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Deciphering Your Patient's Leg Pain

How do you quickly assess for all the possible musculoskeletal, vascular, metabolic, traumatic, infectious, neoplastic, neurologic, and referred causes of leg pain?and be sure not to miss one of the few that require immediate intervention? The authors discuss the key considerations.

By George D. Harris, MD, MS, and Bryan C. Hughes, MD

 

Leg pain is a medical complaint that is difficult for patients to accept and clinicians to treat. The pain can be acute or chronic, mild to severe, occur at rest or with activity, be local or referred, and vary in its sensory presentation. The patient?s age and comorbidities can assist the emergency physician in determining the underlying cause of leg pain.

Common causes of leg pain can be divided into several major categories: musculoskeletal, vascular, metabolic, traumatic, infectious, neoplastic, neurologic, and referred (see table below). In most cases, the underlying cause is not life- or limb-threatening. However, there are some instances in which an early diagnosis is imperative, such as deep vein thrombosis (DVT), acute arterial occlusion, underlying neoplasm or metastatic lytic lesion, and acute compartment syndrome.

In this article, we will discuss the proper evaluation of leg pain, key physical exam findings, and diagnostic testing. We will also review appropriate management strategies.

Causes of Leg Pain

Musculoskeletal

muscle cramps

muscle strain

ligament strain

overexertion or injury

previous knee or hip injury

medial tibial stress syndrome ("shin splints")

stress fractures

compartment syndrome (acute or chronic exertional)

patellofemoral syndrome

degenerative joint disease

rheumatoid arthritis


Vascular

venous insufficiency or stasis and varicose veins

arterial occlusion

superficial or deep vein thrombophlebitis


Metabolic

hypokalemia

gout

diabetes mellitus

Traumatic

soft tissue injury

fracture


Infectious

acute infectious arthritis

osteomyelitis

cellulitis


Neoplastic

osteosarcoma

Ewing's sarcoma

osteoid osteoma

metastatic bone disease (most commonly from lung, breast, or prostate cancer)


Referred

sciatica

hip pain

degenerative disc disease

spinal canal infection

spinal stenosis


Neurologic

nerve entrapment (meralgia paresthetica)

peripheral neuropathy

EVALUATING THE PAIN

Taking a detailed history about the nature of leg pain and related symptoms is very important for generating a differential diagnosis. The pain should be stratified by the patient?s age, the duration of the pain (acute or chronic), and its specific location. The presence of any associated symptoms (such as paresthesias, numbness, throbbing pain, or cramping) or signs (including dependent rubor, cyanosis, pallor, inflammation, pigmentation changes, or altered gait) can provide valuable information to narrow the diagnosis.

Leg pain in children and adolescents is more likely to be secondary to trauma, overuse, infection, neoplasm, or referred pain from the abdomen or spine. Usually, trauma in children is obvious or witnessed, allowing for rapid assessment of the involved extremity.

Leg pain in athletes raises a separate set of diagnostic possibilities. Special consideration must be given to acute versus chronic injury, biomechanical forces involved, anatomy, and the location of the pain. Conditions that cause leg pain in athletes include exertional compartment syndrome, stress fractures, and medial tibial stress syndrome. These are the most common disorders seen in athletes, with an incidence of 33%, 25%, and 13%, respectively. Other less common causes of leg pain in athletes include nerve or popliteal artery entrapment, claudication, tendonitis, or referred pain from the knee or hip.

Exertional compartment syndrome is caused by increased pressure in the anatomical compartments of the lower leg that leads to ischemia and pain. Typically, it is characterized by cramping, burning, or aching that occurs with exercise and is relieved dramatically with rest. It may also cause weakness and paresthesia in the affected nerve distribution. Stress fractures typically occur in the tibia, calcaneus, or metatarsals; patients usually report a history of gradual pain onset that starts as a mild ache and continues to increase in severity during exercise. The pain is usually well localized to the site of the fracture. Medial tibial stress syndrome (or ?shin splints?) is anterior tibial leg pain caused by chronic traction on the periosteum. Often seen in long-distance runners, it is characterized by pain that becomes more apparent after exercise and lasts for several hours. All three of these conditions may present a diagnostic dilemma because of their overlapping clinical presentations.

The type of pain, its duration, timing (constant or intermittent), and quality (dull ache, sharp, or cramping) can all be helpful in making the diagnosis (see table below). Leg pain may occur with walking or at rest (from arterial or venous insufficiency, spinal stenosis, or thrombophlebitis). Constant, dull, achy pain is a frequent symptom of chronic venous insufficiency. Complaints of tiredness or a focal burning or discomfort at the end of the day (or after being on one?s feet for several hours) suggest varicose veins. Acute swelling and constant pain in a leg that is tender to palpation are symptoms of acute DVT. Intermittent pain associated with walking that resolves with rest is a classic symptom of claudication and arterial insufficiency.

Leg Pain Characteristics in Various Diagnoses

occurs with walking or at rest arterial insufficiency
venous insufficiency
spinal stenosis
acute DVT
constant, dull aching chronic venous insufficiency
constant pain with acute swelling acute DVT
intermittent pain associated with walking intermittent claudication
sudden onset of pain acute arterial occlusion
spontaneous pain with leg movement leg cramp

 

RISK OF SEVERE ISCHEMIA

Sudden onset of severe leg pain in a patient with diabetes mellitus or peripheral vascular disease suggests acute arterial occlusion, which must be recognized immediately since peripheral nerves and muscles can suffer irreversible damage after four to six hours of severe ischemia. In addition to the sudden pain, classic symptoms of acute lower extremity ischemia include paresthesias, paralysis (sudden weakness), pallor, and pulselessness.

Referred pain may be due to sciatica, local hip pathology (such as avascular necrosis), osteoarthritis, spinal disc disease, or a spinal canal infection, among other causes.

Leg pain associated with muscle cramps can be due to muscle fatigue or strain from overuse, excessive exercise, or maintaining an extremity in the same position for a prolonged period of time. Muscle cramps can result from dehydration, low potassium, sodium, calcium, or magnesium levels, or certain medications (such as diuretics). Patients describe a leg cramp as unexpected, spontaneous pain during leg movement. Clinically, a cramp is an intense contraction of a large group of motor units; occasionally, it is a sign of underlying disease of the anterior horn cell, nerve roots, or peripheral nerve. Leg cramps are common, particularly in elderly patients, but usually benign. When severe, cramps can produce intense muscle contractions that cause muscle injury and elevation of creatine phosphokinase in the blood.

In a patient with monoarticular pain and inflammation, the three critical diagnoses to consider are trauma, infection, and crystalline diseases such as gout and pseudogout. Acute inflammation of a hip, knee, ankle, or the metatarsophalangeal joints should alert the physician to gouty arthritis, rheumatoid arthritis (RA), or a septic joint. Acute gouty arthritis presents with redness, swelling, and disability of the affected joint and severe pain lasting several hours. In most cases, only a single joint is involved, typically in the lower extremity (most often the first metatarsophalangeal joint or in the knee).

The inflammation may extend beyond the affected joint; the shoulders, hips, sternoclavicular joints, and even the spine and sacroiliac joints may become inflamed, complicating the diagnosis. The clinical picture can be indistinguishable from acute septic arthritis since both can cause fever, leukocytosis, and an elevated erythrocyte sedimentation rate. The diagnosis relies on aspiration of synovial fluid from the affected joint and analysis of the fluid by Gram?s stain, culture, and polarized light microscopic examination, which can distinguish the etiology in the great majority of cases. The light microscopic exam may demonstrate either positively birefringent crystals (pseudogout) or negatively birefringent crystals (gout).

Also, gouty attacks of lesser severity may be mimicked by a stress fracture or traumatic process in the bone or joint. The history and physical exam can assist in deciphering the underlying etiology.

Clinical presentations of RA include a polyarticular disease with a gradual onset, intermittent or migratory joint involvement, and a monoarticular onset. A classic presentation demonstrates predominant symptoms of pain, stiffness and swelling of many joints (in early disease, the metacarpophalangeal and proximal interphalangeal joints of the fingers, interphalangeal joints of the thumbs, the wrists, and metacarpophalangeal joints of the toes). In addition, the elbows, shoulders, ankles, and knees are commonly affected. Clinical features noted to be present for diagnostic and classification purposes include morning stiffness for at least one hour and present for at least six weeks, swelling of three or more joints or the wrist or the metacarpophalangeal or proximal interphalangeal joints in the fingers for at least six weeks, and symmetric joint swelling.

The presence of burning or tingling leg or foot pain suggests paresthetica, nerve entrapment, diabetic or nondiabetic peripheral neuropathy, or meralgia paresthetica. Pain and numbness in the lateral aspect of the thigh without any weakness results from compression of the lateral femoral cutaneous nerve. Obtaining a pertinent medical history of the lower extremity allows the clinician to identify risk factors and assess for vascular symptoms and comorbid conditions.

CLUES ON PHYSICAL EXAMINATION

Performing a thorough physical examination can provide important clues to the diagnosis. Edema in the extremity results from inflammation of the vasculature and can be found in cellulitis, venous thrombosis, musculoskeletal injury, and neoplasm. Skin changes such as erythema, hyperpigmentation, ecchymosis, or rash may result from infection, vasculitis, or trauma. A full neurologic examination of sensation, reflexes, strength, and tone can help differentiate neuropathy from other local tissue injury. Coexistent herniated discs need to be excluded in patients with radicular pain, especially when an ankle or knee tendon reflex is absent.

Several changes may be noted with chronic arterial insufficiency. Blood flow may be significantly reduced at rest, causing symptoms of severe leg ischemia. Unlike in intermittent claudication, where there is a supply-demand mismatch affecting the skeletal muscle, in severe lower extremity ischemia the most distal portion of the extremity (the skin and subcutaneous tissues of the forefoot) is affected. Diminished perfusion to the local tissues eventually produces ischemic changes in the color and temperature of the skin and in any hair on the skin. Patients can develop ischemic rest pain, distal ulceration, and gangrene.

On examination, the leg may have an abnormal pallor after two minutes of elevation and increased rubor on suddenly making the leg dependent. Comparing each leg and the time it takes for normal color to return can indicate the severity of the disease. If normal color does not return in 15 seconds, a moderate degree of arterial insufficiency is present; a delay of 30 seconds indicates marked insufficiency; and a delay of 60 seconds or longer reflects extreme disease.

A recent study demonstrated that patients with peripheral arterial disease, confirmed with noninvasive ankle-brachial index (ABI) testing, had a broad range of symptoms other than classic intermittent claudication. A substantial number of patients were asymptomatic or had exertional leg symptoms other than intermittent claudication. Leg pain on exertion and rest seem to also result from comorbid diseases affecting the legs, such as diabetes mellitus, neuropathy, intervertebral disc disease, spinal stenosis, or degenerative arthritis.

CONFIRMATORY TESTING

The history and physical examination are important for all causes of leg pain and imperative for deciding which diagnostic tests should be ordered for evaluation and confirmation of the pathologic process involved. However, these tests need to be used selectively to be helpful in the diagnosis and management of leg pain.

Synovial fluid analysis. Performing a joint aspiration on an inflamed joint can be both diagnostic and at times therapeutic. The synovial fluid must be sent to the lab for cell count and differential, Gram?s stain and culture, and crystal analysis using polarized microscopy.

Radiographic studies. For a significant number of acute or chronic muscle, ligament, or tendon injuries, radiographic studies may not be necessary to manage the initial problem unless a bone fracture is suspected. For most medical causes of leg pain, plain radiographs, computed tomography, or magnetic resonance imaging are generally not helpful in making the diagnosis.

Ankle-brachial index. There is an increased risk of systemic ischemic events and limb loss in a patient with peripheral artery disease (PAD), even if the patient is asymptomatic. Pulse palpation is not an appropriate screening tool for PAD. However, an appropriate noninvasive screening test is the ABI. It has proven to be the most effective, accurate, and practical method for detecting PAD. The ABI can detect latent disease; it can also evaluate patients with no exertional leg symptoms as well as those with intermittent claudication. Normally, systolic blood pressure readings in the legs and arms are similar. In the presence of hemodynamically significant stenoses, the systolic blood pressure in the leg will be decreased and the ABI less than 1.0. When the ABI is less than 0.85, then the relative risk of death at 10 years is 2.4.

D-dimer testing. Caution must be used when DVT is suspected based on clinical assessment findings. In one study, only 25% of patients with signs and symptoms of DVT had confirmation of the condition on ultrasound. When the quantitative D-dimer level is normal, coupled with a low pretest probability using the Wells criteria, the presence of acute DVT is highly unlikely. Quantitative D-dimers are not very sensitive and should not be used for screening purposes.

Ultrasound. Compression ultrasound is the most cost-effective and reliable test for confirmation of symptomatic proximal DVT, with a sensitivity and specificity of around 95%. However, sensitivity falls to 70% with isolated distal thrombus. Contrast venography is the gold standard but is not used much in clinical practice.

Other laboratory studies. Routine laboratory studies such as a complete blood cell count or metabolic profiles are generally not helpful unless a specific underlying medical cause for leg pain is suspected. The white blood cell count may be elevated in inflammatory, infectious, or neoplastic processes, but it is not very sensitive for confirming cellulitis, DVT, or arterial occlusion. If a patient experiences cramping leg pain, electrolyte studies may be helpful if they show a low potassium, sodium, calcium, or magnesium level.

MANAGEMENT STRATEGIES

One of the most important considerations in the management of leg pain is deciding whether the patient?s condition requires emergent or nonemergent intervention. Most conditions that cause leg pain are not life- or limb-threatening, but there are a few causes that warrant emergent intervention. Examples include arterial thromboembolization, acute compartment syndrome, rapidly spreading soft tissue infections, and severe trauma that compromises nervous or vascular tissue. Patients with sensory or motor neurologic deficits are at high risk for loss of limb and require emergent intervention. If acute ischemic injury is confirmed, prompt consultation with a vascular surgeon is necessary to determine whether the limb can be revascularized with surgery, thrombolytics, or embolectomy (see table below). The benefit of heparin therapy in acute arterial thrombosis has not been proved, but most surgeons will initiate heparin administration perioperatively.

Treatment Modalities

Agent Condition
Pharmacologic
anticoagulants DVT
arterial occlusion
antibiotics

cellulitis
osteomyelitis
infectious arthritis

NSAIDs musculoskeletal injuries
osteoarthritis
Surgical
embolectomy acute embolic ischemia
revascularization peripheral vascular disease
severe trauma
debridement necrotizing fasciitis
gangrene

Acute compartment syndrome is usually seen following severe trauma, particularly crush injury, to the lower extremities. Patients will often present with pain that is out of proportion to the physical exam findings. Classically, acute compartment syndrome is associated with the five P?s of pain, paresthesias, paralysis, pallor, and pulselessness. Patients with these signs and symptoms should have emergent fasciotomy.

Some leg disorders may not require emergent intervention but will require acute inpatient hospitalization for effective management. Deep vein thrombosis requires admission for observation and anticoagulation therapy in some cases. Either unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) can be used successfully. However, LMWH is quickly becoming the standard of care because it is just as effective as UFH and easier to use, with fewer side effects and monitoring parameters. Appropriately selected patients may be instructed to use LMWH safely at home, making hospital admission unnecessary.

Cellulitis that is resistant to outpatient oral treatment, covers a significant portion of soft tissue, or demonstrates any sign of systemic bacterial spread warrants hospital admission for parenteral antibiotic therapy. Most cases of cellulitis that spread proximally are caused by streptococcal infections. Staphylococcal infections should be strongly suspected in patients with diabetes or immunosuppressive disorders; initial antibiotic therapy should cover both organisms. Cephalosporins, macrolides, fluoroquinolones, and clindamycin may all be used empirically. With the increasing prevalence of methicillin-resistant Staphylococcus aureus, the physician must always consider this infection, especially in high-risk populations or in patients who are not improving with conventional antibiotics.

Many cases of peripheral vascular disease can be managed with antithrombotic therapy and risk-factor modification on an outpatient basis. Modifiable risk factors include smoking, obesity, hypertension, hyperlipidemia, and diabetes. Aspirin and clopidogrel have been shown to reduce cardiovascular events, but they do not affect symptoms of claudication. Patients with claudication at rest should be referred for revascularization surgery.

Most musculoskeletal causes of pain are usually alleviated with nonsteroidal anti-inflammatory drugs and physical therapy. If the pain limits ambulation, a proper walking aid, ankle-foot orthotics, and proper seating are critical. With overuse injuries in athletes, alleviation of a specific repetitive movement using braces or orthotics may be necessary.

 

Suggested Reading

Baun J: Evaluating a patient with leg pain: clinical guide. J Diag Med Sono 14(6):267, 1998.

Blackman PG: A review of chronic exertional compartment syndrome in the lower leg. Med Sci Sports Exerc 32(3 Suppl):S4, 2000.

Buller HR, et al.: Antithrombotic therapy for venous thromboembolic disease: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 126(3 Suppl):401, 2004. Erratum in Chest 127(1):416, 2005.

Collins TC, et al.: An absent pulse is not sensitive for the early detection of peripheral arterial disease. Fam Med 38(1):38, 2006.

Cox NH: Management of lower leg cellulitis. Clin Med 2(1):23, 2002.

Edwards PH Jr, et al.: A practical approach for the differential diagnosis of chronic leg pain in the athlete. Am J Sports Med 33(8):1241, 2005.

Ho WK, et al.: Venous thromboembolism: diagnosis and management of deep venous thrombosis. Med J Aust 182(9):476, 2005.

Lacroix P, et al.: Management of acute leg ischemia. Rev Prat 55(11):1205, 2005.

McDermott MM, et al.: Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA 286(13):1599, 2001.

McKenna M, et al.: The ratio of ankle and arm arterial pressure as an independent predictor of mortality. Atherosclerosis 87(2-3):119, 1991.

Shammas NW and Dippel EJ: Evidence-based management of peripheral vascular disease. Curr Atheroscler Rep 7(5):358, 2005.

Wells PS, et al.: Accuracy of clinical assessment of deep-vein thrombosis. Lancet 345(8961):1326, 1995.

 



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