Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
29 Cards in this Set
- Front
- Back
Gestational Hypertension Etiologic theories
|
Multifactorial
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
OR 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 Abruption 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 Eclampsia 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
OR 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 Hemoconcentration |
|
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 Oliguria |
|
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
|
Hemolysis
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 |