Poison g2

Ambo universityDepartment of Medicine

Seminar onApproach to child with poisoning

By

Gelaye Mandefro(C2)

Facilitated by Dr. G

onfa(M.D)

11/15/16 1Approach to child with poisoning

Outline

Introduction

Epidemiology

Approach to poisoned child

Selected poisons:

Drug toxicity(acetaminophen)

Organophosphorous poisoning

Iron Overdose

Management principles of poisoned patient


Introduction

Poison: Any substance (Liquid, Solid or Gas) that is harmful to the body

when Ingested, Inhaled, Injected, or Absorbed through the skin.

Any substance that can harm the body by altering cell structure or functions

Does not include adverse reactions to medications taken correctly.

The majority of poisonings are accidental, especially in the under-5 age group

Intentional overdoses and substance abuse are seen in older children

Poisoning maybe a medical emergency depending on the substance involved.


Intro…

Poison: any agent capable of producing a deleterious response in a

biological system

Toxin: generally refers to toxic substances that are produced by biological

systems such as plants, animals, fungi or bacteria. e.g. zeralanone,

produced by a mold, is a toxin

Toxicant: refers to toxic substances that are produced by or are a by-

product of anthropogenic (human-made) and some times natural activities.

e.g. “dioxin” [2,3,7,8-tetrachlorodibenzop- dioxin (TCDD)], produced

during the combustion of certain chlorinated organic chemicals

Patterns of poisoning

Intentional poisoning: A person taking or giving a substance

with the intention of causing harm, e.g. Suicide and Assault

Unintentional poisoning: If the person taking or giving a

substance did not mean to cause harm, e.g. For recreational

such as in an “Overdose” or Accidentally taken by a toddler

“Undetermined”: When the distinction between intentional

and unintentional is unclear.


Types of Exposure Acute: Exposure < 24 hours

Single: a single or continuous exposure (e.g. carbon monoxide)

Repeated: multiple interrupted exposures where there may be

accumulation (e.g. aspirin overdose)

Chronic: > 24 hours or long-term exposure, for weeks or months (e.g. lead

poisoning)

Acute “on chronic”: Acute exposure against a background of chronic

exposure to the same agent (e.g. organophosphorus pesticide exposure on a

chronically exposed child)

“Hit and run”: Acute exposure leading to delayed effects once the toxicant is

gone (e.g. thalidomide exposure during gestation leading to phocomelia)


Acute Poisoning

Pharmaceuticals: sedatives, analgesics, contraceptives,

cardiovascular drugs

Household products: bleaches, detergents, solvents, kerosene

Cosmetics: perfumes, shampoo, nail products

Substances of abuse: alcohol, tobacco, illicit drugs

Pesticides: insecticides, rodenticides, herbicides

Plants and mushrooms: berries, seeds, leaves

Seafood Poisoning: paralytic shellfish poisoning, fish poisoning

Venomous bites and stings: snake, scorpions, bees, jellyfishes,

spiders11/15/16 7Approach to child with poisoning

Chronic Poisoning

Metals

Lead

Mercury

Pesticides in food or fields

Organophosphates

Carbamates

Warfarins

Organochlorines: Persistent Organic Pollutants (POPs), has potential

developmental neurobehavioral and endocrine effects, e. g. DDT


Factors that contribute to the occurrence of poisoning in children

Developmental stage Gender Child-caring practices Poverty Children with special needs


Epidemiology

Accessibility of the poisoning agent is the single most important

environmental risk factor.

Most drug containers in use in the region are easy to open and do not have

a child lock.

Many pediatric drug preparation are sugar coated or sweetened and may be

mistaken for sweets.

Seasonal variations in poisoning occur.

Illiteracy; unable to follow safety precautions written on the labels of

various drugs and chemicals.

Inadequate labeling of drugs and chemicals increase the risk of poisoning.

Administration of the wrong drug or the wrong dose.


Epidemiology…

Poisoning is the fourth most common cause of accidents in children.

Ages less than 5…accidental.

Ages adolescents…intentional, experimental.

More than 90% of toxic exposures in children occur in the home.

Ingestion is the most common route of poisoning exposure (77% of

cases), with the dermal, inhalation, and ophthalmic routes

accounting for approximately 7.5%, 6%, and 5% of cases,

respectively.

Approximately 50% of cases involve nondrug substances, such as

common household products (cosmetics, personal care items,

cleaning solutions, plants, foreign bodies, hydrocarbons).11/15/16 11Approach to child with poisoning

Shannon M. N Engl J Med 2000;342:186-191

Agents Most Commonly Ingested by Children Less Than Six Years of Age, 1995 to 1998


Shannon M. N Engl J Med 2000;342:186-191


Epidemiology…

One year study done in Tikur Anbessa (2007/2008)

Acute poisoning with in one year was 116.

75 male and 41 female.

Mean age 21 years.

96.5% intentional.

Cause of poisoning

43.1% House hold cleaning agents

20.7% Organophosphate

10.3% Phenobarbital

Mortality 8.6%,death occur by organophosphate and Phenobarbital

poisoning. 11/15/16 14Approach to child with poisoning

Effects of poisoning

The effects of poisoning maybe None, Mild or Severe depending on:

The amount of poison ingested.

The nature of the substance.

The age of the child.

The nutritional status of the child.

The state of the stomach-whether empty or full of food.


Pathophysiology

Toxic substances have seven common major pathophysiologic mechanisms

that may produce symptom

Interfere with the transport or tissue utilization of O2 e.g. CO

Depress or stimulate CNS e.g. MDMA

Affect autonomic nervous system e.g. Organophosphate

Affect the lungs by aspiration e.g. Hydrocarbon

Affect the heart and vasculature myocardial dysfunction e.g.

Antidepressant

Produce local damage e.g. Corrosive

Affect on the liver e.g. Acetaminophen


Approach to the poisoned patient

A detailed history and physical examination serves as the

foundation for a thoughtful differential diagnosis and the formation

of an initial prognosis.

The history and physical examination should not await the

collection of body fluid and the results of a “tox screen.”

Toxicology laboratory analyses, or “screens,” in fact evaluate for

only a small fraction of common pediatric exposures and rarely

make (vs confirm) the diagnosis.


Initial patient evaluation

Identification of the patient and toxic agent.

What? Description of the toxin.

How much? Magnitude of the exposure.

When ?Time of exposure.

Progression of symptoms.

Medical history.


Cont.

Patient historyDescription of Toxins.

Product names (brand, generic, chemical) and ingredients, along with their concentrations, may be obtained from labels.

Several characteristic toxic syndromes, or “toxidromes,” exist for some of the more common exposures and may assist in identifying the offending agent.

Example Increased sympathetic nervous system activity Poison Syndrome Pyrexia Flushing Tachycardia HypertensionAssociated Signs Pupillary constriction Sweating

Cough and decongestant preparations

Amphetamines

Cocaine Possible ToxinEcstasy

Theophylline


Magnitude of Exposure

It is important to attempt to determine as accurately as possible how much

of the substance has been ingested by counting the remaining tablets or

measuring the remaining volume of liquid.

It is better to overestimate than to underestimate.

Estimates can be refined as the patient is assessed over time and initial

laboratory data become available.

Because the toxicity of most agents is dose-related, knowing the age or

weight of the child aids in assessment.

For inhalation, ocular, or dermal exposures, the concentration of the

offending agent and the length of contact time with the material should be

determined, in addition to the time course for associated symptoms to

occur, their progression, and possible resolution.


Time of Exposure.

• For some products, toxic manifestations may be delayed for hr. or

days. Knowing the time lapse between exposure and the onset of

symptoms and/or medical evaluation will markedly influence

decisions about obtaining certain diagnostic testing as well as

therapeutic intervention.

Progression of Symptoms.

• Knowing the nature and progression of symptoms is very helpful for

assessing the need for immediate life support, the prognosis, and the

type of intervention that may be needed.11/15/16 21Approach to child with poisoning

Cont… Medical History

Underlying diseases may make a child more susceptible to the effects

of a toxin.

Concurrent drug therapy may also increase susceptibility because

certain drugs may interact with the toxin.

Pregnancy is a common precipitating factor in adolescent suicide

attempts and can influence the patient evaluation and treatment plan.

At 6 mo of age or younger, it is very unlikely that an infant could

become accidentally exposed to a sufficient quantity of a potentially

harmful product in the absence of other extraneous factors that require

further investigation (social environment).


Signs & Symptoms of Poisoning

Lower level, if any of consciousness.

Altered mood: lethargic, ecstatic,

violent or hostile.

Differed breathing rate.

Increased or lowered heart rate.

Dilated or shrunken pupils

Change of colour around mouth

Cramps

Nausea

Vomiting

Diarrhoea

Vomiting


ODOR

Bitter almonds Cyanide

Acetone Isopropyl alcohol, Methanol, Paraldehyde, Salicylates

Alcohol Ethanol

Wintergreen Methyl Salicylate

Garlic Arsenic, Thallium, Organophosphates

OCULAR SIGNS

Miosis Narcotics (except meperidine), Organophosphates, muscarinic mushrooms, clonidine, phenothiazine's, chloral hydrate, barbiturates (late), PCP

Mydriasis Atropine, alcohol, cocaine, amphetamines, antihistamines, cyclic antidepressants, cyanide, carbon monoxide

Nystagmus Phenytoin, barbiturates, éthanol, carbonmonoxide

Lacrimation Organophosphates, irritant gas or vapors

Retinal hyperemia Methanol

Poor vision Methanol, botulism, carbon monoxide


CUTANEOUS SIGNS

Needle tracks Heroin, PCP, amphetamines

Bullae Carbon monoxide, barbiturates

Dry, hot skin Anticholinergic agents, botulism

Diaphoresis Organophosphates, nitrates, muscarinic mushrooms, aspirin, cocaine

Alopecia Thallium, arsenic, lead, mercury

Erythema Boric acid, mercury, cyanide, anticholinergics

ORAL SIGNS

Salivation Organophosphates, salicylates, corrosives, strychnine

Dry mouth Amphetamines, anticholinergics, antihistamine

Burns Corrosives, oxalate-containing plants

Gum lines Lead, mercury, arsenic

Dysphagia Corrosives, botulism

INTESTINAL SIGNS

Cramps Arsenic, lead, thallium, Organophosphates

Diarrhea Antimicrobials, arsenic, iron, boric acid

Constipation Lead, narcotics, botulism

Hematemesis Aminophylline, corrosives, iron, salicylates11/15/16 25Approach to child with poisoning

CARDIAC SIGNSTachycardia Atropine, aspirin, amphetamines, cocaine, cyclic antidepressants,

theophyllineBradycardia Digitalis, narcotics, mushrooms, clonidine, Organophosphates, β

blockers, calcium channel blockersHypertension Amphetamines, LSD, cocaine, PCPHypotension Phenothiazines, barbiturates, cyclic antidepressants, iron, β blockers,

calcium channel blockersRESPIRATORY SIGNSDepressed respiration Alcohol, narcotics, barbituratesIncreased respiration Amphetamines, aspirin, ethylene glycol, carbon monoxide, cyanidePulmonary edema Hydrocarbons, heroin, Organophosphates, aspirinCNS SIGNSAtaxia Alcohol, antidepressants, barbiturates, anticholinergics, phenytoin,

narcoticsComa Sedatives, narcotics, barbiturates, PCP, Organophosphates, salicylates,

cyanide, carbon monoxide, cyclic antidepressants, leadHyperpyrexia Anticholinergics, quinine, salicylates, LSD, phenothiazine's,

amphetamines, cocaineMuscle fasciculation Organophosphates, theophyllineMuscle rigidity Cyclic antidepressants, PCP, phenothiazines, haloperidolPeripheral neuropathy

Lead, arsenic, mercury, organophosphates11/15/16 26Approach to child with poisoning

Selected poisons


1. 1. Drug toxicity/Acetaminophen Poisoning/Acetaminophen Poisoning/

is the most widely used nonsteroidal anti-inflammatory drug

with potent antipyretic and analgesic actions but with very

weak anti-inflammatory activity

Acetaminophen can be:

Unintentionally ingested by young children

Taken in an intentional overdose by adolescents

Inappropriately dosed in all ages


Acetaminophen toxicity

Results from the formation of a highly reactive intermediate

metabolite, N-acetyl-p-benzoquinone imine (NAPQI)

Acetaminophen metabolism


Acetaminophen toxicity…

In therapeutic use:

Only a small percentage of a dose (approximately 5%) is

metabolized by the hepatic cytochrome P450 enzyme

CYP2E1 to NAPQI, which is then immediately conjugated

with glutathione to form a nontoxic mercapturic acid

conjugate.

In overdose:

Glutathione stores are overwhelmed, and free NAPQI is

able to combine with hepatic macromolecules to produce

hepatocellular damage11/15/16 30Approach to child with poisoning

Acute toxic dose of acetaminophen

The single acute toxic dose of acetaminophen is generally

considered to be >200 mg/kg in children

Supratherapeutic doses ( >75 mg/kg/day for consecutive days)

can lead to hepatic injury or failure in some children

Patients Requiring Management

Acute ingestion of > 200 mg/kg

Ingestion of unknown quantity

Repeated supratherapeutic ingestion of > 100mg/kg/day


Stages of acetaminophen

toxicity

Duration Clinical manifestations

Laboratory findings

Stage 1 Within first 0.5 -24 hr

Anorexia ,Nausea

,Vomiting ,Malaise,

Pallor ,Diaphoresis

Normal except acetaminophen level

Stage 2 Within 24-48 hr Resolution of earlier

symptoms

RUQ abdominal pain

and tenderness

↑↑Bilirubin ,

Prothrombin time

,Hepatic enzymes

Oliguria

Stage 3 Within 72-96 hr Fulminant hepatic

failure

Multisystem organ

failure

Potential death

Peak liver function

abnormalities

Stage 4 Within 4 days – 2 weeks

Clinical recovery precedes histologic recovery

Resolution of liver abnormalities

Clinical & Laboratory manifestations


Ix…

If a toxic ingestion is suspected, a

serum acetaminophen level should

be measured 4 hr after the reported

time of ingestion.

For patients who present to

medical care >4 hr after ingestion,

a stat acetaminophen level should

be obtained.


Ix…

Acetaminophen levels obtained <4 hr

after ingestion are difficult to interpret and

cannot be used to estimate the potential for

toxicity.

Other important baseline labs include :

Hepatic transaminases

Renal function tests

Coagulation parameters


Paracetamol Poisoning…Mgt

Activated charcoal is not useful in liquid ingestions due to rapid absorption

Activated charcoal 1 g/kg may be considered in a cooperative patient seen

within 1 hour of tablet or capsule ingestion.

Serum paracetamol level at (or as soon as possible after) 4 hours post

ingestion determines the need for N-acetyl cysteine (NAC) administration.

Patients who present > 8 hours after a toxic ingestion / symptoms of toxicity

(RUQ pain or tenderness, nausea, vomiting) should be commenced on NAC

immediately.

The decision to continue or cease NAC is then based on the paracetamol

level.






Unknown time of ingestion or a history of chronic supratherapeutic ingestion?

For assessment of such patient, check :

Acetaminophen level

Hepatic transaminases

Coagulation parameters.

If the acetaminophen level is >10 μg /mL,

even with normal liver function tests, this

patient is a candidate to be treated with NAC


Why?

To catch patients in the asymptomatic

phase of toxicity, before hepatotoxicity

develops, because a level of 10 µg/ mL is

potentially toxic at ≥20 hr after ingestion


Paracetamol Poisoning Rx

Initial treatment:

Basic life support (ABCs)

Decontamination with activated charcoal (within 1-2 hr of ingestion)

The antidote for acetaminophen poisoning is N- acetylcysteine (NAC)

( which works primarily via replenishing hepatic glutathione stores )


Treatment…

N- acetylcysteine (NAC)

Most effective when initiated within 8 hr of ingestion

There is no demonstrated benefit to giving NAC before the 4 hr

post-ingestion mark.

NAC is available in oral and intravenous forms

, and both forms are equally efficacious


Treatment…

N- Acetylcysteine (Mucomyst)

Dosage: 140 mg /kg loading ,followed by 70 mg / Kg every 4

hrs. for 17 doses

Route of administration : Oral

Side effects: Nausea ,vomiting

N.B. Most effective if given within 8 hr of ingestion


Treatment…

N- Acetylcysteine (Acetadote)

Dosage: 150 mg /kg over 1 hr ,followed by 50 mg / Kg over 4

hrs. followed by 100 mg /Kg over 16 hrs.

Route of administration : IV

Side effects: Anaphylactoid reactions

(most commonly with loading dose)


What is next?A patient who is being on NAC ,the following lab tests : Transaminases,

synthetic function, and renal function should be followed daily

Patients who develop hepatic failure in spite of NAC therapy may be

candidates for liver transplantation

King’s College criteria

Are used to determine which patients should be referred for consideration of

liver transplant.

These criteria include :

1. Acidosis (pH <7.3) after adequate fluid resuscitation,

2. Coagulopathy (prothrombin time [PT] >100 sec),

3. Renal dysfunction (creatinine >3.4 mg/dL),

4. Hepatic encephalopathy grade III or IV


2. Organophosphate poisoning

Organophosphate (OP) compounds are a diverse group of

chemicals used in both domestic and industrial settings.

Examples of organophosphates include insecticides (malathion,

parathion, dichlorvos, and diazinon)

Worldwide mortality studies report mortality rates from 3-25 %

Mortality rates depend on the type of compound used, amount

ingested, general health of the patient, delay in discovery and

transport, insufficient respiratory management, delay in

intubation, and failure in weaning off ventilatory support.11/15/16 45Approach to child with poisoning

Ops..

Ops are esters of phosphoric acid and its derivatives

comprises a central phosphorus atom P and the characteristic phosphoric( P=O) or thiophosphoric(P=S) bond

The symbol X represent the leaving group, which is replaced by the oxygen of the serine in the AChE active site

The rate of AchE inhibition depends on the leaving group; higher tendency of leaving results in the higher affinity of the inhibitor of the enzyme

11/15/16 Approach to child with poisoning 46

Route of entry:


Pathogenesis:Ops Inactivates acetylcholinesterase by phosphorylation, followed by

accumulation of Ach in the synapses.


Clinical features of organophosphate poisoning Overstimulation of muscarinic receptor

D- diarrhoea & diaphoresis

U- Urinary incontinence

M – Miosis

B – Bradycardia, bronchospasm

E –Emesis

L- Lacrimation

S - Salivation

Overstimulation of Nicotinic receptor

Remember the days of the week!!!!!

Mydriasis

Tachypnea

Weakness

Tachycardia

Fasciculation's

Pediatric patients tend to present with a

predominance of nicotinic symptoms!!!


Investigations

ECG

Oxygen saturation

Blood gas analysis

Renal and hepatic function

Electrolytes

Glucose

Amylase

Urine toxicology


Management of OP Poisoning

Hospitalization/ ICU

1. Initial stabilization

2. Reduction of exposure

3. Administration of specific antidote

4. Supportive treatment

Initial stabilization

Clear airway and

Adequate ventilation because the patient with acute organophosphate

poisoning commonly presents with respiratory distress.

Oxygen- Circulation- iv access


Decontamination

Dermal spills—wash pesticide spills from the patient

with soap and water and remove and discard contaminated clothes,

shoes and any other material made from leather

Gastric lavage—consider for presentations within 1 or 2 hours, when

the airway is protected. A single aspiration of the gastric contents may

be as useful as lavage

Activated charcoal —50 g may be given orally or nasogastrically to

patients who are cooperative or intubated, particularly if they are

admitted within one or two hours or have severe toxicity


Antidotes in the treatment of OP poisoning Atropine- Reverses the muscarinic features.

Oxime- Reactivate cholinesterase and reverses the nicotinic features.

Atropine

Initial dose: 0.5-2 mg IV every 5-10min until atropinization

Continuous infusion (8mg atropine in 100ml NS) at rate of 0.02-

0.08mg/kg/hr (0.25-1.0 ml/kg/hr) with additional 1-5mg bolus

May require about 40-1500mg/day

For at least 5-7days

Watch out for OVER ATROPINIZATION


Target end points for atropine therapy

Clear chest on auscultation with no wheeze

Heart rate> 80/min

Pupils no longer pin point (does not imply that pupils must be

dilated)

Dry axilla

Systolic BP > 80 mm Hg


Pralidoxime An oxime that reactivates phosphorylated cholinesterase

Effects: skeletal-neuromuscular junctions (counteracts weakness,

fasciculation and respiratory depression)

Administration within 48 hours of poison ingestion

IV 1-2gm in 100cc of NS over 30min (at a rate not exceeding

200mg/min), repeat in 1 hour if muscle weakness persist, then at

8-12 hours interval if cholinergic signs recur

Severe case: IV infusion 500mg/hr (max 12gm in 24hours)

Started after maximal atropinization


3. Iron overdose3. Iron overdose

The most common cause of death in toddlers.

Classically taught as having five clinical stages.

Remember prenatal vitamins, supplements, and “natural

products”.

Toxic doses occur at 10-20mg/Kg of elemental iron.

Prenatal vitamins typically contain about 65 mg of

elemental iron.

Children's vitamins contain about 10-18 mg of

elemental iron.11/15/16 56Approach to child with poisoning

Fe toxicity…

Iron has the ability to produce oxygen free radicals under aerobic conditions,

which turns it into a potential harmful component

Free radicals are generated within the cell as part of normal cellular

mechanisms

However, the overproduction of reactive oxygen species (ROS), such as

superoxide (•O2−) and hydroxyl (•OH) radicals may lead to cellular damage

The main sources of OH radicals


Fe toxicity…

The resulting effects are impaired synthesis of proteins, membrane lipids,

and carbohydrates; induction of proteases; and altered cell proliferation

In diseases of iron overload (e.g., HH), the generation of free radicals leads

to tissue damage and organ failure.

excess of free iron has been considered carcinogenic, once the generation

of free radicals by this metal can promote DNA strand breaks, oncogenes

activation, and tumor suppressor genes inhibition

The role of iron in neurodegenerative disorders such as Parkinson’s and

Alzheimer’s diseases suggested to be that iron overload increases brain

oxidative stress status


The Five Stages Stage 1

Nausea, vomiting, abdominal pain and diarrhea.

Stage 2 (quiescent phase)

This is the latent phase often between 6-24 hours as the patient resolves GI

symptoms.

Stage 3(Systemic Toxicity)

Shock stage involving multiple organs including coagulopathy, poor cardiac

output, hypovolemia, lethargy and seizures.

Stage 4

Continuing of hepatic failure and ongoing oxidative damage by the iron in

the reticuloendothelial system.

Stage 5

Gastric outlet obstruction secondary to scarring and strictures.11/15/16 59Approach to child with poisoning

Diagnosis Testing serum iron concentration is the best method to confirm iron

poisoning.Repeat the serum iron test four to six hours after initial measurement.

Total iron-binding capacity An abdominal radiographic examination can be useful to identify

metallic objects. Laboratory testing should include:

Serum electrolytes, blood urea nitrogen (BUN), and glucoseAlanine and aspartate aminotransferases and bilirubinVenous or arterial blood gases in moderately and severely poisoned patientsComplete blood count with differentialProthrombin and partial thromboplastin time


Dx…

Peak serum iron concentrations typically correlate with the following

levels of toxicity:

Less than 350 mcg/dL – Minimal toxicity.

Between 350 and 500 mcg/dL – Mild to moderate GI symptoms

(rarely develop serious complications).

Greater than 500 mcg/dL – Serious systemic toxicity.

Greater than 1000 mcg/dL – Significant morbidity and mortality

The ideal serum iron level is a peak level drawn between 2 and 6 hours

after ingestion


Management of Iron Poisoning: Chelation Therapy

Criteria for initiation of therapy include a history of iron ingestion with:

1. Any clinical sign of shock

2. Lethargy, coma, or altered mental status

3. Persistent vomiting, diarrhea, hematemesis, hematochezia, or other

gastrointestinal symptoms

4. Positive anion-gap metabolic acidosis

5. Large number of pills on abdominal radiograph

6. Serum iron level greater than 500 μg/dL

7. Estimated dose greater than 60 mg Fe+2/kg.


Chelation Therapy…

Deferoxamine is 15 mg/kg per hour as a continuous intravenous

infusion.

Can be given at a dose of 90 mg/kg intramuscularly (If IV

access is not feasible)

Chelation therapy should continue until there is significant

resolution of systemic toxicity, specifically acidosis and shock.

Deferoxamine SE: Hypotension, acute respiratory distress

syndrome (ARDS).


Gastrointestinal decontamination

Any patient with probable or confirmed significant exposure

should have whole bowel irrigation.

polyethylene glycol-electrolyte solution at a rate of 0.5 L/h for

children or 2 L/h for adolescents.

SE: nausea, bloating, vomiting, and diarrhea

Whole bowel irrigation is continued until the effluent is clear.

Magnesium hydroxide might be used to reduce absorption but

no supporting data


GI decont…

Patient with no history of abdominal pain, nausea, vomiting, or diarrhea

& with a normal physical examination and remains asymptomatic for 6

hours, the patient may be safely discharged.

Patients with minimal gastrointestinal symptoms only but an otherwise

normal physical examination should have abdominal radiographs, an

arterial blood gas, and electrolytes.

If there are no pills visible on an abdominal radiograph and there is no

evidence of metabolic acidosis after several hours, the patient is unlikely to

develop systemic toxicity.

A serum iron level less than 500 μg/dL would support identifying this as a

low-risk patient. This patient may be admitted to the hospital for

observation or discharged home with close follow-up.11/15/16 65Approach to child with poisoning

GI decont…

Any patient with more than mild gastrointestinal symptoms or with

evidence of altered mental status, shock, or acidosis should receive

chelation therapy and be admitted to the hospital.

Patients with severe toxicity may require intensive care therapy.

If a hospital has limited pediatric critical care facilities or does not have

access to toxicology consultation, plans to transfer a patient to a tertiary

care hospital should be made early, before the patient becomes unstable

for transfer.

Toxicological consultation should be requested for patients who have

significant toxicity or who are receiving deferoxamine.


Management principles


Management principles of poisoned patient It includes procedures designed to prevent the absorption, minimize the

toxicity, and hasten the elimination of the suspected toxin.

The prompt employment of appropriate emergency management

procedures often can prevent unnecessary morbidity and mortality.

Fundamentals of poisoning management

1. Initial resuscitation and stabilization

2. Removal of toxin from the body

3. Prevention of further poison absorption

4. Enhancement of poison elimination

5. Administration of antidote

6. Supportive treatment

7. Prevention of re - exposure


Mgt principles…1. Initial resuscitation & stabilization:

First priorities are ABC’s

I/V access – I/V fluids

Endo tracheal intubation - to prevent aspiration

Unconscious patients

Respiratory depression/ failure

Convulsions- give anticonvulsants

2.Removal of Toxin : Copious flushing with water or saline of the body including skin folds,

hair Inhalational exposure

Fresh air or oxygen inhalation11/15/16 69Approach to child with poisoning

Mgt principles…3.Prevention of poison absorption

3.1. Gastric Lavage

Done with water,1:5000 potassium permanganate, 4% Tannic acid,

saturated lime water or starch solution with orogastric or Ewald’s tube.

Performed until clear fluid is obtained or a maximum of 3 L

Lavage decreases ingestant absorption by an average of :-

50%- if performed within 5 min. of ingestion

26%- if performed at 30 min.

16%- if performed at 60 min.

Contraindication:

Corrosive poisoning

Recent esophageal / gastric surgery

Unconscious patient Ewald’s tube11/15/16 70Approach to child with poisoning

Mgt principles…

3.2. Ipecac Syrup induced emesis

Administered orally

Dose:

30ml- adults

15ml- children

10ml- small infants

Contraindication

Corrosives

CNS depression or seizures

Rapidly acting CNS poisons ( cyanide, strychnine, camphor )


Mgt principles…3.3. Activated Charcoal:

Charcoal adsorbs ingested poisons within gut lumen allowing charcoal-

toxin complex to be evacuated with stool or removed by induced

emesis / lavage

Dose – 1 g/kg body wt.

Given orally as a suspension ( in water ) or through NG tube

Contraindications:

Mineral acids, alkalis, cyanide, fluoride ,iron


Mgt principles…

3.4.Whole bowel irrigation

Administration of bowel cleansing solution containing electrolytes &

polyethylene glycol

Orally or through gastric tube

Rate – 2 L/hr. ( 0.5 L /hr. in children)

End point- rectal fluid is clear

Position – sitting

Contraindications:

Bowel obstruction

Ileus

Unprotected airway11/15/16 73Approach to child with poisoning

Mgt principles…

4. Enhancement of Elimination of Poison

Forced alkaline diuresis

Infusion of large amount of NS+NAHCO3

Used to eliminate acidic drug that mainly excreted by the kidney

e.g salicylates

Serious fluid and electrolytes disturbance may occur

Need expert monitoring

Acidification of urine:

Enhance elimination of weak bases such as Phencyclidine &

Amphetamine


Mgt principles…

Enhancement of Elimination of Poison… Extracorporeal removal

Dialysis

Acetone, Barbiturates, Bromide, Ethanol, Ethylene glycol, Salicylates,

Lithium

Less effective when toxin has large volume of distribution (>1 L/kg), has

large molecular weight, or highly protein bound.

Peritoneal dialysis

Alcohols , long acting salicylates, Lithium

Chelation

Heavy metal poisoning

Complex of agent & metal is water soluble & excreted by kidneys

Eg. EDTA, BAL – Arsenic, Lead, Copper, Mercury, EDTA- Cobalt, Iron,

Cadmium


Mgt principles…

5. Administration of Antidote:

Antidotes are therapeutic agents that have a specific action against the

activity or effect of a toxicant.

Not all poisons have antidotes

Typical Examples are mentioned only

Types of Antidotes,

Competitive antagonists

Physiological antagonists

Dispositional antidotes


Mgt principles…

Heavy metals………Chelators

Isoniazid……………Pyridoxine

Iron…………………Deferoxamine

Methanol……………Fomepizole or ethanol

Methemoglobinemia…Methylene blue

Opioids………………Naloxone

Organophosphate ….Atropine + pralidoxime

Sulfonylureas………Diazoxide or octreotide

Warfarin……………Vitamin K


Mgt principles…


6. Supportive care

Supportive care includes careful attention to airway support,

ventilator management, blood pressure support, and appropriate

and timely management of seizures, dysrhythmias, conduction

delays, and electrolyte and metabolic derangements.

The goal is to support the vital functions of the patient until the

patient can eliminate the toxin from the system.

Mgt principles…7. Prevention of re - exposure

By following these guidelines you will be able to prevent most poisoning

emergencies:

Keep the household products and medications out of the reach of children.

Use childproof safety caps on containers of medications and other

potentially dangerous substances.

Keep products in their original containers.

Use poison symbols to identify dangerous substances.

Dispose of outdated medications and household products.

Use chemicals only in well-ventilated areas.

Wear proper clothing.


References

Uptodate 21.6

Nelson Text Book of pediatrics 19th edition

Singapore Medical Association. MOH Clinical Practice

Guidelines Dec/2011.Management of Poisoning


Thank youThank you

There is poison in everything.

Only the dose makes a thing not a poison.

--Paracelsus, Father of Toxicology


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