Copper is one of essential trace elements in the human body, but excessive copper is harmful for health. Copper sulfate poisoning is rare and little reported that and is mainly associated with suicide.
Ingestion of a copper substance (> dose of 1g) results in signs and symptoms of copper poisoning.3 Physically, copper is absorbed from the intestine and is stored in the liver lysosome in the form of ceruloplasmin. Once the lysosome is destroyed and liver cells die, copper is released to blood circulation. There have also been reports of lung lesions caused by spraying vineyards with a mixture of copper sulfate and quicklime4. There once reported that copper sulphate had been inserted into the rectum in order to be pregnant5. But there have never been reports of copper sulfate drowning.
The initial manifestations of copper sulfate poisoning include nausea, vomiting, abdominal pain and other nonspecific clinical symptoms, followed by severe complications such as digestive tract mucosal injury, intravascular hemolysis, hemolytic anemia, methemoglobinemia, renal insufficiency, cerebral arterial thrombosis and even die6.
Copper sulphate is an oxidizing agent that as the stimulating effects on mucosa membranes. The patient developed digestive tract symptoms, which consist of a metallic taste in the mouth, nausea, vomiting of blue-green stomach contents, diarrhea, upper abdominal pain, and gastrointestinal nausea, vomiting. After poisoning, the patient does not develop serious gastrointestinal complications, such as gastrorrhagia or perforation, under the protection of gastric mucosal protectant.
Since most of the absorbed copper is deposited in the liver after circulating through the portal vein, liver damage is often seen early in patients with copper sulfate poisoning7 due to cell necrosis and obstruction8. However, the rise of total bilirubin approximately occurred on the 20th hour after poisoning, and reached the peak on the 7th day. After liver protection treatment, the liver enzyme of the patient was not very high, but the indexes of liver function completely returned to normal about four weeks later.
Renal insufficiency usually occurs 3 to 4 days after copper sulfate poisoning. and the causes of renal insufficiency were as follows9: (1) the direct toxic effects of copper sulfate; (2) cohemolytic anemia and rhabdomyolysis; (3) hypotension due to hypovolemia. The toxic effects of copper sulfate on muscles lead to rhabdomyolysis10, which leads to renal insufficiency. Patients may benefit from alkalizing the urine or starting continuous renal replacement therapy (CRRT)as early as possible when patients have progressed to renal insufficiency. Fortunately, this patient did not develop renal damage and rhabdomyolysis. We wondered if this was related to the different routes of copper sulfate into the body, because the vast majority of cases reported in the past were poisoning by oral copper sulfate, and our patient was drowning by copper sulfate. The specific reasons deserve further study.
Copper sulfate is a potent oxidant. In response to copper ions, oxygen-containing hemoglobin is oxidized from ferrous to iron, resulting in methemoglobinemia and reduced oxygen-binding capacity8. Copper sulfate can decrease the stability of erythrocyte membrane, which will lead to in vascular hemolysis in patients, generally occurring 12-24h after poisoning. At high concentrations, copper ions bind to the sulfhydryl group of erythrocyte membrane, reducing glutathione in erythrocyte and reducing the activity of glucose-6-phosphate dehydrogenase2. On the third day after poisoning, the patient experienced a significant decrease in hemoglobin, and we considered the occurrence of intravascular hemolysis. We treated the patient by using reduced glutathione and a large amount of blood transfusions (We had a total of six transfusions, 17 U of red blood cells). The hemoglobin was stable for 17 days after the poisoning. Although jaundice can be secondary to hepatic necrosis and hemolysis8, The absence of jaundice may be related to the lack of severe liver impairment. This patient did not experience another decrease in hemoglobin after treatment with reduced glutathione and blood transfusion, but delayed hemolytic episodes have also been reported in the literature. This released copper is taken up by the erythrocytes and may account for the delayed secondary episode of haemolysis11.
The skin may also be one of the routes through which copper (metals and/or aside salts) enters the body12. The patient accidentally fell into a copper sulphate pool and suffered skin damage, which is reeking Sun Park reported a case of exposing to a hot copper exposing patient had a deep dermal exposing cerebral infarct, which may have been due to hypercoagulability and anemia, caused by severe intravascular hemolysis6. But the skin damage in this case was mainly burns from the explosion. The case we report is a rare case of skin damage caused by direct exposure to copper sulfate. This patient suffered from skin lesions on the right face and back. Since there was no previous case or experience, we only gave iodophor dressing change. Although the patient's skin healed, it left a scar.
The most serious complication in this patient was pulmonary lesions caused by copper sulfate, resulting in respiratory failure. The patient's lungs developed rapidly and ferociously. At the local hospital, the patient showed no symptom of respiratory failure, such as decreased oxygenation, but the emergency physician administered an endotracheal intubation because of the rapid progression of the copper sulfate disease, which was confirmed by subsequent treatment. On the 8th day after the poisoning, the oxygenation could not be maintained and the patient needed pure oxygen ventilation on the ventilator. After antibiotic therapy (initially meropenem, later imipenem and cystatin), tracheoscopy sputum aspiration and irrigation, the tracheobronchial intubation was successfully removed 20 days after poisoning without reintubation, although the right lung was still severely inflamed. The mechanism underlying pulmonary toxicity induced by copper consists of oxidative effects resulting from the generation of reactive oxygen species (ROS)13. In addition, copper blocks antioxidant activities in epithelial cells by inhibiting the activity of catalysts and glutathione reductase sand and increasing the activity of glutathione peroxidase14. Three stages-intra-alveolar desquamation of macrophages, formation of predominantly histiocytic granulomas in the septa, and the healing of these lesions generally under the form of fibro-hyaline nodules very similar to those found in silicosis4. There have been few reports of lung lesions caused by copper sulfate, it has been reported that inhalation of copper sulfate could lead to pulmonary tuberculosis, known as “vineyard lung4”. Elisabetta Giudice15reported a dog exposed to copper sulfate powder leading to acute hypoxemic respiratory failure. In the case of the patient we reported, more copper sulfate choked into the airway during drowning, much more than the two cases previously reported. Therefore, we do not know whether this patient will suffer severe complications such as airway stenosis and lung cavity in the future. We told the patients that he needed long-term follow-up.
The patient suffered corneal injury due to direct contact between the copper sulfate and the cornea during the copper sulfate drowning.. After admission in our hospital, we had an ophthalmological consultation, and applied eye ointment to both eyes. The physical examination revealed scarring of the patient's cornea. Unfortunately, the patient refused toconduct a further eye examination.
The mortality rate from copper sulfate poisoning is high, and the leading cause of early death is shock.. Earl Schwartz16 reported a case of refractory shock after copper sulfate poisoning. Although shock did not appear in this patient, it is still a matter of caution and concern. The cause of shock is still unknown. Some believe that early vomiting, diarrhea, and intravascular concern. There may be other key mechanisms that we don't know about that merit further investigation. This deserves further investigation. Copper sulfate poisoning can also cause heart damage, the cause is unknown and may be related to pulmonary hypertension.
Our patient showed an increase in troponin 20 hours after poisoning, the peak value was 11.1ng/mL on day 11. but repeated ECG reexamination showed no abnormality, and there was no pulmonary hypertension. 22 days after poisoning, the patient's troponin was reduced to normal. Because there are no other symptoms of cardiac insufficiency, we did not give special treatment.
Symptomatic treatment is the common treatment of copper sulfate poisoning, including but not limited to dexamethasone frantic-stress, renal and hepatic support therapy, omeprazole which was given to protect the gastrointestinal mucosa,intravenous fluid infusion༌and special treatment of chelate succinate (dimercaprol). Chelation therapy was administered even though the concentration of copper ions remained within the normal range. Hemodialysis is not very helpful for the removal of copper8. But, early application of plasma replacement (plasmapheresis) is an effective way to block further tissue damage caused by cupric sulfate. The patient underwent a plasmapheresis immediately after admission༌this should be the basis for successful patient care. In addition, our repeated tracheoscopy rinsing reduced the amount of copper sulfate entering the lung, which provided a very important role for the successful removal of tracheal intubation.