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Transcript
DRUG THERAPY OF
ACUTE POISONING
Two of the most dreaded and insidous
mushrooms found in Swedish forests: the
hepatoxic Amanita virosa and the nephrotoxic
Cortinarius speciocissimus
Acute Poisoning in the Emergency
Department
Common - 3-5% of ED attendances
 2000 Deaths per year
 Some of the highest rates of deliberate
poisoning in Europe
 Often multiple drugs
 DON’T FORGET ALCOHOL !!
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Poisoning
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Poisoning can be defined as a chemical injury to body
organs or a chemically induced disturbance of the
functions in biological systems. Such toxic effects may
follow the exposure to exogenous (environmental)
substances. By tradition an agent has been considered
as a poison if it may damage the organism in a very
small dose. The toxic properties of a certain poison are
often specific, and hence the clinical symptoms after
exposure to a poison may be quite characteristic.
Substances that normally are considered as harmless
may also, if the dose is big enough, cause deleterious
effects and thereby act as poisons. Examples of this are
sodium chloride, oxygen and water.
The science devoted to the study of the structures,
effects and fate of poisonous substances is called
toxicology. This is nowadays a wide, heterogeneous and
rapidly expanding discipline. Clinical toxicology is a
subentity that deals with problems related to poisonings
in humans and their treatment.
Biological poisoning


Acute poisoning is exposure to a poison on one occasion
or during a short period of time. Symptoms develop in
close relation to the exposure. Absorption of a poison is
necessary for systemic poisoning. In contrast,
substances that destroy tissue but do not absorb, such
as lye, are classified as corrosives rather than poisons.
Chronic poisoning is long-term repeated or continuous
exposure to a poison where symptoms do not occur
immediately or after each exposure. The patient
gradually becomes ill, or becomes ill after a long latent
period. Chronic poisoning most commonly occurs
following exposure to poisons that bioaccumulate such
as mercury and lead.
Types of poisoning

Deliberate:
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Overdose as self-harm or suicide attempt
Child abuse ± Munchausen's syndrome by proxy
Third party (attempted homicide, terrorist, warfare)
Accidental:
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Most episodes of paediatric poisoning.
Dosage error:
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Recreational use
Environmental:
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Iatrogenic
Patient error
Plants
Food
Venomous stings/bites
Industrial exposures
General Management
A (Airway)
 B (Breathing)
 C (Circulation)
 D (Disability-AVPU/ Glasgow Coma Scale)
 DEFG ( Don’t ever forget the Glucose)
 GET A SET OF BASIC OBSERVATIONS

For effective management of an acutely poisoned
victim, five complementary steps are required:
1. Resuscitation and initial stabilization
2. Diagnosis of type of poision
3. Nonspecific therapy
4. Specific therapy
5. Supportive care
Resuscitation

Airway:


Open, suction, maintain and intubate as
necessary.
Breathing:
Assess work and effectiveness of ventilation.
 Give oxygen ±assisted ventilation (avoid
mouth-to-mouth).
 Respiratory depression - consider opiates,
benzodiazepines, early salicylate poisoning.
 Tachypnoea - consider metabolic acidosis e.g.
salicylates, methanol.

Resuscitation (cont’d)

Circulation:
Attach a cardiac monitor, assess pulse, blood
pressure and perfusion. Establish intravenous
access.
 Tachycardia/irregular pulse - consider
overdose of salbutamol, antimuscarinics,
tricyclics, quinine, phenothiazine, chloral
hydrate, cardiac glycosides, amfetamines,
and theophylline poisoning.
 If hypotensive consider giving fluid bolus
(colloid) or, if necessary, inotropes.

Resuscitation (cont’d)

Disability:

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
Assess consciousness level (Glasgow Coma Scale).
Coma may suggest benzodiazepines, alcohol, opiates, tricyclics,
or barbiturates.
Check pupils and eye movements:
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Large - consider anticholinergics, sympathomimetics, tricyclics.
Small - consider opiates or cholinergics.
If opiates suspected give 0.8-2 mg naloxone iv/im every 2-3mins up
to 10 mg until response (children: 10 mcg/kg iv/im repeated up to
0.2 mg/kg), repeated doses may be required thereafter as it has a
shorter half-life than most opiates.
Unreactive - causes include barbiturates, carbon monoxide,
hydrogen sulphide, cyanide/cyanogens, head injury/hypoxia.
Unequal - slight variation can be normal - but consider head injury.
Strabismus - can be seen with carbamazepine overdose.
Papilloedema - associated with methanol, carbon monoxide and
glutethimide.
Nystagmus - seen with CNS acting agents e.g. phenytoin.
Resuscitation (cont’d)
 Disability:

Check blood glucose - if hypoglycaemic give 50
ml 50% dextrose iv (children: 5 ml/kg of 10%
dextrose iv).



Hyperglycaemia - organophosphates, theophyllines,
MAOIs or salicylate.
Hypoglycaemia - insulin, oral hypoglycaemics, alcohol
or salicylate.
Seizures - if prolonged/recurrent initially give
diazepam 5-10 mg iv (Child: 0.25-0.4 mg/kg iv or
pr) or midazolam (0.15 mg/kg) IM/IV. Many drugs
can induce seizures including tricyclics,
theophylline, opiates, cocaine and amfetamines.
History
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What was taken, how much, when, and by what
route?
Was alcohol consumed too?
Any vomiting since ingestion?
Past medical history, current medications and
allergies.
Was a suicide note left?
Is the patient pregnant?
Histories from others including: family, friends,
paramedics, police and observers.
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General
examination
Directed cardiovascular, respiratory, abdominal and
neurological examination.
Vital signs, pupils etc. mentioned in Resuscitation
section above.
Temperature - hypothermia (phenothiazines,
barbiturates, or tricyclics) or hyperthermia (amfetamines,
ecstasy, MAOIs, cocaine, antimuscarinics, theophylline,
serotonin syndrome).
Muscle rigidity (ecstasy, amfetamines).
Skin - cyanosis (methaemoglobinaemia), very pink
(carboxyhaemoglobinaemia, cyanide, hydrogen
sulphide), blisters (barbiturates, TCAs,
benzodiazepines), needle tracks, hot/flushed
(anticholinergics).
Breath - ketones (diabetic/alcoholic ketoacidosis), "bitter
almonds" (cyanide), "garlic-like" (organophosphates,
arsenic), "rotten eggs" (hydrogen sulphide), organic
solvents.
Mouth - perioral acneiform lesions (solvent abuse), dry
mouth (anticholinergics), hypersalivation
(parasympathomimetics).
Investigations
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12 lead electrocardiogram.
U+E, lab glucose, anion gap ± lactate & osmolal gap.
LFT & clotting
Arterial blood gases.
Drug levels (at appropriate interval: paracetamol,
salicylates; others: theophylline, digoxin, lithium, antiepileptics if it was likely that they had been taken).
Comprehensive toxicology screens not normally
indicated in the emergency treatment.
Carboxyhaemoglobin levels if carbon monoxide
poisoning suspected.
Urinalysis - rhabdomyolysis, save sample for possible
toxicological analysis.
CXR if pulmonary oedema/aspiration suspected.
CT brain may be needed to exclude other causes of
alterations in conscious level.
Laboratory Investigations :
A few simple bedside tests are helpful in diagnosing the
chemical ingested. A pinkish colour of urine occurs in
phenothiazine intoxication, as well as in myoglobinuria
and haemoglobinuria. Chocolatecoloured blood is
indicative of methaemoglobinaemia.
Presence of oxalate crystals in urine is typical of ethylene
glycol ingestion. Ketonuria without any metabolic change
occurs in isopropyl alcohol and acetone intoxication
while ketonuria
with metabolic acidosis is suggestive of salicylate
poisoning.
Abdominal X-ray may be useful in diagnosing certain
radiopaque toxins which include chloral hydrate, heavy
metals, iron, iodides, phenothiazines, sustained-release
preparations and solvents (chloroform, carbon
tetrachloride). However, one must not exclude a
poisoning on the basis of absence of radiopaque density
on X-ray.
Treatment

Initial management
Initial management for all poisonings includes ensuring
adequate cardiopulmonary function and providing
treatment for any symptoms such as seizures, shock,
and pain.
Poisons that have been injected (e.g. from the sting of
poisonous animals) can be treated by binding the
affected body part with a pressure bandage and by
placing the affected body part in hot water (with a
temperature of 50°C). The pressure bandage makes
sure the poison is not pumped troughout the body and
the hot water breaks down the poison. This treatment
however only works with poisons that are composed of
protein-molecules.[5]
Treatment

Decontamination if appropriate:
Avoid contaminating yourself and wear protective
clothing.
 Ensure area is well-ventilated.
 The patient should remove soiled clothing and wash
him/herself if possible.
 Put soiled clothing in a sealed container.
 Wash all contaminated skin/hair with liberal amounts
of warm water ±soap.
Decontamination may be achieved using activated
charcoal, gastric lavage, whole bowel irrigation, or
nasogastric aspiration. Routine use of emetics (syrup
of Ipecac), cathartics or laxatives are no longer
recommended.

Treatment (cont’d)

Decrease absorption:

Gastric emptying - this is contraindicated if the airway
is unprotected or overdose of corrosives or
hydrocarbons taken. Complications include pulmonary
aspiration and oesophageal perforation. Only 30% of
gastric contents are returned and it is proven to be
effective if within 1 hour of ingestion (so this is only
generally done if patients present early having taken a
potentially fatal dose of drug). Controversially this is
sometimes extended if delayed gastric emptying (e.g.
presence of coma or overdose of tricyclics or
salicylates) is thought likely.
Emesis - no longer recommended.
 Gastric lavage - Place patient in left lateral head down (20°)
position, insert large (36-40F) bore tube (children: 16 to 28F)
into stomach. Remove contents with sequential administration
and aspiration of small (200-300 ml) quantities of warm water
or saline (children: 10-20 ml/kg preferably saline). Alternatively
the stomach contents can just be aspirated.

Treatment (cont’d)

Activated charcoal is the treatment of
choice to prevent absorption of the poison.
It is usually administered when the patient
is in the emergency room or by a trained
emergency healthcare provider such as a
Paramedic or EMT. However, charcoal is
ineffective against metals such as sodium,
potassium, and lithium, and alcohols and
glycols; it is also not recommended for
ingestion of corrosive chemicals such as
acids and alkalis.
Treatment (cont’d)

Whole bowel irrigation cleanses the bowel, this
is achieved by giving the patient large amounts
of a polyethylene glycol solution. The osmotically
balanced polyethylene glycol solution is not
absorbed into the body, having the effect of
flushing out the entire gastrointestinal tract. Its
major uses are following ingestion of sustained
release drugs, toxins that are not absorbed by
activated charcoal (i.e. lithium, iron), and for the
removal of ingested packets of drugs (body
packing/smuggling)
Treatment (cont’d)
o Nasogastric aspiration involves the placement of a
tube via the nose down into the stomach, the stomach
contents are then removed via suction. This
procedure is mainly used for liquid ingestions where
activated charcoal is ineffective, e.g. ethylene glycol
poisoning.
o Cathartics were postulated to decrease absorption by
increasing the expulsion of the poison from the
gastrointestinal tract. There are two types of
cathartics used in poisoned patients; saline cathartics
(sodium sulfate, magnesium citrate, magnesium
sulfate) and saccharide cathartics (sorbitol). They do
not appear to improve patient outcome and are no
longer recommended
Enhanced excretion
 In some situations elimination of the
poison can be enhanced using diuresis,
hemodialysis, hemoperfusion, hyperbaric
medicine, peritoneal dialysis, exchange
transfusion or chelation. However, this
may actually worsen the poisoning in
some cases, so it should always be
verified based on what substances are
involved.
Increase elimination:

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Forced diuresis - no longer recommended.
Haemoperfusion and acid/alkaline diuresis - rarely
used now.
Haemodialysis - severe salicylate, ethylene glycol,
methanol, lithium, phenobarbital and chlorate
poisonings.
Multiple doses of activated charcoal - interrupts
enterohepatic or enteroenteric recirculation. Use 50g
4-hourly (children 1g/kg) or 12.5g hourly (children
0.25g/kg) to reduce vomiting, but beware severe
constipation, fluid depletion and avoid repeating
cathartic agent doses within 24hrs. Used with
carbamazepine, dapsone, phenobarbital, quinine,
salicylate, colchicine, dextropropoxyphene, digoxin,
verapamil and theophylline overdoses.
Specific Therapy
If the toxin can be identified, specific therapy
using antidotes should be administered:
Paracetamol
(acetaminophen)
N-acetylcysteine
vitamin K anticoagulants, e.g.
warfarin
vitamin K
opioids
naloxone
iron (and other heavy
metals)
benzodiazepines
desferrioxamine, Deferasirox
or Deferiprone
Organophosphates
Atropine and
flumazenil
SUPPORTIVE THERAPY
Since the antidotes are available only for a few toxins,
treatment of most cases of poisoning is largely
supportive
The aim is to preserve the vital organ functions till
poison is eliminated from the body and the patient
resumes normal physiological functions. Therefore,
functions of central nervous system, cardiopulmonary system
and renal system should be supported with proper care for coma,
seizures, hypotension, arrhythmias, hypoxia, and
acute renal failure. The fluid, electrolyte and acidbase status
should be closely monitored in all patients.
Prevention
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Adult education.
Double-check dosage before administration.
Vigilance by health professionals to recognise
the early signs of abuse and potential suicide.
Put all medicines and household chemicals in a
locked child-proof cupboard >1.5 metres off the
ground.
Safely dispose of medicines, chemicals which
are not needed or out of date.
Keep all medicines and chemicals in their
original containers with clear label