bubble_chart Overview

Puerperal infection refers to the infection of the reproductive tract by pathogens during childbirth and the puerperium period, leading to local and systemic inflammatory responses. The incidence rate is 1% to 7.2%, making it one of the four major causes of maternal mortality. Puerperal morbidity is defined as the occurrence of a temperature of 38°C or higher on at least two occasions within the first 10 days postpartum, measured orally four times daily starting 24 hours after childbirth. It is evident that puerperal infection and puerperal morbidity have different meanings. Although puerperal infection is the primary cause of puerperal morbidity, other postpartum infections and fevers outside the reproductive tract are also included, such as urinary tract infections, mastitis, and upper respiratory infections.

bubble_chart Etiology

1. Types of Pathogens Currently, it is believed that the vaginal ecosystem during pregnancy and the puerperium period is extremely complex, containing a large number of aerobic bacteria, anaerobic bacteria, fungi, as well as Chlamydia, Mycoplasma, and other Chinese Taxillus Herb, with anaerobic bacteria being predominant. Additionally, many non-pathogenic bacteria can become pathogenic under specific conditions.

(1) Aerobic Streptococci: β-hemolytic streptococci can be divided into 18 groups. Group B streptococci (GBS) produce exotoxins and histolytic enzymes, making them highly pathogenic, virulent, and capable of rapid dissemination. They are closely associated with puerperium infections and can cause severe infections. The clinical features include early fever (on average within 11 hours postpartum), body temperature exceeding 38°C, accompanied by shivering, rapid heart rate, abdominal distension and fullness, poor uterine involution, tenderness in the parametrium or adnexal area, and even bacteremia. Aerobic streptococci are the primary pathogens in exogenous infections.

(2) Escherichia coli and Related Species: Escherichia coli and related Gram-negative bacilli, such as Proteus, are major pathogens in exogenous infections and are also the most common causative agents of bacteremia and septic shock. Chinese Taxillus Herb Escherichia coli proliferates rapidly in the vagina, perineum, and around the urethral orifice during the puerperium period, leading to infection. The sensitivity of Escherichia coli to antibiotics varies significantly in different environments, necessitating drug sensitivity tests.

(3) Staphylococci: The main pathogenic species are Staphylococcus aureus and Staphylococcus epidermidis. Their pathogenicity differs significantly. Staphylococcus aureus is mostly associated with exogenous infections and can easily cause severe wound infections. Staphylococcus epidermidis is part of the vaginal flora and causes milder infections. Staphylococci can produce penicillinase, leading to resistance to penicillin's medicinal properties.

(4) Anaerobic Streptococci: Peptostreptococcus and Peptococcus are the most common, existing in the normal vagina. When there is injury in the birth canal and necrotic tissue remains, the local redox potential decreases, allowing these bacteria to multiply rapidly. Mixed infections with Escherichia coli produce an exceptionally foul odor.

(5) Anaerobic Bacteroides: A group of strictly anaerobic Gram-negative bacilli, including Bacteroides fragilis and pigment-producing Bacteroides. These bacteria have the characteristic of accelerating blood coagulation and can cause thrombophlebitis in adjacent infected areas.

Additionally, Clostridium and Neisseria gonorrhoeae can also cause puerperium infections, though these are less common. Mycoplasma and Chlamydia can also be among the pathogens causing puerperium infections.

2. Sources of Infection There are two sources of infection: one is self-infection, where pathogens naturally present in the reproductive tract or other areas of a healthy pregnant woman become pathogenic under predisposing factors; the other is exogenous infection, caused by contact with contaminated clothing, utensils, surgical instruments, or other items.

3. Predisposing Factors The body's response to invading pathogens depends on the type, quantity, virulence of the pathogens, and the body's defense capabilities. Any factor that weakens the maternal reproductive tract or overall defense mechanisms can facilitate pathogen invasion and proliferation. Examples include anemia, malnutrition, chronic diseases, sexual activity near the due date, premature rupture of membranes (amniotic fluid contains bacteriolytic enzymes, whose antibacterial effects weaken after amniotic fluid loss), intra-amniotic infection, various obstetric procedures, birth canal injury, antepartum or postpartum hemorrhage, uterine packing, foreign bodies in the birth canal, prolonged labor, retained placenta, etc. These can all serve as predisposing factors for puerperium infections.

bubble_chart Clinical Manifestations

1. Acute vulvitis, vaginitis, and cervicitis: Infection occurs due to perineal injury or surgical delivery during childbirth, manifesting as localized burning, pain, a sensation of heaviness, and purulent discharge irritating the urethral orifice, leading to dysuria and frequent urination. Infection at the wound site causes sutures to become embedded in swollen tissue, with pus discharge from needle holes. Vaginal and cervical infections present as mucosal congestion, ulcers, and increased purulent discharge, which may later lead to vaginal adhesions or even atresia. If the infection spreads deeper, it can disseminate to the parametrial tissues, causing pelvic connective tissue inflammation.

2. Garden Balsam Seed endometritis and myometritis: Pathogens invade through the placental detachment site and spread to the decidua, leading to endometritis. If the infection reaches the myometrium, it is called myometritis. Endometritis is often accompanied by myometritis. Severe cases present with chills, high fever, headache, tachycardia, leukocytosis, varying degrees of lower abdominal tenderness, and lochia that may not be excessive, making misdiagnosis likely.

3. Acute pelvic connective tissue inflammation and acute salpingitis: Pathogens spread via parametrial lymphatics or blood vessels to the parametrial tissues, causing acute inflammatory reactions and forming inflammatory masses, while also affecting the mesosalpinx and tubal walls. If the entire pelvis is involved, a "frozen pelvis" may develop. Neisseria gonorrhoeae ascends along the genital tract mucosa, reaching the fallopian tubes and pelvic cavity, forming abscesses that can cause persistent high fever.

4. Acute pelvic peritonitis and diffuse peritonitis: The inflammation progresses, spreading to the uterine serosa, forming pelvic peritonitis, which then develops into diffuse peritonitis, presenting with systemic toxic symptoms such as high fever, nausea, vomiting, abdominal distension, and obvious tenderness and rebound tenderness in the lower abdomen upon examination. Due to the relaxation of the postpartum abdominal wall, muscle rigidity is often not pronounced. Inflammatory exudates and fibrin deposits on the peritoneal surface can cause intestinal adhesions or form localized abscesses in the rectouterine pouch. If the abscess involves the intestines or bladder, diarrhea, tenesmus, and dysuria may occur. Inadequate treatment during the acute phase can lead to chronic pelvic inflammatory disease and infertility.

5. Thrombophlebitis: Bacteroides and anaerobic streptococci are common pathogens. On the basis of blood stasis or venous wall damage, bacteria secrete heparinase to break down heparin, promoting coagulation. Infection of the placental attachment site on the uterine wall by these bacteria causes pelvic thrombophlebitis. This can affect the ovarian veins, uterine veins, internal iliac veins, common iliac veins, and inferior vena cava, often unilaterally. Patients typically present 1–2 weeks postpartum, following endometritis, with chills, high fever, and recurrent episodes lasting weeks, making it difficult to distinguish from pelvic connective tissue inflammation. Lower limb thrombophlebitis often involves the femoral, popliteal, and great saphenous veins, causing intermittent fever, persistent lower limb pain, localized venous tenderness, or palpable cord-like structures, obstructing blood return and leading to lower limb edema and pale skin, commonly called "phlegmasia alba dolens." Some cases may have deep, mild lesions without obvious signs, detectable by color Doppler ultrasound. Lower limb thrombophlebitis often secondary to pelvic phlebitis or surrounding connective tissue inflammation.

6. Pyemia and septicemia: When infected thrombi detach and enter the bloodstream, pyemia can occur, leading to abscesses in the lungs, brain, or kidneys, or pulmonary embolism, which can be fatal. If large numbers of bacteria enter the bloodstream and multiply, septicemia develops, which can be life-threatening. {|105|}

bubble_chart Diagnosis

1. Take a detailed medical history, conduct comprehensive and local physical examinations, and pay attention to excluding other diseases that may cause puerperium morbidity, such as wound infections. Perform routine hematuria tests. Detecting C-reactive protein in serum acute-phase reaction substances can aid in the early diagnosis of infection.

2. Identify the pathogen. Pathogen identification is crucial for the diagnosis and treatment of puerperium infections. Methods include: ① Pathogen culture: After routine disinfection of the vagina and cervix, use a cotton swab to collect secretions from the uterine cavity through the cervical canal. Since these are often contaminated by cervical bacteria, secretions or pus from the uterine cul-de-sac should be collected for dual aerobic and anaerobic culture; ② Secretion smear examination: If aerobic culture results are negative but the smear shows a large number of bacteria, anaerobic infection should be suspected; ③ Pathogen antigen and specific antibody testing: Many commercial kits are available for rapid detection.

3. Determine the lesion location. Through comprehensive physical examinations, as well as triplex or bimanual examinations, thickened fallopian tubes or pelvic abscess masses may sometimes be palpated. Auxiliary tests such as B-mode ultrasound, color Doppler ultrasound, CT, and MRI can provide localization and qualitative diagnosis for inflammatory masses, abscesses, and venous thrombosis caused by puerperium infections.

bubble_chart Treatment Measures

1. Supportive therapy to correct anemia and electrolyte imbalances, and enhance immunity.

2. Remove residual tissue in the uterine cavity, perform abscess incision and drainage, and adopt a semi-recumbent position to eliminate pathogenic tissue.

3. The use of antibiotics should consider the issues of aerobic and anaerobic bacteria as well as drug-resistant strains. For severe infections, broad-spectrum and highly effective antibiotics are the first choice for comprehensive treatment. Short-term use of adrenal glucocorticoids may be added if necessary to improve the body's stress response.

4. For thrombophlebitis, in addition to the administration of large doses of antibiotics, heparin should be added for 48–72 hours. Specifically, 50 mg of heparin is administered intravenously with 5% glucose solution every 6–8 hours. After body temperature decreases, the frequency is reduced to twice daily for 4–7 days, accompanied by oral administration of dicoumarol and dipyridamole. Alternatively, Chinese medicinals for invigorating blood and resolving stasis or thrombolytic drugs may be used. If suppurative thrombosis continues to spread, ligation of the ovarian vein or internal iliac vein, or direct thrombectomy via incision of the affected vein may be considered.

5. Severe cases may lead to toxic shock or renal failure, requiring urgent and aggressive treatment. Every second counts in the treatment process, as delay can be fatal.

bubble_chart Prevention

Strengthen prenatal health education, maintain overall cleanliness, avoid baths and sexual intercourse in the advanced stages of pregnancy, enhance nutrition, and improve constitution. Treat complications such as acute vulvovaginitis and cervicitis, prevent premature rupture of membranes, prolonged labor, birth canal injuries, and postpartum hemorrhage. Sterilize maternity supplies, strictly adhere to aseptic techniques, and correctly assess indications for surgical delivery. Conduct close postpartum monitoring, and administer antibiotics prophylactically for those at risk of puerperal infection or puerperal morbidity.