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/div>
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yle
E
C
Module 10:
Common Physical Symptoms
© EPEC Project, 2003
Permission to reproduce for educational purposes granted
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Permission to reproduce for educational purposes granted
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![](3D"master15_background.gif")
![](3D"master15_image001.gif")
![](3D"master15_image002.gif")
E
P
E
C
P
E
C
Common Physical Symptoms
Module=
10
![](3D"master14_background.gif")
![](3D"master14_image003.gif")
Objectives
<=
span
style=3D'mso-special-format:bullet;color:#FF3300;position:absolute;left:-4=
.71%'>•Know
general guidelines for managing nonpain symptoms
•Understand how the
principles of intended / unintended consequences and
double effect apply to symptom management
•Know the assessment,
management of common physical symptoms
General management guidelines
. . .
. . .
General management guidel=
ines
•Provide
ongoing patient, family education, support
•Involve members of the
entire interdisciplinary team
• Reassess frequently
Intended vs unintended consequences
<=
span
style=3D'mso-special-format:bullet;color:#FF3300;position:absolute;left:-4=
.71%'>•Primary
intent dictates ethical medical practice
![](3D"slide0080_image004.gif")
C=
ardiac
arrest, death during surgery =
R=
educe
pain, improve function
Operation to r=
epair
broken hip
E=
lectrolyte
imbalance, death
R=
educe
burden of investiga-tion for p=
atient
Stopping all lab t=
ests
S=
epsis,
death
R=
educe
pain
Epidural administration <=
/span>of
analgesia
P=
romote
arrhythmia, death
P=
revent
arrhythmia
A=
miodarone
I=
mmune
suppression, cytopenias, death
C=
ure
or reduce the burden of cancer
C=
hemotherapy
S=
epsis,
death
I=
mproved
nutritional status
TPN for short g=
ut
syndrome
Potential
Adverse, Secondary Consequences
Intended, Primary Effect
Therapy
Intended=
vs
Unintended Consequences
Breathlessness (dyspnea) . . .
•M=
ay
be described as
shortness of breath
a smothering feeling
inability to get enough air
suffocation
. .
. Breathlessness (dysp=
nea)
•The
only reliable measure is patient self-report
•Respiratory rate, pO2<=
/span>,
blood gas determinations DO NOT always correlate
with the feeling of breathlessness
•Prevalence in the
life-threateningly ill: 12 – 74%
Causes of breathlessness
<=
span
style=3D'font-weight:normal'>•Anxiety
• Airway obstruction
=
;
<=
span
style=3D'font-weight:normal'>•Bronchospasm
<=
span
style=3D'font-weight:normal'>•Hypoxemia
=
<=
span
style=3D'font-weight:normal'>•Pleural effusion
=
<=
span
style=3D'font-weight:normal'>•Pneumonia
=
<=
span
style=3D'font-weight:normal'>•Pulmonary edema=
•Pulmonary embolism
<=
span
style=3D'font-weight:normal'>•Thick secretions
<=
/span>
<=
span
style=3D'font-weight:normal'>•Anemia
<=
span
style=3D'font-weight:normal'>•Metabolic
=
•Family /
financial / legal / spiritual / practical issues=
Management
of breathlessness
of breathlessness
•T=
reat
the underlying cause
•S=
ymptomatic
management
oxygen
opioids
anxiolytics
nonpharmacologic interventions
Oxygen
Opioids
<=
span
style=3D'font-weight:normal'>•Relief not related to
respiratory rate
<=
span
style=3D'font-weight:normal'>•No ethical or professi=
onal
barriers
![](3D"slide0081_image005.gif")
Mild
dyspnea
&m=
iddot;
hydrocodone, 5 mg tab q 4 h with a
breakthrough dose of 5
mg q =
2 h
prn
· acetaminophen, 325 mg, with codeine, 30 mg =
(1
tab) q 4 h
with a
breakthrough dose of 30 mg q 2 h prn
· for children or elderly who may require low=
er
doses,
consi=
der
hydrocodone/acetaminophen syrup, 1–3 mL q 4 h
with a
breakthrough dose equivalent to the q 4 h dose
offer=
ed q 2
h prn
Example of Opioid Prescripti=
ons
![](3D"slide0082_image006.gif")
Example of Opioid Prescripti=
ons
Severe
dyspnea
·
morphine (as elixir or tablets), 5–15 mg q 4 h
and titrate
·
oxycodone, 5–10 mg q 4 h and titrate
·
hydromorphone, 0.5–2 mg q 4 h and titrate
Anxiolytics
•S=
afe
in combination with opioids
lorazepam
0.5-2 mg po q 1 h prn until settled
then dose routinely q 4–6 h to keep settled
![](3D"slide0083_image007.gif")
Example =
of
benzodiazepines include:
·
lorazepam, 0.5–2.0 mg po, SL, against the buccal
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mucosa, or IV q 1 h prn until set=
tled,
then dose
routinely q 4–6 h to keep
settled
·
diazepam, 5–10 mg po, IV q 1 h until settled, then
dose routinely q 6–8 h prn&=
#13;
·
clonazepam, 0.25–2.0 mg po q 12 h
·
midazolam, 0.5 mg IV q 15 min until settled, then
by continuous SC or IV infusion
Nonpharmacologic interventions
. . .
Nonpharmacologic
interventions . . .
<=
span
style=3D'font-weight:normal'>•Eliminate environmental
irritants
. .
. Nonpharmacologic inter=
ventions
•I=
ntroduce
humidity
•R=
eposition
elevate the head of the bed
move patient to one side or other
•E=
ducate,
support the family
Nausea / vomiting
•N=
ausea
subjective sensation
stimulation
gastrointestinal lining, CTZ, vestibular apparatus,
cerebral cortex
•V=
omiting
neuromuscular reflex
Causes
of nausea / vomiting
of nausea / vomiting
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Metastases
•Meningeal
irritation
<=
/span>
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Movement
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Mental
anxiety
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Medications
<=
span
style=3D'font-size:107%;font-weight:normal;visibility:hidden'>•
•Mechanical
obstruction
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Motility
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Metabolic
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Microbes
<=
span
style=3D'font-size:107%;color:yellow;font-weight:normal'>•=
Myocardial
<=
span
style=3D'font-size:107%;font-weight:normal;visibility:hidden'>•
Pathophysiology
of nausea / vomiting
of nausea / vomiting
![](3D"slide0072_image008.gif")
Cortex
Vestibular apparatus
GI tract=
Chemoreceptor
Trigger Zone (CTZ)<= /span>
Trigger Zone (CTZ)<= /span>
![](3D"slide0072_image009.gif")
<=
b>Neurotransmitters
<=
span
style=3D'font-family:Arial;font-size:117%;color:white;mso-color-index:0;
text-shadow:auto'>• Serotonin
![](3D"slide0072_image010.gif")
![](3D"slide0072_image011.gif")
![](3D"slide0072_image012.gif")
![](3D"slide0072_image013.gif")
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<=
span
style=3D'font-family:Arial;font-size:117%;color:white;mso-color-index:0;
text-shadow:auto'>• Dopamine
<=
span
style=3D'font-family:Arial;font-size:117%;color:white;mso-color-index:0;
text-shadow:auto'>• Acetylcholine
<=
span
style=3D'font-family:Arial;font-size:117%;color:white;mso-color-index:0;
text-shadow:auto'>• Histamine
Vomiting
center
Management
of nausea / vomiting
of nausea / vomiting
•Dopamine antagonists
<=
span
style=3D'font-weight:normal'>•Antihistamines
<=
span
style=3D'font-weight:normal'>•Anticholinergics
=
•Seroton=
in antagonists<=
span
style=3D'font-weight:normal'>•Prokinetic agents
=
<=
span
style=3D'font-weight:normal'>•Antacids
<=
/div>
•Cytopro=
tective
agents
<=
span
style=3D'font-weight:normal'>•Other medications
Dopamine antagonists
•Haloperidol
•Prochlorperazine
•Droperidol
•Promethazine
•Trimethobenzamide
•Metoclopramide
Histamine antagonists (antihistamines)
Acetylcholine antagonists
(anticholinergics)
(anticholinergics)
•Scopolamine
Serotonin antagonists
Prokinetic agents
<=
span
style=3D'color:white;mso-color-index:0;mso-special-format:lastCR;display:n=
one'>
Antacids
•Antacids
•H2 receptor antagonists
cimetidine
famotidine
ranitidine
•Proton pump inhibitors
omeprazole
lansoprazole
•Proton pump inhibitors (omeprazole, lansoprazole)
Other medications
<=
span
style=3D'font-weight:normal'>•Dexamethasone
<=
span
style=3D'font-weight:normal'>•Dronabinol
=
<=
span
style=3D'font-weight:normal'>•Lorazepam
<=
/div>
<=
span
style=3D'font-weight:normal;visibility:hidden'>•&=
#13;
<=
span
style=3D'font-weight:normal'>•Octreotide
Constipation
•=
Medications
opioid=
s
calcium-channel
blockers
antich=
olinergic
•D=
ecreased
motility
•=
Ileus
•Mechanical
obstruction
•Metabolic
abnormalities
•Spinal cord compression
=
<=
span
style=3D'font-weight:normal'>•Dehydration
•Autonomic dysfunction
<=
span
style=3D'font-weight:normal'>•Malignancy
Management
of constipation
of constipation
•G=
eneral
measures
establish what is “normal”
regular toileting
gastrocolic reflex
•S=
pecific
measures
stimulants
osmotics
detergents
lubricants
large volume enemas
Stimulant laxatives
Osmotic laxatives
<=
span
style=3D'font-weight:normal'>•Milk of magnesia (othe=
r Mg
salts)
Detergent laxatives
(stool softeners)
(stool softeners)
Prokinetic agents
Lubricant stimulants
•G=
lycerin
suppositories
•O=
ils
mineral
peanut
Large-volume enemas
Constipation
from opioids . . .
from opioids . . .
. .
. Constipation
from opioids
from opioids
•<=
span
style=3D'color:white;mso-color-index:0'>Combination stimulant / softeners =
are useful first-line medications&=
#13;
casanthranol +
docusate sodium
senna + docusa=
te
sodium
•<=
span
style=3D'color:white;mso-color-index:0'>Prokinetic agents
Causes of diarrhea
•Infections
•GI
bleeding
•Malabsorption
•Medications
•Obstruction
•Overflow
incontinence
•Stress
Management of diarrhea
•E=
stablish
normal bowel pattern
•A=
void
gas-forming foods
•I=
ncrease
bulk
•T=
ransient,
mild diarrhea
attapulgite
bismuth salts
Management
of persistent diarrhea
of persistent diarrhea
Anorexia / cachexia
Management
of anorexia / cachexia . . .
of anorexia / cachexia . . .
•Assess,
manage comorbid conditions
• Educate, support
<=
/span>
•Favorite foods /
nutritional supplements
. .
. Management
of anorexia / cachexia=
of anorexia / cachexia=
Management
of fatigue / weakness . . .
of fatigue / weakness . . .
•Promote
energy conservation
•Evaluate
medications
•Optimize
fluid, electrolyte intake
•Permission
to rest
•Clarify
role of underlying illness
•Educate,
support patient, family
•Include
other disciplines
. .
. Management
of fatigue / weakness<= /span>
of fatigue / weakness<= /span>
•D=
examethasone
feeling of well-being, increased energy
effect may wane after 4-6 weeks
continue until death
•M=
ethylphenidate
Fluid balance / edema . . .
•Frequently
associated with advanced illness
•Hypoalbuminemia ® decreased <=
/span>oncotic
pressure
•Venous
or lymphatic obstruction may contribute
. . . =
Fluid
balance / edema
Skin
Pressure (decubitus) =
ulcers
<=
span
style=3D'font-weight:normal'>•Closely associated with
mortality
Odors
•T=
opical
and / or systemic antibiotics
metronidazole
silver sulfadiazine
•K=
itty
litter
•A=
ctivated
charcoal
•V=
inegar
•B=
urning
candles
Insomnia
Management
of insomnia . . .
of insomnia . . .
•Regular
sleep schedule, avoid staying in bed
•Avoid
caffeine, assess alcohol intake
•Cognitive
/ physical stimulation
•Avoid
overstimulation
•Control
pain during the night
•Relaxation,
imagery
. .
. Management
of insomnia
of insomnia
E
P
E
C
P
E
C
End of Module 10:
Common Physical Symptoms
Review Fast Facts
Complete Module 10 Post Assessment
‹header›
‹date/time&=
#8250;
Click to edit Master text styles
Second level
Third level
Fourth level
Fifth level
‹footer›
‹#›
Many symptoms are commonly encou=
ntered
in patients with advanced illness. This module discusses the assessment and
management of breathlessness (dyspnea), nausea and vomiting, constipation,
diarrhea, loss of appetite (anorexia)/weight loss (cachexia), edema, skin
ulcers, insomnia, and fatigue (asthenia).
Each one can both be
debilitating and prevent the patient and family from either continuing the=
ir
lives or completing life closure. As with other aspects of medicine,
management is tailored based on the underlying etiology and pathophysiolog=
y.
When several symptoms occur together, they can be interrelated and managem=
ent
may become complex. The physician requires a working knowledge of therapy,
drug interactions, and
potential adverse effects to effectively relieve
suffering and improve the patient’s quality of life
During advanced stages of illnes=
s,
particularly in end-of-life care, pain management appropriately receives a
great deal of attention and emphasis. However, most patients are likely to
suffer from a number of other symptoms besides pain. At times, these sympt=
oms
can be even more distressing to patients and families than pain. If
unrelieved, they preclude any possibility of relieving psychological, soci=
al,
and spiritual suffering, improving quality of life, or completing life
closure.
Focusing on symptom control may make some physicians uneasy. =
Many
regard symptoms simply as clues to lead the physician to diagnoses, and as=
sume
that the symptoms will improve as the disease gets better. While it is com=
mon
for physicians to direct their efforts at curing or reducing disease, most=
do
not understand the associated pathophysiology, appropriate pharmacology, or
therapeutic interventions. When combined with
misconceptions about the
potential risks, interactions, or adverse effects of appropriate medicatio=
ns,
symptoms are often very poorly controlled.
The general approach to managing=
any
symptom is identical to the standard approach used to manage any illness. A
thorough history, physical examination, and laboratory or radiologic
investigations appropriate for the patient’s situation are used to g=
ain
the best possible understanding of each symptom’s etiology and
underlying pathophysiology.
As symptoms are often interrelated with
multiple concurrent medical problems, management can be challenging. As wi=
th
any other illness, it is not acceptable to have an unthinking approach to
symptom management, as causes and appropriate therapies can
vary widely.
Once the cause(s) and pathophysiology are known, intervention ideally incl=
udes
therapy to relieve the symptom(s) as well as treat underlying causes. As m=
any
journal articles and textbooks have been written on the management of the
underlying causes, this module will focus primarily on relieving the sympt=
om
itself.
When goals for care preclude dis=
ease
management, symptom relief may be all that is required. When symptoms are
debilitating or the patient is too weak, physicians will not be able to wa=
it
for the results of investigations before initiating therapy. Initial
therapeutic trials based on history, examination, and inference about the
pathophysiology may provide both symptom relief and/or additional informat=
ion
as to the etiology and
pathophysiology.
As with pain management, if a symptom is present continuously, medication =
should
be prescribed on a continuous or “around-the-clock” basis. Bre=
akthrough
doses may also be required. Education and involvement of the patient and
family as partners are key to successful management. Encourage patient and
family to keep a diary when symptoms are out of control or adverse effects
occur. When individual patient management becomes complex, physicians are
encouraged to consult with local palliative medicine experts, and other
members of the interdisciplinary team, to optimize therapies and minimize =
the
risk of adverse events and drug interactions.
As etiologies and
pathophysiology may change, frequent reassessment is critical, particularly
when symptoms recur. As changes in the patient’s condition can occur
rapidly, caregivers should be prepared to respond quickly.
Many physicians believe that med=
ications
used to manage symptoms have an unusually or unacceptably high risk of an
adverse event that may shorten a patient’s life, particularly when h=
e or
she is frail or close to the end of his or her life. Instead of fully
understanding and discussing the potential benefits and risks of these
therapies with their patients, taking into account their goals for care, t=
his
fear of an adverse unintended consequence
often leads clinicians to
withhold treatment or dose inadequately, thus leaving their patients suffe=
ring
unnecessarily.
When offering a therapy, the intent in offering a treat=
ment
that greatly determines
whether it is ethical medical practice:
· if the intent in offering a treatment is desirable or helpful to =
the
patient and the primary outcome is good (such as cure or relief of sufferi=
ng),
but there is a potential, adverse, secondary effect (such as death), then =
the
treatment is probably still ethical if there was proper informed consent&#=
13;·
if the intent is not desirable or will harm the patient and the primary
outcome is bad, the treatment is probably unethical
Concerns about
intended vs unintended consequences are most commonly invoked around such
issues as the treatment of pain or dyspnea with opioids. However, all medi=
cal
treatments have both intended effects and the risk of unintended, potentia=
lly
adverse, secondary consequences.
The
principle of double effect refers to an ethical construct when a person ta=
kes
an action with an expected good outco=
me but
with an unavoidable, known bad effect as well. The primary intended effect=
can sometimes justify the action. When a physician=
uses
a treatment for an ethical, intended effect where the potential outcome is good (eg, relief of a sym=
ptom),
knowing that there may also be a dire ,undesired, secondary effect such as
de=
ath,
this principle of double effect is commonly cited. In symptom control,
however, it rarely applies. The secon=
dary
adverse consequence of death is not likely to occur.
Co=
ncerns
that the principle of double effect may be an issue when managing symptoms=
are
raised by the fact that, like other m=
edical
treatments, there is a risk that treatments to control symptoms could prod=
uce adverse consequences including death, either when
improperly used or, very rarely, when properly used. Also, in suffering states of lifethreatening illne=
ss,
death may seem appealing and what is ordinarily intuitive may
be=
come
complex. For many interventions, such as chemotherapy, total parenteral
nutrition (TPN) for short gut syndrom=
e,
surgery, and noninterventions such as stopping all laboratory tests or
avoiding surgery, we make decisions k=
nowing
there is a risk of adverse events, in particular death. As long as (a) the intent is to relieve suffering and not hasten =
death,
(b) death is a possible and not inevitable outcome of the interventions, and
(c=
) there
is fully informed consent, the action need not be ethically suspect.
<=
/span>
In
contrast, if symptom control involves treatments that are intended to cause
death as the means to relieve sufferi=
ng,
then there is ethical concern. If the patient seeks hastened death by
physician-assisted suicide or euthana=
sia,
the clinical and ethical issues are different.
Fo=
rtunately,
these difficult circumstances need not occur. Adequate symptom management =
can
be achieved without causing death. If=
the
reason for offering a medication such as an opioid is to relieve suffering (eg, pain, breathlessness), and accepted
dosing guidelines are followed, the risk of a potentially dangerous adverse secondary effect is minimal. The=
risk
of respiratory depression is vastly over estimated.
Patients will become
dr=
owsy and
confused and lose consciousness long before their respiratory rate is
compromised.
&#=
13;
&#=
13;
M.S. is a 67-year-old accountant=
with
advanced pulmonary fibrosis. She experiences severe breathlessness with
minimal activity around the house. She experiences little benefit from
bronchodilators. She would like to be able to do things for herself.
B=
reathlessness
can be one of the most frightening and distressing symptoms for patients,
families, and caregivers. The sense of drowning or being smothered can be
terrifying for everyone. Fortunately, for the majority of patients, relief=
can
be relatively straightforward.
Yet physicians’ lack of understan=
ding
of breathlessness and the medications to manage it, and the fear of adverse
effects, frequently lead to inadequate relief and unnecessary suffering for
the patient, family, and caregivers.
Thus, as we have no objective
assessments, we must accept the patient’s self-report of his
or =
her
experience. Some patients may not report breathlessness. However, when
asked
Breathlessness, like pain, is a =
symptom,
not a sign. Its prevalence is variable (12%–74%), depending on the
diagnosis and the stage of the illness. Research has shown that measures of
respiratory rate, oxygen saturation, blood gas levels, and professional and
family members’ perceptions do not correlate with the patient’s
perception of breathlessness. about walking, they may indicate that
breathlessness prevents them from walking at their
usual pace or distance.
Families and caregivers need to be aware that what they see may be very di=
fferent
from the patient’s experience. Time spent to understand the
patient’s wishes for symptom control, and to communicate management
strategies to the patient, family, and caregivers, will minimize
misunderstanding and onlookers’ distress.
Many different illnesses can imp=
air
respiration and leave the patient with a sense of being breathless. Some of
the common mechanisms include anxiety, airway obstruction, bronchospasm,
hypoxemia, pleural effusion, pneumonia, pulmonary edema, pulmonary embolis=
m,
thick secretions, anemia, metabolic disorders, and family/financial/legal/
spiritual issues. Each may itself have many different etiologies.
When patients report air hunger,=
it is
frequently not possible to identify and/or correct the underlying etiology.
Therapeutic trials based on known history are frequently focused on
symptomatic relief only. In patients with advanced disease, the burden of
investigations and disease-modifying interventions may outweigh any potent=
ial
benefit.
There are 3 widely used medical approaches for the symptomatic
relief of breathlessness:
oxygen, opioids, and anxiolytics.
Nonpharmacologic interventions may also contribute significantly to the
patient’s and family’s sense of well-being.
As breathlessness is frequently
perceived to be a lack of air, it would seem to be quite reasonable to sup=
pose
that the administration of supplemental oxygen would relieve a patientR=
17;s
sense of air hunger. Yet, research has shown that the majority of patients=
who
report breathlessness are not hypoxemic and measures of hypoxemia (eg, pul=
se
oximetry, blood gas determination) do not correlate with the patient’=
;s
self-report. Thus, do not follow
pulse oximetry or blood gases to asse=
ss
relief. These tests do not reliably reflect breathlessness or its relief. =
They
may be uncomfortable and/or expensive, and divert the focus away from the
symptom. It does not help symptom management to know that the oxygen
saturation is 86% if the patient feels fine.
If a patient is breathles=
s, a
therapeutic trial of supplemental oxygen may be beneficial. After all, the
goal is to make the patient feel better. However, clinicians should be awa=
re
that there is likely a placebo effect in nonhypoxemic patients. Supplement=
al
oxygen is frequently viewed as a potent symbol of contemporary medical car=
e.
In addition, it is important to know that cool air moving across the
patient’s face, eg, from compressed air
or from a fan, may relie=
ve
the sense of breathlessness. This is likely due to the physiologic effect =
of
stimulating the V2 branch of the fifth cranial nerve that has a central
inhibitory effect on the sensation of breathlessness. Portable oxygen is
expensive and is not reimbursed by all insurance payers. Nevertheless, if =
the
patient reports relief, use supplemental oxygen if possible.
Research has demonstrated that o=
pioids
will relieve the distress of breathlessness in many patients without a
measurable effect on their respiratory rate or blood gas concentrations.&#=
13;The
precise mechanism by which opioids exert this effect is unclear. There may=
be
both central and peripheral effects. In the opioid-naive patient, doses lo=
wer
than those used to relieve pain may be effective.
When an effective do=
se
has been established, convert to an extended-release preparation to simpli=
fy
dosing. When using opioids, always anticipate adverse effects, particularly
constipation.
While nebulized opioids have been widely reported to be
effective in anecdotal reports and phase II studies, in placebo-controlled
studies, they have not yet been demonstrated to be superior to nebulized
saline.
When opioids are used to manage breathlessness, pharmacologic
tolerance is not a clinically significant problem. In some patients, the
symptom relief may also be associated with a measurable increase in exerci=
se
tolerance and mobility. If opioid dosing guidelines are followed, respirat=
ory
depression has not been demonstrated at the doses used to relieve
breathlessness.
Concerns that opioids used to manage symptoms will has=
ten
death or cause addiction are not relevant. Opioid treatment for dyspnea is
consistent with good medical practice, and, when widely accepted dosing
guidelines are followed, are unlikely to be associated with hastened death=
or
abuse behaviors.
In patients receiving an opioid =
on a
fixed schedule, an additional dose of a short-acting opioid (eg, morphine)
equivalent to 30%–50% of the amount of the baseline opioid taken ove=
r 4
hours can be tried q 1 h, and titrated to effect. Opioids can be administe=
red
IV or SC for urgent situations or when the oral route is not available or
advisable.
Chlorpromazine and promethazine have both been reported imp=
rove
breathlessness, particularly when combined with opioids.
Breathlessness, particularly whe=
n it is
acute or severe, may cause severe anxiety and panic. Opioid and nondrug
therapies may relieve both breathlessness and resultant anxiety. Consequen=
tly,
their use is recommended as first-line pharmacologic therapy for
breathlessness. However, the opioids themselves, particularly with continu=
ed
dosing, are not particularly anxiolytic.
Benzodiazepines are highly
effective anxiolytic medications. Use formulations that have relatively lo=
nger
half-lives to avoid pronounced peak and trough effects that may lead to
rebound anxiety. Begin with low doses and titrate to effect. These medicat=
ions
may be combined safely with opioids.
Additional relief of breathlessn=
ess may
be provided by a variety of nonpharmacologic interventions. When possible,
coordinate treatments with the family and other caregivers. Work closely w=
ith
the patient and family to provide understanding and support, and explain t=
he
various interventions. Include other members of the interdisciplinary team=
to
increase interaction, minimize loneliness, explore issues of meaning and
value, and provide counseling for family, financial, legal, spiritual, or
practical issues that may be adding to anxiety. Limit the number of people=
in
the patient’s room. Reduce the room temperature (without chilling the
patient). Open a window and keep an unobstructed line of sight between the
patient and the outside. Eliminate environmental irritants such as smoke.
Maintain sufficient humidity in the air the patient is breathing. Repositi=
on
the patient by elevating the head of his or her bed, or moving him or her =
to
one side or another.
Try relaxation, distraction, or hypnotic therapy.
Complementary and alternative medical approaches may help some patients.&#=
13;
In some instances, nonpharmacolo=
gic
therapies may be effective without other medications. However, in the high=
ly
anxious patient, combination therapies are usually necessary.
Family member/caregiver reactions
Standing next to a person who is breathing at 36 breaths/min, with a pulse=
oximeter
beeping and oxygen rushing through tubing, is anxiety producing for almost
anyone. Family members and caregivers frequently take on the anxiety of the
patient. In turn, their anxiety may make the patient’s breathlessnes=
s worse.
When
managing breathlessness, it is important to distinguish between the patien=
t’s
distress and that of family members and caregivers. Minimize the number of
machines and sounds. Titrate medications to relieve the patient’s re=
port
of distress, not someone else’s perception of it.
As patients
approach the last hours of their lives, be sure to educate family members =
and
caregivers about the breathing patterns they may witness. Remind them that
what they see may be very different from what the patient experiences.
P.T. is a 92-year-old farmer wit=
h colon
cancer metastatic to the liver. Right upper quadrant pain is well controll=
ed
with extended-release morphine, 60 mg po bid, and dexamethasone, 4 mg po q=
am.
However, he complains of constant nausea that limits his ability to eat.&#=
13;Nausea
and/or vomiting are commonly associated with many advanced diseases. Nause=
a is
an unpleasant subjective sensation that results from stimulation of the
gastrointestinal lining, the chemoreceptor trigger zone in the base of the
fourth ventricle, the vestibular apparatus, or the cerebral cortex. Vomiti=
ng
is a neuromuscular reflex that constitutes a final common pathway after
stimulation of one or more of these areas. The awareness of nausea, the in=
ability
to keep food or fluids down, the associated acid and bitter tastes, and the
unpleasant smells associated with vomitus can be very distressing for pati=
ents,
families, and caregivers.
While there are multiple potenti=
al
causes for both nausea and vomiting, fortunately, symptomatic relief is
relatively easy to achieve if the right medications are chosen. Unfortunat=
ely,
as with most symptoms, lack of physician understanding and unsophisticated
prescribing frequently lead to inadequate relief and unnecessary suffering=
for
the patient, family, and caregivers.
A thorough assessment of nausea a=
nd
vomiting is crucial to understanding which of the potential etiologies is
operant, what the likely pathophysiology is, and what would be most
appropriate to prescribe. Different causes will require very different
interventions if the symptoms are to be controlled effectively.
There are 2 organ systems that a=
re
particularly important in nausea and vomiting: the brain and the GI tract.
These are shown schematically. The gastric lining, the chemoreceptor trigg=
er
zone in the base of the fourth ventricle, the vestibular apparatus, and the
cortex are all involved in the intricate physiology of nausea. The vomiting
center is where the neuromuscular reflex that constitutes the final common
pathway after stimulation
from one or more of these areas emanates.
Stimulation is mediated through the neurotransmitters serotonin, dopamine,=
acetylcholine,
and histamine. All 4 neurotransmitters can be demonstrated in the
chemoreceptor trigger zone. Although all are present in the lining of the =
GI tract,
serotonin is particularly important. Acetylcholine and histamine are impor=
tant
in the vestibular apparatus.
Nausea and vomiting that is mediated by t=
he
cortex is more complex and is not associated
with specific
neurotransmitters. Cortical responses seem to be learned responses (eg, the
anticipatory nausea associated with chemotherapy, nausea related to anxiet=
y,
etc).
This module focuses on the gener=
al
symptomatic management of nausea and vomiting. It does not provide detail =
of
all the possible causes or specific treatments to reverse each of these
etiologies. In the management of nausea and vomiting, it is frequently not
possible to identify or specifically correct the underlying etiology.
Therapeutic trials may provide both relief and clues to underlying causes.
When causes are known, the burden of the disease-modifying intervention may
also outweigh its potential benefit.
Empiric therapy with antiemetics
usually begins with a single medication targeting the presumed mechanism of
nausea/vomiting. The dose should be optimized before a second medication w=
ith
a different mechanism of action is added. Sequential combination therapy m=
ay
be required in some patients.
Dopamine-mediated nausea is prob=
ably the
most common form of nausea, and the most frequently targeted for initial
symptom management, even when the precise mechanism of nausea is not known.
These medications are phenothiazines or butyrophenone neuroleptics and have
the potential to cause drowsiness and extrapyramidal symptoms, particularl=
y in
young women. Haloperidol is less sedating.
All antihistamines typically use=
d to
control nausea may also cause sedation. In some patients, this adverse eff=
ect
may be an added benefit. Because the antihistamines also have anticholiner=
gic
properties, they may do “double duty” as a single agent and co=
ver
both mechanisms. Consider using:
· diphenhydramine, 25–50 mg po q 6 h
· meclizine, 25–50 mg po q 6 h
· hydroxyzine, 25–50 mg po q 6 h
Opioids and anesthetics can trig=
ger
acetylcholine-mediated nausea in the vestibular apparatus. A medication fr=
om
this class may be added to other antiemetics in empiric therapy.
Consider:
· scopolamine, 0.1–0.4 mg SC, IV q 4 h or
1–3 transdermal patches q 72 h or
10–80 mg/h by continuous IV or SC infusion
Serotonin has been particularly
implicated in chemotherapy-associated nausea. This class of medications ca=
n be
exceedingly effective, but they are very expensive. They can be useful for
refractory nausea of diverse types but are typically tried only when other
medications have failed. They should be promptly stopped if they are not
effective after a short trial. Medication and dosing options include:
· ondansetron, 8 mg po tid
· granisetron, 1 mg po q d or bid
A “sluggish” or dysk=
inetic
gut (due to carcinomatosis, opioid therapy, other medications, etc) may be=
a
profound source of nausea and vomiting in patients with advanced disease. A
large liver may be causing a “squashed stomach.” Ascites or
peritoneal disease may be causing pseudo-obstruction. Constipation can be =
an
exacerbating factor. Medication and dosing options include:
· metoclopramide, 10–20 mg po q 6 h
· cisapride, 10–20 mg po q 6 h
Hyperacidity, with or without
gastroesophageal reflux and/or gastric or duodenal erosions, may produce
considerable nausea, heartburn, acidity, or bitter taste. It may also be
associated with vomiting. Possible therapies include:
· antacids, 1–2 tablespoons q 2 h prn
· H2 receptor antagonists (cimetidine, famotidine,
ranitidine)
· proton pump inhibitors (omeprazole, lansoprazole)
This heterogeneous class of medi=
cations
has unclear mechanisms of action, but uncontested benefits in some patient=
s.
Consider:
· dexamethasone, 6–20 mg daily
· tetrahydrocannabinol, 2.5–5 mg po tid
· lorazepam, 0.5–2 mg po q 4–6 h
The symptoms of bowel obstruction represent a special case. With complete =
obstruction,
accumulation of intraluminal fluid from epithelial sources is principally
response for the symptoms of bloating, crampy abdominal pain, nausea, and
vomiting. Octreotide, a synthetic analog of somatostatin, selectively inhi=
bits
secretion of fluids and electrolytes into the gut lumen. It may be started=
by
continuous IV at 10 mg/hr or intermittent subcutaneous
injection. A standard regimen is:
· octreotide 100 mg q 8-12 h, titrate q 24 to 48 h to effect&#=
13;
A.R. is a 46-year-old mother of =
2 with
advanced ovarian cancer widespread within the abdomen. Ascites is present =
on
examination. Bowel sounds are present. Pain is well controlled with
transdermal fentanyl, 25 mg/h. However, she complains of persistent
constipation.
Constipation can be defined as “discomfort associa=
ted
with reduced frequency of bowel movements.” It is usually associated
with an increase in stool consistency that leads to difficulty in defecati=
ng.
There are many causes of constipation, including medications (eg, opioids,
calcium-channel blockers, anticholinergics), decreased mobility, ileus,
mechanical obstruction, dehydration, metabolic abnormalities, spinal cord
compression, autonomic dysfunction, malignancy, etc.
The cause in a gi=
ven
patient is often not carefully assessed. If left unmanaged, it can lead to
considerable patient distress. The consequences of unmanaged constipation
include abdominal pain, bloating, nausea and vomiting, overflow incontinen=
ce,
tenesmus, fecal impaction, or even bowel obstruction.
General approaches
Examination, investigation, and treatment should be tailored to the presen=
tation,
stage, and context of the person and illness. For most patients near the e=
nd
of life, correction of the underlying pathophysiologic cause of constipati=
on
is often not possible or appropriate. The following general measures may be
helpful.
Establish what the patient considers normal bowel function. T=
here
is a wide range of “normal” number of bowel movements per day =
or
per week, consistency, color, and volume. Have the patient toilet regularl=
y at
the same time each day. Take advantage of the gastrocolic reflex that occu=
rs
after eating. Have the patient sit upright if possible.
Specific approaches
For medical management of constipation, suggested cathartics are listed in=
order
of usual preference in patients with advanced illness, poor mobility, and =
decreased
oral intake. Clinicians frequently fail to dose-escalate a particular moda=
lity.
This leads to the sense that “nothing works” when, in fact,
nothing has been tried to its maximal therapeutic dose.
Stimulant laxatives irritate the=
bowel
and increase peristaltic activity. Consider:
· prune juice, 120–240 mL q d or bid
· senna, 2 po q hs, titrate to effect (up to 9 or more per
day)
· casanthranol, 2 po q hs, titrate to effect (up to 9 or more =
per
day)
· bisacodyl, 5 mg po, pr q hs, titrate to effect
Osmotic laxatives draw water int=
o the
bowel lumen. They maintain or increase the moisture content of stool and
increase the overall stool volume. Consider:
· lactulose, 30 mL po q 4–6 h (sorbitol is cheaper
alternative), then titrate
· milk of magnesia (or other Mg salts), 1–2 tablespoons
1–3 times per day
· magnesium citrate, 1-2 bottles prn
Detergent laxatives facilitate t=
he
dissolution of fat in water and increase the water content
of stool. Consider:
· sodium docusate, 1–2 po q d–bid, titrate to
effect
· calcium docusate, 1–2 po q d–bid, titrate to
effect
· phosphosoda enema prn
Prokinetic agents stimulate the
bowel’s myenteric plexus, and increase peristaltic activity
and stool movement. Consider:
· metoclopramide, 10–20 mg po q 6 h
· cisapride, 10–20 mg po q 6 h
Lubricant stimulants lubricate t=
he stool
and irritate the bowel, thus increasing peristaltic activity and stool
movement. Consider:
· glycerin suppositories
· oils:
- mineral
- peanut
Large-volume enemas soften stool=
by
increasing its water content. They also distend the
colon and induce peristalsis. Consider:
· warm water
The addition of soap suds further irritates the colon and induces peristal=
sis.
(NB. Too
much soap suds may damage the bowel wall.)
· soap suds (irritates colon to induce peristalsis)
Constipation should be expected =
during
opioid treatment, and prophylactic measures should always be considered. T=
he
condition is easier to prevent than treat, and prophylactic laxatives are
reasonable in the elderly, debilitated patient who may have other coexisti=
ng
causes of constipation. An effective regimen to maintain bowel function wi=
ll
enable patients to have both pain relief and normal bowel movements. New-o=
nset
abdominal pain and/or nausea and vomiting in a patient taking opioids may =
be
due to unrecognized constipation. Abdominal x-rays may be needed to confirm
the diagnosis.
Warn the radiologist that you are looking for the volum=
e of
stool present, not just signs of obstruction.
While opioids cause constipation=
, they
are not the only medication to do so. Other medications also commonly cause
constipation, including calcium-channel blockers, and any medication with
anticholinergic adverse effects (such as tricyclic antidepressants) may be
causing or exacerbating the problem
S.D. is a 79-year-old tax attorn=
ey with
advanced congestive heart failure. He is debilitated and has difficulty wi=
th
mobility. Due to a curative resection of a large transverse mass some years
ago, he has chronic diarrhea. Getting up to go to the bathroom 12 to 15 ti=
mes
per day is exhausting.
Diarrhea can be defined as stools that are loos=
er
than normal and that may be increased in numbers. If persistent, diarrhea =
can
lead to dehydration, malabsorption, fatigue, hemorrhoids, and perianal skin
breakdown.
General approaches
· establish normal bowel habits (there is wide variation)
=
· avoid gas-forming foods, particularly lactose
· increase bulk (eg, psyllium, bran, pectin)
Specific approaches
For the medical management of transient or mild diarrhea consider:=
3;
· attapulgite, 30 mL or 2 tabs prn
· bismuth salts, 15–30 mL bid–qid
For persistent and bothersome diarrhea, slow peristalsis consider:=
3;
· loperamide, 2–4 mg po q 6 h, or higher
· diphenoxylate/atropine, 2.5–5.0 mg po q 6 h or higher&=
#13;
· tincture of opium, 0.7 mL po q 4 h and titrate
For persistent, severe secretory diarrhea consider:
· octreotide, 50 mg SC q 8–12 h, then titrate up to 500 mg q =
8 h
SC, or higher, or
10–80 mg q 1 h by continuous SC, IV infusion
· parenteral fluid support, as needed and appropriate
M.C. is a 53-year-old obstetrici=
an with
widely metastatic breast cancer to bone, liver, and lung. Her disease is
slowly progressive despite chemotherapy and hormonal therapy. She has lost=
60
pounds in the past 4 months, and complains of a poor appetite. Anorexia (l=
oss
of appetite) and cachexia (loss of weight) are frequently accompanied by
generalized fatigue (asthenia). These symptoms occur in many illnesses,
particularly
when the disease process is advanced. Wasting syndromes a=
re
often seen with certain malignancies, heart and pulmonary disease, renal a=
nd
hepatic failure, and chronic infections, including Acquired Immune Deficie=
ncy
Syndrome (AIDS).
The specific etiology of these symptoms is not well
understood. However, they are a significant cause of distress to patients =
and,
even more so, to families and caregivers. Loss of appetite and weight in a
patient are often construed as evidence of “failure” to provide
adequate care. Alternately, attentive families may believe that they are d=
oing
something wrong. Many patients and families conclude that, if only the pat=
ient
would eat more,
he/she would resume his/her former weight and vigor.
Sadly, this is not usually possible, even with parenteral or enteral
nutrition.
Loss of appetite, weight, and en=
ergy are
not strictly the result of malnutrition; providing nutrition, even
parenterally, does not change the course of the disease. Helping patients =
and
families understand these distinctions often diminishes guilt, hostility, =
or
conflict. The physician and members of the health care team can then help =
the
patient and family focus on things that may be useful.
Assessing for
dysphagia, odynophagia, medication effects, or infections that may be caus=
ing
or exacerbating the problem may be worthwhile. There are therapies that may
improve appetite and add weight, although none affect longevity.
There are several approaches to =
the
general management of loss of appetite, weight loss, and fatigue. Assess a=
nd
manage comorbid conditions such as anxiety, nausea, dehydration, constipat=
ion,
and oral or systemic infections. Educate and support the family and
caregivers. Help them distinguish between the normal progression of the
disease, over which they have no control, and things they can do to help t=
he
patient feel better. Explore
the emotional components and the meaning =
of
the patient not eating, losing weight, or not having energy. Assess how mu=
ch
the patient (as opposed to family) is bothered by symptoms. Frequently the
patient is comfortable, but the family is distressed.
Offer the patient
favorite foods and nutritional supplements if the patient enjoys them.
Eliminate dietary restrictions. Reduce portion sizes and make food look
appetizing. Avoid odors that the patient finds disagreeable
T.L. is a 97-year-old woman with
osteoarthritis, hypertension, and breast cancer metastatic primarily to bo=
ne.
She lives independently, but complains about not having enough energy to g=
o to
the store.
In multiple series, fatigue/weakness is the most frequent
distressing symptom associated with advanced illness and end-of-life care.
Patients and families will frequently focus on the symptom rather than its
underlying cause. Many believe that a person’s strength is under his=
or
her control, and feel that the patient is “giving up” or
“not fighting.”
The physician can play an instrumental rol=
e in
educating the patient and family about the nature of the symptom and giving
the patient “permission” to rest. The physician can help decre=
ase
the pressure from family or others exhorting the patient to be more alert,
energetic, and conversant. Input from other team members may also be
helpful.
General approaches
There are many general management approaches to fatigue. Help patients and=
families
to adapt activities of daily living that promote energy conservation. Phys=
iotherapy
and occupational therapy can help with assessment, teaching, and assistive
devices. Discontinue routine medications that are no longer appropriate ne=
ar
the end of life and may be making the fatigue worse (particularly
antihypertensives, cardiac medications, diuretics, etc).
Optimize fluid
and electrolyte intake to maintain best possible hydration consistent with
goals of care and the patient’s ability to maintain intravascular hy=
dration
based on the degree of hypoalbuminemia.
Specific approaches
While fatigue/weakness is not easily treated pharmacologically, some patie=
nts respond
to a few of the following approaches. Steroids may have a beneficial effec=
t.
Dexamethasone in doses of 2 to 20 mg po daily is favored because its long
half-life permits once-daily dosing and relative lack of mineralocorticoid=
adverse
effects. Its use is frequently associated with feelings of well-being and =
increased
energy. Dose in the morning for its
activating effect. While it can be
continued until death, the effect may wane after 4 to 6 weeks. As long-term
adverse effects are not a factor for patients who are at the end of their
lives, there is no need to taper the dose if it remains effective.
The
psychostimulants may also be useful. Most experience has been gained with
methylphenidate, although dextroamphetamine and pemoline have been used. B=
egin
methylphenidate at 2.5 to 5 mg po q am and q noon and titrate to effect
(usually 10–30 mg po q am and q noon, but sometimes higher). Extende=
d-release
formulations permit once-daily dosing. Methylphenidate can be used safely =
even
in the debilitated patient.
Adverse effects, including tremulousness,
anorexia, tachycardia, and insomnia, should be monitored.
O.F. is a 78-year-old mathematic=
ian with
alcoholic cirrhosis of the liver with ascites and dependent edema. He
complains of “tight legs and abdomen.” Blood pressure is 110/5=
0 mm
Hg and his wife notes he is not urinating very much. This section will not
cover the management of edema when the causes are easily identifiable
=
and
reversible. Difficult cases may merit interdisciplinary evaluation. This s=
ection
discusses some useful points related to the management of patients with
advanced disease.
In the face of hypoalbuminemia and consequent dimini=
shed
oncotic pressure, patients will be unable to maintain their usual
intravascular physiology. It is normal for some patients to develop relati=
ve
hypotension, tachycardia, and reduced urine output. No amount of intraveno=
us
fluid and salt will return the intravascular volume to normal. Attempts to=
do
so will create or exacerbate edema, resulting in swollen limbs, skin
breakdown, ascites,
pleural effusions, and pulmonary edema. Similarly,
exogenous albumin infusions are ineffective and expensive and may make ede=
ma
worse because of extravasation of denatured albumin into the soft tissues.
Total parenteral nutrition is ineffective for different reasons
Notes on the management of patients with advanced
disease and edema
The following tips and reminders can be helpful.
· hypoalbuminemia leads to reduced oncotic pressure, decreased
intravascular volume
(with relative hemoconcentration), and increased
fluids in interstitial spaces (edema)
· decreased intravascular
volume stimulates antidiuretic hormone secretion and increases
free-water retention. This, in turn, leads to a relative hyponatremia=
as
water
exceeds salt retention
· in patients with hypoalbuminemia, a small amount of peripheral ed=
ema
is indicative of “closer to normal” intravascular volumes, in
contrast to the significantly decreased volumes that will be present when
hypoalbuminemia is not accompanied by peripheral edema
· patien=
ts
with clinical edema are not dehydrated; they have excess quantities of tot=
al
body fluid and salt. With time, they may be able to reabsorb them, though =
not
as efficiently as normal
· urine output of 300–500 ml/d or less is normal and
adequate in this setting
· supplemental fluid (particularly parenteral) should be avoided.
Patients should be encouraged to eat and drink as they usually do. Treat
symptoms that prevent oral intake
· debilitated patients may on=
ly
be drinking free water (such as in tap water, tea, coffee, juices, sodas t=
hat
have no sodium chloride). Encourage them to drink some salt-containingflui=
ds
(soups, club soda, sport drinks, red vegetable juices) to help them mainta=
in
their electrolyte balance
· careful attention to mucous membran=
es
(mouth, lips, eyes, nose, etc) can prevent sense of dryness that
hypoalbuminemia and intravascular hypovolemia may bring
· edema=
tous
skin is fragile. Use other interdisciplinary team members to assess and ma=
nage
it with appropriate supports and protection
· selected patients
with limb edema may benefit from appropriate wrapping with compression
bandages
E.K. is a 103-year-old housewife=
with
advanced dementia. She has been a resident of a nursing home for the past 7
years. She has become progressively bedbound. Several bedsores over bony
prominences have appeared.
Skin care is often overlooked in physician
education. Yet, skin breakdown and ulceration can be a source of significa=
nt
morbidity for both the patient and the family. The associated pain can be
significant. Exudates, particularly purulent ones, can be soiling and
malodorous. Good care requires close collaboration with nurses and other
caregivers, as most cases of skin breakdown are preventable. Prevention is
much easier than treatment
once skin breakdown occurs.
While comprehensive wound management is not the focus of this module, a few
points are worth reviewing, as many require a physician’s order.
Hygiene
Encourage family and caregivers to keep skin clean and dry. A variety of n=
ursing
techniques are appropriate. Absorbent surfaces, urinary catheters and rect=
al
tubes may be of assistance if soiling is constant and/or the patient is hi=
ghly
debilitated. Protection
Cover areas with appropriate dressings where prolonged urine or stool cont=
act may
occur. Cover fragile skin that is at risk for breakdown with clear, occlus=
ive
dressings. Cover pressure points with thin, hydrocolloid dressings.
Supports
Appropriate bed coverings will optimize weight distribution, reduce the ri=
sk
of decubitus ulcer development, and minimize contact pain. Use draw sheets=
to move/turn
cachectic patients. Egg crate foam pads, or other support mattresses, shou=
ld
be thick enough to lift the patient from the bed. One rule of thumb is to =
ensure
that there is at least 1 inch of foam between the patient’s lowest p=
oint
and the surface of the bed. If foam isn’t enough,
air mattresses=
or
other special air-flotation beds may be required to fully support the
patient.
Pressure ulcer management should be consistent with the overa=
ll
goals of care. If overall maintenance or improvement of function is the go=
al,
and prognosis is expected to be weeks to months, then stage and treat the
ulcer with accepted management guidelines (see the AHCPR management guidel=
ines
for pressure ulcers). Avoid all iodine-containing products as they will
inhibit reepithelialization.
If prognosis is limited (days to weeks) a=
nd
intent is to optimize quality of life, then a conservative management stra=
tegy
to minimize morbidity is appropriate. Regular cleaning with saline or Beta=
dine
is helpful. Cover ulcers with appropriate protective dressings that absorb
exudates.
Odors may be very distressing to
patients, families, and caregivers, and may lead to poor quality care, as =
even
professional caregivers avoid sickening smells. Odors are usually the resu=
lt
of anaerobic infections and/or poor hygiene. Treat superficial infections =
with
topical metronidazole or silver sulfadiazine bid or tid. For soft tissue
infections, add systemic metronidazole, 250 to 500 mg q 8 h to topical
management.
To control odors, place open kitty litter or activated
charcoal in a pan under the patient’s bed, provide adequate room
ventilation, place an open cup of vinegar in the room, or burn a candle.
Special charcoal-impregnated dressings placed over the odorous wound may a=
lso
be helpful.
G.E. is a 92-year-old seamstress=
with
progressive dementia. Her daughter, who lives with her but works during the
day, indicates the patient isn’t sleeping well. The caregiver during=
the
day indicates she spends most of the day in a chair in front of the
television, and naps frequently.
Many patients (and their families)
complain that they cannot sleep. Management begins with an assessment of u=
sual
and current sleep patterns. Do they have difficulty falling asleep or are =
they
waking? Are they awakened by nightmares? Are they experiencing early morni=
ng
awakening or nighttime restlessness? What do they think about when they are
awake? Are they afraid? Are they experiencing day-night reversal of sleep
patterns?
What are the associated symptoms (eg, anxiety, pain, nausea =
and
vomiting, breathlessness, medication effects), psychosocial or spiritual
issues, or practical concerns that may be interfering with sleep? Family a=
nd
other team members will often be needed to find answers
General approaches
To manage insomnia, general measures will need to be instituted that suppo=
rt good
sleep patterns. Establish and maintain a regular sleep schedule. If possib=
le,
avoid staying in bed when awake. Avoid caffeine (including analgesics with
caffeine), particularly late in the day. Assess alcohol use. Many patients=
use
alcohol as a soporific or “toddy” at bedtime.
Yet, alcohol
makes a poor sleeping medicine, as it can cause a paradoxical awakening
several hours after falling asleep. Plan for cognitive and physical stimul=
ation
during the day. Avoid overstimulation in the period before going to sleep.
Control bothersome symptoms and use long-acting medication to control pain
during the night. Interventions
such as relaxation and imagery may be helpful.
Specific approaches
A number of pharmacologic measures may be adjuncts to the general measures=
indicated
above.
Antihistamines are frequently used. Examples include diphenhydramine, 25 to
50
mg po q hs, and meclizine, 25 to 50 mg po q hs. However, tolerance =
may develop
quickly,
and some patients find the anticholinergic adverse effects troubling. Benz=
odiazepines
(eg,
lorazepam, 0.5–2 mg po q hs) are frequently used. However, dementia =
and delirium
may be worsened, particularly in the frail or elderly. Imidazopyridines (e=
g,
zolpidem, 5–10 mg po q hs) may have fewer adverse effects.
Neuro=
leptic
medications may be required, particularly if day-night reversal or deliriu=
m is
present. Risperidone or
haloperidol, 1 mg q hs (less sedating), or chlorpromazine, 10–25 mg =
q hs
(more sedating), may be useful.
Debilitated and frail patients require
careful titration and attention to undesired effects of medications. Commo=
nly
used medications may be associated with excessive daytime sedation. Trazod=
one,
25 mg po q hs (titrating to up to 200 mg q hs) may be particularly useful =
in
the frail and/or elderly.
Symptom control requires the phy=
sician
to combine scientific knowledge of pathophysiology, pharmacotherapeutics, =
and
human behavior with communication skills and clinical judgment. It is
challenging and rewarding to help patients feel better in spite of progres=
sive
disease. Careful attention to symptom control may lead to better tolerance=
of
disease-modifying therapies, and may even help prolong life. Continued sym=
ptom
control as patients approach the end of their lives will give them the
opportunity to realize the final goals they are striving for.
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