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DEEP VENOUS
THROMBOSIS
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 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 .
Virchow Triad
 More than 100 years ago, Virchow described a
triad of factors of
 Venous stasis,
 Endothelial damage
 Hypercoagulable state
Venous stasis
 Prolonged bed rest (≥4 days)
 Limb paralysis from stroke or spinal cord
injury
 Extended travel in a vehicle
 Surgery
 Critical illness
Hypercoagulation
Primary Hypercoagulable States
 Factor V Leiden Mutation
 Deficiencies of Protein S, Protein C,
Antithrombin III.
 Inc Prothrombin
Hypercoagulation
Secondary Hypercoagulable States
 Surgery and trauma
 Malignancy
 Increased estrogen (due to a fall in protein S)
- pregnancy
- the first three months postpartum,
- after elective abortion, and
- OCP’s
Hypercoagulation
 Nephrotic Syndrome
 Antiphospholipid Syndrome
 SLE
 Myeloproliferative Disorder(a group of
conditions that cause blood cells -- platelets, white
blood cells, and red blood cells -- to grow abnormally in
the bone marrow. )
 Hyperhomocysteinemia
 HIT Heparin-induced thrombocytopenia
 Chemotherapy
 IBD
Endothelial Injury
 Venous Trauma,
 Surgery
 Iatrogenic – CVC (central venous catheter )
in subclavian and internal jugular lines.
 Malignancy
 C/T
Other Risk Factors
 Age
 H/O DVT or PE
Risk of DVT according to Surgery
 Low risk
a. Minor Surgery(<30 min)no risk other than age
b. Major Surgery (>30 min)age>40,risk factor-
c. Minor trauma or Medical illness
 Medium Risk
a. Major Surgery, Age >40, or other risk
b. Major medical illnes,CA,IBD,cardiopulm dis
c. Major trauma or Burns
d. Minor surgery,trauma,burns,illness ê H/O
DVT,PE
 High Risk
a. Fracture or Major Ortho surgery
b. Major pelvic or abdominal surgery for CA
c. Major surgery,trauma,burns,illness ê H/O
DVT,PE
d. Lower Limb paralysis
e. Major lower limb amputation
CLINICAL
PATHOPHYSIOLOGY
 The nidus for a clot is often an intimal defect
 Usually in venous valves
 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.
 exacerbations of swelling and pain, probably as a result
of venous dilatation and hypertension
 Pulmonary embolism (PE) is a serious complication
of DVT. Many go unrecognized,
SYMPTOMS
 Calf pain
 Swelling
 Pleuritic pain, dyspnea, hemoptysis (PE)
SIGNS
 Tenderness
 Pitting Edema
 Homan’s sign:
 Increased skin temperature
 Superficial venous dilatation
 Cyanosis can occur with severe obstruction
 Phlegmasia Alba Dolens (known as milk leg or white
leg)
blanching of extremeties, edema, discomfort
 Phlegmasia Cerulea Dolens (painful blue edema)
pain and cyanosis. Ileofemoral DVT
 Search for stigmata of PE such as tachycardia
(common), tachypnea or chest findings (rare),
and
 exam for signs suggestive of underlying
predisposing factors.
Well’s Clinical Prediction Guide
 Active cancer (treatment ongoing, or within 6 months
or palliative)
 Paralysis or recent plaster immobilization
 Recently bedridden for >3 days or major surgery <4
weeks
 Localized tenderness along the distribution of the deep
venous system
 Entire leg swelling
 Calf swelling >3 cm compared to the asymptomatic leg
 Pitting edema (greater in the symptomatic leg)
 Collateral superficial veins (nonvaricose)
 Alternative diagnosis (as likely or > that of
DVT) minus 2
 Total of Above Score
High probability: Score ≥3
Moderate probability: Score 1 - 2
Low probability: Score 0
DIAGNOSTIC STUDIES
 Blood Tests
 the D-dimer ( is a fibrin degradation product (or
FDP), a small protein fragment present in the blood
after a blood clot is degraded by fibrinolysis)
 INR. (International normalized ratio (INR) is based
on the ratio of the patient's prothrombin time and the
normal mean prothrombin time.)
Imaging Studies
 INVASIVE
 Venography,
 Radiolabeled fibrinogen
 NONINVASIVE
 USG (color-flow Duplex scanning)
 Plethysmography,
 MRI techniques
DIFFERENTIAL DIAGNOSIS
 Cellulitis
 Suoperficial Thrombophlebitis
 Arthritis
 Asymmetric peripheral edema (CHF, liver disease, renal
failure, nephrotic syndrome, lymphangitis)
 Extrinsic compression of iliac vein (tumor, hematoma,
abscess)
 Calf muscle Hematoma
 Lymphedema
 Ruptured Baker cyst
 Stress fractures or other bony lesions
 Ruptured plantaris tendon
 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.
 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
I. prevent pulmonary embolism,
II. reduce morbidity, and
III. 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 by activation of antithrombin III.
inactivates thrombin and inhibits the activity of
activated factor X in the coagulation process.
 . 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
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.
warfarin
 Interferes with hepatic synthesis of vitamin K-
dependent coagulation factors
 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
1. when anticoagulant therapy is ineffective
2. unsafe,
3. 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
I. Pulmonary embolism with contraindication to
anticoagulation
II. 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 (ie, hematemesis, hematuria,
gastrointestinal hemorrhage) should be investigated
thoroughly since anticoagulant therapy may unmask a
preexisting disease (eg, cancer, peptic ulcer disease,
arteriovenous malformation).
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
exceeding risk of anticoagulation: indefinite duration
(subject to review)
Further Outpatient Care:
 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.
 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
Ideidentify any patiant who is at risk.
GENERAL MEASURES
 Early Mobilization
 Prevent dehydration.
 During operation avoid prolonged calf compression.
 Stop OCP’s 6 wks prior to surgery
 Foot of bed should be elevated to increase venous
return.
SPECIFIC MEASURES
 Graded Elastic Compression Stockings
 Intermittant Pneumatic Calf Compression
 Electrical Calf Muscle Stimulation
 Post op Leg Elevation & Early Ambulation
 Heparin(LMWH)

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Dvt

  • 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 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. Virchow Triad  More than 100 years ago, Virchow described a triad of factors of  Venous stasis,  Endothelial damage  Hypercoagulable state
  • 5. Venous stasis  Prolonged bed rest (≥4 days)  Limb paralysis from stroke or spinal cord injury  Extended travel in a vehicle  Surgery  Critical illness
  • 6. Hypercoagulation Primary Hypercoagulable States  Factor V Leiden Mutation  Deficiencies of Protein S, Protein C, Antithrombin III.  Inc Prothrombin
  • 7. Hypercoagulation Secondary Hypercoagulable States  Surgery and trauma  Malignancy  Increased estrogen (due to a fall in protein S) - pregnancy - the first three months postpartum, - after elective abortion, and - OCP’s
  • 8. Hypercoagulation  Nephrotic Syndrome  Antiphospholipid Syndrome  SLE  Myeloproliferative Disorder(a group of conditions that cause blood cells -- platelets, white blood cells, and red blood cells -- to grow abnormally in the bone marrow. )  Hyperhomocysteinemia  HIT Heparin-induced thrombocytopenia  Chemotherapy  IBD
  • 9. Endothelial Injury  Venous Trauma,  Surgery  Iatrogenic – CVC (central venous catheter ) in subclavian and internal jugular lines.  Malignancy  C/T
  • 10. Other Risk Factors  Age  H/O DVT or PE
  • 11. Risk of DVT according to Surgery  Low risk a. Minor Surgery(<30 min)no risk other than age b. Major Surgery (>30 min)age>40,risk factor- c. Minor trauma or Medical illness  Medium Risk a. Major Surgery, Age >40, or other risk b. Major medical illnes,CA,IBD,cardiopulm dis c. Major trauma or Burns d. Minor surgery,trauma,burns,illness ê H/O DVT,PE
  • 12.  High Risk a. Fracture or Major Ortho surgery b. Major pelvic or abdominal surgery for CA c. Major surgery,trauma,burns,illness ê H/O DVT,PE d. Lower Limb paralysis e. Major lower limb amputation
  • 13. CLINICAL PATHOPHYSIOLOGY  The nidus for a clot is often an intimal defect  Usually in venous valves  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.
  • 14.  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
  • 15.  Edema, sclerosis, and ulceration characterize this syndrome, which develops in 40-80% of patients with DVT.  exacerbations of swelling and pain, probably as a result of venous dilatation and hypertension  Pulmonary embolism (PE) is a serious complication of DVT. Many go unrecognized,
  • 16. SYMPTOMS  Calf pain  Swelling  Pleuritic pain, dyspnea, hemoptysis (PE)
  • 17. SIGNS  Tenderness  Pitting Edema  Homan’s sign:  Increased skin temperature  Superficial venous dilatation  Cyanosis can occur with severe obstruction
  • 18.  Phlegmasia Alba Dolens (known as milk leg or white leg) blanching of extremeties, edema, discomfort  Phlegmasia Cerulea Dolens (painful blue edema) pain and cyanosis. Ileofemoral DVT
  • 19.  Search for stigmata of PE such as tachycardia (common), tachypnea or chest findings (rare), and  exam for signs suggestive of underlying predisposing factors.
  • 20.
  • 21. Well’s Clinical Prediction Guide  Active cancer (treatment ongoing, or within 6 months or palliative)  Paralysis or recent plaster immobilization  Recently bedridden for >3 days or major surgery <4 weeks  Localized tenderness along the distribution of the deep venous system  Entire leg swelling  Calf swelling >3 cm compared to the asymptomatic leg  Pitting edema (greater in the symptomatic leg)  Collateral superficial veins (nonvaricose)
  • 22.  Alternative diagnosis (as likely or > that of DVT) minus 2  Total of Above Score High probability: Score ≥3 Moderate probability: Score 1 - 2 Low probability: Score 0
  • 23. DIAGNOSTIC STUDIES  Blood Tests  the D-dimer ( is a fibrin degradation product (or FDP), a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis)  INR. (International normalized ratio (INR) is based on the ratio of the patient's prothrombin time and the normal mean prothrombin time.)
  • 24. Imaging Studies  INVASIVE  Venography,  Radiolabeled fibrinogen  NONINVASIVE  USG (color-flow Duplex scanning)  Plethysmography,  MRI techniques
  • 25.
  • 26. DIFFERENTIAL DIAGNOSIS  Cellulitis  Suoperficial Thrombophlebitis  Arthritis  Asymmetric peripheral edema (CHF, liver disease, renal failure, nephrotic syndrome, lymphangitis)  Extrinsic compression of iliac vein (tumor, hematoma, abscess)  Calf muscle Hematoma  Lymphedema
  • 27.  Ruptured Baker cyst  Stress fractures or other bony lesions  Ruptured plantaris tendon  Varicose veins
  • 28. 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.
  • 29.  If the duplex study is negative and the patient is low risk, DVT has been ruled out.  If the patient is high risk but the ultrasound study was negative, the patient still has a significant probability of DVT
  • 30.  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
  • 31. EMERGENCY DEPARTMANT CARE  The primary objectives of the treatment of DVT are to I. prevent pulmonary embolism, II. reduce morbidity, and III. prevent or minimize the risk of developing the postphlebitic syndrome.
  • 32.  Anticoagulation  Thrombolytic therapy for DVT  Surgery for DVT  Filters for DVT  Compression stockings
  • 33. Anticoagulation  Heparin prevents extension of the thrombus  Heparin's by activation of antithrombin III. inactivates thrombin and inhibits the activity of activated factor X in the coagulation process.
  • 34.  . 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 arise from the larger higher molecular weight fragments.
  • 35.  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.
  • 36.  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.
  • 37. warfarin  Interferes with hepatic synthesis of vitamin K- dependent coagulation factors  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
  • 38. 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.
  • 39. Thrombolytic therapy does not prevent  clot propagation,  rethrombosis, or  subsequent embolization.  Heparin therapy and oral anticoagulant therapy always must follow a course of thrombolysis.
  • 40.  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
  • 41. Surgery for DVT INDICATIONS 1. when anticoagulant therapy is ineffective 2. unsafe, 3. contraindicated.  The major surgical procedures for DVT are clot removal and partial interruption of the inferior vena cava to prevent pulmonary embolism.
  • 42.  These pulmonary emboli removed at autopsy look like casts of the deep veins of the leg where they originated. 
  • 43. This patient underwent a thrombectomy. The thrombus has been laid over the approximate location in the leg veins where it developed.
  • 44. Filters for DVT INDICATIONS I. Pulmonary embolism with contraindication to anticoagulation II. Recurrent pulmonary embolism despite adequate anticoagulation
  • 45.  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
  • 46.  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
  • 47.
  • 49. 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
  • 50.  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.
  • 51.  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).
  • 52. 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 exceeding risk of anticoagulation: indefinite duration (subject to review)
  • 53. Further Outpatient Care:  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.
  • 54.  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.
  • 55. Complications  Acute pulmonary embolism  Hemorrhagic complications  Chronic venous insufficiency
  • 56. 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
  • 57. 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
  • 58. PROPHYLAXIS Ideidentify any patiant who is at risk. GENERAL MEASURES  Early Mobilization  Prevent dehydration.  During operation avoid prolonged calf compression.  Stop OCP’s 6 wks prior to surgery  Foot of bed should be elevated to increase venous return.
  • 59. SPECIFIC MEASURES  Graded Elastic Compression Stockings  Intermittant Pneumatic Calf Compression  Electrical Calf Muscle Stimulation  Post op Leg Elevation & Early Ambulation  Heparin(LMWH)