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MANAGEMENT OF ACUTE COPPER SULPHATE POISONING

MANAGEMENT OF ACUTE COPPER SULPHATE POISONING. Synonyms of Copper sulphate. Copper (II) sulfate Cupric sulfate Bluestone Blue vitriol Roman vitriol Salzburg vitriol. Uses of Coppersulphate. In agriculture

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MANAGEMENT OF ACUTE COPPER SULPHATE POISONING

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  1. MANAGEMENT OF ACUTE COPPER SULPHATEPOISONING

  2. Synonyms of Copper sulphate • Copper (II) sulfate • Cupric sulfate • Bluestone • Blue vitriol • Roman vitriol • Salzburg vitriol

  3. Uses of Coppersulphate • In agriculture • fungicide, herbicide, algaecide and bactericide, and as a fertilizer additive. • In industry • textile dyeing; preserving hides and wood • tanning leather,electroplating,battery electrolyte; • In veterinary • anthelmintic, emetic and fungicide • Therapeutically • topical antifungal agent • antidote in phosphorus poisoning

  4. Role of Copper in Humans • Adult human content is 100 mg of copper • Co-factor in several metalloproteins, (cytochrome oxidase and superoxide dismutase) • Essential for the utilization of iron and haemoglobin formation

  5. Functions of Cuproenzymes electron transfer reactions in metabolic pathways involving • cellular respiration • iron homeostasis • pigment formation • neurotransmitter production • connective tissue biosyn-thesis • antioxidant defense.

  6. Acute Copper Sulphate poisoning

  7. Epidemiology • Particularly common in India • Cheap and do not have unpleasant smell or taste . • Common in North Chennai • Formed 2.5% of poison cases at GSH(2005) • There is decline in the cuso4 ingestion 1.1%(2006) • Decline in the number of cases is possibly due to easy availability of less painful suicide substances

  8. Absorption and Distribution • 40 to 70 % of ingested copper is absorped • Transported across the intestinal mucosa • Facilitated by enzyme cytosolic metallothionein • Max. blood concentration in 2 hrs as albumin-bound • In the liver it is incorporated into caeruloplasmin • Can penetrate the erythrocyte membrane • Can also absorbed through the skin and lung • Copper can cross the placenta • Highly concentrates in liver, heart, brain, kidneys and muscle

  9. Biliarycannaliculus Trans golgi network Cu apoceruloplasminn Cu Wilson ATPase Cu ceruloplasmin Copper metabolism

  10. Mechanism of Toxicity • Powerful oxidizing capacity and hence Corrosive to mucous membranes • Decreased copper-metallothionein binding and copper clearance from the cell (se free Cu) results in cellular death • Inactivation of enzymes such as G6PD and Glutathione Reductase (GSH) by reduced Cu(I) that binds to SH groups • Production of reactive toxic hydroxyl radicals by copper interacting with oxygen species by catalyzing production hydroxyl ions (e.g. superoxide anions and hydrogen peroxide)

  11. Mechanism of Hemolysis • Direct red cell membrane damage • Indirectly by inactivation of enzymes that protect against oxidative stress (including glutathione reductase)

  12. Gastro Intestinal toxicity • Corrosive to mucous membranes • Ulceration of Gastric and duodenal mucosa • Haematemesis (frequently massive) and melaena • Vomiting, abdominal pain and diarrhoea • Hypersalivation and a metallic taste • Body secretions may be green or blue • Blue staining of the mouth, lips and oesophageal mucosa

  13. Hepatic toxicity • Excessive hepatic Cu produces cellular and obstructive damage. • 25 to 35% develop jaundice • Jaundice may be cholestatic, haemolytic or both • Jaundice, tender hepatomegaly with increased transaminase and alkaline phosphatase activities • Increase in serum caeruloplasmin concentrations until the third day post poisoning • There is decline in the ceruloplasmin level from 7th day

  14. Nephrotoxicity • Acute renal failure is a common complication • Secondary to • Hypovolaemic shock • Intravascular haemolysis.  • Pigmentary nephropathy • Frequently occurs 3 to 4 days post poisoning • Dark-reddish coloured urine and oliguria. • Albuminuria, haematuria and haemoglobinuria

  15. Hemotoxicity • Haemolytic anaemia is another common complication • Direct erythrocyte membrane damage • Indirectly by inhibition of enzymes protecting againstoxidative stress, including G6PD and glutathione reductase • Hyperbilirubinaemia, reticulocytosis, haemo- globinaemia and a fall in haematocrit • Methaemoglobinaemia due to powerful oxidizing capacity

  16. Other toxicities • Pulmonary due to aspiration • Neurological due to hepatic or renal failure • Cardiac due to doubtful myocarditis Peripheral cyanosis,cardiac arrest • Rhabdomyolysis • Hyponatremia and hyperkalemia

  17. ACUTE COPPER SULPHATE POISON MANAGENENT

  18. Traditional Management • Gastric Lavage • Forced alkaline diuresis • D-Pencillamine (250mg PO qid upto – 2gms/ day) for 0-7 days • Inj. Vitamin C 500mgs 8th hrly • H2 Antagonist / PPI • Supportive measures for complications

  19. DISADVANTAGES OF TRADITIONAL MANAGEMENT

  20. Stomach in copper sulphate poisoning • Copper sulphate is a corrosive poisoning • Produces extensive ulceration and bleeding • Raw areas may hasten the absorption of cuso4

  21. Sloughing of the mucosa

  22. Minimizing of corrosive injury of gastric mucosa • Avoidance of gastric lavage as in any corrosive poisons • Egg albumin to coat the mucosa and prevent injury

  23. GASTROPROTECTIVE MEASURES • Stomach wash is to be avoided • Egg albumin to be used as demulcent • H2 blockers or PPIs to hasten the healing of corrosive injury

  24. Role of egg albumin in gastric protection • Coats the mucosa and protects further injury by the cuso4 • Copper combine with albumin to form insoluble cupric albuminate • This reduces the corrosive effect of cuso4

  25. Egg albumin Cuso4 absorption • Cupric albuminate is insoluble ( used for preserving paintings and photography) • Copper requires enzyme cytosolic methionine for its absorption • The enzyme may not act over insoluble Cupric albuminate poor absorption • Possibly by this mechanism systemic manifestations can be prevented

  26. Criteria for urinary alkalinization and forced diuresis • Should be predominantly eliminated unchanged by the kidney • Distributed primarily in the extracellular fluid compartment • Minimally protein-bound • Weak acids with pH ranging from 3.0 to 7.5

  27. Forced alkaline diuresis • Copper sulphate does not fulfill the criteria • Cycles to be properly monitored • Close monitoring of the urine output is required • Fluid overload may occur • Studies indicate that there no advantage

  28. Fluids in cuso4 • Forced alkaline diuresis may be avoided • Adequate replacement of fluids • Close monitoring of the electrolytes • Management of deficit • Blood transfusion if there is hematemesis

  29. Chelating agents • DMPS (Dimercaptopropanesulfonate) is an ideal chelating agent proved in cuso4 poison • D-pencillamine is frequently used since it is useful in Wilson's disease • There is no controlled study to prove the role D-pencillamine in acute cuso4 poisoning • It should not be used in the presence of renal failure

  30. D-pencillamine • DMPS is not available in our country • No absolute contraindication is there except acute renal failure • Considering the above the drug can be continued

  31. Modified management of acute cuso4 poison • Gastric Lavage is to be absolutely avoided • Egg Albumin to be used as demulcent in place of GL • H2 Antagonists/PPI • Adequate IV Fluids • D-Pencillamine • Other supportive measures for complications

  32. ACUTE COPPER SULPHATE POISONINGComparative Study of the methods of treatment conducted atGOVERNMENT STANLEY MEDICAL COLLEGE2004 TO 2006

  33. AIM To compare the mortality and morbidity of the traditional management protocol with modified protocol in acute copper sulphate poison

  34. Protocol-ITraditional Management • Gastric Lavage • Forced alkaline diuresis • D-Pencillamine (250mg PO qid upto – 2gms/ day) for 0-7 days • Inj. Vitamin C 500mgs 8th hrly • H2 Antagonist / PPI

  35. PROTOCOL – IIModified management • Gastric Lavage was Avoided • Egg Albumin was used as demulcent • Adequate IV Fluids • H2 Antagonists/PPI • D-Pencillamine • Management of complications

  36. PATIENTS & METHODS • Total 169 Patients of Acute Copper Sulphate Poisoning • Treated with Protocol – I - 84 Patients • Treated with Protocol – II - 85 Patients • Type of Study - Prospective Study • Period of Study – 30 months (2½ years)

  37. PATIENTS AND METHODS • Detailed history • Quantity and time of ingestion of CuSo4 • History of vomiting (spontaneous or induced) • H/O coexisting disease was also elicitated • UGI endoscopy (within 6 to 12hours) • CBC/urine deposit/hemoglobinuria/blood biochemistry/ met hemoglobin//CPK if needed

  38. OBSERVATIONS

  39. Demographic data 84 85

  40. AGE DISTRIBUTION

  41. AGE DISTRIBUTION

  42. Endoscopic Grading comparison

  43. Endoscopic gradings 6 Protocol I Protocol II

  44. Treatment outcome of the two protocols

  45. Treatment outcome

  46. Mortality comparison

  47. AN ALTERNATE METHOD OF MANAGEMENT

  48. Recommendations • stomach wash to be deferred • 6 – 8 raw egg white to be given orally • H2 blockers / PPIs to heal the corrosive injuries. • Adequate fluid replacement • D-Penicillamine if there is no contraindication • Appropriate Management of complications

  49. ADVANTAGES OF THE MODIFIED TREATMENT • Management can start at the community level at the patient’s house (egg white) • Can be carried out by health worker (does not require instruments and equipments) • Can be managed at the primary care physicians (needs only adequate IV Fluids and observation) • Patients with complications only may require secondary or tertiary care

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