1. DEEP VENOUS THROMBOSIS
Prof. M.C.Bansal
MBBS;MS. MICOG . FICOG.
Founder Principal & Controller,
Jhalawar Medical College & Hospital , Jhalawar.
Ex Principal & controller ,
Mahatma Gandhi Medical College & Hospital,
Sitapura , Jaipur.

2. Definition
Deep venous thrombosis
is the formation of a semisolid coagulum within
flowing blood in any of the deep veins of the
body, usually in the lower limb or Pelvic veins.

3. VEINS OF LOWER LIMB
Superficial veins
Deep veins
Perforating veins
Superficial veins includes great and small sephanous veins and their
tributaries. They drain into deep veins through perforating veins.
The greater saphenous vein joins the femoral vein at a fixed point in
the groin 2.5 cm below and lateral to the pubic tubercle, and the lesser
saphenous vein terminates at a variable site in the popliteal fossa.
Blood passing up the superficial veins enters the deep veins at the
saphenopopliteal and saphenofemoral junctions..

4. Superficial
veins

5. Deep Calf Veins
The deep veins of the lower limb arise from
three pairs of venae commitantes, which
accompany the three cruralarteries(anterior and
posterior tibial and peroneal arteries)
These six veins intercommunicate and join in
the popliteal fossa to form the popliteal vein,
which also receives the soleal and gastrocnemius
veins.
.

6. Deep veins

7. Perforating Veins Of leg
Perforating veins- connect superficial
veins with deep veins.
Perforators- 1-adductor canal
perforator, 2-below knee peforator, 3-
medial perforator, 4-lateral perforator

8. Deep Veins of Thigh
The popliteal vein passes up through the adductor
hiatus to enter the subsartorial canal as the femoral
vein, which receives the deep (profunda) femoral
vein (or veins) in the femoral triangle before passing
behind the inguinal ligament to become the external
iliac vein.

9. Pelvic Veins (MAJOR )
 The internal iliac vein joins with the external
iliac vein in the pelvis to form the common
iliac vein.
The left common iliac vein passes behind the
right common iliac artery to join the right
common iliac vein on the right side of the
abdominal aorta to form the inferior vena cava.

10. ETIOLOGY
DVT usually originates in the lower
extremity venous system ,starting at
the calf vein and progressing proximally
to involve popliteal ,femoral ,or iliac
system.
80 -90 % pulmonary emboli originates
here .

11. Virchow’s triad
More than 100 years ago, Virchow described a triad of
factors for the development of venous thrombosis-
venous stasis,
endothelial damage, and
 hypercoagulable state

12. Venous stasis –Favoured by
 Age---Incidence increases with advancing age
 Obesity-- >BMI > is DVT
 Prolonged bed rest (4 days or more)
 A cast on the leg
 Limb paralysis from stroke or spinal cord injury
 Extended travel in a vehicle/Aeroplane

13. Hypercoagulability
Surgery and trauma are responsible for up to 40% of all
thromboembolic disease
Malignancy
Increased estrogen (due to a fall in protein ‘S) Increased
estrogen occurs during as in pregnancy and HRT,OCP
Taking women.
Hyper coagulabilty status
-Through out pregnancy—
-the first three months postpartum,
-after elective abortion, and
 during treatment with oral contraceptive pills

14. Inherited disorders of coagulation
 deficiencies of protein ‘S,
 protein ‘C,’ and
 antithrombin III.

15. Acquired disorders of
coagulation
nephrotic syndrome –
results in urinary loss of antithrombin III, this
diagnosis should be considered in children
presenting with thromboembolic disease
Antiphospholipid antibodies-
accelerate coagulation and include the lupus
anticoagulant and anticardiolipin antibodies.

16. >Inflammatory processes, such as
• systemic lupus erythematosus (SLE)
•sickle cell disease,
•inflammatory bowel disease (IBD),
also predispose to thrombosis, presumably due
to hyper coagulability
•

17. Endothelial Injury
Trauma,
 surgery, and
 invasive procedure may disrupt venous integrity
Iatrogenic causes of venous thrombosis are increasing
due to the widespread use of central venous catheters,
particularly subclavian and internal jugular lines. These
lines are an important cause of upper extremity DVT,
particularly in children . Femoral vein cannulation and
Vene section for Iv therapy (prolong duration )
predispose for DVT

18. Clinical Pathophysiology
-> An intimal defect often works sThe nidus works as a
nidus for clot is
Formation.
-> initially a platelet aggregate,
-ate develops .
->subsequently
clotting factors through
intrinsic and extrinsic
pathway fibrin and red cells
Cells form a mesh until the lumen
clot occludes the vein. wall occludes.

19. When a clot forms on an intimal defect, the coagulation
cascade promotes clot to growth proximally.
Thrombus can extend
from the superficial
veins into the deep
veins and after
detachment passes
through venacava,
through the right heart
and from which it can
embolize to one or
both the lungs via pulmonary arteries.

20. Opposing the coagulation cascade is the
endogenous fibrinolytic system. After the clot
organizes or dissolves, most veins will recanalize
in several weeks. Residual clots retract as
fibroblasts and capillary development lead to
intimal thickening.
 Venous hypertension and residual clot may
destroy valves, leading to the postphlebitic
syndrome, which develops within 5-10 years

21. Edema, sclerosis, and ulceration characterize this
syndrome, which develops in 40-80% of patients with
DVT.
 patients also can suffer exacerbations of swelling and pain,
probably as a result of venous dilatation and hypertension
Pulmonary embolism (PE) is a serious complication of
DVT. Many episodes of pulmonary embolism go
unrecognized, and at least 40% of patients with DVT have
clinically silent PE.

22. An Organised Clot (c) Thrombus ( T)

24. Presentation and Physical
Examination
Calf pain or tenderness, or both in one or both the lower limbs
Swelling with pitting edema
Swelling below knee in distal deep vein
thrombosis and up to groin in proximal
deep vein thrombosis
Increased skin temperature
Superficial venous dilatation
Cyanosis can occur with severe obstruction

25. DVT Both Legs

26. DVT—Left Leg

28. Venous thrombosis---causing venous
gangrene

29. Palpate distal pulses and evaluate capillary refill to
assess limb perfusion.
Move and palpate all joints to detect acute
arthritis or other joint pathology.
Homan’s test: pain in the posterior calf or knee
with forced dorsi flexion of the foot.

30. Moses Test: tenderness over calf muscles on
squeezing the muscles from side to side. Not
done now for the fear of embolism
Bilateral DVT is common, up to 30% of all
cases of DVT.
Bilateral DVT should be differentiated from
other systemic edema, such as hypo
protienaemia, renal failure and heart failure
etc.

31. Many patients report as they develop
respiratory symptoms of PE so search
for signs of PE such as plueritic chest
pain, haemoptysis,tachycardia
(common),tachypnea and central
cynosis.

35. Pelvic vein
thrombisis

41. venography
gold standard” modality for the diagnosis of
DVT
Advantages
Venography is also 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.

42. side effects
phlebitis
anaphylaxis

43. RADIOACTIVE FIBRINOGEN TEST
A fibrinogen uptake test is a test that
was used to detect deep vein thrombosis.
Radioactive labeled fibrinogen (I-131, I-
125) is given which is incorporated in
the thrombus. The thrombus can then be
detected by scintigraphy.

44. Plethysmography
Plethysmography measures change in lower extremity volume in
response to certain stimuli.
Impedance phlebography,
or impedance plethysmography (IPG), is a non-
invasive medical test that measures small changes in electrical
resistance of the calf.
These measurements reflect blood volume changes, and can
indirectly indicate the presence or absence of venous thrombosis.
This procedure provides an alternative to venography, which is
invasive and requires a great deal of skill to execute adequately
and interpret accurately.

45. 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.

46. Colour Dropller –Aeroes showing DVT

47. clinical limitations
expensive
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

48. Magnetic Resonance Imaging
It detects limb, 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.

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

50. Muscle or soft tissue injury
Neurogenic pain
Postphlebitic syndrome
Prolonged immobilization or limb
paralysis
Ruptured Baker cyst
Stress fractures or other bony lesions
Superficial thrombophlebitis
Varicose veins

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

52. If the patient is at high risk but the ultrasound study
was negative, the patient still has a significant
probability of DVT
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.

53. a venogram is done 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

54. 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.

55. LINE OF MANAGEMENT
Anticoagulation
Thrombolytic therapy for DVT
Surgery for DVT
Filters for DVT
Compression stockings

56. Anticoagulation
Heparin prevents extension of the
thrombus
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 in
the coagulation process.

57. Heparin is a heterogeneous mixture of
polysaccharide fragments with varying molecular
weights but with similar biological activity. The
larger fragments primarily interact with
antithrombin III to inhibit thrombin.
 The low molecular weight fragments exert their
anticoagulant effect by inhibiting the activity of
activated factor X.
The hemorrhagic complications attributed to
heparin are thought to arise from the larger higher
molecular weight fragments.

58. The optimal regimen for the treatment of
DVT is anticoagulation with heparin or a
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.

59. After an initial bolus of 100 U/kg, a
constant maintenance infusion of 20 U/kg is
initiated. The aPTT is checked 6 hours after
the bolus and adjusted accordingly. .
The aPTT is repeated every 6 hours until 2
successive aPTTs are therapeutic.
Thereafter, the aPTT is monitored every 24
hours as well as the hematocrit and platelet
count.

60. Advantages of Low-Molecular-Weight Heparin Over
Standard Unfractionated Heparin
Superior bioavailability
Superior or equivalent safety and efficacy
Subcutaneous once- or twice-daily dosing
Less phlebotomy (no monitoring/no intravenous
line)
Less thrombocytopenia
Results are Earlier

61. At the present time, 3 LMWH
preparations,
Enoxaparin,
Dalteparin, and
Ardeparin

62. 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 2-10 mg/day
caution in active tuberculosis or diabetes;
patients with protein C or S deficiency are at risk
of developing skin necrosis.

63. Duration of anticoagulation in patients with deep
vein thrombosis
Transient cause and no other risk factors:
3 months
Idiopathic: 3-6 months
Ongoing risk for example, malignancy: 6 -
12 months
Recurrent pulmonary embolism or deep vein
thrombosis: 6-12 months
Patients with high risk of recurrent thrombosis :
indefinite duration.

64. COMPLICATIONS
Acute pulmonary embolism
 Hemorrhagic complications
Chronic venous insufficiency

65. Thrombolytic therapy for DVT
Streptokinase
Urokinase
Advantages
prompt resolution of symptoms,
prevention of pulmonary embolism,
restoration of normal venous circulation,
preservation of venous valvular function,
and prevention of postphlebitic syndrome.
Heparin therapy and oral anticoagulant therapy always must
follow a course of thrombolytics.

66. Thrombolytic therapy is not effective once the
thrombus is adherent and begins to organize
The hemorrhagic complications of
thrombolytic therapy are formidable (about 3
times higher), including the small but
potentially fatal risk of intracerebral
hemorrhage.

67. Surgery for DVT
Indications
 when anticoagulant therapy is ineffective
 or unsafe,
 contraindicated.
The major surgical procedures for DVT are clot
removal (venous thrombectomy),femoral vein ligation
and partial interruption of the inferior vena cava
(insertion of inferior venacava filters) to prevent
pulmonary embolism.

68. Filters for DVT
Indications for insertion of an inferior vena
cava filter
Pulmonary embolism with contraindication to
anticoagulation
Recurrent pulmonary embolism despite adequate
anticoagulation

69. Deep vein thrombosis with
contraindication to anticoagulation
Deep vein thrombosis in patients with
pre-existing pulmonary hypertension
Free floating thrombus in proximal vein
Failure of existing filter device
Post pulmonary embolectomy

70. 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

71. Clot Filter in IVC

72. Compression stockings
(routinely recommended

73. Prognosis
All patients with proximal vein DVT are at long-
term risk of developing chronic venous
insufficiency.
About 20% of untreated proximal (above the calf)
DVTs progress to pulmonary emboli, and 10-20%
of these are fatal. With aggressive anticoagulant
therapy, the mortality is decreased 5- to 10-fold.
DVT confined to the calf virtually never causes
clinically significant emboli and thus does not
require anticoagulation

74. PROPHYLAXIS
Identify any patient who is at risk.
Prevent dehydration.
During operation avoid prolonged calf
compression.
Passive leg exercises should be encouraged
whilst patient on bed.
Foot end of bed should be elevated to increase
venous return.

75. VTE in pregnancy

76. Diagnosis

77. D-DIMER

78. Compression ultrasonography

79. CT Pulmonary angiography
vs. V/Q scan

80. CT Pulmonary angiography
vs. V/Q scan

81. Treatment of VTE during pregnancy

82. Treatment of VTE during pregnancy

83. Treatment of VTE during pregnancy

84. Treatment of VTE during pregnancy

85. Treatment of VTE during pregnancy

86. Anticougulant therapy during
labour and delivery

87. Anticougulant therapy during
labour and delivery

89. Thrombolytic therapy

90. Vena cava filters

91. Prevention of VTE in pregnant women
with previousVTE

93. stesis of bloosd flow---Pelvi congestion syndrome
---prone to get thrombosed