1. What is a Kennedy Terminal Ulcer?
A Kennedy Terminal Ulcer is a pressure ulcer some people develop as they are dying.
2. What does a Kennedy Terminal Ulcer look like?
It usually presents on the sacrum.
It can be shaped like a pear, butterfly or horseshoe.
It can have the colors of red, yellow, black or purple.
The borders of the ulcer are usually irregular.
It has a sudden onset.
The two statements you hear most are::
1 “Oh, my gosh, that was not there the other day.”
2 “I worked Friday, it was not there then, I was off the weekend and when I came
back on Monday there it was.
3. How does a Kennedy Terminal Ulcer progress?
It usually starts out as a blister or a Stage II and can rapidly progresses to a
Stage III or a Stage IV. In the beginning it can look much like an abrasion as if
someone took the patient and drug his or her bottom along a black top driveway.
It can become deeper and starts to turn colors. The colors can start out as a red/purple
area then turn to yellow and then black.
4. How are these different than other pressure ulcers?
They can start out larger than other pressure ulcers, are usually more superficial
initially and develop rapidly in size, and depth and color.
5. What kind of treatment is best for a Kennedy Terminal Ulcer?
Treatment for a Kennedy Terminal Ulcer is the same as for any other pressure ulcer
with the same characteristics. What you see is what you treat. When it is in the
blanchable/or non-blanchable intact skin stage the goal would be to relieve the
pressure and protect the area. When it becomes a Stage II or a partial thickness
ulcer usually there is not a lot of drainage and a thin film, hydrocolloid, foam
or gel may be indicated. When it is a full thickness wound, Stage III or IV depending
on the amount of drainage you could use a hydrocolloid, foam, gel, or calcium alginate.
If there is necrotic tissue slough (yellow tissue) or eschar (black, brown, beige
or tan tissue) you may want to use an enzymatic debriding agent. If it becomes clinically
infected you may want to consider a dressing with silver.
6. What causes a Kennedy Terminal Ulcer?
Further research needs to be done on this subject. However, one idea is it may be
a blood perfusion problem exacerbated by the dying process. The skin is an organ,
just like the heart, lungs, kidneys, lungs and liver. It is the largest of the body
organs and is the only one that is on the outside of the body. It can reflect what
is going on inside the human body. One theory is as people are approaching the dying
process the internal organs begin to slow down and go into what is thought of as
multi-organ failure. This is where all the organs start to slow down and not function
as efficiently as previously. No particular symptomatology may be detected except
the skin over bony prominences starts to show effect of pressure in a shorter time
frame. Where as turning a patient every two hours may be enough in somewhat of a
normal situation it now may cause superficial tissue damage.
7. Can a Kennedy Terminal Ulcer get better?
Yes, and no.
The majority of them do not. It is something that is generally thought to be terminal.
However, it has been known for a patient that was terminal or at the end of life
and the patient or family decided they did want intravenous or tube feeding intervention
along with other appropriate modalities to change their mind and decide they did
want all available interventions. At that point I have known of patients to have
this phenomena reversed.
8. When was a Kennedy Terminal Ulcer first described?
In March of 1989 the National Pressure Ulcer Advisory Panel put together their first
conference in Washington D.C.. The conference was to help determine how many pressure
ulcers there were (prevalence) and could you predict who was going to get them.
9. What age group is this prominent in?
Further research needs done but it tends to be a geriatric phenomenon. It does not
seem to be prominent in pediatrics. It is reported frequently in hospice patients
10. What do you mean by the 3:30 syndrome?
In our experience at the Byron Health Center in Fort Wayne, Indiana, a 500-bed long-term
care facility at that time, presented as a subdivision of the Kennedy Terminal Ulcer.
It presents a little different and has a quicker time frame. It can come on quickly,
sometimes in a matter of hours. It comes on as little be-be spots that are black.
They tend to look like a speck of dirt or dried bowel movement most caregivers tend
to try to wash away, finding out it is under the skin and not on the skin. These
can look like suspected deep tissue injuries. As the hours progress it becomes larger
and can in a matter of hours become almost the size of a quarter, fifty-cent piece
or silver dollar. These can look like someone colored the skin with a black or purple
marker. Presenting as a black flat type blister with intact skin presenting in a
unilateral location. The usual story is the patient got up in the morning the skin
was examined by the nurse aid and the skin looked normal and was intact with no
discoloration. At 3:30 PM when the patient was placed back in bed the skin shows
this blackened discoloration. (Thus the name: 3:30 syndrome.) When the nurse comes
to examine the discolored skin it is difficult to believe it actually was not here
in the AM and is as large as it is 6-8 hours later. The life expectancy of the 3:30
syndrome presentation of our patients was within 8-24 hours.
11. How did it get its name?
It was named by the Medical Director of the Byron Health Center is Fort Wayne, Indiana,
Dr. Stephen Glassley. He termed it “The Kennedy Terminal Ulcer”. Naming it after
the first Family Nurse Practitioner, in Fort Wayne, Indiana, Karen Lou Kennedy.
Karen began employment at the Byron Health Center in 1977 and in1983 started one
of the first Skin Care Teams in a Long Term Care facility. Record keeping was initiated
indicating some patients developed pressure ulcers with similar characteristics(see
photos) that went on to die in a short time frame.
As the data was reviewed a pattern developed as to the characteristic and time frame
from onset to death. This data was reviewed by the medical director, Dr. Stephen
Glassley and the attending physician, Dr. Delores Espino, thus naming it the “Kennedy
12. Why have I not heard of this before?
This was first described in modern literature by Karen Lou Kennedy in 1989 in Decubitus
(now know as Advances in Skin & Wound Care) Vol.2, No,2, May 1989. p.44-45
However, in about 2002 Dr. Jeffrey M. Levine, MD, AGSF, found a long lost textbook
published in 1877 by professor Dr. Jean-Martin Charcot called Lectures the Diseases
of The Nervous System. In this textbook were hand drawn pictures and descriptions
of the Kennedy Terminal Ulcer and the three thirty syndrome. The term used by Dr.
Charcot was Decubitus Acutus (Acute Bed-Sore) described as the 3:30 syndrome by
Kennedy and Decubitus Ominosis described as the “Kennedy Terminal Ulcer” at the
Byron Health Center.
Dr. Charcot was a French neurologist considered the father of modern neurology and
the first professor of diseases of the nervous system regarded as one of the most
important researchers in the field of clinical neurology of the 19th century.
Dr. Charcot contributions to neurology were describing a range of neurological diseases
including multiple sclerosis, lateral amyotrophic sclerosis, Parkinson’s disease
and Gilles de la Tourette syndrome to name a few. Other important contributions
by him have been forgotten.