copper sulphate poisoning
TRANSCRIPT
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DR SAQIB PERVEZ1ST YEAR PG TRAINEEMEDICAL C MTI LRH
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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.
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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.
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• 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
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• Tender right and left upper quadrant of abdomen.
• Rest of exam was unremarkable.
ON EXAMINATION
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• Initial FBC in A & E showed Hb 3.8 TLC 27000 PLT 421000 Pt was admitted for work-up and management
INVESTIGATIONS
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• 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
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• 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
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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
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• 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
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ABGs • PH 7.41 • PaO2 75 mmHg • PaCO2 36 mmHg • SO2 93%
INVESTIGATIONS
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INVESTIGATIONS
• ECG sinus tachycardia
• CXR normal
• USG both kidneys increased echogenicity.
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DIAGNOSIS ?
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DIAGNOSIS
COPPER SULPHATE POISONING
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• 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
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Urea Creatinine Date466 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 COURSERFTs
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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
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OGD
• OGD was also done on 17th day of admission in consultation with Gastroenterlogist which reveals gastric erosion.
• Patient managed with I / v PPI
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• 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
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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
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• 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
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HOSPITAL COURSE
• On day of discharge call to Psychiatry was made
• Declared low risk because she was regretting her previous attempt.
• Counseled
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• COPPER SULPHATE POISONING
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• Review of copper sulphate poisoning• Etiology• Physiology• Pathophysiology• Clinical features• Diagnosis• Therapy
OBJECTIVES
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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.
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COPPER SULPHATE
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• 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
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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.
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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.
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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.
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PATHOPHYSIOLOGY & CLINICAL FEATURES
• Common systems affected are GI , Hematological , renal & hepatic.
• Rarely affected systems are CVS , Skeletal muscle , CNS & Endocrine system.
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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.
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GASTROINTESTINAL
• Nausea , vomiting (geenish blue)• Crampy abdominal pain & burning epigastric
sensation• Haemorrhagic enterocolitis ( mucosal erosion)• Hematemesis & malena ( severe cases)
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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+.
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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)
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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.
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HEPATIC
• Hepatitis • ALF• Jaundice (hemolytic or hepatocellular)• May be associated with tender hepatomegaly
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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
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RENAL
• AKI• Urinary abnormalities oliguria anuria albuminuria hemoglobinuria hematuria
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CVS
• Hypotension• Tachycardia• Hypoxia • Dysrythmia• CV collapse
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CNS
• CNS depression (lethargy to coma)• Seizure
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MUSCULAR
• Rhabdomyolysis with high CPK
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CLINICAL MANIFESTATIONS
• Common clinical manifestations include Erosive gastropathy IV hemolysis Methemoglobinemia Hepatitis AKI Hemoglobinuria
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CLINICAL MANIFESTATIONS
• Rarely Arrythmias Pancreatitis Rhabdomyolysis Seizures
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SIGNS OF POOR PROGNOSIS
• Hypotension• Cyanosis• Uremia• Jaundice
• Immediate cause of death (shock)• Death in later stages (hepatic & renal failure)
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DIAGNOSIS
• History & clinical features• Measurement of serum & whole blood copper
level
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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)
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MANAGEMENT
• Centers on four key principles• 1) Reducing absorption• 2) Close observation for complications• 3) Supportive therapy• 4) Chelation therapy
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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).
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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
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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
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SUPPORTIVE TREATMENT AND CARE OF COMPLICATIONS
• AKI• Avoid dehydration• Avoid nephrotoxic drugs• Intake out-put record • Serial monitoring of RFTs• Dialysis
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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)
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CHELATION
• Little clinical experience• BAL• D-penicillamine• EDTA
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CHELATION
Chelating agent Dose Adverse reactionsD-penicillamine 1000 to 1500 mg/day bd to
qid orallyProteinuria, hematuria, renal failure, hepatotoxicity, BM suppression
BAL 3 to 5 mg/kg/dose deep IMEvery 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
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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.
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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.
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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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