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nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1 SUBSTANCE ABUSE DISORDERS DANA BARTLETT, RN, BSN, MSN, MA Dana Bartlett is a professional nurse and author. His clinical experience includes 16 years of ICU and ER experience and over 20 years as a poison control center information specialist. Dana has published numerous CE and journal articles, written NCLEX material and textbook chapters, and done editing and reviewing for publishers such as Elsevier, Lippincott, and Thieme. He has written widely on the subject of toxicology and was recently named a contributing editor, toxicology section, for Critical Care Nurse journal. He is currently employed at the Connecticut Poison Control Center and is actively involved in lecturing and mentoring nurses, emergency medical residents and pharmacy students. ABSTRACT Substance use in the United States and worldwide is a major health concern requiring specially trained health professionals in primary care, public health and treatment centers for the identification of various categories of substance abuse and its prevention. There is high risk of substance abuse among certain groups in society. Although substance abuse is typically thought of as illicit drug use or chronic alcohol abuse, commonly occurring within marginalized, crime ridden sectors of society, in reality, substance abuse is a wide-spread societal problem involving alcohol, tobacco, prescription and illicit drugs, among many individuals indistinguishable from the general population. Substance abuse is explained according to the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition) criteria.

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SUBSTANCE ABUSE

DISORDERS

DANA BARTLETT, RN, BSN, MSN, MA

Dana Bartlett is a professional nurse and author. His clinical experience

includes 16 years of ICU and ER experience and over 20 years as a poison

control center information specialist. Dana has published numerous CE and

journal articles, written NCLEX material and textbook chapters, and done

editing and reviewing for publishers such as Elsevier, Lippincott, and Thieme.

He has written widely on the subject of toxicology and was recently named a

contributing editor, toxicology section, for Critical Care Nurse journal. He is

currently employed at the Connecticut Poison Control Center and is actively

involved in lecturing and mentoring nurses, emergency medical residents and

pharmacy students.

ABSTRACT

Substance use in the United States and worldwide is a major health

concern requiring specially trained health professionals in primary

care, public health and treatment centers for the identification of

various categories of substance abuse and its prevention. There is high

risk of substance abuse among certain groups in society. Although

substance abuse is typically thought of as illicit drug use or chronic

alcohol abuse, commonly occurring within marginalized, crime ridden

sectors of society, in reality, substance abuse is a wide-spread societal

problem involving alcohol, tobacco, prescription and illicit drugs,

among many individuals indistinguishable from the general population.

Substance abuse is explained according to the DSM-5 (Diagnostic and

Statistical Manual of Mental Disorders, Fifth Edition) criteria.

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Continuing Nursing Education Course Director & Planners:

William A. Cook, PhD, Director; Douglas Lawrence, MS, Webmaster;

Susan DePasquale, CGRN, MSN, FPMHNP-BC, Lead Nurse Planner

Accreditation Statement:

This activity has been planned and implemented in accordance with

the policies of NurseCe4Less.com and the continuing nursing education

requirements of the American Nurses Credentialing Center's

Commission on Accreditation for registered nurses.

Credit Designation:

This continuing education (CE) activity is credited for 3.5 hours.

Nurses may only claim credit commensurate with the credit awarded

for completion of this course activity.

Course Author & Planner Disclosure Policy Statements:

It is the policy of NurseCe4Less.com to ensure objectivity,

transparency, and best practice for all continuing nursing education

(CNE) activities. All authors and course planners participating in the

planning or implementation of a CNE activity are expected to disclose

to course participants any relevant conflict of interest that may arise.

Statement of Need:

Nurses need to understand varying patterns of substance use and the

harm caused by each. As members of the health care team, nurses can

assist individuals needing help begin recovery and, hopefully, succeed.

Course Purpose:

This course is designed to provide nurses and health associates with

knowledge about substance abuse and the recommended steps to

support patient recovery.

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Learning Objectives:

1. Identify the diagnostic criteria of a substance abuse disorder.

2. Identify a mechanism of action by which substance abuse occurs.

3. Identify behaviors commonly associated with a substance abuse

disorder.

4. Identify signs/symptoms of substance abuse withdrawal.

5. Identify drugs used for treating substance abuse withdrawal.

Target Audience:

Advanced Practice Registered Nurses, Registered Nurses, Licensed

Practical Nurses, and Associates

Course Author & Director Disclosures:

Dana Bartlett, RN, MA, MSN, William S. Cook, PhD,

Douglas Lawrence, MS, Susan DePasquale, CGRN, MSN, FPMHNP-BC -

all have no disclosures

Acknowledgement of Commercial Support:

There is no commercial support for this course.

Activity Review Information:

Reviewed by Susan DePasquale, CGRN, MSN, FPMHNP-BC.

Release Date: 9/8/2014 Termination Date: 9/8/2017

Please take time to complete the self-assessment Knowledge Questions before

reading the article. Opportunity to self-assess knowledge learned will be

provided at the end of the course.

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1. The term dependency used in relation to substance abuse

means:

a. an intense psychological craving for alcohol or a drug

b. physical need for alcohol or a drug that develops over time.

c. the need for increasing amounts of alcohol or a drug over time.

d. a physical resistance to withdrawal signs and symptoms.

2. One of the central themes of a substance abuse disorder

is:

a. continued use despite significant substance related problems.

b. excessive use of alcohol or an illicit drug.

c. a pattern of use of alcohol or a drug that causes medical harm.

d. alcohol or drug use that has social consequences.

3. One of the diagnostic criteria for substance abuse disorder

is:

a. Self-admitted addiction to alcohol or a drug.

b. Excessive use of alcohol or a drug for > five years.

c. Impaired control relating to use of alcohol or a drug.

d. Use of an illicit drug

4. One of the diagnostic criteria for substance abuse disorder

is:

a. Refusal by the patient to accept professional help.

b. Alcohol or drug use that causes medical harm.

c. Alcohol or drug use that waxes and wanes.

d. Tolerance to alcohol or a drug.

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5. Substance abuse is thought to be caused and reinforced in

part by:

a. Changes in neurotransmitters and their receptors.

b. Decreased function of the endocrine system.

c. Changes in microcirculation.

d. Undiagnosed immune system dysfunction.

6. Withdrawal in most patients who have a substance abuse

disorder:

a. causes significant morbidity and mortality.

b. is relatively benign and self-limiting.

c. is less serious if the duration of use has been many years.

d. typically affects males more than females.

7. One of the serious complications of alcohol withdrawal is:

a. Acute renal failure

b. Delirium tremens

c. Rhabdomyolysis

d. Cardiac arrhythmias

8. Withdrawal from benzodiazepines can cause:

a. Seizures

b. Rhabdomyolysis

c. Hepatic damage

d. Pulmonary edema

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9. Which of the following is the drug of choice for treating

alcohol withdrawal?

a. Antipsychotics

b. Benzodiazepines

c. Selective serotonin reuptake inhibitors

d. Barbiturates

10. Which of the following drugs are often used to treat opioid

withdrawal?

a. Benzodiazepines, clonidine, and methadone

b. Anti-psychotics, barbiturates, and selective serotonin reuptake

inhibitors

c. Non-opioid analgesics, propofol, and tri-cyclic anti-depressants

d. Buprenorphine/naloxone, clonidine, and methadone

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INTRODUCTION

Substance abuse is an enormous problem in the United States, and

even the small sample of statistics outlined below illustrates its

widespread and deeply injurious effects.

A 2102 report issued by the U.S. White House Office of National

Drug Control Policy states that, for the period from 2000-2006,

drug users in the United States spent $100 billion each year on

cocaine, heroin, marijuana, and methamphetamine.1

In 2011, nonmedical use of pharmaceuticals was involved in

greater than 1.4 million emergency department encounters.

Additionally, emergency department encounters was reported to

be 505,224 for the use of cocaine, 455,668 for the use of

marijuana, 258,482 for the use of heroin, and 159,840 for the

use of amphetamines, methamphetamine, and other

psychostimulants.2

Alcohol use is the third leading cause of death in the United

States.3

Approximately 17 million American adults and 855,000

adolescents in the United States have an alcohol use disorder.4

Tobacco use is the leading cause of preventable death in the

United States.5

Substance abuse is typically thought of as illicit drug use or chronic

abuse of alcohol, and it is often assumed that substance abuse is

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primarily an issue for those living on or near the fringe of society and a

problem characterized by aberrant behavior and crime. Yet substance

abuse is a problem that also involves the use of legal substances such

as alcohol and tobacco, prescription drugs such as benzodiazepines

and opioids; moreover, people who are substance abusers are often

indistinguishable from the general population. This module will discuss

substance abuse involving cocaine, opioids, amphetamines/stimulants,

sedative/hypnotics, and alcohol.

Note that this module uses the terms substance abuse and substance

abuse disorder, not addiction or addict. Both of the former terms are

still in common use and there are many professional journals that

have the word addiction as part of their title. But addiction is not a

recognized diagnostic term, and the word addict has negative

connotations and tends to focus attention on the behavior and

character of the individual. The term dependency is also frequently

used when referring to substance abuse. Dependency refers to the

physical need for a drug or substance that develops over time and it is

just one part of the clinical picture of substance abuse.

Part of the commonly accepted definition of a drug is a substance that

will and is intended to, affect the structure or function of the body.6 A

drug is also defined as a substance intended for the cure, diagnosis,

mitigation, prevention, or treatment of a disease.6 Almost all the

classes of drugs that are involved in substance abuse disorders have

some legitimate, albeit occasionally limited medical use, and alcohol

has in the past been used medicinally. However, alcohol is almost

never used as a drug anymore. The illicit forms of cocaine, opioids,

and stimulants are obviously produced without quality control, and

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there are many well-documented cases of dangerous contaminants

and adulterants being added to them. For practical purposes, when

discussing substance abuse disorders, alcohol is considered a

substance and all of the rest are considered drugs.

WHAT IS SUBSTANCE ABUSE?

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition

(DSM-5) lists more than 20 separate substance use disorders,7 and a

partial list is provided in Table 1.

Table 1: DSM-5 Substance Abuse Disorders

Each of the substance abuse disorders has its specific features, but the

DSM-5 does point out that all substance abuse disorders are

characterized by a central theme:

“The essential feature of a substance use disorder is a cluster of

cognitive, behavioral, and physiological symptoms indicating that the

individual continues using the substance despite significant

substance-related problems.”7

Alcohol Use Disorder

Cannabis Use Disorder

Inhalant Use Disorder

Opioid use Disorder

Phencyclidine Use Disorder

Sedative, Hypnotic, or Anxiolytic Use Disorder

Stimulant Use Disorder

Other (or Unknown) Substance Abuse Disorder

Other Hallucinogen Use Disorder

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This can be expanded by noting that the person who has a substance

abuse disorder exhibits the following: 1) has a constant craving for,

and preoccupation with the drug; 2) uses more of the drug than is

necessary to become intoxicated; 3) has a decreased interest in, and

motivation for, normal life activities; 4) develops a tolerance to the

drug so that there is a need for increasingly larger doses and more

frequent use; 5) develops neurological changes that result in craving

and dependency, and; 6) develops withdrawal signs and symptoms if

the drug cannot be obtained.

All of these are further explained by the DSM-5 in the diagnostic

criteria of substance abuse. These criteria are divided into five

categories.7

1. Impaired control:

Impaired control is one of the hallmarks of a substance abuse

disorder. Someone with a substance abuse disorder finds that

over time she/he is taking larger amounts of the drug of

substance, despite expressed intentions to cut down or stop use.

The life of a person with a substance abuse disorder slowly

begins to revolve around drug or substance use, and daily

activities become focused on obtaining, using, and recovering

from use. The individual’s desire for the drug or substance, the

craving, becomes intense and unmanageable.

2. Social impairment:

The second diagnostic criterion of substance abuse disorder is

social impairment. Because of impaired control and the priority

on obtaining and using the drug or substance, the substance

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abuser cannot function at home, at work, or in other areas of

attachment and responsibility. The consequences of the

substance abuse are often quite serious; e.g., divorce, loss of

job and income, estrangement and isolation from friends and

family, or homelessness. However, despite these consequences,

some substance abusers cannot or will not change.

3. Risky use:

A person who has a substance abuse disorder will continue to

use the drug or substance even if doing so involves significant

and obvious risks to health and life. He/she may do some very

risky things to obtain the drug and get high.

4. Tolerance:

A substance abuse disorder is characterized by tolerance.

Tolerance is defined as the need for increasingly higher amounts

of the drug or substance to achieve the desired effect or a

decreased effect from the usual dose or amount. Tolerance is a

complicated phenomenon that involves changes in the central

nervous system (CNS) and the degree of tolerance developed

varies widely from individual to individual

5. Withdrawal:

Withdrawal is the final diagnostic criterion of substance abuse

disorders. Withdrawal is defined as specific signs and symptoms

that occur when someone with a substance abuse disorder

abruptly discontinues or greatly decreases use. The seriousness

of withdrawal depends on the drug or substance that has been

used and the pattern and duration of use.

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Considering these diagnostic criteria, the picture of a substance abuser

begins to emerge. Drug or substance use is compulsive and causes

intense craving. Acquisition and use can become the sole focus of that

person’s life, and recovery from “highs” can be lengthy and

debilitating. Other areas of life suffer and may be completely

neglected, and the substance abuser may lose his/her home, friends

and family, and job. The health risks and social and personal

consequences of the abuse are clear, but the substance abuser feels

compelled to continue and will frequently take ever-increasing risks to

get the drug and get high. The substance abuser may express a desire

to stop use, but the desire to continue is intense and discontinuation is

discouraged because of withdrawal signs and symptoms - further

reinforcement for continued drug or substance abuse.

DRUGS AND SUBSTANCES THAT ARE ABUSED

Certain drugs and substances have strong potential for abuse while

others do not, and it is not clear why. Drugs such as cocaine and

heroin and substances such as alcohol are intensely psychoactive -

using cruder terms, they provide a powerful high - and this is certainly

one of the reasons for why they are the agents of choice for people

who develop a substance abuse disorder. However, the pleasures of

intoxication cannot fully explain substance abuse, and research has

shown that continued and excessive use of these harmful agents

causes changes in the central nervous system, changes that both

cause and reinforce substance abuse. Of course, there are many

people who take illicit or prescription drugs and/or drink alcohol that

do not develop a substance abuse disorder, and these individual

responses to commonly abused drugs and substances further

complicate the efforts at understanding substance abuse.

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The mechanism of action, the signs and symptoms of acute

intoxication, and the medical consequences of long-term use of

alcohol, amphetamines/stimulants, cocaine, opioids, and sedative-

hypnotics will be discussed in this section. The mechanisms of action

by which alcohol and these drugs cause substance abuse disorder and

the withdrawal syndromes associated with each one will be discussed

in separate sections.

Alcohol

Aside from tobacco, alcohol is the most commonly abused

psychoactive drug in our society. There are many types of alcohol,

e.g., ethylene glycol, isopropyl, but the one that is most often

consumed for its intoxicating effects is ethanol.

The exact mechanisms by which ethanol alters consciousness and

causes tolerance and withdrawal are not completely understood. But it

is thought that these effects are due to ethanol changing the activity of

two neurotransmitters and their receptors: a major inhibitory

neurotransmitter called gamma aminobutyric acid (GABA) and a sub-

type of the major excitatory neurotransmitter glutamate called N-

methyl-d-aspartate (NDMA). Gamma aminobuytric acid acts as an

inhibitory neurotransmitter by increasing intracellular chloride

concentration and decreasing intracellular potassium concentration.

This hyperpolarizes the cells and makes them less able to respond. N-

methyl-d-aspartate increases the movement of calcium and sodium

across cell membranes, and this increases the cells’ ability to respond

to a stimulus and depolarize.

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Ethanol binds to receptors that are associated with GABA and NDMA

receptors on cell membranes in the CNS. This binding increases the

affinity of GABA for GABA receptors and it decreases the affinity of

NDMA for DMA receptors. The result is increased inhibition and

decreased excitation. However, when large amounts of alcohol are

abused chronically the body responds by decreasing the number,

sensitivity, and function of GABA receptors and increases the number,

sensitivity, and function of NDMA receptors.11

This effect explains alcohol intoxication as well as tolerance to alcohol,

e.g., the need for larger amounts of alcohol to produce the same

effect; and, it explains withdrawal, the clinical state that is produced

when alcohol intake is stopped. Intoxication is caused by increased

inhibition and decreased excitation in the CNS. Tolerance occurs

because of the effect of chronic alcohol intake on the neurotransmitter

receptors. Furthermore, when the intake of alcohol is stopped,

withdrawal is caused because there are large numbers of highly active

NDMA receptors that can respond to NDMA and a greatly decreased

number of GABA receptors that can respond to GABA.

Alcohol intoxication is characterized primarily by CNS depression and

impairment. Someone who has ingested an excess amount of ethanol

will be drowsy, may be ataxic (incoordination of movement), have

impaired judgment, decreased impulse control, and slurred speech.

Extreme intoxication can cause coma, hypoglycemia, hypotension,

respiratory depression, and death. Long-term use is associated with

liver disease, heart failure, brain atrophy, gastritis and ulcers, anemia,

and various cancers; it is particularly dangerous to the unborn child.

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Amphetamines/stimulants

Amphetamines and stimulants act by directly stimulating the

adrenergic nerve endings. This causes a release into the synapses of

norepinephrine and dopamine, neurotransmitters that stimulate the

peripheral α receptors and β receptors. Acute intoxication causes

anxiety, diaphoresis, hypertension, mydriasis, and tachycardia. More

serious effects such as dysrhythmias, hallucinations, hyperthermia,

myocardial ischemia, myocardial infarction, psychosis, seizures,

stroke, and rhabdomyolysis are possible, as well.

Long-term effects of amphetamine and stimulant use include aortic

and mitral valve regurgitation, cardiomyopathy vasculitis,

cardiomyopathy, pulmonary hypertension, and permanent damage to

the dopaminergic and serotonergic neurons. Amphetamines and

stimulants can be taken as tablets, injected, smoked, or insufflated

(snorted). Probably the most commonly abused amphetamine is

methamphetamine.

Methamphetamine is commercially produced (Desoxyn®), and it has

labeled uses for the treatment of patients who have exogenous obesity

or attention deficit disorder with hyperactivity disorder.

Methamphetamine is lipid-soluble and crosses the blood-brain barrier

more easily than the parent compound amphetamine, making it a

more powerful drug. The great majority of the methamphetamine

involved in substance abuse is illicitly produced, and this form of the

drug is commonly called crank or speed.

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Cocaine

Cocaine causes the release and blocks the re-uptake of the

neurotransmitters dopamine, epinephrine, norepinephrine, and

serotonin. These actions produce a hyper-adrenergic state, and the

common signs and symptoms of cocaine intoxication are agitation,

anxiety, chest pain, diaphoresis, hypertension, hyperthermia,

mydriasis, tachycardia, and tachypnea. Cocaine also acts to stabilize

the cardiac membrane by an effect on the sodium channels in the

myocardium, and it bocks the movement of potassium through cardiac

membrane ion channels.

Blockade of the sodium channels produces cardiac membrane

stabilization, typically called the quinidine-like effect. This can cause a

prolonged QRS and cardiac dysrhythmias. Blockade of the potassium

ion channels can cause QTc prolongation and cardiac dysrhythmias, as

well.

Cocaine abuse has also been associated with serious medical problems

affecting essentially every organ system: acute angle-closure

glaucoma, aortic dissection, coronary artery vasospasm, dystonic

reactions, intestinal infarction, myocardial infarction, pneumothorax,

pulmonary infarction, rhabdomyolysis, seizures, stroke, and transient

ischemic attack. Long-term effects of cocaine abuse include

atherosclerosis, cardiomyopathy, endocarditis, malnutrition, and

behavior that can be characterized as virtually identical to personality

disturbances, paranoia, and schizophrenic syndromes.

Cocaine can be ingested, applied to mucous membranes, insufflated,

smoked, or injected. As mentioned previously, there are many well-

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documented cases of dangerous contaminants and adulterants being

added to cocaine, and these can cause significant harm.

Opioids

The opioids are a class of drugs that are derived from chemical

modification of an opiate, an opiate being one of several alkaloids that

are derived directly from the opium poppy. In common practice the

term opioid is the one used for all drugs that have similar structure

and clinical effects including, but not limited to, buprenorphine,

codeine, dextromethorphan, fentanyl, heroin, hydrocodone,

methadone, morphine, oxycodone, and propoxyphene. In the United

States all of these drugs except for heroin are commercially produced

and are commonly prescribed.

In the United States, heroin is classified as a Schedule 1 drug. A

Schedule 1 drug is defined as a drug: 1) with a high potential for

abuse; 2) that has no currently accepted medical use; and, 3) for

which there is a lack of accepted safety for use of the drug while under

medical supervision. Heroin is commercially available in other

countries and is used for treating people who have severe, intractable

pain.

The opioids act by binding to and stimulating opioid receptors in the

brain, spinal cord, and peripheral sites. Opioid receptor stimulation

causes the cells to become hyperpolarized and thus less active and

less able to respond to stimuli. As with alcohol and other drugs

discussed in this module, chronic use of opioids affects the function

and activity of neurotransmitters and their receptors, and this causes

tolerance and the potential for a withdrawal syndrome. The

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therapeutic effects of the opioids are analgesia and an anti-tussive

effect. Constipation, drowsiness, nausea, and vomiting are common

side effects of the opioids.

Opioid intoxication is characterized by ataxia, central nervous system

depression, euphoria, hypotension, miosis, respiratory depression, and

slurred speech. With profound intoxication coma, hypoxic seizures,

hypoxic brain injury, pulmonary edema, and respiratory arrest are

possible. Propoxyphene intoxication can cause myocardium sodium

channel blockade and arrhythmias. Long-term effects of opioid abuse

include heart valve infections, infectious diseases such as hepatitis B

and C and HIV (human immunodeficiency virus) that occur with

intravenous use, arthritis, collapsed and sclerotic veins, malnutrition,

and a depressed immune system. Opioids can be taken as tablets,

injected, smoked, or insufflated. As mentioned previously, there are

many well-documented cases of dangerous contaminants and

adulterants being added to illicit opioids (typically injectable heroin)

and these can cause significant harm.

Sedative-hypnotics

The sedative-hypnotics are a group of drugs that are used to treat

anxiety and/or agitation (sedatives) or to induce sleep (hypnotics).

There are many drugs that are classified as sedatives or hypnotics, but

the sedative-hypnotics that are most often involved in substance

abuse disorders are the benzodiazepines and the barbiturates.

Table 2A lists the commonly available sedative-hypnotics.

Flunitrazepam is not commercially available in the United States but it

is included here because of its highly publicized status as the date rape

drug, also known as roofies. Midazolam is an injectable benzodiazepine

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that is used for pre-operative sedation. It is seldom a drug of choice

for abuse but it is included here because it is well known and often

used. The non-benzodiazepine hypnotics (Table 2B) have a similar

mechanism of action as the benzodiazepines.

The barbiturates, listed in Table 3, were at one time the drugs of

choice for treating anxiety/agitation or for inducing sleep, but the

benzodiazepines have been shown to have similar effectiveness for

those purposes and a superior safety profile. The barbiturates are now

used to help induce pre-operative sedation or for the treatment of

seizure disorders. The short-acting barbiturate butalbital is available in

prescription analgesics, compounded in various combinations with

acetaminophen, aspirin, caffeine, and codeine. These drugs are almost

always used and abused in tablet or capsule from, but injectable

preparations are available.

Table 2A: Benzodiazepines

Alprazolam (Xanax®)

Chlordiazepoxide (Librium®)

Clonazepam (Klonopin®)

Diazepam (Valium®)

Flunitrazepam (Rohypnol®)

Flurazepam (Dalmane®)

Lorazepam (Ativan®)

Midazolam (Versed®)

Oxazepam (Serax®)

Temazepam (Restoril®)

Triazolam (Halcion®)

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Table 2B: Non-Benzodiazepine Hypnotics

Eszopiclone (Lunesta®)

Zaleplon (Sonata®)

Zolpidem (Ambien®)

Table 3: Barbiturates

Amobarbital (Amytal®)

Butalbital

Pentobarbital (Nembutal®)

Phenobarbital (Luminal®)

Primidone (Mysoline®)

Secobarbital (Seconal®)

Thiopental (Pentothal®)

The mechanism of action differs slightly for the three different

categories, but essentially all these drugs act by binding to specific

receptors that are part of the GABA receptor complex. This binding

increases the affinity of GABA for GABA receptors and, as explained

previously, this increases the inhibitory effect of GABA in the CNS.

Intoxication with a sedative-hypnotic causes ataxia, CNS depression of

varying degrees, from mild drowsiness to coma, hypotension, slurred

speech, and respiratory depression. Death is caused by respiratory

depression. The barbiturates, compared to the benzodiazepines and

the non-benzodiazepine hypnotics, will produce more severe effects: if

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very large amounts are ingested coma and respiratory depression may

last for days.

Compared to alcohol, cocaine, amphetamine/stimulants, and opioids,

the long-term medical consequences of sedative-hypnotic abuse are

relatively mild. Perhaps the biggest risks are the potential for

dependency and development of substance abuse. And although acute

intoxication and the long-term medical consequences of alcohol,

cocaine, amphetamines/stimulants, and opioids are much more

severe, the sedative-hypnotic withdrawal from the benzodiazepines

and the barbiturates is comparatively more severe and can be life

threatening.

THE CAUSES OF SUBSTANCE ABUSE

There is no single cause of substance abuse, and despite many years

of research there are still no answers to the most pressing questions

about substance abuse. Why do some people make the use and

acquisition of alcohol, illicit drugs, or certain prescription medications

the sole focus of their lives? Also, why do some people continue to

abuse substances despite obvious and severe consequences? Although

the term is no longer preferred, another way of asking this question is,

why do some people become addicts while others do not?

There has been a vast amount of effort and research directed towards

uncovering the root cause(s) of substance abuse disorders. Biological,

psychological, and sociological reasons for these afflictions have all

been advanced, and strong arguments can be made for each of these

as major contributors to the genesis of, and continued presence of,

substance abuse disorders.

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Current thinking is that there is no single cause of substance abuse

disorders, and that substance abuse involves complex neuro-

psychological phenomena that are behaviorally expressed within a

social context. However, although there has been much research,

more work needs to be done. Much of the published literature involves

animal experiments or a single drug, and it is clear that the true basis

for substance abuse disorders is not known.

Substance abuse: the process

Substance abuse is a multi-factorial process, and the nuances of how

biology, psychology and sociology contribute to it have not been sorted

out. However, although it is not entirely clear what causes substance

abuse, there is very strong evidence about how substance abuse

develops in, and affects, the neurologic system.

Substance abuse involves changes in several areas of the brain and in

neurotransmitters, but perhaps the most important part of the brain

that is affected by substance abuse is the reward system. Drugs of

abuse stimulate areas of the brain that are involved with very

pleasurable survival behaviors such as eating, sex, and bonding. When

these areas of the brain (there are several, but the mesolimbic

pathway is considered to be the most important) are stimulated, they

receive a surge in the neurotransmitter dopamine. Dopamine is a

neurotransmitter that is found in the areas of the brain that control

emotion, motivation, and pleasure, and increases in dopamine levels

of the CNS have many effects and one of them is the experience of

pleasure.

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Cocaine, heroin, etc. stimulate a direct release of dopamine or prevent

its breakdown and, crudely put, the more dopamine the higher the

level of pleasure. Alcohol, and the drugs that are involved in substance

abuse disorders, cause a higher brain dopamine level than do natural

rewards such as food or sex.

This surge in dopamine and the intensity of the experience - the high -

is especially strong when it is caused by drugs of abuse and the

information about that experience gets stored and remembered: the

drug is associated with pleasure. However, with succeeding exposures

to these drugs, the dopamine surge become less and less, and the

dopamine levels go lower and lower below normal baseline as less is

produced. There is a reduction in dopamine receptors as well. The

result is that the person who is chemically dependent gets less of a

“high” each time he/she use the drug and he/she feels less happy

when they are not intoxicated, which leads to more drug seeking, and

a vicious cycle because the chemically dependent person has now

developed a tolerance.8

Addicts have a term that is called “chasing the dragon.” It means that

there is no high like the first high, and science is proving that to be

correct. There is also evidence that the faster the increases in

dopamine concentration in the brain (which occurs with early, heavy

drug use and with certain drugs such as cocaine) the stronger the

reinforcing effect of the drug. Even worse, long-term use of addictive

drugs produces long-lasting changes in brain structure that make the

person who has a substance abuse disorder susceptible to relapse

months and years after successful rehabilitation and abstinence; a

phenomenon that partially explains the high relapse rate in people who

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have had a substance abuse disorder and they are chemically

dependent. Also, these changes in brain structure make the brain less

able to react to the “weaker” pleasure stimuli such as food, sex,

bonding, etc.

However, it has been shown that increases in brain dopamine

concentrations caused by drugs of abuse happen to people who

become addicted and to people who do not, so the short-term increase

in dopamine cannot explain the development of chemical dependency.

It may be that there is a difference in the dopamine circuits between

those who are chemically dependent and those who are not. The

chemically dependent person may have a particularly “weak” circuit

that doesn’t respond to normal pleasurable activities so she/he needs

strong levels of stimulation to feel good, and there is supporting

evidence for this idea in the literature.

It is also possible that people who develop a substance abuse disorder

have a biological susceptibility to drugs of abuse. Their brains react to

drugs by decreasing the numbers of dopamine receptors and

decreasing the amount of dopamine released, thus inhibiting their

ability to feel pleasure. This may not happen to people who do not

develop a substance abuse disorder.

TREATMENT APPROACHES AND WITHDRAWAL

Treatment for substance abuse disorders is a process as complex as

the disorders themselves. There are many treatment approaches,

some which have strong supporting evidence in the medical literature

and some that do not. It does seem clear though that early

interventions are more likely to be successful. If someone has had a

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substance abuse disorder for a relatively brief period of time the

chances for him/her successfully discontinuing use are much greater.

However, regardless of the specifics of any approach to treating

substance abuse disorders the process must involve the following: 1)

stopping the use of alcohol and or the drug; 2) if possible, administer

the patient an equivalent drug that has a more limited potential for

dependency and tolerance; 3) manage the physical signs and

symptoms of withdrawal; and, 4) provide psychiatric and social

support. Treatment for substance abuse must be a fluid process and

be able to change over time. The patient at times will have a need for

medical support, rehabilitation, and continuing care, and there are a

myriad of personal, social, legal, and medical issues to address.

Withdrawal defined

Discontinuation of alcohol or one of the drugs discussed in this module

will cause withdrawal. Withdrawal is a group of characteristic signs and

symptoms of varying severity, which occur after cessation or reduction

of use of a psychoactive substance. Withdrawal happens when

someone has taken the psychoactive substance in high doses for a

prolonged period of time.9

The intensity and duration of withdrawal depends on many factors. For

some people and for certain drugs the withdrawal process is quite

uncomfortable, but it is self-limiting and poses no serious risk. But for

certain individuals and with some drugs, the withdrawal process can

be dangerous.

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Alcohol withdrawal

The pathophysiology of alcohol withdrawal is not completely

understood, but the primary mechanism is thought to be adaptation

and insensitivity of the CNS to GABA and NDMA.10 In response to

chronic alcohol ingestion and its effects on GABA and NDMA, the body

decreases the number, sensitivity, and function of the GABA receptors

and increases the number, sensitivity, and function of NDMA

receptors.11 When someone who chronically abuses alcohol stops

drinking, the stimulation and inhibition respectively of the GABA and

NDMA receptors is removed and the patient experiences an intense

excitatory state which explains, in part, the signs and symptoms of

alcohol withdrawal syndrome.

Alcohol withdrawal syndrome usually starts within six hours or so after

cessation of drinking, but the onset may be delayed for several days.

It is possible for withdrawal to occur even if the patient still has a

relatively high alcohol level.10 The signs and symptoms of alcohol

withdrawal syndrome are primarily cardiac, neurologic, and

gastrointestinal and can be mild to severe. Commonly noted signs and

symptoms include agitation, anxiety, depression, elevated blood

pressure and heart rate, fever, insomnia, nausea, and tremors.10,11

Patients may present with a relatively mild to moderate clinical picture.

However, there are three serious complications of alcohol withdrawal

syndrome that are possible: 1) withdrawal seizures; 2) alcoholic

hallucinations, and; 3) delirium tremens.

Withdrawal seizures affect approximately 10% of all patients with an

alcohol withdrawal syndrome.11 They typically occur within 12-24 hour

after the last drink is consumed; they are usually single seizures or

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several seizures occurring within a short period of time, and they are

self-limiting.10,11

Alcoholic hallucinations (sometimes called alcoholic hallucinosis) are

usually visual, but auditory and tactile hallucinations are possible.

Alcoholic hallucinations are self-limiting and usually resolve within 24-

48 hours.10 It is important to note that alcoholic hallucinations are a

separate phenomenon from delirium tremens.

Delirium tremens, typically called the DTs, is a specific alcohol

withdrawal syndrome complication. It affects approximately 5% of all

patients who are going through alcohol withdrawal syndrome.10 The

DTs are more likely to occur if the patient 1) has had DTs before, 2)

has been a long-time alcohol abuser, 3) is greater than age 30, 4) is

experiencing alcohol withdrawal and has a high blood alcohol level, 5)

has a concurrent illness, and 6) the onset of alcohol withdrawal is

delayed.10 Delirium tremens produces a clinical picture essentially

identical to mild to moderate alcohol withdrawal syndrome, but the

intensity of the signs and symptoms is much more intense.

Patients who have DTs have severe agitation, confusion and

disorientation, diaphoresis, fluid and electrolyte losses, hallucinations,

fever, hypertension, and tachycardia. Delirium tremens has a mortality

rate of approximately 5%.10 Patients who succumb are those who are

elderly and/or have significant co-morbidities.

Factors that have been correlated with an increased risk of developing

complicated alcohol withdrawal include:12

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The use of alcohol within the past 30 days or a measurable blood

alcohol level

Previous episodes of alcohol withdrawal

A history of alcohol withdrawal seizures

A history of DTs

A history of blackouts caused by alcohol ingestion

Prior admission to an alcohol rehabilitation program

The use of alcohol and a CNS depressant drug such as a

benzodiazepine within the past 90 days

The use of alcohol and a substance of abuse within the past 90

days

A blood alcohol level > 200 mg/dL

Evidence of autonomic hyperactivity, e.g., diaphoresis,

tachycardia.

Opioid withdrawal

The pathophysiology of opioid withdrawal is incompletely understood,

but it is thought to be similar to other withdrawal syndromes, i.e.,

continued excessive use of an opioid causes changes to

neurotransmitters and their receptors; in the case of opioids, GABA

and noradrenaline.13 When the opioid is discontinued the changes in

circulating levels of neurotransmitters and the altered function of the

receptors are no longer inhibited by the opioid, resulting in the clinical

picture of withdrawal.

Opioid withdrawal begins 6-12 hours after last use and the severity of

the signs and symptoms will peak within 24 to 48 hours.14 The clinical

course of opioid withdrawal syndrome often follows the progression

outlined below, starting from the last time the opioid was used.14

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6-12 hours: Diaphoresis, lacrimation, mydriasis, rhinorrhea,

yawning

12-18 hours: Anxiety, insomnia, irritability, nausea

18-24 hours: Abdominal cramps, anorexia, piloerection,

restlessness, tremor

> 24 hours: Chills, diarrhea, hyperthermia, muscle spasms,

severe insomnia, tachycardia

The severity of opioid withdrawal can be evaluated by using the

Clinical Opiate Withdrawal Scale (COWS).14 The use of COWS can help

clinicians make an objective assessment of the severity of withdrawal

and it also involves patient input.

Table 4: Clinical Opiate Withdrawal Scale

1. Resting heart rate:

a. 0 - 80 beats/min or below

b. 1 - 81-100 beats/min

c. 2 - 101-120 beats/min

d. 4 - > 120 beats/min

2. Sweating over the past 30 minutes, not caused by ambient

temperature or physical activity:

a. 0 - No chills or flushing

b. 1 - Subjective reporting of chills or flushing

c. 2 - Observed flushing or moistness on the face

d. 3 – Diaphoresis on the brow or face

e. 4 – Sweat streaming from the face

3. Restlessness:

a. 0 - able to sit still

b. 1 – Reports difficulty sitting still, but can do so

c. 3 – Frequent shifting or extraneous movements of

arms/legs

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4. GI upset within past 30 minutes:

a. 0 - No GI symptoms

b. 1 - Stomach cramps

c. 2 - Nausea or loose stools

d. 3 - Vomiting or diarrhea

e. 5 - Multiple episodes of diarrhea or vomiting

5. Anxiety or irritability:

a. 0 - None

b. 1 - Patient reports increasing anxiousness or irritability

c. 2 - Patient is obviously anxious or irritable

d. 4 - Patient is anxious/irritable and difficult to assess

6. Bone or joint aches:

a. 0 - absent

b. 1 - Mild, diffuse discomfort

c. 2 - Patient reports severe, diffuse aching of muscles, joints

d. 4. - Patient is rubbing joints or muscles and cannot sit still

7. Tremor: observation of outstretched arms

a. 0 - No tremor

b. 1 - Tremor can be felt but not observed

c. 2 - Slight tremor observed

d. 4 - Gross tremor or muscle twitching

8. Yawning:

a. 0 - No yawning

b. 1 - Yawning once or twice during assessment

c. 2 - Yawning three or more times during assessment

d. 4 - Yawning several times a minute

9. Pupils size:

a. 0 - Pupils normal sized for room light or pinned

b. 1 - Pupils possibly (?) than normal size for room light

c. 2 - Pupils moderately dilated

d. 4 - Pupils are dilated to the point that only the rim of the

iris is visible

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10. Runny nose or tearing: Not accounted for by allergy or cold:

a. 0 - Not present

b. 1 - Nasal stuffiness or unusually moist eyes

c. 2 - Nose running or tearing

d. 4 - Nose constantly running or tears streaming down

cheeks

11. Gooseflesh skin:

a. 0 - Absent

b. 3 - Skin piloerection can be felt or hair standing up on arms

c. 5 - Prominent piloerection

A score of 5-12 is considered mild; 13-24 is moderate; 25-36 is

moderately severe, and; > 36 is severe.

Benzodiazepine withdrawal

The benzodiazepines are comparatively old drugs; they are commonly

prescribed and commonly abused, and the most of the medical

literature regarding sedative-hypnotic withdrawal has been about

benzodiazepines. Benzodiazepine intoxication is typically mild to

moderate in severity but paradoxically, withdrawal from

benzodiazepines can produce severe signs and symptoms and can be

life-threatening.15

As with other alcohol and the other drugs discussed in this module,

chronic use of a benzodiazepine changes the affinity of receptors for a

specific neurotransmitter (GABA in the case of benzodiazpines),

causing a compensatory change in the number, function, and activity

of these receptors. When someone who has been chronically using or

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abusing a benzodiazepine stops taking the drug, the inhibitory effect of

GABA is removed, causing excess CNS excitation.

Withdrawal from benzodiazepines occurs when use of the drug is

abruptly stopped or tapering of the drug is done too quickly,15 but mild

withdrawal can occur even if the drug is slowly tapered.16 The onset of

signs and symptoms depends on the half-life of the particular

benzodiazepine. The withdrawal syndrome may begin within 24-48

hours after cessation of the drug, but if the benzodiazepine has a long

half-life (> 24 hours) it may be several weeks before signs and

symptoms are observed.15,17 The severity and duration of the

withdrawal syndrome appears to be related to the duration of

use/abuse and how quickly the drug was stopped. However, severe

withdrawal reactions can occur even after short-term use at low

doses.17

The benzodiazepine withdrawal syndrome is characterized by agitation,

anxiety, dysphoria, insomnia, irritability, muscle tremors, and

restlessness. Other, less common signs and symptoms include

abnormal sensory perceptions, delirium, parathesias, tinnitus,

psychotic symptoms, persistent headaches, myoclonic jerks, and

seizures.16,18 The prevalence of seizures has been estimated to be

2.5%-8%.16 They are usually self-limiting, but deaths have been

reported in association with seizures caused by benzodiazepines.19 The

benzodiazepines that have short (< 1 hours) half-lives such as

diazepam and lorazepam are more likely to cause withdrawal

seizures,17,20 and seizures are more likely to occur during withdrawal if

the prescribed dose is high and the duration of use is long.17,20 The risk

of withdrawal seizures is also increased by other factors that are

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common to the population of substance abusers such a concomitant

alcohol use.17

Amphetamine/stimulant withdrawal

Compared to the amount of literature published about alcohol

withdrawal and opioid withdrawal there is little data about

amphetamine/stimulant withdrawal and much of the research has

been on methamphetamine. The medical effects of methamphetamine

withdrawal appear to be relatively benign and well tolerated, and

several sources identify an acute phase and a sub-acute phase.21,22

The acute phase lasts approximately 7 to 10 days and the signs and

symptoms may include diaphoresis, headache, muscle and joint pain,

and mild, self-limiting gastrointestinal distress.21 Psychological effects

during the acute phase include anxiety, depression, an increased

appetite and an increased need for sleep, and craving for the drug.

Psychosis during the acute phase of withdrawal is relatively common.

Patients who have a long history of methamphetamine use, have more

severe depressive symptoms, and are significantly older than other

users, are more likely to have persistent and severe psychotic

symptoms.23

The sub-acute phase lasts approximately to weeks and is characterized

by a gradual decrease in the number and intensity of symptoms.21

Craving may persist for up to five weeks.22

Cocaine withdrawal

Cocaine withdrawal rarely causes serious medical harm or

consequences, and most patients simply have mild, self-limiting signs

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and symptoms such as chills, non-specific musculo-skeletal pain, and

tremor.24 However, the psychological effects of cocaine withdrawal can

be intense and debilitating. Patients may experience significant levels

of anxiety, depression, fatigue, inability to concentrate, insomnia, and

intense drug cravings.24 The duration of cocaine withdrawal is typically

one to two weeks.24

TREATMENT FOR SUBSTANCE ABUSE

Amphetamine/stimulant abuse and withdrawal and cocaine abuse and

withdrawal are considered to be relatively mild and self-limiting and

treated with symptomatic/supportive care.22, 24-26.

Benzodiazepine abuse and withdrawal is treated by slowly tapering the

use of the drug, administering a long-acting benzodiazepine, and

providing symptomatic/supportive care.15,16 Antihistamines, anti-

psychotics, beta-blockers, selective serotonin reuptake inhibitors, and

tricyclic anti-depressants have been used to treat benzodiazepine

withdrawal, but they have not been shown to be superior to

benzodiazepines.15,16 There has been some evidence supporting the

use of carbamazepine to treat benzodiazepine withdrawal, but a review

considered the data for its use for this purpose insufficient.27 The

optimum rate for tapering has not been determined and it may take

weeks to years to successfully withdraw a patient from a

benzodiazepine.28

Treatment of alcohol abuse and withdrawal has been well studied. The

basic approach is to: 1) make sure the patient is undergoing alcohol

withdrawal by ruling out alternative diagnoses, and; 2) provide

symptomatic/supportive care.10 Symptomatic/supportive care should

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consist of frequent assessments, intravenous hydration and nutritional

support, the use of benzodiazepines to control agitation,10 and this

approach is appropriate for all patients who are undergoing alcohol

withdrawal. Patients in severe withdrawal and having a serious

complication such as DTs may need sedation with a long-acting

barbiturate, such as phenobarbital, or a more powerful sedation with

propofol.10

Assessment

One of the most widely used tools for assessing the severity of alcohol

withdrawal is the Clinical Institute Withdrawal Assessment for alcohol

(CIWA).12 The CIWA scale measures 10 symptoms: Agitation, anxiety,

auditory disturbances, clouding of sensorium, headache,

nausea/vomiting, paroxysmal sweats, tactile disturbances, tremor, and

visual disturbances.

The presence of symptoms in the CIWA is scored on a scale of 0-7,

and the total score is used to determine the severity of withdrawal,

e.g., a score of 8-15 indicates the patient is in moderate withdrawal. If

the patient is determined to be in severe withdrawal and needs

intravenous benzodiazepines, an assessment with the CIWA scale may

be needed every 10-15 minutes.10 If the patient is unable to answer

questions, e.g., he/she is incoherent or endotracheally intubated,

another assessment tool will need to be used.

Intravenous hydration/nutritional support

Careful attention should be given to intravenous (IV) hydration as

patients undergoing alcohol withdrawal are often dehydrated. The IV

fluids provided to patients should contain glucose, supplemental

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thiamine, and multivitamins that contain folate.10 Serum levels of

magnesium, phosphate, and potassium should be measured and

replenishment given as needed.

Benzodiazepines

Benzodiazepines are the cornerstone of treating agitation in patients

who are in alcohol withdrawal.10 Many authorities recommend a

symptom-triggered approach in which benzodiazepines are given

based on the result of the CIWA assessment.10 Benzodiazepines such

as diazepam that have a long half-life are preferred, but

chlodiazepoxide and lorazepam can be used, as well. The patient’s

liver function should be evaluated prior to use as compromised hepatic

function could cause decreased metabolism and clearance of a

benzodiazepine, resulting in prolonged effects.

The treatment of opioid abuse and withdrawal is also well studied and

the treatment approach is relatively standardized. Use of the opioid

should be stopped. A long-acting drug such as methadone that is

pharmacologically similar to the used/abused opioid should be given,

and symptomatic/supportive care should be offered.29

The pharmacological treatment of opioid abuse and withdrawal

typically involves three drugs: methadone, buprenorphine/naloxone,

and clonidine. Methadone is the most commonly used drug for the

treatment of opioid withdrawal. It is a longer-acting opioid agonist and

it produces less CNS depression and euphoria than most opioids. The

drug is given as a tablet or oral solution several times a day, and the

amount of time a patient will need to take methadone is highly

variable. Buprenorphine is a partial opioid agonist that can be used to

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treat opioid withdrawal.30 It is often combined with naloxone in the

form of Suboxone® in order to discourage abuse. Clonidine is a

centrally acting alpha-agonist that decreases sympathetic outflow. This

mechanism of action makes it useful for treating the signs and

symptoms of opioid withdrawal.30

Anxiolytics and hypnotics can also be used for symptomatic care.

Long-acting opioid antagonists such as naltrexone have been used to

treat opioid abuse and withdrawal but without a significant degree of

success.30

Psychological treatment

There is a vast and bewildering array of psychological approaches for

treating chemical dependency, and given the diverse multitude of

treatments, it is not surprising that there is no consensus as to what is

the “best” psychological approach for treating chemical dependency.

Also, there are many methods that are widely used that have little

supporting scientific evidence.

Add to the above the fact that research has indicated that many of the

therapeutic approaches have similar success rates and the selection of

treatment becomes confusing. However, there are common aspects of

successful treatments. The best ones are evidence-based treatments,

and where the practitioners have received extensive training. For

example, there is an organization of physicians who specialize in

treating chemical dependency, the American Society of Addiction

Medicine.

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But although there are many ways to address the psychological needs

of the chemically dependent patient, behavioral therapies are most

often used. Behavioral therapies are a group of approaches

characterized by a concern with the patient’s behavior. The therapist

focuses not on past events that may have led to chemical dependency,

but on what is currently occurring in the patient’s life. There are

different behavioral therapies. Cognitive behavioral therapy has been

proven to work, has been thoroughly tested and there is empirical

evidence for its success.

Cognitive behavioral therapy

Cognitive behavioral therapy (CBT) is grounded in social learning

theories and operant conditioning. In this process, the patient

identifies feelings, thoughts, and situations that are associated with

using the substance of abuse. The patient sees the thinking – the

distorted, inaccurate, maladaptive thinking – that is the underpinning

of negative emotions that lead to his/her chemical dependency

behaviors, and the therapist helps him/her to replace these with

realistic, life-affirming beliefs. Thus, cognitive behavioral therapy has

two parts. The first is a functional analysis, and the second is skills

training. It provides the chemically dependent patient with motivation

for abstinence, teaches coping skills, changes reinforcing

contingencies, and trains interpersonal skills that allow the patient to

build a support network.

The treatment is a one-on-one encounter with a trained therapist and

12-16 weekly sessions are typically scheduled. It is done on an

outpatient basis (typically) because chemical dependency is intimately

connected with the circumstances of the patient’s life, and this gives

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the patient an immediate chance to try new coping skills and get

immediate feedback on their effectiveness. Cognitive behavioral

therapy can be successfully combined with pharmacological treatment

and group, family, and/or couples therapy. It is unique in that it

provides a functional analysis of chemical dependency and concrete

coping skills are taught and practiced during sessions.30

Of course, cognitive behavioral therapy is not the only way to address

the psychological and emotional concerns of the patient with chemical

dependency. Contingency management may be valuable. In this

technique, patients receive rewards for specific behavioral goals, and

there is a lot of very good empirical support for its effectiveness.

However, it should also be noted that there is evidence that the effects

tend to lessen when the contingencies are removed, and that this

approach involves a lot of time and money.

Motivational interviewing is a focused, goal-directed technique that

helps patients explore and resolve ambivalence and helps the patient

towards an acceptable goal. It has been successfully used in treating

chemical dependency on alcohol and research has shown significant

effects, which are very durable. The therapist tries to understand the

patient’s frame of reference, expresses acceptance and affirmation,

and reinforces the patient’s own concerns, desires, and intentions for

change. Finally, couples and family therapy can be used.

There is much research that indicates these psychological treatments

can be effective in adult and adolescent patients with chemical

dependency.

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NURSING CARE OF THE CHEMICALLY DEPENDENT PATIENT

Nursing care of the patient who is chemically dependent is complex.

Nurses may encounter these patients during acute intoxication, the

withdrawal phase, or during the process of rehabilitation and the

patient’s ongoing attempts to maintain a drug-free state. During these

specific periods, the goals of nursing care will be very different and the

needs of the patient will be very different, so it is difficult to provide a

“one size fits all” approach.

This problem is exacerbated by the fact that nurses often receive little

information about the nursing care of the patient with chemical

dependency during their formal education. There is almost nothing in

the nursing literature on the topic, and as the field of addiction

medicine is relatively new, standards of care are still being formed.

Also, nurses – and other health care personnel – also frequently report

that they do not like caring for the patient with chemical dependency,

and they have negative attitudes towards them. This is not surprising.

The typical heath care paradigm is that the patient seeks help for a

health problem that is out of his/her control and is willing to cooperate

willingly with the recommendations of caregivers. However, many

patients with chemical dependency do not fit this paradigm: quite the

opposite. As a result, nurses caring for them experience impatience,

resentment, anger, and the feeling that other patients with

“legitimate” health care concerns are being neglected.

Chemical dependency carries a large negative stigma in our society,

and many nurses feel that the patient with chemical dependency is

simply a “bad person.” Nurses often wonder: why can’t they just stop?

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The solution is education. Nurses must be taught that chemical

dependency is a chronic disease, and that the health issues of these

patients are legitimate, albeit at times confusing and unfamiliar.

Nurses need specific information about drugs and treatments. They

must familiarize themselves with specific nursing diagnoses (e.g.,

ineffective health maintenance, anxiety, risk for injury, etc.) that will

be used when caring for these patients. In addition, nurses must also

cultivate the following characteristics that have been found to be

important for successful care of someone with a chemical dependency.

Hope and optimism:

Given the seemingly self-inflicted nature of chemical dependency

and the high relapse rate, it can be a challenge to remain

hopeful and optimistic, but these attitudes are essential.

A non-judgmental attitude:

It is very easy to form judgments about the patient with

chemical dependency, to view them as weak or lacking in morals

and/or self-control.

A low need to control the patient.

The ability to engage the patient, but still detach.

Patience and tolerance:

Chemical dependency is a chronic disease and relapses are very

common.

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Flexibility.

Recognize that people with chemical dependency often have co-

occurring psychiatric disorders that must be treated.

SUMMARY

Substance abuse disorder involves a wide variety of legal and illicit

substances but the essential feature of a substance use disorder is a

cluster of cognitive, behavioral, and physiological symptoms indicating

that the individual continues using the substance despite significant

substance-related problems. In simpler terms, the person who has a

substance abuse disorder will continue to acquire and use alcohol or

drugs despite very serious consequences. This is further illustrated by

the diagnostic criteria of a substance abuse disorder, e.g., the person

who has a substance abuse disorder has impaired control, exhibits

risky behavior regarding acquisition and use, and his/her substance

abuse disorder and its associated behaviors causes social impairment.

The causes of substance abuse disorder are many and varied, but it is

believed that one of the primary effects of continued use of alcohol or

drugs is a significant increase and/or decrease in the activity and

function of inhibitory and excitatory neurotransmitters. This effect

produces tolerance and withdrawal. The CNS responds by needing

larger amounts of alcohol or drugs to produce the desired effect

(tolerance), and if the alcohol or drug is discontinued the inhibitory

effect of the drug or alcohol is removed and the excitatory effect of

these neurotransmitters is greatly increased, resulting in withdrawal.

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Treatment of substance abuse requires specific interventions and long-

term commitment. It involves cessation of alcohol or the drug,

identification and treatment of complications of withdrawal, and, the

use of specific drugs that can help to decrease craving and treat the

signs and symptoms of withdrawal.

Withdrawal is most often a benign and self-limiting process, albeit

physically and psychologically quite uncomfortable. Follow-up care that

involves social and psychological support is crucial after the withdrawal

period is complete. Substance abuse disorder certainly has a physical

basis but there are emotional and psychological aspects that cause and

reinforce substance abuse that must be addressed.

Please take time to help NurseCe4Less.com course planners evaluate the

nursing knowledge needs met by completing the self-assessment

Knowledge Questions after reading the article, and providing feedback in

the course evaluation.

Correct Answers, pg. 46

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1. The term dependency used in relation to substance abuse

means:

a. an intense psychological craving for alcohol or a drug

b. physical need for alcohol or a drug that develops over time.

c. the need for increasing amounts of alcohol or a drug over time.

d. a physical resistance to withdrawal signs and symptoms.

2. One of the central themes of a substance abuse disorder

is:

a. continued use despite significant substance related problems

b. excessive use of alcohol or an illicit drug.

c. a pattern of use of alcohol or a drug that causes medical harm.

d. alcohol or drug use that has social consequences.

3. One of the diagnostic criteria for substance abuse

disorder is:

a. Self-admitted addiction to alcohol or a drug.

b. Excessive use of alcohol or a drug for > five years.

c. Impaired control relating to use of alcohol or a drug.

d. Use of an illicit drug

4. One of the diagnostic criteria for substance abuse disorder

is:

a. Refusal by the patient to accept professional help.

b. Alcohol or drug use that causes medical harm.

c. Alcohol or drug use that waxes and wanes.

d. Tolerance to alcohol or a drug.

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5. Substance abuse is thought to be caused and reinforced

in part by:

a. Changes in neurotransmitters and their receptors.

b. Decreased function of the endocrine system.

c. Changes in microcirculation.

d. Undiagnosed immune system dysfunction.

6. Withdrawal in most patients who have a substance abuse

disorder:

a. causes significant morbidity and mortality

b. is relatively benign and self-limiting

c. is less serious if the duration of use has been many years.

d. typically affects males more than females.

7. One of the serious complications of alcohol withdrawal is:

a. Acute renal failure

b. Delirium tremens

c. Rhabdomyolysis

d. Cardiac arrhythmias

8. Withdrawal from benzodiazepines can cause:

a. Seizures

b. Rhabdomyolysis

c. Hepatic damage

d. Pulmonary edema

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9. Which of the following is the drug of choice for treating

alcohol withdrawal?

a. Antipsychotics

b. Benzodiazepines

c. Selective serotonin reuptake inhibitors

d. Barbiturates

10. Which of the following drugs are often used to treat opioid

withdrawal?

a. Benzodiazepines, clonidine, and methadone

b. Anti-psychotics, barbiturates, and selective serotonin reuptake

inhibitors

c. Non-opioid analgesics, propofol, and tri-cyclic anti-depressants

d. Buprenorphine/naloxone, clonidine, and methadone

CORRECT ANSWERS:

1. B

2. A

3. C

4. D

5. A

6. B

7. B

8. A

9. B

10. D

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Footnotes:

1. Office of National Drug Control Policy. What America’s users spend on illegal

drugs: 2000-2006. February 2014. Retrieved August 29, 2014 from

http://www.whitehouse.gov/sites/default/files/ondcp/policy-and-

research/wausid_results_report.pdf.

2. Office of National Drug Control Policy. Consequences of illicit drug use in

America. April, 2014. Retrieved August 29, 2014 from

http://www.whitehouse.gov/sites/default/files/ondcp/Fact_Sheets/consequence

s_of_illicit_drug_use_-_fact_sheet_april_2014.pdf.

3. Thompson W. Alcoholism. eMedicine. July 14, 2104. Retrieved August 29, 2014

from http://emedicine.medscape.com/article/285913-overview.

4. National Institute on Alcohol Abuse and Alcoholism. Alcohol use disorder.

Retrieved August 29, 2014 from http://niaaa.nih.gov/alcohol-health/overview-

alcohol-consumption/alcohol-use-disorders.

5. National Cancer Institute. Tobacco statistics snapshot. Retrieved August 29,

2014 from http://www.cancer.gov/cancertopics/tobacco/statisticssnapshot.

6. Food and Drug Administration. Glossary of drug terms. Retrieved August 30,

2014 from http://www.fda.gov/Drugs/InformationOnDrugs/ucm079436.htm.

7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental

Disorders. 5th ed. Arlington, VA; American Psychiatric Publishing: 2013.

8. Hoffman J, Froemke S, ed. Addiction: Why Can’t They Just Stop? Emmaus, PA:

Rodale; 2007.

9. World Health Organization. Management of substance abuse. Retrieved

September 2, 2014 from

http://www.who.int/substance_abuse/terminology/withdrawal/en/

10. Hoffman RS, Weinhouse GL. Management of moderate to severe alcohol

withdrawal syndromes. UpToDate. September 11, 2012. Retrieved September

3, 2014 from http://www.uptodate.com/contents/management-of-moderate-

and-severe-alcohol-withdrawal-

syndromes?source=search_result&search=Management+of+moderate+to+seve

re+alcohol+withdrawal&selectedTitle=1%7E150.

11. Stehman CR, Mycyk MB. A rational approach to treatment of alcohol withdrawal

in the ED. American Journal of Emergency Medicine. 2013;31:734-742.

12. Maldonado JR, Sher Y, Ashouri JF, Hills-Evans K, Swendsen H, Lolak S, et al.

The “Prediction of Alcohol Withdrawal Severity Scale” (PAWSS): systematic

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literature review and pilot study of a new scale for the prediction of complicated

alcohol withdrawal syndrome. Alcohol. 2014;48:375-390.

13. Ashish K. Rehni, Amteshwar S. Jaggi and Nirmal Singh. Opioid withdrawal

syndrome: Emerging concepts and novel therapeutic targets. CNS &

Neurological Disorders – Drug Targets. 2013;12:112-125.

14. Hopper JA. Opioids. In: McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg

JS, eds. Principles and Practices of Hospital Medicine. New York, NY: McGraw-

Hill; 2012. Online edition, retrieved September 2, 2014 from www.UCHC.edu.

15. Greller H, Gupta A. Benzodiazepine poisoning and withdrawal. UpToDate. May

15, 2013. Retrieved September 2, 2014 from

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withdrawal?source=search_result&search=Benzodiazepine&selectedTitle=1%7E

150.

16. Hu, X. Benzodiazepine withdrawal seizures and management. Journal of the

Oklahoma State Medical Association. 2011;104:62-65.

17. Fialip J, Aumaitre O, Eschalier A, Maradeix B, Dordain G, Lavarenne J.

Benzodiazepine withdrawal seizures: analysis of 48 cases. Clinical

Neuropharmacology. 1987;10:538-544

18. Levy AB. Delirium and seizures due to abrupt alprazolam withdrawal: case

report. Clinical Psychiatry. 1984;45:38-39.

19. Haque W, Watson DJ, Bryant SG. Death following suspected alprazolam

withdrawal seizures: a case report. Texas Medicine. 1990;86:44-47.

20. Owen RT, Tyrer P. Benzodiazepine dependence: a review of the evidence.

Drugs. 1982;25:385-398.

21. McGregor C, Srisurapanont M, Jittiwutikarn J, Laobhripatr S, Wongtan T, White

JM. The nature, time course, and severity of methamphetamine withdrawal.

Addiction. 2005;100:1320-1329.

22. Zorick T, Nestor L, Miotto K, Sugar C, Hellemann G, Scanlon G, et al.

Withdrawal symptoms in the abstinent methamphetamine-dependent subjects.

Addiction. 2010;105:1809-181.

23. Lecomte T, Mueser KT, MacEwan W, Thornton AE, Buchanan T, Bouchard V, et

al. Predictors of persistent psychotic symptoms with methamphetamine abuse

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24. Gorelick DA. Cocaine use disorder in adults: Epidemiology, pharmacology,

clinical manifestations, medical consequences, and diagnosis. UpToDate. August

15, 2013. Retrieved September 3, 2014 from

http://www.uptodate.com/contents/cocaine-use-disorder-in-adults-

epidemiology-pharmacology-clinical-manifestations-medical-consequences-and-

diagnosis?source=search_result&search=Cocaine+use+disorder&selectedTitle=

1%7E150.

25. Pennay AE, Lee NK. Putting the call out for more research: the poor evidence

base for treating methamphetamine withdrawal. Drug and Alcohol Review.

2022;30:216-22.

26. Srisurapanont M. Jarusuraisin N. Kittirattanapaiboon P. Treatment for

amphetamine withdrawal. Cochrane Database of Systematic Reviews.

(4):CD003021, 2001.

27. Denis C, Fatseas M, Lavie E, Auriacombe M. Pharmacological interventions for

benzodiazepine mono-dependence management in outpatient settings.

Cochrane Database of Systematic Reviews. 2006;3:CD005194.

28. Lader M, Tylee A, Donoghue J. Withdrawing benzodiazepines in primary care.

CNS Drugs. 2009;23:19-34.

29. Kosten TR. Opioid drug abuse and dependence. In: Longo DL, Fauci AS, Kasper

DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal

Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. Online edition, Retrieved

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The information presented in this course is intended solely for the use of healthcare

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is designed to assist healthcare professionals, including nurses, in addressing issues

associated with healthcare.

The information provided in this course is general in nature, and is not designed to

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