DIABETIC FOOT

Dr Martha Lungu
• Foot problems are an important cause of morbidity in patients with
diabetes mellitus
• The lifetime risk of a foot ulcer for patients with type 1 or 2 diabetes may
be as high as 34 percent , and the worldwide incidence of diabetic foot
ulcer is approximately 18.6 million people per year
• Management of diabetic foot ulcers accounts for a large number of
inpatient stays, has a high rate of hospital readmissions, and is associated
with a 2.5-fold risk of death compared with patients with diabetes
without foot ulcers
• Foot amputations, many of which are preventable with early recognition
and therapy, may be required in up to 20 percent of diabetic foot ulcers
 DIABETIC FOOT
• PVD is common among patients with diabetes
• Intermittent claudication is twice as common among diabetic patients
as among nondiabetic patients
• An increase in hemoglobin A1c by 1% can result in more than a 25%
risk of PAD.
• Major amputation rates are 5 to 10 times higher in diabetics than in
nondiabetics
• Because of these causal relations, the American Diabetes Association
recommends ABI screening every 5 years in patients with diabetes.
• Diabetic foot results from a combination of ischaemia (Peripheral
vascular disease), neuropathy, foot deformity and
immunocompromise that renders the feet of diabetic patients
particularly susceptible to sepsis, ulceration and gangrene.
• It is estimated that 60% to 70% of diabetic ulcers are due to
neuropathy, 15% to 20% are due to ischemia, and another 15% to
20% are due to a combination of both
Diabetic neuropathy affects the motor, sensory and autonomic
nerves.
• Neuropathy, which is present in over 80 percent of diabetes patients
with foot ulcers, promotes ulcer formation by decreasing pain
sensation and perception of pressure, by causing anatomic
deformities (such as hammer toes from greater flexor muscle tone
compared with extensor tone, loss of arch, and/or rocker bottom
feet associated with Charcot foot), and by impairing the
microcirculation and the integrity of the skin.
• Once ulcers form, healing may be delayed or difficult to achieve,
particularly if infection penetrates to deep tissues and bone and/or
there is diminished local blood flow.
Polyol Or Sorbitol Pathways on diabetic neuropathy
In diabetics, when glucose levels are elevated, other pathways like the
sorbital pathway are upregulated to handle the glucose effectively.
The sorbital pathway increases in activity in tissues like the retina,
kidneys, peripheral nerves and blood vessels where insulin is not
required for cellular glucose uptake. These tissues don’t have the
enzyme sorbital dehydrogenase
Extra glucose is shunted into the polyol pathway and converted to
sorbitol and fructose by the enzymes aldose reductase and sorbitol
dehydrogenase.
Accumulation of sorbitol and fructose lead to reduced nerve
myoinositol, decreased membrane Na+/K+ -ATPase activity, impaired
axonal transport, and structural breakdown of nerves, causing abnormal
action potential propagation.
This is the rationale for the use of aldose reductase inhibitors to improve
nerve conduction
Sorbital doesn’t diffuse through cell membranes easily, so it accumulates
and causes osmotic damage and neuropathy develops.
The lack of consensus warrants further research into the indications and
effectiveness of aldolase reductase inhibitors as a potential
breakthrough in diabetic treatment.
Sensory neuropathy
The patient is incapable of feeling pain. Minor trauma – for example,
from a stone in the shoe – remains unnoticed.
Even severe ischaemia and/or tissue loss that would lead a sensate
patient to seek urgent medical advice may be completely painless.
Motor neuropathy
The normal structure and function of the foot depends not only upon ligaments,
but also upon the long and short flexors and extensors of the calf and foot.
The motor neuropathy leads to collapse or dislocation of the interphalangeal or
metatarsophalangeal joints, causing pressure on areas with little protection.
This exposes the metatarsal heads to abnormal pressure, and they are a frequent
site of callus formation and ulceration
There is also severe micro- and macrovascular circulatory impairment. Once
ulceration occurs, the chances of healing are poor
• Motor dysfunction of peripheral nerves in diabetic neuropathy leads
to muscular imbalances in the diabetic foot
• In diabetic people with neuropathy, even if successful management
results in healing of the foot ulcer, the recurrence rate is 66% and the
amputation rate rises to 12%.
Autonomic neuropathy
Autonomic neuropathy involves damage to the nerves that carry
information from the brain and spinal cord
The information is then carried to the heart, blood vessels, bladder,
intestines, sweat glands, and pupils
Major clinical manifestations of DAN include resting tachycardia,
exercise intolerance, orthostatic hypotension, constipation,
gastroparesis, erectile dysfunction
.
This leads to a dry foot deficient in the sweat that normally lubricates the
skin and contains antibacterial substances.
The result is scaling and fissuring of the skin, and the creation of a portal
of entry for bacteria
Lack of autonomic tone in the capillary circulation causes shunting of
blood from arteries directly into veins, bypassing the tissues that need
nutrition.
This results in a foot that feels warm and has distended veins and
bounding pulses. Despite these apparent signs of adequate perfusion, the
foot is vulnerable to local "microvascular" gangrene, will heal very poorly
and slowly, and will be less able to resist infection.
Diabetes-related atherosclerosis
People with diabetes mellitus (DM) have a higher incidence
of atherosclerosis
significant atherosclerotic disease of the infra popliteal segments is
particularly common in the diabetic population.
The pathophysiology of diabetic peripheral neuropathy is
multifactorial and is thought to result from vascular disease occluding
the vasa nervorum; endothelial dysfunction causing edema of nerve
trunks
• diabetic patients often present late, with extensive destruction of the
foot.
• Sensory neuropathy also affects proprioception such that, when
walking, pressure is applied at unusual sites. This leads to ulcer
formation and even joint destruction (Charcot's joint).
• Charcot foot (neuropathic osteoarthropathy), is a condition affecting
the bones, joints, and soft tissues of the foot and ankle,
characterized by inflammation in the earliest phase.
• The hallmark deformity associated with this condition is midfoot
collapse, described as a “rocker-bottom” foot
• Pain or discomfort may be a feature of this disorder at the active
(acute) stage, but the level of pain may be significantly diminished
when compared with individuals with normal sensation and
equivalent degrees of injury.
• Loss of protective sensation will increase the likelihood of trauma to
the foot, while motor neuropathy could result in altered structure of
the foot (with exaggeration of the plantar arch and clawing) and
changed gait with resultant abnormal loading.
• Because the foot is numb, pain from fractures or other traumas can
go unnoticed, leading to additional damage from walking and
standing.
• As the bones continue to weaken, the joints of the foot can become
dislocated or collapse, changing the foot’s shape. The resulting shape
is referred to as rocker-bottom foot, since the arch extends down and
out, creating a rocker-like appearance.
• The care of diabetic patients should start with preventive measures,
and it is important to avoid infections in patients with insensate feet
because of neuropathy
These patients need to wear properly fitted shoes at all times for
protection.
Diabetic patients may be unaware of the presence of infections or
ulcerative lesions because of peripheral neuropathy and a decreased
ability to sense pain
Patients with diabetic neuropathy tend to have decreased vibration
and position sense and decreased reflexes.
 DIAGNOSIS
History
• Diabetics should be questioned about the duration of illness; type of
medication used and compliance; diet; exercise; footwear and
symptoms relating to eyesight, renal status and foot problems.
• Risk factors for atherosclerotic disease should be similarly enquired
about.
• A history of prior foot ulceration is a significant risk factor for
identification of the high risk patient. However since symptoms may
be delayed in the neuropathic foot, every diabetic should have their
feet examined at every clinic visit
Physical exam
• A rapid systematic examination of the foot can be developed. The
condition of the nails should be examined for paronychia, ingrown
nails or onchomycosis; of the skin for fungal infection in the inter-
digital areas, for edema, colour and temperature; for evidence of
foot deformity
Neurologic exam Assessment of the presence of neuropathy is a vital
tool in the identification of the high risk patient
vascular evaluation of the presence and severity of arterial and/or
venous insufficiency
Laboratory evaluation should include
• complete blood count
• blood glucose, electrolytes, and renal function.
• Baseline and subsequent inflammatory markers such as erythrocyte
sedimentation rate (ESR) and C-reactive protein (CRP) can be useful
for monitoring response to therapy.
• samples for Gram stain and culture are appropriate. Aerobic and
anaerobic cultures of deep tissue or bone biopsies should be
obtained at the time of debridement if deep tissue infection or
osteomyelitis is suspected.
Noninvasive vascular assessment
Since vascular insufficiency is a strong risk factor for failure of ulcer
healing and for amputation, every patient with absent pedal pulses
should undergo non-invasive assessment.
Segmental pressures determined by hand held Doppler will be
adequate in the majority of patients. An ankle/brachial index (ABI) <
0.8 is indicative of vascular insufficiency consistent with claudication
ABI<0.4 is indicative of more severe disease associated with rest pain
and limb threatening ischemia
Radiology
• Every foot harboring a diabetic ulcer should be x rayed to assess for
the presence of osteomyelitis or other abnormalities such as
Charcot’s foot. These two entities may be difficult to distinguish
radiologically.
• magnetic resonance imaging (MRI) can be performed to better
evaluate for soft tissue abnormalities and osteomyelitis.
The University of Texas Diabetic Foot
Classification
• The University of Texas Diabetic Foot Classification can be used in the diabetic
clinic as a means of identifying the high risk patient and guiding intervention.
The first 4 categories are entirely lacking foot lesions and intervention here is
preventative.
Category 0: the protective sensation is intact. Patients in this category have 1/5
the risk of developing foot ulcer than subsequent categories. Education on
footcare is given and the patient may be seen annually.
Category 1: LOPS (loss of protective sensation) is found but without history of
previous ulceration. Footcare education and prescription of therapeutic shoes is
recommended and closer follow-up every 6 months.
Category 2: LOPS and deformity mandates closer follow-up every 3 months and
possible elective corrective surgery.
• Category 3: LOPS, deformity and a history of previous ulceration
indicates the highest level of risk and mandates monthly follow-up.
Category 4: The first category with actual ulceration is divided into A –
non-infected, non-ischemic neuropathic ulcer – all U of Texas Stage A
ulcers and B– acute Charcot’s foot. Treatment of 4A is primarily
debridement and orthotic device, such as total contact casting.
Treatment of Charcot’s foot is primarily directed at immobilization
and stress reduction in the acute phase.
Category 5: Infected diabetic foot – treatment directed
towards control of infection as well as underlying
abnormalities.
Category 6: Ischemic foot – ABI<0.6; Toe
pressure<40mmHg; TCO2<30mmHg. A referral to a
vascular surgeon is indicated
Management of Diabetic foot
• Management of diabetic foot infections requires attentive wound management,
good nutrition, appropriate antimicrobial therapy, glycemic control, and fluid and
electrolyte balance
• The treatment of diabetic wounds involves local and systemic measures.
Local Measures
• If the blood supply to the foot is adequate, dead tissue can be excised
(debridement) in the expectation that healing will occur, provided infection is
controlled and the foot is protected
• If there is ischaemia as well, the priority is to revascularize the foot, if possible
(Angioplasty, bypass surgery)
• Many diabetic patients present late, with extensive tissue loss and
‘unreconstructable’ disease, which accounts for the very high amputation rate
Systemic measures
• Most diabetic wounds are infected, and eradication of the infectious
source is paramount to the success of healing
• Treatment should address the possible presence of osteomyelitis and
should employ antibiotics that achieve adequate levels both in soft
tissue and bone
• Glycaemic Control
• Other supportive measures: rehydration…