Third Problem

Emergency Medicine Block

“Disastrous Pills”
Group 1

Tuesday, October 10th 2017

Group’s Identity
• Tutor: dr.Hugo
• Leader: Sugiarto Kamarudy Lay (405140208)
• Writer: Archangela Luisa Keyko (405140173)
• Secretary: Agustina Cynthia Cesari S (405140066)
• Members:
1. Daniel Albar Patterson (405130106)
2. Arliza Prasetya Wati (405130200)
3. Phoenix Hong (405140015)
4. Willyanti (405140035)
5. Elisa Handiwijaya (405140057)
6. Andreas Natan (405140099)
7. Jatinder Pall Singh (405140155)
8. Vinny Desyagiarini (405140182)
9. Richard Cristanto T (405140254)
 Third Prblem
“Disastrous Pills”
A 25 year old female is brought to the ED by her brother for being found
unconscious and breathing very slowly. He found her in her bedroom with some
pills, a can of glue and a bottle of alcohol beside her when he got back from work.
They are living in a small house in an industrial area with a lot of factories. He is
saying that she works at one of the pesticide factory. He also said that she is very
irritable and depressed since a month ago because her fiancee cancelled their
wedding. She seems to be very upset and once said prescribed her an anti-
depressant. One of her friend gave her some unknown pills, which made her seem
happy and “high” after she took them. On her initial physical examination, her
blood pressure is 100/80 mmHg. Heart rate is 60 beats per minute, respiratory rate
is 10 breaths per minute and her temperature is 37 celcius. Physical examinations
on her thyroid, thorax and abdomen are unremarkable. Her pupil is symmetrical
and are reactive to light stimulation with 1.5 mm pupil width.
A 70 year old male is brought to the Emergency Department by his son
for being delirious in the past few days. He has been complaining of pain on his
right knee and received acetaminophen from his physician. He has a history of
chronic heart failure and took digoxin and warfarin daily. His wife usually prepares
his medication, but she had to go out of town for a few days, hence he managed
his medication by himself. He complained of gum bleeding when he brushed his
teeth this morning. On initial examination, his blood pressure is 105/80 mmHg,
heart rate is 60 beats per minute and irregular, respiratory rate is 16 breaths per
minute and his temperature is 37 celcius. His pupils are symmetrical and reactive
to light. There is abdominal tenderness on his right upper quadrant of abdomen

Discuss the case, asses the patient’s condition, and plan proper treatment while
considering all possibilities!
Problems
1. Pada pasien perempuan, adakah hubungan antara umur dan jenis kelamin terhadap
keluhan?
2. Pada pasien perempuan, mengapa setelah diberi pil pasien merasa happy dan “high”? Kira-
kira pil apa yang diberikan?
3. Apa pengaruh dari obat-obatan yang dipakai dengan keluhan?
4. Apakah hubungan antara pekerjaan, lingkungan tempat tinggal terhadap keluhan pada
pasien perempuan? Efek intoksikasi pestisida?
5. DD pasien perempuan dan laki-laki?
6. Apa penyebab frekuensi napas dan denyut jantung menurun pada pasien perempuan?
7. Apakah keluhannya dapat disebabkan oleh antidepresan yang dia minum?
8. Apakah hubungan antara obat yang dipakai dengan keluhan pada pasien laki-laki? Adakah
hubungan dengan riwayat CHF?
9. Kenapa ada nyeri tekan RUQ pada pasien laki-laki?
10. Mengapa gusinya berdarah pada pasien laki-laki?
11. Pada pasien laki-laki, jika pasien ini tidak teratur minum obat, apakah ada hubungan dengan
keluhannya?
12. Pemeriksaan penunjang yang disarankan?
13. Terapi awal yang diberikan?
14. Keracunan apa saja yang dialami oleh pasien perempuan?
Brainstorm
1. Tidak ada hubungan, epidemiologi: wanita, usia 25-39 tahun
2. Golongan benzodiazepin dapat menyebabkan penurunan kesadaran dan menyebabkan
depresi napas, golongan opioid dan stimulan dapat menyebabkan euforia, selain itu
golongan opioid juga dapat menyebabkan depresi napas, bradikardi, dan pinpoint pupil
3. Alkohol, organofosfat  kesadaran menurun
4. Organofosfat  CNS depression
5. Pasien perempuan: intoksikasi Kerosene (bensin), intoksikasi CO  intoksikasi via inhalasi,
intoksikasi organofosfat (melalui inhalasi, kulit, oral), intoksikasi alkkohol, stimulan, tricyclic
antidepressant, SSRI. Pasien laki-laki: intoksikasi digoxin, asetaminofen, warfarin
6. Golongan benzodiazepin  depresi napas, golongan opioid  depresi napas, bradikardi
7. Karena tricyclic antidepressant
8. Digoxin toxicity  bradikardi
9. Gangguan tubular cell dari hepar (>3 gr/day), intoksikasi asetaminofen (fase 3= 72-96 jam) 
hepatotoksik, kombinasi warfain + asetaminofen
10. Riwayat warfarin dan digoxin, warfarin (vit K antagonis  hambat koagulasi), + asetaminofen
(NAPQI  rusak sel  gangguan vit k). Riwayat penggunaan obat ini meningkatkan resiko
perdarahan
11. Tidak ada, kalo ada: heart failure
12. Cek urin, SGOT & SGPT, albumin, cek kadar alkohol
13. ABC  pinpoint pupil: opioid (antidote: naloxone), alkohol  berikan tiamin, asetaminofen
 berikan N-asetilsistein
14. Kerosene (bensin), intoksikasi CO  intoksikasi via inhalasi, intoksikasi organofosfat (melalui
inhalasi, kulit, oral), intoksikasi alkohol, stimulan, tricyclic antidepressant, SSRI
Mindmap
ORGANOFOSFAT &
NARCOTICS
KEROSENE

INTOKSIKASI

HEAVY METALS NON-PSYCHOACTIVE

&INHALED TOXIN

DELIRIUM &
PSYCHOTIC BREAK
Learning Issues
1. MM intoksikasi obat
2. MM intoksikasi bahan kimia
3. MM intoksikasi inhalasi gas
4. MM intoksikasi logam berat
5. MM psychotic break
 LI 1
DRUGS INTOXICATION
Acetaminophen intoxication
• Toxic Dose :
• Acute Ingestion : 150-200 mg/kg (children) ; 6-7 g (adult)
• Chronic Toxicity : Daily consumption of supratherapeutic dose (>4-6
g/day) by alcoholic ps
• Hepatic Injury : product of normal metabolism of
acetaminophen by CYP-450 highly toxic (NAPQI)
• Normally NAPQI rapidly detoxified by glutathione in liver cell ->
overdose : NAPQI > glutathione -> liver injury
• Manifestations :
• Asymptomatic, mild gastrointestinal upset (nausea, vomiting)
• elevated aminotransferase levels and hypoprothrombinemia
(24–36 hours)
• fulminant liver failure occurs  hepatic encephalopathy and
death
• Renal failure may also occur
Serum acetaminophen
concentration

 Determine the need

for antidotal therapy
for acute
intoxication:

• >150 µg/mL at 4
hours
• Reduced to 4,7
µg/mL at 24
hours

Rosen’s emergency medicine. 8th ed..

Acetaminophen Intoxication
Chronic ingestion
• Determining whether
the patient is at risk for
hepatotoxicity

• Evaluating the patient

by measuring a serum
acetaminophen
concentration & AST

• Initiating therapy with

NAC, if:
• AST >50 IU/L
• AST < 50 IU/L, but
serum
acetaminophen ↑↑
Treatment
• Liver transplantation for patients with fulminant
hepatic failure
• Antidote acetylcysteine
• glutathione substitute  binding the toxic metabolite as it is
produced
• most effective when given early and should be started within
8–10 hours if possible
Treatment
N-Acetylcysteine  should not be delayed > 8
hours
Tricyclic Antidepressant Intoxication
Tricyclic Antidepressant
Intoxication
• Mechanism of Toxicity :
• Cardiovascular :
• Anticholinergic effect & inhibition of neuronal reuptake of
catecholamine -> tachycardia & mild hypotension
• Peripheral a-adrenergic blockade -> vasodilatation ->
hypotension
• CNS :
• Anticholinergic toxicity (e.g., sedation & coma)
• Seizure – result of inhibition reuptake NE / serotonin in brain
Tricyclic Antidepressant
Intoxication
3 major toxic syndrome :
• Anticholinergic: sedation, delirium, coma, dilated pupil,
dry skin & mucous membrane, diminished sweating,
tachycardia, diminished/absent bowel sound & urinary
retention
• Cardiovascular : abn cardiac conduction, arrhythmias
& hypotension
• Seizure : common in tricyclic antidepressant toxicity ->
recurrent / persistent
• Muscular hypereactivity from seizure + myoclonic jerking +
diminished sweating -> severe hyperthermia ->
rhabdomyolisis, brain damage, multisystem failure & death
Tricyclic Antidepressant
Intoxication
• Diagnosis : suspected in ps with lethargy, coma /
seizure + QRS interval prolongation
• Specific lv : 0.3 mg/L (therapeutic concentration), 1
mg/L (drug + metabolite)
• Treatment :
• Specific drug & antidotes :
• QRS interval prolongation / hypotension -> Sodium Bicarbonate
1-2 mEq/kg IV -> repeat to maintain arterial pH 7.45-7.55
• Phyosphothygmine
• Decontamination :
• Activated Charcoal
Treatment
Opioid Intoxication
Ex: tramadol, oxycodone, methadone, morphine, buprenorphine, and hydrocodone, morphine.
• Stimulation of the μ-receptors  analgesia, sedation, miosis, respiratory depression, cough suppression, euphoria, and
decreased GI motility.
• Stimulation of κ-receptors  weaker analgesia, sedation, miosis, decreased intestinal motility, dysphoria, and
hallucinations.
• Stimulation of the δ-receptors  some analgesia and antidepressant effect.
• All currently available opioid agonists possess μ-receptor activity and result in some degree of respiratory depression.

Clinical features:
• Respiratory and mental status depression
• Analgesia
• Miosis / could be mydriasis
• orthostatic hypotension,
• nausea and vomiting (especially in opioid-naïve patients),
• histamine release resulting in localized urticaria
• bronchospasm,
• ileus secondary to decreased GI motility
• urinary retention secondary to increased vesical sphincter tone.
Diagnosis:
• Coma
• Miosis
• Respiratory depression / <12x/min
• Auscultatory finding : pulmo edema
• PP : Qualitative urine opioid screen, specific urine assay

Treatment :
- Airway protection and Ventilatory maintainance  bag-valve mask ventilatory support
- After ensured adequate ventilation  naloxone
- Activated charcoal 1 g/kg PO  if opioid ingestion occured within the hour

• Naloxone-responsive injection drug users with presumed heroin intoxication  can be safely
discharged 1 to 2 hours after administration of naloxone if they have independent mobility, oxygen
saturation on room air >92%, respiratory rate >10 breaths/min, pulse rate >50 beats/min, normal
temperature, and a Glasgow coma scale score of 15.
• If exposure to opioids other than heroin  observation period of 4 to 6 hours in the ED is
recommended after the last naloxone administration.
• In long-acting opioid overdose  observation should be extended for a minimum of 8 hours.
Treatment
• Breathing support,
including oxygen, or a tube
that goes through the
mouth into the lungs and
attachment to a breathing
machine
• Intravenous (IV, through a
vein) fluids
• Medicine called naloxone
(Evzio, Narcan) to block the
effect of the opioid on the
central nervous system
(such medicine is called a
narcotic antagonist)
Digoxin Intoxication
Clinical features
• May be asymptomatic
• May produce
dysrhythmias or
conduction block
• Non-cardiac
symptoms

Diagnosis
• Serum digoxin level
(steady-state serum),
in 6-8 hrs
Management
• Digoxin-specific Fab (DigiFab)
• In life threatening dysrhythmias:
• 10 vials (acute ingestion),
administer within 30 mins
• 4-6 vials (chronic ingestion)
• 20 vials (in cardiac arrest)
• Based on the amount ingested,
or
• Based on serum digoxin
concentration
• Electrolyte correction
• Maintenance of serum
potassium level
• Atropine 1 mg IV (adults) for severe
bradycardia & AV block
• Phenytoin & lidocain
Cocaine, Methamphetamine, And
Other Stimulants
• Cocaine and methamphetamine induce euphoria
• Symptoms of sympathomimetic overdose 
hypertension, tachycardia, diaphoresis, and
agitation.
• Complications  dysrhythmias, myocardial
ischemia, aortic rupture, aortic and coronary artery
dissection, seizures, intracranial hemorrhage,
hyperthermia, rhabdomyolysis, and acute renal
failure, which can be life threatening
• “Cocaine chest pain”  with electrocardiographic
changes and hemodynamic complications or with mild
tachycardia and chest discomfort
• Cocaine abuse during pregnancy  spontaneous
abortion, abruptio placentae, fetal prematurity, and
intrauterine growth retardation
• Crack cocaine use  bronchospasm, pneumonitis,
pulmonary hemorrhage, pulmonary edema, and
barotrauma
• Intestinal ischemia, bowel necrosis, ischemic colitis,
gastrointestinal bleeding, and bowel perforation may
result
• Methamphetamine toxicity  hyperthermia,
dysrhythmias, seizures, and hypertension that
results in intracranial infarction or hemorrhage and
encephalopathy
• Stimulants, such as ephedrine and
methylphenidate, produce toxic effects similar to
those of cocaine and amphetamines.
• Ephedrine has been linked to significant
cardiovascular and neurologic toxicities, psychosis,
severe hypertension, and death.
Diagnosis
• Urine drug screening for cocaine is reliable and can
detect exposure within 72 hours.
• Urine screens for amphetamines are less specific and
have high false negative and false positive results.
• Additional laboratory evaluation  a complete
metabolic panel to assess acid/base status and creatine
kinase (CK) to assess for rhabdomyolysis
• The evaluation of altered mental status  a head CT to
exclude intracranial hemorrhage.
• Chest pain  ECG, chest radiograph, and cardiac
enzymes in cocaine- or amphetamine-intoxicated
Treatment
Salicylates Intoxication
Aspirin and other salicylates
(Pediatric)
Rapidly become acidotic and are consequently more
likely to suffer the severe central nervous system
effects of toxicity. Salicylate overdose can be complex
to manage
• Give activated charcoal if available, If charcoal is
not available and a severely toxic dose has been
ingested, perform gastric lavage or induce vomiting,
as above

WHO 2013 pocket book of hospital care for children

• Give IV sodium bicarbonate at 1 mmol/kg over 4 h to
correct acidosis and to raise the pH of the urine above
7.5 so that salicylate excretion is increased.
• Give oral supplementary potassium too (2–5 mmol/kg
per day in three or four divided doses). Monitor urine
pH hourly.
• Give IV fl uids at maintenance requirements unless the
child shows signs of dehydration, in which case give
adequate rehydration
• Monitor blood glucose every 6 h, and correct as
necessary
• Give vitamin K at 10 mg IM or IV.

WHO 2013 pocket book of hospital care for children

 LI 2.
CHEMICAL AGENTS INTOXICATION
Insecticides
• Organophosphorus insecticides include diazinon,
acephate, maalthion, parathion, and chlorpyrofos.
• Most patients become symptomatic within 8 hours
of dermal exposure, though some fat-soluble
agents (eg, fenthion) can cause delayed symptoms
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e
Herbicides
• Herbicides are agents used to kill weeds
Rodenticides
• The most commonly used rodenticides are
superwarfarins, including bordifacoum, diphenacoum,
and bormadoline
• Coagulopathy typically develops within 48 hours and
lasts for weeks to months due to the long half-lives of
these agents
• Acute intentional or repeated ingestions  delayed
hemorrhage, including hematuria, gastrointestinal
hemorrhage, or epistaxis
• Diagnosis  screening for toxic effect can be
performed with an INR obtained 24 to 48 hours after
ingestion
Treatment
• If the INR is elevated (> 2), then start oral vitamin
K1 , typically at doses of 20 milligrams a day in
adults (1 to 5 milligrams for children) and continue
for up to 10 months.
• Acute hemorrhage requires more aggressive
therapy with fresh frozen plasma, IV vitamin K1,
and addition of prothrombin complex or
recombinant activated factor VII for refractory
hemorrhage
Methanol
• Methanol (methyl alcohol; CAS 67-
56-1; H3COH) is a clear, volatile,
colorless, slightly sweet-tasting
alcohol at room temperature.
•  cleaning solutions, adhesives,
enamels, stains, dyes, and paint
removers. windshield wiping fluid,
antifreeze (particularly brake line
antifreeze), embalming fluid, and
fuel for camp stoves.

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e

Methanol
• rapidly absorbed from the gastrointestinal (GI) tract;
half-life of 5 minutes, and reaches peak concentration
in 30 to 60 minutes.
• its metabolism results in toxic metabolites, in particular
formic acid, which dissociates into formate and
hydrogen ions  acidosis.
• Formic acid uniquely targets the optic disk of the retina
and retrolaminar optic nerve, potentially due to the
high amount of blood and cerebrospinal fluid (CSF) flow
through the choriocapillaris.
• The basal ganglia and subcortical white matter are
affected by formic acid in a similar manner to the
ocular toxicity.

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e

Clinical Features
• Abdominal discomfort and vomiting occur from mucosal
irritation, and patients can develop acute pancreatitis.
• As formic acid accumulates, the most characteristic feature
is some degree of visual disturbance, including seeing spots
with blurred vision (such as in a snowstorm), altered visual
fields, and blindness.
• As acidosis progresses, a compensatory tachypnea develops.
Acidosis can be profound, with many patients presenting
with an arterial pH less than 7 (high mortality rate) and
serum bicarbonate level less than10 mEq/L.
• Patients that survive the acute toxicity of methanol can have
permanent complications, including blindness and
neurologic deficits.

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e
Rosen’s Emergency Medicine Concepts and Clinical Practice 9e
Ethylene Glycol
• Ethylene glycol (ethane-1,2-diol, CAS 107-21-1,
C2H6O2) is a colorless, odorless, sweet-tasting
liquid. It is a common component of antifreeze and
de-icing solutions because it lowers the freezing
point of water.
• Ethylene glycol is rapidly absorbed from the GI
tract; peak blood levels occur within 1 to 4 hours
after ingestion.
• Highly water-soluble and, unlike methanol or
isopropanol, is not volatile at room temperature.
Clinical Features
• The acute neurologic stage occurs over 30 minutes
to 12 hours after ingestion with EG, producing
inebriation and euphoria similar to ethanol.
• The cardiopulmonary stage occurs 12 to 24 hours
after ingestion, with patients developing
tachycardia with a severe metabolic acidosis and
compensatory tachypnea
• The renal stage occurs 24 to 72 hours postingestion
with the development of acute renal failure (ARF)
from calcium oxalate crystal deposition.
 LI 3.
INHALED TOXINS
 Carbon Monoxide

• CO interacts with deoxyhemoglobin to form COHb, which cannot carry

oxygen  Hemoglobin binds CO tightly and forms a complex that is only
slowly reversible.
• CO shifts the oxyhemoglobin dissociation curve to the left in such a way
that even if oxygen is bound to hemoglobin, its unloading to tissues is
impaired
• In muscle, CO binds myoglobin, preventing its normal function  a
traumatic rhabdomyolysis.
• CO, similar to cyanide, inhibits the final cytochrome complex involved in
mitochondrial oxidative phosphorylation. This results in a switch to
anaerobic metabolism and ultimately in cellular death.

Rosen's Emergency Medicine-Concepts and Clinical Practice 9th Ed

Clinical Features :
• Altered mental status, coma and
seizures
• Extremely abnormal vital signs,
hypotension and cardiac arrest; and
metabolic acidosis
• Mild CO poisoning  headache,
nausea, vomiting, dizziness,
myalgia, and confusion
• Delayed neurologic  neurologic
syndromes (eg, focal deficits and
seizures) psychiatric or cognitive
findings (eg, apathy and memory
deficits).
• Risk factors that predict the
development of delayed neurologic
sequelae include extremes of age
and loss of consciousness
Rosen's Emergency Medicine-Concepts and Clinical Practice 9th Ed
Diagnostic Testing :
• History and Physical examination
• Co-oximetry
Management :
• First  the half-life of COHb is
inversely related to the Po₂  it can
be reduced from approximately 5
hours on room air to 1 hour
byproviding supplemental 100%
oxygen. HBO therapy (at 3 ATA)
further reduces the half-life to
approximately 30 minutes
• Second  a sufficient Po2 can be
achieved with HBO to sustain life in
the absence of adequately
functioning hemoglobin, but this is
helpful only when the COHb is
extremely elevated.
 Simultaneous Carbon Monoxide and
Cyanide Poisoning (Fire Victims) :
• Nitrite-induced methemoglobinemia,
 reduces the tissue oxygen delivery,
may be detrimental to patients with
elevated COHb levels or otherwise
impaired oxygen delivery.
• Sodium thiosulfate, administered
without nitrites, or hydroxocobalamin
 should be given to all smoke
inhalation victims with coma,
hypotension, severe acidosis, or
cardiovascular collapse in whom
cyanide poisoning cannot be rapidly
excluded.

Rosen's Emergency Medicine-Concepts and Clinical Practice 9th Ed

Clinical Emergency Medicine. LANGE
Clinical Emergency Medicine. LANGE
 LI 4.
HEAVY METALS INTOXICATION
Metals toxicity
• Metals are chemical elements that possess three
general properties: (1) they are a good conductor of
heat and electricity, (2) they are able to form cations,
and (3) they can combine with nonmetals through ionic
bonds.
• In clinical toxicology, the following metals, noted in
ascending atomic weight, are usually considered under
the concept of “heavy” or “toxic” metal poisoning:
beryllium, vanadium, cadmium, barium, osmium,
mercury, thallium, and lead, with lead and mercury
being the metals most clinically significant concerning
human poisoning.
Metalloid toxicity
• Metalloids are chemical elements with properties
intermediate to those of metals and nonmetals,
metalloids tend to have these two general
properties: (1) they are semiconductors of
electricity, and (2) they form amphoteric oxides.
• Boron, silicon, germanium, arsenic, antimony, tellurium,
and polonium; arsenic is the most clinically significant
metalloid.
• Because of their effects on numerous enzymatic
systems in the body, the metals and metalloids
often present with protean manifestations
primarily affecting five systems:
• Neurologic, cardiovascular, GI, hematologic, and renal.
Lead
• Exposure to lead can occur from
inhalation or ingestion, and both inor
ganic and organic forms of lead
produce clinical toxicity
• In the CNS, the toxic effects of lead
include:
• Injuries to astrocytes, with secondary
damage to the microvasculature and
resultant disruption of the bloodbrain
barrier, cerebral edema, and increased
intracranial pressure
• Decreases in cyclic adenosine
monophosphate and protein
phosphorylation, which contribute to
memory and learning deficits
• Alteration with calcium homeostasis,
which leads to spontaneous and
uncontrolled neurotransmitter release.
• In the peripheral nervous system,
lead causes primary segmental
demyelination, followed by
secondary axonal degeneration,
mostly of the motor nerves
• In the cardiovascular system, small
but statistically significant increases
in the prevalence of hypertension
and atherosclerotic vascular disease
are found in individuals with
elevated blood lead levels.
• In the hematopoietic system, lead
interferes with porphyrin metabo-
lism, which may contribute to lead-
induced anemia.
Lead
• In the kidney, lead affects • Lead induced adverse
the proximal tubule, effects on the reproductive
producing Fanconi’s system include increased
syndrome with fetal wastage, premature
aminoaciduria, glycosuria, rupture of membranes,
phosphaturia, and renal depressed sperm counts,
tubular acidosis abnormal or non-motile
• Lead adversely affects sperm, and sterility.
osteoblast and osteoclast
function in bone. With
chronic lead exposure,
increased calcium
deposition at growth plates
may be seen as “lead lines”
on radiographs of long
bones.
Lead
Lead diagnose
• 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.
• Abdominal radiographs may show radiopaque material
in the GI tract.
• The abdominal pains of lead toxicity can mimic sickle
cell crisis, the hepatic porphyrias, and even
appendicitis. Chronic lead toxicity can mimic major
depression, hypothyroidism, polyneuritis, gout, iron
deficiency anemia, and learning disability.
Arsenic
• Arsenic exists in elemental,
inorganic salts, organic salts, and
gaseous forms. Elemental and
organic forms have little to no
toxicity, whereas inorganic
compounds, including arsenite
(trivalent or As3+) and arsenate
(pentavalent or As5+), are highly
toxic
• Arsenic is well absorbed by GI,
respiratory, and parenteral routes
and may be absorbed through
nonintact skin.
• 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. Inhaled arsine
attaches to sulfhydryl groups of
hemoglobin, producing an acute
hemolytic anemia with resulting
jaundice, abdominal pain, and
hemoglobinuria induced acute
renal failure
Arsenic diagnose
• An abdominal radiograph may demonstrate intestinal
radiopaque metallic flecks in cases of arsenic ingestions.
• The ECG often reveals a prolonged QT interval, especially in
subacute poisoning.
• The CBC may reveal a normocytic, normochromic, or
megaloblastic anemia, and/or a thrombocytopenia.
• The WBC count may be elevated in acute toxicity and
decreased in chronic toxicity
• Definitive diagnosis of acute poisoning depends on finding
elevated arsenic levels in a 24-hour urine collection
• Normal urinary arsenic level is below 50 micrograms/L (0.67
micromol/L), and total urinary arsenic excretion in an
unexposed patient typically does not exceed 100
micrograms/d (1.3 micromol/d)
 Mercury
• Mercury occurs in inorganic and
organic forms. Inorganic mercury
compounds are subdivided into
elemental mercury (quicksilver),
mercurous (Hg+) salts
(mercurous chloride or calomel),
and mercuric (Hg2+) salts
cinnabar or mercuric sulfide).
Organic mercurials exist as short
and long chained alkyl and aryl
compounds
• The short chained alkyls, such as
methyl mercury and ethyl
mercury, are more toxic to
humans, with dimethyl mercury
being lethal in small amounts.
• Elemental mercury is absorbed
primarily by vapor inhalation.
Elemental mercury can be
absorbed dermally.
• Inorganic mercury salts are
absorbed primarily through the
GI tract, but they may also be
absorbed across intact skin.
Mercury salts do not enter the
CNS in consequential amounts
nor do they cross the placenta.
• Organic mercury compounds are
also primarily absorbed by the GI
tract. The highly lipid soluble
short chained alkyls easily cross
membranes, accumulating in red
blood cells, the CNS, liver, kidney,
and fetus.
• Longer-chained alkyl and the aryl
compounds are biotransformed
into inorganic mercuric ions in
the body
• The short-chained alkyl
compounds are excreted
primarily in the bile, where they
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 and may produce
symptoms of acetylcholine deficiency.
• Mercuric salts produce proximal renal tubular
necrosis.
Clinical features mercury
• 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.
• In severe cases, patients may
develop acute lung injury
and severe respiratory
distress
• Inorganic Mercury Mercury with
abdominal pain often associated
with a characteristic graying of
the oral mucosa and metallic
taste. Shock and cardiovascular
collapse may rapidly ensue.
Acute kidney injury results from
both direct toxicity of the
mercury ions and from decreased
renal perfusion due to shock.
• 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. Hallmarks
of chronic neurologic toxicity
include tremor, neurasthenia,
and erethism.
Clinical features mercury
• Organic Mercury The short-chained alkyl
compounds, methyl, dimethyl, and ethyl mercury,
have the most devastating effects on the CNS. After
a latent period of weeks to months, orofacial
paresthesias are a common initial symptom:
• Headache, tremor, and fatigue. In severe cases, patients
may develop ataxia, muscle rigidity and spasticity,
blindness, hearing deficits, and dementia
Mercury diagnose
• 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 .
Conclusions and suggestions
• The differential diagnosis of this patients:
 A 25-year old female: kerosene intoxication,
organophospate intoxication, alcohol intoxication, drugs
intoxication
A 70 year old male: drugs intoxication (warfarin, digoxin,
and acetaminophen)
• We suggest the patient to do more supporting
examination
• Do the initial treatment for acute poisoning
(stabilize the patients, decontamination, and give
antidotes)
References
• WHO 2013 pocket book of hospital care for children
• Rosen’s Emergency Medicine Concepts and Clinical Practice 9e
• Tintinalli’s Emergency Medicine 8th Edition
• Clinical Emergency Medicine. LANGE