Diabetic Foot

Clinical Evaluation and Imaging

Dr. Seleno Glauber

2023
 Epidemiology
• U.S. data
– 250 million diabetics by 2025
– 2-5% of diabetics develop foot ulcer annually
– Prevalence of ulceration estimated at 4-10%
– 40-60% of all non-traumatic lower extremity
amputations are in diabetics
– 85% of these preceded by foot ulcer
 Pathogenesis
• Multi-factorial, Complex and still poorly
understood
– Neuropathy
– Vasculopathy
– Immune dysfunction
– Infection
• Prolonged Hyperglycemia contributes to all the
above factors through different mechanisms
 Complex interplay of factors
Vasculopathy
Motor
Neuropathy

Sensory
Neuropathy

Autonomic Immune
Neuropathy dysfunction

Ulbrecht JS, Cavanagh PR. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S73-82.
 Neuropathy
• Sensory
Unaware of minor cuts/bruises
– Loss of protective sensation
– Loss of position sense
Clawed toes
• Motor
– Muscle weakness Poor weight
– Foot deformity distribution
Prominent metatarsals
• Autonomic
– Poor blood flow regulation
Cracked skin allows easy
– Dry, stiff skin entry of bacteria
 Foot Ulcers

Inappropriately
high pressure
distribution

Ulbrecht JS, Cavanagh PR. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S73-82.
 Vasculopathy
• Accelerated atherosclerosis Decreased
local blood flow
– Diabetes
– Hypertension
– Obesity
– Age Poor Poor
antibiotic wound
– Dyslipidemia penetration healing

Heel ulcer is typical of poor blood

circulation due to vasculopathy
 Immune dysfunction
• Impaired defenses against infection
1.  Polymorphonuclear leukocyte migration
2.  Phagocytosis
3.  Intracellular killing
4.  Chemotaxis

2
1

4
3
 Infection
• Foot infections in diabetic patients usually
begin in a skin ulceration

• Most infections remain superficial

• 25% will spread contiguously from the skin to
deeper subcutaneous tissues and/or bone.

• An infected foot ulcer precedes 60% of

amputations.
 Infection
• Infection must be diagnosed clinically by the
presence of systemic signs (e.g., fever, chills, and
leukocytosis), purulent secretions (pus), or 2 local
classical signs or symptoms of inflammation (warmth,
redness, pain or tenderness, and induration).

• In chronic wounds, additional signs suggesting

infection may include delayed healing, abnormal
coloration, friability, or foul odor.
 Microbiology of Diabetic Foot
• Polymicrobial
• Serious infections in hospitalized patients are often caused by 3–5
bacterial species
• Aerobes
• Gram-positive cocci
– S. aureus is the most important pathogen
– Enterococci in patients who have previously received a cephalosporin
• Gram-negative bacilli
– Enterobacteriaceae in patients with chronic or previously treated infections
– Pseudomonas species in patients with wounds that have been soaked or
treated with wet dressings
• Anaerobes
• Wounds with ischemic necrosis or that involve deep tissues

Lipsky BA. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S104-14.
 Evaluation
Check Check
posterior tibial pulse Dorsalis pedis pulse Sensory
examination

Select patients
•Doppler study
X-ray of
• MRI / SPECT
the foot
• Angiography

Watkins PJ. BMJ. 2003 May 3;326(7396):977-9.

 Patient Evaluation
• Semmes-Weinstein Monofilament Aesthesiometer
• 5.07 (10g) seems to be threshold
• 90% of ulcer patients can’t feel it
• Only helpful as a screening tool
• Place a 10g nylon Semmes-Weinstein monofilament at a right angle to the
skin
• Apply pressure until the monofilament buckles, indicating that a specific
pressure has been applied.
• Inability to perceive the 10g of force applied by the monofilament is
associated with clinically significant large fibre neuropathy and an increased
risk of ulceration (sensitivity of 66 to 91%)
• Test 4 plantar sites on the forefoot (great toe and the base of 1st, 3rd and 5th
metatarsals ) to identify 90% of patients with an insensate foot.
 Structural Abnormalities and Deformities
• Structural abnormalities and deformities lead to bony prominences
which are associated with high mechanical pressure on the
overlying skin.
• This results in ulceration, particularly in the absence of a protective
pain sensation and when shoes are unsuitable.
• The deformity should be recognised early and accommodated in
properly fitting shoes before ulceration occurs.

• Common abnormalities / deformities include:

i. Callus
ii. Bunion
iii. Hammer toes
iv. Claw toes
v. Charcot foot
vi. Nail deformities

• Note: It is vital to inspect the patients' shoes as part of the

assessment!
 Charcot foot
deformity
Claw toes

Nail deformity Hammer Toe

 Ulcers
• Several foot ulcer
classifications have been
proposed although none is
universally accepted.

• The simplest classification is

based on the underlying
pathogenesis: neuropathic,
ischaemic or neuroischaemic.

• It is vital to carefully monitor

the progress of an ulcer once
one has developed. A neuropathic ulcer on the
sole of the foot
 Classification

Cerqueira et al. J Vasc Bras. 2020;19:e20190070. https://doi.org/10.1590/1677-5449.190070

 Examples

Hall J, Preventive foot care for diabetes patients in primary care. Pfizer. Data on file.
Lipsky BA, et al. Clinical Infectious Diseases 2012;54(12):132–173
WIFI Classification
WIFI Classification
 Investigation of an Infected Ulcer
Simple investigations include:
• Tissue specimens or material obtained from the bottom of a wound for gram
staining and culture for microbial sensitivity.
• Full blood count, urea and electrolytes, inflammatory markers (ESR and
CRP) for assessing severity of infection
• Plain X-ray of the leg for signs of bone damage, presence of foreign body,
or gas in soft tissue (gas gangrene)

More advanced radiology involves:

• Technetium bone scan and MRIs may be necessary in some patients to
define underlying bony involvement

Invasive investigations include:

• Bone biopsy, as the gold test for diagnosing osteomyelitis.
• Arteriography using contrast dye can be used to visualise leg ischaemia
 Plain X-Ray
Cortical bone abnormalities characteristic of osteomyelitis: cortical erosion, periosteal
reaction, and lucency or osteolysis.
These abnormalities may not be apparent until 7-15 days after the onset of acute
clinical osteomyelitis and the early subtle changes are not easily differentiated from
those due to Charcot osteoarthropathy.

Triangular foot Air Lucency

 Additional Imaging Modalities
• CT can be helpful in visualizing bony anatomy
for abscess, extent of disease
• MRI has a role instead of nuclear medicine
scans in uncertain cases of osteomyelitis
• Duplex-scan / MDCTA / DS Angiography are
reserved for ischemic limbs and for
revascularization strategies
 Charcot’s neuro-osteoarthropathy
• Charcot neuro-osteoarthropathy is a degenerative disease
with progressive destruction of the bones and joints.
• It is seen in neurological disorders with sensory loss of the
feet, including tabes dorsalis, leprosy, diabetic neuropathy,
and other conditions involving injury to the spinal cord.
• In 1868 Jean-Martin Charcot gave the first detailed
description of the neuropathic aspect of this condition in a
patient with syphilis.
• Diabetes mellitus is the most common etiology associated
with Charcot osteoarthropathy, with the joints of the foot and
ankle being most commonly affected.
Charcot’s neuro-osteoarthropathy

Chronic Stage of Charcot Acute Stage of Charcot

Charcot’s neuro-osteoarthropathy
In the acute stage, the
radiographs are normal
and may not exclude the
diagnosis of acute Charcot
neuro-osteoarthropathy.

Within 4 months there is

progressive decrease of
calcaneal inclination with
equinus deformity at the
ankle. There is destruction
of the tarsometatarsal joint
with the typical rocker-
bottom deformity.
Bony debris is seen on the
dorsal aspect of the foot.
 Charcot’s neuro-osteoarthropathy

Typical rocker-bottom deformity of the foot due to collapse of the longitudinal arch.
Abnormal pressure on the cuboid has led to ulceration.
 MRI

Extracted from Miller JC. Radiology Rounds. 2006;4(6)

 Diabetic Foot
Clinical Evaluation and Imaging

Dr. Seleno Glauber

2023