Case
A previously healthy 32-year-old man presented to the ED after unintentionally ingesting a mouthful of concentrated (35%) hydrogen peroxide (H2O2) from an unmarked bottle he kept in his refrigerator. Upon realizing his error, he immediately drank a liter of water, which promptly induced vomiting. In the ED, the patient complained of mild throat and chest discomfort as well as “abdominal fullness.”
His initial vital signs were: blood pressure, 140/92 mm Hg; heart rate, 93 beats/minute; respiratory rate, 18 breaths/minute; temperature, 96.4° F. Oxygen saturation was 98% on room air. Physical examination revealed tenderness in the epigastric region with no peritoneal findings. Oropharynx and chest examination were normal, and standard laboratory investigations were all within normal limits.
What are the potential exposures to hydrogen peroxide?
Hydrogen peroxide is a colorless and odorless liquid. Solutions with concentrations ranging from 3% to 5% have many household applications, including use as a wound disinfectant and dentifrice; dilute solutions are also utilized for similar purposes in the hospital setting. Industrial-strength H2O2 (concentrations of 10% to 35%) is employed to bleach textiles and paper, and higher concentrations (70% to 90%) are used as an oxygen source for rocket engines.
Consumer application of concentrated H2O2 solutions has become increasingly common. Some, like this patient, clean the surfaces of fruits and vegetables with H2O2 to decrease transmission of bacteria during cutting.1 More concerning, however, is the purported medicinal benefits of ingesting “food-grade” (35%) H2O2 mixed with water—touted on many Internet sites as a treatment for illnesses such as emphysema, cancer, anemia, and HIV.2 Sometimes referred to as “hyperoxygenation therapy,” this so-called treatment has not been approved by the US Food and Drug Administration for any such purpose.3 When diluted sufficiently, this concoction is not harmful but unlikely to provide any health benefits.
Dr Lucyk is a fellow of medical toxicology in the department of emergency medicine at the New York University School of Medicine and the New York City Poison Control Center. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.
What are the toxic effects of concentrated hydrogen peroxide?
Injury from concentrated H2O2 consumption is primarily from either direct caustic injury or the embolic obstruction of blood flow. Following ingestion, the enzyme catalase metabolizes the breakdown of H2O2 in accordance with the following equation: 2H2O2(aq) → 2H2O(l) + O2(g) + heat. A single milliliter of 35% H2O2 results in the liberation of 100 mL of O2. (The more common 3% household solution generates 10 mL of oxygen per 1 ml of H2O2.) The creation of a large intragastric pressure gradient from the liberation of gas, coupled with the caustic and exothermic injury of the bowel mucosa, may contribute to the movement of oxygen through epithelial interstices into the circulation.In addition, and perhaps more importantly, absorption of intact H2O2 with subsequent metabolism by catalase in the blood liberates oxygen directly within the vasculature. Oxygen bubbles may coalesce in blood circulation and occlude vascular flow. In canine studies, elevated oxygen tension in the portal venous system led to cessation of mesenteric flow in arteries and veins, though the mechanism of action is unclear.4 Furthermore, coalescence of bubbles can lead to disruption of bowel-cell architecture, fibrin plugging of capillaries, venous thrombosis, and infarction of tissues.4
Cases of cardiac and cerebral gas embolism have been reported, and present similarly to patients with diving-related decompression injuries (eg, stroke-like syndromes).5,6 The proposed mechanism for these latter effects involves the metabolism of H2O2 in the systemic circulation with production of oxygen bubbles. In the presence of an atrial septal defect, bubbles may move from the right atrium to the arterial circulation.7
Toxicity and death from H2O2 exposure associated with the historical treatment of inspissated meconium,4 as well as the irrigation of wounds,8 has been reported in the medical literature. Ingestion of a 3% solution is generally benign, resulting at worst in gastrointestinal symptoms or throat irritation.9 Rarely does significant toxicity occur at this low concentration,5 with the vast majority of such cases involving concentrated solutions of 35%.
Case continuation
Case 2
Based on this patient’s continued symptoms, an abdominal radiograph was obtained to assess the presence of portal venous air. Although radiographic findings were normal, continued abdominal examination findings warranted a subsequent abdominal computed tomography (CT) scan, which revealed the presence of extensive air throughout the portal venous system (Figure.).