598
Views
6
CrossRef citations to date
0
Altmetric
Letter to the Editors

Mercury tissue concentrations in various organs following a fatal intentional poisoning with mercury chloride

, &
Pages 783-784 | Received 24 May 2007, Accepted 17 Aug 2007, Published online: 20 Oct 2008

Acute poisoning with mercury, although rare, can have dramatic consequences due to the cellular effects in different vital organs (Citation1CitationCitation3). This case focuses on acute poisoning by inorganic mercury and more particularly on tissue concentrations following fatality.

A 36-year-old woman, presented to our emergency department after an intentional ingestion of alcohol, tricyclic antidepressants, KCN, and possibly other products. Although she was fully conscious, intubation of the trachea was immediately performed because of an obstructive airway and vomiting. She had a compromised peripheral circulation with mottled extremities and cyanosis, hemorrhagic nasopharyngeal mucosa, but no major hemodynamic instability. Supportive therapy and a diagnostic work-up were started. A gastric tube was placed to perform gastric emptying, administration of 50 g activated charcoal, gastric lavage (recent ingestion) followed by a second administration of 50 g activated charcoal. Central venous and arterial catheters were inserted, and a bladder catheterisation was performed. Intravascular fluid replacement was started and urine, gastric content, and blood were sampled for toxicological investigations.

The following hours, the patient's hemodynamic condition deteriorated rapidly. Artificial ventilation was needed to compensate respiratory and metabolic acidosis, and hypoxemia. There was a generalized bleeding tendency with significant blood loss from nasopharynx, stomach, rectum, and catheter insertion points. Mercury was determined in a specialised laboratory and has previously extensively been described (Citation4). The measurements are accurate to the first decimal place. Toxicological investigation demonstrated the intake of high amounts of mercury chloride but no other substances could be found. Blood and urine samples taken on admission, approximately 2 hours post ingestion, revealed respectively 48.6 μg/ml and 8.6 μg/L. Further intensive therapy included IV fluids, crystalloids, blood products, inotropic support, IV sodium bicarbonate, and hyperventilation. Chelator therapy was started with DMSA (dimercaptosuccinic acid) intravenously in a continuous infusion of 1 g/12 h approximately 4 hours after ingestion. By 6 hours post ingestion, blood and urine mercury levels were 26.9 μg/mL and 1.2 μg/L. The hemodynamic instability remained, renal and liver functions deteriorated, lung oedema appeared. Pieces of mucous membranes were found in the pharynx while suctioning. Twelve hours after ingestion, extra corporal continuous regional haemodialysis was performed with administration of DMSA in a rate of 82 mg / min on the arterial line. Unfortunately, the patient collapsed completely resulting in cardiac arrest and resuscitation attempts were not successful.

A post mortem examination was requested and tissue samples of different organs were harvested for analyses. The post-mortem tissue concentrations were: mucosa of stomach 6624 μg/g: kidney 284.3 μg/g; liver 65.1 μg/g; spleen 56.3 μg/g; lung 38.5 μg/g; myocardium 16.9 μg/g; brain (cortex) 1.4 μg/g and brain (cerebellum) 1.2 μg/g. The highest concentrations, as could be anticipated, are found in the stomach where mercury is absorbed and in the kidneys indicating an important accumulation provoking acute renal failure. Limited mercury accumulation was observed in the brain and cerebellum.

A recent review paper on inorganic vapour inhalation summarizes the available data on mercury concentrations found in different organs following acute and chronic exposure (Citation5). In three fatal cases, 12 to 19 days following exposure, accumulation of mercury was found in the kidneys (between 26 and 60 μg/g). The other organs (brain, lung, liver, spleen, muscle, colon, testis) tissue concentrations were below 4 μg/g. Subjects chronically exposed to mercury vapour demonstrate high tissue concentrations in the brain (10 to 12 μg/g) but inorganic mercury did not seem to damage the neurons.

After acute ingestion, it has been hypothesised that only 7 to 15% of the inorganic mercury is absorbed (Citation6). The highest amount is fixed to the mucous gastric membranes, as demonstrated in this case. The remaining absorbed fraction will then be dissociated in the elements mercury and chloride. The renal accumulation has been demonstrated in an animal model (Citation7). The accumulation is mainly at the level of the distal part of the proximal tubule and is responsible for the acute renal failure which settles within a few hours. Liver, spleen and lungs are reached in lesser extend. In contrast, the brain and cerebellum are relatively spared indicating a limited passage of the inorganic shape through the blood-brain barrier. This case report illustrates the uneven distribution of the toxin following an acute poisoning.

References

  • M Yoshida, H Satoh, M Igarashi, K Akashi, Y Yamamura, and K Yoshida. (1997). Acute mercury poisoning by intentional ingestion of mercuric chloride. J Exp Med 182 (4):347–352.
  • GA McLauchlan. (1991). Acute mercury poisoning. Anaesthesia 46 (2):110–2.
  • S Satar, N Toprak, Y Gokel, and A Sebe. (2001). Intoxication with 100 grams of mercury: a case report and importance of supportive therapy. Eur J Emerg Med 8:245–248.
  • JP Bucket, and RR Lauwerys. (1989). Influence of 2,3-dimercaptopropane-1-sulfonate and dimercaptosuccinic acid on the mobilization of mercury from tissues of rats pretreated with mercuric chloride, phenylmercury acetate or mercury vapors. Toxicology 54:323–333.
  • S Asano, K Eto, E Kurisaki, H Gunji, K Hiraiwa, M Sato, H Sato, M Hasuike, N Hagiwara, and H Wakasa. (2000). Acute inorganic mercury vapour inhalation poisoning. Pathology International 50:169–174.
  • TW Clarkson. (1997). The toxicology of Mercury. Critical reviews in Clinical Laboratory Sciences 34 (3):369–403.
  • T Emanuelli, JB Rocha, ME Pereira, LO Porciuncula, VM Morsch, AF Martins, and DO Souza. (1996). Effect of mercuric chloride intoxication and dimercaprol treatment on delta-aminolevulinate dehydratase from brain, liver and kidney of adult mice. Pharmacol Toxicol 79 (3):136–143.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.