Hypertensive Disorders Of Pregnancy

Description #

This is an Obstetrics and Gynecology unit.

Learning Objectives #

The Students should know:

– The definition and classification of hypertension in pregnancy

– Pathophysiology of Preeclampsia and Eclampsia

– Symptoms, physical findings and diagnostic methods

– The approach to management

– Maternal and fetal complications

Definition and Classification #

Hypertensive disorders of pregnancy remains a leading cause of maternal and perinatal mortality and morbidity.

In the mother they can cause multi-organ cluster of varying clinical dysfunction including renal and hepatic failure, CNS hemorrhage and stroke, pulmonary edema, abruptio placentae and DIC.

In the fetus they can cause Growth restriction, prematurity, low 5 minute APGAR scores, low umbilical artery pH and perinatal death.

Recommendations: Measurement of BP

1. BP should be measured with the woman in the sitting position at 45 degree supported with the upper arm at the level of the heart.

2. An appropriately sized cuff (i.e., length of 1.5 times the circumference of the arm) should be used.

3. Korotkoff phase V (disappearance of pulse sounds) should be used to designate diastolic BP.

4. If BP is consistently higher in one arm, the arm with the higher values should be used for all BP measurements.

5. BP can be measured using a mercury sphygmomanometer, calibrated aneroid device, or an automated BP device that has been validated for use in preeclampsia.

6. Automated BP machines may underestimate BP in women with preeclampsia, and comparison of readings using mercury sphygmomanometry or an aneroid device is recommended.

7. Ambulatory BP monitoring (by 24-hour or home measurement) may be useful to detect isolated office (white coat) hypertension.

8. Patients should be instructed in proper BP measurement echnique if they are to perform home BP monitoring.

The Canadian Hypertension Society currently defines hypertensive disorders of pregnancy in the following categories:

A. Pre-existing Hypertention

 Diastolic hypertension that predates pregnancy or is diagnosed before 20 weeks gestation. Typically persists beyond 42 days postpartum.

1. Essential: Primary

2. Secondary: Secondary to disorders such as renal disease, Cushing syndrome, or sympathetic nervous system disease.

B. Gestational Hypertension

Diastolic pressure >90 mm of Hg on 2 occasions 4 hours apart diagnosed at greater than 20 weeks gestation. Typically resolves before 42 days postpartum.

1. Without Proteinuria:  Protein excretion is < 0.3 g/day in 24 hr urine collection

a. without adverse conditions

b. with adverse conditions :

CNS: visual disturbances, frontal headache,hyperreflexia, convulsions

Cardio/Vascular /Pulmonary: diastolic pressure >110 mmHg, pulmonary edema, shortness of breath, chest pain

Renal: proteinuria ≥0.3g/day, oliguria (<500 ml/day,hypoalbuminemia (albumin <18 g/L)

Hematological: thrombocytopenia (platelet count <100,000 x109/L), hemolysis

Hepatic: elevated liver enzymes, persistent right upper quadrant abdominal pain/chest pain, severe nausea and vomiting

Fetal: placental abruption, intrauterine growth restriction, oligohydramnios, absent or reversed umbilical artery end diastolic flow

2. With Proteinuria: 24hr urine collection: ≥0.3 g/day (Spot protein: creatine ratio: >30 mg/mmol)

a. without adverse conditions

b. with adverse conditions: Same as above, especially with hypoalbuminanemia

C. Preexisting hypertension with superimposed gestational hypertension with proteinuria

Preexisting hypertension associated with increasing hypertension and protein excretion of ≥ 0.3g/d at >20 weeks gestation.

D. Unclassifiable Hypertension: if BP not recorded prior to 20 weeks, with or without systemic manifestations. Reassessment and classification should be made at ≥ 42 days postpartum.

Etiology:  

Genetic, immunologic, vascular, hormonal, nutritional and behavioural factors have all been proposed as causes. The predominant pathophysiologic finding in preeclampsia and gestational hypertension is generalized vasospasm and progressive involvement of essential organs such as the kidney, liver, brain, and haematological systems. Maternal endothelial cell damage associated with the release of substances from the poorly perfused placenta initiates a dysfunctional cascade of coagulation, vasoconstriction and intravascular fluid redistribution that results in the clinical syndrome of pre eclampsia/eclampsia.

Several potential causes for maternal vasospasm are:

1. Vascular changes:

Instead of noting the physiologic trophoblast mediated vascular changes in the uterine vessels (decreased musculature in the spiral arterioles leads to the development of a low-resistance, low-pressure, high-flow system), inadequate maternal vascular response is seen in cases of preeclampsia and/or intrauterine fetal growth restriction. Endothelial damage is also noted within the vessels. 

2. Hemostatic changes:

Increased platelet activation with increased consumption in the microvasculature is noted during the course of preeclampsia. Endothelial fibronectin levels are increased and anti thrombin III and α2-antiplasmin levels are decreased, reflecting endothelial damage. Low anti thrombin III levels are permissive for microthrombi development. Endothelial damage is then thought to promote further vasospasm. 

3. Changes in prostanoids:

Preeclampsia is associated with a disturbance in prostaglandin production, with a decrease in the ratio of the vasodilator prostaglandin E2 and prostacyclin to the vasoconstrictor prostaglandin F series and thromboxanes.

In normal pregnancy prostacyclin and thromboxane (TXA2) are increased during pregnancy, with the balance in favor of prostacyclin. In patients who develop preeclampsia, the balance shifts to favor TXA2.Again, prostacyclin functions to promote vasodilatation and decrease platelet aggregation, and TXA2 promotes vasoconstriction and platelet aggregation. Because of this imbalance, vessel constriction occurs.

4. Changes in endothelium-derived factors:

Nitric oxide, a potent vasodilator and inhibitor of platelet aggregation, is decreased in patients with preeclampsia and may explain the evolution of vasoconstriction in these patients. 

 5. Lipid peroxide, free radicals, and antioxidant release:

It is postulated that uteroplacental ischemia results in oxidative stress leading to the production and release of toxins such as Lipid peroxides and free radicals that enter the circulation and cause inflammation and endothelial damage. This is supported by the fact that preeclampsia is increased in pregnant women with underlying conditions such as obesity and diabetes that are associated with chronic inflammation and dyslipidemia. Decreased antioxidant levels are also noted in pregnancies complicated by preeclampsia.

 Risk factors #

The rate of hypertensive disorders of pregnancy in British Columbia in 2003-2004 was 5.7% according to BCRCP Guideline.

Risk factors of greatest significance:

·                 previous preeclampsia

·                 Anti‐phospholipid antibodies

·                 medical conditions such as pre‐existing hypertension, diabetes mellitus, renal disease, collagen vascular disease

·                 multiple pregnancy

Additional risk factors:

·                 family history of preeclampsia or early‐onset cardiovascular disease

·                 booking sBP ≥130mmHg or d BP ≥80mmHg

·                 maternal age <20 years or >40 years

·                 inter pregnancy interval >10 years or <2 years

·                 primigravida/ first pregnancy with a new partner

·                 lack of mid trimester fall in BP

·                 obesity (BMI ≥35)

·                 excessive weight gain (> 2lbs/week)

·                 finger and facial edema

·                 ethnicity (Nordic, Black, South Asian, Pacific Island)

·                 Low socioeconomic status

·                 Low dietary intake of calcium (<600mg/day); supplement with at least 1000mg/day is recommended

Pre-existing hypertension:

Definition

·                 HTN (>140/90) that predates pregnancy or is diagnosed before 20 weeks gestation(unless a gestational trophoblastic neoplasia ), In most cases hypertension persists >42 d postpartum. It may be primary or secondary to conditions such as renal disease.

·                 essential hypertension associated with an increased risk of gestational HTN, abruptio placenta, IUGR and IUD

Management

·                 alpha-methyldopa 250-500 mg PO tid/qid or labetalol 100-300 mg PO bid/tid

·                 no ACE inhibitors, diuretics or propranolol (teratogens)

·                 monitor progress with serial U/S

Gestational hypertension:  Hypertension developed after 20 weeks gestation. In most cases it resolves <42 d postpartum.

1. Without preeclampsia (without Proteinuria):           

Protein excretion in 24­-hour urine collection is <0.3 g/d.

a) without adverse conditions

b) with adverse conditions

2. With preeclampsia (with Proteinuria)          

Further classified as being:

a) with new proteinuria (protein excretion in 24 hour urine > 3 g/d)

b) with one or more adverse conditions

Evaluation #

The history and physical examination are directed toward detection of pregnancy-associated hypertensive disease and its signs, symptoms and complications.

 review of current obstetric records especially :

• Visual disturbances, especially scotomata
• Unusually severe or persistent headaches (indicative of vasospasm)
• Right-upper-quadrant pain (indicative of liver involvement)
• Any history of loss of conscious-ness or seizures
• Patient’s blood pressure compared before and during this pregnancy
• Patient’s weight compared with her pregravid weight and previous weights during this pregnancy `
• Persistent edema unresponsive to resting in the supine position, especially when it also involves the upper extremities, sacral region, and face

Funduscopic examination may detect vasoconstriction of retinal blood vessels indicative of similar vasoconstriction of other small vessels.

Tendernessover the liver, attributed partly to hepatic capsule distension, may be associated with complaints of right-upper-quadrant pain.

The patellar and Achilles’ deep tendon reflexes should be carefully elicited, and hyperreflexia noted.

The demonstration of clonus at the ankle is especially worrisome.

Maternal liver dysfunction, renal insufficiency, and coagulopathyare significant concerns and require serial evaluation.

The maternal and fetal laboratory evaluations for pregnancy complicated by hypertension:

• CBC and Platelet count
• Coagulation profile
• Liver function studies (ALT, AST, LDH)
• Serum creatinine
• Uric acid
• 24-hour urine Creatinine clearance and total urinary protein
• For fetal evaluation: fetal movement monitoring, Ultrasound examination and checking Fetal weight, growth and Amniotic fluid volume plus NST and/or biophysical profile

Management #

Management of Chronic Hypertension

The management of patients with chronic hypertension in pregnancy involves closely monitoring maternal blood pressure and watching for the superimposition of preeclampsia or eclampsia, and following the fetus for appropriate growth and fetal well-being. 

Antihypertensive medication in women with chronic hypertension is generally not given unless the systolic blood pressure is 150 to 160 mm Hg or the diastolic blood pressure 100 to 110 mm Hg. The purpose of such medications is to reduce the likelihood of maternal stroke. Methyldopa is a commonly used antihypertensive medication, although a combined alpha-and-beta-blocker (such as labetalol) and calcium-channel blockers (such as nifedipine)are also commonly used. It was formerly taught that diuretics were contraindicated during pregnancy, but diuretic therapy is no longer discontinued, and indeed is usually continued, in the patient who already has been on such therapy before becoming pregnant.

Management of Gestational Hypertension

o        Gestational hypertension without preeclampsia

·         bed rest in left lateral decubitus position (LLDP), normal salt and protein intake 

·         avoid diuretics and anti-hypertensives

·         monitor for progression

·         if >37 weeks GA, consider induction of labour

o        Gestational hypertension with preeclampsia

·         stabilize and deliver: regardless of gestational age the only “cure” is delivery  (vaginal delivery preferred)

·         increase maternal monitoring to hourly input and output, urine dip every 12h and neurological vitals every hour

·         increase fetal evaluation to include continuous monitoring

·         anticonvulsant therapy:

–      raises seizure threshold

–      Mg sulfate (4 g IV bolus over 15-20 min) followed by maintenance of 2-4 g/hour

–     monitor for signs of Mg toxicity: depressed deep tendon reflexes, decreased RR, anuric, hypotonic, CNS or cardiac depression

–     antagonist to Mg sulfate: calcium gluconate (10%) 10 mL (1 g) IV over 2 minutes

·         antihypertensive therapy:

–      lowering BP decreases the risk of stroke

–      hydralazine 5-10 mg IV bolus over 5 minutes q15-30 minutes as necessary

–      labetalol 20-50 mg IV q10 minutes

–      2nd line: nifedipine 10 PO q20-60 minutes if needed to a maximum dose of 30 mg  

–     ACE-inhibitors are contraindicated

·         postpartum management

–       risk of seizure highest in first 24 hours postpartum, thus continue Mg sulfate for 12-24 hours

–      vitals q1h

–      consider HELLP syndrome in toxic patients

–       most return to a normotensive BP within 2 weeks

HELLP syndrome, like severe preeclampsia, is an indication for delivery to avoid jeopardizing the health of the woman. HELLP is the presence of Hemolysis, Elevated Liver enzymes and Low Platelets.

o        Gestational hypertension with Seizures

• ABC’s

Seizure control and prevention: Magnesium sulfate is the drug of choice for the prevention and treatment of eclamptic seizures.