Ulcer Classification and Venous Leg Ulcer Treatment Notes

Differential Diagnosis Of Leg Ulcer

Leg ulcers are one of the important topics in surgery. They can occur in children, adults and old people. No age or gender is spared. The varying aetiological factors and the presence of complicated systemic diseases make the treatment of ulcers very difficult.

Read And Learn More: Clinical Medicine And Surgery Notes

Chronic ulcers in old people definitely cause considerable morbidity and diabetic ulcers of the leg can cause life-threatening complications such as diabetic ketoacidosis and septicaemia.

Hence, it is necessary to do a careful clinical examination of the ulcer to arrive at the diagnosis and plan for appropriate treatment.

Differential Diagnosis Of Leg Ulcer Definition

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

Differential Diagnosis Of Leg Ulcer Classification

Pathological Classification

1. Nonspecific

1. Traumatic: Trauma can be mechanical. This is the most common cause of leg ulcers. It can be physical trauma due to burns or radiation. It can also be due to chemicals such as acids.
2. Venous ulcers: They include varicose ulcers and post-thrombotic ulcers which can occur following deep vein thrombosis.
3. Arterial ulcers: The following are a few examples of arterial ulcers.

• • Buerger’s disease—common

Pathological Classification Of Ulcer

1. Nonspecific Ulcers
   • Traumatic
   • Venous
   • Arterial
   • Neurogenic—Trophic
   • Tropic
   • Diabetic
   • Blood dyscrasias
2. Specific Ulcers
3. Malignant Ulcers
   • Atherosclerotic vascular disease — common
   • Vasospastic disorders like Raynaud’s disease—uncommon
   • Martorell’s ulcers or hypertensive ulcers —rare
   • Rheumatoid arthritis patients can 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 the other causes.
5. Tropical ulcer: It is a rare ulcer due to malnutrition associated with infection caused by Vincent’s organisms.
6. Diabetic ulcer foot or diabetic ulcer leg
7. Blood dyscrasias: Sickle cell anaemia, thalassaemia, leukaemia, etc. can produce recurrent ulcerations in the leg.

2. Specific Ulcer: This is due to specific types of organisms, for example, tubercular ulcers, syphilitic ulcers, actinomycotic ulcers, etc.

3. Malignant Ulcers: These are squamous cell carcinoma, basal cell carcinoma, and malignant melanoma. Malignant ulcers are discussed in Chapter 12.

Clinical Examination Of The Ulcer History

• How did it start? Often leg ulcers start after a trauma – Ask a question Did you have trauma? It is but natural agriculturists, field workers, and manual labourers are susceptible. Trivial trauma may be the precipitating factor for the development of ulcers in diabetes patients and in patients with occlusive arterial disorders like TAO.
• Before the onset of the ulcer, were you getting any crampy or catch-like pain in the legs especially while walking? If present it indicates arterial occlusion. Thrombo Angitis Obliterans (TAO) and atherosclerotic disease are the 2 common arterial occlusive disorders affecting the limbs.
• Crampy pain late in the evening may also be due to venous disorders like varicose veins.
• Sudden severe pain in the limbs, followed by a change in colour, then black patches are suggestive of embolic gangrene. Once gangrenous skin is removed, it results in ulcers.
• How is the progress? Is it becoming big or remaining the same or it is healing? An ulcer which is becoming big is a spreading ulcer. Example: Diabetic ulcer. An ulcer which remains the same may be a chronic ulcer.

Example: Callous ulcers. An ulcer which is becoming small are healing ulcer. Examples: Treated diabetic ulcers or venous ulcers. A non-healing and spreading ulcer can also be malignant especially malignant melanoma (Malignant skin tumour arising from melanin pigment) and the leg is one of the common sites of melanoma.

• Do you appreciate sensations in the sole of the foot? Those who have neuropathy may have a loss of sensation. Diabetes is the most common cause of neuropathic foot. Totally anaesthetic foot is classical of Leprosy. Such ulcers are also called Trophic ulcers.

Ulcer Past History

Any history suggestive of chronic illness such as diabetes, should be enquired.

Ulcer General Physical Examination

It is done to check for the general health of the patient.

Chronic anaemia: poor wound healing Jaundice: Sickle cell anaemia.

Ulcer Inspection

1. Location of the ulcer
   • Arterial ulcer—Tip of the toes, dorsum of the foot, malignant melanoma in the sole 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 which is exposed or seen.
   1. Red granulation tissue—Healing ulcer.
   2. Necrotic tissue, slough—Spreading ulcer.
   3. Pale, scanty granulation tissue—Tuberculous1 ulcer.
   4. Wash-leather slough —Gummatous ulcer
   5. Part of the bone—Neuropathic ulcer
   6. Nodular—Epithelioma
   7. Black tissue—Malignant melanoma
3. Discharge from the ulcer
   • Serous discharge—Healing ulcer
   • Purulent discharge—Spreading ulcer
   • Bloody discharge—Malignant ulcer
   • Discharge with bony spicules— Osteomyelitis

It is described as apple jelly granulation tissue.

Greenish discharge —Pseudomonas infection.

4. Edge: This is between the floor of the ulcer and the margin. The margin is the junction between the normal epithelium and the ulcer. These two parts represent the areas of maximum activity. If destruction dominates as in spreading ulcers, the edge is inflamed, oedematous and angry-looking (stage of extension).

When the ulcer shows evidence of healing, the edge will be bluish due to granulation tissue covered with thin epithelium (stage of transition). In a healed ulcer, the outermost part of the edge is whitish due to fibrosis (stage of repair).

• Sloping edge is seen in all healing ulcers like traumatic ulcers, and venous ulcers.
• A punched-out edge is seen in gummatous ulcers and trophic ulcers. Gummatous ulcers have punched out the edge due to endarteritis obliterans caused by syphilitic organisms.
• Chronic nonhealing ulcers also may have punched-out edges.
• Undermined edge is seen in tuberculous ulcers, probably due to more destruction of subcutaneous tissues than the skin. The edge is classically thin and bluish in colour.
• A raised edge (beaded edge) is seen in rodent ulcers or basal cell carcinoma.
• Everted edge (rolled out) is diagnostic of squamous cell carcinoma. The edge grows very rapidly and it occupies the normal skin and thus gets 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
• Pigmentation—malignant melanoma

Ulcer Palpation

Edge: Induration (hardness) of the edge is very characteristic of squamous cell carcinoma.

Some degree of induration can also be seen in chronic ulcers and longstanding varicose ulcers. Induration occurs due to extensive fibrosis. It is said to be a host defence mechanism.

• By causing fibrosis, lymphatic spread is delayed. Tenderness of the edge is characteristic of infected ulcers and arterial ulcers.

Base: It is the area on which the ulcer rests. Pick up the ulcer between the thumb and index finger and tissues beneath are appreciated. If the ulcer cannot be lifted up, the base cannot be made out. The base can be tendons, muscles or bone depending upon the site of the ulcer.

• Marked induration at the house is diagnostic of squamous cell carcinoma. Hunterian chancre is a benign ulcer and produces significant induration. Hence, it is also called a hard chancre.

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

Bleeding: Malignant ulcer is friable like a cauliflower. On gentle palpation, it bleeds. Granulation1 tissue in a healing ulcer also causes bleeding.

Surrounding area: Thickening and induration is found in squamous cell carcinoma. Tenderness and pitting on pressure indicate spreading inflammation surrounding the ulcer. gives a summary of the clinical examination of an ulcer.

Ulcer Palpation Relevant Clinical Examination

1. Regional lymph nodes

• Tender and enlarged—Acute secondary infection.
• Non-tender and enlarged —Chronic infection.
• Non-tender and hard—Squamous cell carcinoma.
• Non-tender, large, firm, multiple — Malignant melanoma.

2. Peripheral vessels: Detailed examination of peripheral vessels is discussed under peripheral vascular disease. However, 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.

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 edge, base and the surrounding area should be examined for induration

Granulation tissue is made up of capillaries and fibroblasts. Hence, it gives rise to fresh blood loss.

Clinical Examination Of An Ulcer Inspection

• Location, size, shape, floor, edge, discharge, surrounding area.

Palpation

• Tenderness, local rise of temperature, bleeding on touch, consistency of the ulcer, edge, surrounding area—oedema, mobility.
• Regional lymph nodes
• Sensations
• Pulsations
• The function of the joint
• Systemic examination

3. Sensations: Loss of vibration sense and loss of ankle jerk occurs early in cases of diabetic neuropathy. Later, touch and pain are lost. Totally anaesthetic feet are characteristic of leprosy.

4. Function of the joint: The involved joint movements are restricted either due to the pain, involvement of the joint or due to infiltration into the joint by malignant ulcers.

5. Varicose veins: If present, it is most probably a varicose ulcer. However, A-V fistula can present as distal ulcers, with arterialisation of veins and a continuous murmur.

Ulcer Systemic Examination

1. Central nervous system (CNS) and spine in neuropathic ulcers. There may be gibbous as in cases of TB spine or operated scar due to myelomeningocele, etc.
2. Splenomegaly in blood dyscrasias like early stages of sickle cell anaemia, etc.
3. Cardiovascular system (CVS) may reveal murmur as in cases of arteriovenous fistula or features suggestive of cardiac diseases.

Ulcer Management

Investigations

1. Complete blood picture: Hb%, TC, DC, ESR, peripheral smear
   • Low Hb% is found in chronic ulcers. It is either nutritional or due to frequent blood loss during dressings as in diabetic ulcers.
   • A high total count indicates an infection
   • Peripheral smear to rule out anaemia and sickle cell disease.
2. Urine and blood examination to rule out diabetes.
3. Chest X-ray—PA view to rule out pulmonary tuberculosis.
4. Pus for culture/sensitivity.
5. Lower limb angiography in cases of arterial diseases.
6. X-ray of the part to see for
   • Osteomyelitis —Common in diabetic ulcers
   • Periostitis tibia—Varicose ulcers
7. Biopsy: Non-healing/malignant ulcers.

Treatment of ulcer

It can be discussed as under:

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 ulcer: After obtaining a pus culture/sensitivity report, appropriate antibiotics are given. Many solutions are available to treat the slough, like hydrogen peroxide and EUSOL1.
   • Hydrogen peroxide (diluted) when poured over the wound, liberates nascent oxygen which bubbles out and helps in separating the slough. EUSOL1 also separates the slough.
   • Partially separated slough needs to be removed daily or on alternate days, in the wards.
   • Excessive granulation tissue or pouting granulation tissue (proud flesh) needs to be decapitated by excision or by application of copper sulphate or silver nitrate solution.
   • Thus, by repeated dressings, the slough gets separated, and discharge becomes minimal resulting in a healing ulcer with healthy red granulation tissue. Management thereafter is like a healing ulcer.
2. Treatment of healing ulcer
   • Regular dressings are done for a few days with antiseptic creams like liquid iodine, zinc oxide or silver sulphadiazine preparation.
   • A swab is taken to rule out the presence of Streptococcus haemolyticus which is a contraindication for skin grafting.
   • If the ulcer is small, it heals by itself with epithelialisation, from the cut edge of the ulcer.
   • If the ulcer is large, a free split skin graft is applied as early as possible.
3. Treatment of chronic ulcers: These are the ulcers which do not respond to conventional methods of treatment. Some special forms of treatment are available; their usefulness is doubtful.
4. They are as follows:

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

• Infrared radiation, short-wave therapy, and ultraviolet rays decrease the size of the ulcer.
• Amnion helps in epithelialisation.
• Chorion helps in the granulation of tissue. These ulcers ultimately may require skin grafting.

4. Treatment of the underlying disease: (vide infra)

Ulcer Differential Diagnosis

The differential diagnosis is given

Traumatic Ulcer

They can occur anywhere in the body. However, they are more common where the skin is closely applied to bony prominences, for example. shin, and 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. Footballer’s ulcer is the name given to those nonhealing ulcers which occur in the leg over the shin due to direct trauma caused by football. If not treated properly, it gets adhered to the bone.

Venous Ulcer

• It occurs due to increased venous hydrostatic pressure.
• Located on the medial side of the lower 1/3 leg in cases of long saphenous varicosity and on the lateral aspect of the leg in short saphenous varicosity.

• It is shallow and superficial.
• Never penetrates deep fascia
• Usually painless unless it is infected or causes periostitis tibia
• Shows evidence of healing
• Usually associated with varicose veins
• Typically lower leg around the ulcer is pigmented.

Arterial Ulcer (Ischaemic Ulcer)

They are very painful and occur in young patients who have Buerger’s disease or in elderly patients due to atherosclerotic vascular disease. It commonly occurs on the tips of toes and fingers. The ulcer is dry, and deep and penetrates deep fascia. Evidence of chronic ischaemia in the rest of the foot clinches the diagnosis.

Neurogenic Ulcer, Neuropathic Ulcer, Trophic Ulcer

This type of ulcer develops in an anaesthetic limb. The causes of neuropathy are:

• Diabetic neuropathy
• Meningomyelocele
• Leprosy
• Alcoholic neuropathy
• Nerve injuries
• Transverse myelitis
• Ulcer develops on the pressure points such as the heel, beneath the first and fifth metatarsals and gluteal region (decubitus ulcer). It develops as a callosity, gets infected, suppurates and leaves a central hole discharging pus. Slowly, it burrows deep inside, may involve bone and cause osteomyelitis. Hence, it is also called a perforating ulcer.
• Trophic ulcers are caused by inadequate blood supply, malnutrition, and neurological deficits. They are also included in this group.

Arterial Ulcer Treatment

Immobilisation 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 is also controlled, for example. leprosy. If the ulcer is non-healing with slough, initial management should include desloughing agents and surgical removal of the slough.

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, fusiformis and Borrelia vincentii. It starts as a pustule with extensive inflammation. The pustule bursts and the ulcer spreads rapidly and causes destruction of surrounding tissue. Hence, it is also called a Phagedenic ulcer¹

The edges are undermined, the floor contains slough, and there is copious seropurulent discharge. Healing is delayed for days to a month. Metronidazole may be quite useful in bringing down the inflammation. 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 it may be due to femoral vein thrombosis. It is an example of a venous ulcer or gravitational ulcer.

Tropical Ulcer Precipitating Factors

• Accidents involving lower leg
• The following childbirth
• After an abdominal operation.

Post-Thrombotic Ulcer

Clinical Features

• Bursting pain in the limb
• Extensive induration of the leg or thigh depending upon the site of thrombosis
• An ulcer is non-healing with scanty granulation tissue.
• An ulcer is deep and always infiltrates deep fascia.

Phagedenic (to eat). Rapidly spreading ulcerative destructive lesion. It can occur in the oral cavity and also over the penis.

• Due to increased hydrostatic venous pressure, the part is significantly indurated (cyanotic induration) pigmented, and thickened with a rise in local temperature.
• An ulcer is not associated with superficial varicosity.
• Homan’s sign is positive in calf vein thrombosis. It is elicited by forcible dorsiflexion of the foot with the knee extended causing pain in the region of the calf.
• Moses sign: Squeezing of the calf muscles from side to side also produces pain.

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 get canalised and the ulcer may heal. The treatment can be very very difficult (Refer varicose veins chapter for details on deep vein thrombosis).

Rare Ulcers – Martorell’s Ulcer

• Affects elderly patients over the age of 50 years.
• Commonly affects hypertensive patients, hence the name hypertensive ulcers.
• Atherosclerosis is also a precipitating factor even though all peripheral pulses are usually present.
• It occurs due to the sudden obliteration of end-arterioles of the skin on the back or outer side of the calf region.
• Severe pain, an ischaemic patch of skin which later develops into a deep punched out nonhealing ulcer are other clinical features.
• Healing is delayed due to vascular insufficiency.

Students should not offer these ulcers as a clinical diagnosis. They are rare ulcers, with rare clinical interest.

Bazin’S Ulcer

• These ulcers occur exclusively in young females and occur in the lower third of the leg and ankle region.
• Usually seen in those patients who are obese with thick ankles and abnormal amounts of subcutaneous fat.
• It begins with erythematous purplish nodules (hence the name erythrocytosis frigid) on the calves which later rupture producing a non-healing ulcer.
• The aetiology of these ulcers is not clear. It is supposed to be due to ischaemia of the lower leg due to spasms of branches of posterior tibial and peroneal arteries. These vessels are abnormally sensitive to hot and cold weather similar to Raynaud’s disease. In some cases, tubercle bacilli have been isolated, with ulcers responding to antituberculous treatment.
• These ulcers are managed conservatively.
• Sympathectomy may be beneficial in those patients who are hypersensitive to weather changes.

Diabetic Ulcer Foot

Diabetic patients are more prone to the development of ulcers in the foot because of the following reasons.

1. It usually produces a Neuropathy which can be distal and diffuse with a stocking type of distribution. It commonly manifests after about 10 years of diabetes. 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, trophic ulcer develops which progresses and can penetrate deeper and deeper.
   • Very often the patient is unaware of this. Diabetic neuropathy of the tibial nerve is dangerous. Clawing of the toes and hammer toe results due to paralysis of the intrinsic muscles of the foot. The sensation is absent over the entire sole of the foot due to the involvement of medial and lateral plantar nerves. These two factors predispose to the pressure sore over the plantar surface of the head of the metatarsals.
2. Resistance to infection is lowered due to diabetes. Uncontrolled diabetic patients 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.
3. Diabetes is usually associated with atherosclerosis involving major vessels resulting in ischaemia of the foot (macroangiopathy). In addition, it also produces small vessel disease in the form of non-specific thickening of the basement membrane. It is described as microangiopathy.

Thus, neuropathy or microangiopathy singly or in combination with secondary infection favours the development of diabetic ulcers. Ulcer starts due to minor trauma like a thorn prick, or trimming of the nail or shoe bite. It may also start as a callosity in the sole of the neuropathic foot.

Sequence Of Events In Diabetic Ulcer Foot

1. Following an injury or due to infection, an ulcer develops along with a swollen, oedematous foot—Stage of cellulitis.
2. The Cellulitis stage takes up a virulent course and spreads deeper and also upwards along fascial planes —Stage of spreading cellulitis.
3. Secondary infection caused by mixed organisms along with anaerobes and non-clostridial gas-forming organisms produce multiple abscesses—Stage of abscesses.
4. Tense oedema along with vascular compromise which is already existing produces ischaemia and gangrenous patches of skin, toes, etc. —Stage of gangrene.
5. Infection involves deeper tissues like bone, producing osteomyelitis — Stage of osteomyelitis.
6. Untreated cases develop rapidly spreading cellulitis and gangrene of the limb producing septicaemia and diabetic ketoacidosis—Stage of septicaemia.

Diabetic Ulcer Foot Investigations

1. A complete blood picture usually demonstrates a high total count with low Hb% (Infection).
2. Blood and urine sugar estimations.
3. Pus for culture/sensitivity.
4. X-ray of the foot to rule out osteomyelitis which may be the cause for chronicity of the ulcer.
5. Liver function test (LFT), ECG, chest X-ray, blood urea, and creatinine a routine in diabetic patients.
6. Lower limb angiography is an important investigation to check the patency of vessels.

Treatment¹Of Diabetic Ulcer Foot

It can be discussed under five headings:

1. Control of diabetes
2. Control of infection
3. Local treatment of the ulcer
4. Various types of surgery for diabetic ulcer foot
5. Care² of the patient as a whole

1. Control of diabetes: It is an important part of the treatment of diabetic ulcer foot. Diabetes precipitates infection and infection worsens the diabetic status. These ulcers are better managed, at least in the initial period by insulin rather than oral antidiabetic drugs. Injection plain insulin is given 3-4 times/ day depending upon the requirement.

• At the time of admission after measuring blood levels of glucose, urine is checked 3–4 times/ day by Benedict’s test and a urine sugar chart is maintained. Depending upon the change in the colour of the reagent, insulin is given. This method is described as a SLIDING SCALE METHOD.
• After starting the dosage, a careful watch is made regarding blood sugar values and urine colour changes in Benedict’s test. If the patient is not improving, insulin dosage is increased every day, at each time, by 4–8 units till all the urine sugar samples show either blue or green colour.

2. Control of infection: Once the culture/ sensitivity report is available, appropriate antibiotics are started. Commonly gram-positive, gram-negative and anaerobic infection exists. Antibiotics may have to be continued for a long time depending upon the nature, type and severity of infection.

• The presence of high-grade fever with chills and rigours suggests the development of multiple abscess pockets which need to be drained rather than indiscriminate change and usage of antibiotics. If infection is not controlled properly, ketoacidosis results.

3. Local treatment of diabetic ulcer foot: Diabetic ulcer is a non-healing ulcer. Hence, initial treatment is with hydrogen peroxide or Eusol or iodine solution and when the ulcer is converted into a healing ulcer, with pink granulation tissue, a split skin graft is applied. Small ulcers heal by granulation tissue.

4. Various types of surgery¹ for diabetic foot.

5. Care of the patient as a whole: Recovery from healing of diabetic ulcer foot may range from a few weeks to a few months. During this period there are various other aspects to be looked after apart from infection and insulin.

¹Even a small negligible diabetic ulcer should be treated properly, otherwise, a patient may have to “Pay through his foot” for it.

²This is an important aspect often forgotten by the treating physicians and surgeons.

Sliding Scale Method-Treatment With Insulin1 (Initial Plan)

Blue

• Noinsulin

Green

• 4 units

Yellow

• 8 units

Orange

• 12 units

Red

• 16 units

Red precipitate

• 20 units

¹Various types of insulin, dosage, resistance to insulin, complications such as hypoglycaemic coma, etc. are given in different textbooks of medicine.

Patient/Public Education To Protect The Foot

• Never walk barefoot, preferably use Microcellular rubber shoes which are not only soft but also allow oxygenation. They also help in minimising the pressure points.
• Keep the foot dry after proper cleaning of the foot. The paring of the nails, and trimming should be done carefully, if infection sets in consult the physician at the earliest.
• Avoid applying herbal/local medicines or lotions to corn. Consult the surgeons for the com.
• Proper and regular control of diabetes by diet, frequent self-examination of urine and regular blood sugar estimation.
• Do not consult the neighbourS².

¹Unfortunately 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.

²Remember, it is the patient’s leg that may have to be amputated and not the neighbour’s.

• Reassurance and good rapport with the treating doctors.
• Since these patients have peripheral neuropathy, they will not be able to appreciate the temperature of the water. Pouring hot water over the foot can cause burns without the patient being aware of it. Hence, a bystander has to check the temperature of the water before being used by the patient. Thus, the best way to avoid complications related to diabetes is by controlling the sugar levels with diet alone or diet with insulin or oral hypoglycaemic agents.

Causes Of Death In Diabetic Ulcer Foot

• Septicaemia with ketoacidosis
• Severe electrolyte abnormalities
• Other causes such as silent myocardial infarction.

Pressure Sore Prevention And Treatment

Pressure ulcers, or bed sores are a serious and frustrating complication for the paralyzed, debilitated or comatose patient confined to a bed or wheelchair.

• The ulcers form when soft tissue is compressed between a bony prominence such as the ischium, sacrum or trochanter and a supporting structure – the bed or wheelchair.
• The growing incidence of spinal cord injuries due to automobile accidents and increased numbers of debilitated geriatric patients admitted to hospitals have drawn more attention to the problem of pressure ulcer prevention and treatment.
• Pressure ulcer is usually the most important factor that delays rehabilitation of the paraplegic or quadriplegic patient.

Factors Predisposing To Formation Of Pressure Sore

The most important factor is pressure, with other factors being paralysis, paresis, shearing forces

malnutrition, anaemia, advanced age and infection. The lack of protective sensation in comatose, debilitated patients prevents them from changing their posture. The localized pressure continues and the skin ulcer develops. Initially, there is tissue anoxia and cell death.

• Later there will be an active inflammation and vasodilatation occurs, resulting in reactive hyperemia. If pressure is removed allowing tissue perfusion and thus wash out toxic byproducts. Initial damage may be reversible. If not, permanent damage will occur. This can happen in one to six hours.

Pressure Sore Clinical features

1. Early superficial ulceration
   • Erythema, oedema and punctate haemorrhage. Moist irregular ulceration with 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
   1. Cicatrization of rolled ulcer edges
   2. Eschar at the base of the ulcer
   3. Spread of inflammation and bacterial invasion
4. Late deep ulceration
   • Breakdown of fascial plane
   • Chronic inflammation and fibrosis of deep tissue (Bursa formation)

Various Aspects Of Diabetic Ulcer Foot

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 larger undermined defect overlying the bone.

Pressure Ulcers Preventive Measures

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

Treatment

1. Superficial ulceration: Debridement and allow it to heal by secondary intention. It will take many weeks to heal.
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 spasms and contractures if present.
  • Once it is ready, the defect is closed. 3. Education of patient and patient attendees to
    prevent pressure sores.

Pressure Ulcers 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 maturation. 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 valuable skin with lanolin lotion
5. Care of perineum and genitalia especially in patients with incontinence
6. Clothing and bedding must be wrinkled free, 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 party education

Pressure Ulcers Methods of Closure

1. Primary closure—undermine and approximate the cut edges
2. Split skin graft (SSG)—in selected cases only.
3. Skin flaps

• • Transposition flap
  • Rotation flap
  • Advancement flap
  • Cultured muscle interposition for severe and ischial pressure sores.