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Pregnancy Induced Hypertension

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1 Pregnancy Induced Hypertension
Hypertensive disorders are among the most common and yet serious conditions seen in obstetrics. These disorders cause substantial morbidity and mortality for both mother and fetus, despite improved prenatal care. Jun Ma Dept. of Obstetrics & Gynecology The First Hospital of Xi’an Jiaotong Univ

2 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 Hypertensive disorders are among the most common and yet serious conditions seen in obstetrics. These disorders cause substantial morbidity and mortality in both the mother and fetus, despite improved prenatal care.

3 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 Although this definition seems quite clear, its use in clinical practice is difficult because of various problems in obtaining a reliable assessment of blood pressure. Position Corrrect size blood pressure cuff BP normally decreases during the second trimester, and the decrease may mask the presence of chronic hypertension .

4 Classification Various classifications of hypertensive disorders in pregnancy have been proposed. Here the commonly used classification of ACOG is proposed.

5 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 Hypertensive disorders in pregnancy represent a spectrum of disease, classification systems should not be considered as rigid markers on which all management decisions are made.

6 Classification (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

7 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

8 Classification (3) Eclampsia Meets the criteria of preeclampsia
Presence of convulsions, not attributable to other neurological disease, Occurrence: %, with 25% occurring in the 1st 72 hs postpartum

9 Classification (4) 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

10 Classification (5) 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. Superimposed preeclampisa: preeclampsia may occur in women with chronic hypertension, the progress is worse for the mother and the fetus than either condition alone. The criteria for it are worsening hypertension before 20 weeks together with either nondependent edema or proteinuria.

11 Classification (6) 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 Gestational hypertension: is further divided into transient hypertension of pregnancy if preeclampsia is present at the time of delivery and the blood pressure is normal by 12 weeks postpartum, and chronic hypertension if the elevation in blood pressure persists beyond 12 weeks postpartum. This condition is often predictive of the later development of essential hypertension.

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

13 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 Preeclampsia has been described as a disease of theories, because the cause is unknown.

14 Pathophysiology Hypertension in pregnancy affects the mother and newborn to varying degrees, depending on the severity of disease. The effect is multisystem. One common pathophysiologic finding in hypertension in pregnancy , especially when there is progression to preeclampsia, is vasospasm.

15 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)

16 Eyes Serous retinal detachment Cortical blindness

17 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

18 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,

19 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

20 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

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

22 Blood (2): coagulation Isolated thrombocytopenia: <150,000/ml
Microangiopathic hemolytic anemia DIC (5%) HELLP syndrome: in severe preeclampsia schistocytes on the peripheral blood smear lactic dehydrogenase > 600 u/L total bilirubin > 1.2 mg/dl aspartate aminotransferase >70 U/L platelet count <100,000/mm3 Misdiagnosis: hepatitis, gallbladder disease, ITP ITP: idiopathic thrombocytopenic purpura

23 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

24 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

25 Clinical findings (1) Symptoms and signs Hypertension
Diastolic pressure ≥ 90 mmHg or Systolic pressure ≥ 140 mmHg or Increase of 30/15 mmHg Proteinuria >300 mg/24-hr urine collection or + or more on dipstick of a random urine Hypertension is the most important criterion for the diagnosis of preeclampsia, and it may occur suddenly. The criteria are as described before. It usually falls during sleep in patients with mild preeclampsia and chronic hypertension, but in severe preeclampsia, BP may increase during sleep, eg, the most severe hypertension may occur at 2 am. Proteinuria is the last sign to develop. Eclampsia may occur without proteinuria. Most patients with proteinuria will have glomeruloendotheliosis on kidney biopsy. Proteinuria in preeclampsia is an indicator of fetal jeopardy. The incidence of SGA infants and perinatal mortality is mardedly increased in patients with proteinuric preeclampsia.

26 Clinical findings (2) 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

27 Clinical findings (3) 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 Preeclampsia-eclampsia is a multisystem dissease with varying clinical presentations.

28 Laboratory findings (1)
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

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

30 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

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

32 Predictive evaluation (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 More than 100 clinical , biophysical and biochemical tests have been reported to predict preeclampsia, unfortunately, most suffer from poor sensitivity and none are suitable for routine use a as screening test in clinical practice.

33 Predictive evaluation (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 Urine calcium/ creatinine < 0.04 Several authors have reported reduced urinary excretion of calcium during preeclampsia and for several weeks prior to the onset of clinically apparent disease. In addition, abnormal intracellular calcium metabolism in platelets and RBC has been demonstrated in women with preeclampsia as compared with normotensive pregnant women.

34 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. As a result, most studies of prevention have used patients with various risk factors for preeclampsia. Aspirin: There is evidence to suggest that thromboxane A2 production is markedly increased, while prostacyclin production is reduced in women with welll established preeclampsia and prior to the onset of preeclampsia. In addition, placental infarcts and thrombosis of the spiral arteries have been demonstrated in pregnancies complicated by preeclampsia, particularly in those with severe fetal growth retardation or fetal demise. As a result of these findings, several authors have used various antithrombotic agents in a an attempt to prevent preeclampsia. The baseline tests include: Hct and Hb, platelet count Serum creatine and uric acid 24-h urine collection for protein and creatinine clearance Early ultrasounds and follow-up scans.

35 Treatment 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 The patient is usually hospitalized upon diagnosis, since this diminishes the possibility of convulsions and enhances the chance of fetal survival. Hospitalization to prevent premature delivery in preeclmapsia is far less expensive than the cost of caring for a premature infant. The mainstay of patients with mild preeclampsia and an immature fetus is bed rest, preferably with as much of the time as possible spent in a lateral decutitus position. In this position cardia function and uterine blood flow are maximized and maternal BP in most cases are normalized. This improves uteroplacental function, allowing normal fetal growth and metabolism.

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

37 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.

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

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

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

41 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: Slow i.v . 10% calcium gloconate Oxygen supplementation Cardiorespiratory support

42 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

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

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

45 Plasma expander Diuretics

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

47 Delivery Induction of labor
First stage: close monitor, rest and sedation Second stage: shorten as much as possible Third stage: postpartum hemorrhage Cesarean section Induction of labor unsuccessful Induction of labor not possible Maternal or fetal status is worsening Postpartum eclampsia can happen at days after delivery.

48 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

49 Management Control of seizure Control of hypertension Delivery
Proper nursing care

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