OBGYN Topic Titles 11/12

Question 1

Physiological changes in pregnancy: renal function,
alimentary system, nutrients in blood, skin, breasts.
Maternal weight gain, endocrine changes.

Answer 1

Question 2

Placental growth, development and function

Answer 2

(Last page) Uteroplacental blood flow

1. Formation of the intervillous space begins with small lacunas of blood dispersed between the decidual cells and eventually are dispersed between the syncytiotrophoblasts.

They are supplied by maternal spiral arteries. Growing of the lacunas is due to their fusion with adjacent lacunasuntil the maternal blood “baths” the blastocyst allowing for further growth of the villi and until the formation of the cotyledon.

8. Trophoblastic invasion to maternal spiral arterioles leads to destruction of smooth muscle and formation of sinusoids which makes the blood circulation more efficient.
9. Uterine blood flow is between 500-750mL/min.
10. Factors influencing uterine blood flowa. Catecholaminesb. Mechanical forcec. Hemorrhagesd. RAASe. Vasodilators
11. Transfer of material is by simple diffusion, facilitated diffusion (passive and active) and pinocytosis.

Placental functions

1. Gas exchange
   a. Simple diffusion of oxygen.
   b. What favors O2 uptake by the fetus and placenta?

(right shift in the oxygen dissociation curve – Bohr’s effect)

i. PO2 of maternal is 90-100mmHg which is higher than the fetal PO2.

ii. The period of high fetal metabolism produces high CO2 levels that promote O2 uptake from the mother.

iii. Fetal hemoglobin has higher affinity for oxygen.

c. The placenta utilizes high amount of oxygen and remaining goes to the fetus.

2. Nutrition and excretiona.

Maternal glucose crosses the placenta and provides 90% of fetal energy.

b. Hormones regulating glucose metabolism do not cross the placenta – insulin, glucagon, human placental lactogen and growth hormone.

c. Glycogen is stored in the placenta and also in the fetal liver which serves as energy source for the period after pregnancy and for asphyxiated fetus.

d. Free fatty acids cross the placenta.e. Proteins are synthesized by the fetus and can cross the placenta via active transporters.

f. Immunoglobulin are synthesized by the fetus and IgM appears first in the fetus by week 20.3.

g. IgG is the only one who can cross the placenta.

Hormones synthesisa.

hCG produced by trophoblasts similar to (LH). It maintains corpus callosum which is responsible for progesterone until the placenta is able to produce it by itself.

b. hPL produced by syncytiotrophoblasts.

It increases free fatty acids and insulin levels. Used to assess placental function (low levels indicate placental failure).

c. Progesterone is formed by the placenta by week 17. About 350mg are formed by full term.

d. Estrogen is mainly formed by the placenta and to lesser extent by the ovaries.

Question 3

Physical examination in obstetrics

Answer 3

There are 2 tables in the note (diameter) check.

8. Pelvisa.

b. c. d. Vulvar lesions
Speculum examination – used during gynecological examination (for complaints about bleedings, abnormal vaginal discharge, Pap test, during labor in cases of bleeding or cervical assessment.

Digital vaginal examination – contraindicated in later pregnancy due to the risk of introducing infection, artificial rupture of membranes.

However, used during labor for evaluation of cervical effacement and assessment of fetal presentation.

Pelvimetry – not a routine anymore but used in cases ofi.

Delayed labor progressionii. Previous fractures

iii. Abnormal development of bony pelvisiv. Includes the following measurements:

• Transverse diameter – line between widest iliopectineal points
• True conjugate – line between the sacral promontory and superior

Inlet*
* pubic symphysis
Obstetric conjugate – line between the sacral promontory and midlinepubic symphysis

Diagonal conjugate diameter – line between inferior margin of the pubic symphysis to sacral promontory (most clinically important)

Midline * Mid-cavity – line between ischial spines

Outlet
* Anteroposterior diameter (least pelvic diameter) - sacrococcygeal joint and the inferior margin of pubic symphysisIntertuberous diameter – line between ischial tuberosities

Anatomy remindersi. Pelvic girdle is a single hip boneii. Bony pelvis is 2 hips + sacrum + coccyxiii.

Pelvic brim (pelvic inlet) is bordered by pubic symphysis, iliopectineal line, margin of ala and sacral promontoryiv.

True pelvis is below pelvic inlet and false pelvis is above pelvic inlet

Palpation of fetal parts
1. Features:
* Head is firm
* Buttocks are soft
* Breech is not ballotable
* Normal fetal altitude is flexion

2. Liea.
   b. Definition: relationship of long axis of fetus to the long axis of uterus

Types:
i. ii. iii. Transverse - poles of fetus palpable in the lumber regions

Oblique - presenting part is palpable in iliac fossa

Longitudinal - presenting part (head or breech) palpable over pelvic inlet

Presentationa.

Definition: the leading body part of the fetus through the birth canal (dilated cervix and vagina)

b. Types:

i. ii. Cephalic presentation (head) – longitudinal lie* * * *

BreechVertex (occipito-) – hyperflexed (most common)
Brow (eyebrows) – partially extended
Forehead – partially flexed
Face (mento-) – hyperextended
* Buttocks (sacro-)
* Feet (podalic-)
iii. iv. Shoulder - transverse or oblique lie

Compound presentation – more than >1 presenting part (e.g. cephalic and an extremity)

c. Positiona.
Diagnosis – vaginal examination in established labor

Definition: relationship of the denominator (the prominent part of the presenting part) to the maternal pelvis (direction the fetus is facing in relation to the mother’s spine.
b. Examples:

c. Stationa.

Diagnosis – vaginal examination in established labor (dilated cervix and palpable fontanelles)

Definition: measurement (cm) of the presenting part above and below the maternal ischial spine.

6. Engagementa.

Definition: when the widest diameter (usually biparietal diameter [BPD]) passed through the pelvic inlet to the true pelvis.

Measurement is described in fifths. “Engaged head” is when ≤ 2/5 of the head is palpable in the abdomen. Palpable head is usually not engaged.

7. Synclitismb.

Definition: parallelism between pelvic inlet plane and fetal plane. Sagittal suture is the in line with the pubic symphysis and sacral promontory.

c. Asynclitism: sagittal suture is in the transverse diameter of the pelvic inlet.

Question 4

Normal pregnancy and antenatal care

Answer 4

a. Some are needed to be stopped or replaced.

7. Fetal anomalya.

Trisomy 21 (Down’s syndrome)

i. Positive results end with either termination of pregnancy or continuation of pregnancy that allows for better preparation for birth by the parents (for those who want to keep the baby)

ii. Ultrasound examination of nuchal translucency and biochemical tests

Risk factors
1. Smokinga. CO has higher affinity for Hemoglobin (200 times greater than oxygen) and shifts dissociation curve to the left

2. b. Nicotine is vasoconstrictor causing narrowing of capillaries of placentac. Placental structure shows thickening of trophoblastic membraned.

Reduces birth weight of infant and crown-heel length.Alcohol abusea.

Fetal alcohol syndromei. Growth retardationii. Structural defects (facial, cardiac and joint anomalies)

b. 3. Drugsa. Interferes also with recommended dietary intake (alcohol is only energy and not a source for proteins, vitamins etc.)

Heroine, amphetamine, cocaine cause:i. IUGRii. Miscarriageb. iii. Placental abruptioniv. Developmental anomaliesv. Cardiac arrhythmiasMarijuana showed to be teratogenic in animal studies

4. Maternal age (both extremes are bad)

Question 5

Hypertensive disorders of pregnancy

Answer 5

Gestational HTN and Pre-eclampsia

Assessment status (fetal and maternal) and necessity for hospitalization and deliver by:

laboratoy values, fetal ultrasound, non-stress test (NTS) – 20-40 minutes of CTG recording fetal movements in relation to heart rate (different from contraction test that is used to assess heart rate in relation to hypoxia).

Depending on results, either monitor or hospitalize with delivery:

Monitor – 1-2 times a week (blood pressure, urine analysis and lab tests), educate patient for identifying symptoms (mentioned above, reduced fetal movements, vaginal bleeding) and start antihypertensive therapy (labetalol, hydralazine, methyldopa, NO ACE inhibitors they are teratogenic)Hospitalize and delivery if: >37 week, suspected placental abruption, oligohydramnios, abnormal lab

Severe pre-eclampsia

Delivery is the only treatment.Delivery if >34 week or <34 week with maternal or fetal instability.Immediate delivery if pulmonary edema, eclampsia, DIC, placental abruptionDelayed (24h – 48h) delivery if HELLP, PROM,

HELLP
Stabilization - blood transfusion and IV fluids. Antihypertensives - methyldopa, hydralazine, alpha and beta blockers, nifedipineDeliveryIf before <34 week or at any gestational age with presence of deteriorating maternal or fetal status → deliver.If no maternal of fetal stress and stabilization has calmed give corticosteroids for 24-48 hours and then deliver

5. Diagnosis:

a. 4-hour monitoring until blood pressure has returned to normal.
b. Urine checks for proteinuria

c. Maternal

d. Blood count (particular platelets)
Renal and liver functions

e. Uric acid

f. Clottingg.
Catecholamines (to rule out pheochromocytoma)

h. Serial ultrasounds (measure fetal growth every 2 weeks and CSF volume twice a week)

j. Fetali.
k. Doppler ultrasound – umbilical and uterine arteries (check absence or reverse of flow)

Cardiotocography – fetal heart rate and uterine contractionUltrasound – fetal growth in relation to gestational age, placental implantation and amniotic fluid

6. Prevention:a. Ca2+ (may reduce risk)b. Low-dose aspirin (COX inhibitor)

Eclampsia

1. Definition: pre-eclampsia and convulsions (fast relaxing and contracting muscles→seizures). It is secondary to pre-eclampsia
2. Featuresa. Manifests when pre-eclampsia is not recognizedb. Can be preventedc. Can occur in pre-, intra- and post-partum periods.
3. Management:

d. Pre-termi. Control seizures* Ensure airway* MgSu (drug of choice) - 4g solution over 20 minutes + maintenance dose 1 g/h.

ii. Control blood pressure* Labetalol 20mg followed by 40mg, 80mg to total of 200mg* Epidural analgesia - to relief pain and cause vasodilation in lower extremities.

iii. Fetus delivery – after controlling blood pressure, oxytocin induced labor or Csection are followed.

b. Post-term – continues up to 7 days after delivery. In case seizures continue, epilepsy or cortical thrombus need to be considered.

i. Constant patient observationii. Maintain levels of sedationiii. Antihypertensive therapy (until returned to normal)

iv. Fluid balance

Question 6

Antepartum haemorrhage

Answer 6

Complications:
1. Fetal hypoxia
2. Maldevelopmenta.
Placenta accerta – attached to myometrium)b. Placenta increta – invades myometrium)c. Placenta precreta – invades parametriumPlacental abruption

Definition:Hemorrhage from premature separation of the placenta from the uterus.

Risk factors:
1. Dietary deficiency (especially folic acid)
2. Smoking
3. HTN
4. Thrombophilia
5. Trauma
Classification (clinically unimportant):
1. Revealed
2. Concealed
3. Mixed

DD from placenta previa

Symptoms:

Painful vaginal bleeding

Increased uterine contractions

Longitudinal lie of fetus

Pathogenesis:

Blood in the uterine wall causes increase in resting tone and onset of contractions as well as clot formation (consumption of maternal clotting factors which promotes further bleeding).

Clinical presentation example:

1. Pregnant woman with sudden onset of abdominal pain with uterine contraction with or without bleeding → might suffer from placental abruption.
2. Assessment of oxygenation and blood pressure. If pulse measure is higher than systolic measure it is suggestive for serious blood loss (e.g pulse 110 and systole 80)
3. Required IV fluids, CTG and ultrasound assessment of fetus4. Prognosis is dependent on extent of placental separation.

Management:
1. General approacha. Blood transfusion and IV fluidsb. Monitor vital signsc. Clotting factorsd. Maintain airwaye. Anti-D Ig antibodies in Rh(-) motherf. Ultrasound – assess fetal growth and placental site

2. Normal findings:a. <34 weeksi. Observe and monitorii. Use corticosteroids and tocolytics to aim for normal deliveryb. >34 weeks

i. If active uterine contractions attempt vaginal delivery ii. If no contractions and no fetal distress and no bleeding → conservative treatment (as in placental previa)

3. Acute symptoms and live fetus:
   a. Induction of labor with syntocinon and vaginal delivery – only when close to termb.

Otherwise, emergency C-section regardless of gestational age4. Acute symptoms and dead fetus:

a. Induction of delivery or emergency C-section in case of maternal risk due to bleeding or slow labor progression.

Complications1. Afibrinogenemia –thromboplastin released to mother circulation resulting in DIC.

2. Hypovolemia
3. Renal tubular necrosis
4. Couvelaire uterus - when blood penetrates the wall causing bruised appearance to the uterus or may reach the peritoneum.

Uterine rupture

Definition: life-threatening obstetric condition with tearing lesion in the uterus. Presents with sudden onset or more commonly during labor.

Symptoms:
1. Severe painful abdominal pain
2. Sudden pause of contractions
3. Fetal distress
4. Vaginal bleeding

Risk factors:1. Previous C-section or other uterine surgery2. Placental abruption

Question 7

Multiple pregnancy

Answer 7

Related to zygosity

Complications:
1. Nausea and vomiting – higher incidence than singlet.
2. Anemia – due to extra metabolic demands
3. Miscarriage – “vanishing twin syndrome”
4. Antepartum hemorrhage – placenta previa and placental abruption.
5. Pre-eclampsia
6. Intra uterine growth restriction (IUGR) – one fetus is smaller than the other
7.
8. Related to zygosity
9. Pre-term labor – due to over distension of uterus (two fetuses and higher amniotic fluid)

Twin-to-twin transfusion syndrome (TTTS) – blood shunting; one fetus (donor) transfuses blood to the other fetus (recipient) via common vascular channels.

The donor is oligouric, anemic,oligohydramnionic and growth restricted compared to the recipient which
is polyhydramnionic and polycythemic.

Types of anastomoses are artery to artery, vein to vein or artery to vein (most dangerous).

Monoamniotic and conjoined twinning

10. Undiagnosed twins – oxytocic drugs are administered after delivery leading for entrapment of the second twin (irreversible even with using tocolytics drugs)
11. Malpresentation (especially transverse lie)
12. Locked twins – twins lock chin to chin

Presentation:

Management:
1. Antenatal ultrasound to detect anomalies (defect growth, TTTS, IUGR)
2. C-section (same indications for singlet pregnancy but when additional complications exist it is chosen – diabetes, pre-eclampsia, subfertility, pervious scar, preterm labor 28-34 weeks)

3. Vaginal delivery

a. Indication – cephalocephalic or cephalobreech.b. Establish IV linec. Monitor both fetusesd. Deliver first fetus. For second fetus delivery, lie and presentation are needed to be verified along with continuous monitoring of heart rate and uterine contractionsi.

In case of transverse lie or other abnormal position – internal podalic version orexternal cephalic version may be attempted.

ii. If contractions are not present – use oxytocin (wait 30 minutes for normal contraction before administration of oxytocin)

TTTS

4.Amniocenteses – removal of amniotic fluid from the recipient

5 Selective feticide
6 Laster ablation of communicating vessels (if one twin dies the other often dies as well due to hemodynamic changes)

Question 8

Medical problems arising in pregnancy

Answer 8

. 75g dose is given and glucose levels are measured 2 hours later

6. Symptoms:

a. Asymptomatic

7. Complications:

a. Maternal:
i. Pre-eclampsiaii.
b. iii. iv. v. vi.
Fetus:i. Recurrent infections

Polyhydramnios
Induced labor

If vaginal birth occurs → shoulder dystocia and extended perineal tears.

Develop type 2 diabetes post-gestational

Neonatal unit admissionii.

Hypoglycemia (due to increased fetal pancreas activity to oppose the uncontrolled maternal glucose that crosses the placenta. Maternal insulin does not cross so fetus is dependent on its own supply.)

iii. IRDSiv.

Jaundicev. Macrosomia8. vi. Management:Increased risk for diabetes and obesity in childhooda.

During pregnancy – control blood glucose levels.

i. Low glycemic index foodsii. Medication – metformin, glibenclamide and insulinb. During labor – fetal blood glucose monitoring.

c. Post labor – stop treatment and continue monitoringi. If values are normalized → true gestational diabetesii.

If values remain elevated → masked (prior to pregnancy) or developed diabetesInfections1. Diseases:a. Chicken poxi. Pathogen: varicella zoster.

ii. Disease: pneumonia (fetal and maternal), congenital varicella syndrome (eye defects, limb hypoplasia and neurological defects)

iii. Management: IgG prophylaxis (for non-immune women) or acyclovir (for infected women)

. Parvovirus 19

i. Pathogen: parvovirus 19

ii. Disease: erythema infectiosum / fifth disease / slapped cheek syndrome, fever, rash, arthropathy, fetal anemia (aplastic anemia), miscarriage, fetal hydrops (heart failure → edema, ascites, pleural effusion, pericardial effusion).

iii. Management:* Maternal: analgesics and antipyretics* Fetal: infection after week 20 → Doppler US of middle cerebral artery can detect fetal anemia → if so utero blood transfusionsc. Influenza H1N1

i. Disease: fever, cough, respiratory failure, secondary infections, preterm birth, stillbirth, neonatal death.

ii. Management: vaccine or antiviral medication (oseltamivir, zanamivir) for infected women.d. HIVi.

ii. Disease: AIDS, secondary infection, cancer development, vertical transmission (transplacental or vaginal birth or breast feeding), miscarriage, stillbirth.

Management: HAART (highly active anti-retroviral therapy), C-section (in women who do not take HAART) and avoid breast feeding.

e. Viral hepatitisi.

Pathogen: Hepatitis A, B, C, D and E

ii. Transmission: A (fecal-oral), B&C (blood)iii. Disease: preterm birth, vertical transmission (perinatally)

iv. Management:
* Prvention (hygiene – Hep. A, vaccine – Hep. B)
* Screening – to reduce vertical transmission and exclude co-infection with HIV

• Vaginal delivery with avoidance of interventions that may increase bleeding (C-section and lack of breast feeding do NOT reduce vertical transmission).

f. * Tuberculosis:Fetal immunization with IgG and vaccinei.

Pathogen: Mycobacterium tuberculosisii. Disease: miscarriage and same as in non-pregnantiii.

Diagnosis: Tuberculin test (in suspected women) → x-ray chest (in positive tests)

iv. Management: RIPE antibiotics (streptomycin is contraindicated as it causes deafness)UTI1.

Features:a. 2-10% of all sexually active women2. b. Causes:30% out of this group develops ascending infections

a. E. coli (most common)
Complications:

a. Pyelonephritis → bacteremia and septic shock

b. Preterm

4. Management: antibioticsThromboembolic disease (VTE)
5. Features:
   a. 10 times more common in pregnancy than non-pregnant
6. b. Causes:a.

b. c. Leading cause of maternal mortality
Increased coagulation factors

Suppressed anticoagulants and fibrinolysisVenous stasis due to compression on pelvic vessels

Prothrombotic pregnancy state

3. Risk factors:a. Family history of VTEb.

Thrombophiliac.

Obesity

d. Smokinge. Sickle cells diseasef. Immobilityg. Operative deliveryh. Multiple pregnanciesi. Pre-eclampsiaj.

Contraceptives (estrogen containing)

4. Diagnosisa. Doppler USb. MRI

c. CT (with caution to fetus)

5. Clinically:

a. DVT: swelling and tenderness of the legi. Compression of left common iliac vein by the right common iliac artery lead to stasis and thrombus formation most commonly in the iliac or femoral veins.

b. PE: dyspnea and pleuritic chest pain

6. Management:

a. Prophylaxis for high risk – elastic compression stock and LMWH.i. LMWH – does not cross placenta

ii. Warfarin – crosses placenta causing abnormalities if used in 1st trimester

iii. Stop treatment briefly perinatally to reduce postpartum hemorrhage but continue again for 6 weeks after delivery.

b. In acute case – heparin therapy

Liver disease

1. Obstetric cholestasisa.

Definition: static bile acids flow commonly in 3rd trimester

b. Risk factors:i.

Genetics

ii. Hormonal pregnancy state (influencing bile acids flow)

iii. Ethnicityc.

Clinically:

i. Itching (especially palms and soles) → cholestatic pruritis (irritation of nerve endings)

ii. Pale stool

iii. Dark urineiv. Jaundiced.

Diagnosis:

i. High serum bile acids

ii. High liver enzymes

iii. Serology – rule out hepatitis and autoimmune hepatitis (anti-SM and antimitochondrial antibodies)

e. Complication:

i. Preterm birth

ii. Still birth

iii. Impaired liver function (prolonged bleeding time)

iv. Recurrence in following pregnancies

f. Management:

i. Medication: ursodeoxycholic acid (for itching and liver function), vitamin K (for bleeding), cholestyramine

2. Acute fatty liver of pregnancy (AFLP)a. Definition: rare disease most common in the third trimester characterized by extensive fatty infiltration of the liver, which can result in acute liver failureb.

Risk factors:

c. i. Multiple pregnancies

ii. Obesity

Pathomechanism:

i. Mutated mitochondrial enzyme (of the fetus) leads to unoxidized fatty acids that enter the maternal circulation and accumulate in her liver.

d. Clinically:

i. Non-specific symptoms – nausea, vomiting, abdominal pain

ii. Jaundicee.

iii. Coagulopathy with risk for DICiv. Hypoalbuminemia and ascites

Diagnosis:i. Symptoms

ii. Exclude other causes

• Pre-eclampsia
• HELLP syndrome (hemolysis, elevated liver enzymes and low platelets).
• Viral hepatitis

iii. iv. v. Hypoglycemia
Elevated liver enzymes
Biopsy

f. Management:

i. Immediate C-sectiong.

Complications:
i. Acute liver failure
ii. Hemorrhage
iii. Hepatic encephalopathy (nitrogen-containing compounds are not excreted because urea cycle is impaired.

These compounds go to the circulation cross the BBB and are consumed by astrocytes that use them to produce glutamate. Glutamate causes increased osmotic pressure and astrocytes are swollen).

Question 9

Pre-existing medical conditions and pregnancy

Answer 9

(Another table in note)

iv. Ophthalmic assessment each semester for diabetic retinopathy

Fetal assessmenti. Chromosomal problems (1st trimester) and routine anatomy check (week 20).

ii. Additional cardiac anatomy scan.

f. Give birth in hospital with neonatal facilities.

Thyroid diseases

1. Features:

a. Estrogen increases TBP (thyroid binding proteins) that reduce levels of T4 and T3 in the

b. c. blood → resulting in increased production by the thyroid to maintain normal levels.

Iodine levels fall due to increased renal loss leading to enlarged thyroid.

TSH levels drop due to hCG.

2. Hyperthyroidism:

a. Causes:

i. Grave’s disease (laboratory shows high T4 and T3 with low TSH)

b. Implications:

i. Pregnancy over disease – increases thyroxine demand so it has less significance in pregnancy, unless there is untreated thyrotoxicosis.

ii. Disease over pregnancy: pre-eclampsia, fetal growth restriction, still birth, fetal thyrotoxicosisc.

Management:

i. Thyroid function tests
ii. Anti-thyroid therapy (methimazole and propylthiouracil)
iii. Assessment of fetal growth and heart rate

3. Hypothyroidism:

a. Causes:

b.
i. Autoimmune (autoantibodies, Hashimoto disease).
ii. Iatrogenic (thyroidectomy, anti-thyroid drugs)

Implications:

i. Pregnancy over disease – few effects.

ii. Disease over pregnancy – spontaneous abortion, pre-eclampsia, low birth weight, reduced IQ, congenital iodine deficiency syndrome (cretinism)

c. Management:

i. Thyroid function test (T4) and TSH levels every trimester.

ii. Iodine supplementation or dietary.

Obesity

1. 2. 3. Definition: BMI > 25 (weight / (height^2)

Features:

a. Co-morbidities of HTN, sleep apnea, cardiovascular disease

Implications:

a. Pregnancy over disease – increased weight gainb. Disease over pregnancy

i. Increased miscarriage and congenital abnormalities (1st trimester)

ii. Pre-eclampsia and gestational diabetes (2nd trimester)

iii. Fetal macrosomiaiv.

Childhood obesity and juvenile diabetes.
v. Induction of labor and C-section.

4. Management:

a. Pre-counseling

b. Diet support.

c. Folic acid (until week 12 due to increased neural defects)

d. Assessment for co-morbidities.e. Low dose aspirin for pre-eclampsia and thromboprophylaxis.

f. OGTT throughout pregnancy.g. Fetal screening – poor ultrasound visualization because of mother

Thrombophilia

1. Features – pregnancy is a prothrombotic state.
2. Implications:

a. Disease over pregnancy:i. Thromboembolism

ii. Factor V Leiden mutation leads to fetal loss

iii. Pre-eclampsia

iv. Placental abruptionv. Growth restriction

vi. Miscarriage

vii. Premature birth

3. Management:

a. Screening for thrombophilia (family history, recurrent miscarriage, early onset of preeclampsia)

b. Obstetrician and hematologist assessmentsc. Prophylactic LMWH (safer in pregnancy) – around time of birth to avoid bleeding

d. Compression stockingse. Hydrationf. Antiphospholipid syndrome

i. Recurrent pregnancy loss before week 10 and the presence of lupus anticoagulant and/or anticardiolipin antibodies.

ii. Therapy with aspirin combined with heparin reduces pregnancy loss.

Epilepsy

1. Definition: neurological disorder in which brain activity is abnormal, causing seizures or periods of unusual behavior and sometimes loss of awareness
2. Implications:

a. Pregnancy over disease – variable. Seizures frequency can increase, decrease or stay the b. same.Disease over pregnancy:

i. Congenital abnormalities (due to anti-epileptic drugs)

ii. Tonic-clonic seizures (muscle contractions and relaxations) associated with fetal loss.

iii. Increased chance for child with epilepsy

3. Management:

a. Pre-counseling to discuss risk and review of taken medications.

b. Risk of uncontrolled epilepsy is greater than risk of taken medications.

c. Aim is to avoid seizures during pregnancy.

Cardiac diseases

1. Features:
2. a. b. Causes:

a. Most common cause for indirect maternal death.

Mostly Acquired
Valvular lesions

b. Congenital heart disease

c. Cardiomyopathies

d. Arrhythmiase. Ischemic heart disease.

3. Implications:

a. Pregnancy over disease:

i. Deterioration of conditions (aortic stenosis, regurgitations etc.) due to increased cardiac demand in pregnancy.

ii. Mimic of normal pregnancy symptoms such as dizziness, syncope, palpitations

iii. Risk for: CHF, hypoxia, bacterial endocarditis, VTE, aortic dissection, angina and ischemia

4. Disease over pregnancy

:a. Depends in the cardiac problem

.b. Increased risk in general: pre-eclampsia, intrauterine growth, preterm birth

5. Management:

a. Pre-counseling as sometimes pregnancy may not be advisable.

Eisenmenger’s syndrome - left-to-right cardiac shunt caused by a congenital heart defect (ventricular septal defect, atrial septal defect or patent ductus arteriosus) causes pulmonary hypertension

b. Medications (may be required)i. Anticoagulants

c. Fetal assessments

i. Growth scans

ii. Cardiac abnormalities

d. Special attention to postpartum period as it is most risky due the hemodynamic changes

Respiratory disorders

1. Asthmaa.

Implications:

i. Pregnancy over disease – variable.
ii. Disease of pregnancy – if well controlled no adverse effects, else, premature birth, pre-eclampsia and growth restrictions.

b. Management:
i. Medications (safe for pregnancies)ii. Avoid triggering agents.

2. iii. Cystic fibrosis:In acute case the treatment is the same as in non-pregnant.

a. Implications:

i. Pregnancy over disease – pregnancy can be tolerated well but risk relate to degree of pulmonary dysfunction which can deteriorate.

ii. Disease of pregnancy – fetal inheritance, gestational diabetes, preterm birth

b. Management

:i. Genetic counseling

ii. Treatment of GI and lung dysfunctions.

iii. Pulmonary function tests at prior and during pregnancy.

iv. High dose folate (5mg/day)v. Nutritional supportvi.

Treat chest infections immediately.

vii. OGTT

Autoimmune

1. Features:

a. b. Some diseases may “benefit” from the suppressed immune state of pregnancy such as Crohn’s disease and RA.

Other diseases include: SLE, APS, scleroderma etc.

2. SLE
   a.
   b. Diagnosis:i. At least 4/11 clinical criteria + serology (positive ANA)

Implications

:i. Pregnancy over disease: increased relapses and deterioration of kidney function.

ii. Disease over pregnancy:

1. Miscarriage
2. Stillbirth
3. Pre-eclampsia
4. Preterm birthc.
   5.
5. Management:If co-existence with APS → increased VTE riskIncreased neonatal lupus and congenital heart block

i. Avoid pregnancy at least 6 months after flare.

ii. Medications:

1. Low dose aspirin for pre-eclampsia
2. LMWH for APS co-existenceiii.
3. Steroids in severe lupus cases (but only non-teratogenic)

Induced labor at weeks 37-38 to avoid thrombotic events.
Hemoglobinopathies

1. Sickle cells anemia:

a. Definition: autosomal recessive disorder of a gene mutation of glutamic acid to valine on the beta-globin subunit.

Polymerization of hemoglobin ensues resulting in sickling of erythrocytes.

2. Implications:

a. Pregnancy over disease – variable according to severity of disease (heterozygous or homozygous).

i. Sickle cell crisis - acute conditions leading most commonly to vaso-occlusive crisis and splenic crisis with splenomegaly presenting with severe pain and limb swelling.

b. Disease over pregnancy:

i. Anemia and infections

ii. Preterm birth
iii. Miscarriage,
iv. VTE
v. Growth restrictions

c. Management:
i. Prenatal diagnosis (of both partners)
ii. High dose folate due to increased hemolysis

. Low dose aspirin for pre-eclampsia.

iv. Prophylactic antibiotics
v. Fetal assessments (growth scans)vi. Blood transfusions if necessary

vii. VTE prophylaxis

Question 10

Congenital abnormalities

Answer 10

g. Tetralogy of Fallot - pulmonary stenosis, ventricular septal defect, right ventricular hypertrophy, overriding aorta (blood from both ventricles enter the aorta)

2. Diagnosis:

a. Ultrasound – 18th-20th weeks using several views:

i. Four chamber view
ii. iii. iv. Abdominal wall defects
Left ventricular outflow view

Right ventricular outflow view

Transverse abdominal view standard fetal echocardiogram consists of several specific views which can be obtained to optimize visualization of different cardiac abnormalities

1. Types:

a. b. Gastroschisis – herniation through rectus abdominis muscle (usually below and to the right from the umbilical cord) and without peritoneal covering.

Size of the hole is variable so sometimes other organs can be seen but mostly only intestines.

Exomphalos (Omphalocele) – large hernia of the umbilical cord with peritoneal covering

Abdominal wall defects
Left ventricular outflow view
Right ventricular outflow view

Transverse abdominal view standard fetal echocardiogram consists of several specific views which can be obtained to optimize visualization of different cardiac abnormalities

1. Types:

a. b. Gastroschisis – herniation through rectus abdominis muscle (usually below and to the right from the umbilical cord) and without peritoneal covering.

Size of the hole is variable so sometimes other organs can be seen but mostly only intestines.

Exomphalos (Omphalocele) – large hernia of the umbilical cord with peritoneal covering

2. Complications:

a. Intrauterine growth restrictions
b. Intestinal atresiac.
Premature birth

3. Management:

a. Postpartum surgery
Chromosomal abnormalities

1. Definition: Structural or numerical abnormality of the chromosomes.

Normal human karyotype is diploid (2 copies of each chromosome) with 22 somatic pairs and 1 sex pair of chromosomes.

Chromosomal abnormalities identified from the culture and karyotyping of fetal or placental cells in the amniotic fluid or from the chorionic plate.

2. Types

a. Down’s syndrome (trisomy 21)

i. Clinically:

• Mental retardation and progressive IQ decline
• Congenital heart diseases
• Flat face and occiput with low flat nose, epicanthal folds
• Short ribs, pelvis, extremities and hands exhibiting simian crease.
• Duodenal stenosis
• Infertilityii.
• Types:*
• High risk for leukemiaNondisjunction (95%) - before conception (all cells are triploid) or after conception (variable severity depending when the nondisjunction occurred – leading to mosaic pattern)Robertsonian translocation (5%)

– between chromosome 14 and 21.

iii. Diagnosis:

• Amniocentesis or chorionic villus sampling
• Nuchal translucency:

o Describes the sonographic appearance of fluid collection under the skin behind the neck.

o Done in weeks 11-13o Measure higher than >3mm is abnormalo

Criteria: sagittal section with certain structures that are needed to be visible, neutral position of fetal head (not hyperflexed or extended), widest thickness is measured (higher value higher risk), depends on crown-rump length (CRL)*

• In case of increased risk additional finding at weeks 14-20 may include no or small nasal bone, large ventricles

Quad test – maternal blood measurements of hCG, AFP, Estriol and Inhibin-Ab.

c. d.

• Post birth – physical appearance and karyotyping

Turner syndrome – sex chromosome monosomy (X0) and fetus usually undergo spontaneous abortion.

Klinefelter syndrome – sex chromosome trisomy (XXY) due to nondisjunction of first meiotic division.

Edward’s syndrome (Trisomy 18) – most infants die postnatally.

Question 11

Assessment of fetal wellbeing

Answer 11

h. Biometry (BPD, OFD, HC, AC, FL) – IUGRWeeks 36-37 (+6 days)i. Fetal presentation

j. Biometry

k. Amniotic fluid volume

l. Placental localization and maturitym.

Previous C-section scar (with full bladder)Blood tests and amniocentesis (screening for Down’s syndrome)

1. Sampling is done by

a. Chorionic villus sampling (CVS)
b. Amniocentesis

2. Combined screening testa. Between weeks 11-13

b. Nuchal translucency (NT) – see criteria for measurement and also needed CRL measures are 45-84mm

c. Biochemical markers hCG and pregnancy-associated plasma protein A (PPPA)

3. Quad test

a. Between weeks 14-20

b. Biochemical markers – hCG, inhibin-A, AFP and unconjugated estradiol (uE3)

Doppler examinations

1. Normal fetal recording (A)
2. Absent end-diastolic velocity (AEDV) is a typical type UPVD.

Usually fatal but early recognition and monitoring until elective term can be performed at 34 weeks (B).

3. Reverse end diastolic velocity (REDV) – leads to fetal death but elective pre-term at 26 weeks or more may be done

(C)
Fetal growth

1. Definition: ultrasound measurements of the head (HC) and abdominal (AC) circumferences.
2. Small fetus – suboptimal fetal growth with values below the lowest centile range.
3. Typical – not high risk for complications and seen usually in short or Asian ethnicity woman.
4. Atypical asymmetric – tends to occur at later pregnancy and associated and associated with UPVD.
5. Atypical symmetric – tends to occur in early pregnancy and associated with severe early onset of pre-eclampsia.
6. Large fetus
7. Typical – usually seen in tall women or Afro-Caribbean ethnicity.
8. Atypical – accelerated growth above the upper limit of the central range.

Mostly seen in diabetic women.Amniotic fluid volume (AFV)

1. Accurate measurement is done with US and two method are used:

a. Single deepest pocket – normal range is 2-8 cm. The deepest longest vertical diameter of echo-free pocket between the fetus and uterus.

Less than 2 is oligohydramnios and more than 8 is polyhydramnios.

b. Amniotic fluid index (AFI) – sum of measurements of the largest pocket in each of the four quadrants. Normal range is 6-24.

Biophysical profile scoring (BPS)

1. Definition:

prenatal evaluation of the fetal well-being involving a scoring system.

Normal score is a fetus presenting at least 4 of the following parameters in a period of 40 minutes.

Parameters are:a. b. c. d. e. Fetal heart rate (FHR) – recorded with cardiotocograph (CTG) maximum recording of 40 minutes.

At least 2 accelerations of 15 bpm lasting for at least 15 seconds.

Normal FHR is 110-160 bpm.

Fetal movements – maximum of 40 minutes fetal observation in ultrasound.

At least 3 separate distinct movementsFetal tone – one of the fetal movements demonstrates full 90-degree flexion-extension flexion cycle of the limb or opening and closing of the hand.

Fetal breathing – maximum of 40 minutes fetal observation in ultrasound. At least one episode of 30 seconds regular fetal breathing movements.AFV - at least 1 vertical measurement between 2 – 8 cm.

Management1. When fetal risk is proven real by fetal surveillance methods mentioned above, there are only two intervention that are in value:

2. Elective deliverya. ≥34 weeks elected delivery is performed.b. <34 weeks if acute measures of health are abnormal then delivery is performed. If normal continuous monitoring to gain time.
3. Maternal steroidsa. In case of elective delivery is set in a high-risk pregnancy and the chronic fetal measures are abnormal then betamethasone is given

Question 12

Normal labour

Answer 12

Uterine activity in labor

1. The 3 P’s of birth progression (power, passages and passenger)

a. Poweri.

Infrequent, low-intensity contraction throughout pregnancy are replaced by the activity of contractions that show an increase in frequency, duration and strength as full-term approaches.

ii. Identification of these contractions by palpitation or tocography and intrauterine pressure by a measuring catheter (normal resting tone is around 10-20mmHg)

iii. Establishment of labor is likely when 2 contractions last >20 seconds in a period of 10 minutes.

iv. Retraction - progressive contractions lead to effacement and dilatation of cervix due to shortening of myometrial fiber in the upper segment and stretching and thinning of lower segment.

As uterus and round ligaments contract the longitudinal axis are pulled towards the abdominal wall and the realignment if the axis is what promotes the descent of the presenting part.

vi. Obstructed labor – an abnormal junction between the upper and lower segments may become visible at the level of the umbilicus called retraction ring (Bandl’s ring)

b. Passagesvii. Structure of bony pelvis (described in earlier chapters)viii. Size and shape of the pelvis varies and effects the outcome of labor.

ix. Softening of sacroiliac ligaments and pubic symphysis allow expansion of pelvic cavity.

Passenger

x.Fetal size, lie and position (described in earlier chapters)

Mechanism of labor
1. Descent – occurs throughout labor.

Engagement of head occurs before onset of labor in the majority of primigravid but not multipara. Provides measure of the progress of labor.

2. Flexion – head flexes towards the chest which reduces the diameter of presentation.

Begins from deflexed occipito-frontal diameter to suboccipitobregmatic diameter which is fully flexed.

3. Internal rotation – head rotates when it reaches pelvic floor and the occiput is facing anteriorly towards the pubic symphysis in most cases but also face-to-pubis delivery may occur.
4. Extension – head extends until it is delivered. The occiput comes in contact with the inferior rami of the pubis.
5. Restitution – after delivery the head, it rotates back to its normal relationship with the shoulders.
6. External rotation – shoulders reach pelvic floor and rotate antero-posteriorly.
7. Delivery of shoulders – final expulsion of trunk occurs after shoulders are delivered.

Question 13

Abnormalities of the third stage labour

Answer 13

• Hysterectomy (last resort)Vaginal wall hematoma

1. Causes:
2. a. Vaginal and perineal lacerations by assisted delivery

Symptoms

a. Anemia
b. Pelvic pain
c. Urine retention

3. Diagnosis

a. Visible bleeding
b. Vaginal examination – in deep bleedings where bleeding is not visible a bulge can be felt
c. Ultrasound

4. Management

a. Venous bleeding controlled by compressionb. Arterial bleedingi.

Superficial – drainage and ligature of vessels.

ii. Deep – incision, drainage, suturing and antibiotics.

Amniotic fluid embolism (AFE)

1. Diagnosisa. Sudden development of ARDS and shock in patients in labor or recently delivered
2. Pathomechanism

a. Amniotic fluid enters maternal circulation via tears in the placental membrane →triggers anaphylaxis shock like response → DIC is followed bleeding to massive bleeding

3. Managementa. Supportive (oxygenation)

Question 14

Postpartum problems

Answer 14

i. Dehiscence

ii. Necrotizing fasciitis

5. Thromboembolisma.

Thrombophlebitis

i. 3-5 days post-delivery

ii. Superficial venous inflammation of the legs

iii. No severe manifestations

iv. Anti-inflammatory drugs

b. Phlebothrombosis (DVT)

i. 7-10 days post-delivery

ii. Risk factors:

• Immobilization

iii. Symptoms
* Chest pain
* Dyspnea
* Hemoptysis

iv. Diagnosis
* Ronchi and pleural rub
* Chest CT

6. Maternal collapse

a. Definition: involving cardiorespiratory system with decreased consciousness up to 6 weeks following pregnancy.

b. Causes: 4 T’s4 H’s

Thromboembolism
Tamponade (cardiac)
Tension pneumothorax
Toxicity (drugs)
Hypoxia
Hypovolemia
Hypothermia
Hypo- or hyperkalemia

Question 15

Psychiatric disorders of childbirth

Answer 15

Screening

1. History taking

a. Family history

b. Drug abuse (substance misuse)

c. Current mental health (early pregnancy and also on later occasions)

d. Whooley questions

i. During the past month have you often been botheredby feeling down, hopeless or depressed?

ii. During the past month have you often been botheredby having little interest or pleasure in doing things?

iii. Do you feel you need or want help with this?

2. Edinburgh Postnatal Depression Scale (EPDS)

a. Management

10 screening questions that can indicate whether mother has symptoms that are common in depression and anxiety.

1. Principles

a. Mild disorders may improve as pregnancy progresses

b. Serious disorders who have not shown relapse in more than 2 years are not consideredto be for high-risk antenatal recurrence (the opposite is also true)

c. Serious disorders who have not shown relapse in more than 2 years are considered to be for high-risk postnatal illnessd.

Women under medications are considered for high-risk of both antenatal and postpartum relapsee. For new-onset symptomatic disorders “watch-and-wait” approach (for 2 weeks)

f. Relapse is common after recent illness or stopping medication intake

g. Some medications are safe to use while others should be stopped before conception or reduced and slowly withdrawn

2. Non-medication

a. Psychological treatment

b. Counselling

c. Cognitive behavior therapy

d. Family and other health professional care providers involvement

e. Lifestyle change

3. Medications

a. Antidepressants

i. Monoamine oxidase inhibitors (MAOIs)

• Not used due to risk of drug and food interactions

ii. Tricyclic antidepressants (TCAs) – amitriptyline, imipramine, clomipramine, doxepin

• No risk for fetal abnormalities (except for clomipramine)

iii. Selective serotonin reuptake inhibitors (SSRIs) – fluoxetine, paroxetine, sertaline

• Risk for cardiac abnormalities (ventricular septal defects)Antipsychotic - for schizophrenia and bipolar illness

i. Typical “older” drugs (chlorpromazine, trifluoperazine)

• No risk for fetal abnormality but associated with poor obstetric outcome (e.g. early delivery and increased C-section rate)

ii. Atypical “newer” drugs (olanzapine, quetiapine, risperidone)

• No risk for fetal abnormality but associated with gestational diabetes, venous emboli and weight gain

c. Mood stabilizers and anti-epileptics – for bipolar disorders

i. Valporate (lithium containing agents)

ii. Risk for cardiac abnormalities, neural tube defects, fetal hypothyroidism and polyhydramnios.

iii. If no evident relapse for the last 2 years medication should not be used. Otherwise it can be used but alternatives should be explored.

Prevention

1. Counsel women with chronic severe mental illness about pregnancy
2. Bipolar illness: consider restarting treatment after delivery
3. Maintain chronic schizophrenic medication throughout pregnancy
4. Previous history of serious mental illness or puerperal psychosis/severe postnatal depression: close contact first weeks
5. Consider prophylaxis after delivery
6. Assess all women at

6 weeks postnatal check for postnatal depression