Archive for November, 2008

Heavy Metal Poisoning: Mercury

Mercury is the only metal which is present in liquid form. The toxicity of low level organic mercury exposure is mainly manifested by neurobehavioral performance. Mercury is excreted in urine and feces and has a ½ life in blood of about 60 days. But, deposits in the kidney and brain may remain for many years. Elemental mercury (Hg°) is not absorbed well. But, it can volatilize into highly absorbable vapor. Inorganic mercury is absorbed through the gastro intestinal tract and skin. Organic mercury is well absorbed by ingestion and inhalation and it is a major source of mercury poisoning.

Sources of Mercury poisoning: Metallic, mercuric mercury (Hg°, Hg+, Hg2+) and mercurous mercury exposures occur in some chemical, metal-processing, electrical equipment industries and automotive industries. Mercury is also present in thermometers, dental amalgams and batteries. Mercury can also be spread by waste incineration. Mercury present in environment is converted to organic mercury from inorganic mercury by bacteria. This organic mercury is than taken up by planktons, algae and fungi which are food for sea fishes like tuna, swordfish, and other pelagic fish. These sea foods when consumed by humans in large amount can lead to slow mercury poisoning.

Toxicity: Acute inhalation of mercury vapor can cause pneumonitis and pulmonary edema (water in lungs) which may cause death. It can also cause polyneuropathy and CNS (central nervous system) symptoms. Acute ingestion of inorganic mercury can cause gastroenteritis, nephritic syndrome, acute renal failure, hypertension, and cardiovascular collapse. Death usually occurs at a dose of 10–42 mg/kg. Acute ingestion of organic mercury causes gastroenteritis, arrhythmias (rhythm disturbance of heart beat), and lesions in the basal ganglia and gray matter. Chronic inhalation of mercury vapor causes CNS toxicity (mercurial erethism) lower exposures impair renal function, motor speed, memory, coordination.

High exposure of mercury during pregnancy can cause severe mental retardation due to derangement of fetal neuronal migration. Mild exposures of mercury during pregnancy (from fish like tuna, swordfish, and other pelagic fish consumption) are associated with reduced neurobehavioral performance in offspring.

Dimethylmercury is highly toxic (supertoxic) and is found in research labs. A few drops of exposure via skin absorption or inhaled vapor can cause severe cerebellar degeneration which lead to death.

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Posted by - November 29, 2008 at 12:46 am

Categories: Heavy Metal Poisoning   Tags:

Scombroid Fish Poisoning: Treatment

Scombroid fishes are mackerel-like fish that include the albacore, yellowfin tuna, blue fin, mackerel, saury, needlefish, wahoo, skipjack and bonito. All the above fishes are included in scombroid fish family. Many non scombroid fishes can also produce scombroid poisoning and they include the dolphinfish, kahawai, sardine, black marlin, pilchard, anchovy, herring, amberjack, and salmon. Now non scombroid fishes are producing scombroid poisoning than scombroid fishes.

Histamine, histamine phosphate, and histamine hydrochloride are the active poisons in scombroid poisoning. All the above poisons are produced by decarboxylation of the amino acid L-histidine during decomposition in improperly preserved fish.

Treatment of scombroid fish poisoning:

The treatment is directed at the histamine and its related compounds. Both first generation and second generation anti histaminics are effective in the treatment of scombroid poisoning. First generation anti histaminics like pheniramine, cinnerazine and second generation anti histaminics like cetirizine, fexofenadine are equally effective in the treatment of scombroid poisoning. But the second generation anti histaminics are preferred because they are less sedative and they can be given as once a day dose and patient compliance is better.

If there is bronchospasm (constriction of bronchus) and it is severe, an inhaled bronchodilator like salbutamol is given and in extremely severe circumstances, injected epinephrine can be used. Glucocorticoids are not useful in scombroid poisoning induced bronchospasm.

If there is severe nausea and vomiting may be controlled with a specific antiemetic, like prochlorperazine. Headache of scombroid poisoning can be treated by simple analgesics. The persistent headache of scombroid poisoning if not controlled by simple analgesic may respond to cimetidine or a similar antihistamine. 

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Posted by - November 15, 2008 at 4:28 pm

Categories: Disease Treatment, Health Information   Tags: , , , ,

Lead Poisoning: Treatment

Clinical manifestations of lead poisoning: Abdominal pain, lethargy, anorexia, irritability, anemia, Fanconi’s syndrome, pyuria (pus in urine), azotemia in children with blood lead level of more than 80µg/100ml. Epiphyseal plate “lead lines” can be seen on X-ray of long bones. Convulsions, coma, and death can occur if blood lead level is more than 120µg/100ml. CDC Atlanta, USA recommends screening of all children at the time of crawling age (about 6 months) source identification and intervention is begun if the BPb (blood lead level) is more than 10 µg/100ml. Neurodevelopmental delays are seen at BPb of 40–80 µg/100ml. Headaches, arthralgias (joint pain), myalgias, depression, impaired short-term memory, loss of libido are common symptoms of lead poisoning. Examination may reveal a “lead line” at the gum-tooth border, pallor, wrist drop.

Diagnosis: Diagnosis is mainly by history, clinical symptoms and blood lead levels.  Laboratory tests may reveal a normocytic, normochromic anemia, an elevated blood protoporphyrin level, and motor delays on nerve conduction. In the U.S., regular testing of lead-exposed workers with removal if BPb is more than 40 µg/100ml is mandatory. K-X-ray fluorescence (KXRF) instruments have made it possible to measure bone lead levels which can diagnose a chronic lead poisoning even if it is at subclinical level.

Treatment: Source of the poisoning should be identified and corrected. Chelation is recommended with oral DMSA (succimer). Severe toxic cases should be hospitalized and IV (intravenous) or IM (intramuscular) chelation with edentate calcium disodium (CaEDTA) is administered. Dimercaprol is given to prevent worsening of encephalopathy. Correction of dietary deficiencies of iron, calcium, magnesium, and zinc lower lead absorption and also can improve the toxic condition. Vitamin C is a weak and natural chelating agent.

Chelation should be done or not in children with asymptomatic lead poisoning (blood lead level 20-40 µg/100ml) are not clear.

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Posted by - November 8, 2008 at 2:00 pm

Categories: Heavy Metal Poisoning   Tags: , ,