Pregnancy Induced Hypertension

Jun Ma

Dept. of Obstetrics & Gynecology

The First Hospital of Xi’an Jiaotong Univ

Introduction

Incidence: China: 9.4%, worldwide: 7-12%

The most common and yet serious conditions seen in obstetrics

cause substantial morbidity and mortality in the mother and fetus

Death due to cerebral hemorrhage, aspiration pneumonia, hypoxic encephalophathy, thromboembolism, hepatic rupture, renal failure

Hypertension in pregnancy

Definition Diastolic BP ≥90 mmHg

Systolic BP ≥140 mmHg

Or as an increase in the diastolic BP of ≥ 15 mmHg or in the systolic blood pressure of 30 mmHg, as compared to previous pressure

The increased blood pressures be present on at least two separate occasions, > 6h apart

Classification

• Pregnancy-induced hypertension

Preeclampsia

Mild

Severe

Eclampsia

• Chronic hypertension preceding pregnancy

• Chronic hypertension with superimposed PIH

Superimposed preeclampsia

Superimposed eclampsia

• Gestational hypertension

Classification of Hypertensive Disorders in Pregnancy (ACOG)

Classification (1)1. Pregnancy-induced hypertension:

Hypertension associated with proteinuria and edema, occurring primarily in nulliparas after the 20th week or near term.

Preeclampsia

【 mild 】 BP ≥ 140/90mmHg Onset after 20 weeks’ gestation Proteinuria (>300mg/24-hr urine collection) or + Epigastric discomfort Thrombocytopenia

Classification (2)【 severe 】 BP ≥ 160/110 mmHg Marked proteinuria (>1-2 g/24-hr urine collection or 2+ or

more), oliguria Cerabral or visual disturbances such as headache and

scotomata Pulmonary edema or cyanosis Epigastric or right upper quadrant pain (probably caused by

subcapsular hepatic hemorrhage) Evidence of hepatic dysfunction, or thrombocytopenia

Classification (3)

Eclampsia

Meets the criteria of preeclampsia

Presence of convulsions, not attributable

to other neurological disease,

Occurrence: 0.5 -4 %, with 25%

occurring in the 1st 72 hs postpartum

Classification (4)

2. Chronic hypertension proceeding pregnancy (essential or secondary to renal disease, endocrine disease, or other causes)

BP ≥ 140/90 mmHg

Presents before 20 wk gestation

Persists beyond 12 wk postpartum

Classification (5)

3. Chronic hypertension with superimposed preeclampsia or eclamptia

Coexistence of preeclampsia or eclampsia with preexisting chronic hypertension

Cause greatest risk

When diagnosis is obscure, it is always wise to assume that the findings represent preeclampsia and treat accordingly.

Classification (6)

4. Gestational hypertension: not mentioned in the

ACOG

Finding of hypertension in late pregnancy in the

absence of other findings suggestive or

preeclampsia

Transient hypertension of pregnancy

May develop into chronic hypertension if elevated

BP persists beyond 12 weeks postpartum

High risk factors

Nulliparous <18ys or >40 ys, multiple pregnancy Has previous gestational hypertensive disorders Chronic nephritis Diabetic Malnutrition Low social status Hydatidiform mole

Etiology: UNCLEAR Immune mechanism (rejection phenomenon, insufficient

blocking Ab)

Injury of vascular endothelium----disruption of the equilibrium between vasoconstriction and vasodilatation, imbalance between PGI and TXA

Compromised placenta profusion

Genetic factor

Dietary factors: nutrition deficiency

Insulin resistance

Increase CNS irritability

Pathophysiology

Central nervous system

Raised BP disrupt autoregulation

Increased permeability due to vasospasm---thrombosis of arterioles, microinfarcts, and petechial hemorrhage

Cerebral edema: increased intracranial pressure

CT scan (1/3-1/2 positive): focal hypodensity

Cerebral angiography: diffuse arterial vasoconstriction

EEG: nonspecific abnormality (75% in eclamptic patient)

Eyes

Serous retinal detachment Cortical blindness

Pulmonary system

Pulmonary edema Cardiogenic or noncardiogenic Excessive fluid retention, decreased hepatic

synthesis of albumin, decreased plasma colloid oncotic pressure,

Often occurs postpartum Aspiration of gastric contents: the most

dreaded complications of eclamptic seizures

Kidneys

Characteristic lesion of preeclampsia: glomeruloendotheliosis

Swelling of the glomerular capillary endothelium

Decreased GFR

Fibrin split products deposit on basement membrane

Proteinuria

Increase of plasma uric acid, creatinine,

Liver

The spectrum of liver disease in preeclampsia is broad

Subclinical involvement

Rupture of the liver or hepatic infarction

HELLP syndrome: hemolysis, elevated liver enzymes and low platelets

Cardiovascular system

Generalized vasoconstriction, low-output, high-resistance state

Untreated preeclamptic women are significantly volume-depleted

Capillary leak

Cardiac ischemia, hemorrhage, infarction, heart failure

Increased sensitivity to vasoconstrictor effects of angiotensin

Blood (1)

Volume: reduced plasma volume Normal physiologic volume expansion

does not occur Generalized vasoconstriction and capillary

leak Hematocrit

Blood (2): coagulation Isolated thrombocytopenia: <150,000/l Microangiopathic hemolytic anemia DIC (5%) HELLP syndrome: in severe preeclampsia

1. schistocytes on the peripheral blood smear

2. lactic dehydrogenase > 600 u/L

3. total bilirubin > 1.2 mg/dl

4. aspartate aminotransferase >70 U/L

5. platelet count <100,000/mm3

Misdiagnosis: hepatitis, gallbladder disease, ITP

Endocrine system

Vascular sensitivity to catecholamines and other endogenous vasopressors such as antidiuretic hormone and angiotensin II is increased in preeclampsia

Disequilibrium of prostacyclin/ thromboxane A2

Placenta perfusion

500 m vs 200 m

Acute atherosis of spiral arteries: fibrinoid necrosis of the arterial wall, the presence of lipid and lipophages and a mononuclear cell infiltrate around the damaged vessel----vessel obliteration---- placental infarction

Fetus is subjected to poor intervillous blood flow

IUGR or stillbirth

Clinical findings (1)Symptoms and signs

1. Hypertension

Diastolic pressure ≥ 90 mmHg or

Systolic pressure ≥ 140 mmHg or

Increase of 30/15 mmHg

2. Proteinuria

>300 mg/24-hr urine collection or

+ or more on dipstick of a random urine

Clinical findings (2)

3. Edema

Weight gain: 1-2 lb/wk or 5 lb/wk is considered worrisome

Degree of edema

Preeclampsia may occur in women with no edema

Most recent reports omit it from the definition

Clinical findings (3)

4. Differing clinical picture in preeclampsia-eclampsia crises: patient may present with

Eclamptic seizures

Liver dysfunction and IUGR

Pulmonary edema

Abruptio placenta

Renal failure

Ascites and anasarca

Clinical findings (4)

Laboratory findings (1)

Blood test: elevated Hb or Hct, in severe cases, anemia secondary to hemolysis, thrombocytopenia, FDP increase, decreased coagulation factors

Urine analysis: proteinuria and hyaline cast, specific gravity > 1.020

Liver function: ALT and AST increase, alkaline phosphatase increase, LDH increase, serum albumin

Renal function: uric acid: 6 mg/dl, serum creatinine may be elevated

Clinical findings (5)

Laboratory findings (2)

Retinal check:

Other tests: ECG, placenta function, fetal maturity, cerebral angiography, etc

Differential diagnosis

Pregnancy complicated with chronic nephritis

Eclampsia should be distinguished from epilepsy, encephalitis, brain tumor, anomalies and rupture of cerebral vessel, hypoglycemia shock, diabetic hyperosmatic coma

Complications

Preterm delivery

Fetal risks: acute and chronic uteroplacental insufficiency

Intrapartum fetal distress or stillbirth

IUGR

Oligohydramnios

Predictive evaluation (1)

1. Mean arterial pressure, MAP= (sys. Bp + 2 x Dia. Bp) /3

MAP> 85 mmHg: suggestive of eclampsia

MAP > 140 mmHg: high likelihood of seizure and maternal mortality and morbidity

Predictive evaluation (2)

2. Roll over test: ROT

Preeclamptic patients are more sensitive to angiotensin II

Difference between Bp obtained at left recumbent position and supine position (at a 5 min interval)

Positive: > 20 mmHg

3. Urine calcium/ creatinine < 0.04

Prevention

Calcium supplementation: not effective in low risk women bur show effect in high risk group

Aspirin (antithrombotic): uncertain

Good prenatal care and regular visits

Baseline test for high-risk women

Eclampsia cannot always be prevented, it may occur suddenly and without warning.

Treatment

A. Mild preeclampsia: bed rest & delivery Hospitalization or home regimen Bed rest (position and why) and daily weighing Daily urine dipstick measurements of proteinuria Blood pressure monitoring Fetal heart rate testing Periodic 24-h urine collection Ultrasound Liver function, renal function, coagulation

A. Mild preeclampsia: bed rest & delivery

Observe for danger signals: severe headache, epigastric pain, visual disturbances

Sedatives: debatable

B. Severe preeclampsia:

Prevention of convulsion: magnesium sulfate or diazepam and phenytoin

Control of maternal blood pressure: antihypertensive therapy

Initiation of delivery: the definitive mode of therapy if severe preeclampsia develops at or > 36 wk or if there is evidence of fetal lung maturity or fetal jeopardy.

Magnesium sulfate

1. Decreases the amount of acetylcholine released at the neuromuscular junction

2. Blocks calcium entry into neurons

3. Vasodilates the smaller-diameter intracranial vessels

Magnesium sulfate

1. Prevent convulsion

2. Virtually ineffective on blood pressure

3. i.v. or i.m. 5g loading dose 5-10 min, i.v. 1-2g/hr constant infusion Total dose: 20-30 g/d

Toxicity: Diminished or loss of patellar reflex Diminished respiration Muscle paralysis Blurred speech Cardiac arrest

How to prevent toxicity?

Frequent evaluation of patellar reflex and respirations

Maintenance of urine output at >25 ml/hr or 600 ml/d

Reversal of toxicity:

1. Slow i.v . 10% calcium gloconate

2. Oxygen supplementation

3. Cardiorespiratory support

Antihypertensive therapy: reduce the Dia. pressure to 90-110 mmHg

Indication Bp> 160/110 mmHg

Dia. Bp > 110 mmHg

MAP > 140 mmHg

Chronic hypertension with previous antihypertensive drugs usage

Antihypertensive therapy

Medications: Hydrolazine: initial choice

Labetolol

Nifedipine

Nimoldipine

Methyldoe

Sodium nitroprusside

Medication Mechanism of action

Effects

hydralazineDirect peripheral vasodilation

CO, RBF maternal flushing, headache, tachycardia

labetalol adrenergic blocker

CO, RBF maternal flushing,headache, neonatal depressed respirations

nifedipineCalcium channel blocker

CO, RBF maternal orthostatic hypotensionHeadache, no neonatal effects

methyldopaDirect peripheral arteriolar vasodilation

CO, RBF maternal flushing,headache, tachycardia

sodium nitroprusside Direct peripheral vasodilation

Metabolite (cyanide) toxic to fetus

Plasma expander Diuretics

Delivery

Indication of termination of pregnancy

1. Preeclampsia close to term

2. <34 wk with decreased placental function

3. 2 hs after control of seizure

Delivery

Induction of labor

1. First stage: close monitor, rest and sedation

2. Second stage: shorten as much as possible

3. Third stage: postpartum hemorrhage

Cesarean section

1. Induction of labor unsuccessful

2. Induction of labor not possible

3. Maternal or fetal status is worsening

Eclampsia

No aura preceding seizure

Multiple tonic-clonic seizures

Unconsciousness

Hyperventilation after seizure

Tongue biting, broken bones, head trauma and aspiration, pulmonary edema and retinal detachment

Management

Control of seizure Control of hypertension Delivery Proper nursing care