OBGYN—PID, TOA, and TSS



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

5) Cytomegalovirus

6) Group B streptococcus

7) Streptococcus faecalis

8) Prevotella bivius

Normal Vaginal Flora

1) Gardnerella vaginalis

2) Haemophilus influenzae

3) Enteric gram-negative organisms (Escherichia coli)

4) Peptococcus and Peptostreptococcus species (anaerobic cocci)

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

5) Nulliparity

6) IUD use

7) History of PID

8) History of STDs

9) Vaginal douching

10) Smoking

History

1) Fever and/or chills

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 beta-hemolytic 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 Strep. pyogenes: females = males

S. aureus: age 15-35 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

6) Osteomyelitis

7) Infection of nasopharynx, vagina, rectum, wounds

8) Nasal packing

9) Immunosuppression – diabetes, HIV

History

1) Abrupt high fever or chills

2) Profuse watery diarrhea

3) Vomiting

4) Prodromal – headache, myalgia, arthralgia, sore throat

5) Erythroderma

6) Conjunctivitis

7) Confusion

8) Lightheadedness or syncope

9) 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

................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download