5. Introduction
Definition:
• National Pressure Ulcer Advisory Panel (NPUAP) and European
Pressure Ulcer Advisory Panel (EPUAP) defined pressure ulcers as
“localized injury to the skin and/or underlying tissue usually over a
bony prominence as a result of pressure, or pressure in combination
with shear and/or friction”
6. Historical perspective
• Pressure ulcers are an ancient problem, observed in bodies found preserved by
mummification in Egypt
• Ambrose Pare in 16th century enlisted ; nutrition, pain relief and debridement as
key factors for pressure ulcers to heal
• Sir James Paget in 1873 recognized the effect of eternal pressure on the
cutaneous circulation and the skin necrosis that ensued if the pressure was not
relieved
• John Staige Davies was the first to suggest replacing unstable scar with flap tissue
in 1938
• Lamon described the first closure of open pressure sore in 1945
• Kostrubala and Greenley recommended excision of bony prominences and
padding the exposed bone with local fascia or muscle flap in 1947
7. Epidemiology
• Highest incidences
-Elderly patients with femoral neck fractures (66%)
-Quadriplegic patients (60%)
-Neurologically impaired young (spinal cord injury [SCI] and
veterans)
-Chronic hospitalization and on palliative care
8. Epidemiology cont’d
• Prevalence
• General acute care setting: 10%-18% (15%)
• Long-term care facilities: 2.3%-28% (15%)
• Home care setting: 0%-29% (15%)
• Incidence
• General acute setting: 0.4%-38%
• Long-term care facilities: 2.2%-23.9%
• Home care setting: 0%-17%
• Over 60,000 death per year
9. Epidemiology cont’d
• Constitute about 25% of total cost of whole patient care
Susceptible areas
Majority of pressure sores
Developed over the bony
Prominence in the lower part
Of the body
Bony prominences
Ischial tuberosity (28%)
Trochanter (19%)
Sacrum (17%)
Heel (9%)
Scalp
10. • Statement of surgical importance
• A major cause of patient morbidity, prolonged hospital stay,
depression, representing a major health burden and drain on
resources
• IT’S PREVENTABLE
12. Risk assessment
• The first step in prevention of pressure ulcers is evaluation of risk
• Several scales have been devised but the Braden scale is widely used
A composite of 6 subscales
1. Sensory perception
-Ability to respond meaningfully to pressure-related discomfort
- Scored 1-4
2. Skin moisture
- Degree to which skin is exposed to moisture
- Scored 1-4
13. Risk assessment
3. Activity
- Degree of physical activity
- Scored 1-4
4. Mobility
- Ability to change and control body position
- Scored 1-4
5. Friction and shear- scored 1-3
6. Nutritional status
- Usual food intake
- Scored 1-4
14. Risk assessment
• Minimum value of 6 and maximum of 23
• Lower scores- increase risk of pressure ulcer development
• Higher scores- decrease risk of development
• Threshold score
- 16 tertiary care facilities
- 19 in veterans hospital
- 18 in skilled nursing care facilities
• Norton scale- used in geriatrics ( 5 greatest risk, 20 least risk)
• General physical condition, mental status, activity, mobility, incontinence
• Nutritional status- Gosnell scale ( modified Norton)
16. Pathology
• Pathogenesis
• Extrinsic and intrinsic factors work together
1. Extrinsic factors
a. Pressure
• Mechanical force/ unit area perpendicular to plane
• Tissue deformation, mechanical damage, blockage of vessels- deep
necrosis
• Pressure of twice the arterial capillary pressure (32mmHg) for 2 hours
produce irreversible ischemia
17.
18. Pathology
b. Friction
• Resistance to movement between two surfaces
• Outermost skin layer lost, resulting in increased water loss ->
increased coefficient of friction
• Most often during patient transfer
c. Shear
• Mechanical stress parallel to tissue plane
• Stretches or compresses muscles perforators to the skin resulting in
ischaemia
19. Pathology
2. Intrinsic factors
• Local ischaemia or fibrosis -> decrease tissue perfusion
• Infection/sepsis -> decrease tissue perfusion
• Decrease autonomic control -> excess perspiration, spasms, and lack
of bladder or bowel control
20. Pathology
• Increased age- decreased skin moisture, tensile strength, increased
skin friability
• Anaemia- decrease wound healing capability and weakness or fatigue
-> prolonged immobilization
• Altered level of consciousness- loss of protective reflexes or voluntary
movement to off-load pressure
• Sensory loss- absent feeling of discomfort from prolonged pressure
• Malnutrition- decrease ability to heal wound
• Vascular disease- PVD, diabetes, smoking
21. Pathology
• Pathophysiology
• High degree of pressure can be tolerated when evenly distributed
• Soft tissue compression (> 32mmHg ) results in ischaemia -> necrosis
-> ulceration
• Accelerated by infection/inflammation, oedema
• Muscles necrosis occur after 4 hours whereas skin after 12 hours
22. Pathology
• Natural history
1. Hyperemia is observed within less than 30 minutes of pressure
• Disappears within an hour after pressure relieve
2. Ischaemia – continuous pressure for 2-6 hours
• Redness requires at least 36 hours to completely disappear after
relieve of pressure
3. Necrosis-unrelieved pressure within 6 hours
• Skin becomes bluish and indurated areas can be felt
23. Pathology
4. Ulceration- within 2 weeks following development of necrosis
typically in bony prominences
• However, other factors (friction, shear) may influence this sequence
• Grade 1 & 2- typically friction and shear
• Grade 3 & 4 may be primarily pressure-time component
24. Classification
Different classification systems exist
• National Pressure Ulcer Advisory Panel developed a four stage
classification
• Modifications- Shea’s and Yarkony-Kirk
• Shea’s- presence of large cavities accessible only through small
sinuses
• Yarkony-Kirk- subclassifies grade 1 and identifies the tissue at the
base of the wound in grade 2 through 6
25. National Pressure Ulcer Advisory Panel Shea classification Yarkony-Kirk classification
Stage I: Non-blanchable erythema
of intact skin; the heralding lesion of
skin ulceration
1 Limited to epidermis, exposing the
dermis
Includes red areas
1 Red area
A Present longer than 30 minutes
but less than 24 hours
B Present longer than 24 hours
Stage II: Partial thickness skin loss
involving epidermis and or dermis. The
ulcer is superficial and present clinically
as abrasion, blister, or crater
2 Full thickness of dermis to the
junction of subcutaneous fat
2 Epidermis and or dermis ulcerated
with no subcutaneous fat observed
Stage III: Full thickness skin loss
involving damage or necrosis of
subcutaneous tissue which may extend
down to, but not through underlying
fascia. The ulcer present clinically as
deep crater with or without
undermining of adjacent tissue
3 Fat obliterated, limited by the deep
fascia undermining skin
3 Subcutaneous fat observed, no
muscle observed
Stage IV: Full thickness skin loss with
extensive destruction, tissue necrosis or
damage to muscle, bone or supporting
structures e.g tendon, joint, capsule
4 Bone at the base of ulceration
5 Close large cavity through a sinus
4 Muscle fascia is observed but no
bone observed
5 Bone is observed but no
involvement of joint space
6 Involvement of the joint space
26.
27. Diagnosis
• Diagnosis of pressure ulcers is clinical
• History and physical examination is focused on:
Determining the etiologic factors
Associated factors that influence wound healing-
31. Treatment
• Surgical
• Goals:
• Prevent progressive osteomyelitis and sepsis
• Reduce protein loss through the wound
• Improve quality of life
• Lower rehabilitation cost
• Improve patient hygiene and appearance
32. • In general, grade 1 & 2 can be managed non-surgically
• Grade 3 & 4 usually is protracted, culminating in non-healing or early
recurrence
34. Treatment
Post-operative care
• Pressure relief bed for 3-6 weeks
• Antispasmodics
• Nutrition optimization
• Active or passive range of motion of the uninvolved extremity
• Culture-directed antibiotics with infectious disease consultation
• Sitting protocol
• Education
36. Follow up
• Prevention begins the management of pressure ulcers
1. Skin care
• Consistent cleaning and bathing of patient and keeping the body dry
• Clean and neatly stretched out powdered bed sheet
• Proper bowel/ bladder program to keep skin clean and dry
2. Control of spasticity
• Proper patient positioning
• Medications- diazepam, baclofen, dantrolene sodium, mephenesin
carbonate
37. 3. Pressure dispersion
• Padding of pressure point-
• Pressure relieve behavior or alternate weight bearing surface
• Seated patient must be lifted for up to 10 seconds every 10 minutes
• Supine patients must be turned every 2 hours
• Support surface
• At least 4 inches of ring foam
• Water bed
38. Prevention
• Alternating air cell mattress (AAC)
• Air cells oriented perpendicular to patient
• Inflates and deflates
• Dispersal of accumulated metabolites via vascular and lymphatic drainages
• Head of bed elevation not > 45 degrees
• Low air loss mattress(LAL)
• Controlled loss of air within the mattress
• Facilitates drying of the skin
• Exerts <25mmHg pressure on any one part of the body
• As bed overlay or multiple pinholes that act to periodically redistribute
pressure
39. Prevention
• Air fluidized beds
• Patient floats on ceramic beads while warm, regulated air is forced through
• Eliminates excessive moisture from skin
• Keeps surface interface pressure at <20mmHg
• May cause dehydration
• Turning and repositioning in bed difficult- large and heavy
• Expensive
• Cushions for wheelchair filled with gel, foam, air, or water for pressure
relieve
• Rigid-based cushion provide lumbar support and decrease ischial pressure
• Optimization of underlying medical conditions
40. Peculiarities of our environment
• Poverty
• Ignorance
• Lack of modern pressure dispersal equipment
41. Conclusion
• Pressure ulcers are here to stay despite all the advances in prevention
and management.
• Management requires a multidisciplinary approach.
• One has to keep abreast with the etio-pathogenesis, risk factors and
staging in detail so as to improve upon the understanding of this
preventable condition.
42. References
1. Karen LP, Linda GP. In: Charles HT. Pressure Sores. Grabb and Smith’s Plastic Surgery.
7th edition. China. Lippincott Williams & Wilkins. 2014: 989- 997
2. Jeffrey EJ, Jeffrey MK. Pressure sores. Selected Reading in Plastic Surgery vol. 9(39).
Dallas. The University of Texas Southwestern Medical Centre2003: 1-43
3. Jeffrey EJ, Eamon BO. In: Jeffrey EJ. Pressure sores. Essentials of Plastic Surgery. 2nd
edition. Columbus, Ohio. CRC Press Taylor & Francis Group. 2014: 641- 649
4. Waterlow J. Pressure sores: A risk assessment card. Nurs Times. 1985;81:49–55.
5. Braden B, Bergstrom N. A conceptual schema for the study of the etiology of pressure
sores. Rehabil Nurs. 1987;12:8–12.
6. Gosnell DJ. Pressure sore risk assessment. Part II. Analysis of risk factors. Decubitus.
1989;2:40–3
7. Defloor T. The risk of pressure sore: A conceptual scheme. J Clin Nurs. 1999;8:206–16.
8. Pressure ulcer prevention: Clinical guideline No. 7. London: NICE; 2003. National
Institute for Clinical Excellence.
