Substance Use Disorders and

Withdrawal I
Saad Chaudhry, MS III
UMHS

Clinical Vignette
65 year-old engineer suffered a femur fracture and some cuts and
bruises after being involved in a MVA. Hes admitted to the medicine
floor and started on oxycodone. The day after admission, he appears
confused with observable tremors in both extremities. He becomes
concerned about bugs on the walls in his room and asks for your
help. What is the most likely explanation for his symptoms?
A Brain concussion
B Alcohol Withdrawal
C Oxycodone intoxication
D Brief Psychotic Disorder
E Schizophrenia

Alcohol (EtOH)
Alcohol activates gamma-aminobutyric acid (GABA) and
serotonin receptors in the central nervous system (CNS)
and inhibits glutamate receptors.
GABA receptors are inhibitory, and thus alcohol has a
sedating effect.
Alcohol is the most commonly abused substance in the
United States.
7-10% of Americans are alcoholics.
Alcohol is the most common co-ingestant in drug overdoses.

Metabolism
Alcohol -> acetaldehyde (enzyme: alcohol dehydrogenase)
Acetaldehyde> acetic acid (enzyme aldehyde
dehydrogenase)
Upregulation of these enzymes in heavy drinkers.
Asian people often have less aldehyde dehydrogenase;
the resultant buildup of acetaldehyde causes flushing and
nausea.
Disulfram (Antabuse) inhibits aldehyde dehydrogenase

CAGE Questionnaire
Have you ever wanted to cut down on your drinking?
Have you ever felt annoyed by criticism of your drinking?
Have you ever felt guilty about drinking?
Have you ever taken a drink as an eye opener (to
prevent the shakes)?

Alcohol Intoxication

Absorption and elimination rates of alcohol are variable

and depend on many factors (zero order kinetics)
Many factors including age, sex, body weight, speed of
consumption, and presence of food in the stomach,
chronic alcoholism, the presence of advanced cirrhosis,
and the state of nutrition.

Clinical Presentation
Effects

Blood Alcohol Level

Decreased fine motor control

20-50 mg/dL

Impaired judgement and coordination

50-100 mg/dL

Ataxic gait and poor balance

100-150 mg/dL

Lethargy; difficulty sitting upright

150-250 mg/dL

Coma in the novice drinker

300 mg/dL

Respiratory depression

400 mg/dL

Treatment
Intoxication (Acute)

Ensure adequate airway, breathing and circulation. Monitor

electrolytes and acid-base status.
Obtain finger-stick glucose level to exclude hypoglycemia.
Thiamine (to prevent or treat Wernickes encephalopathy),
naloxone (to reverse the effects of any opioids that may have
been ingested,) and folate are also administered.

Dependence (Long Term)

Alcoholics Anonymous self-help group
Disulfram (Antabuse) aversive therapy; inhibits
aldehyde dehydrogenase, causing violet retching when the
person drinks
Psychotherapy and selective serotonin reuptake inhibitors
(SSRIs)
Naltrexone- though an opioid antagonist, helps reduce
cravings for Alcohol

Alcohol Withdrawal
Pathophysiology of alcohol withdrawal syndrome poorly understood.
May be related to the chronic depressant effects of alcohol on
the CNS.
When long-term alcohol consumption ceases, the depressant effect
is terminated, and CNS excitation occurs.
Earliest effects of alcohol withdrawal occur between 6-24 hours
after patients last drink and depend on duration and quantity
consumed.
Patients experiencing mild withdrawal may be irritable and complain
of insomnia.
Those in more severe withdrawal may experience fever,
disorientation, seizures, or hallucinations.

Delirium tremens (DTs)

Most serious form of alcohol withdrawal
Often begins within 72 hours of cessation of drinking.
5% of patients hospitalized for alcohol withdrawal
develop DTs
Roughly 15-20% mortality rate if left untreated
Visual or tactile hallucinations, gross tremor, autonomic
instability, and fluctuating levels of psychomotor activity.

Long term complications of Alcohol

Werinicke-Korsakoff syndrome caused by thiamine
(vitamin B1) deficiency resulting from poor diet of
alcoholics.
Werinickes encephalopathy is acute and can be reversed
with thiamine therapy.
If left untreated, Wernickes encephalopathy may
progress into Korsakoffs syndrome, which is chronic and
often irreversible- impaired recent memory, anterograde
amnesia, +/- confabulation

Opiates

Heroin, codeine, dextromethorphan (cough syrup,)

morphine, methadone, meperidine (Demerol)
Stimulate opiate receptors (mu, kappa, and delta) which
are normally stimulated by endogenous opiates and are
involved in analgesia, sedation, and dependence.
Also have effects on the dopaminergic system, which
mediates their addictive and rewarding properties.
Endorphins and enkephalins are endogenous opiates.

Opiate Statistics
Prescribed medications, and not rampant thefts from pharmacies, account
for nearly all overdose incidents caused by prescription pain medications.
An estimated 80 percent of prescription painkillers are prescribed by 20
percent of prescribers.
Medicaid enrollees receive pain prescriptions at twice the rate of nonMedicaid patients.
Results from a Washington state study show Medicaid enrollees accounted
for 45 percent of overdose fatalities in the state.
Between the years 1999 and 2010, sales for prescription painkillers to
hospitals, doctors and pharmacies increased fourfold.
In 2009, the abuse of prescription painkiller drugs accounted for more
than 475,000 emergency room visits.

Clinical Information
Codeine is converted by hepatic metabolism to morphine
and norcodeine with a half-life of 2 to 4 hours.
Morphine is converted by hepatic metabolism to
normorphine with a half-life of 2 to 4 hours.
Half life of Naloxone is approximately 30 to 81 minutes.

Opiate Intoxication

Drowsiness, nausea/vomiting, constipation, slurred

speech, constricted pupils, seizures, and respiratory
depression
May progress to coma or death in overdose
Meperidine and monoamine oxidase inhibitors taken in
combination may cause the serotonin syndrome:
Hyperthermia, confusion, hyper or hypotension, and
muscular rigidity.

Treatment
Intoxication

Ensure adequate airway, breathing, and circulation

Overdose

Administer naloxone or naltrexone (opiate antagonists)

Will improve respiratory depression
Will cause severe withdrawal in an opiate dependent patient
Ventilatory support may be required

Dependence
Oral methadone once daily, tapered over months to years
Psychotherapy, support groups (Narcotics Anonymous, etc.)

Opiate Withdrawal
Not life threatening
Abstinence in the opiate dependent individual leads to an
unpleasant withdrawal syndrome
Dysphoria, insomnia, lacrimation, rhinorrhea, yawning,
weakness, sweating, piloerection, nausea/vomiting, fever,
dilated pupils, and muscle ache.

Treatment
Moderate symptoms: Clonidine and/or buprenorphine
Severe symptoms: Detox with methadone tapered over 7 days

Works Cited
"Acute Alcohol Intoxication".Mount Holyoke College. N.p., 2016. Web.
18 Dec. 2016.
"Alcohol".World Health Organization. N.p., 2016. Web. 18 Dec.
2016.
"Alcohol Toxicity: Background, Pathophysiology,
Epidemiology".Emedicine.medscape.com. N.p., 2016. Web. 18 Dec.
2016.
intoxication, Opioid. "Opioid Intoxication: Medlineplus Medical
Encyclopedia".Medlineplus.gov. N.p., 2016. Web. 18 Dec. 2016.
"Opiate Intoxication".DoveMed. N.p., 2016. Web. 18 Dec. 2016.
"WHO | Acute Intoxication".Who.int. N.p., 2016. Web. 18 Dec.
2016.