THIRD PROBLEM

EMERGENCY
MEDICINE BLOCK
Agustina Cynthia Cesari S
405140066
Group 1
 LI 1.
DRUG INTOXICATION
ACETAMINOPHEN
DIGOXIN
WARFARIN
SULFA
OPIOID
PSYCHOTROPIC AGENTS
 LI 2.
CHEMICAL AGENTS
INTOXICATION
ORGANOPHOSPHATE
Organophosphates
◦ Commonly used: diazinon, acephate, malathion, parathion, and
chlorpyrifos
◦ Organophosphate and carbamate compounds are the
insecticides most commonly associated with systemic illness
◦ Organophosphate poisoning results primarily from accidental
exposure in the home, recently sprayed or fogged areas using
pesticide applicators, agriculture, industry, and the transport of
these products
◦ Systemic absorption of organophosphates occurs by inhalation
and after mucous membrane, transdermal, transconjunctival,
and GI exposure.
Pathophysiology
◦ Organophosphate and carbamate compounds inhibit the enzyme
cholinesterase  acetylcholine accumulation at nerve synapses and
neuromuscular junctions, resulting in overstimulation of acetylcholine
receptors  Excess acetylcholine results in a cholinergic crisis that
manifests as a central and peripheral clinical toxidrome
◦ Aging : the permanent, irreversible binding of the organophosphorus
compound to the cholinesterase
◦ The time to aging is highly variable among different agents and can
range from minutes to a day or more
◦ Once aging occurs, the enzymatic activity of cholinesterase is
permanently destroyed, and new enzyme must be resynthesized over
a period of weeks before clinical symptoms resolve and normal
enzymatic function returns  Antidotes must be given before aging
occurs to be effective
Signs & symptoms
◦ Four clinical syndromes:

ACUTE POISONING
◦ Most poisoned patients are symptomatic within the first 8 hours
and nearly all within the first 24 hours
◦ Acute organophosphate poisoning results in CNS, muscarinic,
nicotinic, and somatic motor manifestations
INTERMEDIATE SYNDROME
◦ May occur 1-5 days after exposure
◦ Clinical features include paralysis of neck flexor muscles, muscles
innervated by the cranial nerves, proximal limb muscles, and
respiratory muscles  respiratory support may be needed

CHRONIC TOXICITY
◦ Is seen primarily in agricultural workers with daily exposure,
manifesting as symmetrical sensorimotor axonopathy  begin
with leg cramps and progress to weaknes and paralysis,
mimicking features of the Guillain-Barre syndrome

ORGANOPHOSPATE-INDUCED DELAYED NEUROPATHY

◦ Characterized by cognitive dysfunction, impaired memory, mood
changes, autonomic dysfunction, and peripheral neuropathy
Diagnosis
◦ Based on history and the presence of a suggestive toxidrome
◦ The cholinergic toxidrome may vary depending on the
predominance of muscarinic, nicotinic, and CNS manifestations
and the severity of the intoxication
◦ Cholinesterase activity is used to assess potential toxicity, with red
cell acetylcholinesterase enzymatic activity a more accurate
indicator of synaptic cholinesterase inhibition, but plasma
butyrylcholinesterase is easier to assay and more available
Treatment
Complications & prognosis
◦ Following an acute exposure, the patient may have neurologic
sequelae, such as paresthesias or limb weakness, along with
nonspecific symptoms lasting days to months
◦ Death form organophosphate poisoning usually occurs in 24 hours
in untreated patients, usually from respiratory failure secondary to
paralysis of respiratory muscles,28 neurologic depression, or
bronchorrhea.
KEROSENE
Kerosene
◦ Hydrocarbons are a diverse
group of organic compounds
consisting primarily of carbon
and hydrogen atoms
◦ The two basic forms of
hydrocarbons are aliphatic
(straight- or branched-chain
carbon arrangement) or
aromatic (carbon arranged in a
ring)
◦ Hydrocarbons are in many
household and occupational
products
Pathophysiology
◦ The toxic potential of hydrocarbons depends on their physical
characteristics (viscosity, surface tension, and volatility), chemical
characteristics (aliphatic, aromatic, or halogenated), presence of
toxic additives (pesticides or heavy metals), routes of exposure,
concentration, and dose
◦ The physical characteristics contribute the most to aspiration risk
◦ Ingestion of liquids with low viscosity and surface tension and high
volatility increases the risk for aspiration because these substance
can flow easily, spreading out widely on the oral mucosa, and
vaporize at body temperature
Signs and symptoms
Diagnosis
◦ History
◦ Physical examination
◦ Bedside cardiac and pumonary monitoring
◦ Laboratory tests
◦ Chest radiography: indicated in a symptomatic patient after
hydrocarbon aspiration
◦ CBC is indicated if anemia, bleeding disorder, hemolysis, or
leukemia is considered
Treatment
 LI 3.
INHALED TOXIN
Inhaled Toxin
◦ Inhalational exposure to systemic toxins can be covert and
indolent (as in occupational exposure to irritant photochemical
smog) or overt and fulminant.
◦ The circumstances of the exposure, the presence of combustion
or odors, and the number and condition of victims assist in the
management.
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1927
Simple Asphyxiants
Principles Of Toxicity
◦ Are inert and produce toxicity only by
displacement of oxygen and lowering of
the fraction of inspired oxygen (Fio2).
◦ Remain asymptomatic if the Fio2 is
normal.
◦ Carbon dioxide and nitrogen are
exceptions in that both can produce
narcosis at elevated partial pressures,
even though their predominant
toxicological effect is simple
asphyxiation.
◦ Most deaths from the intentional
inhalation of automotive exhaust result
from simple asphyxiation, due to
hypoxia, and not from carbon monoxide
(CO) poisoning.
Clinical Features
◦ Acute effects occur within minutes of onset of
hypoxia and are the manifestations of ischemia.
◦ A fall in the Fio2 from normal (21%) to 15% :
◦ Autonomic stimulation :
◦ Tachycardia
◦ Tachypnea
◦ Dyspnea
◦ Cerebral hypoxia :
◦ Ataxia
◦ Dizziness
◦ Incoordination
◦ Confusion
◦ FiO2 falls below 10%  lethargy from cerebral edema
◦ FiO2 below 6%  life is difficult to sustain
◦ Removal from exposure terminates the simple
asphyxiation and allows restoration of oxygenation
and clinical improvement  resolving symptoms
◦ Failure to improve suggests complications of ischemia
(seizures, coma, and cardiac arrest) and is associated
with a poor prognosis
Simple Asphyxiants
Diagnostic Testing Management

◦ Minimally symptomatic or ◦ Removal from exposure

asymptomatic patients 
◦ Supportive care
don’t require chest
radiography or arterial blood ◦ Administration of
gas (ABG) analysis. supplemental oxygen.
◦ Screening for acetaminophen ◦ Psychiatric consultation 
and any other relevant toxin act of deliberate self-harm.
implicated by history, physical
examination, or observation 
asphyxiation was an act of
deliberate self-harm
Disposition
◦ Mild asphyxia who recover after removal from the exposure can
be discharged after 6 hours of observation if they are
asymptomatic or minimally symptomatic and improving.
◦ Patients at risk for complications of hypoxia, such as those
presenting with significant signs or symptoms (coma, chest pain,
ECG changes) or with exacerbating medical conditions (cardiac
disease)  observed for 24 to 48 hours for the development or
progression of post hypoxic complications.
Pulmonary Irritants
Principles of Toxicity
◦ Irritant gases dissolve in the
respiratory tract mucus and
alter the air-lung interface by
invoking an irritant or
inflammatory response
◦ When these gases are
dissolved  produce an acid
or alkaline product, but
several generate oxygen
derived free radicals that
produce direct cellular
toxicity
Clinical Features
◦ Highly water-soluble gases
rapidly impact the mucous
membranes of the eyes 
lacrimation and upper
airway  nasal burning,
cough
◦ Massive or prolonged
exposure can result in life-
threatening laryngeal
edema, laryngospasm,
bronchospasm, or ARDS
Pulmonary Irritants
Diagnostic Testing
◦ Oxygenation and ventilation are
assessed by serial chest
auscultation, pulse oximetry, and
continuous capnography.
◦ Chest radiography is indicated for
patients presenting with cough,
dyspnea, hypoxia, or abnormal
findings, such as rales or wheezes,
on physical examination.
◦ ABGs are reserved for patients who
are more severely symptomatic,
have hypoxia, or do not improve
readily with appropriate therapy.
Management
◦ Evidence of severe tissue irritation, such as oral
or tongue edema, altered voice (raspy or
muffled), or significant odynophagia or
dysphagia  early intubation
◦ Erythema or pain in the oropharynx or
nasopharynx and those with any evidence of
alteration of voice, dysphagia or odynophagia,
or stridor  laryngoscopy.
◦ Erythema with mild edema  repeat
examination 30 to 90 minutes after the initial
examination or earlier, if symptoms or signs are
worsening.
◦ Bronchospasm generally responds to inhaled
beta-adrenergic agonists
◦ Chlorine or hydrogen chloride gas receive
symptomatic relief from nebulized 2% sodium
bicarbonate solution.
Disposition
◦ Exposed to highly water-soluble gases can be discharged if they
are asymptomatic or symptoms are minimal and improving
◦ Exposure to intermediate or poorly water-soluble gases,
asymptomatic patients should be observed for increasing
dyspnea for 6 hours before final disposition
◦ Patients with prolonged gas exposure or exposure to highly
concentrated gases, which may occur in a closed space, even if
asymptomatic, or those in high-risk situations (underlying
pulmonary disease, extremes of age, and poor follow-up) 
observed in an inpatient setting or observation unit for 24 hours.
Smoke Inhalation
Principles of Toxicity
◦ Temperatures between 350°
and 500° C, air has such a low
heat capacity that it rarely
produces lower airway
damage.
◦ The greater heat capacity of
steam (approximately 4000
times that of air) or heated
soot suspended in air (smoke)
can transfer heat and cause
injury deep within the
respiratory tract.
Clinical Features
◦ Thermal and irritant-induced
laryngeal injury  cough,
voice alteration, or stridor, but
these findings are often
delayed.
◦ Soot and irritant toxins in the
airways  early cough,
dyspnea, and bronchospasm.
◦ Deaths that occur rapidly after
exposure are caused by
asphyxia, airway compromise,
or metabolic poisoning (CO).
Smoke Inhalation
Diagnostic Testing
◦ Airway management is as described earlier
for inhaled pulmonary irritants.
◦ If evidence of significant airway exposure is
present, such as carbonaceous sputum or
hoarse voice, the airway should be
examined by rigid or flexible laryngoscopy,
and secured if signs of injury or compromise
are noted.
◦ Pulmonary injury is assessed through
auscultation and chest radiography for signs
of alveolar filling or hyperinflation
◦ Metabolic acidosis, particularly when serum
lactate concentration is greater than 10
mmol/L, suggests concomitant cyanide
poisoning
Management
◦ Early assessment of the airway and
early intubation
◦ Inhaled beta-adrenergics are
widely used for patients with
dyspnea or wheezing  at least
one dose
◦ Optimal supportive care and
maintenance of adequate
oxygenation (suctioning and
pulmonary toilet)
◦ Bronchoscopy with
bronchoalveolar lavage is
frequently recommended to clear
debris and toxins from the distal
airways.
Disposition
◦ Patients who are intubated should be admitted to the ICU or burn
unit, depending on the extent of the cutaneous burns or
respiratory tract injury.
◦ Patients with upper airway symptoms or signs, but without
concerns for airway loss  repeat airway examination for 6 hours
preferably in an ICU
◦ Patients with prolonged closed-space exposure or lower airway
findings  rales or carbonaceous sputum  admitted to an ICU
and observed for at least 24 hours while assessing for the
development of signs of lower respiratory tract injury
Principles of Toxicity :
Cyanide and Hydrogen Sulfide
◦ Instead of directly affecting the airway and lungs, these poisons cause effects at the
cellular level
◦ Hydrogen cyanide is a gas with many commercial uses, particularly in synthetic fiber
manufacture and fumigation
◦ Gaseous hydrogen cyanide is occasionally noted to have the odor of bitter almonds
◦ Cyanide in its salt form (sodium or potassium) is important in the metallurgy (jewelry)
and photography and is much safer to work with because of its low volatility.
◦ When cyanide salts are dissolved in water, hydrogen cyanide can leave the surface,
particularly under acidic conditions.
◦ Cyanide is metabolically released in vivo from precursors (cyanogens) such as
amygdalin, found in apricot and other Prunus species pits, and from nitriles, a group
of chemicals with many commercial uses.
◦ Hydrogen sulfide poisoning most often occurs in petroleum re nery and sewage
storage tank workers
◦ Hydrogen sulfide has a noxious odor similar to rotten eggs, which becomes
unnoticeable with extremely high concentrations or prolonged exposure (a process
called olfactory fatigue).
Principles of Toxicity :
Cyanide and Hydrogen Sulfide
◦ Gaseous cyanide is rapidly absorbed after inhalation and is
immediately distributed to the oxygen-using body tissues.
◦ The poisoned tissue rapidly depletes its adenosine triphosphate
reserves and ceases to function
◦ Hydrogen sulfide exerts its toxic effects both as a pulmonary
irritant and as a cellular poison.
Clinical Features
◦ Tissue hypoxia occurs within minutes, with the exact onset dependent
on the route, dose or concentration, and nature of the exposure.
◦ Dysfunction of the heart and the central nervous system (the organ
systems most sensitive to hypoxia)  cyanide poisoning : coma,
seizures, dysrhythmias, and cardiovascular collapse
◦ Metabolic acidosis develops as a result of diffuse cellular dysfunction
and is associated with an elevated serum lactate concentration
◦ Cyanide and hydrogen sulfide prevent tissue extraction of oxygen
from the blood, the oxygen content of venous blood remains high,
approaching that of arterial blood  “arterialization” or brightening
of venous blood to resemble arterial blood.
◦ Patients surviving cyanide or hydrogen sulfide poisoning may have
persistent or delayed-onset neurologic syndromes
Cyanide and Hydrogen
Sulfide
Diagnostic Testing
◦ Pulse oximetry and ABG
analysis are accurate
◦ An increased anion gap
metabolic acidosis and
elevated serum lactate
concentration are usually
present
◦ A lactate concentration
greater than 10 mmol/L in a fire
victim, low COHb level 
cyanide poisoning.
◦ Testing for hydrogen sulfide is
not clinically available
Management
◦ Therapy is almost always
empirical.
◦ Patients removed from a re
environment who have
cardiovascular instability,
altered mental status, or a
serum lactate greater than
10 mmol/L should receive
cyanide treatment regardless
of the COHb concentration.
 Management for Hydrogen
Cyanide
◦ The accepted goal of
therapy is to reactivate the
cytochrome oxidase system
by providing an alternative
binding site for the cyanide
ion.

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1931

Management for Hydrogen
Sulfide
◦ Because the bond between hydrogen sulfide and cytochrome
oxidase is rapidly reversible, removal from exposure and standard
resuscitative techniques are usually sufficient to reverse hydrogen
sulfide toxicity  use of the nitrite portion of the cyanide antidote
kit is suggested to create MetHb
 Carbon Monoxide
◦ CO is the most common cause of acute poisoning death in developed
nations and the most common cause of fire-related death
◦ Etiology :
◦ Structure fires  wood
◦ Clogged vents for home heating units  methane
◦ Use of gasoline powered generators indoors
◦ CO affects cellular oxygen use at the tissue level  CO, similar to
cyanide, inhibits the final cytochrome complex involved in mitochondrial
oxidative phosphorylation  switch to anaerobic metabolism and
ultimately in cellular death

Tintinalli’s Emergency Medicine

8th. 2016 pg 1437
 Carbon Monoxide
Clinical Features Diagnostic Testing
◦ Altered mental status : coma and
seizures ◦ Co-oximetry : distinguish
◦ Extremely abnormal vital signs : between normal hemoglobin
hypotension and cardiac arrest and COHb (and MetHb)
◦ Metabolic acidosis.
◦ Mild CO poisoning :
◦ Headache
◦ Nausea
◦ Vomiting
◦ Dizziness
◦ Myalgia
◦ Confusion
◦ Postmortem : cherry-red skin color

Tintinalli’s Emergency Medicine 8th. 2016 pg 1438

 Management
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 193

◦ Treatment begins with oxygen

therapy, purpose :
◦ half-life of COHb is inversely
related to the Po2
◦ It can be reduced from
approximately 5 hours on room
air to 1 hour by providing
supplemental 100% oxygen.
◦ Second, a sufficient Po2  HBO
to sustain life in the absence of
adequately functioning
hemoglobin, but this is helpful
only when the COHb is
extremely elevated.
◦ A patient with a neurologic
abnormality or cardiovascular
instability  syncope, altered
mental status, myocardial
ischemia, and dysrhythmias is a
candidate for HBO

Tintinalli’s Emergency Medicine 8th. 2016 pg 1439

 LI 4.
HEAVY METALS INTOXICATION
Heavy metals
intoxication
Lead
◦ The most common cause of chronic metal poisoning
◦ Exposure to lead can occur from inhalation or ingestion, and both
inorganic and organic forms of lead produce clinical toxicity
Signs & symptoms
Diagnosis
◦ Exposure history (occupational or environmental)
◦ The combination of abdominal or neurologic dysfunction with a
hemolysis should raise suspicion for lead toxicity
◦ Consider the diagnosis in all children presenting with encephalopathy
◦ The definitive diagnosis rests on finding an elevated blood lead level,
with or without symptoms
◦ The blood lead level is the best single test for evaluating lead toxicity,
and levels at or >5 micrograms/dL (0.24 micromol/L) are considered
elevated in children
◦ The anemia from lead toxicity can be normocytic or microcytic,
possibly with evidence of hemolysis, such as an elevated reticulocyte
count and increased serum-free hemoglobin
◦ Abdominal radiographs may show radiopaque material in the GI
tract
Treatment
◦ Patients with appropriate signs and symptoms and an elevated
blood lead level are classified as lead toxic and should be
treated
◦ In severely toxic patients, standard life support measures should
be instituted
◦ Seizures are treated with benzodiazepines and general
anesthesia, if necessary
◦ Chelation therapy
Arsenic
◦ Ingested or absorbed arsenic reversibly binds with sulfhydryl
groups found in many tissues and enzyme systems
◦ Acute exposure produces dilatation and increased permeability
of small blood vessels, resulting in GI mucosal and submucosal
inflammation and necrosis, cerebral edema and hemorrhage,
myocardial tissue destruction, and fatty degeneration of the liver
and kidneys
◦ Subacute or chronic exposure can cause a primary peripheral
axonal neuropathy with secondary demyelination
Signs & symptoms
Diagnosis
◦ History of exposure
◦ The diagnosis of acute arsenic poisoning should be considered in
a patient with hypotension that was preceded by severe
gastroenteritis
◦ The diagnosis of chronic arsenic toxicity should be considered in a
patient with a peripheral neuropathy, typical skin manifestations,
or recurrent bouts of unexplained gastroenteritis
◦ Abdominal radiograph  intestinal radiopaque metallic flecks in
cases of arsenic ingestions
◦ CBC: normocytic, normochromic, or megaloblastic anemia,
and/or a thrombocytopenia
◦ Definitive diagnosis of acute poisoning depends on finding
elevated arsenic levels in a 24-hour urine collection
Treatment
◦ Stabilize circulatory function, because hypotension and
dysrhytmias are the chief causes of death
◦ Hypotension: crystalloid volume replacement, and vasopressor
therapy with dopamine or NE may be required
◦ Acute ingestion: gastric lavage and activated charcoal
◦ Whole bowel irrigation should be considered if abdominal
radiographs reveal intestinal radiopaque materials consistent with
arsenic
◦ Seizures can be treated with benzodiazepines and general
anesthesia as necessary
◦ Chelation therapy uses dimercaprol or succimer
Mercury
◦ Mercury binds with sulfhydryl groups, affecting a diverse number
of enzyme and protein systems
◦ Methyl mercury also inhibits choline acetyl transferase, which
catalyzes the final step in the production of acetylcholine  may
produce symptoms of acetylcholine deficiency
◦ Mercuric salts produce proximal renal tubular necrosis
Signs & symptoms
ELEMENTAL MERCURY
◦ Acute symptoms following inhalation of elemental mercury vapor
include shortness of breath, fever/chills, cough, nausea, vomiting,
diarrhea, metallic taste, headaches, weakness, and blurry vision

INORGANIC MERCURY
◦ Mercury salts are caustic, and an acute ingestion produces a
severe hemorrhagic gastroenteritis with abdominal pain often
associated with a characteristic graying of the oral mucosa and
metallic taste
◦ GI symptoms of chronic inorganic mercury toxicity include
metallic taste, burning sensation in the mouth, loose teeth,
mucosal lesions and fissures, excessive salivation, and nausea
ORGANIC MERCURY
◦ After a latent period of weeks to months, orofacial paresthesias
are a common initial symptom, followed by headache, tremor,
and fatigue.
◦ In severe cases, patients may develop ataxia, muscle rigidity and
spasticity, blindness, hearing deficits, and dementia
Diagnosis
◦ History of exposure
◦ 24-hour urine mercury levels: a level >20 micrograms/L (>0.1
micromol/L) may indicate meaningful exposure
◦ Whole blood mercury levels
◦ MRI findings in methyl mercury toxicity from ingestion of
contaminated seafood include marked atrophy of the visual
cortex, cerebellar vermis and hemispheres, and postcentral
cortex
Treatment
◦ Elemental mercury: the severe respiratory failure following
inhalation of volatilized elemental mercury or aspiration of
elemental mercury may require endotracheal intubation and
positive-pressure ventilation
◦ Inorganic mercury salts: treat with aggressive IV hydration and GI
decontamination, including gastric lavage if the patient has not
had significant emesis, and consider activated charcoal
◦ Organic mercury: institute gastric decontamination in the setting
of acute ingestion
◦ Chelation
 LI 5.
PSYCHOTIC BREAK