Anatomical Variations of the Intrapelvic Course of the Superior Gluteal Vessels and their Relationship to the Lumbosacral Plexus: A Cadaver Study

Cancelliere L1, Li A L K1, Marcu I2, Fernandes G L3, Sermer C1, Shaubi M1, Balica A4, Morozov V5, Campian E C2, Solnik M J1, Girão M J B C3, Lemos N6

Research Type

Clinical

Abstract Category

Anatomy / Biomechanics

Abstract 549
Open Discussion ePosters
Scientific Open Discussion Session 28
Friday 31st August 2018
13:10 - 13:15 (ePoster Station 6)
Exhibition Hall
Anatomy Neuropathies: Peripheral Sensory Dysfunction Pain, other Pain, Pelvic/Perineal
1. University of Toronto, Toronto, Canada, 2. Saint Louis University, Missouri, USA, 3. Federal University of São Paulo, São Paulo, Brazil, 4. Rutgers Robert Wood Johnson Medical School, New Jersey, USA, 5. Georgetown University, Washington DC, USA, 6. University of Toronto, Toronto, Canada; Federal University of São Paulo, São Paulo, Brazil
Presenter
Links

Poster

Abstract

Hypothesis / aims of study
The role of malformed or dilated branches of iliac vessels in causing pelvic pain is not well understood. Such vessels may entrap nerves of the lumbosacral plexus against the pelvic sidewalls, producing symptoms not typically encountered in gynecological practice, including sciatica and refractory urinary and/or anorectal dysfunction [1]. Recently, compression of lumbosacral nerve roots by variant superior gluteal veins (SGV) has been identified laparoscopically in patients with sciatica with no clear spinal or musculoskeletal cause. Laparoscopic nerve decompression by superior gluteal (SG) vessel ligation resulted in 92.3% of patients reporting a ≥ 50% improvement in visual analog pain scores [2]. Therefore, in isolating this anatomical variant in symptomatic patients and demonstrating an improvement in symptoms after decompression, we identified this neurovascular conflict – the Superior Gluteal Vein (SGV) Syndrome – as a potential yet previously unrecognized intrapelvic cause of sciatica. Descriptions of anatomical variation in the venous branching pattern of the iliac vessels, which includes the SGV, in the asymptomatic general population, are limited. Therefore, to better understand the clinical significance of this finding, we investigated the characteristics and prevalence of SG vessel variants in a general population of female cadavers. We describe and quantify variants in the SG vessels, particularly in the SGV, to identify those potentially responsible for symptomatic lumbosacral nerve entrapment.
Study design, materials and methods
We performed laparoscopic pelvic dissection in 45 female cadavers, donated to an academic institution for medical education & training. Standard laparoscopic techniques, including closed intraperitoneal entry with Veress needle insufflation and lateral & suprapubic port placement, were employed. Retroperitoneal entry and dissection was performed using sharp and vessel-sealing instruments. Visualization comparable to that obtained intraoperatively was achieved. Dissection was performed by gynecology faculty, fellows, and residents, under the supervision of faculty selected for their experience in minimally invasive gynecologic surgery.

Of the 45 cadavers, 38 were dissected bilaterally. A total of 78 SG vessel sites were dissected – data was collected in native anatomical pairs to identify potential trends & variaton within cadavers. The paths of the SG vessels were followed & documented. Their branching patterns and relationships to nearby lumbosacral nerve roots were documented: originating directly from the internal iliac vessels or from a posterior trunk, and then traveling posterior or anterior to the lumbosacral plexus.  SG variants were defined as those branches coursing anterior to the lumbosacral plexus (Figure 1).

Our main outcome measure was the prevalence of variants in the cadaver population. The path of the variant, nature of vessels involved (arterial, venous, or both), and laterality (left, right, or bilateral) were further described. Other subgroups that were predefined for comparison in those with previous hysterectomy and by internal iliac branching pattern.
Results
SG variants were identified in 35.56% (95% CI 21.57 to 49.54) of specimens. Only 4.44% (95% CI 0.00 to 10.47) of cadavers had bilateral SG variants. Out of the 18 dissections with variants, 8 involved both the SG artery and vein, while 5 only had a variant SG artery, and 5 had a variant SG vein. SG variants were significantly more likely to originate directly from the internal iliac vessels rather than from a posterior trunk (p=0.0458). The presence of an SGV variant was not significantly associated with previous hysterectomy (p=0.8396).
Interpretation of results
Laparoscopic dissection in female cadavers reveals that SG variants previously identified in patients with sciatica, also exist in the general population. In our sample population of 45 cadavers, the prevalence of all SG variants was 35.56% (95% CI 21.57 to 49.54). This suggests that SG variants are present as a potential source of entrapment in a significant portion of the general population. Variant characteristics, including vessel type (arterial, venous, or both) and laterality were heterogeneous. Whereas all SG variants isolated in symptomatic patients were venous, both arterial and venous variants were identified in cadavers. SG variants occurred significantly more in specimens without a distinct posterior trunk, suggesting that these variants may be more likely when the SG vessels originate directly from the internal iliac vessels.
Concluding message
Laparoscopic identification of SG variants in female cadavers confirms that variations in the SGV vessels previously described in symptomatic patients are also present in a general population of female cadavers. Although our sample was limited to female cadavers with undisclosed clinical history, the identification of SG variants in several of these specimens means that anatomical variants vulnerable to neurovascular entrapment exist in about 35% of the general population. This supports our hypothesis that variant SG vessels, particularly aberrant SG veins, can be the source of symptoms of sciatica with lower urinary tract symptoms, anorectal dysfunction, and/or perineal or gluteal pain by compressing the lumbosacral plexus and nerve roots.  This intrapelvic neurovascular conflict – the SGV Syndrome – should be considered in cases of sciatica with no identifiable spinal or musculoskeletal etiology.
Figure 1
References
  1. Lemos N, Possover M. Laparoscopic approach to intrapelvic nerve entrapments. J Hip Preserv Surg. 2015; 0(0): 1-7.
  2. Cancelliere L, et al. Superior gluteal vein syndrome: an intrapelvic cause of sciatica, 2018. Submitted to ICS 2018.
Disclosures
Funding None Clinical Trial No Subjects Human Ethics not Req'd REB approval is not required for this type of study according to Saint Louis University guidelines. Helsinki Yes Informed Consent No
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