The Role of Plasmapheresis in Treating Lethal Cupric Sulfate Poisoning.

The mortality rate of cupric sulfate is relatively high in contrast to that of other heavy metals. Cases of orally ingested cupric sulfate poisoning are very rare, with a reported half lethal dose of 10 g. Cupric sulfate poisoning leads to gastrointestinal corrosion, intravascular hemolysis, hemolytic anemia, methemoglobinemia and acute renal and hepatic impairment. Without proper and prompt treatment, multiple organ failure and death occur. Here, we present the first report that removal of the excessive intravascular copper ions by plasmapheresis was accompanied by complete recovery.

Ingestion of bedding material as a cause of acute copper sulfate poisoning in turkey poults.

The article reports a case of acute copper sulfate (CuSO4) poisoning in 2-day-old turkeys. The first incidences were noticed 2 h after placing the animals in the poultry house, where turkeys were provided with wood shaving bedding. Post-mortem examination showed wood shavings present in gastric and intestinal contents and numerous lesions in the alimentary tract: dark green color of the koilin lining, and surface erosions, deep ulceration, and severe congestion of the gizzard. The copper (Cu) concentration in samples of the liver, kidney, heart, gizzard content, gizzard muscle, gizzard lining, and wood shavings from the bedding was determined. Our results showed that the level of Cu in the livers of affected birds was more than sevenfold higher than the recommended value and the Cu content in bedding material was above the value considered to be toxic to turkeys. Our investigation identified the bedding disinfected using a CuSO4 solution as a possible cause of turkey fatalities.

Successful extracorporeal life support in respiratory failure after copper sulphate ingestion.

A 44-year-old woman intentionally ingested a solution of copper sulphate. She had minimal intravascular haemolysis and methemoglobinaemia but developed acute respiratory distress syndrome (ARDS) 4 hours after acute copper sulphate poisoning. This required extracorporeal membrane oxygenation (ECMO) management in the intensive care unit. Subsequently, she improved clinically and was successfully weaned from ECMO. Acute copper sulphate poisoning can cause severe pulmonary toxicity even in the absence of other serious symptoms. Therefore, a physician treating acute copper sulphate poisoning should look out for respiratory symptoms even in the absence of other common symptoms. We suggest early initiation of venovenous ECMO in those with ARDS following copper sulphate poisoning.

Greenish-blue gastric content: Literature review and case report on acute copper sulphate poisoning.

A literature review of cases of acute poisoning by copper sulfate was conducted, emphasizing therapeutic interventions, and a new fatality case is reported. Specifically, the relevant literature was reviewed for incidence rates, sociodemographic variables, pathophysiology, diagnosis, prognosis, and therapeutic outcome of copper sulfate poisoning. Results conclude that copper sulfate poisoning incidence varies in different regions. It is rare in western countries, while it is very common in South Asian countries. The majority of patients belong to rural populations and are males in the third decade of their lives. The lethal dose of ingested copper is considered to be 10-20 g; 14-36% of the patients pass away within a few hours of ingestion, while the average hospitalization time is more than 20 days. The clinical features of copper sulfate poisoning include erosive gastropathy, intravascular hemolysis, methemoglobinemia, hepatitis, and acute kidney injury. The therapeutic management focuses on absorption reduction, close observation for complications, supportive therapy, and chelation therapy.

Bluish vomiting: a rare clinical presentation of poisoning.

Bluish vomiting is a symptom of poisoning that is rarely seen in Western emergency departments. Consequently, physicians are not aware of the diagnosis, complications, and treatment of this unusual form of intoxication. In this article, we report a case of bluish vomiting that occurred after an accidental ingestion of copper sulphate. In the discussion, we review three life-threatening causes of bluish vomiting (copper sulphate, boric acid, and paraquat ingestion), and we discuss their respective clinical manifestations, specificities, complications, and management therapies.

Blue vitriol poisoning: a 10-year experience in a tertiary care hospital.

BACKGROUND AND AIM: Copper sulphate poisoning, while unusual in the West, is not rare in the Indian subcontinent, and mostly suicidal in intent. Unfortunately, data available on copper sulphate poisoning is limited. This study was planned to identify common presentations and complications of copper sulphate poisoning, and biochemical parameters that predict outcomes in these patients. MATERIALS AND METHODS: A retrospective analysis of 35 patients presenting with copper sulphate poisoning over a period of 10 years (2001-2010) was performed, based on review of their medical records. Paediatric cases and patients with concomitant poisoning with other substances were excluded. Clinical presentation, laboratory parameters, complications and treatment modalities were studied. RESULTS: Of the 35 cases, 23 were females (65.71%). Mean age was 29.18 ± 10.77 years. Vomiting was the commonest symptom (85.71%) followed by diarrhoea (45.71%), epigastric pain (42.86%) and rectal passage of blood (31.43%). Fourteen (40%) patients had pre-existing psychiatric disease. Medical signs included pallor (37.14%) and icterus (37.14%). Major complications included hemolysis (68.57%), renal failure (51.43%), acute hepatitis (45.71%) and upper gastrointestinal bleed (40%). Mean serum copper at presentation was 104.53 ± 56.67 µg/dL; mean methemoglobin level was 9.59 ± 8.28%. Twenty-seven patients survived yielding a mortality rate of 22.9%. Peak serum aspartate and alanine aminotransferases were significantly lower (223.8 ± 247.3 U/L, 66.3 ± 92.2 U/L) in survivors compared to non-survivors (489.6 ± 374.0 U/L, 192.9 ± 168.7 U/L; p = 0.03, p < 0.01, respectively). Analysis by receiver operating characteristic (ROC) curve showed sensitivities of 100% and 85.7%, and specificities of 73.1% and 69.2%, respectively for peak serum alanine aminotransferase levels greater than 55 U/L, and peak serum aspartate aminotransferase levels greater than 234 U/L in predicting mortality. CONCLUSION: Copper sulphate is a potent poison that can involve multiple organ systems. Elevated levels of serum aspartate and alanine aminotransferases beyond the aforementioned values can identify patients at greater risk of mortality, allowing for institution of aggressive treatment.

Copper sulphate toxicity in a young male complicated by methemoglobinemia, rhabdomyolysis and renal failure.

Copper sulphate is a compound prepared by the action of sulphuric acid on copper II. Copper sulphate is widely used asfungicide, herbicide and for photography. In a human being, it can lead to anemia. Medical literature is lacking regarding accidental or suicidal poisoning cases of copper sulphate in Pakistan. We present a case of accidental ingestion of copper sulphate resulting in severe acute toxicity, which was successfully managed by intensive supportive measures and Dimercaprol (BAL).

Acute copper sulphate poisoning: a case report and literature review.

Voluntary copper poisoning is a rare mode of suicide. We report a case of copper sulphate poisoning in a patient presenting delusions with mystic demands for purification. The initial gastrointestinal symptoms were followed by intravascular haemolysis and renal failure. The course was favourable after symptomatic treatment and specific copper chelation therapy. However, the pathogenesis is not fully understood and with the present state of knowledge, no one treatment can be said to be superior to another. The authors discuss the various treatments of this rare poisoning through a review of the available literature.

Severe acute copper sulphate poisoning: a case report.

As copper sulphate pentahydrate (CSP) is a common compound used in agriculture and industry, chronic occupational exposures to CSP are well known, but acute poisoning is rare in the Western world. This case report describes acute poisoning of a 33-year-old woman who attempted suicide by ingesting an unknown amount of CSP. On admission to the hospital, she had symptoms and signs of severe hemorrhagic gastroenteritis, dehydration, renal dysfunction and methaemoglobinaemia with normal serum copper level. Therapy included early gastric lavage, fluid replacement, vasoactive drugs, furosemide, antiemetic drugs, ranitidine, and antidotes methylene blue and 2,3-dimercaptopropane-1-sulphonate (DMPS). However, the patient developed severe intravascular haemolysis, acute severe hepatic and renal failure, as well as adrenal insufficiency. After prolonged, but successful hospital treatment, including haemodialysis and IV hydrocortisone, the patient was discharged with signs of mild renal and liver impairment. Our conclusion is that in severe cases of copper poisoning early supportive measures are essential. In addition, antidotes such as methylene blue for methaemoglobinaemia and chelating agent such as DMPS improve morbidity and survival of severely poisoned victims.

An unusual suicide with parenteral copper sulphate poisoning: a case report.

A 22-year-old unmarried, male painter was found by neighbouring shopkeepers to be rolling on the ground inside his shop due to severe abdominal pain. The man had tried to commit suicide by intravenously injecting a solution of copper sulphate, used as an antifouling agent in paints. He was taken to the local hospital with severe epigastric pain, vomiting and diarrhoea. His condition worsened after three days and he was transferred to the All India Institute of Medical Sciences, New Delhi, but the victim died on his way to the hospital. His relatives and neighbours confirmed that he had recently been suffering from depression.

Acute sheep poisoning from a copper sulfate footbath.

An outbreak of footrot occurred in a flock of Corriedale sheep; 27 animals were treated with antibiotic and footbathed in a 5% copper sulfate solution. Being deprived of water for > 17 h, many sheep drank the footbath solution. After 6 h 16 sheep became ill with acute copper poisoning, 10 animals died within 10 h; 6 were severely ill and were sent to Veterinary Hospital, and 4 had mild signs and recovered without treatment. The sick sheep had anorexia, dullness, grinding teeth, moaning, rumen atony, dehydration, dark blue-green diarrheic feces and congested membranes. They were treated with 3.4 mg tetrathiomolybdate/kg body weight and lactated Ringer's solution iv, oral molybdate, sulfate, kaolin and pectin, and drenched with antacids. Two of the 6 sheep died during hospitalization. The ingestion of copper solution caused an intense gastrointestinal injury that resulted in ulcers, petechial and echymotic hemorrhages in the mucosa, mild hemolysis detected by microscopic hemoglobinuria and a lowered packed cell volume, severe hepatic injury that raised the AST and gammaGT blood values, and moderate kidney lesions with increasing serum blood urea and nitrogen creatinine levels.

[Acute cupric sulfate intoxication: pathophysiology and therapy about a case report]. / Intoxication aiguë au sulfate de cuivre: physiopathologie et traitement d'après un cas.

A case of acute copper sulfate intoxication is presented here, as an illustration of high toxic copper dose. A 38-years-old patient with a light mental deficit ingested half a glass of copper sulfate. This patient first suffered from nausea and vomiting, then an intravascular haemolysis occurred during the hospitalisation in our intensive care unit. The outcome was favourable under aetiologic and symptomatic treatment: administration of D-penicillamine as a copper antidote and packed red cell transfusion. The patient left the intensive care unit after 9 days. Acute copper intoxication is not an exceptional situation, with a potentially severe outcome.

Chronic interstitial nephritis following parenteral copper sulfate poisoning.

A 21-year-old male patient was admitted with acute renal failure and intravascular hemolysis following suicidal parenteral copper sulfate poisoning. He developed metabolic acidosis and septicemia; and was treated with intensive hemodialysis, blood transfusions and antibiotics. After remaining anuric for 4 weeks, his urine output gradually increased. However his renal functions improved only partially. Renal biopsy done 8 weeks after the episode showed chronic tubulo-interstitial nephritis (CIN). This is the first reported case showing CIN following acute copper sulfate intoxication.

Death following cupric sulfate emesis.

CASE HISTORY: A 25-year-old woman who had ingested about 20 tablets of diazepam 2.5 mg in a suicide attempt was given cupric sulfate 2.5 g in 1750 mL water as an emetic, but died 3 days later. On autopsy, death was attributed to acute hemolysis and acute renal failure due to copper poisoning. Copper concentrations were 5.31 microg/mL in whole blood, 19.0 microg/g in the liver, 8.9 microg/g in the kidney, 1.1 microg/L in the brain, 1.1 microg/g in the gastric wall, 1.5 microg/g in the jejunal wall, 0.3 microg/g in the colon wall, 4.6 microg/g in the gastric contents, and 12.6 microg/g in the intestinal contents (fresh weight). This case and 10 others from the Chinese medical literature provide additional evidence that cupric sulfate is a corrosive poison and contraindicated as an emetic.