Lead Poisoning From a Toy Necklace
Jessica L. VanArsdale, MD, MPH*; Richard D. Leiker, MS‡; Mel Kohn, MD, MPH§; T. Allen Merritt, MD, MHA㛳¶; and B. Zane Horowitz, MD#
ABSTRACT. A 4-year-old, previously healthy boy ex-perienced intermittent abdominal pain for several weeks. He was diagnosed with probable gastroenteritis, but his symptoms worsened. Laboratory tests revealed normo-cytic anemia, and an abdominal radiograph showed a metallic foreign body in the stomach, without evidence of obstruction. Endoscopy resulted in the retrieval of a quarter and a medallion pendant from the stomach. A venous blood lead level measurement was extremely el-evated, at 123g/dL (level of concern:>10g/dL). The medallion was tested by the state environmental quality laboratory and was found to contain 38.8% lead (388 000 mg/kg), 3.6% antimony, and 0.5% tin. Similar medallions purchased from toy vending machines were analyzed and were found to contain similarly high levels of lead. State health officials notified the US Consumer Product Safety Commission, which resulted in a national volun-tary recall of>1.4 million metal toy necklaces.Pediatrics
2004;114:1096–1099;lead, lead poisoning, lead foreign bod-ies.
ABBREVIATIONS. LFB, lead foreign body; BLL, blood lead level; EDTA, calcium disodium versenate; ZPP, zinc protoporphyrin; RBC, red blood cell.
P
ediatric lead poisoning remains an important preventable public health problem. Children can be exposed to lead through a variety of sources. Although ingestion of dust from lead-based paint remains the most significant source of lead exposure among children, lead can be present in unsuspected objects that, when ingested, can result in rapid lead poisoning. The diagnosis of lead poi-soning resulting from ingestion of lead foreign bod-ies (LFBs) is often delayed when lead poisoning is not included in the differential diagnosis for the pre-senting symptoms. Appropriate management and follow-up procedures have changed during the years, and it is important for pediatric health careproviders to be aware of these changes. This case report describes a child with lead poisoning after ingestion of a medallion necklace purchased from a toy vending machine. We discuss management and follow-up procedures for children with foreign-body ingestion.
CASE REPORT
A 4-year-old, previously healthy boy was brought to his phy-sician after several days of abdominal cramping, vomiting, and diarrhea without fever. Probable viral gastroenteritis was diag-nosed, and the patient’s symptoms resolved during the following week. The patient remained asymptomatic for 1 to 2 weeks until he experienced another bout of vomiting and abdominal pain. He returned to his physician, and an abdominal ultrasound scan revealed a normal appendix with mesenteric adenitis. The results of a complete blood count and metabolic panel were normal except for normocytic anemia (hemoglobin: 9.9 g/dL; hematocrit: 28.4%; mean corpuscular volume: 83 fL) and mild elevation of liver enzyme levels (aspartate aminotransferase: 76 U/L; alanine aminotransferase: 120 U/L). Probable viral syndrome causing mesenteric adenitis and anemia of undetermined cause were di-agnosed. Two days later, the patient was brought to the local emergency department with symptoms of increasing abdominal pain, protracted vomiting, decreased urine output during the previous 48 hours, no bowel movements for 5 days, and a 4- to 5-lb weight loss during the previous week. The patient exhibited in-creased irritability and was unable to eat or sleep because of the abdominal pain. His physical examination was notable for a some-what emaciated appearance, diminished bowel sounds, and ab-dominal tenderness with deep palpation. An abab-dominal radio-graph showed a metallic foreign body in the stomach, without evidence of obstruction. A repeat blood count and metabolic panel showed persistent normocytic anemia (hemoglobin: 9.5 g/dL; he-matocrit: 27.5%; mean corpuscular volume: 82 fL), with some improvement in liver enzyme levels (aspartate aminotransferase: 50 U/L; alanine aminotransferase: 80 U/L). The patient was ad-mitted to the hospital for intravenous hydration and surgical consultation regarding the gastric metallic foreign body. The ini-tial surgical consultation revealed benign abdominal findings, and it was suggested that the object would most likely pass on its own, without necessitating surgical intervention. The following day, an abdominal computed tomography scan showed that the metallic object was more superiorly located, in comparison with findings from the plain film from the previous day. Endoscopy was per-formed, which resulted in retrieval of a quarter and a medallion pendant from the stomach. The patient was discharged from the hospital but returned to his physician 3 days later, with edema of the left cheek and gingiva. He was thought to have either a dental abscess or excessive biting of the cheek. A pediatric dentist was consulted, and dental radiographs excluded the possibility of a dental abscess. There was concern that the cheek bite could have been attributable to a seizure, which prompted assessment of the blood lead level (BLL). The BLL was extremely elevated at 123
g/dL (level of concern:ⱖ10g/dL). The child was admitted to the pediatric intensive care unit for intravenous chelation therapy. A neurology consultation revealed no evidence of encephalopa-thy, and results of a sleep electroencephalogram were normal. The patient was treated with dimercaprol for 48 hours and with cal-cium disodium versenate (EDTA) for 4 days, and the BLL de-creased to 57g/dL. The patient was switched to orally admin-istered succimer but required a repeat course of EDTA when the From the *Departments of Family Medicine and Public Health and
Preven-tive Medicine and #Oregon Poison Center, Oregon Health and Science University, Portland, Oregon; ‡Oregon Childhood Lead Poisoning Preven-tion Program and §Disease PrevenPreven-tion and Epidemiology, Oregon Depart-ment of Human Services, Oregon Health Services, Portland, Oregon;㛳St Charles Medical Center and Central Oregon Pediatric Associates, Bend, Oregon; and ¶Oregon Commission for Children and Families, Portland, Oregon.
Accepted for publication Jun 14, 2004. doi:10.1542/peds.2004-0361
BLL rebounded to 69g/dL. After three 19-day courses of succi-mer, the BLL remained at⬍40g/dL (Fig 1). Iron studies showed no evidence of iron deficiency anemia. Zinc protoporphyrin (ZPP) levels peaked at 556mol/mol (normal: 25-65mol/mol). Periph-eral blood smears showed basophilic stippling.
Environmental investigation of the child’s home by the public health department did not reveal any additional sources of lead exposure; the home was built in 1996. The child’s 6-year-old sibling had a BLL of⬍5g/dL. The child underwent neurode-velopmental, cognitive, and speech therapy evaluations, which showed appropriate development.
The medallion retrieved from the child’s stomach reportedly had been purchased from a toy vending machine in Deschutes County, Oregon. It was estimated that the patient ingested the medallion⬃3 weeks before it was retrieved. The medallion was tested by the state environmental quality laboratory and was found to contain 38.8% lead (388 000 mg/kg), 3.6% antimony, and 0.5% tin. Two similar medallions purchased from toy vending machines in other parts of Oregon were analyzed and were found to contain similarly high levels of lead (44% and 37%). These medallions are round,⬃7/8 inch in diameter, and gray in color, with a symbol on 1 side (Figs 2 and 3). State health officials notified the US Consumer Product Safety Commission and an investigation was initiated, which resulted in a national voluntary recall of⬎1.4 million metal toy necklaces. A distributor of these medallions reported that they are manufactured in India and distributed throughout the United States.
DISCUSSION
Foreign-body ingestion is a common occurrence in the pediatric population. In 2002, the American As-sociation of Poison Control Centers received⬎80 000 calls regarding ingestion of foreign bodies, toys, and miscellaneous objects by children ⬍6 years of age.1 The findings in this case underscore the fact that lead poisoning can occur as a result of ingestion of seem-ingly innocuous objects. There have been reports of lead poisoning resulting from ingestion of curtain weights, fishing sinkers, lead shot/pellets, key chain emblems, toy sailboat ballasts, and clothing accesso-ries.2–11
In the literature, there are 2 case reports of lead poisoning that was not suspected on the basis of the child’s clinical presentation and resulted in death after ingestion of LFBs. Hugelmeyer et al4described a 23-month-old girl who died as a result of lead encephalopathy after ingestion of a lead curtain weight, which resulted in a BLL of 238g/dL. Al-though the child presented with classic symptoms of lead poisoning, including irritability, lethargy, vom-iting, abdominal pain, and seizures, as well as ane-mia and abdominal radiographic results showing a
metallic foreign body in the right upper quadrant, the possibility of lead poisoning was not entertained until after the child’s death. The lead curtain weight was thought to have been ingested⬃4 weeks before death.4A similar case was reported by Forsby et al,5 who described a 2-year-old girl with a 10-day history of vomiting who died within 24 hours after hospital admission. The postmortem examination revealed evidence of encephalopathy and a lead drapery weight in the patient’s stomach.5Delayed diagnosis and treatment were common among the published case reports, because lead poisoning was not in-cluded in the differential diagnosis for the presenting symptoms.
Acute lead poisoning can cause symptoms such as irritability, lethargy, abdominal pain, constipation, and vomiting, all of which are nonspecific symptoms usually attributed to gastroenteritis. If the condition
Fig 1. Venous BLLs for a 4-year-old child in Oregon, 2003.
Fig 2. Medallion retrieved from the child’s stomach. Analysis by the state environmental quality laboratory found the medallion to contain 38.8% lead (388 000 mg/kg), 3.6% antimony, and 0.5% tin.
Fig 3. Medallions purchased from toy vending machines in Ore-gon. Analysis by the state environmental quality laboratory found the medallions to contain 37% to 44% lead.
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is not recognized in the early phase of gastrointesti-nal symptoms, then lead encephalopathy may ensue, causing ataxia, hyperirritability, stupor, and sei-zures. This may occur at BLLs of⬎70 to 80g/dL.12 Acute levels of ⬎100 g/dL have been associated with coma and death resulting from cerebral edema. As the reported case illustrates, not all children with very high BLLs become encephalopathic; this is be-cause lead follows a multicompartmental model of tissue entry. Acutely absorbed lead is distributed first to the blood, where 98% of the lead becomes bound in the red blood cells (RBCs), leaving only a small fraction available for distribution to soft tissues such as the brain and kidneys. Lead readily and rapidly crosses the blood-brain barrier, however, and is quickly transported into neurons by efficient met-abolic pumps. It is likely that physiologically signif-icant concentrations of lead are deposited in the brain and other soft-tissue compartments even with acute elevations in BLLs. With long-term exposure, lead enters the deeper compartment of bone, which has a prolonged excretion half-life.12 If a BLL mea-sured early after ingestion of an LFB is significantly elevated but the child is asymptomatic, then lead resides mostly in the blood compartment, where it can be easily chelated and removed before it be-comes a chronic source of exposure for the patient. Elevated ZPP levels reflect lead bound to intercellu-lar globins in RBCs; levels increase slowly as RBCs are produced in marrow that has elevated levels of lead stored in it. The reported child’s elevated ZPP levels and frequent rebounds of BLLs after chelation suggest that he had elevated soft-tissue stores, which may reflect either prior unrecognized ingestions of lead or some lead deposition in brain and other soft tissues as a result of delayed recognition of the LFB ingestion.
Recent studies showed that lead can cause intel-lectual impairment even among children with BLLs ofⱕ10g/dL.13The long-term effects of acute lead poisoning, such as described in this report, are un-clear, because long-term follow-up monitoring after acute lead intoxication has not been performed sys-tematically. Current guidelines call for any child who has ever exhibited an elevated BLL (⬎10 g/dL) to receive long-term neurodevelopmental and behav-ioral surveillance, because there may be a lag of several years before problems become evident.14The frontal lobes are particularly vulnerable to the effects of lead poisoning, and lead neurotoxicity can result in disruption of executive functions, attention, social-behavior conduct, and impulse control, which may not be fully appreciated until late childhood or ado-lescence.15 Tests for executive functioning are not available for children as young as the child described in this case report; therefore, close follow-up moni-toring is important. Any child who has ever exhib-ited an elevated BLL should have this listed on their medical problem list, even after the BLL returns to normal.
Recommended management of LFB ingestion has changed over the years, and there may be miscon-ceptions about appropriate management. In 1989, Durback et al16 suggested that solid lead objects
could be retained safely in the bowels for up to 2 weeks without causing lead toxicity. The prevailing thought was that metallic lead and lead alloys were poorly absorbed after ingestion. In a more recent report, Fergusson et al7proposed that management of LFBs depends on the location. Lead objects located in the stomach pose a higher risk of lead poisoning, compared with lead objects located more distally in the gastrointestinal tract. The acidic environment in the stomach aids dissolution of the lead object, al-lowing the dissolved lead to pass into the duode-num, where it is absorbed into the bloodstream. For LFBs located in the stomach, those authors suggested treatment with a proton pump inhibitor, to decrease the rate of dissolution, and a prokinetic agent, to encourage passage of the LFB. Repeat radiographs should be obtained 48 hours after ingestion; if the LFB remains in the stomach, then it should be re-moved endoscopically. Those authors also proposed that other indications for prompt removal include a BLL of⬎55 g/dL or symptoms of lead poisoning. For LFBs located in the small intestine, they sug-gested that the child be given a cathartic agent and observed for passage of the object with abdominal radiographs and BLL measurements every 4 days.7
It may be advisable, however, to monitor BLLs more frequently in the first few days after ingestion, because levels can increase rapidly after ingestion. Published experience suggests that ingestion of LFBs often results in BLLs of ⬎55 g/dL, for which re-trieval is indicated. A case report by Treble and Thompson10suggests that BLLs can increase rapidly even when the LFB is located in the large intestine. Those authors reported a BLL of 56 g/dL for a 2.5-year-old child only 1.5 hours after ingestion of pellets from an air rifle. An abdominal radiograph indicated that the majority of the pellets were located in the large intestine.10McKinney2reported a BLL of 57g/dL for a 5-year-old child 13 hours after inges-tion of lead pellets from a strap-on ankle weight. Two unpublished case reports from the Oregon Childhood Lead Poisoning Prevention Program noted similar findings. The first patient was a 10-year-old child who swallowed a fishing weight and exhibited a BLL of 40g/dL 3 hours after ingestion. The second patient was a 4-year-old child who swal-lowed lead shot and exhibited a BLL of 55 g/dL within 24 hours.
Removal of an LFB located beyond the stomach may include whole-bowel irrigation with a balanced polyethylene glycol solution. Colonoscopic removal should be reserved for objects that remain in the intestine and pose a risk for chronic lead absorption.8 Although it is rare, LFBs can become lodged in the appendix, resulting in appendicitis with or without lead poisoning.6,17
Al-though efforts should be made to remove the in-gested LFB first, the use of chelating agents should not be withheld if endoscopic removal must be de-layed and encephalopathy is present.
On the basis of our review of published case re-ports, it is advisable that all children who ingest metallic foreign bodies undergo BLL testing, which should be repeated within 24 hours if levels are elevated. It may also be prudent to measure BLLs for children with nonmetallic foreign bodies. Wiley et al19found that children⬍6 years of age with foreign bodies in the ear, nose, or gastrointestinal tract had higher mean BLLs, compared with control subjects with similar environmental risk factors for lead ex-posure. This finding suggests that behaviors such as inserting foreign bodies into body orifices represent a risk factor for lead poisoning and children exhibit-ing these behaviors may require BLL tests. In the case described by McKinney,2 the child passed not only 11 lead pellets but also nonmetallic beads and an eraser.
CONCLUSIONS
This case report illustrates several important is-sues. First, it illustrates the presence of lead hazards in objects routinely intended for use by children. Clinicians and caretakers of children should be alerted to the fact that lead can be found in unsus-pected objects, and lead poisoning should be consid-ered for any child who ingests a foreign object. All children who ingest metallic foreign bodies should undergo BLL testing, with frequent monitoring. Sec-ond, pediatric health care providers should include lead poisoning in the differential diagnosis, particu-larly when a child is diagnosed with anemia of un-known cause and/or probable gastroenteritis that does not follow the usual course, warranting addi-tional evaluation, including abdominal radiographs and BLL tests. This case report clearly illustrates the critical advocacy role that health care providers can play in identifying hazards affecting children’s health and the importance of timely reporting of such hazards to public health authorities, so that appropriate actions can be initiated. The recall that resulted from the reporting of this case likely pro-tected other children from exposure to this lead source.
ACKNOWLEDGMENTS
We acknowledge the following people who provided support in the investigation and follow-up monitoring of this case: Barbara
R. Zeal, Marilyn J. Scott, David H. Lew, and Wendy L. Pickner from the Oregon Childhood Lead Poisoning Prevention Program, Oregon Department of Human Services, Oregon Health Services; Daniel W. Peddycord, Elaine Severson, Kathleen M. Moore, and Nadine J. Pusel from the Deschutes County Health Department; M.W. Shannon from Children’s Hospital Boston; and A. Jaffe from Oregon Health and Science University.
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DOI: 10.1542/peds.2004-0361
2004;114;1096
Pediatrics
Horowitz
Jessica L. VanArsdale, Richard D. Leiker, Mel Kohn, T. Allen Merritt and B. Zane
Lead Poisoning From a Toy Necklace
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