In the realm of medicine, misnomers which are erroneous or inappropriate designations are not uncommon. These misnomers can give rise to confusion, misdiagnosis, and misguided treatment approaches, ultimately impacting patient care and increase staff utilization and costs. Within the field of venous diseases, misnomers primarily manifest as erroneous names assigned to conditions or clinical findings. They may arise from a lack of comprehension regarding underlying mechanisms or concepts, or from the uncritical referencing of previous literature. While the ramifications of misnomers in medical research may be less severe, they can still lead investigators astray, resulting in misguided research directions, misinterpretation of findings, and the perpetuation of false concepts and deceptive hypotheses (1). Consequently, the utilization of accurate terminology becomes crucial for facilitating effective communication between healthcare providers and patients. By employing precise and descriptive language, the accuracy of diagnoses can be enhanced, leading to the implementation of appropriate treatment strategies. This article aims to shed light on prevalent misnomers in venous disease, highlighting the significance of employing the correct terminology.

In 2009, the VEIN-TERM transatlantic interdisciplinary consensus document provided a definition for chronic venous insufficiency (CVI) as “any morphological and functional abnormalities of the venous system of long duration manifested either by symptoms and/or signs indicating the need for investigation and/or care” (2). Edema, defined as the accumulation of fluid in the interstitial space resulting in leg swelling, often serves as the initial clinical symptom or sign of CVI. The primary pathophysiologic mechanism behind CVI-associated edema involves increased transcapillary pressures and oncotic attraction, leading to progressive protein accumulation in the interstitial space (3). CVI arises from chronic venous hypertension resulting from venous reflux or obstruction. When venous hypertension extends to the microcirculation, it leads to increased hydrostatic pressure in capillaries, triggering wall remodeling and microvenous valvular insufficiency (4). This process gives rise to secondary enlargement of the capillary bed and excessive trans-capillary filtration, leading to interstitial fluid accumulation and exudation of fibrinogen and proteins into the interstitial space, ultimately resulting in characteristic lipodermatos-clerosis (5).

Therefore, it is recommended that the term CVI be reserved for the description of more advanced disease stages, typically starting with venous edema (C3) but more commonly observed in cases featuring skin changes (C4) or ulceration (C5~6), as outlined in the Clinical, Etiological, Anatomical, and Pathophysiological (CEAP) classification system (6). Instead, the term “chronic venous disease” can be utilized to describe the entire spectrum C0 to C6 while CVI is part of it including CEAP classes 3 to 6.

May-Thurner Syndrome is commonly recognized as a condition resulting from the compression of the left common iliac vein (LCIV) by the right common iliac artery (RCIA) over the fifth lumbar vertebra. However, it is important to note that the term “May-Thurner Syndrome” is both historically and pathophysiologically inaccurate. Physicians May and Thurner were not the first to describe this condition, nor did they define it as a syndrome. The previous literature, as elucidated by Antonio et al., provides a comprehensive account of the historical aspects of this condition (7). Many studies quote erroneously the paper by Virchow in 1851 (8) as the first description but that paper is irrelevant as it never mentions the iliac vein (7). In fact, the first documented description of iliac vein compression syndrome came in 1965 from Cockett and Thomas, who highlighted the discomfort, swelling, pain, and thrombosis that may occur in the iliofemoral veins due to compression of the LCIV by the overlying RCIA (9,10). The first description for the LCIV compression by the RCIA was done in 1906 and 1908, by McMurrich (11,12). Then Ehrich and Krumhaar who performed dissection in 412 cadavers also demonstrated the compression and the collagen formation in that area (13). Subsequently, Dr. May, inspired by Wanke's report in 1950 (14), conducted LCIV surgery in 1955, demonstrating the pre- and post-procedural results through venography (15). Building on these surgical findings, Dr. Thurner conducted a comprehensive study involving 430 cadavers (15) confirming the results of McMcMurrich and that of Ehrich and Krumhaar.

Moreover, the area of extrinsic iliac vein compression is not limited to the LCIV. Similar compression can occur in other structures as well, such as the right common iliac vein (RCIV) by the RCIA, LCIV by the left common iliac artery (LCIA), right external iliac vein (REIV) by the right external iliac artery, REIV by the right internal iliac artery, left external iliac vein (LEIV) by the left external iliac artery, and LEIV by the left internal iliac artery (16). Additionally, compression can occur in the REIV or LEIV by the inguinal ligament (16). Therefore, it is crucial to acknowledge the historical context and rectify the terminology associated with this condition. The term “May- Thurner Syndrome” should be reconsidered, as May and Thurner were not the original discoverers or describers of the condition. Instead, adopting more accurate and descrip-tive terms, such as iliac vein syndrome presenting with signs and symptoms or not, can help clarify the origins and pathophysiology of this vascular disorder.

Pelvic congestion syndrome (PCS) is a relatively uncommon and poorly understood disorder affecting the pelvic venous circulation. It is often misdiagnosed and can cause chronic pelvic pain in premenopausal women (17). Patients with classic PCS commonly experience lower pelvic pain, dyspareunia, postcoital pain, and bladder irritability or urgency. However, due to the existence of various well-known causes of chronic pelvic pain, diagnosing PCS involves a process of exclusion. Conditions such as endometriosis, uterine abnormalities (e.g., leiomyo-mata, adenomyosis, arteriovenous malformations), pelvic inflammatory disease, and adhesions are typically considered as initial possibilities (16,18) A diagnosis of PCS is made when these conditions are ruled out, and the pelvic pain is determined to be originating from pelvic vein reflux or obstruction, or both. It is important to note, however, that the historical term “congestion” is imprecise and no longer appropriate for describing this condition accurately (19,20). Instead, the term “pelvic venous disorder” should be used to describe the spectrum of symptoms and signs arising from the veins of the pelvis (the gonadal veins, the internal iliac veins and their tributaries, and the venous plexuses of the pelvis) and their primary drainage pathways (the left renal vein, the iliac veins, and the pelvic escape points) (21). Patients with pelvic vein disorders may have reflux, obstruction or a combination of the two. A comprehensive understanding of pelvic venous pathology is of utmost importance for physicians practicing in the field of phlebology. This is particularly crucial as venous disorders affecting the pelvis and lower extremities exist on a continuum. When dealing with patients presenting with nonsaphenous venous reflux, it is essential to conduct a thorough evaluation to determine if the reflux originates from the pelvic region.

Medical students universally receive education regarding the underlying mechanisms of venous thrombosis, which are referred to as Virchow’s triad. However, a thorough examination of the historical literature brings forth uncer-tainties regarding the existence of a triad as described by Virchow in its currently quoted form throughout modern medical literature (22). First, in his work, Virchow mentioned “Phenomena due to the irritation of the vessel and its surroundings; Phenomena due to blood coagulation; Phenomena due to the interruption of the blood-stream.” These descriptions can be interpreted as referring to endothelial damage, hypercoagulability, and stasis, which form the basis of Virchow’s triad. However, he did not explicitly connect these phenomena to the de novo formation of clots. Instead, he discussed them in relation to clot propagation and the occurrence of embolism. Secondly, Virchow began to be acknowledged for this triad a hundred years after the publication of his work on venous thrombosis. Third, the notable absence of Virchow’s own acknowledgment serves as significant evidence that he did not formulate a triad in the manner we currently describe it. This is particularly noteworthy considering Virchow's reputation as a scientist who actively advocated for and promoted his own ideas and discoveries.

While Virchow did not directly discover the mechanism of de novo clot formation, his investigations into the factors that promote clot propagation indirectly led to identifying the conditions that contribute to the de novo development of clots. It is worth noting that Virchow himself did not explicitly acknowledge this connection.

Many patients diagnosed with chronic deep vein thrombosis often undergo anticoagulation therapy and, in certain cases, thrombolysis. Nonetheless, these treatments carry a substantial cost and pose a risk of bleeding for the patients. In a study conducted by Comerota et al. (23) histological findings were reported the tissue responsible for the occurrence of chronic post-thrombotic venous obstruction. Histological evaluation of occlusive tissue samples taken from the common femoral vein and femoral vein revealed the predominance of collagen type I in 80~90% of the tissue, with collagen type III observed in 10~20% of the tissue. Thrombus formation triggers an inflammatory response, leading to alterations in both the thrombus itself and the venous wall (24). Notably, wall thickness increases in all lower-extremity venous segments in patients with acute and post-thrombotic diseases (24). Given these insights, it becomes apparent that the term “chronic deep vein thrombosis” is both inaccurate and potentially harmful to patients. Although a definitive terminology has not yet been established, it is recommended to replace it with terms such as “chronic post-thrombotic luminal changes,” “synechiae,” or “chronic venous fibrosis.”

Misnomers in venous disease can have detrimental effects, causing confusion, misdiagnosis, and mistreatment of patients. Therefore, it is crucial to utilize the correct terminology, as it plays a vital role in facilitating accurate diagnosis and appropriate treatment. By employing accurate and descriptive terminology, healthcare professionals can enhance communication, leading to improved patient outcomes. It is important to avoid eponyms use instead topographic anatomy and appropriate terms to eliminate misunderstanding.