WOUND MANAGEMENT
Managing pressure sores Iain A Hunter John Davies
Abstract Management of pressure ulcers accounts for a significant proportion of healthcare resources. Pressure ulcers (or sores) are caused by pressureinduced necrosis of soft tissue and as such should be entirely preventable. Although pressure can be considered as the initiating insult, multiple factors also contribute to progression and development. Prevention and treatment of pressure ulcers requires a multidisciplinary approach. Recognition of at-risk patients and the introduction of preventative measures is the mainstay of prevention. Multiple adjuncts to pressure ulcer resolution such as pressure relief systems, nutritional supplementation, pharmaceutical debridement, antimicrobials, negative wound pressure therapy and surgery can be employed. Category I and II ulcers are treated conservatively with dressings and the removal of precipitating factors. Although the majority of pressure ulcers are managed by nursing staff without any medical intervention, deeper lesions with significant tissue necrosis and secondary infection may require surgical debridement and possibly reconstructive closure. The development of a pressure ulcer is often a reflection of significant comorbidity and treatment should be applied in the context of the patient’s overall likely clinical outcome and prognosis.
Figure 1 Multiple category III and IV pressure ulcers in a paraplegic patient.
previous studies have suggested that the overall annual cost burden for pressure ulcers to the NHS to be as high as £2.1 billion.4 Pressure ulcer development in hospital patients and in the community is now utilized as one of the baseline indicators of the quality of care provided, monitored nationally in the UK by external safety agencies. Patients most at risk tend to be those with pre-existing medical conditions. Surgical intervention in pressure ulcer care must be considered in the context of the patient’s overall situation and likely prognosis. In an end of life situation surgical intervention is unlikely to be successful or have any significant positive impact on a patient’s quality of life and should be avoided.
Keywords Debridement; nutrition; osteomyelitis; pressure sores; pressure ulcers; risk assessment; surgical flaps; wound healing
Introduction
Prevention
A pressure ulcer is localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear.1 These usually occur over weight bearing bony prominences such as the sacrum (most common), ischial tuberosities, greater trochanters and the calcaneum (Figure 1). Necrosis commences in the deeper layers of tissue over the bone. Evident skin changes are usually unrepresentative of the extent of necrosis as they are often only the apex of the underlying pathology. The European Pressure Ulcer Advisory Panel1 classifies pressure ulcer severity according to the degree of tissue loss (Table 1).
Pressure ulcers should be considered a preventable pathology. Recognition of ‘at-risk’ patients and the introduction of preventative measures is the mainstay of treatment.5 Increased pressure stresses are a particular problem in immobile and insensate patients. Extrinsic factors are those that have a detrimental effect on
European Pressure Ulcer Advisory Panel grading system for pressure ulcer classification Category I
Epidemiology In 2012, the prevalence of pressure ulcers in UK was estimated to be approximately 7%.2 Due to the chronicity of such wounds, their management represents a significant demand on healthcare resources. A 2012 UK study estimated the cost of treatment for a category IV pressure ulcer to be approximately £40,0003 and
Category II
Category III Iain A Hunter BMBS FRCS PhD is a Consultant Surgeon at Castle Hill Hospital and Hull Royal Infirmary, UK. Conflict of Interest: none declared.
Category IV
John Davies MBChB MRCS MD is a Higher Surgical Trainee at Castle Hill Hospital, Hull, UK. Conflict of Interest: none declared.
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Intact skin with non-blanchable erythema of a localized area usually over a bony prominence. Discoloration of the skin, warmth, oedema, hardness or pain may also be present. Darkly pigmented skin may not have visible blanching Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum e filled or sero-sanginous filled blister Full-thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. May include undermining and tunnelling Full-thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present. Often include undermining and tunneling
Table 1
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WOUND MANAGEMENT
based on rational theory by experts within the field. New UK NICE guidelines are currently under development. The multifactorial aetiology of pressure ulcers has evident implications for treatment. In order to promote healing, remediable causative factors must be attended to, while contributory metabolic and physiologic abnormalities should be optimized. Such an approach requires a multidisciplinary team of nursing staff, physicians, surgeons, physiotherapists, dieticians, wound care specialists and carers. Complex surgical interventions will be doomed to failure if underlying initiating and potentiating factors are not addressed.
Risk factors for the development of pressure ulcers Intrinsic factors
Extrinsic factors
Age >65 Male gender Caucasian Diabetes Metastatic carcinoma Malnutrition Anaemia Hypotension and use of inotropes Smoking
Urinary incontinence Faecal incontinence Uncontrolled fistula Perspiration Shear and friction forces
Pain Pressure ulcers can be exceedingly painful. Dressing changes can also induce severe discomfort. Good analgesia, especially preemptively before dressing changes, should be instituted as routine.
Table 2
the skin’s tolerance to pressure. These include moisture, shear and friction. Intrinsic factors result in impairment of the skin’s supporting structures, blood supply and lymphatic drainage.6e8 These combined risk factors are illustrated in Table 2. Risk assessment tools such as the Waterlow score7 (Figure 2) have been developed in order to facilitate risk stratification and management after initial assessment of skin integrity by nursing and medical staff.
Pressure relief Pressure is the main initiator of ulcer formation. The effects of pressure can be reduced by regular repositioning, effecting pressure relief for 5 minutes every 2 hours and using suitable beds or cushions. Other basic interventions include patient mobilization, the use of profiling beds to minimize the effect of shear and the use of visco-elastic foam mattresses and cushions. Specialized dynamic pressure-relieving beds/mattresses and overlays are employed in higher risk and immobile patients, supported by randomized controlled evidence.12 Low air loss beds reduce pressure by alternating the inflation of separate air compartments whereas air-fluidized bead beds effectively float the patient on an air-fluidized bed of glass beads in an attempt to eliminate shear, friction and pressure. They also have the
Management Current guidelines on pressure ulcer management (including NICE guidance) are based on limited randomized controlled evidence but mostly derived from non-controlled retrospective data sources6,9e11 However, the basic principles of management are
Copyright J Waterlow 2005. With kind permission.
Figure 2
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advantage of absorbing and filtering exudates reducing the adverse effects of moisture and incontinence. When the patient is out of bed, the use of appropriate cushions, seating and wheelchairs is important. General optimization Correction of physiological abnormalities such as anaemia and diabetes should improve tissue oxygenation and resistance to secondary infection. Local arterial and venous disease may also contribute to the recalcitrant nature of ulcers, especially in the case of heel sores. Procedures to improve arterial inflow should be considered when peripheral vascular disease is a contributing factor.
of moisture or sheer damage and foam dressings can provide extra protection for at-risk areas, although they do not redistribute pressure. Alginates absorb up to 20 times their weight in water and are useful in wounds and cavities with a high exudate. Conversely, hydrogels are mostly composed of water and are of more use in dry, shallow minimally exuding ulcers. Hydrocolloids effectively seal wounds and retain moisture, promoting healing and autolysis.9 Negative wound pressure therapy can be used as an adjunct to the healing of category III and IV ulcers following adequate debridement. Their employment is designed to accelerate the formation of granulation tissue, control exudate and shorten the time required to prepare wounds for surgical closure.11
Nutrition Many patients with pressure ulcers are in a state of chronic malnutrition. Failure to correct nutritional deficits will have an adverse effect on healing. All patients with pressure ulcers should be formally assessed by a dietician and supplementation introduced where appropriate. Vitamin C supplementation may have a positive effect on ulcer healing.11
Minimizing contamination Continued exposure to moisture and faecal material can both contribute to the initiation and potentiation of ulcer formation. If contamination is a problem then urinary diversion can usually be achieved with a convene or urinary catheterization. Faecal contamination may be avoided with the use of transanal faecal diversion catheters or rarely a diverting colostomy.
Dressings Dressings should maintain a moist wound environment to encourage healing while providing adequate control of wound exudate to protect the surrounding skin. As well as maintaining a moist environment, dressings can also facilitate autolytic debridement. When indicated semi-transparent films can be used on category I lesions (unbroken skin). Semi-permeable transparent films are generally used on category I ulcers to protect areas at risk
Infection Distant infections should be treated aggressively in at-risk patients and patients with existing pressure ulcers to prevent secondary infection of compromised tissues. Debridement of necrotic tissue is the primary step in treating infected category III and IV pressure ulcers.13 This removes infected material and provides samples and swabs for culture. Failure of progression after debridement is often an indication of persistent deep
Figure 3 Closure of a sacral category IV pressure ulcer using a gluteal rotation flap. Cavity extent is marked with methylene blue prior to thorough debridement including bone. The defect is then closed with a musculocutaneous gluteal rotation flap.
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Figure 4 Closure of an ischial pressure ulcer with a tensor fascia lata (TFL) fasciocutaneous flap. The pressure ulcer is debrided prior to raising the TFL flap which is then rotated into place. The resulting defect is closed with a split skin graft.
infection or a failure to adequately offload the pressure damaged area. Ulcers with 106 CFU/g of tissue or any level of beta haemolytic streptococci following debridement should be treated with topical antimicrobials. Although systemic antibiotics were historically thought to be ineffective at reducing bacterial levels in granulating tissue, more recent research indicates that adequate tissue levels may be reached with intravenous antibiotics.14
Surgical debridement has the advantage of speed combined with a more accurate definition of cavity extension and the ability to sample deep tissue for microbiological culture, but may result in the exposure of bone or tendon. For eventual closure to be successful debridement must be complete and may necessitate bursectomy, excision of infected bone in cases of osteomyelitis and a radical excision of all non-viable, fibrous and infected tissues. Removal of bony prominences can also remove the initiating pressure point but may also shift pressure elsewhere. Undermined areas must be exposed to ensure adequate debridement. This can be aided by application of a methylene blue soaked gauze at the start of the operation to mark the cavity walls and extensions. Surgical closure should not be attempted in the presence of beta haemolytic streptococci or bacterial counts of >105 CFU/g of tissue. Resection of osteomyelitic bone mandates a 3 week course of appropriate antibiotics as guided by culture and sensitivity results.13 Significant blood loss should be anticipated during such debridement procedures, especially if bone is being removed. Adequate attention to haemostasis is vital. All patients should be blood typed in preparation for potential transfusion.
Surgical intervention The role of surgery in pressure ulcer treatment can be broadly divided into debridement and closure. Debridement Debridement aims to remove all necrotic, infected and fibrous scar tissue as a means of treating infection and to prepare the wound bed for surgical closure. Many non-surgical methods of debridement are available (including conservative sharp, mechanical, autolytic or larval debridement) and at the present time there is no strong evidence to favour one method over another, and methods employed should be tailored to the location of the pressure ulcer and the patient’s requirements.15
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2 CQUIN. Delivering the NHS safety thermometer. http://harmfreecare. org/wp-content/uploads/2012/06/NHS-ST-CQUIN-2012.pdf (accessed Jan 2014). 3 Dealey C, Posnett J, Walker A. The cost of pressure ulcers in the United Kingdom. J Wound Care 2012; 6: 261e6. 4 Bennett G, Dealey C, Posnett J. The cost of pressure ulcers in the UK. Age Ageing 2004; 33: 230e5. 5 Chou R, Dana T, Bougatsos C, et al. Pressure ulcer risk assessment and prevention e a systematic comparative effectiveness review. Ann Intern Med 2013; 159: 28e38. 6 NICE. Pressure ulcers-the management of pressure ulcers in primary and secondary care. http://www.nice.org.uk/nicemedia/live/10972/ 57623/57623.pdf (accessed Jan 2014). 7 Waterlow J. Pressure ulcer prevention manual. 2005 (accessed Jan 2014), www.judy-waterlow.co.uk. 8 Cox J. Pressure ulcer development and vasopressor agents in adult critical care patients: a literature review. Ostomy Wound Manage 2013; 59: 50e60. 9 Langemo DK, Black J, et al. Pressure ulcers in individuals receiving palliative care: a national pressure ulcer advisory panel white paper. Adv Skin Wound Care 2010; 23: 59e72. 10 Beth Smith MO, Totten A, Hickam DH, et al. Pressure ulcer treatment strategies e a systematic comparative effectiveness review. Ann Intern Med 2013; 159: 39e50. 11 Levine SM, Sinno S, Levine JP, et al. Current thoughts for the prevention and treatment of pressure ulcers e using the evidence to determine fact or fiction. Ann Surg 2013; 257: 603e8. 12 McInnes E, Jammali-Blasi A, Bell-Syer SE, et al. Support surfaces for pressure ulcer prevention. Cochrane Database Syst Rev 2011; http:// dx.doi.org/10.1002/14651858.CD001735.pub4. Issue 4. Art. No.: CD001735. 13 The wound healing society. Chronic wound care guidelines. http:// www.woundheal.org/assets/documents/final%20pocket%20guide% 20treatment.pdf (accessed Jan 2014). €ttcher S, Abel R, et al. Tissue and serum concen14 von Baum H, Bo trations of levofloxacin in orthopaedic patients. Int J Antimicrob Agents 2001; 18: 335e40. 15 Diaz S, Li X, Rodrı´guez L, et al. Update in the surgical management of decubitus ulcers. Anaplastology 2013; 2: 3, http://dx.doi.org/10. 4172/2161-1173.1000113 (accessed Jan 2014).
Different types of flaps used to provide tissue cover in pressure ulcers Ischial
Sacral
Trochanteric
Posterior thigh fasciocutaneous (FC) flap Hamstring VeY advancement Tensor fascia lata (TFL) (can be used for simultaneous trochanteric and ischial coverage) Gracilis Gluteus maximus Pedicled VRAM (recurrent sores) Buttock rotation flap Gluteus maximus muscle or musculocutaneous flaps Transverse or Lumbosacral flaps TFL Lateral thigh FC flap Rectus femoris
Table 3
Surgical closure Surgical closure should only be considered following adequate preparation of the wound bed as detailed above. The final method of closure should obliterate all dead space and achieve a tension-free closure using well-vascularized tissue in accordance with basic surgical principles. Suture lines should be kept away from future pressure points. Although the majority of large category III and IV pressure ulcers are managed without surgical intervention, due to the patients underlying medical condition, a proportion may require closure with a local or regional musculocutaneous (Figure 3) or fasciocutaneous (Figure 4) flap and the choice of which type is utilized is made on a case by case basis.10,15 Although free flaps can be considered, these are not a first-line treatment. The donor defect can be closed with a split skin graft but can often be closed directly in thin patients. If refractory spasticity is contributing to pressure ulcer development or threatening the eventual placement of reconstructive grafts, consideration should be given to tenotomy. Amputations, such as hind quarter amputations may be required in cases of resistant osteomyelitis or flap failure. The array of available flap reconstructions is beyond the scope of this article, however, examples of flap options are detailed in Table 3. A
Acknowledgments
REFERENCES 1 European pressure ulcer advisory panel and national pressure ulcer advisory panel. Prevention and treatment of pressure ulcers: quick reference guide. http://www.epuap.org/guidelines/Final_Quick_ Treatment.pdf (accessed Jan 2014).
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The operative images were kindly provided by Mr Nick Hart, Consultant Plastic Surgeon, Castle Hill Hospital.
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