Bubbling up consequences: severe gastric injury in a child after hydrogen peroxide ingestion: a case report
Article information
Abstract
We report a case of a previously healthy 9-year-old boy who presented to the emergency department following accidental ingestion of 35% hydrogen peroxide. He developed emesis and mild abdominal pain and was found to have extensive portal venous gas, severe gastric pneumatosis, and free intraperitoneal air on a computed tomography scan. He was transferred to an outside hospital for hyperbaric oxygen therapy, with no emergency surgical intervention indicated. This case highlights the dangers of ingesting even a small amount of concentrated hydrogen peroxide in children and underscores the safe storage practices at home.
Introduction
Concentration of hydrogen peroxide (H₂O₂) varies from 3% to 70% (1). While 3% H₂O₂ is a common household disinfectant widely available, a highly concentrated one, typically 35% or greater, is less commonly found in the average household, as it is a potent caustic agent with oxidizing properties. While the majority of pediatric ingestions involves diluted (3%) solutions and results in benign outcomes, requiring conservative management, concentrated forms pose a high risk of caustic injury and gas embolism (1-7). We present a case of a school-aged boy with accidental ingestion of 35% H₂O₂, resulting in gastric pneumatosis and portal venous gas. Informed consent was obtained from his legal guardians for publication of this case report.
Case
A previously healthy 9-year-old boy (weight, 31.6 kg) presented to the emergency department (ED) at 9:55 p.m. via an emergency medical technician after accidental ingestion of H₂O₂. Upon arrival at the ED, his initial vital signs were as follows: blood pressure, 113/83 mmHg; heart rate, 82 beats/minute; respiratory rate, 18 breaths/minute; temperature, 36.6 °C; and oxygen saturation, 100% on room air. According to the boy, he drank approximately 10 mL of the chemical from a refrigerator-stored, unlabeled bottle containing the solution, mistaking it for water at around 8:55 p.m. on the same day of the ED visit. Right after the ingestion, he experienced a burning and bubbling sensation in the throat and abdomen and had 3 episodes of emesis. Local governmental poison control was contacted promptly by the family around 9:00 p.m., and the emergency medical technician was dispatched within 6 minutes.
On arrival to the ED, thorough physical examination only showed mild erythema to the posterior oropharynx and epigastric tenderness. The boy was alert, oriented, and in no acute distress, experienced no stridor or drooling, and remained in a lingering epigastric dull pain, 2/10 on the Numerical Rating Scale. In further discussions with his parents, it seemed that the ingested liquid was 35% food-grade H₂O₂. A venous blood gas analysis showed PO2, 280 mmHg; SO2, 100%; carboxyhemoglobin, 97.5%; and total hemoglobin, 12.1 g/dL, while electrolytes were within normal limits.
Considering that the boy was symptomatic following the food-grade ingestion of H₂O₂, it was determined to obtain computed tomography (CT) scans of the chest, abdomen, and pelvis to check the presence of intestinal injuries. The CT showed severe portal venous gas, severe gastric pneumatosis suggestive of gastric wall necrosis, possible duodenal wall thickening, and tiny droplets of free intraperitoneal air anterior to the stomach (Figure 1). The oral cavity was distended with air, possibly from excessive gas production due to the interaction of H₂O₂ with gastric acid. At 11:18 p.m., he remained well-appearing and hemodynamically stable on room air.
Computed tomography findings with axial, sagittal, and coronal scans. An axial scan shows severe portal venous gas (arrows) and severe gastric pneumatosis suggestive of gastric wall necrosis (arrowhead) (A). A sagittal scan shows tiny droplets of free intraperitoneal air anterior to the stomach (arrow) (B). A coronal scan also shows the severe gastric pneumatosis (arrows) (C).
Given the present illness and imaging findings, the boy was determined to require emergency hyperbaric oxygen therapy (HBOT). A consulted pediatric surgeon opined that emergency surgery was not indicated given the small amount of free air and lack of abdominal rigidity. Despite the need for abdominal decompression, no nasogastric tube was placed given the suspected perforation on the CT (Figure 1B). He was placed on a non-rebreather oxygen mask at 15 L/min, with oxygen saturation remaining at 100% while awaiting transfer to a tertiary care facility with a hyperbaric chamber. He developed a fever (38.1 °C) during the observation and was treated with rectal acetaminophen.
The boy was subsequently transferred to the tertiary care facility for HBOT. He spent 12 hours in a hyperbaric chamber and continued to remain overall well-appearing. An abdominal plain radiograph showed the absence of perforation or free air. Approximately 48 hours after time of ingestion, a pediatric gastroenterologist performed an upper endoscopy, showing diffuse severe inflammation characterized by congestion, erosions, erythema, granularity, and diffuse, mildly erythematous mucosa with no stigmata of bleeding in the duodenal bulb (Figure 2).
Upper endoscopic finding showing the diffuse severe inflammation characterized by congestion, erosions, erythema, and granularity in the stomach (arrows).
He was started on intravenous pantoprazole 20 mg every 12 hours and oral sucralfate 600 mg every 6 hours. He progressed from a clear liquid diet to a regular gastritis diet upon discharge. No CT findings are available post-HBOT. He was cleared for discharge at the outside tertiary care facility approximately 5 days after the ingestion of H₂O₂, with close outpatient follow-up and minimal concern for long-term damage.
Discussion
Ingestion of 35% H₂O₂ releases large volumes of oxygen due to catalytic decomposition in the stomach, which may result in gas embolism, gastric distention, pneumatosis, and portal venous gas (2,3,5,8). When ingested, it can lead to significant gastrointestinal injury and multiorgan complications through the 2 primary mechanisms. First, the corrosive properties of H₂O₂ can directly lead to chemical burns of the mucosal surfaces, resulting in esophagitis, gastritis, ulceration, or necrosis (3,9). Second, decomposition of H₂O₂ rapidly releases oxygen, leading to gastric distention and the potential for gas embolism. Gas emboli can migrate to the portal venous system (i.e., portal venous gas) or enter the systemic circulation, leading to cerebral or cardiac gas embolism, or mortality (2,3,4,10).
Even 1 mL of 35% H₂O₂ can release over 100 mL of oxygen, generating sufficient gas to cause serious complications such as gastric distention, portal venous gas, or gas embolism (3). Portal venous gas and gastric pneumatosis are alarming findings and require rapid multidisciplinary evaluation. HBOT is indicated to reduce the risk of gas, as it accelerates the dissolution of gas bubbles and improves oxygenation of ischemic tissues (3,5,8). It helps prevent the development of end-organ damage, such as ischemic stroke, myocardial infarction, or bowel infarction (6). Nasogastric tube decompression may be considered cautiously, while it may be deferred in case of suspected perforation, as in the present case (3,5).
Access to HBOT is limited and may require interfacility transfer. The presence of portal venous gas and gastric pneumatosis should prompt immediate multidisciplinary evaluation and consideration of HBOT, even in clinically stable patients. Air transport was not recommended due to the theoretical risk of bubble expansion at altitude. This highlights the importance of understanding, early planning, and coordination of the physiologic risks associated with altitude in gas-forming ingestions.
This case illustrates the potentially life-threatening consequences of concentrated H₂O₂ ingestion in children. For the prevention of ingestion, it is important to keep the chemical in its original, clearly labeled container and out of children’s reach, as well as being aware of various concentrations of household cleaners. Furthermore, it is critical to recognize the ingestion early, perform CT as well as a multidisciplinary approach, and spot the nearest hyperbaric chamber (8).
Notes
Author contributions
Conceptualization: AY
Data curation: AY, CH, and PP
Formal analysis: AY, CH, and RK
Funding acquisition: not applicable
Investigation: AY, CH, PP, NM, and RK
Methodology: AY, CH, and RK
Project administration: AY
Resources: AY
Software: NM and RK
Supervision: AY
Validation: AY and CH
Visualization: AY, NM, and RK
Writing-original draft: all authors
Writing-review and editing: all authors
All authors read and approved the final manuscript.
Conflicts of interest
No potential conflicts of interest relevant to this article were reported.
Funding sources
No funding source relevant to this article was reported.