Introduction

The acutely swollen leg is a common presenting complaint in the emergency room. It may represent a sudden presentation of an underlying chronic disease, or it may be the manifestation of a new acute problem, in particular deep vein thrombosis (DVT). A number of diseases can be associated with swelling of the lower extremity. It is important to identify the cause of the swelling, as treatment differs greatly depending on the underlying pathology. The underlying diagnosis may be life-threatening and make immediate action necessary and will also influence long-term prognosis and follow-up.

This chapter will help in the evaluation of the acutely swollen leg and will present up-to-date information on the treatment of DVT.

Pathophysiology of oedema

Acute swelling of the leg is caused by tissue oedema. Oedema formation is caused by excess water accumulation in the interstitial space of the tissue. Reasons for accumulation of water in the interstitial space are increased hydrostatic pressure, decreased colloid osmotic pressure, increased capillary permeability and lymphatic obstruction. These factors cause rapid fluid shifts in the body. There are also chronic states that cause oedema, but these are beyond the scope of this chapter. The mechanisms causing the shift in fluids are described later.

Increased hydrostatic pressure forces fluid out of the intravascular space. This is usually seen with any process that increases venous pressure. Central causes for increase of hydrostatic pressure include congestive heart failure, right heart failure and tricuspid insufficiency. Focal or unilateral oedema is often the result of DVT causing venous outflow obstruction.

Decreased colloid osmotic pressure allows passive transfer of intravascular fluid to the interstitial compartment. This is generally the result of reduction of intravascular protein content (i.e., hypoalbuminaemia). This mechanism causes generalised oedema and is rarely acute.

Increased capillary permeability removes the barrier to water moving from the intravascular space to the interstitial space. This is observed with focal trauma, burns, infection, ischaemia and immunological injury. This can cause rapid oedema forming in a single leg or it can present as a generalised oedema.

Lymphatic obstruction (lymphoedema) may be the result of hereditary hypoplasia, acute infection, or a consequence of lymphatic ablation following surgery, trauma or radiation. The trigger is usually identifiable, and presentation is rarely acute.

Medical history

A good medical history from the patient will often raise suspicion regarding the underlying pathology. A previous history of operations on the leg, trauma or a history of DVT may be useful, along with an overview of the patient’s general health. There are often several differential diagnoses despite an accurate history. The correct diagnosis, or exclusion of DVT, is essential to prevent potentially life-threatening complications. Consequently, several decision tools have been developed, including the Wells score. It is important to ascertain the precise time point when symptoms began, as this can influence both treatment and prognosis.

Physical examination

Upon examination of the leg, specific features should be identified. The swollen leg may be accompanied by redness, tenderness in the calf and increased temperature. An entry point may be found in cases of erysipelas. Swelling around a specific muscle or muscle compartment may increase suspicion of muscle rupture. Despite a good medical history and thorough physical examination, additional investigations are usually required to confirm a diagnosis. If DVT is suspected, additional imaging may be necessary. Severe pain and loss of sensory and motor function may point towards a compartment syndrome. Skin changes, varicose veins and ulceration of the leg may point towards a chronic venous insufficiency.

Differential diagnosis

There are a few differential diagnoses for the acutely swollen leg. The most frequent cause is a DVT. If DVT is suspected, it should be ruled out before any other diagnosis is considered. Other possible causes for acute leg swelling include a ruptured Baker’s cyst, erysipelas, cellulitis, fasciitis, muscle rupture or lymphoedema. These causes are mostly limited to one leg. If the patient has swelling of both legs, then alternative causes should be considered, in particular systemic causes such as chronic heart failure, renal failure or sepsis.

Musculotendinous rupture

Sudden intense pain of the calf usually suggests a musculoskeletal aetiology. If associated with sudden dorsiflexion of the foot, rupture of the musculotendinous portion of the medial head of the gastrocnemius muscle or the plantaris muscle (tendon) should be suspected. Localised pain in the medial or mid-calf area and swelling at the ankle level is common. Ecchymotic discolouration at the ankle level often follows 2–5 days later because of blood tracking down the fascial planes when the leg is dependent. Excluding DVT with a venous duplex examination is appropriate.

Treatment consists of symptomatic and supportive care until symptoms resolve. Leg elevation, ice early followed by heat, analgesics and reduced weight bearing may be necessary until symptoms resolve, usually within a month.

Baker’s cyst

Patients presenting with sudden, instantaneously severe calf pain and swelling of the leg may suffer from a ruptured Baker’s cyst. A Baker’s cyst forms as a result of overproduction of synovial fluid secondary to an underlying cause such as degenerative arthritis, meniscal tears, gout or rheumatoid arthritis. It is common among adults but can occur in children. A Baker’s cyst is usually located on the dorsolateral side of the knee. If the cyst bursts, immediate pain occurs, with swelling of the leg and redness, often mimicking a DVT. The Baker’s cyst is usually easily identified with duplex ultrasound. Treatment consists of anti-inflammatory medication, leg elevation and application of cold packs.

Cellulitis and erysipelas

Sudden swelling of the leg, combined with redness, pain and increased warmth, is seen in patients with erysipelas or cellulitis. Accompanying complaints can be nausea, vomiting, headaches and fever. The terms erysipelas and cellulitis are both used. There is, however, a small distinction between the two diagnoses. They differ in that erysipelas involves the upper dermis and superficial lymphatics, whereas cellulitis involves the deeper dermis and subcutaneous fat. This manifests in a different presentation in erysipelas, where there is a clear line of demarcation of the redness and the skin involved. In cellulitis, there is no clear demarcation visible. Upon physical examination, it is important to look for a break in the skin as a portal for entry of bacteria. Common skin barrier breaks are abrasions, insect bites or tinea pedis. Any fluid coming from the wound should be cultured. The most likely causative bacteria are Staphylococcus aureus and Group A streptococci. Treatment comprises antibiotics targeted towards Gram-positive bacteria, rest and elevation. Duplex ultrasound should be considered to exclude DVT. Patients treated for erysipelas or cellulitis should experience symptom improvement within 24–48 hours.

Necrotising fasciitis

Fasciitis is a very serious condition with a high morbidity and mortality. While this may present as excruciating pain, other clinical signs may be absent. Possible clinical signs include erythema, crepitations caused by gas formed by subcutaneous bacteria, fever, nausea, vomiting, local oedema, blisters and necrosis of the skin and underlying structures. The underlying mechanism is a bacterial colonisation of S. aureus or Group A streptococci. The microorganisms produce endotoxins, which cause a severe inflammatory reaction, with destruction of the deep fascia and surrounding structures. Patients with a compromised immune system are more susceptible to infection with opportunistic bacteria. If this situation is left untreated, the destruction of the fascia will spread and eventually lead to the death of the patient. Treatment of necrotising fasciitis consists of aggressive surgical debridement of the infected tissues. Broad-spectrum antibiotics should be given to include coverage for Gram-positive, Gram-negative and anaerobic organisms. Additional intensive care support is vital to improve the chance of survival. Even with optimal treatment, the mortality rate is over 30%.

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