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Pregnancy

Induced
Hypertension
Jun Ma
Dept. of Obstetrics & Gynecology
The First Hospital of Xian 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

Classification of Hypertensive
Disorders in Pregnancy (ACOG)
Pregnancy-induced hypertension
Preeclampsia
Mild
Severe
Eclampsia
Chronic hypertension preceding pregnancy
Chronic hypertension with superimposed PIH
Superimposed preeclampsia
Superimposed eclampsia
Gestational hypertension

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/ml

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 mm vs 200 mm

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 preeclampsiaeclampsia 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

Mechanism
of action

Effects

hydralazine

Direct peripheral
vasodilation

CO, RBF maternal flushing,


headache, tachycardia

labetalol

a, b- adrenergic
blocker

CO, RBF maternal flushing,


headache, neonatal
depressed respirations

Medication

CO, RBF maternal


orthostatic hypotension
Headache, no neonatal
effects

nifedipine

Calcium channel
blocker

methyldopa

Direct peripheral
CO, RBF maternal flushing,
arteriolar vasodilation 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

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