Pregnancy pathophys Flashcards
consequences of dysfunctional early placenta dev
- prematurity
- fetal growth restriction
- stillbirth
- preeclampsia
due date calc
LMP + 280 days ~40wk
EDD often corrected based on crown-rump length in 1st tri, more accurate indication of start of pregnancy
how long conception –> implantation
1 wk
“pregnancy” starts when egg implants
trophoblast differentiation and function
b//c placenta
syncytiotrophoblasts
- produce hormones (hCG to maintain corpus lutem)
- proteases to degrade endometrium
cytotrophoblasts
- direct contact with maternal blood = uteroplacental circulation
- during invasion extravillous trophoblasts seek sPIRal arteries
- remodeling of spiral arteries
preeclampsia mx
- high bp during pregnancy
- risk of eclampsia
- d/t inadequate placental invasion during early pregnancy
mx:
- myometrial spiral arterioles undisturbed by trophoblasts = still responsive to maternal vasomotor
- impaired blood supply to placenta –> increased maternal bp
- sFLT –> endothelial dysfunction (anti-angiogenic)
signalling molecules in placentation
angiogenic:
- support formation of new blood vessels
- PIGF - placental growth factor
- VEGF
anti-angiogenic
- prevent maternal endothelial cells from resealing ends of spiral arteries
- prevent maternal blood vessels from entering fetal compartment
- prevent fetal vessels from growing out into uterus
- sFLT-1
- increased in preeclampsia
placenta accreta spectrum
excessive invasion of placenta into uterus
*hemorrhage risk
- accreta = villi attached to myometrium
- increta = villa invade myometrium
- percreta = villi invade through myometrium
placental hemorrhage ddx
- placenta accreta spectrum (accreta < increta < percreta)
- placenta previa (covering cervix)
- placental abruption (*trauma, smoking, hypertension, preeclampsia, cocaine)
fetal nutrition in pregnancy
first 10-12 weeks = diffusion/histiotrophic
then vascular circulation/hemotrophic
placental hormones
syncytiotrophoblast
- influence maternal physiology
- beta-hCG maintains corpus luteum
- progesterone synthesized de novo from cholesterol, maintains endometrium and pregnancy
- hPL ~ GH, decreases maternal insulin sensitivity and glucose
- CRH –> fetal ACTH, onset of labor
cytotrophoblast
- prevent maternal hormones from entering fetal compartment
hCG testing
- blood detection at 3 weeks (1 wk post-conception)
- urine @ 4 wk
- doubles every 48 hours in early pregnancy
- peaks at 8-10 wk
thyroid hormones in preg
alpha-hCG is identical to TSH, stimulates T3/T4 production
- T3/T4 increases throughout pregnancy and don’t fall much even after hCG has dropped
- TSH inversely proportional to hCG, initial significant dip followed by recovery as hCG peaks and drops ~8-10 wk
progesterone in pregnancy
- initially produced by corpus luteum
- then directly by placenta via de novo synthesis from cholesterol
“pro-gestation”
- immune tolerance to fetus
- hair growth
- inhibits prolactin
- increases respiration (maternal)
- smooth muscle relaxation –> vasodilation (important d/t increase in plasma volume)
- inhibits uterine contraction
sfx:
- GI: constipation, gallstones
- possible orthostatic hypotension
CVD in preg - presentation
htn ≥ 140
HR ≥ 120
crackles, S3, gallop
O2 ≤ 90%
(some or all of above)
estrogens in pregnancy
- increases across gestation
- fetal DHEAs (fetal adrenal) –> estraDIol (E2) and *esTRIol (E3)
- b/c placenta lacks 17alpha hydroxylase only DHEA pathway, no de novo synthesis
low estriol ~ poor outcome
fx
- endometrial and uterine growth
- placental angiogenesis
- breast enlargement
sfx
- nausea
- hepatic clotting factors (increased clotting)
- estriol –> contractions, labor onset
hPL
human placental lactogen similar to GH shunts resources to baby - decreases maternal insulin sensitivity - decreases maternal glucose use - increases maternal lipolysis also mammogenesis
CRH
increases fetal ACTH
involved in immunosuppression
involved in onset of labor
blood changes in pregnancy
increased blood volume by ~50%
- protection from blood loss at delivery
- circulation to baby
- starts at 6-8 wk
- possibly triggered by estrogen stim of RAAS
increased red cell mass by ~20-30%
- EPOesis d/t progesterone, hPL, prolactin
- increase iron demand
- lower blood viscosity – intervillous circulation, protect VTE
dilution anemia (more increase in blood volume than red cell mass)
CV changes in pregnancy
increase ventricular muscle mass and contractility
- dilated heart but no reduction in EF
- starts in 1st trimester
- EDV increases in late pregnancy
CO increase by ~30-50%
- most in first 8 wk
- SV declines somewhat at term
- postural - drops ~25% when supine, postural hypotension in ~8%
- distribution mainly to uterus, kidneys, breast, and skin
- no change in flow to brain, liver
SVR decreases ~35-40%
- starting as early as 5 wk
- ? why, progesterone, NO, low resistance placental circulation
BP decreases 5-10/10-15 mmHg
- ~24 wk
- affected by posture
- except in preeclampsia
CV changes intrapartum (during labor) and postpartum
further increase in CO
- E/NE rise d/t pain
- autotransfusion d/t contractions
- less affected if +epidural, left lateral position
CO increases another ~80% in first 15 min postpartum
- autotransfusion d/t contractions
- relief of aortocaval compression
CO returns to pre-labor ~1 h post-delivery
CO, SV, SVR do not return to pre-pregnancy until 12+ wk PP
PE CV findings in preg
normal:
- 3rd heart sound
- flow murmurs
- up/lateral heart displacement CXR
abnormal:
- systolic murmur >2/4
- chronic hypertension
expected but abnormal:
- decompensation of underlying CVD
respiratory changes in pregnancy
- O2 demand +20-40%
- tidal volume +40%
- minute ventilation +30-50%
- no change in RR
- decreased functional residual capacity d/t shmooshing ~20%
- less reserve but no change in VC
- no change in FEV1
why?
- progesterone is a respiratory stimulant
- increased sensitivity of medulla to CO2
acid-base changes in pregnancy
normal:
- mild respiratory alkalosis
- hyperventilation –> hypOcapnia
- facilitates CO2 fetus –> mom
- partial compensation +bicarb
abnormal:
- mild CO2 elevation PaCO2 >35 is respiratory failure
- requires intubation at that point
- e.g. acute asthma attack
renal changes in pregnancy
structure:
- larger +1-1.5cm
- dilated calyces and pelvis
- dilated ureters
- right > left d/t dextrorotation of uterus
- persists 3-4 mo PP
fx:
- flow +50-85%
- GFR +50% all in 1st tri
- vasodilation of pre and post glomerular vessels w/o change in pressure
- fall in serum creatinine
- saturation of glucose reabsorption –> glucosuria
- no hematuria
- protein loss <300mg/24 h
bladder changes in pregnancy
- upward displacement
- flattening
- urinary frequency
- mechanical + hormonal
- increased bladder capacity by ~1 L
normal renal/urinary lab changes in preg
- low serum Cr (threshold of suspicion for disease also lower)
- more rapid drug ecertion
- glycosuria
- asymptomatic bacteriuria
- – strep B can be problem during cb
GI changes in pregnancy
gastric reflux more likely
- delayed gastric emptying
- relaxation of lower esophageal sphincter
- increase in gastric acid
constipation more likely
- slower transit
also
- stomach displaced upward
- increased mucus
gallbladder changes in pregnancy
stasis –> gallstones
- progesterone inhibits contractions
- decreased contractility = slow emptying
WBC changes in preg
pre-preg ~4500
preg ~5000-12000
labor ~20000-25000
predominant rise in PMNs
platelet and clotting changes in preg
VTE risk 6x
platelets
- increased production
- increased consumption
- sometimes a fall in 3rd tri d/t increase in peripheral consumption
clotting factors
- increase
- fibrinogen, V, VIII, IX, X –> thrombin
- d/t estrogen
- decreased fibrinolysis, protein S activity
venous stasis and deep vein capacitance also increase VTE risk
skin changes pregnancy
- +blood flow
- +pigmentation
- melasma
- darker nevi (rapid changes –> excision)
- less hair loss during preg
- more hair loss pp, regrowth by 6-12 mo
breast changes pregnancy
early
- tenderness
- tingling
- heavyness
- enlargement d/t
- – vascular engorgement
- – estrogen –> ductal growth
- – progesterone –> alveolar hypertrophy
later
- enlargement and pigmentation of areollae
- colostrum late in preg
- milk production
- – estrogen
- – progesterone
- – prolactin
- – hPL
- – cortisol
- – insulin
lactation
- drop in E and P pp
- progesterone inhibits lactation
- maternal prolactin decreases pp, but not as much as progesterone –> lactation
- pulsatile prolactin d/t suckling –> milk
“let down”
- suckling –> oxytocin –> release by myoepithelial cells
thyroid changes in preg
- increased
- alpha hCG = TSH
- thyroid enlargement d/t hyperplasia and vascularity
- TBG (binding globulin) +2-3x d/t estrogen
clinically:
- don’t check total T4 or T3, check ratio FT3/FT4
- low TSH common in 1st tri
- transient hyper-T4 in first tri
metabolism and nutritional requirement in preg
- increased metabolic demands
- 300-400 cal/day in 2nd and 3rd tri
- protein recommendations increase
- carb recommendations increase
- no rec for fat d/t optimal not known
weight gain rec in preg
BMI <18.5
- total +30-40 lb
- 1-4 lb 1st tri
- 1-1.5lb/wk 2nd and 3rd
BMI 18.5-24.9
- total +25-35 lb
- 1-4 lb 1st tri
- 1lb/wk 2nd and 3rd
BMI 25-29.9
- total +15-25 lb
- 1-4 lb 1st tri
- 0.5 lb/wk 2nd and 3rd
BMI ≥30
- total +10-20 lb
- 1-4 lb 1st tri
- > 0.5 lb/wk therafter
miscarriage/spontaneous abortion vs. stillbirth
SAB <20wk or fetus <500g
stillbirth thereafter
G&P
gravida = number of pregnancies, including the current one
para = delivery after 20 wk, abortion prior to 20 wk, living children
SAB incidence
15-20%
80% of which <12 wk
categories of SAB
- threatened
- inevitable
- complete
- incomplete
- missed
- septic
- anembryonic/blighted ovum
threatened SAB
- bleeding
- closed cervical os
- no tissue passage
- watch and wait
- bedrest no longer indicated as no clinical benefit
inevitable SAB
- bleeding or leaking fluids
- dilated cervical os
- imminent fetal loss
- POC not yet passed
- ± fever, pain
- may require medical or surgical intervention
complete SAB
- all POC (products of conception) expelled
- hx of heavy vaginal bleeding
- closed cervical os (b/c already closed again)
- generally no further treatment or f/u needed
incomplete SAB
- some POC expelled
- bleeding, cramping
- open cervical os
- watch and wait
- may need medical or surgical mgmt
missed SAB
- POC retained after demise
- asymptomatic
- pt reports “not feeling pregnant”
- closed cervical os
- requires evacuation
septic SAB
- infection post-demise
- d/t retained POC + ascending bacteria
- possible sepsis
- uterine evacuation + abx
anembryonic preg/blighted ovum
- embryo fails to develop
- empty gestational sac, no fetal pole
- similar presentation to missed or threatened ab (bleeding or asymptomatic, generally no pain, fever, cramping, heavy bleeding)
- d/t aneuploidy (± chromosome)
fetal risk fx for SAB
chromosomal abnormalities, usually aneuploidy (± chromosome) ~75% of 1st tri SA, ~50% overall
- – trisomies ~50%, esp 16
- – monosomy X ~18%
- – polyploidy e.g. 69XXY
other fetal anomalies such as genetic mutations not compatible with life
maternal risk fx for SAB
- advanced maternal age >35
- previous SAB
- smoking, alcohol, cocaine
- maternal chronic disease: diabetes, thyroid, PCOS, etc
- immune disease e.g. APLS (antiphospholipid syndrome)
- TORCH infections
- listeria
- fever
- severely over or underweight
- balanced translocation carrier
SAB > fertility rate at ~ ___ y/o
40
SAB almost 100% >45 y/o
uterine risk fx for SAB
- congenital anomolies
- septet uterus
- fibroids
- IUD
- polyps
- scarring
- cervical insufficiency/incompetence
- conization, LEEP, other cervical procedures (e.g. cancer or biopsy)
other risk fx for SAB
- amniocentesis
- chorionic villi sampling
- direct or indirect trauma
- ovary removal
- subchhorionic hematoma
NOT
- stress
- heavy lifting
- sex
workup for SAB
- H&P
- bleeding, pain, cramping
- UPT
- pelvic US
- ± beta-hCG, CBC, Rh, blood type
management/workup for preg of uncertain viability
- suspect if slow growth, slow hr, large or abnormal sac
- expectant management
- trend beta-hCG - declining, plateau ~ abnormal preg
- repeat US
- serum progesterone <5 ng/ml
- Rhogam blood type and Ab screen
- CBC if heavy bleeding, infection
management of confirmed SAB
- expectant
retained POC:
- medical - prostaglandin E1 (misoprostol)
- – pretreatment w/ mifepristone improves evacuation success
- D&C
- vacuum aspiration
complications
- hemorrhage
- retained POC
- infection
- perforation
- asherman syndrome post-D&C
post-SAB management
- counseling
- future pregnancy planning
optional:
- f/u beta-hCG
- confirmatory US
recurrent pregnancy loss
2-3+ SAB
3+ <1% incidence
~50% unknown cause
w/u:
- thyroid
- HbA1c
- anti-phospholipid Ab
- uterine assessment
- parental karyotype
tx:
- limited options w/o identifiable cause
- possible role for IVF w/ selection of normal embryo
APLS
antiphospholipid syndrome
- 1 clinical and 1 lab indication to make dx
sx:
- VTE
- preg morbidity
- – 1+ loss >10wk
- – preterm <34 wk d/t preeclampsia or IUGR
- – recurrent loss
labs:
- IgG or IgM anticardiolipin
- +lupus anticoagulant
- IgG or IgM beta-2 glycoprotein
tx:
- heparin
- ASA
ectopic pregnancy
- implantation outside endometrial cavity
~98% Fallopian tube
sx:
- pelvic pain
- vaginal bleeding
- +UPT
- high index of suspicion
w/u:
- PE
- transvaginal US
- beta-hCG
- (laparoscopy)
tx:
- expectant
- methotrexate IF hemodynamically stable, asymptomatic, able to comply w/ follow up, no fetal cardiac activity, normal labs
- – folic acid antagonist vs trophoblast
- – nausea, vomiting, diarrhea, dizziness, stomatitis
- – abd pain for a few days
- surgery = definitive
- – laparoscopy
- – laparotomy
- – linear salpingostomy or salpingectomy
risk fx:
- IUD
- previous ectopic
- tubal damage, surgery
- prior tubal infection
- STI
- assisted reproductive technology
- smoking
heteroectopic pregnancy
multiple pregnancy w/ 1+ extrauterine and 1+ intrauterine
increasing incidence d/t assisted repro
molar pregnancy
- placental tumor
- premalignant
complete mole
- no fetus
- vesicles only
- all paternal chromosomes
- bleeding
- size > expected by LMP
- very high beta-hCG
- hyperemesis, PEC, hypERthyroid, theca lutein cysts
- 15-20% risk of neoplasia
partial mole:
- some fetal tissue
- triploid karyotype (69XXY, 69XXX, 69XYY)
- <5% neoplasia risk
- high bleeding risk
- tx: D&C w/ aspiration, f/u weekly beta-hCG monitoring
risk fx:
- prior GTD
- age extremes
3 “P’s” of normal labor
Power - uterine contractions
Passenger - fetus, position, umbilicus
Passage - maternal pelvis
Braxton-hicks
sporadic uterine muscle activity
vs true, synchronized
>37 wk normal
assessment:
- sterile vag exam for dilation and effacement
- fetal heart tones, doppler or electronic monitoring
- fetal presentation, hand or US
- possible contraction monitoring
cervical changes labor
dilation –> 10cm
effacement –> 100%, essentially flattening of cervix as it b//c dilated
station –> -5 to +5, location/orientation, 0 is ischial spine
pliancy
fetal orientations
lie:
- longitudinal (normal)
- transverse
- oblique
presentation
- cephalic (normal)
- breech (butt)
- shoulder/arm
attitude
- flexed
- extended
position
- occiput, sacrum, mentum, A/P
leopards maneuvers
manually turning fetus from abdomen
pelvis shapes & fetal passage
gynecoid - most common, best for passage
may recommend C section:
platypoid - oval, L/R
android - heart
arthoropid - oval, A/P
indications for L&D admission
synchronized contractions every 5 min >1h
fluid leak
bleeding
decreased fetal movements
stages of labor
- dilation and effacement
- - latent = less than 6 cm, hours to days
- - active, more than 6 cm, acceleration, less variable, 1 cm every 1-2 h - complete dilation
- - active pushing
- - minutes to 4h
- - longer in nulliparous, epidural - delivery, baby and placenta
- - delayed cord clamping 30-60s after placing on mom’s chest
- - active mgmt of placenta to minimize pp hemorrhage
- — fundal massage, gentle traction, oxytocin
- signs of placental detachment, hemorrhage risk: gush of blood, umbilical cord lengthening
- placental delivery is up to 30 min
- examine placenta for completeness (no POC), umbilical cord insertion (3 normal vessels), and membranes - postpartum to 6 wk
pain mgmt labor
stage 1
- visceral T10-L1
stage 2
- somatic S2-S4
options
- IV morphine
- inhaled nitrous
- epidural ~60% - continuous injection of local anesthetic (usually bupivacaine) into epidural space
- pudendal nerve block
fetal monitoring labor
intermittent
- handheld doppler
- – every 30 min in stage 1, 15 stage 2 in uncomplicated
- – every 15 in stage 1, 5 stage 2 in complicated
continuous
- electronic fetal heart rate monitoring (EFM) ~85%
- – controversial d/t unreliable assessment of fetal oxygenation, increased use of c-section, no significant change to cerebral palsy (d/t large confidence intervalbut does decrease neonatal seizures), and inter and intra-observer variability
- – no RTC
- – always indicated for high risk pregnancies i.e. preeclampsia, T1DM, IUGR
operative vaginal delivery
- vacuum assisted
- forceps assisted
indications
- prolonged phase II
- FHR requiring expedited delivery
- maternal benefit
requirements
- ≥+2 station
- ≥34 weeks
- no maternal/fetal c/i
benefits
- avoid cesarean
- fetus already in canal
risks
- F/M trauma
indications for primary cesarean
- labor arrest
- abnormal FHR
- fetal malpresentation
- multiple gestations
- F/M risk
- large fetal size
- non-gynecoid pelvis or small pelvic outlet
- maternal request
prevention of primary cesarean
- allow prolonged latent labor
- allow prolonged active labor
- allow prolonged pushing
- use operative vaginal delivery
- avoid excessive maternal weight gain
- encourage labor support such as doulas
- leopards maneuver (external cephalic version)
- trial of labor w/ twins
pre-op cesarean mgmt
- counseling
- consent
- IV - labs and fluids
- foley
- mom vitals, fetal EFM
- prep abx - 2 gm Ancef
- anesthesia consult
pp management
- uterine size and maternal physiology returns to normal by 6 wks
- > 50% maternal deaths are pp
- suicide and self harm among leading causes
- ongoing, not single encounter
preterm birth causes
<37wk #1 cause fetal mortality
F/M stress
- activation of HPA
- physical stress, depression
- fetal stress e.g. inadequate arterial supply
inflammation
- infection of placental membranes OR general e.g. UTI, dental
- autoimmune or inflammatory conditions
abruption
- d/t abnormal placentation in early pregnancy
uterine distension
- multiple gestation
- polyhydroamnosis (too much amniotic fluid)
cervical insufficiency
- short cervical length by TVUS is a strong indicator of preterm labor
management of preterm labor
<34 wk
- betamethasone (steroid) injection –> surfactant
- tocolytic agent –> relaxes uterus, delays continuation of labor
<32 wk
- + mag sulfate to protect against seizures, cerebral palsy
hx of preterm labor
- progesterone supplementation throughout preg
general recommendations
- lifestyle changes, e.g. smoking, cocaine use
when to initiate prenatal care
ideally preconception
- risk assessment
- control underlying disease
- smoking cessation
- prenatal vitamins/folic acid
definitely recommended in 1st tri (~60% ww)
no prenatal care ~1% in US, 5x mortality
frequency prenatal care
- 1x/mo through 28 weeks
- 2x/mo 28-36 wek
- weekly >36 wk
h&p 1st prenatal visit
- LMP
- Gs&Ps, outcome specifics
- PMHx
- risk assessment: genetic disease, teratogens
- EtOH, drugs, smoking
- DV
- STI hx
- viral illness since LMP
- religion/cultural considerations
- allergies
- complete physical exam
- US - TV
Gs&Ps
G = gravitas # of current preg P = parity, outcomes by TPAL - term ≥37wk - preterm 20-36w6d (36 weeks 6 days) - abortion, intentional or spontaneous, <20wk - living children at encounter
examples:
G1P0 = first pregnancy
G3P0020 = 3rd pregnancy, 2 prior SAB or AB
G6P3106 = 6th pregnancy, 4 term births, 1 preterm twin delivery
G2P0100 = 2nd pregnancy, 1 preterm delivery of a now-deceased child
may be abridged in certain settings (e.g. G3P2, G6P4, G2P1 in above examples) but OB will generally use full TPAL
calc gestational age
fastest way - LMP -3 mo, +1y3d
e.g. LMP 3/3/22, EDD 12/31/22
- <9wk US, adjust EDD if >5 days discordant from LMP
- 9-14wk US, adjust EDD if >7 days discordant
- 14+ wk dating by biometry
- after 22 wk dating accuracy drops significantly
genetic carrier screening
- expanded vs targeted
- minimum: CF carrier, SMA carrier
- others if FHx, ethnicity risk fx
- pt counseling
aneuploidy screening
1st tri:
- nuchal translucency
- PAPP-A
- hCG
2nd tri:
- hCG
- AFP
- UE3
- inhibin
T21 (Down’s)
- PAPP-A, AFP, UE3 low
- hCG, inhibin high
T18/T13
- all decreased
information from CVS or amnio
- karyotype
- microarray
- other studies
- PCR for TORCH
- (outdated) fetal lung maturity
prenatal visits 1st tri
- 1st visit: LMP, labs, diabetes screen
- 9-10 wk - NIPT (maternal blood screen for certain genetic conditions), doppler
- 11-14: CVS, nuchal translucency
- 10-14 - 1st tri serum
- teratogen avoidance
- dietary counseling
- – avoid unpasteurized dairy, unwashed raw produce, high mercury fish
- toxoplasmosis avoidance
- SAB signs/sx
- symptoms and concerns
prenatal visits 2nd tri
- 15-20: MSAFP
- 15+ wk: amnio
- 18-22 wk: detailed US
- 24-28 wk: gestational diabetes screen, CBC
- symptoms and concerns
- preterm labor/SAB signs/sx
- fundal height
- fetal movement
- may begin to address birth plan, anesthesia, breastfeeding, future family planning etc but typically more in 3rd tri
prenatal visits 3rd tri
- 28 wk - Rhogam (if Rh-)
- 27-36 wk - Tdap
- flu - any
- 3rd tri labs - CBC, RPR, HIV, GC/CT risk
- 36-37w6d - group B strep
- regular US
- fundal height
- fetal movement
- birth plan
- anesthesia plan
- breastfeeding
- family planning/pp bc
- sterilization consent e.g. desired sterilization, hysterectomy in event of complications
- circumcision
- sx and concerns
prenatal visits near dd
- delivery timing
- consider induction of labor
- fetal surveillance
- cesarean
assess at every prenatal visit
- bp
- ±urine dip
- FHR
- weight
- edema
- labor complaints
- ± cervical exam
- sx and concerns
2nd tri on:
- fundal height
- fetal movement (could ask earlier but generally won’t be present until 2nd tri)
cutoffs for htn and severe htn of preg
mild ≥140/90
severe≥160/110
(systolic, diastolic, or both)
classes of htn in preg
- chronic: <20 wk gestation
- gestational: >20wk, mild (140-160)
- preeclampsia: >20wk, mild w/ proteinuria >300
- preeclampsia w/ severe features: >20wk, severe htn or any end-organ damage
- eclampsia: preeclampsia w/ seizure
preeclampsia etiology
- shallow placental invasion
- failure of spiral artery remodeling
- decreased blood flow to fetus w/o reduction in CO
- inflammatory protein release by hypoxic placenta –> vasoconstriction, endothelial dysfunction
- endothelial dysfunction also results in salt retention by kidneys
maternal endothelial cell d/t preeclampsia
- vasospasm
- capillary leak incl proteinuria and edema
- hypercoag
end organ damage d/t preeclampsia
liver renal headache seizure (tx w/ mag) abruption, poor fetal growth
tx for eclampsia
mag to reduce seizures and reduce contractions
immediate delivery
consequences of severe preeclampsia
- placental abruption
- hemorrhagic stroke
- HELLP ~10-20%
- – hemolysis, elevated liver enzymes, low platelets
- – d/t sheering of RBCs over thromocytic plaques
- systemic, pulmonary, and cerebral edema
- seizures caused by cerebral edema mark eclampsia
postpartum hemorrhage defn and etiology
top reason for maternal mortality ww
>500 ml post vaginal, >1000 post-cesarean
internal bleeding signs: >10% change in Hct, hr, bp, o2 changes
4 T’s::
- tone (atony)
- trauma - uterine, cervical, vaginal, peroneal bleeding d/t childbirth trauma; tx: pressure + surgical repair
- tissue - retained placental fragments e.g. placenta accreta, umbilical traction
- thrombin - poor clotting d/t genetic disorder, eclampsia, abruption –> dic; tx underlying cause, administer platelets and coagulation factors
tx::
- specific to type
for all:
- IV fluids
- blood products
uterine atony
- primary cause of postpartum hemorrhage
- soft, spongy, boggy uterus
- slow, steady blood loss
- little to no uterine contraction after birth = no self-clamping of uterine arteries
- d/t uterine fatigue from prolonged labor, multiple births, multiparous, certain anesthetics, urinary retention
tx:
- fundal massage
- catheter (if d/t retention)
- meds
- surgery
uterine hematoma
- cause of delayed hemorrhage
- can often go unnoticed
- mass or collection of blood d/t trauma of childbirth
- rupture
signs:
- persistent bleeding
- firm uterus
- delayed bleeding
maternal cardiac risk stratification
1- no mortality risk, no to mild morbidity risk
2- small mortality risk, moderate morbidity risk
3- significant risk of M&M, rq expert counseling
4- extreme risk, preg c/i, termination advised, continue as in 3 if continues
calculators:
- mWHO
- CARPREG II
- ZAHARA for congenital
preg termination risks in women w/ cardiac conditions
medical ab:
- unpredictable bleeding, hemodynamic alteration
- esp if mother on anticoags or prone to hemodynamic instability
- monitor closely
surgical ab:
- perform in OR w/ skilled anesthesiologists
contraception in cardiac conditions
risk level 3 and 4 mothers need good contraception so that preg, if desired, can be planned and cardiac conditions stabilized amap
estrogen not advised d/t alterations in coag profile, increased bp, fluid retention, potential prolonged QT (mostly in post-menopausal F)
progestin-only is preferred - *IUD best
- – implant and injection have theoretic risk of hematoma in pt on anti-coags, definite c/i in pts on bosentan for pulm htn
- – injection - use caution w/ A-fib, flutter, PHTN, MI
- – pills, ring interferes w/ anticoag
- – IUD lessens menses, less risk of excessive blood loss :)
- – IUD use caution w/ severe htn, complex chd d/t vasovagal
copper implant not advised if on anti-coags d/t worsening of bleeding
non-cardiac risk factors pregnancy
- AMA ≥40 y/o
- black (mainly structural)
- pre-preg BMI ≥35
- pre-preg diabetes
- htn
- substances
- hx chemo
WHO class 4 cardiac risk conditions
- PAH
- EF <30%
- RV failure
- severe mitral stenosis
- severe symptomatic aortic stenosis
- severe aortic dilation
- vascular ehlers-danlos (other EDS types including hypermobile generally do not carry much risk)
- severe recoarctation
- complicated Fontan (surgical procedure rerouting blood to lungs)
breast development
- starts w/ proliferation of fat and glands @ puberty
- glands not fully developed until pregnancy
- delivery: ducts –> buds and alveoli; proliferation declines
- breastfeeding: alveolar hypertrophy, accumulation of secretory products
stages of lactogenesis
stage 1
- colostrum
- 16+ weeks pregnant, through pp day 3
- high IgA, lymphocytes, plasma cells
- poor nutritional content
stage 2
- day ~3-10 pp
- secretory activation
- increased lactose
- decreased lytes (Na+, Cl-, Mg++)
stage 3
- mature
- day 10+ pp through end of feeding
stage 4
- breast involution following end of feeding
- decreased milk production
- apoptosis of milk-producing cells
hypERprolactinemia
- amenorrhea
- infertility
- osteoporosis
- sx d/t GnRH inhibition
causes
- prolactinoma = benign posterior pituitary tumor
- dopamine inhibitors
hormonal components in breastfeeding
during preg
- high inhibitory estrogen, progesterone
- high prolactin, but not sufficient to overcome inhibition
after placental delivery
- diminished progesterone and estrogen
- high prolactin –> milk production
suckling
- prolactin release d/t neural reflex w/ nipple stim –> milk production
- oxytocin release d/t seeing baby, baby crying, other nursing stimulation –> smooth muscle contraction in breast alveoli –> let-down
