The human oviduct, also known as the fallopian tube, is an essential component of the normal reproductive

process. The tube, which connects the peritoneal space to the endometrial cavity, captures the egg after
ovulation and transports the sperm from the uterus to the fertilization site in the ampulla (the middle portion
of the tube). The ampulla serves as the physiologic site for final gamete maturation, fertilization, and early
embryonic development. This article reviews the morphologic, physiologic, functional, and pathologic
aspects of the human oviduct.
See Medscapes Womens Sexual Health Resource Center.

Embryology
Early in the embryologic life, 2 sets of paired genital ducts exist: the wolffian ducts (mesonephric duct) and
the mllerian ducts (paramesonephric duct). At about 6 weeks' gestation, the wolffian ducts regress in
females because testosterone and mllerian inhibiting substance (MIS) are not secreted in the absence of
testis. The mllerian ducts develop into the female genital tract in a cephalocaudal fashion. The more
cephalad ends of the paired paramesonephric ducts are opened to the peritoneal cavity and develop into
the fallopian tubes, while the more caudal portion fuses in the lower midline to form the uterovaginal
primordium, which later develops into the epithelium and glands of the uterus and cervix. [1]
If one mllerian duct fails to develop (usually associated with lack of development of the mesonephric
system on the same side), a unicornuate uterus results, which consists of one uterine horn with only one
fallopian tube. Complete failure of the mllerian system results in the absence of the fallopian tubes, the
uterus, the cervix, and most of the vagina (Rokitansky-Kster-Hauser syndrome). Also seeMullerian Duct
Anomalies.
Remnants of the paramesonephric or mesonephric ducts may persist in the female as paratubal cysts or
hydatid cysts of Morgagni.

Anatomy
The paired fallopian tubes extend laterally from the cornua of the uterus on each side and end near the
ovaries. They range in length from 10-14 cm and are about 1 cm in external diameter, connecting the
peritoneal space to the endometrial cavity. The ostia or openings of the tube are about 1.5 mm in diameter
at the cornual end and 3 mm in diameter at the peritoneal end. The tubes sit within the abdominal cavity
and are suspended by the mesosalpinx, a free edge of the superior portion of the broad ligament that
contains the blood supply and nerves.[2, 3] Except for their intramural part, the tubes are covered by the
peritoneum.
For descriptive purposes, each fallopian tube is divided into 4 anatomic regions.

The infundibulum, from the Latin word meaning funnel, is the funnel-shaped most distal end of the
tube and is in close relation to the ovary. The peritoneal ostium lies at the base of the infundibulum and is
surrounded by 20-30 irregular fingerlike projections (fimbriae), which spread over the surface of the ovary,
and a single large fimbria (the fimbria ovarica), which is attached to the ovary. The fimbriae trap the
ovulated ovum and sweep it through the tubal ostium into the ampulla. [4] The infundibulum is surrounded
by a thin longitudinal muscular layer.

The ampulla is about 4-6 cm in length and is the longest region of the tube, comprising about half
its length. It is also the widest region, about 6 mm in inner diameter, and the most tortuous region. Its
luminal diameter is wider at its distal end than its proximal end. It is relatively thin walled and surrounded
by 2 smooth muscle layers, an inner longitudinal layer and an outer circular layer. Fertilization occurs in
this region.

The isthmus is short, about 2.5-4 cm, and begins as the tube exits the uterus. Its lumen is narrow,
about 1-2 mm in diameter, and the muscular wall is thick and well developed, consisting of 3 well-defined
layers: an inner longitudinal layer, an outer longitudinal layer, and a middle circular layer. [5, 6]

The interstitial or intramural segment is 1-2 cm long and constitutes the uterine-tubal junction. This
section extends through the wall of the uterus and the ostium opens within the uterine cavity.
Complex coordinated contractions of the musculature are thought to be important for movement of the
ovum from the distal end to the proximal end of the tube, while at the same time aiding in the movement of
sperm from the proximal end to the distal end of the oviduct.
Arterial supply to the tubes is derived from the uterine and ovarian arteries, with the uterine branches
supplying the medial two thirds of the tube. The tubal branches traverse and anastomose between the
layers of the mesosalpinx. The venous system follows a similar path, draining into the uterine and ovarian
veins. The lymphatic system follows the lymphatic drainage of the uterine fundus and the ovary, ascending
along the ovarian veins and draining into the internal iliac and the aortic lymph nodes in the lumbar region.

The tubes are innervated by both sympathetic and parasympathetic nerves, derived partly from the ovarian
plexus and partly from the uterine plexus, and by afferent nerves contained in T11, T12, and L1 nerves. [3, 7]

Physiology
The lumen of the oviduct is formed by a complex interdigitating system of longitudinal mucosal folds
(plicae), lined by mucosal and underlying stromal connective tissue. [6] Plicae are most prominent in the
ampullary region and least prominent in the isthmic region. The stroma is thin, but the lamina propria is
thick, with vascular channels between the epithelial and muscular layers. The adventitia contains blood
vessels and nerves between the muscular layer and the peritoneal surface.
Three different cell types are present in the mucosa of the oviduct. Columnar ciliated epithelial cells are
most prominent near the ovarian end and constitute 25% of the mucosal cells. Secretory cells constitute
60% of the mucosa and are mostly in the isthmic region. Narrow peg cells are located between secretory
and ciliated cells and are believed to be a variant of secretory cells. [7]
The morphology of the epithelium is controlled by female hormones.[8, 9, 10] During the follicular phase, rising
estrogen levels stimulate differentiation of the epithelium into secretory and ciliated cells. At the time of
ovulation, approximately half of the epithelial cells lining the oviductal lumen are secretory cells. The apical
tips of these cells contain secretory granules that release their secretory products by exocytosis.
Estrogen induces both hypertrophy as well as hyperplasia of the oviductal epithelium. It stimulates the
differentiation of the secretory cells, the development of the secretory organelles, and ciliogenesis.
Progesterone antagonizes these processes, resulting in atrophy, regression, and loss of cilia and secretory
activity. As with other reproductive tract tissues, estrogen and progesterone regulate these processes in
part by regulation of their own receptor levels. Estrogen stimulates the production of both estrogen and
progesterone receptors while progesterone has an opposite, suppressive effect on both receptors in the
oviduct.[11, 12]

Oviduct glycoprotein
The lumen of the oviduct is filled with fluid composed of a complex mixture of oviduct-specific secretory
proteins, selective serum transudate, and electrolytes.[13]Albumin, immunoglobulins, and transferrin are the
primary serum proteins present within oviductal fluid. While a number of other proteins, such as growth
factors, enzymes, protease inhibitors, and cytokines, have also been identified in oviductal fluid, only one
oviduct-specific molecule has been well characterized to date. At the time of ovulation, the major oviductspecific protein present in oviductal fluid is oviductal glycoprotein (OGP). [8]
OGP is an estrogen-dependent glycoprotein that is synthesized and secreted by the secretory cells of the
human oviduct.[14, 15] OGP is species-specific but shares a certain homology. Studies suggest that OGP is a
sialomucin involved in forming a protective barrier due to its relative resistance to proteolytic degradation. [16]
The physiologic function of OGP is not known; however, evidence suggests that OGP is involved in
fertilization and potentially in the early embryonic development processes. It has been found to be
associated with the zona pellucida (ZP) and the flocculent material present within the perivitelline space of
oviductal eggs and embryos but not associated with ovarian eggs. [17, 18, 19, 20, 21, 22, 23] Also, inclusion of OGP in in
vitro sperm binding and in vitro fertilization (IVF) assays enhances sperm binding to the ZP, increases
sperm penetration through the ZP, and increases the fertilization rate. [23, 24, 25, 26] Addition of antibodies directed
specifically against OGP has reversed or inhibited the effects of OGP on sperm binding and fertilization. [27]
A limited number of reports are available on OGP effects on embryonic development. These studies
suggest that OGP may enhance embryo cleavage rates and blastocyst formation. As a whole, the
functional studies on OGP strongly support the contention that OGP may play a role as an enhancing factor
in key reproductive events. Moreover, some hypothesize that the addition of OGP to procedures may lead
to better overall outcomes.[28, 29]

Sperm reservoir
In addition to its contribution of oviductal secretions, the oviduct serves as an important reservoir for sperm.
Numerous studies have shown that sperm are retained within the isthmic portion of the oviduct. Of the
millions of sperm present within a normal ejaculate, only thousands enter the isthmus and only a select few
reach the site of fertilization in the ampulla. As sperm enter the isthmus, many of them adhere to the
epithelium.[30, 31, 32, 33] This adherence may be promoted by the extremely narrow lumen at the uterine end of
the isthmus, thus providing a greater chance of contact between the sperm and the mucosa.

Studies have shown that incapacitated sperm bind with higher affinity than capacitated sperm. [34, 35, 36] In both
in vivo studies and in vitro studies, the interaction of sperm with oviductal epithelial cells has been shown to
enhance sperm viability, stabilize the acrosomal membrane, and potentially prevent or reduce polyspermy.
[37, 38, 39, 40]
Sperm-epithelial interaction decreases as sperm become capacitated. This may be due to changes
in molecules present on the sperm plasma membrane as well as hyperactivated motility of sperm in a
capacitated state, which allows them to detach more easily.[37, 38] Soluble factors produced by oviductal cells
may in part account for some of the positive effects of epithelial cells on sperm. [41] Sperm appear to bind to
species-specific carbohydrates present on the surface of oviductal cells via a lectinlike mechanism. As
sperm capacitate, this lectin appears to be lost or masked.
Ne
Salpingitis is the inflammation of the fallopian tube, most commonly caused by an infection.
Acute salpingitis is often used synonymously with pelvic inflammatory disease (PID) because it is the most
common form of PID and because the most common and serious long-term sequelae of PID involve the
tubes.

Epidemiology
Salpingitis is the most common serious infection in women of reproductive age. An estimated 1 million new
cases occur in the United States every year, most commonly in females aged 15-25 years, and about 1-2%
of sexually active young women are affected annually. However, the true incidence of acute salpingitis is
not known because no precise definition of the disease exists and many cases are subclinical. [42, 43, 44, 45]
Acute salpingitis and its sequelae cause a substantial public health burden. In 1994, the total cost of PIDs
exceeded $4 billion and the projected total annual cost for the year 2000 was $10 billion. However, since
that time, the hospitalization rate has declined due to changes in the criteria for hospital admissions, an
increase in outpatient management, and a decrease in incidence of PID. Rein et al estimated that the direct
cost of PID and its sequelae was $1.88 billion in 1998.[7, 46, 47, 48]The decline in PID incidence might be
attributable to an expansion of national and regional programs that screen women for asymptomatic
chlamydial infections, one common cause of PID. [49]
Risk factors for acquiring acute salpingitis are similar to those for acquiring sexually transmitted diseases
(STDs). Age is inversely related to the rate of acute salpingitisand directly related to long-term sequelae.
Sexually active teenagers are 3 times more at risk for acquiring acute salpingitis than women aged 25-29
years. This is due to the biologic and behavioral characteristics of this age group, such as young age at first
sexual intercourse, multiple sexual partners, high frequency of unprotected sexual intercourse, and
increased rate of acquiring new partners within 30 days.[43, 50, 51, 52, 53]
Other risk factors that have been associated with acute salpingitis include never being married, divorced or
separated, and low socioeconomic status as measured by lower level of education, lower income, or
unemployment.[54]

Pathogenesis
Neisseria gonorrhoeae and Chlamydia trachomatis were originally thought to be the only pathogens that
caused acute salpingitis until investigators used laparoscopy to collect specimen from patients with PID.
Culture results revealed that N gonorrhoeae and C trachomatis were inconsistently recovered: C
trachomatis was recovered from the cervix in 5-39% of patients with PID and from the fallopian tubes in
only 0-10%; similarly, N gonorrhoeae was isolated from the cervix in 27-80% of cases and from the
fallopian tubes in only 13-18% of cases. This is probably because of variations among the populations
studied and the severity of infection, differences in the time intervals of the investigations, and methods of
microbial investigation, as well as difficulty of sampling microorganisms from the fallopian tube. [55]
Multiple organisms that usually colonize the lower genital tract were isolated from the normally sterile upper
tract, and most infections were polymicrobial. These organisms included Gardnerella vaginalis, Escherichia
coli, Haemophilus influenzae, group B beta-hemolytic streptococci, nonhemolytic streptococci,Prevotella
bivia, Bacteroides species, Peptostreptococcus species, Mycoplasma hominis, and Ureaplasma
urealyticum.
Salpingitis is believed to be an ascending infection that results from the direct canalicular spread of
organisms from the endocervix to the endometrium and then the fallopian tube mucosa. According to
Stamm et al and Platt et al, 10-40% of women not treated for gonococcal or chlamydial cervicitis develop
clinical symptoms of acute salpingitis.[56, 57]
Four factors are thought to contribute to the ascent of these microorganisms.

Cervical and uterine instrumentation during intrauterine device (IUD) insertion, endometrial biopsy,
and dilation and curettage (D&C) bypassing of the cervical mechanical barrier

Hormonal changes during menses and menstruation causing cervical alterations leading to a loss
of the mechanical barrier including the bacteriostatic cervical mucus

Retrograde menstruation favoring ascent to the fallopian tubes

Virulence factors of the microorganism itself

However, rarely, salpingitis can result from the noncanalicular spread of cervical infection, possibly through
parametrial lymphatics,[58] or by hematologic spread from other infection sites.

Clinical presentation and diagnosis

The clinical presentation of salpingitis is highly diverse, ranging from asymptomatic to severe pelvic pain to
diffuse peritonitis to, rarely, life-threatening illness. Poor correlation exists between the number and
intensity of symptoms and the severity of tubal inflammation. This is seen frequently with C
trachomatis infection where asymptomatic women are found to have severe tubal disease during infertility
workup.
Since the diagnosis is usually based on clinical criteria, a high false-positive rate and a high false-negative
rate can occur. For this reason, the classic clinical triad of fever, elevated erythrocyte sedimentation rate
(ESR), and adnexal tenderness or mass required for the diagnosis of acute salpingitis has been dropped,
as this triad was observed in only 17% of laparoscopically proven cases. [50]
In 1986, Hagdu et al reported no statistically significant difference between the following clinical symptoms
among women with laparoscopically diagnosed acute PID and those who were visually healthy: lower
abdominal pain, vaginal discharge, irregular bleeding, urinary symptoms, vomiting, proctitis symptoms, and
marked tenderness on bimanual examination. The only statistically significant objective differences were
temperature greater than 38C, palpable mass or swelling on bimanual examination, ESR greater than 15
mm/h, and abnormal vaginal discharge.[59]
A low threshold for diagnosing PID is recommended because the clinical diagnosis of acute salpingitis is
imprecise, current evidence indicates that many cases go unrecognized, and significant potential exists for
irreversible damage to the fallopian tubes and associated health consequences.
In 1997, the Centers for Disease Control and Prevention (CDC) established guidelines for the diagnosis of
acute PID and the minimum clinical criteria for initiating treatment.
Minimum criteria for clinical diagnosis of PID
Empiric treatment should be initiated in sexually active young women and others at risk for STDs if all of
the following minimal criteria are met and no other causes of the illness can be identified:

Lower abdominal tenderness

Bilateral adnexal tenderness
Cervical motion tenderness
Additional criteria useful in diagnosing PID
Because incorrect diagnosis and management might cause unnecessary morbidity, the following criteria
should be used to increase the specificity of the diagnosis.

Routine
o
o
o
o

o
o
o

Oral temperature greater than 38.3C

Abnormal cervical or vaginal discharge
Elevated ESR and/or C-reactive protein levels
Culture or nonculture evidence of cervical infection with N gonorrhoeaeor C trachomatis
Elaborate
Histopathologic evidence of endometritis on endometrial biopsy
Tubo-ovarian abscess (TOA) or thickened fluid-filled tubes with or without free-fluid on
ultrasonography or other imaging techniques
Laparoscopic findings

Treatment

Patients can be treated as outpatients; however, according to the 2006 CDC guidelines, patient
hospitalization should be used at the discretion of the physician. Several criteria for inpatient treatment
have been suggested:[45]

Pregnancy
Presence of TOA
Patients are noncompliant or cannot tolerate oral therapy
Symptoms are severe and include nausea, vomiting, and high fever
Response to outpatient regimen is inadequate
Uncertain diagnosis and surgical emergencies cannot be ruled out (eg, appendicitis)
No evidence exists that women who are immunocompromised benefit from inpatient versus outpatient
treatment.
No evidence exists that IUDs should be removed in patients diagnosed with PID. Women who retain IUDs
have similar outcomes to those whose IUDs are removed.[60] Close followup of women who retain IUDs is
mandatory, as removal is warranted in a patient who does not show clinical improvement following 72 hours
of treatment for PID.[60]
Outpatient regimens can be considered in mild to moderate PID. The regimens include the following:

Ceftriaxone 250 mg IM once, plus doxycycline 100 mg PO bid for 14 d, with or

without metronidazole 500 mg PO bid for 14 d

Cefoxitin 2g IM single dose plus probenecid 1 g IM single dose plus doxycycline 100 mg PO bid
for 14 d, with or without metronidazole 500 mg PO bid for 14 d

Other parental 3rd generation cephalosporin plus doxycycline 100 mg PO bid for 14 d, with or
without metronidazole 500 mg PO bid for 14 d
In a critical update on April 12, 2007, the CDC no longer recommends using fluoroquinolones for the
treatment of gonococcal infections and associated conditions such as PID. Consequently, only 1 class of
drugs, the cephalosporins, is still recommended and available for the treatment of gonorrhea. [61]
Inpatient regimens include the following:

Regimen A - Cefotetan 2 g IV q12h, or cefoxitin 2 g IV q6h, plusdoxycycline 100 mg IV or PO

q12h
Discontinue cefoxitin 24 hours after patient's symptoms improve and continue doxycycline 100 mg PO bid
for a total of 14 days. If TOA is present, add clindamycin or metronidazole for better anaerobic coverage.

Regimen B - Clindamycin 900 mg IV q8h, plus gentamicin loading dose 2 mg/kg IV or IM, then 1.5
mg/kg IV q8h
Single daily doses of gentamicin may be substituted.
Alternative IV regimens include the following:

Unasyn 3 g IV q6h, plus doxycycline 100 mg IV or PO q12h

Outcome
According to the PID Evaluation and Clinical Health Study (PEACH), no difference exists in the
effectiveness of inpatient and outpatient treatment strategies for patients with mild-to-moderate PID in
preventing infertility, ectopic pregnancy, chronic pelvic pain, recurrence, and a good quality of life. Patients
with mild-to-moderate PID were characterized by the following: a history of pelvic discomfort for a period of
30 days or less, findings of pelvic organ tenderness on bimanual examination, leukorrhea and/or
mucopurulent cervicitis, and/or untreated, but documented, gonococcal or chlamydial cervicitis. [62]

Complications
Before antibiotics were available, mortality from acute salpingitis was about 1%. However, the mortality rate
is much higher in cases complicated by ruptured TOA and in ectopic pregnancies.
Long-term sequelae include chronic pelvic pain, TOA, hydrosalpinx, tubal infertility, and ectopic pregnancy.

Chronic pelvic pain

The likelihood that a patient with acute salpingitis will develop chronic pelvic pain(20%) is 4 times that of
patients without a pelvic infection (5%). The pain can be caused by resultant pelvic adhesions, TOA, or

hydrosalpinx. Laparoscopy can be considered in these patients to establish the cause of the pain and rule
out other causes, like endometriosis.

Tubo-ovarian abscess
TOA is one of the major and serious complications of acute salpingitis and occurs in up to 15% of women
with PID. Of women with a TOA, 33% require hospitalization.[63] TOA is unilateral in 25-50% of cases. It
forms as a consequence of acute salpingitis with pus collection within an anatomic space created by
adherence of adjacent structures involving the fallopian tubes, ovaries, uterus, and sometimes the
intestines, and, as such, is more precisely defined as a tubo-ovarian complex, while an abscess is a
collection of pus in a newly created space.[7]Clinically, however, these 2 conditions are managed the same
way.
The formation of an abscess in relation to PID increases morbidity and the risk of treatment failure and
subsequent operative intervention.[64] Today, despite modern medical and operative management, mortality
from ruptured TOA is 5-10%, mostly as a result of developing acute respiratory distress syndrome (ARDS).
[65]

Using a rat model, Cox et al demonstrated that N gonorrhoeae and C trachomatisalone did not produce
abscesses; however, when combined with facultative or anaerobic bacteria, synergism with abscess
formation was noted frequently. This finding supports the hypothesis that N gonorrhoeae and C
trachomatis initiate the infection and then aerobic and anaerobic bacteria act synergistically to produce
abscesses. In addition, microorganisms, which were not inoculated, were recruited into the infectious
process, gaining access to the peritoneal cavity via the lower genital tract or from transmucosal migration
from the intestinal flora.[66]
The risk factors for the development of a TOA from PID have not been clearly defined, and the relationship
to IUD use has been difficult to evaluate. Landers et al found no statistical difference between the incidence
of unilateral TOA in women with IUDs and those without IUDs.[67] Charonis et al report that the risk of TOA
with copper IUD used longer than 5 years is significantly higher than in women with IUD used for less than
5 years.[68]
Although most TOAs develop from PID, several case reports exist of rare TOA formation not related to PID.

Canas et al reported TOA in a 12-year-old after total abdominal hysterectomy for cervical
dysplasia, challenging the classic pathogenesis of TOA. [69] Cases also exist of bilateral TOA that
developed 50 days after a thermal ablation,[70] after vaginal hysterectomy, and after colonic vaginoplasty
for high cloacal anomaly in a 13-year-old girl.
Few cases of TOA were reported as resulting directly or indirectly following transvaginal
ultrasonographic-guided oocyte retrieval for IVF and transcervical embryo transfer, [71, 72] some suggesting
that reactivation of latent pelvic infection due to a previous PID was the possible route of infection.
Cases have been reported of pelvic abscesses caused by Enterobius vermicularis, [73] Pasteurella
multocida (which occurs most commonly following an animal bite wound or cat
scratch), [74] and Edwardsiella tardainfections (which have been reported in association with pet
reptiles). [75]
Pompeo et al presented a case of unilateral chronic TOA secondary to ruptured colonic
diverticulum presenting as a brain abscess. [76]

Clinical presentation and diagnosis of TOA

Typically, patients with an abscess present with acute pelvic pain, fever, and an adnexal mass, although the
pelvic pain may be chronic. Patients may also report nausea, vomiting, a change in bowel habits, and
vaginal discharge. Fever and leukocytosis may be absent. This clinical picture is not typically different from
a patient diagnosed with PID alone. However, in severe cases, the patient can present with obstruction of
the ureter and hydronephrosis,[77] intestinal obstruction, or sciatic pain.[78] Halperin et al found that the
presence of a pelvic mass in women older than 42 years with ESR >50 mm/hr is the best predictor of TOA.
[79]

Ultrasonography is the test of choice; it is cheaper and more available than either CT scan or MRI, and it
provides guidance to draining the abscess. Typically, a TOA appears on ultrasound as an elongated,
sausagelike, multiloculated, with thick borders that contain turbid fluid, and with abundant flow seen from
the borders and the septa, with reduced resistance to flow on color Doppler.[80, 81]
On CT scan, the most common appearance of TOA is that of a somewhat tubular septated cystic pelvic
mass with uniform wall thickness and with loss of fat planes between the mass and the adjacent pelvic
organs.[82]

MRI is an excellent radiologic modality in defining tissues and distinguishing between ovarian and tubal
lesions, but it is also more expensive.
In cases of suspected ruptured TOA, culdocentesis can be a valuable diagnostic technique with 70% yield
of purulent material.[83] However, the wide availability of sonography today makes blind culdocentesis a less
desirable approach.

Management and outcome of intact TOA

An initial conservative antimicrobial approach to the management of the unruptured TOA is appropriate if
the antimicrobial agents used can penetrate abscesses, remain active within the abscess environment, and
are active against the major pathogens in TOA, which are predominantly anaerobes, including the resistant
gram-negative anaerobes such as Bacteroides fragilis and Prevotella bivius. Clindamycin penetrates
neutrophils that facilitate its passage inside the abscess and the stability of clindamycin within the
microenvironment of the abscess has been proven. Adding an aminoglycoside completes the gramnegative coverage. This combination is considered the standard treatment of TOA. However, clindamycin
does not cover Enterococcus species and, therefore, ampicillin should be added to that combination
whenever Enterococcus is suspected. Metronidazole is an acceptable alternative to clindamycin. [7]
Landers et al demonstrated that single-agent, broad-spectrum antibiotics, such as cefoxitin, in conjunction
with doxycycline, have efficacy that is equivalent to that of clindamycin-containing regimens. [67] The overall
medical treatment success rate of 75% suggests that conservative treatment of TOAs is warranted. [84]
The CDC STD Treatment Guidelines published in 2006 do not specify any particular treatment of TOA, but
rather use the same parental regimen A and B as for PID. However, once the parental treatment is
discontinued, the CDC suggest using clindamycin or metronidazole with doxycycline orally instead of
doxycycline alone for better anaerobic coverage.[61]
If the patient does not begin to show a response within a reasonable amount of time, usually 48-72 hours,
surgical intervention should be considered. Acute rupture is an indication for immediate operation. Once
operation is undertaken, a conservative approach with unilateral adnexectomy for one-side TOA is
appropriate if future fertility or hormone production is desired. [67] Similarly, drainage of the abscess by either
laparotomy, percutaneous drainage, or a colpotomy incision may preserve the patient's fertility.
Posterior colpotomy is preserved for abscesses in the cul-de-sac. The 3 requirements for colpotomy
drainage[65] are as follows:

Abscess must be in the midline.

Abscess should be adherent to the peritoneum of the cul-de-sac and dissect into the rectovaginal
septum to ensure extraperitoneal drainage of pus.

Abscess should be cystic or fluctuant for adequate drainage.

Cases that do not meet the above criteria can be managed by percutaneous drainage or laparotomy.
Percutaneous aspiration or drainage of a TOA under ultrasonographic or CT guidance can be
accomplished either transvaginally or transabdominally. In a series of 35 pelvic abscesses that resulted
from PID, Worthen and Gunning demonstrated a success rate of 94% by aspiration drainage of 26
abscesses ranging from 2-11 cm in size, while catheter drainage of 9 abscesses ranging from 7.4-14 cm
yielded only a 77% success rate.[85, 86]
In a retrospective study of 27 pelvic abscesses, Corsi et al demonstrated a more than 90% success rate of
transvaginal ultrasonographic-guided aspiration of the pelvic abscess while the patient was on broadspectrum intravenous antibiotics.[87]The perceived adequacy of drainage was correlated with lack of
abscess septation. However, these studies were not randomized and were underpowered; larger studies
need to be performed to claim an advantage of one method over the other, and long-term follow up is
needed to assess the effect of such treatment on the rate of ectopic pregnancy, fertility, recurrence, and
chronic pelvic pain.
Perez-Medina et al randomly distributed 40 women into 2 groups. Both groups received clindamycin and
gentamicin, but in the study group, early transvaginal drainage of the abscess was performed. Both shortterm (48-72 h) and medium-term (4 wk) responses to the treatment were evaluated. In 90% of the study
group, a favorable short-term response was reported in terms of a decrease in leukocytosis, C-reactive
protein, temperature, and size of the abscess evaluated sonographically, whereas only 65% in the control
group responded to the same degree. Moreover, the average length of hospitalization was 3.9 days in the
study group versus 9.1 days in the control group. In the medium-term follow-up, 1 patient in the study group

and 3 in the control group had persistent adnexal mass on transvaginal sonography but no complications
were present in both groups.[88]
Goharkhay et al compared 50 patients treated primarily with IV antibiotics to 8 patients treated primarily
with image-guided drainage. Only 29 patients (58%) in the first group completely responded to treatment
versus all patients (100%) in the second group. Of the 21 patients who failed initial treatment, 2 patients
underwent surgery and 19 had salvage drainage with 18 of the 19 patients having complete recovery.
Those who underwent primary drainage had shorter hospital stay and faster recovery.[89]
Definitive surgical management by exploratory laparotomy with conservative adnexal surgery is indicated in
failed cases when either the abscess does not resolve or the patient does not improve clinically. To
decrease the risk of complications, if possible, surgery should be delayed until after the infection has been
quiescent and radiologic evidence of complete absorption of the inflammatory exudates surrounding the
focus of infection is present. Ideally, the patient should have a normal ESR, WBC count, and hematocrit
level and a relatively nontender pelvis, which usually takes about 2-3 months.
However, when the patient on antibiotics does not improve clinically and the abscess cannot be drained,
surgery should be performed, but in this setting, the risk of complications, including bowel and bladder
injuries, is higher.[65] The serosal surface of the bowel is usually inflamed, edematous, friable and
predisposed to damage and complicating repair. Caution should be used in manipulating the bowel and
lysing the adhesions. Aerobic and anaerobic cultures from the pus or ascitic fluid should be obtained and
copious irrigation should be performed to drain all the pus from the abdominal cavity.

Management and outcome of ruptured TOA

TOAs can rupture spontaneously into the rectum, sigmoid colon, bladder, or peritoneal space, but almost
never into an intact vagina. Rupture can also result from accidental trauma or during bimanual examination.
The major symptom of a ruptured TOA is an acutely worsening pelvic pain that is so severe that the patient
can usually precisely identify the time and location it occurred. On physical examination, the patient may
appear critically ill with tachycardia, fever, distended abdomen, absent bowel sounds, signs of generalized
peritonitis, muscle rigidity, shifting dullness, and direct and rebound tenderness. A pelvic mass is detected
50% of the time. Shock can develop while the patient is under observation due to accumulation of fluids in
peripheral tissues and failure of compensatory vasoconstrictor mechanisms. The patient may be afebrile,
and leukocytosis can be absent. Severe leukopenia is an ominous sign. [65]
A ruptured TOA is a surgical emergency because any delay in operative management increases mortality
risk due to septic peritonitis and shock resulting from systemic absorption of bacterial endotoxins and
significant third spacing into the peritoneal cavity through inflamed tissues. Speed is of the essence; the
preoperative time should be reduced, and the operation should be performed in the fastest way possible.

Surgical treatment of TOA

Preoperative preparation for TOA may include the following:

Blood products should be available, and if the patient is anemic, a transfusion should be done prior
to surgery.
Adequate correction of metabolic acidosis and electrolytes imbalance
Adequate respiratory support
Intravenous broad-spectrum antibiotics
Intestinal tube to decompress dilated intestines
The ideal operation includes removal of pus, abscess, uterus, tubes, and ovaries. If the abscess involves
only 1 adnexa, then a unilateral salpingo-oophorectomy can be attempted in a young patient, although
leaving the uterus increases the risk of recurrence in the unaffected tube. In these cases, hysterectomy
should be consideredusually a supracervical hysterectomy since it is achieved faster. The extent of the
surgery should be weighed against iatrogenic complications; for example, in case of severe bowel
adhesions and edematous tissue, it would be safer to only drain the abscess through gentle blunt
dissection along the anatomical planes and postpone any resection until the inflammation subsides.
Copious irrigation with warm saline prior to closure of the incision removes and dilutes any remaining
bacteria in the peritoneum. The fascia is closed with either delayed absorbable sutures or permanent
sutures.

The postoperative course can be complicated by intestinal obstruction or fistulas, recurrent abscesses,
separation or dehiscence of the incision, septic shock, disseminated intravascular coagulation (DIC),
pulmonary embolus, and ARDS.

Pyosalpinx and hydrosalpinx

Pyosalpinx is defined as pus in the fallopian tube, which usually results from acutesalpingitis. If the infection
is severe and spreads to the adjacent structures, it forms a TOA. On the other hand, if the fimbrial end
becomes occluded, the infection is contained within the tube and it forms a pyosalpinx. Grossly, the tube
appears distended and is filled with pus. Microscopically, the tubal wall is thickened and infiltrated by acute
and chronic inflammatory cells. The plicae of the tube are swollen and edematous.
Hydrosalpinx is a collection of watery sterile fluid inside the fallopian tube. It results from tubal obstruction
as an end stage of pyosalpinx. Grossly, it appears as a dilated tube with a thin wall and is filled with clear,
colorless, watery fluid, which results from proteolysis of neutrophils and debris. The external surface may
have adhesions. Microscopically, the thin and dilated tubes have flattened epithelium, but both ciliated and
secretory cells can be recognized.
On ultrasonography, hydrosalpinx appear as elongated, sausagelike, cystic lesions with thin borders that
contain clear fluid with or without septa. The addition of color Doppler flow helps in distinguishing
hydrosalpinges from ovarian lesions by demonstrating flow from the borders (and usually not from the thin
septa), with a higher resistance than ovarian flow (mean resistive index of 0.752 vs 0.55), while in TOAs the
resistance is much lower (mean resistive index 0.448) secondary to the inflammation. [80]
The major clinical significance of a hydrosalpinx is its adverse effect on fertility. This effect is thought to be
due to more than just the destruction and occlusion of the fallopian tube. The presence of a hydrosalpinx is
associated with up to a 50% reduced implantation and pregnancy rate after IVF.[90] This reduction is thought
to result from the presence of embryo toxin in the hydrosalpinx fluid. These toxins are yet to be identified.
Therefore, excising the hydrosalpinx prior to performing IVF is recommended.
In a Cochrane database systematic review, Johnson et al concluded that laparoscopic salpingectomy
should be considered for all women with hydrosalpinges prior to IVF treatment, although further evaluation
is needed and randomized trials are required to assess other surgical options for hydrosalpinx, such as
salpingostomy, tubal occlusion, or needle drainage of a hydrosalpinx at oocyte retrieval. [91]
A hydrosalpinx, although sterile, can be reinfected leading to a pyosalpinx. Nikolic et al published a case of
the development of a pyosalpinx from a preexisting hydrosalpinx after uterine artery embolization for
leiomyomata.[92]