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8 Medical Management oftheLimb Salvage Inpatient
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Evaluation andExamination
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oftheDiabetic Foot
MichaelEdmonds, RajeshKesavan, andArunBal
9
Introduction
There have been several consensus documents
depicting best practice recommendations for
clinical evaluation of the diabetic foot [1–3]. In
this chapter, we describe a simple practical
approach to the evaluation and examination of
the diabetic foot which informs the practitioner
how to carry out a comprehensive assessment.
From this, a diagnostic classication and staging
of the foot can be made which will enable the
correct treatment to be performed.
The diabetic foot can be classied into two
main clinical groups:
M. Edmonds (*)
King’s College Hospital, London, UK
Diabetic Foot Medicine, King’s College, London, UK
e-mail: michael.edmonds@nhs.net
R. Kesavan
Dr. RK Diabetic Foot and Podiatry Institute and
Rakesh Jhunjhunwala Amputation Prevention Centre,
Chennai, India
SRM Institute of Science and Technology,
Chennai, India
A. Bal
Raheja Fortis Hospital, Mumbai, India
Amrita Institute of Medical Sciences, Kochi, India
Diabetic Foot Society of India, Mumbai, India
International Association of Diabetic Foot Surgeons,
Frederiksberg, Denmark
1. The neuropathic foot
2. The ischaemic foot
It is important to differentiate the neuropathic
foot from the ischaemic foot as management of
each differs in many respects. Usually there will
be little doubt as to which category the foot
should be placed in. However, if the examiner has
any doubt, then the foot should be regarded as
ischaemic, because if an ischaemic foot is
wrongly classied as neuropathic, there may be
resulting failure to do further tests to identify
ischaemia and adapt the care plan accordingly.
This may lead to preventable catastrophe and loss
of the foot.
The neuropathic foot may be further stratied
into two clinical scenarios.
1. Foot with neuropathic ulceration (Fig.9.1)
2. Charcot foot, which may be secondarily com-
plicated by ulceration and infection (Fig.9.2)
The ischaemic foot may be stratied into three
clinical scenarios:
1. Neuroischaemic foot characterised by mild or
moderate ischaemia and neuropathy and often
complicated by ulcer (Fig.9.3)
2. Severely ischaemic foot otherwise known as
the critically ischaemic foot (Fig.9.4)
3. Acutely ischaemic foot (Fig.9.5)
© 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_9
107
108
M. Edmonds et al.
Fig. 9.3 Neuroischaemic ulcer on medial aspect of rst
toe
Fig. 9.1 Neuropathic ulcer
Fig. 9.2 Charcot foot with ulcer over lateral malleolus
Fig. 9.4 Necrosis of toes in critically ischaemic foot
Fig. 9.5 Necrosis and mottling of the foot secondary to
acute ischaemia
9 Evaluation andExamination oftheDiabetic Foot
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109
Fig. 9.6 Simple Staging System showing natural history of the ve scenarios of the diabetic foot
With reference to the ischaemic scenario, the
Global Vascular Guidelines have recently proposed the term Chronic Limb Threatening
Ischaemia to include a broad group of patients
with varying degrees of ischaemia that can often
delay wound healing and increase amputation
risk [4]. This will include both the neuroischaemic and the critically ischaemic scenarios.
Each of the above ve main clinical scenarios
(two neuropathic and three ischaemic) are characterised by having specic stages in their natural
history. These stages have been described in a
Simple Staging System [5] (Fig.9.6).
sion of each scenario from the normal foot through
the stages to necrosis. In particular, it emphasises
the development of the ulcer as a pivotal stage in
the natural history of the diabetic foot demanding
urgent and aggressive management.
The Simple Staging System is thus based on
clinical presentation and clinical assessment and
allows all practitioners, whether experienced in
diabetic foot care or not, to make an initial assess-
ment of the diabetic foot and establish at what stage
the foot may be in its natural history. The stage then
determines treatment. The aim is to keep all dia-
betic feet at as low a stage as possible [5].
The stages are
Simple Staging System
1. Normal foot
2. High-risk foot
The Simple Staging System covers the entire
spectrum of diabetic foot disease. It describes ve
stages in the natural history of each of the ve
clinical scenarios. It also traces the rapid progres-
3. Foot with tissue damage (ulceration, Charcot
foot, or ischaemic tissue)
4. Threatened foot
5. Necrotic foot
110
M. Edmonds et al.
Classications oftheDiabetic Foot
There are various classications of the diabetic
foot which are suited to different circumstances,
such as characterising populations, designing
clinical trials and assessing comparative effectiveness of treatments. Classications such as the
Wagner, the University of Texas and SINBAD
are established classications of ulcers [6–8]. In
a person with diabetes and a foot ulcer, the
SINBAD system has been used for communication among health professionals to convey the
characteristics of the ulcer, and to allow comparisons between institutions on the outcomes of
people with a diabetic foot ulcer in regional/
national/international audits [9, 10].
In the Lower Extremity Threatened Limb
Classication System of the Society for Vascular
Surgery, perfusion of the foot is considered in the
context of wound characteristics and infection. It
straties amputation risk according to wound
extent, the degree of ischaemia, and severity of
foot infection and thus is known as WIfI [11]. It
provides accurate and early risk stratication for
patients with threatened lower limbs. It aids clinical management and predicts risk of amputation at
1 year and the need for limb revascularization. It
has been correlated with the probability of limb
salvage and wound healing following revascularization [12].
In order to classify and stage the diabetic foot,
according to the Simple Staging System, a comprehensive assessment, consisting of full history
and examination and bedside (or chair side)
investigations, should be carried out.
Presenting Complaint (Be Aware That
Some Patients May BeAsymptomatic
DuetoNeuropathy)
The presenting complaint is usually concerning
one or more of the following features:
Skin breakdown
Discharge
Swelling
Colour change
Pain
For skin breakdown, discharge, swelling and
colour change or any other specic presenting
complaints, the following questions may be
helpful:
• Where is the problem?
• When did it start?
• How did it start?
Were there any injuries, burns, rat bites
(Figs.9.7 and 9.8), ant bites (Figs.9.9 and 9.10),
History
The history can be divided into the following
sections:
– Presenting complaint
– Past foot history
– Diabetic history
– Past medical history
– Family history
– Drug history
Fig. 9.7 Rat bites over the third and fth toes
9 Evaluation andExamination oftheDiabetic Foot
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Fig. 9.8 Rat bite with partial amputation of the tip of the
left third toe
Fig. 9.9 Ants attracted to the neuropathic foot
111
Assessment ofPain
It is important for personnel who work in a diabetic
foot clinic or limb salvage clinic to understand the
various causes of pain in the diabetic lower limb.
Pain may be a lone specic complaint or it may
accompany the other problems. It may arise locally
or be diffuse. Local sources may come from bone,
joint or soft tissue including skin and subcutaneous
tissue. Generalised burning pain in both feet suggests a diagnosis of painful neuropathy. Diffuse
localised pain in a single foot at rest suggests ischaemia, classically known as rest pain which is
relieved by dependency such as achieved by hanging the foot over the side of the bed. However, pain
in the mild or moderately ischaemic foot should
not always be blamed on reduced arterial perfusion. It may be caused by infection. In the neuropathic or ischaemic foot, severe infection can still
cause pain, particularly throbbing pain. Pain around
an ulcer also suggests infection or ischaemia.
Neuropathy and ischaemia may co-exist in the
foot, and it is important to understand the presentation of pain in neuropathy and also in ischaemia. It should be noted that, in general,
peripheral neuropathy in diabetes is usually NOT
painful and secondly when painful neuropathy
does occur, it is not usually associated with tissue
loss. Thus caution must be exercised in attributing pain to neuropathy when it is more likely due
to infection or ischaemia.
Pain may be unilateral or bilateral and of neuropathic or ischaemic origin. Pain may also be
caused by focal pathology such as infection. The
following sections will discuss rst the assessment of bilateral and then unilateral pain of neuropathic origin and secondly bilateral and then
unilateral pain of ischaemic origin.
Bilateral Neuropathic Pain
Fig. 9.10 Excoriations due to ant bites over the dorsum
of the left lateral forefoot
Bilateral symmetrical neuropathic pain is usually
due to painful neuropathy. It is important to ask
three questions to aid in the diagnosis of painful
neuropathy.
application of native medicines or chemicals,
self-surgery, massage, treatment from unauthorised personnel or damage caused by footwear
[13].
What is the nature of the pain?
When is the pain worse?
Where is the pain?
112
M. Edmonds et al.
What Is theNature ofthePain?
Pain may be spontaneous or be brought on by a
specic stimulus. Spontaneous pain may comprise one or several of the following:
• Sharp, shooting, stabbing or burning pain
• Paraesthesiae (‘pins and needles’)
• Unpleasant tingling (dysaesthesiae)
• Deep muscular aching pain
• Restless legs
• Cramps
• Sensation of cold
• Sensation of tightness (as if a constricting
band is around the foot)
• Heaviness
Patients may complain of walking on marbles.
The pain may be continuous, varying in intensity
or intermittent and episodic and of short duration,
like electric shocks. Itching may also be a symptom of painful neuropathy. Pain can vary according to the evolution of the disease. The pain often
has an acute early phase which lasts a few months
followed by a gradual reduction in pain over the
subsequent year.
Patients with painful neuropathy may charac-
teristically have pain which may be described in
medical terms as allodynia, hyperalgesia or
hyperpathia.
Allodynia is dened as the patient feeling
painful sensations from stimuli which are not
usually painful to normal individuals such as pain
evoked by contact with bedclothes.
Hyperalgesia refers to increased sensation to
stimuli which are normally painful.
Hyperpathia is a greatly exaggerated painful
sensation to a stimulus after cessation of the stimulus especially a repetitive stimulus.
When Is thePain Worse?
Painful neuropathy is worse in bed at night, and
when the feet and legs are in contact with clothes,
including bedclothes. Pain intensity is altered by
emotion and fatigue. The pain may vary in relation to the temporal evolution of the condition,
being especially painful in the initial stages.
Where Is thePain?
The distribution of pain is usually in both feet
extending into the lower legs in a stocking distribution. Often there is poor localisation and it is
usually diffuse. Pain does not generally extend
above the knees but one limb may be slightly
worse than the other. In severe cases, pain does
extend above the knees and it may also be felt in
the hands and arms and also on the skull.
However, unilateral lower pain with no pain at all
on the contralateral limb does not suggest a classical painful neuropathy. It may be due to a focal
ischaemic neuropathy or compression of a nerve
plexus or root by a prolapsed intervertebral disc.
General Symptoms
Relentless, burning pain and contact discomfort
make patients extremely miserable. Patients in
severe pain cannot sleep and can become profoundly disturbed, confused and depressed. Pain
interferes with the activities of daily living and
the quality of life is reduced. There is a negative
impact on sleep, ability to work, mood, recreational activity, mobility and enjoyment of life
[14, 15].
Patients with painful neuropathy may also
present with the following syndromes.
Diabetic Neuropathic Cachexia
The syndrome of diabetic neuropathic cachexia
is characterised by profound weight loss and
severe pain [16]. The weight loss can be up to
60% of the normal weight and can be so great
that patients often appear cachectic. The weight
loss is not related to diabetic control. The emotional disturbances are severe and depression,
anorexia and often erectile dysfunction may be
present. Depression is an inherent part of the syndrome rather than related to the pain.
The sensory loss is mild or absent. There is
usually no motor weakness but ankle jerks may
be absent. The initial incorrect diagnosis may be
metastatic carcinoma or carcinomatous neuropathy. Usually there is spontaneous resolution with
weight completely restored and the painful neuropathic symptoms resolved.
9 Evaluation andExamination oftheDiabetic Foot
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113
Acute Painful Neuropathy ofRapid
Glycaemic Control
This is often known as insulin neuritis but the
condition is associated with rapid improvement
of glycaemic control whether it results from insulin therapy, oral hypoglycaemic agents or diet
alone. Symptoms are burning pain and
paresthesiae worsening at night. Sensory loss
may be minimal or absent. There is usually resolution of symptoms within about 1 year.
Acute Reversible Neuropathy
This has an acute onset and is characterised by
distal pain and weakness associated with very
high blood glucose levels and often ketosis.
There is a sensory neuropathy but usually complete recovery ensues after improvement in diabetic control.
Painful Neuropathy ofImpaired Glucose
Tolerance
Prediabetic states are associated with neuropathy
that typically is predominantly sensory and painful [17]. It is often known as ‘impaired glucose
tolerance neuropathy’ and may represent the
earliest stage of diabetic neuropathy. Patients
with impaired glucose tolerance usually have
small bre neuropathy, whereas those with diabetes more often have neuropathy involving both
small and large bres.
Unilateral Neuropathic Pain
Neurological symptoms and signs limited to one
leg are indicative of a focal neuropathy. Focal
neuropathy may be due to ischaemic damage to
the nerve from diabetes itself or due to a compression of the nerve or nerve root by external factors
in an entrapment neuropathy. Focal neuropathies
due to ischaemic damage with resulting subsequent infarction have an acute onset but they heal
spontaneously in 6–8 weeks. They must be distinguished from entrapment syndromes which start
slow and progress and persist without treatment.
Pain is a prominent symptom of focal neuropathies. It is present at rest and worse at night. Pain
can be felt both proximal and distal to the com-
pression point. Sensory symptoms are sharp
burning pain associated with paraesthesiae.
Allodynia may also be present. Complex regional
pain syndromes which often present with unilateral neuropathic pain must be considered in the
differential diagnosis.
Focal Nerves Aected intheLeg
• Lateral cutaneous nerve of thigh
• Common peroneal nerve
• Posterior tibial nerve
• Femoral nerve
• Saphenous nerve
Lateral Cutaneous Femoral Nerve ofThighMeralgia Paraesthetica
This is entrapment of the lateral cutaneous femoral nerve of thigh as it exits the pelvis. It is compressed or stretched as it passes through the
lateral end of the inguinal ligament next to the
anterior superior iliac spine. It causes burning,
tingling, itching and numbness over the anterolateral surface of thigh which demonstrates contact sensitivity. Similar symptoms may be caused
by a prolapsed disc which is compressing the
Lumbar 3 nerve root. The causes are surgical
interventions to that area, as well as a tight belt or
corset and weight gain underneath inguinal
ligament.
Posterior Tibial Nerve: Tarsal Tunnel
Syndrome
This is an entrapment neuropathy which develops
from compression of the posterior tibial nerve or
its associated branches as the nerve passes below
the exor retinaculum at ankle level or more distally [18]. There is tingling and burning pain in
the sole and toes which is worse at night. There is
also cramping of the intrinsic muscles of the
plantar region. Weakness of the small muscles of
the foot includes abductor hallucis but not extensor digitorum brevis which is supplied by deep
peroneal nerve. Dysaesthesia, paraesthesia and
contact sensitivity are present in the distribution
of medial and plantar nerves on the sole of the
foot.
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