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Ultrasonography and the Embryo Transfer — 127
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30. Garc´ıa-Velasco JA, Isaza V, Martinez-Salazar J, et al. Transabdominal ultrasound-guided embryo transfer does not increase
pregnancy rates in oocyte recipients. Fertil Steril. 2002;78:534–
539.
31. Flisser E, Grifo JA, Krey LC, NoyesN.Transabdominal ultrasoundassisted embryo transfer and pregnancy outcome. Fertil Steril.In
press.
32. Mirkin S, Jones EL, Mayer JF, Stadtmauer L, Gibbons WE,
Oehninger S. Impact of transabdominal ultrasound guidance on
performance and outcome of transcervical uterine embryo transfer. J Assist Reprod Genet. 2003;20:318–322.
33. Buckett WM. A meta-analysis of ultrasound-guided versus
clinical touch embryo transfer. Fertil Steril. 2003;80:1037–
1041.
34. Sallam HN, Sadek SS. Ultrasound-guided embryo transfer:
a meta-analysis of randomized controlled trials. Fertil Steril.
2003;80:1042–1046.
35. Yovich JL, Turner SR, Murphy AJ. Embryo transfer technique as a
cause of ectopic pregnancies in in vitro fertilization. Fertil Steril.
1985;44:318–321.
36. Pope CS, Cook EKD, Arny M, Novak A, Grow DR. Influence of
embryo transferdepthon in vitro fertilizationandembryo transfer
outcomes. Fertil Steril. 2004;81:51–58.
37. Sieck UV, Jaroudi KA, Hollanders JMG. Ultrasound guided
embryo transfer does not prevent ectopic pregnancies after invitro fertilization. Hum Reprod. 1997;12:2081–2085.
38. Egbase PE, Al-Sharhan M, Grudzinskas JG. Influence of position and length of uterus on implantation and clinical pregnancy
rates in IVF and embryo transfer treatment cycles. Hum Reprod.
2000;15:1943–1946.
39. Nazari A,Askari HA,CheckJH, O’ShaughnessyA.Embryotransfer
technique as a cause of ectopic pregnancy in in vitro fertilization.
Fertil Steril. 1993;60:919–921.
40. Yovich JL, Turner SR, Murphy AJ. Embryo transfer technique as a
cause of ectopic pregnancies in in vitro fertilization. Fertil Steril.
1985;44:318–321.
41. Lesny P, Killick SR, Robinson J, Maguiness SD. Transcervical
embryo transfer as a risk factor for ectopic pregnancy. Fertil Steril.
1999;72:305–309.
42. Baba K, Ishihara O, Hayashi N, Saitoh M, Taya J, Kinoshita K.
Where does the embryo implant after embryo transfer in humans?
Fertil Steril. 2000;73:123–125.
43. Hurley VA, Osborn JC, Leoni MA, Leeton J. Ultrasound-guided
embryo transfer: a controlled trial. Fertil Steril. 1991;55:559–
562.
44. Kojima K, Nomiyama M, Kumamoto T, Matsumoto Y, Iwasaka T.
Transvaginal ultrasound-guided embryo transfer improves pregnancy and implantation rates after IVF. Hum Reprod. 2001;
16:2578–2582.
45. Anderson RE,NugentNL,GreggAT, NunnSL,BehrBR.Transvaginal ultrasound-guided embryo transfer improves outcome in
patients with previous failed in vitro fertilization cycles. Fertil
Steril. 2002;77:769–775.
46. Letterie GS. Three-dimensional ultrasound-guided embryo
transfer: apreliminary study. Am J ObstetGynecol. 2005;192:1983–
1988.
47. Gergely RZ, DeUgarte CM, Danzer H, Surrey M, Hill D, DeCherney AH. Three dimensional/four dimensional ultrasound-guided
embryo transfer using the maximal implantation potential point.
Fertil Steril. 2005;84:500–503.
48. Mansour RT, Aboulghar MA, Serour GI, Amin TM. Dummy
embryo transfer using methylene blue dye. Hum Reprod . 1994;9:
1257–1259.
49. Krampl E, Zegermacher G, Eichler C, Obruca A, Strohmer H,
Feichtinger W. Air intheuterine cavity afterembryo transfer. Fertil
Steril. 1995;63:366–370.
50. Sieck UV, Jaroudi KA, Hollaners JMG.Ultrasound guidedembryo
transfer does not prevent ectopic pregnancies after in-vitro fertilization. Hum Reprod. 1997;12:2081–2085.
51. Woolcott R, Stanger J. Potentially important variables identified
by transvaginal ultrasound-guided embryo transfer. Hum Reprod.
1997;12:963–966.
52. Rosenlund B, Sj¨oblom P, Hillensj¨o T. Pregnancy outcome related
to the site of embryodepositionintheuterus. J Assist Reprod Genet.
1996;13:511–513.
53. Franco JG Jr, Martins AM, Baruffi RL, et al. Best site for embryo
transfer: the upper of lower half of endometrial cavity? Hum
Reprod . 2004;19:1785–1790.
54. Coroleu B,Barri PN, Carreras O, et al.Theinfluenceofthedepthof
embryo replacement into the uterine cavity on implantation rates
after IVF: a controlled, ultrasound-guided study. Hum Reprod.
2002;17:341–346.
55. Prapas Y, Prapas N, Hatziparasidou A, et al. Ultrasound-guided
embryo transfer maximizes the IVF results on day 3 and day
4 embryo transfer but has no impact on day 5. Hum Reprod.
2001;16:1904–1908.
56. Frankfurter D, Trimarchi JB, Silva CP, Keefe DL. Middle to lower
uterine segmentembryotransfer improves implantation and pregnancy rates compared with fundal embryo transfer. Fertil Steril.
2004;81:1273–1277.
57. Knutsen V, Stratton CJ, Sher G, McNamee PI, Huang TT, SotoAlbors C. Mock embryo transfer in early luteal phase, the cycle
before in vitro fertilization and embryo transfer: a descriptive
study. Fertil Steril. 1992;57:156–162.
58. Lesny P, Killick SR, Tetlow RL, Robinson J, Maguiness SD.
Embryo transfer – can we learn anything new from the observation of junctional zone contractions? Hum Reprod. 1998;13:1540–
1546.
59. Lesny P,Killick SR, Robinson J, RavenG,MaguinessSD.Junctional
zonecontractionsandembryotransfer:it issafe touse atenaculum?
Hum Reprod. 1999;14:2367–2370.
60. Fanchin R, Righini C,Olivennes F,Taylor S,deZiegler D, Frydman
R. Uterine contractions at the time of embryo transfer alter pregnancy rates afterin-vitrofertilization. Hum Reprod.1998;13:1968–
1974.
61. Leong M, Leung C, Tucker M, Wong C, Chan H. Ultrasoundassistedembryotransfer.JInVitro FertEmbryoTransf . 1986;3:383–
385.
62. Woolcott R, Stanger J. Ultrasound tracking of the movement of
embryo-associated air bubbles on standing after transfer. Hum
Reprod . 1998;13:2107–2109.
63. Botta G, Grudzinskas G. Is a prolonged bed rest following embryo
transfer useful? Hum Reprod. 1997;12:2489–2492.
64. Amarin ZO, Obeidat BR. Bed rest versus free mobilization following embryo transfer: a prospective randomized study. BJOG.
2004;111:1273–1276.
65. Sharif K, Afnan M, Lashen H, Elgendy M, Morgan C, Sinclair L.
Is bed rest following embryo transfer necessary? Fertil Steril.
1998;69:478–481.
66. Bar-Hava I, Kerner R, Yoeli R, Ashkenazi J, Shalev Y, Orvieto R.
Immediate ambulation after embryo transfer: a prospective study.
Fertil Steril. 2005;83:594–597.
67. Mart´ınez F, Coroleu B, Parriego M, et al. Ultrasound-guided
embryo transfer: immediate withdrawal of the catheter versus a
30 second wait. Hum Reprod . 2001;16:871–874.
68. Lenz S, Leeton J. Evaluating the possibility of uterine transfer by
ultrasonically guided transabdominal puncture. JInVitroFert
Embryo Transf . 1987;4:18–422.
128 — Eric Flisser and Jamie A. Grifo
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69. Parsons JH,BoltonVN,WilsonL,CampbellS. Pregnancies following in vitro fertilization and ultrasound-directed surgical embryo
transfer by periurethral and transvaginal techniques. Fertil Steril.
1987;48:691–693.
70. Kato O, Takatska R, Asch RH. Transvaginal-transmyometrial
embryo transfer: the Towako method; experiences of 104 cases.
Fertil Steril. 1993;59:51–53.
71. Sharif K, Afnan M, Lenton W, Bilalis D, Hunjan M, Khalaf Y. Transmyometrial embryo transfer after difficult imme-
diate mock transcervical transfer. Fertil Steril. 1996;65:1071–
1074.
72. Groutz A,Lessing JB, Wolf Y, Azem F, Yovel I, Amit A. Comparison
of transmyometrial and transcervical embryo transfer in patients
with previously failed in vitro fertilization-embryo transfer cycles
and/or cervical stenosis. Fertil Steril. 1997;67:1073–1076.
73. Sohan K, Woodward B,Ramsewak SS. Successful use of transrectal
ultrasound forembryotransfer in obese women. J ObstetGynaecol.
2004;24:839–840.
Section 7.5. Salpingostomy and Salpingectomy
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Jaime Ocampo, Mary Jacobson, Mario Nutis, and Camran Nezhat
Approximately 25% to 35% of women’s infertility is caused by
tubal disease.[1] The most common cause of tubal disorder is
pelvic inflammatory disease; other causes include endometriosis, salpingitis isthmica nodosa, complicated appendicitis, and
surgery.
Because the fallopian tube may be affected at different sites,
tubal damage is categorized into proximal or distal tubal disease.
Proximal tubal disease accounts for 10% to 25% of tubal infertility. The most common etiology of proximal tubal disease is
salpingitis isthmica nodosa. Other causes of proximal obstruction may be mucus plugs, cornual synechiae, polyps, and tubal
endometriosis. Distal tubal diseasecommonly refers tothe development of hydrosalpinges; however, other anatomic abnormalities, such as fimbrial phimosis or tubal adhesions, may constitute
distal tubal disease. Distal tubal disease may account for up to
85% of tubal infertility.[1]
Surgical treatment for tubal disease waned after the advent
of IVF. However, in recent years it has become evident that for
specific tubal pathologies, specifically hydrosalpinges, surgical
intervention needs to be considered, even in patients undergoing
IVF.[2,3]
SURGICAL TREATMENT
OF HYDROSALPINGES
A hydrosalpinx, or fluid-filledtube, occurs afteran inflammatory
process damages the serosa and mucosaof the fallopian tube, creating an occlusion in the distalpart of the tube.Asaresult, normal
and pathologic secretions may accumulate in the tube. The frequency of hydrosalpinges in distal tubal disease is approximately
10% to 30%.[4]
Hydrosalpinges have been shown to have a negative effect on
pregnancy rates. In 1998, Zeyneloglu et al. [5] presented a metaanalysis of23 studies that looked atthe relation of hydrosalpinges
and IVF outcome. They suggested that the existence of hydrosalpinges reduced the implantation rate and increased the risk of
loss in patients undergoing IVF. Similar findings were presented
in aCochrane review donein 2004 by Johnson et al.[3] They were
able to find only three randomized controlled studies that looked
at surgical treatment of hydrosalpinges. The pooled results of
these studies showed that the odds for pregnancy and live birth
were increased with laparoscopic salpingectomy for hydrosalpinges before IVF. Thispromptedtheauthors to conclude that “the
option of laparoscopic salpingectomy should be considered for
all women with hydrosalpinges who are due to undergo IVF.”[3]
Although the actual mechanism by which hydrosalpinges
decrease pregnancy rates is unknown, there are several proposed
theories. In themurinemodel, multiple studies have documented
that hydrosalpinx fluid is embryotoxic. However, similar studies
have failed to show toxicity in human embryos.[6] Mansour et al.
[7] proposed that a mechanical interference with implantation
occurred as the hydrosalpinx fluid leaked into the uterine cavity. In this study, the presence of fluid in the endometrial cavity reduced pregnancy rates and most women with fluid in the
endometrial cavity had a hydrosalpinx at the time of IVF. Other
studies haveshown that the endometrium may become less receptive to embryo implantation when exposed tohydrosalpinxfluid.
Meyer et al. [8] studied the expression of endometrial integrins
in women with hydrosalpinges. They founda significant decrease
in the integrin marker αvβ3. Deficiency in this marker and two
others (α1β1, α4β1) has been shown to have a deleterious effect
on endometrial receptivity to embryo implantation.
CHOICE OF SURGICAL PROCEDURE
There has been considerable controversy as to the best and most
appropriate surgical intervention for hydrosalpinges. Less invasive procedures like needle aspiration of hydrosalpinx fluid, salpingostomy, fimbriolysis, and proximal tubal occlusion have been
proposed.
The success of these treatments is closely related to the severity of tubal disease. There have been several grading systems for
assessing tubal damage. Tubal factors that affect the success of
tubal surgery include thickness of the fallopian tube wall, adhesions of the tubal mucosa, and in some classifications, serosal
adhesions.[9] In general, tubes classified with mild tubal disease have conception rates of 60% with fimbrioplasty and 81%
with salpingostomy.[1] This is likely the result of an intact tubal
mucosa – there is evidence that a healthy mucosa hasa much better prognosis of success with fimbrioplasty and salpingostomy
because the tube’s ability to retrieve andtransport ooctyes is usually preserved.[9]
Although the proposed systems for assessing tubaldiseaseand
choosing the adequate surgical procedure seem feasible, in practice they are difficult to carry out because most grading systems
require the abilityto perform asalpingoscopyto adequately grade
the extent of tubal disease. These procedures can be carried out
in tertiary centers with surgeons that have extensive experience
with this type of procedure; however, this makes access much
more difficult for the general infertility population.
Other issues to keep in mind are the high risk of ectopic
pregnancy – up to 20% with salpingostomy – with tubal surgery
done on inadequately assessed tubal disease.[9] In a review article on the management of hydrosalpinges, Sabatini et al. [9]
129
130 — Jaime Ocampo, Mary Jacobson, Mario Nutis, and Camran Nezhat
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suggested that tubes with bipolar damage, mucosal adhesions,
dense serosal adhesions, or thick walls as well as any tubes larger
than 3 cm are unsuitable for tubal surgery, and salpingectomy
should be the procedure of choice.
Recently there has been considerable debate over the use of
proximaltubalocclusion for treatment of hydrosalpingesin infertility patients. The most recent study to compare this procedure
with salpingectomy was donebyKontoravdis et al.[10] Thisstudy
found similar improvement in implantation ratesand pregnancy
rates with tubal occlusion. There was a trend toward better outcomes with salpingectomy, but these numbers did not reach statistical significance.
Ultrasound-guided aspiration of hydrosalpinx fluid has also
been proposed. Some researchers have performed this procedure just before an IVF cycle is done. This procedure, however,
Grasping
forceps
has a high rate of recurrence, with some reporting reaccumulation of the hydrosalpinx fluid within 2 days after the procedure.[11]
SALPINGECTOMY
Salpingectomy is the most widely used method for treatment of
hydrosalpinges in infertility patients. The evidence for use of this
procedure is based on two small randomized controlled studies
and multiple retrospective studies. Critics ofthis procedure claim
that the indiscriminate use of salpingectomy for hydrosalpinges
should not be adopted because corrective surgery may be just as
successfulinadequatelyassessedtubaldisease.However,adequate
assessment of tubal disease requires salpingoscopy, a procedure
Coagulation
of tubal isthmus
Hydrosalpinx
Mesosalpinx
Uterus
Ovarian
ligament
Ovary
Endosalpinx
A
Figure 7.5.1. Salpingectomy is done with bipolar electrocoagulation for hemostasis. (A) The isthmic portion of
the tube is coagulated and cut close to the uterus.(Continued)
Grasping
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forceps
Mesosalpinx
Tubal
Isthmus
Ovary
Salpingostomy and Salpingectomy — 131
CO2 laser
B
C
Endoloop
Hydrosalpinx
Grasping
forceps
Scissors
Uterus
Ovary
D
E
Scissors
Figure 7.5.1. (Continued) (B) While thetube is undertraction, themesosalpinx is coagulated andcut. (C) Sharp
scissors (inset) or the ultra-pulse CO
laser are used for cutting. (D) The Endoloop is passed around the tube
2
and the mesosalpinx is ligated with one suture. (E) The mesosalpinx is cut above the tube. An adequate stump
remains to prevent the ligature from slipping (inset).
132 — Jaime Ocampo, Mary Jacobson, Mario Nutis, and Camran Nezhat
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not widely taught or performed. Without assessment of the tubal
mucosa, it would be very difficult to accurately predict the success of salpingostomy or fimbriolysis. The possible impairment
of ovarian blood supply after salpingectomy has been proposed,
raising the possibility of decreased ovarian response undergoing
hyperstimulation for IVF cycles. This theory was proposed after
studies done on women who underwent salpingectomy after an
ectopic pregnancy showed a decrease in follicle formation. However, subsequent studies have shown no impairment in ovarian
response to IVF treatment.[12] Proximal tubal occlusion may
represent another option in the treatment of hydrosalpinges in
infertility patients. However, evidence for adoption of this procedure in place of salpingectomy is still fairly scant.
TECHNIQUE FOR SALPINGECTOMY
Salpingectomy is an easy procedure that requires instruments
commonly used to do tubal electrocoagulation for sterilization.
[13] The necessary instruments are a bipolar electrocoagulator,
grasping forceps, scissors, and a laparoscope. A CO
laser also
2
may be used. The laparoscope and 5-mm suprapubic trocars are
placed, through which the graspers and bipolar electrocoagulator are inserted. Peritubal adhesions are lysed, and the tube is
grasped at the isthmic portion. The proximal portion of the isthmus is coagulated and cut, using either scissors or laser (Figure
7.5.1A–C). If scissors areused,the bipolar electrocoagulator must
be removed and replaced with the scissors through the same secondary trocar, or a third accessory trocar may be placed. The
laser is faster and more precise than the scissors. Cutting is done
in layers so that there is less chance to overshoot the coagulated
area and get into an area beyond the coagulated tissue. Once the
tubal isthmus is transected, the mesosalpinx is coagulated alternately and cut at intervals of 1 to 2 cm in the direction of the
tubo-ovarian ligament.
Alternatives to bipolar electrocoagulation of the mesosalpinx
are the Endoloop sutures (Ethicon) and automated stapling
device (Endopath ELC 35, Ethicon). Before the Endoloop ligature is used, both the proximal portion of the tube and its distal
attachment to theovary (fimbria ovarica) are coagulated andcut.
The Endoloop is passed around the tube, and the mesosalpinx
is ligated with one Endoloop and removed. The mesosalpinx is
cut above the ligature. An adequate stump is left to prevent the
ligature from slipping (Figure 7.5.1D,E). The stapling device is
introduced through a 12-mm trocar incision. Afteradhesions are
lysed and the tube is mobilized, it is pulled up and put under
traction. The stapler is used from the proximal to the distal end
to staple and cut the tube. One or two applications are sufficient
Hydrosalpinx
A
Endoclip
Clips
Mesosalpinx
B
Figure 7.5.2. (A) Salpingectomy is achieved with an automatic stapling device. The first application of the
stapling device is to the proximal portion of the tube across the mesosalpinx. The tube is under traction. (B)
The second application completes the salpingectomy (inset). A view of the mesosalpinx after the tube has been
removed.
Salpingostomy and Salpingectomy — 133
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for the entire tube (Figure 7.5.2A,B). Once detached, the tube
is removed from the pelvis through a suprapubic trocar sleeve
or the operating channel of the laparoscope. Removal of a larger
tube (a ruptured tubal pregnancy or hydrosalpinx) requires an
Endopouch (Ethicon) or another method of removal. The pelvic
cavity is irrigated. The intra-abdominal pressure is decreased to
reveal bleeding temporarily controlled by a pneumoperitoneum.
This is especially important when one is using a stapling device.
REFERENCES
1. Kodaman PH, Arici A, Seli E. Evidence-based diagnosis and management oftubal factor infertility. Curr Opin Obstet Gynecol. 2004;
16(3):221–229.
2. Mansour R, Aboulghar M, Serour GI. Controversies in the surgical management of hydrosalpinx. Curr Opin Obstet Gynecol.
2000;12:297–301.
3. Johnson NP, Mak W, Sowter MC. Surgical treatment for tubal
disease in women due to undergo in vitro fertilisation. Cochrane
Database Syst Rev. 2004;(3):CD002125.
4. Hull MG, Glazener CM, Kelly NJ, etal. Population study of causes,
treatment and outcome of infertility. Br Med J (Clin Res Ed).
1985;291:1693–1697.
5. Zeyneloglu HB, Arici A, Olive DL. Adverse effects of hydrosalpinx
on pregnancy rates afterinvitrofertilization embryo transfer. Fertil
Steril. 1998;70:492.
6. Chen CD, Yang JH, Lin KC, Chao KH, Ho HN, Yang YS. The significance ofcytokines, chemical composition, andmurine embryo
development in hydrosalpinx fluid for predicting the IVF outcome inwomen with hydrosalpinx. Hum Reprod. 2002;17(1):128–
133.
7. Mansour RT, Aboulghar MA, Serour GI, Riad R. Fluid accumulation of the uterine cavity before embryo transfer: a possible hindrance for implantation. J In Vitro Fert Embryo Transf .
1991;8(3):157–159.
8. Meyer WR, Castelbaum AJ, Somkuti S, et al. Hydrosalpinges
adversely affect markers of endometrial receptivity. Hum Reprod .
1997;12(7):1393–1398.
9. Sabatini L, Colin D. The management of hydrosalpinges: tubal
surgery orsalpingectomy? Curr Opin ObstetGynecol. 2005;17:323–
328.
10. Kontoravdis A, Makrakis E, Pantos K, et al. Proximal tubal occlusion and salpingectomy result in similar improvement in in vitro
fertilization outcome in patients with hydrosalpinx. Fertil Steril.
2006;86(6):1642–1649.
11. Bloechle M, Schreiner T, Lisse K. Recurrence of hydrosalpinges after transvaginal aspiration of tubal fluid in an IVF cycle
with development of a serometra. Hum Reprod . 1997;12(4):703–
705.
12. Sacks G, Trew G. Reconstruction, destruction and IVF: dilemmas
in the art of tubal surgery. BJOG. 2004;111(11):1174–1181.
13. Nezhat C, Nezhat F, Winer W. Salpingectomy via laparoscopy: a
new surgical approach. J Laparosc Surg. 1991;1:91.
8 HYSTEROSCOPY
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Section 8.1. Evaluation and Management of the Uterine Septum
Eric J. Bieber and Edie L. Derian
Uterine anomalies area relatively common congenitalabnormality,with uterine septum beingthemost common (Table 8.1.1).[1]
This is even truer in patients with recurrent pregnancy loss, in
whom rates of uterine abnormalities may approach 15% to 27%.
Historically, the uterine septum has been approached via laparotomy through either a Tompkins or Jones procedure. These successful but highly morbid procedures required laparotomy, significant hospital stays, and subsequent cesarean delivery and had
a high risk of adhesion formation. More recently, this surgery
has been supplanted by hysteroscopic or other minimally invasive methodologies for treatment. This section focuses on the
embryologic development of the genital tract that may lead to
mullerian abnormalities, discussesthework-up of patients before
treatment, evaluates the appropriate candidates for surgical procedures,and discusses the technical aspects of the procedure itself,
postoperative recommendations, and results of various modalities of treatment. In addition, complications specific to these
procedures are reviewed.
EMBRYOLOGY
It is unclear what the exact rate of mullerian abnormalities is in
the general population as there have been nogood cross-sectional
studies of normal patients.Itisbelieved that the incidence is inthe
range of 1%to6%,and there are numerous variations. The American Fertility Society(nowthe American Society forReproductive
Medicine) has published aclassification system to standardize the
nomenclature among surgeons (Tables 8.1.1, 8.1.2).[2] Women
with recurrentpregnancyloss(RPL)appeartohave a muchhigher
incidence of anomalies relative to the general population. Salim
et al. [3] in evaluating patients with and without RPL noted an
anomaly rate of 1.7% in patients without RPL and a rate of 6.9%
in those with three or more losses. Several hypotheses have been
proposed to explain the wide range of abnormalities that may
occur. The most prominent theory suggests the mullerian ducts
initially fuse together as one structure and that this begins caudally at the mullerian tubercle and proceeds unidirectionally in a
cephalad manner. The ultimate result is one cavity that is divided
in the midline by a septum, which is then reabsorbed. Given the
wide range of abnormalities, early in the century it was suggested
that resorption of theseptummaybegin anywherewithin the septum and proceed in either or both directions. Uterine anomalies
were thus attributed to either failures of the mullerian elongation process, abnormal fusion, canalization, or resorption. More
recently, several case reports of patients with a uterine septum
and cervical duplication with a vaginal septum have been published – casesthat would be inconsistent with theaforementioned
hypothesis.[4,5] Muller et al. [6] proposed an alternate theory
suggesting that at the beginning of the 10th week, the lowermost
portions of the mullerian ducts (between the isthmus cranially
and theurogenital sinus caudally) fuse at the medialaspects. This
creates a single cavity thatcomprisestheupper vagina, cervix, and
isthmus. Interestingly,they suggest that at the upper aspects there
is not true fusion, but rather at the triangular junction between
the two mullerian ducts, there is rapid division of cells that then
connects the two ductsand convergeswith the lower septum. Like
the original hypothesis, resorption then follows. In this model,
if the initial fusion did not occur correctly but the upper fusion
did occur, a patient might have both a vaginal septum and two
cervices but a unified cavity separated by a septum, as the prior
case reports suggest.
Patients with uterine anomalies may also have associated
anomalies ofthe urogenital tract.It has beenestimated that in the
case of aunicornuateuterus, up to 40%of patients may have renal
anomalies. These are generally noted on the side of the remnant
uterine horn.[7] In an early report, Valle and Sciarra [8] found
two of 12patients with auterine septum tohavea urologic abnormality. More recently, Heinonen [9], in evaluating patients with
a complete septum and vaginal septum, found 11 of 55 patients
(20%) had genitourinary abnormalities, with five patients who
had ipsilateral renal agenesis and six with a double ureter.
MORPHOLOGY
The actual morphology of the uterine septum has been suggested
as the reason for poor reproductive function in patients with this
abnormality. The most common hypothesis suggests a decrease
in vascularity to the septum that may decrease the likelihood of
implantation and functional placentation. Several groups have
investigated these tenets to ascertain if differences exist within
the structure of the septum versus normal uterine tissue that
might lead to reproductive loss. Sparac et al. [10] performed
resectoscopic biopsy of septa in 63 women undergoing metroplasty. They noted preoperatively that evaluation of the uterine
septum with transvaginal color Doppler imaging demonstrated
vascularity consistent with radial arteries. Histopathology of
the septum specimens demonstrated both connective tissue and
myometrial tissue. They proposedthatthe muscular tissue within
the septum might create irregular contractile patterns that may
increase the risk of abortion.Fedele et al.[11] evaluated theultrastructural aspects of the uterine septum by discretely sampling
endometrium overlying the septum as well asendometrium from
the nonseptal lateral wall. Using scanning electron microscopy,
they demonstrated the following changes in the tissue overlying
134
Evaluation and Management of the Uterine Septum — 135
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Table 8.1.1: Incidence of Uterine Anomalies
Anomaly Incidence, %
Septate uterus 55
Unicornuate uterus 20
Bicornuate uterus 10
Uterus didelphys 5–7
Data from Troiano RN.[1]
Table 8.1.2: American Society for Reproductive Medicine
Classification of Mullerian Anomalies
Class Anomaly
I Mullerian agenesis or hypoplasia
II Unicornuate uterus
III Didelphys uterus
IV Bicornuate uterus
V Septate uterus
VI Arcuate uterus
VII Diethylstilbestrol (DES)-exposed uterus
From The American Fertility Society.[2]
the septum: reduced number of glandular ostia, irregular nonciliated cells with rare microvilli, incomplete ciliogenesis on ciliated cells, and a decrease in the ciliated/nonciliated ratio. They
believe these changes represent a decrease in the sensitivity of the
endometrial cells overlying the uterineseptum, which might have
an impact on the receptivity to embryos.
WORK-UP
Many individuals will have a uterine septum diagnosed as part
of an evaluation for repetitive loss. In these settings, a complete
work-up and evaluation for the underlying issues of reproductive
loss should be performed.
Hysterosalpingography(HSG)isonetechniqueused foridentifying a uterine/mullerian abnormality.The testis relatively easy
to perform, with low cost compared with surgery. Uterine subcavities generally are well visualized, and often the extent of the
uterine septum may be estimated (Figure 8.1.1).[12] Unfortunately, the radiographic appearance of the uterine septum is not
significantly different from a bicornuate uterus, which is managed in a much different fashion. One study found only 55%
accuracy in differentiating these entities via HSG, with the difficulty being that the uterine fundus cannot be evaluated to assess
whether an indentation exists.[13] In addition, smaller uterine
septa may also be missed if a significantly anteverted or retroverted uterus is not brought into an axial plane or if medium is
injected too quickly to outline the uterine cavity. The advantage
of HSG besides simplicity is the ability to concomitantly evaluate
the fallopian tubes. HSG has also been used in the postoperative
evaluation after septoplasty to evaluate if a residual septum is still
present.
Ultrasonography is the simplest and least invasive methodology for evaluating the uterus as well as other pelvic structures.
More recently, the addition of saline infusion sonohysterography
(SHG) has also been used to aid in further evaluating the uterine
cavity. Transvaginal ultrasound may be superior to transabdominal ultrasound, although both have been effectively used. The
ultrasound appearance of a septate uterus demonstrates little or
no indentation at the fundusasonescansfromonecornualregion
to the next. The septum itself appears as a different echogenic
area within the endometrium and extending cephalad. Pellerito
et al. [14] noted 100% sensitivity and 80% specificity for diagnosing a uterine septum. Alborzi et al. [15] performed a small
prospective trial and noted the ability of SHG to differentiate a
bicornuate from a septate uterus. They questioned if laparoscopy
would be necessary given these findings. Most recently,
A
Figure 8.1.1. Hysterosalpinographic (HSG)images from three patients with recurrentearlypregnancy loss. The three images show varying degrees
of division of the uterine cavity. (A) HSG diagnosis: normal uterus; surgical diagnosis: uterine septum extending one third the length of uterine
cavity. (B) HSG diagnosis: septum versus bicornuateuterus; operative diagnosis: uterine septum extending three quarters the length of the uterine
cavity. (C) HSG diagnosis: septum versus bicornuate uterus; operative diagnosis: long uterine septum. From Proctor JA and Haney AF.[12]
B
C
136 — Eric J. Bieber and Edie L. Derian
https://t.me/med1917
A
Figure 8.1.2. (A) Three-dimensional ultrasound longitudinal view of the uterus demonstrating a complete uterine septum. (B) Hysteroscopic
view of the uterus demonstrating a uterine septum reaching approximately 40% of the uterine cavity. From Weissman A et al.[16]
three-dimensional ultrasound hasbeen suggested as animproved
tool for accessing mullerian abnormalities (Figure 8.1.2).[16]
Raga et al. [17] evaluated three-dimensional ultrasound and
found a91.6%correlationwithlaparoscopicfindings.Otherstudies are less compelling regarding three-dimensional ultrasound
in adding additional information above and beyond that noted
with standard two-dimensional imaging.[18] Given the high sensitivity and specificity as well as the relative ease to perform SHG,
B
(Figures 8.1.3, 8.1.4).[4] Several studies have suggested that MRI
has a high ability to noninvasively differentiate uterine anomalies, especially in complex anatomic situations.[19,20] Fedele
et al. [21] suggested that uterine septa have MRI findings of
maximal fundal indentation of 10 mm or less and an angle
◦
of 60
or less between the medial margins of the hemicavities. Doyle [22] evaluated ultrasound, HSG, and MRI for diagnosing mullerian abnormalities and noted the correct anatomic
it may be difficult to ascertain that the further expense and lack
of wide availability of this newer technology are justifiable.
Magnetic resonance imaging (MRI) is yet one more imag-
ing modality available for evaluating mullerian abnormalities
CC
Figure 8.1.3. Axial magnetic resonance image demonstrating double
uterine cavities (white arrows) and uterine septum (black arrow). The
ovaries are the circular structures on either side of the uterine cavities.
From Hundley AF et al.[4]
Figure 8.1.4. Magnetic resonance–based three-dimensional image of
the uterus and pelvic organs (superior view). The double cavities are
labeled C, and the dimmed-out uterine muscle outline is shown with
the black arrow. Color legend: pale yellow, ovaries; brown, levator ani;
beige-pink, vagina; white, pelvic bones; yellow, urethra; pink-brown,
obturator internus. From Hundley AF et al. [4] and Scott P and Magos
A.[23]
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