CTVS 64 Venous Diseases Deep Vein Thrombosis

• Venous stasis
• Endothelial injury
• Hypercoagulable state

• A) Inherited (Primary hypercoagulable state)
• - Antithrombin III deficiency 
• - Protein C,S deficiency 
• - Factor V Leiden mutation
• - Prothrombin gene mutation 
• - Elevated homocysteine

• B) Acquired (secondary) hypercoagulable state 
• - Antiphospolipid syndrome 
• - Pregnancy and post-partum period 
• - Estrogen use, advancing age 
• - Immobiliation, injury 
• - Clinical disorders - Malignancy, Nephrotic syndrome, congestive heart failure

• Major abdominal or orthopedic surgery
• Major trauma
• Prolonged immobility (>3 days)
• Malignant disease
• Increased body mass index
• Increasing age (especially >60 years)
• Pregnancy
• Tobacco use
• Prior deep vein thrombus

• Most calf thrombi may be asymptomatic unless there is proximal propagation.
• Pain and swelling, especially in the calf – usually in one lower limb; however, bilateral deep vein thromboses are common.
• When the swelling is bilateral, deep vein thromboses must be differentiated from other causes of systemic oedema, such as hypoproteinaemia, renal failure and heart failure.
• Some patients have no symptoms of thrombosis and may first present with signs of a pulmonary embolism, e.g. pleuritic chest pain, haemoptysis and shortness of breath
• Homan sign - pain in the calf on dorsiflexion of the foot.
• Major venous thrombosis involving the iliofemoral venous system results in a massively swollen leg, with pitting edema, pain, and blanching, a condition known as phlegmasia alba dolens.
• With further progression of disease, there may be such massive edema that arterial inflow can be compromised. This condition results in a painful blue leg, a condition called phlegmasia cerulea dolens.
• With this evolution of the condition, venous gangrene can develop unless flow is restored.
• Post thrombotic syndrome (PTS) - common manifestation of deep venous thrombus - chronic edema, pain, venous claudication and venous ulceration.

• Ruptured Baker’s cyst
• Calf muscle haematoma
• Ruptured plantaris muscle
• Thrombosed popliteal aneurysm
• Arterial ischaemia

• Variable // Points
• Clinical signs and symptoms of DVT (minimum of leg swelling and pain on palpation of deep veins) // 3.0
• Alternative diagnosis less likely than PE // 3.0
• Heart rate >100 // 1.5
• Immobilisation >3 days or surgery within past 4 weeks // 1.5
• Previous DVT or PE // 1.5
• Haemoptysis // 1.0
• Malignancy (treatment or palliation within past 6 months) // 1.0

• A score of <4 means PE is unlikely; >4 is suggestive of PE

High index of suspicion form history and physical examination 

Fibrin and fibrinogen assays

• Imaging studies - 
• - Duplex ultrasound - investigation of choice
• - Magnetic resonance venous imaging - for imaging the iliac veins and IVC, an area where the use of duplex ultrasound is limited

• 1. Mechanical
• - Ask the patient to walk
• - Graduated elastic compression stockings
• - External pneumatic compression

• 2. Pharmacological
• - Use of low-dose unfractionated heparin - 5000 units every 8 hours (5000 units sc BD is no more effective than placebo)
• - LMWX

• LMWH has a longer plasma half-life and significantly higher bioavailability.
• The consistent bioavailability and clearance of LMWH do not require monitoring of factor Xa levels, which facilitates use by the patient.
• Dosing is merely based on the patient’s weight.
• There is a more predictable anticoagulant response than with unfractionated heparin.
• No laboratory monitoring is necessary because the partial thromboplastin time (PTT) is unaffected

• If unfractionated heparin is used, it is important to use a nomogram-based dosing therapy.
• The PTT needs to be checked 6 hours after any change in heparin dosing.
• Warfarin is started on the same day. If warfarin is initiated without heparin, the risk for a transient hypercoagulable state exists because protein C and protein S levels fall before the other vitamin K–dependent factors are depleted.
• With the advent of LMWH, it is no longer necessary to admit the patient for IV heparin therapy. It is now accepted practice to administer LMWH on an outpatient basis, as a bridge to warfarin therapy, which is also monitored on an outpatient basis.

• 1. Treatment with heparin
• - to maintain the PTT at 60 to 80 seconds, followed by warfarin therapy to obtain an INR of 2.5 to 3.0.
• - Duration - minimum treatment time of 3 months. If the patient has a known hypercoagulable state, lifetime anticoagulation is required in the absence of contraindications.
• - During pregnancy, LMWH is the treatment of choice. Warfarin is teratogenic.

• 2. Thrombolysis
• - should be considered in patients with an iliac vein thrombosis, especially if they are seen early and the limb is extremely swollen
• - tissue plasminogen activator is administered directly into the thrombus, either via the popliteal vein or by direct puncture in the groin.

3. Endovascular reconstruction - Balloon dilation of the lesion, and a stent is placed across the dilated segment. Endovascular iliac therapy has evolved to become first-line therapy for iliac occlusions.

4. Thrombectomy -may be attempted in patients with threatened venous gangrene and phlegmasia cerulia dolens. If performed, a venous thrombectomy should be accompanied by an arteriovenous fistula to increase venous flow through the vein that has had the thrombus removed

• CTPA (CT pulmonary angiogram)
• Ventilation—perfusion scan.

Insertion of IVC filter. This filter is usually inserted via the internal jugular or via femoral vein by interventional radiology.

• They are dilated, tortuous, elongated veins in the leg.
• There is reversal of blood flow through its faulty valves.

• C — Clinical signs (grade 0-6); (A) for asymptomatic or (S) for symptomatic presentation.
• E — Etiologic classification (congenital, primary, secondary).
• A — Anatomic distribution (superficial, deep or perforator).
• P — Pathophysiologic dysfunction (reflux or obstruction).

• a. Primary varicosities - intrinsic abnormalities of the venous wall
• 1. Congenital incompetence or absence of valves.
• 2. Weakness or wasting of muscles—defective connective tissue and smooth muscle in the venous wall.
• 3. Stretching of deep fascia.
• 4. Inheritance (family history) with FOXC2 gene.
• 5. Klippel – Trenaunay syndrome

• b. Secondary varicosities associated with deep and/or superficial venous insufficiency.
• 1. Recurrent thrombophlebitis,
• 2. Occupational – standing for long hours (traffic police, guards).
• 3. Obstruction to venous return like abdominal tumour, retroperitoneal fibrosis, lymphadenopathy.

• • Dragging pain
• • Heaviness in the legs
• • Night time cramps – usually late night
• •  These symptoms worsen with prolonged standing and sitting and are relieved by elevation of the leg above the level of the heart.
• • Oedema feet
• • Discolouration/ulceration in the feet/painful walk
• • Pruritus, and early fatigue of the affected leg.

More severe signs include thrombophlebitis, hyperpigmentation, lipodermatosclerosis, ulceration, and bleeding from attenuated vein clusters.

• 1. Venous Doppler
• 2. Duplex scan
• 3. MRV
• 4. Phlebography/Venography
• 5. Plethysmography: It is a noninvasive method which measures volume changes in the leg

• 1. Conservative treatment:
• • Elastic compression stocking 
• • Elevation of the limb—relieves oedema.
• • Pneumatic compression method—provide dynamic sequential compression.

• 2. Drugs used for varicose veins:
• • Calcium dobesilate—500 mg BD. Calcium dobesilate improves lymph flow; improves macrophage mediated proteolysis; and reduces oedema.

• 3. Injection—sclerotherapy: (Fegan’s technique)
• - Act by destroying venous endothelium
• - Successful in varicose veins <3 mm in diameter and in telangiectatic vessels
• - e.g - hypertonic saline, sodium tetradecyl sulfate, and polidocanol
• - Elastic bandages are wrapped around the leg after injection and worn continuously for 3 to 5 days to produce apposition of the inflamed vein walls and prevent thrombus formation
• - After the bandages are removed, elastic compression stockings should be worn for a minimum of 2 weeks.
• - Complications from sclerotherapy include allergic reaction, local hyperpigmentation, thrombophlebitis, DVT, and possible skin necrosis.

• 4. Endovenous ablation techniques
• - Endo venous laser ablation (EVLA)
• - Radiofrequency ablation (RFA) techniques

• 5. Surgical procedures
• - Saphenous vein ligation and stripping (Trendelenburg operation) - for GSVs >2 cm
• -  Surgical excision using the “stab avulsion” technique - for Larger varicose veins. Stab avulsions are performed by making 2-mm incisions directly over branch varicosities, and the varicosity is dissected from the surrounding subcutaneous tissue as far proximally and distally as possible through the small incisions.

• Using Myer’s stripper vein is stripped off. Stripping from below upwards is technically easier. Immediate application of crepe bandage reduces the chance of bleeding and haematoma formation. Stripping avulses the vein as well as obliterates the tributaries.

Complications - ecchymosis, lymphocele formation, DVT, infection, and saphenous nerve injury (occurs more frequently when the great saphenous vein is stripped from the ankle to the groin).

GSV stripping is associated with a lower rate of recurrence of varicose veins and a better quality of life than saphenofemoral junction ligation alone.

• - It is done as an outpatient procedure or as day- care surgery.
• - Supine position with external rotation of leg and knee slightly flexed. 
• - Patient in reverse trendelenberg position (to dilate vein)
• - Painting and draping
• - Under USG guidence, distal thigh or proximal calf GSV is punctured with 21G needle. 
• - A guide wire is passed beyond SFJ and 5- French catheter is passed over guide wire and tip of the ablation catheter is placed 2 to 3 cm distal to the saphenofemoral junction to minimize the chance of heat transmission into the femoral vein.
• - Tumescent anesthesia is infiltrated along the length of GSV.
• - Laser fibre is inserted up to the tip of the catheter and catheter is withdrawn for 2 cm and laser fibre protrudes for 2 cm.
• - Laser fibre is fired step by step using diode laser, one mm withdrawal in 2 seconds.
• - Once procedure is over catheter is removed and pressure bandage is applied for 2 weeks.

• - Heat produced (729°C – 1000°C at tip) by the laser produces steam bubbles with thermal damage of endothelium leading into occlusion of the vein.
• - Laser energy acts on the blood within the vein rather directly through the wall and heats the blood and in turn heats the vein wall.
• - Drawback of laser therapy is inability to create flush occlusion allowing tributaries to open up to cause possible recurrence.

• • Haemorrhage: Venous haemorrhage can occur from the ruptured varicose veins or sloughed varicose veins, often torrential, but can be controlled very well by elevation and pressure bandage.
• • Eczema and dermatitis.
• • Periostitis causing thickening of periosteum.
• • Venous ulcer.
• • Marjolin’s ulcer.
• • Lipodermatosclerosis.
• • Ankylosis of the ankle joint.
• • Deep venous thrombosis.
• • Calcification.
• • Thrombophlebitis.

• • Measures to reduce oedema, increase venous drainage, so as to promote ulcer healing.
• • Elevation.
• • Massage of the indurated area and whole calf.
• • Passive and active exercise
• • Pressure bandage (crepe bandage).
• • Care of ulcer by regular cleaning with povidone iodine, H2O2.
• • Dressing with EUSOL.
• • Four layer bandage (45 mm Hg pressure) technique to achieve high compression pressure. It is changed once a week.
• • Antibiotics depending on culture and sensitivity of the discharge.

Once ulcer bed granulates well, split skin graft (SSG) is placed (Thiersch Graft).

• • Haemorrhage
• • Marjolin’s ulcer (in unstable scar of long duration) 
• • Infection
• • Talipes equino varus
• • Periostitis is common over the tibia
• • Disability
• • Calcification