Deep venous thrombosis

Lucid discussion on the risk factors, clinical presentation and prevention of deep venous thrombosis in surgical patients

1. DEEP VENOUS THROMBOSIS
DR ITAMAN, USIFOH
surgery registrar
Presented 0n 30/6/2019 to the Department of
Surgery, ISTH, as part of the requirements for the
Part 1 Post-graduate Training Programme in
Surgery

2. OUTLINE
•Introduction
•Relevant anatomy and physiology
•Epidemiology
•Risk factors
•Classification
•Pathogenesis
•Clinical features
•Diagnosis
•Prevention
•Treatment
•Complications
•Conclusion

3. INTRODUCTION
•Venous thromboembolism (VTE) is a spectrum of
clinical manifestations that includes deep venous
thrombosis (DVT) and pulmonary embolism (PE)
•Thrombosis is the formation of a clot (thrombus)
from blood constituents within the vessels of a
living body.
•When this phenomenon occurs in the deep veins,
it is called DVT
•Results from imbalance between the pro
coagulant and anticoagulant factors .

4. •Commonly occurs in the deep veins of the
lower limbs but can occur in the pelvic,
subclavian/axillary .
•It is a preventable cause of morbidity and
mortality .
•Clinical diagnosis is insufficient

5. HISTORICAL BACKGROUND :
•1644, Schenk first observed venous thrombosis
•1819, Laennec described PE
•1846, Virchow recognized the association btw DVT in
the leg and PE
•1877, first embolectomy by Trendelenburg
•1937, Heparin was introduced
•1948 Warfarin was synthesized by Karl Link
•1976 First IVC filter (Mobin-Uddin) approved for use
•2010 Rivarobaxan
•2014 Dabigatran

6. RELEVANT ANATOMY

8. VASCULAR PHYSIOLOGY
Haemostasis:
Keeps blood within the blood vessels
Achieved by
Vessel wall contraction
Platelets adhesion & aggregation
Coagulation activation

11. Anticoagulation process
Prevents excessive coagulation
Antithrombin III
Thrombomodulin
Protein C & S(inactivate factors Va and VIIIa)
Fibrinolysis
Fibrinolysins
Inactivate Va & VIIIa
Lysis clot deposits
Recanalization
•Equilibrium between these processes maintains blood in the fluid state
within the vessels

12. EPIDEMIOLOGY
Exact incidence is unknown;
•About 80 cases per 100,000 population annually
•In US, DVT accounts for 600,000
hospitalizaton/ yr
•M:F –1.2:1
•Age >40yrs
•Less common in the pediatric population; about
1 in 100,000 people

13. EPIDEMIOLOGY cont’d
•Clinically recognised disease accounts for 1 in
20 deaths in patients above 50 years
•Autopsy shows that ≈ 80% DVT & PE are
undiagnosed
•Prevalence highest in
–Hospitalised patients
–Post operative and traumatized patients
–Severe co-existing illness

14. RISK FACTORS

16. IMMEDIATE PERIOP RISK FACTORS
•Nature and duration of operation
•The anaesthetic technique used
•The degree and duration of immobility
•Dehydration or sepsis
•Surgery
–70% after non-elective hip surgery
–48% after elective hip surgery
–12% after elective general surgery

17. CLASSIFICATION
1.Based on location
•Proximal
•Distal
Proximal versus distal (70%)
2. Based on etiology
•Primary (idiopathic)
•Secondary

18. PATHOGENESIS
ActivationofClottingcascadeinavesselleadstothrombusformation.
•Virchow’s Triad –stasis
-hypercoagulability
-vascular endothelial injury
Contrasting pathogenesis of Arterial & Venous thrombus
Unlike with arterial thrombus where endothelial damage initiates the
clot, venous clots mostly occur without any endothelial injury.
Low flow + Tissue factor !!

20. Diagnosis
•Risk assessment
•Clinical presentation
•Investigations

21. RISK ASSESSMENT
•Wells
•Rogers
•Caprini
•Padua
•VTE-BLEED score
•IMPROVE risk assessment model

22. RISK ASSESSMENT

23. CLINICAL PRESENTATION
Two-third are asymptomatic
Symptomatic patients present with:
•Fever
•Unilateral leg swelling
•Leg Pain
•Phlegmasia alba dolens
•Phlegmasia cerulea dolens
•Symptoms of PE

24. EXAMINATION
-Stretched and shiny skin
-Differential warmth positive
-Tense and tender limb swelling
-Unilateral pitting oedema (usually below the point of obstruction. )
-Superficial venous dilatation(varicose vein) may be observed
-Signs:
Homan’s sign
Moses sign
Neuhof
Lowenberg
These signs are non-specific and largely condemned.

26. INVESTIGATION
•Diagnostic; Invasive/ non invasive
Duplex USS,
Venography
CT, MRI
Intravascular USS
I
125
Fibrinogen uptake
•D-dimer
•Clotting profile: PT, aPPT, INR
•FBC+ absolute Platelet count
•Assay: Protein c, Protein S, ATIII, Factor V.
•CXR in view of PE

27. D-DIMER ASSAY
Degradation product of fibrin
Measured via: ELISA, LLA, SimpliRED
Highly sensitive > 95%
Poor specificity

28. VENOUS ULTRASONOGRAPHY
-DVT likely patient
-Non invasive ,safe, available and inexpensive
-There are 3 types:
Compression ultrasound (B mode imaging)
Duplex ultrasound (doppler wave form analysis)
Colour doppler imaging
-Limitations

30. CONTRAST VENOGRAPHY
Definitive diagnostic test for DVT
-cannulation of pedal vein with
injection of a contrast medium
-Identifies location, extent and
attachment of a clot
-constant intraluminal filling
defect evident in 2 or more
views and abrupt cut off of
deep veins
-Abrupt cut off of a deep vein
-Limitations

31. IMPEDANCE PLETHYSMOGRAHY
Rate of change in impedance between 2
electrodes on the calf when a venous occlusion
cuff is deflated
-Delay in outflow of venous blood leads to a
more gradual change in the presence of DVT
-Its safe and non invasive
-Limitation: Not sensitive to small proximal
thrombi

32. MRI VENOGRAPHY
CT VENOGRAPHY

33. Diagnosis algorithm

34. DIFFERENTIAL DIGNOSIS

35. PREVENTION OF DVT
PRE-OP
•General measures
–Identify patient at risk
–Reduce weight before surgery
–Stop oral contraceptives 4 weeks before elective surgery
–Stop smoking
–Short pre-op hosp stay (< 72hrs)
–Deep breathing exercises
–Adequate hydration
•Mechanical
–Graduated compression stockings
–Intermittent pneumatic compression of calf
–Electrical calf muscle stimulation
•Chemical-drugs (high risk pts)
–Anticoagulation eg subcut Clexane

36. INTRA OP
•Pad pressure points
•Anaesthesia: Epidural
•Electrical stimulation of calf muscles
•External passive leg exercise using foot
paddling machine
•Adequate hydration

37. POST OP
•General measures
–Adequate hydration
–Deep breathing exercises
–Adequate analgesia
–Early mobilization
•Mechanical
–Graded elastic compression stockings
–Intermittent pneumatic leg compression
•Chemical-drugs
–Heparin-unfractionated, LMWH
–Warfarin; Fondaparinux
–Aspirin; Dextran

38. Unfractionated heparin (UFH)
Natural; porcine intestine & bovine lung mucosa.
Enhances Antithrombin III activity
-inactivates Xa, IIa, IXa, XIIa, antiplatelet activity, HIT
Dose 5000units SC 8HRLY
•Monitoring with aPTT required; target 1.5×control.
reversed with protamine sulphate(1mg/100units)
Heparin prophylaxis is usually given for at least five days (the
minimum duration of prophylaxis in RCTs) or until hospital
discharge if earlier.
safe throughout pregnancy & renal failure.

39. LMWH
•Natural source
•Indirect inhibitor of Xa by ↑ antithrombin III
•Enoxaparin, certoparin, tinzaparin, dalteparin etc.
•No monitoring of aPTT or INR required
•Safe in pregnancy, ↓ dose in renal failure
•OD dosing, S.C
•No antiplatelet activity, less HIT
•Less bleeding compared to UFH
•Partial reversal by protamine sulphate. ≠ FFP !!
•Expensive, but cost effective.
•Meta-analyses of RCTs have shown that subcutaneous
LMWHs have similar prophylactic efficacy to UFH

40. Warfarin
•Oral, OD dosing, 5mg, synthetic.
•Inhibits synthesis of Vit. K –dependent factors.
•Absolute C/I:pregnancy, non-compliance to Px or INR monitoring
•First,establish baseline INR, Initial therapy, Monitoring frequency.
•Target 2.5 (range: 2-3)
•Diverse drug, food interaction.
↓ dosing in renal failure
•Slow onset; 3-5 days
•Reversal with Vit.K –5mg i.v slowly; 6hr onset. (-FFP 15mls/kg; immediate
onset.)

41. Rivaroxaban
•1
st
Direct Xa inhibitor, synthetic.
•Oral, O.D dosing, 10mg
•No lab monitoring required
•No reversal agent
•Cost of Enoxaparin
↓ dosing in renal failure

42. Dabigatran
•Direct thrombin inhibitor
•Oral, synthetic
•O.D dosing, 220mg
•No specific antidote
•Lab monitoring not reqd.
•↓ dosing in renal failure
•Cost of Enoxaparin

43. Fondaparinux ( ULMWH )
•Synthetic pentasaccharide
•Indirect Xa inhibitor, by ↑ antithrombin III activity
•No monitoring reqd
•OD dosing, Start 6hrs post-op, S.C, 2.5mg
•2×cost of Enoxaparin
•No reversal agent. FFP ineffective ! !
•↓ dosing in renal failure
•More effective, more bleeding > LMWH

44. Antiplatelets
•Low dose aspirin etc.
•Inhibits platelet activation & aggregation
•Cheap, oral.
•Reversal with platelet concentrate
•Low risk of bleeding
•Lab monitoring not required
•Effect continues for 7-10 days
•↓ risk of PE > DVT.
•POOR RESULTS V. LMWH
•NOT RECOMMENDED ALONE FOR VTE IN ANY PATIENT GROUP

45. Dextrans
•DEXTRAN-70, DEXTRAN –40
•Plasma expander, ↓ viscosity, ↓stasis, Antiplatelet
•No monitoring reqd
•Effective for medium risk patients
Easy & convenient, effective during surgery
•Risk of anaphylaxis.

46. Early ambulation
•Traditional method
•Ambulation addresses
only one component of
Virchow's triad, namely
venous stasis.
•Although desirable, it is
by itself not an
adequate prophylactic
measure for patients at
moderate or high risk.

47. GRADUATED ELASTIC COMPRESSION STOCKING
•Among the simplest of physical measures used.
•Properly fitted ES increase the velocity of blood
flow through the femoral veins.
•Effective in reducing the incidence of venous
clots, but only for patients at low risk.
•Thigh-length stocking should be preferred to
knee-length, substantial DVT develop above the
knee.
•Should be used in the appropriate manner

49. INTERMITTENT PNEUMATIC COMPRESSION(IPC)
•Important means of DVT prophylaxis.
•Made up of inflatable garment for the limb and electrical
pneumatic pump that fills the garment with compressed
air.
•Compare favorably with low-dose heparin.
•Pooled data show an incidence of DVT in 10 percent of
patients protected with IPC, representing a risk reduction
of 60 percent
•Not practicable in patients with fractures, plaster casts or
external fixation devices.

51. Venous foot pumps
•Useful when IPC devices or
stockings cannot be worn e.g.
trauma pts.
•It flattens metatarsal arch and
empties the plantar venous
plexus,reproducing the effect
of a normal weight bearing.
•Pt compliance better than in
the IPC devices.
•Risk of vessel injury is less,
pumps differ in speed and
pressure.

52. Inferior vena cava filters
•Inserted percutaneously under USS guidance
usually via the femoral vein.
•Placed in the IVC below the renal veins.
•Useful when anticoagulation is
contraindicated or pts who develop recurrent
VTE despite anticoagulation.
•Filters only prevent PE but do not halt the
thrombotic process.

54. Treatment
•Non operative:
-General measures
-Anticoagulation
-Thrombolysis (fribrinolysis)
•Operative:
-Minimally invasive
-Open venous thrombectomy

55. Non operative
•ANTI-COAGULATION
Heparin-Warfarin
Doses :
•Unfractionated Heparin 333units/kg subcut.followed by
250 units/kg twice daily
•Enoxaparin 1 mg/kg 12h hourly
•Enoxaparin 1.5 mg/kg daily
•Tinzaparin 175 IU/kg daily
•Dalteparin 100 IU/kg 12hourly
•Dalteparin 200 IU/kg daily

56. •FIBRINOLYSIS
–Now mainstay of therapy esp in early presentation
–However large thrombi and recent surgery are
unsuitable
–Two forms of recombinant tissue plasminogen
activator
•t-PA (alteplase)
•r-PA (reteplase)
–Urokinase
–Streptokinase

57. Operative
•Surgical Therapy
Preservation of patency AND valve function are the
main goals
Minimally invasive
–Venous thrombectomy with Fogarty catheter
–Angioscopic thromboembolectomy
–Aspiration thromboembolectomy
–With/without adjunctive fibrinolytic infusion
Open surgery

58. Fogarty catheter

60. Treatment timeline
Duration of therapy Indication
3-6months First event with reversible* or
time-limited risk factor
6 months or more Idiopathic venous
thromboembolism, first event
1 year to lifetime First event
†
with:
-Cancer, until resolved
-Anticardiolipin antibody
-Antithrombin deficiency
Recurrent event,
idiopathic or with
thrombophilia
* Surgery, trauma, immobilization, estrogen use.

61. Complications
•Pulmonary embolism
•Phlegmasia alba dolens
•Phlegmasia cerulea dolens
•Chronic Venous insufficiency
•Post phlebitic syndrome
•Recurrent DVT
•Varicose veins
•Complications of treatment

63. New trends
•M R A is being increasingly used to diagnose
DVT involving popliteal, common iliac and IVC
•Percutaneous retrievable IVC filters
•Newer agents : hirudin, lepirudin, idraparinux,
Bivalirudin, ximelagatran

64. Conclusion
•DVT is a common cause of morbidity and
mortality.
•Best prophylactic protocol for each patient
must be individualized, taking into account the
risk –benefit ratio.
•Even with optimal prophylaxis, VTE can & does
occur.
•VTE and DVT will remain a topical issue for
years to come.

65. References
•Brunicard F.C., Dana K.A., David L.D et al, 2015. Schwartz Principles Of Surgery .10
th
Edn. McGraw Hill, New York.
•John L.C., Andrew M.C. , 2014. Current Surgical Therapy. 11
th
Edn, Elsevier Sanders,
Philadephia.
•E. Kesieme, C. Kesieme, E. Irekpita, A. Dongo. 2012. Deep Vein Thrombosis: A Clinical
Review , Journal of Blood Medicine 2012:2 .
https://www.researchgate.net/publication/221789439
•Kesieme E B, Arekhandia B J, Inuwa I M, Akpayak I C, Ekpe E E, Olawoye O A, Umar A,
Awunor N S, Amadi E C, Ofoegbu I J. 2016. Knowledge and practice of prophylaxis of
deep venous thrombosis: A survey among Nigerian surgeons. Niger J Clin Pract
2016;19:170-4
•Andre Biuckians; George H. Meier III. Treatment of Symptomatic Lower Extremity
Acute Deep Venous Thrombosis: Role of Mechanical Thrombectomy
http://www.medscape.com/viewarticle/567031_2

66. Thanks for listening