Proudfoot A T, Simpson D, Dyson E H
Med Toxicol. 1986 Mar-Apr;1(2):83-100. doi: 10.1007/BF03259830.
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)
急性铁中毒在5岁以下儿童中最为常见。虽然毫无疑问它可能致命,但最近的调查显示,死亡仅发生在极少数病例中,而且铁盐导致的药物过量致死案例占少数。同样,在过去三十年中,严重病例的比例似乎有所下降,这可能是由于治疗更及时、更积极,但更可能是由于报告的轻微接触病例数量增加。铁盐对胃肠道有直接毒性,可引起呕吐、腹泻、腹痛,偶尔还会导致大量失血。它们还通过干扰中间代谢、引发休克和减少组织灌注导致代谢性酸中毒。急性铁中毒的临床过程分为4个阶段。摄入后6小时内,急性胃肠道刺激症状为主,大多数患者不会出现其他症状,也不会进展到下一阶段。很少有失血严重到导致低血压的情况。严重中毒的特征是意识障碍、抽搐和代谢性酸中毒。第二阶段是摄入后6至12小时,症状有所缓解。第三阶段从摄入后12至48小时,只有少数患者会进入此阶段。通常会再次出现或发生休克和代谢性酸中毒,还可能发展为肾衰竭和广泛肝细胞坏死的症状。最后(第四)阶段是摄入后2至6周,仅在幼儿中可能出现,其特征是由于铁诱导的黏膜溃疡愈合导致胃或十二指肠狭窄而再次呕吐。人类急性铁中毒尚未得到充分研究,而且由于病例罕见且分散,现在也不太可能进行充分研究。因此,许多传统治疗方法的证据并不令人满意。评估中毒严重程度是最佳治疗的必要前提,但却很困难。摄入的元素铁量难以确定,因为很少能准确得知,而且由于呕吐和腹泻,吸收情况也不可预测。常见的临床特征也不可靠,尽管一般认为昏迷、休克和代谢性酸中毒表明中毒严重。(摘要截断于400字)