Do people near the end “starve to death” or “die of thirst”?

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This is an excerpt of a post recently published on the Society for PSP’s Forum, an online discussion group.  The author is my online friend Ed Plowman.  Though he writes about his wife Rose with progressive supranuclear palsy, his comments apply to those nearing the end with any disorder.  Ed addresses whether those nearing the end suffer from starvation or thirst.

Robin

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Excerpt of a post by Ed Plowman
Society for PSP Forum
Mon May 05, 2008 11:05 pm

Two hospice doctors and a hospice nurse explained to me what the final days for Rose will be like if she no longer can swallow or take fluid, and remains adamant about no feeding tube or IV hydration. Morphine likely will be administered. (I was with a dying friend recently who was on morphine; he seemed completely normal, not in a “drugged stupor” — a common misconception about the effects of morphine, as I understand it — and we conversed normally for hours with each other and members of his family. He knew the end was near, he seemed relaxed and calm.)

My youngest daughter said she could not stand by while her mother starves to death or dies of thirst. The hospice docs explained that with morphine, that doesn’t happen. The patient has no desire to eat, and often has no sensation of thirst. Moistening the lips and mouth will alleviate discomfort from “dryness.” After the patient stops eating, the body normally will begin the shutdown process; it will produce and release from the pituitary gland endorphins, or endomorphines — a natural form of morphine. These biochemicals give the patient a calming sense of wellbeing. Eventually, in many cases, when the respiratory system begins to shut down, the patient falls asleep, breathing becomes shallow, and the end is peaceful. (That’s how it was with the dying friend I mentioned above.)

The end script is not exactly the same for everyone, of course. But the hospice staff said they’ve not seen any of their patients, many of whom could not eat or drink at the end, die of hunger or thirst as many people commonly envision.

I think it’s important that the family gather together in harmony, compassion, and loving appreciation as the end nears. It wouldn’t hurt to recount a few unforgettable positive memories involving the loved one. Some families sing favorite hymns; someone may feel led to say a prayer of thankfulness for what the loved one has meant in the lives of family members. The loved one with PSP may not be able to speak or even move. But he or she will hear and understand all that is said and done. This can be a precious, joyful time for him or her.

I believe we are fast approaching this time of transition at our house.

ed p.

“Compassionate Communication” – do’s and don’ts

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Recently I attended a workshop on dementia caregiving.  This wonderful handout on compassionate communicate was shared.  Though written by an Alzheimer’s support group leader and addressed to caregivers of those with “memory impairment,” the suggestions of “do’s” and “don’ts” apply to all dementia types, even without memory impairment.

Here’s a link to the handout:

www.ocagingservicescollaborative.org/wp-content/uploads/2013/03/Compassionate-Communication-with-the-Memory-Impaired.pdf

Compassionate Communication with the Memory Impaired
Liz Ayres, Alzheimer’s Support Group Leader, former Caregiver, Orange County, CA
Copyright 2008

[Editor’s Note, 2013: handout link from 2008 no longer working.]

I’ve copied much of the handout below.  Page 2 of the handout contains lots of examples.

Robin

Compassionate Communication with the Memory Impaired
Liz Ayres, Alzheimer’s Support Group Leader, former Caregiver, Orange County, CA
©1995, 2001, 2005, 2007, 2008

DON’T

Don’t reason.
Don’t argue.
Don’t confront.
Don’t remind them they forget.
Don’t question recent memory.
Don’t take it personally.

DO

Give short, one sentence explanations.

Allow plenty of time for comprehension, then triple it.

Repeat instructions or sentences exactly the same way.

Eliminate ‘but’ from your vocabulary; substitute ‘nevertheless.’

Avoid insistence. Try again later.

Agree with them or distract them to a different subject or activity.

Accept the blame when something’s wrong (even if it’s fantasy.)

Leave the room, if necessary, to avoid confrontations.

Respond to the feelings rather than the words.

Be patient and cheerful and reassuring. Do go with the flow.

Practice 100% forgiveness. Memory loss progresses daily.

My appeal to you: Please elevate your level of generosity and graciousness.

REMEMBER

You can’t control memory loss, only your reaction to it. Compassionate communication will significantly heighten quality of life. They are not crazy or lazy. They say normal things, and do normal things, for a memory impaired, dementia individual. If they were deliberately trying to exasperate you, they would have a different diagnosis. Forgive them…always. For example: they don’t hide things; they protect them in safe places…and then forget. Don’t take ‘stealing’ accusations personally.

Their disability is memory loss. Asking them to remember is like asking a blind person to read. (“Did you take your pills?” “What did you do today?”) Don’t ask and don’t test memory! A loss of this magnitude reduces the capacity to reason. Expecting them to be reasonable or to accept your conclusion is unrealistic. (“You need a shower.” “Day care will be fun.” “You can’t live alone.”) Don’t try to reason or convince them. Give a one sentence explanation or search for creative solutions. Memory loss produces unpredictable emotions, thought, and behavior, which you can alleviate by resolving all issues peacefully. Don’t argue, correct, contradict, confront, blame or insist.

Reminders are rarely kind. They tell the patient how disabled they are––over and over again. Reminders of the recent past imply, “I remember, I’m okay; you don’t, you’re not.” Ouch! Refer only to the present or the future. (If they’re hungry, don’t inform them they ate an hour ago, offer a snack or set a time to eat soon.) They may ask the same question repeatedly, believing each time is the first. Graciously respond as if it’s the first time. Some days they seem normal, but they’re not. They live in a different reality. Reminders won’t bring them into yours. Note: For vascular dementia, giving clues may help their recall. If it doesn’t work, be kind…don’t remind.

Ethical dilemmas may occur. If, for instance, the patient thinks a dead spouse is alive, and truthful reminders will create sadness, what should you do? To avoid distress, try these ways of kindness: 1) distract to another topic, or 2) start a fun activity, or 3) reminisce about their spouse, “I was just thinking about ___. How did you meet?” or you might try, “He’s gone for a while. Let’s take our walk now.”

Open ended questions (“Where shall we go?” “What do you want to eat/wear/do?”) are surprisingly complex and create anxiety. Give them a simple choice between two items or direct their choice, “You look great in the red blouse.”

They are scared all the time. Each patient reacts differently to fear. They may become passive, uncooperative, hostile, angry, agitated, verbally abusive, or physically combative. They may even do them all at different times, or alternate between them. Anxiety may compel them to shadow you (follow everywhere). Anxiety compels them to resist changes in routine, even pleasant ones. Your goal is to reduce anxiety whenever possible. Also, they can’t remember your reassurances. Keep saying them.

 

Back rash

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This was posted on 1/6/06 by Pauline:

ed,

It was not discovered what made the raging rash on Greg’s back, but I believe it was from severe sweating against the wheelchair back which is Naugahyde. We were in Florida at the time of the rash showing up.

Doctor prescribed the benedryl-like drug to allow Greg to sleep at night. The doctor had me wash and rinse his back, mix half & half white vinegar and warm water and rinse again, pat dry thoroughly and apply a very thin layer of Triamcinolone Acetonide Ointment USP, 0.1% as prescribed. I think that the doctor prescribed the vinegar/water solution to dissolve any possibility of soap or other residue and cause a drying effect on the nearly blistered skin.

We were lucky Greg only had it on his back. In the past, this same ointment has been prescribed for me by a dermatologist for itchy, scaly patches on my lower leg and it cleared it up completely. That doctor told me if I could see the ointment on my skin I had used too much, so it is a very thin layer that is used.

Pauline

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I received the following via email today (4/13/08):

I would like to copy an email I sent to Pauline in Maine in case you can answer my question.

Here goes:
Hello Pauline in Maine,
I was wondering if you ever discovered the cause of the back rash. My husband has complained of this off and on since his hip replacement surgery a few years ago. At first I thought it was chemicals used to launder the sheets in the hospital coupled with the heat he generated by laying on them for so long. It’s been a few years now, since his surgeries, and he still complains. I’ve tried changing laundry soaps, given him benedryl, nothing seems to make it go away. Also, his symptoms seemed to appear soon after the surgery as well. I must add that prior to his surgeries (double hip replacement), he was also diagnosed with high blood pressure and started taking toprol. Several months later vytorin, plavix, cozaar and norvask were added.
Do you think there is any connection to this? Do you have any suggestions on how this can be treated?

Thank you.

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I’m posting this here because others have had experiences with rashes and can be helpful.

Many with PD and PD-related disorders get seborrheic dermatitis (a form of eczema). A dermatologist should be able to look at the rash and tell what sort of rash it is.

If it’s seborrheic dermatitis, dermatologists often prescribe hydrocortisone (some strengths are available OTC), Elidel, and Protopic. A relatively new product is Xolegel.

For my father, for seborrheic dermatitis on his arms and chest, we used Elidel, and it worked very well.

“Clinical outcomes” paper – PSP and MSA

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This is a very interesting article written by some of Europe’s top PSP researchers (and presumably top MSA researchers too).  The first author is O’Sullivan.  This is also a very important paper because it includes analysis of brains donated to the University College of London brain bank.

110 pathologically-confirmed PSP cases and 83 pathologically-confirmed MSA cases were examined for early clinical features and survival.  PSP cases were divided according to the D. Williams criteria of Richardson’s syndrome (RS) and PSP-parkinsonism.  MSA cases were divided according to the presence of early autonomic failure.

The PSP findings confirms what D. Williams has told us before:

“In PSP an RS phenotype, male gender, older age of onset and a short interval from disease onset to reaching the first clinical milestone were all independent predictors of shorter disease duration to death. Patients with RS also reached clinical milestones after a shorter interval from disease onset, compared to patients with PSP-P.”

The MSA findings are new to me (though maybe not to many of you):

“In MSA early autonomic failure, female gender, older age of onset, a short interval from disease onset to reaching the first clinical milestone and not being admitted to residential care were independent factors predicting shorter disease duration until death. The time to the first clinical milestone is a useful prognostic predictor for survival.”

Interesting (and scary?) that “not being admitted to residential care” predicts *shorter* disease duration in MSA.

I’ve copied below the abstract.

Update:  the full paper is now available at no charge.  See our post here with links.

Robin

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Brain. 2008 Apr 2 [Epub ahead of print]

Clinical outcomes of progressive supranuclear palsy and multiple system atrophy.

O’Sullivan SS, Massey LA, Williams DR, Silveira-Moriyama L, Kempster PA, Holton JL, Revesz T, Lees AJ.

Reta Lila Weston Institute of Neurological Studies, Institute of Neurology, Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, Sara Koe PSP Research Centre, Institute of Neurology, University College London, London, UK, Faculty of Medicine (Neuroscience), Monash University (Alfred Hospital Campus) and Department of Neurosciences, Monash Medical Centre, Melbourne, Australia.

Prognostic predictors have not been defined for progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). Subtypes of both disorders have been proposed on the basis of early clinical features. We performed a retrospective chart review to investigate the natural history of pathologically confirmed cases of PSP and MSA.

Survival data and several clinically relevant milestones, namely: frequent falling, cognitive disability, unintelligible speech, severe dysphagia, dependence on wheelchair for mobility, the use of urinary catheters and placement in residential care were determined.

On the basis of early symptoms, we subdivided cases with PSP into ‘Richardson’s syndrome’ (RS) and ‘PSP-parkinsonism’ (PSP-P).

Cases of MSA were subdivided according to the presence or absence of early autonomic failure.

Sixty-nine (62.7%) of the 110 PSP cases were classified as RS and 29 (26.4%) as PSP-P.

Of the 83 cases of MSA, 42 (53.2%) had autonomic failure within 2 years of disease onset.

Patients with PSP had an older age of onset (P < 0.001), but similar disease duration to those with MSA. Patients with PSP reached their first clinical milestone earlier than patients with MSA (P < 0.001). Regular falls (P < 0.001), unintelligible speech (P = 0.04) and cognitive impairment (P = 0.03) also occurred earlier in PSP than in MSA.

In PSP an RS phenotype, male gender, older age of onset and a short interval from disease onset to reaching the first clinical milestone were all independent predictors of shorter disease duration to death. Patients with RS also reached clinical milestones after a shorter interval from disease onset, compared to patients with PSP-P.

In MSA early autonomic failure, female gender, older age of onset, a short interval from disease onset to reaching the first clinical milestone and not being admitted to residential care were independent factors predicting shorter disease duration until death. The time to the first clinical milestone is a useful prognostic predictor for survival.

We confirm that RS had a less favourable course than PSP-P, and that early autonomic failure in MSA is associated with shorter survival.

PMID: 18385183

“Frontal-subcortical dementias” (PSP, CBD, LBD, and MSA)

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This newly-published abstract reviews the clinical presentation of frontal-subcortical dementias, lists them, and suggests how they relate to cortical dementias. The classic “cortical dementia” is Alzheimer’s Disease. Three dementias in our atypical parkinsonism group are mentioned as frontal-subcortical dementias — Parkinson disease dementia (also called Lewy body dementia), progressive supranuclear palsy, and corticobasal degeneration.

Interestingly, multiple system atrophy is listed as a frontal-subcortical dementia though dementia is exclusionary for MSA.

Robin

The Neurologist. 2008 Mar;14(2):100-107.

Frontal-Subcortical Dementias.

Bonelli RM, Cummings JL.
>From the *Department of Psychiatry, Graz Medical University, Graz, Austria; and the †Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA.

Frontal-subcortical dementias are a heterogeneous group of disorders that share primary pathology in subcortical structure and a characteristic pattern of neuropsychologic impairment. Their clinical presentation is characterized by memory disorders, an impaired ability to manipulate acquired knowledge, important changes of personality (apathy, inertia, or depression), and slowed thought processes (or bradyphrenia). It also has marked frontal dysfunction.

Classic frontal-subcortical dementias include Huntington chorea, Parkinson disease dementia, progressive supranuclear palsy, thalamic degeneration, subcortical vascular dementia, multiple sclerosis, the acquired immunodeficiency syndrome dementia complex, depressive pseudodementia, and some other rare dementias like spinocerebellar degenerative syndromes, Hallervorden-Spatz disease, choreoacanthocytosis, idiopathic basal ganglia calcification, Guamanian parkinsonism-dementia complex, corticobasal degeneration, multiple system atrophy, Wilson disease, metachromatic leukodystrophy, adrenoleukodystrophy, hypoparathyroidism, sarcoidosis, and other CNS inflammatory disorders.

Anatomic data suggest that the frontal signs result from a disconnection of the frontal cortex from the basal ganglia. However, most frontal-subcortical dementias show cortical atrophy in later stages, and cortical dementias have subcortical pathology at some point. In fact, the concept might be seen as a continuum, and only the 2 extremes would be represented by pure cortical or subcortical pathology. Anyway, subcortical disorders may still be more similar to one another than they are to AD. Possibly, frontal-subcortical and cortical dementias are the description of the prior main target of the disease process, ending up in both cases in a global dementia. Although the dichotomy cortical versus frontal-subcortical dementia is not strict, the 2 concepts still seem to have advantages.

PubMed ID#: 18332839 (see pubmed.gov for abstract only)