Published online: 27.11.

2019

Review Article

Pressure ulcers: Back to the basics

Karoon Agrawal, Neha Chauhan

Department of Burns, Plastic and Maxillofacial Surgery, VM Medical College and Safdarjang Hospital, New Delhi, India

Address for correspondence: Dr. Karoon Agrawal, Department of Burns, Plastic and Maxillofacial Surgery, VM Medical College and
Safdarjang Hospital, New Delhi, India E-mail: [email protected]

ABSTRACT
Pressure ulcer in an otherwise sick patient is a matter of concern for the care givers as well as the
medical personnel. A lot has been done to understand the disease process. So much so that USA
and European countries have established advisory panels in their respective continents. Since
the establishment of these organizations, the understanding of the pressure ulcer has improved
significantly. The authors feel that the well documented and well publicized definition of pressure
ulcer is somewhat lacking in the correct description of the disease process. Hence, a modified
definition has been presented. This disease is here to stay. In the process of managing these
ulcers the basic pathology needs to be understood well. Pressure ischemia is the main reason
behind the occurrence of ulceration. Different extrinsic and intrinsic factors have been described in
detail with review of literature. There are a large number of risk factors causing ulceration. The risk
assessment scales have eluded the surgical literature and mostly remained in nursing books and
websites. These scales have been reproduced for completion of the basics on decubitus ulcer. The
classification of the pressure sores has been given in a comparative form to elucidate that most of
the classifications are the same except for minor variations. The management of these ulcers is
ever evolving but the age old saying of “prevention is better than cure” suits this condition the most.

KEY WORDS
Bed sore; decubitus ulcer; pressure ulcer; prevention; risk factors; ulcer

HISTORY In Persia, Avicenna used a variety of topical applicants on

wounds. In Arabia, Maimonides recommended nutritional

P
ressure ulcers have been recognized as a disease support to promote ulcer healing. A wide variety of
entity since ages. Pressure sores have been found topical remedies like honey, moldy bread, meat, animal
in Egyptian mummies, some of which are more than and plant extracts, copper sulfate, zinc oxide and alum
5,000 years old. Egyptians used honey for the treatment have been used in the past.[1]
of such ulcers and wounds.
Hippocrates (460-370 B.C) had described pressure ulcer
in association with paraplegia with bladder and bowel
Access this article online dysfunction.[2] During the renaissance, Ambrose Paré, a 16th
Quick Response Code: century French army barber-surgeon and founding father
Website:
of medical surgical practice, wrote in his autobiography
www.ijps.org
about a wounded French aristocrat developing a pressure
DOI: ulcer. He mentioned cure with good nutrition, pain relief
10.4103/0970-0358.101287 and debridement; which is no different than the present
modality to some extent.[3]
Indian Journal of Plastic Surgery May-August 2012 Vol 45 Issue 2 244
 Agrawal and Chauhan: Pressure ulcers: Back to the basics

In 19th century, Jean-Martin Charcot studied decubitus PRESSURE ULCER ADVISORY PANELS
ulcers and subscribed to the “neurotrophic theory” for
the causation of ulcer rather than the “pressure” as we The National Pressure Ulcer Advisory Panel (NPUAP) is
believe today. Charcot directly related the occurrence of an independent American organization established in
ulcer to the damage to central nervous system. ‘Decubitus 1987. This non-profit organization deals with prevention,
ominosus’ was the term given to ulcer covered with management and research on pressure ulcers. Similarly
eschar as it caused high mortality. Charcot described EPUAP was formed in December 1996 in London to support
the decubitus ulcer in detail with its complications like prevention and prepare guidelines for the management
‘gangrenous pulmonary metastasis (infiltration)’ and of pressure ulcer in all the European countries. Their
spinal cord invasion. However, Brown-Sequard opposed mission statement reads as “to provide for the relief of
this theory and proved that if the pressure is avoided in persons suffering from or at risk of pressure ulcers, in
guinea pigs with spinal cord injury, the ulcer does not particular through research and the education of the
develop and the existing ulcer heals on relieving the public.”
pressure.[4] According to Ayurveda bed-sore is termed as
“SayyajVrava”; ‘Sayyaj’ meaning bed and ‘vrava’ is ulcer EPIDEMIOLOGY
or wound. Due to pressure ‘mamsadhatu’ (circulation) is
affected and results in bedsore. Pressure ulcers have been described as one of the most
costly and physically debilitating complications in the 20th
During the nineteenth century, discovery of bacteria by century.[6] Pressure ulcers are the third most expensive
Pasteur, antisepsis by Lister and X-ray by Roentgen changed disorder after cancer and cardiovascular diseases.
the understanding of these ulcers in general. The twentieth
century brought in antibiotics which changed the scenario In Japanese Geriatric Health Services facility, the immobile
further. The later part of twentieth century witnessed geriatric patients represent 91% of total population with
studies on nutrition, trace elements, biomechanics and pressure ulcer in the Geriatric Health Service facility.[7]
newer methods of management of these ulcers.
The incidence of pressure ulcers is different in each clinical
DEFINITIONS setting. Incidence rates of as low as 0.4% to as high as 38%
have been reported in the inpatient department while
Pressure ulcer is commonly termed as bed-sore, decubitus prevalence has been reported as 3.5% to 69%.[8-11] In long
ulcer or pressure sore and sometimes as pressure term care facilities, the reported incidence is between
necrosis or ischemic ulcer. The term pressure ulcer was 2.2% to 23.9% while in home care setting the incidence
popularized by the Agency for Healthcare Research and varies from 0 to 17%.[8] In a study from Ankara, Turkey it was
Quality. Pressure ulcer has been defined as “an area of found that 59.2% of these ulcers occur in patients admitted
unrelieved pressure usually over a bony prominence to the intensive care unit. The acceptable incidence rates
leading to ischemia, cell death and tissue necrosis”. for all settings should ideally be less than 2%. Two thirds of
This definition has been further refined by the National pressure sores occur in the elderly above 70 years of age.
Pressure Ulcer Advisory Panel (NPUAP) and European They are also common in young patients with neurological
Pressure Ulcer Advisory Panel (EPUAP) as “localized impairment. In Indian setting, the prevalence of pressure
injury to the skin and/or underlying tissue usually over a ulcers in hospitalized patients has been reported to be
bony prominence as a result of pressure, or pressure in 4.94% in a study conducted by Chauhan et al.[12]
combination with shear and/or friction”.[5]
There are many studies on the incidence of pressure
Both these definitions fall short of the complete ulcer. In spinal cord injury patients, pressure ulcer occurs
description of pressure ulcer. So, we have proposed a in 30-85% of patients during the first month of injury.[13-16]
modification of this definition. We define pressure ulcer Also, paraplegics and quadriplegics are likely to have
as “an area of localized soft tissue ischemic necrosis multiple ulcers.[17,18]
caused by prolonged pressure higher than the capillary
pressure with or without shear, related to posture which Patients with pressure ulcers have high mortality rates.
usually occurs over a bony prominence”. Ueda et al, 1990 have reported 22% mortality over 6

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 Agrawal and Chauhan: Pressure ulcers: Back to the basics

years follow up of 23 patients with pressure ulcers.[19] skin, subcutaneous fat, muscle and fascia if any between
Kuwahara et al. 2005 reported 68.8% mortality amongst the bony prominence and the pressure causing surface. If
elderly patients with NPUAP stage 3 and 4 pressure ulcers, subcutaneous necrosis occurs, ulceration will be clinically
because of secondary systemic complications.[20] seen when the necrotic skin gives way. Hussain reported
that for a specific pressure the obliteration of skin and
These data indicate that presence of pressure ulcer subcutaneous vessels is more as compared to those of
hampers quality of life and prevention of pressure ulcer the underlying muscle.[21] But the tissue damage is more in
is an important goal. Not surprisingly the hospital stay is the muscle after mechanical loading than in the skin.[22,23]
longer in these patients with increased risk of nosocomial Because of this the existing staging of pressure sores may
and renal infections. The hospital re-admission rate is also not be justifiable. This needs to be studied further before
very high. Pressure ulcers result in an exponential increase any change in the prevailing staging is recommended.
in the healthcare burden and financial requirement for these
patients. This brings us to the information on etiology and One may question why different points in the body have
risk factors so that one can work on these factors for the different prevalence of ulceration. The variation in the
prevention of pressure ulcers in susceptible patients. pressure at different points during common postures is
one explanation. The average pressure over the ischial
ETIOPATHOGENESIS tuberosity and the surrounding area exceeds 100 mm Hg
during sitting,[24] at the sacral region it is 40-60 mm Hg
Pressure between the bony prominence and external in the supine position, while it is 70-80 mm Hg over the
surface occludes the capillaries. The normal capillary trochanteric region in the lateral lying down position.
pressure ranges from 16 to 33 mm Hg in different
segments. External pressure of more than 33 mm Hg Another reason for the differential incidence is the
occludes the blood vessel so that the underlying and difference in the amount of soft tissue between the skin and
surrounding tissues become anoxic and if the pressure the bony prominences. Sacrum and trochanters are devoid
continues for a critical duration, cell death will occur, of much soft tissue covering. Effectively the skin directly
resulting in soft tissue necrosis and eventual ulceration. covers these pressure points with very little interposition
of soft tissue cushion, thus increasing the risk of ulceration
As the new definition suggests, prolonged pressure is as compared to the rest of the body [Figures 1-3].
the leading contributing factor. It has been proven that
there is an inverse relationship between the degree of The “sling effect” of the skin and subcutaneous tissue over
pressure and the duration of pressure. Uninterrupted the bony prominence is another interesting explanation.
higher pressure requires shorter time while continuous This sling effect prevents transmission of full pressure at
lower pressure will require longer time to cause tissue deeper level, hence the impact of body pressure on the
necrosis and pressure ulceration. subcutaneous tissue is reduced to some extent.[25]

Application of high pressure for shorter duration not PATHOPHYSIOLOGY

only causes tissue necrosis due to blockage of capillaries
but also produces pressure effect on the larger vessels A lot of research has been undertaken to study the
causing thrombosis, more often venous thrombosis. mechanism of tissue necrosis. It has been found that
Hence, the deleterious effect of high pressure for short many intrinsic and extrinsic factors have an impact on the
duration is much more than that of low pressure for a level and extent of tissue trauma. Extrinsic factors remain
longer duration. This has been proven by the observation the main causative factors or the primary factors with
that when the high pressure is relieved, ischemia persists “pressure” heading the list while intrinsic factors also called
because of effects on the adjacent larger vessels; while on secondary factors contribute to it. The factors contributing
relief from low pressure, the normal hyperemic response to the formation of pressure ulcers are enlisted in Table 1.
compensates for the temporary ischemia and the tissue
does not undergo degeneration. The dermal collagen fibers are also likely to protect
against external pressure. Similarly the interstitial fluid
Due to the effect of pressure, the ischemic degenerative acts as buffer and maintains the tissue hydrostatic
changes occur at all the levels simultaneously affecting the pressure.[26--35]
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 Agrawal and Chauhan: Pressure ulcers: Back to the basics

a b
Figure 1: (a) Left sided ischial pressure ulcer with multiple sinuses in a paraplegic patient. Sinuses are highlighted with arrows. Gluteus maximus muscle has been
marked for raising as a muscle flap (b) Complete excision of the ulcer with excision of sinuses has been done. The gluteus maximus muscle flap has been used to
cover the ischial tuberosity and for filling the cavity

a b
Figure 2: (a) A large sacral ulcer(b) Sacral ulcer has been managed with transverse back flap

a b c
Figure 3: (a) Left trochanteric pressure ulcer with a small external wound (b) The ulcer after debridement of the ulcer edge and the underlying bursa. One can
notice the large wound under a small and deceptive pressure ulcer (c) Bilateral Trochanteric pressure ulcers have been resurfaced with bilateral tensor fascia lata
myocutaneous flaps

Pressure Pressure effect is directly proportional to the body weight

Pressure is the perpendicular load or force exerted on a and the duration for which it is applied and is inversely
unit area of the body. proportional to the surface area of the skin in contact. The
unit pressure is determined not only by the body weight
Pressure = body weight/skin contact surface area. but by the stiffness and composition of the tissues too.

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 Agrawal and Chauhan: Pressure ulcers: Back to the basics

Table 1: Factors contributing to the formation of operation table because of gravity or when the patient
pressure ulcers
is turned and pushed on the bed without lifting him/her
Extrinsic factors (etiological /patho -mechanical/primary factors)
Undue and prolonged pressure off the surface.
Shear
Friction So, shear causes tissue damage differently, however,
Moisture
the damage is produced concomitant with pressure. It
Abnormal posture
Impaired mobility is difficult to create pressure without shear and shear
Intrinsic factors (pathophysiological/secondary factors) without compression.[37]
Altered consciousness
Decreased or absent sensations
Friction
Nutritional factors (under- or over-nutrition)
Anemia
Friction between the skin and the stationary, surfaces,
Edema such as bed clothes results in the loss of stratum corneum.
Atherosclerosis This seems to be a trivial factor. However, this may
Age-related changes initiate the breach in the epidermis. Repeated friction
Acute illness
may lead to deeper injury. When there is loss of the
Sleep
Medications stratum corneum, there is a breach in the barrier against
Cardiovascular changes infection. If the underlying tissue is relatively ischemic, it
Emotional stress will get infected and result in deeper ulceration.
Smoking
Other factors
Recurrence of pressure ulcer
Moisture
Prolong hospital stay This is an important extrinsic factor. The extrinsic
Long duration of surgery (surgical immobility) moisture from perspiration, urine, feces and discharge
causes maceration of the skin surface. The macerated
What is the resultant critical capillary pressure below which skin forms blisters and is susceptible to breakdown.
ischemia occurs is still questionable. Constant pressure for Excessive moisture on the skin surface also weakens the
long period induces ischemia and causes reactive hyperemia. skin barrier and makes it more susceptible to pressure,
Muscles and subcutaneous tissues are more susceptible to shear and friction. This promotes the occurrence of
pressure induced injury than the skin, therefore pressure ulceration.
ulcers are generally worse than what they appear on the
skin surface. It has been rightly said that the wound that Position of the patient
is seen on the surface is just the tip of the iceberg and the This is an extrinsic factor which determines the pressure
major injury lies under the skin defect.[24] points which are likely to cause pressure ulceration.
Changes in body posture generates pressure at different
Apart from the direct effect of pressure causing ischemic
anatomical points in the body making them susceptible
tissue necrosis, the reperfusion after relieving the pressure
to pressure ulceration [Figures 4a-d].
leading to inflammatory tissue destruction by macrophages
also participates in the causation of ulceration.[36]
These bony points transmit the body weight and hence,
Shearing bear the brunt of pressure [Figures 5, 6]. In one of the
When the body tends to glide with gravity over a surface, studies ischial ulcer was the most common as the wheel
the skin and the subcutaneous tissue remain stationary chair bound patients spend long hours sitting, thus
and there is a differential movement of the underlying causing pressure on the ischial region. Trochanteric and
soft-tissue like muscle and fascia. This shearing is an sacral ulcers were the next common.[38]
important patho- mechanical factor. This forceful inter-
tissue plane movement causes stretching and tearing of Studies have measured the transcutaneous oxygen
blood vessels, reduced blood flow, stasis and ischemic tension at specific high risk pressure points during
tissue necrosis. This shearing may not directly cause any various postures on conventional as well as specialized
trauma to the skin surface. This usually occurs when beds. It has been proved that specialized beds maintain
a semi-reclining patient glides on the bed or on the better tissue oxygen tension in weight bearing tissues.[39]
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 Agrawal and Chauhan: Pressure ulcers: Back to the basics

a d
Figure 4: (a-d) Pressure points in sitting, supine, lateral and prone postures

Immobility vitamins and trace elements are critical factors in the

This is inter-related with posture/position of the patient. prevention of pressure ulceration. The patients with
Normal individual changes the posture frequently. Even negative nitrogen balance are at a high risk of tissue
during sleep, due to sensorimotor feedback system, a breakdown and delayed healing [Figure 7]. A patient
normal person periodically changes the posture in bed. with rapid weight loss needs close observation. Patients
This results in intermittent relief from pressure effect. with pressure ulceration or those prone to it should
This feedback system is impaired in neurologically have an intake of 30-35 kcal/kg/day with 1.25-1.5 gram
compromised patients and in those who have received of protein/ kg/day. Specific supplementation with vitamin
prolonged anesthesia or in sedated patients. The C, zinc and other trace elements needs to be assessed
body fails to make postural adjustments in response periodically in high risk patients.
to prolonged pressure and ischemia. The patients
undergoing prolonged surgery of more than 4 hours are Hemoglobin is a good indicator of the patient’s
at a higher risk of developing pressure ulcer as they tend nutritional status. Good hemoglobin is required for
to stay immobile for a much longer period during the tissue oxygenation. In anemic patients, oxygen carrying
perioperative period.[40] capacity of blood is reduced and hence, there is decreased
supply of oxygen to the tissues. This will precipitate
Neurological factors tissue necrosis in ischemic tissue because of mechanical
The loss of sensory perception or impaired level of pressure. Hence, well-nourished patients with good
consciousness prevents the patient from perceiving the pain hemoglobin will be able to tolerate the deleterious
of pressure and the need to relieve it. Similarly neurological effects of pressure better as compared to emaciated and
conditions causing paralysis or motor weakness prevents anemic patients.
change of posture when pressure is exerted. Surprisingly
poliomyelitis affected patients are less prone to pressure Edema
ulceration indicating that sensory loss is a more important An edematous tissue has a compromised circulation and it
factor. The sensation of pain and pressure prevents is poor in nutrition. Increased tissue fluid also decreases
prolonged pressure and hence, the ischemia. the tissue oxygenation and is more prone to ulceration.One
may think that edema fluid should have a cushioning effect
Metabolic and nutritional factors and decrease the unit pressure over the pressure point.
Adequate nutrition, positive nitrogen balance, hydration, However, increased interstitial tissue fluid causes increased
249 Indian Journal of Plastic Surgery May-August 2012 Vol 45 Issue 2
 Agrawal and Chauhan: Pressure ulcers: Back to the basics

Figure 5: Pressure ulcer over the lateral border of heal, lateral malleolus and
lateral border of fibula due to pressure in lateral posture
Figure 6: Pressure ulcer over the knee and thigh because of the pressure in
prone position

group in the unit. There are three scales in vogue. They

are Norton, Braden and Waterlow scales. These scales are
being reproduced from the original description.

An ideal risk assessment scale should have a high

sensitivity and specificity for being able to correctly
predict the risk of ulcer development. It should be easy
to use and the criteria should be clear and definitive and
applicable to different healthcare settings.[41]

Norton scale
Figure 7:Sacral pressure ulcer in a patient with 60% total body surface burn
Norton scale was developed by Doreen Norton et al. in
1962 [Table 2].[42]
pressure over the blood vessels, decreases the pressure
difference between the capillary blood and the tissue fluid The Norton scale does not consider nutritional factors,
and hence, decreases blood flow and oxygenation to the shearing forces and does not have a functional definition
tissues. Hence, edema does not prevent rather enhances of the applied parameters.
the deleterious effect of pressure.
‘Norton plus scale’ is a modified scale in which the
RISK FACTORS AND PRESSURE ULCER RISK presence of the following are noted.[29,43]
ASSESSMENT SCALES • Diabetes
• Hypertension
This aspect of pressure ulcer is not discussed adequately • Hematocrit – in males < 41%, in females < 36%
amongst surgeons. These are more often deliberated • Hemoglobin – in males <14gm %; in females < 12gm %
upon in nursing literature. However, the treating surgeons • Serum albumin level < 3.3 gm%
should also be well aware of the various risk factors and • Fever - temperature >99.6°F
the Risk Assessment Scales. • Prescription of  5 medications
• Changes in mental state within 24 hours to confused,
The extrinsic and intrinsic factors discussed above are lethargic.
the causative factors. There are a large number of other
factors which are called risk factors. These factors should Waterlow scale
be looked for during the pre-ulcer period for a proper Waterlow scale was devised by Judy Waterlow et al.
assessment of the risk of development of a pressure ulcer in 1987.[31,44,45] This is an incremental positive scoring
in a given patient. This is usually done by the nursing system. [Table 3] Waterlow scale has the risk of over
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 Agrawal and Chauhan: Pressure ulcers: Back to the basics

Table 2: Norton pressure ulcer risk assessment scale

Factor/score 4 3 2 1
Physical condition Good Weak Ill Very ill
Mental state Alert Apathetic Confused Stuporous
Activity Ambulant Walks with help Chair bound Bed-ridden
Mobility Full Slightly impaired Very limited Immobile
Incontinence No Occasional Usually urinary incontinence Double incontinence
Interpretation of scale Score of >18 – low risk
Score of 14-18 – medium risk
Score of 10-<14 – high risk
Score of <10 – very high risk

Table 3: Waterlow pressure ulcer risk assessment scale

Build/Weight for Height Score Skin type visual risk areas Score Sex & age Score Special risks
(Years)
Average 0 Healthy 0 Male 1 Tissue Malnutrition Score
(BMI= 20-24.9)
Above average (BMI= 25-29.9) 1 Tissue paper (Frail) 1 Female 2 Terminal Cachexia 8
Obese BMI= >30 2 Dry 1 14-49 1 Multiple organ failure 8
Below average 3 Oedematous 1 50-64 2 Single organ failure (Resp, 5
(BMI = <20) Renal, Cardiac)
(BMI=Wt in kg/Ht in m2) Clammy, Pyrexia 1 65-74 3 Peripheral vascular disease 5
Discoloured grade I 2 75-80 4 Anemia <8gm% 2
Broken/Spots grade 2-4 3 81+ 5 Smoking 1
Continence Score Mobility Score Appetite Score Neurological deficit Score
Complete/ Catheterised 0 Fully 0 Normal 0 Diabetes, MS, CVA 4 to 6
Urine Incontinence 1 Restless/Fidgety 1 Scarce/Feeding 1 Motor/Sensory 4 to 6
tube
Fecal Incontinence 2 Apathetic 2 Liquid IV 2 Paraplegia 4 to 6
Urinary + Fecal Incontinence 3 Restricted 3 Anorexia/ 3
Absolute diet
Bed bound e.g. traction 4 Major surgery or trauma
Chair bound e.g. wheel chair 5 Orthopedic/Spinal 5
On table >2 Hrs 5
Interpretation On table >6 Hrs 8
10+ At Risk
15+ High Risk
20+ Very High Risk

assessment. There are a large number of parameters 17-21- moderate risk

making it complex. It states that women are at a higher ≤ 16 – high risk
risk of developing pressure ulcer than men.
This scale is rated in scientific journals as having the best
Braden scale sensitivity and specificity. This scoring system is technically
This risk assessment scale has been devised by Bergstrom demanding and requires some training to use it properly.
et al. in 1987 [Table 4]. It is an inverse scoring tool
implying that the lower the score, the greater is the risk CLASSIFICATION OF PRESSURE ULCER
of developing ulcer. Score 1 is poor and 4 is normal.
The first well described classification of pressure sores
The same scale has been modified for predicting pressure was given by an orthopedic surgeon, Darrell Shea in
ulcer risk in pediatric patients of  9 years of age, which 1975. It was a landmark paper in which Shea classified
is popularized as Modified Braden scale. In this scale only these ulcers into five categories defined by the anatomic
the interpretation score differs from the original Braden depth of the soft tissue damage.[48] After Shea, the
scale. literature has been flooded with classifications. Amongst
22-25 – mild risk several, only a few classifications became popular. The
251 Indian Journal of Plastic Surgery May-August 2012 Vol 45 Issue 2
 Agrawal and Chauhan: Pressure ulcers: Back to the basics

Table 4: Braden scale for predicting risk of pressure ulcer[32,46,47]

1 2 3 4
1. Sensory perception Completely limited Very limited Slightly limited No impairment
2. Moisture Constantly moist Very moist Occasionally moist Rarely moist
3. Activity Bedfast Chair-fast Walks occasionally Walks frequently
4. Mobility Completely immobile Very limited Slightly limited No limitation
5. Nutrition Very poor Probably inadequate Adequate Excellent
6. Friction and shear Problem Potential problem No apparent problem
Interpretation of scores for 15-18 - Mild risk of developing pressure ulcer
development of pressure ulcer 12-14 - Moderate risk of developing pressure ulcer
≤11 - Severe risk of developing pressure ulcer

Table 5: Comparative table of common classifications of pressure ulcers

Grade/stage Shea (1975) Yarkony-Kirk (1990) EPUAP (1996) US- NPUAP (2007)
I Limited to epidermis exposing dermis Red area Erythema Redness
II Full thickness skin loss exposing fat Involvement of epidermis Partial thickness skin loss Partial thickness loss of skin
and dermis, no
subcutaneous fat observed
III Full thickness skin and fat defect Exposed subcutaneous fat Full thickness skin and Full thickness skin loss exposing
exposing deep fascia with no muscle observed subcutaneous necrosis subcutaneous fat
IV Full thickness defect exposing bone Exposed muscle without Extensive destruction with Full thickness tissue loss
bone involvement or without skin loss exposing bone, tendon or muscle
V - Exposed bone - -
VI - Joint space involvement - -
Closed pressure sores. Subcutaneous - - Suspected deep tissue injury
necrosis without skin ulceration with discolored intact skin.
- - - Un-stageable: Full thickness
tissue loss with base covered
with slough/ eschar.

most commonly used is the one presented by NPUAP. of pressure ulcer as a wound. Many agents and methods
For the interest of readers the important classifications have been used to take care of these wounds. The list
are reproduced along with a comparative table for easy is never-ending. Broadly these therapies can be enlisted
understanding. [Table 5] under topical agents for debridement, topical therapeutic
agents for infection control, therapeutic agents for
Popular classifications of pressure ulcer and comparison wound healing, nutritional support, 2-hourly change of
of various stages and grades [Table 2]. posture, avoidance/reduction of pressure with the use of
special mattress and cushion, surgical management and
International classification of diseases (ICD-10) education to patients and care givers.
codes
ICD-10-AM codes are categorized into four stages as CONCLUSIONS
defined in the Australian Wound Management Guidelines
but analysis is limited as there is no mechanism to identify Pressure ulcers are here to stay despite all the
the origin of the ulcer. advances in prevention and management. One has
to keep abreast with the etio-pathogenesis, risk
MANAGEMENT factors and staging in detail so as to improve upon
the understanding of this preventable condition. A
Detailed management of pressure ulcer is beyond the more precise and wholesome definition has been
scope of this article. “Prevention is better than cure” is best suggested as the existing definition falls short of the
emphasized in the case of pressure ulcer. This condition true description of the disease process.
is cent percent preventable with care, compassion and
dedication towards the care of patients. Prevention is ACKNOWLEDGEMENT
directed towards taking care of the extrinsic and intrinsic
factors. There are innumerable methods of management The authors thank Dr. Aparna Agrawal, MD, Director Professor

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 Agrawal and Chauhan: Pressure ulcers: Back to the basics

LHMC and Associated Hospitals, New Delhi for her suggestions, operation for elderly long-term bedridden patients. Ann Plast
editing and correction of English transcript. We acknowledge the Surg 2005;54:629-32.
contribution of Ms. Shrreya Agrawal for preparing the line diagram. 21. Husain T. An experimental study of some pressure effects
on tissues, with reference to the bedsore problem. J Pathol
Bacteriol 1953;66:347-58.
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How to cite this article: Agrawal K, Chauhan N. Pressure ulcers:
47. Bergstrom N, Demuth PJ, Braden BJ. A clinical trial of the Braden
Back to the basics. Indian J Plast Surg 2012;45:244-54.
scale for predicting pressure sore risk. Nurs Clin North Am
Source of Support: Nil, Conflict of Interest: None declared.
1987;22:417-28.

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