Pressure Ulcer

Syed Rafay H. Zaidi; Sandeep Sharma.

Author Information and Affiliations

Last Update: August 9, 2022.

Go to:

Continuing Education Activity

Pressure ulcers are skin or soft tissue injuries that form due to
prolonged pressure exerted over specific areas of the body. They should
receive prompt treatment; otherwise, complications associated with
these injuries can be fatal. The cornerstone of treatment is to reduce the
pressure exerted at the site of the lesion. Treatment options vary
according to the stage/grade of the pressure ulcer. This activity involves
the etiology, pathophysiology, and histopathology of the pressure
ulcers, as well as highlighting evaluation and treatment options based
on an interprofessional approach, so that patient care and outcomes are
optimal.
Objectives:
 Describe different etiological factors that cause pressure ulcers.
 Identify various medical conditions that lead to pressure ulcers.
Explain complications that result from these ulcers.
 Outline treatment options based on grade and complication of
pressure ulcer.
 Explain the importance of coordination and communication
amongst the interprofessional team to enhance optimum patient
care and improve patient outcomes.
Access free multiple choice questions on this topic.
Go to:

Introduction
Decubitus ulcers, also termed bedsores or pressure ulcers, are skin and
soft tissue injuries that form as a result of constant or prolonged
pressure exerted on the skin. These ulcers occur at bony areas of the
body such as the ischium, greater trochanter, sacrum, heel, malleolus
(lateral than medial), and occiput. These lesions mostly occur in people
with conditions that decrease their mobility making postural change
difficult. Jean-Martin Charcot was a French doctor in the 19th century
who studied many diseases, including decubitus ulcers. He noticed that
patients who developed eschar of the buttocks and sacrum died after
some time. He named this lesion "decubitus ominous," which meant
death was inevitable after developing this lesion.[1]
Go to:

Etiology
The development of decubitus ulcers is complex and multifactorial.
Loss of sensory perception, locally and general impaired loss of
consciousness, along with decreased mobility, are the most important
causes that aid in the formation of these ulcers because patients are not
aware of discomfort and hence do not relieve the pressure.[2] Both
external and internal factors work simultaneously, forming these ulcers.
External factors; pressure, friction, shear force, moisture, and internal
factors; fever, malnutrition, anemia, and endothelial dysfunction speed
up the process of these lesions.[3]
Immobility of as little as two hours in a bedridden patient or patient
undergoing surgery is sufficient to create the basis of a decubitus ulcer.
[3]
The dysfunction of nervous regulatory mechanisms responsible for the
regulation of local blood flow is somewhat culpable in the formation of
these ulcers.[4] Prolonged pressure on tissues can cause capillary bed
occlusion and, thus, low oxygen levels in the area. Over time, the
ischemic tissue begins to accumulate toxic metabolites. Subsequently,
tissue ulceration and necrosis occur.
Patients with the following conditions exhibit a predisposition to
decubitus ulcers:
  Neurologic disease
 Cardiovascular disease
 Prolonged anesthesia
 Dehydration
 Malnutrition
 Hypotension
 Surgical patients
Go to:

Epidemiology
Decubitus ulcers are a significant health care problem worldwide,
which affects several thousand people each year.[3] Their management
costs billions of dollars per annum, burdening the already scarce health
economy.
Sacral decubitus ulcers usually occur in elderly patients. Patients who
are incontinent, paralyzed, or debilitated are more prone to getting
them. Patients with normal sensory status, mobility, and mental status
are less likely to form these ulcers because their normal physiologic
feedback system leads to frequent physical positional shifts. As stated
above, elderly patients are more prone to sacral decubitus ulcers; two-
thirds of ulcers occur in patients who are over 70 years old. There is
data that shows 83% of hospitalized patients with ulcers developed
them within five days of their hospitalization.[3]
A study done in a medical research center in Turkey concluded that 360
patients out of 22834 admitted patients developed one or more pressure
ulcers. Most of the patients who developed pressure ulcers were
admitted to the intensive care unit (ICU).[5]
Go to:

Pathophysiology
Decubitus ulcer formation is multifactorial (external and internal
factors), but all of these result in a common pathway leading to
ischemia and necrosis. Tissues can sustain an abnormal amount of
external pressure, but constant pressure exerted over a prolonged period
is the main culprit. External pressure must exceed the arterial capillary
pressure (32 mmHg) to impede blood flow and must be greater than the
venous capillary closing pressure (8 to 12 mmHg) to impair the return
of venous blood. If the pressure above these values is maintained, it
causes tissue ischemia and further results in tissue necrosis.[6] This
enormous pressure can be exerted due to compression by a hard
mattress, railings of hospital beds, or any hard surface with which the
patient is in contact.
Friction caused by skin rubbing against surfaces like clothing or
bedding can also lead to the development of ulcers by contributing to
breaks in the superficial layers of the skin. Moisture can cause ulcers
and worsen existing ulcers via tissue breakdown and maceration.
Go to:

Histopathology
Histological studies of the decubitus ulcer extent, which include blanch
able erythema, non-blanch able erythema, decubitus dermatitis,
decubitus ulcer, and black scab/gangrene, show a dynamic process. The
initial change occurs in the vessels of the papillary dermis. After this
follows the necrosis of skin structures. The scab/gangrene is a full-
thickness defect that is due to either persistent ischemia and anoxemia
or a sudden occlusion of large vessels due to shear injury.[7]
Detailed analysis of chronic pressure ulcers showed the presence of
densely aggregated bacterial colonies, often present in the extracellular
matrix, but these findings were not present in acutely developed ulcers.
[8]
Go to:

History and Physical

In most instances, decubitus ulcers are reported by a patient’s attendant.
This is because the lack of sensation at the site of the lesion makes the
patient unaware of his injury. There might be staining of the patient’s
clothes or bedsheets due to pus or blood discharge. The clinical
presentation may vary between different sites of the body as skin, soft
tissue, and muscle resist differently to external pressure. The muscle
becomes ischemic and necrotic before skin breakdown can occur,
which can be deceiving to the clinician’s observation undermining the
depth or extent of the ulcer.
The following require examination in a patient with a decubitus ulcer:
 Ulcer history, including etiology, duration, and previous
treatment (if any)
 Staging by thoroughly examining the depth of the wound, which
this activity will cover in detail under "staging."
 Size (length, width)
 Sinus tracts, undermining, and tunneling
 The presence of drainage
 The presence of necrotic tissue
A detailed discussion of the history and associated conditions follows
under "evaluation."
Go to:

Evaluation
The initial evaluation of patients with pressure injuries involves a
detailed history, and the clinician should gather the following:
 Duration of immobility or being bedridden
 Duration of hospital stay
 Associated medical cause that has caused the injury (e.g.,
paraplegia, quadriplegia, stroke, road traffic accident (RTA) that
might have resulted in immobility
  The natural history of the injury; the site at which it first
developed. Did it increase in size? How long has the injury been
present?
 A brief history of any systemic diseases is also necessary.
Diseases like diabetes mellitus, peripheral vascular disease, and
malignancy prevent or slow down wound healing.
 If the patient can precisely localize the site of the ulcer or localize
any associated pain because most of the time, the ulcers are
painful, but the patient is unaware because either he has
paraplegia or is in a critical condition.
 Is there any discharge or foul odor from the ulcer site? These may
specify the worsening of the lesions.
Go to:

Treatment / Management
Managing decubitus ulcers is complicated as there is no fixed treatment
regime or algorithm. Once it has developed, there should be no delay in
treatment, and management should start immediately.[9] Treatment
varies between site, stage, and associated complications of the ulcer.
The goal of all the various treatment options is to; minimize the
pressure exerted on the ulcer, minimize contact of the ulcer with a hard
surface, decrease moisture, and to keep it as aseptic or least septic as
possible. The choice of treatment options should be according to the
stage/grade of the ulcer, and what the purpose of the treatment should
be (decreasing moisture, removal of necrotic tissue, controlling
bacteremia).
Prevention is clearly the best treatment with excellent skincare,
pressure dispersion cushions, and support surfaces. Support surfaces
decrease the amount of pressure on the wound. Support surfaces can be
either static (e.g., air, foam, and water mattress overlays) or dynamic
(e.g., alternating air overlay). Repositioning and turning the patient
every two hours can also lessen pressure on the area, but some patients
may require more frequent repositioning, while others may require less
frequent repositioning.[10]
In some cases, urinary and fecal diversion may be necessary depending
on the site of the ulcer, being prone to urine or fecal contamination.
Hydrocolloid dressings should be used. Good antibiotic cover decreases
septicemia.
The depth and severity of the ulcer determine whether surgical
management may be required. The ulcer must be thoroughly cleaned
and drained to remove any dead tissue and debris. Vacuum-assisted
closure (VAC) may be a preoperative option to provide a favorable
wound for the surgical closer.[11] Surgical management aims to fill the
dead space and provide durable skin through flap reconstruction.
There is also some evidence to suggest that hyperbaric oxygen therapy
can help with wound healing, as it improves oxygenation in and around
the area of the wound.[12]
Thus, the treatment of decubitus ulcers has its basis on the following:
 Prevention of additional ulcers
 Decreasing pressure on the wound
 Wound management
 Surgical intervention
 Improving the nutritional status
For the most part, stage I and II ulcers do not require operative
measures. Stage 3 and 4 ulcers may require surgical intervention.
Go to:

Differential Diagnosis
The differential diagnosis of sacral decubitus ulcers include[2]:
 Diabetic ulcers
 Venous ulcers
 Pyoderma gangrenosum
 Osteomyelitis
 Go to:

Staging
There are many different ways to stage sacral decubitus ulcers. The
most widely accepted classification system is the National Pressure
Ulcer Advisory Panel (NPUAP) system.[3] It uses ulcer depth as a way
to classify these ulcers.
The stages are as follows:
 Stage I: The skin is intact with the presence of non-blanchable
erythema.
 Stage II: There is partial-thickness skin loss involving the
epidermis and dermis.
 Stage III: There is a full-thickness loss of skin that extends to the
subcutaneous tissue but does not cross the fascia beneath it. The
lesion may be foul-smelling.
 Stage IV: There is full-thickness skin loss extending through the
fascia with considerable tissue loss. There might be possible
involvement of the muscle, bone, tendon, or joint.
Go to:

Prognosis
There have been many studies researching the prognosis and outcomes
for patients with sacral decubitus ulcers, but given the different
treatment regimens, the prognosis varies. One showed that 53% of
pressure ulcers healed within 42 days when "sheng-ji-san"-a Chinese
herbal medicine, was used as a dressing.[13] Another study showed
that no ulcer ever healed completely.[14]
Although outcomes have been difficult to study, there is general
agreement that most of the time, lifelong treatment and prevention
measures are necessary for these patients. Patients with sacral decubitus
ulcers are at high risk of recurrence.[15]
Go to:
Complications
Complications often develop with decubitus ulcers. The most common
problem is infection. Grade III and IV ulcers require management
intensively as their complications can be life-threatening. Microbial
analysis has shown that both aerobic and anaerobic bacteria are present
in the lesions.[16] If the infection spreads to deeper tissues and the
bone it can result in; periostitis (infection of the layer covering the
bone), osteomyelitis (infection of a bone), septic arthritis (infection of a
joint), and formation of sinuses (abnormal cavity formed by loss of
tissue). The invasion of the infective agent results in fatal consequences
because septicemia is challenging to manage in an already debilitated
patient.
These wounds are catabolic (meaning that they use up a lot of energy).
The catabolic nature of these ulcers causes severe fluid and protein
loss, which can result in hypoproteinemia or malnutrition. Up to 50
grams of body protein can be lost daily due to a draining ulcer.[16]
Chronic decubitus ulcers can cause chronic anemia or secondary
amyloidosis. Anemia also occurs secondary to chronic water loss and
bleeding.[16]
If there is inadequate postoperative care complications secondary to
reconstructive surgery can occur. These include hematoma or seroma
formation, wound dehiscence, abscess formation, or postoperative
wound sepsis.
Go to:

Postoperative and Rehabilitation Care

Postoperative care of patients who have undergone reconstructive
surgery is of utmost significance as these ulcers have high rates of
recurrence. A study done on characteristics of recurrent pressure ulcers
showed that patients who underwent reconstructive surgery and
developed post-operative, had an 11% to 19% chance of recurrence.
Those without any postoperative complications had recurrence as high
as 61%.[17]
When medical staff shift patients from the operating table to their air-
fluid beds, they must avoid excessive shearing, and stretch on skin
flaps. For the first four weeks, patients are positioned flat on their
support surfaces, after which they can place themselves in a semi-
sitting position. The patient starts to sit for 10 minutes only after six
weeks of the surgical procedure. After these sitting periods, the flap
should be examined for discoloration and wound edge separation. Over
two weeks, the sitting periods will increase to 2 hours in 10-minute
increments. Patients will also learn to lift for 10 seconds every 10
minutes to relieve pressure. Meticulous skin care is necessary.
Go to:

Consultations
Managing decubitus ulcers should always be done with an
interprofessional approach. Usually, a general surgery consultation is
necessary for patients with sacral decubitus ulcers, especially for those
with deep ulcers. A wound care specialist or a dermatologist is
involved in non-healing ulcers. If any associated medical conditions
affect the wound healing process, an internal medicine specialist should
have involvement in the management of the case. Patients who have
contractures or have spastic paralysis have regular physiotherapies.
Go to:

Deterrence and Patient Education

Patients and their family members should have a clear idea that
preventing recurrence requires commitment and responsibility. They
should receive education on how to manage their condition in the
hospital and as well as in their homes. They should be familiar with
warning signs like skin discoloration, ulceration, discharge, or a foul
smell from the ulcer site and body areas with decreased or no sensation.
The patient should move or turn every 2 hours; it could not be done by
themselves, or they should ask someone to help them. Air or water
mattress should be used in their homes too. Their food intake should be
adequate and should consist of a balanced and healthy diet. Active
mattress use leads to significant improvements in resting blood flow,
post-occlusive reactive hyperemia, and baseline skin temperature.
These results suggest that active mattress use can improve endothelial
function.[18]
Go to:

Pearls and Other Issues

Decubitus ulcers occur when there is prolonged pressure on specific
areas of the body that are susceptible to friction and shear force
injuries. Pressure ulcers vary in size, depth, and chronicity. There is a
grading system in place for pressure ulcers, which helps guide
treatment. Consulting with a wound care specialist and/or general
surgery can also help guide treatment.
Go to:

Enhancing Healthcare Team Outcomes

The main goal is to prevent a decubitus ulcer by decreasing the
pressure acting on the affected site. This goal requires an
interprofessional team, including primary care providers, wound care
specialists, surgeons, specialty-trained wound nurses, physical
therapists, and nurses aides. Nurses provide care, monitor patients, and
notify the team of issues. Nurses aides are often responsible for turning
and repositioning patients. [Level 5] Air-fluidized or foam mattresses
should be used, frequent postural changes, provision of adequate
nutrition, and treatment of any underlying systemic illnesses.
Debridement should take place to remove dead tissue that serves as the
optimum medium for the growth of bacteria. Hydrogels or hydrocolloid
dressing should be used, which aid in wound healing.[19] Tissue
cultures are necessary, so the most directed antibiotic can be
administered, which can involve the pharmacist and the latest
antibiogram data. The patient should be kept pain-free by giving
analgesics. They should try to increase physical activity if possible,
which a nurse's aide, medical assistant, or rehab nurse can facilitate.
Frequent follow-ups are an absolute necessity and a team approach to
patient education and management involving the wound care nurse and
wound care clinician will lead to the best results. These
interprofessional activities can help drive better outcomes for patients
with decubitus ulcers. [Level 5]
Each year around 60000 patients die due to complications of decubitus
ulcers.[19] Therefore patients with these injuries should get prompt
treatment, as worsening of this condition increases the risk of mortality
and increased healthcare costs.
Go to:

Review Questions
 Access free multiple choice questions on this topic.
 Comment on this article.

Figure

Photo of pressure ulcer with ischium protruding. Contributed From

Wikimedia User Noles1984 (Public Domain) Noles1984 grants anyone
the right to use this work for any purpose, without any conditions,
unless such conditions are required by law.

Figure

Close up shot of Stage 4 Ulcer. Contributed From Wikimedia User

Essent (Public Domain) Essent grants anyone the right to use this work
for any purpose, without any conditions, unless such conditions are
required by law.

Figure
Example of a pressure ulcer. Contributed From Pflegewiki-User
Mennfield (CC BY-SA 3.0 https://creativecommons.org/licenses/by-
sa/3.0/deed.en)

Figure

Stages of Ulcers. Contributed by Wikimedia User Sadegh

Babagolzadeh (CC BY-SA 3.0
https://creativecommons.org/licenses/by-sa/3.0/deed.en)
Go to:

References
1.
Levine JM. Historical perspective on pressure ulcers: the
decubitus ominosus of Jean-Martin Charcot. J Am Geriatr
Soc. 2005 Jul;53(7):1248-51. [PubMed]
2.
Anders J, Heinemann A, Leffmann C, Leutenegger M, Pröfener
F, von Renteln-Kruse W. Decubitus ulcers: pathophysiology and
primary prevention. Dtsch Arztebl Int. 2010 May;107(21):371-
81; quiz 382. [PMC free article] [PubMed]
3.
Bansal C, Scott R, Stewart D, Cockerell CJ. Decubitus ulcers: a
review of the literature. Int J Dermatol. 2005 Oct;44(10):805-
10. [PubMed]
4.
van Marum RJ, Meijer JH, Ribbe MW. The relationship between
pressure ulcers and skin blood flow response after a local cold
provocation. Arch Phys Med Rehabil. 2002 Jan;83(1):40-
3. [PubMed]
5.
Leblebici B, Turhan N, Adam M, Akman MN. Clinical and
epidemiologic evaluation of pressure ulcers in patients at a
university hospital in Turkey. J Wound Ostomy Continence
Nurs. 2007 Jul-Aug;34(4):407-11. [PubMed]
 6.
Gefen A. Reswick and Rogers pressure-time curve for pressure
ulcer risk. Part 1. Nurs Stand. 2009 Jul 15-21;23(45):64, 66, 68
passim. [PubMed]
7.
Witkowski JA, Parish LC. Histopathology of the decubitus
ulcer. J Am Acad Dermatol. 1982 Jun;6(6):1014-21. [PubMed]
8.
Rhoads DD, Wolcott RD, Percival SL. Biofilms in wounds:
management strategies. J Wound Care. 2008 Nov;17(11):502-
8. [PubMed]
9.
Pressure ulcer treatment. Agency for Health Care Policy and
Research. Clin Pract Guidel Quick Ref Guide Clin. 1994 Dec;
(15):1-25. [PubMed]
10.
McInnes E, Jammali-Blasi A, Bell-Syer SE, Dumville JC,
Middleton V, Cullum N. Support surfaces for pressure ulcer
prevention. Cochrane Database Syst Rev. 2015 Sep
03;2015(9):CD001735. [PMC free article] [PubMed]
11.
Batra RK, Aseeja V. VAC Therapy in Large Infected Sacral
Pressure Ulcer Grade IV-Can Be an Alternative to Flap
Reconstruction? Indian J Surg. 2014 Apr;76(2):162-4. [PMC free
article] [PubMed]
12.
Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus
SE, Weibel S. Hyperbaric oxygen therapy for chronic
wounds. Cochrane Database Syst Rev. 2015 Jun
24;2015(6):CD004123. [PMC free article] [PubMed]
13.
Hsu YC, Chang HH, Chen MF, Chen JC. Therapeutic effect of
sheng-ji-san on pressure ulcers. Am J Chin Med. 2000;28(3-
4):391-9. [PubMed]
14.
Ferrell BA. Pressure ulcers. Assessment of healing. Clin Geriatr
Med. 1997 Aug;13(3):575-86. [PubMed]
 15.
Qaseem A, Humphrey LL, Forciea MA, Starkey M, Denberg
TD., Clinical Guidelines Committee of the American College of
Physicians. Treatment of pressure ulcers: a clinical practice
guideline from the American College of Physicians. Ann Intern
Med. 2015 Mar 03;162(5):370-9. [PubMed]
16.
Teasell R, Dittmer DK. Complications of immobilization and bed
rest. Part 2: Other complications. Can Fam Physician. 1993
Jun;39:1440-2, 1445-6. [PMC free article] [PubMed]
17.
Bates-Jensen BM, Guihan M, Garber SL, Chin AS, Burns SP.
Characteristics of recurrent pressure ulcers in veterans with spinal
cord injury. J Spinal Cord Med. 2009;32(1):34-42. [PMC free
article] [PubMed]
18.
Baker G, Bloxham S, Laden J, Gush R. Vascular endothelial
function is improved after active mattress use. J Wound
Care. 2019 Oct 02;28(10):676-682. [PubMed]
19.
Al Aboud AM, Manna B. StatPearls [Internet]. StatPearls
Publishing; Treasure Island (FL): Apr 19, 2023. Wound Pressure
Injury Management. [PubMed]
20.
Chou R, Dana T, Bougatsos C, Blazina I, Starmer AJ, Reitel K,
Buckley DI. Pressure ulcer risk assessment and prevention: a
systematic comparative effectiveness review. Ann Intern
Med. 2013 Jul 02;159(1):28-38. [PubMed]
21.
Gaspar S, Peralta M, Marques A, Budri A, Gaspar de Matos M.
Effectiveness on hospital-acquired pressure ulcers prevention: a
systematic review. Int Wound J. 2019 Oct;16(5):1087-
1102. [PMC free article] [PubMed]
22.
Mervis JS, Phillips TJ. Pressure ulcers: Pathophysiology,
epidemiology, risk factors, and presentation. J Am Acad
Dermatol. 2019 Oct;81(4):881-890. [PubMed]
 23.
Kottner J, Cuddigan J, Carville K, Balzer K, Berlowitz D, Law S,
Litchford M, Mitchell P, Moore Z, Pittman J, Sigaudo-Roussel D,
Yee CY, Haesler E. Pressure ulcer/injury classification today: An
international perspective. J Tissue Viability. 2020
Aug;29(3):197-203. [PubMed]
Disclosure: Syed Rafay Zaidi declares no relevant financial relationships
with ineligible companies.

Disclosure: Sandeep Sharma declares no relevant financial relationships

with ineligible companies.
Copyri