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cervicovaginal ora migration into the uterine cavity, resulting in infection. The
uterus is typically a sterile environment until the amniotic sac ruptures. During
labor, and particularly during cesarean sections, the uterus and amniotic uid
become contaminated with anaerobic and aerobic bacteria. These bacteria are prone
to colonizing devitalized tissues, hematomas, and incision sites. Of all postpartum
infections, endometritis is the most common and accounts for 27% of all postnatal
complications [4].
The incidence of postpartum endometritis following normal spontaneous vaginal
delivery is low (1–2%). For patients with risk factors, which include prolonged
labor, multiple cervical exams, premature rupture of membranes, internal fetal/uter-
ine monitoring, manual removal of the placenta, maternal diabetes or obesity, low
socioeconomic status, HIV infection, or colonization with group B streptococcus,
the incidence increases to 5–6% [5]. The route of delivery is the most important risk
factor for developing postpartum endometritis, with cesarean deliveries carrying the
highest risk [6]. Rates of postpartum endometritis have been reported to be 5 to 30
times higher following cesarean section compared to vaginal delivery [7, 8].
Unscheduled cesarean deliveries that are performed after the onset of labor are par-
ticularly high risk.
Most cases of postpartum endometritis (60–70%) involve both aerobic and
anaerobic organisms from the lower genital tract [9]. The most common aerobic
organisms include Groups A and B Streptococcus, Staphylococcus, Klebsiella,
Enterobacter, and Escherichia coli. The most common anaerobic species include
Peptostreptococcus, Bacterioides, Fusobacterium, and Clostridium. In patients
infected with HIV, the microbiology can include less common pathogens such as
herpes simplex virus and cytomegalovirus. Devitalized tissue is particularly suscep-
tible to streptococcus pyogenes and staphylococcus aureus, which are the most
common causes of post-cesarean section endometritis [10].
The diagnosis of postpartum endometritis is largely clinical. Patients may pres-
ent with multiple symptoms, including fever (often the rst sign), tachycardia, mid-
line lower abdominal pain, uterine tenderness, foul-smelling lochia, and purulent
vaginal discharge [11]. Most patients will develop symptoms within 5days follow-
ing delivery [6, 12]. Patients that present more than 7days postpartum may have
Chlamydia trachomatis endometritis [1
]. If the patient is in shock, very ill- appearing,
or has diarrhea or abdominal pain that appears out of proportion to the physical
exam, infection with group A Streptococcus (GAS) should be considered. These
patients are at risk for the development of toxic shock syndrome, necrotizing fasci-
itis, or death and need emergent antimicrobial treatment and possible surgical
debridement [11, 13].
Though the diagnosis of endometritis is clinical, some laboratory tests such as a
complete blood count (CBC) may be useful and show an elevated white blood cell
count with neutrophilia and a left shift. However, this is non-specic, and endome-
tritis cannot be ruled out if all laboratory tests are unremarkable. Certain imaging
tests may be useful to rule out other causes of postpartum fever and abdominal pain.
Ultrasound can diagnose retained products of conception and infected intrauterine
blood or uid collections [14, 15]. In endometritis, ultrasound may show a
S. van Terheyden et al.
117
thickened, heterogeneous endometrium or uid collection in the uterus; however,
these can also be normal postpartum ndings [6, 10]. Computed tomography (CT)
may show an enlarged uterus, endometrial uid, and/or gas, all of which are non-
specic ndings and seen in normal postpartum patients. CT with intravenous con-
trast may be helpful if there is suspicion for a pelvic abscess or necrotizing soft
tissue infection [16].
Treatment of postpartum endometritis depends on the clinical stability of the
patient and the mode of delivery. Most patients, including those who developed
endometritis post-cesarean section, will require admission for intravenous antibiot-
ics. The rst-line choice for intravenous treatment is clindamycin 900mg every 8h
plus gentamicin 5mg/kg every 24h (preferred) or gentamicin 1.5mg/kg every 8h
[17]. This regimen is preferred for patients with normal renal function and no
recorded group B streptococcus (GBS) colonization and is considered the gold stan-
dard. There is data that clindamycin is developing increasing resistance to GBS.For
patients who are known to be colonized with GBS, it is recommended to add ampi-
cillin 2 g every 6 h to the above clindamycin/gentamicin regimen or consider
piperacillin- tazobactam 3.375g intravenous every 6h, or piperacillin-tazobactam
4.5g intravenous every 8h [18]. A small number of patients who had a vaginal
delivery and are very well-appearing may be appropriate candidates for oral antibi-
otics and close outpatient follow-up (within 24–48h). Options for these patients
include amoxicillin-clavulanate 875–125 mg every 12 h or amoxicillin 500 mg
every 8h plus metronidazole 500mg every 8h or doxycycline 100mg every 12h
plus metronidazole 500mg every 12h or levooxacin 500mg every 24h plus met-
ronidazole 500mg every 8h [11, 19] (Table9.1).
Table 9.1 Antimicrobial treatment for postpartum endometritis
Intravenous (IV) regimens Considerations
Clindamycin 900mg IV every 8h
AND
Gentamicin 5mg/kg IV every 24h
(preferred) or 1.5mg/kg IV every 8h
Gold standard for patients with normal renal
function and no GBS colonization
Ampicillin 2g IV every 6h AND the above
clindamycin/gentamicin regimen
Patients with documented or unknown GBS
colonization or if enterococcus suspected
piperacillin- tazobactam 3.375g IV every 6h
OR
piperacillin-tazobactam 4.5g IV every 8h
Oral regimens
Amoxicillin-clavulanate 875–125mg every
12h
Amoxicillin 500mg every 8h
AND
metronidazole 500mg every 8h
Doxycycline 100mg every 12h
AND
metronidazole 500mg every 12h
Doxycycline compatible with breastfeeding for
short time periods
(<3weeks)
Levooxacin 500mg every 24h
AND
metronidazole 500mg every 8h
Levooxacin not recommended for breastfeeding
patients
9 Postpartum Complications: Endometritis, Mastitis, andBreast Abscesses
118
Mastitis
Mastitis is dened as inammation of the breast parenchyma and occurs most com-
monly during lactation. Mastitis affects between 2 and 20% of breastfeeding patients
and typically occurs within the rst 12weeks postpartum [20–22]. During preg-
nancy, the breasts undergo signicant changes. Pre-pregnancy, breasts are mostly
adipose tissue with some glandular tissue interspersed. With hormonal changes
associated with pregnancy, this ratio changes, with the amount of dense, glandular
tissue increasing and the amount of adipose tissue decreasing [23]. The glandular
tissue consists of branching milk ducts that end in alveoli where milk is excreted [21].
Breastfeeding mastitis occurs when milk ducts become obstructed. During lacta-
tion, the ductal lumens can become hyperemic and edematous, leading to narrowing
[24]. Disruption of the ductal microbiomes from genetic factors, breast pumping, or
use of antibiotics or probiotics may also contribute to ductal narrowing [24]. Ductal
narrowing leads to engorgement of the alveoli, resulting in erythema and pain, and
subsequently, breastfeeding mastitis. Breastfeeding mastitis can be infectious or
non-infectious [20–22]. Inammatory (non-infectious) mastitis develops when the
local ductal narrowing leads to increased inammation of the breast tissue. This
typically presents as unilateral breast erythema, pain, and warmth. Patients may also
experience systemic symptoms such as fevers, chills, and malaise [3, 24]. Erythema
may spread to involve the entire breast, and areas of induration may develop.
Approximately 3–11% of patients will develop a breast abscess from untreated lac-
tation mastitis [21].
Breast engorgement, common with pregnancy, may cause a similar presentation
to mastitis in the absence of systemic symptoms. Engorgement typically peaks on
postpartum day 5 and may be uncomfortable for the mother. Vital signs should be
normal, and there are no focal areas of erythema or warmth on breast exam, differ-
entiating engorgement from mastitis [24]. Plugged milk ducts, another common
breast concern postpartum, occur when the milk duct is obstructed, allowing milk to
build up distally. If this plug is unrelieved, a patient may develop mastitis or a galac-
tocele (a buildup of milk that is aseptic) [24]. Other important etiologies for post-
partum breast pain include malignancy (uncommon) and other forms of mastitis
such as idiopathic granulomatous mastitis and periductal mastitis [21].
Risk factors for the development of mastitis include overstimulation of milk pro-
duction (more common with breast pumping and hyperlactation) and the use of
antibiotics, which causes an imbalance of the normal skin ora. Nipple trauma,
more common in babies with latching issues, is also associated with an increased
risk of mastitis, likely due to the cracked nipple serving as an entry point for bacte-
ria. Furthermore, breast inammation may also make the nipple more prone to
cracking [25]. Nipple shields also predispose women to mastitis as they can be a
surface where bacteria can adhere and then become transmitted [25]. Primiparity,
poor maternal nutrition, history of prior mastitis, and wearing tightly tted clothing
are also risk factors for the development of mastitis [20, 25].
On exam, patients with mastitis will have unilateral breast erythema, pain, and
warmth. Systemic symptoms such as fevers, chills, or generalized malaise may also
S. van Terheyden et al.
119
be present. Depending on the severity of the infection, patients may be febrile,
tachycardic, or even hypotensive, although this is less common [26]. If not properly
treated, mastitis can spread to involve the entire breast.
Lactation mastitis typically does not require laboratory testing or imaging for
diagnosis, as it is a clinical diagnosis. If bloodwork is obtained, patients may have
an elevated white blood cell count, signifying an active inammatory or infectious
process. If there is concern for a breast abscess, a breast ultrasound should be
obtained [27].
Recommendations for the treatment of mastitis have changed over time, tending
to favor initial watchful waiting over immediate antibiotic prescription. For patients
with mild systemic symptoms and focal breast erythema without induration or
edema, careful monitoring for the rst 24 to 36 h of symptoms is favored over
immediate antibiotic use [20, 21, 26]. In addition to careful monitoring, patients
with mild symptoms should continue physiologic breastfeeding (either feeding
infants as needed or expressing breast milk) and use nonsteroidal anti-inammatory
medications for symptom management. Patients should be careful not to overstimu-
late the affected breast tissue through excessive pumping or expression, as this can
worsen symptoms. Careful breast massage is recommended while avoiding causing
additional trauma to the breast or nipple, which could worsen symptoms and pos-
sibly lead to abscess formation [26]. Furthermore, warm and cool compressions,
depending on patient preference, can be helpful for symptomatic management as
well. If symptoms do not improve after a short period of watchful waiting, or if
patients have more severe systemic symptoms on presentation, antibiotics should be
administered.
Infectious mastitis is typically caused by Staphylococcus (namely Staph aureus)
and Streptococcus. Antibiotic selection should be effective against these two com-
mon pathogens. Typically, dicloxacillin or cephalexin dosed for 10–14 days is
appropriate. Both medications are safe for breastfeeding babies, and patients should
continue to breastfeed throughout the treatment course [21]. If there is a concern for
methicillin-resistant S aureus, either by patient history of colonization or symptoms
on presentation, antibiotics should be tailored to be effective against MRSA.Typically,
clindamycin or trimethoprim/sulfamethoxazole for 10 to 14days is prescribed [20].
Trimethoprim/sulfamethoxazole should be avoided in mothers who are breastfeed-
ing premature infants, infants with hyperbilirubinemia or if there is a history of
glucose-6-phosphate-dehydrogenase deciency [26] (Table9.2).
Parenteral antibiotics are necessary for patients with severe systemic symptoms
(tachycardia, hypotension, persistent fevers) or patients who have failed to improve
or who have worsened despite 5–6days of oral antibiotics. The regimen should be
effective against both Gram-positive and Gram-negative organisms. Vancomycin in
addition to either ceftriaxone or piperacillin/tazobactam is recommended. These
patients, if showing signs of sepsis, may require resuscitation as well, in the form of
intravenous uids and possibly vasopressors.
It is important to counsel the patient on how to prevent recurrent mastitis in the
future. Patients should be advised to avoid hyperlactation, which can spur mastitis
recurrence. This includes avoiding excessive breast pumping and medications or
9 Postpartum Complications: Endometritis, Mastitis, andBreast Abscesses
120
Table 9.2
Antimicrobial treatment for lactation mastitis [21]
Oral regimens Considerations
Dicloxacillin 500mg PO every 6h for 10–14days First line treatment
Cephalexin 500mg PO every 6h for 10–14days
Augmentin 875/125mg PO every 12h for 10–14days
Clindamycin 300mg PO every 6h for 10–14days Penicillin-allergic patients
Patients MRSA concerns/colonization
Trimethoprim/sulfamethoxazole 800mg/160mg PO
every 12h 10–14days
Penicillin-allergic patients
Patients with MRSA concerns/
colonization
Caution in G6PD, infants with
hyperbilirubinemia, infants <1month
of age
IV regimens Considerations
Vancomycin 20–35mg/kg (actual body weight) IV up
to 3000mg, then 15–20mg/kg (actual body weight)
IV every 8–12h
AND
Ceftriaxone 2g IV every day
OR
Piperacillin/tazobactam 3.375mg IV every 6h
supplements that increase lactation. Furthermore, encouraging direct breastfeeding
may be protective as the baby’s mouth ora may create a more balanced microbiota
environment [20]. Breast pumps should be carefully cleaned with soap and water or
placed in the dishwasher [26].
With persistent hyperlactation, patients can experience recurrent mastitis, which
is managed slightly differently than an initial presentation of infectious mastitis. In
this patient population, a clean catch breast milk culture is recommended to assist
with tailoring antibiotics. Care should be taken to ensure the sample is placed in a
sterile container, and sterile gloves must be used to express milk from the breast.
Patients should be discharged home on antibiotics that are sensitive to Staphylococcus
and Streptococcus while they await culture sensitivities.
Subacute mastitis is suspected with weeks of aching, often shooting breast pain,
and no evidence of erythema, induration or systemic symptoms on exam. The nip-
ple may have a biolm or blebbing, which suggests an underlying infectious pro-
cess [24]. A sterile breast milk culture should be obtained, as well, for this subset of
patients. Patients should initially be started on empiric antibiotics until the breast
milk culture results with antibiotic sensitivities.
Lactational Breast Abscess
A breast abscess is a walled-off collection of pus that can develop secondary to
mastitis or from a sterile galactocele that becomes infected. The incidence of breast
abscesses is low in lactating women (approximately 0.4–3%) but has signicant
maternal morbidity. For most women, the development of a breast abscess leads to
S. van Terheyden et al.
121
Fig. 9.1 Ultrasound image
of breast abscess in
lactating woman showing
mild skin thickening
measuring 4mm (bracket),
edematous hyperechoic
broglandular tissue
(chevrons) and a discrete
complex uid collection
measuring 4.4cm
(asterisk). (From Bhatt
etal. [30])
interruption or discontinuation of breastfeeding. Furthermore, treatment of breast
abscesses with incision and drainage can lead to undesirable cosmetic outcomes due
to scarring and wound granulation [28, 29]. Patients with breast abscesses may pres-
ent with the typical signs of mastitis such as breast pain, warmth, and redness, plus
an indurated or uctuant mass. Lactational breast abscesses are frequently located
peripherally on the breast, with the most common site being the upper outer quad-
rant [29]. The diagnosis is clinical and can be conrmed with ultrasound, which will
demonstrate a discrete uid collection with surrounding edema [30] (Fig.9.1).
Breast abscesses require drainage in addition to antibiotics. Drainage can occur
either by traditional incision and drainage (I&D) or through needle aspiration using
ultrasound guidance. I&D is performed using a scalpel to cut open the abscess and
release the infected uid (pus). Needle aspiration is a less invasive procedure per-
formed by inserting a needle (18–19 gauge) into the cavity of the breast abscess and
using a syringe to draw out the pus [31]. Repeat or serial aspiration may be required.
A recent review of 25 studies comparing needle aspiration to I&D found that needle
aspiration was associated with a shorter mean healing time, higher success rate,
acceptable cosmetic results, minimal effects on breastfeeding, and acceptable
patient satisfaction, particularly for women with smaller breast abscesses (<3–5cm
in diameter) [29]. Patients with larger abscesses (>5cm diameter or >50mL of pus
aspirated) or with abscesses near the center of the breast have higher rates of failure
of needle aspiration [32].
Following drainage, well-appearing patients without severe systemic symptoms
and who are able to tolerate oral antibiotics can be safely discharged home with
close follow-up either with their obstetrician or primary care physician. In patients
with recurrent or large abscesses, consultation or follow-up with a breast surgeon
may also be warranted.
9 Postpartum Complications: Endometritis, Mastitis, andBreast Abscesses
122
Summary
Following delivery, women remain at risk for developing pregnancy-related compli-
cations including endometritis, mastitis, and breast abscesses and often present to
an emergency department for evaluation. Postpartum infections such as lactational
mastitis are typically mild and can be managed conservatively as outpatients. Breast
abscesses and endometritis are more severe and can lead to fulminant sepsis requir-
ing intravenous antibiotics and operative source control. The route of delivery is the
most important risk factor for developing postpartum endometritis, with cesarean
deliveries having the highest risk. Emergency clinicians must be prepared to
promptly recognize and treat common postpartum infections and their
complications.
Key Points
• Patients are at much higher risk for developing postpartum endometritis follow-
ing cesarean delivery.
• Most patients with postpartum endometritis will require admission for IV
antibiotics.
• Mastitis is common in breastfeeding patients and can usually be managed
conservatively.
• Lactational breast abscesses require drainage plus antimicrobial treatment.
• Ultrasound-guided needle aspiration is an appropriate rst-line treatment for
most lactational breast abscesses.
References
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© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
J. Borhart (ed.), Emergency Department Management of Obstetric
Complications, https://doi.org/10.1007/978-3-032-10261-4_10
10
Management ofPostabortion
Complications
MariaLawrynowicz andJeffreyUribe
Introduction
Induced abortions performed under the supervision of a physician are safe outpa-
tient procedures. In the United States in 2021, there were approximately 11.6 abor-
tions per 1000 women aged 15–44 years [4]. In 2020, six women died of
complications from legally induced abortion [4]. According to the Center for
Disease Control (CDC), the national case-fatality rate in 2013-2020 for legal
induced abortions was 0.45 per 100,000 reported legal abortions [4]. Major compli-
cations or those requiring admission, transfusion, or surgery are rare and quoted as
low as 0.16% [1]. Most induced abortions were medical (53.0%) performed at
≤9 weeks’ gestation followed by surgical (37.6%) at ≤13 weeks’ gestation [4].
Surgical abortions at >13weeks gestation (6.4%) and medical abortions >9weeks’
gestation (3%) were both relatively uncommon [4]. While emergency department
(ED) visits after abortion are rare, representing only 0.1% of all ED visits in women
15 to 49years of age (2009-2013), certain populations are overrepresented. 27.5%
of patients were from zip codes in the lowest national income quartile, while 20.5%
presented from the highest national income quartile [2]. Those seeking postabortion
care in the ED were most frequently Medicaid users (45.2%), followed by private
insurance (31.4%) and self-pay (17.1%) [2].
Medication abortions in the United States are primarily performed before 70days
(10weeks) gestation usually with a combined drug regimen [5, 6]. This includes an
initial dose of mifepristone 200mg, which acts as a synthetic progesterone antago-
nist that disrupts pregnancy growth and sensitizes the myometrium to prostaglan-
dins to induce contractions [6, 7] followed by self-administration of misoprostol
800μg buccally in 24–48h [6, 8]. Misoprostol acts as a synthetic prostaglandin
M. Lawrynowicz (*) · J. Uribe
Department of Emergency Medicine, Medstar Washington Hospital Center, Washington, DC,
USA
e-mail: maria.lawrynowicz@medstar.net; jeffrey.uribe@medstar.net
126
analog that induces myometrial contraction [8]. An alternative is taking misoprostol
800 ug either vaginally, sublingually, or buccally every 3h, up to 3 doses [9].
Surgical abortions are considered more effective for pregnancy termination;
however, they are more invasive and pose different risks depending on the timing of
the procedure [10]. First-trimester uterine aspiration often involves treatment with
misoprostol as a cervical ripening agent, followed by mechanical dilation with
sequentially larger cervical dilators [10]. This allows insertion of cannula into the
uterine cavity and vacuum aspiration of fetal tissue. Second-trimester dilation and
evacuation (D&E) is a short procedure (<30min) performed under procedural seda-
tion or general anesthesia [11]. Patients will rst be treated with osmotic dilators
and medications to prepare the cervix. This is followed by mechanical dilation and
uterine evacuation using aspiration, extraction with forceps, or curettage [11].
Management
In evaluating postabortion complications, obtain gestational history, estimated ges-
tational age at time of abortion, details of the procedure, current symptoms, and
comorbidities. For any procedure, obtain date, medical vs. surgical, medications
used, and any complications [12]. If available, contact the facility that performed
the abortion.
ED workup includes laboratories (complete blood count, comprehensive meta-
bolic panel, blood type and screen, coagulation factors, beta-hCG level), pelvic
exam, and initial point- of-care ultrasound to assess for retained products of concep-
tion or free uid. Advanced radiologic ultrasound or computer tomography (CT)
scan may be required to assess for more complex ndings.
Immediate Complications
The most common pharmacologic side effects of medication-assisted abortions are
reported with both mifepristone and misoprostol and include dizziness, headache,
gastrointestinal symptoms, and thermoregulatory effects such as fever, warmth, hot
ashes, or chills [11]. These are usually self-limited and may only require support-
ive care. Moderate-to-severe reactions to misoprostol are less common and include
hypotension, myocardial infarction, pulmonary embolism, anaphylactoid reactions,
and thrombosis [8]. Moderate reactions to mifepristone may present with adreno-
cortical insufciency while severe reactions (<0.01%) include toxic epidermal
necrolysis, anaphylaxis, thromboembolism, and angioedema [7, 13].
Vaginal bleeding is a common and expected immediate complication of induced
abortion. Bleeding can be difcult to quantify but is considered heavy if patients are
soaking through more than 2 pads per hour for 2 consecutive hours. Most bleeding
after misoprostol administration begins within 1–4h with moderate to heavy bleed-
ing within 3–8h [11, 14]. Bleeding is more severe with increased gestational age
and generally improves after passage of fetal tissue. Median duration of mild
M. Lawrynowicz and J. Uribe