medical complications in pregnancy Flashcards
Pregnancy induced HTN (PIH)
HTN that develops AFTER 20 wks of gestation in the absence of proteinuria & returns to nml postpartum.
Chronic HTN
HTN present before 20th wk of pregnancy or HTN present before pregnancy
mild HTN
systolic >/= 140-180 mmHg or
diastolic >/= 90-100 mmHg or
both
severe HTN
SBP >/= 180 mmHg or
DBP >/= 100 mmHg
what is the major risk factor w/ chronic HTN?
development of preeclampsia/ eclampsia later in pregnancy
preeclampsia
develop of HTN w/ proteinuria & edema fter 20wks gestation
BP in preeclampsia
SBP > 140 mmHg or DBP > 90 mmHg
2 occasions > 6 hrs but < 7 days apart
after 20 wks gestation w/ previously nml BP
Proteinuria in preeclampsia
urinary excretion of 0.3 g protein or higher in 24 hr urine or >/= 1+ protein on UA dipstick
severe preeclampsia
SBP > 160 mmHg or DBP > 110 mmHg marked proteinuria -> 5g/24 hr urine or 3+ on 2 dipstick of random urine samples collected at least 4 hrs apart oliguria-> < 500 mL in 24 hrs cerebral/visual distrubances (HA & scotomata) pulmonary edema/cyanosis epigastric/RUQ pain evidence of hepatic dysfunction thrombocytopenia IUGR
eclampsia
presence of convulsions (grand mal seizures) in a woman w/ preeclampsia not explained by neuro d/o
most cases occur w/in 24 hrs of delivery but can also occur 2-10 days postpartum
risk factors for preeclampsia
nulliparity age 35 yo new paternity FH of preeclampsia CRD, chronic HTN prolonged interpregnancy interval antiphospholipid syndrome DM multi-fetal gestation high BMI connective tissue d/o (RA, SLE) vit D insufficiency?
what is the predominant pathophysiological finding in preeclampsia
maternal vasospasm
what are some potential causes of maternal vasospasm
vascular changes
hemostatic changes
changes in prostanoids
dysfunctional changes in endothelium-derived factors
lipid peroxide, free radicals & antioxidant release
vascular changes
theorized that a shallowly implanted placenta becomes hypoxic-> upregulates placental inflammatory mediators->acts on vascular endothelium
- decreased musculature in spinal arterioles leads to development of low-resistance, low pressure, high-flow system
- inadequate maternal vascular response
- endothelial damage w/in vessels
Hemostatic changes
- increased platelet activation w/ increased consumption in microvasculature
- endothelial fibronectin levels are increased & anti-thrombin III 7 a2- antiplsmin levels are decreased (reflects endothelial damage)
changes in prostanoids
-prostacycline (PG12) & thromboxane (TXA2) increased during pregnancy
PG12 promotes what?
vasodilation
TXA2 promotes what?
vasoconstriction
platelet aggregation
during pregnancy, balance is in favor of PG12 or TXA2?
PG12
pts w/ preeclampsia, balance is in favor of PG12 or TXA2?
TXA2
dysfunctional changes in endothelium-derived factors (may be placental in origin)
nitric oxide (potent vasodilator) is decreased–may explain evolution of vasoconstriction
lipid peroxide, free radicals & antioxidant release
lipid peroxide & free radicals implicated in vascular injury & increased in women who develop preeclampsia
decreased antioxidant levels noted
proposed theories regarding preeclampsia
endothelial cell injury immune rejection of the placenta compromised placental perfusion imbalance bet. prostacyclin & thromboxane decreased glomerular filtration rate w/ retention of salt & H2O decreased intravascular vol. increased CNS irritability disseminated intravascular coagulation uterine m. stretch (ischemia) dietary factors, including vit. def. genetics air pollution obesity unfamiliar sperm theory thyroid dysfunction
evaluation of preeclampsia
detailed H&P- hx of HTN, previous preeclampsia
review of OB records if applicable
BP (tends to decline 2nd trimester)
wt- rapid wt gain (2 lbs/wk)
edema
DTRs- hyperreflexia or clonus at ankle worrisome
S&S’s of preeclampsia
visual disturbances severe/persistant HA RUQ pain hx of LOC/seizures dizziness
edema in preeclampsia
unresponsive to rest in supine position esp. in upper extremities, sacral egion & face
evaluation of the mother
CBC, esp. Hct platelet count- thrombocytopenia coag profile (PT, PTT)- coagulopathy LFTs- hepatocellular dysfunction SCr- decreased renal function uric acid 24 hr urine CrCl total urinary protein
Hct in preeclampsia
Hct signals worsening vasoconstriction & intravascular volume or hemolysis
lab studies of fetus
ULS for fetal wt, growth, amniotic fluid vol.
NST &/or biophysical profile- indirect assessment of placental status
Biophysical profile (BPP)
BPP has 5 components: 4 ULS assessments & a nonstress test (NST). The NST evaluates fetal HR & response to fetal mvnt. The 5 discrete biophysical variables:
- fetal mvnt
- fetal tone
- fetal breathing
- amniotic fluid volume
- fetal HR
NST/ Reactive FHR
nml= at least 2 accelerations in 30 min abnml= <2 accel. to satisfy the test in 30 min
ULS: fetal breathing mvnt
nml= at least 1 episode of breathing that lasts >30 seconds or >20s in 30 mins
abnml: none or < than 30s or 20s
ULS: fetal activity/ gross body mvnts
@ least 2 movnts of the torso or limbs
abnml: < 3 or 2 mvnts
ULS: fetal muscle tone
@ least 1 episode of active bendign & straightening of the limb/trunk
abnml: no mvnts or mvnts slow & incomplete
ULS: qualitative AFV/AFI
@ least 1 vertical pocket > 2cm or more in the vertical axis
abnml: largest vertical pocket </= 2 cm
BPP <2
labor induction