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12/23/25

 


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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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OB37 Obstetrics Toronto Notes 2023

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

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