Caring for the patient in Alcohol Withdrawal

Cortney K. Muns, BSN,RNAlverno College MSN Candidate

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Instructions for navigating the tutorial

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You will be given opportunities throughout to test your knowledge

At the end of the tutorial, the learner will

be able to.. 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

SectionsClick on individual sections to jump to that

section

Case Study (1) Neurological Pathophysiology(2) Hypothalamic-pituitary-adrenal Axis(HPA Axis), “f

ight 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)

Case Study

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

Case Study Continued

Feels intense anxiety Denies hallucinations Denies agitation Knows the current place and time

We will come back to this case study later in the tutorial

Click here to return to

data

Brain Communication

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

Lovinger, 2008

Neurotransmitters: The Heavy Hitters

gamma-Aminobutyric acid (GABA)

Glutamate

GABA

Glutamate

Microsoft, 2007

GABA 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

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

Lovinger, 2008

Neurotransmitter binding

NIAAA, 2009

Benzodiazepines bind here

glutamate

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

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

Lovinger, 2008

Neurotransmitter Basics: a quick review

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

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)

Hypothalamic-Pituitary-Adrenal (HPA) Axis

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

Hutchison & Spencer, 1999

Hypothalamic-Pituitary-Adrenal (HPA) Axis

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.

Stressful situation(alcohol intoxication)

Hypothalamus Pituitary Gland

Adrenal Glands Hint: Roll mouse over body parts to reveal what they release.

Hutchison & Spencer, 1999 & Microsoft 2007

Adrenal Gland

HPA Axis & Alcohol Use

Alcohol use stimulates the HPA Axis Length of stimulation depends on

amounts of alcohol consumed or blood alcohol level (BAC)

Hutchison & Spencer, 1999 & Microsoft 2007

HPA Axis Activation & Genetics

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

Hutchison & Spencer, 1999

HPA Axis and Aging

Aging people are more at risk for HPA Axis overstimulation

Why?

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

Hutchison & Spencer, 1999

Fight or FlightNorepinephrine/Noradrenaline

Released

Alpha1

Alpha2

Beta1

Beta2

Diaphoretic

Increased Blood Pressure

Dilated Pupils

GI Tract off

LowersInsulin

Increased HR

IncreasedRespirations

Case Question #1A 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

Nursing Sensitive Outcomes

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

McKinley, 2005

Alcohol Withdrawal Syndrome Tremors Sweating Nausea Vomiting

Agitation Anxiety Auditory

disturbances Clouding of

sensorium Visual/Tactile

disturbances

Autonomic Hyperactivity

NeuropsychiatricAlterations

McKinley, 2005

Alcohol Withdrawal Syndrome

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

McKinley, 2005

Kindling

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

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

Becker, 1998

Alcohol Withdrawal Assessment Tools

Clinical Institute Withdrawal Assessment (CIWA)

Selective Severity Assessment (SSA)

CAGE questions Alcohol Withdrawal Syndrome Type

Indicator Alcohol Use Disorders Identification

Test

CIWA

CIWA is a 10 item rating scale that discriminates symptoms of gastric distress, perceptual distortions, cognitive impairment, anxiety, agitation, and headache

Ragasis,2004

Sig

ns/s

ym

pto

ms

Nause

a/V

om

iting

Parox

ysm

al S

weats

0 No Nausea/Vomiting 1-3 Mild nausea 4-6 Intermittent Nausea with Dry

Heaves 7-Constant Nausea, Dry Heaves,

Vomiting

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

Sig

ns/s

ym

pto

ms

Trem

ors

Anxie

ty

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

Sig

ns/s

ym

pto

ms

Agita

tion

Headach

e/Fu

llness

0-Normal activity 1-3 Somewhat more than usual 4-6 Moderately fidgety/restless 7-Paces back and forth, thrashing about

None 1-Very mild 2-Mild 3-Moderate 4-Moderately sever 5-Severe 6-Very severe 7-Extremely severe

Click here to return to data

Visual Hallucinations

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

Auditory Hallucinations

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?

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

Tactile Hallucinations

Do you feel any itching, or pins and needles?

Any numbness or burning?

Do you feel bugs crawling on or under your skin?

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

Clouding of Sensorium/Orientation

“ What day is it? Where are you? Who am I?”

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? Patient is sweating profusely Exhibits moderate tremors w

hen asked to extend arms Appears to be restless and jit

tery during assessment

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

Objective Data Subjective Data

Click here to review the case study!

Click here to return to case study

Scores

Profuse sweating 4-7

Moderate tremors 4 Moderate agitation

4-6

Moderate headache 4-6

Intense anxiety 4-6 No hallucinations 0 Oriented 0 Mild nausea 1-3

Score range is 21-32Now what?

Objective Data

Subjective Data

Click on individual signs/symptoms to take you to the scores

Treatment for alcohol withdrawal

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!

Alcohol Abuse, Genetics, & Metabolism

The processing of alcohol involves….

1. Gastrointestinal tract absorption2. Alcohol distribution in the body3. Liver metabolismGenetics and Environmental factors

influence these processes

NIAAA, 2007

Environmental influences GI Surgeries

Concentration of alcohol in beverage

Rate of consumption Presence of food in the stomach

Genetic Influences

Liver Enzymes

(Needed for alcohol breakdown)

Cytosolic alcohol

dehydrogenase(ADH)

Mitochondrial aldehyde

dehydrogenase(ALDH2)

NIAAA, 2007

Genetics and Metabolism

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

Alcohol Abuse and Associated Health Conditions

Alcoholic Liver Disease (ALD) Alcoholic Cardiomyopathy Alcohol Related Dementia Peripheral Neuropathy Gastritis Pancreatitis

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

Is inflammation important?

What do you think? Click on a box to find out?

No Yes

So, what happens with inflammation in ALD?

Repeated

Alcohol Abuse

Cytokines

Released

Endotoxins

Produced

Promote Scar

Formation

Stimulate More

Cytokines

Activate Immune System

Roll mouse over underlined words for more information.

Chronic inflammation from chronic alcohol exposure can cause

hepatocyte apoptosis

Neuman, 2001

What if inflammation continues?

Increased numbers of cytokines continue to be activated

Increased scarring occurs Cell injury increases Increase in cell death Compromised organ function Organ failure

Treating ALD….depends on what is going on.

Alcoholic Liver Disease

(ALD)

Fatty Liver Alcoholic Hepatitis Cirrhosis

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)

Nursing Considerations

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.)

What can you do as a nurse?

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

References

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/arh313/196-214.htm.

References

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.arh27-4/307-316.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.

Correct!

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

Think Again!

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

Correct!

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