THROMBOSIS

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DR. OKEKE CHINEDU

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6/18/2022

OUTLINE

• INTRODUCTION
• EPIDEMIOLOGY
• PATHOGENESIS
• CLINICAL PRESENTATION
• INVESTIGATION AND DIAGNOSIS
• TREATMENT
• COMPLICATION

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• INTRODUCTION
• The term thrombosis refers to the formation, from constituents of the blood, of a mass within the venous or arterial vasculature of a living animal
• Hemostatic thromboses, namely, self-limited and localized thromboses that prevent excessive blood loss, represent the body's natural and desired response to acute vascular injury
• Pathologic thromboses such as deep venous thrombosis (DVT), pulmonary embolism (PE), coronary arterial thrombosis leading to myocardial infarction (MI), and cerebrovascular thrombotic occlusion represent the body's undesired response to acute and chronic perturbations of the vasculature, blood, or both

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• The terms coagulated blood and clot are not synonymous with thrombosis and refer to the formation of a solid mass of blood components outside of the vascular tree
• Examples of clots include soft tissue, body cavity (e.g., peritoneal), and visceral hematomas
• Coagulated blood best describes clots formed ex vivo
• Formation of solid mass of blood constituents within vascular system
• WHY IS THIS A PROBLEM?
• Classified broadly into
• Venous thromboembolism
• Deep venous thrombosis (DVT)
• Pulmonary embolism (PE)
• Arterial thrombosis (this is usually managed by the cardiologist)

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PHYSIOLOGY AND PATHOPHYSIOLOGY OF THROMBOSIS

• The human hemostatic system consists of multiple independent, yet integrally related, cellular and protein components that function to maintain blood fluidity under normal conditions and promote localized, temporary thrombus (hemostatic thrombus) formation at sites of vascular injury
• A normal hemostatic system is the human physiologic defense against exsanguination
• An abnormal hemostatic system can result in pathologic bleeding, vascular thrombosis, or both

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• The hemostatic system is comprised of six major components: Platelets, vascular endothelium, procoagulant plasma protein “factors,” natural anticoagulant proteins, fibrinolytic proteins, and antifibrinolytic proteins
• Each of these six hemostatic components must be present in fully functional form, in adequate quantity, and at the proper location to prevent excessive blood loss after vascular trauma and, at the same time, to prevent pathologic thrombosis
• The hemostatic system is highly regulated and maintains a delicate balance between a prohemorrhagic state and a prothrombotic state
• Any significant acquired or congenital imbalance in the hemostatic “scales” can lead to a pathologic outcome.

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• Normal hemostasis in response to vascular injury can be divided into two major processes of equal importance, known as primary and secondary hemostasis
• Primary hemostasis comprises the reactions needed to form a platelet plug at a site of vascular damage, whereas secondary hemostasis comprises a series of reactions (coagulation cascade) needed to generate cross-linked fibrin required to stabilize the platelet plug and form a durable thrombus
• Natural anticoagulants (antithrombin [AT] and activated protein C [APC]) function to confine thrombus formation to the sites of vascular injury and limit thrombus size to prevent vessel occlusion and flow interruption in the affected vessel

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• The activity of AT is greatly enhanced by endothelial cell heparan sulfate and pharmacologic heparins
• The function of APC is enhanced by its cofactor, protein S
• Physiologic fibrinolysis is initiated by endothelial-cell-derived tissue-type plasminogen activator (t-PA), which converts plasminogen to plasmin
• Plasmin can degrade cross-linked fibrin, limit thrombus size, and help dissolve a thrombus once the vascular injury has been repaired
• The fibrinolytic system is regulated and localized by antiplasmin and PA inhibitor (PAI)-1.

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• Specific alterations in the quantitative and qualitative status of any hemostatic cellular or protein element can lead to pathologic thrombosis
• A marked increase in the platelet count (thrombocytosis) and accentuated platelet aggregation (“sticky platelet syndrome”) are associated with thromboembolic events
• Elevated levels of procoagulant factors such as fibrinogen, factors VIII, IX, XI, and VII, as well as resistance to inactivation of factor Va by APC, are recognized risk factors for vascular disease and thrombosis

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• Deficiency of a natural anticoagulant protein such as protein C, protein S, or AT is associated with venous thromboembolic disease.
• Deficiency of a fibrinolytic cascade component, such as t-PA or plasminogen, and excess plasma levels of the fibrinolytic inhibitor PAI-1 have been linked to hypercoagulability and thrombosis
• It is the net balance between the participating and, at times, opposing groups of proteins and not the level of any individual factor that is most critical to hemostatic regulation

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THROMBOSIS - EPIDEMIOLOGY

DEEP VENOUS THROMBOSIS

• In western countries 1 per 1000 population
• Predominantly a disease of middle age and the elderly, hence incidence increases with age
• Very rear in childhood
• Low incidence in the Chinese and Koreans

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THROMBOSIS - EPIDEMIOLOGY

• There is a relative paucity of information about DVT in most African populations including Nigeria

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PULMONARY EMBOLISM

• Incidence is unknown
• 90% or more originates from deep veins of the leg
• Other sites: deep pelvic veins, renal veins, inferior vena cava, right side of the heart, and axillary veins

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THROMBOSIS - INTRODUCTIOIN

• Venous thrombosis affects the deep veins of the upper and lower limbs
• NB: Superficial veins
• Lower limb DVT can be divided into two prognostic categories
• Calf vein thrombosis
• Proximal vein thrombosis - popliteal, femoral, or iliac veins

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THROMBOSIS - PATHOGENESIS

• OVERVIEW OF THE PROCESS OF HAEMOSTASIS
• It reflects a disruption of the balance between procoagulant and anticoagulant mechanism
• Important factors involve therefore include
• Endothelium
• Prothrombotic
• antithrombotic
• Platelets
• Caogulation factors

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THROMBOSIS - PATHOGENESIS

• Virchow’s Triad suggested that there are three component’s that are important in thrombus formation
• Endothelial injury
• Hypercoagulability
• Abnormal blood flow

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• VIRCHOW TRIAD
• In the mid-19th century (1854), German pathologist Rudolph Virchow postulated that vascular obstruction was precipitated by, and thrombosis resulted from, three interrelated factors:
• P.1219
• (a) “Decreased blood flow” (stasis of blood flow), (b) “inflammation of or near the blood vessels” (vascular endothelial injury), and (c) “intrinsic alterations in the nature of the blood itself” (hypercoagulability)

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Virchow's triad in thrombosis. Integrity of endothelium is the most important factor. Injury to endothelial cells can also alter local blood flow and affect coagulability. Abnormal blood flow (stasis or turbulence), in turn, can cause endothelial injury. The factors may act independently or may combine to promote thrombus formation

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THROMBOSIS - PATHOGENESIS

• Increased systemic coagulability and stasis are the most important for venous thrombosis
• Endothelial injury is important for arterial thrombosis.

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• RISK FACTORS FOR ARTERIAL THROMBOSIS (ATHEROSCLEROSIS)
• Positive family history
• Male sex
• Hyperlipidaemia
• Hypertension
• Diabetes mellitus
• Gout
• Polycythaemia
• Hyperhomocysteinaemia
• Cigarette smoking
• ECG abnormalities
• Elevated CRP, IL6, fibrinogen, lipoprotein‐associated phospholipase A2
• Lupus anticoagulant
• Collagen vascular diseases
• Behcet’s disease

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THROMBOSIS – RISK FACTORS

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• HEREDITARY AND ACQUIRED RISK FACTORS FOR VENOUS THROMBOSIS.
• Hereditary Haemostatic Disorders
• Factor V Leiden
• Prothrombin G20210A variant
• Protein C deficiency
• Antithrombin deficiency
• Protein S deficiency
• Dysfibrinogenaemia
• Non-O ABO blood group
• DVT in close relative (especially if unprovoked)

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• Hereditary Or Acquired Haemostatic Disorders
• Raised plasma levels of factor VIII
• Raised plasma levels of fibrinogen
• Raised plasma levels of homocysteine

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Acquired Disorders

• Lupus anticoagulant
• Oestrogen therapy (oral contraceptive and HRT)
• Heparin‐induced thrombocytopenia
• Pregnancy and puerperium
• Surgery, especially abdominal, hip and knee surgery
• Major trauma
• Malignancy
• Acutely ill hospitalized medical patients including cardiac or respiratory failure, infection, inflammatory bowel disorders
• Myeloproliferative disease

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Acquired disorders

• Hyperviscosity, polycythaemia
• Stroke
• Pelvic obstruction
• Nephrotic syndrome
• Dehydration
• Varicose veins
• Previous superficial vein thrombosis
• Age
• Obesity
• Paroxysmal nocturnal haemoglobinuria
• Behcet’s disease

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• Factor V Leiden gene mutation
• This is the most common inherited cause of an increased risk of venous thrombosis
• It occurs in approximately 3–7% of factor V alleles in white people
• There is failure of activated protein C (APC) to prolong the activated partial thromboplastin time (APTT) test when added to plasma and the phenotype is sometimes referred to as ‘activated protein C resistance’
• Activated protein C normally breaks down activated factor V and so it should slow the clotting reaction and prolong the APTT
• APC resistance is caused by a genetic polymorphism in the factor V gene, which makes factor V less susceptible to cleavage by APC
• Presumably, individuals with this allele have been ‘selected’, probably because of a reduced bleeding tendency (e.g. post‐partum)
• It does not increase the risk of arterial thrombosis

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• A small minority of patients with APC resistance do not have factor V Leiden but have other mutations of factor V.
• Patients who are heterozygous for factor V Leiden are at an approximately five‐ to eight‐fold increased risk of venous thrombosis compared to the general population, but only 10% of carriers develop thrombosis during their lifetime
• Individuals who are homozygous have a 30–140‐fold risk
• Following venous thrombosis they have a higher risk of re‐thrombosis than individuals with DVT but normal factor V.
• The incidence of factor V Leiden in patients with venous thrombosis is approximately 20–40%
• Genetic screening is relatively easy and is widely performed.
• However, even if a patient with DVT is a carrier of factor V Leiden their absolute risk of thrombosis is still very low in the absence of other risk factors
• At present it is not recommended to start anticoagulation therapy in individuals with the Leiden mutation, even if homozygous, if they have no history of thrombosis.

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• Antithrombin deficiency
• Inheritance is autosomal dominant
• There are recurrent venous thromboses usually starting in early adult life and arterial thrombi may occur.
• Antithrombin concentrates are available and are occasionally used to prevent thrombosis during surgery or childbirth
• Many molecular variants of antithrombin have been categorized and are associated with varying degrees of risk of thrombosis
• Protein C deficiency
• Inheritance is autosomal dominant with variable penetrance.
• Protein C levels in heterozygote individuals are approximately 50% of normal
• Characteristically, many patients develop skin necrosis as a result of dermal vessel occlusion when treated
• with warfarin, thought to be caused by a further reduction of protein C levels in the first day or two of warfarin therapy
• Rarely, infants may be born with homozygous deficiency and characteristically present with severe disseminated intravascular coagulation (DIC) or purpura fulminans in infancy.

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• Protein S deficiency
• Protein S deficiency has been found in a number of families with a thrombotic tendency
• It is a cofactor for protein C
• The clinical features of protein S deficiency are similar to those of protein C deficiency, including a tendency to skinnecrosis with warfarin therapy
• The inheritance is autosomal dominant

Prothrombin allele G20210A

• G20210A is an allele of the prothrombin gene that has a prevalence of 2–3% in the population
• It leads to increased plasma prothrombin levels and increases thrombotic risk five‐fold
• It is probable that the cause of venous thrombosis with this mutation is that sustained generation of thrombin results in prolonged down‐regulation of fibrinolysis through activation of thrombin‐activated fibrinolysis inhibitor

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• Hyperhomocysteinaemia
• High levels of plasma homocysteine may be genetic or acquired and are associated with increased risk for both venous and arterial Thrombosis
• Trials show little evidence that lowering the levels reduces these risks.
• Homocysteine is derived from dietary methionine and is removed by either remethylation to methionine or conversion to cysteine via a trans‐sulphuration pathway
• Classic homocystinuria is a rare autosomal recessive disorder caused by deficiency of cystathione β‐synthase, the enzyme responsible for trans‐sulphuration.
• Vascular disease and thrombosis are major features of the disease

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• Methylenetetrahydrofolate reductase is involved in the remethylation of tetrahydrofolate (THF), methylTHF being responsible for methylating homocysteine to methionine
• A common thermolabile variant of the enzyme may be responsible for mild homocysteinaemia
• In people homozygous for this mutation and who have had a DVT, long‐term folic acid therapy is indicated
• Other acquired risk factors for hyperhomocysteinaemia include deficiency of vitamin B6, drugs (e.g. ciclosporin), renal damage and smoking
• The levels also increase with age and are higher in men and post‐menopausal females.

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• Defects of fibrinogen
• Defects of fibrinogen are usually clinically silent or cause excess bleeding
• Thrombosis is a rare association.
• ABO blood group
• Non‐O blood group carriers have a higher risk of venous thrombosis or embolism than O carriers
• This is relatedto their higher plasma levels of von Willebrand factor and factor VIII
• Hereditary or acquired disorders of haemostasis
• High plasma factor VIII or fibrinogen levels are associated with venous thrombosis
• The combination of multiple risk factors is associated with increased risk of thrombosis
• If these are persistent they may represent a reason for extended anticoagulation.

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• Acquired risk factors
• These may cause thrombosis in patients without another identifiable abnormality but are more likely to do so if an inherited predisposing abnormality such as factor V Leiden is also present.
• Hospital‐acquired thrombosis (HAT)
• Hospital‐acquired thrombosis is responsible for up to 50% of cases of DVT and PE
• Thrombosis may occur many weeks after discharge from hospital
• HAT is now regularly defined as venous thromboembolism occurring within 90 days of hospitalization
• Thromboprophylaxis is typically given for the duration of admission and is extended after discharge in very high‐risk patients such as those having had hip or knee replacement

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• Postoperative venous thrombosis
• This is more likely to occur in the elderly, obese, those with a previous or family history of venous thrombosis, and in those in whom major abdominal or hip operations are performed
• Elasticated stockings or mechanical methods are used to reduce the risk of DVT.
• Venous stasis and immobility
• These factors are probably responsible for the high incidence of postoperative venous thrombosis and for venous thrombosis associated with congestive cardiac failure, myocardial infarction and varicose veins
• In atrial fibrillation, thrombin generation from accumulation of activated clotting factors leads to a high risk clot formation in the atrial appendage and consequent systemic embolization
• The use of muscle relaxants during anaesthesia may also contribute to venous stasis
• Venous thrombosis also has a higher frequency after prolonged journeys
• Malignancy
• Patients with carcinoma of the ovary, brain and pancreas have a particularly increased risk of venous thrombosis or its recurrence but there is an increased risk with all cancers and myeloproliferative diseases
• The tumours produce tissue factor and a procoagulant that directly activates factor X

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• Inflammation
• This up‐regulates procoagulant factors and down‐regulates anticoagulant pathways, particularly protein C
• Thrombosis is particularly likely in inflammatory bowel disease, Behcet’s disease, systemic tuberculosis, systemic lupus erythematosus (SLE) and diabetes
• Superficial venous thrombosis
• The risk of DVT is increased in those who have had a previous superficial venous thrombosis or thrombophlebitis, especially if there are additional risk factors.
• Blood disorders
• Increased viscosity, thrombocytosis and enhanced platelet functional responses are possible factors for the high incidence of thrombosis in patients with polycythaemia vera and essential thrombocythaemia
• There is a high incidence of venous thrombosis in patients with paroxysmal nocturnal haemoglobinuria, including thrombi in large veins such as the hepatic vein
• An increased tendency to venous thrombosis has been observed in patients with sickle cell disease, during post‐splenectomy thrombocytosis and those with a paraprotein

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• Oestrogen therapy
• Oestrogen therapy, particularly high‐dose therapy, is associated with increased plasma levels of factors II, VII, VIII, IX and X, and depressed levels of antithrombin and tissue plasminogen activator in the vessel wall
• There is a high incidence of postoperative venous thrombosis in women on high‐dose oestrogen therapy and full‐dose oestrogen‐containing oral contraceptives.
• The risk is much less with low‐dose oestrogen contraceptive preparations
• Hormone replacement therapy also increases the risk of thrombosis, largely obviated by the use of low‐oestrogen preparations.

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• The antiphospholipid syndrome
• The antiphospholipid syndrome (APS) can be defined as the occurrence of venous and arterial thrombosis and/or recurrent miscarriage in association with laboratory evidence of persistent antiphospholipid antibody
• One antiphospholipid is the lupus anticoagulant (LA) which was initially detected in patients with SLE and is identified by a prolonged plasma APTT which does not correct with a 50 : 50 mixture of normal plasma
• Paradoxically, in view of its name, it is associated with venous and arterial thrombosis
• Antiphospholipid antibodies are also found in other autoimmune disorders particularly of connective tissues, lymphoproliferative diseases, post‐viral infections, with certain drugs including phenothiazines and as an ‘idiopathic’ phenomenon in otherwise healthy subjects.
• Collagen vascular diseases and Behcet’s syndrome are also associated with arterial and venous thrombosis, whether or not the lupus anticoagulant is present.

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• Investigation of thrombophilia
• Tests that may be abnormal in patients with a tendency to venous thrombosis include:
• 1 Blood count and erythrocyte sedimentation rate – to detect elevation in haematocrit, white cell count, platelet count, fibrinogen and globulins
• 2 Blood film examination – may provide evidence of myeloproliferative disorder; leucoerythroblastic features may indicate malignant disease
• 3Prothrombin time (PT) and APTT – a shortened APPT is often seen in thrombotic states and may indicate the presence of activated clotting factors
• A prolonged APTT test, not corrected by the addition of normal plasma, suggests an LA or an acquired inhibitor to a coagulation factor
• 4 Anticardiolipin and anti‐β2‐GPI antibodies

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• 5 Thrombin time (and reptilase time) – prolongation suggests an abnormal fibrinogen.
• 6 Fibrinogen assay.
• 7 DNA analysis for factor V Leiden.
• 8 Antithrombin – immunological and functional assays.
• 9 Protein C and protein S – immunological and functional assays.
• 10 Prothrombin gene analysis for the G20210A variant.
• 11 Plasma homocysteine estimation.
• 12 Test for CD59 and CD55 expression (paroxysmal nocturnal haemoglobinuria) in red cells if paroxysmal nocturnal haemoglobinuria is suspected.
• 13 Test for JAK2 (V617F) mutation if portal or hepatic vein thrombosis.
• 14 Protein electrophoresis for paraprotein.

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CLINICAL FEATURES

• Approximately one-half of those with a venous thrombosis never have recognizable symptoms and hence are asymptomatic
• These symptoms can develop slowly or suddenly.

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CLINICAL FEATURES - DVT

DVT

• Sudden swelling of one limb
• Pain or tenderness
• Skin that is warm to the touch
• Fullness of the veins just beneath the skin
• Change in color (blue, red or very pale)

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NB: Homan’s sign

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CLINICAL FEATURES - DVT

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CLINICAL FEATURES - PE

PE- dependent on the size, location and number of embolus as well as the patients underlying cardiorespiratory reserve

• Dyspneoa
• Cough +/- haemoptysis
• Chest pain (pleuritc)
• Clinical findings of tachypneoa, tachycardia pleural effusion and arrythmias

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CLINICAL FEATURES – ARTERIAL THROMBOSIS

ARTERIAL THROMBOSIS

• Ischaemia – compromised blood flow
• Complete obstruction – ischaemia and finally infarction

NB; presentation is dependent on location of blockage.

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CLINICAL FEATURES – ARTERIAL THROMBOSIS

• Pain
• Tingling and numbness
• Pale skin
• Coldness
• Absent pulses
• Weakness or absence of movement

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THROMBOSIS - DIFFERENTIAL DIAGNOSIS

DVT

• Superficial thrombophlebitis
• Cellulitis
• Ruptured Baker cyst
• Lymphagitis/Lymphoedema
• Other musculoskeletal conditions

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DIFFERENTIAL DIAGNOSIS

PE

• Pneumonia
• Acute pulmonary oedema
• Atelectasis
• Pneumothorax

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INVESTIGATION AND DIAGNOSIS

• Base line investigation cannot be underplayed
• Patient is managed as a whole and not just concentrating on the obvious pathology
• These base line investigations can help in pointing or confirming the presence of a risk factor for thrombosis
• NB : Screening test for thrombophilia and other possible risk factors.

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DIAGNOSIS

DVT

• Clinical pretest probability score A.K.A WELL’S SCORE
• Initial objective testing:

- D-dimer testing

- Venous ultrasonography

• Contrast venography

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DIAGNOSIS – CLINICAL PROBABILITY

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DIAGNOSIS

• Because the clinical diagnosis is insensitive and nonspecific, confirmation with objective investigations is essential.

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DIAGNOSIS

D-dimers

• D-dimers are products of fibrin degradation.
• Raised serum concentrations are considered to reflect the presence of intravascular thrombosis.
• Therefore, measuring serum values provides a highly sensitive method of detecting acute venous thromboembolism with a reported sensitivity of up to 100% depending on the assay.
• However, specificity is very low with reported figures of 35%-60%. This is due to other co-morbid conditions increasing D-dimer concentrations-for example, infection, trauma, pregnancy and malignancy.

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DIAGNOSIS

Venous ultrasonography

• Venous ultrasonography is our first objective test of choice in patients with high or moderate pretest probabilities.
• Non-compressibility of the common femoral vein or popliteal vein or both is diagnostic for proximal DVT.
• Sensitivity of 95% and a specificity of 96% for diagnosing symptomatic, proximal DVT

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DIAGNOSIS – VENOUS ULTRASONOGRAPHY

• sensitivity and specificity of 60% to 70% for isolated calf vein thrombosis
• It can be combined with spectral, colour or power Doppler scanning which improve accuracy by focusing on individual veins.
• Therefore, when the clinical likelihood and ultrasound evaluations of the proximal venous system are concordant, the accuracy and predictive values of the positive and negative combinations approach 100%.

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DIAGNOSIS – DOPPLER USS

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DIAGNOSIS – DOPPLER USS

• Fortunately, calf vein thrombosis embolize so rarely that they are considered to be clinically unimportant so long as they do not extend proximally.
• A repeat ultrasound at one week to examine the proximal and popliteal veins is currently used to further evaluate the patient.

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DIAGNOSIS – DOPPLER USS

• The advantages of ultrasound include
• non-invasive
• cheaper
• acceptable to patients
• It is however, very operator dependent and partial obstructions are more difficult to assess.

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DIAGNOSIS - VENOGRAPHY

• This is an invasive technique requiring the injection of contrast medium into one of the pedal veins. It may be painful and can cause allergy or other side effects.
• It is an expensive test that is not easily repeatable and itself carries a 2%-5% chance of causing a DVT.

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DIAGNOSIS - OTHERS

Impedeance plethysmography

• Another diagnostic procedure still used in some centers is impedance plethysmography.
• It is an electrical signal technique that compares the electrical impedance of patent and obstructed veins.
• Again it is non-invasive, quick and cheap, but relies heavily on the cooperation of the patient.
• It has largely been superseded by ultrasound and Doppler techniques.

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DIAGNOSIS - OTHERS

Magnetic resonance imaging

• Very expensive
• Has a good sensitivity

Fibrinogen ¹²⁵I leg scanning

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Figure 1. Algorithm for diagnosing DVT using clinical assessment, venous ultrasonography, and D-dimer testing. #Reevaluate history and review ultrasound for features suggestive of old rather than new thrombosis. If ultrasound findings are inconclusive, venography should be considered. *In patients with a high clinical probability or who cannot return for serial ultrasonography, venography is recommended. Venography can also be considered in patients with cardiorespiratory compromise.

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DIAGNOSIS

PE

• Clinical pretest probability score
• D – dimer
• CTPA – Computed Tomography Pulmonary Angiography
• Ventilation – Perfussion (V/Q) Lung Scanning

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DIAGNOSIS - CLINICAL SCORE FOR PE

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THROMBOSIS – TREATMENT

Goals of treatment includes :

• To prevent progression of thrombus
• To prevent a pulmonary embolism (if not already present)
• To prevent death from pulmonary embolism
• To prevent a recurrent DVT
• To prevent the post-phlebitic syndrome

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THROMBOSIS –TREATMENT

TREATMENT MODALITIES INCLUDE

• Anticoagulation
• Parenteral – unfractionated heparin (UFH)/low molecular weight heparin (LMWH)
• oral anticoagulants: VKA and Direct Oral Anti-coagulants (DOAC)
• Preventive / prophylaxis mechanisms
• Graduated compression stockings
• Intermittent compression stockings
• Inferior vena caval filter
• Thrombolytic agents
• Antiplatelet drugs

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TREATMENT

VENOUS EMBOLECTOMY

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Preventive / prophylaxis mechanisms

• Graduated compression stockings
• Intermittent compression stockings
• Inferior vena caval filter

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NB : LIMB ELEVATION

LIMIT MOBILISATION

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• Graduated compression stockings
• These are often used postoperatively, past‐partum and during long aeroplane flights to reduce the risk of DVT
• After a DVT, they have been recommended for 1–2 years to reduce the risk of the post‐thrombotic syndrome
• Knee‐high stockings have been used in the vast majority of cases, compression class II, and are worn except when the patient is recumbent
• Intermittent compression devices
• Intermittent pneumatic compression and mechanical foot pumps are used in high‐risk patients in whom bleeding as a result of LMWH is likely
• They reduce the risk of thrombosis in both medical and surgical patients.
• Inferior vena cava filter
• This can provide protection against pulmonary embolism when a DVT in the legs is diagnosed but anticoagulation is contraindicated (e.g. ongoing or very recent intracranial or gastrointestinal bleeding or where there is recurrent PE despite adequate anticoagulation)

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THROMBO EMBOLIC DISORDER STOCKINGS

COMPLICATION

• Due to complication of treatment
• Heparin induced thrombocytopenia
• Osteoporosis
• Warfarin overdosage
• Execessive bleeding
• Due to progression of the disease
• Embolisation (pulmonary thromboembolism)
• Complete occlusion of the limb with subsequent wet gangrene.

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COMPLICATION

• Post thrombotic (Phlebitic) syndrome

A common complication of deep vein thrombosis. It results from damage to the valves in the deep veins, causing pain, redness, and thickening of the skin. It can lead to chronic leg ulceration. Up to 60% of patients with deep vein thrombosis develop post-thrombotic syndrome, frequently occurring within two years. Graduated elastic compression stockings or pneumatic compression boots and anticoagulant therapy are often used to reduce the risk of post-thrombotic syndrome after deep vein thrombosis.

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TREATMENT

DURATION OF TREATMENT

• PROVOKED VENOUS THROMBOSIS
• Treat/remove the inciting factor
• Anticoagulation for 3 – 6 months after (a) above
• UNPROVOKED VENOUS THROMBOSIS
• Handle the stimulating factor if present
• Possibility of anticoagulation for life
• RECURRENT VENOUS THROMBOSIS
• Anti coagulation for life.

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THANK YOU

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