# Neurological impairment and hyperglycemia following acute copper sulfate poisoning: a case report

## TL;DR

A 14-year-old girl who ingested copper sulfate developed rare complications like neurological impairment and hyperglycemia, highlighting the need for early monitoring in such cases.

## Contribution

The paper reports neurological impairment and hyperglycemia as uncommon complications of acute copper sulfate poisoning.

## Key findings

- Neurological impairment and hyperglycemia occurred in a patient with acute copper sulfate poisoning.
- Early monitoring and treatment improved outcomes, but some complications only partially resolved.
- Plasma exchange and chelation therapy were part of the successful treatment regimen.

## Abstract

Generally, clinical manifestations of copper sulfate intoxication include acute gastroenteritis, hemolytic anemia, and hepatorenal failure. Herein, we reported the case of a patient who developed neurological impairment and hyperglycemia following massive oral ingestion of copper sulfate. The article was to characterize these uncommon complications that extend beyond the typical toxicological spectrum, thereby enhancing the clinical understanding of copper sulfate toxicity.

A 14-year-old girl ingested approximately 50 grams of copper sulfate. Following initial resuscitation at a local hospital, she developed rapidly progressive tachypnea and hypoxemia. She was immediately transferred to Jinhua Central Hospital for further treatment.

The patient was diagnosed with acute severe copper sulfate intoxication, complicated by hemolytic anemia, hepatorenal failure, and two rare sequelae: neurological impairment and hyperglycemia.

The patient received gastric lavage with 15,000 mL of isotonic solution at a local hospital. Due to the subsequent deterioration of respiratory function (tachypnea and hypoxemia), she was transferred to our hospital. Based on experience from previously reported successful cases of copper sulfate poisoning, we immediately implemented a comprehensive therapeutic regimen, including plasma exchange, copper chelation therapy (sodium dimercaptopropane sulfonate combined with calcium disodium edetate), and continuous renal replacement therapy. During hospitalization, the patient developed epileptic seizures, lower extremity neurological impairment, and persistent hyperglycemia. After symptomatic treatment with neurotrophic agents and insulin for glycemic control, clinical manifestations improved, with no recurrence of epilepsy. However, hyperglycemia and lower extremity neurological dysfunction showed only partial remission and were not fully resolved at discharge.

Acute massive copper sulfate poisoning may induce neurological impairment and hyperglycemia. Importantly, early monitoring and heightened vigilance for the delayed onset and protracted course of such complications are imperative.