HUMAN IMMUNODEFICIENCY VIRUS (HIV)



 

Refer to Obstetrics, Chapter 7, Perinatal Infections.

 

 

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PELVIC INFLAMMATORY DISEASE (PID)

A 19-year-old nulligravida presents to the emergency department with bilateral lower abdominal pelvic pain. The onset was 24 hours ago after she had just finished her menstrual period. She is sexually active but using no contraception. Speculum examination reveals mucopurulent cervical discharge. Bimanual pelvic examination shows bilateral adnexal tenderness and cervical motion tenderness. She is afebrile. Qualitative urinary b-hCG test is negative. Complete blood cell count shows WBC 14,000. ESR is elevated.

 

 

Definition. PID is a nonspecific term for a spectrum of upper genital tract conditions rangingfrom acute bacterial infection to massive adhesions from old inflammatory scarring.

The most common initial organisms are chlamydia and gonorrhea. With persistent infection, secondary bacterial invaders include anaerobes and gram-negative organisms.

 

Pathophysiology

 

Cervicitis. The initial infection starts with invasion of endocervical glands with chla-mydia and gonorrhea. A mucopurulent cervical discharge or friable cervix may be noted. Cervical cultures will be positive, but symptoms are usually absent.

 

Acute salpingo-oophoritis. Usually after a menstrual period with breakdown of thecervical mucus barrier, the pathogenic organisms ascend through the uterus, causing an endometritis, and then the bacteria enter the oviduct where acute salpingo-oophoritis develops.

 

Chronic PID. If the salpingo-oophoritis is not appropriately treated, the body’simmune defenses will often overcome the infection but at the expense of persistent adhesions and scarring.

 

Tubo-ovarian abscess (TOA). If the body’s immune defenses cannot overcome theinfection, the process worsens, producing an inflammatory mass involving the ovi-ducts, ovaries, uterus, bowel, and omentum.

 

Risk Factors. The most common risk factor is female sexual activity in adolescence, with multiplepartners. PID is increased in the month after insertion of an IUD, but this is probably exacerbation of preexisting subclinical infection.

 

 

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GYN Triad

Acute Salpingo-Oophoritis

 

• Bilateral abdominal/pelvic pain

 

• Mucopurulent cervical discharge

 

• Cervical motion tenderness

 

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Cervicitis

Symptoms. Often there are no symptoms except vaginal discharge.

 

Examination. The most common finding is mucopurulent cervical discharge or a friable cer-vix. No pelvic tenderness is noted. The patient is afebrile.

 

Investigative Findings. This can be either a laboratory diagnosis or a clinical diagnosis. SeeDiagnosis section for chlamydia. WBC and ESR are normal.

 

Management. Single dose orally of cefixime and azithromycin.

 

 

Acute salpingo-oophoritis

 

Symptoms. Bilateral lower abdominal-pelvic pain may be variable ranging from minimal tosevere. Onset may be gradual to sudden, often after menses. Nausea and vomiting may be found if abdominal involvement is present.

 

Examination. Mucopurulent cervical discharge, cervical-motion tenderness, and bilateraladnexal tenderness are present. Fever, tachycardia, abdominal tenderness, peritoneal signs, and guarding may be found depending on the extent of infection progression.

 

Investigative Findings. WBC and ESR are both elevated. Pelvic sonography is usually unremark-able. Laparoscopy will show erythematous, edematous, purulent oviducts. Cervical cultures will come back positive for chlamydia or gonorrhea.

 

Differential Diagnosis. Adnexal torsion, ectopic pregnancy, endometriosis, appendicitis, diver-ticulitis, Crohn disease, and ulcerative colitis.

Diagnosis. This is a made on clinical grounds using the following:

 

Minimal criteria:

Sexually active young woman

Pelvic or lower abdominal pain

Tenderness: cervical motion or uterine or adnexal

Supportive criteria (but not necessary for diagnosis):

– Oral temperature >101°F (>38.3°C)

– Abnormal cervical or vaginal mucopurulent discharge

– Presence of abundant WBC on vaginal fluid saline microscopy

– Elevated erythrocyte sedimentation rate

– Positive lab findings of cervical N. gonorrhoeae or C. trachomatis

– Most specific criteria for diagnosis:

– Endometrial biopsy showing endometritis

– Vaginal sono or MRI imaging showing abnormal adnexae

– Laparoscopic abnormalities consistent with PID

 

Management is often based on a presumptive diagnosis. Empiric broad spectrum coverageneed to include N. gonorrhoeae or C. trachomatis as well as anaerobes (e.g., B. fragilis).

 

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Outpatient treatment is equivalent to inpatient in mild to moderate cases.

 

Criteria: absence of inpatient criteria

Antibiotics: Ceftriaxone IM x 1 plus doxycycline po bid for 14 days with/without met-ronidazole po bid for 14 days

Inpatient treatment is essential with severe cases

 

Criteria: Appendicitis cannot be ruled out; failed outpatient therapy; unable to tolerate oralmedications; severe illness, high fever, nausea/vomiting; tubo-ovarian abscess or pregnancy

Antibiotics: (1) Cefotetan IV 12 h plus doxycycline po or IV q 12 h or (2) clindamycinplus gentamicin IV q 8 h

     

Cervicitis

               
                             
       

 

                 
 

Acute salpingo-oophoritis

         
                             
 

 

     

 

   

 

     
                             

Treatment

     

No treatment

   
                             
                             
                             

Heals without

   

Heals with

       

Gets

adhesions

   

adhesions

       

worse

Normal pelvis

 

Chronic PID

       

TOA

                             

Figure II-8-1. Pelvic Inflammatory Disease

 

Tubo-ovarian abscess (TOA)

 

TOA is the accumulation of pus in the adnexae forming an inflammatory mass involving the oviducts, ovaries, uterus, or omentum.

 

Symptoms. The patient looks septic. Lower abdominal-pelvic pain is severe. Often the patient hassevere back pain, rectal pain, and pain with bowel movements. Nausea and vomiting are present.

 

Examination. The patient appears gravely sick. She has high fever with tachycardia. She maybe in septic shock with hypotension. Abdominal examination shows peritoneal signs, guarding, and rigidity. Pelvic examination may show such severe pain that a rectal examination must be performed. Bilateral adnexal masses may be palpated.

 

Investigative Findings. Cervical cultures are positive for chlamydia or gonorrhea. Blood cul-tures may be positive for gram-negative bacteria and anaerobic organisms such as Bacteroides fragilis. Culdocentesis may yield pus. WBC and ESR are markedly elevated. Sonography or CTscan will show bilateral complex pelvic masses.

 

Differential Diagnosis. Septic abortion, diverticular or appendiceal abscess, and adnexal torsion.

 

 

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GYN Triad

Chronic Salpingo-Oophoritis

 

• Bilateral abdominal/pelvic pain

 

• No cervical discharge

 

• Cervical motion tenderness

 

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Management. Inpatient IV clindamycin and gentamicin should result in fever defervescencewithin 72 hours. If the patient does not respond or there is rupture of the abscess exposing free pus into the peritoneal cavity, significant mortality can occur. Exploratory laparotomy with pos-sible TAH and BSO or percutaneous drainage through a colpotomy incision may be required.

Chronic PID

 

Symptoms. Chronic bilateral lower abdominal-pelvic pain is present, varying from minimal tosevere. Other symptoms may include history of infertility, dyspareunia, ectopic pregnancy, and abnormal vaginal bleeding. Nausea and vomiting are absent.

 

Examination. Bilateral adnexal tenderness and cervical-motion tenderness is present, butmucopurulent cervical discharge is absent. Fever and tachycardia are absent.

 

Investigative Findings. Cervical cultures are negative. WBC and ESR are normal. Sonographymay show bilateral cystic pelvic masses consistent with hydrosalpinges.

 

Diagnosis. This is based on laparoscopic visualization of pelvic adhesions.

 

Management. Outpatient mild analgesics are used for pain. Lysis of tubal adhesions may behelpful for infertility. Severe unremitting pelvic pain may require a pelvic clean-out (TAH, BSO). If the ovaries are removed, estrogen replacement therapy is indicated.

 

 

PRIMARY DYSMENORRHEA

A 15-year-old girl comes to the outpatient office complaining of severe menstrual-period pain that started 6 months ago. Onset of menarche was age 13. The pain can be so severe that she is unable to attend school or carry on normal activities. She describes it as cramping in nature, and it is associated with nausea, vomiting, and diarrhea. When her menses are completed, the pain is gone. She is not sexually active. General exam is normal for age. Pelvic exam is unremarkable.

 

 

Definition. Primary dysmenorrhea refers to recurrent, crampy lower abdominal pain, alongwith nausea, vomiting, and diarrhea, that occurs during menstruation in the absence of pelvic pathology.

 

It is the most common gynecologic complaint among adolescent females. (Secondary dysmen-orrhea refers to painful menstruation in the presence of pelvic pathology. It is more common among women in the fourth and fifth decades of life.)

 

Findings

 

• Onset of pain generally does not occur until ovulatory menstrual cycles are estab-lished. Maturation of the hypothalamic-pituitary-gonadal axis leading to ovulation occurs in half of teenagers within 2 years postmenarche, and the majority of the remainder by 5 years postmenarche.

 

• The symptoms typically begin several hours prior to the onset of menstruation and continue for 1 to 3 days.

 

• The severity of the disorder can be categorized by a grading system based on the degree of menstrual pain, presence of systemic symptoms, and impact on daily activities.

 

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Pathogenesis

 

• Symptoms appear to be caused by excess production of endometrial prostaglandin F2α resulting from the spiral arteriolar constriction and necrosis that follow progesterone withdrawal as the corpus luteum involutes. The prostaglandins cause dysrhythmic uterine contractions, hypercontractility, and increased uterine muscle tone, leading to uterine ischemia.

 

• The effect of the prostaglandins on the gastrointestinal smooth muscle also can account for nausea, vomiting, and diarrhea via stimulation of the gastrointestinal tract.

 

Management. Suppression of prostaglandins is the objective of treatment. Nonsteroidal antiinflam-matory drugs (NSAIDs, i.e., prostaglandin synthetase inhibitors) are the first choice in treatment.

 

• Continuous combination estrogen-progesterone steroid agents (e.g., oral contracep-tives) are the second choice for suppressing prostaglandin release.

 

SECONDARY DYSMENORRHEA

 

Endometriosis

 

A 34-year-old woman complains of painful periods, painful sex, painful bowel movements, and infertility for 2 years. She had used combination oral contraceptive pills from age 25 to 30. Pelvic examination reveals a tender, 5-cm cul-de-sac mass, along with tenderness and nodularity of the uterosacral ligaments.

Definition. Endometriosis is a benign condition in which endometrial glands and stroma areseen outside the uterus. This is not a premalignant condition.

 

Pathophysiology. Although the etiology of endometriosis is not known, the most acceptedtheory of explanation is that of Sampson, which is retrograde menstruation.

 

• The most common site of endometriosis is the ovary, and because this is functioning endometrium, it bleeds on a monthly basis and can create adnexal enlargements known as endometriomas, also known as a chocolate cyst.

 

• The second most common site of endometriosis is the cul-de-sac, and in this area the endometriotic nodules grow on the uterosacral ligaments, giving the characteristic uterosacral ligament nodularity and tenderness appreciated by rectovaginal examina-tion. Menstruation into the cul-de-sac creates fibrosis and adhesions of bowel to the pelvic organs and a rigid cul-de-sac, which accounts for dyspareunia.

 

Clinical Findings

 

Symptoms. Pelvic-abdominal pain is not necessarily related to the extent of disease. Painfulintercourse (dyspareunia) is often experienced along with painful bowel movements (dys-chezia). Infertility of endometriosis is not necessarily related to the extent of disease.

 

Examination. Pelvic tenderness is common. A fixed, retroverted uterus is often causedby cul-de-sac adhesions. Uterosacral ligament nodularity is characteristic. Enlarged adnexa may be found if an endometrioma is present.

 

Investigative findings. WBC and erythrocyte sedimentation rate (ESR) are normal.CA-125 may be elevated. Sonogram will show an endometrioma if present.


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GYN Triad

Endometriosis

 

• Chronic pelvic pain

 

• Painful intercourse

 

• Painful bowel movements


 

 

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Diagnosis. The diagnosis of endometriosis is made by laparoscopy. There is a suspicion ofthe disease based on history and physical examination; however, laparoscopic identification of endometriotic nodules or endometriomas is the definitive way of making the diagnosis.

Medical therapy of endometriosis seeks to prevent shedding of the ectopic endometrial tissue,thus decreasing adhesion formation and pain.

 

Pregnancy can be helpful to endometriosis because during pregnancy there is nomenstruation and also the dominant hormone throughout pregnancy is progesterone, which causes atrophic changes in the endometrium. However, infertility may make this impossible.

 

Pseudopregnancy achieves this goal through preventing progesterone withdrawalbleeding. Continuous oral medroxyprogesterone acetate (MPA [Provera]), subcutane-ous medroxyprogesterone acetate (SQ-DMPA [Depo Provera]), or combination oral contraceptive pills (OCPs) can mimic the atrophic changes of pregnancy.

 

Pseudomenopause achieves this goal by making the ectopic endometrium atrophic.The treatment is based on inhibition of the hypothalamic–pituitary–ovarian axis to decrease the estrogen stimulation of the ectopic endometrium. Several medications can be used to achieve inhibition of the axis.

 

\endash Testosterone derivative (Danocrine or Danazol)

 

\endash Gonadotropin-releasing hormone (GnRH) analog (leuprolide or Lupron)

 

The best inhibition of the hypothalamic–pituitary–ovarian axis is achieved by GnRH analogs. GnRH stimulates the pituitary in a pulsatile fashion, and GnRH analogs stimulate by continu-ous stimulation, which produces a condition known as down-regulation of the pituitary.

Although regression of the endometriotic nodules can be achieved, the patient can become symptomatic with menopausal complaints. Patients on Lupron therapy for >3–6 months can complain of menopausal symptoms, such as hot flashes, sweats, vaginal dryness, and personal-ity changes. Lupron medication is continued for 3–6 months’ duration, and then a more accept-able medication for the inhibition of the axis can be used, such as birth control pill medication. An alternative to Lupron is DMPA (Depo Provera), which also suppresses FSH and LH but does not result in vasomotor symptoms.

 

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Surgical management may be conservative or aggressive.

Conservative. If preservation of fertility is desired, the procedures can be performedin many cases through laparoscopic approach. Lysis of paratubal adhesions may allow adherent fimbria to function and achieve pregnancy. Ovarian cystectomies as well as oophorectomies can be treatment for endometriomas. Laser vaporization of visible lesions is also performed laparoscopically.

 

Aggressive. If fertility is not desired, particularly if severe pain is present becauseof diffuse adhesions, definitive surgical therapy may be carried out through a total

 

abdominal hysterectomy (TAH) and bilateral salpingo-oophorectomy (BSO). Estrogen replacement therapy is then necessary.

 

Follow-Up. Endometriosis is not considered a premalignant condition; however, patients withthis disease should be followed up with yearly gynecologic evaluation.

 

 

Adenomyosis

 

Refer to Chapter 4, Disorders of the Cervix and Uterus.

 

 

Ectopic Pregnancy

 

Refer to Obstetrics, Chapter 2, Failed Pregnancy.

 

 

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Fertility Control

 

 


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