OBGYN—PID, TOA, and TSS
Pelvic Inflammatory Disease (PID)
Pelvic inflammatory disease (PID) usually comes from infection, most
commonly Cervicitis. It is a general term for acute, subacute, recurrent, or chronic
genital tract and pelvic infection. Acute salpingitis is the most important subtype and
most common presentation of PID. Infection of the upper female genital tract is most
commonly the result of direct spread of bacteria (most commonly Chlamydia trachomatis
and Neisseria gonorrhoeae) along mucosal surfaces from an initial cervical infection. It
is an ascending pelvic infection, starting from the cervix and heading upwards. The
normal protective endocervical mucus may be directly breached by bacteria, or may ride
on sperm or trichomonads, or via the string of an intrauterine device. Cervical infection
may then easily spread to the uterus (endometritis), then subsequently to the fallopian
tubes (salpingitis), ovaries (oophoritis), pelvic and abdominal peritoneum, and adjacent
tissues.
Etiology
1) *Chlamydia trachomatis*
2) *Neisseria gonorrhoeae*
3) Mycoplasma hominis
4) Ureaplasma urealyticum
Normal Vaginal Flora
1) Gardnerella vaginalis
2) Haemophilus influenzae
3) Enteric gram-negative organisms
(Escherichia coli)
4) Peptococcus and
Peptostreptococcus species
(anaerobic cocci)
5)
6)
7)
8)
Cytomegalovirus
Group B streptococcus
Streptococcus faecalis
Prevotella bivius
5) Streptococcus agalactiae
6) Bacteroides fragilis (anaerobic)
7) Lactobacillus is the most
common finding in the vagina
Epidemiology
1) Incidence: 1 million (200,000 require hospitalization)
2) 11% of all reproductive-aged females
Risk Factors
1) Young age
2) Sexually active, recent
intercourse, unprotected sex
and young age of first sexual
intercourse
3) Multiple sexual partners
4) Unmarried
History
1) Fever and/or chills
5) Nulliparity
6) IUD use
7) History of PID
8) History of STDs
9) Vaginal douching
10) Smoking
2) Abdominal/pelvic pain - May be insidious or acute, but diminishes within 1
week. Constant, and of a dull and aching character; usually bilateral. May
manifest as back pain with radiation down one or both legs
3) Right upper quadrant pain – Fitz-Hugh-Curtis perihepatitis syndrome. Usually
stems from an upper abdominal peritonitis, causing fibrosis of the liver. Leads to
“violin-string” fibrosis.
4) Pelvic pressure
5) N/V
6) Headache
7) Lassitude
8) Vaginal discharge and abnormal vaginal bleeding
9) Of recent menses – when menstruation occurs, there is a reduction in the amount
of cervical mucus, which is protective. There is also dilatation of the
endocervical canal. This all increases the risk of PID cervicitis.
10) Of underlying STD
Physical
Abdominal Exam
1) Abdominal distension
2) Hypoactive/absent bowel sounds
3) Bilateral lower abdominal tenderness
4) Abdominal muscle guarding and/or rebound tenderness
Pelvic Exam
1) Periurethral (Skene) or Bartholin gland inflammation
2) Purulent cervical discharge
3) Adnexal and uterine mass/fullness and/or tenderness
4) Chandelier sign – cervical motion tenderness
5) Urethral discharge
Differential
1) Appendicitis
2) Diverticulitis
3) Regional ileus
4) Ulcerative colitis
5) UTI pyelonephritis
6) Ectopic pregnancy
7) Endometriosis
8) Ovarian tumors and ruptured
cysts
9) Adnexal torsion
10) Degenerating leiomyoma
Diagnosis
1) CBC with differential
2) Urine or β-hCG
3) ESR/CRP
4) Syphilis screening – RPR and VDRL
5) Vaginal wet mounts may show WBCs
6) Gonorrhea and chlamydia cervical cultures – usually positive
7) Abdominal plain films – abscess may develop and eventually rupture, showing
free air under the diaphragm
8) Transvaginal sonography – thickened fluid-filled tubes, with or without free
pelvic fluid or tubo-ovarian abscess
9) Pelvic MRI
10) Culdocentesis – blood (acute salpingitis) or pus (acute salpingitis with
progression to ruptured tubo-ovarian abscess). Rarely done.
11) Endometrial biopsy – endometritis
12) Laparoscopy – when suspecting abscess formation
CDC Clinical Criteria for Diagnosis of Acute Salpingitis
Must be present:
1) Abdominal tenderness with/without rebound
2) Uterine/adnexal tenderness
3) Cervical motion tenderness
Plus one or more of the following:
1) Gram stain of endocervix positive for gram negative, intracellular diplococci
or laboratory documentation of cervical infection with Neisseria gonorrhoeae
or Chlamydia trachomatis
2) Temperature > 38.3oC
3) WBC > 10,000
4) Elevated erythrocyte sedimentation rate
5) Elevated C-reactive protein level
6) Pus on culdocentesis or laparoscopy or abnormal cervical or vaginal
mucopurulent discharge
7) Presence of white blood cells (WBCs) on saline microscopy of vaginal
secretions
8) Pelvic abscess on bimanual exam or sonogram
Treatment
1) Outpatient: patient characteristics include minimal lower abdominal findings,
fever < 39oC, nontoxic, able to tolerate PO medication – Ofloxacin 400mg BID or
levofloxacin 500mg PO QD x 14 days + Metronidazole 500mg PO BID or
clindamycin 450mg PO QID x 14 days to cover anaerobes OR Ceftriaxone
250mg IM once (or equivalent cephalosporin: cefoxitin 2g IM once or
ceftizoxime or cefotaxime) and probenecid 1g PO + doxycycline 100mg PO BID
x 14 days + Metronidazole 500mg PO BID (preferred modality)
Hospitalization Indications
1) Uncertain diagnosis, or surgical emergencies (i.e. appendicitis) that cannot be
ruled out
2) Ultrasonic evidence of tubo-ovarian abscess
3) Upper abdominal peritonitis
4) Pregnant
5) Nulliparity
6) WBCs > 20,000 or < 4,000
7) Failure to improve clinically after 72 hours with outpatient therapy
8) Unable to follow (unreliable) or tolerate outpatient oral regimen
9) All adolescents
10) Severe course of illness, nausea, vomiting, high fever
11) Immunodeficient – HIV with low CD4 count, immunosuppressive therapy, or
other immunosuppressant disease
Inpatient
1) Suggested if toxic appearance, temperature > 39oC, abdominal guarding and
rebound tenderness
2) Supportive – bed rest, restrict PO intake, IV resuscitation, nasogastric suction
3) Cefoxitin 2g IV q6hr or cefotetan 2g IV q12hr + doxycycline 100mg PO/IV q12h,
for at least 24 hours following clinical improvement, then doxycycline 100mg PO
BID x 14 days (preferred modality)
4) Clindamycin 900mg IV q8hr + Gentamicin 2mg/kg loading dose IV or IM
followed by a maintenance dose of 1.5mg/kg q8hr IV, for at least 24 hours
following clinical improvement, then doxycycline 100mg PO BID x14 days or
clindamycin 450mg PO QID x 14 days
Complications
1) Pelvic peritonitis or generalized peritonitis
2) Prolonged adynamic ileus – no bowel function
3) Severe pelvic cellulitis with thrombophlebitis
4) Abscess formation – pyosalpinx, tubo-ovarian, cul-de-sac
5) Adnexal destruction
6) Infertility – 12% incidence following first episode of salpingitis, 25% following
second, and 50% following third
7) Ectopic pregnancy
8) Chronic pelvic pain and chronic PID
9) Intestinal adhesions
10) Intestinal obstruction
11) Rare – dermatitis, gonococcal arthritis, bacteremia, septic shock
Teaching Points
1) Treat patient's sexual contacts within last 60 days
2) Start empiric therapy if minimal criteria present
3) Delay > 3 days increases ectopic pregnancy and infertility risk
4) Correct underlying risk factors
Tubo-Ovarian Abscess (TOA)
Tubo-Ovarian Abscess (TOA) is a purulent inflammatory mass arising from
untreated or inadequately treated acute salpingo-oophoritis. Its formation may occur
following an initial episode of acute salpingitis, but more commonly is seen with
recurrent infection superimposed on chronically damaged adnexal tissue. The
pathogenesis of TOA is due to fallopian tube necrosis and epithelial damage by bacterial
pathogens causing a favorable environment for anaerobic invasion and growth. TOA
may involve the uterus, oviducts, ovaries, bowel, and omentum. Disease may be
bilateral, but is usually unilateral.
Etiology
1) Polymicrobial with abundance of anaerobes
2) Actinomyces israelii associated with IUD usage
History
1) Asymptomatic
2) Fever
3) Abdominopelvic pain – acute and often diffuse
4) N/V
5) Of previous pelvic infection
6) Menses > 2 weeks prior
Physical
1) Fever
2) Tachycardia
3) Abdominal exam – guarding, rebound tenderness, ileus, rigidity
4) Pelvic exam – adnexal mass
5) Of underlying PID
Presentation of Ruptured Tubo-Ovarian Abscess
1) Impending or actual septic shock – Fever or hypothermia, chills, tachycardia,
disorientation, hypotension, tachypnea, oliguria
Diagnosis
1) CBC with differential – leukocytosis/leukopenia
2) Urinalysis will show WBCs
3) ESR/CPR will be elevated
4) Cervical cultures – positive for gonorrhea and chlamydia
5) Kidney-ureter-bladder (KUB) – adynamic ileus, adnexal mass, free air under the
diaphragm (rupture)
6) Pelvic ultrasonography – complex adnexal masses with thickened walls and
central fluid
7) Culdocentesis – blood (as in acute salpingitis), purulent material (in leaking or
ruptured TOA)
Treatment: Unruptured Symptomatic TOA
1) Immediate hospitalization – Bed rest in semi-Fowler position, Intravenous
rehydration, Frequent abdominal assessment, Nasogastric suction
2) Antibiotic therapy – Penicillin G or ampicillin + gentamycin + clindamycin or
Metronidazole x 48-72 hrs.
3) Complications – rupture with sepsis, reinfection, bowel obstruction, infertility,
ectopic pregnancy
Ruptured TOA - an acute life-threatening catastrophe requiring immediate surgical
intervention
1) Laparoscopy with laparotomy: lysis, irrigation, drainage or dissection of all
abdominal and pelvic abscesses
2) Complications: septic shock, intra-abdominal abscess (e.g., subphrenic,
subhepatic abscess), septic emboli with renal, lung, or brain abscess
3) Prognosis – 2% mortality
Toxic Shock Syndrome (TSS)
Toxic shock syndrome (TSS) has been linked to endotoxin production by
bacteria, most often toxic shock syndrome toxin-1 (TSST-1). The toxins activate
production of superantigens, such as tumor necrosis factor, interleukin-1, M protein, and
gamma-interferon. Coagulase-positive staphylococci (S aureus) and group A betahemolytic streptococci (S pyogenes) contribute to TSS; bacterial invasiveness does not
contribute to the syndrome. Historically, it has been associated with tampon use in
women, however, there are now as many non-menstrual causes of TSS. Non-menstrual
causes are usually not caused by strains producing TSST-1. Almost every organ system
can be involved, including the cardiovascular, renal, skin, mucosa, GI, musculoskeletal,
hepatic, hematologic, and central nervous systems.
Epidemiology
S. aureus: females > males
S. aureus: age 15-35
Strep. pyogenes: females = males
Strep. pyogenes: age 50-70
Etiology
1) Staphylococcus aureus (TSST-1)
2) Streptococcus pyogenes exotoxin A (SPEA)
3) Streptococcus pyogenes exotoxin B (SPEB)
Risk Factors
1) Use of superabsorbent tampons
2) Post-surgery – wound
colonization
3) Postpartum
4) Diaphragm use
5) Soft tissue abscesses
History
1) Abrupt high fever or chills
2) Profuse watery diarrhea
3) Vomiting
4) Prodromal – headache, myalgia,
arthralgia, sore throat
5) Erythroderma
6) Osteomyelitis
7) Infection of nasopharynx, vagina,
rectum, wounds
8) Nasal packing
9) Immunosuppression – diabetes,
HIV
6)
7)
8)
9)
Conjunctivitis
Confusion
Lightheadedness or syncope
Use of tampons or
menstruating
10) Of underlying infection
Physical
1) High fever > 39oC
2) Hypotension: endotoxin-mediated or orthostatic
3) Tachycardia
4) Dry mucus membranes
5) Toxic appearance
6) Diffuse erythematous “sunburn-like” rash – trunk initially, then to extremities
(including palms and soles), and face
7) Desquamation of palms and soles
8) Erythema of conjunctivae or pharynx
9) Muscle tenderness
10) Abdominal tenderness
11) Pelvic exam – evidence of tampon
12) Of multisystem involvement – DIC, ARDS, hepatic or renal failure, cardiac
dysrhythmias, altered consciousness, necrotizing fascitis and/or myositis
13) Of underlying infection
Differential
1) Scarlet fever
2) Kawasaki disease
3) Measles
4) Rocky Mountain spotted fever
5) Leptospirosis
6) Gram-negative sepsis
Diagnosis
1) CBC with differential – leukocytosis, mild anemia, thrombocytopenia
2) CMP - Hyponatremia, hypokalemia, hypocalcemia, hypophosphatemia, and
hypomagnesemia, elevated BUN and creatinine
3) Serum albumin – hypoalbuminemia
4) Liver profile – increased AST, ALT, hyperbilirubinemia
5) Coagulation studies – increased aPTT and fibrin split products (normal fibrinogen
levels and PT)
6) Arterial blood gas – metabolic acidosis
7) Urinalysis – pyuria, myoglobinuria, red cell casts
8) Creatine phosphokinase
9) Pertinent cultures
10) Lumbar puncture
11) EKG – ventricular arrhythmias, bundle-branch or first-degree heart block, ST-T–
wave changes, with ischemia
12) Plain films – chest, affected site
13) Serologic testing
14) Rapid streptococcal test
Treatment
Aggressive supportive therapy
1) Fluid and electrolyte therapy up to 12 L/d
2) Packed RBCs and coagulation factors
3) Dopamine
4) Mechanical ventilation
5) Hemodialysis
6) Corticosteroids – dexamethasone or methylprednisolone
Antibiotics
1) β-lactamase inhibitor – nafcillin, oxacillin (2g IV q4hr)
2) PCN-allergic – vancomycin
3) Add aminoglycoside until gram-negative sepsis ruled out – Gentamicin
Also:
1) Intravenous immunoglobulin G (IVIG)
2) Treat underlying causes, complications/remove underlying offending agent