How to Draw a Low Power Tissue Plan

• Journal List
• Indian J Plast Surg
• v.48(1); January-Apr 2015
• PMC4413488

Indian J Plast Surg. 2015 January-Apr; 48(1): iv–16.

Pressure ulcers: Current agreement and newer modalities of treatment

Surajit Bhattacharya

ⁱDepartment of Plastic & Reconstructive Surgery, Sahara Hospital, Lucknow, Uttar Pradesh, Bharat

R. K. Mishra

Section of Plastic & Reconstructive Surgery, SIPS Hospital, Lucknow, Uttar Pradesh, Republic of india

Abstract

This article reviews the mechanism, symptoms, causes, severity, diagnosis, prevention and present recommendations for surgical as well every bit non-surgical management of pressure ulcers. Particular focus has been placed on the current understandings and the newer modalities for the treatment of pressure ulcers. The paper likewise covers the function of diet and pressure-release devices such as cushions and mattresses as a office of the treatment algorithm for preventing and quick healing process of these wounds. Force per unit area ulcers develop primarily from pressure and shear; are progressive in nature and most oft found in bedridden, chair bound or immobile people. They frequently develop in people who have been hospitalised for a long time generally for a different problem and increase the overall fourth dimension as well as cost of hospitalisation that accept detrimental effects on patient'due south quality of life. Loss of sensation compounds the problem manifold, and failure of reactive hyperaemia cycle of the force per unit area decumbent area remains the nearly important aetiopathology. Pressure ulcers are largely preventable in nature, and their management depends on their severity. The available literature near severity of pressure ulcers, their classification and medical care protocols have been described in this paper. The present treatment options include various approaches of cleaning the wound, debridement, optimised dressings, role of antibiotics and reconstructive surgery. The newer treatment options such as negative pressure wound therapy, hyperbaric oxygen therapy, cell therapy have been discussed, and the advantages and disadvantages of current and newer methods have also been described.

KEY WORDS: Bedsore, decubitus ulcer, force per unit area sore, pressure level ulcer

INTRODUCTION

Pressure ulcers are a blazon of injury that breaks down the skin and underlying tissue when an area of skin is placed under constant force per unit area for certain period causing tissue ischaemia, cessation of nutrition and oxygen supply to the tissues and eventually tissue necrosis. Constant pressure level resulting in 'distortion or deformation impairment' is probably the most accurate description of a pressure level ulcer.[1] There is a localised, acute ischaemic impairment to any tissue caused by the application of external force (either shear, compression or a combination of the ii).

"Pressure sores" is the term used commonly in the UK but again pressure injuries that are not open wounds (such as blisters and non-blanching erythema) are not true sores, but simply "pressure harm" and still belong to this family unit of pressure ulcers. "Pressure ulcers" is a term used widely in the USA and other countries and has been accustomed as the Europe-wide term by the European Force per unit area Ulcer Informational Panel (EPUAP). They are also known as 'bedsores', 'decubitus ulcers' although these names are now rarely used as it is recognised that the ulcers are not acquired by lying or being in bed. The areas that are particularly prone to pressure sores are those that embrace the bony areas such as occiput, trochanters, sacrum, malleoli and heel.

AETIOLOGY

There are many factors that tin can contribute to the development of pressure ulcers, only the final mutual pathway to ulceration is tissue ischaemia. The tissues are capable of sustaining pressure on the arterial side of effectually 30-32 mm hg for only a small duration of time. Just when pressure increases even slightly above this capillary filling force per unit area, it causes microcirculatory occlusion and this in turn initiates a downward spiral toward ischaemia, tissue death and ulceration.[2,3]

Pressure ulcers can develop when a large corporeality of pressure is applied to an expanse of pare over a curt flow. They tin can too occur when less pressure is applied over a longer period. The tissue baloney occurs either because the soft tissues are compressed and/or sheared betwixt the skeleton and a support, such as a bed or chair when the person is sitting or lying, or because something is pressing into the body, such as a shoe, a prosthesis, a surgical appliance or article of clothing rubberband. Blood vessels inside the distorted tissue are compressed, angulated or stretched out of their usual shape and claret is unable to pass through them.[iv] The tissues supplied by these blood vessels become ischaemic. Besides occluding the blood flow, tissue distortion also obstructs lymphatic flow, which in turn leads to accumulation of metabolic waste products, proteins and enzymes in the affected tissue. This too can compound the tissue harm.[5,6]

The majority of people affected with pressure sores are those having health conditions (mental or concrete) that encourage immobility, peculiarly those who are confined to bed or chair for prolonged periods of time. Several other wellness conditions that influence blood supply and capillary perfusion, such as type-2 diabetes, can make a person more vulnerable to pressure ulcers. Age is also a factor that the majority (approximately two-third) of pressure level ulcers occur in old historic period people (60-80 years of age).[7] To put it more simply, whatever individual, with or without a medical condition, who is incapable of avoiding prolonged periods of an uninterrupted compression, is at a take chances of pressure ulcers. Bulk of the patients affected with pressure level ulcers frequently develop it over a bony prominence. Bulk of the cases reportedly are afflicted over the area where pare covers bones such as sacral, ischial and trochanteric pressure level ulcers[8] and the lower extremities these are seen in the malleolar, heel, patellar and pretibial locations — account for approximately 25% of all pressure level sores.[nine] Table one describes the diverse straight and indirect causes of pressure level ulcers.

Table 1

Cause of force per unit area ulcer

Force per unit area

Equally the living tissues are non static, the way they are distorted change over fourth dimension. When constant force per unit area is maintained, soft tissues mould themselves to adjust the external shape. This is known as tissue creep.[10] This may reduce the external pressures but may also exaggerate internal distortions of soft tissues that further reduce the vascular supply of already compromised area due to vascular kinking. This distortion of internal conjugation of soft tissues are significantly loftier in paraplegic patients[11] and peculiarly in these susceptible patients, If ischaemia persists for 1-2 h, necrosis takes place and pressure level ulcers can occur inside i-2 h.[12] Due to prolonged and constant pressure, the chances of cloudburst of the skin with thinning of this protective barrier, making the skin more susceptible to modest pinch.

The peak of the available tissue cover over the bony prominence is not the only determining factor for developing pressure sores. Although the soles of the anxiety accept a thin covering of soft tissue, they accept a vasculature that is especially well-adapted to withstand considerable distorting forces. On the sacrum and ischial tuberosity on the other hand, although at that place is a relatively thick roofing of soft tissue and a wide supporting surface, the blood vessels are not adapted for weight-begetting, which means that even with fairly light compression, pressure ischaemia can develop rapidly. Hence, soles of feet do non develop pressure level sores even afterwards prolong weight bearing in ambulatory patients unless in that location are underlying causes making them insensate and more prone to pressure harm.

Shear

Shearing occludes flow more easily than compression (for example, it is easier to cut off catamenia in a h2o hose by bending than past pinching information technology), so shear can be considered to exist even more significant than pressure in the causation of pressure ulcers.[13] Areas of the body particularly susceptible to shearing include ischial tuberosities, heels, shoulder blades and elbows. These are areas on which the trunk is frequently supported when in a position (such every bit sitting or lying semi-recumbent) which allows forward slide. Superficial pressure ulcers caused by shearing tend to have uneven appearance.

Friction

Friction, along with pressure level and shear, is also oft cited as a cause of pressure ulcers.[14] Friction can cause pressure ulcers both indirectly and directly. In the indirect sense, friction is necessary to generate the shearing forces. Skin weakened past force per unit area ischaemia may be more susceptible to friction, and the two volition act together to hasten skin breakup.

Immobility

Immobility is not a principal cause of pressure ulcers but in the presence of additional factors it can initiate them. Patients with a profound immobility only intact sensation rarely develop force per unit area ulcers when they tin still communicate. Conversely, asleep patients, even with intact sensation, tin can develop pressure ulcer, every bit they cannot communicate regarding pain of increased pressure threshold. The pain of tissue ischaemia ensures that these patients oftentimes inquire for their position to exist changed. Patients with orthopaedic casts should be encouraged to report whatsoever discomfort and hurting in gild to prevent iatrogenic pressure ulcers.

Failure of reactive hyperaemia cycle

It is a known fact that tissue baloney causes ischaemia that in turn stimulates protective movements to relieve pressure and circulatory activity to restore normal blood flow in the affected areas. These protective movements are often reflexes as the person is unaware of making them. All the same, if these prompt actions prove bereft to relieve ischaemia, the fundamental nervous system is stimulated by constant signals of discomfort and pain to make sure that the pressure is relieved before whatsoever permanent damage occurs. Once the force per unit area is relieved, and the apportionment restored, local capillaries begin to dilate and increased blood menstruation takes identify, referred to every bit reactive hyperaemia. As a issue, a bright pink transitory patch appears on the pare, often called blanching erythema because it blanches on pressure level different the boring red non-blanching erythema that indicates tissue impairment[fifteen] [Figure 1a]. Reactive hyperaemia ensures a rapid restoration of oxygen and carbon dioxide remainder; it likewise flushes out waste products. Erythema subsides as presently as tissues are restored to their resting state.

(a-d) Various grading of force per unit area ulcer [Table 2]. (due east) A very severe trochanteric force per unit area ulcer where destruction is and so severe that the femoral caput dislocated and came out

Patients who fail to produce reactive hyperaemia cannot recover from the pressure induced ischaemic episodes resulting permanent damage to the tissues. Clinically, this presents equally white patches in pressure areas, which practice not change colour apace to the red of reactive hyperaemia, every bit they would in a healthy person. Rather, the white patches remain for many minutes before slowly returning directly to a more than normal peel color with little or no reactive hyperaemia being appreciable.

Combined pathology

When the reactive hyperaemia bicycle ceases to function adequately, a pressure ulcer will almost certainly develop unless preventive action is taken. There are iii predisposing factors for pressure ulcers:

• Loss of motility

• Failure of reactive hyperaemia

• Loss of sensation.

The creation of a pressure ulcer tin involve one or a combination of these factors. The diabetic patient with neuropathy of the anxiety is probable to take abnormal circulatory function in the involved surface area. On the other hand, the paralysed patient with a spinal injury loses sensation and the ability to move the afflicted areas and the ventilated patient doesn't able to feel or move due to anaesthesia while the peripheral apportionment may be compromised by the assistants of inotropes.

Indirect causes (associated factors)

1. Age-related physiological alterations can lower the threshold for pressure-induced injury in elderly patients. For instance, an increase in the fragility of blood vessels and connective tissue and a loss of fat and muscle leading to a reduced capacity to dissipate pressure.

2. Whatever condition that is associated with prolonged, impaired wound healing such as diabetes mellitus, which affects eleven% of adults over the age of lxx years.[16]

3. Oxygen is required for all stages of wound healing thus whatsoever condition that is associated with a low tissue oxygen tension is a major cause of pressure level ulcers. These include: Heart failure, atrial fibrillation, myocardial infarction, and chronic obstructive pulmonary illness.

4. Peripheral vascular disease, which affects 20% of older adults,[17] has a negative impact on wound healing.

5. Contractures and spasticity can contribute by repeatedly exposing tissues to pressure through flexion of a articulation.

6. Loss of sensations, the pain point that would normally crusade an immobile individual to change position is lost.

7. Paralysis and insensibility may produce atrophy of the skin leading to a thinning. This renders the skin more susceptible to the friction and shear forces a patient experiences when being moved.

8. Nutritional conditions such as malnutrition,[xviii] hypoproteinemia,[nineteen] and anaemia[xx] can cause pregnant delays in wound healing and hasten the formation of pressure ulcers.[21]

9. Moisture causes maceration, which predisposes the peel to injury. De-epithelialisation caused by trauma leads to transdermal water loss that creates maceration and adherence of the pare to clothing and any other supports in contact, resulting into further injury.[10]

10. Mental wellness conditions - people with severe mental wellness conditions such as schizophrenia or severe depression have an increased risk of pressure ulcers for a number of reasons:

    • Their diet tends to be poor, resulting in hypoproteinemia.

    • They often have other physical health conditions, such as diabetes or incontinence.

    • They may neglect their personal hygiene, making their skin more vulnerable to injury and infection that help an ulcer to form.

SEVERITY OF Pressure level ULCERS

Healthcare professionals use several grading systems to depict the severity of pressure level ulcers; most common is the EPUAP grading system. Pressure sores are categorised into four stages [Table 2] corresponding to the depth of damage.[22,23,24] It must even so be emphasised that when an eschar is present, accurate staging is not possible.

Table 2

Grades of pressure ulcer [Figure i]

Grade one

A grade one pressure ulcer is the most superficial type of ulcer. The affected surface area of pare appears discoloured and is red in white people, and purple or blueish in people with darker coloured skin [Effigy 1a]. 1 important thing to think is that Form 1 pressure ulcers do non plough white when pressure is placed on them. The pare remains intact, only it may hurt or crawling. It may also experience either warm and spongy or hard.

The characteristics are:

• Non-blanchable erythema of intact skin can be difficult to assess in patients with darkly pigmented skin.

• Oedema, induration.

• Warmth over a bony prominence.

• When an eschar is present, authentic staging is non possible.

Grade 2

In Grade two pressure ulcers, some of the outer surface of the pare (the epidermis) or the deeper layer of peel (the dermis) is damaged, leading to skin loss [Effigy 1b]. The ulcer looks like an open wound or a blister. The characteristics are:

• Partial thickness skin loss involving epidermis, dermis or both, for instance, abrasion, blister or shallow crater.

Course 3

In Course 3 pressure ulcers, peel loss occurs throughout the entire thickness of the peel. The underlying tissue is likewise damaged, just the underlying musculus and bone are not damaged. The ulcer appears as a deep cavity like wound [Effigy 1c]. The characteristics are:

• Full thickness skins involving harm to or necrosis of, subcutaneous tissue that may extend down to, but not through, underlying fascia.

• Presents clinically every bit a deep crater with or without undermining.

Course 4

A Grade 4 pressure level ulcer is the most severe blazon of pressure ulcer. The skin is severely damaged, and the surrounding tissue begins to dice (tissue necrosis). The underlying muscles, os or articulation may also exist damaged [Figure 1d], sometimes very severely [Figure 1e]. People with grade iv pressure ulcers have a loftier risk of developing a life-threatening infection. The characteristics are:

• Total thickness skin loss with extensive destruction, tissue necrosis, or damage to musculus, bone, or supporting structures, for example, tendon or joint capsule. Undermining and sinus tracts may exist associated with this stage of wound progression

• Similar to grading a fire with the addition of a stage 4 that is deeper than a phase three ulcer or iii^rd caste burn.

TREATMENT

Where possible, treatment of ulcers is planned with an aim to contrary the factors that accept originally caused the ulcer. Ulcers are often the event of combined pathology (similar diabetes, pressure, loss of sensation). Careful assessment is needed before planning for treatment. In full general the possible causative factor should be removed (pressure, shear, friction) and the associated general condition should be taken into the control (similar treatment of associated co-morbid illness and improvement in the nutrition). The affected area requires thorough cleaning and dressing. The limb must be elevated to improve the venous and lymphatic drainage, and the part must be given some rest from the weight begetting, pressure and friction. Still, since the full range of move and active physiotherapy of joints do meliorate circulation, fifty-fifty not-weight begetting physiotherapy is desirable.

Wound healing requires adequate protein, iron, Vitamin-C and zinc. Supplements may be prescribed if they are deficient in the diet.[25]

Remainder of the management of ulcer depends on many factors, and Tabular array iii illustrates an algorithm to help formulate a treatment plan. Various treatment options are available to care for pressure level ulcers, they include:

Tabular array 3

Algorithm for management of pressure level ulcers

Cleaning and debridement

Cleaning of the wound and meticulous peel care are the most essential part of the handling. The procedure involves removal of surface contagion and meticulous excision of all dead tissue. This is debridement. Besides the conventional surgical debridement other types of debridement similar mechanical debridement which includes use of repeated moisture to dry out dressings to removes slough,[26] enzymatic debridement using enzymes to liquefy dead tissue in the wound and remove them with the dressings,[27] and biological debridement or maggots and larval therapy[28,29] (in which the larvae swallow all the expressionless tissue and brand the wound make clean without harming the living tissues) also observe a mention in literature. Maggots also help to fight infection by releasing substances that impale bacteria and stimulate the healing process.[29] Abrupt surgical debridement using bract or scissors is the most commonly used and most effective method of debridement in able surgical easily. Dead tissue may be removed using mechanical means. Some mechanical debridement techniques include:

Cleansing and pressure irrigation

Where expressionless tissue is removed using high-pressure water jets. There is no bear witness bachelor to support any specific and effective cleansing techniques or solution, in detail.[30]

Ultrasound

Expressionless tissue is removed using depression-frequency energy waves.[31,32]

Light amplification by stimulated emission of radiation

Dead tissue is removed using focused beams of light.[33]

Basically, debridement is done for converting the chronic wound into an astute wound so that information technology tin progress through the normal stages of healing.

Wound dressings

The dressing used for various stages of wound healing is specialised for every stage; in fact at that place is a whole range of dressings available to assist with the different stages of wound healing. These are classified equally non-absorptive, absorbent, debriding, cocky-adhering and many others. It is vital to determine the most appropriate dressing as it ultimately depends on the site/type of ulcer, for hospital care or domicilic management, personal preference and toll to the patient.

Dressings are ordinarily occlusive, and then the ulcers heal meliorate in a moist environment. If the ulcer is clean and dry, occlusive dressings are usually inverse weekly, and more than frequent changes are avoided every bit dressing changes remove healthy cells forth with debris. Contaminated or weeping wounds may require more frequent dressing changes, sometimes every few hours. Heavily contaminated ulcers are treated with negative pressure wound therapy (NPWT).[34]

Specialised dressings and bandages are used to protect and speed upwardly the healing process of the pressure ulcers. These dressings include:

Hydrocolloid dressings

These contain a special gel that encourages the growth of new skin cells in the ulcer and keeps the nearby healthy area of skin dry.[35,36]

Alginate dressings

These are made from seaweed that contains sodium and calcium known to speed up the healing process. Dear-impregnated alginate dressings are known to reach total wound healing to pressure ulcers.[37]

Nano argent dressings

These apply the antibacterial property of silver to make clean the ulcer.[38,39]

Creams and ointments

To foreclose further tissue harm and aid speed up the healing process, topical preparations, such equally cream and ointments are frequently used.

Antibiotics

All pressure sores do not require antibiotics.[4] Antibiotics are usually just prescribed to treat an infected pressure ulcer and prevent the infection from spreading. If tissue infection exists, antibiotics are necessary to care for the infection, but endeavor must be made to debride the ulcer thoroughly and go out all viable tissues but, otherwise antibiotics solitary will non clean up the ulcer. Antibiotics are adjunct to surgical debridement and not an alternative to it.

Topical antibiotics should be avoided considering their use may increase antibiotic resistance and allergy. Antiseptic cream may as well exist applied topically to pressure ulcers to clear out any bacteria that may be present.

Biofilm

It has been noticed that the longstanding pressure level ulcers are oftentimes colonised past micro-organisms in a biofilm. The biofilm may be composed of bacteria, fungi or other organisms, which are embedded in and adherent to the underlying wound. The organisms are protected from the issue of conventional antibiotics; unnecessary prescription of antibiotics may, in fact, select more resistant organisms. We address the problem of biofilm by irresolute the pH of the wound — dressing with dilute ascetic acid if it is alkaline, which it usually is and curetting out all the underminings, cracks and crevices of the ulcer or by surgical debridement.

NEGATIVE PRESSURE WOUND THERAPY

This is an invaluable tool in the management of pressure sores and involves the application of sub-atmospheric pressure to a wound using a computerised unit of measurement to intermittently or continuously convey negative force per unit area to promote wound healing. NPWT, is constructive for deep, cavitating, infected and copiously discharging pressure ulcers, particularly with exposed bone.[40] With growing clinical feel[41] it can be said with certainty that information technology assists wound healing, and its benefits can be summarised thus:

• Assists granulation.

• Applies controlled, localised negative pressure level to help uniformly draw wounds airtight.

• Helps remove interstitial fluid allowing tissue decompression.

• Helps remove infectious materials and quantifies exudates loss.

• Provides a closed, moist wound healing environment

• Promotes flap and graft survival.

• Both hospital and domiciliary use.

• Reduces hospital/dressings/nursing cost (if we tin discharge the patient to habitation).

Newer research

There are many supportive therapies to promote healing of pressure ulcers. While some are in clinical use others are in the realm of inquiry. Many products are available to aid wound healing but should be prescribed simply under strict medical advice, as they still require further enquiry to determine their effectiveness. These include:

1. Growth factors and cytokines.[42]

2. Hyperbaric oxygen (HBO) to increase tissue oxygen tension.[43]

3. Skin graft substitutes (bioengineered pare).[44]

   1. Connective tissue matrix.

   2. Expanded epidermis.

   3. Epidermal stem cells.[45]

4. Os marrow (BM) or adipose tissue derived stem cell (ASC) therapy.[46]

Cytokines and growth factors

Chronic pressure ulcers display high levels of inflammation and disruption of the collagen matrix, forth with increased indications of apoptosis and decreased levels of growth factors and their receptors. These characteristics can exist used to comprehensively evaluate the aetiology and handling of these ulcers.[47] Contemporary authors hadl. compared the healing response of sequential topically applied cytokines to that of each cytokine alone and to a placebo in pressure ulcers, and evaluated the molecular and cellular responses.[48] Ulcers treated with cytokines had greater closure than those in placebo-treated patients. Patients treated with basic fibroblast growth cistron (bFGF) alone did the best, followed by the granulocyte-macrophage colony-stimulating factor (GM-CSF)/bFGF group. Patients treated with GM-CSF or bFGF had college levels of their respective cytokine after handling. Patients with the greatest amount of healing showed higher levels of platelet-derived growth factor on day 10 and transforming growth-factor beta-1 on solar day 36. Message for the bFGF factor was upregulated afterward treatment with exogenous bFGF, suggesting autoinduction of the cytokine. Both cytokines and growth factors may have a big role to play in the treatment of pressure ulcers in hereafter.

Hyperbaric oxygen therapy

Hyperbaric oxygen therapy (HBO) is being used for treatment of pressure sores. Peculiarly constructed devices equipped with controlled pressure sealings, and automatic relief valves are fitted in HBO chambers. A constant pressure of 22 mm Hg (1.03 atmospheres absolute) is maintained inside the chamber using pure oxygen at a flow-rate of 2-eight L/min with direct discharge to temper.[47] It has proven to exist very successful and prophylactic adjunctive treatment to daily wound dressing,[49] assistants of antibiotics and surgical debridement because:

1. Information technology increases oxygen transport to wound area stopping further tissue damage

2. It facilitates growth of new capillaries (angiogenesis) improving the microcirculation

3. It speeds upwards wound healing by reducing inflammation and swelling

4. It relieves pain

5. It reduces infection past eliminating bacteria direct and increasing capacity of white claret cell to fight infection

6. It improves microcirculation and emptying of toxins in the claret

7. It enhances the result of some antibiotics

8. Information technology stimulates the release of stem cells from the BM

9. It decreases blood viscosity and risk of thrombosis and stroke

10. It improves lymphatic circulation

11. It improves bone density and mineralisation and speeds upwards bone healing

12. It enhances peripheral nerve regeneration for improved sensitivity

13. Information technology prepares tissue and os for grafting before surgery

14. Information technology speeds up healing after surgery and improves chances of graft survival.

Skin substitutes (bio-engineered skin)

Cultured keratinocytes take been used for the treatment of diverse types of wounds for more than a decade.[50] Researches explain that in patients with fractional/total-thickness skin defects, the nigh effective therapy is cultured dermal substitute (CDS), while cultured epidermal substitute, and cultured skin substitute have likewise been used as biological wound dressings.[51] The artificial dermis induces angiogenesis and fibroplasia in deep, poorly vascularised tissue defects with fewer vascular invasions. Yet, it is difficult to apply collagen matrix to pressure level ulcers, considering they are usually accompanied by infection with discharge of excessive amounts of exudate or pus and generally exposed to external forces that prevent graft fixation.[52] The allogeneic CDS effectively treats intractable ulcers while BM cell implantation combined with allogeneic CDS is used in treating severely ischaemic ulcers.[53]

Bone marrow/adipogenic stem cells

"Jail cell therapy" tin be defined equally a set of strategies, which use live cells for therapeutic purposes. The aim of such therapy is to repair, supervene upon or restore the biological function of a damaged tissue or organ. Bone Marrow (BM)-mono nuclear cells (MNCs) can exist easily obtained in big numbers past aspiration without extensive manipulation or tillage before transplant and cells can be transplanted directly without in vitro expansion. Using the entire mononuclear fraction, no potentially beneficial cell type is omitted and MNCs from a patient's own BM promote angiogenesis[46] and this seems to exist a primal factor for optimal healing of pare wounds. Marrow stem cells (MSCs), which make up a minor proportion of BM-MNCs, secrete paracrine factors that could recruit macrophages and endothelial cells to enhance wound healing.[54] The repair functions of MSC are thought to involve the secretion of factors such as vascular endothelial growth factor[55] or FGF[56] which could help prevent apoptosis, promote angiogenesis, aid in matrix reorganisation, and increase the recruitment of circulating MSCs.[57] BM harvesting is rather invasive and painful. In 2001, Zuk et al.[57] identified and characterised adipose tissue derived stalk cellsASCs from lipoaspirates and fifty-fifty a department of whole fatty (biopsy). A very small percentage of the nucleated cells, which compose the BM, are actually MSCs, whereas the amount of ASCs is approximately 500-fold greater when isolated from an equivalent amount of adipose tissue.[58,59] Even though jail cell therapy is a relatively new tool, several studies prove these types of cells may be used safely, and they have demonstrated their efficacy in healing wounds and sores.

RECONSTRUCTIVE SURGERY

Sometimes the severe force per unit area ulcer (Grade Three or 4) fail to heal, in such cases, surgery is required to fill up the wound and forestall whatever further tissue damage. This is commonly done by cleaning the wound and closing it by bringing together the edges of the wound (straight closure), awarding of diverse type skin grafts or using local and regional flaps and gratuitous tissue transfer. It is prudent to remember and use the reconstructive ladder during planning of reconstructive surgery for pressure ulcers [Table 3].

There are many risks and complications that can occur after surgery, including infection, necrosis of flap, musculus weakness, blisters, recurrence of the pressure ulcers, septicaemia, infection of the bone (osteomyelitis), haemorrhage, abscesses, and deep vein thrombosis. Despite the risks, surgery is often a necessity and the only option to prevent limb and life-threatening complications.

The available reconstructive options are

Dissever thickness skin grafting

When the ulcer is superficial and vital tissues such equally os, vessels, nerves or tendons are not exposed, and the ulcer is not copiously discharging, skin grafting is the first pick for surgical treatment. The slimy layer over the surface of ulcer is sharply debrided to become a healthy vascular bed for skin grafting.

Local flaps

Variety of local flaps can be used to reconstruct the defect created by excision of force per unit area ulcers. Local transposition, rotation, limberg flap are the available options [Figures ​ ii and ​ 3]. Biceps femoris V-Y advancement (in paraplegics but) for ischial force per unit area sore[60,61] and perforator based V-Y advancement is another good options if the anatomy permits [Effigy 4].

Occipital pressure ulcer (a) managed by marginal debridement and coverage using Limberg's flap (b and c). A 2-calendar week post-operative motion picture of flap (d)

Sacral pressure ulcer (a) managed past marginal debridement and cover past Limberg's flap (b). 3-months follow-up (c) and two years follow-upward (d) shows that flap is stable without recurrence

Sacral pressure sore (a), debridement and cover by local perforator based Five-Y advancement flaps (b and c), 1-month post-operative (d), recurrence on the flap after eleven years (e) due to loss of family unit support and subsequent improper intendance. Some other patient with the same flap after xvi-year of follow-up (f) with a proper weight shifting and intendance showing stable coverage

Regional flaps

Sometimes the local or limberg flap cannot close the larger defects due to their size or location resulting in need for regional flaps. For Sacral pressure sores there are many flap options such every bit gluteus maximus myo-cutaneous flap, Sup gluteal avenue based rotation fascio-cutaneous flap, superior gluteal artery perforator flaps [Figure five], perforator based 5-Y advancement flap, lumbogluteal sensory flap. For lower extremity pressure level ulcer reconstruction; Islanded Medial planter flap [Figure 6], lateral or medial calcaneal flaps, Reverse sural flap [Figure 7], varieties of fascio-cutaneous flaps may provide a huge reconstructive option.

Class iv sacral force per unit area ulcer (a) managed past right-sided superior gluteal artery perforator flap (b), and 2-year follow-up (c)

Medial planter flap for heel sore: A long-standing deep trophic ulcer of heel (a). The islanded medial planter flap was transposed to the defect and the resultant donor site was covered past dissever thickness skin graft (b). The 1-calendar week (c) and iii-calendar month (d) post-operative pictures showing stable coverage. Patient allowed total weight bearing from half-dozen^th week along with silicone footpad protection

Reverse sural flap for posterior heel ulcer: A full thickness (Grade-4) acute pressure ulcer of posterior heel (a). The ulcer was sharply excised and covered with the contrary sural flap (b). The donor site and distal half of the island pedicle were covered with separate skin graft in this one phase repair. At 36-months post-operative follow-up (c)

Microvascular free flaps

Microvascular gratuitous flaps are usually reserved for some selected cases where the local and regional flap options are either not available or have failed, and the depth of the force per unit area ulcer demands acceptable book restoration for proper weight bearing. In fact, the latter reason is so vital that many large pressure level ulcers on weight bearing soles or on tip of amputation stumps are today being primarily treated with microvascular free tissue transfer.

Prevention: Mattresses and cushions

Protection is the all-time way to prevent ulcers. Patients who are at risk of developing pressure ulcers should accept the skin carefully inspected for any damage or redness (particularly over bony areas) twice daily. The skin should be kept clean and dry out. Any pressure causing damage to skin or tissue should be immediately eliminated. This tin can be washed with the assist of special mattresses, cushions and by many protective devices that can save the external force per unit area on vulnerable areas of body limbs. These peculiarly designed protective devices can be very helpful in patients who thought to be at chance of developing pressure ulcers, or who have pre-existing Grade ane or ii pressure ulcers. Classified past their static or dynamic nature, many advanced low tech and high tech back up surfaces and overlays are available for patients bound to lie on bed for long periods of time. Static surfaces (such as foam filled mattresses, air-filled mattresses, fluid-filled mattresses) do non require electrical ability, while dynamic surfaces (such as alternating air pressure level mattresses or pneumatic ripple beds) require electrical power for shifting and redistributing the pressure within the surface.[62] Other integrated electronic beds similar air fluidised beds (Clinitron or KinAir bed)[63] and electronic moving air mattresses crave high technology and heavy machinery to let air and ceramic sphere particles support the object on a stream mechanically; are often plush, noisy and not easily available. Due to lack of substantial evidences and researches, it is difficult to firmly conclude nigh relative effects of support surfaces.

We are using pneumatic ripple beds (alternating air pressure mattresses) that consist of several air-filled chambers that are separately inflated and deflated at an alternate bike of 5-10 min with the aid of a pneumatic pump. This helps in fugitive continuous contact of whatsoever body part with bed and prevents pressure sores. Owing to unique pressure redistributing properties, affordable cost, easy availability and effectiveness; pneumatic ripple beds are now most commonly used for pressure ulcer prevention worldwide. Many nursing homes and hospitals have turned to pneumatic beds from standard beds to make the overall stay of immobile or critically ill patients more comfortable and therefore, these beds form mainstay of pressure ulcer prevention at most places. For small areas like manus, ankle and foot, nosotros use h2o filled tied surgical hand gloves [Effigy 8a] as pressure relieving devices at infirmary setups and we advise the patients to use these at their home equally a very like shooting fish in a barrel to make, very low-cost pressure relieving device.

Pressure ulcers put a greater health risk to regular users of wheelchairs or those who are bound for prolonged sitting. The near often involved areas while seating are sacrum, coccyx, ischial tuberosities and greater trochanters. These sites tend to develop pressure ulcers more quickly every bit these are bony areas, and the fat that works as natural cushion is less in these areas. But pressure level ulcers are said to be largely preventable with the help of protective devices and proper management. At that place are custom designed gel and pneumatic wheelchair cushions which are easily available, and they aid to distribute the load more evenly and aid in preventing ulcer formation. Further, patients or their caretakers are taught to conduct force per unit area release movements or weight shifts on regular intervals to prevent force per unit area concentration and tissue impairment. Patients who sit for a long fourth dimension demand to employ protective cushioning/made air mattresses for protection of bony points and do periodic alter of postures and offloading of pressure points by side bending, forward bending and lifting off the chair with powerful upper body muscles. Other pressure level management tools include protective padding, pillows or cushions to separate body surfaces from difficult seats.

Many soft silicone elastomer based commercially bachelor devices may exist effectively used to avoid the pressure level from the affected or at risk area of limb. The commonly used are: Fractional or full silicone sole, silicone pads and digital caps, toes separators etc., [Figure 8].

Nutrition plays a very important role in whatever wound healing procedure so in force per unit area ulcers, compounding the effect of older historic period, diabetes and many other medical conditions hampering adequate intake of nutrition.[64] Poly peptide energy malnutrition is direct related to the occurrence equally well equally healing of the pressure ulcer. Though the serum albumin <3.5 mg/dl is traditionally considered as clinical indicator of malnutrition,[65] recent researches relates low level of serum albumin and pre-albumin to inflammatory procedure or to disease rather than malnutrition straight.[66,67] Rising level of serum albumin indicates improvement in clinical status and is desirable. Apart from biochemical data nutritional assessment should be done by other changes, such as weight changes, fluid intake, wound healing or progression. Pressure ulcer prevention and treatment guidelines should include guidelines that have nutritional recommendation too similar National Pressure level Ulcer Informational Panel/EPUAP guidelines.[68]

Footnotes

Source of Back up: Zilch

Conflict of Involvement: None declared.

REFERENCES

1. Gebhardt KS. Function one. Causes of pressure ulcers. Nurs Times. 2002;98:4. [PubMed] [Google Scholar]

2. Gefen A. Reswick and Rogers pressure-time curve for pressure level ulcer adventure. Part i. Nurs Stand up. 2009;23:64. 66, 68. [PubMed] [Google Scholar]

3. Gefen A. Reswick and Rogers pressure-fourth dimension bend for pressure ulcer risk. Part ii. Nurs Stand. 2009;23:twoscore–4. [PubMed] [Google Scholar]

4. Callam MJ, Ruckley CV, Harper DR, Dale JJ. Chronic ulceration of the leg: Extent of the problem and provision of care. Br Med J (Clin Res Ed) 1985;290:1855–6. [PMC free article] [PubMed] [Google Scholar]

5. Krouskop TA, Reddy NP, Spencer WA, Secor JW. Mechanisms of decubitus ulcer formation — An hypothesis. Med Hypotheses. 1978;4:37–nine. [PubMed] [Google Scholar]

6. Reddy NP, Patel Thousand. A mathematical model of menstruum through the terminal lymphatics. Med Eng Phys. 1995;17:134–xl. [PubMed] [Google Scholar]

vii. Leblebici B, Turhan N, Adam M, Akman MN. Clinical and epidemiologic evaluation of force per unit area ulcers in patients at a university infirmary in Turkey. J Wound Ostomy Continence Nurs. 2007;34:407–11. [PubMed] [Google Scholar]

8. Vasconez LO, Schneider WJ, Jurkiewicz MJ. Pressure sores. Curr Prob Surg. 1977;62:1–62. [PubMed] [Google Scholar]

nine. Cannon BC, Cannon JP. Management of pressure level ulcers. Am J Health Syst Pharm. 2004;61:1895–905. [PubMed] [Google Scholar]

10. Dodd KT, Gross DR. Three-dimensional tissue deformation in subcutaneous tissues overlying bony prominences may assistance to explain external load transfer to the interstitium. J Biomech. 1991;24:eleven–9. [PubMed] [Google Scholar]

eleven. Jay R. Force per unit area and shear: Their effects on support surface selection. Ostomy Wound Manage. 1995;41:36–8. 40. [PubMed] [Google Scholar]

12. Kuffler DP. Techniques for wound healing with a focus on force per unit area ulcers emptying. Open Circ Vasc J. 2010;3:72–84. [Google Scholar]

13. Goossens RH, Snijders CJ, Holscher TG, Heerens WC, Holman AE. Shear stress measured on beds and wheelchairs. Scand J Rehabil Med. 1997;29:131–half-dozen. [PubMed] [Google Scholar]

14. Allman RM. Pressure ulcer prevalence, incidence, risk factors, and impact. Clin Geriatr Med. 1997;13:421–36. [PubMed] [Google Scholar]

fifteen. Bliss MR. Hyperaemia. J Tissue Viability. 1998;8:iv–13. [PubMed] [Google Scholar]

16. Kaveeshwar SA, Cornwall J. The current state of diabetes mellitus in Republic of india. Australas Med J. 2014;7:45–8. [PMC free article] [PubMed] [Google Scholar]

17. Premalatha G, Shanthirani S, Deepa R, Markovitz J, Mohan Five. Prevalence and hazard factors of peripheral vascular affliction in a selected South Indian population: The Chennai Urban Population Written report. Diabetes Care. 2000;23:1295–300. [PubMed] [Google Scholar]

18. Langemo D, Anderson J, Hanson D, Hunter S, Thompson P, Posthauer ME. Nutritional considerations in wound care. Adv Pare Wound Care. 2006;19:297–eight. 300, 303. [PubMed] [Google Scholar]

19. Scivoletto G, Fuoco U, Morganti B, Cosentino E, Molinari M. Pressure sores and blood and serum dysmetabolism in spinal cord injury patients. Spinal String. 2004;42:473–6. [PubMed] [Google Scholar]

20. Keast DH, Fraser C. Treatment of chronic skin ulcers in individuals with anemia of chronic disease using recombinant human erythropoietin (EPO): A review of four cases. Ostomy Wound Manage. 2004;fifty:64–70. [PubMed] [Google Scholar]

21. Narsete TA, Orgel MG, Smith D. Pressure level sores. Am Fam Physician. 1983;28:135–9. [PubMed] [Google Scholar]

22. Ferrell BA, Josephson K, Norvid P, Alcorn H. Pressure ulcers amid patients admitted to habitation care. J Am Geriatr Soc. 2000;48:1042–seven. [PubMed] [Google Scholar]

23. Berlowitz DR, Brandeis GH, Anderson J, Brand HK. Predictors of pressure ulcer healing among long-term care residents. J Am Geriatr Soc. 1997;45:thirty–4. [PubMed] [Google Scholar]

24. Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM. Preventive foot care in people with diabetes. Diabetes Care. 1998;21:2161–77. [PubMed] [Google Scholar]

25. Desneves KJ, Todorovic BE, Cassar A, Crowe TC. Treatment with supplementary arginine, vitamin C and zinc in patients with pressure ulcers: A randomised controlled trial. Clin Nutr. 2005;24:979–87. [PubMed] [Google Scholar]

26. Mosher BA, Cuddigan J, Thomas DR, Boudreau DM. Outcomes of 4 methods of debridement using a determination analysis methodology. Adv Wound Care. 1999;12:81–eight. [PubMed] [Google Scholar]

27. Ramundo J, Grayness M. Enzymatic wound debridement. J Wound Ostomy Continence Nurs. 2008;35:273–eighty. [PubMed] [Google Scholar]

28. Mumcuoglu KY, Lipo M, Ioffe-Uspensky I, Miller J, Galun R. Maggot therapy for gangrene and osteomyelitis. Harefuah. 1997;132:323–five. 382. [PubMed] [Google Scholar]

29. Sherman RA. Maggot versus conservative debridement therapy for the treatment of pressure ulcers. Wound Repair Regen. 2002;10:208–14. [PubMed] [Google Scholar]

30. Moore ZE, Cowman S. Wound cleansing for force per unit area ulcers. Cochrane Database Syst Rev. 2005;3:CD004983. [PubMed] [Google Scholar]

31. Ramundo J, Greyness M. Is ultrasonic mist therapy effective for debriding chronic wounds? J Wound Ostomy Continence Nurs. 2008;35:579–83. [PubMed] [Google Scholar]

32. Kavros SJ, Liedl DA, Benefaction AJ, Miller JL, Hobbs JA, Andrews KL. Expedited wound healing with noncontact, low-frequency ultrasound therapy in chronic wounds: A retrospective analysis. Adv Skin Wound Intendance. 2008;21:416–23. [PubMed] [Google Scholar]

33. Graham JS, Schomacker KT, Glatter RD, Briscoe CM, Braue EH, Jr, Squibb KS. Efficacy of laser debridement with autologous split-thickness skin grafting in promoting improved healing of deep cutaneous sulfur mustard burns. Burns. 2002;28:719–30. [PubMed] [Google Scholar]

34. Webb Threescore. New techniques in wound management: Vacuum-assisted wound closure. J Am Acad Orthop Surg. 2002;10:303–xi. [PubMed] [Google Scholar]

35. Wasiak J, Cleland H, Campbell F. Dressings for superficial and fractional thickness burns. Cochrane Database Syst Rev. 2008;4:CD002106. [PubMed] [Google Scholar]

36. Fletcher J. The benefits of using hydrocolloids. Nurs Times. 2003;99:57. [PubMed] [Google Scholar]

37. Molan PC. The evidence supporting the utilize of honey as a wound dressing. Int J Low Extrem Wounds. 2006;v:forty–54. [PubMed] [Google Scholar]

38. Toy LW, Macera L. Evidence-based review of silver dressing employ on chronic wounds. J Am Acad Nurse Pract. 2011;23:183–92. [PubMed] [Google Scholar]

40. Lorée S, Dompmartin A, Penven Chiliad, Harel D, Leroy D. Is Vacuum Assisted Closure a valid technique for debriding chronic leg ulcers? J Wound Care. 2004;13:249–52. [PubMed] [Google Scholar]

41. Al Fadhli A, Alexander G, Kanjoor JR. Versatile utilise of vacuum-assisted healing in 50 patients. Indian J Plast Surg. 2009;42:161–eight. [PMC free commodity] [PubMed] [Google Scholar]

42. Payne WG, Ochs DE, Meltzer DD, Colina DP, Mannari RJ, Robson LE, et al. Long-term outcome study of growth cistron-treated pressure level ulcers. Am J Surg. 2001;181:81–6. [PubMed] [Google Scholar]

43. Marston WA. Dermagraft, a bioengineered man dermal equivalent for the treatment of chronic nonhealing diabetic foot ulcer. Skillful Rev Med Devices. 2004;1:21–31. [PubMed] [Google Scholar]

44. González Sarasúa J, Pérez López S, Álvarez Viejo M, Pérez Basterrechea M, Fernández Rodríguez A, Ferrero Gutiérrez A, et al. Treatment of pressure ulcers with autologous bone marrow nuclear cells in patients with spinal cord injury. J Spinal Cord Med. 2011;34:301–7. [PMC free article] [PubMed] [Google Scholar]

45. Kamata Y, Takahashi Y, Iwamoto Thou, Matsui Grand, Murakami Y, Muroi M, et al. Local implantation of autologous mononuclear cells from bone marrow and peripheral claret for handling of ischaemic digits in patients with connective tissue diseases. Rheumatology (Oxford) 2007;46:882–4. [PubMed] [Google Scholar]

46. Robson MC, Hill DP, Smith PD, Wang X, Meyer-Siegler One thousand, Ko F, et al. Sequential cytokine therapy for pressure ulcers: Clinical and mechanistic response. Ann Surg. 2000;231:600–11. [PMC free article] [PubMed] [Google Scholar]

47. Fischer BH. Topical hyperbaric oxygen handling of force per unit area sores and skin ulcers. Lancet. 1969;two:405–9. [PubMed] [Google Scholar]

48. Chen L, Tredget EE, Wu PY, Wu Y. Paracrine factors of mesenchymal stem cells recruit macrophages and endothelial lineage cells and enhance wound healing. PLoS 1. 2008;three:e1886. [PMC gratuitous article] [PubMed] [Google Scholar]

49. Bhutani S, Vishwanath G. Hyperbaric oxygen and wound healing. Indian J Plast Surg. 2012;45:316–24. [PMC costless article] [PubMed] [Google Scholar]

50. Schönfeld One thousand, Moll I, Maier K, Jung EG. Keratinocytes from cell culture for therapy of skin defects. Review and personal results. Hautarzt. 1993;44:281–nine. [PubMed] [Google Scholar]

51. Kuroyanagi Y, Yamada N, Yamashita R, Uchinuma E. Tissue-engineered production: Allogeneic cultured dermal substitute composed of spongy collagen with fibroblasts. Artif Organs. 2001;25:180–6. [PubMed] [Google Scholar]

52. Ichioka Southward, Ohura N, Sekiya N, Shibata One thousand, Nakatsuka T. Regenerative surgery for sacral pressure ulcers using collagen matrix substitute dermis (artificial dermis) Ann Plast Surg. 2003;51:383–nine. [PubMed] [Google Scholar]

53. Mizuno H, Miyamoto One thousand, Shimamoto Chiliad, Koike South, Hyakusoku H, Kuroyanagi Y. Therapeutic angiogenesis by autologous bone marrow cell implantation together with allogeneic cultured dermal substitute for intractable ulcers in critical limb ischaemia. J Plast Reconstr Aesthet Surg. 2010;63:1875–82. [PubMed] [Google Scholar]

54. Tang YL, Zhao Q, Zhang YC, Cheng L, Liu Yard, Shi J, et al. Autologous mesenchymal stem prison cell transplantation induce VEGF and neovascularization in ischemic myocardium. Regul Pept. 2004;117:3–10. [PubMed] [Google Scholar]

55. Ono I, Yamashita T, Hida T, Jin HY, Ito Y, Hamada H, et al. Local administration of hepatocyte growth factor gene enhances the regeneration of dermis in acute incisional wounds. J Surg Res. 2004;120:47–55. [PubMed] [Google Scholar]

56. Caplan AI, Dennis JE. Mesenchymal stem cells every bit trophic mediators. J Jail cell Biochem. 2006;98:1076–84. [PubMed] [Google Scholar]

57. Zuk PA, Zhu M, Ashjian P, De Ugarte DA, Huang JI, Mizuno H, et al. Human being adipose tissue is a source of multipotent stem cells. Mol Biol Cell. 2002;13:4279–95. [PMC free commodity] [PubMed] [Google Scholar]

58. Strioga Grand, Viswanathan S, Darinskas A, Slaby O, Michalek J. Same or not the same? Comparing of adipose tissue-derived versus bone marrow-derived mesenchymal stem and stromal cells. Stem Cells Dev. 2012;21:2724–52. [PubMed] [Google Scholar]

59. Jiang L, Dai Y, Cui F, Pan Y, Zhang H, Xiao J, et al. Expression of cytokines, growth factors and apoptosis-related signal molecules in chronic pressure ulcer wounds healing. Spinal Cord. 2014;52:145–51. [PubMed] [Google Scholar]

60. Hurteau JE, Bostwick J, Nahai F, Hester R, Jurkiewicz MJ. 5-Y advancement of hamstring musculocuataneous flap for coverage of ischial pressure sores. Plast Reconstr Surg. 1981;68:539–42. [PubMed] [Google Scholar]

61. Tobin GR, Sanders BP, Homo D, Weiner LJ. The biceps femoris myocutaneous advocacy flap: A useful modification for ischial pressure level ulcer reconstruction. Ann Plast Surg. 1981;vi:396–401. [PubMed] [Google Scholar]

62. International review. London: Wounds International; 2010. Pressure ulcer prevention: Pressure, shear, friction and microclimate in context. A consensus document. [Google Scholar]

63. Hargest TS, Artz CP. A new concept in patient care: The air-fluidized bed. AORN J. 1969;10:50–three. [PubMed] [Google Scholar]

64. Allman RM, Laprade CA, Noel LB, Walker JM, Moorer CA, Dear MR, et al. Pressure sores among hospitalized patients. Ann Intern Med. 1986;105:337–42. [PubMed] [Google Scholar]

65. Bergstrom N, Bennett MA, Carlson CE. Rockville, MD: AHCPR Publication -, Bureau for Health Care Policy and Research; 1994. Treatment of Force per unit area Ulcers. Clinical Practice Guideline, No.15. [Google Scholar]

66. Ferguson RP, O'Connor P, Crabtree B, Batchelor A, Mitchell J, Coppola D. Serum albumin and prealbumin as predictors of clinical outcomes of hospitalized elderly nursing home residents. J Am Geriatr Soc. 1993;41:545–ix. [PubMed] [Google Scholar]

67. Friedman FJ, Campbell AJ, Caradoc-Davies Th. Hypoalbuminemia in the elderly is due to affliction non malnutrition. Clin Exp Gerontol. 1985;7:191–203. [Google Scholar]

68. Washington DC: National Pressure Ulcer Advisory Panel; 2009. National Pressure level Ulcer Advisory Panel and European Pressure Ulcer Advisory Console. Prevention and Handling of Pressure level Ulcers: Clinical Do Guideline. [Google Scholar]

---

Manufactures from Indian Journal of Plastic Surgery : Official Publication of the Association of Plastic Surgeons of India are provided here courtesy of Thieme Medical Publishers

---

hartleyfromin.blogspot.com

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413488/