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Laparoscopic Treatment of Endometriosis — 267
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adenocarcinoma may develop after bilateral oophorectomy, even
at sites far from the pelvis.[74] Unopposed estrogen stimulation
may lead to premalignant or malignant transformation in the
residual foci of endometriosis. Therefore, the addition of progestins to estrogen replacement therapy should be considered in
women who have undergone hysterectomy with oophorectomy
because of endometriosis, especially if they are known to have
residual endometriosis.
APPEARANCES OF ENDOMETRIOSIS
Laparoscopic assessment in combination with histologic examination of the excised lesions remains the gold standard for diagnosis of endometriosis. Knowledge of the most common locations of endometriosis is required for accurate visual inspection
of the pelvic and abdominal cavities. Three different forms
of endometriosis must be considered during laparoscopic
visualization: peritoneal implants, endometriomas, and deep
infiltrating lesions of the rectovaginal septum. An increased
awareness of the variations in the appearance of endometriotic
lesions hasresulted in an almost twofoldincrease in the diagnosis
of endometriosis at laparoscopy.[75] Peritonealimplantsaremost
commonly localized in the uterosacral ligaments, cul-de-sac,
ovarian fossa, and adjacent pelvic side walls. Less frequently,
implants may also be found in the upper abdomen as well as
on the surface of the bladder and the bowel (predominantly rectum, sigmoid colon, appendix, and cecum). Hence, careful and
close inspection of the entire peritoneal cavity should be performed. Magnification obtained during laparoscopy depends on
the distance between the laparoscope and the area inspected; for
example, the magnification rateis approximately3.2and 1.7 from
a distance of 10 and 20 mm, respectively. Magnification allows
the recognition of lesions as small as 400 μm for red and 180 μm
for clear lesions.
Complete removal of endometriotic implants is difficult
because of their variability in appearance and visibility. Powder
burn lesions represent foci of inactive disease containing stroma
and glands embedded in hemosiderindeposits.[76] These lesions
are more common in older women and may not cause pain or
infertility.[77] When implants involve the uterosacral ligaments,
they are palpable as tender nodularities and can cause dysmenorrhea and dyspareunia. Atypical andnonpigmented lesions, which
are seen as clear vesicles, pink vascular patterns, white scarred
lesions, red lesions, yellow-brown patches, and peritoneal windows, represent active endometriosis and secrete prostaglandin
in the peritoneal fluid.[78] The peritoneum must be examined
from different angles and at different degrees of illumination to
see vesicles or whitish lesions and the peritoneal folds must be
stretched and searched for small, atypical lesions.
Deep nodular endometriosis is usually localized in the rectovaginal and uterovesical septum, in other fibromuscular pelvic
structures (e.g., uterosacral ligaments), and in the muscular wall
of pelvic structures. Rectovaginal nodules are histologically similar to an adenomyoma, being composed of smooth muscle,
endometrial glands, and stroma. They probably constitute an
entity distinct from peritoneal and ovarian endometriosis and
are thought to originate from the mullerian rests present in
the rectovaginal septum.[79] Deep endometriotic lesions may
be predominantly retroperitoneal, with little or no superficial
peritoneal involvement. The depth of endometriotic implants
may be related to the level of disease activity and symptoms
(Figure 10.3.1). Cornillie and coworkers [80] reported that cellular activity of endometriosis was greater for both superficial
and deep implants (58% and 68%, respectively) than for intermediate implants (25%). They postulated that earlylesions result
from proliferation of retrograde menstrual tissue and present as
superficial implants. These lesions progress to an intermediate
depth, where they either become inactive or progress and infiltrate deeper layers, usually more than 5 mm. Implants continue
their biologic activity and proliferate, being stimulated by circulating steroid hormones because they are no longer dependent
on the steroids in the peritoneal fluid.[78,81]
Microscopic endometriosis may be overlooked during surgical exploration but is identified by light and electron microscopy
in normal-appearing peritoneum. This finding has been noted
in patients with visible endometriosis in other areas of the pelvis
[52,53] and patients with unexplained infertility in whom no
endometriosis was seen at laparoscopy.[54,82] Microscopic presentation may preclude total resection, but two techniques can
enhance visual detection. Near-contactlaparoscopymagnifiesthe
peritoneal area. In a series of 20 women with pelvic endometriosis, biopsy specimens were taken from peritoneum that appeared
normal. The histologic studies of this tissue revealed only one
case of microscopic endometriosis, and an additional two cases
were suspicious for endometriosis.[53] The second technique
for improved detection of microscopic endometriosis is “painting” the peritoneum and broad ligament with blood or serosanguineous fluid to render atypical lesions more evident.[83]
Retroperitoneal hydrodissection of the anterior cul-de-sac, posterior broad ligaments, and pelvic side wall sometimes facilitates
the identification of lesions (Figure 10.3.2).
At the time of laparoscopy, endometriomas may be identified as smooth-walled, dark-brownish cysts, usually strongly
associated with the presence of adhesions. Upon incision, dense,
brown, chocolate-like fluid is released. As reported by Vercellini
et al.[84], careful visual inspection of the ovariesis usually highly
reliable in identification of endometriomas, with 97% sensitivity and 95% specificity. Normal-appearing ovaries may contain
endometriosis under an apparently normal cortex. By inserting
a needle deep in the stroma and aspirating the ovary, Candiani
and coworkers [85] identified small endometriomas in 48% of
otherwise normal-appearing or slightly enlarged ovaries. They
suggested that preoperative ultrasonographic evaluation is useful to screen for small subcortical ovarian cysts, which should
be explored surgically with needle aspiration. The diagnosis of
endometriosis is missed in at least 7% of patients and understaged inas many as 50%.[53] Acareful examination of the pelvis
is essential to diagnose and stage endometriosis and to be aware
of its various appearances, including its presence as microscopic
implants on visually normal peritoneal surfaces or as small, deep
endometriomas within slightly enlarged but otherwise normal
ovaries.
Using patient-assisted laparoscopy, Demco [86] studied the
relationship of lesions of endometriosis to pelvic pain. He found
that pain from endometriosis has little relationship to the location or color of lesions. However, red and vascular lesions were
268 — Bulent Berker, Thomas H. S. Hsu, Keith L. Lee, Ceana Nezhat, Farr Nezhat, and Camran Nezhat
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Symphysis
Pouch of Douglas
Pubic bone (cut)
Bladder
Ureter
Vagina
Rectum
Uterosacral ligament
Peritoneal defect
Superficial endometriosis
Peritoneal defect
Superficial endometriosis
(sagittal section)
A
Figure 10.3.1. (A) A peritoneal defect in the pouch of Douglas has an endometriotic implant at its base. The
inset reveals a healed peritoneal defect with infiltrating endometriosis beneath it.
Peritoneal defect is healed
Retraction of peritoneum and rectum
toward the uterosacral ligament
Peritoneal defect is healed
Infiltrating endometriosis
B
Figure 10.3.1. (Continued )(B) Sagittal view of endometriotic implants involving the uterosacral ligament. The
inset shows infiltrating endometriosis beneath the peritoneum.
Laparoscopic Treatment of Endometriosis — 269
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The bowel is retracted over the uterosacral ligaments
Vagina
Rectum
Infiltrating endometriosis
Uterosacral ligament
A
Figure 10.3.2. (A) Anatomic representation of the pelvic structures involved with implants of endometriosis.
(Continued )
the most painful, followed by clear and white scar lesions. Least
painful were black lesions. Pain extended beyond lesions to
normal-looking peritoneum for up to 27 mm but was not consistent with respect to the type of lesion.
TREATMENT OF ENDOMETRIOTIC IMPLANTS
Diagnostic Laparoscopy
Initially,the surgeon exploresthe pelvic cavity to assess the extent
of disease and identify abnormalities or distortions of the pelvic
organs. Photographs and video recordings have been very useful for documenting the surgeon’s findings. In a recent opinion statement, however, the American College of Obstetricians
and Gynecologists’ Committee on Professional Liability advised
against physicians recording proceduresbecause of a growing fear
among clinicians that procedural tapes can be edited, enhanced,
or otherwise manipulated for the purposes of winning liability
suits against doctors.[87] Thecommittee further cautionedthatif
a recording is made, the health care facility should keep the original tape and provide an exactcopy tothepatient.Thelocationand
boundaries of the bladder, ureter, colon, rectum, pelvic gutters,
uterosacral ligaments, and major blood vessels are noted. The
upper abdominal organs, abdominal walls, liver, and diaphragm
should be evaluated for endometriosis or any other condition
that may contribute to the patient’s symptoms. The omentum
and the small bowel are evaluated for disease and to ensure that
they were not injuredduring insertionof the Veress needle or trocar. A rectovaginal examination is accomplished to evaluate deep
and retroperitoneal endometriosis found in the lower pelvis at
the rectovaginal septum, uterosacral ligament, lower colon, and
pararectal area. Deep retroperitoneal endometriosis is rare without a connection to the surface peritoneum.
In 15% of patients with endometriosis, the appendix is
involvedand should be examined.[88] An implant that has penetrated retroperitoneally several centimeters is called an “iceberg”
lesion. It can be detected laparoscopically by palpating areas of
the pelvis and bowel with the suction–irrigator probe. With the
forceps or probe, endometriotic implants are examined to gauge
size, depth, and proximity to normal pelvic structures. The diagnostic laparoscopy is extended to an operative procedure if the
patient has been advised of this possibility.
Operative Laparoscopy
The operative procedure begins by lysing adhesions between the
bowel and the pelvic organs to expose the pelvic cavity adequately. The ovaries are dissected from the cul-de-sac or pelvic
side wall,and the tubes are freed fromadhesions and chromopertubated. Endometrial implants and endometriomas are resected
or vaporized, and if thepatienthassignificantmidline pelvic pain,
uterosacral nerve ablation or presacral nerve resection is done.
Lysis of Bowel Adhesions
Bowel adhesions vary in thickness, vascularity, and cohesiveness. Some adhesions are stretched without tearing the tissue,
excised with a laser harmonic scalpel or electrosurgery at the
points of attachment to the pelvic organs, and removed. Dense
adhesions are excised with scissors or any other cutting instrument. The CO
laser has more controlled penetration than do
2
electrosurgery and fiber lasers. The structures requiring separation arepulled apart with forceps, and a cleavage planeis formed.
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Superior rectal artery
Inferior rectal artery
B
Figure 10.3.2. (Continued )(B) The ureters are at risk because of infiltrating endometriosis.
Hydrodissection is useful to identify and develop the dissection
plane, which is ablated or excised, using a laser or dissecting scissors or any other cutting instrument.
Peritoneal Implants
In treating peritoneal endometriosis, the implants should be
destroyed in the most effective and least traumatic manner to
minimize postoperative adhesions. Although different modalities
have been used, hydrodissection and a high-power superpulse or
ultrapulse CO
laser are the best choices for treatment.[89] This
2
laser doesnot penetrate water, anda fluid backstop (hydrodissection) allows the surgeon to work on selected tissue with a greater
safety margin than would otherwise be available (Figure 10.3.3).
A small opening is made in the retroperitoneum with the laser
or scissors, and lactated Ringer’s solution is injected beneath the
lesion to provide a protective cushion of fluid between the lesion
to be excised and the underlying ureter or blood vessels. The
fluid under the implant absorbs the CO
laser energy, buffering
2
the underlying tissue. For retroperitoneal disease, the lesion is
picked up with grasping forceps, pulled medially, and removed,
using sharp or blunt dissection.
Bifurcation
Middle sacral artery
Middle rectal artery
Superficial peritoneal endometriosis is vaporized with the
laser, coagulated with monopolar or bipolar current, or excised.
Implants less than 2 mm are coagulated, vaporized, or excised.
When lesions exceed 3 mm, vaporization or excision is needed. For lesions greater than 5 mm, deep vaporization or excisional techniques are used. Superficial implants on the pelvic
side wall are ablated with the CO
laser (3500 to 5500 W/cm2).
2
Low-power densities cause greater damage and more charring.
High-power densities penetrate too deeply and injure underlying normal structures or cause unnecessary bleeding. Firing in
a continuous mode will ablate the lesion from the surface to its
base, where the peritoneal fat should appear as unpigmented and
soft rather than fibrotic, like endometriosis or scars. To suction
the laser plume and irrigate the lesion base, the suction–irrigator
is placed next to or behind the lesion, removing char and identifying any vascular structure within the operative field. If carbon
is allowed to accumulate, the field is obscured. In either situation, carbon may be mistaken for endometriosis. Therefore, if
vaporization is chosen, it is important to copiously irrigate and
remove the charred areas to confirm complete removal of the
lesion and avoid confusing endometriosis with a carbon deposit.
Laparoscopic Treatment of Endometriosis — 271
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Without Hydrodissection With Hydrodissection
0.5cm. opening
Round
ligament
Fallopian tube
Ovary
Wheal formed by
injection of lactated
Ringer’s solution
Peritoneum
Pararectal
space
Injection site 1
Paravesical
space
Inj. site 2
Ureter
Bladder
Inj. site 3
Rectum
Uterus
Uterosacral
ligament
Peritoneum raised
off of pararectal space
and rectum
Peritoneum raised
from the bladder
Peritoneum raised
off of ureter
Peritoneum raised
from pelvic wall
Ringer’s solution
infused
Ureter
Figure 10.3.3. Hydrodissection protects retroperitoneal structures such as the bladder, ureter, and blood vessels from the CO2laser. The insets
show the creation of retroperitoneal space.
When used in the superpulse/ultrapulse mode, this laser achieves
more rapid vaporization and decreased carbonization.
The accepted histologic criterion for the diagnosis of
endometriosis is the presence of endometrial glands and
stroma.[93] Chernobilsky and Morris [94] described a vari-
Resection of Ovarian Endometriosis
The ovaries are a common site for endometriosis. Ovarian
endometriosis causes adhesions between the ovarian surface and
the broad ligament. In 1921, Sampson [90] noted that the histologic findings varied in different portions of the same cyst.
Some implants also developed from spilling of the contents of
endometriomas after rupture, resulting in the invasion of functional cysts by these surface implants. Large endometriomas
could develop because of secondary involvement of follicular
or luteal cysts by surface implants. Ovarian implants are similar to endometriosis in extra-ovarian sites and are limited in size
by fibrosis and scarring. Endometriomas might originate from
metaplasia of the celomic epithelium that lines the cystic epithelial
inclusions that frequently are found in the ovaries.[91,92] Sampson [90] believed that there was local spread of endometriosis by
salpingeal reflux.
ety of epithelial characteristics found in ovarian endometriosis. Nissole-Pochet and associates [95] studied 113 instances of
ovarian endometriosis before and after hormone therapy. Those
authors could identify typical endometrial glandular epithelium
and stroma. In 18%, only the endometrial epithelium lined the
cyst. Areas with ciliated cells representing oviduct-like epithelium were observed in 47%. In the others, flattened endometrial
epithelium and typical glandular and stromal structures were
seen. Martin and Berry [96] examined 41 “chocolate” cysts and
found that 61% were endometriomas, 27% were corpora lutea,
and in 12%, no lining was found. Vercellini and coworkers [84]
confirmed 97.7% of visually diagnosed endometriomas by using
at least two of the following microscopic patterns to diagnose
them: (1) the presence of endometrial epithelium, (2) endometrial glands or glandlike structures, or (3) endometrial stroma
and hemosiderin-laden macrophages.
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and are difficult to excise. Microscopically, endometrial tissue is
seen in all of them. Although small, these endometriomas are
difficult to remove intact because of associated fibrosis and adhesions. They can be biopsied, drained, and vaporized by using a
laser or electrosurgery or removed in pieces.
Type IIA endometriomas are hemorrhagic cysts and grossly
look like endometriomas. The cyst wall is separated easily from
the ovarian tissue. Endometriotic implants are superficial and
adjacent to a hemorrhagic cyst, which is either follicular or luteal
in origin; microscopically, no endometrial lining is seen.
In type IIA lesions, the peri-ovarian adhesions are lysed, the
ovarian cortex is evaluated, and the cyst is aspirated. Superficial
ovarian implants adjacent to the cyst are vaporized or excised.
The cyst is opened, its wall is examined, and a biopsy specimen is
taken for frozen section. If it has a yellowish appearance, removal
is easy (Figure 10.3.6). Postoperatively,either danazol 800 mg/day
or a gonadotropin-releasing hormone (GnRH) analogue may be
used for 6 to 8 weeks.
In type IIB lesions, the cyst lining is separated easily from the
ovarian capsule andstroma,except near the endometrialimplant.
Intype IIC lesions, surface endometrial implantspenetratedeeply
into the cyst wall, making excision difficult. Histologic findings
of endometriosis are seen in the cyst wall in these two subtypes.
The basis for differentiating between these two subtypes is the
progressive difficulty in removing the cyst wall.
Type IIB and type IIC endometriomas are large and are
associated with peri-ovarian adhesions that attach them to the
pelvic side wall and the back of the uterus. When suction and
Superficial endometriosis of the ovary
Figure 10.3.4. Superficial implants are seen on this ovary.
irrigation are alternated, the contents are removed. The inside of
the cyst is examined, and the portion of ovarian cortex involved
with endometriosis is removed. Using the grasping forceps and
the suction–irrigator probe,the cyst wall isgrasped and separated
from the ovarian stroma by traction and countertraction.[101]
Endometriotic implants or endometriomas less than 2 cm in
diameter are coagulated, laser ablated, or excised, using scissors,
biopsy forceps, lasers,orelectrodes (Figure 10.3.4).Forsuccessful
eradication, all visible lesions and scars must be removed from
the ovarian surface. Entrapment of oocytes within the luteinized
ovarian follicle,as reported in experimental animalmodels, must
be avoided.[97]Drainingtheendometrioma or partially resecting
its wall is inadequate because the endometrial tissueliningthecyst
can remain functionaland may cause the symptomsto recur.[98]
However, photocoagulation of the cyst wall has been equally
therapeutic and occasionally less difficult.[41,99,100] Brosens
and Puttemansi [99] recommended cytology and biopsy of the
cyst wall before ablating the cyst. When a double optic laparoscope,whichinvolvesthepassageofasmalleroperative endoscope
through thechannel of the main laparoscope, is used, theovarian
cyst is punctured and drained, the fluid is sent for cytology, and
the lining is inspected visually. Any suspicious area is biopsied,
and the specimen is sent for frozen section. Once it has been
ascertained that the cyst is not malignant, its wall is ablated to a
depth of 3 to 4 mm using a laser or an electrocoagulator introduced through the operative channel of the second laparoscope.
This procedure is analogous to endometrial ablation and seems
to be successful, with no recurrence on follow-up ultrasound or
second-look laparoscopy.
Endometriomas can be classified as types I to IV. Type I
endometriomas are 1 to 2 cm in size and contain dark fluid (Figure 10.3.5). They develop from surface endometriotic implants
Small blood vessels from the ovarian bed and bleeding from the
ovarian hilum are controlled with bipolar electrocoagulation.
In type IIC lesions, it is difficult to develop a cleavage plane
between the cyst wall and the ovarian stroma. The portion of the
ovary attached tothecyst wall is removeduntil a clear boundaryis
found so that the entire cyst can be extirpated. The remainder of
the procedure is similar to that which was described earlier. The
edges of theovarian defect are brought together with a low-power
laser or electrosurgery. Low-power, continuous laser or bipolar
coagulation applied to the inside wall of the redundant ovarian
capsule causes it to invert. Excessive coagulation of the adjacent
ovarian stroma must be avoided. If sutures are needed, they are
placed inside the capsule, and 4-0 polyglycolic material is used.
Fewer sutures result in fewer adhesions.[102]
The least invasive and technically simplest approach to
endometriomas involves laparoscopic fenestration and removal
of “chocolate” fluid without cystectomy or ablation of the cyst
wall. However, fenestration and irrigation are ineffective, as evidenced by a 50% recurrence rate. Fayez and Vogel [103] made
a wide opening in the cyst wall to drain its contents. They
claimed that their technique created fewer periadnexal adhesions
(27%). Vercellini andassociates[99]showedthataspirationofthe
cyst and irrigation of the endometriomas were ineffective. In 33
women, most endometriomas recurred, although many patients
took GnRH analogues postoperatively. Hasson [98] noted recurrences in eight of nine endometriomas treated by fenestration
alone.
Laparoscopic Treatment of Endometriosis — 273
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Ovarian ligament
Type I endometrioma
Ovary
AB
Figure 10.3.5. (A) Type I endometriomas are small,contain dark fluid, and develop from surface implants. (B) They are difficult to remove intact
because of associated adhesions and fibrosis.
Endometrial implant on the
ovarian cortex with no
attachment on the cyst wall
Functional cyst
Endometrial implant
Type IIA
Cyst wall
Figure 10.3.6. A functional cyst with a small endometriotic implant.
Ovarian cortex
For endometriomas over 2 cm in diameter, the cyst is punctured with the 5-mm trocar and aspirated with the suction–
irrigator probe. Using high-pressure irrigation at 500 to 800 mm
Hg, thecyst is irrigated, causing it to expand, andis aspirated several times.[104] This procedure allows examination of the cyst
wall. After the repeated expansion and shrinkage with irrigation
and suction, the cyst wall should separate from the surrounding
ovarian stroma(Figure10.3.7).Ifitdoesnot,5to20 mLoflactated
Ringer’ssolution is injected between thestroma and the cyst wall.
The cyst wall is removed by grasping its base with laparoscopic
forceps and peeling it from the ovarian stroma (Figure 10.3.8). If
this isnot successful, thewall is separatedfrom the ovarian cortex
with forceps at the puncture site. A cleavage plane is created by
pulling the two forceps apart and cutting between the structures.
Use of the laser or electrosurgery minimizes bleeding because
the blood vessels supplying the endometrioma are usually small
enough to be cutandcoagulatedsimultaneously. Anothermethod
involves hydrodissection of the plane between the cyst wall and
the ovarianstroma.[23,43] These techniques may beapplied successfully to completely remove the cyst wall, whichshould be sent
for histologic evaluation to rule out malignancy. If the entire cyst
cannot be separated from the ovary, the adherent sections are
ablated or coagulated.[98–100,104] When the entire cyst wall
is ablated, representative biopsy specimens are taken for histologic diagnosis. These endometriomas tend to rupture during
separation because of their adherence to other pelvic structures.
Because it is difficult to develop a plane between the cyst wall
and the ovarian stroma, the portion of the ovary attached to the
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Endometrial implant has reached the cyst wall
Functional cyst
Endometrial implant
A
Functional cyst
Type IIB
Ovarian cortex
Cyst wall
Uterus
Filmy adhesions
Pelvic sidewall
Ovary
Type IIB
Endometrial implant
B
Figure 10.3.7. (A) A type IIB endometrioma with features of a functional cyst involved deeply with histologic
findings of endometriosis in the cyst wall. The cyst wall is separated easily from the ovarian capsule and stroma
except where adjacent to the areas of endometriosis. (B) In this type IIB lesion, the endometriotic implant has
reached the cyst wall. (Continued )
Functional cyst
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Laparoscopic Treatment of Endometriosis — 275
Uterus
Dense adhesions
Ovary
Type IIC
Endometrial implant
C
Figure 10.3.7. (Continued )(C) Extensiveperi-ovarianadhesionsarepresent, andthere ismoreextensive involve-
ment of the cyst wall with endometriotic implants. When suction and irrigation are alternated, the inside of the
cyst can be explored.
cyst wall is removed until an area is located to produce a line of
cleavage.
Cyst wall closure is not necessary, according to animal experiments [105] and clinical experience.[106] For large defects that
result from resecting endometriomas larger than 5 cm, the edges
of the ovariancortexare approximatedwith a singlesutureplaced
within the ovarian stroma. The knot is tied inside the ovary so
that no part of the suture penetrates the ovarian cortex or is
exposed to the ovarian surface to minimize adhesion formation.
Fibrin sealant has been described to atraumatically approximate
the edges of large ovarian defects (Figure 10.3.9).[107]
Rare patients present with localized symptoms and severe
involvement of the ovary with disease and adhesions while
the opposite ovary is normal, requiring unilateral salpingooophorectomy. When the diseased ovary is removed, the risk
of disease recurrence is minimized, and the fertility potential is
improved by limiting ovulation to the healthy side. In a prospective trial, Beretta and coauthors [108] randomly allocated 64
patients with advanced stages of endometriosis toundergo either
cystectomy of the endometrioma or drainage of the endometrioma and bipolar coagulation of the inner lining. The 24-month
cumulative recurrence rates of dysmenorrhea, deep dyspareunia,
and nonmenstrual pelvic pain were lower in the patients who
underwent cystectomy than in those who did not (dysmenorrhea, 15.8% vs. 52.9%;deep dyspareunia, 20% vs. 75%;nonmenstrual pelvic pain, 10% vs. 52.9%). The median interval between
the operation and the recurrence of moderate to severe pelvic
Pelvic sidewall
pain was longer after cystectomy: 19 months compared with 5
months. The 24-month cumulative pregnancy rate was higher
after cystectomy: 66.7%comparedwith 23.5%.For the treatment
of ovarian endometriomas, a better outcome with a similar rate
of complications is achieved with laparoscopic cystectomy than
with drainage and coagulation.
The efficacy of laparoscopy done by applying the stripping
technique was compared retrospectively with that of microsurgery by laparotomy in 132 women under 40 years of age with
ovarian endometriotic cysts at least 3 cm in diameter, stages III
and IV endometriosis, rAFS classification.[109] The recurrence
rate of ovarian cysts, symptomatic improvement, and the reproductive outcomewerefound to be comparable for thetwogroups.
However, as was expected, laparoscopy resulted in less postoperative febrile morbidity and a significantly shorter duration of
hospitalization. The long-term results of laparoscopic fenestration and coagulation of ovarian endometriomas were investigated
in a case-control study and compared with the results of ovarian cystectomy done by either laparotomy or laparoscopy.[110]
The study enrolled 156 premenopausal women with ovarian
endometriomas at least 3 cm in diameter, stages III and IV
endometriosis, rAFS classification. The mean time to first pregnancy wasshorter in the 80 patientswho underwent laparoscopic
ovarian fenestration and coagulation (1.4 years) than it was in
the 23 patients who underwent laparoscopic ovarian cystectomy
(2.2 years) or the 53 patients who underwent ovarian cystectomy by laparotomy and a microsurgical technique (2.4 years).
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Cortical endometrial implant has reached
the cyst wall and is firmly attached
Cyst wall
Type IIB
Endometrial implant
A
Figure 10.3.8. (A) The lining is separated easily from the ovarian capsule and stroma except where adjacent to
the areas of endometriosis.
Cyst wall has been removed
from the ovarian stroma
Ovarian cortex with
the endometrial implant
has been removed
Removing type IIB
B
Figure 10.3.8. (B) The cyst wall has been removed, and a piece of the ovarian cortex with the endometrial
implant has been excised. Using the grasping forceps and the suction–irrigator probe, the cyst wall is separated
from the ovarian cortex by traction and countertraction.
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