ACUTE DEEP VENOUS

THROMBOSIS:
PREVENTION AND MEDICAL TREATMENT

Sqn Ldr Deepak Kumar

Guide: Col CP Singh
 Deep Vein Thrombosis
DVT of the
legs three
types:

Proximal DVT Iliofemoral

Calf DVT: DVT :
: involving the
involving the involving
proximal leg
infra popliteal proximal DVT
veins up to the
venous system that extends
inguinal
ligament above the
inguinal
ligament
Risk factors for VTE

 Acquired
 Advanced age
 Hospitalization/im Inherited Mixed Etiology
mobilization •Factor V Leiden •Homocysteinemia
 Hormone
•Prothrombin 20210A •Factor VII, VIII, IX,
replacement XI elevation
therapy and oral •Antithrombin
contraceptive use •Hyperfibrinogenemia
deficiency •Activated protein C
 Pregnancy and
puerperium •Protein C deficiency resistance without
 Prior venous
•Protein S deficiency factor V Leiden
thromboembolism •Factor XI elevation
 Malignancy •Dysfibrinogenemia
Risk factors for VTE

 Acquired
 Major surgery
 Obesity Inherited
 Nephrotic syndrome
 Trauma or spinal cord
injury
 Long-haul travel (>6
hours)
 Varicose veins
 Antiphospholipid
antibody syndrome
 Myeloproliferative
disease
 Polycythemia
Mixed Etiology
•Factor V Leiden •Homocysteinemia
•Prothrombin 20210A •Factor VII, VIII, IX,
XI elevation
•Antithrombin
•Hyperfibrinogenemia
deficiency •Activated protein C
•Protein C deficiency resistance without
•Protein S deficiency factor V Leiden
•Factor XI elevation
•Dysfibrinogenemia
Prophylaxis
 Goal : Reduce the mortality
and morbidity associated with
VTE.
 Based on
 Caprini Risk Assessment
Model
Caprini Score
Rogers Score
Methods of Prophylaxis
 Can be mechanical or pharmacologic.
 Simplest method  to walk.
 Activation of the calf pump mechanism

 Patients walking within 24 to 48 hours

Low risk of DVT

Methods of Prophylaxis
 CAUTION:
 Patient  out of bed into a chair is one of the most thrombogenic
positions.

 Sitting in a chair with the legs in a dependent position

Venous pooling

Predisposing factor for the development of thromboembolism.

 IPC( Intermittent Pneumatic Compression)
 Periodically compress the calves
 Replicates the calf bellows mechanism.
 Has reduced the incidence of VTE in the surgical
patient.
 MECHANISM :
 Prevention of venous stasis.

 ?? Fibrinolytic activity systemically is enhanced by

a sequential compression device.
Ref: Killewich LA, Cahan MA, Hanna DJ, et al: The effect of external pneumatic compression on regional
fibrinolysis in a prospectiverandomized trial. J Vasc Surg 36:953–958, 2002.
 Treatment
 Once VTE is diagnosed: antithrombotic therapy should be
initiated promptly.
 Goals: Prevention of
 Mortality and morbidity associated with PE

 Post thrombotic syndrome (PTS).

 Any venous thrombosis involving the femoropopliteal system

is treated with full anticoagulation.
 Traditionally heparin treatment to maintain the PTT at 60
to 80 seconds
 Presently warfarin therapy : (INR) of 2.5 to 3.0.
May include..

Temporary or Catheter-directed
Antithrombotic permanent vena or systemic Operative
therapy cava filter thrombolytic thrombectomy
placement therapy
Antithrombotic Therapy- General Considerations
 Most often, antithrombotic therapy for VTE is initiated with
 IV or subcutaneous (SC) unfractionated heparin
 SC low molecular weight heparin.
 Fondaparinux : Alternative to heparin to initiate therapy.
 An oral vitamin K antagonist (sodium warfarin) is begun shortly after
initiation of IV or SC therapy.
 Either SC or IV therapy is continued until effective oral anticoagulation
with warfarin is achieved as indicated by an international normalized
ratio (INR) ≥2 for 24 hours.
Antithrombotic Therapy- General Considerations
 Incidence of recurrent VTE
increases if the time to therapeutic
anticoagulation is prolonged.

Important to reach therapeutic

levels within 24 hours.
Antithrombotic Therapy- General Considerations
 Unfractionated heparin : An initial bolus
of 80 U/kg or 5000 units IV bolus is
administered, followed by 18 U/kg/ hr.
 Rate is dependent on a target PTT
corresponding to anti-factor Xa level of 0.3
to 0.7 unit/mL.
 PTT : Checked 6 hours after any change in
heparin dosing.
Antithrombotic Therapy- General Considerations

 Warfarin is started on the same day.

 Ifwarfarin is initiated without heparin, the risk for a
transient hypercoagulable state exists because
protein C and S levels fall before the other vitamin
K–dependent factors are depleted.
 Now accepted practice
 LMWH on an OPD basis
 As a bridge to warfarin therapy
Unfractionated Heparin
 Heterogenous mixture of polysaccharide chains
 MW 3k to 30k
 Active in vitro and in vivo
 Administration - parenteral- Do not inject IM - only IV or deep s.c.
 Half-life 1 - 2 hrs - monitor APTT
 Antidote - Protamine sulphate
Mechanism of action
 The antithrombin-heparin complex
 Primarily inhibits factor IIa (thrombin) and factor Xa and
 To a lesser degree, factors IXa, XIa, and XIIa of the coagulation
cascade.
 Also binds to tissue factor pathway inhibitor, which inhibits
the conversion of factor X to Xa, and factor IX to IXa.
Heparin: Mechanism of Action
Accelerates antithrombin III activity
Antithrombin III
(Heparin)
Factor X
Factor IXa
Ca 2+, PL
Factor VIIIa

Factor Xa
Prothrombin Thrombin
Factor Va
Ca2+, PL
 Un-fractionated Heparin
SIDE EFFECTS CONTRAINDICATIONS-
• Bleeding • Bleeding disorders,
• Severe hypertension,
• Osteoporosis threatened abortion, piles,
• Thrombocytopenia • large malignancies,
• Skins lesions- urticaria, papules, tuberculosis
necrosis • Ocular surgery and
neurosurgery
• Hypoaldosteronism, • Chronic alcoholics,
hyperkalemia • cirrhosis, renal failure
Unfractionated Heparin- Dose

Analyses of trials
The dosage comparing placebo 08 hrs Regimen ,
traditionally used versus fixed-dose rather than every 12
was 5000 U of heparin  dose of hoursreduction in
unfractionated 5000 U SC every 12 the development of
heparin every 12 hours is no more venous
hours. effective than thromboembolism.
placebo.
LMWH ( Low molecular weight heparin)

 Standard (Unfractionated) heparin 3k to 30k

 LMWH contains polysaccharide chains MW 5k
 Enriched with short chains with higher anti-Xa:IIa ratio
LMWH- Regimen
 The optimal regimen for the treatment of DVT is anticoagulation
with heparin or an LMWH followed by full anticoagulation with
oral warfarin for 3-6 months

 Warfarin therapy is overlapped with heparin for 4-5 days until the
INR is therapeutically elevated to between 2-3.
LMWH- Advantages
 Longer plasma half-life
 Significantly higher bioavailability.
 Do not require monitoring of factor Xa levelswhich facilitates patient
use (Consistent bioavailability and clearance )
 Dosing is merely based on the patient’s weight.
 More predictable anticoagulant response than with unfractionated heparin.
 No laboratory monitoringis necessary (partial thromboplastin time (PTT) is
unaffected)
LMWH
 Significant reduction : Venous thromboembolism compared with other
methods.
 Considered the optimal method of prophylaxis for moderate- and high-
risk patients.
 Thromboprophylaxis should continue until discharge, except
 Malignancy Patients : up to 4–6 weeks

 Patients with significant risk for bleeding : Mechanical prophylaxis until

this risk subsides.
 Gould MK, Garcia DA, Wren SM, et al. Prevention of venous thromboembolism in nonorthopedic
surgical patients. American College of Chest Physicians Evidence- Based Clinical Practice Guidelines,
9th ed. Chest. 2012;141:227S.
Complications of Heparin
 Haemorrhage
 Heparin-induced thrombocytopaenia (HIT)
 Osteopenia/ Osteoporosis (long-term only)
 Complications of Heparin
 Heparin-Induced Thrombocytopaenia:
 Most significant adverse effect of heparin after haemorrhage

 Most common drug-induced thrombocytopenia

 Results from heparin-associated antiplatelet antibodies (HAAbs)

directed against platelet factor 4 complexed with heparin
 Occurs in 1% to 5% of patients being treated with heparin.

 Repeat heparin exposure the incidence of HAAbs= 21%

 Occurs most frequently in the second week of therapy.

Complications of Heparin
 Non-immune heparin-associated thrombocytopaenia (“HIT Type I”)
 Benign
 Up to 10% patients on heparin
 Rapid decline in platelet count within first 2 days of heparin
administration
 Platelet count >100 000/ul
 Returns to normal within 5 days despite continued heparin use (or within
2 days if heparin is stopped).
 Complications of Heparin
 Heparin-induced thrombocytopaenia: “HIT type 2”
 Potentially catastrophic thrombosis (Heparin-induced thrombocytopenia
and thrombosis)
 1-5% patients on heparin develop thrombocytopaenia
 Of those with thrombocytopaenia, 30% develop venous and/or arterial
thrombosis
 Bleeding uncommon
Management of HIT
 Discontinue all heparin
 If need to continue anti-coagulation, use Danaparoid (orgaran).
 Avoid platelet transfusions
 Thrombosis: Use Danaparoid or thrombin inhibitor
Complications of Heparin
 Osteopenia 
 Another complication of prolonged high-dose heparin therapy is
osteopenia.
 Heparin-induced osteopenia results from

 Impairment of bone formation

 Enhancement of bone resorption
Fondaparinux
 Fondaparinux is a synthetic pentasaccharide.
 Recently approved by the FDA : Initial treatment of DVT and PE.
 MOA:
 Binds and activates antithrombin,causing specific inhibition of
factor Xa.
 Administered: SC once daily with a weight-based dosing protocol: 5 mg,
7.5 mg, or 10 mg for patients weighing <50 kg, 50 to 100 kg, or >100
kg,respectively.
 Half-life : 17 hours
Direct thrombin inhibitors (DTIs)
 Include recombinant hirudin, argatroban, and bivalirudin.
 MOA:
 These antithrombotic agents bind to thrombin, inhibiting the conversion
of fibrinogen to fibrin as well as thrombin-induced platelet activation.
 These actions are independent of antithrombin.
Direct thrombin inhibitors (DTIs)
 The DTIs should be reserved for
 (a) patients in whom there is a high clinical suspicion or confirmation
of HIT
 (b) patients who have a history of HIT or test positive for heparin-
associated antibodies.
 In patients with established HIT, DTIs should be administered for at least 7
days, or until the platelet count normalizes.
 Warfarin may then be introduced slowly, overlapping therapy with a DTI
for at least 5 days.
Direct thrombin inhibitors (DTIs)

Bivalirudin is approved primarily for patients

undergoing percutaneous coronary intervention.
Hirudin
 Manufactured using recombinant DNA technology.
 Indication:
 Prophylaxis and treatment of patients with HIT.

 Administration:
 IV bolus dose of 0.4 mg/kg

 Followed by a continuous IV infusion of 0.15 mg/kg per hour.

 The half-life ranges from 30 to 60 minutes.

Hirudin
 The aPTT is monitored, approximately 4 hours after initiation of therapy.
 Dosage is adjusted : Maintain aPTT of 1.5 to 2.5 times the laboratory
normal value.
 Elimination:
 Eliminated via renal excretion dosage adjustments in patients with
renal insufficiency.
Argatroban
 Indication:
 Prophylaxis and treatment of thrombosis in HIT.

 It also is approved for patients with, or at risk for, HIT undergoing

percutaneous coronary intervention.
 Administration:
 Antithrombotic prophylaxis and therapy are initiated with a continuous
IV infusion of 2 μg/kg per minute, without the need for a bolus.

 The half-life ranges from 39 to 51 minutes

 The dosage is adjusted to maintain an aPTT of 1.5 to 3 times normal.
Argatroban
 Monitoring:
 Using the activated clotting time.

 Elimination:
 Metabolized and excreted by the liver  dosage adjustments in
patients with hepatic impairment.
 No reversal agent.
Vitamin K antagonists
 Include warfarin and other coumarin derivatives.
 The mainstay of long-term antithrombotic therapy in patients with
VTE.
 MOA:
 Warfarin inhibits the γ-carboxylation of vitamin K–dependent
procoagulants (factors II, VII, IX, and X) and anticoagulants (proteins
C and S)

 Formation of less functional proteins.

Vitamin K antagonists
 Warfarin usually requires several days to achieve full effect because
normal circulating coagulation proteins must first undergo their
normal degradation.
 Factors X and II have the longest half-lives, in the range of 36 and 72
hours, respectively.
 A steady-state concentration of warfarin is usually not reached for 4 to 5
days.
Vitamin K antagonists
 Warfarin therapy is monitored by measuring the INR, calculated using the
following equation:
 INR = Patient Prothrombin time ISI
Laboratory normal Prothrombin time
 The ISI (international sensitivity index) describes the strength of the
thromboplastin that is added to activate the extrinsic coagulation
pathway.
 The therapeutic target INR range2.0 to 3.0.
Vit K Antagonists- Complications
 Common:
 Hemorrhage
 Risk is related to INR prolongation.
 Reversed by:
 Omitting or decreasing subsequent dosages
 Administering oral or parenteral vitamin K
 Administering fresh-frozen plasma, prothrombin complex
concentrate, or recombinant factor VIIa
 Holbrook A, Schulman S, Witt DM, et al. Evidence based management of
anticoagulant therapy. American College of Chest Physicians Evidence-Based
Clinical Practice Guidelines,9th ed. Chest. 2012;114:152S.
 Vit K Antagonists- Complications
 Rare complication
 Skin necrosis / Limb gangrene.
 M: F (1:4)
 Commonly involves breast, buttocks, and thighs
 Occurs in the first days of therapy, associated with
 protein C or S deficiency
 malignancy
 Treatment:
 Restart on low-dose warfarin (2 mg) while receiving concomitant therapeutic
heparin.
 The warfarin dosage is then gradually increased over a 1- to 2-week period
 Holbrook A, Schulman S, Witt DM, et al. Evidence based management of anticoagulant therapy.
American College of Chest Physicians Evidence-Based Clinical Practice Guidelines,9th ed. Chest.
2012;114:152S.
ACCP recommendation
 3 months of anticoagulation are sufficient to prevent recurrent VTE : Transient
risk factor
 Hospitalization
 Orthopedic or major general surgery
 In VTE related to malignancy:
 Longer-term therapy with LMWH (up to 6 months) is associated with a
lower VTE recurrence than treatment using conventional vitamin K
antagonists.
 Lee AYY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a coumarin for the
prevention of recurrent venous thromboembolism in patients with cancer. N Engl J Med. 2003;349:146.
 Akl EA, Barba M, Rohilla S, et al. Anticoagulation for the long term treatment of venous
thromboembolism in patients with cancer. Cochran Database Syst Rev. 2008;2:CD006650.
Summary of ACCP recommendations :Duration of
long-term antithrombotic therapy DVT
Duration of Anticoagulant drugs
 The recommended duration  continues to evolve.
 A minimum treatment time of 3 months is advocated in most cases.
 Recurrence rate is the same with 3 versus 6 months of warfarin therapy.
 If the patient has a known hypercoagulable state or has experienced
episodes of venous thrombosis lifetime anticoagulation is required in
the absence of contraindications.
Anticoagulants in Pregnancy
 Oral anticoagulants are teratogenic
 In pregnant patient : DOC: LMWH
 Continued through delivery
 Can be continued postpartum, as indicated.
2. Thrombolysis
 Benefit :
 Preservation of valve function  lesser chance of developing CVI.

 Few definitive convincing studies to support the use of thrombolytic

therapy for DVT.
 Exception : Phlegmasia :
 Thrombolysis relief of significant venous obstruction.
 Better relief of symptoms
 Less long-term sequelae than heparin anticoagulation alone.
 Alternative surgical venous thrombectomy.
Systemic and Catheter-Directed Thrombolysis.

CDT as compared to
anti-coagulation
alone:

Potentially reduces
acute congestive Decreases the
More effective
lower extremity development of PTS
symptoms
Recombinant tissue plasminogen activator

Streptokinase Alteplase Reteplase Tenecteplase Urokinase

MOA:  They differ with regard to their

• Convert plasminogen to • Half-lives

plasmin • Potential for inducing
fibrinogenolysis (generalized
lytic state)
• Degradation of fibrin. • Potential for antigenicityFDA-
approved indications for use.
Streptokinase
Purified from β-hemolytic Streptococcus

Treatment:
• Acute myocardial infarction
• PE
• DVT
• Arterial thromboembolism
• Occluded central lines and arteriovenous shunts
Fevers and shivering occur in 1% to 4% of patients.
Urokinase
 Derived from Human neonatal kidney cells grown in tissue culture.
 Approved Uses:
 lysis of massive PE or PE associated with unstable hemodynamics.
Tissue plasminogen activators
 Alteplase
 Indication: Treatment of
 acute MI
 acute ischemic stroke
 acute massive PE.

 However, it often is used for CDT of DVT.

 Reteplase and Tenecteplase: Acute MI.
 Catheter directed thrombolysis

 CDT techniques were developed:

 To minimize bleeding complications
 Increase efficacy of treatment of
symptomatic primarily iliofemoral DVT
 Includes
 CDT
 Balloon Angioplasty
 Stenting
Catheter directed thrombolysis
 With catheter-directed therapy, venous access
may be achieved through percutaneous
catheterization of
 Ipsilateral popliteal vein
 Retrograde catheterization through the contralateral
femoral vein
 Retrograde cannulation from the internal jugular
vein
 Delivery of lytic agent directly into the
thrombus:
 Multi-side-hole infusion catheters with or without
infusion wires
Endovascular Mechanical Thrombectomy
ANGIOJET™ ULTRA Thrombectomy System

MECHANISM OF ACTION
1. The AngioJet Ultra Console 4. Thrombus is drawn into the 5. Thrombus is evacuated
monitors and controls the in-flow windows and the from the body and into
system. jets push the thrombus back the collection bag.
2. The Console energizes the down the catheter.
pump which sends
pressurized saline to the
catheter tip.
3. Saline Jets travel backwards
to create a low pressure zone
causing a vacuum effect.
Endovascular Mechanical Thrombectomy
 CDT vs Pharmacomechanical thrombolysis with the AngioJet catheter was
associated with
 Significantly fewer phlebograms
 Shorter ICU stays
 Shorter hospital stays
 Fewer blood transfusions.
 Bleeding complications were not different between the two groups
 Lin PH, et al: Catheter-direct thrombolysis versus pharmacomechanical thrombectomy for
treatment of symptomatic lower extremity deep venous thrombosis. Am J Surg 192:782–
788, 2006.
 Pharmaco-mechanical thrombolysis
 Lytic agents + catheter-based methods
 physically break up the clot
 Vedantham et al evaluated the
effectiveness of mechanical thrombectomy
alone or in combination with
pharmacologic thrombolysis in 28 limbs of
patients with acute DVT.
 26%- mechanical thrombectomy alone,

 82%%- Pharmaco-mechanical
thrombolysis
Post CDT in a case of DVT Left Lower limb
 3.Vena Cava Filter
 Placed to prevent significant PE from
deep veins of the leg, pelvis or IVC
 Relevance:
 30% of patients with venous TED die
within 30 days
 1 in 5 die of PE

 Isolated calf vein thrombosis not

always benign
Indications:
RELATIVE RECOMMENDATIONS FOR VENA CAVA FILTER
USE AS VENOUS THROMBOEMBOLISM PROPHYLAXIS

PROPHYLAXIS IN HIGH- PROPHYLAXIS IN INCREASED BLEEDING

RISK PATIENTS
• Critically ill
• Previous DVT
• Family history of DVT
• Morbid obesity
• Malignancy
• Known hypercoagulable state
• Prolonged immobility
TRAUMA RISK
• Multiple traumatic • Major operation
injuries • Intracranial hemorrhage
• Spinal cord injury • Solid intra-abdominal organ
• Closed-head injury injury
• Complex pelvic • Pelvic or retroperitoneal
fractures hematoma
• Multiple long-bone • Ocular injury
fractures • Medical problem (cirrhosis,
end-stage renal disease, peptic
ulcer
disease, medication, coagulation
disorder)
Vena Cava Filters
 Modern filters are
placed percutaneously
over a guidewire.
 The Greenfield filter
 Most extensively used
and studied
 Has 95% patency rate
 4% recurrent embolism
rate.
Device related Complications

Device-related
complications

Caval
Migration of
occlusion
Wound the device into In the latter
caused by
hematoma the pulmonary situation,
trapping of a
artery
large embolus.
PE vs Caval Occlusion
 The dramatic hypotension that accompanies acute caval occlusion can be
mistaken for a massive pulmonary embolism.
 The distinction between the hypovolemia of caval occlusion and the right
heart failure from pulmonary embolism can be made by measuring filling
pressures of the right side of the heart.
 The treatment of caval occlusion volume resuscitation.
Retrievable IVC filters

The Recovery filter (Bard,

Helsingborg, Sweden),

There are three retrievable

IVC filters that have U.S.
OptEase filter (Cordis, Johnson &
Food and Drug
Johnson Gateway, Piscataway, NJ)
Administration (FDA)
approval—

Gunther-Tulip filter (Cook Medical,

Bloomington,Ind).
Retrievable IVC filters

Deployed from: Retrieved from:

• The internal jugular • The right jugular vein

vein (Gunther- Tulip and
• Femoral vein Recovery)
• Right femoral vein
(OptEase).
 Retrievable IVC filters
•Before retrievalvenography

Patients that Benefit:

• Multiple trauma patients
• High-risk surgical
patients.
Advantage : May be removed when the
patient no longer requires pulmonary
Insertion embolism protection or can undergo
complications:
• Vena cava perforation
anticoagulation.
• Filter migration
• Venous thrombosis at the
insertion site.
Retrievable IVC filters

Retrieval
complications

Failure to Thrombus
Vein retrieval Groin
retrieve the embolization
site thrombus hematoma
filter from the filter
4. Operative Venous Thrombectomy.

who worsen with anticoagulation

therapy

Surgical therapy : Those with phlegmasia cerulea

Reserved for: dolens  Fasciotomy

Impending venous gangrene

Operative Venous Thrombectomy.
 In iliofemoral DVT
 A longitudinal venotomy is made in the common femoral
vein
 A venous balloon embolectomy catheter is passed through
the thrombus & pulled back.
 Old femoral thrombus cannot be extracted, the vein
may be ligated.
 For a thrombus extending into IVC
 The IVC is exposed transperitoneally
 Controlled below the renal veins.
 Operative Venous Thrombectomy.
 The IVC is opened : Thrombus is removed by gentle massage.
 An intraoperative completion venogram Residual thrombosis or stenosis
 If a residual iliac vein stenosis Intraoperative Angioplasty and Stenting
 In most cases, an arteriovenous fistula is then created by
 Anastomosing the great saphenous vein (GSV) end to side with the
superficial femoral artery.
 An effort to maintain patency of the thrombectomized iliofemoral
venous segment.
Post-op
 Heparin is administered postoperatively for several days.
 Warfarin anticoagulation is maintained for at least 6 months after
thrombectomy.
 Complications include :
 PE in up to 20% of patients

 Death in <1% of patients.

Longitudinal inguinal incision to expose the common
femoral vein, femoral vein, saphenofemoraljunction,
and profunda femoris vein
The balloon catheter is guided distally through the
thrombosed venous valves and clotted veins to the
level of the posterior tibial venotomy.
Performance of infrainguinal venous thrombectomy, with passage of the
balloon catheter repeated as necessary.
 Proximal posterior tibial vein

Flushing with heparin-saline

solution

Bulb syringe.
 Caval thrombectomy
•Alternative to vena caval filtration if a clot is
present in the vena cava

protective balloon catheter

Upper Extremity DVT
Upper extremity DVT  thrombosis of the axillary or subclavian veins.

Paget-
Schroetter
primary syndrome
idiopathic Idiopathic
Two categories upper extremity
DVT.
secondary
Paget-Schroetter syndrome
 Patients develop effort
thrombosis of the extremity

Caused by compression of
the subclavian vein
 The venous component of
thoracic outlet syndrome
Venous TOS
Clinical Features
Investigations
 Plain films are one of the first diagnostic tests used to confirm thoracic
outlet syndrome.

 Duplex Ultrasound: Duplex ultrasound has become the recommended

imaging study for initial diagnostic purposes. It has both a high
 Sensitivity (78–100%) and specificity (82–100%) for diagnosis of
thrombus.
Investigations
 Venography:
 Previously the recommended initial test for diagnosis.

 Now it is indicated in :

 patients with symptoms who have demonstrated pathology on duplex

ultrasound and in whom an initial endovascular intervention is
planned
 Venography is also useful to demonstrate venous stenosis.
Investigations
 Magnetic Resonance and Computed Tomographic Venography
 Used infrequently.
 Even though these tests can offer slightly higher anatomic detail of the
adjacent structures, it often does not impact management.
Treatment
 Initial thrombolysis followed by first rib resection is the standard of care.
 Idiopathic upper extremity DVT:
 `Attributed to an occult malignancy
 warrants evaluation for an undetected malignancy.
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