A patient presents with an ulcer that progresses to gangrene.

1. A Diabetic Patient with
wound on foot
A Presentation by:
Abdullah Mohammad 2014-001

2. Case
Mr. XYZ is a 50 year old gentleman who presented to the OPD clinic with chief complaint of
lesion on the right foot and swelling for one week.
HOPC: Mr. XYZ who is a known case of type 2 diabetes mellitus for the last 18 years was in his
usual state of health 1 week back when he noticed a lesion on his right foot. He doesn’t know
when the lesion actually appeared. At first he did not bother with it and thought it is just a result
of some trauma but for the last 1 day he has also noticed redness and swelling around the lesion
which brought him to the clinic today. It does not interfere with his walking. There is no history
of fever, rigors or chills. There is no history of trauma.
ROS: Unremarkable
Past Medical Hx: On insulin for the control of his blood sugar. He monitors it occasionally and it
is not properly controlled. He does not complain of decrease in vision or frothy urine. There are
no other co-morbids
Past Surgical Hx: Nil
Social Hx: He smokes 1-2 cigarettes per day for the last 10 years. There are no other addictions

3. Physical Examination
• Vital signs are stable.
• On inspection of the right foot a purulent ulcer was present on the 5th metatarsal
head with about 1 cm induration and erythema around the ulcer. The ulcer had a
punched out edge. There was no visible deformity of the foot. The color and hair
distribution of the rest of the foot was normal. On palpation of the ulcer, it was
warm as compared to the surrounding skin and non-tender to touch. It measured
0.5 cm in length, 1 cm in width and 3 mm in depth. The base of the ulcer was
pink and granulating surrounded by callus. There was no visible or palpable bone
with probing. Peripheral pulses were Palpable. Light touch, vibration, and
monofilament pressure perception was greatly diminished. Deep tendon reflexes
were normal. There was no inguinal lymphadenopathy.
• Examination of the left foot was unremarkable

4. Investigations
• CBC
• Fasting Blood Sugar
• Gram Stain and Culture of the discharge from the ulcer
• XRAY / MRI foot
• Arterial Duplex scanning
• Angiography if required

5. Results
• CBC revealed total WBC of 7000, Hb of 13.5 gm/dl, MCV of 85 and Plt
count of 210,000
• Fasting blood sugar was 180 mg/dl
• Culture of the discharge grew Staphylococcus Aureus sensitive to
vancomycin, linezolid and ceftazidime
• XRAY of the foot showed no evidence of osteomyelitis
• Arterial Duplex scanning revealed good flow in all the peripheral pulses

6. Treatment
• Foot ulcers in diabetes require multidisciplinary assessment, usually by
diabetes specialists and surgeons.
• Treatment consists of
• Appropriate bandages
• Antibiotics (against staphylococcus, streptococcus and anaerobe strains)
• Debridement,
• Arterial revascularisation
• Platelet-rich fibrin therapies.

8. Typical features of Diabetic foot ulcer
according to etiology
Feature Neuropathic Ischemic Neuroischemic
Sensation Sensory loss
Painless
Painful Degree of sensory loss and
painless
Callus/necrosis Callus present and often thick Necrosis common Minimal callus
Prone to necrosis
Wound bed Pink and granulating,
surrounded by callus
Pale and sloughy with poor
granulation
Poor granulation
Foot temperature and pulses Warm with pulses present Cool with absent pulses Cool with absent pulses
Other Dry skin and fissuring Delayed healing High risk of infection
Typical location Weight bearing areas of the
foot such as metatarsal heads,
the heel and over the dorsum of
clawed toes
Tips of toes, nail edges and
between the toes and lateral
borders of the foot
Margins of the foot and toes

9. STAGES OF ULCER DEVELOPMENT

10. STAGES OF ULCER DEVELOPMENT

11. Assessment of a Diabetic Foot Ulcer
• Examination of the ulcer
• Testing for loss of sensation. 10g Semmes-Weinstein monofilament and standard 128Hz
tuning fork are simple and effective screening tool
• Testing for vascular status. This can be done by palpation of the peripheral pulses, Duplex
ultrasound, Angiography
• Identifying infection and taking culture
• Full blood count, electrolytes, inflammatory markers (ESR, CRP)
• Assessing bone involvement (Using XRAY or MRI)
• Inspecting feet for deformities

12. Monofilament for pressure sensation (pinprick
sense)
• 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.
Monofilament test

14. Assessment Infected Ulcers
• Assessing foot ulcers for the presence of infection is vital. All open wounds are likely to
get colonised with microorganisms, such as Staphylococcus aureus, and not necessarily
infected. Therefore, the presence of infection needs to be defined clinically rather
than microbiologically.
An infected ulcer
Signs suggesting
infection include;
1. purulent
secretions
2. presence of friable
tissue
3. undermined edges
4. foul odour

16. Assessment 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.
• Ideally, 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!
Callus on plantar
surface
Bunion on the medial
border of the foot

17. Claw toes
Charcot foot
deformity
Nail deformity
Assessment - Some Common Foot Deformities

18. Classification of Diabetic Foot 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 neuroischemic.
• It is vital to carefully monitor the progress of an ulcer once one has developed.
• The University of Texas system shown on the next slide can be used to predict outcome
by grading wound depth and presence of infection and/or ischemia. However there is no
measure of neuropathy.

19. Ulcer Grade ( depth )
0 I. II. III.
Ulcer
stage
A Pre / postulcerative lesion
completely epethelialised
Superficial lesion, not involving
tendon, capsule or bone
Wound penetrating to tendon or
capsule
Wound penetrating to bone or
joint
B Pre / postulcerative lesion with
Infection
Superficial lesion, not involving
tendon, capsule or bone with
Infection
Wound penetrating to tendon or
capsule with Infection
Wound penetrating to bone or
joint with Infection
C Pre / postulcerative lesion with
ishaemia
Superficial lesion, not involving
tendon, capsule or bone with
ischaemia
Wound penetrating to tendon or
capsule with ishaemia
Wound penetrating to bone or
joint with ishaemia
D Pre /postulcerative lesion with
infection and ishaemia
Superficial lesion, not involving
tendon, capsule or bone with
infection and ischaemia
Wound penetrating to tendon or
capsule with infection and
ischemia
Wound penetrating to bone or
joint with infection and
ischemia
University of Texas system for classification
of ulcers

20. WAGNER CLASSIFICATION FOR DIABETIC FOOT
LESIONS
• Grade 0 – No open lesion(callus may be present)
• Grade 1 – Superficial Ulcer
• Grade 2 – Deep Ulcer to Tendon, Capsule or Bone
• Grade 3 – Deep Ulcer with abscess, osteomyelitis, joint sepsis
• Grade 4 – Localized gangrene
• Grade 5 – Gangrene of entire foot
Non Surgical
Management
Surgical and
Medical
Management

21. Managing a Diabetic Foot Ulcer
• General Principles of Therapy:
1. Stabilize the patient
• Restoration of fluid and electrolyte balance
• Correction of hyperglycemia, hyperosmolarity, acidosis, and azotemia
• Treat other exacerbating factors
Note – improving glycemic control may aid in eradicating the infection and healing the wound
• Cardiovascular risk factors such as smoking, dyslipidaemia and hypertension should be addressed to
reduce risks of Peripheral Vascular Disease, acute coronary syndrome and chronic renal failure
• Education of patients on proper foot care and on the importance of seeking medical advice early is very
important
• Ensure an adequate blood supply
• Local wound care (tissue debridement, inflammation and infection control, moisture balance)

22. • Choose an antibiotic regimen
• Severe infection:
• start broad spectrum IV abx (ensure Gram Positive Coverage, gram negative and
anaerobic coverage)
• Mild-Moderate infection:
• Relatively narrow spectrum only covering aerobic Gram Positive Coverage
• No evidence for anti-anaerobic therapy
• Oral therapy with highly bioavailable agents is appropriate
• Mildly infected open wounds with minimal cellulitis:
• Limited data support the use of topical antimicrobial therapy (B-I)

25. • “It’s an ulcer..what now!?”-Don’t panic, be methodical.
• Treatment of diabetic foot ulcers largely depends on the underlying causes: ischaemia,
neuropathy or a combination of both. Treatment approaches for ischaemia include:
Ischaemic necrosis of a
toe and an extensive
plantar ulcer
Medical: reduce cardiovascular risk factors
Surgical: revascularisation to achieve timely and durable wound
healing is sometimes necessary. Patients with supra-inguinal (aorta-
iliac) disease may be amenable to angioplasty (+/- stenting), with good
long-term results being achieved at a low risk. Open bypass surgery
may be considered for those patients who do not have an
endovascular option.

26. • The best method is some form of cast.
• If not available, temporary ready-made shoes with a plastozote insole such as Drushoe
can off-load the site of ulceration. Alternatively, weight-relief shoes and felt pads may
also be used.
• Other weight-relieving measures such as the use of crutches, wheelchairs and zimmer
frames should be encouraged.
• Heeled ulcers also need off-loading by foam wedges, heel protector splints or rings.
The common site for
a neuropathic ulcer
The key to treatment here is to redistribute plantar
pressure.

27. • “These cast things sound useful...what are they?”
• Various casts are available and all aim to relieve plantar pressure. Their use is governed by
local experience and expertise
• Air cast (walking brace)
• A bivalved cast with the halves joined together with Velcro strapping. The cast is lined with
4 air cells which can be inflated with a hand pump to ensure a close fit. The cast can be
removed easily by patients to check their ulcers and before going to bed.
• Scotch cast boot
• A simple, removable boot made of stockinette, soffban bandage, felt and fibreglass tape.
• Total contact cast
• It is a close-fitting plaster of paris and fibreglass cast applied over minimum padding. It is
very efficient method of redistributing plantar pressure, and should be reserved for plantar
ulcers that have not responded to other casting treatments.
An air cast
A scotch cast boot

28. Casts should be removed every week for wound inspection and then renewed.
Cast problems to be aware of:
• Iatrogenic lesions (rubs, pressure sores, infections) which often go undetected
• Cast are often heavy and uncomfortable and reduce the patient’s mobilty
• Patients may not drive a car in a cast
• The leg may develop immobilisation osteoporosis
• Danger of fracture and the development of a Charcot foot when coming out of a cast if patient walks
too far too soon
• A few patients develop a cast phobia and will not wear them

29. • “What can we do to treat the ulcer?”
• In both isacheamic and neuropathic ulcers, treatment is based on debridement of the wound and
dressing application.
Debridement is the removal of necrotic and dead tissue in order to enhance healing.
Debridement is undertaken to:
• Remove callus in neuropathic foot to lower plantar pressure
• Assess the true dimension of the ulcer
• Drain exudate and remove dead tissue to render infection less likely
• Take a deep swab for culture
• Encourage healing and restore a chronic wound to an acute wound
Forcep and a scalpel is the
usual technique by cutting
away of all slough and non-
viable tissue.

30. )
• The larvae of the green bottle fly (which feed on dead flesh) are sometimes used to debride ulcers,
especially in the ischaemic foot. Only sterile maggots obtained from a medical maggot farm should be
used!
• Maggots produce a mixture of proteolytic enzymes that breakdown slough and necrotic tissue which they
ingest as a source of nutrients. During this process, they also ingest and kill bacteria including antibiotic
resistant strains.
• As a result of their wound cleansing activity, the application of maggots has been found to reduce wound
odour, and it has also been reported that their presence within a wound stimulates the formation of
granulation tissue.
• Contra-indications to maggot therapy:
• Free range maggots should not be introduced into wounds that communicate with the body cavity or
any internal organ
• They should not be applied to wounds that have a tendency to bleed easily or contain exposed large
blood vessels
• They should not be applied to patients with clotting disorders, or individuals receiving anticoagulant
therapy unless under constant medical supervision in a health facility.

31. • Maggots are available in 2 forms.
1. ‘Free Range’ maggots
• applied directly to the wound
• roam freely over the surface seeking out areas of slough or necrotic
tissue
• generally left on wound for a maximum of 3 days.
2. BioFOAM Dressing
• Maggots enclosed in net pouches containing pieces of hydrophilic
polyurethane foam
• dressing is placed directly upon the wound surface
• BioFOAM Dressing can be left for up to 5 days then the wound is
reassessed.
BioFOAM dressing with
maggots inside

32. Management - Wound Dressings
• A sterile, non-adherent dressing should cover all open diabetic foot lesions to protect them from
trauma, absorb exudate, reduce infection and promote healing.
• Dressings should be lifted every day to ensure that problems or complications are detected quickly,
especially in patients who lack nociception.
• Additional approaches include
• Skin graft:
•A split-skin graft may be harvested and applied to the ulcer to speeds healing of the ulcer which
if has a clean granulating wound bed
•Vacuum-Assisted closure (VAC) pump:
•This is an innovative measure to close diabetic foot wounds. It applies gentle negative pressure
to the ulcer via a tube and foam sponge which are applied to the ulcer over a dressing and
sealed in place with a plastic film to create a vacuum. Exudate from the wound is sucked along
the tube to a disposable collecting chamber. The negative pressure improves the vascularity and
stimulates granulation of the wound.

33. “Are there any new interesting aids for wound healing?” –Yes, three here;
 Hyperbaric oxygen therapy: Poor tissue oxygenation with diabetic microangiopathy reduces wound healing.
Therefore hyperbaric oxygen therapy (HBOT) would theoretically aid in faster wound healing, there is however little
evidence for this at present.
 Growth factor therapy: Recombinant platelet derived growth factor (PDGF) was the first growth factor approved by
the Food and Drug Administration (FDA) for the treatment of lower extremity diabetic neuropathic ulcers that extend
into the subcutaneous tissue and have adequate blood supply. PDGF, applied as a gel , theoretically acts to enhance
granulation tissue formation and facilitate epithelialisation . It may be useful in small, low-grade so may have a role
in chronic neuropathic ulcers that are refractory to conventional therapy but there is no evidence to support this
theory.
 Bioengineered human dermis transplantation: Dermagraft is a cultured human dermis produced by seeding dermal
fibroblasts on a biodegradable scaffold. After culture, a living dermal tissue is created which can later support the
formation of an epidermis. Furthermore, dermatograft can generate growth factors, cytokines, matrix proteins and
glycosaminoglycan, thus aiding the healing process. There have been a limited number of trials have confirmed the
efficacy of dermagraft in healing chronic ulcers in a significantly shorter time.

34. • “And when the bone gets infected?”
• Lastly, treating underlying osteomyelitis is an important therapeutic challenge. Presence of
osteomyelitis warrants long-term treatment of at least 4 – 6 weeks duration with antibiotics that
penetrate well into bone such as fluoroquinolones, clindamycin or fusidic acid.
• Surgical ressection still remains the most definitive treatment for osteomyelitis especially for
patients not responding to antibiotics.
Treating Charcot’s neuro-osteoarthropathy
“Charcot foot” refers to bone and joint destruction that occurs in the neuropathic foot or rarely just the toe. It can be
divided into three phases:
•Acute onset;
•Bony destruction / deformity;
•Stabilistion;
1. Acute onset
Characterised by unilateral erythema and oedema and the foot is at least 2˚C hotter than the contralateral foot. About
30% of patients may complain of pain or discomfort which is rarely severe. X-ray may be normal, but a technnetium
methylene diphosphonate bone scan will detect early evidence of bony destruction.
An infected
ulcer
draining
pus

35. • Patients awaiting bone scan should be treated as if the diagnosis has been confirmed;
• Initially the foot is off-loaded and immobilised in a non-weight-bearing cast to prevent
deformity. After 1 month, a total-contact cast is applied and the patient may mobilise for
brief period. However, the patient is given crutches and encouraged to keep walking to a
minimum.
• If given early, these measures can prevent bony destruction. Bisphosphonates are potent
inhibitors of osteoclast activation and may also be used in this phase.
• 2. Bony destruction
• Clinical signs are swelling, warmth, a temperature 2˚C greater than the contralateral foot
and deformities
• X-ray reveals fragmentation, fracture, new bone formation, subluxation & dislocation.
• The aim of treatment is immobilisation until there is no X-ray evidence of continuing
bone destruction and the foot temperature is within 2˚C of contra lateral foot.
A photo showing a charcot foot
with an ulcer on the sole

36. • 3. Stabilisation
The foot is no longer warm and red. There may still be oedema but the difference in skin temperature
between the feet is less than 2˚C. the X-ray shows fracture healing, sclerosis and bone remodelling.
The patient can now progress from a total-contact cast to an orthotic walker. Cautious rehabilitation should
be the rule, beginning with a few short steps in a new footwear.
Regular reduction of callus can prevent ulceration.
During the acute stage, charcot foot’s foot may be misdiagnosed as;
 Cellulitis
 Osteomyelitis
 Deep vein thrombosis
 Inflammatory arthropathy
Therefore a high index of suspicion is very important at this stage!

37. Gangrene
• Gangrene is a serious condition that arises when a considerable mass of body tissue dies (necrosis). The
primary cause of gangrene in a diabetic patient is reduced blood supply to the affected tissues which
results in cell death.
• There are different types of gangrenes i.e. wet gangrene, dry gangrene, gas gangrene
• Necrosis in chronic ischemia may be patchy and localized if there is a developed collateral circulation.
Such necrosis is usually confined to toes or a limited part of the forefoot. The necrotic area slowly
becomes hard, black and mummified (dry gangrene) and may eventually separate spontaneously from the
viable tissue. However, there is always a risk that the necrotic area can become infected. The tissue then
becomes ulcerated and the infection and gangrene spread proximally. This wet gangrene requires urgent
treatment often with a combination of revascularization and amputation.
• Treatment options include debridement, amputation, antibiotics, vascular surgery, maggot therapy or
hyperbaric oxygen therappy

39. Amputation
• Indications for amputation are:
1. If revascularization is technically impossible
2. If there is substantial tissue necrosis and functionally useless foot or spreading
infection is present
3. A non healing ulcer that is accompanied by a higher burden of disease than would
result from amputation.
4. Ischemic rest pain that cannot be managed by analgesics or revascularization
5. As part of debridement (minor amputation)
6. Spreading cellulitis

40. Level of Amputation
Two principles guide the level of amputation
1. The amputation must be made through healthy tissue. If not, there is a high risk of
wound breakdown and chronic ulceration, requiring further amputation at a higher
level. When amputation is for (uncorrected) peripheral ischemia, it is almost always
necessary to amputate at mid-tibial level or above to ensure healing
2. The choice of amputation level must take into account the fitting of a prosthetic limb.
For this purpose, the mid-tibia (below-knee) and lower femoral levels (above-knee)
are preferred. If the knee joint can be saved, the functional success of a prosthesis is
much better.

41. Types of Amputation
• Minor
This involves simple amputation at the base of the digit or ‘ray’ amputations where, e.g. in
the foot, the metatarsal head and tendons are removed. Occasionally for ischemia of all
toes, transmetatarsal amputation may be undertaken.
• Major
1. Below Knee amputation: This provides the patient with the best chance of mobilizing
with a prosthesis. This is suitable in diabetics with a palpable popliteal pulse. The
standard tibial stump is 8-12 cm long
2. Above Knee amputation: This is a common amputation in patients with
arteriosclerosis. The stump of the femur is 25 cm long measured from the greater
trochanter

43. Postoperative care
• Pain relief
• Care of the good limb: This involves physiotherapy. It is important to avoid pressure
ulcers by nursing on air bed
• Physiotherapy: Build up muscle power and coordination. Start as soon as the patient is
comfortable and continue in gymnasium. The aim is to prevent contractures and ensure
rapid mobilization with prosthesis
• Prosthesis: Measure patient as soon as stump shrinks and volume of stump is stable

44. Complications
• Early: These include hemorrhage, hematoma, abscess, gas gangrene, wound dehiscence,
ischemic flaps and fat embolism
• Late: These include pain, sinus formation, osteomyelitis, phantom limb and ulceration of
the skin (pressure from prosthesis or continuing ischemia)