A 17-year old girl presented with abdominal pain, vomiting, black stools, and weakness after ingesting copper sulfate. She was diagnosed with copper sulfate poisoning based on her symptoms and laboratory results showing kidney and liver damage. She received supportive care including dialysis and blood transfusions. After 12 dialysis sessions over one month, her kidney function recovered and she was discharged.

1. DR SAQIB PERVEZ
1ST
YEAR PG TRAINEE
MEDICAL C MTI LRH

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. 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. • 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. • Tender right and left upper quadrant of
abdomen.
• Rest of exam was unremarkable.
ON EXAMINATION

6. • Initial FBC in A & E showed
Hb 3.8
TLC 27000
PLT 421000
Pt was admitted for work-up and management
INVESTIGATIONS

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. • 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. 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. • 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. ABGs
• PH 7.41
• PaO2 75 mmHg
• PaCO2 36 mmHg
• SO2 93%
INVESTIGATIONS

12. INVESTIGATIONS
• ECG sinus tachycardia
• CXR normal
• USG both kidneys increased echogenicity.

13. DIAGNOSIS ?

15. DIAGNOSIS
COPPER SULPHATE POISONING

16. • 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

17. 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

18. 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

19. OGD
• OGD was also done on 17th
day of admission in
consultation with Gastroenterlogist which
reveals gastric erosion.
• Patient managed with I / v PPI

20. • 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

21. 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

22. • 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

23. HOSPITAL COURSE
• On day of discharge call to Psychiatry was
made
• Declared low risk because she was regretting
her previous attempt.
• Counseled

24. • COPPER SULPHATE POISONING

25. • Review of copper sulphate poisoning
• Etiology
• Physiology
• Pathophysiology
• Clinical features
• Diagnosis
• Therapy
OBJECTIVES

26. 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.

27. COPPER SULPHATE

28. • 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

29. 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.

30. 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.

31. 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.

32. PATHOPHYSIOLOGY & CLINICAL
FEATURES
• Common systems affected are GI ,
Hematological , renal & hepatic.
• Rarely affected systems are CVS , Skeletal
muscle , CNS & Endocrine system.

33. 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.

34. GASTROINTESTINAL
• Nausea , vomiting (geenish blue)
• Crampy abdominal pain & burning epigastric
sensation
• Haemorrhagic enterocolitis ( mucosal erosion)
• Hematemesis & malena ( severe cases)

35. 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+.

36. 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)

37. 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.

38. HEPATIC
• Hepatitis
• ALF
• Jaundice (hemolytic or hepatocellular)
• May be associated with tender hepatomegaly

39. 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

40. RENAL
• AKI
• Urinary abnormalities
oliguria
anuria
albuminuria
hemoglobinuria
hematuria

41. CVS
• Hypotension
• Tachycardia
• Hypoxia
• Dysrythmia
• CV collapse

42. CNS
• CNS depression (lethargy to coma)
• Seizure

43. MUSCULAR
• Rhabdomyolysis with high CPK

44. CLINICAL MANIFESTATIONS
• Common clinical manifestations include
Erosive gastropathy
IV hemolysis
Methemoglobinemia
Hepatitis
AKI
Hemoglobinuria

45. CLINICAL MANIFESTATIONS
• Rarely
Arrythmias
Pancreatitis
Rhabdomyolysis
Seizures

46. SIGNS OF POOR PROGNOSIS
• Hypotension
• Cyanosis
• Uremia
• Jaundice
• Immediate cause of death (shock)
• Death in later stages (hepatic & renal failure)

47. DIAGNOSIS
• History & clinical features
• Measurement of serum & whole blood copper
level

48. 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)

49. MANAGEMENT
• Centers on four key principles
• 1) Reducing absorption
• 2) Close observation for complications
• 3) Supportive therapy
• 4) Chelation therapy

50. 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).

51. 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

52. 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

53. SUPPORTIVE TREATMENT AND
CARE OF COMPLICATIONS
• AKI
• Avoid dehydration
• Avoid nephrotoxic drugs
• Intake out-put record
• Serial monitoring of RFTs
• Dialysis

54. 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)

55. CHELATION
• Little clinical experience
• BAL
• D-penicillamine
• EDTA

56. 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

57. 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.

58. 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.

59. 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