Portal gas embolism after bleach ingestion: the role of hyperbaric oxygen therapy: a case report

Introduction

Hydrogen peroxide (H₂O₂) is commonly found in household formulations for its disinfectant, oxidizing, and bleaching properties. Ingestion can lead to severe consequences, including mucosal damage and the release of oxygen, causing portal gas embolism, a rare but potentially life-threatening condition. When H₂O₂ interacts with catalase in the gastrointestinal tract, it produces tiny oxygen-filled bubbles that bring blood out of intramural vascularity, resulting in ischemic injury and damage from free radicals (1). Deeper tissue involvement by H₂O₂ can result in severe conditions such as gangrene, colon rupture, fulminant colitis, and gas embolism (2). From the venous circulation, gas bubbles traverse the pulmonary arteries, reaching the lungs. A significant volume or rapid transit of gas bubbles in the pulmonary arteries can cause multiple severe complications. These include compromised alveolar gas exchange (3,4), cardiac arrhythmias (5), the development of pulmonary hypertension (4), and subsequent cardiac failure (6,7). Conventional treatment options are limited, and hyperbaric oxygen (HBO₂) therapy has been proposed to mitigate these complications (8).

We report a case of portal gas embolism due to the deliberate ingestion of a significant amount of a bleach formulation containing 10% H₂O₂ by a 29-year-old female patient with the intent of self-harm who achieved successful outcomes after HBO₂ therapy. We present this article in accordance with the CARE reporting checklist (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-24-83/rc).

Case presentation

In November 2023, a 29-year-old female patient presented to the emergency room after deliberate ingesting approximately 100 mL of bleach containing 10% H₂O₂, for anti-conservative purposes, with the intent of self-harm. She had no relevant medical and pharmacological histories. The patient complained of abdominal pain, dyspnea, nausea, and vomiting. On admission, her vital signs were: Glasgow Coma Scale (GCS) 15, non-invasive blood pressure (NIBP) 120/70 mmHg, SpO₂ 99% in room air, heart rate (HR) 98 bpm, Numeric Pain Rating Scale (NPRS) 0. Routine laboratory tests showed: white blood cell (WBC) 9.300/µL, red blood cell (RBC) 4.76 M/µL, haemoglobin (Hb) 13.1 g/dL, C-reactive protein (CRP) 0.28 mg/dL, glutamic pyruvic transaminase (GPT) 11 U/L, creatinine 0.71 mg/dL, international normalized ratio (INR) 1.11. Electrocardiogram (ECG) indicated sinus tachycardia at 107 bpm. Esophagogastroduodenoscopy (EGDS) revealed Zargar’s grade I mucosal gastro-duodenal lesions from caustics (9); abdomen computed tomography (CT) showed intrahepatic air mainly in the left segments, at the hilum and, to a lesser extent, in the right segments due to gas embolism from the portal circle (Figure 1A). Chest CT didn’t show signs of pulmonary embolism (PE). Given the patient’s GCS score of 15 and the absence of neurological deficits and signs of PE, there was no suspicion of cerebral involvement, so brain CT wasn’t performed. Intravenous omeprazole was administered along with hydration and gastric lavage. On the advice of the poison control center, the patient underwent HBO₂ therapy according to US Navy Treatment Table 5 protocol, involving 2.5 atmosphere absolute (ATA) pressure with O₂ administration for 60 minutes (10). The patient showed clinical improvement without complications. In fact, following the first HBO₂ session, gastrointestinal symptoms resolved completely, neurological examination was negative, and vital parameters stabilized (NIBP: 115/75 mmHg, HR 70 bpm, SpO₂ 99% in room air). The patient was hospitalized in the internal medicine ward and received a second HBO₂ treatment the following day as a precaution to avoid possible delayed recurrence of symptoms. After the second HBO₂ session, the patient reported complete regression of symptoms, and an abdominal CT scan confirmed the disappearance of the portal embolus (Figure 1B). She was discharged home after three days without any functional impairment, with recommendations for regular follow-ups by a gastroenterologist to monitor for any delayed mucosal lesions of the gut.

Figure 1 Abdominal CT scans (liver sections). (A) Intrahepatic air in the left segments, at the hilum and, to a lesser extent, in the right segments, due to gas embolism of the portal circle; (B) total resolution of symptoms after HBO₂ therapy. CT, computed tomography; HBO₂, hyperbaric oxygen.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

H₂O₂ is a potent oxidizing agent that can cause significant tissue damage if ingested. Even small volumes (1–5 mL) can be harmful (11). Henry et al. suggested to reserve imaging and other invasive diagnostic exams to patients ingesting more than 10% H₂O₂ (12). Its toxicity is attributed to different mechanisms: the direct caustic effect on mucosa, the impairment of membrane by peroxidation, the oxygen gas production (13). Catalase enzyme, found in tissues, leads to the dissociation of H₂O₂ in mucous membranes resulting in the production of oxygen and water and in the formation of oxygen bubbles in the systemic circulation. In particular, during H₂O₂ ingestion, oxygen can penetrate gastric wall and reach the portal venous system. When oxygen solubility is exceeded by its high concentration in blood, bubbles form and obstruct the vessels, leading to ischemia (6).

The ingestion of 100 mL of 10% H₂O₂ can produce approximately 6.58 liters of oxygen. To date, there is no known antidote for H₂O₂ ingestion (14). Although portal gas embolism could rarely occur after H₂O₂ ingestion, if not treated properly and promptly, it can result in complications such as portal venous thrombosis, pulmonary gas exchange impairment, pulmonary hypertension (3,4), cardiac arrhythmias (5), and cardiac failure. Initially, ischemia is induced by vascular occlusion due to gas emboli. Subsequently, gas bubbles adhere to the vessel walls, triggering an inflammatory cascade that further exacerbates tissue injury (15).

Due to the rarity of the event, there are only few studies in the literature about the treatment of portal venous gas emboli. We identified 27 cases of portal gas embolism due to H₂O₂ ingestion (8,15,16): almost all patients (21/25) ingested 35% H₂O₂ and only 10 patients didn’t undergo HBO₂. On the contrary, our patient ingested 10% H₂O₂ demonstrating that even low concentrations may also cause serious tissue damage. Moreover, the U.S. Navy Treatment Table 6 protocol was applied in 6 cases, while the protocol used in the other cases is not known. In our case, we have applied the U.S. Navy Treatment Table 5 protocol, that demonstrated its effectiveness in relieving symptoms within 10 minutes at a maximum pressure of 60 feet sea water (fsw). So, this protocol ensured clinical improvement faster (2 hours and 16 minutes) than expected with U.S. Navy Treatment Table 6 protocol (4 hours and 45 minutes), with less discomfort of the patients. Lee et al. reported a case of ingestion of 35% H₂O₂ resulting in portal venous embolism (17). In this case, the authors performed an HBO₂ protocol other than those in Table 5 and Table 6: 2.8 ATA compression for 45 minutes without air breaks followed by 2.0 ATA compression for 60 minutes with 5 minutes of air break. Compared to U.S. Navy Treatment Table 5 protocol, Lee’s protocol results more challenging to tolerate, despite its equal effectiveness.

In literature, patients who didn’t receive HBO₂ therapy after H₂O₂ ingestions had different outcomes: some authors like French et al. and Luu et al. reported a complete resolution (6,18), while others like Ashdown et al. reported permanent paresis or hemiparesis, and seizure disorder (19). The studies suggested to perform HBO₂ treatment compared to wait and see strategy since it ensures greater probability of complete resolution, without residual impairment (6,8).

HBO₂ therapy represents the main treatment in case of arterial gas embolism (AGE). However, if HBO₂ therapy is widely used and recognized for treatment of AGE, its use for portal venous gas emboli is off label. So, the use of U.S. Navy Treatment assumes that HBO₂ works on the venous gas emboli like on AGE. HBO₂ therapy acts through various mechanisms. First, in accordance with Boyle’s Law, it decreases the volume of gas emboli. Second, it promotes gas solubility in tissue and plasma (20), facilitating the rapid resolution of ischemic vascular occlusion or inflammatory lesions and reducing endothelial damage (3,6,14,21). In the end, the expelled gas is eliminated via respiration.

H₂O₂ ingestion can impair different organs. We reported a case of portal venous gas emboli promptly diagnosed and treated without multi-organ impairment. Mullins et al. (20) reported the case of full resolution of ischemic stroke symptoms after ingestion of 35% H₂O₂ thanks to HBO₂ treatment. Vander et al. (2) documented a case marked by altered mental state due to ingestion of H₂O₂, with rapid recovery post-HBO₂ therapy. Rider et al. (5) presented a case involving the ingestion of a 33% H₂O₂ leading to hemiplegia, confusion, and hemianopia that resolved after HBO₂ treatment.

However, it’s crucial to acknowledge that this therapy isn’t without risk. HBO₂ treatment heightens the risk of barotrauma, such as damage to the tympanic membrane or sinuses, and may lead to oxygen toxicity, potentially triggering seizures (7). Additionally, oxygen bubbles in the portal venous system can precipitate acute portal vein obstruction, resulting in acute inflammation, portal hypertension, and intestinal edema. Therefore, the decision to pursue treatment should be approached cautiously and made under the guidance of experienced physicians.

Conclusions

This case underscores the potential effectiveness of HBO₂ therapy in treating portal gas embolism resulting from H₂O₂ ingestion. Despite the positive outcome observed in our patient, the rarity of this condition and the limited number of documented cases highlight the need for further research. Comprehensive studies are essential to establish standardized treatment protocols, assess long-term outcomes, and evaluate the safety and efficacy of HBO₂ therapy in similar cases. The prompt diagnosis and intervention in this case emphasize the importance of early recognition and treatment of H₂O₂ ingestion complications to prevent severe outcomes and ensure complete recovery.

Acknowledgments

Funding: None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-24-83/rc

Peer Review File: Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-24-83/prf

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-24-83/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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