Transcript VENOUS THROMBOSIS

VENOUS
THROMBOSIS
Dr Narisha Ramparsad
Department of Haematology and
Molecular Medicine
Normal haemostasis
 Ensures fluid state of blood in vasculature
 Prevents blood loss – site of injury – by
forming haemostatic plug
 Clot removal – when healing is complete
Overview of Haemostasis
THROMBOSIS
BLEEDING
Definitions
 A blood clot that forms in a blood vessel or within the
heart and remains there is called a thrombus. A
thrombus that travels from the blood vessel or heart
to another location in the body is called an embolus,
and the disorder, an embolism. For example, an
embolus that occurs in the lungs is called a
pulmonary embolism.
 Sometimes, a piece of atherosclerotic plaque, small
pieces of tumor, fat clumps, air, amniotic fluid, or
other materials can act in the same manner as an
embolus. (MEDLINE PLUS)
Pathogenesis -Thrombosis
 Normally - balance between clotting and bleeding
 With thrombosis - imbalance with procoagulant state
manifesting
 Risk increases when > 1 risk factor present
 Venous thrombi – fibrin & RBCs mainly, leucocytes &
plts also present
 Virchow’s triad
1) vessel wall damage
2) blood flow (stasis)
3) hypercoaguability of
blood
Venous thrombosis can affect any part of venous
system but deep veins most commonly affected.
Acquired Risk Factors
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Malignancy
Presence of a central venous catheter
Surgery, especially orthopedic
Trauma
Pregnancy
Oral contraceptivesHormone replacement therapyTamoxifen
Immobilization
Congestive failure
Antiphospholipid antibody syndrome
Myeloproliferative disorders Polycythemia vera,Essential thrombocythemia
Paroxysmal nocturnal hemoglobinuria
Inflammatory bowel disease
Nephrotic syndrome
Hyperviscosity e.g Waldenstrom's macroglobulinemia, Multiple myeloma
Marked leukocytosis in acute leukemia
Sickle cell anemia
Acquired Risk Factors
 NB in South Africa – effect of HIV
 Decrease Protein S, Protein C
 Increase Factor VIII
Inherited Risk Factors
 Factor V Leiden mutation
 Prothrombin gene mutation
 Protein S deficiency
 Protein C deficiency
 Antithrombin (AT) deficiency
 Rare disorders: Dysfibrinogenemia
Coagulation Cascade – Inherited Risk
factors – thrombosis
Venous thromboembolism (VTE)
 VTE = Deep Vein Thrombosis (DVT) and/or
Pulmonary Embolism (PE)
 Incidence increases with age
 117 cases/100 000
 Increasing health problem – prevention
important, potentially fatal
VTE
VTE
 Thrombosis commonly occurs in deep veins of limbs.
Can also affect superficial veins
 Venous system leg – 2 important categories
1- deep calf vein involvement only
2- proximal vein thrombosis (involving popliteal,
femoral or iliac veins) – give rise to clinically
significant PE
 Pulmonary emboli ( majority arise from deep veins of
leg >90%)
 Other sources of PE include – upper extremity
thrombosis, deep pelvic veins, renal veins, IVC
DEEP VEINS OF THE LEG
DEEP VEIN THROMBOSIS – clinical
features
 Leg pain, swelling, tenderness, palpable cord
(thrombosed vessel), phlegmasia cerulea
dolens in occasional patients.
Non specific signs and
symptoms.
Differential Diagnosis DVT
 Cellulitis
 Popliteal cyst
 Lymphatic obstruction
 Muscle strain/tear
 Direct twisting injury to leg
 If think about DVT – MUST objectively
exclude
Pulmonary Embolism – Clinical
Features
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Symptoms variable
Transient Dyspnoea, tachypnoea
Tachycardia
Pleuritic chest pain, cough, haemoptysis,
CVS collapse with hypotension, syncope (
massive pulmonary embolism)
 Clinically silent
 Clinical features are non specific
 ONCE again must objectively exclude
Laboratory investigations
 D-Dimer assay
 Compression ultrasound(DVT)
 Venography (DVT)
 Spiral CT (highly sensitive for PE
 MRI
 Work up for thrombophilic state when confirm
diagnosis
Clinical course
 Untreated proximal vein thrombosis –
potentially lethal – fatal PE
 Extension of thrombus proximally
 Post thrombotic syndrome frequent
complication of deep DVT. Heaviness,
swelling cramps, itching, ulceration
 Chronic thromboembolic pulmonary
hypertension.
Treatment – Anticoagulant Therapy
 Heparin: Unfractionated or Low Molecular
Weight Heparins e.g Enoxaprin(Clexane),
Dalteprin,
 Fondaparinux
 Vitamin K antagonists e.g Warfarin
 Oral anti Xa (clinical trials)
 Direct thrombin inhibitors
Initiation of treatment
 Must cover with Clexane when initiating Rx
with Warfarin – Why? ( short T1/2, Protein C)
– relative prothrombotic state
Treatment – how long?
 Individualise each case
 Look at risk factors present
 Transient vs permanent vs no risk factors
 1st episode vs recurrent thrombosis
 Reassess
 D-Dimer levels
 Risk –Benefit ratio of anticoagulant therapy
Treatment – how long ?
First onset ,transient risk factor – 6 months ,
recheck D-Dimer levels . If raised continue ?
Indefinite therapy.
First onset, idiopathic thrombosis – consider
life long Warfarin. Reassess risk-benefit ratio
Recurrent DVT – indefinite anticoagulation
Patients with APL antibodies or 2 more
inherited risk factors – 12 months
anticoagulation and reassess
Treatment how long
 First episode thombosis – with deficiency of
natural anticoagulants e.g. antithrombin, Prot
C, Prot S or FVLeiden/Prothrombin gene
mutation – 12 months and reassess ?
indefinite therapy
Side effects of anticoagulant therapy
 Bleeding
 Heparin Induced thrombocytopenia and
thrombosis
 Heparin induced osteoporosis, increased
transaminase levels, hypersensitivity
reactions e.g. necrosis, alopecia,
hyperkalaemia
Treatment – Thrombolytic therapy –
When?
 Indicated in patients with PE –
haemodynamically unstable , evidence of R
ventricular failure
 Threatened limb in setting of DVT
Prophylaxis – venous thrombosis
 Important to identify those patient at
increased risk of thrombosis
 Prevention
 Use of LMWH, compression stockings
 Awareness – patients and health care
professionals
CONCLUSION
 Venous thromboembolism – major cause of
morbidity and mortality
 Identify risk factors early -institute prophylaxis
 Prophylaxis imperative measure to decrease
incidence of thrombotic events
 If suspect thrombosis must objectively test
 Duration of treatment – varies -individualise