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 containers
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)
Doesnt 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

contd

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 life = 60 min
Small children ingest crack shock ALTE
passive inhal./breast milk seizure

Cocaine / Crack

contd

blocks reuptake of neurotransmitters

on presyn, nerves (Accumulation of Epi,
Nor, Dopa, Serot)
and is a fast Na channel blocker
(prolongs QRS) (lidocaine, blocker,
procainamide, propranolol, quinidine,
carbamazepine, doxepin)

Cocaine / Crack, Clinical

CNS: mood elevation, exhilaration,
hallucination, movement disorder, tremor,
hyper , 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 -blocker (antagonize
cocaine 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

contd

Bradyarrhytmia / Hypotension
Pulm-edema, GI mobility CNS
(coma, syncope)
Immediate
Delayed (slow release)

Ca-Channel Blockers Treatment

contd

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

-Adrenergic Blockers
Compete with sympathetic (Epi, Nor) neurot.
At receptor sites
(1 Cardiac, renal adipose
2 Lower airway, vessels, GI)
intracellular CAMP (brady, contractility)
release of Ca from endo retriculum
( conduction)

-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

-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

-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 g/hr (2.5mg 100mg)
Dm cough syrup
Methadone (long life)
Clonidine (central 2 agonist)

OPIOD OD

contd

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 life
Now. GO-SLOW. GO-LOW
(1)

OPIOD OD, Treatment

contd

Naloxone (0.1 mg/kg up to 2 mg for 2 hours)

short 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, - 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.