Pemicu 3: Muhammad Fahmi Rosyadi 405140220

Pemicu 3
Muhammad Fahmi Rosyadi

405140220
Principles of toxicity
• Most poisoned patients in ED = adults with intentional oral
drug overdoses.
• Other common clinical scenarios:
– accidental poisoning in children, which represent the majority of calls
to regional poison control centers
– Illicit drugs of abuse
– chronic poisoning from supratherapeutic pharmaceutical agents
– environmental, industrial, and agricultural chemical exposures;
envenomation
– medication interactions
• In the ED, it is important to evaluate and recognize scenarios
where there may be immediate or delayed toxicity, as well as
initiating decontamination, enhanced drug elimination, and
administering more focused antidotal strategies, when
indicated
Rosen's Emergency Medicine-Concepts and Clinical Practice
• In regards to a specific patient with a
particular ingestion, essential historical points
:
– the agent itself,
– the route of exposure,
– the amount ingested,
– possible co-ingestants,
– timing of the exposure.
• Knowing these facts can help make a
determination regarding the expected course
of care in the ED and help to mobilize
resources.

Clinical Features
• Historical information must be • A patient attempting suicide may
pulled from all available sources. intentionally mislead the ED staff, or
– A family member or friend may offer medications may have been stored in
insight into the circumstances behind mislabeled containers.
the patient’s exposure, (eg, • Other sources of potentially useful
intentional or accidental).
information: state controlled-
• medications or substances were substance registries, pharmacy
available to the patient, and the records, previous medical records.
timing of ingestion also is important.
• Accessing the patient’s text-
• Paramedics routinely will bring in all messaging history also may be
medication bottles present at the helpful, if the patient or guardian
scene—not just the patient’s consents to this.
prescribed medications or alleged
ingestion.

• For chemical exposures in either • Poisoned patients = unwilling or
the home or workplace, avoid unable to participate in an
exposure to other individuals in interactive physical examination.
the ED. – Toxicologic physical examination,
• Proper identification of the therefore, rests upon observing
substance is important to initiate factors that do not require
cooperation to elicit.
care and obtain product safety
information • Many ingestants can cause
derangement of the pulse and
• One could consider taking a
respiratory rates, as well as blood
picture of the label including any
pressure.
precise chemical numbers; if a
substance is brought to the ED, • Thus, rapid and accurate
then take appropriate steps to recording of the patient’s vital
avoid further exposure, such as signs, including a rectal core
sealing in an airtight container. temperature and pulse oximetry,
should be done and repeated at
appropriate intervals.

• Examination of the skin
and mucous membranes =
particular attention toward
discoloration and level of
moisture may suggest
poisoning by any of several
agents
• it may also reveal evidence
of injection drug abuse,
such as “track marks” or
ulcerations from “skin
popping.”

• A careful neurologic
examination focusing on
the level of muscle tone,
clonus, or hyperreflexia
can assist in the
diagnosis of serotonin
syndrome or neuroleptic
malignant syndrome
(NMS).
• Finally, certain
intoxicants may have
particular odors
associated with them;
the presence of such an
odor ought alert the
clinician to the
possibility of poisoning
by one of these agents
However, the absence of a characteristic smell is not accurate in excluding poisoning

Toxidromes
• Toxidromes = constellations of signs & symptoms based on
autonomic and neurochemical processes that can suggest a
particular class of exposure and direct management and
therapy.
• The 5 traditionally described entities:
– sympathomimetic
– anticholinergic
– cholinergic,
– sedative/hypnotic,
– opioid toxidromes.
• In addition, serotonin syndrome and NMS have been well
described

Sympathomimetics
• Toxidrome = state of sympathomimetic excess  typically causing
those effects expected from the “fight or flight” reaction.
• Patients are often altered & may be delusional
– Esp ingestion of substituted amphetamines: N-methyl-3,4-
methylenedioxyamphetamine (MDMA)
• Vital signs are typically elevated, (+) hypertension, tachycardia &
tachypnea.
• May also be hyperthermic
– consequence of an increased metabolic rate
• Mydriasis & diaphoresis
• In severe overdoses:
– derangement of cardiac output can occur—decreased diastolic
filling time coupled with arrhythmogenesis—resulting in
circulatory collapse and shock, which may be refractory to fluid
resuscitation and pressor agents.
Anticholinergic
• Toxidrome: antimuscarinic properties
• Alteration in (N) homeostatic balance
between the sympathetic & parasympathetic
arms of the autonomic nervous system
occurs.
• This allows the sympathetic side to function
unopposed  generates a state of relative
sympathomimesis.

• Toxidrome: symptoms attributable to the
anticholinergic:
– delirium,
– hyperthermia,
– mydriasis,
– cutaneous flushing
– In contrast, as the secretory glands of the skin and
mucous membranes are cholinergically innervated,
these systems are typically dry (not diaphoretic as
found in the sympathomimetic toxidrome)
• The typical signs and symptoms can be recalled
by the mnemonic “mad as a hatter, hot as a hare,
blind as a bat, red as a beet, and dry as a bone.

Cholinergic
• The cholinergic toxidrome results from overstimulation of the
parasympathetic portion of the autonomic nervous system,
which maintains the “rest and digest” functions.
• These patients typically have:
– “fluids coming from every orifice” as a consequence of increased
glandular secretion
– diaphoresis, urination
– miosis,
– bronchorrhea,
– emesis,
– lacrimation, lethargy
– Salivation

• Agents of concern are primarily anticholinesterase
agents:
– organophosphates and carbamate insecticides
(pesticides; but they have also been engineered as
weapons of mass destruction, typically referred to as
nerve gases)
• Important to rapidly recognize this toxidrome:
patients frequently die from excessive
bronchorrhea, effectively drowning in their own
secretions
– unless timely antidotal therapy and cholinesterase
regenerators can be given.

• Nicotine poisoning from tobacco can occur in
children who ingest detritus
– cigarettes or chewing tobacco,
– liquids from electronic cigarettes
• Role of nicotine: both the central & peripheral
autonomic nervous systems
– Clinical picture in these poisonings resemble both
sympathomimetic & cholinergic toxidromes

Sedative/Hypnotics
• Hallmark of this toxidrome = sedation.
– Typically occurs on a spectrum depending on the particular
ingestant, route, and potency.
• Severe ingestions = state of general anesthesia (loss of tone and
airway protective reflexes)
• May cause hypothermia through suppression of muscle metabolism.
• It is well known in the ED, because ethanol intoxication is frequently
seen.
• Other agents: barbiturates & benzodiazepines cause a similar picture,
as will illicit substances such as gamma-hydroxybutyrate (GHB).
• The coincidence of traumatic injuries may be high, and one should
have a low threshold for evaluating to exclude their presence.

Opioid
• Similar to sedative/hypnotics, toxidrome also involves
sedation & diminished respiratory drive.
– Exception of pentazocine & propoxyphene, this toxidrome causes
pupillary miosis.
• Dx is confirmed by noting a response to naloxone, a direct
opioid receptor antagonist.
– However, because certain opioids have higher potencies, a lack of
response does not exclude opioid intoxication.
• Furthermore, this is a clinical diagnosis because not all opioids
will be detectable by the standard drug screen

Serotonin syndrome
• Toxidrome = state of serotonergic excess
• Often precipitated by the addition of a new serotonergic agent or a
substance that interferes with the metabolism of a previously tolerated
agent.
• Typically described with selective serotonin reuptake inhibitors (SSRIs)
and monoamine oxidase inhibitors (MAOIs), it has been reported with
cyclic antidepressants and atypical antipsychotics.
• Consequently, serotonin syndrome typically occurs within hours to days
of introduction to a new medication; although it has been described in a
delayed fashion due to the prolonged half-lives of some antidepressants.
• The manifestations of serotonin syndrome:
– altered mental status,
– hyperthermia,
– agitation;
– hyperreflexia, clonus, & diaphoresis.

Neuroleptic Malignant Syndrome
• Similar to serotonin syndrome, NMS also presents
with altered mental status, hyperthermia, and
agitation;
– however, unlike serotonin syndrome, peripheral muscular
effects tend toward rigidity and decreased reflexes rather
than clonus and hyperreflexia.
• It is due to dopaminergic depletion due use of dopamine
antagonists, such as antipsychotics.

• Frequently, poisoned patients
have some level of delirium as
part of their presentation.
• As such, excluding other causes
of altered mental status while
initiating appropriate toxicologic
therapy should be considered
• Any “intoxicated” patient
presenting to the ED should have
the reversible causes of altered
mental status excluded:
hypoglycemia & nutritional
deficiencies.
• Trauma is frequently coincident
with intoxication, so a careful
unclothed examination looking
for evidence of traumatic injury Rosen's Emergency Medicine-Concepts and Clinical Practice
should be investigated as well.
• The thorough physical examination may also reveal
findings that could suggest specific intoxicants,
• The most important diagnostic approach =
maintaining a broad differential diagnosis of both
toxicologic & non-toxicologic causes for the patient’s
presentation, & avoid premature conclusion.
• The differential diagnosis may be extremely broad,
particularly when ingestion of a toxin is not known,
or felt unlikely, or much more specific, when a
certain agent, or class of agent is known to be
involved

Diagnostic testing
• When a patient presents with altered mental status
& hyperthermia, testing may focus on
differentiating a toxic cause from thyrotoxicosis or
acute infectious disease.
• Patients with intoxication & evidence of trauma may
require evaluation for head trauma as a cause of
their altered mental status.
• In most instances, however, it is known that the
patient has a potentially toxic exposure and some or
all of the involved toxins have been implicated or
identified.
• Unknown overdose or exposure 
broad array of laboratory testing
used to screen for abnormalities &
potentially elucidate clinical
picture.
• diagnostic studies routinely
checked are:
– CBC
– serum chemistry with renal
function
– liver function tests
– urinalysis (with a pregnancy test if
appropriate)
– urine toxicology screen
– serum alcohol concentration,
– serum lactate
– bedside glucose.
• Based on these results, or when the
ingestion is known, other tests such
as specific serum concentrations
may be obtained
• When assays for a particular agent are not
available, or are not performed on site,
empirical treatment generally begins before
these results are available.
• If the blood gas shows (+) metabolic acidosis,
calculating the anion gap  further refine
possible etiologies.
• [Na] − ([HCO3] + [Cl])
– (N) range = 8 to 12 mEq/L.

• Metabolic acidosis w/
(x) anion gap :
– << bicarbonate
(diarrhea, renal tubular
acidosis) or
– >> chloride-containing
compounds (ammonia,
calcium chloride).
• Metabolic acidosis (+)
anion gap =
– >> in unmeasured
serum anions 
suggests several specific
toxins and disease states

• When ingestion of a toxic • Toxicology “screens” = helpful in
alcohol (methanol, ethylene diagnosing an unknown ingestion
glycol, or isopropanol) is – Blood toxicology screens can be
suspected, calculating the falsely negative if the ingested drug
osmole gap may be helpful; has a short half-life and the sample
because early in the poisoning is not drawn soon enough after
course the patient may be exposure.
minimally or non-acidemic. – Urine toxicology screens are more
• Urine fluorescence is not reliable, because they typically
sufficiently sensitive to be have a longer time period for
reliable and its absence positive detection (24 - 72 hours)
cannot be used to “rule out” – Urine toxicology screens include:
said ingestion.
• phencyclidine (PCP),
• cocaine,
• opioids,
• amphetamines,
• cannabinoids;

• Urine screen = qualitative,
• positive result does not necessarily imply acute toxicity.
• A urine toxicology screen can be falsely positive due to cross-
reactivity between agents (e.g: “positive” PCP screen +
dextromethorphan ingestion).
• Alternatively, urine screens can be falsely negative if the
substance ingested does not cross-react with the tested
analyte: case w/ methadone, which will not cross react with
the opioid component of the urine toxicology screen
• Ultimately, the diagnosis of intoxication is clinical;
– urine drug screening may be confirmatory but should not
supplant clinical evaluation and judgment.

• In addition to the blood work, should obtain
electrocardiogram (ECG) if the patient is tachycardic
or bradycardic, or may have ingested a cardiotoxic
agent that can prolong the QRS or QT intervals

Management
• General management of a poisoned patient:
– Providing appropriate supportive care
– Undertaking decontamination or enhancing
elimination if indicated
– Providing specific antidotal therapy where an
antidote exists and is indicated.

• Antidotes do not exist for every potential poisoning,
and thus supportive care is the cornerstone of
managing the poisoned patient.
• Basic “ABCs” of resuscitation
– ensuring airway protection and adequacy of ventilation
while maintaining the circulatory status of the patient
with fluid resuscitation and vasopressor support = prime
focus.
– If the airway is compromised or in danger of becoming so,
or if the respiratory effort is insufficient to maintain
appropriate ventilation, intubation is usually the preferred
course

• Vascular access  obtain!
– peripheral & central venous catheters
• Intraosseous lines are also viable access
points from the toxicologic perspective,
because there are no known
contraindications to antidotal therapy
through this route.
• Supportive care (+); immediate threat to the ABCs
(+), one should then progress  systematic
assessment of decontamination strategies,
enhanced elimination, focused therapy (antidotes),
and getting help (consultation).

Decontamination
• The process of preventing systemic absorption
into the body.
• Ocular or dermal exposure = copious irrigation
with water, after removal of contaminated
clothing to expose the area.
– Water irrigation is not used for metallic potassium,
magnesium, or sodium (such as, found in “tracer”
ammunition)  ignite on contact with water.
• Instead, in these very rare exposures, the area should be
covered with petroleum jelly or mineral oil.

Syrup of Ipecac Gastric Lavage
• Emesis with syrup of ipecac • Process of directly removing an ingested
is not indicated in the care substance from the stomach
of any poisoned patient in – using a 30 Fr or larger orogastric tube
the ED. – little data or evidence showing its
• significant side effects (eg, efficacy and should not be performed
dehydration due to routinely for the treatment of
intractable vomiting) & poisoned patients.
complications (eg, • Given the risks of aspiration and
aspiration pneumonitis, esophageal trauma,
Mallory-Weiss tears, and – American Association of Poison Centers
gastric rupture). suggests = only (+) “within an hour of
• Insufficient data and ingestion of a potentially life-
evidence showing threatening poison which does not
improvement in clinical adsorb to activated charcoal or for
outcomes which no antidote exists” and, even
then, in a center with “sufficient
expertise” to perform the procedure
safely
Single-dose activated charcoal
• Historically, SDAC = mainstay of gastric decontamination in medical
toxicology.
• Benefits: decreasing primary absorption, or binding during enterohepatic
recirculation of a potentially toxic xenobiotic.
• These benefits are more likely to occur if:
– Activated charcoal (+) within 1 hour post ingestion
– Patient is alert, able, willing to cooperate with administration,
anticipated to remain alert & protective of airway reflexes
– Either substance ingested has high toxicity (eg, verapamil, colchicine),
or is a toxic, sustained–release agent (eg, bupropion SR),
– Evidence of a massive ingestion of a toxic agent (eg, salicylates)
• sedated, unprotected airway, unwilling to drink charcoal suspension =
contraindicated.
– This may be particularly true for young children with limited ability to drink the slurry.
• should not place NGT solely to administer activated charcoal  risk of
aspiration or direct instillation of activated charcoal into lungs rises

• Considering all of this information, how does one decide
whether activated charcoal is indicated in a specific overdose?
• First, the ingested drug must have a high potential for toxicity
and lethality.

Whole Bowel Irrigation
• Certain ingestions:
– extended-release preparations,
– illicit drug packets, or metals (eg, iron & lead),
continuous whole bowel irrigation may be indicated.
• WBI is performed with a balanced polyethylene glycol
solution that does not participate in fluid exchange nor
become absorbed into the body.
• To be effective, requires a rate of 2 L/ hr in adult;
consequently, require NGT
• However, if a patient is critically ill, (+) hypoperfusion of the
gut, or has obstruction of the bowel = WBI is contraindicated
– reports of worsened morbidity and mortality in these clinical settings.

Enhanced Elimination
• Once a toxin has been absorbed into the
body, it undergoes metabolism and
elimination; typically via hepatic & renal
pathways.
• Certain substances are amenable to
enhancing these elimination pathways
– ex vivo: hemodialysis
• best suited to remove poisons of
low molecular weight, low
protein binding, and high water
solubility; (toxic alcohols, lithium,
salicylates)
– in vivo: multipledose activated
charcoal (MDAC) & urinary
alkalinization.
• All forms of extracorporeal removal have
been studied and found to be efficacious
Multiple-dose activated charcoal
• MDAC is intended to facilitate removal of a toxin that has
already been absorbed.
• MDAC decreases xenobiotic absorption & elimination half-
life when large amounts of the toxin are ingested and
dissolution is delayed (eg: concretions, bezoars (solid mass of
indigestible material accumulates digestive tract), or
extended release formulations).
• It also is believed to create a hemoperfusion substrate for the
gut wall microcirculation  permit “gastrointestinal
dialysis,” which generates a concentration gradient into the
stool or certain poisons, which are then be eliminated by
defecation

• Certain drugs excreted in the bile, then reabsorbed by the gut,
only to be re-excreted in the bile (enterohepatic circulation)
– MDAC also interfere with reabsorption of these drugs by binding
them during their transit of the GIT
• Drugs with significant enterohepatic circulation

• MDAC administration  pulmo aspiration  best avoided by
applying same conditions for SDAC:
– patient awake, alert, and cooperating and is anticipated to remain
awake and alert.
• Obstruction  avoidance in situations w/ delayed gut motility
(eg, critical illness, opioid or anticholinergic effects) is
recommended to reduce this risk.
• When MDAC is indicated, initial loading dose of an activated
charcoal–to-xenobiotic ratio of 10 :1  subsequent doses of
50% of the initial dose @4 - 6 hours up to 24 hours.
• Discontinued when the patient’s measureable serum levels
are no longer considered in the toxic range.

Serum Alkalinization
• Certain water-soluble ingestants: salicylates, methotrexate,
phenobarbital will undergo ion-trapping & enhanced urinary
elimination if serum is sufficiently alkalinized.
• Especially important w/ salicylate poisonings  alkalinization not
only promotes elimination but also prevents salicylate crossing
BBB to CNS
• Monitor the serum pH & bicarbonate level, + urinary pH = goal
serum pH ~7.5 & a urinary pH ~ 8.0.
• Also ensure that the serum K+ lvl is (N), because alkalinization will
cause an intracellular shift of potassium  >> urine reabsorption
of potassium by excreting hydrogen ions into the urine (eliminate
the pH gradient and dissipate the benefits of this process)
• To accomplish this, combine 150 mEq (3 amps) of 8.4% sodium
bicarbonate into a liter of dextrose 5% in water (D5W) + potassium
(20 to 40 mEq total) to IV fluid; rate (x) >> 250 cc/hour.
Intravenous Fat Emulsion (Intralipid)
• Intravenous fat emulsion (IFE) is a newly
introduced therapy for poison-induced
cardiogenic shock.
• This therapy was first described for treatment of
toxicity from local anesthetics, such as
bupivacaine.
• IFE is proposed to work primarily by two
separate mechanisms:
– (1) the lipid sink
– (2) enhanced cardiac metabolism.

• The lipid sink theory posits that fat-soluble drugs are soaked
up and removed from the site of toxicity, effectively
increasing the volume of distribution for a fat-soluble drug.
– This is the predominant theory behind the use of IFE.
• A second theory involves optimization of cardiac metabolism.
• The heart under physiologic circumstances prefers free fatty
acids; in times of stress, it switches to glucose metabolism for
energy.
– A dose of IFE theoretically provides a large supply of free fatty acids
to optimize energy use in the heart.
– IFE may also enhance activation of cardiac calcium channels

• Indications for IFE are not universally agreed upon.
– only in consultation with a medical toxicologist or poison center.
• In addition to anesthetic agents, successful resuscitations have
been described with refractory B-blocker overdose, calcium
channel blockers, cyclic antidepressants, and bupropion and
cocaine toxicity.
• Dosing for IFE also varies in the literature.
– If indicated = initial bolus of 1.5 mL/kg of 20% lipid solution
given over 2 - 3 minutes is most commonly recommended,
followed by an infusion of 0.25 mL/kg/min.
• Despite recent enthusiasm for IFE, its use has associated
complications:
– extreme lipemia resulting in lab interference with blood tests
(complete blood counts, chemistries, and coagulations studies),
as well as acute pancreatitis, and acute respiratory distress
syndrome

Focused Therapy
• Although the majority of

poisonings require
supportive care alone, in
selected ingestions
specific antidotal therapy
may be available.
• Antidotes, which should
be available either
immediately (eg, stocked)
or in a rapid fashion (eg,
transported within a few
hours).

Disposition
• Patients with severe toxicity (such as, seizures, persistent
cardiovascular instability, airway compromise, or significant
metabolic derangements) should be admitted to an intensive
care setting.
• Patients who are asymptomatic on arrival but have ingested a
potentially dangerous substance or an extended-release
preparation that could cause significant deterioration in their
clinical status, are admitted to either an inpatient setting or a
observation unit for 24 hours, or until peak toxicity has
obviously passed and the patient is physiologically normal or
near normal.
• For patients who are asymptomatic after an ingestion of a
minimally toxic substance and for whom other ingestions and
psychiatric issues have been addressed, discharge after the ED
visit, which typically takes at least 4 to 6 hours, is appropriate.
Narcotics & Other substance
abuse
LI 1
“Dependency" = severe form of substance abuse and drug
addiction characterized by the triad of:
1. a psychological dependence or craving and the behavior
involved in procurement of the drug;
2. physiologic dependence, with withdrawal symptoms on
discontinuance of the drug;
3. tolerance, ie, the need to increase the dose to obtain the
desired effects.
• Terms "dependency" and "abuse" were dropped in DSM-5 in
favor of the single term "substance use disorder;’ ranging
from mild to severe.
• Many patients could have a severe and life-threatening abuse
problem without ever being dependent on a drug.
Stimulants
• User has improved sense of Excessive use:
alertness – Irritability
• Enhanced energy – Mood swings
• Excitability – Hallucinations
• Euphoria/improved sense of – Heart palpitations
well-being/mood elevation – Dizziness
• Physiological responses: – Headache
– Increased heart rate – Chest pain
– Increased blood pressure – Death
– Flushed skin Example: Cocaine
– Perspiration
Depressants
• Used to induce sleep or • Excessive use:
relaxation • – Slow, shallow
• Physiological responses: breathing
• – Reduction of tension • – Clammy skin
• – Anxiety relief • – Weak, rapid pulse
• – Speech slurring • – Coma
• – Staggered gait • – Death
• – Relaxed muscles • Example: Alcohol
Narcotics (Opiates)
• Generally used to reduce Excessive Use:
pain, dull senses, induce • – Increased risk for STD’s
sleep with needle use
• Narcotics are generally a • – Nausea/vomiting
derivative of opium • – Convulsions
Physiological Responses: • – Respiratory arrest
• – Pain relief • – Coma, death
• – Euphoria Example: Heroin
• – Confusion
• – Drowsiness
• – Respiratory depression
Hallucinogens
• Used to change perceptions Excessive Use:
• Used to change mood • – Memory loss
• – Difficulties with speech,
Physiological Responses: thinking
• – Hallucinations • – Depression
• – Erratic behavior • – Weight loss
• – Paranoia • – Medical emergencies are
• – Depersonalization (“I am not rare
real”)
• – Impaired social/occupational
functioning
• – Elevations in heart rate,
blood pressure
Cannabis
• Cannabis sativa is a plant (a hemp Excessive Use (may be
plant) growing in more temperate
regions of the world. controversial):
• The plant contains chemicals-- • – Respiratory irritation
"cannabinoids"--which are
responsible for its characteristic • – Fluctuating emotions
psychoactive effects.
• – Impaired memory
Physiological Responses:
• – Euphoria • – Psychosis
• – Relaxation (schizophrenia link)
• – Impaired memory,
concentration
• – Loss of coordination Example:Marijuana
• – Enhancement of senses
• – Appetite changes
• – Lowered blood pressure
https://facweb.northseattle.edu/troot/HEA150/week8/hea150_wk8_drug_classifications.pdf
Ethanol, Benzodiazepines, other
Sedative-Hypnotic Agents
• Sedative-hypnotic drugs includes a variety of products used
for the treatment of anxiety, depression, insomnia, and
epilepsy.
– common benzodiazepines: lorazepam, alprazolam, clonazepam,
diazepam, oxazepam, chlordiazepoxide, and triazolam,
– newer benzodiazepine like hypnotics zolpidem and zaleplon,
– the muscle relaxant carisoprodol.
• Ethanol & other selected agents are also popular recreational
drugs.
• All of these drugs depress CNS
– Reticular activating system, cerebral cortex, cerebellum.
Clinical Findings
• Mild intoxication:
– euphoria, slurred speech, ataxia.
• Ethanol intoxication:
– hypoglycemia
even at relatively low concentrations, in children and in fasting adults.
• More severe intoxication:
– stupor, coma, respiratory arrest
• Carisoprodol (Soma)  muscle jerking or myoclonus.
• Death or serious morbidity  result of pulmonary aspiration of gastric contents.
• Bradycardia, hypotension, hypothermia are common.
• Massive intox  appear to be dead: (x) reflex responses & absent
electroencephalographic activity.
• Dx & assessment of severity of intoxication are usually based on clinical findings
– Ethanol serum levels > 300 mg/dL (0.3 g/dL; 65 mmol/L)
• coma in persons who are not chronically abusing the drug
• Regular users may remain awake at much higher levels.
Treatment
Emergency and Supportive Measures
• Activated charcoal if the patient has ingested a massive dose and the airway is
protected
– Repeat-dose charcoal may enhance elimination of phenobarbital, but it has not
been proved to improve clinical outcome.
• Hemodialysis = patients with severe phenobarbital intoxication.
Specific Treatment
• Flumazenil = benzodiazepine receptor-specific antagonist;
– No effect on ethanol, barbiturates, or other sedative-hypnotic agents.
– given slowly IV, 0.2 mg over 30-60 seconds, repeated in 0.2-0.5 mg addition as
needed up to a total dose of 3-5 mg.
Caution: Flumazenil should rarely be used because it may induce seizures in
patients with preexisting seizure disorder, benzodiazepine addiction, or
concomitant tricyclic antidepressant or other convulsant overdose.
• If seizures occur, diazepam and other benzodiazepine anticonvulsants will not be
effective.
• As with naloxone, the duration of action of flumazenil is short (2-3 hours) and
resedation may occur, requiring repeated doses
Alcoholism
• Alcohol use disorder is a syndrome consisting of 2
phases:
– at-risk drinking
• Repetitive use of alcohol, often to alleviate anxiety or solve other
emotional problems.
– moderate to severe alcohol misuse.
• repeated use of other sedative-hypnotics and is characterized by
recurrent use of alcohol despite disruption in social roles (family
and work), alcohol-related legal problems, and taking safety risks
by oneself and with others.
The National Institute on Alcohol Abuse and Alcoholism formally
defines at-risk drinking as
• >4 drinks/day or 14 drinks/week for men
• >3 drinks/day or 7 drinks/week for women
• Depression is often present and should be evaluated carefully.

• The majority of suicides and intrafamily homicides involve
alcohol.
• Alcohol is a major factor in rapes and other assaults.
• There are several screening instruments that may help
identify an alcohol use disorder.
– One of the most useful is the Alcohol Use Disorder Identification Test
(AUDIT)
ACUTE INTOXICATION
• Signs of alcoholic intoxication = overdosage of CNS depressant:
– drowsiness, errors of commission, psychomotor dysfunction, disinhibition,
dysarthria, ataxia, nystagmus.
70-kg person, an ounce of whiskey, a 4- to 6-oz glass of wine, or a 12-oz bottle of beer (roughly 15, 1 1,
and 13 grams of alcohol, respectively) may raise the level of alcohol in the blood by 25 mg/ dL. For a 50-
kg person, the blood alcohol level would rise even higher (35 mg/dL) with the same consumption.
Blood alcohol levels:
Blood level (mg/dL)

<50 rarely cause significant motor dysfunction (legal limit for driving under the influence is
commonly 80 mg/dL)
>150 Intoxication as manifested by ataxia, dysarthria, and nausea and vomiting
350 - 900 lethal blood levels
• In severe cases, overdosage is marked by respiratory depression, stupor,

seizures, shock syndrome, coma, and death.
• Serious overdoses are frequently due to a combination of alcohol with other
sedatives.
Opiates & Opioids
• Prescription & illicit opiates & opioids (morphine, heroin,
codeine, oxycodone, fentanyl, hydromorphone, etc) are
popular drugs of misuse & abuse; cause of frequent
hospitalizations for overdose.
• Widely varying potencies & durations of action;
– Some of the illicit fentanyl derivatives are up to 2000 x >> potent than
morphine.
• All of these agents << CNS activity & sympathetic outflow by
acting on opiate receptors in the brain.
• Tramadol = analgesic; unrelated chemically to the opioids but
acts on opioid receptors.
• Buprenorphine is a partial agonist-antagonist opioid =
outpatient treatment of opioid addiction.
Clinical Findings • Methadone is associated with QT
• Mild intoxication: interval prolongation & torsades
– euphoria, de pointes.
– drowsiness, • While the duration of effect for
heroin is usually 3-5 hours,
– constricted pupils. methadone intoxication may last
• More severe intoxication: for 48-72 hours or longer.
– hypotension, • Tramadol, dextromethorphan, &
– bradycardia, meperidine also occasionally
– hypothermia, cause seizures.
– coma, • Meperidine, the metabolite
– Respiratory arrest. normeperidine is probably the
cause of seizures & is most likely
– Pulmonary edema may occur. to accumulate with repeated
– Death is usually due to apnea dosing in patients w/ CKD
or pulmonary aspiration of
gastric contents.
• Propoxyphene prolongs QRS interval & may cause
seizures;
• Wound botulism has been associated with skin-
popping, especially involving "black tar" heroin.
• Buprenorphine added to an opioid regimen may
produce acute narcotic withdrawal symptoms.
• Many opioids: fentanyl, tramadol, oxycodone,
methadone, are not detected on routine urine
toxicology "opiate" screening.
Treatment
• Protect the airway and assist ventilation. Administer activated
charcoal for recent large ingestions.
Specific Treatment
• Naloxone is a specific opioid antagonist that can rapidly reverse
signs of narcotic intoxication.
– Structurally related to the opioids, it has no agonist effects of its own.
– (+) 0.2-2 mg IV, repeat as needed to awaken the patient & maintain airway
protective reflexes & spontaneous breathing.
– Very large doses (10-20 mg) for patients intoxicated by some opioids (eg,
codeine, fentanyl derivatives).
• Caution: The duration of effect of naloxone is only about 2-3
hours; repeated doses may be necessary for patients
intoxicated by long-acting drugs, e.g: methadone.
• Continuous observation for at least 3 hours after the last
naloxone dose is mandatory.
Amphetamines & cocaine
• Both widely abused for their • Amphetamine derivatives & related drugs:
euphorigenic & stimulant – methamphetamine ("crystal meth;’ "crank"),
properties. • Methcathinone derivatives & related
• Smoked, snorted, ingested, synthetic chemicals:
or injected. methylenedioxypyrovalerone (MDPV)
• Both produce CNS have become popular drugs of abuse
stimulation & generalized and are often sold as purported "bath
salts:’
increase in central &
peripheral sympathetic – MDMA ("Ecstasy"),
activity. – ephedrine ("herbal ecstasy"),
• Toxic dose of each drug is – methcathinone ("cat" or "khat").
highly variable & depends on • Amphetamine-like reactions = synthetic
the route of administration & cannabinoids (eg, "Spice” & "K2").
individual tolerance. • Nonprescription medications & nutritional
• Onset of effects is most rapid supplements contain stimulant or
after IV injection or smoking. sympathomimetic drugs: ephedrine, yohimbine,
or caffeine
Clinical findings:
• Anxiety, tremulousness, tachycardia, hypertension, diaphoresis, dilated
pupils, agitation, muscular hyperactivity, psychosis.
– Muscle hyperactivity  metabolic acidosis & rhabdomyolysis.
• Severe intoxication = seizures & hyperthermia may occur.
• Sustained or severe hypertension  intracranial hemorrhage, aortic
dissection, or myocardial infarction.
• Ischemic colitis has been reported.
• Hyponatremia after MDMA use;
– Mech not known; may involve >> water intake, syndrome of
inappropriate antidiuretic hormone (SIADH), or both.
• Supporting dx = (+) amphetamines or cocaine metabolite
benzoylecgonine in urine.
• Note that many drugs can give a false-positive result on the immunoassay
for amphetamines.
Specific Treatment
Treatment
• Treat agitation, psychosis, or seizures =
Emergency and Supportive Measures benzodiazepine (diazepam, 5-10 mg,
• Maintain a patent airway and assist lorazepam, 2-3 mg IV)
ventilation, if necessary. • + phenobarbital 15 mg/kg IV for
• Treat seizures persistent seizures.
• Rapidly lower the body • Hypertension
temperature in patients who are – vasodilator (phentolamine (1-5 mg
intravenously))
hyperthermic (>39-40°C).
– Nitroprusside
• Give IV fluids: prevent – combined alpha- and beta-adrenergic
myoglobinuric kidney injury in (+) blocker labetalol (l0-20 mg IV).
rhabdomyolysis. • (X) administer pure beta-blocker:
propranolol alone,  paradoxic
worsening of hypertension (unopposed
alpha-adrenergic effect)
• Tachycardia or tachyarrhythmias 
Short-acting B-blocker: esmolol (25-100
meg/kg/min by IV infusion).
• Treat hyperthermia. Treat hyponatremia
LSD & Hallucinogens
• A variety of substances-ranging from naturally occurring plants &
mushrooms to synthetic substances: phencyclidine (PCP), toluene and
other solvents, dextromethorphan, and lysergic acid diethylamide (LSD)-
are abused for their hallucinogenic properties.
• Mechanism of toxicity & the clinical effects vary for each substance.
• >> hallucinogenic plants & mushrooms  anticholinergic delirium,char:
– flushed skin,
– dry mucous membranes,
– dilated pupils,
– tachycardia,
– urinary retention.
• Plants & mushrooms contain hallucinogenic indoles: mescaline & LSD,
typically cause:
– marked visual hallucinations and perceptual distortion,
– widely dilated pupils,
– mild tachycardia.
• PCP = anesthetic agent similar to ketamine, can
produce fluctuating delirium & coma, often
associated with vertical & horizontal nystagmus.
• Toluene & other hydrocarbon solvents (butane,
trichloroethylene, "chemo;' etc) cause euphoria and
delirium and may sensitize the myocardium to the
effects of catecholamines  fatal dysrhythmias.
• Newer drugs used for their psychostimulant effects:
synthetic cannabinoid receptor agonists (street
names include "spice" and "K2"), Salvia divinorum,
and mephedrone and related cathinone derivatives.
Treatment
• Monitor patients who
have sniffed solvents for
• Maintain a patent airway and assist respirations if cardiac dysrhythmias
necessary. (most commonly
• Treat coma, hyperthermia, hypertension, and seizures premature ventricular
• For recent large ingestions, consider giving activated contractions, ventricular
charcoal orally or by gastric tube tachycardia, ventricular
fibrillation);
Specific Treatment – (+) th beta-blockers:
propranolol (1-5 mg
• (+) anticholinergic delirium  physostigmine, 0.5- 1 intravenously) or
mg IV, (X) >1 mg/min. esmolol (250-500 meg/
• Dysphoria, agitation, psychosis associated with LSD kg intravenously, then 50
or mescaline intoxication may respond to: mcg/kg/min by infusion)
may be more effective
– benzodiazepines (eg, lorazepam, 1-2 mg orally or
than lidocaine or
intravenously) or
amiodarone.
– haloperidol (2-5 mg intramuscularly or intravenously)
or
– another antipsychotic drug (eg, olanzapine or
ziprasidone).
Theophylline & Caffeine
• Theophylline may cause intoxication after:
– an acute single overdose,
– chronic accidental repeated overmedication
– reduced elimination  result from hepatic dysfunction or
interacting drug (eg, cimetidine, erythromycin).
• The usual serum T ½ theophylline = 4-6 hours,
– increase to >20 hours after overdose.
• Caffeine in energy drinks, herbal or dietary
supplement products can produce similar toxicity.
Clinical Findings
• Mild intoxication  nausea, vomiting, tachycardia,
tremulousness.
• Severe intoxication is characterized by ventricular and
supraventricular tachyarrhythmias, hypotension, and
seizures.
• Status epilepticus is common and often intractable to the
usual anticonvulsants.
• After acute overdose (but not chronic intoxication),
hypokalemia, hyperglycemia, metabolic acidosis are common.
• Seizures & manifestations of toxicity may be delayed for
several hours after acute ingestion, especially if a sustained-
release preparation such as Theo-Dur was taken
• Tea, cocoa, & cola drinks also contribute to an intake of caffeine that is
often astoundingly high in a large number of people.
• Low to moderate doses (30-200 mg/day) tend to improve some aspects
of performance (eg, vigilance).
• Caffeine-containing analgesics usually contain ~30 mg per unit.
• Symptoms of caffeinism (usually ingestion >500 mg/day):
– anxiety, agitation, restlessness, insomnia, a feeling of being "wired;’ & somatic
symptoms referable to the heart & GIT
• Common for a case of caffeinism to present as an anxiety disorder.
• It is stimulants to precipitate severe symptoms in compensated
schizophrenic & manic-depressive patients.
• Chronically depressed patients often use caffeine drinks as self-
medication.
– This diagnostic clue may help distinguish some major affective disorders.
Treatment
Specific Treatment
• Seizures  benzodiazepines
• Acute ingestion  (+) activated
charcoal
(lorazepam, 2-3 mg IV, or
diazepam, 5-10 mg IV) or
• Repeated doses of activated charcoal
 enhance theophylline elimination
phenobarbital (10-15 mg/kg
by "gut dialysis:' IV).
• (+) of whole bowel irrigation = for large • Phenytoin is not effective.
ingestion; sustained-release • Hypotension & tachycardia:
preparations mediated through excessive
• Hemodialysis = removing theophylline; B-adrenergic stimulation 
indicated for patients with status
respond to beta-blocker
epilepticus or markedly elevated serum
therapy even in low doses.
theophylline levels
– + esmolol, 25-50 meg/kg/min
– (eg, >100 mg/L [555 mcmol/L] after
acute overdose or >60 mg/L [333
by IV infusion, or propranolol,
mcmol/L] w/ chronic intoxication).
0.5- 1 mg IV
Tricyclic & Anti-depressants
• Tricyclic & related cyclic antidepressants = among most
dangerous drugs involved in suicidal overdose.
• (+) anticholinergic & cardiac depressant properties
("quinidine-like" sodium channel blockade).
• Tricyclic antidepressants produce >> marked membrane-
depressant cardiotoxic effects than phenothiazines.
• Newer generation antidepressants:
– trazodone, fluoxetine, citalopram, paroxetine, sertraline, bupropion,
venlafaxine, and fluvoxamine  not chemically related to the tricyclic
& do not generally produce quinidine-like cardiotoxic effects.
– However, they may cause seizures in overdoses and they
may cause serotonin syndrome
Clinical Findings • Quinidine-like cardiotoxic
• Signs of severe intoxication effects:
may occur abruptly & without – QRS interval widening (>0.12
warning w/in 30-60 minutes s),
after acute tricyclic overdose. – ventricular arrhythmias, AV
• Anticholinergic effects: block, Rightward axis
– Dilated pupils, tachycardia, deviation
dry mouth, flushed skin, – hypotension
muscle twitching, << – Prolongation QT interval &
peristalsis. tosades de pointes = several
of the newer
antidepressants.
• Seizures & coma are common
with severe intoxication.
• Life-threatening hyperthermia
 status epilepticus &
anticholinergic induced
impairment of sweating
• Among newer agents, bupropion and venlafaxine have been
associated with a greater risk of seizures.
• The diagnosis should be suspected in any overdose patient
with anticholinergic side effects, esp (+) widening of the QRS
interval or seizures.
• For intoxication by most tricyclic antidepressants, the QRS
interval correlates with the severity of intoxication more
reliably than the serum drug level.
• Serotonin syndrome should be suspected if:
– agitation, delirium, diaphoresis, tremor, hyper reflexia, clonus
(spontaneous, inducible, or ocular), fever develop in a patient taking
serotonin reuptake inhibitors.
Treatment
Emergency & Supportive Measures
• Observe patients for at least 6 hours
• Admit all patients with evidence of anticholinergic
effects (eg, delirium, dilated pupils, tachycardia) or
signs of cardiotoxicity.
• (+) activated charcoal and consider gastric lavage 
recent large ingestions.
• All of these drugs are highly tissue-bound & are not
effectively removed by hemodialysis procedures.
Specific Treatment
• Cardiotoxic Na+ channel-depressant effects of tricyclic antidepressants =
respond to boluses of NaHCO3(50- 100 mEq IV).
– NaHCO3 provides large Na load  << depression of Na-dependent
channel.
• Reversal of acidosis may also have beneficial effects at this site.
– Maintain the pH between 7.45 and 7.50.
• Prolongation of the QT interval or torsades de pointes  intravenous
magnesium or overdrive pacing.
• Severe cardiotoxicity in patients with overdoses of lipid-soluble drugs (eg,
amitriptyline, bupropion) has responded to intravenous lipid emulsion
(Intralipid),1.5 mL!kg repeated one or two times if needed.
• Plasma exchange using albumin has been reported successful in a few
cases.
• Mild serotonin syndrome th/ w/
benzodiazepines & withdrawal of
antidepressant.
• Moderate cases may respond to
cyproheptadine (4 mg oral or via gastric tube
hourly for 3-4 doses) or chlorpromazine (25
mg IV).
• Severe hyperthermia should be treated with
neuromuscular paralysis and endotracheal
intubation in addition to external cooling
measures.
Antipsychotic drugs
• Promethazine, prochlorperazine,
chlorpromazine, haloperidol, droperidol,
risperidone, olanzapine, ziprasidone,
quetiapine, and aripiprazole are used as
antipsychotic agents, and sometimes as
antiemetics and potentiators of analgesic and
hypnotic drugs.
• Therapeutic doses phenothiazines • Therapeutic or toxic doses  acute
(esp chlorpromazine)  drowsiness extrapyramidal dystonic rxn may
& mild orthostatic hypotension (50% develop in some patients:
pts) – spasmodic contractions of face &
– Larger doses  obtundation, miosis, neck muscles,
severe hypotension, tachycardia, – extensor rigidity of the back
convulsions, coma. muscles,
– Abnormal cardiac conduction may – carpopedal spasm,
occur  prolongation QRS or QT – motor restlessness.
intervals (or both) & ventricular
>>common with haloperidol & other
arrhythmias.
butyrophenones
• Among the newer agents, quetiapine << common with newer atypical
is more likely to cause coma and antipsychotics: ziprasidone, lurasidone,
hypotension. olanzapine, aripiprazole, and
quetiapine.
• Severe rigidity + hyperthermia +
metabolic acidosis ("neuroleptic
malignant syndrome”) occasionally
occur ; life-threatening
Specific Treatment
Treatment
• Prolongation QT interval & torsades
Emergency and de pointes  IV magnesium or
overdrive pacing.
Supportive Measures • Extrapyramidal signs 
• Administer activated diphenhydramine, 0.5- 1 mg/kg
intravenously, or benztropine
charcoal for large or mesylate, 0.01-0.02 mg/kg IM
recent ingestions. – Treatment with oral doses of these
agents should be continued for 24-48
• Severe hypotension = hours.
• Bromocriptine (2.5-7.5 mg orally
IV fluids & vasopressor daily) may be effective for mild or
agents moderate neuroleptic malignant
syndrome.
• Treat hyperthermia • Dantrolene (2-5 mg/kg intravenously)
has also been used for muscle
• Cardiac monitoring. rigidity but is not a true antidote.
• For severe hyperthermia, rapid
neuromuscular paralysis is preferred.
Marijuana
• Cannabis sativa, a hemp plant, is • High doses  transient psychotomimetic
effects.
the source of marijuana.
• Marijuana frequently aggravates existing
• Mercury may be a contaminant in mental illness and adversely affects
marijuana grown in volcanic soil. motor performance.
• The drug is usually inhaled by • Long-term usage:
smoking. – depression of plasma testosterone
levels and reduced sperm counts
• Effects occur in 10-20 minutes – Abnormal menstruation and failure
and last 2-3 hours. to ovulate have occurred in some
• Moderate dosage: marijuana women
– abnormalities in the pulmonary tree.
produces 2 phases:
• Laryngitis and rhinitis are related
– mild euphoria  sleepiness to prolonged use, along with
– Acute state: altered time chronic obstructive pulmonary
disease.
perception, less inhibited
– Cognitive impairments are common.
emotions, psychomotor
• Detection periods span 4-6 days in short
problems, impaired term users and 20-50 days in long-term
immediate memory, & users.
conjunctival injection.
Non-psychoactive drug abuse
LI 2
Selected Posioning
1. Acetaminophen
• Acetaminophen • Acute acetaminophen overdose (>150-200
(paracetamol) = common mg/kg, or 8-10 g average adult) 
analgesic (nonprescription hepatocellular glutathione <<  reactive
& prescription) intermediate attacks other cell proteins 
• Absorption  metabolized necrosis.
by glucuronidation & • Patients (+) enhanced P450 2E1 activity:
sulfation + small fraction chronically abuse alcohol & taking INH = >> risk
met via P450 mixed- hepatotoxicity.
function oxidase system – Hepatic toxicity may also occur after overuse of
(2E1)  highly toxic acetaminophen
reactive intermediate  • Eg: taking 2 or 3 acetaminophen-containing
normally detoxified by products concurrently or >> recommended max
dose 4 g/day for several days.
cellular glutathione.
• # of acetaminophen oral prescription
combination products
(hydrocodone/acetaminophen) is limited by the
CURRENT Medical Diagnosis & Treatment 2017
FDA to (X) > 325 mg/tablet.
Clinical Findings
• Shortly after ingestion  nausea or vomiting, but
(no other signs of toxicity)  24-48 hrs after
ingestion, hepatic aminotransferase levels begin to
increase.
• Severe poisoning  fulminant hepatic necrosis may
occur  jaundice, hepatic encephalopathy, acute
kidney injury, death.
• Rarely, massive ingestion (serum levels >500-1000
mg/L)  early onset of acute coma, seizures,
hypotension, metabolic acidosis unrelated to
hepatic injury.

• Dx after acute overdose = based on measurement of serum acetaminophen level.
• Plot serum level vs time since ingestion (acetaminophen nomogram)
• Ingestion of sustained release products or co ingestion of an anticholinergic agent,
salicylate, or opioid drug  delayed elevation of serum levels  difficult to interpret
nomogram.
• Nomogram (x) useful after repeated overdose.

Treatment: • Oral treatment:
Emergency and Supportive – loading dose of N-
Measures acetylcysteine, 140 mg/kg  70
mg/kg @ 4 hours.
• (+) activated charcoal if it can
Dilute the solution to about 5%
be given within 1 -2 hours of with water, juice, or soda.
the ingestion. • vomiting interferes with oral N-
– Charcoal may interfere with acetylcysteine administration  IV
absorption of the oral antidote
acetylcysteine  not considered
Conventional oral N-acetylcysteine US
clinically significant.
= 72 hours of treatment. Other
Specific Treatment regimens have equivalent success w/
• If the serum or plasma 20-48 hours of treatment.
acetaminophen level falls • N-acetylcysteine most effective
started w/in 8-10 hrs after
above the line on the ingestion.
nomogram; treatment N-
acetylcysteine is indicated;
PO/IV
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.
Treatment Specific Treatment
Emergency and Supportive • Warfarin and "superwarfarin''
Measures overdose  (X) treat
• Discontinue the drug at 1st sign prophylactically with vitamin K-
of gross bleeding  determine wait for evidence of
PT (international normalized anticoagulation (elevated PT).
ratio, INR). • If the INR is elevated  (+)
– prothrombin time >> within 12- phytonadione (vitamin K1)
24 hours (peak 36-48 hours) – 10-25 mg orally & increase dose
after overdose of warfarin or as needed = restore PT to (N)
"superwarfarins:' – 200 mg/day required after
• newer oral anticoagulants
ingestion of "superwarfarins:'
(dabigatran, rivaroxaban, apixiban,
and edoxaban) (X) alter the • (+) fresh-frozen plasma,
prothrombin time; but normal INR
suggests no significant toxicity.
prothrombin complex
concentrate, or activated Factor
• Pts ingested an acute overdose,
VII as needed to rapidly correct
 (+) activated charcoal
the coagulation factor deficit if
there is serious bleeding.

• 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.

Anticonvulsants
• Anticonvulsants (carbamazepine, phenytoin,
valproic acid, and many newer agents) = as
management of seizure disorders & some are
treatment of mood disorders or pain.

Phenytoin (oral/IV) Carbamazepine intoxication
• Rapid IV injection phenytoin  acute • drowsiness, stupor,
myocardial depression & cardiac arrest. • high levels = atrioventricular block,coma,
• Phenytoin intoxication can also occur following seizures.
acute intentional or accidental overdose. • Dilated pupils and tachycardia are common.
• Overdose syndrome is usually mild even with • Toxicity seen in serum levels >20 mg/L (85
high serum levels. mcmol/L)
• most common manifestations: ataxia, • severe poisoning [] >30-40 mg/L (127- 1 69
nystagmus, drowsiness. Choreoathetoid mcmol/L).
movements have been described. • Erratic slow absorption, intoxication progress
over several hours - days.
Valproic acid intoxication  unique Newer anticonvulsants: gabapentin,

syndrome: levetiracetam, vigabatrin, and
• hypernatremia (from the sodium component of the zonisamide
salt),
• metabolic acidosis, • somnolence,
• hypocalcemia, • confusion and dizziness;
• elevated serum ammonia, • Felbamate  overdose: crystalluria & kidney
• mild liver aminotransferase elevation. injury; th/ use: idiosyncratic aplastic anemia
• Hypoglycemia may occur as a result of hepatic • lamotrigine, topiramate, tiagabine overdose 
metabolic dysfunction. seizures
• Coma with small pupils  mimic opioid poisoning.
• Encephalopathy and cerebral edema can occur.
Emergency and Supportive Measures • No specific antidotes.
• Recent ingestions= (+) charcoal • Naloxone was reported to have
orally or by gastric tube reversed valproic acid overdose in
• Large ingestions of carbamazepine one anecdotal case.
or valproic acid-especially of • Carnitine may be useful in
sustained release formulation = patients with valproic acid
whole bowel irrigation induced hyperammonemia.
• Combined multiple-dose activated • Consider hemodialysis for
charcoal + whole-bowel irrigation massive intoxication with
may be beneficial in ensuring gut valproic acid or carbamazepine
decontamination for selected (eg, carbamazepine > 60 mg/L
large ingestions. [254 Mcmol/L] or valproic acid >
800 mg/L [5544 mcmol/L] ).

Atropine & Anticholinergics
• Atropine, scopolamine, • Physical signs:
– dilated pupils,
belladonna, diphenoxylate
– flushed skin,
with atropine, Datura – tachycardia,
stramonium, Hyoscyamus – fever,
niger, some mushrooms, – delirium,
– myoclonus,
tricyclic antidepressants,
– ileus
antihistamines = – May induce convulsions.
antimuscarinic agents + • Antihistamines are commonly
CNS effects available with or without
• Symptoms of toxicity: prescription  Diphenhydramine
commonly causes delirium,
– dryness of the mouth,
tachycardia, and seizures.
– thirst,
– Massive diphenhydramine overdose
– difficulty in swallowing, may mimic tricyclic antidepressant
– blurring of vision. cardiotoxic poisoning

Treatment
• (+) activated charcoal
• External cooling & sedation, or neuromuscular paralysis
(rare) to control high temperatures
Specific Treatment
• Severe anticholinergic syndrome (eg, agitated delirium) = (+)
physostigmine salicylate, 0.5-1 mg slowly IV over 5 minutes +
ECG monitoring; repeat as needed to a total dose <2 mg.
• Caution:
– Bradyarrhythmias & convulsions are a hazard with physostigmine
administration, the drug should be avoided in patients with
cardiotoxic effects from tricyclic antidepressants or other sodium
channel blockers.

B-adrenergic blockers
• The most toxic beta-blocker = propranolol
– (blocks beta -1, beta-2 adrenoceptors; (+) direct membrane-depressant & CNS effects)
Clinical Findings
• Most common findings mild - moderate intoxication = hypotension &
bradycardia.
• Cardiac depression = severe poisoning is often unresponsive to
conventional therapy with beta-adrenergic stimulants: dopamine, NE
• Propranolol & other lipid-soluble drugs: seizures & coma may occur.
• Propranolol, oxprenolol, acebutolol, alprenolol also have membrane-
depressant effects and can cause conduction disturbance
– (wide QRS interval) similar to tricyclic antidepressant overdose.
• The diagnosis is based on typical clinical findings.
Routine toxicology screening does not usually include beta-blockers.

Emergency and Supportive Measures • Persistent bradycardia &
hypotension = (+) glucagon
• Attempts to treat bradycardia or – 5-10 mg intravenously  infusion of 1-5
heart block: mg/h.
– Atropine (0.5-2 mg IV), – Glucagon = inotropic agent acts at
different receptor site; therefore not
– isoproterenol (2-20 meg/min IV affected by beta-blockade.
infusion, titrated to the desired • High-dose insulin (0.5- 1 units/kg/h
heart rate) intravenously) + glucose
• Ingested within 1 hour of supplementation = reverse severe
presentation (or longer after cardiotoxicity.
ingestion extended-release • Membrane-depressant effects (wide
formulation) = (+) activated QRS interval) = (+) boluses of
charcoal NaHCO3 (50- 100 mEq IV) as for
tricyclic antidepressant poisoning.
• Intravenous lipid emulsion (Intralipid
20%, 1.5 mL/kg) = successfully in
severe propranolol overdose.

CCB
• In therapeutic doses
– nifedipine, nicardipine, amlodipine, felodipine, isradipine, nisoldipine,
and nimodipine act mainly on blood vessels
– Verapamil & diltiazem act mainly on cardiac contractility and
conduction.
However, selective effects lost after acute overdose.
• Patients may present with:
– bradycardia,
– atrioventricular (AV) nodal block,
– Hypotension,
combination of these effects.
• Hyperglycemia is common due to blockade of insulin
release. With severe poisoning, cardiac arrest may occur.

Treatment
• administer activated charcoal
• (+) whole bowel irrigation should be initiated as soon as possible if the patient has ingested
a sustained-release product.
Specific Treatment
• Bradycardia = atropine (0.5-2 mg intravenously), isoproterenol (2-20 meg/min by
intravenous infusion), or a transcutaneous cardiac pacemaker.
• Hypotension = (+) CaCl 10%, 10 mL, or calcium gluconate 10%, 20 mL. Repeat @3-5 min
Optimum (or maximum) dose has not been established, but many toxicologists recommend
raising the ionized serum calcium level to as much as twice the normal level.
• Calcium = most useful in reversing negative inotropic effects
• High doses Insulin ( 0.5-1 units/kg IV bolus  0.5- 1 units/kg/h infusion) + Dextrose to
maintain euglycemia = beneficial (no controlled studies)
• Infusion of Intralipid 20% lipid emulsion improve hemodynamics in animal models and case
reports of calcium channel blocker poisoning.
• Methylene blue ( 1 -2 mg/kg) was reported to reverse refractory shock due to profound
vasodilation in a patient with amlodipine poisoning.

Clonidine & Other sympatholytics
Antihypertensives
• Overdosage of these agents ( donidine, guanabenz, guanfacine,
methyldopa):
– bradycardia, hypotension, miosis, respiratory depression, and
coma.
Usually resolved in < 24 hours, deaths are rare.
• Similar symptoms (+) after ingestion of topical nasal decongestants
chemically similar to donidine (oxymetazoline, tetrahydrozoline,
naphazoline).
• Brimonidine & apraclonidine = ophthalmic preparations for glaucoma.
• Tizanidine = centrally acting muscle relaxant structurally related to
clonidine; it produces similar toxicity in overdose.

Treatment
• Activated charcoal
• Maintain the airway & support respiration if necessary.
• Symptomatic treatment sufficient even in massive
overdose.
– Maintain blood pressure = IV fluids & dopamine
– Atropine for bradycardia.
Specific Treatment
• no specific antidote.
• Tolazoline recommended for clonidine overdose, but
effects are unpredictable and it should not be used.
• Naloxone has been reported to be successful in a few
anecdotal and poorly substantiated cases.

Salicylates
• Salicylates (aspirin, methyl salicylate, bismuth subsalicylate,
etc) = OTC & prescription medications.
• Salicylates uncouple cellular oxidative phosphorylation 
anaerobic metabolism & >> prod of lactic acid &heat;
interfere with several Krebs cycle enzymes.
• Single ingestion >200 mg/kg  acute intoxication.
• Poisoning may also occur as a result of chronic excessive
dosing over several days.
• T ½ of salicylate is 2-3 hours after small doses
– increase to >> 20 hours in patients with intoxication.

Clinical Findings
• Acute ingestion  nausea & vomiting, (+/-) • Dx of salicylate poisoning =
gastritis. suspect in metabolic acidosis 
• Moderate intoxication: confirm = measure serum
– hyperpnea (deep and rapid breathing), salicylate level.
– tachycardia,
– >100 mg/dL (1000 mg/L or 7.2
– tinnitus,
mcmol/L) after an acute
– elevated anion gap metabolic acidosis.
overdose  likely severe
• Serious intoxication:
poisoning.
– agitation, confusion, coma,
– Subacute or chronic intoxication
– seizures,
may suffer severe symptoms
– cardiovascular collapse,
with levels of only 60-70 mg/dL (
– pulmonary edema,
4.3-5 mcmol/L).
– Hyperthermia,
– death. • ABG typically reveals a
• PT often elevated  salicylate induced respiratory alkalosis + underlying
hypoprothrombinemia. metabolic acidosis.
• CNS intracellular glucose depletion can
occur despite normal measured serum
glucose levels
Treatment
• (+) activated charcoal oral
• Gastric lavage  (+) extra doses activated charcoal in
patients who ingest >10 g aspirin
• The desired ratio of charcoal to aspirin ~10:1 by weight;
– cannot always be given as a single dose, administered over 1st 24
hours divided doses @2-4 hours + whole bowel irrigation
• (+) glucose-containing fluids to << risk of cerebral
hypoglycemia.
• Th/ metabolic acidosis  IV sodium bicarbonate.
– CRITICAL! because acidosis (especially acidemia, pH < 7.40) >> entry of
salicylate into cells, worsening toxicity.
Warning: Sudden & severe deterioration can occur after rapid sequence
intubation and controlled ventilation if the pH is allowed to fall during
the apneic period.

Specific Treatment
• Alkalinization of the urine enhances renal salicylate
excretion by trapping the salicylate anion in the urine.
– + 100 mEq (2 ampules) of NaHCO3 to 1 L of 5% dextrose in 0.2% saline
 infuse IV w/ rate ~150-200 mL/h.
– + 20-30 mEq of KCl to each liter of IV fluid; Unless the patient is
oliguric or hyperkalemic
• Patients who are volume-depleted often fail to produce an
alkaline urine (paradoxical aciduria) unless K+ given.
• Hemodialysis = lifesaving; is indicated for:
– patients with severe metabolic acidosis,
– markedly altered mental status,
– significantly elevated salicylate levels
• (eg, greater than 100- 120 mg/dL [1000- 1200 mg/L or 7.2-8.6 mcmol/L] after acute
overdose or >60-70 mg/ dL [600-700 mg/L or 4.3-5 mcmol/L] + subacute or chronic
intoxication).

Isoniazid
• Antibacterial drug; treatment & prevention of tuberculosis.
• Cause hepatitis with long-term use,
– especially in alcoholic patients and elderly persons.
• It produces acute toxic effects by competing w/ pyridoxal 5-
phosphate  lowered brain gammaaminobutyric acid (GABA)
levels.
• Acute ingestion of as little as 1.5-2 g of INH cause toxicity
• Severe poisoning is likely to occur after ingestion > 80- 100
mg/kg.

Clinical Findings
• Confusion, slurred speech, seizures occur abruptly after
acute overdose.
• Severe lactic acidosis out of proportion to the severity of
seizures-is probably due to inhibited metabolism of lactate.
• Peripheral neuropathy and acute hepatitis may occur with
long-term use.
• Diagnosis is based on a history of ingestion and the presence
of severe acidosis associated with seizures.
INH is not usually included in routine toxicologic screening, and

serum levels are not readily available.

Emergency and Supportive Measures • Pyridoxine (vitamin B6) is a
specific antagonist of the acute
• Seizures may require higher than toxic effects of INH, usually
usual doses of benzodiazepines successful in controlling
(eg, lorazepam, 3-5 mg convulsions that do not respond
intravenously) or administration to benzodiazepines.
of pyridoxine as an antidote . – 5 g IV over 1-2 minutes
• # ingested is known, give a
• Administer activated charcoal gram-for-gram equivalent
after large recent ingestion, but amount of pyridoxine.
with caution because of the risk – Patients taking INH are

usually given 25-50 mg of
of abrupt onset of seizures.
pyridoxine orally daily to
help prevent neuropathy.

Heavy metals & Inhaled toxins
LI 3
Acid, Corrosive
• Strong mineral acids  primarily • Hydrofluoric acid  highly toxic
local corrosive effect on skin & fluoride ion  penetration 
mucous membranes. Severe deep destructive tissue
• Symptoms: damage
– Severe pain in throat & upper • Systemic hypoCa2+ & hyperK+
GIT; after fluoride absorption, even
• bloody vomitus; difficulty in following skin exposure.
swallowing, breathing, speaking;
• Inhalation of volatile acids,
discoloration and destruction of
skin and mucous membranes in fumes, or gases (chlorine,
and around the mouth; and fluorine, bromine, or iodine) 
shock. severe irritation of throat &
– Severe systemic metabolic larynx  upper airway
acidosis due to: obstruction & non cardiogenic
• result of cellular injury
pulmonary edema.
• systemic absorption of the acid.

Ingestion Eye Contact
• Dilute = (+) glass (4-8 oz) of water to drink. • Anesthetize the conjunctiva and corneal
• (x) + bicarbonate or neutralizing agents, (x) induce surfaces topical local anesthetic drops (eg,
vomiting. proparacaine).
• Some suggest: Immediate (+) small flexible gastric • Flood with water 15 minutes, holding
tube & removal of stomach contents  lavage, esp eyelids open.
corrosive liquid or (+) important systemic toxicity. • Check pH  6.0-8.0 test paper  repeat
• In symptomatic patients  flexible endoscopic irrigation 0.9% saline, until pH is near 7.0.
esophagoscopy: determine presence & extent injury. • Check corneal damage = fluorescein and
• CT scan or plain radiographs of the chest and slit-lamp exam; consult an
abdomen  reveal the extent of injury: Perforation, ophthalmologist about further treatment.
peritonitis, major bleeding = indications for surgery.
Skin Contact
• Flood with water (15 minutes)
Treatment • Use no chemical antidotes; heat reaction  additional injury.
• Hydrofluoric acid burns = soak affected area in benzalkonium chloride
solution or apply 2.5% calcium gluconate gel
• 3.5 g calcium gluconate + 5 oz of water-soluble surgical lubricant, eg, K-Y
Inhalation Jelly)  arrange immediate consultation with a plastic surgeon or other
• Remove from further specialist.
exposure to fumes or gas. • Inject 0.5 mL of 5% calcium gluconate/cm2 under burned area  Binding
of fluoride ion (Caution: (X) use calcium chloride.)
• Check skin and clothing. • intra-arterial infusion of calcium = for extensive burns or involving nail
• Treat pulmonary edema. bed; consult with a hand surgeon or poison control center
Alkalies
• Strong alkalies = common ingredients in household cleaning compounds;
suspected by their "soapy" texture.
• Alkalinity > pH 12.0 = corrosive.
• Disk (or "button") batteries are also a source.
• Alkalies  liquefactive necrosis, which is deeply penetrating.
• Symptoms:
– burning pain in Upper GIT, nausea, vomiting, difficulty in swallowing &
breathing.
• Examination: destruction & edema of the affected skin and mucous
membranes and bloody vomitus and stools.
• Radiographs may reveal evidence of perforation or the presence of
radiopaque disk batteries in the esophagus or lower gastrointestinal
tract.
Ingestion
Treatment
Skin Contact
• Dilute immediately + glass of water; (x) induce emesis!
• Immediate cautious small flexible gastric tube & removal
of stomach contents  gastric lavage (remove residual
material) • Wash with running water
• Prompt endoscopy in symptomatic patients  evaluate
extent of damage;
until the skin no longer feels
• CT scanning & Radiography may also aid in assessment. soapy.
• (+) location of ingested disk batteries in the esophagus,
immediate endoscopic removal is mandatory. • Relieve pain and treat shock.
• Corticosteroid to prevent stricture = no proved benefit;
contraindicated in esophageal perforation.
Eye Contact
• Anesthetize conjunctival & corneal surfaces  topical
anesthetic (eg, proparacaine).
• Irrigate with water or saline continuously 20-30 minutes,
holding lids open.
• Amphoteric solutions effective >> water or saline
• available in Europe (Diphoterine, Prevor).
• Check pH w/ test paper  repeat irrigation +30-minute 
until pH ~7.0.
• Check corneal damage w/ fluorescein & slit-lamp
examination; consult an ophthalmologist for further
treatment.
Carbon Monoxide
• CO = colorless, odorless gas Clinical Findings
(by the combustion of carbon- • Low CO levels (HbCO 10-20%)
containing materials) – headache, dizziness,
• Poisoning as a result of – abdominal pain, and nausea.
suicidal or accidental • Higher levels:
exposure to automobile – Confusion,
exhaust, smoke inhalation in a – Dyspnea,
fire, or accidental exposure to – syncope may occur.
an improperly vented gas • Lvl > 50-60%
heater, generator, or other – Hypotension, coma, and seizures
appliance. • Survivors of acute severe
poisoning = permanent obvious
• CO avidly binds to
or subtle neurologic &
hemoglobin, affinity 250x >>
neuropsychiatric deficits.
O2  reduced oxygen-
• Fetus & newborn more
carrying capacity; altered
susceptible; high CO affinity for
delivery of oxygen to cells fetal hemoglobin.
• CO poisoning should be suspected in any person with severe
headache or acutely altered mental status, esp in cold
weather  improperly vented heating systems
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
• Maintain a patent airway and assist ventilation, if necessary.
• Remove from exposure.
• Treat patients with coma, hypotension, or seizures
Specific 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
• 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.
Petroleum Distillates & Solvents
• Petroleum distillate toxicity occur from inhalation of vapor or as
result of pulmonary aspiration of liquid during or after ingestion.
• Acute manifestations of aspiration pneumonitis:
– vomiting, coughing, bronchopneumonia.
• Hydrocarbons (those w/ aromatic or halogenated subunits) can
also cause severe systemic poisoning after oral ingestion.
• Hydrocarbons can also cause systemic intoxication by inhalation.
• Vertigo, muscular incoordination, irregular pulse, myoclonus,
seizures occur with serious poisoning  may be due to hypoxemia
or the systemic effects of the agents.
• Chlorinated & fluorinated hydrocarbons (trichloroethylene, Freons,
etc) and many other hydrocarbons can cause ventricular
arrhythmias due to increased sensitivity of the myocardium to the
effects of endogenous catecholamines.
Treatment
• Remove patient to fresh air.
• For simple aliphatic hydrocarbon ingestion, gastric emptying &
activated charcoal not recommended  but these procedures
indicated if preparation contains toxic solutes (eg, insecticide) or
aromatic or halogenated product.
• Observe victim 6-8 hours for signs of aspiration pneumonitis
(cough, localized crackles or rhonchi, tachypnea, infiltrates on CXR)
• Corticosteroids are not recommended.
• Fever occurs, (+) specific AB only after identification of bacterial
pathogens by laboratory studies.
• Risk of arrhythmias  use bronchodilators w/ caution in patients
with chlorinated or fluorinated solvent intoxication.
• Tachyarrhythmias occur, use esmolol IV 25- 100 mcg/kg/min.
Lead
• Lead is used in industrial & commercial products:
storage batteries, solders, paints, pottery, plumbing,
and gasoline & is found in some traditional Hispanic
and Ayurvedic ethnic medicines.
• Lead toxicity = chronic repeated exposure; rare after
a single ingestion.
• Adverse effects on cellular function & primarily
affects nervous system, GIT, and hematopoietic
system.
Clinical Findings
• Lead poisoning often goes undiagnosed initially because presenting symptoms
and signs are nonspecific and exposure is not suspected.
• Common symptoms: colicky abdominal pain, constipation, headache, and
irritability.
• Severe poisoning  coma and convulsions.
• Chronic intoxication  learning disorders (in children) and motor neuropathy
(eg, wrist drop).
• Lead containing bullet fragments in or near joint spaces  chronic lead toxicity.
• Diagnosis = measurement of the blood lead level.
• Whole blood lead levels < 10 mcg/dL considered nontoxic, 5 mcg/dL in children.
– 10 - 25 mcg/dL  impaired neurobehavioral development in children.
– 25-50 mcg/dL  headache, irritability, &subclinical neuropathy.
– 50-70 mcg/dL  moderate toxicity,
– >70- 100 mcg/dL  severe poisoning.
• Other laboratory findings of lead poisoning: microcytic anemia with basophilic
stippling and elevated free erythrocyte protoporphyrin.
Treatment
• Pts (+) encephalopathy = maintain a patent airway and treat
coma and convulsions
• Recent acute ingestion: large lead-containing object (eg,
fishing weight) is still visible in the stomach on abdominal
radiograph, whole bowel irrigation, endoscopy, or even
surgical removal may be necessary to prevent subacute lead
poisoning.
– (The acidic gastric contents may corrode the metal surface, enhancing lead
absorption. Once the object passes into the small intestine, the risk of
toxicity declines.)
• Conduct an investigation into the source of the lead exposure.
• Workers with a single lead level >60 mcg/dL (or 3 successive
monthly levels >50 mcg/dL) or construction workers with any
single blood lead level >50 mcg/dL  removed from the site
of exposure.
Specific Treatment
• Indications for chelation depend on the blood lead level and the patient's
clinical state.
– It is impermissible under the law to treat asymptomatic workers with elevated blood lead
levels in order to keep their levels <50 mcg/dL rather than remove them from the exposure.
1. Severe toxicity-severe intoxication (encephalopathy or levels >70- 100
mcg/dL):
– edetate calcium disodium (ethylenediaminetetraacetic acid, EDTA), 1500
mg/m2 /kg/day (approximately 50 mg/kg/day) in 4-6 divided doses or as
a cont IV infusion.
– Most clinicians also (+) dimercaprol (BAL), 4-5 mg/kg IM @4 hours for 5
days, for patients with encephalopathy.
2. Less severe toxicity-less severe symptoms & asymptomatic w/ blood lead
levels b/w 55 - 69 mcg/dL may be treated with edetate calcium disodium
alone in dosages as above.
• An oral chelator, succimer (DMSA), is available for use in patients with mild
to moderate intoxication
– 10 mg/kg orally every 8 hours for 5 days,
– then every 12 hours for 2 weeks.
Iron
• Widely used therapeutically = treatment of anemia and daily
supplement in multiple vitamin preparations.
• Most children's preparations ~12-15 mg of iron (sulfate,
gluconate, or fumarate salt)/dose
• 60-90 mg in most adult-strength preparations.
• Iron is corrosive to GIT  once absorbed (+) depressant
effects on the myocardium and on peripheral vascular
resistance.
• Intracellular toxic effects = disruption of Krebs cycle
enzymes.
• Carbonyl iron is a powdered form of elemental iron. It is not
as irritating to the gastrointestinal tract as the iron salts and
appears safer
Clinical Findings
• Ingestion <30 mg/kg of iron usually  mild GI upset.
• Ingestion >40-60 mg/kg  vomiting (sometimes with
hematemesis), diarrhea, hypotension, and acidosis.
• Death = result of profound hypotension due to massive fluid
losses & bleeding, metabolic acidosis, peritonitis from
intestinal perforation, or sepsis.
• Fulminant hepatic failure may occur.
• Survivors of the acute ingestion  permanent GI scarring.
• Serum iron levels > 350-500 mcg/dL = potentially toxic,
• Levels >1000 mcg/ dL  associated w/ severe poisoning.
• A plain abdominal radiograph may reveal radiopaque tablets.
Emergency & Supportive • Deferoxamine = selective iron chelator.
Measures – It is not useful as an oral binding agent.
• Hypotension  IV – pts w/ established manifestations of toxicity-
& those with markedly elevated serum iron
crystalloid (0.9% saline or
levels (eg, >800-1000 mcg/dL) (+) 10-15
lactated Ringer solution). mg/kg/h by constant IV infusion
– Fluid losses may be – higher doses (up to 40-50 mg/kg/h) have
massive owing to been used in massive poisonings.
vomiting and diarrhea • Hypotension may occur.
as well as third-spacing • Deferoxamine is safe for use in pregnant
into injured intestine. women with acute iron overdose.
• Whole bowel irrigation  • Caution: Prolonged infusion of deferoxamine
remove unabsorbed pills (>36-48 hours) has been associated with
from the intestinal tract development of acute respiratory distress
syndrome (ARDS)-the mechanism is not
known.
Lithium
• Treatment of bipolar depression and other
psychiatric disorders.
• The only normal route of lithium elimination =
kidney,
– chronic kidney disease >> risk for accumulation of lithium
 gradual onset (chronic) toxicity.
• Intoxication resulting from chronic accidental
overmedication or renal impairment is more
common and usually more severe than that seen
after acute oral overdose.
Clinical Findings
• Mild - moderate toxicity = lethargy, confusion, tremor, ataxia,
and slurred speech  progress to myoclonic jerking,
delirium, coma, and convulsions.
• Recovery may be slow & incomplete in severe intoxication.
• Laboratory studies in patients with chronic intoxication:
– elevated serum creatinine
– elevated BUN/creatinine ratio
due to underlying volume contraction.
– The white blood cell count is often elevated.
• ECG findings: T-wave flattening or inversion, and sometimes
bradycardia or sinus node arrest.
• Nephrogenic diabetes insipidus can occur with overdose or
with therapeutic doses.
• Lithium levels may be difficult to interpret.
• Lithium has a low toxic:therapeutic ratio & chronic
intoxication can be seen in levels only slightly above the
therapeutic range (0.8- 1 .2 mEq/L).
• In contrast, patients with acute ingestion may have
transiently very high levels (up to 10 mEq/L) w/out any
symptoms before the lithium fully distributes into tissues.
• Note: Falsely high lithium levels (as high as 6-8 mEq/L) can be
measured if a green-top blood specimen tube (containing
lithium heparin) is used instead of a red- or marbled-top tube
Treatment
• After acute oral overdose, consider gastric lavage or whole
bowel irrigation to prevent systemic absorption (lithium is
not adsorbed by activated charcoal).
• In all patients, evaluate renal function + volume status, and
give IV saline-containing fluids as needed.
• Monitor serum lithium levels, and seek assistance
– with their interpretation & need for dialysis from a medical
toxicologist or regional poison control center
• Consider hemodialysis if the patient is markedly
symptomatic or if the serum level >4-5 mEq/L
– esp if renal function is impaired.
• Continuous renal replacement therapy may be an effective
alternative to hemodialysis.
Mercury
• Poisoning occur by ingestion of inorganic mercuric salts,
organic mercury compounds, or inhalation of metallic
mercury vapor.
• Ingestion of the mercuric salts  burning sensation in the
throat, discoloration and edema of oral mucous membranes,
abdominal pain, vomiting, bloody diarrhea, and shock.
• Direct nephrotoxicity  AKI
• Inhalation of high concentrations of metallic mercury vapor
 acute fulminant chemical pneumonia.
• Chronic mercury poisoning  weakness, ataxia, intention
tremors, irritability, and depression.
• Exposure to alkyl (organic) mercury derivatives from highly
contaminated fish or fungicides used on seeds  ataxia,
tremors, convulsions, catastrophic birth defects.
– Nearly all fish have some traces of mercury contamination; the US
Environmental Protection Agency (EPA) advises consumers to avoid
swordfish, shark, king mackerel, tilefish because they contain higher
levels.
• Fish & shellfish that are generally low in mercury content:
shrimp, canned light tuna, salmon, pollock, catfish.
• Dental fillings composed of mercury amalgam pose a very
small risk of chronic mercury poisoning and their removal is
rarely justified.
• Some imported skin lightening creams contain toxic
quantities of mercury.
Treatment Chronic Poisoning
Acute Poisoning • Remove from
• There is no effective specific treatment for exposure.
mercury vapor pneumonitis.
• Remove ingested mercuric salts by lavage, and • Neurologic
administer activated charcoal toxicity is not
• For acute ingestion of mercuric salts, give considered
dimercaprol (BAL) reversible with
• Unless the patient has severe gastroenteritis, chelation
consider succimer (DMSA), 10 mg/kg orally
every 8 hours for 5 d  12 hours for 2 weeks.
• Unithiol (DMPS) = chelator (orally or
parenterally)
• Maintain urinary output.
• Treat oliguria and anuria if they occur.
Organophosphates
LI 4
Pesticides: Cholinesterase Inhibitor
• Organophosphorus & carbamate • There are a variety of
insecticides chemical agents in this
– organophosphates: parathion, group, with widely
malathion, etc; varying potencies.
– carbamates: carbaryl, aldicarb, etc • Most of them are poorly
widely used in commercial agriculture & water-soluble, are often
home gardening largely replaced older, formulated with an
environmentally persistent aromatic hydrocarbon
organochlorine compounds (DDT & solvent such as xylene,
chlordane) well absorbed through
• Organophosphates & carbamates-also intact skin.
called anticholinesterases: both inhibit • Most chemical warfare
enzyme acetylcholinesterase  >> "nerve agents" (such as
acetylcholine activity at nicotinic & GA [tabun] , GB [sarin] ,
muscarinic receptors & in CNS 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
• 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.
Arsenic
• (+) in some pesticides & industrial chemicals, used as a
chemotherapeutic agent.
• Symptoms of acute poisoning appear within 1 hour after
ingestion
but may be delayed as long as 12 hours:
– abdominal pain, vomiting, watery diarrhea, skeletal muscle cramps.
– Profound dehydration and shock may occur.
• Chronic poisoning, symptoms can be vague but often include:
– pancytopenia,
– painful peripheral sensory
– Neuropathy,
– skin changes: melanosis, keratosis, desquamating rash.
• Urinary arsenic levels may be falsely elevated after certain meals
(eg, seafood) that contain large quantities of a nontoxic form of
organic arsenic.
Treatment
Emergency Measures
• After recent ingestion (within 1-2 hours), perform gastric lavage
• Activated charcoal is of uncertain benefit because it binds arsenic poorly.
• (+) IV fluids  replace losses due to vomiting and diarrhea.
Antidote
• For patients with severe acute intoxication (+) chelating agent.
• 2,3-dimercaptopropanesulfonic acid (DMPS, Unithiol) (3-5 mg/kg IV @4
hours)
• Alternative parenteral chelator = dimercaprol (British antiLewisite, BAL),
which comes as a 10% solution in peanut oil, given 3-5 mg/kg IM @4-6
hours 2 days.
• Side effects: nausea, vomiting, headache, hypertension.
• GI ssx  switch to oral chelator succimer (dimercaptosuccinic acid,
DMSA), 10 mg/kg @8 hours, 1 week.
• Consult a medical toxicologist or regional poison control center for advice
regarding chelation.
Seafood Poisoning
• A variety of intoxications may occur after
eating certain types of fish or other seafood.
– scombroid, ciguatera, paralytic shellfish, puffer
fish poisoning.
• Majority of cases, seafood has a normal
appearance & taste (scombroid may have a
peppery taste).
Emergency and Supportive Measures • There is no specific
• Caution: Abrupt respiratory arrest antidote for paralytic
may occur in patients with acute shellfish or puffer fish
paralytic shellfish and puffer fish poisoning.
poisoning. – Ciguatera-There are
anecdotal reports of
• Observe patients for at least 4-6 successful treatment of acute
hours. neurologic symptoms with
• Replace fluid and electrolyte mannitol, 1 g/kg
intravenously, but this
losses from gastroenteritis with
approach is not widely
intravenous saline or other accepted.
crystalloid solution. – Scombroid-Antihistamines
• For recent ingestions, it may be such as diphenhydramine, 25-
possible to adsorb residual toxin in 50 mg intravenously, and the
H2-blocker cimetidine, 300
the gut with activated charcoal, mg intravenously, are usually
50-60 g orally effective.
Dietary Supplements & Herbal Products
• Dietary supplements do not require FDA approval, do not undergo the same
premarketing evaluation of safety and efficacy as drugs, and purveyors may or may
not adhere to good manufacturing practices and quality control standards.
• Supplements may cause illness as a result of intrinsic toxicity, misidentification or
mislabeling, drug-herb reactions, or adulteration with pharmaceuticals.
Methanol & Ethylene Glycol
• Methanol (wood alcohol) commonly found in: solvents, duplicating fluids,
record cleaning solutions, paint removers.
• Sometimes ingested intentionally by alcoholic patients as substitute for
ethanol & may also be found as a contaminant in bootleg whiskey.
• Ethylene glycol = major constituent in most antifreeze compounds.
• Toxicity of both agents = metabolism to highly toxic organic acids-
methanol to formic acid; ethylene glycol to glycolic & oxalic acids.
• Diethylene glycol = nephrotoxic solvent that has been improperly
substituted for glycerine in various liquid medications (cough syrup,
teething medicine, acetaminophen) causing numerous deaths in Haiti,
Panama, and Nigeria.
Clinical Findings
• Shortly after ingestion of methanol or ethylene glycol,
patients usually appear "drunk:'
• Serum osmolality (measured w/ freezing point device) is
usually increased, acidosis is often absent early.
• After several hours, metabolism to toxic organic acids leads
to a severe anion gap metabolic acidosis, tachypnea,
confusion, convulsions, and coma.
• Methanol intoxication  visual disturbances,
• Ethylene glycol  oxalate crystalluria & acute kidney injury.
Note: Point-of-care analytical devices common used in the
emergency department may falsely measure glycolic acid (a toxic
metabolite of ethylene glycol) as lactic acid.
• Significant toxicity (severe metabolic
Emergency and Supportive acidosis, altered mental status,
Measures markedly elevated osmol gap) 
hemodialysis ASAP to remove parent
• For patients presenting compound & toxic metabolites.
within 30-60 minutes after • Th/ w/ folic acid, thiamine,
ingestion, empty the pyridoxine  enhance breakdown of
stomach by aspiration toxic metabolites.
• Ethanol blocks metabolism of parent
through a nasogastric tube compounds: competing for enzyme
– Charcoal is not very effective alcohol dehydrogenase.
but should be administered if • Fomepizole (4-methylpyrazole;
other poisons or drugs have Antizol) blocks alcohol
also been ingested. dehydrogenase  much easier to
use > ethanol.
• If started before onset of acidosis,
fomepizole may be used as the sole
treatment for ethylene glycol
ingestion in some cases.
MetHb-inducing agents
• Chemical agents capable of oxidizing ferrous hemoglobin to its ferric
state (methemoglobin); form that (x) carry O2
• Drugs & chemicals known to cause methemoglobinemia:
– Benzocaine (a local anesthetic found in some topical anesthetic sprays and a
variety of nonprescription products),
– aniline,
– propanil (an herbicide),
– nitrites, nitrogen oxide gases, nitrobenzene,
– dapsone,
• Long elimination T ½
• may produce prolonged or recurrent methemoglobinemia
– phenazopyridine (Pyridium)
Many others
Clinical Findings
• Methemoglobinemia << O2-carrying capacity  dizziness, nausea,
headache, dyspnea, confusion, seizures, coma.
• Severity of symptoms depends on % of Hb oxidized  methemoglobin;
severe poisoning (+) when methemoglobin fractions > 40-50%.
• Low levels (15-20%), victims appear cyanotic due to "chocolate brown"
color of methemoglobin w/ normal P02 results on arterial blood gas
determinations.
• Conventional pulse oximetry gives inaccurate oxygen saturation
measurements; the reading is often between 85% and 90%.
– (A newer pulse oximetry device [Masimo Pulse CO-oximeter] is capable of estimating
the methemoglobin level.)
• Severe metabolic acidosis may be present.
• Hemolysis may occur, especially in patients susceptible to oxidant stress
(ie, those with glucose-6-phosphate dehydrogenase deficiency).
Treatment
• Administer high-flow oxygen.
• Agent recently ingested  (+) activated charcoal
– Repeat-dose activated charcoal may enhance dapsone elimination.
Specific Treatment
• Methylene blue = convert methemoglobin  hemoglobin (increasing
activity of enzyme methemoglobin reductase)
– Symptomatic patients = 1-2 mg/kg (0.1 -0.2 mL/kg of 1% solution) IV
– The dose may be repeated once in 15-20 minutes if necessary.
– Patients with hereditary methemoglobin reductase deficiency or
glucose-6-phosphate dehydrogenase deficiency  (x) respond to
methylene blue treatment.
• In severe cases where methylene blue is not available or is not effective,
exchange blood transfusion may be necessary.
Delirium & Psychotic Breaks
LI 5
Delirium
• Acute change in • 3 main types of delirium:
cognition; fluctuates – hypoactive,
• “quiet delirium”; patients have <<
rapidly over time, psychomotor activity and can appear
often reversible. somnolent.
• Frequently 1st sign of – If hypoactive delirium is
confused for depression
underlying acute
– hyperactive,
medical illness. • >> psychomotor activity, patients are
• Signs: often agitated, anxious, sometimes
combative.
– Altered levels of
– Mixed
consciousness,
inattention, • combination of both hyperactive &
hypoactive states that fluctuate over
disorganized thinking,
time
altered perception.
most common types: hypoactive & mixed
delirium  highest potential to be missed
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition

• Environmental risk factors for delirium:
– functional dependence,
– living in a nursing home,
– hearing impairment.
• Delirium = independent marker for mortality and is
associated with a longer length of hospital stay,
increased hospital complications, discharge to long-
term care facilities, and lasting cognitive deficits.
• Even though delirium is a common disorder in the
elderly • Differential diagnosis of delirium:
• dementia,
• Depression,
• another underlying psychiatric disorder.
• Such conditions can also be comorbidities of each
other. However, first assess for delirium  then
consider the possibility of the other disorders.
History
• Focus history taking on identifying the patient’s baseline
mental status and level of functioning and the time course of
changes.
• Ask about past medical history and recent illness.
• Obtain an accurate medication list, and ask about over-the-
counter medications, medications with anticholinergic
properties, or any new medications.
• Ask about substance abuse to assess the likelihood of
intoxication or withdrawal.
• Any past psychiatric history requires close investigation of
prior diagnoses, hospitalizations, and medications.
• Determine the patient’s ability to make informed medical
decisions, and determine whether another individual has
legal power of attorney for medical decision making.
• When attempting to differentiate delirium
from dementia, consider several key factors
(more consistent in delirium):
– Acute change in mental status
– Fluctuating course over time
– Altered level of consciousness, inattention,
disorganized thinking

Physical Examination should be thorough.
• Vital signs must be complete, to include oxygen saturation and
temperature.
• Determine the blood glucose level.
• Baseline blood pressures may be higher than in younger age groups, and
tachycardia can be masked by pharmacologic and/or physiologic
limitations.
• Older patients have lower basal temperatures
• Look for evidence of trauma, as patients may not recall falling or injuring
themselves.
• Examine the entire body, making sure to look at the patient’s back and
heels for evidence of decubitus ulcers.
• Perform a complete neurologic exam, checking for focal findings,
abnormal posturing, or difficulty with gait, coordination, or vision.
• A normal physical examination does not exclude the diagnosis of
delirium.

Mental Status
• Mental status examination is performed to identify delirium and differentiate it
from other conditions.
• The examination consists of an assessment of 6 mental-behavioral components
• 2 of most common screening tests used to detect delirium:
– Confusion Assessment Method for general use
– Confusion Assessment Method–Intensive Care Unit for intubated patients who are
not heavily sedated.

Laboratory Testing and Imaging
• Obtained to identify the treatable causes of delirium
• In geriatric patients: infections (urinary tract infections and pneumonia), are
associated with nearly half of cases of delirium, and medications may
account for another 40%
• Check point-of-care glucose ASAP after patient arrival in the ED.
• Obtain CBC and basic metabolic studies: calcium, phosphorus, hepatic
enzymes.
• Urinalysis is necessary because urinary tract infections are a frequent cause
of delirium.
• Obtain cardiac markers.
• Consider an arterial blood gas analysis, especially in patients with chronic
lung disease, because hypercarbia can cause delirium.
• Obtain thyroid function studies.
• Urine or serum toxicologic studies may be in order.

• Lumbar puncture may be necessary (after CT scan) if
there is suspicion for meningitis or encephalitis or
the patient has had a new-onset seizure
• Further studies may be needed depending on the
results of history, examination, and basic tests.
Imaging/Ancillary Tests
• Electrocardiogram & chest radiograph are essential.
• Head CT scan is advised for patients with signs of, or
a history of, trauma, focal neurologic deficits,
impaired level of consciousness, or an otherwise
unrevealing evaluation.

TREATMENT
• Medical Treatment Direct treatment to the
underlying cause of delirium.
• Withhold or remove medications that are
responsible for delirium.
• Treat infection, provide IV fluids for dehydration,
correct hypoglycemia, and treat pain.
• Select doses of analgesics and narcotics for each
individual patient and monitor for adverse effects.

The Medical Environment • Precipitating factors in the
• Provide the patient with his/her glasses or development of delirium in the
hearing aids, allow family or caregivers at hospital:
the bedside, provide frequent – the use of physical restraints,
reorientation about surroundings and
– malnutrition,
course of care, and make sure there is
access to a bathroom. – use of a bladder catheter,
• The Multicomponent Intervention to – > 3 medications added,
Prevent Delirium in Hospitalized Older – any iatrogenic event.
Patients identified 6 risk factors for the
development of delirium:
Preventing and minimizing these
factors are especially important
– cognitive impairment,
when long ED stays are
– sleep deprivation,
unavoidable.
– immobility,
– visual impairment,
– hearing impairment,
– dehydration
targeted each risk factor with specific
interventions carried out by a
multidisciplinary team.
Agitation
• If the patient is agitated, begin with a non-pharmacologic approach:
– addressing patient needs (such as using the restroom and, if possible,
allowing the patient to eat or drink),
– providing comfortable surroundings,
– having the family close by.
• Avoid bladder catheters.
• Physical restraints should be an absolute last resort.
If basic interventions are not successful, consider medication
• Avoid benzodiazepines in elderly if at all possible, unless alcohol
withdrawal is the cause
– Benzodiazepines can cause paradoxical disinhibition (excitement or
altered mental state) & increased agitation in the elderly.
– If a benzodiazepine is used, consider a short-acting, glucuronidated
agent such as lorazepam, oxazepam, or temazepam to minimize
prolonged benzodiazepine effects.
• Avoid antihistamines, because this drug class has strong anticholinergic
effects and can induce or worsen delirium in the elderly.
DISPOSITION AND FOLLOW-UP
• The vast majority of patients with delirium should be
hospitalized.
• Criteria for possible discharge:
– identification and treatment of the source of delirium;
– the patient returns to baseline function and mentation in the ED;
– the patient is discharged to the care of an active, capable individual
or to a responsible facility;
– the patient has access to follow-up in 24 hours or has the ability to
return immediately to the ED if conditions deteriorate.

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.

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

• ED staff must be educated and • If necessary, isolate and restrain
equipped with a range of skills to threatening patients before they
protect themselves. are disrobed, gowned, and
• These skills: searched for weapons.
– enhanced awareness of risk • Medical and nursing staff should
factors and warning signs of stay distant from the patient;
violent behavior avoid excessive eye contact;
– verbal de-escalation techniques maintain a calm, controlled
– Quick access to rapidly posture and tone of voice; and
tranquilizing or neuroleptic stand in a location that neither
medications threatens the patient nor blocks
– Emergency strategies for getting the exit of the healthcare worker
help quickly in explosive from the room.
circumstances.
• Approach patients with
potentially dangerous behavior
cautiously and with a
nonthreatening attitude, with
adequate security nearby.
–
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).

• Seclusion rooms may be used to • Keep the patient advised of each
protect patients and staff. action and the expected duration,
• Remove or carefully secure any and explain the consequences of
objects that could be used for self- violent behavior.
injury or against staff. • Monitor the patient in a seclusion
• Austere seclusion rooms may be room with a personal guard or
useful for some agitated patients nurse-monitor, by closed circuit
by providing relief from external television, or by individual checks
stimuli. about every 10 minutes.
• Search patients before entry, and • Give the patient opportunities to
remove potentially dangerous comply with staff demands for
objects, clothing, or weapons. acceptable behavior  release
• Make sure staff are aware of the from seclusion.
location of exits and of panic • If violent behavior persists,
buttons. physical restraint is justified.
• Initially, leave the door open  • Document all steps in the use of
remains agitated  lock the door. 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.

Physical Restraints
• In many cases, there is no substitute • Be careful to avoid injury.
for the application of physical limb • Elevate the patient’s head, if
restraints. possible, to minimize risk of
• Restraints should be applied rapidly aspiration.
and safely by individuals trained and • Once the patient is restrained, offer
skilled in their use. medications, and if refused,
• A team of 5 staff members is administer medications involuntarily
recommended: • Once the patient is calm and
– one team leader compliant, restraints can be removed
– one person for each limb. one at a time, while staff carefully
• The patient and any family members monitor the patient to ensure the
present should be provided with safety of all concerned.
clear, ongoing explanations of all
procedures.
• Place the patient on a bed or
stretcher, and secure all four limbs
with leather restraints.


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Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

Rosen's Emergency Medicine-Concepts and Clinical Practice

• Although the majority of

Rosen's Emergency Medicine-Concepts and Clinical Practice

• Depression is often present and should be evaluated carefully.

Blood alcohol levels:

Blood level (mg/dL)

>150 Intoxication as manifested by ataxia, dysarthria, and nausea and vomiting

350 - 900 lethal blood levels

• In severe cases, overdosage is marked by respiratory depression, stupor,

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

• Excessive anticoagulation may cause:

CURRENT Medical Diagnosis & Treatment 2017

• Specific reversal agents have been developed and are now

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

Valproic acid intoxication  unique Newer anticonvulsants: gabapentin,

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017

CURRENT Medical Diagnosis & Treatment 2017