Swollen leg I: Deep vein thrombosis

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216 Swollen leg I

Deep vein thrombosis

Instruction

Look at this patient’s leg.

Salient features

History

• Recent history of immoblization including recent surgery, stroke, myocardial infarction

• Whether onset was acute or chronic

• Pain

• Past and family history of thromboses including deep vein thrombosis (DVT), pulmonary embolism

• Drug history: oral contraceptives

• Air travel; the evidence is circumstantial (BMJ 2001;322:188).

Examination

• Painful calf

• Redness

• Engorged superficial veins

• Unilateral swollen leg with pitting oedema (Fig. 216.1)

• Pain on the calf on dorsiflexion of the foot: Homans’ sign (not diagnostic).

image

Fig. 216.1 Deep venous thrombosis: acutely swollen left leg with dilation of the superficial veins.

(With permission from Forbes, Jackson 2003.)

Proceed as follows:

• Check for pitting oedema on both sides (look at the patient’s eyes while eliciting this sign to ensure that you are not hurting the patient).

• Compare the temperature of both the legs (use the dorsum of your fingers to elicit this sign).

• Check the arterial pulses in the leg.

• Comment on the heparin pump by the bedside.

• Remember to collect your thoughts when asked to examine the legs: do not rush in to grab the patient’s legs.

Diagnosis

This patient has a swollen leg resulting from deep vein thrombosis (lesion), which may be caused by the oral contraceptives she is taking (aetiology); the leg is oedematous and the patient is at risk of pulmonary embolism (functional status).

Questions

What are the complications of deep vein thrombosis?

• Pulmonary embolism

• Venous gangrene

• Pain, particularly in iliofemoral thrombosis.

What are the predisposing factors for venous thrombosis?

• Surgery (particularly of leg or pelvis, or after prostatectomy)

• Following cerebrovascular accident (about half of the patients develop DVT)

• Following myocardial infarction (one-third of patients have DVT)

• Obesity

• Malignancy (Lancet 1998;351:1077–80)

• Varicose veins

• Oral contraceptives

• Older age (exponential increase above the age of 50 years)

• Immobilization (paralysed limbs in stroke, paraplegia)

• Previous DVT (risk increases two- to three-fold)

• Pregnancy (risk increased in postpartum period)

• Hypercoagulable states: antithrombin III deficiency, protein C deficiency, protein S deficiency, antiphospolipid syndrome, excessive plasminogen activator inhibitor, polycythaemia vera, erythrocytosis

• Tissue trauma.

How would you investigate a patient with suspected deep vein thrombosis?

As clinical diagnosis is unreliable, it is essential to perform the following investigations to assess the extent of thrombosis:

• Duplex ultrasonography scanning and color Doppler studies

• D-dimer

• Venography: by injecting contrast into one of the leg veins.

What is the risk of pulmonary embolism in patients with below-knee thrombi?

The risk in such cases is low and many physicians refrain from prescribing anticoagulation to these patients.

How would you treat patients with below-knee thrombi?

• Pain relief

• Control of oedema

• Intermittent elevation of foot and elevation of foot during the night above the level of the heart

• Avoid long periods of standing

• Elastic support stockings from the midfoot to just below the knee, worn during the day.

The main aim is to prevent pulmonary emboli and restore venous patency and valvular function in order to prevent postphlebitic syndrome.

How would you treat patients with above-knee thrombi?

All patients with thrombi above the knee must receive anticoagulation therapy:

• Low-molecular-weight heparin has been shown to be more effective than unfractionated heparin in reducing size of thrombus and prevention of recurrence. It requires subcutaneous injection but does not require bolus or laboratory monitoring. Examples include enoxaparin, dalteparin or tinzaparin.

• Parenteral synthetic pentasaccharide analogues (e.g. fondaparinux) are factor Xa inhibitors that can also be used as first-line therapy.

• Unfractionated heparin is preferred in patients with iliofemoral thrombosis:

• Initial therapy aims to maintain the activated partial thromboplastin time (APTT) at 1.5–2.5 times the normal value within the first 24 h. Failure to achieve this target APTT within 24 h increases the risk of recurrent venous thromboembolism by 15-fold. Heparin therapy is continued for about 5–10 days.
• This is followed by warfarin therapy aiming to maintain the international normalized ratio (INR) at 2.0–3.0, which is recommended for the treatment of venous thromboembolic disease; however, substantially less intensive anticoagulation may be effective.

Remember: Anticoagulants do not affect thrombus that is already present.

• When anticoagulation is contraindicated, inferior vena caval filters may be required when there is a high risk of pulmonary embolism.

• Thrombolysis should be considered when the thrombosis is ‘limb threatening’.

There is no consensus on duration of therapy but the following are broad guidelines:

• 3–6 months with first episode

• 6 weeks to 3 months postoperatively if no other risk factors

• 6–12 months if persistent risk factors and recurrent venous thromboembolic events

• lifelong only rarely.

How would you prevent deep venous thrombosis?

• Subcutaneous low-dose heparin or low-molecular-heparin should be given to patients:

• undergoing surgery to the leg, pelvis or prostatectomy
• with myocardial infarction
• with cardiac failure.

• Stop oral contraceptives prior to surgery

• Early ambulation within 72 h after surgery

• Encourage leg exercise following surgery

• Elastic supports to patients with a history of thrombosis or obesity

• Aspirin 160 mg every day reduces the risk of pulmonary embolism and DVT by at least a third particularly after hip surgery (Lancet 2000;355:1295–302).

Advanced-level questions

How is bleeding risk from warfarin calculated?

The HEMORR2HAGES score is computed by adding 1 point for each bleeding risk factor:

Hepatic or renal disease

Ethanol abuse

Malignancy

Older (age >75 years)

Reduced platelet count (<75 × 109/l) or function

Rebleeding risk (2 points for major bleed and 1 point for minor bleed)

Hypertension (uncontrolled), systolic BP >160 mmHg

Anaemia (hematocrit <30)

Genetic factors

Excessive fall risk

Stroke.

The risk of bleeding is then predicted by the following table (Am Heart J 2006;151:713–19):

Hemorr2hages score Bleeds per 100 patient-years warfarin (95% confidence interval)
0 1.9 (0.6–4.4)
1 2.5 (1.3–4.3)
2 5.3 (3.4–8.1)
3 8.4 (4.9–13.6)
4 10.4 (5.1–18.9)
≥5 12.3 (5.8–23.1)

What are causes of recurrent venous thrombosis?

• Pregnancy, surgery, trauma, oral contraceptives

• Abnormalities in antithrombin III, protein C, protein S, fibrinogen or factor V

• Acquired conditions such as anti-phospholipid antibody syndrome, occult cancer, myeloproliferative disorders, some vasculitides

• Potential abnormalities include thrombomodulin, tissue factor pathway inhibitor, vitronectin associated with heparin and antithrombin III and fibrinolytic receptors.

What do you know of the anti-phospholipid antibody syndrome?

The diagnosis of this syndrome requires that a patient have recurrent clinical events (such as thromboses or foetal loss) and an anti-phospholipid antibody (such as anti-cardiolipin antibody or lupus anticoagulant). The ‘primary’ syndrome has no accompanying autoimmune disease, whereas it is ‘secondary’ if the patient also has SLE or lupus-like disease. Many patients with this syndrome have livedo reticularis, thrombocytopenia and neurological symptoms (Lancet 1999;353:1348–53).

The clinical course of the secondary syndrome is independent of the activity and severity of the lupus, but the presence of anti-phospholipid antibody worsens the prognosis of the lupus. Warfarin therapy with an INR of ≥3 offers the best protection against recurrent thrombosis for patients who have a confirmed major thrombosis.

Note: The anti-phospholipid antibody can occur in certain drug reactions and infectious diseases, but only those that occur in patients with autoimmune disease are associated with the clinical syndrome.

Further reading

Gorman WP, Davis KR, Donnelly R. ABC of arterial and venous disease. Swollen lower limb 1: general assessment and deep vein thrombosis. BMJ. 2000;320:1453-1456. (review)

Prins MH, Büller HR. Deep-vein thrombosis. Lancet. 1999;353:479-485. (review)

J Homans (1877–1954) was an American surgeon who worked at Johns Hopkins Hospital with Cushing, initially on experimental hypophysectomy and later on vascular disease. He first reported venous thrombosis related to airtravel in a 54-year old physician who develop DVT after a 14-hour flight (N Engl J Med 1954;250:148–59).

GRV Hughes, contemporary London physician, Raynes Institute, St Thomas’ Hospital, first described the anti-phospholipid antibody syndrome (N Engl J Med 1995;332:993–7).

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