Hemorrhage: a Rare Neuroimaging Pitfall
Al-Yamany, John Deck and Mark Bernstein
Objective: We report an unusual case of the CT
appearance of diffuse subarachnoid hemorrhage in a patient with
anoxic encephalopathy, a situation which neurosurgeons, neurologists,
and neuroradiologists should be aware of. Clinical presentation:
A young man collapsed unconscious in jail after abusing
an unknown quantity and variety of drugs. CT scan showed a picture
compatible with diffuse subarachnoid hemorrhage. Intervention:
As the patient had a Glasgow Coma Score of 3 no heroic
intervention was undertaken. An autopsy performed 40 hours after
the initial ictus and 24 hours after death revealed no evidence
of subarachnoid hemorrhage but gross and microscopic evidence
of anoxic encephalopathy. Conclusion: Anoxic encephalopathy
can mimic diffuse subarachnoid hemorrhage on CT.
Pseudo-hemorragie sousarachnoïdienne: une embûche
rare à la neuro-imagerie. But: Nous rapportons
un cas inusité d'apparition à la tomodensitométrie
d'une hémorragie sousarachnoïdienne chez un patient
présentant une encéphalopathie anoxique, une situation
que les neurochirurgiens, les neurologues et les neuroradiologues
devraient connaître. Présentation clinique:
Un jeune prisonnier est devenu inconscient après avoir
utilisé une quantité et une variété
inconnues de drogues. La tomodensitométrie a montré
une image compatible avec une hémorragie sousarachnoïdienne
diffuse. Intervention: Comme le patient avait
un score de 3 à l'échelle de coma de Glasgow,
aucune intervention héroïque n'a été
tentée. Une autopsie faite 40 heures après l'ictus
initial et 24 heures après le décès n'a
révélé aucune évidence d'hémorragie
sousarachnoïdienne, mais des manifestations macroscopiques
et microscopiques d'encéphalopathie anoxique. Conclusion:
Une encéphalopathie anoxique peut simuler une
hémorragie sousarachnoïdienne à la tomodensitométrie.
J. Neurol. Sci. 1999; 26:57-59
only condition we are aware of which can mimic the appearance
of diffuse subarachnoid hemorrhage (SAH) on unenhanced computed
tomography (CT) is pyogenic meningitis.(1) However, in most
of these cases the clinical progression would distinguish it
from subarachnoid hemorrhage. We report a case of sudden collapse
with CT appearance compatible with diffuse SAH in a patient
who in fact suffered from anoxic encephalopathy due to respiratory
arrest secondary to drug overdose.
35-year-old man with a known history of substance abuse was
arrested and taken to a detention centre following a domestic
dispute. He was drowsy and had consumed an unknown quantity
of alcohol and drugs. While in jail he suddenly became comatose
and was taken to a local hospital where he was intubated and
resuscitated. Glasgow Coma Score (GCS) was 3. Plain CT of the
head was interpreted by a neurologist and a general radiologist
as demonstrating subarachnoid hemorrhage in the basal cisterns,
convexity, and interhemispheric fissure (Figures
1, 2, 3). The patient was transferred to our neurosurgical
centre where the CT was again interpreted as showing SAH by
neurosurgery residents and staff, and neuroradiologists. As
his GCS was 3, further therapy was discontinued and the patient
expired several hours later.
coroner's autopsy was performed by a forensic neuropathologist
about 40 hours after the patient's collapse. The general autopsy
was normal except for congestion in the lungs. The brain was
swollen with generalized flattening of the gyri, effacement
of the sulci, and bilateral herniation of the hippocampal unci.
There was absolutely no evidence of subarachnoid blood. There
were no gross lesions on sectioning of the brain and microscopic
examination revealed evidence of acute hypoxic ischemic changes
consisting of selective neuronal necrosis, patchy infarction,
and cortical edema. Pre-mortem toxicology studies revealed toxic
levels of alcohol, codeine, morphine, alprazolam, and acetaminophen.
cause of death was attributed to anoxic encephalopthy due to
respiratory arrest secondary to central nervous system depression
induced by a drug overdose.
clinical presentation in this case was compatible with spontaneous
SAH and the CT appearance was interpreted as showing diffuse
SAH by every doctor who encountered the case pre-mortem and
by numerous others who were presented the case at post-mortem
conference. In this case the "mis-diagnosis" had no negative
clinical implications for the management of the patient whose
treatment was appropriate given his neurological condition.
The incidence of the erroneous diagnosis of an apparent SAH
is indeterminate as many cases like the one described herein
do not undergo autopsy. This situation has been alluded to,(2)
and increased density of the dura on CT mimicking subarachnoid
hemorrhage has been reported in an autopsy study in patients
who had increased intracranial pressure of non-SAH etiology.(3)
scans of normal patients show the cranial bone lined by a thin
layer of dura mater which overlies the subarachnoid space filled
with cerebrospinal fluid (CSF). The average width of this space
varies, increasing with age. In the case of brain swelling due
to acute hypoxic anoxic encephalopathy the cerebral cortex becomes
displaced into areas normally occupied by CSF and veins become
congested. The increased average tissue density immediately
deep to the dura and superficially within the cerebral sulci
results in hyperdensity on unenhanced CT, simulating the appearance
of SAH. Another plausible explanation(2) is that with severe
ischemia the density of the brain on CT decreases relative to
the density in the congested veins in the superficial cortex
again giving a relatively hyperdense appearance to superficial
tissues. Yet another explanation incriminates impairment of
the vascular circulation of the dura(3) although the latter
could not account for the appearance of the sylvian fissure
and cortical sulci seen in our case.
spite of the frequency of anoxic encephalopathy in patients
studied with CT, the incidence of the CT appearance of subarachnoid
hemorrhage in these patients is either extremely rare or under-recognized
and/or under-reported. We feel that this rare imaging pitfall
should be known to all neurosurgeons, neurologists, and neuroradiologists,
as well as residents and emergency room physicians caring for
patients with unexplained unconsciousness. It could have clinical
implications if a patient with anoxic or other metabolic encephalopathy
with GCS greater than 3 were inappropriately treated as a case
of SAH. Furthermore, there could possibly be medico-legal implications
of the misdiagnosis of SAH.
DB, Moss ML, Chason DP, Muphree S, Casey S. Acute purulent
leptomeningitis mimicking subarachnoid hemorrhage on CT.
J Comput Assist Tomogra 1994; 18: 126-128.
A. Diagnostic Neuroradiology. Baltimore: Mosby, 1994;
SM, Fox AJ, Vinuela F, Pelz DM. Increased density of tentorium
and falx: a false positive CT sign of subarachnoid hemorrhage.
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the Division of Neurosurgery (M.A-Y, M.B.), The Toronto
Hospital, and Forensic Pathology Branch (J.D.), Ministry
of the Solicitor General and Correctional Services,
Government of Ontario, Toronto, Canada.
July 2, 1998. Accepted in final form September 16, 1998.
requests to: Mark Bernstein, Division of Neurosurgery,
The Toronto Hospital, Suite 2-405 McL, 399 Bathurst
Street, Toronto, Ontario, Canada M5T 2S8
J. Neurol. Sci. 1999; 26:57-59