Hubbry Logo
Postpartum infectionsPostpartum infectionsMain
Open search
Postpartum infections
Community hub
Postpartum infections
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Postpartum infections
Postpartum infections
Postpartum infections
View on Wikipedia
from Wikipedia

Postpartum infections
Other namesPuerperal fever, childbed fever, maternal sepsis, maternal infection, puerperal infections
Streptococcus pyogenes (red-stained spheres) is responsible for many cases of severe puerperal fever.
SpecialtyObstetrics
SymptomsFever, lower abdominal pain, bad-smelling vaginal discharge[1]
CausesTypically multiple types of bacteria[1]
Risk factorsCaesarean section, premature rupture of membranes, prolonged labour, malnutrition, diabetes[1][2]
TreatmentAntibiotics[1]
Frequency11.8 million[3]
Deaths17,900[4]

Postpartum infections, also known as childbed fever and puerperal fever, are any bacterial infections of the female reproductive tract following childbirth or miscarriage.[1] Signs and symptoms usually include a fever greater than 38.0 °C (100.4 °F), chills, lower abdominal pain, and possibly odorous vaginal discharge.[1] It usually occurs after the first 24 hours and within the first ten days following delivery.[5]

The most common infection is that of the uterus and surrounding tissues known as puerperal sepsis, postpartum metritis, or postpartum endometritis.[1][6] Risk factors include caesarean section (C-section), the presence of certain bacteria such as group B streptococcus in the vagina, premature rupture of membranes, multiple vaginal exams, manual removal of the placenta, and prolonged labour among others.[1][2] Most infections involve a number of types of bacteria.[1] Diagnosis is rarely helped by culturing of the vagina or blood.[1] In those who do not improve, medical imaging may be required.[1] Other causes of fever following delivery include breast engorgement, urinary tract infections, infections of an abdominal incision or an episiotomy, and atelectasis.[1][2]

Due to the risks following caesarean section, it is recommended that all women receive a preventive dose of antibiotics such as ampicillin around the time of surgery.[1] Treatment of established infections is with antibiotics, with most people improving in two to three days.[1] In those with mild disease, oral antibiotics may be used; otherwise, intravenous antibiotics are recommended.[1] Common antibiotics include a combination of ampicillin and gentamicin following vaginal delivery or clindamycin and gentamicin in those who have had a C-section.[1] In those who are not improving with appropriate treatment, other complications such as an abscess should be considered.[1]

In 2015, about 11.8 million maternal infections occurred.[3] In the developed world about 1% to 2% develop uterine infections following vaginal delivery.[1] This increases to 5% to 13% among those who have more difficult deliveries and 50% with C-sections before the use of preventive antibiotics.[1] In 2015, these infections resulted in 17,900 deaths down from 34,000 deaths in 1990.[4][7] They are the cause of about 10% of deaths around the time of pregnancy.[2] The first known descriptions of the condition date back to at least the 5th century BCE in the writings of Hippocrates.[8] These infections were a very common cause of death around the time of childbirth starting in at least the 18th century until the 1930s when antibiotics were introduced.[9] In 1847, Hungarian physician Ignaz Semmelweiss decreased death from the disease in the First Obstetrical Clinic of Vienna from nearly 20% to 2% through the use of handwashing with calcium hypochlorite.[10][11]

Signs and symptoms

[edit]

Signs and symptoms usually include a fever greater than 38.0 °C (100.4 °F), chills, low abdominal pain, and possibly bad-smelling vaginal discharge.[1] It usually occurs after the first 24 hours and within the first ten days following delivery.[5]

Causes

[edit]

After childbirth, the female genital tract has a large bare surface, which is prone to infection. Infection may be limited to the cavity and wall of the uterus, or it may spread beyond to cause sepsis or other illnesses, especially when resistance has been lowered by long labour or severe bleeding. Puerperal infection is most common on the raw surface of the interior of the uterus after separation of the placenta (afterbirth), but pathogenic organisms may also affect lacerations of any part of the genital tract. By whatever portal, they can invade the bloodstream and lymph system to cause sepsis, cellulitis (inflammation of connective tissue), and pelvic or generalized peritonitis (inflammation of the abdominal lining). The severity of the illness depends on the virulence of the infecting organism, the resistance of the invaded tissues, and the general health of the woman. Organisms commonly producing this infection are Streptococcus pyogenes; staphylococci (inhabitants of the skin and of pimples, carbuncles, and many other pustular eruptions); the anaerobic streptococci, which flourish in devitalized tissues such as may be present after long and injurious labour and unskilled instrumental delivery; Escherichia coli[12] and Clostridium perfringens (inhabitants of the lower bowel); and Clostridium tetani.[13]

Risk factors

[edit]

Causes (listed in order of decreasing frequency) include: endometritis, urinary tract infection, pneumonia/atelectasis, wound infection, and septic pelvic thrombophlebitis. Sepsis risk factors for each condition are listed in order of the postpartum day (PPD) on which the condition generally occurs.[citation needed]

  • PPD 0: atelectasis risk factors include general anesthesia, cigarette smoking, and obstructive lung disease.
  • PPD 1–2: urinary tract infection risk factors include multiple catheterization during labor, multiple vaginal examinations during labor, and untreated bacteriuria.
  • PPD 2–3: endometritis ( the most common cause ) risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examinations during labor.
  • PPD 4–5: wound infection risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examinations during labor.
  • PPD 5–6: septic pelvic thrombophlebitis risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and diffuse difficult vaginal childbirth.
  • PPD 7–21: mastitis risk factors include nipple trauma from breastfeeding.

Diagnosis

[edit]

Puerperal fever is diagnosed with:

  • A temperature rise above 38 °C (100.4 °F) maintained over 24 hours or recurring during the period from the end of the first to the end of the 10th day after childbirth or abortion. (ICD-10)
  • Oral temperature of 38 °C (100.4 °F) or more on any two of the first ten days postpartum. (USJCMW)[14]

Puerperal fever (from the Latin puer, male child (boy)), is no longer favored as a diagnostic category. Instead, contemporary terminology specifies:[15]

  1. the specific target of infection: endometritis (inflammation of the inner lining of the uterus), metrophlebitis (inflammation of the veins of the uterus), and peritonitis (inflammation of the membrane lining of the abdomen).
  2. the severity of the infection: less serious infection (contained multiplication of microbes) or possibly life-threatening sepsis (uncontrolled and uncontained multiplication of microbes throughout the bloodstream).

Endometritis is a polymicrobial infection. It frequently includes organisms such as Ureaplasma, Streptococcus, Mycoplasma, and Bacteroides, and may also include organisms such as Gardnerella, Chlamydia, Lactobacillus, Escherichia, and Staphylococcus.[16]

Differential diagnosis

[edit]

Several other conditions can cause fevers following delivery, including: urinary tract infections, breast engorgement, atelectasis, and surgical incisions, among others.[1]

Management

[edit]

Antibiotics have been used to prevent and treat these infections; however, the misuse of antibiotics is a serious problem for global health.[2] It is recommended that guidelines be followed that outline when it is appropriate to give antibiotics and which antibiotics are most effective.[2]

Atelectasis: mild to moderate fever, no changes or mild rales on chest auscultation.[17]

Management: pulmonary exercises, ambulation (deep breathing and walking).

Urinary tract infection: high fever, malaise, costovertebral tenderness, positive urine culture.[18]

Management: antibiotics as per culture sensitivity (cephalosporin).

Endometritis: moderate fever, exquisite uterine tenderness, minimal abdominal findings.[19]

Management: multiple agent IV antibiotics to cover polymicrobial organisms: clindamycin, gentamicin, and addition of ampicillin if no response, no cultures are necessary.

Wound infection: persistent spiking fever despite antibiotics, wound erythema or fluctuance, wound drainage.[20]

Management: antibiotics for cellulitis, open and drain wound, saline-soaked packing twice a day, secondary closure.

Septic pelvic thrombophlebitis: persistent wide fever swings despite antibiotics, usually normal abdominal or pelvic exams.[21]

Management: IV heparin for 7–10 days at rates sufficient to prolong the PTT to double the baseline values.

Mastitis: unilateral, localized erythema, edema, tenderness.[22]

Management: antibiotics for cellulitis, open and drain the abscess if present.

Epidemiology

[edit]

The number of cases of puerperal sepsis per year shows wide variations among published literature—this may be related to different definitions, recordings etc.[14] Globally, bacterial infections are the cause of 10% of maternal deaths—this is more common in low income countries but is also a direct cause of maternal deaths in high-income countries.[2][23]

In the United States, puerperal infections are believed to occur in between 1% and 8% of all births. About three die from puerperal sepsis for every 100,000 births. The single most important risk factor is caesarean section.[24] The number of maternal deaths in the United States is about 13 in 100,000. They make up about 11% of pregnancy-related deaths in the United States.[1]

In the United Kingdom from 1985 to 2005, the number of direct deaths associated with genital tract sepsis per 100,000 pregnancies was 0.40–0.85.[25] In 2003–2005, genital tract sepsis accounted for 14% of direct causes of maternal death.[26]

Puerperal infections in the 18th and 19th centuries affected, on average, 6 to 9 women in every 1,000 births, killing two to three of them with peritonitis or sepsis. It was the single most common cause of maternal mortality, accounting for about half of all deaths related to childbirth, and was second only to tuberculosis in killing women of childbearing age. A rough estimate is that about 250,000–500,000 died from puerperal fever in the 18th and 19th centuries in England and Wales alone.[27]

History

[edit]

Although it had been recognized from as early as the time of the Hippocratic corpus that women in childbed were prone to fevers, the distinct name "puerperal fever" appears in historical records only from the early 18th century.[28]

The death rate for women giving birth decreased in the 20th century in developed countries. The decline may be partly attributed to improved environmental conditions, better obstetrical care, and the use of antibiotics. Another reason appears to be a lessening of the virulence or invasiveness of Streptococcus pyogenes. That organism is also the cause of scarlet fever, which declined over the same period but has seen a rise in the last decade worldwide, especially in Asia, with smaller outbreaks in the US and Canada. The UK reported 12,906 cases between September 2015 and April 2016, which is the largest outbreak since 1969.[29]

"The Doctor's Plague"

[edit]
In his 1861 book, Ignaz Semmelweis presented evidence to demonstrate that the advent of pathological anatomy in Vienna in 1823 (vertical line) was correlated to the incidence of fatal childbed fever there. Onset of chlorine handwash in 1847 marked by vertical line. Rates for the Dublin maternity hospital, which had no pathological anatomy, are shown for comparison (view rates). His efforts were futile, however.

From the 17th century through to the mid-to-late 19th century, the majority of childbed fever cases were caused by the doctors themselves. With no knowledge of germs, doctors did not believe hand washing was needed.[30]

Hospitals for childbirth became common in the 17th century in many European cities. These "lying-in" hospitals were established at a time when there was no knowledge of antisepsis or epidemiology, and women were subjected to crowding, frequent vaginal examinations, and the use of contaminated instruments, dressings, and bedding. It was common for a doctor to deliver one baby after another, without washing his hands or changing clothes between patients.[citation needed]

The first recorded epidemic of puerperal fever occurred at the Hôtel-Dieu de Paris in 1646. Hospitals throughout Europe and America consistently reported death rates between 20% and 25% of all women giving birth, punctuated by intermittent epidemics with up to 100% fatalities of women giving birth in childbirth wards.[31]

In the early 19th century, Ignaz Semmelweis noticed that women giving birth at home had a much lower incidence of childbed fever than those giving birth in a maternity ward. His investigation discovered that washing hands before a delivery with a calcium hypochlorite solution reduced childbed fever fatalities by 90%.[32] His findings were not well received by the medical profession, because they conflicted both with existing medical concepts, and with the image doctors had of themselves.[33] The scorn and ridicule of doctors was so extreme that Semmelweis moved from Vienna and, following a breakdown, eventually died in a mental asylum.[34]

Semmelweis was not the only doctor ignored after sounding a warning about the problem. In his Treatise on the Epidemic of Puerperal Fever (1795), ex-naval surgeon and Aberdonian obstetrician Alexander Gordon (1752–1799) warned that the disease was transmitted from one case to another by midwives and doctors. Gordon wrote, "It is a disagreeable declaration for me to mention, that I myself was the means of carrying the infection to a great number of women."[35][36]

In 1842, Thomas Watson (1792–1882), a professor of medicine at King's College Hospital, London, wrote: "Wherever puerperal fever is rife, or when a practitioner has attended any one instance of it, he should use most diligent ablution." Watson recommended handwashing with chlorine solution and changes of clothing for obstetric attendants "to prevent the practitioner becoming a vehicle of contagion and death between one patient and another."[37][38]

Hygienic measures

[edit]

In 1843, Oliver Wendell Holmes Sr. published The Contagiousness of Puerperal Fever and controversially concluded that puerperal fever was frequently carried from patient to patient by physicians and nurses. He suggested that clean clothing and avoidance of autopsies by those aiding birth would prevent the spread of the disease.[39][40] Holmes quoted Dr. James Blundell as stating, "... in my own family, I had rather that those I esteemed the most should be delivered unaided, in a stable, by the mangerside, than that they should receive the best help, in the fairest apartment, but exposed to the vapors of this pitiless disease."[41]

Holmes' conclusions were ridiculed by many contemporaries, including Charles Delucena Meigs, a well-known obstetrician, who stated, "Doctors are gentlemen, and gentlemen's hands are clean."[42] Richard Gordon states that Holmes' exhortations "outraged obstetricians, particularly in Philadelphia".[43] In those days, "surgeons operated in blood-stiffened frock coats—the stiffer the coat, the prouder the busy surgeon", "pus was as inseparable from surgery as blood", and "cleanliness was next to prudishness". He quotes Sir Frederick Treves on that era: "There was no object in being clean. Indeed, cleanliness was out of place. It was considered to be finicking and affected. An executioner might as well manicure his nails before chopping off a head."[44][45]

In 1844, Ignaz Semmelweis was appointed assistant lecturer in the First Obstetric Division of the Vienna General Hospital (Allgemeines Krankenhaus), where medical students received their training. Working without knowledge of Holmes' essay, Semmelweis noticed his ward's 16% mortality rate from fever was substantially higher than the 2% mortality rate in the Second Division, where midwifery students were trained. Semmelweis also noticed that puerperal fever was rare in women who gave birth before arriving at the hospital. Semmelweis noted that doctors in the First Division performed autopsies each morning on women who had died the previous day, but the midwives were not required or allowed to perform such autopsies. He made the connection between autopsies and puerperal fever after a colleague, Jakob Kolletschka, died of sepsis after a student accidentally cut his hand while performing an autopsy.[citation needed]

Semmelweis began experimenting with various cleansing agents and, from May 1847, ordered all doctors and students working in the First Division to wash their hands in chlorinated lime solution before starting ward work and later ordered this before each vaginal examination. The mortality rate from puerperal fever in the division fell from 18% in May 1847 to less than 3% in June–November of the same year.[46] While his results were extraordinary, he was treated with skepticism and ridicule (see Response to Semmelweis).

He did the same work in St. Rochus hospital in Pest, Hungary, and published his findings in 1860, but his discovery was again ignored.[47]

In 1935, Leonard Colebrook showed Prontosil was effective against haemolytic streptococcus and hence a cure for puerperal fever.[48][49]

Notable cases

[edit]
See also: List of women who died in childbirth

Elite status was no protection against postpartum infections, as the deaths of several English queens attest. Elizabeth of York, queen consort of Henry VII, died of puerperal fever one week after giving birth to a daughter, who also died. Her son Henry VIII had two wives who died this way, Jane Seymour[citation needed] and Catherine Parr.[50]

Suzanne Barnard, mother of philosopher Jean-Jacques Rousseau, contracted childbed fever after giving birth to him and died nine days later. Her infant son was also in perilous health following the birth; the adult Rousseau later wrote that "I came into the world with so few signs of life that little hope was entertained of preserving me". He was nursed back to health by an aunt.[51] French natural philosopher Émilie du Châtelet died in 1749. Mary Wollstonecraft, author of Vindication of the Rights of Woman, died ten days after giving birth to her second daughter, who grew up to write Frankenstein. Other notables include African-American poet Phillis Wheatley (1784), British housekeeping authority Isabella Beeton (1865),[52][53] and American author Jean Webster in 1916 died of puerperal fever.[citation needed]

In Charles Dickens' novel A Christmas Carol, it is implied that both Scrooge's mother and younger sister perished from this condition, explaining the character's animosity towards his nephew Fred and also his poor relationship with his own father[citation needed].

See also

[edit]

References

[edit]

Further reading

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Postpartum infections

View on Grokipedia
from Grokipedia
Postpartum infections, also known as puerperal infections or puerperal fever, are bacterial infections of the female reproductive tract following childbirth or miscarriage that occur within six weeks (42 days) postpartum, posing a major risk for maternal morbidity, sepsis, and death if untreated. These infections most commonly manifest as endometritis (infection of the uterine lining), surgical site infections after cesarean delivery, urinary tract infections, or mastitis (breast infection), arising primarily from endogenous bacteria such as group B streptococci, ''Escherichia coli'', or anaerobes that ascend from the vagina or are introduced iatrogenically during labor and delivery. These bacterial infections are generally localized to the mother and are not contagious to the infant through casual contact or breastfeeding. Mastitis, in particular, is not transmissible to the baby, and breastfeeding is safe and encouraged during treatment. However, if the fever is due to a separate viral illness, such as influenza, transmission may occur via close contact or respiratory droplets. Globally, infections account for approximately 7% (ranging from 5% to 9%) of maternal deaths as of 2023, with higher burdens in low-resource settings due to limited access to hygiene and antibiotics. The of postpartum infections, detailed in later sections, shows varying incidence by region and delivery mode, with key risk factors including cesarean delivery, prolonged , and . In low- and middle-income regions, inadequate care contributes to higher mortality, with from postpartum infections causing up to 12% of pregnancy-related deaths in areas like .

Definition and overview

Definition

Postpartum infections, also known as puerperal infections, are bacterial infections affecting the genital tract, , or surgical wounds that develop following . They are characterized by the ascension of microorganisms from the lower genital tract into the upper reproductive organs or adjacent sites, leading to localized or . These infections occur during the puerperium, the defined as the time from placental expulsion through the ensuing 6 weeks, during which the reproductive organs undergo involution and return to their pre- state. This timeframe distinguishes postpartum infections from antenatal infections, which arise during prior to delivery. The term "puerperal" originates from the Latin puerperus, derived from puer (child) and parere (to bring forth), denoting conditions related to the process of . Common manifestations include , though other sites such as the urinary tract or cesarean incisions may also be involved.

Types of infections

Postpartum infections are classified primarily by their anatomical location and clinical presentation, encompassing a range of bacterial infections that occur within the six-week period following delivery. The most prevalent types include , wound infections, urinary tract infections, and , with rarer manifestations such as septic pelvic thrombophlebitis and . These infections collectively affect approximately 5% to 7% of postpartum individuals, with variations based on delivery mode and risk factors. Endometritis, the inflammation and infection of the uterine lining (), represents the most common form of postpartum infection, often referred to as puerperal when associated with fever. It typically arises from ascending bacterial during or after delivery and accounts for a significant portion of postpartum morbidity. The incidence is estimated at 1% to 3% following vaginal deliveries, increasing to 5% to 30% after cesarean sections due to surgical disruption of uterine barriers. Wound infections involve bacterial invasion at surgical or perineal sites, categorized as surgical site infections (SSIs) following cesarean delivery or infections at or laceration sites after vaginal birth. Cesarean infections occur in 3% to 15% of cases, manifesting as superficial or deep tissue involvement at the incision line. infections are less frequent, affecting 0.1% to 2% of cases, particularly when third- or fourth-degree tears are present. Urinary tract infections (UTIs) in the commonly present as cystitis or, less often, , frequently linked to catheterization during labor or delivery. These infections affect 1% to 5% of postpartum individuals, with rates varying by delivery mode; some studies report higher incidence after cesarean sections due to catheterization. Mastitis, an of the breast tissue during , typically involves staphylococcal or streptococcal pathogens and can progress to formation in severe instances. It occurs in 3% to 10% of individuals, most commonly within the first three months postpartum, with pooled estimates indicating an incidence of about 4.4% in the early weeks. Rarer types include septic pelvic , an infection-induced of pelvic veins, which complicates approximately 1 in 800 cesarean deliveries and 1 in 9,000 vaginal deliveries, often in the context of . , a rapidly progressive , is exceptionally uncommon postpartum, primarily reported in isolated cases following cesarean sections or complications.

Clinical features

Signs

Postpartum infections manifest through various objective clinical signs that healthcare providers can observe during , aiding in the identification of infection sites such as the , surgical wounds, or breasts. A hallmark sign is fever, defined as an oral temperature of 38.0°C (100.4°F) or higher on two occasions at least 6 hours apart (excluding the first 24 hours postpartum), which often occurs within the first few days postpartum and may be accompanied by chills and rigors indicating an inflammatory response. In more severe cases, particularly when the infection progresses to , patients may exhibit (heart rate greater than 90 beats per minute) and (systolic blood pressure less than 90 mmHg), reflecting systemic involvement and potential hemodynamic instability. For uterine infections like , key observable signs include tenderness of the upon , often with subinvolution (failure of the to return to its pre-pregnancy size), and foul-smelling , which is the that appears abnormal in odor and color due to bacterial overgrowth. In cases of surgical site infections following cesarean delivery or , reveals (redness), swelling, and purulent drainage at the incision site, sometimes accompanied by or induration. Postpartum mastitis presents with localized breast engorgement, characterized by firm, swollen tissue, along with and warmth over the affected area, distinguishing it from physiologic engorgement.

Symptoms

Patients with postpartum infections commonly report lower abdominal or , cramping, or discomfort, particularly in cases of , where diffuse is a frequent complaint due to uterine . This pain may be accompanied by gastrointestinal symptoms such as discomfort with bowel movements or . In urinary tract infections (UTIs), women often experience , urinary frequency, urgency, and lower abdominal discomfort, which can persist or worsen postpartum. For pyelonephritis, a more severe form of UTI, additional symptoms include flank or , along with and . In , breast pain and tenderness are hallmark subjective complaints, often described as sharp or aching in the affected area, accompanied by a sensation of fullness or engorgement. across various postpartum infections can lead to general , , myalgias, and flu-like , contributing to overall debilitation in affected individuals. These symptoms may vary in intensity depending on the infection type and timeliness of recognition, with patients occasionally noting persistent discomfort despite initial recovery from delivery. Accompanying objective signs such as fever are common but are detailed separately.

Pathophysiology and causes

Pathophysiology

Postpartum infections, particularly , arise primarily from the ascension of endogenous from the lower genital tract into the endometrial cavity or surgical wounds following delivery. This process is facilitated by the physiological changes during labor and delivery, including , which creates a pathway for microbial translocation, and tissue trauma that compromises local barriers. The normal cervicovaginal , including both aerobic and anaerobic species, ascends into the , leading to infection in the , , or adjacent structures. These infections are typically polymicrobial, involving a mix of aerobes such as Group B Streptococcus and Gram-negative bacilli like , alongside anaerobes including Bacteroides species. The follows pregnancy-associated and involves a rapid shift to a proinflammatory state (immune reconstitution), which, combined with hormonal changes, tissue trauma, and bacterial exposure, increases susceptibility to infection. Cervical dilation and peripartum tissue trauma further exacerbate this by disrupting mucosal integrity and promoting bacterial adherence and entry. Once established, the infection elicits a robust inflammatory response, characterized by the release of pro-inflammatory cytokines such as interleukin-6 and , which can lead to local tissue damage and, if unchecked, systemic dissemination resulting in . This dysregulated inflammation contributes to and organ injury, hallmarks of maternal . The risk is notably higher following cesarean delivery compared to vaginal birth, as the provides a direct breach in the uterine wall, allowing easier bacterial ingress and a 5- to 20-fold increased incidence of .

Risk factors

Cesarean delivery significantly increases the risk of postpartum infections compared to vaginal birth, with women undergoing cesarean section facing a five- to twenty-fold higher likelihood of developing conditions such as or wound infections. Without antibiotic prophylaxis, the infection rate following cesarean delivery can reach 10-15% for alone, highlighting the procedure's role in breaching natural barriers and introducing potential pathogens. Intrapartum factors further elevate susceptibility. exceeding 24 hours, (particularly lasting more than 18 hours), and multiple vaginal examinations during labor are associated with higher infection rates by facilitating bacterial ascension into the genital tract. Complications such as chorioamnionitis, , and postpartum hemorrhage also contribute substantially, as they promote tissue trauma, bacterial proliferation, and impaired uterine clearance. Maternal conditions play a key role in immune compromise and healing. , , , and immunosuppression—such as in HIV-positive individuals—increase the odds of by weakening host defenses and promoting hyperglycemia-related . For instance, is linked to a higher incidence of surgical site infections post-cesarean, with excessive gestational exacerbating this risk. Socioeconomic elements, particularly in low-resource settings, amplify vulnerability through limited access to sterile procedures and timely care. Poor during delivery and inadequate healthcare infrastructure correlate with elevated postpartum infection rates, which are higher in low- and middle-income countries (often 2-5% overall, up to 7-10% post-cesarean) compared to 1-6% in high-resource areas. These factors interact with clinical risks to heighten overall susceptibility, as noted in pathophysiological models of ascending infections.

Diagnosis

Clinical evaluation

Clinical evaluation of postpartum infections begins with a thorough to establish suspicion and guide further assessment. Symptoms typically onset within 24 to 48 hours postpartum, often linked to recent delivery events, though delayed presentations up to several weeks may occur in cases like wound or breast infections. Key historical elements include delivery mode (vaginal versus cesarean section), labor duration, number of vaginal examinations, use of internal fetal monitoring, premature , and postpartum interventions such as retained placental fragments or excessive bleeding. Patients often describe progressive symptoms starting with or localized , escalating to fever, , and systemic discomfort if advances. A comprehensive physical examination follows to confirm clinical suspicion and identify focal signs. Vital signs assessment is paramount, with fever (temperature ≥38°C on two occasions at least 4 to 6 hours apart), (>100 beats per minute), and signaling potential . Abdominal and uterine detects tenderness, guarding, or rebound, alongside evaluation for uterine subinvolution (fundus >2 cm above the umbilicus by postpartum day 2). For cesarean sections, incision sites require inspection for , induration, dehiscence, or purulent drainage. Breast examination identifies through focal , warmth, , and tenderness, often with axillary . Laboratory evaluation supports the clinical findings and helps identify complications. A often shows with , while blood cultures are recommended if is suspected. with culture is useful for suspected urinary tract s. C- or levels may aid in assessing severity. Imaging, such as pelvic or CT, is indicated for suspected abscesses or to evaluate for retained . To stratify sepsis risk, clinical scoring systems like the quick Sequential Organ Failure Assessment (qSOFA) are employed; scores ≥2 (altered mentation, ≥22/min, systolic ≤100 mmHg) indicate poor and necessitate rapid intervention. Early recognition within the first postpartum week is essential to halt progression to severe illness, emphasizing prompt evaluation of at-risk patients. Routine postpartum check-ups, ideally at 1 to 2 weeks and 6 weeks, facilitate detection of subclinical infections via targeted and examination.

Differential diagnosis

Postpartum infections, particularly those presenting with fever, must be differentiated from a variety of other conditions that can mimic infectious symptoms in the puerperium, such as , fever, and systemic signs. A thorough clinical is essential to distinguish infectious etiologies, which typically respond to antibiotics, from non-infectious or alternative infectious causes that may require different management strategies. Key differentiators include the presence of uterine tenderness and foul in gynecologic infections, urinary symptoms in renal issues, localized in surgical complications, and imaging findings like thrombi on CT for vascular conditions. Non-infectious causes of postpartum fever include , often seen shortly after cesarean delivery due to , which presents with mild fever and resolves with respiratory support without antibiotics; , causing transient low-grade fever without focal tenderness; and drug reactions, such as to antibiotics or analgesics, identifiable by timing and on labs. Postpartum hemorrhage may mimic infection through but lacks fever unless secondary infection occurs. Other infections to consider include urinary tract infections or , which feature , flank pain, and positive urine cultures, contrasting with the uterine focus of ; , marked by unilateral breast erythema, warmth, and tenderness; , with cough, dyspnea, and chest imaging abnormalities; and viral infections like , which may cause prolonged fever without bacterial response but are rarer in this context. Wound infections post-cesarean present with localized redness and purulent discharge, differing from deep pelvic infections by site. Surgical complications without overt infection encompass , where serosanguinous drainage occurs without fever resolution on antibiotics, and such as pelvic vein or ovarian vein , both presenting with persistent fever despite antimicrobial therapy and diagnosed via Doppler or CT showing vascular filling defects; the latter often mimics with right lower quadrant pain but lacks peritoneal signs. Rare mimics include , which can coincide postpartum and presents with rebound tenderness and elevated white count, confirmed by CT; and ovarian vein thrombosis, differentiated from by lack of and positive imaging for . These require prompt imaging to avoid misdiagnosis as infection.

Treatment

Pharmacological management

The pharmacological management of postpartum infections primarily involves targeted antibiotic therapy to address the polymicrobial nature of these conditions, which often include aerobic and anaerobic bacteria from genital tract . For postpartum , the standard empiric regimen consists of intravenous broad-spectrum antibiotics such as clindamycin (900 mg every 8 hours) combined with gentamicin (5 mg/kg/day divided every 8 hours), providing coverage against gram-positive, gram-negative, and anaerobic organisms. This combination has demonstrated efficacy in resolving symptoms in approximately 90% of cases. Therapy is typically continued intravenously until the patient remains afebrile for 48 hours, at which point step-down to oral antibiotics, such as amoxicillin-clavulanate (875 mg twice daily), is recommended for an additional 3 to 7 days to complete treatment and prevent relapse. Adjustments are necessary for patients with , where alternatives like plus clindamycin or (for suspected MRSA) may be used; renal dosing for gentamicin involves monitoring levels to avoid , particularly in postpartum women with impaired clearance. For specific infection types, regimens are tailored accordingly. Postpartum wound infections, often involving and anaerobes, are managed with cephalosporins such as (2 g intravenously every 8 hours) for initial therapy, transitioning to oral cephalexin if improving. Postpartum mastitis, primarily caused by , responds to (500 mg orally four times daily for 10 to 14 days), which is safe during . Resistance monitoring is essential, with MRSA coverage added via or if cultures indicate. In low-resource settings, the 2025 (WHO) guidelines emphasize affordable regimens for maternal peripartum infections, recommending lincosamide (e.g., clindamycin) plus (e.g., gentamicin) as the first-line option for , with plus as an alternative, due to cost-effectiveness and broad coverage while minimizing resistance risks. These antibiotics are administered alongside supportive measures to optimize recovery.

Supportive and surgical care

Supportive care for postpartum infections focuses on stabilizing the patient, managing symptoms, and preventing progression to severe complications such as . Fluid resuscitation is a , particularly in cases of or hypoperfusion, where isotonic crystalloids are administered to restore volume and support organ perfusion. For patients developing , immediate resuscitation includes fluids alongside respiratory and circulatory support, often requiring (ICU) monitoring to track and response to therapy. Pain management typically involves acetaminophen as a first-line agent, providing relief without interfering with or increasing risk, and can be combined with non-pharmacologic measures like rest. Surgical interventions are reserved for localized or infections unresponsive to initial measures. In postpartum complicated by formation, is performed to evacuate , often under , followed by continued milk expression to promote healing. For wound infections at cesarean sites, removes necrotic tissue and facilitates drainage, reducing the risk of deeper spread. In rare cases of leading to and overwhelming infection despite conservative therapy, emergency may be to source control and halt progression. Nutritional support plays a vital role in recovery, especially in , where early enteral is preferred to meet protein needs (1.2–2.0 g/kg/day) and correct deficiencies while avoiding overfeeding. should continue whenever possible, as it supports maternal recovery and provides immune benefits to the , with precautions such as frequent milk removal in cases and hygiene to prevent transmission. A multidisciplinary approach enhances outcomes, involving obstetricians, infectious disease specialists, intensivists, and consultants to coordinate care, particularly in severe where collaborative decision-making guides and source control alongside antibiotic therapy.

Prevention

Prophylactic measures

Prophylactic measures aim to mitigate the risk of postpartum infections by targeting key pathogens and vulnerabilities during labor and delivery. For cesarean deliveries, the American College of Obstetricians and Gynecologists (ACOG) recommends administering a single intravenous dose of (2 g standard; 3 g for patients >120 kg; 1 g may be considered for ≤80 kg) within 60 minutes prior to skin incision to optimize tissue concentrations and reduce surgical site infections. This timing ensures effective prophylaxis against common endometritis-causing organisms like group A and , particularly in patients with risk factors such as or chorioamnionitis. In high-risk vaginal deliveries, intrapartum antibiotic prophylaxis is indicated for women who test positive for group B (GBS) colonization, typically with penicillin G or administered intravenously at the onset of active labor or . This intervention not only prevents early-onset GBS disease in the neonate but also lowers maternal chorioamnionitis rates by approximately 49%, thereby reducing the subsequent risk of postpartum . Screening for (BV) during early pregnancy, particularly in women at high risk for , followed by treatment with oral (500 mg twice daily for 7 days), can help eradicate BV-associated biofilms and polymicrobial overgrowth that predispose to ascending infections. Although routine screening is not recommended for low-risk pregnancies due to insufficient of benefit, targeted treatment in symptomatic or high-risk cases has been associated with reduced postpartum infectious morbidity in select cohorts. Evidence from meta-analyses supports the efficacy of these measures, with cesarean prophylaxis reducing incidence by 60-80% compared to no prophylaxis, as per ACOG guidelines derived from randomized trials. ACOG guidelines recommend weight-adjusted prophylaxis for obese patients ( ≥30 kg/m²), including adjunctive dosing of alongside to address anaerobic coverage gaps and further decrease rates in this population, particularly for nonelective cesareans.

Hygienic and postpartum practices

Hand hygiene is a cornerstone of prevention in postpartum care, with caregivers required to perform it before and after contact with patients and newborns using and or alcohol-based hand rubs. Mothers should also practice strict hand hygiene before breastfeeding, handling their breasts, or touching the newborn to minimize pathogen transmission. This practice significantly reduces the transmission of pathogens that can lead to or wound infections. For patients, perineal care involves gentle cleansing with warm and mild after each voiding or to minimize bacterial in the genital area, particularly following . Patients are advised to pat the area dry and avoid harsh wiping to prevent and potential entry points for . Early ambulation is encouraged within 6-12 hours post-delivery to promote circulation, reduce stasis-related , and lower the risk of urinary tract infections by facilitating regular voiding. Bladder emptying should be monitored closely, with patients prompted to urinate every 2-3 hours and assessed for complete voiding to avoid retention, which can lead to overdistention and ascending infections. For cesarean deliveries, proper care of incisions includes regular cleaning and dressing changes following standardized protocols, typically involving removal of the initial dressing within 24-48 hours if dry and intact, followed by daily inspections and cleansing with saline to detect early signs of while maintaining a moist environment. Promoting breastfeeding initiation within the first hour after birth supports uterine involution and immunity transfer, while proper latching techniques—ensuring the baby's mouth covers most of the —help prevent trauma and milk stasis that contribute to . Mothers should practice good breastfeeding techniques, including correct latching, feeding on demand (at least 8-12 times per 24 hours), alternating breasts, ensuring complete emptying to avoid engorgement, and expressing milk if needed to prevent clogged ducts and cracked nipples. Mastitis is not contagious to the infant, and continued breastfeeding is recommended as it can help resolve inflammation. Support from consultants is advised to correct shallow latches. In high-risk scenarios, such as , these practices complement prophylactic measures outlined elsewhere. Hospital protocols emphasize aseptic techniques during vaginal exams or insertions, including the use of sterile gloves, drapes, and single-use instruments to limit microbial introduction into the reproductive tract. For cases of confirmed , such as group A streptococcal , isolation precautions are implemented, including contact isolation with dedicated equipment and cohorting of affected patients to prevent nosocomial spread. Staff training on these protocols ensures compliance, with regular audits to maintain standards. Community education focuses on empowering women and families to recognize early signs of postpartum infection, such as fever above 38°C (100.4°F), foul-smelling , severe abdominal pain, or chills, and to seek immediate medical care if these occur. Women should be advised to seek prompt medical attention for postpartum fever exceeding 38°C (100.4°F) and to receive prompt treatment of any infections with antibiotics as prescribed to prevent complications. Programs delivered through antenatal classes or discharge counseling stress prompt reporting of symptoms like uterine tenderness or excessive bleeding, which can indicate , to facilitate timely intervention and reduce morbidity. This education extends to danger signs in the newborn, such as poor feeding alongside maternal illness, reinforcing the need for integrated family care-seeking behaviors.

Complications and prognosis

Complications

Postpartum infections, if untreated or inadequately managed, can escalate to severe systemic complications, with and representing the most critical threats. arises from the spread of infection into the bloodstream, leading to a dysregulated inflammatory response that can progress to characterized by profound , tissue hypoperfusion, and multi-organ failure. This condition is a leading cause of maternal mortality worldwide, accounting for approximately 11% of maternal deaths globally, and is particularly prevalent in resource-limited settings where access to timely care is restricted. Endometrial and pelvic infections may result in scarring of the uterine lining, potentially causing , a condition involving intrauterine adhesions that impairs endometrial regeneration and leads to or secondary amenorrhea. Chronic , in particular, has been associated with uterine factor due to persistent and , reported in approximately 30-50% of women with recurrent implantation failure in assisted reproduction, depending on diagnostic criteria. Additionally, ascending infections can damage fallopian tubes, resulting in tubal occlusion and further risks. Severe postpartum infections often culminate in abscess formation within the , such as tubo-ovarian or pouch of Douglas es, occurring in less than 1% of cases but requiring surgical intervention if antibiotics fail. These es can cause persistent localized , leading to chronic that persists beyond the acute phase and impacts . In cases of maternal , the condition is not considered contagious to the infant, transmission risks are minimal, and breastfeeding remains safe and encouraged during treatment, as it helps resolve the infection and poses no significant risk to healthy term infants. In severe untreated cases, mortality rates from postpartum range from 10% to 20%, driven by delays in and , underscoring the need for vigilant monitoring to avert fatal outcomes.

With early initiation of appropriate , the vast majority of uncomplicated postpartum , such as , resolve within 48 to 72 hours, achieving cure rates exceeding 85% in early cases. Delays in and treatment, with multidrug-resistant organisms, and underlying comorbidities like or are associated with poorer outcomes, including progression to (with mortality around 20%) or (mortality up to 40%). Severe postpartum infections can have lasting psychological effects, elevating the risk of , anxiety, and (PTSD), particularly when the episode involves intensive care or life-threatening complications. The risk of recurrence in subsequent pregnancies may be elevated for women with a history of postpartum infection, particularly with risk factors like prior cesarean delivery, though prophylactic measures can mitigate this. Antimicrobial resistance is an emerging challenge, potentially worsening outcomes by increasing treatment failure rates and mortality, particularly in regions with limited access to advanced diagnostics and alternative therapies. In high-income settings, recent advancements in prophylaxis and rapid management have reduced mortality from postpartum infections to less than 1%, reflecting improved overall maternal outcomes as of 2023-2025 data. Complications such as pelvic abscesses or , if present, further influence prognosis by necessitating additional interventions.

Epidemiology

Incidence and prevalence

Postpartum infections affect approximately 5% to 7% of women globally following delivery. The overall incidence is higher after cesarean section (approximately 5% to 20% with standard prophylaxis) compared to 3% to 6% after . In the United States, the Centers for Disease Control and Prevention (CDC) reports an overall postpartum rate of about 6% (based on mid-1990s data that includes both inpatient and post-discharge cases). Rates are notably higher among women from low (SES) groups, where barriers to timely care and higher underlying risk factors contribute to increased vulnerability. In developed countries, incidence has declined over recent decades primarily due to widespread adoption of prophylaxis during cesarean deliveries and improved hygienic practices. However, this progress is threatened by rising , with studies showing increasing prevalence of multidrug-resistant pathogens such as methicillin-resistant Staphylococcus aureus (MRSA) and extended-spectrum beta-lactamase (ESBL)-producing in postpartum cases, particularly in low- and middle-income settings but also emerging in high-resource areas. Specific types of postpartum infections exhibit varying incidences. , an inflammation of the uterine lining, occurs in 1% to 5% of postpartum women overall, with higher rates following cesarean section. , a breast infection common in women, affects 2% to 10% during the early postpartum period, often peaking within the first few weeks after delivery. for postpartum infections relies on standardized methods, including hospital discharge codes such as those from the (ICD) system to track cases via administrative data, which has proven effective in identifying both inpatient and outpatient infections. The (WHO) supports global tracking through maternal sepsis surveillance frameworks, which integrate postpartum infection data into broader monitoring to inform policy and intervention strategies.

Global impact

Postpartum infections represent a significant contributor to global maternal mortality, accounting for approximately 11% of all maternal deaths worldwide and up to 15% in low- and lower-middle-income countries, where limited healthcare infrastructure exacerbates outcomes. In 2023, infections contributed to approximately 11% of the estimated 260,000 global maternal deaths. These infections, often manifesting as sepsis or endometritis, are the third leading cause of maternal death globally, with the majority occurring in the postpartum period due to delays in diagnosis and treatment. In low-income settings, this burden is amplified by factors such as inadequate sanitation and antimicrobial resistance, leading to higher case fatality rates compared to high-income regions. Regionally, stark disparities highlight the uneven global impact, particularly in , where the prevalence of postpartum infections is estimated at 11.5% and associated maternal reaches up to 19%, driven by restricted access to sterile delivery environments and timely medical interventions. This elevated incidence contrasts with rates of 5-7% in high-income countries, underscoring how socioeconomic barriers perpetuate higher morbidity and mortality in resource-poor areas. Economically, postpartum infections impose a substantial burden through hospitalizations and ; in the United States, severe maternal morbidity—including infections—costs an estimated $32.3 billion annually, with per-case hospitalization expenses averaging $50,000 for affected women. The global ramifications of postpartum infections directly impede progress toward (SDG 3), which aims to reduce the maternal mortality ratio to less than 70 deaths per 100,000 live births by 2030 and ensure universal access to reproductive health services. By increasing preventable deaths and complications, these infections hinder equitable health outcomes and strain healthcare systems in vulnerable populations. Recent developments, including the , have worsened this impact through disrupted care pathways, with indirect effects leading to a 38.6% rise in maternal mortality globally due to delayed prenatal and postpartum monitoring, potentially elevating infection risks from untreated complications.

History

"The Doctor's Plague"

In the 1840s, , a Hungarian physician working at , observed the devastating outbreaks of puerperal fever—also known as childbed fever—that ravaged maternity wards. Postpartum infections were sometimes referred to as "The Doctor's Plague" by women and observers, attributing the infections directly to practices by medical professionals. Semmelweis noted stark disparities in mortality rates between the hospital's two clinics: the first clinic, staffed by doctors and medical students, saw puerperal fever death rates as high as 18%, while the second clinic, attended solely by midwives, experienced rates around 1%. Investigating the cause, Semmelweis hypothesized that the elevated risk stemmed from doctors performing autopsies on deceased patients and then delivering babies without washing their hands, thereby transferring cadaveric particles—decomposing organic matter laden with infectious agents—to vulnerable postpartum women. In 1847, following the death of a colleague from a similar infection acquired during an autopsy, Semmelweis mandated handwashing with a chlorinated lime solution before patient examinations; this intervention swiftly reduced mortality in the first clinic from approximately 18% to under 2%, demonstrating the preventable nature of the epidemic. Despite these compelling results, Semmelweis encountered fierce opposition from the medical establishment, who viewed his emphasis on as an insult to their professionalism and dismissed his lack of a full germ theory explanation; this resistance culminated in his forced resignation from the hospital in 1849 and his institutionalization in a Viennese asylum in 1865, where he died shortly thereafter from a gangrenous wound.

Hygienic measures

In 1847, , building on his earlier observations of puerperal fever's contagious nature in the General Hospital's maternity wards, instituted a mandatory hand-washing protocol for medical staff using a chlorinated lime solution before examining patients. This simple hygienic measure reduced mortality from puerperal fever in the First Obstetrical Clinic from approximately 18% to under 2% within months, demonstrating the role of hand contamination in disease transmission. Despite these compelling results, Semmelweis's protocol faced widespread rejection from the medical community, who resisted the implication that physicians themselves were vectors of infection, leading to his professional isolation and the protocol's limited adoption at the time. Independently, in 1843, American physician published an essay, "The Contagiousness of Puerperal Fever," arguing that the disease spread through contact with infected individuals or materials, advocating handwashing, isolation of cases, and precautions by attendants to prevent transmission. The acceptance of principles gained momentum two decades later through Joseph Lister's work. In 1867, inspired by Louis Pasteur's germ theory, Lister pioneered the use of carbolic acid (phenol) as an in surgical settings, including obstetric procedures, by applying it to wounds, instruments, and dressings. This approach dramatically lowered postoperative infection rates, including puerperal fever, with one early series showing compound fracture mortality dropping from 45% to 15%. Lister's methods marked a pivotal shift toward systematic in , influencing global obstetric practices and reducing the epidemics of postpartum that had plagued hospitals. Advancements accelerated in the with the advent of antibiotics. Sulfonamides, introduced in the mid-1930s following Gerhard Domagk's 1932 discovery of Prontosil's against streptococcal infections, became the first widely used agents for treating puerperal fever and other postpartum infections, halving maternal mortality rates in affected cases by the late 1930s. , discovered by in 1928 and mass-produced during the 1940s, further transformed outcomes by effectively combating resistant bacterial strains in severe postpartum , contributing to a steep decline in infection-related maternal deaths. Contemporary hygienic standards build on these foundations, emphasizing standardized protocols for surgical interventions common in modern . The World Health Organization's Surgical Safety Checklist, launched in 2009, incorporates critical steps such as antibiotic prophylaxis timing and site preparation for cesarean deliveries, reducing surgical site infections by up to 50% in implementing facilities. This tool promotes a multidisciplinary approach to , ensuring verification of sterile techniques and patient allergies before incision. Collectively, these developments in hygienic and practices have profoundly impacted global . Maternal mortality from all causes, heavily influenced by postpartum infections in earlier eras, fell from an estimated 800 deaths per 100,000 live births around 1900 to 197 per 100,000 in 2023, reflecting the widespread adoption of antisepsis, antibiotics, and safety protocols.

Notable cases

One of the earliest notable cases highlighting the dangers of postpartum infections occurred in 1817 with the death of Princess Charlotte of Wales, the only child of the future King George IV, following the of her son. After a , she suffered severe postpartum hemorrhage, potentially complicated by , leading to her death just hours later. This tragedy prompted immediate royal inquiries, including a detailed medical examination published in 1818 that scrutinized the obstetric management and contributed to early discussions on improving maternal care practices. Ignaz Semmelweis, the Hungarian physician renowned for his 1847 advocacy of handwashing with chlorinated lime to prevent puerperal fever—a bacterial postpartum —ironically met his end in 1865 from a similar infectious cause. Committed to a asylum amid professional rejection and possible decline, Semmelweis sustained a hand injury during his confinement that developed into a gangrenous wound and , resulting in his death at age 47. His case underscored the resistance to reforms he championed, which later became foundational to modern control. Recent cases in the 2020s from have drawn attention to (AMR) in postpartum infections, where multidrug-resistant pathogens such as extended-spectrum beta-lactamase-producing have elevated maternal mortality risks in resource-limited settings. A 2024 systematic review identified pooled AMR prevalence exceeding 50% for key antibiotics in , including , prompting the to reinforce antibiotic stewardship guidelines in its 2021 recommendations for maternal management and global AMR action plans. Disparities in postpartum infection outcomes are exemplified by anonymized cases among underserved populations, particularly in the United States, who face 3-4 times higher maternal mortality rates from infections compared to white women due to systemic barriers like delayed care access and biased treatment. For instance, infection accounts for up to 12% of maternal deaths in this group.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK560804/
  2. https://emedicine.medscape.com/article/796892-overview
  3. https://pmc.ncbi.nlm.nih.gov/articles/PMC7465810/
  4. https://www.cdc.gov/sepsis/media/pdfs/CDC-Sepsis-pregnant-postpartum-508.pdf
  5. https://www.thelancet.com/journals/langlo/article/PIIS2214-109X(24)00560-6/fulltext
  6. https://journals.plos.org/globalpublichealth/article?id=10.1371/journal.pgph.0003109
  7. https://www.ncbi.nlm.nih.gov/books/NBK555904/
  8. https://emedicine.medscape.com/article/260187-overview
  9. https://www.etymonline.com/word/puerperal
  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC4934978/
  11. https://www.ncbi.nlm.nih.gov/books/NBK553124/
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC5322852/
  13. https://wwwnc.cdc.gov/eid/article/7/5/01-0511_article
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC5857667/
  15. https://obgyn.onlinelibrary.wiley.com/doi/10.1080/00016340903147405
  16. https://pubmed.ncbi.nlm.nih.gov/39172675/
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC8020511/
  18. https://www.merckmanuals.com/home/women-s-health-issues/postpartum-care/infections-after-childbirth
  19. https://www.acog.org/womens-health/experts-and-stories/the-latest/3-conditions-to-watch-for-after-childbirth
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC8288480/
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC8381608/
  22. https://www.ncbi.nlm.nih.gov/books/NBK615369/
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC5497372/
  24. https://www.ncbi.nlm.nih.gov/books/NBK557782/
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC4860650/
  26. https://www.ncbi.nlm.nih.gov/medlineplus/ency/article/001484.htm
  27. https://www.acog.org/clinical/clinical-guidance/clinical-consensus/articles/2023/08/urinary-tract-infections-in-pregnant-individuals
  28. https://www.ncbi.nlm.nih.gov/books/NBK519537/
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC3253187/
  30. https://www.merckmanuals.com/professional/gynecology-and-obstetrics/postpartum-care-and-associated-disorders/postpartum-endometritis
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC12187610/
  32. https://academic.oup.com/cid/article/45/9/1192/370158
  33. https://www.who.int/teams/sexual-and-reproductive-health-and-research-(srh)/areas-of-work/maternal-and-perinatal-health/maternal-sepsis
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC9758935/
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC7227107/
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC5980779/
  37. https://pmc.ncbi.nlm.nih.gov/articles/PMC7571565/
  38. https://bmcpregnancychildbirth.biomedcentral.com/articles/10.1186/s12884-018-1891-1
  39. https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002984
  40. https://emedicine.medscape.com/article/796892-clinical
  41. https://emedicine.medscape.com/article/796892-workup
  42. https://www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2018/05/optimizing-postpartum-care
  43. https://tools.apgo.org/wp-content/uploads/2016/05/TC28.pdf
  44. https://www.unboundmedicine.com/5minute/view/5-Minute-Clinical-Consult/816959/1.1/Postpartum_Fever
  45. https://emedicine.medscape.com/article/796892-differential
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC6605948/
  47. https://www.sciencedirect.com/science/article/pii/S1930043325003000
  48. https://emedicine.medscape.com/article/254169-treatment
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC7050613/
  50. https://www.msdmanuals.com/professional/gynecology-and-obstetrics/postpartum-care-and-associated-disorders/postpartum-endometritis
  51. https://www.droracle.ai/articles/30283/treatment-for-endometritis-post-partum
  52. https://emedicine.medscape.com/article/796892-medication
  53. https://www.aafp.org/pubs/afp/issues/2008/0915/p727.html
  54. https://www.ccjm.org/content/91/5/283
  55. https://www.who.int/publications/i/item/9789241549363
  56. https://app.magicapp.org/summary/guideline_7963.html
  57. https://www.ogmagazine.org.au/21/4-21/managing-the-septic-postnatal-patient/
  58. https://www.acog.org/clinical/clinical-guidance/clinical-consensus/articles/2021/09/pharmacologic-stepwise-multimodal-approach-for-postpartum-pain-management
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC3900741/
  60. https://www.glowm.com/section-view/heading/diagnosis-and-management-of-postoperative-infection/item/32
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC6447319/
  62. https://emedicine.medscape.com/article/796892-treatment
  63. https://saferbirth.org/psbs/sepsis-in-obstetric-care/
  64. https://www.acog.org/clinical/clinical-guidance/practice-bulletin/articles/2018/09/use-of-prophylactic-antibiotics-in-labor-and-delivery
  65. https://journals.lww.com/greenjournal/fulltext/2018/09000/acog_practice_bulletin_no__199__use_of.67.aspx
  66. https://www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2020/02/prevention-of-group-b-streptococcal-early-onset-disease-in-newborns
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC10733553/
  68. https://www.cdc.gov/std/treatment-guidelines/bv.htm
  69. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/bacterial-vaginosis-in-pregnancy-to-prevent-preterm-delivery-screening
  70. https://pmc.ncbi.nlm.nih.gov/articles/PMC4164464/
  71. https://jamanetwork.com/journals/jama/fullarticle/2654382
  72. https://www.cdc.gov/flu/hcp/infection-control/peri-post-settings.html
  73. https://www.glowm.com/article/heading/vol-15--the-puerperium--perineal-care-and-postpartum-urogynecology/id/416523
  74. https://www.nursetogether.com/postpartum-nursing-diagnosis-care-plan/
  75. https://www.cdc.gov/infant-toddler-nutrition/breastfeeding/what-to-expect-while-breastfeeding.html
  76. https://www.tmh.org/blogs/how-to-prevent-mastitis
  77. https://llli.org/breastfeeding-info/mastitis/
  78. https://www.bfmed.org/assets/ABM%20Protocol%2036.pdf
  79. https://www.publichealthontario.ca/-/media/documents/B/2015/bp-ipac-perinatology.pdf
  80. https://www.cdc.gov/infection-control/hcp/core-practices/index.html
  81. https://www.who.int/news-room/fact-sheets/detail/maternal-mortality
  82. https://imsear.searo.who.int/bitstreams/8f80382b-6a43-4691-890b-ae100a4898a2/download
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC9355436/
  84. https://www.ncbi.nlm.nih.gov/books/NBK448088/
  85. https://pubmed.ncbi.nlm.nih.gov/25385744/
  86. https://www.mayoclinic.org/diseases-conditions/mastitis/diagnosis-treatment/drc-20374834
  87. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2023.1126807/full
  88. https://patient.info/doctor/obstetrics/postpartum-endometritis-pro
  89. https://pmc.ncbi.nlm.nih.gov/articles/PMC11176113/
  90. https://womensmentalhealth.org/posts/serious-complications-delivery-increase-risk-postpartum-ptsd/
  91. https://emedicine.medscape.com/article/254169-overview
  92. https://www.who.int/news-room/fact-sheets/detail/antimicrobial-resistance
  93. https://pmc.ncbi.nlm.nih.gov/articles/PMC6891249/
  94. https://www.kff.org/racial-equity-and-health-policy/racial-disparities-in-maternal-and-infant-health-current-status-and-efforts-to-address-them/
  95. https://www.sciencedirect.com/science/article/pii/S1701216325002075
  96. https://pubmed.ncbi.nlm.nih.gov/38630391/
  97. https://www.dynamed.com/condition/endometritis-postpartum
  98. https://www.who.int/teams/sexual-and-reproductive-health-and-research-%28srh%29/areas-of-work/maternal-and-perinatal-health/maternal-sepsis
  99. https://bmcpregnancychildbirth.biomedcentral.com/articles/10.1186/s12884-025-07409-2
  100. https://www.thelancet.com/journals/langlo/article/PIIS2214-109X%2824%2900560-6/fulltext
  101. https://stratfordjournalpublishers.org/journals/index.php/Journal-of-Medicine-Nursing-P/article/view/1487
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC10847291/
  103. https://www.commonwealthfund.org/publications/issue-briefs/2021/nov/high-costs-maternal-morbidity-need-investment-maternal-health
  104. https://pmc.ncbi.nlm.nih.gov/articles/PMC8524749/
  105. https://www.who.int/data/gho/data/themes/topics/sdg-target-3-1-maternal-mortality
  106. https://www.thelancet.com/journals/langlo/article/PIIS2214-109X%2821%2900079-6/fulltext
  107. https://www.nature.com/articles/s41390-023-02651-w
  108. https://pmc.ncbi.nlm.nih.gov/articles/PMC2870773/
  109. https://www.npr.org/sections/health-shots/2015/01/12/375663920/the-doctor-who-championed-hand-washing-and-saved-women-s-lives
  110. https://www.sciencehistory.org/education/scientific-biographies/ignaz-semmelweis/
  111. https://embryo.asu.edu/pages/ignaz-philipp-semmelweis-1818-1865
  112. https://pmc.ncbi.nlm.nih.gov/articles/PMC6053623/
  113. https://www.idcmjournal.org/semmelweis-and-hand-hygiene
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC11568873/
  115. https://www.cdc.gov/mmwr/pdf/rr/rr5116.pdf
  116. https://pmc.ncbi.nlm.nih.gov/articles/PMC3881728/
  117. https://www.nejm.org/doi/full/10.1056/NEJM18430425a00001
  118. https://pmc.ncbi.nlm.nih.gov/articles/PMC3468637/
  119. https://pmc.ncbi.nlm.nih.gov/articles/PMC8902014/
  120. https://pubmed.ncbi.nlm.nih.gov/3511335/
  121. https://www.journals.uchicago.edu/doi/10.1086/686035
  122. https://www.fda.gov/about-fda/fda-history-exhibits/drug-therapeutics-regulation-us
  123. https://pmc.ncbi.nlm.nih.gov/articles/PMC10867741/
  124. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm4838a2.htm
  125. https://data.unicef.org/topic/maternal-health/maternal-mortality/
  126. https://archive.org/details/criticalinquiryi00pric
  127. https://www.who.int/publications/i/item/9789240027992
Add your contribution
Related Hubs
User Avatar
No comments yet.