Basic teaching on wound management seen in home care / domiciliary palliative care in Malaysia. Spesifically describe management of pressure ulcer at home.

1. WOUND MANAGEMENT IN
DOMICILIARY PALLIATIVE CARE
Dr Wan Zuraini, MD
Tissue Viability
Clinician

2. SLIDE WITH CROSSMARK
HAS HIGH VALUE FOR CLINICAL
PRACTICE

3. WOUNDS IN DOMI / PALLIATIVE
Pressure wound
Diabetic foot ulcer
Venous leg ulcer
Primary malignancy wound
Secondary malignancy wound
Post radio/chemo wound / chemo port wound
Thomas & Gregory 2014

5. OUTLINE
1. THE BIOLOGY OF WOUND HEALING
2. INCIDENCE AND PREVALENCE OF PRESSURE INJURY
3. PREVENTION OF PRESSURE INJURY
4. GENERAL PRINCIPLES OF PRESSURE INJURY MANAGEMENT
5. PALLIATIVE WOUND CARE

6. 1. THE BIOLOGY OF WOUND
HEALING

7. SKIN CHANGES, WOUND & AGING
1. Decrease and flattening of dermal thickness, decline collagen, loss
of elastin  epidermal-dermal shear type injury  skin tear
2. Reduce tensile strength  poor scar, increase post-surgical wound
dehiscence
0.9% at age 30-39
2.5% at age 50-59
5.0% at age > 80 Ref: Mendoza 1970
3. The rate of epithelialization differs with age (1.9 days slower in
mean age of 72) Ref Linstedt 1975
4. Slow keratinocytes migration Ref Stanulis P 1986
5. Poor fibroblast support for extracellular matrix build
secondary to decrease TGF-Beta 1 (2 vs 6 fold in young donor)
Ref Reed MJ 1994

8. 2. INCIDENCE & PREVALENCE OF
PRESSURE INJURY
- Varies by settings, varies by stage
- Cost involved – 1.1Billion annually in USA
Thomas & Gregory
2014

9. INCIDENCE OF PRESSURE ULCERS VARIES BY
SETTING
7%–9%
0
2
4
6
8
10
12
14
16
18
Hospital Home Care Nursing Home
11%
0–17% Ref NPUAP 2007

10. PREVALENCE OF PRESSURE ULCERS VARIES
BY STAGE
Stage I, 47%
Stage II, 33%
Stages III &
IV, 20%
Stage I Stage II Stages III & IV
Ref NPUAP 2007

11. ANATOMICAL
SITE
18% sacral, ischial
12% heel

12. PRESSURE ULCERS – MECHANISM OF
DEVELOPMENT
12
INTERFACE
PRESSURE
FRICTION
SHEAR
EXCESSIVE
MOISTURE

13. INTERFACE PRESSURE
SHEAR & FRICTION

14. Hayashi & Bruce 2014

15. NURSING HOMES
3837 residents in 30 care homes -
39% possesses stage 2 or deeper PU,
13.2% develops new ulcer Ref Lechner 2017
Dry skin and pressure ulcer risk: A multi-centre cross-sectional prevalence study in
German hospitals and nursing homes
Anna Lechnera, , , Lahmannb, c, Konrad Neumannd, Ulrike Blume-Peytavia, Jan Kottnera

16. 3. PREVENTION OF PRESSURE
ULCERS
- Not all PUs are avoidable, but > 90% is
avoidable
- Focus on
1. Skin assessment
2. PU Risk Assessment Scale
3. Associated risk factors
Thomas & Gregory
2014

17. Recommendation from National Institute of Health & Clinical Excellence
Pressure Ulcer Guideline (NICE, UK 2003), for outpatient setting:
- Check at first contact
- Reviewed at least weekly
- Reassess if there is a change in mental/physical status of the patient or
if conditions deteriorate
- Classified the injury, according to the NPUAP (updated 2016) stage
3. PREVENTION OF PRESSURE ULCERS –
SKIN ASSESSMENT

18. CLASSIFICATION
New Components
 Use validated system
NPUAP-EPUAP Pressure Ulcer
Classification System
We agree on:
 Definition of pressure ulcer
 Definition of four “categories or stages”
 Additional categories
 Deep Tissue Injury
 “Unstageables”

19. STAGE 1: PRESSURE INJURY: NON-
BLANCHABLE ERYTHEMA OF INTACT SKIN
Intact skin with a localized area of
non-blanchable erythema, which
may appear differently in darkly
pigmented skin. Presence of
blanchable erythema or changes in
sensation, temperature, or
firmness may precede visual
changes. Colour changes do not
include purple or maroon
discoloration; these may indicate
deep tissue pressure injury.

20. STAGE 2 PRESSURE INJURY: PARTIAL-
THICKNESS SKIN LOSS WITH EXPOSED
DERMIS
Partial-thickness loss of skin with
exposed dermis. The wound bed is
viable, pink or red, moist, and may
also present as an intact or ruptured
serum-filled blister. Adipose (fat) is
not visible and deeper tissues are not
visible. Granulation tissue, slough and
eschar are not present. These injuries
commonly result from adverse
microclimate and shear in the skin over
the pelvis and shear in the heel. This
stage should not be used to describe
moisture associated skin damage
(MASD) including incontinence
associated dermatitis (IAD),
intertriginous dermatitis (ITD), medical
adhesive related skin injury (MARSI), or
traumatic wounds (skin tears, burns,
abrasions).

21. STAGE 3 PRESSURE INJURY: FULL-
THICKNESS SKIN LOSS
Full-thickness loss of skin, in which
adipose (fat) is visible in the ulcer
and granulation tissue and epibole
(rolled wound edges) are often
present. Slough and/or eschar may
be visible. The depth of tissue
damage varies by anatomical
location; areas of
significant adiposity can develop
deep wounds. Undermining and
tunneling may occur. Fascia, muscle,
tendon, ligament, cartilage and/or
bone are not exposed. If slough or
eschar obscures the extent of tissue
loss this is an Unstageable Pressure

22. STAGE 4 PRESSURE INJURY: FULL-
THICKNESS SKIN AND TISSUE LOSS
Full-thickness skin and tissue
loss with exposed or directly
palpable fascia, muscle,
tendon, ligament, cartilage or
bone in the ulcer. Slough
and/or eschar may be visible.
Epibole (rolled edges),
undermining and/or
tunneling often occurs. Depth
varies by anatomical location.
If slough or eschar obscures
the extent of tissue loss this
is an Unstageable Pressure
Injury.

23. UNSTAGEABLE PRESSURE INJURY:
OBSCURED FULL-THICKNESS SKIN AND
TISSUE LOSS
Full-thickness skin and tissue loss in which the extent
of tissue damage within the ulcer cannot be confirmed
because it is obscured by slough or eschar. If slough
or eschar is removed, a Stage 3 or Stage 4 pressure
injury will be revealed. Stable eschar (i.e. dry,
adherent, intact, without erythema or fluctuance) on
the heel or ischaemic limb should not be softened or
removed.

24. UNSTAGEABLE

25. DEEP TISSUE PRESSURE INJURY:
PERSISTENT NON-BLANCHABLE DEEP
RED, MAROON OR PURPLE
DISCOLORATIONIntact or non-intact skin with localized areas of persistent
non-blanchable deep red, maroon, purple discoloration or
epidermal separation revealing a dark wound bed or blood
filled blister. Pain and temperature change often precede
skin colour changes. Discoloration may appear differently
in darkly pigmented skin. This injury results from intense
and/or prolonged pressure and shear forces at the bone-
muscle interface. The wound may evolve rapidly to reveal
the actual extent of tissue injury, or may resolve without
tissue loss. If necrotic tissue, subcutaneous tissue,
granulation tissue, fascia, muscle or other underlying
structures are visible, this indicates a full thickness
pressure injury (Unstageable, Stage 3 or Stage 4). Do not
use DTPI to describe vascular, traumatic, neuropathic, or
dermatologic conditions.

26. DEEP TISSUE
INJURY

27. PRESSURE ULCER RISK
ASSESSMENT SCALE (PURAS)
1. NORTON SCALE (England 1962, 5 parameters) – physical condition,
mental state, activity, mobility, incontinence
2. WATERLOW SCALE (England 1984, 8 parameters) – BMI, skin visual,
sex, age, continence, mobility, appetite, medication
3. BRADEN SCALE (USA 1987, 6 subscales) – sensory, perception,
mobility, activity, nutrition, friction & shear
4. GOSNELL SCALE (USA1973, 5 parameters) – mental status,
continence, mobility, activity, nutrition
5. RAMSTADIUS TOOL (AUSTRALIA 2000, 2 questions) – skin integrity,
mobility

30. PATIENT
SPECIFIC
RISK FACTOR

31. GENERAL PRINCIPLES OF
PRESSURE INJURY MANAGEMENT
1. Manage patient comorbidities
2. Reduce pressure, shear, friction
3. Address nutritional status
4. Assess the ulcer
5. Manage infection
6. Measure progress towards healing
7. Surgical considerations

32. 1. MANAGING PATIENT
COMORBIDITIES AND SKIN CARE
1. Optimize comorbid disease – DM, Hypertension, arterial disease
Daily systematic skin inspection and cleansing
 Especially bony prominences
 Use warm water and a mild cleanser
Reduce factors that promote dryness
 Avoid low humidity and exposure to cold
 Moisturize dry skin
Avoid massaging over bony prominences
TEACH TO
CARER

33. Reduce moisture
Incontinence
Perspiration
Drainage

34. 2. REDUCE PRESSURE, FRICTION,
SHEAR
• Reposition at least every 2 h (may use pillows, foam wedges)
• Use lubricants and protective dressings/pads
• Keep the head of bed at the lowest elevation possible
• Use lifting devices to decrease friction and shear
• Remind patients in chairs to shift weight every 15 mins
• “Doughnut” seat cushions are contraindicated, as they may
cause pressure ulcers
• Pay special attention to heels (account for 20% of all pressure

35. PREVENTION OF HEEL PRESSURE
INJURY
- Second most common from the sacrum, accounted 22.5% in long
term care facilities Ref Vanglider 2005
- 3 associated factors – 1. Low ABI, 2. Duration confined to bed, 3.
Male gender Ref Okuwa 2006
- Using pressure relief boots – foam, air, plastic, fibre, synthetic
sheepskin OR pillow

36. PREVENTING HEEL ULCERS
(1 OF 2)
Assess heels of high-risk patients every day
Use moisturizer on heels (no massage) twice a day
Apply dressings to the heels:
 Transparent film for patients prone to friction problems (eg,
stroke patients)
 Single or extra-thick hydrocolloid dressing for those with pre-
stage I reactive hyperemia

37. PREVENTING HEEL ULCERS
(2 OF 2)
Have patients wear:
Socks to prevent friction (remove at bedtime)
Properly fitting sneakers or shoes when in wheelchair
Place pillow under legs to keep heels off the bed
Turn patients every 2 hours, repositioning heels

38. 3. NUTRITIONAL STATUS
Ensure adequate diet; prevent malnutrition
Weak evidence for nutritional support that achieves 30 to 35
calories/kg/day and 1.25 to 1.5 g of protein/kg/day
Weak evidence for supplemental vitamins and minerals

39. Decision tree on
nutrition in
pressure ulcer

40. MALNUTRITION
UNIVERSAL
SCREENING
TOOL (MUST)

41. 4. ASSESS THE ULCER
Using Triangle of Wound Assessment –
TOWA
Then develop wound dressing prescription
Wounds International
2015

42. TRIANGLE OF WOUND
ASSESSMENT
Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International
2015

43. The Triangle of Wound Assessment
extends the current concepts of wound
bed preparation (WBP) and TIME beyond
the wound edge
It divides assessment of the wound into
three areas:
• the wound bed
• the wound edge
• the periwound skin
The Triangle of Wound Assessment
Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International
2015

44. TRIANGLE OF WOUND ASSESSMENT –
MANAGEMENT PLAN
Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International
2015

45. TEST
1. WOUND BED
Tissue type, infection,
exudates
2. WOUND EDGE
Dehydration, rolled
edges, undermining.
Maceration
3. PERIWOUND
Callus, hyperkeratosis,
excoriation, maceration,

46. Type of Dressing
Materials

47. 5. MANAGING INFECTION IN
PRESSURE ULCER

48. WOUND BED
PREPARATION
APPROACH IN
WOUND CARE

49. SIGNS AND
SYMPTOMS IN
SYSTEMIC
PRESSURE ULCER
INFECTION

50. BIOFILM IN
CHRONIC WOUNDS
- Aggregation of microbes and dwell
in protective carbohydrate matrix
-Adapted well to the environment
-Blocks phagocytic activity of
neutrophil
-Resistant to invasion by host
defence cell, topical or systemic
antibiotic (lack of elimination by
PMNs)
-The fact that bacteria in biofilms
not in motile state are the reason
why cellulite and bacteremia
uncommon complications in chronic
wound
-polymicrobial colonized
Wolcott 2008

51. IDENTIFYING TRUE
INFECTION IN
CHRONIC WOUNDS
With fever, UTI and pneumonia
are much more common
Lazarus 1994

52. PERIWOUND
CANDIDA
INFECTION
- Satellite lesion
- especially to patient on
antimicrobials and corticosteroid
-May also have thrush, intertrigo,
denture stomatitis
- Caused by Candida albicans
- Treatment short course of steroid

53. CELLULITIS
- Sudden in onset
-erythema, edema, pain, tenderness
-Systemic symptom – infrequent –
fever uncommon
-Treatment – systemic antibiotic

54. OSTEOMYELITIS
COMPLICATING
PRESSURE
ULCERS
-Not common, always over treated
-Exposed bone in pressure ulcer
does not establish the diagnosis of
OM
-Probe to bone test – low predictive
value
-Require X-ray and ESR (>70mh/h)
-best test – MRI
-Suspicious if sinus tract present
-Refer surgical to remove
involucrum if healing is about to
occur
Donlan 2002

55. TO CULTURE OR
NOT? - Often misleading
- No clinical value, doesn’t reflect
the true colonization ecology
-Alginate matrix of biofilms requires
a special process to break the
carbohydrate bonds
-Most reliable method – BIOPSY –
bur require skill, facilities and
expensive
-Alternative – LEVINE method
Davies 2001

56. DEBRIDEMENT
SHARP DEBRIDEMENT IS MAINSTAY
FOR PRESSURE ULCER WITH
NECROSIS
Option mechanical debridement,
surgical, chemical
Maggot debridement therapy and
has a beneficial effect on
disruption of biofilm
Dressings with autolytic
component are not known to
disrupt biofilm
Dovi 2004

57. ROLE OF TOPICAL
ANTIBIOTIC
-Limited role
-Most studies on DFU and VLU

58. 5. MEASURE PROGRESS TOWARDS
HEALING
Document all observations over time
Describe each ulcer to track progress of healing
Do not use “reverse staging”
 For example, stage IV cannot become stage III
 Ulcers are filled with granulation tissue (endothelial cells, fibroblasts,
collagen, extracellular matrix)
 Ulcers do not replace lost muscle, subcutaneous fat, or dermis before re-
epithelializing
Use validated tools (e.g., PUSH, see next slide)

59. PUSH (PRESSURE ULCER SCALE
FOR HEALING) TOOL
A method to document healing over time
Observe and measure the ulcer’s:
 Surface area: measure with centimetre ruler
 Exudate: estimate portion of the ulcer bed covered by drainage
 Appearance: estimate portion of ulcer for each tissue type (epithelial,
granulation, slough, necrotic)
Assign a weighted score to obtain a total score; total scores over time indicate
healing or deterioration

61. PALLIATIVE WOUND CARE
SCALE (Skin Changes at Life’s End) Consensus
Document Ref Krasner & Sibbald 2012
Goal of palliative wound care – integrating
wound care in palliative continuum

64. LOCAL WOUND MANAGEMENT FOR
CANCER WOUND
Minimize trauma
Control odor
Manage excess exudates
Prevent deterioration and infection

65. MINIMIZE TRAUMA
-Granulation tissue in malignant
wound always friable and easily
bleeds (VEG-F) stimulated
-Reduce fibroblast disrupts collagen
matrix
-periwound care – proper use of
adhesive tape, skin sealants and
barrier, spray and gel

66. CONTROL ODOR -Due to increase bacterial burden
(Pseudomonas)
-Metabolic by product (fatty acids –
propionic, butyric, valeric,
isobutyric, isovaleric), sulphur
compounds, putrescine, cadaverine
-Treatment
Topical metronidazole
Metronidazole soaks
Activated charcoal dressing
Woo & Sibbald 2010

67. EXUDATES
Foams , alginates, hydrofiber
hydrogel, hydrocolloid
contraindicated
Prevent maceration, contact
dermatitis

68. OVERALL RECOMMENDATION –
NPUAP/EPUAP
1. COMPLETE PURAS ON FIRST VISIT AND REASSESS ON EVERY CHANGE
CONDITION
2. USE PRESSURE REDUCTION MATTRESS AND CUSHIONS AS INDICATED
3. MINIMIZE CHRONIC MOISTURE EXPOSURE FROM URINARY AND FECAL
INCONTINENCE
4. USE OF PRESSURE REDUCTION DEVICES INCLUDING PILLOW OR BOOTS
FOR REDUCTION OF PRESSURE ON HEEL
5. OPTIMIZE NUTRITIONAL STATUS INCLUDING PROTEIN INTAKE AND
HYDRATION
6. REPOSITIONING 4HRLY AND IN HIGH RISK PATIENT 2HRLY

69. THANK YOU
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