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Prepared by : Dr.Mohamed Shekhani . References: Davidson PP of Medicine .

Poisoning introduction 2012

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Page 1: Poisoning introduction 2012

Prepared by:

Dr.Mohamed Shekhani.

References: Davidson PP of Medicine.

Page 2: Poisoning introduction 2012

Introduction:• Poisoning is a major cause of death in young adults& 10% of hospital

admissions.• Most deaths occur before patients reach medical attention&

mortality is much <1% in those admitted to hospital.• In developed countries, the most frequent cause is intentional drug

overdose in the context of self-harm& usually involves prescribed or ‘over-the-counter’ OTC medicines.

• Accidental poisoning is also common, esp in children& elderly.• Toxicity also may occur as a result of alcohol or recreational

substance use, or following occupational or enviro exposure. • In developing countries household /agricultural products such as

pesticides/ herbicides are common sources of poisoning &associated with a much higher case fatality.

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General approach:Triage/resuscitation:

• Those seriously poisoned must be identified early so that appropriate management is not delayed.

• Vital signs: • Identifying the poison(s) by obtaining adequate information.• Prevent reattempt by identifying those at risk.• Those with external contamination with chemical or environmental

toxins should undergo appropriate decontamination. • Critically ill patients must be resuscitated.• (GCS) is commonly employed to assess conscious level or AVPU

(alert/verbal/painful/unresponsive).

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General approach:Triage/resuscitation:

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• An (ECG) should be performed & cardiac monitoring instituted in all patients with CV features or where exposure to potentially cardiotoxic substances is suspected.

• Those who need antidotes given according to weight.• Substances that are unlikely to be toxic in humans should be

identified so that inappropriate admission & intervention are avoided

General approach: Triage/resuscitation:

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General approach: Triage/resuscitation:

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General approach: Triage/resuscitation:

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Clinical assessment:• History &examination . • Patients may be unaware or confused about what they have

taken, or may exaggerate (or less commonly underestimate) the size of the overdose, &rarely mislead medical staff deliberately.

• Toxic causes of abnormal physical signs SHOULBE BE KNOWN.• Cluster of clinical features (‘toxidrome’) suggestive of poisoning

with a particular drug type IDENTIFIED. • Poisoning is a common cause of coma, especially in younger people,

but it is important to exclude other potential causes, unless the aetiology is certain.

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• Anticholinergic–Hot As Hades–Blind As A Bat–Dry As A Bone–Red As A Beet–Mad As A Hatter

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Investigations:

• Urea, electrolytes, creatinine should be measured in most patients. • Arterial blood gases should be checked in those with significant

respiratory or circulatory compromise, or when poisoning with substances likely to affect acid–base status is suspected.

• Calculation of anion and osmolar gaps may help to inform diagnosis for a limited number of specific substances.

• Management may be facilitated by measurement of the amount of toxin in the blood.

• Qualitative urine screens or potential toxins including near-patient testing kits have a limited clinical role.

• Occasionally, for medicoegal reasons, it is useful to save blood and urine for subsequent measurement of drug concentrations.

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psychiatric assessment• All patients presenting with deliberate drug overdose should

undergo psychosocial evaluation by a health professional with appropriate training prior to discharge ,once the patient has recovered from any features of poisoning, unless there is an urgent issue such as uncertainty about his or her capacity to decline medical treatment.

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• Patients presenting with eye or skin contamination should undergo appropriate local decontamination procedures.

General management

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Gastrointestinal decontamination• Patients who have ingested potentially life- threatening

quantities of toxins may be considered for GIT decontamination if poisoning has been recent.

• Induction of emesis using ipecacuanha is now never recommended.

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Activated charcoal• Given orally as slurry, activated charcoal absorbs toxins in the

bowel as a result of its large surface area.• If given sufficiently early, it can prevent absorption of an

important proportion of the ingested dose of toxin. • The efficacy decreases with time.• Current guidelines do not advocate use >1 hour after overdose in

most circumstances,EXCEPT when delayed-release preparation has been taken or when gastric emptying may be delayed.

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Activated charcoal• Some toxins do not bind to activated charcoal so it will not affect

their absorption.• In patients with an impaired swallow or a reduced level of

consciousness, the use of activated charcoal, even via a nasogastric tube, carries a risk of aspiration pneumonitis.

• This risk can be reduced but not completely removed by protecting the airway with a cuffed endotracheal tube.

• Multiple doses of oral activated charcoal (50 g every 4 hours) may enhance the elimination of some drugs at any time after poisoning and are recommended for serious poisoning with some substances .

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Activated charcoal• They achieve their effect by interrupting enterohepatic circulation

or by reducing the concentration of free drug in the gut lumen, to the extent that drug diffuses from the blood back into the bowel to be absorbed on to the charcoal: so-called ‘GIT dialysis’. A laxa-tive is generally given with the charcoal to reduce the risk of constipation or intestinal obstruction by charcoal ‘briquette’ formation in the gut lumen.

• Recent evidence suggests that single or multiple doses of activated charcoal do not improve clinical outcomes after poisoning with pesticides or oleander.

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SUBSTANCES NOT BOUND BY CHARCOAL

• Alcohols And Glycols

• Corrosives– Alkalis– Acids

• Cyanide• Saline Cathartics

• Heavy Metals– Iron– Lead– Lithium– Mercury

• Hydrocarbons

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Gastric aspiration & lavage• Gastric aspiration and/or lavage is now very infrequently

indicated in acute poisoning, as it is no more effective than activated charcoal, and complications are common, especially aspiration.

• Use may be justified for life-threatening overdoses of some substances that are not absorbed by activated charcoal

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Whole bowel irrigation• This is occasionally indicated to enhance the elimination of ingested

packets or slow-release tablets that are not absorbed by activated charcoal (e.g. iron, lithium), but use is controversial.

• It is performed by administration of large quantities of polyethylene glycol and electrolyte solution (1–2 L/hr for an adult), often via a nasogastric tube, until the rectal effluent is clear.

• Contraindications include inadequate airway protection, haemodynamic instability, gastrointestinal haemorrhage, obstruction or ileus.

• Whole bowel irrigation does not cause osmotic changes but may precipitate nausea and vomiting, abdominal pain and electrolyte disturbances

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Urinary alkalinisation• Urinary excretion of weak acids& bases is affected by urinary pH, which

changes the extent to which they are ionised. • Highly ionised molecules pass poorly through lipid membranes and

therefore little tubular reabsorption occurs and urinary excretion is increased.

• If the urine is alkalinised (pH > 7.5) by the administration of sodium bicarbonate (e.g. 1.5 L of 1.26% sodium bicar-bonate over 2 hrs), weak acids (e.g. salicylates, methotrexate , herbicides 2,4-dichlorophenoxyacetic acid and mecoprop) are highly ionised and so their uri-nary excretion is enhanced.

• This technique should be distinguished from forced alkaline diuresis, in which large volumes of fluid with diuretic are given in addi-tion to alkalinisation.

• This is no longer used because of the risk of fluid overload.

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Urinary alkalinisation

• Urinary alkalinisation is currently recommended for patients with clinically significant salicylate poi-soning when the criteria for haemodialysis are not met

• It is also sometimes used for poisoning with methotrexate. • Complications include alkalaemia, hypokalaemia, occasionally

alkalotic tetany. • Hypocalcaemia is rare.

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Haemodialysis & haemoperfusion

• These can enhance the elimination of poisons that have a small volume of distribution and a long half-life after overdose, and are useful when the episode of poisoning is sufficiently severe to justify invasive elimination methods.

• The toxin must be small enough to cross the dialy-sis membrane (haemodialysis) or must bind to activated charcoal (haemoperfusion) .

• Haemodialysis may also correct acid–base and metabolic disturbances associated with poisoning

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Antidotes • are available for some poisons and work by a variety of

mechanisms: for example, by specific antago-nism (e.g. isoproterenol for β–blockers), chelation (e.g. desferrioxamine for iron) or reduction (e.g. methylene blue for dapsone).

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Supportive care • For most poisons, antidotes & methods to accelerate elimination

are inappropriate, unavailable or incompletely effective. • Outcome is dependent on appropriate nursing & supportive care,

& on treatment of complications.• Patients should be monitored carefully until the effects of any

toxins have dissipated.

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