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DEEP VENOUS THROMBOSIS
DR.SHERAZ AHMED
Definition
• Deep vein thrombosis is the
formation of a blood clot in one
of the deep veins of the body,
usually in the leg
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 .
Virchow tried
• More than 100 years ago, Virchow
described a triad of factors of
–venous stasis,
–endothelial damage, and
–hypercoagulable state
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
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
Inherited disorders of
coagulation
Deficiencies of
 protein ‘S’,
 protein ‘C’, and
 antithrombin III.
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.
Inflammatory processes, such as
• systemic lupus erythematosus (SLE),
• sickle cell disease, and
• inflammatory bowel disease (IBD),
also predispose to thrombosis, presumably
due to hypercoagulability
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.
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.
• 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
• 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
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
• 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
• Search for stigmata of PE such as
tachycardia (common), tachypnea or
chest findings (rare), and
• Exam for signs suggestive of underlying
predisposing factors.
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
• 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)
• 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
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)
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
• 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
Imaging Studies
• Invasive
venography,
radiolabeled fibrinogen and.
• Noninvasive
ultrasound,
plethysmography,
MRI techniques
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.
side effects
• phlebitis
• anaphylaxis
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.
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.
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
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.
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
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
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.
• 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
• 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
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.
• Anticoagulation
• Thrombolytic therapy for DVT
• Surgery for DVT
• Filters for DVT
• Compression stockings
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.
• 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.
• 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.
• 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.
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
At the present time, 3 LMWH
preparations,
• Enoxaparin,
• Dalteparin, and
• Ardeparin
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
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.
Thrombolytic therapy does not prevent
 Clot propagation,
 Rethrombosis, or
 Subsequent embolization.
 Heparin therapy and oral anticoagulant therapy
always must follow a course of thrombolysis.
• 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
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.
• These pulmonary emboli removed at autopsy
look like casts of the deep veins of the leg
where they originated.
This patient underwent a thrombectomy.
The thrombus has been laid over the
approximate location in the leg veins where
it developed.
Filters for DVT
Indications for insertion of an inferior vena cava
filter
• Pulmonary embolism with contraindication to
anticoagulation
• Recurrent pulmonary embolism despite
adequate anticoagulation
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
• 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
Compression stockings
(routinely recommended
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
• 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.
• 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 (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).
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
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.
• 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.
Complications
• Acute pulmonary embolism
• Hemorrhagic complications
• Chronic venous insufficiency
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
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
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.

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  • 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.
  • 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
  • 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.