eMedicine Specialties > Plastic Surgery > Pressure Ulcers

Pressure Ulcers, Surgical Treatment and Principles

Author: Bradon J Wilhelmi, MD, Professor and Endowed Leonard J Weiner, MD, Chair of Plastic Surgery, Residency Program Director, University of Louisville School of Medicine
Coauthor(s): Michael Neumeister, MD, FRCSC, Professor & Chairman - FACS - Director Hand/Microsurgery Fellowship - Division of Plastic Surgery, Southern Illinois University School of Medicine
Contributor Information and Disclosures

Updated: Jan 29, 2010

Introduction

Found during autopsies on Egyptian mummies, pressure sores are an ancient medical problem. The terms decubitus ulcer and pressure sore have been interchanged inappropriately over the years. Technically, the term decubitus ulcer refers to wounds developed over bony prominences while in the recumbent position (ie, sacrum, heel, occiput); the Latin decumbere means "to lie down." Therefore, semantically, wounds acquired from extended pressure in the seated or turned position (ie, ischial or trochanteric ulcers) are not decubitus ulcers. Therefore, in general, wounds acquired from pressure over bony prominences can always be called pressure sores.

History of the Procedure

In 1938, Davis was the first to suggest replacing the unstable scar of a healed pressure sore with a flap of tissue.1 In 1947, Kostrubala and Greeley recommended excising the bony prominence and adding padding for the exposed bone with local fascia or muscle-fascia flaps.2

Problem

Overall, patients with pressure sores are important users of medical resources. They require 50% more nursing time, remain hospitalized for significantly longer periods, and incur higher hospital charges.

Frequency

Pressure sores are common conditions among patients hospitalized in acute- and chronic-care facilities. Studies have suggested that, at any given time, 3-10% of hospitalized persons have pressure sores and 2.7% develop new pressure sores.3 Among a selected population, the incidence rate for the development of a new pressure sore has been demonstrated to be much higher, with a range of 7.7-26.9%.

Two thirds of pressure sores that develop in hospitalized patients occur in patients older than 70 years.4 As elderly individuals become the fastest-growing segment of the population, with an estimated 1.5 million people living in extended-care facilities, the problem of pressure sores will have an even more profound influence on the American economy.5 Most studies found the prevalence rate of pressure sores in patients in nursing homes to be 3-6%. However, other studies reported prevalence rates as high as 25-33%.

Pressure sores also occur with a higher frequency in young patients who are neurologically impaired.5 Immobility and lack of sensation make these patients susceptible to developing pressure sores. The incidence rate of pressure sores in these patients has been demonstrated to be approximately 5-8% annually, and 25-85% of these patients develop a pressure sore at some time. Once again, the treatment of pressure sores in this patient population represents a financial challenge, with an average cost per admission of a patient with a pressure sore of $78,000 at one hospital.

Etiology

Several theories exist on the etiology of pressure sores, mostly based on ischemia and hypoxia resulting in decreased oxygen delivery to the tissues. In 1879, Charcot suggested that injury to CNS trophic centers decreases tissue tolerance to local pressure and leads to skin necrosis.6 However, Brown Sequard demonstrated that pressure ulcers can heal equally well in paralyzed and nonparalyzed animals.7

The pressure ischemia theory maintains that pressure sores result from constant pressure sufficient to impair local blood flow to soft tissue for an extended period. This external pressure must be greater than arterial capillary pressure of 32 mm Hg to impair inflow and greater than venous capillary closing pressure of 8-12 mm Hg to impede the return of flow for an extended time. Constant external pressure for 2 hours or more produces irreversible changes in tissues in animal model studies. One study demonstrated no histologic changes with pressure release at 5-minute intervals.

Lindan et al documented ranges of pressure applied to various anatomic points in certain positions.8 The points of greatest pressure with the patient supine included the sacrum, heel, and occiput, at 40-60 mm Hg. With the body in prone position, the chest and knees absorbed the greatest pressure, at 50 mm Hg. When the patient is sitting, the ischial tuberosities are under the most pressure, at 100 mm Hg. Obviously, these pressures are greater than end capillary pressure, indicating why these are the most common areas to develop pressure sores.

Furthermore, studies have demonstrated the pathologic changes caused by pressure to be more severe in muscle than in skin and subcutaneous layers.9 These histologic studies revealed that early signs of damage occur in the upper dermis, with dilation of capillaries and venules and swelling and separation of endothelial cells.10 Then, perivascular infiltrates, platelet aggregates, and perivascular hemorrhage develop in the dermis. Additionally, subcutaneous fat demonstrates signs of necrosis along with early vascular changes. Interestingly, the epidermis shows no signs of necrosis until late because epidermal cells are able to withstand a prolonged absence of oxygen both in vivo and in vitro.

Others have postulated that pressure ulcers result from metabolic deficits. Muscle has the highest nutritional demands, which helps explain this deeper tissue involvement preferential to skin.

Presentation

Patient history

In obtaining a history from the patient with a pressure sore, determine the associated medical cause for the ulcer (eg, paraplegia, quadriplegia, spina bifida, immobilization in hospital, multiple sclerosis). Other factors that should be elicited in the patient's history include onset, duration, other ulcers, prior medical treatment, wound care, and prior surgical treatment.

The patient's social situation also can impact treatment. Determine if the patient has a pressure-reducing mattress for the wheelchair and bed and an appropriate support system at home to minimize the risk of recurrence. Also, obtain a complete review of systems, including the presence of fevers, night sweats, rigors, weight loss, weakness, and loss of appetite.

Physical examination

In addition to the patient history, perform a physical examination. Describe the specific location of the pressure sore based on the underlying bony prominence (eg, sacral, ischial, trochanteric). Infection of the pressure sore is suggested by wound edge erythema, foul odor, purulent discharge, and necrotic bone. Determine the level of tissue injury (ie, to epidermis, dermis, subcutaneous fat, muscle, bone, joint). Several classification systems of pressure sores are available based on this level of injury. One widely accepted classification system has 4 stages.11 Pressure sore staging from Barczak et al12 is as follows:

  • Stage 1 - Skin intact but reddened for greater than 1 hour after relief of pressure
  • Stage 2 - Blister or other break in dermis with or without infection
  • Stage 3 - Subcutaneous destruction into muscle with or without infection
  • Stage 4 - Involvement of bone or joint with or without infection

Also, note the character of the wound base and if it has granulation tissue or necrotic tissue. Verrucous heaps of white tissue within or around the wound suggest malignant transformation, as is observed with Marjolin ulcers (see images below). Document the size of the wound, wound edge undermining, additional pockets, and sinus tract communication with the hip joint or urethra. Note existing scars and the presence of colostomy and cystostomy. Also assess the extent of associated spasm.

Heaps of verrucous white tissue around the ulcer ...

Heaps of verrucous white tissue around the ulcer suggest malignant transformation as observed with Marjolin ulcers.

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Heaps of verrucous white tissue around the ulcer ...

Heaps of verrucous white tissue around the ulcer suggest malignant transformation as observed with Marjolin ulcers.


Pressure ulcers. Close-up view of area with heaps...

Pressure ulcers. Close-up view of area with heaps of verrucous white tissue around the ulcer, the presence of which suggests malignant transformation as observed with Marjolin ulcers.

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Pressure ulcers. Close-up view of area with heaps...

Pressure ulcers. Close-up view of area with heaps of verrucous white tissue around the ulcer, the presence of which suggests malignant transformation as observed with Marjolin ulcers.


Indications

Despite the susceptibility of muscle to early injury with pressure over bony prominences (see Relevant Anatomy), classification schematics recognize muscle involvement as a later stage in the process of wounding. The classification scheme is most useful in determining treatment.

The decision to reconstruct a pressure ulcer is complex and based on several considerations. Stage 1 and 2 pressure sores are treated conservatively. In general, stage 3 and 4 pressure sores may require flap reconstruction, although some patients with stage 3 and 4 pressure sores must be treated conservatively because of coexisting medical problems.

Wound reconstruction can be considered once the bacterial load has been minimized to fewer than 100,000 organisms to reduce the risk of infectious complications. Furthermore, the patient's social situation and nutritional status must be optimized (albumin level >3.5 g/mL) to reduce risk of an adverse outcome.

Relevant Anatomy

Pressure ulcers are described by location and the depth of involvement. Pressure sores can be found over the occiput, scapula, ischium, sacrum, trochanter, heels, and posterior iliac spine. These wounds can involve different levels of tissue. Muscle has been proven to be most susceptible to pressure. However, Daniel and Faibisoff found muscle to rarely interpose bone and skin in normal weightbearing positions in cadaver and clinical dissections.13

Contraindications

Because the complication rate of pressure sore reconstruction can be extremely high, poor candidates for operations in general should not undergo pressure reconstruction. Patients without the proper support network and pressure-release bed at home are not good candidates for pressure sore reconstruction because of the risk for recurrence or other complications. Patients who are noncompliant with nonoperative measures used to promote healing by secondary intention are also poor candidates for reconstruction.

Wound infections and osteomyelitis must first be aggressively debrided. Patients with significant fecal soiling into the pressure sore should be considered for diverting colostomy prior to reconstruction. Also, pressure sores with urethral fistulas should be diverted and healed prior to reconstruction.

More on Pressure Ulcers, Surgical Treatment and Principles

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References
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Further Reading

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Keywords

pressure ulcer, decubitus ulcer, bed sore, pressure sore, nonhealing wound, non-healing wound, wound healing complication, wound-healing complication, pressure ischemia, paraplegia, quadriplegia, spina bifida, immobilization, multiple sclerosis, MS, Marjolin ulcers, pressure sore reconstruction, flap procedures, chronic wound, pressure sore carcinoma

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Contributor Information and Disclosures

Author

Bradon J Wilhelmi, MD, Professor and Endowed Leonard J Weiner, MD, Chair of Plastic Surgery, Residency Program Director, University of Louisville School of Medicine
Bradon J Wilhelmi, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Hand Surgery, American Association of Clinical Anatomists, American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Society for Aesthetic Plastic Surgery, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, American Society of Plastic Surgeons, Association for Surgical Education, Plastic Surgery Research Council, and Wound Healing Society
Disclosure: Nothing to disclose.

Coauthor(s)

Michael Neumeister, MD, FRCSC, Professor & Chairman - FACS - Director Hand/Microsurgery Fellowship - Division of Plastic Surgery, Southern Illinois University School of Medicine
Michael Neumeister, MD, FRCSC is a member of the following medical societies: American Association for Hand Surgery, American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Medical Association, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, American Society of Plastic Surgeons, Association of Academic Chairmen of Plastic Surgery, Canadian Society of Plastic Surgeons, Illinois State Medical Society, Illinois State Medical Society, Ontario Medical Association, Plastic Surgery Research Council, Royal College of Physicians and Surgeons of Canada, and Society of University Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Albert E Cram, MD, FACS, Professor Emeritus, Departments of Surgery, Otolaryngology Head & Neck Surgery and Orthopedic Surgery, University of Iowa College of Medicine; Consulting Staff, Iowa City Plastic Surgery
Albert E Cram, MD, FACS is a member of the following medical societies: American Association of Tissue Banks, American Burn Association, American College of Surgeons, American Heart Association, American Society for Aesthetic Plastic Surgery, and American Society of Plastic Surgeons
Disclosure: ethicon Grant/research funds Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Wayne Karl Stadelmann, MD, Stadelmann Plastic Surgery, PC
Wayne Karl Stadelmann, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society of Plastic Surgeons, New Hampshire Medical Society, Northeastern Society of Plastic Surgeons, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Nicolas (Nick) G Slenkovich, MD, Director, Colorado Plastic Surgery Center
Nicolas (Nick) G Slenkovich, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Society of Aesthetic Plastic Surgery, American Society of Plastic Surgeons, and Colorado Medical Society
Disclosure: Nothing to disclose.

Chief Editor

Lars M Vistnes, MD, FRCSC, FACS, Professor of Surgery, Emeritus, Stanford University Medical Center
Lars M Vistnes, MD, FRCSC, FACS is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

 
 
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