Premature rupture of membranes

　　1. Etiology

　　The etiology of premature rupture of membranes is not very clear. Initially, it was explained from the traditional mechanical point of view, and then it was found that the structural changes of the amniotic membrane itself and the infection factors are very important for premature rupture of membranes. In recent years, further exploration has been made on the role of enzymes and cytokines in the process of premature rupture of membranes.

　　1. There are many causes of poor amniotic membrane development, including factors related to the amniotic membrane itself, such as vitamin C deficiency, copper deficiency, and smoking during the early pregnancy of pregnant women, which are related to poor amniotic membrane development.

　　2. Premature rupture of membranes leading to uterine cavity infection is the traditional causal relationship between premature rupture of membranes and infection. In recent years, it has been widely recognized that infection and premature rupture of membranes are interrelated, and infection is the most important cause of premature rupture of membranes.

　　3. Incompetence of the cervical os Under non-pregnant conditions, the cervical os can be dilated without resistance to 8.0 cm, which can be diagnosed as cervical incompetence. The main manifestations of cervical incompetence are relaxation of the os and deficiency of the isthmus.

　　4. Abnormal uterine cavity pressure is common in malpresentation of the head and pelvis and abnormal fetal position; excessive uterine cavity pressure is common in twin pregnancy, polyhydramnios, severe cough, and difficulty in defecation.

　　5. Trauma and mechanical stimulation are mainly divided into two types: iatrogenic and non-iatrogenic. Non-iatrogenic common cases include sexual intercourse in the late stage of pregnancy; iatrogenic cases include multiple amniocentesis, multiple vaginal examinations, and membrane stripping induction of labor, etc.

　　Second, pathogenesis

　　1. Maldevelopment of the membranes The normal membranes have epithelial-fibrosis maturation or metaplasia, and finally evolve into membranes with certain elasticity and tensile strength. Maldevelopment of the membranes mainly refers to the abnormal development of the amniotic layer and chorionic layer of the membranes, and the reduction of type III gelatin is of great significance for premature rupture of membranes.

　　2. Incomplete cervical function Currently, there are many studies on the causes of premature rupture of membranes due to infection, the mechanism is complex, and can be summarized as follows: (1) Bacteria and bacterial inflammation destroy the structure of the membranes: bacteria themselves and the inflammatory reaction process induced by bacteria can produce a large number of enzymes, especially proteolytic enzymes and metalloproteinases, which can destroy the gelatin of the membranes, and finally lead to a decrease in the tensile strength and elasticity of the amnion; (2) Inducing uterine contraction, increasing the pressure in the amniotic cavity: the mechanism of inducing uterine contraction is mainly divided into the products of bacteria themselves and the maternal inflammatory reaction process induced by bacteria. The main products of bacteria themselves refer to phospholipase A2 produced by the破碎 or cracking of the cell wall, which can induce uterine contraction. The mechanism of uterine contraction caused by the maternal inflammatory reaction process is relatively complex and mainly involves: immune cells involved in the immune response in the inflammatory process produce interleukin-like cytokines, interleukins can induce uterine contraction; inflammatory mediators involved in the inflammatory process, such as prostaglandins such as PGE2 and PGF2 produced by the arachidonic acid system, can induce strong uterine contraction.

　　3. As the membranes are stretched with the progression of pregnancy, the uterus increases in size, the intrauterine pressure increases, the cervix cannot withstand the gradually increasing normal pressure and dilate, and the membranes also stretch and protrude towards the external os of the cervix and the vagina to form the anterior amniotic sac. The diameter of the anterior amniotic sac gradually increases, and the tension and elasticity of the membranes are stretched more and more, finally exceeding the elastic strength of the membranes and rupturing.

　　4. Abnormal intrauterine pressure includes uneven intrauterine pressure and excessive intrauterine pressure.

　　1. Uteroplacental thrombosis

　　The formation of placental posterior hematoma, especially in concealed abruption, where the blood does not flow out of the uterus, due to increased local pressure, the blood can渗入uterine muscular layer, causing muscle fiber separation and rupture. The blood can also infiltrate and affect the uterine serous membrane, causing purple ecchymosis on the uterine surface, especially prominent at the placental implantation site, known as uteroplacental thrombosis. This phenomenon was discovered by Courelaire in the early 20th century, hence also known as Courelaire uterus (Courelaireuterus). The blood can also infiltrate the serous layer of the fallopian tube or the broad ligament, even the substance of the ovary. Sometimes, there may be free blood in the peritoneal cavity, possibly due to blood flowing into the abdominal cavity through the fallopian tube. The incidence of uteroplacental thrombosis is difficult to accurately calculate, as it is only visible during cesarean section, and thus its actual incidence should be higher than that reported. Uteroplacental thrombosis rarely affects uterine contraction, and therefore, it is rare to cause severe postpartum hemorrhage, and thus it is not an indication for hysterectomy.

　　2. Fetal-maternal hemorrhage

　　In traumatic placental abruption, hemorrhage from fetus to mother can occur. In general, in non-traumatic placental abruption, bleeding from fetus to mother is only 20%, and the amount is also less than 10ml; but in severe trauma, Stettler reported in 1992 that 8 cases of fetal maternal hemorrhage reached 80-100ml.

　　3. Disseminated Intravascular Coagulation (DIC)

　　Abnormal coagulation function and placental abruption in early pregnancy are the most common causes of coagulation dysfunction during pregnancy. Severe placental abruption, especially cases with intrauterine fetal death, are likely to develop disseminated intravascular coagulation (DIC) and coagulation dysfunction. The placenta and decidua are rich in tissue thromboplastin. During placental abruption, procoagulant substances enter the maternal blood circulation through damaged blood vessels, activate the coagulation system, and lead to DIC. Microthrombi can form in the capillaries of organs such as the lungs and kidneys, causing organ damage. A large number of coagulation factors such as platelets and fibrinogen are consumed. Therefore, the longer the time of placental abruption, the more procoagulant substances enter the maternal blood circulation, and DIC continues to develop, activating the fibrinolysis system, producing a large amount of fibrin degradation products (FDP). Due to the excessive consumption of coagulation factors, in addition to the anticoagulant effect of FDP, coagulation dysfunction is exacerbated, which is manifested clinically as bleeding under the skin, submucosal bleeding, or at injection sites. Uterine bleeding may not clot or only soft clot formation, and even hematuria, hemoptysis, or vomiting of blood may occur. In 1987, the First Chinese Hemostasis Society proposed that the laboratory examination of DIC (amended version) with 3 or more of the following abnormalities can be diagnosed: (1) platelet count of 20mg/L; (3) prothrombin time (PT) shortened or prolonged by more than 3 seconds, or dynamic change, or activated partial thromboplastin time (APTT) shortened or prolonged by more than 10 seconds; (4) shortened euglobulin lysis time, or decreased plasminogen, indicating the occurrence of DIC. DIC occurs in 30% of cases sufficient to cause fetal death, and DIC without fetal distress is uncommon.

　　4. Acute renal failure

　　Severe early placental detachment is often caused by severe preeclampsia. During severe preeclampsia, the small arteries in the body spasm, and the small arteries in the kidneys also spasm, causing tissue hypoxia. The glomerular vascular endothelial cells in the kidneys swell and increase in volume, causing blood flow obstruction; renal ischemia. In addition, excessive blood loss during early placental detachment, prolonged shock time, and DIC and other factors cause a sudden decrease in renal blood flow. In severe cases, it can cause ischemic necrosis of the renal cortex or renal tubules. Or due to the large amount of fibrin deposition in the afferent arterioles, blocking the blood supply to the kidneys, causing acute renal ischemic necrosis and acute renal failure. The clinical manifestations are: (1) oliguria or anuria, oliguria (7mmol/L), hyperkalemia is one of the causes of death during oliguria; (3) azotemia, due to oliguria, the kidneys cannot excrete urea nitrogen and creatinine, causing an increase in blood urea nitrogen and creatinine levels; (4) metabolic acidosis, due to the accumulation of acidic metabolic products in the body and the consumption of alkali reserves, the blood pH value decreases, leading to the inhibition of intracellular enzyme activity and the increase of intermediate metabolic products, resulting in metabolic acidosis.

　　5. Amniotic fluid embolism

　　During early placental detachment, the uterine blood sinus at the detachment surface is open. If the bleeding behind the placenta penetrates the amnion, the blood enters the amniotic fluid, the amniotic fluid can also reflux into the open uterine blood vessels and enter the maternal circulation, forming clots in the lungs causing pulmonary embolism, thus leading to pulmonary hypertension, respiratory and circulatory failure, DIC, multiple organ damage, and a series of amniotic fluid embolism symptoms. Most of these occur before the fetus is delivered. If not treated in time, it may endanger the patient's life.

　　6. Postpartum hemorrhage

　　Postpartum uterine atony and coagulation dysfunction can lead to postpartum hemorrhage, which is manifested clinically as a large amount of vaginal bleeding after the placenta is delivered. The blood often does not clot. During examination, it is found that the fundus is unclear, the uterine contour is not obvious, the patient's face is pale, the expression is indifferent, cold sweat is produced, the heart rate increases, and blood pressure decreases, showing symptoms of hemorrhagic shock.

　　7. Fetal intrauterine death

　　When the placental detachment area reaches 1/3, the fetus may experience intrauterine distress and even death; when the detachment area reaches 1/2, the majority of fetuses will die. Even if the atypical symptoms of early placental detachment are mild, the harm to perinatal infants is great. Therefore, even if the clinical symptoms are not severe, and there is a suspicion of early placental detachment, close monitoring of the fetus's intrauterine condition and active treatment should be provided.

　　1. Symptoms

　　Sudden vaginal discharge due to various reasons, the amount of discharge can be more or less, and the discharge is usually persistent with varying durations. The initial amount is large and then gradually decreases, and a few are intermittent discharges. Vaginal discharge is usually related to changes in the position of the pregnant woman and whether she is active.

　　2. Signs

　　Lying on the back, fluid may be seen to flow out of the vaginal orifice, or there may be no fluid at all. If there is no fluid, when performing digital rectal examination, the posterior fornix of the vagina is elevated, the fetal head is pushed up, the fundus is pressed, or the position of the pregnant woman is changed, and fluid may flow out of the vaginal orifice. Pay attention that after these auxiliary operations, fluid may still not be seen to flow out. The fluid that flows out is usually thin and may contain meconium or fetal fat. Emergency inpatients may bring their内衣, sanitary napkins, or toilet paper to the hospital, and should be examined carefully.

　　Amnion premature rupture is a common obstetric complication that can lead to pre-and postpartum infections in mothers and infants, affect fetal maturity, and increase the incidence and mortality rate of perinatal infants. Preventing and actively treating amnion premature rupture can effectively improve the prognosis of mothers and infants. Amnion premature rupture is often diagnosed by the alkaline pH of vaginal fluid test, and when the diagnosis is unclear, it can be confirmed by auxiliary examinations such as vaginal fluid smear. Since amnion premature rupture occurs at different gestational weeks, the principles of treatment are different. Generally, when the gestational age is 28 to 35 weeks and the conditions for preserving the pregnancy are allowed, active measures should be taken to preserve the pregnancy and promote fetal lung maturity. For gestational ages above 35 weeks, it can be allowed to deliver spontaneously.

　　1. Vaginal secretion pH detection

　　The pH of amniotic fluid is greater than 7.0, and the pH of vaginal secretions is 4.5 to 5.5. The acidity and alkalinity of the vaginal fluid are measured with litmus paper. If the pH value is greater than 7.0, it indicates amnion premature rupture. A pH of 7.0 can cause a false positive result and must be distinguished from amniotic fluid; (2) Most physicians or midwives measure the pH value of the liquid at the vaginal orifice, especially the posterior joint, with a paper. If there is little or no amniotic fluid during the examination, it can cause a false negative result; (3) According to the acidity and alkalinity of vaginal secretions and amniotic fluid, mix 1ml of vaginal secretion with 10ml of amniotic fluid. Theoretically, the pH value of the mixed liquid

　　2. Vaginal fluid smear

　　The difference between amniotic fluid and vaginal secretions lies in the fact that inorganic salts are the main component in amniotic fluid, and it also contains some fetal components such as fetal cells shed, while vaginal secretions contain a large amount of protein. The liquid from the posterior fornix or cervical os is smeared, and the following checks after smearing are helpful for diagnosis. Amnion premature rupture can be diagnosed by observing the fern-like crystals or primrose-like crystals after slowly drying the smear. If the smear is heated for 30 seconds over an ethanol lamp and the crystals are white or grayish inorganic salts, it indicates amnion premature rupture; vaginal secretions are usually brown or black carbonized protein. Sudan III staining of the smear can reveal orange-red fetal sebaceous gland cells in amniotic fluid.

　　3. Vaginal speculum examination

　　Routine disinfection before examination; diagnosis can be made when amniotic fluid is present in the posterior fornix and exceeds 3ml; amniotic fluid can also be diagnosed by the amniotic fluid flowing out from the cervical os due to uterine contractions or fundal pressure.

　　4. Ultrasound examination

　　B-ultrasound diagnosis of PROM mainly assists in the diagnosis by observing the changes in amniotic fluid volume and distribution through B-ultrasound, such as a significant decrease in amniotic fluid volume compared to recent or recent days, which can help diagnose PROM; if the distribution of amniotic fluid is limited, such as a large difference in the diameter of the first and second largest amniotic fluid pools, it can assist in the diagnosis of PROM.

　　5. Examination of other components of amniotic fluid

　　Amniotic fluid contains a large amount of fetal cells, cytokines secreted by the amnion or decidua, and various methods of detecting cytokines in vaginal secretions are very helpful for the diagnosis of PROM. Common cytokines include alpha-fetoprotein, fetal-type fibronectin, and insulin-like growth factor binding protein-1. The determination of these factors usually requires enzyme-linked immunosorbent assay, which is relatively complicated and needs to be simplified for wider application.

　　To prevent PROM and the birth of premature infants, pregnant women should consume more foods high in copper content, such as nuts, seafood, animal liver, wheat, dried beans, tuber vegetables, and oysters.

　　In the late pregnancy period, the husband is required to cooperate, and sexual activity is prohibited. During pregnancy, attention should be paid to a reasonable diet, comprehensive nutrition, and appropriate supplementation of foods rich in vitamin C and trace elements such as copper and zinc. For those with severe cephalopelvic disproportion, floating fetal head, and abnormal lie, it is appropriate to be admitted to the hospital in advance. Once PROM occurs, the patient should lie flat immediately to prevent umbilical cord prolapse, and emergency hospitalization should be sought.

　　1. Treatment

　　Premature rupture of membranes before term can be treated with expectant management or termination of pregnancy according to the situation. For term PROM, the method of termination of pregnancy should be chosen according to the situation, including induction of labor or cesarean section. In any case, prophylactic application of antibiotics should be considered if the membranes are ruptured for more than 12 hours.

　　1. Determining the treatment principles for PROM: Once PROM is diagnosed, a treatment plan needs to be formulated based on the characteristics of the patient, and many factors determine the treatment plan, such as gestational age, whether there is a concurrent infection, whether there is fetal distress, whether there is oligohydramnios, and neonatal level of care, among which the most important are gestational age and whether there is amniotic cavity infection.

　　(1) The important issues of premature rupture of membranes (PROM) include preterm birth and related problems of premature infants: the survival rate of premature infants is mainly determined by the maturity of vital organs, especially the lungs, and the maturity of the lungs increases with the increase of gestational weeks. The following relationship between the maturity of the lungs and gestational age is the main basis for formulating treatment plans for PROM based on gestational age: by 37 weeks of gestation, the fetal lung function is fully developed; from 34 to 36 weeks of gestation, the fetal lung function is basically fully developed, except for gestational diabetes or women with gestational diabetes mellitus; for those with gestational age from 29 to 33 weeks, extending the gestational age and using drugs to promote fetal lung maturity can improve lung maturity and significantly reduce the incidence of neonatal hyaline membrane disease; for those with gestational age from 24 to 28 weeks, using drugs to promote fetal lung maturity and appropriately extending the gestational age can reduce the neonatal mortality rate, but whether it can reduce neonatal hyaline membrane disease is not yet certain; there is little research before 23 weeks of gestation, and the survival rate of neonates is almost zero.

　　(2) Infection: Refers to amniotic cavity infection, and the combination of premature rupture of membranes and amniotic cavity infection is an indication for termination of pregnancy. According to the causal relationship or time sequence between amniotic cavity infection and premature rupture of membranes, infection can be divided into primary infection and secondary infection. Primary amniotic cavity infection already exists before the rupture of the membrane and is the main cause of premature rupture of membranes. Secondary infection appears after a certain period of time after the rupture of the membrane and can be the exacerbation of an existing infection that was not diagnosed at the time of membrane rupture and was observed, or it can be an ascending infection of bacteria in the cervix or vagina after the rupture of the membrane. Whether or not secondary infection appears is an important indicator that needs to be observed during the expectant therapy period for patients with premature rupture of membranes. Secondary infection usually appears within 12 hours after the rupture of the membrane and increases with the extension of the time of membrane rupture. Amniotic cavity infection is divided into subclinical and clinical types, and the specific diagnostic criteria are see the section on amniotic cavity infection syndrome.

　　(3) Basic treatment principles: ① Premature rupture of membranes complicated with amniotic cavity infection is an indication for termination of pregnancy, without considering the size of gestational age; ② Gestational age over 37 weeks or 36 weeks, observe for 12 hours, and add antibiotics for those who have not gone into labor; 24 hours later, if still not in labor, induction of labor can be performed; ③ Gestational age over 34 weeks, the treatment plan is the same as that for 36 weeks, unless it is clear that the fetal lung development is not mature; ④ For those between 29 and 33 weeks of gestation, try to extend the gestational age as much as possible by inhibiting uterine contractions, preventing infection with antibiotics, and administering drugs to promote fetal lung maturation, so that the gestational age reaches 34 weeks or 48 hours after the administration of drugs to promote fetal lung maturation, which is what is called expectant therapy; ⑤ Before 28 weeks of gestation, the decision to terminate pregnancy is based on the level of neonatal medicine, and it can be chosen for those who are not yet 24 weeks pregnant.

　　2. Expectant therapy is a general term for a comprehensive treatment method adopted to continue the growth and development of the fetus in utero for patients before 34 weeks of pregnancy, especially those between 28 and 34 weeks of pregnancy, with the aim of improving the survival rate of the fetus after delivery. Expectant therapy includes various treatment measures such as general treatment, inhibiting uterine contractions, promoting fetal lung maturation, and preventing infection, and is suitable for patients with premature rupture of membranes without infection, without fetal distress, and without oligohydramnios.

　　(1) General treatment measures: Include absolute bed rest, lying flat or on the side, raising the foot of the bed, maintaining cleanliness of the perineum, and avoiding vaginal examination and rectal examination, etc.

　　(2) Fetal monitoring: Regular fetal electronic monitoring, and necessary biophysical scoring to judge the condition of the fetus in utero; regular ultrasound examination to record amniotic fluid volume and the growth and development of the fetus.

　　(3) Promoting fetal lung maturation: The main methods for promoting fetal lung maturation include adrenocortical hormones, thyroid-stimulating hormone, and beta-agonists such as salbutamol and ritodrine (hydroxybenzhydrazine). The most commonly used are two types of adrenocortical hormone drugs, dexamethasone and betamethasone, with similar usage and dosage. The main application scheme of dexamethasone outside China: ① Dexamethasone 6mg intramuscular or intravenous injection, twice a day, for a total of 2 days; ② Dexamethasone 10mg intramuscular or intravenous injection once, for a total of 3 days; ③ Dexamethasone 10mg amniotic cavity injection once.

　　Precautions for the use of adrenocorticotropic hormones to promote fetal lung maturation: ① Suitable for gestational weeks

　　(4) Inhibition of uterine contractions: The inhibition of uterine contractions is an important treatment measure of the expectant therapy, which is divided into preventive and therapeutic inhibition of uterine contraction treatment. The former is a routine inhibition of uterine contraction treatment regardless of whether uterine contractions occur, and the latter is only used when uterine contractions occur. There are many methods to inhibit uterine contractions when the amniotic membrane is prematurely ruptured, mainly including magnesium sulfate, beta-agonists, nitric oxide (NO) donors, calcium channel blockers, and non-steroidal anti-inflammatory analgesics, etc.

　　①Magnesium sulfate: The effective blood concentration of magnesium sulfate needed to inhibit uterine contractions needs to reach 2-4mmol/L, and the dosage and administration speed require high requirements. The common method is: the initial dose is an intravenous bolus of 4g, and the maintenance dose is 1.5-2.0g/h intravenously. The above regimen is a common regimen in China, and the regimen reported in foreign literature is usually an initial intravenous bolus of 6g; maintenance dose of 2.0-3.0g/h, intravenously. Due to the close proximity of the effective dose and the dose of poisoning and even death, it is necessary to monitor closely when using it and prepare for detoxification. Clinical work has found that patients with renal insufficiency are prone to magnesium sulfate poisoning, even if the urine volume of the patient exceeds 600ml/d. The reason may be that the glomerular filtration rate of the patient is low, and the concentrating ability of the renal tubules is poor, so the total amount of magnesium sulfate in the actual excreted urine is low, leading to the accumulation of magnesium sulfate in the body, and even magnesium poisoning. On the contrary, for patients with normal renal function, such as patients after appendectomy for acute appendicitis, the use of magnesium sulfate to suppress uterine contractions, the renal function of such patients is usually normal, with about 3000ml of fluid replacement per day, urine volume of about 2500ml, due to the strong ability of the kidneys to excrete magnesium, it is difficult for the blood magnesium concentration of such patients to reach the ideal concentration. In recent years, foreign research has found that the excessive use of magnesium sulfate to suppress uterine contractions is easy to cause perinatal pulmonary edema, which is usually benign pulmonary edema. If attention is paid to improving the colloid osmotic pressure of patients and preventing infection, it can usually regress within 72 hours.

　　②Beta-agonists: The mechanism of action of these drugs is to excite the beta receptors, especially beta 2 receptors, of the uterine smooth muscle cells, and inhibit the contraction of the uterine smooth muscle. Sulbutamol is commonly used in China, while sulbutamol (metaproterenol) and ritodrine (bendrofluorohydrochloride) are commonly used abroad, and only ritodrine (bendrofluorohydrochloride) has been certified by the U.S. Food and Drug Administration. The usage of sulbutamol: The first method is 2.4mg every 12 hours, which can be used for several months; the second method is the initial dose of 4.8mg, relief or disappearance of uterine contractions within 15 minutes, supplemented with 4.8mg every 6 hours for several days, then gradually reduced to 2.4mg every 8 hours, and if the initial dose is ineffective, 2.4mg or 4.8mg can be added. The usage of ritodrine (bendrofluorohydrochloride): Firstly, 100mg is added to a 5% glucose solution for intravenous infusion, with an initial rate of 5 drops/min, increasing by 5 drops every 10 minutes until the uterine contractions disappear, with a maximum rate of 35 drops/min, and the heart rate of pregnant women should be

　　③ Nonsteroidal Anti-inflammatory Analgesics: The mechanism of action of this class of drugs is to inhibit the production of prostaglandins by acting on the arachidonic acid system, thereby inhibiting uterine contractions. Commonly used drugs include indomethacin, aspirin, and sulindac (Sulindac), with specific usage as follows: indomethacin 25mg, 3 times a day; aspirin 0.5 to 1.0mg, 3 times a day; sulindac (Sulindac) 200mg, 2 times a day.

　　④ Nitric Oxide (NO) Donor Drug - Nitroglycerin: The research on the use of nitroglycerin to inhibit uterine contractions has a history of only a few decades, and it can meet the needs of inhibiting uterine contractions during prelabor, labor, and postpartum. Prelabor use is mainly for the inhibition of uterine contractions in cases of preterm labor and cervical insufficiency, with the dosage form being topical - nitroglycerin patch, administered through the skin, with a permeation dose of 0.4 to 0.8mg/h, usually effective within 24 to 48 hours, one patch is ineffective, and an additional patch can be used every hour. If nitroglycerin patches are not available, they can be administered intravenously at a rate of 0.4 to 0.8mg/h. During labor and postpartum, it is mainly used for situations where uterine contractions are too strong, leading to fetal distress, and for surgical procedures in the following situations, such as inversion of the uterus, placental retention, internal or external version, and dysynchronous uterine contractions. Dosage: 50 to 200μg of nitroglycerin, administered intravenously within 1 minute, can take effect, and can be repeated every 3 to 5 minutes. Attention should be paid to the headache symptoms and hypotensive reactions in pregnant women. The same effect can be achieved by placing the above dose of nitroglycerin under the tongue.

　　⑤ Calcium Channel Blockers: Nifedipine is commonly used, with a dose of 10mg per time, which can be taken multiple times a day.

　　(5) Prevention and Treatment of Infection: Infection prevention and treatment should include both prevention and treatment. Prevention of infection refers to the use of antibiotics from the moment the amniotic membrane ruptures without infection, with the aim of preventing or delaying the occurrence of amniotic cavity infection. Treatment of infection mainly targets amniotic cavity infection, placental inflammation, and infections of the cervix and vagina that have already occurred but have not been diagnosed before the amniotic membrane rupture. Women who have not gone into labor within 12 hours after the amniotic membrane rupture need to be administered antibiotics, with penicillin, cephalosporins, and erythromycin being the first choices, with attention to a broad spectrum of antibacterial activity. Because modern theories suggest that infection is an important cause of premature rupture of membranes, most patients with premature rupture of membranes may have subclinical infection, so it is recommended to first administer antibiotics intravenously for 2 to 3 days, and then switch to oral antibiotics to maintain treatment.

　　3. Termination of Pregnancy: The method of termination of pregnancy due to premature rupture of membranes is mainly vaginal delivery, and cesarean section can be performed if there are obstetric indications.

　　Second, Prognosis

　　Impact on Mother and Child:

　　1. Infection: Infection and premature rupture of membranes are interrelated. Infections of the amniotic cavity, cervical canal, and placental membranes can lead to premature rupture of membranes, and premature rupture of membranes can also cause infection. Infections caused by premature rupture of membranes refer to the upward spread of pathogenic bacteria that寄生 in the cervical canal and vagina after the membrane rupture, leading to fetal, pregnancy tissues (umbilical cord, membrane, and placenta), uterus, and even pelvic and abdominal cavity infections. Fetal infections are common, including lung infections, sepsis, and enterocolitis. Maternal infections mainly refer to amniotic fluid infection syndrome before delivery and puerperal infection after delivery. The risk of maternal and fetal infections caused by premature rupture of membranes increases with the extension of the latent period. The infections caused by premature rupture of membranes may be new infections, or the exacerbation of existing infections, or the combination of new infections.

　　2. Umbilical Cord Abnormalities: The main umbilical cord abnormalities caused by premature rupture of membranes are umbilical cord prolapse and umbilical cord compression. Umbilical cord prolapse is common in cases of premature rupture of membranes combined with malpresentation, abnormal position, and excessive amniotic fluid. Umbilical cord compression is mainly caused by the continuous outflow of amniotic fluid, leading to less amniotic fluid. Under various conditions such as fetal rest, fetal movement, and uterine contraction, umbilical cord compression can occur, and in severe cases, it can cause fetal distress.

　　3. Difficult Labor: Premature rupture of membranes can lead to difficult labor due to the disappearance of the anterior amniotic sac and the loss of the effect of the anterior amniotic sac on dilating the cervix during labor. At the same time, the disappearance of the posterior amniotic fluid combined with infection can also cause difficult labor.

　　4. Fetal Malformation: Fetal malformation is mainly seen when the gestational age is small at the time of membrane rupture, conservative treatment takes a long time, and there is less amniotic fluid. Common malformations include limb, facial organ, and respiratory system malformations.

　　5. Premature Birth and Premature Babies: Premature rupture of membranes accounts for 40% of all premature births. The mortality rate of premature babies with premature rupture of membranes is doubled, and the main cause of death is neonatal respiratory distress syndrome.