestational HTN
- Anemia
- Increased physiological stress on all systems
- Increased compressive symptoms
- C/S

- Increased PROM/PTL
- Polyhydramnios
- Placenta Previa
- Placental abruption
- PPH (uterine atony)
- Umbilical cord prolapse
- Cord anomalies (velamentous insertion, 2 vessel cord)

- Prematurity
- Malpresentation
- Congenital anomalies
- Twin-twin anomalies
- Increased perinatal morbidity and mortality
- Twin interlocking (twin A breech, twin B vertex)
- Single fetal demise
Management of twin pregnancies
- U/S determination of chorionicity must be done within the first trimester (ideally 8-12 weeks GA)
- Increased antenatal surveillance
+ NST weekly from 24 weeks GA
+ Serial U/S Q 2-3 weeks from 28 weeks GA to assess growth
+ Doppler flow studies weekly if discordant fetal growth
+ BPP as needed

- Vaginal examination in 3rd trimester to check for cervical dilatation
- May attempt vaginal delivery if twin A delivered vaginally and twin B delivered by C/S
- Mode of delivery depends on fetal weight, GA, presentation
Twin Twin transfusion syndrome
10% of monochorionic twins

- arterial blood from donor twin passes through placenta into vein of recipient twin

Clinical features
- donor twin : IUGR, hypovolemia, hypotension, anemia, oligohydramnios
- recipient twin : hypervolemia, hypertension, CHF, polycythemia, edema, polyhydramnios, kernicterus in neonatal period
Management of twin twin transfusion
Therapeutic serial amniocentesis to decompress polyhydramnios of recipient twin and decrease pressure in cavity and on placenta

Intrauterine blood transfusion to donor twin if necessary

Laparoscopic occlusion of placental vessels
Definition of IUGR
Infant weight <10th percentile for a particular GA

Weight not associated with any constitutional or familial causes
Risk factors for IUGR
- malnutrition
- smoking
- drug abuse
- alcoholism
- heart disease
- type 1 DM
- pulmonary insufficiency
- previous IUGR

- any disease causing placental insufficiency (GHTN, chronic HTN, CRF, gross placental morphological abnormalities)

- Multiple gestation
- Congenital anomalies
Classification and features of IUGR
Symmetric (type I(
- occurs early in pregnancy
- inadequate growth of head and body
- head : abdomen ratio may be normal
- usually associated with congenital anomalies or TORCH infections

Asymmetric (type II)
- occurs late in pregnancy
- brain is spared, therefore head:abdomen ratio increased
- usually associated with placental insufficiency
- more favorable prognosis than type I
Complications of IUGR
Prone to meconium aspiration, asphyxia, polycythemia, hypoglycemia and mental retardation

Greater risk of perinatal morbidity and mortality
Investigations for IUGR
- Symphysis-fundus height (SFH) measurements at every antepartum visit
- if mother at high risk or SFH lags >2cm behind GA
+ anatomy U/S exam should include assessment of biparietal diameter (BPD), head and abdomen circumference, femur length and fetal weight, amniotic fluid
- Doppler analysis of umbilical cord blood flow as needed
Differential diagnosis of incorrect uterine size for dates
Inaccurate dates
Maternal diabetes mellitus
Polyhydramnios, oligohydramnios
Multiple gestations
Abnormal karyotype
Fetal anomaly
Abnormal lie
Definition of macrosomia
Infant weight > 90th percentile for a particular GA or > 4000 g
Risk factors of macrosomia
Maternal diabetes
Maternal obesity
Past history of macrosomic infant
U/S predictors of macrosomia
Third trimester abdominal circumference (AC) >1.5 cm/week
Head circumference (HC)/AC ratio <10th percentile
Femur length (FL)/AC ratio <20th percentile
Definition of polyhydramnios
Amniotic fluid volume (AFV) >2000 cc at any stage in pregnancy
U/S criteria L >8x8 cm pocket of amniotic fluid volume
Etiology of polyhydramnios
Maternal type 1 DM
- chorioangiomas
- multiple gestation
- fetal hydrops
- chromosomal anomaly (up to 2/3 of fetuses with severe polyhydramnios)
- respiratory : cystic adenamatoid malformed lung)
- CNS : anencephaly, hydrocephalus, meningocele
- GI : TE fistula, duodenal atresia, facial clefts (interfere with swallowing)
Features of polyhydramnios
Pressure symptoms from overdistended uterus (dyspnea, edema, hydronephrosis)
Uterus large for dates, difficulty palpating fetal parts and hearing fetal heart tones

- cord prolapse
- placenta abruptio
- malpresentation
- preterm labour
- uterine dysfunction
- postpartum hemorrhage
- increased perinatal mortality rate
Management of polyhydramnios
1- determine underlying cause
+ screen for maternal disease / infection
+ complete fetal U/S evaluation

2- depends on severity
+ mild to moderate cases require no treatment
+ if severe, hospitalize and consider therapeutic amniocentesis
Definition of oligohydramnios
Amniotic fluid index of 5 cm or less
An important sign of chronic placental insufficiency
Etiology of oligohydramnios
Early onset oligohydramnios
- Decreased production : renal agenesis or dysplasia, urinary obstruction, posterior urethral valves (male), chronic hypoxemia leading to IUGR results in shunting away from the kidneys to ensure profusion of the brain
- Increased loss : prolonged amniotic fluid leak (although most often labour ensues)

Late onset oligohydramnios
- amniotic fluid normally decreases after 35 weeks
- common in post-term pregnancies
- U/S Doppler studies (umbilical cord and uterine artery Dopplers)
Clinical features of oligohydramnios
Cord compression
Increased risk of fetal adverse outcomes

Early onset
- 15-25% have fetal anomalies
- Amniotic fluid bands (T1) can leat to Potter's facies, limb deformities, abdominal wall defects

Late onset
- pulmonary hypoplasia
- marker for infants who may not tolerate labour well
Management of oligohydramnios
- Maternal hydration with oral or IV fluids to help increase amniotic fluid
- Vesicoamniotic shunt : if etiology is related to fetal obstructive uropathy, however, pulmonary function may not be restored with restoration of amniotic fluid.
- Injection of fluid via amniocentesis will improve condition for 1 week
- Consider delivery if at term
- Amnio infusion may be considered during labour via intra-uterine catheter, evidence to show improved fetal outcomes is equivocal
Definition of puerperium
6 week period of adjustment after pregnancy when pregnancy induced changes are reversed
Definition of postpartum hemorrhage
Loss of > 500 ml of blood at the time of vaginal delivery or > 1000 ml with C/S

Early : within first 24 hours postpartum
Late : after 24 hours but within 6 weeks
Etiology of postpartum hemorrhage
4 Ts

1. Tone
- Uterine atony, due to:
+ labour (prolonged, precipitous, induced, augmented)
+ uterus (infection, over-distention)
+ placenta (abruption, previa)
+ maternal factors (grand multiparity, gestational HTN)
+ halothan anesthesia

2. Tissue
- Retained placenta
- Retained blood clots in atonis uterus
- Gestational trophoblastic neoplasia

3. Trauma
- Laceration
- Episiotomy
- Hematoma (vaginal, vulvar, retroperitoneal)
- Uterine rupture
- Uterine inversion

4. Thrombin
- coagulopathy
+ most identified prior to delivery (low platelets inreases risk)
+ includes hemophilia, DIC, aspirin use, ITP, TTP, vWD
+ do not forget therapeutic anti-coagulation
Uterine atony
Most common cause of PPH

Avoid by giving oxytocin with delivery of the anterior shoulder

Occurs within first 24 hours
Management of postpartum hemorrhage
Medical therapy
- Oxytocin 20 U/L NS or RL IV continuous IV - in addition can give 10 U intramyometrial after delivery of the placenta
- Ergotamine 0.25 mg IM/IMM Q5min up to 1.25 mg; can be given as IV bolus
- Carboprost (PGF-2 alpha analog) 0.25 mg IM/IMM Q15min to max 2 mg (major prostaglandin effect side effects and contraindicated in CN, pulmonary, renal and hepatic dysfunction)

Local control
- Bimanual compressions
- Uterine packing (mesh with antibiotic treatment)
- Intrauterine Senstake-Blakemore catheter for balloon tamponad - may slow hemorrage

Surgical therapy
- D&C (beware of vigorous scraping which may cause Asherman's syndrome)
- Laparotomy with bilateral ligation of uterine artery,ovarian artery or hypogastric artery
- Hysterectomy (last option) with angiographic embolization if post-hysterectomy bleeding
Definition of retained placenta
Placenta undelivered after 30 minutes postpartum
Etiology of retained placenta
Placenta separated but not delivered
Abnormal placental implantation i.e. placenta accreta, placenta increta, placenta percreta
Risk factors for retained placenta
Placenta previa
Prior C/S
Post-pregnancy curettage
Prior manual placental removal
Uterine infection
Management of retained placenta
2 large bore IVs, type and screen

Brant maneuver (firm traction on umbilical cord with one hand applying suprapubic pressure to hold uterus in place)

Oxytocin 10 IU in 20 mL NS into umbilical vein

Manual removal if above fails

D&C if required
Etiology of uterine inversion
Often iatrogenic (excess cord traction with fundal placenta)
Excessive use of uterine tocolytics
More common in grand multiparous (lax uterine ligaments)
Features of uterine inversion
Can cause profound vasovagal response with vasodilation and hypovolemic shock
Shock may be disproportionate to maternal blood loss
Management of uterine inversion
Urgent management essentials, call anesthesia
ABCs - initiate IV crystalloids
Can use tocolytic drug or nitroglycerin IV to relax uterus and aid replacement
Replace uterus without removing placenta
Remove placenta manually and withdraw slowly
IV oxytocin infusion (only after uterus replaced)
Re-explore uterus
May require GA +/- laparotomy
Definition of postpartum pyrexia
Fever > 38 on any 2 of the first 10 days postpartum, except the first day
Etiology of postpartum pyrexia

Breast : engorgement, mastitis
Wind : atelectasis, pneumonia, PE
Water : UTI
Wound : C/S incision or episiotomy site
Walking : pelvic thrombophlebitis, DVT
Womb : endomtritis