Hypertensive Disorders in Pregnancy
Department of Obstetrics and Gynecology

Hypertensive Disorders in Pregnancy
• Gestational Hypertension
• Preeclampsia
- Mild
- Severe
• Eclampsia
• Preeclampsia superimposed on hypertension
• Chronic hypertension

Gestational Hypertension
• BP >140/90 mm Hg for 1st time during pregnancy
• No proteinuria
• BP returns to normal < 12 weeks postpartum
• Final diagnosis made only postpartum
• May have other signs and symptoms of preeclampsia (ex. Epigastric pain or thrombocytopenia)


Preeclampsia
• Minimum criteria
- BP >140/90 mm Hg after 20 weeks gestation
- Proteinuria > 300mg/24 hours or > 1+ dipstick
• Increased certainty of preeclampsia
- BP > 160/110 mm Hg
- Proteinuria > 2.0g/24 hours or > 2+ dispstick
- Serum creatinine > 1.2 mg/dL unless known to be previously elevated
- Platelets < 100,000/mm3
- Microangiopathic hemolysis (increased LDH)
- Increased ALT or AST
- Persistent headache or other visual disturbances
- Persistent epigastric pain

Severity of Preeclampsia
Mild:
Diastolic blood pressure = < 100 mmhg
Proteinuria = trace to +1
Headache = absent
Visual Disturbances = absent
Upper Abdominal pain = absent
Oliguria = absent
Convulsion (Eclampsia) = absent
Serum Creatinine = normal
Thrombocytopenia = absent
Liver enzyme elevation = minimal
Fetal Growth Restriction = absent
Pulmonary Edema = absent

Severe:
Diastolic blood pressure = 110 mmhg or higher
Proteinuria = persistent 2+ or more
Headache = present
Visual Disturbances = present
Upper Abdominal pain = present
Oliguria = present
Convulsion (Eclampsia) = present
Serum Creatinine = elevated
Thrombocytopenia = present
Liver enzyme elevation = marked
Fetal Growth Restriction = obvious
Pulmonary Edema = present




Eclampsia
• Seizures that cannot be attributed to other causes in a woman with preeclampsia


Superimposed preclampsia on Chronic Hypertension
• New-onset proteinuria > 300mg/24 hours in hypertensive women but no proteinuria before 20 weeks gestation
• A sudden increase in proteinuria or blood pressure or platelet count < 100,00mm3 in women with hypertension and proteinuria before 20 weeks gestation


Chronic Hypertension
• BP > 140/90 mm Hg before pregnancy or diagnosed before 20 weeks gestation not attributable to gestational trophoblastic disease or Hypertension first diagnosed after 20 weeks gestation and persistent after 20 weeks postpartum

Risk Factors
• Nulligravid
• Advancing age
• Chronic hypertension
• Multifetal gestation
• Obesity
• African-American ethnicity

Etiology
• More likely to develop in women who:
1.Exposed to chorionic villi for the 1st time
2. Exposed to superabundance of chroionic villi
3. Preexisting vascular disease
4. Genetically predisposed to hypertension during pregnancy

Potential Causes
• Abnormal trophoblastic invasion of uterine vessels
• Immunologic intolerance between maternal and fetoplacental tissues
• Maternal maladaptation to cardiovascular or inflammatory changes during pregnancy
• Dietary deficiencies
• Genetic influences

Abnormal Trophoblastic Invasion
• Incomplete Trophoblastic Invasion
• Decidual vessels but not myometrial vessels become lined with endovascular trophoblast
• Endothelial Damage
• Insudation of plasma constituents in vessel wall
• Proliferation myointimal cells
• Medial Necrosis

Immunological Factors
• Formation of blocking antibodies to placental antigenic sight might be impaired
• Number of antigenic site might be great compared with amount of antibodies
• Lower proportion of helper T cells

Vasculopathy and Inflammatory Changes
The decidua can release noxious agents - endothelial cell injury
• Extreme state of activated leukocyte in the maternal circulation
• Cytokines such as TNF-a and interleukins contribute to oxidative stress
• Highly toxic radicals are then produced that injure endothelial cells




PATHOGENESIS

Vasospasm
• Vascular constriction causes resistance and subsequent hypertension
• Endothelial cell damage causes interstitial leakage through which blood constituents, including platelets and fibrinogen are deposited subendothelially
• This leads to necrosis , hemorrhage and end-organ disturbances

Endothelial Cell Activation

Increased Pressor Responses
• Pregnant women develop refractoriness to infused vasopressors
• Women with early preeclampsia have increased vascular reactivity to infused norepinephrine and angiotensin II