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Basil Tumaini, MD
May Shoo, MD
MMED Residents
02 June 2016
Muhimbili University of Health and Allied Sciences
1Basil Tumaini, May Shoo
Outline
• Introduction
• Epidemiology
• Pathophysiology
• Diabetic foot infections
• Diabetic skin conditions
• Diabetic neuropathies and foot deformities
• Peripheral vascular disease
• Patient evaluation
• Management and Prevention
• References
2Basil Tumaini, May Shoo
Introduction: DM
 Diabetes mellitus (DM) is a group of metabolic diseases
characterized by hyperglycemia resulting from defects in
insulin secretion, insulin action, or both
 Chronic hyperglycemia is associated with long-term
damage, dysfunction &failure of various organs & tissues
such as eyes, kidneys, heart, nerves & blood vessels
3Basil Tumaini, May Shoo
Introduction: Diabetic foot
Diabetic foot is defined as any foot pathology
that results directly from diabetes or its long
term complications
4Basil Tumaini, May Shoo
EPIDEMIOLOGY
5Basil Tumaini, May Shoo
Epidemiology: DM
• 1 in 11 adults have diabetes (415 million)
• By 2040, 1 adult in 10 (642 million) will have
diabetes
• 1 in 7 births is affected by gestational
diabetes
• Every 6 seconds a person dies from diabetes
(5.0 million deaths)
6Basil Tumaini, May Shoo
Epidemiology: DM foot
• The lifetime risk of a foot ulcer for diabetic
patients (type 1 or 2) may be as high as 25%1
• Foot ulcerations are the commonest cause of
hospital admission in diabetics
• Atherosclerosis rarely seen in type I diabetics
< 40 yrs while it may be present even before
diagnosis in type II
7Basil Tumaini, May Shoo
An amputation
every 30 seconds
due to diabetes
8Basil Tumaini, May Shoo
Epidemiology: amputations
• Half of all limb amputations are caused by
diabetes
• Risk is 40 times increased in diabetes
• 70% of people die five years following an
amputation
• Foot problems account for 40% of healthcare
resources in developing countries; 15% in
developed countries
9Basil Tumaini, May Shoo
• 85% of all amputations begin with an
ulcer
• Foot problems cost USD 6 billion/year in
the USA
• 49-85% of amputations can be prevented
10
Epidemiology: amputations …
Basil Tumaini, May Shoo
Epidemiology: DM foot in Tanzania
• In a study done between 2004 -2007, it was
pointed out that foot complications cause
substantial morbidity in Tanzania where 70%
of leg amputations occur in diabetic patients2
• In a study done among 404 DM patients in Dar
es Salaam in 2008, 15% had foot ulcers, 44%
had peripheral neuropathy and 15% had PVD3
11Basil Tumaini, May Shoo
Epidemiology – risk factors
• Peripheral neuropathy (loss of protective
sensation – LOPS)
• Foot deformity
• Peripheral arterial disease (PAD)
• H/o previous ulceration / amputation1
• DM > 10 years duration
• Smoking
• Poor glycemic control (HbA1c > 7%)
• Male sex
12Basil Tumaini, May Shoo
Risk category Definition
Treatment
recommendations
Suggested follow-
up
0 No LOPS, no PAD,
no deformity
Patient education
including advice on
appropriate footwear.
Annually (by
generalist and/or
specialist)
1 Loss of protective
sensation (LOPS)
± deformity
Consider prescriptive
or accommodative
footwear.
Every three to six
months (by
generalist or
specialist)Consider prophylactic
surgery if deformity is
not able to be safely
accommodated in
shoes. Continue
patient education.
2 Peripheral arterial
disease (PAD) ±
LOPS
Consider prescriptive
or accommodative
footwear.
Every two to
three months (by
specialist)
Consider vascular
consultation for
combined follow-up.
3 History of ulcer or
amputation
Same as category 1. Every one
to two months (by
specialist)
Consider vascular
consultation for
combined follow-up if
PAD present.
RISK CLASSIFICATION AND RECOMMENDATIONS1
13Basil Tumaini, May Shoo
Pathophysiology
• Factors leading to development of diabetic foot:
– Diabetic macroangiopathy – peripheral arterial
occlusive disease
– Diabetic microangiopathy – thickening of basement
membranes
– Diabetic polyneuropathy
– Diabetic osteoathropathy – abnormal foot
biomechanics
– Reduced resistance to infection
– Delayed wound healing
– Reduced rate of collateral vessel formation
14Basil Tumaini, May Shoo
Diabetic foot disease –the high-risk foot
Peripheral vascular
disease
Peripheral neuropathy
Peripheral neuropathy and
peripheral vascular disease
15Basil Tumaini, May Shoo
Spectrum of diabetic foot disorders
• Diabetic foot infections: skin, SC tissue, bones;
bacterial, fungal
• Diabetic skin manifestations: callus, corns,
warts, ingrown nails
• Diabetic joint deformities: bunion,
hammertoes, Charcot joint, claw toe
• Diabetic neuropathy: sensory, motor,
autonomic
• Peripheral vascular disease
16Basil Tumaini, May Shoo
DIABETIC FOOT INFECTIONS
• Compromise of the blood supply from
microvascular disease, often in association with
lack of sensation because of neuropathy,
predisposes persons with diabetes mellitus to
foot infections.
• These infections span the spectrum from
simple, superficial cellulitis to chronic
osteomyelitis.
17Basil Tumaini, May Shoo
Increased infection rate
• Skin fissurations predisposes to penetration of
infectious microbes
• Polymorphonuclear granulocyte chemotaxis and
phagocytosis is impaired
• Polyneuropathy predisposes to deep seated infections
due to impaired pain sensation
• Both anaerobe and aerobe infections are implicated in
diabetic foot infections
• Decreased immunity
18Basil Tumaini, May Shoo
IMMUNE DYSFUNCTION
1 Decrease polymorphonuclear leucocyte
migration
2 Decrease phagocytosis
3 Decrease intracellular killing
4 Decrease chemotaxis
19Basil Tumaini, May Shoo
Signs and symptoms
• Diabetic foot infections typically take one of the
following forms:
• Cellulitis
• Deep-skin and soft-tissue infections
• Acute osteomyelitis
• Chronic osteomyelitis
20Basil Tumaini, May Shoo
Cellulitis
• Tender, erythematous, non raised skin lesions
are present, sometimes with lymphangitis
• Lymphangitis suggests group A streptococcal
infection
• Bullae are typical of Staphylococcus aureus
infection, but occasionally occur with group A
streptococci
• No ulcer or wound exudate is present
21Basil Tumaini, May Shoo
Cellulitis
22Basil Tumaini, May Shoo
• The WBC and ESR are slightly or moderately
elevated, but these elevations are not diagnostic
• Blood culture results are usually negative; if
positive, they usually indicate the presence of
group A or group B streptococci
• Cultures of skin via aspiration or biopsy are
generally unrewarding;
– aspiration of a sample from the leading edge of the
erythematous border has a low yield (likely < 5%) but
may be used if the likely organism must be identified
on initial presentation
23
Diagnosis
Basil Tumaini, May Shoo
Deep-skin and soft-tissue infections
• The patient may be acutely ill, with painful
induration of the soft tissues in the extremity
• Wound discharge is usually not present
• In mixed infections that may involve anaerobes,
crepitation may be noted over the afflicted area
• Extreme pain and tenderness may indicate
compartment syndrome or clostridial infection
(ie, gas gangrene)
• The tissues are not tense, and bullae may be
present
• Discharge, if present, is often foul
24Basil Tumaini, May Shoo
• The WBC and ESR are mildly or moderately elevated
• If bullae are present,
– Gram stain and culture results from aspirated exudate from a bullous lesion
may help identify the pathogen
• Blood culture results may be positive
• In suspected deep soft-tissue infection,
– plain radiography, CT, or MRI may be performed to evaluate for
compartment syndrome or for gas or a foreign body in the deep tissues
– excessive gas signifies a mixed aerobic-anaerobic infection, in contrast to
gas gangrene (clostridial myonecrosis)
• Gram stains and/or cultures of samples aspirated from deep-skin
and soft-tissue infections may be used to identify the organism
25
Diagnosis – skin & soft tissue infections
Basil Tumaini, May Shoo
• The patient's temperature is usually less than 102°F
• Discharge is commonly foul
• No lymphangitis is observed
• Pain may or may not be present, depending on the degree
of peripheral neuropathy
• Deep, penetrating ulcers and deep sinus tracts (diagnostic of
chronic osteomyelitis) are usually located between the toes or on
the plantar surface of the foot
• The medial malleoli, shins, or heels are not usually sites of
involvement
26
Chronic osteomyelitis
Basil Tumaini, May Shoo
Diagnosis - Osteomyelitis
• Acute osteomyelitis
• The WBC usually reveals leukocytosis, and the ESR is
moderately or highly elevated[4]
• Blood culture results are usually negative; when positive, the
findings most frequently indicate the presence of S aureus
• For affected long bones, plain radiographic findings generally
become abnormal after 10-14 days; soft-tissue swelling and
periosteal elevation are the earliest signs
• Bone scans are preferred to gallium or indium scans; bone-
scan findings are positive within 24 hours
• Bone biopsy is not necessary
27Basil Tumaini, May Shoo
Diagnosis - Osteomyelitis
Chronic osteomyelitis
• The WBC is often within the reference range; the ESR is usually
very highly elevated and may exceed 100 mm/hr[4] ; the platelet
count is also often elevated
• Blood culture results are usually negative
• Plain X-ray findings are invariably abnormal
• Bone scans -usually unnecessary unless diagnostic confusion
exists with another disorder (eg, bone tumor); an MRI scan would
also be helpful in such a situation
• Bone biopsy under aseptic conditions -preferred way to identify
the causative pathogen
• Important pathogens- Bacteroides fragilis, E coli, Proteus
mirabilis, and Klebsiella pneumoniae; Pseudomonas aeruginosa is
usually not the causative organism
28Basil Tumaini, May Shoo
Management
• Treatment of diabetic foot infections varies by type, as follows:
• Cellulitis – Most responsive to antibiotics
• Deep skin and soft-tissue infections – Usually curable, but
additional debridement is usually indicated
• Acute osteomyelitis – Infecting microorganisms and the likelihood
of successful treatment with antimicrobial therapy are essentially
the same as in patients without diabetes
• Chronic osteomyelitis – Surgical debridement is essential, in
addition to antibiotics; amputation may be necessary
29Basil Tumaini, May Shoo
Fungal nail infection
• Nails infected with a fungus become discolored (yellowish-
brown or opaque), thick and brittle, and may separate from
the rest of the nail.
– In some cases, the nail may crumble.
– The dark, moist, and warm environment of shoes
can promote fungal growth.
– In addition, an injury to the nail put the patient at
an increased risk for a fungal infection.
– Fungal nail infections are difficult to treat.
– Drugs applied directly to the nail only help a small
number of fungal nail problems.
• Pills may be used, and periodic removal of the damaged nail
tissue."
30Basil Tumaini, May Shoo
Fungal nail infection
31Basil Tumaini, May Shoo
Athlete's foot
• "Athlete's foot is a fungus that causes
itching, redness, and cracking. Germs can
enter through the cracks in your skin and
cause an infection.
• Antifungal are used to treat athlete's foot-be
pills and/or creams applied directly *
32Basil Tumaini, May Shoo
Athlete's foot
33Basil Tumaini, May Shoo
Calluses
• "A callus is a build-up of hard skin, usually on
the underside of the foot.
• Calluses are caused by an uneven distribution
of weight, generally on the bottom of the
forefoot or heel.
• Calluses also can be caused by improperly
fitting shoes or by a skin abnormality.
• Keep in mind that some degree of callus
formation on the sole of the foot is normal.
34Basil Tumaini, May Shoo
35Basil Tumaini, May Shoo
Calluses
• After bath, use a pumice stone to gently
remove the build-up of tissue.
• Use cushioned pads and insoles in your shoes.
• Medication also may be used to soften
calluses.
• DO NOT try to cut the callus or remove it with
a sharp object.“
36Basil Tumaini, May Shoo
Localized callus
• When an increase in pressure and discomfort occurs,
people with normal sensation change their gait.
• People with neuropathy do not feel pain and continue
to walk in the same way.
• This leads to a build up of callus at the site of most
pressure.
• Ultimately this hard, localized callus can cause the
tissue underneath to breakdown forming ulceration.
• As a preventive measure, all callus should be removed.
• It is particularly important to note that bleeding callus is
indicative of possible ulceration and should be removed
immediately.
37Basil Tumaini, May Shoo
Localized callus
38Basil Tumaini, May Shoo
Pumice stone
39Basil Tumaini, May Shoo
Corns
• "A corn is a build-up of hard skin near a bony
area of a toe or between toes.
• Corns may be the result of pressure from shoes
that rub against the toes or cause friction
between the toes.
• Use a pumice stone to gently remove the build-
up of tissue.
• Do not use over-the-counter remedies to
dissolve corns. Or cut the corns with a sharp
object.
40Basil Tumaini, May Shoo
Corns
41Basil Tumaini, May Shoo
Bunions
• "A bunion forms when the big toe angles in toward the
second toe. Often, the spot where big toe joins the rest of
the foot becomes red and callused.
• The area may begin to stick out and become hard.
Bunions can form on one or both feet.
• Bunion may run in the family, but most often are caused
by wearing high-heeled shoes with narrow toes. The shoes
put pressure on the big toe, pushing it toward the second
toe.
• The use of felt or foam padding on the foot may help
protect the bunion from irritation.
• A device also may be used to separate the big and second
toes. If the bunion causes severe pain and/or deformity,
surgery to realign the toes may be necessary
42Basil Tumaini, May Shoo
Blisters
• Wearing shoes that do not fit properly or
wearing shoes without socks can cause blisters,
which can become infected.
• When treating blisters, it's important not to
"pop" them.
• The skin covering the blister helps protect it from
infection.
• Use an antibacterial cream and clean, soft
bandages to help protect the skin and prevent
infection.
43Basil Tumaini, May Shoo
Plantar warts
• "Plantar warts look like calluses on the ball of
the foot or on the heel.
• They may appear to have small pinholes or tiny
black spots in the centre.
• The warts are usually painful and may develop
singly or in clusters.
• Plantar warts are caused by a virus that infects
the outer layer of skin on the soles of the feet.
• Over-the-counter medications to dissolve the
wart should not used.
44Basil Tumaini, May Shoo
Plantar warts
45Basil Tumaini, May Shoo
46Basil Tumaini, May Shoo
Hammertoes
47Basil Tumaini, May Shoo
Ingrown toenail
• "Ingrown toenails occur when the edges of the
nail grow into the skin.
• They cause pressure and pain along the nail
edges.
• The edge of the nail may cut into the skin, causing
redness, swelling, pain, drainage, and infection.
• The most common cause of ingrown toenails is
pressure from shoes.
• Other causes include improperly trimmed nails,
crowding of the toes, and repeated trauma to the
feet from activities such as running, walking, or
doing aerobics. 48Basil Tumaini, May Shoo
Ingrown toenail
• Keeping your toenails properly trimmed is the
best way to prevent ingrown toenails.
• Surgery to remove part of the toenail and
growth plate may be needed.
49Basil Tumaini, May Shoo
Ingrown toenail
50Basil Tumaini, May Shoo
Diabetic neuropathy
Can affect:
sensory
motor and
autonomic fibers
51Basil Tumaini, May Shoo
Peripheral neuropathy–Sensory motor
• Most common form of neuropathy
• The prevalence of peripheral neuropathy is very
dependent on the sensitivity of the test used.
• However, it is generally accepted that with standard
clinical examination and objective testing,
approximately 50% of people will have neuropathy
after 15 years of diabetes
• The long nerves of the feet and hands are affected
in what is commonly known as a ‘glove and
stocking distribution’. When the neuropathy has
reached the knees, usually the hands become
involved.
52Basil Tumaini, May Shoo
Causes/risk factors of DN
1. Metabolic factors, such as high blood glucose, long duration of
diabetes, abnormal blood fat levels, and/or low levels of
insulin
2. Neurovascular factors, leading to damage to the BV that carry
oxygen and nutrients to nerves
3. Autoimmune factors that cause inflammation in nerves
4. Mechanical injury to nerves, such as carpal tunnel syndrome
5. Inherited traits that increase susceptibility to nerve disease
6. Lifestyle factors, such as smoking or alcohol use
53Basil Tumaini, May Shoo
Pathophysiology
• Among the metabolic factors that contribute to dev. of
neuropathy , Polyol pathway activity has been most important
• The polyol pathway is comprised of two steps:
– (1) the conversion of glucose to sorbitol by aldose reductase
(localized to paranodal Schwann cells and endoneurial
microvessels )
– (2) the conversion of sorbitol to fructose by sorbitol
dehydrogenase.
• Glucose is converted to the sugar-alcohol (polyol)
sorbitol using NADPH as a coenzyme, which has a close
affinity to aldose reductase
54Basil Tumaini, May Shoo
Pathophysiology …
• Accumulation of sorbitol, perturbation of phosphoinositide
metabolism, as well as alterations of coenzymes, leads to
neural lesions
• Increased non enzymatic glycation of structural proteins is
also considered to be another factor in pathogenesis of DN.
• Advanced glycation end products resulting from
hyperglycemia act on specific receptors, inducing
monocytes and endothelial cells to increase the production
of cytokines and adhesion molecules which also, have an
effect on matrix metalloproteinases, which might damage
nerve fibers.
55Basil Tumaini, May Shoo
Peripheral neuropathy–Sensory motor
• Bilateral- Unlike peripheral vascular disease,
which can involve only one limb, peripheral
neuropathy affects both feet, with
approximately equal symptoms in each limb.
• Unlike peripheral vascular disease, which can
involve only one limb, peripheral neuropathy
affects both feet, with approximately equal
symptoms in each limb.
56Basil Tumaini, May Shoo
Diabetic peripheral neuropathy – risk
factors
• The poorer the glycaemic control, and
• the longer the duration of diabetes, the higher the risk of
developing foot problems.
• These are the two most important risk factors.
• The older the person, the higher the risk.
• Interestingly, the taller the person, the higher their chance of
developing neuropathy. This appears to be explained by the fact
that the most distal part of the nerve is damaged first. Diabetic
neuropathy is also known as the ‘dying back’ disease.
• Excessive alcohol
57Basil Tumaini, May Shoo
Sensory neuropathy
Deep sensory perception is reduced resulting
in loss of protective reflexes against physical
injury.
Overshooting due to loss of joint position 
Joint injuries
Typically, manifests in a sock - like distribution.
58Basil Tumaini, May Shoo
Manifestations of sensory neuropathy
• Painful with these symptoms:
–burning
–pins and needles
–pain
• Painless (or insensate) - No symptoms
59Basil Tumaini, May Shoo
Nerve damage – neuropathy
• Symptoms of painful neuropathy include
– numbness,
– burning,
– pins and needles, and
– pain that can be excruciating,
– distressing and difficult to treat satisfactorily.
– These symptoms occur bilaterally and tend to be worse at night.
• The majority of people with neuropathy, however, experience no
symptoms, despite having significant disease. These people are more
likely to develop problems as they are not aware of their feet, having
lost their sensation of pain.
60Basil Tumaini, May Shoo
Most of us experience pain when we injure our foot.
This alerts us to examine the foot and treat it as necessary
61Basil Tumaini, May Shoo
Painless nature of diabetic foot
disease • However, in the insensate foot, pain
sensation is absent.
• A significant amount of damage can
occur; people are completely oblivious
to this until they notice blood or
swelling.
• For this reason it is often said that
people with insensate neuropathy can
have quite major surgical procedures
performed without the need for
anaesthetic.
Basil Tumaini, May Shoo
Sensory nerve damage
• This slide shows a person who
attended a foot clinic for
treatment of ulceration,
completely unaware that they
were walking with a thumb-
tack stuck into their foot.
• Had the tack not been found,
this injury could quite easily
have become infected, leading
to serious consequences
63Basil Tumaini, May Shoo
Sensory nerve damage
64Basil Tumaini, May Shoo
Motor nerve damage
• As well as affecting the sensory nerves, peripheral
neuropathy affects the motor nerves of the feet.
• This causes weakness in the intrinsic muscles of the feet,
leading to contraction of the muscles and clawed toes.
• As the toes claw back, the fat pads are pulled forward from
under the metatarsal heads, increasing the pressure under
these metatarsal heads and on the tips of the toes
(common places for neuropathic ulceration).
65Basil Tumaini, May Shoo
66Basil Tumaini, May Shoo
Motor neuropathy
Denervation and atrophy of small foot muscles
leading to malum perforans, transverse foot
arch instability with clawing and splay foot
Hammer toe
Claw toe
Hallux valgus, hammer toes, erythema over
pressure points 67Basil Tumaini, May Shoo
68Basil Tumaini, May Shoo
Motor nerve damage
69Basil Tumaini, May Shoo
Charcot’s arthropathy
• Charcot’s arthropathy is a condition that is associated with end stage peripheral
neuropathy.
• While the pathogenesis of this condition is still under debate, one reasonable
explanation is that with the onset of autonomic neuropathy, a ‘shunting’
between the arteries and veins occurs.
• This leads to an increase in blood flow to the foot – hence the term ‘warm
neuropathic foot’.
• This increase in blood flow provokes the demineralization of the bones, making
them soft and weak.
70Basil Tumaini, May Shoo
Charcot’s arthropathy
• Insensate people can easily damage these weak bones, leading to
dislocation and/or fracture.
• People do not feel pain and continue walking on the damaged foot,
causing the bony architecture of the foot to collapse.
• This condition is often misdiagnosed as gout, septic arthritis or
osteomyelitis.
• A good rule of thumb is that if a person has a unilateral hot, swollen
foot, with no obvious portal for infection, consider Charcot’s
arthropathy.
71Basil Tumaini, May Shoo
Charcot’s arthropathy
• Artery-vein shunting
• Increased blood flow
• Bone resorption
• Commonly misdiagnosed
72Basil Tumaini, May Shoo
Acute vs chronic Charcot’s arthropathy
• It is very important to understand that there are two phases in Charcot’s. The acute
phase, and the burnt out or chronic phase.
• If a patient comes to you with a
– unilateral warm swollen foot that is
– relatively pain free,
– with bounding pulses and
– with or without some deformity,
– and if there is no obvious portal for infection, an acute Charcot’s needs to be considered.
This will be a very different foot from the burnt out Charcot’s where there is little or no
temperature difference and the foot is rigid and misshapen.
73Basil Tumaini, May Shoo
Acute vs chronic Charcot’s
arthropathy• Unilateral
• Warm, swollen
• Relatively pain free
• Bounding pedal
pulses
• Deformity may be
present
• No temperature
difference
• Rigid foot deformity
• Grossly misshapen foot
74Basil Tumaini, May Shoo
Charcot’s arthropathy
75Basil Tumaini, May Shoo
76Basil Tumaini, May Shoo
The typical
appearance of a later-
stage Charcot foot
with a rocker-bottom
deformity4
77Basil Tumaini, May Shoo
Lateral X-ray of a Charcot foot deformity
Dislocation of the tarsometatarsal joint with break in the talo-first
metatarsal line (dashed lines) and a reduced calcaneal inclination
angle
4
78Basil Tumaini, May Shoo
79
Lee C. Rogers, et al. The Charcot Foot in Diabetes. Diabetes Care Sep 2011, 34 (9)
2123-2129; DOI: 10.2337/dc11-0844
Basil Tumaini, May Shoo
Charcot’s arthropathy –
treatment
• Acute phase
– Non weight-bearing
– Total contact cast
• Chronic phase
– Orthopaedic surgery
80Basil Tumaini, May Shoo
Management4
Offloading
• Offloading at the acute active stage of the Charcot foot
is the most important management strategy
• could arrest the progression to deformity
• the foot should be immobilized in an irremovable total
contact cast (TCC)
• the patient should use crutches or wheelchair and
should be encouraged to avoid weight bearing on the
affected side
Others: Surgical
81Basil Tumaini, May Shoo
Autonomic neuropathy
• Vasodilation  Oedema
• ↓Sweating thus foot is warm, dry, scaly
which predisposes to fissure formation
Callus formation at pressure points
and dry skin are substrate for
ulceration
Pes cavus resulting in callus formation
over the pressure points
82Basil Tumaini, May Shoo
83Basil Tumaini, May Shoo
AUTONOMIC NERVE DAMAGE
84Basil Tumaini, May Shoo
85Basil Tumaini, May Shoo
Peripheral vascular disease
• Cause: decreased perfusion
due to macrovascular disease
• Sites: more distal
Tibial and peroneal arteries
(segment between the knee and
the ankle but aortic-illiac to knee
less frequently)
86Basil Tumaini, May Shoo
Peripheral vascular disease in
diabetes
• 15-40 times more likely to
have lower limb amputation
• People over 70 years have a
70-fold increased risk of
amputation
87Basil Tumaini, May Shoo
Risk factors characteristics of
atherosclerosis in diabetes
• More common
• Affects young age group
• No sex difference
• Smoking
• Faster in progress
88Basil Tumaini, May Shoo
Pathogenesis of atheroschlerosis
89Basil Tumaini, May Shoo
Peripheral vascular disease
• Symptoms
– Intermittent claudication
– Rest pain
• No symptoms
– Inactivity
– Neuropathy
90Basil Tumaini, May Shoo
Signs of vascular disease
• Diminished or absent
pedal pulses
• Coolness of the feet
and toes
• Poor skin and nails
• Absence of hair on feet
and legs
91Basil Tumaini, May Shoo
Peripheral vascular disease
and diabetes
• Symptoms and signs of peripheral
vascular disease
• There are four stages:
1. Occlusive disease without symptoms
2. Intermittent claudication
3. Ischaemic rest pain (nighttime)
4. Ulceration/gangrene
92Basil Tumaini, May Shoo
Vascular assessment
Palpation of foot pulses
– Dorsalis pedis (10% absent
due to anatomical reasons)
– Tibialis posterior
93Basil Tumaini, May Shoo
Peripheral vascular disease
non-invasive evaluation
• Methods
– Doppler pressure studies (ABI)
– Duplex arterial imaging
• Rationale- The degree of vascular disease can
be used to:
– Identify and confirm presence of disease
– predict whether the ulcer will heal without
surgical intervention.
– determine need for early surgical intervention
94Basil Tumaini, May Shoo
Peripheral vascular disease
non-invasive evaluation
• Doppler ultrasound
– |The ABI- Measures pressure at brachial, pedal and
toe arteries
– The ABI is an estimate of the lower limb blood flow
– The SBP of the brachial artery is divided into the SBP
of the pedal arteries.
– Ankle Brachial Index (ABI)
<0.9 abnormal
0.9 to 1.0 normal
>1.3 non-compressible
95Basil Tumaini, May Shoo
Peripheral vascular disease
non-invasive evaluation
• Duplex arterial imaging – allows narrowing or
obstruction of blood vessels to be localized
• through the detection of either disturbance or
absence of flow.
• An accurate roadmap of all the arteries in the
leg can be generated using this technique,
which avoids the pitfalls associated with the
interpretation of Doppler pressure
measurements and calcification
96Basil Tumaini, May Shoo
Peripheral vascular diseaseTreatment
• Quit smoking
• Walk through pain
– Surgical intervention Studies have shown that the results from angioplasty
and a formal exercise programme – ‘walking through the pain barrier’ –
are similar.
• People should be reassured that walking with claudication is not
dangerous.
97Basil Tumaini, May Shoo
Peripheral vascular disease
• They should be asked to continue walking after the onset of
claudication to encourage the development of collateral blood
supply to the limbs.
• If this fails, bypass surgery is required.
• In the past this has always been considered unsatisfactory in
people with diabetes because the vessels that are involved in the
lower limbs are smaller.
• In recent times, however, the success rate has improved.
98Basil Tumaini, May Shoo
Patient evaluation
99Basil Tumaini, May Shoo
Examination
 Neurological examination
◦ Vibration perception – tuning
fork at 128 Hz
◦ Light pressure - Simmes –
Weinstein 10 gram
monofilament
◦ Light touch
◦ Two point discrimination
◦ Pain
◦ Temperature perception
◦ Deep tendon reflexes
◦ Clonus
◦ Babinski test
◦ Romberg test
 Vascular Examination
◦ Palpation of pulses
◦ Skin/limb colour changes
◦ Presence of edema
◦ Temperature gradient
◦ Skin changes
 Abnormal wrinkling
 Absence of hair
 Onychodystrophy
◦ Venous filling time
100Basil Tumaini, May Shoo
Examination
 Dermatological
◦ Skin appearance
◦ Calluses
◦ Fissures
◦ Nail appearance
◦ Hair growth
◦ Ulceration/infection/
gangrene
◦ Interdigital lesions
◦ Tinea pedis
◦ Markers of diabetes
 Musculoskeletal
◦ Biomechanical
abnormalities
◦ Structural deformities
◦ Prior amputation
◦ Restricted joint mobility
◦ Tendo Achilles contractures
◦ Gait evaluation
◦ Muscle group strength
testing
◦ Plantar pressure assessment
101Basil Tumaini, May Shoo
Do not forget the shoes !
102Basil Tumaini, May Shoo
Neuropathic vs Ischemic Ulcer
Neuropathic Ischaemic
Position Pressure areas
Plantar Aspect
Lateral and medial aspects
due to compression
Swelling Dry Swollen
Pain Painless Very painful
Warmth No Yes
Necrosis +/- Yes
Appearance Clean Ulcer Pus & Smelling
103Basil Tumaini, May Shoo
Classification - Wagner
• Grade 0 - Skin intact, no foot deformity
• Grade 1 - Superficial ulcer
• Grade 2 - Deep ulcer
• Grade 3 - Deep ulcer with infection
• Grade 4 - Limited necrosis
• Grade 5 - Necrosis of the entire foot
104Basil Tumaini, May Shoo
Wagner grade 0
105Basil Tumaini, May Shoo
Wagner grade 1
106Basil Tumaini, May Shoo
Wagner grade 2
107Basil Tumaini, May Shoo
Wagner grade 3
108Basil Tumaini, May Shoo
Wagner grade 4
109Basil Tumaini, May Shoo
Wagner grade 5
110Basil Tumaini, May Shoo
INVESTIGATIONS
Can be group into 4 categories.
1) Biochemical
2) Vascular
3) Neurological
4) Foot imaging
111Basil Tumaini, May Shoo
Laboratory evaluation
• FBS/RBS
• Glycosylated hemoglobin (HbA1C)
• FBP + ESR
• Wound and Blood cultures
• Serum Chemistry: CRP
• Urinalysis
112Basil Tumaini, May Shoo
Imaging
Plain X-rays
- Osteomyelitis, fractures
- Soft tissue gas
- Dislocations in neuropathic arthropathy
CT Scan
Technetium bone scans - osteomyeletis
MRI - osteomyelitis
113Basil Tumaini, May Shoo
VASCULAR AND NEUROLOGICAL
INVESTIGATIONS
• Indicated to evaluate the extend of occlusive vascular
disease and assessment of healing potential
 Doppler segmental arterial pressure
 Ankle brachial Index(ABI) normal is 1.1 while <0.9 abnormal
 Toe pressure measurement,
• Sensory examination with a 5.07 Semmes Weinstein
monofilament wire
 Single most practical measure of risk assessment
 BUT is cost effective
114Basil Tumaini, May Shoo
MANAGEMENT
• Five aspect of patient treatment
1. Mechanical control
2. Metabolic control
3. Microbial control
4. Vascular management
5. Education
115Basil Tumaini, May Shoo
Management
• Preventative foot care
• Diabetic foot ulcer (DFU) care
• Ischemia management
• Neuropathy management
• Surgery
116Basil Tumaini, May Shoo
Preventative foot care
 Podiatry - Regular inspection of the foot, appropriate nail
care, warm (32oC) soaks, moisturizing creams, early
detection of new lesions
 Optimally fitted footwear – well cushioned sneakers,
custom molded shoes
 Pressure reduction – cushioned insoles, custom orthoses
 Patient education — need for daily inspection and
necessity for early intervention, avoidance of barefoot
walking
 Physician education — significance of foot lesions,
importance of regular foot examination, and current
concepts of diabetic foot management
117Basil Tumaini, May Shoo
Diabetic Foot Ulcer care
 Debridement – of callus and necrotic tissue using sharp
debridement till bleeding tissue, lavage with 0.9%NaCl
 Dressing  Honey, Mabble cream or Paraffin gauze
 Open dressing advisable
 Avoid corrosive solutions like – Eusol, H2O2, Spirit or Iodine
 Offloading of the ulcer site to reduce ischaemia via total
contact cast, non weight bearing (crutches, bedrest, wheel
chair)
 Wound management – maintenance of a moist wound with
regular cleaning and dressing
 Infections treated with broad spectrum antibiotics based on
culture results. Clindamycin/flouroquinolone/metronidazole
suitable empiric therapy
118Basil Tumaini, May Shoo
Ischemia/neuropathy
• Angiography evaluates for chance of catheter
intervention or vascular surgery
• Vascular bypass surgery successful if occlusion is
supramalleolar but less so in inframalleolar PAOD
• Aspirin is useful for primary and secondary
prevention
• Neuropathy treated pharmacologically with
agents such as carbamazepine, gabapentin and
pregabalin and prevention of minor trauma that
will go undetected due to insensate foot
119Basil Tumaini, May Shoo
Surgery
• Sharp debridement
• Local procedures to remove areas of
chronically elevated pressure (deformities)
causing non healing ulcers
• Sequestrectomies
• Amputation
• Correct structural deformities — hammer
toes, bunions, Charcot
120Basil Tumaini, May Shoo
Indications for amputation
• Uncontrollable infection or sepsis
• Inability to obtain a plantar grade, dry foot
that can tolerate weight bearing
• Non ambulatory patient
121Basil Tumaini, May Shoo
Common pathway Cause of diabetic amputation
A person with diabetes has neuropathy and/or peripheral
vascular disease.
Trauma may occur that causes ulceration.
If this fails to heal, infection and osteomyelitis can ensue.
If the infection is not arrested, the patient might ultimately
require an amputation.
However in
some hot and humid countries,
in people with poor glycaemic control,
underlying neuropathy and/or vascular disease do not
need to be present;
people can progress quickly from trauma to infection to
amputation.
Basil Tumaini, May Shoo
Cause of diabetic amputation
Pecararo
Trauma
Ulcer
Failure to heal
Infection
Amputation
Neuropathy or vascular disease
123Basil Tumaini, May Shoo
This slide says it all…
• This figure is terrifying especially when we
know that up to 85% of amputations are
preventable with early identification of the
• at-risk foot and prompt treatment by a
skilled multidisciplinary footcare team.
124Basil Tumaini, May Shoo
Lessons from The Step by Step Foot Project2
• Training personnel in diabetic foot management,
facilitating transfer of knowledge and expertise,
and improved patient education improves:
• foot ulcer management
• reduces the incidence of foot ulcers
• reduces amputation rates
125Basil Tumaini, May Shoo
References
1. Boulton AJM, et al. Comprehensive Foot Examination and
Risk Assessment: A report of the Task Force of the Foot Care
Interest Group of the American Diabetes Association, with
endorsement by the American Association of Clinical
Endocrinologists. Diabetes Care 2008; 31:1679.
2. Abbas ZG, Lutale JK et al, The ‘Step by Step’Diabetic Foot
Project in Tanzania: a model for improving patient outcomes
in less-developed countries. Int Wound J. 2011 Apr;8(2):169-
75 availabe at
http://www.ncbi.nlm.nih.gov/pubmed/21266010 Accessed on
01/06/2016.
126Basil Tumaini, May Shoo
References ...
3. Chiwanga, Faraja S., and Marina A. Njelekela. Diabetic Foot:
Prevalence, Knowledge, and Foot Self-Care Practices among
Diabetic Patients in Dar Es Salaam, Tanzania – a Cross-
Sectional Study. Journal of Foot and Ankle Research 8
(2015): 20. PMC. Web. 1 June 2016.
4. Lee C. Rogers, et al. The Charcot Foot in Diabetes. Diabetes
Care Sep 2011, 34 (9) 2123-2129; DOI: 10.2337/dc11-0844
5. Previous slides from Prof. Lutale and former students.
127Basil Tumaini, May Shoo
THE END
128Basil Tumaini, May Shoo

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Diabetic foot by Dr. Basil Tumaini and Dr. May Shoo

  • 1. Basil Tumaini, MD May Shoo, MD MMED Residents 02 June 2016 Muhimbili University of Health and Allied Sciences 1Basil Tumaini, May Shoo
  • 2. Outline • Introduction • Epidemiology • Pathophysiology • Diabetic foot infections • Diabetic skin conditions • Diabetic neuropathies and foot deformities • Peripheral vascular disease • Patient evaluation • Management and Prevention • References 2Basil Tumaini, May Shoo
  • 3. Introduction: DM  Diabetes mellitus (DM) is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both  Chronic hyperglycemia is associated with long-term damage, dysfunction &failure of various organs & tissues such as eyes, kidneys, heart, nerves & blood vessels 3Basil Tumaini, May Shoo
  • 4. Introduction: Diabetic foot Diabetic foot is defined as any foot pathology that results directly from diabetes or its long term complications 4Basil Tumaini, May Shoo
  • 6. Epidemiology: DM • 1 in 11 adults have diabetes (415 million) • By 2040, 1 adult in 10 (642 million) will have diabetes • 1 in 7 births is affected by gestational diabetes • Every 6 seconds a person dies from diabetes (5.0 million deaths) 6Basil Tumaini, May Shoo
  • 7. Epidemiology: DM foot • The lifetime risk of a foot ulcer for diabetic patients (type 1 or 2) may be as high as 25%1 • Foot ulcerations are the commonest cause of hospital admission in diabetics • Atherosclerosis rarely seen in type I diabetics < 40 yrs while it may be present even before diagnosis in type II 7Basil Tumaini, May Shoo
  • 8. An amputation every 30 seconds due to diabetes 8Basil Tumaini, May Shoo
  • 9. Epidemiology: amputations • Half of all limb amputations are caused by diabetes • Risk is 40 times increased in diabetes • 70% of people die five years following an amputation • Foot problems account for 40% of healthcare resources in developing countries; 15% in developed countries 9Basil Tumaini, May Shoo
  • 10. • 85% of all amputations begin with an ulcer • Foot problems cost USD 6 billion/year in the USA • 49-85% of amputations can be prevented 10 Epidemiology: amputations … Basil Tumaini, May Shoo
  • 11. Epidemiology: DM foot in Tanzania • In a study done between 2004 -2007, it was pointed out that foot complications cause substantial morbidity in Tanzania where 70% of leg amputations occur in diabetic patients2 • In a study done among 404 DM patients in Dar es Salaam in 2008, 15% had foot ulcers, 44% had peripheral neuropathy and 15% had PVD3 11Basil Tumaini, May Shoo
  • 12. Epidemiology – risk factors • Peripheral neuropathy (loss of protective sensation – LOPS) • Foot deformity • Peripheral arterial disease (PAD) • H/o previous ulceration / amputation1 • DM > 10 years duration • Smoking • Poor glycemic control (HbA1c > 7%) • Male sex 12Basil Tumaini, May Shoo
  • 13. Risk category Definition Treatment recommendations Suggested follow- up 0 No LOPS, no PAD, no deformity Patient education including advice on appropriate footwear. Annually (by generalist and/or specialist) 1 Loss of protective sensation (LOPS) ± deformity Consider prescriptive or accommodative footwear. Every three to six months (by generalist or specialist)Consider prophylactic surgery if deformity is not able to be safely accommodated in shoes. Continue patient education. 2 Peripheral arterial disease (PAD) ± LOPS Consider prescriptive or accommodative footwear. Every two to three months (by specialist) Consider vascular consultation for combined follow-up. 3 History of ulcer or amputation Same as category 1. Every one to two months (by specialist) Consider vascular consultation for combined follow-up if PAD present. RISK CLASSIFICATION AND RECOMMENDATIONS1 13Basil Tumaini, May Shoo
  • 14. Pathophysiology • Factors leading to development of diabetic foot: – Diabetic macroangiopathy – peripheral arterial occlusive disease – Diabetic microangiopathy – thickening of basement membranes – Diabetic polyneuropathy – Diabetic osteoathropathy – abnormal foot biomechanics – Reduced resistance to infection – Delayed wound healing – Reduced rate of collateral vessel formation 14Basil Tumaini, May Shoo
  • 15. Diabetic foot disease –the high-risk foot Peripheral vascular disease Peripheral neuropathy Peripheral neuropathy and peripheral vascular disease 15Basil Tumaini, May Shoo
  • 16. Spectrum of diabetic foot disorders • Diabetic foot infections: skin, SC tissue, bones; bacterial, fungal • Diabetic skin manifestations: callus, corns, warts, ingrown nails • Diabetic joint deformities: bunion, hammertoes, Charcot joint, claw toe • Diabetic neuropathy: sensory, motor, autonomic • Peripheral vascular disease 16Basil Tumaini, May Shoo
  • 17. DIABETIC FOOT INFECTIONS • Compromise of the blood supply from microvascular disease, often in association with lack of sensation because of neuropathy, predisposes persons with diabetes mellitus to foot infections. • These infections span the spectrum from simple, superficial cellulitis to chronic osteomyelitis. 17Basil Tumaini, May Shoo
  • 18. Increased infection rate • Skin fissurations predisposes to penetration of infectious microbes • Polymorphonuclear granulocyte chemotaxis and phagocytosis is impaired • Polyneuropathy predisposes to deep seated infections due to impaired pain sensation • Both anaerobe and aerobe infections are implicated in diabetic foot infections • Decreased immunity 18Basil Tumaini, May Shoo
  • 19. IMMUNE DYSFUNCTION 1 Decrease polymorphonuclear leucocyte migration 2 Decrease phagocytosis 3 Decrease intracellular killing 4 Decrease chemotaxis 19Basil Tumaini, May Shoo
  • 20. Signs and symptoms • Diabetic foot infections typically take one of the following forms: • Cellulitis • Deep-skin and soft-tissue infections • Acute osteomyelitis • Chronic osteomyelitis 20Basil Tumaini, May Shoo
  • 21. Cellulitis • Tender, erythematous, non raised skin lesions are present, sometimes with lymphangitis • Lymphangitis suggests group A streptococcal infection • Bullae are typical of Staphylococcus aureus infection, but occasionally occur with group A streptococci • No ulcer or wound exudate is present 21Basil Tumaini, May Shoo
  • 23. • The WBC and ESR are slightly or moderately elevated, but these elevations are not diagnostic • Blood culture results are usually negative; if positive, they usually indicate the presence of group A or group B streptococci • Cultures of skin via aspiration or biopsy are generally unrewarding; – aspiration of a sample from the leading edge of the erythematous border has a low yield (likely < 5%) but may be used if the likely organism must be identified on initial presentation 23 Diagnosis Basil Tumaini, May Shoo
  • 24. Deep-skin and soft-tissue infections • The patient may be acutely ill, with painful induration of the soft tissues in the extremity • Wound discharge is usually not present • In mixed infections that may involve anaerobes, crepitation may be noted over the afflicted area • Extreme pain and tenderness may indicate compartment syndrome or clostridial infection (ie, gas gangrene) • The tissues are not tense, and bullae may be present • Discharge, if present, is often foul 24Basil Tumaini, May Shoo
  • 25. • The WBC and ESR are mildly or moderately elevated • If bullae are present, – Gram stain and culture results from aspirated exudate from a bullous lesion may help identify the pathogen • Blood culture results may be positive • In suspected deep soft-tissue infection, – plain radiography, CT, or MRI may be performed to evaluate for compartment syndrome or for gas or a foreign body in the deep tissues – excessive gas signifies a mixed aerobic-anaerobic infection, in contrast to gas gangrene (clostridial myonecrosis) • Gram stains and/or cultures of samples aspirated from deep-skin and soft-tissue infections may be used to identify the organism 25 Diagnosis – skin & soft tissue infections Basil Tumaini, May Shoo
  • 26. • The patient's temperature is usually less than 102°F • Discharge is commonly foul • No lymphangitis is observed • Pain may or may not be present, depending on the degree of peripheral neuropathy • Deep, penetrating ulcers and deep sinus tracts (diagnostic of chronic osteomyelitis) are usually located between the toes or on the plantar surface of the foot • The medial malleoli, shins, or heels are not usually sites of involvement 26 Chronic osteomyelitis Basil Tumaini, May Shoo
  • 27. Diagnosis - Osteomyelitis • Acute osteomyelitis • The WBC usually reveals leukocytosis, and the ESR is moderately or highly elevated[4] • Blood culture results are usually negative; when positive, the findings most frequently indicate the presence of S aureus • For affected long bones, plain radiographic findings generally become abnormal after 10-14 days; soft-tissue swelling and periosteal elevation are the earliest signs • Bone scans are preferred to gallium or indium scans; bone- scan findings are positive within 24 hours • Bone biopsy is not necessary 27Basil Tumaini, May Shoo
  • 28. Diagnosis - Osteomyelitis Chronic osteomyelitis • The WBC is often within the reference range; the ESR is usually very highly elevated and may exceed 100 mm/hr[4] ; the platelet count is also often elevated • Blood culture results are usually negative • Plain X-ray findings are invariably abnormal • Bone scans -usually unnecessary unless diagnostic confusion exists with another disorder (eg, bone tumor); an MRI scan would also be helpful in such a situation • Bone biopsy under aseptic conditions -preferred way to identify the causative pathogen • Important pathogens- Bacteroides fragilis, E coli, Proteus mirabilis, and Klebsiella pneumoniae; Pseudomonas aeruginosa is usually not the causative organism 28Basil Tumaini, May Shoo
  • 29. Management • Treatment of diabetic foot infections varies by type, as follows: • Cellulitis – Most responsive to antibiotics • Deep skin and soft-tissue infections – Usually curable, but additional debridement is usually indicated • Acute osteomyelitis – Infecting microorganisms and the likelihood of successful treatment with antimicrobial therapy are essentially the same as in patients without diabetes • Chronic osteomyelitis – Surgical debridement is essential, in addition to antibiotics; amputation may be necessary 29Basil Tumaini, May Shoo
  • 30. Fungal nail infection • Nails infected with a fungus become discolored (yellowish- brown or opaque), thick and brittle, and may separate from the rest of the nail. – In some cases, the nail may crumble. – The dark, moist, and warm environment of shoes can promote fungal growth. – In addition, an injury to the nail put the patient at an increased risk for a fungal infection. – Fungal nail infections are difficult to treat. – Drugs applied directly to the nail only help a small number of fungal nail problems. • Pills may be used, and periodic removal of the damaged nail tissue." 30Basil Tumaini, May Shoo
  • 31. Fungal nail infection 31Basil Tumaini, May Shoo
  • 32. Athlete's foot • "Athlete's foot is a fungus that causes itching, redness, and cracking. Germs can enter through the cracks in your skin and cause an infection. • Antifungal are used to treat athlete's foot-be pills and/or creams applied directly * 32Basil Tumaini, May Shoo
  • 34. Calluses • "A callus is a build-up of hard skin, usually on the underside of the foot. • Calluses are caused by an uneven distribution of weight, generally on the bottom of the forefoot or heel. • Calluses also can be caused by improperly fitting shoes or by a skin abnormality. • Keep in mind that some degree of callus formation on the sole of the foot is normal. 34Basil Tumaini, May Shoo
  • 36. Calluses • After bath, use a pumice stone to gently remove the build-up of tissue. • Use cushioned pads and insoles in your shoes. • Medication also may be used to soften calluses. • DO NOT try to cut the callus or remove it with a sharp object.“ 36Basil Tumaini, May Shoo
  • 37. Localized callus • When an increase in pressure and discomfort occurs, people with normal sensation change their gait. • People with neuropathy do not feel pain and continue to walk in the same way. • This leads to a build up of callus at the site of most pressure. • Ultimately this hard, localized callus can cause the tissue underneath to breakdown forming ulceration. • As a preventive measure, all callus should be removed. • It is particularly important to note that bleeding callus is indicative of possible ulceration and should be removed immediately. 37Basil Tumaini, May Shoo
  • 40. Corns • "A corn is a build-up of hard skin near a bony area of a toe or between toes. • Corns may be the result of pressure from shoes that rub against the toes or cause friction between the toes. • Use a pumice stone to gently remove the build- up of tissue. • Do not use over-the-counter remedies to dissolve corns. Or cut the corns with a sharp object. 40Basil Tumaini, May Shoo
  • 42. Bunions • "A bunion forms when the big toe angles in toward the second toe. Often, the spot where big toe joins the rest of the foot becomes red and callused. • The area may begin to stick out and become hard. Bunions can form on one or both feet. • Bunion may run in the family, but most often are caused by wearing high-heeled shoes with narrow toes. The shoes put pressure on the big toe, pushing it toward the second toe. • The use of felt or foam padding on the foot may help protect the bunion from irritation. • A device also may be used to separate the big and second toes. If the bunion causes severe pain and/or deformity, surgery to realign the toes may be necessary 42Basil Tumaini, May Shoo
  • 43. Blisters • Wearing shoes that do not fit properly or wearing shoes without socks can cause blisters, which can become infected. • When treating blisters, it's important not to "pop" them. • The skin covering the blister helps protect it from infection. • Use an antibacterial cream and clean, soft bandages to help protect the skin and prevent infection. 43Basil Tumaini, May Shoo
  • 44. Plantar warts • "Plantar warts look like calluses on the ball of the foot or on the heel. • They may appear to have small pinholes or tiny black spots in the centre. • The warts are usually painful and may develop singly or in clusters. • Plantar warts are caused by a virus that infects the outer layer of skin on the soles of the feet. • Over-the-counter medications to dissolve the wart should not used. 44Basil Tumaini, May Shoo
  • 48. Ingrown toenail • "Ingrown toenails occur when the edges of the nail grow into the skin. • They cause pressure and pain along the nail edges. • The edge of the nail may cut into the skin, causing redness, swelling, pain, drainage, and infection. • The most common cause of ingrown toenails is pressure from shoes. • Other causes include improperly trimmed nails, crowding of the toes, and repeated trauma to the feet from activities such as running, walking, or doing aerobics. 48Basil Tumaini, May Shoo
  • 49. Ingrown toenail • Keeping your toenails properly trimmed is the best way to prevent ingrown toenails. • Surgery to remove part of the toenail and growth plate may be needed. 49Basil Tumaini, May Shoo
  • 51. Diabetic neuropathy Can affect: sensory motor and autonomic fibers 51Basil Tumaini, May Shoo
  • 52. Peripheral neuropathy–Sensory motor • Most common form of neuropathy • The prevalence of peripheral neuropathy is very dependent on the sensitivity of the test used. • However, it is generally accepted that with standard clinical examination and objective testing, approximately 50% of people will have neuropathy after 15 years of diabetes • The long nerves of the feet and hands are affected in what is commonly known as a ‘glove and stocking distribution’. When the neuropathy has reached the knees, usually the hands become involved. 52Basil Tumaini, May Shoo
  • 53. Causes/risk factors of DN 1. Metabolic factors, such as high blood glucose, long duration of diabetes, abnormal blood fat levels, and/or low levels of insulin 2. Neurovascular factors, leading to damage to the BV that carry oxygen and nutrients to nerves 3. Autoimmune factors that cause inflammation in nerves 4. Mechanical injury to nerves, such as carpal tunnel syndrome 5. Inherited traits that increase susceptibility to nerve disease 6. Lifestyle factors, such as smoking or alcohol use 53Basil Tumaini, May Shoo
  • 54. Pathophysiology • Among the metabolic factors that contribute to dev. of neuropathy , Polyol pathway activity has been most important • The polyol pathway is comprised of two steps: – (1) the conversion of glucose to sorbitol by aldose reductase (localized to paranodal Schwann cells and endoneurial microvessels ) – (2) the conversion of sorbitol to fructose by sorbitol dehydrogenase. • Glucose is converted to the sugar-alcohol (polyol) sorbitol using NADPH as a coenzyme, which has a close affinity to aldose reductase 54Basil Tumaini, May Shoo
  • 55. Pathophysiology … • Accumulation of sorbitol, perturbation of phosphoinositide metabolism, as well as alterations of coenzymes, leads to neural lesions • Increased non enzymatic glycation of structural proteins is also considered to be another factor in pathogenesis of DN. • Advanced glycation end products resulting from hyperglycemia act on specific receptors, inducing monocytes and endothelial cells to increase the production of cytokines and adhesion molecules which also, have an effect on matrix metalloproteinases, which might damage nerve fibers. 55Basil Tumaini, May Shoo
  • 56. Peripheral neuropathy–Sensory motor • Bilateral- Unlike peripheral vascular disease, which can involve only one limb, peripheral neuropathy affects both feet, with approximately equal symptoms in each limb. • Unlike peripheral vascular disease, which can involve only one limb, peripheral neuropathy affects both feet, with approximately equal symptoms in each limb. 56Basil Tumaini, May Shoo
  • 57. Diabetic peripheral neuropathy – risk factors • The poorer the glycaemic control, and • the longer the duration of diabetes, the higher the risk of developing foot problems. • These are the two most important risk factors. • The older the person, the higher the risk. • Interestingly, the taller the person, the higher their chance of developing neuropathy. This appears to be explained by the fact that the most distal part of the nerve is damaged first. Diabetic neuropathy is also known as the ‘dying back’ disease. • Excessive alcohol 57Basil Tumaini, May Shoo
  • 58. Sensory neuropathy Deep sensory perception is reduced resulting in loss of protective reflexes against physical injury. Overshooting due to loss of joint position  Joint injuries Typically, manifests in a sock - like distribution. 58Basil Tumaini, May Shoo
  • 59. Manifestations of sensory neuropathy • Painful with these symptoms: –burning –pins and needles –pain • Painless (or insensate) - No symptoms 59Basil Tumaini, May Shoo
  • 60. Nerve damage – neuropathy • Symptoms of painful neuropathy include – numbness, – burning, – pins and needles, and – pain that can be excruciating, – distressing and difficult to treat satisfactorily. – These symptoms occur bilaterally and tend to be worse at night. • The majority of people with neuropathy, however, experience no symptoms, despite having significant disease. These people are more likely to develop problems as they are not aware of their feet, having lost their sensation of pain. 60Basil Tumaini, May Shoo
  • 61. Most of us experience pain when we injure our foot. This alerts us to examine the foot and treat it as necessary 61Basil Tumaini, May Shoo
  • 62. Painless nature of diabetic foot disease • However, in the insensate foot, pain sensation is absent. • A significant amount of damage can occur; people are completely oblivious to this until they notice blood or swelling. • For this reason it is often said that people with insensate neuropathy can have quite major surgical procedures performed without the need for anaesthetic. Basil Tumaini, May Shoo
  • 63. Sensory nerve damage • This slide shows a person who attended a foot clinic for treatment of ulceration, completely unaware that they were walking with a thumb- tack stuck into their foot. • Had the tack not been found, this injury could quite easily have become infected, leading to serious consequences 63Basil Tumaini, May Shoo
  • 64. Sensory nerve damage 64Basil Tumaini, May Shoo
  • 65. Motor nerve damage • As well as affecting the sensory nerves, peripheral neuropathy affects the motor nerves of the feet. • This causes weakness in the intrinsic muscles of the feet, leading to contraction of the muscles and clawed toes. • As the toes claw back, the fat pads are pulled forward from under the metatarsal heads, increasing the pressure under these metatarsal heads and on the tips of the toes (common places for neuropathic ulceration). 65Basil Tumaini, May Shoo
  • 67. Motor neuropathy Denervation and atrophy of small foot muscles leading to malum perforans, transverse foot arch instability with clawing and splay foot Hammer toe Claw toe Hallux valgus, hammer toes, erythema over pressure points 67Basil Tumaini, May Shoo
  • 69. Motor nerve damage 69Basil Tumaini, May Shoo
  • 70. Charcot’s arthropathy • Charcot’s arthropathy is a condition that is associated with end stage peripheral neuropathy. • While the pathogenesis of this condition is still under debate, one reasonable explanation is that with the onset of autonomic neuropathy, a ‘shunting’ between the arteries and veins occurs. • This leads to an increase in blood flow to the foot – hence the term ‘warm neuropathic foot’. • This increase in blood flow provokes the demineralization of the bones, making them soft and weak. 70Basil Tumaini, May Shoo
  • 71. Charcot’s arthropathy • Insensate people can easily damage these weak bones, leading to dislocation and/or fracture. • People do not feel pain and continue walking on the damaged foot, causing the bony architecture of the foot to collapse. • This condition is often misdiagnosed as gout, septic arthritis or osteomyelitis. • A good rule of thumb is that if a person has a unilateral hot, swollen foot, with no obvious portal for infection, consider Charcot’s arthropathy. 71Basil Tumaini, May Shoo
  • 72. Charcot’s arthropathy • Artery-vein shunting • Increased blood flow • Bone resorption • Commonly misdiagnosed 72Basil Tumaini, May Shoo
  • 73. Acute vs chronic Charcot’s arthropathy • It is very important to understand that there are two phases in Charcot’s. The acute phase, and the burnt out or chronic phase. • If a patient comes to you with a – unilateral warm swollen foot that is – relatively pain free, – with bounding pulses and – with or without some deformity, – and if there is no obvious portal for infection, an acute Charcot’s needs to be considered. This will be a very different foot from the burnt out Charcot’s where there is little or no temperature difference and the foot is rigid and misshapen. 73Basil Tumaini, May Shoo
  • 74. Acute vs chronic Charcot’s arthropathy• Unilateral • Warm, swollen • Relatively pain free • Bounding pedal pulses • Deformity may be present • No temperature difference • Rigid foot deformity • Grossly misshapen foot 74Basil Tumaini, May Shoo
  • 77. The typical appearance of a later- stage Charcot foot with a rocker-bottom deformity4 77Basil Tumaini, May Shoo
  • 78. Lateral X-ray of a Charcot foot deformity Dislocation of the tarsometatarsal joint with break in the talo-first metatarsal line (dashed lines) and a reduced calcaneal inclination angle 4 78Basil Tumaini, May Shoo
  • 79. 79 Lee C. Rogers, et al. The Charcot Foot in Diabetes. Diabetes Care Sep 2011, 34 (9) 2123-2129; DOI: 10.2337/dc11-0844 Basil Tumaini, May Shoo
  • 80. Charcot’s arthropathy – treatment • Acute phase – Non weight-bearing – Total contact cast • Chronic phase – Orthopaedic surgery 80Basil Tumaini, May Shoo
  • 81. Management4 Offloading • Offloading at the acute active stage of the Charcot foot is the most important management strategy • could arrest the progression to deformity • the foot should be immobilized in an irremovable total contact cast (TCC) • the patient should use crutches or wheelchair and should be encouraged to avoid weight bearing on the affected side Others: Surgical 81Basil Tumaini, May Shoo
  • 82. Autonomic neuropathy • Vasodilation  Oedema • ↓Sweating thus foot is warm, dry, scaly which predisposes to fissure formation Callus formation at pressure points and dry skin are substrate for ulceration Pes cavus resulting in callus formation over the pressure points 82Basil Tumaini, May Shoo
  • 84. AUTONOMIC NERVE DAMAGE 84Basil Tumaini, May Shoo
  • 86. Peripheral vascular disease • Cause: decreased perfusion due to macrovascular disease • Sites: more distal Tibial and peroneal arteries (segment between the knee and the ankle but aortic-illiac to knee less frequently) 86Basil Tumaini, May Shoo
  • 87. Peripheral vascular disease in diabetes • 15-40 times more likely to have lower limb amputation • People over 70 years have a 70-fold increased risk of amputation 87Basil Tumaini, May Shoo
  • 88. Risk factors characteristics of atherosclerosis in diabetes • More common • Affects young age group • No sex difference • Smoking • Faster in progress 88Basil Tumaini, May Shoo
  • 90. Peripheral vascular disease • Symptoms – Intermittent claudication – Rest pain • No symptoms – Inactivity – Neuropathy 90Basil Tumaini, May Shoo
  • 91. Signs of vascular disease • Diminished or absent pedal pulses • Coolness of the feet and toes • Poor skin and nails • Absence of hair on feet and legs 91Basil Tumaini, May Shoo
  • 92. Peripheral vascular disease and diabetes • Symptoms and signs of peripheral vascular disease • There are four stages: 1. Occlusive disease without symptoms 2. Intermittent claudication 3. Ischaemic rest pain (nighttime) 4. Ulceration/gangrene 92Basil Tumaini, May Shoo
  • 93. Vascular assessment Palpation of foot pulses – Dorsalis pedis (10% absent due to anatomical reasons) – Tibialis posterior 93Basil Tumaini, May Shoo
  • 94. Peripheral vascular disease non-invasive evaluation • Methods – Doppler pressure studies (ABI) – Duplex arterial imaging • Rationale- The degree of vascular disease can be used to: – Identify and confirm presence of disease – predict whether the ulcer will heal without surgical intervention. – determine need for early surgical intervention 94Basil Tumaini, May Shoo
  • 95. Peripheral vascular disease non-invasive evaluation • Doppler ultrasound – |The ABI- Measures pressure at brachial, pedal and toe arteries – The ABI is an estimate of the lower limb blood flow – The SBP of the brachial artery is divided into the SBP of the pedal arteries. – Ankle Brachial Index (ABI) <0.9 abnormal 0.9 to 1.0 normal >1.3 non-compressible 95Basil Tumaini, May Shoo
  • 96. Peripheral vascular disease non-invasive evaluation • Duplex arterial imaging – allows narrowing or obstruction of blood vessels to be localized • through the detection of either disturbance or absence of flow. • An accurate roadmap of all the arteries in the leg can be generated using this technique, which avoids the pitfalls associated with the interpretation of Doppler pressure measurements and calcification 96Basil Tumaini, May Shoo
  • 97. Peripheral vascular diseaseTreatment • Quit smoking • Walk through pain – Surgical intervention Studies have shown that the results from angioplasty and a formal exercise programme – ‘walking through the pain barrier’ – are similar. • People should be reassured that walking with claudication is not dangerous. 97Basil Tumaini, May Shoo
  • 98. Peripheral vascular disease • They should be asked to continue walking after the onset of claudication to encourage the development of collateral blood supply to the limbs. • If this fails, bypass surgery is required. • In the past this has always been considered unsatisfactory in people with diabetes because the vessels that are involved in the lower limbs are smaller. • In recent times, however, the success rate has improved. 98Basil Tumaini, May Shoo
  • 100. Examination  Neurological examination ◦ Vibration perception – tuning fork at 128 Hz ◦ Light pressure - Simmes – Weinstein 10 gram monofilament ◦ Light touch ◦ Two point discrimination ◦ Pain ◦ Temperature perception ◦ Deep tendon reflexes ◦ Clonus ◦ Babinski test ◦ Romberg test  Vascular Examination ◦ Palpation of pulses ◦ Skin/limb colour changes ◦ Presence of edema ◦ Temperature gradient ◦ Skin changes  Abnormal wrinkling  Absence of hair  Onychodystrophy ◦ Venous filling time 100Basil Tumaini, May Shoo
  • 101. Examination  Dermatological ◦ Skin appearance ◦ Calluses ◦ Fissures ◦ Nail appearance ◦ Hair growth ◦ Ulceration/infection/ gangrene ◦ Interdigital lesions ◦ Tinea pedis ◦ Markers of diabetes  Musculoskeletal ◦ Biomechanical abnormalities ◦ Structural deformities ◦ Prior amputation ◦ Restricted joint mobility ◦ Tendo Achilles contractures ◦ Gait evaluation ◦ Muscle group strength testing ◦ Plantar pressure assessment 101Basil Tumaini, May Shoo
  • 102. Do not forget the shoes ! 102Basil Tumaini, May Shoo
  • 103. Neuropathic vs Ischemic Ulcer Neuropathic Ischaemic Position Pressure areas Plantar Aspect Lateral and medial aspects due to compression Swelling Dry Swollen Pain Painless Very painful Warmth No Yes Necrosis +/- Yes Appearance Clean Ulcer Pus & Smelling 103Basil Tumaini, May Shoo
  • 104. Classification - Wagner • Grade 0 - Skin intact, no foot deformity • Grade 1 - Superficial ulcer • Grade 2 - Deep ulcer • Grade 3 - Deep ulcer with infection • Grade 4 - Limited necrosis • Grade 5 - Necrosis of the entire foot 104Basil Tumaini, May Shoo
  • 105. Wagner grade 0 105Basil Tumaini, May Shoo
  • 106. Wagner grade 1 106Basil Tumaini, May Shoo
  • 107. Wagner grade 2 107Basil Tumaini, May Shoo
  • 108. Wagner grade 3 108Basil Tumaini, May Shoo
  • 109. Wagner grade 4 109Basil Tumaini, May Shoo
  • 110. Wagner grade 5 110Basil Tumaini, May Shoo
  • 111. INVESTIGATIONS Can be group into 4 categories. 1) Biochemical 2) Vascular 3) Neurological 4) Foot imaging 111Basil Tumaini, May Shoo
  • 112. Laboratory evaluation • FBS/RBS • Glycosylated hemoglobin (HbA1C) • FBP + ESR • Wound and Blood cultures • Serum Chemistry: CRP • Urinalysis 112Basil Tumaini, May Shoo
  • 113. Imaging Plain X-rays - Osteomyelitis, fractures - Soft tissue gas - Dislocations in neuropathic arthropathy CT Scan Technetium bone scans - osteomyeletis MRI - osteomyelitis 113Basil Tumaini, May Shoo
  • 114. VASCULAR AND NEUROLOGICAL INVESTIGATIONS • Indicated to evaluate the extend of occlusive vascular disease and assessment of healing potential  Doppler segmental arterial pressure  Ankle brachial Index(ABI) normal is 1.1 while <0.9 abnormal  Toe pressure measurement, • Sensory examination with a 5.07 Semmes Weinstein monofilament wire  Single most practical measure of risk assessment  BUT is cost effective 114Basil Tumaini, May Shoo
  • 115. MANAGEMENT • Five aspect of patient treatment 1. Mechanical control 2. Metabolic control 3. Microbial control 4. Vascular management 5. Education 115Basil Tumaini, May Shoo
  • 116. Management • Preventative foot care • Diabetic foot ulcer (DFU) care • Ischemia management • Neuropathy management • Surgery 116Basil Tumaini, May Shoo
  • 117. Preventative foot care  Podiatry - Regular inspection of the foot, appropriate nail care, warm (32oC) soaks, moisturizing creams, early detection of new lesions  Optimally fitted footwear – well cushioned sneakers, custom molded shoes  Pressure reduction – cushioned insoles, custom orthoses  Patient education — need for daily inspection and necessity for early intervention, avoidance of barefoot walking  Physician education — significance of foot lesions, importance of regular foot examination, and current concepts of diabetic foot management 117Basil Tumaini, May Shoo
  • 118. Diabetic Foot Ulcer care  Debridement – of callus and necrotic tissue using sharp debridement till bleeding tissue, lavage with 0.9%NaCl  Dressing  Honey, Mabble cream or Paraffin gauze  Open dressing advisable  Avoid corrosive solutions like – Eusol, H2O2, Spirit or Iodine  Offloading of the ulcer site to reduce ischaemia via total contact cast, non weight bearing (crutches, bedrest, wheel chair)  Wound management – maintenance of a moist wound with regular cleaning and dressing  Infections treated with broad spectrum antibiotics based on culture results. Clindamycin/flouroquinolone/metronidazole suitable empiric therapy 118Basil Tumaini, May Shoo
  • 119. Ischemia/neuropathy • Angiography evaluates for chance of catheter intervention or vascular surgery • Vascular bypass surgery successful if occlusion is supramalleolar but less so in inframalleolar PAOD • Aspirin is useful for primary and secondary prevention • Neuropathy treated pharmacologically with agents such as carbamazepine, gabapentin and pregabalin and prevention of minor trauma that will go undetected due to insensate foot 119Basil Tumaini, May Shoo
  • 120. Surgery • Sharp debridement • Local procedures to remove areas of chronically elevated pressure (deformities) causing non healing ulcers • Sequestrectomies • Amputation • Correct structural deformities — hammer toes, bunions, Charcot 120Basil Tumaini, May Shoo
  • 121. Indications for amputation • Uncontrollable infection or sepsis • Inability to obtain a plantar grade, dry foot that can tolerate weight bearing • Non ambulatory patient 121Basil Tumaini, May Shoo
  • 122. Common pathway Cause of diabetic amputation A person with diabetes has neuropathy and/or peripheral vascular disease. Trauma may occur that causes ulceration. If this fails to heal, infection and osteomyelitis can ensue. If the infection is not arrested, the patient might ultimately require an amputation. However in some hot and humid countries, in people with poor glycaemic control, underlying neuropathy and/or vascular disease do not need to be present; people can progress quickly from trauma to infection to amputation. Basil Tumaini, May Shoo
  • 123. Cause of diabetic amputation Pecararo Trauma Ulcer Failure to heal Infection Amputation Neuropathy or vascular disease 123Basil Tumaini, May Shoo
  • 124. This slide says it all… • This figure is terrifying especially when we know that up to 85% of amputations are preventable with early identification of the • at-risk foot and prompt treatment by a skilled multidisciplinary footcare team. 124Basil Tumaini, May Shoo
  • 125. Lessons from The Step by Step Foot Project2 • Training personnel in diabetic foot management, facilitating transfer of knowledge and expertise, and improved patient education improves: • foot ulcer management • reduces the incidence of foot ulcers • reduces amputation rates 125Basil Tumaini, May Shoo
  • 126. References 1. Boulton AJM, et al. Comprehensive Foot Examination and Risk Assessment: A report of the Task Force of the Foot Care Interest Group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care 2008; 31:1679. 2. Abbas ZG, Lutale JK et al, The ‘Step by Step’Diabetic Foot Project in Tanzania: a model for improving patient outcomes in less-developed countries. Int Wound J. 2011 Apr;8(2):169- 75 availabe at http://www.ncbi.nlm.nih.gov/pubmed/21266010 Accessed on 01/06/2016. 126Basil Tumaini, May Shoo
  • 127. References ... 3. Chiwanga, Faraja S., and Marina A. Njelekela. Diabetic Foot: Prevalence, Knowledge, and Foot Self-Care Practices among Diabetic Patients in Dar Es Salaam, Tanzania – a Cross- Sectional Study. Journal of Foot and Ankle Research 8 (2015): 20. PMC. Web. 1 June 2016. 4. Lee C. Rogers, et al. The Charcot Foot in Diabetes. Diabetes Care Sep 2011, 34 (9) 2123-2129; DOI: 10.2337/dc11-0844 5. Previous slides from Prof. Lutale and former students. 127Basil Tumaini, May Shoo