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DR SAQIB PERVEZ
1ST
YEAR PG TRAINEE
MEDICAL C MTI LRH
CASE HISTORY
17 year old unmarried girl presented to A & E
with 3 days history of
pain abdomen
vomiting (blackish)
black s...
CASE HISTORY
• Seen 5 days back in peripheral hospital with hx
of some poisonous substance ingestion.
• Gastric lavage don...
• On exam. pt was conscious , communicative
• BP 100/60 Pulse 90/min Temp 98.6F
• RR 18 O2 sat. 88%
• On GPE
• Severe pall...
• Tender right and left upper quadrant of
abdomen.
• Rest of exam was unremarkable.
ON EXAMINATION
• Initial FBC in A & E showed
Hb 3.8
TLC 27000
PLT 421000
Pt was admitted for work-up and management
INVESTIGATIONS
• After admission basic investigation were sent.
• Blood grouping & cross match done and packed
RBCs were arranged.
• Pati...
• Subsequent investigations in the ward showed
• Special smear
• Hb 4.4 gm/dl
• MCV 85
• HCT 15%
• Retic count 3.8%
TLC 22...
Investigations Results
Urea 466
Creatinine 15.13
Na 125
K 4.66
ALT 81
ALP 62
Bil 2.7
RBS 117
Amylase 473
LDH 452
INVESTIGA...
• PT 17 sec control 13 sec
• APTT 35 sec control 27 sec
• INR 1.3
• Urine R/E = albumin 2+
• RBCs 3-4 /hpf
INVESTIGATIONS
ABGs
• PH 7.41
• PaO2 75 mmHg
• PaCO2 36 mmHg
• SO2 93%
INVESTIGATIONS
INVESTIGATIONS
• ECG sinus tachycardia
• CXR normal
• USG both kidneys increased echogenicity.
DIAGNOSIS ?
DIAGNOSIS
COPPER SULPHATE POISONING
• Call to nephrology for urgent H/D was made.
• Left femoral D/L passed and one session of H/D
done.
• Her post dialysis u...
Urea Creatinine Date
466 15.13 24/04/16
1 308 11.18 25/04
2 290 9.4 26/04
3 230 8.07 27/04
4 136 7.56 28/04
5 111 7.12 29/...
After her last dialysis her serum creatinine and
blood urea gradually decreased over the next
few days without HD as the k...
OGD
• OGD was also done on 17th
day of admission in
consultation with Gastroenterlogist which
reveals gastric erosion.
• P...
• After passing left subclavian double lumen
catheter for dialysis on 19th
day of admission she
develop SOB and chest pain...
HOSPITAL
COURSE/COMPLICATIONS
• As the effusion was persistant despite intubation
& U/S chest showed left sided loculated
...
• At discharge her urea 37, creatinine 1.30,
11 days after her last H/D session.
• She received total of 10 units of packe...
HOSPITAL COURSE
• On day of discharge call to Psychiatry was
made
• Declared low risk because she was regretting
her previ...
• COPPER SULPHATE POISONING
• Review of copper sulphate poisoning
• Etiology
• Physiology
• Pathophysiology
• Clinical features
• Diagnosis
• Therapy
...
INTRODUCTION
• Copper sulphate commonly known as “blue
vitriol” or “blue stone” or “Neela Thotha”.
• Exists as bright blue...
COPPER SULPHATE
• Ingestion of > 1gm of copper sulphate results in
manifestations of symptoms of toxicity.
• Lethal dose of ingested coppe...
PHYSIOLOGY OF COPPER
• Copper is an essential trace element in
humans.
• Human body contain 50 – 120 mg of copper.
• Daily...
PHYSIOLOGY OF COPPER
• Copper transport 90 % is carried by
ceruloplasmin small amount by albumin
• Also transported by ami...
MECHANISM OF TOXICITY
• Copper sulphate is a powerful oxidizing agent.
• Corrosive to mucous membranes.
• Free reduced cop...
PATHOPHYSIOLOGY & CLINICAL
FEATURES
• Common systems affected are GI ,
Hematological , renal & hepatic.
• Rarely affected ...
GASTROINTESTINAL
• Being a corrosive acid results in caustic burns of
the esophagus , superficial & deep ulcers in the
sto...
GASTROINTESTINAL
• Nausea , vomiting (geenish blue)
• Crampy abdominal pain & burning epigastric
sensation
• Haemorrhagic ...
HEMATOLOGICAL
• Intravascular Hemolysis is caused by
Inhibition of G6PD and oxidative damage to
RBCs
Inhibition of Na / K ...
HEMATOLOGICAL
• Intravascular hemolysis can be rapid & severe
with drastic drops in Hb.
• Methemoglobinemia leads to cyano...
HEPATIC
• Liver gets damaged early in copper poisoning
as the majority of absorbed copper is deposited
in liver after bein...
HEPATIC
• Hepatitis
• ALF
• Jaundice (hemolytic or hepatocellular)
• May be associated with tender hepatomegaly
RENAL
• AKI much more common.
• Mechanisms include
1.hemoglobinuria
2.rhabdomyolysis
3.direct copper toxicity on proximal ...
RENAL
• AKI
• Urinary abnormalities
oliguria
anuria
albuminuria
hemoglobinuria
hematuria
CVS
• Hypotension
• Tachycardia
• Hypoxia
• Dysrythmia
• CV collapse
CNS
• CNS depression (lethargy to coma)
• Seizure
MUSCULAR
• Rhabdomyolysis with high CPK
CLINICAL MANIFESTATIONS
• Common clinical manifestations include
Erosive gastropathy
IV hemolysis
Methemoglobinemia
Hepati...
CLINICAL MANIFESTATIONS
• Rarely
Arrythmias
Pancreatitis
Rhabdomyolysis
Seizures
SIGNS OF POOR PROGNOSIS
• Hypotension
• Cyanosis
• Uremia
• Jaundice
• Immediate cause of death (shock)
• Death in later s...
DIAGNOSIS
• History & clinical features
• Measurement of serum & whole blood copper
level
INVESTIGATIONS
• Baseline & serial monitoring of
• FBC
• LFTs , RFTs , S/E
• Coagulation profile
• Methemoglobin level (in...
MANAGEMENT
• Centers on four key principles
• 1) Reducing absorption
• 2) Close observation for complications
• 3) Support...
REDUCING ABSORPTION
• In the pre-hospital set up , immediate dilution
with water or milk.
• Activated charcoal
• Gastric l...
SUPPORTIVE TREATMENT AND
CARE OF COMPLICATIONS
• Corrosive upper GI burns
upper GI endoscopy (ideally within 12 – 24 hr
to...
SUPPORTIVE TREATMENT AND
CARE OF COMPLICATIONS
• Methemoglobinemia
Methylene blue (1 – 2 mg/kg/dose IV)
(Dose may be repea...
SUPPORTIVE TREATMENT AND
CARE OF COMPLICATIONS
• AKI
• Avoid dehydration
• Avoid nephrotoxic drugs
• Intake out-put record...
SUPPORTIVE TREATMENT AND
CARE OF COMPLICATIONS
• IV hemolysis
• If the pt is anemic and symptomatic packed
RBCs
• Hypotens...
CHELATION
• Little clinical experience
• BAL
• D-penicillamine
• EDTA
CHELATION
Chelating agent Dose Adverse reactions
D-penicillamine 1000 to 1500 mg/day bd to
qid orally
Proteinuria, hematur...
CONCLUSIONS
• Copper sulphate poisoning though rare , can be
life threatening.
• Mortality is variable (14 – 19%).
• Mains...
REFRENCES
• 1) www.researchgate.net/publication/5368476
• 2) Gamakaranage et al. Journal of Occupational
Medicine and Toxi...
REFRENCES
• 5) Meena MC, Bansal MK. Acute Copper Sulfate
Poisoning: Case Report and Review of Literature. Asia
Pac J Med T...
Copper sulphate poisoning
Copper sulphate poisoning
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Copper sulphate poisoning

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Copper sulphate poisoning

  1. 1. DR SAQIB PERVEZ 1ST YEAR PG TRAINEE MEDICAL C MTI LRH
  2. 2. CASE HISTORY 17 year old unmarried girl presented to A & E with 3 days history of pain abdomen vomiting (blackish) black stools oliguria with dark color urine & generalised weakness and fatigue.
  3. 3. CASE HISTORY • Seen 5 days back in peripheral hospital with hx of some poisonous substance ingestion. • Gastric lavage done and iv fluids were given there. • Was observed for few hours and then sent home as patient was vitally stable at that time.
  4. 4. • On exam. pt was conscious , communicative • BP 100/60 Pulse 90/min Temp 98.6F • RR 18 O2 sat. 88% • On GPE • Severe pallor , jaundice, pedal edema , bluish- brown discoloration of lips ON EXAMINATION
  5. 5. • Tender right and left upper quadrant of abdomen. • Rest of exam was unremarkable. ON EXAMINATION
  6. 6. • Initial FBC in A & E showed Hb 3.8 TLC 27000 PLT 421000 Pt was admitted for work-up and management INVESTIGATIONS
  7. 7. • After admission basic investigation were sent. • Blood grouping & cross match done and packed RBCs were arranged. • Patient was started on • O2 inhalation • IV fluids • IV PPI • IV anti-emetic's HOSPITAL COURSE
  8. 8. • Subsequent investigations in the ward showed • Special smear • Hb 4.4 gm/dl • MCV 85 • HCT 15% • Retic count 3.8% TLC 22000 PLT 365000 INVESTIGATIONS
  9. 9. Investigations Results Urea 466 Creatinine 15.13 Na 125 K 4.66 ALT 81 ALP 62 Bil 2.7 RBS 117 Amylase 473 LDH 452 INVESTIGATIONS
  10. 10. • PT 17 sec control 13 sec • APTT 35 sec control 27 sec • INR 1.3 • Urine R/E = albumin 2+ • RBCs 3-4 /hpf INVESTIGATIONS
  11. 11. ABGs • PH 7.41 • PaO2 75 mmHg • PaCO2 36 mmHg • SO2 93% INVESTIGATIONS
  12. 12. INVESTIGATIONS • ECG sinus tachycardia • CXR normal • USG both kidneys increased echogenicity.
  13. 13. DIAGNOSIS ?
  14. 14. DIAGNOSIS COPPER SULPHATE POISONING
  15. 15. • Call to nephrology for urgent H/D was made. • Left femoral D/L passed and one session of H/D done. • Her post dialysis urea 308 creatinine 11.18 • She had 12 H/D session during her 1 month stay in ward. • After her last H/D urea 46 creatinine 5.74 HOSPITAL COURSE
  16. 16. Urea Creatinine Date 466 15.13 24/04/16 1 308 11.18 25/04 2 290 9.4 26/04 3 230 8.07 27/04 4 136 7.56 28/04 5 111 7.12 29/04 6 108 8.01 30/04 7 100 7.5 01/05 8 52 7 04/05 9 86 7.2 05/05 10 73 6.96 07/05 11 58 6.2 10/05 12 46 5.74 12/05 HOSPITAL COURSE RFTs
  17. 17. After her last dialysis her serum creatinine and blood urea gradually decreased over the next few days without HD as the kidneys were recovering its function. HOSPITAL COURSE
  18. 18. OGD • OGD was also done on 17th day of admission in consultation with Gastroenterlogist which reveals gastric erosion. • Patient managed with I / v PPI
  19. 19. • After passing left subclavian double lumen catheter for dialysis on 19th day of admission she develop SOB and chest pain • CXR = Left sided large pleural effusion. • Diagnostic tap = hemorrhagic effusion • Left sided intubation was done by pulmonologist HOSPITAL COURSE/COMPLICATIONS
  20. 20. HOSPITAL COURSE/COMPLICATIONS • As the effusion was persistant despite intubation & U/S chest showed left sided loculated Pl.Effusion with multiple septations • Two doses of Streptokinase were given • Repeat U/S after two days showed left sided minimal PE about 90 ml. • Chest tube was then removed
  21. 21. • At discharge her urea 37, creatinine 1.30, 11 days after her last H/D session. • She received total of 10 units of packed RBCs. • At discharge her Hb was 10.8 gm/dl HOSPITAL COURSE
  22. 22. HOSPITAL COURSE • On day of discharge call to Psychiatry was made • Declared low risk because she was regretting her previous attempt. • Counseled
  23. 23. • COPPER SULPHATE POISONING
  24. 24. • Review of copper sulphate poisoning • Etiology • Physiology • Pathophysiology • Clinical features • Diagnosis • Therapy OBJECTIVES
  25. 25. INTRODUCTION • Copper sulphate commonly known as “blue vitriol” or “blue stone” or “Neela Thotha”. • Exists as bright blue crystals (CuSO4.5H2O). • Commonly used as pesticide & fungiside. • Also used in adhesive glue making , photography & dye industry. • Medically , was used as an emetic & antidote for phosphorous poisoning.
  26. 26. COPPER SULPHATE
  27. 27. • Ingestion of > 1gm of copper sulphate results in manifestations of symptoms of toxicity. • Lethal dose of ingested copper sulphate is • 10 – 20 gm. • Suicidal ingestion • Accidental • Chronic HUMAN POISONING
  28. 28. PHYSIOLOGY OF COPPER • Copper is an essential trace element in humans. • Human body contain 50 – 120 mg of copper. • Daily recommended intake is about 2mg/day. • Most of copper is absorbed from stomach & duodenum. • Enterohepatic cycle and excreted mainly through bile. • <3% in urine.
  29. 29. PHYSIOLOGY OF COPPER • Copper transport 90 % is carried by ceruloplasmin small amount by albumin • Also transported by amino acids , vitamin. • In acute poisoning albumin rather than the ceruloplasmin binds the excess copper.
  30. 30. MECHANISM OF TOXICITY • Copper sulphate is a powerful oxidizing agent. • Corrosive to mucous membranes. • Free reduced copper in the cell binds to sulfhydryl groups & inactivates enzymes such as G6PD & glutathione reductase. • Also alters cellular membranes by lipid peroxidation & cellular proteins by denaturation.
  31. 31. PATHOPHYSIOLOGY & CLINICAL FEATURES • Common systems affected are GI , Hematological , renal & hepatic. • Rarely affected systems are CVS , Skeletal muscle , CNS & Endocrine system.
  32. 32. GASTROINTESTINAL • Being a corrosive acid results in caustic burns of the esophagus , superficial & deep ulcers in the stomach & small intestine. • Changes of acute gastritis , hemorrhages & necrosis in the intestinal mucosa & perforation have been reported.
  33. 33. GASTROINTESTINAL • Nausea , vomiting (geenish blue) • Crampy abdominal pain & burning epigastric sensation • Haemorrhagic enterocolitis ( mucosal erosion) • Hematemesis & malena ( severe cases)
  34. 34. HEMATOLOGICAL • Intravascular Hemolysis is caused by Inhibition of G6PD and oxidative damage to RBCs Inhibition of Na / K ATPase pump leading to Increases cell permeability  Methemoglobinemia is caused by oxidation of Fe 2+ to Fe 3+.
  35. 35. HEMATOLOGICAL • Intravascular hemolysis can be rapid & severe with drastic drops in Hb. • Methemoglobinemia leads to cyanosis & loss of oxygen carrying capacity. • Coagulopathy (liver injury or direct effect of free copper)
  36. 36. HEPATIC • Liver gets damaged early in copper poisoning as the majority of absorbed copper is deposited in liver after being delivered from the portal circulation. • ALF following tissue necrosis can occur due to direct copper toxicity.
  37. 37. HEPATIC • Hepatitis • ALF • Jaundice (hemolytic or hepatocellular) • May be associated with tender hepatomegaly
  38. 38. RENAL • AKI much more common. • Mechanisms include 1.hemoglobinuria 2.rhabdomyolysis 3.direct copper toxicity on proximal tubules 4.pre renal failure due to dehydration 5.secondary effects of MOD
  39. 39. RENAL • AKI • Urinary abnormalities oliguria anuria albuminuria hemoglobinuria hematuria
  40. 40. CVS • Hypotension • Tachycardia • Hypoxia • Dysrythmia • CV collapse
  41. 41. CNS • CNS depression (lethargy to coma) • Seizure
  42. 42. MUSCULAR • Rhabdomyolysis with high CPK
  43. 43. CLINICAL MANIFESTATIONS • Common clinical manifestations include Erosive gastropathy IV hemolysis Methemoglobinemia Hepatitis AKI Hemoglobinuria
  44. 44. CLINICAL MANIFESTATIONS • Rarely Arrythmias Pancreatitis Rhabdomyolysis Seizures
  45. 45. SIGNS OF POOR PROGNOSIS • Hypotension • Cyanosis • Uremia • Jaundice • Immediate cause of death (shock) • Death in later stages (hepatic & renal failure)
  46. 46. DIAGNOSIS • History & clinical features • Measurement of serum & whole blood copper level
  47. 47. INVESTIGATIONS • Baseline & serial monitoring of • FBC • LFTs , RFTs , S/E • Coagulation profile • Methemoglobin level (in cyanotic patients) • Urine R/E • Abdominal Xray (to rule out perforation) • Serum Cu level (if history is not clear)
  48. 48. MANAGEMENT • Centers on four key principles • 1) Reducing absorption • 2) Close observation for complications • 3) Supportive therapy • 4) Chelation therapy
  49. 49. REDUCING ABSORPTION • In the pre-hospital set up , immediate dilution with water or milk. • Activated charcoal • Gastric lavage ?? • (Risk of perforation? Cautious placement of narrow NG tube).
  50. 50. SUPPORTIVE TREATMENT AND CARE OF COMPLICATIONS • Corrosive upper GI burns upper GI endoscopy (ideally within 12 – 24 hr to gauge the severity.Period of wound softening 2nd or 3rd day post injury & last for roughly two weeks). PPI Sucralfate
  51. 51. SUPPORTIVE TREATMENT AND CARE OF COMPLICATIONS • Methemoglobinemia Methylene blue (1 – 2 mg/kg/dose IV) (Dose may be repeated if cyanosis does not disappear within one hour). Alternatives Hyperbaric oxygen Ascorbic acid (100 – 500 mg bd orally or IV) Exchange transfusion or packed RBCc
  52. 52. SUPPORTIVE TREATMENT AND CARE OF COMPLICATIONS • AKI • Avoid dehydration • Avoid nephrotoxic drugs • Intake out-put record • Serial monitoring of RFTs • Dialysis
  53. 53. SUPPORTIVE TREATMENT AND CARE OF COMPLICATIONS • IV hemolysis • If the pt is anemic and symptomatic packed RBCs • Hypotensive episodes (Fluids , dopamine & nor- adrenaline) • Rhabdomyolysis (judicious fluid replacement , mannitol & urine alkalinization)
  54. 54. CHELATION • Little clinical experience • BAL • D-penicillamine • EDTA
  55. 55. CHELATION Chelating agent Dose Adverse reactions D-penicillamine 1000 to 1500 mg/day bd to qid orally Proteinuria, hematuria, renal failure, hepatotoxicity, BM suppression BAL 3 to 5 mg/kg/dose deep IM Every 4 hr for 4 days then every 12 hr for 7 days Urticaria , persistent hyper pyrexia EDTA 75 mg/kg/day deep IM or slow IV infusion in 3 to 6 divided doses for 5 days Renal tubular necrosis
  56. 56. CONCLUSIONS • Copper sulphate poisoning though rare , can be life threatening. • Mortality is variable (14 – 19%). • Mainstay of treatment is supportive , including careful fluid therapy & methylene blue in symptomatic methemoglobinemia. • Commonly used copper chelators are D- penicillamine , BAL or EDTA.
  57. 57. REFRENCES • 1) www.researchgate.net/publication/5368476 • 2) Gamakaranage et al. Journal of Occupational Medicine and Toxicology 2011, 6:34 http://www.occup-med.com/content/6/1/34 • 3) Indian J Crit Care Med Apr-Jun 2007 Vol 11 Issue 2 • 4) International Journal of Current Medical And Applied Sciences, vol.5. Issue 3, February: 2015. PP: 178-180.
  58. 58. REFRENCES • 5) Meena MC, Bansal MK. Acute Copper Sulfate Poisoning: Case Report and Review of Literature. Asia Pac J Med Toxicol 2014;3:130-3. • 6) Sinkovi~ A, et al. ACUTE COPPER SULPHATE POISONING Arh Hig Rada Toksikol 2008;59:31-35

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