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Pressure Ulcer

Bed Sore

A pressure ulcer (decubitus ulcer, pressure sore) is a localized injury to the skin and underlying tissue at sites of constant tissue pressure, recurring friction and resulting inadequate perfusion. Impaired mobility is an important contributing factor. A pressure ulcer occurs most frequently on the sacrum, elbows, heels, outer ankles, inner knees, hips and occipital bone of high-risk patients, especially elderly individuals, persons who are neurologically impaired and patients who are acutely hospitalized.


Presentation

To make the diagnosis of a pressure ulcer requires suspicion [3] [4]. To the inexperienced healthcare provider a deep soft tissue ulcer may easily be missed. One needs to get a comprehensive history from the patient or care provider [5] which should include overall health, medical history, medications, allergies, diet, use of tobacco and alcohol and level of mobility.

The pressure ulcer should be staged as follows:

  • Suspected injury to deep tissues or skin. May present as skin discoloration, blister or injury to soft tissue underneath. Overlying skin is intact.
  • Stage I: Skin is intact with non-blanchable erythema, impending skin breakdown. It may be painful, firm or soft, warmer or cooler compared with the surrounding skin. 
  • Stage II: There is partial-thickness dermal loss characterized by an open shallow ulcer which is pink and fresh without slough or bruising.
  • Stage III: There is full-thickness loss of skin with a deep ulcer extending to the subcutaneous tissue but the fascia is spared. The bone, tendon and other deeper tissues are not yet exposed.
  • Stage IV: There is a full-thickness ulcer with tissue loss. Ulcer extends to fascia, muscle, bone or tendon. Sloughing or eschar may be present and presence of sinus tracts is common.
  • Unstageable: There is full-thickness tissue and the ulcer base is covered with eschar to such an extent that the ulcer cannot be staged accurately. The only way to stage this ulcer is to completely debride the necrotic tissues and reassess.
Fever
  • The case of a 78-year-old woman with high fever and severe inflammation caused by iliopsoas abscess secondary to a sacral pressure ulcer is reported.[ncbi.nlm.nih.gov]
  • The disease was thereafter also known as boutonneuse fever (spotted fever) because of the manifestation of a papular rather than a macular rash.[dx.doi.org]
  • Risk Factors Immobility or limited mobility Spinal cord injury Diseases that affect blood flow such as diabetes or atheroscelerosis Fragile skin Urinary or fecal incontinence Poor nutrition or dehydration Decreased mental awareness Obesity Neuropathy Fever[woundsource.com]
  • Get immediate care if you notice signs of infection (fever, spreading redness, swelling, or pus). Treatments Your Physician May Prescribe In addition to self-care, your doctor might prescribe special pads or mattresses.[skinsight.com]
  • Get medical advice immediately if there is: red, swollen skin pus coming from the pressure ulcer or wound cold skin and a fast heartbeat severe or worsening pain a high temperature (fever) of 38C (100.4F) or above These symptoms could be a sign of a serious[nhs.uk]
Recurrent Urinary Tract Infection
  • She was known to have recurrent urinary tract infection. Contrast study through the fistula revealed a communicating fistula between the left buttock ulcer and the bladder.[ncbi.nlm.nih.gov]
Blister
  • It may also appear as an enclosed or open serum-filled blister. Stage lll: Full-thickness loss of skin with the epidermis and dermis gone and damage to or necrosis of subcutaneous tissues.[visualdx.com]
  • Stage II : An open wound The pressure ulcer may look like a shallow, pinkish red bowl-like wound, or it may appear as an intact or ruptured blister. Stage III : A deep wound The pressure ulcer has a crater-like appearance.[woundcarecenters.org]
  • The pressure ulcer is superficial and presents clinically as an abrasion, blister or shallow crater. • GRADE 3: Full thickness skin loss involving damage of subcutaneous tissue but not extending to the underlying fascia.[judy-waterlow.co.uk]
  • The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose (fat) is not visible and deeper tissues are not visible. Granulation tissue, slough and eschar are not present.[npuap.org]
Skin Ulcer
  • Malignant degeneration (Marjolin's ulcer) in chronic pressure ulcers and other chronic skin ulcerations may become more widespread as the life span of spinal cord injured patients increases.[ncbi.nlm.nih.gov]
  • ulcers Skin conditions resulting from physical factors Complications of bedridden Versteckte Kategorie: Uses of Wikidata Infobox[commons.wikimedia.org]
  • […] of ulcer ( L97.4- , L97.5- ) E09.621 , ICD-10-CM Diagnosis Code E09.622 Drug or chemical induced diabetes mellitus with other skin ulcer 2016 2017 2018 2019 Billable/Specific Code E09.622 , ICD-10-CM Diagnosis Code E10.621 Type 1 diabetes mellitus with[icd10data.com]
  • Rarely, a skin ulcer leads to sepsis. Prevention You can help prevent bedsores by frequently repositioning yourself to avoid stress on the skin.[mayoclinic.org]
Grieving
  • Those with a Stage IV pressure ulcer and flap repair and/or those with a spinal cord injury experienced the grieving process in some form.[ncbi.nlm.nih.gov]
Overflow Incontinence
  • Overflow incontinence Involuntary loss of urine secondary to over distension of the bladder; results in the leakage of small amounts of urine due to an outflow obstruction or a hypotonic bladder Common causes include medications, neurological conditions[nursingceu.com]
Foot Drop
  • Physical examination revealed loss of sensation and foot drop in the right foot.[ncbi.nlm.nih.gov]
Lower Extremity Spasticity
  • It was not until the successful control of his lower extremity spasticity that the pressure ulcers showed signs of healing. Neuroablation nay be considered for spasticity control when more conservative approaches fail or are not feasible.[ncbi.nlm.nih.gov]

Workup

Laboratory workup of pressure ulcer may include the following:

  • Complete blood count
  • C-reactive protein (CRP)
  • ESR
  • Albumin 
  • Transferrin

Other studies

  • Urine analysis and culture
  • Stool examination 
  • Blood cultures
  • Tissue or bone biopsy 

Imaging studies

  • Plain X-rays of the ulcer area may suggest osteomyelitis
  • Bone scan is more sensitive for osteomyelitis
Ischemic Changes
  • However, 1 week later, ischemic change of the wound edges and wound dehiscence were observed.[ncbi.nlm.nih.gov]

Treatment

Treatment of pressure ulcer is multidisciplinary. The type of treatment for pressure ulcer depends on the ulcer stage, status of patient and other comorbidities. General principles of pressure ulcer include nonsurgical or surgical wound care. Non-surgical treatment is usually used for early stage ulcers. For late stage ulcers, surgery may be required.

First the cause of pressure, friction or shear forces have to be determined and eliminated. The fundamental premise of treating pressure ulcers is frequent patient turning and positioning. When treating a pressure ulcer, it is vital to use antibiotics that cover the bacteria isolated. Indiscriminate use of antibiotics is not recommended as it leads to resistance and adverse effects.

In many patients with long standing pressure ulcers, osteomyelitis of the underlying bone can occur. The diagnosis of osteomyelitis requires a bone scan or a bone biopsy. Osteomyelitis should always be suspected when the pressure ulcer overlies a bony prominence does not heal despite pressure relief. When osteomyelitis is confirmed, antibiotic treatment for 6 to 8 weeks may be needed. In chronic osteomyelitis, surgery may be required.

Early stage ulcer when treated with non-surgical treatment may heal in most cases. Successful treatment of pressure ulcer includes the following:

  • Relieving pressure
  • Thorough debridement of devitalized and necrotic tissues
  • Prompt control of infection
  • Regular wound care
  • Use of innovative mattresses
  • Barrier creams, ointments and solutions
  • Other adjunctive treatments include UV light or heat
  • Before the patient is discharged, an interdisciplinary meeting should be held to ensure that the patient receives adequate homecare. The family or caregiver must be educated on prevention of ulcers.

General measures 

  • Use medications like baclofen, diazepam to control spasticity. Patients with spasticity who do not respond to medications may benefit from neurosurgical ablation. Treat flexion contractures surgically but ensure patient gets rehab to prevent recurrence.
  • Obtain a dietary consult and optimize nutritional status. Malnutrition is one very common reason why pressure ulcers never heal. Diets supplemented with vitamin C, arginine and zinc are recommended. Try enteral nutrition first because more invasive delivery of nutrition is like to result in more complications. Try to aim for a protein intake of 1.5-2.0g/kg/day [6].
  • Ensure adequate pain control and maintain hydration.
  • Correct anemia and all electrolyte deficiencies. Reversing anemia also improves oxygen delivery to the tissues.
  • Keep skin around the ulcer clean by regular skin care.
  • Obtain a urology consult if patient suffers from urinary incontinence. Treat all reversible causes of urinary incontinence such as a urinary tract infection
  • Add fiber in the diet to prevent constipation and overflow fecal incontinence.
  • Diapers and similar incontinence pads can help remove moisture away from skin but they need to be continually checked for soiling, leaving wet and dirty diapers in a patient with a pressure ulcer only aggravates skin maceration and promoted worsening of infection.
  • Bacterial contamination is common in pressure ulcers and must be assessed and treated appropriately.

Wound management

  • Debridement of the pressure ulcer is vital. When done regularly, it prevents infection and promotes healing. In addition, an ulcer can never be accurately staged until all necrotic tissue has been removed. Debridement may be done via proteolytic enzymes, mechanical debridement using surgical instruments, whirlpool, forceful irrigation or wet to dry dressing. Use of povidine iodine is recommended but hydrogen peroxide solution should be avoided as it is toxic to fibroblasts in the long run. Once the ulcer is clean and granulating use of debriding agent must be discontinued but the site must be kept clean.
  • When the wound is clean and not infected, normal saline is preferred. Saline can help irrigate the wound, keep it moist and minimize and fluid shifts that occur within newly growing tissue cells. Povidone iodine has antibacterial, antifungal and mild antiviral effects and can be used in infected wounds. A dilute solution should be used to prevent damage to the healing tissues. When granulation tissue started to appear, it should be discontinued. If pseudomonas is cultured, the use of acetic acid (0.5%) is recommended. Acetic acid is known to discolor the tissues and can make superinfect ion with other organism. Thus, each time acetic acid is used, the tissue should be rinsed with saline. Sodium hypochlorite (2.5%) can be used to debride necrotic tissue. However, prior to use, zinc oxide paste should be applied on the wound edges to prevent irritation to normal skin. After using sodium hypochlorite, the wound should be rinsed with saline
  • There are hundreds of dressings for pressure ulcer. While dressings are not required for intact skin, most advanced ulcers do require. The type of dressing depends on the wound status and goal [8]. Hydrocolloid dressings are commonly used because they form an occlusive barrier over the ulcer [7]. The dressings also maintain a moist wound and prevent bacterial contamination and enhance wound healing. The other benefit of these dressing is that they also prevent friction and minimize shear forces. These dressings need to be kept moist all the time. Finally hydrophilic dressings can be removed without causing discomfort to the patient. Transparent adhesive and alginate dressings can be used and provide occlusion and allow gas exchange. They prevent maceration of skin and lower the risk of secondary bacterial infection.
  • Silver sulfadiazine is often applied on wounds to lower the bacterial load. It is an effective agent with low toxicity, easy to apply and causes minimal pain. The agent has activity against a broad group of bacteria. Mafenide is also used and is active against pseudomonas it has the ability to penetrate eschar and cause softening of scar tissue. The problem with use of systemic and topical antibiotics is development of resistance. Thus antibiotics use should be limited and only used when cultures reveal that the organism is sensitive to that particular agent.
  • For chronic pressure wounds, other novel therapies include electrotherapy, growth factors, hyperbaric oxygenation and negative pressure wound therapy.

Surgery

If surgery is to be done the patient’s medical status and nutrition (albumin >3.5g/ml) must be optimized, otherwise any reconstruction will fail. The wound must be clean, nutritional state must be improved and spasticity must be relieved. Any urinary or fecal soiling must be improved by diversion. Further before surgery is undertaken, the patient must have social and family support, proper mattress to prevent recurrence. After surgery, avoidance of pressure is vital to prevent breakdown and recurrence [8]. Patients will need to be positioned on an air fluid mattress for weeks and carefully turned [9] [10]. Physical therapy is highly recommended. The skin must be checked and cleaned daily. The area should be kept clean and drug and moisturizers may help

Complications as a result of reconstructive surgery are, unfortunately, considerable. Such complications may include hematoma, flap necrosis, seroma, wound dehiscence or infection. As soon as the musculocutaneous flap show signs of healing ambulation should be started. Strenuous physical activity should be delayed for at least 4-6 weeks. The physical theory should begin by getting out of bed and sitting on a chair. Gradually ambulation should be started and continued until patient is able to carry our independent daily living activities.

Prognosis

When a pressure ulcer develops the prognosis is guarded. Death is often a direct result of a pressure ulcer in hospitalized patients. It is estimated that nearly 1/3rd of hospitalized patients who develop a pressure ulcer die during the same admission. Many of the patients are repeatedly admitted for further treatment of the pressure ulcer. Unfortunately, despite advanced therapy and use of muscle flaps, recurrence and breakdown of pressure ulcers is very common. In many cases, the cause of death is a concomitant bacterial infection. With advanced ulcer, renal failure is often a common occurrence. 

Other complications of pressure ulcer include:

Complications

Complications of pressure ulcer include the following:

Etiology

The most common cause of pressure ulcer is impaired mobility. This results in prolonged and uninterrupted pressure on a part of the body that eventually results in breakdown of tissues. Immobility may occur in patients with neurological impairment, those who are restrained, anesthetized, heavily sedated, recovering from a long injury or demented. These individuals are unable to alter their body positions frequently to relieve the pressure. The prolonged immobility creating pressure over a certain part of the body leads to skin and soft tissue atrophy over time. The muscles over the bony prominences also start to decline in size.

Another common cause of pressure sores is spasticity and contractures. Failing to sense pain whether from use of medications or neurological deficits also contributes to development of pressure ulcers. The reason is that there are no stimuli to the brain from the body to reposition for pressure relief. In addition, if the patient has pain from a fracture or surgical incision he or she may not be able or willing to change body position for fear of making the pain worse.

Presence of fistulas or incontinence (urine or fecal) can also lead to skin ulceration. The excess fluid and harsh acid/alkaline body secretions continually keep the skin moist lead to maceration. Further fecal soiling of the open wound introduces microorganisms into the wound. Presence of bacteria must be a consideration when evaluating pressure ulcers. Overgrowth of bacteria can lead delay in wound healing and a bacterial infection may spread causing osteomyelitis, gangrene and necrotizing fasciitis.

Organisms isolated from pressure ulcers include the following:

Risk factors for pressure ulcer including anemia and malnutrition. Poor nutrition is a major contribution factor for pressure ulcers because it leads to a depressed immune system and promotes bacterial infection. Other risk factors include peripheral vascular disease and hypovolemia, which impairs blood flow to the area of ulceration.

Other risk factors include:

Epidemiology

Pressure ulcers are common in hospitalized patients and nursing homes. In the USA at least a million pressures are seen in healthcare facilities each year. Unfortunately there are many other patients in nursing homes and acute care facilities who never come to attention in hospitals. The incidence of pressure sores is highest in patients who are paralyzed and in those with spinal cord injury. The higher the level of spinal cord injury, the higher the risk of developing pressure sores. 

The problem of pressure ulcers is a global phenomenon reported in all countries. The incidence of pressure sores varies from 3-30% with the higher numbers seen in long-term care facilities and intensive care units. The numbers of people with pressure ulcers outside the hospital are often under reported to prevent a negative stigma by the public. Pressure sores are thought to be more common in African Americans. This is speculated to be due to the difficulty in recognizing mild erythema in people with dark skin color.

Pressure ulcers have a bimodal distribution. There is a small peak in the 3rd decade of life probably reflecting individuals involved in traumatic neurological injury which makes them unable to sense pressure and are immobile, leading to pressure ulcers. The other age group that is prone to pressure ulcers are those individuals between the ages 70 and older. These are patients with numerous comorbidities, are frail and are not ambulatory. The younger individuals suffering from pressure ulcers are often males, but in the older population, most patients are females. 

Sex distribution
Age distribution

Pathophysiology

Pressure ulcers are most common around the buttock and hip areas. The next most common sites are the heels, patella, malleolar and pretibial regions. Some individuals may develop pressure ulcers on the chin, occiput, chest, back and elbow. There is no surface of the body that may not be affected by a pressure ulcer.

The pathophysiology of pressure ulcers is dependent on many factors but prolonged pressure is the one necessary component. The unrelenting pressure leads to impairment of the local blood supply to the soft tissues and muscles resulting in ischemia. The external pressure required to impair normal capillary filling is about 32 mmHg. Because most body tissues are able to withstand high pressure for a short period, prolonged pressure is required to produce a pressure ulcer. In many cases, the tissue is compressed by a rigid structure like a mattress or wheel chair and pressures of 45 mmHg to 75 mmHg over bony prominences are generated. 

When these high pressures for more than 2 hours are combined with friction, humidity and microcirculatory ischemia, tissue anoxia occurs with resultant ischemia, necrosis and ulceration. It is suggested that reperfusion may be the cause of additional injury to the ulcer. Often when patients with ulcer are repositioned to relieve pressure, the ulcer gets bigger and appears worse; this is believed to be due to reperfusion injury caused by an influx of calcium and generation of free radicals.

Prevention

The best way to treat pressure ulcers is to prevent them in the first place. All hospitals now have preventive measures for patients at high risk for pressure ulcers. The Braden or Norton scales are widely used to assess for risk of pressure ulcer. Both these tools assess the physical and mental state of the patient, ambulation, incontinence, sensory perception and comorbidities. Management and prevention of pressure ulcers is vital because they carry a high morbidity and mortality. 

Summary

Pressure ulcers, also referred to as decubitus ulcers or pressure sores, are common in hospital settings, nursing homes and long-term care facilities. The majority of pressure ulcers occur at anatomical sites where bony structures are prominent especially when a patient is supine. No matter where on the body a pressure ulcer occurs, the common denominator is constant pressure at the site. Over time the unrelenting pressure results in ischemia, necrosis and ulceration.

In general, patients with normal mentation, sensitivity and mobility do not develop pressure ulcers, because the feedback mechanisms to the brain lead the individual to change position before any type of tissue damage occurs. Individuals who are unable to avoid prolonged uninterrupted pressure such as those with neurological impairment or the elderly are at the highest risk for pressure ulcer.

Patient Information

Pressure ulcer, also known as pressure sore or decubitus ulcer, occurs when there is prolonged pressure on certain parts of the body, which is unrelieved. The ulcers tend to develop over bony prominences such as heels or the hips. People at the highest risk for pressure ulcers are those with stroke, paraplegia, spinal cord injury or bed ridden people. Other factors that increase the risk of a pressure ulcer include malnutrition, cancer, incontinence, and lack of ambulation.

The treatment of pressure ulcer requires frequent turning of the patient and improving nutrition. Specialized mattresses and physical therapy can help. At the first sign of a pressure ulcer, the preventive steps should be immediately taken to prevent skin break down.

References

Article

  1. Krupp AE, Monfre J. Pressure ulcers in the ICU patient: an update on prevention and treatment. Curr Infect Dis Rep. 2015 Mar;17(3):468.
  2. Hagen EM, Acute complications of spinal cord injuries. World J Orthop. 2015 Jan 18;6(1):17-23.
  3. Gadd MM, Morris SM. Use of the Braden Scale for pressure ulcer risk assessment in a community hospital setting: the role of total score and individual subscale scores in triggering preventive interventions. J Wound Ostomy Continence Nurs. 2014 Nov-Dec;41(6):535-8.
  4. van Rijswijk L, Beitz JM. Pressure Ulcer Prevention Algorithm Content Validation: A Mixed-methods, Quantitative Study. Ostomy Wound Manage. 2015 Apr;61(4):48-57.
  5. Richardson A, Barrow I. Part 1: Pressure ulcer assessment - the development of Critical Care Pressure Ulcer Assessment Tool made Easy (CALCULATE). Nurs Crit Care. 2015 Mar 19.
  6. Posthauer ME, Banks M, Dorner B, Schols JM. The role of nutrition for pressure ulcer management: national pressure ulcer advisory panel, European pressure ulcer advisory panel, and pan pacific pressure injury alliance white paper. Adv Skin Wound Care. 2015 Apr;28(4):175-88.
  7. Dumville JC, Stubbs N, Keogh SJ, Walker RM, Liu Z. Hydrogel dressings for treating pressure ulcers. Cochrane Database Syst Rev. 2015 Feb 17;2:CD011226
  8. Kuffler DP. Improving the Ability to Eliminate Wounds and Pressure Ulcers. Wound Repair Regen. 2015 Mar 20.
  9. Pittman J, Beeson T, Kitterman J, Lancaster S, Shelly A. Medical device-related hospital-acquired pressure ulcers: development of an evidence-based position statement. J Wound Ostomy Continence Nurs. 2015 Mar-Apr;42(2):151-4
  10. Moore ZE, Cowman S. Repositioning for treating pressure ulcers. Cochrane Database Syst Rev. 2015 Jan 5;1:CD006898.

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Last updated: 2019-06-28 12:28