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Laparoscopic Myomectomy
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Fig. 4 Making an incision with a harmonic scalpel
223
transverse incision. It would be extremely difcult repairing a vertical incision via ipsilateral
ports just as it would be difcult repairing a
transverse incision using contra-lateral ports. The
incision is continued until it reaches the broid
capsule; usually, the glistening white capsule can
be visualized, and the broid bulges out.
6.6 Enucleation oftheFibroid
Commence enucleation by grasping the broid
with either a laparoscopic tenaculum or a myoma
screw and apply traction while holding the edge
of the myometrium with traumatic grasping forceps such as an Alice forceps (Fig.5). A suction
irrigation tubing, Maryland dissector, or the harmonic scalpel can then be used to shell out the
broid. The uterine defect is irrigated, and any
visible bleeder coagulated with bipolar forceps.
6.7 Suturing theDefect
Fig. 5 Enucleation of the broid seedlings. (Image cour-
tesy of Dr. Joseph Njagi)
monocryl 3-0in a single layer, either by continuous or interrupted stitches. Next, repair the myometrium ensuring symmetry of both sides of the
myometrium. The authors commonly use vicryl 1
or 2-0 sutures in a continuous fashion taking bites
about 1cm apart. One or two layers of closure are
applied depending on the depth of the uterine
wound. Finally, the serosa layer is closed, typically in a continuous manner, preferably using
monocryl 3-0 sutures (Fig. 6a–c). Suturing is
generally performed using intracorporal suturing
techniques, albeit, some surgeons prefer extracorporal suturing
The introduction of the barbed suture, V-loc,
and Quill sutures has made suturing much easier
as they obviate the need for tying knots. The quill
(Stratax) suture is bidirectional. Suturing therefore begins from the middle of the wound, and
each half is run in the opposite direction until
they reach the edge of the defect.
This is a crucial aspect of laparoscopic myomectomy. Whether re-approximating the myometrium via laparoscopic suturing gives the uterine
wall the same strength as multilayer closure at
laparotomy is still debatable [13, 19]. While there
seems to be no agreement in terms of the number
of layers of suturing that could prevent future
uterine rupture, it is essential however to close
dead spaces to prevent haematoma formation,
which can potentially lead to wound breakdown
or future rupture of the uterus. First start by suturing any endometrial defect with vicryl 3-0 or
6.8 Removal ofFibroids
This is achieved with the use of a morcellator
preferably via the left lower quadrant port
(Fig.7a, b), or via a posterior colpotomy. In using
a morcellator, the risk of an occult malignancy
and risk of spread should be borne in mind and
steps taken toward preventing this. Morcellation
within a retrieval bag helps reduce the dissemination of broid tissues within the abdominal cavity. Proper irrigation is mandatory thereafter.

224
a
b
a b
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c
Fig. 6 (a, b) Suturing. (c) Suturing of the broid cavities
J. E. Okohue et al.
Fig. 7 (a, b) Morcellation
7 Special Situations
7.1 Hand-Assisted Laparoscopic
Myomectomy (HALM)
This helps to overcome some of the limitations of
laparoscopic surgery, such as multiple or massive
broids, as well as diverse pelvic adhesions. It takes
advantage of the benets of laparoscopy as well as
that of a tactile feel. In the year 2000, Pelosi reported
hand-assisted laparoscopic surgery (HALS) with
the evacuation of a broid mass that reached the
level of the liver and weighed 3120g [20].
Typically, an incision is made in the patient’s
abdomen, and the size of the incision is based on
the surgeon’s hand and the size of the tumour. A
special appliance is introduced into the abdomen
via the incision. This prevents leakage of gas.
The surgeon introduces his hands via this device
and takes advantage of the feedback of tactile
sensation which seems to make HALS safer and
more accurate [11, 21].

Laparoscopic Myomectomy
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225
8 Postoperative
Considerations
We usually would discharge the patient the following day on non-steroidal anti-inammatory
drugs. She is seen 2 weeks postoperatively and
counselled against conception for at least
3months.
Uterine rupture during subsequent pregnancies is one of the feared complications of laparoscopic myomectomy. The risk of uterine rupture
has been reported to be 0.6–1% [22]. Parker etal.
[23] reviewed 19 cases of reported uterine rupture following laparoscopic myomectomy and
found that the excessive use of electrocautery and
single-layer closure were risk factors for subsequent uterine rupture, albeit, it was also suggested that individual wound healing
characteristics might predispose to uterine
rupture.
Learning Points
• While submucous broids might impair fertil-
ity, the effect of intramural broids on fertility
remains controversial.
• Patient selection is key to an effective laparo-
scopic myomectomy.
• As a rule, ensure that the primary port is above
the uterine fundus.
• Use vasopressin to control bleeding with care.
• Ensure adequate suturing of the defect with
the appropriate suture.
• Do not use a morcellator in suspected
malignancies.
References
1. Baird DD, Dunson DB, Hill MC, Cousins D,
Schectman JM. High cumulative incidence of uterine leiomyoma in black and white women: ultrasound evidence. Am J Obstet Gynecol. 2003;188(1):
100–7.
2. Metwally M, Cheong YC, Horne AW. Surgical
treatment of broids for subfertility. Cochrane
Database Syst Rev 2012(11):CD003857. https://doi.
org/10.1002/14651858.CD003857.pub3.
3. Jayakrishnan K, Menon V, Nambiar D. Submucous
broids and infertility: Effect of hysteroscopic myo-
mectomy and factors inuencing outcome. J Hum
Reprod Sci. 2013;6(1):35–9.
4. Carranza-Mamane B, Havelock J, Hemmings R.The
management of uterine broids in women with otherwise unexplained infertility. J Obstet Gynaecol Can.
2015;37(3):277–5.
5. Purohit P, Vigneswaran K. Fibroids and infertility.
Curr Obstet Gynecol Rep. 2016;5:81–6.
6. Semm K, Mettler L.Technical progress in pelvic surgery via operative laparoscopy. Am J Obstet Gynecol.
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7. Nezhat C, Nezhat F, Silfen SL, Schaffer N, Evans
D. Laparoscopic myomectomy. Int J Fertil.
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8. Sizzi O, Rosetti A, Malzoni M, Minelli L, La Grotta
F, Soranna L, etal. Italian multicenter study on complications of laparoscopic myomectomy. J Minim
Invasive Gynecol. 2007;14:453–62.
9. Holub Z. Surgical results of myomectomy using
laparoscopic and minilaparotomic access. Womens
Health. 2007;3(5):537–9.
10. Cittadini E. Laparoscopic myomectomy: the
Italian experience. J Am Assoc Gynecol Laparosc.
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indication and curative effect of hysteroscopic and
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12. Frascà C, Tuzzato G, Arena A, Degli Esposti E,
Zanello M, Raimondo D, Seracchioli R.The role of
pelvic ultrasound in preoperative evaluation for laparoscopic myomectomy. J Minim Invasive Gynecol.
2018;25(4):679–3.
13. Dubuisson JB, Chapron C, Fauconnier A, BabakiFard K. Laparoscopic myomectomy fertility result.
Ann N Y Acad Sci. 2001;943:269–75.
14. Campo S, Garcea N.Laparoscopic myomectomy in
premenopausal women with and without preoperative
treatment using gonadotrophin-releasing hormone
analogues. Hum Reprod. 1999;14(1):44–8.
15. Hobo R, Netsu S, Koyasu Y, Tsutsumi O.Bradycardia
and cardiac arrest caused by intramyometrial injection of vasopressin during a laparoscopically assisted
myomectomy. Obstet Gynecol. 2009;113(2):484–6.
16. Frishman G. Vasopressin: if some is good, is more
better? Obstet Gynecol. 2009;113(2):476–7.
17. Butala BP, Shah VR, Parikh BK, Jayaprakash J, Kalo
J.Bradycardia and severe vasospasm caused by intramyometrial injection of vasopressin during myomectomy. Saudi J Anaesth. 2014;8:396–8.
18. Liu L, Li Y, Xu H, Chen Y, Zhang G, Liang
Z.Laparoscopic transient uterine artery occlusion and
myomectomy for symptomatic uterine myoma. Fertil
Steril. 2011;95(1):254–8.
19. Wallach EE, Vlahos NF.Uterine myomas: an overview of development, clinical features, and management. Obstet Gynecol. 2004;104(2):393–406.
20. Pelosi MA, Pelosi MA 3rd, Elim J. Hand-assisted
laparoscopy for megamyomectomy: a case report. J
Reprod Med Obstet/Gynaecol. 2000;45(6):519–25.

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21. Wu Y, Wang X.Hand-assisted laparoscopic surgery
and its applications in gynaecology. Gynecol Minim
Invasive Ther. 2016;5(1):12–5.
22. Koo YT, Lee JK, Lee YK, Kwak DW, Lee IH, Lim
KT, etal. Pregnancy outcomes and risk factors for
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23. Parker HP, Eionarsson J, Istre O, Dubuisson JB.Risk
factors for uterine rupture after laparoscopic myomectomy. JMIG. 2010;17(5):551–4.

Laparoscopic Management
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ofEndometriosis
UcheA.Menakaya andVadunemeKingsleyOriji
1 Denition
Endometriosis is a clinical condition characterized by the presence of endometrial glands and
stroma in sites other than the endometrial cavity
[1, 2]. Endometriosis principally involves the
structures within the female pelvis, but it can also
affect tissues beyond the pelvis, resulting in
endometriosis of gastrointestinal tract, the thoracic cavity and cutaneous endometriosis.
Although endometriosis is a benign disease, it
has the capacity to cause signicant pelvic pain,
patient suffering and reduced quality of life for
women living with endometriosis.
2 Prevalence
The reported overall prevalence of endometriosis
varies between 10% and 15% of reproductive age
women [3]. Globally, there are nearly 176 million
women living with endometriosis [4]. The disease affects up to 50% of women with infertility
U. A. Menakaya (*)
JUNIC Specialist Imaging and Women’s Centre and
Calvary Hospitals, Canberra, ACT, Australia
e-mail: info@junicimaging.com.au
V. K. Oriji
University of Port Harcourt Teaching Hospital,
Port Harcourt, Rivers State, Nigeria
e-mail: vaduneme.oriji@uniport.edu
and up to 5% of fertile women [3, 5, 6]. Studies
have suggested ethnic variations in the prevalence of endometriosis with the disease being
more prevalent among Oriental women and least
in African American women [7, 8].
Epidemiological data on the prevalence of
endometriosis among African indigenous
women are meagre [9]. In some of the few published studies, endometriosis constituted the
third most common nding at laparoscopies and
was reported in 15.7% of laparoscopies performed for infertility assessment [10]. In South
Africa, Wiswedel et al. (1989) [11] reported a
prevalence of 2% among African indigenous
women presenting to an infertility clinic compared to a prevalence of 4–6% among South
Africans of mixed and white race. In Nigeria, a
prevalence of 4–8% has been reported among
women also presenting for assisted reproductive
programmes [10, 12, 13].
The low prevalence of endometriosis reported
among indigenous African women has been
attributed to different cultural and lifestyle factors [14]. In particular, early age at rst pregnancy, shorter inter pregnancy intervals with
large size families, taboos around menstruation
and pain, increased risk of pelvic inammatory
disease and blocked fallopian tube [14–16].
These factors contribute to delays in expression
of symptoms and limit the cumulative number of
menstrual cycles with retrograde menstruation
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
J. E. Okohue et al. (eds.), Gynaecological Endoscopic Surgery,
https://doi.org/10.1007/978-3-030-86768-3_22
227

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U. A. Menakaya and V. K. Oriji
[14–16]. Others have attributed the lower prevalence of endometriosis among indigenous African
women to the low awareness of the disease in
sub-Saharan Africa, the poor access to diagnostic
and therapeutic facilities and the limited training
available for the management of endometriosis in
the region [12, 17, 18].
3 Pathogenesis
A number of theories have been proposed for the
pathogenesis of endometriosis [19–22]. A common theory for the pathogenesis of ectopic endometrium is the retrograde menstruation theory
where blood from menstruation ows through
the fallopian tubes into the pelvis, the viable
endometrial tissues in the reux gets implanted
into the pelvic peritoneum and is with under the
inuence of the cyclical hormonal interplay of
the female reproductive system and bleed just
like the eutopic endometrium during menstrua-
tion [23] (see Fig. 1). This bleeding results in
inammation, adhesions, cysts and other changes
within the pelvis that manifest the symptoms and
signs of endometriosis [19].
Other theories include the metaplasia of coelomic epithelium, seeding of endometrial cells
through the lymphatic channels and blood to
ectopic sites [24]. A genetic predisposition with
possible polygenic inheritance, hormonal as
well as immunologic theories has all been
advocated to explain the pathogenesis of endometriosis [20, 25, 26]. Iatrogenic endometrial
tissue seedling during caesarean sections, episiotomy scars and during myomectomies is also
possible [27].
The biologic mechanisms that link endometriosis and infertility include altered peritoneal,
hormonal and cell mediated function, endocrine
and ovulatory abnormalities, distorted pelvic
anatomy, impaired implantation, poor oocyte and
embryo quality and abnormal uterotubal transport [28].
Fig. 1 Deposition of
endometrial tissue
through retrograde
menstruation and the
different forms of
peritoneal
endometriosis. (Image
from Atlas of operative
hysteroscopy and
laparoscopy, 3rd edition
by Jacques Donnez)
Attachment
Proliferation Partial shedding – migration
Neovascularization
Inflammatory
reaction
fibrosis
Red
Black
White

Laparoscopic Management ofEndometriosis
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4 Clinical Features
Pelvic endometriosis is a known cause of chronic
pelvic pain and infertility. The disease may be
asymptomatic or present as cyclical spasmodic
dysmenorrhea, dyspareunia, dyschezia, dysuria
and/or infertility. Other symptoms include noncyclical lower abdominal pain, chronic pelvic
pain, low back pain, menorrhagia and irregular
menses. Cyclical nonspecic symptoms like
insomnia, fatigue, malaise, nausea and vomiting
have been described in patients with endometriosis [29, 30].
Additionally, cyclical pain or tender swelling
and bloody discharge from the umbilicus and surgical scars as in laparotomy or episiotomy scars
may relate to cutaneous endometriosis. The
severity and chronicity of the pain induced by
endometriosis impact negatively on the general
quality of life of women with endometriosis
affecting their sexual life, efciency and productivity at work [7, 8, 31].
Risk factors for endometriosis include early
menarche, reduced cycle length, prolonged inter
pregnancy interval, nulliparity, family history of
endometriosis and exposure to diethylstilbesterol
in utero [32]. Conversely, the use of oral contraceptive pills and parity reduce the risk of endometriosis [33, 34].
Physical examination may not be helpful in
making diagnosis as vast majority of patients
with endometriosis have no signicant physical
ndings. However, a pelvic examination could
reveal discrete tender nodules in the adnexa or
pouch of Douglas. Cervical motion tenderness
may be present as well, and the uterus may be
immobile from adhesions. This may suggest the
presence of deep inltrating endometriosis in the
pouch of Douglas. A pelvic examination is mandatory to rule out other possible causes of symptoms including pelvic inammatory disease.
The European Society of Human Reproduction
and Embryology (ESHRE) recommends a diagnosis of endometriosis in the presence of gynaecological symptoms such as dysmenorrhoea,
non-cyclical pelvic pain, deep dyspareunia, infertility and non-gynaecological cyclical symptoms
like dyschezia, dysuria, haematuria and rectal
bleeding, shoulder tip pain and fatigue in women
of reproductive age [35].
5 Histological Phenotypes
ofEndometriosis
Endometriosis is a heterogenous, multiforme disease. Three principal histological phenotypes of
endometriosis are recognized. These include the
supercial (peritoneal) disease, deep inltrating
endometriosis (DE) and ovarian endometrioma
[36, 37]. These subtypes can occur alone or in
combination presenting additional phenotypes of
endometriosis that include ovarian adhesions
and/or pouch of Douglas obliteration. The severity of symptoms, best treatment option and recurrence rates vary signicantly among these various
phenotypes of endometriosis [29, 30].
6 Diagnosis
Delays in the diagnosis of endometriosis are a
signicant challenge in the management of endometriosis worldwide. For example, diagnostic
delays of up to 10years have been reported in a
number of European countries [38, 39]. In
Nigeria, diagnostic delays of 5–7years have been
reported [38].
These delays mainly occur at the primary level
of care with women reporting an average of seven
visits before specialist referral [38]. The “discrediting” nature of menstrual irregularities and associated risk of stigmatization may also delay women
from seeking help [40, 41]. These delays contribute to unnecessary patient sufferings, reduced
quality of life and signicant personal and societal
costs associated with endometriosis [38].
Laparoscopic visualization of endometriotic
lesions is considered the current gold standard in
the diagnosis of endometriosis, and limited
access to expensive laparoscopic services in
resource-restricted countries is another contributor to the delay in the diagnosis of endometriosis
in these countries.

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6.1 Preoperative Diagnosis
A number of preoperative strategies are now utilized in clinical practice to reduce the delays in
the diagnosis of women with endometriosis. For
example, some symptom-based models have
demonstrated good accuracy with predicting
moderate to severe endometriosis [42]. Predictive
tools based on these symptoms-based models
could help prioritize women for surgical investigation and treatment in clinical practice [42].
Pelvic ultrasound is another strategy for
improving the preoperative diagnosis of endometriosis. There is evidence in support of the performance of transvaginal pelvic ultrasound in the
diagnosis of ovarian and extra-ovarian endometriosis as well as their markers of local invasiveness when compared to gold standard laparoscopy
[43]. A major advantage of pelvic ultrasound is
its ease of use, availability and accessibility to
women in resource-restricted countries [44].
6.2 Intraoperative Diagnosis
Intraoperative diagnosis of endometriosis can be
made with laparotomy or laparoscopy.
Laparoscopy is a preferred modality for diagnosing endometriosis because it is usually associated
with better intraoperative magnication, less
pain, less postop adhesions, shorter hospital stay,
quicker recovery and better cosmetics.
Irrespective of the modality of surgery, intraoperative recognition of the three principal phenotypes of endometriotic lesions and their markers
of local invasiveness are critical to the diagnosis
of endometriosis.
Ovarian endometriomas are the most recognized form of endometriosis (see Fig. 2g, h).
They are typically described as chocolate cysts
and occur in 17–44% of women with endometriosis [45]. DE are endometriosis implants
Table 1 Types of peritoneal endometriosis [49]
Colour Appearance
Black Typical puckered black lesions
Red Red ame-like lesions
Glandular excrescences
Petechial peritoneum
Areas of hyper-vascularization
White White opacications
Sub-ovarian adhesions
Yellow brown peritoneal patches
Circular peritoneal defects
that extend deeper than 5mm under the peritoneum surface or those involving or distorting
bowel, bladder, ureter or vagina [46] (see
Fig.2i, m–p). They occur in 1–5% of women
with endometriosis and are commonly found
on the uterosacral ligaments [47]. They can
also be found on other pelvic organs like the
bowel, appendix, bladder and pelvic sidewall
and less commonly on the diaphragm and
upper abdomen (see Fig.2q, r).
Peritoneal endometriosis refers to lesions that
involve only the peritoneum and do not invade
the underlying tissue. It is the most common
type of endometriosis occurring in up to 66% of
women undergoing laparoscopy for endometriosis [48]. Peritoneal endometriosis is multiforme
and can appear as black, red, white, yellow
brown peritoneal lesions or circular peritoneal
defects [49] (see Table1 and Fig.2a–d). The red
lesions are highly vascular, bleed into the peritoneal cavity during menstruation and are associated with early neoangiogenesis, adhesion
formation and inammation (see Fig. 2c, e).
Dark or white lesions are correlated with higher
amounts of brosis, decreased vascularity and
decreased bleeding [50] (see Fig.2a, b, d and f).
Peritoneal endometriotic implants can change
appearance and even regress with medical treatment but often reappear after cessation of treatment and return of the menstrual cycle [50].

ab
cd
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6.3 Visual vs. Histological
Diagnosis ofEndometriosis
Laparoscopy with or without histological verication is widely used to diagnose and rule out the
presence of endometriosis. Without histological
verication, the experience, skill and knowledge
of the surgeon are critical to a diagnosis of endometriosis at laparoscopy [35].
Current evidence recommends that clinicians
conrm a positive laparoscopy by histology
since positive histology conrms the diagnosis
of endometriosis and rules out rare forms of
malignancy [35]. The combination of laparoscopy and the histological verication of endometrial glands and/or stroma are considered to
be the gold standard for the diagnosis of the disease [35].
Fig. 2 Laparoscopic images of different types of endo-
metriosis. (a) Supercial ovarian endometriosis (black).
(b) Peritoneal endometriosis at left pelvic brim (black).
(c) Widespread peritoneal endometriosis endometriosis in
utero vesical space (red). (d) Another form of peritoneal
endometriosis (yellow brown). (e) Another form of peritoneal endometriosis (red). (f) Another form of peritoneal
endometriosis (white). (g) Left endometrioma. (h) Right
endometrioma with spillage of content. (i) Uterovesical
endometrioma. (j) Rectal endometriosis adherent to left
USL DIE. (k) Endometriosis with POD obliteration. (l)
Bowel involvement in POD obliteration. (m) Bladder
endometriosis. (n) Isolated left uterosacral DE. (o) Large
sigmoid nodular endometriosis. (p) Rectal endometriosis
in POD. (q) Diaphragmatic DE endometriosis. (r)
Peritoneal endometriosis on diaphragm. (Images courtesy
of Junic Laparoscopy Australia)

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Fig. 2 (continued)
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