DVT (Deep Vein Thrombosis)

DVT (Deep Vein Thrombosis)

How to investigate and treat DVT (Deep Vein Thrombosis) – for doctors, medical students and medical exams

 

Types of deep vein thrombosis

  • Most deep vein thromboses (DVTs) occur in a leg. These are divided into:
    • Above-knee (proximal) DVT if present in the popliteal, superficial femoral (despite the name, still a deep vein), deep femoral, common femoral or external iliac veins
    • Below knee (distal) DVT if present in the soleal or peroneal veins
  • DVT can also more rarely affect an arm.
  • Note thromboses in the saphenous veins or other superficial veins are not DVTs
  • ‘Venous thromboembolism’ (VTE) is used to collectively refer to DVT and pulmonary embolism (PE).

 

Epidemiology of deep vein thrombosis

 

Click here for all the causes of deep vein thrombosis

 

Prevention of deep vein thrombosis

 

Presentations of DVT

  • History
    • Unilateral leg pain and/or swelling, usually of insidious onset
    • Symptoms may be confined to the calf or the thigh, or affect the whole leg
    • The location of symptoms is an unreliable guide to the location of the thrombus
    • May be asymptomatic (incidental finding)
    • Ask about symptoms of pulmonary embolism
    • Bilateral leg swelling is very rarely due to DVT – only if clot has extended around the iliac bifurcation to the other leg, or in the context of pulmonary embolism and right heart failure.
    • Rarely presents with fever or sweats
  • Examination findings
    • Swelling, often tender
    • Pitting oedema
    • Redness
    • Dilated collateral veins (not varicose veins)
    • Evidence of the primary cause:
      • Inguinal lymphadenopathy
      • Inguinal sinus / discharging abscess from intravenous drug abuse
      • Abdominal mass
    • Signs of pulmonary embolism
      • Tachycardia
      • New atrial fibrillation
      • Dullness and reduced breath sounds if pulmonary infarction

 

Video overview of DVT

 

Differential diagnosis of deep vein thrombosis

  • Ruptured Baker’s cyst (though may co-exist with DVT)
  • Cellulitis
  • Lymphoedema
  • Asymmetric oedema due to cardiac failure or renal failure
  • Muscle haematoma

 

Scoring of deep vein thrombosis

Active cancer+1
Recently bedridden ≥3 days or major surgery in the past 12 weeks+1
Paralysis, paresis or recent plaster immobilization of affected leg+1
Previously documented DVT+1
Calf swelling >3cm more than contralateral leg +1
Swelling of whole leg+1
Localised tenderness along deep venous system+1
Dilated collaterals present (NOT varicose veins)+1
Pitting oedema confined to symptomatic leg+1
An alternative diagnosis is at least as likely-2

 

Initial management of deep vein thrombosis

  • After history and examination, calculate the Wells score:
    • If <2, perform a D-dimer test – if negative, DVT is excluded. Consider alternative diagnoses.
    • If Wells score ≥2, or if the D-dimer is positive, proceed to Doppler and compression ultrasound examination of the venous system. If scanning is delayed, start precautionary anticoagulation whilst it is awaited.
  • Proximal DVT requires treatment
    • There are no trial data to inform whether below-knee DVT requires treatment, and some centres will not scan below the knee for that reason.
    • If diagnosis confirmed, bloods prior to treatment:
      • FBC
      • PT and APTT
      • U+E
      • LFT
  • Treatment with anticoagulation
    • Initial treatment with one of the following:
    • Low molecular weight heparin (enoxaparin, dalteparin, or tinzaparin at a therapeutic dose, depending on weight, given sub-cutaneously)
    • Apixaban (an oral Xa inhibitor, given at a dose of 10mg twice daily for 7 days, then 5mg twice daily thereafter. It is contraindicated if eGFR<15ml/min.)
    • Rivaroxaban (an oral Xa inhibitor, given at a dose of 15mg twice daily for 21 days with food, then 20mg once daily thereafter. It is contraindicated if eGFR<15ml/min)

 

Further management of deep vein thrombosis

Anticoagulation
  • After initial treatment, anticoagulation can continue with one of the above anticoagulants, or switch to warfarin or dabigatran.
    • Warfarin initiation requires frequent INR monitoring, and concurrent LMWH at a therapeutic dose until INR>2 for 24 hours. This is because warfarin also inhibits synthesis of proteins C and S, which have a shorter half life than other vitamin K-dependent clotting factors, and so the initial effect of warfarin is prothrombotic.
    • Dabigatran (an oral thrombin inhibitor) is given at a dose of 150mg twice daily, or 110mg twice daily if elderly, if eGFR<50ml/min or receiving concurrent verapamil. It is contraindicated if eGFR<30ml/min.
  • Duration of anticoagulation depends on previous history and whether the DVT was provoked by a transient risk factor e.g. surgery.
    • Patients with recurrent unprovoked VTE should receive long-term anticoagulation.
    • A first episode of provoked VTE requires anticoagulation for at least 3 months, and consider re-scanning for residual thrombus, in which case extend anticoagulation to 6 months.
    • Use clinical judgement to assess risk of recurrence in those with first unprovoked VTE or recurrent provoked VTE. In general, most patients do not need anticoagulation beyond 6 months but some will be at high risk of recurrence.
Other options
Investigation for underlying causes
  • Most risk factors will become apparent in the history, examination and initial testing.
  • Consider investigation for underlying malignancy in those over 55yrs with first unprovoked DVT
  • Testing for inherited thrombophilias is generally not recommended, as it does not alter management. Furthermore acute thrombus and anticoagulant drugs affect levels of clotting factors so tests are not interpretable.
  • In those with recurrent unprovoked DVT or thrombosis in unusual sites (e.g. arm, cerebral sinuses, splanchnic veins)  consider testing for antiphospholipid syndrome (Lupus anticoagulant, anti-cardiolipin and anti-β2 glycoprotein 1), myeloproliferative neoplasms (for JAK2 mutations) and paroxysmal nocturnal haemoglobinuria (by flow cytometry).

 

Complications of deep vein thrombosis

  • The major complication is pulmonary embolism, which may be fatal. This is why treatment is needed even if there are no symptoms, urgently.
  • A post-thrombotic syndrome is described, including chronic pain, oedema, haemosiderin deposition and varicose veins can develop. Compression stockings are ineffective in preventing it.
  • Thrombus can be a nidus for infection, particularly in intravenous drug users, in whom chronic endovascular infection may initially present as occult fever.

 

Prognosis of deep vein thrombosis

  • Isolated DVT generally has a good prognosis, with rates of post-thrombotic syndrome of 5-15% depending on the definition used.
  • Recurrent rates depend on the severity of ongoing risk factors.

 

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Common exam questions and answers for doctors and medical students

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Questions about DVT (Deep Vein Thrombosis)

DVT (Deep Vein Thrombosis) Questions

Common DVT exam questions and answers for doctors, medical students and exams

 

What is the definition of a proximal DVT?

  • A thrombus in the popliteal, superficial femoral, deep femoral, common femoral or external iliac vein.

What is Virchow's Triad?

  • Blood stasis, procoagulant tendency, and endothelial injury. Each of these can lead to thrombosis.

Give 4 transient risk factors for DVT?

  • Immobilisation
  • Surgery
  • Trauma
  • Acute infectious or inflammatory illness

What is the Wells score?

The Wells score quantifies the pre-test probability of DVT and guides further investigation:

Active cancer+1
Recently bedridden ≥3 days or major surgery in the past 12 weeks+1
Paralysis, paresis or recent plaster immobilization of affected leg+1
Previously documented DVT+1
Calf swelling >3cm more than contralateral leg +1
Swelling of whole leg+1
Localised tenderness along deep venous system+1
Dilated collaterals present (NOT varicose veins)+1
Pitting oedema confined to symptomatic leg+1
An alternative diagnosis is at least as likely-2

How does the Wells score guide further investigation?

  • If <2, perform a D-dimer test – if negative, DVT is excluded. Consider alternative diagnoses.
  • If ≥2, or if the D-dimer is positive, proceed to Doppler and compression ultrasound examination of the venous system.

Is treatment indicated for a below-knee DVT?

  • It is not known whether a below-knee DVT confers increased risk of PE; it is certainly a common incidental finding in otherwise well individuals.
  • If local symptoms are thought to be due to the DVT, offer treatment. If not, consider repeat scanning in one week to see if the clot has extended proximally.

Which patients with DVT should undergo investigation for an underlying cause?

  • Those aged >55yrs with unprovoked DVT, and those with recurrent unprovoked DVT or DVT at an unusual site.

 

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Anaemia – Exam questions and answers

Questions about anaemia

Common anaemia exam questions for doctors and medical students 

 

How can causes of haemolysis be classified?

  • Congenital or acquired
  • Immune-mediated or non-immune mediated
  • Intravascular or extravascular

What are the common causes of a microcytic anaemia?

  • Overwhelmingly the most common is iron-deficiency
  • Thalassaemia
  • Sideroblastic anaemia
  • Lead poisoning

What are the common causes of a macrocytic anaemia?

  • B12 or folate deficiency
  • Myelodysplastic syndrome
  • Brisk bleeding or haemolysis
  • Hypothyroidism and alcohol cause macrocytosis, but not typically anaemia

What are the common causes of normocytic anaemia?

  • Renal failure
  • Chronic inflammation
  • Bone marrow failure

What proportion of the healthy population have a positive DAT?

  • Approximately 5%, so a positive DAT is not evidence of haemolytic anaemia, in the absence of other findings such as a raised bilirubin, LDH and reticulocyte count.

 

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Anaemia

Anaemia

How to investigate and treat anaemia – for doctors, medical students and exams

 

Causes of anaemia

  • May be classified as inherited vs. acquired, or disorders of red cell production vs. excessive loss, although there is some overlap, e.g. chronic bleeding leads to iron deficiency and chronic haemolysis leads to folate deficiency.
  • Note in pregnancy plasma volume rises and therefore Hb concentration falls, but this is physiological and not a disease state.
Inherited causes due to defective production
  • Thalassaemia (inadequate production of alpha or beta chains of haemoglobin)
  • Other inherited anaemias (congenital dyserythropoietic anaemia, Diamond-Blackfan anaemia, Schwachman-Diamond syndrome, sideroblastic anaemia)
Inherited causes due to increased destruction (haemolysis)
  • Structural haemoglobin defects (sickle cell anaemia, HbC disease, HbE disease)
  • Red cell membrane defects (hereditary spherocytosis, elliptocytosis, and pyropoikilocytosis)
  • Red cell enzyme defects (G6PD deficiency, pyruvate kinase deficiency)
Acquired causes due to defective production
  • Deficiencies
    • Iron, vitamin B12 or folate deficiency
    • Low erythropoietin due to chronic kidney disease
  • Inflammation
    • ‘Anaemia of chronic disease’
    • HIV infection
  • Marrow issues
    • Bone marrow poisoning due to alcohol, cytotoxic drugs, antibiotics
    • Bone marrow infiltration (by haematological malignancy or solid organ malignancy)
    • Myelofibrosis
    • Myelodysplastic syndrome
    • Bone marrow aplasia due to viral infection (transient) or idiopathic aplastic anaemia (persistent)
  • Liver disease
Acquired causes due to excessive loss or destruction
  • Bleeding
  • Haemolysis, immune-mediated
    • Warm autoimmune haemolytic anaemia
    • Cold agglutinin disease
    • Paroxysmal cold haemoglobinuria
    • Drug-induced haemolytic anaemia
    • Haemolytic disease of the newborn
    • Post-transfusion haemolytic reactions
  • Haemolysis, non-immune mediated
    • Mechanical heart valves
    • Congenital heart defects
    • March haemoglobinuria
    • Spur cell anaemia
    • Paroxysmal nocturnal haemoglobinuria
    • Microangiopathic haemolytic anaemia (DIC, HUS, TTP)
    • Infection (malaria, C. perfringens)
    • Burns
    • Oxidant drugs (dapsone, primaquine, sulfonamides, sulfasalazine)
    • Hypersplenism
  • Note causes of haemolysis may also be categorised as intravascular or extravascular

 

Video on the basics of anaemia

 

History in anaemia

  • Presenting complaint
    • Shortness of breath
    • Fatigue
    • Dizzyness
    • Angina (where co-incident coronary artery disease)
    • Incidental finding (commonly)
  • History of presenting complaint
    • Duration and onset of symptoms
    • History of bleeding [menstrual most commonly, also traumatic, epistaxis, oral bleeding, melaena/PR bleeding, haematuria]
    • Recent infection [cold agglutinin following Mycoplasma infection, red cell aplasia following viral infections esp. Parvovirus B19]
    • Associated symptoms [renal failure and low platelets suggest HUS,
  • Past medical history
    • Chronic kidney disease or liver disease
    • Previous cancers and previous chemotherapy or radiotherapy
    • Lymphoproliferative disease (increased risk of autoimmune haemolytic anaemia)
    • Congenital, ischaemic or valvular heart disease
    • Gastrointestinal malabsorption [coeliac disease, inflammatory bowel disease] or malnutrition
    • Gallstones (increased bile pigments in chronic haemolysis)
    • Ischaemic or valvular heart disease (will exacerbate symptoms)
  • Medications
    • Marrow aplasia [trimethoprim, penicillamine, carbimazole, propylthiouracil, carbamazepine]
    • Drug-induced autoimmune haemolysis [beta lactam antibiotics, NSAIDs, co-trimoxazole]
    • Haemolysis via oxidative damage to erythrocytes [dapsone, ribavirin, rifampicin, primaquine, paraquat]
    • Proton pump-inhibitors and H2 antagonists impair iron absorption by increasing gastric pH.
  • Family history
    • There may be a family history in autosomal dominant inherited anaemias (hereditary spherocytosis) or common autosomal recessive anaemias (sickle cell and thalassaemias)
    • G6PD deficiency is X-linked recessive, so affected males may have an affected maternal grandfather.
  • Social history
    • Alcohol excess
    • Diet (vegetarian / vegan), tea (inhibits iron absorption)

 

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Examination in anaemia

  • Signs of anaemia
    • Pallor, particularly conjunctival
    • Hyperdynamic circulation [bounding pulse, flow murmur]
  • Signs of iron, vitamin B12 and folate deficiency
    • Kolionychia (iron deficiency only)
    • Atrophic glossitis
    • Angular chelitis
  • Signs of haemolysis
    • Jaundice & scleral icterus
    • Dark urine
  • Signs of bleeding
    • Excessive bruising
    • Petechiae
    • Telangiectasiae or larger vascular malformations
  • Signs of malignancy
    • Muscle wasting
    • Oedema
    • Organomegaly
    • Lymphadenopathy
    • Palpable soft tissue masses

 

Investigation of anaemia

  • FBC
    • MCV (low in iron deficiency/thalassaemia/sickle cell, raised in B12 or folate deficiency, myelodysplasia, liver disease and brisk bleeding or haemolysis)
    • MCH (low in iron deficiency and thalassaemia, usually falls earlier than MCV)
    • Platelets (raised in iron deficiency, low in bone marrow failure)
    • White cell count (raised in inflammatory states, low in bone marrow failure)
  • Reticulocyte count (raised in bleeding/haemolysis, low in bone marrow failure or haematinic deficiencies)
  • Blood film
    • Pencil cells in iron deficiency
    • Oval macrocytes and polylobated neutrophils in B12/folate deficiency
    • Spherocytes and polychromasia in extravascular haemolysis
    • Schistocytes in intravascular haemolysis
    • Target cells and acanthocytes in liver disease
    • Stomatocytes in alcohol toxicity
    • Target cells, Howell-Jolly bodies in hyposplenism
    • Bite cells (oxidative stress such as G6PD deficiency)
    • Basophilic stippling in thalassaemia, alcohol toxicity and lead poisoning
    • Tear drop cells and nucleated red cells in myelofibrosis
    • Sickle cells
    • Burr cells/echinocytes in renal failure
    • Rouleux in myeloma
  • U&E, LFT, B12, folate, ferritin
  • If haemolysis is suspected: LDH, unconjugated bilirubin, haptoglobin (falls in intravascular haemolysis)
  • If haemolysis is proven: direct antiglobulin test (DAT; Coombs test)
  • If myeloma is suspected: serum electrophoresis and urinary free light chains (Bence-Jones protein) or serum free light chains
  • If an inherited haemoglobinopathy is suspected: haemoglobin electrophoresis
  • If a primary bone marrow pathology is suspected, bone marrow aspirate and trephine

 

Further investigation of iron deficiency anaemia

  • The gold standard test for iron deficiency is a bone marrow aspirate but this is rarely practical.
  • In otherwise well patients, serum ferritin closely corresponds to iron stores and so is  useful test for iron deficiency.
  • In the setting of acute inflammation, serum ferritin rises so it loses its utility as a test.
  • Serum iron concentration fluctuates with diurnal rhythm and falls in inflammation, so it and transferrin saturation are also rarely helpful. Soluble transferrin receptor levels are less influenced by inflammation but not widely available.
  • Acquired hypochromia, and to a lesser extent microcytosis, is almost always due to iron deficiency.
  • In the absence of menorrhagia, proven iron-deficiency anaemia should be investigated with upper and lower GI endoscopies.

 

Management of anaemia

  • Find and treat cause if possible. Specific management includes:
  • Emergencies
  • Deficiencies
    • Replace haematinics
    • e.g. folic acid 5mg PO once daily, hydroxocobalamin 1mg IM three times a week for two weeks, or ferrous fumarate 210mg twice daily with orange juice.
  • Warm autoimmune haemolytic anaemia
    • Steroid e.g. prednisolone 1mg/kg PO once daily and then wean slowly.
  • Cold haemolytic anaemias
    • Often be managed by avoiding cold exposure.
  • Anaemia in renal failure
    • Treated with iron supplementation if reticulocyte Hb <29pg, and erythropoietin if necessary, to maintain Hb between 100-120g/L.
  • Myelodysplasia
    • In myelodysplasia with isolated anaemia, erythropoietin therapy may avoid transfusion-dependence.
  • Irreversible bone marrow failure
    • Should be treated with transfusion aimed at minimising symptoms of anaemia.

 

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Questions and answers on anaemia diagnosis and management

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Questions about myeloma and MGUS

Questions about myeloma and MGUS

Example exam questions and answers about myeloma and MGUS (monoclonal gammopathy of undetermined significance) – for doctors and medical student exams

 

Is there a fundamental difference between MGUS and myeloma?

  • No. In both MGUS and myeloma, there is a clonal population of plasma cells in the bone marrow, which share an abnormal immunophenotype (CD38+ CD138+ CD45- CD19- CD11a-).
  • The difference is in the burden of disease (<10%, or >10% plasma cells in marrow), and hence the presence of complications. However many patients with MGUS only progress very slowly and it may take years for myeloma to develop, which justifies the different diagnostic categories.

Is a polyclonal raised IgG level evidence of myeloma?
  • No. Polyclonal raised immunoglobulins are seen in various inflammatory states, but do not indicate a primary plasma cell disorder such as myeloma, MGUS or amyloidosis.
Is a bone scan a useful investigation in myeloma?
  • No. The isotopes used in bone scans to detect metastatic solid organ cancers, such as breast and prostate, are taken up in response to osteoblast activity.
  • In myeloma only osteoclasts are stimulated, so the lesions do not appear on bone scans. The skeletal imaging modalities of choice are MRI or CT, to detect lytic lesions.
Does alkaline phosphatase go up in myeloma?
No. Again it is secreted by osteoblasts, not osteoclasts, so is not raised in myeloma bone disease, although it is in the presence of bone metastases from solid organ primaries.
How is it determined whether end-organ damage is attributable to myeloma?

  • This sometimes involves a degree of judgement, if for example there are multiple possible causes of anaemia.
  • Myeloma kidney disease can usually be demonstrated on a renal biopsy, though this is not always necessary, and is much more likely in the presence of very elevated serum free light chains (>1000 mg/L).
  • Discrete bony lytic lesions are easily attributable to myeloma, but more diffuse bone density loss may be due to osteoporosis.

 

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