Pediatrics Dr.

Sawsan Ali

"Poisoning" lecture 2

Iron Poisoning
 Historically, iron was a common cause of childhood poisoning deaths. The
severity of an exposure is related to the amount of elemental iron ingested,
moderate to severe toxicity is typically seen with ingestions of >60 mg/kg.

Pathophysiology:
 Iron is directly corrosive to the GI mucosa, leading to hematemesis, melena,
ulceration, infarction, and potential perforation.

 Early iron-induced hypotension is due to massive volume losses, increased

permeability of capillary membranes, and venodilation mediated by free iron.

Clinical and Laboratory Manifestations:

Iron toxicity is classically described in 5, often overlapping, stages:

Stage Time after ingestion Characteristics

profuse vomiting and diarrhea (often bloody),

I 30 min to 6 hr. abdominal pain, and significant volume losses
leading to potential hypovolemic shock
"quiescent phase", as GI symptoms typically
II 6 to 24 hr.
resolve.
multisystem organ failure, shock, hepatic and
cardiac dysfunction, acute lung, and profound
III 12 to 24 hr.
metabolic acidosis. Death occurs most
commonly during this stage.

IV 2-5 days fulminant liver failure and coagulopathy

marked by formation of strictures and signs of

V 4-6 wk.
GI obstruction.

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  Symptomatic patients and patients with a large exposure by history should have
serum iron levels drawn 4-6 hrs. after ingestion.

 Investigations should include blood gas, complete blood count, serum glucose
level, liver function tests, and coagulation parameters. An abdominal x-ray might
reveal the presence of iron tablets.

 Careful attention should be paid to ongoing monitoring of the patient's

hemodynamic status.

Treatment
 Close clinical monitoring, combined with aggressive supportive and
symptomatic care, is essential to the management of iron poisoning.

 Activated charcoal does not adsorb iron, and WBI remains the decontamination
strategy of choice.

 Deferoxamine, a specific chelator of iron, is the antidote for moderate to severe

iron intoxication.

 Indications for deferoxamine treatment include a serum iron concentration of

>500 mg/dL or moderate to severe symptoms of toxicity, regardless of serum
iron concentration.

Lead Poisoning
Several hundred products contain lead, including batteries, cable sheathing,
cosmetics, mineral supplements, plastics, toys, lead-based paint. As paint deteriorates,
it chalks, flakes, and turns to dust. The dust can coat all surfaces, including children's
hands. All of these forms of lead can be ingested.
The nonnutritive hand-to-mouth activity of young children is the most common
pathway by which lead enters the body. In nearly all cases, lead is ingested.

After absorption, lead is disseminated throughout the body. Most retained lead
accumulates in bone, where it may reside for years. It circulates bound to erythrocytes;
about 97% in blood is bound on or in the red blood cells.

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 Previously, Blood Lead Levels (BLL) of 10 microg/dL or greater regarded as a
level of concern for public health purposes. The Centers for Disease Control and
Prevention (CDC), recognizing that a BLL of 10 μg/dL qualifies neither as a threshold
of toxicity nor as a protective parameter of children with lead exposure, changed its
standard. It no longer refers to a level of concern or toxicity but has designated 5 μg/dL
as the “reference value based on the 97.5th percentile of the population BLL in children
aged 1-5 years to identify children living or staying for long periods in environments
that expose them to lead hazards.”
Protoporphyrin is readily measurable in red blood cells. Levels of protoporphyrin
higher than 35 microg/dL are abnormal and are consistent with lead poisoning, iron
deficiency, or recent inflammatory disease. Measurement of the erythrocyte
protoporphyrin (EP) level is, therefore, a useful tool for monitoring biochemical lead
toxicity.

Clinical effects
Hearing and height are inversely related to BLLs in children.
Higher BLLs have adverse effects on cognitive functions.

Clinical Symptoms
GI symptoms of lead poisoning include anorexia, abdominal pain, vomiting, and
constipation, often occurring and recurring over a period of weeks.
CNS symptoms are related to worsening cerebral edema and increased
intracranial pressure. Headaches, change in mentation, lethargy, papilledema,
seizures, and coma leading to death are rarely seen at levels lower than
100 microg/dL but have been reported in children with a BLL as low as
70 microg/dL. There is no clear cutoff BLL value for the appearance of
hyperactivity, but it is more likely to be observed in children who have levels
higher than 20 microg/dL.
At high levels (>100 microg/dL), renal tubular dysfunction is observed.
At high BLLs, red blood cell survival is shortened, possibly contributing to a
hemolytic anemia.
Older patients may develop a peripheral neuropathy.

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Diagnosis:
 Screening: It is estimated that 99% of lead-poisoned children are identified by
screening procedures rather than through clinical recognition of lead-related
symptoms.
 Radiographs of long bones may show dense bands at the metaphyses, which may
be difficult to distinguish from growth arrest lines but, if caused by lead, are
indicative of months to years of exposure.

 For children with acute symptoms, a kidneys-ureters-bladder (KUB) radiograph

may reveal radiopaque flecks in the intestinal tract, a finding that is consistent
with recent ingestion of lead-containing plaster or paint chips.

Treatment:
 Once lead is in bone, it is released only slowly and is difficult to remove even
with chelating agents. Because the cognitive/behavioral effects of lead may be
irreversible, the main effort in treating lead poisoning is to prevent it from
occurring and to prevent further ingestion by already-poisoned children.

 Drug treatment to remove lead is lifesaving for children with lead

encephalopathy. In non-encephalopathic children, it prevents symptom
progression.

 Four drugs are available:

1. 2,3-dimercaptosuccinic acid (DMSA [succimer])

2. CaNa2EDTA (versenate)

3. Penicillamine

4. British antilewisite (BAL [dimercaprol]),

 Early screening remains the best way of avoiding and therefore obviating
the need for the treatment of lead poisoning.

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 Hydrocarbons Poisoning
Hydrocarbons include a wide array of chemical substances found in thousands of
commercial products.

Pathophysiology
 The most important manifestation of hydrocarbon toxicity is aspiration
pneumonitis via inactivation of the type II pneumocytes and resulting surfactant
deficiency.
 Compounds with low viscosity, such as mineral spirits, naphtha, kerosene,
gasoline, and lamp oil, spread rapidly across surfaces and cover large areas of the
lungs when aspirated
 Only small quantities (<1 mL) of low-viscosity hydrocarbons need be aspirated
to produce significant injury.
 Pneumonitis does not result from dermal absorption of hydrocarbons or from
ingestion in the absence of aspiration. Gasoline and kerosene are poorly
absorbed, but they often cause considerable irritation of the GI mucosa as they
pass through the intestines.

Clinical and Laboratory Manifestations

 Transient, mild CNS depression.
 Aspiration is characterized by coughing, which usually is the first clinical
finding.
 Chest radiographs may initially be normal, but they often show abnormalities
within 6 hr of exposure in patients who have aspirated. Pneumatoceles can appear
on the chest radiograph 2-3 wks. after.
 Respiratory symptoms. can remain mild or progress rapidly to ARDS.
 Fever and leukocytosis.

Treatment
 Emesis and lavage are contraindicated, given the risk of aspiration.
 Activated charcoal is not useful because it does not bind the common
hydrocarbons and can also induce vomiting.
 Respiratory treatment is supportive, neither corticosteroids nor prophylactic
antibiotics have shown any clear benefits.
 Patients with dysrhythmias should be treated with β-blockers (usually esmolol).

*** Good Luck ***