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M. Edmonds et al.
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 rst metatarsophalangeal
joints. Limited mobility at the subtalar joint leads
to reduced dorsiexion of the ankle and also
plantar exion of the foot resulting in increased
plantar pressures on the foot.
Limited joint mobility of the rst metatarsal-
phalangeal joint, so-called hallux rigidus, results
in loss of dorsiexion of this joint and excessive
forces on the plantar surface of the rst toe. This
leads to overloading of the plantar aspect of the
forefoot in the toe off phase of the gait cycle,
causing callus formation and ulceration. It is
often seen in barefooted and sandal-wearing
populations. Furthermore an unbending toe is
exposed to repeated traumas.
soft. Callus can also occur in the mild or moderately ischaemic foot, when it is glazed in nature.
In contrast to callus, corns are discrete areas, usually not more than 1 cm in diameter and can
extend to a depth of several millimetres. 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
(Figs.9.21 and 9.22).
Callus andCorns
Callus is a thickened area of epidermis which
develops at sites of pressure, shear and friction. It
should not be allowed to become excessive as
callus is a common precursor of ulceration in the
presence of neuropathy. Callus is caused by high
pressures and is suggestive of unsuitable footwear or unprotected walking and its most common site is under the metatarsal-phalangeal
joints, commonly the rst metatarsal-phalangeal
joint. Interdigital callus is due to crowding of the
toes and friction and injury due to adjoining toenail. Callus is a classical feature of the neuropathic foot, forming diffuse plaques. It can be
proliferative and hard with a peculiar smell which
attracts insects [13]. When proliferation is excessive it may look like a malignant growth. If the
neuropathic foot gets wet or infected, it becomes
Fig. 9.21 Callus with underlying haemorrhage on medial
side of left rst toe
Fig. 9.22 Callus under second metatarsal head with
underlying haemorrhage
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Oedema
Oedema of the tissues of the foot is a major factor
predisposing to ulceration, and often exacerbates
a tight t inside poorly tting shoes. It also
impedes healing of established ulcers. Oedema
already suspected on inspection can be conrmed
by gentle digital pressure applied for a few seconds. Oedema may be unilateral or bilateral.
Unilateral Oedema
This is usually associated with local pathology in
the foot or leg.
Causes are:
• Infection, when it is usually associated with
erythema and skin breakdown
• Charcot foot (a unilateral hot, red, swollen
foot is often the rst sign and the oedema can
extend to the knee)
• Gout, which may also present as a hot, red,
swollen foot
• Trauma, sprain or fracture
• Deep vein thrombosis
• Venous insufciency
• Lymphoedema caused by lymphatic obstruction secondary to malignancy
• Venous obstruction by a pelvic mass, malignancy or ovarian cyst
• Localised collection of blood or pus which
may present as a uctuant swelling
Bilateral Oedema
This is usually secondary to:
• Cardiac failure
• Hypoalbuminaemia
• Renal failure
• Venous insufciency (sometimes unilateral)
• Inferior vena caval obstruction
• Lymphoedema
• Neuropathic oedema
Nails
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
• Colour of the nail bed
• Abnormalities under the nail
• Signs of nail infections
Structure oftheNails
Thickened nails is a common feature in the general population. If the shoe presses on the nail, it
may cause bleeding under the nail. Eventually
this may lead to ulceration.
Nails in the neuropathic foot may be hard and
brittle. The nails in an ischaemic foot may also be
brittle but ivory in appearance [13]. Alternatively,
nails may become atrophic in patients with neuropathy and ischaemia.
An ingrowing toenail (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 inammation.
Eventually, usually after incorrect nail cutting or
trauma, the nail penetrates the esh.
Colour oftheNail 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-tting shoes.
In acute ischaemia, the nail beds are very pale.
Abnormalities Under theNail
Discharge of uid 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.
Neuropathic oedema secondary to diabetic
neuropathy is rare and is related to increased arterial blood ow and arteriovenous shunting. It
often responds to the drug, ephedrine.
Nail Infections
Fungal infection of the nail usually invades the
nail plate dorsally causing onycholysis. The hallux is the most common nail affected. Infection
126
M. Edmonds et al.
starts in one corner and over a period of years it
spreads to involve the entire toenail and may
affect other nails.
Paronychia is associated with a nail that has a
convex nail bed with tendency to incurve in the corners. Recurring 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 inammatory response with secondary inammation and localised infection.
Neuropathy
Peripheral neuropathy is the most common complication of diabetes affecting 50% of all diabetic
patients. Although neuropathy may present with
tingling and a feeling of numbness, it is asymptomatic in the majority of patients and neuropathy will only be detected by clinical examination.
An important indication of neuropathy will be a
patient who has no pain even when signicant
foot lesions are present. Painless ulceration is
denite evidence of a peripheral neuropathy. In
practice, any patient who walks on a foot with
ulceration or heavy plantar callus without discomfort has signicant neuropathy.
Peripheral neuropathy can involve sensory,
motor and autonomic nerves. Simple inspection
will usually reveal signs of motor and autonomic
neuropathy of the feet but sensory neuropathy
must be detected by a simple sensory assessment.
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. In severe cases, pressure points
also develop over the apices and dorsal interphalangeal joints of associated claw toes. However,
claw toe is a common deformity and may not
always be related to a motor neuropathy. It may
be caused by wearing unsuitable shoes or trauma
or may be congenital.
Complicated assessment of motor power in
the lower limb is not usually necessary, but it is
advisable to assess dorsiexion 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 a painful mononeuropathy is suspected from the history, a more
detailed neurological examination is indicated to
detect a femoral neuropathy or a diabetic amyotrophy and to rule out compressive lesions of
nerve roots supplying the lower limb.
Autonomic Neuropathy
The classical signs of autonomic neuropathy are:
• Dry skin with ssuring secondary to decreased
sweating (Figs.9.11 and 9.15). (The sweating
loss normally occurs in a stocking distribution, which can extend up to the knee.)
• Distended veins over the dorsum of the foot
and ankle, secondary to arteriovenous
shunting.
Sensory Neuropathy
Sensory neuropathy can be simply detected by:
• Clinical examination
• Monolaments examination
• Neurothesiometry
Clinical Examination
A simple clinical examination detecting sensation to light touch using a cotton wisp and vibration using a 128-Hz tuning fork may sufce,
comparing a proximal site with a distal site to
conrm a symmetrical stocking-like distribution
of the neuropathy. It is preferable to avoid the use
of ‘pin-prick’ to detect sensory loss.
Initially, vibratory sensation should be
assessed over the tip of the great toe. An abnormal response is determined when the patient can
no longer feel the vibratory sensation but the
examiner still perceives it. Absence of ankle
reex even after reinforcement conrms a
peripheral neuropathy. Small bre function may
be evaluated using quantitative sensory tests of
thermal and pain perception [27] or by measuring the axon reex-mediated Laser Doppler
Imager are response (LDIare) [28].
The Ipswich Touch Test (IpTT) is an alterna-
tive neurologic test that requires only the physician’s index nger. During the IpTT, the physician
instructs the patient to close his or her eyes while
the physician lightly rests his or her nger on
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127
each of the patient’s rst, third, and fth toes for
1–2secs. Patients are instructed to respond with a
‘yes’ when they feel the physician’s touch. In a
head-to-head trial, diagnostic results of the IpTT
directly paralleled those of the monolament in
detecting Loss of Protective Sensation (LOPS);
IpTT was also equally sensitive and specic [29].
Monolaments Examination
It is important to detect patients who have sufcient neuropathy to render them susceptible to
foot ulceration. This can be carried out using a
monolament which, when applied perpendicular to the foot, buckles at a given force of 10g
[30]. Ability to feel that level of pressure provides protective sensation against foot ulceration.
It is helpful rst to demonstrate the technique on
the patient’s forearm.
The number of sites used varies according to
different protocols. Sites examined include the
plantar aspects of the rst toe, the rst, third and
fth metatarsal heads, the plantar surface of the
heel and the dorsum of the foot. The lament
should not be applied at any site until callus has
been removed. If the patient cannot feel the lament at any of the tested areas, then protective pain
sensation is lost, indicating susceptibility to foot
ulceration [31]. The 10g monolament may
become inaccurate after use on numerous occasions and should be replaced regularly. There are
differences in the performance of commercially
available 10g monolaments. Monolaments were
tested using a calibrated load cell. Each monolament was subjected to ten mechanical bucklings.
The monolaments were mounted vertically and
were compressed in the vertical plane by 10mm
while the load cell detected the maximal buckling
force. Longevity testing was performed on the
monolaments by subjecting them to continuous
compression until the buckling force was less than
9g. Longevity and recovery testing suggested that
each monolament would be reliable on 10 consecutive patients before needing a recovery time of
24hours before further usage [32].
threshold (VPT) is a measure of large bre function that can be semi-quantied by the use of the
neurothesiometer (Fig. 9.23). The stylus of the
instrument is placed over the pulp of the hallux.
The amplitude of vibration is increased until the
patient can detect the vibration. The mean of
three readings is taken over the hallux. The vibration threshold increases with age and thus should
be corrected for age. Standards for normal subjects, their satisfactory reproducibility and relationship to age have been described. However, a
VPT >25V is regarded as abnormal and has been
shown to be highly predictive of subsequent foot
ulceration.
Determination of an abnormal VPT is important for two reasons. First, it identies patients
with large bre dysfunction who are susceptible
to foot ulceration and second, it identies a population with increased cardiovascular risk.
A small number of patients have a small-bre
neuropathy with impaired pain and temperature
perception but with intact touch and vibration.
They are prone to ulceration and thermal traumas but test normal with laments, and a clinical
assessment of light touch and vibration is normal. As yet, there is no simple inexpensive
method of detecting and quantifying small bre
neuropathy. However, a simple temperature
assessment of cold sensation can be made by
placing a cold tuning fork on the patient’s foot
and leg.
Neurothesiometry
Quantitative sensory testing can be used to evaluate vibration perception threshold as well as thermal sensory thresholds. Vibration perception
Fig. 9.23 Neurothesiometer measuring vibration perception threshold
128
M. Edmonds et al.
Examination ofPainful Neuropathy
On examination, there may be few objective neurological decits and the feet and legs may be
normal, although some patients may show a
stocking distribution of loss of sensation of pain
and temperature. Autonomic dysfunction is not
prominent. Vibratory sensation can be mildly
reduced at the toes. Motor strength, tendon
reexes, and proprioception, however, may be
preserved because they are functions of large
nerve bres. There may be an increased sensation
to a normal stimulus such as light touch conrming allodynia.
Gait
There may be high stamping gait due to loss of
proprioception [13].
Patients with distal symmetrical neuropathy
may walk with a wide gait.
In the presence of foot drop, the foot scrapes
along the oor or there is a high stamping gait.
Footwear Assessment
It is important to examine both shoes and socks.
Examination ofPatient’s Footwear
The following enquiries should be made:
• Is the shoe long enough?
• Is the toe box broad and deep enough?
• Are the heels too low?
• Does the shoe fasten with a lace or strap (slipons are unsuitable for everyday wear).
• If using a velcro strap, is it too tight or loose?
• Is the sole thick enough to provide protection
from puncture wounds?
• Is the shoe lining worn, with rough areas that
may prove irritating and warrant
replacement?
• Are there foreign bodies within the shoes?
• Is there excessive wear under hallux suggesting a hallux rigidus?
• Is there wear across whole of tread suggesting
pes cavus?
• Do the insoles show excessive wear and tear?
• Are there exudates/blood stains?
Examination ofPatient’s Socks
• Are the socks large enough?
• Are the seams too prominent?
• Is there a tight band at the top?
• Are the socks in good repair—no holes or
lumpy darns?
• Are the socks made of absorbent material?
• Are the socks very thick, taking up too much
space in the shoe?
• Are the socks nonelastic and impede lymphatic and venous drainage causing oedema of
feet?
General Examination
• As part of the diabetic foot assessment and
indeed the diabetic assessment, all patients
should have a physical examination including
the following systems:
• Cardiovascular
• Respiratory
• Abdomen
• Eyes:
• Visual acuity
• Fundi (A patient lacking necessary visual acuity to give himself a daily foot examination is
a patient at risk, and his family or caregiver
should help him.)
Classication andStaging
oftheDiabetic Foot
Evaluation and examination of the foot will facilitate classication and staging. As previously discussed, the neuropathic foot may be stratied
into two clinical groups: the foot with neuropathic ulceration and the Charcot foot, which
may be secondarily complicated by ulceration
and infection. The ischaemic foot may be stratied into three clinical groups: the neuroisch-
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aemic foot characterised by mild or moderate
ischaemia and neuropathy and often complicated
by ulcer, the severely ischaemic foot otherwise
known as the critically ischaemic foot and the
acutely ischaemic foot (Fig.9.6).
Staging
Stage 1
At this stage, the patient does not have the risk
factors of neuropathy, ischaemia, deformity, callus and swelling rendering him vulnerable to foot
ulcers. The normal foot is characterised by no
symptoms, including no pain, and examination is
normal.
Stage 2
The patient has developed one or more of the risk
factors for foot ulceration including neuropathy,
ischaemia, deformity, callus and oedema and the
foot may be divided into the neuropathic foot and
the ischaemic foot.
Stage 3
The neuropathic and the ischaemic foot have
developed tissue damage mainly skin breakdown.
This is usually an ulcer, but because some minor
injuries such as blisters, splits of skin or grazes
have a propensity to become ulcers, they are
included in Stage 3. Ulceration is usually on the
plantar surface in the neuropathic foot and usually
on the margin in the ischaemic foot but can occur
on the plantar surface in mild distal ischaemia.
Other forms of tissue damage included in this
stage are the bone and joint disruption of Charcot
osteoarthropathy and severe tissue ischaemia in the
critically ischaemic and acutely ischaemic foot.
Stage 4
The foot has become threatened and is in danger
of its tissue being destroyed and losing its function. In the neuropathic foot, infection has developed and is the threat driving the foot to tissue
necrosis. In the Charcot foot, it is usually infection that is the threat but in some cases severe
mechanical instability threatens the integrity of
the foot. In the neuroischaemic foot, the threat is
predominantly infection together with mild or
moderate ischaemia. In the critically ischaemic
foot and the acutely ischaemic foot, severe ischaemia is the threat, driving the foot towards
necrosis.
Stage 5
Necrosis has supervened. In the neuropathic foot,
infection is usually the cause. In the ischaemic
foot, infection is still the most common reason
for tissue destruction although ischaemia contributes. In some cases, ischaemia alone can lead to
necrosis of a previously intact foot. The foot in
Stage 5 is at risk of becoming unsalvageable with
overwhelming necrosis, or has intractable pain or
gross instability and there is a risk a major
amputation.
Conclusion
We have described a practical approach to the
evaluation and examination of the diabetic foot.
Using this approach, the practitioner should be
able to carry out a comprehensive assessment to
allow an accurate diagnostic classication and
staging of the foot. This should enable the correct
treatment to be carried out.
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Frailty andMobility Degeneration
inDiabetes andDiabetic Foot
Ulceration
BijanNaja andGuEonKang
10
Aging, Diabetes, andFrailty
More than 700million people were aged 65years
or over worldwide in 2019, according to a report
by the United Nations, and the number of people
aged 65years or over will increase to 1.5billion
by 2050 [1]. One serious concern regarding the
rapid increase in aging population is growing
challenges in the clinical management of chronic
health conditions such as diabetes in the population [2]. For example, in 2017, 123million people aged 65years or over had diabetes worldwide,
and the number will be doubled by 2045 [3].
Diabetes is a group of metabolic disorders that
occurs due to decits in insulin secretion, insulin
action, or both [4]. The World Health Organization
estimated 1.5 million people died directly from
diabetes in 2019 [5]. Diabetes heightens the risk
B. Naja (*)
Interdisciplinary Consortium on Advanced Motion
Performance (iCAMP), Division of Vascular Surgery
and Endovascular Therapy, Michael E.DeBakey
Department of Surgery, Baylor College of Medicine,
Houston, TX, USA
e-mail: Bijan.Naja@bcm.edu
G. E. Kang
Neuromuscular and Musculoskeletal Biomechanics
Laboratory, Department of Bioengineering, Erik
Jonsson School of Engineering and Computer
Science, University of Texas at Dallas,
Richardson, TX, USA
e-mail: GuEon.Kang2@utdallas.edu
of cardiovascular disease and strokes two- to
threefold and further reduces the life expectancies and quality of life of the affected individuals
[6]. Studies also demonstrated diabetes accelerates the aging process such as cognitive decline
and functional decline at a younger age compared
to those without diabetes [7, 8], which raises concerns about the onset of frailty in older adults
with diabetes.
Frailty is a geriatric syndrome, dened as
increase in vulnerability in older adults to poor
resolution of homeostasis after stressful events
[9] (Fig. 10.1). Although a gradual decline in
cognitive function and physical function is normal with aging, frailty signicantly speeds up the
decline and starts to fail the homeostatic reserve
mechanism [11]. Frailty is also considered a
measure of resilience, and increases adverse
health outcomes such as falls, pressure ulcers,
and disability even after a small insult such as a
minor surgical procedure and a minor infection,
and results in dramatic decrease in health state
[10, 12, 13].
In this chapter, we will review current knowledge of the pathway to develop frailty in diabetes. We will also summarize strategies on how to
screen frailty and its impact on adverse outcomes
in people with diabetes and will discuss potential
treatments to improve health outcomes among
frail older adults.
© Springer Nature Switzerland AG 2023
C. E. Attinger, J. S. Steinberg (eds.), Functional Limb Salvage,
https://doi.org/10.1007/978-3-031-27725-2_10
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Fig. 10.1 Frailty is a
measure of resilient or
measures of inability to
cope with acute stressors
like surgery or an acute
illness such as u or a
fall. (This gure is built
based on the Figure
from [10])
B. Naja and G. E. Kang
Pathways ofFrailty inDiabetes
The two “storms” of aging and diabetes are
associated with a greater risk of developing
frailty [14]. In people with diabetes, the prevalence of frailty signicantly increases by nearly
50% (the prevalence of frailty of 5–10% in nondiabetic individuals) [15]. Although the true
pathways from diabetes to frailty are still
unclear, one commonly considered pathway is
insulin resistance [16] (Fig.10.2). Insulin resistance might result in muscle loss (i.e., sarcopenia) particularly in people with type 2 diabetes
by reducing stimulation of protein synthesis
and mitochondrial function and increasing protein degradation [17].
Arteriosclerosis may be another pathway to
frailty in diabetic individuals. Diabetes accelerates arteriosclerosis [18]. For example, studies
showed peripheral arteriosclerosis, peripheral
chronic ischemia with impaired oxygen supply
caused by arteriosclerosis can cause muscle atrophy and muscle loss and weakness [19].
Several studies also identied chronic inammation and increased oxidative stress may be
other causes of frailty in diabetes. Chronic
inammation induces anabolic resistance in muscle, which leads to sarcopenia because of reduced
production of growth factors and necessary signaling for muscle recovery [20]. Similarly,
increased oxidative stress in diabetes can lead to
muscle atrophy and sarcopenia by reducing mitochondrial function [21].
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