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Briefly discuss a rational ED approach to
poisoning patients
Assess level of evidence of toxicologic
interventions to provide rational ED
management
Updates on management of specific
xenobiotics requiring critical care at ED
Poisoning has been likened to trauma on the
cellular level, destroying the natural workings of a
victim’s physiology
Vanden Hoek et al (2010) Circulation:
http://circ.ahajournals.org
Emergency Department Intervention of acute
poisoning: 90% of cases in a nutshell
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Gastrointestinal decontamination
techniques
Investigations
Antidotes
Increasing Elimination
Disposition
10% Immediate care: BLS and
Acute cardiac life support
The evidence for recommendations :
I: Definitely recommended.
Definitive, excellent evidence provides
support.
II: Acceptable and useful. Good
evidence provides support.
III: May be acceptable,
possibly useful. Fair-to-good evidence
provides support.
Indeterminate: Continuing area of
research.
Determine the need for lavage or
charcoal
 Serious overdose presenting to the
ED within one hour?
 Potentially serious overdose
presenting to ED after one hour?
 Determine whether toxin is
adsorbed to charcoal
 Routine administration in nontoxic
ingestion is not indicated
Determine the need for whole bowel
irrigation:
• Large ingestion of iron, heavy metals,
lithium and other drugs poorly
adsorbed by activated charcoal
• Drug packets (body packers)
Suicide attempt
•
•
•
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Gather lavage if life-threatening
overdose within one hour of ED arrival
(carries risk of aspiration , esophageal
perforation) Class Interderminate
Activated Charcoal 1 g/kg or 10:1 ratio
of charcoal to toxin (Class II)
MDAC: Antimalarials, Aminophylline,
Barbiturates, Beta Blockers (Class II-III)
Polyethelene glycol (1-2L in adults, 25
cc/kg in children orally by NG Tube
(Class III)
Determine suicide risk (Class I-II)
Restrain as needed (Class II)
Drug levels
ECG?
Yes, if
Yes, if
Xray ?
• Cardiotoxin ingestion (known or
potential
• Chest pain or shortness of breath
• Abnormal heart rate or hypotension
• Any unstable patient (Class II)
Chest x-ray (Class I-II)
• Dyspnea , tachynea, coma, or
obtundation
• Cyanosis
• Symptomatic patients who ingest:
opiods, phenobarbital, phenothiazines
and salicylates
KUB – suspected metals or drug packets
(Class II)
Enteric coated preparations
Cocaine /opiate packets
Arsenic other heavy metals
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Diagnostics/Labs
Abnormal vital signs
Altered mental status
Symptomatic patients and unknown
toxin
Ingestion of substance that can
produce metabolic acidosis
Toxic alcohol?
Cyanosis or respiratory distress
Suspected rhabdomyolysis
Female of childbearing age
CBG
Electrolytes
Serum osmolality, anion gap
ABG
CPK
Pregnancy test, urinalysis
Yes, if
TOXICOLOGY SCREEN?
Yes, if
Need for antidote?
Yes, if
Dialysis?
Yes, if
Toxicology Screen
Qualitative/Quantitative:
plasma drug concentrations of :
o Paracetamol
o
Salicylates
:Symptomatic
patient with
o Iron of (Class II)
ingestion
Isopropanol
o Lithium
Specific
Agents
Salicylates
o Ethylene
glycol
Theophylline
Uremia
o MEDICOLEGAL PURPOSES
Methanol
Barbiturates, beta blockers
Lithium
Ethylene Glycol
AGENT
paracetamol
Anticholinergics
benzodiazepines
Beta blockers
carbamates
digoxin
Ethylene glycol
ANTIDOTES
N-Acetylcysteine
Physostigmine
Flumazenil
Glucagon
Atropint
AGENT
ANTIDOTES
iron
Deferoxamine
Isoniazid
Pyridoxine
metals
BAL, EDTA, DMSA
Nitrates/nitrites
Methylene blue
opiates
Naloxone,
nalmeferne
Fab Fragments
organophosphates Atropine,
pralidoxime
Ethanol, fomefizole snales
Antivenin,crofab
TOXICOLOGY UPDATES:
Caveats:
 Patients may not be able to provide acute
history of exposure to a toxic substance
 In cases of suicide attempts, multiple
substance exposure
 Comprehensive toxicology laboratory testing
is never available on time
Basic life support and ACLS current standards
should be followed, except for toxin-specific
interventions recommended once with ROSC
 Hypotension
 Arrhythmia
 seizures
A clinical syndrome – a
constellation of signs ,
symptoms, and laboratory
findings – suggestive of the
effects of a specific toxin.
THINK!
Toxidrome
Approach:
Tachycardia/
hypertention
Bradycardia/
hypotention
Cardiac
conduction delays
(wide QRS)
• Amphetamines* anticholinergic
drugs*antihistamines*cocaine*theophylline/caffeine
• Beta blockers/calcium channel blockers; clonidine,
digoxin, and related glycosides, organophosphates and
carbamates
• Cocaine/ tricyclic antidepressants, local anethetics,
antiarrythmics (quinidine, flecanide)
seizures
• Cyclic antidepressants;isoniazid; selective
and nonselective norepinephrine
reuptake inhibitors; withdrawal states
CNS or
respiratory
depression
• Antidepressants, benzodiazepines,
carbon monoxide, ethanol, methanol,
opiods, oral hypoglycemics
Metabolic
acidosis
• Cyanide, ethylene glycol, metformin,
methanol and salicylates
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Intravenous fluids
NOREPINEPHRINE
 Peripheral vasodilation
Opioids
Beta blockers
digoxin
 Epinephrine for
myocardial depressants
Greene et al (2005) Postgrad Med J; 81:204216
Naloxone
Glucagon
Digoxin specific
antibodies
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Anti arrythmics :
 not first line agents
 Proarrythmics
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Electrical Cardioversion
 May produce asystole in a
poisoned myocardium
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Correction of:
Acidosis
Hypokalemia
Hypomagnesemia
Hypoxia
Immediate antidotal
therapy
Watch out for :
 conduction delays (widened
QRS)
 Torsade de pointes
Greene et al (2005) Postgrad
Med J; 81:204-216
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Benzodiazepines as first
line agents
Agitation: avoid
phenothiazines or
butyrophenones
Resistant seizures:
 General anesthetics: IV
barbiturates
 Supportive care
(intubation and
mechanical ventilation)
Caveats:
NO PHENYTOIN
for: TCAs and
cocaine
•has sodium
channel blocking
properties
 Benzodiazepines (BZD) exert their action by
potentiating the activity of Gamma-aminobutyric acid
(GABA) is the major inhibitory neurotransmitter in the
CNS
 Flumazenil as an antidote
 Evidence: administration of flumazenil to patients
with undifferentiated coma confers risk and is not
recommended (Class III, LOE B) : seizures,
hypotension and arrhythmia with TCAs
 Indication: reversal of excessive sedation during
procedural sedation
Lheureux P, Vranckx M, Leduc D, Askenasi R. Flumazenil in mixed benzodiazepine/tricyclic antidepressant overdose: a placebo-controlled study in the dog. Am J
Emerg Med. 1992;10:184 –188.
Pitetti RD, Singh S, Pierce MC. Safe and efficacious use of procedural sedation and analgesia by nonanesthesiologists in a pediatric emergency
department. Arch Pediatr Adolesc Med. 2003;157:1090 –109
β-Blockers: myocardial membrane-stabilizing
activity >>> QRS widening and decreased
myocardial contractility
 Cardiovascular complications of B-blocker
toxicity: include hypotension, bradycardia, AV
blocks of different degrees, and CHF with or
without pulmonary edema.
 Most common: propranolol
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 seizure is highest with propranolol, particularly when
the QRS complex is > 100 ms
Beta Blockers
Glucagon
Drug of choice for -blocker (& CCB) O.D.
• Secreted by pancreas secondary to hypoglycemia
• Glucagon Receptors found in heart muscle
• Acts by stimulating adenylate cyclase.
 independent of -receptor
glucagon
-blocker
+
Glucagon
receptor
Beta Blockers: Glucagon
The final outcome:
 positive chronotropic and inotropic effects despite
-adrenergic blockade.
 Onset within minutes, peak levels in 5-7 minutes,
duration of action of 10-15 minutes.
Beta Blockers
Glucagon - precautions
1. Diluent contains 2 mg/ml phenol as preservative
i.
ii.
Max 10-h dose of phenol = 50 mg = 5mg glucagon
Use sterile water instead of diluent
2. Side effects from glucagon include:
i. dose-dependent nausea and vomiting 
aspiration
ii. hyperglycemia, hypokalemia (not clinically
important)
iii. Some Reports of treatment failure
Beta Blockers: Insulin
Insulin??
Shown to have positive inotropic effects
on animal and human myocardium
Kerns, et al. Ann Em Medicine. 1997. 29:748-757
24 dogs, anesthetized and infused with propanol.
Hemodynamics before & after treatment with:
i.
ii.
iii.
iv.
Normal Saline (n=6)
Insulin (4IU/min) + glucose PRN (n=6)
Glucagon (50 ug/kg) + infusion (n=6)
Epinephrine (1ug/kg/min) + titrated (n=6)
Beta Blockers
Results:
6/6 Controls died within 150 min
5/6 Epinephrine animals died after 240 min
2/6 Glucagon animals died “
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“
0/6 Insulin animals died “
“
“
Kaplan-Meier Survival Curve
Insulin vs. Glucagon (p<0.05)
Insulin vs. Epinephrine (p<0.02)
Beta Blockers
Insulin in Acute Beta Blocker OD.
Pathophysiology ?:
1. May enhance catecholamine release
2. May enhance myocardial substrate use
In normal myocardium, FFA are preferred
substrate. In poisoned myocardium, glucose becomes 1o
substrate
3. May increase cytosolic calcium
Supportive therapy : activated charcoal for
decontamination; combinations of fluid resuscitation,
vasopressor agents, atropine, transvenous pacing
Specific antidotes:
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glucagon bolus of 3 to 10 mgadministered slowly over 3 to
5 minutes, followed by an infusionof 3 to 5 mg/h (0.05 to
0.15 mg/kg followed by an infusion of 0.05 to 0.10 mg/kg per
hour) (Class IIb, LOE C)
 high-dose IV insulin, accompanied by IV dextrose
supplementation (Class IIb,LOE C)
 Other: Calcium, 0.3 mEq/kg of calcium (0.6 mL/kg of 10%
calcium gluconate solution or 0.2 mL/kg of 10% calcium
chloride solution) IV over 5 to 10 minutes,followed by an
infusion of 0.3 mEq/kg per hour.
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hypotension and bradycardia
extended-release (ER) formulations can result in
delayed onset of arrhythmias, shock, sudden
cardiac collapse, and bowel ischemia.
 Treatment:
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 IV insulin/Dextrose
 Calcium (Calcium chloride (1-4 g IV; preferably via central line; (30 mL)
of 10% calcium gluconate can be administered IV over 10-15 minutes
in adults. Boluses may be repeated every 15-20 minutes for a total of 3
doses)
Haddad LM. Resuscitation after nifedipine overdose exclusively with intravenous calcium chloride. Am J
Emerg Med. Oct 1996;14(6):602-3
Hung YM, Olson KR. Acute amlodipine overdose treated by high dose intravenous calcium in a patient with
severe renal insufficiency. ClinToxicol (Phila). 2007;45(3):301-3
Arrhythmia, hypertension, acute coronary syndrome
HX: Onset and duration of symptoms depend on route
of administration, dose, and patient
tolerance
 Clinical Presentation
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 Central Nervous System: agitation, psychosis, AMS etc
 Cardiovascular: ACS (6% ), hypertension, hyperthermia
 Acute Pulmonary Syndrome: y dyspnea, diffuse infiltrates,
and hemoptysis
Can act as a Vaughan-Williams class Ic antiarrhythmic,
producing wide-complex tachycardia through several
mechanisms, including blockade of cardiac sodium channels
>>> Wide complex tachycardia
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Methamphetamine – MDAC
Ascorbic acid no longer recommended
Cocaine related ACS
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Diagnosis of cocaine related MI is difficult as 84% of patients
with cocaine related chest pain have abnormal ECGs
 Half of all cocaine users have increased creatinine kinase
concentrations in the absence of myocardial infarction
 Troponin concentrations are more sensitive and specific
 Pathophysiology: sympathomimetic action of cocaine
produces an increase in myocardial oxygen demand and
direct cocaine induced coronary artery vasospasm
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Benzodiazepines (lorazepam, diazepam),
calcium channel blockers (verapamil),
morphine, and sublingual nitroglycerin (Class
IIb, LOE B)
Aspirin for Cocaine ACS ; Lidocaine?
Supportive: rapid cooling measures
Caveats: phentolamine can be used but not
propranolol, labetalol ineffective ( Class IIb,
LOE C)
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(+) Wide complex tachycardia
Sodium bicarbonate 1 mL/ kg (cocaine) IV as a
bolus, repeated as needed until
hemodynamic stability is restored and
QRS duration is < 120 ms
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cyanide can be found in jewelry cleaners,
electroplating solutions; fire smoke
Joint DOH-DENR Advisory: Series of 2010001 on reporting of cases to DOH-FDA
Clinical Manifestations:
 causes rapid cardiovascular collapse, which
manifests as hypotension, lactic acidosis, central
apnea, and seizures
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Enhancement of body’s natural mechanisms for dealing
with cyanide:
i. oxygen
ii. Sodium thiosulphate
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Cyanide will also bind to methaemoglobin formed after
administration of:
i. Amyl nitrite;
ii. Sodium nitrite, or;
iii. 4-dimethylaminophenol
(4-DMAP)
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Cobalt containing drugs:
i.
ii.
Hydroxocobalamin, or
Dicobalt edetate.
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Approach using evidenced based toxicologic
interventions and supportive care guided by
expert referrals on intervention and
disposition from poison control centers
Consider the toxidromes
In critical care situations utilize standard
AHA/ECC guidelines for BLS and ACLS
 Consider exceptions among severely poisoned
individuals with exposure to specific toxic agents
UP PGH NPMCC:
02-5218451 loc 2311
Department of Health:
East Avenue Medical Center: (02) 4342511
Rizal Medical Center: (02) 5241078
Batangas Regional Medical Center: (043) 7233578
“Give a man a fish, and he can eat for a
day. But teach a man how to fish, and
he’ll be dead of mercury poisoning
inside of three years.”
—Charlie Haas (1889-1964)