pregnancy induced hypertension
Introduction
Introduction Pregnancy-induced hypertension syndrome (pregnancy-induced hypertension), pregnancy-induced hypertension, known as pregnancy toxicosis, pre-eclampsia, etc., is a unique disease for pregnant women, most of which occur in 20 weeks of gestation and two weeks after delivery, accounting for all 5% of pregnant women. Some of them are accompanied by proteinuria or edema, which is called pregnancy-induced hypertension syndrome. If the condition is severe, symptoms such as headache, blurred vision, and upper abdominal pain may occur. If not treated properly, it may cause generalized paralysis or even coma. The disease is a systemic disease unique to pregnant women. This disease is a serious threat to maternal and child health and is the leading cause of maternal and perinatal death.
Cause
Cause
Etiology theory
(1) Uterus-placental ischemia theory: This theory was first proposed by Young (1918). It is believed that this disease is prone to occur in the first trimester, multiple pregnancy, and polyhydramnios. It is due to the increased uterine tension and affects the blood supply to the uterus. Caused by uterus-placental ischemia and hypoxia. In addition, the systemic blood circulation can not adapt to the needs of the uterus-placenta, such as pregnant women with severe anemia, chronic hypertension, diabetes, etc., is also easy to accompany this disease. Some scholars believe that utero-placental ischemia is not the cause of disease, but the result of vasospasm.
(2) Neuroendocrine theory: The imbalance of the renin-angiotensin-prostaglandin system may be related to the occurrence of this disease. In the past, it was thought that there was a large amount of renin in the blood circulation of patients with pregnancy-induced hypertension, which increased the content of angiotensin II (AII). AII caused vasoconstriction, increased blood pressure, and promoted the secretion of aldosterone. , thereby increasing glomerular recovery of sodium ions. However, in recent years, it has been confirmed that the levels of plasma renin and AII in patients with pregnancy-induced hypertension are lower than those in normal pregnant women, especially in critically ill patients. Therefore, it is believed that the onset of pregnancy-induced hypertension may be related to the increased sensitivity of the body to AII.
Prostaglandin (PG) is associated with the onset of pregnancy-induced hypertension, except that prostaglandin E2 (PGE2) has been shown to have anti-AII effect on vascular wall muscle fibers and vasodilation and prostaglandin F2a (PGF2a) has strong vasoconstriction. In addition, in recent years, two new prostaglandin analogues, prostacycline (PGI2) and thromboxane A2 (thoboxane, TXA2) have been found to be more important for the pathogenesis of pregnancy-induced hypertension. PGI2 has platelet inhibition. Agglutination and enhancement of vasodilatation; TXA2 has the effect of inducing platelet aggregation and enhancing vasoconstriction. In normal pregnancy, both levels increase with pregnancy progression, but are in equilibrium. At the time of pregnancy-induced hypertension, the amount of PGI2 decreased significantly, while the amount of TXA2 increased, resulting in vasoconstriction, elevated blood pressure, and possibly coagulation dysfunction. There is data suggesting that the reduction of PGI2 precedes the occurrence of clinical symptoms of pregnancy-induced hypertension, suggesting that the reduction of PGI2 may be involved in the occurrence of pregnancy-induced hypertension.
(3) Immunology: Pregnancy is considered a successful natural allograft. The maintenance of normal pregnancy depends on the establishment and stability of the immune balance between the mother and the mother. From the point of view of immunology, it is considered that the cause of pregnancy-induced hypertension is an allergic reaction to the immune response of certain antigenic substances in the placenta, which is very similar to the viewpoint of transplantation immunity. Immunological studies from pregnancy-induced hypertension found that the IgG and complement valence of maternal plasma were low, and the incompatibility of histocompatibility antigen (HLA) between husband and wife was increased. This HLA incompatibility may be related to the occurrence of pregnancy-induced hypertension. There is data showing that the detection rate of HLA antibodies in patients with pregnancy-induced hypertension is significantly higher than that in normal pregnancy. However, not every patient with pregnancy-induced hypertension can detect HLA antibodies, and even patients with severe disease cannot detect HLA antibodies. Therefore, the relationship between this disease and immunity is still not completely clear.
(4) Chronic disseminated intravascular coagulation (DIC) theory: In pregnancy-induced hypertension, especially in critically ill patients, there is a tendency to hemorrhage, various clotting factors are reduced to varying degrees, and fibrinogen degradation products (FDP) are obvious. Increased, renal pathological examination found that glomerular vascular endothelial cells and basement membrane have pre-fibrin deposition and changes in chronic DIC caused by placental infarction. However, DIC is the cause or result of this disease, it is still difficult to determine.
(5) Others: In recent years, new research has been made on the etiology of pregnancy-induced hypertension, such as endothelin, calcium, atrial natriuretic peptide and trace elements. Among them, the relationship between plasma endothelin and calcium deficiency and pregnancy-induced hypertension is more noticeable.
1. Pregnancy-induced hypertension and plasma endothelin: Endothelin (ET) is a polypeptide hormone secreted by vascular endothelial cells and is a powerful vasoconstrictor. ET and TXA2 and endothelium-derived relaxing factors (EDRFs) and PGI2 maintain a dynamic balance during normal control and control the blood pressure and local blood flow of the body. In pregnancy-induced hypertension, ET and TXA2, which regulate vasoconstriction, increase in patients, while EDRFs and PGI2, which regulate vasodilation, decrease, making the regulation of vasoconstriction and diastole imbalance.
2, calcium deficiency and pregnancy-induced hypertension: In recent years, the occurrence of pregnancy-induced hypertension may be related to calcium deficiency. It has been shown that calcium deficiency in humans and animals can cause an increase in blood pressure. Pregnancy is easy to cause maternal calcium deficiency, leading to the occurrence of pregnancy-induced hypertension, and calcium supplementation during pregnancy can reduce the incidence of pregnancy-induced hypertension. Therefore, it is believed that calcium deficiency may be an important factor in the occurrence of pregnancy-induced hypertension, and its mechanism is still unclear. In addition, the detection of urinary calcium excretion can be used as a predictive test for pregnancy-induced hypertension.
Examine
an examination
Related inspection
Blood pressure urine routine fundus examination
Pregnancy-induced hypertension is complicated and rapid. The purpose of monitoring and evaluation is to understand the severity and progress of the disease and to treat it promptly and reasonably.
1. Basic examination: Understand headaches, chest tightness, vertigo, upper abdominal pain and other symptoms, check blood pressure, urine routine, weight, urine volume, fetal heart rate, fetal movement, fetal heart monitoring.
2. Special examination of pregnant women: including fundus examination, coagulation function, heart, liver and kidney function tests.
3. Special examination of the fetus: including fetal development, B-ultrasound monitoring of intrauterine conditions and umbilical arterial blood flow.
Diagnosis
Differential diagnosis
Should be differentiated from the following diseases: pregnancy with chronic hypertension, pregnancy with nephrotic syndrome, pregnancy with pheochromocytoma, pregnancy with cholelithiasis and cholecystitis, pregnancy with cerebrovascular disease, pregnancy with seizures, pregnancy with hand and foot convulsions Acute fatty liver during pregnancy, peripartum cardiomyopathy, immune thrombocytopenic purpura, etc.
Clinical manifestation
(1) mild pregnancy-induced hypertension
The main manifestation is a mild increase in blood pressure, possibly accompanied by mild edema and microalbuminuria. This phase can last for several days to several weeks and can gradually develop or deteriorate rapidly.
1. Edema: It is the earliest symptom of pregnancy-induced hypertension. At the beginning, it only showed weight gain (recessive edema), and gradually developed into clinically visible edema. The edema starts from the crotch and gradually develops upwards. It is divided into four levels according to its degree and is represented by +. (+) Depression edema below the calf, does not subside after rest; (++) edema extends to the thigh; (+++) edema extends to the vulva or abdomen; (++++) systemic edema, or even chest and ascites.
2. Hypertension: The blood pressure is not high before 20 weeks of pregnancy, and the blood pressure rises above 17.3/12KPa (130/90mmHg) after 20 weeks of pregnancy, or 4/2KPa (30/15mmHg) compared with the baseline blood pressure.
3. Proteinuria: occurs after the increase in blood pressure, no or trace.
(2) Moderate pregnancy-induced hypertension
The blood pressure is further increased, but does not exceed 21.3/14.7KPa (160/110mmHg), the urine protein is increased, accompanied by edema, and there may be mild symptoms such as dizziness.
(3) Severe pregnancy-induced hypertension
Includes pre-eclampsia and eclampsia. The blood pressure is more than 21.3/14.7KPa (160/110 mmHg), the urine protein is more than ten to ++, the degree of edema is different, and there are symptoms such as headache and vertigo, and severe convulsions and coma.
Pre-eclampsia
In addition to the above three main symptoms, dizziness, headache, visual disturbance, upper abdominal discomfort, chest tightness and nausea and vomiting, etc., indicate further development of intracranial lesions. At this time, the blood pressure is more than 21.3/147 KPa (160/110 mmHg), the edema is heavier, the urine is less, the urine protein is increased, convulsion may occur at any time, and active treatment should be taken to prevent eclampsia.
Preeclampsia
On the basis of each of the above serious symptoms, seizures occur, or accompanied by coma. A small number of patients progress rapidly, pre-eclampsia symptoms can not be significant, and sudden convulsions occur more often in late pregnancy and before labor, a few at birth, less can occur within 24 hours after delivery.
diagnosis
Normal people's blood pressure has a certain fluctuation range under different physiological conditions. When anxiety, nervousness, stress state or physical activity, blood pressure can be increased. In addition, the systolic blood pressure increases with age, so the boundary between hypertension and normal blood pressure is not easy to divide. In 1979, China revised blood pressure measurement methods and diagnostic criteria for hypertension as follows:
1. After 15 minutes of rest, take the sitting position and measure the blood pressure of the right arm. It should be measured several times until the blood pressure value is relatively stable. The diastolic pressure is based on the disappearance of the sound. If the sound does not disappear, the value at the time of the change is used. One hour apart on the same day, or verified again every other day.
2, where systolic blood pressure 21.2kPa (160mmHg) and / or diastolic blood pressure 12.6kPa (95mmHg), can be confirmed by verification. Blood pressure 18.7 ~ 21.2 / 12 ~ 12.6kPa (140 ~ 160 / 90 ~ 95mmHg) for clinical hypertension.
3, in the past there is a history of hypertension, not treated for more than 3 months, this check for normal blood pressure, not listed as high blood pressure; such as the usual medication and this check blood pressure is normal, should still be diagnosed as high blood pressure.
Repeated measurement of blood pressure above 18.7/12 kPa (140/90 mmHg) before 20 weeks of gestation, or diagnosis of hypertension before pregnancy, is called pregnancy with essential hypertension. About 59% of patients have a family history.
Pregnancy with essential hypertension and lower blood pressure in the second trimester, or lower than 21.2/13.3 kPa (160/100 mmHg), the fetal survival rate is high; if the blood pressure is higher than 21.2/13.3 kPa (160/100 mmHg), the fetus The mortality rate has increased significantly. About 10% to 20% of pregnant women with essential hypertension develop pregnancy-induced hypertension syndrome in the third trimester. The baseline blood pressure is >24/14.6 kPa (180/110 mmHg), and the fetal mortality rate is 23%. If the pregnancy-induced hypertension syndrome is added, the fetal mortality rate is as high as 41.3%. The earlier the pregnancy hypertension sign, the worse the fetal pre-existing, the pregnancy-induced hypertension syndrome before the 32 weeks of gestation, 75% fetal death. In addition, in patients with pregnancy-induced hypertension based on essential hypertension, the incidence of early placental ablation was 2%, higher than that of patients with pregnancy-induced hypertension.
