HYPERTENSION IN PREGNANCY

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There are four major hypertensive disorders related to pregnancy: -Pre- eclampsia Eclampsia HELLP-Chronic/preexisting hypertension-Preeclampsia superimposed upon chronic/preexisting hypertension-Gestational hypertension

DEFINITIONS OF PREGNANCY-RELATED DEFINITIONS OF PREGNANCY-RELATED HYPERTENSIVE DISORDERS: — HYPERTENSIVE DISORDERS: —

CHRONIC/PREEXISTING HYPERTENSION

Systolic pressure ≥140 mmHg

and/or diastolic pressure ≥90 mmHg

-That antedates pregnancy or is present beforethe 20th week of pregnancy (on at least twooccasions) or persists longer than 12 weekspostpartum. -It can be primary (essential hypertension) orsecondary to a variety of medical disorders

PREECLAMPSIA SUPERIMPOSED UPON CHRONIC/PREEXISTING HYPERTENSION

Superimposed preeclampsia is defined by thenew onset of proteinuria after 20 weeks ofgestation in a woman with chronic/preexisting hypertension.

GESTATIONAL HYPERTENSION

Gestational hypertension refers to hypertension without proteinuria or other signs/symptoms of preeclampsia that develops after 20 weeks of gestation.

It should resolve by 12 weeks postpartum. If it persists beyond 12 weeks postpartum,

the diagnosis is revised to chronic/preexisting hypertension that was masked by the physiologic decrease in blood pressure that occurs in early pregnancy.

CRITERIA FOR GESTATIONAL HYPERTENSION

Systolic blood pressure ≥140 mmHg OR Diastolic blood pressure ≥ 90 mmHg AND no proteinuria Developing

AFTER the 20th week of gestation in womenknown to be normotensive before pregnancy.

- Blood pressure should be elevated on at leasttwo occasions at least six hours apart.

PRE-ECLAMPSIA

DEFINITIONS:

Preeclampsia — refers to the new onset of hypertension and proteinuria after 20 weeks of gestation in a previously normotensive woman.

DEFINITIONS:

Preeclampsia can be classified as ‘severe’ when:- Severe hypertension, - or severe proteinuria, - or other signs/symptoms of end-organ injury are

present. In the absence of any of these findings,

preeclampsia can be classified as ‘mild.’ In this commonly used system, there is no ‘moderate’ classification.

CRITERIA FOR DIAGNOSIS OF PREECLAMPSIA:

Systolic blood pressure ≥140 mmHg

or Diastolic blood pressure ≥90 mmHg

and Proteinuria ≥0.3 grams in a 24-hour urinespecimen

INCIDENCE

Preeclampsia occurs in up to 7.5 percent of pregnancies worldwide

RISK FACTORS OF PRE-ECLAMPSIA

Maternal Factors:

1. Demographic criteria:o Primagravidao Age extremes (<18 years, > 34 years).o Black race o High body mass index (≥26.1)o Male partner whose mother had preeclampsia

2- Medical complications:o DM , Chronic HTN, Pre-existing renal disease , thrombophilia ,

Antiphospholipid antibody syndrome.

3- Past Hx or FHx of pregnancy-induced HTN.

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RISK FACTORS OF PRE-ECLAMPSIA Fetal factors:

o Hydatidiform mole

o > 1 fetus

o fetal hydrops

o Unexplained fetal growth restriction

RISK FACTORS OF PRE-ECLAMPSIA

-A past history of preeclampsia – Risk 7-fold

-Primigravid state is a significant predisposing factor. One theory is thatthese women may have had limited recent exposure to paternal antigens,which may play a role in the pathogenesis of the disease.

-A family history of preeclampsia in a first degree relative, suggesting aheritable mechanism in some cases. The father of the baby may contribute

tothe increased risk, as the paternal contribution to fetal genes may have a

rolein defective placentation and subsequent preeclampsia.

-Women who smoke cigarettes have a lower risk of preeclampsia than

nonsmokers.

MECHANISMS BEHIND PREECLAMPSIA

Not certain. Numerous maternal, paternal, and fetal

factors have been implicated in development.

The factors currently considered to be the most important include the following: Maternal immunologic intolerance Abnormal placental implantation Genetic, nutritional, and environmental factors Cardiovascular and inflammatory changes

PATHOGENESIS OF PRE-ECLAMPSIA As the term toxemia indicates, the search for

a toxin has been long fruitless.

Uteroplacental ischemia is the center to the development of disease, results in production of toxin that enters circulation widespread endothelial dysfunction.

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SEVERE PRE-ECLAMPSIA Less common.

Can be diagnosed on basis of: Severe HTN (BP ≥ 160 / 110 mm Hg) on two

occasions at least six hours apart.OR Severe proteinuria (3-4+ dipstick OR > 5 g / 24

hr) alone without symptoms. OR Only mild HTN + proteinuria if signs and

symptoms are present:

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CON’T Resp: Plum. Edema, cyanosis. Renal: Proteinuria, ↑ Serum creatinine,

Oliguria <500 mL in 24 hours. Hepatic: ↑ LFTs Neurologic: visual disturbance (i.e.

scotomas, loss of peripheral vision), headache, convulsions.

Symptoms of liver capsule distention: Right upper quadrant or epigastric pain Nausea, vomiting.

Hematologic: thrombocytopenia, microangiopathic hemolysis.

Fetal growth restriction 19

ECLAMPSIA

[Latin = convulsions] = Unexplained tonic-clonic seizures

+ Mild / severe pre-eclampsia.

Most often occurs intra-partum, but can also occur ante-partum & post-partum.

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An eclamptic seizure is typically tonic-clonic – lasts60 to 75 seconds.

Symptoms that may occur before the seizureinclude persistent frontal or occipital headache,blurred vision, photophobia, right upper quadrantor epigastric pain, and altered mental status.

In up to one-third of cases, there is no proteinuriaor blood pressure is less than 140/90 mmHg priorto the seizure

SUMMARY OF MATERNAL AND NEONATAL OUTCOMES IN ECLAMPISA

Abruption 7 to 10 % DIC 7 to 11% Pulmonary edema 3 to 5 % Acute renal failure 5 to 9%

Aspiration pneumonia 2 to 3 % Cardiopulmonary arrest 2 to 5 % Liver hematoma 1% HELLP syndrome 10 to 15% Perinatal death 5.6 to

11.8% Preterm birth 50%

CON’T

HELLP syndrome:

o Type of severe pre-eclampsia.

o Hemolysis + Elevated Liver enzymes + Low Platelets.

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SIGNS AND SYMPTOMS Severe hypertension (systolic blood pressure

≥160 mm Hg or diastolic ≥110 mm Hg on two occasions at least six hours apart)

Persistent and/or severe headache, Visual abnormalities (scotomata, photophobia,

blurred vision, or temporary blindness [rare]) Upper abdominal or epigastric pain Nausea, vomiting Oliguria Dyspnea, retrosternal chest pain Fetal growth restriction Oligohydramnios Altered mental status

LABORATORY ABNORMALITIES

Hemoconcentration Microangiopathic hemolytic anemia

(abnormal peripheral smear, elevated bilirubin, or low serum haptoglobin levels U/L)

Thrombocytopenia (<100,000/microL) Elevated serum creatinine concentration

(>1.3 mg/dL) Elevated liver enzymes (twice the upper

limit of normal) Severe proteinuria (≥5 grams in 24 hours)

ATYPICAL PRESENTATION

Include any of the following:

Onset of signs/symptoms at <20 weeks of gestation

Hypertension or proteinuria (but not both) with or without characteristic signs and symptoms of severe preeclampsia

Delayed postpartum onset or exacerbation of disease (>2 days postpartum)

COMPLICATIONS Maternal:

1. Cerebral hemorrhage (50% of deaths).2. LVF / Pulm. edema.3. Liver / renal dysfunction.4. Seizures.5. DIC.6. Abruptio placenta: ante-partum painful vaginal

bleeding. Fetal: Mainly due to placental insufficiency:

1. Fetal loss.2. IUGR.3. Prematurity.

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MANAGEMENT OF PRE-ECLAMPSIA

The optimal management of a woman withpreeclampsia depends on:

- Gestational age.- Disease severity.

Because delivery is the only cure forpreeclampsia, clinicians must try to minimizematernal risk while maximizing fetal maturity.

MANAGEMENT OF PRE-ECLAMPSIA

Deliveries with mild preeclampsia are often induced after 37 weeks' gestation.

Before this, the immature fetus is treated with expectant management with corticosteroids to accelerate lung maturity in preparation for early delivery.

In patients with severe preeclampsia, induction of delivery should be considered after 34 weeks' gestation.

In these cases, the severity of disease must be weighed against the risks of infant prematurity.

CARE IN MILD PREECLAMPSIA

Hospitalized and monitored carefully A pregnancy complicated by mild

preeclampsia at or beyond 37 weeks should be delivered

Delivery is recommended if a patient is at 34 weeks' gestation or more and has:

Ruptured membranes, Abnormal fetal testing, Progressive labor, or Fetal growth restriction in the setting of mild

preeclampsia.

CARE IN MILD PREECLAMPSIA

Expectant management of women with mild preeclampsia consists of: Frequent laboratory monitoring (platelet count,

liver and renal function tests), Assessment of maternal blood pressure and

symptoms, and Evaluation of fetal growth and well-being.

TREATMENT OF HYPERTENSION

The use of antihypertensive drugs to control mildly elevated blood pressure in the setting of preeclampsia does not alter the course of the disease or diminish perinatal morbidity or mortality, and should be avoided.

Sodium restriction and diuretics have no role in routine therapy

CARE IN SEVERE PREECLAMPSIA

When severe preeclampsia is diagnosed after 34 weeks' gestation, delivery is most appropriate.

But if patient appears to be stable, and if the fetal condition is reassuring, expectant management may be considered.

CRITERIA FOR DELIVERY

Women with severe preeclampsia who are managed expectantly must be delivered under the following circumstances: Nonreassuring fetal heart status Uncontrollable BP Oligohydramnios, with amniotic fluid index (AFI) of less than

5 cm Severe intrauterine growth restriction in which the estimated

fetal weight is less than 5% Oliguria (< 500 mL/24 h) Serum creatinine level of at least 1.5 mg/dL Pulmonary edema Shortness of breath or chest pain with pulse oximetry of <

94% on room air Headache that is persistent and severe Right upper quadrant tenderness Development of HELLP syndrome

ACUTE TREATMENT OF SEVERE HYPERTENSION IN PREGNANCY Hydralazine: Direct peripheral arteriolar vasodilator In the past, was widely used as the first-line

treatment for acute hypertension in pregnancy.

Slow onset of action (10-20 min), peaks approximately after 20 minutes

IV bolus dose of 5-10 mg, depending on the severity of hypertension, may be administered every 20 minutes up to a maximum dose of 30 mg.

S/E: headache, nausea, and vomiting. May result in maternal hypotension, resulting in nonreassuring fetal heart rate tracing

ACUTE TREATMENT OF SEVERE HYPERTENSION IN PREGNANCY Labetalol: Selective alpha blocker and nonselective beta blocker;

produces vasodilatation. 20 mg IV with repeat doses (40, 80, 80, and 80 mg) every

10 minutes. Maximum dose of 300 mg. Decreases in BP after 5 minutes (in contrast to hydralazine). Decreases supraventricular rhythm and slows the heart

rate, reducing myocardial oxygen consumption. No change in afterload is observed after treatment with

labetalol. S/E dizziness, nausea, and headaches. Oral maintenance dose can be started after IV

ACUTE TREATMENT OF SEVERE HYPERTENSION IN PREGNANCY Calcium channel blockers: Arteriolar smooth muscle; vasodilatation by

blocking calcium entry into the cells. Nifedipine is the oral calcium channel blocker that

is used in the management of hypertension in pregnancy.

10 mg PO every 15-30 minutes, max 3 doses. S/E: tachycardia, palpitations, and headaches. Avoid CCB with MgSO4 Postpartum in patients with preeclampsia, for BP

control.

ACUTE TREATMENT OF SEVERE HYPERTENSION IN PREGNANCY

Sodium Nitroprusside In a severe hypertensive emergency, given

when others failed to lower BP, Release of nitric oxide; vasodilation. Preload and afterload decreased. Onset of action is rapid Severe rebound hypertension may result. Cyanide poisoning may occur in the fetus.

Should be reserved for postpartum care or just before the delivery of the fetus

SEIZURE PROPHYLAXIS

Recommended for women with severe preeclampsia

Less clear benefit in mild preeclampsia Magnesium sulfate rather than phenytoin is

recommended for seizure prophylaxis. A loading dose of 6 grams magnesium

sulfate intravenously over 15 to 20 minutes followed by 2 grams per hour as a continuous infusion.

The maintenance dose (but not the loading dose) should be adjusted in women with renal insufficiency.

MGSO4 TOXICITY

Calcium gluconate (1 gram intravenously over 5 to 10 minutes) should be administered to counteract life-threatening symptoms of magnesium toxicity.

Magnesium toxicity is related to serum concentration:

Loss of deep tendon reflexes occurs at 8 to 10 mEq/L,

Respiratory paralysis at 10 to 15 mEq/L, Cardiac arrest at 20 to 25 mEq/L.

PROGNOSIS

Morbidity and Mortality Worldwide, preeclampsia and eclampsia

responsible for approximately 14% of maternal deaths/year (50,000-75,000).

Morbidity and mortality in preeclampsia and eclampsia are related to the following conditions: Systemic endothelial dysfunction Vasospasm and small-vessel thrombosis leading to

tissue and organ ischemia CNS events, such as seizures, strokes, and

hemorrhage Acute tubular necrosis Coagulopathies Placental abruption in the mother

RECURRENCE

Recurrence risk of preeclampsia: approximately 10%.

Previous history of severe preeclampsia (including HELLP syndrome and/or eclampsia), recurrence risk of preeclampsia is 20%.

Recurrence risk of HELLP syndrome is 5%

and of eclampsia is 2%. Earlier disease during the index pregnancy,

higher chance of recurrence. If before 30 weeks' gestation, recurrence may be

as high as 40%

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