Silas Henry Ismanto

Department of Psychiatry
Faculty of Medicine
Gadjah Mada University

DRUG ABUSE AND OVERDOSE

Substance (Drug) Use

 Substance Use Disorder are devided into 2

groups
 Substance Dependence
 Substance Abuse
Drug Dependence

 is a maladaptive pattern use leading to

impairment or distress, as manifested by one
(more) of the following
 Tolerance
 Withdrawal
 taken in larger amounts or over longer periode
 persistent unsuccessful effort s to cut down or
control drug use
  A great deal of time is spent to obtain the drug
 Important activities are reduced because of drug use
 Continued use despite of having persistent or recurrent
social or interpersonal problems caused or exacerbated
by the effects of the drug
Drug (Substance) Abuse

 is a maladaptive pattern use leading to

impairment or distress, as manifested by one
(more) of the following
 Recurrent use resulting in a failure to fulfill major role
obligation
 Recurrent use in situations in which it is physically
hazardous
 Recurrent substance-related-legal problems
 Continued use despite having persistent or recurrent
social or interpersonal problems caused or
exacerbated by the effects of the substance
Emergency Clinical Condition
of Drug Use

 Acute Intoxication (Overdose)

 Drug Withdrawal
 Physical/Psychiatric Comorbidity
 There are substances that most often be
abused and cause OD/Intoxication
 Amphetamines
 Ethanol, Methanol
 Opiates
 Sedative-hypnotic
Amphetamines

 All drugs of this class are central nervous

system stimulants
 Predominant symptom is sympathetic
hyperactivity
 Treatment of intoxication is supportive; no
specific antidote is available
 General Considerations
 Easily abused
 Sympathetic hyperactivity
 May produce vasoconstriction, hypertention
 Short half-lives
 Peak effect, toxicity within 30’ after iv/im adm and
2-3 h after oral ingestion
 Clinical Findings
 “high feeling”, euphoria, enhanced vigor
 Restlessness, hyperactivity
 Talkativeness
 Anxiety, tension
 Anger, fighting
 Toxic psychosis
 Tachycardia
 Mydriasis
 Hypertension
 Arrhytmias
 Hyperthermia, seizures
rhabdomyolysismyoglobinuria
 Treatment
 Agitation, psychotic behavior
 Diazepam 5-10 mg i.v , repeat every 5’-10’ until
sedation; or
 Haloperidol 0,1-0,2 mg/kg i.m
 Seizure
 Diazepam, followed by phenobarbital, phenytoin, or
both if seizure uncontrollable
  Hypertension
 Generally transient
 Often responds to benzodiazepine
 Arrhythmias
 Tachycardia and ventricular tachyarrhythm may
respond to propanolol 0.05-0.1 mg/kg i.v
 Disposition
 Hospitalize patients with complications
 Psychotic, hypertension, hyperthermia, chest pain,
arrhythmias, prolonged symptoms
Ethanol

 Ethanol is c.n.s depressant

 Treatment of ethanol intoxication is
supportive and includes glucose and thiamine
 Clinical Findings
 Inappropriate sexual or aggressive behavior
 Mood lability
 Impaired judgment
 Ataxia
 Dysarthria
 Nystagmus
 Depressed sensorium, stupor, coma
 The breath may smell alcohol
 Frequently seen with trauma
 Treatment
 Thiamine 100 mg im/iv
 Glucose 50 mL of 50% solution over 3-5 minute, if
needed
Methanol

 Methanol is highly toxic alcohol

 It is metabolized by alcohol dehidrogenase
formaldehyde & formic acid
 Optic neuritis that result in blindess has been
described after overdose
 Clinical Findings
 Central nervous system depression
 Agitasi
 Stupor, coma
 Breathlesness
 Headache
 Dizziness
 Seizure
 Methanol is metabolized to formic acid  visual
disturbances
 Hyperemia of the optic disc
 Retinas appear suffused and bright red
 Treatment
 Blocking the metabolism of methanol by alcohol
dehydrogenase
 Fomepizole
 Ethanol
 Correct metabolic acidosis with sodium
bicarbonat
 Folate replacement
 Hemodialysis
Opiates

 Sedation, hypotension, bradycardia,

hypothermia, and respiratory depression
 Diagnosis is confirmed if patient regains
consciousness after naloxone
 General Consideration
 Opiates with varying potencies and durations of
action are found in wide range of prescription
analgesic preparations and illicit drugs
 The opiates act on c.n.s receptor and cause
sedation, hypotension, bradycardia, hypothermia,
& respiratory depression
 Most opiates have half-life of 3-6 hours (the major
exceptions are methadone, 15-20 hours)
 Receptors
 Mu-1 :analgesic, euphoria, hypothermi
 Mu-2 :bradycardia, depresi pernafasan, myosis,
euphoria, penurunan aktivitas usus, ketergantungan
fisik
 Kappa :depresi nafas, myosis, hypothermi,
analgesic
 Delta :depresi pernafasan, disforia, halusinasi
 Gamma :inhibisi otot polos
 Clinical Finding
 Lethargic, coma
 Pinpoint pupils
 Signs of parenteral drug abuse
 Pulmonary edema may occur
 Regains consciousness after administration of
naloxon
 Treatment
 Give naloxon, start with 0.4-2 mg i.v; repeat 3 or 4
times if no response occurs
Sedative-Hypnotics

 Symptom include nystagmus, atonia,

lethargy, somnolence, respitarory depression,
and hypothermia
 Sedative-hypnotics may be associated with
symptoms ranging from respiratory
depression and coma to seizurelike activity
with aggressive behavior
 Clinical Findings
Manifestation of overdose, include:
 Nystagmus
 Ophthalmoplegia
 Ataxia
 Dysarthria
 Lethargy
 Somnolence
 Respiratory depression
 Hypotension
 hypothermia
 Treatment
 Flumazenil 0,2 mg iv repeated 5-10 minutes as
needed, up to maximum 3-5 mg
Reference

 Stone C Keith, Humphries RL: Current

Emergency Diagnosis & Treatment. New York:
McGraw-Hill, 2004
 Martin PR: Substance Related Disorder. In:
Current Diagnosis & Treatment Psychiatry.
Boston: McGraw-Hill, 2008
 Jaffe Jerome H: Substance Related Disorder.
Baltimore: Williams & Wilkins, 1994