DEEP VEIN

THROMBOSIS
P resenter – D r. SA M R AT S H R E ST HA
DEFINITION
• DVT is formation of blood clot in one of deep veins
of body, usually in leg.

• Acute DVT is a major cause of morbidity and

mortality in hospitalized patient, particularly in
surgical patient.

• Triad of venous stasis, endothelial injury, and

hypercoagulable state, first posited by Virchow in
1856

• Most dreaded sequel to acute DVTPulmonary

embolism
 EPIDEMIOLOGY

• Venous thromboembolism occurs for the first time in

approximately 100 persons/100,000 each year in US.

• Incidence increases with increasing age, with an

incidence of 0.5%/100,000 at 80 years of age.

• More than 2/3RD of these patients have DVT alone,

and rest have evidence of PE
• Recurrence rate with anticoagulation has been
noted to be 6% to 7% in the ensuing 6 months.

• In US, PE causes 50,000 to 200,000 deaths

annually.

• A 28-day case-fatality rate of 9.4% after first-time

DVT and of 15.1% after first-time PE.
Without prophylaxis the incidence of DVT
is about

 14% in gynaecological surgery

 22% in neurosurgery

 26% in abdominal surgery

 45%-60% in patients undergoing hip and

knee surgeries.

 15% to 40% Urologic surgery.

V IR C H OW TR IA D
𝗈 More than 100 years ago, Rudolf Virchow
described a triad of factors of -
 V E N O U S S TA S I S
• Labeled fibrinogen studies in patients as well as in
autopsy studies have demonstrated convincingly that
soleal sinuses are the most common sites of initiation
of venous thrombosis.

• Stasis may contribute to endothelial cellular layer

contacting activated platelets and procoagulant factors,
thereby leading to DVT.

• Stasis, in and of itself, has never been shown to be a

causative factor for DVT.
HYPERCOAGULABILIT
Y

• Postoperative patient, after major surgery, is predisposed

to formation of DVT.

• After major operations, large amounts of tissue factor may

be released into bloodstream from damaged tissues.
• Tissue factor is a potent procoagulant expressed on
leukocyte cell surface as well as in a soluble form
in bloodstream.

• Factor for increased risk for thrombosis.

1. Increase in platelet count
2. Adhesiveness
3. Changes in coagulation cascade
4. Endogenous fibrinolytic activity result from
physiologic stress, such as major operation or
trauma
E N D O T H E L I A L I N J U RY
• Mechanical injury to the vein:

1. Trauma
2. Surgery
3. Peripherally inserted venous catheters
4. Previous DVT
5. Intravenous drug abuse
P R E S E N TAT I O N A N D
P H Y S I C A L E X A M I N AT I O N
• Calf pain or tenderness, or both

• Swelling with pitti ng edema

• Increased skin temperature and fever

• Superficial venous dilatation

• Cyanosis can occur with severe obstruction

Less frequent manifestations of venous
thrombosis include
• Phlegmasia alba dolens

• Phlegmasia cerulea dolens

• Venous gangrene.
PHLEGMASIA ALBA DO LENS

Thrombosis in only major deep venous

channels sparing collateral veins

Causing painful congestion and oedema of

leg, with lymphangitis

Which further increases

Oedema
PHLEGMASIA CERULEA DOLENS

Thrombosis extends to collateral veins.

congestions, massive fluid sequestration, edema

40-60% also have capillary involvement
irreversible venous gangrene

Hydrostati c pressure in arterial and

venous capillaries exceeds the oncoti c
pressure

fl uid sequestration in the interstitium

Circulatory shock, and arterial

insuffi ciency which causes gangrene.
Clinical Feature:
• Sudden severe pain , swelling, cyanosis and
edema of the affected limb.
• High risk of massive pulmonary embolism, even
under anti coagulati on.
• Foot gangrene may also occur.
• Underlying malignancy is found in 50% of cases
C L I N I C A L E X A M I N AT I O N
𝗈 Palpate distal pulses and evaluate capillary refill to
assess limb perfusion.
𝗈 Move and palpate all joints to detect acute
arthritis or other joint pathology.
𝗈 Neurologic evaluation may detect nerve root
irritation; sensory, motor, and reflex deficits
should be noted
 Homans sign
Pain in posterior calf or knee with forced dorsiflexion of foot.

Absence of this sign is not a reliable indicator of absence of

venous thrombus

Presence of Homan sign should prompt one to attempt to

confirm diagnosis.
❑ Moses sign
Gentle squeezing of lower part of calf from side to
side.

❑ Neuhofs sign
Thickening and deep tenderness elicited while
palpating deep in calf muscles.

❑ Lintonssign
After applying torniquet at SFJ patient made to
walk ,then limb is elevated in supine position
prominent superficial veins will be observed.
WELLS CLINICAL PREDICTION GUIDE

𝗈 It pre-test probability score

𝗈 H elps in early risk stratification and appropriate

use of laboratory tests and imaging modalities.

𝗈 wells criteria is an additional tool to diagnosis

rather than being a stand-alone test.
Interpretati on

𝗈 High probability: ≥ 3 (Prevalence of DVT - 53%)

𝗈 Moderate probability: 1-2 (Prevalence of DVT -

17%)
𝗈 Low probability: ≤ 0 (Prevalence of DVT - 5%)

𝗈 Adapted from Anand SS, et al. JAMA. 1998; 279

[14];1094
 DIAGNOSTIC STUDIES

𝗈 C linical examination alone is able to

confirm only 20-30% of cases of DV T

𝗈 B lood Tests
D-dimer

𝗈 Imaging
Studies
D -DIM E R
❑ Itspecific degradation product of cross-linked
fibrin.

❑ Because concurrent production and breakdown of

clot characterize thrombosis, patients with
thromboembolic disease have elevated levels of
D-dimer.

❑ Three major approaches for measuring D-dimer

➢ ELISA
➢ latex agglutination
➢ blood agglutination test
𝗈 Various kits have a 93-95% sensitivity and about 50%
specificity in the diagnosis of thrombotic disease.

 False-positi ve D-dimers occur in patients with

➢ recent (within 10 days) surgery or trauma,

recent myocardial infarction or stroke, acute
➢
infection,
➢ disseminated intravascular coagulation,
➢ pregnancy or recent delivery,
➢ active collagen vascular disease, or metastatic cancer
➢
ALGORITHM FOR
DIAGNOSTIC IMAGING
IMAGING
STUDIES
𝗈Invasive
➢ venography,

➢ radiolabeled fibrinogen
𝗈 Noninvasive

➢ Ultrasound,

➢ Plethysmography,

➢ M RI techniques
Venography

VENOGRAM:
POPLITEAL VEIN
TH R O M B O S IS
VENOGRAPHY

𝗈It detects thrombi in both calf and thigh

𝗈 It can conclude and exclude the diagnosis of DVT
when other objective testings are not conclusive.

𝗈 Advantages
𝗈 It is useful if patient has a high clinical probability of

thrombosis and a negative ultrasound.

𝗈 It is also valuable in symptomatic patients with a

history of prior thrombosis in whom ultrasound is
non-diagnostic.
D I S A D VA N TA G
E

𝗈 It can primary cause of DVT in 3% of patients

who undergo this diagnostic procedure.

𝗈 An invasive and expensive.

Nuclear Medicine Studies
NUCLEAR MEDICINE
STUDIES

❑ Because the radioactive isotope incorporates into a

growing thrombus, this test can distinguish new
clot from an old clot.

❑ Nuclear medicine studies done with I125-labeled

fibrinogen .

❑ More commonly used in research.

PLETHYSMOGRAPH
Y
𝗈 Plethysmography measures change in lower
extremity volume in response to certain stimuli.
 IMPEDANCE
P L E THYS M O G R AP H Y
▪ Principle- Blood volume changes in leg lead to
changes in electrical resistance.
• Venous return in lower extremity is occluded by
inflation of a thigh cuff

• Cuff is released, resulting in a decrease in calf

blood volume.

• Any obstruction of proximal veins diminishes

volume change, which is detected by measuring
changes in electrical resistance (impedance) over
calf.
U LTR AS ON O G R AP H Y
• Color-flow Duplex scanning is imaging test of
choice for patients with suspected DVT

• Inexpensive, noninvasive, widely available

• Ultrasound can also distinguish other causes of

leg swelling, such as tumor, popliteal cyst,
abscess, aneurysm, or hematoma.
C L I N I C A L L I M I TAT I O N S
• Reader dependent

• Duplex scans are less likely to detect non- occluding

thrombi.

• During second half of pregnancy, ultrasound

becomes less specific, because the gravid uterus
compresses the inferior vena cava, thereby changing
Doppler flow in lower extremities.

• An inability to distinguish old clots from a newly

forming clot
MAGNETIC RESONANCE IMAGING
• It detects leg, pelvis, and pulmonary thrombi and is 97%
sensitive and 95% specific for DVT.

• It distinguishes a mature from an immature clot.

• M R I is safe in all stages of pregnancy.

• Test may not be appropriate for patients with pacemakers

or other metallic implants, it can be an effective diagnostic
option for some patients.
D I F F E R E N T I A L DI AGNOSI S
o Cellulitis
o Thrombophlebitis
o Arthritis
o Asymmetric
peripheral edema
secondary to
C H F, liver
disease, renal
failure, or
nephrotic
syndrome
o Lymphangitis
o Extrinsic
EM ER G E NC Y D E P A R TM A N T C A R E

The primary objecti ves of the treatment of

DV T are to:

• Prevent pulmonary embolism

• Reduce morbidity, and

• Prevent or minimize the risk of developing

postphlebitic syndrome.
GENERAL THERAPEUTIC MEASURES :

𝗈 Bed rest .

𝗈 Encourage the patient to perform gentle foot & leg

exercises every hour.

𝗈 Increase fluid intake upto 2 l/day unless

contraindicated.

𝗈 Avoid deep palpation .

S P E C I F I C TREATMENT :

𝗈 Anticoagulation

𝗈 Thrombolytic therapy for DVT

𝗈 Surgery for DVT

𝗈 Filters for DVT

𝗈 Compression stockings
𝗈 Initial treatment of D V T:
Low- molecular-weight heparin or
unfractionated heparin for at least 5 days,
followed by warfarin (target INR, 2.0–3.0)
for at least 3 months.
 A N T I C O A G U L AT I O
N
 Heparin prevents extension of the thrombus

 Heterogeneous mixture of polysaccharide fragments

with varying molecular weights but with similar
biological activity.
MECHANISM OF
ACTION
𝗈 Heparin's anticoagulant effect is related directly to
its activation of antithrombin III.

𝗈 Antithrombin III, the body's primary anticoagulant,

inactivates thrombin and inhibits activity of
activated factor X , factor I X in coagulation process.
Heparin: Mechanism of Action
Accelerates antithrombin III activity
Antithrombin III
(Heparin)
Factor X
Factor IXa
Factor VIIIa Ca 2+, PL

Factor Xa
Prothrombin Thrombin
Factor Va
Ca2+, PL
 S i d e eff ects
• Bleeding
Osteoporosis
•
Thrombocytopenia
• Skins lesions- urticaria, papules, necrosis
• Hypoaldosteronism, hyperkalemia
•
C O N T R A I N D I C AT I O N S -
• Bleeding disorders,
Severe hypertension, threatened abortion, piles,
•
large malignancies, tuberculosis’
• Ocular surgery and neurosurgery, Chronic
• alcoholics, cirrhosis, renal failure
DOSE
❑ IV bolus dose of 5,000 to 10,000 units
followed by an infusion of 1,000 units per hour.

Other method of initiating therapy is to begin

with
❑ Loading dose of 50-100 units/kg of heparin

followed by a constant infusion of 15-25

units/kg/hr.
LOW M O L E C U L A R W E I G H T H E PA R I N

𝗈 Selectively inhibit factor X a .

𝗈 Superior bioavailability

𝗈 Superior or equivalent safety and efficacy

𝗈 Subcutaneous once- or twice-daily dosing

𝗈 No laboratory monitoring

𝗈 Less phlebotomy (no monitoring/no intravenous

line)
𝗈 Less thrombocytopenia
𝗈 The optimal regimen for the treatment of DVT is
anticoagulation with heparin or an L M W H
followed by full anticoagulation with oral warfarin
for 3-6 months

𝗈 Warfarin therapy is overlapped with heparin for 4-5

days until the I N R is therapeutically elevated to
between 2-3.
W A R FA R I N

𝗈 Interferes with hepatic synthesis of vitamin K-

dependent coagulation factors

𝗈 Dose must be individualized and adjusted to

maintain I N R between 2-3

𝗈 Oral dose of 2-10 mg/d

𝗈 Caution in active tuberculosis or diabetes; patients

with protein C or S deficiency are at risk of
developing skin necrosis
D R A W B A C K S O F WA R FA R I N
THERAPY
𝗈 Delayed onset and offset of action.

❑ Frequent blood test monitoring required:

- the dose response is unpredictable,
- has a narrow therapeutic range

𝗈 Reversibility of anticoagulant affect is slow.

𝗈 Requires intensive follow up, Expert dose

management, Frequent patient communication.
T H R O M B O LY T I C T H E R A P Y F O R
DV T

Advantages include
𝗈 Prompt resolution of symptoms,
𝗈 Prevention of pulmonary embolism,

𝗈 Restoration of normal venous circulation,

𝗈 Preservation of venous valvular function,

𝗈 Prevention of postphlebitic syndrome.

𝗈 Thrombolytic therapy is also not effective once thrombus is
adherent and begins to organize

𝗈 The hemorrhagic complications of thrombolytic therapy

are about 3 times higher, including small but potentially
fatal risk of intra-cerebral hemorrhage.
At present, therefore, thrombo-lysis should be
𝗈 reserved for exceptional circumstances, such as
patients with limb-threatening ischemia caused by
phlegmasia cerulea dolens.
S U R G E RY F O R
DVT
Indications
𝗈 when anticoagulant therapy is ineffective

𝗈 unsafe,

𝗈 contraindicated.

𝗈 The major surgical procedures for DVT are clot

removal and partial interruption of the inferior

vena cava to prevent pulmonary embolism.
𝗈 These pulmonary emboli removed at autopsy
look like casts of the deep veins of the leg where
they originated.
T H I S PATIENT U N D E RW E N T A T H RO M B E C TO M Y. T H E
T H RO M B U S H AS B E E N LA I D O V E R T H E A P P ROX I M AT E
L O C AT I O N I N T H E L E G V E I N S W H E R E IT D E V E L O P E D.
CATHETE R-
D IR E C T E D
T H R O M B O LY S I S

𝗈 Successful clot lysis in > 85%

𝗈 Better 1-yr patency,

𝗈 Long-term symptom resolution.

F I R S T- G E N E R AT I O N P C D T ( Pharmacomechanical,
catheter-directed thrombolysis)
 NEW: S I N G L E - S E S S I O N
PCDT

PowerPulse Isolated Thrombolysis

F I LT E R S F O R DV T

• IVC Filters reduce the rate of PE but have no effect on

the other complications of DVT.

• Thrombolysis should be considered in patients with

major proximal vein thrombosis and threatened
venous infarction
PR OPH YLAXI
S

𝗈 Indicated in who underwent major abdominal

trauma or orthopaedic surgery or patient having
prolonged immobolization (> 3 days).

𝗈 Benefits of V T E Prophylaxis
● Improved patient outcomes

● Reduced costs
METHODS OF VTE PROPHYLAXIS
𝗈 Mechanical:
●Graduated Compression Stockings (GCS)
●Intermittent Pneumatic Compression
Devices (IPC)

𝗈 Pharmacologic
Low molecular weight Heparin.(5000u sc
8hourly ) It inhibits factor Xa and IIA activity.
THANK YOU