and etiologic (E) features of patient disease PVDAHE
.3
The symptoms and
varices are then broken down into what anatomic zone they involve as seen in Figure 1. For example, a patient with primary left ovarian vein reflux is S2
V2 PLGV, R, NT (left gonadal
vein, reflux, nonthrombotic). Having a standardized classification system will allow for homogeneous patient populations for upcoming disease- specific clinical trials targeted at improving clinical decision-making.
Although I have not changed any major practice patterns based on SIR Connect threads, I do feel I have expanded my armamentarium based on the insights of my colleagues across the country.
When working up CPP, it is important to do a thorough history and physical, which likely includes high-level external gynecological assessment, as there is a broad differential diagnosis for CPP that can include multifactorial components.4
Often the first imaging
test obtained in a woman with pelvic pain is a pelvic ultrasound, which may show periovarian and para-uterine varicosities. Additional cross-sectional imaging is often obtained to look for pelvic varices >5 mm or ovarian veins measuring >6 mm due to its association with reflux leading to pelvic venous hypertension.5 Diagnostic venography remains the gold standard approach in evaluating for venous reflux and measurement of pressure gradients.
The pathophysiology of PeVD is complex, and the relevant venous anatomy has many interconnections and anastomosis which leads to a broad spectrum of presenting symptoms. Often the pelvic veins can be thought of as “blood reservoirs” divided into the left renal vein, the
superficial and deep veins of lower extremity and the parietal and visceral veins of the pelvis as seen in Figure 1. PeVD is secondary to venous incompetence leading to distension of a venous reservoir and venous hypertension. This activates nociceptors generating pain and generally occurs in the ovarian or internal iliac tributary veins. There are several venous “escape points” or communications between the pelvic veins and the superficial veins of the legs which can lead to vulvar and lower extremity varicosities. Symptom type and location depend on whether the distal reservoir affected has compensated or uncompensated physiology. For example, uncompensated reflux in the left ovarian vein will be transmitted to pelvic distal reservoir and can cause CPP. However, if compensation occurs via flow through “pelvic escape points” this may result in no CPP and
instead pelvic origin vulvar and lower extremity varicosities.2,5,6,7,8
Ovarian vein and internal iliac vein embolization have been shown to be safe and effective for management of CPP. A large systematic review of 762 patients with CPP who underwent embolization and/or sclerosis of the internal iliac or ovarian veins reported symptomatic improvement in 697 (91.4%) of patients.9
Nonthrombotic
iliac vein lesion (NIVL) can be associated with CPP and classically involves compression/occlusion of the left iliac vein between right iliac artery and the lumbar vertebrae. In a 2015 retrospective study reviewing outcomes of 18 patients with NIVL and 1 with suprarenal IVC stenosis, all who were treated with venous stenting, 15 of the 19 patients had complete resolution of their CPP.10
A similar
retrospective study of 18 patients treated with stents for left renal vein stenosis or compression resulted in
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