ACUTE SALPINGITIS

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ACUTE SALPINGITIS Liang Gu Pathology Case
Discussion and Presentation
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An 18-year-old female presents to the emergency
room with severe abdominal pain, which has been
progressive over the last 3 days. Her menstrual
period was due about the time her symptoms
started. She admits to being sexually active with
several partners in the past 2 months with
inconsistent use of birth control. Physical
examination reveals marked lower abdominal/pelvic
tenderness and a purulent vaginal discharge. She
is febrile (39 C) at the time of exam. Her CBC is
significant for a white blood cell (WBC) count of
15 x 103/µL with 82 polymorphonuclear
neutrophils (PMN) and 6 bands and
metamyelocytes.
Normal Lab Values
WBC 4.1-10.9x103/µL PMN 35-80 Immature Polys
(Bands) 0-10
Other Lab Values of Interest Erythrocyte
Sedimentation Rate (ESR) - Measures the distance
that erythrocytes have fallen after one hour in
a vertical column of anti-coagulated blood under
the influence of gravity C-Reactive Protein -
Indicative of acute inflammation Cultures
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Band cells or band neutrophils are those which
have unsegmented nuclei. This is the
developmental stage of the neutrophil immediately
preceding the mature segmented form. An increased
proportion of bands in the peripheral blood is
often referred to as a 'left shift', and may
indicate the presence of infection.
http//meds.queensu.ca/medicine/deptmed/hemonc/a
nemia/band.htm
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Differential
Cervicitis The cervix appears red and bleeds
easily (when touched with a spatula or cotton
swab). Mucopurulent discharge is yellow-green and
contains gt 10 polymorphonuclear WBCs per oil
immersion field (using Gram stain). Salpingitis
Inflammation of the fallopian tube. When the
ovaries are involved, it is termed Pelvic
Inflammatory Disease (PID). Acute salpingitis
Onset is usually shortly after menses. Lower
abdominal pain becomes progressively more severe,
with guarding, rebound tenderness, and cervical
motion tenderness. Involvement is usually
bilateral. Nausea and vomiting occur with severe
infection. In the early stages, acute abdominal
signs are often absent. Bowel sounds are present
unless peritonitis with ileus (temporary absence
of the normal contractile movements of the
intestinal wall) has developed. Fever,
leukocytosis (elevation of WBCs), and
mucopurulent cervical discharge are common
irregular bleeding and bacterial vaginosis often
accompany the pelvic infection. A fibrinous
exudate may also appear. Chronic salpingitis
Untreated or inadequately treated acute infection
can lead to chronic salpingitis, with tubal
scarring and possible adhesion formation. Chronic
pelvic pain, menstrual irregularities, and
infertility are long-term sequelae. Other
Ectopic pregnancy, acute appendicitis,
endometriosis (endometrial tissue adheres to
other organs in the abdominal cavity such as the
ovaries and fallopian tubes), symptomatic ovarian
rupture, ovarian neoplasm, and uterine fibroids.
The Merck Manual
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Normal Fallopian Tube - Low Power
M Mucosal Folds L Lumen W Wall of Tube
Note the delicate mucosal folds lined by
epithelium and a vascularized stroma. There are
no inflammatory cells in the lumen or in the
mucosa.
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Normal Fallopian Tube - Medium Power
M Tubal Mucosa S Stroma
Note the darkly staining nuclei in the
subepithelial layer. They are the normal
resident lymphocytes and macrophages that can be
found at many mucosal sites.
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Uterus, Bilateral Fallopian Tubes, and Ovaries
U Uterus C Cervix F Fallopian Tube O Normal
Ovary M Inflamed Tubo- Ovarian Mass
Note the hemorrhagic, edematous fallopian tubes,
so much so that the architecture of the right
tube and ovary is obscured. The surface of the
tubo-ovarian mass is not only red but also
somewhat shaggy. What cardinal signs of
inflammation are present? Rubor (Redness) and
Tumor (Swelling) What chemical mediators increase
the blood flow to an area of inflammation?
Histamine, Nitric Oxide, PGI2, PGE, PGD2 What is
responsible for the shaggy appearance? Fibrinogen
exudate deposited as fibrin. Sign of increased
vascular permeability.
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Inflamed Fallopian Tubes http//www.meddean.luc.e
du/lumen/MedEd/Radio/curriculum/Mechanisms/acute_s
alpingitis1.htm
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Look at how profoundly edematous all aspects of
this fallopian tube are.  We are going to focus
on the mucosal folds, but the inflammatory
features are present throughout this
specimen. http//bl-msci-007c.ads.iu.edu/c602web/
602/c602web/repro/sl86_1.htm
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Fallopian Tube - Low Power
W Muscular Wall M Inflamed Mucosa L Lumen with
Inflammatory Cells
Notice the inflammatory infiltrate in the mucosa
and muscular wall. Inflammatory cells have
nearly obscured the lumen. What is responsible
for the leukocytosis? In patients with acute
inflammation, the blood neutrophil count is
increased, because these cells are mobilized from
the storage pool of neutrophils in the bone
marrow by the action of IL-1 and TNF. Later in
the course of inflammation, there is increased
production of neutrophils in the bone marrow,
due to the production of GM-CSF (Granulocyte
Macrophage-Colony Stimulating Factor ).
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Fallopian Tube - Pelvic Inflammatory Disease
Note the extensive neutrophil infiltrate present
in the lumen with infiltration of mucosa.
How do neutrophils exit from the blood to the
tissues? First, margination, rolling, and firm
adhesion in the vessel lumen. Second,
transmigration across the endothelium. Last,
migration in tissue toward the chemotactic
stimulus. What adhesion molecules are relevant
for emigration of inflammatory cells? E-selectin
and P-selectin on the endothelium bind to
sialyl-Lewis X on neutrophils. L-selectin on
neutrophils binds to mucin-like molecules on
endothelium. ICAM-1 and VCAM-1 (Ig family) on
endothelium bind to integrins (LFA-1, Mac-1, and
VLA-4) on leukocytes. When do they function?
Rolling involves selectins while firm adhesion
requires integrins. PECAM-1 (Expressed on
leukocytes and endothelial cells) is involved in
transmigration.
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Neutrophil Killing Mechanisms
Oxygen-Dependent utilizes superoxide (O2-) via
the NADPH system giving rise to H2O2 and OH-.
Also generated are myeloperoxidase-dependent HOCl
radicals. Most important. Oxygen-Independent
defensins, lysozyme, and lactoferrin. Lesser
importance. Defects in Neutrophil Killing
Mechanisms 1. Defect in adhesion (LAD-1)
Defective synthesis of leukocyte integrins LFA-1
and Mac-1. (LAD-2) Absence of sialyl-Lewis X.
2. Defects in chemotaxis or phagocytosis
(Chediak-Higashi syndrome) Inherited impairment
in assembly of microtubules causing impaired
movement and lysosomal degranulation into
phagosomes. 3. Defects in microbicidal
activity (Chronic Granulomatous Disease) Genetic
deficiency of the NADPH oxidase system or
genetic deficiency of myeloperoxidase
A remnant of tubal epithelium is seen here
surrounded and infiltrated by numerous
neutrophils. http//medlib.med.utah.edu/WebP
ath/FEMHTML/FEM041.html
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Fallopian Tube - Pelvic Inflammatory Disease
L Lumen M Mucosa S Sub-Mucosa P Plasma
Cell N Neutrophil
The fallopian tube lumen contains an abscess-like
collection of neutrophils and necrotic debris.
The mucosal epithelium itself is infiltrated by
neutrophils and shows histologic evidence of
damage. The submucosa is infiltrated by both
neutrophils and plasma cells. What does the
presence of plasma cells tell us? Chronic
inflammation is present
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Lung - Chronic Inflammation
L Lymphoid Nodule F Fibrosis A Alveolar Space
Lymphocytes have aggregated to form a lymphoid
nodule. They are also scattered in the areas of
fibrosis. The fibrous tissue has replaced the
normal lung parenchyma that has been destroyed.
Only a few alveolar spaces separated by markedly
fibrotic septa remain.
Characteristics of Chronic Inflammation 1.
Infiltration by mononuclear cells (plasma cells,
monocytes, lymphocytes) 2. Inflammatory-cell
mediated tissue injury 3. Scarring as a result
of repair by granulation tissue with angiogenesis
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Mixed Inflammatory Infiltrate - High power
E Eosinophil P Plasma Cell M Macrophage
Activated macrophages cause fibrogenesis,
deposition of ECM, and angiogenesis.
Macrophage Secretions Enzymes (Acid and neutral
proteases) causing tissue damage Plasma proteins
(Complement components and coagulation
factors) Reactive oxygen species and nitric
oxide Arachidonic acid Cytokines (IL-1, TNF,
FGF, PDGF, EGF) Eosinophils Prominent in
infiltrate during allergic, parasitic, and at
times, chronic inflammation. Granules contain
major basic protein and eosinophil cationic
protein. Major basic protein and eosinophil
cationic protein are toxic to tissue.
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Chronic inflammation need not require a history
of acute inflammation. It may arise de novo.
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Pathogenesis of Acute Salpingitis Pelvic
infection due to Neisseria gonorrhoeae is usually
more acute and typical than that due to Chlamydia
trachomatis onset is rapid, and pelvic pain
develops shortly after menses starts. Although
the pain is often localized to one side, both
tubes are probably infected. The infection
produces a diffuse exudate, leading to
agglutination, adhesions, and tubal occlusion.
Peritonitis may occur, causing upper abdominal
pain and adhesions. C. trachomatis produces
symptoms that often seem mild, but it can cause
more damage than N. gonorrhoeae in the long term.
Chlamydial organisms may remain in tubal mucosa
for many months before clinical manifestations of
acute disease appear.
The Merck Manual
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Complications of Acute Salpingitis Tubo-ovarian
abscess develops in about 15 of women with
salpingitis. It can accompany acute or chronic
infection and may require prolonged
hospitalization, sometimes with surgical
percutaneous drainage. Rupture of the abscess is
a surgical emergency, rapidly progressing from
severe lower abdominal pain to nausea, vomiting,
generalized peritonitis, and septic shock.
Pyosalpinx, in which one or both fallopian
tubes are filled with pus, may also be present.
The fluid may be sterile, but WBCs predominate in
it. Hydrosalpinx (fimbrial obstruction and
tubal distention with nonpurulent fluid) develops
if treatment is late or incomplete. The
consequent mucosal destruction leads to
infertility. Hydrosalpinx is generally
asymptomatic but can cause pelvic pressure,
chronic pelvic pain, or dyspareunia (painful
sexual intercourse). Fitz-Hugh-Curtis Syndrome
can be a complication of gonococcal or chlamydial
salpingitis. It is characterized by right upper
quadrant pain in association with acute
salpingitis, indicating perihepatitis
(inflammation of the liver capsule). Acute
cholecystitis may be suspected, but symptoms and
signs of PID are present or develop rapidly.
The Merck Manual
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Treatment of Acute Salpingitis Therapeutic
Goals Complete resolution of the infection and
prevention of infertility and ectopic pregnancy.
Immediate and vigorous treatment with
antibiotic therapy should be started as soon as
cultures are obtained. Traditional indications
for inpatient treatment include nulliparity
(borne no children) or low parity, severe illness
(eg, significant fever, leukocytosis, pain),
suspected pregnancy, and mass noted during the
pelvic examination in these cases, IV therapy
should continue until the patient has been
afebrile for 24 h. Percutaneous or transvaginal
drainage of a tubo-ovarian abscess can be
performed using ultrasound guidance. For
uncomplicated infection due to N. gonorrhoeae,
options include Ceftriaxone 125 mg
IM Cefixime 400 mg po Ciprofloxacin 500 mg
po Because C. trachomatis often accompanies N.
gonorrhoeae, the following may be
used Doxycycline 100 mg po bid for 7
days Azithromycin 1 g po in a single dose
Ofloxacin 300 mg bid for 7 days Partners of
patients with infection also need to be treated.
The Merck Manual
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