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DR.FAZAL HUSSAIN KHALIL
TMO SURGICAL B WARD
KTH
Venous thromboembolism (VTE)
A condition in which a blood clot (thrombus) forms in a vein, which
in some cases then breaks free and enters the circulation as an
embolus, finally lodging in and completely obstructing a blood
vessel, e.g., in lungs causing a PE
The most common type of venous thromboembolism is deep vein
thrombosis, which occurs in veins deep within the muscles of the
leg,arm and pelvis.
A superficial venous thrombosis (also called phlebitis or superficial
thrombophlebitis) is a blood clot that develops in a vein close to
the surface of the skin. These types of blood clots do not usually
travel to the lungs unless they move from the superficial system
into the deep venous system first.
 Deep

vein thrombosis is the
formation of a blood clot in one of
the deep veins of the body, usually
in the leg
 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 .
More than 100 years ago, Virchow describes the
three broad categories of factors that are
thought to contribute to thrombosis
 venous stasis,
 endothelial damage,


hypercoagulable state
 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
Surgery and trauma (responsible for up to 40% of all
thromboembolic disease) injury which damages veins, or
surgery can slow down the flow of blood, thus raising the
chances of blood clots. General anesthetics can dilate the
veins, which makes it more likely that blood pools and clots
form.
 Malignancy…some types are associated with a higher risk of
DVT, as are some cancer therapies.
 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

deficiencies of protein ‘S,
 ’ protein ‘C,’ and
 antithrombin III.

 nephrotic syndrome results in urinary loss of

antithrombin III,
 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, causing
hypercoagulability
 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.
The beginning of venous thrombosis is thought to
be caused by tissue factor, which leads to
conversion of prothrombin to thrombin, followed by
fibrin deposition.The fibrin appears to attach to the
endothelial lining , a surface that normally acts to
prevent clotting.
 When a clot forms, 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.
• But in presence of risk factors this clot propagates
proximally and may lodge an emboli to lung
• Residual clots and venous hypertension due to
narrowing of lumen 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.
Dvt Deep Venous Thrombosis










In the majority of cases, only one leg is affected.
However, on rare occasions both legs may have a
DVT.
Calf pain or tenderness, or both
The skin of the affected leg may feel warm
Swelling below knee in distal deep vein thrombosis
and up to groin in proximal deep vein thrombosis
Superficial venous dilatation
The skin may go red, especially below the knee
behind the leg. The skin may be discolored.
Cyanosis can occur with severe obstruction
Leg fatigue
• Palpate distal pulses and evaluate capillary refill to assess
limb perfusion.
• Move and palpate all joints to detect acute arthritis or other
joint pathology.
• Homans'’ sign: pain in the posterior calf or knee with forced
dorsiflexion of the foot while the knee is fully extended. This
is not a commonly used test and should not be done. This test
is less used today because it can potentially dislodge the deep
vein thrombosis (DVT) and travel to the lung.
• exam for signs suggestive of underlying
predisposing factors
Signs of pulmonary embolism:
• Breathlessness - this may develop slowly, or come on suddenly
• Chest pain, pain is usually more severe during inhalation,
eating, coughing, stooping or bending over. During exertion
the pain will get worse, and will not go away when the patient
rests.
• Coughing may produce bloody or bloodstained sputum
• Wheezing
• Lightheadedness, and sometimes even fainting (collapse)
• Unexplained anxiety
• Accelerated heartbeat
•

Wells Clinical Prediction Guide

The Wells clinical prediction guide incorporates risk factors, clinical signs,
and the presence or absence of alternative diagnoses.A high score is 3 or
more, a moderate score 1−2 and a low score 0.
 Total of Above Score

High probability: Score 3 or more
Moderate probability: Score = 1 or 2
Low probability: Score 0
Clinical examination alone is able to confirm only
20-30% of cases of DVT
 Two important investigations are
A)Blood Tests i.e d-dimers and INR
B)Imaging Studies

 the D-dimer

INR.
 Currently 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 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 Ddimer
 ELISA
 latex agglutination
 blood agglutination test
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
 Invasive

venography,
 radiolabeled fibrinogen and.
 noninvasive
 ultrasound,
 plethysmography,
 MRI techniques

 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.
 phlebitis
 anaphylaxis
 Because the radioactive isotope incorporates

into a growing thrombus, this test can
distinguish new clot from an old clot
 Mercury-filled strain gauges used to

continuously measure circumference of the
extremity to determine circulatory capacity,
e.g. at mid calf. It is a non-invasive method
used to detect venous thrombosis in these
areas of the body.
 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.
 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
 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.
o
o
o
o
o
o
o
o
o
o
o
o

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
Ruptured Baker cyst
Stress fractures or other bony lesions
Superficial thrombophlebitis
Varicose veins
 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 well:
 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
 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
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
Two types
1) Heparin
2) Warfarin
 Mechanism of action

Heparin binds to the enzyme inhibitor
antithrombin III (AT), causing a
conformational change that results in its
activation which then inactivates thrombin
• After an initial bolus of 80 U/kg, a constant
maintenance infusion of 18 U/kg is initiated.
The aPTT(all clotting factors except seven and
thirteen) is checked 6 hours after the bolus
and adjusted accordingly. .it is said that text
references refer to a therapeutic aPTT target
of 1.5- 2.0 times the mean of the reference
range
• 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.
• Heparin induced thrombocytopenia(HIT)
Heparin occurs naturally in the human body, but the development
of HIT antibodies suggests heparin sulfate act as a hapten, and thus
targeted by the immune system, their development usually takes
about five days. These antibodies form a complex with heparin in
the bloodstream. The tail of the antibody then binds to a protein
on the surface of the platelet. This results in platelet activation
,which initiate the formation of blood clots and the consumption of
platelets; the platelet count falls as a result, leading to
thrombocytopenia. Three agents are used to provide
anticoagulation in patients with strongly suspected or proven HIT:
danaparoid(LMW heparin), lepirudin, and argatroban.(direct
thrombin inhibitor)
At the present time, 3 LMWH preparations,
 Enoxaparin,
 Dalteparin, and
 Ardeparin
Interferes with hepatic synthesis of vitamin
K-dependent coagulation factors i.e factors II,
VII, IX and X (and proteins C, S, and Z)
 Dose must be individualized and adjusted to
maintain INR between 2-3
 2-10 mg/d PO

 for the first three days of "warfarinization", the

levels of protein C and protein S (proteins of
anticoagulation) drop faster than procoagulation proteins such as factor II, VII, IX and
X. Therefore bridging anticoagulant therapies
(such as enoxaparin) are often used to reverse
this temporary hypercoagulable state
 caution in active tuberculosis or diabetes;
patients with protein C or S deficiency are at risk
of developing skin necrosis
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)

A mechanical thrombectomy device can remove venous clots,
but it is recommended only as an option when the following
conditions apply: "iliofemoral DVT, symptoms for < 7 days
(criterion used in the single randomized trial), good
functional status, life expectancy of ≥ 1 year, and both
resources and expertise are available
Thrombolytic therapy does not prevent
 clot propagation,
 rethrombosis, or
 subsequent embolization.
 Heparin therapy and oral anticoagulant therapy always must
follow a course of thrombolysis.
Open surgical thrombectomy has a very limited role in
the management of acute DVT. The limitations to the
procedure are obvious, and the results are
ambiguous at best. For this reason, open surgical
thrombectomy for DVT is reserved as a last resort for
those patients with threatened limb loss secondary
to extensive DVT




Indications
when anticoagulant therapy is ineffective
unsafe,
contraindicated.
 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.
 this tiny umbrella-like device is inserted into

the vein to catch blood clots and stop them
moving up into the lungs, while allowing
blood flow to continue. It is inserted in the
vena cava
 Indications for insertion of an inferior vena

cava filter









Pulmonary embolism with contraindication to anticoagulation
Recurrent pulmonary embolism despite adequate
anticoagulation
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
Dvt Deep Venous Thrombosis







Acute pulmonary embolism
Postthrombotic Syndrome
Blood clot in the kidney, called renal vein
thrombosis
Blood clot in the heart, leading to heart
attack
Blood clot in the brain, leading to stroke
Chronic venous insufficiency
 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
 Advise women taking estrogen of the risks

and common symptoms of thromboembolic
disease.
 Discourage prolonged immobility,
particularly on plane rides and long car trips
 Advise patient at risk to use compression
stockings
Identify 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.

Dvt Deep Venous Thrombosis

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Dvt Deep Venous Thrombosis

  • 1. DR.FAZAL HUSSAIN KHALIL TMO SURGICAL B WARD KTH
  • 2. Venous thromboembolism (VTE) A condition in which a blood clot (thrombus) forms in a vein, which in some cases then breaks free and enters the circulation as an embolus, finally lodging in and completely obstructing a blood vessel, e.g., in lungs causing a PE The most common type of venous thromboembolism is deep vein thrombosis, which occurs in veins deep within the muscles of the leg,arm and pelvis. A superficial venous thrombosis (also called phlebitis or superficial thrombophlebitis) is a blood clot that develops in a vein close to the surface of the skin. These types of blood clots do not usually travel to the lungs unless they move from the superficial system into the deep venous system first.
  • 3.  Deep vein thrombosis is the formation of a blood clot in one of the deep veins of the body, usually in the leg
  • 4.  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 .
  • 5. More than 100 years ago, Virchow describes the three broad categories of factors that are thought to contribute to thrombosis  venous stasis,  endothelial damage,  hypercoagulable state
  • 6.  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
  • 7. Surgery and trauma (responsible for up to 40% of all thromboembolic disease) injury which damages veins, or surgery can slow down the flow of blood, thus raising the chances of blood clots. General anesthetics can dilate the veins, which makes it more likely that blood pools and clots form.  Malignancy…some types are associated with a higher risk of DVT, as are some cancer therapies.  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 
  • 8. deficiencies of protein ‘S,  ’ protein ‘C,’ and  antithrombin III. 
  • 9.  nephrotic syndrome results in urinary loss of antithrombin III,  Antiphospholipid antibodies accelerate coagulation and include the lupus anticoagulant and anticardiolipin antibodies.
  • 10. Inflammatory processes, such as • systemic lupus erythematosus (SLE), • sickle cell disease, and •inflammatory bowel disease (IBD), also predispose to thrombosis, causing hypercoagulability
  • 11.  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.
  • 12. The beginning of venous thrombosis is thought to be caused by tissue factor, which leads to conversion of prothrombin to thrombin, followed by fibrin deposition.The fibrin appears to attach to the endothelial lining , a surface that normally acts to prevent clotting.  When a clot forms, 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. 
  • 13. • 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. • But in presence of risk factors this clot propagates proximally and may lodge an emboli to lung • Residual clots and venous hypertension due to narrowing of lumen 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.
  • 15.         In the majority of cases, only one leg is affected. However, on rare occasions both legs may have a DVT. Calf pain or tenderness, or both The skin of the affected leg may feel warm Swelling below knee in distal deep vein thrombosis and up to groin in proximal deep vein thrombosis Superficial venous dilatation The skin may go red, especially below the knee behind the leg. The skin may be discolored. Cyanosis can occur with severe obstruction Leg fatigue
  • 16. • Palpate distal pulses and evaluate capillary refill to assess limb perfusion. • Move and palpate all joints to detect acute arthritis or other joint pathology. • Homans'’ sign: pain in the posterior calf or knee with forced dorsiflexion of the foot while the knee is fully extended. This is not a commonly used test and should not be done. This test is less used today because it can potentially dislodge the deep vein thrombosis (DVT) and travel to the lung. • exam for signs suggestive of underlying predisposing factors
  • 17. Signs of pulmonary embolism: • Breathlessness - this may develop slowly, or come on suddenly • Chest pain, pain is usually more severe during inhalation, eating, coughing, stooping or bending over. During exertion the pain will get worse, and will not go away when the patient rests. • Coughing may produce bloody or bloodstained sputum • Wheezing • Lightheadedness, and sometimes even fainting (collapse) • Unexplained anxiety • Accelerated heartbeat
  • 18. • Wells Clinical Prediction Guide The Wells clinical prediction guide incorporates risk factors, clinical signs, and the presence or absence of alternative diagnoses.A high score is 3 or more, a moderate score 1−2 and a low score 0.
  • 19.  Total of Above Score High probability: Score 3 or more Moderate probability: Score = 1 or 2 Low probability: Score 0
  • 20. Clinical examination alone is able to confirm only 20-30% of cases of DVT  Two important investigations are A)Blood Tests i.e d-dimers and INR B)Imaging Studies 
  • 21.  the D-dimer INR.  Currently 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 Ddimer  ELISA  latex agglutination  blood agglutination test
  • 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.
  • 27.  Because the radioactive isotope incorporates into a growing thrombus, this test can distinguish new clot from an old clot
  • 28.  Mercury-filled strain gauges used to continuously measure circumference of the extremity to determine circulatory capacity, e.g. at mid calf. It is a non-invasive method used to detect venous thrombosis in these areas of the body.
  • 29.  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.
  • 30.  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
  • 31.  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.
  • 32. o o o o o o o o o o o o 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 Ruptured Baker cyst Stress fractures or other bony lesions Superficial thrombophlebitis Varicose veins
  • 33.  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 well:  If the patient is high or moderate risk and the duplex ultrasound study is positive, treat for DVT.
  • 34.  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  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. 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
  • 38.  Mechanism of action Heparin binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation which then inactivates thrombin
  • 39. • After an initial bolus of 80 U/kg, a constant maintenance infusion of 18 U/kg is initiated. The aPTT(all clotting factors except seven and thirteen) is checked 6 hours after the bolus and adjusted accordingly. .it is said that text references refer to a therapeutic aPTT target of 1.5- 2.0 times the mean of the reference range • 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.
  • 40. • Heparin induced thrombocytopenia(HIT) Heparin occurs naturally in the human body, but the development of HIT antibodies suggests heparin sulfate act as a hapten, and thus targeted by the immune system, their development usually takes about five days. These antibodies form a complex with heparin in the bloodstream. The tail of the antibody then binds to a protein on the surface of the platelet. This results in platelet activation ,which initiate the formation of blood clots and the consumption of platelets; the platelet count falls as a result, leading to thrombocytopenia. Three agents are used to provide anticoagulation in patients with strongly suspected or proven HIT: danaparoid(LMW heparin), lepirudin, and argatroban.(direct thrombin inhibitor)
  • 41. At the present time, 3 LMWH preparations,  Enoxaparin,  Dalteparin, and  Ardeparin
  • 42. Interferes with hepatic synthesis of vitamin K-dependent coagulation factors i.e factors II, VII, IX and X (and proteins C, S, and Z)  Dose must be individualized and adjusted to maintain INR between 2-3  2-10 mg/d PO 
  • 43.  for the first three days of "warfarinization", the levels of protein C and protein S (proteins of anticoagulation) drop faster than procoagulation proteins such as factor II, VII, IX and X. Therefore bridging anticoagulant therapies (such as enoxaparin) are often used to reverse this temporary hypercoagulable state  caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis
  • 44. 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) 
  • 45. A mechanical thrombectomy device can remove venous clots, but it is recommended only as an option when the following conditions apply: "iliofemoral DVT, symptoms for < 7 days (criterion used in the single randomized trial), good functional status, life expectancy of ≥ 1 year, and both resources and expertise are available 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. Open surgical thrombectomy has a very limited role in the management of acute DVT. The limitations to the procedure are obvious, and the results are ambiguous at best. For this reason, open surgical thrombectomy for DVT is reserved as a last resort for those patients with threatened limb loss secondary to extensive DVT    Indications when anticoagulant therapy is ineffective unsafe, contraindicated.
  • 47.  These pulmonary emboli removed at autopsy look like casts of the deep veins of the leg where they originated. 
  • 48. This patient underwent a thrombectomy. The thrombus has been laid over the approximate location in the leg veins where it developed.
  • 49.  this tiny umbrella-like device is inserted into the vein to catch blood clots and stop them moving up into the lungs, while allowing blood flow to continue. It is inserted in the vena cava
  • 50.  Indications for insertion of an inferior vena cava filter        Pulmonary embolism with contraindication to anticoagulation Recurrent pulmonary embolism despite adequate anticoagulation 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.       Acute pulmonary embolism Postthrombotic Syndrome Blood clot in the kidney, called renal vein thrombosis Blood clot in the heart, leading to heart attack Blood clot in the brain, leading to stroke Chronic venous insufficiency
  • 53.  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
  • 54.  Advise women taking estrogen of the risks and common symptoms of thromboembolic disease.  Discourage prolonged immobility, particularly on plane rides and long car trips  Advise patient at risk to use compression stockings
  • 55. Identify 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. 