Calf Pain

This pain is usually muscle and its mechanism may be ischemic, inflammatory, or metabolic. For understanding the pain of muscular origin, we can also see chapter Myalgia and cramps.

But sometimes the pain of bone origin or joint.

Three situations are possible:

– The pain is acute and brutal, and it is often a medical emergency;

– Pain is intermittent, usually brought on by exercise;

– The pain is chronic, and it is especially in this case it must be wary of non muscle pain.

Calf AnatomyACUTE PAIN:

Acute muscle ischemia by arterial occlusion:

This must be the obsession of the doctor called urgently for a sudden calf pain occurring at rest, because every minute counts. The clinical criteria of acute ischaemia of arterial origin are the 5 P Anglo-Saxon authors: pain, paleness,paresia, paresthesia, pulseness.

In practice, the calf and foot pain are pale and cold, and distal pulses were abolished; the painful leg is more or less paralyzed and seat paresthesia. if we then sought to determine arterial occlusion is embolic origin: concept of heart disease and especially atrial fibrillation; aortic lesions (atheroma or sometimes traumatic); unusually paradoxical embolism from phlebitis, thrombus through a patent foramen ovale due to excessive pressure in the right cavities, transient. We must immediately begin treatment with heparin, low molecular weight heparin at curative dose, or unfractionated heparin (syringe if one is in hospital). You must then assign the patient to the radiologist who will opacify the arterial bed (the scanner with injection supplanted angiography) and the vascular surgeon who will remove the thrombus with a Fogarty catheter.

If was removed arterial embolism, there is an in situ thrombosis, usually on pathological arteries (atherothrombosis) but sometimes on healthy arteries (antiphospholipid syndrome, paraneoplastic syndrome Trousseau).

In young and smoking topic, we think of the juvenile arteritis Buerger. In these situations, it is usually impossible to surgically reperméabiliser the or occluded arteries. Treatment is essentially medical and uses heparin, or infusions of prostacyclin or analogue (or Ilomédine® Iloprost®). In the case of diabetic arteritis or Buerger these acute ischemias quite often lead to a more or less limited amputation.


The pain is less intense, walking is possible, but awake pain. The coloring of the calf and foot is normal (excluding exceptional phlegmasia coerulea where the leg is purple). The calf is rather hot and pulse are perceived. There are no reliable clinical signs of sural phlebitis and the least bad sign is the increase in volume of the calf, especially if it is accompanied by an increase in volume of the thigh. The famous sign Homans can be forgotten because it has no semiotic value.

It is essential to confirm the clinical suspicion for venous doppler ultrasonography, because the penalty is an anticoagulant treatment for at least three months. We begin, after checking the blood count, a heparin low molecular weight heparin (LMWH) Lovenox®, Fraxiparine® or Fraxodi® Inohep® or if you want to settle for a single injection per day.

In the elderly (over 75 years) and / or renal failure, it is prudent to prefer calciparine to LMWH. The relay is taken from the first day by anti-vitamin K (Coumadin® or Previscan in an evening taking, Sintrom® in two doses) so as to interrupt the LMWH to the 5th day (there is virtually no thrombocytopenia heparin before 5 days of treatment).

During that establishes treatment, we look for a cause for this phlebitis. Some triggering circumstances are obvious: pregnancy, contraception, orthopedic surgery or plaster, prolonged bed rest). In other cases you must check the list of drugs, eliminate in young patients with lupus, a disorder antiphospholipid or Behcet’s disease, and looking at the older patient with cancer.

The biological investigation comprises systematically, further NFS + platelets, fibrin and CRP, electrophoresis of the protein, the protein assay protein C and S, (before the AVK), the measurement of the resistance protein C activated, the dosage of factor VIII and homocysteine, research anticardiolipin antibody or a circulating lupus anticoagulant (aPTT not corrected by adding control plasma).

Venous Doppler ultrasound is necessary before the start of anticoagulants because there are many differential diagnoses. In particular, think if known knee pathology (rheumatoid arthritis, osteoarthritis of the knee, …) to a ruptured popliteal cyst Baker. There is usually an increase in volume of the calf and in 30% of cases, internal above-ankle hematoma “crescent” that is very characteristic. If calf pain occurs suddenly after exercise, even very moderate, we must think of a muscle strain. In both cases, the anticoagulant therapy may aggravate the symptoms. lodges syndrome often occurs after prolonged exercise and requires stopping the effort. The pain is usually limited to a bilateral muscle compartment but when unilateral the differential diagnosis with phlebitis arises. The pain is due to the increase in volume of the calf in a box osteo fascial inextensible.

Measuring the intramuscular pressure, often greater than 30 mmHg confirms the diagnosis. Fasciotomy discharge is sometimes necessary.

Primitive muscle pain, the mechanism is not unequivocal:

Infectious myositis:

Infectious myositis often staphylococcal, are extremely painful. The diagnosis is made by the discovery of other septic foci, the finding of an inflammatory syndrome, blood cultures. It is urgent to establish appropriate antibiotic treatment for antibiotic susceptibility. If snow crackling calf, a search anaerobic germ responsible for gas gangrene or necrotizing cellulitis.

Ischemic myositis:

Myositis can be reached by coronary arterioles, during a nodosa or Wegener’s granulomatosis. The existence of a segmental edema, mononeuritis or systemic manifestations is evocative. This is corticosteroids (bolus Solumedrol®) that will relieve the patient.

Inflammatory myositis:

Inflammatory myositis include polymyositis, dermato-myositis syndrome the antisynthetase and inclusion body myositis. It is the increase of creatine phosphokinase (CPK) and / or myogenic electromyogram which leads to muscle biopsy and it is this that distinguishes these different varieties of inflammatory myositis. In the particular case of anti-synthetase syndrome, there are usually hand anomalies (called trucker hand) and pulmonary fibrosis.

The existence of antibodies against soluble nuclear antigens and anti-Jo type 1 precisely confirms the diagnosis.

It is important to search an associated neoplasia, especially if there is a dermatomyositis (almost 25% of them are paraneoplastic).

Treatment is based on first-line Prednisone® (1 mg / kg / day) which must usually involve intravenous immunoglobulin (2 g / kg in 48 hours monthly courses) and / or immunosuppressants (Methotrexate®, Cellcept®, anti-CD20 antibody or Mabthera®, …). Inclusion body myositis are particularly amenable to treatment.

Sometimes muscle biopsy shows granulomatous myositis and in this case we must eliminate trichinosis (eosinophilia, serology) and essentially seek sarcoidosis (CT scan, lip biopsy) or Behcet’s disease (bipolar aphtose pseudo folliculitis, ocular ).


Pain related to exertion:

It is usually intermittent claudication and accurate perimeter walking possible before the onset of pain. Lameness can be arterial, neurological or muscular.

Claudication of arterial origin:

The most characteristic is limping calf linked to atherothrombosis of the arteries of the legs. The first review involves comparing the systolic blood pressure measured in the arm and the ankle (with a DINAMAP® type of automatic device or better a Doppler probe). The systolic pressure index (ABI), which is the ratio between the systolic pressure at the ankle on the systolic pressure to the arm, is physiologically between 1.3 and 0.9. IPS <0.9 sign occlusive peripheral arterial disease (PAD) and arterial Doppler ultrasound and scanner with injection or MR angiography will clarify the level or obstacles. The classic lesion is the occlusion of the superficial femoral artery in the Hunter’s canal. IPS <0.5 is a poor prognostic factor. It is important to clarify the vascular risk factors (foremost among them smoking) and seek other localizations of atheromatous disease (Doppler ultrasound of the supra-aortic trunks and the renal arteries, ECG and, if necessary myocardial scintigraphy).

Treatment is based on smoking cessation, correction of other risk factors and walking (at least 30 minutes morning and evening). The antiplatelet drugs (Aspirin, Plavix), incidentally vasodilators (pentoxyphilline or Torental®). We can hope to regress atherosclerosis if we reduce total cholesterol audessous of 1.80 g / L, hence the frequent prescription of statin. In severe intermittent claudication not improved by medical treatment, it may be necessary to perform angioplasty, often with stent placement, or intervention (aorto-femoral bypass, femoral-femoral bypass, coronary bifemoral prosthesis , …).

Exceptionally limping calf is not related to PAD but a rare anatomic lesion (trapped popliteal artery, popliteal cyst adventitious) or iliac arterial endofibrose. This occurs in cyclists who make over 8000 km per year, by bicycle. It is linked to a progressive elongation of the iliac artery which becomes tortuous and fibrous. The treatment is surgical.

Claudication of neurological origin (in bilateral principle):

The possible cause is lumbar spinal stenosis is due to the combination of a genetically narrow spinal canal and lumbar osteoarthritis affecting particularly facet joints, possibly combined with a protrusion or a true herniated disc.

The scanner and lumbar MRI to measure the dimensions of the spinal canal, knowing these facts examinations supine underestimate the importance of the canal narrowing.

We can make some epidural infiltrations Hydrocortancyl® but if lameness is severe, it will resort to surgery. It seems prudent to settle for a simple act of laminectomy on a three-stage, without set up equipment. Postoperative improvement is progressive, three to six months.

Claudication of muscular origin (in bilateral principle):

The compartment syndrome can achieve intermittent pain in the calves, but limping slowly gives in to stop the effort.Rhabdomyolysis metabolic myopathies are usually delayed compared to the effort and yield in hours or days after stopping the effort. They may be accompanied by the emission of very dark urine, by myoglobinuria.

CPK is very high (more than 5 times the normal value). The two major metabolic myopathies are responsible rhabdomyolysis glycogenosis McArdle and mitochondrial cytopathies. In the first case, the venous lactate do not increase the effort; in the second case, they rise considerably, commonly than 5 mmol / L after effort.

Metabolic MRI with spectroscopy virtually allows for diagnosis but this review is difficult to obtain. It is the muscle biopsy with special stains that show muscle enzyme deficiency. If mitochondrial cytopathy, there is usually an aspect of ragged red fibers (ragged red fibers); the metabolic abnormality can affect one of the steps of the mitochondrial respiratory chain; treatment may include ubiquinone (if there is an exceptional challenge cit coenzyme Q) and carnitine. But more commonly delayed muscle soreness after exercise correspond to simple minor aches (delayedonset muscle soreness or DOMS).

Muscle pain not related to the effort:

These are muscle cramps, usually nocturnal and bilateral. Usually trivial, they can be improved by taking Hexaquine® (2-6 cp / d) or Vitamin B2 (beflavine). If they are intense and rebels, they have to seek a metabolic abnormality (do a chemistry panel, a dosage of the serum magnesium and phosphate).

Paralysis dyskaliémiques, mostly genetic but sometimes associated with hyperthyroidism, can be painful.


Joint pain, tendon or bone radiating in the calf:

A diagnostic trap is to ignore joint pain, tendon or bone radiating in the calf. We must especially beware of painful irradiation of a synovial cyst knee, tendinitis of the crow’s feet, or bone damage (osteonecrosis tibia or knee osteosarcoma). Bone scan and, if necessary MRI knee will confirm the diagnosis.

Muscle pain:

But more often the pain is muscular.

Post-traumatic pain:

Pain can be post-traumatic. It is easy to raise this hypothesis when the notion of a direct hit, often occurred during a sports activity, but it can also be an intrinsic muscle injury (bruise, encysted hematoma, myositis ossificans). Muscle ultrasound of good technical quality allows to visualize these lesions.

In the absence of trauma:

We must first think of the drug and causes first statin. CPK are usually increased, but not always.

Some connective can be complicated by muscle injuries or chronic subcutaneous: myositis ossificans in consecutive dermatomyositis, mainly in adolescents; calcinose subcutaneous scleroderma.

Unusually there is a muscle tumor, localized by MRI and confirmed by biopsy (rhabdomyosarcoma, malignant fibrous histiocytoma, clear cell tumor of the tendon and sheath, haemangiopericytoma).

If questioning, examination and imaging are not contributing, we can evoke a chronic polymyositis or myofasciitis macrophages. It blames vaccines containing aluminum (especially hepatitis B vaccine) and biopsy is usually done in the deltoid and possibly the side where the patient has been vaccinated.

Generally muscle biopsy is hardly profitable if the CPK and electromyography are normal.

When you have nothing found and the pain is more diffuse, involving the tendon insertion areas we will discuss fibromyalgia (see chronic widespread pain).

Warning: there may be two muscle diseases and intricate example is the muscle from statin intolerance reveal mitochondrial cytopathy. One can also observe the association of polymyositis and a myofasciitis macrophages. Only the muscle biopsy done in a specialized laboratory will establish these difficult diagnoses.