Severe neurotoxicity following ingestion of tetraethyl lead.

Organic lead compounds are potent neurotoxins which can result in death even from small exposures. Traditionally, these compounds are found in fuel stabilizers, anti-knock agents, and leaded gasoline. Cases of acute organic lead intoxication have not been reported for several decades. We report a case of a 13-year-old Iraqi male who unintentionally ingested a fuel stabilizer containing 80-90% tetraethyl lead, managed at our combat support hospital. The patient developed severe neurologic symptoms including agitation, hallucinations, weakness, and tremor. These symptoms were refractory to escalating doses of benzodiazepines and ultimately required endotracheal intubation and a propofol infusion. Adjunctive therapies included chelation, baclofen, and nutrition provided through a gastrostomy tube. The patient slowly recovered and was discharged in a wheelchair 20 days after ingestion, still requiring tube feeding. Follow-up at 62 days post-ingestion revealed near-resolution of symptoms with residual slurred speech and slight limp. This case highlights the profound neurotoxic manifestations of acute organic lead compounds.

Intoxicação por chumbo no ambiente de trabalho / Lead poisoning in the workplace

O presente estudo tem por objetivo abordar a intoxicação por chumbo no ambiente ocupacional. Inicialmente, buscou-se contemplar a etiopatogenia do saturnismo, onde se pode afirmar que os efeitos tóxicos do chumbo dependem não só da quantidade absorvida como da tolerãncia individual e de sua distribuição no organismo: foi visto o processo de absorção, distribuição e eliminação do chumbo, sua epidemiologia, quadro clínico, diagnóstico, tratamento e prevenção. O estudo conclui qua as medidas de primeira linha na prevenção das exposições a chumbo estão no plano da prevenção primária, ou seja, trata-se de medidas que buscam eliminar ou reduzir a exposição excessiva. A quelação com EDTA (Ácido Etileno Diamino tetra-acético) é o que melhores resultados apresentam para o tratamento da intoxicação por chumbo, sendo considerado o de escolha principalmente nas intoxicações graves.

Ayurvedic medicine: patients in peril from plumbism.

Heavy metals are commonly incorporated into Ayurvedic preparations as ashes or 'bhasmas'. A widely disseminated belief within Ayurvedic medicine is that these heavy metals can be valuable therapeutic components. Western toxicology refutes this contention. We report eight cases of lead poisoning occurring in or near the Auckland region of New Zealand. In all cases, poisoning was attributable to consumption of Ayurvedic 'herbal medicines'. Whole blood lead levels ranged from 1.5 to 6.9 micromol/L. Six patients had symptomatic lead poisoning, requiring treatment with chelation therapy. A high index of suspicion is required to detect lead poisoning, which should be suspected in people taking Ayurvedic remedies, especially if they have associated anaemia or abdominal symptoms.

Neuropathies associated with excessive exposure to lead.

Exposure to lead is a ubiquitous problem of the modern era. The majority of cases of all forms of lead intoxication, especially lead neuropathy, result from industrial exposure. In the Western world meticulous monitoring in industry has reduced the risk of overt lead neuropathy. The classic form of lead neuropathy consists of weakness that primarily involves the wrist and finger extensors but which later spreads to other muscles. There is only minimal sensory involvement. Less commonly, there is a more typical toxic neuropathy with distally accentuated sensory and motor involvement. The motor neuropathy is more likely to develop following relatively short-term exposure to high lead concentrations and evolves in a subacute fashion. Prognosis for recovery is good as long as exposure is terminated promptly. The distal sensory and motor neuropathy develops after many years of exposure, evolves more slowly, and recovery is less certain. There is a generally weak relationship between the development of lead neuropathy and blood lead levels, at least for the subacute motor neuropathy, leading to speculation that the metabolic basis for the neuropathy is interference with porphyrin metabolism. Lead intoxication in humans causes axonal degeneration, but in some other species it causes a primarily demyelinating neuropathy. It should be possible to prevent lead neuropathy by good industrial hygiene. Close monitoring should identify excessive lead exposure before it causes overt neuropathy. If evidence of excessive exposure is found or if overt neuropathy develops, exposure must be terminated immediately. The role of chelation therapy in the treatment of lead neuropathy is controversial.

Lead poisoning.

Understanding of lead toxicity has advanced substantially over the past three decades, and focus has shifted from high-dose effects in clinically symptomatic individuals to the consequences of exposure at lower doses that cause no symptoms, particularly in children and fetuses. The availability of more sensitive analytic methods has made it possible to measure lead at much lower concentrations. This advance, along with more refined epidemiological techniques and better outcome measures, has lowered the least observable effect level until it approaches zero. As a consequence, the segment of the population who are diagnosed with exposure to toxic levels has expanded. At the same time, environmental efforts, most importantly the removal of lead from gasoline, have dramatically reduced the amount of lead in the biosphere. The remaining major source of lead is older housing stock. Although the cost of lead paint abatement is measured in billions of dollars, the monetized benefits of such a Herculean task have been shown to far outweigh the costs.