Puerperal infection refers to local or systemic infections caused by pathogenic invasion of the genital tract during childbirth or the puerperium, with an incidence rate of approximately 6%. Puerperal fever is defined as a fever of 38°C or higher occurring at least twice within 10 days after delivery (excluding the first 24 hours), with measurements taken at intervals of at least 4 hours. Puerperal fever is often caused by puerperal infections but can also result from infections unrelated to the genital tract, such as acute mastitis, upper respiratory tract infections, urinary tract infections, or thrombophlebitis.
Etiology
Predisposing Factors
Under normal conditions, the female vagina possesses a natural defense mechanism against external pathogens. The response to invading pathogens depends on their type, quantity, virulence, and the host's immune response. Vaginal self-cleaning mechanisms and the presence of antimicrobial substances in the amniotic fluid provide additional protection. Pregnancy and normal delivery typically do not increase the risk of infection. Infection occurs when the balance between the host's immunity and the pathogenic load or virulence is disrupted. Factors such as poor maternal health, malnutrition, anemia during pregnancy, inadequate hygiene during pregnancy, premature rupture of membranes, amniotic cavity infection, chronic illnesses, obstetric surgeries, prolonged labor, excessive pre- or postpartum hemorrhage, and multiple cervical examinations can act as predisposing factors for puerperal infections.
Pathogenic Microorganisms
The normal vaginal microbiota comprises various microorganisms, including aerobic bacteria, anaerobic bacteria, fungi, chlamydia, and mycoplasma. These microorganisms are classified into pathogenic and non-pathogenic types. Certain non-pathogenic microorganisms can become opportunistic pathogens under specific conditions, while even pathogenic microorganisms require sufficient quantity or a weakened immune system to cause disease.
Aerobic Bacteria
Streptococci
Group B beta-hemolytic streptococci are highly virulent, producing pyrogenic exotoxins and tissue-destroying enzymes, which cause infections to spread rapidly and result in severe complications. Aerobic streptococci may reside in the vagina or be introduced into the reproductive tract through contamination from healthcare workers or other maternal sites. Clinical features include early onset of fever, chills, body temperature exceeding 38°C, tachycardia, abdominal distension, incomplete uterine involution, tenderness in the uterine or adnexal regions, and potentially secondary sepsis.
Bacilli
Common bacilli include Escherichia coli, Klebsiella species, and Proteus species. These bacteria are often found around the vagina, perineum, and urethral opening. They produce endotoxins and are common causes of bacteremia and septic shock. Their antibiotic sensitivities vary widely across different settings.
Staphylococci
The two main pathogens are Staphylococcus aureus and coagulase-negative Staphylococcus epidermidis. S. aureus is often associated with external contamination and can lead to severe wound infections. Due to its ability to produce penicillinase, it frequently exhibits resistance to penicillin. S. epidermidis, a normal vaginal flora component, typically causes milder infections.
Anaerobic Bacteria
Gram-Positive Cocci
Peptostreptococcus and Peptoniphilus species are part of the normal vaginal flora. When birth canal injuries, retained placenta, or necrotic tissue hypoxia occur, these bacteria multiply rapidly. Mixed infections with E. coli may result in abnormal malodorous discharges.
Bacilli
Common anaerobic bacilli include Bacteroides fragilis. These bacteria frequently cause mixed infections involving aerobic and anaerobic cocci, leading to localized abscesses with purulent discharge and a foul odor. Infections may also result in suppurative thrombophlebitis, with infected thrombi disseminating via the bloodstream to other organs, forming abscesses.
Clostridium Species
Clostridium perfringens is a notable anaerobe that produces exotoxins capable of lysing proteins, generating gas, and inducing hemolysis. Infections range from mild endometritis, peritonitis, or sepsis to severe complications like hemolysis, jaundice, hemoglobinuria, acute renal failure, circulatory collapse, gas gangrene, and even death.
Mycoplasma
Ureaplasma urealyticum and Mycoplasma hominis are common vaginal commensals that can lead to reproductive tract infections. These infections are often asymptomatic, with mild clinical manifestations.
Other pathogens, including Chlamydia trachomatis and Neisseria gonorrhoeae, can also contribute to puerperal infections.
Routes of Infection
Exogenous Infection
Exogenous infections occur when external pathogens enter the birth canal. These pathogens may be introduced through inadequate disinfection by healthcare workers or contaminated clothing, instruments, surgical tools, and maternal sexual activity in the late stages of pregnancy.
Endogenous Infection
Endogenous infections arise from microorganisms that reside within the reproductive tract of healthy pregnant women. Although these normal flora are typically non-pathogenic, they can become pathogenic when factors such as reduced immunity, an increased number of microorganisms, or heightened virulence are present. Endogenous infections are considered more significant than exogenous ones because they can not only lead to puerperal infections but also cross the placenta, fetal membranes, or amniotic fluid to infect the fetus. This may result in complications such as miscarriage, preterm birth, fetal growth restriction, premature rupture of membranes, or stillbirth.
Pathology and Clinical Manifestations
Fever, pain, and abnormal lochia are the three main symptoms of puerperal infection. The most common cause of early puerperal fever is dehydration, but the sudden onset of high fever following 2–3 days of low-grade fever strongly suggests the possibility of infection. Clinical manifestations vary depending on the location, severity, and extent of the infection. Based on the site of infection, puerperal infections are classified into localized infections of the perineum, vagina, cervix, abdominal wound, uterine incision; acute endometritis; acute pelvic cellulitis or peritonitis; thrombophlebitis; and septicemia.
Acute Vulvitis, Vaginitis, and Cervicitis
Perineal injuries during delivery are prone to infection, commonly caused by Staphylococcus aureus and Escherichia coli.
Infections of perineal tears or episiotomy wounds present with perineal pain and difficulty sitting. Local symptoms include redness, swelling, induration, wound dehiscence with tenderness, and purulent discharge. Severe cases may show low-grade fever.
Vaginal laceration or contusion infections cause mucosal hyperemia, edema, ulceration, and an increase in purulent discharge. Deeper infections may result in para-vaginal cellulitis.
Cervical laceration infections can extend deeply into the parametrium, leading to pelvic cellulitis.
Uterine Infections
This category includes acute endometritis and myometritis. Pathogens invade through the placental detachment site, spreading to the decidua (endometritis) or the myometrium (myometritis), and the two conditions often coexist:
- In endometritis, the endometrium becomes congested and necrotic, with foul-smelling, purulent vaginal discharge.
- Myometritis causes abdominal pain, increased purulent lochia, marked uterine tenderness, and subinvolution of the uterus, often accompanied by high fever, chills, headaches, leukocytosis, and systemic signs of infection.
Acute Pelvic Cellulitis and Acute Salpingitis
Pathogens can reach the parametrium via lymphatic or hematogenous routes, triggering an acute inflammatory response that forms inflammatory masses, which often affect the fallopian tubes as well, leading to acute salpingitis. Clinical features include lower abdominal pain with a sense of rectal pressure, accompanied by chills, high fever, tachycardia, and headache. Physical findings may show significant lower abdominal tenderness, rebound tenderness, and muscle guarding. Thickened or tender pelvic connective tissue and/or palpable inflammatory masses may be detected on one or both sides of the parametrium. Severe cases present as a "frozen pelvis" involving widespread pelvic inflammation. Infections caused by Neisseria gonorrhoeae may ascend along the mucosa of the reproductive tract to the fallopian tubes and pelvis, resulting in abscess formation, persistent high fever, leukocytosis, and a visible shift in neutrophil nuclear segmentation (left shift).
Acute Pelvic Peritonitis and Diffuse Peritonitis
As the infection progresses, it can spread to the uterine serosa, causing pelvic peritonitis, and subsequently evolve into diffuse peritonitis. Systemic symptoms become pronounced, with high fever, nausea, vomiting, abdominal distension, and prominent lower abdominal tenderness with rebound tenderness on examination. Large volumes of peritoneal exudate are produced, and fibrin deposition may lead to intestinal adhesions. Abscesses may form in the rectouterine pouch (Douglas pouch); if the abscess involves the intestines or bladder, symptoms such as diarrhea, tenesmus, or difficulty urinating may occur. Inadequate treatment during the acute phase can lead to pelvic inflammatory disease (PID) sequelae, increasing the risk of infertility.
Thrombophlebitis
Pelvic thrombophlebitis typically involves the uterine, ovarian, internal iliac, or common iliac veins, as well as the vaginal veins, with anaerobic bacteria being the common pathogens. The condition is usually unilateral and most frequently occurs 1–2 weeks postpartum. Symptoms include chills and high fever that can persist for weeks or recur intermittently. Local examination may not reliably distinguish between thrombophlebitis and pelvic cellulitis.
Thrombophlebitis in the lower extremities is often secondary to pelvic vein thrombophlebitis and commonly affects the femoral, popliteal, or great saphenous veins. Features include intermittent fever, persistent leg pain, localized venous tenderness, or palpable cord-like structures. Impaired venous return can cause leg edema and pallor, referred to as "milk leg." Mild cases may lack obvious findings, but color Doppler ultrasound can assist in the diagnosis.
Septicemia
Detached infected thrombi entering the bloodstream can cause bacteremia, which may progress to septicemia and metastatic abscesses (e.g., in the lungs or kidneys). Large quantities of pathogens entering the bloodstream can proliferate and release toxins, leading to severe septicemia, septic shock, and/or multi-organ failure. Clinical manifestations include persistent high fever, chills, marked systemic toxicity, multi-organ dysfunction, and potentially life-threatening complications.
Diagnosis
Medical History
A detailed patient history and a thorough review of the childbirth process are essential. For patients presenting with puerperal fever, puerperal infection should be the primary consideration while excluding other causes of fever during the puerperium.
Physical and Local Examination
Comprehensive evaluations of the abdomen, pelvis, and perineal wounds are necessary to identify the infection site and assess severity.
Imaging and Laboratory Investigations
Ultrasonography, CT, or MRI can aid in localizing and characterizing inflammatory masses or abscesses. Elevated serum C-reactive protein (CRP) levels can support the early diagnosis of infection.
Identification of Pathogens
Pathogens can be identified through bacterial cultures and sensitivity testing of uterine secretions, abscess aspirates, or cul-de-sac punctures. Blood cultures may also be required. Rapid antigen or specific antibody tests can aid in the quick identification of pathogens.
Differential Diagnosis
The main conditions requiring differentiation from puerperal infection include upper respiratory tract infection, acute mastitis, and urinary tract infection.
Management
Once puerperal infection is diagnosed, broad-spectrum, adequate, and effective antimicrobial therapy is typically employed. The treatment regimen is adjusted according to the identified pathogen. For cases involving abscess formation or retained infected tissue within the uterus, addressing the source of infection is essential.
Supportive Therapy
Nutritional supplementation and adequate vitamin intake can enhance systemic resistance. Correcting water and electrolyte imbalances is crucial. For severe illness or cases of anemia, repeated small-volume transfusions of fresh blood or plasma can help improve resistance. A semi-recumbent position may facilitate lochia drainage and help confine the inflammation to the pelvic region.
Management of Retained Placental or Membrane Tissue
In tandem with effective anti-infective treatment, uterine cavity remnants should be removed. In cases of acute infection with a high fever, infection control should be prioritized. This may involve clamping infected intrauterine tissue, followed by comprehensive uterine curettage once the infection is fully controlled and the patient's temperature has stabilized. This approach helps prevent the spread of infection, endometrial damage, and uterine perforation during curettage.
Use of Antimicrobial Agents
When the pathogen has not been identified, broad-spectrum and high-efficacy antimicrobial agents are selected based on clinical presentation and experience. Subsequent adjustments to drug type and dosage are determined by bacterial culture and susceptibility testing, ensuring maintenance of effective plasma drug concentrations. For patients with severe systemic toxicity, short-term administration of corticosteroids may be employed to enhance stress response and improve tolerance to infection.
Anticoagulant Therapy
In cases of thrombophlebitis, anticoagulants can be used alongside large doses of antibiotics.
Heparin sodium, at a dose of 150 IU/(kg·day), is typically diluted in 500 mL of 5% glucose injection and administered via intravenous infusion every 6 hours. Once the fever subsides, the dosage frequency is reduced to twice daily, continuing for 4–7 days.
Urokinase (400,000 units) may be diluted in 0.9% sodium chloride or 5% glucose injection (500 mL) and infused intravenously over a 10-day period.
Coagulation function should be closely monitored throughout the course of therapy. Oral anticoagulants such as dicoumarol or aspirin may also be used concomitantly.
Surgical Treatment
Infected perineal or abdominal surgical wounds may require timely incision and drainage.
Pelvic abscesses can be drained via an abdominal route or through posterior fornix aspiration or incision.
For severe uterine infections unresponsive to aggressive treatment, where inflammation continues to spread or complications such as uncontrollable bleeding, septicemia, or septic shock develop, hysterectomy may be performed to eliminate the source of infection and save the patient’s life.
Prevention
Improved nutrition and enhanced physical fitness contribute to reducing infection risks. Promoting hygiene awareness during pregnancy and maintaining perineal cleanliness are vital for prevention. Timely treatment of vulvovaginitis and cervicitis can minimize complications. Strict adherence to aseptic techniques is encouraged, with efforts to minimize unnecessary vaginal examinations and surgical interventions. Properly determining surgical indications is essential. For cesarean sections, prophylactic antimicrobial agents are recommended prior to the skin incision to reduce the risk of infection.