Diagnosis
ICD-9-CM
ICD-9-CM code 985.8 Toxic effect of other specified metals includes acute & chronic copper poisoning (or other toxic effect) whether intentional, accidental, industrial etc. In addition, it includes poisoning and toxic effects of other metals including tin, selenium, nickel, iron, heavy metals, thallium, silver, lithium, cobalt, aluminum and bismuth. Some poisonings, e.g. zinc phosphide, would/could also be included as well as under 989.4 Poisoning due to other pesticides, etc. Excluded are toxic effects of mercury, arsenic, manganese, beryllium, antimony, cadmium, and chromium. ICD-10-CM
SNOMED
Treatment
In cases of suspected copper poisoning, penicillamine is the drug of choice, and dimercaprol, a heavy metal chelating agent, is often administered. Vinegar is not recommended to be given, as it assists in solubilizing insoluble copper salts. The inflammatory symptoms are to be treated on general principles, as are the nervous ones. Treatment can also look like ozone oxidation for environmental toxicity problems, as well as removing sediment in water areas because sediment can be a home for toxicants to reside. There is some evidence that alpha-lipoic acid (ALA) may work as a milder chelator of tissue-bound copper. Alpha lipoic acid is also being researched for chelating other heavy metals, such as mercury. Aquatic life
Too much copper in water may damage marine and freshwater organisms such as fish and molluscs.
Hennekam syndrome also known as intestinal lymphagiectasia–lymphedema–mental retardation syndrome, is an autosomal recessive disorder consisting  of intestinal lymphangiectasia, facial anomalies, peripheral lymphedema, and mild to moderate levels of growth and intellectual disability.It is also known as "lymphedema-lymphangiectasia-mental retardation syndrome".Hennekam Syndrome is subdivided according to the causative genetic lesion, most (or all) of which are affecting the VEGF-C/VEGFR-3 signaling pathway:

Type 1 (mutations in CCBE1) 
Type 2 (mutations in FAT4)
Type 3 (mutations in ADAMTS3)The first recognition of a genetic association was with CCBE1, published by its namesake, Raoul Hennekam. The molecular mechanism of the lymphedema phenotype in CCBE1-associated cases was identified as a diminished ability of the mutated CCBE1 to accelerate and focus the activation of the primary lymphangiogenic growth factor VEGF-C. Mutations in the FAT4 gene had previously been only associated with van Maldergem syndrome, but the pathogenetic molecular mechanism and the function of FAT4 within lymphangiogenesis are still unknown. References


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