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Acute zinc chloride ingestion in a young child
CASE REPORT
Acute Zinc Chloride Ingestion In a Young Child Joseph L. Potter, MD, PhD Akron, Ohio
This brief report describes the clinical course and management of a child who ingested a zinc chloride solution used in a lead soldering process. Injury was limited to bleeding from esophageal erosions and hematemesis. No adverse systemic effects were observed, although serum zinc levels were markedly elevated. A single small dosage of calcium disodium edetate (150 mg dissolved in 75 ml 1:5 normal saline) was effective in normalizing the serum zinc level. Potter JL: Acute zinc chloride ingestion in a young child. Ann Emerg Med 10:267-269, May 1981.
ingestion, zinc chloride; toxicology, zinc chloride INTRODUCTION Although the medical literature is abundant with respect to zinc deficiency and its treatment, and consideration has been accorded the so-called "fume fever" due to inhalation, 1 very little has been recorded regarding the toxicity and management of patients who ingest soluble salts of zinc. Several recent reviews of zinc metabolism devote almost negligible consideration to zinc toxicity in man. 24 We report a case of zinc chloride ingestion and discuss its clinical presentation, course, and management. CASE REPORT The patient was a 28-month-old white infant who ingested 4 oz of an acid soldering flux which his mother was using in the process of making lead-lined windows and which she knew contained zinc chloride. The patient vomited twice at home within five to ten minutes of ingestion, and was then brought to the emergency department of Children's Hospital where he vomited Hematest ~positive material several times. Atomic absorption spectrophotometry of a sample of the ingested fluid provided by the mother immediately revealed a zinc content of 11%. An intravenous line of lactated Ringer's solution was started at a rate of 75 ml/hr and the patient was hospitalized. He weighed 13.1 kg. Physical examination revealed a slightly lethargic child in no apparent distressl He was sleepy, but easily arousable. His blood pressure was 132/88 mm Hg; pulse, 108 beats per minute; respirations, 28 per minute; and temperature, 37 C. No burns of the lips, mouth, or pharynx were seen. Admission studies were as follows (normal ranges in parentheses): sodium, 139 mEq/L; potassium, 3.5 mEq/L; chloride, 104 mEq/L; calcium, 4.4 mEq/L; pH, 7.39; PCO2, 35 mm Hg; PO2, 88 mm Hg; bicarbonate, 20.5 mEq/L; alkaline phosphatase, 197 IU (100-350); SGOT, 48 IU (10-30); GGTP, 8 IU (10-90); total protein, 7.0 gm/dl; hemoglobin, 12.6 gm/dl; a n d white blood cells, 18,000/cu ram. Urinalysis was normal. Serum zinc level was 1,644 ~g/dl on admission, rose to 1,944 ~g/dl after an hour, and then dropped to 1,230 ~g/dl three hours later just prior to the institution of therapy. From the Department of Pathology, Children's Hospital Medical Center of Akron, Akron, Ohio. Address for reprints: Joseph L. Potter, MD, PhD, Children's Hospital Medical Center of Akron, 281 Locust Street, Akron, Ohio 44308
10:5 (May) 1981
Ann Emerg Med
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A single dosage of 150 mg calcium disodium edetate dissolved in 75 ml of 1:5 normal saline containing 5% glucose was administered intravenously over a period of one hour. Two hours later, serum zinc was 450 ~g/dl and his blood pressure had normalized. Six hours after administration, serum zinc was 270 ~g/dl; 12 hours later, serum zinc was 134 ~g/dl (77-137) and serum copper was 150 ~g/dl (30-150). At this time, esophagoscopy revealed a small amount of bleeding from mucosal abrasions. The esophagus was otherwise entirely normal. Radiologic examination of the chest and a skeletal survey were unremarkable. An electrocardiogram on the following day was within normal limits. A detailed neurological evaluation showed no effect of the hyperzincemia. A complete urinalysis on the day of discharge was entirely normal and with a zinc content of 531 ~g per 24-hr collection (140800) ~g/day. No late complilcations h a v e occurred in the two years since ingestion.
DISCUSSION The h u m a n daily requirement for zinc ranges from 3 mg to. 15 mg per day, depending on its bioavailability in the dietary sources and increasing as a function of age. Zinc is absorbed in the small intestine and transported in the blood, bound predominantly to plasma proteins and to a small extent as amino acid complexes. The primary route of excretion of zinc is via the feces, with small amounts excreted in urine and sweat. The biologic importance of zinc resides in its role as a cofactor for many enzymes and in its function in nucleic acid and protein metabolism. Zinc deficiency may be due to inadequate intake or excessive losses due to steatorrhea or malabsorption syndromes. Zinc deficiency is associated with failure of growth and development, hypogonadism, skin lesions, skeletal changes, and altered vitamin A metabolism. An uncommon inherited disease, acrodermatitis enterohepatica, is due to zinc deficiency and responds dramatically to oral zinc supplementation. Zinc also forms biologically important complexes with insulin. Alcohol dehydrogenase, carbonic anhydrase, and carboxypeptidase are examples of enzymes requiring zinc as a cofactor. Flux is a generic term for a variety of formulations of zinc salts used
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in soldering processes, and the composition of the flux may vary depending on the manufacturer. 5 According to the vendors of the product ingested in this case, two formulations of flux were sold: one containing 20% zinc chloride and 2% a m m o n i u m chloride, and the other containing 10% zinc chloride and 2% ammonium chloride. Our analysis indicated that the child had ingested the former solution. If the total dosage had been absorbed, the child would have received 13.2 gm of zinc, or 1 gm/kg of body weight. The powerful emetic property of zinc chloride must l~ave reduced substantially the magnitude of the intake, but it was not possible to estimate this in the absence of zinc measurements of the vomitus. At blood levels of almost 2,000 ~g/dl, symptomatology, apart from hematemesis, was mild. The toxicity of zinc generally has been considered mild in comparison with other metals such as copper, mercury, lead, and iron. 24 The almost complete absence of systemic toxicity in our patient seems to confirm this view. The major adverse effect of acute zinc chloride ingestion appears to reside in its corrosive effect on the tissues of the gastrointestinal tract which it bathes. 6 Anemia secondary to hyperzincemia has been reported in patients on hemodialysis, 7,s and another group has reported a fatality in a 72-year-old woman with Crohn's disease who received an inadvertent overdose of zinc. 9 The precise role of the elevated zinc levels in these patients is somewhat complicated by the fact that all had chronic, debilitating diseases. Treatment of acute zinc salt ingestion should include dilution of the poison with water or milk and gastric lavage, unless the p a t i e n t is vomiting or there is evidence of severe corrosive damage. 6 Few recommendations exist in the toxicology literature regarding the dosage of calcium disodium edetate specifically for hyperzincemia, 1° and physicians generally have adopted and applied the guidelines for lead poisoning, ie, 50 mg/kg/day to 75 mg/kg/day. 11 In o u r p a t i e n t , a s i n g l e intravenous dosage of calcium disodium edetate at 10 mg/kg of body weight was sufficient to lower rapidly and r e t u r n to normal the zinc level due to the high stability constant of the chelate 12 relative to that of zinc proteinate. ~3 The serum zinc level peaked and then dropped precipitously while the patient was re-
Ann Emerg Med
ceiving intravenous fluids and prior to the administration of calcium disodium edetate. It would have been of interest to follow the zinc levels in this patient with intravenous fluids alone and in the absence of chelation therapy, as the zinc level may have continued to increase toward or to normality. Our results indicate that the calcium disodium edetate dosage recommended for lead is much higher than that required for zinc. In view of the rather low systemic toxicity of zinc TM and the danger of renal injury due to high levels of the chelating agent, 11 it is recommended that overly aggressive chelation therapy be avoided in patients with hyperzincemia. However, there should be careful observation for the possible caustic and corrosive effects of the ingestion, and v i t a l signs s h o u l d be m o n i t o r e d closely.
CONCLUSION Zinc is an easily chelatable meta l which, in excess, can be eliminated from the body by the administration of a small dosage of calcium disodium edetate. At s e r u m zinc levels of almost 2,000 ~g/dl, little adverse systemic effect was noted. Injury was limited to the corrosive action of zinc on the e s o p h a g u s . Rapid d i a g n o s i s and a p p r o p r i a t e management require the immediate a v a i l a b i l i t y of l a b o r a t o r y backup with the instrumentation capable of carrying out the determination of zinc and other metals.
REFERENCES 1. Papp JP: Metal fume fever. Postgrad Med 43-'160-163, 1968.
2. Praesad AS: Clinical, biochemical, and pharmacological role of zinc, in George R, Cho AK, (eds): Annual Review of Pharmacology and Toxicology, vol 19. Palo Alto, California, Annual Reviews, Inc, 1979, pp 393-426. 3. Underwood EJ: Zinc, in Trace Elements in Human and Animal Nutrition,
ed 4. New York, Academic Press, 1977, pp 196-242. 4. Burch RE, Sullivan JF: Clinical and nutritional aspects of zinc deficiency and excess, in Burch RE, Sullivan JF (eds): The Medical Clinics of North America, vol 60. Philadelphia, WB Saunders Co, 1976, pp 675-685. 5. Gosselin PE, Hodge HC, Smith RP, et al: Clinical Toxicology of Commercial Products, ed 4, Baltimore, Williams and Wilkins Company, 1976, p 130. 6. Rumack BH (ed): Zinc and zinc compounds. Poisindex. Micromedex, Inc, 1980.
10:5 (May) 1981
7. Petrie JJB, Row PG: Dialysis anemia caused 'by subacute zinc toxicity. Lancet 2:1178-1180, 1974. 8. Gallery EDM, Blomfield J, Dixon SR: Acute zinc toxicity in haemodialysis. Br Med J 4:331-333, 1972. 9. Brocks A, Reid H, Glazer G: Acute intravenous zinc p o i s o n i n g . Br Med J 1:1390-1391, 1977.
10:5 (May) 1981
10. Lovejoy FH: Poisoning, in Graef JW, Cone TE (eds): Manual of Pediatric Therapeutics, ed 1. Boston, Little, Brown, and Co, 1974, p 71. 11. Physicians Desk Reference, ed 35. Oradell, New Jersey, Medical Economics Co, 1981, pp 1453-1454. 12. Peterg DT, Hayes JM, Hieftje GM: Chemical Separations and Measurements,
Ann Emerg Med
ed 1. Philadelphia, WB S a u n d e r s Co, 1974, p 173. 13. Parisi AF, Vallee BL: Isolation of a zinc a 2 - m a c r o g l o b u l i n f r o m h u m a n serum. Biochem 9:2421-2426, 1970. 14. Hallbook T, Lanner E: Serum zinc and healing of venous leg ulcers. Lancet 2:780-782, 1972.
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Acute Zinc Chloride Ingestion In a Young Child Joseph L. Potter, MD, PhD Akron, Ohio
This brief report describes the clinical course and management of a child who ingested a zinc chloride solution used in a lead soldering process. Injury was limited to bleeding from esophageal erosions and hematemesis. No adverse systemic effects were observed, although serum zinc levels were markedly elevated. A single small dosage of calcium disodium edetate (150 mg dissolved in 75 ml 1:5 normal saline) was effective in normalizing the serum zinc level. Potter JL: Acute zinc chloride ingestion in a young child. Ann Emerg Med 10:267-269, May 1981.
ingestion, zinc chloride; toxicology, zinc chloride INTRODUCTION Although the medical literature is abundant with respect to zinc deficiency and its treatment, and consideration has been accorded the so-called "fume fever" due to inhalation, 1 very little has been recorded regarding the toxicity and management of patients who ingest soluble salts of zinc. Several recent reviews of zinc metabolism devote almost negligible consideration to zinc toxicity in man. 24 We report a case of zinc chloride ingestion and discuss its clinical presentation, course, and management. CASE REPORT The patient was a 28-month-old white infant who ingested 4 oz of an acid soldering flux which his mother was using in the process of making lead-lined windows and which she knew contained zinc chloride. The patient vomited twice at home within five to ten minutes of ingestion, and was then brought to the emergency department of Children's Hospital where he vomited Hematest ~positive material several times. Atomic absorption spectrophotometry of a sample of the ingested fluid provided by the mother immediately revealed a zinc content of 11%. An intravenous line of lactated Ringer's solution was started at a rate of 75 ml/hr and the patient was hospitalized. He weighed 13.1 kg. Physical examination revealed a slightly lethargic child in no apparent distressl He was sleepy, but easily arousable. His blood pressure was 132/88 mm Hg; pulse, 108 beats per minute; respirations, 28 per minute; and temperature, 37 C. No burns of the lips, mouth, or pharynx were seen. Admission studies were as follows (normal ranges in parentheses): sodium, 139 mEq/L; potassium, 3.5 mEq/L; chloride, 104 mEq/L; calcium, 4.4 mEq/L; pH, 7.39; PCO2, 35 mm Hg; PO2, 88 mm Hg; bicarbonate, 20.5 mEq/L; alkaline phosphatase, 197 IU (100-350); SGOT, 48 IU (10-30); GGTP, 8 IU (10-90); total protein, 7.0 gm/dl; hemoglobin, 12.6 gm/dl; a n d white blood cells, 18,000/cu ram. Urinalysis was normal. Serum zinc level was 1,644 ~g/dl on admission, rose to 1,944 ~g/dl after an hour, and then dropped to 1,230 ~g/dl three hours later just prior to the institution of therapy. From the Department of Pathology, Children's Hospital Medical Center of Akron, Akron, Ohio. Address for reprints: Joseph L. Potter, MD, PhD, Children's Hospital Medical Center of Akron, 281 Locust Street, Akron, Ohio 44308
10:5 (May) 1981
Ann Emerg Med
267/61
A single dosage of 150 mg calcium disodium edetate dissolved in 75 ml of 1:5 normal saline containing 5% glucose was administered intravenously over a period of one hour. Two hours later, serum zinc was 450 ~g/dl and his blood pressure had normalized. Six hours after administration, serum zinc was 270 ~g/dl; 12 hours later, serum zinc was 134 ~g/dl (77-137) and serum copper was 150 ~g/dl (30-150). At this time, esophagoscopy revealed a small amount of bleeding from mucosal abrasions. The esophagus was otherwise entirely normal. Radiologic examination of the chest and a skeletal survey were unremarkable. An electrocardiogram on the following day was within normal limits. A detailed neurological evaluation showed no effect of the hyperzincemia. A complete urinalysis on the day of discharge was entirely normal and with a zinc content of 531 ~g per 24-hr collection (140800) ~g/day. No late complilcations h a v e occurred in the two years since ingestion.
DISCUSSION The h u m a n daily requirement for zinc ranges from 3 mg to. 15 mg per day, depending on its bioavailability in the dietary sources and increasing as a function of age. Zinc is absorbed in the small intestine and transported in the blood, bound predominantly to plasma proteins and to a small extent as amino acid complexes. The primary route of excretion of zinc is via the feces, with small amounts excreted in urine and sweat. The biologic importance of zinc resides in its role as a cofactor for many enzymes and in its function in nucleic acid and protein metabolism. Zinc deficiency may be due to inadequate intake or excessive losses due to steatorrhea or malabsorption syndromes. Zinc deficiency is associated with failure of growth and development, hypogonadism, skin lesions, skeletal changes, and altered vitamin A metabolism. An uncommon inherited disease, acrodermatitis enterohepatica, is due to zinc deficiency and responds dramatically to oral zinc supplementation. Zinc also forms biologically important complexes with insulin. Alcohol dehydrogenase, carbonic anhydrase, and carboxypeptidase are examples of enzymes requiring zinc as a cofactor. Flux is a generic term for a variety of formulations of zinc salts used
62/268
in soldering processes, and the composition of the flux may vary depending on the manufacturer. 5 According to the vendors of the product ingested in this case, two formulations of flux were sold: one containing 20% zinc chloride and 2% a m m o n i u m chloride, and the other containing 10% zinc chloride and 2% ammonium chloride. Our analysis indicated that the child had ingested the former solution. If the total dosage had been absorbed, the child would have received 13.2 gm of zinc, or 1 gm/kg of body weight. The powerful emetic property of zinc chloride must l~ave reduced substantially the magnitude of the intake, but it was not possible to estimate this in the absence of zinc measurements of the vomitus. At blood levels of almost 2,000 ~g/dl, symptomatology, apart from hematemesis, was mild. The toxicity of zinc generally has been considered mild in comparison with other metals such as copper, mercury, lead, and iron. 24 The almost complete absence of systemic toxicity in our patient seems to confirm this view. The major adverse effect of acute zinc chloride ingestion appears to reside in its corrosive effect on the tissues of the gastrointestinal tract which it bathes. 6 Anemia secondary to hyperzincemia has been reported in patients on hemodialysis, 7,s and another group has reported a fatality in a 72-year-old woman with Crohn's disease who received an inadvertent overdose of zinc. 9 The precise role of the elevated zinc levels in these patients is somewhat complicated by the fact that all had chronic, debilitating diseases. Treatment of acute zinc salt ingestion should include dilution of the poison with water or milk and gastric lavage, unless the p a t i e n t is vomiting or there is evidence of severe corrosive damage. 6 Few recommendations exist in the toxicology literature regarding the dosage of calcium disodium edetate specifically for hyperzincemia, 1° and physicians generally have adopted and applied the guidelines for lead poisoning, ie, 50 mg/kg/day to 75 mg/kg/day. 11 In o u r p a t i e n t , a s i n g l e intravenous dosage of calcium disodium edetate at 10 mg/kg of body weight was sufficient to lower rapidly and r e t u r n to normal the zinc level due to the high stability constant of the chelate 12 relative to that of zinc proteinate. ~3 The serum zinc level peaked and then dropped precipitously while the patient was re-
Ann Emerg Med
ceiving intravenous fluids and prior to the administration of calcium disodium edetate. It would have been of interest to follow the zinc levels in this patient with intravenous fluids alone and in the absence of chelation therapy, as the zinc level may have continued to increase toward or to normality. Our results indicate that the calcium disodium edetate dosage recommended for lead is much higher than that required for zinc. In view of the rather low systemic toxicity of zinc TM and the danger of renal injury due to high levels of the chelating agent, 11 it is recommended that overly aggressive chelation therapy be avoided in patients with hyperzincemia. However, there should be careful observation for the possible caustic and corrosive effects of the ingestion, and v i t a l signs s h o u l d be m o n i t o r e d closely.
CONCLUSION Zinc is an easily chelatable meta l which, in excess, can be eliminated from the body by the administration of a small dosage of calcium disodium edetate. At s e r u m zinc levels of almost 2,000 ~g/dl, little adverse systemic effect was noted. Injury was limited to the corrosive action of zinc on the e s o p h a g u s . Rapid d i a g n o s i s and a p p r o p r i a t e management require the immediate a v a i l a b i l i t y of l a b o r a t o r y backup with the instrumentation capable of carrying out the determination of zinc and other metals.
REFERENCES 1. Papp JP: Metal fume fever. Postgrad Med 43-'160-163, 1968.
2. Praesad AS: Clinical, biochemical, and pharmacological role of zinc, in George R, Cho AK, (eds): Annual Review of Pharmacology and Toxicology, vol 19. Palo Alto, California, Annual Reviews, Inc, 1979, pp 393-426. 3. Underwood EJ: Zinc, in Trace Elements in Human and Animal Nutrition,
ed 4. New York, Academic Press, 1977, pp 196-242. 4. Burch RE, Sullivan JF: Clinical and nutritional aspects of zinc deficiency and excess, in Burch RE, Sullivan JF (eds): The Medical Clinics of North America, vol 60. Philadelphia, WB Saunders Co, 1976, pp 675-685. 5. Gosselin PE, Hodge HC, Smith RP, et al: Clinical Toxicology of Commercial Products, ed 4, Baltimore, Williams and Wilkins Company, 1976, p 130. 6. Rumack BH (ed): Zinc and zinc compounds. Poisindex. Micromedex, Inc, 1980.
10:5 (May) 1981
7. Petrie JJB, Row PG: Dialysis anemia caused 'by subacute zinc toxicity. Lancet 2:1178-1180, 1974. 8. Gallery EDM, Blomfield J, Dixon SR: Acute zinc toxicity in haemodialysis. Br Med J 4:331-333, 1972. 9. Brocks A, Reid H, Glazer G: Acute intravenous zinc p o i s o n i n g . Br Med J 1:1390-1391, 1977.
10:5 (May) 1981
10. Lovejoy FH: Poisoning, in Graef JW, Cone TE (eds): Manual of Pediatric Therapeutics, ed 1. Boston, Little, Brown, and Co, 1974, p 71. 11. Physicians Desk Reference, ed 35. Oradell, New Jersey, Medical Economics Co, 1981, pp 1453-1454. 12. Peterg DT, Hayes JM, Hieftje GM: Chemical Separations and Measurements,
Ann Emerg Med
ed 1. Philadelphia, WB S a u n d e r s Co, 1974, p 173. 13. Parisi AF, Vallee BL: Isolation of a zinc a 2 - m a c r o g l o b u l i n f r o m h u m a n serum. Biochem 9:2421-2426, 1970. 14. Hallbook T, Lanner E: Serum zinc and healing of venous leg ulcers. Lancet 2:780-782, 1972.
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