Pediatric emergency medicine trisk 3072 3072
Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (102.79 KB, 1 trang )
Iron
CLINICAL PEARLS
Iron toxicity begins with vomiting and progresses to metabolic acidosis
and multisystem organ failure.
Serum iron levels contribute to evaluation, but do not correspond well
with severity of illness.
Treatment for patients with suspected serious iron toxicity begins with
aggressive supportive care and early institution of deferoxamine.
Current Evidence
In the 1990s, iron poisoning was one of the most common, potentially fatal
intoxications in children. Most serious childhood poisonings result from ingestion
of maternal prenatal vitamins or ferrous sulfate tablets (which unfortunately often
look much like candy) that were intended for adults. A common scenario is that
the patient is a toddler whose mother has just had a new baby; the increased
demands on the mother’s attention and almost universal prescription of iron to
pregnant women combine to set the stage for this ingestion. In addition, numerous
exposures result from ingestion of iron-fortified children’s vitamins, but these
tend to be far less toxic.
Sufficient data to define a safe lower limit for toxic iron ingestions are not
available. As little as 20 mg/kg of elemental iron has caused GI toxicity, whereas
ingestions of more than 40 mg/kg often produce moderate toxic effects with
profound toxicity seen after doses of 60 mg/kg. Of course, it is often impossible
to know the exact number of tablets ingested. As few as ten 300-mg FeSO4
tablets have been fatal to a young child. Furthermore, the elemental iron content
of whole bottles of chewable vitamins is usually about 1,200 mg. Industry
standards typically lead to the use of child resistant caps for vitamin bottles that
contain more than 250 mg of elemental iron. Unit dose (blister) packaging has
been advised for pills with high iron content. These measures have led to a
dramatic reduction in deaths due to exploratory iron poisoning.
Iron toxicity results from direct caustic effect on the GI mucosa and the
presence of free iron in the circulation. Pathologic changes include hemorrhagic
necrosis of stomach and intestinal mucosa and lesions in the liver that range from
cloudy swelling to areas of complete necrosis. Occasionally, pulmonary
congestion and hemorrhage are noted. Excess free iron is believed to act as a
