Pelvic vein thrombosis in patients with pelvic venous disorders

Abstract

Objective

To assess the incidence of pelvic vein thrombosis (PVT) and outcomes of anticoagulant therapy for PVT in patients with pelvic venous disorders (PeVDs).

Methods

This prospective cohort study included 588 female patients with PeVDs underwent clinical examination followed by duplex ultrasound of the pelvic veins in 2021-2023. Patients with PVT were administered with anticoagulant therapy in an outpatient setting using low molecular weight heparins at a therapeutic dose.

Results

PVT was detected in 7.6% of patients with PeVDs and was symptomatic in 28.8% of them. The majority of asymptomatic patients had thrombosis in only one of the parametrial veins (90.6%). Anticoagulant therapy resulted in the PVT symptoms relief in all patients within 10 days and recanalization of the pelvic veins in 1-3 months.

Conclusion

In our study, PVT was diagnosed in 7.6% of patients with PeVDs. Anticoagulant therapy is effective and safe in resolving PVT symptoms.

Keywords

Pelvic venous disorders pelvic vein thrombosis duplex ultrasound anticoagulant therapy

Introduction

The most recent consensus documents define pelvic veins as ovarian veins, pelvic venous plexuses (pampiniform, uterine, parametrial veins) and tributaries of the internal iliac veins.^1,2 Published data suggest that pelvic vein thrombosis (PVT) is a rare disorder with a prevalence of 0.05 to 3% in various cohorts.^3–5 Ovarian vein thrombosis (OVT) is most often detected in the postpartum period, in patients with inflammatory diseases of the internal reproductive organs, and after surgical interventions on the pelvic organs and vessels.^6–10 There are mainly sporadic case or small series reports of the PVT development.^11–14 Labropoulos et al. indicated rare incidence of symptomatic forms of PVT and reported benefits of anticoagulant treatment.¹⁴ Rottenstreich et al. presented results of examination and treatment of 74 females with pregnancy- and non-pregnancy related OVT and indicated that short-term use of anticoagulants leads to rapid resolution of the OVT symptoms and recanalization of the veins.¹⁵ Amin et al. stated that idiopathic PVT does not require anticoagulation.¹⁶

Currently, the data on the prevalence of PVT, diagnosis and treatment approaches in this condition are scattered and contradictory. There is no convincing evidence of the need and optimal regimen of anticoagulant treatment in patients with PVT.

This study aimed to assess the incidence of PVT, as well as efficacy and safety of anticoagulant therapy in patients with pelvic venous disorders (PeVDs).

Methods

This single-center prospective cohort study included 588 female patients with PeVDs aged 21 to 52 years (median 36, IQR 17), which were treated at the University Surgical Clinic in 2021-2023. The study was approved by the local ethics committee of the University. All patients signed a voluntary informed consent to participate in the study.

Inclusion criteria were the detection of pelvic varicose veins with reflux in them for more than 1 s and/or visualization of blood clots in pelvic varicose veins during duplex ultrasound study (DUS). Exclusion criteria were pregnancy and the postpartum period, neoplasms, acute inflammatory diseases of the pelvic organs, receiving chemotherapy or hormonal therapy, and recent surgical or endovascular intervention on the pelvic organs and veins.

Patients

Over a period of 3 years, 588 female patients with PeVDs were examined. Out of them, 217 patients without symptoms and signs of PeVDs or PVT were referred to our clinic from gynecological consultation centers, where the presence of pelvic varicose veins and PVT was suspected based on the results of a routine ultrasound examination of the pelvic organs. The remaining 371 patients sought medical help in our clinic due to the presence of symptoms and signs of PeVDs (chronic pelvic pain, heaviness in the hypogastric region, dyspareunia, vulvar varicose veins, varicose veins of the posteromedial aspect of the thigh, dysuria) or with clinical manifestations of PVT. Symptoms of PVT included sudden, acute pain in the lower abdomen, which did not change its intensity in different positions of the patient, or a sudden increase in existing chronic pelvic pain (CPP), fever up to 37–39°C, and chills. Pain syndrome was assessed using a visual analogue scale (VAS).¹⁷ All patients were examined for competing comorbidities by a gynecologist and urologist.

The diagnosis of PeVDs and TPV was verified using transabdominal and transvaginal duplex ultrasound (DUS) of the pelvic veins and retroperitoneum. All patients with detected PVT were administered with anticoagulant therapy. Follow-up clinical examinations and DUS were performed after 10, 30 and 90 days. Computed tomography was not used to diagnose PVT. The assessment in all patients with confirmed PVT included complete blood count, urinalysis and coagulation testing for measuring international normalized ratio (INR), prothrombin time (PT), activated partial thromboplastin time (aPTT) and fibrinogen level. The study design is presented in Figure 1.

Figure 1.

Study flowchart. PeVDs, pelvic venous disorders; DUS, duplex ultrasound; PVT, pelvic veins thrombosis; LMWH, low molecular weight heparins; OACs – oral anticoagulants.

Ultrasound studies

Ultrasound studies of the pelvic and lower limb veins were performed using Philips EPIQ 5 device (Philips, Amsterdam, Netherlands) according to the procedures described earlier.¹⁸ The study protocol included a sequential evaluation of the status of superficial and deep veins of the lower extremities, perineal veins, iliac veins, inferior vena cava and renal veins, parametrial (PVs), uterine (UVs) and ovarian veins (OVs). To detect reflux in the veins of the lower extremities, perineum and pelvis, the Valsalva manoeuvre and compression test were used during DUS. An increase in the diameter of PVs, UVs and OVs of greater than 5 mm was considered pathological.² Reflux in the pelvic veins and deep veins of the lower extremities was considered abnormal if it persisted for more than 1 s.² The pelvic venous reflux (PVR) severity was assessed by its duration using a previously developed classification as follows: type I (mild), 1-2 s; type II (moderate), 2.1-5 s; and type III (severe), >5 s or spontaneous reflux without loading tests.¹⁸

Hemodynamic significance of the left renal vein (LRV) stenosis was evaluated using the ratios of LRV diameter (D) and maximum velocity (V) at the site of stenosis and in the renal hilum area (D_hilum/D_stenosis and V_stenosis/V_hilum). The ratios D_hilum/D_stenosis >4 and V_stenosis/V_hilum >4.9 were considered ultrasonic signs of nutcracker syndrome (NS), while lower values were indicative of the nutcracker phenomenon (NF). Additionally, the angle of superior mesenteric artery (SMA) with aorta was measured, and its value of less than 41° was considered abnormal.

Ultrasound signs of PVT were the detection of hypoechoic inclusions in the venous lumen with no or parietal blood flow in the studied vein. Restoration of the patency of pelvic veins was assessed using DUS according to the degree of recanalization as follows: weak (single isolated blood flows in the lumen or close to the venous wall); medium (multiple multi-directional blood flows occupying up to half of the lumen; residual mural thrombi in the lumen); and complete (more than half of the lumen of the vein is visualized, the blood flow is recorded as a single flow, and there are parietal cord-like intravascular structures). The absence of blood flow in the venous segment indicated its occlusion.

The polymerase chain reaction (PCR) testing for thrombophilia was not performed because patients and their relatives had no history of venous thromboembolism (VTE), and current guidelines do not recommend routine screening of thrombophilia in patients with VTE.¹⁹ The D-dimer level was not measured as the PVT diagnosis was verified using DUS.

Anticoagulant therapy

All patients with PVT received anticoagulant therapy (ACT) on an outpatient basis. Low molecular weight heparins (LMWH) were used in therapeutic doses (enoxaparin sodium 100 IU/kg or nadroparin calcium 86 IU/kg twice daily subcutaneously into the abdomen) for 10 days. If the thrombotic process had a stable course and there was no increase in the size of thrombus according to repeated DUS of the pelvic veins, the patients were switched from LMWH to oral anticoagulants (OACs) rivaroxaban 15 mg or apixaban 5 mg twice a day for 3 weeks. After this period, it was recommended to take rivaroxaban 20 mg or apixaban 5 mg once a day for 2 months. The total duration of ACT was 3 months.

Outcomes

The study outcomes were the incidence of PVT in patients with PeVDs, peculiarities of clinical manifestations of PVT, changes in the PVT symptoms and signs, the PVR duration and thrombotic process characteristics (recanalization or occlusion grades) after 10, 30 and 90 days from the start of ACT.

Statistical analysis

Statistical analysis was performed using Microsoft Excel (Microsoft Corp., Redmond, WA, USA), Statistica 10 software (StatSoft, Tibko, USA) and VassarStats online calculator (open-source online project; https://vassarstats.net/). Data are presented as the mean value with corresponding 95% confidence interval (CI) for quantitative variables or as odds ratio (OR) with a 95% CI for categorical variables. Comparisons were made using the Student's t-test and Mann-Whitney test, where appropriate, for quantitative variables, and the Chi-square test for categorical variables. Differences were considered statistically significant at p < .05. To analyse correlations between various parameters, the Spearman’s coefficient was calculated.

Results

Diagnosis of PVT

At baseline, there were no abnormalities in the blood, urine or coagulation tests in the study population. Demographic, clinical and ultrasound characteristics of patients are shown in Table 1.

Table 1.

Demographic, clinical and ultrasound characteristics of patients at baseline (N = 588).

Parameter	PeVD with PVT (n = 45)	PeVD without PVT		p value
Parameter	PeVD with PVT (n = 45)	Symptomatic PeVD (n = 349)	Asymptomatic PeVD (n = 194)	p value
Age, years, M ± SD	31.9 ± 2.4	33.6 ± 1.7	35.2 ± 1.3	NS
BMI, kg/m², M ± SD	21.3 ± 1.1	20.1 ± 2.3	24.8 ± 1.6^*	.003
Pregnancies, range [min-max]	1–5	0–6	1–7	NA
Childbirths, range [min-max]	1–4	0–5	1–4	NA
CPP, n (%)	4 (8.9)	295 (84.5)	0	.001
CPP intensity, VAS scores, M ± SD	6.7 ± 1.2	7.1 ± 2.3	0	NS
APP, n (%)	9 (20)	0	0	NA
APP intensity, VAS scores, M ± SD	8.2 ± 0.6	0	0	NA
Dyspareunia, n (%)	10 (22.2)	281 (80.5)	0	.001
Heaviness in the hypogastric region, n (%)	11 (24.4)	259 (74.2)	0	.001
Vulvar varicose veins, n (%)	1 (2.2)	92 (26.4)	0	.001
Gluteal varicose veins, n (%)	0	5 (1.4)	0	-
Dysuria, n (%)	0	67 (19.2)	0	-
Haematuria, n (%)	0	0	0	-
Fever, n (%)	10 (22.2)	0	0	-
Chills, n (%)	7 (15.6)	0	0	-
Left flank pain, n (%)	1 (2.2)	0	0	-
Reflux in OVs, n (%)	3 (6.7)	43 (12.3)	55 (28.3)	NS
Duration of reflux in OVs, s, M ± SD	3.3 ± 0.5	4.9 ± 1.7	1.5 ± 0.6^*	.002
Reflux in PVs, n (%)	45 (100)	349 (100)	194 (100)	-
Duration of reflux in PVs, s, M ± SD	3.7 ± 1.1	4.3 ± 1.2	1.7 ± 0.9^*	.01
Reflux in UVs, n (%)	19 (42.2)	211 (60.5)	15 (7.7)^*	.001
Duration of reflux in UVs, s, M ± SD	2.1 ± 0.6	2.5 ± 0.8	1.3 ± 0.4	NS
LRV compression stenosis, n (%)	3 (6.7)^**	83 (23.8)	72 (37.1)	.001
D_hilum/D_stenosis ratio	2.7 ± 0.6	3.1 ± 1.4	2.5 ± 0.8	NS
V_stenosis/V_hilum ratio	2.9 ± 0.5	3.4 ± 1.3	3.2 ± 1.1	NS
History of VTE, n (%)	0	5 (1.4)	3 (1.5)	NS
Small uterine fibroids, n (%)	1 (2.2)	32 (9.2)	27 (13.9)	NS
Polycystic ovaries, n (%)	0	21 (6)	34 (17.5)	.001
History of salpingoophoritis, n (%)	0	2 (0.6)	3 (1.5)	NS
Adenomyosis, n (%)	0	2 (2)	7 (3.6)	NS

Abbreviations: BMI, body mass index; CPP, chronic pelvic pain; APP, acute pelvic pain; OV, ovarian vein; PV, parametrial vein; UV, uterine vein; LRV, left renal vein; D_hilum, the left renal vein diameter near the renal hilum; D_stenosis, the left renal vein diameter in the area of stenosis; V_stenosis, maximum linear blood flow velocity in the left renal vein in the area of stenosis; V_hilum, maximum linear blood flow velocity in the left renal vein near the renal hilum; NS, not significant; NA, not applicable; PP, pampiniform plexus; ACT, anticoagulant therapy.

*, statistically significant difference between group 3 and groups 1 and 2;

**, statistically significant difference between group 1 and groups 2 and 3.

PVT was detected in 45 (7.6%) patients with PeVDs and had symptomatic form in 13 (28.9%) and asymptomatic form in 32 (71.1%) of them. Of these 45 patients, clinical manifestations of PeVD (CPP, dyspareunia, etc.) were present in only 4 (8.9%) patients. Thrombi were located in only the PVs in 36 (80%) patients (left-sided in 34 and bilateral in 2 patients), in the left PVs and MVs in 7 (15.6%) patients, in the left PVs and pampiniform plexus (PP) in 1 (2.2%) patient, and in the left OVs, PVs and PP in 1 (2.2%) patient (Figure 2).

Figure 2.

Ultrasound images. A. Thrombus in one of the parametrial veins; B. Thrombi in several parametrial veins; C. Thrombus in the pampiniform plexus; D. Thrombus in the initial (caudal) section of the left ovarian vein. Indicated by arrows.

The typical length of thrombi in the pelvic veins was 5 to 11 mm, and the width was 4 to 10 mm. Of note that all thrombi in PVs, MVs, GVs and PP had a segmental nature, i.e. thrombosed sections of veins alternated with non-thrombosed ones, which made it possible to determine reflux in the pelvic veins by DUS. In one patient with a combination of thrombosis in the left PVs, OVs and PP, an occlusive thrombus in the ovarian vein extended from PP to the lower third of the vessel, and its dimensions were 55x7 mm. In the PVT group, the PVR duration was >1 s (type I) in 60% and >2 s (type II) in 40% of patients. The majority of patients with asymptomatic PVT had type I PVR (84.4%, or 27 out of 32 patients), while patients with symptomatic PVT had either type II or III PVR. Out of 45 patients with PVT, 30 (66.7%) had thrombus in one of PVs, and 6 (13.3%) had thrombi in two or more PVs. The prevalence rates of PVT symptoms and characteristics of the thrombotic lesions of the pelvic veins are presented in Table 2.

Table 2.

Clinical and ultrasound characteristics of patients with PVT (N = 45).

Parameter	Symptomatic PVT (n = 13)	Asymptomatic PVT (n = 32)	p value
APP, n (%)	9 (69.2)	0	-
APP intensity, VAS scores, M ± SD	8.2 ± 0.6	0	-
Sudden increase in CPP, n (%)	4 (30.8)	0	-
Fever, n (%)	10 (76.9)	0	-
Chills, n (%)	7 (53.8)	0	-
Thrombi in one PV, n (%)	1 (7.7)	29 (90.6)	.001
Thrombi in two or more PVs, n (%)	5 (38.5)	1 (3.1)	.002
Thrombi in the left PVs and MVs, n (%)	5 (38.5)	2 (6.3)	.01
Thrombi in the left PVs and PP, n (%)	1 (7.7)	0	-
Thrombi in the left OVs, PVs and PP, n (%)	1 (7.7)	0	-
Occlusive thrombi, n (%)	7 (53.8)	19 (59.4)	NS
Parietal thrombi, n (%)	6 (46.2)	13 (40.6)	NS
Type I PVR, n (%)	0	27 (84.4)	-
Type II PVR, n (%)	4 (30.7)	3 (9.4)	.001
Type III PVR, n (%)	9 (69.3)	2 (6.2)	.001
LRV compression stenosis, n (%)	1 (7.7)	2 (6.3)	NS

For abbreviations see Table 1.

Symptoms and signs suggestive of PVT were identified in 13 patients, of whom 7 had APP (or increase in CPP) in combination with fever and chills, 4 had APP with fever, and 2 had only pelvic pain. Hyperthermia ranged from 37.3 to 38.5°C. The APP severity varied from 7 to 9 VAS scores. The pain was permanent, resistant to analgesics, and was not associated with static loads or exercises. These characteristics were considered specific features of APP in PVT.

Chronic pelvic pain in PeVD differed from APP in terms of duration (more than 1 year in all patients), description (dull and aching pain), and aggravating/relieving factors (increase in intensity with prolonged static loads and decrease after an overnight rest). In addition, patients with PeVD and PVT reported an increase in the CPP intensity from 5 to 6 to 8-9 VAS scores, a permanent and intense pain syndrome, and its combination with hyperthermia and chills. As shown in Table 2, typical clinical manifestations of PVT were present in 28.8% of patients with PeVDs. Symptomatic course of PVT was reported most often in patients with lesions of two or more pelvic venous collectors and type II or III PVR (Figure 3). Type III PVR was more prevalent in symptomatic versus asymptomatic patients (69.3% and 6.2%, respectively, p = .001). The majority of patients with asymptomatic PVT (90.6%) had blood clots in one of the parametrial veins and PVR of mainly type I. Thrombi in the pelvic veins were obstructive in 57.8% or parietal in 42.2% of patients, and these rates did not differ significantly between symptomatic and asymptomatic patients. Thrombosis of both occlusive and parietal nature was considered occlusive because of a greater significance of this feature in the venous outflow impairment.

Figure 3.

Ultrasound images. Reflux in the pelvic veins. A. Reflux in the parametrial vein lasting 3.5 s (type II); B. Reflux in the parametrial vein lasting more than 5 s (Type III).

Correlation analysis revealed high correlations between the occurrence of PVT symptoms and both the number of pelvic veins involved in the pathological process (r = 0.69) and the PVR reflux of types II and III (r = 0.73) (all p < .05). There was no relationship between the LRV compression stenosis and the incidence of PVT symptoms. The LRV narrowing was not hemodynamically significant and had similar prevalence in patients with symptomatic and asymptomatic PVT (7.7% and 6.3%, respectively, p > .05).

Outcomes of anticoagulant therapy

All patients with PVT received ACT for 3 months regardless of whether they had clinical manifestations of the disease or not. In symptomatic patients, clinical manifestations of PVT decreased in severity within the first 3-5 days and almost completely resolved by Day 10 of ACT (Table 3).

Table 3.

Clinical and ultrasound characteristics of patients with PVT during anticoagulant therapy (N = 45).

Parameter	Before treatment	Days of ACT			p value
Parameter	Before treatment	Day 10	Day 30	Day 90	p value
APP, n (%)	9 (20)	2 (4.4)	0	0	-
APP intensity, VAS scores, M ± SD	8.2 ± 0.6	2.5 ± 0.5	0	0	.001
Increase in CPP, n (%)	4 (8.9)	3 (6.7)	3 (6.7)	3 (6.7)	NS
CPP intensity, VAS scores, M ± SD	8.6 ± 0.5	5.4 ± 0.5*	4,7 ± 0.4*	5.1 ± 0.3*	.001
Fever, n (%)	10 (22.2)	0	0	0	-
Chills, n (%)	7 (15.6)	0	0	0	-
Thrombi in one PV, n (%)	30 (66.7)	Weak recanalization	Complete recanalization	Complete recanalization	-
Thrombi in two or more PVs, n (%)	6 (13.3)	Weak recanalization	Complete recanalization	Complete recanalization	-
Thrombi in the left PVs and MVs, n (%)	7 (15.6)	No changes	Weak recanalization	Complete recanalization	-
Thrombi in the left PVs and PP, n (%)	1 (2.2)	No changes	Weak recanalization	Complete recanalization	-
Thrombi in the left OVs, PVs and PP, n (%)	1 (2.2)	No changes	LGV occlusion;weak recanalization of PP and PVs	LGV occlusion; complete recanalization of PP and PVs	-
Reflux in OVs, n (%)*	3 (6.7)	3 (6.7)	3 (6.7)	3 (6.7)	NS
Duration of reflux in OVs, s, M ± SD	3.3 ± 0.5	3.1 ± 0.5	3.5 ± 0.3	3.5 ± 0.5	NS
Reflux in PVs, n (%)*	45 (100)	45 (100)	45 (100)	45 (100)	NS
Duration of reflux in PVs, s, M ± SD	3.7 ± 1.1	3.3 ± 0.8	3.8 ± 0.7	3.6 ± 0.8	NS
Reflux in UVs, n (%)*	19 (42.2)	19 (42.2)	20 (44.4)	20 (44.4)	NS
Duration of reflux in UVs, s, M ± SD	2.1 ± 0.6	2.2 ± 0.5	2.3 ± 0.5	2.4 ± 0.6	NS
Increase in thrombus size, n (%)	-	0	0	0	-
Pulmonary embolism	0	0	0	0	-

For abbreviations see Table 1. * Reflux in veins free of thrombi.

A characteristic feature was a substantial relief or complete elimination of APP. In 4 patients with PVT that developed on the top of symptomatic PeVD, the pelvic pain decreased in intensity, but was not completely resolved with ACT. In isolated thrombosis of PVs, the complete recanalization was observed within 30 days of ACT. In patients with a combined thrombosis of PVs, UVs and PP, complete recanalization of the veins was observed only after 3 months. In one patient with the combined thrombosis of OVs, PVs and PP, the left OV occlusion and complete recanalization of the left PVs and PPs was developed after completing the ACT course. No worsening of the PeVD clinical manifestations or an increase in the PVR duration was observed during the 3-months follow-up period.

Discussion

The issues of diagnosis and treatment of PVT have not been sufficiently studied.^19,20 The medical literature provides rather contradictory data on the diagnostic and treatment approaches for PVT.^7,21,22 The vast majority of studies were focused on the ovarian venous thrombosis,^6,23 which is understandable, because ovarico-caval and ovarico-renal thrombosis can be sources of pulmonary embolism (PE).²⁴ Real clinical practice shows that 90% of PVT cases are diagnosed accidentally during a routine gynecological examination or search for sources of PE, which is explained by the latent course of PVT. Obviously, the true prevalence of PVT is unknown, and its significance in the PE development and role in the disturbances of the pelvic venous hemodynamics cannot be comprehensively assessed nowadays.

Taking into account basic concepts of hemostasis, spontaneous formation of intravascular blood clots is an obvious pathological condition.²⁵ Moreover, if this occurs in the presence of varicose veins of the pelvis and reflux in them in patients with PeVDs, when at least two components of the Virchow’s triad are involved²⁶: slowing down of blood flow with deposition of blood in the dilated veins of the pelvis, and endothelial lesion due to the varicose vein transformation and vein-specific inflammation.^27–30 These considerations were taken into account when planning and conducting the present study.

The study did not include patients in the immediate postpartum period, taking hormonal drugs, undergoing any surgical interventions on the abdominal or pelvic organs or vessels, and with neoplasms or inflammatory diseases of the pelvic organs.

We evaluated the PVT occurrence in patients with PeVDs, and pelvic varicose veins were the only known risk factor. Among patients with PeVDs, pelvic vein thrombosis turned out to be quite rare (7.6%). In the general population, PVT is found in 0.05%–3% of patients.^5,31 It is important to note that the literature data refer to patients in the early postpartum period who underwent surgery or had gynecological or oncological diseases. In patients with PeVDs, pelvic varicose veins with reflux are the only but predetermining factor in the development of PVT.

Almost every third patient had a symptomatic course of PVT. The most common clinical manifestations were APP and fever. When analysing published data, it is difficult to understand which patients had symptoms of PVT and which were asymptomatic. Thus, Amin et al.⁵ reported that pelvic pain (not specified as acute or chronic) was present in 25.6% of patients with thrombosis of the uterine venous plexus. In patients with ovarian vein thrombosis, according to the literature data, clinical symptoms were present in 100% of cases.^6–8

Patients in the present study had no simultaneous organ disorders or surgical interventions that could impact on the PVT occurrence; however, all patients had pelvic varicose veins with reflux in them. The PVR duration was found to be more than 2 s in 100% of symptomatic patients with PVT, and among them 30.8% had clinical manifestations of PeVDs. A characteristic finding was that patients with symptomatic PVT tended to have blood clots in two or more pelvic venous collectors and also had moderate or severe PVR (>2 s). The relationships between the occurrence of PVT symptoms and these parameters were proven by correlation analysis (r = 0.68 and 0.73, accordingly).

None of patients with asymptomatic PVT had symptoms or signs of PeVDs. Majority of them had thrombosis of one of the parametrial veins (90.6% of cases) and PVR of less than 2 s. The data obtained suggest that the PVT occurrence is not associated with the presence or absence of symptoms and signs of PeVDs or the PVR duration. It can be speculated that the fundamental factors in the PVT development in this population of patients are pathomorphological changes in the wall of pelvic varicose veins and the deposition of blood in them.

All patients with PVT in our study received anticoagulant therapy. It is well-known that a venous thrombus can «grow» and extend to nearby venous segments. Studies have demonstrated that isolated deep vein thrombosis (calf DVT) spreads proximally in 2%–30% of cases.^32–34 Similarly, it is quite expected that in PVT the thrombus can spread to the ovarian veins and the internal iliac vein (IIV) tributaries and trunk and result in pulmonary embolism. In our study, no cases of the thrombus size increase, involvement of other pelvic veins in the pathological process, or episodes of PE were observed on the top of ACT. Recanalization of the pelvic veins occurred within 1 to 3 months after the start of ACT, and only one patient had developed occlusion of the left OV. Probably, the weak «inflow» of blood into the LGV due to thrombotic lesions of the left parametrial veins and the PP veins was a cause of the left OV occlusion. There were no complications of ACT.

Limitations

The study was not randomized, and there was no control group of patients without ACT. The follow-up period for patients in this study was limited to 3 months, which did not allow assessment of the long-term consequences of PVT. The patients did not undergo PCR testing for thrombophilia, so the significance of this prothrombotic factor was not taken into account.

Conclusion

In our study, the incidence of PVT in patients with PeVDs was 7.6%, which is significantly higher than the incidence rates reported for other cohorts of patients. The symptomatic course of PVT was observed in 28.8% of patients with PeVDs and was associated with the duration of PVR and the number of pelvic collectors involved in the thrombotic process. Anticoagulant therapy is an effective and safe for treating PVT. It provides rapid relief of clinical manifestations of PVT and restores the patency of the pelvic veins.

Footnotes

Author Contributions

Concept and design of the work by SG, analysis and interpretation - SG, YeM, AK, AA, writing of the text by SG, YeM, AK, AA, statistical analysis - YeM, AA, critical revision and final approval of the manuscript by all authors.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Ethical statement

Guarantor

SG.

ORCID iD

Sergey G Gavrilov

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