This document discusses various drugs of abuse, including their epidemiology, pharmacology, clinical effects, and emergency management. It covers stimulants like amphetamines and cocaine, opioids, inhalants, marijuana, and others. For each drug class, it describes the typical symptoms of intoxication as well as treatments for associated complications like seizures, hyperthermia, arrhythmias, and respiratory depression. Naloxone is discussed as an antidote for opioid overdose that can precipitate withdrawal symptoms in dependent patients.

1. DRUGS OF ABUSE
Dr abdullah alzahrani
Pediatric emergency F1
KKUH

2. Drugs of abuse
■ non permissive consumption of certain substance
that lead to physical and psychological dependence
■ Substance abuse and addiction is a major burden to
the societies.
■ In the USA, Economic costs alone are estimated to
exceed half a trillion dollars annually, including
health, crime related costs, and losses in productivity

3. Epidemiology in Saudi Arabia
■ hospital based survey
■ June 95 to December 96
■ From the Department of Psychiatry, Al-Amal Hospital, Jeddah, Kingdom of SaudiArabia

4. Epidemiology in Saudi Arabia

5. Drug of abuse Symptoms and signs
CNS stimulants
(Amphetamines,Cocaine )
Pupils dilated. Increased BP, pulse, temperature, sweating; tremors; confused;
paranoid ideation; impulsivity; hyperactivity; convulsions; cardiac arrhythmias
CNS sedatives
(Barbiturates, Opioids)
BP decreased, respirations depressed; drowsy, coma, lateral nystagmus,
confusion,
ataxia, slurred speech, delirium; convulsions , Pupils constricted
Cannabis group
(marijuana,hashish )
Pupils unchanged; injected conjunctiva; euphoria, anxiety; dreamy; fantasy
state ,Toxic delirium (disorientation, confusion, memory impairment)
Hallucinogens (LSD ,
PCP)
Pupils dilated (normal or small with PCP); BP elevated, heart rate increased,
amnesia, analgesia, nystagmus, increased temperature, flushed face, euphoria,
paranoid thought, time and visual distortions, visual hallucinations.
Anticholinergic Pupils dilated and fixed, heart rate increased, temperature increased,
BP increased; drowsy, coma, flushed, dry skin and mucous membranes,
erythematous skin, amnesia, disoriented, visual hallucinations

6. Amphetamines
■ used to treat
narcolepsy, ADHD,
obesity, fatigue, and
nasal congestion
■ decongestant nasal
inhalers contains
amphetamine that can
be extracted and
ingested by drug-
seeking adolescents.

7. Amphetamines
■ Methamphetamine (“Ice,”
“Crystal Meth”).
■ rapid onset of desired
euphoria.
■ Dextroamphetamine
■ Methylphenidate
(Concerta )
■ legally prescribed
■ It is used for the
treatment of (ADHD) and
narcolepsy.

8. Amphetamines
■ Fenethylline
■ a codrug of amphetamine
and ththeophylline

9. Amphetamines
■ MDMA (Ecstasy)
■ popular at concerts,
and music festivals
■ Qat
■ contains the alkaloid
cathinone, an
amphetamine-like
stimulant,

10. Amphetamines : pharmacology
■ CNS stimulant, peripheral adrenergic actions .
■ Oral , injection , nasal insufflation
■ act by releasing endogenous biogenic amines from the
presynaptic neurons. MDMA has more serotonergic
activity
■ The half-life of the amphetamines is about 3 hours,
with much of the drug excreted in the urine

11. Amphetamines : clinical
■ 10 to 30 mg cause wakefulness, alertness, a decreased sense of
fatigue, and an elevation of mood.
■ increased initiative, self-confidence, ability to concentrate,
euphoria, increased motor and speech activity.
■ improved physical performance in athletes.
■ appetite-suppressant effect through an action on the lateral
hypothalamic feeding center. However, tolerance to this effect
also develops
■ consider the diagnosis of Amphetamines intoxication in any
diaphoretic patient with hypertension, tachycardia, severe
agitation, and psychosis.

12. Amphetamines : clinical
■ acute toxic effects
– euphoria, restlessness, dizziness, tremor, hyperactive reflexes,,
irritability, weakness, insomnia, and fever.
– confusion, assaultiveness, anxiety, delirium, paranoid hallucinations,
panic states, and suicidal or homicidal tendencies, especially in patients
who have underlying mental illnesses.
– Violent behavior can cause or worsen hyperthermia, hyperkalemia, and
rhabdomyolysis.
– pulmonary problems :acute pulmonary edema, pulmonary hypertension
– Cardiotoxic effects :, anginal pain, hypertensive crisis or circulatory
collapse.
– GI effects : anorexia,, vomiting, diarrhea, and abdominal cramps.
– Severe overdoses may cause convulsions, coma, and cerebrovascular
accidents.

13. Amphetamines : clinical
■ Chronic amphetamine abuse
– causes symptoms similar to acute overdose.
– The most common serious effect is a psychotic reaction
with hallucinations and paranoid delusions, often
mistaken for schizophrenia.
– associated with cerebral vasculitis.
■ In addition to sympathomimetic features, MDMA toxicity may
cause hyponatremia, serotonin syndrome, and
hepatotoxicity.

14. Amphetamines : ED
Management
■ Initial stabilization is based on clinical presentation and vital
signs.
■ finger-stick glucose (evaluation of altered mental status)
■ serum electrolytes; serum lactate; creatinine phosphokinase
(CPK); liver function studies (ALT,AST); arterial blood gas; PT,
PTT; renal function studies (creatinine, BUN);
■ acetaminophen and salicylate levels (possible co-ingestion)
■ ECG (possible additional drug ingestion that causes prolonged
QRS or QTc intervals)
■ toxicological screen will pick up amphetamines

15. Amphetamines : Management
of Complications
■ Airway Management.
– When indicated, patients may require intubation. Succinylcholine is
contraindicated because of potential for hyperkalemia.
■ Seizures.
– These usually are brief, but if prolonged, use lorazepam or diazepam and seek
other causes (hypoglycemia, intracranial hemorrhage).
■ Hyperthermia.
– Aggressive sedation, neuromuscular paralysis, and fluid resuscitation are
used to control methamphetamine-induced hyperthermia
– external cooling blankets or evaporative cooling techniques.
– Dantrolene has been recommended for the treatment of hyperpyrexia
associated with MDMA use
■ Hypertension.
– Hypertension is managed as other hypertensive crisis

16. Amphetamines : Management
of Complications
■ Agitation.
– benzodiazepines (lorazepam 4 mg or diazepam 5 to 10 mg IV) to control
agitation.These doses may need to be repeated at frequent intervals based
on clinical response.
– Second-generation antipsychotic agents (e.g., ziprasidone 10 mg IM),
butyrophenones (e.g., droperidol 2.5 to 5 mg, or haloperidol 10 mg given
IM or IV), can be used as adjunctive therapy when benzodiazepines do not
control symptoms.
■ Rhabdomyolysis.
– volume expansion, normal saline and sodium bicarbonate for metabolic
acidosis
■ Electrolyte Abnormalities.
– Hyperkalemia: if there is ECG changes, requires calcium to prevent
arrhythmias, followed by measures to shift potassium intracellular.

17. Cocaine
■ Cocaine from leaves
of Erythroxylum coca lives mainly in south
America
■ injection, inhalation, nasal insufflation, and
rarely, ingestion
■ body packer
■ body stuffer
■ Body stuffers are typically at greater risk of
cocaine intoxication because they do not take
enough protection.

18. Cocaine pharmacology
■ Cocaine potentiates the excitatory responses of innervated
organs to norepinephrine and epinephrine by blocking the
reuptake of catecholamines at adrenergic nerve endings.
■ vasoconstriction and mydriasis.
■ Cocaine is still occasionally used as a local anesthetic for
ophthalmologic or otorhinolaryngologic procedures
■ Cocaine metabolites are readily detected in urine for
approximately 3 days after exposure

19. Cocaine clinical
■ CNS stimulation : euphoria, restlessness, excitement, tremors, forced speech,
agitation, and tonic–clonic convulsions.
■ Larger doses :hypertension followed by cardiovascular collapse, myocardial
ischemia and infarction.
■ Rhythm disturbances : ventricular or supraventricular tachyarrhythmias.
Arrhythmias are the most common cause of death after severe cocaine
exposure.
■ bronchospasm, hemoptysis, pneumothorax, and pneumomediastinum.
■ Coke fever (or pyrexia) after acute cocaine use. muscle rigidity (resembling
neuroleptic malignant syndrome) , rhabdomyolysis (the result of agitation
and/or physical restraint).
■ Infants exposed to cocaine :CNS excitation that includes hyperactivity,
dystonic posturing, altered mental status, or frank seizures.

20. Cocaine management
■ seizures requires immediate airway control as well as anticonvulsant
therapy by Benzodiazepines
■ Benzodiazepines should also be administered to the patient with
mild to moderate toxicity (agitation, hypertension, tachycardia)
because of their efficacy in reversing many of these clinical
manifestations.
■ hypertensive crises : benzodiazepine use may be combined with a
short-acting antihypertensive (e.g., nitroprusside).
■ Cardiac arrhythmias are treated according to advanced cardiac life
support protocols
■ Hyperthermia must be recognized and treated promptly to prevent
its complications.

21. Cocaine management
■ Patients with CNS depression or a lateralizing neurologic examination
should receive head imaging to rule out an intracranial vascular
event.
■ need for GI decontamination is confined to body packers/stuffers or
when drug coingestion is suspected.
■ With body stuffers :
– Gastric emptying maneuvers and endoscopic removal of cocaine
bags are relatively contraindicated because of the risk of bag
rupture.
– Instead, decontamination is confined to administration of
activated charcoal and WBI, though in some cases surgical
removal may be indicated.
■ In the event of severe intoxication or ingestion of more than 1 to 2 g
of cocaine, transfer to the intensive care unit is essential

22. Opioids
■ include illegal drug heroin as well as pain
relievers available legally by prescription,
such as oxycodone ,hydrocodone ,codeine,
morphine and Fentanyl

23. Opioids pharmacology
■ analgesia, drowsiness, change in mood, respiratory
depression, decreased GI motility, nausea, and vomiting.
■ clinical toxicity (excessive sedation) appear with doses that
exceed 5 mg in the adolescent.
■ (neurogenic) pulmonary edema
■ mast cell degranulation (which leads to histamine release and
an “anaphylactoid” reaction)
■ cardiac disturbances (with propoxyphene or methadone
intoxication),
■ neurotoxicity with seizures (with meperidine intoxication).

24. Opioids clinical
■ Miosis and Respiratory depression is hallmark of opioid toxicity
■ blood pressure changes as result from histamine release.
■ sitting or standing may produce orthostatic hypotension.
■ GI tract
– decrease the secretion of hydrochloric acid, GI motility, and
pancreatic secretions
– increasing colonic tone to the point of spasm
– Therapeutic doses of morphine and codeine can increase biliary
tract pressure, producing epigastric distress and biliary colic.
■ Neonates may develop the neonatal abstinence syndrome due to
maternal use of illicit or prescription opioids

25. Opioids management
■ ensure adequate ventilation of the patient. Endotracheal
intubation may be necessary if there is severe respiratory
depression or pulmonary edema.
■ GI decontamination should be considered if large amount of
oral opioids has been ingested, (heroin body-packing)
■ When patients who are addicted to opiates are hospitalized,
small doses of an opiate may be necessary to prevent severe
withdrawal. Methadone substitution is often the preferred
agent, because in small doses, it is less euphorigenic and its
long elimination half-life permits once- or twice-daily dosing.

26. Opioids management:
naloxone
■ dose depends on the severity of the patient’s symptoms and
whether or not they chronically use opioids.
■ Naloxone can precipitate an abstinence syndrome in those who
have developed physical dependence
■ for those patients, smaller initial doses of 0.2 to 0.4 mg with
upward titration as needed.
■ full reversal dose in a pediatric patient is 0.1 mg/kg IV.
■ If there is no response despite the suspicion of opiate
intoxication, the naloxone dose should be repeated (up to a
total dose of 8 to 10 mg)

27. Inhalants
■ prevalence of inhalant abuse among young children and adolescents has
been related to the ready availability of these products

28. Inhalants

29. Inhalants clinical
■ all inhalants possess the pharmacologic property of narcosis, leading
to euphoria and light-headedness after inhalation.
■ halogenated hydrocarbons increase sensitize of the myocardium to
catecholamines, leading to myocardial irritability and cardiac
arrhythmias.
■ sudden sniffing death has been described in adolescents who abuse
inhalants and is most commonly reported with use of halogenated
hydrocarbons.
■ act of bagging is associated with the risk of simple asphyxia.
■ acute exposure to inhalants that contain nitrites lead to
methemoglobinemia
■ chronic inhalant abuse : abdominal pain, muscle wasting, electrolyte
disturbances (hypokalemia), and renal tubular acidosis.
leukoencephalomalacia with cerebral atrophy.

30. Inhalants management
■ Because inhalant abuse may lead to the development of life-
threatening symptoms, close attention to the vital signs and
their stability.
■ Patients with depressed levels of consciousness may require
airway support and ventilation.
■ Arrhythmias should be treated according to the standard
protocol however, the use of epinephrine is relatively
contraindicated because it has been associated with
worsening of rhythm disturbances.

31. Marijuana
■ active constituent,
tetrahydrocannabinol
(THC)
■ Recent marijuana
contain 5% to 8%THC
by weight
Therefore, smoking a
joint is now likely to lead
to a greater degree of
altered mental status
than previously.

32. Marijuana pharmacology
■ When smoked ,THC is absorbed via the lungs. Pharmacologic
effects begin immediately.
■ Oral ingestion of cannabis typically results in decreased
bioavailability due to hepatic first pass metabolism but more
prolonged effects due to ongoing slow absorption by the GI
tract. the onset of effects occurs in 30 minutes to 1 hour, and
peak effects may not occur until the second and third hours
after ingestion
■ THC crosses the blood–brain barrier and binds to endogenous
cannabinoid receptors in the CNS and periphery in order to
exert its clinical effects.

33. Marijuana clinical
■ effects on mood, memory, motor coordination, cognitive ability,
sensorium, time sense, and self-perception.
■ short-term memory is impaired, and the capacity to carry out tasks
that require multiple mental steps to reach a specific goal
deteriorates.
■ Depersonalization, a sense of strangeness and unreality about one’s
self
■ Marijuana may cause an acute exacerbation of symptoms in
stabilized schizophrenics.
■ tachycardia, hypertension, and marked conjunctival injection.
■ Chronic smoking of marijuana and hashish is associated with
bronchitis and asthma, even thoughTHC is a mild bronchodilator.

34. Marijuana management
■ In general, the only treatment required is discontinuation of
the drug.
■ In the adolescent patient with a psychotic reaction or acute
toxic delirium, a sedative such as diazepam, 5 to 10 mg by
mouth or 0.1 mg per kg IV, may be necessary.
■ These acute symptoms should improve with drug abstinence
over 4 to 6 hours.

35. References
■ Fleisher & Ludwig'sTextbook of Pediatric Emergency
Medicine Seventh Edition by Richard G Bachur MD
■ Pediatric Emergency Medicine Reports /Volume 17, Number
12 / December 2012 / Drugs of Abuse 2012 Update