Total Contact Cast - Guide to Clinical Practice

PRACTICAL GUIDE The Total Contact Cast (TCC) can be used for the bloodless treatment of neuropathic plantar ulcers and has good results in their closure. It is an easy-to-perform, low-cost, low-morbidity method that allows walking with full weight bearing without walking aids.

This guide helps orthopedic professionals understand the disease and make the TOTAL CONTACT CAST with quality and efficiency, reducing the risk of amputations and infections.

DIABETIC FOOT / CHARCOT ARTHROPATHY / PLANTAR INJURY /

TOTAL CONTACT CAST

FRANCISCO SÉRGIO DE OLIVEIRA

First, I thank God for allowing me the opportunity to do this work, it was a lot of work to research everything there is in the world on the subject with the intention of enabling professionals who care for orthopedic patients with problems caused by diabetes.

To my children and grandchildren who are the reason for my existence and it's for them that I wake up every morning.

I thank the friends who readily volunteered to help with the translations of the work: Mr. Charles Barocas CEO of the American Society of Orthopedic Professionals - USA Allen Garita Orthopedic Technologist San Jose - Costa Rica Massimo Menchella Nurse, Santi cosma and damiano - Italy

dream on dream until your dream come true (Aerosmith)

A thousand will fall at your side, and ten thousand at your right hand, but it will not come to you.

Psalm 91:7

Francisco Sérgio de Oliveira graduated in nursing in 1993, graduated as a orthopedic technician in 1994 from the Brazilian Society of Orthopedics and Traumatology and a orthopedic technologist from the American Society of Professionals in Orthopedics in 2016.

Specialist in Trauma Nursing by the Brazilian Nursing Association, specialist in cardiac surgery perfusion by the Santa Lucinda hospital, specialist in endoscopic procedures by Olympus and by Santa Casa de São Paulo.

Master Caster by the American Society of Orthopedic Professionals - ASOP He has worked for 28 years at Sorocaba Hospital Center as an orthopedic technician in an orthopedic clinic.

INDEX

Introduction (Charcot's Neuropathy) ----------------------------------------------------------- 02 Types of Neuropathies ------------------------------------------------------------------------------- 03 Causes / risk factors / symptoms of neuropathies ----------------------------------------- 04 Pathogenesis -------------------------------------------------------------------------------------------- 07 Clinical presentation and diagnosis ------------------------------------------------------------- 08 Loss of protective sensation and deformities with and without ulcer -------------- 09 Classification (clinical and anatomical) --------------------------------------------------------- 12 Conclusion ------------------------------------------------------------------------------------------------ 14 Neuropathic plantar ulcers ------------------------------------------------------------------------- 15 Skin Anatomy and Physiology --------------------------------------------------------------------- 16 Healing Process ----------------------------------------------------------------------------------------- 17 Factors that interfere with healing --------------------------------------------------------------- 18 Ulcers (classification) --------------------------------------------------------------------------------- 19 Neurotrophic Ulcer ------------------------------------------------------------------------------------ 20 Application of full contact plaster in neuropathic ulcers --------------------------------- 22 Indications and technique of the total contact plaster ----------------------------------- 26 Indications / contraindications -------------------------------------------------------------------- 29 Ulcer evaluation / debridement / dressings -------------------------------------------------- 31 Characteristics of an ideal dressing / Ulcer cleaning / Coverings --------------------- 33 Main types of roofs ------------------------------------------------------------------------------------ 34 Technique of making full contact plaster ------------------------------------------------------ 36 Iatrogenic complications the full contact plaster ------------------------------------------- 40 References ----------------------------------------------------------------------------------------------- 41

INTRODUCTION

Charcot's Neuroarthropathy (CNA) Charcot neuroarthropathy (CNA) is a bone and joint deformity of the neuropathic foot, in which the architecture and structural organization of the bones are altered, with radiographic alterations characterized by bone destruction and remodeling, joint destruction, subluxation and dislocation.

Despite recognizing that Mitchell was the first physician to describe osteoarticular destruction associated with neurological dysfunction, it was Charcot who, in 1868, made the first detailed histopathological description of the alterations present in Tabes Dorsalis. In 1881, Paget, at an international medical congress in London, suggested the definition of Charcot's disease for this pathological entity that has several definitions.

Although Diabetes is currently the main cause of CNA worldwide, it was only in 1936 that this pathology was described for the first time as a complication of Diabetes.

Although recognized for over 300 years, CNA remains a complex and difficult entity when it comes to diagnosis and treatment. Therefore, healthcare professionals should be aware of this pathology given the growing trend of Diabetes and its complications.

Diabetic neuropathy is a nervous disorder caused by diabetes. People with the disease can, over time, experience nerve damage throughout the body. Some people may not have any symptoms, others may experience pain, tingling or loss of sensation especially in the hands, arms, feet and legs. However, these problems can also occur in the digestive system, heart and reproductive organs.

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TYPES

There are four main types of diabetic neuropathy. You may have only one type or symptoms of several types. Most develop gradually and may go unnoticed until considerable damage occurs: Peripheral neuropathy Peripheral neuropathy is the most common form of diabetic neuropathy. As the name implies, it affects the extremities of the body, such as feet, legs, hands and arms.

Autonomic neuropathy The autonomic nervous system controls the heart, bladder, lungs, stomach, intestines, sex organs and eyes. Diabetes can affect the nerves in any of these areas, giving rise to autonomic diabetic neuropathy.

Diabetic amyotrophy Rather than affecting nerve endings like peripheral neuropathy, diabetic amyotrophy affects nerves in the thighs, hips, buttocks and legs. Also called femoral neuropathy or proximal neuropathy, this condition is more common in people with type 2 diabetes and older adults.

SICK NERVE

SOUND NERVE

Mononeuropathy Mononeuropathy involves damage to a specific nerve. The nerve can be in the face, trunk or leg. Also called focal neuropathy, diabetic mononeuropathy often happens suddenly. It is more common in older adults. Although it can cause severe pain, the disease usually doesn't bring any long-term complications. Sometimes mononeuropathy occurs when a nerve is pinched. Carpal tunnel syndrome is a common type of compression neuropathy in people with diabetes.

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CAUSES

Diabetes is a disease that affects blood vessels, both large and small. Our nerves, which can be understood as small electrical wires that transmit information about heat, pain, cold or pressure to our brain, need to receive blood with oxygen to function properly. In the case of diabetes, there is a decrease in oxygen reaching the nerves through small blood vessels, and an inflammatory process also forms, both leading to malfunction of the nerves and causing diabetic neuropathy.

The exact causes of this damage differ depending on the type of diabetic neuropathy.

The damage to the nerves is likely due to a combination of factors: Metabolic factors such as high blood glucose, long-term diabetes, abnormal blood fat levels, and possibly low insulin levels Neurovascular factors leading to damage to blood vessels that deliver oxygen and nutrients to nerves Autoimmune Factors That Cause Nerve Inflammation Mechanical damage to nerves such as carpal tunnel syndrome Inherited traits that increase susceptibility to nerve disease Lifestyle factors such as smoking or alcohol use

RISK FACTORS

Uncontrolled blood sugar levels: This is the biggest risk factor for all complications from diabetes, including diabetic neuropathy. Keeping blood sugar levels under control is the best way to prevent complications.

Long-term diabetes: The risk of diabetic neuropathy increases the longer you have diabetes, especially if your blood sugar is not well controlled. Diabetic neuropathy is more common in people who have had diabetes for at least 25 years.

Kidney disease: Diabetes can damage the kidneys, which can build up toxins in the blood and contribute to nerve damage.

Smoking: Smoking narrows and hardens the arteries, reducing blood flow to the legs and feet. This can damage the integrity of peripheral nerves.

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SYMPTOMS

Diabetic Neuropathy Symptoms The signs and symptoms of diabetic neuropathy vary depending on the type of neuropathy and nerves that are affected.

Peripheral neuropathy Numbness Reduced ability to feel pain or changes in temperature, especially in the feet and fingers Tingling or burning sensation Pain when walking Extreme sensitivity to the lightest touch - for some people, even the weight of a sheet can be distressing Muscle weakness and difficulty walking Serious foot problems such as ulcers, infections, deformities and bone and joint pain. This condition is called diabetic foot.

Autonomic neuropathy No symptoms of hypoglycaemia when blood sugar levels are low Bladder problems, including frequent urinary infections or urinary incontinence Constipation, uncontrolled diarrhea or a combination of the two Slow emptying of the stomach (gastroparesis), leading to nausea, vomiting and loss of appetite Difficulty in swallowing Erectile dysfunction Vaginal dryness Increase or decrease in sweating Inability of the body to adjust blood pressure and heart rate, leading to sharp drops in blood pressure when standing up, for example Problems with regulating body temperature Changes in the way the eyes adjust to a light or dark environment Increased heart rate at rest

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Diabetic amyotrophy Symptoms usually occur on one side of the body. In some cases, symptoms can spread to the other side as well. Most people improve at least partially over time.

However, the symptoms may get worse before they get better. This condition is often marked by: Sudden severe pain in hip, thigh or buttock Thigh muscles that may be weak or atrophied difficulty getting up Abdominal bloating if the abdomen is affected Weight loss Mononeuropathy Symptoms usually subside and go away on their own over a few weeks or months.

Signs and symptoms depend on which nerve is involved and may include: Difficulty focusing vision, double vision or pain behind one eye Paralysis of one side of the face (Bell's palsy) leg or foot pain Pain in the front of the thigh chest or abdominal pain Sometimes mononeuropathy occurs when a nerve is pinched. Carpal tunnel syndrome is a common type of compression neuropathy in people with diabetes.

Signs and symptoms of carpal tunnel syndrome include: Numbness or tingling in your fingers or hand, especially in your thumb, index finger, middle finger and ring finger A feeling of weakness in your hand and a tendency to drop things

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PATHOGENESIS

The exact mechanism of the pathogenesis of NAC is not yet established.

Two theories try to explain its pathogenesis: the Neurotraumatic theory (German) and the Neurovascular theory (French). It is currently considered that both theories may play an important role in the pathogenesis of CNA. According to the Neurotraumatic theory, bone destruction is due to sensory loss associated with repetitive mechanical traumas of the foot.

Imperceptible trauma combined with weight bearing on the affected limb will cause fractures and joint destruction characteristic of this pathology.

On the other hand, in the Neurovascular theory, joint destruction will be caused by a vascular reflex secondary to an autonomous neurological dysregulation (sympathectomy) that will cause hyperemia and periarticular osteopenia through the activation of osteoclasts, which facilitates the occurrence of fractures with trauma.

Autonomic neuropathy results in osteopenia that, associated with the loss of protective sensation caused by sensory neuropathy, predisposes to bone destruction that occurs during gait, as the patient is not aware of the trauma. Thus, CNA results from this vicious cycle in which the patient continues to walk on the diseased foot, allowing for more lesions to appear.

It should be noted that the resulting dysfunction of the intrinsic muscles of the foot causes overload in certain areas, leading to the appearance of microfractures, ligament laxity and progression to bone destruction.

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CLINICAL PRESENTATION AND DIAGNOSIS

HOW TO DIAGNOSE THE DIABETIC FOOT...

NEUROPATHIC? ISCHEMIC? INFECTIOUS? PATHOPHYSIOLOGY - Algorithm adapted from: Boulton AJM, 1988; IWGDF, 1999a; Armstrong et al., 1996; Lavery et al., 1998

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LOSS OF PROTECTIVE FEELING WITH DEFORMITIES WITH AND WITHOUT ULCERA

Clinically, Charcot's arthropathy can present itself in two forms, the acute phase and the chronic phase.

The diagnosis of acute CNA is predominantly clinical and this pathological entity should be suspected in the presence of a foot with signs suggestive of inflammation, in the absence of fever and a visible port of entry, such as interdigital wounds or plantar ulcers.

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Acute Charcot's foot presents with hyperemia, edema, temperature rise of more than 2 degrees when compared to the other foot, very dry skin and sensory neuropathy.

Proprioceptive sensitivity and reflexes are diminished or absent. Pain may be present in varying degrees or even absent, depending on the degree of nerve dysfunction. Arterial pulses of the affected foot are maintained or even increased due to peripheral vasodilation characteristic of CNA. The acute presentation of CNA may mimic a crisis of gout, DVT or cellulite, hence the importance of measuring certain serological parameters, such as uric acid, and of imaging in distinguishing these different pathological entities.

The clinical diagnosis of the acute phase is difficult and radiography is often unable to identify or distinguish this entity from other conditions, thus failing to diagnose fracture and/or dislocation. In turn, bone scintigraphy with technetium radioisotope has good sensitivity and low specificity for this pathology.

It should be noted, however, that only magnetic resonance imaging (MRI) is able to reveal, in greater detail, the nature of the damage and inflammation of the bone and surrounding soft tissue (subchondral bone marrow edema with or without microfractures). Thus, MRI is particularly useful in the early stages of the disease, with a significant correlation between the intensity of bone marrow edema and certain clinical parameters such as soft tissue edema and pain.

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The diagnosis of acute CNA is therefore based on history and clinical examination but must be confirmed by imaging methods. X-ray of the foot should be the first imaging exam to be performed in order to verify the occurrence of fractures or subtle subluxations. When, despite clinical suspicion, the X-ray of the foot is apparently normal, MRI and nuclear imaging can sometimes confirm the diagnosis.

It is noteworthy that the delay in the correct diagnosis of acute CNA has serious consequences, as the patient, by continuing to load the affected foot, will increase bone destruction and the appearance of foot deformities characteristic of the chronic phase.

In the chronic phase of CNA, the foot does not show signs of inflammation, although the edema remains. At this stage, there is deformity of the foot due to the shortening of the plantar arch and equinism caused by the shortening of the Achilles tendon. These deformities resulting from osteoarticular and muscle involvement give rise to hyperpressure sites and increase the likelihood of the occurrence of ulcers and amputation, in symbiosis with the ischemia characteristic of this phase.

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CLASSIFICATION

Different classification systems for CNA have been proposed, with the SandersFrykberg anatomical classification being one of the most popular. NAC can be classified according to various parameters such as clinical status, anatomical location and stage in the natural history of the disease. Existing classifications have no prognostic value and do not influence treatment.

CLINICAL CLASSIFICATION

Clinically, CNA can be divided into the acute or chronic stage. In the acute or active phase, the foot presents marked inflammatory signs (redness, edema and heat) most frequently affecting the midfoot. Pain may be absent depending on the degree of neuropathy. At this stage the foot has no deformities and imaging is typically normal.

On the other hand, in the chronic or inactive phase, local inflammatory signs progressively regress, however, the foot remains flushed, but with a temperature similar to that of the contralateral foot. It is at this stage that the foot can develop characteristic deformities such as plantar arch collapse in the midfoot, causing the “rocker-bottom deformity” and the medial convexity of the midfoot.

ANATOMIC CLASSIFICATION

Several authors have proposed anatomical classifications of CNA according to the patterns of involvement of the foot and ankle, because although this disease has been verified in other body locations, in diabetic patients it affects almost exclusively the foot and ankle.

In 1991 Sanders and Frykberg proposed the currently most used anatomical classification of the CNA. According to this classification, CNA can be divided into five different patterns according to the articulations involved.

Type I, present in 15% of feet with CNA, affects the metatarsophalangeal and interphalangeal joints of the foot.

Type II, the most common, accounting for 40% of Charcot's feet, affects the tarsometatarsal joints or Lisfranc joint. The second most common pattern, type III, present in 30% of CNA, is characterized by involvement of the naviculocuneiform, talonavicular and calcaneocuboid joints.

The type IV pattern (10%) affects the ankle and subtalar joints. Finally, type V, present in 5%, affects the calcaneus region. Types IV and V have a poor prognosis due to the abnormal load distribution during gait.

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There is also a more simplistic anatomical classification that characterizes this entity in 3 different types according to the location of the foot strike: forefoot (metatarsophalangeal and interphalangeal joints), midfoot (tarsal and tarsometatarsal joints) and hindfoot (ankle and heel joint).

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CONCLUSION

CNA (Charcot's Neuro Arthropathy) syndrome is a major complication resulting from diabetes and neuropathy. The exact mechanism of its pathogenesis is still unclear, although it is considered, at present, that both the Neurotraumatic and Neurovascular theories may play an important role.

Although this condition is considered one of the important complications of diabetes, it is only identified in a small percentage of diabetics. Due to the delay in the diagnosis and treatment of CNA, it progresses to the formation of ulcers, thus increasing the risk of amputation, hence the importance of an early diagnosis and treatment.

Although several authors have presented different classification systems with some clinical importance, they do not have a prognostic value or influence the treatment.

It is a neuroarthropathy with important individual and social consequences, which is predominantly associated with the Diabetes epidemic, deserves special attention in order to diagnose and treat this complication arising from this serious public health problem early.

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NEUROPATHIC PLANTAR ULCERS

The foot reflects in a very special way all the damage caused by diabetes mellitus to the patient's body. The association of vascular involvement due to atherosclerosis and microangiopathy, sensory and motor peripheral neuropathy and foot deformities favors the appearance of ulcers, infection and gangrene.

One of the biggest fears of diabetic patients is the total or partial loss of their lower limb, due to amputation. This fear is well founded, as 50% to 75% of non-traumatic lower limb amputations are related to complications from diabetes, with approximately 35,000 major amputations (above the ankle) occurring annually in the United States. Foot infection is the most common cause of hospitalization in diabetic patients, among all complications of the disease, accounting for 25% of total admissions (about 200,000 admissions/year).

In the study of the results of the treatment of diabetic foot ulcers, classified as Wagner grades I and II using Total Contact cast (TCC) and the analysis of factors that interfere with the healing of these lesions, we understand that the closure of foot ulcers Grades I and II diabetics, without active infection, is a fundamental step in the prevention of deep infections and amputations. The classification and treatment proposal advocated by Wagner are used due to their comprehensiveness, simplicity and reproducibility. The use of TCC is recommended as an effective method to close neuropathic ulcers of grades I and II.

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Neurotrophic ulcers can cause various stigmas, leading the patient to marginalization.

To prevent this from happening, the multidisciplinary team must provide them with global assistance, meeting their biopsychosocial needs, to improve their living conditions. The professionals of this team must be cohesive, value the diversity of roles in search of the patient's integrality, to ensure their adherence to the treatment, emphasizing that their participation in the healing process is essential. They should also encourage the patient to activities of daily living, pointing out the importance of self-care in their recovery. The relationship between professionals and the patient must be based on mutual respect and dignity. Team members must be aware of their responsibility to indicate adequate treatment, as well as have the humility to recognize their own limitations and make referrals to other professionals, whenever necessary. Patient care must be focused on the prevention and treatment of the disease, when it is already installed, seeking to guide self-care activities in pursuit of improving quality of life.

SKIN ANATOMY AND PHYSIOLOGY

For professionals to provide adequate care to patients with ulcers, the skin layers and the healing process must be known, as described below. The skin is the largest organ that covers and delimits our body, represents 15% of body weight and is composed of three layers: epidermis, dermis, hypodermis or subcutaneous tissue. The epidermis is the outer layer, without vascularization, formed by several layers of cells. Its main function is to protect the body and constantly regenerate the skin. It prevents the penetration of microorganisms or destructive chemicals, absorbs ultraviolet radiation from the sun and prevents fluid and electrolyte losses. The dermis is the intermediate layer, made up of dense fibrous tissue, collagen, reticular and elastic fibers. In it are located the vessels, nerves and skin appendages (sebaceous glands, sweat glands and hair follicles). The hypodermis is the deepest layer of the skin, also called the subcutaneous cellular tissue. Its main function is the nutritional reserve deposit, working as a thermal insulator and mechanical protection against external pressure and trauma, facilitating the mobility of the skin in relation to the underlying structures. The skin's functions are: to control body temperature and establish a barrier between the body and the environment, preventing the penetration of microorganisms. The sensory nerve fibers are responsible for the sensation of heat, cold, pain, pressure, vibration and touch, essential for survival. The sebaceous secretion acts as a lubricant, emulsifier, and forms the lipid mantle of the skin surface, with antibacterial and antifungal activity. Under the action of sunlight, the skin synthesizes vitamin D, which has effects on the calcium metabolism in bones.

Skin structure.

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HEALING PROCESS

The skin, when injured, immediately begins the healing process. Skin restoration occurs through a dynamic, continuous, complex and interdependent process, comprising a series of overlapping phases, called healing. To better understand this process, its various phases will be discussed below. a) Immediate reaction It is the first stage of this process, constituted by the body's initial response to trauma. It occurs with a vascular and inflammatory reaction, which leads to hemostasis, the removal of cell debris and microorganisms. Immediately after the trauma, vasoconstriction occurs, which stops the bleeding. This process involves the presence of platelets, fibrin clots that activate the coagulation cascade, resulting in the release of substances to form the temporary extracellular matrix that supports the migration of inflammatory cells, followed by the activation of protection and preparation mechanisms tissue for the development of healing. Inflammation leads to known clinical manifestations of heat, pain, edema and loss of function, signs that can be minimal, transient or lasting. Infection intensifies and prolongs inflammation. b) Proliferation It's the second step. It occurs after the initial inflammatory reaction and comprises the following stages: granulation, epithelialization and contraction. Granulation is the formation of new tissue, composed of new capillaries (angiogenesis), proliferation and migration of fibroblasts responsible for collagen synthesis. With the production of collagen, there is an increase in the strength of the ulcer, called traction force, characterized as the ability of the ulcer to resist external forces and not break. At the end of this phase, epithelialization occurs, which is the step that will lead to the closure of the ulcer surfaces, through the multiplication of epithelial cells at the edge, characterized by the reduction of capillarization and the increase in collagen. At this point, the contraction reduces the size of the ulcers, with the specialized action of fibroblasts. c) Maturation and remodeling It is the third step in the healing process. It is a slow process, which begins with the formation of granulation tissue and the reorganization of proliferated collagen fibers, extending for months after re-epithelialization. It is responsible for increasing the traction force. During remodeling, there is a decrease in cell activity and the number of blood vessels, loss of the fibroblast nucleus, leading to scar maturation. In this phase, the lesion repair process is reorganized, with collagen deposition. Initially, the healing has a flat appearance; later, it stiffens and rises. After a certain time, the scar becomes lighter, less rigid and flatter, causing its reduction.

INFLAMMATORY

PROLIFERATIVE

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MATURATION

FACTORS THAT INTERFERE WITH HEALING

Among the various factors that make healing difficult, some stand out, such as: the longer the evolution of the ulcer, as well as its extension and depth, the longer the time required for healing.

Continuous pressure on the injured area by bony prominences, calluses and/or continuous immobilization leads to interruption of the blood supply, preventing blood flow from reaching the tissues.

In infection, the presence of foreign bodies and devitalized or necrotic tissues prolong the inflammatory phase of the healing process, causing tissue destruction, inhibiting angiogenesis, delaying collagen synthesis and preventing epithelialization. These must be removed by mechanical or autolytic process, for the repair phase to occur.

Edema is characterized by the accumulation of fluid in the body (blood, lymph and others), due to trauma, infections, iatrogenic, infectious and inflammatory diseases. It interferes with oxygenation and nutrition of tissues in formation, prevents collagen synthesis, reducing cell proliferation and reducing tissue resistance to infection.

The dressing technique can cause mechanical trauma, caused by aggressive cleaning (friction with gauze, liquid jets with excess pressure), dry coverings adhered to the ulcer bed and/or inadequate, which interfere in the healing process, delaying healing.

Age is an important factor in healing. In children, scarring occurs quickly, but they are prone to hypertrophic scarring. Among young people, healing can be delayed by systemic processes added to the psychosocial process and activities of daily living.

With advancing age, the inflammatory response decreases, reducing collagen metabolism, angiogenesis and epithelialization, especially if associated with conditions that often accompany senility such as malnutrition, vascular insufficiency and systemic diseases.

An adequate nutritional intake of proteins and calories, in addition to vitamins such as vitamin C and zinc. This contribution may be compromised in cases of malnutrition, gastrointestinal malabsorption and inadequate diets. Obesity makes mobilization and walking difficult, leading to a sedentary lifestyle, which can cause disorders such as venous hypertension, which makes it difficult for ulcers to heal. On the other hand, it is known that obesity acts as an immunosuppressive disease, which can inhibit the inflammatory reaction and, consequently, alter healing. Anemia has been referred to as an interfering factor in ulcer repair.

Smoking reduces functional hemoglobin and causes pulmonary dysfunction, predisposing to tissue oxygen deprivation. Nicotine produces vasoconstriction, which increases the risk of necrosis and peripheral ulcers. Alcoholism can damage the brain, heart, liver and pancreas, and interfere with treatment adherence.

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ULCERS

Ulcer is any interruption in the solution of continuity of the cutaneous-mucosal tissue, causing alterations in the anatomical structure or physiological function of the affected tissues.

CLASSIFICATION OF ULCERS Ulcers can be classified, according to the cause, into: surgical, non-surgical; according to the repair time, in acute and chronic, and, according to the depth, in relation to the extension of the tissue wall involved (epidermis, dermis, subcutaneous tissue and deeper tissues such as muscles, tendons, bones and others), in degrees , I, II, III and IV. Grade I: there is an involvement of the epidermis; the skin is intact but shows signs of redness, discoloration, or induration.

Grade II: partial tissue loss involving the epidermis or dermis occurs; the ulceration is superficial and presents in the form of an excoriation or blister.

Grade III: there is involvement of the epidermis, dermis and hypodermis (subcutaneous tissue).

Grade IV: involvement of the epidermis, dermis, hypodermis and deeper tissues.

Grade 0: ulcers have intact skin.

Grade 1: ulcers are superficial with exposed subcutaneous tissue.

Grade 2: ulcers have a deeper extension.

Grade 3: ulceration implies the formation of an abscess or osteomyelitis.

Grade 4: ulcers involve partial gangrene of the forefoot.

Grade 5: ulcers involve extensive gangrene.

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NEUROTROPHIC ULCER

This ulcer is caused by peripheral neuropathy, due to some underlying pathologies, such as: leprosy, diabetes mellitus, alcoholism and others. People with these pathologies, which affect the peripheral nerves, are at greater risk of developing injuries to the autonomic, sensory and motor fibers, which can result in primary injuries, such as claw hand, foot drop and ankylosis (hardened joints); and secondary, such as muscle paralysis, fissures, plantar ulcers and traumatic injuries The autonomic fibers responsible for the maintenance of the sebaceous and sweat glands, when affected, lead to a reduction in the production of their secretions. The skin becomes dry, inelastic and can easily cause cracks which, if left untreated, will compromise the structures of the hands and feet, increasing the risk of infection.

Loss of protective sensation (thermal, painful and tactile) or anesthesia in the hands and feet influence the appearance of skin lesions. This compromise leads to an increased risk of burns, the appearance of blisters and calluses, resulting from continuous pressure on support points, requiring the use of insoles and appropriate shoes. Other factors that influence the appearance of these ulcers are changes in motor fibers, due to muscle weakness and paralysis. This imbalance leads to deformities, compromising function and increasing the risk of triggering these ulcers. In the country's primary healthcare services, a higher incidence of plantar ulcers caused by peripheral neuropathies has been observed. The basic cause of neurotrophic ulcer is loss of protective sensation or anesthesia in the plantar region, due to damage to the posterior tibial nerve. However, there are other factors that influence the appearance of an ulcer, such as: paralysis of the intrinsic foot muscles, loss of the normal pad under the metatarsal head and dry (anhydrous) skin. Anhidrosis resulting from dysfunction of the sweat and sebaceous glands makes the palm and sole of the foot dry and its horny layer, hard and thick, tends to break. “Cracks” or fissures in the upper and lower limbs are very common and often act as an entry point for infectious agents.

Changes in the anatomy of the foot caused by changes in the bone structure create abnormal pressures, facilitating the appearance of ulcers. The other functional factor is gait, that is, in addition to the lack of sensitivity, the foot is subjected to efforts, such as long walks, strides or jogging, the presence of foreign objects in the shoes (stones, nails), which contributes to the ulcer development. Neurotrophic ulcers are classified in degrees, according to tissue involvement, from a superficial lesion to deeper lesions, with involvement of the joint, tendons and bones, osteomyelitis being very common, with subsequent necrosis, gangrene and loss of bone segments .

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Callosity (thickening of the keratin caused by the pressure of the tissues to friction) and tension in areas that support the greatest weight are also a risk for ulcers.

When the calluses are thin, they can be considered protective, but when they are thick and located in areas with reduced sensitivity, they damage the soft tissues and become predisposing factors for ulcers, in addition to being common on the edges of neurotrophic ulcers. Considering the loss of sensitivity and increased pressure as risk factors for the development of ulcers, some measures can be taken to monitor the evolution of pressure in these risk areas, such as: guidance on the use of footwear, special insoles, on daily activities and adaptation of work instruments.

Neurotrophic ulcers can be described based on the following characteristics: they are anesthetic lesions, circular, usually hot and showing no signs of infection. They develop over areas of bony prominences, more frequently in the lower limbs. They are usually preceded by hyperkeratosis (callosities).

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APPLICATION OF TOTAL CONTACT CAST IN NEUROPATHIC ULCERS

Total contact cast are recognized as the gold standard treatment for neuropathic plantar diabetic foot ulceration, endorsed by all national and international consensus documents. Despite this, research has shown that there is a division between the existing evidence supporting the use of total contact models in the treatment of diabetic foot ulcers and their use in clinical practice.

A cornerstone in the management of DFU (Diabetic Foot Ulcers) is the reduction of pressure through unloading. There are many products available for the physician to reduce the pressure of an DFU, including removable devices below the knee and non-removable full contact molds. A total contact cast is a rigid or semi-rigid molded cast that extends from the patient's foot to just below the knee, maintaining contact with the entire plantar surface of the foot and leg and immobilizing the surrounding joints and soft tissue, allowing the patient to remain in outpatient treatment. A total contact mold uses minimal padding to protect the malleolus, tibial shaft and DFU. The use of padding provides full contact with the entire foot while isolating the DFU and significantly reduces peak pressure (p = 0.008) and pressure-time integral (p -0.0012).

The DFU is expensive to run, with an estimated annual expenditure of between $9-$13 billion in the US. Hospitalization of patients with DFU represents between 73.7% and 80% of the overall overall cost, and leads to longer hospital stays. Private health insurance payments nearly double in patients with DFU compared to patients without DFU ($28,031 vs $16,320 respectively). The estimated cost of a lower limb amputation is between $35,000-$45,000, although these numbers do not include past DFU management or indirect costs associated with lost productivity, family status, or quality of life.

On the other hand, the use of total contact models showed substantial cost savings when compared to other treatments ($11,946 vs $22,494 per patient, respectively). In addition, a recent publication highlighted the cost-effectiveness of walkers with non-removable totalcontact cast compared to removable walkers due to the impossibility of removing the appliance, forcing its constant use.

In addition, cure of DFU from all causes has been reported between 60% and 77%.

However, total contact models have shown improved cure rates when compared to other offloading devices in the treatment of plantar neuropathic DFU, with cure rates ranging from 89% to 92%, and in some cases over significantly shorter period.

Despite these benefits, Sinacore reported that 45% of the clinics did not offer an efficient service with qualified and experienced professionals in the management of DFU and in the making of the full contact plaster.

More recently, studies have shown that total contact molds are not regularly used in the management of plantar DFU and shoe modification is the preferred method of unloading despite its ineffectiveness in reducing plantar pressure and shear forces.

This is despite the fact that total contact models are recognized as the gold standard treatment for plantar DFU by all consensus committees.

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Traditionally, it was believed that a total contact cast worked by equalizing plantar pressure, as the entire plantar surface of the foot was in contact with the inner surface of the cast, creating a larger surface area, redistributing pressure across the entire foot. However, other authors have reported a reduction in the plantar contact area as the load capacity of the fused rigid wall lifts the foot. Total contact models also showed a greater reduction in plantar load when compared to ankle or below-theankle devices and below-the-knee removable walkers. The cast shank has been shown to remove 30%-36% of foot pressure when compared to a cast shoe.

Frictional shear forces are also controlled when the foot is held firmly in position.

When compared to shear-reduced walkers, total contact casts are associated with improved cure rates. This suggests that there are several mechanisms that reduce pressure and shear forces and improve DFU outcome and cure time.

It is widely accepted that total contact casts "force compliance and enhance treatment" as patients are unable to remove the cast, maintaining plantar load distribution and decreasing pressure points at ulcer sites. Armstrong and colleagues evaluated the difference between computerized accelerometers worn at the waist and those hidden in removable plaster walkers in the same patients. The results showed that participants recorded higher levels of daily activity on the waist accelerometer compared to that found on the removable walker, which recorded only 28% of daily activity.

This suggests that patients use removable below-the-knee walkers less than a third of the time thus reducing treatment efficiency; whereas a non-removable device enforces continued use compliance. Patients treated with a total contact cast are also significantly less active compared to other discharging devices, thus reducing the number of repetitive stress cycles and improving DFU healing. Shorter stride lengths and reduced walking speeds have also been recorded using total contact casts, reducing vertical forces through the foot.

Total contact models may be contraindicated under certain circumstances. Some authors recommend its use only in uninfected neuropathic ulcers in the absence of PAD (Peripheral Arterial Disease).

However, Nabuurs-Franssen and colleagues conducted a study involving 98 patients with a combination of DPN (Diabetic Peripheral Neuropathy), moderate PAD (Peripheral Arterial Disease), and infection (PEDIS grade ≤2).

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In this prospective, nonrandomized study, researchers aimed to determine the outcome and complications of total contact models in patients with DFU complicated by DPN, DPN and PAD, DPN and infection or DPN, DAP and infection.

They treated the patients in one or a combination of traditional full contact cast, removable bi-valve contact cast and shoe model cast. The authors found that patients with DPN or DPN and infection or DPN and PAD cured 90%, 87%, and 69% of the time, respectively. Importantly, the authors reported rates of new ulcerations and pre-ulcer changes of 9% and 29%, respectively. Although none of these were related to PAD or infection and resolved before the main ulcer healed, suggesting that patients with moderate PAD or infection are no more at risk of developing full plaster complications than patients without PAD or infection. Patients with the triad of DPN, PAD, and infection had worse outcomes, with cure occurring in only 36% of DFUs. The authors did not allude to the reason for this significant difference.

However, it is well established that DFU with PAD and infection have the worst treatment outcomes. Although this trial was non-blinded and non-randomized, the use of full contact casts was found to improve DFU outcome in the presence of moderate PAD and infection and has now been endorsed by the International Working Group on the Diabetic Foot. However, patients must be monitored carefully, and the clinician must have a high degree of experience in managing these types of wounds.

The decision to use a cast may depend on the level of exudate around the wound. Highly exudative wounds may require daily dressing changes. In these circumstances, a bivalve or removable plaster may be considered or the creation of a window at the DFU site.

The most common side effects resulting from the use of a full contact cast are skin abrasion or iatrogenic ulceration. However, a study evaluating the development of iatrogenic ulceration found only 22 new ulcers in a sample of 398 devices, which equates to an iatrogenic ulceration rate of 5.52%, as important, the author reported no deterioration in pre DFU -existing. It has also been found that the iatrogenic ulcer heals before the primary ulcer. To reduce the risk of iatrogenic ulceration, padding should be used to protect the bony prominences, and patients should be advised to check for signs of bleeding or redness in the exposed toes and to protect the contralateral leg with a long sock or pillowcase when in bed to reduce contact with fiberglass mold. Patients should also be taught to check the integrity of the cast and the treating physician should review any problems.

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Long-term use of total contact cast has been associated with muscle atrophy and reduced bone density. To eliminate these problems, Carvaggi et al. (2000) first applied two layers of fiberglass for flexibility and strength (Softcast 3M; 3M Health Care, St. Paul, MN). A second high load-resistance fiberglass bandage was used to reinforce the design (Scotchcast 3M; 3M Health Care). This was placed first between and extended beyond the two malleolus. A second layer was then applied to the plantar aspect of the plaster, which gave the plaster a rigid construction. They found that using a combination of rigid and semi-rigid casting materials minimized these complications. Furthermore, the introduction of a gait rehabilitation program can reduce the adverse effects of muscle atrophy and loss of bone density, although this has not yet been examined.

A leg-length discrepancy can also occur, resulting in further postural instability or worsening. This must be considered during patient selection. Low-profile plasters can be used with a lightweight material to minimize instability, or patients can purchase shoe balancers for the contralateral limb.

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INDICATION AND TECHNIQUE OF MAKING THE TCC

Peripheral neuropathy ultimately leads to numb feet and loss of proprioceptive ability, which reduces the reflex arc of defense against trauma.

Repetitive trauma or even gait itself, when associated with loss of protective sensitivity, can trigger capsuloligamentous injuries, collapse of the medial arch, predisposing to fractures and dislocations not perceived by the patient.

The resulting deformity can lead to the appearance of abnormal pressure zones predisposing to the development of ulcers. The formation of ulcers creates a highrisk situation, as they can become contaminated, evolving with involvement of adjacent soft tissues, reaching the bone, progressing to amputations, sepsis or death.

Several methods have been proposed for the treatment of this type of ulcers, including bed restriction, local wound care with debridement, changing shoes, topical agents and surgical interventions such as: ostectomy, arthrodesis and amputations.

The concept of total contact cast, first described by Brand in 1950, created a new trend in the treatment of this pathology, based on the principle of load distribution across the surface in contact with the soil. Remembering that Pressure=Force/Area, increasing the area of ​contact with the ground will decrease the vertical pressure in the plantar region, distributing it evenly.

Regarding the technique for making the plaster cast, we observed that it is fundamentally important to model the sole of the entire plantar area of ​the foot, including the support of all the toes, providing load distribution over the largest possible contact area. Thus, there is no load concentration in the ulcerated region, allowing local tissue regeneration and progressive healing.

Originally, the TCC was described and is still widely used today in its "closed" form, that is, covering all fingers and leaving no opening for them. Sometimes, for varied needs such as the patient's feeling of "claustrophobia", dorsal lesions on the skin of the fingers, skin irritations or erythema in the areas of bony prominences, we use the "open" form of the TCC, maintaining an opening for the fingers.

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In this way, we obtained the claustrophobic patient's collaboration and adherence in continuing the treatment and we were able to better monitor the evolution of the dorsal lesions of the toes, as well as the general condition of the forefoot, without having noticed any damage or delay in the healing of these ulcers.

Another advantage observed in open plaster is the possibility of ventilation, which greatly reduces the unpleasant odor that invariably accompanies closed TCC. In addition, the association of the foul odor with the non-visualization of the toes generates in the patient and family members the constant doubt about "whether the foot is not rotting in the plaster", often contributing to giving up or avoiding the continuity of the plastered treatment.

Literature is vague when referring to the mean time to closure of ulcers treated with the TCC. Usually, an average period of six to eight weeks for the ulcer to heal is mentioned. Walker et al reported closure around 30.6 days for forefoot ulcers and 42.1 days for hindfoot ulcers. Myerson et al reported a mean healing time of 5.5 weeks for ulcers with a mean diameter of 3.5 cm. Bridges and Deitch reported a mean period of six to eight weeks, without reporting the mean ulcer size.

In our survey, the mean healing time of ulcers was 46.3 days, and the mean size was 2.1 cm for grade I lesions and 5.2 cm for grade II. Thus, we believe that the adjusted model for calculating the healing time based on the size of the ulcer or the use of the adjusted table for this purpose is extremely valuable, as it allows the individualization of each case and informing the patient and their families of the most accurate period. when healing should occur and, consequently, when everyone will be involved in the ulcer closure process.

Such information provides greater involvement and collaboration on the part of the patient and their families, allowing for family, social and economic planning that are important in the routine of patients undergoing long-term treatments.

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The analysis of the variable grade (ulcer depth) was significant, showing that patients with grade II ulcers took longer to heal. The average size of grade II ulcers was greater (5.2cm) than that of grade I ulcers (2.1cm), explaining the longer healing time due to their larger size and not due to their greater depth.

Regarding the use of closed and open casts, the statistical tests showed that the means and medians of the ulcer size versus plasters needed for healing did not show any significant difference (Student's test with p value = 0.42 and the test of Mood with p value = 0.666). Thus, the use of closed or open cast does not change the healing time.

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INDICATIONS

The TCC is indicated in patients with peripheral neuropathy presenting superficial plantar ulcers, grades I and II of Wagner (and in cases of neuroarthropathy of Charcot in phases I and II of Eichenh0ftz).

CONTRAINDICATIONS

The absolute contraindications are: deep infection, dermatoses, arterial insufficiency and grades III, IV and V of Wagner. Relative contraindications include diseases that lead to edema in the lower limbs such as heart failure and kidney disease, blindness and morbid obesity.

CONSTRUCTION TECHNIQUE

The first cast is applied for approximately 1 week or less if excessive drainage is anticipated. Subsequent molds are changed every 2 weeks. Average healing time is 6 weeks.

Charcot fractures are cast for up to 3 months or when surface temperatures are within 2 degrees centigrade.

Indications: Plantar ulcers of the insensitive foot Neuropathic Fractures (Charcot Fractures) Contraindications: Acute infection Wound tracking, ulcer depth greater than width Overdraining wound Claustrophobia Fragile skin Excessive edema Benefits: Immobilization Protects tissue from further trauma Reduces / controls edema Keep walking Disadvantages: Possible joint stiffness if immobilization is prolonged Possible secondary abrasions if cast is incorrectly applied or not carefully monitored

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It is important that the person responsible for placing the TCC is a qualified professional and that the monitoring of the patient is strict in order to reduce risks and avoid complications.

The TCC is applied differently from other casts, as the filling is only used on the anterior part of the tibia, instep and malleolus, thus achieving close contact with the leg, foot and ulcers on the bony prominences are also avoided.

It is applied with the patient placed in a prone position, with the leg flexed at 90º in relation to the thigh, and the ankle in a neutral position. In this position, the gastrocnemius muscles are relaxed and better contact with the leg can be obtained and the excess soft tissue is directed towards the knee, which facilitates maximum use of the "cone effect"; also, in this position, the professional has more access to the plant, which is the most important area, and the formation of edema decreases during application.

The wound is first covered with a sponge dressing, then the cotton layer is placed over the feet and extends to the base of the knee, pulling on its distal part to cover the toes.

Subsequently, a pad or several layers of cotton is placed on the anterior aspect of the tibia, the instep, the sole, heel and malleolus to prevent pressure ulcers. Lie the patient in the prone position and two bandages are placed, in plaster or fiberglass, in a spiral from distal to proximal, covering the fingers and rising to 3 cm below the knee. The base of the cast is molded carefully and intimately with the sole of the foot.

All folds made must be over padding. Later, two splints are formed with plaster or fiberglass covering of the fingers in the proximal part of the plaster; when placing them one on top of the other, the excess is folded to fill the plantar arch and, therefore, the sole is completely flat.

The splints are fixed with a plaster or fiberglass bandage placed in a spiral shape.

Plaster has to be left to dry for 15 min, or until it cools and becomes hard.

The first change in the TCC is made after 7 days, which is when there is a greater reduction in the edema, and the plaster loses its fit, favoring friction. Subsequent changes will ideally be made fortnightly if TCC is used in Charcot foot.

It may be that patients with ulcers with profuse exudate require more frequent exchanges to prevent ulcer maceration; Likewise, very active patients may need more frequent changes due to deterioration of the cast.

TCC discharge should be continued, as with any discharge method, for a week or two after healing so that the foot is ready to change to shoes with special insoles or orthosis.

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Preparation for cast placement includes debridement of all necrotic wound tissue and callus removal. If the tissue is devitalized, scraping until there is bleeding from the wound may be evaluated.

ULCER ASSESSMENT, DEBRIDEMENT AND DRESSING

The assessment of the wound must be done in detail, checking the depth, diameter, tissue types and the presence and type of exudate.

Characteristics of the ulcer and the skin around it: may indicate skin changes, such as: hyperemia, heat, edema, pain, maceration, dryness, desquamation, eczema, hyperpigmentation, or other changes, which are also valuable to guide the treatment.

Exudate characteristics: can be valuable indicators to determine treatment. The color and consistency of this may vary. Serous and bloody fluids are considered normal. Purulent exudate indicates an infectious process.

Appearance of the ulcer: the type of tissue present indicates the stage of the healing process in which the ulcer is: Necrotic tissue: varies in color, from black, gray, whitish, brown, to greenish and black. It corresponds to dead, dehydrated tissue, and pus and fibrous material may also be present.

Fibrinous tissue: yellow in color, with a creamy consistency, due to the amount of cell degradation. Fibrin may cover the entire length of the ulcer or appear as fibrin points partially covering the lesion.

Grain fabric: It looks red, shiny and moist. The diseased tissue has a pale-dark appearance, may bleed spontaneously and has a friable appearance (which breaks easily), indicating an ongoing infectious process.

Epithelialization tissue: it has a pinkish-white appearance, which migrates from the margin to the center of the ulcer.

Measurement of the ulcer: allows you to follow the evolution of the healing process.

The frequency of this procedure will depend on the type of ulcer.

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Excess tissue from the bora should be removed to prevent the callus from macerating the wound and delaying healing.

The cleaning of the wound bed should be done until vitalized tissue is noted, to favor spontaneous granulation. The ulcer must be measured at its largest and smallest diameter.

The ulcer is covered with an appropriate dressing and also gases are placed between the fingers to minimize lateral-medial pressure, preventing maceration of the interdigital space.

BAND AID

Dressing is the set of care given to an injury or ulcer, aiming to provide safety and comfort to the patient and promote healing.

PURPOSES OF DRESSINGS A dressing, to be effective, must serve the following purposes: Be impermeable to water and other fluids, allowing gas exchange.

Be easy to apply and remove, without causing trauma.

Assist in hemostasis.

Protect the ulcer against mechanical trauma and infections.

Limit tissue movement around the ulcer.

Promote a moist environment.

Absorb secretions.

Treat the existing ulcer cavities.

Promote debridement.

Relieve pain.

Provide favorable conditions for the patient's activities of daily living.

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CHARACTERISTICS OF AN IDEAL DRESSING Remove exudate.

Keep high humidity between wound and dressing.

Allow gas exchanges.

Be impervious to bacteria.

Provide thermal insulation.

Be free of contaminated particles and toxic substances from ulcers.

Allow removal without causing local trauma.

Ulcer cleaning The ulcer cleaning technique consists of removing cell debris, foreign materials, necrotic or devitalized tissue and reducing the amount of microorganisms present on the surface. This cleaning must be performed with proper technique, using sterile material.

The handling of the ulcer must be carried out carefully and rigorously, in all its extension and depth, and may be carried out with mechanical cleaning and irrigation.

Mechanical cleaning, with gauze or cotton balls, is currently not indicated, as it can traumatize newly formed cells, triggering inflammatory reactions and increasing healing time. Cleaning with gentle irrigation with saline or saline solution of 0.9% sodium chloride is recommended, because this solution does not harm the tissues and cleans the ulcer, removing all exudate and/or foreign body present, without traumatizing the cells of the bed of it, accelerating the healing process.

The ulcer bed must be kept moist, and the entire surrounding skin must be cleaned with gauze moistened with saline solution. After cleaning the area around the ulcer, dry it with gauze to avoid maceration of the intact skin and facilitate the fixation of the cover.

Covers As we consider the term curative as the process of topical care for the ulcer, we will adopt the term coverage to designate the product used to cover the ulcer bed.

Covers can be classified as primary, secondary and mixed. The primary coverage is the product that remains in direct contact with the ulcer bed on the adjacent skin, in order to absorb its exudate, facilitating the free flow of drainage, preserving the moist environment and non-adherence. This type of dressing requires permeability to fluids, non-adherence and impermeability to bacteria. The secondary covering is the product that covers the primary covering, in order to absorb excess drainage, providing protection and compression. This type of dressing needs to have satisfactory absorption and protection capacity. Mixed coverage is the product that has two layers, one in contact with the ulcer bed and the other in contact with the external environment.

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MAIN TYPES OF COVERAGE DRESSING WITH MOISTED GAUZE IN PHYSIOLOGICAL SOLUTION Composition: sterile gauze and 0.9% saline solution.

Mechanism of action: maintains moisture in the ulcer, favors the formation of granulation tissue, softens devitalized tissues, stimulates autolytic debridement, absorbs exudate.

Indication: maintenance of moist ulcer, indicated for all types of ulcer.

Contraindications: none.

HYDROCOLOIDS Hydrocolloids are dressings that can be presented in the form of a plaque, paste, gel and granules.

Composition: hydrocolloid in plaque is a synthetic dressing derived from natural cellulose, which contains hydrophilic particles that form a self-adhesive elastic plaque.

Mechanism of action: Cellulose particles expand when absorbing liquids and create a moist environment, which allows cells in the ulcer microenvironment to provide self-lytic debridement. This condition stimulates the growth of new vessels, granulation tissue and protects nerve endings.

Indication: plaques are indicated for ulcers with a small or moderate amount of secretion.

Contraindication: they are contraindicated in cases of infection, mainly by anaerobes.

TRANSPARENT FILM Composition: the transparent film is a sterile dressing made up of a polyurethane membrane, covered with a hypoallergenic adhesive and has a certain degree of permeability to water vapor.

Mechanism of action: maintains a moist environment between the ulcer and the dressing, favors autolytic debridement, protects against trauma, favoring healing.

Indication: it should be used in superficial ulcers with minimal drainage, in grade I, and in the prevention of pressure ulcers.

Contraindications: not recommended for exudative, deep and infected ulcers.

CALCIUM ALGINATE Composition: alginate is a polysaccharide composed of calcium, derived from some algae.

Mechanism of action: this type of dressing has debriding properties. Before use, it is dried and, when the alginate fibers come into contact with the liquid medium, they carry out an ion exchange between the calcium ions of the dressing and the sodium ions of the ulcer.

Indication: can be used on infected and exudative ulcers.

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ACTIVATED CHARCOAL Composition: this type of dressing has a covering made up of a pillow containing a fabric of activated carbon whose surface is impregnated with silver, which exerts a bactericidal activity, reducing the number of bacteria present in the ulcer, especially gram negative ones.

Mechanism of action: this dressing has a high degree of absorption and elimination of ulcer odor. Activated carbon fabric removes and retains exudate molecules and bacteria, exerting a cleansing effect.

Indication: it is indicated in exudative ulcers, infected with accentuated odors, in fistulas and gangrene.

Note - In little exudative ulcers and in cases of osteotendinous exposure, it should be used with restrictions, due to the possibility of dryness of the lesion site SILVER SULFADIAZINE Composition: 1% silver sulfadiazine, hydrophilic.

Mechanisms of action: the silver ion causes protein precipitation and acts directly on the cytoplasmic membrane of the bacterial cell, and has residual bacteriostatic action, by releasing this ion.

Indication: colonization prevention and burn treatment.

Contraindication: hypersensitivity.

Note - There is silver sulfadiazine with cerium nitrate, which can be used on burns, infected and chronic ulcers, reducing infection and acting against a wide variety of microorganisms.

ESSENTIAL FATTY ACIDS OR MEDIUM CHAIN ​TRIGLICERIL Composition: it is a product originating from polyunsaturated vegetable oils, mainly composed of essential fatty acids that are not produced by the body, such as: linoleic acid, caprylic acid, capric acid, vitamin A, E, and soy lecithin.

Mechanism of action: promote chemotaxis (attraction of leukocytes) and angiogenesis (formation of new blood vessels), keep the environment moist and accelerate the tissue granulation process.

Indication: prevention and treatment of dermatitis, pressure ulcers, venous and neurotrophic; treatment of open ulcers with or without infection.

Note - Essential Fatty Acids may be associated with calcium alginate, activated carbon and other types of coatings.

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A cotton stockinette is worn down to the infra patellar region, taking care to avoid creases. Distally the mesh is folded over the fingers and secured with tape. Carefully so that there are no wrinkles that could cause secondary lions.

A 1.3 cm layer of foam is pre-molded and cut to avoid creases and overlaps.

This is used to close the forefoot, if you want to opt for a closed cast.

A long rectangular piece is applied to the pretibial crest, two circular segments are applied to the malleolus and a platform with an orifice for the ulcerated region is fixed to the plantar region.

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The technician should stand in front of the patient, with the patient sitting with the leg dangling and the knee bent at 90 degrees. The cotton is rotated from the tibial tubercle to the forefoot.

Cotton stockinette should be applied evenly with thin layers and without wrinkles or accumulation of material. From the distal region to the proximal region, from the fingers to 3 cm below the knee.

Cotton should be applied with extra layers on the bony protrusions to avoid friction.

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Placing plaster bandages from the distal part to the proximal part is started with enough tension for a good fit in the segment and a good impression, paying attention to the 90-degree angle of the ankle joint and the functional position of the fingers.

The plaster must be molded in every segment so that the contact with the plaster is total.

A plaster base is placed in the plantar region to reinforce the support area with the soil. After fixing it, the patient must stand and step with the plaster still wet on the floor so that there is an increase in the contact area of the plaster with the ground, distributing the force evenly and relief in the region of the ulcer where a circular segment was made in the foam.

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The plaster must be molded again along the entire length of the segment, increasing the contact with the entire surface.

The TCC allows charging as soon as it is dry, after 48h.

Plaster application leads to a significant reduction in edema. The patient will have to return in one week to change the first plaster, subsequently it will have to be changed every one to two weeks, depending on factors such as wound size, drainage and edema.

Afterwards, it is possible to adapt a specific shoe for insensitive feet that must be extra deep, wide anterior chamber, without internal seams and with an insole molded to the patient's foot.

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IATROGENIC COMPLICATIONS OF FULL CONTACT PLASTER

A frequently changed total contact cast is a safe modality for unloading and immobilizing the neuropathic foot, albeit with an expected steady rate of minor reversible complications. Patients should be informed of these complications and risks prior to plaster application.

Contraindications and complications include infection, poor foot hygiene including elongated toenails, ischemia, non-compliance and claustrophobia.

With respect to infection, the dark, humid and warm atmosphere inside this device is an excellent environment for bacterial growth.

There are other ways in which offloading should be used until the infection is resolved before applying the TCC. Xerotic skin should be treated with emollient lotions to avoid cracking and hyperkeratosis, if present, debrided.

Circumferences should be avoided in bandages. Cut the bandage where reduced blood flow to the foot can occur. As Kominsky puts it "It is much more important to be concerned about what is being removed from the ulcer, ie pressure, than what is being put in."

Before applying the plaster, the ulcer must be evaluated for width and depth.

Ulcers that are deeper than their width can create a problem as epithelialization can occur before the depth of the wound is properly healed, possibly allowing an abscess to form. These ulcers must be uncapped, treated with an open package, and then TCC applied.

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