HYPERTENSION IN PREGNANCY

Classification of Hypertensive
disorders in Pregnancy
1. Gestational Hypertension
2. Preeclampsia
3. Eclampsia
4. Preeclampsia superimposed on chronic
Hypertension
5. Chronic Hypertension
 Gestational Hypertension
BP 140/90 mmHg for the first time during
pregnancy
No proteinuria
BP returns to N < 12 weeks postpartum
 Preeclampsia
Minimum Criteria
BP 140/90 mmHg after 20 weeks gestation
Proteinuria 300mg/24 hours or 1+
dipstick
 Preeclampsia
Increased certainty of preeclampsia
BP 160/110 mmHg
Proteinuria 2.0g/24 hours or 2 + dipstick Serum
creatinine 1.2 mg/dL
Platelets < 100,000/mm3
Microangiopathic hemolysis (increased LDH)
Elevated ALT or AST
Persistent headache or other cerebral or visual
disturbance
Persistent epigastric pain
 Indications of Severity of
Hypertensive Disorders During
Pregnancy
ABNORMALITY MILD SEVERE
Diastolic BP 100 mmhg 110mmhg
Proteinuria Trace to 1 + 2+
Headache Absent Present
Visual disturbance Absent Present
Upper abdominal pain Absent Present
Oliguria Absent Present
Convulsion (eclampsia) Absent Present
Serum creatinine Normal Elevated
Thrombocytopenia Absent Present
Liver enzyme elevation Minimal Marked
Fetal growth restriction Absent Obvious
Pulmonary edema Absent Present
 Eclampsia
Seizures/convulsions + preeclampsia
 Preeclampsia superimposed on
chronic HPN
New-onset proteinuria 300mg/24 hours in
hypertensive women but no proteinuria
before 20 weeks gestation
A sudden in proteinuria or BP or platelet
count < 100,000mm3 in women with HPN and
proteinuria before 20 weeks gestation
 Risk Factors
Nulliparity
Chronic HPN
Maternal age > 35
Obesity
Genetic predisposition
Hyperplacentosis states (multifetal pregnancy, H-
mole, hydrops)
African-american ethnicity
Renovascular disease
Dietary factors (low protein, low calcium)
Low socioeconomic status
 Etiology
HPN disorders due to pregnancy are likely to
develop in women who:
Are exposed to chorionic villi for the first time
Are exposed to superabundance of chorionic villi,
as with twins or H. mole
Have preexisting vascular disease
Are genetically predisposed to HPN developing
during pregnancy
 Mechanisms
Abnormal trophoblastic invasion
Immunological factors
Vasculopathy & inflammatory changes
Dietary deficiencies
Genetic influences
 Associated Changes
plasma uric acid
plasma creatinine
Glomerular endotheliosis
Periportal hemorrhagic necrosis of the liver
SGOT, SGPT
Subcapsular hemorrhage of the liver
Brain edema, hemorrhages
Blurring of vision due to edema; retinal
detachment
 Objectives of Treatment
Control Hypertension
Prevent convulsion
Delivery of healthy, if possible term baby
Avoid residual effects
 Drugs for Management
Magnesium Sulfate
Control & prevention of convulsions
Hydralazine, Nifedipine, Ca-channel blockers
Symptomatology of Gestational HTN
 3 Cardinal Principles
1. Control of convulsions
2. Control of hypertension
3. Optimum mode and time of delivery
Management Protocol
 Control of Convulsions
Anticonvulsant Therapy
MgSo4
Diazepam
Phenytoin
Magnesium sulfate drug of choice
Given in 2 ways :
1. continuous IV infusion
2. intermittent IM injections
MOA
cerebral vasodilator
increases uterine blood flow
reduces level of plasma endothelin 1
increases renal and extrarenal prostacyclin central anticonvulsant effect
increases levels of endothelium-derived relaxing factor precursors
 Control of Convulsions
MgSO4
Therapeutic Level: 4-7 mEq/L
Loss of Patellar Reflex: 10 mEq/L
Respiratory Depressions: > 10 mEq/L
Respiratory Paralysis and Arrest: >12 mEq/L
 Control of Convulsions
Precautions for succeeding doses:
Presence of patellar reflex
Respirations are not depressed
Urine output 30 ml for the past hour or 100 ml
for the past 4 hours
IV Calcium gluconate ( 10 ml of 10% solution)
available at bedside for MgS04 overdose
MgS04 therapy is continued for 24 hours after
delivery and is administered for 24 hours after
the onset of convulsions if eclampsia develops
postpartum.
 Control of Hypertension
Hydralazine (initial dose 5 mg IV Bolus
followed by 5 mg increments every 30 min to
total 20 mg IF DBP does not improve
Labetaloladverse effects of fetal growth and
hemodynamics
Nifedepine
Nicardipine
ACE Inhibitors NOT USED (Teratogenic)
 Optimum time and mode of delivery
Five considerations in terminating pregnancy:
Age of gestation
Disease severity
Status of fetus
Condition of the mother
Nursery capabilities
Optimum time and mode of delivery
Optimum time and mode of delivery