Multiple brain gas
embolism after
ingestion of
concentrated
hydrogen peroxide

Article abstract-We present a 63-year-old man who developed multiple
brain infarction after ingesting a 35% hydrogen peroxide solution. Neurologic
examination revealed left hemiparesis, primarily affecting the lower limb,
and mild weakness of the right lower limb. Gadolinium-enhanced MRI revealed patchy bilateral brain lesions. Oxygen gas embolization is the likely
cause of the brain infarctions.
NEUROLOGY 1997:48:277-279

T. Ijichi, MD; T. Itoh, MD; R. Sakai, MD; K. Nakaji, MD; T. Miyauchi, MD; R. Takahashi, MD;
S. Kadosaka, MD; M. Hirata, MD; S. Yoneda, MD; Y. Kajita, MD; and Y. Fujita, MD

Concentrated hydrogen peroxide solution, an industrial bleaching or oxidizing agent, is a clear and
odorless ubiquitous liquid used in many industries.
Accidental exposures to the solution sometimes occur. Because the main route of exposure is
inge~tion,'.~
gastrointestinal tract involvement is the
most common ~omplication.~
Although there have
been reports of brain inv~lvement,'.~,~
only one case
report has documented neuroimaging findings.6 We
report a patient who developed multiple brain infarction with unusual MRI findings after ingestion of
concentrated hydrogen peroxide.
Case report. A 63-year-old left-handed man was working in a brewery as a seasonal laborer when he unintentionally ingested three cups of 35% hydrogen peroxide (approximately 120 ml) stored in a Japanese rice wine bottle
in the factory kitchen. His past medical history was notable only for partial gastrectomy for gastric ulcer a t the age
of 57 years.
Soon after the ingestion, the patient vomited three
times and complained of general malaise and was taken to
our emergency room. He arrived approximately 45 minutes
after the ingestion. On presentation, the patient's consciousness level was decreased (Glasgow Coma Scale score
of 5). Vital signs were as follows: blood pressure 164/112
mm Hg, pulse 100/min, respiratory rate 18 breathdmin,
and body temperature 36.0" C. Subcutaneous emphysema
was not noted. The patient's lungs were clear and heart
sounds were normal; the abdomen was slightly distended.
Complete neurologic examination could not be performed
because of the patient's decreased level of consciousness.
Routine blood test results were normal except for a slight
increase in the serum glucose and liver enzyme concentrations. Arterial blood gas analysis showed pH 7.463, PCO,
39.0 Torr, and PO, 69.6 Torr.
Radiographs of the abdomen and chest revealed a
crescent-shaped region of air under the left diaphragm,
suggesting intra-abdominal free air (figure 1).Preoperative esophagogastroduodenoscopy 1 hour later showed diffuse hemorrhage of the gastric mucosa. The esophagus and
duodenum appeared normal. At laparotomy 5 hours after
the ingestion, severe erythema, edema, and emphysema of
the gastric serosa were noted; however, a visible perforation was not detected.
The patient's level of consciousness gradually improved.
On the fifth hospital day, the patient became alert and
complained of numbness of the extremities. Neurologic examination demonstrated a left hemiparesis predominantly

affecting the lower limb while sparing the face and a mild
weakness of right lower limb. A left Babinski sign was
present. Unenhanced axial brain MRI on the tenth hospital day showed patchy areas of low intensity on TIweighted images and high intensity on T,-weighted images, mainly in the gray matter of the frontal and parietal
lobes bilaterally. Five days later, a coronal MRI with gadolinium demonstrated multiple enhancing lesions in the
premotor, motor, and sensory cortices bilaterally (figure 2,
A through C). Although the abdominal symptoms had rapidly improved, recovery from the neurologic deficits was
only partial. Four weeks later, follow-up MRI revealed that
the gadolinium-enhancing lesion had almost disappeared
(figure 2, D through F). The TI-weighted images showed
low intensity in some areas previously enhancing.

Discussion. There are multiple reports of oxygen
embolization associated with the use of dilute hydrogen peroxide to irrigate tissues during ~ u r g e r y ,but
~-~
ingestion of the dilute form is usually benign. Ingestion of industrial-strength hydrogen peroxide can
cause venous or arterial oxygen embolization. 1,3,4,6
Giberson et al.' reported a case of embolic brain injury in an adult woman who ingested an unknown
volume of 35% hydrogen peroxide. Christensen et al.3
described portal venous and possible cerebral venous
oxygen embolization in a 2-year-old boy who ingested
4 to 6 ounces of 35% hydrogen peroxide. They
showed a chest radiograph demonstrating gas in the
portal venous system and documented marked diffuse cerebral edema with cerebellar and uncal tonsillar notching on autopsy, suggesting the presence of
severe brain venous oxygen embolism. Sherman et
al.'j reported a case of multiple brain infarction documented by neuroimaging in an elderly man who had
ingested 30 ml of 35% hydrogen peroxide. Brain MRI
in this patient showed the characteristic distribution
of lesions consistent with brain gas embolism.
The clinical signs in our patient were consistent
with bihemispheric brain infarction. The patchy distribution of the brain infarction and the predominance of lesions in the gray matter with relatively
sparing of the white matter as shown by TI-and
T,-weighted MRI of our patient is consistent with
brain arterial gas embolism.1° Moreover, the presence of enhancing lesions on brain MRI on the 15th
hospital day and the resolution of the enhancement
on subsequent MRI suggest that these lesions were
Copyright 0 1997 by the American Academy of Neurology 277

Figure 1. Chest radiograph demonstrating a crescentshaped region of gas under the left diaphragm (arrowheads).

subacute. The distribution of the lesions favoring
parasagittal areas is well correlated with the predominant lower limb paresis. Thus, we propose that
the multiple foci of brain infarction in our patient
were due to oxygen gas embolization after ingestion
of concentrated hydrogen peroxide solution. This
may be the first report demonstrating gadoliniumenhancing MRI lesions produced by brain gas embolism.
One hundred twenty milliliters of 35% hydrogen
peroxide can release about 14 liters of oxygen gas on
contact with organic tissue in the presence of catalase.2 Although our patient vomited soon after the
ingestion, a sufficient amount of hydrogen peroxide
could have entered into the blood vessels through the

erosive stomach mucosa as noted during esophagogastroduodenoscopy. We speculate that a substantial
amount of hydrogen peroxide was catalyzed in the
blood vessels or the tissue as evidenced by the presence of subdiaphragmatic air and subserosal emphysema without visible perforation during laparotomy.
Previous reports proposed at least three mechanisms of oxygen gas embolization due to hydrogen
peroxide. First, oxygen bubbles are formed in or
brought into right atrium or ventricle by way of the
portal system.3 These bubbles may move to left
atrium through a patent foramen ovale, causing arterial oxygen gas embolization. Second, pulmonary
aspiration of hydrogen peroxide can cause direct arterial oxygen gas embolization.6 Third, undissociated
hydrogen peroxide absorbed in the gastrointestinal
system may catalyze in the arterial circulation after
crossing the lung, causing arterial oxygen gas embolization.6 In our patient, the last mechanism seems
the most plausible, because he did not develop circulatory or respiratory failure during his clinical
course.
Although there have been no reports concerning
hyperbaric therapy for the treatment of brain oxygen
gas embolism caused by hydrogen peroxide, theoretically it should decrease the bubble size as suggested
by some author^.^,^ Armon et al.") emphasized that
this therapy is effective for brain air embolism complicating cardiac surgery even if administered during
the subacute phase. In addition to hyperbaric therapy, vasodilators, such as prostaglandin El analogues, may be beneficial to remove oxygen bubbles
in arterioles.
Our case re-emphasizes the hazard of concentrated hydrogen peroxide solution and suggests that
physicians should be alert to the possibility of CNS
involvement in patients after ingestion. As suggested
by previous report^,^.^ the accident of our patient
could have been avoided if the solution was stored
appropriately. Therefore, we further recommend that
concentrated hydrogen peroxide solution should have

Figure 2. Gadolinium-enhanced
brain MRI on the 15th hospital day
showing enhancing lesions involving
premotor (A), motor (B),and sensory
cortices (C). Involvement of the premotor and motor cortex is more severe on the right side. The white
matter is relatively spared. On
follow-up M R I on the 43rd hospital
day, the enhancement appears almost resolved (D-F).
278 NEUROLOGY 48 January 1997

a distinct color or odor if possible and should be
labeled and stored as a toxic agent.
From the Division of Neurology (Dr. Ijichi), Department of Surgery (Drs. Itoh, Nakaji, and Miyauchi), and Department of Internal Medicine (Drs. Sakai, Takahashi, Kadosaka, Hirata, Yoneda,
Kajita, and Fujita), Nantan General Hospital, Funai-gun, Kyoto,
Japan.
Received March 28, 1996. Accepted in final form May 22, 1996.
Address correspondence and reprint requests to Dr. T. Ijichi, Division of Neurology, Nantan General Hospital, Yagi-cho, Funai-gun,
Kyoto 629-01, Japan.

References
Giberson TP, Kern JD, Pettigrew DW 111, Eaves CC, Haynes
J F J r . Near-fatal hydrogen peroxide ingestion. Ann Emerg
Med 1989;18:778-779.
Humberston CL, Dean BS, Krenzelok EP. Ingestion of 35%
hydrogen peroxide. Clin Toxicol 1990;28:95-100.
Christensen DW, Faught WE, Black RE, Woodward GA, Tim-

Unusual MRI and
pathologic findings of
progressive multifocal
leukoencephalopathy
complicating adult
Wiskott-Aldrich
syndrome

mons OD. Fatal oxygen embolization after hydrogen peroxide
ingestion. Crit Care Med 1992;20:543-544.
4. Luu TA, Kelley MT, Strauch JA, Avradopoulos K. Portal vein
gas embolism from hydrogen peroxide ingestion. Ann Emerg
Med 1992;21:1391-1393.
5. Dickson KF, Martin Caravati E. Hydrogen peroxide exposure-325 exposures reported to a regional poison control center. Clin Toxicol 1994;32:705-714.
6. Sherman SJ, Boyer LV, Sibley WA. Cerebral infarction immediately after ingestion of hydrogen peroxide solution. Stroke
1994;25:1065-1067.
7. Shaw A, Cooperman A, Fusco J. Gas embolism produced by
hydrogen peroxide. N Engl J Med 1967;277:238-241.
8. Basson MM, Dudai M, Shalev 0. Near-fatal systemic oxygen
embolism due to wound irrigation with hydrogen peroxide.
Postgrad Med J 1982;58:448-450.
9. Morikawa H, Mima H, Fujita H, Mishima S. Oxygen embolism due to hydrogen peroxide irrigation during cervical spinal
surgery. Can J Anaesth 1995;42:231-233.
10. Armon C, Deschamps C, Adkinson C, Fealey RD, Orszulak
TA. Hyperbaric treatment of cerebral air embolism sustained
during a n open-heart surgical procedure. Mayo Clin Proc
1991;66:565-571.

Article abstract-We present a long-surviving patient with Wiskott-Aldrich
syndrome complicated by atypical progressive multifocal leukoencephalopathy (PML). MRI showed multiple tiny spots o f Gd-DTPA-enhanced lesions on
the TI-weighted image. Pathologic findings for brain biopsy were patchy
demyelinated vascularized lesions infiltrated by a surprising number of eosinophils. The presence of polyomavirus J C was confirmed by in situ hybridization and polymerase chain reaction. PML should be included in the differential diagnosis when Gd-DTPA-enhanced spotty lesions are present in the
white matter, especially in patients who have a mild immunologic defect.
NEUROLOGY 1997:48:279-282

T. Matsushima, MD; K. Nakamura, MD; T. Oka, MD; N. Tachikawa, MD; T. Sata, MD; S. Murayama, MD;
N. Nukina, MD; and I. Kanazawa, MD

Wiskott-Aldrich syndrome (WAS) is a n X-linked recessive combined immune deficiency that manifests
the triad of thrombocytopenia, eczema, and recurrent infection. Several reports have described patients with variant forms of WAS, with milder clinical features of bleeding and infection. Patients
survived into adulthood; however, it is very rare for
patients to survive longer than 10 years.'
In contrast, progressive multifocal leukoencephalopathy (PML) is typically a rapidly progressive degenerative disease, resulting from CNS infection by
polyomavirus JC (JC virus). This infection results in
continued neurologic decline, mostly in immunocompromised hosts, and is usually relentlessly progressive with death within 9 months of the onset of
symptoms. Typical MRI features of PML involve
multiple asymmetrical lesions, predominantly in the
white matter, without mass effect or enhancement.2
We present a patient with WAS who has survived
more than 35 years and then developed PML. Unusual MRI and pathologic findings are discussed.

C a s e report. A 36-year-old man was hospitalized because of slowly progressive dementia that included anomia, alexia, and agraphia. He had a history of idiopathic
thrombocytopenic purpura at the age of 1 month, atopic
dermatitis at 1 year, and pulmonary tuberculosis a t age
20. At age 34, 2 years before admission, a sudden epileptic
attack occurred, and treatment with antiepileptic drugs
was begun. Thereafter, his mental symptoms gradually
worsened. In January 1994, he was hospitalized for a complete medical examination.
His family history disclosed that a maternal uncle had a
bleeding tendency combined with a n immunodeficiency
and died of malignant lymphoma a t age 31. A granddaughter of this uncle also showed thrombocytopenia. This family history strongly suggests a disease of X-linked recessive
inheritance. On physical examination, erythema with teleangiectagia on the face and eczema over the entire body
were noted. Neurologic and neuropsychological examinations revealed mild anomia, aphasia with phonemic paraphasia, alexia, and agraphia. He showed slight right hemiparesis. Deep tendon reflexes, however, were reduced in
Copyright 0 1997 by the American Academy of Neurology 279

Multiple Brain Gas Embolism After Ingestion of Concentrated Hydrogen Peroxide
T. Ijichi, T. Itoh, R. Sakai, et al.
Neurology 1997;48;277-279
DOI 10.1212/WNL.48.1.277
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