Accidental Ingestion of Potassium Permanganate in a Child: Effects, Toxicity, and Management

A 22-month-old boy presented to the emergency department following an accidental ingestion of potassium permanganate (KMnO₄).

Accidental ingestion of hazardous substances remains a significant concern for pediatric populations. Among these substances, KMnO₄ poses a unique challenge due to its easy availability. KMnO₄ is commonly used in various settings, ranging from water treatment to medicinal purposes. Its ingestion can lead to severe complications, particularly in children, making prompt identification, evaluation, and management crucial. By shedding light on this specific incident, we hope to enhance the medical community's understanding of the potential risks and guide appropriate management strategies in similar cases.

Case description. A 22-month-old boy was brought to the emergency department by his babysitter with complaints of sudden onset of hoarseness of voice, shortness of breath, and difficulty in breathing. Before this development, the patient had been playing alone in the storeroom. When the babysitter entered the room, she found that the patient was having trouble breathing. She immediately brought the patient to the hospital.

His past medical history was unremarkable and he was on no medications. His immunizations were up to date. He had no known allergies.

He was conscious, alert, and nontoxic appearing. His temperature was 35.0° C. His blood pressure was 100/70 mm Hg and his pulse was 137 beats/min. Oxygen saturation was 97% on room air and respiratory rate was 28 breaths/min. His tongue, gums, and perioral area had black discoloration. The patient was crying often and a mild hoarseness of voice was noted but there was no stridor or drooling present. The tonsils were erythematous. Breath sounds were heard equally bilaterally and there was no use of accessory respiratory muscles. The heart sounds were within normal limits and no murmurs were heard. The abdomen was soft, non-distended, non-tender, and with normative bowel sounds. A neurological examination was within normal limits with grossly intact cranial nerves and reflexes. There were a few marks of brownish-black discoloration, suggestive of splash marks, on the face and hands. The eyes were not injected. Fluorescent staining of both eyes showed punctate areas of increased uptake at the 1 o'clock position in the right eye and the 11 o'clock position in the left eye. 

He was given 250 ml of normal saline bolus. His laboratory investigations revealed an elevated white cell count (15,000/µL with 23% neutrophils, 7% monocytes, & 67% lymphocytes) with a hemoglobin of 13.7 g/dL, and a platelet count of 364,000/μL. His serum electrolytes were within normal limits with 142 mmol/L of sodium, 4.6 mmol/L of potassium, 107 mmol/L of chloride, and a bicarbonate of 18 mmol/L. His kidney function tests (blood urea nitrogen 13 mg/dL; creatinine 0.5 mg/dL) and liver function tests (aspartate aminotransferase 31 U/L; alanine transaminase 36 U/L; alkaline phosphatase 233 U/L; albumin 3.7 g/dL; total bilirubin 0.2 mg/dL) were within normal limits. His blood glucose level was 116 mg/dL.

The patient was admitted to the pediatric intensive care unit for further investigations and observations. An upper gastrointestinal (GI) endoscopy was conducted, which revealed an esophageal mucosa within normal limits with a good vascular pattern and no evidence of burns. Erythema was noted in the fundus of the stomach with no ulcerations or erosions. The antrum was within normal limits. Erythema was also seen on the retroflex of the stomach at the lower esophageal sphincter (LES) on the gastric side. The duodenum appeared to be within normal limits. A gastroenterologist was consulted to assess the severity of the lesions. He was kept nil per oral as he was unable to tolerate oral feeds, was administered intravenous fluids, and began an infusion of esomeprazole 40 mg. Since the patient had hoarseness, he was kept under close observation for any sign of impending airway obstruction.

The differential diagnosis for this case included caustic ingestion, foreign body ingestion, laryngotracheobronchitis, and epiglottitis. Laryngotracheobronchitis and epiglottitis were both ruled out through the patient’s history. The results of the upper GI endoscopy pointed towards a diagnosis of caustic ingestion.

The parents were asked if they’d noticed any tell-tale signs of possible ingestion. It was then revealed that the patient’s grandmother stored her foot soak, an undiluted solution of KMnO₄, in the storeroom and the patient had easy access to it. Soon after the incident, the grandmother complained that some of the foot soak was missing. Additionally, some spillage was also noted in the storeroom where the patient was playing alone. It was concluded that the signs and symptoms were a result of accidental ingestion of KMnO₄-containing foot soak.

Over the next 2 days, his condition improved and he was able to tolerate oral feeds. After 3 days of hospitalization, he was discharged. On a regular outpatient follow-up, the patient was healthy and with no residual problems.

Discussion. KMnO₄ is a widely available, highly caustic chemical compound with a strong oxidizing property. Dilute solutions of it are used to treat ulcers, dermatitis, and fungal infections of the hands or feet and in water treatment systems.^1,2 Weak dilutions of it are safe for use in topical and external applications to the skin only, and KMnO₄ baths are commonly used to treat dermatologic conditions. Additionally, KmnO₄ has excellent bactericidal properties, so it is commonly used as a disinfectant.³ It is used as a reagent for the synthesis of ascorbic and pyrazinoic acids, as well as a preservative.⁴

Toxicity could be intentional or unintentional. In children, ingestion is mostly accidental.^5,6 Cases of accidental ingestion in children can be avoided by adding barriers to accessing salts containing this compound.⁶ In some other cases, medication misuse have led to KMnO₄-associated burns and toxicity.⁷

The pure chemical form of KMnO₄ is rated as highly toxic by the US EPA product label.⁸ KMnO₄ causes injury to the skin and mucous membranes and its ingestion can lead to esophageal and stomach damage.⁹ When consumed in large doses, it can lead to cardiovascular toxicity and cardiovascular depression with shock and collapse.¹⁰

The symptoms of its toxicity depend on the mode of ingestion and the amount of chemicals involved. KMnO₄, being a strong oxidant, reacts with tissues to produce coagulative necrosis.¹¹ The toxicity can be reduced by organic matter, such as milk or egg white. The probable lethal dose for adults who ingest KMnO₄ is 10 grams, equal to 1.5 teaspoons of crystals.¹²

The main concern with KMnO₄ toxicity is its potential to cause acute laryngeal edema, which should be a health care practitioner’s immediate concern following ingestion. This necessitates early endotracheal intubation.¹² Gastrointestinal manifestations include nausea and vomiting in mild cases.¹² Burns and ulcerations of the mouth, esophagus, and stomach are due to its caustic action.¹³ It combines with proteins to form proteinates and with fats to form soaps, which results in necrotic ulcers and may lead to perforation.¹² Telltale signs would include brownish-black splash marks, as seen in our patient. Early esophagoscopy is needed to assess the severity of esophageal burns and in our patient, erythema was noted in the fundus and on the retroflex of the stomach at the LES on the gastric side. There were no erosions or ulcerations. Late complications of upper GI ulceration include the formation of esophageal strictures and pyloric stenosis.¹⁴

The mainstay in treatment is supportive.¹² Securing the airway level should be the immediate priority in treatment.¹² Some practitioners have recommended gastric lavage. However, this treatment is potentially dangerous as there is a risk of perforation.¹⁵ The use of activated charcoal, as used in some cases of poisoning, is considered controversial due to insufficient data on its effectiveness in KMnO₄ poisoning.¹² Consuming milk or water may dilute and neutralize the effects of KMnO₄.¹⁶ Early esophagoscopy can be used to determine the extent of upper GI injury.^5,16 Diagnostic testing in cases of suspected ingestion should include liver and renal function tests, methemoglobin level, serum manganese, and serum amylase values.¹² Other supportive treatments include methylene blue and vitamin C for methemoglobinemia and broad-spectrum antibiotics for perforation and subsequent peritonitis. The use of steroids has been controversial in prior cases of KMnO₄ poisoning.¹⁶

Conclusion. KMnO₄, a powerful oxidizing agent, is readily available without a prescription and is used for various purposes. Upper GI endoscopy is key to understanding the extent of injury following ingestion. A thorough history and prompt management can help improve morbidity and mortality.

References:

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AFFILIATIONS:
¹Vardhman Mahavir Medical College & Safdarjung Hospital, Delhi, India
²Medical Director, Pediatric Emergency Department, Cleveland Clinic Fairview Hospital, Cleveland, OH

CITATION:
Kumar M, Grover P. Accidental ingestion of potassium permanganate in a child: effects, toxicity, and management. Consultant. 2023;63(12):e1. doi:10.25270/con.2023.12.000005.

Received August 30, 2023. Accepted October 25, 2023. Published online December 27, 2023. 

DISCLOSURES:
The authors report no relevant financial relationships.

ACKNOWLEDGEMENTS:
None.

CORRESPONDENCE:
Manya Kumar, MBBS, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India, 110029 (manyakumar15@gmail.com)

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