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114
M. Edmonds et al.
Common Peroneal Nerve
The nerve is compressed around the head of the
bula. External compression can be caused by
squatting, leg crossing or a tight plaster cast in
circumstances of diminished consciousness. The
common peroneal nerve splits into two branches:
the supercial branch supplies the skin of lateral
side of lower leg and the lateral calf muscles that
evert the foot and the deep peroneal branch,
which supplies the toe and ankle dorsiexors
and an area of skin on dorsum between rst and
second toes. The nerve can further be compressed as it splits and passes through the origin
of the peroneus longus muscle 1inch inferior to
the bular neck.
Injury to the common peroneal nerve leads to
a painless foot drop with weakness of tibialis
anterior and the evertors and also numbness over
the dorsal aspect of the ankle and foot There may
be pain over the lateral aspect of the shin and the
dorsum of the foot. The sensory impairment over
the lateral leg and dorsum of the foot must be distinguished from an Lumbar 5 nerve root lesion.
Femoral Nerve
The femoral nerve arises from Lumbar 2,3,4 roots
which pass through the psoas muscle and beneath
the inguinal ligament to supply the anterior thigh
muscles. It may be compressed by a psoas abscess,
retroperitoneal haematoma, particularly in
patients on anticoagulants, or by a pelvic tumour.
A femoral nerve lesion produces weakness of
knee extensors of the quadriceps group, with muscle wasting, a depressed or absent knee jerk and
sensory loss in anterior thigh and medial part of
knee. Diabetic amyotrophy and upper lumbar
radiculopathy (Lumbar 2,3,4) can present in a
similar way to entrapment of the femoral nerve.
Diabetic amyotrophy is a focal neuropathy
of the lumbosacral radiculoplexus and presents
with severe pain in the proximal lower limb,
usually involving the thigh, sensory loss, significant weight loss and weakness of thigh
muscles. The knee reflex is also absent. There
is usually a spontaneous resolution of diabetic
amyotrophy by 1 year with return of the knee
reflex. It is important to differentiate between
diabetic amyotrophy and root compression.
Saphenous Nerve
The saphenous nerve is compressed as it pierces
the roof of the subsartorial fascia in the lower
third of the thigh. The nerve is commonly damaged during the stripping of the long saphenous
vein. There is pain in thigh and lower leg on
walking.
Lumbar Spinal Stenosis
This is a common cause of leg pain and results
from the narrowing of the spinal canal or neural
foramina leading to root ischaemia and neurogenic claudication. Stenosis of the spinal canal is
most often caused by loss of disc space, osteophytes and a hypertrophic ligamentum avum.
Lumbar stenosis can be caused by other pathologies that decrease the space of the spinal canal,
including tumours and infection.
There is gradual onset of unilateral or bilateral leg pain (with or without back pain), numbness, and weakness which develop after the
patient walks a certain distance. Painful sensations shoot down the legs with continued walking and diminish with resting. Standing and
bending backwards can exacerbate the symptoms because bending forward increases the
space in the spinal canal and vertebral foramen,
while bending backward decreases the space.
The pain is usually decreased by sitting, leaning forward, putting the foot on a raised cushion or stool. Walking uphill may be easier than
downhill. The patient may have leg fatigue, and
numbness or paraesthesiae of the leg.
If not treated, there can be increasing weakness and dysfunction of the bladder and bowel
leading to a cauda equina syndrome. This results
in lower back pain, severe bilateral pain radiating
down the legs, weakness of legs and feet, retention of urine, bowel dysfunction and impotence
with sensory decits and reduced or absent
reexes in the legs. The cauda equina syndrome
is a surgical emergency.
Complex Regional Pain Syndrome
Another cause of unilateral neuropathic pain is
complex regional pain syndrome (CRPS), previously called Reex Sympathetic Dystrophy
(RSD). It is a chronic, painful and progressive
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neurological condition that affects the skin,
muscles, joints and bones [19, 20]. The syndrome usually develops in an injured limb but
often there is only a minor injury or no precipitating event at all. Typically, there is burning
pain, excessive sweating, swelling and sensitivity to touch. The presentation of swollen hot
foot may be mistaken for an acute Charcot neuroarthropathy. Although CRPS does demonstrate sensory loss, it is characterised by severe
neuropathic pain compared with the Charcot
foot which is relatively painless [19]. Both conditions demonstrate areas of bone marrow
oedema on MRI although in CRPS, it is diffuse,
patchy and uctuating. Pain may begin in one
area or limb and then spread to other limbs. In
some cases, symptoms of RSD/CRPS diminish
for a period and then reappear with a new
injury.
Bilateral ischaemic pain.
Ischaemic pain rarely develops in both legs
simultaneously but can occur in the following
circumstances.
1. Saddle embolus in the lower aorta.
Patients with acute embolic occlusion of
the aortic bifurcation appear marble white or
mottled to the waist. They may also present
with paraplegia due to ischaemia of the cauda
equina, which can be irreversible. Immediate
bilateral embolectomy restores lower limb
perfusion.
2. Acute aortic dissection extending into the
iliac arteries can lead to acute lower extremity
ischaemia which can accompany the predominant symptom of chest pain.
3. Rupture of an abdominal aortic aneurysm
may also lead to acute lower limb ischaemic
pain. Nevertheless, severe pain in the back or
abdomen is the dominant symptom.
4. Leriche syndrome is claudication of the glu-
teal muscles due to severe disease at the aortic
bifurcation.
Other Causes ofBilateral Leg Pain
Osteoarthritis of hips, knees and feet
Rheumatoid arthritis
Venous hypertension of the legs
Polymyalgia rheumatica
Polymyositis
Restless legs syndrome
Unilateral Ischaemic Pain
Pain in the lower limb due to ischaemia is
known as rest pain and by this stage the ischaemia is severe and has been previously termed
critical ischaemia. Rest pain is usually a constant pain, occurring in the toes and the forefoot, often worse at night. It is exacerbated after
lying down because of the loss of gravityassisted ow and is relieved by sitting or standing. Rest pain is eased by hanging the leg down
outside the bed.
Although atherosclerosis is usually present in both limbs, marked deterioration of the
occlusive disease leading to critical ischaemia
often occurs in one leg at any one time leading
to the classical presentation of rest pain predominantly in one leg. This is commonly due to
a thrombosis on top of existing atherosclerosis.
It can lead to the pink painful foot or in cases
of sudden complete occlusion a pale mottled
foot. Claudication of the calf is another sign
of ischaemia but may be absent in people with
diabetes because of the very distal site of atherosclerosis in the tibial vessels of the diabetic
leg as well as the presence of neuropathy. Thus
diabetic patients do not usually go through the
classical natural history in peripheral vascular
disease of claudication, then rest pain and then
tissue loss.
Dierentiation ofNeuropathic Pain
fromIschaemic Pain
Most patients with painful neuropathy have palpable dorsalis pedis and posterior tibial pulses,
thus ruling out signicant ischaemia. However,
when both these pulses are absent, it is necessary
to assess how much pain is due to neuropathy and
how much may be due to ischaemia. One helpful
clinical point is that ischaemic rest pain initially
presents unilaterally although background
peripheral vascular disease may be present in
both legs, whereas painful neuropathy is usually
bilateral.
116
M. Edmonds et al.
The rest of the history is devoted to gathering
important relevant information about the patient
to aid diagnosis and management.
Past Foot History
• Previous ulcers and treatment
• Previous surgery to the lower limb
• Amputations Major/Minor
– Peripheral angioplasties
– Peripheral arterial bypass
Diabetes History
• Type of diabetes
• Duration of diabetes
• Treatment of diabetes:
– Insulin
– Oral hypoglycaemics
– Diet
Complications of diabetes
Retinopathy
• Background
• Proliferative
• Previous laser therapy
• Vitrectomy
• Cataract
Nephropathy
• Proteinuria
• Renal replacement therapy:
– Continuous ambulatory peritoneal dialysis
(CAPD)
– Haemodialysis
– Renal transplant
Cardiovascular
• Angina
• Heart failure
• Myocardial infarction
• Coronary artery angioplasty
• Coronary artery bypass
Cerebrovascular
• Transient ischaemic attack
• Stroke
Past Medical History
• Serious illness
• Accidents
• Injuries
• Hospital admissions
• Operations
Drug History
– Present medication
– Known allergies
Family History
– Diabetes
– Other serious illness
– Cause of death of near relatives
Psychosocial History
• Occupation
• Number of cigarettes smoked per day
– Number of cigarettes previously smoked
per day and for number of years
• Number of units of alcohol per day
• Recreational drugs
• Psychiatric illness
• Home circumstances:
• Type of accommodation
• Lives alone
Examination
This comprises three parts:
• Simple inspection
• Palpation
• Special assessments that can be carried out at
the bedside/chairside
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In practice, these are often integrated into a
comprehensive examination with the aim to look
for and assess particular diagnostic features that
will enable the practitioner to accurately classify
and stage the feet [20, 21]). Examination of the feet
should be carried out in a systematic fashion: rst
the right and then the left, including dorsum, sole,
medial border, lateral border, back of the heel, malleoli and interdigital areas. It is useful to compare
the feet particularly when assessing colour and
temperature. The examination should particularly
focus on the following aspects of the foot.
Skin andSkin Breakdown
Skin
In the initial inspection, the general features of
the skin including colour and temperature should
be examined. The skin under the metatarsal heads
should be specically assessed, looking for any
redness as sign of inammation, particularly in
the neuropathic foot in which the skin is dry and
ssured. Prominent dilated veins secondary to
autonomic neuropathy may be visible. Signs of
pruritus may indicate dryness (Fig. 9.11). Hair
loss can be a sign of ischaemia or neuropathy.
117
Fig. 9.11 Scratch marks due to itching secondary to dryness of skin complicated by cellulitis
Colour oftheSkin ofFoot
It is important to observe the colour of the foot
including the toes. Colour changes may be localised or diffuse. Common colour changes are red,
blue, pale (white) or black. In dark skins, the red
colour may present as a tawny (orange-brown)
hue (Fig.9.12).
Causes of the red foot/toe
• Cellulitis
• Critical ischaemia, especially on dependency
(dependent rubor—may be dusky red
(Fig.9.13)
• Charcot foot
• Gout
• Burn or scald
• Chilblain
• Dermatitis/eczema
Fig. 9.12 Cellulitis of right foot, with tawny (orangebrown) hue on the dorsum of the foot and ulcer on dorsum
of right great toe with infection of the extensor hallucis
longus tendon
118
Fig. 9.13 Red discolouration of the dependent critically
ischaemic foot
Causes of the blue foot/toe
• Peripheral arterial disease
• Severe infection
• Cardiac failure
• Chronic pulmonary disease
• Venous insufciency (often with brownish
pigmentation due to haemosiderosis)
M. Edmonds et al.
• Blood blister
• Shoe dye
• Application of Henna Black
• Tumour (melanoma)
Temperature oftheSkin Foot
Skin temperature is compared between both feet
with the back of the examining hand. The temperature gradient is checked by gently moving
the back of the hand from the pretibial region of
the leg towards the dorsum of the foot and then to
the toes while keeping in contact with the
patient’s skin. An asymmetric gradient may indicate either unilateral ischaemia on the colder side
or unilateral inammatory response such as
Charcot’s osteoarthropathy or infection on the
warmer side.
It is helpful to follow up the clinical assessment of skin temperature by measuring skin temperature using a digital skin thermometer. An
infrared thermometer is ideal and skin temperatures can be compared between similar areas on
each foot. This is particularly helpful in the management of the Charcot foot. Warm areas or hot
spots indicate inammation which may be due to
infection, fracture, Charcot’s osteoarthropathy or
soft tissue trauma. Unilateral temperature increase
in the foot especially in the absence of ulceration
is best presumed to be Charcot’s osteoarthropathy
until proved otherwise. 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 pale foot/toe
• Critical ischaemia, especially on elevation.
• Acute ischaemia, the foot is pale, often with
purplish mottling.
Causes of the black foot/toe
• Wet necrosis
• Dry necrosis
• Severe chronic ischaemia
• Acute ischaemia
• Emboli
• Bruise
Causes of the hot foot [22]
• Cellulitis
– Charcot foot
– Gout
• Venous insufciency
• Deep vein thrombosis
Causes of the cold foot
• Chronic ischaemia
• Acute ischaemia
• Low output cardiac failure
• Deep vein thrombosis
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Skin Breakdown
An active search should be made for breaks in the
skin or wounds over the entire surface of the foot
and ankle, not forgetting the areas between the
toes and at the back of the heel. Toes should be
gently held apart for inspection (Fig.9.14). This
may reveal web space fungus infection.
• Abrasions, bullae and ssures also represent
breakdown of the skin. Bullae are often the
rst sign of skin breakdown in the ischaemic
foot. They are also a feature of fungal skin
infections (tinea pedis), as is web space maceration. Bullae at pressure points may indicate
an impending ulcer.
• Dry skin around the heel will form deep ssures (Fig.9.15) unless an emollient is applied
regularly.
• In assessing any wound, it is important to note
the size, edge, shape, nature of the base of
ulcer, any slough, discharge, exposure of
bones and tendons and the characteristics of
the surrounding tissue.
• As well as skin lesions specic to the diabetic
foot, it is important to recognise inammatory
skin disease such as psoriasis, eczema and
dermatitis, which may complicate the diabetic
foot and leg.
119
Fig. 9.14 Toes gently stretched apart to reveal interdigital ulcer
Fig. 9.15 Dry ssured heel in neuroischaemic foot
Infection
beneath the surrounding skin and tracking of uid
When skin breakdown develops, it may act as a
portal of entry for infection which develops in 50%
of ulcers. A close examination for signs of infection
should be made. These include purulent discharge
from the lesion and cellulitis as indicated by erythema, swelling and warmth of the toe or foot
although in the presence of neuropathy, these classical signs of infection may be diminished. Signs of
infection may also be limited in the presence of
ischaemia as the inammatory response to infection needs increased blood supply.
Thus, it is important to look for subtle signs of
infection including increased friability of granulation tissue, wound odour, wound breakdown and
delayed healing. There may be tracking of the ulcer
underneath callus. Deep infection may spread from
the site of skin breakdown along tendons and their
sheaths (Fig.9.12). This may not be obvious.
In the presence of infection, it is important to
look for signs suggestive of necrotising fasciitis
including purpuric rash and blistering. Palpation
may reveal crepitus as a ne crackling sensation
indicating gas in the tissues.
Osteomyelitis may be suspected by an exposed
or visible bone at the base of the ulcer or the appearance of the ‘sausage toe’ as a red fusiform swelling
(Fig.9.16). It is often associated with an ulcer on
the dorsum of the toe which probes to bone.
The probe-to-bone involves inserting a sterile
metal probe into the suspected ulceration. A
120
Fig. 9.16 Sausage-shaped discoloured toe suggesting
osteomyelitis
‘click’ (solid or gritty end point) indicates a positive nding. Osteomyelitis is unlikely after a
negative test in the outpatient or low-risk location. However, it is likely after a positive test in a
high-risk or inpatient situation [23, 24].
Ischaemia
On inspection the foot has thin atrophic shiny
skin without hair. There is atrophy of the subcutaneous tissue. Ulcers may be present on the margin of the foot and the toes and there may be
patches of necrosis.
The most important manoeuvre to detect isch-
aemia is the palpation of foot pulses.
• The dorsalis pedis pulse is felt lateral to the
extensor hallucis longus tendon on the dorsum
of the foot.
• The posterior tibial pulse is felt below and
behind the medial malleolus.
M. Edmonds et al.
A small handheld Doppler can be used to conrm the presence of pulses and to assess the vascular supply and with a sphygmomanometer, it
can be utilised to measure the brachial systolic
pressure and ankle systolic pressure. The ankle
brachial pressure index (ABI), which is the ratio
of ankle systolic pressure to brachial systolic
pressure, can then be calculated. In normal subjects, the ABI is usually >0.9 but in the presence
of ischaemia is <0.9. Thus, absence of pulses and
an ABI of <0.9 conrms ischaemia. Conversely,
the presence of pulses and an ABI of >1 essentially rules out ischaemia in the leg but not in the
foot in which arterial disease may be located in
diabetes. Furthermore, the calf arteries in diabetes
typically show diffuse medial calcication which
renders the vessel incompressible and can limit
the utility of assessing the ABI.If arteries are calcied, the ABI may be artifactually raised but the
test is still important as long as one understands
its interpretation. Thus, if the ABI is 0.5, then it is
low, and indicates severe ischaemia, whether the
foot arteries are calcied or not. Indeed, if it is
calcied, the true ABI may be lower. Furthermore,
absence of foot pulses would be an indication to
investigate popliteal and femoral arteries.
Further information about the circulation can
be obtained from assessing the Doppler waveform which normally is pulsatile with a positive
forward ow in systole followed by a short
reverse ow and a further forward ow in diastole. In the presence of arterial narrowing, the
waveform shows a reduced forward ow and is
described as damped and monophasic.
It is now accepted that ischaemia may occur
very peripherally in the foot arteries and may not
be detected by ABI.Thus it is advisable to measure either the transcutaneous oxygen pressure
on the dorsum of the foot or the toe pressures.
Recent studies suggest that toe pressure is more
sensitive than ankle pressure in the diagnosis of
limb threatening ischaemia and is more predictive of amputation risk [25, 26].
As adjunctive tests, it is possible to perform
the capillary lling time (also known as the
blanch test). In the capillary rell test, pressure is
applied to the pulp of the toe until the digit loses
colour. On release of pressure, the rell time
should be less than 3secs if the patient has good
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121
cardiac output and digital perfusion. A capillary
rell time of more than 5secs is abnormal and
suggests poor peripheral perfusion.
From the history, examination and investigations it is possible to assess the severity of the
ischaemia. However, the ischaemic foot covers a
wide spectrum ranging from the neuroischaemic
foot with mild or moderate ischaemia to the critically ischaemic foot and the acute ischaemic
foot. It is important to recognise these two particular presentations, those of critical ischaemia
and acute ischaemia.
Critically Ischaemic Foot
The colour of the skin is bright pink or a dusky
red. The foot is cool and the pulses absent. In the
foot with such severe ischaemia, Buerger’s test is
positive. This is performed by elevating the leg
with the patient supine and within 30 secs it
becomes pale. The foot is then allowed to hang
over the side of the couch and the dependent limb
becomes red due to the chronic dilatation of the
microcirculation distal to the arterial occlusion
(Fig.9.12) A positive Buerger’s sign is indicative
of severe ischaemia which needs urgent vascular
investigations. Another sign of critical ischaemia
is the leg being held in the knee exed position.
Acute Ischaemia
Acute ischaemia results from a sudden occlusion
of a major artery, usually popliteal or supercial
femoral. Classically there are ve features of
acute limb ischaemia (5 P’s):
suddenly decreases. Acute ischaemia is a clinical
emergency with severe morbidity and mortality.
If ischaemia is not treated within 6 hours, then
mottling becomes xed, leading to blistering and
then digital necrosis.
Necrosis
Areas of necrosis or gangrene can be identied
by the presence of black or brown devitalized tissue. Such tissue may be wet (usually related to
infection) or dry. Wet necrosis is usually secondary to a septic vasculitis accompanying severe
soft tissue infection and ulceration and is the
commonest cause of necrosis in the diabetic foot.
In the neuropathic foot, necrosis is usually wet
and is caused by infection complicating a digital,
metatarsal or heel ulcer, and leading to a septic
vasculitis of the digital and small arteries of the
foot (Fig.9.17). Wet necrosis is also prominent in
the infected neuroischaemic foot and has a similar pathology of septic vasculitis. However, in the
neuroischaemic foot, reduced arterial perfusion
to the foot resulting from occlusive disease of the
leg and foot arteries is also an important predisposing factor.
Dry necrosis is hard, blackened, mummied
tissue and there is usually a clean demarcation
line between necrosis and viable tissue. It may be
1. Pain
2. Pulselessness
3. Pallor
4. Paresthesiaes
5. Paralysis
Signs are:
• Pallor of the foot
• White or blueish nail beds
• Blueish-grey discolouration with mottling or
‘bruised’ appearance (Fig.9.5)
If a hand is run down the leg, a ‘cut-off’ point
will be found where the temperature of the skin
Fig. 9.17 Wet necrosis of right third toe secondary to a
septic vasculitis of the digital arteries
122
M. Edmonds et al.
difcult to diagnose in the patient with a dark
skin. Dry necrosis can be seen usually in three
situations, in the ischaemic foot namely in critical ischaemia (Fig.9.4), in acute ischaemia and
in emboli to the toes.
Deformity (Including Limited Joint
Mobility)
Deformity often leads to bony prominences,
which are associated with high mechanical pressures on the overlying skin. This results in ulceration, particularly in the absence of protective
pain sensation and when the shoes are unsuitable.
When assessing deformity it is important to
assess whether it is xed or mobile.
Common deformities include:
• Pes cavus
• Trigger toe
• Hammer toes
• Claw toes
• Hallux valgus
• Fibrofatty padding depletion (FFPD)
• Charcot foot
• Deformities related to previous trauma and
surgery
Hammer Toe
A hammer toe is a exible or rigid deformity in
which there is buckling of the toe with extension
at the metatarsal-phalangeal joint, exion of the
proximal interphalangeal joint and extension of
the distal interphalangeal joint. In people with
diabetic neuropathy, hammer toes are commonly
caused by weakness of the small intrinsic muscles (interossei and lumbricals) of the foot
(Fig. 9.18). This deformity results in increased
pressure over the metatarsal head, over the prominent interphalangeal joint and at the tip of the
toe. There is a risk of the toe rubbing against the
uppers of the shoe.
Claw Toes
Claw toes are similar to hammer toes, but with
more buckling. There is hyperextension at the
metatarsal-phalangeal joint and exion defor-
Pes Cavus
Normally the dorsum of the foot is domed due to
the medial longitudinal arch, which extends
between the rst metatarsal head and the calcaneus. When it is abnormally high, the deformity
is called pes cavus and results in a reduction of
the area of the foot in contact with the ground
during walking and an abnormal distribution of
pressure. This 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 the lesser
toes or a trigger rst toe.
Trigger Toe
A trigger toe is a exion or contraction at the
interphalangeal joint of the hallux leading to
increased vertical pressure on the rst metatarsal
head.
Fig. 9.18 Typical neuropathic foot demonstrating hammer toes, wasting of lumbricals, xerosis and crowding of
toes
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123
mity at the proximal and distal interphalangeal
joints. This results in callus formation and ulceration of the apex and dorsal aspect of the interphalangeal joints. Although claw toes may be
associated with 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 rst
metatarsal- phalangeal 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.
Fibrofatty Padding Depletion (FFPD)
There is reduction of the thickness of the brofatty padding over the metatarsal heads
(Fig. 9.19). Normal feet contain cushions of
brofatty padding over the metatarsal heads
which absorb plantar pressures. In diabetic neu-
ropathy, the brofatty padding may be displaced forward or destroyed by infection or
ulceration reducing the foot’s capacity to absorb
pressure.
Charcot Foot
Bone and joint damage in the tarso-metatarsal
joints and mid-tarsal joints leads to two classical
deformities: the rocker bottom deformity, in
which there is displacement and subluxation/
dislocation of the tarsus downwards, and the
medial convexity (Fig.9.20) 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. When the ankle and subtalar
joints are involved, instability of the hindfoot
can result.
Deformities Related toPrevious
Trauma andSurgery
Deformities of the hip and fractures of the tibia or
bula lead to shortening of the leg and abnormal
gait, which predisposes to foot ulceration. Ray
Fig. 9.19 Distal migration of plantar metatarsal fat pad,
callus and prominent metatarsal heads
Fig. 9.20 Medial convexity deformity of Charcot foot
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