DR SAQIB PERVEZ1ST YEAR PG TRAINEEMEDICAL C MTI LRH

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.

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.

• 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

• 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.• Patient was started on • O2 inhalation• IV fluids • IV PPI• IV anti-emetic's

HOSPITAL COURSE

• 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

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

• 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 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

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

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

OGD

• OGD was also done on 17th day of admission in consultation with Gastroenterlogist which reveals gastric erosion.

• Patient managed with I / v PPI

• 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

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

• 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

HOSPITAL COURSE

• On day of discharge call to Psychiatry was made

• Declared low risk because she was regretting her previous attempt.

• Counseled

• COPPER SULPHATE POISONING

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

OBJECTIVES

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.

COPPER SULPHATE

• 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

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.

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.

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.

PATHOPHYSIOLOGY & CLINICAL FEATURES

• Common systems affected are GI , Hematological , renal & hepatic.

• Rarely affected systems are CVS , Skeletal muscle , CNS & Endocrine system.

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.

GASTROINTESTINAL

• Nausea , vomiting (geenish blue)• Crampy abdominal pain & burning epigastric

sensation• Haemorrhagic enterocolitis ( mucosal erosion)• Hematemesis & malena ( severe cases)

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+.

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)

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.

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 tubules 4.pre renal failure due to dehydration 5.secondary effects of MOD

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 Hepatitis AKI Hemoglobinuria

CLINICAL MANIFESTATIONS

• Rarely Arrythmias Pancreatitis Rhabdomyolysis Seizures

SIGNS OF POOR PROGNOSIS

• Hypotension• Cyanosis• Uremia• Jaundice

• Immediate cause of death (shock)• Death in later stages (hepatic & renal failure)

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 cyanotic patients)• Urine R/E• Abdominal Xray (to rule out perforation)• Serum Cu level (if history is not clear)

MANAGEMENT

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

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).

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

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

SUPPORTIVE TREATMENT AND CARE OF COMPLICATIONS

• AKI• Avoid dehydration• Avoid nephrotoxic drugs• Intake out-put record • Serial monitoring of RFTs• Dialysis

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)

CHELATION

• Little clinical experience• BAL• D-penicillamine• EDTA

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

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.

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.

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