eclampsia
Introduction
Introduction Late pregnancy or at the time of labor or new postpartum, dizziness, headache, sudden fainting, two eyes, convulsions, hand and foot convulsions, shortness of the body, wake up, relapse after waking, and even coma, called "eclampsia", Also known as "pregnancy epilepsy." The disease is caused by the development of symptoms and signs of pre-eclampsia. Eclampsia can occur during pregnancy, childbirth or 24 hours after delivery, and is called prenatal eclampsia, postpartum pain and postpartum eclampsia, respectively. It is one of the four major causes of death in obstetrics.
Cause
Cause
It may involve a variety of factors including maternal, placenta and fetus, including abnormal trophoblastic invasion, abnormal immune regulation, endothelial cell damage, genetic factors and nutritional factors. But no single factor can explain the etiology and mechanism of all preeclampsia.
Trophoblastic invasion
May be an important factor in the pathogenesis of pre-eclampsia. The patient's trophoblasts invade the spiral arterioles, and the myometrial spiral arterioles do not recast. The abnormally narrow spiral artery reduces placental perfusion and hypoxia, which eventually leads to preeclampsia.
Abnormal immune regulation
Maternal immunodeficiency or dysregulation of the maternal-derived placenta and fetal antigens is an important component of the preeclampsia etiology.
Vascular endothelial injury
Oxidative stress, anti-angiogenic and metabolic factors, as well as other inflammatory mediators, can cause vascular endothelial damage leading to pre-eclampsia.
genetic factors
Preeclampsia is a multi-factor polygenic disease with a family genetic predisposition: mothers with pre-eclampsia have a pre-eclampsia incidence of 20-40%, and women with pre-eclampsia have a pre-eclampsia prevalence rate. 11-37%, the incidence of pre-eclampsia in women with pre-eclampsia in twins was 22-47%. But so far, its genetic model is still unclear.
Nutritional factors
Lack of vitamin C increases the risk of pre-eclampsia-eclampsia.
Examine
an examination
(1) Blood test: including complete blood count, hemoglobin content, hematocrit, blood viscosity, blood coagulation function, according to the severity of the disease can be repeatedly checked.
(2) Determination of liver and kidney function: impaired hepatocyte function can lead to elevated ALT and AST. Albumin deficiency-based hypoproteinemia may occur, and the white/globulin ratio is inverted. When renal function is impaired, serum creatinine, urea nitrogen, and uric acid increase, and creatinine increases parallel to the severity of the disease.
(3) urine test: urine specific gravity 1.020 indicates urine concentration, urine protein (+) protein content 300mg/24h, urine protein (++++) urine protein content 5g/24h, severe pre-eclampsia patients Urine protein should be checked once a day.
(4) Fundus examination: The degree of retinal arteriolar spasm reflects the degree of small vascular vasospasm, which can reflect the severity of the disease. Retinal arteriolar spasm, retinal edema, flocculation or bleeding may occur, and retinal detachment may occur in severe cases. Patients may have blurred vision or blindness.
(5) Others: ECG, echocardiography, placental function, fetal maturity check, cerebral blood flow chart examination, etc., depending on the condition.
Special examination of fetal placenta
1. Fetal electronic monitoring to understand the presence of intrauterine hypoxia, such as NST (non-stress test), OCT (oxytocin load test). Note that NST is non-responsive and the baseline is straight, bradycardia, and late deceleration are predictive of fetal hypoxia.
2. B-mode ultrasound scan to understand the fetal biparietal diameter and abdominal circumference, calculate the fetal weight, and estimate the possibility of intrauterine growth retardation. Understand the maturity of the placenta and the amount of amniotic fluid in order to terminate the pregnancy at the right time.
3. Determination of 24-hour urine or serum estriol and HPL (human placental lactogen) estimated placental fetus.
Diagnosis
Differential diagnosis
Need to be differentiated from other tonic-sexual convulsions, such as rickets, hypertensive encephalopathy, cerebrovascular accidents (including bleeding, thrombosis, abnormal vascular rupture, etc.), epilepsy, intracranial tumors, metabolic diseases (hypoglycemia, hypokemia Calcium, white matter lesions, cerebral vasculitis, etc.
(1) Seizures Patients with epilepsy have a history of seizures in the past. There are often auras before the onset, and the attack time is short. After the loss of the mind, they fall, and the whole body licks for 1 to 2 minutes. It can also bite the tongue and incontinence. However, most of them are awake immediately after convulsions, and even if there is a short coma or confusion, they can return to normal in a short time. No high blood pressure, edema and proteinuria. There is no change in the fundus at the fundus. The patient pays attention to the relevant medical history after convulsion and emergency treatment, checks the urine protein in time, and measures the blood pressure for rapid diagnosis.
(B) Hypertensive encephalopathy and cerebral hemorrhage patients should have a history of chronic hypertension before pregnancy, often without edema and proteinuria. Sudden coma, loss of consciousness, soft hemiplegia, positive pathological reflex, and asymmetry of pupil. When the cerebral hemorrhage has special changes in the cerebrospinal fluid, it can be diagnosed.
(C) encephalitis encephalitis has a seasonal onset, Japanese encephalitis is seen in summer and autumn, epidemic encephalitis is more common in spring. Although the onset is urgent, but there are fever, headache, neck discomfort, rapid high fever, nausea, vomiting, irritability, coma, can also occur convulsions, convulsions. Patients with eclampsia had no fever, no neck stiffness and meningeal irritation, and no pathological reflex. Patients with encephalitis have no hypertension, edema, proteinuria, and typical inflammatory changes in cerebrospinal fluid examination.
