UPDATES IN TOXICOLOGY: Critical Appraisal and updates of Interventions in the ED
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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

Objectives Interventions in the ED

  • 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 destroying the natural workings of a victim’s physiology

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) destroying the natural workings of a victim’s physiology& 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.

Level of evidence clinical toxicology
Level of evidence & Clinical destroying the natural workings of a victim’s physiologyToxicology

Clinical pathway basic toxicologic interventions
Clinical Pathway: destroying the natural workings of a victim’s physiology 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 destroying the natural workings of a victim’s physiology

  • 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

  • Diagnostics/Labs destroying the natural workings of a victim’s physiology

  • 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

Antidotes destroying the natural workings of a victim’s physiology

Disposition destroying the natural workings of a victim’s physiology

Toxicology updates

TOXICOLOGY UPDATES: destroying the natural workings of a victim’s physiology

Initial approach to Critically poisoned patient

Approach to critically ill patients
Approach to critically ill patients destroying the natural workings of a victim’s physiology


  • 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

toxidromes ingestion

A clinical syndrome – a constellation of signs , symptoms, and laboratory findings – suggestive of the effects of a specific toxin.

Toxidrome approach
Toxidrome ingestion Approach:

THINK! Toxidrome Approach:

Toxidromes cardiovascular and central nervous system
Toxidromes ingestion: cardiovascular and Central Nervous System

hypotension ingestion


Beta blockers


  • Intravenous fluids


    • Peripheral vasodilation

    • Epinephrine for myocardial depressants



Digoxin specific antibodies

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

Arrythmias ingestion

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 ingestion

  • 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 ingestion

  • 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 ingestion :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 ingestion


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 ingestionBlockers: 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 ingestion

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 ingestionBlockers: 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 ingestion


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 ingestion

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 ingestion

  • 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 ingestion

  • 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 ingestionderivaties

  • 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 ingestion

  • 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 ingestion

  • 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 ingestion

  • (+) 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 ingestion

  • 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

management ingestion

  • 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 ingestion

  • 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 ingestion: 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)