KMCTH

1. Dr. Uttam Laudari
3/3/2015
Venous Thromboembolism

2.  Major cause of morbidity and mortality in the
hospitalized patient, particularly in the surgical patient.
 The triad of venous stasis, endothelial injury, and
hypercoagulable state first posited by Virchow in 1856

3.  The most dreaded sequel to acute DVT is that of
pulmonary embolism, a condition of potentially lethal
consequence.
 The late consequence of DVT, particularly of the
iliofemoral veins, can be CVI and ultimately post-
thrombotic syndrome, as a result of valvular
dysfunction in the presence of luminal obstruction

4.  Hepercoagulbility-
 Most impotant in most cases of spontaneous VTE (Idiopathic
VTE)
 Stasis and endothelial damage
 Greater role in secondary VTE( provoked VTE)
 Occurs in association with risk factors like immobilasation,
surgical procedures and trauma

5. The Hypercoagulable State
 Factor V Leiden mutation
 Prothrombin gene mutation
 Protein C deficiency
 Protein S deficiency
 Antithrombin III deficiency
 Homocysteine
 Antiphospholipid syndrome

6.  After major operations
 Damaged tissue tissue factor may be released into the
bloodstream
 potent procoagulant expressed on the leukocyte cell surface as
and as soluble form in the bloodstream
•Increases in platelet count,
•adhesiveness,
•changes in coagulation
cascade,
•endogenous fibrinolytic
activity
Thrombosis

7. Stasis
 soleal sinuses are the most common sites of initiation
of venous thrombosis.
 stasis may contribute to the endothelial cellular layer
contacting activated platelets and procoagulant
factors, thereby leading to DVT.
 Stasis, in and of itself, has never been shown to be a
causative factor for DVT.

8. Venous Injury
 venous thrombosis occurs in veins that are distant from the site
of operation
 multiple microtears noted within the valve cusps that resulted in
the exposure of the subendothelial matrix

9. Initial Evaluation
1. Approximately 75% of patients with suspected DVT
or PE turn out not to have these condition
2. Assessment of Risk factor

10. Initial Evaluation
3. Clinical presentation
• Extremity pain
• Increased cicumference with respect to
contralateral extremity
• Dilatation of supeficial veins of suspected
extremity only

11. • Phlegmasia cerulea dolens
o Extensive DVT of major axial deep venous channels
o Relative sparing of collaterals
o Pain, pitting oedema and cyanosis
• Phlegmasia alba dolens
 Thrombous extension to collateral system
 Massive fluid sequestrationsignificant oedema
 Extremely painful and oedematous, pale secondary
to arterial insufficiency increases in below in
compartment pressue

12. Differential diagnosis
 Ruptured Baker’s cyst
 Calf muscle hematoma
 Ruptured plantaris muscle
 Thrombosed popliteal aneurysm
 Arterial ischemia

13. Assessing Clinical likelyhood
Clinical Variable Score
Active cancer 1
Paralysis, paresis, or recent cast 1
Bedridden for >3 days; major surgery
<12 weeks
1
Tenderness along distribution of deep
veins
1
Entire leg swelling 1
Unilateral calf swelling >3 cm 1
Pitting edema 1
Collateral superficial nonvaricose veins 1
Alternative diagnosis at least as likely
as DVT
–2
Low Clinical Likelihood of DVT if Point Score Is Zero
or Less
Moderate-Likelihood Score Is 1 to 2
High-Likelihood Score Is 3 or Greater

14. Assessing Clinical likelyhood
Clinical Variable Score
Signs and symptoms of DVT 3.0
Alternative diagnosis less likely than PE 3.0
Heart rate >100/min 1.5
Immobilization >3 days; surgery within 4
weeks
1.5
Prior PE or DVT 1.5
Hemoptysis 1.0
Cancer 1.0
High Clinical Likelihood of PE if Point Score Exceeds
4

15. Nonimaging Diagnostic Modalities
 Blood test
 D-Dimer rises in the presence of DVT or PE because of the
breakdown of fibrin by plasmin.
 The sensitivity of the d-dimer is >80% for DVT (including
isolated calf DVT) and >95% for PE.
 The d-dimer is less sensitive for DVT than for PE because
the DVT thrombus size is smaller.
 The d-dimer is a useful "rule out" test.
 More than 95% of patients with a normal (<500 ng/mL) d-
dimer do not have PE.

16. • The d-dimer assay is not specific.
 Levels increase in patients with
 myocardial infarction,
 pneumonia, sepsis,
 cancer,
 the postoperative state
 those in the second or third trimester of pregnancy.
• Therefore, d-dimer rarely has a useful role among
hospitalized patients, because levels are
frequently elevated due to systemic illness.

17. Noninvasive Imaging Modalities

19.  USG rules out other D/ds
 Baker's cyst (also known as a popliteal or synovial
cyst
 hematoma
 technically poor or nondiagnostic venous
ultrasound alternative imaging modalities CT
and MRI

20. Duplex ultrasound
 Real time B mode USG +pulse doppler capability
 Lack of spontaneous flow
 Incompressibility
 Absence of color filling of lumen by color flow DUS
 Loss of respiratory flow variation and venous
distension

21. Chest CT
 RV enlargement on chest CT indicates an
increased likelihood of death within the next 30
days compared with PE patients who have
normal RV size on chest CT.
 imaging is continued below the chest to the
knee pelvic and proximal leg DVT also can be
diagnosed by CT scanning.
 Rules out other
 pneumonia, emphysema, pulmonary fibrosis,
pulmonary mass, and aortic pathology.

22. Lung Scanning
 second-line diagnostic test for PE
 used mostly for patients who cannot tolerate intravenous
contrast
 Small particulate aggregates of albumin labeled with a
gamma-emitting radionuclide are injected intravenously
and are trapped in the pulmonary capillary bed
 perfusion scan defect indicates absent or decreased
blood flow, possibly due to PE.
 Ventilation scans, obtained with a radiolabeled inhaled
gas such as xenon or krypton, improve the specificity of
the perfusion scan.

23.  A high-probability scan for PE is defined as one
that indicates two or more segmental perfusion
defects in the presence of normal ventilation

24. Magnetic Resonance (MR)
 suspected VTE patients with renal insufficiency or
contrast dye allergy.
 may detect large proximal PE but is not reliable for
smaller segmental and subsegmental PE.

25. Echocardiography
 useful diagnostic tool for detecting conditions that
may mimic PE, such as acute myocardial infarction,
pericardial tamponade, and aortic dissection
 The best-known indirect sign of PE on transthoracic
echocardiography is McConnell's sign: hypokinesis
of the RV free wall with normal motion of the RV apex

26. Pulmonary angiography
 technically unsatisfactory chest CTs
 interventional procedure such as catheter-directed
thrombolysis or embolectomy is planned.
 visualization of an intraluminal filling defect in more
than one projection.
 Secondary signs of PE include abrupt occlusion
("cut-off") of vessels, segmental oligemia or
avascularity, a prolonged arterial phase with slow
filling, and tortuous, tapering peripheral vessels.

27. Management
 Goal of VTE Management
 Prevention of mortality and morbidity associated
with PE and prevention of post thrombotic
syndrome
 Treatment option
 Antithrombotic therapy
 Temporary or permanent venacaval filter placement
 Catheter directed or systemic thrombolytic therapy
 Operative thrombectomy

28. Antithrombotic therapy
 IV or SC UFH
 SC LMWH
 Foundaparinux
 Warfarin
 Begun after initiation IV/SC therapy
 IV/SC continued until oral anticoagulatio achieved
( INR>2)
 Minimum 5 days of heparin or fondaparinux recommended

29. UFH
 Binds to antithombin III
 inhibits factor IIa ( Thrombin) and facto Xa and also F
IXa,XIa and XIIA of coagulation cascade
 Dose-
 IV bolus- 80u/kg
 Followed by continious IV drip at 18units/kg/hr
 T1/2- 45-90min (dose dependent)
 Monitoring- aPTT 6hourly
 aPTT goal- 1.5 to 2 times the control value

30. Complication of UFH
1.Hemorrahage
 Fatal, intracranial hemorrhage, retroperitoneal or
requiring >2 unit of packed red cell is aprox 5 % in
hospitalized patient
 Management
 Discontinue UFH
 Protamine sulphate
 1mg protamine neutralizes 90-115 unit of heparin
 Dose not to exceed 50mg IV over any 10 min

31.  Protamine sulphate side effect
 Hypotension
 Pulmonary edema
 Anaphylaxis
 Patient on NPH and allergic to fish

32. Complication of UFH
2. HIT
 Results due to heparin associated antiplatelets
antibody complex
 Repeted heparin exposure( vascular Sx- 21%)
 Occurs m/c in 2nd week of therapy
 Platelet counts to be monitored periodically
 Dx- exposure to Heparin + platelets <100,000 and/ or
decline in 50% of platelet following exposure

33. Complication of UFH
3. Heparin induced osteopenia
impairment of bone formation and enhancement of
bone resorption by heparin

34. LMWH(enoxaparin)
 Derived from polymerization of porcine UFH
 Act more on F Xa
 Increased bioavailability
 2-4 times longer half life
 Can be administered S.C without lab monitoring
 Partially reversible by protamine (60%)
 Patient requiring monitoring
 Severe renal impairment, pediatrics,pregnants, wt>120kg
 HIT <2%
 Established HIT- not be used
 Outpatient treatment
 Reduce hospital stay

35. Fondaparinux
 Synthetic petasaccharide
 Activated antithrombin and Xa inhibiion
 Recurrent VTE- 3.8-5%
 Major bleeding- 2-2.6%
 Administered – SC once daily dose
 Half life 17 hour

36. Direct thrombin inhibitors
 Hirudin,argatroban and bivalirudin
 Binds thrombin and inhibiting conversion of fribrinogen to
fibrin and fribrin induced thrombocytopenia
 Used for high suspicion/confirmed HIT or with
history of HIT or HAAb positive cases
 Requires aPTT adjustment

37. Vitamin K antagonist
 Main stay of long term antithrombotic therapy
 Warfarin and other coumarin derivatives
 Inhibits gamma carboxyaltion of Vit K dependent factors and
protein C and S
 Requires several days to achieve full effect ( 4-5 days)
 Monitored by INR
 INR= (patient PT/lab normal PT)*ISI
 ISI- international senstivity index- strength of thromboplastin
that is added to activate the extrinsci coagualtion pathway

38. warfarin
 Therapeutic range- 2-3
 To be started on same day of starting parenteral
anticoagualation ( except with concominant thrombolysis
and venous thrombectomy)
 Usual starting dose 50-10mg
 Smaller dose for older, malnourished, liver disease and
CHF
 Variability of response
 Depends upon Liver funtion, diet, age and medicaitons used

40.  Primary complication- hemorrhage
 Reversal- VIT-K, FFP, prothrombin factor complex,
Recombinant F VIIa
 Warfarin therapy rarely causes skin necrosis and limb
gangrene
 M:F=1:4
 Breat, buttock, thigh

41. Systemic and catheter directed
lysis(CDT)
 Indication
 Extensive proximal, iliofemoral DVT
 Streptokinase
 B-hemolytic streptococcus
 Acute MI,PE,DVT, arterial thromboembolism, occulded
central lines
 Limited use- antigenicity (fever/shiver-1-4%)
 Urokinase
 Human neonatal kidney
 Alteplase,reteplase
 Recombinant variants of tissue plasminogen activator
 CDT of DVT, PE, acute MI

42. Systemic thrombolysis/ CDT
 Systemic thrombolysis
 More clot lysis
 Less PTS
 More bleeding complication
 CDT
 Administer lytic agent alone
 Pharmacomechanical clot lysis

43. Inferior Venacaval filters
Patients with proven VTE with
 contraindication for anticoagulation
 complication of anticoagulation
 or recurrent VTE despite of anticoagulaiton

44. Operative thrombectomy
 ileofemoral DVT
 Worsening with anticoagulation therapy
 Phlegmasia cerulea dolens
 Impending venous gangrene
 Pulmonary thormobectomy
 Massive pulmo emboli with failed thrombolysis or
contraindication to thrombolytics
 Posterolateral thoracotomy
 Percutaneous catheter based technique- mechanical
clot fragmentation followed by CDT

45. Prophylaxis
 Use of one or more pharmacologic or mechanical
modalities

46. Elastic compression stockings
 Assist calf muscle pump and reduce venous
hypertension and venous valvular reflux
 Reduces leg edema, aids the microcirculaiton,
prevents ischemia
 Regular use of ECS reduced the Post thrombotic
syndrome by 50%
 30- to 40-mmHg vascular compression
 When patients are in bed, the stockings need not be
worn

47. Ambulation
 ACCP Concensus Conference on antithrombotic and
thrombolytic therapy for VTE (2012)
 Ambulation as tolerated for patient with DVT
 Early ambulaiton on day 2 after initiation of outpatient anticoagulant
therapy in addtion to ECS is strongly recommended
 Early ambulation without ECS is not recommended due to fear of
dislodging clots and precipititing fatal PE
 The practice of having a patient “out of bed into a chair” is one of the
most thrombogenic positions.
 Sitting in a chair with the legs in a dependent position causes venous
pooling thromboembolism.

48. Level of Risk Approx DVT Risk
without
Thromboprophylaxis
(%)
Thromboprophylaxi
s option
Very low risk
General or abdominopelvic
surgery
<0.5%
(Rogers
score<7;Caprini score
0)
No specific drugs
Early ambulation
low risk
General or abdominopelvic
surgery
~1.5%
(Rogers score 7-10
Caprini score 1-2)
Mechanical
Prohpylaxis
Moderate risk
General or abdominopelvic
surgery
~3%
(Rogers score>10
7;Caprini score 3-4)
LMWH,LDUH or
mechanial
prophylaxis
High Bleeding risk Mechanical
prophylaxis
High Risk
General or abdominopelvic
surgery
~6%(Rogers
score<7;Caprini score
>5)
LMWH, fondaparinux,
mechanical
prophylaxis

49. References
 Schwartz’s Principles of Surgery 10th edition
 Sabiston Text book of Surgery 19th Edition
 Harrison’s Principle of Internal Medicine 18th
edition
 Bailey and Love’s short Practice of Surgery ( 25th)
 Washington Manual of Surgery 6th Edition
 Medscape

50.  Thank you