An intravenous (IV) cannula represents the most common source of venous trauma leading to SVT. Erythema, warmth, and tenderness along the course of the cannulated vein usually indicate the presence of SVT. Treatment starts with removal of the cannula and warm compresses. After the acute inflammation resolves, a lump may persist for months afterward.

Suppurative SVT (SSVT) is a rare form of SVT characterized by pus and intense pain at an IV site that is often associated with systemic signs of infection such as fever and leukocytosis [6]. Although both SVT and SSVT can be triggered by an IV cannula, the more common clinical scenario for SSVT is a patient with a history of IV drug abuse. In contrast to uncomplicated SVT which typically resolves on its own, SSVT can be fatal if it deteriorates into septicemia. Treatment for SSVT begins with prompt removal of the foreign body and IV antibiotics. Excision of the vein is rarely needed to clear infection; however, it should be considered in a patient with purulence at an IV site who fails to improve with noninterventional management.

In 1845, Jadioux first described migratory thrombophlebitis as repeated superficial venous thrombosis at varying sites, most commonly in the lower extremity [7]. Migratory thrombophlebitis has been associated with underlying malignancy and may be present several years before the cancer is diagnosed. Consequently, the diagnosis of migratory thrombophlebitis often warrants an evaluation for occult malignancy.

Mondor’s disease is defined as thrombophlebitis of the thoracoepigastric vein of the breast and chest wall. This diagnosis has been associated with breast carcinoma or a hypercoagulable state; however, cases with no identifiable cause have also been reported [8]. Recently, the term “penile Mondor’s disease” has been used to describe SVT of the dorsal vein of the penis [9]. Treatment consists of noninterventional measures including warm compresses and nonsteroidal anti-inflammatory drugs.

Although it does not receive as much attention as SVT of the GSV, small saphenous vein (SSV) SVT can have significant clinical consequences. SSV SVT can extend proximally and become a popliteal DVT. In a group of 56 patients with SSV SVT, 16 % suffered from PE or DVT [2]. Therefore, patients with SSV SVT should be managed using a similar approach to those diagnosed with GSV SVT. Treatment includes a thorough duplex ultrasound examination, vigilant follow-up, and anticoagulation or ligation of the SSV if the thrombus approaches the popliteal vein.

Patients with SVT and varicose veins may have a different underlying pathophysiology compared to those without varicose veins. In several studies, only 3–20 % of SVT patients with varicose veins developed a DVT, compared to 44–60 % of patients without varicose veins [10, 11, 12]. In contrast, a more recent study showed no difference in the incidence of DVT or PE among 186 SVT patients with and without varicose veins [2]. Therefore, it remains unclear if SVT patients with and without associated varicose veins should be classified as belonging to different patient subsets.

SVT involving varicose veins may remain localized to a cluster of tributary varicosities or extend into the GSV [2]. SVT of varicose vein tributaries can occur without antecedent trauma and is frequently found in varicosities surrounding venous stasis ulcers. The diagnosis should be confirmed by duplex ultrasound scan as the clinical exam often underestimates the true extent of SVT. Treatment consists of noninterventional therapy including warm compresses and nonsteroidal anti-inflammatory drugs.

Upper extremity SVT often results from intravenous cannulation and infusion of caustic substances that damage the endothelium. In contrast to lower extremity SVT, upper extremity SVT does not have a tendency to progresses into a DVT and rarely becomes the source of a PE [13]. Initial treatment of symptomatic upper extremity SVT associated with a catheter requires catheter removal followed by warm compresses and nonsteroidal anti-inflammatory medications.

Peripheral inserted central catheters (PICCs) have become nearly ubiquitous in modern medical practice. Their accessibility, cost-effectiveness, and perceived safety profile have led to widespread use of PICCs across all specialties in both the inpatient and outpatient setting. The proliferation of PICCs has focused attention on their potential complications, the most common of which are infection and venous thrombosis. The exact incidence and relative risk of PICC-associated thrombotic episodes remains unclear because some studies have reported on only symptomatic patients, while others have included asymptomatic patients diagnosed by ultrasound screening. Periard et al. prospectively compared PICCs to peripheral IV cannulas in patients requiring IV therapy for at least 5 days [14]. Ultrasound screening of all 60 patients demonstrated a high but similar rate of upper extremity SVT in both the PICC and peripheral IV groups (29 % vs. 34 %). In a review of symptomatic upper extremity venous thrombosis, Liem et al. found a much lower incidence of PICC-associated SVT: 1.9 % for basilic PICCs and 7.2 % for cephalic PICCs [15]. Despite the low incidence, the large number of PICCs placed per year makes PICC-associated venous thrombosis an important and commonly encountered clinical problem. According to Liem et al. PICCs were associated with 20 % of all upper extremity SVTs diagnosed by their vascular lab in 1 year. PICC-associated DVT had an even greater clinical impact accounting for over 35 % of all upper extremity DVTs diagnosed in 1 year.

PICC-associated SVT usually results from catheter-induced trauma to the venous endothelium. Any patient with a current or recent PICC who has upper extremity edema, pain, or a palpable cord warrants a complete ultrasound exam to evaluate for thrombus and determine its extent. The presence of the catheter often impairs sonographic evaluation of the veins and may obscure direct visualization of the thrombus. Obtaining multiple views, changing the angle of insonation, and using a combination of gray imaging, spectral wave analysis and color flow imaging can usually overcome these technical challenges. As the previously cited studies show, clinical symptoms occur in only a minority of patients with PICC-associated SVT. Screening ultrasonography has not been widely adopted since the clinical significance of detecting SVT in an asymptomatic patient remains unclear.