Transcript Caring for the patient in Alcohol Withdrawal

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You will be given opportunities throughout
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Identify keys components to the pathophysiology of alcohol
withdrawal and neurological involvement
Identify the body’s responses to stress and how the HPA axis
relates to aging
Identify the signs, symptoms, and behaviors of alcohol
withdrawal
Apply learned concepts to a case study involving the care of
the patient in alcohol withdrawal
Identify how genetics and metabolism are related in alcohol
abuse
Identify inflammation and it’s role in comorbidities associated
with alcohol abuse
Sections
Click on individual sections to jump to that
section
Case Study (1)
 Neurological Pathophysiology(2)
 Hypothalamic-pituitary-adrenal Axis(HPA Axis),
“fight or flight”, & Generalized Stress Response(3)
 Signs & Symptoms of alcohol withdrawal(4)
 Symptom Management(5)
 Nursing Interventions(6)
 Genetics & Metabolism (7)
 Alcoholic Liver Disease & Inflammation (8)
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31 year old male, admitted to your unit for
alcohol detox, states he had his last drink
over 24 hours ago, and exhibits the
following signs and symptoms Complains of nausea but no vomiting
 Tremulousness
 States he has a tight “rubber band”
feeling around his head
 Profuse sweating
Click here
to return to
data
Feels intense anxiety
 Denies hallucinations
 Denies agitation
 Knows the current place and time
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Click here
to return to
data
We will come back to this case study later
in the tutorial
Neurons- nerve cells that communicate to
each other using electrical and chemical
signals (neurotransmitters)
 Synapse- giving and receiving ends where
neurotransmitters are transported from one
neuron to the next
 Presynaptic neurons release
neurotransmitters to receptors on the
postsynaptic neuron
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Lovinger, 2008
gamma-Aminobutyric acid (GABA)
GABA
Glutamate
Glutamate
Microsoft, 2007
Main inhibitory
neurotransmitter in the human
body
 Found in all areas of the brain
 Regulates neuronal
excitability throughout the
body
 Binds to GABA receptors in the
presynaptic and postsynaptic
phases of transmission
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Lovinger, 2008
Alcohol enhances GABA by
increasing the inhibitory
effects (sedative effect)
 Current drugs in the
benzodiazepine and
barbiturate families can
replace alcohol in the brain
for successful and non life
threatening alcohol
withdrawal treatment
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Benzodiazepines
bind here
NIAAA, 2009
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Exhibits excitatory effects on
the brain
Like GABA, is found all over
the brain
Binds to NMDA receptors in the
brain
Acute alcohol exposure
inhibits glutamate
transmission, causing neuronal
excitability (leading to
seizures)
Chronic alcohol exposure
increases the number of
NMDA receptors
Lovinger, 2008
Increased numbers of NMDA
receptors leads to withdrawal
hyper excitability and alcohol
induced neuronal damage
when GABA cannot produce
inhibitory effects
 Involved in cognitive functions
such as learning and memory
 Drugs that act to reduce
receptors involved with
glutamate such as memantine
and topiramate are either
being studied or used for
treatment
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GABA is an inhibitory
neurotransmitter
GABA and alcohol bind to
the same receptors
In alcohol withdrawal
treatment,
benzodiazepines bind to
those same receptors,
preventing neurological
withdrawal symptoms
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Glutamate in an excitatory
neurotransmitter
Alcohol binds to certain
receptors to produce
sedating effects and long
term use causes increased
NMDA receptors
In the absence of alcohol,
NMDA and glutamate
create excitability since
GABA is not present to
inhibit this (seizures)
Neuroendocrine response to stress
(Brain)(Hormones)
 Contributes to psychological and physiological
responses to alcohol
 Ultimately stimulates glucocorticoid secretion
 Three way relationship exists between alcohol use,
glucocorticoid secretion, and aging
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Hutchison & Spencer, 1999
Adrenal
Gland
Stressful
situation
(alcohol
intoxication)
Hypothalamus
Pituitary Gland
Hint: Roll mouse over body parts
to reveal what they release.
Adrenal Glands
So now what?
Cortisol released from the adrenal glands of the kidneys prevent
further release of CRH and ACTH.
Is this a negative or positive feedback loop? Think about it and
save it for the end of the section.
Hutchison & Spencer, 1999 & Microsoft 2007
Alcohol use stimulates the HPA Axis
 Length of stimulation depends on
amounts of alcohol consumed or blood
alcohol level (BAC)
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Hutchison & Spencer, 1999 & Microsoft 2007
Blood alcohol levels (BAC) and HPA Axis
activation have a strong genetic
component
 Strong evidence exists of a defective
gene, not allowing the correct
metabolism of alcohol
 People with this gene have significant
high cortisol levels
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Hutchison & Spencer, 1999
Aging people are more
at risk for HPA Axis
overstimulation
Why?
Hutchison & Spencer, 1999
Recovery is slower
 The feedback loop
takes longer to get the
message back
 Getting rid of
catecholamines takes
longer
 Cortisol levels
eventually will cause
neuronal death
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Norepinephrine/
Noradrenaline
Released
Alpha
1
Diaphoretic
Alpha
2
Dilated
Pupils
Increased
Blood Pressure
GI Tract
off
Lowers
Insulin
Beta
1
Increased
HR
Beta
2
Increased
Respirations
A patient in acute alcohol withdrawal is
experiencing sweats (diaphoresis) and an increase in
heart rate (tachycardia). What is causing this?
Click on the correct answer
Sympathetic
Nervous
System
HPA Axis
Delirium
Accurate nursing assessment of patients
with alcohol dependence can help to
eliminate or minimize negative patient
outcomes
 Recognizing/identifying
signs/symptoms/behaviors of those at risk
for alcohol withdrawal syndrome
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McKinley, 2005
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Tremors
Sweating
Nausea
Vomiting
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Autonomic
Hyperactivity
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Agitation
Anxiety
Auditory
disturbances
Clouding of
sensorium
Visual/Tactile
disturbances
Neuropsychiatric
Alterations
McKinley, 2005
Signs/symptoms can appear within 24 hours
of last drink
 Peak of s/s happen as early as 24 hours and
stop around 48 hours
 Delirium tremens typically occur between
48-72 hours after last drink
 Delirium tremens is considered an
emergency and can end in death
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McKinley, 2005
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Excessive activation of
NMDA increases the
chance of seizures
Long term exposure to
alcohol depresses GABA,
making brain more
vulnerable to seizures
For nurses, the implication
would be to assess patient
history of withdrawal/detox
and treat more
aggressively those who are
most at risk
Becker, 1998
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48% of inpatient alcoholics
who suffered seizures had
gone through several
detoxifications in their pasts
In the same study, 12% of
alcoholics who had seizures
during detoxification had
little to no history of
detoxification
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Clinical Institute Withdrawal
Assessment (CIWA)
Selective Severity Assessment (SSA)
CAGE questions
Alcohol Withdrawal Syndrome Type
Indicator
Alcohol Use Disorders Identification
Test
CIWA is a 10 item rating scale that
discriminates symptoms of gastric
distress, perceptual distortions,
cognitive impairment, anxiety,
agitation, and headache
Ragasis,2004
Nausea/Vomiting
0 No Nausea/Vomiting
 1-3 Mild nausea
 4-6 Intermittent Nausea with Dry Heaves
 7-Constant Nausea, Dry Heaves, Vomiting
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Paroxysmal Sweats
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0-No sweat visible
1-3 Barely Sweating
4-6 Beads of Sweat Obvious on Forehead
7- Drenching Sweats
Click here to return to data
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Anxiety
Tremors
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0-No tremors
1-3 Not visible, but can be felt fingertip to
fingertip
4- Moderate with arms extended
7-severe, even without arms extended
“Do you feel nervous?”
 0-No anxiety/at ease
 1-3 Mildly anxious
 4-6 Moderately anxious
 7-Acute panic, anxiety
Click here to return to data
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Agitation
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None
1-Very mild
2-Mild
3-Moderate
4-Moderately sever
5-Severe
6-Very severe
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7-Extremely severe
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Headache/Fullness
0-Normal activity
1-3 Somewhat more than usual
4-6 Moderately fidgety/restless
7-Paces back and forth, thrashing about
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Click here to return to data
Does the light appear to
be too bright?
Is the color different?
Does it hurt your eyes?
Are you seeing anything
that is disturbing to
you?
Are you seeing things you
know aren’t there?
0-None
 4-Mild sensitivity to
light to
occasionally seeing
things you can’t
 7-Constant visual
hallucinations
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Are you aware of sounds
around you?
Are they harsh?
Do they frighten you?
Are you hearing anything
disturbing?
Are you hearing things
you know aren’t
there?
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0-None
2-Very mild harshness of
ability to frighten
3-Moderate
4-Moderately severe
hallucinations
5-Severe hallucinations
6-Extremely severe
hallucinations
7-Continuous
hallucinations
Do you feel any
itching, or pins and
needles?
Any numbness or
burning?
Do you feel bugs
crawling on or
under your skin?
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0-None
1-Very mild itching
2-Mild itching
3- Moderate itching
4-Moderate
hallucinations
5-Severe hallucinations
6-Extremely severe
hallucinations
7-Continuous
hallucinations
“ What day is it?
Where are you?
Who am I?”
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0-oriented
1-Cannot do serial
additions or uncertain of
dates
2-Disoriented to date but
not by more than 2 days
3-Disoriented for date by
more than 2 days
4-Disoriented to
time/place
Case Study
Prepare to use your critical thinking skills
and assess your patient in alcohol
withdrawal!
What is going on?
Objective Data
Subjective Data
Patient is sweating profusely
 Exhibits moderate tremors
when asked to extend arms
 Appears to be restless and
jittery during assessment
Click here to review the case study!
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Patient complains of intense
headache, a “rubber band” is
tight around his head
Patient complains of intense
anxiety
Patient denies
audio/visual/tactile
hallucinations
Patient is alert and oriented to
self, place and time
Patient complains of
moderate nausea, no
vomiting
Click here to return to case study
Subjective Data
Objective Data
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Profuse sweating 4-7
Moderate tremors 4
Moderate agitation
4-6
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Moderate
headache 4-6
Intense anxiety 4-6
No hallucinations 0
Oriented 0
Mild nausea 1-3
Click on individual
signs/symptoms to take
you to the scores
Score range is 21-32
Now what?
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Benzodiazepines are given, to meet receptors in the brain
alcohol is no longer binding to, to prevent hyperexcitibility and
seizures
Intravenous fluids
Anti inflammatory medications for the headache
Thiamine (patients often malnourished)
Multivitamin (patients often malnourished)
Folic Acid (patients often malnourished)
Therapeutic relations with patient (support)
Always remember to continue to use the nursing process for
outcomes and continued care!
The processing of alcohol involves….
Gastrointestinal tract absorption
2. Alcohol distribution in the body
3. Liver metabolism
Genetics and Environmental factors
influence these processes
1.
NIAAA, 2007
GI Surgeries
 Concentration of alcohol in
beverage
 Rate of consumption
 Presence of food in the stomach
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Liver Enzymes
(Needed for alcohol
breakdown)
Cytosolic
alcohol
dehydrogenase
(ADH)
Mitochondrial
aldehyde
dehydrogenase
NIAAA, 2007
(ALDH2)
The amount of alcohol metabolized in the body relies
on:
Liver Size & Body Mass
Genetics have influences on ADH & ALDH and affect
how people metabolize alcohol
This can help to explain why certain groups of people
have variances in levels of alcohol abuse
NIAAA, 2007
Alcoholic Liver Disease (ALD)
 Alcoholic Cardiomyopathy
 Alcohol Related Dementia
 Peripheral Neuropathy
 Gastritis
 Pancreatitis
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Alcoholic
Liver Disease
(ALD)
Fatty Liver
Alcoholic
Hepatitis
Cirrhosis
Long term alcohol abuse is leading cause of liver disease in the U.S.
Alcohol, Research, & Health, 2000
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What do you think? Click on a box to
find out?
No
Yes
Repeated
Alcohol
Abuse
Endotoxins
Produced
Activate
Immune
System
Roll mouse over
underlined words
for more
information.
Neuman, 2001
Cytokines
Released
Promote
Scar
Formation
Stimulate
More
Cytokines
Chronic inflammation
from chronic alcohol
exposure can cause
hepatocyte apoptosis
Increased numbers of cytokines continue
to be activated
 Increased scarring occurs
 Cell injury increases
 Increase in cell death
 Compromised organ function
 Organ failure
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Alcoholic
Liver Disease
(ALD)
Fatty Liver
Alcoholic
Hepatitis
Depending on what is happening to the liver,
interventions lie in decreasing the
inflammation, resting the organ, preventing
hepatic encephalopathy, preventing ascites,
and abstaining from the stressor (alcohol)
Cirrhosis
One role of the nurse is to provide safe patient care that contributes to
ideal patient outcomes. In caring for the patient in alcohol
withdrawal these include:
 Keeping safety in mind (seizure pads)
 Eliminate extraneous stimuli (keep it quiet)
 Prevent falls (bed/chair alarms, rounding)
 Watching for s/s of bleeding (since the liver might be compromised)
 Critical thinking for s/s of other disease processes that might mimic
AWS, as to avoid mistreating (medicating for AWS when patient
might have a low blood sugar)
 Monitor all values related to liver function (coagulation, enzymes,
etc.)
Promote healing through
nursing/medical interventions
 Be familiar with the pathophysiology of
what is going on with the patient
 Look at the “whole” picture
 Advocate for the patient
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Animated images not otherwise specified, Microsoft Clip Art, (2009), obtained at
http://office.microsoft.com/en-us/clipart/default.aspx
Axen, D., Koranda, A., & McKay, A., (2004). Using a Symptom-Triggered Approach to
Manage Patients in Acute Alcohol Withdrawal. Medsurg Nursing, February 2004, (13)1.
Author unknown., Medical Consequences of Alcohol Abuse. (2000). Alcohol Research &
Health., Vol. 24, No. 1.
Becker, H.C., Kindling in Alcohol Withdrawal. (1998). Alcohol Health & Research World. Vol. 22,
No. 1.
Hutchison, K.E. & Spencer, R.L., Alcohol, Aging, and the Stress Response. (1999). Alcohol
Research & Health. Vol. 23, No. 4.
Lovinger, D.M., Communication Networks in the Brain: Neurons, Receptors, Neurotransmitters,
and Alcohol.(2008). Alcohol Research & Health. Vol. 31 No. 3. Retrieved on the world
wide web on March 31st, 2009 at http://pubs.niaaa.nih.gov/publications/arh313/196214.htm.
McKinley, M.G., (2005). Alcohol Withdrawal Syndrome: Overlooked and Mismanaged?
Critical Care Nurse. Vol. 25, No. 3.
National Institute on Alcohol Abuse and Alcoholism., (2007). Alcohol Metabolism: An Update.
Retrieved on the world wide web on April 16th, 2009 at
http://pub.niaaa.nih.gov/publications/AA72/AA72.htm
National Institute on Alcohol Abuse and Alcoholism, 2009, Permission obtained for use of
pictures/graphics.
Neuman, M. G., (2001). Cytokines-Central Factors in Alcohol Liver Disease. Retrieved on the
world wide web on May 2nd, 2010 at http://pubs.niaaa.nih.gov/publications.arh274/307-316.htm.
Ragaisis K.M., (2004). Alcohol Screening in the Acute Care Hospital. Journal of Addictions
Nursing, 15: 171-175.
Saitz, R., (1998). Introduction to Alcohol Withdrawal. Alcohol Health & Research World. Vol.
22, No. 1.
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As you have seen in previous slides, the
sympathetic nervous (SNS) system, part
of the GSR, is responsible for many signs
and symptoms of alcohol withdrawal
Click here to return to the tutorial
Without inflammation , injuries would not
be localized and the immune system
would not be able to do its job,
preventing healing and further
infections.
Click here to return to inflammation slide
When the body has an “injury”,
inflammation occurs, attempts to
localize the injury, and calls the immune
system to work as a team to heal the
injury and prevent further spread or
damage.
Click here to return to inflammation slide