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UPDATES IN TOXICOLOGY: Critical Appraisal and updates of Interventions in the ED Cherie Grace G. Quingking,MD. Objectives. Briefly discuss a rational ED approach to poisoning patients Assess level of evidence of toxicologic interventions to provide rational ED management

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UPDATES IN TOXICOLOGY: Critical Appraisal and updates of Interventions in the EDCherie Grace G. Quingking,MD

  • 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

Alteration of function of a cellular receptor, ion channel, organelle, or chemical pathway to the extent that critical organ systems can no longer support life.

VandenHoek et al (2010) Circulation:

general ed management
GENERAL ED Management

Emergency Department Intervention of acute poisoning: 90% of cases in a nutshell

10% Immediate care: BLS and Acute cardiac life support

  • Gastrointestinal decontamination techniques
  • Investigations
  • Antidotes
  • Increasing Elimination
  • Disposition
level of evidence cebm clinical toxicology
Level of evidence (CEBM) & Clinical Toxicology

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.

clinical pathway basic toxicologic interventions
Clinical Pathway: Basic Toxicologic Interventions
  • 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
  • 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 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)

Determine suicide risk (Class I-II)

Restrain as needed (Class II)

Drug levels

Suicide attempt

Yes, if
  • 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

Yes, if

Xray ?

KUB – suspected metals or drug packets (Class II)

Enteric coated preparations

Cocaine /opiate packets

Arsenic other heavy metals

  • 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



Serum osmolality, anion gap



Pregnancy test, urinalysis

Yes, if

  • Toxicology Screen
  • Qualitative/Quantitative: plasma drug concentrations of :
  • Paracetamol
  • Salicylates
  • Iron
  • Lithium
  • Ethylene glycol

:Symptomatic patient with ingestion of (Class II)






Barbiturates, beta blockers


Ethylene Glycol


Yes, if

Specific Agents

Need for antidote?

Yes, if


Yes, if

approach to critically ill patients
Approach to critically ill patients


  • 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
worst case scenario cardiac arrest associated with toxic ingestion
Worst case scenario: cardiac arrest associated with toxic ingestion

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.

toxidrome approach
Toxidrome Approach:

THINK! Toxidrome Approach:



Beta blockers


  • Intravenous fluids
    • Peripheral vasodilation
    • Epinephrine for myocardial depressants



Digoxin specific antibodies

Greene et al (2005) Postgrad Med J; 81:204-216


Correction of:





Immediate antidotal therapy

  • Anti arrythmics:
    • not first line agents
    • Proarrythmics
  • Electrical Cardioversion
    • May produce asystole in a poisoned myocardium
  • Watch out for :
    • conduction delays (widened QRS)
    • Torsade de pointes

Greene et al (2005) Postgrad Med J; 81:204-216

seizures and agitations
Seizures and agitations
  • Caveats:
  • NO PHENYTOIN for: TCAs and cocaine
  • has sodium channel blocking properties
  • Benzodiazepines as first line agents
  • Agitation: avoid phenothiazines or butyrophenones
  • Resistant seizures:
    • General anesthetics: IV barbiturates
    • Supportive care (intubation and mechanical ventilation)
  • 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.

PitettiRD, Singh S, Pierce MC. Safe and efficacious use of procedural sedation and analgesia by nonanesthesiologists in a pediatric emergency

department. Arch PediatrAdolesc Med. 2003;157:1090 –109

antihypertensives blockers
Antihypertensives :β-Blockers
  • 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
    • seizure is highest with propranolol, particularly when the QRS complex is > 100 ms
Beta Blockers


Drug of choice for -blocker (& CCB) O.D.

  • Secreted by pancreas secondary to hypoglycemia
  • Glucagon Receptors found in heart muscle
  • Acts by stimulating adenylatecyclase.
    • independent of -receptor






Beta Blockers: Glucagon
  • The final outcome:
    • positive chronotropic and inotropiceffects despite
    • -adrenergic blockade.
    • Onset within minutes, peak levels in 5-7 minutes, duration of action of 10-15 minutes.
Beta Blockers

Glucagon - precautions

  • Diluent contains 2 mg/ml phenol as preservative
      • Max 10-h dose of phenol = 50 mg = 5mg glucagon
      • Use sterile water instead of diluent
  • Side effects from glucagon include:
      • dose-dependent nausea and vomiting  aspiration
      • hyperglycemia, hypokalemia (not clinically important)
      • Some Reports of treatment failure
Beta Blockers: 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.
  • Hemodynamicsbefore & after treatment with:
  • 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


6/6 Controls died within 150 min

5/6 Epinephrine animals died after 240 min

2/6 Glucagon animals died “ “ “

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 1osubstrate

3. May increase cytosolic calcium

blockers management
:β-Blockers: Management
  • Supportive therapy : activated charcoal for decontamination; combinations of fluid resuscitation, vasopressor agents, atropine, transvenouspacing

Specific antidotes:

    • glucagonbolus of 3 to 10 mgadministeredslowly over 3 to 5 minutes, followed by an infusionof3 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,LOEC)
    • 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,followedby an infusion of 0.3 mEq/kg per hour.
calcium channel blockers
Calcium Channel Blockers
  • hypotension and bradycardia
  • extended-release (ER) formulations can result in delayed onset of arrhythmias, shock, sudden cardiac collapse, and bowel ischemia.
  • Treatment:
    • 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
cocaine and methamphetamine and derivaties
Cocaine and methamphetamine and derivaties
  • Arrhythmia, hypertension, acute coronary syndrome
  • HX: Onset and duration of symptoms depend on route of administration, dose, and patient


  • Clinical Presentation
    • 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

treatment and caveats
Treatment and Caveats
  • Methamphetamine – MDAC
  • Ascorbic acid no longer recommended

Cocaine related ACS

  • 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
treatment and caveats1
Treatment and Caveats
  • 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)

cocaine induced arrhythmia
Cocaine induced Arrhythmia
  • (+) 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

  • cyanide can be found in jewelry cleaners,

electroplating solutions; fire smoke

  • Joint DOH-DENR Advisory: Series of 2010-001 on reporting of cases to DOH-FDA
  • Clinical Manifestations:
    • causes rapid cardiovascular collapse, which manifests as hypotension, lactic acidosis, central apnea, and seizures
  • Enhancement of body’s natural mechanisms for dealing with cyanide:

i. oxygen

  ii. Sodium thiosulphate

  • Cyanide will also bind to methaemoglobin formed after administration of:

i. Amyl nitrite;

ii. Sodium nitrite, or;

iii. 4-dimethylaminophenol


  • Cobalt containing drugs:

i. Hydroxocobalamin, or

ii. Dicobaltedetate.

in summary
In summary
  • 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
hotlines information services
Hotlines: Information Services

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)