Accidental poisonings

Accidental Poisoning
Presented by: Shalini Mehta
Department of Child Health Nursing
BPKIHS, Dharan

Introduction
Children are curious and explore their world with all their
senses, including taste.
As a result, the home and its surroundings can be a dangerous
place when poisonous substances are inadvertently ingested
Acute exposure is a single contact that lasts for seconds,
minutes or hours, or several exposures over about a day or
less.

Introduction…
Chronic exposure is contact that lasts for many days, months
or years.
Most of the poisonings in children is accidental in nature.
Accidental poisoning in children is a global problem.
 It is one of the leading causes of death in children.
10/21/2020Shalini Mehta
3

Defination
Poisoning is when cells are injured or destroyed by the
inhalation, ingestion, injection or absorption of a toxic
substance.
Key factors that predict the severity and outcome of
poisoning are the nature, dose, formulation and route of
exposure of the poison; co-exposure to other poisons;
state of nutrition of the child or (fasting status); age and
pre-existing health conditions.

Scale of the problem
Mortality
 In 2004, acute poisoning caused more than 45 000 deaths in
children and youth under 20 years of age – 13% of all fatal
accidental poisonings worldwide.
 In 16 high-income and middle-income countries, poisoning is
the fourth biggest cause of unintentional injury after road
traffic injuries, fires and drowning.

Scale of the problem…
The rate of fatal poisoning is highest for children under one
year, with another slight peak around 15 years.
 Fatal poisoning rates in low-income and middle-income
countries are four times that of high-income countries.
Africa and low-income and middle-income countries in
Europe and the Western Pacific Regions have the highest
rates.

Scale of the problem…
Common poisoning agents in high-income countries include
pharmaceuticals, household products (e.g. bleach, cleaning
agents), pesticides, poisonous plants and bites from insects
and animals.
Common poisoning agents in low-income and middle income
countries are fuels such as paraffin and kerosene,
pharmaceuticals and cleaning agents.

Research Article
Title: Pattern of acute poisoning in children in a
tertiary care hospital in eastern Nepal
By: Satish Yadav, Shankar Prasad Yadav, Jyoti Agrawal, Gaurishankar Shah
in 2 July 2016 .
Results: A total number of 64 children (36 males & 28 females)
were admitted with acute poisoning.
• It constituted 3.4% of the total admissions and 4.4% of the
total deaths. The maximum number of children 25 (39.1%)
was of the age group 1 to 5 years.
8

Results…
• Fifty-one (79.7%) were admitted in Ward and 13 (20.3%) in
Pediatric Intensive Care Unit (PICU) among which 4 (6.25%)
patients were put in mechanical ventilation.
• The most common poison involved was organophosphorus
compounds 24 (37.5%) followed by mushroom 16 (25%) and
kerosene 11 (17.2%).
• Mean time interval between ingestion and admission to
hospital was 6.87 ±8.33 hours.
9

Results…
• The majority of the poisoning 28 (44%) occurred between
2pm to 7 pm.
• Forty-nine (76.6%) of the poisonings were non-intentional and
14 (21.6%) were intentional.
• Average duration of hospital stay was 4.14±1.94 days and
vomiting was the commonest clinical manifestation.
• Of all the patients, 28 (43.8%) received pre-referral treatment,
44 (68.8%) antidotes and 22 (34.4%) gastric lavage.
10

Conclusions: In our study, most of the poisoning was
non-intentional and 1 to 5 years old children were at
greater risk for poisoning.
The main substance was organophosphorus .
11

Risk factors
Young children are particularly susceptible to the ingestion of
poisons, especially liquids, because they are very inquisitive,
put most items in their mouths and are unaware of
consequences.
Adolescents, on the other hand, are more aware of the
consequences of their actions but peer pressure and risk taking
behaviour can lead them to misuse alcohol or illicit drugs,
leading to a fatality rate higher than in younger children.

Risk factors …
 Younger children are more susceptible to poisoning because
of their smaller size and less well-developed physiology,
particularly as the toxicity of most substances relates to dose
per kilogram of bodyweight.
Most common agents involved in childhood poisoning:
Over-the-counter preparations such as paracetamol, cough/
cold remedies, vitamins and iron tablets, antihistamines and
anti inflammatory drugs.

Risk factors …
Prescription medications such as antidepressants,
narcotics, analgesics and illicit drugs.
Household products such as bleach, disinfectants,
detergents, cleaning agents, cosmetics, vinegar.
Paraffin/kerosene.
15

Risk factors …
Pesticides, including insecticides, rodenticides and herbicides.
Poisonous plants.
Animal or insect bites.
Boys have higher rates of poisoning than girls in all regions of
the world, probably because of differences in socialization.

Risk factors …
 Fatal and non-fatal poisonings are strongly associated with
lower socioeconomic status, between and within countries.
 The prevalence and types of poisoning vary in different parts
of the world.

Risk factors …
They depend on industrial development, agricultural activities,
cultural practices relating to supervision of children and local
beliefs and customs.
For example, medicinal drugs are the leading cause of non-
fatal poisoning in children in middle income to high-income
countries, and ingestion of fuels such as kerosene is a common
cause in low-income countries.
23

Risk factors …
 Other risk factors for poisoning include those related to the
poisoning agent itself, including toxicity, nature, physical
appearance and storage; season and weather conditions;
policies, standards and laws governing the manufacture,
labelling, distribution, storage and disposal of poisoning
agents; and access to quality health care for treatment.

Ecology of poisoning
Age: About 40 percent of all cases of accidental poisoning in
children are reported in the second year of life; about 12 percent
of the cases occur in the first and 20 percent in the third years.
Large families: In large families, there may be carelessness in
storage of potentially poisonous household substances.
25

Ecology of poisoning…
Small accommodation: In smaller houses, there is little
storage facility. Poisonous substances may be stored in easily
accessible places.
Environment: Lead poisoning is common in children living
in areas where there are workshops for repair of old
automobile lead storage batteries or for manufacture of lead
typesets for printing presses.
Rural or urban areas
26

Presenting features of common
poisonings
Seizures: Organochlorines, chlorinated hydrocarbons, cocaine,
isoniazid, phenothiazine, carbon monoxide, theophylline
Respiratory embarrassment: Narcotics, organophosphates,
barbiturates, benzodiazepines
Cardiac arrhythmias: Tricyclic antidepressants, amphetamine,
aluminium phosphide, digitalis, theophylline, arsenic, cyanide,
chloroquine.
27

features of common poisonings…
Metabolic acidosis: Isoniazid, methanol, salicylates,
phenformin, iron, cyanide.
GIT disturbances: Organophosphorus, arsenic, iron, lithium,
mercury.
Cyanosis: Nitrobenzene compounds, aniline dyes, and dapsone.
28

Basic management of a poisoned
patient:
Antidotes are available for very few commonly encountered
poisons, and treatment is usually non-specific and
symptomatic.
 In such cases management consists of emergency first aid and
stabilization measures, appropriate treatment to reduce
absorption, measures to enhance life support followed by
psychiatric counseling.
29

Emergency stabilization measures
The unconscious patient should be transported in the head-
down semi prone position to minimize the risk of inhalation of
gastric contents.
 A clear airway is established and ventilation is maintained.
Potentially serious abnormalities such as metabolic acidosis,
hyperkalemia and hypoglycemia may require correction as a
matter of urgency.
 Neurological assessment is made by calculating the Glasgow
Coma Score (GCS).
30

Emergency stabilization measures…
• Many drugs and poisons can cause grand malconvulsions,
which, if repeated, should be controlled with intravenous
diazepam.
• Hypotension with peripheral circulatory failure is treated first
by correction of hypoxia and acidosis, and by elevation of foot
end of the bed.
31

Emergency stabilization measures…
• If adequate perfusion is not restored by these
measures, the circulating volume should be increased
by administration of plasma expander intravenously.
• Cardiac arrhythmias are often improved or abolished
by correction of hypoxia, acidosis and electrolyte
imbalance.
32

VIDEO
33

Identification of poison
• Identify the poison by careful history and helpful clues.
Determine what, when and how much of the poison was
ingested or inhaled.
• Find the supporting evidence for your diagnosis from the
nature of the symptoms and physical signs.
34

Removal of toxin
The aim of decontamination procedures is to reduce
the absorption of poison. It can be achieved by:
Eye decontamination
Ocular exposure to solvents, e.g. hydrocarbons,
detergents and alcohol, or corrosive agents, e.g. acid
or alkalis require immediate local decontamination.
35

Eye decontamination…
This is achieved by copious irrigation with
neutralizing solution (e.g. normal saline or water) for
at least 30 minutes.
Do not use acid or alkaline irrigating solution.
36

Dermal decontamination
Absorption of organophosphorous and related compounds
through cutaneous route can prove to be as fatal as oral route
absorption.
Remove all decontaminated clothes and irrigate the whole
body including nail, groin, skinfolds with water or saline as
soon as possible after exposure and continue irrigating for at
least 15 minutes.
Water should not be used to decontaminate skin in exposures
to sodium and phosphorus.
37

Gut decontamination
This includes gastric evacuation, adsorbent administration and
catharsis.
Emesis is the preferred method of emptying the stomach in
conscious children.
 Induction of vomiting is contraindicated in corrosive or
kerosene poisoning and in comatose patients or those with
absent gag reflex.
38

Gastric lavage
If the vomiting does not occur quickly, gastric lavage should
be done promptly to remove the poison.
In a symptomatic but alert child with minor ingestion,
activated charcoal alone by mouth is sufficient for
gastrointestinal decontamination.
39

Adsorbent administration
An agent capable of binding to a toxic agent in the GIT is
known as adsorbent.
Activated charcoal is the most widely used adsorbent.
 For the comatosed child with potentially serious overdose,
gastric lavage is followed by administration of activated
charcoal via an orogastric or nasogastric tube within 1-2 hours
of ingestion.
 Dose of activated charcoal administered should be at least 10
times the dose of ingested toxic material.
40

Catharsis
Laxative and purgatives may be given in poisoning with
substances which do not cause corrosive action on
gastrointestinal mucosa.
Increased motility of may reduce absorption. Commonly used
cathartics include sorbitol and mannitol (1-2 g/kg), and
magnesium or sodium sulfate (200-300 mg/kg).
Do not give magnesium salt cathartics in cases with renal
failure.
41

Specific antidotal therapy
Specific antidotes may be lifesaving but unfortunately they are
not often available and are effective for less than 5% of
poisoning cases.
Chemical antidotes combine with the poison and render it
innocuous.
42

Promotion of excretion of toxin
Forced diuresis
Diuresis alone has relatively little effect on drug elimination
because at best the renal clearance is only proportional to the
urine flow rate.
 In the cases of drugs which are weak organic acids and bases,
a much greater effect on clearance can be obtained by
manipulation of the urine pH.
43

Supportive therapy
Keep the airway open, give oxygen for inhalation and be
prepared for intermittent positive pressure respiration.
Fluid and electrolyte balance is maintained.
Circulatory failure should be managed to sustain life.
44

Supportive therapy…
Anemia is treated with packed cell transfusion.
Severe convulsions and status epilepticus are treated with
diazepam or midazolam.
Renal failure is managed as per standard protocol; dialysis
may be needed.
 Infections are treated with antibiotics.
Fever and pain are relieved with antipyretics and analgesics.
45

Prevention of poisoning
1. Protection of the child from the poisonous
substances.
2. Education of parents about the potential household
poisons.
3. Need for parental supervision.
46

Prevention of poisoning…
4. Safety regulations by the state should be enforced.
5. Establishment of the poison control centers to
collect, compile and disseminate information on
poisons and their management. These should
promote research on prevention and treatment.
47

Some specific poisons and antidotes
48

ORGANOPHOSPHOROUS
COMPOUNDS AND CARBAMATES
Organophosphorus compounds and Carbamates are used as
insecticides in agriculture and in domestic usage.
Some of the commonly used compounds are
Organophosphosohates: Tetraethyl pyrophosphate (TEPP),
Ethyl parathion, Dichlorofos, Fenthion (Baytex), Malathion,
Temephos (Abate), Endosulphan (Endrin)
Carbamates: Methocarb (Nudrin), Propoxur (Baygon),
Carbaryl (Sevin)
49

Clinical Features
Muscarinic effect: This is characterized by excess salivation,
lacrimation, urination and diarrhea.
• The pupils are pinpoint and there is marked bradycardia.
• GI symptoms consist of nausea, vomiting, pain abdomen and
diarrhea. Tightness of chest , bronchospasm, wheezing and
pulmonary edema may occur.
54

Clinical Features…
Nicotinic effects: These are seen in severe poisoning chiefly
causing muscle twitching, fasciculation, and cramps followed by
muscle weakness and paralysis particularly of the respiratory
muscles.
56

Central effects: These are seen in severe cases and include
restlessness, confusion, headache, slurred speech, ataxia,
seizures and coma.
The signs and symptoms of Carbamates are similar except that
they are milder and of short duration.
58

Diagnosis
History and typical clinical findings.
The RBC cholinesterase level is less than 50% in cases where
exposure has occurred and less than 20% in case symptoms
are present.
 X-ray chest may be required to document the presence of
pulmonary edema.
59

Management
Further exposure to the insecticide must be avoided by moving
to a safer environment.
The clothes to be removed and skin to be washed with
adequate amount of soap and water.
 If ingested, gastric decontamination should be done. If
conscious, by vomiting followed by lavage, and if
unconconcious by lavage after protecting the airway with a ET
tube.
60

Management…
Activated charcoal slurry can be left in the stomach after
lavage.
Atropine is the specific antidote which neutralizes the CNS
and Muscarinic effect but not the Nicotinic effect.
It is given in a loading dose of 0.02-0.05mg/Kg followed by
maintenance dose of the same dose every 10-30 min.
Child should be watched for signs of Atropinisation in the
form of dryness of mouth, dry skin, decrease in bronchial
secretions, pupillary dilatation and tachycardia.
61

Management…
The patient is kept Atropinised till the enzymes regenerates or
is reactivated.
Pralidoxime, a cholinesterase enzyme reactivator is a specific
antidote for Organophosphorus compounds.
Enzyme activation occurs most rapidly at the neuromuscular
junction with rapid restoration of skeletal muscle response.
The Muscarinic or central effects are not significantly reversed
with this drug and hence concomitant use of atropine is
essential.
63

Management…
The dose of Pralidoxime is 25-50 mg/Kg for a child less than
12 years and for children above 12 years adult dose of 1-2 gm
is given over 15 to 30 min IV followed by repeat dose after 1-
2 hours.
Following recovery the child should be observed closely for
24 to 48 hours to ensure that cholinergic signs do not recur as
Pralidoxime and Atropine effects wear off.
64

Management…
• Intermediate syndrome can develop 24 to 96 hours after
Organophosphorus poisoning which is characterized by
weakness in the proximal motor muscles, motor cranial
nerves, neck flexors and respiratory muscles.
• A combination of pre-synaptic and post synaptic impairment
of neuromuscular transmission probably causes this syndrome.
• Enzyme activation has no role in Carbamates poisoning and
may be harmful.
65

Symptoms :
Muscarinic- Skin, Resp., Pupils, GIT, Urinary
Nicotinic- Skeletal muscles, Resp. muscles CNS- Confusion, coma
Management : Decontamination of Surface and GIT
Atropinisation, Pralidoxime
66

Management of OP Poisoning in
Children (BPKIHS)
Inj. atropine 0.05mg/kg IV every 5-10 minutes till full
atropinization (the best sign of atropinization is chest
devoid of any secretions , detected by chest auscultation.
i.e. end point of atroponization is clear chest on
auscultation).
 Once patient is atropinized give the maintenance dose at
0.08mg/kg/hour. Decrease the dose of atropine by 0.02
mg/kg every 12-24 hours till it reaches 0.02 mg/kg/hr.
(Range of atropine infusion: 0.02-0.08mg/kg/hr).
Once the infusion reaches 0.02mg/kg/hr then stop
atropine infusion.
Also pralidoxime should be given.
67

Hydrocarbon poisoning
68
SOURCES
• Petrol
• Kerosene
• Lighter Fluid
• Paraffin Oil
• 2 Stroke Fuel
• Diesel Fuel
• Solvents
• White Spirit
• Lubricating Oil
• Furniture Polishes
• Essential oils
• Mineral Turpentine

Risk Assessment
History
• Was exposure intentional or accidental?
Dose:
Type of compound
Quantity ingested
Duration of exposure in inhalation
Co-ingestants (eg paracetamol)
71

Examination
Respiratory
Coughing / gagging / choking indicates aspiration
Wheeze, tachypnoea, hypoxia, hemoptysis and pulmonary
edema are signs of evolving chemical pneumonitis.
Cardiovascular
Dysrhythmias occur early in exposure
72

CNS
CNS depression, coma and seizures may occur with large acute
exposures. Onset is usually within 2 hours
GIT
Nausea, vomiting and diarrhoea
Excessive burping, heartburn, epigastric pain
73

Acute Management
1. Resuscitation
• Standard procedures and supportive care
• Intubate early for progressive CNS depression
• Ventricular dysrhythmias:
▫ Commence advance life support
▫ Intubate, hyperventilate, correct hypoxia
▫ Correct electrolyte disturbances
▫ Withhold catecholamine inotropes if possible
74

Seizures – Benzodiazepines remain standard first line treatment.
• Chemical pneumonitis is managed supportively (Oxygen &
bronchodilators – may require non invasive ventilation or
intubation if severe).
• Fever is common following aspiration with pneumonitis –
antibiotics should be withheld until there is objective evidence
of bacterial infection
75

2. Decontamination
• Activated charcoal is specifically contraindicated in
hydrocarbon poisoning as they do not bind hydrocarbons and
increase the risk of hydrocarbon aspiration.
• Ongoing care and monitoring
Asymptomatic children with normal vital signs should be
observed for 6 hours post exposure before discharge
Patients with milder respiratory or CNS symptoms should be
admitted for a longer period of observation +/- supportive
care.
76

BARBITURATE
Poisoning is likely to occur in children who suffer
from epilepsy or where a family member is on such
medication.
Ingestion of over 1 gm of any barbiturate should be
viewed with concern and over 3 gm is potentially
lethal.
77

Clinical Features
The clinical features are characterized by CNS
depression. The respiration may be shallow and
progress to respiratory arrest.
Hypotension occurs with severe poisoning and the
pupils are constricted but later dilate. There is loss of
light and corneal reflex.
 The bullous lesions on the skin are more due to
pressure effects on the skin rather than toxicity due to
the drug.
78

On recovery there is headache, dizziness, diplopia, ptosis and
ataxia. Cause of death in barbiturate poisoning is due to
respiratory arrest.
Serum levels of barbiturate are useful in confirming toxicity
with levels more than 10 mg/dl for long acting, 7 mg for
intermediate acting and more than 3 mg for short acting drugs
considered to be in the toxic range.
 EEG changes correlate with severity with fast activity in mild
poisoning to slowing and progressing to flat EEG with severe
poisoning.
80

Treatment
• Gastric lavage is useful if done within 6 hours of
ingestion.
• Activated charcoal adsorbs barbiturates and is used as
slurry after the lavage.
• Supportive treatment for respiratory failure,
hypotension and hypothermia is to be provided.
• Forced alkaline diuresis enhances drug excretion.
81

IRON
Iron is an important toxicological hazard because of easy
availability and bright coloured formulations.
Ingestion up to 25 mg/Kg of elemental iron does not cause any
problem.
Higher ingestions are potentially serious.
82

Clinical Features
The earliest symptoms of Iron ingestion are nausea, vomiting
and diarrhea with onset within 30 min and up to 6 hrs post
ingestion.
Following this is a quiescent phase. Subsequently, GI losses
due to increased capillary permeability and systemic effect in
tissues causing metabolic acidosis and myocardial dysfunction
lead to circulatory failure characterized by shock.
83

Thrombocytopenia and hypoprothrombinemia may also occur.
Hepatocellular necrosis leading to hepatic failure is a
significant cause of mortality.
 The corrosive effect of iron leads to gastric scarring causing
outlet obstruction as a late feature of the poisoning.
84

Toxic dose: More than 25 mg/Kg or serum levels above 300
mcg/dl
Symptoms: GI symptoms (Vomiting & diarrhea), shock, hepatic
failure
Management: General measures-lavage, bowel wash, IV fluids,
Inotropes
Antidote: Desferroxamine
85

Lab Investigations
Serum level of iron greater than 300 mcg/dl are associated
with toxicity and levels greater than 500 mcg/ dl are
considered severe poisoning and levels above 1000 mcg/dl are
invariably fetal.
Blood glucose may be elevated and liver functions may be
derranged.
 X-ray abdomen may be valuable prior to and after lavage to
see the quantum of radio opaque tablets if ingested.
86

Treatment
Ingestion up to 25 mg/Kg of elemental iron need not be
treated.
 Children if symptomatic or with serum levels above 300
mcg/dl may be managed with specific antidote.
 All other children should receive general measures of poison
management.
Lavage is indicated even if emesis has occurred though the
iron tablets may have become a gel in the acid medium of the
stomach and not likely to be fully removed even with lavage.
87

Treatment…
100 ml of Milk of Magnesia or 100 ml of Soda bi carb may be
left in the stomach after lavage.
 Bowel irrigation with Polyethylene glycol may be useful in
Iron elimination from the GI tract.
The excretion of free circulating iron can be enhanced by
chelating with Desferroxamine, the complex of
Desferroxamine-Iron being more water soluble gets excreted
by the kidney.
88

Treatment…
Desferroxamine is added to normal saline and infused at the
rate of 15 mg/Kg/hr.
The Desferroxamine-iron complex colours the urine a distinct
pink(vin-rose) hue to the urine.
The infusion is continued for a period of 24 hrs after the urine
becomes clear or the serum Iron level is below 300 mcg/dl.
89

Treatment…
The child may require supportive therapy in the form of IV
fluids, inotropic support, maintaining glucose levels and
correction of the metabolic acidosis.
Gastrostomy may be required if radiological visualization
confirms persistence of large number of radio opaque shadows
even after lavage.
 Hemodialysis is not useful unless associated renal failure is
present.
90

91
Research Article

Title: Hospital Based Study of Poisoning
Among Children, 1 to 18 Years of Age in
Eastern Nepal
By: Rimal HS et al; May 2017 Birat Journal of Health Sciences
Introduction: The poisoning among children had been a major
cause of hospital admission and also a significant global health
problem throughout the world including Nepal. There are
various studies suggestive of incidence rate of poisoning in
children ranging from 0.74% to 3%. In older children, poisoning
is usually intentional where as in infants and younger children it
is accidental in nature. There are few studies done in Nepal and
they are mainly from Kathmandu valley, this study will add
more information from eastern region of Nepal.
92

Objective:
This study aimed to find out the type of poisoning among
children and adolescents, manner of poisoning and its outcomes.
93

Methodology:
 This was a retrospective study carried out at Nobel Medical
College Teaching Hospital over a period of one year starting
from 1 August 2014 to 31July 2015.
 This study included all the children and adolescents of 1 to 18
years of age admitted to pediatric ward and ICU for the
management of poisoning.
 The information including name of poisons, manner of
poisoning, socio-economic and demographic factors related to
poisoning, geographical distribution of sample population,
durations of hospital stay and outcome of treatment were
retrieved from the records.
 The data was analyzed using SPSS.
94

Results:
 A total of 64 cases were studied. It included almost the same
number of males (n=31) and females (n=33).
 The age group of 13-18 years had the largest prevalence of
poisoning (n=22).
 Organo-phosphorus (n=25) was the commonest poison.
95

Results…
 As the study was conducted in a tertiary care center of eastern
Nepal located at Biratnagar, Morang district, a majority of the
cases (39) were from Morang.
 A total of 41% children required hospital stay for more than 7
days where as 37% of them required 5-7 days of hospital stay
and only 22% children stayed for 1-4 days in the hospital. No
mortality was noted.
96

Conclusion:
• The pediatric poisoning in eastern Nepal is a significant public
health issue and nature of poisoning was accidental followed
by suicidal.
• The commonest age group involved is adolescence, which
highlights the need for education and implementation of
suicidal prevention program in this region.
• The higher prevalence of accidental poisoning in first two year
of life necessitates the need of child safety and injury
prevention program in the community
97

98
Any
Query?

References
• Ghai, O.P., Ghai Essential Pediatrics, 6th edition, CBS
Publishers and distributors; 2007
• Gupta, Piyush, Textbook of Pediatrics, 1st edition, CBS
publishers, New Delhi, 2013
• Mayo Clinic. 2020. Poisoning: First Aid. [online] Available at:
<https://www.mayoclinic.org/first-aid/first-aid-
poisoning/basics/art-20056657> [Accessed 17 October 2020].
• Who.int. 2020. WHO | Poisoning. [online] Available at:
<https://www.who.int/environmental_health_emergencies/pois
oning/en/> [Accessed 17 October 2020].
99

• Melbourne, T., 2020. Clinical Practice Guidelines : Poisoning - Acute
Guidelines For Initial Management. [online] Rch.org.au. Available at:
<https://www.rch.org.au/clinicalguide/guideline_index/Poisoning_-
_Acute_Guidelines_For_Initial_Management/> [Accessed 18 October
2020].
• Rwimal, H., Tiwari, U., Ghimire, K. and Thapa, M., 2017. Hospital Based
Study of Poisoning Among Children, 1 to 18 Years of Age in Eastern
Nepal. Birat Journal of Health Sciences, [online] 2(1), pp.138-141.
Available at:
<https://www.researchgate.net/publication/316840255_Hospital_Based_St
udy_of_Poisoning_Among_Children_1_to_18_Years_of_Age_in_Eastern_
Nepal> [Accessed 15 October 2020].
100

References…
• Dhakal, A., Shrestha, D., Shakya, A., Shah, S. and Shakya, H., 2014.
Clinical Profile of Acute Poisoning in Children at a Teaching Hospital in
Lalitpur. Journal of Nepal Paediatric Society, [online] 34(2), pp.100-103.
Available at:
<https://www.researchgate.net/publication/267927778_Clinical_Profile_of
_Acute_Poisoning_in_Children_at_a_Teaching_Hospital_in_Lalitpur>
[Accessed 15 October 2020].
• Yadav, S., Yadav, S., Agrawal, J. and Shah, G., 2016. Pattern of acute
poisoning in children in a tertiary care hospital in eastern
Nepal. International Journal of Contemporary Pediatrics, [online]
pp.1001-1005. Available at:
<https://www.ijpediatrics.com/index.php/ijcp/article/view/61> [Accessed
15 October 2020].
101

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