Deep vein thrombosis is a blood clot that forms in the deep veins, usually of the legs. Risk factors include prolonged bed rest, surgery, trauma, cancer, and genetic hypercoagulable states. Symptoms include leg pain, swelling, and shortness of breath. Ultrasound is commonly used for diagnosis. Treatment involves anticoagulation with heparin or warfarin to prevent pulmonary embolism complications.
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
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
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,
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.)
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.
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
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.
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)