HEAVY METAL POISONING Medical Presentation

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HEAVY METAL POISONING (Hg,Pb,Fe) DR AFOLABI O.F
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OUTLINE INTRODUCTION -Definition -History EPIDEMIOLOGY PATHOPHYSIOLOGY MANAGEMENT -Mercury poisoning -Lead poisoning -Iron poisoning CONCLUSION
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INTRODUCTION Metals are electropositive elements characterised by properties such as luster, malleability and the ability to conduct electricity. Heavy metals are defined as those metals with atomic weight of >5.0 Also regarded as metals or semi metals with potential human or environmental toxicity. However, some metals are essential to human biochemical processes e.g Zn,Fe,Cu,Mn,Se etc or used therapeutically in medicine e.g Aluminium, Bismuth,Gold etc.
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HISTORY Dated back to era of Hippocrates who noticed abdominal colic in a man who extracted metals. Theophrastus of Erebus(370-287BC) noted pernicious effects of Ar and Hg poisoning among smelters. Arsenic was the component of spray called Lewisite used by British during trench warfare in WW1.
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Minamata bay disaster in Japan(1930’s-1960’s ) due to mercury poisoning from methylmercury bioaccummulation in local fish from dumping of industrial waste. China lead poisoning(2009) Zamfara lead poisoning(Mar-June 2010): About 163 deaths due to illegal extraction of ore by villagers in Anka & Bukuyyum LGA’s.
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EPIDEMIOLOGY Commonest is lead poisoning though incidence is reducing in the developed world. Toxicity of heavy metals depend on -Type of metal -Total dose absorbed -Whether exposure is acute or chronic -Age of the patient -Route of exposure No sex or race predilection.
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Sources of exposure include -Diet -Drugs -Environment -Occupational exposure Common routes of exposure are -Ingestion -Inhalation -Absorption via skin and mucous membranes -Vertical transmission
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PATHOPHYSIOLOGY Common toxic mechanisms of action include Enzyme inhibition/activation :due to interaction between metal & sulfhydryl (SH) groups on the enzyme or metal displacing an essential cofactor of the enzyme e.g lead Subcellular organelles :disruption of structure or function of organelles such as ER, lysosomes, mitochondria affecting cellular function. Carcinogenicity:some metals are known human carcinogens e.g Arsenic, chromium,nickel.
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Common systems where heavy metals exert their toxic effects include: Renals :as kidneys are the main excretory organs e.g cadmium,mercury. R.S :effects via inhalation include irritation/inflammation, fibrosis (aluminium), carcinogenesis(arsenic,chromium,nickel) Nervous system:profound neurological effects esp. organic heavy metals e.g mercury
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4. Endocrine & Reproductive systems : via effects on neuroendocrine and hormonal control. Moreover, some metals act directly on sex organs e.g cadmium, lead.
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MERCURY POISONING AKA Hydrargyria,mercurialism. 80th element on periodic table with an atomic mass of 201 and classified as a transition metal. Exist in 3 forms: Elemental Mercury -found in liquid form & readily vapourises @ room temp. with 80% absorbtion via inhalation. -Exerts main effects on the CNS and RBC’s. -Has very poor GI absorption therefore mildly toxic when ingested.
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-found in thermometers, barometers, batteries, dental amalgams, flourescent and mercury lamps. 2. Inorganic Mercury -Exists as metallic mercury(Hg),mercurous mercury(HG+) and mercuric mercury(Hg2+). -Highly toxic & corrosive -Route of exposure is mainly orally or dermally. -Has poor lipid solubility allowing for slow elimination with potential for CNS & renal accummulation.
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-Found in cosmetics,explosives,disinfectants,fur hat processing,ink manufacturing etc. 3.Organic Mercury -Exists as aryl,short chain alkyl(methylmecury) and long chain alkyl compounds. -Readily absorbed in the GI & has high lipid solubility causing profound CNS ,haematologic and teratogenic effects. -Major exposure is via ingestion of contaminated seafood.
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-Also found in fungicides,antiseptics,embalming products,diaper products etc -A very controversial source of organic mercury is THIMEROSAL,which is a preservative used in vaccines to prevent bacterial contamination (DPT,HIB,HBV). -Unsubstantiated claims suggest a link of thimerosal containing vaccines to childhood autism. -No study reports harmful effects @ doses used in vaccines except local redness & swelling @ injection site.
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-However,in recent times thimerosal has been removed in vaccines. Toxic Effects of mercury include: Binds to sulfhydryl,amide,carboxyl,phosphoryl groups incapacitating enzymes, transport membranes & structural proteins. Inactivates Na+/K+ ATPase Membrane depolarisation Ca2+ entry cell death. Displaces Selenium as an enzymatic cofactor disrupting cellular biochemical pathways. -All these lead to multiorgan toxicity of mercury.
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CLINICAL FEATURES Acute inhalation of Elemental Mercury -Acute onset cough,dyspnea,chest pain, fever, chills,headaches & visual blurring. -Extent of exposure determine illness being self limiting or progressing to complications e.g interstitial pneumonitis, necrotising bronchiolitis, pulm. edema, resp. failure. -Renal & CNS features may develop subacutely. -Long term pulm. complications are restrictive lung diseases e.g interstitial fibrosis.
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Acute ingestion of Inorganic Mercury -Presents as corrosive gastroenteritis (oropharyngeal burns,metallic taste, nausea, hematemesis, haematochezia,severe abd.pains) -other feat. are ATN, CVS collapse. Chronic Inorganic Mercury ingestion -presents as a triad of tremors,neuropsychiatric disturbances & gingivostomatitis. -Tremors initially intention tremors later progressing to choreoarthetosis & spasmodic ballismus.
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-Neuropsychiatric features are emotional lability, delirium, insomnia, headaches etc -Renal features may range from asymptomatic proteinuria to nephrotic syndrome. Acrodynia(Pink’s Disease) -Rare idiosyncratic hypersensitivity reaction mainly occuring in children. -Features are acral rash that may involve face, usually pink,papular,pruritic with morbiliform, vesicular & haemmorrhagic variants. -Also apathy,hypotonia (pelvic & pectoral girdles)
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-Inability to degrade catecolamines diaphoresis, tachycardia,hypertension,tremors etc
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Minamata Disease -Name derived from Methylmercury poisoning from Minamata bay,Japan. -Causes profound CNS effects after a latent period of wks to mnths such as ataxia, dysarthrias, paresthesias,memory loss, progressive dementia,death. -Also neuronal atrophy in utero LBW, microcephaly ,cerebral palsy, profound delayed milestones, deafness, blindness, seizures.
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DIAGNOSIS Based on Hx of exposure, clinical features and elevated blood(>10mcg/L) & urine (>20mcg/L) mercury levels. Abdominal xrays show ingested mercury. Others include CT scan,MRI,nerve conduction tests.
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TREATMENT Acute ingestion may require fluid resuscitation, pressor agents,mechanical ventilation,dialysis. Gastric lavage & use of activated charcoal NOT recommended. Chelation is most effective treatment. Dimercaprol aka 2,3 dimercaptopropanol or British antilewisite(BAL) is chelator of choice. Suitable for ill pxs that cannot tolerate orally. Dose is 5mg/kg stat,then 2.5mg/kg q12-24 for 10days(IM)
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C/I for methylmercury poisoning due to exacerbation of CNS effects. Side effects are pain, hypertension, tachycardia, abd.pains,hemolysis in G6PD deficient pxs. Other chelators include -DMSA (2,3 dimercaptosuccinic acid/succimer). -DMPS (2,3 dimercapto-1-propanesulfonic acid). -D-penicillamine.
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LEAD POISONING AKA plumbism,painters colic,colica pictonum etc 82nd element on periodic table with an atomic mass of 207. Commonest form of heavy metal poisoning. Exists as organic and inorganic forms. Suitable for use in production of many chemical products due to its low melting point and ability to form stable compounds. However,it is purely a toxicant clinically.
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Sources of lead include batteries, lead pipes, paint, cosmetics, cable sheathing, mineral supplements, plastics, toys etc A significant occupational hazard in industries and also a common environmental pollutant. Exposure can be via contact, ingestion, inhalation or vertical transmission. Absorption depends on PH,presence of other elements(e.g Ca2+,Fe) or materials in the gut. Mainly bound to RBC’s after absorption.However, in lead accummulation about 95% is found in bone.
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Toxic effects are via -Inhibition of enzyme activity due to binding of sulfhydryl groups.(esp. Delta-aminolevulenic acid dehydratase,ferrochelatase) -Displaces Ca2+ altering many intra- & inter -cellular functions e.g neurotransmitter release. -Prevents development of the tertiary structure of the brain.
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CLINICAL FEATURES Acute poisoning -Neurological effects e.g paraesthesias,muscle weakness,encephalopathy. -GI effects e.g metallic taste, nausea, vomiting, diarrhoea, abd. pain etc. -CVS collapse if large amounts are ingested. -Hemolysis anemia,haemoglobinuria. -Fanconi syndrome,acute renal insufficiency.
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Chronic poisoning -Memory loss, depression, insomnia, headaches, slurred speech. -Psychiatric disturbances e.g hyperkinetic or aggressive behaviour. -Loss of coordination, paraesthesias -Pallor with ‘lead hue’. -Bluish line along the gum called Burton Line. -In utero poisoning leads to LBW, mental retardation,learning disabilities.
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-Other features are testicular degeneration, inhibition of spermatogenesis, leydig cell atrophy etc.
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DIAGNOSIS Hx of exposure, clinical signs and lab.analysis of blood lead levels(BLL). Ideal BLL is 0 mcg/dl,acceptable levels below 10. Erythrocyte protoporphyrin levels. FBC & PBF -Microcytic,hypochromic anemia -Basophilic stippling X rays of long bones show ‘Lead lines’@ the metaphysis.
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TREATMENT Mainstay of treatment is chelation therapy. Chelators used include: -Edetate disodium calcium (EDTA) -Dimercaprol (BAL) -Succimer -D-penicillamine Other treatment modalities are -Treatment of Fe,Ca,Zn deficiencies . -Whole bowel irrigation in cases of ingestion.
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PREVENTION Mainly by avoiding exposure to lead Major preventive strategies are Individual level -Frequent hand washing. -Adequate intake of calcium and iron. -Eliminating household lead containing objects. -Use of lead testing kits. Preventive medicine -Routine screening of high risk individuals.
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Public health level -By reducing risk on population @ national and state levels such as a)Regulations limiting amount of lead in products e.g paint, toys, furniture etc b)Evacuation of residents in highly lead contaminated areas.
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IRON POISONING
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26th element on periodic table with atomic mass of 56. One of the most common causes of childhood poisoning. Usually refers to acute iron overload caused by ingestion of iron supplements. Chronic iron toxicity occurs in children with anemias requiring frequent blood transfusions e.g SCD, thalassemias, MDS etc
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Different iron salts contain different amounts of elemental Fe e.g Fumarate(33%), Gluconate(12% ), Sulfate(20%). Toxic effects of iron include: -Corrosive toxicity to GI mucosa. -Cellular toxicity via impairment of oxidative phosphorylation & mitochondrial dysfunction cellular death. -Also causes venodilation & capillary permeability hypotension.
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Doses >20mg/kg : GI toxicity >40mg/kg : Moderate intoxication >60mg/kg : Toxic dose
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CLINICAL FEATURES Iron poisoning is classified into 5 stages Stage 1(GI Phase) -occurs within 6hrs after exposure. -Vomiting, diarrhoea, abdominal pain. -GI bleeding haematochezia in severe cases. -Shock due to 3rd spacing and blood loss. Stage 2 (Latent/Quiescent Phase) -6 -24hrs -Characterised by resolution of GI symptoms.
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-A deceptive phase to the clinician. -some skip this phase directly to stage 3. Stage 3 (Metabolic/CVS Phase) -48-96hrs. -Characterised by metabolic acidosis & CVS symptoms. -CNS features e.g stupor,coma. -Multiple organ failure.
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Stage 4 (Hepatic Phase) -Hepatic failure from hepatic necrosis -Characterised by liver enzymes & bilirubin levels. -Coagulopathy,Hypoglycemia may occur due to the above. Stage 5 (Delayed Phase) -2-6 wks after ingestion. -GI obstruction(GOO,intestinal obst.) due to scarring of healing GI tract. Death can occur from any of the stages .
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DIAGNOSIS Serum iron levels -Measured about 4hrs after ingestion. -If measured > 6hrs toxicity may be underestimated due to ferritin binding & redistribution of iron. -Levels < 500mcg/dl indicate low risk of toxicity. -Levels > 500mcg/dl indicate significant toxicity. -Levels > 800mcg/dl are assoc.with severe toxicity.
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RBS -Hypoglycemia seen in hepatic dysfunction. FBC -WBC >15 x109/L associated with severe iron poisoning. -Anemia from blood loss. LFT’s Coagulation studies. Arterial blood gases. -To determine existence & severity of metabolic acidosis.
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E/U/Cr, Anion gap. Lipase and Amylase levels(pancreatic injury) Imaging studies such as plain abd. Xray to show radioopacities .
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TREATMENT Good supportive & symptomatic care is essential. IV access for aggressive hydration to maintain urine output. Gastric decontamination done within few hrs of ingestion via: -Gastric lavage -Ipecac induced emesis -Whole bowel irrigation Activated charcoal NOT useful.
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Chelation is the mainstay of treatment. -Indicated for iron levels >350mcg/dl + signs of toxicity OR > 500mcg/dl regardless of signs of toxicity. DEFEROXAMINE is chelator of choice. -Stable pxs :40mg/kg IM/IV -Unstable pxs :15mg/kg IV over 1 hr then continuous infusion of 15mg/kg/hr untill ‘vin rose’ urine colour disappears. (‘vin rose’is reddish urine colour due to deferoxamine-iron complexes)
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PREVENTION Safeguarding off ALL medications from children. Use of child resistant packaging.
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CONCLUSION Heavy metal poisoning is an uncommon diagnosis which results in significant morbidity & mortality if unrecognised or inappropriately treated. Prevention is key to exposure to most of these heavy metals hence the need for surveillance & routine screening of individuals @ risk for prompt diagnosis and management.
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THANKS FOR YOUR TIME!