CLASSES OF SUBSTANCES

• Alcohol • Opioid
• Amphetamine • Phencyclidine
• Caffeine • Sedative, hypnotic,
• Cannabis anxiolytics
• Cocaine • Prescribed drugs and
• Hallucinogen OTC medications
• Inhalant • Anabolic-Androgenic
steroids
• Nicotine

Kaplan and Sadock’s Pocket Handbook of Clinical Psychiatry 5th Ed

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1814
Rosen’s Emergency Medicine Concepts
and Clinical Practice 9e pg 1814
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1815
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1816
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1816
Specific antidote

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology.

11th edition. US: McGraw-Hill, 2007
Specific antidote

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology.

11th edition. US: McGraw-Hill, 2007
 OPIOIDS
• Opioids are a class of drugs
that have actions similar to
opium. Opioids act on the
brain.
• Effects:
– Drowsiness: due to
‘depressant’ effect on the brain
– Suppression of cough: due to
the effect of opioids on the
brain cough centre
– Constriction of the pupils in the
eyes
– Constipation: due to the effect
of opioids on the gut system
• Overdose occurs when a
person takes opioid drugs or
opioids in combination with
other drugs, in quantities that
the body cannot handle.
• As a result, the brain is not
able to carry out normal body
functions  The person may
pass out and stop breathing,
and in extreme cases, have
heart failure, or experience
convulsions.
• Overdose can be fatal, and is
one of the most common
causes of death among opioid
dependent users
DSM IV-TR CRITERIA FOR OPIOID
INTOXICATION

Kaplan and Sadock’s Synopsis of Psychiatry 10th Ed

 OPIOIDS
Some of the commonly used
opioids include:
• Morphine
• Codeine
• Heroin
• Buprenorphine (commonly
available as Tidigesic, Lupigesic
2)
• Pentazocine (commonly
available as Fortwin )
• Dextropropoxyphene
(commonly available as
Proxyvon, Spasmoproxyvon,
Parvon Spas )
Risks factors for Opioid Overdose
• Staying away from drugs
• Change in the purity of the
opioids
• Mixing different type of drugs
• Physical illness or recent
infections
• Mental health
• Past overdose events
• Using other drugs while on Opioid
Substitution Therapy
• Drug Interactions with
antiretroviral and other
prescription medications
 OPIOIDS
Signs & Symptoms of Opioid
Overdose Preventing Overdose
• Coma • Avoid mixing drugs, and mixing drugs with alcohol.
If you are drinking alcohol and injecting together,
• Pinpoint pupils inject first and wait for it to take effect before you
• Respiratory depression start drinking
• When your tolerance is low divide the normal dose
Warning Signs of Opioid in half, do a tester shot and allow the drugs to take
overdose effect before you try more. Try changing the route
of administration, that is, if you usually inject, try
• Can’t be woken up by noise or pain snorting
• Blue lips and fingernails due to lack • If you have a new dealer or unfamiliar supply, try a
of oxygen small amount at first to check how strong it is
• Slow breathing (less than 1 breath • Understand that medications prescribed by a doctor
may interact with street drugs and cause an
every 5 seconds) overdose
• Gasping, gurgling, or snoring • Avoid using alone; if you overdose, you need
• Choking sounds someone around to help. For example, put together
a support team of people who know that you are
• Passing out going to use drug alone and ask them to check on
• Vomiting you
• Pale face • Take care of your health. Eat well, drink plenty of
water, and sleep properly.
• Tired body
 Acetaminophen
• Acute ingestion of more than 150–200 mg/kg
(children) or 7 g total (adults)
– highly toxic metabolite is produced in the liver

• Manifestations
– Asymptomatic, mild gastrointestinal upset (nausea,
vomiting)
– elevated aminotransferase levels and
hypoprothrombinemia (24–36 hours)
– fulminant liver failure occurs hepatic
encephalopathy and death
– Renal failure may also occur
Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology.
Clinical Stage of Acute Acetaminophen
Toxicity
 Acetaminophen
• Treatment
– antidote acetylcysteine
• glutathione substitute  binding the toxic
metabolite as it is produced
• most effective when given early and should be
started within 8–10 hours if possible
– Liver transplantation for patients with
fulminant hepatic failure

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology.

 DIGOXIN
• Used therapeutically:
– To increase the force of myocardial
contraction to increase cardiac
output in patients with heart
failure
– To decrease atrioventricular (AV)
conduction to slow the ventricular
rate in atrial fibrillation.
• The basis for its first effect is
inhibition of membrane sodium-
potassium–adenosine
triphosphatase (Na+,K+-ATPase),
which increases intracellular
sodium and extracellular
potassium concentrations
• Digoxin exerts direct and indirect
effects on sinoatrial (SA) and AV
nodal fibers
• Digoxin also exerts three primary
effects on Purkinje fibers:
– Decreased resting potential,
resulting in slowed phase 0
depolarization and conduction
velocity
– Decreased action potential
duration, which increases
sensitivity of muscle fibers to
electrical stimuli
– Enhanced automaticity resulting
from increased rate of phase 4
repolarization and delayed after
depolarizations
• The volume of distribution (Vd) of
digoxin is 5 L/kg for adults but
varies from 3.5 L/kg in premature
infants to 16.3 L/kg in older
infants.
 Anticoagulants
• Warfarin & related compounds (include ingredients commercial
rodenticides: "superwarfarins” [brodifacoum, difenacoum, related
compounds]) inhibit clotting mechanism = blocking hepatic
synthesis vitamin K-dependent clotting factors.
– "superwarfarins;' inhibition synthesis persist for several weeks or months
after a single dose.
• Newer oral anticoagulants:
– direct thrombin inhibitor: dabigatran
– factor Xa inhibitors: rivaroxaban, apixiban, edoxaban.
• especially dabigatran, largely eliminated by kidney  may accumulate in patients with
renal insufficiency.
• Excessive anticoagulation may cause:
– hemoptysis, gross hematuria, bloody stools, hemorrhages into organs,
widespread bruising, and bleeding into joint spaces.

CURRENT Medical Diagnosis & Treatment 2017

 Anticoagulants
Treatment
Emergency and Supportive Measures
• Discontinue the drug at 1st sign of
gross bleeding  determine PT
(international normalized ratio,
INR).
– prothrombin time >> within 12-24
hours (peak 36-48 hours) after
overdose of warfarin or
"superwarfarins:'
• newer oral anticoagulants (dabigatran,
rivaroxaban, apixiban, and edoxaban)
(X) alter the prothrombin time; but
normal INR suggests no significant
toxicity.
• Pts ingested an acute overdose, 
(+) activated charcoal
CURRENT Medical Diagnosis & Treatment 2017
Specific Treatment
• Warfarin and "superwarfarin''
overdose  (X) treat
prophylactically with vitamin K-wait
for evidence of anticoagulation
(elevated PT).
• If the INR is elevated  (+)
phytonadione (vitamin K1)
– 10-25 mg orally & increase dose as
needed = restore PT to (N)
– 200 mg/day required after
ingestion of "superwarfarins:'
• (+) fresh-frozen plasma,
prothrombin complex concentrate,
or activated Factor VII as needed to
rapidly correct the coagulation
factor deficit if there is serious
bleeding.
 Anticoagulants
• Chronically anti-coagulated + strong medical indications for
being maintained (eg, prosthetic heart valve)  (+) much
smaller doses of vitamin K (1 mg orally) & fresh-frozen
plasma (or both) to titrate to the desired PT
• (+) ingested brodifacoum or a related superwarfarin,
prolonged observation (over weeks) & repeated
administration of large doses of vitamin K may be required.
• Specific reversal agents have been developed and are now
approved by the FDA:
– idarucizumab for dabigatran reversal and andexanet for reversal of
the factor Xa inhibitors.

CURRENT Medical Diagnosis & Treatment 2017

 Inhaled Toxin
• Inhalant drugs – volatile
substances / solvents  volatile
hydrocarbons that vaporize to
gaseous fumes @ room temp,
inhaled to enter bloodstream via
transpulmonary route
• 4 commercial classes
– Solvents for glues &
adhesives
– Propellants (aerosol paint
sprays, hair sprays, shaving
cream)
– Thinners (paint products,
correction fluids)
– Fuels (gasoline, propane)
• Ppl like to inhale these products
for their intoxicating effect
• Conduct disorder, mood disorder,
suicidalitym physical & sexual
abuse / neglect
• Inhalant = CNS depressants
– Effect appear within 5 mins
and can last for 30 min-hr,
depending on the inhalant
substance & dose
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1927
 Diagnosis
• Inhalant intoxication
– Presence of maladaptive
behavioral changes & at least 2
physical sx
– Intoxicated state: apathy,
diminished social & occupational
functioning, impaired judgment,
impulsive/aggressive behavior
– + nausea, anorexia, nystagmus,
depressed reflexes, diplopia
– High doses & long exp: stupor &
unconsciousness
– Rashes around pt’s nose &
mouth, unusual breath odors,
residue of inhalant substances
on pt’s face, hand or clothing
– Irritation of eye, throat, lungs,
nose
• Inhalant intoxication delirium
– Bc pharmacodynamic interaction
w/ other substances
– Hypoxia that may be associated
w/ inhalant or its method of
inhalation
– If delirium results in severe
behavioral disturbance  short
term tx w/ dopamine receptor
antagonist (haloperidol) might be
necessary
– Avoid benzodiazepine bc ⬆pt’s
respiratory depression
• Inhalant-induced persisting
dementia
– Bc neurotoxic effect of inhalant
– Prolonged period of hypoxia
 Inhaled Toxin
Clinical features
• Small initial dose inhalant
disinhibiting & produce feelings of
euphoria & excitement, pleasant
floating sensation
• High dose  fearfulness, sensory
illusions, auditory & visual
hallucinations, distortion of body size
– Neurological sx: slurred speech, decreased
speed of talking, ataxia
• Long term use: irritability, emotional
lability, impaired memory
• Withdrawal syndrome: sleep
disturbance, irritability, jittery, N/V,
tachycardia, (sometimes) delusion &
hallucinations
Treatment
• Resolves spontaneously
• Effect of intoxication: coma,
bronchospasm, laryngospasm,
cardiac arrhythmias, trauma, or
burns need treatment.
• Course & tx of inhalant-induced
psychotic disorder is brief
• Confusion, panic, psychosis 
mandate special attention to pt
safety
• Severe agitation haloperidol (5
mg IM per 70 kg body weight)
• Avoid sedative bc can aggravate
psychosis
 Carbon Monoxide
• CO = colorless, odorless gas (by
the combustion of carbon-
containing materials)
• Poisoning as a result of suicidal or
accidental exposure to
automobile exhaust, smoke
inhalation in a fire, or accidental
exposure to an improperly
vented gas heater, generator, or
other appliance.
• CO avidly binds to hemoglobin,
affinity 250x >> O2  reduced
oxygen-carrying capacity; altered
delivery of oxygen to cells
Clinical Findings
• Low CO levels (HbCO 10-20%)
– headache, dizziness,
– abdominal pain, and nausea.
• Higher levels:
– Confusion,
– Dyspnea,
– syncope may occur.
• Lvl > 50-60%
– Hypotension, coma, and seizures
• Survivors of acute severe poisoning
= permanent obvious or subtle
neurologic & neuropsychiatric
deficits.
• Fetus & newborn more susceptible;
high CO affinity for fetal
hemoglobin.
 Diagnosis
• Specific measurement arterial or venous HbCO saturation,
– level may have declined if high-flow oxygen therapy has already been
administered
– levels do not always correlate with clinical symptoms.
• Routine arterial blood gas testing and pulse oximetry are not
useful because they give falsely normal Pa02 and
oxyhemoglobin saturation determinations, respectively.
– (A specialized pulse oximetry device, Masimo pulse CO-oximeter, is
capable of distinguishing oxyhemoglobin from carboxyhemoglobin.)
 Treatment
Emergency and Supportive
Measures
• Maintain a patent airway
and assist ventilation, if
necessary.
• Remove from exposure.
• Treat patients with coma,
hypotension, or seizures
Spesific Treatment
• T ½ HbCO complex ~4-5 hrs(room air)  <<
dramatically in high [] of O2
• (+) 100% oxygen by tight-fitting high-flow
reservoir face mask or endotracheal tube.
• Hyperbaric oxygen (HBO) = in chamber
provide 100% oxygen under higher than
atmospheric pressures  shorten T ½ ; also
reduce incidence of subtle neuropsychiatric
sequelae.
– Commonly recommended indications
for HBO:
• history of loss of consciousness,
• HbCO >25%,
• metabolic acidosis,
• age > 50 years,
• cerebellar findings on neurologic
examination
 Cyanide
• Highly toxic chemical for research,
commercial laboratories and
industries.
• Its gaseous form (hydrogen cyanide) =
important component of smoke in
fires.
• Cyanide-generating glycosides found in
pits of apricots and other related
plants. Cyanide is also formed by
metabolism of acetonitrile, a solvent
found in some over-the-counter
fingernail glue removers.
• Cyanide is rapidly absorbed by
inhalation, skin absorption, or
ingestion.
• It disrupts cellular function by
inhibiting cytochrome oxidase and
preventing cellular oxygen utilization.
Clinical Findings
• Onset of toxicity =
– instantaneous after inhalation of
hydrogen cyanide gas
– delayed for minutes - hours after
ingestion of cyanide salts or
cyanogenic plants or chemicals.
• Effects:
– Headache, dizziness, nausea,
abdominal pain, anxiety 
confusion, syncope, shock,
seizures, coma, death.
– Odor of "bitter almonds" may be
detected on the victim's breath or
in vomitus, though this is not a
reliable finding.
– The venous oxygen saturation may
be elevated (>90%) in severe
poisonings because tissues have
failed to take up arterial oxygen .
 Treatment
Emergency and Supportive
Measures
• Remove the victim from
exposure, taking care to
avoid exposure to rescuers.
• For cyanide ingestion,
administer activated
charcoal
– Although charcoal has a
low affinity for cyanide,
doses of 60- 100 g are
adequate to bind
typically ingested lethal
doses (100-200 mg).
Specific Treatment
• Cyanide antidote regimens:
– Conventional cyanide antidote package
(Nithiodote) = sodium nitrite (induce
methemoglobinemia, binds free cyanide)
& sodium thiosulfate (promote conversion
of cyanide  less toxic thiocyanate).
• Administer 3% sodium nitrite
solution, 10 mL intravenously
followed by 25% sodium thiosulfate
solution, 50 mL intravenously ( 1 2.5
g). Caution: Nitrites may induce
hypotension and dangerous levels of
methemoglobin.
• Other approved cyanide treatment =
hydroxocobalamin (Cyanokit, EMD
Pharmaceuticals), newer; potentially safer
antidote.
– Adult dose = 5 g IV
– Children's dose = 70 mg/kg
Note: Hydroxocobalamin causes red
discoloration of skin and bodily fluids that
may last several days and can interfere with
some laboratory tests.
 Management for Hydrogen Cyanide
• The accepted goal
of therapy is to
reactivate the
cytochrome
oxidase system by
providing an
alternative
binding site for
the cyanide ion.
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1931
Pesticides: Cholinesterase Inhibitor
• Organophosphorus & carbamate
insecticides
– organophosphates: parathion,
malathion, etc;
– carbamates: carbaryl, aldicarb,
etc
widely used in commercial
agriculture & home gardening
largely replaced older,
environmentally persistent
organochlorine compounds (DDT &
chlordane)
• Organophosphates & carbamates-
also called anticholinesterases: both
inhibit enzyme acetylcholinesterase
 >> acetylcholine activity at
nicotinic & muscarinic receptors & in
CNS
• There are a variety of
chemical agents in this group,
with widely varying potencies.
• Most of them are poorly
water-soluble, are often
formulated with an aromatic
hydrocarbon solvent such as
xylene, well absorbed through
intact skin.
• Most chemical warfare "nerve
agents" (such as GA [tabun] ,
GB [sarin] , GD [soman] and
VX) are organophosphates.
 Clinical Findings
• Inhibition of cholinesterase:
– abdominal cramps, diarrhea, vomiting
– excessive salivation, sweating, lacrimation
– miosis (constricted pupils)
– Wheezing & bronchorrhea
– seizures, & skeletal muscle weakness.
• Initial tachycardia  bradycardia.
• Profound skeletal muscle weakness, aggravated excessive bronchial
secretions & wheezing  respiratory arrest & death.
• S&S of poisoning persist or recur over several days
– esp w/ highly lipid-soluble agents: fenthion or dimethoate.
• Dx should be suspected in patients w/ miosis, sweating, hyperperistalsis.
• Serum & RBC cholinesterase activity is usually depressed at least 50%
below baseline in those w/ severe intoxication.
 Treatment :
Emergency and Supportive Measures
• If the agent was recently ingested  gut decontamination by
aspiration of the liquid using a nasogastric tube followed by
administration of activated charcoal
• If the agent is on the victim's skin or hair, wash repeatedly
with soap or shampoo and water.
– Providers should take care to avoid skin exposure by wearing gloves
and waterproof aprons.
• Dilute hypochlorite solution (eg, household bleach diluted 1
:10) is reported to help breakdown organophosphate
pesticides & nerve agents on equipment or clothing.
 Specific Treatment
• Atropine reverses excessive
muscarinic stimulation &
effective for salivation, bronchial
hypersecretion, wheezing,
abdominal cramping, and
sweating.
– However, it does not interact with
nicotinic receptors at autonomic
ganglia & at NMJ & has no direct
effect on muscle weakness.
– (+) 2 mg IV  no response after 5
minutes  (+) epeated boluses in
rapidly escalating doses ( eg, 2x
dose each time) as needed to dry
bronchial secretions & decrease
wheezing; as much as several
hundred milligrams of atropine has
been given to treat severe
poisoning.
• Pralidoxime (2-PAM, Protoparn) = more
specific antidote that reverses
organophosphate binding to the
cholinesterase enzyme  effective at NMJ
as well as other nicotinic & muscarinic sites.
• Clinically effective if started very soon after
poisoning, prevent permanent binding of
the organophosphate to cholinesterase.
– (+) 1-2 g IV (loading dose)  begin
continuous infusion (200-500 mg/h, titrated
to clinical response).
• Continue to (+) pralidoxime as long as (+)
evidence of acetylcholine excess.
• Pralidoxime is of questionable benefit for
carbamate poisoning, because carbamates
have only a transitory effect on the
cholinesterase enzyme.
• Other, unproven therapies for
organophosphate poisoning: magnesium,
sodium bicarbonate, clonidine,
extracorporeal removal.
 Singkong (Cassava)
• Patofisiologi :
– Singkong mengandung
glikosida sianogenik linamarin
(C10H17O6N) lapisan luar 
glukosa,aseton dan asam
sianida (HCN)
– HCN :
sianmethemoglobin,keracunan
protoplasmik  melumpuhkan
pernafasan sel
• Uji Guinard  uji singkong
tersangka  warna asam
pikrat kuning mjd kemerahan
dalam 15mnt-3 jam
Buku Ajar Anak - IDAI
Manifestasi klinis
• Tergantung jumlah kandungan HCN
dalam singkong
• Jumlah besar : kematian dalam
waktu singkat akibat gagal nafas
• Mula-mula : panas pada
perut,mual,pusing,sesak,lemah 
nafas cepat dg inspirasi pendek &
bau bitter almond (bau nafas dan
muntahan)
• Sesak disusul pingsan,kejang 
lemas,berkeringat,mata
menonjol,pupil melebar tanpa
reaksi
• Busa pada mulut tercampur warna
darah dan warna kulit mjd merah
bata
• Tidak ada sianosis
 Tatalaksana
Awal •Eliminasi racun  muntah / bilas lambung
•Pemberian antidotum

Amil/Na Nitrit dan •Proses detoksifikasi

Na-tiosulfat •Na-Nitrit : metHb cukup banyak  mengikat NaCN
 tidak merusak enzim pernafasan dan sel
ferisitokrom oksidase
• 3 % ml iv pelan-pelan
•Na-tiosulfat : iket NaCN  terbentuk tiosianat 
keluar melalui paru,ludah,kencing
•10% iv dg dosis 0,5 ml/kgbb/kali

Resusitasi dan •Cairan IV dan Oksigenasi dengan tekanan tinggi

suportif (hiperbarik/CPAP)
Buku Ajar Anak - IDAI
 Jengkol
Patofisiologi Manifestasi Klinis
• jengkol mengandung asam • Sakit pinggang, nyeri perut,
muntah,akit waktu kencing
jengkolat (AA yang
• Air kemih keluar sedikit-sedikit
mengandung belerang)  dg butir-butir putihm urin
bertumpuknya asam berbau jengkol dg hematuria
jengkolat dalam tubulis • Oliguri – anuria
distal ginjal (kristal),ureter • Muntah
dan uretra • Pegal
• Infiltrat pada
• Pada anak keluhan mulai penis,skrotum,daerah
timbul 5-12 jam setelah suprapubik
makan • GGA

Buku Ajar Anak - IDAI

 Jengkol
Tatalaksana Pencegahan
• Eliminasi racun : muntah/bilas • masak biji jengkol dg soda/
lambung
bikarbonat lain
• Tidak ada antidotum yang
khas
• Ringan : minum banyak air
soda/Na Bikarbonat + Na
Bikarbonat 1-2 gr/hr dalam 4
dosis pH urin mjd alkalis
(±pH 8)
• Cairan IV  bila px tidak dapat
minum banyak
• GGA : dialisis

Buku Ajar Anak - IDAI

 DELIRIUM
• Delirium is an acute change in cognition that
fluctuates rapidly over time and is often
reversible
• Delirium  Altered levels of consciousness,
inattention, disorganized thinking, and altered
perception
• Types of delirium: hypoactive (most common),
hyperactive, and mixed
• RF  functional dependence, living in a nursing
home, and hearing impairment
Precipitating factors Predisposing factors
CLINICAL FEATURES
 HISTORY
• Assests Patient’s
baseline mental, level of
functioning and the
time course of changes
• Past medical history and
recent illness
• Substance abuse to
assess the likelihood of
intoxication or
withdrawal
• Past psychiatric history
 PHYSICAL EXAMS
• Vital signs + oxygen saturation and temperature
• Blood glucose level
• Blood pressures (baseline > in younger age groups)
• Tachycardia
• Fever  lower basal Temperature
• Examine entire body
– Backs and heels  decubitus ulcers
– Full neurologic exam
– Check focal findings, AbN posturing or difficulty w/ gait
coordination and vision
 LABORATORY TESTING
• Geriatric ps  associated w/ infx (urinary tracts
infx & pneumonia)
• Lab  point of care glucose as soon as arrival,
CBC, basic metabolites studies (Ca2+, fosfor,
hepatic enzymes), urinalisis, cardiac marker, AGD
(esp : chronic lung disease), (+)
meningitis/encephalitis/seizure : LP
• Imaging  ECG, chest radiography , CT (If (+)
sigsn/history of trauma, focal neurologic deficits,
impaired consiousness, unrevealing exam)
 Treatment
• Reorientation  glasses or hearing aids, access of the
bathroom
• six risk factors (cognitive impairment, sleep
deprivation, immobility, visual impairment, hearing
impairment, and dehydration)  th/ the RF
• Preventing and minimizing in the hospital (Use of
physical restraints, malnutrition, use of a bladder
catheter, > three medications)
• (+) agitation  nonpharmacological approach , avoid
benzodiazepine (ex OH intoxication) and AH drugs
• Treat insomsia and psychoses
 Mental Health disorders:
ED Evaluation & Disposition
• ED visit increases are especially notable for
older persons and those living in urban areas,
and with visits related to mood and anxiety
disorders, suicide attempts, and substance
abuse.
• ED visits in children are often related to
substance use, anxiety and attention deficit
disorders, disruptive behavior, and psychosis.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
 Safety First
• Mental health emergencies include situations in which
patients are highly distressed, suicidal, and/or homicidal.
• Patients with suicidal or homicidal ideation, suicide or
violence plans, or suicide or homicide attempts require
measures to minimize the possibility of harm to themselves
or others
• Mental health disorders coexisting with substance abuse are
also a recipe for violence.
• Violent incidents have been associated with dementia,
court-ordered admission, and mood disorder.
• Violent and aggressive behavior frequently demands
immediate chemical or physical restraint to protect the
patient, other patients, staff, and visitors

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

 • ED staff must be educated and
equipped with a range of skills to
protect themselves.
• These skills:
– enhanced awareness of risk
factors and warning signs of
violent behavior
– verbal de-escalation techniques
– Quick access to rapidly
tranquilizing or neuroleptic
medications
– Emergency strategies for getting
help quickly in explosive
circumstances.
• Approach patients with
potentially dangerous behavior
cautiously and with a
nonthreatening attitude, with
adequate security nearby.
–
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
• If necessary, isolate and restrain
threatening patients before they
are disrobed, gowned, and
searched for weapons.
• Medical and nursing staff should
stay distant from the patient;
avoid excessive eye contact;
maintain a calm, controlled
posture and tone of voice; and
stand in a location that neither
threatens the patient nor blocks
the exit of the healthcare worker
from the room.
 Examination Rooms & Seclusion
• Waiting rooms & examination rooms need to
be designed to ensure safety.
• Steps that promote safety:
– security staff, metal detectors, rooms with doors
that permit rapid and easy exit, panic buttons, and
the removal of any objects that could be used in
violent attacks or suicide attempts
• (including neckties of both staff and patient, large
earrings, patient belts or belt buckles, shoes, shoelaces,
stethoscopes, blood pressure cuffs, and cutting
instruments).

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

 • Seclusion rooms may be used to
protect patients and staff.
• Remove or carefully secure any
objects that could be used for self-
injury or against staff.
• Austere seclusion rooms may be
useful for some agitated patients
by providing relief from external
stimuli.
• Search patients before entry, and
remove potentially dangerous
objects, clothing, or weapons.
• Make sure staff are aware of the
location of exits and of panic
buttons.
• Initially, leave the door open 
remains agitated  lock the door.
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
• Keep the patient advised of each
action and the expected duration,
and explain the consequences of
violent behavior.
• Monitor the patient in a seclusion
room with a personal guard or
nurse-monitor, by closed circuit
television, or by individual checks
about every 10 minutes.
• Give the patient opportunities to
comply with staff demands for
acceptable behavior  release
from seclusion.
• If violent behavior persists,
physical restraint is justified.
• Document all steps in the use of
seclusion and medical and physical
restraints.
 Chemical
Restraints
• Tool score (SATS) = grading
behavior & assessing medication
options.
• Ketamine has been used for acute
agitation or depression,
– but concerns about hypoxia or
oversedation, & lack of large clinical
ED studies, limit its use in the ED at
the present time.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

 Physical Restraints
• In many cases, there is no substitute
for the application of physical limb
restraints.
• Restraints should be applied rapidly
and safely by individuals trained and
skilled in their use.
• A team of 5 staff members is
recommended:
– one team leader
– one person for each limb.
• The patient and any family members
present should be provided with
clear, ongoing explanations of all
procedures.
• Place the patient on a bed or
stretcher, and secure all four limbs
with leather restraints.
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
• Be careful to avoid injury.
• Elevate the patient’s head, if
possible, to minimize risk of
aspiration.
• Once the patient is restrained, offer
medications, and if refused,
administer medications involuntarily
• Once the patient is calm and
compliant, restraints can be removed
one at a time, while staff carefully
monitor the patient to ensure the
safety of all concerned.
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
 ORGANOPHOSPHATES POISONING
Pathophysiology
• Organophosphate and carbamate compounds inhibit the
enzyme cholinesterase.
• Inhibition of cholinesterase leads to acetylcholine accumulation
at nerve synapses and neuromuscular junctions, resulting in
overstimulation of acetylcholine receptors.
• Excess acetylcholine results in a cholinergic crisis that manifests
as a central and peripheral clinical toxidrome.
• Once aging occurs, the enzymatic activity of cholinesterase is
permanently destroyed
• Antidotes must be given before aging occurs to be effective.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

 Clinical Features

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

 Clinical Features
CNS symptoms of cholinergic excess include
• anxiety,
• restlessness,
• emotional lability,
• tremor,
• headache, dizziness,
• mental confusion,
• delirium,
• hallucinations, and seizures.
• Coma with depression of respiratory and circulatory
centers may result.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
 Hydrocarbon Poisoning

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

 DIAGNOSIS
• Diagnosis of hydrocarbon toxicity incorporates the
findings of the history, physical examination, bedside
cardiac and pulmonary monitoring, laboratory tests,
and chest radiography.