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DEFINITION to be absorbed into the cells.

Consequently the blood glucose levels
Defined as a group of syndromes in within nerve axons will be directly
which neuropathy, ischemia and proportional to that of blood. Glucose
infection lead to tissue breakdown is then transformed into sorbitol and
resulting in morbidity and amputation. fructose which eventually leads to
numerous biochemical and functional
EPIDEMIOLOGY abnormalities. As the rate of polyol
pathway is directly dependent on the
The lifetime risk that a diabetic patient level of glucose, persistent
will acquire foot lesions hyperglycemia feeds the process.
(ulcers/gangrene) has been estimated
at 15% to 25%, with an annual SENSORY NEUROPATHY
incidence of 1.0% to 4.1%. The
incidence of these lesions appears There is a symmetrical sensory loss in
similar in type 1 vs. type 2 diabetic glove and stocking distribution.
patients, although type 2 diabetic Patients can present with numbness,
patients comprise approximately 90% paresthesia or burning under the feet.
of the total diabetic population. Ulcers commonly occur with minor
Diabetics are 15X more likely to have wounds that the patient is unaware of
an amputation than non-diabetics. e.g. improper trimming of nails,
thermal injuries (hot water bottles) and
In>15% of these patients, ulcers will foreign bodies entering the foot.
ultimately lead to amputation.
The risk for an initial foot ulcer is MOTOR NEUROPATHY
increased in patients who have had
diabetes for>10 years, are male, have With diabetics there is weakness and
poor glycemic control, and already wasting of the intrinsic muscles of the
have other cardiovascular, renal, or foot, which in turn leads to imbalance
retinal co morbidities between the long flexor tendons and
the extensor tendons resulting in the
AETIOLOGY/PATHOPHYSIOLOGY flexors dominating .Ultimately the
changes seen in the feet that of pes
The aetiology and pathophysiology of cavus(high arched foot) and clawing of
diabetic foot ulcer usually has many the toes(hammer toes).With the
components. Multicenter trial attributed clawing of the toes there is drawing of
63% of diabetic foot ulcers to the the fat pad normally under the
critical triad of peripheral sensory metatarsal heads forward, which
neuropathy, trauma and deformity. reduces the cushioning effect under
Other risk factors include ischaemia; the metatarsal head as a result there
callus and oedema .The risk factors for is increased pressure leading to
ulceration are also predisposing calluses which in turn act as foreign
factors for amputation. bodies and resulting in ulceration with
the clawing of the toes the toes
NEUROPATHY become non weight bearing which
further increases the pressure under
There are two theories the metatarsal heads and heels
1. Vascular-decreased blood supply to predisposing to ulceration.
the nerves leads to hypoxia of the
2. Metabolic-nerve tissue is unique as
it does not require insulin for glucose
AUTONOMIC NEUROPATHY There is an increased risk of infection
due to an impaired immune system.
This leads to loss of sweating and Impaired humoral immunity
changes in the normal microcirculation Impaired PMN function
auto regulation. Loss of sweating Loss of protective skin barrier
leads to a dry foot that may cause
fissures and cracks which predisposes CONNECTIVE TISSUE CHANGES
to ulceration. With the loss of
microcirculation auto regulation there Due to enzymatic glycosylation of
is increased peripheral blood flow collagen, it leads to stiffening of the
which leads to arterio-venous shunting connective tissue surrounding the
which leads to ischaemia of the joint. As a result there is limited joint
deeper tissues. mobility which leads to
· Stiffness of the joints of the foot
The shunts are about 20-70um in · Abnormal gait
diameter and are under sympathetic With continued hyperglycemia there is
control, with loss of tone the shunts continued catabolism with a negative
open and blood bypasses the capillary nitrogen balance. Synthesis of proteins
bed. such as fibroblasts and collagen is
impaired resulting in poor wound
ISCHAEMIA healing.

The incidence of PVD in diabetics is DIABETIC CHARCOT`S OSTEO-

4X more than non-diabetics. In ARTHROPATHY
diabetics the occlusive disease
involves primarily the tibial and It is a rare but serious complication. It
peroneal vessels between the ankle was first described by Dr Jean Charcot
and the knee. The distal vessels are in 1868.
usually spared. It affects <1% of diabetics. It is usually
Arterial disease in diabetics is due to unilateral, but 20% are bilateral.
atherosclerosis and medial sclerosis. It involves the following:
Atherosclerosis is 20x more common · Midtarsal joint 60%
than in non-diabetics. Diabetics have · Metatarsophalangeal joint 30%
decreased ability to develop collateral · Ankle joint 10%
circulation and as a result of
neuropathy, claudication or rest pain is PATHOPHYSIOLOGY
absent due to the neuropathy. The
critically ischaemic foot may be The exact aetiology of neuro-
relatively warm with little discoloration. arthropathy remains ill-defined.
Calcification of the tunica media The two major theories are:
produces a rigid tube as a result can · Neurotraumatic: proposes
falsely elevate arterial blood pressure. decreased protective sensation
Medial sclerosis does not cause allows cumulative mechanical
ischaemia. trauma to result in fractures
and joint destruction.
OEDEMA · In contrast the neurovascular
theory proposes that a neurally
Is common in diabetics and is usually initiated vascular reflex of
related to cardiac, renal or venous autosympatectomy leads to
disease. It impairs cutaneous increased bone blood flow and
circulation and impairs healing. It active bone resorption by
predisposes to ulcer formation. osteoclasts.
Four factors are essential for ASSESSMENT OF THE DIABETIC
arthropathy to develop FOOT
· Peripheral neuropathy
· Unrecognized injury 1. General assessment
· Increased local blood flow. 2. Assess comorbid condition
· Repetitive stress in injured · CVS
structures · Renal
· Neurological
The exact interplay between these · Eyes
factors has not been determined but it · Metabolic, water and
is believed that the process starts with electrolytes
ligamentous failure and proceeds to 3. Assessment of the foot.
subluxation or dislocation, with · Neuropathy
fractures or results in fixed deformity. · Ischaemia
· Deformity
Usually presents with painless o Callus
deformity of the foot which is hot o Swelling
swollen and erythematous. The o Skin breakdown and
differential to consider is gout, cellulitis ulcer evaluation
and osteomyelitis. o Infection
o Necrosis
The Charcot foot in the diabetic is
progressive condition that is not ASSESSMENT OF NEUROPATHY
confined to the bones but also affects
all the tissues in the lower extremity. It Up to 35% of patients have
is often confused with infection and asymptomatic neuropathy. The
osteomyelitis of the foot. Early classical neuropathic foot is warm, dry,
identification and management to insensitive, dilated veins, good pulses,
prevent amputation is essential. pes cavus, clawed toes and
hyperkeratosis under the forefoot and

General or systemic contributions: 1. Assess pain and touch with a pin

· Uncontrolled hyperglycemia and cotton wool
· Duration of diabetes 2. Ankle reflexes
· Peripheral vascular disease 3. Vibration sense with a tuning fork at
· Blindness or visual loss 128HZ.Three readings are taken at the
· Chronic renal disease medial malleolus and pulp of the great
· Older age toe. Inability to feel vibration at that
frequency indicates peripheral
Local issues neuropathy.
· Peripheral neuropathy 4. Nylon monofilament test
· Structural foot deformity o 10 point monofilament test
· Trauma and improper fitted used. Inability to feel more than
shoes 4 out of 10 points on the foot
· Callus indicates presence of sensory
· History of prior ulcer or neuropathy.
· Prolonged elevated pressure
· Limited joint mobility
The purely ischaemic foot will feel cool
· Previous ulcer and or amputation have absent pulses and trophic
changes. If any of the peripheral
pulses are felt significant ischaemia is
unlikely. If the pulses are absent or o Rocker bottom feet
asymmetrical then further tests are o Pes cavus
required. Approximately 60% of non- o Hallux valgus and hallux rigidis
healing ulcers are due to PAD. o Charcot’s foot
o Fixed flexion deformity of pip
o Flexion deformity of pip joints
1. Measurement of ankle
brachial index Deformity usually leads to a bony
prominence which results in high
o Normal is 0.9-1.1 pressure and ulceration.
o <0.45 is limb threatening
o Medial sclerosis can falsely ASSESSMENT OF PLANTAR
elevate the result PRESSURE
o A dampened waveform with a
normal ABI suggests calcified Normally the metatarsal heads and
vessels and a falsely elevated heels are the greatest weight bearing
ABI area. In diabetics there is loss of
protection of fat pads and reduced
2. Arterial Duplex: structural ankle joint dorsiflexion. This causes
location of stenosis, early lifting of the heels resulting in
occlusions and velocity and premature loading of the forefoot and
waveform of the blood increased duration of pressure.
These and other structural defects
3. Toe pressure measurements causes increase in pressure of forefoot
o This reflects blood flow more during the static and contact phases of
accurately in patients with the gait. Peak pressures maybe
diabetes. several folds higher than non-
o An absolute systolic measure diabetics. Foot pressure can be
<45mmHg is abnormal measured in the following ways:
1. Podotrack
4. Transcutaneous oxygen o Footprint mat that quantifies
measurements plantar pressure by visual
o A normal TcP02 is >55mmHg comparison between greyness
o A TcP02 <30mmHg suggests of the foot print and a
that wound healing is less calibration card
likely. o It is shown to identify 90% of
o It is an independent predictor high risk areas correctly
of ulceration and wound
healing. 2. Optical pedograph
o This is a computerized
INVASIVE VASCULAR TESTS pressure measurement device
o The system consists of a glass
A carefully performed arteriogram plate and is illuminated at its
must show the appropriate inflow edge by strip lights and
source and outflow target artery and covered with a thin sheet of
must incorporate the complete opaque reflective plastic
infrapopliteal circulation, including foot o >12.3kg/cm2 are at risk of
vessels. ulceration


o Skin cracks, fissures, calluses Look for bacterial and fungal

o Claw toes. Hammer toes infections. Fissures or cracked skin
between the toes and heels can act as o Detect subcutaneous air (non-
portal of entry for infection. Ulcers clostridial)
should also be probed to detect sinus o Detect foreign bodies
tracts, dissection of the ulcer into o Detect osteomyelitis
tendon sheaths and bone or joints. A XR are not sensitive for acute
positive probe to bone has a high infections of bone
predictive value for osteomyelitis. The o latent period of 10-14 days
existence of odour and exudates o needs 50% of bones loss
should be noted and if exudates are If the XR is negative but there is strong
present, they should be sent for MCS. suspicion of osteomyelitis then other
Generally limb threatening infections modalities available to make the
can be defined by cellulitis extending diagnosis.
beyond 2cm from the ulcer perimeter o Bone scan-falsely positive due
as well as a deep abscess, to hyperemia
osteomyelitis or critical ischaemia. o CT-scan can localize infection
Polymicrobial infections usually but cannot define proximal
predominate i.e.: extent of sepsis
· gram positive
cocci(Staphylococcus, MANAGEMENT
Streptococcus, Enterococcus)
· gram negative ( E.Coli, A multidisciplinary approach must be
Pseudomonas, Klebsiella, taken for patients with diabetic feet
Proteus) due to multifaceted nature of the co-
· anaerobes.(Bacteroides, morbidities that can occur in these
Clostridium perfringens, patients. This approach has
Peptostreptococcus) demonstrated significant improvement
in outcomes including reduction in
The typical inflammatory signs of incidence of major amputations.
infection, including erythema, rubor,
cellulitis, or tenderness, may be Treatment based on the Wagner
absent or diminished. Also frequently classification
absent are the usual systemic Grade 0: foot at risk, no ulceration
manifestations of infection, including Grade 1: superficial diabetic ulcer, no
fever, tachycardia, or elevated white infection
blood cell count. Unexplained Grade 2: extension of ulcer to deeper
hyperglycemia should prompt an tissue i.e. tendons, joints or fascia.
aggressive search for a source of Grade 3: deep ulcer with abscess or
infection because the patient’s osteomyelitis involving joints, bone, etc
elevated glucose level may be the only Grade 4: localized gangrene (wet/dry)
sign of impending problems. toe/foot
Grade 5: extensive gangrene
Careful palpation of the foot for areas
of tenderness or fluctuance is University of Texas Wound
important to detect undrained Classification System of Diabetic
abscesses in deeper tissue planes. All
Foot Ulcers
ulcers must be carefully inspected and
probed and superficial eschars Grade I-A: non-infected, non-ischemic
unroofed, to look for potential deep superficial ulceration
space abscesses
Grade I-B: infected, non-ischemic
RADIOLOGICAL EVALUATION superficial ulceration
Grade I-C: ischemic, non-infected
Should be done to: superficial ulceration
o Monitor bone and joint changes
Grade I-D: ischemic and infected and detect underlying abscesses or
superficial ulceration
Foot at risk:
The first step in the treatment of any
Identify patients at risk i.e. look at risk
neuropathic ulcer is restriction of
factors. Patients with foot at risk are
weight bearing of the involved
classed into the following categories
extremity. Patients with limb-
threatening foot infections and
Category 0: no sensory neuropathy-
noncompliant patients will require
once a year follow up
hospitalization and bed rest, followed
Category 1: sensory neuropathy –
by evaluation and management of
twice a year follow up
arterial ischemia.
Category 2: signs of neuropathy and
Uncomplicated neuropathic ulcers will
PAD and or foot deformities-once
often heal with topical therapy and
every 3 months
non-weight bearing, and a trial of
Category 3: previous ulcers-once a
outpatient care is warranted. Topical
dressings should be aimed at
maintaining a moist environment with
saline impregnated gauze, topical
antibiotic ointments, or other similar
The primary goal in treating ulcers is to
agents. The ulcer should be protected
obtain wound closure. Management of
from excessive pressure by placing of
the foot is determined by
an accommodative pad around the
· Severity(grade)
lesion to distribute pressure to
· Vascularity surrounding tissues.
· Infection Heavy callus around the edges of the
lesion should be trimmed away to
Rest and elevation should be instituted reduce peak plantar pressure, and
at the first presentation. shoes should be replaced with a stiff-
soled “healing sandal.”
Relief of pressure by “off-loading”: Custom-molded orthotics and extra-
· bed rest depth shoes, running shoes, or
· crutches custom-molded shoes in the case of
· wheelchair maybe severe foot deformity, are also
recommended to totally off load prescribed to prevent future
pressure from the foot recurrence.
· TCC (total contact cast) is
considered the optimal Hyperbaric oxygen therapy facilitates
management of neuropathic wound healing for diabetic foot ulcers
ulcers. Problem-must be and thus lower amputation rates by
reapplied weekly and requires promoting wound healing through anti-
considerable experience to edema, antibacterial, and
avoid iatrogenic lesions. neovascularization effects.
· Acceptable alternatives are
removable braces and half INFECTIONS
In the absence of deep infection or
Mainstay of treatment is debridement necrosis, minor infections or ulcers
of all necrotic tissue, callus and fibrous may be managed conservatively with
tissue local wound care, antibiotics, or both.
Unhealthy tissue must be debrided In patients with salvageable ischemic
back to bleeding tissue to allow full foot lesions and concomitant active
visualization of the extent of the ulcer infection, the infection needs to be
controlled before vascular surgical · amputation
In addition to instituting broad- VASCULARITY
spectrum antibiotics, options include
open debridement and drainage or Each operation must be individualized
partial foot amputation. A short delay according to the patient’s available
(usually <5 days) before venous conduit and arterial anatomy.
revascularization to control active Options include open surgical bypass
infection is justified; however, longer or endovascular intervention.
waits to “sterilize wounds” is Treatment of underlying ischaemia is
inappropriate and may result in further critical to a successful outcome
necrosis and a lost opportunity to save regardless of topical therapies.
the foot. Vascular consultation should be
sought when the patient presents with
Patients with limb-threatening · ischaemic wound
infections (Abscess, Cellulitis, · non healing ulcer despite
Osteomyelitis, Gangrene) require appropriate management
immediate hospitalization, A major component of limb salvage
immobilization, and intravenous surgery in these patients is to restore
antibiotics. Cultures from the depths of pulsatile flow to the foot.
the ulcer should be sent; wound swabs
are unreliable and should not be MEDICAL TREATMENTS
performed. .
Empiric broad-spectrum antibiotic Primary prevention involves
therapy should be initiated to cover the aggressive glycemic control (goal
poly-microbial infections usually seen hemoglobin A1C <6.5% to 7.0%);
in diabetic patients. Empiric antibiotic management of associated risk factors
regimens are dictated by institutional such as smoking, hypertension,
preferences, local resistance patterns, hyperlipidemia, and obesity; periodic
availability, and cost. physical examinations, including a
· Penicillin + Gentamycin + vascular examination; and probably
Metronidazole. most important, proper foot care and
· Augmentin hygiene strategies.
· Clindamycin+ Ciprofloxacin · Zero smoking
Patients with abscess formation or · Physical activity of 180
necrotizing fasciitis must undergo minutes/ week
prompt incision, drainage, and · BP < 140/90 mm Hg
debridement, including partial open · Cholesterol: Total < 5.0mmol/l
toe, ray, or forefoot amputation. LDL
cholesterol < 2.2 mmol / l
Wounds should be packed open with HDL
saline-moistened gauze, and cholesterol >1.0mmol/l fasting TG <
dressings should be changed two to 2.0 mmol/l
three times a day. Wounds should be · HbA1c < 6.5% in diabetics
examined daily, and additional bedside · BMI < 25
or operative debridement should be
repeated as needed. THE MANAGEMENT GOALS OF
Adequate dependent drainage is CHARCOT FOOT
crucial, and limited incisions with
closed-suction or Penrose drains Aim is to offload the affected
should be avoided. extremity, prevent further collapse and
Underlying osteomyelitis requires deformity, and protect the opposite
· bony resection foot. The first step of treatment is an
· antibiotics (culture driven) extended period of non-weight bearing
and castor splint immobilization to OFF LOADING
promote eventual healing of the joint.
The use of accommodative footwear is A final aspect of managing diabetic
essential to long-term management. foot ulcers is offloading to decrease
Surgery is rarely indicated, and a pressure on the extremity. Offloading
stabilizing procedure is done most strategies involve combinations of bed
safely after the disease has reached a rest, crutches or wheelchairs, casting,
quiescent stage. Amputation is foams or padding, and healing shoes
reserved for those rare patients with or walking boots.
severe uncorrectable deformities, Only after wound healing has been
those with chronic ulcers plagued by achieved should weight bearing be
such extensive osteomyelitis that the reinstituted back to baseline levels,
foot is unsalvageable, or after failed and consultation with a physical
open reconstructions. therapist should be obtained when
AMPUTATIONS The last alternative remains
amputation. Closed minor toe or
Certain patients may not be transmetatarsal amputations are
appropriate candidates for arterial practical after infection control and
reconstruction because of their overall revascularization and typically leave
health status. the patient with a functional foot for
Elderly patients with severe dementia walking.
who are non-ambulatory or bedridden, In situations involving extensive tissue
or who have severe flexion loss precluding a functional foot, when
contractures of the knee or hip, have there are non-healing wounds in the
no prospect of rehabilitation and are setting of patent grafts and for control
inappropriate candidates for traditional of sepsis, amputation below the knee
vascular procedures and will require is necessary.
primary amputation.
Patients with terminal cancer with a PREVENTION
very short life expectancy or similar
lethal co-morbidities do poorly with Foot examination should be performed
open revascularization and are in diabetic patients at least once a
probably better served by year and more frequently in those
endovascular intervention or primary patients at high risk of foot ulceration.
amputation. Identification of patients at risk is the
Patients with an unsalvageable foot most important aspect of amputation
due to extensive necrosis from prevention. Education is an integral
ischemia or infection also require part of prevention, should be simple
primary amputation. and repetitive. Education should be
targeted at both healthcare providers
Natural history of amputations: and patients. Several studies have
30 day post op mortality: shown that foot care programs
– AKA 13-16%, BKA including education, regular
6-9 % examinations and risk categorization
– Up to 50% can reduce the occurrence of foot
Survival (3 years): lesions in up to 50% of patients.
– AKA 39% BKA 57%
– BKA : 60%, AKA :
40% DO’s:
• wash feet daily, dry well,
• check hidden areas carefully
• anti-fungal powder
• careful nail hygiene
• early treatment of wounds
• wear comfortable, well fitted
• natural fibre socks are best

• walk barefoot EVER
• wear new shoes without
“breaking in”
• leave wounds untreated
• burn your feet
• cut nails too short
• ignore discomfort


• Callus formation
• Ulceration
• Ischaemic change
• Acute local sepsis
• Non-healing trauma

• recurrent callus / ulceration
• worsening deformity
• worsening neuropathy
• deteriorating sugar control
• onset of ischaemic symptoms

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