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Jewelry bismuth
Atomic number 83
Atomic weight 208.980
Melting point 271 °C
Discovered by GERMANY
BI
O
OO OH
 Solid
 Colour Crystalline, with pink tint .
 No Odour
 No thermal conductivity
 high electrical resistance
 Diamagnetic
 Free in nature
 Earth crust
 Seawater
 In soil with lead
 Found in fire detection
device
 fire sprinklers.
 Ceramic glaze
 Hunting shot
 Pharmacy products
 cosmetics
 Paints
 A catalyst in rubber production
 it was distinct from lead in 1753 .
 Elemental bismuth is nontoxic.
 bismuth salt have therapeutic uses
and responsible the toxicities.
 In the early 20th century acute kidney
was reported in children administered
IM bismuth salt for the treatment of
gingivostomatitis Historically bismuth
tartrate were used to treat syphilis,
while bismuth sodium triglycollamate
has been used to treat warts,
stomatitis and upper respiratory tract
infections.
Bismuth got its
name from the
German word
*wissmuth
*meaning white
mass
 Xenobiotic
 Inorganic bismuth compound ’’ subnitrate ’ subcarbonat”
used for gastrointestinal disorder (diarrhea ,flatulence
,constipation ,cramp ,dyspepsia )
 Lipid soluble organic Colloidal bismuth subcitrate
’subgallate ‘subsalicylate (pepto bismol) ranitidin
bismuth citrate ‘ used to treat peptic ulcer and H.pylori
associated with gastritis
 Potential application include the use of bismuth subnitrate
to prevent cisplatin nephrotoxicity but not have been
applied in practice
 The use of a particle emitting bismuth compounds as
radiotherapeutics agent and as anti-tumor agent .
 ‘Bismuth iodoform paraffin paste’ surgical packing past
for treatment of flatus and odor associated with
ileostomies & colostomies and treatment of ulcer.
 transdermal application of a bismuth-containing skin
cream.
 Antimicrobial Anti-inflammatory antisecretory
action
 The first, a distribution half-life, is
approximately 1 to 4 hours.
 The second, the apparent plasma half life ,
lasts 5 to 11 days.
 The third is the apparent half-life of urinary
excretion lasting between 21 and 72 days
 urinary bismuth detected as late as 5 months
after the last oral dose
NormalconcentrationToxicandlethalconcentration
plasma half life 5-11 d
blood 0.003 -0.5 mg/l
brain 0.6mg/kg
blood 1–100mg/l
brain 3–25mg/kg
Acute:
 Abdominal pain
 Nausea
 Vomating
 Oliguric,anuria , renal insufficiency
secondary to acute tubular necrosis 111
Chronic:
 signs of Encephalopathy
i. Sever confusion may developed over weeks but
develop over 24-48 hr. lead to coma
ii. Myoclouns
iii. poor coordination ,loss of memory ,problem with
language
iv. Less common visual hallucination .*
 renal failure
 Generalized pigmentation of the skin Deposition of
bismuth sulfied into the mucosa cause a Blue-black
discoloration of the gumline (bismuth line )a blackening of
the stool.
 Patient on chronic bismuth therapy with a lipid soluble
group xenobiotic.
 The main target organs for bismuth toxicity are kidney,
brain, and bone
 Bismuth enter the body by ingestion of bismuth –
containing medication .
 99% eliminated and 1 % absorbed
 peak absorption ranges between 15 and 60 minutes
 Once in the circulation, bismuth binds to α2-macroglobulin,
IgM, β-lipoprotein, and haptoglobin. Bismuth rapidly enters
liver, kidney, lungs, and bone.
 Bismuth can cross the placenta and B.B.B.
Absorption
 The gastrointestinal absorption of bismuth
salts depends on their water solubility.
 peak bismuth concentration within 1 hour of
ingestion , with no detectable bismuth in the
blood
 Repeated dose daily increase its
concentration in plasma level.
. Distribution
 in the kidney ,lung, spleen, liver, brain and muscle .
 In the kidney, bismuth is bound to a protein which is
distinct from metallothionein.
 The brain concentration of bismuth higher when
ingestion of lipid soluble compounds
 The tissue distribution of the metal also is affected by its
physical form.
 In rats, co-administration of selenium with bismuth
produced a 50 percent reduction in the kidney bismuth
concentration possibly because synthesis of the
bismuth-binding protein was inhibited by selenium
Excretion
 90% of absorbed bismuth is eliminated
through the urine and feces
 A six week course of colloidal bismuth
subcitrate 480 mg daily, significantly
increased urine bismuth excretion continued
for at least (three month)after cessation of
therapy .
 The elimination half-life is reported to be
about 21 days, depending on bismuth
compounds.
For encephalopathy :
I. History of exposure
II. Blood or urine test( Icp-ms)
III. Abdominal X-ray may detect radiopaque
material .*
IV. Black stool and negative test for blood
V. Salcylate level should be obtained in case
of bismuth subsalicylate exposure .
For acute kidney injury :
I. Hematuria and proteinuria
II. On renal biopsy or postmortem examination
of the kidney identified nuclear inclusion
bodies
1. withdrawal of the bismuth containing compound
2. Gastric lavage
3. Replace fluids and electrolytes*
4. Benzodiazepin may be used for myoclonic activity
5. BAL and ( DMPS) have been used with some success
as chelating agents *.
6. (BAL) in doses of 3 mg/kg may be tried within 8 to 12
hours of a bismuth poisoning. Later administration may
be ineffective due to rapid absorption.
7. The use of EDTA contraindicated .
8. Hemodialysis in patient with renal failure .
 A 76 year-old man died nine days after taking 80
"De-Nol" tablets (9.6 g CBS) The admission blood
bismuth concentration was 1600 µg/L. Within hours
this patient developed MELENA and became
oliguric with rapidly deteriorating renal function
requiring dialysis. He developed an acute abdomen
on day five but was deemed unfit for surgery and
died. A perforated duodenal ulcer was found at
autopsy and the kidneys contained bismuth in
concentrations of 11 mg/g and 16 mg/g
respectively. Bismuth nephropathy had contributed
to renal failure precipitated by acute gastrointestinal
hemorrhage
 Handbook of Forensic Toxicology for Medical by d.kimberley molina Exa
miners/Metals and Metalloids
 gold frank toxicology emergency
 casarett and doulls toxicology the basic scince of poison
 ASPET
Bismuth toxicity

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Bismuth toxicity

  • 1.
  • 3.
  • 4. Atomic number 83 Atomic weight 208.980 Melting point 271 °C Discovered by GERMANY BI O OO OH
  • 5.  Solid  Colour Crystalline, with pink tint .  No Odour  No thermal conductivity  high electrical resistance  Diamagnetic
  • 6.  Free in nature  Earth crust  Seawater  In soil with lead
  • 7.  Found in fire detection device  fire sprinklers.  Ceramic glaze  Hunting shot  Pharmacy products  cosmetics  Paints  A catalyst in rubber production
  • 8.  it was distinct from lead in 1753 .  Elemental bismuth is nontoxic.  bismuth salt have therapeutic uses and responsible the toxicities.  In the early 20th century acute kidney was reported in children administered IM bismuth salt for the treatment of gingivostomatitis Historically bismuth tartrate were used to treat syphilis, while bismuth sodium triglycollamate has been used to treat warts, stomatitis and upper respiratory tract infections. Bismuth got its name from the German word *wissmuth *meaning white mass
  • 9.  Xenobiotic  Inorganic bismuth compound ’’ subnitrate ’ subcarbonat” used for gastrointestinal disorder (diarrhea ,flatulence ,constipation ,cramp ,dyspepsia )  Lipid soluble organic Colloidal bismuth subcitrate ’subgallate ‘subsalicylate (pepto bismol) ranitidin bismuth citrate ‘ used to treat peptic ulcer and H.pylori associated with gastritis  Potential application include the use of bismuth subnitrate to prevent cisplatin nephrotoxicity but not have been applied in practice  The use of a particle emitting bismuth compounds as radiotherapeutics agent and as anti-tumor agent .
  • 10.  ‘Bismuth iodoform paraffin paste’ surgical packing past for treatment of flatus and odor associated with ileostomies & colostomies and treatment of ulcer.  transdermal application of a bismuth-containing skin cream.
  • 11.
  • 12.  Antimicrobial Anti-inflammatory antisecretory action  The first, a distribution half-life, is approximately 1 to 4 hours.  The second, the apparent plasma half life , lasts 5 to 11 days.  The third is the apparent half-life of urinary excretion lasting between 21 and 72 days  urinary bismuth detected as late as 5 months after the last oral dose
  • 13.
  • 14. NormalconcentrationToxicandlethalconcentration plasma half life 5-11 d blood 0.003 -0.5 mg/l brain 0.6mg/kg blood 1–100mg/l brain 3–25mg/kg
  • 15. Acute:  Abdominal pain  Nausea  Vomating  Oliguric,anuria , renal insufficiency secondary to acute tubular necrosis 111
  • 16. Chronic:  signs of Encephalopathy i. Sever confusion may developed over weeks but develop over 24-48 hr. lead to coma ii. Myoclouns iii. poor coordination ,loss of memory ,problem with language iv. Less common visual hallucination .*  renal failure  Generalized pigmentation of the skin Deposition of bismuth sulfied into the mucosa cause a Blue-black discoloration of the gumline (bismuth line )a blackening of the stool.
  • 17.  Patient on chronic bismuth therapy with a lipid soluble group xenobiotic.  The main target organs for bismuth toxicity are kidney, brain, and bone  Bismuth enter the body by ingestion of bismuth – containing medication .  99% eliminated and 1 % absorbed  peak absorption ranges between 15 and 60 minutes  Once in the circulation, bismuth binds to α2-macroglobulin, IgM, β-lipoprotein, and haptoglobin. Bismuth rapidly enters liver, kidney, lungs, and bone.  Bismuth can cross the placenta and B.B.B.
  • 18.
  • 19. Absorption  The gastrointestinal absorption of bismuth salts depends on their water solubility.  peak bismuth concentration within 1 hour of ingestion , with no detectable bismuth in the blood  Repeated dose daily increase its concentration in plasma level.
  • 20. . Distribution  in the kidney ,lung, spleen, liver, brain and muscle .  In the kidney, bismuth is bound to a protein which is distinct from metallothionein.  The brain concentration of bismuth higher when ingestion of lipid soluble compounds  The tissue distribution of the metal also is affected by its physical form.  In rats, co-administration of selenium with bismuth produced a 50 percent reduction in the kidney bismuth concentration possibly because synthesis of the bismuth-binding protein was inhibited by selenium
  • 21. Excretion  90% of absorbed bismuth is eliminated through the urine and feces  A six week course of colloidal bismuth subcitrate 480 mg daily, significantly increased urine bismuth excretion continued for at least (three month)after cessation of therapy .  The elimination half-life is reported to be about 21 days, depending on bismuth compounds.
  • 22.
  • 23. For encephalopathy : I. History of exposure II. Blood or urine test( Icp-ms) III. Abdominal X-ray may detect radiopaque material .* IV. Black stool and negative test for blood V. Salcylate level should be obtained in case of bismuth subsalicylate exposure .
  • 24. For acute kidney injury : I. Hematuria and proteinuria II. On renal biopsy or postmortem examination of the kidney identified nuclear inclusion bodies
  • 25. 1. withdrawal of the bismuth containing compound 2. Gastric lavage 3. Replace fluids and electrolytes* 4. Benzodiazepin may be used for myoclonic activity 5. BAL and ( DMPS) have been used with some success as chelating agents *. 6. (BAL) in doses of 3 mg/kg may be tried within 8 to 12 hours of a bismuth poisoning. Later administration may be ineffective due to rapid absorption. 7. The use of EDTA contraindicated . 8. Hemodialysis in patient with renal failure .
  • 26.  A 76 year-old man died nine days after taking 80 "De-Nol" tablets (9.6 g CBS) The admission blood bismuth concentration was 1600 µg/L. Within hours this patient developed MELENA and became oliguric with rapidly deteriorating renal function requiring dialysis. He developed an acute abdomen on day five but was deemed unfit for surgery and died. A perforated duodenal ulcer was found at autopsy and the kidneys contained bismuth in concentrations of 11 mg/g and 16 mg/g respectively. Bismuth nephropathy had contributed to renal failure precipitated by acute gastrointestinal hemorrhage
  • 27.  Handbook of Forensic Toxicology for Medical by d.kimberley molina Exa miners/Metals and Metalloids  gold frank toxicology emergency  casarett and doulls toxicology the basic scince of poison  ASPET

Editor's Notes

  1. stimulating absorption of fluid and electrolytes across the intestinal wall (antisecretory action) but also, when hydrolyzed to salicylic acid, by inhibiting synthesis of a prostaglandin responsible for intestinal inflammation and hypermotility
  2. from group III water soluble bismuth salts.
  3. Type II lipophilic bismuth salts.
  4. After 8 month
  5. Neurological feature may unlikely to occur in a patient who has no initial gastrointestinal
  6. Icp –ms using thalium (spectrometry )
  7. Monitor renal and liver function