Chapter 66: Pain in the leg

Pain in the leg has many causes, varying from a simple cramp to an arterial occlusion. Overuse of the legs in the athlete can lead to a multiplicity of painful leg syndromes, ranging from simple sprains of soft tissue to compartment syndromes. A major cause of leg pain lies in the source of the nervous network to the lower limb, namely the lumbar and sacral nerve roots of the spine. It is important to recognise radicular pain, especially from L5 and S1 nerve roots, and also the patterns of referred pain, such as from apophyseal (facet) joints and sacroiliac joints (SIJs).

A summary of the diagnostic strategy model is presented in TABLE 66.1.

Probability diagnosis

Many of the causes, such as foot problems, ankle injuries and muscle tears (e.g. hamstrings and quadriceps), are obvious and common. There is a wide range of disorders related to overuse syndromes in athletes.

A very common cause of acute severe leg pain is cramp in the calf musculature, the significance of which escapes some patients as judged by middle-of-the-night calls.

One of the commonest causes is nerve root pain, invariably single, especially affecting the L5 and S1 nerve roots. Tests of their function and of the lumbosacral spine for evidence of disc disruption or other spinal dysfunction will be necessary. Should multiple nerve roots be involved, other causes, such as compression from a tumour, should be considered. Remember that a spontaneous retroperitoneal haemorrhage in a patient on anticoagulant therapy can cause nerve root pain and present as intense acute leg pain. The nerve root sensory distribution is presented in FIGURE 66.1.

Other important causes of referred thigh pain include ischiogluteal bursitis (weaver’s bottom) and gluteus medius tendonitis or trochanteric bursitis.

Serious disorders not to be missed

Neoplasia

Malignant disease, although uncommon, should be considered, especially if the patient has a history of one of the primary tumours, such as breast, lung or kidney. Such tumours can metastasise to the femur. Consider also osteogenic sarcoma and multiple myeloma, which are usually seen in the upper half of the femur. The possibility of an osteoid osteoma should be considered with pain in a bone relieved by aspirin.

Infections

Severe infections are not so common, but septic arthritis and osteomyelitis warrant consideration. Superficial infections such as erysipelas and lymphangitis occur occasionally.

Vascular problems

Acute severe ischaemia can be due to thrombosis or embolism of the arteries of the lower limb. Such occlusions cause severe pain in the limb and associated signs of severe ischaemia, especially of the lower leg and foot.

Chronic ischaemia due to arterial occlusion can manifest as intermittent claudication or rest pain in the foot due to small vessel disease.¹

Various pain syndromes are presented in FIGURE 66.2. It is important to differentiate vascular claudication from neurogenic claudication (see TABLE 66.2).

Venous disorders

The role of uncomplicated varicose veins as a cause of leg pain is controversial. Nevertheless, varicose veins can certainly cause a dull aching ‘heaviness’ and cramping, and can lead to painful ulceration.

Superficial thrombophlebitis is usually obvious, but it is vital not to overlook deep venous thrombosis. These more serious conditions of the veins can cause pain in the thigh or calf.

Pitfalls

There are many traps and pitfalls in the painful leg. Herpes zoster at the pre-eruption phase is an old trap and more so when the patient develops only a few vesicles in obscure parts of the limbs.

In future we can expect to encounter more cases of spinal canal stenosis (secondary to the degenerative changes) in the elderly. The early diagnosis can be difficult, and buttock pain on walking has to be distinguished from vascular claudication due to a high arterial obstruction.

The many disorders of the SIJ and hip region can be traps, especially the poorly diagnosed yet common gluteus medius tendonitis. Another more recent phenomenon is the ‘hip pocket nerve syndrome’, where a heavy wallet crammed with credit cards can cause pressure on the sciatic nerve.

One of the biggest traps, however, is when hip disorders, particularly osteoarthritis, present as leg pain, especially on the medial aspect of the knee.

Nerve entrapments (see FIG. 66.3) are an interesting cause of leg pain, although not as common as in the upper limb. Some entrapments to consider include:

• lateral cutaneous nerve of thigh, known as meralgia paraesthetica

• common peroneal nerve

• posterior tibial nerve at ankle (the ‘tarsal tunnel’ syndrome)

• obturator nerve, in obturator canal

• femoral nerve (in inguinal region or pelvis)

Then there are the rare causes. One overlooked problem is complex regional pain syndrome I (sympathetic dystrophy), which may follow even minor trauma to the limb. This ‘causalgia’ syndrome manifests as burning or aching pain with vasomotor instability in the limbs. The essential feature is the disparity between the intensity of the pain and the severity of the inciting injury.

General pitfalls

• Overlooking beta blockers and anaemia as a precipitating factor for vascular claudication

• Overlooking hip disorders as a cause of knee pain

• Mistaking occlusive arterial disease for sciatica

• Confusing nerve root syndromes with entrapment syndromes

Seven masquerades checklist

The outstanding cause of leg pain in this group is spinal dysfunction. Apart from nerve root pressure due to a disc disruption or meralgia paraesthetica, pain can be referred from the apophyseal (facet) joints. Such pain can be referred as far as the mid-calf (see FIG. 66.4).

The other checklist conditions—depression, diabetes, drugs and anaemia—can be associated with pain in the leg. Depression can reinforce any painful complex.

Diabetes can cause discomfort through a peripheral neuropathy that can initially cause localised pain before anaesthesia predominates. Drugs such as beta blockers, and anaemia, can precipitate or aggravate intermittent claudication in a patient with a compromised circulation.

Psychogenic considerations

Pain in the lower leg can be a frequent complaint (maybe a magnified one) of the patient with non-organic pain, such as the malingerer, the conversion reaction patient (hysteria) and the depressed. Sometimes regional pain syndrome (reflex or post-traumatic) is incorrectly diagnosed as functional.

Careful attention to basic detail in the history and examination can point the way of the clinical diagnosis.

History

In the history it is important to consider several distinctive aspects, outlined by the following questions.

• Is the pain of acute or chronic onset?

• If acute, did it follow trauma or activity?

  • – If not, consider a vascular cause: vein or artery; occlusion or rupture.

• Is the pain ‘mechanical’ (related to movement)?

  • – If it is unaltered by movement of the leg or a change in posture, it must arise from a soft tissue lesion, not from bone or joints.

• Is the pain postural?

  • – Analyse the postural elements that make it better or worse.

  • – If worse on sitting, consider a spinal cause (discogenic) or ischial bursitis.

  • – If worse on standing, consider a spinal cause (instability) or a local problem related to weight-bearing (varicose veins).

  • – If worse lying down, consider vascular origin, such as small vessel peripheral vascular disease. If worse lying on one side, consider greater trochanteric pain syndrome.

  • – Pain unaffected by posture is activity-related.

• Is the pain related to walking?

  • – No: Determine the offending activity (e.g. joint movement with arthritis).

  • – Yes: If immediate onset, consider local cause at site of pain (e.g. stress fracture). If delayed onset, consider vascular claudication or neurogenic claudication.

• Is the site of pain the same as the site of trauma?

  • – If not, the pain in the leg is referred. Important considerations include lesions in the spine, abdomen or hip and entrapment neuropathy.

• Is the pain arising from the bone?

  • – If so, the patient will point to the specific site and indicate a ‘deep’ bone pain (consider tumour, fracture or, rarely, infection) compared with the more superficial muscular or fascial pain.

• Is the pain arising from the joint?

  • – If so, the clinical examination will determine whether it arises from the joint or juxtaposed tissue.

Examination

The first step is to watch the patient walk and assess the nature of any limp.

Note the posture of the back and examine the lumbar spine. Have both legs well exposed for the inspection.

Inspect the patient’s stance and note any asymmetry and other abnormalities, such as swellings, bruising, discolouration, or ulcers and rashes. Note the size and symmetry of the legs and the venous pattern. Look for evidence of ischaemic changes, especially of the foot.

Palpate for local causes of pain and if no cause is evident examine the spine, blood vessels (arteries and veins) and bone. Areas to palpate specifically are the ischial tuberosity, trochanteric area, hamstrings and tendon insertions. Palpate the superficial lymph nodes. Note the temperature of the feet and legs. Perform a vascular examination, including the peripheral pulses and the state of the veins if appropriate.

If evidence of peripheral vascular disease (PVD), remember to auscultate the abdomen and adductor hiatus, and the iliac, femoral and popliteal vessels.

A neurological examination may be appropriate, particularly to test nerve root lesions or entrapment neuropathies.

Examination of the joints, especially the hip and SIJs, is very important.

Investigations

A checklist of investigations that may be necessary to make the diagnosis is as follows:

• FBE and ESR

• radiology:

  • – leg X-rays, especially knee, hip

  • – plain X-ray of lumbosacral spine

  • – CT scan of lumbosacral spine

  • – ultrasound or MRI of greater trochanteric area

  • – MRI scan of lumbosacral spine

  • – bone scan

• electromyography

• vascular:

  • – arteriography

  • – duplex ultrasound scan

  • – ankle brachial index

  • – venous pool radionuclide scan

  • – contrast venography

  • – air plethysmograph (varicose veins)

  • – D-dimer test

Aches and pains in the legs are a common complaint in children. The most common cause is soreness and muscular strains due to trauma or unaccustomed exercise. One cause of bilateral leg pain in children is leukaemia. Consider osteomyelitis (refer CHAPTER 69).

It is important to consider child abuse, especially if bruising is noted on the back of the legs.

‘Growing pains’

So-called ‘growing pains’, or idiopathic leg pain, is thought to be responsible for up to 20% of leg pain in children.² Such a diagnosis is vague and often made when a specific cause is excluded. It is usually not due to ‘growth’ but related to excessive exercise or trauma from sport and recreation, and probably emotional factors.

The pains are typically intermittent and symmetrical and deep in the legs, usually in the anterior thighs or calves. Although they may occur at any time of the day or night, typically they occur at night, usually when the child has settled in bed. The pains usually last for 30–60 minutes and tend to respond to attention such as massage with an analgesic balm or simple analgesics (refer to CHAPTER 91).

Serious problems

It is important to exclude fractures (hence the value of X-rays if in doubt), malignancy (such as osteogenic sarcoma, Ewing tumour or infiltration from leukaemia or lymphoma), osteoid osteoma, osteomyelitis, scurvy and beriberi (rare disorders in developed countries) and congenital disorders such as sickle-cell anaemia, Gaucher disease and Ehlers–Danlos syndrome.

The older the patient, the more likely it is that arterial disease with intermittent claudication and neurogenic claudication due to spinal canal stenosis will develop. Other important problems of the elderly include degenerative joint disease, such as osteoarthritis of the hips and knees, muscle cramps, herpes zoster, Paget disease, polymyalgia rheumatica (affecting the upper thighs) and sciatica.

Spinal causes of leg pain

Problems originating from the spine are an important, yet at times complex, cause of pain in the leg.

Important causes are:

• nerve root (radicular) pain from direct pressure

• referred pain from:

  • – disc pressure on tissues in front of the spinal cord

  • – apophyseal joints

  • – SIJs

• spinal canal stenosis causing claudication

Various pain patterns are presented in FIGURES 66.3 and 66.4.

Nerve root pain

Nerve root pain from a prolapsed disc is a common cause of leg pain. A knowledge of the dermatomes of the lower limb (see FIG. 66.1) provides a pointer to the involved nerve root, which is usually L5 or S1 or both. The L5 root is invariably caused by an L4–5 disc prolapse and the S1 root by an L5–S1 disc prolapse. The nerve root syndromes are summarised in TABLE 66.3.

A summary of the physical examination findings for the most commonly involved nerve roots is presented in TABLE 66.3.

Sciatica

See CHAPTER 38. Sciatica is defined as pain in the distribution of the sciatic nerve or its branches (L4, L5, S1, S2, S3) caused by nerve pressure or irritation. Most problems are due to entrapment neuropathy of a nerve root, in either the spinal canal (as outlined above) or the intervertebral foramen.

It should be noted that back pain may be absent and peripheral symptoms only will be present.

Treatment

A protracted course can be anticipated, in the order of 12 weeks (see CHAPTER 38). The patient should be reassured that spontaneous recovery can be expected. A trial of conservative treatment would be recommended thus:

• back care education

• relative bed rest if very painful only (2 days is optimal)—a firm base is ideal

• return to activities of daily living ASAP

• analgesics (avoid narcotic analgesics if possible)

• NSAIDs (2 weeks is recommended)

• basic exercise program, including swimming

• traction can help, even intermittent manual

Referral to a therapist of your choice (e.g. physiotherapist) may be advisable. Conventional spinal manipulation is usually contraindicated for radicular sciatica. If the patient is not responding or the circumstances demand more active treatment, an epidural anaesthetic injection is appropriate. Surgical consultation is indicated for a severe or progressive neurological deficit.

If a trial of NSAIDs, rest and physiotherapy has not brought significant relief, an epidural anaesthetic (lumbar or caudal) using half-strength local anaesthetic (e.g. 0.25% bupivacaine HCl) and a depot corticosteroid (e.g. triamcinolone) is advisable. The lumbar route under image intensification is preferred.

LSS is narrowing of the spinal canal resulting in pressure on the sciatic nerve roots and possibly the spinal canal and cord. It typically occurs in people aged over 50 years with a history of spinal degenerative changes, including osteoarthritis (see FIG. 38.9), but LSS may be congenital.

The symptoms are as outlined for neurogenic claudication in TABLE 66.2. Pain, which is usually bilateral, is in the proximal-leg buttocks, thighs and legs, radiating distally. Some 50% remain clinically stable, 25% deteriorate and about 25% improve with time. Conservative treatment includes relative rest, specific exercises, analgesics and agents for neuropathic pain. There is no evidence of the value of epidural corticosteroid injections or oral corticosteroids. Surgical consultation is indicated for severe or progressive neurological deficit or progressive pain,. The risk of surgical complications increases with age.

Referred pain

Referred pain in the leg can arise from disorders of the SIJs or from spondylogenic disorders. It is typically dull, heavy and diffuse. The patient uses the hand to describe its distribution compared with the use of fingers to point to radicular pain.

Spondylogenic pain

Non-radicular or spondylogenic pain originates from any of the components of the vertebrae (spondyles), including joints, the intervertebral discs, ligaments and muscle attachments. An important example is distal referred pain from disorders of the apophyseal joints, where the pain can be referred to any part of the limb as far as the calf and ankle but most commonly to the gluteal region and proximal thigh (see FIG. 66.4).

Another source of referred pain is that caused by compression of a bulging disc against the posterior longitudinal ligament and dura. The pain is typically dull, deep and poorly localised. The dura has no specific dermatomal localisation, so the pain is usually experienced in the low back, sacroiliac area and buttocks. Less commonly, it can be referred to the coccyx, groin and both legs down to the calves. It is not referred to the ankle or the foot.

Sacroiliac dysfunction

This typically causes a dull ache in the buttock, but it can be referred to the iliac fossa, groin or posterior aspects of the thighs (see CHAPTER 65). It rarely radiates to or below the knee. It may be caused by inflammation (sacroiliitis) or mechanical dysfunction. The latter must be considered in a postpartum woman presenting with severe aching pain present in both buttocks and thighs.

Nerve entrapment syndromes

Entrapment neuropathy can result from direct axonal compression or can be secondary to vascular problems, but the main common factor is a nerve passing through a narrow rigid compartment where movement or stretching of that nerve occurs under pressure.

Clinical features

• Pain at rest (often worse at night)

• Variable effect with activity

• Sharp, burning pain

• Radiating and retrograde pain

• Clearly demarcated distribution of pain

• Paraesthesia may be present

• Tenderness over nerve

• May be positive Tinel sign

Meralgia paraesthetica

This is the commonest lower limb entrapment and is due to the lateral femoral cutaneous nerve of the thigh being trapped under the lateral end of the inguinal ligament, 1 cm medial to the ASIS.⁴

The nerve is a sensory nerve from L2 and L3. It occurs mostly in middle-aged people, due mainly to thickening of the fibrous tunnel beneath the inguinal ligament, and is associated with obesity, pregnancy, ascites or local trauma such as belts, trusses and corsets. Its entrapment causes a burning pain with associated numbness and tingling (see FIG. 66.3).

The distribution of pain is confined to a localised area of the lateral thigh and does not cross the midline of the thigh.

Differential diagnosis

• L2 or L3 nerve root pain (L2 causes buttock pain also)

• Femoral neuropathy (extends medial to midline)

Treatment

• Injection of corticosteroid medial to the ASIS, under the inguinal ligament

• Surgical release (neurolysis) if refractory

• Treat the cause (e.g. weight reduction, constricting belt, corset)

Note: Meralgia paraesthetica often resolves spontaneously.

Peroneal nerve entrapment

The common peroneal (lateral popliteal) nerve can be entrapped where it winds around the neck of the fibula or as it divides and passes through the origin of the peroneus longus muscle 2.5 cm below the neck of the fibula. It is usually injured, however, by trauma or pressure at the neck of the fibula.

Symptoms and signs

• Pain in the lateral shin area and dorsum of the foot

• Sensory symptoms in the same area

• Weakness of eversion and dorsiflexion of the foot (described by patients as ‘a weak ankle’)

Differential diagnosis

• L5 nerve root (similar symptoms)

Treatment

• Shoe wedging or other orthotics to maintain eversion

• Neurolysis is the most effective treatment

Tarsal tunnel syndrome

This is an entrapment neuropathy of the posterior tibial nerve in the tarsal tunnel beneath the flexor retinaculum on the medial side of the ankle. The condition is due to dislocation or fracture around the ankle or tenosynovitis of tendons in the tunnel from injury, or rheumatoid arthritis and other inflammations.

Symptoms and signs

• A burning or tingling pain in the toes and sole of the foot, occasionally the heel

• Retrograde radiation to the calf, perhaps as high as the buttock

• Numbness is a late symptom

• Discomfort often in bed at night and worse after standing

• Removal of shoe may give relief

• Sensory nerve loss variable, may be no loss

• Tinel test (finger or reflex hammer tap over nerve below and behind medial malleolus) may be positive

• Tourniquet applied above ankle may reproduce symptoms

The diagnosis is confirmed by electrodiagnosis.

Treatment

• Relief of abnormal foot posture with orthotics

• Corticosteroid injection into tunnel

• Decompression surgery if other measures fail

Vascular causes of leg pain

Occlusive arterial disease

Risk factors for peripheral vascular disease (for development and deterioration):

• smoking

• diabetes mellitus

• hypertension

• hypercholesterolaemia

• family history

• atrial fibrillation (embolism)

Aggravating factors:

• beta-blocking drugs

• anaemia

Acute lower limb ischaemia

Sudden occlusion is a dramatic event that requires immediate diagnosis and management to save the limb.

Causes

• Embolism—peripheral arteries

• Thrombosis: major artery, popliteal aneurysm

• Traumatic contusion (e.g. postarterial puncture)

The symptoms and signs of acute embolism and thrombosis are similar, although thrombosis of an area of atherosclerosis is often preceded by symptoms of chronic disease (e.g. claudication). The commonest site of acute occlusion is the common femoral artery (see FIG. 66.5).

Signs and symptoms—the 6 Ps

• Pain

• Pallor

• Paraesthesia or numbness

• Pulselessness

• Paralysis

• ‘Perishing’ cold

The pain is usually sudden and severe and any improvement may be misleading. Sensory changes initially affect light touch, not pinprick. Paralysis (paresis or weakness) and muscle compartment pain or tenderness are most important and ominous signs.

Other signs include mottling of the legs, collapsed superficial veins, and no capillary return. If the foot becomes dusky purple and fails to blanch on pressure, irreversible necrosis has occurred.

Note: Look for evidence of atrial fibrillation.

Examination of arterial circulation

This applies to chronic ischaemia and also to acute ischaemia.

Note colour changes, hair distribution and wasting. Note the temperature of the legs and feet with the backs of your fingers.

It is important to assess four pulses carefully (see FIG. 66.6). Note that the popliteal and posterior tibial pulses are difficult to feel, especially in obese subjects.

Femoral artery. Palpate deeply just below the inguinal ligament, midway between the ASIS and the symphysis pubis. If absent or diminished, palpate over abdomen for aortic aneurysm.

Popliteal artery. Flex the leg to relax the hamstrings. Place fingertips of both hands to meet in the midline. Press them deeply into the popliteal fossa to compress artery against the upper end of the tibia (i.e. just below the level of the knee crease). Check for a popliteal aneurysm (very prominent popliteal pulsation).

Posterior tibial artery. Palpate, with curved fingers, just behind and below the tip of the medial malleolus of the ankle.

Dorsalis pedis artery. Feel at the proximal end of the first metatarsal space just lateral to the extensor tendon of the big toe.

Look for evidence of oedema: pitting oedema is tested by pressing firmly with your thumb for at least 5 seconds over the dorsum of each foot, behind each medial malleolus and over the shins.

Raise both legs to about 60° for about 1 minute, when maximal pallor of the feet will develop. Then get the patient to sit up on the couch and hang both legs down.⁴

Note: Comparing both feet, check the time required for return of pinkness to the skin (normally less than 10 seconds) and filling of the veins of the feet and ankles (normally about 15 seconds). Look for any unusual rubor (dusky redness) that takes a minute or more in the dependent foot. A positive Buerger test is pallor on elevation and rubor on dependency and indicates severe, chronic ischaemia.

Listen over abdomen and femoral area for bruits.

Note: Neurological examination (motor, sensory, reflexes) is normal unless there is associated diabetic peripheral neuropathy.

Treatment

Golden rules: Occlusion is usually reversible if treated within 4 hours (i.e. limb salvage). It is often irreversible if treated after 6 hours (i.e. limb amputation).

• Intravenous heparin (immediately) 5000 U

• Emergency embolectomy (ideally within 4 hours):

  • – under general or local anaesthesia

  • – through an arteriotomy site in the common femoral artery

  • – embolus extracted with Fogarty balloon or catheter

  or

• Stenting of vessels (a good modern option)—discuss this with an interventional cardiovascular physician or interventional radiologist (less invasive and less expensive)

• Angioplasty

• Arterial bypass if acute thrombosis in chronically diseased artery

• In selected cases, thrombolysis with streptokinase or urokinase appropriate

• Amputation (early) if irreversible ischaemic changes

• Lifetime anticoagulation with warfarin will be required

Note: An acutely ischaemic limb is rarely life-threatening in the short term. Thus, even in the extremely aged, demented or infirm, a simple embolectomy is not only worthwhile but also is usually the most expedient treatment option.

Chronic lower limb ischaemia

Chronic ischaemia caused by gradual arterial occlusion can manifest as intermittent claudication, rest pain in the foot or overt tissue loss—ulceration, gangrene (see FIG. 66.7).

Intermittent claudication is a pain or tightness in the muscle on exercise (Latin claudicare, to limp), relieved by rest. Rest pain is a constant severe burning-type pain or discomfort in the forefoot at rest, typically occurring at night when the blood flow slows down.

The main features are compared in TABLE 66.4.

Intermittent claudication

The level of obstruction determines which muscle belly is affected (see FIGS 66.2 and 66.6).

Proximal obstruction (e.g. aortoiliac)

• Pain in the buttock, thigh and calf, especially when walking up hills and stairs

• Persistent fatigue over whole lower limb

• Impotence is possible (Leriche syndrome)

Obstruction in the thigh

• Superficial femoral (the commonest) causes pain in the calf (e.g. 200–500 m), depending on collateral circulation

• profunda femoris → claudication at about 100 m

• multiple segment involvement → claudication at 40–50 m

Causes

• Atherosclerosis (mainly men over 50, smokers)

• Embolisation (with recovery)

• Buerger disease: affects small arteries, causes rest pain and cyanosis (claudication uncommon)

• Popliteal entrapment syndrome (<40 years of age)

Note: The presence of rest pain implies an immediate threat to limb viability.

Investigations

• FBE: exclude polycythaemia and thrombocytosis

• Colour Doppler ultrasound: measure resting ankle systolic BP; determine ankle/brachial index; normal value 0.9–1.1

• Angiography: the gold standard, reserved for proposed intervention

• Digital subtraction angiography (developing)

Prevention (for those at risk)

• Smoking is the risk factor and must be stopped.

• Other risk factors, especially hyperlipidaemia, must be attended to and weight reduction to ideal weight is important.

• Exercise is excellent, especially walking.

Diagnostic plan

• Check if patient is taking beta blockers.

• General tests: blood examination, random blood sugar, urine examination, ECG.

• Measure blood flow by duplex ultrasound examination or ankle brachial index.

• Arteriography should be performed only if surgery is contemplated.

Treatment

• General measures (if applicable): control obesity, diabetes, hypertension, hyperlipidaemia, cardiac failure.

• Achieve ideal weight.

• There must be absolutely no smoking.

• Exercise: daily graduated exercise to the level of pain. About 50% will improve with walking; so advise as much walking as possible.

• Try to keep legs warm and dry.

• Maintain optimal foot care (podiatry).

• Drug therapy: aspirin 150 mg daily.

  Note:

• Vasodilators and sympathectomy are of little value.

• About one-third progress, while the rest regress or don’t change.⁵

When to refer to a vascular surgeon

• ‘Unstable’ claudication of recent onset; deteriorating

• Severe claudication—unable to maintain lifestyle

• Rest pain

• ‘Tissue loss’ in feet (e.g. heel crack, ulcers on or between toes, dry gangrenous patches, infection)

Surgery. Reconstructive vascular surgery is indicated for progressive obstruction, intolerable claudication and obstruction above the inguinal ligament:

• endarterectomy—for localised iliac stenosis

• bypass graft (iliac or femoral artery to popliteal or anterior or posterior tibial arteries)

Percutaneous transluminal dilation. This angioplasty is performed with a special intra-arterial balloon catheter for localised limited occlusions. An alternative to the balloon is laser angioplasty.

Venous disorders

Varicose veins

Varicose veins are dilated, tortuous and elongated superficial veins in the lower extremity.

The veins are dilated because of incompetence of the valves in the superficial veins or in the communicating or perforating veins between the deep and superficial systems (see FIG. 66.8). The cause is a congenital weakness in the valve and the supporting vein wall, but there are several predisposing factors (TABLE 66.5), the most important being family history, female sex (5:1), pregnancy and multiparity. Previous DVT can also damage valves, especially calf perforators, and cause varicose veins.

Dilated superficial veins, which can mimic varicose veins, may be caused by extrinsic compression of the veins by a pelvic or intra-abdominal tumour (e.g. ovarian cancer, retroperitoneal fibrosis). Uncommonly, but importantly, superficial veins dilate as they become collaterals following previous DVT, especially if the iliofemoral segment is involved.

Symptoms

Varicose veins may be symptomless, the main complaint being their unsightly appearance. Symptoms include swelling, fatigue, heaviness in the limb, an aching discomfort and itching.

Varicose veins and pain

They may be painless even if large and tortuous. Pain is a feature where there are incompetent perforating veins running from the posterior tibial vein to the surface through the soleus muscle.

Severe cases lead to lower leg venous hypertension syndrome,⁶ characterised by pain that is worse after standing, cramps in the leg at night, irritation and pigmentation of the skin, swelling of the ankles and loss of skin features such as hair.

A careful history will usually determine if the aching is truly due to varicose veins and not to transient or cyclical oedema, which is a common condition in women.⁷

The complications of varicose veins are summarised in TABLE 66.6.

Examination

The following tests will help determine the site or sites of the incompetent valves.

Venous groin cough impulse. This helps determine long saphenous vein incompetence. Place the fingers over the line of the vein immediately below the fossa ovalis (4 cm below and 4 cm lateral to the pubic tubercle).⁸ Ask the patient to cough—an impulse or thrill will be felt expanding and travelling down the long saphenous vein. A marked dilated long saphenous vein in the fossa ovalis (saphena varix) will confirm incompetence. It disappears when the patient lies down.

Trendelenburg test. In this test for long saphenous vein competence, the patient lies down and the leg is elevated to 45° to empty the veins (see FIG. 66.9a). Apply a tourniquet with sufficient pressure to prevent reflux over the upper thigh just below the fossa ovalis. (Alternatively, this opening can be occluded by firm finger pressure, as originally described by Trendelenburg.)

The patient then stands. The long saphenous system will remain collapsed if there are no incompetent veins below the level of the fossa ovalis. When the pressure is released, the vein will fill rapidly if the valve at the saphenofemoral junction is incompetent (see FIG. 66.9B). This is a positive Trendelenburg test.

Note: A doubly positive Trendelenburg test is when the veins fill rapidly before the pressure is released and then with a ‘rush’ when released. This indicates coexisting incompetent perforators and long saphenous vein.

Short saphenous vein incompetence test. A similar test to the Trendelenburg test is performed with the pressure (tourniquet or finger) being applied over the short saphenous vein just below the popliteal fossa (see FIG. 66.10).

Incompetent perforating vein test. Accurate clinical tests to identify incompetence in the three common sites of perforating veins on the medial aspect of the leg, posterior to the medial border of the tibia, are difficult to perform. The general appearance of the leg and palpation of the sites give some indication of incompetence here.

Note: Venous duplex ultrasound studies will accurately localise sites of incompetence and determine the state of the functionally important deep venous system.

Prevention

• Maintain ideal weight.

• Eat a high-fibre diet.

• Rest and wear supportive stockings if at risk (pregnancy, a standing occupation).

Treatment

• Keep off legs as much as possible.

• Sit with legs on a footstool.

• Use supportive stockings or tights (apply in morning before getting out of bed and standing up).

• Avoid scratching itching skin over veins.

• Use a small volume of sclerosant (e.g. sodium tetradecyl sulphate—Fibro-vein 3%).

• It is ideal for smaller, isolated veins, particularly below the knee joint.

• This is the best treatment when a clear association exists between symptoms and obvious varicose veins (i.e. long saphenous vein incompetence).

• Remove obvious varicosities and ligate perforators.

Note: Surgery for varicose veins may not relieve heavy, aching legs.

Superficial thrombophlebitis

Clinical features

• Usually occurs in superficial varicose veins

• Presents as a tender, reddened subcutaneous cord in leg

• Usually localised oedema

• No generalised swelling of the limb or ankle

• Requires symptomatic treatment only (see below) unless there is extension above the level of the knee, when there is a risk of pulmonary embolism

• Venous duplex scan is diagnostic and also determines:

  • – extent of superficial thrombosis

  • – if coexisting, unsuspected DVT is present

Treatment

The objective is to prevent propagation of the thrombus by uniform pressure over the vein.

• Cover whole tender cord with a thin foam pad.

• Apply a firm elastic bandage (preferable to crepe) from foot to thigh (well above cord).

• Leave pad and bandage on for 7–10 days.

• Bed rest with leg elevated if severe, otherwise keep active.

• If complication of IV infusion: prescribe a NSAID (e.g. diclofenac 75 mg bd or diclofenac 1% gel topically tds).⁹

• If spontaneous: LMWH (e.g. dalteparin 5000 units SC daily for 4 weeks).⁹

• The traditional glycerin and ichthyol dressings are still useful.

• Consider association between thrombophlebitis and deep-seated carcinoma.

• If the problem is above the knee, ligation of the vein at the saphenofemoral junction is indicated.

Deep venous thrombosis

Refer to CHAPTER 131.

Iliofemoral thrombophlebitis (phlegmasia dolens)¹⁰

This rare but life-threatening condition is when an extensive clot obstructs the iliofemoral veins (following an acute DVT) so completely that subcutaneous oedema and blanching occurs. This initially causes a painful ‘milky white leg’, previously termed phlegmasia alba dolens (used to be seen in late pregnancy or early puerperium). It may deteriorate and become cyanotic—phlegmasia cerulea dolens—representing incipient venous infarction. Massive iliofemoral occlusion is an emergency as such patients may develop ‘shock’, gangrene and pulmonary embolus. Limb amputation will usually follow.

Other painful conditions

Cellulitis and erysipelas

The causative organisms are Streptococcus pyogenes (commonest) and Staphylococcus aureus. Others include Haemophilus influenzae, Aeromonas and fungal infection (especially in the immunocompromised). Predisposing factors include cuts, abrasions, ulcers, insect bites, foreign matter, IV drug use and skin disorders such as eczema and tinea pedis of toe webs. Look for evidence of diabetes.

• Rest in bed.

• Elevate limb (in and out of bed).

• Use aspirin or paracetamol for pain and fever.

• Wound cleansing and dressing with non-sticking saline dressings.

Streptococcus pyogenes¹¹

• If S. pyogenes confirmed:

  • phenoxymethylpenicillin 500 mg (o) 6-hourly for 5–10 days or procaine penicillin 1.5 g IM daily for 5 days

• If organism doubtful:

  • flu/dicloxacillin 500 mg (o) 6-hourly for 7–10 days

• If penicillin hypersensitive/allergic:

  • cephalexin 500 mg (o) 6-hourly

  • or (if severe)

  • cefazolin 2 g IV 6-hourly

Staphylococcus aureus¹¹

• Severe, may be life-threatening:

  • flucloxacillin/dicloxacillin 2 g IV 6-hourly for 7–10 days

• Less severe:

  • flucloxacillin/dicloxacillin 500 mg (o) 6-hourly for 5–10 days

    or

    cephalexin 500 mg (o) 6-hourly

Furuncle (boil) of groin

A painful furuncle caused by S. aureus in the hairy area of the groin is common. The aim is to treat conservatively.

• Localised:

  • – local antiseptics

  • – hot compresses

  • – drain when ‘ripe’

• Deep/extensive:

  • – dicloxacillin 500 mg (o) 6-hourly for 5–7 days

  • – drain when ‘ripe’, not before

Pain in the calf

Calf pain is usually not serious except if swelling is present. Some of the uncommon causes have serious implications and necessitate careful assessment.

Common causes: cramp, muscle stiffness, muscle injury e.g. gastrocnemius tear, claudication (PVD).

Not to be missed: deep venous thrombosis, cellulitis, thrombophlebitis, popliteal artery entrapment.

Other: ruptured Baker cyst, referred pain (back, knees), Achilles tendon rupture.

Torn ‘monkey muscle’

The so-called torn ‘monkey muscle’ or ‘tennis leg’ is a rupture of the medial head of the gastrocnemius muscle in the lower calf. Symptoms include a sudden sharp pain in the calf with an inability to comfortably put the heel to the ground and a need to walk on tiptoe. There is localised tenderness and hardness, possible local bruising and painful dorsiflexion of the ankle. Treatment includes RICE treatment for 48 hours, ice packs every 2 waking hours, a firm elastic bandage (toes to below the knee), crutches if severe, a raised heel, active mobilisation after 48 hours’ rest and physiotherapist-supervised stretching massage and exercises.

Nocturnal muscle cramps

Note: Treat cause (if known)—tetanus, drugs, sodium depletion, hypothyroidism, hypocalcaemia, pregnancy.

Physical measures

• Muscle stretching and relaxation exercises: calf stretching for 3 minutes before retiring,¹¹ then rest in chair with the feet out horizontal to the floor with cushion under tendoachilles for 10 minutes.

• Massage and apply heat to affected muscles.

• Try to keep bedclothes off feet and lower part of legs—a doubled-up pillow at the foot of the bed can be used.

Medication for idiopathic cramps

• Tonic water before retiring may help.

• Drug treatment:

  Consider:

  biperiden 2–4 mg nocte

  magnesium complex tablets (e.g. Crampeze)

Quinine sulphate is effective, but with a 1–3% incidence of haematological abnormalities, especially thrombocytopenia, it is no longer recommended in Australia. It is very toxic to children. More severe idiopathic cramps may respond to magnesium.¹²

Roller injuries to legs

A patient who has been injured by a wheel passing over a limb, especially a leg, can present a difficult problem. A freely spinning wheel is not so dangerous, but serious injuries occur when a non-spinning (braked) wheel passes over a limb and these are compounded by the wheel then reversing over it. This leads to a ‘degloving’ injury due to shearing stress. The limb may look satisfactory initially, but skin necrosis may follow.

• Admit to hospital for observation.

• Fasciotomy with open drainage may be an option for compartment syndrome.

• Surgical decompression with removal of necrotic fat is often essential.

• Rehydrate the patient and monitor renal function.

• The sudden onset of pain, pallor, pulselessness, paralysis, paraesthesia and coldness in the leg

• Worsening intermittent claudication

• Rest pain in foot

• Presence of popliteal aneurysm

• Superficial thrombophlebitis above knee

• Evidence of DVT

• Suspicion of gas gangrene in leg

• Worsening hip pain

• Evidence of disease in bone (e.g. neoplasia, infection, Paget disease)

• Severe sciatica with neurological deficit (e.g. floppy foot, absent reflexes)

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Calf muscle injury

• Cramp

• Deep vein thrombosis

• Sciatica