Chemical and drug poisoning
Epidemiology:
It is common emergency problem in the community. More than 50% occur in
children 5 yr of age or younger. More than 90% of toxic exposure in children occur in
the home, and most involve single substance. Ingestion is the most common route of
poisoning exposure (77% of cases). 50% of cases involve non drug substances such as
common household products. 85% of childhood poisoning can be managed without
direct medical intervention, because the product is not very toxic or the amount ingested
is not sufficient to produce clinically toxic effect.
Poisoning in children may be accidental, non-accidental, and iatrogenic, in older child
deliberate. With 2 main age groups:1. Those below 6 years old: they are exposed to plants, household, products,
medication, gases, usually it occurs accidentally, but may occur due to
child abuse. The peak between 1 and 4years, boy more than girls. Also it
more common in poor social circumstances and in summer.
2. Those above 6 years old: It involve 6% of all pediatric exposures. mainly
the adolescent’s girls who exposed more frequently to medication and
occur mainly in suicidal attempts or during occupation. Also occur in boys
who ingest alcohol.
Prevention:
1. Public awareness by TV, radio, news paper,…etc.
2. Improvement of social awareness,
3. Use of child proof celled components of medication (put these drugs out of
reach of children.
Clinical feature:
Poison may affect one system or more:
1. C.N.S.: direct insult to the brain or by causing hypoglycemia, or
electrolyte disturbance. It leads to convulsion, cyanosis, paresis, ataxia…
2. Respiratory system: very acute mostly occur in CO poison, narcotics,
organophosphorus compounds, and morphine. They cause tachypnea, apnea,
chocking, coughing,…etc.
3. Cardiovascular system: cause hypotension or hypertension, tachycardia or
bradycardia, arrhythmia, heart failure (large dose of digoxin).
4. Renal: oligurea, heamaturia, anuria, and proteinuria.
Management:
Patient History: involving description of toxins, time of exposure, and progression of
symptoms.
Medical History: involving underlying diseases, and concurrent drug therapy.
Demographic information: about the patient and caller addresses.
Children who take poison deliberating or iatrogenic or non accidental should be
admitted to hospital.
Accidental Poisoning classified into:
a- accidental poisoning with low toxicity substance: treated at home.
B-intermediate toxicity substance: should be admitted.
C-high toxicity substance: should be admitted.
 resuscitation: focusing on airways potency which may need intubations,
maintain breathing which may need artificial massage (mouth to mouth
breathing, and then circulation.
 evaluation of severity: regarding the weight and the age of the patient, type,
and amount of ingested poison. The product container which may be related
to the exposure should be brought with the patient and if the patients get
vomiting, the emesis should be brought with the patient.
● blood, urine, and gastric leavage samples for chemical analysis.
1- Prevention of absorption, by:
Prompt action to remove the toxin and minimize contact with the absorptive
surface. Dermal and ocular decontamination by flushing with tepid water. It is
better to irrigate one eye for 20-30 sec and then to switch to the other affected eye,
and so forth, for 10 min. For dermal exposures, copious irrigation, followed by a
mild soap wash. For inhaled toxins, by immediately moving the child to fresh air,
and if necessary, administering oxygen. Most liquid drug products are almost
completely absorbed within 30-45 min of ingestion, and most solid dosage forms
are absorbed within 1-2 hr. When a large overdose involves solid dose forms,
complete intestinal absorption can be delayed for 3-6 hr, and for drugs with anti
cholinergic properties, absorption can be delayed by up to 8-12 hr.
a- Activated charcoal: it is the most effective and safest procedure. it can
adsorb almost all drugs, and many chemicals, it is given by water slurry with
the dose of 15-50 gm in children, and 50-100 gm in adolescent. It is
ineffective in many metals, iron, lithium, cyanide or volatile hydrocarbon
poisoning. Repeat doses may be given every 2-4 hr, accompanied by cathartic
for the first dose, and terminated with the first charcoal stool. Its use in
children is limited by its poor acceptance in children. Activated charcoal used
in aspirin, carbamazepine, digoxine, mefenamic acid, phenytoin,
phenobarbitol, quinine, theophylline, and particulary usuful in tricyclic
antidepressant poisoing.
b- Cathartics: sorbitol 1 gm/kg or Mg sulphate, Na citrate or phosphosoda in a
dose of 250 mg/kg to fasten emptying of G.I.T. it is used with caution in
young children, because of the risk of dehydration and electrolyte imbalance.
c- Whole bowel irrigation: involves instilling large volumes ( 30ml/kg/hr) of a
nonabsorbed polyethelyene glycol electrolyte solution in to the stomach to
flow through the entire length of the bowel to cleanse the entire GIT. It is used
to remove slowly absorbed products, such as iron,and foreign bodies
2- Enhancing elimination, which is done by:
a- Emesis: By using syrup of ipecac, which induce emesis in 20-30 min after
dosing, with vomiting in 90- 95% of patients. The dose is10 ml in those
between 6-12 mo of age, 15-30 ml for children between 1-12 yr of age, and
30 ml for older children and adults. It should not be used in patients before 6
mo. It should be followed by at least 6-8 oz of water or other clear fluid. It is
not recommended for routine ingestions . It removes 1l3 of the stomach
contents. We must put the patient on the left side with the head downward.
Emesis is contraindicated in: coma, convulsion, ingestion of strong acid or
base or when there is significant risk of aspiration like kerosene poisoning.The
initial emesis should be send for diagnostic analysis.
b- Gastric Lavage: it is usually unnecessary in children, it may be useful with
drugs like ( iron, calcium channel blockers, tricyclic antidepressants, and
lithium), it is effective only within 1 hour of exposure, it may be complicated
by oesophageal perforation, it is done by washing the stomach with the
normal saline and we suck the contents frequently until we get clear fluid.
c- Diuresis: increasing the pH of urine with IV bicarbonate can augment the
elimination of weak acids, such as salicylates and Phenobarbital. Acidifying
the urine to increase the elimination of weak bases, such as, amphetamine and
phencyclidine, is rarely useful.
d- Dialysis: hemodialysis and peritoneal dialysis are indicated in toxic alcohols,
methanol, and ethylene glycol as well as large symptomatic ingestion of
salicylates, theophylline, or lithium.
e- Hemoperfusion: it is a dialytic technique in which blood is passed through a
column of activated charcoal or resin. It is indicated in sever theophyline or
salicylate poisoning.
3- Laboratory evaluation: serum level of poison is important in changing pattern
of management in salicylate, acetaminophine, iron, methanol, and ethylene glycol
poisoning.
4- antidotes:
a. CO: we give 100% O2.
b. Cyanide: we give kit contains  amyl nitrate inhalers which may be
broken under the patient's nose for 30 seconds every minute while
preparing  Na nitrate 3% solution which given in a dose of 0.33
ml/kg (10 mg/kg) to maximum dose of 10 ml  Na thiosulfate 25%
solution in a dose of 1.65 ml/kg. the alternative antidote is
hydroxycobalamine thiosulfate mixture.
c. Acetaminophen: we give N-acetyle cystein (NAC).
d. Opiates: we give naloxone 0.4 mg can be given to any patient
regardless of his age, and weight. If fail to respond, up to 2 mg should
be given rapidly I.V. to larger children, and adolescent which may be
repeated as necessary. In newborn up to 6 month age, the dose is 0.2
mg/kg.
e. Cholinergic agents: example organophosphorus which cause
salvation, lacrimation, urination, defecation, and fasciculation, the
antidote is atropine 0.05 mg/kg to maximum initial dose of 2.5 mg and
washing the body with soap, and water. Repeated doses may be
necessary. In severe cases or when cholinesterase level falls to 25% of
normal or lower we give pralidoxime which is cholinesterase
regenerator, the dose is 25-50 mg/kg over 30 minute I.V. and given
each 8-12 hours.
f. Methanol or ethylene glycol: we give ethanol
g. Substance that that produce methemoglobinemia like aniline dyes,
nitrobenzene: which diagnosed by putting drop of blood on filter paper
which change to brown colour when dried if the blood contain 20% of
methemoglobinemia then we give methylin blue which is the antidote
0.1-0.2 ml/kg which equal to 1-2 mg/kg in 1% solution. If 2 doses are
non successful then we do exchange transfusion.
h. Β- blocking agents: we give glucagons to improve the blood sugar
level.
i. Iron salt: the antidote is deferoxamine.
j. Isoniazide: the antidote is pyridoxine.
k. Lead poising: the antidote is EDTA or BAL and depending on the
severity.
Specific drugs and chemical poisoning
Acetaminophen:
The acute toxic dose is >200 mg/kg in children below 12 yr of age; a single ingestion
of 7.5g is considered a minimum toxic dose in adolescents and adults. Repeated
administrations of (> 60 mg/kg/day)for consecutive days may lead to hepatic injury or
failure in some children. Children less than 6yr of age are unlikely to have toxicity
after a single ingestion of even relatively large doses. It affect the liver by causing
hepatic injury that lead to increase liver enzymes and prolongation of prothrombin
time, which should be followed daily if the drug level in the toxic range. Chronic use
of it might lead to renal damage, especially in adults.
Clinical manifestations:
Stage
Time after ingestion Characteristics
I
0.5-24 hr
Anorexia, nausea, vomiting, pallor, diaphoresis
II
24-48 hr
Resolution of earlier symptoms, right upper
quardent abdominal pain and tenderness, elevated
biliruibin, PT, hepatic enzymes, oliguria
III
72-96 hr
Peak liver functions abnormalities, earlier
symptoms may reappear
IV
4 days-2 wk
Resolution of hepatic dysfunction or complete
liver failure
Treatment:
Treatment should be started as soon as possible, including within 1-2hr of ingestion.
Oral NAC(N-acetyl cystien) : It is most effective when initiated within 8hr, but may
have value even if it is started 24-36 hr after ingestion in sever cases. I.V. N-acetyl
cystien may be used.
Salicylate:
The incidence of ingestion of salicylate has gradually dropped, because of increase
use of paracetamol. Poisoning may occur accidentally or therapeutically. The acute
toxic dose is generally considered > 150 mg/kg for mild symptoms and > 300-500
mg/kg for moderate to sever intoxication.
Clinical features:
The clinical presentation after acute poisoning differ significantly from that of chronic
toxicity. Young children are more susceptible to toxic effects because they are less
able to buffer the acid load produced by salicylate. Young infants will develop
dehydration, hyperpnoea, and temperature elevation, leading to increase doses of
salicylate.
Older children develop hyperpnoea, vomiting, progressive lethargy, tinnitus, and
sudden deafness.
In adolescence: get hyperventilation syndrome.
Manifestations pass in 3 phases:
Phase I: respiratory center stimulation that lead to respiratory alkalosis, and obligate
alkaluria as compensatory mechanism. There will be loss of K+, Na+, and HCO3- in
the urine. This phase may last for 12 hours after ingestion in adolescent, and may be
missed in infants.
Phase II: there will be sever hypokalemia with paradoxical aciduria. This phase may
last for 12-24 hours, in an adolescent.
Phase III: sever dehydration; sever hypokalemia, metabolic acidosis, and aciduria,
pulmonary edema, hypoglycemia (chronic), or hyperglycemia (acute). This phase
may begin 4-6 hours after ingestion in infants or 24 hours, or more in adolescent.
Local effect of aspirin of G.I.T. is bleeding, and gastric ulceration.
Death results from pulmonary edema and respiratory failure, cerebral edema,
hemorrhage, sever electrolyte imbalance, or cardiovascular collapse.
Serial serum salicylate concentration, initially at 4 hr post ingestion and then every 34 hr., should be monitored.
Urine pH and volume should measured hourly in all seriously poisoned children,
plasma pH, glucose, K, and other electrolytes should be monitored at regular
intervals. Clotting studies and liver function tests should also be monitored in all
seriously poisoned children.
Treatment:
Aggressive rehydration, and correction of electrolyte abnormalities ( large quantities
of K and HCO3 may be needed) after initiating active charcoal emesis, and other
general measures like: forced alkaline diuresis, hemodialysis, and peritoneal dialysis.
The treatment depends on phase, and serum level of salicylate.
Lead:
It is a common serious public health problem. The sources are paints, fumes from
battery burning, toys, some tubes used for water supply, Kohl, and children with pica.
Clinical features:
There's no precise direct correlation between blood lead level and clinical feature, but
the severity of symptoms increase with increase exposure to the lead and its level.
The most serious manifestation is encephalopathy or lead colic (vomiting, abdominal
pain and constipation).
CSF will reveal mild pleocytoses, increase protein and pressure. There will be
hypochromic microcytic anemia with basophilic stippling.
Some times lead deposition in the gum lead to formation of blue line in the teeth and
gingiva, some times it is precipitated in the long bones leading to transverse line on
metaphysic, which seen by X-rays, or precipitated in the abdomen and seen as flecks
in the plane X-rays of the abdomen.
Diagnosis:
A confirmed venous blood lead level ≥ 45 μg/dL requires prompt chelation therapy
Supportive measures: which include increase in erythrocytes protoporphyrine, X-rays
of abdomen, and long bones.
Treatment:
 Removing source of exposure.
 Chelating agent like, pencilamine, DMSA , EDTA, , and dimercaprol( BAL)
depending on blood level.
 Fluid therapy, and electrolyte correction.
 Correction of anemia.
 Phenytoin if the patient get convulsion.
In mild cases pencilamine should be used orally.
In severe cases (EDTA) by i.v infusion. The effectiveness of EDTA can be enhanced
by deep I.M injection of (BAL) .
Organophosphorous:
Its mostly occur in agricultural areas because the source is mainly the insecticide. It is
very dangerous.
It is absorbed by inhalation, ingestion, or through skin, small doses can kill the
patient.
Its main action is suppression of choline-estrase which lead to increase acetylcholine
lead to pinpoint pupil, irritability, excess secretion, muscle cramps, bradycardia, and
increase respiratory rate.
Treatment:
Supportive measures like O2, suctioning, positioning. Then we give atropine until
atropinization occur (flushing of the face), and then stop slowly within 2-3 days until
the enzyme start to built itself. In sever cases we use pralidoxime to breaks the bond
between the organophosphate and the enzyme, and liberating the enzyme, so it is
effective only if used within 18 hr after ingestion. For significant poisoning both
atropine and pralidoxime are used. Even with treatment neurological symptoms may
occur and persist.