Chapter 69: Walking difficulty and leg swelling

The clinical evaluation of the patient presenting with difficulty walking can be very complex, especially for abnormal gaits caused by neurological conditions. Not all gaits fall into a single category; gait disturbances may be multifactorial, especially in the elderly.

Non-neurological conditions are the most common cause of walking difficulties. They include various arthritic conditions of the lower limbs, usually presenting as a limp, other mechanical factors, such as swelling of the legs, disorders of circulation such as intermittent claudication, and general debility (e.g. malignancy, anaemia and endocrine disorders such as hyperparathyroidism).

It is important for the general practitioner not to overlook hypokalaemia and drugs or the myopathies as a cause of walking difficulty. The drugs that require special consideration include alcohol, corticosteroids, chloroquine, colchicine, clofibrate, bretylium, HMG-CoA reductase inhibitors (the statins), gemfibrozil, penicillamine, diuretics, beta blockers and general anaesthetic agents.

It is convenient to classify abnormal gaits as painless or painful (antalgic). With antalgic gaits the rhythm is disturbed; with painless abnormal gaits the contour is affected. One type of skeletal mechanical abnormality is described as arthrogenic (due particularly to hip disorders) and a second type as osteogenic (due to a shortened limb).

Neurogenic gaits and myogenic gaits are considered together below, under the heading ‘Neurological disorders of gait’.

Psychogenic or ‘hysterical’ gait may have to be considered if the gait is bizarre or seems greatly exaggerated. On the other hand, loss of confidence, especially in the elderly, is an important cause of gait disturbance. However, many abnormal gaits that are caused by neurological disease may also appear bizarre, and caution is advised. Doubtful cases should be referred for an expert opinion.

Disorders of gait and posture go hand in hand because of a common physiological process.

The source of the abnormality is indicated.

1. Ask the patient to stand.

   Note any difficulty in reaching a standing position. Difficulty = proximal muscle weakness.

2. Ask the patient to stand with eyes closed (Romberg test).

   If positive (sways or falls) = loss of proprioception (e.g. peripheral neuropathy).

3. Ask the patient to walk (ensure sufficient testing length).

   Table Graphic Jump Location

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   Gait initiation:	hesitancy = basal ganglia or frontal cortex
   Stride length:	very short = basal ganglia or frontal cortex irregular = cerebellar
   Narrow or broad base:	narrow = UMN, muscle weakness, basal ganglia
   	broad = cerebellum, proprioception, vestibular
   Stiff or ‘sloppy’:	stiff = UMN, basal ganglia sloppy = LMN, muscle weakness
   Heel strike:	loss of normal strike = UMN, LMN, myopathy
   High stepping:	positive = LMN (distal), proprioception, muscle weakness
   Arm swing:	decreased = basal ganglia, UMN (frontal lobes)
   Pelvis control:	Trendelenburg gait = proximal muscle weakness

4. Ask the patient to walk using provocation tests.

   Table Graphic Jump Location

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   ‘Tightrope’ walk:	tests proprioception
   Stand on tiptoes and back on the heels:	tests distal muscle weakness

   Note: Peripheral neuropathy is a common cause of LMN lesion.

Cerebellar (ataxic) gait

The patient has difficulty standing, has a broad-based stance and an unsteady gait, with swaying from side to side. It has been described as the ‘dirty diaper’ gait. The patient may stagger or bump into walls and may be accused of being drunk. When asked to walk in a straight line the patient tends to veer towards the side of the lesion. Ask the patient to walk ‘heel to toe’ in a straight line and perform a heel–knee–shin test to demonstrate cerebellar ataxia. Significant causes are multiple sclerosis, alcoholic cerebellar degeneration and space-occupying lesions. Cannot climb stairs.

Basal ganglia gait (Parkinson type)

Identifying this disorder in its early stages can be difficult as the first sign may be a limp with one leg being described as weak or stiff or slow.² However, the typical gait is a shuffling of the feet with small steps in a forward flexed posture, rather like a person walking with a belt around the ankles. This leads to a hurrying (festinant) gait as though there is an impending feeling of falling forward. There is hesitation in starting.

Spastic gait

Spastic gait may be regarded as the typical bilateral or paraplegic gait, or as a hemiplegic gait. With the former the gait affects both legs—they are stiff or weak, leading to slow, jerking walking, dragging of the feet and scraping of the toes. This scuffing can be heard as the front of the shoe drags along the ground. Every step can be a struggle and the patient may appear as though walking through glue on the floor.

A scissor-type gait will develop with bilateral hip adduction. Spasticity is caused by a UMN lesion, including multiple sclerosis and spinal cord compression. The typical UMN posture is of a flexed upper limb and an extended lower limb.

With hemiplegia the patient drags the affected leg stiffly with the hips adducted, the knee extended and the foot plantar flexed, leading to scraping of the toes. Mounting stairs can be very difficult, especially if clonus is induced with dorsiflexion of the foot.

Foot drop gait

The patient cannot dorsiflex the foot, leading to a high-stepping gait with extra flexion of the hip and knee to lift the foot off the ground. The foot then slaps down on the ground.

Vestibular gait

If unilateral the patient tends to veer off to the side of the lesion.

Apraxia

With apraxia of gait (due to a prefrontal lobe lesion) there is a failure of control of the legs. The patient may stand up and try to walk but looks with bewilderment at the legs (the ‘glued to the floor’ effect) and moves them in an inappropriate manner with a broad-based, small-stepping unsteady gait. Turning is difficult. Apraxia is caused by bilateral cortical involvement, such as normal pressure hydrocephalus, multi-infarct states and tumours of the corpus callosum.²

Neurogenic claudication

With intermittent claudication of the cauda equina, due to spinal canal stenosis, the patient develops pain in the leg after walking a certain distance. However, weakness and numbness are usually more prominent than pain.

Drop attacks

In a drop attack the patient suddenly falls to the ground, without other symptoms, and gets up almost immediately. There is no loss of consciousness. Drop attacks can be caused by disorders such as epilepsy, Parkinson disease and vertebrobasilar insufficiency. However, in most cases, particularly middle-aged and elderly women, there is no obvious cause. (See CHAPTER 54.)

Waddling (myopathic) gait

A waddling gait is usually caused by muscular dysfunction affecting the pelvic girdle muscles and trunk. There is a wide-based gait with a marked ‘rocking and rolling’ body swing from side to side and related compensatory movements of the pelvis, that is, a bilateral Trendelenburg gait. Cannot climb stairs.

Proximal muscle weakness

The patient may complain when getting out of a low chair or going up or downstairs. The weakness can be demonstrated by asking the patient to squat down and, after a second, rise from the squatting position.² Waddling of gait reflects extreme cases. Causes include myopathies, motor neurone disease and Guillain–Barré syndrome.

Distal muscle weakness

This causes a high-stepping gait as the foot is floppy and tends to flap, with walking similar to foot drop gait. Causes include peripheral neuropathy, myotonic dystrophy and peroneal muscular atrophy.

Limp is a symptom commonly associated with painful disorders of the lower limb, especially of the hip and knee joints. A limp implies an asymmetrical gait pattern caused by one of four general factors:

1. unequal leg length

2. antalgic (painful) gait (e.g. hip disorder)

3. restricted joint movement (e.g. ankylosed knee)

4. neuromuscular weakness (e.g. poliomyelitis)

Limp has an inseparable relationship with painful hip and buttock conditions, especially those of the hip. Painful hip and pelvic conditions that cause limp are presented in CHAPTER 65.

Limp in adults

In adults the cause of limp is usually more obvious than in children and is commonly due to degenerative osteoarthritis of the hip or knee, to spinal disorders, especially sciatica caused by a disc prolapse, or to overuse disorders of the knee, ankle or foot. Other causes to consider are trauma to the back and legs, vestibular ataxia, Parkinson disease and intermittent claudication.

Limp in children

The child who limps presents an interesting diagnostic dilemma. The limp must be considered to be due to a definite organic cause, although conversion reactions can be a factor.³ It is appropriate to focus initially on the hip. The diagnostic strategy is presented in TABLE 69.1.

Limp can be considered as acute, subacute or chronic. An acute limp may be due to injury, infection (osteomyelitis, septic arthritis), spinal injuries, a fracture or an irritable hip (transient synovitis). Subacute causes include juvenile rheumatoid arthritis and tumour or leukaemia. Chronic causes include cerebral palsy, DDH, Perthes disease and chronic SCFE.

History

The age of the patient gives a diagnostic pointer. A careful history, especially of trauma, may lead to the diagnosis. A history of injury is usually but not always available. The relationship of the limp to exercise and footwear is significant. The location of any associated pain is relevant: low back pathology can refer to the buttocks and hip pathology can cause knee pain.

Examination

The hip and knee joints should be carefully examined if the source of limp has no specific localisation. Get the child to walk and run on the toes and heels (if appropriate). Note the gait and check whether it is antalgic (painful), hemiplegic (the arm is held out in a balancing action) or Trendelenburg (classic for DDH). Look for evidence of muscular dystrophy. Never forget to examine the soles of the feet and between the toes.

Investigations

The following have to be considered:

• FBE and ESR

• blood culture

• needle aspiration of joint

• radiological: plain X-ray, ultrasound, bone scan, CT or MRI scan

Management

Management is based on the cause. Surgical drainage supplemented with antibiotics is essential for septic arthritis. If the child initially has a limp and cannot walk, admit to hospital for:

• skin traction

• FBE and ESR

• ultrasound of hip

• blood culture

Specific conditions

Osteomyelitis

Acute haematogenous osteomyelitis is mainly a disease of childhood, occurring in the proximal ends of long bones, particularly the femur and tibia. It should be suspected in a child with an acute febrile illness, unwillingness to move the limb and ‘fingertip’ tenderness near one of the large points (the metaphysis). Main organisms—S. aureus, S. pneumonia, Kingella kingae, Propionibacterium acnes. Sources of infection—boils, abscesses, septic toes, surgical procedures. Consider impaired immunity and diabetes.

Blood should be collected for FBE, ESR and culture (positive in 60%). A plain X-ray and nuclear scan are valuable but may not provide immediate confirmation of the diagnosis (may be normal for the first 10 days). The child should be admitted to hospital, an IV line should be inserted and IV antibiotics commenced to cover the organisms involved—empirical therapy:

• di(flu)cloxacillin:⁴ 50 mg/kg up to 2 g IV 6-hourly; adjust according to the site of infection, patient’s age and particularly to culture and sensitivity results⁴

Septic arthritis

Septic arthritis should be suspected in a child with pyrexia and an acute arthritis with limited motion. Manage as for osteomyelitis as causative organisms are similar.

Bone tumour

Chronic limp is a common presentation of malignant bone tumours. Radiological investigation is mandatory.

Irritable hip syndrome (transient synovitis)

Typical age is 3–8 years and the child presents with an acute limp with restricted hip motion. Plain X-ray is normal. Orthopaedic assessment is recommended.

Perthes disease, SCFE and DDH

Refer to CHAPTER 65.

Paget disease

Paget disease of bone (osteitis deformans) is a chronic focal disorder of the adult skeleton in which new soft bone replaces localised areas of normal bone. The cause is unknown but a viral aetiology is suspected. There is a great increase in bone turnover with osteoclastic resorption followed by increased but disorganised osteoblastic activity. The disorder is quite common:

• 1 in 200 of the population at 40 years

• 1 in 10 of population at 90 years

Paget disease is usually asymptomatic but some patients may present with deep aching pain in the lower back and lower limbs. They may also present with a disturbance of gait due to unequal leg length, osteoarthritis of associated joints such as the knee or hip, or a change in the distribution of mechanical forces in the lower extremities (see FIG. 69.1).

Clinical features⁵

• Male:female ratio = 2:1.

• 95% asymptomatic (discovered by X-ray or raised serum alkaline phosphatase [ALP] level).

• Symptoms may include joint pain and stiffness (e.g. hips, knees), bone pain (usually spine), deformity, headache and deafness.

• Bone pain is typically deep and aching; it occurs at rest, particularly at night.

• Signs may include deformity, enlarged skull (‘hats don’t fit any more’), bowing of tibia, waddling gait, hyperdynamic circulation (see FIG. 69.2).

• Bones most commonly affected, in decreasing order, are the pelvis, femur, skull, tibia, vertebrae, clavicle and humerus.

• Sensory disability—taste, smell, vision, hearing, loss or reduction of feeling in areas of the face if cranial nerves involved.

Diagnosis

• Raised serum ALP level (often very high >1000 U/L). A result >125 U/L suggests active disease.⁶

  Note: calcium and phosphate normal.

• Plain X-ray: dense expanded bone—best seen in skull and pelvis.

  Note: Can mimic prostatic secondaries, so every male Pagetic patient should have a DRE and serum PSA test.

• Bone isotopic scans: useful in locating specific areas.

• Watch for the uncommon complication of osteogenic sarcoma.

  Note: screen siblings and children every 5 years after the age of 40.⁶

Treatment^5,6

The major goals are relief of pain, normal biochemical indices of bone turnover and prevention of long-term complications (e.g. deafness, deformities). Treatment is required for symptomatic features such as bone pain and neurological complications, and for selected asymptomatic patients such as those with active disease and <50 years.

Localised disease and most patients with asymptomatic disease require no treatment.

Three groups of drugs are currently available:

• the calcitonins

• the bisphosphonates—e.g. etidronate, pamidronate disodium (APD), alendronate, risedronate

• various antineoplastic agents (e.g. mithramycin)

Bisphosphonates have become the preferred drugs for first-line therapy, with intravenous preparations shown to be superior, including:⁶

• alendronate 40 mg (o) daily for 6 months (oesophagitis can be problematic)

• pamidronate disodium 30–60 mg IV infused over 2–4 hours (usually the preferred option)

• risedronate 30 mg (o) daily for 2 months

• tiludronate 400 mg (o) daily for 3 months

• zoledronic acid 5 mg IV over at least 15 minutes, once yearly (certain biomedical parameters must be met e.g. eGFR >35)

All oral agents should be taken on an empty stomach.

Repeated doses may rarely be required in severe cases as judged by symptoms and disease activity (e.g. monitoring with serum ALP usually 6 months post-therapy and then 2-yearly; X-rays also help monitor response).

Diagnostic features and pitfalls

• Not all swollen legs require investigation and treatment.

• The significance of leg swelling varies according to the age group, whether it is bilateral or unilateral, and whether the onset is sudden or gradual (see TABLE 69.2).

• If the onset of oedema is acute (often <72 hours) suspect DVT.⁷

• DVT must be considered in all unilateral cases and ultrasound examination performed if appropriate.

• If a DVT is present, consider occult malignancy (e.g. pancreatic cancer).

• Consider pelvic cancer causing lymphatic obstruction in a woman >40 years presenting with painless unilateral leg oedema.

• A drug history is essential as several drugs can cause oedema.

• Pitting oedema is a feature of venous thrombosis or insufficiency, not lymphatic obstruction.

Investigations

Select from these first-line tests:

• urinalysis (? albumin)

• FBE and ESR

• serum electrolytes, urea and creatinine

• blood sugar

• serum albumin/LFTs

• TSH level

• ultrasound (DVT screen)

• other radiographs (e.g. CT scan, venogram)

Calf swelling of sudden onset

Causes to consider:

• acute arterial occlusion

• ruptured Baker cyst

• ruptured medial head of gastrocnemius

• DVT (usually gradual)

• cellulitis/erysipelas

• compartment syndrome

Pain accompanies most of these conditions but the absence of pain does not exclude DVT or thrombophlebitis. Refer to CHAPTER 66.

Lipoedema

Lipoedema or lipedema is the development of bilateral leg swelling that does not involve the feet (in lymphoedema the swelling develops in the most distal part of the foot). Lipoedema is fat and fluid.

Clinical features

• Exclusive to obese women

• Spares the feet

• Bilateral and symmetrical distribution of fat

• The legs are often painful and bruise easily

• The Stemmer sign (the ability to pick up a fold of skin at the base of the large toe) is usually negative⁸

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

• Deep venous thrombosis

• Paget’s disease of bone

• Parkinson disease

A physician’s guide to the management of Paget disease of bone. Brooklyn NY: The Paget Foundation. <pagetfdn@aol.com>