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
repair of 4th degree laceration
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
26
forceps and vacuum
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
27
intercourse pain at 12w pp
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
28
variable deceleration
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
29
HSV in pregnancy Hep B serology
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
30
Varicella in pregnancy
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
Parvovirus and CMV in pregnancy
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
chorio and endometritis
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
GBS
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
mastitis
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
ddx of fevers on POD#2 s/p CD
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
PP hematoma
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
pyelo in preganncy
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
twins
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
HTN disorder of pregnancy
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
ecclampsia
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
preGDM
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
gestational DM
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
IUGR
<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
44
shoulder dystocia
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
ECV
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
vaginal breech
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
abnormal presentation
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
operative vaginal delivery
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
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38w, previous vaginal delivey of 4100gm infant; c-section for previa, now has 4490g EFW, what is cousneling
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
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maternal risk factors for macrosomia
preGDM, GDM, pre-pregnancy obesity, excessive gestational weight gain, abnormal fasting and PP glucose levels, dyslipidemia, prior macrosomic infant and post-term pregnancy
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isoimmunization ddx of non immune fetal hydrops at 24w etiology, evaluation and management
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
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28w gestation, now has + Ab screen, didn't have before
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
PTL/PPROM
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
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evaluation of PTL
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
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cerclage
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
PPROm
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
previous deliveries at 16w and 18w, what is DDX?
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)
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DIC and placental abruption
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
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1st trimester bleeding
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
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abnormal placentation
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
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3w pp with heavy vaginal bleeding, difficult placental removal
ddx of delayed hemorrhage infection/endomyometritis subinvolution of the placental site retained products of conception retained intrauterine clot
62
ureter and c section
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
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vasa previa
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
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AFE
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
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pregnancy physiology
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
failed labor
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
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massive transfusion
>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
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changes in clotting in normal pregnancy
increase thrombotic activity increase F5, 7, 9, 10, 12 and fibrinogen decrease in fibrinolytic activity increase in plasminogen activator inhibitor
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lidocaine
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
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MOA of magnesium
works at neuromuscular jxn by inhibiting presynaptic release of acetylcholine and desensitizing the post synaptic membrane
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pathophysiology of preE
absence ofnormal hypervolemia of pregnancy resultant hemoconcentration thrombocytopenia hemolysis elevated liver enzymes oliguria elevated uric acid risk of PTL
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endocarditis ppx
not generally recommended can consider: prosthetic valve, unrepaired cyanotic disease, previous endocarditis (amp 2g x1 or vanco)
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cardiac disease in pregnancy
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