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OB28 Obstetrics Toronto Notes 2023
Medical Complications of Pregnancy
Iron and Folate Deficiency Anemia
Table 13.Iron Deficiency and Folate Deficiency Anemia
Iron Deficiency Anemia Folate Deficiency Anemia
Etiology
Epidemiology
See Hematology.H15
Responsible for 80% of non-physiologic anemia during
pregnancy
See Hematology. H15
See Hematology.H15
Prevention (non-anemic):30 mg elemental iron daily (met by
most prenatal vitamins)
Treatment(anemic): 30-120 mg elemental iron daily
325 mg ferrous fumarate - 106 mg elementalFe:32S
mg ferrous sulfate - 65 mg elemental Fe;325 mg ferrous
gluconate - 36 mg elemental Fe
Polysaccharide-Iron Complex - 150 mg elemental Feicapsule
Maternal:angina.CHF.infection,slower recuperation,and PTL Maternal:decreased blood volume.HV.andanorexia
Fetal:decreased oxygen carrying capacity leading to fetal Fetal:neural tube defects in11.low birth weight,and
distress.IUGR.low birth weight,and fetal neurodevelopment prematurity
Mother needs1g of elemental iron per fetus:this amount
exceeds normal stores + dietary intake
Iron requirements increase during pregnancy due to fetal/
placental growth (500 mg),increased maternal R8C mass
(500 mg),and losses (200 mg) -more needed for multiple
gestations
See Hematoloov.H26
Incidencevanes from 0.5-25% depending on region,
population,and diet
See Hemalnisov.H26
See Hematology.H26
Prevention:0.4-1mg folic addP0 daily for1-3mo
preconceplually and throughoutII
Clinical Features
Investigations
Management
Complications
Minimum daily requirementis 0.4 mg
Most often associatedwithirondeficiency anemia
Folic acidis necessary for closure ofneural lube during
early fetal development (by 28 d GA)
Notes
Diabetes Meilitus
Epidemiology
• 2-6% of pregnancies are complicated by DM
Classification of Diabetes Meilitus
• T1DM and T2DM (see Endocrinology. E9)
• GDM:onset of DM during pregnancy (usually tested for around 24-28 wk GA)
Etiology
• pre-existing T1DM and T2DM
• GDM: anti-insulin factors produced by placenta and high maternal cortisol levels create increased
peripheral insulin resistance -> leading to GDM and/or exacerbating pre-existing DM
Management
Monitoring Glucose Levels
• Frequent measurements of blood
glucose during pregnancy are
advised foe women with T1DM or
T2DMto help prevent or treat both
hypoglycemia and hyperglycemia,
and also improve neonatal outcomes
• Aim for
. FPG <5.3 mmolI(95 mg'
dL)
• 1hpostprandial PG <7.8 mmol1
(140 mg/dL)
• 2 h postprandial PG <6.7mmoll
(120 mg/dL)
• Most women can be followed with
monthly HbAlc determinations
A. T1DM and T2DM
Preconception
• pre-plan and refer to high-risk clinic for interprofessional care
• commence folic acid (1.0 mg daily) 3 mo prior to conception
• optimize glycemic control (HbAlc <7%), counsel and assess for risks and complications (retinopathy,
neuropathy, CKD,CVD), review medications (discontinue ACE1, ARBs,statins)
Pregnancy
• for T2DM,switch to insulin therapy and discontinue non-insulin antihyperglvcemic agents
continuing glyburide or metformin is controversial
teratogenicity unknown for other oral antihvperglycemics
• tight glycemic control
insulin dosage may need to be adjusted as pregnancy advances due to increased demand and
increased insulin resistance
• monitor as for normal pregnancy, plus initial 24 h urine protein and creatinine clearance, retinal
exam, and HbAlc (aim for <6.5% during pregnancy)
• increased fetal surveillance (fetal growth, BPP, NST) starting in late T2 and 13 and perform weekly at
34-36 wk GA, consider fetal echocardiogram in T2 (if high HbAlc in T1 or just prior to pregnancy) to
look for cardiac abnormalities
• Start 162 mg ASA at night before 16 wk GA to reduce risk of preeclampsia
Postprandial blood glucose values seem
to be the most effective at determining
the likelihood of macrosomia or other
adverse pregnancy outcomes
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OB29 Obstetrics Toronto Notes 2023
Labour
• timing of deliver)’depends on fetal and maternal health and risk factors (Le.must consider size of
baby, lung maturity, maternal blood glucose)
• induce by 38-39 wk GA for uncomplicated pre-existing diabetes,induce earlier if indicated (poor
glycemic control, end-organ involvement)
• increased risk of CPD and shoulder dystocia with babies >4000 g,consider elective CD for predicted
birth weight >4500 g (controversial)
• monitoring:
• during labour, monitor blood glucose ql h with patient on insulin and dextrose drip
aim for blood glucose between 4.0-7.0 mmol/L to reduce the risk of neonatal hypoglycemia
Postpartum
• insulin requirements dramatically drop with expulsion of placenta (source of insulin antagonists)
• monitor glucose q6 h, restart insulin at two-thirds of pre-pregnancy dosage when glucose >8 mmol/L
B. GESTATIONAL DM
Screening and Diagnosis
• all pregnant women between 24-28 wk GA
• 2 screening options
preferred 2-step screening (recommended by theCanadian Diabetes Association)
step 1: perform a random non-fasting 50 g OGCT
- 1 h PG <7.8 mmol/L is normal
- I hPG >11.1 mmol/L is GDM
- if 1 h PG 7.8-11.0 mmol/L, proceed to Step 2
step 2:perform a fasting 75gOGTT,GDM if >1 of:
- PPG >5.3 mmol/L
- IhPG >10.6 mmol/L
- 2 hPG >9.0 mmol/L
alternative 1-step screening with fasting 75 gOGTT;GDM if >I of:
PPG >5.1 mmol/L
1 hPG >10.0 mmol/L
2 h PG >8.5 mmol/L
Risk Factorsfor GDM
• Age >35yr
• Obesity (BMI >30 kgfm2)
• Increased risk in Indigenous,
Hispanic,Asian,and African
populations
. FHx of DM
Management
• first line:diet modification and increased physical activity
• initiate insulin therapy if glycemic targets not achieved within 2 wk oflifestyle modification alone
glycemic targets:PPG <5.3mmol/L, 1 h PG <7.8 mmol/L, 2 h PG <6.7 mmol/L
• metformin can be used in pregnancy but is off-label and should be discussed with patient
• serial BPP/growth starting at 28 wk GA q3-4 wk
• starting at 36 wk,weekly assessment of fetal well-being with either BPP or NST until delivery
• stop insulin and diabetic diet postpartum
« follow up with 75 g OGTT between 6 wk-6 mo postpartum,counsel about lifestyle modifications
Labour
• offer 10L between 38-40 wk GA for GDM on insulin or metformin
• intrapartum glucose management and maternal glucose maintenance between 4.0-7.0 mmol/L
• Previous history of GDM
• Previous child with birthweight
>4.0 kg
• Polycystic ovarian syndrome
• Current use of glucocorticoids
• Essential HTN or pregnancy-related
K I N
Metformin and glyburide are safe
during breastfeeding.Other anti-insulin
antihyperglycemic agentsshould not be
used due to lack of safety data
Postpartum
• encourage breastfeeding for 3-4 mo postpartum to present childhood obesity and diabetes
• repeat testing for women with previous pregnancy affected by GDM before planning another
pregnancy or every 1-3 yr
Prognosis
• most maternal and fetal complications are related to hyperglycemia and its effects
• long-term maternal complications
• TT DM and T2D.V1: risk of progressive retinopathy and nephropathy
• GDM: 50% risk of developingT2DM in next 20 yr
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OB30 Obstetrics Toronto Notes 2023
Table 14.Complications of DM in Pregnancy
Maternal Fetal
Obstetric
HIN/precclampsia (especially il pre existing ncpluopiilhy/protcrnuria ):
insulin resistance is implicated in etiology of KIN
Polyhydramnios: maternal hyperglycemia leadsto fetal hypeiglycemia.
which leads to fetal polyuria (a majorsource of amniotic fluid)
Diabetic Emergencies
Hypoglycemia
Ketoacidosis
Diabetic coma
End -Organ Involvementor Deterioration
(occur in I1DM and I2DM , not in COM)
Retinopathy
Nephropathy
Growth Abnormalities
Microsomia:maternal hyperglycemia leadsto fetal liyperinsulinism
resulting in accelerated anabolism
IUGR: dueto placental vascular insufficiency
Delayed Organ Maturity
Fetal lungimmaluiily: hyperglycemia interfeies with surfactant
synthesis (RDS)
Congenital Anomalies (occur in T1DM and 12DM, not in COM)
2-7« increased risk of cardiac (ventricular seplal defect ).HTO.GU (cystic
kidneys). G!(anal atresia),and MSK (sacral agenesis) anomalies due to
hyperglycemia
Note: Pregnancies complicated by GDM do not manifest an increased
risk of congenital anomalies because GDM develops after the critical
period oforganogenesis (in T1)
labour and Delivery
Pll/prematunty: most commonly in patients with HIN/piecdampsia
PIL is associated with poor glyccmic control but the exact mechanism
is unknown
Increased incidence of stillbirth
Birth trauma:due to macrosomia, can lead to difficult vaginal delivery
and shoulder dystocia
Neonatal
Hypoglycemia: due to pancieatic hyperplasia and excess insulin
seciction in the neonate
Hyperbilirubinemia and|aundice: due to premaUnity and polycythemia
Hypocalcemia:exact pathophysiology not undeistood, may be related
to functional hypoparathyroidism
Polycythemia:hyperglycemia stimulatesfetal erythropoietin
production
Other
PyelonephriUsIDII: glucosuria provides a culture medium for f. coh and
other bacteria
Increased incidence of spontaneousaboition (in UDMand I2DM. notin
GDM):related to preconception glycemic control
Early-Onset Group B Streptococcus Disease
Indications for Intrapartum Antibiotic
GBS Prophylaxis
Prevention of Perinatal Group B
Streptococcal Disease:Revised
Guidelines from CDC, 2010. MMWR
Recomm Rep 2010:59:1-36
• Previous infant with invasive GBS
disease
• G8S bacteriuria during any trimester
of the current pregnancy
• Positive GBS vaginal-rectal screening
culture in late gestation during
current pregnancy
• Unknown GBS status at the onset
of labour (culture not done,
incomplete, or results unknown)
and any of the following:
• Delivery at <37 wk GA
• Amniotic membrane rupture
>18 h
• Intrapartum temperature
>38.0”C (>100.4"F)
• Intrapartum nucleic-acid
amplification test positive
for GBS
Epidemiology
• 15-40% recto-vaginal carrier rate
Risk Factors (for Neonatal Disease)
• <37 completed wk GA at birth
• prolonged RDM £18 h
• maternal intrapartum CiBS colonization during current pregnancy
• GBS bacteriuria at any time during current pregnancy
• previous infant with invasive GBS disease
• maternal fever (temperature >38"C)
Clinical Features
• increases risk of endometritis
• risk of vertical transmission (neonatal sepsis, meningitis or pneumonia, and death)
Investigations
• offer screening to all women at 35-37 wk GA with vaginal and anorectal swabs for GBS culture
Treatment
• prophylactic treatment of maternal GBS at delivery decreases neonatal morbidity and mortality
• antibiotics for CiBS prophylaxis (should be given 4 h prior to delivery to be considered adequate)
• penicillin G 5 million IU IV, then 2.5 million 1 U IV q4 h until delivery
• penicillin allergy but low risk for anaphylaxis: cefazolin 2 g IV', then 1 g q8 h
penicillin allergy and at risk of anaphylaxis: vancomycin 1 g IV ql 2 h or clindamycin 900 mg q8 h
(only if isolate known to be susceptible to clindamycin) until delivery
vancomycin and clindamycin levels in amniotic fluid do not reach therapeutic levels, all babies
should be screened for CiBS despite treatment
• if maternal fever, broad spectrum antibiotic coverage regardless of CiBS status and GA is advised
• if <37 wk GA and in labour or with ROM, IV CiBS antibiotic prophylaxis for a minimum of 48 h
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OB.M Obstetrics Toronto Notes 2023
Urinary Tract Infection
Epidemiology
• most common medical complication of pregnancy
• asymptomatic bacteriuria in 2-7% of pregnant women, more frequently in multiparous women
• note: asymptomatic bacteriuria should be treated in pregnancy due to increased risk of pyelonephritis
andPTl
Treat asymptomatic bacteriuria In
pregnancy because o( increased risk ot
progression to cystitis,pyelonephritis,
Etiology and probable Increased risk of PTl
• increased urinary stasis from mechanical and hormonal (progesterone) factors
• organisms include GBS as well as those that occur in non-pregnant women
Clinical Features
• may be asymptomatic
• dvsuria, urgency, and frequency in cystitis
• fever, flank pain, and costovertebral angle tenderness in pyelonephritis
Major organisms responsible for
pyelonephritis:C.coli. klebsiella.
eiterobocter. proleus
Investigations
• urinalysis, urine CSS
• renal function tests in recurrent infections
Management
• uncomplicated U IT
first line: amoxicillin (250-500 mg PC) q8 h x 7 d)
alternatives: nitrofurantoin (100 mg PC) BID x 7 d) or cephalosporins
follow with monthly urine cultures
• pyelonephritis
• hospitalization and IV antibiotics
Prognosis
• complications if untreated: acute cystitis, pyelonephritis, and possible PTL
• recurrence is common
Infections During Pregnancy
• infant immunity begins to develop at 9-15 wk GA
• initial response to infection is Ig.M production
• transplacental IgG provides passive immunity
Table 15, Infections During Pregnancy
Infection Source of
Transmission
Greatest
Transmission Risk
to Fetus
Agent Effects on Fetus Effects on Mother Diagnosis Management
Chicken Pox Varicella roster To mother:direct,
virus (herpes respiratory
family) To baby:
transplacental
13-30 wkGAand 5
d pre- to 2 d postdelivery
Congenital
varicella syndrome
(limb aplasia,
chorioretinitis,
cataracts, cutaneous
scars, cortical atrophy.
IUGR, hydrops),PTl
Fever,malaise,
vesicular pruritic lesions fluid culture.*
serology
Clinical,±vesicle Varicella-roster
immunoglobulin (VZIG)
for mother if exposed,
decreases congenital
varicella syndrome
If maternal infection 5 d
before delivery,give infant
VZIG for passive immunity
Note:donoladminister
vaccine during pregnancy
(live attenuated vaccine)
No specific treatment:
maintain good hygiene
and avoid high-risk
situations
’Cytomegalovirus DNAvirus Tomother:blood/
(herpes family) organ transfusion,
sexual contact
To baby:
transplacental,
during delivery,
bieasl milk
T1-T3 5-10% develop CNS Asymptomatic or flu-like Serologic screen:isolate
involvement (mental (fever,pharyngitis,
retardation, cerebral lymphadenopathy,
polyarthritis)
virus from urine or
secretion culture
calcification,
hydrocephalus,
microcephaly,
deafness,
chorioretinitis)
Erythema
Infectiosum (Fifth
Disease)
Parvovirus 619 Tomother:
respiratory.infected
blood products
To baby:
transplacental
DNA virus Tomother:blood.
saliva,semen,
vaginal secretions
fo baby:
transplacental,
bieasl milk
10-20 v/k GA Spontaneous abortion Flu-like,rash,arthritis: Serology,viral PCS,
ISA),stillbirth,hydrops often asymptomatic
inutero
If hydrops occurs,consider
maternal AFP:if IgM fetal transfusion
present,follow fetus with
U/S for hydrops
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T3 Serologic screening for all fix neonate with HBIG and
vaccine (at birth.1,6 mo):
90% effective
Hepatitis 6 Prematurity,low birth Fever.N/ V,fatigue,
weight, neonatal jaundice,elevated liver pregnancies
death
10% vertical
transmission
if asymptomatic and
HBsAq *ve: 85-90%il
HBsAgandH6eAg *
ve
enrymes +
* Indicates TORCH intection
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OB32 Obstetrics Toronto Notes 2023
Table 15. Infections During Pregnancy
Infection Source of
Transmission
Greatest
Transmission Risk
to Fetus
Agent Effects on Fetus Effects on Mother Diagnosis Management
'Herpes Simplex DMA virus
Virus
To mother:intimate
mucocutaneous
contact
To baby:
transplacental,
during delivery
Delivery (if genital
lesions present):less
commonly muieio
Disseminated herpes
(20%); CNS sequelae
(3S%);self-limited
infection
Fa nful vesicular lesions Clinical diagnosis Acyclovir for symptomatic
women,suppressive
therapy at 36 wk 6A
controversial
Suggested CD if active
genital lesions,even if
remote from vulva
1/3 in siltro.V3
at delivery.1/3
breastfeeding
To mother:blood,
semen,vaginal
secretions
Tobabyrrffufero.
during delivery,
breast milk
IUGR.PIl. PR0M See Infectious Diseases. Serology,viral PCR
All pregnant women are
offered screening
Triple antiretroviral therapy
decreases transmission
to
'
1%
Elective CD:no previous
antiviral
Rx or monotherapy only,
viral load unknown or >500
RNA copies/mL.unknown
prenatal care,pabent
request
No specific treatment:
offer vaccine following
pregnancy
Do not administer during
pregnancy (live attenuated
vaccine)
HIV RNA retrovirus
1027
SA or congenital
rubella syndrome
(hearing loss,
cataracts.CV lesions,
mitral regurgitation.
IUGR. hepatitis.CNS
defects,osseous
changes)
Risk of PTL.
multisystem
involvement,fetal
death
Rash(50%).lever,
posterior auricular
or occipital
lymphadenopathy,
arthralgia
Serologic testing:all
pregnant women screened
(immuneif litre>1:16):
infectionifIgM present or
>4x increaseinIgG
ssRHAtogavrrus To mother:
respiratory droplets
(highly contagious)
To baby:
transplacental
'Rubella II
Spirochete
( Ireponemc
pallidum)
Syphilis Tomother:sexual
contact
To baby:
transplacental
T1-T3 See Infectious Diseases. VORL screening for all
1024 pregnancies:if positive.
requires confirmatory
testing
Benzathine penicillin6
2.4 million IU IMildose
if early syphilis.3 doses if
late syphilis,monitor VDRl
monthly
No approved alternatives
in pregnancy:if 6-lactam
allergy,recommendto
desensitize then beat with
penicillin
Self-limiting in mother;
spiramycin decreases fetal
morbidity bulnotrate of
transmission
'Toxoplasmosis Protozoa
(foxop/osmo
gondii]
To mother raw meat. 13 (but most severe
unpasteurized goal's if infectedin11);only
milk,cat feces/urine concern if primary
To baby: infection during
bansplacental
Congenital
toxoplasmosis
(chorioretinitis.
hydrocephaly.
intracranial
calcification,mibal
regurgitation.
microcephaly).
NB:75%initially
asymptomatic at birth
Majority subdinical;may IgM andIg6 serology:PCR
have Du-like symptoms of amwotic fluid
pregnancy
Congenital possible Cough,sore throat.
N1D if exposed in early malaise,headaches,
pregnancy as a result myalgia
of high fevers
Clinical diagnosis,viral
swab
Influenza ssRNA virus Tomother:
respiratory droplets
To baby:
transplacental
Earty pregnancy Immunization with
inactivated influenza
vaccine
If infected: symptomatic
treatment,antivirals,
supportive therapy
Complications include
pneumonia
'Indicates TORCH infection
Venous Thromboembolism
Epidemiology
• incidence of 12.1 in lOOOO (DVT) and 5.4 in 10000 (PE)
• increased risk of V I E throughout pregnancy ( highest risk of DVT in T3) and postpartum period
(highest risk of PE postpartum first 6 wk)
Virchow's Triad for VTE
• Hypercoagulable slate
• Venous stasis
• Endothelial damage
Risk Factors
previous VTE, age >35,obesity,infection, bedrest/immobility,shock/dehydration,smoking, pre
eclampsia, and thrombophilias (see Hematology. H36)
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Table 16. Risk Factors for VTE Specific to Pregnancy
Hypercoagulability Stasis Endothelial Damage
Increased Factors:
H.V.VII.VIII.IX.X.XII,fibrinogen
Increased platelet aggregation
Decreased protein S,tPA.factors XI.Till
Increased resistance to activated protein C
Anbthrombin can be normal or reduced
Vascular damage at delivery (CD or SVD)
Uterine instrumentation
Perrpartum pelvic surgery
Increased venousdistensibility
Decreased venous tone
50%decrease invenous flow inlower
extremity by T3
Uterus is mechanical impediment to venous
return
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OB33Obstetrics Toronto Notes 2023
Clinical Features
• most DVTs occur in the iliofemoral or calf veins with a predilection for the left leg
• signs of a PE are non-specific
Investigations
• duplex venous Doppler sonography for DVT
• CT angiography preferred for PE
Management
• before initiating treatment,obtain a baselineCBC including platelets and aPTT
• treatment with LMWH preferred
dosing varies depending on specific LMW H used
should he discontinued at least 24 h prior todelivery
• unfractionated heparin
80 lU/kg bolus (max 5000 IU) followed by 18 lli/kg/h infusion
• measure aPTT 6 h after the bolus
maintain aPTT at a therapeutic level (1.5-2x normal)
repeat q24 h once therapeutic
• heparin-induced thrombocytopenia (HIT) uncommon (3%), but serious complication
• warfarin is contraindicated during pregnancy due to its potential teratogenic effects
• poor evidence to support a recommendation for or against avoidance of prolonged sitting
• VTE prophylaxis
women on long-term anticoagulation:full therapeutic anticoagulation throughout pregnancy and
for 6-12 wk postpartum
• women with a non-active PMHx of VTE:unfractionated heparin regimenssuggested
• postpartum thromboprophylaxisshould be considered if absolute risk is over 1.0%,defined as:
any two of the following:BMI >30 at first antepartum visit,smoking >10 dgarettes/d,
preeclampsia,IUGR, placenta previa,emergencyCD,peripartum/postpartum blood loss >1
L, any low-risk thrombophilia, maternal cardiacdisease/SLE/SCD/lBD/varicose veins/GDM,
preterm delivery,stillborn
any three or more of the following:age >35, parity >2, use of ART,multiple gestation,
placental abruption,PROM, elective CD,maternal cancer
current prophylaxis regimensfor acquired thrombophilias (e.g.APS) include low dose ASA in
conjunction with prophylactic heparin
Normal Labour and Delivery
Definition of Labour
• true labour:regular, painful contractions of increasing intensity associated with progressive dilatation
and effacement of cervix and descent of presenting part,or progression ofstation
preterm (20-36+6 wk GA)
term (37-41+6 wk GA)
postterm (>42 wk GA)
• false labour (Braxton-Hicks contractions):irregular contractions with unchanged intensity and long
intervals, occur throughout pregnancy and not associated with any cervical dilatation, effacement,or
descent
• often relieved by rest or hydration
Maternal Triage Assessment
ID:Age.6PA, EDD, GA, GBS, Rh,
Serology
Chief Complaint (CC)
HPI: 4 key questions:
• Contractions:Since when, how close
(q x min), how long (x s), how painful
- Bleeding:Since when, how much
(pads), colour (pinky vs, brownish vs.
bright red), pain, last U/S, trauma/
intercourse
. Fluid (ROM):Since when, large gush
vs.trickle,soaked pants, clear vs.
green vs. red. continuous
• FM:As much as usual, time since last
movement, kick counts(lie still for 1-2
h, cold juice,feel FM -should have 6
movements in 2 h)
PregHx: Any complications (HTN, GDM.
infections). IPS/FTS. last U/S (BPP score,
growth. EFW, presentation),last vaginal
exam
POBHx: Every previous pregnancy and
outcome: year,SVD/CD/miscarriage/
abortion, baby size, length of labour, use
of vacuum or forceps, complications
PMHx. Meds. Allergies. SHx
0/E:Maternal vitals,fetal heart tracing
(baseline,variability, presence of
accelerations/decelerations), Leopold's,
vaginal exam.U/S
The Cervix
• see Bishop Score (see Table 20, OB3S )
• dilatation:latent phase (0-4 cm, variable time);active phase (4-10 cm)
• effacement: thinning of the cervix by percentage or length of cervix (cm)
• consistency:firm, medium,or soft
position:posterior, mid, or anterior
• other consideration
application: contact between the cervix and presenting part (i.e. well or poorly applied)
The Fetus
• fetal lie: orientation of the long axis of the fetus with respect to the long axis of the uterus
(longitudinal, transverse,or oblique)
• fetal presentation: fetal body part closest to the birth canal
breech (complete, frank,footling and incomplete) (see Figure5, OB25)
cephalic (vertex/occiput,face,or brow)
transverse (shoulder)
compound (fetal extremity7
prolapses along with presenting part)
all except vertex are considered malpresentations(see Obstetrical Complications, OBI 7 )
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OB34 Obstetrics Toronto Notes 2023
• fetal position:position of presenting part of the fetus relative to the maternal pelvis
OA:most common presentation (“normal") -left OA most common
OP:most rotate spontaneously to OA; may cause prolonged second stage of labour
OT:leads to arrest of dilatation
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:tlexion/extension of fetal head relative to shoulders
• brow presentation: head partially extended (requires CD)
face presentation: head fully extended
mentum posterior always requires C.
'
D, mentum anterior can deliver vaginally
• station: position of presenting bony part relative to ischial spines- determined by vaginal exam
• at ischial spines = station 0
= engaged
-5 to -1 cm above ischial spines
• +1 to +5cm below ischial spines
• asynclitism:alignment of the sagittal suture relative to the axis of the birth canal
• lateral tilt seen with either anterior or posterior asynclitism and may impact descent
Reference Point for Describing Fetal
Position
• Occiput for cephalic presentation
• Sacrum for breech presentation
• Mentum for face presentation
Frontal Fontanelle or Anterior Fontanelle
Biparietal
Diameter
9.5 cm
Occipital Fontanelle or Posterior Fontanelle Right Occiput Transverse
Occiput Anterior Occiput Posterior
=•
Figure 7.Synditism and asynclitism
CO
Left Occiput Anterior Right Occiput Posterior
Figure 6. Fetal positions
Four Stages of Labour o
Course of Normal Labour’
First Stage of Labour (0-10 cm cervical dilatation)
• latent phase
uterine contractions typically infrequent and irregular
slow cervical dilatation (usually to 4 cm) and effacement
• active phase
• rapid cervical dilatation to full dilatation (nulliparous >1.0 cm/h, multiparous >1.2 cm/h)
• phase of maximum slope on cervical dilatation curve
• painful, regular contractions q2-3 min, lasting 45-60 s
• contractionsstrongest at fundus
Stage Nulliparous Multiparous
First 6-181 MOh
Secure 30 tu-3 h 5-30 min
Th.
-d 5-30 min 5-30 no
Second Stage of Labour (10 cm dilatation - delivery of the baby)
• from full dilatation to delivery of the baby; duration varies based on parity, contraction quality, and
type of analgesia
• mother feels a desire to bear down and push with each contraction
• women may choose a comfortable position that enhances pushing efforts and delivery
upright (semi-sitting,squatting) and LLDP are supported in the literature
• progress measured by descent
Signs of Placental Separation
• Gush of blood
. Lengthening of cord
• Uterus becomes globular
• Fundus rises
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OB35Obstetrics Toronto Xotes 2023
Third Stage of Labour (delivery of the baby - delivery of the placenta)
• from baby’s birth to separation and expulsion of the placenta
• can last up to 30 min before intervention is indicated
• demonstrated by gush of fresh blood, umbilical cord lengthening, uterine fundus changing shape
(firm and globular), and rising upward
• active management:start oxytocin IV drip, or give 101U L\1 or 5 mg IV push,after delivery’
of anterior
shoulder in anticipation of placental delivery, otherwise give after delivery of placenta
• routine oxytocin administration in third stage of labour can reduce the risk of PPH by >40%
Coa'
jcioosSupport for Women During Childbirth
Codira:
*
DBSjst Rev 201/:?:CO 003766
SMr Systematic review ot 2? trialsfront17
countriessnoring a total of 15158 women
Htmtioa:Corneoussupport vs.usual cae
feriwg labour
Outcoae: Effects on notbers audtheir babies
lesiltr Women receiving continuoussupport were
sight!) note Eketjf ID have a spontaneous vaginal
both it!108.95% Cl 1.08 to 1.12) a nd shorter laoow
(mean d ffevence 0.69 h ,95% Cl -1.04 to -0 341aed
were lessikeIp to use intrapartum analgesia (It
000.95% Cl 0.84 to 0.961.report dissatisfaction with
tteirchidbirth eioener.ee|«t 0.69.95% a 0.59 hi
0-751-
and bavea baby with a low 5 min APUIstore
(U0.52.95% CI 0.46 to0.8S)
Fourth Stage of Labour
• first postpartum hour
• monitor vital signs and bleeding, repair lacerations
• ensure uterus is contracted (palpate uterus and monitor uterine bleeding)
• inspect placenta for completeness and umbilical cord for presence of 2 arteries and 1 vein
• 3rd and 4th stages of labour most dangerousto the mother (i.e. hemorrhage)
The Cardinal Movements of the Fetus During Delivery
2.Engagement
descent,flexion
3.Further descent,
internal rotation
1. Head floating,
before engagement
4.Complete rotation,
beginning extension
5. Complete extension 6. Restitution 8. Delivery ot (external rotationl posterior shoulder
Figure 8.Cardinal movements of fetus during delivery
Adapted from illustration in Williams Obstetrics,t9th ed
Analgesic and Anesthetic Techniques in Labour and Birth
• pain or anxiety leads to high endogenous catecholamines,which produce a direct inhibitory'effect on
uterine contractility
Non-Pharmacologic Pain Relief Techniques
• reduction of painfulstimuli
• maternal movement, position change, counter-pressure, and abdominal compression
• activation of peripheralsensory receptors
• superficial heat and cold
• immersion in water during labour
touch and massage,acupuncture, and acupressure
• TENS
intradermal injection ofsterile water
aromatherapy
• enhancement of descending inhibitory pathways
• attention focusing and distraction
w hypnosis
music and audio analgesia
• biofeedback
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Pharmacologic Methods (see Anesthesia. A26)
• nitrous oxide (e.g.self-administered Entonox')
• narcotics(usually combined with anti-emetic)
• pudendal nerve block
• perineal infiltration with local anesthetic
• regional anesthesia (epidural block, combined spinal-epidural, and spinal)
Fetal Monitoring in Labour
• see online Fetal Heart Kate Tutorial
Vaginal Exam
• membrane status, as indicated by amniotic fluid (clear, pink, bloody, and meconium)
• cervical etTacement (thinning), dilatation, consistency, position, and application
• fetal presenting part, position, and station
• bony pelvis size and shape
• monitor progress of labour at regular intervals and document in a partogram
Intrapartum Fetal Monitoring
• intermittent fetal auscultation with Doppler device q15-30 min for 1 min in active phase of first stage
following a contraction, q5 min during second stage when pushing has begun
• continuous electronic I
'
HR monitoring reserved for abnormal auscultation, prolonged labour, labour
which is induced or augmented, meconium present, multiple gestation/fetal complication, and
concerns about the fetus tolerating labour
• use of continuous electronic monitoring shown to lead to higher intervention rates and no
improvement in outcome for the neonate when used routinely in all patients (i.e. no risk factors)
techniques for continuous monitoring include external (Doppler) vs. internal (fetal scalp
electrode) monitoring
• fetal scalp sampling should be used in conjunction with electronic FHR monitoring and contraction
monitoring (CFG) to resolve the interpretation of abnormal or atypical patterns
Electronic FHR Monitoring
• FHR measured by Doppler; contractions measured by tocometer
• described in terms of baseline FHR, variability (short-term, long-term), and periodicity (accelerations,
decelerations)
• see t able 5, OB10
• Baseline FHR
normal range is 110-160 bpm
• parameter of fetal well-being vs. distress
• Variability
• physiologic variability is a normal characteristic of 1 HR
• variability is measured over a 15 min period and is described as; absent, minimal (<6 bpm),
moderate (6-25 bpm), or marked (>25 bpm)
• normal variability indicates fetal acid-base status is acceptable
• can only be assessed by electronic contraction monitoring (CFG)
variability decreases intermittently even in a healthy fetus
• Periodicity
• accelerations: increase of 15 bpm for 15 s (or 10 bpm for 10 s if <32 wk GA)
• decelerations: 3 types,described in terms of shape, onset, depth, duration recovery, occurrence,
and impact on baseline FHR and variability
Approach to the Management of
Abnormal FHR
POISON- ER
Pos ition (LLDP)
02 (100% by mask)
IV fluids (corrects maternal
hypotension)
Fetal scalp stimulation
Fetal scalp electrode
Fetal scalp pH
Stop oxytocin
Notify physician
Vaginal exam to rule out cord prolapse
Rule out fever,dehydration,drug
effects,and prematurity
•N 4tottMv.<e>tu4nCt)
Continuous Cardiotocography (CTG) isI form
ol Electron it Fetal Monitoring|EFM ) for Felal
Assessment Darin;labom
CochraneOB Syst ter 201)
:$:CD006066
Pnipose loeurme the effectiveness of continuous
electronic fetal monitoring or cardiotocography
during labour
Selection Criteria: Randorriiedand quasirandor red controlled trials comparing continuous
CIC (with and withoutfetal blood sampling!to a) no
fetal monitoring.b) interrittertauscultation, or c)
intermittent CIC
Results:13 trials.37000 women.Continuous CIG
compared with intermittent auscultation showed no
difference in overall perinatal death rate oi cerebral
palsy rates,nonetheless, neonatal seizures ware
hatred (HR 0.50.95% Cl 0.310.80) and there was a
Significant increase in C0(RR 1.63,95% Cl 1.29-2.07 )
and nstrmnental vaginal birth (RR 115.95% Cl
1.01-1.33) with CTG
Conclusion:Cnobnuous CIG may reduce the
incidence of neonatalseizures, but has no effect
on cerebral palsy rates,infant mortality, or other
measures of neonatal well-ber.g.Continuous CIG
was alsoassociated with an increase a CD and
instrumental delvenes
Table 17. Factors Affecting Fetal Heart Rate
Fetal Tachycardia
(FHR >160 bpm)
Fetal Bradycardia
(FHR <110 bpm)
Decreased Variability
Maternal Factors Fever,hyperthyroidism,anemia, Infection
dehydration
Hypothermia, hypotension,
hypoglycemia, position,umbilical Dehydration
cord occlusion
Fetal Factors Arrhythmia,anemia,infection,
prolonged activity, chronic
hypoxemia,congenital anomalies (head compression),hypothermia. Inactivity/sleep cycle, preterm
acidosis
P-blockers
Anesthetics
Late hypoxia (abruption. HTN)
Acute cord prolapse
Hypercontractility
Rapid descent,dysrhythmia, heart CHS anomalies
block,hypoxia,vagal stimulation Dysrhythmia
fetus
Drugs Sympathomimelics Narcotics,sedatives
Magnesium sulphate,
^
-blockers
Hypoxia
r T
Early hypoxia (abruption. HTN)
Chotioamnionifis
Uteroplacental l. J
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Table 18. Comparison of Decelerations
Comparisons
Early Decelerations
• Uniform shape with onset early in contraction,returns to baseline
by end of contraction,mirrors contraction ( nadir occurs at peak of
contraction)
• Gradual deceleration and return to baseline
• Often repetitive; no effect on baseline f HR or variability
• Benign , due to vagal response to head compression
BPM Early Deceleration
180 Onset of deceleration
/
» Nadir of
s. deceleration
160
140 FHR (baseline)
I 120
100
"
/AcmB ofN
contraction Uterine contraction
Onset % (baseline) of
contraction
nd of
contraction
Variable Decelerations
. Variable in shape,onset, and duration
• Most common type ol periodicity seen during labour
• Often with abrupt drop In FHR >15 bpm below baseline|*15 s. «
2
min): usually no effect on baseline FHR or variability
• Due to cord compression or, in second stage,forceful pushing with
contractions
Variable Deceleration
FHR
Variant,in duration.
mtansitY. and timing
Uterine contraction
Complicated Variable Decelerations
• FHR drop > 60 bpm lor >60 s
. loss of variability or decrease in baseline alter deceleration
• Biphasic deceleration
> Slow return to baseline
• Baseline tachycardia or bradycardia
• May be associated with fetal acidemia
Rule of 60s Suggesting Severe Variable
Decelerations
Deceleration to <60 bpm
>60bpm below baseline
>60 s in duration with slow return to
baseline
Late Decelerations
• Uniform shape with onset, nadir,and recovery occurring alter peak of
contraction,slow return to baseline
• May cause decreased variability and change in baseline FHR
• Due to fetal hypoxia and acidemia,maternal hypotension, or uterine 120
hypertonus
• Usually a sign ol uteroplacental insufficiency (an ominous sign)
BPM Late Deceleration
nset of deceleration
Nadir of
deceleration _ 140 /
FHR
30 seconds 4
of lag time
100 >
Recovery time
/
Acmu ol
contraction Uterine contraction
4
Onset of \
contraction
nd of
contraction
Fetal Scalp Blood Sampling
• cervix must be adequately dilated
• indicated when atypical or abnormal FHR is suggested by clinical parameters including heavy
meconium or moderately to severely abnormal FHR patterns(including unexplained low variability,
repetitive late decelerations, complex variable decelerations, and fetal cardiac arrhythmias)
• done by measuring pH or more recently fetal lactate
• pH S7.25, lactate <4.2 mmol/L: normal, repeat if abnormal FHR persists
• pH 7.21-7.24, lactate 4.2- 4.8 mmol/L:repeat assessment in 30 min or consider delivery if rapid fall
since last sample
pH <7.20, lactate >4.8 mmol/L indicates fetal acidosis, delivery is indicated
• contraindications:
known or suspected fetal blood dyscrasia (hemophilia, VWD)
• active maternal infection (HIV, genital herpes. Hep B)
Fetal Oxygenation
• uterine contractions during labour decrease uteroplacental blood flow, which results in reduced
oxygen delivery to the fetus
• most fetuses tolerate this reduction in flow and have no adverse effects
• fetal response to hvpoxia/asphyxia:
decreased movement, tone, and breathing activities
• anaerobic metabolism (decreased pH)
transient fetal bradycardia followed by fetal tachycardia
• redistribution of fetal blood flow
• increased flow to brain, heart, and adrenals
• decreased flow to kidneys, lungs, gut, liver, and peripheral tissues
• increase in blood pressure
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Table 19. Factors Affecting Fetal Oxygenation
Factor Mechanism Example
Maternal Decreased maternal oxygen carrying capacity Significant anemia (iron deficiency, hemoglobinopathies),
carboxyhemoglobin {smokers)
Hypotension (blood loss,sepsis),regional anesthesia,maternal positioning
Vasculopathies (SLE, T1DM, chronic HTH), APS, cyanotic heart disease.COPD
Placental abruption, tachysystole secondary to oxytocin, prostaglandins, or
normal labour
Placental abruption, placental infarction (dysfunction marked by IUGR ,
oligohydramnios, abnormal Doppler studies), chorioamnionitis, placental
edema ( DM, hydrops), placentalsenescence (post-dates)
Oligohydramnios, cord prolapse, or entanglement
Significant anemia (isoimmunization, fetomaternal bleed),
carboxyhemoglobin (exposure to smokers)
Decreased uterine blood flow
Chronic maternal conditions
Uteroplacental Uterine hypertonus
Uteroplacental dysfunction
Cord compression
Decreased fetal oxygen carrying capacity
Fetal
Induction and Augmentation of Labour
Induction of Labour
Definition
• artificial initiation of labour in a pregnant woman prior to spontaneous initiation to deliver the fetus
and placenta
Induction is indicated when the risk of
continuing pregnancy exceeds the risks
associated with induced Labour and
delivery
Prerequisites for Labour Induction
• capability for CD if necessary
• maternal:
inducible/ripe cervix:short, thin,soft, anterior cervix with open os
if cervix is not ripe, use prostaglandin vaginal insert (Cervidil*), prostaglandin gel (Prepidil*),
misoprostol (Cytotec*), or l
'
oley catheter
Induction vs. Augmentation
Induction is the artificial initiation of
labour
Augmentation promotes contractions
when spontaneous contractions are
inadequate
• fetal:
• normal fetal heart tracing
cephalic presentation
adequate fetal monitoring available
• likelihood of success determined by Bishop score:
cervix considered unfavourable if <6
cervix favourable if >6
Consider the Following Before
Induction
• Indication for induction
• Contraindications
score of 9-13 associated with high likelihood of vaginal delivery
Table 20. Bishop Score GA
Cervical favourability
Fetal presentation
Potential for CPD
Fetal wellbeing/FHR
Membrane status
Cervical
Characteristic
0 1 2 3
Position
Consistency
Effaccmcnt (
"„)
Dilatation (cm)
Station of Fetal Head
Poslerior Mid Anterior
firm Medium Soft
030 4050 60-70 >80
0 1-2 3-4 >5
•3 •2 •1.0 -1.-2.-3
Indications
• late term and postterm pregnancy = most common reason for induction
• 39-41 wk GA especially with risk factorssuch as advanced maternal age (>40 yr): consideration should
be given to 10L due to increased risk of stillbirth
• >41 wk GA: offer l()L if vaginal delivery is not contraindicated
• 10L shown to decrease CD, I HR changes, meconium staining, macrosomia, and death when
compared with expectant management
• >41 wk GA and expectant management elected:serial fetal surveillance
• h
'M count by the mother
BPP q3-4 d
• maternal factors:
• DM = second most common reason for induction
• gestational HTN 238 wk GA
preeclampsia 237 wk GA
• other maternal medical problems, (e.g. renal or lung disease, chronic HTN, and cholestasis)
• significant but stable antepartum hemorrhage
• labour induction may be offered to patients age 240 at 239 wk GA due to increased risk of
stillbirth
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OB39 Obstetrics Toronto Notes 2023
• maternal-fetal factors:
• isoimmunization, PROM, and chorioamnionitis
• fetal factors:
• suspected fetal jeopardy as evidenced by biochemical or biophysical indications
• macrosomia, fetal demise, RJCiR, oligo/polyhvdramnios, anomalies requiring surgical
intervention, and twins
previous stillbirth or low PAPP-A
Evidence loi Cervical Ripening Methods (S06C
Guidelines)
•Meta -analysis of five trials has concluded that the
use of ocytocin to ripen the termis not effect
•Since the best dose and route of m isoprostot for
labour induct on with a live fetus are not known and
there are concerns regarding hyperstaolation.the
use of misoprostol for lotshould be in cases of IUFD
to initiate labour
Risks
• failure to achieve labour and/or vaginal birth
• tachvsvstole with fetal compromise or uterine rupture
• maternal side effects to medications
• uterine atony and PPH if labour is prolonged
Vaginal Prostaglandin (PGE2 and PGI 2a) for
Induction of labour at term
Cochrane OS Syst Rev 2014.6 C0003101
This analysis enam nedthe results ol TO RCIs (n-IUS)
women ]. Use ol vaginal PGE 2 in creased the risk of
uterine hy perstimulation with f HR changes|RR 3.16:
95% Cl 1.67-5.98) aud likely reducesthe CO rate
slightly (RR 0.91; 95% Cl 0.81-1.02) compared to
placebo omo treatment,(here were no detectable
differences in effectiveness between gel or tablet
forms of PGE2 or between sustained release pessaries
end PGE2 gel/tablets
Theoretical advantages between mtreveginal PGE2
(Cervidil;
) compared to Intravaginal Prostaglandin
Contraindications
• maternal
• prior classical or Inverted T-lndslon CD or uterine surgery (e.g. myomectomy)
• unstable maternal condition
• active maternal genital herpes
invasive cervical carcinoma
pelvic structure deformities
previous uterine rupture
• maternal-fetal
placenta previa or vasa previa
cord presentation
fetal Gel:
fetal distress or malpresentation/abnormal lie •Slow, continuous release
•Ability to use oxytocin 30 mm after re moral vs.
filllor gel
•Abi lily to remove insect If required (e.g. etcessive
uterine aclivityl
Methods for Induction of Labour
CERVICAL RIPENING
Definition
• use of medications or other means to soften, efface, and dilate the cervix; increases likelihood of
successful induction
• ripening of an unfavourable cervix (Bishop score <6) is warranted prior to IOL
Labouc Induction vs. Expectant Manageneot in
Low-Risk Multiparous Women
NEJM 2018;379:513-523
Purpose: fo assess whether induction of labour
between 39*0 wk GAand 40*
6 wk GA implores
perinatal and maternal outcomes
Methods: 6106 low-risk nulliparous women were
randomized to the elective indaction oc the expectant
management groups.Ihe primary outcome wasa
composite outcome of perinatal death orsenre
neonatal complications.The mam secondary outcome
wasthe rale afCO
Results: Ihe primary per natal outcome occurred
in 4.3% ol neonalesfrom Ihe elective induction
group and 5.4% ol neonalesfrom ihe eipectant
management group (RR: 0.80:95% Ct 0.64-1.00:
P*
0.049, P«0.04G lorsign 4i cancel This result was
consistent after adjusting for other maternalfactois.
CD occurred In 18.6% of Induction group mothers
compared to 22.3% of eipectant management group
mothers (RR:0.84:95% Cl:0.76-0.93. P <0.001).
there were no sigmheant differencesin primacy or
secondary outcomes m subgroup analyses
Conclusion: Elective induction of tatcour between
39-0 and 41-0 wk Gi did not resu lt in increased
incidence ofadverse perinatal outcoresand resulted
in fewer CDs
Methods
• intravaginal prostaglandin PGE2 gel (Frostin’gel):long and closed cervix
recommended dosing interval of prostaglandin gel is ever)'6-12 h up to 3 doses
• intravaginal PGH2 (Cervidil*):long and closed cervix,may use if ROM
continuous release, can be removed if needed
• controlled release PGE2
• intraccrvical PGE2 (Prepidil*)
• intravaginal PGE1 misoprostol (Cytotec*):long and closed cervix
inexpensive,stored at room temperature
• more effective than PGK2 for achieving vaginal delivery and less epidural use
• l-
'
oley catheter placement to mechanically dilate the cervix
INDUCTION OF LABOUR
Amniotomy
• artificial ROM (amniotomy) to stimulate prostaglandin synthesis and secretion; may try this as initial
measure if cervix is open and soft, the membranes can be felt, and if the head is well applied to the
cervix
• few studies address the value of amniotomy alone for IOL
• amniotomy plus IV oxytocin: more women delivered vaginally at 24 h than amniotomy alone
(RR=0.03) and had fewer instrumental vaginal deliveries (RR=5.5)
Oxytocin
• oxytocin ( Pitocin*): 10 U in I L normal saline, run at 0.5*2 mll/min IV increasing by 1-2 mU/min q20-
60 min
• reduces rate of unsuccessful vaginal deliveries within 24 h when used alone (8.3% vs. 54%, RR=0.I6)
• ideal dosing regimen of oxytocin is not known
• current recommendations: use the minimum dose to achieve active labour and increase q30 min as
needed
• reassessment should occur once a dose of 20 mU/min is reached
• potential complications
tachysystole/tetanic contraction (may cause fetal distress or uterine rupture)
uterine muscle fatigue, uterine atony (may result in PPH)
vasopressin-like action causing anti-diuresis
Oxytocin t
’
/j- 3-5 min
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Augmentation of Labour
• augmentation of labour with amniotomy and/or oxytocin may be used to promote stronger and
more frequent contractions when spontaneous contractions are inadequate and cervical dilatation or
descent of fetus fails to occur
Provided there are no contraindications,
oxytocin is used to improve uterine
contraction strength and/or frequency
Abnormalities and Complications of Labour and
Delivery
Abnormal Progression of Labour (Dystocia)
Definition
• expected patterns of descent of the presenting part and cervical dilatation fail to occur in the
appropriate time frame;can occur in allstages of labour
• during active phase:>4 h of <0.5 cm/h
• during 2nd stage: >1 h with no descent during active pushing
Etiology
• power (leading cause):contractions (hypotonic, uncoordinated), inadequate maternal expulsive
efforts
• passenger:fetal position, attitude,size, anomalies(hydrocephalus)
• passage: pelvic structure (CPU), maternalsoft tissue factors (tumours, full bladder or rectum, vaginal
septum)
• psyche:hormones released in response to stress may contribute to dystocia; psychological and
physiologicalstressshould be evaluated as part of the management once dystocia has been diagnosed
The 4 Ps of Dystocia
Power
Passenger
Passage
Psyche
Management
• confirm diagnosis of labour (rule out false labour)
• search for factors of (.
'
PD
• concern for dystocia if adequate contractions measured by intrauterine pressure catheter with no
dcscent/dilatation for >2 h
• management: if CPD ruled out, IV oxytocin augmentation ± amniotomy, optimize fetal position,
optimize pain control
Risks of Dystocia
• inadequate progression of labour is associated with an increased incidence of:
maternalstress
• maternal infection
PPH
need for neonatal resuscitation
• fetal compromise (from tachysystole)
• uterine rupture
hypotension
Shoulder Dystocia
Definition
• fetal anteriorshoulder impacted above pubic symphysis after fetal head has been delivered
• life threatening emergency
Etiology/Epidemiology
• incidence 0.15-1.4% of deliveries
• occurs when breadth of shoulders is greater than biparietal diameter of the head
Risk Factors
• maternal: obesity, DM, multiparity, and previousshoulder dystocia
• fetal: prolonged gestation or macrosomia (especially if associated with GDM)
• labour:
prolonged 2nd stage
instrumental midpelvic delivery
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Presentation
• “turtle sign"
:head delivered but retracts against perineum
• complications:
fetal:
Approach to the Management of
Shoulder Dystocia
hypoxic ischemic encephalopathy (chest compression by vagina or cord compression by pelvis
can lead to hypoxia)
brachial plexus injury'(Hrb s palsy:C5-C7; Klumpke’
s palsy:C8-T1),90% partially resolve
within 6 mo
fracture (clavicle,humerus, and cervical spine)
death
maternal:
perineal injury
PPH (uterine atony orlacerations)
uterine rupture
ALARMER
Ask for help
Legs in full flexion (McRoberts
maneuver)
Anterior shoulder disimpaction
(suprapubic pressure)
Release posterior shoulder by rotating
it anteriorly with hand in the vagina
under adequate anesthesia
Manual corkscrew i.e.rotate thefetus
by the posteriorshoulder until the
anteriorshoulder emergesfrom behind
the maternalsymphysis
Episiotomy
Rollover (on hands and knees)
'Note that suprapubic pressure and
McRoberts maneuver together will
resolve 90% of cases
Treatment
• goal:to displace anteriorshoulder from behind symphysis pubis;follow a stepwise approach of
maneuvers until goal achieved (see sidebar)
• other options:
cleidotomy (deliberate fracture of neonatal clavicle)
• Zavanelli maneuver:replacement of fetus into uterine cavity and emergent CD
symphysiotomy
Prognosis
• 1% risk of long-term disability for infant
Umbilical Cord Prolapse
•
Definition
descent of the cord to a level adjacent to or below the presenting part, causing cord compression
O
between presenting part and pelvis
Umbilical Cord Accident Causes
• Nuchal cord
• Type A (looped)
. Type B (hitched)
• Body loop
• Single artery
• True knot
• Torsion
• Velamentous cord insertion
• Short cord <35cm
• Long cord >80 cm
Etiology/Epidemiology
• increased incidence with prematurity/PROM,fetal malpresentation (
-50% of cases),low-lying
placenta,polyhydramnios,multiple gestation, and CPD
• incidence:1 in 200 to 1 in 400 deliveries
Presentation
• visible or palpable cord
• 1 H R changes(variable decelerations, bradycardia, or both)
Treatment
• emergency CD if not fully dilated and vaginal delivery not imminent
• O:to mother,monitor fetal heart
• alleviate pressure of the presenting part on the cord by elevating fetal head with a pelvic exam
(maintain this position until CD)
• keep cord warm and moist by replacing it into the vagina ± applying warm saline soaks
• roll mother onto all fours or position mother in Trendelenburg or knee-to-chest position
• if fetal demise or too premature (<22 wk GA), allow labour and delivery
1/3of protraction disorders develop into
2° arrest of dilatation due to CPD
2/3of protraction disorders progress
through labour to vaginal delivery
Uterine Rupture
Definition
• associated with previous uterine scar (in 40% of cases), tachysystole with oxytocin,grand multiparity,
and previousintrauterine manipulation
• generally occurs during labour, but can occur earlier with a classical incision
• 0 5-0.8% incidence,up to 12% with classical incision
Presentation
• prolonged fetal bradycardia (most common presentation)
• acute onset of constant lower abdominal pain, may not have pain if receiving epidural analgesia
• hyper/hvpotonic uterine contractions
• abnormal progress in labour
• vaginal bleeding
• intra-abdominal hemorrhage
• loss of station of the presenting fetal part
• maternal tachycardia, hypotension, or shock
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Risk Factors
• uterine scarring (e.g. previous uterine surgeries including CD (especially classical incision),
perforation with D&C, and myomectomy)
• excessive uterine stimulation (e.g. protracted labour, oxytocin, and prostaglandins)
• uterine trauma (e.g. operative equipment, ECV )
• multiparity
• uterine abnormalities
• malpresentation
• placenta accreta
Treatment
• rule out placental abruption
• maternal stabilization (may require hysterectomy), treat hypovolemia
• immediate delivery for fetal survival
Complications
• maternal mortality 1-10%
• maternal hemorrhage,shock, D1C
• amniotic fluid embolus
• hysterectomy if uncontrollable hemorrhage
• fetal distress, associated with infant mortality as high as 15%
w
Maternal Mortality Causes
• Thromboembolism
• Cardiac event
. Suicide
. Sepsis
• Ectopic pregnancy
. HTN
• Amniotic fluid embolism
• Hemorrhage
*
ln Canada (2013), lifetime risk of
maternal death is1/5200
Amniotic Fluid Embolism
Definition
• amniotic fluid debris in maternal circulation triggering an anaphylactoid immunologic response
Etiology/Epidemiology
• rare intrapartum or immediate postpartum complication
• 13-30% maternal mortality rate
• leading cause of maternal death in induced abortions and miscarriages
. 1 in 8000 to 1 in 80000 births
Risk Factors
• placental abruption
• rapid labour
• multiparity
• uterine rupture
• uterine manipulation
• induction medication and procedures
Differential Diagnosis
• pulmonary embolus, drug-induced anaphylaxis, septic shock, eclampsia, HELLP syndrome,
abruption, and chronic coagulopathy
Presentation
• sudden onset of respiratory distress, cardiovascular collapse (hypotension, hypoxia), and
coagulopathy
• seizure in 10%
• ARDS and left ventricular dysfunction seen in survivors
Management
• should be managed in the ICU by a multidisciplinary team
• supportive measures (high flow 02, ventilation support, fluid resuscitation, inotropic support, ±
intubation) and coagulopathy correction
Chorioamnionitis
Definition
• infection of the chorion, amnion, and amniotic fluid
Etiology/Epidemiology
• incidence: 1-5% of term pregnancies and up to 25% in preterm deliveries
• ascending infection (microorganisms from vagina)
• predominant microorganisms include: GBS, Bacteroides and Prevotclla species, E. coli,and anaerobic
Streptococcus
r T
LJ
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