OB Flashcards

1
Q

Patients who are candidates for VBAC

A

documetnation that previous uterine incision is low transverse or low vertical; unknown scar can be candidate unless high clinical suspicion of previous classical
one prior CD–2 prior can be considered
clinically adequate pelvis
no other prior uterine scars or uterine trauma

contraindications
prior classical or T incision on uterus
prior uterine rupture
non vertex presentation; can try ECV
prescence of medical/obstetrical complication that would preclude vaginal delviery
prior transfundal surgery

increased risk of rupture
induced rather than spontaneous labor
GA >40w
multiple gestations
clinical fetal macrosomia in setting of no prior vaginal delivery
higher maternal age
non white

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2
Q

characteristic signs of uterine rupture

A

NRFHR (recurrent significant decelerations, bradycardia)
significant abdominal pain
loss of station of the presenting part
vginal bleeding

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3
Q

thyroid changes in pregnancy

A

natrual increase in estrogen produces increases in binding globulins including thyroid hormone binding globulin
total T4 and T3 increase, no net effect on FT4
TSH may appear decreased in 1st tri due to hCG but in general unchanged otherwise

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4
Q

hyperthyroid meds

A

PTU in 1st tri, preferred for T3 thyrotoxicosis
Methimazole 2nd/3rd tri–has risk for methimazolw embryopathy (esophageal or choanal atresia, aplasia cutis)

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5
Q

thyroid storm in pregnancy

A

ICU admission
PTU 1g Po load, 200mg PO q6hrs
followed 1-2hrs later by idine; lugols 10 drops PO q8hrs sodium iodid 1g IV q8hrs
propranolol to control tachycardia
steroids
IVF

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6
Q

NV pregancny

A

common before 9w: normal NV, hyperemesis, gestational transient hyperthyroidism, molar pregnancies and GTN

transient hyperT will have elevated LFTs, absent in Grave’s disease; do not need thyroid treatment

2nd tri n/v: GERD, gastritis, pancreatitis, chronic cholecystitis

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7
Q

rheumatic fever

A

mitral valve, aortic stenosis–most cases of aortic stenosis in persons under 65 involve congenital stenotic aortic valves or bicuspid valves wtih development of stenosis

AS: LVH, increase is LV diastolic pressure with high pressure gradient across the aortic valve–leads to decrease in coronary artery flow and increase in the risk of ischemia under stress; cardiac function is very sensitive to small volume changes

monitoring of weight gain, vital signs, O2 saturation
febrile illness is themost common cause of deterioratio in these patient
avoid anemia
shortened second stage with operative assistance preferred

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8
Q

asthma and pregnancy, some things

A

Peak expiratory flow meter
FEV>70% for outpatient management; acute management ofcuses on prevention of hypoxia
continuous o2 monitoring with sats and vitals; aim >95%
CEFM
oxygen by facemask with:
-albuterol 10-15mg/hr continuously or dosed as 5mg q20min for 3 doses then 2.5-5mg q1-4hrs as needed
-if inadequate response, ipratropium bromide inhaler 500mcg q20min for 3 doses then prn
-poor response, systemic corticosteroid

FEV1<50% heralds impending respiratory arrest and is managed emergently
-ICU admission and intubation for ventilatory support, 100% O2 initially
nebulized albuterol, ipratropium bromide and systemic corticosteroids

maternal risks with systemic steroids: increase risk of PTD and preE
fetal risks with systemic steroids: 3x increase in risk of cleft lip if used 1st tri, increase in low birth weight

BUDESONIDE IS PREFERRED STEROID INHALER IN PREGNANCY

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9
Q

PP blues v PP depression

A

blues: emotional lability experienced by women following delivery of the infant; typically develops 2-3 days after delivery, peaks several days later and resolves by 2w

depression: can arise up to 12 months following delivery; pathogenesis unknown; occurs more often in women who experienced complications in delivery and with underlying mental illness–suspect when woman expresses extreme anxiety about the health ofthe infanct, concern about her ability to care for the infant, has a negative perception of infant temperament and behavior, lack of interest in the infant’s activities and has nonadherence to postnatal care

ACOG recommends screening for depression at least once during pregnancy and postpartum using a validated screening test

mild-moderate symptoms: psychotherapy is firt line; SSRIs, SNRIs, buproprion are reasonable
severe symptoms: need referral to psychiatrist

SSRIs during pregnancy: decrease in birth weight, increased NICU admission, poor neonatal adjustment, small increase in Primary Pulmonary Hypertension

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10
Q

RLQ pain ddx in pregnancy

A

pregnancy: PTL, abruption, infection
appendicities
local muscular reaction–rectus abdominis trigger point
obstipation, R ureteral lithiasis, R ovarian abnormality (hemorrhagic expansion, rupture of cyst, symptomatic mass, torsion)
inguinal hernia

US or MRI in pregnancy

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11
Q

cholecystitis in pregnancy

A

episodes tend to be recurrent and progressively more severe
in-ductal obstruction or gallstone pancreatitis are more common
gallstone pancreatitis is dangerous; maternal mortality is significant and fetal loss may exceed 50%

surgery in the second trimester is preferred, after 14w

adnexal mass in pregnancy; 10cm complex–can be observed if no symptoms; operate in pregnancy for appearance of tosion, suspicion of malignancy, symptoms

no c-section unless obstetric indication; if c-section done don’t remove unless appears like cancer

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12
Q

anemia and pregnancy

A

hematologic changes such as blood volume expansion may create appearance of anemia or unmask a subtle or compensated existing hematologic abnormality

blood volume increases 40-50% in pregnancy and RBC mass increases only 15-25%
typical diet 15mg elemental iron; in pregnancy 27mg/day is required

acquired causes of anemia in pregnancy: iron deficiency, anemia of blood loss, megaloblastic anemia, chronic renal disease, pyelonephritis, acquired hemolytic anemia, auto immune, malignancy, hypoplastic or aplastic anemia, drug induced

hereditary: sickle hemoglobinopathy, thalassemia, other hemoglobinopathies, hereditary hemolytic anemia

evaluation of anemia in pregnancy: FH for suggestion fo hereditary factors, physical exam, CBC iron/TIBC/ferritin, reticulocyte count, folate and B12, hemoglobin electrophoresis
Ferritin has highest sensitvity for dx of Fe deficiency anemia (<30 diagnostic)

post-malabsorptive/restrictive gastric bypass–decreased absorption of iron B12 and folate
hgbAS–give iron; need to assess hgb status of father as well

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13
Q

homozygous factor V in pregnancy

A

VTE history
severity of inherited thrombophilia
additional RF (obesity, CD, prolonged immobilization)

prophylactic anticoagulation:
antithrombin III deficiency
leiden factor V homozygous
prothrombin G20210A homozygous
double heterzygous for prothrombin and facto V leiden
antiphospholipid antibodysyndrome

strict heterozygotes, protein S and C deficiency don’t need anticoagulation unless history of clots

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14
Q

contraindications to exercise in pregnancy

A

hemodynamically significant heart disease; restrictive lung disease, incompetent cervix/cerclage, multiple gestation at risk for PTL, persistent second/third trimester bleeding, placenta previa after 24-26w, preterm labor, PPROM, preE or gHTN

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15
Q

pt is 10w and presents iwth n/v; she measures 14w

A

ddx: incorrect dates, multiple gestation, uterine mass, molar pregnancy

molar pregnancy: hydropic placenta with or without fetus
twin gestation: confirm viability and chorionicity and amnionicity

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16
Q

previous bariatric surgery and early pregnancy

A

normal pregnancy 25-35lb weight gain; 2200-2900 calories per day
best to defer pregnancy for 12-24mo after surgery
morbid obesity carries risk of fetal compromise or IUFD prior to term

obesity in pregnancy: low birth weight, congenital malformation is increased and US detection is less acurate

gastric dumping syndrome may occur with ingestion of refined sugars; may not tolerated GTT and may be evaluated for GDM iwth home glucose monitoring fastin and 2hr PP x5-7d

third trimester antenatal testing

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17
Q

recurrent pregnancy loss

A

genetic: recurrent autosomal aneuploidy, balanced rearrangement/translocation, mosaicism
uterin anomalies: contenital–septate/bicornuate; aquired–myomas polyps
metabolic: DM, thyroid
environmental: smoking drugs obesity
immune disorders: antiphospholipid syndrome
unexplained: 50% of cases

work up: karyotype of the parents, karyotype of abortus; HSG; labs: hgb A1c, TSH, TPO Ab, lupus anticoagulant/anticardiolipin/anti-beta 2 glycoprotein

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18
Q

maculopapular rash in pregnancy

A

ddx: contact allergic reaction, pruritic urticarial papules and plaques of pregnancy (PUPP), parvovirus, varicella, rubella

cholestasis: itching in the absence of rash

30-60% of adults have IgG to parvovirus from early childhood exposure; those without immunity and are exposed, 1/3 probability of transmission to the fetus, most don’t have an adverse outcome

PUPPs: topical steroids, oatmeal baths etc, short course of oral steroids in severe cases

ICP: most common pregnancy induced liver condition; itching without rash, itching on palms and soles
labs: bile acids >10, mild tranaminitis, prolonged PTT and increase in conjugated bili

fetal risk: stillbirth, premature delivery, meconium stained AF
do fetal surveillance from 32w gestation by BPP/NST
ursodeoxycholic acid for itching, does not reduce risk of stillbirth

delivery at 36/0w for bile acids >100; if <100, delvier 36-39w
most fetal mortaility occurs after 37w

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19
Q

seizure disorders and pregnancy

A

pregnancy increases incidence of seizures by 30-50%
management in coordination with patient’s neurologist or internistg

fetal risks: increasein IUGR, increase in stillbirth, possible increase in risk of preE

attempt to convert multi-agent therapy to single agent therapy prior to pregnancy
Lamotrigine and levetiracetam are preferred anti-seizure drugs

anticonvulsants interfere with folate metabolisma nd can decrease levels–1-4mg daily starting before pregnancy and vit D supplementation

fetal complications
NTD (valproate/carbamazepine)–resistant to folate
cardiac defects (ASD/VSD)
palatal clefting
valproate is teratogenic–multiple congenital anomalies
dilantin can cause fetal hydantoin syndrome

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20
Q

1st tri screening

A

indications: should be offered to all women

1st tri screen: sono assessment of fetal nuchal translucency and serum markers is more sensitive than second tri triple screen

women with abnormal first tri screen/NT assesssment should be offered genetic counseling and either amnio or cvs

integrated screen: first and second tri serum marker assossment without sonographic NT–more sensitive and has a lower false positive incidence than the 1st tri screen with markers alone (no NT)

cffDNA

AFP offered to all women who elect the first trimester screen only

1st tri screen with NT: T21 85%
quad screen: T21 80%, T18 65% open NTD 80-85%

1st tri screen: serum assays for hcg and papp-a; T21 hcg increased t18 hcg decreased; papp-a levels are decreased below 0.43 MOMs and add to the sensitvity and specificity

2nd tri screen: hcg, AFP, inhibin, estriol

US: T13, T18 have major structural anomalies; T21 duodenal atresia, ASD/VSD, clinodactyly)

finding of abnormal AFP and PAPPA in setting of normal karyotyping is associated with adverse pregnancy outcomes–IUFD after 24w, FGR, PTL, spontaneous less <245w, gHTN, preE

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21
Q

abdominal wall defect on 20w US

A

gastroschisis and omphalocele

gastroschisis: R para-umbilical abdominal wall defect which involves free evisceration of bowel into the amniotic cavity and may also involve herniation of stomach or liver; NOT associated with other anatomic abnormalities, sporadic

omphalocele: ventral midline abdominal wall defect in which a membrane surrounds the herniated bowelstomach/liver; associated with other abnormalities in 50-75% of cases and with chromosomal abnormalities in 25% of cases (trisomy)

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22
Q

amniocentesis, now leakage of fluid from vagina

A

ddx: PPROM, PTL with cervical mucus drainage due to cervical dilation, urinary incontinence, physiologic effect of pregnancy, UTI, leukorrhea of pregnancy, BV

evaluation: vaginal speculum exam to assess fluid or cervical change, nitrazine testing and fern testing, US to assess amniotic fluid index, amnio with instillation of dye

2nd tri amniocentesis leakage can occur in 1.7% cases

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23
Q

cleft palate

A

congenital abnormality occuring 9-10w gestation
palate closure is complete by 56-58 days post conception
50% are syndromic and
5 genes associated with cleft lip/palate
evaluation is by advanced US

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24
Q

screening for fetal aneuploidy

A

1st tri screening, 2nd tri screening (quad and penta), combined (integrated, sequential and contigent), US, cff DNA

1st tri: 10-13w, T21 80%, NT, hcg, pappa–assessed in conjunction with maternal age, prior aneuploidy, weight, race, # of fetus; will not detect open NTD

2nd tri: T21, T18, open NTD; triple screen 15-22w, comprises hcg, AFP and estriol, T21 70%; quad screen 15-22w (best at 16-18w), T21 80%, comprises hcg, AFP, unconjugated estriol, inhibin A–assessed in conjunction with maternal age, weight, race, DM

combined 1st and 2nd triscreening–higher down detection rate, requires more follow up–integrated, sequential, contingent

US better at detecting T13 and T18

cffDNA: detect fetal sex, Rh status, T21, 18, 13; T21 rate 98%, any positive result must be followed by a definitive diagnostic test prior to making any irreversible decisions

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25
Q

repair of 4th degree laceration

A

rectal mucosa and submucosa are repaired with running absorbable suture
anal sphincter is carefully repaired with interrupted suture and reinforcemetn
bulbocavernosus musculature is repaired with interrupted suture
vaginal mucosa and submucosa are reapproximated with runing or interruptred absorbably sutre
closure of perineal skin accomplished with runing/interrupted sture in subcuticular fashion if neeed
single dose of abx can be considered

early breakdown: debride any necrotic tissue and cleanse, obtain cultures if indicated; if evidence of cellulitis, treat with abx

NPO and enema prior to repair

risk of subsequent OASIS is 3%; consider CD if anal incontinence present after delivery, wound infection occurred and/or repeat laceration repair was done, psychological trauma and patient requests it

prevention: perineal massage or support, intrapartum warm perineal compresses

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26
Q

forceps and vacuum

A

simpson forceps: fenestrated blades and a cephalic curve designed for application to the molded fetal head

tucker McLane: shorter solid blades with more rounded cephalic curve for the unmolded head

forceps are more successful but more risk to mom

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27
Q

intercourse pain at 12w pp

A

repair should be all healed and suture material gone
approach to initial penetration dyspareunia including vestibulitis, vaginismus, local infections, estrogen deficiency due to breast feeding, pp depression

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28
Q

variable deceleration

A

abrupt in onset and also return to baseline <30s; duration is at least 15s and at least 15bpm below baseline but is less than 2 minutes

mild: duration less than 30s any depth
moderate: depth of <80bpm
severe: depth of <70bpm and duration greater than 60s

fetal scalp stimulation that shows >15bpm acceleration and lasting >15s for >32w, almost always shows absence of fetal acidemia 90% will have pH >7.2

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29
Q

HSV in pregnancy

Hep B serology

A

1st episode, valacyclovie 1gm BID x7-10 days
start daily suppressive therapy at 36w
if outbreak in labor, do C-section

HBsAg indicates either present acute infection or chronic carrier
vaccinated will have HBsAb
Ab to Hep B core antigen are present only in persons who have been infected with Hep B at some point–IgM indicates active acute, positive IgG and negative IgM requires HBsAg status to decide

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30
Q

Varicella in pregnancy

A

Maternal risks: varicella pneumonia (esp in 3rd tri)–ICU admission intubation if necessary

fetal risks: congenital varicella syndrome (msk) limb hypoplasia, muscular atrophy, digital malformation (brain) microcephaly, cortical atrophy, psychomotor retardation (ocular) cataracts, micro-ophthalmia, chorio-retinitis

highest risk fo malformations is at 13-20w; uncommon if before 13w

intrauterine varicella: hydramnios, fetal hydrops, echogenic foci in abdominal viscera, FGR

maternal treatment with acyclovir in pregnancy does NOT prevent congential varicella infection

if maternal clinical varicella infection develops between 5 days prior to delivery and 2 days after delivery, neonatal varicella infection risk may be reduced by VZIG administration–if neonate develops varicella, IV acyclovir is recommended

neonatal varicella may carry a 20-30% mortality, delivery should be delayed for a week following onset of maternal clinical infection, if possible, as this will further reduce the risk of maternal infant transmission

31
Q

Parvovirus and CMV in pregnancy

A

parvovirus: 50% of pregnant women have lifetime immunity
symptoms of new maternal infection: flu like myalgias and arthralgias, low fever, slapped face rash, reticular rash on the trunk
fetal effects: 20-30% vertical transmission rate–MOST COMMON INFECTIOUS CAUSE OF NON IMMUNE HYDROPS
abortion, IUFD are complications in he hydrops group

if suspicious, get IgM and IgG ab to parvovirus; if both are negative, repeat in 4w–if IgM positive at 4w, serial weekly US and doppler MCA for 8 weeks to evaluate for development of fetal anemia and hydrops

if hydrops: doppler MCA systolic peak velocity, PUBS for severity of anemia, fetral tranfusions if needed

CMV in pregnancy: most common perinatal infection worldwide
85% of woemn with new infection are asymptommatic 15% have fever, pharyngitis, polyarthritis
to diagnose get serology 3-4w apart test for anti CMV igG ab–if negative initially, but positive in 3-4w or if there is a 4x increase in titer diagnosis is made
maternal immunity does NOT prevent reinfection with fetal transmission, infection by new strain
fetal effects: (like toxo) more transmission later in pregnancy, more severe disease early in pregnancy; only 5-10% of infected fetuses exhibit congenital CMV

congential CMV syndrome (like toxo): low birth weight, intracranial calcifications, chorioretinitis, hepatosplenomegaly, icterus, anemia, low IQ; UNLIKE TOXO CMV HAS MICROCEPHALY

32
Q

chorio and endometritis

A

primary bugs are e coli and GBS

abx: amp/gent; if pcn allergic clinda/gent

decision to perform CD based on:
evidence of evolving maternal sepsis or deterioration in maternal condition
NRFHT
failure of progress in augmented labor

after vaginal delivery, don’t need to continue abx
after c-section continue x1 dose

33
Q

GBS

A

screening for all women 36-38w
don’t have to screen if previous GBS bacteruria in pregnancy or previous GBS infected infant
avx: ampicillin 2g followedb y 1g q4hrs; pcn 5 million u followed by 2.5-3 q4hrs until delivery

if pcn allergic–give clinda if sensitivity confirmed
otherwise give vanc (direct resistance to clinda or resistance to erythromycin)

cx good for 5 weeks

34
Q

mastitis

A

dicloxicillin 500mg qid x10-14d or cephalexin 500mg qid x10-14d if no improvement in 48hrs, consider b-lactam resistant strain and substitue augmentin , consider MRSA, abscess

35
Q

ddx of fevers on POD#2 s/p CD

A

pelvic infection>endomyometritis
breast engorgement
atelectasis or pulm infection
UTI or pyelo
viral syndrome

get: CBC with dif, chemo profile, UA and Ucx
pp endomyometriitis: fever, pain or tenders with no other recognized cause, purulent drainage from uterus (need 2 of 3)

septic thrombophlebitis is more common in patients with chorioamnionitis or pp endometritis, usually occurs on the R side, diagnosis of exclusion after abx therapy for 5-7d without improvement and in the absence of another suspected source

36
Q

PP hematoma

A

vulva: usually drain and close dead space
vaginal: don’t open; packing important; does have potential to expand in the retroperitoneal space so monitor vitals closely and trend labs if appropriate
anterior wall: do diagnostic cysto to r/o bladder trauma

place foley

37
Q

pyelo in preganncy

A

IV abx until 48hrs afebrile; complete PO course x7-10 days total; daily macrobid suppression

do suppressive therapy after 2nd UTI in pregnancy, after any diagnosis of pyelonephritis, any prior surgery of the kidney/ureter/bladder

38
Q

twins

A

monochorionic twin gestations carry a significantly increased risk of poor outcomes–1st/2nd tri loss; FGR, TTTS, UFD, congenital anomalies

TTTS monochorionic/diamniotic pregnancies; they have separate sacs but share blood flow; one twin may become under perfused and will develop FGR and oligo, other twin becomes over perfused and develops hydrops and polyhydramnios

management of TTTS: serial reduction amnio to the polyhydramnios amniotic sac; amniotic septostomy, laser ablation of placental anstomoses via fetoscopy

TTTS occurs in 10-15% of mono/di twins–watch fetal growth, amniotic fluid volumes, umbilical doppler flows thorughout pregnancy
US q2w starting at 16w; fetal echo at 18-22 weeks; antenatal testing at 32w–delivery considered when absent or reversed end-diastolic flow is identified in one twin

di/di twins: serial growth q4w from 20w on; consider antental testing at 36w

monochorionic: death of one twin poses high risk to surviving twin; maternal DIC low

growth discordance: most common complications of twin gestations and should be watched with serial US; two risks for multiple gestation include preterm birth and FGR

discordant=smaller twin >20% smaller than larger twin; once diagnosed follow with serial growths and UA dopplers and antenatal testing with BPPs

delivery timing of uncomplicated twins
di/di: 38w
mono/di: 34-37w
mono/mono: 32-34 must be by CD

39
Q

HTN disorder of pregnancy

A

cHTN: elevated BP >140/90 on two separate measurements at least 4hrs apart BEFORE 20w
ic cHTN: assess for other diseases with risk for HTN (DM, thyroid, CAD), serial blood pressure, serum lytes, liver enzymes, renal function, spot urine P:C (if >0.15 get 24hr urine protein), ekg
give them aspirin

maternal risks of cHTN: increase risk of preE/E; CVA/MI/Pulm edema, worsenign renal function, GDM, CD and PPH, placental abruption
fetal risks: FGR, IUFD, PTD
3rd tri growth US and antenatal testing usualy starting at 32w

low dose aspirin should be recommended to women at high risk for preE and should be considered for women wiht moret han one moderate RF
HR: h/o preE, cHTN, renal disease, multfetal gestation, DM, autoimmune disease
moderate: age >35yo, nullip, obesity, AA, low SES, FH of preE, previous adverse pregnancy outcome, low birthweight, IVF
start at 12w-16w

MOA: reduces production of thromboxane by platelets–thromboxane promotes vasoconstriction and platelet aggregation

contraindications to asa: allergy, high risk for bronchospasm due to aspirin–nasal polyps or asthma with history of aspirin bronchospasm, h/o GI bleed or peptic ulcer

40
Q

ecclampsia

A

initial management:
notification of staff
assessment of mother’s airway
lateral decubitus position to maintain airway and prevent aspiration
treat HTN
pad bedrails
establish pulse ox
supplemental o2
suctio at bedside to clear secretions

Mg bolus 6->2; if still seizing at 5 min, give benzo–lorazepam 4mg IV over 2 min; diazepam 5-10mg IV; phenytoin 300-400mg IV

following seizure, control BP; assess maternal status regarding oxygenation and return to consciousness (get ABG)

deliver once stabilized; can do induction with favorable cervix. if not favorable consider CD as want to avoid prolonged induction

post ictal state may be present for 10-15min; if no return to baseline, consider Mg tox or CVA event

after eclamptic episode fetal bradycardia for 3-5 min is expected; then fetal tachycardia and transient deceleration, minimal variabiltiy

41
Q

preGDM

A

fetal malformations: increased with hyperglycemia during organogenesis; CNS anomalies (hydrocephalus, NTD-spina bifida, anencephaly); skeletal anomalies with caudal regression syndrome considered the classic sign; complex cardiac anomalies; renal anomalies, macrosomia, FGR, hydramnios, IUFD risk

A1C 5-6% risk is baseline to non DM; A1C 10% associated with 20-25% anomaly rate

get retinal exam by ophthalmologist, 24hr urine for protein excretion and Cr clearance, EKG, metabolic profile and lipids

42
Q

gestational DM

A

all pregnancies screen at 24-28w; do at new OB if risk factors, if normal repeat at 24-28w

if 1hr>200, get fasting, if >95–diagnosis made–fasting >105 suggests underlying hyperglycemia

3hr: 95/180/155/140–need 2 of 4 abnormal

insulin preferred; usually started at 0.7-1u/kg daily

oral hypoglycemics can be used if declines insulin or can’t safely use it; metformin start at 500mg qhs; increase after 1 week, max is 2500-3000mg/d in divided doses

AM fasting goal 60-90; 2hr pp <120

intrapartum management: hourly FS, IVF with NS, switch to D5NS when in active labor or BS <70, if BS >140 insulin gttat a rate of 1u/hr

if continues on insulin after delivery start at 1/3 to 1/2 pregancny doses

43
Q

IUGR

A

<10% for GA OR AC <10% for GA

constitutionally small fetus: variance from normal size int he 3rd trimester, more so approaching term; identification prior to 32 weeks more likelyt o be FGR

causes
maternal: cHTN, preGDM, renal insufficiency, autoimmune, cyanotic heart disease, HTN disease of pregnancy, substance abuse, teratogen exposure
placental: placental infarcation, umbilical cord abnormalities (velamentous or marginal cord insertion), circumvallate placenta, chorioangioma, TTTS/vascular anastomoses
fetal: multiple gestation, chromosoaml anomalies, structural anomalies, infections

when to deliver
EFW 3-10%, normal uA doppler, 38w
EFW <3% and normal UA doppler 37w or at diagnosis if earlier
earlier delivery is indicated in cases of absent or reverse UA flow

doppler measurements of umbilical vessel flow cm/sec and S/D ratio

if FGR is diagnosed before 32w or in combination with polyhydramnios or fetal malformation, genetic counseling nad testing should be offered

S<D at 20w, likely a dating error; but if truly FGR, r/o chromosomal etiology and structural anomalies

risks of FGR: IUFD, for SGA newborn, increased risk of hypoglycemia, hypothermia, IVH, NEC, seizures, sepsis RDS, hyperbilirubinemia and neonatal death

44
Q

shoulder dystocia

A

call for help
drain bladder
mom stop pushing
mcroberts
suprapubic pressure
posterior arm
rotational maneuver; rubin maneuver or wood corkscrew
episiotomy for hand
fracture clavicle–upward traction
repeat above maneuvers
fracture other clavicle
repeat above maneuvers
frature humerus
repeat above maneuvers
replace head, proceed with c-section

45
Q

ECV

A

risks of ECF intself which require emergency CS: fetal or placental compromise abruption, NRFHR, cord accident, PROM, uterine scar separation

contraindications to ECV: multiple gestation, IUGR/FGR, previous classical c-section, congenital uterine malformations or large submucous fibroid, presence of PROM, signficant fetal anomaly, abnormal FHT, severe oligo, hyperextended fetal head, active labor with fetal descent, placental abruption

make sure to look at Rh status; give RhoGam
informed consent!
IV access
terb 0.25mg or similar tocolytic

fetal bradycardia can be observed for 5 min after version

intrapartum ECV can be attempted if membranes intact and fetus is not engaged

46
Q

vaginal breech

A

would prefer emergent c section
if not possible move to OR alert all staff
FHR monitoring, US to see if any anatomic anomalies like hydrocephalus and type of breech
IV, maternal O2, pain control
hands off until fetal umbilicus present–Pinard meaneuver; press finger into popliteal fossa
wrap fetus in towel to cushion legs and abdomen; hold at hips, support don’t pull
Lovset’s maneuver when scapulae present
now rewrap fetus so arms are secured
hands off again, observe for delivery of head (10-15s)
attempt to keep head flexed (suprapubic pressure)
if mouth delivers, suction to creat open airway
veit maneuver–aygomatic arches, finger in mouth, occiput to press down
Pippers forceps–kneel, someone else holds baby; L blade, then R blade, articulate, J shape pull
Duhrssen’s incsions 10, 2, 6 o oclock

47
Q

abnormal presentation

A

2nd stage arrest is common with brow presentation–don’t correct with manual manipulation or forceps
expectant management can be considered if large maternal pelvis, small fetus, consistent adequate progess in labor/descent
CD is appropriate in all other circumstances

face presentation: mentum anterior can continue laboring and may successfully deliver vaginally; mentum posterior or transverse need CD

transverse lie with back down means c-section with vertical incision

48
Q

operative vaginal delivery

A

indications for operative vaginal delivery
prolonged second stage of labor: nullip 3hrs (4hrs iwth epidural); multip 2hrs (3hrs with epidural)
concern for immediate or impending fetal compromise
shorten second stage for maternal indications

outlet forceps: fetal scalp visible at introitus without separating the labia; skull is at pelvic floor, head at perineum
low: leading point of skull at2+
mid: would not perform this; fetal skull above 2+ station but engaged

requirements for operative vginal delivery:
cervix fully dilated and retracted
membranes ruptured
engaged fetal head
known position
pelvis though to be adequate
EFW performed
adequate analgesia
empty bladder
appropriate patient positioning
ability to perform emergent c section
patient consent

contraindications:
<34w (vacuum)
position of fetal head unknown or unengaged
fetal conditions: bleeding disorder, bone demineralization disorder

complications
fetal (vacuum): scalp laceration, cephalohematoma, retinal hemorrhage, subaleal hematoma, intracranial hemorrhage
fetal (forceps): facial lacerationsa nd facial nerve palsy, corneal abrasions and external ocular trauma, skull fracture, intracraial hemorrhage

maternal: obstetrical laceration, pelvic hematoma

positioning of vacuum: 2cm anterior to posterior fontanelle, over sagital suture
positioning of forceps: sagittal suture aligned in midline, posterior fontanelle 1 finger breath above the shanks and lambdoid sutures are equidistant from te forceps blades

49
Q

38w, previous vaginal delivey of 4100gm infant; c-section for previa, now has 4490g EFW, what is cousneling

A

absence of diabetes, EFW >5000g consider c-section
vaginal delivery possible but with increased risk of shoulder dystocia
operative vaginal delivery has higher risk of shoulder dystocia but lower risks than c section
if EFW >4500g, if prolonged second stage or arrest of descent above 2+–CD indicated
macrosomia is not a contra indication to a TOLAC but has a lower chance of success

50
Q

maternal risk factors for macrosomia

A

preGDM, GDM, pre-pregnancy obesity, excessive gestational weight gain, abnormal fasting and PP glucose levels, dyslipidemia, prior macrosomic infant and post-term pregnancy

51
Q

isoimmunization
ddx of non immune fetal hydrops at 24w
etiology, evaluation and management

A

parvovirus B19 maternal infection; most women are immune, new infection can result in fetal effects in up to 1/3 cases; vertical transmissin rate ranges from 17-33%; worse in earlier GA–most severe <20w; evaluation is by serial US by 8-12w after maternal illness documented; if no evidence of fetal hydrops, then fetus likely not affected; if hydrops is identified, then do fetal assessment by serial middle cerebral artery peak systolic velocimetry; cordocentesis and fetal RBC transfusion may be performed; maternal infection confirmed wiht serology; fetal infection can be confirmed with PCR testing of amniotic fluid–other infections CMV, Toxo, Syphilis

alpha thalassemia major, hemoglobin Bart
cardiac anomalies–structural and arrhythmias
aneuploidies (45XO)
severe anemia due to massive fetomaternal hemorrhage
certain congenital syndromes
congenital cystic adenomatous formation

52
Q

28w gestation, now has + Ab screen, didn’t have before

A

minor antigens that cause significant iso-immumization include Duffy, Kell, Kidd, Lewis

if positive, immediately test the father – if negative, no risk to the pregnancy as the fetus cannot be antigen positive
if father positive–repeat maternal titers and fetal surveillance (including MCA dopplers)
don’t monitor titers with Kell–they don’t correlate with fetal status/anemia; serial US and MCA doppler studies are indicated

Lew antigen is not a RBC antighen, it is expressewd in other tissues–not associated with isoimmunization

don’t give rhogam, she is already sensitizied
follow with titers, US and MCA dopplers

what causes maternal alloimmunization: transplacental fetomaternal bleeding during any pregnancy, injection with needles contaminated with RhD pos blood, inadvertent transfusion of RhD blood

53
Q

PTL/PPROM

A

previous PTD; do serial ultrasound surveillance of cervical length q2w from 16-24w; if CL <25mm identified, then a cerclage can be placed OR vaginal progesterone

modifiable maternal risk factors for PTD: low maternal pre-pregnancy weight, smoking, substance abuse, short interva pregnancy

27w 1cm dilated what next?
evaluate on L&D–is evidence of PTL (cervical exam), fetal status and presentation, collect FFN to assess if delivery eminent–consider Mg, BMTZ, GBS ppx, tocolysis for BMTZ

54
Q

evaluation of PTL

A

review obstetrical history; look for history of PTD and risk factors in current pregnancy (infections, cervical shortening, cerclage, congenital uterine anomalies, etc)
careful pelvic examination with speculum and bimanual exam to include assessment of any possible inflammatory infection source implicated in the onset of PTL
EFM/TOCO continuously
US for assessment of cervical length, EFW/EGA and amniotic fluid volume, fetal presentation
UA, cervical and vaginal cx including GBS
FFN

tocolysis: beta adrenergic agonists, CCB, NSAIDs

MgSo4 tox:8-10 nausea, lossof DTRs; 14-16 respiratory arrest, >30 cardiac arrest

contraindications to tocolysis: IUFD, lethal fetal anomaly, NRFHT, server preE, maternal bleeding with hemodynamic instability, choio, pprom

in multifetal gestation; give steroids and Mg, no tocolysis

tocolytics: terbutaline–can have maternal cardiac complications; nifedipine–maternal flushing, headaches, nausea, hypotension; indomethacin–contraindicated in women with gastritis, h/o GI bleed, aspirin hypersensitivity, >32w cant give bc of risk of closure of PDA

55
Q

cerclage

A

candidates: singleton pregnancy and history of cervical insufficiency, painless cervical dilationon exam, cervical length <25mm with prior spontaneous preterm birth before 34w; can consider in low risk patient with very short cervix of <1cm

high risk patient (prior spontaneous PTD<34w) should be offered progesterone supplementation from 16-36w and cervical length measurement every 2w
–cerclage placement between 16-24w if CL <25mm

cerclage is removed at 36w EGA or for development of active PTL prior to 36w

56
Q

PPROm

A

48hrs of IV ampicillin and azithromycin
5 days oral amoxicllin and azithromycin
avoid augmentin due to risk fo necrotizing enterocolitis

management: once ROM confirmed, evaluate GA, fetal presentation, wellbeing, signs of infection/abruption; get GBS cx and other cx if indicated

PPROM without evidence of chorio, preterm labor or fetal compromise is not an indication for removal of a cerclage

57
Q

previous deliveries at 16w and 18w, what is DDX?

A

incompetent cervix, occult preterm labor, occult PPROm, chorioamnionitis, anomalous condition of the fetus, congenital uterine anomalies

dx of cervical insufficiency=painless cervical dilation after the first trimester with expulsion of the pregnancy in the 2nd trimester (usually before 24w) in the absence of ctx, labor or other pathology (bleeding, infection or ruptured membranes)–a shortened cervical length in the 2nd trimester is a marker for increased risk fo PTD but has not been shown to identify cervical insufficiency

indications for cerclage:
history of >1 second trimester losses related to painless cervical dilation in the absence of labor or abruption
current isngleton pregnancy, prior spontaneous PTD <34w and cervical length <25mm before 24w
presence of painless cervical dilation in 2nd tri (r/o labor, infection, abruption)

58
Q

DIC and placental abruption

A

preterm: stabilize mother–maintain volume status with FFP

if fetal demise: vaginal birth preferred if mom is hemodynamically stable without coagulopathy and if vaginal birth imminent
CD is preferable when vaginal birth is not imminent and rapid control of bleeding is required due to maternal hemodynamic instability OR significant coagulopathy

if cat 3–expeditious delivery indicated; vaginal birth if imminent (spontaneous or instrument assisted vaginal birth) whether or not mom is stable; otherwise CD

59
Q

1st trimester bleeding

A

physiologic chagnes within the endometrial/placental interface (implantation bleeding)
threatened spontaneous abortion
pregnancy loss
ectopic
molar
cervicitis or vaginitis

2nd/3rd tri:
cervicitis or vaginitis
dilation (labor or incompetent cervix)
abnormal placentation
abruption, marginal separation
PPROm
FDIU
uterine rupture
ruptured vasa previa

60
Q

abnormal placentation

A

placenta accreta may be diagnosed by US: loss of the hypoechoic placental/myometrial boundary zone, loss of the uterine serosa/bladder interface, focal intraplacental masses, numerous intraplacental vascular lakes

MRI mayb e useful in cases of equivocal US findings, posterior placental location

most important risk factor is presence of placenta previa which is present in 80% of accretas

antepartum fetal surveillance in 3rd tri appropriate; antenatal coticosteroid for lung maturity, optimize blood count, c-hyst with placenta left in situ after delivery of fetus at 34w-35w

61
Q

3w pp with heavy vaginal bleeding, difficult placental removal

A

ddx of delayed hemorrhage
infection/endomyometritis
subinvolution of the placental site
retained products of conception
retained intrauterine clot

62
Q

ureter and c section

A

risk of injury usual if broad ligament extension
to minimize risk of injury to ureter:
understand where ureter is
open broad ligament and attempt to find it
you can open dome of bladder and feed stents up UOs

you can give methylene blue or fluorescein IV and look for spillage in abdomen

63
Q

vasa previa

A

serial US every 4-6w starting at 24w
admit to the hospital at 30-34w for maternal and fetal surveillance
steroids
planned CD at 34-35w
prompt CD if persistent variables on NST; NR NST, PROm, suspected PTL, vaginal bleeding with fetal tachycardia, sinusoidal pattern or evidence of fetal bleeding

64
Q

AFE

A

rapidly fatal in 80% cases
clinical diagnosis and should be suspected in pregnant or recently PP with sudden cardiovascular collapse, severe respiratory difficulty, hypoxemia especially when followed by DIC

thought to arise from entrance of amniotic fluid, fetal cellular debris or other antigenic material into the maternal cirulcation causing a massive anaphylacitc reaction and activation of the complement cascade
phase 1: pulmonary artery vasospasm, RV failure, LV failure and systemic hypotension leading to hypoxia, cardiogenic pulmonary edema and is often fatal as cardiac arrest may occur
phase 2: DIC, massive hemorrhage, noncardiogenic pulmonary edema

SMFM definition: sudden onset cardiorespiratory arrest OR hyptension with evidence of respiratory compromise; documentaiton of overt DIC; clinical onset during labor or within 30 min of placental delivery, absence of fever during labor

65
Q

pregnancy physiology

A

water metabolism: water retention

carbohydrate metabolism: mild fastin hypoglycemia, postprandial hyperglycemia and hyperinsulinemia

blood volume: hypervolemia with 40-45% increase in blood volume; increase red blood cell but not as much as volume; hgb 11 is abnormal late in pregnancy

respiratory: diaphragm rises about 4cm; RR unchanged; but TV and resting minute ventilation increase significantly–enhanced due to progesterone, low expiratory reserve volume and compensated respiratory alkalosis ; functional residual capacity and the residual volume are decreased; peak expiratory flow rates decline progressivley as gestation advances; lung compliance is unaffected

66
Q

failed labor

A

failed induction: failure to generate regular ctx q3 min and cervcial change after 24hrs pitocin (ideally with AROM)

arrest of dilation (1st stage arrest): dilation of greater than 6cm with ROM and no cervical change for 4 hours with adequate contractions or 6hrs of inadequate contractions

arrest of descent (2nd stage arrest): 2hrs multip without epidural; 3hrs multip with epidural or primip without epidural; 4hrs primip with epidural

67
Q

massive transfusion

A

> 10u prbcs in 24hrs or 4u pRBCs in 1 hour

1:1:1 add cryo for consuptive coagulopathy

massive transfusion: increases K, decreases calcium, cirtrate toxicity and can lead to pulm edema

FFP (good in DIC): figrinogen and AT3, F5 and F8
cryo (vWB and hemophilia) figrinogen F8, F13 and vWB

68
Q

changes in clotting in normal pregnancy

A

increase thrombotic activity
increase F5, 7, 9, 10, 12 and fibrinogen
decrease in fibrinolytic activity
increase in plasminogen activator inhibitor

69
Q

lidocaine

A

with epi: 7mg/kg up to 60cc
withou epi: 4mg/kg up to 30cc

toxicity: metallic taste in mouth, perioral numbness, tinnitus, slurred speech, blurred vision, altered consciousness, vonvulsions, arrthymia, death

70
Q

MOA of magnesium

A

works at neuromuscular jxn by inhibiting presynaptic release of acetylcholine and desensitizing the post synaptic membrane

71
Q

pathophysiology of preE

A

absence ofnormal hypervolemia of pregnancy resultant hemoconcentration
thrombocytopenia
hemolysis
elevated liver enzymes
oliguria
elevated uric acid
risk of PTL

72
Q

endocarditis ppx

A

not generally recommended
can consider: prosthetic valve, unrepaired cyanotic disease, previous endocarditis

(amp 2g x1 or vanco)

73
Q

cardiac disease in pregnancy

A

mitrial stenosis: most common rheumatic heart condition, fixed C due to narrowed valve; normal physiologic changes in pregnancy lead to back up in lungs bc narrowed valve cant puh it forward; 25% present with heart failure for first time in pregnancy; enlarged LA predisposes to afib
avoid fluid overload and valsalva shorten 2nd stage

marfan syndrome with dilated aortic root >40mm do CD

highest risk in pregnancy
pulmonary HTN
severe cardiomyopathy
severe aortic stenosis
marfan with dialted aortic root
NYHA class 4