CASE REPORT
gas embolism hydrogen peroxide
Portal Vein Gas Embolism From Hydrogen Peroxide Ingestion From the Department of Emergency _Medicine, The Ohio State University Hospitals;* Central Ohio Poison Center, Children's Hospital;t and Department of Surgery, Riverside Methodist Hospitals,¢ Columbus, Ohio. Received for publication February 24, 1992. Revision received May 6, 1992. Accepted for publication May 29, 1992.
Tuan A Luu, MD* Michael T Kelley, MD *t Jean A Strauch, RNt Konstantine Avradopoulos, MD~
A 40-year-old woman who ingested a 35% hydrogen peroxide solution presented to the emergency department with abdominal pain. Acute abdominal series showed gas in the portal vein system. The patient was admitted and treated conservatively. She was released after five days in the hospital with no major sequelae. [Luu TA, Kelley MT, Strauch JA, Avradopoulos K: Portal vein gas embolism from hydrogen peroxide ingestion. Ann EmergMed November 1992;21:1391-1393.] INTRODUCTION Hydrogen peroxide is a fairly common household product. A 3% solution is available over the counter and is used as a disinfectant and deodorant. Higher percentages, up to 85%, are also available for industrial use, as bleaching or oxidizing agents. Concentrated hydrogen peroxide also is promoted as a health aide to be used in "hyperoxygen" t h e r a p y J Hydrogen peroxide releases oxygen and water when it makes contact with organic tissue. 2 We r e p o r t the case of a 40-year-old woman who accidentally ingested two mouthfuls of 35% hydrogen peroxide, which p r o d u c e d gas embolism of the portal veins.
CASE
REPORT
The patient r e p o r t e d mistakenly drinldng two mouthfuls of a liquid that she thought was water from a clear plastic container in her refrigerator. She stated that she did not experience any adverse effects until after the second swallow, when she noticed epigastric pain and gas escaping from her nostrils. She then re-examined the label of the bottle and realized that it was H202 instead of H20. The hydrogen peroxide was stored in the refrigerator by one of her relatives who ingested two drops a day for "hyperoxygen" therapy. The relative h a d p u r c h a s e d the 35% hydrogen peroxide in a health food store. The patient contacted the emergency medical service system, was administered about 200 mL of milk by mouth, and was t r a n s p o r t e d to the emergency department. On presentation, the patient's vital signs were blood pressure of 108/80 mm Hg; temperature, 36.9 C; pulse on room air, 80; and respirations, 20. Oxygen saturation by pulse oximeter was 100%. Her main complaint was a b u r n -
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GAS EMBOLISM Luu et al
I
ing sensation in her throat, epigastrium, and substernal area. She r e p o r t e d vomiting twice soon after the ingestion and complained of persisting nausea. She denied shortness of breath or hematemesis. She was not taking any medications and reported no allergies. Her medical history was significant 0nly for irritable bowel syndrome. On physical examination, the patient's oral p h a r y n x was without blisters or erythema. H e r lungs were clear to auscultation. Her cardiac examination was normal. Her abdomen was soft and nondistended. Bowel sounds were present, and she was moderately tender in the epigastric area. The remainder of her examination was unremarkablc. L a b o r a t o r y results for serum electrolytes, coagulation, liver enzymes, and CBC were within normal limits. The treating physician gave the patient approximately 100 mL of water to drink, after which she complained of a sharp pain in her stomach. The treating physician then passed a nasogastric tube to decompress her stomach and check the p H of the gastric contents. The p H was 6, and the gastric contents were Gastroccult ® positive. Esophagealgastroduodenal endoscopy performed in the ED showed severe diffuse hemorrhagic gastritis. The hypopharynx, o r o p h a r y n x , esophagus, and duodenum were normal. The endoscopist aspirated as much fluid out of the stomach as possible during the procedure. An acute abdominal series obtained before the endoscopy showed a large amount of gas in the stomach and gas in the venous system throughout the liver including the left lobe. (The p e r i p h e r a l pattern of gas distribution in the liver indicated that the gas was in the portal venous system and was consistent with the direction of blood flow. In contrast, a biliary gas p a t t e r n would concentrate centrally because of the flow characteristics of bile.) The r a d i o g r a p h also revealed retroperitoneal gas along the psoas muscles and gas in the stomach wall (Figure). The patient was admitted to a monitored bed; administered nothing by mouth; and started on IV antibiotics, corticosteroids,
Figure. Flat (.4) and upright (B) views of the abdomen. The liver portal system is well delineated by gas. Retroperitoneal gas can also be seen along paraspiual muscles.
NOVEMBER 1992
21:1
ANNALSOF EMERGENCY MEDICINE
and cinletidine. Serial abdonfinal examinations were performed, and an acute abdominal series was done every 12 hours. The patient's gastric burning sensation subsided after 24 hours. Her leukocyte count returned to normal, and her hemoglobin and hematocrit remained stable. The subsequent abdominal radiographs showed complete resolution of the p o r t a l vein and retroperitoneal gas by 24 hours. The patient began tolerating oral intake by day 3 of her hospital stay. She had another endoscopic study before discharge, which showed subsiding gastritis. Liver enzymes and p r o t h r o m b i n time were normal before her discharge. She went home after five days in good condition on cimetidine. DISCUSSION
Hydrogen peroxide is a cleat-, colorless liquid. It decomposes into water and oxygen on contact with organic tissue, some metals, and alkaline solutions. A 35% solution contains 35% hydrogen peroxide in an aqueous solution with a stabilizing agent. One milliliter of hydrogen peroxide solution can release about 115 mL of oxygen. High concentrations of hydrogen peroxide are caustic to the skin and mucous membranes and can result in a white eschar. 2 The 1990 Annual Report of the American Association of Poison Control Centers listed 10,140 r e p o r t e d cases of hydrogen peroxide ingestion; most were accidental. About one third of the cases were in persons older than 17 years. One fatality occurred in a 2-year-old boy who ingested an unknown amount of 35% hydrogen peroxide that was used to treat raw- milk for drinking. 3 In our case, a relative of the patient used the hydrogen peroxide to "hyperoxygenate" himself. Because the m a n u f a c t u r e r of that p r o d u c t recommends that this high-concentration solution be refrigerated, the potential for accidental ingestion is increased. There have been other reports of fatal ingestion with high concentrations of hydrogen peroxide in children.a, 5 In these cases, death usually was caused by respiratory complications. Ingestion of high-concentration hydrogen peroxide in adults usually is not fatal but often requires hospitahzation.6, 7 A low-concentration (3%) hydrogen peroxide ingestion in a child also caused gas embolism to the p o r t a l venous system. The child was observed, discharged home with oral antibiotics, and reportedly had no sequelae. 8 Hydrogen peroxide, administered under pressure, has been reported to cause subcutaneous gas. No adverse sequelae were observed. 9 Other uses of hydrogen peroxide have produced more severe consequences. 9-11 Small bowel perforation, coma, and respir a t o r y distress have been attributed to gas embolism after irrigation of wounds with hydrogen peroxide. The patient in this r e p o r t d r a n k approximately 60 mL of a 35% hydrogen peroxide solution. This relatively small amount of hydrogen peroxide could release 6.9 L of oxygen in the stomach. Some of this oxygen escaped through the esophagus as reported by the patient. Oxygen also could have been forced into the duodenum; diffuse, small bowel gas was noted on the abdominal radiograph. The portal venous gas seen in
1392/!31
GAS E M B O L I S M L u u et al
this patient could have resulted from oxygen forced into the gastric circulation through the bleeding vessels damaged by the caustic effects of the hydrogen peroxide. Oxygen has been shown to be absorbed by mesenteric circulation after irrigation by 0.75% or higher hydrogen peroxide solution even without mncosal interruption. 9 Anothei~ mechanism to explain the portal venous gas pattern would be direct absorption of hydrogen peroxide with subsequent release of oxygen. Diffusion of hydrogen peroxide into the surrounding tissues could account for the retroperitoneal gas. Fortunately, this patient recovered without any serious sequelae. However, had her clinical picture been worse at the initial presentation, hyperbaric oxygen therapy might have been therapeutic. Hyperbaric oxygen therapy theoretically would be able to decrease the size of the gas emboli and provide benefits similar to those achieved in the treatment of diving accidents. SUMMARY
We present a case of portal vein gas embolism resulting from ingestion of 35% hydrogen peroxide. The patient recovered with nfinor sequelae. With the availability of this substance, other accidental or intentional ingestions should be treated appropriately. Hyperbaric oxygenation may be of benefit in patients with respiratory compromise or central nervous system symptoms from gas embolism in hydrogen peroxide ingestion.
132/1393
REFERENCES 1. Department of Health and Human Services: Newsletter, P89-18,United States Food and Drug Administration Federal-States Relations, Rockville, Maryland, April 1989. 2. Reynolds JEF, Parfitt K, Parsons AV, et at: The Extra Pharmacopeia, ed 29. London, The Pharmaceutical Press, 1989,p 1578-1579. 3. Litovitz TL, Bailey KM, Schmitz BF, et al: 1990Annual Report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1991;9:461-509. 4. Giusti GV: Fatal poisoning with hydrogen peroxide. Forens Sci1973;2:99-100. 5. Zecevic D, 6asparec Z: Death caused by hydrogen peroxide. ZRechtsmed1979;84:5759. 6. Humberston CL, Dean BS, Krenzelok EP: Ingestion of 35% hydrogen peroxide. J Toxicol Clin Toxico11990;28:95-100. 7.6iberson TP, Kern JD, Pettigrew DW, et al: Near-fatal hydrogen peroxide ingestion. Ann Emerg Med 1989;18:778-779. 8. Rackoff WR, Merton DF: Gas embolism after ingestion of hydrogen peroxide. Pediatrics 1990;85:593-594. 9. Shaw A, CoopermanA, Fusco J: Gas emborism produced by peroxide. NEnglJMed 1967;277:238-241. 10. Bassan MM, Duda[ M, Shalev O: Near-fatal systemic oxygen embolism due to wound irrigation with hydrogen peroxide. PostgradMedJ 1982;58:448-450. 11. Sleigh JW, Linter SPK: Hazards of hydrogen peroxide. Br Med J 1985;291:1706, Address for reprints: Michael T Kelley, MD Children's Hospital Pharmacology/Toxicology 700 Children's Drive Columbus, Ohio 43205
ANNALS OF EMERGENCY MEDICINE 21:11 NOVEMBER1992
gas embolism hydrogen peroxide
Portal Vein Gas Embolism From Hydrogen Peroxide Ingestion From the Department of Emergency _Medicine, The Ohio State University Hospitals;* Central Ohio Poison Center, Children's Hospital;t and Department of Surgery, Riverside Methodist Hospitals,¢ Columbus, Ohio. Received for publication February 24, 1992. Revision received May 6, 1992. Accepted for publication May 29, 1992.
Tuan A Luu, MD* Michael T Kelley, MD *t Jean A Strauch, RNt Konstantine Avradopoulos, MD~
A 40-year-old woman who ingested a 35% hydrogen peroxide solution presented to the emergency department with abdominal pain. Acute abdominal series showed gas in the portal vein system. The patient was admitted and treated conservatively. She was released after five days in the hospital with no major sequelae. [Luu TA, Kelley MT, Strauch JA, Avradopoulos K: Portal vein gas embolism from hydrogen peroxide ingestion. Ann EmergMed November 1992;21:1391-1393.] INTRODUCTION Hydrogen peroxide is a fairly common household product. A 3% solution is available over the counter and is used as a disinfectant and deodorant. Higher percentages, up to 85%, are also available for industrial use, as bleaching or oxidizing agents. Concentrated hydrogen peroxide also is promoted as a health aide to be used in "hyperoxygen" t h e r a p y J Hydrogen peroxide releases oxygen and water when it makes contact with organic tissue. 2 We r e p o r t the case of a 40-year-old woman who accidentally ingested two mouthfuls of 35% hydrogen peroxide, which p r o d u c e d gas embolism of the portal veins.
CASE
REPORT
The patient r e p o r t e d mistakenly drinldng two mouthfuls of a liquid that she thought was water from a clear plastic container in her refrigerator. She stated that she did not experience any adverse effects until after the second swallow, when she noticed epigastric pain and gas escaping from her nostrils. She then re-examined the label of the bottle and realized that it was H202 instead of H20. The hydrogen peroxide was stored in the refrigerator by one of her relatives who ingested two drops a day for "hyperoxygen" therapy. The relative h a d p u r c h a s e d the 35% hydrogen peroxide in a health food store. The patient contacted the emergency medical service system, was administered about 200 mL of milk by mouth, and was t r a n s p o r t e d to the emergency department. On presentation, the patient's vital signs were blood pressure of 108/80 mm Hg; temperature, 36.9 C; pulse on room air, 80; and respirations, 20. Oxygen saturation by pulse oximeter was 100%. Her main complaint was a b u r n -
130/1391
ANNALSOF EMERGENCYMEDICINE 21:11 NOVEMBER1992
GAS EMBOLISM Luu et al
I
ing sensation in her throat, epigastrium, and substernal area. She r e p o r t e d vomiting twice soon after the ingestion and complained of persisting nausea. She denied shortness of breath or hematemesis. She was not taking any medications and reported no allergies. Her medical history was significant 0nly for irritable bowel syndrome. On physical examination, the patient's oral p h a r y n x was without blisters or erythema. H e r lungs were clear to auscultation. Her cardiac examination was normal. Her abdomen was soft and nondistended. Bowel sounds were present, and she was moderately tender in the epigastric area. The remainder of her examination was unremarkablc. L a b o r a t o r y results for serum electrolytes, coagulation, liver enzymes, and CBC were within normal limits. The treating physician gave the patient approximately 100 mL of water to drink, after which she complained of a sharp pain in her stomach. The treating physician then passed a nasogastric tube to decompress her stomach and check the p H of the gastric contents. The p H was 6, and the gastric contents were Gastroccult ® positive. Esophagealgastroduodenal endoscopy performed in the ED showed severe diffuse hemorrhagic gastritis. The hypopharynx, o r o p h a r y n x , esophagus, and duodenum were normal. The endoscopist aspirated as much fluid out of the stomach as possible during the procedure. An acute abdominal series obtained before the endoscopy showed a large amount of gas in the stomach and gas in the venous system throughout the liver including the left lobe. (The p e r i p h e r a l pattern of gas distribution in the liver indicated that the gas was in the portal venous system and was consistent with the direction of blood flow. In contrast, a biliary gas p a t t e r n would concentrate centrally because of the flow characteristics of bile.) The r a d i o g r a p h also revealed retroperitoneal gas along the psoas muscles and gas in the stomach wall (Figure). The patient was admitted to a monitored bed; administered nothing by mouth; and started on IV antibiotics, corticosteroids,
Figure. Flat (.4) and upright (B) views of the abdomen. The liver portal system is well delineated by gas. Retroperitoneal gas can also be seen along paraspiual muscles.
NOVEMBER 1992
21:1
ANNALSOF EMERGENCY MEDICINE
and cinletidine. Serial abdonfinal examinations were performed, and an acute abdominal series was done every 12 hours. The patient's gastric burning sensation subsided after 24 hours. Her leukocyte count returned to normal, and her hemoglobin and hematocrit remained stable. The subsequent abdominal radiographs showed complete resolution of the p o r t a l vein and retroperitoneal gas by 24 hours. The patient began tolerating oral intake by day 3 of her hospital stay. She had another endoscopic study before discharge, which showed subsiding gastritis. Liver enzymes and p r o t h r o m b i n time were normal before her discharge. She went home after five days in good condition on cimetidine. DISCUSSION
Hydrogen peroxide is a cleat-, colorless liquid. It decomposes into water and oxygen on contact with organic tissue, some metals, and alkaline solutions. A 35% solution contains 35% hydrogen peroxide in an aqueous solution with a stabilizing agent. One milliliter of hydrogen peroxide solution can release about 115 mL of oxygen. High concentrations of hydrogen peroxide are caustic to the skin and mucous membranes and can result in a white eschar. 2 The 1990 Annual Report of the American Association of Poison Control Centers listed 10,140 r e p o r t e d cases of hydrogen peroxide ingestion; most were accidental. About one third of the cases were in persons older than 17 years. One fatality occurred in a 2-year-old boy who ingested an unknown amount of 35% hydrogen peroxide that was used to treat raw- milk for drinking. 3 In our case, a relative of the patient used the hydrogen peroxide to "hyperoxygenate" himself. Because the m a n u f a c t u r e r of that p r o d u c t recommends that this high-concentration solution be refrigerated, the potential for accidental ingestion is increased. There have been other reports of fatal ingestion with high concentrations of hydrogen peroxide in children.a, 5 In these cases, death usually was caused by respiratory complications. Ingestion of high-concentration hydrogen peroxide in adults usually is not fatal but often requires hospitahzation.6, 7 A low-concentration (3%) hydrogen peroxide ingestion in a child also caused gas embolism to the p o r t a l venous system. The child was observed, discharged home with oral antibiotics, and reportedly had no sequelae. 8 Hydrogen peroxide, administered under pressure, has been reported to cause subcutaneous gas. No adverse sequelae were observed. 9 Other uses of hydrogen peroxide have produced more severe consequences. 9-11 Small bowel perforation, coma, and respir a t o r y distress have been attributed to gas embolism after irrigation of wounds with hydrogen peroxide. The patient in this r e p o r t d r a n k approximately 60 mL of a 35% hydrogen peroxide solution. This relatively small amount of hydrogen peroxide could release 6.9 L of oxygen in the stomach. Some of this oxygen escaped through the esophagus as reported by the patient. Oxygen also could have been forced into the duodenum; diffuse, small bowel gas was noted on the abdominal radiograph. The portal venous gas seen in
1392/!31
GAS E M B O L I S M L u u et al
this patient could have resulted from oxygen forced into the gastric circulation through the bleeding vessels damaged by the caustic effects of the hydrogen peroxide. Oxygen has been shown to be absorbed by mesenteric circulation after irrigation by 0.75% or higher hydrogen peroxide solution even without mncosal interruption. 9 Anothei~ mechanism to explain the portal venous gas pattern would be direct absorption of hydrogen peroxide with subsequent release of oxygen. Diffusion of hydrogen peroxide into the surrounding tissues could account for the retroperitoneal gas. Fortunately, this patient recovered without any serious sequelae. However, had her clinical picture been worse at the initial presentation, hyperbaric oxygen therapy might have been therapeutic. Hyperbaric oxygen therapy theoretically would be able to decrease the size of the gas emboli and provide benefits similar to those achieved in the treatment of diving accidents. SUMMARY
We present a case of portal vein gas embolism resulting from ingestion of 35% hydrogen peroxide. The patient recovered with nfinor sequelae. With the availability of this substance, other accidental or intentional ingestions should be treated appropriately. Hyperbaric oxygenation may be of benefit in patients with respiratory compromise or central nervous system symptoms from gas embolism in hydrogen peroxide ingestion.
132/1393
REFERENCES 1. Department of Health and Human Services: Newsletter, P89-18,United States Food and Drug Administration Federal-States Relations, Rockville, Maryland, April 1989. 2. Reynolds JEF, Parfitt K, Parsons AV, et at: The Extra Pharmacopeia, ed 29. London, The Pharmaceutical Press, 1989,p 1578-1579. 3. Litovitz TL, Bailey KM, Schmitz BF, et al: 1990Annual Report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1991;9:461-509. 4. Giusti GV: Fatal poisoning with hydrogen peroxide. Forens Sci1973;2:99-100. 5. Zecevic D, 6asparec Z: Death caused by hydrogen peroxide. ZRechtsmed1979;84:5759. 6. Humberston CL, Dean BS, Krenzelok EP: Ingestion of 35% hydrogen peroxide. J Toxicol Clin Toxico11990;28:95-100. 7.6iberson TP, Kern JD, Pettigrew DW, et al: Near-fatal hydrogen peroxide ingestion. Ann Emerg Med 1989;18:778-779. 8. Rackoff WR, Merton DF: Gas embolism after ingestion of hydrogen peroxide. Pediatrics 1990;85:593-594. 9. Shaw A, CoopermanA, Fusco J: Gas emborism produced by peroxide. NEnglJMed 1967;277:238-241. 10. Bassan MM, Duda[ M, Shalev O: Near-fatal systemic oxygen embolism due to wound irrigation with hydrogen peroxide. PostgradMedJ 1982;58:448-450. 11. Sleigh JW, Linter SPK: Hazards of hydrogen peroxide. Br Med J 1985;291:1706, Address for reprints: Michael T Kelley, MD Children's Hospital Pharmacology/Toxicology 700 Children's Drive Columbus, Ohio 43205
ANNALS OF EMERGENCY MEDICINE 21:11 NOVEMBER1992
