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Lead Toxicity in a 14-Year-Old Female With Retained Bullet Fragments

^a Darnall Army Community Hospital, Fort Hood, Texas
^b Poison Control Center, University Medical College, University of Arizona, Tucson, Arizona

	ABSTRACT

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In the past 3 decades, lead levels in North American children have been declining. Despite the decline in lead exposure, lead toxicity remains a significant childhood environmental health hazard. The usual route of lead exposure is through ingestion, but lead toxicity secondary to retained bullet fragments has been well documented in the adult literature. The diagnosis of lead toxicity is often difficult and delayed secondary to vague and transient symptoms. Recognizing high-risk characteristics of bullet fragments can improve clinician awareness to the possibility of lead toxicity. The primary management of patients with continued lead exposure is to remove the source of exposure. However, in the case of retained bullet fragments, initiation of chelation therapy before surgical removal may be essential in preventing systemic toxicity. We present the case of a 14-year-old female with lead toxicity who presented with an 18-month course of chronic abdominal pain, vomiting, and anorexia 2 years after sustaining a gunshot wound to the right leg. The patient was treated with oral succimer and operative removal of bullet fragments.

Key Words: adolescent health • gunshot injuries • lead poisoning • lead toxicity • toxicology

Abbreviations: CT, computed tomography

In the past 3 decades, lead levels in North American children have been declining.¹ Despite the decline in lead exposure, lead toxicity remains a significant childhood environmental health hazard. The usual route of lead exposure occurs through ingestion of lead-contaminated household dust and soil containing lead-based paint.² Lead intoxication secondary to retained bullets or shrapnel is uncommon, but an in-depth review of case reports in the medical literature has illustrated the importance of retained bullet fragments in lead toxicity. Between 1993 and 1998 there were >475000 nonfatal firearm-related injuries in the United States, but the association and incidence of retained bullet fragments and lead toxicity among children has not been well studied.^{3, 4}

Without a high suspicion for lead toxicity, the diagnosis is often difficult and delayed.⁵ A presentation plagued by vague and transient symptoms and an unpredictable time interval to the onset of symptoms may contribute to a delay in diagnosis.⁶ Lead toxicity may affect the neurologic, hematologic, gastrointestinal, musculoskeletal, renal, and reproductive systems and produce a wide array of vague symptoms including abdominal pain, vomiting, constipation, fatigue, arthralgias, headache, decreased libido, hypertension, and anorexia.^{3, 5} The onset of symptoms from the initial gunshot wound has been reported from 2 days to 52 years.⁷ Transient symptoms may reflect fluctuations of blood lead concentrations. Blood lead levels may fluctuate with rapid bone growth, pregnancy, lactation, or stressful events such as sepsis, shock, or thyrotoxicosis.⁶

Here we present the case of a 14-year-old female with a delayed diagnosis of lead toxicity 2 years after sustaining a gunshot wound to the right leg. She suffered 18 months of recurrent abdominal pain, vomiting, and anorexia. She also had a decrease in school performance and rate of growth. The patient was treated with oral succimer for lead chelation followed by surgical debridement of the right knee.

	CASE REPORT

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A 14-year-old female was admitted to the pediatric service for lead toxicity 2 years after being shot in the right lower extremity. The patient had complained of diffuse colicky abdominal pain over the previous 18 months that was always associated with nausea, vomiting, and anorexia. The patient's abdominal pain was often severe, lasting 2 consecutive weeks every month, usually straddling her menses. In addition, the patient reported a 20-pound weight loss over the previous 18 months. Her primary care physician saw her on 1 previous occasion, and over the last 10 months she had 3 separate hospital admissions.

On all 3 previous admissions she presented for chronic abdominal pain, vomiting, and weight loss, and on the last of the 3 admissions she was noted to have altered mental status and a presumed initial diagnosis of hypertensive encephalopathy. A history of eating disorders was negative, and a review of systems revealed no infectious, endocrine, genitourinary, or neurologic etiologies. She denied any tobacco, alcohol, or drug use, sexual activity, and home abuse. A review of available past medical records did not reveal any notation of a previous gunshot wound.

Physical examination was positive for systolic blood pressures running from 140 to 150 mm Hg on all 3 prior admissions. Radiologic evaluation for hypertension was performed with a normal renal ultrasound and Doppler, MRI/magnetic resonance angiography of the kidneys, and echocardiography.

The laboratory workup for hypertension was unremarkable. Her height was measured as being in the 10th percentile (148 cm), and her weight was below the 5th percentile (33.3 kg) on her first admission 10 months earlier with a discharge weight of 34.9 kg after total parenteral nutrition. Abdominal examination showed diffuse nonspecific tenderness felt to be nonsurgical by general surgery and obstetric consultations. An abdominal computed tomography (CT) scan was normal, and an esophagogastroduodenoscopy was grossly normal but provided a biopsy diagnosis of gastritis and Helicobacter pylori. Triple-drug therapy for H pylori was given at that time. The patient was noted to be thin and cachectic but otherwise pleasant, alert, and willing to interact and answer questions appropriately. The remainder of her physical examination was normal. The inpatient laboratory workup consisted of testing for normal electrolytes, liver function, and hepatic enzymes. No complete blood count could be located for her previous admissions, and on each admission her pain was treated with intravenous morphine. During each hospitalization, the patient's vomiting ceased after pain control. During her third admission, a workup for acute intermittent porphyria was ordered to include a lead level. Her blood pressure had returned to normal (100s/50s mm Hg) before discharge on each admission, and she was asymptomatic and tolerating an oral diet. All labs for porphyria and lead were pending when she was discharged after this third hospitalization.

Two days after discharge the patient's lead level returned at 83 µg/dL, and arrangements were made for the patient's readmission to the hospital. On admission she again was symptomatic, with abdominal pain and intermittent vomiting. Her blood pressure at admission was 100/80 mm Hg, and she was alert and oriented. A small right knee effusion and a healed entrance wound to the posterior right calf were noted. The remainder of the physical examination was unremarkable and included a benign abdominal examination and a grossly normal neurologic and mental-status examination. At admission her lead level was 113 µg/dL, white blood cell count was 6.8 x 10³, platelet count was 292 x 10³, and hemoglobin and hematocrit was 8.1 g/dL and 24.0%, respectively, with a mean corpuscular volume of 85 fL and a peripheral smear that demonstrated no basophilic stippling. A radiograph of the right knee revealed an arthrogram of the synovium with multiple bullet fragments within and surrounding the knee joint (Fig 1). A CT of the right knee further illustrated bullet fragments within the joint space (Fig 2). Our toxicology service was consulted at this time for inpatient management.

View larger version (75K): [in this window] [in a new window]   FIGURE 1 Retained bullet fragments and arthrogram of the right knee.

View larger version (66K): [in this window] [in a new window]   FIGURE 2 CT of the right knee with retained bullet fragments.

	DISCUSSION

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Relationship Between Lead Toxicity and Bullet Location
Patients with a history of retained bullet fragments and symptoms of lead toxicity should have a complete clinical workup and blood lead levels obtained.³ The pathophysiology of lead absorption from retained bullets is not well explained. Many factors contribute to increased lead levels from retained bullets, the presence of which should increase clinical suspicion and dictate follow-up. Bullet fragmentation increases the surface area for lead absorption and has been reported to increase blood lead levels by 25.6%.⁴ The correlation between bullet location and lead toxicity has been well described. Synovial and bony interfaces, bony fractures (especially of the thorax), and contact with synovial fluid, pleural fluid, and cerebrospinal fluid have all been associated with elevated absorption rates and lead toxicity.^{3, 4} In this case, both the fragmentation of the bullet and proximity of the fragments close to a major joint likely played a major role in the resulting high blood lead levels.

Surveillance for Known Gunshot Wounds and Retained Bullet Fragments
Recommended surveillance for patients with known retained bullet fragments is based on the above-mentioned high-risk characteristics and the potential for surgical intervention. Removal of bullet fragments status post gunshot wounds is not common practice, but consultation with a toxicologist and surgeon should be considered when determining the benefit/risk ratio.^{4, 6} All children with retained bullet fragments should be considered for routine serum lead levels at admission, discharge, or 2 weeks after injury, monthly intervals up to 3 months, 1 year postinjury, and yearly thereafter.⁴

Importance of Physician Awareness and Documentation
No documentation was found in this case that demonstrated any awareness of a prior gunshot wound by either the primary care physician or the inpatient services, and surveillance was not initiated. Awareness and early surveillance is critical when considering the vague presentation and difficult diagnosis of lead toxicity. The need for proper documentation and flagging of patient charts with retained bullet fragments or gunshot wounds should be promoted to prevent a delay in diagnosis.

Neurobehavioral Effects
In addition to lead-level surveillance, it is important to recognize the need for serial neurobehavioral testing in patients with lead toxicity. This patient had a decrease in school performance over the previous 18 months, and on discharge it was unclear whether this was secondary to a large number of medical absences from school or secondary to the neurobehavioral effects of lead toxicity. Intellectual and behavioral functioning may be decreased even at low lead levels, and the ability to reverse such effects with chelation therapy is currently unknown.^{8, 9} On the opposite end of the spectrum, acute encephalopathy associated with lead poisoning is usually profound but potentially reversible with proper treatment and the lowering of lead levels.^{10, 11}

Treatment for Lead Toxicity and Retained Bullet Fragments
Treatment of patients with elevated lead levels and retained bullet fragments is not clear cut. The Centers for Disease Control and Prevention considers blood lead levels of <10 µg/dL to be safe in children, but no evidence exists demonstrating a threshold of no adverse effects, and a decrease in IQs has been noted at levels as low as 10 µg/dL.^{1, 6} In symptomatic patients with retained bullet fragments, definitive treatment must involve removal of lead fragments. Whether to perform this removal before or after the initiation of chelation therapy, unfortunately, is ill defined. Systemic toxicity after surgery without the initiation of chelation therapy has been reported.³ In this case, chelation therapy was initiated before surgery. The risk for redistribution and systemic toxicity with surgery was felt to be to great without first lowering the serum levels with some form of chelation therapy. Operative and chelation-therapy timing should be made on an individual basis in consultation with both a toxicologist and surgeon. Considering the worst possible outcome, encephalopathy with increased intracranial pressure, precautions should also be taken to ensure that critical care management is readily available.

Chelation Therapy
The American Academy of Pediatrics recommends the use of parenteral chelators (dimercaprol and calcium disodium ethylenediamine tetraacetate) for lead levels >70 µg/dL or encephalopathy. This case, however, was complicated by the presence of retained bullet fragments, a very large body burden of lead, and the patient's age.¹⁰ Calcium disodium ethylenediamine tetraacetate has been associated with the redistribution of lead from soft tissue to brain, increasing the risk of encephalopathy in patients with continued lead absorption and high body burdens of lead.^{10, 12} Dimercaprol is only given intramuscularly, and up to 50% of patients experience some form of adverse events. Succimer can be given orally, is not believed to cause redistribution to the brain, and has a much lower adverse-effect profile when compared with dimercaprol, and previous reports have demonstrated successful chelation with oral succimer before surgical removal of retained bullet fragments.^{3, 10}

	CONCLUSIONS

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This case illustrates the difficult and often delayed diagnosis of lead poisoning. Recognition of multiple bullet fragments and their proximity to the right knee may have lead to earlier surveillance. However, the location of the gunshot wound may have mislead the initial physicians and provided a false sense of security. Management of the patient reflected prior case reports using succimer chelation before surgical removal and may have avoided the theoretical redistribution phenomenon and many of the adverse effects associated with parenteral chelators. The importance of proper documentation and flagging the charts of patients who have gunshot wounds cannot be overstated, because the diagnosis of lead poisoning is already quite difficult. The patient was discharged on standard succimer chelation therapy, and outpatient neurobehavioral testing was established. A final key factor to note is the requirement for continued surveillance of blood lead levels and monitoring for rebound lead toxicity from bone redistribution. All patients with prolonged lead exposure may have high lead body burdens and require multiple chelation treatments to deplete bone lead levels.¹³

	FOOTNOTES

 
Accepted Oct 3, 2005.

Address correspondence to Troy Coon, MD, Department of Emergency Medicine, Darnall Army Community Hospital, 36000 Darnall Loop, Fort Hood, TX 76544. E-mail: tcoon1{at}hotmail.com

	REFERENCES

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1. Sanborn MD, Abelsohn A, Campbell M, Weir E. Identifying and managing adverse environmental health effects: 3. Lead exposure. CMAJ. 2002;166 :1287 –1292[Abstract/Free Full Text]
2. Campbell C, Osterhoudt KC. Prevention of childhood lead poisoning [review]. Curr Opin Pediatr. 2000;12 :428 –437[CrossRef][ISI][Medline]
3. Meggs WJ, Gerr F, Aly MH, et al. The treatment of lead poisoning from gunshot wounds with succimer (DMSA). J Toxicol Clin Toxicol. 1994;32 :377 –385[ISI][Medline]
4. McQuirter JL, Rothenberg SJ, Dinkins GA, Kondrashov V, Manalo M, Todd AC. Change in blood lead concentration up to 1 year after a gunshot wound with a retained bullet. Am J Epidemiol. 2004;159 :683 –692[Abstract/Free Full Text]
5. John BE, Boatright D. Lead toxicity from gunshot wound. South Med J. 1999;92 :223 –224[CrossRef][ISI][Medline]
6. McQuirter JL, Rothenberg SJ, Dinkins GA, Manalo M, Kondrashov V, Todd AC. The effects of retained lead bullets on body lead burden. J Trauma. 2001;50 :892 –899[ISI][Medline]
7. Farrell SE, Vandevander P, Schoffstall JM, Lee DC. Blood lead levels in emergency department patients with retained lead bullets and shrapnel. Acad Emerg Med. 1999;6 :208 –212[ISI][Medline]
8. US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention. Preventing lead poisoning in young children: effects of lead on children and fetuses. Available at: http://wonder.cdc.gov/wonder/prevguid/p0000029/p0000029.asp#head007001000000000. Accessed May 4, 2005
9. Dietrich KN, Ware JH, Salganik M, et al. Effect of chelation therapy on the neuropsychological and behavioral development of lead-exposed children after school entry. Pediatrics. 2004;114 :19 –26[Abstract/Free Full Text]
10. American Academy of Pediatrics, Committee on Drugs. Treatment guidelines for lead exposure in children. Pediatrics. 1995;96 :155 –160[Abstract/Free Full Text]
11. Sachs HK, Blanksma LA, Murray EF, O'Connell MJ. Ambulatory treatment of lead poisoning: report of 1,155 cases. Pediatrics. 1970;46 :389 –396[Abstract/Free Full Text]
12. Cory-Slechta Da, Weiss B, Cox C. Mobilization and redistribution of lead over the course of calcium disodium ethylenediamine tetraacetate chelation therapy. J Pharmacol Exp Ther. 1987;243 :804 –813[Abstract/Free Full Text]
13. Bolanos AA, Demizio JP Jr, Vigorita VJ, Bryk E. Lead poisoning from an intra-articular shotgun pellet in the knee treated with arthroscopic extraction and chelation therapy: a case report. J Bone Joint Surg. 1996;78 :422 –426[Free Full Text]

This Article Abstract P3Rs: Submit a response Alert me when this article is cited Alert me when P3Rs are posted Alert me if a correction is posted Services E-mail this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to My File Cabinet Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Coon, T. Articles by Sullivan, J. Search for Related Content PubMed Articles by Coon, T. Articles by Sullivan, J. Related Collections Therapeutics & Toxicology

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