TASHKENT MEDICAL ACADEMY
DEPARTMENT OF OBSETRICS AND GINECOLOGY
Hypertensive states in pregnancy
Lector prof.,doctor of medicine Babadjanova G.S
TASHKENT-2013
Purpose:
To make out the questions of diagnostics and new methods of
treatment,profilactics.
Object:
To give the new classification
To say theories of etiology and patogenesis
Clinics of difference
Methods of treatment
Bases of profilactic
Gestational hypertension or pregnancy-induced hypertension (PIH) is defined as
the development of new arterial hypertension in a pregnant woman after 20
weeks gestation without the presence of protein in the urine.
Conditions
There exist several hypertensive states of pregnancy:
 Gestational hypertension
 Gestational hypertension is usually defined as having a blood pressure
higher than 140/90 without the presence of protein in the urine.
Preeclampsia
 Preeclampsia is gestational hypertension (blood pressure greater than
140/90) plus proteinuria (>300 mg of protein in a 24-hour urine sample).
Severe preeclampsia involves a blood pressure greater than 160/110, with
Eclampsia

This is when tonic-clonic seizures appear in a pregnant woman with high
blood pressure and proteinuria.
 HELLP syndrome
 This is a dangerous combination of three medical conditions: hemolytic
anemia, elevated liver enzymes and low platelet count.
 additional medical signs and symptoms.
Risk factors
 Family history of preeclampsia
 Pre-existing hypertension
 Renal disease
 Diabetes mellitus
 Obesity
 Multiple gestation (twins or triplets, etc.)
 Age 35 or greater
 Adolescent pregnancy
Chronic Hypertension in Pregnancy
 The latest article in our Clinical Practice review series, Chronic Hypertension
in Pregnancy, reviews the potential risks associated with pregnancy among
women with chronic hypertension and recommended treatment before
and during pregnancy. Current recommendations regarding medications
are reviewed.
 The prevalence of chronic hypertension in pregnancy in the United States is
estimated to be as high as 3%, which represents a substantial increase over
time. This increase in prevalence is primarily attributable to the increased
prevalence of obesity, a major risk factor for hypertension, as well as the
delay in childbearing to ages when chronic hypertension is more common.
What are the risks associated with chronic hypertension in pregnancy?
 Women with chronic hypertension have an increased frequency of
preeclampsia (17 to 25% vs. 3 to 5% in the general population), as well as
placental abruption, fetal growth restriction, preterm birth, and cesarean
section. Preeclampsia is a leading cause of preterm birth and cesarean
delivery in this population.
How does the blood pressure of women with chronic hypertension change during
pregnancy?
Most women with chronic hypertension have a decrease in blood pressure during
pregnancy, similar to that observed in normotensive women; blood pressure falls
toward the end of the first trimester and rises toward prepregnancy values during
the third trimester. As a result, antihypertensive medications can often be
tapered during pregnancy
What blood pressure targets are generally recommended during pregnancy?
Various professional guidelines provide disparate recommendations regarding
indications for starting therapy (ranging from a blood pressure >159/89 mm Hg to
>169/109 mm Hg) and for blood-pressure targets for women who are receiving
therapy (ranging from <140/90 mm Hg to <160/110 mm Hg). For women whose
antihypertensive therapy is continued, aggressive lowering of blood pressure
should be avoided, though prospective controlled trials to support these
recommendations are not available.
What medications are recommended to manage hypertension in pregnancy?
 The antihypertensive agent with the largest quantity of data regarding fetal
safety is methyldopa, which has been used during pregnancy since the
1960s. Labetalol, a combined alpha- and beta-receptor blocker, is often
recommended as another first-line or second-line therapy for hypertension
in pregnancy. Long-acting calcium-channel blockers also appear to be safe
in pregnancy, although experience is more limited than with labetalol.
Angiotensin-converting-enzyme inhibitors
blockers are contraindicated in pregnancy.
and
angiotensin-receptor
Risks to the Mother and Fetus
 Pregnant women with chronic hypertension are at increased risk for
superimposed preeclampsia and abruptio placentae, and their babies are at
increased risk for perinatal morbidity and mortality.8 The likelihood of
these complications is particularly increased in women with long-standing
severe hypertension and those with preexisting cardiovascular or renal
disease.13-16 In addition, fetal and maternal morbidity and mortality are
higher than normal when pregnant women have a diastolic pressure of 110
mm Hg or higher during the first trimester.14,15 Conversely, the outcomes
of women with mild, uncomplicated chronic hypertension during
pregnancy and of their babies are similar to those of normal pregnant
women.
 Preeclampsia has traditionally been described as the occurrence of
hypertension, edema, and proteinuria after 20 weeks' gestation in a
previously normotensive woman. The differences between preeclampsia
and gestational hypertension are summarized in Table 1. In general,
preeclampsia is defined as hypertension plus hyperuricemia or proteinuria,
and it is categorized as mild or severe primarily on the basis of the degree
of elevation in blood pressure, the degree of proteinuria, or both. At
present, there is no consensus regarding the definition of mild
hypertension, severe hypertension, or severe proteinuria.1-6 Nonetheless,
emphasis on either hypertension or proteinuria may minimize the clinical
importance of a number of other disturbances in various organ systems.4
For example, some women with the syndrome of hemolysis, elevated
serum liver-enzyme concentrations, and low platelet counts (HELLP) have
life-threatening complications (pulmonary edema, acute renal failure, or
liver rupture) but little or no hypertension and minimal proteinuria.
 There are 2 categories of preeclampsia, mild and severe. Severe
preeclampsia is defined as the following: (1) blood pressure greater than
160 mm Hg systolic or 110 mm Hg diastolic on 2 occasions 6 hours apart;
(2) proteinuria exceeding 2 g in a 24-hour period or 2-4+ on dipstick testing;
(3) increased serum creatinine (> 1.2 mg/dL unless known to be elevated
previously); (4) oliguria ≤500 mL/24 h; (5) cerebral or visual disturbances;
(6) epigastric pain; (7) elevated liver enzymes; (8) thrombocytopenia
(platelet count < 100,000/mm3); (9) retinal hemorrhages, exudates, or
papilledema; and (10) pulmonary edema.
Pathophysiology
 One of the earliest abnormalities noted in women in whom preeclampsia
later develops is the failure of the second wave of trophoblastic invasion
into the spiral arteries of the uterus. As a result of this defect in
placentation, there is failure of the cardiovascular adaptations (increased
plasma volume and reduced systemic vascular resistance) that are
characteristic of normal pregnancy. In preeclampsia, both cardiac output
and plasma volume are reduced, whereas systemic vascular resistance is
increased.1 These changes result in reduced perfusion of the placenta,
kidneys, liver, and brain. Endothelial dysfunction (resulting in vasospasm,
altered vascular permeability, and activation of the coagulation system)
could explain many of the clinical findings in women with preeclampsia.4
Indeed, many of the abnormalities described in such women are due
primarily to reduced perfusion rather than to hypertensive vascular injury.
Mild Preeclampsia
 Women with preeclampsia require close observation because the disorder
may worsen suddenly. The presence of symptoms (such as headache,
epigastric pain, and visual abnormalities) and proteinuria increases the risks
of both eclampsia and abruptio placentae; women with these findings
require close observation in the hospital. Outpatient management may be
considered if compliance is expected to be good, hypertension is mild, and
the fetus is normal. The management should include close monitoring of
the mother's blood pressure, weight, urinary protein excretion, and platelet
count, as well as of fetal status.1 In addition, the woman must be informed
about the symptoms of worsening preeclampsia. If there is evidence of
disease progression, hospitalization is indicated.
Severe Preeclampsia
 Severe preeclampsia may be rapidly progressive, resulting in sudden
deterioration in the status of both mother and fetus, so that prompt
delivery is recommended regardless of the duration of gestation. Prompt
delivery is clearly indicated when there is imminent eclampsia, multiorgan
dysfunction, or fetal distress or when severe preeclampsia develops after
34 weeks.Early in gestation, however, prolongation of pregnancy with close
monitoring may be indicated in order to improve neonatal survival and
reduce short-term and long-term neonatal morbidity. In three recent
clinical trials in women with severe preeclampsia remote from term,
neonatal morbidity and mortality were reduced with conservative
management. Nevertheless, because only 116 women were assigned to
conservative management in these trials, and because such management
entails risk to the mother and fetus, conservative management must be
considered only at tertiary perinatal centers and must include very close
monitoring of both mother and fetus
Risks of Preeclampsia to the Mother and Fetus
 The chief risks to the woman entailed by preeclampsia are convulsions,
cerebral hemorrhage, abruptio placentae with disseminated intravascular
coagulopathy, pulmonary edema, renal failure, liver hemorrhage, and
death. The risks to the fetus include severe growth retardation, hypoxemia,
acidosis, prematurity, and death. The frequency of these complications
depends on the duration of gestation at the onset of preeclampsia, the
presence or absence of associated medical complications, the severity of
the preeclampsia, and the quality of medical management. In women with
mild preeclampsia who are closely followed,45-48 the risk of convulsions is
0.2 percent, that of abruptio placentae is 1 percent, and that of fetal or
neonatal death is less than 1 percent. The incidence of fetal growth
retardation (birth weight, <10th percentile) is 5 to 13 percent, and that of
preterm delivery ranges from 13 percent to 54 percent — depending on the
duration of gestation at onset and the presence or absence of proteinuria.
Conversely, maternal and fetal or neonatal morbidity and mortality are
substantial among women with eclampsia,those with the HELLP syndrome
and those in whom preeclampsia occurs before 34 weeks' gestation.
Management of Preeclampsia
 Early diagnosis, close medical supervision, and timely delivery are the
cardinal requirements of the management of preeclampsia; delivery is the
ultimate cure.1,3 Once the diagnosis is established, subsequent
management should be based on the initial evaluation of maternal and
fetal well-being. On the basis of the results of this evaluation, a decision is
then made regarding hospitalization, expectant management, or delivery,
with the following factors taken into account: the severity of the disease
process, the status of mother and fetus, and the length of gestation.
Irrespective of the management strategy chosen, the ultimate goal must
first be the safety of the mother and, second, the delivery of a live infant
who will not require intensive and prolonged neonatal care.
Conclusions
 In caring for pregnant women with hypertension, it is important to
differentiate among chronic hypertension, gestational hypertension, and
preeclampsia. Maternal and neonatal outcomes are usually good among
pregnant women who have either mild chronic hypertension or gestational
hypertension. In addition, antihypertensive drug therapy may permit such
women to continue their pregnancies to term. In contrast, preeclampsia is
a unique syndrome of pregnancy that is potentially dangerous for both
mother and fetus; it does not respond well to the conventional
antihypertensive therapy used in nonpregnant patients. Close medical
supervision and timely delivery are the keys to the treatment of
preeclampsia.
Eclampsia
 The mechanism of the cerebral damage in eclampsia is unclear. The
pathologic findings are similar to those of hypertensive encephalopathy.
These abnormalities include fibrinoid necrosis and thrombosis of arterioles,
microinfarcts, and petechial hemorrhages. In both hypertensive
encephalopathy and eclampsia, the lesions are widely distributed
throughout the brain, but the brainstem is more severely affected in the
former, while the cortex is more severely affected in the latter. Other
differences in the two conditions are that eclampsia may be seen in the
absence of hypertension and that retinal hemorrhages and infarcts are rare
in eclampsia. Two theories have been proposed to explain the pathogenesis
of hypertensive encephalopathy, vasospasm, and forced dilation. In the
first, vasospasm causes local ischemia, arteriolar necrosis, and disruption of
the blood-brain barrier. According to the second, as blood pressure rises
above the limit of autoregulation, cerebral vasodilation occurs. Initially,
some vessel segments dilate, and some remain constricted. Overdistention
of the dilated segments results in necrosis of the medial muscle fibers and
damage to the vessel wall. It is possible that both mechanisms are operant.
 The presence of cerebral edema in preeclampsia-eclampsia is controversial.
One set of researchers stated that cerebral edema was not present in
eclamptic patients when autopsy was performed within 1 hour of death
and that such edema was a late postmortem change. In contrast, some
others found generalized cerebral edema in some autopsy specimens and
confirmed increased intracranial pressure in eclamptics with prolonged
coma (> 6 hours). Early studies of cerebrospinal fluid opening pressure
showed elevated pressures; however, more recent studies have failed to
confirm this.
 Most patients with preeclampsia-eclampsia have normal clotting studies. In
some, a spectrum of abnormalities may be found, ranging from isolated
thrombocytopenia to microangiopathic hemolytic anemia to disseminated
intravascular coagulation (DIC). Thrombocytopenia is the most common
abnormality; a count of less than 150,000/uL is found in 15-20% of patients.
Fibrinogen levels are actually elevated in preeclamptic women as compared
with normotensive patients. Low fibrinogen levels in preeclampsiaeclampsia are usually associated with abruptio placentae or fetal demise.
Elevated fibrin split products are seen in 20% of patients (usually in the
range of 10-40 uL/mL). Microangiopathic hemolytic anemia without other
signs of DIC may be seen in about 5% of patients, and evidence of DIC is
also present in about 5%. In the past, DIC was thought to be the cause of
preeclampsia; now it is regarded as a sequela of the disease.
 The HELLP syndrome describes patients with hemolytic anemia, elevated
liver enzymes, and low platelet count. Criteria for the diagnosis at the
authors' institution are schistocytes on the peripheral blood smear, lactic
dehydrogenase > 600 U/L, total bilirubin > 1.2 mg/dL, aspartate
aminotransferase > 70 U/L, and platelet count < 100,000/mm3. This
syndrome is present in about 10% of patients with severe preeclampsiaeclampsia. It is frequently seen in Caucasian patients with delay in diagnosis
or delivery and in patients with abruptio placentae. The syndrome may
occur remote from term (eg, at 31 weeks) and with no elevation of blood
pressure. The syndrome is frequently misdiagnosed as hepatitis, gallbladder
disease, idiopathic thrombocytopenic purpura, or thrombotic
thrombocytopenic purpura. Most hematologic abnormalities return to
normal within 2-3 days after delivery, but thrombocytopenia may persist
for a week.
Differential Diagnosis
 Hypertensive states of pregnancy other than preeclampsia-eclampsia.
 Chronic essential hypertension
 Chronic hypertension due to renal disease
 Interstitial nephritis
 Acute and chronic glomerulonephritis
 Systemic lupus erythematosus
 Diabetic glomerulosclerosis
 Scleroderma
 Polyarteritis nodosa
 Polycystic kidney disease
 Renovascular stenosis
 Chronic renal failure with treatment by dialysis
 Renal transplant
 Chronic hypertension due to endocrine disease
 Cushing's disease and syndrome
 Primary hyperaldosteronism
 Thyrotoxicosis
 Pheochromocytoma
 Acromegaly
 Chronic hypertension due to coarctation of the aorta