Case Report

Accidental Ingestion of 35% Hydrogen Peroxide Resulting in Air in the Soft Tissues of the Neck and Significant Esophageal Injury

Leslie R. Dye, M.D., F.A.C.M.T.
Dan W. Dobler, MD

Corresponding Author:
Leslie R. Dye, M.D., F.A.C.M.T.
5364 Elbon Road
Waynesville, Ohio 45068

Int J Med Toxicol 2002; 5(2): 7



This case report is supported by an unrestricted educational grant from Orphan Medical, Inc. For more information, please call 1-888-8ORPHAN.

ABSTRACT

Introduction: Hydrogen peroxide, H2O2, is a readily available substance with multiple household and industrial uses, with concentrations varying from 3% to 70%. Ingestion of the over-the-counter, 3% solution, is usually benign, but ingestion of more concentrated forms (>10%) may have catastrophic effects.

Case Report: The following case represents an unusual presentation of air in the soft tissue of the neck in a patient upon arrival to the ED after the accidental ingestion of a solution of 35% H2O2. The patient also developed significant esophageal injury.

Conclusion: This report demonstrates air in the soft tissues of the neck following H2O2 ingestion. As the use of H2O2 for various illnesses increases, toxicologists should be familiar with the signs and symptoms of toxicity.

INTRODUCTION

Hydrogen peroxide, H2O2, is a readily available substance with multiple household and industrial uses. Concentrations vary from 3% to 70%. Ingestion of the over-the-counter, 3% solution is usually benign, but serious consequences have been reported. Ingestion of more concentrated forms (>10%) may have catastrophic effects. Multiple cases report gas embolism in the vascular circulation.1-5 Gastrointestinal injury most commonly occurs in the stomach, but the esophagus is usually spared. There have been no reported cases of esophageal rupture or air in the soft tissue of the neck following H2O2 ingestion. The following case represents an unusual presentation of air in the soft tissue of the neck in a patient upon arrival to the ED after the accidental ingestion of a 35% solution of H2O2. The patient also developed significant esophageal injury. As the use of H2O2 for various illnesses increases, the toxicologist and emergency physician should be familiar with the signs and symptoms of toxicity.

CASE REPORT

A 68-year-old female accidentally ingested one cup of 35% H2O2. She was instructed that the ingestion of 3 drops of the substance mixed with distilled water would improve her arthritis. She confused containers and accidentally ingested a solution of 35% concentrated H2O2, instead of the recommended mixture. She immediately developed shortness of breath and sore throat. She vomited and coughed up a foamy substance with a small amount of blood. Shortly following ingestion, she developed severe pain between the scapulae.

Upon arrival to the ED, the patient was anxious with moderate discomfort, but in no acute respiratory distress. She was afebrile with a pulse of 76, blood pressure of 120/87 and a respiratory rate of 20. The tongue was swollen with a markedly edematous and erythematous uvula. The pharynx was also slightly edematous and erythematous. There were no mucosal or lip burns. The neck was supple with crepitus in the soft tissue. Lung exam revealed mild inspiratory stridor and rhonchi, without wheezing. Abdomen was soft with mild diffuse tenderness. The remainder of the physical exam was unremarkable.

Laboratory examination revealed a white blood cell count of 14.9/mm3 with 47% segmental neutrophils, 47% lymphocytes, and 2% monocytes. Hemoglobin, hematocrit, and platelet counts were normal. An arterial blood gas on 44% oxygen showed pH of 7.37, p CO2 of 36 mmHg, pO2 of 68 mmHg, with an oxygen saturation of 91%. Chest radiograph showed no infiltrates, but pneumomediastinum and air in the soft tissues of the neck was noted. A lateral neck film showed abnormal gas in the soft tissue with a normal epiglottis and cervical spondylosis. (Figure 1).

The patient initially received broad-spectrum antibiotics and steroids in the Emergency Department. A barium swallow obtained after admission showed no obvious perforation but slight aspiration. A Computerized Axial Tomogram of the neck and chest revealed gas in the mediastinum and subcutaneous emphysema in the neck. Diffuse edema of the esophagus was seen and a perforation was suspected, but the exact site could not be determined. Due to the high suspicion of esophageal perforation, the patient was taken to surgery for exploration of the cervical esophagus with drainage, exploratory laparotomy with exploration of the distal esophagus, and right thoracotomy with exploration of the mediastinal esophagus with drainage.

Upon intubation in the operating suite, laryngeal edema was noted. On examination of the neck, the cervical tissue surrounding the carotid sheath was edematous, as was the area surrounding the esophagus. A moderate amount of purulent fluid was also noted. The esophagus was extremely friable, edematous, and hyperemic on the external surface. Crepitus was noted, but no full-thickness necrosis or perforation was identified. On laparotomy, there was edema within the peritoneal folds on the lesser curvature of the stomach, but the gastric mucosa appeared normal without inflammation. The esophageal hiatus was significantly inflamed and had several areas of petechial hemorrhage. There was no esophageal necrosis, but the color was noted to be pale. As with the cervical esophagus, no perforation was identified. Thoracotomy revealed mediastinal tissues that were grossly edematous and inflamed. Similar to findings in the upper esophagus, the lower esophagus showed small areas of petechial hemorrhage, and the color was pale. No gross area of perforation was noted.

The patient did well postoperatively and was discharged on postoperative day fifteen. Esophagogastroduodenoscopy (EGD) one month after the initial ingestion showed a single erosion in the extreme proximal esophagus, and the esophageal mucosa was scalded and denuded from the proximal portion to a few centimeters above the gastroesophageal junction. Linear erosions, similar to those seen from peptic esophagitis, were noted in the mid-esophagus, but the extreme distal esophagus and stomach were normal.

DISCUSSION

Hydrogen peroxide is a clear, colorless, odorless, oxidizing liquid. The 1% solution has a pH of 5-6.5 When it contacts organic tissue containing catalase, it is degraded to oxygen and water in an exothermic reaction. For every one ml of 3% H2O2, ten ml of oxygen is produced.6 This amount greatly increases, up to 115 ml, with more concentrated solutions.2 H2O2 is available over the counter in 3% concentration, but a 35% solution can be obtained in health food stores.

Industrial uses of concentrated H2O2 include bleaching textiles, wool and paper and use in the production of foam rubber, rocket fuel and electroplating.5 Medical professionals used H2O2 in the 1950's for colonic irrigation to treat meconium ileus in newborns. This practice has been abandoned due to serious complications, including gas emboli and bowel perforation.7 It also was extensively used to irrigate wounds during surgical procedures, which can also result in gas emboli and subcutaneous emphysema.3 Currently H2O2 is used as a mild antiseptic, an aid in loosening crusted secretions, and as an aid for cerumen removal. It has been used as a mouthwash, a vaginal douche, and for enemas. H2O2 can also be used for bleaching hair, teeth, and clothes.5,8 Addition of H2O2 to milk and other products, although not FDA-approved, has been performed to prolong the shelf-life.9

Other non-approved uses that have been suggested include "hyperoxygenation therapy" for various conditions ranging from cancer to HIV infections.8 Intravenous H2O2 is believed by some to relieve allergic reactions, influenza symptoms and acute viral infections. Other medical conditions purported to be improved by H2O2 therapy include: Alzheimer's disease, cardiovascular disease, chronic obstructive pulmonary disease, asthma, herpes zoster and simplex, type II diabetes, multiple sclerosis, rheumatoid arthritis, parkinsonism, migraine headaches and various bacterial, viral, and parasitic infections.10

While some proclaim H2O2 to be a "medical miracle," 10 there are multiple reports of both minor and serious complications as well as death resulting from ingestion of this substance.9 A study reviewing 670 cases of 3% H2O2 exposures reported to a poison control center found that most ingestions were benign, and the majority of patients were asymptomatic. Of those that had symptoms, gastrointestinal complaints such as nausea and vomiting were the most common.8 Other symptoms reported in a study that reviewed 122 ingestions of all strengths were sore throat, abdominal distention, seizures, and chest pain.7 In one case report, a 2-year-old boy ingested an unknown amount of 3% H2O2 and developed portal venous gas embolism. The child also experienced severe gastritis with hematemesis, but an EGD revealed no esophageal abnormalities.3

More serious complications have been reported from ingestion of concentrated forms of H2O2. A 40-year-old woman who ingested 2 mouthfuls of a 35% solution developed a portal gas embolism. She also suffered severe diffuse hemorrhagic gastritis with a normal esophagus.2 Gas emboli are not limited to the portal system. A 2-year-old male ingested four to six ounces of 35% H2O2 and died. He not only had portal air but also had a gas embolism in the right ventricle. As with the other cases reported, the patient had hemorrhagic gastritis with a normal esophagus.4 A 63-year-old who ingested 35% H2O2 developed neurological findings and was found to have multiple cerebral gas emboli. Once again, hemorrhagic gastric mucosa was present with a normal esophagus.1 Seizure and respiratory arrest were reported in a 33-year-old woman who ingested an unknown amount of 35% H2O2. Her gastric mucosa showed diffuse hemorrhages and edema with only mild erythema of the esophagus.6

The most common gastrointestinal injury that occurs after ingestion of concentrated H2O2 is in the stomach.11 There has been laboratory evidence of esophageal tissue injury in dogs when denture cleanser containing H2O2 was applied directly to the tissue,12 however, in our literature review only two clinical cases of mild esophageal erythema were reported after H2O2 ingestion. In one of these cases, only the lower esophageal sphincter was involved. 5, 6 All other cases showed only gastric injury.1-4, 8 Our case demonstrated not only gastric damage, but also severe esophageal injury with free air in the soft tissue around the esophagus. The emergency physician, toxicologist, gastroenterologist, and the surgeon all were suspicious of esophageal perforation, however, extensive surgery did not demonstrate any gross perforation. The possibility exists that the oxygen generated when the H2O2 came in contact with the esophageal mucosa escaped into the surrounding tissue directly through the extensive diffusely damaged esophageal wall. Another possible explanation is that the H2O2 entered the tissue first and then was catalyzed producing the gas in the soft tissue. There have been similar reports of free air seen under the diaphragm without a perforated viscous.1, 6 The reason for these findings remains unknown.

Toxicologists need to be aware that any patient who ingests H2O2 and is symptomatic requires a complete history and thorough physical exam. It is important to note that significant esophageal injury can occur in addition to gastric injury and vascular embolism. In addition to routine laboratory and radiographic exams, a soft tissue radiograph of the neck should be obtained in patients complaining of throat, neck, or upper chest pain, to screen for esophageal injury.

REFERENCES

  1. Ijichi T, Itoh T, Sakai R, et al: Multiple Brain Gas Embolism After Ingestion of Concentrated Hydrogen Peroxide. Neurology 1997;48:277-279.
  2. Luu TA, Kelley MT, Strauch JA, et al: Portal Vein Gas Embolism From Hydrogen Peroxide Ingestion. Annals of Emergency Medicine 1992;21:1391-1393.
  3. Rackoff WR, Merton DF: Gas Embolism After ingestion of Hydrogen Peroxide. Pediatrics 1990;85:593-594.
  4. Christensen DW, Faught WE, Black RE, et al: Fatal Oxygen Embolization After Hydrogen Peroxide Ingestion. Critical Care Medicine 1992;20:543-544.
  5. Jackson SB, Rusyniak DE, Mowry JR, et al: Troubles with Bubbles: Air Gas Embolus from Concentrated Hydrogen Peroxide Ingestion. Journal of Toxicology Clinical Toxicology 2001;39:521-522.
  6. Humberston CL, Dean BS, Krenzelok EP: Ingestion of 35% Hydrogen Peroxide. Clinical Toxicology 1990;28:95-100.
  7. Giberson TP, Kern JD, Pettigrew DW, et al: Near-Fatal Hydrogen Peroxide Ingestion. Annals of Emergency Medicine 1989;18:778-779.
  8. Dickson KF, Caravati EM: Hydrogen Peroxide Exposure - 325 Exposures Reported to a Regional Poison Control Center. Clinical Toxicology 1994;32:705-714.
  9. Henry MC, Wheeler J, Mofenson HC, et al: Hydrogen Peroxide 3% Exposures. Clinical Toxicology 1996;34:323-327.
  10. Cina SJ, Downs JCU, Conradi SE: Hydrogen Peroxide: A Source of Lethal Oxygen Embolism. The American Journal of Forensic Medicine and Pathology 1994;15:44-50.
  11. Douglass WC: Hydrogen Peroxide - Medical Miracle. Phoenix Arizona, Second Opinion Publishing, 1992, p6, 136-138
  12. Goldfrank LR, Flonnenbaum NE, Lewin NA, et al: Toxicologic Emergencies, ed 5. Norwalk Connecticut, Appleton and Lange, 1994, p1088-1089.
  13. Abramson AL: Corrosive Injury of the Esophagus. Archives of Otolaryngology 1978;104:514-516.


Journals Home  | Past Issues | Search | Send Comments to ACMTNet

Copyright 1999-2003, American College of Medical Toxicology.