ppt

1. DEEP VENOUS THROMBOSIS
DR.SHERAZ AHMED

2. Definition
• Deep vein thrombosis is the
formation of a blood clot in one
of the deep veins of the body,
usually in the leg

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

4. Virchow tried
• More than 100 years ago, Virchow
described a triad of factors of
–venous stasis,
–endothelial damage, and
–hypercoagulable state

5. Venous stasis
• Prolonged bed rest (4 days or more)
• Extended travel in a vehicle
• Limb paralysis from stroke or spinal cord
injury
• A cast on the leg

6. Hypercoagulability
• Surgery and trauma responsible for up to 40%
of all thromboembolic disease
• Malignancy
• Increased estrogen (due to a fall in protein ‘S)
Increased estrogen occurs during
• All stages of pregnancy—
• The first three months postpartum,
• After elective abortion, and
• During treatment with oral contraceptive pills

7. Inherited disorders of
coagulation
Deficiencies of
 protein ‘S’,
 protein ‘C’, and
 antithrombin III.

8. 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.

9. Inflammatory processes, such as
• systemic lupus erythematosus (SLE),
• sickle cell disease, and
• inflammatory bowel disease (IBD),
also predispose to thrombosis, presumably
due to hypercoagulability

10. 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.

11. Clinical Pathophysiology
• The nidus for a clot is often an intimal
defect
• When a clot forms on an intimal defect,
the coagulation cascade promotes clot
growth proximally.
• Thrombus can extend from the superficial
veins into the deep system from which it
can embolize to the lungs.

12. • 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

13. • 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 on VQ
scanning

14. Presentation and Physical
Examination
• Calf pain or tenderness, or both
• Swelling with pitting oedema
• Swelling below knee in distal DVT and
up to groin in proximal DVT
• Increased skin temperature
• Superficial venous dilatation
• Cyanosis can occur with severe
obstruction

15. • 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
• Homans'’ sign: pain in the posterior calf or
knee with forced dorsiflexion of the foot

16. • Search for stigmata of PE such as
tachycardia (common), tachypnea or
chest findings (rare), and
• Exam for signs suggestive of underlying
predisposing factors.

17. Wells Clinical Prediction Guide
• The Wells clinical prediction guide
incorporates risk factors, clinical signs, and
the presence or absence of alternative
diagnoses
• Wells Clinical Prediction Guide for DVT
Clinical Parameter Score
• Active cancer (treatment ongoing, or within
6 months or palliative)1
• Paralysis or recent plaster immobilization 1
• Recently bedridden for >3 days or major
surgery <4 weeks1

18. • Localized tenderness along the distribution
of the deep venous system1
• Entire leg swelling1
• Calf swelling >3 cm compared to the
asymptomatic leg 1
• Pitting edema (greater in the symptomatic
leg)1
• Collateral superficial veins (nonvaricose)1
• Alternative diagnosis (as likely or > that of
DVT)

19. • Total of Above Score
High probability: Score >3
Moderate probability: Score = 1 or 2
Low probability: Score = 0
• Adapted from Anand SS, et al. JAMA.
1998; 279 [14];1094

20. Diagnostic Studies
• Clinical examination alone is able to confirm
only 20-30% of cases of DVT
• Blood Tests
• The D-dimer
• INR.
• Current D-dimer assays have predictive value
for DVT, and the
• INR is useful for guiding the management of
patients with known DVT who are on
warfarin (Coumadin)

21. D-dimer
• D-dimer is a 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 (SimpliRED

22. • 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

23. Imaging Studies
• Invasive
venography,
radiolabeled fibrinogen and.
• Noninvasive
ultrasound,
plethysmography,
MRI techniques

24. 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.

25. side effects
• phlebitis
• anaphylaxis

26. Nuclear Medicine Studies
• Because the radioactive isotope incorporates
into a growing thrombus, this test can
distinguish new clot from an old clot
Plethysmography
• Plethysmography measures change in lower
extremity volume in response to certain
stimuli.

27. 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.

28. 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

29. 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.

30. Differential diagnosis
Cellulitis
Thrombophlebitis
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

31. Hematoma
Lymphedema
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

32. 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.

33. • 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

34. • 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

35. 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.

36. • Anticoagulation
• Thrombolytic therapy for DVT
• Surgery for DVT
• Filters for DVT
• Compression stockings

37. 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.

38. • 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.

39. • The hemorrhagic complications attributed
to heparin are thought to arise from the
larger higher molecular weight fragments.
• 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.

40. • After an initial bolus of 80 U/kg, a
constant maintenance infusion of 18
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.

41. Advantages of Low-Molecular-
Weight Heparin Over
Standard Unfractionated Heparin
• 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
• Earlier/facilitated

42. At the present time, 3 LMWH
preparations,
• Enoxaparin,
• Dalteparin, and
• Ardeparin

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

44. Thrombolytic therapy for DVT
• Advantages include:
Prompt resolution of symptoms,
Prevention of pulmonary embolism,
Restoration of normal venous circulation,
Preservation of venous valvular function,
And prevention of postphlebitic syndrome.

45. Thrombolytic therapy does not prevent
 Clot propagation,
 Rethrombosis, or
 Subsequent embolization.
 Heparin therapy and oral anticoagulant therapy
always must follow a course of thrombolysis.

46. • Thrombolytic therapy is also 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.
• The uncertainty regarding thrombolytic therapy likely
will continue

47. 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.

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

49. This patient underwent a thrombectomy.
The thrombus has been laid over the
approximate location in the leg veins where
it developed.

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

51. Controversial indications:
• 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

52. • 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

53. Compression stockings
(routinely recommended

54. Further Inpatient Care
• Most patients with confirmed proximal vein DVT may be
treated safely on an outpatient basis.
• Exclusion criteria for outpatient management are as follows:
– Suspected or proven concomitant pulmonary embolism
– Significant cardiovascular or pulmonary comorbidity
– Morbid obesity
– Renal failure
– Unavailable or unable to arrange close follow-up care

55. • Patients are treated with a low molecular
weight heparin and
• instructed to initiate therapy with warfarin 5
mg PO the next day.
• Low molecular weight heparin and warfarin
are overlapped for about 5 days until the
international normalized ratio (INR) is
therapeutic.

56. • If inpatient treatment is necessary, low
molecular weight heparin is effective and
obviates the need for IV infusions or serial
monitoring of the PTT.
• With the introduction of low molecular weight
heparin, selected patients qualify for
outpatient treatment only if adequate home
care and close medical follow-up care can be
arranged.

57. • Platelets also should be monitored and
heparin discontinued if platelets fall below
75,000.
• While on warfarin, the prothrombin time (PT)
must be monitored daily until target achieved,
then weekly for several weeks.

58. • When the patient is stable, monitor monthly.
• Significant bleeding (i.e., hematemesis,
hematuria, gastrointestinal hemorrhage)
should be investigated thoroughly
• since anticoagulant therapy may unmask a
preexisting disease (e.g., cancer, peptic ulcer
disease, arteriovenous malformation).

59. Duration of anticoagulation in patients with
dDVT
• Transient cause and no other RFs: 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
exceeding risk of anticoagulation: indefinite duration

60. Further Outpatient Care:
• Patients with suspected or diagnosed isolated calf
vein DVT may be discharged safely on a NSAID or
aspirin with close follow-up care and repeat
diagnostic studies in 3-7 days to detect proximal
extension.
• At certain centers, patients with isolated calf vein
DVT are admitted for full anticoagulant therapy.

61. • Patients with suspected DVT but negative
noninvasive studies need to be reassessed by their
primary care provider within 3-7 days.
• Patients with ongoing risk factors may need to be
restudied at that time to detect proximal extension
• because of the limited accuracy of noninvasive tests
for calf vein DVT.

62. Complications
• Acute pulmonary embolism
• Hemorrhagic complications
• Chronic venous insufficiency

63. 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

64. Patient Education:
• Advise women taking estrogen of the
risks and common symptoms of
thromboembolic disease.
• Discourage prolonged immobility,
particularly on plane rides and long car
trips

65. 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 of bed should be elevated to increase venous
return.
• Early mobilization should be rule for all surgical patients.