Pt. Khushilal sharma govt.(auto.) ayurveda college and institute , Bhopal(M.P.

Department of Shalya tantra

Diabetic foot Ulcerl

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प्रमेह पिड़िका
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Payal Sindel
Year -2022-23
BAMS Final year
 Introduction
A diabetic foot ulcer is an open sore or wound on the foot of a person
with diabetes, most commonly located on the plantar surface, or bottom
of the foot.

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Diabetic foot ulcers occur in approximately 15% of persons with

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diabetes. Of those who develop a foot ulcer, 6% will be hospitalized

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due to infection or other ulcer-related complication.

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The risk of foot ulceration and limb amputation increases with age and

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the duration of diabetes.

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Diabetes is the leading cause of non-traumatic lower extremity

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amputations in the U.S. Between 14-24% percent of patients with

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diabetes who develop a foot ulcer will require an amputation, and foot
ulceration precedes 85% of diabetes-related amputations.
In the U.S., 82,000 amputations are performed each year on persons
with diabetes, half of those age 65 or older.
The good news is that a foot ulcer is preventable if the underlying
conditions causing it, diabetic peripheral neuropathy and/or
peripheral arterial disease, are appropriately diagnosed and treated.
 Epidemiology

The annual incidence of diabetic foot ulcer worldwide is

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between 9.1 to 26.1 million.

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Around 15 to 25% of patients with diabetes mellitus will

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develop a diabetic foot ulcer during their lifetime.

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As the number of newly diagnosed diabetics are

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increasing yearly, the incidence of diabetic foot ulcer is

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also bound to increase.

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Diabetic foot ulcers can occur at any age but are most

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prevalent in patients with diabetes mellitus ages 45 and

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over.
Latinos, African Americans, and Native Americans have
the highest incidence of foot ulcers in the US.
 Aetiology
Slight injury to glucose laden tissue may cause chronic infection and
ulcer formation.
Ulceration in diabetes may be precipitated by ischaemia due to diabetic

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atherosclerosis.

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More prone to infection of glucose ladden tissue may cause ulceration.

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Diabetic polyneuropathy or peripheral neuritis may also cause ulcer
formation.

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The etiology for diabetic foot ulcer is multifactorial. The common

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underlying causes are poor glycemic control, calluses, foot deformities,

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improper foot care, ill-fitting footwear, underlying peripheral

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neuropathy and poor circulation, dry skin, etc.

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About 60% of diabetics will develop neuropathy, eventually leading to a

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foot ulcer. The risk of a foot ulcer is increased in individuals with a flat
foot as they have disproportionate stress across the foot, leading to
tissue inflammation in high risk areas of the foot.
Peripheral neuropathy (nerve damage) and lower extremity ischemia
(lack of blood flow) due to peripheral artery disease are the primary
causes of diabetic foot ulcers.
 Diabetic Peripheral Neuropathy
Diabetic peripheral neuropathy is a precipitating factor in almost 90% of diabetic foot ulcers.
Chronically high glucose (blood sugar) levels damage nerves, including the sensory, motor and autonomic
nerves.
Diabetic neuropathy also damages the immune system and impairs the body's ability to fight infection.

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Sensory nerves enable people to feel pain, temperature, and other sensations. When sensory nerves of a

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diabetic person are damaged (sensory neuropathy), they may no longer be able to feel heat, cold, or pain

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in their feet.

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A cut or foot sore, a burn from hot water, or exposure to extreme cold might go completely unnoticed

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because of numbness and lack of sensation.

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Diabetic Peripheral Neuropathy
The sore or exposed area may then become infected and not heal
properly due to the body's impaired ability to fight infection.
Peripheral neuropathy also causes muscle weakness and loss of

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reflexes, especially at the ankle.

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This may change the way a person walks and lead to foot

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abnormalities and deformities such as bunions, hammertoes, and

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charcot foot.

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These play an important role in the pathway of diabetic foot ulcers

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since they contribute to abnormal pressures in the plantar area

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Shoes that no longer fit due to abnormalities and deformed foot

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structure may rub against toes causing blisters and ulcers on areas

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of the foot that are numb due to sensory neuropathy.
If not treated promptly, an ulcer may become infected and spread
to the bone causing osteomyelitis, a serious complication that
might require surgery.
Autonomic dysfunction causes decreased sweating resulting in
cracked skin and ulceration, making the skin vulnerable to infection.
Peripheral Artery Disease
Diabetes also damages blood vessels by causing inflammation and
atherosclerosis, or hardening of the arteries. Narrowing of the arteries causes
ischemia, a condition in which the blood circulation in the arteries is

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restricted and the availability of oxygen, glucose, and critical nutrients to

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tissues in the body is substantially reduced. When poor circulation affects

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the arteries of the feet and hands, it is called peripheral artery disease, or
PAD.
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By restricting the supply of oxygenated, nutrient-rich blood to the site of the

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ulcer, peripheral artery disease increases the risk an ulcer will become

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infected and heal slowly--or not at all.

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Peripheral artery disease (PAD) is 2–8 times more common in patients with

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diabetes, and about half of patients with a diabetic foot ulcer will also be

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found to have co-existing PAD.
Identifying PAD in patients with foot ulceration is important because its
presence is associated with slower (or lack of) healing of foot ulcers as well as
other serious complications.
Diagnosing PAD is challenging in patients with diabetes, as they frequently
lack typical symptoms, such as intermittent claudication (rest pain), even in
the presence of severe tissue loss.
 Pathophysiology
The development of a diabetic ulcer is usually in 3 stages. The initial stage is the development of a callus. The
callus results from neuropathy.
The motor neuropathy causes physical deformity of the foot, and sensory neuropathy causes sensory loss
which leads to ongoing trauma.

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Drying of the skin because of autonomic neuropathy is also another contributing factor.

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Finally, frequent trauma of the callus results in subcutaneous hemorrhage and eventually, it erodes and
becomes an ulcer.[2]

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Patients with diabetes mellitus also develop severe atherosclerosis of the small blood vessels in the legs and

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feet, leading to vascular compromise, which is another cause for diabetic foot infections.

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Because blood is not able to reach the wound, healing is delayed, eventually leading to necrosis and gangrene.

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 Types of Diabetic Ulcers
1. Neuropathic ulcers occur where there is peripheral diabetic neuropathy, but no ischemia
caused by peripheral artery disease.
2. Ischemic ulcers occur where there is peripheral artery disease present without the

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involvement of diabetic peripheral neuropathy.

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3. Neuroischemic ulcers occur where the person has both peripheral neuropathy and

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ischemia resulting from peripheral artery disease.

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 Risk Factors
Diabetic peripheral neuropathy and peripheral artery
disease (PAD) are strong risk factors associated with the
development of diabetic foot ulcers.

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Other risk factors include cigarette smoking, poor

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glycemic (sugar) control, and previous foot ulcerations.

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In addition, certain groups have a greater risk of

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developing foot ulcers including Native Americans,

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African Americans, Hispanics, older men, insulin-

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dependent diabetics, and persons with diabetes-related
kidney, eye, and heart disease.

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Sites

1. Toes and feet particularly the sole is the

commonest site.
2. Leg is also affected.
3. Any other part of the body may be affected.
 Signs and Symptoms

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Appearance of drainage on the person's socks
Redness and swelling in the area
Odor if the ulcer has progressed significantly
Diabetic ulcer is deep and spreading.
Staging After the diagnosis of the ulcer, it should undergo
staging. One of the commonly used classifications is by
Wagner from 1981. It classifies wounds into six grades
based on the depth

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Grade/ Features

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1/Superficial ulcer

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2/Deep ulcer involving tendon bone or joint

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3/Deep ulcer with abscess or osteomyelitis

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4/Gangrene involving the forefoot

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grading merely the depth of the ulceration and not
incorporating other factors known to influence the
outcome. Among others, one of the most commonly
used classification today is The University of Texas
Classification, which not only includes assessment of
the depth, but also the type of infection, and ischemia
based on the eventual outcome of the wound.
 History and Physical
1. Getting a good history is vital in the care of patients with a diabetic ulcer. The history
should include the duration of diabetes, glycemic control, other pre-existing complications
of diabetes including sensory neuropathy, history of peripheral vascular disease, callus,
previous ulcer, prior treatment, and the outcome. The detailed history should also include

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information regarding the footwear and foot.

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2. The clinical examination should include examining the peripheral pulses of the feet, looking

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for any anatomical anomalies, the presence of callus, signs of vascular insufficiency, which

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may indicate loss of hair, muscle atrophy, and location of the ulcer. Also assess for the

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presence of purulence, scabs, and evidence of neuropathy by examining with a

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monofilament.

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3. Features indication neuropathy include:

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Paresthesia

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Hypo or hyperesthesia
Dysesthesia
Anhydrosis
4. Ulcers are most common in the weight-bearing areas such as the plantar metatarsal head,
heel, tips of hammer toes and other prominent areas. Other physical features include
hammertoes, brittle nails, calluses, and fissures.
 Evaluation
1. The most common laboratory investigations done during evaluation of the ulcer include a
fasting blood sugar,
glycated hemoglobin levels,
complete metabolic panel,

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a complete blood count,
erythrocyte sedimentation rate (ESR),

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C-reactive protein (CRP).

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2. Recent guidelines and the literature suggest that in patients with diabetic foot ulcers, results of specimens

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for culture taken by swabbing do not correlate well with those obtained by deep tissue sampling; this

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suggests that superficial swab specimens may be less reliable for guiding antimicrobial therapy than deep

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tissue specimens.

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3. Radiological investigations include plain x-rays to look for any underlying osteomyelitis, the presence of air

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in the subcutaneous tissue, any signs of underlying fractures, and presence of a foreign body.
4. If osteomyelitis is suspected, MRI is the most preferred test.
5. A bone scan with technetium can also be used to diagnose underlying osteomyelitis.
6. Arterial Doppler with ankle-brachial index (ABI) is useful to rule out underlying peripheral vascular disease.
7. The probe-to-bone test (PTB) is performed by probing the ulcer with a sterile metal probe is a bedside test
that can help with the diagnosis of underlying osteomyelitis. If the probe hits the bone, it is a positive test.
Positive probe-to-bone test results are helpful especially when conducted on patients with diabetes mellitus.
 Treatment / Management
1. A diabetic foot ulcer acts as a portal for systemic infections such as cellulitis, infected foot ulcers, and
osteomyelitis. These are especially dangerous to patients with diabetes, whose impaired immunity

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increases their risk for local and systemic infection. Therefore, debridement and antibiotic therapy should

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be initiated as soon as possible.

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2. Blood sugar should also be monitored closely and controlled, because hyperglycemia may increase the

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virulence of infectious microorganisms.

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3. The goal of treatment is to accelerate the healing process and decrease the chance for infection (or

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prevent a recurrence of infection). Treatment usually consists of:

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Optimal glucose control.

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Debridement - removal of all hyperkeratotic (thickened) skin, infected and nonviable, including necrotic

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(dead), tissue, slough, foreign debris, and residual material from dressings.

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Systemic antibiotics for deep infection, drainage, and cellulitis.
Off-loading - Relieving the pressure from the ulcerated areas by having the patient wear special foot gear, a
brace, specialized castings, or using a wheelchair or crutches.
Creating a moist wound environment.
Treatment with growth factors and/or cellular therapy if the wound is not healing.
 Treatment / Management
STEP 1 Treatment of diabetic foot ulcer should be systematic for an optimal outcome. The most important
point is to identify if there is any evidence of ongoing infection, by obtaining a history of chills, fever, looking
for the presence of purulence or presence of at least two signs of inflammation that includes, pain, warmth,

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erythema or induration of the ulcer. It should is noteworthy that even in the presence of severe diabetic foot

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infection, there can be minimal systemic signs of infection.

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The next step is to decide if the patient’s ulcer can is manageable in the outpatient setting or inpatient

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setting. Need for parenteral antibiotics, concern for noncompliance, inability to care for the wound, ability to

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offload pressure, are few points to be considered for hospitalization. Both categories of patients should have

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treatment with antibiotics.

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The common organisms seen in a diabetic foot ulcer are Staphylococcus aureus, Streptococcus,

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Pseudomonas aeruginosa, and rarely E. coli. Diabetes patients have higher carriage rate of Staphylococcus

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aureus in the nares and skin, and this increases the chances of infection of the ulcer. Antibiotics are only
needed if there is a concern for infection. The severity of the infection dictates the dose, duration, and the
type of antibiotic.
The typical outpatient antibiotics regimen includes oral cephalosporins, and amoxicillin-clavulanic acid
combination, (If MRSA is not of concern). If MRSA is suspected, then the oral regimens include linezolid,
clindamycin or cephalexin plus doxycycline or a trimethoprim-sulphamethoxazole combination.
 Treatment / Management
Parenteral antibiotic regimens include piperacillin-tazobactam, ampicillin-sulbactam, and if penicillin-allergic,
then carbapenems including ertapenem or meropenem. The other combinations regimen including adding
metronidazole for anaerobic coverage along with quinolones like ciprofloxacin or levofloxacin, or with
cephalosporins like ceftriaxone, cefepime or ceftazidime. Intravenous agents which cover MRSA include

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vancomycin, linezolid or daptomycin.

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The next therapeutic step is to treat any underlying peripheral vascular disease. Inadequate blood supply limits

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the oxygen supply and the delivery of the antibiotics to the ulcer; hence revascularization improves both, and

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there is a better chance for the healing of the ulcer. The subsequent step is to perform local debridement or

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removal of calluses.

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Vacuum assisted closure can be undertaken for clean non healing wounds. Others may benefit from

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hydrotherapy to get rid of infected debris.

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If the patient has charcot foot, then the initial treatment is immobilization with braces or specially made shoes,

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but most will require a surgical procedure like arthrodesis or an osteotomy.

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Finally, efforts should be made for the prevention of new ulcers or worsening of the existing ulcer, which occurs
by offloading the pressure from the site by using walkers or therapeutic shoes.If the wound fails to heal in 30
days, then hyperbaric oxygen therapy can be considered. Since the wound has low oxygen supply, there is often
delay in healing of the wound. Hyperbaric oxygen therapy improves the rate of wound healing and also reduces
the rate of complications.
To have the best outcome a team of health care providers including primary care physician, podiatrist, a vascular
surgeon, an infectious disease specialist and wound care nursing staff are imperative.
 Wound Care
Wounds and ulcers heal faster and have a lower risk of infection if they are kept covered and
moist, using dressings and topically-applied medications.
Products including saline, growth factors, ulcer dressings, and skin substitutes are highly
effective in healing foot ulcers.

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There should be adequate circulation to the ulcerated area.

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Tight control of blood glucose is critical during to the effect treatment of a diabetic foot ulcer.

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This will enhance healing and reduce the risk of complications.

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 Surgical Options

Many non-infected foot ulcers are treatable without surgery.

However, surgery may be required to:

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Remove pressure on the affected area, including shaving or

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excision of bone(s).

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Correct deformities, such as hammertoes, bunions, or bony

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“bumps.”

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Treat infections such as osteomyelitis, an infection of the

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bone, by surgically removing the infected bone.

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Healing time may range from weeks to several months,
depending on:

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Wound size and location
Pressure on the wound from walking or standing
Degree of swelling
Issues with proper circulation
Blood glucose levels
 Prognosis
The prognosis these ulcers is good if identified early and
optimal treatment initiated. Unfortunately, delays in care can
have detrimental effects which can lead even to amputation of

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the foot. Patients who have chronic diabetic ulcer have a high

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risk of rehospitalization and prolonged hospitalization.

Complications
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The most feared complication is amputation of the extremity.

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The other complications include gangrene of the foot,

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osteomyelitis, permanent deformity, and risk of sepsis.

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Postoperative and Rehabilitation Care
Patients who end up with amputation will need comprehensive
therapy including physical therapy, occupational therapy and
also will need a prosthesis.
 Risk Reduction

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The risk of developing a foot ulcer can be reduced by:

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Smoking cessation

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Lowering consumption of alcohol

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Reducing high cholesterol

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Controlling blood glucose levels

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Wearing the appropriate shoes and socks

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Inspecting feet every day—especially the sole and between

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the toes—for cuts, bruises, cracks, blisters, redness, ulcers,
and other signs of abnormality
 Prameha pidika
Prameha Piḍakā are complications occuring in patients afflicted with Prameha due to prolonged
presence of vitiated Doṣas. Prameha Piḍakā are diabetic carbuncles / boils.

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Bheda: (Ā. Sushruta & Ā. Vāgbhaṭa)

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1) Sharāvikā are the boils which resemble Sharāva (curved earthen pan) in shape.

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2) Sarṣapikā are the boils which resemble white mustard in colour and size.

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3) Kacchapikā are the boils which are elevated like a tortoise shell, with a rough surface, and causing

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burning sensation.

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4) Jālinī are the boils which cause severe burning sensation and appear like a network of fibres on the

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skin.

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5) Vinatā are the boils which are deep rooted, large, painful, moist and appear on the back and

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abdomen.
6) Putriṇī are the boils which are spread over a large area with multiple blisters at the center.
7) Masūrikā are the boils which resemble red lentils.
8) Alajī are the boils which are red or white in color, appear as they are about to rupture and cause
severe pain.
9) Vidārikā are the boils which resemble the tubers of Vidārī.
10) Vidradhikā are the boils which possess similar features like Vidradhi Roga.
 Prameha pidika
Sādhyāsādhyatā

Sādhya -> Sarṣapikā, Vinatā, Masūrikā, Alajī, Vidradhikā

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Kṛcchrasādhya -> Sharāvikā, Kacchapikā, Jālinī, Putriṇī, Vidārikā; Piḍakā which are associated with burning

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sensation, excessive thirst, fever, hallucinations, which spread easily, and have red or black
discolouration.

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Chikitsā
Prameha should be controlled.

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Apakva Piḍakā -> Raktamokṣaṇa / Jalaukāvacharaṇa

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Pakva Piḍakā -> Pāṭana & Vraṇa Chikitsā

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Nyagrodhādi Gaṇa Kaṣāya with Gomūtra is administered internally.
Āragvadhādi Gaṇa Kaṣāya should be used internally and externally for Udvartana.
Mudgaparṇyādi Kvātha, Anantādi Kvātha
Prameha Piḍakāhara Lepa (Udumbara kṣīra & Bākuchī chūrṇa)
Gandhaka chūrṇa with Guḍa is taken internally; it cures 20 types of Prameha and 10 types of Prameha
Piḍakā.
Sārivādi Lauha (250-500 mg) with Madhu and Ghṛta is indicated in 10 types of Prameha Piḍakā, all types
of Ashas, and Tvak vikāra.
Ayurvedic Perspective

Ayurvedic texts
describes the ulcers of diabetic patients as
‘Madhumehaj vrana

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Samprapti of diabetic ulcer

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In Madhumeha ,the lower limbs vessels become weakened and unable to

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expel

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doshas.

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This leads to accumulation of doshas(meda and rakta along with other

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dosha-dushyas)followed by formation of Prameha Pidika which converts into

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wounds after purification i.e. Diabetic Ulcer.( This samprapti has been presumed

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on bases of samprapti of madhumeha as prameha pidika is a complication of

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madhumeha and they arecommonly found over lower limbs clinically.)

Prognosis:

During description of prognosis of vrana, Acharya Sushruta hasstated that

“madhumehaja vrana” i.ediabetic ulcers are kashtsadhya (difficult or management).
Further, Sushruta
specified that the wounds over the lowerlimbs too delays its healing.
Leech therapy

Leech therapy (Jalauka avacharan) has been mentioned as a type

of bloodletting ( Raktavsechan ).It is aneffective, safer and non-
surgical way ofblood-letting and can be used in children,females,
pregnant patients and elderly7

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References of Leech Therapy in wounds

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Sushruta has advocated that bloodletting by means of Leech can

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bepractised in all inflammatory, suppurative and painful conditions to

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relieve pain andinhibit suppuration including that ofdiabetic

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ulcerative lesions8.Sushrutafurther describes that in case of

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diabetes, ifsanshodhan is not done,the doshas get

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aggravated ,vitiates blood and muscles andproduce swelling or other

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complications.
The treatment prescribed for swelling anvene-puncture should be
done. If these are
not done, the swelling increases greatly,give rise to pain and burning
sensation,then it should be treated by sharpinstruments followed
by treatment ofwound
 Leech therapy
Probable Mechanism of Action of LeechTherapy

Leech application improves blood circulation and reduces congestiondue to

presence of carboxy-peptidase-A inhibitor, histamine like substances andAch;

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thus it corrects Diabetic Microangiopathy.It has peripheralvasodilator effect

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due to presence ofvasodilator constituent in saliva, whichimproves blood

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circulation and correctsischaemia due to diabetic atherosclerosis.Ithas anti-

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inflammatory action on nerves,hence corrects diabetic neuropathy.

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Probable Mechanism of Action of LeechTherapy (Ayurvedic Perspective)

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Vrana Shodhak Effect: expulsion of impure blood leads to removal of

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local vitiated doshas (dushit rakta ,toxins,metabolites ,etc).

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Vrana Ropan: fresh blood supply is facilitated which promotes healing

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andhealthier, newer tissues.

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Madhumeha Pacifying Effect: Bloodletting with leech applicationpacifies
madhumeha i.e. it breaks thepathogenesis at cellular level andinhibition
of infection, thus promotes wound healing(in diabetes, the tissues
areglucose laden which promotes propensityof bacteria to multiply).
 REFERENCES

1. M. Sriram bhatt,:SRB’s manual of surgery 4th edition

2. Boon Nicholas A., Colledge Nicki R., Walker Brian R.: Davidson’s principles and

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practice of medicine

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3. Charak Samhita , By Dr BrahmaNand Tripathi , Chaukhambha Surbharati
Prakashan ,Var anasi

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4. Kaviraj Ambikadatta Shastri. Sushruta Samhita, Varanasi, Chaukhambha
Sanskrit Sansthan,

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5. Vagbhata, Astanga Hridayam (Vidyotani Hindi commentary of Kaviraj Atrideva
Gupta).

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6. International Journal of Applied Ayurved Research ISSN: 2347- 6362

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7. WIKIPEDIA
Thank
you!!