gestational hypertension
Introduction
Introduction to pregnancy-induced hypertension Hypertensive disorders of pregnancy are diseases specific to pregnancy, including gestational hypertension, pre-eclampsia, eclampsia, chronic hypertension complicated by pre-eclampsia, and chronic hypertension. The incidence rate in China is 9.4%, and foreign reports are 7% to 12%. The disease seriously affects maternal and child health and is one of the main causes of maternal and perinatal morbidity and mortality. basic knowledge The proportion of illness: 30% Susceptible people: pregnant women Mode of infection: non-infectious Complications: placental abruption pulmonary edema renal failure fetal distress acute heart failure cerebral palsy
Cause
Causes of pregnancy-induced hypertension
Vasospasm (35%):
Cervical placenta ischemic multiple pregnancy, excessive amniotic fluid, primipara, excessive uterine enlargement, abdominal wall tension, etc., will increase the pressure of the uterine cavity, reduce or slow down the blood flow of the uterus, causing ischemia and hypoxia, vasospasm and blood pressure Raise. It has also been suggested that after ischemia or hypoxia of the placenta or decidua tissue, a pressurized substance can be produced, causing vasospasm and raising blood pressure.
Prostaglandin deficiency (30%):
Prostaglandins can cause blood vessels to dilate. Generally, the body's pressurized substances and antihypertensive substances are in equilibrium, keeping blood pressure at a certain level. The vasodilator prostaglandin is reduced, and the reactivity of the blood vessel wall to the pressurized substance is increased, so that the blood pressure is increased.
Immunity and heredity (15%):
Clinically, maternal pregnancy-induced hypertension is less common. Women with pregnancy-induced hypertension have more pregnancy-induced hypertension. Some people think that it is related to the recessive gene or recessive immune response gene in pregnant women.
Pathogenesis
Pathogenesis
(1) Immunological theory: Pregnancy is successful with allogeneic transplantation. Pregnancy maintenance depends on the immune balance between mother and child. Once the immune balance is imbalanced, it can cause immune rejection and lead to pre-eclampsia.
1 Correlation between pre-eclampsia and human leukocyte antigen (HLA): Some studies have found that the frequency of HLA-DR4 antigen in patients with pre-eclampsia, the maternal-fetal HLA-DR4 antigen sharing rate is higher than that of normal pregnancy, resulting in maternal versus HLA-D region The immune response of the antigen - that is, the blocking antibody, the action of an IgG subclass of HLA antibody is disrupted, the immune balance is dysregulated, and eventually leads to pre-eclampsia.
2 Changes in cellular immunity during pre-eclampsia: Th decreased and Ts increased significantly during pregnancy, which reduced the ratio of Th/Ts to maintain normal maternal-fetal immune relationship and protect the fetus from rejection. TS in patients with severe pre-eclampsia decreased to non-pregnant women The level, while the function is reduced, and the Th/Ts ratio is increased, indicating that the maternal-fetal immune imbalance protection response is weakened in pre-eclampsia.
3 Immune complex (IC) changes in preeclampsia: During priming, the trophoblasts in the uterine vein enter the mother circulation in large amounts, and the IC formation with the parent antibody increases significantly, and deposits in the kidney and placenta of the patient, IC makes the placenta Impaired blood vessels in the attachment, causing blood flow disorder in the placenta, IC deposition in the glomerular basement membrane, increasing its permeability, a large amount of protein leaking, IC deposition in the blood vessels of various organs, activation of coagulation and fibrinolysis system DIC.
(2) Ischemia of the placenta: In normal pregnancy, the fixed villus trophoblasts are retrogradely infiltrated along the spiral artery, gradually replacing the vascular endothelial cells, and replacing the elastic layer of the vascular smooth muscle with a fibrous substance to enlarge the lumen of the blood vessel. Increased blood flow to better nourish the fetus. This process is called remould of vascular. The depth of invasion can reach 1/3 of the myometrium. When pre-eclampsia, trophoblast invasion only reaches the decidual blood vessel. A small number of blood vessels do not remodel, this phenomenon is called superficial implantation of placenta, leading to hypoxia in early trophoblast cells, affecting fetal development.
(3) abnormality of the vasoactive compounds: there are regulatory factors regulating blood vessels in plasma, such as vasoconstrictor, endothelin (ET) and thromboxane (thromboxane A2, TXA2), together Vasoconstriction, vasodilating factor nitric oxide (NO), prostaglandin (PGI2), atrial natriuretic peptide (ANP), etc., with normal pregnancy progress, PGI2 and TXA2, vitamin E ( There is an anti-peroxide activity) and lipid peroxide, the ratio of ET to ANP increases. In pre-eclampsia, the above ratio decreases, and increased TXA2, peroxide, ET, etc. aggravate the destruction of vascular endothelium. It induces platelet aggregation and is sensitive to vasoconstriction factors, further contraction of blood vessels, and further destruction of vascular endothelium, leading to clotting and fibrinolysis disorders. Therefore, patients with severe pre-eclampsia have subclinical or clinical manifestations of DIC.
(4) Genetic predisposition: It is known from clinical observation that pregnant women with a family history of pre-eclampsia have a higher incidence of pre-eclampsia than pregnant women without family history. In hereditary manner, pre-eclampsia is currently considered. It is a single gene recessive inheritance, a single gene can come from the mother, the fetus, or can be combined by two genes; but multi-factor inheritance can not be excluded.
(5) Nutritional deficiency theory: In recent years, it is believed that calcium deficiency may be related to the onset of pre-eclampsia. During pregnancy, 2 g of calcium is added every day, and the prevalence of pre-eclampsia can be reduced from 18% to 4%. The effect may be supplemental regulation of pre-eclampsia. In the case of epilepsy, the kidney absorbs calcium, but some scholars have observed that even after 2 g/d of calcium supplementation for mild pre-eclampsia, it cannot prevent its progression to severe pre-eclampsia.
2. Pathophysiology The basic pathological condition of pre-eclampsia is systemic small arterial spasm, which leads to poor blood flow in the whole body, insufficient blood supply to the microcirculation, damage to tissues and organs due to ischemia and hypoxia, and severe necrosis of various organs. obstacle.
(1) Placenta: There is no change in the placenta itself in pre-eclampsia, but the spiral arterioles in the myometrium and aponeurosis are uneven, the thickness is uneven, the lumen is thin, and it is acute atherosclerosis. Sinusoidal ischemia, placental sinus volume is significantly reduced, which affects fetal growth and development, clinical manifestations of placental dysfunction and fetal growth restriction (FGR), if there is spiral artery embolism, decidual necrosis and post-placental bleeding It can lead to placental abruption and premature birth. If the placenta is infarct due to ischemia, it can cause stillbirth.
(2) brain: cerebral arteriolar spasm, brain tissue ischemia, edema can cause cerebral edema, severe cerebral palsy, MAP 140mmHg, cerebral vascular autoregulation loss, brain microvascular thrombosis, can cause limitations Or diffuse cerebral infarction, when the blood vessels rupture, there may be cerebral hemorrhage, half of the autopsy of factor epilepsy death has cerebral edema and cerebral palsy.
(3) Heart: due to small vasospasm, increased peripheral resistance, increased cardiac afterload, increased heart rate, reduced effective circulation, increased blood concentration and blood viscosity, increased myocardial burden, coronary artery spasm, myocardial ischemia and hypoxia, Interstitial edema and hemorrhagic necrosis occur. Severe pre-eclampsia is prone to acute pulmonary edema and heart failure.
(4) Kidney: renal arteriolar spasm, which reduces renal blood flow, produces a large amount of renin in renal ischemia and hypoxia, causes Ang II to increase, blood pressure to rise further, renal hypoxia also causes glomerular swelling, and filtration function is reduced. Metabolic wastes such as urea nitrogen and uric acid excretion in the body are reduced, but accumulate in the body, hypoxia also increases glomerular permeability, and renal tubular absorption function is reduced, resulting in protein leakage in the blood to form proteinuria, urine protein content and The condition is directly proportional, and acute renal cortical necrosis can occur in patients with severe renal hypoxia, which is characterized by acute renal failure.
(5) Liver: hepatic arteriolar spasm, tissue ischemia and hypoxia, hepatocyte damage, serum alanine aminotransferase may increase, jaundice occurs in severe cases, and autopsy found localized hemorrhage around the hepatic portal vein and even large necrosis, severe aura Eclampsia can occur subhepatic hemorrhage and hematoma formation, or even rupture, leading to intra-abdominal hemorrhage and death, liver damage and coagulopathy occur simultaneously, that is, HELLP syndrome (hemolysis, elevated liver enzymes and thrombocytopenia), will seriously endanger the mother Child life.
(6) abnormal blood coagulation mechanism: the blood is hypercoagulable at the end of normal pregnancy. In severe pre-eclampsia, due to severe vasospasm, the ischemia and hypoxia of various organs, vascular endothelial cells and intravascular red blood cells are destroyed, not only the PGI2 synthesis declines, but also Coagulation substances enter the blood circulation, consume the mother's blood coagulation factors and platelets, placental ischemia, release a large amount of blood coagulation substances and blood concentration, hyperlipidemia, etc. all affect the aggravation of DIC.
Prevention
Pregnancy-induced hypertension prevention
The cause of PIH is unknown, but it cannot be completely prevented. However, the following measures can be taken to reduce the occurrence and development of pre-eclampsia into severe cases.
1. Establish and improve maternal and child health care networks at all levels, and do a good job in pregnancy care. Blood pressure should be measured early in pregnancy, and regular checkups should be performed. Blood pressure, body weight and urine routine must be measured every time. Abnormal findings and timely treatment can significantly reduce eclampsia. Incidence.
2. Pay attention to strengthen the nutrition of pregnant women and rest during pregnancy. Eat more protein, vitamins and various nutrients. In the past, it was considered that calcium supplementation (600-2000mg/d) and/or low-dose aspirin (50-150mg/d) could be added after 20 weeks of pregnancy. Reduce the incidence of pre-eclampsia, but Levine et al (1997) summarized 3 cases of 13 231 cases of calcium and 3 cases of a total of 22064 cases of aspirin pregnant women, found that no reduction in pre-eclampsia.
3. Strengthen the monitoring of high-risk population in the middle of pregnancy. The average arterial pressure is >85mmHg and the roll over test is positive. It is prone to pre-eclampsia in the third trimester. The patients with primary hypertension or kidney disease are prone to pre-eclampsia during pregnancy. Pre-eclampsia is more likely to occur in the next pregnancy. The above-mentioned population should be strengthened during pregnancy.
Complication
Complications of pregnancy-induced hypertension Complications, placental abruption, pulmonary edema, renal failure, fetal distress, acute heart failure, cerebral palsy
1. The harm to maternal mothers The prevalence of maternal mortality in China is 7.5/100,000 (1989), accounting for the second cause of maternal mortality, severe pre-eclampsia combined with placental abruption, coagulopathy, HELLP syndrome, liver Membrane rupture, cerebral vascular disease, pulmonary edema, heart, renal failure, operative and postpartum hemorrhage increase maternal morbidity and mortality, maternal mortality of eclampsia is 1% to 20%, and HELLP syndrome 2% to 4%.
2. Harm to the fetus Severe pre-eclampsia due to insufficient blood supply to the placenta, fetal distress, FGR, premature birth, low birth weight, stillbirth, neonatal death rate, perinatal mortality can be as high as 150 ~ 300 .
Pregnant women may have suffocation due to convulsions, fractures, self-injury, pulmonary edema, acute heart failure, acute renal insufficiency, cerebral palsy, cerebrovascular accident, aspiration pneumonia, placental abruption, fetal distress, fetal death, etc. disease.
Symptom
Symptoms of pregnancy- induced hypertension disease Common symptoms Pregnancy-induced hypertension, convulsions, hypertension, pregnancy-induced hypertension, close-closed ascites, proteinuria, fetal distress, pre-eclampsia, coma
History
Inquire patients in detail before pregnancy and 20 weeks before pregnancy whether there is hypertension, proteinuria and (or) edema, and convulsions and other symptoms; previous high blood pressure, chronic kidney disease, adrenal disease and other secondary hypertension; this pregnancy After the presence or absence of an abnormality.
2. Signs
Appears after 20 weeks of pregnancy:
(1) Hypertension: If blood pressure is measured, it needs to rest for 0.5~1h and then retest. WHO experts believe that blood pressure should be increased for more than 4h to diagnose, but in emergency delivery or low pressure >110mmHg, although the rest is less than 4h It can be diagnosed. In the past, the blood pressure was increased by 130/90mmHg, and it is now changed to 140/90mmHg to be in line with international standards. At the same time, no abnormal diagnosis is made for those whose blood pressure is 30/15mmHg higher than the basic blood pressure but still lower than 140/90mmHg. Because more than 5,700 prospective studies conducted by North et al (1999) and Levine (2000) confirmed that blood pressure increased but remained below 140/90 mmHg, there was no abnormality in maternal and child outcomes, so it is not listed as a diagnostic criterion.
(2) proteinuria: should be left in the middle of the clean urine test, such as 24h urine protein 0.3g, it is abnormal.
(3) Edema: There may be physiological edema during pregnancy. If there is no disappearance after rest, it is pathological edema, and there is concave edema in the ankle and calf, which is represented by 1+; the edema extends to the thigh with 2+ Indicates; edema extends to the vulva and abdominal wall, expressed as "3+"; "4+" is systemic edema or associated with ascites, such as edema is not obvious, but the weight gain of more than 0.5kg per week should pay attention to the presence or absence of recessive edema, Because of the many factors that cause pregnancy edema, the incidence is high, and there is no specificity, it is not used internationally as a feature to diagnose pre-eclampsia.
Examine
Examination of pregnancy-induced hypertension
Blood test
(1) Hematocrit (HCT) <0.35 during normal pregnancy and >0.35 during pre-eclampsia, suggesting blood concentration.
(2) The platelet count is <100×109/L, and it progressively decreases as the condition worsens.
(3) Severe pre-eclampsia If the large amount of protein in the urine is lost, the plasma protein is low and the albumin/globulin ratio is inverted.
(4) elevated blood uric acid, creatinine and urea nitrogen suggest impaired renal function; elevated alanine aminotransferase (ALT) and decreased fibrinogen suggest impaired liver function; myocardial zymogram abnormalities indicate cardiac involvement.
(5) Hemolysis can occur in severe pre-eclampsia, which is characterized by morphological changes of red blood cells and blood bilirubin >20.5 mol/L, and the increase of LDH is the earliest. If DIC occurs, there will be a corresponding change.
(6) For patients with eclampsia, blood, electrolyte and blood gas analysis should be performed to understand whether there is electrolyte metabolism disorder and acid-base balance disorder.
2. Urine check
The severity of the disease is determined based on the degree of abnormal urine protein. If the specific gravity of urine is >1.020, it indicates that there is blood concentration. If it is fixed at 1.010 or so, it indicates renal insufficiency. Urinary examination of patients with pre-eclampsia is mostly normal. If there are most red blood cells and casts, it should be considered as acute renal failure or serious disease in the kidney itself.
3. Fundus examination
Retinal arterioles can reflect the condition of the small arteries of the whole body. The diameter of the retinal arteriovenous tube is 2:3 than normal, and 1:2 or even 1:4 for pregnancy-induced hypertension. Severe cases with retinal edema, exudation and hemorrhage, and even retinal stripping.
4. Heart and brain monitoring
For patients with severe pre-eclampsia and eclampsia, ECG and EEG can be found in time. For patients with suspected intracranial hemorrhage or cerebral embolism, CT (or MRI) examination should be helpful for early diagnosis.
5.B type ultrasound examination
Regular B-mode ultrasound examination of fetal growth and development, FGR can be found in time, and the amount of amniotic fluid and placental maturity can be understood. The amount of amniotic fluid is reduced, such as amniotic fluid index (AFI) 5cm, fetal development is less than gestational age, uterine artery, umbilical artery blood flow high resistance, all suggest fetal hypoxia, should be actively treated.
6. Fetal heart monitoring
Fetal heart monitoring should be performed weekly after 32 weeks of pregnancy to understand the fetus. If the results of non-stress test (NST) or oxytocin challenge test (OCT) are suspicious, the test should be repeated within 3 days.
In patients with labor, if the contraction stress test (CST) is abnormal, suggesting that the fetus is hypoxic, and is intolerant to contractions during labor, it should be promptly cesarean section to terminate the pregnancy.
7. Tire maturity
Fetal lung maturation is the basic condition for the survival of the fetus after birth. Whether the fetal lung is mature has a great influence on the treatment of pre-eclampsia. Understanding the maturity of the fetal lung and terminating the pregnancy in a timely manner is beneficial to reducing maternal complications and reducing perinatal death caused by premature birth. At present, amniocentesis is used for amniocentesis for amniocentesis test (FST) and amniotic fluid lecithin/sphingomyelin ratio (L/S) determination. If the fetal lung is mature, the pregnancy can be terminated.
According to the medical history and clinical signs, the diagnosis of pre-eclampsia can be basically made, but the above-mentioned various examinations are required to determine the damage of the whole body organs, whether there are complications, to determine the clinical category and to formulate the correct treatment plan.
Diagnosis
Diagnosis and diagnosis of pregnancy-induced hypertension
Diagnostic criteria
Compared with the international standard, the classification and diagnostic criteria of pregnancy-induced hypertension syndrome in China lack comprehensive evaluation of maternal and fetus and the connection with pregnancy outcome. In order to better communicate with the international community, the internationally accepted naming and diagnostic criteria are in place. It must be done.
1. Hypertension in pregnancy refers to the first time after 20 weeks of pregnancy, blood pressure 140/90mmHg, but no proteinuria, the final diagnosis needs to be determined after 4 weeks postpartum visual blood pressure returned to normal.
2. Pre-eclampsia
(1) Mild: blood pressure 140/90mmHg, with proteinuria 300mg / 24h or 1 + test paper method.
(2) Severe: systolic blood pressure 160mmHg or diastolic blood pressure 110mmHg; proteinuria 2.0g / 24h or 2+ test paper; serum creatinine > 106mol / L or higher; platelets <100 × 109 / L; microvascular hemolysis Anemia (higher lactate dehydrogenase); elevated ALT or AST; headache or other brain or visual symptoms; persistent upper abdominal discomfort.
3. eclampsia: convulsions and coma on the basis of pre-eclampsia, clinically common for eyeball fixation, pupil dilation, head twisted to one side, closed jaw, followed by mouth and facial muscles twitching, limbs straight, hands clasped, double The arm is straight and rapidly develops into strong convulsion. When convulsions, the patient pauses and his face is bruising. The twitching amplitude is weakened in about 1 minute, the muscles of the whole body are gradually loosened, and a deep voice of the pregnant woman makes a deep inhalation and resumes breathing, such as frequent convulsions and duration. Long, there may be coma, at this time pregnant women may have suffocation due to convulsions, fractures, self-injury, and may have various complications such as pulmonary edema, acute heart failure, acute renal insufficiency, cerebral palsy, cerebrovascular accident, aspiration pneumonia , placental abruption, fetal distress, fetal death and other serious complications.
Differential diagnosis
Mainly differentiated from primary pregnancy such as hypertension and kidney disease. If the identification is really difficult, you can first treat with pre-eclampsia, and make a diagnosis after the postpartum follow-up.
