National University of Rwanda Family and Community Medicine

Hypertensive Disorders in Pregnancy

KABERA Ren,MD PGY IV Resident Family and Community Medicine National University of Rwanda

Introduction
Hypertensive disorders complicating pregnancy are common and form one of the deadly triad, along with hemorrhage and infection, that contribute greatly to maternal morbidity and mortality.

Classification
Gestational hypertension Preeclampsia. Eclampsia. Preeclampsia superimposed on chronic hypertension. Chronic hypertension.

Gestational hypertension
BP 140/90 mm Hg for first time during pregnancy No proteinuria BP returns to normal < 12 weeks' postpartum Final diagnosis made only postpartum May have other signs or symptoms of preeclampsia, for example, epigastric discomfort or thrombocytopenia Gestational hypertension has replaced the term pregnancyinduced hypertension to describe women who develop hypertension without proteinuria after 20 weeks of gestation.

Gestational hypertension
Gestational hypertension is a provisional diagnosis that includes women eventually diagnosed with preeclampsia or chronic hypertension, as well as women retrospectively diagnosed with transient hypertension of pregnancy. Fifty percent of women diagnosed with gestational hypertension between 24 and 35 weeks develop preeclampsia

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

Preeclampsia
Described as a pregnancy-specific syndrome of reduced organ perfusion secondary to vasospasm and endothelial activation. Proteinuria is an important sign of preeclampsia Significant proteinuria is defined by 24-hour urinary protein exceeding 300 mg per 24 hours, or persistent 30 mg/dL (1+ dipstick) in random urine samples. Renal biopsy specimens: glomerular lesion. The minimum criteria for the diagnosis of preeclampsia are hypertension plus minimal proteinuria. The more severe the hypertension or proteinuria, the more certain is the diagnosis of preeclampsia

Preeclampsia
Epigastric or right upper quadrant pain is thought to result from hepatocellular necrosis, ischemia, and edema that stretches the Glisson capsule. This characteristic pain is frequently accompanied by elevated serum hepatic transaminase levels and usually is a sign to terminate the pregnancy. The pain presages hepatic infarction and hemorrhage or catastrophic rupture of a subcapsular hematoma. Fortunately, hepatic rupture is rare.

Preeclampsia
Thrombocytopenia is characteristic of worsening preeclampsia Thrombocytopenia is due platelet activation and aggregation as well as microangiopathic hemolysis induced by severe vasospasm. Evidence of gross hemolysis such as hemoglobinemia, hemoglobinuria, or hyperbilirubinemia is indicative of severe disease. Other factors indicative of severe hypertension include cardiac dysfunction with pulmonary edema as well as obvious fetal growth restriction.

Preeclampsia
Exact mechanism not known Immunologic Genetic Placental ischemia Endothelial cell dysfunction Vasospasm Hyper-responsive response to vasoactive hormones (e.g. angiotensin II & epinephrine)

Preeclampsia
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Abnormality Diastolic blood pressure Proteinuria Headache Visual disturbances Upper abdominal pain Oliguria Convulsion (eclampsia) Serum creatinine Thrombocytopenia Liver enzyme elevation Fetal growth restriction Pulmonary edema Mild < 100 mg Trace to 1+ Absent Absent Absent Absent Absent Normal Absent Minimal Absent Absent Severe Hg 110 mm Hg or higher Persistent 2+ or more Present Present Present Present Present Elevated Present Marked Obvious Present

Eclampsia
Seizures that cannot be attributed to other causes in a woman with preeclampsia The seizures are generalized and may appear before, during, or after labor. Recent study reported that a fourth of eclamptic seizures developed beyond 48 hours postpartum

Superimposed Preeclampsia
New-onset proteinuria 300 mg/24 hours in hypertensive women but no proteinuria before 20 weeks' gestation A sudden increase in proteinuria or blood pressure or platelet count < 100,000/mm3 in women with hypertension and proteinuria before 20 weeks' gestation All chronic hypertensive disorders, regardless of their cause, predispose to development of superimposed preeclampsia and eclampsia. The diagnosis of chronic underlying hypertension is made when: Hypertension (140/90 mm Hg or greater) is documented antecedent to pregnancy. Hypertension (140/90 mm Hg or greater) is detected before 20 weeks, unless there is gestational trophoblastic disease.

Chronic Hypertension
BP 140/90 mm Hg before pregnancy or diagnosed before 20 weeks' gestation not attributable to gestational trophoblastic disease Hypertension first diagnosed after 20 weeks' gestation and persistent after 12 weeks' postpartum.

Etiology
Chorionic villi for the first time. Superabundance of chorionic villi, as with twins or hydatidiform mole. Preexisting vascular disease. Genetically predisposed to hypertension developing during pregnancy. Abnormal trophoblastic invasion of uterine vessels. Immunological intolerance between maternal and fetoplacental tissues. Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy. Dietary deficiencies. Genetic influences.

Diagnosis
Hypertension is diagnosed when the resting blood pressure is 140/90 mm Hg or greater. Edema has been abandoned as a diagnostic criterion because it occurs in too many normal pregnant women to be discriminant.

Pathophysiology

Pathophysiology
Prostacyclin is produced by endothelial cells and thromboxane A2 by platelets from their common precursor arachidonic acid via the cyclooxygenase pathway. Thromboxane A2 promotes platelet aggregation and vasoconstriction, whereas prostacyclin inhibits platelet aggregation and promotes vasodilation. The balance between platelet thromboxane A2 and prostacyclin fosters localized platelet aggregation and consequent clot formation while preventing excessive extension of the clot and maintaining blood flow around it. The thromboxane A2-prostacyclin balance can be shifted toward prostacyclin by administration of low doses of aspirin.

Pathophysiology
Aspirin produces irreversible inhibition of cyclooxygenase by acetylating serine residue in its active site. Obviously, this reduces production of both thromboxane A2 and prostacyclin. Endothelial cells produce new cyclooxygenase in a matter of hours whereas platelets cannot manufacture the enzyme, and the level rises only as new platelets enter the circulation. This is a slow process because platelets have a half-life of about 4 days. Administration of small amounts of aspirin for prolonged periods reduces clot formation and has been shown to be of value in preventing myocardial infarctions, unstable angina, transient ischemic attacks, and stroke.

Pathophysiology
Brain There are two distinct but related types of cerebral pathology. The first is gross hemorrhage due to ruptured arteries caused by severe hypertension The second type of cerebral lesion is variably demonstrated with preeclampsia but probably is universal with eclampsia. These are more widespread, focal, and seldom fatal. The principal postmortem lesions are edema, hyperemia, ischemias, thrombosis, and hemorrhage

Pathophysiology
Cardiac/Pulmonary Increased CO & SVR CVP normal or slightly increased Plasma volume reduced Pulmonary edema
Decrease oncotic/collid pressure Capillary/endothelial damage leak Vasoconstriction increase PWP and CVP Occurs 3 % of preeclamptic patients

Pathophysiology
Liver Usually mild Severe PIH or preeclampsia complicated by HELLP periportal hemorrhages ischemic lesion generalized swelling hepatic swelling epigastric pain

Pathophysiology
Kidney Adversely affected proteinuria GFR and CrCl decrease BUN increase, may correlate w/ severity RBF compromised ARF w/ oliguria PIH, esp. w/ abruption, DIC, HELLP

Pathophysiology
Uterus Activity increased Hyperactive/hypersensitive to oxytocin Preterm labor frequent Uterine/placental blood flow decreased by 50-70% Abruption incidence increased

Management
Basic management objectives for any pregnancy complicated by preeclampsia are: Termination of pregnancy with the least possible trauma to mother and fetus. Birth of an infant who subsequently thrives. Complete restoration of health to the mother.

Antepartum Hospital Management

Hospitalization is considered at least initially for women with new-onset hypertension, especially if there is persistent or worsening hypertension or development of proteinuria. A systematic evaluation is instituted to include the following: Detailed examination followed by daily scrutiny for clinical findings such as headache, visual disturbances, epigastric pain, and rapid weight gain. Weight on admittance and every day thereafter.

Management
Analysis for proteinuria on admittance and at least every 2 days thereafter. Blood pressure readings in the sitting position with an appropriate-size cuff every 4 hours, except between midnight and morning. Measurements of plasma or serum creatinine, hematocrit, platelets, and serum liver enzymes, the frequency to be determined by the severity of hypertension. Frequent evaluation of fetal size and amnionic fluid volume either clinically or with sonography.

Management of chronic hypertension

Methyldopa (Aldomet),labetalol, and nifedipine (Procardia) are oral agents commonly used to treat chronic hypertension in pregnancy. The beta blocker atenolol (Tenormin) has been associated with IUGR, Women in active labor with uncontrolled severe chronic hypertension require treatment with intravenous labetalol or hydralazine.

Management of Severe Preeclampsia

Magnesium sulfate: Loading dose of 4 to 6 g diluted in 100 mL of normal saline, given IV over 15 to 20 minutes, followed by a continuous infusion of 2 g per hour Assess serum magnesium level if urine output is < 30 mL per hour or there is a loss of deep tendon reflexes, decreased respiratory rate, or altered mental status Therapeutic range for serum magnesium is 4 to 7 mg per dL Corticosteroids (if between 24 and 34 weeks of gestation and not previously administered) Betamethasone (Celestone), 12 mg IM initially, then repeat in 24 hours or Dexamethasone, 6 mg IM initially, then repeat every 12 hours for three additional doses

Management of Severe Preeclampsia

For systolic blood pressure > 160 mm Hg or diastolic > 110 mm Hg, one of the following should be given to achieve a systolic measurement of 140 to 155 mm Hg and/or a diastolic measurement of 90 to 105 mm Hg: Hydralazine, 5 to 10 mg IV every 15 to 30 minutes (maximal dose: 30 mg) Labetalol, 20 mg IV initially; if the initial dose is not effective, double the dose to 40 mg and then 80 mg at 10minute intervals until target blood pressure is reached or a total of 220 mg has been administered; the maximal dose of IV labetalol is 220 mg in a 24-hour period Calcium gluconate, 1 g IV; keep at bedside in case of respiratory depression from magnesium sulfate use

Management Eclampsia
Protecting the airway and minimizing the risk of aspiration by placing the woman on her left side, suctioning her mouth, and administering oxygen. intubations should be immediately available. Close observation, soft padding, and use of side rails on the bed may help prevent trauma from falls or violent seizure activity. After the convulsion has ended and the patient is stabilized, plans should be made for prompt delivery. In rural or remote areas, physicians need to consider the risk of transfer versus the benefits of tertiary maternal and neonatal care.

Management of eclampsia
Magnesium sulfate is the drug of choice because it is more effective in preventing recurrent seizures than phenytoin (Dilantin) or diazepam (Valium). If a patient has already received a prophylactic loading dose of magnesium sulfate and is receiving a continuous infusion, an additional 2 g should be given intravenously. Otherwise, a 6-g loading dose is given intravenously over 15 to 20 minutes, followed by maintenance infusion of 2 g per hour. A total of 8 g of magnesium sulfate should not be exceeded over a short period of time

References
American Academy of Family Physician : www.aafp.org Williams obstetrics Review of Medical Physiology

End

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