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164
Manipal Manual of Surgery
DIABETIC FOOT
“Diabetic foot is a complex disease with many complications
and every effort should be made to understand and treat it in
as simple way as possible”—Dr Amit Jain, Founder of
Modern Diabetic Foot Surgery.
Diabetes is extremely common worldwide, is
increasing day by day and it has various complications.
Diabetic foot is a distressing, devastating complication
of diabetes and is common neglected problem that can
lead to amputation which can result in patient becoming
handicap. The numerous problems (Amit Jain’s
categorization) associated with diabetic foot are listed
in Key Box 26.5.
Key Box 26.5
Amit Jain’s classification of problems of diabetic foot*
Categories of Type Examples
foot problems
Category 1 Preponderant Diabetes mellitus
Category 2 Current Abscess, ulcer, gangrene,
etc.
Category 3 Concurrent Hypertension, heart disease,
kidney disease, etc.
Category 4 Recurrent Re-amputation, re-ulcera-
tion, re-admissions, etc.
Category 5 Subsequent Mortality, major amputa-
tions, stump complications,
etc.
Category 6 Supplement Depression, loss of job,
financial issues, etc.
• Various risk factors are given in Key Box 26.6.
Diabetic foot is a triad that mainly consists of
neuropathy, infection and ischemia.
1
1. Neuropathy:
It commonly manifests after about
10 years of diabetes though it can occur early if there
is uncontrolled diabetes and it can be sensory, motor
or autonomic. Neuropathy may be distal and diffuse
with a stocking type of distribution. Nerve damage
is due to the formation of sorbitol from sugar.
Sorbitol causes demyelination of large fibres. New
arteriovenous communications open beneath skin,
diverting nutrient flow away from it. This ischaemic
tissue is vulnerable to infection, causing nerve
ischaemia. Loss of vibration sense and deep tendon
reflexes occur early. Later, joint position, touch, pain,
and temperature sensations are lost. As a result of
this, a trophic ulcer develops. It progresses and may
penetrate deeper and deeper. The patient is often
unaware of this as he has no pain and he continues
walking on it and ultimately the ulcer may get infected.
• Diabetic neuropathy of the tibial nerve is
dangerous. Clawing of the toes and hammer toe
result due to the paralysis of intrinsic muscles of
the foot. Sensation is absent over the entire sole
due to involvement of the medial and lateral
plantar nerves. These two factors predispose to the
development of pressure sores over the plantar
surface of the head of the metatarsals.
• Charcot’s arthropathy (joints) is a form of arthritis
seen in neuropathic foot with good vascularity and
it leads to severe deformity. Often midfoot bones
and joints are affected.
• Autonomic neuropathy leads to absence of sweat-
ing and gives rise to anhydrotic skin (Key Box 26.7).
Key Box 26.7
Key Box 26.6
Risk Factors for Diabetic Ulcer Foot
Male above 50 years
DM of more than 10 years duration
Blood glucose levels not controlled
Peripheral neuropathy
Abnormal structure of foot
Peripheral vascular disease
Smoking and hypertension
Increased level of lipids
Genetic factors
*If a patient has gone through any 5 problems, then the patient is said to have a “Diabetic Foot Storm” in his life. This term was recently coined by Amit
Jain. Once he gets any 3 problems, he should be warned of diabetic foot storm and preventive strategies are advised including screening and education.
Professor of Surgery, Shri Raj Rajeshwari Medical College, Bengaluru
1
Burning or tingling in plantar aspect of forefoot radiating to toes—Morton’s interdigital neuroma.
Section II • General Surgery
Loss of vibration and touch
Loss of pain and temperature
Dead like feeling in the feet
Sensation of walking on the ‘sand’
Susceptible for repeated trauma
Nylon monofilament test is routinely used to test
neuropathy by pressing in on the foot/sole
Autosympathectomy is a feature of diabetic foot ulcers.
Diabetic Neuropathy
Differential Diagnosis of Leg Ulcer and Pressure Sore
165
• Various factors of neuropathy contribute to
changes in the configuration of the foot and a
change in gait. The foot becomes shorter and wider.
The longitudinal arch becomes flat. New pressure
points develop, resulting in ulcers in the foot
(Key Box 26.8).
Key Box 26.8
Effects of Diabetic Neuropathy
Loss of sensation
Loss of sweating
Loss of muscle strength
Loss of curvature of foot
Loss of normal joint position
Loss of elasticity of skin
2. Resistance to infection is reduced in patients with
diabetes mellitus. Patients with uncontrolled diabetes
are more susceptible to infection. Even though leukocytosis occurs in diabetic patients with infection, the
phagocytic activity of the leukocytes is greatly
reduced.
• In ketoacidosis, granulocyte mobilisation is
impaired and chemotaxis is reduced. Thus, these
patients are more susceptible to polymicrobial and
fungal infections.
3. Atherosclerosis: Diabetic angiopathy involving major
vessels results in ischaemia of the foot (macroangio-
pathy). These patients have accelerated atherosclerosis.
In addition, it also produces small vessel disease in
the form of nonspecific thickening of the basement
membrane (microangiopathy) (Key Box 26.9).
Different Sequence of Events in
Diabetic Foot P
atients (Fig. 26.16)
1. Stage of cellulitis: Following an injury or trivial
trauma, redness can develop along with swelling and
oedema of the leg.
2. Stage of spreading cellulitis: Cellulitis takes up a
virulent course and spreads deeper and upwards along
fascial planes. When infection is severe, necrotising
fasciitis may occur with renal failure and septic
shock.
3. Stage of abscesses: Secondary infection caused by
mixed organisms along with anaerobes and nonclostridial gas-forming organisms produce multiple
abscesses.
4. Stage of gangrene: Tense oedema and the existing
vascular compromise produce ischaemia and
gangrenous patches of skin, toes, etc. The gangrene
can be wet gangrene or dry gangrene.
5. Stage of osteomyelitis: Infection involves deeper
tissues like the bone, leading to osteomyelitis.
6. Stage of septicaemia: Some patient can present in
emergency with septicemia. This is due to untreated
cases of gangrene, abscess, cellulitis, etc. which can
spread locally and systemically producing septicaemia and diabetic ketoacidosis.
Amit Jain’s Staging for Cellulitis (Table 26.5)
This new staging system consists of 4 sequential
progressive clinical stages of primary cellulitis and gives
a corresponding treatment guide. This is extremely
simple, easy to remember, practical staging that can be
Key Box 26.9
Diabetes and Atherosclerosis
16% of diabetic patients have PVD (peripheral vascular
diseases)
Collateral circulation is reduced in diabetics
Atherosclerotic plaque causes increased ulceration and
cracking
More severe the diabetes, more severe will be peroneal
occlusive disease
Thus, neuropathy or microangiopathy singly or in
combination with secondary infection favours the
development of a diabetic ulcer. The ulcer forms due to
minor trauma, such as from a thorn prick, trimming of
the nail, or a shoe bite. It may also start as a callosity in
the sole of the neuropathic foot. Hence, utmost care
should be taken to protect the feet of patients with
diabetes mellitus.
Fig. 26.16: Various stages of infection of the leg in diabetic
patients. (Events need not follow the same order)
Section II • General Surgery
166
Table 26.5 Amit Jain’s staging system for cellulitis
Stage of Clinical description Treatment guideline
cellulitis
Stage 1 Cellulitis without Broad spectrum antibiotics,
any abscess or limb elevation, and crepe
necrosis bandage.
Monitor the patient daily
Stage 2 Cellulitis with either Requires some form of
localized abscess or surgical intervention, like
skin necrosis drainage of abscess or
debridement.
Stage 3 Necrotizing fasciitis Extensive radical debride-
without myonecrosis ment of all the devitalized
tissues/amputation based
on extensiveness
Stage 4 Necrotizing fasciitis Radical debridement and
with myonecrosis some form of amputation is
invariably performed at this
stage
Fig. 26.17: Stage 1
cellulitis
Fig. 26.18: Stage 3 wherein necrotizing
fasciitis has occurred
Manipal Manual of Surgery
Fig. 26.19: Destruction of metatarsal bone and dislocation of
metatarsal joint
5. Liver function test (LFT), ECG, chest X-ray, blood
urea, and serum creatinine to be done as a routine
(remember diabetes is a systemic disease).
6. Lower limb arterial duplex scan is an important
investigation to check for the patency of vessels. It is
useful investigation if foot pulses are not felt
• Normally, the flow is laminar and triphasic
• In patients with diabetic foot, the flow becomes
turbulent and there is loss of diastolic forwards
flow.
. Hand held Doppler and measurement of ankle
7
brachial index (ABI) is a bedside test. ABI of less than
0.9 indicates ischemia.
CT angiogram is done in case of ischemic ulcer not
healing or presence of dry gangrene. If vessels are
extensively calcified or if there is elevated creatinine,
then MR angiogram can be considered. Often it is seen
that below popliteal vessels are involved (Fig. 26.20).
used for extremities and also in nondiabetics. The stage 1
cellulitis (Fig. 26.17) should be managed conservatively
with good antibiotics and one should prevent it from
progressing to more serious stages (Fig. 26.18). Stage 4
is associated with amputation.
Investigations
1. Complete blood picture usually demonstrates a high
total count (infection).
.
Blood—fasting blood sugar, postprandial blood sugar
2
and glycosylated haemoglobin to be done.
3. Pus should be sent for culture/sensitivity. Deep
tissues can also be sent intraoperatively. Common
microbes seen in diabetic foot are Escherichia coli,
Staphylococcus aureus, Klebsiella, etc.
4. X-ray of the foot to be done to rule out osteomyelitis,
which may be the cause for chronicity of the ulcer
(Fig. 26.19). It takes weeks for visible changes of
osteomyelitis on radiograph. Today in all such
Section II • General Surgery
doubtful cases, MRI of the foot/leg is done.
Fig. 26.20: Lower limb angiogram. Note the bilateral
infrapopliteal arterial disease
DIABETIC FOOT CLASSIFICATION (see K
ey Box 26.10)
There are several classification for diabetic foot ulcer
which is a common clinical focal pathology. The
commonly used diabetic foot ulcer classification from
West is Meggit-Wagner classification (Key Box 26.10).
Another modern diabetic foot ulcer classification is Amit
Differential Diagnosis of Leg Ulcer and Pressure Sore
Key Box 26.10
167
Grading of Diabetic Ulcer Foot
Modified Wagner grading system of diabetic ulcer foot
Grade 0: No skin changes
Grade 1: Superficial ulcer
Grade 2: Ulcer extension
a. Involves ligament, tendon, joint capsule or
fascia
b. No abscess, no osteomyelitis
Grade 3: Deep ulcer with abscess or osteomyelitis
Grade 4: Gangrene of the portion of forefoot
Grade 5: Extensive gangrene of foot
Fig. 26.21: Infected ulcer. This is class 3 diabetic foot ulcer
(AJ S1A1C3)
Jain’s ulcer classification (Key Box 26.11). This is a new
original diabetic foot ulcer classification from India that
divides ulcers into 3 types that are extremely easy to
remember (Fig. 26.21). It also has an Amit Jain’s ulcer
Key Box 26.11
scoring system that predictis amputation and a coding
system (Amit Jain’s SAC coding) to be used in lines of
TNM system (Key Box 26.12).
Amit Jain’s diabetic foot ulcer classification
Class of diabetic foot ulcer Description Causation Examples
Class 1 Simple ulcers There is no intrinsic cause of Trophic ulcers
non-healing
Class 2 Complex ulcers There is intrinsic cause of Claw toe ulcers, ischemic
non-healing like bony or ischemia ulcers, etc
Class 3 Complicated ulcers These ulcers have underlying Ulcers with osteomyelitis
infection
Key Box 26.12
Amit Jain’s SAC coding for diabetic foot ulcer
Size (S) Anatomical area involved (A) Amit Jain’s class of ulcer (C)
S1–Less than 2 cm A1–Forefoot C1–Class 1
S2–2–4 cm A2–Midfoot C2–Class 2
S3–More than 4 cm A3–Hindfoot C3–Class 3
Amit Jain’s Universal Classification for Diabetic Foot
Complications
This is a new, simple, easy-to-remember, practical, open,
complete, descriptive, modern diabetic foot classification
which is also from India that includes almost all the
complication of diabetic foot seen worldwide. It divides
diabetic foot into 3 simple types (Table 2
6.6). It has a sequel
(Amit Jain’s surgical scoring system) that predicts major
amputation and is governed by Amit Jain’s law of
classification which suggest using combination of classification like universal classification and surgical scoring,
as a single classification cannot be made for diabetic foot
complications that has many pathological entities.
Amit Jain’s DIABETIC FOOT acronym covers all the
lesions seen in this universal classification (Key Box 26.13)
Table 26.6 Amit Jain’s universal classification for diabetic
foot
Type of diabetic foot Lesions
complication
Type 1 diabetic foot Cellulitis, abscess, wet gangrene,
complications [infective] necrotizing fasciitis, etc.
Type 2 diabetic foot Trophic ulcers, dry gangrene,
complications ischaemic ulcer, claw toe, hammer
[noninfective] toe, charcot foot, diabetic bullae, etc.
(Figs 26.22 and 26.23)
Type 3 diabetic foot When type 2 complications get
complications [mixed] infected
Classical examples—trophic ulcer
with osteomyelitis, dry gangrene
with secondary infection, etc.
Section II • General Surgery
168
Manipal Manual of Surgery
Key Box 26.13
Amit Jain’s DIABETIC FOOT
Dry gangrene
Infective gangrene (Fig. 26.22)
Abscess (Fig. 26.23)
Bullosis diabeticorum
Erysipelas
Trophic ulcer
Ischemic ulcer
Cellulitis
Flesh eating bacterial disease, Fungal infections
Osteoarthropathy (Charcot foot)
Osteomyelitis
Toe deformities
on the requirement. With the availability of glucometers and the estimation of GRBS, the sliding scale
method based on urine sugar estimation has become
obsolete.
2. Control of infection: Commonly used empirical
antibiotics are fluoroquinolones and cephalosporins.
Often metronidazole is added if severe infection.
Once the culture/sensitivity report is available,
appropriate antibiotics should be started. Commonly,
gram-positive, gram-negative, and/or anaerobic
infections exist. Antibiotics may have to be continued
for a long time based on the nature, type, and severity
of infection. Presence of high-grade fever with chills
and rigors suggests the development of multiple
abscess pockets that need to be drained, rather than
an indiscriminate change in antibiotics. If infection
is not controlled properly, ketoacidosis may occur.
3. Local treatment of diabetic foot ulcer: Diabetic ulcer
is a nonhealing ulcer. Hence the aim should be
towards healing of that ulcer. Management of these
ulcers involves debridement, dressings, using iodine
solution in infections and offloading the ulcer. Once
the ulcer is granulating well, then it can be allowed
to heal on its own if small or one can do split skin
grafting. One should avoid using povidone iodine
or hydrogen peroxide on good granulating wound
as they can delay wound healing.
There are numerous modern wound dressing pro-
Fig. 26.22: Wet gangrene left
foot. This is type 1 diabetic foot
complication
Fig. 26.23: Abscess. This is also
type 1 diabetic foot complication
ducts available that can be used during the course of
ulcer management like hydrogels, foams, hydrocolloid, alginates, etc. Hydrogels are commonly used
nowadays and are also affordable. It provides mois-
Treatment1of Diabetic Foot Ulcers
It may be discussed under the following headings:
ture of wounds. Diabetic wounds heal very slowly
or delayed healing (Fig. 26.24).
• Control of diabetes
• Control of infection
• Local treatment of the ulcer—debridement
• Amit Jain’s grading of debridement
• Various types of surgery for diabetic foot ulcer
2
• Care
of the patient as a whole
• Revascularisation of the foot
• Vacuum assisted closure (VAC) therapy
• Limited access dressing (LAD)
1. Control of diabetes: It is an important part of the
treatment of diabetic foot ulcer. Diabetes precipitates
infection, which worsens the diabetic status. These
ulcers are better managed, at least in the initial period,
with insulin rather than oral antidiabetic drugs alone.
Inj. plain insulin is given 3–4 times/day depending
1
Even a small diabetic ulcer should be treated properly. Otherwise, a patient may have to ‘pay through his foot’ for it.
2
Section II • General Surgery
This is an important aspect often forgotten by the treating physicians and surgeons.
Fig. 26.24: Delayed healing of diabetic ulcers
Differential Diagnosis of Leg Ulcer and Pressure Sore
There are numerous products being launched yearly and one
should be cautious in using them blindly. Remember, many
patients are already in financial misery and one should avoid
adding further financial burden through expensive products.
4. Amit Jain’s modified grading1 for debridement
(Table 26.7): Debridement is an essential and key
surgery to prevent the spread of infection. It is
frequently performed for abscesses, infected ulcers,
necrotizing fasciitis, etc. The new Amit Jain’s grading
system divides surgical debridement into 4 grades
[G1–4] based on the tissues removed, extent of
regions debrided [E1–3], and repetitions of
169
Fig. 26.25: Showing status post-debridement (Amit Jain’s G3 E2 R0)
Table 26.7 Amit Jain’s modified grading for debridement
Grade of Description Modified
debride- coding
ment [G]
Grade 1 Removal of sloughs from G1
the ulcer, callus removal,
deroofing the large
blisters/blebs, removal of
desiccated tendons, etc.
Grade 2 Removal of necrotic/ G2
unhealthy skin and
subcutaneous tissue
Grade 3 Removal of infected/ G3
necrotic skin, subcutaneous
tissue along with either
tendons/retinaculum/deep fascia
Grade 4 Removal of infected/necrotic G4
skin, subcutaneous tissue,
tendon/retinaculum/deep
fascia along with necrotic/
infected muscle
Extent of debridement [E]
Only 1 site [foot/leg/thigh] E1
2 Sites [foot + leg or leg + thigh] E2
3 Sites [foot + leg + thigh] E3
Repetition of debridement [R]
Debridement not repeated R0
Debridement repeated once R1
Debridement repeated twice R2
Debridement repeated thrice R3
Debridement repeated … R …
debridement [R1, 2, 3,...] performed in the operation
theatre. Debridement may be coded as GER (like
TNM staging). This grading system is simple, easy,
practical, reproducible, and applicable in day-to-day
practice and may be used for upper extremities as
well (Fig. 26.25).
The other types of nonsurgical debridement are
enzymatic debridement wherein papain urea is used,
mechanical debridement and biological debridement
wherein sterile maggots are used to remove necrotic
tissue.
2
5. Various types of surgery
for diabetic foot (Table 26.8).
Debridement is the commonly performed procedure.
Amputation becomes necessary if tissues are
destroyed or part is not salvageable. Always try to
save limb as much as possible. There are different
types of foot amputation (Table 26.9). Type 1 foot
amputations are most commonly performed in clincal
practice.
Table 26.8 Aim—to save the leg
Spreading ulcer with slough Debridement
Healing ulcer Skin grafting/flaps (reverse
sural flap)
Incision and drainage
Abscess Disarticulate toe
Gangrene toe Excision of metatarsal bones
Involvement of metatarsal bones Forefoot amputation
Gangrene confined to toes Multiple fasciotomy/de-
compression/debridement
Spreading cellulitis/necrotising Amputation below knee or
fasciitis above knee
Spreading cellulitis with gangrene Revascularisation, infraIschaemic limb inguinal bypass
1
This is a new classification and new grading system applied in diabetic foot. However, students are requested to verify the procedures with your
senior faculty in the institution.
2
Unfortunately in some patients, in an attempt to save the limb, all these surgeries will be done and at last, they may end up with amputation of the
leg.
Section II • General Surgery
170
Table 26.9 Amit Jain’s classification for foot amputation
Type of foot amputations Description Examples
Type 1 foot amputations Simple Toe amputation, transmetatarsal amputation
Type 2 foot amputations Complex Lisfranc, Chopart
Type 3 foot amputations Complicated Syme’s amputation
Manipal Manual of Surgery
All the amputations below malleoli are considered
to be minor amputation, whereas amputation above
malleoli are major amputations like below knee
amputation. Amit Jain’s destructive/amputation
ladder (Fig. 26.26) provides various types of amputation available for extremity starting from distal to
proximal most amputation (Key Box 26.14).
Fig. 26.26: Amit Jain’s amputation ladder
Key Box 26.14
Remember following ladders
Reconstructive ladder: Wound closure options
Destructive ladder (Amit Jain’s): Amputation options
WHO analgesic ladder: Pain relief options
Revascularization is done if limb is ischemic and
wound is nonhealing. Today, peripheral angioplasties
are more commonly done compared to peripheral
bypass procedure.
Once the wound has good granulations, then it can
be allowed to close by secondary healing, sutured,
split skin grafting can be done in case of large wounds
or flaps may be required (reconstructive ladder).
6. Care of the patient as a whole (Table 26.10): Recovery
and healing of diabetic foot ulcer may range from a
few weeks to a few months. During this period, there
are various other aspects to be looked after, other than
infection and insulin. Ensure patient’s blood pressure
and lipids are under control. If patients are on blood
thinning agents like aspirin, then they should be
stopped prior to surgery and restarted later.
7. Revascularisation of the foot:
• Ankle brachial pressure index is misleading because
of calcified vessels (incompressible).
• Duplex ultrasound assesses both anatomical and
functional abnormality. If there is stenosis, the peak
systolic velocity ratio will be >2 across the arterial
lesion.
• Angiography is still the gold standard.
• For short stenotic lesions, balloon angioplasty with
or without stent placement is performed.
• Infrainguinal bypass surgery—popliteal to tibial
or pedal artery using the long saphenous vein.
• Even after successful surgery, the amputation rate
is about 35%. The 2-year patency rate is around
70%.
Patients are given aspirin and lipid lowering agents
like Atorvastatin in post-revascularization period.
Table 26.10 Various problems and their solutions
Problems Solutions
Nutritional factors Diabetic diet should be given
A bedridden patient may have difficulty in passing urine, Catheterisation (Foley’s catheter) under aseptic measures,
situation worsened by pre-existing benign prostatic hypertrophy frequent change of catheter and catheter care
Chest infection such as pulmonary tuberculosis or static Control of tuberculosis, pneumonia, chest physiotherapy
pneumonia
Development of bedsores Frequent change of position and nursing care
More sensitive to carbohydrate metabolism, protein Frequent checking of Hb%, total proteins, blood glucose
depletion and changes in water and electrolyte metabolism and electrolyte levels, etc.
Section II • General Surgery
Differential Diagnosis of Leg Ulcer and Pressure Sore
171
8. Vacuum assisted closure (VAC) therapy: It is also
called vacuum therapy, vacuum sealing, or topical
negative pressure therapy. It is used to drain blood
or serous fluid from a wound or operation site.
Technique
• Necrotic tissue in eschar
• Malignancy
9. Limited access dressing (LAD): A simple plastic
sheet covers the wound and intermittent suction is
applied. It is cheaper than VAC (Fig. 26.28).
• Foam with an open-cell struc-
ture is introduced into the
wound and a drain is kept
and brought out by multiple,
lateral holes. The entire area
is then covered with a transparent adhesive membrane,
which is firmly secured to the
normal healthy skin around
the wound margin. The drain
tube is connected to a vacuum
and fluid is drawn from the
wound through the foam into
a bag (Fig. 26.27).
Fig. 26.27: VAC
• The plastic membrane prevents the inflow of air and
bacteria. It also allows a partial vacuum to form
within the wound, facilitating the removal of fluid.
How does it work?
• Negative pressure assists with the removal of
interstitial fluid, decreasing localised oedema and
increasing blood flow.
• This, in turn, decreases tissue bacterial levels.
• Mechanical deformation of cells occurs, which results
in protein and matrix molecule synthesis, which
increases the rate of cellular proliferation.
• Equipment: Microprocessor-controlled vacuum unit
capable of providing controlled levels of continuous or
intermittent sub-atmospheric pressure (25–200 mmHg).
Indications
• Venous ulcers, diabetic ulcers, large ulcers following
Patient Education to Protect the Feet of
Patients with Diabetes Mellitus (Key Box 26.15)
• Never walk barefoot. Preferably use microcellular
rubber sandals, which are not only soft, but also allow
oxygenation.
• Keep the foot dry after proper cleaning.
• Paring and trimming of toenails should be done care-
fully. If infection sets in, consult a physician at the
earliest.
• Avoid applying herbal medicines or lotions to a
corn. Consult surgeons for the treatment of corns.
• Proper and regular control of diabetes by diet and
frequent measurement of blood sugar.
• Do not consult neighbours
• Reassurance and good rapport with the treating
doctors is needed.
• Since these patients have peripheral neuropathy, they
will not be able to appreciate the temperature of water.
Pouring hot water over the foot may cause burns
without the patient being aware of it. Hence, a
bystander has to check the temperature of water before
it is used by the patient. Avoid dipping leg in hotwater.
necrotising fasciitis, and any chronic ulcers.
• Patients with open fractures.
Key Box 26.15
• Soft tissue injuries, including sacral pressure ulcers,
acute traumatic soft tissue defects, and infected soft
tissue defects following rigid stabilisation of lower
limb fractures.
• Treatment of burns and wounds in the perineum,
hand, or axilla.
Contraindications
• Osteomyelitis—first treat osteomyelitis and then
apply VAC
• Internal fistula
1
Remember it is the patient’s leg that may have to be amputated and not the neighbour’s!
Barefoot walking should be avoided
Avoid herbal/local ointment application
Regular and rigorous control of diabetes with diet
Exercises
Foot care—dry, frequent cleaning and corn care
Oxygenation to toes/foot, proper shoes (MCR)
O Do not consult Others
Trimming of nail should be done carefully
Remember as BAREFOOT
Fig. 26.28: Limited access dressing
1
.
Public Education in DiabetIc Patients
Section II • General Surgery
172
Manipal Manual of Surgery
VARIOUS ASPECTS OF DIABETIC ULCER FOOT (Figs 26.29 to 26.39)
VARIOUS ASPECTS OF DIABETIC ULCER FOOT
Fig. 26.29: Cellulitis leg Fig. 26.30: Clawing of toes Fig. 26.31: Wet gangrene with abscess foot
Fig. 26.32: This patient had heat burns
following barefoot walking resulting in ulcers
Fig. 26.35: Diabetic ulcer
with moist gangrene. Patient
had ketoacidosis with septicaemia. In spite of amputation, patient died
Fig. 26.36: Extensive diabetic
ulcer of the foot—needed
below knee amputation
Fig. 26.33: Pale granulation tissue and
purulent discharge
The best way to avoid complications related to diabetes
is by controlling the sugar levels by diet alone or by
diet with insulin or oral hypoglycaemic agents.
Screening of foot in diabetes: Diabetic foot is one such
disease where prevention is better than treatment and
as far as possible one should see that the feet should
not be affected. Although physicians are the one to see
diabetes patient often, it is responsibility of surgeons
also to screen the foot as and when possible. Screening
the foot in diabetes can prevent most complications for
long period and a diabetic foot storm can be prevented
Section II • General Surgery
in his life.
Fig. 26.34: Red granulation tissue-healing
after control of diabetes and regular dressings
Fig. 26.37: Artificial
limb prosthesis
Fig. 26.38: Microcellular
rubber (MCR) chappals
specially designed for
patients with neuropathic
. They avoid pressure
foot
points
Fig. 26.39: Below
knee amputation
(see Chapter 70 on
amputation under
operative surger
more details)
Amit Jain’s triple assessment for foot: Screening of the
foot in diabetic patients should be mandatory by the
treating doctor. Amit Jain’s screening tool is the simplest
and fastest screening tool from India for diabetic foot.
It can be performed by any healthcare professional, easy
to remember and perform and requires minimal
expertise and time for a clinician. It is also known as
Amit Jain’s linear foot test (LFT) and it has 3 components
that address the triad of diabetic foot. It has a look
component [check for ulcer/infection over dorsum,
plantar and interdigital region], feel component [pulses
of foot are palpated] and test component [for sensation].
y for
Differential Diagnosis of Leg Ulcer and Pressure Sore
173
One can use simple methods to testing sensation like
tuning fork, monofilament, pin prick, etc.
The triple assessment should be done annually in
every diabetic patient. In case patient comes for followup in between, then the look component is enough. This
screening tool also has Amit Jain’s scoring system and
it divides patients into low risk and high risk group
Causes of Death due to Diabetic Foot Ulcer
• Ketoacidosis with septicaemia
• Severe electrolyte abnormalities
• Other causes like silent myocardial infarction, renal
failure, etc.
Further Reading (as they are advanced)
1. Amit Jain’s Modern Diabetic Foot Surgery Principle
and Practice.
. Amit Jain’s Rule of 3 for Diabetic Foot.
2
3. Amit Jain’s Destructive Elevator.
4. Amit Jain’s Diabetic Foot Ulcer Scoring.
PRESSURE SORES
Pressure ulcers or bedsores are a serious and frustrating
complication for paralysed, debilitated, or comatose
patients confined to a bed or wheelchair. These ulcers
form when soft tissue is compressed between a bony
prominence (such as the ischium, sacrum, or trochanter)
and a supporting structure (such as a bed or wheelchair)
(Figs 26.40 and 26.41).
The growing incidence of spinal cord injuries due to
automobile accidents and the increased number of
debilitated geriatric patients admitted to hospitals have
drawn more attention to the prevention and treatment
of pressure ulcers. A pressure ulcer is usually the most
important factor for delayed rehabilitation in a
paraplegic or quadriplegic patient.
Factors Predisposing to the Formation of a
Pressure Sore
The most important factor is pressure. Other factors are
paralysis, paresis, shearing forces, malnutrition,
anaemia, advanced age, and infection. A lack of protec-
tive sensations in comatose or debilitated patients prevents them from changing posture. The localised
pressure continues and a skin ulcer develops. Initially,
there is tissue anoxia and cell death. Later, active
inflammation and vasodilatation occur, resulting in
reactive hyperaemia. If the pressure is removed to allow
tissue perfusion and the washing out of toxic byproducts,
initial damage may be reversible. If not, permanent
damage occurs. This may happen within six hours.
Clinical Features
1. Early Superficial Ulceration
• Erythema, oedema, and punctate haemorrhage
• Moist irregular ulceration with a surrounding erythe-
matous halo
2. Late Superficial Ulceration
• Full thickness skin ulceration
• Spreading necrosis of subcutaneous tissue
• Deep inflammatory response spreads in a cone-
shaped fashion to deeper tissues
3. Early Deep Ulceration
• Cicatrization of rolled ulcer edges
• Eschar at ulcer base
• Spread of inflammation and bacterial invasion
4. Late Deep Ulceration
• Breakdown of fascial plane
• Chronic inflammation and fibrosis of deep tissue
(bursa formation)
There is no such thing as a small pressure ulcer.
The visible skin wound is merely the “tip of the
iceberg.” 70% of the ulcer is below the skin. Pressure is
transmitted in a cone-shaped or pyramidal manner from
the skin through each layer of tissue to the bony prominence, so that a cone of tissue destruction is created.
The point of the cone is at the skin surface, and base is
formed by the larger undermined defect overlying the
bone.
Fig. 26.40: Pressure sore
Fig. 26.41: Pressure
gangrene—sore over
heel
Preventive Measures
Pressure ulcers may be avoided by meticulous skin
care and relief of pressure over the bony prominence
(Key Box 26.16).
Section II • General Surgery