Diabetic Foot - Dr Rohit Bhaskar

DIABETIC FOOT
©2020 Rohit Bhaskar PT https://www.pt-pedia.com/

©2020 Rohit Bhaskar PT https://www.pt-pedia.com/ 2
• Local trauma and/or pressure
• Prior ulcers or amputations
• Infection
• Effects of chronic ischemia, due to
peripheral artery disease
• Patients with diabetes also have an
increased risk for nonhealing related
to mechanical and cytogenic factors

• Peripheral neuropathy and peripheral
arterial disease (PAD) (or both) play a
central role
• Diabetic Foot Ulcers are classified as:
– Neuropathic
– Ischaemic
– Neuroischaemic

• Sensory Neuropathy
• Motor Neuropathy
• Autonomic Neuropathy

• Loss of pain sensation
• Unnoticed and trivial trauma (thermal,
chemical , mechanical )
• Progressive callous formation
• Tissue damage and necrosis
• Subcutaneous fluid collection and
hemorrhage
• Tissue breakdown
• Ulceration

• Weakness of intrinsic foot muscles
• Progressive muscle wasting
• Foot deformities and joint
subluxations
• Limited joint mobility
• Abnormal gait
• Chronic Internal pressure
• ulceration

• Decreased sweating
• Dry and brittle skin
• Fissures and cracks
• Secondary infections
• Ulceration

> People with diabetes are twice as likely to
have PAD as those without diabetes.
Macroangiopathy : atherosclerosis of arteries
> Microangiopathy : increased and
abnormal basement membrane thickening
and endothelial proliferation Leads to
capillary damage and release of ROS
> Leading to decreased blood flow - poor
antibiotic penetration - poor wound healing

Hyperglycemia impairs neutrophil function
and reduces host defenses.
• Persistently high pro-inflammatory
cytokines and proteases concentration
• Degrade growth factors, receptors and
matrix proteins
• Decreased PMNs migration and
phagocytosis
• Decreased chemotaxis and intracellular
killing

• Most diabetic foot infections are
polymicrobial
• Superficial diabetic foot infections :likely
due to aerobic gram-positive cocci.
• Ulcers that are deep, chronically infected
and/or previously treated with antibiotics
are more likely to be polymicrobial.

• Wounds with extensive local
inflammation, necrosis, malodorous
drainage, or gangrene with signs of
systemic toxicity should be presumed
to have anaerobic organisms in
addition to the above pathogens.

• MRSA: Prior antibiotic use, previous
hospitalization, and residence in a long-
term care facility.
• Pseudomonas aeruginosa :Macerated
ulcers, foot soaking, and other exposure
to water or moist environments.
• Resistant enteric gram-negative rods:
patients with prolonged hospital stays,
prolonged catheterization, prior antibiotic
use, or residence in a long-term care
facility.

University of Texas system
Grade 0: Pre- or postulcerative
Grade 1:Full-thickness ulcer not involving tendon,
capsule, or bone Grade 2: Tendon or capsular
involvement without bone palpable Grade 3: Probes to
bone
• STAGE:
●A: Noninfected
●B: Infected
●C: Ischemic
●D: Infected and ischemic

©2020 Rohit Bhaskar PT https://www.pt-pedia.com/
Diabetic Foot Stages

• Measures 3 factors:
– Wound
– Ischemia
– Foot Infection

Diabetic foot infections typically
take one of the following forms:
• Localized superficial skin involvement
at the site of a preexisting lesion
• Deep-skin and soft-tissue infections
• Acute osteomyelitis
• Chronic osteomyelitis

Assessment for the presence of
• existing ulcers
• peripheral neuropathy
• loss of protective sensation
• peripheral artery disease, and
• foot deformities
– claw toes and
– Charcot arthropathy

• Predominantly neuropathic,
ischaemic or neuroischaemic?
• Is there critical limb ischaemia?
• Any musculoskeletal deformities?
• Ulcer Characteristics:
size/depth/location/woun
d bed
• wound infection
• status of the wound edge

• Vibration sensation
• Pressure sensation
• Superficial pain (pinprick) or
temperature sensation
• Scoring Systems

• 128Hz tuning Fork used
• Placed on the interphalangeal joint
of the right hallux and compared
with dorsal wrist.
– Severe Deficit: no senation in hallux
– Mild/Moderate: vibration feels stronger
at the wrist
– Normal: vibration feels no different at the
wrist.

• Primarily based on suggestive clinical
manifestations
• The presence of two or more features of
inflammation (erythema, warmth, tenderness,
swelling, induration and purulent secretions) can
establish the diagnosis
• Presence of microbial growth from a wound
culture in the absence of supportive clinical
findings is not sufficient to make the diagnosis of
infection

• Grossly visible bone or ability to probe to bone
• Ulcer size larger than 2 cm2
• Ulcer duration longer than one to two weeks
• Erythrocyte sedimentation rate (ESR) >70 mm/h
• A conventional radiograph with consistent
changes can be helpful in making the
diagnosis ((MRI), which is highly sensitive and
specific for osteomyelitis )
• Culture of bone biopsy specimens is also
important for identifying the causative organisms

• Trauma
• crystal-associated arthritis
• acute Charcot arthropathy
• fracture
• thrombosis
• venous stasis

Management of diabetic foot
infections requires:
• Attentive wound management
• Good nutrition
• Appropriate antimicrobial
therapy
• Glycemic control, and
• fluid and electrolyte balance.

• Local wound care for diabetic foot infections
typically includes debridement of callus and
necrotic tissue, wound cleansing, and relief of
pressure on the ulcer
DEBRIDMENT:
• Debridement is essential for
ulcer healing
• choice of debridement
– sharp,
– enzymatic,
– autolytic,
– mechanical, and
– biological)

DRESSINGS
• After debridement, ulcers should be kept
clean and moist but free of excess fluids
• Dressings should be selected based upon
ulcer characteristics, such as the extent
of exudate, desiccation, or necrotic
tissue
Adjunctive local therapies :
• negative pressure wound therapy (NPWT)
• use of custom-fit semipermeable
polymeric membrane dressings
• cultured human dermal grafts
• application of growth factors

Required for cure of infections complicated by
• abscess,
• extensive bone or joint involvement,
• crepitus, necrosis, gangrene or necrotizing fasciitis
• And for source control in patients with severe sepsis
In addition to surgical debridement, revascularization
(via angioplasty or bypass grafting) and/or
amputation may be necessary.

EMPERIC THERAPY:
Mild infection: Outpatient oral
antimicrobial therapy.
Should include activity against skin
flora including streptococci and S.
aureus
Agents with activity against methicillin-resistant
S. aureus (MRSA) should be used in patients
with purulent infections and those at risk for
MRSA infection

• Moderate infection: Deep ulcers with
extension to fascia. Should include
activity against streptococci, S. aureus
(and MRSA if risk factors are present),
aerobic gram-negative bacilli and
anaerobes
– can be administered orally
• Empiric coverage for P. aeruginosa may
not always be necessary unless the
patient has particular risk for involvement
with this organism, such as a macerated
wound or one with significant water
exposure

Severe infection: Limb-threatening
diabetic foot infections and those
that are associated with systemic
toxicity should be treated with broad-
spectrum parenteral antibiotic
therapy
In most cases, surgical
debridement is also necessary.

Diabetic Foot - Dr Rohit Bhaskar

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