Diabetic foot - diagnosis and management

1. Dr. Joe M Das
DIABETIC FOOT

2. - Bahara, Mills et al. International Wound Journal 2009.

4. The theme – Diabetes
education and prevention
(2009 – 2013)

5. Statistics
 60-70% of those with diabetes will develop
peripheral neuropathy, or lose sensation in their
feet.
 Up to 25% of those with diabetes will develop a
foot ulcer.
 More than half of all foot ulcers (wounds) will
become infected, requiring hospitalization and 1 in
5 will require an amputation.
 After a major amputation, 50% of patient will have
their other limb amputated within 2 years.

6. The History of Diabetes
 1552 BC: the first known mention of diabetes
– found on the Ebers Papyrus
 Egyptian physician Hesy-Ra of the 3rd
Dynasty makes
 Lists remedies to combat the
‘passing of too much urine’
Wood Carving of
Hesy-Ra

7. The History.. Contd…
 250 BC: Diabetes described as ‘the
melting down of flesh and limbs into
urine’
 By Greek physician Aretaeus of
Cappodocia who gives the first
complete medical description of
diabetes
 1425 AD: Diabetes first appears in the
English language as the Middle
English word ‘diabete’.

8.  16th Century: Swiss physician Phillipus Aureolus
considered the ‘Martin Luther of Medicine’ –
identifies diabetes as a serious general disorder.
1776: English physician Mathew Dobson of Liverpool
 evaporates two quarts of urine from a patient with
diabetes.
 The resulting residue is granulated and smells and
tastes like sugar, conclusively establishing the presence
of ‘saccharine materials’ as a diagnosis of diabetes.
The History… Contd…
Phillipus Aureolus

9.  1869
 German medical student
 Paul Langerhans
 The islet cells of the pancreas but is unable to explain
their function.
 The find is dubbed the ‘islets of Langerhans.”
The History Continues..

10.  1871: French physician Apollinaire Bouchardat
notices the disappearance of glycosuria in his
diabetes patients during food rationing of
food under the Siege of Paris in the Franco-
Prussian War, and formulates individualized
diets to treat the condition.
 1889: Scientists Oskar Minkowski and Joseph
von Mering of the University of Strasbourg,
France demonstrate how removing a dog’s
pancreas produces diabetes.
The History Continues..
Apollinaire Bouchardat
Oskar Minkowski

11.  1901: American pathologist Eugene Opie of
John Hopkins University in Baltimore
establishes a connection between the
failure of the islets of Langerhans in the
pancreas and the occurrence of diabetes.
 1913: Prof. John J.R. Macleod writes a
monograph on diabetes entitled
‘Diabetes: Its Pathological Physiology.’
The History Continues..

12.  Dec. 1916: Boston pathologist Elliott Joslin
 compiles 1,000 of his own cases and creates the
textbook The Treatment of Diabetes
Mellitus.
 In it he reports that ‘the mortality of patients
was approximately 20 per cent lower than for
the previous year’, due to ‘the introduction of
fasting and the emphasis on regular
exercise.’
 1919: Dr. Frederick Allen of the Rockefeller
Institute in New York publishes
 “Total Dietary Regulations in the
Treatment of Diabetes” that introduces a
therapy of strict dieting – dubbed the
‘starvation treatment’ –- as a way to manage
diabetes
The History Continues..
Dr. Frederick Allen
Elliott Joslin

13. Oct. 31, 1920
Sir Frederick Grant Banting
 conceives of the idea of insulin after reading an
article in The Journal Surgery, Gynecology and
Obstetrics by Moses Barron, by an American
pathologist, titled ‘The Relation of Islets of
Langerhans to Diabetes with Special Reference to
Cases of Pancreatic Lithiasis.’
 With the support of Prof.. Macleod of the
University of Toronto, and the assistance of
 Best, a medical student he starts his research
using a variety of different extracts on
depancreatized dogs.
The History Continues..

14.  Summer 1921: Banting’s work leads to the discovery of insulin. On July
30, Dog 410 is the first to receive the extract. On August 4 the extract
is called ‘Isletin’ for the first time.
 Nov. 14, 1921 Dr. Banting and Charles Best deliver a preliminary report
of their research to the Journal Club of the University of Toronto,
Department of Physiology.
 Nov. 17, 1921: Banting and Best discover that extract from cattle foetal
pancreas lowers blood sugar levels of depancreatized dogs, leading
them toward plentiful, cheap sources for insulin. Experiments begin
to test the long-term effectiveness of insulin treatment.
 Dec. 30, 1921 :Banting, Macleod, Best and Dr. James Bertram
Collip, a biochemist present the results of their research at a session
of the American Physiological Society at Yale University. The paper
initially generates little interest.
 The paper – ‘The Internal Secretion of the Pancreas’ – is published two
months later in the prestigious Journal of Laboratory and Clinical
Medicine
More Of Banting & Best…

15. Oct. 25, 1923
 Banting and Macleod
 The Nobel Prize in Physiology or Medicine.
 Banting shares his award with Best
 Macleod shares his with Collip.
The Nobel Prize Goes To….
Banting & Macleod
Banting's and Best's laboratory, where
insulin was discovered.

16.  11th January 1922
 Leonard Thompson, 14,
 A ‘charity patient’ at the Toronto General Hospital,
 First person to receive and injection of insulin to treat Type 1
diabetes.
 Thompson lives another 13 years before dying of pneumonia
at age 27.
The History Continues..

17.  May 3, 1922: The word ‘insulin’ is used in public for the
first time when Macleod presents the paper ‘The Effect
Produced on Diabetes by the Extracts of Pancreas’ to the
 May 30, 1922: Pharmaceutical manufacturer Eli Lilly & Co.
of Indianapolis and the University of Toronto enter a deal
for the mass production of insulin.
The History Continues..

18.  1966
 First pancreas transplant
 University of Manitoba
The History Continues..

19.  July 7, 1989: Her Majesty Queen Elizabeth The Queen Mother
kindles the
 Flame of Hope at Banting House National Historic Site – ‘The
Birthplace of Insulin’ – in London, Ontario.
 As a symbol of hope, the flame will burn until a cure for
diabetes is found.

20.  March 1999
 Scientists conduct the first
successful islet transplant at the
University of Alberta Hospital.
 The Edmonton Protocol.
isolating islets from a cadaveric
donor pancreas using a mixture
of enzymes called Liberase
The History Continues..

21.  Dec. 20, 2006: The United Nations recognizes diabetes as a
global threat and designates World Diabetes Day,
November 14 – in honour of Frederick Banting’s birthday –
as a UN Day to be observed every year starting in 2007.

22. Pathogenesis
 Chronic hyperglycaemia
 Nerve microvascular dysfunction
 ↑ free radical formation (due to ↓ NADPH)
 Polyol pathway hyperactivity (Glucose → ↑sorbitol
→ ↓ myoinositol → ↓ Na-K ATPase)
 PKC hyperactivity
 Nonenzymatic
 Abnormalities of nerve growth

23.  Pathology:
 Axonal loss distally, with a “dying back”
phenomenon
 A reduction in myelinated fiber density and
 Focal areas of demyelination on teased fiber
preparations.

26. Neuropathy
Motor Sensory Autonomic
↓ nociception
↓ Proprioception,
Unawareness
of foot position
A-V Shunt* open
Permanent
Increase foot
Blood flow
Bulging foot veins,
Warm foot
Reduced
sweating
Dry skin
Fissures and
cracks
Muscle wasting
Foot weakness
Postural deviation
Deformities, stress
and shear pressures
Trauma
Stress on bones & joints
Plantar pressure
Callus formation
InfectionUlcer

27. Symmetrical neuropathies Asymmetrical neuropathies
Distal sensory and sensory-
motor neuropathy
Mononeuropathy
Large-fiber type Mononeuropathy multiplex
Small-fiber type Radiculopathies
Distal small-fiber neuropathy Lumbar plexopathy or
radiculoplexopathy
“Insulin neuropathy” CIDP
CIDP

28.  Distal Symmetrical Neuropathy
 The commonest neuropathic syndrome
 “Diabetic neuropathy”
 A “length-related” pattern of sensory loss
 Toes → Feet → Leg (stocking pattern)
 Later motor
 Autonomic neuropathy is less common

29.  Autonomic neuropathy:
 ↓ sweating → dry skin that is likely to crack easily →
risk of infection.
 Warm because of the arterio-venous shunting →
Distension of foot veins that fail to collapse even
when the foot is elevated
 A gangrenous toe in a foot that has bounding
arterial pulses may be seen as there is impairment of
the nutritive capillary circulation because of
arteriovenous shunting.
 The oxygen tension of the blood in these veins is
typically raised.
 Neuropathic edema, which is resistant to treatment
with diuretics but may respond to treatment with
ephedrine

30.  High blood sugar expedites
artherosclerosis giving peripheral
vascular disease (reduction of blood
supply to the foot).
 The delivery of essential nutrients
and oxygen to the foot is
compromised leading to anaerobic
infections and tissue necrosis.
Peripheral arterial disease
Artherosclerosis
narrows or blocks
the arterial lumen
Foot ischaemia
Foot ulcer
Necrosis/ Gangrene
Infection
Artheroma plaque
narrowing the arterial
lumen
Ischaemic toes due to
artherosclerosis
Peripheral Arterial Disease

31. Clinical features (Contd..)
 Ulcers
 ↓ vibration sense
 Glove and stocking distribution of sensory loss
 +ve Romberg’s sign; ↓ ankle tendon reflex
 Wasting of small muscles of feet → Unopposed
pulling of long extensors and flexors → Clawing
of toes → Elevated plantar pressure points at the
metatarsal heads→ Callus formation & foot
ulceration

32. Charcot arthropathy
 A progressive condition of the musculoskeletal system
that is characterized by joint dislocations, pathologic
fractures, and debilitating deformities.

33. Charcot Foot
 More dramatic – less common 1%
 Severe non-infective bony collapse with secondary
ulceration
 Two theories
 Neurotraumatic
 Neurovascular

34. Charcot Foot
 Neurotraumatic
 Decreased sensation + repetitive trauma = joint and
bone collapse
 Neurovascular
 Increased blood flow → increased osteoclast activity →
osteopenia → Bony collapse
 Glycolization of ligaments → brittle and fail →
Joint collapse

35. Charcot’s Foot-- Classification
Eichenholtz
1 – acute inflammatory process
Often mistaken for infection
2 – coalescing phase
3 - consolidation
Location
Forefoot, midfoot (most
common) , hindfoot
Atrophic or hypertrophic
•Radiographic finding
•Little treatment implication

36. Wagner’s classification
Depth of penetration
Extent of tissue necrosis
Treatment given

37. Grade 1
 No open lesion, skin intact
 Potential site for ulceration like prominent
metatarsal heads, hammer toes, Charcot’s
deformity
 Treatment:
 Education & prevention
 Self foot care & proper shoes
 Antibiotics for cellulitis

38. Grade 2
 Superficial ulcer – extension to subcutaneous
adipose tissue
 Treatment:
 Wound care + antibiotics
 Radiological evaluation
 Modified weight bearing bone resection

39. Grade 3
 Ulcer penetrating joint, deep abscess, OM,
tendon sheath infection
 No digital gangrene
 Treatment:
 Hospitalisation
 Debridement and IV antibiotics
 Joint and bone resection

40. Grade 4
 Some part of the foot gangrenous
 Most part salvagable
 Treatment:
 Similar to that for grade 3 + Local amputation

41. Grade 5
 Extensive gangrene
 Limb not salvagable
 Treatment:
 Major amputation

42. University of Texas Diabetic Wound Classification
 Stages
 Stage A: No infection or ischemia
 Stage B: Infection present
 Stage C: Ischemia present
 Stage D: Infection and ischemia present
 Grading
 Grade 0: Epithelialized wound
 Grade 1: Superficial wound
 Grade 2: Wound penetrates to tendon or capsule
 Grade 3: Wound penetrates to bone or joint

43. Depth
Classification
Definition Treatment
0 At-risk foot, no
ulceration
Patient education,
accommodative
footwear, regular
clinical examination
1 Superficial ulceration,
not infected
Offloading with total
contact cast (TCC),
walking brace, or
special footwear
2 Deep ulceration
exposing tendons or
joints
Surgical debridement,
wound care, offloading,
culture-specific
antibiotics
3 Extensive ulceration
or abscess
Debridement or partial
amputation, offloading,
culture-specific
antibiotics

44. Ischemia
Classification
Definition Treatment
A Not ischemic
B Ischemia without
gangrene
Noninvasive vascular
testing, vascular
consultation if symptomatic
C Partial (forefoot)
gangrene
Vascular consultation
D Complete foot
gangrene
Major extremity
amputation, vascular
consultation

45. International Working Group on Diabetic Foot
Classification System
 On the basis of the scientific literature and expert
opinion, five categories were identified,
which were considered the most relevant items for
research projects in diabetic foot ulcers:
 Perfusion
 Extent/size
 Depth/ tissue loss
 Infection
 Sensation

46. PEDIS Classification System

47. History taking
 Age
 Mode of onset
 Bare foot walking
 Paraesthesia
 Claudication pain
 Fever
 H/o DM – Duration, controlled/uncontrolled
 Treatment history
 H/o impotency

48.  Diabetics present to the surgeon in a number of scenarios:
 with any foot and ankle problem and diabetes as an
incidental part of the past medical history - important to
assess how much diabetes increases the risk of any
proposed surgical or non-surgical treatment
 with an acutely inflamed where the main differential
diagnosis is between infection and Charcot arthropathy
 with an ulcer which may or may not be complicated by
deep infection or ischemia
 with a deformity which has led to recurrent ulceration, or
is felt to be a risk factor for ulceration - important to assess
the relative risks of corrective surgery and continuing
protective care

49. Whatever the initial presentation, it is important to ask
about
 what type of diabetes does the patient have (type 1 or type 2)
 how is it managed - diet, oral hypoglycaemics, insulin - and
what agents and regime
 who normally looks after the patient's diabetes - GP/practice
nurse/hospital diabetic clinic and therefore who is likely to
have the patient's diabetic records
 how well controlled is the diabetes - review the patient's
glucose monitoring record and ask when the last HbA1c test
was done and what was the result and the previous trend
 does the patient have any of the major complications of
diabetes
 cardiovascular disease
 renal disease
 eye disease
 has the patient had an ulcer or Charcot arthropathy before - the
single biggest risk factor for either of these conditions is to have
had them before

50. Clinical Examination
 Nourishment, pallor
 A) Limb affected
B) Type of lesion:
 Ulcer
 Gangrene
 Cellulitis / abscess

51. Ulcer: “Malperforant ulcer”
 Site
 Size, shape, margin
 Floor: Slough ±
 Edge: Punched out
 Surrounding skin
 Base: May be bone
 Infected – foul smell
 Local anesthesia of skin

52. Gangrene:
 Usually wet
 Forefoot → Leg
 Edema
 Foul smell
 Skip lesion
 No line of demarcation
 Bone may be exposed

53. Cellulitis / abscess:
 Diffuse tender
 Swelling ±

54. Regional examination:
Deformity of foot
High arching
Local anaesthesia
Regional pulsations: Posterior tibial & Dorsalis
pedis
Lymphadenopathy
Local thrombophlebitis
Local fracture

55. Nylon monofilament test
 For identifying loss of
protective sensation
 Failure to feel the
filament at four of 10
sites is 97 percent
sensitive and 83
percent specific

56. Procedure of NMT
 10 gram Semmes-Weinstein nylon monofilament
 The patient must not watch
 Test the monofilament on the patients hand so that
he/she knows what to anticipate.
 Apply the monofilament perpendicular to the
 Apply sufficient force to cause the filament to bend or
buckle, using a smooth, not a jabbing motion.
 Apply the filament along the perimeter and NOT
ON an ulcer site, callus, scar or necrotic tissue

57. • Apply a vibrating 128 Hz tuning fork to the bony
prominence of the big toe
• If the patient cannot feel the vibration, gradually
move the fork upwards
• The sensitivity of this test for demonstrating a deficit
is ~53%
• A biothesiometer is a portable device that measures
the vibration perception threshold. A vibration
threshold of more than 25V has a sensitivity of 83%.
Tuning fork
test
Either an abnormal 10g monofilament test or a vibration
threshold of more than 25V predicts foot ulceration with a
sensitivity of 100% , hence the rationale for combining these
two tests in clinical practice.
Tuning Fork (vibration)

58. Biothesiometer
 To measure simply and accurately the
threshold of appreciation of vibration in
human subjects.
 An "electrical tuning fork" whose amplitude
may be set to any predetermined level or whose
amplitude may be gradually increased until the
threshold of vibratory sensation is reached.
 Conversely, the amplitude may be lowered
until the vibration is no longer discernible.
 To detect neurological changes that are not
disclosed with a tuning fork.

59. Thermal Exam
 Taking temperature readings on both the plantar and dorsal surfaces of the foot
 may be a good indicator of foot condition. A wide difference of temperatures
between left and
 right feet can indicate possible infection, injury or circulatory problems. Done with
gloves and
 the patient sitting comfortably, shoes and socks off.
 a. Dorsal Temp: Take a reading on the dorsum of the foot near the dorsalis pedis
artery.
 Plantar Temp: Take a reading on the plantar aspect of the foot in the medial arch
area.
Skin & Nail Exam:
 Done with gloves and the patient sitting comfortably, shoes and socks off.
 a. Corns & Calluses: Metatarsal heads, Dorsal aspect of 5th toe, Lateral aspect of 1st
toe, Heel, Plantar surface
 b. Skin appearance: Shiny, thin, fragile
 c. Hair: Normal hair growth / no hair growth
 d. Skin Features: Bruises, Cracks/breaks in skin, Soggy skin, Dry skin, Blisters,
 Discoloration, Ulcerations, Previous surgeries, Tinea Pedis (Fungus)
 e. Nails: Ingrown, Improperly cut, Sharp, Long, Absent

60. Footwear assessment
 Examine the inside of the shoes
 Look at the type of footwear
 Look at the fit of the footwear
 Are there any areas of increased pressure?
 Are there any accommodations made for any
deformities if already present?
 Is the footwear appropriate in size & shape for the
patients feet?
 Would the patient benefit from corrective footwear?
 From inserts?

61. Evaluation of Diabetic foot
 Urine – sugar, acetone
 FBS, PPBS
 Local –
 Radiology – deformity, osteomyelitis, #,
infection
 Doppler & Duplex
 Transcutaneous oximetry
 Mapping of pressure areas by foot prints
 C&S
 MRI, MRA
 Angiography

64. Transcutaneous oximetry
 Application of heat to skin → Localised hyperemia →
If O2 present in excess of skin requirement (depends
on oxygen delivery & blood flow) → O2 diffuses across
skin → Measured by electode
 TcPO2 - 40 – 70 mm Hg (normal)
 TcPO2 <20 mm Hg – Limb threatening ischaemia

65. MRI foot
 Most specific
 Differentiates between bony destruction from OM and
that from Charcot’s arthropathy
 Iridium – labelled white cell studies

66. Risk Stratification

67. Guidelines

68. Interventions in diabetic ulcer
Offloading
Debridement
Wound dressing
Antibiotics
Revascularisation
Limited amputation

69. Offloading

70. Offloading Devices
 Offloading devices are devices used to decrease the
pressure over a wound and protect wounds, thereby
giving the wound a good chance of healing.
 Although many offloading modalities are currently
utilized, only small numbers of case series exist
describing the frequency and rate of wound healing
associated with these devices.

71.  Reduction of pressure and shear forces on the foot
may be the single most important-and most
neglected-aspect of treating neuropathic ulceration.
 Off-loading therapy is a key part of the treatment
plan for diabetic foot ulcers.
 The goal is to off-load (reduce) the pressure at the
ulcer while keeping the patient ambulatory.
Offloading Devices Contd

72. Total Contact Casts (TCCs):
 Most common modality for offloading used by diabetic
foot specialists. This type of offloading was first described
by Milroy Paul in treating cases of neuropathic foot
wounds and became more popular by Dr.Paul Brand at
the Hansen's disease Center in Carville, Louisiana
 This modality of offloading is known as total contact cast
(TCC) due to the technique used to make it. It employs a
well-moulded, minimally padded cast that maintains
contact with the entire planter aspect of the foot and lower
leg.
 TCCs have been shown to reduce pressure at the site of
ulceration by 84 - 92%(7). It is also effective in treating a
majority of non-infected, non-ischemic plantar diabetic
foot wounds, with healing rates ranging from 72% - 100%
over a course of 5 - 7% weeks(8)

73. TCC
Gait modification
 Total contact casts
(TCCs) – gold standard

74. Advantages of TCCs
 Offloading the foot(mainly the anterior aspect)
 Protect the foot from infection
 Help in reduce or control edema

75. Disadvantages of TCCs
 Adds pressure on posterior aspect of foot hence not useful in
case of heal ulcers
 Technically difficult to apply, need special skills.
 Consuming time on its application & Improper cast application
can cause skin irritation.
 Improper cast application can cause frank ulceration
 Loss of flexibility of daily wound assessment.
 Difficulty in daily life activity such as bathing without wetting
the cast
 Users may have difficulty in sleeping comfortably.
 Some designs of TCCs may affect gait stability

76. Contraindications for use of TCCs
 For wounds with ischemia
 For infected wounds
 For wounds with osteomylitis

77. Removable Cast Walkers

78. Advantages of the Removable Cast Walkers
 Easily removed for self inspection of the wound
 Easily removed for local application of topical
therapies
 Easier to do activities such as bathing, sleeping
comfortably.
 Can be used for infected wounds
 Can be used for superficial ulcers.

79.  The amount of pressure reduction for certain RCW is equivalent to
TCCs
 Although some RCWs reduce the pressure as well as TCCs other data
showed that healing with TCCs is more readily achieved than healing
with other modalities.
 Because patients can remove RCWs easily, the best feature of this
device is potentially the most hazardous point.
 In a recently conducted study evaluated the activity of patients with
diabetic foot ulcers and their adherence to their offloading regime.
This study suggests that it is less than 30% of their total daily activity
 Due to the disadvantages of the TCCs it has been suggested to make
an alternative which might make the RCWs difficult to remove.This
alternative called instant total contact cast (iTCC). Wrapping the
RCW with either a layer of cohesive bandage or plaster / fiberglass,
making it more difficult for patients to remove.
The great advantage of iTCC is that it binds the benefit of offloading
plus the benefit of forced compliance.

81. Scotch Cast Boot
 Finishing below ankle
 It was developed when
fiberglass materials
were introduced. Its
development was to
alternate with the
plaster of Paris casts.
 The boot is made to fit
each individual foot
and a window cut at
the site of ulceration

82. Advantages of Scotch Cast boot
 Light in weight
 Removable and allowing regular inspection of the
wound and facilitates the redressing of the wound.
 Reduces pressure on the lesion
 Maintains patient mobility
 Protects the wound and remaining foot

83. Some other offloading devices
 The Neuropathic CROW
(Charcot Restraint
Orthotic Walker)
 The off-loading of foot
ulcers, unstable Charcot
foot/ankle
 This model provides a
total contact interface,
pretibial shell, and
rocker bottom

84. Pneumatic
walker – air cast

85. HALF SHOES
 To relieve pressure on
forefoot post
operatively
 ADVANTAGES
Easy to apply
Inexpensive
Removable
 DISADVANTAGES
Efficacy decreased
Unstable gait

86.  Double H boot
 Pressure relieving ankle
foot orthosis (PRAFO)

87. Healing Sandals
Therapeutic Footwear
Silicon Insoles
Sandal with a rigid rocker limiting
dorsi flexion of MCP joint

88. CRUTCHES, WALKERS, WHEELCHAIRS
The best!!...but
 Requires upper body
strength
 Endurance
 Pressure on opposite
foot increased

89. Hyperbaric Oxygen therapy
 Adjunctive therapy in
 Persistent critical limb ischemia, soft tissue infection,
and impaired wound healing from osteomyelitis
 If TcPO2 > 200 mmHg close to the trophic lesion in 2.5
ATA hyperbaric oxygen.
 Peri-wound TcPO2 > 400 mmHg in 2.5 ATA hyperbaric
oxygen or > 50 mmHg in normobaric pure oxygen ═>
Healing chance very high

90. MOA of hyperbaric oxygen
 ↑ angiogenesis
 ↓ infection by killing bacteria
 ↓ pain and inflammation
 Releases stem cells from bone marrow
 ↓ risk of thrombosis
 Enhances nerve regeneration
 Improves bone density
 Eliminates toxins from blood

92. Advice to patients
 Inspect your feet daily
 Wash your feet in lukewarm water
 Be gentle when bathing your feet
 Moisturize your feet—but not between your toes
 Cut nails carefully—and straight across
 Never trim corns and calluses
 Wear clean, dry socks
 Avoid open-toe / open-heel shoes

93. Advice to patients Contd
Wear socks to bed
Shake out shoes and inspect the inside before wearing
Keep your feet warm and dry
Never walk barefoot
Take care of your diabetes
Don't smoke
Get periodic foot exams

94. Annual foot examination
 Assess
 Blood flow
 Sensation (monofilament testing, pin prick, tuning fork)
 Ankle reflex
 Nail care
 Look for foot deformities
 Identify sites of potential ulceration

95. Lower Extremity Amputation Prevention
(LEAP) Program
 The L.E.A.P. Program consists of five relatively simple
activities:
 Annual foot screening
 Patient education
 Daily self inspection of the foot
 Appropriate footwear selection
 Management of simple foot problems

96.  Check his/her feet daily for
early lesion

97. New developments
 Bioengineered skin (Apligraf)
 Human dermis (Dermagraft)
 are new types of biologically active implants for ulcers
that are derived from fibroblasts of neonatal foreskins
 PDGF
 Hyaluronan
 Epalrestat (Aldose reductase inhibitor)
 Lipoic acid, Thioptic acid
 VAC
 Hydrocolloid dressing

98. Apligraf
 Apligraf® is a unique, advanced treatment for healing. It is
created from cells found in healthy human skin. Which explains
why it looks like a thin, piece of real skin.
 It is used to heal ulcers such as diabetic foot and venous leg
ulcers that are not healing after 3-4 weeks, despite treatment
with conventional therapies.
 When healthy skin gets wounded, the proteins and growth
factors in the skin stimulate the body to regenerate new skin.
This is the normal wound healing process.
 However with diseases like diabetes the skin is missing these
biological substances, and the healing cycle is broken. This leads
to the development of non-healing ulcers and wounds.

99. Apligraf
 Apligraf® contains two types of cells – an outer layer of
protective skin cells, and an inner layer of cells contained
within collagen. Both types of cells contain substances
similiar to those found in human skin.
 Apligraf® plays an active role in healing by providing to the
wound living cells, proteins produced by the cells, and
collagen, which are important for healing.

100. Apligraf
•Apligraf® is placed directly on the
wound.
•The wound is then covered with a
non-adhesive dressing to keep
Apligraf® in place.
•The area is then wrapped with other
dressings that are changed weekly
by the doctor
•The healing process now begins,
and improvement of the wound can
usually be seen within weeks.

102. Apligraf: How is it Made?
 Human keratinocytes and fibroblasts are derived from
neonatal foreskins obtained for use under informed-
consent guidelines
 The foreskin is decontaminated with antibiotics,
antifungals, and an ethyl alcohol rinse.
 Production of cell stocks involves enzymatic digestion
of the foreskin tissue and fibroblast/keratinocyte
isolation1

103. Dermagraft
 Advanced BioHealing is a The Company that currently
manufactures and markets Dermagraft®, a bio-engineered
skin substitute that assists in restoring damaged tissue and
supports the body’s natural healing process.
 Dermagraft is approved by the FDA for the treatment of
diabetic foot ulcers.
 It is a Cryopreserved human fibroblast-derived dermal
substitute, approved by the FDA for the treatment of
diabetic foot ulcers.
 A combination of living fibroblasts, matrix proteins,
and bound factors that protect the wound and
stimulate dynamic events that promote regeneration
and repair.

104. Dermagraft
To treat Diabetic foot ulcers that have
been present for more than 6 weeks
It is used together with standard methods
of treating foot ulcers, including cleaning
and preparing the wound, applying cover
dressings to hold it in place, and offloading
devices.

106.  Dermagraft is indicated for use in the treatment of full-
thickness diabetic foot ulcers greater than 6 weeks
duration, which extend through the dermis, but without
tendon, muscle, joint capsule, or bone exposure..
 In a trial, a 64% relative increase in complete wound
closure was seen in the Dermagraft-treated patients; 30.0%
of Dermagraft and 18.3% of conventional therapy patients
achieved complete wound closure at 12 weeks.
 The most frequently reported adverse events experienced
by patients in the Dermagraft group (terms ≥ 5%) included
infection, accidental injury, skin dysfunction/blister, flu
syndrome, osteomyelitis, surgeries involving study ulcer,
wound enlargement/skin ulcer, cellulitis and peripheral
edema/localized swelling. These adverse events were
similar to those seen in the control group.

107. PDGF
 Platelet-derived growth factor is mainly secreted by the
platelets’ α-granule, but it is also produced by other cells
involved in early wound healing, ie, macrophages,
endothelial cells, fibroblasts, and keratinocytes
 PDGF is a powerful chemoattractant and mitogen, exerting
its action on fibroblasts, smooth muscle cells, and
endothelial cells
 It also induces production of fibronectin and hyaluronic
acid.
 There is a synergistic effect between PDGF and EGF, as well
as TGF-β, and so PDGF has a pivotal role at all stages of
wound healing

108. PDGF
 At present, recombinant PDGF
 by DNA technology via incorporation of the gene for
the β-chain of human PDGF into the yeast
Saccharomyces cerevisiae.
 The resultant homodimeric protein, Becaplermin, has
a biological activity similar to the endogenous PDGF-
BB
 Approved by the US Food and Drug Administration
for the treatment of diabetic neuropathic ulcers with
adequate peripheral circulation

109. Hydrocolloid Dressing
 Duoderm[1], Granuflex[2], and 3M Tegaderm Hydrocolloid)
 An opaque dressing to provide a moist wound-healing
environment, while protecting from contamination.
 Hydrocolloids were initially utilized in medicine as a reliable,
skin-friendly adhesive, useful for securing colostomy appliances
to the patient's abdomen
 Clinicians observed that acute abdominal wounds from
colostomy operations healed more rapidly when a hydrocolloid
was used.
 It is biodegradeable, nonbreathable and adheres to the skin so
no separate taping is needed.

110. Hydrocolloid Dressing Contd
 The active surface of the dressing is coated with a cross-linked
adhesive mass containing a dispersion of gelatin, pectin and
carboxy-methylcellulose together with other polymers and
adhesives forming a flexible wafer.
 In contact with wound exudate, the polysaccharides and other
polymers absorb water and swell, forming a gel which is held
within the structure of the adhesive matrix.

111. Hydrocolloid Dressing Contd
 The moist conditions produced under the dressing promote
fibrinolysis, angiogenesis and wound healing, without causing
softening and breaking down of tissue.
 The gel which is formed as a result of the absorption of wound
exudate is not mobile and free running but held within the
structure of the adhesive matrix.
 Most hydrocolloid dressings are waterproof, allowing normal
washing and bathing. [2]
 Dressings may be used even if aerobic infection is present

112. Colloidal Silver
 Silver -- colloidal or ionic silver, silver in solution -- is a
potent antibacterial product. It has been demonstrated as
such for well over 100 years.
 Silver is incorporated into the wound pad of the new
bandages which come in a variety of sizes
 Eg: Hydroheal AM Gel & Dressings

113. Colloidal Silver
 Silver interferes with the bacteria in at least three ways:
 by interacting with the cell membrane,
 binding to the DNA of cells, and
 blocking the metabolism of the bacteria.
 It reduces the growth of hundreds of different types of
bacteria, including some that do not normally react to
pharmaceutical antibacterial agents.
 Because silver blocks the growth and spread of germs through
multiple mechanisms, it is hard for bacteria to build up
resistance