Deep vein thrombosis

DVT

1. DR. NAWIN KUMAR

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

3. DVT ususally 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. More than 100 years ago, Virchow described
a triad of factors of
venous stasis,
endothelial damage, and
 hypercoagulable state

5. 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

6. 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. 
deficiencies of protein ‘S,
’ protein ‘C,’ and
 antithrombin III.

8. 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. 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. 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. Calf pain or tenderness, or both
Swelling with pitting oedema
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

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.

18. The Wells clinical prediction guide
incorporates risk factors, clinical signs,
and the presence or absence of
alternative diagnoses
. Wells Clinical Prediction Guide for
DVTClinical ParameterScore
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

19. 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)

20. Total of Above Score
High probability: Score ³3
Moderate probability: Score = 1 or 2
Low probability: Score £0
Adapted from Anand SS, et al. JAMA. 1998;
279 [14];1094

21. 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)

22. 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

23. 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

24. Invasive
 venography,
radiolabeled fibrinogen and.
 noninvasive
ultrasound,
plethysmography,
MRI techniques

25. 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.

26. phlebitis
anaphylaxis

28. Because the radioactive isotope incorporates
into a growing thrombus, this test can
distinguish new clot from an old clot

29. Plethysmography measures change in lower
extremity volume in response to certain
stimuli.

30. 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.     

31. 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

32. 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.

33. oCellulitis
Thrombophlebitis
oArthritis
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

34. 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

35. 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.

36. 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

37. 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

38. 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.

39. Anticoagulation
Thrombolytic therapy for DVT
Surgery for DVT
Filters for DVT
Compression stockings

40. 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.

41. 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.

42. 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.

43. 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.

44. 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

45. At the present time, 3 LMWH preparations,
Enoxaparin,
Dalteparin, and
Ardeparin

46.  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

47. 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.

48. Thrombolytic therapy does not prevent
clot propagation,
 rethrombosis, or
 subsequent embolization.
 Heparin therapy and oral anticoagulant
therapy always must follow a course of
thrombolysis.

49. 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

50.  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.

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

53. Indications for insertion of an inferior vena
cava filter
Pulmonary embolism with contraindication to
anticoagulation
Recurrent pulmonary embolism despite
adequate anticoagulation

54. 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

55. 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

58. 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

59. 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.
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.

60. 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. When the patient is
stable, monitor monthly.
Significant bleeding (ie, hematemesis, hematuria,
gastrointestinal hemorrhage) should be investigated
thoroughly since anticoagulant therapy may unmask
a preexisting disease (eg, cancer, peptic ulcer
disease, arteriovenous malformation).

61. 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 exceeding risk of anticoagulation:
indefinite duration (subject to review)

62. Patients with suspected or diagnosed isolated
calf vein DVT may be discharged safely on a
nonsteroidal anti-inflammatory drug (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.

63. 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.

64. Acute pulmonary embolism
 Hemorrhagic complications
Chronic venous insufficiency

65. 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

66. Advise women taking estrogen of the risks
and common symptoms of thromboembolic
disease.
Discourage prolonged immobility,
particularly on plane rides and long car trips

67. Ideidentify any patiant who is at risk.
Prevent dehydration.
During operation avoid prolonged calf
compression.
Passive leg exercises should be encourged
whilst patient on bed.
Foot of bed should be elevated to increase
venous return.
Early mobilization should be rule for all
surgical patients.