Pathophysiology: The most frequent sources of mercury prior to the legislated removal of the heavy metal from these preparations were calomel-containing anthelminthics, laxatives, diaper rinses, teething powders, fungicides in paint, repeated gamma-globulin injections, termite-protected wood (mercury bichloride), watch batteries (ie, via ingestion), mercurial antibacterial ointments, mercurial skin-lightening creams, and dental amalgam. This legislation corresponded to the virtual disappearance of acrodynia. Present-day cases reveal more novel exposure, such as mercuric oxide used to treat eyelid mites. Some have suggested the disease may represent a delayed allergic or hypersensitivity reaction because not all persons exposed to mercurial compounds develop the disease.
Because the metal can be stored in the body to some extent and intolerance may develop long after exposure, morbid symptoms may appear weeks or months after the drug administration (ie, exposure), with its cause escaping recognition. The deleterious effects of relatively small doses of mercury on the nervous system that are sometimes seen in the course of acrodynia add to the acrodynic reaction. In acrodynia, no reflex dilatation of the peripheral vessels occurs in response to heat. Vasoconstriction is abolished only when the nerve supply to the arterioles is interrupted.
Frequency:
- In the US: Acrodynia was once widely prevalent; however, it is rare today, owing to the discontinued use of mercury in different preparations.
- Internationally: Acrodynia was especially common in Australia. Epidemics of mercury poisoning have followed the release of mercury into the environment from industrial activity, with uptake of methyl mercury from eating fish from Minamata Bay, Japan, and uptake of both inorganic and methyl mercury following the release of mercury vapor and its subsequent deposition in waterways from gold recovery procedures in the Amazon basin. The ingestion of wheat and barley seed treated with an alkyl mercury fungicide for sowing, by a largely illiterate population in Iraq, led to a major outbreak of poisoning with a high fatality rate.
Mortality/Morbidity: Older children tend to have less morbidity. Death can result in 10% of cases.
Treatment
Medical Care: Removal of the inciting agent is the goal of treatment. Correcting fluid and electrolyte losses and rectifying any nutritional imbalances (vitamin-rich diets, vitamin-B complex) are of utmost importance in the treatment of the disease.
- Recently, the chelating agent meso 2,3-dimercaptosuccinic acid has been shown to be the preferred treatment modality. It can almost completely prevent methylmercury uptake by erythrocytes and hepatocytes.
- In the past, dimercaprol (British antilewisite; 2,3-dimer-capto-l-propanol) and D-penicillamine were the most popular treatment modalities. Disodium edetate (Versene) was also used.
- Neither disodium edetate nor British antilewisite has proven reliable. British antilewisite has now been shown to increase CNS levels and exacerbate toxicity.
- N-acetyl-penicillamine has been successfully given to patients with mercury-induced neuropathies and chronic toxicity, although it is not approved for such uses. It has a less favorable adverse effect profile than meso 2,3-dimercaptosuccinic acid.
- Hemodialysis with and without the addition of L-cysteine as a chelating agent has been used in some patients experiencing acute renal failure from mercury toxicity.
- Peritoneal dialysis and plasma exchange also may be of benefit.
- Tolazoline (Priscoline) has been shown to offer symptomatic relief from sympathetic overactivity.
- Antibiotics are necessary when massive hyperhidrosis, which may rapidly lead to miliaria rubra, is present. This can easily progress to bacterial secondary infection with a tendency for ulcerating pyoderma.
The goals of pharmacotherapy are to remove the causing agent, to reduce morbidity, and to prevent complications.
Drug Category: Chelating agents -- Succimer almost completely prevents methylmercury uptake by erythrocytes and hepatocytes.
| Drug Name | Succimer (Chemet) -- Metal chelating agent, analog of dimercaprol, used in lead poisoning. Recommended treatment course is 19 d. Blood mercury levels should be monitored at least qwk after therapy to determine if a repeat course is indicated. A minimum of 2 wk between courses is recommended. |
|---|---|
| Adult Dose | 10 mg/kg IV q8h for 5 d; then q12h for 2 wk |
| Pediatric Dose | Administer as in adults |
| Contraindications | Documented hypersensitivity |
| Interactions | Do not administer concomitantly with edetate calcium disodium or penicillamine |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Caution in renal or hepatic impairment; to prevent toxicity, patient should be well hydrated; adverse effects include rash, GI symptoms (eg, nausea, vomiting, diarrhea, appetite loss, metallic taste in mouth), and increases in serum transaminases |
| Drug Name | Tolazoline (Priscoline) -- Alpha-adrenoliticum, vasodilatins peripherica. IV medication used only in hospital. Directly dilates blood vessels and is a competitive antagonist of alpha-receptors. |
|---|---|
| Adult Dose | 3-5 mg IV q4h |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; renal failure, low blood pressure, or endocranial bleeding |
| Interactions | Do not coadminister with epinephrine because hypotensive effect may be potentiated from unopposed beta-adrenoceptor stimulation; may cause disulfiramlike reaction if given with ethanol |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Stimulates gastric acid secretion and should not be used in peptic ulcer disease; caution in mitral stenosis |
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