Jun Ma
Dept. of Obstetrics & Gynecology
The First Hospital of Xi’an Jiaotong Univ


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

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 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 .

Preeclampsia 【mild 】 BP ≥ 140/90mmHg  Onset after 20 weeks’ gestation Proteinuria (>300mg/24-hr urine collection) or +  Epigastric discomfort  Thrombocytopenia  .Classification (1) 1.  Pregnancy-induced hypertension: Hypertension associated with proteinuria and edema. occurring primarily in nulliparas after the 20th week or near term.

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 .

5 -4 %.  Occurrence: 0.Classification (3) Eclampsia  Meets the criteria of preeclampsia  Presence of convulsions. not attributable to other neurological disease. with 25% occurring in the 1st 72 hs postpartum .

endocrine disease. or other causes)  BP ≥ 140/90 mmHg  Presents before 20 wk gestation  Persists beyond 12 wk postpartum .Classification (4) 2. Chronic hypertension proceeding pregnancy (essential or secondary to renal disease.

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 (5) 3.

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 .

multiple pregnancy  Has previous gestational hypertensive disorders  Chronic nephritis  Diabetic  Malnutrition  Low social status  Hydatidiform mole .High risk factors  Nulliparous  <18ys or >40 ys.

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 .

decreased plasma colloid oncotic pressure. decreased hepatic synthesis of albumin.Pulmonary system  Pulmonary edema  Cardiogenic or noncardiogenic  Excessive fluid retention.  Often occurs postpartum  Aspiration of gastric contents: the most dreaded complications of eclamptic seizures .

. creatinine.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.

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 .

hemorrhage. infarction.Cardiovascular system  Generalized vasoconstriction. heart failure  Increased sensitivity to vasoconstrictor effects of angiotensin . high-resistance state  Untreated preeclamptic women are significantly volume-depleted  Capillary leak  Cardiac ischemia. low-output.

Blood (1) Volume: reduced plasma volume  Normal physiologic volume expansion does not occur  Generalized vasoconstriction and capillary leak  Hematocrit  .

platelet count <100.000/mm3  Misdiagnosis: hepatitis. aspartate aminotransferase >70 U/L 5. schistocytes on the peripheral blood smear 2. total bilirubin > 1.2 mg/dl 4. gallbladder disease. lactic dehydrogenase > 600 u/L 3. ITP .Blood (2): coagulation  Isolated thrombocytopenia: <150.000/ml  Microangiopathic hemolytic anemia  DIC (5%)  HELLP syndrome: in severe preeclampsia 1.

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 .

placental infarction  Fetus is subjected to poor intervillous blood flow  IUGR or stillbirth . the presence of lipid and lipophages and a mononuclear cell infiltrate around the damaged vessel---vessel obliteration---.Placenta perfusion  500 mm vs 200 mm  Acute atherosis of spiral arteries: fibrinoid necrosis of the arterial wall.

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 .

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 (3) 4.

alkaline phosphatase increase. serum albumin Renal function: uric acid: 6 mg/dl. thrombocytopenia. FDP increase. anemia secondary to hemolysis. decreased coagulation factors Urine analysis: proteinuria and hyaline cast.Clinical findings (4) Laboratory findings (1) Blood test: elevated Hb or Hct.020 Liver function: ALT and AST increase. in severe cases. LDH increase. serum creatinine may be elevated . specific gravity > 1.

Clinical findings (5) Laboratory findings (2) Retinal check: Other tests: ECG. fetal maturity. cerebral angiography. placenta function. etc .

encephalitis. anomalies and rupture of cerebral vessel.Differential diagnosis  Pregnancy complicated with chronic nephritis  Eclampsia should be distinguished from epilepsy. brain tumor. diabetic hyperosmatic coma . hypoglycemia shock.

Complications  Preterm delivery  Fetal risks: acute and chronic uteroplacental insufficiency  Intrapartum fetal distress or stillbirth  IUGR  Oligohydramnios .

Bp) /3  MAP> 85 mmHg: suggestive of eclampsia  MAP > 140 mmHg: high likelihood of seizure and maternal mortality and morbidity . MAP= (sys. Bp + 2 x Dia.Predictive evaluation (1) 1. Mean arterial pressure.

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 3.04 . Urine calcium/ creatinine < 0.

. it may occur suddenly and without warning.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.

renal function. coagulation .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.

epigastric pain.A. visual disturbances  Sedatives: debatable  . Mild preeclampsia: bed rest & delivery Observe for danger signals: severe headache.

.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.

Blocks calcium entry into neurons 3. Decreases the amount of acetylcholine released at the neuromuscular junction 2. Vasodilates the smaller-diameter intracranial vessels .Magnesium sulfate 1.

or i.Magnesium sulfate 1. Prevent convulsion 2.v.  1-2g/hr constant infusion  Total dose: 20-30 g/d .m. Virtually ineffective on blood pressure 3.v. i. i.  5g loading dose 5-10 min.

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

Cardiorespiratory support . Oxygen supplementation 3.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.v . Slow i. 10% calcium gloconate 2.

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: reduce the Dia.

Antihypertensive therapy Medications:  Hydrolazine: initial choice  Labetolol  Nifedipine  Nimoldipine  Methyldoe  Sodium nitroprusside .

no neonatal effects nifedipine Calcium channel blocker methyldopa Direct peripheral CO. tachycardia labetalol a. RBF maternal orthostatic hypotension Headache. RBF maternal flushing. b. RBF maternal flushing. headache. headache.Mechanism of action Effects hydralazine Direct peripheral vasodilation CO. neonatal depressed respirations Medication CO. tachycardia sodium nitroprusside Direct peripheral vasodilation Metabolite (cyanide) toxic to fetus . RBF maternal flushing. arteriolar vasodilation headache.adrenergic blocker CO.

Plasma expander  Diuretics  .

<34 wk with decreased placental function 3. Preeclampsia close to term 2.Delivery  Indication of termination of pregnancy 1. 2 hs after control of seizure .

Second stage: shorten as much as possible 3. Maternal or fetal status is worsening . rest and sedation 2. First stage: close monitor.Delivery  Induction of labor 1. Induction of labor not possible 3. Third stage: postpartum hemorrhage  Cesarean section 1. Induction of labor unsuccessful 2.

pulmonary edema and retinal detachment . broken bones. head trauma and aspiration.Eclampsia  No aura preceding seizure  Multiple tonic-clonic seizures  Unconsciousness  Hyperventilation after seizure  Tongue biting.

Management Control of seizure  Control of hypertension  Delivery  Proper nursing care  .