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VENOUS THROMBOEMBOLISM Composite
term for DVT &PE
 The presence of thrombus with in deep veins
is termed as deep vein thrombosis
 It is a life threatening condition that may lead
to sudden death in the short term or long
term morbidity due to the development of
post thrombotic limb and venous ulceration
 1846 virchow recognised association of
thrombus in leg and PE.
 1916 J McLean ,a medical student discovered
heparin
 1937 Heparin introduced to clinical practice.
 Last 25 years significant progress made in our
understanding of DVT.
 CLASSIFICATION :
PROXIMAL DVT :thrombus formed in veins
above the knee jt (femoral, iliac, popliteal)
DISTAL DVT : those formed below the knee jt
(calf veins)
Venous thrombosis are difficult
to recognize clinically. The
documented cases probably
represent only tip of the Ice
Berg.
SILENT KILLER
 M:F 1.2:1
 Age more than 40 years.
 VT occur in more than 50% of patient’s having
orthopaedic surgical procedures.
 10 to 20% of patient with idiopathic DVT have or
develop cancer.
 1/3rd
to 1/4th
patient having proximal DVT may
develop PE.
 About 10% of hospital deaths attributable to PE
(from DVT)
 Calf vein - most common
 Ilio femoral - most symtomatic
 IVC - most lethal
 Blood clots occurring in people sitting at the
computer for prolonged periods of time.
AIR TRAVEL AND DVT
 Up to 1 out of 10 air line passengers develop small
asymptomatic blood clots.
 Due to hypoxia and reduced cabin pressure.
 VT occurs in patients regularly without any damaged
to the blood vessels.
VTE Risk Stratification
Patient Factors: Clinical
 Age
 Previous VTE
 Malignancy
 Advancing age
 Obesity
 Prolonged immobility
 Trauma
 Surgery (THR, TKR, HFS)
 Pregnancy/ postpartum
 Indwelling central venous catheter
 Thrombophilia
 Deficiency of anti-thrombin III
Protein C or S
Contd...
 Paralysis of lower limbs
 Polycythaemia
 Paraproteinaemia
 PNH Antibody or lupus anticoagulant
 Medical illness
◦ stroke
◦ MI
◦ CHF
◦ pneumonia
◦ COPD
◦ infections
◦ nephrotic syndrome
◦ inflammatory bowel disease
 Oral contraceptives
 Varicose veins
 Pregnancy and postpartum period.
 Immoblisation longer than 3 days
 Major surgery in previous 4weeks
 Long air or car trips >4hrs in previous 4 weeks
 Predisposing Factors :
1. Stasis
2. Vascular damage
3. Hyper coagulability
 Imbalance between thrombogenesis &
thrombolytic agents
1. Propagation
2. Embolization
3. Dissolution
4. Organization & recanalisation
 ORGIN
DVT usually originates from veins of calf
around the valve cusps or with in soleal
plexus
 A minority of cases occurs directly in ilio
femoral veins
 In practical terms the development of VT is
best understood as activation of coagulation in
areas of reduced blood flow.
 Majority of calf vein thrombus dissolve
completely.
 Only 20% progress proximally.
 Propagation occurs before embolisation.
 The process of adherence and organisation of
venous thrombus does not begin until 5 to 10
days after thrombus formation.
 This non adherent thrombus may propagate or
embolise.
 Propagation or organisation of venous
thrombus  destruction of valves & varying
degree of venous outflow obstruction 
chronic venous insufficiency.
1. Fatal PE
2. Non-fatal PE
3. Post-thrombotic syndrome
 Rate of fatal PE in gen population >65yrs is .
003%
 In ortho pts (THR,TKR) it is 0.3%
 10 fold increase in risk of having fatal PE
 Consequence of recanalisation of major
venous thrombus
 Due to incompetence of valves
 Long term morbidity
 Causes chronic edema &venous ulcers
 Swelling/edema
most specific sign
unilateral
 Leg pain (50%)
non specific
 Redness/erythema
over the thrombus
 Tenderness(75%)
calf or along the involved veins
does not correlate size, site, extent
 Low grade pyrexia
 Signs and symptoms of PE

 Pain or discomfort in leg on forceful dorsiflexion
of foot with knee straight
 Time honoured sign
 Present only in 10% of confirmed DVT
 Highly non-specific
 Present in 50%of cases with out DVT
 Misleading sign
 No longer used
 Pts with superficial thrombophlebitis with out
coexisting varicose veins & with no other
etiology (IV Catheter) are at high risk of having
DVT (40%)
 Pts with ST extending to sapheno-femoral jn
are at high risk of associated DVT
 Painful blue inflammation
PHLEGMASIA ALBA DOLENS
 Painful white inflammation
 Massive IVF thrombus with arterial spasm
In approximately 70% of patients with clinically suspected
DVT, alternate diagnoses are ultimately found as follows:
Arthritis
Cellulitis, lymphangitis
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
D-DIMER STUDY
 D-dimer fibrin fragments are present in fresh fibrin clots and
fibrin dehydration products of cross linked fibrin.
 Monoclonal antibodies specific to D-dimer fragment are used to
differentiate fibrin specific clots from noncrosslinked fibrin and
from fibrinogen. These specific attributes of the D-dimer
antibodies account for their high sensitivity for venous
thromboembolism.
 Elevated in any medical condition where clots form.
 Rised in trauma, recent surgery, haemorrhage, cancer and
sepsis.
 It has high sensitivity and low specificity for VTE.
 Levels elevated in DVT for seven days.
 After clot organisation and adherence the levels decrease.
 Current evidence strongly supports the use of a D-
dimer assay in the clinical algorithm of suspected
DVT.
A negative D-dimer assay R/O DVT in patients
with low-to-moderate risk (Wells DVT score <2).
All patients with positive D-dimer assay and all
patient with a moderate-to-high risk of DVT ( Wells
DVT score >=2) require a diagnostic study.
 Protein S, protein C, anticromin III, factor V Leyden,
prothrombin 20210A mutation, antiphospholipid
antibodies and homocysteine levels can be measured.
 investigations for these abnormalities are primarily
indicated when DVT is diagnosed in patients younger that
35 years or when venous thrombosis is detected in
unusual sites.
CONTRAST VENOGRAPHY
 Gold standard for DVT.
 Used when other test are inconclusive.
 It is either contra indicated or non diagnostic in as many as 20-25%
of patients.
 Drawbacks : Allergic reactions, contrast induced DVT, technical
problems, inter observer variability and lack of availability.
 It is replaced by non invasive studies as initial diagnostic test.
 Combination of real – time ultrasonographic
imaging with Doppler flow studies.
 Sensitivity for proximal DVT is 97% for calf
veins is 73%.
 Overall specificity is 95%.
 Helpful to differentiate from haematoma,
baker cyst, abscess and other causes of leg
pain and edema.
 Primary disadvantage : Inherent inaccuracy in
diagnosis of calf vein thrombosis.
Those proximal to the inguinal ligament are also
difficult to visualize. Non occluding thrombi may be
difficult to detect.
Not able to differentiate to old and new clots in
patients with acute recurrent DVT.
Depends on experience of radiologist
 Based on recording changes in blood volume of an
extremity, which are directly related to venous outflow.
 Sensitive and specific for proximal vein thrombosis.
 Cannot differentiate between thrombotic occlusion and
extra vascular compression of the vein.
 Insensitive for calf vein thrombosis, non-occluding
proximal DVT and ileofemoral DVT.
 Increasingly used.
 Accuracy approaches to that of contrast venograghy.
 Diagnostic test of choice for suspected iliac vein & IVC
thrombosis.
 2nd
&3rd
trimester of pregnancy (gravid uterus alters
doppler flow characteristics).
 In suspected calf vein thrombosis it is more sensitive
than other non invasive study.
 Expense, lack of general availability and technical issues
limit its use.
 Used for pelvis vein thrombosis.
NUCLEAR MEDICINE IMAGING STUDIES
 I125
labeled fibrinogen.
 Takes longer than 24 hrs.
 No longer used.
PRIMARY OBJECTIVES
1. To prevent PE.
2. Reduce morbidity.
3. Prevent or minimize risk of developing the postphletic
syndrome.
SURGICAL TREATMENT
1. Indicated when anticoagulant therapy is ineffective, unsafe or
contraindicated.
2. Major surgical procedures : clot removal and partial
interruption of IVC to prevent PE.
 To restore venous patency and valvular function.
 Alone it is not indicated because rethrombosis is frequent.
 Heparin therapy is a necessary adjunct.
 Best reserved for patients with massive IF vein thrombosis
when limb viability is at risk.
FILTERS FOR DVT
 First suggested by Trousseau in 1868.
 Today introducing intracaval devices percutaneosly and floating
them into position with fluoroscopy is the procedure of choice
for filter placement.
 Severe hemorrhage complications of
anticoagulant therapy.
 Absolute contra indications to anticoagulation.
 Failure of anticoagulation such us new or
recurrent VTE or PE.
 Bed rest
 Affected limb is elevated above the level of heart.
 Anticoagulant prevent thrombus propagation and
allow the endogenous lytic system to operate
 Pain relief.
 Initial bolus 7500 to 10000 IU followed by
continuous in infusion to 1000 to 1500 IU/hr.
 Infusion rate adjusted so that aPTT is approx
twice the control value
 Every 6 hrs aPTT monitered till therapeutic
range is reached
 Duration :5 days
 Discontinue when platelet count <75,000
 Effective and better than conventional heparin.
 Different preparations available.
 Administered SC in fixed doses once or twice
daily.
 Duration -7 to 14 days
 Anticoagulant effect by inhibiting the activated
factor X.
 Hemorrhagic complications doesn’t occur
 LMWHs are individual, distinct compounds
that exhibit unique physical, pharmacokinetic
and pharmacodynamic profiles
 LMWHs exhibit distinct non-antithrombin III-
mediated effects, including unique tissue
factor pathway inhibition and von Willebrand
factor release profiles.
 Currently four LMWH are available.
Enoxaparin
Tinazaparin
Dalteparin
Nadroparin
 Only enoxaparin and tinazaparin are
approved by FDA for DVT prophylaxis.
 To be taken along with heparin for initial 4 to5
days.
 Dose adj to maintain prothrombin time at INR
2.0 to3.0
 Continued for 3 to6 months for pts with acute
idiopathic DVT
 For recurrent DVT/PE low intensity warfarin
continued indefinitely maintaining INR 1.5 to2.0
 Early administration
a) Prompt resolution of symptoms
b) Accelerate clot lysis
c) Preserve venous valves
d) Decrease the potential for developing post-
phlebitic syndrome
 Does not prevent clot propagation or
rethrombosis.
 Heparin and oral anti coagulant therapy must
follow a course of thrombolysis.
 Haemorraghic complications reduced by
regionally administering with flouroscopic
control.
 Streptokinase,urokinase,tPA (alteplase)
 Lepirudin or aragatroban
 Used when heparin is contra indicated due to
HIT(heparin induced thombocytopenia)
 LOW RISK: young pts ,minor illness, surgery
lasting <30 mt with no risk factors
 MODERATE RISK: >40yrs with deblitating
illness undergoing major surgery but no risk
factors
 HIGH RISK: >40 yrs with serious medical
condition undergoing major surgery with
additional risk factors
 YES - Overall reduction in DVT and PE is by 40%
to 60%
 Three pronged approach
 Designed to address stasis & coagulation
 Usually combination of therapies
I. EARLY MOVT & REHABLITATION
II. MECHANICAL METHODS
lower extremity exercises
graded compression stockings
intermittent pneumatic compression devices
CPM
III PHARMACOLOGICAL PROPHYLAXIS
a) ASPIRIN
easy to administer
low cost
few bleeding complications
 Most commonly used
 Takes 36 hrs to start action
 Started day before surgery
 Low doses are used
LOW MOLECULAR WT HEPARIN
 More effective than conventional
 Lesser bleeding
 Low molecular wt heparinoid
 For pts with HIT
Fondaparinux
 Synthetic pentasaccharide
 Graduated compression stockings
 Exercise
 Avoid alcohol &sleeping tablets
HIGH RISK PATIENTS
 LMWH ,single dose SC before the flight
 PAGET VON SCHROTTER DISEASE
 Axillary and sub clavian vein thrombosis
 Reduced incidence
 Thoracic outlet synd &cervical ribs
 Thrombolytic therapy is treatment of choice
 Since restoring venous patency more important
in upper limb
 Early - Progression
Pulmonary
embolism Paradoxical
embolism Acute
compartment syndrome venous gangrene
 Late - Rec DVT, Post phlebitic syndrome
 Special group of pts
 very high risk for DVT & may reach up to 60 to 80% with
out prophylaxis (THR)
 Assymptomatic DVT common in >50% of all patients
 PE develop in 10 to 20 %of pts
 Even with prophylaxis DVT & PE remains the most
common cause for emergency readmission and
death in joint replacement pts
 •Pre-op Immobilization (stasis)
•Trigger of tissue factor
reamed products (THR)
tissue debris ,fat  activation of
coagulation
• Distortion of Femoral and Poplietal viens
retraction,twisting,manipulation –
damage to vessel wall
•Prolonged post-op Immobilization.
 THR, TKR
 Hip fracture surgery
 Spine surgery [ malignancy, neurological deficit]
 Although thromboprophylaxis is routinely given
to patients who undergo major orthopedic
surgery, it is usually stopped at discharge.
 Coagulation cascade remains abnormal upto 4
weeks.
 Risk of propagation of the DVT, and PE,
remains active during this period.
 Patients undergoing THA TKA or HFS receive
Thromboprophylaxis with LMWH Fondaparinux
or VKA for a minimum of ten days. [can be cont.
for 4 – 5 wks]
 Not an uncommon condition in clinical practice
 DVT OCCURS ONLY IN POST-OP PATIENTS’ IS A MYTH
 Awareness is most important for early diagnosis
 Prompt treatment can prevent lethal complications
 Diagnosis can be made using noninvasive methods
 Long term follow up is necessary to identify patients
who develop chronic venous insufficiency.

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Deep vein thrombosis

  • 1.
  • 2. VENOUS THROMBOEMBOLISM Composite term for DVT &PE  The presence of thrombus with in deep veins is termed as deep vein thrombosis  It is a life threatening condition that may lead to sudden death in the short term or long term morbidity due to the development of post thrombotic limb and venous ulceration
  • 3.  1846 virchow recognised association of thrombus in leg and PE.  1916 J McLean ,a medical student discovered heparin  1937 Heparin introduced to clinical practice.  Last 25 years significant progress made in our understanding of DVT.
  • 4.  CLASSIFICATION : PROXIMAL DVT :thrombus formed in veins above the knee jt (femoral, iliac, popliteal) DISTAL DVT : those formed below the knee jt (calf veins)
  • 5. Venous thrombosis are difficult to recognize clinically. The documented cases probably represent only tip of the Ice Berg. SILENT KILLER
  • 6.  M:F 1.2:1  Age more than 40 years.  VT occur in more than 50% of patient’s having orthopaedic surgical procedures.  10 to 20% of patient with idiopathic DVT have or develop cancer.  1/3rd to 1/4th patient having proximal DVT may develop PE.  About 10% of hospital deaths attributable to PE (from DVT)
  • 7.  Calf vein - most common  Ilio femoral - most symtomatic  IVC - most lethal
  • 8.  Blood clots occurring in people sitting at the computer for prolonged periods of time. AIR TRAVEL AND DVT  Up to 1 out of 10 air line passengers develop small asymptomatic blood clots.  Due to hypoxia and reduced cabin pressure.  VT occurs in patients regularly without any damaged to the blood vessels.
  • 9. VTE Risk Stratification Patient Factors: Clinical  Age  Previous VTE  Malignancy  Advancing age  Obesity  Prolonged immobility  Trauma  Surgery (THR, TKR, HFS)  Pregnancy/ postpartum  Indwelling central venous catheter  Thrombophilia  Deficiency of anti-thrombin III Protein C or S Contd...
  • 10.  Paralysis of lower limbs  Polycythaemia  Paraproteinaemia  PNH Antibody or lupus anticoagulant  Medical illness ◦ stroke ◦ MI ◦ CHF ◦ pneumonia ◦ COPD ◦ infections ◦ nephrotic syndrome ◦ inflammatory bowel disease  Oral contraceptives  Varicose veins
  • 11.  Pregnancy and postpartum period.  Immoblisation longer than 3 days  Major surgery in previous 4weeks  Long air or car trips >4hrs in previous 4 weeks
  • 12.  Predisposing Factors : 1. Stasis 2. Vascular damage 3. Hyper coagulability  Imbalance between thrombogenesis & thrombolytic agents
  • 13. 1. Propagation 2. Embolization 3. Dissolution 4. Organization & recanalisation  ORGIN DVT usually originates from veins of calf around the valve cusps or with in soleal plexus  A minority of cases occurs directly in ilio femoral veins
  • 14.  In practical terms the development of VT is best understood as activation of coagulation in areas of reduced blood flow.  Majority of calf vein thrombus dissolve completely.  Only 20% progress proximally.  Propagation occurs before embolisation.
  • 15.  The process of adherence and organisation of venous thrombus does not begin until 5 to 10 days after thrombus formation.  This non adherent thrombus may propagate or embolise.  Propagation or organisation of venous thrombus  destruction of valves & varying degree of venous outflow obstruction  chronic venous insufficiency.
  • 16. 1. Fatal PE 2. Non-fatal PE 3. Post-thrombotic syndrome  Rate of fatal PE in gen population >65yrs is . 003%  In ortho pts (THR,TKR) it is 0.3%  10 fold increase in risk of having fatal PE
  • 17.  Consequence of recanalisation of major venous thrombus  Due to incompetence of valves  Long term morbidity  Causes chronic edema &venous ulcers
  • 18.  Swelling/edema most specific sign unilateral  Leg pain (50%) non specific  Redness/erythema over the thrombus  Tenderness(75%) calf or along the involved veins does not correlate size, site, extent  Low grade pyrexia  Signs and symptoms of PE 
  • 19.  Pain or discomfort in leg on forceful dorsiflexion of foot with knee straight  Time honoured sign  Present only in 10% of confirmed DVT  Highly non-specific  Present in 50%of cases with out DVT  Misleading sign  No longer used
  • 20.  Pts with superficial thrombophlebitis with out coexisting varicose veins & with no other etiology (IV Catheter) are at high risk of having DVT (40%)  Pts with ST extending to sapheno-femoral jn are at high risk of associated DVT
  • 21.  Painful blue inflammation PHLEGMASIA ALBA DOLENS  Painful white inflammation  Massive IVF thrombus with arterial spasm
  • 22. In approximately 70% of patients with clinically suspected DVT, alternate diagnoses are ultimately found as follows: Arthritis Cellulitis, lymphangitis 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
  • 23. D-DIMER STUDY  D-dimer fibrin fragments are present in fresh fibrin clots and fibrin dehydration products of cross linked fibrin.  Monoclonal antibodies specific to D-dimer fragment are used to differentiate fibrin specific clots from noncrosslinked fibrin and from fibrinogen. These specific attributes of the D-dimer antibodies account for their high sensitivity for venous thromboembolism.  Elevated in any medical condition where clots form.  Rised in trauma, recent surgery, haemorrhage, cancer and sepsis.  It has high sensitivity and low specificity for VTE.  Levels elevated in DVT for seven days.  After clot organisation and adherence the levels decrease.
  • 24.  Current evidence strongly supports the use of a D- dimer assay in the clinical algorithm of suspected DVT. A negative D-dimer assay R/O DVT in patients with low-to-moderate risk (Wells DVT score <2). All patients with positive D-dimer assay and all patient with a moderate-to-high risk of DVT ( Wells DVT score >=2) require a diagnostic study.
  • 25.  Protein S, protein C, anticromin III, factor V Leyden, prothrombin 20210A mutation, antiphospholipid antibodies and homocysteine levels can be measured.  investigations for these abnormalities are primarily indicated when DVT is diagnosed in patients younger that 35 years or when venous thrombosis is detected in unusual sites.
  • 26. CONTRAST VENOGRAPHY  Gold standard for DVT.  Used when other test are inconclusive.  It is either contra indicated or non diagnostic in as many as 20-25% of patients.  Drawbacks : Allergic reactions, contrast induced DVT, technical problems, inter observer variability and lack of availability.  It is replaced by non invasive studies as initial diagnostic test.
  • 27.  Combination of real – time ultrasonographic imaging with Doppler flow studies.  Sensitivity for proximal DVT is 97% for calf veins is 73%.  Overall specificity is 95%.  Helpful to differentiate from haematoma, baker cyst, abscess and other causes of leg pain and edema.
  • 28.  Primary disadvantage : Inherent inaccuracy in diagnosis of calf vein thrombosis. Those proximal to the inguinal ligament are also difficult to visualize. Non occluding thrombi may be difficult to detect. Not able to differentiate to old and new clots in patients with acute recurrent DVT. Depends on experience of radiologist
  • 29.  Based on recording changes in blood volume of an extremity, which are directly related to venous outflow.  Sensitive and specific for proximal vein thrombosis.  Cannot differentiate between thrombotic occlusion and extra vascular compression of the vein.  Insensitive for calf vein thrombosis, non-occluding proximal DVT and ileofemoral DVT.
  • 30.  Increasingly used.  Accuracy approaches to that of contrast venograghy.  Diagnostic test of choice for suspected iliac vein & IVC thrombosis.  2nd &3rd trimester of pregnancy (gravid uterus alters doppler flow characteristics).  In suspected calf vein thrombosis it is more sensitive than other non invasive study.  Expense, lack of general availability and technical issues limit its use.
  • 31.  Used for pelvis vein thrombosis. NUCLEAR MEDICINE IMAGING STUDIES  I125 labeled fibrinogen.  Takes longer than 24 hrs.  No longer used.
  • 32. PRIMARY OBJECTIVES 1. To prevent PE. 2. Reduce morbidity. 3. Prevent or minimize risk of developing the postphletic syndrome. SURGICAL TREATMENT 1. Indicated when anticoagulant therapy is ineffective, unsafe or contraindicated. 2. Major surgical procedures : clot removal and partial interruption of IVC to prevent PE.
  • 33.  To restore venous patency and valvular function.  Alone it is not indicated because rethrombosis is frequent.  Heparin therapy is a necessary adjunct.  Best reserved for patients with massive IF vein thrombosis when limb viability is at risk. FILTERS FOR DVT  First suggested by Trousseau in 1868.  Today introducing intracaval devices percutaneosly and floating them into position with fluoroscopy is the procedure of choice for filter placement.
  • 34.  Severe hemorrhage complications of anticoagulant therapy.  Absolute contra indications to anticoagulation.  Failure of anticoagulation such us new or recurrent VTE or PE.
  • 35.  Bed rest  Affected limb is elevated above the level of heart.  Anticoagulant prevent thrombus propagation and allow the endogenous lytic system to operate  Pain relief.
  • 36.  Initial bolus 7500 to 10000 IU followed by continuous in infusion to 1000 to 1500 IU/hr.  Infusion rate adjusted so that aPTT is approx twice the control value  Every 6 hrs aPTT monitered till therapeutic range is reached  Duration :5 days  Discontinue when platelet count <75,000
  • 37.  Effective and better than conventional heparin.  Different preparations available.  Administered SC in fixed doses once or twice daily.  Duration -7 to 14 days  Anticoagulant effect by inhibiting the activated factor X.  Hemorrhagic complications doesn’t occur
  • 38.  LMWHs are individual, distinct compounds that exhibit unique physical, pharmacokinetic and pharmacodynamic profiles  LMWHs exhibit distinct non-antithrombin III- mediated effects, including unique tissue factor pathway inhibition and von Willebrand factor release profiles.
  • 39.  Currently four LMWH are available. Enoxaparin Tinazaparin Dalteparin Nadroparin  Only enoxaparin and tinazaparin are approved by FDA for DVT prophylaxis.
  • 40.  To be taken along with heparin for initial 4 to5 days.  Dose adj to maintain prothrombin time at INR 2.0 to3.0  Continued for 3 to6 months for pts with acute idiopathic DVT  For recurrent DVT/PE low intensity warfarin continued indefinitely maintaining INR 1.5 to2.0
  • 41.  Early administration a) Prompt resolution of symptoms b) Accelerate clot lysis c) Preserve venous valves d) Decrease the potential for developing post- phlebitic syndrome
  • 42.  Does not prevent clot propagation or rethrombosis.  Heparin and oral anti coagulant therapy must follow a course of thrombolysis.  Haemorraghic complications reduced by regionally administering with flouroscopic control.  Streptokinase,urokinase,tPA (alteplase)
  • 43.  Lepirudin or aragatroban  Used when heparin is contra indicated due to HIT(heparin induced thombocytopenia)
  • 44.  LOW RISK: young pts ,minor illness, surgery lasting <30 mt with no risk factors  MODERATE RISK: >40yrs with deblitating illness undergoing major surgery but no risk factors  HIGH RISK: >40 yrs with serious medical condition undergoing major surgery with additional risk factors
  • 45.  YES - Overall reduction in DVT and PE is by 40% to 60%
  • 46.  Three pronged approach  Designed to address stasis & coagulation  Usually combination of therapies I. EARLY MOVT & REHABLITATION II. MECHANICAL METHODS lower extremity exercises graded compression stockings
  • 47. intermittent pneumatic compression devices CPM III PHARMACOLOGICAL PROPHYLAXIS a) ASPIRIN easy to administer low cost few bleeding complications
  • 48.  Most commonly used  Takes 36 hrs to start action  Started day before surgery  Low doses are used LOW MOLECULAR WT HEPARIN  More effective than conventional  Lesser bleeding
  • 49.  Low molecular wt heparinoid  For pts with HIT Fondaparinux  Synthetic pentasaccharide
  • 50.  Graduated compression stockings  Exercise  Avoid alcohol &sleeping tablets HIGH RISK PATIENTS  LMWH ,single dose SC before the flight
  • 51.  PAGET VON SCHROTTER DISEASE  Axillary and sub clavian vein thrombosis  Reduced incidence  Thoracic outlet synd &cervical ribs  Thrombolytic therapy is treatment of choice  Since restoring venous patency more important in upper limb
  • 52.  Early - Progression Pulmonary embolism Paradoxical embolism Acute compartment syndrome venous gangrene  Late - Rec DVT, Post phlebitic syndrome
  • 53.  Special group of pts  very high risk for DVT & may reach up to 60 to 80% with out prophylaxis (THR)  Assymptomatic DVT common in >50% of all patients  PE develop in 10 to 20 %of pts  Even with prophylaxis DVT & PE remains the most common cause for emergency readmission and death in joint replacement pts
  • 54.  •Pre-op Immobilization (stasis) •Trigger of tissue factor reamed products (THR) tissue debris ,fat  activation of coagulation • Distortion of Femoral and Poplietal viens retraction,twisting,manipulation – damage to vessel wall •Prolonged post-op Immobilization.
  • 55.  THR, TKR  Hip fracture surgery  Spine surgery [ malignancy, neurological deficit]
  • 56.  Although thromboprophylaxis is routinely given to patients who undergo major orthopedic surgery, it is usually stopped at discharge.  Coagulation cascade remains abnormal upto 4 weeks.  Risk of propagation of the DVT, and PE, remains active during this period.  Patients undergoing THA TKA or HFS receive Thromboprophylaxis with LMWH Fondaparinux or VKA for a minimum of ten days. [can be cont. for 4 – 5 wks]
  • 57.  Not an uncommon condition in clinical practice  DVT OCCURS ONLY IN POST-OP PATIENTS’ IS A MYTH  Awareness is most important for early diagnosis  Prompt treatment can prevent lethal complications  Diagnosis can be made using noninvasive methods  Long term follow up is necessary to identify patients who develop chronic venous insufficiency.