1. DEEP VEIN
THROMBOSIS
Guide – Dr. Prof. P. M. Luka(MS)
Presented by – Dr. Abhinandan Patil

2. What Is Deep Vein
Thrombosis ?

3. DEFINITION
Deep vein thrombosis is the
formation of a blood clot in one
of the deep veins of the body,
usually in the leg.

4. IT IS LIKE ICEBERG DISEASE
Symptomatic deep vein thrombosis is
"tip of the iceberg"

5. EPIDEMIOLOGY
 Venous ThromboEmbolism related deaths
3,00,000/anum
 7% diagnosed and treated
 34% sudden pulmonary embolism
 59% as undected

6. INCIDENCE
 An annual incidence of symptomatic Venous
ThromboEmbolism as 117 per 100,000
persons .
 Venous ThromboEmbolism in hospitalized
patients has increased from 0.8% to 1.3% over a
period of 20 years (reported in 2005).

7. Without prophylaxis the incidence of deep vein
thrombosis 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.

8. ETIOLOGY

9. Virchow's triad
describes
three factors that are thought to
contribute to thrombosis

10. VIRCHOW TRIAD
 More than 100 years ago, Rudolf Virchow
described a triad of factors of -

12. VENOUS STASIS
 prolonged bed rest (4 days or more)
 A cast on the leg
 Limb paralysis from stroke
 spinal cord injury
 extended travel in a vehicle

13. HYPERCOAGULABILITY
 Surgery and trauma - 40% of all thrombo embolic
disease
 Malignancy
 increased estrogen
 Inherited disorders of coagulation -Deficiencies of
protein-S, protein-C, anti-thrombin III.
 Acquired disorders of coagulation- Nephrotic syndrome,
Anti-phospholipid antibodies


14. ENDOTHELIAL INJURY
 Trauma
 Surgery
 Invasive procedure
 Iatrogenic causes –
central venous catheters
 Subclavian
 Internal jugular lines
These lines cause of upper extremity DVT.

15. HYPERCOAGULABLE STATE OF
MALIGNANCY
 Up to 15% of cancer patients presents with VTE
VTE is not equally common in all types of
cancer.
 The highest incidence is found in mucin-
producing adenocarcinomas, pancreas and
gastrointestinal tract, lung cancer, and
ovarian cancer.

16. Cancer Site Prevalence (% )
Pancreas 28
Lung 27
Stomach 13
Colon 13
Breast premenopausal 1 –2
Breast postmenopausal 3 –8
Prostate 2
Unknown primary tumor 1

17. PATHOPHYSIOLOGY
 Vessel trauma stimulates the clotting cascade.
 Platelets aggregate at the site particularly when
venous stasis present
 Platelets and fibrin form the initial clot
 RBC are trapped in the fibrin meshwork

18.  The thrombus propagates in the direction of the
blood flow.
 Inflammation is triggered, causing tenderness,
swelling, and erythema.
 Pieces of thrombus may break loose and travel
through circulation- emboli.
 Fibroblasts eventually invade the thrombus,
scarring vein wall and destroying valves. Patency
may be restored valve damage is permanent,
affecting directional flow.

20.  Thrombophlebitis - a thrombus accompanied
by inflammation of the vein (phlebitis).
 Phlebothrombosis - refers to a thrombus with
minimal inflammation.
 Dislodgment and migration of a thrombus are
known as thromboembolism. Which is common
in phlebothrombosis.

21. PRESENTATION AND
PHYSICAL EXAMINATION
 Calf pain or tenderness, or both
 Swelling with pitting oedema
 Increased skin temperature and fever
 Superficial venous dilatation
 Cyanosis can occur with severe obstruction

22. Less frequent manifestations of venous thrombosis
include
 Phlegmasia alba dolens,
 Phlegmasia cerulea dolens, and
 Venous gangrene.
These are clinical spectrum of the same disorder.

23. PHLEGMASIA ALBA DOLENS
Thrombosis in only major deep venous
channels sparing collateral veins
Causing painful congestion and oedema of
leg, with lymphangitis
Which further increases
Oedema

24. PHLEGMASIA CERULEA DOLENS
Thrombosis extends to collateral veins.
congestions, massive fluid sequestration, edema

25. 40-60% also have capillary involvement
irreversible venous gangrene
hydrostatic pressure in arterial and venous
capillaries exceeds the oncotic pressure
fluid sequestration in the interstitium
Circulatory shock, and arterial insufficiency
which causes gangrene.

26.  c/f
 sudden severe pain , swelling, cyanosis
and edema of the affected limb.
 There is a high risk of massive
pulmonary embolism, even under
anticoagulation.
 Foot gangrene may also occur.
 An underlying malignancy is found in 50%
of cases. Usually, it occurs in those afflicted
by a life-threatening illness.

28. CLINICAL EXAMINATION
 Palpate distal pulses and evaluate capillary refill
to assess limb perfusion.
 Move and palpate all joints to detect acute
arthritis or other joint pathology.
 Neurologic evaluation may detect nerve root
irritation; sensory, motor, and reflex deficits
should be noted

29.  Homans sign: pain in the posterior calf or knee
with forced dorsiflexion of the foot.

30.  Moses sign
Gentle squeezing of the lower part of the
calf from side to side.
 Neuhofs sign
Thickening and deep tenderness elicited
while palpating deep in calf muscles.
 Lintons sign
After applying torniquet at
saphenofemoral junction patient made to
walk , then limb is elevated in supine
posation prominent superficial veins will
be observed.

31. Search for stigmata of PE such as
tachycardia (common)
tachypnea
chest findings (rare),
 exam for signs suggestive of underlying
predisposing factors.

32. WELLS CLINICAL PREDICTION
GUIDE
 It pre-test probability score
 Helpsin early risk stratification and
appropriate use of laboratory tests and
imaging modalities.
 wellscriteria is an additional tool to
diagnosis rather than being a stand-alone
test.

33. Variable Wells
Active cancer (rx within last 6 months or palliative) 1
Calf swelling >3 cm compared to other calf 1
Collateral superficial veins (non-varicose) 1
Pitting edema 1
Swelling of entire leg 1
Localized pain along distribution of deep venous system 1
Paralysis, paresis, or recent cast immobilization of lower extremities 1
Recently bedridden > 3 days, or major surgery requiring regional or
1
general anesthetic in past 12 weeks
Previously documented DVT 1
-2
Alternative diagnosis at least as likely deep vein thrombosis

34. Interpretation
 High probability: ≥ 3 (Prevalence of DVT - 53%)
 Moderate probability: 1-2 (Prevalence of DVT -
17%)
 Low probability: ≤ 0 (Prevalence of DVT - 5%)
 Adapted from Anand SS, et al. JAMA. 1998; 279
[14];1094

35. LIMITATIONS OF WELLS SCORE
It useful in secondary and tertiary care
centers, has not been properly validated for use
in primary care centers patients with the
suspicion of DVT.
 The performance of Wells score was decreased
when evaluating elderly patients or those with a
prior DVT or having those having other
comorbidities, which might be equivalent to
what is found in a primary care setting.

36. DIAGNOSTIC STUDIES
 Clinical examination alone is able to
confirm only 20-30% of cases of DVT
 Blood Tests
The D-dimer
 Imaging Studies

37. D-DIMER
 It specific 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

38. S OF FIBRIN,
PLASMIN
CLEAVES
FACTOR
XIIIA–CROSS-
LINKED
FIBRIN INTO
AN ARRAY OF
INTERMEDIA
TE FORMS.
THE D-DIMER
AND E
FRAGMENTS
ARE THE
RESULT OF
TERMINAL
FIBRIN
DEGRADATIO
N

39.  Various kits have a 93-95% sensitivity and about 50%
specificity in the diagnosis of thrombotic disease.
 False-positive 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

40.  It should be noted that since D-dimer assays
present a low specificity for DVT, the value of
this test should be limited to ruling out rather
than confirming the diagnosis of a DVT.

41. ALGORITHM FOR DIAGNOSTIC
IMAGING

42. IMAGING STUDIES
 Invasive
 venography,
 radiolabeled fibrinogen
 noninvasive
 ultrasound,
 plethysmography,
 MRI techniques

43. Venograph
y
VENOGRAM:
POPLITEAL
VEIN
THROMBOSIS

44. VENOGRAPHY
It detects thrombi in both calf and thigh
 It can conclude and exclude the diagnosis of DVT
when other objective testings are not conclusive.
 Advantages
 It is useful if the patient has a high clinical
probability of thrombosis and a negative
ultrasound.
 It is also valuable in symptomatic patients with
a history of prior thrombosis in whom the
ultrasound is non-diagnostic.

45. DISADVANTAGE
 It can primary cause of DVT in 3% of patients
who undergo this diagnostic procedure.
 An invasive and expensive.
 Although Venography was once considered the
gold standard for diagnosis of DVT, today it is
more commonly used in research environments
and less frequently utilized in clinical practice.

46. Nuclear Medicine Studies

47. 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.

48. PLETHYSMOGRAPHY
 Plethysmography measures change in lower
extremity volume in response to certain stimuli.

49. IMPEDANCE
PLETHYSMOGRAPHY
 Principle- Blood volume changes in the leg lead
to changes in electrical resistance.
 Venous return in the lower extremity is occluded
by inflation of a thigh cuff, and then the cuff is
released, resulting in a decrease in calf blood
volume. Any obstruction of the proximal veins
diminishes the volume change, which is detected
by measuring changes in electrical resistance
(impedance) over the calf.

50. ULTRASONOGRAPHY
 color-flow Duplex scanning is the 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.

51. CLINICAL LIMITATIONS
 Reader dependent
 Duplex scans are less likely to detect non-
occluding thrombi.
 During the second half of pregnancy, ultrasound
becomes less specific, because the gravid uterus
compresses the inferior vena cava, thereby
changing Doppler flow in the lower extremities.
 An inability to distinguish old clots from a
newly forming clot

52.  Lack of accuracy in detecting DVT in the pelvis
or the small vessels of the calf
 Lack of accuracy in detecting DVT in the
presence of obesity or significant edema

53. 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.
 MRI 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.

54. DIFFERENTIAL DIAGNOSIS
o Cellulitis
Thrombophlebitis
o Arthritis
Asymmetric peripheral edema secondary
to CHF, liver disease, renal failure, or
nephrotic syndrome
lymphangitis
Extrinsic compression of iliac vein
secondary to tumor, hematoma, or abscess
Hematoma
Lymphedema

55.  Muscle or soft tissue injury
Neurogenic pain
Postphlebitic syndrome
Ruptured Baker cyst
Stress fractures or other bony lesions
Superficial thrombophlebitis

56. MANAGEMENT
 Using the pretest probability score calculated
from the Wells Clinical Prediction rule, patients
are stratified into 3 risk groups—high, moderate,
or low.
 The results from duplex ultrasound are
incorporated as follows:
 If the patient is high or moderate risk and the
duplex ultrasound study is positive, treat for
DVT.

57.  If the duplex study is negative and the patient is low
risk, DVT has been ruled out.
• When discordance exists between the pretest
probability and the duplex study result, further
evaluation is required.
 If the patient is high risk but the ultrasound study
was negative, the patient still has a significant
probability of DVT

58.  a venogram to rule out a calf vein DVT
 surveillance with repeat clinical evaluation and
ultrasound in 1 week.
 results of a D-dimer assay to guide management
 If the patient is low risk but the ultrasound
study is positive, some authors recommend a
second confirmatory study such as a venogram
before treating for DVT

59. EMERGENCY DEPARTMANT
CARE
The primary objectives of the treatment of
DVT are to -
 prevent pulmonary embolism,
 reduce morbidity, and
 prevent or minimize the risk of developing the
postphlebitic syndrome.

60. GENERAL THERAPEUTIC
MEASURES :
 Bed rest .
 Encourage the patient to perform gentle foot &
leg exercises every hour.
 Increase fluid intake upto 2 l/day unless
contraindicated.
 Avoid deep palpation .

61. SPECIFIC TREATMENT :
 Anticoagulation
 Thrombolytic therapy for DVT
 Surgery for DVT
 Filters for DVT
 Compression stockings

62.  Initialtreatment of DVT is with 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.

63. ANTICOAGULATION
 Heparin prevents extension of the thrombus
 It is a heterogeneous mixture of polysaccharide
fragments with varying molecular weights but
with similar biological activity.

64. MECHANISM OF ACTION
 Heparin's anticoagulant effect is related directly
to its activation of antithrombin III.
 Antithrombin III, the body's primary
anticoagulant, inactivates thrombin and inhibits
the activity of activated factor X, factor IX in the
coagulation process.

65. Heparin: Mechanism of Action
Accelerates antithrombin III activity
Antithrombin III
(Heparin)
Factor X
Factor IXa
Ca2+, PL
Factor VIIIa
Factor Xa
Prothrombin Thrombin
Factor Va
Ca2+, PL

66. Side effects
• Bleeding
• Osteoporosis
• Thrombocytopenia
• Skins lesions- urticaria, papules, necrosis
• Hypoaldosteronism, hyperkalemia
CONTRAINDICATIONS-
• Bleeding disorders,
• Severe hypertension, threatened abortion, piles,
• large malignancies, tuberculosis’
• Ocular surgery and neurosurgery,
• Chronic alcoholics, cirrhosis, renal failure

67. 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.

68. LOW MOLECULAR WEIGHT
HEPARIN
 Selectively inhibit factor Xa .
 Superior bioavailability
 Superior or equivalent safety and efficacy
 Subcutaneous once- or twice-daily dosing
 No laboratory monitoring
 Less phlebotomy (no monitoring/no intravenous
line)
 Less thrombocytopenia

69.  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.

70. WARFARIN
 Interferes with hepatic synthesis of vitamin K-
dependent coagulation factors
 Dose must be individualized and adjusted to
maintain INR between 2-3
 Oral dose of 2-10 mg/d
 caution in active tuberculosis or diabetes;
patients with protein C or S deficiency are at risk
of developing skin necrosis

71. WARFARIN—MECHANISM OF ACTION
Vitamin K
VII
Synthesis of
IX Dysfunctiona
X l Coagulation
Factors
II
Warfarin

72. DRAWBACKS OF WARFARIN
THERAPY
 Delayed onset and offset of action.
 Frequent blood test monitoring required:
- the dose response is unpredictable,
- has a narrow therapeutic range
 Reversibility of anticoagulant affect is slow.
 Requires labor-intensive follow up, Expert dose
management, Frequent patient communication.

73. THROMBOLYTIC THERAPY FOR
DVT
Advantages include
 Prompt resolution of symptoms,
 Prevention of pulmonary embolism,
 Restoration of normal venous circulation,
 Preservation of venous valvular function,
 Prevention of postphlebitic syndrome.

74. DISADVANTAGE
Thrombolytic therapy does not prevent
clot propagation,
 rethrombosis, or
 subsequent embolization.
 Heparin therapy and oral anticoagulant therapy
always must followed after a course of
thrombolysis.

75.  Thrombolytic therapy is also not effective once the
thrombus is adherent and begins to organize
 The hemorrhagic complications of thrombolytic
therapy are about 3 times higher, including the small
but potentially fatal risk of intra-cerebral
hemorrhage.
 At present, therefore, thrombo-lysis should be
reserved for exceptional circumstances, such as
patients with limb-threatening ischemia caused by
phlegmasia cerulea dolens.

76. SURGERY FOR DVT
Indications
 when anticoagulant therapy is ineffective
 unsafe,
 contraindicated.
 The major surgical procedures for DVT are clot
removal and partial interruption of the inferior
vena cava to prevent pulmonary embolism.

77.  These pulmonary emboli removed at autopsy
look like casts of the deep veins of the leg where
they originated.

78. THIS PATIENT UNDERWENT A THROMBECTOMY. THE
THROMBUS HAS BEEN LAID OVER THE APPROXIMATE
LOCATION IN THE LEG VEINS WHERE IT DEVELOPED.

79. CATHETER-DIRECTED
THROMBOLYSIS
 Successful clot lysis in > 85%
 Better 1-yr patency,
 Long-term symptom resolution.

80. FIRST-GENERATION PCDT

81. NEW: SINGLE-SESSION PCDT
PowerPulse Isolated Thrombolysis

82. FILTERS FOR DVT
 Indications
 Contraindication to anticoagulation.
 Significant bleeding complication of
anticoagulation therapy.
 Pulmonary embolism with contraindication to
anticoagulation.
 Recurrent thrombo-embolic complication despite
adequate anticoagulation therapy.

83.  Inferior vena cava filters reduce the rate of
pulmonary embolism but have no effect on the
other complications of deep vein thrombosis.
Thrombolysis should be considered in patients
with major proximal vein thrombosis and
threatened venous infarction

85. PROPHYLAXIS
 Indicated in who underwent major abdominal
trauma or orthopaedic surgery or patient having
prolonged immobolization (> 3 days).
 Benefits of VTE Prophylaxis
 Improved patient outcomes
 Reduced costs

86. METHODS OF VTE PROPHYLAXIS
 Mechanical:
Graduated Compression Stockings
(GCS)
Intermittent Pneumatic Compression
Devices (IPC)
 Pharmacologic
Low molecular weight Heparin.(5000u sc
8hourly ) It inhibits factor Xa and IIA activity.

87. THANKS …