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Parity : the number of pregnancies that have been carried to > 20 weeks
Trimesters
o T1: 0 to 12 weeks
o T2: 12 to 28 weeks
o T3: 28 to 40 weeks
Stillbirth : loss of intrauterine pregnancy after 20 weeks and/or > 500 g fetal weight
Stillbirth Rate : the annual number of stillbirths per 1000 total births
Perinatal Mortality Rate : the annual number of stillbirths and early neonatal deaths (in the
first seven days of life) per 1000 total births
causes
prematurity
congenital anomalies
Neonatal Mortality Rate : the annual number of deaths of liveborn infants within 28 days per
1000 live births
Infant Mortality Rate the annual number of deaths of liveborn infants in the first year of life
per 1000 live births (includes neonatal mortality)
Maternal Mortality Rate the annual number of deaths of women while pregnant or within 90
days of pregnancy per 100 000 live births
Birth Rate : the annual number of live births per 1000 population
Fertility Rate : the annual number of live births per 1000 women aged 15-44 years
DIAGNOSIS OF PREGNANCY
Symptoms
1. amenorrhea
2. nausea and/or vomiting
3. breast tenderness
4. urinary frequency fatigue
Signs
Investigations
1. Beta hCG
2. Transvaginal ultrasound
o 5 weeks: gestational sac visible (Beta hCG = 1200 -1500 mIU/mL)
o 6 weeks: fetal pole seen
3. Transabdominal U/S
intrauterine pregnancy visible at Beta hCG = 5000 mIU/mL
General Principles
Cardiovascular System
1. increased cardiac output, heart rate, and blood volume (hyperdynamic circulation)
2. decreased blood pressure (especially diastolic, maximal in T2) due to decreased
peripheral vascular resistance
3. blood flow to the uterus, kidneys, breasts, and skin increases with
gestational age
4. enlarging uterus compresses IVC and pelvic veins leading to risk of hypotension (by
decreasing venous return) as well as varicose veins, hemorrhoids and leg edema (because
of increased venous pressure)
Hematologic System
*** Placenta and the foetus are made up of different genetic components, the immune
tolerance that is necessary for the non-rejection of the foetus
Respiratory System
** This maintain higher concentration gradient of CO2 between mother and Foetus
Gastrointestinal System
1. increased gastroesophageal reflux ,due to
Neurologic System
Integumentary System
o spider angiomas
o palmar erythema
chloasma
linea nigra
spider angiomas
striae gravidarum
Genitourinary System
1. increased GFR 50% (therefore decreased BUN and serum creatinine) but no change in
urine output because of increased reabsorption in tubules glycosuria can be physiologic;
with increase in GFR the threshold for glucose reabsorption can be surpassed
2. increased urinary frequency
3. physiologic dilatation of ureters and renal pelvis (R > L) due to progesterone-induced
smooth muscle relaxation and uterine enlargement
4. increased incidence of UTI and pyelonephritis due to stasis
Endocrine System
1. estrogen
2. progesterone
6. levels below expected by dates suggest an ectopic pregnancy, abortion or wrong dates
7. levels higher than expected suggest multiple gestation, molar pregnancy, trisomy 21, or
wrong dates
4. thyroid
6. prolactin
7. relaxin
Ca++ metabolism
1. folic acid to prevent NTD s (0.4 to 1 mg daily in all women, 4 mg if past NTD)
2. genetic history and risk factors
3. modify medications, alcohol, smoking
4. rubella immunity
5. proper nutrition
6. use of prenatal vitamin and iron supplementation
7. impact on family and occupation (maternity/paternity leave)
8. domestic violence (50% of domestic violence begins in
pregnancy) depression / mental health
INITIAL VISIT
History
1. determine GA by dates from the first day of the LMP (if regular periods and sure dates)
2. if LMP unsure, get a dating ultrasound
3. determine EDC using the Naegele Rule
Physical
1. complete physical exam
2. baseline BP (very important for relating subsequent changes)
3. baseline weight
4. pelvic exam
Investigations
1. blood work
2. urine
R&M (Routine and Microscopy), C&S (Urine culture and sensitivity)
asymptomatic bacteriuria in 5% of pregnant women
if untreated 25-30% will get a UTI in pregnancy (increased risk of preterm labour)
3. pelvic exam
Pap smear (if none within 6 months), culture for GC and Chlamydia
1. estimate GA
2. urine dip for glucose and protein
3. weight gain
4. blood pressure
5. symphyseal-fundal height measurement:
6. differential diagnosis of uterus incorrect size for dates (accurate dates essential)
maternal--> DM
maternal-fetal--> polyoligo-hydramnios, multiple gestation
fetal--> abnormal karyotype, IUGR, fetal anomaly
Gestation-Dependent Management
1. offers a risk estimate of whether the fetus may be affected with Downs
syndrome, trisomy 18, or a NTD
2. to make accurate diagnosis, positive MSS should be followed up with U/S and/or
amniocentesis
3. three markers
missed abortion
chromosomal anomalies (e.g. Trisomy 18, 21)
6. 80% of Downs babies born to women under 35 years, so MSS is a valuable screening tool
8. detection rate of Trisomy 21 with the 3 markers is 2-3 times higher than with MSAFP alone,
however will still miss 20-30% of Trisomy 21 pregnancies in older women and will not reliably
detect other chromosomal anomalies that occur more frequently in older women so
amniocentesis should still be offered to high risk women
Group B Streptococcus
o preterm labour
o PROM > 12 hours
o fetal tachycardia
PRENATAL DIAGNOSIS
Indications
Amniocentesis
L/S ratio: if > 2:1, fetal lungs are mature enough that RDS less likely to occur
used to quantitate amniotic fluid bilirubin concentration in Rh-isoimmunized pregnancies
advantages
disadvantages
disadvantages
ANTENATAL MONITORING
Fetal Movements
Assessed by
Ultrasound
routinely done at 4-5 month to assess fetal growth and anatomy
earlier or subsequent U/S only when medically indicated
constant fetal heart rate (FHR) tracing using an external doppler to assess fetal heart rate
and its relationship to fetal movement (see Intrapartum Fetal Cardiotocography)
indicated when there is any suggestion of uteroplacental insufficiency or suspected fetal
distress
reactive NST (normal)
observation of two accelerations of FHR > 15 bpm from the baseline lasting >15 seconds in 20
minutes
nonreactive NST (abnormal)
consists of NST and 30 minute ultrasound assessment of the fetus five scored parameters
of BPP (see Table 2)
scores
INTRA-PARTUM MONITORING
Vaginal Exam
1. membrane status
2. cervical effacement (thinning), dilatation, consistency, position, application
3. fetal presenting part, position, and station
4. bony pelvis size and shape
periodicity
accelerations
excursion of 15 bpm or more lasting for at least 15 seconds, in response to fetal movement or
uterine contraction
decelerations
describe in terms of shape, onset, depth, duration, recovery, occurrence, and impact on baseline
FHR and variability
early decelerations
1. uniform shape with onset early in contraction, returns to baseline by end of contraction;
slow gradual deceleration
2. often repetitive, no effect on baseline FHR or variability
3. due to vagal response to head compression
4. benign, usually seen with cervical dilatation of 4-7cm
variable decelerations
late decelerations
1. uniform (symmetric) in shape, with onset late in contraction, lowest depth after peak of
contraction, and returns to baseline after end of contraction
2. may cause decreased variability and change in baseline FHR
3. must see 3 in a row, all with the same shape to define as late deceleration
4. due to fetal hypoxia and acidemia, maternal hypotension, or uterine hypertonus
5. usually a sign of uteroplacental insufficiency (ominous)
6. manage with position change to left lateral decubitus,oxygen, stopping oxytocin, C/S
consistency
MULTIPLE GESTATION
1. rest in T3
2. increased antenatal surveillance
3. close monitoring for growth (serial ultrasounds)
4. vaginal examinations in third trimester to check for cervical dilatation
5. may attempt vaginal delivery if twin A presents as vertex, otherwise C-section
6. twin B should be delivered within 15-20 minutes after twin A (may be longer if FHR
tracing adequate)
1. occurs more frequently in pregnancy and puerperium (time immediately after the delivery
of a baby)
2. most common medical complication of pregnancy due to increased urinary stasis from
mechanical and hormonal (progesterone) factors
3. organisms : same as non-pregnant woman, also GBS
4. may be symptomatic or asymptomatic; treat all
5. risk of acute cystitis, pyelonephritis, and possible PPROM (Preterm Premature Rupture
of Membranes)
6. recurrence common treatment of pyelonephritis during pregnancy requires
hospitalization and IV antibiotics
7. treatment of asymptomatic bacteruria or acute cystitis
ron requirements increase during pregnancy (mother needs 1000 mg of elemental iron per fetus;
this amount exceeds normal stores)
Etiology
Complications
Diagnosis
1. CBC, blood film, serum ferritin (changes in ferritin stores first sign of anemia)
2. microcytic, hypochromic anemia with decreased ferritin
3. morphology not good indicator because of RBC half life
4. TIBC not reliable because increased during pregnancy
Treatment
1. Prevention :
o dietary iron and iron mobilized from stores insufficient to meet demands
o adequate iron intake (30 mg elemental iron/day) for all women
2. oral supplement of 200 mg/day of elemental iron if anemic
3. monitor
Etiology
1. malnutrition
2. malabsorption (e.g. sprue) c
3. hronic hemolytic anemia (e.g. SCD)
4. multiple gestation medications (i.e. phenytoin, trimethoprim-sulfamethoxazole, oral
contraceptives)
Complications
Diagnosis
Treatment
1. 1 mg folic acid PO daily
2. 4 mg folic acid per day with past history of neural tube defect
DIABETES MELLITUS IN PREGANACY
Incidence
Fetal
Neonatal
Treatment of DM in Pregnancy
T1
1. see prior to pregnancy to optimize glycemic control (will reduce risk of congenital
anomalies)
2. since oral hypoglycemics are contraindicated, Type IIs must be switched to insulin
3. counsel : potential complications and risks
4. advise preconception folic acid
5. see early and date pregnancy
6. consult internist and dietitian to manage insulin and diet
7. measure hemoglobin A 1C early in T1 or preconception if possible; this gives an
indication of glycemic control during embryogenesis and can be used to estimate risk of
birth defects
8. initial evaluations: 24 hour urine (protein and creatinine clearance), retinal exam, ECG,
urine C&S, hemoglobin A 1C
9. throughout pregnancy monitor BP, urine dip (protein/glucose/ketones), weight gain,
blood glucose (self-monitor) every visit and occasional urine C&S and hemoglobin A1 C
10. in early pregnancy transfer of glucose and amino acids to the fetus results in a tendency
toward maternal hypoglycemia
11. nausea and vomiting may reduce food intake, therefore may need to decrease insulin dose
T2
T3
Labor
Postpartum
GESTATIONAL DIABETES
Risk Factors
1. age > 30
2. previous history of high blood glucose, GDM, or macrosomic infant (> 4.5 kg) p
3. ositive family history (GDM, Type II DM, macrosomic infant)
4. excessive weight gain in pregnancy, prepregnancy obesity
5. baby > 4.5 kg or large for GA
6. previous unexplained stillbirth
7. previous congenital anomaly
8. early preeclampsia or polyhydramnios
9. repeated vaginal candidiasis
10. member of high risk ethnic group
11. multiple gestation
Diagnosis
1. screen at 26 weeks (or earlier) with 50 g oral glucose challenge test if risk factors or
glycosuria are present
2. > 7.8 mmol/L at 1 hour is abnormal
3. confirm with 3 hour 100 g oral glucose tolerance test (OGTT)
4. need 2 out of 4 values to be abnormal to diagnose GDM
o fasting: > 5.8 mmol/L
1. controversial
2. aim to achieve normal blood sugars post-prandial (i.e. < 6.7 mmol/L)
3. start with diabetic diet
4. if blood sugars 2 hours post-prandial are > 6.7, add insulin
5. oral hypoglycemic agents contraindicated in pregnancy
6. fetal monitoring and timing of delivery same as for DM above
7. insulin and diabetic diet should be stopped post-partum
8. follow-up testing recommended postpartum because of increased risk of overt diabetes
(i.e. OGTT at 6 weeks postpartum)
Classification
1. preeclampsia/eclampsia
2. chronic hypertension
3. chronic hypertension with superimposed preeclampsia/eclampsia
4. transient or gestational hypertension
Maternal factors
Fetal factors
1. IUGR
2. hydatidiform mole
3. > 1 fetus
4. fetal hydrops
Fetal Complications
1. fetal loss
2. IUGR
3. prematurity
4. abruptio placentae
Maternal Complications
o low platelets
1. maternal evaluation
2. history and physical examination
3. laboratory
o CBC and electrolytes
Severe Preeclampsia
.
Management of Severe Preeclampsia
Maternal monitoring
1. hourly input and output, check urine 12 hours for protein
2. vitals and DTR 1 hour
Fetal evaluation
1. NST followed by continuous electronic fetal monitoring until delivery
Anticonvulsant therapy
1. given to increase seizure threshold
2. baseline magnesium blood level
3. magnesium sulphate (4g IV push) followed by maintenance of 2-4 g/hour
4. excretion of magnesium sulfate is via kidney therefore patients with oliguria require a
lower infusion rate
Antihypertensive therapy
1. decreasing the BP decreases the risk of stroke (indicated only if BP > 140-170/90-110)
2. first line: hydralazine 5 - 10 mg IV push over 5 minutes q 15 - 30 minutes until desired
effect (an arteriolar vasodilator with minimal venous effect)
3. controls BP for hours not days (deliver as soon as possible)
4. next dose is given ~6 hours later with BP readings 15 minutes duration
5. also used in postpartum state if BP remains elevated and urinary output < 25 mL/hour
6. second line: labetalol 20 - 50 mg IV q 10 minutes
7. third line: nifedipine 10 -20 mg po q 20 - 60 minutes (puncture capsule and swallow
liquid)
Postpartum management
1. all antepartum therapy and monitoring continued until stable
2. risk of seizure highest in first 24 hours postpartum
3. continue magnesium sulfate for 12-24 hours after delivery
4. the patient who continues to remain in serious condition may have HELLP
5. most women return to a normotensive BP within 2 weeks but BP may worsen transiently
in that time
Eclampsia
Management of Eclampsia
Chronic Hypertension
Features
Management
1. hypertension alone that develops during the latter half of pregnancy or during the first 24
hours after delivery and disappears within 10 days following parturition
2. monitor for signs of preeclampsia/eclampsia
HYPEREMESIS GRAVIDARUM
Definition
1. intractable nausea and vomiting to extent of weight loss, dehydration and electrolyte
imbalance, acid-base disturbance and if severe, hepatic and renal damage
2. usually present in T1 then diminishes or persists throughout pregnancy
in a minority
Etiology
Maternal Complications
Fetal Complications
1. usually none
2. IUGR is 15x more common in women losing > 5% of prepregnant weight
o cholecystitis
o hepatitis
o gastroenteritis
o pancreatitis
o PUD
3. pyelonephritis
4. thyrotoxicosis
5. multiple gestation
6. GTN
7. HELLP syndrome
Investigations
Treatment
General
Pharmacological options
1. dimenhydrinate (Gravol)
2. vitamin B6 and doxylamine succinate (Diclectin)
Non-pharmacological options
1. accupressure at inner aspect of the wrists, just proximal to the flexor crease has been
shown to significantly reduce symptoms of nausea and vomiting
2. avoid triggers (i.e. certain smells)
Rh ISOIMMUNIZATION
Pathogenesis
4. complications
o anti-Rh Ab can cross the placenta and cause fetal hemolysis resulting in fetal
anemia, CHF, edema, and ascites
o severe cases can lead to fetal hydrops (total body edema), or erythroblastosis
fetalis
Diagnosis
1. routine screening at first visit for blood group, Rh status, antibodies
2. Ab titres < 1:16 considered benign
3. Ab titres > 1:16 necessitates amniocentesis (correlation exists between amount of biliary
pigment in amniotic fluid and severity of fetal anemia) from 24 weeks onwards
4. Liley curve is used to determine bilirubin level and appropriate
management
5. Kleihauer-Betke test can be used to determine extent of feto-maternal
hemorrhage
o fetal red blood cells are identified on a slide treated with citrate phosphate buffer
Prophylaxis
o antepartum hemorrhage
3. if Rh neg and Ab screen positive, follow mother with serial monthly Ab titres throughout
pregnancy +/- serial amniocentesis as needed (Rhogam of no benefit)
Treatment
TORCH is an acronym that is used to describe the more common fetal infections :
T oxoplasmosis
O ther, which refers to syphilis and HIV infection principally, but may also refer to
gonorrhoea and varicella
R ubella
C ytomegalovirus
H erpes, and also hepatitis
Toxoplasmosis
Rubella
1. RNA togavirus with transmission by respiratory droplets (highly contagious)
2. maternal infection during pregnancy (greatest in T1) may cause spontaneous abortion or
Congenital Rubella Syndrome: hearing loss, cataracts, cardiovascular lesions, MR,
symmetric IUGR, hepatitis, CNS defects and osseous changes
3. diagnosis best made by serologic testing
4. all pregnant women screened for rubella immunity (rubella titer > 1:16 = immune)
5. non-immune
o should be offered vaccination following pregnancy (not a contraindication for
breast feeding)
o rubella vaccine should be avoided before (3 months) or during pregnancy
since it is an attenuated live vaccine
Cytomegalovirus
o organ transplant
o sexual contact
o breast milk
o transplacental
Herpes
Syphilis
1. Treponema pallidum
2. may have transplacental transmission
3. serological tests
o VDRL screening done at first prenatal visit (non-specific)
Hepatitis B
1. parvovirus B19
2. febrile illness with bilateral erythema of cheeks (slapped cheek rash) followed by
maculopapular rash of trunk and extremities
3. fetus of infected woman may develop hydrops in utero
o follow fetus with weekly U/S (if hydrops occurs, consider fetal transfusion)
HIV
o acute cholecystitis
o acute pancreatitis
o abdominal trauma
o pelvic abcess
o bowel obstruction
o intracranial hemorrhage
o thromboembolic disease
1. surgery in first trimester has highest risk of teratogenicity and spontaneous abortion
2. surgery for nonemergent conditions usually delayed until the more stable second
trimester
3. EX :
o adnexal tumours
o cervical cancer
o breast cancer
o gastrointestinal trauma
o melanoma, osteosarcoma
Differential Diagnosis
Differential Diagnosis
1. placenta previa
2. abruptio placentae
3. vasa previa
4. bloody show (shedding of cervical mucous plug)
5. marginal sinus bleeding
6. cervical lesion (cervicitis, polyp, ectropion, cervical cancer)
7. uterine rupture
8. other: bleeding from bowel or bladder, placenta accreta, abnormal
coagulation
9. NB - do NOT perform a vaginal exam until placenta previa has been ruled out by U/S
VASA PREVIA
1. incidence 1 in 5000
2. occurs with velamentous insertion of cord into membranes of placenta; unprotected fetal
vessels pass over the cervical os
3. since bleeding is from fetus a small amount of blood loss can have catastrophic
consequences
4. presents with painless vaginal bleeding and fetal distress (tachy- to bradyarrhythmia)
5. Apt test (NaOH mixed with the blood) can be done immediately to determine if the
source of the bleeding is fetal (supernatant turns pink) or maternal (supernatant turns
yellow)
6. Wright stain on blood smear and look for nucleated red blood
cells (in cord not maternal blood)
7. management is STAT C-section
8. 50% perinatal mortality, increasing to 75% if membranes rupture (most infants die of
exsanguination)
Types of Abortions
THERAPEUTIC ABORTIONS
Medical management
< 9 weeks use methotrexate plus misoprostol (experimental)
> 12 weeks use prostaglandins intra- or extra-amniotically, or IM
Surgical management
< 12-16 weeks use dilatation and curettage
> 16 weeks use dilatation and evacuation
Complications
1. perforation of uterus
2. hemorrhage
3. laceration of cervix
4. risk of sterility
5. infection - usually due to retained products, occasionally endometritis
6. Asherman's syndrome (fibrosis of the uterus)
ABRUPTIO PLACENTAE
Classification
Etiology
Fetal Complications
1. perinatal mortality 25-60%
2. prematurity
3. intrauterine hypoxia
Maternal Complications
Clinical Features
Diagnosis
clinical
U/S NOT helpful except to rule out placenta previa
Management
Initial management
1. hydrate and restore blood loss and correct coagulation defect if present
2. vaginal delivery if no evidence of fetal or maternal distress and if cephalic presentation
OR with dead fetus
3. labour must progress actively
1. C-section if fetal or maternal distress develops with fluid/blood replacement, labour fails
to progress or non-cephalic fetal presentation
PLACENTA PREVIA
Classification
Etiology
1. multiparity
2. multiple pregnancy
3. increased maternal ageterine scar due to previous abortion, C-section, D&C,
myomectomy
4. uterine tumour (e.g. fibroids) or other uterine anomalies
5. history of placenta previa (4-8% recurrence risk)
Fetal Complications
1. perinatal mortality low but still higher than with a normal pregnancy
2. prematurity (bleeding often dictates early C/S)
3. intrauterine hypoxia (acute or IUGR)
4. fetal malpresentation
5. PPROM
6. risk of fetal blood loss from placenta, especially if incised during C/S
Maternal Complications
1. < 1% maternal mortality
2. hemorrhage and hypovolemic shock
3. anemia
4. acute renal failure
5. pituitary necrosis (Sheehan syndrome)
6. PPH (because lower uterine segment is atonic)
7. hysterectomy
8. placenta accreta
Clinical Features
Management
o uterine activity
7. expectant management and observation of mother and fetus if the initial bleeding episode
is slight and GA < 37 weeks
o admit to hospital
Definition
Maternal causes
1. poor nutrition,
2. cigarette smoking,
3. drug abuse, alcoholism,
4. cyanotic heart disease,
5. severe DM,
6. SLE,
7. pulmonary insufficiency
Maternal-fetal
Fetal causes
1. TORCH infections,
2. multiple gestation,
3. congenital anomalies
Clinical Features
Symmetric/Type I (20%)
Asymmetric/Type II (80%)
Diagnosis
1. clinical suspicion
2. SFH measurements at every antepartum visit
3. more thorough assessment if mother is in high risk category or if SFH lags > 2 cm behind
GA
4. U/S exam should include assessment of BPD, head and abdomen circumference,
head:body ratio, femur length and fetal weight
5. doppler analysis of umbilical cord blood flow
Management
OLIGOHYDRAMNIOS
Definition
1. decreased production
o renal agenesis or dysplasia,
o urinary obstruction,
2. increased loss
o prolonged amniotic fluid leak (although most often labour ensues)
Fetal Complications
1. cord compression
2. T1 onset
o Potters facies
o limb deformities
PRETERM LABOUR
Definition
Etiology
Maternal
1. preeclampsia/hypertension
2. placenta previa or abruption
3. uncontrolled diabetes
4. recurrent pyelonephritis and untreated bacteriuria
5. maternal genital tract infection
6. chorioamnionitis
7. other medical illness (heart disease, renal disease, severe anemia, systemic infection,
chronic vascular disease)
8. maternal age < 18 years or > 40 years
9. fibroids or other uterine anomalies
10. incompetent cervix
11. history of abortions or stillbirths
12. surgical (intra-abdominal surgery, cholecystitis, peritonitis)
13. previous incision into uterus or cervix (C/S, conization)
14. low socioeconomic class
15. lack of prenatal care
16. poor nutrition
17. low prepregnancy weight
18. smoking
19. drug addiction (alcohol, cocaine)
20. stress/anxiety/fatigue
21. prior history of premature delivery (recurrence risk of 17-40%)
Maternal-fetal
Fetal
1. multiple gestation
2. congenital abnormalities of fetus
1. erythroblastosis fetalis
2. severe congenital anomalies
3. fetal distress/demise IUGR,
4. multiple gestation (relative)
Diagnosis
Prevention
1. good prenatal care
2. identify pregnancies at risk
3. treat silent vaginal infection or UTI
4. patient education
5. the following may help but evidence for their effectiveness is lacking
6. rest, time off work, stress reduction
7. improved nutrition
8. U/S measurement of cervical length or frequent vaginal exams to assess cervix; this
would catch PTL earlier so tocolysis would be more effective
Management
Initial
1. have no impact on neonatal morbidity or mortality but may buy time to allow celestone
use or to transfer to appropriate centre
2. beta-mimetics: ritodrine, terbutaline
3. magnesium sulphate (if diabetes or cardiovascular disease present)
4. calcium channel blockers: nifedipine
5. PG synthesis inhibitors (2nd line agent): indomethacin
o viral keratosis
o maternal DM
RUPTURE OF MEMBRANES
Premature ROM
Prolonged ROM
Preterm ROM
PPROM
preterm premature rupture of membranes (not in labour)
Associated Conditions
congenital anomaly
infection
Causes
Complications
1. cord prolapse
2. intrauterine infection (chorioamnionitis)
3. premature delivery
Diagnosis
Management
o 34-36 weeks: grey zone" where risk of death from RDS and neonatal sepsis is the
same
o > 36 weeks: induction of labour since the risk of death from sepsis is greater than
RDS
3. assess fetal lung maturity by L/S ratio of amniotic fluid
4. consider administration of betamethasone to accelerate maturity
5. if not in labour or labour not indicated, consider antibiotics (controversial)
6. admit and monitor vitals q4h, daily BPP and WBC count
ANTENATAL COMPLICATIONS
1. descent of the cord to a level adjacent to or below the presenting part causing cord
compression between presenting part and pelvis
2. visible or palpable cord FHR changes (variable decelerations, bradycardia or both)
3. increased incidence with prematurity/PROM, fetal malpresentations,low-lying placenta,
polyhydramnios, multiple gestation, CPD
Management
1. STAT C-section
2. adjunctive measures
3. alleviate pressure of the presenting part on the cord
4. keep cord warm and moist by replacing it into the vagina and/or applying warm saline
soaks
CHORIOAMNIONITIS
Risk factors:
1. prolonged ROM,
2. long labour,
3. multiple vaginal examsduring labour,
4. internal monitoring,
5. bacterial vaginosis and other vaginal infections
Clinical features:
1. maternal fever,
2. maternal or fetal tachycardia,
3. uterine tenderness,
4. foul cervical discharge,
5. leukocytosis,
6. presence of leukocytes or bacteria in amniotic fluid
Management:
POST-DATE PREGNANCY
Complications
Management
incidence = 1% of pregnancies
Etiology
1. unknown in 50%
2. hypertension,
3. DM
4. erythroblastosis fetalis
5. congenital anomalies
6. umbilical cord or placental complications
7. intrauterine infection
8. antiphospholipid Abs
Management
1. labour induction
2. must monitor for maternal coagulopathy (10% risk of DIC)
3. psychologic aspects of fetal loss
4. investigations to determine cause
5. subsequent pregnancies high risk
THE FETUS
Fetal Lie
1. refers to the orientation of the long axis of the fetus with respect to the long axis of the
uterus
o longitudinal
o transverse
o oblique
Fetal Presentation
1. vertex
2. brow
3. face
4. sinciput ( Forehead and above it )
o shoulder
Fetal Position
2. normally, fetal head enters maternal pelvis and engages in OT position subsequently
rotates to OA position or OP (in a small percentage of cases)
Attitude
Station
THE CERVIX
1. Dilatation
o latent phase: 0-3 cm