17 CME REVIEWARTICLE Volume 62, Number 6

OBSTETRICAL AND GYNECOLOGICAL SURVEY

Copyright © 2007
by Lippincott Williams & Wilkins

CHIEF EDITOR’S NOTE: This article is part of a series of continuing education activities in this Journal through which a total
of 36 AMA/PRA Category 1 CreditsTM can be earned in 2007. Instructions for how CME credits can be earned appear on the
last page of the Table of Contents.

Puerperal Pyrexia: A Review. Part II

Dushyant Maharaj, MBBS, Dip Tert Teach, FCOG (SA), FRANZCOG
Senior Lecturer, Department of Obstetrics and Gynecology, Wellington School of Medicine, University of
Otago, Wellington. New Zealand; and Consultant, Wellington Women’s Hospital, Wellington, New Zealand

Puerperal pyrexia and sepsis are among the leading causes of preventable maternal morbidity
and mortality not only in developing countries but in developed countries as well. Most postpartum
infections take place after hospital discharge, which is usually 24 hours after delivery. In the
absence of postnatal follow-up, as is the case in many developing countries, many cases of
puerperal infections can go undiagnosed and unreported. Besides endometritis (endomyometritis
or endomyoparametritis), wound infection, mastitis, urinary tract infection, and septic thrombo-
phlebitis are the chief causes of puerperal infections. The predisposing factors leading to the
development of sepsis include home birth in unhygienic conditions, low socioeconomic status,
poor nutrition, primiparity, anemia, prolonged rupture of membranes, prolonged labor, multiple
vaginal examinations in labor, cesarean section, obstetrical maneuvers, retained secundines within
the uterus and postpartum hemorrhage. Maternal complications include septicemia, endotoxic
shock, peritonitis or abscess formation leading to surgery and compromised future fertility. The
transmissions of infecting organisms are typically categorized into nosocomial, exogenous, and
endogenous. Nosocomial infections are acquired in hospitals or other health facilities and may
come from the hospital environment or from the patient’s own flora. Exogenous infections come
from external contamination, especially when deliveries take place under unhygienic conditions.
Endogenous organisms, consisting of mixed flora colonizing the woman’s own genital tract, are
also a source of infection in puerperal sepsis. Aseptic precautions, advances in investigative tools
and the use of antibiotics have played a major role in reducing the incidence of puerperal infections.
Part II of this review describes the best management of wound infection, pelvic abscess, episiot-
omy infection, thrombophlebitis, mastitis, urinary tract infection, and miscellaneous infections.
Target Audience: Obstetricians & Gynecologists, Family Physicians
Learning Objectives: After completion of this article, the reader should be able to recall that world wide
puerperal sepsis is a leading cause of maternal mortality, state that many of the predisposing factors are
preventable, explain that both nosocomial infections as well as exogenous infections are serious factors,
and relate that septic techniques and antibiotics can play a major role in reducing the incidence of
puerperal infections.

The basic clinical approach to prevention, diagnosis,
and treatment of puerperal sepsis has not changed;
however, recent technological advances have con-
tributed to improving access and increasing the effi-
The author has disclosed that he has no financial relationships
with or interests in any commercial companies pertaining to this
educational activity.
Lippincott Continuing Medical Education Institute, Inc. has
identified and resolved all faculty conflicts of interest regarding
this educational activity.
400
ciency of infection management. Current technology
mostly relates to developments in the method of
administration of antiseptics and antibiotics, the use
of equipment for infection control, and the formula-
tion of clinical, surgical, and laboratory-based pro-
cedures, techniques, and protocols (Table 1).
Reprint requests to: D. Maharaj, Department of Obstetrics and
Gynecology, Wellington School of Medicine, University of Otago,
PO Box 7343 Wellington South 6021, New Zealand. E-mail:
dean.maharaj@otago.ac.nz.
 Puerperal Pyrexia. Part II Y CME Review Article 401

TABLE 1
Strategies for prevention and treatment of puerperal sepsis
Methods Standard
General Hand-cleansing agents*
Sharps disposal and systems to reduce horizontal
transmission of infections
Use of disposable supplies and equipment
Antibiotics Prophylactic use of antibiotics for cesarean section
Prophylactic use of antibiotics for preterm prelabor
rupture of membranes
Therapeutic treatment with antibiotics for
established infections
Nutritional supplements
Protocols and procedures Surgical drainage of abscesses
Clinical audit and monitoring methods
Rapid microbiological diagnostic techniques
Infection prevention procedures and protocols
Ionotropic support & fluid replacement for treatment
of septic shock
*Italics indicate relatively new technological developments.
Modified from Hussein J, Fortney JA. Puerperal sepsis and maternal mortality: what role can new technologies play? Int J Gynecol
Obstet 2004;85:S52–S61, Copyright ©2004, with permission from Elsevier.
Controversial
Vaginal, peritoneal and uterine installation of
antiseptic preparations
Lubricant to reduce birth trauma
Vaginal application of antibiotics
Different antibiotic combinations
Nitroglycerine for septic shock
Vitamin A
Zinc
Routine wound drainage at cesarean section
Ultrasound, computed tomography, magnetic
resonance angiography for diagnosis
Training of traditional birth attendants
Antenatal screening of genital tract infections
in asymptomatic women viz. endocervical
and high vaginal swabs
Type of suture material used

The current literature describes 2 main techniques
for puerperal sepsis prevention. The first, hand hy-
giene, is the most important component of infection
control, and can be achieved by standard hand wash-
ing with soap and water, or a hand-cleansing agent
that obviates the need for water and for hand drying.
This hand rub, containing alcohol and antiseptics, has
been studied for use in developed countries and
found to be microbiologically effective with few side
effects (1,2). The second technique, intravaginal ap-
plication of antiseptics such as chlorhexidine and
iodine, has also been proposed for routine use before
labor or cesarean delivery to reduce maternal and
neonatal postpartum infections (3). However, the ef-
ficacy of vaginal preparation with antiseptics is not
universally accepted (4,5).
Antibiotics are traditionally used for treating in-
fections and are recommended for prophylactic use
during elective and nonelective cesarean section. A
systematic review of 81 trials from developed and
developing countries showed that antibiotic use con-
sistently reduced the incidence of puerperal infec-
tions (6). In addition to systemic administration of
antibiotics, this review included studies comparing
irrigation of the peritoneal or uterine cavity with
various antibiotic regimens. The authors could not
draw a conclusion on the relative effectiveness of
these local applications of antibiotics. Others have
proposed supplementary administration of antibiotics
in the form of preoperative vaginal instillation of
metronidazole gel (7). Other systematic reviews in-
dicate that the prophylactic administration of antibi-
otics to women with preterm, prelabor rupture of
membranes is recommended to reduce puerperal in-
fection (8). Prophylactic antibiotics in the second and
third trimester of pregnancy are also effective in
reducing postpartum endometritis in “high-risk”
women (i.e., those with previous spontaneous pre-
term delivery, history of low birth weight, prepreg-
nancy weight less than 50 kg, or bacterial vaginosis
in the current pregnancy), although data are insuffi-
cient to recommend the routine use of antibiotics for
pregnant women in general (9).
Surgical interventions during delivery are known
to increase the risk of infection (10,11).
To minimize these risks, improvements to tradi-
tional procedures have been proposed. These include
1) replacement of presurgical hand-scrubbing proto-
cols with alcohol-based hand rubs; 2) routine wound
drainage at cesarean section, which has been tried but
found to be ineffective; and 3) the choice of suture
materials in episiotomy and cesarean section scar
repair, which is believed to affect wound inflamma-
tion and healing. One study has shown that a deriv-
ative of polyglycolic acid (Vicryl Rapid®, Ethicon)
may be superior to catgut in episiotomy repair, but no
402 Obstetrical and Gynecological Survey
conclusive evidence is available with regard to type
of suture material in the prevention of puerperal
sepsis (12–14). The value of antenatal screening of
the genital tract for streptococcal colonization in
asymptomatic women accompanied by use of pro-
phylactic antibiotics antenatally or in the intrapartum
period has been debated (15). Antibiotic administra-
tion during labor appears to be favored, primarily for
its benefits to the newborn rather than the mother
(16). The role of vitamin A and zinc as anti-infective
therapy has been suggested. The investigators con-
cluded that daily low-dose vitamin A given during
the second and third trimesters of pregnancy reduced
the risk of maternal postpartum infections or mortal-
ity in populations of women deficient in vitamin A.
Zinc supplementation was not found to be effective
(17–19).
A common treatment for postpartum endometritis
involves the use of combination antimicrobial cov-
erage, including an aminoglycoside for coverage of
Gram-negative organisms and clindamycin phos-
phate for coverage of Gram-positive and anaerobic
organisms (20). Although regimens effective against
penicillin-resistant anaerobic bacteria (a combination
of gentamicin and clindamycin) are recommended
in systematic reviews, other regimens and proto-
cols are used. Second or third-generation cephalo-
sporins in combination with metronidazole is another
widespread and popular choice (21,22). Irrespective
of which regimen is used it is now recognized that
intravenous therapy for puerperal sepsis need not be
followed routinely with oral therapy (23–25).
Gram staining of uterine cavity fluid postcesarean
section to expedite diagnosis of postpartum endo-
metritis has been proposed (26). An endometrial
culture obtained with a flexible endometrial catheter
(Pipelle®) aids in formulating a diagnosis of endo-
metritis (27). Unfortunately, the difficulty in obtain-
ing an endometrial culture without contamination
from the cervicovaginal canal limit the value of these
particular diagnostic modalities (28). The diagnosis
is therefore made clinically, particularly when risk
factors are prominent. Treatment is initiated on the
assumption that a polymicrobial infection with 2 or 3
organisms exists (27).
Ultrasound, computed tomography, and magnetic
resonance angiography for diagnosis of endometritis
and septic puerperal ovarian thrombosis are areas of
topical research (29).
Clinical response to antibiotic treatment dictates
further management. If there is no improvement,
alternative antibiotic combinations should be used. It
has been widely appreciated for many years among
physicians and microbiologists that blood cultures
are among the most important laboratory tests per-
formed in the diagnosis of serious infections (30,31).
The possibility of other causes as well as hospital
acquired infections due to resistant organisms should
be borne in mind. If there is clinical improvement but
a persistent low-grade fever, the possibility of pelvic
thrombophlebitis, connective tissue disease, or drug
fever should be considered. In the event of deterio-
ration in the patient’s condition, the situation be-
comes life-threatening, and a hysterectomy may be
an option.
WOUND INFECTION
Wound infection occurs in 2% to 16% of women
who have had a cesarean section. This rate is related
to factors such as the length of labor, duration of
internal monitoring, number of vaginal examinations,
and use of antibiotic prophylaxis (32–34). Other risk
factors implicated in the increased incidence of cae-
sarean section wound infections are chorioamnioni-
tis, obesity, prolonged surgical time, and significant
blood loss at surgery (35,36).
Wound infections complicating abdominal deliver-
ies are generally caused by direct contamination by
skin flora or by spread from the amniotic cavity at the
time of surgery. The frequency of infecting organ-
isms varied in different studies, with clostridial in-
fection resulting in cellulitis, myofascial necrosis,
hemolysis, renal failure, and cardiovascular collapse
(32,33,37).
Examination of the wound will reveal erythema,
swelling, tenderness, and a discharge. In wound in-
fections following cesarean section, the integrity of
the fascia must be checked, and any defects repaired
to prevent possible evisceration. Necrotizing fasciitis
must be considered whenever infection of the fascia
is suspected. This is a rare, life-threatening infection
that usually is caused by group A beta-hemolytic
streptococci, Staphylococcus aureus and anaerobic
streptococci, although other organisms may be in-
volved. It is more common in persons with preex-
isting tissue susceptibility, such as persons with
diabetes and those with vascular insufficiency disor-
ders. Mortality rates in these patients are generally
quoted as between 30% and 60% (38). The diagnosis
of necrotic fasciitis can be made if the patient has a
high fever resistant to antibiotics, with associated
systemic toxicity and a hard, “wooden” feel to the
infected area. The infected area quite often has an-
esthetic areas. In the presence of crepitations, bullae,
and an offensive discharge, a clostridial infection
 Puerperal Pyrexia. Part II Y CME Review Article
with possibly necrotizing fasciitis must be consid-
ered, and subcutaneous gas on radiograph will aid in
the diagnosis. In all cases of wound discharge, a
Gram stain and a culture with sensitivity testing
should be performed. Treatment requires surgical
excision of the involved fascia and other necrotic
tissue, appropriate antibiotic use, drainage and irri-
gation. Once the wound is determined to be suffi-
ciently clean, closure by secondary intention may be
undertaken.
PELVIC ABSCESS
Pelvic abscess should be suspected in patients with
persistent spiking fever despite antibiotic coverage
(39). An ultrasound examination or computed tomo-
graphic (CT) scan aids in formulating the diagnosis
(40). Ultrasound may confirm an abscess when fluid
and gas collections are associated with shaggy walls
and fluid in the cul-de-sac. The treatment of choice is
surgical drainage.
EPISIOTOMY INFECTION
Episiotomy infection is usually confined to the skin
and surrounding subcutaneous tissue, and limited by
Camper’s fascia. An infection of the episiotomy site
should be suspected in patients with significant per-
ineal pain, hip pain, or erythema and swelling beyond
the episiotomy site. Pelvic examination may detect
the presence of hematomas or abscesses. If no ab-
scess or extension is suspected, Sitz baths are usually
sufficient treatment. Deeper involvement to Colle’s
and Scarpa’s fascia may result in necrotizing fasciitis
(41). If an abscess is suspected, CT scanning may be
necessary to determine if the abscess is located in the
retroperitoneal or gluteal muscle areas, as severe
infections may spread to the levator ani, lumbosacral
nerve plexus, hip capsule, and retropsoas space
(42,43). Treatment consists of exploration of the
episiotomy, drainage, and debridement. The wound
is then allowed to heal secondarily.
THROMBOPHLEBITIS
Septic pelvic thrombophlebitis is an uncommon
cause of postpartum pyrexia, occurring in 1 in 2000
deliveries (44). The incidence increases to 1% to 2%
among women with postcesarean section endometri-
tis (45). The risk of thrombosis increases during
pregnancy secondary to the prevalent hypercoagula-
ble state. These changes worsen around the puerpe-
rium, particularly after cesarean section (46,47). The
403
entity of septic pelvic thrombophlebitis has evolved
profoundly over the last century. By the end of the
19th century, von Recklinhausen described an entity
in which pelvic infection was characterized by throm-
bosis of one or both ovarian veins while the remain-
ing pelvis was normal, proposing surgical excision as
the therapeutic approach (48).
Reviews by Williams and Miller (49) reported an
average mortality of roughly 50% during the first
quarter of the twentieth century in patients undergo-
ing surgery. In the 1980s, mortality was reported to
be 4.4%. A 1999 study found that, of a total of
44,922 deliveries, 69 patients carried the diagnosis of
prolonged infection. Fifteen patients were found to
have pelvic thrombophlebitis; however, no compli-
cation or death was reported in either group (50).
Septic pelvic thrombophlebitis is more common after
cesarean section than after vaginal delivery (51). The
mechanism of action involves the presence of a hy-
percoagulable state and ascent of infection spreading
from the myometrium to the pelvic and ovarian veins
(49). The pathophysiology of pelvic thrombophlebi-
tis as the progression of a pelvic infection was first
elucidated by Collins (49,52,53). The pathogenesis is
thought to include injury to the intima of the pelvic
vein caused by spreading uterine infection, bactere-
mia, endotoxins, or the trauma of delivery or surgery.
In this setting, Virchow’s triad is completed since
pregnancy is a well-known hypercoagulable state and
there is reduced blood flow in dilated uterine and
ovarian veins during the postpartum period which
causes venous stasis. Phlebographic studies have
demonstrated a left to right venous flow in upright
position, which may explain the dextroprevalence of
ovarian vein thrombosis (49).
Patients often complain of flank and lower abdom-
inal pain, typically described as noncolicky and con-
stant. Pain may be of variable intensity and may
radiate to the groin or upper abdomen, and paralytic
ileus may occur. Frequently, the first sign is a pul-
monary embolus. When thrombophlebitis is recog-
nized early, the risk of pulmonary embolism can be
greatly reduced with appropriate anticoagulant ther-
apy (47). On physical examination, the patient usu-
ally does not appear toxic, there may be tenderness in
the lower abdomen, and an occasional tender abdom-
inal mass described as “rope-” or “sausage-shape”
may rarely be identified. The diagnosis is suspected
when a patient responds poorly to antibiotic treat-
ment of endometritis and a mass is palpable on pelvic
examination. The diagnosis is confirmed by CT of
the pelvis or magnetic resonance imaging (40). When
diagnostic imaging is negative but the diagnosis is
404 Obstetrical and Gynecological Survey
highly suspected, a positive response to a trial of
anticoagulation therapy with heparin supports the
diagnosis.
CT and magnetic resonance imaging (MRI) are
used to provide confirmation of pelvic thrombophle-
bitis. Tomographic criteria for diagnosis include 1)
enlargement of the vein involved, 2) low density
lumen within the vessel wall, and 3) sharp enhance-
ment of the vessel wall. When using MRI, the throm-
bosed vessel will appear bright, whereas a vessel
with normal blood flow looks dark (49). It is believed
that both methods are comparable. MRI offers a
better visualization of soft tissue changes and allows
evaluation of edema and inflammatory signs. How-
ever, both techniques allow only limited visualiza-
tion of smaller vessels such as uterine, cervical, and
other smaller pelvic branches. Color Doppler ultra-
sonography may have a role in the diagnosis of
pelvic thrombophlebitis and in monitoring of treat-
ment response (49,54,55). Laboratory tests that may
aid in the diagnosis and management of the disease
include a complete blood count with blood cultures.
However, blood cultures provide identification of a
microorganism in less than 35% of cases (49,52,53).
The mainstay of treatment is anticoagulation with
heparin along with broad-spectrum antibiotics for 7
to 10 days (37,51). Low-molecular-weight heparins
have replaced traditional heparin therapy for both
prophylaxis and treatment of thromboembolism in
many clinical scenarios. Although LMWH has proven
anticoagulation efficacy and fewer complications
than heparin, there is little data to support its routine
use in ovarian vein thrombophlebitis. Several case
reports have described favorable outcomes with
LMWH treatment in ovarian vein thrombophlebitis
(44,48,54,56–60). Treatment regimens in one of
these cases included therapeutic dosing of enoxapa-
rin (1 mg/kg twice daily) for 1 week as an inpatient,
followed by once-daily dosing at 1 mg/kg for 8
weeks as an outpatient (60). Alternatively, 1 mg/kg
enoxaparin twice daily as an inpatient until fever
resolution, followed by 60 mg twice daily for 7 days
has been suggested (58). In summary, an evidence-
based treatment protocol for patients with ovarian
vein thrombophlebitis is not available at the present
time, nor any randomized control trials comparing
LMWH and unfractionated heparin (57).
Surgical ligation of infected veins is reserved for
patients who fail to respond to medical therapy. If
there is caval extension or pulmonary embolism de-
spite anticoagulation, ligation of the inferior vena
cava is undertaken. Complications of this procedure
may include transient lower limb edema and persis-
tent postphlebitic syndrome (61).
MASTITIS
Mastitis is usually caused by Staphylococcus au-
reus, Group A or B streptococci, or Hemophilus
organisms. The clinical findings include fever, local-
ized breast tenderness, and erythema. Microscopy
and Gram staining of expressed breast milk may
reveal polymorphonuclear cells and the causative
organism. Mastitis should be distinguished from late
engorgement caused by milk stasis, which can cause
inflammation of the breast but is not associated with
high fever or cracked nipples, and does not require
antibiotic therapy (62). Therapy for the treatment of
mastitis includes local care such as ice-packs, anal-
gesia and breast support, in addition to a penicillinase-
resistant antibiotic. Breast-feeding should be continued
unless an abscess develops. The treatment of a breast
abscess requires incision and drainage.
URINARY TRACT INFECTION
Urinary tract infection with classic symptoms and
signs of urinary frequency, dysuria, and fever is a
common cause of puerperal fever. The diagnosis is
based on clinical findings and a urine specimen con-
taining greater than 105 colony forming U/mL.
The majority of urinary tract infections (UTIs) are
caused by gastrointestinal organisms. Even with ap-
propriate treatment, the patient may experience a
reinfection of the urinary tract from the rectal reser-
voir. The organisms that cause UTIs during preg-
nancy and the postpartum period are the same as
those found in nonpregnant patients. Escherichia coli
accounts for 80% to 90% of infections. Other Gram-
negative rods such as Proteus mirabilis and Kleb-
siella pneumoniae are also common. Enterococci,
Gardnerella vaginalis and Ureaplasma ureolyticum,
as well as Gram-positive organisms such as group B
streptococcus and Staphylococcus saprophyticus are
less common causes of UTI (63–65).
In pregnancy and the puerperium, increased blad-
der volume, and decreased bladder tone, along with
decreased ureteral tone, contribute to increased uri-
nary stasis and ureterovesical reflux. Increases in
urinary progestins and estrogens may lead to a de-
creased ability of the lower urinary tract to resist
invading bacteria (66). Bacteriuria in the postpartum
period is often asymptomatic, with only 21% of
culture-positive women reporting symptoms (67). Of
all risk factors, urethral catheterization contributes
 Puerperal Pyrexia. Part II Y CME Review Article
most to the incidence of nosocomial urinary tract
infections. Failure to treat a urinary tract infection in
the postpartum period results in persistence of the
bacteriuria in about 30% of cases. A 3-day course of
antibiotics is usually sufficient to eradicate the infec-
tion in uncomplicated cases (67).
Acute pyelonephritis during the puerperium is a
serious systemic illness that can progress to maternal
sepsis. The diagnosis is made when the presence of
bacteriuria is accompanied by systemic symptoms or
signs such as fever, chills, nausea, vomiting, and
flank pain. Symptoms of lower tract infection (, i.e.
frequency and dysuria) may or may not be present.
Early, aggressive treatment with appropriate antibi-
otics is important in preventing complications from
pyelonephritis. Hospitalization, although often indi-
cated, is not always necessary. However, hospitaliza-
tion is indicated for patients who are exhibiting signs
of sepsis and who are vomiting and unable to remain
hydrated (68). Parenteral antibiotic treatment of py-
elonephritis should be continued until the patient
becomes afebrile. Most patients respond to hydration
and prompt antibiotic treatment within 24 to 48
hours. The most common reason for initial treatment
failure is resistance of the infecting organism. If fever
continues or other signs of systemic illness remain
after appropriate antibiotic therapy, the possibility of
a structural or anatomic abnormality should be in-
vestigated. Persistent infection may be caused by
urolithiasis, which occurs in 1 of 1500 pregnancies or
less commonly, congenital renal abnormalities, or a
perinephric abscess (69).
MISCELLANEOUS CAUSES
As with any patient with fever, the possibility of
other causes, such as viral infection, connective tis-
sue disease, malignancy, human immunodeficiency
virus infection, or subacute bacterial endocarditis,
should be considered if the course of illness is atypical
or the patient is unresponsive to standard therapy.
CONCLUSION
It is evident from the literature that enormous
strides have been made over the past few centuries in
reducing maternal mortality from puerperal infec-
tions. In the past decades this has evolved to reducing
maternal morbidity as well. While this may be true
for developed countries, postpartum infections are
still an issue in less developed nations. The principles
of management in cases of puerperal infection in-
clude assessment of risk factors, a detailed history, a
405
“head-to-toe” examination, appropriate laboratory
and radiologic tests, and treatment of the cause.
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