鉛中毒

Lead Poisoning-A Case Report

余福祺(Fu-Chi Yue)

《Acta Paediatrica Sinica》 4卷2期 (1963/06) Pp. 143-148

摘要

鉛中毒對於小孩來說，是一種相當嚴重的疾病。因爲若不做早期診斷及適當的治療，則可引起死亡或留下中樞神經系統的後遺症。此疾病例數之多寡，似乎和醫務人員及一般社會人士的關心與興趣成平行的關係，即愈有興趣及關心，則所能找到的病例就愈多。反之，若沒有興趣和關心，則許多病例都在錯誤的診斷下被忽略過去。例如Mellins & Jenkins報告他們在發現第一個病例以後，在一年內陸續發現了21個病例，而在第一個病例被發現以前，有好幾年都沒有做過鉛中毒的診斷。
自本省光復後臺大小兒科曾於民國35年8月及民國42年3月各發現壹個病例。第一病例係4歲之女孩，第二病例係兩歲之男孩，兩病例經治療後皆痊癒，惟未曾提出報告。而光復後之文獻，亦只有張建彬於民國43年12月之第17屆小兒科學術演講會時所報告之一例而已。
最近我們發現一鉛中毒的病例，茲報告如下。

並列摘要

A case of lead poisoning is presented and the literature is reviewed briefly.
The patient, a 15 years old boy and being a workman in a storage battery factory for about one and half a year, was admitted to the Pediatric Ward of the National Taiwan University Hospital because of intermittent abdominal cramp and generalized convulsive seizures on February 2, 1963.
The main signs and symptoms were pallor, abdominal cramp, vomiting, mental cloudiness, restlessness and irritability, generalized convulsive seizures, lead line, hypochromic microcytic anemia with basophilic stippling of erythrocyte, coproporphyrinuria, positive skin test with sodium sulfide and increased density at the epiphysis of long bones on x-ray film. The patient was treated with BAL and other supportive measures but there was no clinical improvement and the patient died on February 5, 1963.
Of greatest importance in the diagnosis of lead poisoning remains the clinical identification of a source of lead. It is also important to ask the parents about the presence of pica in babies and small children under their care. The diagnosis of lead poisoning is usually established when the patient presents the features of hypochromic microcytic anemia with basophilic stippling, coproporphyrinuria, positive skin test with sodium sulfide and increased density at epiphysis of long bones on x-ray film, together with the evidence of contact with chemically demonstrable source of lead.
Ca-EDTA which has been reported to have a high effectiveness in the treatment of lead intoxication was formerly considered to be of no side effect, yet deaths from renal failure caused by inadequate us of Ca-EDTA have been reported. The treatment should be started with smaller dosage of Ca-EDTA and the patient should be kept under close observation. BAL may be used if there is no Ca-EDTA available.
Lead encephalopathy should be treated with intravenous urea with dose of 1gm/kg per 24 hours and the use of Ca-EDTA should be delayed for 12 to 24 hours. The urea therapy may be repeated 8 to 12 hours later if the condition remains critical but blood urea nitrogen should be checked before the use of urea and it should be discontinued if blood urea nitrogen rises above 75mg%. Hypothermia is also worthwhile to try. The surgical decompression is indicated for those who are refractory to medical treatment.
Metabolic disturbance caused by toxic action of lead remains far from understanding, but two groups of mechanism, one responsible for the abnormal concentrations of coproporphyrin and protoporphyrin in erythrocytes, and another underlying urinary coproporphyrin, appear to have been elucidated.