Deep Venous Thrombosis
Anatomy of lower limb venous system
• The anatomic border of the lower extremity venous system is the fascial
plane. The veins that lie on the subcutaneous fat layer belongs to the
superficial venous system, and the veins that lie inside the deep fascia
belongs to the deep venous system.
• In the lower extremity, the main route of venous flow is the deep veins
rather than the superficials. Therefore, cases of DVT may present with
severe disorders in the lower extremity venous return, which can cause
extremity swelling, discomfort, and gait disorders.
Introduction
• Deep venous thrombosis (DVT) occurs when a blood clot forms in a
deep vein.
Epidemiology
• Between 2.5% and 5% of the population is affected by DVT at some
point in their lives.
• Lower extremity deep venous disease is the third most common
cardiovascular disease and is associated with significant individual
morbidity and high societal cost.
• Within two years of DVT occurrence, over 50% patients develop
postthrombotic syndrome (PTS), manifested by leg pain, swelling, skin
pigmentation, or venous ulceration, despite the use of
anticoagulation treatment.
Risk Factors
• Thrombosis is essentially caused by the Virchow’s triad— alteration in blood flow (i.e.,
stasis), vascular endothelial injury, and alteration in the constituents of the blood (i.e.,
hypercoagulation state).
• The risk factors for DVT are divided into inherited and acquired causes.
• Inherited causes include inherited thrombophilia, such as Factor V Leiden mutation,
prothrombin gene mutation, protein C or protein S deficiency, and antithrombin
deficiency.
• Acquired causes include immobilization, prolonged hospitalization, recent surgery or
trauma, obesity, previous venous thromboembolism,age over 65 years, family history
of DVT, heart failure, inflammatory bowel disease, pregnancy, malignancy, use of oral
contraceptives, myeloproliferative disorder, antiphospholipid syndrome, and
placement of central venous catheterization.
• In addition, there are some anatomic risk factors, such as May-Thurner syndrome and
inferior vena cava (IVC) abnormalities (including agenesis, hypoplasia, and
malformation).
Category of DVT
• Based on the popliteal vein, the DVT occurring in the popliteal vein or above it
(i.e., femoral vein, deep femoral vein, common femoral vein, iliac vein, and/or
IVC) is called a proximal DVT. Conversely, thrombosis of one or more deep calf
veins, including the anterior tibial vein, posterior tibial vein, peroneal vein,
and/or deep muscular vein, is called distal DVT.
• Most acute cases of PE is associated with proximal DVT.
• The mortality rate of proximal DVT is higher than that of distal DVT.
• Iliofemoral DVT differs from femoropopliteal DVT in that the fomer is
associated with more frequent recurrent DVT, and more frequent and severe
PTS. Compared to femoropopliteal DVT or distal DVT, which are more easily
compensated by collateralization to the deep or superficial vein, an iliofemoral
occlusion has poor chances of sufficient collateralization
• Based on symptom duration, DVT can be categorized into acute,
subacute, and chronic DVT.
• Acute DVT refers to the presence of symptoms for less than 14 days.
• Subacute DVT refers to cases in which symptoms have been present for
15–28 days.
• Chronic DVT refers to cases in which symptoms have been present for
more than 28 days
Clinical presentation
• DVT usually presents with unilateral extremity swelling, warmth, pain,
and erythema.
• Symptoms are aggravated by walking and standing, leading to limited
activity and inability to work.
• Additionally, many patients experience non-healing venous ulcers.
Wells criteria for DVT
• Active cancer (ongoing treatment or treatment within last 6 months)
• Paralysis or recent plaster immobilisation of the legs.
• Recently bedridden for >3 days or major surgery within the last 12
weeks requiring general or local anaesthetics.
• Localised tenderness along the distribution of the deep venous system.
• Entire leg swelling.
• Calf swelling >3cm compared with the asymptomatic leg (measured at
10cm below the tibial tuberosity).
• Pitting edema
• Collateral superficial veins (non-varicose).
• Previously documented DVT.
Radiographic features
Ultrasound
• Venous duplex ultrasound (VDUS) uses two main components to assess for DVT,
specifically, the brightness mode (B-mode) imaging—using probe compression and
Doppler evaluation in addition to color flow Doppler imaging and spectral Doppler
waveform analysis.
• Characteristics that define “definitely acute” includes a hypoechoic thrombus,
thrombus loosely attached to a vessel wall or is mobile, a distended vein lumen,
and a compressible thrombus.
• Characteristics of the classification “definitely chronic” must have following
features; hyperechoic thrombus, a thrombus firmly adherent to the vessel wall,
venous wall thickening and scaring with or without calcium deposition, standard
size or smaller than average-sized vein lumen, recanalization of the thrombus, or a
thrombus that is noncompressible or partially compressible.
Computed Tomography
• Computed tomography venography (CTV) permits routine evaluation of the US’s deep veins
not routinely evaluated, including the iliac veins and inferior vena cava (IVC). The clot is
identified as a filling defect within a deep vein.
• Acute DVT often expands the vein and may demonstrate venous wall enhancement or
perivenous edema.
• CT venography has drawbacks as it requires iodinated contrast media and exposure to ionizing
radiation.
Magnetic Resonance Imaging
• MR-DTI may distinguish between an acute recurrent thrombus and a persisting (evolving) clot
in the exact location. The technique is based on the paramagnetic properties of
methemoglobin, formed in a fresh thrombus, which decreases the longitudinal relaxation time
(T1), resulting in a high signal on T1-weighted images. The MR-DTI highlights this bright
thrombus signal by nulling the signals from fat (using a water-selective excitation) and blood
(due to its extended T1 property).
• MR venography are limited as it requires a high level of patient cooperation with a long
examination time.
Management
• Patient work-up should include a complete blood count, basic metabolic panel, and
coagulation parameters, with particular attention paid to renal function, platelet count, and
the international normalized ratio
• Management depends on multiple factors such as location, duration of symptoms, cause of
the thrombosis, and recurrence rate.
• Anticoagulation should be started immediately upon diagnosis due to increased embolization
risks if treatment is delayed.
• Parenteral anticoagulation (unfractionated heparin, a low molecular weight heparin or
fondaparinux) with subsequent transition to long term oral vitamin K antogonist therapy
often for atleast 3 months in duration.
• Interventional management options includes catheter-directed lysis, mechanical
thrombectomy, pharmaco-mechanical directed lysis, IVC filter placement, and venous
stenting.
• The widely accepted indications for endovascular thrombus removal for lower extremity DVT
include massive proximal acute DVT (i.e., iliofemoral or femoropopliteal thrombosis)
accompanied by severe symptomatic leg swelling.
Indication for anticoagulation
• Patients with distal DVT (calf veins).
• Older patients with serious comorbidities (unlikely to be active and
have diminshed longevity).
Catheter directed thrombolysis
Indications:
• Ileofemoral or femoral DVT (increased risk of PTS and recurrent VTE).
• Symptoms for <14 days.
• Inadequate response to initial anticoagulation.
• Good functional status (to lie prone and receive sedation for the procedure)
• Life expectancy >1year.
• Low risk of bleeding.
• Patients with markedly severe symptoms (massive swelling, phlegmasia)
caused by extensive venous obstruction to reduce morbidity and prevent
progression to venous gangrene.
• CDT refers to the slow administration of a thrombolytic agent over several hours for
intrathrombus infusion via multiple side-holes of an infusion catheter embedded
within the thrombosed vein.
• Ideally, a vein with blood flow below the thrombosed venous segment should be
accessed, if possible.
• Following this, stenosis is treated with angioplasty or stenting, if applicable.
• Thrombolytic agents activate serum plasminogen to form plasmin, which
accelerates the lysis of thrombus.
• The most representative thrombolytic agent was urokinase, a second-generation
plasminogen activator. However, it is no longer used because of discontinuation of
production.
• Recently, alteplase (a tissue plasminogen activator [tPA]), a recombinantly derived
analog of human tPA, has predominantly replaced urokinase. Moreover, two tPA
variants, reteplase (recombinant plasminogen activator) and tenecteplase (TNK), are
also used.
• Reteplase has a longer half-life than alteplase.
• The commonly used dosing schemes are alteplase (0.5–1.0 mg/h), reteplase
(0.25–0.75 units/h), and TNK (0.25–0.5 mg/h) for CDT.
Limitations:
• Complications such as significant bleeds, intracranial bleeds, and the need for
monitoring in the ICU for 1–3 days.
Percutaneous mechanic thrombectomy
• PMT refers to the percutaneous use of catheter-based mechanical devices
that contribute to thrombus removal via fragmentation, maceration, and/or
aspiration, without administering a thrombolytic agent.
• It eliminate the need of thrombolytic drugs that carry inherent risks such as
bleeding and prolonged ICU stays.
Pharmacomechanical catheter-directed
thrombolysis
• The venous thrombus is primed with the fibrinolytic drugs, which
increases the susceptibility to mechanical fragmentation and allows
for more effective removal, preventing residual fragment embolizing
to the lungs.
• Due to its effectiveness, this method reduces the thrombolytic drug
dose, treatment time, and hospital costs significantly.
• The patient then undergoes radiolytic thrombectomy utilizing saline
jets to create a localized low pressure zone by the Bernoulli effect to
macerate a clot.
IVC filter
• IVC filters are used in patients with contraindication to
anticoagulation therapy or failure to avoid iatrogenic pulmonary
embolism.
Venous angioplasty/Stenting
• This treatment is classically utilized in May-Thurner syndrome, which refers to
chronic compression of the left common iliac vein against a lumbar vertebra
secondary to the overlying, pulsating, right common iliac artery causing DVT.
• Criteria for angioplasty in acute DVT include iliofemoral DVT and evidence of
residual thrombosis or obstruction following mechanical thrombolysis. In
contrast, measures in chronic DVT include established PTS with significant
symptoms and evidence of iliofemoral stenosis or obstruction confirmed by
imaging amenable to stent placement.
• Venous stent placement is indicated when the block is >50%, there is
apparent formation of superficial collaterals, and evidence of reflux in deep
and superficial veins.
Complications
• If not managed properly, these thrombi can embolize, causing further
complications.
• Delay in management may lead to pulmonary embolization or stroke.
• Another common complication is posted thrombotic syndrome (PTS),
which manifests as chronic limb fatigue/heaviness, swelling, pain, and
paresthesia, occurring in 50% of patients, accompanied by severe
quality of life impairment.
The most important factors leading to PTS include the development
of valvular reflux and late venous obstruction when the clot is not
entirely cleared.
• Phlegmasia cerulea dolens is a severe form of DVT characterized by complete
lower extremity venous occlusion of deep and superficial channels. Associated
edema causes a rise in interstitial tissue pressure overcoming arterial closing
pressure, causing collapse.
• Phlegmasia cerulea dolens is potentially life-threatening complication of acute
DVT characterized by marked swelling of the extremities with pain,
motor/sensory defecit and cyanosis. This may lead to arterial ischemia and
ultimately cause gangrene, with high amputation and mortality rates.
Endovascular treatments include catheter-directed thrombolysis and
pharmacomechanical /mechanical thrombectomy.
• Progression can also lead to death or major disability as a result of pulmonary
embolism, postthrombotic syndrome, or limb amputation.
Case 1
• Patient presented with right lower limb pain and swelling since 1 week,
progressive in nature, aggravated by walking and relieved on rest.
• Peripheral pulses were present.
• Past history of left lower limb DVT and underwent angioplasty.
• Known case of May Thurner syndrome. IVC filter insertion done. Left common
iliac vein stenting
• No comorbities.
• History of blood transfusion 2 pint.
• Pallor present.
• Murmurs present at tricuspid and pulmonary region.
• Medication started, Tablet Ecosprin (antiplatelet drug), Tablet Rivaroxaban
(Factor Xa inhibitor), Injection Heparin 5000IU 6 hourly.
• CT venogram of bilateral lower limb was planned.
• During CT venogram, extravasation of IV contrast occurred. Patient developed
swelling in forearm. On examination, non pitting edema was noted. No signs
of inflammation were present. Radial and ulnar pulses were present.
• Patient was suggseted for doppler of left forearm,limb elevation and cold
compression.
• Decided to do ,CBC, PT, INR, GRBS, HbA1C, Blood grouping , Serum creatinine
and 2D Echo.
• Hb came out be low (7.7gm/dl).
• Medicine team decided to do peripheral smear and transfuse 1 pint of PRBC.
• After procedure Tablet Clexane (Factor Xa inhibitor and antithrombin
complex).
• Bilateral lower limb DVT thrombolysis and thrmbectomy with Tenecteplase
(tissue plasminogen activator) was done.
• After procedure Tablet Clexane (Factor Xa inhibitor and antithrombin
complex), strict immobilisation was suggested, heparin was withold and
proper hydration was maintained.
• After procedure patient developed chest pain. However, BP, PR and SPO2
were normal. Medicine team suggested for serial ECG and Troponin I. ECG
showed sinus tachycardia and flat T wave. Troponin I was normal. Pain
subsided after 1 day.
• Patient complained right lower limb pain and swelling. Elastic compression
bandages were suggested.
mov-series-001-Abdomen 3 fps.wmv mov-series-003-Fluoroscopy.wmv mov-series-005-Fluoroscopy.wmv mov-series-009-Abdomen 3 fps.wmv mov-series-015-Abdomen 3 fps.wmv mov-series-019-Fluoroscopy.wmv
mov-series-031-Abdomen 3 fps.wmv
Case 2
• Complain of pain and swelling in left leg for 4 days. Peripheral pulses were normal.
• History of recurrent cerebral venous thrombosis (2016)
• No comorbities.
• He was on medication, acitrom (acenocoumarol, inhibits vitamin K epoxide
reductase) 2mg OD (irregular treatment)
• History of chronic smoking for 2 years (3-4cigarettes/day).
• Occasional alcoholic since 6-7years (once weekly).
• On 2D Echo : Trivial MR, Grade I left ventricular diastolic dysfunction.
• Venous doppler done : DVT in left SFV and popliteal vein. Varicose veins,
incompetent perforators at SFJ.
• Investigations done : PT, APTT, INR, Thrombophilia profile (Vitamin B12,
Homocysteine etc), complete haemogram, Blood group, RFT, LFT, HIV, HbsAg, HCV
• Injection Heparin 5000 IU I.V stat, followed by 1000 IU/hour. Morning dose
should skipped on day of procedure. Patient should be NPO from midnight.
• IVC filter placement and thrombolysis of left lower limb DVT was performed.
• Post procedure injection heparin 5000 IU continued every 6 hourly. CBC, PT,
APTT and INR was repeated.
mov-series-009-Fluoroscopy.wmv mov-series-010-Fluoroscopy.wmv mov-series-012-Fluoroscopy.wmv mov-series-014-Fluoroscopy.wmv mov-series-015-Abdomen 3 fps.wmv mov-series-016-Abdomen 3 fps.wmv
mov-series-018-Abdomen 3 fps.wmv mov-series-019-Fluoroscopy.wmv mov-series-023-Fluoroscopy.wmv mov-series-026-Fluoroscopy.wmv mov-series-030-Abdomen 3 fps.wmv
References
• Endovascular Interventions for Acute and Chronic Lower Extremity Deep Venous Disease: State of the Art. Radiology,
276(1), 31–53.
Sista, A. K., Vedantham, S., Kaufman, J. A., & Madoff, D. C. (2015).
• Endovascular Treatment for Lower Extremity Deep Vein Thrombosis: An Overview. Kyung Ah Kim,Sun Young Choi, and
Ran Kim
Korean J Radiol. 2021 Jun;22(6):931-943.
• Imaging findings and interventional management of deep venous thrombosis. Hussam Hindi​
, Gauthier Dongmo, Alyssa Goodwin, Sean Jones, Kristian Loveridge.

Deep Venous Thrombosis Presentation 19.8.22.pptx

  • 1.
  • 2.
    Anatomy of lowerlimb venous system
  • 3.
    • The anatomicborder of the lower extremity venous system is the fascial plane. The veins that lie on the subcutaneous fat layer belongs to the superficial venous system, and the veins that lie inside the deep fascia belongs to the deep venous system. • In the lower extremity, the main route of venous flow is the deep veins rather than the superficials. Therefore, cases of DVT may present with severe disorders in the lower extremity venous return, which can cause extremity swelling, discomfort, and gait disorders.
  • 4.
    Introduction • Deep venousthrombosis (DVT) occurs when a blood clot forms in a deep vein.
  • 5.
    Epidemiology • Between 2.5%and 5% of the population is affected by DVT at some point in their lives. • Lower extremity deep venous disease is the third most common cardiovascular disease and is associated with significant individual morbidity and high societal cost. • Within two years of DVT occurrence, over 50% patients develop postthrombotic syndrome (PTS), manifested by leg pain, swelling, skin pigmentation, or venous ulceration, despite the use of anticoagulation treatment.
  • 6.
    Risk Factors • Thrombosisis essentially caused by the Virchow’s triad— alteration in blood flow (i.e., stasis), vascular endothelial injury, and alteration in the constituents of the blood (i.e., hypercoagulation state). • The risk factors for DVT are divided into inherited and acquired causes. • Inherited causes include inherited thrombophilia, such as Factor V Leiden mutation, prothrombin gene mutation, protein C or protein S deficiency, and antithrombin deficiency. • Acquired causes include immobilization, prolonged hospitalization, recent surgery or trauma, obesity, previous venous thromboembolism,age over 65 years, family history of DVT, heart failure, inflammatory bowel disease, pregnancy, malignancy, use of oral contraceptives, myeloproliferative disorder, antiphospholipid syndrome, and placement of central venous catheterization. • In addition, there are some anatomic risk factors, such as May-Thurner syndrome and inferior vena cava (IVC) abnormalities (including agenesis, hypoplasia, and malformation).
  • 7.
    Category of DVT •Based on the popliteal vein, the DVT occurring in the popliteal vein or above it (i.e., femoral vein, deep femoral vein, common femoral vein, iliac vein, and/or IVC) is called a proximal DVT. Conversely, thrombosis of one or more deep calf veins, including the anterior tibial vein, posterior tibial vein, peroneal vein, and/or deep muscular vein, is called distal DVT. • Most acute cases of PE is associated with proximal DVT. • The mortality rate of proximal DVT is higher than that of distal DVT. • Iliofemoral DVT differs from femoropopliteal DVT in that the fomer is associated with more frequent recurrent DVT, and more frequent and severe PTS. Compared to femoropopliteal DVT or distal DVT, which are more easily compensated by collateralization to the deep or superficial vein, an iliofemoral occlusion has poor chances of sufficient collateralization
  • 8.
    • Based onsymptom duration, DVT can be categorized into acute, subacute, and chronic DVT. • Acute DVT refers to the presence of symptoms for less than 14 days. • Subacute DVT refers to cases in which symptoms have been present for 15–28 days. • Chronic DVT refers to cases in which symptoms have been present for more than 28 days
  • 9.
    Clinical presentation • DVTusually presents with unilateral extremity swelling, warmth, pain, and erythema. • Symptoms are aggravated by walking and standing, leading to limited activity and inability to work. • Additionally, many patients experience non-healing venous ulcers.
  • 11.
    Wells criteria forDVT • Active cancer (ongoing treatment or treatment within last 6 months) • Paralysis or recent plaster immobilisation of the legs. • Recently bedridden for >3 days or major surgery within the last 12 weeks requiring general or local anaesthetics. • Localised tenderness along the distribution of the deep venous system. • Entire leg swelling. • Calf swelling >3cm compared with the asymptomatic leg (measured at 10cm below the tibial tuberosity). • Pitting edema • Collateral superficial veins (non-varicose). • Previously documented DVT.
  • 12.
    Radiographic features Ultrasound • Venousduplex ultrasound (VDUS) uses two main components to assess for DVT, specifically, the brightness mode (B-mode) imaging—using probe compression and Doppler evaluation in addition to color flow Doppler imaging and spectral Doppler waveform analysis. • Characteristics that define “definitely acute” includes a hypoechoic thrombus, thrombus loosely attached to a vessel wall or is mobile, a distended vein lumen, and a compressible thrombus. • Characteristics of the classification “definitely chronic” must have following features; hyperechoic thrombus, a thrombus firmly adherent to the vessel wall, venous wall thickening and scaring with or without calcium deposition, standard size or smaller than average-sized vein lumen, recanalization of the thrombus, or a thrombus that is noncompressible or partially compressible.
  • 15.
    Computed Tomography • Computedtomography venography (CTV) permits routine evaluation of the US’s deep veins not routinely evaluated, including the iliac veins and inferior vena cava (IVC). The clot is identified as a filling defect within a deep vein. • Acute DVT often expands the vein and may demonstrate venous wall enhancement or perivenous edema. • CT venography has drawbacks as it requires iodinated contrast media and exposure to ionizing radiation. Magnetic Resonance Imaging • MR-DTI may distinguish between an acute recurrent thrombus and a persisting (evolving) clot in the exact location. The technique is based on the paramagnetic properties of methemoglobin, formed in a fresh thrombus, which decreases the longitudinal relaxation time (T1), resulting in a high signal on T1-weighted images. The MR-DTI highlights this bright thrombus signal by nulling the signals from fat (using a water-selective excitation) and blood (due to its extended T1 property). • MR venography are limited as it requires a high level of patient cooperation with a long examination time.
  • 18.
    Management • Patient work-upshould include a complete blood count, basic metabolic panel, and coagulation parameters, with particular attention paid to renal function, platelet count, and the international normalized ratio • Management depends on multiple factors such as location, duration of symptoms, cause of the thrombosis, and recurrence rate. • Anticoagulation should be started immediately upon diagnosis due to increased embolization risks if treatment is delayed. • Parenteral anticoagulation (unfractionated heparin, a low molecular weight heparin or fondaparinux) with subsequent transition to long term oral vitamin K antogonist therapy often for atleast 3 months in duration. • Interventional management options includes catheter-directed lysis, mechanical thrombectomy, pharmaco-mechanical directed lysis, IVC filter placement, and venous stenting. • The widely accepted indications for endovascular thrombus removal for lower extremity DVT include massive proximal acute DVT (i.e., iliofemoral or femoropopliteal thrombosis) accompanied by severe symptomatic leg swelling.
  • 19.
    Indication for anticoagulation •Patients with distal DVT (calf veins). • Older patients with serious comorbidities (unlikely to be active and have diminshed longevity).
  • 21.
    Catheter directed thrombolysis Indications: •Ileofemoral or femoral DVT (increased risk of PTS and recurrent VTE). • Symptoms for <14 days. • Inadequate response to initial anticoagulation. • Good functional status (to lie prone and receive sedation for the procedure) • Life expectancy >1year. • Low risk of bleeding. • Patients with markedly severe symptoms (massive swelling, phlegmasia) caused by extensive venous obstruction to reduce morbidity and prevent progression to venous gangrene.
  • 22.
    • CDT refersto the slow administration of a thrombolytic agent over several hours for intrathrombus infusion via multiple side-holes of an infusion catheter embedded within the thrombosed vein. • Ideally, a vein with blood flow below the thrombosed venous segment should be accessed, if possible. • Following this, stenosis is treated with angioplasty or stenting, if applicable. • Thrombolytic agents activate serum plasminogen to form plasmin, which accelerates the lysis of thrombus. • The most representative thrombolytic agent was urokinase, a second-generation plasminogen activator. However, it is no longer used because of discontinuation of production. • Recently, alteplase (a tissue plasminogen activator [tPA]), a recombinantly derived analog of human tPA, has predominantly replaced urokinase. Moreover, two tPA variants, reteplase (recombinant plasminogen activator) and tenecteplase (TNK), are also used. • Reteplase has a longer half-life than alteplase.
  • 25.
    • The commonlyused dosing schemes are alteplase (0.5–1.0 mg/h), reteplase (0.25–0.75 units/h), and TNK (0.25–0.5 mg/h) for CDT. Limitations: • Complications such as significant bleeds, intracranial bleeds, and the need for monitoring in the ICU for 1–3 days.
  • 28.
    Percutaneous mechanic thrombectomy •PMT refers to the percutaneous use of catheter-based mechanical devices that contribute to thrombus removal via fragmentation, maceration, and/or aspiration, without administering a thrombolytic agent. • It eliminate the need of thrombolytic drugs that carry inherent risks such as bleeding and prolonged ICU stays.
  • 29.
    Pharmacomechanical catheter-directed thrombolysis • Thevenous thrombus is primed with the fibrinolytic drugs, which increases the susceptibility to mechanical fragmentation and allows for more effective removal, preventing residual fragment embolizing to the lungs. • Due to its effectiveness, this method reduces the thrombolytic drug dose, treatment time, and hospital costs significantly. • The patient then undergoes radiolytic thrombectomy utilizing saline jets to create a localized low pressure zone by the Bernoulli effect to macerate a clot.
  • 31.
    IVC filter • IVCfilters are used in patients with contraindication to anticoagulation therapy or failure to avoid iatrogenic pulmonary embolism.
  • 32.
    Venous angioplasty/Stenting • Thistreatment is classically utilized in May-Thurner syndrome, which refers to chronic compression of the left common iliac vein against a lumbar vertebra secondary to the overlying, pulsating, right common iliac artery causing DVT. • Criteria for angioplasty in acute DVT include iliofemoral DVT and evidence of residual thrombosis or obstruction following mechanical thrombolysis. In contrast, measures in chronic DVT include established PTS with significant symptoms and evidence of iliofemoral stenosis or obstruction confirmed by imaging amenable to stent placement. • Venous stent placement is indicated when the block is >50%, there is apparent formation of superficial collaterals, and evidence of reflux in deep and superficial veins.
  • 34.
    Complications • If notmanaged properly, these thrombi can embolize, causing further complications. • Delay in management may lead to pulmonary embolization or stroke. • Another common complication is posted thrombotic syndrome (PTS), which manifests as chronic limb fatigue/heaviness, swelling, pain, and paresthesia, occurring in 50% of patients, accompanied by severe quality of life impairment. The most important factors leading to PTS include the development of valvular reflux and late venous obstruction when the clot is not entirely cleared.
  • 35.
    • Phlegmasia ceruleadolens is a severe form of DVT characterized by complete lower extremity venous occlusion of deep and superficial channels. Associated edema causes a rise in interstitial tissue pressure overcoming arterial closing pressure, causing collapse. • Phlegmasia cerulea dolens is potentially life-threatening complication of acute DVT characterized by marked swelling of the extremities with pain, motor/sensory defecit and cyanosis. This may lead to arterial ischemia and ultimately cause gangrene, with high amputation and mortality rates. Endovascular treatments include catheter-directed thrombolysis and pharmacomechanical /mechanical thrombectomy. • Progression can also lead to death or major disability as a result of pulmonary embolism, postthrombotic syndrome, or limb amputation.
  • 36.
    Case 1 • Patientpresented with right lower limb pain and swelling since 1 week, progressive in nature, aggravated by walking and relieved on rest. • Peripheral pulses were present. • Past history of left lower limb DVT and underwent angioplasty. • Known case of May Thurner syndrome. IVC filter insertion done. Left common iliac vein stenting • No comorbities. • History of blood transfusion 2 pint. • Pallor present. • Murmurs present at tricuspid and pulmonary region.
  • 37.
    • Medication started,Tablet Ecosprin (antiplatelet drug), Tablet Rivaroxaban (Factor Xa inhibitor), Injection Heparin 5000IU 6 hourly. • CT venogram of bilateral lower limb was planned. • During CT venogram, extravasation of IV contrast occurred. Patient developed swelling in forearm. On examination, non pitting edema was noted. No signs of inflammation were present. Radial and ulnar pulses were present. • Patient was suggseted for doppler of left forearm,limb elevation and cold compression. • Decided to do ,CBC, PT, INR, GRBS, HbA1C, Blood grouping , Serum creatinine and 2D Echo. • Hb came out be low (7.7gm/dl). • Medicine team decided to do peripheral smear and transfuse 1 pint of PRBC. • After procedure Tablet Clexane (Factor Xa inhibitor and antithrombin complex).
  • 38.
    • Bilateral lowerlimb DVT thrombolysis and thrmbectomy with Tenecteplase (tissue plasminogen activator) was done. • After procedure Tablet Clexane (Factor Xa inhibitor and antithrombin complex), strict immobilisation was suggested, heparin was withold and proper hydration was maintained. • After procedure patient developed chest pain. However, BP, PR and SPO2 were normal. Medicine team suggested for serial ECG and Troponin I. ECG showed sinus tachycardia and flat T wave. Troponin I was normal. Pain subsided after 1 day. • Patient complained right lower limb pain and swelling. Elastic compression bandages were suggested.
  • 39.
    mov-series-001-Abdomen 3 fps.wmvmov-series-003-Fluoroscopy.wmv mov-series-005-Fluoroscopy.wmv mov-series-009-Abdomen 3 fps.wmv mov-series-015-Abdomen 3 fps.wmv mov-series-019-Fluoroscopy.wmv mov-series-031-Abdomen 3 fps.wmv
  • 40.
    Case 2 • Complainof pain and swelling in left leg for 4 days. Peripheral pulses were normal. • History of recurrent cerebral venous thrombosis (2016) • No comorbities. • He was on medication, acitrom (acenocoumarol, inhibits vitamin K epoxide reductase) 2mg OD (irregular treatment) • History of chronic smoking for 2 years (3-4cigarettes/day). • Occasional alcoholic since 6-7years (once weekly). • On 2D Echo : Trivial MR, Grade I left ventricular diastolic dysfunction. • Venous doppler done : DVT in left SFV and popliteal vein. Varicose veins, incompetent perforators at SFJ. • Investigations done : PT, APTT, INR, Thrombophilia profile (Vitamin B12, Homocysteine etc), complete haemogram, Blood group, RFT, LFT, HIV, HbsAg, HCV
  • 41.
    • Injection Heparin5000 IU I.V stat, followed by 1000 IU/hour. Morning dose should skipped on day of procedure. Patient should be NPO from midnight. • IVC filter placement and thrombolysis of left lower limb DVT was performed. • Post procedure injection heparin 5000 IU continued every 6 hourly. CBC, PT, APTT and INR was repeated.
  • 42.
    mov-series-009-Fluoroscopy.wmv mov-series-010-Fluoroscopy.wmv mov-series-012-Fluoroscopy.wmvmov-series-014-Fluoroscopy.wmv mov-series-015-Abdomen 3 fps.wmv mov-series-016-Abdomen 3 fps.wmv mov-series-018-Abdomen 3 fps.wmv mov-series-019-Fluoroscopy.wmv mov-series-023-Fluoroscopy.wmv mov-series-026-Fluoroscopy.wmv mov-series-030-Abdomen 3 fps.wmv
  • 43.
    References • Endovascular Interventionsfor Acute and Chronic Lower Extremity Deep Venous Disease: State of the Art. Radiology, 276(1), 31–53. Sista, A. K., Vedantham, S., Kaufman, J. A., & Madoff, D. C. (2015). • Endovascular Treatment for Lower Extremity Deep Vein Thrombosis: An Overview. Kyung Ah Kim,Sun Young Choi, and Ran Kim Korean J Radiol. 2021 Jun;22(6):931-943. • Imaging findings and interventional management of deep venous thrombosis. Hussam Hindi​ , Gauthier Dongmo, Alyssa Goodwin, Sean Jones, Kristian Loveridge.