Substance Abuse Ray Taylor Valencia Community College Department of Emergency Medical Services.
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Transcript of Substance Abuse Ray Taylor Valencia Community College Department of Emergency Medical Services.
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Substance Abuse
Ray TaylorValencia Community College
Department of Emergency Medical Services
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Notice
All rights reserved. Slide show used with permission only for the
purposes of educating emergency medical providers (EMTs and Paramedics)
No portion of this presentation may be reproduced, stored in a retrieval system in any form or by any means (including but not limited to electronic, mechanical, photocopying etc.) without prior written permission from the author
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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
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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
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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
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Approach to the Overdose patient
ABC’s Coma cocktail
• narcan, D50• thiamine
Assessment: history and physical
Monitoring Unbiased approach
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Approach to the Overdose PatientGut Decontamination
Ipecac Gastric Lavage Activated
Charcoal Whole Bowel
Irrigation Dialysis
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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
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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)
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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)
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Ipecac/Family Guy
Family Guy - Who Wants Chowder-.flv
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Gastric Lavage
Lavage is rarely recommended
Gastric aspiration
30 minutes post ingestion < 40% removed
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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
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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
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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
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Toxins
Toxidromes• Similar toxins typically have similar
signs and symptoms.• In some cases it may be difficult to
identify a specific toxin.
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Toxic Syndromes (1 of 5)
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Toxic Syndromes (2 of 5)
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Toxic Syndromes (3 of 5)
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Toxic Syndromes (4 of 5)
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Toxic Syndromes (5 of 5)
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Toxic Syndromes
Anticholinergic• dry as a bone….
Sympathomimetic Opiate/ Sedative Cholinergic
• SLUDGE Serotonin
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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
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Substance Abuse and Overdose
Addiction• Habituation• Physiological dependence• Psychological dependence• Tolerance
Withdrawal Drug Overdose
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Common Drugs of Abuse
Narcotics CNS Depressants CNS Stimulants Hallucinogens
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Drugs of Abuse
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Common Drugs of Abuse (1 of 4)
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Common Drugs of Abuse (2 of 4)
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Common Drugs of Abuse (3 of 4)
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Common Drugs of Abuse (4 of 4)
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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
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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)
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Narcotics
Depending on the narcotic preparation, these drugs may be • Taken orally• Injected intradermally (skin popping)• Injected intravenously (mainlining)• Taken intranasally (snorted)• Smoked
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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
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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
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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
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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
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Benzodiazepines
Relatively nontoxic, but may accentuate the effects of other sedative-hypnotic agents
Common benzodiazepines• Valium• Librium• Versed• Klonipin
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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
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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
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CNS Stimulants
Amphetamines are drugs frequently used to produce general mood elevation, improve task performance, suppress appetite, and prevent sleepiness
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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
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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
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CNS Stimulants
Amphetamines, cocaine, PCP Symptoms: euphoria, stimulant,
delirium, SZ, ICH, MI, CVA The Scope of Cocaine
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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
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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
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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
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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
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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
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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
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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
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Cocaine
Major CNS stimulation that causes profound sympathetic discharge
Increased circulating levels of catecholamines result in excitement, euphoria, talkitiveness, and agitation
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Cocaine
Effects of cocaine can precipitate cardiovascular and neurological complications• Cardiac dysrhythmias• MI• Seizures• Strokes (intracranial hemorrhage)• Hyperthermia• Psychiatric disorders
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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
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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
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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
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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
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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
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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
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PCP
High dose toxicity (More than 10mg)• Respiratory depression• Hypertensive crisis• Tachycardia• Coma • PCP psychosis• Treatment
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ECSTASY
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Methamphetamine Lab
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Names XTC X
LOVER’S SPEED CLARITY
E ADAM
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What is Ecstasy?
3,4-Methylenedioxymethamphetamine
“MDMA”
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What does it look like?
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MDMA ????
PMA or PMMA Amphetamine LSD 2-CB Aspirin
Ketamine Atropine 4-MTA DXM Caffeine
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How does it work?
Responds by releasing Serotonin, Dopamine and Norepinephrine.
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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
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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
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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
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Neutral Effects
Visual distortion Pupil dilation Appetite loss Nystagmus Restlessness, nervousness Change in body temp regulation
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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
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Long-Term Effects
Psychological difficulties- ? permanent brain damage- confusion- memory loss- depression- sleep disorders- drug craving- severe anxiety- paranoia
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Treatment and Care
Treatment is related to symptoms- Tachycardia- Hypertension- Hyperthermia- Dehydration- Hyponatremia
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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
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Hallucinogens
Substances that cause perceptual distortions
Most common hallucinogens are PCP and lysergic acid diethylamide (LSD)
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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
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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
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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
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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
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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
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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
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TCAs
Commonly prescribed TCAs• Clomipramine – anafranil• Doxepin – sinequan, zonalon, triadapin• Imipramine – trofinal, impril• Nortriptyline – aventyl, pamelor, norventyl• Desipramine - norpramin• Protriptyline – vivactil• Trimipramine - surmontil
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TCAs
Symptoms of overdose• Early
•Dry mouth, blurred vision, confusion, inability to concentrate, and occasionally visual hallucinations
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TCAs
Severe symptoms• Hypotension• Anticholinergic effects
• Tachycardia, altered mental status• Miadriasis
• AV conduction blocks• Prolonged QT interval
• Wide QRS, VT, VF
• Seizures• Coma• Death
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TCAs
Treatment• Airway and ventilation support• Oximetric monitoring• Cardiac monitoring/BP• Alkalinization (Sodium Bicarbonate),
anticonvulsants, physotigimine when appropriate
• Magnesium for torsades
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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
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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
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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
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Salicylates
CNS stimulation• After this period, there is an
accumulation of intermediate acids involved in energy metabolism resulting in profound metabolic acidosis
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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
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Salicylates
Coagulation effects• Alter normal platelet fuction
Treatment• ABCs, oxygen• Cardiac monitoring• IV NS – large amounts• Activated charcoal• Possible IV glucose and sodium bicarbonate
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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
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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
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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
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Acetaminophen
Toxic effects of acute ingestion•Severe – Liver function disruption•Critical – Liver failure•Antidotal therapy begun with 16-24
hours complete recovery should occur
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Acetaminophen
Emergency care• Respiratory, cardiac, and
hemodynamic support• Ingestion <4 hours gastric
decontamination• Definitive care
• In-hospital administration of N-acetylcysteine (Mucomyst)
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Iron
Forms of Iron Stages of toxicity Decontamination Treatment
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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
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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
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Organophosphates
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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
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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
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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
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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
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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)
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Alcoholism
Major US problem High comorbidity Metabolism Medical consequences Alcoholic Emergencies Disulfiram reaction
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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
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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
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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
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ETOH
CNS depressant Peripheral vasodilator Suppresses ADH secretion Low doses have excitatory and
stimulatory effect High doses to acute intoxication;
respiratory arrest; hypotension; hypothermia
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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
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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)
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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
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The END