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mercury

mercury poisoning

see also:

introduction

  • mercury is a heavy metal which accumulates in the body and also becomes more concentrated in animals higher in the food chain
  • high levels may cause toxicity and can affect babies in utero as well as during lactation
  • mercury was frequently used in medicines such as diuretics, antiseptics, laxatives and to treat syphilis, as well as use in the home and industry
  • in the late 19th century, the term “mad as a hatter” was used to denote mercury poisoning in hat makers
  • in 1961, it was found to be the cause of Minamata disease in Japan due to a factory discharged inorganic mercury into the water where bacteria methylated it and fish ingested it
  • prior to 1990, many paints contained mercury as an antimildew agent
  • the classic triad found in chronic mercury toxicity is tremors, gingivitis, and erethism

toxic effects of mercury

  • inorganic mercurial salts are often caustic when ingested
  • mercury damages the nervous system through several potential mechanisms:
    • binds to sulfhydryl groups and incapacitates key enzymes involved in the cellular stress response, protein repair, and oxidative damage prevention
    • methylmercury disrupts the muscarinic cholinergic systems in the brainstem and occipital cortices
    • methylmercury also inactivates sodium-potassium adenosine triphosphatase (Na+/K+-ATPase), which leads to membrane depolarization, calcium entry, and eventual cell death
    • methylmercury may sequester selenium and thus disrupt cellular biochemical pathways that use selenium as an enzymatic cofactor
    • dysregulation of the nitric oxide system in rodents
    • several pathways may be simultaneously activated to cause apoptosis
  • direct renal toxic effect

mechanisms of poisoning

GIT absorption

  • ingested elemental mercury is not absorbed at all hence swallowing a mercury thermometer is not going to cause mercury poisoning HOWEVER, oral ingestion of elemental mercury may lead to significant environmental contamination as the mercury is passed unabsorbed through the GI tract and expelled in the faeces
  • mercurial compounds are variably absorbed with usual absorption rates of 2-10%, although some organic forms such as methylmercury (eg. in fish from contaminated waters) has ~90% absorption!
    • organic mercurial compounds are mainly excreted in the faeces
    • biological half-life of methylmercury is approximately 65 days
  • inorganic mercurial salt poisoning and caustic burns may occur with ingestions of button batteries
  • mercury has been detected in 45% of high-fructose corn syrup samples
  • mercury is also present in some uncontrolled substances such as skin-lightening creams and Chinese herbal medicines

inhalation

  • mercury vapour is well absorbed through inhalation and as it is lipid soluble, it is easily transported:
    • into RBC's where catalase converts it to inorganic mercuric form which is not lipid soluble and does not readily cross the BBB
    • across the blood brain barrier where it becomes trapped in the CNS by ionisation to mercuric forms
  • inhalation of mercury vapour may lead to metal fume fever
  • inhalational exposure may occur when people vacuum or sweep mercury spills in an enclosed space
  • newer compact, energy-efficient fluorescent lights contain substantial mercury concentrations, making breakages with subsequent release a source of exposure

dermal absorption

  • long term exposure to dermal inorganic mercurial salts can cause toxicity

metal fume fever

  • acute onset:
    • fatigue, weakness
    • fever, chills
    • dizziness, headache
    • abdominal cramping
    • dyspnea
    • dysuria
    • ejaculatory pain

clinical features of acute inorganic mercuric salts ingestion

  • acute onset:
    • ashen-gray mucous membranes secondary to precipitation of mercuric salts
    • hematochezia
    • vomiting
    • severe abdominal pain
    • hypovolemic shock
  • systemic effects onset several hours and may last days:
  • chronic phase - erethism:
    • irritability
    • excitability
    • anxiety
    • insomnia
    • social withdrawal

clinical features of chronic organic mercury poisoning

  • onset is usually days to weeks after exposure when the target enzymes become depleted
  • organic mercury targets various parts of the brain - mainly the cerebral cortex and cerebellum
  • most are neurologic features:
    • paraesthesiae occurs early esp. perioral and facial
    • peripheral neuropathy with preferential loss of large myelinated nerve fibers
    • headache
    • scotomata
    • ataxia
    • hearing loss
    • dysarthria
    • cognitive impairment and memory loss
    • tremor
    • movement disorders
    • psychiatric disturbances
    • severe exposure results in paralysis and death
  • in utero exposure:
    • low birth weight
    • seizure disorders
    • profound developmental delay
    • incomplete visual loss (eg. tunnel vision) or total blindness
    • hearing loss
  • childhood exposure:
    • use of calomel-containing teething powders prior to 1955 has been implicated as a cause of Young's syndrome
    • motor impairment
    • visual loss
    • hearing loss
    • developmental delay
    • seizure disorders

acrodynia or pink disease

  • possibly a HS reaction to mercury
  • erythema of the palms and soles
  • oedema of the hands and feet
  • desquamating rash
  • alopecia
  • pruritus
  • diaphoresis, tachycardia, hypertension
  • photophobia, irritability, anorexia, insomnia
  • poor muscle tone
  • constipation or diarrhoea

Mx of suspected mercury poisoning

  • remove from contaminated air if inhalational, and remove contaminated clothing
  • activated charcoal and whole bowel irrigation may be indicated for acute ingestions or inorganic or organic mercurial compounds
  • FBE to help exclude GIT blood loss
  • U&E to help exclude renal tubular acidosis (RTA)
  • blood mercury levels are useful in acute poisonings but not chronic poisonings
  • hair mercury levels are more inicative of chronic poisonings
  • surgical removal of subcutaneous metallic mercury or ingested mercury that has become ledged in bowel may be indicated
  • chelation Rx may be indicated
    • 2,3-dimercaptosuccinic acid (DMSA or succimer)
    • polythiol is a nonabsorbable resin that can theoretically help in facilitating the removal of methylmercury
    • BUT note that chelation removes only a small portion of the body's mercury stores and risks may outweigh its benefits
  • neostigmine may help motor function in methylmercury toxicity as this toxicity may lead to acetylcholine deficiency
  • avoid further exposures - ie. avoid eating fish high in mercury content such as larger fish / sharks
mercury.txt · Last modified: 2014/04/07 16:19 (external edit)