Emergency
Medicine in
Toxicology
Basics
Definitions
A poison is any substance that can cause
illness or death when it is absorbed into the
body.
An antidote is a substance that acts against a
poison to offset its effects.
Prevention: most accidental poisonings can
be prevented if the presence of poisons is
recognized and proper care is takenin their
use and storage.
Poisioning may be acute or chronic
Signs and symptoms vary widely and are
dependent about the quantity and
route of of administered poison
Types of poisons:
• Ingested poisons
• Inhaled poisons
• Absorbed posions
• Injected poisons
Acute poisonings
• Aimed (suicides)
• Accidental
– Self-treatment
– Misuse of chemicals and drugs
• At home
• In medicine
Acute poisoning may occur despite all
reasonable precautions and when it
does, act quikly but do not panic.
Four basic facts should be known to
give appropriate first aid for poisoning.
Four basic steps:
• Identify the poisonous substance. Look for bottles, pills,
containers or remnants of poisonous material, even vomitus,
that can be used to identify the toxic agent.
• Determine the quantity taken. Estimate, from the container’s
size, the number of pills or amount of chemical available and,
from remaining chemical or pills, how much of poisonous
substance may have been taken.
• Determine the route of entry into the body. First aid will
vary according to whether the substance was ingested into the
stomach, inhaled into lungs, absorbed through the skin, injected
into the bloodstream, or taken by combination of two or more
of these.
• Determine the time elapsed since the poisoning occurred
Intoxication with drugs
Every drug is poison if used in too high quantities.
• Trankvillisators, antidepressants
• Cardiovascular drugs
• Paracetamol, etc.
Try to identify
• The poisonous substance
• Quantity taken
• Rout of entry into body
• Time elapsed since appearance of symptoms
First aid
• Unresponsive patient – recovery position
• Concious patient – induce vomiting
“Restaurant method”
Patient is concious and clear-mind, provokes itself the
reflex of vomiting and is able to control the airways
Drink water and vomit
Never induce vomiting if victim has swallowed corrosive
chemicals.
Emergency ward
management
Decontamination:
Toxic inhalation:
Air – skin decontamination = useful
Dermal (insecticide, organophosphate)
(protocol for rescuer themselves)
Gastro-intestinal
Decontamination
(ipecac, charcoal, bowel irrigation) not
shown to change the outcome, follow
regional poison center:
(National: 800-222-1222)
Investigations
Always check blood glucose.
Send blood & urine for toxicology screening.
ALWAYS measure paracetamol & salicylate
levels
Failure to diagnose & treat is negligent.
U&Es, LFTs, glucose, ABG, clotting, bicarbonate
ECG, CXR
Specific blood levels
Management
Supportive
Correct hypoxia, hypotension, dehydration, hypohyperthermia, and acidosis
Control seizures
Monitor
TPR, BP, ECG, Oxygenation, GCS
General
↓ Absorption
↑ Elimination
Specific antidotes
↓ Absorption
Gastric lavage
Only if within 1 hour & life-threatening
amount
Never for corrosives
If ↓ LOC intubate
Activated charcoal
50 g single or repeated dose (↑ elimination)
Doesn’t bind heavy metals, ethanol, acids
↑ Elimination
Multiple dose activated charcoal
Quinine, phenobarbitone
Charcoal haemoperfusion
Barbiturates, theophylline
Diuresis (fluids!, furosemide)
Urinary alkalinization
Dialysis
CVVHDF
Continuous VenoVeno-Venous Hemodiafiltration
Dialysate
Access
Fluid removal
Solute removal
(small and larger
solutes)
Return
Replacement
Diffusion
S
Convection
Effluent
Syrup of Ipecac ???
Within 30 min of ingestion
For low risk substance
In alert, responsive victim
Activate Charcoal
Absorbs numerous drugs
↓ the bioavailability by
70% within 30 minutes of ingestion
30% within 60 minutes of ingestion
Activated Charcoal
cont’d
1 gm/kg up to 1 year
25 – 50 gm 1 – 12 years
If stable airway, with protective reflex
Contraindicated if no bowel sound
(TCA – Ca blocker – Opiate)
Gastric Lavage
Complication – hypoxia – pneumothorax
– GI perforation
Symptoms and
treatment
Carbon monoxide intoxication
Moderate headache initially
Disturbancies of consiousness
(…unconsiousness)
Vomiting
Death if not rescued
Treatment
Oxygen
Mechanical Ventilation
Cardiovascular system`s support
Hyperbaric chamber
Blood transfusion
Cocaine / Crack
1/3 fatal injury in young adults
Absorbs from mucous mbr, IV – onset 1-2
minutes ½ life = 60 min
Small children ingest crack → shock “ALTE”
passive inhal./breast milk → seizure
Cocaine / Crack
cont’d
→ blocks reuptake of neurotransmitters
on presyn, nerves (Accumulation of Epi,
Nor, Dopa, Serot)
→ and is a fast Na channel blocker
(prolongs QRS) (lidocaine, ß blocker,
procainamide, propranolol, quinidine,
carbamazepine, doxepin)
Cocaine / Crack, Clinical
CNS: mood elevation, exhilaration,
hallucination, movement disorder, tremor,
hyper θ, mydriasis
Resp.CV: Hypertension, ACS (Acute
Coronary Syndrome) ↑ 02 demand, coronary
artery const. Myocardial infarction, chest
pain. Prolonged QRS, QT, VT, VF
Platelets: Aggregation, activation
Cocaine / Crack Treatment
AW, V, O2
ECG monit (troponin)
Benzodiazepine (no
phenothiazine)
“MONA” greets all
patients: Morphine,
O2, Nitroglycerin
0.2 – 0.5 mcg/kg/min
Phentolamine
0.05 mg/kg
ASA / Heparin
Na H CO3 1 – 2 mcg/Kg
No ß-blocker (antagonize
cocaine ß adrenergic
stimulation and
vasodilation)
Ca – Channel Blockers
Affect transmembrane, and intracellular
movement of Ca
↓ Conduction in slow channel (SA, AV node)
↓ Myocardial excit contract
↓ Vascular smooth muscle tone
Ca – Channel Blockers
cont’d
Bradyarrhytmia / Hypotension
Pulm-edema, ↓ GI mobility – CNS
(coma, syncope)
Immediate
Delayed (slow release)
Ca-Channel Blockers Treatment
cont’d
AW – V – O2
ECG monit
Vascular access
(treat shock)
N/S small bolus
5-10 ml/kg
High dose Epi/Nor
CaCl 10% 20mg/kg,
infusion, monitor Ca++
Insulin/Glucose (0.5 g/kg)
0.1u/kg – Glucagon 0.050.1mg/kg bolus, infusion
01.mg/kg/hr
Cardiac pacing, ECMO
Isopro/Abropine/Dopamin
e Amrinore
ß-Adrenergic Blockers
Compete with sympathetic (Epi, Nor) neurot.
At receptor sites
(ß1 Cardiac, renal adipose
ß2 Lower airway, vessels, GI)
↓ intracellular CAMP (brady, ↓ contractility)
↓ release of Ca from endo retriculum
(↓ conduction)
ß-BlockerCardio-Vasc Toxicity
Propranolol-atenolol-metroprolol = 90%
Bradycardia, hypotension
Prolonged PR, QRS, block
Intravent conduction defect
Acebutolol → torsade de pointe, VF- asystole
Na blocking effect (propan. – sotalol)
Prolonged QRS - QT
ß-Blocker, Clinical
CNS=altered mental status, seizures,coma
(2o to hypoperfusion, high lipid solubility (propranolol)
CV/ECG
- Brady – hypot
- Prolonged QRS, QT – block
- arrhythmia
- ↓ contractility
Resp bronchospasm
Hypoglycemia
ß-Blocker Treatment
AW, O2, V
ECG monitor
Vascular Access (Treat shock)
* Epinephrine infusion – high dose
* Glucagon 0.05 to 0.1 mg/kg up to 1
mg (∅ phenol)
* Glucose / insulin
* Nabic
* Ca?
* Cardiac pacing - ECMO
OPIOD OD
Recreational
Analgesic
Morphine, codeine, hydrocodone, fentanyl
patch 25-100 µg/hr (2.5mg – 100mg)
Dm cough syrup
Methadone (long ½ life)
Clonidine (central ą2 agonist)
OPIOD OD
cont’d
Respiratory depression-apnea-non
cardiogenic pulm edema (inhibition of
medulla receptors)
Coma, seizure (meperidone)
Miosis pin-point)
Hypotension-brady/tacky-cardiac arrest
GI delay
Potentiated by benzodiazepine-alcohol
(glutamate-GABA neurotransm)
Drug / Coma / Miosis
88% narcotics
72% phenothiazine
35% ethanol
31% barbiturate
Heroin - symptoms
Small eye pupils
Coma
Stop of breathing
Signs of needle sticks
Ecstazy - symptoms
Restless
Difficult, fast speech
Fever up to 41
Disturbancies of conciuousness
Seizures
Amphethamine - symptoms
•
•
•
•
•
Hyperactivity, restless,insomnia
Fast, disturbed, speech
Disturbancies of consiousness
Seizures
Pulse is fast, high blood pressure
OPIOD OD, Treatment
AW – V – O2 (Correct CO2)
ECG monitoring (treat arrhythmia)
Vascular Access (treat shock)
Naloxone (0.1 mg/kg up to 2 mg for 2
hours) – short ½ life
Now. GO-SLOW. GO-LOW
(1)
OPIOD OD, Treatment
cont’d
Naloxone (0.1 mg/kg up to 2 mg for 2 hours) –
short ½ life
Now. GO-SLOW. GO-LOW
(1) Normaliza pCO2 (to prevent ↑ epinephrine)
(2) 0.01 mg/kg up to 0.4 mg Naloxone
IM, SC, IV, ET
Narcan drip 6-48 hrs (if methadone OD) watch for
cyclical emesis, coma, hypo/hypertension, pupil
dilation, pulm edema, arrhythmia
Paracetamol Overdose
Most common drug taken in overdose
Few symptoms or early signs
As little as 12g can be fatal
Hepatic and renal toxin
Centrolobular necrosis
More toxic if liver enzymes induced or
reduced ability to conjugate toxin
Paracetamol Metabolism
Management
General measures including
U&Es, LFTs, glucose, clotting ABG, bicarbonate,
paracetamol and salicylate levels
Activated charcoal
<8 hours
Take level after four hours
Start N-aceylcysteine if above treatment line
Patients are usually declared fit for discharge from
medical care on completion of its administration.
However, check INR, creatinine and ALT before
discharge. Patients should be advised to return to
hospital if vomiting or abdominal pain develop or
recur
Management 2
>8 hours
Urgent action required because the efficacy of
NAC declines progressively from 8 hours after the
overdose
Therefore, if > 150mg/kg or > 12g (whichever is
the smaller) has been ingested, start NAC
immediately, without waiting for the result of the
plasma paracetamol concentration
>24 hours
Still benefit from starting NAC
Treatment Graph
N-acetylcysteine
Supplies glutathione
Dosage for NAC infusion - ADULT
(1) 150mg/kg IV infusion in 200ml 5% dextrose
over 15 minutes, then
(2) 50mg/kg IV infusion in 500ml 5% dextrose
over 4 hours, then
(3) 100mg/kg IV infusion in 1000ml 5% dextrose
over 16 hours
Side-effects
Flushing, hypotension, wheezing, anaphylactoid
reaction
Alternative is methionine PO (<12 hours)
Aspirin Overdose
Early features
hyperventilation, sweating, tremor, tinnitus,
nausea / vomiting, or hyperpyrexia
Metabolic features
Hypo- or hyper-glycaemia, hypokalaemia,
respiratory alkalosis, metabolic acidosis
Others
renal failure, pulmonary oedema, seizures, coma,
death
Management
General measures
Bloods
Salicylate (paracetamol) level >2 hours, and after
2hrs
>700 potentially lethal
>500 moderate-severe poisoning
U&Es, glucose, ABG, bicarbonate
Activated charcoal
Rehydrate, monitor glucose, correct acidosis and
K+
If levels >500mg/L alkalanize urine (HCO3-)
Levels > 700 mg/L before rehydration, renal
failure or pulmonary oedema consider
haemodialysis
Tricyclic Antidepressant
(and other Na+ blocker)
“TCA” (Three C, A, coma, convulsion+++,
cardiac arrhythmia, acidosis)
Na blocker
* Propranolol, sotalol
* Procain, quinidine
* Lidocaine / cocaine
* Antiarrhythmic
* Benadryl - doxepin
2 Effects
•Anticholinergic (mad as a hatter, red as a beet,
blind as a bat, hot as a hare, dry as a bone)
•Na blocker – quinide like on myocardium K blocker
First anticholin effect → CNS stim – agitation,
confusion, hallucination. Seizure, θ↑ - coma
CV – sinus tacky, then wide complex QRS >0.1. Sec,
brady, block, VF ↑ wave lead a VR > 3mm
RESP: Pulm edema
TCAs -Introduction
Potentially fatal (2.5 to 3.5g of amitriptyline)
Neurological and cardiac problems common
Toxicity due to anticholinergic actions, and direct
quinidine-like effect on the myocardium
Serious toxicity results from:Ventricular dysrhythmias
Seizures
Hypotension
Respiratory depression
Initial symptoms at presentation may be
trivial, and most major problems occur within
6hrs
TCAs-Features of poisoning
Peripheral
Sinus tachycardia, hot dry skin, dry mouth, urinary
retention, hypotension and hypothermia may
occur
CNS
Dilated pupils, ataxia, nystagmus, squint, ↓LOC,
coma, seizures, respiratory depression, ↑tone, ↑
↓reflexes, ↑ plantars
ECG
prolonged PR and QRS interval, ↑ QT
ventricular dysrhythmias
TCAs -Management
GCS and QRS, best indicators of toxicity
Supportive
do not use flumazenil if benzo taken
Check airway, maintain ventilation, correct
hypoxia
Check ABG, if ↑ CO2 requires ventilation
Correct hypotension (crystalloids)
Gastric lavage if within 1 hr, and activated
charcoal
Rx fits and agitation with diazepam
Rewarm slowly if hypothermic
Close monitoring for 24hrs
Tricyclic Antidepressant,
Treatment
AW, V, O2
ECG monitor
Vascular Access (Shock) – Epin
Nabic: 1 meq/kg/bolus inusion (ph7.45-7.5)
Benzodiazepine – no physostigmine
no phenytoin
Anticholinergic: Mydriasis
Antihistamine
Antiparkinson
Belladone
Jimson weed
Carbamazepine - phenothiazine
TCAs- Dysrhythmias
Carful ECG monitoring is required
QRS interval is a guide to cardiac toxicity
(>100ms)
Avoid antidysrhythmic drugs. They may make
matters worse
Correct hypoxia and acidosis. Aim for a pH of
7.45-7.50 (no higher)
use iv boluses of sodium bicarbonate
Sodium loading may also help
Prolonged CPR may be of use
Tricyclic OD – Initial ECG
Tricyclic OD – Recovery ECG
Benzodiazepine Overdose
Deaths from poisoning with benzodiazepines alone are
rare, but may be lethal in combination with other CNS
depressants
Treatment is supportive and aimed at maintaining
adequate ventilation whilst supporting cardiovascular
depression
Benzodiazepine Overdose
Flumazenil (specific benzodiazepine antidote)
is not licensed (in the UK) for routine use in
benzodiazepine overdoses
Flumazenil may induce seizures; particularly
dangerous where tricyclic antidepressants
have been taken
Flumazenil, may however, be used in the
differential diagnosis of unclear cases of
multiple overdoses but expert advice is
ESSENTIAL.