Substance Abuse

Ray TaylorValencia Community College

Department of Emergency Medical Services

Notice

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purposes of educating emergency medical providers (EMTs and Paramedics)

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Objectives

Approach to the overdose patient Recognize toxic syndromes Discuss common drugs of abuse Recognize patterns of substance abuse Discuss Alcohol Abuse

Drug Abuse

Refers to the use of prescription drugs for nonprescribed medical use

Emergencies resulting from drug abuse• Adverse effects caused by the drug or impurities

mixed with drugs• Life threatening infections from IV or intradermal

injection• Accidents during intoxication• Drug dependence or withdrawal syndrome

Background

2.4 to 4 million per year Accidental vs. Suicidal Over half are children 1-5

• Only5% of fatalities Conservatively estimated

that 45 million Americans use drugs in a reactional way

Adults: chemical exposure vs. suicidal

Approach to the Overdose patient

ABC’s Coma cocktail

• narcan, D50• thiamine

Assessment: history and physical

Monitoring Unbiased approach

Approach to the Overdose PatientGut Decontamination

Ipecac Gastric Lavage Activated

Charcoal Whole Bowel

Irrigation Dialysis

Ipecac

Should not be administered routinely Highly variable Effectiveness decreases with time Administration in the ED should be

abandoned Delays charcoal, antidotes, and whole

bowel irrigation

Why Talk About It Then

Can mask signs of toxicity Most useful when unknown or toxic

amount of substance AND Not close to the ED Within 60 minutes (solids) Within 30 minutes (liquids)

Dose:

6 to 12 months: • 5 to 10 cc (with

water) 1 to 12 years:

• 15 cc (with water) 12 years and older:

• 15 to 30 cc (with water)

Ipecac/Family Guy

Family Guy - Who Wants Chowder-.flv

Gastric Lavage

Lavage is rarely recommended

Gastric aspiration

30 minutes post ingestion < 40% removed

Activated Charcoal

Not routinely administered

Will be used most often within 1 hour post ingestion

No data to support or exclude its use

Recommended dose of 1g/kg

Don’t need sorbitol• Makes “shit” come out

faster

Whole Bowel Irrigation

Should not be administered routinely Toxic ingestions of SR or EC drugs Body packers Stuffers Start within 4 hours Polyethylene glycol electrolyte solution N/G tube needed

Whole Bowel Irrigation

Adults:• 1000 cc/hr and increase to 2000cc/hr

Children ( 9 months and up):• 250 cc/hr and increase to 500 cc/hr

Until rectal effluent is clear May give AC prior Do not give MDC during. MDC after WBI

Toxins

Toxidromes• Similar toxins typically have similar

signs and symptoms.• In some cases it may be difficult to

identify a specific toxin.

Toxic Syndromes (1 of 5)

Toxic Syndromes (2 of 5)

Toxic Syndromes (3 of 5)

Toxic Syndromes (4 of 5)

Toxic Syndromes (5 of 5)

Toxic Syndromes

Anticholinergic• dry as a bone….

Sympathomimetic Opiate/ Sedative Cholinergic

• SLUDGE Serotonin

Drug Abuse

DSM IV criteria:• Maladaptive pattern of substance use

leading to impairment manifested by:• recurrent use resulting to fulfill obligations• recurrent use in a way that is physically hazardous• recurrent legal problems related to usage• continued use despite persistent social or

interpersonal problems

Substance Abuse and Overdose

Addiction• Habituation• Physiological dependence• Psychological dependence• Tolerance

Withdrawal Drug Overdose

Common Drugs of Abuse

Narcotics CNS Depressants CNS Stimulants Hallucinogens

Drugs of Abuse

Common Drugs of Abuse (1 of 4)

Common Drugs of Abuse (2 of 4)

Common Drugs of Abuse (3 of 4)

Common Drugs of Abuse (4 of 4)

Narcotics

Heroin accounts for approximately 90% of the narcotic abuse in U.S.

Pure heroin is a bitter-tasting white powder that is usually adulterated (cut) • Lactose• Sucrose• Backing soda• Starch

Narcotics

A typical “bag” is the single dose unit of heroin and may weigh 100mg, which on average is only 5% pure

Other narcotics include:• Morphine, methadone, meperidine, codeine,

oxycodone, propoxyphene• Designer opiates: alpha fentanyl (China White)

Narcotics

Depending on the narcotic preparation, these drugs may be • Taken orally• Injected intradermally (skin popping)• Injected intravenously (mainlining)• Taken intranasally (snorted)• Smoked

Narcotic

CNS depression, drowsiness, euphoria, miosis?, slow RR, N,V

W/D symptoms- not life threatening

Other considerations: infection, abscess, NCPE, epidural abscess, embolization,

Lomotil Treatment: Naloxone

2mg IV or IM to an 8mg total

CNS Depressants

Sedatives/Hypnotic agents Include benzodiazepines and

barbiturates Usually taken orally, but may be diluted

and injected intravenously Use with alcohol increases their effects

CNS Depressants

Benzodiazepines are among the best known and most widely prescribed drugs to control anxiety, stress, and insomnia

Work by depressing brain function and are often abused for their sedative effects

Benzodiazepines

Stimulate Gamma-aminobutyric acid (GABA) receptors

GABA receptors are predominant inhibitory neuroreceptors in CNS

Stimulation produces sedative effects• Alters synaptic transmission in spinal cord

leading to skeletal muscle relaxation

Benzodiazepines

Relatively nontoxic, but may accentuate the effects of other sedative-hypnotic agents

Common benzodiazepines• Valium• Librium• Versed• Klonipin

Barbiturates

General CNS depressants that inhibit impulse conduction in the ascending reticular activating system• Once widely prescribed, but have been

replaced by benzodiazepines• Commonly prescribed barbiturates

• Phenobarbitol• Amobarbitol• Secobarbital

CNS Depressant

Benzos, Barbituates, GABA agonists in the CNS Coma, resp depression, CV depression W/D: restlessness, irritable, seizures BZD are safer GHB, Rohybnol, Treatment: Supportive, Flumazenil

CNS Stimulants

Amphetamines are drugs frequently used to produce general mood elevation, improve task performance, suppress appetite, and prevent sleepiness

CNS Stimulants

Structurally, amphetamines are similar to endogenous catecholamines, but differ in their pronounced effects on the CNS

Adverse effects include:• Tachycardia• Increased BP• Tachypnea• Agitation• Dilated pupils• Tremors, disorganized behavior

CNS Stimulants

Severe cases, patients may exhibit psychosis and paranoia, and experience hallucinations

Sudden withdrawl of amphetamine use may result in “crash” stage• Patients become depressed, suicidal,

incoherent or comatose

CNS Stimulants

Amphetamines, cocaine, PCP Symptoms: euphoria, stimulant,

delirium, SZ, ICH, MI, CVA The Scope of Cocaine

Cocaine

One of the most popular illegal drugs in U.S.

4 million Americans use drug regularly Cocaine related deaths are third leading

cause of drug-related fatalities, proceeded only by heroin and drug-alcohol combinations

Cocaine

Most commonly used as a fine white powder crystalline powder• Street forms are usually adulterated and

vary in purity from 25%-90%• Doses vary from near 0 to 200mg• Usually inhaled intranasally by snorting a

“line” containing 10-35mg of the drug

Cocaine

After absorption through the mucus membranes, effects begin within minutes

Peak effects occur in 15-60 minutes after use

Half life of 1-2.5 hours

Cocaine

Parenteral administration• SQ, IV, IM routes• IV route provides immediate

absorption and intense stimulation• Peak occurs within 5 minutes and a

half life within 50 minutes

Cocaine

Feebase or “crack” cocaine• More potent formulation prepared by mixing

powdered street cocaine with an alkaline solution and then adding a solvent such as ether

• Combination separates into 2 layers with top layer containing the dissolved cocaine

• Evaporation of solvent results in pure cocaine crystals which are smoked and absorbed via lungs

Cocaine

Cocaine in its crystallized form is called “rock” or “crack”

Popping sound produced when the crystals are heated

Freebase is often combined with marijuana or tobacco and smoked in a water pipe

Equal to IV use in intensity and pleasure

Cocaine

Blocks reuptake of NE Use *benzodiazepine (diazepam 5-20 mg) Lidocaine (also a sodium channel blocker

like cocaine) – competes with cocaine at the sodium channel; risk of seizure due to synergistic toxic effect of Lidocaine in presence of cocaine

Bicarb early if coded

Cocaine

Major CNS stimulation that causes profound sympathetic discharge

Increased circulating levels of catecholamines result in excitement, euphoria, talkitiveness, and agitation

Cocaine

Effects of cocaine can precipitate cardiovascular and neurological complications• Cardiac dysrhythmias• MI• Seizures• Strokes (intracranial hemorrhage)• Hyperthermia• Psychiatric disorders

Cocaine

Can occur with any form of the drug and route of administration

Adult fatal dose is thought to be about 1200mg

Fatalities from cocaine induced cardiac dysrhythmias have been reported with a single dose of 25-30mg

Cocaine

Treatment• Airway and ventilation• Oxygen administration and monitor saturation• Cardiac monitoring

• Treat dysrhythmias• Beta blockade

• IV NS• Control and treat seizures• Sympathomimetic toxidrome

(hypertension, tachycardia, agitation)Valium/Versed

Phencyclidine Overdose

A dissociative analgesic with sympathomimetic and CNS stimulant and depressant properties

PCP illegally sold in tablet or powder form to be taken orally, intranasally or with other drugs to be smoked

PCP

Most tablets contain about 5mg PCP

As a rule, PCP in powder from is relatively pure (50-100%)

Chronic use results in permanent memory impairment and loss of higher brain functions

PCP

Low dose toxicity (less than 10mg)• Produces an unpredictable state of

drunkeness, euphoria, confusion, disorientation, agitation, or sudden rage

• Intoxicated patient often has blank stare, stumbling gait, and is dissociative

PCP

Low dose toxicity is best managed by keeping sinsory stimulation to a minimum

Violent and combative patients require protection from self-injury

Closely monitor vital signs Increasing motor activity and muscle

rigidity of often precedes seizures

PCP

High dose toxicity (More than 10mg)• Respiratory depression• Hypertensive crisis• Tachycardia• Coma • PCP psychosis• Treatment

ECSTASY

Methamphetamine Lab

Names XTC X

LOVER’S SPEED CLARITY

E ADAM

What is Ecstasy?

3,4-Methylenedioxymethamphetamine

“MDMA”

What does it look like?

MDMA ????

PMA or PMMA Amphetamine LSD 2-CB Aspirin

Ketamine Atropine 4-MTA DXM Caffeine

How does it work?

Responds by releasing Serotonin, Dopamine and Norepinephrine.

How much does one take?

Standard oral dose is 80 – 150 mg• Most good quality pills contain generally 80-

120mg

Once the “sweet spot” is obtained, a higher dosage is not necessarily more desirable

Lethal dose 106mg/kg or 6000 mg

Onset and Duration

Onset 30 – 60 minutes• Coming up 5-20min.• Plateau 2-3 hours• Coming down 1-2

hours• Duration 3-4 hours• After affects 3-24

hours

Positive Effects

Extreme mood lift Increased willingness

to communicate Increased energy Ego softening Feeling of love,

comfort & empathy

Increased appreciation of music

Profound life-changing spiritual experience

Urge to hug & kiss Neurotically based

fear dissolution

Neutral Effects

Visual distortion Pupil dilation Appetite loss Nystagmus Restlessness, nervousness Change in body temp regulation

Negative Effects

Increased HR & B/P Hyperthermia Dehydration Hyponatremia Nausea & vomiting Headache, dizziness Jaw clenching,

tongue & cheek chewing

Post-trip CRASH Depression Hangover Inappropriate &/or

unintended emotional bonding

Say inappropriate things

Muscle tension

Long-Term Effects

Psychological difficulties- ? permanent brain damage- confusion- memory loss- depression- sleep disorders- drug craving- severe anxiety- paranoia

Treatment and Care

Treatment is related to symptoms- Tachycardia- Hypertension- Hyperthermia- Dehydration- Hyponatremia

Hallucinogen

15 million Americans PCP: nystagmus, agitation-sz coma LSD: paranoia, anxiety-flashbacks Peyote (Mescaline): N/V, diaphoresis,

anxiety Causes sensory experiences outside the

mind Marijuana: Euphoria, relaxation Mushrooms: N/V

Hallucinogens

Substances that cause perceptual distortions

Most common hallucinogens are PCP and lysergic acid diethylamide (LSD)

GHB

Gamma-Hydroxybutyrate Grievous Bodily Harm; Georgia Home Boy;

Liquid Ecstasy; Liquid X; Liquid E; Liquid G; G-Riffick; Organic Quaalude; Somatomax; Scoop; Easy Lay; Fire Water and Blue Nitro, Invigorate or Longevity

Naturally occurring component of metabolism, highest levels found in basal ganglia & hypothalamus, but also in major organs

GHB

Synthesized in 1960s – thought to be beneficial

Crosses blood-brain barrier turning into GABA

Stimulates Growth Hormone release aiding in fat reduction & body building

Now popular among recreational users & violent criminals

“Date Rape” drug & deadly when mixed with ETOH

GHB

GHB ingested, 20-30 mins to brain and binds with GABA-B receptors inhibiting noradrenaline release in hypothalamus & mediating release of an opiate-like substance in the striatum

GHB also produces a biphasic dopamine response, increasing the release of dopamine at high GHB concentrations & inhibiting its release at lower doses

GHB

CNS depression (10 mg/kg = short-term amnesia & hypotonia; 20-30 mg/kg = drowsiness & sleep; 50-70 mg/kg = hypnosis, then continue to deep coma) and seizure activity

Narcan, Charcoal, Atropine for bradycardia, Physostigmine for coma

Tricyclic Antidepressants

TCAs are commonly prescribed in the treatment of depression• Drugs work by blocking the uptake of

norepinephrine, serotonin, or both into the presynaptic neuron

• Alters sensitivity of brain tissue to actions of these chemicals

• Tetracyclic Antidepressants

TCAs

TCA toxicity is thought to result from central and peripheral atropine like anticholinergic effects and direct effects on myocardial functions

Commonly prescribed TCAs• Amitriptyline – elavil, endep, etrafon,

vanatrip, levatate

TCAs

Commonly prescribed TCAs• Clomipramine – anafranil• Doxepin – sinequan, zonalon, triadapin• Imipramine – trofinal, impril• Nortriptyline – aventyl, pamelor, norventyl• Desipramine - norpramin• Protriptyline – vivactil• Trimipramine - surmontil

TCAs

Symptoms of overdose• Early

•Dry mouth, blurred vision, confusion, inability to concentrate, and occasionally visual hallucinations

TCAs

Severe symptoms• Hypotension• Anticholinergic effects

• Tachycardia, altered mental status• Miadriasis

• AV conduction blocks• Prolonged QT interval

• Wide QRS, VT, VF

• Seizures• Coma• Death

TCAs

Treatment• Airway and ventilation support• Oximetric monitoring• Cardiac monitoring/BP• Alkalinization (Sodium Bicarbonate),

anticonvulsants, physotigimine when appropriate

• Magnesium for torsades

Salicylates

Widely available in prescription and over-the-counter• Acetylasalicylic acid (aspirin)• Cold preparations (oil of wintergreen)

methyl salicylates• Combination with other analgesics

• Oxycodone, propoxphene

Salicylates

Mechanism• Complex and includes interference

with cellular glucose uptake and inhibition of enzymes that effect energy production, amino acid metabolism and acid buffering in the body.

• Complications result from chronic and acute ingestions

Salicylates

CNS stimulation• Salicylates initially produce direct

stimulation of the respiratory center causing and increase in rate and depth

• This early respiratory alkalosis is followed by a compensatory elimination of bicarbonate ions by the kidneys and subsequent compensatory metabloic acidosis

Salicylates

CNS stimulation• After this period, there is an

accumulation of intermediate acids involved in energy metabolism resulting in profound metabolic acidosis

Salicylates

GI irritation Glucose metabolism

• Interference with cellular glucose uptake causes accumulation of serum glucose followed by its loss

Fluid and electrolyte imbalance Neurological dysfunction

Salicylates

Coagulation effects• Alter normal platelet fuction

Treatment• ABCs, oxygen• Cardiac monitoring• IV NS – large amounts• Activated charcoal• Possible IV glucose and sodium bicarbonate

Acetaminophen

Commonly prescribed analgesic and antipyretic agent available in both prescription and nonprescription preparations• Due to its widespread availability,

there is a high incidence of accidental and intentional poisionings

Acetaminophen

Hepatic toxicity• Formation of hepatotoxic

intermediate if not managed within 16-24 hours post ingestion

• 30 standard size (325mg) tablets are toxic in the average adult

• Causes hepatic necrosis

Acetaminophen

Toxic effects of acute ingestion• Doses of (140mg/kg or greater) can

be classified in 4 stages•Mild symptoms – often masked by

other ingested agents•Moderate – Nausea, vomiting,

abdominal pain, weakness, fatigue, elevated liver enzymes

Acetaminophen

Toxic effects of acute ingestion•Severe – Liver function disruption•Critical – Liver failure•Antidotal therapy begun with 16-24

hours complete recovery should occur

Acetaminophen

Emergency care• Respiratory, cardiac, and

hemodynamic support• Ingestion <4 hours gastric

decontamination• Definitive care

• In-hospital administration of N-acetylcysteine (Mucomyst)

Iron

Forms of Iron Stages of toxicity Decontamination Treatment

Iron Overdose

Approximately 10% of ingested iron (mainly ferrous sulfate) is absorbed each day by the small intestines• After absorption, iron is converted

and stored in iron storage protein and transported to liver, spleen, and bone marrow for incorporation into hemoglobin

Iron Overdose

Ingested iron exceeds the body’s ability to store it, the free iron circulates in blood and is deposited into other tissues

Over ingestion of iron is corrosive to GI tract mucosa and may produce bloody vomitus, diarrhea, and dark stools

Prehospital Treatment: Supportive

Organophosphates

OrganophosphatesOrganophosphates

Organophospates are very common and can be absorbed readily thru dermis

Cause over stimulation and disrupts transmissions in the central and peripheral nervous systems• acetylcholine (neurotransmitter

substance)• acetylcholinesterase (enzyme)

blocked hyperactivity ensues

Organophospates are very common and can be absorbed readily thru dermis

Cause over stimulation and disrupts transmissions in the central and peripheral nervous systems• acetylcholine (neurotransmitter

substance)• acetylcholinesterase (enzyme)

blocked hyperactivity ensues

SLUDGESLUDGE

•Salivation•Lacrimation•Urination•Defecation•GI cramping•Emesis• Miosis (pinpoint pupils) and

muscle fasciculation

•Salivation•Lacrimation•Urination•Defecation•GI cramping•Emesis• Miosis (pinpoint pupils) and

muscle fasciculation

TreatmentTreatment

• Protect yourself• Surface Decontamination• ABC’s

• Aggressive airway management, suctioning and PPV

• Warn the ED, complete decontamination

• Protect yourself• Surface Decontamination• ABC’s

• Aggressive airway management, suctioning and PPV

• Warn the ED, complete decontamination

TreatmentTreatment

•Drug Administration•Atropine (2mg every 5-15 min. in adults and .05 mg/kg in Peds)•Dries secretions, increases HR

•Diazepam/Lorazepam if seizures are present

•Drug Administration•Atropine (2mg every 5-15 min. in adults and .05 mg/kg in Peds)•Dries secretions, increases HR

•Diazepam/Lorazepam if seizures are present

MonitoringMonitoring

• ECG monitoring (may see all types of dysrhythmias)

• GI decontamination followed by activated charcoal if ingested

• Transport immediately• Surface decontamination is

essential early in the evaluation and management (Warn the hospital)

• ECG monitoring (may see all types of dysrhythmias)

• GI decontamination followed by activated charcoal if ingested

• Transport immediately• Surface decontamination is

essential early in the evaluation and management (Warn the hospital)

Alcoholism

Major US problem High comorbidity Metabolism Medical consequences Alcoholic Emergencies Disulfiram reaction

ETOH

Most common substance of abuse in US

Over 10 million in US; 200,000 die annually

Involved in 1/2 of MVC fatalities, most homicides and 1/3 suicides

1/5 total national expenditure for hospital care

Alcoholism

Causes – 3 factors interact• Personality• Environment• Addictive nature of drug

Also thought genetic and hormonal factors play a significant part

Anyone can become dependent with ETOH consumption for long periods

Alcohol Metabolism

80-90% metabolized in 30 minutes Constant rate 20 mg/dL per hour Rate may increase in chronic alcoholic 3-5% excreted unchanged through

lungs and kidneys Remainder metabolized in liver to CO2

and H2O

ETOH

CNS depressant Peripheral vasodilator Suppresses ADH secretion Low doses have excitatory and

stimulatory effect High doses to acute intoxication;

respiratory arrest; hypotension; hypothermia

Chronic Alcohol Abuse

Drinks early in day/alone/secretly Periodic binges/blackouts GI problems/ “green tongue”

syndrome Cigarette burns on clothing, linens Chronically flushed face/palms

Alcohol Abuse

Consequences of Chronic Alcohol Ingestion• Poor nutrition• Alcohol hepatitis• Liver cirrhosis,

pancreatitis• Sensory loss in

hands/feet• Loss of balance and

coordination• Upper GI hemorrhage• Hypoglycemia• Falls (fractures and

subdural hematoma)

ETOH Withdrawal Syndrome

1st – 24-36 hrs – “rum fits”; seizures 2nd – 3rd day (*48-72 hrs after

deprivation) Delerium Tremens DTs – decreased LOC with

hallucinations Rx: ABC; chemstrip/BGL; IV; D50 and

Thiamine 100 mg if hypoglycemic/Ativan for seizures

The END