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NEET SS MEDICINE

General medicine

Heavy Metal Poisoning

May 22, 2024

Lead Poisoning

Occupational toxin.

Clinical Features of Heavy Metal Poisoning

Severe toxicity. Blood lead levels >60–80 mcg/dL (adults): gastrointestinal distress, nausea, and vomiting; >80 mcg/dL: encephalopathy. Acute lead nephropathy: condition similar to Fanconi

Chronic poisoning, GI distress; anemia (basophilic stippling);
Lead poisoning precipitated saturnine gout; Nephrotoxicity (proximal tubular damage, interstitial fibrosis); Peripheral motor neuropathy (wrist drop > foot drop). The line of Bruce. A pale line on the gingiva.

Lead line on X-ray (deposition of calcium in metaphysis).

Haemoglobin reduces due to d-ALA dehydratase and ferrochelatase.

Diagnosis Of Lead Poisoning

Blood lead levels (over 45 in kids and above 80 in adults)
The amounts of erythrocyte zinc protoporphyrin, blood d-ALA dehydratase, and lead line.

Cortical bone lead levels, basophilic stippling.

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Treatment Of Lead Poisoning

Acute poisoning; supportive care; chelation; chronic; vitamin C (interferes with absorption of lead); iron and calcium.

Chelation Therapy

Indications: Lead concentrations >45 mcg/dL in kids; >80 mcg/dL in adults; DMSA; Simplimer; Dimercaprol; British anti-Levicide (BAL); D-penicillamine; Not FDA authorized.
used in the illness Wilson.

Medication	Dose	Indication to use	Adverse Effects	Comments
Dimercaprol (BAL)	25 mg/kg per day deep intramuscularly divided in six doses per day for at least 3 days	BLL ≥ 70 mcg/dL (3.4 mmol/L) or lead encephalopathy	· Hemolysis in G6PD deficiency Kidney dysfunction · Zinc depletion· Nausea, vomiting, hypertension, headache, tachycardia, hyperpyrexia, leukopenia	· If administered with CaNa2 EDTA, first BAL dose usually given 4 hours prior· Dissolved in peanut oil; therefore, contraindicated in patients who have peanut allergy· Alkalinize urine during therapy
Calcium disodium-ethylenediaminetetraacetic acid (caNa2 EDTA)	50 mg/Kg per dose single – dose continuous infusion in normal saline or D5W, maximum 1 g/day for 5 days	BLL ≥ 45 mcg/dL (2.2 mmol/L) or lead encephalopathy	· Renal dysfunction· Hypokalaemia	· Hospitalize; monitor of adequate hydration, electrolyte status
Succimer (DMSA, 2-3 mesodimercaptosuccinic acid)	10 mg/kg per dose every 8 hours for 5 days, then every 12 hours for 14 days for a totally of 19 days orally	BLL 45 to 69 mcg/dL (2.2 to 3.3 mmol/L	· Transient liver function test abnormalities· Reversible neutropenia	· G6PD deficiency is not a contraindication· Availability of oral route makes this an appealing first-line pediatric option
D-penicillamine	10 to 15 mg/kg per day orally for 4 to 12 weeks	BLL 45 to 69 mcg/dL (2.2 to 3.3 mmol/L)	· Renal dysfunction· Reversible leukopenia and thrombocytopenia	· Oral chelator approved for Wilson disease; not specially approved for chelation of lead· Monitor complete blood count, renal function· Third-line drug

Q. Which of the following is the preferred chelating agent for managing a patient who has lead-induced encephalopathy?

Dimercaprol

Q. Which of the following routes of exposure to elemental mercury carries highest risk of acute toxicity?

Inhalation

2. Mercury Poisoning

Mercury

Elemental Mercury(vaporizable),
Methyl mercury
Mercury salts

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Acute Mercury Poisoning

Inhalation (basic): ARDS, sickness resembling Kawasaki disease . Ingestion (inorganic): corrosive; can result in renal failure, ARDS, esophagitis, and gastritis; systemic shock.

Chronic toxicity

Inhaled, Danbury tremor: Cerebellar signs: Hatter's shakes, ataxia, reeling gait, Mercuria lentis; inorganic mercury ingestion; colitis, melanosis coli, renal injury; Acrodynia (painful erythema), commonly known as pink disease; Erethism (mad hatter) - a neuropsychiatric condition.

Methyl mercury poisoning caused by organic mercury . Minimata disease (dysarthria, ataxia, coma > death, visual and hearing loss, tremors) , observed in brain lesions. Originated from fish tainted with industrial contaminants; reported from Japan.

Diagnosis

• Blood mercury levels: used to treat acute poisoning; normal <10 mcg/L.
• Urine mercury: normal <50 mcg/L; used to treat long-term toxicity.

Q. Which is the best specimen for diagnosis of mercury poisoning in the following settings?

Methyl Mercury Poisoning- Chronic

Acute poisoning

Mercury interacts with sulfhydryl groups during decontamination, supportive care, gastric lavage with milk or egg, and other processes.

Chronic Toxicity: chelation (DMSA, DMPS, BAL, D-penicillamine)

Q. Which of the following chelating agent is not useful for management of methylmercury poisoning?

Ans. DMSA

3. Aluminium Phosphide Poisoning

Death rate of 100%, Phoxine is a toxic metabolite. When water or HCL come into touch with aluminum phosphate. The release of phosphone gas, leaving behind aluminum chloride or hydroxide.

Phosphine is a cell poison; Cyt C oxidase inhibition. Superoxide dismutase is induced., catalase is inhibited., depletes reserves of glutathione. A rise in damage from free radicals. Paralysis of the breathing. Causes the demise of cells.

Clinical Manifestation

Shock, As a result of shock and increased lactic acid generation; severe metabolic acidosis; myocardial depression; arrhythmias (ST-T alterations).

Diagnosis Of ALP Poisoning

Triadic symptoms include: metabolic acidosis; garlicky smell (OP poisoning); hypotension; breath; gastric aspirate; GC-NPD; gas chromatography-nitrogen and phosphate detector; and most sensitive and specific.

Management Of ALP Poisoning

Assistance with care. Magnesium sulfate , NMDA receptor inhibition.
Lower the incidence of arrhythmia (does not lower mortality) . Reduce the formation and absorption of phosphine gas in coconut oil and other fat-rich products.

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