Plantar vein thrombosis

Introduction and background

Thrombosis of the lower leg is well researched with clear guidelines for diagnosis and therapy. ¹ Unfortunately, this is not the case for plantar vein thrombosis (PVT). PVT is a rare venous disorder affecting the deep plantar veins that presents with non-specific pain, swelling, and a heavy sensation in the affected foot. ² PVT may be an under-diagnosed cause of inferior heel pain.^3,4

Although most studies suggest that venous thrombosis starts in the calf veins, in theory they may arise in any part of the deep venous system, including the sole of the foot ² . Historically, a 10% incidence of PVT amongst patients undergoing phlebography for suspected deep vein thrombosis (DVT) was reported, ⁵ yet there are no clear guidelines regarding its diagnosis, management and treatment.

This under-researched entity has important implications and the paucity of evidence requires consolidation to better inform on its diagnosis and management. Herein, we systematically summarise evidence published between 1978 and 2020. The aim of this review is to provide an update on PVT research and its sequelae to guide clinical professionals and researchers.

Review

PVT appears to be a frequently misdiagnosed condition in the clinical setting and can be included as a differential diagnosis. Statistically, plantar fasciitis is the most common cause of unilateral foot pain, with up to 10% of the population experiencing this pathology at least once in their lifetime. ⁴ Other causes of pain include plantar fibromatosis, morton’s neuroma, stress fractures of the metatarsals, tendon abnormalities and ganglionic cysts. ⁴ On ultrasound (US), plantar fasciitis exhibits hypoechogenicity and thickening of the fascia. ⁶

Pulmonary embolism (PE) is a potentially lethal condition. In fatal PE, the correct diagnosis is made in only one third of patients and it is estimated that only 11 to 25% of all proven emboli are diagnosed during life. ⁷ Patients who present with pain and swelling of the foot with concomitant respiratory symptoms should undergo US examination and careful evaluation. ⁴ Whether PVT is a starting point of an ascending DVT and is unclear ⁸ and its relationship to pulmonary embolism (PE) is unrecognised. Barros & Labropoulos ⁹ felt that people with PTV who are not on anticoagulation therapy could theoretically disrupt plantar thrombi via repeated compression of the foot determined by the musculovenous foot pump action. PVT shares common risk factors with DVT, however, mechanical strain is a unique risk factor which may be a distinct variant in venous thromboembolic disease. PVT appears to carry a low risk of symptomatic PE and post-thrombotic syndrome. ⁸

Historically, less than 30 cases of PVT have been reported since the mid 1970s.^4,9,10 The time between symptom onset and diagnosis averages 8.8 days (range 1-21 days). ⁸ In 1978, Thomas & O’Dwyer ⁵ described thrombus formation in 10% of patients in the plantar veins compared to 44% above the ankle. 46% of thrombi were present in both areas, leading them to recommend the inclusion of at least one view of the foot veins in a standard phlebogram in patients suspected of having a DVT or PE.

Predisposing factors

The exact cause of PVT is unknown ⁹ and it is uncertain whether it is increased by genetic or acquired risk factors. In most cases, PVT has traditional DVT risk factors (recent surgery, trauma, infection, malignancy, airplane travel, and oral contraceptives). ⁴ Physical strain to the sole of the foot seems to be a unique cause, as excessive mechanical stress to the plantar veins during exercise may theoretically lead to microtrauma of the plantar veins, causing repeated activation of the coagulation cascade. ⁸ Other causes include athletic activity, ⁴ post-operative immobilisation,^3,11 coagulation disorder anticardiolipin antibody syndrome, ¹² prothrombin G20210A mutation, ¹³ paraneoplastic syndrome in a patient with bone metastasis, ¹⁴ pressure from orthotics ¹⁵ and pressure from footwear. ¹⁶

Assessment

PVT presents as unilateral non-specific plantar foot pain and swelling that mimics other conditions, notably plantar fasciitis (PF) however, patients often report a “heavy” feeling in the affected foot. ⁴

US is the principle method used for diagnosing DVT,^{3,5,11–14,17,18} yet investigation of the plantar veins is not routinely performed. ⁴ US allows easy visibility of the plantar veins and is useful in PVT diagnosis. ¹⁹ In 17 out of 19 cases recently reported,^3,9,11,12,14 diagnosis was made initially by US. US findings of PVT included hypoechoic enlarged venous structures in the transverse plane and hypoechoic enlarged veins in the longitudinal plane.^11–14

Magnetic resonance imaging (MRI) may also be a relevant adjunct diagnostic tool. Findings for PVT on MRI are tissue oedema, enhancement of bordering soft tissue, and filling defects of the plantar veins. ¹³

Management

No standardised therapy exists for PVT and treatment is controversial. Some authors used only non-steroidal anti-inflammatory medication (NSAIDs). ⁹ Czihal et al. ⁸ treated patients with low-molecular weight heparin (LMWH) or fondaparinux for 4–6 weeks combined with concomitant knee-length compression stockings. Patients whose thrombus extended to the deep veins above the ankle were treated according to current DVT guidelines for three months with LMWH overlapping with vitamin-K antagonists. Heparin therapy has been instituted with additional concomitant elastic compression of the ankle^11,14 and another patient was treated with rest, NSAIDS, and acetaminophen. ¹³ Karam et al. ⁴ recommended the use of anticoagulation therapy for a three month period.

Plantar vein thrombosis in the literature

To our knowledge, there have been 44 reported cases of PVT in the literature (Table 1). Vansevenant & Vanhoenacker ¹⁵ reported an 80 year old male exhibiting five days of progressive medial and plantar left heel pain. US and MRI identified thrombosis of the medial plantar vein. He reported that wearing certain shoes, especially a specific pair with a sole defect aggravated his pain. No intralesional flow on US was observed and MRI confirmed thrombosis of the medial plantar vein. The patient’s symptoms disappeared after treatment with NSAIDs and a change to his footwear, and a follow-up US two months later exhibited no residual thrombus.

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Table 1.

Characteristics of previously reported cases of plantar vein thrombosis. F, female; R, Right; L, Left; CP, contraceptive pills; DVT, deep vein thrombosis; PE, Pulmonary embolism; PV, plantar vein; GSV, great saphenous vein; PTV, posterior tibial veins; LPV, lateral plantar veins; MPV, medial plantar veins; NSAIDs, non-steroidal anti-inflammatory drugs; LMWH, low molecular weight heparin.

Authors	N	Mean age	Risk factors	Diagnostic	Segment	Treatment	Evolution	Follow-up
Swellengrebel et al. (2019)	1	61	Mechanical strain (orthoses)	USMRI	PV	NSAIDsRest	No thrombus extension	NA
Barros et al. (2015)	1F	45	Hormone therapy	US	LPV	LMWHWarfarin for 6 months	PE	Partial recanalisation at 6 months
Czihal et al. (2015)	22(13F)	58.2	Mechanical strain Post-menopauseCPImmobilisationSurgeryIdiopathic (*occult malignancy)	USMRI	PVPVT + PTVPVT + GSV	LMWHcompressionfondaparinuxVitamin K	NA	Residual thrombus (11) and PV insufficiency (6) at 22.6 months
Vansevenant & Vanhoenacker (2015)	1	80	Mechanical strain (shoe defect)	USMRI	MPV	Footwear changeNSAIDs	No thrombus extension	Complete recanalisation at 2 months
Barros & Labropoulos (2010)	11(7F)	46.6	SurgeryCPMalinancyAirplane travelHIV-AIDsDVT	US	PV + GSV+ PTV	NSAIDs LMWH	Thrombus extensionNo thrombus extension	Partial recanalisation at 6 monthsComplete recanalisation
Geiger et al. (2009)	1F	32	Busy night dutyCP	MRI	LPV	NSAIDs	Switched to LMWH after 1 week of no amelioration	Total repermabilization at 6 weeks
Siegal et al. (2008)	1F	32	AthleteCPprothrombin gene mutation	MRI	LPV	NSAIDs	Complete clinical resolution	Not done
Berthanova et al. (2005)	3	–	–	US	PV	NA	NA	NA
Long et al. (2004)	1	–	anticardiolipin antibody syndrome	US	PV	LMWH	NA	NA
Cavezzi et al. (1999)	1	–	Surgery	US	PV	LMWH+ compression	NA	NA
Legrand et al. (1997	1	–	Surgery	US	PV	–	NA	NA

Swellengrebel et al. ¹⁶ reported a 61 year old male who presented to an outpatient clinic with severe pain of the medial plantar aspect of his right foot. The pain started abruptly five days prior without any preceding trauma. Initially, pain occurred only during weight-bearing but soon worsened into a continuous discomfort that necessitated the use of crutches. He was a non-smoker with hypercholesterolaemia treated with atorvastatin and had no family history of coagulation disorders. Physical examination revealed intense pain on palpation of the medial-plantar aspect of the foot with no swelling, calf pain, or other visible abnormality. US identified complete thrombosis of the medial and lateral plantar veins and subsequent MRI exhibited segmental thrombosis of these structures, extending 9cm from the medial calcaneus to the level of the metatarsals. Mechanical strain from his orthotics was hypothesized, and the patient was advised to rest his foot and to refrain from wearing his orthotics or hiking shoes. An internal medicine specialist was consulted, advising NSAIDs and rest, without anticoagulant therapy. The patient reported a complete resolution of his symptoms at his 30 day follow-up consultation.

Czihal et al. ⁸ presented a retrospective case series of 22 patients who underwent compression US extended to the plantar veins due to local symptoms in the sole of the foot. 65% of those studied were women, with a mean age of 58.2 (32–79 years). All patients reported “heavy” pain in the sole of the foot. The lateral plantar veins (96%) were more commonly affected than the medial (41%). Extension of the thrombus into the deep calf was common (27%). Eleven (50%) had an idiopathic onset with subsequent diagnosis of occult malignancy in two of these patients. Seven (32%) occurred in association to mechanical strain to the foot. All patients were treated with anticoagulants. No reports of PE occurred and during a mean follow-up of 21 months and post-thrombotic syndrome did not occur. Recurrences of PVT were common (27%). Clinical symptoms resolved after 15.9 days (4-42 days). Repeat US of the plantar veins was performed on 17 (77%) of patients after a mean follow-up time of 22.6 months, showing residual thrombus and plantar vein insufficiency in 11 (50%) and 6 (27%) patients, respectively.

Karam et al. ⁴ reported an 82 year old male who went to his general practitioner reporting left foot pain. He was diagnosed with plantar fasciitis and sent home with NSAIDs, however his clinical condition continued to deteriorate over the following week. Recurrent anamnesis revealed no history of recent trauma, surgery, infection, airplane travel or malignancy and no family history of thromboembolic disease. Swelling and tenderness on the plantar side of the foot with retro-malleolar tenderness and slight redness extending below and above the medial malleolus was exhibited. Duplex US identified non-compressible lateral plantar veins with a 10cm extension of the thrombus to the posterior tibial vein. LMWH therapy was initiated followed by vitamin-K for a three month period. Clinically, he experienced complete resolution of his symptoms. A follow-up US three months later showed partial re-permeabilization of the affected veins. The authors also reported a 57 year old female with a one week history of spontaneous plantar foot pain. No history of mechanical trauma, recent surgery or thromboembolic events were reported and she was not undergoing hormonal treatment. Tenderness along the plantar-lateral aspect of the foot was exhibited with some discrete swelling. MRI examination identified filling defects in the lateral plantar vein. Further confirmation was achieved via US showing this vein to be non-compressible. She was placed on LMWH followed by vitamin-K for three months. At her three month review, complete re-permeabilization of this vein was observed.

Geiger et al. ¹⁸ reported discrete swelling along the medial aspect of the right foot and painful plantar arch in a 32 year old woman after she worked a long shift of night duty at a hospital. Her only risk factor appeared to be her current use of contraception with NuvaRing® (etonogestrel/ethinyloestradiol). MRI with intravenous gadolinium showed filling defects in her lateral plantar vein. Doppler US further showed this vein to be non-compressible without flow signals. Therapy was initiated with LMWH and compression stockings. An US performed six weeks later showed potency of this vein.

Barros et al. ¹⁹ presented a case-series involving 11 patients with PVT. Treatment was initialised with NSAIDs in five patients (45%) and LMWH in six (55%). Evidence of thrombosis extension was observed in three patients (27%). After six months US showed partial recanalisation in nine patients (82%) and complete recanalization in two (19%). Patients who developed thrombosis extension proximal to the ankle demonstrated mild calf swelling associated with posterior tibial vein and/or solar vein reflux ⁹ . The authors specifically mentioned that patients diagnosed with PVT who have chest symptoms should be anticoagulated for three months and re-evaluated at the end of this time-period.

Barros & Labropoulous ⁹ described characteristics and clinical outcomes amongst patients diagnosed with PVT. Patients presenting with sudden pain and/or swelling of the foot were evaluated by duplex US. All major plantar veins were imaged with high resolution multi-linear array transducers and the location and extent of thrombosis formation was recorded in detail. All patients were scheduled for clinical and US follow-up within one week of diagnosis and at various intervals thereafter. Acute thrombosis of the plantar veins was found in 11 patients of whom 7 (63%) were female. Pain was present in all patients and swelling in 8 (72%). The most common risk factors were recent surgery in four (36%), contraception in three (27%), followed by malignancy, airplane travel, HIV-AIDS, and past history of DVT (one each). The plantar veins were exclusively affected in eight (72%), the lower segment posterior tibial vein in two (18%) and the great saphenous vein in one (9%). Evidence of thrombosis extension was observed in three (27%). At six months post-diagnosis, partial recanalisation was observed in nine (81%) and complete recanalisation in two (18%). These results could suggest that PVT may move proximally, eliciting potential post-thrombotic events.

In summary (Table 2), 44 cases of PVT have been reported in the literature, 23 of whom were female. The mean age of the individuals was 50.6 years. Diagnosis was made with US (13), MRI (29) or a combination of both (2). Treatment involved anticoagulation therapy (31) of whom seven achieved partial or total recanalisation, with 17 cases of residual thrombi and one of PE. Nine were treated with NSAIDs, with six reporting partial or total recanalisation, and four received no treatment and no follow up.

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Table 2

Summary of findings.

Cases	N = 44 (23 F)
Predisposing factor	Mechanical strain = 10
	Hormone replacement therapy = 3
	Immobilisation = 1
	Recent surgery = 6
	Ulcerative colitis = 1
	Contraceptive pill = 3
	Malignancy = 3
	Airplane travel = 1
	HIV/AIDS = 1
	Prothrombin gene mutation = 1
	Anticardiolopin antibody syndrome = 1
Diagnosis	US = 29
	MRI = 13
	US & MRI = 2
Treatment & Follow-up	No Treatment = 4	No follow-up = 4
	NSAIDs = 9	No follow-up = 2
		Thrombus extension = 1
		Partial recanalisation = 4
		Complete recanalisation = 2
	Anticoagulation therapy = 31	No follow-up = 2
		Residual thrombus/PV insufficiency = 17
		Pulmonary embolism = 1
		Partial recanalisation = 4
		Complete recanalisation = 7

Conclusion

PVT is an overlooked and under-diagnosed condition and a degree of suspicion should be maintained in patients presenting with spontaneous unilateral foot pain, especially when they report a ‘heavy’ sensation. The foot veins are almost never routinely explored and this diagnosis appears frequently missed. Diagnosis can be made easily via US or MRI. The presence of PVT in patients with no known coagulation disorder may be suggestive of thrombophilic disease. Further research is required regarding treatment and the relationship between PVT and occult malignancy.