Management of acute iron poisoning.

A T Proudfoot, D Simpson, E H Dyson
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Abstract

Acute iron poisoning is most common in children below the age of 5 years. While there is no doubt that it may be fatal, recent surveys show that death occurs in only a very small percentage of cases and that iron salts are responsible for a small minority of fatalities due to overdosage with drugs. Similarly, the proportion of severe cases seems to have fallen over the last thirty years, possibly due to earlier and more aggressive treatment but more probably due to an increase in the number of minor exposures reported. Iron salts are directly toxic to the gastrointestinal tract causing vomiting, diarrhoea, abdominal pain and occasionally significant blood loss. They also cause metabolic acidosis by interfering with intermediary metabolism and producing shock and reduced tissue perfusion. The clinical course of acute iron poisoning is divided into 4 phases. Features of acute gastrointestinal irritation dominate the period up to 6 hours after ingestion and most patients do not develop other features or progress beyond this stage. Rarely, blood loss may be sufficient to cause hypotension. Severe poisoning is characterised by impairment of consciousness, convulsions and metabolic acidosis. The second phase, 6 to 12 hours after ingestion, is one of remission of features. Phase 3 comprises the period 12 to 48 hours from ingestion and is reached only by a small minority of patients. Recurrence or development of shock, and metabolic acidosis are usual and renal failure and features of extensive hepatocellular necrosis may develop. The last (fourth) phase, 2 to 6 weeks after ingestion, is only likely to develop in young children and is characterised by recurrence of vomiting due to gastric or duodenal stenosis caused by healing of iron-induced mucosal ulcers. Acute iron poisoning in humans has not been adequately studied and is unlikely to be so now because of the infrequent and sporadic occurrence of cases. The evidence for many conventional aspects of management is therefore unsatisfactory. Assessment of severity of poisoning is an essential prerequisite to optimum management but is difficult. The amount of elemental iron ingested is unacceptable since it is seldom known with accuracy and absorption is unpredictable because of vomiting and diarrhoea. The commonly encountered clinical features are also unreliable although it is generally accepted that coma, shock and metabolic acidosis indicate severe poisoning.(ABSTRACT TRUNCATED AT 400 WORDS)

急性铁中毒的处理。
急性铁中毒最常见于5岁以下儿童。毫无疑问,铁盐可能是致命的,但最近的调查显示,死亡只发生在很小比例的病例中,而铁盐是少数因过量服用药物而死亡的原因。同样,在过去三十年中,严重病例的比例似乎有所下降,这可能是由于更早和更积极的治疗,但更可能是由于报告的轻微接触数量的增加。铁盐对胃肠道有直接毒性,引起呕吐、腹泻、腹痛和偶尔大量失血。它们还通过干扰中间代谢、产生休克和减少组织灌注而引起代谢性酸中毒。急性铁中毒的临床过程可分为4个阶段。特征的急性胃肠道刺激主导时期摄入6小时后,大多数病人不开发其他功能或进步超越这个阶段。少数情况下,失血足以引起低血压。严重中毒的特征是意识受损、抽搐和代谢性酸中毒。第二阶段,摄入后6至12小时,是症状缓解期之一。第3阶段包括从摄入后12至48小时,只有少数患者达到。复发或发展的冲击,代谢性酸中毒,肾功能衰竭和功能广泛的肝细胞坏死可能发展。最后(第四)期,在摄入后2至6周,仅可能发生在幼儿中,其特征是由于铁诱导的粘膜溃疡愈合引起的胃或十二指肠狭窄导致呕吐复发。人类急性铁中毒尚未得到充分的研究,而且由于病例的罕见和零星发生,现在也不太可能得到充分的研究。因此,管理的许多传统方面的证据并不令人满意。中毒严重程度的评估是最佳管理的必要前提,但也是困难的。铁元素的摄入量是不可接受的,因为它很少被准确地知道,吸收是不可预测的,因为呕吐和腹泻。虽然昏迷、休克和代谢性酸中毒被普遍认为是严重中毒的表现,但常见的临床特征也不可靠。(摘要删节为400字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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