580 Case Report / Journal of Clinical Neuroscience 15 (2008) 580582

and travel, entering into the ventricles, and becoming at-
tached to the ventricular wall. This hypothesis could be indi-
rectly supported by this case.
Since the rst report in which Maravilla5 presented nd-
ings on intraventricular fat-uid level secondary to the
spontaneous rupture of a dermoid cyst, a number of
reports have noted the spread of fat globules into CSF
pathways in patients with fat-containing tumors such as
epidermoid or a dermoid tumors.5,6 To the best of our
knowledge, there has been no prior report regarding ecto-
pic recurrent tumor tissue within the ventricle, which has
been histologically proven to be an epidermoid cyst. Epi-
dermoid cysts in the CSF pathways secondary to spontane-
ous rupture may be widespread. In cases of multiple
intracranial epithelial cysts, dissemination of the epithelial
clusters into the CSF could reasonably be explained by
asymptomatic rupture or spontaneous breakdown of the
cyst wall.
In summary, we report an unusual case of ectopic ven-
tricular recurrence of an epidermoid cyst in the middle fos-
sa with conrming histological characteristics. Care should
be taken to prevent the spread of cystic content into the
CSF pathways during epidermoid removal.
References
1. Wasenko JJ, Rosenbloom SA, Estes M, et al. Magnetic resonance of
intracranial epidermoids. Eur J Radiol 1991;13:1036.
2. Lopes M, Capelle L, Duau H, et al. Surgery of intracranial
epidermoid cysts. Report of 44 patients and review of the literature.
Neurochirurgie 2002;48:513.
3. Samii M, Tatagiba M, Piquer J, et al. Surgical treatment of
epidermoid cysts of the cerebellopontine angle. J Neurosurg 1996;84:
149.
4. Guidetti V, Gagliardi FM. Epidermoid and dermoid cysts: Clinical
evaluation and late surgical results. J Neurosurg 1977;47:128.
5. Maravilla KR. Intraventricular fat-uid level secondary to rupture
of an intracranial dermoid cyst. AJR Am J Roentgenol 1977;128:
5001.
6. Kwon TH, Park YK, Chung HS, et al. Accumulation of intraventric-
ular fat in an intracranial epidermoid tumor: Case report. Neurosurgery
2001;49:4502.

doi:10.1016/j.jocn.2007.02.010

Tension pneumothorax complicating apnea testing during

brain death evaluation
Joseph D. Burns *, James A. Russell
Department of Neurology, Lahey Clinic Medical Center, Burlington, MA 01805, USA

Received 3 November 2006; accepted 4 February 2007

Abstract

Tension pneumothorax is a rare complication of the apnea test using the apneic oxygenation method. In reported cases, it has been
attributed to massive air trapping beyond a supplemental oxygen cannula that was obstructing the airway. We report a case of tension
pneumothorax, pneumomediastinum, and pneumoperitoneum that developed during the apnea test as a result of direct airway perfora-
tion by the supplemental oxygen cannula. We review the literature concerning catastrophic airway complications associated with the
apneic oxygenation method and suggest ways to avoid them.
2007 Elsevier Ltd. All rights reserved.

Keywords: Apnea test; Brain death; Pneumothorax

Apnea testing is an essential element of the evaluation
for death by neurological criteria. The apneic-oxygenation
method, during which supplemental oxygen is provided by
*
Corresponding author. Address: 3074 Avalon Cove Court NW
Rochester, Minnesota 55901, USA. Tel.: +1 781 744 5102; fax: +1 781
744 5243.
E-mail addresses: joseph.d.burns@lahey.org (J.D. Burns), james.a.
russell@lahey.org (J.A. Russell).
a cannula placed in the endotracheal tube (ETT), is the
recommended method for performing this test.1 A high
incidence of complications has been described in asso-
ciation with this method, primarily hypotension and
hypoxemia.24 Infrequently, more serious complications
including cardiac arrest, cardiac arrhythmia, and pneumo-
thorax have been reported.27 We describe the incidence of
 Case Report / Journal of Clinical Neuroscience 15 (2008) 580582
tension pneumothorax, pneumomediastinum, and pneu-
moperitoneum leading to pulseless electrical activity that
occurred during performance of apnea testing using the
apneic-oxygenation method. We review the literature
regarding such airway catastrophes and suggest methods
to avoid them.
1. Case report
A 55-year-old woman with a past medical history
notable for type 2 diabetes, pancreatitis, chronic renal
insuciency, myocardial infarction, and a cryptogenic left
occipital ischemic stroke, was admitted for abdominal
pain. She was found to have a small bowel infarction
and underwent resection of the infarcted segment on hos-
pital day 1. Her postoperative course was complicated by
failure to wean from the ventilator. On post-operative
day 4 she was noted to have decreased arousal and new
left hemiparesis. A CT scan of the brain revealed a large
right middle cerebral artery infarct with substantial ede-
ma and mass eect. Over the next 2 days, her alertness
progressively declined and spontaneous breathing
stopped. On post-operative day 6, the neurology service
was asked to determine if the patient was dead by neuro-
logical criteria.
At the time of brain death evaluation, she was normo-
thermic and unresponsive to loud verbal and noxious tac-
tile stimuli. The pupils were 5 mm diameter, round, and
did not react to light. The oculocephalic reex was absent
and sequential irrigation of each external auditory canal
with 60 cc of ice water did not cause deviation of the eyes.
The corneal reex was absent bilaterally, there was no gri-
mace or limb movement to noxious styloid pressure, and
there was no cough or gag to endobronchial suctioning
or manipulation of the ETT.
Apnea testing using the apneic oxygenation method
was attempted. Pre-apnea test arterial blood gas analysis
showed a pH of 7.43, a carbon dioxide tension (PCO2) of
43 mmHg, and an oxygen tension (PO2) of 144 mmHg.
Pre-oxygenation with FiO2 (fraction of inspired oxygen)
of 100% was performed for approximately 5 min before
the ETT was disconnected from the ventilator. Next, a
nasal cannula from which the nasal prongs had been re-
moved was inserted into the number 7 ETT. Oxygen was
delivered at a rate of 10 L/min. Rapidly expanding sub-
cutaneous emphysema in the neck and chest wall oc-
curred immediately after insertion of the cannula.
Within seconds, the patient developed pulseless electrical
activity.
The ETT was immediately reconnected to the ventilator,
which measured very high inspiratory pressures. Manual
ventilation was initiated. An emergency chest lm revealed
a large left pneumothorax, pneumomediastinum, pneumo-
peritoneum, and extensive subcutaneous emphysema
(Fig. 1). The distal end of the ETT was within 1 cm of
the carina. Autopsy results conrmed the presence of pneu-
581
Fig. 1. Portable anterior-posterior chest X-ray showing a left pneumo-
thorax, pneumomediastinum, pneumoperitoneum, extensive subcutaneous
air, and a low-lying endotracheal tube.
mothorax, pneumomediastinum, and pneumoperitoneum.
No overt breach was found in the wall of the trachea or
proximal mainstem bronchi.
2. Discussion
Apnea testing is technically challenging and has been
associated with a high rate of complications. In the few
studies that have examined this topic, complication rates
as high as 68% have been found.4 Hypotension attributed
to hypoxemia is one of the most common of these compli-
cations.2 Accordingly, methods to minimize hypoxemia
have been devised. One such method, described in the
American Academy of Neurology Practice Parameters
on determining brain death in adults and known as apneic
oxygenation, involves the provision of high-ow oxygen
into the endotracheal tube by means of a cannula placed
at the level of the carina.1
We believe that the insertion of an oxygen cannula
into a deeply positioned ETT led to the complications de-
scribed in our patient. She had no history of chronic
obstructive pulmonary disease, elevated peak airway pres-
sures, bullae or other lung pathology noted on prior chest
lms that would have predisposed her to lung rupture.
Rather, because subcutaneous emphysema became mani-
fest immediately after insertion of the oxygen cannula,
it is likely that the cannula went beyond the distal end
of the ETT and perforated either the distal trachea or
the left mainstem bronchus. The deep position of the
ETT may have predisposed this patients carina to recur-
rent trauma during routine suctioning, thus rendering it
susceptible to puncture by the blunt, silastic oxygen
cannula.
582 Case Report / Journal of Clinical Neuroscience 15 (2008) 582585

This mechanism is dierent from that postulated in pre- Acknowledgement

viously published reports of similar cases. In the two cases
described by Bar-Joseph et al., the development of brady-
cardia and hypotension lagged behind the introduction of
the oxygen cannula by 12 min.5 This led the authors to
conclude that in their cases, tension pneumothorax devel-
oped as the result of massive air trapping beyond a cannula
that was obstructing the airway. A similar explanation was
used to explain the development of subcutaneous emphy-
sema and thoracic ination reported by Marks and Zisf-
ein as part of a case series examining the ecacy of the
apneic oxygenation method in preventing hypoxemia.6
Similarly, Saposnik et al. describe the onset of pneumotho-
rax and pneumoperitoneum followed by cardiac arrest that
occurred 2 min after the oxygen cannula was inserted
during apneic oxygenation.7 The onset of subcutaneous
emphysema immediately after insertion of the oxygen can-
nula makes this mechanism extremely unlikely in our
patient.
Our patient serves as a dramatic example of the poten-
tial for serious complications during apnea testing. Given
the high rate of complications associated with the apneic
oxygenation method, some of which are catastrophic, other
potentially safer apnea testing methods such as articial
carbon dioxide augmentation should continue to be inves-
tigated.2,8 If the apneic oxygenation method is used, we
strongly discourage the insertion of an oxygen cannula into
the ETT. Safer, yet equally eective methods for providing
supplemental oxygen, including bulk diusion, T-piece sys-
tems, and continuous positive airway pressure systems
should be used instead.9,10
The authors thank Dr. Allan Ropper for his thoughtful
guidance and support in the preparation of this paper.
References
1. The Quality Standards Subcommittee of the American Academy of
Neurology. Practice parameters for determining brain death in adults.
Neurology 1995;45:10124.
2. Goudreau JL, Widjicks EFM, Emery S. Complications during apnea
testing in the determination of brain death: predisposing factors.
Neurology 2000;55:10458.
3. Melano R, Adum ME, Scarlatti A, et al. Apnea test in diagnosis of
brain death: comparison of two methods and analysis of complica-
tions. Transplant Proc 2002;34:112.
4. Saposnik G, Rizzo G, Vega A, et al. Problems associated with the
apnea test in the diagnosis of brain death. Neurol India 2004;52:3425.
5. Bar-Joseph G, Bar-Lavie Y, Zonis Z. Tension pneumothorax during
apnea testing for the determination of brain death. Anesthesiology
1998;89:12501.
6. Marks SJ, Zisfein J. Apneic oxygenation in apnea tests for brain
death. A controlled trial. Arch Neurol 1990;47:10668.
7. Saposnik G, Rizzo G, Deluca JL. Pneumothorax and pneumoperi-
toneum during the apnea test: how safe is this procedure? Arq
Neuropsiquiatr 2000;58:9058.
8. Sharpe MD, Young BG, Harris C. The apnea test for brain
death determination: an alternative approach. Neurocrit Care
2004;1:3636.
9. al Jumah M, McLean DR, al Rajeh S, et al. Bulk diusion apnea test
in the diagnosis of brain death. Cri Care Med 1992;20:15647.
10. Levesque S, Lessard MR, Nicole PC, et al. Ecacy of a T-piece
system and a continuous positive airway pressure system for
apnea testing in the diagnosis of brain death. Crit Care Med
2006;34:22136.

doi:10.1016/j.jocn.2007.02.009

Malignant cerebellar ganglioglioma

Marguerite Harding *, Brian Brophy, Timothy Geake
Department of Neurosurgery, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia 5000, Australia

Received 27 September 2006; accepted 5 February 2007

Abstract

We present a 62-year-old man with a high-grade cerebellar ganglioglioma with ataxia. Gangliogliomas are rare tumours which usually
occur in the rst 3 decades of life. There have only been a small number of grade IV gangliogliomas reported in the literature.
Crown Copyright 2007 Published by Elsevier Ltd. All rights reserved.

Keywords: Ganglioglioma; Cerebellar; Glioblastoma multiforme; High grade

*
Corresponding author. Tel.: +61 0434603319; fax: +61 882225886.
E-mail addresses: mhardin1@mail.rah.sa.gov.au (M. Harding).