Practical Assessment

This can be divided into three parts:

• Examination

• Investigations.


Every attempt should be made to encourage the patient to be open and non-defensive. The history can be divided into the following sections:

• Presenting complaint

• Past foot history

• Diabetic history

• Past medical history

• Family history

• Psychosocial history.

Presenting complaint

Be aware that some patients may be asymptomatic due to neuropathy.

The presenting complaint is usually one or more of the following:

• Skin breakdown

• Colour change

For skin breakdown, swelling and colour change or any other presenting complaints, the following questions may be helpful:

As regards pain, this maybe a specific complaint alone or it may accompany the above problems.

Pain may arise locally or it may be diffuse. Local sources may originate from bone, joint and soft tissue including skin and subcutaneous tissue. Generalized pain in both feet suggests neuropathy. Diffuse pain in a single foot suggests ischaemia. However, pain in the ischaemic foot should not always be blamed on reduced arterial perfusion because it may be caused by infection. In the neuropathic foot, severe infections can still cause pain, particularly throbbing pain. Pain around an ulcer suggests infection or ischaemia. The following questions should be asked about pain:

• What aggravates the pain?

• What relieves the pain?

• Is it related to time of day or activity?

• What treatments have been given so far?

Clinical tips to diagnose pain due to neuropathy and ischaemia are shown in Table 1.2.

Table 1.2 Clinical tips on pain Pain due to neuropathy

■ Burning pain with contact discomfort in both feet and lower legs which may also involve the thighs

• Sharp shooting (lancinating) or lightning pains like electric shocks, lasting a few seconds

• Pain relieved by cold

■ Pain worse during periods of rest

• Unilateral burning pain in the leg with muscle wasting suggests a focal neuropathy, commonly a femoral neuropathy

Pain due to ischaemia

■ Persistent pain, worse on elevation and relieved by dependency (hanging the leg out of bed)

• Pain in the calf on exercise relieved by rest (claudication). However, claudication is often absent in ischaemia because of concurrent neuropathy and the distal distribution of the arterial disease

• Feet with severe ischaemia may have little pain because of neuropathy

Patients may not complain of pain itself but of other abnormal sensations which would suggest neuropathy.

• Pins and needles (paraesthesiae)

• Unpleasant tingling (dysaesthesiae)

• Tightness (as if a constricting band is around the foot)

• Numbness ('my feet feel as if they don't belong to me'). After discussing the presenting complaint, the rest of the history is devoted to gathering important relevant information about the patient to aid diagnosis and management. This information can be acquired from various sources including direct questioning of the patient, the patient's medical notes and the referral letter.

Past foot history

• Previous ulcers and treatment

• Amputations: Major Minor

• Peripheral angioplasties

• Peripheral arterial bypasses.

Diabetic history

• Type of diabetes

• Duration of diabetes

• Treatment of diabetes: Insulin

Oral hypoglycaemics.

Complications of diabetes


• Background

• Proliferative

• Previous laser therapy

• Vitrectomy


• Proteinuria

• Severe renal impairment (creatinine > 250 (Xmol/L, 2.83 mg/dL)

• Renal replacement therapy:

Continuous ambulatory peritoneal dialysis (CAPD)


Renal transplant.


• Heart failure

Myocardial infarction

• Coronary artery angioplasty

• Coronary artery bypass.


• Transient ischaemic attack

Past medical history

• Serious illness (e.g. cancer, rheumatoid arthritis, etc.)

• Hospital admissions

Drug history

• Present medication

• Known allergies.

Family history

• Other serious illness

• Cause of death of near relatives.

Psychosocial history

• Occupation

• Number of cigarettes smoked per day

• Number of units of alcohol per day

• Psychiatric illness

• Home circumstances: Type of accommodation Lives alone

Lives with friends or relatives.


There is a need for sensitivity on the part of the examiner. Many patients will be fearful and anxious at their first visit. If, rarely, they have ischaemia but no neuropathy, or they have a severely infected foot, then they will be afraid that the examination will be painful. Other patients may be embarrassed about their feet, or may have very sensitive and ticklish feet. Before the feet are handled the patient should be reassured that the examination will not be painful and that everything will be explained. The feet should be grasped gently but firmly, and poking, prodding and tickling should be avoided. The toes should be separated gently: if they are pulled apart violently the skin may split.

The examination should be performed systematically. It consists of five parts:

• Inspection

• Neurological assessment

• Footwear assessment

• General examination.


The feet should be fully examined in a systematic fashion: first the right and then the left, including dorsum, sole, medial border, lateral border, back of the heel, malleoli and interdigital areas, with a full assessment of the following:

• Limited joint mobility


The general features of the skin should be assessed, especially looking for signs of skin breakdown.

In the neuropathic foot, the skin is dry and fissured and prominent dilated veins secondary to autonomic neuropathy may be visible. Hair loss can be a sign of neuropathy as well as ischaemia. Atrophy of the subcutaneous layer with a thin, shiny, wrinkled skin may indicate ischaemia.

The classical sign of skin breakdown is the foot ulcer. Ulcer assessment is described in Chapter 4. Abrasions, bullae and fissures also represent breakdown of the skin. Bullae are often the first sign of skin breakdown in the ischaemic foot. They are also a feature of fungal skin infections (tinea pedis), as is webspace maceration. Dry skin around the heel will form deep fissures unless an emollient is applied regularly (Fig. 1.1).

Look for other skin lesions, on the leg as well as the foot, including:

• Necrobiosis lipoidica diabeticorum

• Shin spots (diabetic dermopathy).

Necrobiosis lipoidica diabeticorum (NLD) is characterized as well-circumscribed red papules that extend radially with waxy atrophic telangiectatic centres (Fig. 1.2a,b). NLD evolves to ulceration in about one-third of cases.

The round or oval macular hyperpigmented lesions of diabetic dermopathy are found in the anterior tibial region.

As well as skin lesions specific to the diabetic foot, it is important to recognize inflammatory skin disease such as psoriasis, eczema and dermatitis, which also occur in

Fig. 1.1 Fissures are a portal of entry for infection and can lead to severe ulceration.

non-diabetic patients but may complicate the diabetic foot and leg.

Corns and calltis

These are thickened areas of keratosis which develop at sites ofhigh pressure and friction (Fig. 1.3). Corns are discrete areas, usually not more than 1 cm in diameter, and can extend to a depth of several millimetres. Callus forms diffuse plaques. Neither should be allowed to become excessive as this can be a forerunner of ulceration (usually in the presence of neuropathy). Haemorrhage within callus is an important precursor of ulceration.


It is important to inspect the nails closely as the nail bed and periungual tissues may become the site of ulceration. The following should be assessed: ' Structure of the nails

• Abnormalities under the nail

• Signs of nail infections.

Structure of the nails

Thickened nails are common in the population at large. If the shoes press on the nails they may cause bleeding under the nail. Eventually this may lead to ulceration. Atrophic nails may be present in patients with neuropathy and ischaemia.

Ingrowing toe nail (onychocryptosis) arises when the nail plate is excessively wide and thin, or develops a convex deformity, putting pressure on the tissues at the nail edge. Callus builds up in response to pressure and inflam-

Fig. 1.2 (a) Necrobiosis lipoidica diabeticorum (NLD) on dorsum of foot and (b) close up of NLD.

mation. Eventually, usually after incorrect nail cutting or trauma, the nail penetrates the flesh.

Colour of nail bed

Red, brown or black discolouration of the nails may indicate subungual haematoma. The cause may be acute trauma or chronic trauma such as pressure from ill-fitting shoes (Fig. 1.4a).

In acute ischaemia the nail beds are very pale (Fig. 1.4b).

Diabetic Foot Hyperpigmentation

Fig. 1.1 Fissures are a portal of entry for infection and can lead to severe ulceration.

non-diabetic patients but may complicate the diabetic foot and leg.

Fig. 1.3 Corn on the 5th toe.
Fig. 1.4 (a) Subungual haematoma and red marks on toes resulting from wearing tight shoes, (b) Acute ischaemia—pale nail beds.

Fig. 1.5 Pressure on the sulcus from a convex nail has resulted in inflammation with secondary infection.

Abnormalities under the nail

Discharge of fluid from beneath or around the nail, and any maceration or softness of the nail plate, may indicate the presence of a subungual ulcer or infection.

Nail infections

Fungal infection of the nail usually invades the nail plate dorsally causing onycholysis. The hallux is the most common nail affected. Infection starts in one corner and over a period of years it spreads to involve the entire toe nail and may affect other nails.

Paronychia is associated with a nail that has a convex nail bed with tendency to incurve in the corners. Repetitive pressure in the insensitive foot can cause repetitive microtrauma in the nail groove, causing the nail to act as a foreign body creating a foreign body inflammatory response with secondary inflammation and localized infection (Fig. 1.5).


Swelling of the foot is a major factor predisposing to ulceration, and often exacerbates a tight fit inside poorly fitting shoes. It also impedes healing of established ulcers. Swelling may be bilateral or unilateral. It may involve the foot or be limited to the toes.

Causes of bilateral foot swelling include:

• Cardiac failure

• Renal impairment secondary to diabetic nephropathy

Chronic venous insufficiency (sometimes unilateral)

• Rarely, neuropathic oedema secondary to diabetic neuropathy, when it is related to increased arterial blood flow and arteriovenous shunting

• Primary lymphoedema

Gout And Tophi

Fig. 1.6 Gout with tophi on second toe.

Fig. 1.6 Gout with tophi on second toe.

• Severe ischaemia associated with dependency (often unilateral).

Causes of unilateral foot swelling are usually associated with local pathology in the foot or leg. These include:

• Infection, when it is usually associated with erythema and a break in the skin

• Charcot foot (a unilateral hot, red, swollen foot; sometimes the swelling can extend to the knee)

• Gout, which may also present as a hot, red, swollen foot

• Trauma, fracture, muscle or tendon rupture, often associated with bruising

• Deep vein thrombosis

• Venous insufficiency

• Secondary lymphoedema commonly due to malignancy

• Common peroneal nerve palsy

• Localized collection of blood or pus in the foot, which may present as a fluctuant swelling

• Revascularization of a limb. Swelling of the toe can be due to:

• Soft tissue infection

• Osteomyelitis


Common deformities include:

• Fibrofatty padding depletion (FFPD)

• Hammertoes

• Hallux valgus

• Deformities related to previous trauma and surgery.

Fig. 1.7 (a) Amputation specimen from 29-year-old non-diabetic patient showing thick fibrofatty padding, (b) Amputation specimen from 29-year-old diabetic patient with history of neuropathy and ulceration showing great reduction in fibrofatty padding.

Pes cavus

Normally the dorsum of the foot is domed due to the medial longitudinal arch, which extends between the first metatarsal head and the calcaneus. When it is abnormally high, the deformity is called pes cavus and leads to reduction of the area of the foot in contact with the ground during walking. Resulting abnormal distribution of pressure leads to excessive callus formation under the metatarsal heads. This deformity is a sign of a motor neuropathy but may be idiopathic. It is often associated with clawing of lesser toes or a trigger first toe.

Fibrofatty padding depletion (FFPD) A common complication is reduction of the thickness of the fibrofatty padding over the metatarsal heads (Fig. 1.7a,b).

Normal feet contain cushions of fibrofatty padding over the metatarsal heads which absorb plantar pressures.

In diabetic neuropathy the fibrofatty padding may be pushed forward or depleted by previous ulceration, rendering the plantar metatarsophalangeal area prone to ulceration.

Hammer toe

A hammer toe is a flexible or rigid deformity characterized by buckling of the toe. The toe takes on the configuration of a swan's neck. In people with diabetic neuropathy, hammer toes are commonly caused by weakness of the small intrinsic muscles (interossei and lumbricals) of the foot, which can no longer stabilize the toes on the ground. Muscle imbalance results in the affected toes sitting slightly back and up on the metatarsal head. This deformity results in increased pressure over the metatarsal head, over the prominent interphalangeal joint and at the tip of the toe.

Claw toes

Claw toes are similar to hammer toes, but with more buckling and greater deformity. There is fixed flexion deformity at the interphalangeal joint, associated with callus and ulceration of the apex and dorsal aspect of the interphalangeal joint. Although claw toes may be related to neuropathy, they are often unrelated, especially when the clawing is unilateral and associated with trauma or surgery of the forefoot. Claw toes may rarely result from acute rupture of the plantar fascia.

Hallux valgus

Hallux valgus is a deformity of the first metatarsophalangeal joint with lateral deviation of the hallux and a medial prominence on the margin of the foot. This site is particularly vulnerable in the neuroischaemic foot and frequently breaks down under pressure from a tight shoe.

Charcot foot

Bone and joint damage in the tarsometatarsal joints and mid-tarsal joints leads to two classical deformities: the rockerbottom deformity, in which there is displacement and subluxation of the tarsus downwards, and the medial convexity, which results from displacement of the talonavicular joint or from tarsometatarsal dislocation. Both are often associated with a bony prominence which is very prone to ulceration and healing is notoriously difficult.

When the ankle and subtalar joints are involved, instability of the hindfoot can result.

Deformities related to previous trauma and surgery Deformities of the hip and fractures of the tibia or fibula lead to shortening of the leg and abnormal gait, which predisposes to foot ulceration. Ray amputations remove the toe together with part of the metatarsal. They are usually very successful but disturb the biomechanics of the foot leading to high pressure under the adjacent metatarsal heads. After amputation of a toe, deformities are often seen in adjoining toes.

Limited joint mobility (including hallux rigidus)

Limited joint mobility can affect the feet as well as the hands. The range of motion is diminished at the subtalar and first metatarsophalangeal joints. Limited joint mobility of the first metatarsophalangeal joint results in loss of dorsiflexion and excessive forces on the plantar surface of the first toe, causing callus formation and ulceration. It is commonly seen in barefooted and sandal-wearing populations.


It is important to observe the colour of the foot including the toes. Colour changes may be localized or diffuse. Common colour changes are red, blue, white or black.

Causes of the red foot

• Cellulitis

• Critical ischaemia, especially on dependency (dependent rubor)

Causes of the red toe

• Cellulitis

• Osteomyelitis

• Chilblains

• Dermatitis/eczema.

Causes of the blue foot

• Cardiac failure

• Chronic pulmonary disease

• Venous insufficency (often with brownish pigmentation —haemosiderosis).

Causes of the blue toe

• Severe infection

The foot may have a pale white appearance in severe ischaemia, especially on elevation. In acute ischaemia, the foot is pale, often with purplish mottling. The cause of black appearances are discussed under necrosis.


Areas of necrosis and gangrene can be identified by the presence of black or brown devitalized tissue. Such tissue may be wet (usually related to infection) or dry.

Causes of the black toe

• Severe chronic ischaemia

• Acute ischaemia

• Blood blister

• Application of henna


Palpation should take place to assess:

• Temperature of the foot


The most important manoeuvre to detect ischaemia is the palpation of foot pulses, an examination which is often undervalued.

• The dorsalis pedis pulse is palpated, using the index, middle and ring fingertips together, lateral to the extensor hallucis longus tendon on the dorsum of the foot (Fig. 1.8)

• The posterior tibial pulse is palpated below and behind the medial malleolus (Fig. 1.9).

If either of these foot pulses can be felt then it is highly unlikely that there is significant ischaemia in the foot.

If both pulses are absent, a full examination should include palpation for popliteal and femoral pulses.

Temperature of the foot

Skin temperature is compared between both feet with the back of the examining hand. Warm areas or hot spots indicate inflammation which may be due to infection, fracture, Charcot's osteoarthropathy or soft tissue trauma. Unilateral pedal temperature increase, especially in the absence of ulceration, is best presumed to be Charcot's osteoarthropathy.

The temperature gradient is checked by using the back of the hands and gently moving them from the pretibial region of the leg distally over the dorsum of the foot to the toes while keeping in contact with the patient's skin. An asymmetric gradient may indicate either unilateral

Fig. 1.8 Palpation of the dorsalis pedis pulse.
Fig. 1.9 Palpating the posterior tibial pulse.

ischaemia on the colder side or unilateral inflammatory response such as Charcot's osteoarthropathy or infection on the warmer side.

In the neuroischaemic foot, coexisting autonomic neuropathy may keep the foot relatively warm, although an ice-cold foot is indicative of acute ischaemia.

Causes of the hotfoot ' Cellulitis

• Venous insufficiency

• Deep vein thrombosis.

Causes of the cold foot

• Chronic ischaemia

• Acute ischaemia

• Cardiac failure.


Oedema already suspected on inspection can be confirmed by gentle digital pressure applied for a few seconds.


Very occasionally palpation may reveal gas in tissues as a fine crackling sensation.

Neurological assessment

Simple inspection will usually reveal signs of motor and autonomic neuropathy but sensory neuropathy must be detected by a sensory screening test or a simple sensory examination.

Motor neuropathy

The classical sign of a motor neuropathy is a high medial longitudinal arch, leading to prominent metatarsal heads and pressure points over the plantar forefoot (Fig. 1.10a,b).

Complicated assessment of motor power in the foot or leg is not usually necessary, but it is advisable to test dorsiflexion of the foot to detect a foot drop secondary to a common peroneal nerve palsy, which is usually unilateral and will affect the patient's gait. If painful mono-neuropathy is suspected from the history, a more detailed neurological examination is indicated to rule out compressive lesions of nerve roots supplying the lower limb-see under Painful neuropathy in Chapter 3.

Autonomic neuropathy

Signs of an autonomic neuropathy include a dry skin with Assuring and distended veins over the dorsum of the foot.

The dry skin is secondary to decreased sweating. The sweating loss normally occurs in a stocking distribution, which can extend up to the knee. The distended veins are secondary to arteriovenous shunting associated with autonomic neuropathy (Fig. 1.11).

Sensory neuropathy

An important indication of neuropathy will be a patient who has no pain even when significant foot lesions are present. Painless ulceration is definite evidence of a peripheral neuropathy. It is important to detect patients who have sufficient neuropathy to render them susceptible to foot ulceration. This can be carried out using a monofilament which, when applied perpendicular to the foot,

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