Management of pressure ulcer

Pressure ulcers are areas of local tissue trauma, usually developing where soft tissues are compressed between bony prominences and any external surface for prolonged time periods. Thus, they are most commonly found over bony prominences subject to external pressure. A pressure ulcer is a sign of local tissue necrosis: The skin may be involved or there may be major muscle and subcutaneous fat tissue destruction underneath intact skin.

 Incidence  of  Pressure  Ulcers

The exact incidence and prevalence of pressure ulcers remain unclear. Data from the National Pressure Ulcer Advisory Panel (NPUAP) in the United States  indicate that the incidence varies widely, from 0.4 to 38 % in acute care, 2.2–23.9 % in long-term care, and 0–17 % in home care. Prevalence rates show the same variability: 10–18 % in acute care, 2.3–28 % in long-term care, and 0–29 % in home care. Therefore, the incidence of pressure ulcers is high, especially among certain high-risk groups of patients. These groups include elderly patients admitted to a hospital for femoral fractures (66 %) and critical care patients (33 %); in a study of quadriplegic patients, the prevalence was 60 % . In spinal cord injury (SCI) patients, the pressure ulcer prevalence rate ranged from 8 % in the first year following the onset of spinal cord injury to 33 % for community resident individuals with SCI.


Cost  of  Pressure  Ulcer Management

The cost of managing pressure ulcers has increased dramatically in hospitals and in the community due to the overall increase in health-care costs worldwide. The impact of pressure ulcers is significant in terms of both financial and nonmonetary costs. Its reported that the cost to heal complex pressure ulcers was $100,000; less serious pressure ulcers cost $20,000 to $30,000 to heal (National Pressure Ulcer Advisory Panel 1989, U.S. Department of Health and Human Services 1990).


    Medico-Legal  Implications

The medico-legal implications of pressure ulcer development are an urgent issue all worldwide. Pressure ulcers are viewed as a quality indicator of care. Hence, the development of pressure ulcers can constitute a failure in the healthcare system. In the United States, federal health agencies regard pressure ulcers as a surrogate for how well the healthcare team is functioning in monitoring the quality of care for the patient. The increasing recognition of pressure ulcer development as a marker for quality of care has led to a greater number of pressure ulcer litigations against clinicians and their employers. The public has been made aware through the media like television and Internet that pressure ulcers can be prevented and treated effectively. The development of pressure ulcers is considered to be the result of negligence by the healthcare provider. Pressure ulcers can cause sepsis and even death in certain groups of patients, in addition to causing changes in patients’ quality of life. A number of lawsuits have been brought against hospitals, nursing homes, physicians, and even plastic surgeons. If greater attention were paid to preventing development of pressure ulcers and to enforcing some basic rules of prevention, there would be fewer of these litigations


  Advances  in  Prevention

In the twenty-first century, pressure ulcers are seen as a preventable disease, and thus, prevention is a priority and a necessity in their management. This can be accomplished through continuing education for all healthcare staff on detecting the early signs of pressure ulcers and assessing patients for the risk of pressure ulcer development. In hospitals, nursing homes, convalescent homes, and patients’ homes, measures for prevention include: the patient’s repositioning and turning schedule; preventing and treating excessive body moisture and fecal and urinary incontinence; using advanced equipment, such as special beds, mattresses, and wheelchair cushions; attention towards the patient’s nutritional intake; and patient and family education. All of these measures are today’s standard of care and have become the foundation for pressure ulcer prevention.

 Complications and Life- Threatening Risks of Pressure Ulcers

Fifty years ago, pressure ulcers were among the major diseases predisposing in shortening the life expectancy in the spinal cord injury patient. In the twenty-first century, advances in antibiotics, local wound care, and early surgical  interventions have tremendously reduced the morbidity and mortality rates and prolonged life expectancy in spinal cord injury patients. However, the medical literature documents many complications that can occur in patients with chronic pressure ulcers, including acute sepsis, amyloidosis, heterotopic ossification, septic joint,  perineal and urethral fistula , squamous cell carcinoma changes in pressure ulcers, and the most common complication, acute or chronic osteomyelitis of the bone underlying the ulcer. To avoid and prevent these complications, prevention and early detection of pressure ulcers in spinal cord patients are important for the patients’ healthcare and to provide quality of life and longer life expectancy. This responsibility falls on all healthcare providers.



It has been observed that the application of constant pressure of 70 mmHg for more than 2 h produced irreversible tissue damage.  Minimal tissue damage was observed when the pressure exceeded 240 mmHg, providing there was intermittent pressure relief.

Pressure ulcers are the result of mechanical injury to the skin and underlying tissues. Traditionally, pressure (stress), shear, and friction were considered the primary external factors involved in pressure ulcer development. More recently, deformation (strain), heat, reperfusion injury, and impaired lymphatic function have been considered as additional primary forces involved in pressure damage.

Four hypotheses for the pathophysiology behind pressure ulcer development include

  1. Ischemia caused by capillary occlusion
  2. Impairment in lymphatic flow with increase in metabolic waste products.
  3. Reperfusion injury (damage that occurs because of the inflammatory response that occurs when blood flow resumes to the ischemic tissues).
  4. Deformation of tissue cells.

Shear forces are an etiologic factor in development of pressure, and ulcers are caused by movement of boney prominence against the subcutaneous tissues. This occurs when the position of the patient, for example, in bed, is shifted in a way that the skin remains stationary in relation to the support of the body and, as a result of the movement, the subepidermal vessels are bent at a right angle. Shear alone does not cause tissue necrosis; however, it is a predisposing factor in causing pressure ulcers. Shear forces are seen more frequently in clinical practice when a patient loses weight and tissue sliding can occur over the boney prominences. Friction forces relate to rubbing of the skin against linen or clothing, or even when lifting a patient on a sling. Most abrasion injuries are caused by friction, although friction does not lead to all pressure ulcers; it can damage the epidermis and make the skin susceptible to pressure ulcers.

    Significant Factors in Development of Pressure Ulcers

The most important factor in the development of pressure ulcers is skin moisture. The skin is the largest organ of the body and one of its important functions is to protect the body. There are many factors that can alter and decrease the resistance of the skin. Moisture is a contributing factor in the etiology of pressure ulcers because it macerates the epidermis. The epidermis becomes easily eroded and tissue necrosis can occur. Moisture is a condition that can be seen clinically with incontinence of urine and stool, excessive sweating, excessive vaginal discharge, wound discharge, and sometimes wound dressings that can cause. skin irritation. Uncontrolled skin moisture by itself is considered a risk factor in developing pressure ulcers in certain patients.  Because the skin is an organ, poor nutrition has shown to be a factor in its breakdown. In addition, loss of fat and muscle increases the pressure of the boney prominences. In aging skin, changes take place in collagen synthesis that result in the tissue of the body having lower mechanical strength and increased stiffness . There are also changes in the barrier properties in aging skin, reduced immunity, slower wound healing, and diminished pain reception. The patient’s physique also plays a role; if pressure is distributed evenly, the patient is less likely to develop pressure ulcers. A thin patient with little subcutaneous fat and poor muscle bulk will be inclined to develop pressure ulcers over the boney prominences. An extremely obese individual has much greater weight but better padding to distribute the weight; however, these patients have poor circulation and are more liable to be affected by shear and friction.

  Site of  Pressure  Ulcer Development

A study by the model system of spinal cord injury patient care in the United States  found that during early treatment in the acute phase of the spinal cord injury at  trauma centers, for stabilization of the spinal shock and the spine, patients were kept in the supine position in bed for numerous medical reasons. The findings for the common ulcer site areas were occipital = 2.6 %, scapular = 4.3 %, spinous process = 1.3 %, iliac crest = 1.8 %, sacrum = 37.4 %, trochanteric = 3.8 %, ischium = 9.2 %, elbow = 2.0 %, knee = 1.5 %, and malleolar = 3 %. The anatomical distribution of the ulcer sites somewhat changed when patients were followed in the first year post injury, when the common sites were the sacrum = 20 %, ischium = 18.3 %, trochanteric = 12.4 %, heel = 16.6 %, elbow = 2.6 %, and malleolar 8.7 %. The reasons for the ulcer distribution at this phase of a patient’s life were sitting in a wheelchair and resuming normal life without practicing pressure relief as instructed in rehabilitation post injury. Laying down in bed in the supine position or lateral position without a pressure relief mattress can predispose to ulcer development in the sacrococcygeal area and trochanteric area.


pressure ulcer sites


Early Pressure-Induced Tissue Damage

The immediate response of the tissues to a sustained period of pressure are related to the inflammatory response and are manifest as elevated temperature, subepidermal edema, and erythema. Skin temperature and subepidermal edema are reflections of the nonvisible spectrum of pressure-induced tissue damage. Elevated skin surface temperature, as compared with that of healthy tissues can be evaluated by palpation, skin thermistors, or thermography. Subepidermal edema can be assessed using ultrasound and surface electrical capacitance methods. If pressure is not relieved, pressure-induced tissue damage progresses to the visible spectrum. The first visible indicator of pressure damage is blanchable erythema. Erythema presents as redness of a flat, nonraised area of the skin larger than 1 cm. The discoloration varies in intensity from pink to bright red in persons with light skin tones. In persons with dark skin tones, the discoloration appears as a deeper than normal pigmentation or a purple or blue-gray hue to the skin.

Stage I Pressure Ulcers

If pressure is not relieved, the damage progresses to stage I category, with additional temperature, coloration, and texture changes seen. As the tissues become more disturbed, the temperature may decrease, signaling underlying tissue damage. Nonblanchable erythema develops, in which the color of the skin becomes more intense, varying from dark red to purple or cyanotic in both light- and dark-skinned patient In addition, skin texture changes. The skin may feel hard and indurated, and observation may reveal heightened skin features or an orange-peel appearance. This stage of tissue destruction is also reversible, although tissues may take 1 to 3 weeks to return to normal. Additionally, the patient may report pain at the site.

Stage II Pressure Ulcers

Stage II category pressure ulcers are superficial ulcers most often the result of the mechanical force of friction on the epidermis. Stage II pressure ulcers involve damage to the epidermis and part of the dermis, they are partial-thickness lesions. The ulcer is superficial, with indistinct margins and a red pink, shiny base . It is usually surrounded by blanchable or nonblanchable erythema. If not dealt with aggressively, stage II ulcers can progress to involve deeper tissues. Still, if properly treated, the situation may resolve in 2 to 4 weeks.


Stage III and IV Pressure Ulcers

Whereas superficial or partial-thickness ulcers such as stage II ulcers begin at the skin surface and progress to deeper layers, deep, full-thickness ulcers do not originate at the skin surface; they begin at the bony prominence–soft tissue interface at the muscle tissue layer and spread to involve the skin structures.The chronic deep ulcer usually has a dusky red wound base and does not bleed easily.It is surrounded by blanchable or nonblanchable erythema or deepening of normal skin tone, induration, possible edema, change in temperature compared to healthy tissues, and possible mottling with or without hemosiderin staining. Undermining and tunneling may be present with a large necrotic cavity.

Unstageable Pressure Ulcers

Pressure ulcers that present covered with devitalized necrotic tissue are classifi ed as unstageable because the depth of tissue destruction is not visible. The necrotic tissue may be slough or eschar. Eschar is the formation of an acellular dehydrated compressed area of necrosis, usually surrounded by an outer rind of blanchable or nonblanchable erythema  Eschar formation indicates a full-thickness loss of skin and may be the result of both pressure and shear forces. Slough is devitalized tissue with a higher water content than eschar. Slough appears as yellow or tan material that is thickly adherent to wound bed tissues . Slough also indicates full-thickness tissue damage.

Suspected Deep Tissue Injury

Pressure-induced skin damage that manifests as purple, blue, or black areas of intact skin may be suspected DTI areas. These lesions commonly occur on the sacrum and heels and signal more severe tissue damage below the skin surface . DTI lesions reflect tissue damage at the bony tissue interface and may progress rapidly to large tissue defects.

pressure ulcer grades

 Comprehensive  Clinical Wound Evaluation

With pressure ulcers, like any other wounds or illnesses, a complete medical history prior to examination of the wound is important to understanding the nature of the wound. The pressure ulcer is always secondary to the primary illness or trauma, and consequently a management plan is developed according to the information obtained from the patient or the caregiver. Therefore, examining a wound without a comprehensive medical history is considered incomplete diagnosis or management. History of spinal cord injury, level of injury, and whether it’s a complete or incomplete injury should be ascertained to determine the level of sensation in the patient, the level of muscle function, and whether the patient is ambulatory, walks with aids, or is wheelchair confined. Other primary diagnosis, for example, spina bifida, stroke, or neurological disease, will help determine how to treat the wound, either by conservative or surgical treatment. The medical history should include a complete history of illnesses and the medications the patient is taking. Illnesses such as heart disease, lung disease, diabetes, and vascular disease  affect healing and the ability of the patient to tolerate general anesthesia if surgery is indicated. History of bowel and urinary control is important knowledge for the postoperative management of the patient. History of the existing of muscle spasms should be investigated and controlled to avoid postoperative morbidities. Psychosocial evaluation is important for the success of the surgery, as the compliance of patient is important in the postoperative period.

Assessment of the Individual with a Pressure Ulcer

  1. Complete an initial assessment of the individual with a pressure ulcer, to include: The individual’s and family’s goals of care. If the individual is unable to participate, consult with family and/or significant others.
  • A complete health/medical and social history.
  • A focused physical examination that includes:
  • Factors that may affect healing (e.g., impaired perfusion,impaired sensation, systemic infection)
  • Vascular assessment in the case of extremity ulcers (e.g.,physical examination, history of claudication, and ankle brachial index or toe pressure)
  • Laboratory tests and x-rays as needed
  • Nutritional assessment
  • Pain related to pressure ulcers
  • Risk for developing additional pressure ulcers
  • Psychological health, behavior and cognition.
  • Social and financial support systems.
  • Functional capacity, particularly in regard to positioning, posture,and the need for assistive equipment and personnel.
  • The employment of pressure-relieving maneuvers.
  • Adherence to pressure-relieving maneuvers.
  • Integrity of seating and bed surfaces (wear and tear).
  • The individual’s/family member’s knowledge and belief about developing and healing pressure ulcers.
  • Reassess the individual if the ulcer does not show signs of healing as expected despite adequate local wound care, pressure redistribution, and nutrition.
  • Expect some signs of healing in most individuals within 2 weeks.
  • Adjust expectations in the presence of multiple factors (particularly unmodifiable factors) that impair wound healing (e.g., persistent undernutrition, poor perfusion, and co-morbidities known to impair wound healing).
  • Teach the individual and his/her family about the normal healing process and keep them informed about progress (or lack of progress) toward healing, including signs and symptoms that should be brought to the professional’s attention.

Pressure Ulcer Assessment

  1. Assess the pressure ulcer initially and re-assess it at least weekly, documenting findings.
  2. With each dressing change, observe the pressure ulcer for developments that may indicate the need for a change in treatment (e.g., wound improvement, wound deterioration, more or less exudate, signs of infection, or other complications).
  3. Assess and accurately document physical characteristics such as location, Category/Stage, size, tissue type(s), wound bed and periwound condition, wound edges, sinus tracts, undermining, tunneling, exudate, necrotic tissue, odor, presence/absence of granulation tissue, and epithelialization.
  4. Use a validated tool such as the Pressure Ulcer Scale for Healing (PUSH©) Tool or the Bates-Jensen Wound Assessment Tool (BWAT), formerly known as the Pressure Sore Status Tool (PSST).

Role of Nutrition in Pressure Ulcer Healing

  1. Screen and assess nutritional status for each individual with a pressure ulcer at admission and with each condition change — and/or when progress toward pressure ulcer closure is not observed.
  2. Provide 30-35 kcalories/kg body weight for individuals under stress with a pressure ulcer. Adjust formula based on weight loss, weight gain, or level of obesity. Individuals who are underweight or who have had significant unintentional weight loss may need additional kcalories to cease weight loss and/or regain lost weight.
  3. Offer 1.25 to 1.5 grams protein/kg body weight daily for an individual with a pressure ulcer when compatible with goals of care, and reassess as condition changes
  4. Provide additional fluid for individuals with dehydration, elevated temperature, vomiting, profuse sweating, diarrhea, or heavily draining wounds.
  5. Offer vitamin and mineral supplements when dietary intake is poor or deficiencies are confirmed or suspected

Manage General Pain

  1. Organize care delivery to ensure that it is coordinated with pain medication administration and that minimal interruptions follow. Set priorities for treatment.
  2. Encourage individuals to request a ―time out‖ during any procedure that causes pain.
  3. Reduce pressure ulcer pain by keeping the wound bed covered and moist, and using a non-adherent dressing.
  4. Use dressings less likely to cause pain and/or those likely to require less frequent dressing changes (e.g., hydrocolloids, hydrogels, alginates, polymeric membrane foams, foam, soft silicone dressingsNote: Gauze dressings are more likely to cause pain.
  5. For an individual with pain from a pressure ulcer, music, meditation, distraction, conversations, and guided imagery are sometimes beneficial.
  6. Administer pain medication regularly, in the appropriate dose, to control chronic pain following the World Health Organization Dosing Ladder.
  7. Use adequate pain-control measures, including additional dosing at times of wound manipulation, wound cleansing, dressing change, debridement, etc.
  8. Manage persistent pressure ulcer pain (neuropathic) with a local anesthetic or an adjuvant (antidepressant or antiepileptic), as well as with transcutaneous nerve stimulation, warm applications, or tricyclic antidepressants.

Support Surfaces for Treatment of Pressure Ulcers

Support  surfaces  alone  neither  prevent  nor  heal  pressure  ulcers.  They  are  to  be used as part of a  total program of prevention and  treatment. When pressure ulcers deteriorate  or fail  to heal,  the professional should consider  replacing  the existing support surface with  one  that  will  improve  pressure  redistribution  and  microclimate  (heat  and moisture  control)  for  the  individual.  Changing  the  support  surface  is  only  one  of several  strategies  to  consider. The  individual and his/her pressure ulcer  should be re-evaluated.  Preventive  interventions  and  local  wound  care  should  also  be intensified as needed. A significant increase in risk status may also prompt such re-evaluation of the individual and the support surface.

  1. Replace the  existing mattress with  a  support  surface  that provides better pressure  redistribution,  shear  reduction,  and microclimate  control  for  the individual if she or he:
  • Cannot be positioned off of the ulcer
  • Has pressure ulcers on two or more  turning surfaces  (e.g.,  the sacrum and trochanter), limiting turning options
  • Fails to  heal  or  demonstrates  ulcer  deterioration  despite  appropriate comprehensive care
  • Is at high risk for additional ulcers
  • Bottoms out‖ on the existing support surface
  1. Inspect the skin for additional damage each time the individual is turned or repositioned while in bed. Do not  turn  the  individual onto a body  surface that  is  damaged  or  still  reddened  from  a  previous  episode  of  pressure loading,  especially  if  the  area  of  redness  does  not  blanch
  2. Limit head-of-bed  elevation  to  30  degrees  for  an  individual  on  bedrest, unless  contraindicated  by  medical    Encourage  individuals  to sleep  in  a  30-  to  40-degree  side-lying  position  or  flat  in  bed  if  not contraindicated.
  3. Use transfer  aids  to  reduce  friction  and    Lift —  don’t  drag —  the individual  while  repositioning.
  4. Do not use ring- or donut-shaped devices.
  5. Consider higher-specification  foam  or  similar  nonpowered  pressure redistribution support surfaces for Category/Stage I and II pressure ulcers. Use hydrocolloid or silicone foam dressing for sensitive skins.
  6. Relieve pressure under the heel(s) with Category/Stage  I or  II pressure ulcers by  placing  legs  on  a  pillow  to  ―float  the  heels‖  off  the  bed  or  by  using pressure-reducing devices with heel suspension. Use foam or silicone heal guards to prevent pressure sores.


  1. Debride devitalized tissue within the wound bed or edge of pressure ulcers when appropriate to  the  individual’s condition and consistent with overall goals of care.
  2. Select the  debridement  method(s)  most  appropriate  to:  the  individual’s condition; goals of care; ulcer/periulcer status; type, quantity, and location of  necrotic
  3. Use mechanical,  autolytic,  enzymatic,  and/or  biosurgical  methods  of debridement when there  is no urgent clinical need for drainage or removal of necrotic tissue.
  4. Perform surgical  debridement  in  the  presence  of  advancing  cellulitis, crepitus,  fluctuance,  and/or  sepsis  secondary  to  ulcer-related
  5. Use sharp  debridement  with  caution  in  the  presence  of:  immune incompetence,  compromised  vascular  supply  to  the  limb,  or  lack  of antibacterial  coverage  in  systemic    Relative  contraindications include  anticoagulant  therapy  and  bleeding  disorders.
  6. Perform  a  thorough  vascular  assessment  prior  to  debridement  of  lower extremity pressure ulcers
  7. Do not  debride  stable,  hard,  dry  eschar  in  ischemic


Wound dressings are a central component of pressure ulcer care. The selection of the dressing should be based on the tissue in the ulcer bed, the condition of the skin around  the  ulcer  bed,  and  the  goals  of  the  person  with  the  ulcer.  Generally maintaining  a  moist  ulcer  bed  is  the  ideal  when  the  ulcer  bed  is  clean  and granulating  to promote healing or closure. Several moisture-retentive dressings are available. However, the type of dressing may change over time as the ulcer heals or deteriorates.

Hydrocolloid Dressings

  1. Use hydrocolloid dressings for clean Category/Stage  II pressure ulcers  in body areas where they will not roll or melt.
  2. Consider using  hydrocolloid  dressing  on  noninfected,  shallow  Stage  III pressure ulcers.
  3. Change the  hydrocolloid  dressing  if  feces  seep  beneath  the  dressing.
  4. Consider using  filler  dressings  beneath  hydrocolloid  dressings  in  deep ulcers to fill in dead space.
  5. Consider using  hydrocolloid  dressings  to  protect  body  areas  at  risk  for friction injury or risk of injury from tape.

Transparent Film Dressings

  1. Consider using  film  dressings  to  protect  body  areas  at  risk  for  friction injury or risk of injury from tape.
  2. Consider using  film  dressings  for  autolytic  debridement  when  the individual is not immunocompromised.
  3. Consider using film dressings as a  secondary dressing  for ulcers  treated with alginates or other wound  filler  that will  likely  remain  in  the ulcer bed for an extended period of time (e.g., 3-5 days).
  4. Do not use film dressings as the cover dressing over enzymatic debriding agents, gels, or ointments.

Alginate Dressings

  1. Consider alginate  dressings  for  the  treatment  of moderately  and  heavily exudating ulcers.
  1. Consider alginate  dressings  in  infected  pressure  ulcers  when  there  is proper concurrent treatment of infection.
  2. Consider lengthening the dressing-change interval or changing the type of dressing if the  alginate  dressing  is  still  dry  at  the  scheduled  time  for dressing change.

Foam Dressings

  1. Consider using foam dressings on exudative Category/Stage II and shallow Category/Stage III pressure ulcers.
  2. Avoid using  single  small  pieces  of  foam  in  exudating  cavity  ulcers.
  3. Consider using  foam  dressings  on  painful  pressure  ulcers.
  4. Consider placing foam dressings on body areas and pressure ulcers at risk for shear injury.

Silver-Impregnated Dressings

  1. Consider use  of  silver  dressings  for  pressure  ulcers  that  are  infected  or heavily colonized.
  2. Consider use  of  silver  dressings  for  ulcers  at  high  risk  of  infection.
  3. Avoid prolonged use of silver dressings; discontinue when the infection is controlled.
  4. Consider use of silver sulfadiazine in heavily contaminated or infected pressure  ulcers  until  definitive  debridement  is  accomplished.

Silicone Dressings

  1. Consider using  silicone  dressings  as  a  wound  contact  layer  to  promote atraumatic dressing changes.
  2. Consider using silicone dressings to prevent  tissue  injury when  the ulcer or periwound tissue is fragile or friable.

Assessment and Treatment of Infection

Bacteria  are  present  on  all  skin  surfaces. When  the  primary  defense  provided  by intact skin is lost, bacteria reside on the wound surface also. When the bacteria (by numbers or virulence) cause damage  to  the body,  infection  is present. An  impaired host  has  a  reduced  ability  to  combat  bacteria.  The  number  of  bacteria  and  their effect  on  the  host  can  be  categorized  as  contamination,  colonization,  critical colonization,  or  infection.  Infection  is  not  common  in Category/Stage  I  or  II  ulcers, and  assessment  of  infection  should  focus  on  Category/Stage  III  and  IV  ulcers. Infection  may  spread  beyond  the  pressure  ulcer,  resulting  in  serious  systemic infections such as cellulitis,  fasciitis, osteomyelitis, systemic  inflammatory  response syndrome (SIRS), or sepsis.

  1. Have a high index of suspicion for local wound infection in individuals with diabetes mellitus,  protein-calorie  undernutrition,  hypoxia  or  poor  tissue perfusion,  autoimmune  disease,  or
  2. Have a high index of suspicion  for  local  infection  in pressure ulcers when there  are  no  signs  of  healing  for  2  weeks,  or  when  friable  granulation tissue,  foul odor,  increased pain  in  the ulcer,  increased heat  in  the  tissue around  the ulcer,  increased drainage  from  the wound, an ominous change in  the  nature  of  the wound
  3. Consider a diagnosis of spreading acute infection if the pressure ulcer has signs of acute infection, such as erythema extending  from  the ulcer edge, induration,  new  or  increasing  pain,  warmth,  or  purulent    The acutely  infected  ulcer  may  also  be  increasing  in  size  or  have  crepitus, fluctuance,  or  discoloration  in  the  surrounding  skin.  The  individual  may also  have  systemic  signs  of  infection  such  as  fever, malaise,  and  lymph node enlargement. Elderly  individuals may develop confusion/delirium and anorexia.
  4. Determine the bacterial bioburden of the pressure ulcer by tissue biopsy or quantitative swab technique.

The gold standard method for examining microbial load is quantitative culture of viable wound tissue. Surface swabs will only reveal the colonizing organism, and may not reflect deeper tissue infection. An acceptable alternative to quantitative tissue culture is the Levine quantitative swab technique:

  • Cleanse wound with normal saline. Blot dry with sterile gauze.
  • Culture the healthiest-looking tissue in the wound bed.
  • Do not culture exudate, pus, eschar, or heavily fibrous tissue.
  • Rotate the end of a sterile alginate-tipped applicator over a 1 cm x 1 cm area for 5 seconds.
  • Apply sufficient pressure to swab to cause tissue fluid to be expressed.
  • Use sterile technique to break tip of swab into a collection device designed for quantitative cultures.

Consider  a  diagnosis  of  pressure  ulcer  infection  if  the  culture  results indicate bacterial bioburden of > 105 CFU/g of tissue and/or the presence of beta hemolytic streptococci.

  1. In general, topical antibiotics are not recommended for pressure ulcers. Reasons for this  include  inadequate penetration  for deep  skin  infections, development of antibiotic resistance, hypersensitivity reactions, systemic absorption when applied to large wounds, and local irritant effects, all of which can lead to further delay in wound    However,  short  courses  of  silver  sulfadiazine,  topical  antibiotic solutions, or  topical metronidazole can be useful  in certain circumstances —  for example,  on  wounds  that  have  been  debrided  and  cleansed,  yet  still  have  a bacterial  bioburden  of  >  105 CFU/g  of  tissue  and/or  the  presence  of  beta hemolytic streptococci. Topical metronidazole might be used for the treatment of malodor in fungating wounds or wounds with anaerobic infection.
  2. Use systemic antibiotics for  individuals with clinical evidence of systemic infection, such as positive blood cultures, cellulitis, fasciitis, osteomyelitis, systemic  inflammatory  response syndrome  (SIRS), or sepsis.

Biophysical Agents in Pressure Ulcer Management

  • Consider the use of direct contact  (capacitative) electrical stimulation  (ES)  in the management of recalcitrant Category/Stage II, as well as Category/Stage III and IV pressure ulcers to facilitate wound healing.
  • Consider a  course  of  ultraviolet  light  as  an  adjunctive  therapy  to  reduce bacterial burden  in clean, but critically colonized Category/Stage  III and  IV pressure ulcers.
  • Negative Pressure Wound Therapy Consider  NPWT  as  an  early  adjuvant  for  the  treatment  of  deep, Category/Stage III and IV pressure ulcers.   Debride  the  pressure  ulcer  of  necrotic  tissue  prior  to  the  use  of
  • There is insufficient evidence to support the use of biological dressings in the treatment of  pressure
  • The combined  clinical  evidence  on  platelet-derived  growth  factor  (PDGF) suggests that PDGF-BB may improve healing of pressure ulcers.
  • There is  insufficient  evidence  to  recommend  hyperbaric  oxygen  therapy  for the treatment of pressure ulcers.
  • There is  insufficient evidence  to recommend  topical oxygen  for  the  treatment of pressure ulcers.
  • Consider use  of  high-frequency  (MHz)  ultrasound  as  an  adjunct  for  the treatment of infected pressure ulcers

Surgery for Pressure Ulcers

  • Evaluate the  need  for  surgical  consultation  for  operative  repair  in individuals with Category/Stage III or IV pressure ulcers that are not closing with  conservative  treatment,  or  for  individuals  who  desire  more  rapid closure of the ulcer.
  • Wound which shows no signs of healing at 2 wks must be evaluated for usage of alternative therapy if no signs of healing present despite complete patient optimization and patient mobilizing consider surgical closure.