Clinics in Dermatology (2010) 28, 527–532

The decubitus ulcer: Facts and controversies

Caren Campbell, BA, Lawrence Charles Parish, MD, MD (Hon) ⁎
Department of Dermatology, Jefferson Medical College of Thomas Jefferson University, 1760 Market St, Ste 301,
Philadelphia, PA 19103, USA

Abstract Defining the decubitus ulcer proves as difficult as agreeing on a name for the condition.
Causes include pressure over bony prominences, shearing force, destruction of skin, and compromised
blood flow. Evidence is emerging of the importance of ischemia as a primary causative agent, rather
than pressure, which needs further investigation. Scales, staging, and treatment and prevention
guidelines should be used with caution due to their arbitrary implementation and lack of evidence-based
support. Unfortunately, much of the research and expert opinion developed by the government and
touted as regulation lacks appropriate strength-of-evidence. Although decubitus ulcers should be
prevented and treated to the best of our abilities, recognizing the possibility that the skin, like any other
organ in the body, may fail is crucial.
© 2010 Elsevier Inc. All rights reserved.

Introduction: Defining the decubitus ulcer Nomenclature

The difficulty in defining the decubitus ulcer based on Naming is just as problematic as formulating a conscience
previous research highlights the ongoing debate on the topic. definition. Names for the decubitus ulcer have included:
After an extensive literature review of the subject, four main
points emerged, either independently or combined, when pressure ulcer, decubitus ulcer, bedsore, bed-sore, pressure sore,
defining decubitus ulcers: tissue necrosis, decubiti (grammatically incorrect) or decubitus,
trophic ulcer, chronic ulcer, decubitus omniosus/acutus/chron-
• Pressure over bony prominences icus, erythema gangraenosum, cuticular necrosis, and skin ulcer
• Shearing force
• Destruction of skin Ignoring hyphenation, the term bedsore/bed-sore is most
• Compromised blood flow commonly used, followed by pressure ulcer, pressure sore,
decubitus ulcer, and finally decubiti. Despite the frequency
Forming an accurate and complete definition of the of use, proper nomenclature should accurately capture and
decubitus ulcer may be impossible, but these four compo- describe that for which it is named. In this case, bedsore/bed-
nents may be used to craft a definition that defines, in sore implies that the bed is the causative agent, and similarly,
simplistic terms, the decubitus ulcer as a breakdown of skin, pressure ulcer/sore assigns pressure as the causative agent. In
usually over a bony prominence, due to compromised blood reality, the causes include pressure, shearing force, destruc-
flow caused by pressure. tion of skin, and compromised blood flow. The term
decubitus ulcer captures the essential nature of the ulcer,
⁎ Corresponding author. Tel.: +1 215 563 8333; fax: +1 215 563 3044. lying down or resting on the skin, which accurately describes
E-mail address: caren.campbell@jefferson.edu (C. Campbell). all four potential causes of the ulcer.

0738-081X/$ – see front matter © 2010 Elsevier Inc. All rights reserved.
doi:10.1016/j.clindermatol.2010.03.010
528 C. Campbell, L.C. Parish

As far back as 1913, it was argued that, “the term Types of patients
pressure sore best described these complex wounds because
they are multifactorial in nature and can occur anywhere Some studies, although questionable, have shown 60% to
in the body.”1 Although pressure is a principle cause, using 70% of all pressure ulcers occur in persons aged older than
pressure ulcer or sore “conveys the notion that pressure is 65 years,4,6 especially those newly admitted to a geriatric
the only factor and disregards friction, shear, moisture, unit, where ulcers will develop in 8% to 20%. 11,21
temperature, sensory impairment, or oxygenation in its Regardless of statistics, elderly people are most at risk for
pathogenesis.”2 We prefer the term decubitus ulcer, derived developing decubitus ulcers.6,7,12,14,15,17,22-24 Patients with
from the Latin decumbere meaning to lie down, believing paralysis are also at risk.5,6,12,13,16,22,25,26 Although not
that the term best captures the multifactorial nature of mutually exclusive from elderly or paralytic persons, bed- or
the etiology. wheelchair-bound persons are predisposed to ulcers.10,12
In addition to the elderly and paralytic patient, others at
increased risk are those with severe, acute illness in the
intensive care unit,22 and neurologic patients with amyo-
Etiology trophic lateral sclerosis and multiple sclerosis who have
impaired sensory perception and poor mobility.27 Much like
Decubitus ulcers are “caused when tissue is devitalized”3 paralytic or neurologic patients, those lying on operating
by a number of factors, including but not limited to tables for extended time periods are also at high risk of
pressure, friction,4,5 shear,4,6 moisture,4 and ischemia.7,8 In developing decubitus ulcers. Finally, no gender difference
regards to pressure, one must consider the intensity, dura- exists among those most a risk for developing decubitus
tion, and the tissue's tolerance for pressure.9 Not only ulcer. In summary, patients at increased risk include:
intense pressure, but also moderate pressure acting contin-
uously over a long period of time can result in ulcer • Elderly
formation.10 Pressure is the most important factor in the • Neurologic
formation of decubitus ulcers, but not without other • Trauma (including spinal injury)
components being involved.4-6,9,11-13 • Patients in lengthy operations
Friction is defined as rubbing, whereas shear is produced
by sheet pulling, and both can lead to the formation of ulcers.
Also, moisture can exacerbate the effects of friction and
shear. Both forces are increased when sweating or Measurements: Scales and staging
incontinence creates a moist environment, macerating the
skin. Since 1850, it has been recognized that prolonged In an effort to prevent decubitus ulcer formation, risk
contact with urine can be the primary source of mois- assessment scales have been developed. The Braden scale
ture,4,5,11,14-16 and more recently, fecal incontinence has was created to predict the formation of decubitus ulcers
been identified as even more important in ulcer formation.17 based on grading of risk factors—sensory perception, mois-
Basic pathogenesis involves pressure, but other factors ture, activity, mobility, nutrition, friction, and shear. The
include ischemia, which leads to tissue necrosis and ulcer Norton scale evaluates physical condition, activity, mobility,
formation6-8,10,12,15,18 and can be caused by pressure incontinence, and mental status. In addition to these, the
between a hard surface and a bony prominence,6 denerva- Douglas scale builds on the Norton scale to also include
tion,15 or thrombosis of smaller vessels.10 Prolonged pain, skin conditions, and special risk factors. Finally, the
pressure may stretch soft tissues and blood vessels, causing Waterlow scale uses body mass index, continence, skin type,
multiple microthrombi around the point of maximum mobility, gender, age, appetite, tissue malnutrition, neuro-
compression, leading to ischemia and a plaque of dead logic deficit, trauma/surgery, and medication.
tissue surrounded by microthrombi.19 Like any other organ A methodologic review of the risk assessment scales
in the body without proper perfusion, the skin fails, which found the most commonly used scales, Norton, Waterlow,
potentially leads to an ulcer. and Braden, had insufficient predictive validity and poor
A new body of evidence suggests that ischemia, rather reliability.9 Of all the scales, the Braden scale showed the
than pressure, may be the principal culprit in decubitus ulcer best validity, reliability, and better risk prediction than
formation. Some have suggested that most ulcers are the clinical judgment of nurses alone22; however, the Braden
result of deep tissue injury.20 These injuries are incurred scale does not apply to all patient populations. To maintain
from ischemia and the resultant reperfusion injury and its validity, the critical cutoff score and the timing of the
impaired lymphatic function; although pressure does play a assessment vary in different settings for the Braden scale.28
primary role in the mechanical deformation of tissue cells. Clinical judgment may serve as the most valid and effective
Ulcers have been defined as “evidence of pathologic changes means of predicting decubitus ulcer formation. Risk
in blood supply to dermal tissues.”17 The evolving role of assessment scales may prove useful in situations where
ischemia in ulcer formation deserves further assessment. clinical experience is lacking or insufficient.
Decubitus ulcer 529

Once a decubitus ulcer has formed, staging is used to healing in those receiving antibiotics. Antibiotics must be
classify ulcers based on the amount of tissue loss. used with caution and when infection is undoubtedly
present.32 Potentially, a tissue biopsy would be performed
• Stage I involves no tissue loss and is termed and a standard of greater than 105 bacteria would justify the
nonblanchable erythema use of antibiotics,6 but this process still does not ensure
• Stage II is a superficial, partial-thickness ulcer with proper use of antibiotics. The standard of greater than 105
skin breakdown and minimal tissue necrosis bacteria or colony forming units is arbitrary. Skin flaps with
• Stage III is a full-thickness ulcer displaying breakdown more than 105 bacteria survive and commensal protective
extending through the dermis, exposing subcutaneous bacteria present at these levels do not indicate infection, but
tissue normal levels of bacteria. Identifying infected ulcers is
• Stage IV extends through the deep fascia, damaging important.33 Surgical débridement should be postponed
underlying muscle and bone until infection is under control. 15 When infection is
suspected, using 105 bacteria may serve as a guideline, but
Although staging was created to provide a universal caution should be used on a case-by-case basis.
language in which to discuss decubitus ulcers, its necessity is Occlusive dressings using hydrocolloid provide a moist
questionable. Most important in describing an ulcer is environment which accelerates healing. During a 6-month
location, shape, and length, width, and depth, which serve as timeframe, decubitus ulcers covered in moisture/exudate-
less subjective measures of the ulcer. The grading system management dressings in adults older than 50 healed, whereas
created by Lowthian includes not only the tissue involved but those covered with gauze dressing did not. As far back as 1849,
also the shape, depth, and presence of necrotic tissue. For patients with ulcers were treated with collodion, moist dressings
instance, a potential ulcer is more than 15 mm in diameter, dipped in solution. Hydrocolloid dressings represent the gold
while a medium ulcer is open, includes destruction to the standard in decubitus ulcer care.32
dermis, and is more than 5 mm in diameter.29 Pressure relief using repositioning schedules and spe-
Another option to consider when discussing an ulcer cialty beds is essential in treating decubitus ulcers.4,15 Since
is the Pressure Ulcer Scale for Healing (PUSH) tool, the mid-19th century, pressure-relieving devices, including
which is used to monitor wound healing by recording the water cushions and pillows, caoutchouc pillows, and
changes in surface area, the extent of necrotic tissue and hydrostatic beds, have been used in decubitus ulcer
exudate, and the presence of granulation tissue.12 The fact treatment.34-36 Today, large-celled alternating pressure air
remains that staging is arbitrary and often provides mattresses have been shown in controlled trials to heal
confusing information. pelvic and heel sores without repositioning.18 Another
randomized controlled trial found that decubitus ulcers in
patients on air fluidized beds repositioned four times per
day healed faster than they did in patients on regular
Treatment hospital beds repositioned every 2 hours. With the use of
pressure-relieving beds, the frequency and even the
If necrotic tissue is present, débridement is often necessity of repositioning needs to be evaluated. The notion
needed3,4,6 because the presence of devitalized or contam- that patients should be shifted every 2 hours is antiquated
inated tissue interferes with healing by mechanically and based on folklore rather than valid, clinical evidence.
obstructing wound contraction and serves as a barrier to Of the several trials attempting to increase healing using
reepithelialization.30,31 Initially, nonselective methods are nutritional supplements, none have found an increased
used, including complete surgical débridement, mechanical healing rate in decubitus ulcers. 32 Although proper
abrasion, wet-to-dry dressing, or forceful irrigation. As nutrition is unarguably critical to overall patient care,
necrotic material decreases, selective methods can be used, optimal nutrition may not improve the treatment of pressure
including partial surgical débridement, autolytic, enzymatic, ulcers.6 One study found that supplementation of ascorbic
chemical, or even maggot débridement, and the whirlpool or acid (500 mg twice daily) given orally to pressure ulcer
Hubbard tank.30 One study found that in patients aged older patients increased the healing rate of the ulcers compared
than 50, failure to débride wounds with yellow slough with control patients given placebo.37 Unfortunately, the
decreased odds of healing.32 Randomized controlled trials study only looked at 20 surgical patients, a small, select
examining débridement vs no débridement would be sample that may not apply to the critically ill patients that
unethical; therefore, current evidence suggests a need for are often afflicted with decubitus ulcers.
ongoing débridement in chronic wounds with necrotic One report went so far as to recommend lysine and proline
tissue,31 but constant débridement can interfere with any for collagen synthesis; oxygen, iron, vitamin C, and α-
wound healing capabilities the patient might have. ketoglutarate to form triple helix procollagen; calcium for
Antibiotic therapy can retard healing and is only useful conversion of procollagen to fibrillar collagen; iron, folate,
in decubitus ulcers with gross contamination.3,4 A study of and vitamin B12 supplementation to optimize erythropoiesis
Medicaid patients aged older than 50 found lower odds of in anemic patients; and vitamin K for blood clotting.15 The
530 C. Campbell, L.C. Parish

usefulness and validity of giving patients with decubitus regulatory oversight and improvements in prevention
ulcers eight supplements and oxygen has not been properly technology.12,42,43 Decubitus ulcers may not be preventable
evaluated and would likely prove useless. For instance, the or curable, because there is no way to sustain or enhance
use of vitamin C to speed wound healing dates back to the cutaneous function. Skin failure may represent a terminal
1940s,38,39 and like many recommendations for decubitus event in some patients, like the terminally ill. 44 An
ulcer treatment, its use seems based more on tradition than examination of a sample of nursing homes with high and
its utility. low prevalence rates for pressure ulcers found few
At this point, it is important to distinguish between differences in the processes of care, not only by medical
treatment and cure.40 Although decubitus ulcers can be record review but also by direct observation.45
treated with a number of methods, as detailed above, it is In light of the onslaught of lawsuits spurned by decubitus
questionable whether we can cure a decubitus ulcer, ulcer formation, a comment by Worley is worth highlighting:
especially in terminally ill patients.12 Like any other organ The presence of a pressure ulcer in the elderly and
in the body, the skin can fail, and even with best practices in acutely ill person should not be used as a measure of the
treating decubitus ulcers, they can not be cured. We can only quality of care. In some patient populations, no amount
do our best the treat the ulcer. of attention or skill on the part of health care providers
will prevent the occurrence of a pressure ulcer. The
“blame” of the occurrence may lie in the history of the
disease process.46
Prevention
Even the revised guidelines from the Centers for
Pressure-relieving devices are crucial in the alleviation Medicare and Medicaid Services recognize that decubitus
of pressure, the major cause of decubitus ulcers. One ulcers are unavoidable under certain circumstances, espe-
randomized controlled trial showed that the use of an cially those resulting from skin failure and particularly
alternating air mattress or a waterbed lowered the incidence from hypoperfusion.46,47
of ulcers by more than 50% among hospitalized patients.41
As far back as 1883, physicians recognized the importance
of pressure diffusion with waterbeds or cotton wool Stress and decubitus ulcer formation
padding.5 Even foam alternatives in hospital patients and
polymers pads for surgical patients reduce the risk that a Compared with other patients with acute wounds, patients
decubitus ulcers will develop.22 Certainly, air mattresses, with acute wounds under increased stress, defined as
waterbeds, and air-fluidized beds should be used in the psychologic stress due to such burdens as being a caregiver
prevention of ulcers.15 or an upcoming examination, have increased levels of
Repositioning is also important in very sick patients to glucocorticoids and decreased levels proinflammatory local
prevent the formation of deep sores caused by high cytokines. In one study, these differences led to increased
interstitial pressures and capillary deformation produced healing time.48 These results may imply a causative link
by bony prominences. Superficial sores associated with between stress and repair of decubitus ulcers, but no direct
humidity and friction can be prevented with soft pressure- studies have been conducted.
relieving mattresses that rely on low interface pressures.18 The One study found that leg ulcers in elderly patients with
frequency of repositioning is debatable, ranging from 1 to greater anxiety and depression healed more slowly,49 but the
2 hours by day and 2 to 3 hours at night,5,13,21 but these validity of the study is in question. The cross-sectional study
schedules are arbitrary, and further investigation into the time- design does not demonstrate a causal relationship, and
consuming strategy should be conducted. Kinetic therapy despite statistically significant results, the sample size was
bed technologies do exist that assist in patient turning,15 and small. The Hospital Anxiety and Depression scale used to
their utility and cost-effectiveness should be evaluated. evaluate anxiety and depression still needs to be evaluated
Nutritional status is important in overall patient health and for patients aged older than 65, and most of the patients were
certainly influences the formation of decubitus ulcers. older than 65. In addition, the Likert scale used to evaluate
Protein may be important,3,17 as well as use of oral wound healing is insufficient.
supplements. One study of improving nutrition with the The findings that have come from extensive research on
administration of two oral supplements daily in acutely ill acute wounds should not be applied to chronic wounds like
patients older than 65 found decreased decubitus ulcer decubitus ulcers. For instance, matrix metalloprotease-9 is
development in these patients.22 The ability of acutely ill elevated in chronic wounds and reduced in acute
patients to absorb or benefit from nutritional supplementa- wounds.50,51 Such differences make it impossible to link
tion should be examined. directly those results cited in acute wound studies to
It is vital to recognize that no intervention has consistently decubitus ulcer patients. There is a need for studies
and reproducibly reduced decubitus ulcer incidence to zero. that directly evaluate the role of stress in the healing of
Epidemiologic data show a stable incidence of ulcers despite chronic wounds.52
Decubitus ulcer 531

12. Maklebust J. Pressure ulcers: the great insult. Nurs Clin North Am
U.S. Department of Health and Human Services 2005;40:365-89.
Treatment of Pressure Ulcers Clinical 13. “Baking” chronic ulcers of the leg. Lancet 1915;185:143.
Practice Guidelines 14. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic
review. JAMA 2006;296:974-84.
15. Bass MJ, Phillips LG. Pressure sores. Curr Probl Surg 2007;44:101-43.
The Clinical Practice Guidelines indicate the strength of 16. Hitch S. Chemical means for the prevention of bed-sores. Lancet
evidence with ratings A, B, and C. The A rating is supported 1851;57:307.
by two or more randomized clinical control trials, B by two 17. Thomas DR. Prevention and treatment of pressure ulcers: what works?
or more controlled clinical trials, and C by one controlled what doesn't? Cleve Clin J Med 2001;68:704-7, 710-4, 717-22.
18. Preventing pressure sores. Lancet 1990;335:1311-2.
trial, two or more case series or descriptive studies, or expert 19. Parish LC, Lowthian P, Witkowski JA. The decubitus ulcer: many
opinion. All but one of the 15 recommendations for questions but few definitive answers. Clin Dermatol 2007;25:101-8.
assessment were ranked with a C, 14 of the 16 guidelines 20. Berlowitz DR, Brienza DM. Are all pressure ulcers the result of deep
for managing tissue loads were ranked with C, 6 of 22 for tissue injury? A review of the literature. Ostomy Wound Manage
2007;53:34-8.
ulcer care were C, 10 of 12 for managing bacterial
21. Bedford P. Prevention of pressure sores. Lancet 1961;278:1257.
colonization and infection, all 5 of operative repair guide- 22. Pressure ulcers—prevention of pressure related damage. Aust Nurs J
lines, and all 14 of education and quality improvement 2008;15:27-9.
guidelines were ranked C. Thus, the overwhelming majority 23. Livesley B. Prevention of pressure sores. Lancet 1990;335:1595.
of recommendations lack any strength of evidence. Expert 24. The doctor and the old person. Lancet 1948;251:815-6.
opinion in no way validates a recommendation without 25. Levine JM. Historical perspective on pressure ulcers: the decubitus
ominosus of Jean-Martin Charcot. J Am Geriatr Soc 2005;53:1248-51.
further supporting evidence. 26. Gowlland E. The diary of a paraplegic patient. Lancet 1926;207:
529-30.
27. Hayashi T, Narita Y, Okugawa N, Hamaguchi E, Shibahara M,
Kuzuhara S. Pressure ulcers in ALS patients on admission at a
Conclusions university hospital in Japan. Amyotroph Lateral Scler 2007;8:310-3.
28. Bergstrom N, Braden B, Kemp M, Champagne M, Ruby E. Predicting
pressure ulcer risk: a multisite study of the predictive validity of the
Much like King Canute, who commanded the tides to roll
Braden Scale. Nurs Res 1998;47:261-9.
out and learned the limitations of his power, this “so let it be 29. Lowthian P. The classification and grading of pressure ulcers 1987.
written, so let it be done” attitude in regards to decubitus J Tissue Viability 2005;15:15-8.
ulcers may prove severely limited. It has no place in public 30. Witkowski JA, Parish LC. Rational approach to wound care. Int J
policy. Demanding a stop to the incidence of decubitus Dermatol 1992;31:27-8.
ulcers may prove as unsuccessful as requiring an end to 31. Beitz JM. Wound debridement: therapeutic options and care considera-
tions. Nurs Clin North Am 2005;40:233-49.
global warming.53 Although prevention and treatment of 32. Jones KR, Fennie K. Factors influencing pressure ulcer healing in adults
ulcers are feasible, demanding their complete eradication is over 50: an exploratory study. J Am Med Dir Assoc 2007;8:378-87.
as futile a cause as controlling the tides. 33. Parish LC, Bolton L. Wound infection: facts to face. Skinmed 2007;6:
53-4.
34. Ashton T. The prevention of bed-sores. Lancet 1852;60:430.
35. Hooper W. The water-cushion. Lancet 1850;55:317-8.
36. Hawkins C. On the use of water-pillows. Lancet 1849;54:466.
References 37. Taylor TV, Rimmer S, Day B, Butcher J, Dymock IW. Ascorbic acid
supplementation in the treatment of pressure-sores. Lancet 1974;2:
1. Treatment of bedsores by application of hot air. Lancet 1913;181:1684. 544-6.
2. Parish LC, Witkowski JA. Controversies about the decubitus ulcer. 38. Bourne G. Effect of vitamin-C deficiency on experimental wounds
Dermatol Clin 2004;22:87-91. tensile strength and histology. Lancet 1944;243:688-92.
3. Anthony D. The treatment of decubitus ulcers: a century of 39. Lund CC, Crandon JH. Ascorbic acid and human wound healing. Ann.
misinformation in the textbooks. J Adv Nurs 1996;24:309-16. Surg 1941;114:776-90.
4. Alvarez OM. Pressure ulcers: critical considerations in prevention and 40. Parish LC, Ramos-e-Silva, Campbell C. Expectations of the dermato-
management. Clin Mater 1991;8:209-22. logic patient. Eur Rev Dermatol 2009:29-30.
5. Browne T. On the formation and prevention of bedsores in nervous 41. Andersen KE, Jensen O, Kvorning SA, Bach E. Decubitus prophylaxis:
diseases. Lancet 1883;121:631-2. a prospective trial on the efficiency of alternating-pressure air-
6. Levi B, Rees R. Diagnosis and management of pressure ulcers. Clin mattresses and water-mattresses. Acta Derm Venereol (Stockh)
Plast Surg 2007;34:735-48. 1983;63:227-30.
7. Bliss MR. Acute pressure area care: Sir James Paget's legacy. Lancet 42. Thomas DR. Are all pressure ulcers avoidable? J Am Med Dir Assoc
1992;339:221-3. 2003;4(2 Suppl):S43-8.
8. Stekelenburg A, Gawlitta D, Bader DL, Oomens CW. Deep tissue 43. Thomas DR, Osterweil D. Is a pressure ulcer a marker for quality of
injury: how deep is our understanding? Arch Phys Med Rehabil care? J Am Med Dir Assoc 2005;6:228-30.
2008;89:1410-3. 44. Witkowski JA, Parish LC. The decubitus ulcer: skin failure and
9. Papanikolaou P, Lyne P, Anthony D. Risk assessment scales for destructive behavior. Int J Dermatol 2000;39:894-6.
pressure ulcers: a methodological review. Int J Nurs Stud 2007;44: 45. Bates-Jensen BM, Cadogan M, Osterweil D, et al. The minimum data
285-96. set pressure ulcer indicator: does it reflect differences in care processes
10. Spiesman MG. Bedsores (decubitus). Am J Surg 1937;36:17-21. related to pressure ulcer prevention and treatment in nursing homes?
11. Extonsmith A. Prevention of pressure sores. Lancet 1961;278:1364. J Am Geriatr Soc 2003;51:1203-12.
532 C. Campbell, L.C. Parish

46. Worley CA. Skin failure: the permissible pressure ulcer? Dermatol Nurs 50. Lobmann R, Ambrosch A, Schultz G, Waldmann K, Schiweck S,
2007;19:384-5. Lehnert H. Expression of matrix-metalloproteinases and their inhibitors
47. U.S. Department of Health and Human Services. The treatment of in the wounds of diabetic and non-diabetic patients. Diabetologia
pressure ulcers. Rockville (Md): U.S. Dept. of Health and Human 2002;45:1011-6.
Services, Public Health Service, Agency for Health Care Policy and 51. Broadbent E, Petrie KJ, Alley PG, Booth RJ. Psychological stress
Research; 1994. Available at: http://www.ncbi.nlm.nih.gov/bookshelf/ impairs early wound repair following surgery. Psychosom Med
br.fcgi?book=hsahcpr&part=A5124. Accessed: April 13, 2010. 2003;65:865-9.
48. Christian LM, Graham JE, Padgett DA, Glaser R, Kiecolt-Glaser JK. 52. Vileikyte L. Stress and wound healing. Clin Dermatol 2007;25:49-55.
Stress and wound healing. Neuroimmunomodulation 2006;13:337-46. 53. Wall Street Journal. Opinion: King Canute at the G-8. WSJ July 13, 2009,
49. Cole-King A, Harding KG. Psychological factors and delayed healing A-11. Available at: http://online.wsj.com/article/SB124718309166920285.
in chronic wounds. Psychosom Med 2001;63:216-20. html. Accessed: Feb 5, 2010.