Transcript Document

SKIN CHANGES AT LIFE’S
END: THE KENNEDY
TERMINAL ULCER
Anna Nesovic, RN, BSN
DNP Student
MSU Bozeman: College of Nursing
Objectives
Participants will:
• understand the normal skin changes with aging
• be able to describe the pathology and usual presentation of a
pressure ulcer
• be able to list two patient scenarios where pressure ulcers are
unavoidable
• understand how skin failure presents and the underlying
pathology
• be able to state two types of skin changes at life’s end that
maybe expected with hypoperfusion
• be able to differentiate between a pressure ulcer and a
Kennedy terminal ulcer
Geriatrics
• The United States population is aging.
• The United States life expectancy is increasing.
• The Baby Boomer generation is aging.
• Caring for geriatrics is complex due to
comorbidities.
• (CDC, 2013)
Skin
• Skin is the largest organ of the body.
• Skin can also fail.
• Basic Functions:
• Protection
• Sensory Function
• Regulates temperature
• Vitamin D Synthesis
• Psychological Function
• (McLafferty, Hendry, Farley, 2012).
Normal Skin Changes with Aging
• The Epidermis layer thins and the dermoepidermal
junction flattens.
• At the dermoepidermal junction there is a loss of
undulations.
• Decrease in sweat and sebaceous gland activity.
• The Dermis thins and there is decreased vascularity
and a decrease in fibroblasts.
• Reduction in collagen fibers.
• (Taffet, 2015).
Delayed Wound Healing in Geriatrics
•Decreased elasticity
•Altered immune response
•Decreased collagen synthesis
•Increased degradation
•Slower epilthialization
•Multiple comorbidities
• (Watkins, 2011).
Pressure Ulcers
• Pressure ulcers are defined as skin lesions that result from
unrelieved pressure that causes damage to the underlying tissue.
• Pathogenesis: Excess pressure (greater than 32mmHg) for an
extended amount of time over one area prevents oxygen and
nutrients to be delivered to the tissue. This results in tissue
hypoxia, waste buildup, and free radical generation.
• Pressure is greatest over bony prominences (sacrum, heels,
elbows).
• Pressure, friction, shearing forces and moisture all contribute to
pressure ulcer formation.
• (Berlowitz, 2014)
Recognizing Pressure Ulcers
Pressure Ulcer
Shape
Color
Progression
Consistency
Pathology
Round, imaging bony prominence that is
underneath
Red, yellow, brown, and black
Steady and slow progression
Firm and/or boggy
Unrelieved Pressure
(Yastrub, 2010).
Pressure Ulcer
Courtesy of Photo: Karen Zulkowski,
DNS, RN
Pressure Ulcer Risk Factors
• Age greater than 65 years old • Length of stay at a facility
• Terminal illness
• Malnutrition
• Dialysis
• Stroke
• Radiation and oxygen therapy • Renal Failure
• History of pressure ulcer
• Friction/shear
• Functional impairment
• Decreased sensation
• Incontinence
• Sedation
• (Berlowizt, 1997; Ferrell, 2000;
Kwong, 2009; Cox, 2011;
Nonnemacher, 2008; Lahmann,
2012; & Cacon, 2010).
Pressure Ulcer Prevention is Paramount
• The Centers for Medicare and Medicaid Services
(2012) mandated that long-term care facilities report
pressure ulcer prevalence within their facility
publically.
• In 2008 the Department of Health and Human
Services announced that CMS will not reimburse
facilities if a patient develops stage III or IV pressure
ulcer under their care.
Unavoidable Pressure Ulcers
• The National Pressure Ulcer Advisory Panel (2011) agreed that not
all pressure ulcers are preventable. The panelists unanimously
voted that not all pressure ulcers are avoidable.
• “An unavoidable pressure ulcer can develop even though the
provider evaluated the individual’s clinical condition and pressure
ulcer risk factors; defined and implemented interventions
consistent with individual needs, goals, and recognized standards
of practice; monitored and evaluated the impact of the
interventions; and revised the approaches as appropriate” (Black,
2011, p. 30).
• Patient scenarios: perfusion/hemodynamic instability, critical illness,
and comfort care.
Skin Failure
• Skin failure is the result of hypoperfusion of the skin.
• Skin failure can be acute, chronic or end-stage.
• When patients experience multiple organ dysfunction syndrome
the blood is shunted away from the skin and to the vital organs.
• Skin failure can occur in areas under stress (buttock, hips).
• It is not limited to tissue loading areas and can occur on fingers and
toes as necrosis also. This is usually the result of chronic skin
failure, usually seen in geriatrics with several comorbidities.
• No formal diagnostic criteria for skin failure.
• (Beldon, 2011).
• (Black, 2011).
Skin Changes at Life’s End
• Skin changes at life’s end is the term used to describe unusual
wounds at the end of life.
• Skin change at life’s end is associated with hypoperfusion.
• May present as pressure ulcers, unavoidable pressure injury,
ischemic wounds, mottling, tumors or deep tissue injury.
• Minor trauma to the skin can cause: hemorrhage, gangrene,
infection, skin tears and ulcers.
• With vascular compromise the fingers, toes, ears and nose may
have dusky erythema, mottled discoloration, local cooling, infarct
and gangrene appearance.
• (Krasner, 2015)
• (Sibbald, 2010)
Skin Changes at Life’s End Risk Factors
• Hypoperfusion
• Limited mobility
• Malnutrition (weight loss, low serum albumin and hemoglobin
levels, dehydration)
• Decrease tissue perfusion (hypotension and hypoxia)
• Loss of skin integrity
• Decreased immune function
• (Sibbald, 2010)
The Kennedy Terminal Ulcer
• End-stage skin failure can present itself as the Kennedy Terminal Ulcer.
• The Kennedy Terminal Ulcer usually appears at the end of life in some
patients. It develops rapidly, usually located over the sacrococcygeal
area, can be purple, red, blue or black, and has irregular borders.
• Name was developed from Karen Kennedy from the study conducted at
the Byron Health Center.
• During the five year period pressure ulcer prevalence increased from 1.95%
to 3.36%.
• The data from this study showed that 55.7% of people who developed a
pressure ulcer died within six weeks of pressure ulcer onset.
• The life expectancy after this ulcer is identified is approximately two days
to six weeks. There have been a few cases where patients have lived
longer than six weeks.
• (Kennedy-Evans, 2009)
• (Lepak, 2012)
Recognizing Kennedy Terminal Ulcers
Kennedy Terminal Ulcer
Shape
Butterfly or pear shape usually over the
sacrum and over the buttock
Color
Ranges from yellow, red, purple, blue to
black
Progression
Consistency
Pathology
Rapid, usually over 24-48 hours
Firm
Hypoperfusion
(Yastrub, 2010).
Differentiating between Pressure Ulcer and
Kennedy Terminal Ulcer
Pressure Ulcer
Kennedy Terminal Ulcer
Shape
Round, imaging bony
prominence that is
underneath
Butterfly or pear shape usually over
the sacrum and over the buttock
Color
Red, yellow, brown, and
black
Ranges from yellow, red, purple,
blue to black
Progression
Consistency
Pathology
Steady and slow progression
Rapid, usually over 24-48 hours
Firm and/or boggy
Firm
Unrelieved Pressure
Hypoperfusion
(Yastrub, 2010).
Communication is Key
• Communicate with the family and patient about the Kennedy
Terminal Ulcer.
• Educate the family and patient on how this type of ulcer is formed
due to hypoperfusion related to the end of life disease process.
• Spend time with the family and explain the connection of the
patient’s rapidly deteriorating health and its effect on the
circulatory system.
• Use the skin as a visual aide to help make this connection.
• (Beldon, 2011; Yastrub, 2010; Langemo, 2006; Sibbald, 2010).
Treatment
• Discuss the overall condition of the patient with the family and
patient to help put the whole picture together.
• Develop treatment goals with the family and patient.
• If the patient and family want aggressive treatment then the
underlying disease process needs to be treated. Therefore,
perfusion can be restored to the skin. The Kennedy terminal ulcer
will be treated the same as a pressure ulcer with dressings.
• Some families and patients may choose comfort care.
• Always, have thorough charting.
Case Study
• J.S. is a 92 year old female that was admitted to the hospital with
left sided weaknesses, expressive and receptive aphasia. MRI
shows patient to have had a large CVA. Pt does not qualify for tPA.
Patient also was diagnosed with pneumonia.
• Pt’s neuro status continues to decline during her hospitalization.
First, she fails her swallow evaluation. She is unable to get out of
bed without the use of lifts. She is incontinent of stool and has a
foley catheter placed. A few days after admission to the hospital
the patient is only responsive to pain. Further imaging shows
swelling in the brain.
Case Study Continued
• A family meeting is held and it is explained to the family that the
patient is not going to recover from this stroke.
• The family decides not to start artificial feedings and decides to
make the patient a no CPR but is not ready to stop antibiotics and
place the patient on comfort care.
• Pt is turned every two hours and pericare is completed at a
minimum of every two hours.
• Six days after admission to the hospital the morning skin
assessment shows blanchable redness on the patients sacrum. Pt is
turned every two hours throughout the shift and on the evening
assessment the patient’s buttock is purple.
Case Study Continued
• Upon the next morning there are two small areas of skin
breakdown. The borders are irregular and the ulcer bed is red and
pear shaped.
• What do you think the pathology is behind this?
• The family is educated on the significance of the skin breakdown.
• The patient is placed on comfort care and passes away that evening
surrounded by family and friends.
Conclusion
• Our geriatric population is growing.
• There is a general consensus in the literature that not all pressure
ulcers are preventable.
• The Kennedy terminal ulcer pathology is related to the end of life
disease process and hypoperfusion.
• The Kennedy terminal ulcer usually presents over the sacrum is a
butterfly/pear shape is purple, red, blue or black, has a rapid onset,
and has irregular borders.
• Communication is key during this time to explain the disease
process to the family and helping them understand the patient’s
rapidly deteriorating health.
• Thorough documentation is extremely important.
Questions
References
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Beldon, P. (2011). Skin changes at life’s end: SCALE ulcer or pressure ulcer? British
Journal of Community Nursing, 16(10), 491-494.
Berlowitz, D. (2014). Epidemiology, pathogenesis and risk assessment of pressure
ulcers. In K.E. Schamder & H. Sanfey (Eds.), UptoDate. Retrieved from
www.uptodate.com/home
Berlowitz, D.R., Brandeis, G.H., Anderson, J., Du, W., & Brand, H. (1997). Effect of
pressure ulcers on the survival of long-term care residents. Journal of Gerontology,
52A(2), M106-M110.
Black, J.M., Edsberg, L.E., Baharestani, M.M., Langemo, D., Goldberg, M, & Cuddigan, J.
(2011). Pressure ulcers: Avoidable or unavoidable? Results of the national pressure
ulcer advisory panel consensus conference. Ostomy Wound Management, 57(2), 24-37.
Chacon, J.M.F., Nagaoka, C., Blanes, L., & Ferreira, L.M. (2010). Pressure ulcer risk
factors among the elderly living in long-term institutions, Wounds: A Compendium Of
Clinical Research & Practice, 22(4),106-113.
Centers for disease control and prevention. (2013). The state of aging and health in
America 2013. National Center for Chronic Disease prevention and Health Promotion.
Available from http://www.cdc.gov/aging/pdf/state-aging-health-in-america-2013.pdf
References Continued
• Centers for Medicare and Medicaid Services. (2012). Centers for medicare and Medicaid
services long-term care hospital quality reporting program guidance. Centers for
Medicare and Medicaid Services. Available from http://www.cms.gov/Medicare/QualityInitiatives-Patient-Assessment-Instruments/LTCH-Quality-Reporting/Downloads/LTCHQuality-Reporting-QGP-Guidance.pdf
• Cox, J. (2011). Predictors of pressure ulcers in adult critical care patients. American
Journal of Critical Care, 20(5), 364-374.
• Department of Health and Human Services. (2008). Center for Medicaid and state
operations. Centers for Medicare and Medicaid Services. Available from
http://downloads.cms.gov/cmsgov/archiveddownloads/SMDL/downloads/SMD073108.pdf
• Ferrell, B.A., Josephson, K., Norvid, P., & Alcorn H. (2000). Pressure ulcers among
patients admitted to home care. Journal of The American Geriatrics Society, 48, 10421048.
• Kennedy-Evans, K. (2009). Understanding the Kennedy terminal ulcer. Ostomy Wound
Management, 55(6), 6.
• Krasner, D.L., & Stewart, T.P. (2015). SCALE wounds: Unavoidable pressure injury.
Wounds, 27(4), 92-94.
References Continued
• Krasner, D.L., & Stewart, T.P. (2015). SCALE wounds: Unavoidable pressure
injury. Wounds, 27(4), 92-94.
• Kwong, E.W., Pang, S.M., Aboo, G.H. & Law, S.S. (2009). Pressure ulcer
development in older residents in nursing home: Influencing factors. Journal
of Advanced Nursing, 65(12), 2608-2620.
• Lahmann N.A., Kottner, J., Dassen, T., & Tannen, A. (2012). Higher pressure
ulcer risk on intensive care? Comparison between general wards and intensive
care units. Journal of Clinical Nursing, 21, 354-361.
• Lepak, V. (2012). Avoidable & inevitable? Skin failure: The Kennedy terminal
lesion. Journal of legal Nurse Consulting, 2(1), 24-27.
• McLafferty, E., Hendry, C., & Farley, A. (2012). The integumentary system:
anatomy, physiology and function of skin. Nursing Standard, 27(3), 35-42.
• Nonnemacher, M., Stausberg, J., Bartoszek, G., Lottko, B., Neuhaeuser, M., &
Maier, I. (2008). Predicting pressure ulcer risk: a multifactorial approach to
assess risk factors in a large university hospital population. Journal of Clinical
Nursing, 18, 99-107.
• Sibbald, R.G., Krasner, D.L., & Lutz, J. (2010). SCALE: Skin changes at life’s end:
Final consensus statement. Advances in Skin and Wound Care, 23, 225-2236.
References Continued
• Taffet, G.E. (2015). Normal aging. In K.E. Schmader (Ed.), UptoDate.
Retrieved from www.uptodate.com/home
• Watkins, J. (2011). Ageing skin, part 1: normal ageing. Practice
Nursing, 22(5), 250-257.
• Yastrub, D.J. (2010). Pressure or pathology: Distinguishing pressure
ulcers from the Kennedy terminal ulcer. Journal of Wound Ostomy &
Continence Nursing, 37(3), 249-250.