Endometriosis

Jamie A. M. Massie MD
Ruth B. Lathi MD
Lynn M. Westphal MD
Basics
Description
The presence of endometrial glands and stroma at any site outside the uterine cavity.
Age-Related Factors
 Occurs during the active reproductive period
 Rare in postmenopausal women

Pediatric Considerations
 Rare in pre- or recently postmenarchal girls, but can occur
 25–38% of adolescents with chronic pelvic pain affected

 The development of endometriosis during childhood or adolescence may

indicate some degree of genital tract obstruction (i.e., uterine or vaginal
septum).

Staging
Staging is based on site(s) and severity of involvement at the time of surgery:
 Stage I (minimal): Isolated implants, no significant adhesions
 Stage II (mild): Superficial implants with <5 cm of total disease, no significant
adhesions
 Stage III (moderate): Multiple superficial and deep implants, with or without
peritubal and periovarian adhesions
 Stage IV (severe): Multiple superficial and deep implants, large ovarian
endometrioma(s), with presence of adhesions

Epidemiology
Present in 7–10% of women in the general population
Risk Factors
 Delayed childbearing
 1st-degree relative with endometriosis

 Short menstrual cycles

 Delayed parity may increase risk

 Increased incidence in women with uterine anomalies leading to outflow

obstruction (i.e., transverse vaginal septum)

Genetics
 Familial disposition is suggested by current data.
 Concordance in twins has been observed.

Pathophysiology
Controversial, but theories include:
 Retrograde menstruation (Sampson's theory)
  Dissemination of endometrial cells through lymphatics/blood vessels
(Halban's theory)
 Direct transplantation

 Coelomic metaplasia

Associated Conditions
 Adenomyosis
 Uterine leiomyomata

 Chronic pain syndromes

 Infertility

 Müllerian anomalies

 Autoimmune diseases (i.e., hypothyroidism)

 Ovarian cancer (independent risk factor for epithelial ovarian cancer)

Diagnosis
Signs and Symptoms
History
 Dysmenorrhea and/or back pain: Cyclic
 Dysmenorrhea is usually secondary; pain typically begins before the onset of
menstrual flow and may be severe
 Deep dyspareunia

 Premenstrual spotting

 Infertility

Review of Systems
 Primary complaint not GI related
 Denies fever/chills

 Denies anorexia or nausea/vomiting

 Absence of urinary frequency or dysuria

 Absence of purulent vaginal discharge

Physical Exam
 Pelvic exam is nonspecific. The following may be present:
o Uterus of normal size, but mobility limited

o Uterosacral nodularity and tenderness

o Adnexal mass

 Abdominal exam usually benign, unless ruptured endometrioma produces

peritoneal signs
Tests
 Direct visualization via laparoscopy with biopsy confirmation of
endometriosis is required for definitive diagnosis.
 Vesicular lesions on peritoneal surfaces may be black, brown, red, clear, or
white.
 Clear or red flame lesions (“atypical” lesions) are more common in
adolescents.
 Lesions outside of the pelvis can be present (e.g., appendix, diaphragm,
bowel).
 Pelvic adhesions vary from none to severe.

Labs
Serum CA-125:
 May be elevated (>35 IU/mL) in women with endometriosis
 Sensitivity and specificity are low

 Also elevated in other gynecologic disorders (i.e., ovarian cancer)

Imaging
 Rarely helpful in diagnosis of disease
 Vaginal/Abdominal US can be used to diagnose endometrioma.

 MRI can be used to map extent of disease if bladder or bowel involvement is

suspected.
 Hysterosalpingography is useful only in evaluation of fallopian tube occlusion.

Differential Diagnosis
 Adenomyosis
 Uterine leiomyomata

 Interstitial cystitis

 Pelvic adhesive disease

 PID

 Primary dysmenorrhea

 Ovarian torsion

 Ectopic pregnancy

 IBS

 Appendicitis

 Diverticulitis

Treatment
General Measures
Treatment plans should be individualized and based on patient age and desire for
future fertility.
Medication (Drugs)
 First-line therapies below should be combined with NSAIDs to obtain
maximum benefit:
o COCs daily

o Medroxyprogesterone acetate (MPA) 150 mg IM every 3 months

 If symptoms persist after 3 months of OCPs or MPA and NSAIDs:

o Empiric therapy with a 3-month course of GnRH agonist may be

initiated:
 Duration of therapy should be limited to 6 months unless add-
back therapy is started
o Danazol 600–800 mg/d for a course of 6 months is a lower-cost option
than GnRH agonist, however side-effect profile less favorable
 Levonorgestrel IUS: Limited data suggest improvement in dysmenorrhea and
menorrhagia with use

P.97

Surgery
 Patients with persistent pain despite appropriate medical therapies or those
with infertility should pursue surgical treatment.
 Laparoscopy with destruction of identifiable lesions via one of the following
mechanisms:
o Excision

o Laser vaporization

o Electrocautery

o Endocoagulation

 Hysterectomy with/without bilateral salpingo-oophorectomy can be offered to

women who have completed childbearing.
 Postoperatively, use of GnRH agonists for a period of 3–6 months may extend
the painfree interval.

Followup
Disposition
Issues for Referral
 Patients with unexplained infertility should be referred to board-certified
reproductive endocrinologist or gynecologist with expertise in infertility.
  Patients with endometriosis resulting in severe adhesive disease with
significant distortion of the pelvic anatomy may benefit from referral to a
gynecologic oncologist or laparoscopic specialist for surgical treatment.
 Patients with persistent or inadequately treated pain may benefit from
consultation with an interdisciplinary pain management team or service.

Prognosis
 Up to 80% of women have improvement in pain with medical treatment alone,
although there is a high rate of recurrent symptoms after cessation of therapy.
 80–90% of women have improvement in pain after surgery.

 Pregnancy rates are improved after surgical treatment of endometriosis in

patients with infertility.
 Endometriosis often improves or resolves after pregnancy.

Patient Monitoring
 For those patients on extended therapy with a GnRH agonist, vasomotor
symptoms and/or bone loss can develop.
 Add-back therapy with progestins or low-dose OCPs may be utilized to
minimize bone loss and limit vasomotor symptoms.

Bibliography
ACOG Practice Bulletin. Medical management of endometriosis. Clinical
Management Guidelines for Obstetrician-Gynecologists. Number 11, December 1999.
Kennedy S, et al. ESHRE guideline for the diagnosis and treatment of endometriosis.
Hum Reprod. 2005;20(10):2698–2704.
Schenken RS. Pathogenesis. In: Schenken RS, ed. Endometriosis: Contemporary
Concepts in Clinical Management. Philadelphia: JB Lippincott; 1989.
Vercellini P, et al. Endometriosis and pelvic pain: Relation to disease stage and
localization. Fertil Steril. 1996;65(2):299–304.
Miscellaneous
Abbreviations
• COC—Combined oral contraceptives
• GnRH—Gonadotropin releasing hormone
• IBS—Irritable bowel syndrome
• IUS—Intrauterine system
• MPA—Medroxyprogesterone acetate
• NSAIDs—Nonsteroidal anti-inflammatory drugs
• OCP—Oral contraceptive pill
• PID—Pelvic inflammatory disease
Codes
ICD9-CM
• 617.0 Endometriosis of uterus
• 617.1 Endometriosis of ovary
• 617.3 Endometriosis of pelvic peritoneum
• 617.5 Endometriosis of intestine
• 617.9 Endometriosis, site unspecified
Patient Teaching
• Endometriosis Patient Education Pamphlet, American College of Obstetricians and
Gynecologists, November 2001
• The Endometriosis Association www.endo-online.org