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DEEPVEINTHROMBOSISDEEPVEINTHROMBOSIS
Prepared by : Maria Devi
Adlin
Supervisor : Dr Hasmali
OUTLINEOUTLINE
 Definition
 Epidemiology
 Anatomy
 Pathophysiology
 Risk factor
 Approach to DVT
 Management
 complication
 Prevention
 Take home message
DefinitionDefinition
Deep venous thrombosis (DVT) is a
formation of blood clots or thrombus
in the deep vein of legs or pelvic.
Anatomy of deepAnatomy of deep
veinsveins
 In the lower leg, three pairs of deep veins
exist:
 anterior tibial vein (ATV), draining the
dorsum of the foot;
 posterior tibial vein (PTV), draining the
medial aspect of the foot;
 the peroneal vein, draining the lateral aspect
of the foot.
 Just below the knee, all the deep veins joint
to become the single large popliteal vein.
 In the proximal thigh, the FV and the DFV
join together to form the common femoral
vein (CFV), which passes upward and form
the iliac vein.
Superficial Vein :Superficial Vein :
 The Great Saphenous Vein originates from the 
dorsal venous arch of the foot.
 After passing anterior to the medial malleolus, it
runs up the medial side of the leg.
 At the knee, it runs over the posterior border of
the medial epicondyle of the femur bone.
 The great saphenous vein then courses medially
to lie on the anterior surface of the thigh before
entering the saphenous opening.
 It joins with the femoral vein in the region of the 
femoral triangle at the saphenofemoral junction.
AetiologyAetiology
Virchow’s triad:
a) Endothelial injury
b) Stasis or turbulence of blood flow
c) Hypercoagulability of the blood
ENDOTHELIAL INJURY
Reduced or stagnant blood flow HYPERCOAGULABILITY
THROMBOSIS
Virchow’s triadVirchow’s triad
In extremely sluggish flow ,thrombus formation
in the vein valve pockets is. Thrombus formation occurs
when the natural antithrombotic mechanisms are overcome.
By production of
• prostacyclin, nitric oxide and tissue plasminogen activator
• cell-surface glycosaminoglycans (e.g. heparin sulphate)
• the physiological inhibitors of clotting (e.g. antithrombin,
protein
C, protein S, see below).
Endothelial damage (due to direct
trauma and/or damage to endothelial cells by hypoxia caused
by stasis) in the presence of activated clotting factors initiates
thrombosis
there are four main anticoagulant mechanisms
in the coagulation cascade that maintain blood flow
and restrict thrombosis only to site of injury:
• antithrombin
• protein C and protein S
• tissue factor pathway inhibitor
• the fibrinolytic system
Risk FactorsRisk Factors
STASIS/ENDOTH
ELIAL INJURY
THROMBOPHILIA MEDICAL
CONDITION
DRUGS OTHER
Indwelling venous
device
Surgery (most
common pelvic and
orthopedic)
Major trauma,
fracture
Prolonged travel
Paralysis (including
anaesthesia > 30
min)
Varicose vein
Activated protein C
resistance
Prothrombin gene
mutation
Factor V Leiden
Dysfibrinogenemia
Dysplasminogenemia
Hyperhomocysteinemia
Anticardiolipin
antibodies
Lupus anticoagulant
Elevated factor VIII level
Protein C deficiency
Protein S deficiency
Malignancy (solid
tumor &
myeloproliferative
disorder)
Pregnancy
MI
CHF
Stroke
Obesity
IBD
Nephrotic syndrome
History of DVT
Heparin-induced
thrombocytopenia
Paroxysmal nocturnal
hemoglobinuria
Oral
contraceptive
use
Hormone
replacement
therapy
Chemotherapy
(inclding
Tamoxifen)
Increasing
age
How to Approach DVTHow to Approach DVT
• History
• Presenting complaint – pain, swelling
• Time of onset
• Is it both legs?
• Has there been any trauma?
• Is there any pain? (65% below knee DVT are asyptomatic)
• Is there any swelling? How recent?
• Have there been any skin changes?
• Any odema anywhere else?
• Is the patient mobile?
• Recent surgery or trauma/fractures
• Paralysis/paresis
• Plaster immobilisation of lower limb
• Recently bedridden for >3 days or major surgery <4 weeks.
• Look for Symptoms of PE
– Pleuritic, sharp chest pain
– Acute onset of breathlessness
– Haemoptysis
• Previous Medical History
– DVT or PE. Arthritis. Malignancy (ongoing treatment, within 6 months
or palliative)
– Thrombophilia. Recurrent miscarriages. Diabetes. MI. AF. CVA
• Family History
– DVT or PE. Cardiac problems. CVA. Clotting disorders
• Risk Factors
– Age, smoker, pregnancy, long haul travel, obesity, immobility
• Drug history & Allergies
– Immunosuppressant drugs. Contraceptive pill. Warfarin. IV drug user
Clinical featuresClinical features
half of all DVT cases do not cause symptoms
depend on the location and size
swelling
redness
Tenderness
muscle induration
Mild pyrexia
Homan’s sign - tenderness during passive dorsiflexion of
foot.
Pratt’s sign - Squeezing of posterior calf elicits pain
Phlegmasia alba dolens - pale, pulseless cold limb
due to concurrent arterial spasm
Phlegmasia caerulea dolens - cyanosed limb due to
obstructed vein
Clinical PresentationClinical Presentation
Phlegmasia alba dolensPhlegmasia caerulea dolens
DiagnosisDiagnosis
• InvestigationsInvestigations
»Complete blood count – Hb, PCV,
Platlet count and White cell count
»Primary coagulation study
»Liver enzymes
»Renal function and electrolytes
»D – Dimer – fibrin degradation
product) is increasingly being used
as a screening adjunct. It has a
sensitivity of >90% and a specificity
of 30–40%.
»ECG
• ImagingImaging
– Chest radiograph
– B-mode ultrasound
–is the first-line non-invasive investigation
–a non-compressible thrombus in the thigh and
popliteal veins can be diagnosed with 97%
sensitivity and 94% specificity
– Venography
–invasive, uncomfortable and requires injection of
contrast.
– Spiral CT and CT pulmonary angiography
–investigations to diagnose pulmonary embolism.
Well’s CriteriaWell’s Criteria
Clinical feature Points
Active cancer (treatment within 6
months, or palliation)
1
Paralysis, paresis, or immobilization
of lower extremity
1
Bedridden for more than 3 days
because of surgery (within 4 weeks)
1
Localized tenderness along
distribution of deep veins
1
Entire leg swollen  1
Unilateral calf swelling of greater
than 3 cm (below tibial tuberosity)
1
Unilateral pitting edema 1
Collateral superficial veins 1
Alternative diagnosis as likely as or
more likely than DVT
-2
Total points  
Wells Clinical Prediction Rule
for Deep Venous Thrombosis
(DVT)
Risk score interpretation
(probability of DVT):
•>/=3 points: high risk (75%);
•1 to 2 points: moderate risk
(17%);
•<1 point: low risk (3%).
• not universally used, still
debatable
ComplicationsComplications
• Pulmonary Embolism
» The clot from lower limb become detached & passes via
IVC & right heart to the pulmonary arteries and may
totally occlude the perfusion to part or all of one or both
lungs
• Post-thrombotic Limb
» Valves in the deep venous channels of the lower leg have
been damaged by thrombotic process
» Recanalized deep veins are functionally inadequate because of
the damaged valve.
» bidirectional flow & abnormally high ambulatory venous
pressure in the deep vein transmitted to subcutaneous vein→ →
edema, pigmentation, fibrosis, and later, dermatitis,edema, pigmentation, fibrosis, and later, dermatitis,
cellulitis and ulcerationcellulitis and ulceration
TAKE HOME MESSAGES :TAKE HOME MESSAGES :
 DVT is one of those things that has a number of predisposing causes, so it is
in fact mostly preventable
 Clinical predictive rule : Well’s criteria

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Deep vein thrombosis maria

  • 1. DEEPVEINTHROMBOSISDEEPVEINTHROMBOSIS Prepared by : Maria Devi Adlin Supervisor : Dr Hasmali
  • 2. OUTLINEOUTLINE  Definition  Epidemiology  Anatomy  Pathophysiology  Risk factor  Approach to DVT  Management  complication  Prevention  Take home message
  • 3. DefinitionDefinition Deep venous thrombosis (DVT) is a formation of blood clots or thrombus in the deep vein of legs or pelvic.
  • 4. Anatomy of deepAnatomy of deep veinsveins  In the lower leg, three pairs of deep veins exist:  anterior tibial vein (ATV), draining the dorsum of the foot;  posterior tibial vein (PTV), draining the medial aspect of the foot;  the peroneal vein, draining the lateral aspect of the foot.  Just below the knee, all the deep veins joint to become the single large popliteal vein.  In the proximal thigh, the FV and the DFV join together to form the common femoral vein (CFV), which passes upward and form the iliac vein.
  • 5. Superficial Vein :Superficial Vein :  The Great Saphenous Vein originates from the  dorsal venous arch of the foot.  After passing anterior to the medial malleolus, it runs up the medial side of the leg.  At the knee, it runs over the posterior border of the medial epicondyle of the femur bone.  The great saphenous vein then courses medially to lie on the anterior surface of the thigh before entering the saphenous opening.  It joins with the femoral vein in the region of the  femoral triangle at the saphenofemoral junction.
  • 6. AetiologyAetiology Virchow’s triad: a) Endothelial injury b) Stasis or turbulence of blood flow c) Hypercoagulability of the blood
  • 7. ENDOTHELIAL INJURY Reduced or stagnant blood flow HYPERCOAGULABILITY THROMBOSIS Virchow’s triadVirchow’s triad In extremely sluggish flow ,thrombus formation in the vein valve pockets is. Thrombus formation occurs when the natural antithrombotic mechanisms are overcome. By production of • prostacyclin, nitric oxide and tissue plasminogen activator • cell-surface glycosaminoglycans (e.g. heparin sulphate) • the physiological inhibitors of clotting (e.g. antithrombin, protein C, protein S, see below). Endothelial damage (due to direct trauma and/or damage to endothelial cells by hypoxia caused by stasis) in the presence of activated clotting factors initiates thrombosis there are four main anticoagulant mechanisms in the coagulation cascade that maintain blood flow and restrict thrombosis only to site of injury: • antithrombin • protein C and protein S • tissue factor pathway inhibitor • the fibrinolytic system
  • 8. Risk FactorsRisk Factors STASIS/ENDOTH ELIAL INJURY THROMBOPHILIA MEDICAL CONDITION DRUGS OTHER Indwelling venous device Surgery (most common pelvic and orthopedic) Major trauma, fracture Prolonged travel Paralysis (including anaesthesia > 30 min) Varicose vein Activated protein C resistance Prothrombin gene mutation Factor V Leiden Dysfibrinogenemia Dysplasminogenemia Hyperhomocysteinemia Anticardiolipin antibodies Lupus anticoagulant Elevated factor VIII level Protein C deficiency Protein S deficiency Malignancy (solid tumor & myeloproliferative disorder) Pregnancy MI CHF Stroke Obesity IBD Nephrotic syndrome History of DVT Heparin-induced thrombocytopenia Paroxysmal nocturnal hemoglobinuria Oral contraceptive use Hormone replacement therapy Chemotherapy (inclding Tamoxifen) Increasing age
  • 9. How to Approach DVTHow to Approach DVT • History • Presenting complaint – pain, swelling • Time of onset • Is it both legs? • Has there been any trauma? • Is there any pain? (65% below knee DVT are asyptomatic) • Is there any swelling? How recent? • Have there been any skin changes? • Any odema anywhere else? • Is the patient mobile? • Recent surgery or trauma/fractures • Paralysis/paresis • Plaster immobilisation of lower limb • Recently bedridden for >3 days or major surgery <4 weeks.
  • 10. • Look for Symptoms of PE – Pleuritic, sharp chest pain – Acute onset of breathlessness – Haemoptysis • Previous Medical History – DVT or PE. Arthritis. Malignancy (ongoing treatment, within 6 months or palliative) – Thrombophilia. Recurrent miscarriages. Diabetes. MI. AF. CVA • Family History – DVT or PE. Cardiac problems. CVA. Clotting disorders • Risk Factors – Age, smoker, pregnancy, long haul travel, obesity, immobility • Drug history & Allergies – Immunosuppressant drugs. Contraceptive pill. Warfarin. IV drug user
  • 11. Clinical featuresClinical features half of all DVT cases do not cause symptoms depend on the location and size swelling redness Tenderness muscle induration Mild pyrexia Homan’s sign - tenderness during passive dorsiflexion of foot. Pratt’s sign - Squeezing of posterior calf elicits pain Phlegmasia alba dolens - pale, pulseless cold limb due to concurrent arterial spasm Phlegmasia caerulea dolens - cyanosed limb due to obstructed vein
  • 12. Clinical PresentationClinical Presentation Phlegmasia alba dolensPhlegmasia caerulea dolens
  • 13. DiagnosisDiagnosis • InvestigationsInvestigations »Complete blood count – Hb, PCV, Platlet count and White cell count »Primary coagulation study »Liver enzymes »Renal function and electrolytes »D – Dimer – fibrin degradation product) is increasingly being used as a screening adjunct. It has a sensitivity of >90% and a specificity of 30–40%. »ECG
  • 14. • ImagingImaging – Chest radiograph – B-mode ultrasound –is the first-line non-invasive investigation –a non-compressible thrombus in the thigh and popliteal veins can be diagnosed with 97% sensitivity and 94% specificity – Venography –invasive, uncomfortable and requires injection of contrast. – Spiral CT and CT pulmonary angiography –investigations to diagnose pulmonary embolism.
  • 15. Well’s CriteriaWell’s Criteria Clinical feature Points Active cancer (treatment within 6 months, or palliation) 1 Paralysis, paresis, or immobilization of lower extremity 1 Bedridden for more than 3 days because of surgery (within 4 weeks) 1 Localized tenderness along distribution of deep veins 1 Entire leg swollen  1 Unilateral calf swelling of greater than 3 cm (below tibial tuberosity) 1 Unilateral pitting edema 1 Collateral superficial veins 1 Alternative diagnosis as likely as or more likely than DVT -2 Total points   Wells Clinical Prediction Rule for Deep Venous Thrombosis (DVT) Risk score interpretation (probability of DVT): •>/=3 points: high risk (75%); •1 to 2 points: moderate risk (17%); •<1 point: low risk (3%). • not universally used, still debatable
  • 16. ComplicationsComplications • Pulmonary Embolism » The clot from lower limb become detached & passes via IVC & right heart to the pulmonary arteries and may totally occlude the perfusion to part or all of one or both lungs • Post-thrombotic Limb » Valves in the deep venous channels of the lower leg have been damaged by thrombotic process » Recanalized deep veins are functionally inadequate because of the damaged valve. » bidirectional flow & abnormally high ambulatory venous pressure in the deep vein transmitted to subcutaneous vein→ → edema, pigmentation, fibrosis, and later, dermatitis,edema, pigmentation, fibrosis, and later, dermatitis, cellulitis and ulcerationcellulitis and ulceration
  • 17. TAKE HOME MESSAGES :TAKE HOME MESSAGES :  DVT is one of those things that has a number of predisposing causes, so it is in fact mostly preventable  Clinical predictive rule : Well’s criteria

Editor's Notes

  1. False positive readings can be due to various causes: liver disease, high rheumatoid factor, inflammation, malignancy, trauma, pregnancy, recent surgery False negative readings can occur if the sample is taken either too early after thrombus formation or if testing is delayed for several days. Additionally, the presence of anti-coagulation can render the test negative because it prevents thrombus extension.