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HTN in Pregnancy


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Gestational Hypertension Etiologic theories

a)Disordered placentation
b)Inflammatory disorder – prostaglandin imbalance
c)Immunologic disorder
Disordered placentation
Normally uteroplacental bed is a low resistance, low pressure, high flow system
Normally maternal immune cells facilitate deep invasion of the trophoblast
If poor remodeling of spiral arteries by trophoblast then>>>
Decreased dilatation of spiral arteries>>>increased resistance>>>decreased flow
Risk ratios for developing preeclampsia
Factor Risk Ratio
Nulliparity 3:1
Age>40 3:1
African-American Race 1.5:1
Family hx of htn in pregnancy 5:1 
Chronic hypertension 10:1
Chronic renal disease 20:1 
Risk ratios for developing preeclampsia (2)
Antiphospholipid syndrome 10:1
Diabetes mellitus 2:1 
Twin gestation 4:1 
Angiotensinogen gene T235
Homozygous 20:1
Heterozygous 4:1
Obesity: The risk of preeclampsia doubles with each 5-7 kg/m2 increase in prepregnancy body mass index
Definitions: chronic hypertension
BP >= 140/90 before pregnancy or before 20 weeks gestation
hypertension first diagnosed after 20 weeks and persistent after 12 weeks postpartum
Definitions: gestational hypertension
BP >= 140/90 for first time during pregnancy
No proteinuria
BP return to normal < 12 weeks postpartum
Non-specific diagnosis
will include women with preeclampsia who have not yet developed proteinuria as well as women who will not develop preeclampsia
Final diagnosis only made postpartum
Gestational hypertension
If other symptoms of preeclampsia are present, clinical management may be as for preeclampsia
Most frequent cause of hypertension in pregnancy
6-17% frequency in healthy nulliparous patients
2-4% frequency in healthy multiparas
Risks of gestation hypertension
With mild gestational hypertension:
Increased rates of induction
Increased rates of C/S (failed induction and dystocia)
With severe gestational hypertension:
Increased maternal and fetal/neonatal morbidity and mortality including
Preterm birth
Small for gestational age
Definitions: pre-eclampsia
Minimum criteria: BP >= 140/90 after 20 wks gestation plus proteinuria >=300mg/24hrs or >= 1+ on dipstick
Increased certainty of preeclampsia: BP >= 160/110, 2g proteinuria/2+dip, creatinine > 1.2, platelets < 100K, hemolysis, elevated AST/ALT, persistent HA/visual changes or epigastric pain
Severe preeclampsia per ACOG
BP > (BPs 6 hours apart while on bedrest)
Persistent 3+ protienuria on 2 random dip samples 4 hours apart or >5 gm protein in 24 hour urine collection
Decreased platelet count
Increased transaminases
Persistent headache or visual changes or RUQ or epigastric pain or persistent N&V
Fetal growth restriction
Pulmonary edema or cyanosis
Oliguria: < 500 cc/24 hours
Definitions: eclampsia
Seizures that cannot be attributed to other causes in a woman with preeclampsia
Definitions: superimposed preeclampsia (on chronic hypertension)
New onset proteinuria >= 300mg/24h in hypertensive women but no proteinuria before 20 weeks gestation
a sudden increase in proteinuria or BP or plts < 100K in women with HTN and proteinuria before 20 weeks gestation
What might influence BP?
Size of BP cuff in relation to size of arm
Accuracy of equipment
Rest or activity before BP taken
Posture and position
“White coat syndrome”
Korotkoff sound used (phase IV (muffling) or phase V (disappearance)—use phase V
Caffeine, smoking, other drugs
Clinical manifestations of preeclampsia
cardiovascular changes
Increased BP
Alterations in cardiac output
Decreased intravascular volume
Clinical manifestations of preeclampsia
hematologic changes
Mild coagulopathy
Thrombocytopenia – may result from platelet activation and consumption. Lower plts associated with worse outcomes; reflects severity of disease
Fragmentation hemolysis
Clinical manifestations of preeclampsia
renal changes
Reduced GFR
Elevated creatinine secondary to vasospasm
Proteinuria – note that dipsticks do not correspond well with 24 hour urine results
Clinical manifestations of preeclampsia
liver changes
Liver changes
Elevated transaminases – likely secondary to periportal hemorrhagic necrosis
Rarely, bleeding may lead to subcapsular hematoma or hepatic rupture
Clinical manifestations of preeclampsia
CNS changes
Eclampsia/grand mal seizures
Cerebral hemorrhage, cerebral edema, blindness from retinal artery vasospasm, brainstem herniation
Patients with unusual neurologic symptoms should be promptly evaluated – get urgent consultation
Clinical manifestations of preeclampsia
fetal effects
Uteroplacental insufficiency
Prematurity (iatrogenic)
Intrauterine growth restriction
Worst outcomes seen in women with chronic hypertension and superimposed preeclampsia
HELLP syndrome
microangiopathic hemolysis with an abnormal smear (schistocytes, burr cells, echinocytes)
LDH (>2x upper limits of normal), indirect bili
Significant drop in hemoglobin
ELevated liver enzymes
Transaminase >2x upper limits of normal
Low Platelets (<100,000)
Considered a variation of severe preeclampsia
Increased maternal morbidity and mortality
Prevention of preeclampsia – low-dose aspirin
50-150 mg aspirin per day, starting at ~12 weeks until delivery
Aspirin therapy reduced the risk of perinatal death, spontaneous preterm birth, and preeclampsia, with no increase in abruption/bleeding
Management of preeclampsia Goals (3)
Three goals:
1) Delivery with the least possible trauma to mother and fetus
2) Birth of a healthy infant
3 )Complete restoration of health to the mother
Management of preeclampsia
Early prenatal detection
Increased visits in 3rd trimester
“Maybe developing preeclampsia”…
e.g., DBP 81-89, increase in BP 30 systolic, 15 diastolic over first trimester or non-pregnant baseline
outpatient surveillance with office visits every 3-4 days for urine dip and BP check
consider antenatal testing
Consider baseline preeclampsia labs (CBC with platelets, AST, ALT, creatinine)
Management of preeclampsia
Diagnosis of mild preeclampsia at term:
If cervix is favorable, consider induction
If cervix is not favorable, induction is still preferred – but if mild preeclampsia may consider:
Daily blood pressure and urine checks
Fetal monitoring (daily NST/AFI)
If condition worsens, induce.
If it stabilizes or improves may wait for favorable cervix
Management of preeclampsia
when contemplating induction consider:
Disease severity
Fetal gestational age
Maternal and fetal status
Bishop’s score
Parental wishes
Management of preeclampsia
preterm patients
Mild preeclampsia can be managed by close inpatient or outpatient observation
serial BP checks
weekly preeclampsia labs
antenatal testing twice weekly
ultrasound every 3 weeks
No evidence that bedrest is helpful
Antihypertensives may decrease the rate of progression to severe preeclampsia, but do not improve perinatal outcome
Balance risks of prematurity vs. risk of disease to mother and fetus
If lung maturity can be documented, delivery is indicated
Management of preeclampsia
32-34 weeks --Consider delivery, amnio for lung maturity, betamethasone with delivery in 48hours
Less than 32 weeks – if mild disease, may hospitalize and observe. May transiently improve with bedrest, but close maternal and fetal observation is essential
If evidence of severe disease persists, delivery is usually indicated, although perinatologists may occasionally use expectant management
Management of gestational hypertension
No clear guide in terms of whether or not to induce
Need close f/u with BP checks, urine dips, antenatal testing, baseline preeclampsia labs
Preeclampsia and gestational hypertension
morbidity and mortality
Mild preeclampsia and gestational hypertension at or near term is associated with minimal maternal/neonatal morbidity
Severe preeclampsia or gestational hypertension at < 35 weeks associated with significant maternal and perinatal complications

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