When inflammation occurs in the female internal genitalia, its surrounding connective tissue, and the pelvic peritoneum, it is called pelvic inflammatory disease (pelvic inflammatory disease). Pelvic inflammatory disease is a common disease in gynecology. The inflammation can be confined to one site or several sites at the same time. It can be divided into acute and chronic according to its pathogenesis and clinical manifestations. Acute inflammation may cause serious consequences such as diffuse peritonitis, sepsis and even infectious shock; chronic inflammation is recurrent due to prolonged treatment. The patient must pay attention to the prevention and treatment of pelvic inflammatory disease because it affects the physical and mental health of women and causes pain to patients.
Due to the anatomical and physiological characteristics of the female genital tract, there is a relatively well-developed natural defense function that enhances the defense against infection, thus certain pathogens can be present in the vagina of healthy women, but do not necessarily cause inflammation.
[Natural defenses of the female genitalia]
I. The labia majora on both sides naturally close together to conceal the vaginal opening and urethral opening.
Second, due to the action of pelvic floor muscles, the mouth of the obstruction is closed and the front and back walls of the vagina are close together, which can prevent external pollution. In PMS, this defense function is poorer due to vaginal laxity.
3. Under the influence of estrogen secreted by ovaries, the vaginal epithelium thickens and increases its resistance to the invasion of pathogens. Meanwhile, the epithelial cells are rich in glycogen, which is decomposed into lactic acid by Bacillus vaginalis to maintain the normal acidic environment of the vagina (pH 4.2-5), so that pathogens adapted to reproduction in an alkaline environment are inhibited, which is called the role of vaginal self-cleaning.
Fourth, the mucus secreted by the endocervical lining forms mucus plugs that block the cervical canal, and the endocervical opening is usually tightly closed, which helps to prevent the invasion of pathogens. It is reported that the lower 1/3 of the cervical mucus plug can detect bacteria, while the upper 2/3 cannot detect bacteria.
V. Periodic exfoliation of the endometrium in women of childbearing age is also favorable to eliminate official infection.
Sixth, the oscillation of the cilia of the mucous membrane epithelium of the fallopian tubes in the direction of the uterine cavity and the peristalsis of the fallopian tubes are favorable to stop the invasion of pathogens.
[The main pathogenic seedlings and their susceptibility to antibiotics] The main pathogens causing pelvic genital inflammation are Staphylococcus, Streptococcus, Escherichia coli, and anaerobic bacteria.
I. Streptococcus Gram-positive streptococci are many types, there are three categories A, B and C. Category B hemolytic streptococci
Streptococcus haemolyticus is highly pathogenic, can produce hemolysin and a variety of enzymes, so that the infection is easy to spread and cause sepsis, the pus is relatively thin, light red, the amount is more, but generally not complicated by metastatic abscesses. Before the introduction of antibiotics, about 75% of maternal deaths due to septic deficiency of puerperal infections were caused by group A hemolytic group B streptococcal infections. This bacteria is sensitive to penicillin, the application of penicillin, maternal mortality is basically controlled.
Second, staphylococcus Gram-positive, is the pathogenic bacteria of postpartum, post-surgical genital inflammation and wound infection, often along the vagina, uterus, fallopian tube mucosa upstream infection. There are three types of Staphylococcus aureus, white and lemon, all of which are pathogenic, with Staphylococcus aureus being the most pathogenic. The pus is yellow, thick, not smelly, often accompanied by metastatic abscesses, and is easily resistant to commonly used antibiotics, and it is better to use drugs according to drug sensitivity tests. Penicillin-resistant Staphylococcus aureus is sensitive to vanguardycin I, vancomycin, clindamycin, chloramphenicol.
Third, E. coli Gram-negative, normal parasitic bacteria of the intestine, generally not pathogenic, but when the body is extremely weak or due to trauma and other invasion of extraintestinal tissues or organs can cause serious infections, and even endotoxin shock, often mixed with other pathogenic bacteria. The pus of E. coli does not smell, when there is a mixed infection, produce silk thick pus and fecal odor. Can be applied kanamycin, gentamicin, pioneeromycin I, carbenicillin, etc., but easy to produce drug-resistant strains, it is best to make drug sensitivity test, select sensitive drugs. Gram-positive bacteria mixed with serious infection can also be combined with penicillin G, ampicillin, tetracycline, etc.
Fourth, anaerobic bacteria Due to the progress of anaerobic culture technology, since the 70s, more and more attention to the importance of anaerobic bacteria in pelvic infections, mainly peptic streptococcus (peptostreptococcus), peptococcus (peptococcus) and fragile bacilli (bacteroidisfragilis). These bacteria are mainly from the colon, rectum, vagina and oral mucosa. General sampling and culture techniques are not easy to obtain positive results. In the past, some pelvic abscesses had no colony growth in the pus culture, which was probably an anaerobic infection, but positive results were not obtained due to the limitations of anaerobic culture technology at that time. According to the literature, 70% to 80% of pelvic abscesses can be cultured with anaerobic bacteria. Anaerobic bacteria in pelvic infections can be infected alone or mixed with aerobic bacteria, therefore, attention should be paid to the selection of antibiotics to take into account the need to control anaerobic bacteria. Streptococcus digestiveis is sensitive to penicillin, cephalosporins (cepha 10thin) in vanguardomycins (cephalosporins), chloramphenicol, and metronidazole.
Fifth, sexually transmitted pathogens such as gonorrhea, Chlamydia trachomatis, other may have mycoplasma, herpes virus.
Infection route
I. Spread through the lymphatic system Bacteria invade the pelvic connective tissue and other parts of the internal genitalia through the lymphatic vessels of the vulva, vagina, cervix and uterine body trauma, which is the main way for the spread of puerperal infection, post-abortion infection and infection related to certain intrauterine devices.
The pathogen first invades other systems of human body and then infects genitalia through blood circulation.
It is the main route of tuberculosis infection.
The pathogen invades the vulva and vagina, and then spreads along the mucosal surface through the cervix, endometrium and fallopian tubes to the ovaries and abdominal cavity. Staphylococcus and gonococcus spread along this route.
Direct spread The infection of other organs in the abdominal cavity spreads directly to the internal genitalia, such as appendicitis can cause tubal inflammation.
Acute pelvic inflammatory disease
[Etiology
The main etiological factors causing acute pelvic inflammatory disease are as follows.
The main causes of acute pelvic inflammatory disease are as follows.
Secondly, postoperative infections of surgical operations in the official cavity, such as intrauterine device placement, curettage, tubal aeration, tubal hysterosalpingography, official cavity microscopy, etc., can cause acute attacks and spread due to surgical sterilization or improper selection of preoperative indications, and chronic inflammation of the reproductive tract caused by surgical interference. –
The endometrial exfoliation surface of the menstrual period, with dilated blood sinus and clot, is a good breeding environment for bacteria, such as lack of hygiene, the use of unclean menstrual pads, menstrual intercourse, etc. can make pathogens invade and cause inflammation.
V. Acute attack of chronic pelvic inflammatory disease
[Pathology
I. Acute endometritis and acute myometritis Most often seen after abortion, childbirth.
Acute tubal inflammation, tubal abscess, tubo-ovarian abscess Acute tubal inflammation is mainly caused by septic bacteria, which spread through the lymph of the cervix to the parametrial coarse tissue, first invading the plasma membrane layer, and then involving the peri-tubal inflammation, and then the muscular layer, while the endometrial layer of the fallopian tube may not be involved very lightly. The lumen may be narrowed by pressure due to thickening of the muscular wall, but it can still be kept open. In mild cases, the fallopian tubes are only mildly congested, swollen and slightly thickened; in severe cases, the fallopian tubes are significantly thickened and thinned with fibrinous purulent exudate, resulting in surrounding adhesions.
If the inflammation extends upward through the endometrium, it first causes endometritis of the fallopian tubes with swelling of the endometrium and interstitial edema. In severe cases, the epithelium may degenerate or fall off in pieces, causing adhesions in the mucosa of the fallopian tubes, resulting in occlusion of the tubal lumen and the umbilical end, and if pus accumulates in the tubal lumen, tubal pus is formed.
The ovaries are rarely inflamed alone, and the white membranes are a good defense barrier. The ovaries are mostly adherent to the umbilical ends of the inflamed fallopian tubes and perivitellitis occurs, which is called tubo-ovarianitis, also known as adnexitis. Inflammation can invade the ovarian parenchyma through the ovarian ovulatory breach to form an ovarian abscess, and if the abscess wall is adherent to the tubal pus collection and penetrates, a tubo-ovarian abscess is formed. Tubo-ovarian abscesses can occur after the initial onset of acute tubo-ovarianitis, but are often formed on the basis of repeated episodes of chronic adnexitis. The abscesses are mostly located in the posterior aspect of the uterus or in the adhesions between the uterus, the posterior lobe of the broad ligament and the intestinal canal, and may break into the rectum or vagina, or cause diffuse peritonitis if they break into the peritoneal cavity.
In acute inflammation of the internal genitalia, or trauma to the vagina or cervix, pathogens can enter the pelvic connective tissue via the lymphatic vessels and cause congestion, edema, and neutrophil infiltration of the connective tissue. The most common is parametrial connective tissue inflammation, which starts with local tissue thickening, soft texture and unclear borders, and later becomes fan-shaped infiltration to both pelvic walls, forming retroperitoneal abscesses if the tissue is purulent, which can spontaneously break into the rectum or vagina.
Acute pelvic peritonitis When serious infection occurs in the pelvic organs, it often spreads to the pelvic peritoneum, the inflamed peritoneum is congested, edematous and has a small amount of plasma fibrous exudate, forming adhesions between the pelvic organs. When there is a large amount of purulent exudate accumulating in the interstices of the adhesions, small scattered abscesses can be formed, and accumulation in the rectal recess of the uterus to form pelvic abscesses is more common. The abscess is in front of the uterus, behind the rectum, and at the top of the intestinal canal and large omentum, and the abscess can break into the rectum and cause sudden relief of symptoms; it can also break into the abdominal cavity and cause diffuse peritonitis.
V. Sepsis extremely septicemia Sepsis often occurs when the pathogen is virulent and numerous and the patient’s resistance is low. Most often seen in severe puerperal infections, infected abortion, in recent years, there are also reports of sepsis caused by the placement of intrauterine devices, tubal ligation surgery damage to organs, if not timely control, often soon appear infected shock or even death. After the occurrence of infection, if multiple inflammatory lesions or abscesses are found in other parts of the body, the presence of sepsis should be considered, but still needs to be confirmed by the culture.
Clinical manifestations
It may vary depending on the severity and extent of inflammation. The onset of pain in the lower abdomen, accompanied by fever, if the disease is serious, there may be high fever, chills, headache, loss of appetite. If peritonitis is present, digestive system symptoms such as nausea, vomiting, abdominal distention, diarrhea, etc. may occur. If there is abscess formation, there may be lower abdominal mass and local pressure irritation symptoms; if the mass is located in the front, there may be bladder irritation symptoms, such as difficulty in urination, frequent urination, and painful urination if it causes cystitis; if the mass is located in the back, there may be rectal irritation symptoms, and if it is outside the peritoneum, it may cause diarrhea and a feeling of urgency and difficulty in defecation.
The patient is acutely ill with high temperature, rapid heart rate, abdominal distension, muscle tension in the lower abdomen, pressure and rebound pain, and diminished or absent bowel sounds. Pelvic examination: the obstruction tract may be congested with a large amount of purulent discharge, and there is significant tenderness in the fornix. The uterine cervix is congested, edematous, and painful to lift is obvious. The body of the uterus is slightly large, with tenderness and limited mobility. There is significant pressure pain in both guillotines of the uterus, and sometimes a mass can be retrieved. In case of parametrial connective tissue infection, a lamellar thickening on one or both sides of the lower abdomen can be felt. If there is abscess formation and the position is low, a mass with fluctuating sensation can be found in the posterior or lateral fornix.
Diagnosis] The diagnosis can be made based on the medical history, symptoms and signs. In addition. Some necessary laboratory tests must be done, such as blood, urine routine, blood and cervical canal secretion culture (including anaerobic bacteria culture) and drug sensitivity test, although non-pus direct culture, also has a certain reference value for clinical. If necessary, a posterior ^ fornix or lateral ^ fornix with a mass and a fluctuating sensation.
Differential diagnosis】 Acute pelvic inflammatory disease should be differentiated from acute appendicitis, ectopic pregnancy, ovarian Z-tumor torsion or rupture and other acute abdominal conditions.
Prevention
A good menstruation, pregnancy and puerperium hygiene propaganda
Second, strict mastery of obstetrics, gynecological surgery indications to make good preoperative preparations, pay attention to the aseptic operation, including abortion, placement of intrauterine device, diagnostic scraping and other procedures. The first thing you need to do is to take care of yourself after surgery to prevent infection.
Three, complete cure of acute pelvic inflammatory disease, to prevent the transformation into chronic.
Treatment
A general supportive therapy bed rest, L semi-recumbent position to facilitate the accumulation of pus in the rectal sink of the uterus and confine the inflammation. Give adequate nutrition and fluid intake, correct the disorder of turtle solution and acid-base balance, transfuse small amount of blood if necessary, use physical cooling when high fever, avoid unnecessary gynecological examination to avoid the spread of inflammation. If there is abdominal distension, gastrointestinal decompression can be given.
The antibiotic treatment is reasonable according to the drug sensitivity test, before the laboratory results, if the disease is not too serious can be used penicillin hydrogen streptomycin; if the disease is serious, you need to use a broad-spectrum antibiotics, the combination of drugs with good efficacy, the combination must be reasonable, less drug types, less toxic, after the results of bacterial culture, according to the situation to be replaced antibiotics. The route of administration is intravenous drip with fast results. The application of antibiotics must reach the full amount, and must pay attention to toxic reactions. After the disappearance of symptoms continue to give two weeks to consolidate the effect, and strive to completely cure, in order to avoid the formation of chronic pelvic inflammatory disease.