Heavy Metal Toxicity Clinical Presentation

  • Author: Samara Soghoian, MD, MA; Chief Editor: Asim Tarabar, MD   more...
 
Updated: May 6, 2011
 

History

  • A history of exposure is the most critical aspect of diagnosing heavy metal toxicity. A complete history includes questions about potential occupational exposures, hobbies, recreational activities, and potential environmental exposure.
  • A complete dietary history should be taken, especially the ingestion of fish, seafood, and seaweed products since these will frequently be implicated as dietary sources of organic (and relatively nontoxic) mercury, arsenic, or both. The timing of ingestion relative to the collection of urine samples is critical to interpreting the results.
  • Herbal medications and dietary supplements are also potential sources of heavy metal exposure. Many Ayurvedic and Chinese patent medicines contain heavy metals.
  • Most acute presentations of heavy metal toxicity involve industrial exposure.
  • The ingestion of nonfood items such as paint chips, toys, and ballistic devices has also been implicated as the source of metal exposure in several cases.
  • Retained lead shot may ultimately lead to toxicity as well, although generally the shot must be bathed in relatively acidic body compartments like the stomach or joints in order for significant absorption of metal ions to occur.
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Physical

  • General: The physical examination of patients with suspected metal toxicity should focus on the most commonly involved organ systems: the nervous, gastrointestinal, hematologic,[7] renal, and integumentary systems. See the Table for common presentations of acute and chronic exposures to specific metals.
  • Nausea, persistent vomiting, diarrhea, and abdominal pain are the hallmark of most acute metal ingestions. Dehydration is common. Metal salts are generally corrosive.
  • Encephalopathy, cardiomyopathy, dysrhythmias, acute tubular necrosis, and metabolic acidosis are also commonly seen with acute, high-dose exposures to most metals.
  • Patients with chronic metal toxicity tend to have more prominent involvement of the CNS and PNS, although encephalopathy and peripheral neuropathies may occur within a few hours to days of acute high-dose exposure.
  • A classic presentation of chronic metal exposure includes anemia, Mees lines (horizontal hypopigmented lines across all nails), and subtle neurologic findings. These findings should prompt suspicion of heavy metal toxicity in any patient regardless of chief complaint.
  • Because it is relatively common, any combination of GI complaints, neurologic dysfunction, and anemia should prompt a search for lead toxicity.
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Contributor Information and Disclosures
Author

Samara Soghoian, MD, MA  Clinical Assistant Professor of Emergency Medicine, New York University School of Medicine, Bellevue Hospital Center

Samara Soghoian, MD, MA is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO  Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mark Louden, MD, FACEP  Assistant Medical Director, Emergency Department, Duke Raleigh Hospital

Mark Louden, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM,  Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM, is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References
  1. Schwartz BS, Hu H. Adult lead exposure: time for change. Environ Health Perspect. Mar 2007;115(3):451-4. [Medline].

  2. Bowler RM, Roels HA, Nakagawa S, et al. Dose-effect relationships between manganese exposure and neurological, neuropsychological and pulmonary function in confined space bridge welders. Occup Environ Med. Mar 2007;64(3):167-77. [Medline].

  3. Roney N, Osier M, Paikoff SJ, et al. ATSDR evaluation of the health effects of zinc and relevance to public health. Toxicol Ind Health. Nov 2006;22(10):423-93. [Medline].

  4. Parry J. Metal smelting plants poison hundreds of Chinese children. BMJ. Aug 24 2009;339:b3433. [Medline].

  5. Watts J. Lead poisoning cases spark riots in China. Lancet. Sep 12 2009;374(9693):868. [Medline].

  6. Hornung RW, Lanphear BP, Dietrich KN. Age of greatest susceptibility to childhood lead exposure: a new statistical approach. Environ Health Perspect. Aug 2009;117(8):1309-12. [Medline].

  7. Prozialeck WC, Edwards JR, Nebert DW, et al. The vascular system as a target of metal toxicity. Toxicol Sci. Apr 2008;102(2):207-18. [Medline].

  8. [Guideline] Caravati EM, Erdman AR, Christianson G, Nelson LS, Woolf AD, Booze LL, et al. Elemental mercury exposure: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). Jan 2008;46(1):1-21. [Medline]. [Full Text].

  9. [Guideline] Manoguerra AS, Erdman AR, Booze LL, Christianson G, Wax PM, Scharman EJ, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-70. [Medline]. [Full Text].

  10. Ball H. Arsenic Poisoning and Napoleon's Death. New Scientist. October 1982;101-104.

  11. Ellenhorn MJ. Ellenhorn's Medical Toxicology. 2nd ed. Williams & Wilkins: 1997:1532-1613.

  12. Ford M. Arsenic. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS, eds. Goldfrank's Toxicologic Emergencies. 8th ed. McGraw-Hill; 2006:1251-1264.

  13. Henretig FM. Lead. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS, eds. Goldfrank's Toxicologic Emergencies. 8th ed. McGraw-Hill; 2006:1308-1324.

  14. Kaye P, Young H, O'Sullivan I. Metal fume fever: a case report and review of the literature. Emerg Med J. May 2002;19(3):268-9. [Medline].

  15. Meulenbelt J, van Zoelen GA, Vries de I. Cadmium intoxication: features and management. J Toxicol Clin Toxicol. Apr 2001;39:223-226.

  16. Petersdorf RG, Martin JB, Fauci AS, et al. Harrison's Principals of Internal Medicine. Vol 2. 12th ed. McGraw-Hill; 1991:2182-7.

  17. Sue YJ. Mercury. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS, eds. Goldfrank's Toxicologic Emergencies. 8th ed. McGraw-Hill; 2006:1334-1344.

  18. Tintinalli JE, Ruiz E, Krome RL. Emergency Medicine: A Comprehensive Study Guide. 4th ed. McGraw-Hill; 1996:833-41.

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Table. Typical Presentation of the Most Commonly Encountered Metals and Their Treatment
Metal Acute Chronic Toxic Concentration Treatment
ArsenicNausea, vomiting,



"rice-water" diarrhea,



encephalopathy,



MODS, LoQTS,



painful neuropathy



Diabetes,



hypopigmentation/ hyperkeratosis,



cancer: lung, bladder, skin, encephalopathy



24-h urine:



≥50 µg/L urine, or



100 µg/g creatinine



BAL (acute, symptomatic)



Succimer



DMPS (Europe)



BismuthRenal failure; acute tubular necrosisDiffuse myoclonic encephalopathyNo clear reference standard*
CadmiumPneumonitis (oxide fumes)Proteinuria, lung cancer, osteomalaciaProteinuria and/or ≥15 µg/ g creatinine*
ChromiumGI hemorrhage, hemolysis, acute renal failure (Cr6+ ingestion)Pulmonary fibrosis, lung cancer (inhalation)No clear reference standardNAC (experimental)
CobaltBeer drinker’s (dilated) cardiomyopathyPneumoconiosis (inhaled); goiterNormal excretion:



0.1-1.2 µg/L (serum)



0.1-2.2 µg/L (urine)



NAC



CaNa2 EDTA



CopperBlue vomitus, GI irritation/ hemorrhage, hemolysis, MODS (ingested); MFF (inhaled)vineyard sprayer’s lung (inhaled); Wilson disease (hepatic and basal ganglia degeneration)Normal excretion:



25 µg/24 h (urine)



BAL



D-Penicillamine



Succimer



IronVomiting, GI hemorrhage, cardiac depression, metabolic acidosisHepatic cirrhosisNontoxic: < 300 µg/dL



Severe: >500 µg/dL



Deferoxamine
LeadNausea, vomiting, encephalopathy (headache, seizures, ataxia, obtundation)Encephalopathy, anemia, abdominal pain, nephropathy, foot-drop/ wrist-dropPediatric: symptoms or [Pb] ≥45 µ/dL (blood); Adult: symptoms or [Pb] ≥70 µ/dL[1] BAL



CaNa2 EDTA



Succimer



ManganeseMFF (inhaled)Parkinson-like syndrome,



respiratory, neuropsychiatric[2]



No clear reference standard*
MercuryElemental (inhaled): fever, vomiting, diarrhea, ALI;



Inorganic salts (ingestion): caustic gastroenteritis



Nausea, metallic taste, gingivo-stomatitis, tremor, neurasthenia, nephrotic syndrome; hypersensitivity (Pink disease)Background exposure "normal" limits:



10 µg/L (whole blood); 20 µg/L (24-h urine)



BAL



Succimer



DMPS (Europe)



NickelDermatitis; nickel carbonyl: myocarditis, ALI, encephalopathyOccupational (inhaled): pulmonary fibrosis, reduced sperm count, nasopharyngeal tumorsExcessive exposure:



≥8 µg/L (blood)



Severe poisoning:



≥500 µg/L (8-h urine)



*
SeleniumCaustic burns, pneumonitis, hypotensionBrittle hair and nails, red skin, paresthesia, hemiplegiaMild toxicity: [Se] >1mg/L (serum); Serious: >2 mg/L*
SilverVery high doses: hemorrhage, bone marrow suppression, pulmonary edema, hepatorenal necrosisArgyria: blue-grey discoloration of skin, nails, mucosaeAsymptomatic workers have mean [Ag] of 11 µg/L (serum) and 2.6 µg/L (spot urine)Selenium, vitamin E (experimental)
ThalliumEarly: Vomiting, diarrhea, painful neuropathy, coma, autonomic instability, MODSLate findings: Alopecia, Mees lines, residual neurologic symptomsToxic: >3 µg/L (blood)MDAC



Prussian blue



Zinc[3] MFF (oxide fumes); vomiting, diarrhea, abdominal pain (ingestion)Copper deficiency: anemia, neurologic degeneration, osteoporosisNormal range:



0.6-1.1 mg/L (plasma)



10-14 mg/L (red cells)



*
*No accepted chelation regimen; contact a medical toxicologist regarding treatment plan.



MODS, multi-organ dysfunction syndrome; LoQTS, long QT syndrome; ALI, acute lung injury; ATN, acute tubular necrosis; ARF, acute renal failure; DMPS, 2,3-dimercapto-1-propane-sulfonic acid; CaNa2 EDTA, edetate calcium disodium; MDAC, multi-dose activated charcoal; NAC, N -acetylcysteine.



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