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A 32-year-old man presents to the emergency department with mild throat pain, chest discomfort, and “abdominal fullness” after inadvertently ingesting concentrated hydrogen peroxide (35%).
A previously healthy 32-year-old man presented to the emergency department (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 included a blood pressure of 140/92 mm Hg; heart rate, 93 beats/min; respiratory rate, 18 breaths/min; and temperature, 96.4°F. His O2 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 FDA for any such purpose.3 When diluted sufficiently, this concoction is not harmful but is unlikely to provide any health benefits.
Continue reading for the toxic effects of concentrated hydrogen peroxide...
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%.
Continue reading for the case continuation...
CASE CONTINUATION
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 CT scan, which revealed the presence of extensive air throughout the portal venous system (see the figure).
DO ALL PATIENTS PRESENTING WITH H2O2 INGESTION REQUIRE IMAGING TO ASSESS FOR THE PRESENCE OF PORTAL VENOUS AIR?
Reportedly, ingestion of as little as a “sip” or “mouthful” of 35% H2O2 has resulted in venous and arterial gas embolism,6 occasionally with severe consequences, but no current consensus guidelines exist regarding imaging requirements. Some toxicologists and hyperbaric physicians believe that the presence of portal venous air does not adversely impact a patient’s prognosis or necessitate treatment, and therefore a work-up is unnecessary.
Others, however, suggest that the presence of portal venous air indicates oversaturation of oxygen in the blood, placing the patient at increased risk for cardiac and cerebral air embolism. Neither one of these theories is well supported in the literature. Although practice patterns vary by institution, it is reasonable that all patients presenting with abdominal complaints after ingestion of H2O2 undergo CT imaging to assess for portal venous air.
Continue reading to find out what to do if portal venous air is detected...
IF PORTAL VENOUS AIR IS DETECTED, DO PATIENTS REQUIRE HYPERBARIC OXYGEN THERAPY?
The management of patients with portal venous gas following H2O2 ingestion is controversial and has not been established. Hyperbaric oxygen therapy involves increasing the ambient pressure by several atmospheres inside a specially designed chamber—the same therapy used for diving-related bubble injury.
Hyperbaric therapy increases the amount of oxygen that can be dissolved in the blood, thereby decreasing bubble formation and allowing transport of dissolved oxygen to the lungs, where it can be exhaled. Some patients with portal venous air experience significant pain and portal venous hypertension, which may respond rapidly to this therapy.10
Based on available literature, hyperbaric therapy is reasonable for patients with significant abdominal pain and portal venous air following H2O2 ingestion; less controversial is the role of hyperbaric therapy in those with cerebral air embolism. Multiple case reports of patients with significant neurologic findings demonstrate resolution of symptoms following hyperbaric therapy.6
Continue reading for the case conclusion...
CASE CONCLUSION
Hyperbaric oxygen therapy was recommended for the patient in this case, but transfer to a hyperbaric facility was not possible. He was instead admitted to the hospital for continuous monitoring. Over the next 12 hours, his symptoms gradually resolved, and a repeat CT the following day showed complete resolution of the portal venous gas. The patient was subsequently discharged without any sequelae.
REFERENCES
1. Ukuku DO, Bari ML, Kawamoto S, Isshiki K. Use of hydrogen peroxide in combination with nisin, sodium lactate and citric acid for reducing transfer of bacterial pathogens from whole melon surfaces to fresh-cut pieces. Int J Food Microbiol. 2005;104(2):225-233.
2. 35% H2O2 hydrogen peroxide food grade certified benefits. The One Minute Miracle Web site. www.theoneminutemiracleinc.com/pages/h2o2-benefits/. Accessed January 20, 2013.
3. FDA. FDA warns consumers against drinking high-strength hydrogen peroxide for medicinal use: ingestion can lead to serious health risk and death [news release]. July 27, 2006. www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2006/ucm108701.htm. Accessed January 20, 2013.
4. Shaw A, Cooperman A, Fusco J. Gas embolism produced by hydrogen peroxide. N Engl J Med. 1967;277(5):238-241.
5. Cina SJ, Downs JC, Conradi SE. Hydrogen peroxide: a source of lethal oxygen embolism. Case report and review of the literature. Am J Forensic Med Pathol. 1994;15(1):44-50.
6. Rider SP, Jackson SB, Rusyniak DE. Cerebral air gas embolism from concentrated hydrogen peroxide ingestion. Clin Toxicol (Phila). 2008;46(9):815-818.
7. French LK, Horowitz BZ, McKeown NJ. Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature. Clin Toxicol (Phila). 2010;48(6):533-538.
8. Bassan MM, Dudai M, Shalev O. Near-fatal systemic oxygen embolism due to wound irrigation with hydrogen peroxide. Postgrad Med J. 1982;58(681):448-450.
9. Henry MC, Wheeler J, Mofenson HC, et al. Hydrogen peroxide 3% exposures. J Toxicol Clin Toxicol. 1996;34(3):323-327.
10. Papafragkou S, Gasparyan A, Batista R, Scott P. Treatment of portal venous gas embolism with hyperbaric oxygen after accidental ingestion of hydrogen peroxide: a case report and review of the literature. J Emerg Med. 2012;43(1):e21-e23
A 32-year-old man presents to the emergency department with mild throat pain, chest discomfort, and “abdominal fullness” after inadvertently ingesting concentrated hydrogen peroxide (35%).
A 32-year-old man presents to the emergency department with mild throat pain, chest discomfort, and “abdominal fullness” after inadvertently ingesting concentrated hydrogen peroxide (35%).
A previously healthy 32-year-old man presented to the emergency department (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 included a blood pressure of 140/92 mm Hg; heart rate, 93 beats/min; respiratory rate, 18 breaths/min; and temperature, 96.4°F. His O2 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 FDA for any such purpose.3 When diluted sufficiently, this concoction is not harmful but is unlikely to provide any health benefits.
Continue reading for the toxic effects of concentrated hydrogen peroxide...
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%.
Continue reading for the case continuation...
CASE CONTINUATION
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 CT scan, which revealed the presence of extensive air throughout the portal venous system (see the figure).
DO ALL PATIENTS PRESENTING WITH H2O2 INGESTION REQUIRE IMAGING TO ASSESS FOR THE PRESENCE OF PORTAL VENOUS AIR?
Reportedly, ingestion of as little as a “sip” or “mouthful” of 35% H2O2 has resulted in venous and arterial gas embolism,6 occasionally with severe consequences, but no current consensus guidelines exist regarding imaging requirements. Some toxicologists and hyperbaric physicians believe that the presence of portal venous air does not adversely impact a patient’s prognosis or necessitate treatment, and therefore a work-up is unnecessary.
Others, however, suggest that the presence of portal venous air indicates oversaturation of oxygen in the blood, placing the patient at increased risk for cardiac and cerebral air embolism. Neither one of these theories is well supported in the literature. Although practice patterns vary by institution, it is reasonable that all patients presenting with abdominal complaints after ingestion of H2O2 undergo CT imaging to assess for portal venous air.
Continue reading to find out what to do if portal venous air is detected...
IF PORTAL VENOUS AIR IS DETECTED, DO PATIENTS REQUIRE HYPERBARIC OXYGEN THERAPY?
The management of patients with portal venous gas following H2O2 ingestion is controversial and has not been established. Hyperbaric oxygen therapy involves increasing the ambient pressure by several atmospheres inside a specially designed chamber—the same therapy used for diving-related bubble injury.
Hyperbaric therapy increases the amount of oxygen that can be dissolved in the blood, thereby decreasing bubble formation and allowing transport of dissolved oxygen to the lungs, where it can be exhaled. Some patients with portal venous air experience significant pain and portal venous hypertension, which may respond rapidly to this therapy.10
Based on available literature, hyperbaric therapy is reasonable for patients with significant abdominal pain and portal venous air following H2O2 ingestion; less controversial is the role of hyperbaric therapy in those with cerebral air embolism. Multiple case reports of patients with significant neurologic findings demonstrate resolution of symptoms following hyperbaric therapy.6
Continue reading for the case conclusion...
CASE CONCLUSION
Hyperbaric oxygen therapy was recommended for the patient in this case, but transfer to a hyperbaric facility was not possible. He was instead admitted to the hospital for continuous monitoring. Over the next 12 hours, his symptoms gradually resolved, and a repeat CT the following day showed complete resolution of the portal venous gas. The patient was subsequently discharged without any sequelae.
REFERENCES
1. Ukuku DO, Bari ML, Kawamoto S, Isshiki K. Use of hydrogen peroxide in combination with nisin, sodium lactate and citric acid for reducing transfer of bacterial pathogens from whole melon surfaces to fresh-cut pieces. Int J Food Microbiol. 2005;104(2):225-233.
2. 35% H2O2 hydrogen peroxide food grade certified benefits. The One Minute Miracle Web site. www.theoneminutemiracleinc.com/pages/h2o2-benefits/. Accessed January 20, 2013.
3. FDA. FDA warns consumers against drinking high-strength hydrogen peroxide for medicinal use: ingestion can lead to serious health risk and death [news release]. July 27, 2006. www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2006/ucm108701.htm. Accessed January 20, 2013.
4. Shaw A, Cooperman A, Fusco J. Gas embolism produced by hydrogen peroxide. N Engl J Med. 1967;277(5):238-241.
5. Cina SJ, Downs JC, Conradi SE. Hydrogen peroxide: a source of lethal oxygen embolism. Case report and review of the literature. Am J Forensic Med Pathol. 1994;15(1):44-50.
6. Rider SP, Jackson SB, Rusyniak DE. Cerebral air gas embolism from concentrated hydrogen peroxide ingestion. Clin Toxicol (Phila). 2008;46(9):815-818.
7. French LK, Horowitz BZ, McKeown NJ. Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature. Clin Toxicol (Phila). 2010;48(6):533-538.
8. Bassan MM, Dudai M, Shalev O. Near-fatal systemic oxygen embolism due to wound irrigation with hydrogen peroxide. Postgrad Med J. 1982;58(681):448-450.
9. Henry MC, Wheeler J, Mofenson HC, et al. Hydrogen peroxide 3% exposures. J Toxicol Clin Toxicol. 1996;34(3):323-327.
10. Papafragkou S, Gasparyan A, Batista R, Scott P. Treatment of portal venous gas embolism with hyperbaric oxygen after accidental ingestion of hydrogen peroxide: a case report and review of the literature. J Emerg Med. 2012;43(1):e21-e23
A previously healthy 32-year-old man presented to the emergency department (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 included a blood pressure of 140/92 mm Hg; heart rate, 93 beats/min; respiratory rate, 18 breaths/min; and temperature, 96.4°F. His O2 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 FDA for any such purpose.3 When diluted sufficiently, this concoction is not harmful but is unlikely to provide any health benefits.
Continue reading for the toxic effects of concentrated hydrogen peroxide...
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%.
Continue reading for the case continuation...
CASE CONTINUATION
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 CT scan, which revealed the presence of extensive air throughout the portal venous system (see the figure).
DO ALL PATIENTS PRESENTING WITH H2O2 INGESTION REQUIRE IMAGING TO ASSESS FOR THE PRESENCE OF PORTAL VENOUS AIR?
Reportedly, ingestion of as little as a “sip” or “mouthful” of 35% H2O2 has resulted in venous and arterial gas embolism,6 occasionally with severe consequences, but no current consensus guidelines exist regarding imaging requirements. Some toxicologists and hyperbaric physicians believe that the presence of portal venous air does not adversely impact a patient’s prognosis or necessitate treatment, and therefore a work-up is unnecessary.
Others, however, suggest that the presence of portal venous air indicates oversaturation of oxygen in the blood, placing the patient at increased risk for cardiac and cerebral air embolism. Neither one of these theories is well supported in the literature. Although practice patterns vary by institution, it is reasonable that all patients presenting with abdominal complaints after ingestion of H2O2 undergo CT imaging to assess for portal venous air.
Continue reading to find out what to do if portal venous air is detected...
IF PORTAL VENOUS AIR IS DETECTED, DO PATIENTS REQUIRE HYPERBARIC OXYGEN THERAPY?
The management of patients with portal venous gas following H2O2 ingestion is controversial and has not been established. Hyperbaric oxygen therapy involves increasing the ambient pressure by several atmospheres inside a specially designed chamber—the same therapy used for diving-related bubble injury.
Hyperbaric therapy increases the amount of oxygen that can be dissolved in the blood, thereby decreasing bubble formation and allowing transport of dissolved oxygen to the lungs, where it can be exhaled. Some patients with portal venous air experience significant pain and portal venous hypertension, which may respond rapidly to this therapy.10
Based on available literature, hyperbaric therapy is reasonable for patients with significant abdominal pain and portal venous air following H2O2 ingestion; less controversial is the role of hyperbaric therapy in those with cerebral air embolism. Multiple case reports of patients with significant neurologic findings demonstrate resolution of symptoms following hyperbaric therapy.6
Continue reading for the case conclusion...
CASE CONCLUSION
Hyperbaric oxygen therapy was recommended for the patient in this case, but transfer to a hyperbaric facility was not possible. He was instead admitted to the hospital for continuous monitoring. Over the next 12 hours, his symptoms gradually resolved, and a repeat CT the following day showed complete resolution of the portal venous gas. The patient was subsequently discharged without any sequelae.
REFERENCES
1. Ukuku DO, Bari ML, Kawamoto S, Isshiki K. Use of hydrogen peroxide in combination with nisin, sodium lactate and citric acid for reducing transfer of bacterial pathogens from whole melon surfaces to fresh-cut pieces. Int J Food Microbiol. 2005;104(2):225-233.
2. 35% H2O2 hydrogen peroxide food grade certified benefits. The One Minute Miracle Web site. www.theoneminutemiracleinc.com/pages/h2o2-benefits/. Accessed January 20, 2013.
3. FDA. FDA warns consumers against drinking high-strength hydrogen peroxide for medicinal use: ingestion can lead to serious health risk and death [news release]. July 27, 2006. www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2006/ucm108701.htm. Accessed January 20, 2013.
4. Shaw A, Cooperman A, Fusco J. Gas embolism produced by hydrogen peroxide. N Engl J Med. 1967;277(5):238-241.
5. Cina SJ, Downs JC, Conradi SE. Hydrogen peroxide: a source of lethal oxygen embolism. Case report and review of the literature. Am J Forensic Med Pathol. 1994;15(1):44-50.
6. Rider SP, Jackson SB, Rusyniak DE. Cerebral air gas embolism from concentrated hydrogen peroxide ingestion. Clin Toxicol (Phila). 2008;46(9):815-818.
7. French LK, Horowitz BZ, McKeown NJ. Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature. Clin Toxicol (Phila). 2010;48(6):533-538.
8. Bassan MM, Dudai M, Shalev O. Near-fatal systemic oxygen embolism due to wound irrigation with hydrogen peroxide. Postgrad Med J. 1982;58(681):448-450.
9. Henry MC, Wheeler J, Mofenson HC, et al. Hydrogen peroxide 3% exposures. J Toxicol Clin Toxicol. 1996;34(3):323-327.
10. Papafragkou S, Gasparyan A, Batista R, Scott P. Treatment of portal venous gas embolism with hyperbaric oxygen after accidental ingestion of hydrogen peroxide: a case report and review of the literature. J Emerg Med. 2012;43(1):e21-e23
