DEEP VEIN THROMBOSIS

Dr. Iman Haryana SpJP

Deep vein thrombosis

Common femoral vein

Thrombus

Proximal
Knee
Distal
What Is Deep Vein Thrombosis (DVT)?
 Deep vein thrombosis (DVT) is a blood clot that
forms in a vein deep in the body.

 Blood clots occur when blood thickens and

clumps together.

 Most deep vein blood clots occur in the lower

leg or thigh.
• A blood clot in a deep vein can break off and
travel through the bloodstream
• Blood clots in the thigh are more likely to break
off and cause PE than blood clots in the lower
leg.
• Blood clots also can form in veins closer to the
skin’s surface.
• However, these clots won’t break off and cause
PE.
 DVT (deep vein thrombosis) and PE (pulmonary
embolism) are collectively referred to as venous
thromboembolism (VTE)
 DVT and PE are a single clinical entity
 Risk of early death in DVT + PE is 18 X higher than in DVT alone
 ¼ of PE cases present with sudden death
 Other predictors of poor survival in DVT are :
o older age,
o male gender,
o confinement to hospital,
o CHF,
o chronic lung disease,
o neurological disease,
o active malignancy.
Risk factors
Inheriting a blood-clotting disorder..
Prolonged bed rest, such as during a long hospital stay, or paralysis.
Injury or surgery.
Pregnancy.
Birth control pills (oral contraceptives) or hormone replacement therapy.
Being overweight or obese.
Smoking.
Cancer.
Heart failure.
Inflammatory bowel disease.
A personal or family history of DVT or PE.
Age.
Sitting for long periods of time, such as when driving or flying.
5. Fragmentation of the thrombus
(computer graphics superimposed on in-body
photograph)
As the size of the thrombotic mass increases,
it becomes more of a threat. Especially if the
heart rate is normalised, fragments of the
thrombus may break away to be swept into
the circulation.
DVT/PE/VTE
Venous Thrombosis Mechanism

Endothelial Damage

Coagulation
IX a
VII
PF 3
VIII
Ca +
stasis

Xa
Prothrombin Thrombin

Fibrinogen Fibrin
 Virchow Triad
3 primary components:
• venous stasis
• injury to the intima
• changes in the coagulation properties of the
blood
 Pathogenesis of DVT

Virchow’s triad :

 Damage to the vessel wall : prevents the endothelium

from inhibiting coagulation and initiating local fibrinolysis.
 venous stasis : due to immobilization or venous
obstruction inhibits the clearance and dilution of activated
coagulant factors.
 hypercoagulability : congenital or acquired
thrombophilia promotes coagulation
Signs and Symptoms of a DVT
 Swelling, usually in one leg (or arm)
 Leg pain or tenderness often described as a cramp
 Reddish or bluish skin discoloration
 Leg (or arm) warm to touch

Signs and Symptoms of a PE

 Sudden shortness of breath
 Chest pain-sharp, stabbing; may get worse with deep breath
 Rapid heart rate
 Unexplained cough, sometimes with bloody mucus
 Venous thromboembolism –
LIFEBLOOD
THE
Thrombosis
CHARITY
Treatment and secondary prevention

DVT

PE Deep vein
insufficiency

Pulmonary Death Post-thrombotic

hypertension syndrome

Chronic PE Ulcus cruris

 PE

 Sudden shortness of breath

 Chest pain that worsens when you take a deep breath or when you cough
 Feeling lightheaded or dizzy, or fainting
 Rapid pulse
 Coughing up blood
DIAGNOSIS: The diagnosis of DVT is based on
1) Pre-test probability (clinical suspicion)
 The Wells Score is the most widely used.
2) Venous Compression Ultrasound (CUS)
3) D-dimer

DIAGNOSTIC STRATEGY:
TWO-LEVEL WELLS SCORE FOR DVT DIAGNOSIS

CLINICAL FINDINGS POINTS

Paralysis, paresis or recent orthopedic casting of lower extremity 1
Bedridden >3 days recently or major surgery within past 12 weeks 1
Localized tenderness of the deep veins 1
Swelling of entire leg 1
Calf swelling 3 cm greater than other leg (measured 10 cm below
the tibial tuberosity) 1
Pitting edema greater in the symptomatic leg 1
Non‐varicose collateral superficial veins 1
Active cancer or cancer treated within 6 months 1
Previously documented DVT 1
Alternative diagnosis at least as likely as DVT (Baker's cyst, cellulitis,
muscle damage, superficial vein thrombosis, post‐thrombotic syndrome,
inguinal lymphadenopathy, extrinsic venous compression) ‐2

WELLS SCORE PROBABILITY OF DVT STRATA

<2 6% Unlikely
≥2 28% Likely
 Special Investigations
Test Advantages Disadvantages
Contrast “Gold standard” Invasive
Venography Sensitivity approaches 100% Requires specialized equipment
Easily interpretable Rare, but serious side effects

Magnetic Resonance Highly accurate Expensive

Imaging Safe during pregnancy Not readily available
Non-invasive
Computed Tomography Non-invasive Limited data
Can diagnose pelvic DVT
Concurrently exclude PE
Ultrasonography Highly accurate Not accurate for calf or pelvic DVT
Non-invasive Complete study is time consuming
D-Dimer Rapid laboratory study Only used to rule-out DVT
Can aide in exclusion of DVT
Ultrasonography
 Complications of DVT

 Risk factors for PTS

 Recurrent DVT
 Distal vein thrombosis
 Recently, persistently elevated D- dimers
 Pulmonary embolism
Postphlebitic syndrome/ Post Thrombotic
Syndrome (PTS)
Develops in 20- 30% of DVT
 A common complication that can occur after deep vein
thrombosis is known as postphlebitic syndrome, also called
postthrombotic syndrome.
 Damage to your veins from the blood clot reduces blood
flow in the affected areas, which can cause:
Persistent swelling of your legs (edema)
Leg pain
Skin discoloration
Skin sores
Differential diagnosis of DVT

 Hematoma
 Baker’s cyst
 Pulled muscle or tendons
 PTS
 Lymphedema
 Compartment syndrome
 Cardial, renal , hypoproteinemic edema
 Lymphangitis
 Erysipelas
 Superficial thrombophlebitis
 Lumbar and ischiatic pain
 Treatment of DVT
Initial Anticoagulation for Patients With
Acute DVT of the Leg

In patients with acute DVT of the leg treated with VKA therapy,
we recommend :
Initial treatment with parenteral anticoagulation
(LMWH, fondaparinux, IV UFH, or SC UFH) over
no such initial treatment (Grade 1B).
Treatment of DVT .

1. Blood thinners : Anticoagulants.

 Heparin is typically given intravenously
 Enoxaparin (Lovenox), dalteparin (Fragmin) or fondaparinux
(Arixtra), are injected under the skin.
 You might receive an injectable blood thinner for a few days,
after which pills such as warfarin (Coumadin, Jantoven) or
dabigatran (Pradaxa) are started. Once warfarin has thinned your
blood, the injectable blood thinners are stopped. If you take
warfarin, you'll need periodic blood tests to check how long it
takes your blood to clot.
 Other blood thinners can be given in pill form without the need
for an injectable blood thinner. These include rivaroxaban
(Xarelto), apixaban (Eliquis) or edoxaban (Savaysa).
2. Clot busters.
 If you have a more serious type of deep vein thrombosis
or pulmonary embolism, or if other medications aren't
working, your doctor might prescribe drugs that break up
clots quickly, called clot busters or thrombolytics.

3. Filters.
 A vena cava filter prevents clots that break loose
from lodging in your lungs.

4. Compression stockings.
 To help prevent swelling associated with
deep vein thrombosis, these are worn on your legs from
your feet to about the level of your knees.
In general :
 patients should be treated with anticoagulant therapy for a
minimum of 3 months.
 Patients with a reversible risk factor have a low risk of
recurrence after 3 months of anticoagulant therapy.
 In contrast, patients with idiopathic or unprovoked DVT who
are treated for only 3 months have a 10% to 27% risk of
recurrence in the year after anticoagulants are discontinued.
 Continuing warfarin after this period protects the patient
against future recurrence but also exposes the patient to the
risk of anticoagulant‐related bleeding.
Deep vein thrombosis (DVT) can be a killer.
That’s why you have to understand and
prevent DVT—at any age.
THANK YOU