OBSTETRICS - Puerperal Infection

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OBSTETRICS:
Puerperal
Infection

PUERPERAL INFECTION:
Introduction
PUERPERAL INFECTION
a general term used to describe any bacterial
infection of the genital tract after delivery
-PAST: constitutes the LETHAL TRIAD of maternal
death, along with preeclampsia and obstetrical
hemorrhage
-PRESENT: maternal deaths from infection have
become uncommon due to effective
antimicrobials (13% of maternal deaths)

Puerperal Fever
Puerperal Fever
-A temperature of 38.0°C or higher in the puerperium
-Common causes of puerperal fever:
1. Genital tract infection
-Cause most persistent fevers after childbirth
2. Breast engorgement
-in 15% of women who don’t breastfeed
-rarely exceeds 39.0°C
3. Pyelonephritis
-fever: first sign of renal infection
-signs and symptoms that follow: costovertebral
angle tenderness, nausea and vomiting

Puerperal Fever
Puerperal Fever
-Common causes of puerperal fever:
4. Respiratory complications after cesarean delivery
-atelectasis: caused by hypoventilation and
best prevented by coughing and deep
breathing on a fixed schedule following
surgery
-fever: follows infection by normal flora that
proliferate distal to obstructing mucus plugs
5. Superficial or deep-venous thrombosis of the legs
-occasionally cause minor temperature
elevations in the puerperium

Uterine Infection
-Postpartum uterine infection has been called
variously endometritis, endomyometritis and
endoparametritis
-Preferred term: metritis with pelvic cellulitis
-because infection does not only involve the
decidua but also the myometrium and parametrial
tissues

Uterine Infection
Predisposing Factors
1. Route of delivery
-single most significant factor for the development of uterine
infection
-25-fold increased infection-related mortality with cesarean versus
vaginal delivery
-manual removal of the placenta increase puerperal metritis 3-fold
-metritis following vaginal delivery is relatively uncommon
RISK FOR METRITIS
Low risk women without complications 1-2%
High risk women due to membrane rupture,
prolonged labor, and multiple cervical exams
5-6%
Women with intrapartum chorioamnionitis 13%

Uterine Infection
1. Route of delivery
-single-dose perioperative prophylaxis is given almost universally at
cesarean delivery
-Risk factors for infection following surgery include:
-prolonged labor
-membrane rupture
-multiple cervical examinations
-internal fetal monitoring
-Increased risk of infection include cesarean delivery for:
-multifetal gestation
-young maternal age
-nulliparity
-prolonged labor induction
-obestiy
-meconium-stained amnionic fluid

Uterine Infection
2. Lower socioeconomic status
3. Anemia and Poor Nutrition
-in very rare cases
4. Previous bacterial colonization if the lower genital
tract with certain microorganisms like:
-Group B streptococcus
-Chlamydia trachomatis
-Mycoplasma hominis
-Ureaplasma urealyticum
-Gardnerella vaginalis

Uterine Infection
Bacteriology
-Most female pelvic infections are caused by bacteria indigenous to
the female genital tract
-Reports show that group A -hemolytic streptococcus may cause
toxic shock-like syndrome and life-threatening infection
-Prematurely ruptured membranes is a prominent risk
-Women in whom group A streptococcal infection was manifested
before, during, or within 12 hours of delivery had a maternal
mortality rate of almost 90% and fetal mortality rate of >50%
-Skin and soft-tissue infections due to community-acquired
methicillin-resistant Staphylococcus aureus—CA-MRSA—have
become common  NOT for puerperal metritis, but for
incisional wound
-Study: A woman with episiotomy cellulitis with CA-MRSA had
hematogenously spread necrotizing pneumonia

Uterine Infection
Common Pathogens
-Infections are polymicrobial which promotes bacterial synergy
-Other factors that promote virulence are hematomas and
devitalized tissue
-The cervix and vagina routinely harbor such bacteria BUT the
uterine cavity is usually sterile before rupture of the amnionic
sac
-The amnionic fluid and uterus commonly become contaminated
with anaerobic and aerobic bacteria as the consequence of
labor and delivery and associated manipulations
-Cultured amnionic fluid obtained at cesarean delivery in women in
labor with membranes ruptured more than 6 hours  all had
bacterial growth and an average of 2.5 organisms was identified
from each specimen

Uterine Infection
Common Pathogens
-Anaerobes included Peptostreptococcus and Peptococcus species,
Bacteroides species and Clostridium species
-Aerobes included Enterococcus, group B streptococcus, and
Escherichia coli
-Chlamydial infections have been implicated in late-onset, indolent
metritis
-When cervical colonization of U. urealyticum is heavy, it may
contribute to the development of metritis
- Threefold risk of puerperal infection in women in whom
bacterial vaginosis was identified in early pregnancy

Uterine Infection
NORMAN FLORA
CERVICOVAGINAL BACTERIA
Cervical Examinations
Internal Monitoring
Prolonged Labor
Uterine incision
INNOCULATION
ANAEROBIC CONDITIONS
Surgical Trauma
Sutures
Devitalized Tissue
Blood and Serum
CLINICAL INFECTION
BACTERIAL PROLIFERATION

Uterine Infection
Aerobes
-Gram-positive cocci — group A, B, and D streptococci,
enterococcus, Staphylococcus aureus, Staphylococcus
epidermidis
-Gram-negative bacteria — Escherichia coli, Klebsiella,Proteus
species
-Gram-variable — Gardnerella vaginalis
Others
-Mycoplasma and Chlamydia species, Neisseria gonorrhoeae
Anaerobes
-Cocci — Peptostreptococcus and Peptococcus species
-Others — Clostridium and Fusobacterium species Mobiluncus
species

Uterine Infection
Bacterial Cultures
-Routine pretreatment genital tract cultures are of
little clinical use and add significant costs
-Routine blood cultures seldom modify care
-Before perioperative prophylaxis: blood cultures
were positive in 13 percent of women with
postcesarean metritis
-Bacteremia in only 5 percent of almost 800 women
with puerperal sepsis.

Pathogenesis
-Puerperal infection following vaginal delivery primarily
involves:
-placental implantation site
-decidua and adjacent myometrium
-cervicovaginal lacerations
-The pathogenesis of uterine infection following cesarean
delivery is that of an infected surgical incision
-Bacteria that colonize the cervix and vagina gain access to
amnionic fluid during labor and invade devitalized uterine
tissue postpartum
-Parametrial cellulitis next follows with infection of the pelvic
retroperitoneal fibroareolar connective tissue
-With early treatment, infection is contained within the
paravaginal tissue but may extend deeply into the pelvis

Clinical Course
-Fever is the MOST IMPORTANT criterion for the diagnosis of postpartum
metritis
-Degree of fever is believed proportional to the extent of infection and sepsis
syndrome
-Temperatures commonly are 38 to 39°C
-Chills that accompany fever suggest bacteremia
-Women usually complain of:
-abdominal pain
-parametrial tenderness on abdominal and bimanual examination
-offensive odor of lochia (but many women have foul-smelling lochia
without evidence for infection)
*those due to group A -hemolytic streptococci, are frequently
associated with scanty, odorless lochia
-Leukocytosis may range from 15,000 to 30,000 cells/L
*cesarean delivery itself increases the leukocyte count

Treatment
-Mild metritis following vaginal delivery: outpatient treatment with an oral
antimicrobial agent is usually sufficient
-Moderate to severe infections: intravenous therapy with a broad-spectrum
antimicrobial regimen is indicated
-Improvement follows in 48 to 72 hours in nearly 90% of women treated
with one of several regimens
-Persistent fever after 48 to 72 hours mandates a careful search for causes
of refractory pelvic infection including:
-Parametrial phlegmon—an area of intense cellulitis
-Abdominal incisional or pelvic abscess
-Infected hematoma
-Septic pelvic thrombophlebitis
-Antimicrobial-resistant bacteria or drug side effects  SELDOM
-Patient may be discharged home after she has been afebrile for at least 24
hours and further oral antimicrobial therapy is NOT needed

Treatment
Choice of Antimicrobials
-Although therapy is empirical, initial treatment
following cesarean delivery is directed against
most of the mixed flora which typically cause
puerperal infections
-Anaerobic coverage is included for infections
following cesarean delivery
-Such broad-spectrum antimicrobial coverage is
often not necessary to treat infection following
vaginal delivery  respond to regimens such as
ampicillin plus gentamicin

Treatment
Antimicrobial Regimens for Pelvic Infection
Following Cesarean Delivery
Regimen Comments
Clindamycin 900 mg + gentamicin 1.5
mg/kg, q8h intravenously
"Gold standard" 90–97% efficacy, once-
daily gentamicin dosing acceptable
+
Ampicillin added to regimen with sepsis
syndrome or suspected enterococcal
infection
Clindamycin + aztreonam Gentamicin substitute with renal
insufficiency
Extended-spectrum penicillins Piperacillin, ampicillin/sulbactam
Extended-spectrum cephalosporins Cefotetan, cefoxitin, cefotaxime
Imipenem + cilastatin Reserved for special indications

Treatment
-Clindamycin-gentamicin – 95% response rate, and this regimen
-still considered by most to be the standard by which others are
measured
-Enterococcal infections: add ampicillin to the clindamycin-gentamicin
regimen, either initially or if there is no response by 48 to 72 hours
-Serum gentamicin levels be periodically monitored or only with altered
renal function
*Once-daily dosing has a cure rate similar to 8-hour dosing
-Gentamicin: potential nephrotoxicity and ototoxicity in the event of
diminished glomerular filtration
-Alternatives in altered renal function:
-Clindamycin and a second-generation cephalosporin
-Clindamycin and aztreonam (monobactam with aminoglycoside-like
action)

Treatment
-The spectra of -lactam antimicrobials include activity against many anaerobic
pathogens and are inherently safe and free of major toxicity except for allergic
reactions
-cephalosporins such as cefoxitin, cefotetan, and cefotaxime
-extended-spectrum penicillins such as piperacillin, ticarcillin, and mezlocillin
-The -lactamase inhibitors, clavulanic acid, sulbactam, and tazobactam, have been
combined with ampicillin, amoxicillin, ticarcillin, and piperacillin to extend
spectra of lactams
-Metronidazole has superior in vitro activity against most anaerobes
-Given with ampicillin and an aminoglycoside to provide coverage against most
organisms encountered in serious pelvic infections
-Imipenem is a carbapenem that has broad-spectrum coverage against most
organisms associated with metritis
-Used with cilastatin, which inhibits renal metabolism of imipenem
*Combination is effective in most cases of metritis, it seems reasonable
from both a medical and an economic standpoint to reserve it for more serious
infections

Prevention
Perioperative Antimicrobial Prophylaxis
-Administration of antimicrobial prophylaxis at the time of cesarean
delivery  reduce the rate of pelvic infection by 70 to 80
*Observed benefit applies to both elective and nonelective
cesarean delivery and also includes a reduction in abdominal
incisional infections
-Single-dose prophylaxis with ampicillin or a first-generation
cephalosporin is ideal, and both are as effective as broad-spectrum
agents or a multiple-dose
-Extended-spectrum prophylaxis with azithromycin added to standard
single-dose prophylaxis showed a significant reduction in
postcesarean metritis
-Women known to be colonized with methicillin-resistant
Staphylococcusaureus—MRSA—are given vancomycin in addition
to a cephalosporin

Prevention
Perioperative Antimicrobial Prophylaxis
-Infection rate is lowered more if the selected antimicrobial is given
before the skin incision compared with cord clamping
-A number of locally applied antimicrobials have been evaluated to
prevent puerperal infection
-Intrapartum vaginal irrigation with chlorhexidine did not reduce
the incidence of postpartum infection
-Conflicting studies on use of Povidone-iodine:
-vaginal irrigation before cesarean delivery had no effect on
the incidence of fever, metritis, or abdominal incisional infection
-Preoperative vaginal cleansing with povidone-iodine had
a significantly lower infection rate following cesarean
delivery—7 versus 14 percent
-Metronidazole gel: reduction in rate of metritis but no significant
effect on febrile morbidity or wound infections

Prevention
Treatment of Vaginitis
-Prenatal treatment of asymptomatic vaginal infections has
not been shown to prevent postpartum pelvic infections
-No beneficial effects for women treated for asymptomatic
bacterial vaginosis
-Similar postpartum infection rate in women treated for 2nd
trimester asymptomatic Trichomonas vaginalis infection
compared with that of placebo-treated women

Prevention
Operative Technique
-Allowing the placenta to separate spontaneously compared with
removing it manually lowers the risk of infection
-Changing gloves by the surgical team after placental delivery DOES
NOT lower infection rates
-Exteriorizing the uterus to close the hysterectomy may decrease
febrile moridity
-Single versus 2-layer uterine closure: no difference in
postoperative infection rate
-Closure versus Non-closure of Peritoneum: no effect on infection
rates
-Closure of subcutaneous tissue in obese women: does NOT lower
infection rate but LOWERS incidence of wound separation

Complications of Pelvic Infections
Wound Infection
-When prophylactic antimicrobials are given, incidence of
abdominal incisional infections following Cesarean delivery is
less than 2%
-Wound infection is a common cause of persistent fever in women
treated for metritis
-Risk factors:
-Obesity
-Diabetes
-Corticosteroid therapy
-Immunosuppression
-Anemia
-Hypertension
-Inadequate hemostasis with hematoma formation

Wound Infection
-Incisional abscesses that develop following cesarean delivery
usually cause fever or cause persisting fever beginning on the 4th
day – may be accompanied by wound erythema and drainage
-Treatment for abscess include antimicrobials and surgical
drainage, with careful inspection to ensure that fascia is intact
-Wound care given 2-3 times daily: secondary en bloc closure at 4-
6 days of tissue involved in superficial wound infection
-After closure: polypropylene or nylon suture of appropriate gauge
enters 3 cm from one wound edge  crosses the wound to
incorporate the full wound thickness  emerges 3 cm from the
other wound edge – placed in series to close the opening
-Sutures may be removed on postprocedural day 10

Wound Dehiscence
-Disruption or Dehiscence refers to separation of the fascial
layer
-Requires secondary closure of the incision in the operating
room
-Most disruptions manifested on 5th postoperative day and
is often accompanied by a serosanguineous discharge
-May be associated with concurrent fascial infection and
tissue necrosis

Necrotizing Fasciitis of Abdominal Wall Incisions
-Uncommon, severe wound infection with necrosis associated with
high mortality
-may involve abdominal incisions, or may complicate episiotomy or
other perineal lacerations
-Risk factors: Diabetes, Obesity, Hypertension
-Usually are polymicrobial and are caused by organisms that
comprise normal vaginal flora
-Can also be caused by single virulent bacterial species such as
group A β-hemolytic streptococcus
-Treatment consists of broad-spectrum antibiotics along with
prompt fascial debridement until healthy bleeding tissue is
encountered
-In extensive resection, synthetic mesh may be required

Peritonitis
-unusual to develop following cesarean delivery
-invariably preceded by metritis and uterine incisional necrosis and
dehiscence
-may be due to:
-inadvertent bowel injury at cesarean delivery
-after rupture of parametrial or adnexal abscess
-vaginal delivery (very rare)
-Abdominal rigidity MAY NOT be prominent with puerperal peritonitis
because of abdominal wall laxity from pregnancy
-Severe pain may be experienced, but FIRST SYMPTOM is frequently
adynamic ileus
-Bowel distention may develop
-Treatment: antimicrobial treatment alone may suffice for infections that
begin with an intact uterus and extend to peritoneum
-surgical treatment is for peritonitis caused by uterine incisional necoris or
bowel perforation

Adnexal Infections
-Ovarian abscess rarely develops in the puerperium
-Presumed to be caused by bacterial invasion through a rent
in the ovarian capsule
-Usually unilateral
-Present 1-2 weeks after delivery
-Rupture is common and peritonitis may be severe

Parametrial Phlegmon
-Phlegmon: an area of induration within the leaves of the
broad ligament in those with parametrial cellulitis
-Develops following cesarean delivery in women with
metritis
-Considered when fever persists after 72 hours despite IV
antibiotics
-Phlegmons are usually unilateral, frequently limited to the
parametrial area at the base of the broad ligament
-In intense cases, cellulitis extends along natural lines of
cleavage – most common of which is laterally along broad
ligament with tendency to extend to pelvic sidewall
-Posterior extension may involve rectovaginal septum,
producing a firm mass on the cervix

Parametrial Phlegmon
-Severe cellulitis of uterine incision may lead to
necrosis and separation
-Puerperal metritis with cellulitis: typically a
retroperitoneal infection  evidence of peritonitis
suggests possibility of uterine incisional necrosis,
bowel injury, or other lesions
-Treatment: broad-spectrum antimicrobial regimen
*Fever resolves in 5-7 days but may last longer
-surgery is reserved for uterine incisional necrosis
-uterine debridement and resuturing are feasible

Imaging Studies
-Persistent puerperal infections can be evaluated using
computed tomography (CT) or magnetic resonance (MR)
imaging
-Uterine incisional dehiscence is sometimes suspected by CT
scanning images but these must be interpreted within the
clinical context because apparent uterine incisional
defects thought to represent edema can be seen even on
images after uncomplicated cesarean delivery

Pelvic Abscess
-Rarely, a parametrial phlegmon suppurates, forming a
fluctuant broad ligament mass that may point above the
inguinal ligament
-Abscesses may dissect:
-anteriorly - amenable to CT-directed needle drainage
-posteriorly to the rectovaginal septum - surgical drainage
is easily effected by colpotomy incision
-Psoas abscess: rare, may require percutaneous drainage
despite antimicrobial therapy

Septic Pelvic Thrombophlebitis
-common complication in the preantibotic era
-Pathogenesis: puerperal infection may extend along venous routes
and cause thrombosis
-Lymphangitis often coexists
-Ovarian veins may become involved because they drain the upper
uterus and therefore, the placental implantation site
-Puerperal septic thrombophlebitis is likely to involve one or both
ovarian venous plexuses
-Clot may extend into the inferior vena cava and occasionally to the
renal vein

Septic Pelvic Thrombophlebitis
-Incidence:
-1:9000 - following vaginal delivery
-1:800 - with cesarean delivery
-Overall incidence of 1:3000
-Management:
-Women with septic thrombophlebitis usually have clinical
improvement of pelvic infection with antimicrobial treatment but
they continue to have fever
-Occasionally there is pain in one or both lower quadrants but
patients are usually asymptomatic except for chills.
-Diagnosis can be confirmed by either pelvic CT or MR imaging
-Before imaging methods were available, the heparin challenge test
was advocated

Infections of the Perineum, Vagina, and Cervix
-Episiotomy infections are NOT common because the operation is
performed much less frequently now than in the past
-With infection, dehiscence is a concern - 0.5% of episiotomy wounds
dehisced and 80% of these were due to infection
-Infection of a fourth-degree laceration is likely to be more serious
-Although life-threatening septic shock is rare, it may still occur as a
result of an infected episiotomy
-Pathogenesis and Clinical Course:
-Factors associated to episiotomy dehiscence:
-infection
-coagulation disorders
-smoking
-HPV infection

-Common symptoms of episiotomy dehiscence:
-Local pain 65%
-Purulent discharge 65%
-Fever 44%
-dysuria, with or without urinary retention
-Edema, ulceration and exudation of the vulva

-Vaginal lacerations may become infected directly or by extension
from the perineum  mucosa becomes red and swollen and may
then become necrotic and slough
-Parametrial extension may result in lymphangitis.
-Cervical lacerations are common but seldom are noticeably
infected and may manifest as metritis
-Deep lacerations which extend directly into the tissue at the base
of the broad ligament may become infected and cause
lymphangitis, parametritis, and bacteremia

-Treatment:
-Infected episiotomies are managed like other infected surgical
wounds
-Drainage is established
-Sutures are removed
-Infected wound debrided
-Cellulitis but NO purulence: broad-spectrum antimicrobial therapy
with close observation
-Dehiscence: local wound care is continued along with intravenous
antimicrobials
-Early repair after infection subsided is advocated - average
duration of 6 days from dehiscence to episiotomy repair
-Rarely, intestinal diversion may be required to allow healing

-Technique for Early Repair:
Before performing early repair, diligent preparation is essential
PREOPERATIVE PROTOCOL for Early Repair of Episiotomy Dehiscence
1. Open wound, remove sutures, begin intravenous antimicrobials
2. Wound care
-Sitz bath several times daily or hydrotherapy
-Adequate analgesia or anesthesia—regional analgesia or general anesthesia
may be necessary for the first few debridements
-Scrub wound twice daily with a povidone-iodine solution
-Debride necrotic tissue
3. Closure when afebrile and with pink, healthy granulation tissue
4. Bowel preparation for fourth-degree repairs

-Technique for Early Repair:
-Most important is that the surgical wound must be properly
cleaned and free of infection
-Surface of the episiotomy wound free of infection & exudate and
covered by pink granulation tissue  secondary repair can be done
-Tissue must be adequately mobilized, with special attention to
identify and mobilize the anal sphincter muscle
-Secondary closure of the episiotomy is accomplished in layers
-Postoperative care includes:
-local wound care
-low-residue diet
-stool softeners
-nothing per vagina or rectum until healed

-Necrotizing Fasciitis of Perineal and Vaginal Wound Infections
-Fatal complication of perineal and vaginal wound infections is deep
soft-tissue infection involving muscle and fascia
-Common in women with diabetes or those immunocompromised
but may develop in otherwise healthy women
-Microbiology is similar to those of other pelvic infections, as well
as necrotizing fasciitis of the abdominal wall incision
-Necrotizing fasciitis of the episiotomy site may involve any of the
several superficial or deep perineal fascial layers  may extend to
the thighs, buttocks, and abdominal wall
-Early Postpartum: Group A β-hemolytic streptococci infections
typically do NOT cause symptoms until 3 to 5 days after delivery

-Necrotizing Fasciitis of Perineal and Vaginal Wound Infections
-If myofasciitis progresses, the woman may become ill from
septicemia  profound hemoconcentration from capillary leakage
with circulatory failure commonly occurs  death
-Early diagnosis, surgical debridement, antimicrobials, and intensive
care are of paramount importance in the successful treatment of
necrotizing soft-tissue infections
-Surgery includes extensive debridement of all infected tissue, leaving
wide margins of healthy tissue including extensive vulvar
debridement with unroofing and excision of abdominal, thigh, or
buttock fascia
-Mortality is virtually universal without surgical treatment, and rates
approach 50% even if extensive debridement is performed

Toxic Shock Syndrome
-Acute febrile illness with severe multisystem derangement has a
case-fatality rate of 10-15%
-Presents usually with:
-Fever
-Headache
-Mental confusion
-Diffuse macular erythematous rash
-Subcutaneous edema
-Nausea and vomiting
-Watery diarrhea
-Marked hemoconcentration
-Renal failure followed by hepatic failure, disseminated intravascular
coagulation, and circulatory collapse may follow in rapid sequence

-During recovery, the rash-covered areas undergo desquamation
-Staphylococcus aureus has been recovered from almost all afflicted
persons specifically, a staphylococcal exotoxin, termed toxic
shock syndrome toxin-1
-TSST-1—causes the clinical manifestations by provoking profound
endothelial injury
-A very small amount of TSST-1 has been shown to activate 5-30%
of T cells to create a "cytokine storm”
-Other possible causes: Clostridium sordellii colonization, group A β-
hemolytic streptococcal infection (more virulent serotypes: M1,
M3)

-Delayed diagnosis and treatment may be associated with fetal or
maternal mortality
-Principal therapy for toxic shock is supportive, while allowing
reversal of capillary endothelial
-Antimicrobial therapy to include staphylococcal and streptococcal
coverage is given
-With evidence of pelvic infection, antimicrobial therapy must also
include agents used for polymicrobial infections
-Women with these infections often require extensive wound
debridement and possibly hysterectomy

OBSTETRICS - Puerperal Infection

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