I.

CARDIOVASCULAR DISEASE AND PREGNANCY

1) Hypertensive disorders are the most frequent⭐ cardiovascular disorders during pregnancy, occurring in 5-10% of all pregnancies
a) Among the other disease conditions, congenital heart disease is the most frequent CVD present during pregnancy in the western world⭐ (75-
82%)
b) Rheumatic valvular disease dominates in non-western⭐ countries, comprising 56-89% of all CVDs in pregnancy
1st 2nd 3rd Stage 2 3-6 months
Stage 1 Labor Early Postpartum⭐
Trimester Trimester Trimester Labor Postpartum
 60-80% immediately,
Cardiac
 5-10%  35-45%  30%  50% then rapidly decreases
output
within the first hour⭐
During uterine  5-10% within 24 hours,
Heart rate  3-5%  10-15%  15-20% contractions: continues to decrease
 40-50% Return to pre-
throughout the first 6 weeks
pregnancy
During uterine
contractions:  SBP 5-10% within 48 hours; values
Blood
 10%  5%  5% may increase again between
pressure  SBP 15-25%
days 3-6 due to fluid shifts
 DPB 10-15%
Plasma  500 mL due to
  40-50%  
volume autotransfusion

2) Women with underlying cardiac disease may not always accommodate these changes, and ventricular dysfunction leads to cardiogenic heart failure⭐
3) Maternal cardiac dysfunction is related to:
a) Impaired uteroplacental flow – can lead to IUGR and oligohydramnios
b) Suboptimal fetal outcome – IUGR and oligohydramnios can lead to pre-term delivery
4) Heart failure timing
a) A few women with severe cardiac dysfunction can experience evidence of heart failure before mid-pregnancy
b) In others, heart failure may develop after 28 weeks’ gestation, when pregnancy-induced hypervolemia and cardiac output reach their maximum
c) Most cases of heart failure develops PERIPARTUM, when labor, delivery, and several common obstetrical conditions add undue cardiac burdens
i) Preeclampsia, Hemorrhage and anemia (particularly during postpartum), Sepsis
A. DIAGNOSIS OF HEART DISEASE
1) Pregnancy-induced symptoms that may confound the diagnosis of
Symptoms⭐ Clinical Findings⭐
heart disease: ⭐
● Progressive dyspnea or ● Cyanosis
a) Functional systolic heart murmurs are common (not considered
orthopnea ● Clubbing of fingers
abnormal: Diastolic murmurs – abnormal)
● Nocturnal cough ● Persistent neck vein distention
b) Respiratory effort is accentuated (due to rise of diaphragm)
● Hemoptysis ● Systolic murmur grade 3/6 or greater
c) Edema in lower extremities after mid-pregnancy (due to compression
● Syncope ● Diastolic murmur⭐
of the great vessels, not CHF)
● Chest pain ● Cardiomegaly
d) Fatigue and exercise intolerance often develop
● Persistent tachycardia and/or arrhythmia
B. PRE-PREGNANCY COUNSELING ● Persistent split second sound
1) Ideally done in ALL women with known cardiac or aortic disease who ● Fourth heart sound
wish to embark on pregnancy. ● Criteria for pulmonary hypertension
2) For risk estimation, a minimum of ECG, echocardiogram, and exercise testing Congenital heart disease in fetus (%)
Cardiac lesion
should be performed. ⭐ Father affected Mother affected
3) Women with severe heart disease will benefit greatly from counseling before Marfan syndrome⭐ 50 50
pregnancy: Aortic stenosis 3 15-18
a) Advise patients not to get pregnant if there are signs that the pregnancy may Pulmonary stenosis 2 6-7
become difficult VSD 2 10-16
b) Some women have life-threatening cardiac abnormalities that can be ASD 1.5 5-11
reversed by corrective surgery, and subsequent pregnancy becomes less PDA 2.5 4
dangerous Coarctation of the aorta NS 14
c) In women with mechanical valves taking warfarin, fetal teratogenic
TOF 1.5 2-3
concerns predominate
d) Many congenital heart lesions are inherited as polygenic characteristics
II. DIAGNOSTIC STUDIES
1) ECG:
a) Normal electrocardiograph (ECG) adaptations during pregnancy: ⭐
i) Left axis deviation, Reduced mean PR interval, Increased heart rate, Inverted or flattened T waves and A Q wave in lead III
ii) Changes may mimic LV hypertrophy and other structural heart diseases

2) 2D ECHO
a) Transthoracic – most common and preferred
b) Transesophageal
i) Useful in some situations, such as complex congenital heart disease
ii) Fetal monitoring performed (as a precautionary measure)
iii) Done by inserting a probe with a transducer down the esophagus.
(1) May induce gag reflex that is why there is risk of vomiting/aspiration and sudden increases in intraabdominal pressure
c) Normal pregnancy-induced changes:
i) Small increase in dimensions of all cardiac chambers
(1) Particularly in ventricles - Due to adaptation to the increased preload and CO
ii) Slight but significant growth in left ventricular mass
iii) Greater tricuspid and mitral valve regurgitation

MNTM 2022 1
3) EXERCISE TESTING
a) Physiological exercise testing
i) Should be performed in patients with known heart disease who plan pregnancy
ii) Known to have congenital heart disease or valvular disease
(1) If this was not done and the patient becomes pregnant (as long as she’s asymptomatic), a submaximal exercise testing should be
done instead.
iii) Suspected to have heart disease - pregnant, asymptomatic
(1) submaximal exercise testing (80% of predicted maximal heart rate) in asymptomatic patients with suspected heart disease is
recommended
b) Dobutamine stress test
i) Ordinarily done among patients who can’t exercise
ii) Rarely indicated during pregnancy⭐
iii) Use should be avoided when other options are available
4) CHEST X-RAY
a) Not contraindicated during pregnancy
i) Only concern is the exposure of the baby to radiation, although by itself is not significant
ii) When a lead apron shield is used, fetal radiation exposure is minimal
b) Gross cardiomegaly can usually be excluded, but slight heart enlargement cannot be detected accurately because the heart silhouette normally
is larger in pregnancy
5) CARDIOVASCULAR MRI
a) Advised if other non-invasive diagnostic measures are not sufficient for definitive diagnosis
i) NO CONTRAST SHOULD BE USED
b) Evidence regarding gadolinium-based contrast in pregnancy is controversial and its use should be avoided, if possible, especially in the first
trimester
III. CLASSIFICATION OF HEART DISEASE
A. RISK OF MATERNAL CARDIOVASCULAR COMPLICATIONS
1) Depends on: FUNCTIONAL CLASSIFICATION OF HEART DISEASE⭐
a) Underlying cardiac diagnosis Uncompromised – no limitation of physical activity
b) Ventricular and valvular function CLASS
These women do not have symptoms of cardiac insufficiency or
I
c) Functional class (NYHA) experience anginal pain
d) Presence of cyanosis Slight limitation of physical activity
e) Pulmonary artery pressures CLASS These women are comfortable at rest, but if ordinary physical activity
f) Presence of comorbidities II is undertaken, discomfort in the form of excessive fatigue,
2) RISK ESTIMATION SHOULD BE INDIVIDUALIZED⭐⭐⭐ palpitation, dyspnea, or anginal pain results
Marked limitation of physical activity
a) Risk estimation needs to be re-evaluated during each prenatal CLASS
These women are comfortable at rest, but less than ordinary activity
visit because the risk of complications may change overtime III
causes excessive fatigue, palpitation, dyspnea, or anginal pain
b) Disease specific⭐ risk should be assessed using the MODIFIED Severely compromised – inability to perform any physical
WHO (mWHO) CLASSIFICATION – most accurate CLASS activity without discomfort
c) Risk prediction estimation should be further defined by taking into IV Symptoms of cardiac insufficiency or angina may develop even at
account predictors that have been identified in studies such as rest. If any physical activity is undertaken, discomfort is increased
CARPREG and ZAHARA
CARPREG (CARdiac disease in PREGnancy) ZAHARA (Zwangerschap bij Aangeboren Hartafwijking)
● Predictors of primary cardiac events during Predictors of cardiac complications during pregnancy Points
pregnancy: Systemic atrioventricular valve regurgitation (moderate/severe) 0.75
→ Prior cardiac event or arrythmia Baseline New York Heart Association Class  II 0.75
→ Reduced systemic ventricular systolic function (Ejection Cardiac medication usage pre-pregnancy 1.5
Fraction < 40%) Left heart obstruction (aortic valve area <1.0 cm2, peak LV outflow
→ Left heart obstruction (in echocardiography) 2.5
gradient >50 mm Hg)
■ Aortic valve area < 1.5 cm2
History of arrhythmia 1.5
■ Mitral valve area < 2 cm2
■ Peak left ventricular outflow gradient > 30 mmHg Pulmonary AV valve regurgitation (moderate/severe) 0.75
→ Baseline New York Heart Association Class > II or Mechanical valve prosthesis 4.25
cyanosis (resting saturation < 92%) Repaired or unrepaired cyanotic heart disease 1.0
● One point is assigned for each risk factor present:
Risk Score Risk of Cardiac Event Risk Score Risk of Cardiac Event
0 5% 0 – 0.5 2.9%
1 27% 0.51 – 1.5 7.5%
1.51 – 2.5 17.5%
>1 75%
2.51 – 3.5 43.1%
>3.51 70%
B. RISK OF OBSTETRIC AND OFFSPRING COMPLICATIONS
1) Women with cardiac diseases have an increased risk of obstetric complications: Predictors of Neonatal Events
a) Preterm labor (any chronic disease predisposes to preterm labor)
● NYHA Class III/IV or cyanosis during baseline prenatal visit
b) Preeclampsia
● Maternal left heart obstruction
c) Postpartum hemorrhage
● Smoking during pregnancy
i) Patients with cardiac diseases undergoing anticoagulation treatment
● Low maternal O2 sat (<90%)
during pregnancy
● Multiple gestation
(1) If anticoagulation not withheld prior to delivery, increased risk of
● Use of anticoagulants throughout the pregnancy
hemorrhage
● Cardiac medication before pregnancy
ii) Use of oxytocin for labor induction
● Mechanical valve prosthesis
2) Offspring complications: 18-30%
● Maternal cardiac event during pregnancy
3) Neonatal mortality: 1-4%
● Maternal decline in cardiac output during pregnancy
● Abnormal uteroplacental Doppler flow

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 III. MANAGEMENT CONSIDERATIONS
WARNING SIGNS OF HEART FAILURE FETAL EFFECTS OF CARDIAC MEDICATIONS⭐
● Always assess for this every prenatal checkup ● ACE Inhibitors and ARBs
→ Paroxysmal nocturnal dyspnea → Associated with fetal renal failure⭐, growth restriction,
→ Chest pain malformations and death.
→ Nocturnal cough ● Phenytoin
→ Increasing dyspnea on exertion → Potential for early hemorrhagic disease of the
→ Pulmonary crackles newborn.
→ Other clinical findings: ● Warfarin
■ Hemoptysis, Progressive edema, Tachycardia → Risk of fetal hemorrhage.
INTRAPARTUM HEART FAILURE ● Amiodarone
● Cardiovascular decompensation during labor may manifest as pulmonary edema → May be associated with fetal thyroid toxicity.
with hypoxia or as hypotension, or both. ● First three are TERATOGENIC. Amiodarone is not
● The proper therapeutic approach depends on the specific hemodynamic status and teratogenic but has fetal effects (fetal thyroid toxicity) 🗐
the underlying cardiac lesion

ANTENATAL MANAGEMENT LABOR AND DELIVERY PUERPERIUM

● All women with congenital heart disease
should be offered fetal echocardiography
between 19th -22nd weeks of pregnancy⭐
● Consider antenatal steroids in anticipation
of preterm delivery (24 – 34 AOG ) ⭐
● Fetal growth assessment by either serial
clinical examination or ultrasonography
should be considered because fetal growth
restriction occurs in many types of maternal
congenital and acquired cardiac lesions
● Antenatal surveillance: NST, BPS with or
without Doppler
→ Doppler if considering IUGR
Epidural anesthesia
● Preferred gravidocardiac patients ⭐
● Decreases the sympathetic oxygen
consumption
● Fewer hemodynamic changes :
→ minimizes catecholamine release and
resultant cardiac output fluctuations
→ Spinal anesthesia: more hemodynamic
changes such as sudden drop in BP
which could compromise the fetus
● Slower onset allows maternal
cardiovascular system to compensate
resulting in lower risk of both hypotension
and decreased uteroplacental blood flow
● Since epidural anesthesia is given in
increments, hypotension is controlled or
slower in onset.
● In general, vaginal delivery is preferred, ⭐
and labor induction is usually safe
→ During the 2nd stage utilize vacuum or
forceps⭐ to prevent maternal effort in
pushing.
■ intraabdominal pressure exerts
negative effects on the heart
● Cesarean delivery is usually limited to
obstetrical indications
→ Dilated aortic root >4 cm or aortic
aneurysm
→ Acute severe congestive heart failure
→ Recent myocardial infarction
→ Severe symptomatic aortic stenosis
→ Warfarin administration within 2 weeks of
delivery
→ Need for emergency valve replacement
immediately after delivery
● Timing of Delivery
→ Induction of labor should be considered at
40 weeks⭐ of gestation in all women with
cardiac disease
● Endocarditis prophylaxis no longer
recommended
● Reasons why puerperium has highest
change in cardiac output and hence
highest risk of heart failure
→ Fluid mobilized into the intravascular
compartment and reduced peripheral
vascular resistance place higher
demands on myocardial performance.
■ When baby and placenta has been
delivered, all the blood that circulates
here goes back to the mother hence
increase in cardiac output
→ Postpartum hemorrhage, anemia,
infection, and thromboembolism⭐ are
much more serious complications with
heart disease
■ Often act in concert to precipitate
postpartum heart failure
■ To control:
− Postpartum hemorrhage: Do active
management of third stage of labor
− Infection: give antibiotics
− Thromboembolism: Prevention via
compression stockings and early
ambulation.

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 I. PRETERM LABOR
1) Preterm labor is the presence of uterine contractions of sufficient strength and frequency to effect
progressive effacement and dilatation of the cervix between 20 and 37 weeks gestation
a) before 20 weeks AOG or <500g is categorized as abortion
b) This should be accompanied by cervical change, including (+) effacement and (+) dilatation, which
may be observed through internal examination or through early detection using transvaginal
ultrasound
i) Early Preterm⭐
(1) Those delivered < 34 weeks⭐
(2) Gestational age at delivery is inversely related to neonatal morbidity and mortality
(a) Early preterm infants experience a significantly higher rate of prematurity-related
complications
ii) Late Preterm Classification⭐ Weight in Grams (g)
(1) Those delivered between 34 and 36 weeks ⭐ Low (LBW) 1,500 – 2,500
(2) Has a better survival rate, lesser infant mortality rate (Lung maturity of infants Very low (VLBW) 1,000 – 1,500
will already be okay at 34-36 weeks AOG) Extremely low (ELBW) 500 – 1,000
2) The lower the birth weight, the higher the chances of morbidity and complications (regardless of AOG)
A. PRETERM BIRTH STATISTICS

Distribution of Preterm Obstetrical Complications

Incidence Mortality per gestational age Births by Gestational associated with Late-preterm
Age Births at Parkland Hospital

2) The reason why we deliver at 39 weeks (term)

1) Based on the local (PH) data,
preterm birth is leading cause
3)
of neonatal morbidity and
mortality
a) If we want to target this, we
need to know the different
causes of the preterm birth
1) Most of the preterm
is because it has the lowest incidence
birth are in the late 2) Most are spontaneous labor. If
Though neonatal death rate is low at 1.1% at
we can identify the cause of
34 weeks AOG, it is significantly higher than preterm and with
spontaneous labor and
those born at 39 weeks AOG. This is the corresponding lower
spontaneous ROM we can then
reason why when we do CS delivery, we mortality rates.
avoid preterm labor.
would want them to be delivered at 39 weeks
or more of infant deaths

● Presence of significant difference between preterm births versus 39 weeks (as presented in
the table above):
→ Respiratory distress
■ In need of ventilator
■ Transient tachypnea
→ Intraventricular hemorrhage
→ Sepsis
→ In need of phototherapy
→ Necrotizing enterocolitis
→ Intubation in the delivery room

Neonatal complications Long term complications

● Major complications: ● Cerebral palsy
→ Respiratory Distress Syndrome (RDS) – → Increased incidence
lack of surfactant → Reason why we give MgSO4 to severe preterm, to prevent cerebral palsy
→ Necrotizing Enterocolitis (NEC) – leak into ● Visual and hearing deficits
abdomen and blood stream → When you see children (3 years old and younger) with eyeglasses, high probability the child
→ Intraventricular Hemorrhage (IVH) was born preterm
→ Sepsis ● Learning disabilities
→ Retinopathy ● Adult problems
→ Bronchopulmonary dysplasia → If they survive the neonatal and childhood problems, we expect adult problems to come in
→ Periventricular leukomalacia ■ Type II DM
● Minor complications: ■ Hypertension
→ Phototherapy ■ Chronic lung diseases
→ Low APGAR score ■ Cardiovascular diseases
→ Intubation at delivery room → In babies delivered preterm or with IUGR, when they grow old, these are the expected
complications
→ This is what we call the Barker’s Phenomenon aka Barker’s Hypothesis
■ A hypothesis proposed in 1990 by the British epidemiologist David Barker (b. 1939) that
intrauterine growth retardation, low birth weight, and premature birth have a causal
relationship to the origins of hypertension, coronary heart disease, and non-insulin-
dependent diabetes, in middle age

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 II. CAUSES OF PRETERM DELIVERY
1) Spontaneous unexplained preterm labor with intact membranes ⭐ (40-45%)
a) Uterine distention - twins, hydramnios, macrosomic babies ● Risk factors for spontaneous preterm labor
b) Maternal-fetal stress - psychological and emotional → Multifetal pregnancy, Intrauterine infection
c) Premature cervical ripening - cervical dysfunction and incompetence → Bleeding, Placental infarction, Premature cervical dilation,
d) Infection⭐ Cervical insufficiency
2) Idiopathic PPROM (30-35%) → Hydramnios, Uterine fundal abnormalities
3) Delivery for maternal or fetal indications (30-35%) → Fetal anomalies (esopahegal atresia causing hydramnios →
distention)
a) E.g. fetal distress, IUGR, hypertension → Maternal illness from infections, autoimmune diseases, and
4) Multiple coexistent genetic alterations and environmental factors may lead to gestational hypertension
preterm birth ● All culminate in a common end point: premature cervical dilation
and effacement and premature activation of uterine contractions

UTERINE DISTENTION
● Those with multifetal⭐
pregnancy, macrosomic babies
like in DM, or in hydramnios
● Stretch will result to an
increase in Contraction
Associated Proteins (CAPs)
→ uterine contractility
1. Uterine stretch
2. Release of contraction
associated proteins (CAPs) ⭐
like gap junction proteins,
connexin 43, oxytocin receptors,
prostaglandins and gastrin
releasing peptides
3. Promote myometrial contractility
resulting to preterm labor.
1. Uterine stretch
2. Early activation of the
placental-fetal endocrine
cascade
3. Increase corticotropin
releasing hormones (CRH)
4. Release of estrogen and
enhance release of CAPs
5. Increased uterine contractility
PATHOMECHANISM
MATERNAL-FETAL STRESS
● There is release of cortisol followed
by activation of the fetal adrenal-
placental endocrine axis
→ Results in an increase in the
secretion of placental CRH⭐
● (+) Stimulation of adult (maternal)
and fetal adrenal steroid hormone
→ Resulting in an increase in
maternal plasma estrogen
● (+) Loss of uterine quiescence and
increased cervical ripening
● Stressors: Nutrient restriction,
obesity, infection, diabetes,
psychological stress
1. Increased cortisol⭐ from maternal
stress
2. Early activation of the fetal
adrenal- placental endocrine axis
3. Cascade of CRH⭐ secretion and
increase maternal estrogen
resulting to increased CAPs. This
will increase cervical ripening and
increase uterine contractility.
1. There is premature aging of fetal
and decidual cells
2. This increases release of uterotonic
signals.
3. This would result to uterine
activation that causes preterm labor.
INFECTION
1) Transplacental transfer of maternal systemic infection
a) Any infection in the mother can go to the baby (UTI, pneumonia,
sepsis, dental carries)
2) Retrograde flow infection into the peritoneal cavity via fallopian tubes
3) Ascending infection from vagina and cervix
a) Most common⭐; ascending microorganisms colonize the cervix,
decidua, and possibly the membranes, where they then may enter
the amniotic sac
4) Cervical dysfunction of either the epithelia or stromal extracellular matrix
a) Compromise of an intact cervical epithelial barrier increases the risk
of ascending infection by bacteria such as group B streptococci
b) Mucous plug
i) Found in the cervix; prevents the microorganisms in the vagina
and the cervix to enter the uterus
ii) If the mucous plug is removed or dislodged, any
microorganism in the vagina and the cervix can now enter the
uterus
5) Anatomical predisposition: The lower pole of the fetal membrane-
decidual junction is contiguous with the cervical canal orifice, which
provides a passageway for microorganisms
● The earlier the onset of preterm labor, the greater the likelihood of
underlying infection
● Inflammatory responses drive the pathogenesis of infection induced preterm
labor
→ Lipopolysaccharide (LPS) and other toxins from bacteria are recognized
by pattern-recognition receptors (TLRs)
● Induces a signaling cascade that activates production of chemokines such
as IL-8 and cytokines such as IL-1β
→ IL-1β promotes prostaglandin formation that induces cervical ripening
and loss of myometrial quiescence (inc contractions)
→ IL-1β also induce proteases such as matrix metalloproteinases (MMPs)
which breakdown extracellular matrix components, resulting in the
disruption of the structural integrity of fetal membranes and cervix →
PPROM

III. ANTECEDENTS AND CONTRIBUTING FACTORS TO PRETERM LABOR

● Threatened abortion (during the first trimester) ● Prior preterm labor
→ Associated with higher rates of later adverse outcomes → Most important risk factor for preterm labor, confers highest risk
→ Both light and heavy bleeding were shown to be associated with → The recurrent preterm delivery risk for women with a preterm first
subsequent preterm labor, placental abruption, and pregnancy delivery was threefold greater than that of women whose first
loss before 24 weeks neonate was born at term
● Lifestyle factors → The risk of recurrent preterm birth is influenced by three factors:
→ The following affect the incidence and outcome of low birthweight The frequency of prior preterm deliveries, severity as measured
neonates: by gestational age, and the order in which the prior preterm
■ Cigarette smoking, Inadequate maternal weight gain, Illicit drug delivery occurred
use ● Infection
→ Extremes of maternal weight and l age → Antibiotic prophylaxis: Not recommended in women with preterm
→ Poverty, Short stature labor and intact membranes to prevent preterm birth
→ Vitamin C deficiency, Psychological factors → Bacterial vaginosis: Associated with spontaneous abortion,
● Genetic factors preterm labor, PPROM, chorioamnionitis, and amniotic fluid
→ There is a recurrent, familial, and racial nature of preterm birth infection
suggesting that genetics may play a role ● Periodontal diseases
● Birth defects → Due to anaerobic bacteria in gums
● Interval between pregnancies
→ < 18 months and >59 months interval between pregnancies were
associated with greater risks for both preterm birth and small-for-
gestational age newborns
→ Optimum is 18-23 months – WHO

MNTM 2022 2
 IV. DIAGNOSIS OF PRETERM LABOR
● Uterine contractions → Braxton Hicks contractions may be misleading
SYMPTOMS
● Pelvic pressure, Menstrual-like cramps, Watery vaginal discharge, Lower back pain
● Cervical dilatation : If the patient is contracting, we do internal ● T Cervix - Normal
examination to see cervical dilatation (+ → labor) → Horizontal line –
● Via ultrasound : Detect preterm labor even if the cervix is still endocervical canal
closed in the external os level → Curved vertical line –
■ Since, dilatation of the cervix begins in the internal os. internal os
Measure from internal to external os 3x and record ● Y Cervix / Y Funneling
shortest.(?)
CERVICAL → Initial cervical
CHANGES → Normal: At 24 weeks, mean Cervical Length = 35 mm dilatation - Happens in the internal os
(3.5 cm)
→ Short cervical length
■ If at 24 weeks, the cervical
● V Funneling
length is < 25 mm (2.5 cm),
→ Further funneling seen, Shorter cervical length
then these are the patients
that more or less will ● U Funneling
eventually have preterm → Further cervical dilatation and funneling, with increased
labor cervical length shortening
FETAL ● Not present locally
FIBRO ● > 50 ng/mL by ELISA is considered positive
NECTIN ● Marker of impending preterm labor (PTL)
● Present locally : The only thing available in our country
● An immunochromatographic dipstick test for detecting the presence of phosphorylated IGFBP-1 (insulin-like growth factor binding
protein-1) in cervical secretions
● IGFBP-1 - Produced in the decidual cells, Main protein in the amniotic fluid
ACTIM ● The presence of phosphorylated IGFBP-1 during weeks 24-34 of pregnancy, along with symptoms of labor, suggests the
PARTUS possibility of a preterm labor
● Clinical application: Patient with contractions (around 2 to 3 per hour), with a closed cervix on both IE and ultrasound (long cervix),
then we can use this to detect for IGFBP-1
■ If negative, we can send the patient home
■ If positive, then the patient has a possibility to go into preterm labor
V. PRETERM BIRTH PREVENTION
A. CERVICAL CERCLAGE
● Used for incompetent cervix : Recurrent pregnancy loss during the 2nd trimester
■ Can we treat it? Yes, using cervical cerclage
■ 16th, 17th week: Patient delivers the baby without uterine contractions
● Contraindications (substantially raises the likelihood of failure):
→ Bleeding
→ Contractions
→ Ruptured membranes
TYPE OF CERCLAGE AOG (weeks) Definition of Indication
Historical criteria (recurrent ≥3 early PTBs or second trimester losses)
● Women sonographically diagnosed with a short cervix (< 25 mm)
● Surgery between 12 and 14 weeks gestation
→ To make sure the baby is viable; that everything is okay with regards to the baby (ex. Ruling out miscarriage at 8 (earlier)
History indicated weeks, due to chromosomal abnormalities) - at 12-14 weeks, the product of conception still will NOT be able to dilate
12 - 14 the cervix anyway
(Prophylactic cerclage)
→ Allows this early intervention
→ It avoids surgery in a woman with a first trimester pregnancy destined for spontaneous loss
→ The product of conception will still not be able to dilate the cervix
● Studies have shown that this is the better management
Ultrasound indicated Short CL (<25mm) before 24 weeks in singleton gestations with prior PTB
14 - 23
(Therapeutic cerclage)
Cervical changes (≥1 cm dilated or prolapsed membranes on physical examination)
PE indicated ● “Rescue” cerclage; done emergently
16 - 23
(PE cerclage) ● When cervical insufficiency is recognized in women with symptoms (threatened PTL)
● Cervix is found to be dilated, effaced, or both (waited for signs and symptoms to be present)
Transabdominal 11 - 12 Prior history indicated cerclage that resulted in PTB at <33 weeks

Cervical Length Screening

1) If the clinical indication for cerclage is questionable, a woman may instead be observed
a) Most undergo cervical examination weekly or every 2 weeks via ultrasound to assess effacement and dilatation
2) Recommended (in US) for women with prior preterm birth:
a) Between 16 and 24 weeks gestation, sonographical measurement is completed every 2 weeks
i) If an initial or subsequent cervical length is 25 to 29 mm, then a weekly interval is considered
ii) If the cervical length measures < 25 mm, cerclage is offered
3) Women without a history of preterm birth but with a short cervix incidentally identified sonographically, progesterone therapy is offered
instead of cerclage
a) “We can offer either a micronized progesterone or cerclage”
i) 17-OHPC is not available in the Philippines

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 B. PROGESTERONE THERAPY
Prenatal Administration of Progesterone for Preventing Preterm Birth in Women Considered to be At Risk of Preterm Birth
● From the Cochrane Database of Systematic Reviews 2013
→ Benefits of progesterone therapy on patients with history of preterm birth are the ff:
■ ↓ Delivery – < 34 weeks and < 37 weeks
■ Reduced LBW, NEC, admission to NICU, and neonatal deaths
17-alpha-hydroxyprogesterone caproate (17-OHPC) Micronized progesterone
● Benefits women with:
● With a history of prior spontaneous preterm birth⭐
→ Short cervix⭐
● Given at 16 weeks, 250 mg IM every week until 36 weeks; the
→ History of prior preterm birth⭐ → CHECK TPAL
problem is that it’s not available in PH
● Given to women 16-36 weeks AOG to prevent preterm delivery
● First and only drug approved by the FDA for prevention of
● Given as nightly 200 mg micronized progesterone vaginal capsules
recurrent PTL with a preferred primary end-point of delivery <
35 weeks ● Since 17 OHCP is not available in the Philippines, micronized progesterone
is offered instead since it is readily available

VI. MANAGEMENT OF PRETERM LABOR WITH INTACT MEMBRANES

A. ANTENATAL CORTICOSTEROIDS
1) A single course of corticosteroids is recommended for pregnant women between 24 - 34 weeks of gestation who are at risk for preterm
delivery within 7 days | 
a) Betamethasone 12 mg given IM 24 hours apart for 2 doses
b) Dexamethasone 6 mg given IM every 12 hours apart for 4 doses (cheaper)
i) For COVID-19 patients, dexamethasone is the preferred anti-inflammatory drug
ii) Both decreases risk of Respiratory Distress Syndrome (RDS), Necrotizing Enterocolitis (NEC), and Intraventricular Hemorrhage
(IVH)
2) Uterine contractions but no cervical dilatation → you can control uterine contractions by using tocolytics
a) We don’t want to use steroids because its effect only lasts for 2 weeks
3) A “rescue course” of ACS may be considered if:
a) Antecedent therapy was given >2 weeks prior
b) Gestational age < 34 weeks
c) Women are judged by the clinician to be likely to give birth within the next week

B. MAGNESIUM SULFATE
1) Give MgSO4 if there is a risk of delivery within 1 week
2) Protocol (24 0/7 – 32 0/7 weeks) ⭐
a) MgSO4 administration (initial dose)
i) 4 gm loading dose IV
ii) 1 gm/hr continuously for 24 hrs
3) VLBW neonates whose mothers were treated with MgSO4 for preterm labor or
preeclampsia have reduced incidence of cerebral palsy ⭐ at 3 years (Grether, 2000;
Nelson, 1995) → Neuroprotection⭐
4) Adverse Effects
a) Maternal: Hypotension, Decease urine output, Bradypnea, Absent patellar reflex
Flushing, sweating, sensation of warmth, nausea and vomiting, headache, palpitations, pulmonary edema
Concentration above therapeutic range: respiratory depression and cardiorespiratory arrest
b) Fetal: Hypermagnesemia – hyporeflexia, poor suckling, respiratory depression need mechanical ventilation
FDA (2013) warned prolonged use of magnesium sulfate due to bone thinning and fractures in fetuses exposed for more than 5 to 7
days attributed to low calcium levels in the fetus
c) In patients being given MgSO4, there’s always Calcium gluconate (antidote) bedside since this is the antidote for MgSO4 toxicity
i) We have to monitor our patient for deep tendon reflexes or respiratory rate so we know whether there’s MgSO 4 toxicity
C. ANTIMICROBIAL PROPHYLAXIS⭐
1) In a randomized study of placebo or metronidazole + erythromycin between 20 – 24 weeks’ gestation followed by ampicillin + metronidazole
during labor (Goldenberg, 2006)
a) Antimicrobial regimen DID NOT REDUCE the rate of preterm birth or histological chorioamnionitis ⭐
2) Antibiotic prophylaxis to prevent preterm birth is NOT RECOMMENDED⭐ in women with preterm labor and intact membranes⭐
3) ORACLE Collaborative Study: No benefit or harm on neonatal outcomes
D. BED REST
1) There’s no evidence that support or refute bedrest, but clinical common sense would tell you that going on bed rest will decrease pressure
on the cervix
2) Adverse effect of bedrest: increased thromboembolic complications
a) Increased thromboembolic complications⭐
b) Significant bone loss in pregnant women prescribed outpatient bed rest (Promislow et al., 2004)
E. CERVICAL PESSARIES
1) Silicone rings, such as the Arabin pessary, are being used as prophylaxis to support the cervix in women with a sonographically short cervix
2) Studies show conflicting published reports and lack of an FDA- approved pessary for the indication of preterm birth prevention
3) Currently recommend pessary prophylaxis only within research protocols

MNTM 2022
F. TOCOLYTICS
CLASS DESCRIPTION
Most commonly used in the Philippines
→ Two types of β-adrenergic receptor
■ β1 receptors are prevalent in the heart, small intestine, and adipose tissue
■ β2 receptors predominates in the smooth muscle of blood vessels, uterus, bronchioles, and diaphragm
■ Increase in cAMP causes decrease in Ca which lessens contractions
● Ritodrine (withdrawn from market) and Terbutaline (most commonly used)
BETA MIMETICS → Both causes pulmonary edema
● Used to:
→ Reduce intracellular ionized calcium levels
→ Prevent activation of myometrial contractile proteins
● Maternal SE: Palpitations, tremor, nausea, vomiting, headaches, nervousness, anxiety, chest pain, shortness of breath,
hyperglycemia⭐, hypokalemia, pulmonary edema
● Fetal SE: fetal tachycardia, hypoglycemia, hyperinsulinism after birth⭐
• Most commonly used in the Philippines, First Line! CCB > Beta agonists⭐⭐⭐
• Increases AOG at birth, reduces, RDS, NEC, IVH, decreases deliveries before 24 weeks
CALCIUM • Dihydropyridine: Nifedipine > Nicardipine
BLOCKERS • Dangerous to combine with MgSO4 because it can interfere with pulmonary and cardiac function
• Has less side effects than beta mimetics
→ Maternal SE: Flushing, headache, dizziness, nausea, transient hypotension (rare)
Studies have shown it is not as effective
● Magnesium decreases the frequency of depolarization of smooth muscle by modulating calcium uptake binding and
MGSO4
distribution in smooth muscle cells OR by competitive antagonism to calcium for entry into myocytes
● No beneficial effect on reducing deliveries at <34 weeks or <37 weeks, or risk of RDS, NEC, IVH
• COX inhibitors inhibit cyclooxygenase that decreases prostaglandin synthetase and blocks conversion of free arachidonic
acid to prostaglandin → ↓ prostaglandin results in decrease contractile activity
PROSTAGLANDIN • COX inhibitors compared to other tocolytics (ritodrine or magnesium sulfate) showed no difference in their efficacy to forestall
SYNTHETASE preterm delivery
INHIBITORS • Given only for 2 days because of AE: premature closure of the ductus arteriosus and oligohydramnios⭐ (best drug of
there is hydramnios)
o Other AE: renal failure, NEC, IVH⭐
ORA OXYTOCIN RECEPTOR ANTAGONIST : Effective but it is not readily available; very expensive
● Potent smooth-muscle relaxants affect the vasculature, gut, and uterus
● In randomized clinical trials, nitroglycerin (orally, transdermally, IV) was ineffective or showed no superiority over
NO DONORS
other tocolytics
● Common side effect: Maternal hypotension

● Allow time for in-utero transfer to a tertiary center with neonatal intensive care facilities
→ Most authorities do not recommend use of tocolytics at or after 34 weeks
→ Do not use if there are no contractions⭐
Contraindications for Tocolytic Use in Preterm Labor⭐⭐⭐
● If present, there is no need to temporize or delay delivery; proceed to either labor induction/augmentation or CS
→ Fetal distress (non-reassuring fetal status)
→ Chorioamnionitis
→ Eclampsia or severe preeclampsia
→ Fetal demise – no use
→ Fetal maturity (at 37 weeks or near term we can already go away with tocolytics)
→ Maternal hemodynamic instability
→ Lethal fetal anomalies

MNTM 2022
 VII. PRETERM PRELABOR RUPTURE OF MEMBRANES
● A history of vaginal leakage of fluid, either as a continuous stream or a gush, speculum examination visualizes gross vaginal pooling of amniotic
fluid, clear fluid from the cervical canal, or both
● Confirmation of PPROM is usually accompanied by sonographic examination
A. MANAGEMENT OF RUPTURED MEMBRANES ⭐
Gestational Age Management⭐⭐⭐ ANTIMICROBIAL THERAPY
• Proceed to delivery⭐ • Fewer women developed chorioamnionitis (usually a histopath
• Group B streptococcal (or diagnosis)
≥ 34 weeks⭐
antimicrobial) prophylaxis to prevent • Fewer newborn developed sepsis
chorioamnionitis • Pregnancy was more often prolonged
• Single corticosteroid course⭐ (may o Prolonged 7 days in women given antimicrobials
be considered up to < 37 weeks)
• Fewer RDS
• Expectant management unless • Fewer necrotizing enterocolitis
pulmonary maturity is documented
• Fewer composite adverse outcomes
32 – 33 completed • Group B streptococcal prophylaxis
Corticosteroids (delay for at least 2 • IV Ampicillin + Erythromycin⭐ every 6 hours for 48 hours
weeks followed by oral amoxicillin + erythromycin every 8 hours for
days then administer; induce labor at
34 weeks) 5 days
• Antimicrobials to prolong latency o OR Ampicillin-Sulbactam⭐ for 7 days
• Expectant management o Amoxicillin-Clavulanate - NOT RECOMMENDED because
• Group B streptococcal prophylaxis it increases the incidence of of Necrotizing Enterocolitis
• Corticosteroids (NEC)
• Antimicrobials to prolong latency Antibiotics Dosage
• Tocolytics: No consensus For Ampicillin: 2 g IV every 6 hours
24 – 31 completed (administered ONLY if patient is in
weeks⭐ labor so we can still give Ampicillin and
corticosteroids and MgSO4) For Gentamicin: 2 mg/kg IV load followed by
Gentamicin
• Magnesium sulfate for 1.5 mg/kg every 8 hours OR
neuroprotection 5 mg/kg IV every 24 hours
• Deliver if there are signs of fetal For Cefazolin: 2 g IV every 8 hours
distress (if none, wait up until 34 weeks For mild penicillin
to deliver) allergy:
For Gentamicin: 2 mg/kg IV load followed by
Cefazolin and
• Expectant management or Gentamicin
1.5 mg/kg every 8 hours OR 5 mg/kg IV
induction of labor every 24 hours
• Group B streptococcal prophylaxis Alternative Regimens
is not recommended Ampicillin- 3 g IV every 6 hours
< 24 weeks • Corticosteroids may be sulbactam
considered as rescue course Piperacillin- 3.375 g IV every 6 hours or 4.5 g IV
BUT standard is still 24-34 weeks tazobactam every 8 hours
• Antimicrobials may be considered Cefotetan 2 g IV every 12 hours
Cefoxitin 2 g IV every 8 hours
• Tocolytics: No consensus
Ertapenem 1 g IV every 24 hours

B. SIGNS OF CHORIOAMNIONITIS
● ALWAYS DELIVER if the patient has CHORIOAMNIONITIS⭐
● Fever: > 38 °C; most reliable sign⭐
→ Infected group increase incidence of sepsis, RDS, early onset seizure, cerebral palsy,
● Maternal tachycardia: > 100/min and IVH
● Fetal tachycardia: > 160/min → Visual inspection: AF pooling visible in the posterior fornix during speculum exam
● Uterine tenderness → Nitrazine testing: Amniotic fluid is considerably more alkaline than vaginal discharge
● Malodorous vaginal discharge → AmniSure®: Identifies presence of the placental alpha fluid (ferning); confirms
● Maternal leukocytosis: > 15,000 cells/mm3 amniotic fluid microglobulin (PAMG-1) protein
● Elevated CRP: 12-40 mg/L (cut-off level)
C. CATEGORIES OF INTRAAMNIOTIC INFECTION

Isolated ● Any temperature between 38 – 38.9 °C with no other clinical

Maternal criteria indicating intraamniotic infection, and with or without SEQUELAE OF INTRAAMNIOTIC INFECTION
Fever⭐ persistent temperature elevation
● Based on clinical criteria; includes maternal intrapartum fever Neonatal Effects: ⭐
and one or more of the following: ● Neonatal pneumonia
→ Maternal leukocytosis ● Neonatal meningitis
→ Purulent cervical drainage OR ● Sepsis
Suspected
→ Fetal tachycardia ● Death
Intraamniotic
● Patients with a temperature of ≥ 39 °C with no other clinical risk ● Bronchopulmonary dysplasia
Infection⭐ ● Cerebral palsy⭐
factors
● 38 – 39 C and one additional risk factor: Low parity, multiple digital
exam, use of internal uterine and fetal monitors, meconium Maternal Effects:
stained fluid, presence of genital tract pathogens ● Dysfunctional labor
● Postpartum uterine atony with hemorrhage
● Based on a positive amniotic fluid test result (gram stain, ● Endometritis
Confirmed glucose level, or culture results consistent with infection) or ● Sepsis
Intraamniotic placental pathology demonstrating histologic evidence of ● Adult respiratory distress syndrome
Infection⭐ placental infection or inflammation ● Death
● Chorioamnionitis – histopath diagnosis

MNTM 2022
 HYPERTENSION IN PREGNANCY
● During pregnancy
→ Hypertension: SBP ≥ 140 mmHg and/or DBP ≥ 90 mmHg | 
→ Severe hypertension: SBP ≥ 160 mmHg and/or DPB ≥ 110 mmHg | 
A. GESTATIONAL HYPERTENSION
● Hypertension without proteinuria or other signs/symptoms of preeclampsia-related end-organ dysfunction that develops after 20 weeks of gestation⭐
→ Development of proteinuria → preeclampsia
→ Even without proteinuria, patients who develop severe hypertension or other features of severe disease are managed in the same way as those
with preeclampsia with severe features
● True gestational hypertension should resolve by 12 weeks postpartum
→ If it persists > 12 weeks postpartum, the diagnosis is revised to chronic hypertension that was masked by the physiologic decrease in blood
pressure that occurs in early pregnancy
→ If it resolves postpartum and signs and symptoms of preeclampsia did not develop, the diagnosis can be revised to transient hypertension of
pregnancy
B. PREECLAMPSIA
● A multisystem progressive disorder characterized by: | 
→ New onset of hypertension and proteinuria; OR
→ New onset of hypertension and significant end-organ dysfunction with or without proteinuria after 20 weeks of gestation or postpartum in a
previously normotensive woman
■ It is important to note that the diagnosis can still be made in the absence of proteinuria if the new-onset hypertension is accompanied by specific
signs or symptoms of significant end-organ dysfunction
PRE ECLAMPSIA PRE ECLAMPSIA WITH SEVERE FEATURES
● SBP ≥ 140 mm Hg or DBP ≥ 90 mm Hg on at least 2 Severe Blood Pressure Elevation
occasions at least 4 hours apart after 20 weeks of gestation ● Systolic blood pressure ≥ 160 mmHg or diastolic blood pressure ≥ 110 mmHg on
in a previously normotensive patient AND the new onset of 2 occasions at least 4 hours apart while the patient is on bedrest (antihypertensive
1 or more of the following: therapy may be initiated upon confirmation of severe hypertension, in which case criteria
for severe blood pressure elevation can be satisfied without waiting until 4 hours have
→ Proteinuria ≥ 0.3 g in a 24-hr urine specimen or protein/ elapsed)
creatinine ratio ≥ 0.3 (mg/mg) (30 mg/mmol) in a random Symptoms of Central Nervous System Dysfunction
urine specimen or dipstick ≥ 2+ if a quantitative ● New-onset cerebral or visual disturbance, such as: Photopsia, scotomata, cortical
measurement is unavailable blindness, retinal vasospasm
→ Platelet count < 100,000/μL ● Severe headache (I.e., incapacitating, "the worst headache I've ever had") or headache
→ Serum creatinine > 1.1 mg/dL (97.2 μmol/L) or doubling that persists and progresses despite analgesic therapy and not accounted for by
of the creatinine concentration in the absence of other alternative diagnoses
renal disease Hepatic Abnormality
→ Liver transaminases at least 2x ULN of the normal ● Impaired liver function not accounted for by another diagnosis and characterized by
concentrations for the local laboratory serum transaminase concentration >2x ULN range or severe persistent right upper
⭐

quadrant or epigastric pain unresponsive to medication and not accounted for by an

⭐

→ Pulmonary edema
alternative diagnosis
→ New-onset and persistent headache not accounted for Thrombocytopenia < 100,000 platelets/μL
by alternative diagnoses and not responding to usual Renal Abnormality
doses of analgesics ● Renal insufficiency (serum creatinine > 1.1 mg/dL [97.2 μmol/L] or a doubling of the
→ Visual symptoms (e.g. blurred vision, flashing lights or serum creatinine concentration in the absence of other renal disease)
sparks, scotomata) Pulmonary edema

1) Eclampsia - refers to occurrence of a grand mal seizure in a woman with preeclampsia in the absence of other neurologic conditions that could
account for the seizure
2) HELLP - Hemolysis, Elevated Liver enzymes, Low Platelets
a) Represents a subtype of preeclampsia with severe features in which hemolysis (Increased LDH ≥ 600 U/L (NV: < 200 U/L), elevated liver
enzymes (ALT, AST (NV: up to 30 U/L)) , and thrombocytopenia (< 100,000/mL) are the predominant features
3) Chronic Hypertension
a) Defined as hypertension that precedes pregnancy or is present on at least 2 occasions before the 20th week of gestation or persists > 12
weeks postpartum
b) It can be primary or secondary (to chronic kidney disease, adrenal tumors or renovascular hypertension).
4) Superimposed preeclampsia on chronic hypertension
a) Preeclampsia is considered superimposed when it occurs in a woman with preexisting chronic hypertension
b) Characterized by worsening or resistant hypertension (especially acutely), the new onset of proteinuria or a sudden increase in
proteinuria, and/or significant new end-organ dysfunction after 20 weeks of gestation or postpartum in a woman with chronic hypertension

I. PREECLAMPSIA
A. RISK FACTORS
● Nulliparity (+ primipaternity) ⭐ ● Poorly controlled hyperthyroidism ● In vitro fertilization (IVF)
● Preeclampsia in a previous pregnancy ● Woman herself was small for gestational ● Obstructive sleep apnea (OSA)
● Age > 40 years or < 18 years (extremes age (SGA) ● Elevated blood lead level
of age) ● Fetal growth restriction, abruptio ● Posttraumatic stress disorder (PTSD)
● Family history of preeclampsia placentae, or fetal demise in a previous
● Chronic hypertension pregnancy
● Chronic renal disease ● Prolonged interpregnancy interval if the
● Autoimmune disease (APS, SLE) previous pregnancy was normotensive; if
● Diabetes mellitus (pregestational and the previous pregnancy was
gestational) preeclamptic, a short interpregnancy
● Multifetal gestation interval increases the risk of recurrence
● Obesity⭐ ● Partner-related factors (new partner,
● Black race limited sperm exposure [e.g., previous
● Hydrops fetalis use of barrier contraception])
B. ETIOPATHOGENESIS
● May be: Normal Abnormal
→ Exposed to chorionic villi for the first time (primiparity) ⭐ Uterine spiral arterioles are Incomplete trophoblastic
→ Exposed to a superabundance of chorionic villi (twins, higher-ordered invaded by endovascular invasion⭐
pregnancies, or hydatidiform mole) trophoblasts ↓
→ Have preexisting conditions (e.g. diabetes, APAS, SLE) associated with ↓ Shallow invasion of the decidual
endothelial cell activation or inflammation These cells replace the vessels with endovascular
→ Genetically predisposed to hypertension during pregnancy vascular endothelial and trophoblasts, but not the
● Regardless of precipitating etiology, the cascade of events leading to the muscular linings to enlarge myometrial vessels
preeclampsia syndrome is characterized by abnormalities that result in the vessel diameter ↓
systemic vascular endothelial damage with resultant vasospasm, ↓ Myometrial arterioles do not lose
transudation of plasma, and ischemic and thrombotic sequelae |  Converts the narrow lumen, their endothelial lining and
● “Two-stage disorder” theory of preeclampsia pathogenesis⭐ muscular spiral arteries into musculoelastic tissue
→ STAGE 1: Faulty endovascular trophoblastic remodeling dilated, low resistance ↓
→ STAGE 2: Clinical syndrome uteroplacental vessels Impairs placental blood flow
(small caliber vessel with high
Etiology |  resistance to flow)
1) Placental implantation with abnormal trophoblastic invasion of uterine Gene (Polymorphism) Function Affected
vessels MTHFR (C677T) Methylene tetrahydrofolate reductase
2) Immunological maladaptive tolerance between maternal, paternal F5 (Leiden) Factor VLeiden
(placental), and fetal tissues AGT (M235T) Angiotensinogen
a) Because it is more common in primiparas than mutliparas⭐ HLA (Various) Human leukocyte antigens
b) Prior pregnancy with the same partner are “immunized” against NOS3 (Glu 298 Asp) Endothelial nitric oxide
preeclampsia (primipaternity) - new consort have an increased risk⭐ F2 (G20210A) Prothrombin (factor II)
of preeclampsia ACE (I/DatIntron 16) Angiotensin-converting enzyme
3) Maternal maladaptation to cardiovascular or inflammatory changes of CTLA4 Cytotoxic T-lymphocyte-associated protein
LPL Lipoprotein lipase
normal pregnancy
SERPINE1 Serine peptidase inhibitor
4) Genetic factors including inherited predisposing genes and epigenetic
GNA promoter Decreased methylation
influences

Pathogenesis
1) Vasospasm
a) Increased resistance → Hypertension
b) Endothelial cell injury → Interstitial leakage; Blood constituents including platelets and fibrinogen are deposited sub endothelially
c) Diminished blood flow → Ischemia of tissues; Necrosis, hemorrhage, and other end-organ disturbances
2) Endothelial Cell Injury
a) Protein factors are secreted into the maternal circulation and provoke activation and dysfunction of the systemic vascular endothelium
b) Decreased placental perfusion causes endothelial cell damage by
i) inflammatory mediators : cytokines (TNF-a and IL)
ii) antiangiogenic factors
c) These will cause oxidative stress producing free radicals, reactive O2 species, and lipid peroxides
d) Toxic radicals injures and causes endothelial cells to produce less nitric oxide⭐ and may secrete substances that promote coagulation
(prostaglandin balance) and greater sensitivity to vasopressors

3) Increased Pressor Responses

a) Increased sensitivity to angiotensin II
b) Prostaglandin (Imbalance between prostacyclin and thromboxane)
(1) Endothelial prostacyclin (PGI2) production is lower⭐ (decreased vasodilatation)
(2) Thromboxane A2 by platelets is increased⭐ (causes increased
vasoconstriction)
(3) Prostacyclin:thromboxane A2 ratio decreases⭐
(4) What we want is for prostacyclin to be high because it causes dilatation.
c) Nitric oxide⭐
i) Decreased nitric oxide synthase expression
d) Endothelins
i) Potent vasoconstrictor which is increased⭐ in preeclampsia
4) Angiogenic and Antiangiogenic Proteins
a) Placental vasculogenesis is evident by 21 days after conception
i) Imbalance of antiangiogenic and proangiogenic factors
ii) (Antiangiogenic predominance leads to preeclampsia) ⭐

Proangiogenic Antiangiogenic
• Vascular endothelial growth factor (VEGF) • Soluble Fms-like tyrosine kinase 1 (sFlt-1)
• Placental growth factor (PLGF) • Soluble endoglin (sEng)
 Clinical manifestations
● ↑ Cardiac afterload caused by Hypertension
● ↓ Cardiac preload secondary to ↓ diminished volume expansion in pregnancy and ↑ Cardiac preload secondary to ↑ IV
Cardiovascular
crystalloids
● Endothelial activation: extravasation of intravascular fluid into the extracellular space → Pulmonary edema
● Preeclampsia is frequently accompanied by hemolysis
→ Elevated serum LDH, Reduced haptoglobin, Presence of reticulocytosis, spherocytosis, histiocytosis on PBS
● Hemoconcentration: Hallmark of eclampsia | 
Blood volume
→ Vasospasm that follow endothelial activation and leakage of plasma in the interstitial space
and
coagulation
● Thrombocytopenia (<100,000) from increased activation
● Hemolysis (microangiopathic)
● HELLP Syndrome (any one of the ff: partial HELLP. Complete – full HELLP)
→ Hemolysis, Elevated liver enzymes, Low platelets

● Reversible as long as the underlying cause is managed

● ↓ Renal Blood Flow & Glomerular Filtration Rate⭐
→ In normal pregnancy GFR is elevated
● Glomerular capillary endotheliosis
→ Filtration is “blocked” due to the swelling of the glomerular capillary endothelium
Kidneys ● ↑ Serum creatinine (>1.1)
→ Cut of value of 1.1. If more than 1.1, it is already a severe form of eclampsia⭐
● ↑ Uric acid
● Proteinuria – due to decreased absorptive capacity
● Oliguria – due to contraction of intravascular space secondary to vasospasm → renal sodium and water retention
● Acute renal failure or acute kidney injury → results to further kidney insult
● Clinically display 3 manifestations:
→ Pain (epigastric, retrosternal) – severe sign of preeclamspia (end of disease spectrum) ⭐
→ Elevation of liver enzymes (AST, ALT) – markers for severe preeclampsia, HELLP syndrome
→ Hemorrhagic infarction – may extend to form hepatic hematoma
Liver
→ Subcapsular hematoma – rupture; worst case scenario
● Hepatocellular necrosis (manifested as right upper quadrant pain) ⭐ , ischemia, and edema that stretches the Glisson
capsule
● Periportal hemorrhage
● Due to generalized endothelial cell dysfunction
● Headaches, visual symptoms (may be temporary)
Brain
● Convulsions, Intracerebral hemorrhage, Cortical and subcortical petechial hemorrhages, Subcortical edema
● Stroke – give antihypertensives to avoid

● May be transient once underlying causes are addressed

● Scotomata, blurred vision, diplopia
Visual ● Blindness (rare) ; temporary, vision returns within a week but important to still monitor
Changes and a) Amaurosis: Occipital lobe vasogenic edema
Blindness i) Lasting 4 hours to 8 days (may be reversible; rarely cause blindness)
b) Retinal lesions: Ischemia or infarction
c) Retinal detachment: Cause altered vision, usually unilateral
i) Seldom causes total blindness. returns to normal within a week
Uteroplacental
Vasospasm leads to decreased uteroplacental perfusion
perfusion
Other Peripheral edema, pulmonary edema, abruptio placenta

C. SCREENING
1) Maternal Risk factors – screen for risk factors
2) Blood pressure – measure at every encounter
3) Laboratory Tests
a) CBC w PC, Serum creatinine, LFTs
b) Urinary Proteins - Once a diagnosis of preeclampsia is established, testing for proteinuria is no longer useful
i) 24hr Urine total protein – gold standard: 200mg is significant proteinuria
ii) Protein:Creatinine ratio (random urine) – if 24h not available
iii) Dipstick: Protein is ≥ 2 + (30 mg/dL)
4) Assessment of Fetal Status
a) Nonstress test
b) Biophysical profile
c) Ultrasound (AF volume and estimate fetal weight → increased risk of oligohydramnios and fetal growth restriction)
d) Uterine artery⭐ doppler velocimetry (usually done at 23-24 weeks AOG)
i) a notch in early diastole and decreased flow in late diastole at 20-23 weeks should be monitored
5) Biomarkers
a) PAPP-A, Inhibin-A, Activin-A
6) Angiogenic Markers
a) Antiangiogenic factors: sFlt-1 and sEng
b) Angiogenic factors: PLGF and VEGF
c) sFlt-1:PLGF⭐
i) Distinguishing preeclampsia from other hypertensive-proteinuric disorders
ii) Determining whether a woman with signs of preeclampsia requires medical intervention, such as hospitalization or delivery
D. PREVENTION
1) Low dose aspirin⭐
a) Low-dose aspirin (60-150 mg daily) at 2nd and 3rd trimester is the only drug⭐ for which there is proven evidence
b) Low-dose aspirin for preeclampsia prevention at ≥ 12 weeks⭐ of gestation, and ideally prior to 16 weeks
c) MOA: increases productions of prostacyclin over thromboxane which causes inhibition of platelet aggregation and increases
vasodilation
2) Calcium supplementation
a) Low dietary Ca – associated with hypertension
b) Elemental calcium is 1000 mg/day⭐ in pregnant and lactating women
i) Decreases PTH release, decreased INTRACELLULAR Ca, decreased smooth muscle reactivity → vasodilation
3) Investigational
a) Statins
b) Anticoagulation
c) Probably ineffective approaches: Vitamin C, D, E supplement, folic acid or fish oil supplement, nitric oxide donors
E. MANAGEMENT
● Basic Management Objectives
→ Termination of pregnancy with the least possible trauma to the mother and fetus
→ Birth of a healthy newborn that subsequently thrives
→ Complete restoration of health to the mother
Preeclampsia With Severe Features
● Asymptomatic: base on BP, controlled with hypertensive drugs and fetal monitoring
Aggressive Expectant
< 24 weeks Termination of pregnancy to reduce the mother’s ● High neonatal mortality ● Fetal death
risk of developing life-threatening morbidity or death and morbidity due to ● Asphyxial damage in
≥ 24 weeks and < 34 weeks expectant management of selected cases prematurity utero
≥ 34 weeks delivery for ALL women with preeclampsia with ● Prolonged NICU stay ● Increased maternal
severe features ● Long term morbidity
disability/sequalae
Antihypertensive Medications
● Indicated for women with severe hypertension: SBP ≥ 160 mmHg and/or DBP ≥ 110 mmHg) persisting for ≥ 15 minutes
● Treatment initiated within 30-60 mins
● Target BP: ↓ Mean Arterial Pressure by no more than 25% over two hours to achieve target BP of 130-150 mmHg systolic and 80-100 mmHg
diastolic (lower than this may cause uteroplacental insufficency)
→ All hypertensive drugs cross the placenta
■ Beta blocker – Labetalol – FIRST LINE⭐
■ CCB – Oral Nifedipine⭐
■ 2-Adrenergic Agonist – Methyldopa, Vasodilator – Hydralazine, Thiazide diuretics
■ ACEIs, ARBs, and direct renin inhibitors are contraindicated in pregnancy⭐
Initial Management (≥ 24 weeks and < 34 weeks) Continuing expectant management
1. Admission to a Maternal Fetal Unit 1. Hospitalize until delivery
● Transferred to a setting with less intensive care if ALL of the 2. Monitor BP every 4 hrs on waking hours
following are present: 3. Assess maternal symptoms – if present, terminate pregnancy
→ She is asymptomatic, stable, normal or improving ● Headache
laboratories, reassuring fetal status ● Vision changes
2. Administration of a course of antenatal corticosteroids ● Epigastric or abdominal pain
● Betamethasone 2 doses of 12 mg given IM 24 hrs apart OR ● Decreased fetal activity
● Dexamethasone 4 doses of 6 mg given IM 12 hrs apart ● Vaginal bleeding
3. Seizure prophylaxis: Magnesium sulfate (DOC) 4. Continue fluid input and output
● 6 g of a 10% solution IV over 15-20 mins followed by a 2 g/hr as ● Identify oliguria (< 500 mL over 24 hrs)
a continuous infusion ● Serum creatinine and liver chemistries at least 2x weekly
● 5 g of a 50% solution IM into each buttock (total of 10 g) followed → Deteriorating kidney function (rising creatinine to > 1.1
by 5 g IM every 4 hrs mg/dL) and persistent oliguria over 24-48 hrs would
● It is usually continued for 24 hrs postpartum warrant delivery
4. BP monitoring at least every 1-2h 5. Monitor laboratory tests (at least 2x weekly)
5. Fluid intake and urine output monitoring ● Including:
6. Laboratory studies → CBC
● Repeated every 6-12 hrs (to know if px is improving or → Serum creatinine
deteriorating) → Liver chemistries
● Include: CBC with platelet count, Electrolytes, Creatinine. ALT, ● If laboratory abnormalities worsen after an initial improvement,
AST, LDH repeat the tests in 12-24 hrs
● PT, PTT, and fibrinogen are obtained if ALT and AST are > 2x 6. Complete antenatal corticosteroids
ULN, if platelet count < 100,000 cells/μL, or if placental 7. Assess fetal well being
abruption is suspected ● Fetal kick counts and NST: Daily
7. Assessment of fetal well-being ● Ultrasound assessment of AF volume: 1-2x/week
● Nonstress test ● Ultrasound estimation of fetal growth: every 2-3 weeks
● AF volume determination → If the fetus is growth-restricted: weekly Doppler velocimetry
● Estimation of fetal weight of the umbilical artery and ductus venosus
● Umbilical artery and ductus venosus doppler velocimetry if the
fetus is growth restricted⭐
Delivery
Conditions that indicate Termination of Pregnancy
● Goal: 34 weeks AOG
Fetal Maternal Obstetrical
● Vaginal delivery
→ Cervical ripening agents may be used if the ● Hemodynamic instability (shock)
cervix is not favorable prior to induction ● Fetal demise ● Persistent severe hypertension
● CS delivery is reserved for standard obstetric ● Abnormal fetal testing unresponsive to medical therapy
● Placental
● Estimated fetal ● Symptoms of severe disease
indications abruption
weight < 5 th
● Motor deficit or altered sensorium
→ Some experts recommend scheduled CS ● Preterm labor
percentile for AOG ● Pulmonary edema, kidney
delivery for women with preeclampsia with ● PPROM
● Oligohydramnios failure
severe features < 28-30 weeks AOG, especially ● Stroke, MI, Eclampsia
● Fetus with congenital
if they have an unfavorable cervix anomalies ● Laboratory abnormalities
● Anesthesia – Neuraxial is OK, preferred. ● HELLP syndrome
■ Spinal
■ Combined spinal-epidural (CSE)
■ Epidural: risk of epidural hematoma is exceptionally low, in patients with platelet counts 70 x 109/L
Preeclampsia Without Severe Features
● Delivery: 37+0 weeks AOG⭐, even without features of severe disease
● Preterm pregnancies
→ Mother and fetus are stable and have no findings of serious end-organ dysfunction – Expectant management
→ Late Preterm (34+0 to 36+6 weeks): Expectant management until 37+0 weeks AOG
Expectant Management

1. Inpatient vs outpatient care 5. Antihypertensive drugs and BP monitoring

● Hospitalization: establish disease severity and the rate of
progression
● Outpatient care: Cost-effective option for women found to be
stable over a period of several days and with no severe features
of preeclampsia
2. Patient education
● Signs and symptoms of the severe features
● Report if (+) vaginal bleeding, abdominal pain, rupture of
membranes, or regular uterine contractions
● Monitor fetal movements daily
3. Restricted activity (NOT bed rest)
● No heavy lifting, 8 hrs rest/day, Avoid supine sleep position
4. Laboratory follow-up (repeated at least 2x weekly)
● Platelet count, Serum creatinine, Liver enzymes
● Markers for hemolysis
→ Hematocrit: Hemoconcentration
■ Falling hematocrit may be a sign of hemolysis
→ LDH concentration – better marker for hemolysis
→ Haptoglobin – specific marker of hemolysis (< 25 mg/dL)
● BP monitoring: 2x/day at home, 2x/week in the clinic
● For women with SBP ≥ 150 mmHg or DBP ≥ 100 mmHg that
persist for ≥ 15 minutes
● Methyldopa
→ Widely used in pregnant women and its long-term safety for
the fetus has been demonstrated
→ Only a mild antihypertensive agent and has a slow onset of
action (3-6 hrs)
→ Sedative effect at high doses
→ Dose: 250-500 mg PO BID-QID (max 2g/day)
6. Assessment of fetal growth
● Sonography to estimate fetal weight and assess AF volume
for evaluation. If normal, repeat every 3-4 weeks | 
7. Assessment of fetal well-being
● Daily fetal movement counting
● 2x/week NST + assessment of AF volume OR
● 2x/week BPP beginning at the time of diagnosis of
preeclampsia
● Evaluation of umbilical artery⭐ Doppler velocimetry indices
is useful if fetal growth restriction is suspected ⭐
8. Antenatal corticosteroids : When delivery within the next 7 days
is likely and neonatal resuscitation is planned

F. POSTPARTUM
1) Antihypertensives
a) For women with preeclampsia who have taken antihypertensive treatment and have given birth: continue antihypertensive treatment
b) If on methyldopa, switch within 2 days, preferably to CCB
i) Maternal depression⭐ has been reported following methyldopa administration and postpartum women are already at risk for postpartum
depression
2) Analgesia
a) NSAIDs – may increase BP and diminish anti-HTN efficacy (except CCBs)
b) NSAIDs > opioid analgesics
3) Magnesium sulfate
a) Magnesium decreases the frequency of depolarization of smooth muscle by modulating calcium uptake bindingand distribution in smooth muscle
cells.
b) The net result is inhibition of uterine contractions
Table 6. Antihypertensive agents used for urgent BP control in pregnancy
Drug
Labetalol
(FIRST LINE, not available
in the PH)
Hydralazine
(drug usually used to
manage preeclampsia)
Cheap and readily
available, usually used in
government institutions
Nifedipine immediate
release (immediate-
release rapid-acting
formulation)
(second-line drug)
Different formulations:
• 10mg immediate
release
o will bring down
the BP right away
• 20mg intermediate
release
• 30mg slow release
Nifedipine extended
release (extended-
release formulations)
(for maintenance)
Nicardipine (parenteral)
(given if patient is
unresponsive to treatment)
Onset of action Initial dose Follow-up
1-2 mins 20 mg IV gradually Repeat BP measurement at 10-min intervals:
over 2 mins ● If BP remains above target level at 10 mins, give 40 mg IV over 2
or mins
A continuous IV ● If BP remains above target level at 20 mins, give 80 mg IV over 2
infusion of 1-2 mg/min mins
can be used instead of ● If BP remains above target level at 30 mins, give 80 mg IV over 2
intermittent therapy or mins
started after 20 mg IV ● If BP remains above target level at 40 mins, give 80 mg IV over 2
dose mins
Cumulative maximum dose is 300 mg. If target BP is not achieved,
switch to another class of agent
10-20 mins 5 mg IV gradually over Repeat BP measurement at 20-min intervals:
1-2 mins ● If BP remains above target level at 20 mins, give 5 or 10 mg IV
over 2 mins, depending on the initial response
Adequate reduction of ● If BP remains above target level at 40 mins, give 10 mg IV over 2
BP is less predictable mins, depending on the previous response
than with IV labetalol
Cumulative maximum dose is 30 mg. If target BP is not achieved,
switch to another class of agent
5-10 mins 10 mg orally Repeat BP measurement at 20-min intervals:
● If BP remains above target level at 20 mins, give 10 or 20 mg
orally, depending on the initial response
● If BP remains above target at 40 mins, give 10 or 20 mg orally,
depending on the previous response
● If target BP is not achieved, switch to another class of agent
Maximum daily dose of 180 mg
• You have to be careful because the BP might drop quickly
● An intermediate-acting tablet 10 or 20 mg in some countries,
this is known as Nifedipine retard, which has a more delayed
onset and is usually prescribed 2-3x/day as maintenance dose
Within 1 hour 30 mg orally ● If target BP is not achieved in 1-2 hrs, another dose can be
administered
● If target BP is not achieved, switch to another class of agent
Maximum daily dose: 120 mg
Delayed by 5-15 The initial dose is 5 Adjust dose within this range to achieve target BP
mins mg/hr IV by infusion ● Increased to a maximum dose of 15 mg/hr
pump ● Infusion pump or Soluset
→ The release is sustained or controlled
● In general, rapid titration is avoided to minimize risk of
overshooting dose
● Requires use of a programmable infusion pump and continuous
noninvasive monitoring of BP and HR
 POST TERM PREGNANCY AND IUGR
I. POSTTERM PREGNANCY
A. DEFINITION, RISK FACTORS, OUTCOMES
1. Definition
a. Postmature - Reserved for relatively uncommon specific clinical fetal syndrome in which the newborn has recognizable features indicating
a pathologically prolonged pregnancy
b. Post-term⭐ or prolonged - 42 completed weeks (294 days) or more from the first day of LMP
2. Predisposing Factors and Outcomes
a. Fetal factors - the signal which indicates that the pregnancy should already be delivered (or initiates parturition) usually comes from the
baby (problems in CNS -anencephaly or fetal hormone production -adrenal hypoplasia causing dec signals for parturition)
Maternal Risk Factors⭐ Fetal Risk Factors⭐ Adverse Maternal Outcomes⭐ Adverse Perinatal Outcomes⭐
• Nulliparity / Primiparity • Anencephaly • Fetal macrosomia: • Induced labor
• Previous post-term • Adrenal hypoplasia o cesarean delivery • Uteroplacental insufficiency
pregnancy • X-linked placental sulfatase (dystocia and fetal o Stillbirth / perinatal mortality
• BMI > 25 deficiency (⬇ESTROGEN) jeopardy) o Hypoxic-ischemic encephalopathy
• Cervical length at the 3rd or o Male fetus (since X- o shoulder dystocia • Post maturity syndrome
4th quartile at mid pregnancy linked) o postpartum hemorrhage • Meconium aspiration (oligohydramnios)
• Genetic (Maternal only) o perineal laceration • Birth injuries
• Oligohydramnios • Childhood obesity
• Cord compression
• Preeclampsia
3. Increased rates of stillbirth, neonatal death, and infant morbidity
a. Major causes of death: gestational HPN, prolonged labor with CPD, birth injuries, hypoxic-ischemic encephalopathy, diabetes (should be
delivered at 39 weeks)
b. Higher rates of: cerebral palsy, lower IQ scores at age 6.5, NICU admission, neonatal seizures
c. Delivery at 38 weeks – lowest risk for perinatal death

B. Placental Dysfunction and Complications

1. Placental Dysfunction – compromised nutrition and oxygen supply leading to IUGR, oligohydramnios⭐, chronic hypoxia/anoxia
a. Placental Senescence – main problem in post-term pregnancy: as placenta ages, wear and tear → poor function
b. Placental Apoptosis – kisspeptin gene (pro-apoptotic) upregulated in postterm placentas
c. Dysfunctional syncytiotrophoblast – greater risk of the post-maturity syndrome

2. Complications of Placental Dysfunction

a. Postmaturity Syndrome⭐ – due to placental senescence and insufficiency
i. A post-mature newborn: The skin changes of postmaturity are due to loss of the protective effects of vernix caseosa
1. Wrinkled, patchy peeling skin, Skin wrinkling can be particularly prominent on the palms and soles
2. Long, thin body suggesting wasting, nails are long
3. Advanced maturity: Infant is open-eyed, unusually alert, and appears old and worried
b. Fetal distress and oligohydramnios⭐ – physiologic decline of amniotic fluid at 38 weeks
i. Cord compression⭐: decreased AF means decreased cushion to prevent compression of uterine internal surface
and fetal structures
ii. Decelerations secondary to cord compressions
1. Saltatory baseline – Characteristic sawtooth appearance of the fetal heart rate is also associated with cord compression
(specifically in cases with oligohydramnios)
2. Compression is permanent : prolonged decels (most common in post term)⭐
Compression is mild or intermittent : variable decels
Prolonged decel – more than 2 minutes
c. Meconium Aspiration syndrome
i. Mature GI tract or Fetal distress causes release of meconium to reduced AF⭐ → thick, viscous fluid which is worse for physiologic fetal
swallowing of AF as it may lead to an increase degree of pulmonary dysfunction → respiratory distress → neonatal asphyxia and death
ii. Prevention:
1. Amnioinfusion – saline injected into intrauterine cavity to dilute meconium stained AF
a. Has no actual effect on aspiration but increased AF reduces cord compression, which would prevent fetal distress. This
lessens release of meconium.
2. Intrapartum management – For nulliparous woman who is in early labor with thick meconium-stained AF and remote from delivery
(e.g., 6 or 7 cm), strong consideration should be given to prompt CSD⭐ (due to risk of pulmonary dysfunction)
d. Fetal growth restriction - association between intrauterine growth restriction and placental dysfunction, may lead to stillbirth

3. Macrosomia – placenta function WITHOUT AGING: velocity of fetal weight gain peaks at 37 weeks but most continue to gain weight
a. Associated complications:
i. Mother: uterine atony and hemorrhage from overdistention, birth canal lacerations
ii. Baby: shoulder dystocia, clavicular fracture (assisted delivery), brachial plexus injury and Erb’s palsy (excessive traction)
b. No evidence for LABOR INDUCTION in SUSPECED MACROSOMIA
i. Vaginal delivery is not contraindicated for women with estimated fetal weight of up to 5,000 g (in the absence of diabetes)
ii. Do CS for babies > 4,500 g ONLY if prolonged 2nd stage of labor or arrest of descent

MNTM 2022 1
C. MANAGEMENT
1. Correct assessment of AOG⭐
a. Surveillance - Especially for moms who do not know their LMP, do BPS (already includes AFI determination) or twice a week NST
b. The most precise and reproducible method for assessing AOG is fetal biometry by ultrasound in early pregnancy (if you can’t find
ultrasound evidence done during the 1st trimester) - LMP is not reliable in terms of predicting accurate AOG
i. Early UTZ in pregnancy (1st trimester) is the basis for early gestation (if the patient is regularly menstruating),
1st trimester: measure Crown Rump Length (5-7 days error)
ii. AOG sonography computation is most accurate: Error is ± 3 weeks, for 3rd trimester, ± 2 weeks error
c. < 41 weeks
Test Frequency Notes
⭐⭐⭐
1. Not compressed/reassuring: ≥ 10 fetal movements/ 2 hrs or 5 in 1
hour (Dr. Yu, 2023)
Fetal
daily (within 2 hours 2. Any perception of any movement within the abdominal cavity is
movement taken note of
after meals)
counting
3. Decreased FM: Contact obstetrician or go to the hospital to get it
checked ⭐
Biophysical ONLY ONCE 1. To monitor AFI: Be alarmed if + oligo- or anhydramnios
score 2x / week if >42 weeks 2. Take note of estimated fetal weight: IUGR or macrosomia
FW = (FH - N) x 155
Fetal weight Johnson’s Formula i. N = 12 : If head is engaged
ii. N = 11 : If head is unengaged
1. Should be reactive; with each fetal movement, there is FHR
NST 3x a week
acceleration
AFI 2-3x a week NV: 5-25 cm

d. > 41 weeks – we follow the algorithm (determine if complicated on uncomplicated)

2. Complicated vs. Uncomplicated
Uncomplicated
SURVEILLANCE OR DELIVER
1. Fetal surveillance
a. Although not considered mandatory, initiation of surveillance at 41
weeks is a reasonable option
b. Disadvantage: When you choose expectant management, it is
expensive since antenatal surveillance should be done frequently
(Fetal movement counting done daily, NST 3x/ week, AFI 2-3x/week)
2. Internal exam for bishop score and labor induction:
a. Low (<4) - Cervical ripening⭐: If the patient does not want to do labor
induction
i. Membrane sweeping - prostaglandins to be released and
hopefully that would soften and ripen the cervix in a natural way
ii. Prostaglandins – ideal is dinoprostone (PGE2) ⭐
b. >4 – labor induction
i. You can induce labor even with the presence of co-morbids
(chorioamnionitis, HPN, GDM) if the cervical dilation is near 10
cm and with a favorable Bishop score
ii. Evidence for labor induction: No uterine contractions (usually
what is said in quizzes, but still consider the mother and fetus’
presentation and sxs/sx)
iii. When is the patient expected to give birth? Check EDC
iv. Ultimate complication if the baby is not delivered? IUFD
Complicated: hypertension or oligohydramnios or 42 weeks+
DELIVER
1. Complications:
a. Gestational hypertensive disorder and diabetes mellitus – consider
delivery at 38 weeks
b. Prior cesarean delivery
c. Preeclampsia: 37 weeks for preeclampsia WITHOUT severe features
34 weeks for preeclampsia WITH severe features (No reason for
preeclampsia to reach 42 weeks)
d. Oligohydramnios⭐: AFI <5cm or LSVP <2cm
2. Depending on bishop score, cervical ripening or labor induction - No need to
delay further the delivery of the baby
3. In the event of a medical or other obstetrical complication, it is generally not
recommended that a pregnancy is allowed to continue past 42 weeks⭐:
a. At 42 weeks: patient reached 42 weeks but hindi pa rin nagimprove
or wala pa rin contractions → depending on bishop score, CR or LI
already because of increased morbidity and mortality past these
weeks

Cesarean section delivery

● Indications: Non-reactive NST, (+) CST (+)⭐
→ Baby may be sleeping if NST is non-reactive, so try to wake it up with vibroacoustic stimulation
→ The higher the station at the time of labor induction, the higher the rate of CSD: If fetus still floating (Station -3), higher rate of CSD
● Meconium aspiration syndrome is also managed with CS⭐
● Intrapartum management – continuous EFM
● Amniotomy – detect thickly stained AF (aspiration may cause severe pulmonary dysfunction and neonatal death → go for CS already) ⭐
● ACOG – amnioinfusion does not prevent meconium aspiration however it remains reasonable treatment for repetitive variable decels

II. FETAL GROWTH DISORDERS

● Abnormally diminished fetal growth due to placental lesions and infections

A. FETAL GROWTH
1. Fetal growth - Sequential patterns of tissue and organ growth, differentiation and maturation
2. Fetal growth rates – determination of poor growth or totally no growth
a. Rate or velocity of fetal growth can be estimated by serial sonographic anthropometry (BW does not define the rate of fetal growth)
b. Fetal development governed by maternal provision of nutrition while fetal growth potential is determined by the genome
c. Hormones for fetal growth: insulin and IGF-1
i. Excessive glycemia → macrosomia
ii. Excessive transfer of lipids → fetal overgrowth
d. Lipolysis is augmented in pregnancy (FA increased in non-obese women in 3rd trimester)
i. Abnormal accumulation of lipids – placental inflammation and dysfunction
ii. In growth restriction, reversed pattern: amino acid maternal levels > fetal levels
Phases of fetal growth Fetal growth rates⭐
Hyperplasia – rapid increase in cell number First Trimester 35 grams per week 5 g/day
1st 16 weeks
15 weeks
16th to 32nd Hyperplasia and hypertrophy 100 grams per week: Determined by ultrasound 15-20 g/day
≥24 weeks
week
32 weeks Hypertrophy - Most fetal fat and glycogen are accumulated ≥34 weeks 200 grams per week 30-35 g/day

MNTM 2022 2
 III. FETAL GROWTH RESTRICTION
1. Small for gestational age (SGA: Used to describe fetuses with an estimated fetal weight or abdominal
circumference that is less than the 10th percentile for gestational age (small-for-gestation age) : Normal
limits defined by +/-2 standard deviations (< 3 rd /5th percentile) if <10th, need to investigate
a. Constitutional SGA: small father, small mother - Many neonates with birthweights <10th
percentile are NOT pathologically restricted but instead are small simply because of biological
factors (constitutionally small)
b. Growth restricted SGA (FGR): baby did NOT reach its growth potential - There is lag in baby’s
growth
i. Differentiated from constitutional SGA – MONITOR FETAL GROWTH EVERY 2-3
WEEKS
ii. Monitoring on chart, constitutional would have consistent growth with little deviation to
normal curve. In FGR, there is a lag or plateau in growth.
c. Most of the babies with chromosomal abnormalities are SGA
i. Any patient with SGA diagnosis needs congenital anomaly scan
2. Based on gestational age and birthweight should be plotted on the Colorado growth chart : Head and
abdominal circumference
Symmetrical⭐ Asymmetrical⭐
■ Baby is proportionally small ■ Disproportionately lagging abdominal growth
− Small HC and small AC − Normal HC and femur length but small AC⭐
− ALL biometrical parameters are SMALL: BPD, HC, AC, femur − AC is affected
length all small ○ Liver is a major part of the abdomen
■ Insult occurs early⭐ in pregnancy ○ Small baby will have small AC because there is a small reserve in the liver
− Chemical exposure - during the period of organogenesis − HC and femur length are normal
− Viral infection⭐ ■ Brain-sparing⭐: Preferential shunting of oxygen and nutrients to the brain
− Cellular maldevelopment − Instead of normal blood flow to the abdominal organs, blood flow are
■ The timing of the insult is not absolute preferentially sent to the more vital organ, the brain
− The association is just noted because of it being more common ■ Insult occurs late in pregnancy⭐
but not all will present as the same − Placental insufficiency from HPN - Most common
− Meaning, not all early insults (chromosomal) will have − There are also patients with placental insufficiency from HPN that presents
symmetrical IUGR, some may present as asymmetric with symmetrical IUGR
− Diabetes (uncontrolled), preeclampsia
Perinatal risks Long-term sequelae
● Stillbirth : fail to recognize IUGR and you did not do appropriate management early on: fare better if ● Barker Hypothesis : adult metabolic
they are delivered compared to leaving them in-utero syndrome
■ HTN, DM, and other chronic insults can lead to stillbirth ● Suboptimal fetal nutrition is associated with an
● Birth asphyxia ~ placental insufficiency and oligohydramnios increased risk of subsequent adult:
→ If mom undergoes labor, assuming the placenta is not okay and coupling it with contractions, hypertension, atherosclerosis, type 2 DM or
vessels get compressed any glucose intolerance, dyslipidemia
● Meconium aspiration ● Low birthweight: Cardiac structural changes
and dysfunction
● Neonatal hypoglycemia and hypothermia → Admission to NICU because of neonatal comorbidities
(Dr. Ong, 2021) ● Deficient fetal growth → postnatal structural and
functional renal changes
● Abnormal neurological development → placental insufficiency and oligohydramnios
● Also causes long term sequelae of neurologic
→ When there is chronic exposure to hypoxia or anoxia development
→ Developmental milestones are not at par
● Fetal pulmonary maturation is accelerated in pregnancies complicated by growth restriction
→ Fetus responds to a stressed environment by increasing adrenal glucocorticoid secretion leading
to accelerated fetal lung maturation

A. RISK FACTORS and ETIOLOGIES

MATERNAL⭐ PLACENTAL / UTERINE⭐ FETAL

1. Constitutionally small mothers : small uterus and abdominal cavity 1. Placental and cord abnormalities
2. Gestational weight gain and nutrition: maternal weight and nutrition a. Chronic placental abruption,
may be insufficient extensive infarction,
a. Check fundic height in periods of no weight gain. If low weigh chorioangioma, placenta previa,
gain and fundic height – probable IUGR and umbilical artery thrombosis
b. Social issues: smoking, alcohol, substance use may affect b. Marginal or velamentous cord
maternal weight gain insertion (common) - Not the ideal
3. Chronic hypoxia, anemia insertion or placement of the cord
a. Pre-eclampsia, chronic hypertension, asthma, smoking, living 2. Uterine malformations – limiting the
in high altitude space
b. Anemia – more commonly associated with sickle cell diseases
and other inherited anemias
1. Drugs with teratogenic and fetal effects
2. Infections – Rubella and CMV > TB,
syphilis, Toxoplasma, malaria
3. Chromosomal aneuploidies
a. Trisomy 18, trisomy 21, Turner
syndrome, and confined placental
mosaicism
b. Turner syndrome and Down syndrome
– most commonly identifiable
chromosomal abnormalities associated
with IUGR

3. Vascular and renal disease: HPN, DM, SLE, APAS, chronic renal insufficiency, 5. Multiple fetuses – limited space and placental sharing
nephropathies (non-placental sharing – different growth for each baby)
a. Especially when complicated by superimposed preeclampsia
b. Compromised diameter of blood vessels (specifically the placental
vessels) may compromise fetoplacental blood flow
4. Antiphospholipid antibody syndrome – placental thrombosis compromises uteroplacental
blood flow
6. Pregestational diabetes
a. Primary effect is fetal overgrowth, low prevalence of serious vascular disease
i. Uncontrolled DM – compromised blood vessels – uteroplacental insufficiency
b. Pregestational > gestational DM - congenital malformations (highly assoc. with IUGR)
i. Congenital malformations : more severe the malformation, the more likely the fetus to be SGA

MNTM 2022 3
B. RECOGNITION OF FETAL GROWTH RESTRICTION
● Definitive diagnosis frequently cannot be made until delivery - When we have the actual weight of the baby
Low-Risk Women Women With Risks (HPN, DM or history of IUGR)
● Early establishment of accurate gestation age (1st trimester UTZ) ● An initial sonographic measurement at 16 to 20 weeks
→ Fetal biometry: BPD, HC, AC to get estimated fetal weight → Early if necessary
→ AC most important to monitor growth. Repeated every 2-3 weeks ● Followed by an examination at 32 to 34 weeks
● Ascertainment of maternal weight gain (1 lb/wk during the 2nd & 3rd trimester) → Or when otherwise clinically indicated
● Careful measurement of uterine fundal growth → @ 32-34 weeks because there is already expected significant fetal growth
→ Between 18 and 30 weeks’ gestation: weeks = FH ± 2 cm rate at 200 grams/ week due to hypertrophy.
■ (+) Linear correlation: 18 weeks AOG = 18 cm fundic height ± 2 cm ● UTZ evaluation is done together with the examinations for low risk women.
→ Serial measurement of FH can be used as a screening method to detect IUGR
■ Imprecise and dependent on examiner
Sonographic measurement of fetal size
● The most common method for identifying poor fetal growth is estimation of
Pre-Pregnancy Weight Gain in weight using multiple fetal biometric measurements
Recommended Range
Weight BMI
of Total Weight (lbs)
Trimesters 2 ● Combines head, abdomen, and femur dimensions
Category and 3 (lbs/week)
→ Femur length measurement
Underweight < 18.5 28 – 40 lbs 1 (1.0 – 1.3) ■ Technically the easiest and most reproducible
Normal Weight 18.5 – 24.9 25 - 35 1 (0.8 – 1.0) → Abdominal circumference
Overweight 25 – 29.9 15 - 25 0.6 (0.5 – 0.7) ■ Most frequently abnormal with fetal growth restriction
Obese ≥ 30 11 -20 0.5 (0.4 – 0.6) ■ Because soft tissue predominates in this dimension
● Managing IUGR with no other complications but only lagging of growth
Other parameters for recognition of FGR:
● Amniotic fluid volume measurement ● Umbilical Artery Doppler Velocimetry⭐
→ Oligohydramnios → Recommended in the management of fetal-growth restriction as an adjunct
■ Chronic uteroplacental insufficiency to standard surveillance techniques such as NST and BPS
→ Reflection of uteroplacental blood flow → Can be used to predict IUGR, at 23-24 weeks
● Early changes in placenta based growth are detected in peripheral vessels such as → Characterized by absent or reversed end-diastolic flow
UmA and MCA ■ Treatment: Deliver the baby immediately
● Ductus venosus – with IUGR and cardiac decompensation
● Uterine Artery Doppler – surveillance of fetuses already diagnosed IUGR⭐
C. MANAGEMENT
● There is no evidence that diminished activity and bed rest results in accelerated growth or improved outcomes
● Nutrient supplementation (specifically amino acids), attempts at plasma volume expansion, oxygen therapy, heparin, and aspirin have all been shown
to be ineffective
< 24 weeks 24 to <34 weeks 34 weeks to <38 weeks ≥38 weeks⭐
• Repeat UTS every 3 to 4 • Continue pregnancy: fetal growth and • Same as 24 to 34 weeks • No more antenatal surveillance
weeks until you reach 24 surveillance are normal except no more steroids since you will deliver already! ⭐
weeks • Corticosteroids⭐: since we don’t know when • Deliver if: (In addition to o Vaginal delivery – reassuring
• Presence of maternal the baby will be delivered indications in 24-34 weeks) FHR, usually via labor
indication like severe • Antenatal surveillance: ⭐ o Clinically significant induction
uncontrolled HTN – need to o NST – daily oligohydramnios o CS – abnormal FHR, cannot
deliver prior to 24 weeks (The o BPS with Doppler – weekly tolerate vaginal delivery
priority during the stage o Fetal growth monitoring by UTZ –
where viability is still every 3-4 weeks
unfavorable, would be the • Delivery if:
mother) o Non-reassuring fetal tracing
o Oligohydramnios
o Reversed end-diastolic flow⭐
o Maternal and obstetrical indications for delivery
D. PREVENTION
1. Ideally begins before conception:
a. Optimization of maternal medical conditions: Controlling poor medical conditions
b. Medications
c. Nutrition : Advice on starting to eat right
2. Accurate dating is essential during early pregnancy
3. Prophylaxis: Low-dose aspirin (80 mg/day)
a. If there is a risk factor, particularly associated with hypertension, then we can give low dose aspirin
b. Not recommended: Previous history of IUGR
c. Current recommendation: 150 mg/day
i. Note: We’ll follow the book that recommends 80 mg/day
4. Limit physical activities when suspecting IUGR to not compromise available oxygen for the baby
a. Ensure flow from mom to placenta is unimpeded by asking them to do left lateral decubitus
IV. FETAL OVERGROWTH
1. Diagnosis: Risk Factors Maternal and Perinatal Morbidity
a. May use fundic height and ultrasound ● Obesity ● Higher CS rates
b. Clinical fetal weight estimates are just accurate as sonographic ones ● Diabetes ● Traumatic neonatal morbidity
i. Inaccuracy in clinical estimates of fetal weight by PE is often ● Postterm → Shoulder dystocia
attributable to maternal obesity
● Multiparity ● Dystocia
ii. Sonographic estimation of fetal weight is less reliable in predicting the
● Large size of parents ● Postpartum hemorrhage
weight of large fetuses
● Advancing maternal age ● Perineal lacerations
2. Macrosomia cannot be definitively diagnosed until delivery
● Previous macrosomic infant ● Maternal infections
a. Actual weight must be determined
b. Fetal weight: > 90th percentile ● Racial and ethnic factors
c. Birthweight: > 4,500 g or 4.5 kilos

MNTM 2022 4
 3. Management
a. Fetal growth monitoring upto 39 weeks
a. Prophylactic labor induction or delivery before 39 weeks’ gestation is not recommended (ACOG, 2017)
i. At 39 weeks, we can consider labor induction depending on the Bishop score
ii. To obviate further fetal growth and reduce potential delivery complications
b. Elective CS
i. Acceptable when estimated fetal weight is:
1. Without diabetes: > 5,000 g or 5 kilos
2. With diabetes: > 4,500 g or 4.5 kilos
b. When the macrosomia and shoulder dystocia (can result to persistent brachial plexus injury) are major concerns
c. If the patient has DM, aim to control the blood sugar as well
d. Control maternal weight gain during pregnancy

V. SAMPLE CASES
Case 1 → Notice that the weight gain from 23-24 weeks to 27-28 weeks is only 0.5 lbs
AF, 21 year old G1P0, 29 weeks, mall, employee, married from Pasig, came for per week (2lbs in one month)
routine prenatal checkup. → Normally at this AOG, 1 lb per week weight gain is normal
(-) danger signs of pregnancy ● What is the diagnosis at this point?
With good fetal movements
→ G1P0, 29 weeks, with bronchial asthma, to consider IUGR
ROS: unremarkable
PMHx: (+) asthma – last attack 6 months ago (1-2x/year); (-) HPN, DM ● What are the plans?
PSHx: Smoker – 7 pack years; 1 stick per day during pregnancy → No indication for immediate delivery
Sexual Hx: Coitarche 18 years old; 2 partners; No FP method → Give corticosteroids, continue with antepartum surveillance
FH: (+) asthma – sister ■ Doppler, NST, AFI checking every week
PE: ■ Check fetal weight gain every 2 weeks
BP 100/70, PR 89, RR 19, T36.7
Prepregnant weight 127 lbs; current weight 126 lbs, Ht 1.6 meters; BMI – 22; FH Case 2
– 26 cm; FHR – 145/min; LM1 breech, LM2 FB, L; LM3 cephalic; No UCs
A 42 year old G3P2 (1-1-0-2) 29-30 week gestation came in for prenatal check
PNCU:
up
1st PNCU (8-9 weeks): unremarkable; BP 110/70. Weight 120 lbs
Present medical hx: (+) chronic hypertension on Methyldopa 250 mg TID.
→ CBC, urinalysis, FBS, HbsAg, VDRL -> normal; BT: O+ VS: BP – 130/80; PR – 79/min, RR- 21/min, T – 36.5 deg C; HT – 5’2”; Wt –
→ TVS: SLIUP 8 weeks 4 days; Normal ovaries 120 lbs; FH – 26 cm. FHR -150 bpm
→ Given folic acid for 2 months then shifted to prenatal MVP thereafter
→ Given FeSO4 starting 16 weeks Salient features
Subsequent PNCUs unremarkable except during the 23rd to 28th week → Chronic hypertension
→ Poor maternal weight gain → FH is 26 cm – suspect IUGR
→ 23-24 weeks 133 lbs; FH 21 cm
■ OGTT normal Diagnosis
→ 27-28 weeks 135 lbs; FH 24 cm → G3P2 (1-1-0-2)(pregnancy uterine?) 29-30 weeks AOG with controlled
chronic hypertension to consider IUGR
■ Advised to have an ultrasound done
■ TCB as soon as results are available What will be the appropriate management?
th
BPS: SLIUP of about 27 to 28 weeks, cephalic BPS 8/8; SWFW 10 percentile;
→ Ultrasound, Biophysical profile (fetal aging, weight, placental location),
antenatal surveillance (fetal movement, NST, doppler)
AFI 12.6 cm; normal doppler studies
● Salient features What is the management when doppler is normal and NST is reactive?
→ Asthma → Continue monitoring, and control maternal hypertension
→ Poor fetal weight gain
→ Smoker What if ultrasound shows 1600 g then repeat after 2 weeks, what do you expect
→ Fundic height is 26 cm (normal: 29 cm =/- 2cm) the weight?
● What is the normal weight gain during pregnancy? → 100 grams per week appropriate weight gain per week
→ At least minimum of 1800 g is what you expect after 2 weeks

MNTM 2022 5
 I. MULTIFETAL PREGNANCY
1. Uncommon and rare - higher rates of preterm birth, congenital
anomalies, hemorrhage, and peripartum hysterectomy Type of Pregnancy Incidence
2. As the number of fetus increases, there is an exponential Twins 1:80
logarithmic decrease in incidence Triplets 1:802
3. Females > Males
a. Female twins tend to survive better Quadruplets 1:803
b. Fertilized ovum (if its female) tends to split/divide
more

A. TYPES OF MULTIPLE PREGNANCY

Types of Multiple Pregnancy
Monozygotic/Identical Dizygotic/Fraternal
From a single fertilized ovum (1 sperm cell + 1 egg cell) that divides From fertilization of two separate ova (2 sperm cells + 2 egg cells) ⭐
Same Placentas Separate placentas, 2 different genders⭐
Incidence is dependent on race, heredity, maternal age, parity, and especially, fertility
Incidence is generally independent of race, heredity, age, and parity
treatment
(one exception is that zygotic splitting is increased following ART) ⭐
More common than monozygous splitting
Types of Monozygotic Twins Factors Affecting Dizygotic Twinning
Diamnionic Monoamnionic → Race : highest in African-American women
● Diamnionic, Dichorionic ● Monoamnionic, Monochorionic → Maternal age
→ Zygotes divide within the first 3 → Division occurring 8-12 days ■ peaks after 37 years of age; increases with advancing maternal age (due to
days (72 hours) after after fertilization use of Assisted Reproductive Techniques)
fertilization → Results in two embryos within ■ Can be an independent risk factor
→ Two embryos, two amnions, a common amniotic sac → Maternal nutrition - Bigger women (taller, built on a heavier side) are more prone
and two chorions develop → Most number of complications to having twins
→ Two distinct placentas or a ● Conjoined twins → Parity - 20-fold increase if parity ≥ 5
single fused placenta → Result if twinning is initiated → Heredity : Maternal > paternal side history of twinning
● Diamnionic, Monochorionic later (> 13 days) → Infertility therapy – increased follicles from FSH and ovulation induction drugs
→ If division occurs between the → Incomplete division of ■ Pituitary Gonadotropin (FSH levels (increased FSH, inducing ovulation)
4th and 8th day embryonic disk ■ higher rate - conceive within 1 month after stopping oral contraceptives
→ Two sacs, one placenta
■ sudden greater than normal release of pituitary gonadotropin in the first
spontaneous cycle after stopping OCPs
Type of Monozygous Twins Genesis / Time of Division⭐
Diamnionic, Dichorionic 3 days
■ Advanced maternal age – exaggerated pituitary release of FSH in response to
decreased negative feedback from impending ovarian failure
Diamnionic, Monochorionic 4-8 days
Monoamnionic, Monochorionic 8-12 days ■ Monozygotic twinning is unaffected by the above-listed factors
Conjoined >13 days → Only affected by infertility/ART therapy (uses ovulation- inducing drugs)
■ In general with in vitro fertilization (IVF), the greater the number of embryos
that are transferred, the greater the risk of twins and other multifetal gestations

Dichorionic Division at this early stage creates two chorions and two amnions
0 to 4 days
diamnionic (dichorionic, diamnionic). Placentas may be separated or fused

formation of blastocyst with two separate embryoblast (inner cell

monochorionic
4 to 8 days masses). Each embryoblast will form its own amnion within a shared
diamnionic
chorion (monochorionic , diamnionic).

the amnion and amnionic cavity form above the germinal disc.
8 and 12 Monochorionic
Embryonic division leads to two embryos with a shared amnion and
days monoamnionic
shared chorion

One describes an incomplete splitting of one embryo into two. The

>13 days Conjoined other describes fusion of a portion of one embryo from a monozygotic
pair onto the other.

Rates of Twin-Specific Complications in Percent

Fetal-Growth Placental Vascular Perinatal
Type of Twinning Twins Preterm Delivery
Restriction Anastomosis Morbidity
Dizygotic 80 25 40 0 10-12
Monozygotic 20 40 50 15-18
Diamnionic/ dichorionic 6-7 30 40 0 18-20
Diamnionic/ monochorionic 13-14 50 60 100 30-40
Monoamnionic/ monochorionic <1 40 60-70 80-90 58-60
Conjoined 0.002 to 0.008 – 70-80 100 70-90

Dizygotic twinning has higher incidence and lower complications. However, as you progress from a diamnionic/dichorionic monozygotic pregnancy to
conjoined twins, you would see the rate of perinatal mortality would actually increase
→ If you would also notice in monochorionic type of twin pregnancies, the problem would be the occurrence of placental vascular anastomosis
→ Perinatal mortality is highest among conjoined twins
→ There is a high risk of preterm delivery on all types of twinning
→ You won’t be able to tell the chorionicity or zygocity during pregnancy. You will only know afterwards.

MNTM 2022 1
 II. DIAGNOSIS OF MULTIPLE FETUSES
Signs Symptoms
1. Anemia is more pronounced - Higher iron and folate requirements predispose to anemia 1. Minor symptoms of pregnancy are often exaggerated (because of
2. Edema (leg swelling), varicosities, hemorrhoids (secondary to enlarged uterus higher β-hCG levels due to larger placenta) – hyperemesis
3. Abnormal weight gain gravidarum⭐
a. Faster and more than expected a. Nausea and vomiting in early months due to elevated β-
b. Normal: 1 lb/wk during the 2nd and 3rd trimester hCG levels, can be prolonged but hormones would usually
4. Fundic height > AOG - Most obvious decrease by the second trimester
a. Fundic height – approximates AOG by 20th w with ±2 weeks margin, upto 36w 2. Cardio-respiratory embarrassment
b. The uterus and its non-fetal contents may achieve a volume of 10L or more and a. Cardiac output was increased another 20 percent above
weigh more than 20 pounds than in women with a singleton pregnancy
c. Typically, between 16-32 weeks, there is a linear correlation between fundic height b. Increased dyspnea of pregnancy and change in cardiac
and age of gestation output due to enlarged uterus
d. In multifetal pregnancies, between 20 and 30 weeks, fundic heights averaged c. Cardiac changes: Hypervolemia, decreased vascular
approximately 5 cm greater than expected for singletons of the same fetal age resistance, increased cardiac output compared to singleton
5. Leopold’s Maneuver or palpation of 2 separate heads or > 2 fetal poles pregnancies
6. Auscultation: 2 FHRs with difference of at least 10 beats on 2 sides of the uterus, at 3. Excessive fetal movements
least 6 inches away
7. Excessive amounts of amniotic fluid may rapidly accumulate

1. In women with a uterus that appears large for gestational age, the following should be considered:
a. Multiple fetuses
b. Elevation of the uterus by a distended bladder (empty before measurement)
c. Inaccurate menstrual history – (Make sure px recalls LMP correctly and is regular (if irregular: UTZ on first trimester)
d. Hydramnios
e. Hydatidiform mole
f. Uterine leiomyomas
g. A closely attached adnexal mass
h. Fetal macrosomia (late pregnancy)
2. Radiography and MRI
a. Abdominal radiography can be used if fetal number in a higher-order multifetal gestation is uncertain
i. May lead to an incorrect diagnosis if there is hydramnios, obesity, fetal movement during the exposure, or inappropriate
exposure time
ii. Fetal skeletons before 18 weeks’ gestation are insufficiently radio-opaque and may be poorly seen
b. MRI may help delineate complications in monochorionic twins
c. These tests are not often requested. The availability and skilled sonologists has made detection of multifetal pregnancies easier in
practice
3. ⭐Sonography - Separate gestational sacs (confirmation as early as 10 weeks)
a. Two fetal heads or two abdomens should be seen in the same image plane
b. Note that when reporting results, report chorionicity first before the amnionicity.
i. Amnion – sac
ii. Chorion – placenta

CHORIONICITY (Best: 10-14 wks) Monochorionic Dichorionic

Dividing Chorion (If 1 or 2 placentas) Thin Thick

• Determination of chorionicity is most accurate

during the first trimester

Weeks best for ultrasound: ⭐

• Best time for chorionicity (10-14 wks)
• Best for aging (7-8 weeks)
• Detecting congenital abnormalities (22-24 wks)
• Assessing fetal growth, amniotic fluid (26-28 wks)

• After 10-14 weeks, sonographic assessment of

chorionicity may be determined using four features:
1. Number of placental masses
2. Thickness of the membrane dividing the
sacs
3. Presence of an intervening membrane
4. Fetal gender
• T sign
• Thin dividing membrane (< 2 mm)
• May not be seen until the second
trimester and magnification reveals only
two layers
• Right-angle relationship between the
membranes and placenta and lack of
apparent extension of placenta between
the dividing membranes
• Twin peak/Lambda sign
• Thick dividing membrane (≥2 mm)
• 2 different genders
• 2 different placental implantation
• Seen by examining the point of origin of the
dividing membrane on the placental surface
• Appears as a triangular projection of
placental tissue extending a short distance
between the layers of the dividing
membrane
• Best seen between 10th to 14th week since
it disappears after the 20th week

MNTM 2022 2
 III. COMPLICATIONS ASSOCIATED WITH MULTIPLE PREGNANCY
Pregnancy complications
● Spontaneous abortion (1st trimester)
→ Monochorionic placentation was more common in multiple gestations
ending in miscarriage than in those resulting in a livebirth
● Bleeding: Uterine overdistention → atony → postpartum hemorrhage
● Maternal hemodynamic changes → 20% higher cardiac output and 10-
20% greater increase in plasma volume than women with singleton
pregnancy
→ Increases risk of pulmonary adema
● Hypertension, preeclampsia post 20 weeks⭐
→ Fetal number and placental mass are involved in preeclampsia
pathogenesis (due to trophoblast proliferation), earlier and more
severe HTN
● Preterm birth⭐
→ Duration of gestation decreases with increasing fetal number, due to
overdistension
● Long-term infant development: Same cognitive outcomes in singletons
and twins
→ Normal-birthweight neonates: cerebral palsy risk is higher among
twins and higher-order multiple pregnancies.
→ Thought to be related to an increased risk of fetal growth restriction,
congenital anomalies, twin-to-twin transfusion syndrome, and fetal
demise of a co-twin
● Prolonged pregnancy: Twin pregnancy of 40+ wks should be considered
post-term
● Frequency of PPROM increases with increasing plurality (causes
distention of the sac making it thinner)
B. UNIQUE FETAL COMPLICATIONS
Fetal complications
● Monoamnionic Twins
→ Cord Entanglement⭐ most common, more common in early part
■ Diagnose by color flow doppler (overlapping or crossing of the cord, may
compromise blood flow)
■ Monitoring is severely ineffective (can develop in a day)
■ Deliver immediately
→ Twin-twin Transfusion Syndrome monoamnionic < diamnionic
→ Preterm Birth
→ Congenital Anomalies
● Aberrant Twinning Mechanisms (uncommon)
→ Conjoined Twins - Survival depends on whether each twin has their own internal
organs
→ External Parasitic Twins
→ Fetus-in-fetu
● Monochorionic Twins and Vascular Anastomoses
→ Conditions that may arise from chronic feto-fetal transfusion:
■ Twin-twin Transfusion Syndrome (TTTS)
■ Twin Anemia Polycythemia Sequence (TAPS)
■ Twin-reversed Arterial Perfusion (TRAP) Sequence a.k.a. acardiac twinning
● Complete H mole with co-existing fetus
● Congenital malformations : correlates with increased availability of ART and the drugs
used for ART
→ sharing of genetic material and having not enough room for growth
● Low birthweight: ⭐ Due to restricted fetal growth and preterm delivery⭐
→ degree of growth restriction increases with fetal number, mono > di

1. Recommended Management for monoamniotic twin complications

a. 1 hour of daily FHR monitoring, beginning at 26 to 28 weeks
b. Betamethasone is given to promote pulmonary maturation at 26-28 weeks
i. If at risk for preterm labor
ii. Supported by an ultrasound finding of a short cervix or a cervical length of < 2.5 cm
c. If fetal testing remains reassuring, cesarean delivery is performed at 34 weeks after a second course
of betamethasone is given.
i. Rescue dose can be given if it’s more than 2 weeks since the last dose and if the baby is less than 34 weeks AOG
2. Monochorionic twins and vascular anastomoses
a. Number, size, and direction of anastomoses seemingly haphazard connections vary markedly
b. Can arise when monozygotic twinning results in two amnionic sacs and a common surrounding chorion
c. Anastomoses:
i. AA and VV anastomoses are on the surface of the placenta and usually have bidirectional flow
ii. AV anastomoses are typically deep within the placenta and are at least partially responsible for unbalanced transfer of fluid
volume to the recipient twin because they are unidirectional → TTTS
1. Surviving twin with a heart experiences heart failure since it also supports the twin with no heart
2. These deep arteriovenous anastomoses create a common villous compartment or “third circulation” that has been
identified in approximately half of monochorionic twin placentas
C. TWIN-TWIN TRANSFUSION SYNDROME
1. 15-20% of monomorphic pregnancies
Donor⭐ Recipient⭐
2. Higher risk among patients with monochorionic type of placentation
Anemic Polycythemic
(sharing one placenta)
Pale Plethoric
3. Also called Stuck Twin or Polyhydramnios-Oligohydramnios
Growth Restricted Severe hyperbilirubinemia and kernicterus
Syndrome (Poly-Oli) Oliguric Occlusive thrombosis
4. Pathophysiology Oligohydramnios Hydrops
a. Results from unidirectional flow through AV anastomoses • Contractures Hydramnios
(essential part) • Pulmonary Hypoplasia PROM
b. Clinically important TTTS frequently is chronic and results Heart Failure
from significant vascular volume differences between the twins
(typically presents in mid-pregnancy)
c. There is a donor twin and recipient twin
5. Anemia-polycythemia can also happen in TAPS (Twin Anemia Polycythemia Sequence)
i. TTTS: Anastomosis is central in location (big vessels involved)
1. Discordancy is worse such that there’s difference already in amniotic fluid
ii. TAPS: Anastomosis in periphery (small vessels) that’s why manifestation is milder
compared to TTTS
1. Presence of anemia and polycythemia ONLY
6. Diagnosis is based on two criteria:
a. Presence of a monochorionic, diamnionic pregnancy⭐ AND
b. Hydramnios defined if the largest vertical pocket is > 8cm in one twin and Oligohydramnios
defined if the largest vertical pocket is < 2cm in the other twin
7. Serial fetal biometry: From 16 weeks until delivery, monochorionic twin pregnancies should be screened for TTTS every 2 weeks
a. Every 1 or 2 weeks upon diagnosis or discrepancy of fetal weight between twins
b. Note that at 16 weeks you won’t be able to appreciate TTTS yet, despite this being the recommendations of ACOG as seen in Williams.
In our setting, we do it at 24 weeks.- Doc Santiago.
8. Prognosis - Higher stage, lower AOG = poor prognosis
a. If TTTS is left untreated, mortality is 80-100% in severe cases

MNTM 2022 3
9. Management
a. Laser ablation of vascular anastomoses (fetoscopic laser photocoagulation)
i. Best and definite management
ii. Preferred for severe TTTS (Stages II-IV)
iii. Patients with TTTS before 26 weeks AOG should be referred to a center for fetal intervention for FLP
b. Ultrasound-guided serial amnioreduction - palliative
i. Needle drainage of excess fluid
ii. Address polyhydramnios of one sac and reduce it to normal levels
iii. Prevents preterm labor which may result from polyhydramnios
iv. May have a role in TTTS identified too late for fetoscopic laser treatment
c. Septostomy - palliative
i. Intentional creation of a communication in the dividing amnionic membrane
d. Selective Reduction/Feticide
i. Done in other countries but not an acceptable option in our setting for ethical reasons
10. Death of one twin
a. The demise of one twin puts the surviving twin at risk for death (15%) and significant neurologic morbidity (26%)
b. However, once the death of one twin is identified, immediate delivery of the surviving twin has not been shown to improve outcomes
i. Surviving twin usually has problems of its own, hence early delivery does not show significant improvement

IV. DISCORDANT GROWTH OF TWIN FETUSES

1. Monochorionic twins have greater rates of discordant growth than dichorionic twins (A SIGNIFICANT difference in the size and weight between the
two fetuses that would probably compromise the smaller of the twin.)
2. Pathogenesis:
a. Monochorionic: unequal placental sharing
b. Dichorionic: different genetic growth potential (one placenta has suboptimal implantation site – better blood supply above)
3. Diagnosis: sonography (fetal biometry to compute estimated fetal weight)
𝑊𝑡. 𝑜𝑓 𝑙𝑎𝑟𝑔𝑒𝑟 𝑡𝑤𝑖𝑛 − 𝑊𝑡. 𝑜𝑓 𝑠𝑚𝑎𝑙𝑙𝑒𝑟 𝑡𝑤𝑖𝑛
% Discordancy 𝑋 100 (+) discordance if fetal weight difference is ≥ 20%
𝑊𝑡. 𝑜𝑓 𝑙𝑎𝑟𝑔𝑒𝑟 𝑡𝑤𝑖𝑛
Abdominal circumference⭐ AC = AC of larger twin – AC of smaller twin (+) discordance if the AC measurements differ ≥ 20mm
*Either parameters above would suffice but fetal weight is the basis in most cases (almost always reported in utz requests—easily accessible parameter)
4. Management
a. Serial sonographic monitoring of growth within twin pair and calculating discordancy has become a mainstay in management
i. Monochorionic: Every 2-4 weeks
ii. Dichorionic: Every 4-6 weeks
b. Antepartum testing should be performed in multifetal gestations for the same indications as in singleton fetuses (NST, BPS, Doppler)
c. Royal College of Obstetrics and Gynecology (RCOG)
i. Advocates timing of delivery for:
1. Monochorionic twins at 37 weeks
2. Dichorionic twins at 38 weeks

V. PRENATAL CARE AND ANTERPARTUM MANAGEMENT

1. Goals: prevent preterm delivery and close perinatal follow up of high risk pregnancies
2. Diet: 37- to 54-lb weight gain for women with a normal BMI
a. The daily recommended increased caloric intake for women with twins is 40 to 45 kcal/kg/day
i. Composed of 20% protein, 40% carbohydrate, and 40% fat divided into three meals and three snacks daily
ii. 300 kcal/d more than in singleton pregnancy
b. Increased requirements for calories, protein, minerals, and vitamins
c. Take iron (60 to 100 mg) and folate (300 ug) after the 12th week of gestation
3. Serial sonographic examinations to monitor fetal growth or discordancy
a. Routine fetal anomaly ultrasound at 18-20 weeks | 🗐
i. Dr. Mallen’s lecture: Congenital anomaly scan is done between 22-24 weeks
ii. Congenital malformation in 4.9% of cases
b. Assessment of amniotic fluid volume
i. SVP more commonly used than AFI
1. Oligohydramnios: SVP < 2 cm
2. Hydramnios: SVP ≥ 8 cm
c. NST, BPS, Doppler (as necessary, especially if there is growth discordancy)
VI. PRETERM BIRTH
1. Complicates 50% of twin pregnancies, 75% of triplets, and 90% of quadruplets
2. Predictors of preterm birth:
a. Cervical length < 25 mm at 24 weeks AOG - Routine to check for cervical length ⭐
b. Elevated fetal fibronectin level at 28 weeks AOG
3. Prevention: Most schemes have been ineffective
a. Bed rest, prophylactic tocolytics
b. Progesterone therapy (micronized progesterone)
i. Recommended for prevention of preterm labor only among those with short cervix (only < 2.5 cm)
ii. If normal cervical length in a twin pregnancy, do not give
c. Prophylactic cerclage, pessary
4. Treatment
a. Tocolytic therapy in women with a multifetal pregnancy entails higher risk than in singleton pregnancy
i. Because of the augmented pregnancy-induced hypervolemia and its increased cardiac demands and susceptibility to
iatrogenic pulmonary edema
b. Bed rest, Antenatal corticosteroids
i. Especially if you’re considering that pregnancy might be delivered soon and it’s between 24-34 weeks
ii. Guidelines for use similar to singleton pregnancies

MNTM 2022 4
 VII. LABOR AND DELIVERY

ROUTE OF DELIVERY
Cephalic-Cephalic Mono-chorionic, mono-amniotic
Cephalic-Non-cephalic presentation Breech
presentation pregnancy
• Cesarean delivery of both twins • Only type of twin pregnancy that would
• Most obstetricians
• Vaginal delivery with intrapartum external cephalic version of the warrant outright indication for CS
perform CS (uniquely multifetal indication for CS)
second twin or breech extraction of second twin (faster)
o Multigravids: high success rate for ECV (external Locked twins • Even if presentation is cephalic-cephalic
cephalic version) because abdomen is lax already • CS at 34 weeks (Williams) because
o Vaginal breech extraction: usually partial breech cord entanglement⭐ can be a problem
Delivery can usually
extraction (spontaneously deliver until umbilicus) • Usually occurs with a during labor
be accomplished breech-cephalic
spontaneously
o Non-cephalic Twin B: consider VD if term (late pre-term • Rupture of membrane during labor
would have bigger heads, more difficult) presentation
can predispose to cord entanglement
(vaginal delivery) ⭐
▪ • The chin of the 1st twin
or with forceps
Internal podalic version of Twin B • Deliver at a time when fetus already has
o Early pre-term (29-30 weeks): No problem in vaginal locks between the neck
mature lungs and labor has not yet set
delivery because a small baby is expected and chin of the second
in (chance for cord entanglement is less)
• cephalic-presenting co-
Least desirable: Vaginal delivery of the first but cesarean • Higher order multiple pregnancy (3 or
delivery of the second twin twin
more fetuses) – CS routine
o May be required due to intrapartum complications such as • CS should be
• Conjoined – CS routine
umbilical cord prolapse, placental abruption, contracting considered
• Unique complications – CS routine
cervix, and fetal distress
Timing of delivery Increased Rates of:
Type Timing of delivery⭐ → Uterine contractile dysfunction: Prepare oxytocin or uterotonics
Uncomplicated dichorionic⭐ 38 weeks → Abnormal fetal presentation
Uncomplicated monochorionic, → Umbilical cord prolapse
34-37 weeks → Placenta previa
diamnionic
34 weeks (32-24 weeks), delivery → Placental abruption
Monochorionic, monoamnionic
by CS ■ Once the first twin is delivered, uterus might contract already (Intertwin
delivery time should be < 30 mins )
Post-term 40 weeks or more → Emergent operative delivery
→ Postpartum hemorrhage from uterine atony
VIII. CONJOINED TWINS

1. A targeted examination, including a careful evaluation of the connection and organs involved, is
necessary before counseling can be provided
2. MRI can play an important adjunctive role in clarifying shared organs
3. Surgical separation of an almost completely joined twin pair may be successful if essential organs
are not shared
4. Viable conjoined twins should be delivered via CS

IX. CASE
• A.V. 28 y/o G1P0 18-19 weeks AOG consulted for excessive nausea and 3. The patient asks you “What does dichorionic, diamnionic mean?”
vomiting • In this case, there are 2 chorions and 2 amnions. Two distinct placentas or a
• VS: BP 120/70, PR 89, RR 21, Temp 36.5 single fused placenta may develop
• FH 21 cm, FHT 153 bpm • Dichorionic, diamnionic twinning results when the zygote divides within the first
• IE: cervix soft, long, and closed; uterus is enlarged to 5-6 months size 72 hours after fertilization
1. What obstetric condition/s should be considered in this case?
Differentials for this case include the following: 4. What advise should you give the patient regarding her pregnancy?
→ Multifetal pregnancy • The patient should be advised re the following:
→ Molar pregnancy: Bigger for gestational age uterine size is expected here → Prenatal care and frequency of visits
→ Pregnancy with uterine or ovarian mass – least likely → Proper diet and nutritional requirements
■ Uterine leiomyomas may cause an inc. in fundic height → Need for close monitoring and surveillance
■ big ovarian cyst- say an endometrial cyst that is intimately attached to → Risks associated with multiple pregnancy
the uterus, which may be mistaken for being part of the uterus itself. ■ Preterm labor and delivery
■ Hydramnios would also lead to bigger uterine size. ■ Low birthweight infants
2. What findings seen in the patient will support your answer in number 1? ■ Congenital malformations
• Excessive nausea and vomiting, Discrepancy in the measured fundic height ■ Growth discordance
and computed AOG, Discrepancy in the palpated uterine size and computed ■ Hypertension in the mother
AOG
→ Timing and route of delivery
• NOTE: In cases where there is a discrepancy in the computed AOG and
• NOTE: TTTS and other similar conditions are not considered in this case
physical examination findings (i.e. based on FH, uterine size, etc.) ALWAYS
because this is a dichorionic, diamnionic pregnancy. Problems related to deep
re-check and validate the LMP of your patient
anastomoses of vessels are found only in monochorionic cases
• UTZ: Results showed the following: Twin intrauterine pregnancy, dichorionic,
diamnionic 5-6. When is the proper timing of delivery in this case? What is the route of
Twin A Twin B delivery in this case?
■ Live, breech, 18 weeks and 4 ■ Live, breech, 18 weeks and 2 • The timing of delivery in this case is at 38 weeks AOG if uncomplicated. Earlier
days age of gestation by fetal days age of gestation by fetal timing of delivery may be done depending on maternal and/or fetal indications
biometry with good cardiac and biometry with good cardiac and
somatic activity somatic activity • The best route of delivery for this case is CS. First, the patient is primigravid.
Second, following the ultrasound given in this case, the first twin is in a breech
■ Adequate amniotic fluid, ■ Adequate amniotic fluid presentation. Given both conditions, CS may be the best choice for the patient
Placenta anterior, grade I, high- ■ Placenta anterior, grade I, high-
lying lying
■ SEFW appropriate for ■ SEFW appropriate for
gestational age gestational age

MNTM 2022 5
 OB2- DIABETES MELLITUS IN PREGNANCY
I. INTRODUCTION
1) Diabetes Mellitus is the most common medical complication in pregnancy
2) Worldwide: 7% of all pregnancies
3) Philippines:
a) 4.1% in low-risk patients (No risk factors but still developed diabetes)
b) 38.9% in high-risk patients (with risk factors)
CARBOHYDRATE METABOLISM
1) Mild fasting hypoglycemia - Fetus continuously extracts nutrients from the mother even when the
mother is not eating
a) decreased plasma glucose and some amino acids
b) free fatty acids, triglycerides, and cholesterol are also higher in the fasting rate
c) pregnancy-induced switch in fuels from glucose to lipids has been called accelerated starvation
2) Postprandial hyperglycemia - elevated and sustained glucose levels
a) Generally, there is an increased in the glucose level and corresponding insulin level of the pregnant
woman compared to the non-pregnant women
b) Hyperinsulinemia – in response to postprandial hyperglycemia
i) Insulin resistance – start during the mid-pregnancy
(1) Brought about by the interplay of various hormones (i.e., estrogen, cortisol, progesterone,
prolactin, and human placental lactogen)
(2) HPL – starts to increase at the start of pregnancy (the larger the placenta, the greater amount
of HPL)
(3) Ensures post prandial supply of glucose to the fetus even if mother is not eating
3) Suppression of glucagon - increases glucose and fatty acids in the bloodstream, glycogenolysis
CLASSIFICATION OF DIABETES MELLITUS
Type 1 Type 2 Gestational
Insulin deficiency Insulin resistance
Glucose intolerance identified during pregnancy
(insulin-dependent) (non-insulin-dependent)
Increase in secretion of cortisol, GH, HPL, progesterone, and prolactin
↓
● Most common form of diabetes Insulin resistance starting in mid-pregnancy
Autoimmune disease ● INSULIN RESISTANCE → Cells in (Reaches its peak at the 2nd or 3rd trimester/20-24 weeks AOG)
↓ muscles, fats, and the liver become ↓
Destruction of pancreatic b-cells resistant to insulin, glucose stays in Resistance compensated by an increase in insulin secretion and most women
↓ remain normoglycemic due to adequate b-cell compensation
the maternal circulation → ↓
No insulin production
↓ Hyperglycemia GDM develops if b-cell function is decreased or fails to compensate
Insulin Deficiency ● Inadequate insulin secretion in the
(In the absence of exogenous and face of increased insulin resistance ● Glucose or carbohydrate tolerance of variable severity that begins or is first
endogenous deficiency) ● Aggravated by obesity and recognized during pregnancy
sedentary lifestyle ● Preclinical Type 2 DM, have the tendency to be type 2 unmasked by the
hormonal stress of pregnancy
● Undiagnosed Type 2 DM

II. SCREENING AND DIAGNOSIS

SCREENING RISK FACTORS POGS CPG on Diabetes Mellitus in Pregnancy, 2018
● Universal screening for DM is recommended for ALL Filipino gravidas → Age > 25 y/o → Previous GDM
● All Filipino gravidas should be screened for Type 2 DM in the first prenatal visit → Diabetes mellitus in first-degree → Precious delivery of baby with
→ GDM occurs due to increase in hormones usually in the first trimester (20- relatives birthweight ≥ 9 lbs
24 weeks) → Maternal obesity → Congenital malformations
→ To identify those with undiagnosed T2DM not just GDM → Current use of corticosteroids → Unexplained intrauterine death
● Determine if the patient is high-risk based on historical and pregnancy risk factors → Glucosuria → Multiple gestation
→ PCOS → Hypertension
A. PROTOCOL FOR EVALUATION OF DIABETES IN PREGNANT FILIPINO WOMEN⭐⭐⭐
FIRST PRENATAL VISIT LOW RISK (FBS <92) HIGH RISK (FBS <92)
1ST TRIMESTER - FBS OR AT 24-28 WEEKS first prenatal check up – 75 OGTT

● All pregnant patient during the first prenatal visit ● If FBS is normal and labelled as low risk (no risk ● If FBS is normal but labelled as high risk (w/ risk factor),
(ideally during first trimester), request for FBS factor), request 75 g OGTT at 24-28 weeks immediately request for 75 g OGTT.
→ If FBS ≥ 126 mg/dL = Overt DM AOG. → If any of the ff = GDM
→ If FBS < 92 mg/dL = Normal → If any of the ff = GDM FBS ≥ 92 mg/dL
→ If FBS between 92-126 mg/dL = GDM FBS ≥ 92 mg/dL 1 hr ≥ 180 mg/dL
1 hr ≥ 180 mg/dL 2 hr ≥ 153 mg/dL
● If with diagnosis of Overt DM or GDM - monitor
2 hr ≥ 153 mg/dL
patient with CBG. → If 75 g OGTT is normal repeat 75 g OGTT at
● If patient is normal, identify whether the patient
→ If 75 g OGTT is normal, repeat 75 g OGTT ■ 24-28 weeks and if still normal
at ■ repeat at 32 weeks or
is high risk or low risk for DM.
■ 32 weeks or ■ anytime if with maternal/fetal signs of DM
■ anytime if with maternal/fetal signs of DM ● If 75 g OGTT becomes abnormal, stop and proceed to
management of DM.
Fetal signs: macrosomia, polyhydramnios, IUGR
Maternal signs: Polydipsia, polyphagia, polyuria, sudden increase in weight gain

MNTM 2022 1
 GESTATIONAL DM OVERT DM
We are only using FBS and 75 g OGTT, label as overt diabetes (most probably
Only need one value to label the patient as GDM⭐ T2DM) if FBS or 2HPPG is above threshold
Measure of Glycemia Threshold⭐
Plasma Glucose mmol/L mg/dL Fasting plasma glucose 126 mg/dl (7.9 mmol/L)
Fasting 5.1 92 Random plasma glucose 200 mg/dl (11.1 mmol/L)
1-hr OGTT 10.0 180 Hemoglobin A1c 6.5%
2-hr OGTT 8.5 153 2-hr Postprandial glucose 200 mg/dl (11.1 mmol/L)
IV. DIABETES IN PREGNANCY
FETAL EFFECTS
● Up to 25% of diabetic gravidas have an early pregnancy loss
Spontaneous
Abortion ● Those whose HBA1c concentrations where >12% or whose pre-prandial glucose concentrations were persistently >120mg/dL had
an elevated risk
● >26% were delivered preterm compared with 6.8% in the general obstetrical population
Preterm Delivery
● Almost 60% were indicated preterm births, that is, due to obstetrical or medical complications (not due to diabetes)
● Diabetic pregnancies are often complicated by excess amnionic fluid
Hydramnios
● patients with hyperglycemia, they tend to be polyuric - Babies would urinate a lot which causes hydramnios
● Diminished growth⭐ may result from congenital malformations or from substrate deprivation due to advanced maternal
vascular disease
→ More common in type 1 and type 2 diabetes wherein the mother has prolonged diabetes, and the blood vessels are already
Altered Fetal affected
Growth ● MACROSOMIA⭐: Fetal overgrowth is more typical of pregestational diabetes
→ Maternal hyperglycemia prompts fetal hyperinsulinemia, and this in turn stimulates excessive somatic growth
→ Newborns are described as being anthropometrically different from other large-for-gestational age (LGA) neonates
■ Have excessive fat deposition on the shoulders and trunk, which predisposes to shoulder dystocia or CS delivery
● If blood sugar levels were uncontrolled specially during the first trimester, there is a higher risk for congenital malformations
● Incidence of major malformations in women with type 1 diabetes is at least doubled and approximates 11%
Congenital
Malformation ● Cardiovascular malformations⭐ accounted for more than ½ of the anomalies (AV septal defect most common) ⭐⭐⭐
● Etiological mechanisms: excess production of superoxide radicals, altered cell signalling pathways, upregulation of some genes
by hyperglycemia, activation of programmed cell death.
● Hyperglycemia -> chronic aberration in oxygen and fetal metabolite transport -> fetal demise
Unexplained Fetal ● Poor glycemic control → elevated lactic acid, mean umbilical venous blood pH was lower and was related to fetal insulin levels
Demise → Happens usually in babies that are macrosomic, with hydramnios, near-term and and even at term
● Stillbirth: Maternal ketoacidosis, Placental insufficiency, Severe preeclampsia - because of the vascular complications
NEONATAL EFFECTS
● Gestational age (being delivered preterm) ⭐ rather than overt diabetes is likely the most significant factor associated with RDS
Respiratory Distress ● In one analysis of 19,399 very-low-birth-weight neonates delivered between 24 and 33 weeks AOG, rates of RDS in newborns of
Syndrome diabetic mothers were not higher compared with rates in neonates of nondiabetic mothers
● In mothers with uncontrolled blood sugar levels, this can result to delayed fetal lung maturity
● Newborns of a diabetic mother experience a rapid drop in plasma glucose concentration after delivery ⭐
Hypoglycemia → Attributed to hyperplasia of the fetal beta-islet cells induced by chronic maternal hyperglycemia
→ The baby continues to secrete insulin after delivery but the amount of glucose is not increased which causes hypoglycemia
Hypocalcemia⭐
Hyperbilirubinemia
● Pathogenesis is uncertain
● Fetal response to relative hypoxia (brought about by hyperglycemia-mediated elevations in maternal affinity for oxygen and fetal
Polycythemia oxygen consumption)
● Hypoxia + IGF-1 leads to elevated fetal erythropoietin levels and red cell production
Cardiomyopathy ● Hypertrophic cardiomyopathy (due to insulin excess) that primarily affects the interventricular septum
Long-term Cognitive ● IQ of those whose mothers had diabetes during pregnancy averaged 1-2 points lower
Development ● Autism spectrum disorders or developmental delay were also more common in children of diabetic women
● Risk of developing type 1 diabetes if either parent is affected is 3-5%
Inheritance of DM ● Type 2 diabetes has a much stronger genetic component. If both parents have type 2 diabetes, the risk of developing it
approaches 40%
MATERNAL EFFECTS
● Pregnancy-associated hypertension is the complication that most often forces preterm delivery in diabetic women
Preeclampsia
● Aspirin is given to prevent preeclampsia
● Clinically detectable nephropathy begins with micro-albuminuria (30-300 mg/day)
Diabetic → May manifest as early as 5 years after diabetes onset
Nephropathy ● Macroalbuminuria (>300 mg/day)
→ Develops in patients destined to have end-stage renal disease
● First and most common visible lesions: small microaneurysms followed by blot hemorrhages that form when RBCs escape from the
aneurysms (background or non-proliferative retinopathy
Diabetic → Leak serous fluid that creates hard exudates
Retinopathy ● With increasingly severe retinopathy, the abnormal vessels of background eye disease become occluded, leading to retinal ischemia
and infarctions that appear as cotton wool exudates (pre-proliferative retinopathy)
● Peripheral symmetrical sensorimotor diabetic neuropathy is uncommon in pregnant women
Diabetic neuropathy ● Diabetic gastropathy
→ Causes nausea and vomiting, nutritional problems, and difficulty with glucose control
Diabetic ● Develops in approximately 1% of diabetic pregnancies and is not often encountered in women with type 1 diabetes
Ketoacidosis ● Increasingly being reported in women with type 2 or even those with gestational diabetes
Infections ● Common infections include candida vulvovaginitis, urinary and respiratory tract infections, and puerperal pelvic sepsis
Cardiovascular Disease

MNTM 2022 2
 V. MANAGEMENT
A. PRECONCEPTIONAL CARE Parameter Optimal level
● Optimal medical care and education before conception Preprandial glucose level ≤ 95 mg/dL (5.3 mmol/L)
● Adequate glycemic control Premeal ≤ 100 mg/dL
● Management of complications such as hypertension, retinopathy, or nephropathy 1-hour Postprandial glucose ≤ 140 mg/dL (7.8 mmol/L)
● Discontinue unsafe and teratogenic medications (e.g. ACEI) 2-hour Postprandial glucose ≤ 120 mg/dL (6.7 mmol/L)
● Folate supplementation (5 mg/day) 3 months preconceptionally and during early Mean 100 mg/dL
pregnancy Glycosylated hemoglobin (HbA1c) < 6.0 % (<6.5%)
B. ANTEPARTUM MANAGEMENT
NON PHARMACOLOGIC
Medical Nutrition Therapy (MNT) Exercise Self-Monitoring of Blood Glucose (SMBG)
● Daily caloric intake: 30-35 ● ACOG: 30 minutes or more of moderate exercise ● GDM on diet
kcal/kg/day daily (e.g., brisk walking) at least 5 days a week or → Initially monitored through 7-point
● Caloric composition minimum of 150 min per week monitoring (prebreakfast, after breakfast,
→ Complex carbohydrates – 40% ● Muscles will use the glucose during exercise, pre-lunch, after lunch, pre-dinner, after
→ Proteins – 20% lowering blood glucose levels dinner, and at bedtime)
→ Fats – 40% → Increased insulin levels → inhibition of the normal → If confirmed with 7-point monitoring that
● Given as 3 meals and 3 snacks increase in hepatic glucose production and patient is controlled on diet, then 4 point can
daily increased muscle glucose uptake → lowers be done
→ Given equally for the blood sugar blood glucose level → Now: 4-point monitoring is pre breakfast,
to be stable and maintained ● ADA: program of moderate exercise in women after breakfast, after lunch, and after
→ If there is stable and maintained without medical or obstetrical contraindications dinner. (1 fasting, 3 post prandial)
blood sugar throughout the day, ● Type of exercises ● Women on pharmacologic therapy
insulin secretion will also be → Safe, non-contact: Treadmill, swimming, → Patients taking insulin or anti diabetic drugs
stable throughout the day stationary bike, walking, stretching, planks, yoga → SMBG 4-6x/day and include pre-prandial
● Important to note that fruits with → Not tennis, taekwondo, MMA values
high glycemic index (banana, ● Contraindications ● Urine ketone testing
apple, grapes) should not be given → Significant cardiovascular or pulmonary disease → Indications: Severe hyperglycemia, weight
to diabetic patients → Significant risk for preterm labor loss during treatment, or during starvation
■ Cerclage, multiple pregnancy, significant → During treatment, some patients prefer not
bleeding, threatened PTL, PROM to have insulin shots so they resort to
→ Obstetrical complications weight loss if they try to diet and those who
■ Preeclampsia, placenta previa, anemia, don’t diet, weight gain
poorly controlled diabetes, morbid obesity, → Presence of urine ketones in severe
IUGR starvation
PHARMACOLOGIC
Insulin treatment Metformin vs Insulin⭐⭐⭐ Metformin / OHA
● If after 2 weeks of diet and exercise, blood → Lower weight gain and AOG at birth ● If a patient cannot take insulin or declines:
glucose levels are still not controlled, insulin with metformin ● Metformin
must be started⭐ → Preterm birth rate was significantly → Increases insulin sensitivity
● First line and Standard therapy for uncontrolled more in metformin group* → Reduces hepatic gluconeogenesis
DM ■ Only draw back of Metformin → Enhances peripheral glucose uptake
→ DM is uncontrolled if despite following dietary → Pregnancy-induced hypertension → Lowers blood glucose level with minimal
prescription, blood sugar level is still (Preeclampsia) rate was significantly risk of hypoglycemia and weight gain
uncontrolled with at least 3 abnormal values in less in the metformin group ● Counsel about metformin risks including
the 7-point monitoring → No significant difference in: placental cross over and no long term studies
● It does not cross the placenta ■ LGA infants rate in offspring available
● Multiple daily doses of insulin and proper diet ■ SGA infants rate ■ May be associated with preterm birth
● Subcutaneous insulin infusion may be used, but ■ Hypoglycemia rate ■ Pre eclampsia is less
there is scarcity of evidence on pregnancy ■ No effect on SGA, LGA, hypoglycemia
effects ■ Does not cause congenital
● Insulin therapy (POGS CPG on Diabetes malformation even at first trimester
Mellitus in Pregnancy 2011) → Starting dose: 500mg nightly for 1 week,
→ Maintain CBG levels as close to normal increase to 500 twice daily
→ 1st trimester – 0.7-0.8 u/kg/d ■ Check baseline creatinine
→ 2nd trimester – 0.8-1.0 u/kg/d → Adverse events include abdominal pain and
→ 3rd trimester – 0.9-1.2 u/kg/d diarrhea (Recommend with meals)
→ 2/3 of daily dose- before breakfast → Maximal dose is 2,500-3,000mg per day, in
→ 1/3 of daily dose – before dinner two or three divided doses

● Oral hypoglycemic agents (OHA)ACOG and

Insulin Type Onset Peak (hr) Duration (hr) ADA acknowledge the several on the safety
Short acting (SC) and efficacy of metformin and glyburide
Lispro <15 min 0.5-15 3-4 ● Metformin and glyburide crosses the
Glulisine <15 min 0.5-15 3-4 placenta and reaches concentration in the
Aspart <15 min 0.5-15 3-4 fetus that are more than 2/3 of maternal
Regular 30-60 min 2-3 4-6 levels
Long acting (SC) ● FDA has not approved glyburide and
Detemir 1-4 hr Minimal* Up to 24 metformin use for treatment of GDM
Glargine 1-4 hr Minimal* Up to 24 → ACOG recognizes both as reasonable
NPH 1-4 hr 6-10 10-16 choices for second-line glycemic control in
women with GDM

MNTM 2022 3

FIRST TRIMESTER
● Establish age of gestation
● Careful glucose monitoring
→ Diabetes tends to be unstable
during 1st trimester
● Initiate an individualized glucose
control program and provide
education
● Pre-gestational DM: Assess extent
of diabetic vascular complications
TIMING
BY 40 WEEKS
● Patients with well-controlled⭐ ● In
DM on diet with no complicating
factors must be delivered by 40
weeks AOG.
→ Antenatal testing must remain ● Significant factors like extent of
reassuring
→ No evidence of macrosomia
● Expectant management beyond
the due date (40 weeks AOG) is
not recommended
TRIMESTER (OF DIAGNOSIS)BASED MANAGEMENT
SECOND TRIMESTER THIRD TRIMESTER
● Congenital anomaly scan ● Start Antepartum surveillance on:
→ American College of Obstetrics and → 28 WEEKS⭐: if with risk factors risk factors
Gynecology: 18-22 weeks ■ Pregestational DM
→ Philippine Society of Ultrasound in OB- ■ GDM with poor glycemic control
GYN: 24-26 weeks* ■ Diabetes on insulin or oral hypoglycemic agents
● Second trimester fetal echocardiography ■ Presence of other risk factors
→ Most common congenital anomaly is → 37 WEEKS⭐: GDM well controlled and on diet
the heart only
● Continue self-monitoring of glucose level ● Frequency of monitoring is dependent on:
● Adequate glycemic control → Degree of metabolic control
→ Increase insulin requirement due to → Presence of other risk factors like hypertension
increase insulin resistance → Ideally, every week with risk factors or reached 37
weeks
● Antepartum fetal surveillance:
→ Fetal movement, NST, Biophysical profile, Biometry,
Doppler velocimetry
VI. TIMING AND ROUTE OF DELIVERY
ROUTE
BY 37 WEEKS VAGINAL CS
patients with poorly ● Diabetic patients may be ● Elective CS at 39-40 weeks in
controlled⭐ DM, delivery at 37 delivered by outright CS if EFW patients with previous CS
weeks AOG may already be ≥ 4000g (macrosomic baby). ● Diabetes mellitus is NOT an
undertaken ● If the patient is G5P4 and indication for CS
malalaki naman previous → In macrosomic babies, there
glycemic control, hydramnios, babies, you may opt to do is truncal obesity
pregnancy comorbidities and vaginal delivery. ■ The head is smaller than
EFW must be taken into account → CS is not indicated if patient is the trunk of the baby,
in the decision of timing of not diabetic which may result in
delivery. If with hypertension – → Increased shoulder dystocia shoulder dystocia
aim is 37 weeks. due to truncal obesity in ● Diabetes Mellitus in itself is not
diabetic patient an indication for CS

VII. MANAGEMENT OF DIABETES IN PREGNANCY

INTRAPARTUM MANAGEMENT →
● Insulin requiring diabetes
→ Target values: monitor blood
sugar levels hourly (100 mg/dL –
Doc Mongon)
■ Capillary glucose: 70-110
mg/dL or
■ Plasma glucose 80-120
mg/dL
→ Give short-acting insulin via IV
infusion at a dose of 0.5-1 unit
per hour for plasma glucose
above 120 mg/dL
DELIVERY → POSTPARTUM
● Insulin Management for Cesarean Section ● Request for 75 g OGTT 4-12 weeks
→ The last insulin dose is given the night before postpartum
(evening dose of insulin) → If elevated, patient is no longer GDM but
→ Withhold morning dose and determine random already T2DM
plasma glucose immediately prior to CS ● If normal, advise testing every 1-3 years
● If glucose levels >100 mg/dL: → More than 50% of patients diagnosed to
→ Infuse regular insulin at a dose of 1 – 1.25 unit/ hour be GDM will end up to be diabetic later on
for plasma glucose > 100 mg/dL in life
→ Infuse IV normal saline at 100-125 mL/hr → Serves as warning
● If with active labor or if glucose level >70 mg/dL : ■ Patient should be advised for diet,
→ IV 5% dextrose 100-150 mL/hr instead of normal exercise and lifestyle change to
saline to target 100 mg/dL glucose level prevent development of DM
→ Discontinue IV insulin right after the delivery ● Advise breastfeeding
→ Check plasma glucose 2 hours after the CS

CATEGORIES FOR INCREASED RISK OF DIABETES⭐

TEST FPG (mg/dL) 2HR PG (mg/dL) HbA1c
CUT-OFFS 100-125 140-199 5.7-6.4%
CATEGORY Impaired Impaired Glucose
Fasting Tolerance (IGT)
Glucose (IFG)

APPENDIX FIGURES⭐⭐⭐

MNTM 2022 4
 THYROID GLAND AND PREGNANCY
1) Anatomically – moderately enlarged thyroid: glandular hyperplasia and increased vascularity
a) Increased thyroid binding globulin (TBG) concentrations from both higher hepatic synthesis rates and lower metabolism rates
i) Increases total T4 and T3 but not the physiologically important FT4 and FT3 (no symptoms because free form is not increased)
b) TRH levels – not increased during normal pregnancy, TSH levels decrease⭐ in pregnancy
Trimester TSH Level⭐
i) Misdiagnosis of subclinical hyperthyroidism → Caution has to be taken in interpreting the value 1st 0.1 to 2.5 mIU/L
of TSH during pregnancy because there naturally would be some degree of decrease in TSH 2nd 0.2 to 3.0 mIU/L
levels. 3rd 0.3 to 3.0 mIU/L
2) Antibodies Non-pregnant 0.5 to 4.5 mIU/L
a) Thyroid-stimulating autoantibodies, also called thyroid-stimulating immunoglobulins (TSIs): bind to Normal FT4⭐ 0.7 -1.9 ng/mL
the TSH receptor and activate it, causing thyroid hyperfunction and growth → Grave’s Normal FT3⭐ 2.3 – 4.1 ng/mL
b) Thyroid peroxidase (TPO): thyroid gland enzyme for production of thyroid hormones. → Hashimoto’s
I. HYPERTHYROIDISM IN PREGNANCY
• Maternal outcome and pregnancy outcome: Increased incidence of preeclampsia, heart failure, and maternal death
• Clinical manifestation of hyperthyroidism would be the same regardless of whether the patient is pregnant or not
→ Clinical: tachycardia, thyromegaly, exophthalmos, failure to gain weight despite adequate food intake, heat intolerance, tremors 
→ Labs: depressed TSH level, elevated FT4
→ T3 toxicosis – only FT3 is elevated (specifically give a diagnosis of T3 thyrotoxicosis)
→ Thyroid function test is not routinely done during pregnancy; only done when thyroid problems are suspected
• Grave’s Disease
→ Most common cause of thyrotoxicosis in pregnancy, Organ specific autoimmune process
A. TREATMENT OF THYROTOXICOSIS IN PREGNANCY
Goal: Make the level of the thyroid hormones slightly above the normal level while TSH levels remain suppressed.
Propylthiouracil Methimazole SIDE EFFECTS OF ANTI-THYROID DRUGS
First trimester⭐ use increases the risk of • Hepatotoxicity: A more concerning side
Preferred especially during the 1st trimester embryopathy: Esophageal and choanal atresia, effect of PTU 0.1-0.2%
Aplasia cutis • Transient leukopenia
Does not readily cross the placenta : less effects on baby
⭐
Crosses placenta more readily than PTU • Agranulocytosis – 0.3% (normal WBC
Blocks peripheral conversion of T4 to T3 Partially inhibits the conversion of T4 to T3 – 4.0-11.0) ⭐
Dosage: 50 to 150 mg orally three times daily may be Dosage: initial higher daily dose of 10 to 20 mg • Development of antineutrophil
initiated depending on clinical severity followed by a lower maintenance dose of 5 to 10 cytoplasmic antibodies (ANCA) – 20%
If they started high because of severe symptoms and mg after 1 month • Aplasia Cutis is when the skin does not
eventually the disease is controlled, they may opt to taper If the severity of the disease has improved form properly (commonly occurs in the
this for a minimum of 50 mg once a day significantly, you can maintain the dose at 5-10 mg scalp, though other parts of the body
Methimazole can still be used during pregnancy except on first trimester ⭐ but PTU is preferred. may be affected). underlying structures
You have to make use of PTU in the 1st trimester, then probably after the 1st trimester, you can shift to within the skin are absent, sometimes
methimazole the skull is visible.
1) Thyroid surveillance: serum free T4 concentrations are measured every 4 to 6 weeks (to adjust the dose of medication accordingly)
a) This is done all throughout pregnancy. Even after pregnancy, for about 6 weeks, we have to repeat the thyroid hormones
b) ACOG = monitor fT4 only but in reality, monitoring consists of fT4 and TSH
2) Subtotal thyroidectomy
a) Can be performed after thyrotoxicosis is medically controlled, preferably in the 2nd trimester (best time)
i) 1st trimester - stress leads to abortion
ii) 3rd trimester - stress leads to preterm labor
b) Appropriate for failure of medical management or treatment, or in whom drug therapy proves toxic effects
c) Indicated only when patient cannot adhere to medical management due to toxicity
3) Total thyroidectomy is not usually done to avoid its adverse effects (removal of parathyroid glands and injury to the recurrent laryngeal nerve)
a) Drawback: inadvertent resection of parathyroid glands and injury to the recurrent laryngeal nerve which may lead to manifestations of vocal
cord paralysis such as changes in pitch as well as development of voice hoarseness.
4) Thyroid ablation with therapeutic radioactive iodine is contraindicated during pregnancy
a) May also cause fetal thyroid gland destruction
b) If patient is not yet pregnant and underwent RAI therapy, advise her to not get pregnant within 6 months after ablation.
c) There should also be a delay of 3 months between lactation and ablation.
B. ASSOCIATED COMPLICATIONS OF THYROTOXICOSIS IN PREGNANCY
• Minor spontaneous abortion
• Minor congenital anomalies
• Preeclampsia⭐
• Preterm Birth
• LBW
• Abruption (Attachment is disrupted)
• Neonatal thyroid dysfunction
• Perinatal mortality
• Maternal complication of uncontrolled hyperthyroidism are primarily related: thyroid storm,
arrythmia, and congestive heart failure
C. PREGNANCY OUTCOMES
● In untreated women or in those who remain hyperthyroid despite therapy, there is a higher
incidence of preeclampsia, heart failure, and adverse perinatal outcomes⭐
● Other associated complications include: Spontaneous abortion, minor congenital anomalies,
preterm labor and delivery, LBW, and Abruptio placenta (especially when associated with
preeclampsia) ⭐

MTNM 2022 1
D. FETAL AND NEONATAL EFFECTS
• In most cases: perinate is euthyroid
• Others: hyper/hypothyroidism can develop with/without goiter
• 4 possible presentations of a neonate exposed to excessive maternal thyroxine: ⭐
Goitrous thyrotoxicosis⭐ Goitrous hypothyroidism⭐ Non-goitrous hypothyroidism⭐ Fetal thyrotoxicosis⭐
Due to placental transfer of TSI ⭐ Due to placental transfer of Thionamides
Transplacental passage of
PTU or MMT block thyroid hormone transplacental thyroid
Best predictor of perinatal maternal TSH- receptor blocking
production of baby. Goiter is trying to stimulating antibodies
thyrotoxicosis is the presence of antibodies
compensate, kaya enlarged
thyroid-stimulating TSH receptor
No abnormal intellectual or physical
antibodies in women with Grave’s
development, unlike those with overt
disease (>3-fold higher)
hypothyroidism TSH is blocked → thyroid gland is after maternal thyroid gland
Can be treated by a reduced maternal unresponsive ablation with RAI
Non-immune hydrops and fetal
antithyroid medication dose and injection of
demise may occur or death
intra-amnionic thyroxine
Acute and life-threatening:
1) Thyroid storm is an exaggerated, hypermetabolic state and is rare in pregnancy
a) Hypermetabolic state: rapid heartbeats (palpitations), greatly increased temperature, shortness of breath, chest pain, anxiety, irritability,
disorientation, increased sweating, weakness, heart failure
b) Clinical manifestations: Unexplained fever, Tachycardia, Neurologic changes, Arrhythmias, Heart failure
2) Heart failure
a) Develops in 8% of women with uncontrolled hyperthyrotoxicosis
b) Patients may develop thyrotoxic cardiomyopathy: high output state, dilated cardiomyopathy
c) Decompensation is precipitated by preeclampsia, anemia, and sepsis. Important to rule these out first!
i) In contrast, pulmonary hypertension and heart failure from cardiomyopathy caused by the profound myocardial effects of thyroxine, is
common in pregnant women
(1) Thyroxine-induced cardiomyopathy are reversible.
3) Management:
a) Give IV fluids, oxygen, antipyretics, cooling blankets⭐
b) 1st step for pregnant patient with thyroid storm: try to address the excess production
i) Give Thionamide (PTU) ⭐ 1000mg load PO or through NGT, then 200mg every 6
hours
c) Most bothersome manifestations are the tachycardia and arrhythmia
i) Give Propranolol⭐ 10-40mg PO every 8 hours
ii) Other B-blockers that can be used: Labetalol, Esmolol
d) Once the production of the hormones is stopped (1-2hrs), think of the hormones that it
has produced before PTU was given:
i) Give Iodide⭐: inhibit thyroid release⭐ of T3 and T4
(1) Sodium Iodide 500-1000mg IV every 8 hrs
(2) SSKI 5 drops every 8 hrs
(3) Lugol’s solution 10 drops every 8 hrs
ii) Give Lithium Carbonate⭐ 300mg PO every 6 hours: if allergic to Iodine – inhibit
release and synthesis of thyroid hormone
e) Now address those in the periphery which have been released already
i) Give Corticosteroid⭐ therapy for 24 hours (Hydrocortisone or Dexamethasone):
prevent the peripheral conversion of T4 to T3)
f) Manage coexisting problems. Preeclampsia, infection, and anemia - should be aggressively managed
OTHER THYROTOXICOSIS
THYROTOXICOSIS AND GESTATIONAL TROPHOBLASTIC SUBCLINICAL HYPERTHYROIDISM
DISEASE
• Abnormally high hCG levels lead to overstimulation of the TSH • Earliest stage of hyperthyroidism
receptor • TSH is abnormally low, thyroxine hormone levels within the normal
→ hCG and TSH have similar structure; body gets confused reference range
• The prevalence of increased thyroxine levels in women with • In cases of chronic subclinical hyperthyroidism (present even
molar pregnancy is around 25-65% before pregnancy), osteoporosis, CV morbidity, and can progress to
• With definitive treatment, serum FT4 levels usually normalize overt thyrotoxicosis or thyroid failure.
rapidly in parallel with the decline in hCG concentrations • Subclinical Hyperthyroidism in general is not associated with any
→ Don’t give thionamides! Treat the cause of adverse pregnancy outcomes.
hyperthyroidism which is GTD • No need to treat, but periodic surveillance for FT4 and TSH is
→ Suction curettage, hysterectomy recommended every 4-6 weeks.
• Long-term effects:
• Osteoporosis, cardiovascular morbidity, progression to overt
thyrotoxicosis or thyroid failure
GESTATIONAL TRANSIENT THYROTOXICOSIS
• Results from TSH-receptor stimulation from massive, but normal for pregnancy - concentrations of hCG (not GTD levels)
• Results to hyperemesis gravidarum

MTNM 2022 2
 II. HYPOTHYROIDISM IN PREGNANCY
A. HYPOTHYROIDISM
1) Clinical features of thyroid disease, whether it’s hypo- or hyper-are similar to non-pregnant patients
a) Clinical: fatigue, constipation⭐, cold intolerance, muscle cramps, weight gain, edema, dry skin, hair loss, and prolonged relaxation phase of
deep tendon reflexes
b) A pathologically-enlarged thyroid gland is seen in women in areas of endemic Laboratory Results Disease⭐
↓TSH, ↑FT3, FT4 Overt Hyperthyroidism
iodine deficiency or those with Hashimoto’s thyroiditis
2) Clinical or overt hypothyroidism is confirmed when an abnormally high serum TSH ↓TSH, Normal FT3, FT4 Subclinical Hyperthyroidism
level is accompanied by an abnormally low thyroxine level ↓TSH, ↑FT3, Normal FT4 T3 thyrotoxicosis
a) High TSH, low T3 and T4 ↓TSH, ↓FT3, Normal FT4 Euthyroid Sick Syndrome
↑TSH, ↓FT3, FT4 Overt Hypothyroidism
3) Subclinical hypothyroidism is defined by an elevated serum TSH level and normal
↑TSH, Normal FT3, FT4 Subclinical Hypothyroidism
serum thyroxine concentration
a) TSH screening in pregnancy: for any kinds of thyroid disorder (whether hypo or hyper)
i) Not routinely done, Clinical screening is done, not biochemical screening
ii) Request only for TSH screening if there is high suspicion for thyroid disease
4) Causes:
a) Hashimoto’s thyroiditis – most common⭐ (chronic lymphocytic thyroiditis)
i) glandular destruction from autoantibodies (Anti-TPO antibodies)
b) Post-RAIU
i) destruction of thyroid gland - patients treated for thyrotoxicosis before
c) Post-thyroidectomy
5) Treatment
a) Levothyroxine 1 to 2 μg/kg/day (approx. 100 μg daily)
b) Surveillance is with TSH levels measured at 4-to 6-week intervals⭐, and the thyroxine dose
is adjusted by 25- to 50-μg increments until TSH values become normal
i) To assess whether treatment is successful, need for dose adjustment
6) Outcomes⭐
a) Maternal: preeclampsia, placenta abruptio, cardiac dysfunction, LBW (<2000kg), stillbirth,
IUGR, abruptio placenta and preterm delivery
b) Perinatal: Impaired psychomotor development⭐, decreased school performance, decreased
IQ
B. SUBCLINICAL HYPOTHYROIDISM AND PREGNANCY
1) Lab: elevated TSH, normal thyroid hormones
a) TSH values 10-15MIU/L: 19 out of 100 patients will develop eventually overt hypothyroidism
b) TSH values < 10 MIU/L: 2 out of 100 patients will develop eventually overt hypothyroidism
2) Associated with increased risk of severe preeclampsia, GDM, stillbirth
a) Currently no evidence that identification and treatment of subclinical hypothyroidism during pregnancy improves these outcomes
b) Limit treatment to those with clinical or overt hypothyroidism, monitor thyroid hormone levels nalang
c) Doc Mon Gon: give Levothyroxine even if Subclinical.
C. IODINE DEFICIENCY
1) Dietary iodine requirements are increased during pregnancy due to increased thyroid
hormone production, increased renal losses, and fetal iodine requirements.
a) Adequate iodine is requisite for fetal neurological development
b) Can manifest with both maternal and fetal goiter
2) Levels of Severity:
a) MILD: causes intellectual impairment although supplementation prevents fetal goiter
b) MODERATE: intermediate and variable effects: Still try to attempt to correct the iodine
deficiency in the hope that it would not progress to severe iodine deficiency and eventually
endemic cretinism
c) SEVERE: Almost already impossible to recover from iodine deficiency; usually result to
endemic cretinism to the baby
3) Recommended daily iodine intake:
a) Institute of Medicine: (values are what we usually see in supplementation of multivitamins)
i) during pregnancy - 220μg/day
ii) lactating women - 290 μg/day
b) Endocrine society:
i) 250 μg during pregnancy and breastfeeding
ii) 5 micronutrients that need to be supplemented in pregnancy: (Don’t worry about giving separately the iodine because usually the prenatal
multivitamins that we prescribe to the pregnant patients would already contain enough iodine to try to prevent the patient from having the
deficiency)
(1) Iron
(2) Ferrous sulfate
(3) Vitamin B complex
(4) Calcium
(5) Iodine
4) REMEMBER:
a) Clinical screening instead of TSH screening is performed. TSH is requested when clinical screening reveals suspicion for thyroid disease.
b) Overt types of hypo and hyperthyroidism is treared. We don’t treat the subclinical. However, it’s imperative that you repeat the thyroid function
test every 4-6 weeks for monitoring regardless of whether you have subclinical or overt thyroid disorder during pregnancy
i) Overt types = whether to taper down or increase the dose of the drugs that we are giving.
ii) Subclinical = to see if there would be progression to the overt type of thyroid disease because anytime the overt type would arise, that
would warrant the medical treatment.
c) Almost same effects of hypo and hyperthyroidism in pregnancy outcome
i) Increased risk of pre-eclampsia, low birth weight, and preterm birth

MTNM 2022 3
 I. PULMONARY PHYSIOLOGY IN PREGNANCY
1) Enlarging uterus: Diaphragm elevates by 4 cm, widening of the subcostal angle (transverse diameter of the thoracic
cage lengthens by 2 cm) | 
a) increase in a thoracic circumference of about 6 cm
b) Lung volumes⭐
i) ↓Functional residual capacity (FRC) = ↓Expiratory Reserve Volume (ERV) + ↓Residual Volume (RV)
ii) ⭐Tidal volume ↑ by 40% due to respiratory stimulation by progesterone
iii) Resting minute ventilation↑ - respiratory stimulation by progesterone
iv) Total lung capacity (TLC) and respiratory rate (RR) is unchanged
c) Compensated for by an increase in both the AP and transverse diameters of the chest wall | 
d) Diaphragmatic excursions in pregnant women is greater than nonpregnant women
2) ↑ O2 consumption⭐
a) Increases incrementally from 20 to 40 mL/min in the second half of pregnancy
3) Physiologic dyspnea
a) Increased respiratory effort caused by progesterone and to a little extent, estrogen
b) Increased awareness of a desire to breathe - Not necessarily an increase in RR
c) To compensate for respiratory alkalosis (mild), plasma HCO3 levels ↓ from 26 to 22 mmol/L | 
i) progesterone that increases the tidal volume = lowered pCO2
4) End result: substantively increased ventilation due to deeper but not more frequent breathing
II. BRONCHIAL ASTHMA
1) Estimated prevalence ranges between 4-8% and appears to be rising
2) Chronic inflammatory airway syndrome with a major hereditary component
a) Characterized by infiltration with eosinophils, mast cells, and T lymphocytes
b) Secondary to an increased responsiveness to numerous stimuli
3) Hallmark: Reversible airway obstruction
a) Bronchial smooth muscle contraction
b) Vascular congestion
c) Tenacious mucus
d) Mucosal edema
4) IMPLICATED STIMULI
a) Allergens, including pollens, house-dust mites, cockroach antigen, animal dander, molds, and Hymenoptera stings
b) Irritants, including cigarette smoke, wood smoke, air pollution, strong odors, occupational dust, and chemicals
c) Medical conditions, including viral upper respiratory tract infections, sinusitis, esophageal reflux, and Ascaris infestations
d) Drugs and chemicals, including aspirin, nonsteroidal anti-inflammatory drugs, beta-blockers, radiocontrast media, and sulfites
i) F-series prostaglandins and ergonovine maleate can exacerbate asthma thus should be avoided in pregnant asthmatics
e) Exercise, Cold air, Emotional stress
A. CLINICAL COURSE
1) Findings range from mild wheezing to severe bronchoconstriction, and sometimes status epilepticus
2) ↓ FEV1/FVC, PEFR
3) Even early asthma stages may be dangerous for the pregnant woman and her fetus
a) Smaller FRC and increased pulmonary shunting render the woman more susceptible to hypoxia and hypoxemia that translates to the baby
i) If this persists, it would lead to IUGR or fetal demise
Severity⭐
Component Intermittent Persistent
Mild Moderate Severe
> 2 days/wk not
Symptoms ≤ 2 days/wk Daily Throughout day
daily
Nocturnal >1/wk, not
≤ 2x/mo 3-4x/mo Often 7x/wk
awakenings nightly
SABA for > 2 days/wk, Several times
≤ 2 days/wk Daily
symptoms but not >1x/day daily
Interference with Some Extremely
None Minor limitation
normal activity limitation limited
Normal between
Lung function
exacerbations
60-80% < 60%
FEV1 > 80% predicted
predicted predicted
FEV1/FVC Normal Reduced 5% Reduced > 5%
1) Hypoxia initially is mitigated by hyperventilation, which maintains arterial pO2 within a normal range but lowers pCO2, creating respiratory alkalosis
2) As airway narrowing worsens, ventilation-perfusion defects increase, and arterial hypoxemia ensues. With severe obstruction, ventilation becomes
impaired as fatigue causes early CO2 retention. Because of hyperventilation, this may only be seen initially as an arterial pCO2 returning to the normal
range
3) With continuing obstruction, respiratory failure follows from fatigue = ↓ pO2, ↑ pCO2 = acidosis
B. CLINICAL EVALUATION
Clinical signs indicating severity Pulmonary function testing Arterial Blood Gas
• Labored breathing • Routine in the management ● Objective: pH, pO2, pCO2, HCO3
• Tachycardia • Sequential measurement of the FEV1 or the ● Results should be interpreted in relation to normal
• Pulsus paradoxus PEFR⭐ (Peak expiratory flow rate) are the best values for pregnancy
• Prolonged expiration measures of severity ● Not routinely done because of difficulty of
• Use of accessory muscles o Assess: stagnation, improvement, or interpretation due to the associated changes that
• Signs of potentially fatal attack: worsening (need serial determination) happen during pregnancy (i.e. physiologic increase
• Central cyanosis • FEV1 less than 1L, or less than 20% of in pH, pCO2, HCO3)
• Altered consciousness predicted value, correlates with severe disease ● (❗Pulmonary function testing is preferred)

MNTM 2022 1
C. CLINICAL OUTCOMES
Effects of Pregnancy on Asthma Pregnancy Outcome Fetal Effects
● No evidence that pregnancy has a ● Unless disease is severe or is ● Perinatal outcomes are generally good if control is adequate
predictable effect on underlying asthma poorly-controlled, pregnancy ● Medical comorbidities during pregnancy, the usual adverse
→ (1/3) of patients would have an outcomes are generally effect expected on the pregnancy would be preterm labor and
unchanged status of asthma excellent delivery and low birth weight infant.
→ (1/3) would have worsening of → Ensure that if there’s an ● Fetal response to maternal hypoxemia – decreased
asthma symptoms exacerbation, it won’t be too umbilical blood flow, increased systemic and pulmonary
→ (1/3) would have improvement severe and ensure that it will vascular resistance, and decreased cardiac output
→ Probably what we have to do is be addressed right away → Could manifest as poly- or oligohydramnios⭐
patient education and on the role of ● For chronic diseases in → Incidence of IUGR increases with asthma severity⭐
the obstetrician, it would be pregnancy, the most common No evidence that commonly used anti-asthmatic drugs are
anticipation of possible complications are IUGR and harmful to the fetus. The incidence of congenital malformations
complications preterm delivery would still be equal to the general population
D. MANAGEMENT OF CHRONIC ASTHMA
CHRONIC ASTHMA ACUTE ASTHMA
1) Management guidelines: 1) Treatment is similar to that for the non-pregnant asthmatic,
a) Patient education – general asthma management and its effect on although the threshold for hospitalization is lowered
pregnancy, prenatal check up a) First-line therapy: b-agonist, given subcutaneously, taken
i) antenatal surveillance tests frequently orally, or inhaled
(1) Fetal movement counting should be performed i) 3 doses within 60-90 mins
ii) She has to watch out for signs of preterm labor ii) Ex: terbutaline, albuterol, epinephrine, isoetharine,
b) Environmental precipitating factors – avoidance or control; viral infections isoproterenol, metaproterenol | &
include the common cold are frequent triggering events b) For maintenance: b-agonist + inhaled corticosteroids
c) Objective assessment of pulmonary function and fetal status – monitor with c) For severe exacerbations: b-agonist + inhaled
PEFR or FEV1 and fetal surveillance tests | & corticosteroids + oral or parenteral corticosteroids
d) Pharmacological therapy – in appropriate combinations and doses to i) Methylprednisolone, 40-60 mg, every 6 hours for 4
provide baseline control and treat exacerbations; compliance may be a doses is commonly used
problem, and periodic medication reviews are helpful ii) Oral corticosteroids are the very last resort drug to give,
2) Treatment depends on disease severity ⭐ reserved for very severe forms of asthma | 4
a) No therapeutic regimen for management of pregnant asthmatics is 2) Therapeutic aim is to maintain the pO2 > 60 mmHg, and preferably
universally accepted normal, along with 95% O2 saturation
i) b-agonists help abate bronchospasm 3) Baseline pulmonary function testing includes FEV1 or PEFR
ii) Corticosteroids treat the inflammatory component 4) Advise admission if:
b) The more severe the asthma, the more drugs are given a) Patient is in respiratory distress
c) Mild asthma – inhaled b-agonists as needed are usually sufficient b) FEV1 or PEFR is < 70% of predicted after 3 doses of b-
d) Persistent asthma – inhaled corticosteroids administered every 3-4 hours agonist
3) Goal: Reduce the use of b-agonists for symptomatic relief 5) Discharge is considered if there is improvement of FEV1 or PEFR
4) Women with moderate to severe to above 70% of baseline
asthma: STATUS EPILEPTICUS
a) Measure and record either ● Severe asthma of any type not responding after 30-60 mins of
FEV1 or PEFR 2x/day intensive therapy
b) FEV1 ideally is > 80% of → Intensive therapy includes inhaled b-agonists, IV corticosteroids,
predicted and close observation for worsening respiratory distress or fatigue
i) In gauging whether the in breathing
patient is improving or ● Consider early intubation when maternal respiratory status worsens
not, FEV1 should despite aggressive treatment to ensure adequate oxygenation is
ideally be > 80% of
achieved
predicted value | 4
c) Predicted values of PEFR =
→ Indications for mechanical ventilation:
380-550 L/min ■ Fatigue
d) Each woman has her own ■ CO2 retention
baseline value and ■ Hypoxemia
therapeutic adjustments can
be made using this

E. LABOR AND DELIVERY

1) Maintenance medications are continued through delivery
2) Labor itself is a form of stress. Asthmatic patients can have exacerbations when they are under stress. In order to address this give stress-dose
corticosteroids | 
a) Stress-dose corticosteroids are administered to any woman given systemic corticosteroid therapy within the preceding 4 weeks
i) 100 mg hydrocortisone IV every 8 hrs during labor and for 24 hrs after delivery
ii) To control the inflammatory aspect of the pathophysiology of the disease | 
b) Take serial measurements of FEV1 or PEFR
c) Meperidine is not given⭐ for labor analgesia
i) Has a histamine-releasing effect that can trigger an asthma attack
3) Route of delivery: can undergo NSD
a) CS is limited to usual indications in obstetric patients
i) For surgical delivery, conduction/regional analgesia (epidural) is preferred because tracheal intubation (like in general anesthesia)
can trigger severe bronchospasm
4) Postpartum hemorrhage: treated with oxytocin⭐ or prostaglandin E1 or PGE2 (dinoprostone) ⭐
a) PGF2 (carboprost) ⭐ or ergotamine derivatives (methergine) ⭐ are contraindicated because they may cause significant bronchospasm

MNTM 2022 2
 III. PNEUMONIA
A. BACTERIAL PNEUMONIA (50%)
1) Streptococcus pneumoniae is the most Severity Classification
common cause Low risk Moderate risk High risk
2) Pregnancy itself does not predispose to Stable vital signs: Unstable vital signs: Any of the clinical
pneumonia ● RR < 30/min ● RR ≥ 30/min features of moderate
3) Symptoms: ⭐ ● PR < 125/min ● PR ≥ 125/min risk CAP
a) Fever plus any of the
● SBP > 90 mmHg, DBP > 60 ● Temp ≤ 36 °C or ≥ 40 °C following:
b) Productive cough mmHg ● SBP < 90 mmHg, DBP ≤ 60 mmHg
c) Dyspnea ● Temp > 36 °C or < 40 °C ● Severe sepsis and
Altered mental state of acute onset septic shock; OR
d) Pleuritic chest pain
4) Diagnosis:
No altered mental state of acute Suspected aspiration ● Need for mechanical
onset Unstable/decompensated comorbid ventilation
a) CXR⭐ is essential for diagnosis No suspected aspiration
condition/s:
i) Exposure to radiation from a CXR is No or stable co-morbid condition
not that high to cause any adverse ● Uncontrolled diabetes mellitus
effect on the fetus especially if it was CXR findings: ● Active malignancies
done only once or done after the first ● Localized infiltrates ● Neurologic disease in evolution
trimester No evidence of pleural ● Congestive heart failure (CHF) Class
effusion II-IV
ii) Radiographic abnormalities may take
up to 6 weeks to completely resolve ● Unstable coronary artery disease
b) Sputum cultures, serological testing, cold ● Renal failure on dialysis
agglutinin identification, and tests for ● Uncompensated COPD
bacterial antigens are not recommended⭐ ● Decompensated liver disease
i) If antibiotics did not work, a blood culture is helpful to know if there are any antibiotic resistance or incorrect dosing
5) Management
a) Antimicrobial treatment is empirical
i) Macrolide⭐ (azithromycin, clarithromycin, or erythromycin)
ii) For women with severe disease:
(1) Fluoroquinolone (levofloxacin, moxifloxacin) – avoided in the first trimester
(2) Macrolide + a b-lactam (high-dose amoxicillin or amoxicillin-clavulanate)
(a) b-lactam alternatives include ceftriaxone, cefpodoxime, or cefuroxime
iii) Oseltamivir may be added for suspected influenza A infection
(1) Not common but if you are suspecting a viral and bacterial infection, you may add this to the treatment
b) Clinical improvement is usually evident in 48-72 hrs with resolution of fever in 2-4 days
c) Pneumonia treatment for uncomplicated cases lasts for 5-7 days Empirical Antimicrobial Treatment for CAP
d) Criteria for Severe Pneumonia (requires hospitalization)⭐ Treatment
i) RR ≥ 30/min Macrolidesb: clarithromycin or azithromycin
ii) PaO2/FiO2 ratio ≤ 250 Uncomplicated,
plus
iii) Multilobular infiltrates otherwise healthya
Oseltamivir for suspected influenza A infection
iv) Confusion/disorientation Respiratory fluoroquinolones: moxifloxacin,
v) Uremia Severe pneumonia gemifloxacin, or levofloxacin
vi) Leukopenia (WBC < 4000 μL) or
a: Use as inpatient or -lactams: amoxicillin/clavulanate, ceftriaxone,
vii) Thrombocytopenia (< 100,000/μL) outpatient regimen
viii) Hypothermia (core temp < 36 °C) ⭐ b: Doxycycline may be cefotaxime, or cefuroxime plus a macrolide
ix) Hypotension requiring aggressive fluid resuscitation given if postpartum plus
6) Pregnancy Outcome Oseltamivir for suspected influenza A infection
a) Frequent complications: Premature rupture of membranes, Preterm delivery, Chronic diseases⭐
b) Consequently, IUGR and low birthweight infants are common
7) Prevention
a) Pneumococcal vaccine is 60-70% protective against 23 serotypes
b) 13-serotype vaccine is not recommended⭐ for otherwise healthy pregnant women
i) Recommended for: Immunocompromised, including those with HIV infection, Significant smoking history, Diabetes, Cardiac, pulmonary,
or renal disease, Asplenia, such as with sickle cell disease
B. INFLUENZA PNEUMONIA
1) Agents: Influenza A and B
2) Difficult to distinguish clinically from bacterial pneumonia
3) Management:
a) Supportive (antipyretics and bed rest)
b) Early antiviral therapy may have some benefit (oseltamivir for 5 days)
i) Shortens the course of illness by 1-2 days
4) Prevention: Vaccination for influenza A is recommended
IV. PULMONARY TUBERCULOSIS
1) About a million Filipinos have PTB – this is the 3rd highest prevalence in the world (WHO)
2) Mycobacterium tuberculosis – most common etiologic agent
3) Characterized by a granulomatous pulmonary reaction
4) Clinical features:
a) Chronic cough⭐ with minimal sputum production (may be blood-tinged)
b) Intermittent, Low-grade fever⭐
c) Night sweats, Weight loss⭐
5) CXR: (+) Infiltrates, cavitation, mediastinal lymphadenopathy
6) Pregnancy Outcome
a) Active pulmonary tuberculosis is associated with increased incidences of ⭐
i) Preterm delivery
ii) LBW infants
iii) IUGR
iv) Perinatal morbidity

MNTM 2022 3
 Skin testing or IGRA testing of pregnant women who are in any of the high-risk groups be done
(Healthcare workers, Contact with infectious person/s, HIV-infected individuals, Alcoholics, Drug users)
Tuberculin Skin Test (TST) Interferon-Gamma Release Assay (IGRA)
● Helpful for countries where TB is not prevalent
● Still used here in the PH since IGRA is not readily available, but the ● Preferred because it measures interferon-gamma release response to
size of induration is important antigens present in M. tuberculosis, but not BCG vaccine
● Preferred antigen: 5 units of PPD given intradermal → No interference (due to BCG vaccine) in the results
● Positive result requires evaluation for active disease, including a chest → More specific
radiograph Other Essential Tests Used for Verification of TB Infection
Risk Population Size limit to treat
HIV positive
VERY
abnormal CXR 5 mm or greater ● Chest x-ray (with abdominal shield)
HIGH RISK ● Microscopy (AFB staining) ⭐
recent contact with an active case
Foreign-born individuals ● Culture and sensitivity
IV drug users (HIV negative) ● Nucleic acid amplification assay (e.g. PCR, sputum GeneXpert)
HIGH RISK Low income populations 10 mm or greater ● In our setting in the Philippines, we usually go for clinical, tuberculin
Medical conditions that increase the
risk for tuberculosis
skin test, and chest x-ray for the diagnosis. ⭐
NO RISK 15 mm or greater

A. TREATMENT
Active TB Latent TB
1) First-line: Quadruple anti-Koch’s
a) Isoniazid (H), Rifampicin (R), Pyrazinamide (Z), Ethambutol (E) 1) (+) TST but there’s no evidence of active disease
i) Isoniazid – most hepatotoxic⭐ 2) Isoniazid 300 mg OD x 9 months
b) Preferably by directly observed therapy (DOTS) – high cure rates 3) Most recommend that isoniazid therapy be delayed until
c) 2HRZE/4HR⭐ after delivery
i) First 2 months (bactericidal phase): All 4 are given 4) Exceptions (treatment is given antepartum):
ii) Next 4 months (continuation phase): Only Isoniazid and Rifampicin are a) Known recent skin-test convertors
given b) Skin test positive women exposed to active
2) Second-line regimens: Ototoxic to the fetus therefore are contraindicated infection
a) Aminoglycosides⭐ (streptomycin, kanamycin, amikacin, and capreomycin) c) HIV-positive women
i) Streptomycin has a known teratogenic effect⭐
3) Breastfeeding is not prohibited⭐ during anti-TB therapy

Final Remarks from Dr. Mallen Review of Pulmonary Physiology in Pregnancy

● In terms of pregnancy outcomes, is not hard to recall the effects of Vital Capacity and Increase by ~20% by late pregnancy
pulmonary disorders to the baby Inspiratory Capacity
→ Preterm delivery Expiratory Reserve Decreases from 1.3 L to 1.1 L
→ IUGR Volume
→ Low birth weight Tidal Volume Increases ~40% (secondary to respiratory
● Infections must be treated immediately stimulation by progesterone)
● If experiencing mild symptoms, physical activity should be limited Minute Ventilation Increases 30-40% due to increased tidal
● As the obstetrician, make sure to assess the patient for possible growth volume
restrictions, maternal weight gain, FH via ultrasound, doppler, etc. Arterial PO2 Increases from 100-105 mmHg
● The manner of delivery, despite the presence of a concomitant pulmonary Arterial PCO2 Decreases from 40 to 32 mmHg
disorder, does not automatically mean that CS is indicated Residual Volume Decreases ~20% from 1.5 L to 1.2 L
→ Patients with asthma, pneumonia, or controlled TB may still have a trial Chest Wall Reduced by 1/3 (due to the expanding
of normal delivery Compliance uterus and increased intraabdominal
pressure)
Functional Residual Decreases ~10-25%
Capacity

MNTM 2022 4
 I. PREGNANCY-INDUCED URINARY TRACT CHANGES
1) Kidneys become larger, dilatation of the renal calyces and ureters
a) Develops before 14 weeks and likely is due to progesterone- induced relaxation of the muscularis
b) More marked dilatation is apparent beginning in mid- pregnancy because of ureteral compression, especially on the right side
i) The uterus becomes dextro-rotated causing compression in one of the tract of the ureters
2) Certain degree of vesicoureteral reflux occurs
a) An important consequence of these physiological changes is an increased risk of upper urinary infection, and occasionally erroneous
interpretation of studies done to evaluate obstruction
3) Plasma flow ↑ 40% and glomerular filtration ↑ 65%
a) Substances excreted more rapidly, fewer are left in the bloodstream
b) Consequently, serum concentrations of creatinine and urea (BUN) decrease substantively across pregnancy, and values within a non-
pregnant normal range may be abnormal for pregnancy
i) Thus lower cut-off are used for pregnant women because creatinine and BUN are decreased during pregnancy
ii) If the serum creatinine level in pregnancy persistently exceeds 0.9 mg/dL (75 μmol/L), intrinsic renal disease should be suspected
II. ASSESSMENT OF RENAL FUNCTION DURING PREGNANCY
1) Urinalysis is essentially unchanged during pregnancy, except for occasional glucosuria, regardless if pre pregnancy or during the course of
pregnancy
a) Proteinuria must exceed 300 mg/day to be considered abnormal
i) Urinary albumin-to-creatinine ratio (ACR) in a spot urine sample – ideally from a first-morning void – is helpful in estimating a 24-hour
albumin excretion rate (AER), in which ACR (mg/g) approximates AER (mg/24h)
(1) ≥ 0.3 correlates with a 24-hr urine CHON ≥ 300 mg | U
2) Sonography (KUB or kidney, ureters, and urinary bladder) provides imaging of renal size, relative consistency, and elements of obstruction
3) Full-sequence IV pyelography is not done routine
a) Makes use of an abdominal ultrasound radiograph → IV contrast dye → 20-30 mins → X-ray
b) One shot of IVP dye is given instead of 4 and 5
c) Usually done on the 2nd or 3rd trimester
d) Limited IVP – makes use of only 2 or 3 films
4) Renal biopsy is relatively safely performed during pregnancy, but is usually postponed unless results may change therapy
III. URINARY TRACT INFECTIONS
1) Asymptomatic bacteriuria is the most common bacterial infection during pregnancy
2) Organisms that cause urinary infections are those from the normal perineal flora
a) E. coli in non-obstructive nephritis
b) + Adhesin – P or S fimbriae enhance bacterial adherence
3) Risk factors that predispose a woman to UTI in the puerperium
a) Episiotomy, periurethral lacerations, or vaginal wall hematomas : Sensation of bladder distention can be diminished by discomfort
i) Labor and trauma or conduction analgesia → bladder sensitivity to intravesical fluid tension is decreased
b) Catheterization to relieve retention commonly leads to urinary infection – due to inoculation of bacteria (skin flora)
c) Epidural, regional, spinal anesthesia
i) Return of the bladder function is not brisk → don’t perceive the urge to urinate → stasis
A. ASYMPTOMATIC BACTERIURIA
1) Persistent, actively multiplying bacteria within the urinary tract in asymptomatic women Treatment of Asymptomatic Bacteriuria
2) Present in 2-7% of pregnant women, more common in diabetics
Single-dose Treatment 3-day course
3) Etiology:
a) E. coli (63%), Klebsiella pneumonia (12%), Enterococcus (12%), Staphylococcus
● Amoxicillin, 3 g ● Amoxicillin, 500 mg TID
saprophyticus (7%), Staphylococcus aureus (4%), Klebsiella ozanae (2%) ● Ampicillin, 2 g ● Ampicillin, 250 mg QID
4) If not treated: 25% of infected women will develop symptomatic infection (cystitis and ● Cephalosporin, 2 g ● Cephalosporin, 250 mg
pyelonephritis) - associated with preterm delivery and low birthweight infants
● Nitrofurantoin, 200 mg QID
● Trimethoprim- ● Ciprofloxacin, 250 mg BID
5) Diagnosis sulfamethoxazole, ● Levofloxacin, 250 or 500
a) Screening at first prenatal visit (9th-17th week AOG; 16th week most preferred) 320/1600 mg mg QD
i) Urine culture (clean-catch) – test of choice ● Nitrofurantoin, 50-100 mg
(1) >100,000 organisms/mL is diagnostic (presence of > 100,000 CFU/mL of QID or 100 mg BID
the same pathogen in 2 consecutive midstream urine specimens OR ≥ 100 ● Trimethoprim-
CFU/mL of a single uropathogen in one catheterized urine specimen) sulfamethoxazole, 160/800
(2) Susceptibility determination is not necessary because initial treatment is mg BID
empirical Others
ii) Alternative test: Urine gram stain of uncentrifuged urine (>1 organism in OIF) ● Nitrofurantoin, 100 mg QID for 10 days
iii) Not acceptable: Urinalysis, urine dipstick ● Nitrofurantoin, 100 mg BID for 5-7 days
b) Urine culture may be requested, but it is not routinely done, so empiric therapy is ● Nitrofurantoin, 100 mg at bedtime for 10 days
actually given ● Nitrofurantoin, 100 mg QID for 21 days – treatment failure
6) Treatment ● Nitrofurantoin, 100 mg at bedtime for pregnancy remainder
– suppression for recurrence
a) Empiric antibiotic treatment is given regardless of whether urine culture is
Local guidelines: preferred regimen
requested or not
b) Treat even if low concentration – 20,000 to 50,000 can develop pyelonephritis ● Nitrofurantoin macrocrystals 100 mg QID x 7 days
• BID formulation is not locally available
c) Penicillins and Cephalosphorins – safest • Limit use to 2nd trimester to 32 weeks only due to risk of
d) Limit Levofloxacin – given with caution hemolytic anemia & birth defects
e) Nitrofurantoin – given if there is treatment failure ● TMP-SMX 160/800 mg BID x 7 days
f) Fosfomycin - Available single dose treatment locally • Avoid in 1st & 3rd trimester due to teratogenicity and
* As much as possible, avoid single dose treatment (Dr. Ong, 2021) → Comes in kernicterus
sachet, can be mixed with juice or water ● Cefalexin 500 mg BID x 7 days
7) Fluoroquinolones are contraindicated in pregnancy ● Cefuroxime 500 mg BID x 7 days
8) Follow-up ● Amoxicillin-clavulanate 625 mg BID x 7 days
a) Repeat urine CS 1 week after treatment • Avoid for those at risk for pre-term delivery due to
b) Do monitoring (using urine culture) every trimester (Because of 30% recurrence possible NEC complication
rate) ● Fosfomycin 3 g single-dose sachet

MNTM 2022 1
B. CYSTITIS
1) Characterized by dysuria, urgency and frequency, but with few associated systemic findings Cystitis: preferred regimen
(usually without fever)
● Cefalexin 500 mg QID x 7 days
a) (+) Pyuria and bacteriuria
● Cefadroxil 1 g BID x 7 days
b) ± Microscopic hematuria
● Cefaclor 500 mg TID x 7 days
c) Gross hematuria common in hemorrhagic cystitis
● Cefuroxime 500 mg BID x 7 days
d) Upper urinary tract may become involved by ascending infection ● Cefixime 200 mg BID x 7 days
2) Etiology: E. coli, other Enterobacteriaceae, Group B Streptococcus ● Cefpodoxime 100 mg BID x 7 days
3) Diagnosis ● Nitrofurantoin macrocrystals 100 mg QID x 7 days
a) Midstream urine specimen for urinalysis and/or urine C/S ● TMP-SMX 160/800 mg BID x 7 days
i) Significant pyuria: ● Amoxicillin-clavulanate 625 mg BID x 7 days
(1) ≥ 8 pus cells/mm of uncentrifuged urine; OR
3
● Pivmecillinam 400 mg BID x 7 days
(2) ≥ 5 pus cells/HPF of centrifuged urine AND (+) leukocyte esterase and nitrite ● Fosfomycin 3 g single-dose sachet
test on dipstick
ii) Even without significant pyuria (e.g. only 7 pus cells), still treat if symptomatic
4) Follow-up
a) Repeat urine culture 1-2 weeks after completion of treatment
b) Monthly urine CS tests until delivery of pregnant patients with any of the ff:
i) Pyelonephritis, recurrent UTIs, concurrent GDM, concurrent nephrolithiasis/urolithiasis, preeclampsia
ii) Urethritis
(1) Lower urinary tract symptoms with pyuria accompanied by a sterile urine culture may be from urethritis caused by Chlamydia
trachomatis
(2) Mucopurulent cervicitis may coexist
(3) Treatment: Azithromycin
C. ACUTE PYELONEPHRITIS
1) Renal infection is the most common serious medical complication of pregnancy
a) Leading cause of septic shock during pregnancy
Differential Diagnosis (due to pain)
b) Urosepsis is related to increased incidence of cerebral palsy in preterm infants
2) Clinical findings • Labor
a) Urinalysis: many leukocytes, usually in clumps; (+) bacteria • Chorioamnionitis
b) Urine c/s: E. coli is isolated from urine or blood in 70-80% • Appendicitis
c) Spiking fever, shaking chills, nausea and vomiting, and flank pain (in one or both lumbar o Appendix gets dislodged and can be
regions) directed upwards during the 2nd and
i) Flank pain: Unilateral and right-sided in more than ½ of cases 3rd trimester
(1) Right side has more dilatation and stasis due to the dextrorotation of the uterus, • Placental abruption
compressing it more on the right compared to the left PE: (+) CVA tenderness • Infarcted leiomyoma
3) Risk factors: nulliparity, young age, more frequently in 2nd trimester
4) Complications
a) Endotoxin-induced hemolysis – common, a third of patient with pyelonephritis develop anemia
b) Varying degrees of respiratory insufficiency from endotoxin- induced alveolar injury manifest in some and may result to frank pulmonary edema
i) Pulmonary injury may be severe in some cases that it causes acute respiratory distress syndrome
c) Uterine activity from endotoxin → related to fever severity
5) Diagnosis IV antimicrobial therapy is usually empirical : until afebrile
(change to oral antimicrobials once afebrile)
a) Urinalysis and gram stain are recommended
DOC: Ampicillin + Gentamicin
i) Many WBCs, usually in clumps; (+) numerous bacteria Alternative: Cefazolin or Ceftriaxone, Extended-spectrum antibiotic
ii) ≥ 5 WBC/HPF of centrifuged urine in urinalysis ✓ Preferred PARENTERAL ✓ Preferred ORAL regimen:
b) Urine C/S should be performed routinely regimen 14-day treatment
i) It is imperative that we do Urine C/S to adjust the appropriate treatment ● Ceftriaxone 1-2 g IV q24h ● Cefalexin 500 mg QID
(Dr. Santiago, 2021) ● Cefotaxime 1-2 g IV q8h ● Cefuroxime 500 mg BID
ii) E. coli is isolated from urine or blood in 70-80% ● Ceftazidime 2 g IV q8h ● Cefixime 200 mg BID
iii) > 10,000 CFU/mL on urine C/S
● Ampi-Sulbactam 1.5 g IV ● Amoxicillin-clavulanate 625
c) Blood C/S is not routinely recommended q6h mg BID
i) May be done in patients presenting with signs of sepsis ● Pip-Tazo 2.25 g IV to 4.5 g
d) Routine renal ultrasound is of limited clinical benefit IV q6-8h
i) Reserved for patients who do not respond to initial treatment ● Ampicillin + Gentamicin
6) Management Follow up
a) Indications for admission: ● Repeat urine culture 1-2 weeks after antimicrobial therapy
i) Inability to maintain oral hydration or take medications completed
ii) Concern about patient compliance ● Monthly urine C/S until delivery
iii) Presence of comorbid conditions Obstruction and Abscess
iv) Severe illness: High-grade fever, severe pain, marked debility With persistent spiking fever or lack of improvement by 48-72 h
v) Signs of preterm labor, sepsis Obstruction: Renal sonography (pelvocaliceal dilatation)
b) Admit patient (because patient needs to be monitored) • Cystoscopic placement of double J ureteral stent – encrusted
i) Obtain urine and possibly blood cultures and need replacement
• Percutaneous nephrostomy – preferred
ii) Evaluate CBC, serum creatinine, and electrolytes
Intrarenal or perinephric abscess or phlegmon:
iii) Monitor vital signs frequently, including urinary output • Extend IV antibiotics
(1) Establish urinary output ≥ 50 mL/hr with IV crystalloid solution • Ultrasound-guided drainage if large
iv) Obtain chest X-ray if there is dyspnea or tachypnea
v) Repeat hematology and chemistry studies in 48 hours
c) IV hydration to ensure adequate urinary output – cornerstone of treatment
d) Paracetamol or Acetaminophen for fever
e) Discharge when afebrile for 24 hours
i) After discharge, most recommend oral therapy for a total of 7- 14 days
f) Other diagnostic procedures:
i) Non-diagnostic UTZ – X-ray abdomen or one-shot IV pyelogram (30 mins after contrast injection)
ii) MRI – can be done to determine cause of persistent infection

MNTM 2022 2
 IV. NEPHROLITHIASIS
1) Most stones in pregnancy are calcium phosphate or hydroxyapatite
a) Rule out hyperparathyroidism
b) A low-calcium diet promotes stone formation
c) Thiazide diuretics diminish stone formation
2) Indications for stone removal (by flexible basket via cystoscopy)
a) Obstruction, infection, intractable pain, heavy bleeding/gross hematuria
3) Daily calcium allowance in pregnancy = 1-1.2 g (Most common is 600 mg/tab; give 1 tab, BID throughout pregnancy)
A. NEPHROLITHIASIS DURING PREGNANCY
1) Pregnant women may have fewer symptoms with stone passage because of urinary tract dilatation
a) 90% present with pain
2) DIAGNOSIS
a) Sonography may be used to visualize stones, but many are not detected because hydronephrosis may obscure findings
i) Less exposure to radiation
b) If there is abnormal dilatation without stone visualization, then the limited IVP (one shot pyelogram) may be useful
i) Not all stones are visible during US: CT stonogram (in non-pregnant); but since CT is contraindicated in pregnancy, then we can do the
one-shot pyelogram
ii) IV urography (IVU/IVP) consists of initial KUB xray followed by a 2nd radiograph obtained 20-30 mins after the IV injection of a contrast
medium
(1) Initial KUB radiograph exposes the fetus to 0.002 Gy; however, because the standard IVU necessitates 4 or 5 films, the patient may
be exposed to a total of 0.004-0.01 Gy
(2) Dose of radiation during IVU has been reported to be safe to the fetus during the 2nd and 3rd trimesters
iii) Limited IVP, however, has been shown to successfully reveal calculi without the high radiation dose of full IVP
(1) Stothers and Lee (1992) recommend a scout film, a 30-sec film, and a 20-min film
3) MANAGEMENT
a) If stone is few and patient is asymptomatic: Observe or conservative management by adequate hydration
b) Majority of symptomatic women will have improvement with conservative therapy, and the stone usually passes spontaneously
i) IV hydration + analgesics (Acetaminophen, Paracetamol, Meperidine, Morphine)
(1) NSAIDs are associated with cardiac malformations, early spontaneous abortions, premature closure of ductus arteriosus, and neonatal
pulmonary hypertension
(a) Risks vs benefits of these medications must be weighed, can instead give paracetamol or tramadol
c) Temporizing measures to relieve obstruction:
i) Ureteral stenting or percutaneous nephrostomy
d) Definitive:
i) Transurethral laser lithotripsy
ii) Ureteroscopic stone removal – most common indication is to treat upper urinary tract calculi, particularly those that are either unstable for
extracorporeal shockwave lithotripsy
(1) Flexible telescope inserted into the bladder
iii) Extracorporeal shockwave lithotripsy (ESWL) is contraindicated in pregnancy

MNTM 2022 3
 I. HEMATOLOGIC CHANGES IN PREGNANCY
1) Hypervolemia associated with normal pregnancy averages 40 to 45 percent above the nonpregnant blood volume after 32 to 34 weeks
a) Metabolic demands of the enlarged uterus and hypertrophied vascular system, support the rapidly growing placenta and fetus
b) Protects against impaired venous return in the supine and erect positions (IVC compression)
c) Safeguards mother against the adverse effects of parturition- associated blood loss
2) Blood volume expansion → both plasma > erythrocytes (Hgb and Hct slight decrease from dilution)
a) Platelets decrease⭐ from inherent platelet consumption and hemodilution
b) Leukocytes = Neutrophilic Leukocytosis; Coagulation Factors = Hypercoagulable State; ESR = increase will cause a decrease in blood viscosity
3) The disproportion between the rates at which plasma and erythrocytes are added to the maternal circulation is greatest during the second trimester
4) One of the most common cause of anemia during pregnancy is IDA, that’s why iron supplementation is routinely given among pregnant women
→ Iron requirement during pregnancy ACQUIRED
■ 1000 mg Iron deficiency anemia*
− 300 mg – fetus and placenta Anemia caused by acute blood loss*
− 500 mg – maternal hemoglobin expansion Anemia of inflammation of malignancy
− 200 mg – obligatory losses, primarily through the GIT Megaloblastic anemia
■ 6-7 mg/day Acquired hemolytic anemia
Aplastic or hypoplastic anemia
Hemoglobin Cut-off Trimester ⭐ HEREDITARY
11 g/dL First Trimester
Thalassemias
10.5 g/dL Second Trimester
Sickle-cell hemoglobinopathies
11 g/dL Third Trimester
Other hemoglobinopathies
A. EFFECTS ON PREGNANCY OUTCOME Hereditary hemolytic anemias
1) The specific cause of anemia is important when evaluating effects on
pregnancy outcome
a) Maternal and perinatal outcomes are seldomly affected by moderate iron deficiency anemia, yet they are altered markedly in women with
sickle cell anemia
b) Children born to iron-deficient women and without iron supplementation reported to have lower mental development scores
2) Incidence of preterm delivery, LBW, and lower APGAR scores increases as anemia becomes more severe
3) Significant effect on maternal heath → Increased fatigue, risk of infection, risk of post-partum hemorrhage due to uterine atony
II. IRON DEFICIENCY ANEMIA
● The amount of iron diverted to the fetus is similar in a normal and in an iron-deficient mother
→ Newborn infant of a severely anemic mother does not suffer from iron deficiency anemia
→ Neonatal iron stores are related to maternal iron status and to timing of cord clamping
→ In the third trimester, additional iron is needed to augment maternal hemoglobin and for transport to the fetus

A. DIAGNOSIS
1) Initial evaluation should include:
a) CBC – ↓ Hgb, Hct, red cell indices, best to screen
b) Peripheral blood smear (hypochromia, microcytosis)
i) Hypochromia and microcytosis is a characteristic finding that is less prominent in
pregnant than in non-pregnant women with IDA
c) Iron Studies
i) Total Iron Binding Capacity (TIBC) ↑⭐
(1) Refers to the maximum amount of iron that can be bound to transferrin if it
were 100% saturated
ii) Serum Fe↓
iii) Transferrin Saturation (TS) ↓
(1) How much iron is bound to transferrin
iv) Serum ferritin levels↓
(1) Serum ferritin levels <10 to 15 mg/L confirm IDA⭐
v) Hepcidin ↓ – master regulator of iron availability; decreased normally in pregnancy but in iron deficiency, levels follow those of serum ferritin

B. TREATMENT
1) Regardless of anemia status, daily iron oral supplementation with 30-60 mg of elemental iron (60 mg usual preparation) ⭐ and 400 μg or 4mg (if
at risk for neural tube defects) of folic acid is recommended in normal pregnancy (during the second trimester, when the effects of nausea and
vomiting aren’t present)
a) Iron-rich diet
i) Most easily absorbed iron is from red meat, fish, and poultry
ii) Vegetarian options include lentils, fortified cereals, and green leafy vegetables
iii) Factors affecting absorption (acidic promotes while alkaline decreases)
(1) Iron absorption enhancers – vitamin C (citrus, kiwi, strawberries, tomatoes)
(2) Iron absorption inhibitors (red wine, eggs, coffee, tea, and food containing calcium such as milk) should not be taken concomitantly
with iron supplements
2) For iron-deficiency anemia, resolution and restitution of iron stores can be accomplished with simple iron compounds – ferrous sulfate, fumarate,
or gluconate that provide about approximately 200 mg daily of elemental iron (2-3x of 60mg) ⭐
a) Parenteral therapy⭐ is given IF oral iron is not tolerated (gastric irritation, constipation, black stools, nausea, and occasionally diarrhea)
i) Ferrous sucrose > iron-dextran in terms of safety
3) Response
4) A hematological response is detected by an elevated reticulocyte count – 1ST WEEK
5) The rate of increase of hemoglobin concentration or hematocrit is typically slower than in nonpregnant women due to increasing and larger
blood volumes during pregnancy – 2ND WEEK, 1 g/dL per week

MNTM 2022 1
 III. THALASSEMIA
● Impaired synthesis of one or more of the normal globin peptide chains
→ Heme group is made up of ⍺ and β globin chains
→ There could be hundreds of mutations affecting those genes that encode for the globin peptide chains which would lead to the manifestation of
negative effects
■ Example: Point mutation, deletion, transmutations, etc.
● Characterized by varying degrees of ineffective erythropoiesis, hemolysis, and anemia
● Classified according to the globin chain that is deficient (⍺ and β thalassemia

A. DIAGNOSIS
1) CBC - Low Hgb, Hct, MCV, normal RDW, normal serum ferritin⭐
2) Peripheral blood smear - Microcytic, polychromatic, target cells
3) Hemoglobin electrophoresis (commonly used) or high-performance liquid
chromatography is used
a) Fractions of hemoglobin A, A2, F, H, E, and other variants are measured
4) Genetic analysis for both β-thalassemia and ⍺-thalassemia mutations are
necessary
a) Reason: Mutations may overlap on the screening test, resulting in
incorrect diagnosis or a false negative
Fetal Diagnosis
1) DNA analysis using molecular techniques – invasive: chronic villous sampling or amniocentesis
2) Fetal cardiothoracic ratio (↑) at 12 to 13 weeks gestation can be used to identify affected fetuses (sonographically)
3) Doppler velocimetry of the middle cerebral artery – severe anemia can be detected
B. CLASSIFICATIONS
⍺-thalassemias
● Two main groups of ⍺-thalassemia determinant | 
→ ⍺0-thalassemia – deletion of both loci from one chromosome (--/⍺⍺)
→ ⍺+-thalassemia – loss of a single locus from one allele (-⍺/⍺⍺ heterozygote) or loss from each allele (-⍺/-⍺)
● Frequency
→ All these variants are encountered in Asians
→ In those of African descent, hemoglobin H disease is rare and hemoglobin Bart disease is unreported
Phenotype Genotype # DEL Pregnancy Outcome
Normal ⍺⍺/⍺⍺
-⍺/⍺⍺
Normal; silent carrier 1 No consequence
⍺⍺/-⍺
⍺-thalassemia -⍺/-⍺
2 Minimal to moderate hypochromic microcytic anemia of no maternal consequence
minor --/⍺⍺
Newborn will have abnormal red cells containing a mixture of Hgb Bart (𝝲4), Hgb H (β4), and Hgb A
HgB H (β4)
Neonate appears normal but soon develops hemolytic anemia as most of the Hgb Bart is replaced by
With moderate to
--/-⍺ 3 Hgb H
severe hemolytic
Anemia is moderate to severe and it usually worsens during pregnancy
anemia
Compound heterozygous type
Incompatible with survival; usually results in stillbirth or neonates die very soon after birth, fetus at risk
HgB Bart of IUGR
disease, Hydrops --/--⭐ 4 Neonates exhibit the typical features of non-immune hydrops fetalis
fetalis⭐ Increased affinity for oxygen
Maternal complications: early onset severe pre-eclampsia, shoulder dystocia, postpartum hemorrhage
β-thalassemias
● Secondary to impaired β-globin chain production or a-chain instability, decreased β-chain production
● Excess ⍺-chains precipitate to cause cell membrane damage (Due to a-chain instability)
β-thalassemia minor β-thalassemia major “Cooley anemia”
Heterozygous (one gene is defective)
2 genes are defective
Composed of two alpha and two delta globin chains
• Heterozygous (one gene is defective) • Serious and frequently fatal disorder
• Composed of two alpha and two delta globin ■ Failure to thrive, Poor brain development
chains |  ■ Characteristic “chipmunk” facie
• Most cases encountered have elevated − Poor bone development due to hypoplastic bone marrow, resulting in frontal
hemoglobin A2 levels bossing
• Some patients do not have anemia; others have • Due to a reduced or non-existent β-globin chain
mild to moderate microcytic hypochromic ■ Intense hemolysis and severe anemia
anemia − Transfusion dependent → increased iron load → hemochromatosis (diffuse)
− Hemosiderosis → focal and no tissue damage
• Transfusions⭐ are given throughout pregnancy to maintain hemoglobin
• Iron and folate⭐ supplements are given
concentration at 10 mg/dL⭐, every 3 months or depending on severity
• Folic acid may be given at 5 mg/day ⭐
■ Every time the hemoglobin drops to less than 10, start the transfusion of around
(recommended dose) 2 to 3 bags to increase the hemoglobin to more than 10
■ Folic acid deficiency has been reported as a ■ increased risk for iron overload → iron chelation therapy
result of increased erythropoiesis
• Fetal growth surveillance
• Pregnancy is considered advisable if there is normal maternal cardiac function

MNTM 2022 2
C. MANAGEMENT AND COMPLICATIONS
Oral Iron Therapy Iron Chelation
Only if serum ferritin is <30 mg/dL, otherwise may lead to iron overload 3 months prior to conception - Desferasirox and Deferiprone (DFP)
No parenteral option for pregnant + B-thalassemia⭐ (okay for non must be ideally discontinued, converted to DFO iron chelation
pregnant with B-thalassemia) 1ST TRIMESTER – Teratogenic, contraindicated
2ND AND 3RD TRIMESTER - Desferrioxamine IV (DFO)
Delivery: Thalassemia is not an indication for cesarean section, not required in the absence of an obstetric indication
Complications: Cardiac failure, alloimmunization, thrombosis, osteoporosis
New endocrinopathies: DM, hypothyroidism, hypoparathyroidism (increasing iron burden)
IV. THROMBOCYTOPENIA
1) <150,000/μL platelets (quantitative platelet count)
a) Gestational thrombocytopenia (75%) – most common
b) Preeclampsia and HELLP syndrome (20%)
i) HELLP – Hemolysis, Elevated Liver enzymes, Low Platelet
c) Obstetrical coagulopathies – DIC, massive transfusion protocol (MTP)
i) DIC occurs in several obstetrical emergencies such as sepsis from an infected abortion and a result of end -of-the-spectrum in HELLP
syndrome
ii) MTP which is given in patients with DIC can even aggravate the thrombocytopenia
d) Immune thrombocytopenic purpura
e) Other
i) Systemic lupus erythematosus and antiphospholipid antibody syndrome (APAS)
ii) Infections – viral and sepsis syndrome
iii) Drugs, Hemolytic anemias, Thrombotic microangiopathies and malignancies
GESTATIONAL THROMBOCYTOPENIA
● Usually evident in the third trimester⭐ and is thought to be predominantly due to hemodilution (increased splenic mass may contribute)
● A platelet count of < 80,000/μL⭐ should trigger an evaluation for etiologies other than incidental or gestational thrombocytopenia⭐
● Management:
→ < 150 000 Observe, serial platelet monitoring
→ < 80 000 , signs of bleeding : Do more diagnostic tests OR Possibly a platelet concentrate transfusion⭐
IMMUNE THROMBOCYTOPENIC PURPURA
1) “Idiopathic Thrombocytopenic Purpura” (ITP) - Caused by a cluster of IgG antibodies directed against one or more platelet glycoproteins
a) Secondary forms of chronic thrombocytopenia appear in association with systemic lupus erythematosus, lymphomas, leukemias, and several
systemic diseases
b) No irrefutable evidence that pregnancy increases the risk of relapse in women with previously diagnosed ITP or worsens thrombocytopenia in
women with active disease
2) Patient presents with low platelet and common clinical signs like petechiae or gum bleeding, chronic that resolves spontaneously
3) Diagnosis
a) Platelet counts usually range from 10,000 to 100,000/μL
i) Range overlaps with gestational thrombocytopenia and thus diagnosis of ITP requires a high degree of suspicion
b) Abnormal antiplatelet antibody test
i) Best diagnostic test
c) Bone Marrow Aspiration (BMA) which will show very low platelet and precursor cells
4) Management
a) Therapy is considered if the platelet count is less than 30,000 to 50,000/μL⭐
b) Primary treatment includes IVIG or corticosteroids⭐
Prednisone, 1 mg/kg daily⭐ IVIG given in a total dose of 2⭐ g/kg for 2 to 5 days
MoA: Delay destruction of platelets, suppress the phagocytic activity MoA: neutralizes anti=platelet antibodies
of the splenic monocyte-macrophage system More rapid (1-2 days)
Less rapid (2-3 weeks) More effective but more expensive
c) Open or laparoscopic splenectomy may be effective if no response
i) In late pregnancy, surgery is difficult and cesarean delivery may be necessary for exposure
d) Thrombopoietin agonist, Romiplostim, has improved responses
5) Pregnancy complications: Stillbirth, IUFD, fetal loss, preterm birth
6) Fetal and Neonatal Effects
a) Thrombocytopenia: Platelet-associated IgG antibodies cross the placenta
i) Direct fetal blood sampling is necessary
(1) Done to detect fetal thrombocytopenia
(2) More invasive procedures should be done to do this
ii) Severe neonatal thrombocytopenia is defined as < 50,000/μL
(1) We have to watch out for bleeding (intracranial or other sites) in the baby
b) Fetal death from hemorrhage occurs occasionally (really severe thrombocytopenia)
c) The severely thrombocytopenic fetus is at increased risk for intracranial hemorrhage with labor and delivery, but this is unusual
i) Intracranial hemorrhage may be exacerbated or triggered by labor and delivery
ii) NSD or vaginal birth is not a contraindication for these patients

MNTM 2022 3
 I. CONNECTIVE DISSUE DISORDERS IN PREGNANCY
1) Also termed as “collagen vascular disorders”
2) Two basic underlying causes:
a) Autoantibody-mediated immune complex disease (Rheumatic diseases)
i) CT damage is caused by deposition of immune complexes in specific tissues or organs
ii) Manifests as sterile inflammation – predominantly of the skin, joints, blood vessels, and kidneys
iii) Ex. SLE, RA – more prevalent in women
b) Inherited Disorders of bones, skin, cartilage, blood vessels, and basement membranes
i) Ex. Marfan syndrome, osteogenesis imperfecta, Ehlers-Danlos syndrome
II. IMMUNE-MEDIATED CONNECTIVE TISSUE DISEASES
1) Two types:
a) Rheumatoid factor (RF)-associated
i) RF: Auto-antibody found in many autoimmune inflammatory conditions
ii) Ex. SLE, RA, scleroderma, mixed connective tissue disease, dermatomyositis, polymyositis, various vasculitis syndromes
b) RF-seronegative spondyloarthropathies
i) Associated with HLA-B27 antigen
ii) Ex. Ankylosing spondylitis, psoriatic arthritis, Reiter disease
2) Pregnancy may lessen the activity of some of these conditions as a result of immunosuppression that also allows successful engraftment of fetal
and placental tissues
a) Fetal cells and free fetal DNA are detectable in maternal blood beginning early pregnancy
i) Fetal cell microchimerism
(1) Persistence of fetal cells in the maternal circulation and organs following pregnancy → may stimulate autoantibodies or become
engrafted in maternal tissues
(2) Explains why some immune-mediated diseases may either be caused or activated as a result of previous pregnancies
b) On the other hand, immune-mediated disease may contribute to obstetrical complications
c) The two most common connective tissue disorder which are common during pregnancy are Systemic Lupus Erythematosus (SLE) and
Antiphospholid syndrome (APS)
III. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
● Heterogeneous autoimmune disease with a complex pathogenesis that results in interactions between susceptibility genes and environmental factors
● Multisystem, chronic inflammatory autoimmune disease with a high prevalence in females of child-bearing age
→ Prevalence in those of childbearing age ~ 1 in 500
→ Encountered relatively frequently during pregnancy
● Almost 90% of SLE cases are women
● Causes of SLE-associated mortality:
→ Infection, Lupus flares, End-organ failure, Hypertension, Stroke, Cardiovascular disease
Organ System Manifestations %
Clinical Criteria Description
Systemic Constitutional symptoms: Fatigue, hair loss, malaise, 95
unexplained fever, weight loss Discoid rash Erythematous patches, scaling, follicular
plugging
Musculoskeletal Arthritis, arthralgias, inflammatory myositis, myalgias, 95
polyarthritis, myopathy Oral ulcers Usually painless oral and nasopharyngeal ulcers
Hematological Coombs positive hemolytic anemia, lymphopenia, hemolysis, 85 Photosensitivity Exposure to UV light causes rash
leukopenia, thrombocytopenia, lupus anticoagulant, Arthritis Non-erosive, involving ≥ 2 peripheral joints with
splenomegaly tenderness, swelling or effusion
Cutaneous Photosensitive rash or the Malar (butterfly) rash, discoid rash, 80 Malar rash Malar erythema
(Mucocutaneous) photosensitivity, oral/nasal ulcers, alopecia, skin rashes Immunologic Anti-dsDNA or anti-Sm antibodies, or false
Neurological Cognitive dysfunction, mood disorder, headache, seizures, 60 positive VDRL, abnormal level of IgM or IgG
stroke, coma anticardiolipin antibodies, or lupus anticoagulant
Cardiopulmonary Pleural effusion, Pericardial effusion, Pulmonary fibrosis, 60 Neurologic Seizures or psychosis without other cause
pleuritis, pericarditis, myocarditis, endocarditis, pneumonitis, Renal Proteinuria > 0.5 g/day or > 3+ dipstick, or
pulmonary hypertension cellular casts
Renal Glomerulonephritis, Lupus nephritis, Proteinuria, nephrotic 30- ANA Abnormally elevated ANA titers
syndrome, renal failure 50 Serositis Pleuritis or pericarditis
Gastrointestinal Nausea, pain , diarrhea, abnormal liver enzyme levels 40 Hematologic Hemolytic anemia, leukopenia, lymphopenia, or
Vascular Thrombosis: venous (10%), arterial (5%) 15 thrombocytopenia
Ocular Conjunctivitis, sicca syndrome 15
● If equal??? to or > 4 criteria are present at any time during disease course (serially or simultaneously), SLE can be diagnosed with 75% specificity and
95% sensitivity
Diagnosis
1) Signs and symptoms of normal pregnancy must be differentiated from those of SLE exacerbations
2) Physiological changes in pregnancy that may overlap with features of active disease: ⭐
Drug Induced Lupus⭐
a) Chloasma⭐, Transient facial blush, Palmar erythema, Alopecia
● Procainamide, Quinidine,
b) Edema
Hydralazine, -Methyldopa,
i) Especially those around the knee joints⭐ can occur in the late stages⭐ of pregnancy
Phenytoin, Phenobarbital
ii) Should be differentiated from arthritis of SLE
● Rarely associated with
3) Identification of antinuclear antibodies (ANA) → Best screening test |  glomerulonephritis and usually
a) Positive result is not specific for lupus regresses when the medication is
4) Antibodies to double-stranded DNA (anti-dsDNA) ⭐ and to Smith (anti-Sm) antigens are relatively discontinued
specific for lupus |  ● (+) Anti-Histone in 95%
5) Other laboratory findings:
a) False-positive syphilis serology (VDRL)
b) Prolonged PTT
c) Higher rheumatoid factor levels
d) Elevated serum D-dimer levels often follow a flare or infection
i) Unexplained persistent elevations are associated with a high risk for thrombosis

MNTM 2022 1
Lupus and Pregnancy
1) During pregnancy, lupus can unchanged, improve, or worsen without warning
2) Newly diagnosed lupus during pregnancy tends to have a severe course
3) Effect of SLE on pregnancy:
a) Significantly higher risk of thrombosis, infection, thrombocytopenia, and blood transfusion
b) Maternal mortality was 20-fold higher compared to healthy women
c) Preeclampsia complicate 16-30% of women with SLE compared to around 4.6% of pregnancies in the general obstetric population
d) Preterm birth (15-50%) – most common obstetric complications in women with SLE
i) Increased incidence (up to 50%) in women with lupus nephritis or high disease activity
ii) Majority are medically indicated due to preeclampsia, maternal SLE activity, presence of lupus nephritis, and active disease (these are the
strongest risk factors or predictors for early preterm delivery)
4) Factors which favor the best pregnancy outcome in lupus: ⭐
a) Lupus activity has been quiescent for at least 6 months prior to conception (best)
b) No lupus nephritis (manifest by proteinuria or renal dysfunction) = good sign
c) No evidence of the antiphospholipid antibody syndrome (APAS) or lupus anticoagulant = good sign⭐
d) Superimposed preeclampsia does not develop = favor pregnancy
5) Active nephritis is associated with adverse pregnancy outcomes
a) Higher incidence of gestational hypertension and pre-eclampsia (if disease flares)
i) Can cause renal insufficiency, which is more common if there are antiphospholipid antibodies
b) Most recommend continuation of immunosuppressive therapy for nephritis during pregnancy
Lupus vs Preeclampsia-Eclampsia⭐
● Chronic hypertension complicates up to 30% of pregnancies in women with SLE
● Superimposed preeclampsia is encountered more often, and earlier, in those Factor Lupus Preeclampsia
with nephritis or antiphospholipid antibodies Clinical findings Fatigue, headache, extra- Headaches,
renal signs (rash, confusion, visual
● Reasons why it is difficult to differentiate: serositis, arthritis) changes, convulsions
■ CNS involvement with lupus may culminate in convulsions similar to those Blood pressure Normal or high High
of eclampsia Anemia Hemolytic Absent
■ Thrombocytopenia, with or without hemolysis, may confuse the diagnosis Proteinuria Present
because of its similarity to the HELLP syndrome Creatinine Normal or high
■ Share similar clinical features: Edema, Anemia, Hypertension, Transaminases Normal Normal or high
Proteinuria, Hematuria, Renal impairment, Thrombocytopenia Complement  Decreased⭐ Normal
● In terms of management, lupus nephritis is usually treated with immunosuppression and severe preeclampsia/eclampsia would require delivery
● The use of SLE disease activity indices faces similar issues because there are physiologic pregnancy changes which are not accounted for in these
tools
→ Global score systems:
■ SLEDAI – instrument incorporating history, PE, and laboratory measures to gauge lupus activity; not specific for pregnancy
■ SLEDAI-2K, SELENA-SLEDAI, ECLAM, SLAM, SRI
→ Organ/system assessment scales: BILAG, BILAG-2004
→ Clinical judgment of an experienced physician may be the best tool to evaluate disease activity in some scenarios
Management of SLE in Pregnancy
1) SLE-Pregnancy Disease Activity Index (SLEPDAI) and Lupus Activity Index may be used to assess disease activity
2) Fetal well-being monitoring
a) Antenatal testing - BPS, NST, fetal movement counting
b) The fetus should be closely observed for adverse effects such as IUGR and oligohydramnios
3) Labs commonly requested to monitor disease activity:
a) CBC, platelet count – anemia, thrombocytopenia, leukopenia
b) ESR – elevated, non-specific
c) C3 levels - indicates active disease
d) Coomb’s test, reticulocyte count, bilirubin – positive Coomb’s, reticulocytosis, and unconjugated hyperbilirubinemia characterize hemolysis
e) Liver function test
f) Kidney function test, Urinalysis – proteinuria
i) Overt proteinuria that persists is an ominous sign, even more so if accompanied by other evidence of nephrotic syndrome or abnormal
creatinine levels | 
g) Anti-SS-A (anti-Ro) and anti-SS-B (anti-La) antibodies →associated fetal complications such as congenital heart block⭐
h) Confusion which may arise in interpreting lab results:
i) Pregnancy-induced thrombocytopenia and proteinuria resemble lupus disease activity
ii) ESR may be misleading because of pregnancy-induced hyperfibrinogenemia
iii) Serum complement levels are also normally increased in pregnancy
iv) Azathioprine therapy also may induce enzyme elevations
4) Unless hypertension develops or there is evidence of fetal compromise or growth restriction, pregnancy is allowed to progress to term
i) Trial of vaginal delivery should be attempted, CS is done only for appropriate indications

MNTM 2022 2
Pharmacologic Treatment of SLE in Pregnancy
1) Arthralgia and serositis can be managed by occasional doses of NSAIDs
a) Chronic or large intermittent dosing of NSAIDs is avoided due to related oligohydramnios or ductus arteriosus premature closure⭐
i) Discontinue the use of NSAIDs during 3rd trimester to prevent premature closure of the ductus arteriosus
b) Low-dose aspirin can be used throughout gestation to prevent preeclampsia
2) Corticosteroid therapy
a) Prednisone 1-2 mg/kg orally per day – severe disease
i) After the disease is controlled, this dose is tapered to a daily monitoring dose of 10-15 mg (maintenance dose)
ii) Corticosteroid therapy can lead to GDM – monitor the patient’s blood sugar
b) Methylprednisolone 1000 mg IV over 90 mins daily for the next 3 days (Pulse therapy)
i) When severe disease supervenes – usually a lupus flare – high-dose glucocorticoid therapy is given
3) Hydroxychloroquine may be continued⭐ if the patient has been taking it prior to pregnancy: 200-400 mg/day
a) Reduces dermatitis, arthritis, and fatigue
b) Although these agents cross the placenta, hydroxychloroquine is not associated with congenital
malformations
c) Long half-life and discontinuing therapy can precipitate a lupus flare, most recommend their continuation
during pregnancy
4) Immunosuppressive agents (Azathioprine)⭐ may be used in controlling active disease
a) Usually reserved for lupus nephritis or disease that is corticosteroid- resistant
b) Has a good safety record; recommended daily oral dose: 2-3 mg/kg
5) Teratogenic medications to be avoided⭐
a) Mycophenolate mofetil, Methotrexate
b) Cyclophosphamide
i) Teratogenic; not usually recommended during the first trimester of pregnancy
ii) May be used to treat severe disease after 12 weeks’ AOG
Fetal complications Neonatal Lupus Syndrome
● Adverse perinatal outcomes: ⭐ ● Characterized by lupus dermatitis (newborn skin lesion), variable
→ Stillbirth hematologic and systemic derangements, and occasionally congenital
→ IUGR⭐ heart block
→ Neonatal lupus syndrome ● Request numerous antibody tests with specific diagnosis
→ Preterm delivery → Anti-dsDNA, anti-Sm
● Worsen in mothers with a lupus flare, significant proteinuria, or → Anti-SS-A, Anti-SS-B
renal impairment and in those with chronic hypertension, → Anti-histone
preeclampsia, or both → ANA
● Adverse outcomes are more common: neuropsychiatric lupus ● Presence of Anti-Ro (Anti-SS-A) and Anti-La (Anti-SS-B)
● Reasons at least partially responsible for adverse fetal consequences: predisposes to neonatal lupus with heart block⭐
→ Decidual vasculopathy with placental infarction → Even in the presence of such antibodies, however, the incidence of
→ Decreased perfusion fetal myocarditis is only 2-3% but rises to 20% with a prior affected
child
IV. ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS)
1) Autoimmune multisystem disorder characterized by arterial, venous, or small vessel thromboembolic events and/or pregnancy morbidity in the
presence of persistent antiphospholipid antibodies
a) Mediated by one or more of the following: ⭐
i) Activation of various procoagulants
ii) Inactivation of natural anticoagulants
iii) Complement activation
iv) Inhibition of syncytiotrophoblast differentiation
b) In pregnancy: Phospholipid-containing endothelial cell or syncytiotrophoblast membranes may be damaged directly by the APA or indirectly by
antibody binding to either 2-glycoprotein I or annexin V
i) Prevents cell membranes from protecting the syncytiotrophoblast and endothelium
ii) Exposed basement membrane to which damaged platelets can adhere and form a thrombus
c) End result: Arterial or venous thromboses which may involve any/all organ system/s or pregnancy morbidity.
2) Catastrophic Antiphospholipid Antibody Syndrome (CAPS) or Asherson syndrome
a) Rapidly progressive thromboembolic disorder simultaneously affecting 3 or more organ systems or tissue
b) High mortality rate from activation of a cytokine storm
Specific Antiphospholipid Antibodies
1) 2-glycoprotein I (apolipoprotein H)
a) Inhibits procoagulant binding; prevents coagulation cascade activation
b) Reverse anti-coagulant activity and promote thrombosis
c) Important in obstetrical view point since it is expressed in high concentrations on the syncytiotrophoblast surface
2) Lupus anticoagulant (LAC)
a) Induces prolongation of PT, PTT, and Russell viper venom time (in vitro)
b) Powerful thrombotic in vivo
c) Heterogenous group of antibodies directed against phospholipid-binding proteins | 
3) Anticardiolipin antibodies (ACA)
a) Directed against one of the many phospholipid cardiolipins found in mitochondrial membranes and platelets
Clinical Features of APAS Obstetric Complications of APAS
● Venous thrombosis – thromboembolism, thrombophlebitis, livedo reticularis ● Recurrent miscarriage
● Arterial thrombosis – stroke, transient ischemic attack, Libman-Sacks cardiac vegetations, ● Early severe preeclampsia
myocardial ischemia, distal extremity and visceral thrombosis, and gangrene ● Placental insufficiency
● Hematological – thrombocytopenia, autoimmune hemolytic anemia ● Intrauterine growth restriction (IUGR) ⭐
● Others – neurological manifestations, migraine headaches, epilepsy; renal artery, vein, or ● Prematurity
glomerular thrombosis; arthritis and arthralgia ● Intrauterine fetal death
MNTM 2022 3
Diagnosis of APAS
1) Antiphospholipid syndrome is present if at least one of the clinical criteria and one of the laboratory criteria that follow are met:
Clinical Criteria Laboratory Criteria
• Vascular thrombosis • LAC (Lupus anticoagulant) –
• Pregnancy morbidity⭐ dRVVT, aPTT
o ≥ 1 unexplained deaths of a morphologically normal fetus at or beyond the 10 week AOG, with
th
• ACA (Anticardiolipin antibody) –
normal fetal morphology documented by ultrasound or by direct examination of the fetus; OR IgG, IgM (medium to high titer)
o ≥ 1 premature births of a morphologically normal neonate before the 34 week AOG because of:
th
• Anti-2-glycoprotein I – IgG,
(i) eclampsia or severe preeclampsia defined according to standard definitions, or IgM
(ii) recognized features of placental insufficiency; OR
• On 2 or more occasions at
o ≥ 3 unexplained consecutive spontaneous abortions before the 10th week AOG, with maternal
anatomic or hormonal abnormalities and paternal and maternal chromosomal causes excluded least 12 weeks apart⭐
Management of APAS
● Goal:
→ Prevention of thrombosis is the major role of therapy in patients with antiphospholipid antibodies | 
→ All pregnant women with APAS should be managed within a specialist obstetric unit with ready access to neonatal care
PRIMARY APAS SECONDARY APAS
Without an associated CT disorder⭐ With an associated CT disorder (SLE) or for those that are being
1) Low-dose unfractionated heparin⭐ – 5,000-10,000 units is used SC 2x treated for APAS who developed SLE
daily or LMW heparin: enoxaparin 1) Aspirin, heparin⭐ + corticosteroids (prednisone) ⭐
a) Heparin binds to 2-glycoprotein I, which coats the a) Steroids to address SLE
syncytiotrophoblast → prevents binding of ACAs and anti-2- b) Prednisone maintained at the lowest effective dose to
glycoprotein I antibodies to their surfaces, which likely prevents prevent flare from occurring
cellular damage
b) Throughout pregnancy up to 6 weeks⭐ postpartum using either FOR REFRACTORY CASES
heparin or warfarin 1) Immunoglobulin therapy - overt disease or heparin-
c) Prevent venous and arterial thrombotic episodes, thrombosis in induced thrombocytopenia, or both
microcirculation, including decidual-trophoblastic interface a) Used when other first-line therapies (heparin and
d) Heparin AE: bleeding, thrombocytopenia, osteopenia, and aspirin) have failed, especially in the setting of
osteoporosis preeclampsia and IUGR
2) Concurrently, low-dose aspirin⭐ – 60-80 mg PO once daily is given b) Expensive
a) Blocks conversion of arachidonic acid to thromboxane A2 while c) Recent literature found that there is no benefit in adding
sparing prostacyclin production IVIG to low dose aspirin and heparin.
i) Reduces TXA2 which causes platelet aggregation and 2) Without treatment, live birth rate of APAS pregnancy is
vasoconstriction approximately 20%
ii) Spares prostacyclin, which normally has the opposite effect 3) With proper management, > 70% of pregnant women with
b) AE: small-vessel bleeding during surgical procedures APAS will deliver a viable live infant
c) Low-dose aspirin does not reduce adverse pregnancy outcomes
in APA-positive women
V. RHEUMATOID ARTHRITIS
● Cardinal feature: Inflammatory synovitis that usually involves the peripheral joints (hands, wrists, knees, and feet are commonly involved)
→ Chronic polyarthritis
→ Pain, aggravated by movement, is accompanied by swelling and tenderness
● 90% of women with RA will experience improvement during pregnancy
● Postpartum exacerbation is common
Management of Rheumatoid Arthritis
1) Treatment is directed at pain relief, inflammation reduction, protection of articular structures, and preservation of function
2) COX-2 inhibitors + low-dose prednisone + DMARDs are often all the pharmacotherapy needed for RA flares
a) Aspirin and other NSAIDs are the cornerstone of symptomatic therapy
i) NSAIDs are associated with cardiac malformations, early spontaneous abortions, ductus constriction, and neonatal pulmonary hypertension
b) Glucocorticoid therapy (prednisone) may be added to NSAIDs
c) DMARDs have the potential to reduce or prevent joint damage
i) Sulfasalazine and hydroxychloroquine are safe for use in pregnancy
d) Azathioprine treatment may be used if immunosuppressive drugs are warranted

MNTM 2022 4

ORGANISM CLINICAL MANIFESTATION
• 90% of women are asymptomatic
TOXO • Flu-like symptoms + non-tender
PLASMOSIS posterior cervical adenopathy
T. gondii (resembles Infectious
Mononucleosis)
• Incubation period: 14-21 days
• Infective period: 7 days before to 10
days after the onset of rash
• Fever, body malaise (prodrome)
RUBELLA
• Maculopapular rash that begins on
Rubivirus
the head & neck and spreads down
to the trunk and extremities
• Post-auricular lymphadenopathy,
arthralgia
• Most patients are asymptomatic
Fever, pharyngitis,
lymphadenopathy, polyarthritis (non-
specific symptoms)
CYTO • Primary - Highest risk in 3rd
MEGALO trimester⭐
VIRUS • Secondary – equal in all trimesters
HHV-5
• HSV-1 – oral infections; childhood
• HSV-2 – genital lesions; sexual
intercourse
HERPES
• Incubation: 3-7 days
SIMPLEX
HSV-1 • Constitutional symptoms: fever,
HSV-2 headache, malaise, and myalgia
• Local symptoms: pain, itching,
dysuria, vaginal and urethral
discharge, and tender
lymphadenopathy
TORCH ORGANISMS
PREGNANCY DIAGNOSIS TREATMENT PREVENTION
• Maternal: Spiramycin
• M: Toxoplasma retinitis (rare) Encephalitis, infection confirmed until
• Do not eat
myocarditis, pneumonitis, or hepatitis in • M: Serologic (IgM and delivery (3-4g a day
undercooked meat or
immunocompromised women IgG) 2 weeks apart concentrates in the placenta
seafood
• F: Congenital toxoplasmosis • F: PCR of amniotic • Fetal: Pyrimethamine and
• Change cat litter box
o Tetrad: Chorioretinitis, hydrocephalus, fluid in 2nd trimester sulfadiazine + folinic acid
daily (needs 1-5 days in
intracranial calcification, convulsion or 4 weeks after once infection confirmed
cat feces to be
o Other: LBW, hepatosplenomegaly, jaundice, maternal infection (folic acid since both 2 are
infectious)
anemia folic acid antagonists –
penetrate fetal brain)
• Prenatal screen: IgG
Rubella status
• Preterm labor
• If neg: advice
• M: Arthritis • + IgM rubella specific
• Symptomatic: Hydration immunization after
• F: Congenital rubella syndrome Ab
and antipyretics if pregnancy
o Highest risk during first 12 weeks • 4-fold increase in IgG
uncomplicated • MMR vaccine 2 doses
o Triad⭐: sensorineural deafness (58%), eye acute and
• Preterm labor: tocolytics after pregnancy (0. 4
abnormalities (43%), Congenital heart convalescent serum
• NO EVIDENCE for Ig use weeks)
disease (50%) specimens
• Avoid pregnancy
o Low birth weight
within 3 months of
last dose of vaccine⭐
• M: Myocarditis, pneumonitis, hepatitis, retinitis,
gastroenteritis, meningoencephalitis
• Screening if woman
• CMV-specific IgG
presents with
• F: congenital CMV infection and IgM (for the • CMV hyperimmunoglobulins
mononucleosis like
o Most asymptomatic but 5-10% will present mother) lowers the risk
illness, or congenital
with: growth restriction, chorioretinitis, • NAAT of amniotic • IV ganciclovir for 6 weeks to
infection is suspected
mental and motor retardation, sensorineural fluid for the baby neonates with symptomatic
based on sonography
deficits, jaundice, hemolytic anemia, TTP (gold standard to CNS disease prevents
o Generalized hemorrhagic purpuric eruptions determine fetal deterioration
• Strict observance of
(dermal erythropoiesis) infection)
proper hygiene
o Sonography: microcephaly, ventriculomegaly,
cerebral calcification, hepatosplenomegaly
• Spontaneous abortion, IUGR, preterm labor
• M; Recurrent HSV infection (more common), • Maternal signs and
aseptic meningitis (if severely symptoms
immunocompromised) • IgG and IgM for HSV • Avoid sexual contact
• HSV culture – 48-72 • Acyclovir or Valacyclovir with infected individuals
• F: Congenital and neonatal herpes infection hours after • Delivery: CS if active • Suppression decreases
1. 5% In utero: rare, skin blisters, scarring, CNS appearance of genital lesions recurrent genital
hydranencephaly, microcephaly, intracranial lesions • Vaginal - if with history lesions at term, and
calcification, chorioretinits, micropthalmia • PCR assay of genital only, CS not inidicated) viral shedding
2. 85% Peripartum⭐: SEM disease (40%), CNS lesions
w encephalitis (30%), disseminates with • Tzanck smear – MNG
involvement of multiple organs (32%) and viral inclusions
3. 10% Postpartum: like peripartum
MNTM 2022 1
 TORCH - OTHER ORGANISMS
ORGANISM CLINICAL MANIFESTATION PREGNANCY DIAGNOSIS TREATMENT PREVENTION
• Preterm labor, PPROM/PROM, Risk factors: Universal screening for all pregnant women between
chorioamnionitis • Prolonged rupture of membranes 35-37 weeks AOG⭐
• M: Bacteriuria, pyelonephritis, (>18 hours) Anal and vaginal swabs for culture studies are
• No signs and symptoms seen osteomyelitis, postpartum mastitis, • Preterm delivery
recommended⭐
GROUP B
among infected pregnant women puerperal infection • Temperature >38°C
STREP
• Asymptomatic GBS anovaginal • F: Neonatal sepsis (early & late onset)
S. • Maternal chorioamnionitis
colonization in women with preterm
agalactiae • Young maternal age
labor is 20%
• African-American race
• Hispanic ethnicity
• GBS bacteriuria in pregnancy
• VZIG should be given to
• Incubation period: 10-20 days (13- neonates born to mothers
17) who have clinical evidence
• Infective period: 1-2 days prior to of varicella 5 days before
onset of rash and until the lesions and up to 2 days after • Varicella vaccine 2
have dried and crusted delivery⭐ doses after
• Fever, dry cough, • Miscarriage, preterm birth Criteria for hospitalization: • VZIG who already pregnancy (0. 4
tachypnea/dyspnea, pleuritic chest • M: Bacterial infection of the skin • Chest symptoms
developed chickenpox weeks)
pain lesions, varicella pneumonia, rash • Avoid pregnancy
• Neurological symptoms (other than
• Lesions progress from encephalitis headache)
within 3 months of
maculopapular to vesicular • F: Preterm birth, fetal loss, Congenital • Oral acyclovir (5 days) – last dose of vaccine
CHICKEN • Severe varicella disease → >100
• Complications: Secondary bacterial Varicella Syndrome, Neonatal lesions → Numerous mucosal
to shorten infection
POX • IV acyclovir (7days)
infection of the skin, necrotizing Varicella, purpura fulminans lesions
Varicella pregnant with severe
fasciitis, varicella gangrenosis, • Significant immunosuppression
Zoster infection
benign cerebellar ataxia, Congenital varicella syndrome:
(HHV-3) • In pregnant women:
meningoencephalitis, vasculitis, DIC, • 5 days before and 2 days after
• Near term
thrombocytopenia, vesicular delivery
• Poor OB history
hemorrhage • Delivery should be delayed until 5-7
days after onset of maternal • History of smoking
• Varicella pneumonia⭐ (need good varicella⭐ • Chronic lung disease
history and PE for early diagnoses)
• CXR: nodularities and interstitial
pneumonitism 1-6 days after rash
onset
• Higher mortality in pregnant host
VZIG within 96 hours of exposure
• Supportive: for the
mother
• Incubation period: 14-21 days
• Monitor for hydrops • Avoid exposure to
• Infective period: 10 days before until
fetalis: weekly utz for 12 erythema infectiosum is
day of the rash onset
• M: Arthropathy, aplastic crisis, weeks (usually seen 4- the only method of
PARVO • Fever, headache, sore throat, 6 weeks post infection)
myocarditis prevention
VIRUS B19 “slapped cheek” appearance,
• F: Hydrops fetalis⭐, fetal death⭐ • If hydrops fetalis • High-risk groups: school
muscle and joint pains
detected: teachers, workers in
• Maculopapular rash with generalized
• Percutaneous blood daycare centers
distribution
sampling
• Doppler MCA

MNTM 2022 2
ORGANISM CLINICAL MANIFESTATION
• Asymptomatic or mild (80%)
• Severe (5%)
• Incubation: 3-14 days
DENGUE
Serotypes • Characteristic symptoms:
1-4 sudden-onset fever, headache
(typically located behind the
eyes), muscle and joint pains
“break-bone fever”, and a rash
• Fever, cough, headache,
muscle pain, loss of sense of
smell (anosmia) or taste
COVID-19 (ageusia), shortness of breath
• •
• Vertical transmission: 3rd
trimester
• Primary: Firm, round and
painless ulcers or chancres
(vs. painful chancroid in H.
ducreyi) single or multiple
• Secondary: rash,
mucocutaneous lesions
(usually on the palms and
soles of the feet),
lymphadenopathy
SYPHILIS • Tertiary: Cardiac (dilation of
T. pallidum aortic ring, LVH, coronary
stenosis), gummatous lesions,
tabes dorsalis, general paresis
• Latent: no clinical
manifestation but positive
serologic testing
• early if acquired in the past
year
• late if more than a year or
unknown duration
• Mucocutaneous external
HPV genital warts which may be
6 and 11 flat, endophytic, or exophytic
(condyloma acuminata)
PREGNANCY DIAGNOSIS TREATMENT PREVENTION
• Adverse pregnancy outcomes: preterm birth, • Day 1-4: RNA detection: • Vaccination
LBW, CS deliveries, high risk vertical PCR, Viral isolation • Minimize exposure by
transmission, severe bleeding⭐ during • Days 1-7: Antigen detection: avoiding areas with high
parturition NS1 and E/M antigen • Supportive: IV hydration, incidence rates of
• M: Dengue without warning signs, dengue with antipyretic, serial CBC infection
warning signs, severe dengue • Day 4+ :Antibody detection monitoring • Use of DET-containing
• F: Neonatal dengue infection • Hemagglutination inhibition repellants
• Febrile illness of mother just before delivery • ELISA IgG/IgM • Use of mosquito nets
• Fetal distress, IUFD, preterm delivery • Rapid test IgG/IgM • Environmental sanitation
• Wash and sanitize your
• Precaution on drug safety: hands frequently
• Remdesivir – • Disinfect high-touch
• Asymptomatic, Mild, Moderate, Severe/Critical noestablished studies on surfaces
illness
• RT-PCR – gold standard
pregnant women • Wear a mask if you’re
• Pregnant women are not at increased risk of • Close monitoring of sick or advised to
• Term pregnant patient
infection but higher risk of severe illness maternal and fetal status • Self-isolate and practice
undergo testing prior to
• Delivery: CS is not social distancing → If
delivery
• Obstetric complications: preterm labor, indicated mother is working, opt for
neonatal ICU admission, CS • Breastfeeding is work from home if the
recommended (observe option is available to
infection protocols)⭐ minimize contact with
other people
• Can transfer to placenta as early as 6 weeks,
also during labot if w active genital lesions
• Complications miscarriage, stillbirth, preterm • Benzathine Penicilin G IM
labor,LBW, neonatal death shortly after birth o 1 dose: 1, 2, and early
• Gold standard: darkfield latent
•
microscopy o 3 doses: 1 week apart –
• Congenital syphilis:
tertiary and late latent
• Early (<2 years): Maculopapular rash, • Initial screen: non-treponemal
• Monitor response: non-
snuffles, mucous patches in the oral cavity, (RPR, VDRL) treponemal test titers (6
hepatosplenomegaly, jaundice, • Screen: all pregnant
• If + → request confirmatory and 12 months after
lymphadenopathy, pseudoparalysis of Parrot women in first prenatal
• If - → retest quantitative treatment)
(osteochondritis), chorioretinitis visit, retest at 3rd
• Quantitative titers: o Monthly for first 3
• & iritis trimester if high risk
• Baseline documented, dictate months and every 3
• months after if high risk
response to treatment
• Late (2-5 years): Hutchinson’s triad: and pregnant
Hutchinson’s teeth, keratitis, CN8 deafness • Adequate response: 4 fold
• Confirm: treponemal tests
• Mulberry molars, saddle nose, rhagades, decline in titer in:
(TPPA, FTA-ABS)
saber shins o 6 mo: primary and sec
• Neurologic symptoms – mental retardation, o 12-24 mo: latent
hydrocephalus, general paresis, optic nerve
atrophy & Clutton’s joints
• Patient applied treatment
(3x a week for 16 weeks) • Vaccines: Cervarix,
• Neonates at risk: → Born to
– imiquimod, podofilox, Gardasil-4, Gardasil-9
• Increased presence of HPV infection & genital mothers who have active HPV
sinecatecins are all
warts, as well as other immunocompromised • Exposed longer to the
states
CONTRAINDICATED⭐ • Vaccination during
infection (e.g., prolonged
• ACCEPTABLE during pregnancy is not
• M: Genital warts multifocal or multicentric labor)
pregnancy: (provider recommended⭐
• F: Juvenile onset recurrent respiratory • Gross clinical exam, aceto-
applied) Cryotherapy, although there are no
papillomatosis⭐ whitening, colposcopy
surgical removal, associated pregnancy
trichloroacetic acid or outcomes
bichloroacetic acid
MNTM 2022 3
ORGANISM CLINICAL MANIFESTATION
• Fatigue, nausea, vomiting,
HBV fever, hepatomegaly, jaundice,
dark urine, anorexia, rash
• Patients are initially
HIV
asymptomatic or may have
1 AND 2
non-specific symptoms
serotypes
• • Transmission: blood products,
⭐⭐⭐
PREGNANCY
• Preterm birth (conflicting results
in studies)
• M: Chronic hepatitis B infection
(if left untreated) Liver cirrhosis,
liver malignancy
• F: Vertical transmission of the
virus Chronic hepatitis B
infection
• M: HIV Clinical Stage I-IV
Acquired Immunodeficiency
Syndrome (AIDS)
• F: Vertical transmission:
• IUGR, stillbirth, low APGAR
score
• • Screening: ELISA
sexual intercourse, perinatally,
breastmilk
• HIV-1 viral load – main
determinant of transmission
DIAGNOSIS TREATMENT PREVENTION
• All pregnant women –
• Lamivudine<Tenofovir – to
screened at the first
decrease vertical transmission in
prenatal visit
those with high viral loads or
• Initial screening: HBsAg • Hepatitis B vaccine⭐ –
HBeAg positive
• Hepatitis B panel - to determine if given to high-risk
• Hepatitis B Immunoglobulin
acute or chronic mothers who are
(HBIG) – given antepartum to
• HBV-DNA by quantitative PCR – seronegative
women at high risk for
required before initiating
transmission⭐
• Treatment • Hepatitis B vaccine – not
• For infants of infected mothers:
• LFT, Liver utz, fibroscan, biopsy routinely given during
HBIG at birth accompanied by the
pregnancy (1ml at 0,1,6
first of 3 doses of HBV
months) recommended for
recombinant vaccine
high risk populations
• Continue ART in pregnancy
• Indicated to initiate treatment which would lower viral load and
perinatal transmission (goal: <1000 copies/mL)
• Combination of at least 3 ARTs (antiretroviral therapy)
• 2 NRTIs + either a Ritonavir-boosted protease inhibitor or an
integrase inhibitor
• Opt-out approach: HIV testing is
routine but may be declined
• Delivery: scheduled CS at 38 weeks ⭐if load >1000 (vaginal if
<1000)
• Confirmed: Western blot or IFA
• Infant prophylaxis: zidovudine asap after delivery (6-12 hours) and
continued through age of 6 weeks
• Breastfeeding: DO NOT breastfeed if there is access to formula
milk and clean water
• Exclusive breastfeeding (both on ART) if no access
• MIXED FEEDING – STRONGLY DISCOURAGED
MNTM 2022 4
 OBSTETRICS 2 AY 20-21

NATURAL FAMILY PLANNING

Andrea C. Santiago, MD, FPOGS
2.23
26 NOV 21

TABLE OF CONTENTS ● Lessens the number of days when the couple can have safe
I. NATURAL FAMILY PLANNING (NFP) .................................... 1 intercourse
A. ADVANTAGES OF NFP.................................................... 1 ● Does not provide complete protection from sexually
B. DISADVANTAGES OF NFP .............................................. 1 transmitted diseases (STDs)
II. MENSTRUAL CYCLE ............................................................. 1
A. PHASES OF THE MENSTRUAL CYCLE .......................... 1 II. MENSTRUAL CYCLE
B. RELATIONSHIP OF CHANGES IN THE OVARY,
HORMONES, AND ENDOMETRIUM ........................................... 1 A. PHASES OF THE MENSTRUAL CYCLE
III. METHODS USED IN NFP ....................................................... 3
A. CALENDAR/RHYTHM METHOD ...................................... 3
B. CERVICAL MUCUS OR BILLING’S METHOD.................. 4
C. SALIVA OVULATION MONITOR ...................................... 4
D. BASAL BODY TEMPERATURE........................................ 4
E. SYMPTO-THERMAL METHOD ........................................ 4
F. STANDARD DAYS/CYCLE BEADS METHOD ................. 5
G. TWO-DAY METHOD ......................................................... 5
H. LACTATION AMENORRHEA METHOD (LAM) ................ 5
IV. COMPARATIVE EFFICACY OF NFP METHODS ................... 6
V. REASONS FOR DISCONTINUATION OF NFP ...................... 6
VI. NFP SAVES ............................................................................ 6
REFERENCES.................................................................................. 6

MUST KNOW BOOK PREVIOUS TRANS

Additional notes from Dr. Santiago’s recent lecture (November 26, 2021) are in
blue.
Figure 1. Seasons = Phases of the Menstrual Cycle.
I. NATURAL FAMILY PLANNING (NFP) Table 1. Comparison of Seasons to the Phases of the Menstrual Cycle
● AKA fertility awareness-based methods
● “For planning and preventing pregnancy by observation of WINTER ● Begins with cold, dry ground
the naturally occurring signs and symptoms of fertile and (cold, dry) ● First part of the menstrual cycle
infertile phases of the menstrual cycle; with the avoidance of → Basal body temperature (BBT) is lower
intercourse during the fertile phase of pregnancy” – World Health → Note sensation of dryness
Organization (WHO)
SPRING ● Just as the rain moistens the ground, making
A. ADVANTAGES OF NFP (moist, fertile) it fertile and ready for planting
● Effective when accurately and consistently practiced ● Fertile phase
● Creates an awareness of the body and its reproductive functions → Sense wetness
→ Since she will be monitoring herself throughout the menstrual → Observe fluid secretions that are produced
cycle from the cervix
● Helps enhance the relationship of the married couple ● Reflects rising estradiol levels
→ Encourages a more intimate communication and shared
decision making in matters involving sexuality and fertility
regulation between the couple SUMMER ● Warmth allows flowers to bloom
● No physical side effects (warm, growth) ● BBT will rise after ovulation creating a warm
→ Biggest advantage environment for a new baby to grow (if
fertilization has occurred)
→ Does not involve any chemicals (drugs) or physical devices
● Sexual relations can be spontaneous as possible during the FALL ● Trees shed their leaves
safe period (shedding) ● If a woman has not gotten pregnant, she will
→ So long as the woman correctly tracks her menstrual cycle shed the bloody lining of the uterus which we
● Prevention of: know to be her period or menses
→ Pregnancy in very young mothers and older mothers
→ Pregnancy in high-risk women with concurrent serious
disease or other medical problems B. RELATIONSHIP OF CHANGES IN THE OVARY,
→ Unwanted pregnancy HORMONES, AND ENDOMETRIUM
→ Illegal/induced abortion
● The signs and symptoms caused by the ovarian hormones
B. DISADVANTAGES OF NFP (estrogen, progesterone) form the basis of natural family planning
● Requires will power, cooperation, and commitment
→ Takes 3-6 menstrual cycles to learn effectively and entails
daily recording on the part of the woman
● Effectiveness depends on the accurate determination of the
fertile period
→ Changes in the life of the woman (e.g. illness, lifestyle, stress
and travel) can alter fertile indicators and make it harder for
the woman to interpret what is happening to her body
IBE, A. | CUNANAN, A., CUSTODIO, C., DEL ROSARIO, K., IBARRIENTOS, C., LABAD, P. TC: DY, H. Page 1 of 6
 OB 2.23 – Natural Family Planning (26 NOVEMBER 2021) Page 2 of 6

Figure 2. Menstrual Cycle Hormones. Here we see the rise and fall of the
hormones, particularly estrogen and progesterone throughout the menstrual
cycle, which causes the different signs and symptoms of the woman that form
the basis of NFP. Figure 6. Cervical and mucus changes.
● At first secretions are thick, whitish, or cloudy
● Then become clearer, wetter, slippery and stretchy
→ This is the most fertile time
● After ovulation, the secretions go back to sticky then dry
Table 2. Changes in the Cervix and Mucus Secretions |
CERVIX MUCUS
INFERTILE Low, firm, closed Opaque, flaky, sticky,
PHASE not elastic, cloudy white,
(first half) thick, dry
FERTILE High, soft, open Smooth, slippery,
PHASE stretchy, distinct wet
(second half) feeling, thinner, clearer
● Days after menstruation: Dry days |
→ Early, infertile days
→ Characterized by G type of mucus
Figure 3. Relationship between the ovary, endometrium, and hormones during
the menstrual cycle. The growth and maturation of ovarian follicles take a
■ Made up mostly of protein fibers, make it very hostile to the
variable time sperm
■ Does not facilitate the transport of the sperm
■ Infertile type of mucus – lacks the slippery, lubricative
quality of the fertile-type
● As ovulation progresses: S type of mucus |
→ Fertile type of mucus
→ Feelings of fullness, softness, and swelling in the tissues
around the opening of the vagina
→ Provides the sperm cells with protective envelope and
facilitates its transport
Table 3. Types and function of mucus |
MUCUS TYPE FUNCTION
G Mucus • Lower crypts
• Dense, impermeable to sperm
• Mucus plug
L Mucus • Loaf/lump
• Middle crypts
• Lumpy type, support to S mucus
Figure 4. Mid-cycle. During mid-cycle, the LH surge causes the rupture of the
follicle at ovulation. What will be left will be the corpus luteum cyst, that has a • Filtering defective sperm
consistent lifespan of 10-16 days. S Mucus • Most helpful
Cervical Changes • Slippery, stretchy, stringy
• Highest crypts
• Swimming lanes, lubricant
• Provides channel and protective to sperm,
nourishing

Figure 5. Cervical Changes. Low, firm, closed during infertile period. High soft
open during ovulation
 OB 2.23 – Natural Family Planning (26 NOVEMBER 2021) Page 3 of 6

Basal Body Temperature Changes

Figure 7. Basal Body Temperature Changes. Fertile period starts at first sign of
secretion, and ends after the 3rd highest temperature is recorded, provided that
all high temperatures occurred after peak day (last day of wetness or slippery
secretions)
● Rises at approximately 0.4 °F or 0.2 °C
→ Occurs after ovulation
→ Due to the effect of progesterone, since it has higher levels
until the next period
■ Responsible for the biphasic pattern of temperature during
the menstrual cycle
● Days before fertile time -> only relatively infertile
● Days after fertile time -> definitely infertile
→ Most effective time to avoid pregnancy
Figure 9. Changes in the Uterus. Once the ovum has been extruded
out/released, it survives for another 24-48 hours. The sperm can last longer
for about 48-72 hours. When secretions are present (as you can see in the
yellow oval), the lifespan can last for about 8-9 days. (+) Secretions: The
sperm can actually fertilize a woman’s egg up to 7 days after the intercourse.
|
Dr. Santiago Nov. 2021 lecture:
● The ovum survives for 24-48 hours
● The sperm survives longer for 48-72 hours
→ It can fertilize the woman’s egg for up to 7 days after
intercourse when secretions are present
● Allowing for the lifespan of the egg, the fertile time last for a
maximum of 8-9 days
III. METHODS USED IN NFP

A. CALENDAR/RHYTHM METHOD
● Probable days of fertility are estimated based on the average
cycle lengths of the patient in the past 6-12 months
→ We have to ask the patient to take note of her cycle length
during the past 6-12 months before we are able to compute
for the fertile or infertile days |
● For regularly menstruating women |
→ Subtract 14 from the cycle length
Figure 8. Menstrual Cycle. This is an example of a regular 28-day cycle. The ■ Predictive ovulation period, mid-cycle
first 6 days of this cycle is considered as the menstrual phase which is → Once you get the difference
characterized by bleeding or period. The days immediately after (day 7-9) is ■ Subtract 5
what we call as the relatively infertile time, this is the pre-ovulatory phase,
meaning that if they have intercourse there’s a low chance of a woman − Basis: 2 days to allow possible early ovulation; 3 days
getting pregnant. During the ovulatory phase (day 10-18), it spans about 8-9 for the lifespan of the sperm
days. The post-ovulatory phase (day 19-28) is the absolutely infertile time, ■ Add 4
which is the most effective time to avoid pregnancy. | − Basis: 2 days allowance for late ovulation; 2 days for the
lifespan of the sperm

Figure 10. Example of the Calendar Method (regular). A woman’s menstrual

cycle is 28 days. Her fertile days would be from the 9-18th day, while the
remaining are infertile days.
Figure 10 example:
● Regular 28 day cycle
1. Subtract 14 (28-14=14)
2. Subtract 5 (14-5=9)
3. Add 4 (14+4=18)
● Fertile days will be from day 9-18
 OB 2.23 – Natural Family Planning (26 NOVEMBER 2021)
Figure 11. Example of the Calendar Method (irregularly menstruating).
● For women with irregular cycles |
→ Get the shortest and longest cycle length
■ Subtract 20 from the shortest cycle
■ Subtract 10 from the longest cycle
■ TAKE NOTE: These are constant numbers that take into
consideration the ff. factors which are predicted ovulation
time, sperm and ovum lifespan, and the six-day variation in
the cycle lengths
→ Entail longer periods of abstinence
■ That’s why they want to discontinue NFP
B. CERVICAL MUCUS OR BILLING’S METHOD
Figure 12. Billing’s Method.
● Requires a woman to observe the quality and quantity of her
vaginal mucus discharge throughout the cycle
● Useful for women with irregular cycles (< 26 or > 32 days) |
→ The calendar method may not be that reliable for women with
irregular cycles
● Observation is usually done at the end of the day or during the
afternoon and not during the start of the day
Figure 13. Mucus Changes. First half (left): Infertile type of mucus; Second half
(right): Fertile type of mucus (Spinnbarkeit)
Table 4. Features of cervical mucus throughout the cycle
MUCUS
INFERTILE • Opaque, flaky, sticky, not elastic, cloudy white,
PHASE thick, dry
(first half) • Lacks the slippery, lubricating property of fertile
type of mucus that is necessary for sperm transport
FERTILE • Smooth, slippery, stretchy, distinct wet feeling,
PHASE thinner, clearer
(second • Egg white appearance
half) • Facilitates sperm transport and provides cells with
protective envelope
• Women feel fullness, softness, and swelling on the
tissues around the vagina
Figure 14. Peak Day (red bar). Peak day is defined as the last day of slippery
mucus.
● Refrain from vaginal intercourse once there is clear, wet,
slippery, mucus secretion until the 4th day after the peak day
of wetness or the last day of slippery mucus |
Page 4 of 6
● PEAK DAY RULE |
→ Count three days after the peak day
→ During the post-peak days, the woman will feel dry and see
sticky mucus or no mucus at all
→ On the 4th day after the peak day, intercourse is available to
the couple night or day until the next menstruation without
resulting in pregnancy
C. SALIVA OVULATION MONITOR
● Saliva is collected everyday and should be started at the end of
menses
● No food or water for an hour
● Collection of saliva best under the tongue and placed on the
microscope slide examined under a commercially available kit
with lens
→ Allowed to dry for 5-10 minutes
● Presence of ferning pattern: Indicates ovulation
→ Don’t have intercourse if you see this (that’s if you don’t want
to get pregnant)
● 98% higher than the other methods not using the mucus
parameter |
D. BASAL BODY TEMPERATURE
● BBT: Waking temperature of the body before any activity
→ You get the temperature immediately upon waking up
● Lowest point is appreciable within 1-2 days before the LH surge
● Following ovulation, the BBT generally increases by 0.2-0.5 °C
(creates a biphasic pattern throughout the cycle)
→ The increase is due to the thermogenic effect of pregnanediol
■ Metabolite of progesterone
■ Increased after ovulation and is secreted by the corpus
luteum
● Chart daily BBT (from the first day of menstruation)
● Refrain from vaginal intercourse from the first day of menses
until 3 days after the temperature rise of 0.2 to 0.5 °C
Figure 15. Basal Body Temperature Chart. The woman would record her BBT
starting from day 1 of her period.
● Components of the BBT chart: |
→ Cover line: Point of reference for determining the thermal
shift that occurs during ovulation (highest temperature on
days 6-10)
→ Thermal shift: Indicated by the four consecutive
temperatures above the cover line
→ Vertical line: Drawn in between days 3 and 4 of the thermal
shift
→ Fertile days: Days to the left of the vertical line
→ Infertile days: All days to the right of the vertical line
● Very tedious, but very effective (even for women with irregular
cycles) |
E. SYMPTO-THERMAL METHOD
● Requires identification of fertile and infertile days by combining
BBT, cervical secretion observations, and other signs and
symptoms of ovulation
→ Abdominal pain/cramps
→ Breast tenderness
→ Changes in the position and firmness of the cervix
● Who may use? |
→ Women with menstrual cycles of any length
→ Women willing to take their BBT daily, record them, and
interpret their temperature patterns as well as observe and
record their cervical mucus changes
→ Women with normal cervical mucus secretions
 OB 2.23 – Natural Family Planning (26 NOVEMBER 2021)
Figure 16. Sympto-T Chart.
Figure 17. Fertile Time in the Menstrual Cycle. Rise in BBT (known as the
thermal shift) generally occurs during the mid-cycle, coinciding with the peak
mucus symptom and other symptoms that may indicate ovulation
● Patient is instructed to refrain from vaginal intercourse once with
cervical secretions, until the 4th day after peak cervical
secretions and the 3rd full day after the rise in BBT |
F. STANDARD DAYS/CYCLE BEADS METHOD
Figure 18. Cycle Beads. The RED bead marks the first day of menstruation. The
WHITE beads represent the fertile period. The BROWN beads are the infertile
days. The DARK BROWN (day 26) bead and BLACK (day 32) bead determine if
the woman is within the cycle range.
● Avoid intercourse on fixed days of the cycle mainly from day 8-
19 (12-day fertile window) of the cycle |
● Recommended ONLY for women with cycle lengths of 26-32
days (78% efficacy) |
● Advantages:
→ May have unprotected intercourse on all other days
→ Does not need to monitor temperature, cervical secretions or
any bodily symptoms
● The color of the bead lets her know if today is the day that she is
highly fertile or not
● How to use the cycle beads:
→ On the first day of menstruation, move the band to the RED
bead
Page 5 of 6
→ Every morning, move the band to the next bead
■ Always move the band in the same direction, from the
narrow to wide end
■ Move the band even on days when you have your
menstruation
→ The day the patient’s menstruation starts again, move the
band to the RED bead
■ A new cycle has started
→ On WHITE bead days, abstain from intercourse
■ These are the days when the patient can get pregnant
→ On BROWN bead days, the patient can have intercourse
■ These are the days when the patient does not get pregnant
G. TWO-DAY METHOD
Figure 19. Two-day Method.
● Check for the presence of cervical secretions, ideally every
afternoon and/or evening
● As soon as secretions are observed, the patient is considered
fertile on that day and the day after
→ Should avoid vaginal intercourse on these days
● Sounds easy but it can be quite tricky especially if the woman is
not yet used to characterizing her secretions or she has
concomitant vaginal infections that can obscure her findings |
● Any secretions noted within the day or the day before points to a
higher possibility of getting pregnant if sexual contact ensues |
● Start by asking if there are any secretions noted from yesterday
and today, rather than the other way around for this method to be
more successful |
H. LACTATION AMENORRHEA METHOD (LAM)
● Taking advantage of breastfeeding as a means of birth control
→ Can be initiated any time during the first 6 months postpartum
● Pathophysiology:
→ Breast suckling (especially with active stimulation of nipple,
areola, and structures that underlie them) inhibits pulsatile
release of GnRH from the hypothalamus
■ Decreases LH (and FSH) = suppresses development and
release of a viable follicle and ovum
→ Prolactin and oxytocin: plays a minor/lesser contributory role
● Prerequisites of LAM:
→ Lactational: Means exclusive or fully breastfeeding
■ No other liquid or solid food is being given to the infant
→ Amenorrhea: Means not having menstrual bleeding
■ Should not have had menstruated yet from the time of
delivery
→ Method: Used when baby is 6 months or less
● Exclusive breastfeeding |
→ Must feed baby only breastmilk
→ Intervals between feedings should not be longer than 4
hours during the day and 6 hours at night
→ The baby should always be fed on demand
→ The more feedings and longer suckling periods = less
chances of ovulation
→ Infant formula feeding may reduce the woman’s hormonal
response = increases chance of failure on this method
● Disadvantages |
→ Only a temporary, short-term method (for 6 months max.)
→ If mother and child are separated for extended periods of time
because of work, LAM effectiveness may decrease
 OB 2.23 – Natural Family Planning (26 NOVEMBER 2021) Page 6 of 6

→ Exclusive breastfeeding may be difficult to maintain for up to

6 months due to a variety of social circumstances
→ Like all other NFP methods, LAM does not protect a client from
STDs and HIV/AIDS
● LAM could also be combined with the Billing’s method to better
assess if ovulation has occurred
→ So that the woman can anticipate when to avoid sexual
contact
IV. COMPARATIVE EFFICACY OF NFP METHODS
Table 5. Efficacy of NFP methods
METHOD PERFECT USE (%) TYPICAL USE (%)
Standard days 95 88
BBT 99 80
Sympto-T 98 80
Two-day 96.5 86
Billing’s 97 80
● In assessing efficacy, the time needed to learn the method and
to use it correctly must be considered
→ Perfect use efficacy: Method is used correctly at ALL TIMES
■ Ideal, but it never really happens in the real world
→ Typical use efficacy: Reflective of what happens in the real
world
→ BBT: Most effective with perfect use
→ Standard days: Best if typical use
● In the Philippines the most popular NFP among reproductive-age
women as of 2005 at least was the calendar/rhythm method
V. REASONS FOR DISCONTINUATION OF NFP
● Trouble learning a particular method
● Lack of confidence
● Challenge of sexual abstinence
● Shifting to another family planning method
VI. NFP SAVES
● We have to remember that NFP is still very effective and should
be a viable option for all women
● REMEMBER SAVES
→ S – spacing pregnancies
→ A – achieving pregnancies
■ If that is the goal of the couple
→ V – value-based marital bonding
■ Centered on patience, determination and tolerance (to
endure the difficulties that come with the different
methods), and generosity (because the couple must be
willing to give support to each other) of the couple
→ E – empowerment
■ Gives the couple the right to decide when to have
intercourse depending on their fertility or intention
→ S – safe motherhood
■ In the very young, old and high-risk pregnancies
END OF TRANSCRIPT

REFERENCES
A-MED 2021., (2019), Family Planning [Trans]. Manila, Philippines: Faculty of
Medicine and Surgery, University of Santo Tomas, OB 2
Santiago, A.C., (2021), Natural Family Planning [PowerPoint Presentation].
Manila, Philippines: Faculty of Medicine and Surgery, University of Santo
Tomas, OB 2

Original transcriber: Martinez