Differential Diagnosis Of Leg Bazin’s Ulcer And Pressure Sore Notes

Differential Diagnosis Of Leg Ulcer And Pressure Sore Introduction

Leg ulcers are one of the important topics in surgery. They occur in children, adults, and the elderly. No age or sex is spared. Varying aetiological factors and the presence of complicated systemic diseases make the treatment of ulcers very difficult.

Read And Learn More: General Surgery Notes

Chronic ulcers in the elderly definitely cause considerable morbidity, and diabetic ulcers of the leg may cause life-threatening complications such as diabetic ketoacidosis and septicemia. Hence, it is necessary to do a careful clinical examination of the ulcer to arrive at the diagnosis and plan the appropriate treatment.

Differential Diagnosis Of Leg Ulcer And Pressure Sore Definition

An ulcer is a discontinuity of the skin or mucous membrane that occurs due to the microscopic death of the tissues. Thus, ulcers may occur anywhere in the body (skin), oral cavity, penis (mucous membrane), duodenum, intestine, etc. In this chapter, lower limb ulcers will be discussed.

Differential Diagnosis Of Leg Ulcer And Pressure Sore Classification

Ulcers may be classified based on the pathology or clinical features.

Pathological Classification of Ulcer

• Nonspecific ulcers
  • Traumatic
  • Venous
  • Arterial
  • Neurogenic—trophic
  • Tropical
  • Diabetic
  • Blood dyscrasias
• Specific ulcers
• Malignant ulcers

Pathological Nonspecific ulcers

1. Traumatic: This is the most common cause of leg ulcers. Trauma may be mechanical, physical due to burns or radiation, or chemical due to acids.

2. Venous ulcers: They include varicose ulcers and postthrombotic ulcers, which may occur following deep vein thrombosis.

3. Arterial ulcers: Following are a few examples of arterial ulcers:

• • Buerger’s disease—common
  • Atherosclerotic vascular disease—common
  • Vasospastic disorders such as Raynaud’s disease—uncommon
  • Martorell’s ulcers or hypertensive ulcers—rare
  • Patients with rheumatoid arthritis may develop leg or foot ulcers due to vasculitis.

4. Neurogenic ulcer (neuropathic ulcer, trophic ulcers)

• • Leprosy and diabetes are the common causes
  • Paraplegia, meningomyelocele, posterior tibial nerve injury, and tabes dorsalis are other causes.

5. Tropical ulcer: It is a rare ulcer due to malnutrition associated with infection caused by Vincent’s organisms—Borrelia vincentii and Fusiforme organisms.

6. Diabetic foot ulcer or diabetic leg ulcer.

7. Blood dyscrasias: Sickle cell anemia, thalassemia, leukemia, etc. may produce recurrent ulcerations over the leg.

Pathological Specific ulcers

These are due to a specific type of organism (for example. tubercular ulcer, syphilitic ulcer, actinomycotic ulcer).

Pathological Malignant ulcers

These are squamous cell carcinoma, basal cell carcinoma, and malignant melanoma. Malignant ulcers.

Pathological Clinical Classification

Clinical Examination Of An Ulcer

Clinical Examination Of An Ulcer Inspection

1. Location of the ulcer

• Arterial ulcer: Tip of the toes,1 dorsum of the foot.
• Long saphenous varicosity with ulcer: Medial side of the leg.
• Short saphenous varicosity with ulcer: Lateral side of the leg just above the lateral malleolus.
• Perforating ulcers: Over the sole at pressure points.
• Nonhealing ulcer: Over the shin and lateral malleolus.

2. Floor of the ulcer: This is the part of the ulcer that is exposed or seen.

• Red granulation tissue: Healing ulcer
• Necrotic tissue and slough: Spreading ulcer
• Pale, scanty granulation tissue: Tubercular2 ulcer
• Wash-leather slough: Gummatous ulcer
• Part of the bone: Neuropathic ulcer
• Nodular: Epithelioma
• Black tissue: Malignant melanoma

3. Discharge from the ulcer

• Serous: Healing ulcer
• Purulent: Spreading ulcer
• Bloody: Malignant ulcer
• Discharge with bony spicules: Osteomyelitis
• Greenish: Pseudomonas infection

4. Edge: This is between the floor and the margin of the ulcer. The margin is the junction between the normal epithelium and the ulcer. It represents the area of maximum cellular activity.

• If destruction dominates, as in spreading ulcers, the edge is inflamed, oedematous, and angry-looking (stage of extension). When an ulcer shows evidence of healing, the edge will be bluish due to granulation tissue covered by thin epithelium (stage of transition).
• In a healed ulcer, the outermost part of the edge is whitish due to fibrosis (stage of repair). The types of ulcer edges are presented.

Sloping edge is seen in all healing ulcers such as traumatic ulcers and venous ulcers.

A punched-out edge is seen in gummatous ulcers and trophic ulcers. Gummatous ulcers have punched-out edges due to endarteritis obliterans caused by syphilitic organisms. Chronic, nonhealing ulcers may also have punched-out edges.

Undermined edge is seen in tubercular ulcers, probably due to more destruction of the subcutaneous tissues than the skin. The edge is classically thin and bluish in color.

A raised (beaded) edge is seen in rodent ulcers or basal cell carcinoma.

Everted (rolled out) edge is diagnostic of squamous cell carcinoma. The edge grows very rapidly and occupies the normal skin and, thus, becomes everted.

5. Surrounding area

• Thick and pigmented: Varicose ulcer.
• Thin and dark: Arterial ulcer.
• Red and oedematous: Spreading ulcers like diabetic ulcers.
• The scar around the ulcer: Marjolin’s ulcer.

Palpation

1. Edge: Induration (hardness) of the edge is characteristic of squamous cell carcinoma. Some degree of induration may also be seen in chronic ulcers and long-standing varicose ulcers. Induration occurs due to extensive fibrosis.

• It is said to be a host defense mechanism. Because of fibrosis, lymphatic spread is delayed.
• Tenderness of the edge is characteristic of infected ulcers and arterial ulcers.

2. Base: It is the area on which the ulcer rests. Pick up the ulcer between the thumb and index finger to appreciate the tissues underneath. If the ulcer cannot be lifted up, the base cannot be made out.

• The base may be tendon, muscle, or bone, depending on the site of the ulcer. Marked induration at the base is diagnostic of squamous cell carcinoma.
• Hunterian chancre is a benign ulcer and produces significant induration. Hence, it is also known as hard chancre.

Base Induration

• It means hardness
• Maximum induration: Squamous cell carcinoma
• Minimal induration: Malignant melanoma
• Brawny induration: Abscess
• Cyanotic induration: Chronic venous congestion as in varicose ulcer
• The base and the surrounding area should be examined for induration

3. Mobility: A gentle attempt is made to move the ulcer to know its fixity to the underlying tissues. Malignant ulcers are usually fixed, whereas benign ulcers are not.

4. Bleeding: A malignant ulcer is friable, like a cauliflower. On gentle palpation, it bleeds. Granulation tissue, as present in a healing ulcer, also bleeds.

5. Surrounding area: Thickening and induration are found in squamous cell carcinoma. Tenderness and pitting on pressure indicate spreading inflammation surrounding the ulcer.

Relevant Clinical Examination

1. Regional lymph nodes

• Tender and enlarged: Acute secondary infection
• Nontender and enlarged: Chronic infection
• Nontender and hard: Squamous cell carcinoma
• Nontender, large, firm, multiple: Malignant melanoma.

2. Peripheral vessels:

Detailed examination of peripheral vessels is discussed under peripheral vascular disease. However, the dorsal pedis, posterior tibial, popliteal, and femoral arteries should be palpated in cases of lower limb ulcers. The presence of weak pulses or absent pulses indicates peripheral vascular disease.

3. Sensations:

Loss of vibration sense and loss of ankle jerk occur early in cases of diabetic neuropathy. Later, touch and pain are lost. Totally anesthetic feet are characteristic of leprosy.

4. Function of the joint:

Movements of the involved joint are restricted either due to pain, involvement of the joint, or infiltration into the joint by malignant ulcers.

5. Varicose veins:

If present, it is most probably a varicose ulcer. However, A-V fistulas may present as distal ulcers, with arterialisation of veins and a continuous murmur.

Relevant Systemic Examination

• Central nervous system (CNS) and spine in neuropathic ulcers. There may be gibbous, as in cases of TB spine, or an operated scar due to myelomeningocele, etc. See clinical notes.
  • An 18-year-old girl with a nonhealing trophic ulcer was examined by a postgraduate student. He gave a diagnosis of a trophic (neuropathic) ulcer due to leprosy as the first diagnosis followed by polyneuropathy.
  • He failed. It was a case of myelomeningocele. The candidate had not examined the spine! The patient had an operated myelomeningocele.
• Splenomegaly in blood dyscrasias, such as in the early stages of sickle cell anemia.
• Cardiovascular system (CVS) may reveal a murmur, as in cases of arteriovenous fistula or features suggestive of cardiac diseases.

A summary of the clinical examination of an ulcer is given.

Clinical Examination of an Ulcer

• Inspection
  • Location, size, shape, floor, edge, discharge, the surrounding area
• Palpation
  • Tenderness, the local rise of temperature, bleeding on touch, consistency of the ulcer, edge, surrounding area—edema, mobility
  • Regional lymph nodes
  • Sensations
  • Pulsations
  • The function of the joint
  • Systemic examination

Relevant Clinical Examination Investigations

1. Complete blood picture: Hb%, TC, DC, ESR, peripheral smear.
   • Low Hb% is found in a chronic ulcer. It may be nutritional or due to frequent blood loss during dressings as in a diabetic ulcer.
   • A high total count indicates infection.
   • Peripheral smear is done to rule out anemia and sickle cell disease.
2. Blood sugar estimation: Both fasting and postprandial.
3. Chest X-ray: Many of these patients are smokers. They may have restricted pulmonary diseases.
4. Pus for culture or sensitivity.
5. Doppler or duplex scan or lower limb angiography in cases of arterial diseases and venous diseases. More details are given in the respective chapters.
6. X-ray of the part: It is done to look for osteomyelitis— common in diabetic ulcers.
7. MRI foot may be required to know the extent of the disease as in spreading ulcers or chronic ulcers due to diabetes (rocker bottom foot) or due to Madura mycosis. In these types of cases, saving of foot becomes difficult. Amputation may be required.
8. Biopsy: Nonhealing or malignant ulcers.

Treatment Of Ulcers

It may be discussed under the following headings:

1. Treatment of spreading ulcers
2. Treatment of healing ulcers
3. Treatment of chronic ulcers
4. Treatment of the underlying disease

1. Treatment of Spreading Ulcers

• After obtaining a pus culture or sensitivity report, appropriate antibiotics are given. Many solutions are available to treat the slough, such as hydrogen peroxide and EUSol.
• Hydrogen peroxide (diluted), when poured over the wound, liberates nascent oxygen which bubbles out and helps in separating the slough. EUSol also separates the slough. Because there are reports that H₂O₂ and EUSol may cause more damage, they are no longer used.
• Partially separated slough needs to be removed daily or on alternate days.
• Excessive granulation tissue or pouting granulation tissue (proud flesh) needs to be decapitated by excision or by the application of copper sulfate or silver nitrate solution.

By repeated dressings, the slough separates and the discharge minimizes, resulting in a healing ulcer with healthy red granulation tissue. Management thereafter is like that of a healing ulcer. Presents the various ulcer dressings that are available today.

Management classes of wound dressings, debridement agents, and skin replacements are currently available

2. Treatment of Healing Ulcers

• Regular dressings for a few days with antiseptic creams (liquid iodine, zinc oxide, silver sulphadiazine, etc.).
• Swab to rule out the presence of Streptococcus haemolyticus, which is a contraindication for skin grafting.
• If the ulcer is small, it heals on its own by epithelialization from the cut edge.
• If the ulcer is large, a free split skin graft is applied as early as possible.
• Advantages of Split Skin Graft
  • Wound healing occurs fast
  • Secondary infection is avoided because of early skin cover
  • It prevents contractures
  • It prevents Marjolin’s ulcer—squamous cell carcinoma arising from scar tissues

3. Treatment of Chronic Ulcers

• These are the ulcers that do not respond to conventional methods of treatment. Some special forms of treatment are available, but their efficacy is doubtful.
• Infrared radiation, short-wave therapy, and ultraviolet rays decrease the size of the ulcer.
• Amnion helps in epithelialization.
• Chorion helps in the formation of granulation tissue. These ulcers may ultimately require skin grafting.

4. Treatment of the Underlying Disease (vide infra)

Differential Diagnosis of Causes of Ulcers

Traumatic Ulcer

It may occur anywhere over the body. However, it is more common in areas where the skin is close to bony prominences (for example. shin, malleoli), over which there are no muscles.

• They are usually single, very painful ulcers of healing type. With proper dressings and antibiotics, they usually heal within 5–7 days.
• A footballer’s ulcer refers to a nonhealing ulcer over the shin due to direct trauma caused by a football. Sometimes, these ulcers may take a long time to heal. If not treated properly, they may become adherent to the bone.

Venous Ulcer

Occurs due to increased venous hydrostatic pressure

• Usually associated with varicose veins
• Located on the medial side of the lower one-third of the leg in cases of long saphenous varicosity and on the lateral aspect of the leg in cases of short saphenous varicosity
• Shallow and superficial
• Never penetrates the deep fascia
• Usually painless, unless it is infected or causes periostitis tibia
• Shows evidence of healing
• Typically surrounded by pigmented skin

Arterial Or Ischaemic Ulcer

It is very painful and occurs in young patients with Buerger’s disease or in elderly patients with atherosclerotic vascular disease. It commonly occurs on the tips of toes and fingers. The ulcer is dry, and deep, and penetrates the deep fascia. Evidence of chronic ischemia in the rest of the foot clinches the diagnosis.

Differences between arterial and venous ulcers

Neurogenic Ulcer Neuropathic Ulcer Trophic Ulcer

This type of ulcer develops in an anesthetic limb, which may be caused by:

• • Diabetic neuropathy
  • Meningomyelocele
  • Leprosy
  • Alcoholic neuropathy
  • Nerve injuries
  • Transverse myelitis
• Trophic ulcers are caused by inadequate blood supply, malnutrition, and neurological deficits.
• The ulcer develops over pressure points such as beneath the heel, beneath the first and fifth metatarsals, and the gluteal region (decubitus ulcer). It develops as a callosity, gets infected, suppurates, and leaves a central hole that discharges pus.
• Slowly, it burrows deep inside and may involve the bone and cause osteomyelitis. Hence, it is also known as a perforating ulcer. The end stage is Charcot’s foot syndrome with varying degrees of bone and joint destruction and disorganization secondary to neuropathy, trauma, and changes in bone metabolism.

Neurogenic Ulcer Neuropathic Ulcer Trophic Ulcer Treatment

Immobilization of the foot in a plaster of Paris posterior slab with a walking boot almost cures the ulcer within 2–3 weeks, provided the primary disease (For example leprosy) is also controlled.

• If the ulcer is nonhealing with slough, initial management should include de-sloughing agents and surgical removal of the slough.
• The limb which does not serve any purpose for walking necessitates amputation as in advanced cases of Charcot’s foot.

Tropical Ulcer

It occurs in tropical countries. The precipitating factors are:

• Malnutrition
• Humid zones
• Poor immunity
• Trauma or insect bite

The infection is caused by Vincent’s organisms like Bacteroides, B. fusiformis, and Borrelia vincentii. It starts as a pustule with extensive inflammation.

• The pustule bursts and the ulcer spreads rapidly and causes destruction of the surrounding tissue. Hence, it is also known as a phagedenic ulcer.
• The edges are undermined, the floor contains slough, and there copious seropurulent discharge is present. Healing is delayed for up to a month.
• Metronidazole may be useful in bringing down the inflammation. Broad-spectrum antibiotics may also be required in cases of secondary infections. If healing takes place, it leaves behind a scar.

Post Thrombotic Ulcer

It occurs due to deep vein thrombosis. It may affect calf veins or may be due to femoral vein thrombosis. It is an example of a venous ulcer or a gravitational ulcer.

Post Thrombotic Ulcer Precipitating Factors

• Accidents involving the lower leg
• Childbirth
• Abdominal operation.

Post Thrombotic Ulcer Clinical Features

• Bursting pain in the limb
• Extensive induration of the leg or thigh depending on the site of thrombosis
• Nonhealing with scanty granulation tissue
• Deep—always infiltrates the deep fascia
• Due to increased hydrostatic venous pressure, the part is significantly indurated (cyanotic induration), pigmented, and thickened with a rise in local temperature.
• The ulcer is not associated with superficial varicosity.
• Homan’s sign: It is positive in calf vein thrombosis (pain in the calf region on forcible dorsiflexion of the foot with the knee extended).
• Moses’ sign: Squeezing of the calf muscles from side to side produces pain. These two signs are positive in acute cases.

Post Thrombotic Ulcer Treatment

• Rest and elevation of the leg
• Appropriate antibiotics
• Elastic crepe bandage

With conservative treatment for a few days to a few weeks, veins may recanalize and the ulcer may heal. The treatment is often very difficult.

Rare Ulcers

Martorell’S Ulcer

• Affects elderly patients over the age of 50 years.
• Commonly affects hypertensive patients (hence, the name hypertensive ulcer).
• Atherosclerosis is also a precipitating factor, even though peripheral pulses are usually present.
• It occurs due to the sudden obliteration of end-arterioles of the skin on the back or lateral side of the calf region.
• Severe pain
• Ischaemic patch of skin which develops into a deep, punched out, nonhealing ulcer.
• Delayed healing due to vascular insufficiency.

Bazins Ulcer

Exclusively occurs in young females in the lower third of the leg and ankle region.

• Usually seen in obese patients who have thick ankles and an abnormal amount of subcutaneous fat.
• It begins with reddish-purplish nodules (hence, the name erythrocyanosis frigida) on the calves, which later rupture and produce a nonhealing ulcer.
• The etiology of these ulcers is unclear. It may be due to ischemia of the lower leg due to spasm of branches of the posterior tibial and peroneal arteries.
• These vessels are abnormally sensitive to hot and cold weather, similar to Raynaud’s disease. In some cases, tubercular bacilli have been isolated, with ulcers responding to antitubercular treatment.
• These ulcers are managed conservatively.
• Sympathectomy may be beneficial in those patients who are hypersensitive to weather changes.

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 a commonly neglected problem that can lead to amputation.
• Which can result in the patient becoming handicapped. The numerous problems (Amit Jain’s categorization) associated with diabetic foot are listed.

Amit Jain’s classification of problems of diabetic foot

Various risk factors are given

Risk Factors for Diabetic Ulcer Foot

• Males above 50 years
• DM of more than 10 years duration
• Blood glucose levels not controlled
• Peripheral neuropathy
• Abnormal structure of the foot
• Peripheral vascular disease
• Smoking and hypertension
• Increased level of lipids
• Genetic factors

Diabetic foot is a triad that mainly consists of neuropathy, infection, and ischemia.

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 fibers. New arteriovenous communications open beneath the skin, diverting nutrient flow away from it. This ischaemic tissue is vulnerable to infection, causing nerve ischemia. 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 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 results due to the paralysis of intrinsic muscles of the foot. Sensation is absent over the entire sole due to the 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 the neuropathic feet with good vascularity and it leads to severe deformity. Often midfoot bones and joints are affected.
• Autonomic neuropathy leads to the absence of sweating and gives rise to anhydrotic skin.
• Diabetic Neuropathy
  • Loss of vibration and touch
  • Loss of pain and temperature
  • Dead-like feeling in the feet
  • The sensation of walking on the ‘sand’
  • Susceptible for repeated trauma
  • The nylon monofilament test is routinely used to test neuropathy by pressing in on the foot or sole.

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.

• Effects of Diabetic Neuropathy
• • Loss of sensation
  • Loss of sweating
  • Loss of muscle strength
  • Loss of curvature of the foot
  • Loss of normal joint position
  • Loss of elasticity of the 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 mobilization 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 ischemia of the foot (macroangiopathy). These patients have accelerated atherosclerosis. In addition, it also produces small vessel disease in the form of nonspecific thickening of the basement membrane (microangiopathy).

• Diabetes and Atherosclerosis
  • 16% of diabetic patients have PVD (peripheral vascular disease)
  • Collateral circulation is reduced in diabetics
  • Atherosclerotic plaque causes increased ulceration and cracking
  • The more severe the diabetes, the more severe be peroneal occlusive disease

Thus, neuropathy or microangiopathy singly or in combination with secondary infection favors 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.

Different Sequence Of Events In Diabetic Foot Patients

1. Stage of cellulitis: Following an injury or trivial trauma, redness can develop along with swelling and edema of the leg.

2. Stage of spreading cellulitis: Cellulitis takes up a virulent course and spreads deeper and upwards along the fascial planes. When infection is severe, necrotizing 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 produces multiple abscesses.

4. Stage of gangrene: Tense edema and the existing vascular compromise produce ischemia 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 septicemia: Some patients can present in an emergency with septicemia. This is due to untreated cases of gangrene, abscess, cellulitis, etc. which can spread locally and systemically producing septicemia and diabetic ketoacidosis.

Diabetic foot Amit Jain’s Staging For Cellulitis

This new staging system consists of 4 sequential progressive clinical stages of primary cellulitis and gives a corresponding treatment guide.

• This is an extremely simple, easy-to-remember, practical staging that can be used for extremities and also in nondiabetics.
• Stage 1 cellulitis should be managed conservatively with good antibiotics and one should prevent it from progressing to more serious stages. Stage 4 is associated with amputation.

Diabetic foot Investigations

1. A complete blood picture usually demonstrates a high total count (infection).

2. Blood—fasting blood sugar, postprandial blood sugar, and glycosylated hemoglobin to be done.

3. Pus should be sent for culture or sensitivity. Deep tissues can also be sent intraoperatively. Common microbes seen in diabetic feet 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 of the chronicity of the ulcer. It takes weeks for visible changes of osteomyelitis on the radiograph. Today in all such doubtful cases, an MRI of the foot or leg is done.

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 to investigate 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 a loss of diastolic forward flow.

7. Hand-held Doppler and measurement of ankle-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 the presence of dry gangrene.
• If vessels are extensively calcified or if there is elevated creatinine, then an MR angiogram can be considered. Often it is seen that below popliteal vessels are involved.

Diabetic Foot Classification

There are several classifications for diabetic foot ulcer which is a common clinical focal pathology. The commonly used diabetic foot ulcer classification from the West is the Meggit-Wagner classification.

Diabetic Foot 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
  • Involves ligament, tendon, joint capsule, or fascia
  • No abscess, no osteomyelitis
• Grade 3: Deep ulcer with abscess or osteomyelitis
• Grade 4: Gangrene of the portion of the forefoot
• Grade 5: Extensive gangrene of the foot

Another modern diabetic foot ulcer classification is Amit Jain’s ulcer classification.

• This is a new original diabetic foot ulcer classification from India that divides ulcers into 3 types that are extremely easy to remember.
• It also has an Amit Jain ulcer scoring system that predicts amputation and a coding system (Amit Jain’s SAC coding) to be used in lines of the TNM system.

Amit Jains diabetic foot ulcer classification

Amit Jains SAC coding for diabetic foot ulcer

 

Amit Jains 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 and includes almost all the complications of diabetic foot seen worldwide.

• It divides diabetic feet into 3 simple types. 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 suggests using a combination of classification like universal classification.
• Surgical scoring, as a single classification, cannot be made for diabetic foot complications that have many pathological entities. Amit Jain’s DIABETIC FOOT acronym covers all the lesions seen in this universal classification.

Amit Jain’s DIABETIC FOOT

• Dry gangrene
• Infective gangrene
• Abscess
• Bullosis diabeticorum
• Erysipelas
• Trophic ulcer
• Ischemic ulcer
• Cellulitis
• Flesh-eating bacterial disease, Fungal infections
• Osteoarthropathy (Charcot foot)
• Osteomyelitis
• Toe deformities

Amit Jain’s Universal Classification for Diabetic Foot

Treatment of Diabetic Foot Ulcers

It may be discussed under the following headings:

• 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
• Care2 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 ulcers. 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 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 or 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.
• The 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: A 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 wounds as they can delay wound healing.
• There are numerous modern wound dressing products available that can be used during the course of ulcer management like hydrogels, foams, hydrocolloids, alginates, etc.
• Hydrogels are commonly used nowadays and are also affordable. It provides moisture for wounds. Diabetic wounds heal very slowly or delayed healing.

4. Amit Jain’s modified grading1 for debridement: 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, the extent of regions debrided [E1–3], and repetitions of 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.
• 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.
• Amit Jain’s modified grading1 for debridement

5. Various types of surgery for diabetic foot. Debridement is a commonly performed procedure. Amputation becomes necessary if tissues are destroyed or part is not salvageable. Always try to save limbs as much as possible. There are different types of foot amputation. Type 1 foot amputations are most commonly performed in clinical practice.

Amit Jains Universal Classification For Diabetic Foot Aim to save the leg

Amit Jain’s classification for foot amputation

All the amputations below the malleoli are considered to be minor amputations, whereas amputations above the malleoli are major amputations like below-knee amputations. Amit Jain’s destructive or amputation ladder provides various types of amputation available for extremities starting from distal to proximal most amputation.

Amit Jains Universal Classification For Diabetic Foot 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 the limb is ischemic and the wound is nonhealing.

• Today, peripheral angioplasties are more commonly done compared to peripheral bypass procedures. 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 large wounds or flaps may be required (reconstructive ladder).

6. Care of the patient as a whole: Recovery and healing of diabetic foot ulcers 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 the 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:

• The 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 a 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 the post-revascularization period.

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.

Amit Jains Universal Classification For Diabetic Foot Technique

Foam with an open-cell structure 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.
• 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.

Amit Jains Universal Classification For Diabetic Foot How does it work?

• Negative pressure assists with the removal of interstitial fluid, decreasing localized edema 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).

Amit Jains Universal Classification For Diabetic Foot Indications

• Venous ulcers, diabetic ulcers, large ulcers following necrotizing fasciitis, and any chronic ulcers.
• Patients with open fractures.
• Soft tissue injuries, including sacral pressure ulcers, acute traumatic soft tissue defects, and infected soft tissue defects following rigid stabilization of lower limb fractures.
• Treatment of burns and wounds in the perineum, hand, or axilla.

Amit Jains Universal Classification For Diabetic Foot Contraindications

• Osteomyelitis—first treat osteomyelitis and then apply VAC
• Internal fistula
• 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.

Patient Education to Protect the Feet of Patients with Diabetes Mellitus

• 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 carefully. If infection sets in, consult a physician at the earliest.
• Avoid applying herbal medicines or lotions to 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 neighbors.
• 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 your leg in hot water.
• Public Education in Diabetic Patients
  • Barefoot walking should be avoided
  • Avoid herbal or local ointment application
  • Regular and rigorous control of diabetes with diet
  • Exercises
  • Foot care—dry, frequent cleaning, and corn care
  • Oxygenation to toes or foot, proper shoes (MCR)
  • O Do not consult Others
  • Trimming of nails should be done carefully
  • Remember as BAREFOOT

Various Aspects Of Diabetic Ulcer Foot

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 ones to see diabetes patients often. It is the responsibility of surgeons to screen the foot as and when possible.
• Screening the foot for diabetes can prevent most complications for a long period and a diabetic foot storm can be prevented in his life.

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, is 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 or infection over the dorsum, plantar and interdigital region], a feel component [pulses of the foot are palpated], and a test component [for sensation].
• One can use simple methods to test sensation like a tuning fork, monofilament, pinprick, etc. The triple assessment should be done annually in every diabetic patient. In case a patient comes for follow-up 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)
  • Amit Jain’s Modern Diabetic Foot Surgery Principle and Practice.
  • Amit Jain’s Rule of 3 for Diabetic Foot.
  • Amit Jain’s Destructive Elevator.
  • Amit Jain’s Diabetic Foot Ulcer Scoring.

Pressure Sores

Pressure ulcers or bedsores are a serious and frustrating complication for paralyzed, 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).

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.

Pressure Sores Factors Predisposing to the Formation of a Pressure Sore

The most important factor is pressure. Other factors are paralysis, paresis, shearing forces, malnutrition, anemia, advanced age, and infection.

• A lack of protective sensations in comatose or debilitated patients prevents them from changing their 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 hyperemia.
• 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.

Pressure Sores Clinical Features

1. Early Superficial Ulceration

• Erythema, edema, and punctate hemorrhage
• Moist irregular ulceration with a surrounding erythematous 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 the 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 the base is formed by the larger undermined defect overlying the bone.

Pressure Sores Preventive Measures

Pressure ulcers may be avoided by meticulous skin care and relief of pressure over the bony prominence.

Pressure Sores Skin Care

1. Regular, periodical skin inspection, especially over the bony prominences.
2. Any sign of redness, irritation, or abrasion—if noted— all pressure must be taken off the area immediately.
3. Keeping the skin clean and dry: Moist areas lead to maceration. Fine talcum powder may be applied to areas where moisture tends to develop. It must be dusted every day after drying the skin.
4. Gentle massage of vulnerable skin with lanolin lotion.
5. Care of perineum and genitalia, especially in patients with incontinence.
6. Clothing and bedding must be wrinkle-free and made of porous absorbent material to allow air circulation and avoid accumulation of perspiration.
7. Pressure relief—in bedridden patients.

• • Frequent change of posture round the clock every 2 hours.
  • Avoid localized pressure by proper body alignment.
  • The use of air or fluid-filled floatation mattresses also lessens the risk of ulcer formation.
  • Patient and patient’s family education.

Pressure Sores Treatment

1. Superficial ulceration: Debridement and allowing it to heal by secondary intention (takes many weeks)

2. Deep ulceration or large superficial ulceration

• Bedside debridement of obviously necrotic material
• ‘Wet to dry’ dressing
• Use of desloughing agents
• Systemic antibiotics
• Nutritional consideration
• Correction of spasm and contractures, if present
• Once it is ready, the defect is closed

Pressure Sores Methods of Closure

• Primary closure—undermine and approximate the cut edges
• SSG—in selected cases only
• Skin flaps
  • Transposition flap
  • Rotation flap
  • Advancement flap
• Cultured muscle interposition for severe and ischial pressure sores.

3. Education of the patient and patient attenders to prevent pressure sores.

Miscellaneous Maggot Therapy

A maggot is the larva of a fly, such as a house fly. In practice, any neglected wound on the body, especially over the legs, may get contaminated with maggots. Within 1–2 days, there may be a colony of maggots.

• It is a type of biotherapy involving the introduction of live, disinfected maggots into nonhealing wounds.
• The ugly look and feeling of a crawling creature on the body drive the patient to reach the hospital in our country. Maggots may be removed by using turpentine.
• Mode of action:
  • Debride wounds by dissolving necrotic, infected tissue.
  • Disinfection of the wound by killing bacteria and healing—doubtful.
  • Maggot therapy may also reduce the need for antibiotics in people with complex, chronic wounds.
  • Maggot therapy has been shown to accelerate the debridement of necrotic wounds.

Miscellaneous Maggot Therapy Indications

Maggots inhibit and destroy a wide range of pathogenic bacteria including methicillin-resistant Staphylococcus aureus (MRSA), group A and B streptococci, and gram-positive aerobic and anaerobic strains.

• Maggot therapy, therefore, represents a cost-effective method for managing MRSA infection.
• Maggot therapy may also reduce the need for antibiotics in people with complex, chronic wounds.

Diabetic Foot Ulcer And Research

Aldose reductase is the first enzyme in the sorbitol aldose reductase pathway responsible for the reduction of glucose to sorbitol, as well as the reduction of galactose to galactitol.

• Too much sorbitol trapped in the retinal cells, lens cells, and Schwann cells may damage them, leading to retinopathy, cataracts, and peripheral neuropathy, respectively.
• Aldose reductase inhibitors are currently being investigated as a way to prevent or delay these complications.