Deep Vein Thrombosis and Pulmonary Embolism

Background

  • DVT and PE are really a single disease- venous thromboembolism.
  • It is fairly common: DVT occurring in 1/1000- most commonly in the lower limbs (calf)
  • PE is an extremely common cause of mortality, accounting for around 10% of all hospital deaths (1% of admissions).
  • Both PE and DVT can be associated with morbidity also.

Risk factors

Virchow’s triad is a group of three categories that contribute to venous thrombosis:

  1. Haemodynamic status i.e. stasis/turbulence of blood flow
  2. Hypercoagulability
  3. Endothelial injury/dysfunction
  • Intrinsic
    • Previous DVT/PE (strongest factor- previous DVT increases risk by 5 fold; previous PE increases risk of post-operative DVT to almost 100% without prophylaxis)
    • Age (incidence increases with age- >60 considered risk factor)
    • Obesity/overweight and metabolic syndrome
    • Smoking
    • Cancer
    • Acquired or hereditary thrombophilia
      • e.g. hereditary- Factor V lieden or prothrombin gene mutation, protein C/S deficiency; acquired- antiphospholipid syndrome (linked with SLE or other connective tissue disease or not), liver disease, nephrotic syndrome, DIC, pregnancy
    • Hypertension
    • Stroke/paralysis of the leg
  • Extrinsic
    • Immobilisation e.g. long-haul travel; hospitalisation/bed-bound (can increase the rate of DVT to 10%)
    • Major surgery (particularly to lower limbs/pelvis/abdo) (up to 40% if not given prophylaxis)
    • Trauma
    • Oral Contraceptive
    • Pregnancy
    • Dehydration

Presentation

DVT

  • NB Some patients will progress to PE without DVT being apparent.
  • Classic symptoms include
    • Unilateral Limb pain and tenderness
      • this may be along the line of the vein or may be generalised
    • Swelling (oedematous) of the calf/thigh (unilateral)
    • Hot, erythematous skin
    • There may also be distension of the superficial veins
  • It may be difficult to distinguish between DVT and cellulitis and DVT with cellulitis

Well’s Score (two-level) for DVT

wells2

wells
Algorithm for the diagnosis of DVT taken from NICE guidelines
  • D-dimer testing: D-dimer is a degredation product of fibrin which is produced when a blood clot is degraded by plasmin during fibrinolysis.  If it is negative- DVT is highly unlikely (High sensitivity).  However, if it is positive- it DOES NOT CONFIRM DVT (may be raised in patients with liver disease, rheumatoid disease, inflammation, cancer, trauma, pregnancy, recent surgery etc)
  • Other forms of imaging may be of use where there is clinical evidence of DVT but both USS and D-dimer are negative.  Consider MRI or, more rarely, CT venography.

PE

  • Acute onset
    • Dyspnoea (Shortness of breath)
    • Pleuritic, often central chest pain
    • Cough and haemoptysis
  • In severe cases, the patient may present with syncope or collapse due to hypotension secondary to excessive strain on the right heart which can lead to tricuspid regurgitation and impaired filling of the left side of the heart.
    • Strain may be auscultated either as a prominent second heart sound/widely split second heart sound (gallop rhythm), a tricuspid regurgitation murmur (high pitched early-pan-systolic murmur best heard in the 4th IC space, parasternally).
  • The patient may by tachypnoeic, tachycardic and hypoxic
  • There may be signs of an elevated JVP

Well’s score for PE

wells2

Diagnosis of PE taken from NICE guidelines
Diagnosis of PE taken from NICE guidelines
  •  A chest x-ray and blood tests e.g. FBC (Check WCC), CRP, U&Es (check for any signs of electrolyte imbalance or kidney failure which may prevent CTPA), LFTs (check for liver failure that may cause bleeding abnormalities of be a sign of cancer), coagulation screen, ABG etc should be done as part of the initial workup to rule in/out alternative diagnoses.  Troponins could also be considered.
  • ECG should also be done to check for heart strain (dilation), heart shift due to the strain, right ventricular ischaemia and increased heart rate- signs may include a
    • sinus tachycardia
    • Complete or incomplete RBBB (tall R wave in V1 ‘M’; slurred S wave in V6 ‘W’; MaRRoW)
    • Right ventricular strain- T wave inversions in right (v1-4) and inferior (II, III, aVF) leads
    • Right axis deviation (negative QRS in lead I and aVL and positive in lead III and aVF)
    • Dominant R wave in V1 (right ventricular dilation)
    • Right atrial enlargement (P pulmonale) (>2.5mm peaked P waves in inferior leads (II, III and aVF) and >1.5mm peaked P wave in V1 and V2)
    • S1Q3T3 pattern: deep S wave in lead I, Q wave in III, and inverted T wave in lead III.
    • Shift of R/S transition towards V6 with a persistent S wave in V6.
  • In patients allergic to CTPA contrast; with renal failure or whose radiation risk is high, consider a V/Q (SPECT or planar) scan.
  • Echocardiogram can be useful in excluding significant PE if negative.
  • Consider a thrombophilia screen in patients who have had unprovoked PE and who have a first degree relative who has had a DVT/PE (only absolutely necessary if the patient is not planned to be on long-term anticoagulation treatment).

Management

(Treatment of the thrombus/thromboembolism is essentially the same in DVT and PE)

  • For massive PE, thrombolyse unless there are any contraindications
    • Alteplase 50mg stat IV (if imminent cardiac arrest) or 10mg stat IV then 90mg infusion over 120mins
    • Contraindications include
      • Major surgery/trauma in previous 2 weeks; aortic dissection; acute internal bleeding; known cerebral tumour; hx of cerebral bleed/AVM; prolonged/traumatic CPR; pregnancy
      • Relative CI include BP>180/110mmHg; severe renal/liver failure; INR>1.5 from warfarin use or liver disease; current use of warfarin with unknown INR; current use of rivaroxiban; stroke/TIA in last 12 months
  • Newer agents (mainly factor Xa inhibitors e.g. rivaroxaban) are now being used in treating DVT/PE
    • 15mg BD for 3 weeks then 20mg BD until 3 or 6 months (provoked/unprovoked respectively)
    • Not used if eGFR<30
    • Note- no known method of reversal- contraindicated in those at risk of bleeding.  Also not used for >12 months – consider warfarin in those requiring longer term anticoagulation
  • Offer low molecular weight heparin injection e.g. dalteparin (usually 10000-15000 units per day- based on weight), (or fondaparinux) to those unsuitable for rivaroxiban
    • Contraindicated in patients with a recent bleed or at risk of bleed (e.g. GI ulcer, cerebral bleed, haemorrhage diathesis)
    • Also, unfractionated heparin may be preferred in patients with severe renal failure or are haemodynamically unstable.
  • Continue for 5 days or until the INR has been >2 for at least 24 hours (whichever is longer).
    • In patients with cancer, ideally LMWH should be continued for 6 months
  • Offer a vitamin K antagonist e.g. warfarin, within 24 hours and continue for 3 months minimum. (see warfarin prescribing)
    • Reassess risk at 3 months- consider further 3 months, particularly if the DVT/PE was unprovoked

Prognosis

  • DVT
    • Aside from increasing the risk of further DVT/PE, DVT can result in a ‘post-thrombotic syndrome’
      • Chronic, minor skin changes, pain, swelling, hyperpigmentation, leg ulceration
      • More common in elderly, obese, and patients with recurrent disease
  • PE
    • There is a risk that chronic, recurrent, silent PE can cause long-term pulmonary hypertension, right heart strain and eventually heart failure.
    • Mortality is associated with age and comorbidity (particularly cancer, COPD, heart failure, hypertension)
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