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Recognizing and Managing Lead and Mercury Poisonings

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Recognizing and Managing Lead and Mercury Poisonings URGENT CARE Special Section Recognizing and Managing Lead and Mercury Poisonings After iron, which was covered in EM’s May issue, lead and mercury are the two metals most likely to be implicated in heavy metal toxicity syndromes. The authors review the diagnostic considerations and update guidelines for detoxification. hat constitutes a heavy metal? It de- W pends on who you ask. In industrial and environ- mental studies, heavy metals are generally defined as those elements that have high atomic weights—elements with a spe- cific gravity of 5 or higher. A strict chemistry definition classifies ev- Urgent Care Section Urgent Care erything between copper and bis- muth on the periodic table as a heavy metal. Medical usage of the term, however, is much more lib- Inc Researchers, Associates/Photo © 2009 Biphoto eral, encompassing lighter metals Chronic Effects of Lead Poisoning. Dark or bluish discoloration and metalloids that are excluded of the gum-tooth line, known as a “lead line,” may be noted on exam and is the result of a chemical reaction between lead and dental plaque. by other definitions. The list of medically recognized toxic met- als and metalloids includes (but is not limited to) aluminum, arse- poisonings can often result in sig- nic, barium, bismuth, cadmium, nificant morbidity and mortality if cobalt, copper, chromium, gold, unrecognized and inappropriately lead, manganese, mercury, sele- treated. The physician also needs Christian Balmadrid, MD nium, silver, thallium, and zinc.1 to be prepared for the postdiag- Staff Physician Heavy metal or metalloid tox- nostic responsibility of identifying Durham Emergency Physicians Durham Regional Hospital icity is relatively uncommon in possible exposures to the same Durham, North Carolina urgent care centers, but for that toxin within the patient’s family, very reason it is important to workplace, or community that Michael J. Bono, MD Professor of Emergency Medicine maintain familiarity with its signs, may warrant testing, treatment, Eastern Virginia Medical School symptoms, and treatment. These or both. Norfolk, Virginia www.emedmag.com SEPTEMBER 2009 | EMERGENCY MEDICINE 35 HEAVY METAL POISONING According to nationwide data collected by the monly during activities such as removing leaded American Association of Poison Control Centers, paints from surfaces or certain smelting or burn- there were almost 13,000 exposures to heavy ing processes. Gastrointestinal absorption is sec- metals other than iron in 2005.2 (Iron in its min- ondary, at a rate of 10% to 15%, but gastrointesti- eral form and as an ingredient in multivitamins nal absorption rates and efficiency can increase in accounted for nearly 35,000 cases in 20041; for pregnancy and malnourished states (particularly our recent discussion of iron toxicity diagnosis diets low in calcium, iron, phosphorus, or zinc). and management, see EMERGENCY MEDICINE, May Conversely, in children the predominant route of 2009, page 36). absorption is through the gastrointestinal tract, at The aim of this article is to provide a brief re- a rate of 50%. The organic lead found in gasoline fresher course on the epidemiology, biochemis- can also be absorbed through the skin.6 try, and clinical aspects of toxic exposures to lead In the bloodstream, 99% of lead is bound to and mercury—after iron, the most likely causes of erythrocytes, while the remaining 1% is in a free heavy metal toxicity. We would caution, though, form, able to affect tissues such as kidney, brain, that even the best-informed urgent care physi- liver, and bone marrow. Lead is primarily excreted cian should consult a toxicologist or the regional by the kidneys and has a half-life of 30 days in poison control center whenever there is any sus- individuals with normal renal function.7 However, picion of metal toxicity. lead can be stored in bone, where its half-life can extend to decades,7 and may be released during LEAD: A LINGERING THREAT times of bone turnover, as in hyperthyroidism,8 Lead toxicity is considered a disease of industrial- menopause, pregnancy,9 and breastfeeding.10 ization, with the majority of poisonings worldwide Pathophysiology. Lead primarily affects the resulting from exposure to lead-based paints and hematopoietic, neurologic, and renal systems. leaded gasoline. Fortunately, the use of those In the hematopoietic system, lead inhibits heme products in the United States was banned in the biosynthesis, causing anemia. In the neurologic 1970s. However, it is estimated that more than system, it induces demyelination and axonal 30 million homes still contain lead-based paints,3 degeneration that result in peripheral neuropa- and an unknown number have lead pipes or al- thies and wrist and foot drop. It also increases loys in their plumbing systems. Toxic levels of brain capillary permeability and cerebral edema, Urgent Care Section Urgent Care serum lead have been found in screening assess- resulting in acute lead encephalopathy. In chil- ments of as many as 4 million children in a year dren, chronic lead exposures have been found in US households, and about 3 million industrial to correlate with neuropsychiatric disorders as workers are at risk for lead exposure in such jobs manifested in decreased IQ scores, hyperactiv- as lead smelting, battery manufacturing, radiator ity, overaggressive or criminal behavior, learning repair, bridge and ship construction, welding, and disabilities, and other signs.3 Lead also causes glass production.3 Other vehicles for lead expo- nephropathy and renal impairment due to fibro- sure include lead-contaminated soils (especially sis of the proximal tubules. in countries still using Clinical features. Patients will typically pre- >>FAST TRACK<< leaded gasoline), buck- sent with either a known lead exposure, suspi- Toxic levels of serum shot, fishing weights, cious symptoms with a possible history of expo- lead have been found in moonshine whiskey, sure, or a referral from a provider who found a screening assessments lead-glazed pottery, and toxic blood lead level (BLL) on a screening exami- of as many as 4 million some ethnic medications nation. Adults with chronic exposures may have children in a year in US and folk remedies.4,5 only a mildly elevated BLL (less than 10 μg/dL)3 households. Lead has no biological and may be asymptomatic or have an insidious role. It can be absorbed onset of vague symptoms such as myalgias, fa- through the lungs, the gastrointestinal tract, or the tigue, irritability, insomnia, anorexia, impaired skin. In adults, it is absorbed primarily through the short-term memory, and difficulty concentrating. respiratory system at a rate of about 40%, com- Prolonged exposure may cause renal disease that 36 EMERGENCY MEDICINE | SEPTEMBER 2009 www.emedmag.com HEAVY METAL POISONING continued from page 36 can progress to renal failure, hypertension (inde- of standard measures to control cerebral edema, pendent of lead’s effects on the kidneys),11 neu- including intubation (to hyperventilate) and inva- rocognitive dysfunction,12,13 white matter brain sive intracranial pressure monitoring.3 In moder- lesions, loss of brain volume,14 distal sensory ate to severe toxicity, the goals of therapy are to and motor neuropathies,15 and cardiac conduc- prevent further exposure, minimize absorption, tion delays.16 enhance elimination, and prevent or reverse cel- Patients with acute exposure will present with lular pathology. In acute ingestions, whole bowel higher BLLs, which will generally correlate with irrigation can decrease the amount of lead ab- the severity of the presenting symptoms. Patients sorbed through the gastrointestinal tract.18 typically complain of gastrointestinal effects such To enhance elimination, chelating agents have as colicky abdominal pain (“lead colic”), constipa- been used, but controlled clinical trials have not tion, nausea, vomiting, and anorexia. They may been performed to assess their efficacy. The the- also present with central nervous system dysfunc- ory behind their use is that they will bind to lead to tion ranging from mild headache or personality form nontoxic complexes that can undergo biliary changes to full-blown encephalopathy with coma and renal excretion. The chelating agents available and convulsions. This can be rapidly fatal or result include dimercaprol (also called British antilewisite in permanent neurologic and behavioral changes. or BAL), calcium disodium EDTA (ethylenediami- As previously noted, peripheral neuropathies pre- netetraacetic acid), DMSA (2,3-dimercaptosuccinic senting as wrist or ankle drop may also occur.15 acid), and D-penicillamine. Which chelating agent Assessment. An occupational and environmental to use is dictated by the patient’s BLL and the se- history to assess the risk and severity of lead expo- verity of symptoms. The first two agents listed sure is essential. The most important laboratory test come in intramuscular or intravenous form and to obtain is a BLL. The Centers for Disease Control are used for severe toxicities that require admis- and Prevention has defined a BLL greater than 10 sion, while the latter two agents are oral chelators μg/dL to be toxic in children.3 In acute exposures, and can be used for outpatient therapy. BLL can be greater than 100 μg/dL. Other tests that Consensus guidelines have not been proposed may be helpful in the evaluation of lead poison- for the treatment of lead poisoning, but the fol- ing include a complete blood count with peripheral lowing have been recommended in some texts. smear (which may
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