Inorganic Mercury

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Pathogenesis and Pathophysiology. Elemental mercury is transported in blood plasma, proteins, and hemoglobin. In the appropriate conditions, mercury may be incorporated rapidly into the brain. Once incorporated into the body, mercury can be found in the urine as long as 6 years after exposure has ceased. Inorganic mercury has the greatest affinity for the kidney. Although concentrations are lower in the CNS, they may still be significant. In the brain, animal studies have shown that the highest concentrations of mercury occur in the brain stem, followed by the cerebellum, cerebral cortex, and hippocampus.

Inorganic mercury exerts its neurotoxic effects by altering membranes. A paucity of information is available on the pathological events resulting from inorganic mercury intoxication. Very few postmortem studies have been published, and results vary from normal to slight neuronal damage with evidence of intracellular mercury.

Epidemiology and Risk Factors. Historically, inorganic mercury compounds have been used as antiseptics, disinfectants, purgatives, and components in the industrial manufacture of felt. Mercury was also used formerly in the form of cinnabar, a red pigment used for painting and coloring. Works of art containing cinnabar can be found in ancient Egyptian and Pakistanian ruins.

By current NIOSH estimates, 65,000 workers are potentially exposed to mercury. The occupations significantly at risk for mercury intoxication are listedin TabJ.e39.il . Mercury is also one of the most serious environmental pollutants in air and water. Between 1953 and 1956, an epidemic of methyl mercury poisoning occurred in Japan when a large number of villagers developed chronic mercurialism (Minamata disease) from ingesting fish contaminated with methyl mercury from industrial waste. There appears to be a wide range of individual susceptibility to the toxic effects of mercury; these may depend on the form of mercury involved, hygiene, diet (including vitamin deficiency), and some intrinsic differences in mercury metabolism. Metallic mercury becomes volatile at room temperature and thus generally enters the body through the inhalation of mercury vapors.

Clinical Features and Associated Findings. Acute mercury poisoning usually results from accidental ingestion of an antiseptic in the medicine cabinet. Symptoms of acute inorganic mercury poisoning consist of massive gastrointestinal vomiting and colitis with renal failure. The breath has a metallic odor. A brownish mercurial linear streak may be visible along the margin of the teeth. Symptoms of irritability, rapid onset of weakness in the lower limbs, psychotic episodes with delirium, hallucinations, and motor hyperactivity have been reported. The major threat to these patients is gastrointestinal hemorrhage, but after 24 hours renal failure becomes the predominant cause of morbidity.

Chronic mercury toxicity can result in tremor and weakness of the limbs or progressive personality changes. Mercury-induced tremors, also known as "hatter's shakes" or "Danbury shakes," consist of fine and regular tremors interrupted by much coarser myoclonic jerks. These tremors can be seen at rest and often diminish with activity. In the later stages of intoxication, gait and balance may be altered because of the continuous trembling. In addition, dyskinetic movements, pareses, and convulsions have been reported. At times, these patients present a typical picture of parkinsonism. Mercury can also cause peripheral polyneuropathy (sensorimotor axonopathy), which affects the lower extremities more than the upper ones. Paresthesias with extreme pain or peripheral neuropathy with muscle atrophy may also occur. Cognitive decline, vertigo, nystagmus, blurred vision, narrowing of the visual fields, optic neuritis, optic atrophy, sensory ataxia with a positive Romberg's sign, seizures, and vegetative disturbances have also been observed.

Personality changes can develop before neurological signs appear. So-called "mercurial neurasthenia" may develop for weeks or months before the patient seeks treatment. This syndrome consists of extreme fatigue, hyperirritability, insomnia, pathological shyness, and depression. The hyperirritability may become so severe that extremely violent behavior develops, possibly including homicidal acts.

Acrodynia, chronic mercury toxicity in children, is a syndrome consisting of painful neuropathy that involves significant autonomic changes. This syndrome includes redness and coldness in the hands and feet, pain in the limbs, profuse sweating of the trunk, severe constipation, and weakness. Tremors similar to those found in adults and personality changes may also occur.

Differential Diagnosis and Evaluation. Serum concentrations of mercury are unreliable indicators of inorganic and organic mercury toxicity because blood levels vary greatly between individuals and in the same individual. The threshold biological exposure index (BEI) for blood is 15 pg/L, and for urine it is 35 pg/g creatine. However, urinary excretion is not a good measure of toxicity, since there seems to be little correlation between symptomatology and the amount of mercury excreted in the urine. Although the early differential diagnosis might include Parkinson's disease, the tremor seen with mercurial intoxication is not solely a resting tremor and is usually coarser than that found in patients with Parkinson's disease. Because the signs of mercury intoxication may mimic those of some common neurological syndromes, the correct diagnosis is dependent on a good occupational history, clinical symptomatology, and documentation of mercury in the patient's blood, urine, or hair.

Management and Prognosis. Removal of the patient from the sources of exposure and chelation with W-acetyl-D-penicillamine is recommended.

Prognosis and Future Perspectives. Follow-up of the survivors with Minamata disease years after poisoning occurred revealed decreased bilateral attenuation on CT scans in the visual cortex and diffuse atrophy of the cerebellum, especially the vermis.

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