At first, the bleeding will probably be heavy enough that you’ll need to wear a hospital pad. Your nurse may give you some of these extra-absorbent pads when you’re discharged.
As the bleeding slows, you can transition to a regular menstrual pad.
Make sure to change your pads often to prevent infection. Don’t use tampons until your doctor says it’s fine to do so. Once the bleeding is light enough, or you’re only seeing discharge, you can switch to a panty liner.
Shop for postpartum pads.
Delivery by cesarean section is the single most important risk factor for postpartum maternal infection. In the absence of antimicrobial prophylaxis, women who have a cesarean delivery have a five to 20-fold greater chance of a postpartum infection compared to those who delivery vaginally. [28] Therefore ACOG recommends the routine administration of prophylactic antibiotics in women undergoing cesarean section. [29] In a large Cochrane review of 95 studies including over 15,000 women who had cesarean deliveries, there was a 60-70% reduction in postpartum complications after the use of prophylactic antibiotics including wound infection and endometritis. [28]
The American College of Obstetricians and Gynecologist recommend a single dose of a targeted antibiotic, such as a first-generation cephalosporin, as first-line antimicrobial prophylaxis in women undergoing a cesarean section due to its narrow spectrum of activity, efficacy, and low cost. [29] Guidelines set forth by the Society of Health-System Pharmacists (ASHP), the Infectious Diseases Society of America (IDSA), the Surgical Infection Society (SIS), and the Society for Healthcare Epidemiology of America (SHEA) recommend cefazolin 2 grams for patients < 120 kg and 3 grams for patients ≥120 kg. [30]
In those individuals with a severe allergy to penicillin or cephalosporin (ie a history of anaphylaxis, angioedema, respiratory distress or urticarial reaction) a combination of clindamycin (900 mg) with an aminoglycoside (ie gentamicin 5 mg/kg IV) is recommended for broad coverage antibiotic prophylaxis. [29, 30] The prophylactic agent should be administered within 60 minutes prior to skin incision to ensure adequate drug tissue levels; in emergent cases when this is not possible antibiotic administration should occur as soon as possible after the start of the cesarean delivery. [29] Compared to multidose therapy, single-dose antibiotic administration is preferred because it just as effective with a reduction in costs, associated toxicity and risk of colonization with resistant organisms.
The results of a Cochrane review indicated that cleansing the vagina with a povidone-iodine or chlorhexidine solution immediately before cesarean delivery decreases the risk of postoperative endometritis, fever, and wound infection. No adverse effects were reported from cleansing with either of the solutions. [31]
Endometritis is an ascending polymicrobial infection. The causative agents are usually normal vaginal flora or enteric bacteria.
Endometritis is the primary cause of postpartum infection. The most common organisms are divided into 4 groups: aerobic gram-negative bacilli, anaerobic gram-negative bacilli, aerobic streptococci, and anaerobic gram-positive cocci. Specifically, Escherichia coli, Klebsiella pneumoniae, and Proteus species are the most frequently identified organisms.
Endometritis occurring on postpartum day 1 or 2 most frequently is caused by group A streptococci. If the infection develops on day 3 or 4, the causative organism is frequently enteric bacteria, most commonly E coli, or anaerobic bacteria. Endometritis that develops more than 7 days after delivery is most frequently caused by Chlamydia trachomatis. Endometritis following cesarean delivery is most frequently caused by anaerobic gram-negative bacilli, specifically Bacteroides species.
Known risk factors for endometritis include cesarean delivery, young age, low socioeconomic status, prolonged labor, prolonged rupture of membranes, multiple vaginal examinations, placement of an intrauterine catheter, preexisting infection or colonization of the lower genital tract, twin delivery, and manual removal of the placenta. It has also been shown that manual removal of the placenta at cesarean delivery increases the incidence of endometritis.
Endometritis complicates less than 3% of all vaginal deliveries. Cesarean delivery is the most important risk factor for development of postpartum endometritis and therefore significantly increases the risk of endometritis after delivery, particularly when performed after the onset of labor and without antibiotic prophylaxis. Among women who receive standard antibiotic prophylaxis prior a cesarean section delivery in the absence of labor, the frequency of postpartum endometritis is 1.7%; this increases to 11% in patients have a cesarean delivery after the onset of labor and 28% in those who do not receive antibiotic prophylaxis after the onset of labor that resulted in a cesarean section. [28]
Following 48-72 hours of intravenous antibiotic therapy, 90% of women clinically improve. Fewer than 2% of patients develop life-threatening complications such as septic shock, pelvic abscess, or septic pelvic thrombophlebitis. [32]
A patient may report any of the following symptoms: fever, chills, lower abdominal pain, malodorous lochia, increased vaginal bleeding, anorexia, and malaise.
A focused physical examination is important and should include vital signs, an examination of the respiratory system, breasts, abdomen, perineum, and lower extremities. A patient with endometritis typically has a fever of 38°C or greater, tachycardia, and fundal tenderness. Some patients may develop mucopurulent vaginal discharge, whereas others have scant and odorless discharge.
See the list below:
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Lower genital tract infection
See the list below:
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Laboratory tests: The appropriate tests for a febrile postpartum patient may include a CBC count with differential, urinalysis, urine culture, and blood cultures.
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Imaging: If a respiratory process is high on the differential, obtain a chest radiograph.
Treatment of endometritis is with intravenous antibiotics. Parenteral antibiotics are usually stopped once the patient is afebrile for 24-48 hours, tolerating a regular diet, and ambulating without difficulty. [33] In general, an extended course of oral antibiotics has not been found to be beneficial, [34] although 2 exceptions have been noted. In patients who respond quickly to intravenous antibiotics and who desire early discharge, a short course of oral antibiotics may be substituted for continued intravenous therapy. The other exception includes patients with staphylococcal bacteremia requiring an extended period of treatment.
Broad spectrum coverage with a combination of clindamycin and gentamicin is a commonly used and highly effective regimen for the treatment of endometritis with a cure rate of greater than 90%. [35] Clindamycin is typically administered as 900 mg intravenously every eight hours. The most cost efficient and convenient gentamycin regimen is extended interval dosing of gentamicin with 5mg/kg every 24 hour, however 1.5mg/kg every 8 hours is also an acceptable regimen with equal efficacy. Gentamicin should be avoided in those with impaired renal function; instead reasonable alternative regimens include ampicillin-sulbactam (1.5g every 6 hours) or clindamycin and a second-generation cephalosporin. Ampicillin-sulbactam should also be considered in regions with a significant clindamycin resistant B. fragilis. [36] Ampicillin (or vancomycin for patients with a penicillin allergy) should be considered when the patient does not respond to the initial therapy of gentamicin and clindamycin to cover Enterococcus faecalis, which may be the cause of up to 25% of postpartum endometritis infections. [37] In a Cochrane review of endometritis treatment regimens, there were significantly more treatment failure rates in those treated with a regimen with poor activity against penicillin-resistant anaerobic bacteria as compared to those treated with a regimen with coverage against penicillin-resistant anaerobic bacteria with no difference in side effects. [35]
A urinary tract infection (UTI) is defined as a bacterial inflammation of the bladder or urethra. Greater than 105 colony-forming units from a clean-catch urine specimen or greater than 10,000 colony-forming units on a catheterized specimen is considered diagnostic of a UTI.
Risk factors for postpartum UTI include cesarean delivery, forceps delivery, vacuum delivery, tocolysis, induction of labor, maternal renal disease, preeclampsia, eclampsia, epidural anesthesia, bladder catheterization, length of hospital stay, and previous UTI during pregnancy. [38]
The most common pathogen is E coli. [39] In pregnancy, group B streptococci are a major pathogen. Other causative organisms include Staphylococcus saprophyticus, E faecalis, Proteus, and K pneumoniae.
Postpartum bacteruria occurs in 3-34% of patients, resulting in a symptomatic infection in approximately 2% of these patients.
A patient may report frequency, urgency, dysuria, hematuria, suprapubic or lower abdominal pain, or no symptoms at all.
On examination, vital signs are stable and the patient is afebrile. Suprapubic tenderness may be elicited on abdominal examination.
See the list below:
Appropriate laboratory tests include urinalysis, urine culture from either a clean-catch or catheterized specimen, and CBC count.
Treatment is started empirically in uncomplicated infection because the usual organisms have predictable susceptibility profiles. When sensitivities are available, use them to guide antimicrobial selection. Treatment is with a 3- or 7-day antibiotic regimen. [38] Commonly used antibiotics include trimethoprim/sulfamethoxazole, ciprofloxacin, and norfloxacin. Amoxicillin is often still used, but it has lower cure rates secondary to increasing resistance of E coli. The quinolones are very effective but are considerably more expensive than amoxicillin and trimethoprim/sulfamethoxazole and should not be used in breastfeeding mothers.
Mastitis is defined as inflammation of the mammary gland.
Milk stasis and cracked nipples, which contribute to the influx of skin flora, are the underlying factors associated with the development of mastitis. Mastitis is also associated with primiparity, incomplete emptying of the breast, and improper nursing technique. The most common causative organism, isolated in approximately half of all cases, is Staphylococcus aureus. [40] Other common pathogens include Staphylococcus epidermidis, S saprophyticus, Streptococcus viridans, and E coli.
In the United States, the incidence of postpartum mastitis is 2.5-3%. [41, 40] Mastitis typically develops during the first 3 months postpartum, with the highest incidence in the first few weeks after delivery.
Neglected, resistant, or recurrent infections can lead to the development of an abscess, requiring parenteral antibiotics and surgical drainage. Abscess development complicates 5-11% of the cases of postpartum mastitis and should be suspected when antibiotic therapy fails.
The diagnosis of mastitis is solely based on the clinical picture.
Fever, chills, myalgias, erythema, warmth, swelling, and breast tenderness characterize this disease.
Focus examination on vital signs, review of systems, and a complete examination to look for other sources of infection. Typical findings include an area of the breast that is warm, red, and tender. When the exam reveals a tender, hard, possibly fluctuant mass with overlying erythema, a breast abscess should be considered.
See the list below:
No laboratory tests are required. Expressed milk can be sent for analysis, but the accuracy and reliability of these results are controversial and aid little in the diagnosis and treatment of mastitis.
Milk stasis sets the stage for the development of mastitis, which can be treated with moist heat, massage, fluids, rest, proper positioning of the infant during nursing, nursing or manual expression of milk, and analgesics.
When mastitis develops, penicillinase-resistant penicillins and cephalosporins, such as dicloxacillin or cephalexin, are the drugs of choice. Erythromycin, clindamycin, and vancomycin may be used for infections that are resistant to penicillin. Resolution usually occurs 48 hours after the onset of antimicrobial therapy. Lactation efforts should continue and the milk is still safe for newborn ingestion.
Wound infections in the postpartum period include infections of the perineum developing at the site of an episiotomy or laceration, as well as infection of the abdominal incision after a cesarean birth. Wound infections are diagnosed on the basis of erythema, induration, warmth, tenderness, and purulent drainage from the incision site, with or without fever. This definition can be applied both to the perineum and to abdominal incisions.
Perineal infections: Infections of the perineum are rare. In general, they become apparent on the third or fourth postpartum day. Known risk factors include infected lochia, fecal contamination of the wound, and poor hygiene. These infections are generally polymicrobial, arising from the vaginal flora.
Abdominal wound infections: Abdominal wound infections are most frequently the result of contamination with vaginal flora. However, S aureus, either from the skin or from an exogenous source, is isolated in 25% of these infections. [42] Genital Mycoplasma species are commonly isolated from infected wounds that are resistant to treatment with penicillins. [43] Known risk factors include diabetes, hypertension, obesity, treatment with corticosteroids, immunosuppression, anemia, development of a hematoma, chorioamnionitis, prolonged labor, prolonged rupture of membranes, prolonged operating time, abdominal twin delivery, and excessive blood loss.
The incidence of perineal infections is 0.35-10%. The incidence of incisional abdominal wound infections is 3-15% and can be decreased to approximately 2% with the use of prophylactic antibiotics.
The most common consequence of wound infection is increased length of hospital stay or hospital readmission. About 7% of abdominal wound infections are further complicated by wound dehiscence. More serious sequelae, such as necrotizing fasciitis, are rare, but patients with such conditions have a high mortality rate.
Patients with perineal infections may complain of an inordinate amount of pain, malodorous discharge, or vulvar edema.
Abdominal wound infections develop around postoperative day 4 and are often preceded by endometritis. These patients present with persistent fever despite antibiotic treatment.
Perineal infections: An infected perineum often looks erythematous and edematous and may be accompanied by purulent discharge. Perform an inspection to identify hematoma, perineal abscess, or stitch abscess.
Abdominal wound infections: Infected incisions may be erythematous, warm, tender, and indurated. Purulent drainage may or may not be obvious. A fluid collection may be appreciated near the wound, which, when entered, may release serosanguineous or purulent fluid.
The diagnosis of wound infection is often made based on the clinical findings. Serial CBC counts with differentials may be helpful, especially if a patient does not respond to therapy as anticipated. CT imaging of the abdomen may be indicated if an abscess is suspected after a cesarean delivery.
Perineal infections: Treatment of perineal infections includes symptomatic relief with NSAIDs, local anesthetic spray, and sitz baths. Identified abscesses must be drained, and broad-spectrum antibiotics may be initiated.
Abdominal wound infections: These infections are treated with antibiotics as well as drainage and inspection of the fascia to ensure that it is intact. Antibiotics may be used if the patient is afebrile.
Most patients respond quickly to the antibiotic once the wound is drained. Antibiotics are generally continued until the patient has been afebrile for 24-48 hours. Patients do not require long-term antibiotics unless cellulitis has developed. Studies have shown that closed suction drainage or suturing of the subcutaneous fat decreases the incidence of wound infection when the subcutaneous tissue is greater than 2 cm in depth. [44, 45]