(Stroke. 1995;26:696-698.)
© 1995 American Heart Association, Inc.
Brain Abscess as a Complication of Stroke
Sien-Tsong Chen, MD;
Lok-Ming Tang, MD, MSc
Long-Sun Ro, MD, PhD
From the Department of Neurology, Chang Gung Memorial Hospital and
Medical College, Taipei, Taiwan.
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Abstract
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Background Systemic infection is a common complication of
stroke.
However, brain abscess as a complication of stroke has never
been
reported.
Case Descriptions We report two patients, one with a
hypertensive intracerebral hemorrhage and the other with nonseptic
cerebral infarction. In both patients, brain abscess developed at the
stroke lesion site after an infectious complication. After surgical
aspiration and antibiotic treatment, one patient recovered and the
other died.
Conclusions These two cases demonstrate that brain abscess
may occur in a previous hemorrhage or infarction area as a complication
of systemic infection. Recognition of the risk is important for early
diagnosis and proper treatment of this potentially fatal complication
of stroke.
Key Words: brain abscess cerebral infarction complications intracerebral hemorrhage
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Introduction
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Stroke is the most common neurological
disease. Systemic infection,
such as pneumonia, sepsis, and urinary
tract infection, is a
common complication of acute stroke
1
and is an important cause
of death after the first week
poststroke.
2 3 Although brain
abscess may arise from
septic embolism secondary to bacterial
endocarditis,
4
transformation of a hypertensive intracerebral
hematoma or a nonseptic
infarct into an abscess after an infectious
complication has never been
documented. We report two patients
who, in the subacute stage of
stroke, developed a brain abscess
subsequent to a systemic
infection.
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Case Reports
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Case 1
A 56-year-old woman with a 10-year history of hypertension
suffered
from a sudden onset of headache and weakness of the right
extremities.
She was sent to a local hospital where cranial computed
tomography
(CT) showed a left putaminal hemorrhage (Fig 1

). She lost consciousness
and was transferred to our
hospital on the same day. On admission,
the patient was drowsy with a
blood pressure of 160/100 mm Hg
and a body temperature of 36.8°C.
She had motor aphasia
and right hemiplegia with Babinski's sign. On
day 4 of hospitalization,
she developed fever (38°C), chills, and
dysuria. Intravenous
amikacin (600 mg/d) and cephalothin (6 g/d) were
given as soon
as blood culture showed
Klebsiella
pneumoniae, which was sensitive
to both antibiotics. The
patient's condition improved gradually
within 2 weeks of
treatment.

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Figure 1. Computed tomography without contrast
enhancement in case 1 patient showing an intracerebral hemorrhage in
the left putamen.
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Two weeks after antibiotic treatment was discontinued, the patient
experienced a frontal headache, and fever (39°C) recurred. She was
fully conscious, but her neck was stiff. Results of chest radiograph
and urinalysis were normal. A cerebrospinal fluid (CSF) examination
revealed an initial pressure of 250 mm H2O, a leukocyte
count of 3100x106/L with 97% neutrophils, a
glucose level of 0.2 mmol/L, and a protein level of 6.11 g/L; Gram's
stain and bacterial culture were negative. No microorganism was found
on blood culture. A repeated CT scan, 5 weeks after stroke, showed a
slightly hyperdense area in the left putamen with mass effect (Fig 2A
). After contrast-medium injection, there was a ring
enhancement surrounding the mass (Fig 2B
). After neurosurgical
consultation for the possibility of brain abscess, the lesion was still
considered to be a partially resorbed hematoma. The patient was treated
for bacterial meningitis with a 4-week course of intravenous penicillin
(24x106 IU/d) and chloramphenicol (4 g/d). Fever
and headache subsided soon after antibiotic treatment. However, 2 days
after discontinuation of the antibiotics, fever (39°C) recurred, and
the patient became drowsy. An emergency CT, 9 weeks after stroke,
showed a hypodense area in the left putamen (Fig 2C
) with a
well-defined, thin-walled ring enhancement (Fig 2D
). Given the
possibility of brain abscess, a stereotactic aspiration was performed
immediately. The pus culture grew K pneumoniae that was
sensitive to cefotaxime. The patient recovered after 8 weeks of
cefotaxime treatment and remained well at follow-up examination 3 years
later.

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Figure 2. Computed tomography in case 1 patient: A and B, 5
weeks after stroke showing a slightly hyperdense area in the left
putamen (A) and a ring enhancement surrounding the mass (B); C and D, 9
weeks after stroke showing a low-density area in the left putamen (C)
and a well-defined, thin-wall ring enhancement (D). Note the prominent
mass effect with compression of the ipsilateral lateral ventricle.
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Case 2
A 70-year-old man suffered from a sudden onset of weakness of the
left limbs and was admitted to a local hospital, where a cranial CT
scan revealed a large hypodense area in the territory of the right
middle cerebral artery (Fig 3A
and B). The patient
developed aspiration pneumonia during hospitalization. After
tracheostomy and 2 weeks of antibiotic treatment, his condition became
stable. However, upper gastrointestinal tract bleeding occurred, and he
was transferred to our hospital.

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Figure 3. Computed tomography in case 2 patient: A and B, 1
day after stroke showing a large low-density area in the territory of
the right middle cerebral artery; C and D, 5 weeks after stroke showing
deep low-density areas in the previous infarction site (C) and two
well-defined, thin-walled rings of enhancement with marked midline
shift (D).
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On admission, the patient was semicomatose with tracheostomy. His body
temperature was 36.3°C, blood pressure was 150/90 mm Hg, pulse rate
was 90/min, and respiratory rate was 18/min. There was flaccid
paralysis of the left limbs with Babinski's sign. The patient's neck
was supple. Blood chemistry tests revealed hyponatremia (121 mmol/L)
and hyperglycemia (8.2 mmol/L). A two-dimensional echocardiogram was
normal, and chest radiograph was negative for pneumonic patch. The
gastrointestinal bleeding stopped soon after admission. Because there
was occasional low-grade fever, intravenous penicillin
(12x106 IU/d) was given for 2 weeks. Three weeks
after admission to our hospital, the patient had a sudden onset of
vomiting, and his pupils became anisocoric (right, 6 mm; left, 3 mm).
An emergency CT, 5 weeks after stroke, revealed that the previously
infarcted area became very low in density, and there were two
well-defined, thin-walled rings of enhancement (Fig 3C
and D) with
marked midline shift. Because brain abscess with herniation was
suspected, an emergency CT-guided stereotactic aspiration was
performed, and approximately 40 mL puslike fluid was drained out.
Intravenous penicillin (24x106 IU/d),
ceftriaxone (2 g/d), and metronidazole (2 g/d) were
administered before and after the surgery. CSF cultures for aerobic and
anaerobic bacteria, fungi, and tubercle bacilli were all negative. The
patient died 1 month later despite vigorous treatment for the
infection.
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Discussion
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Our two cases are unique and worth noting in that both patients,
admitted
for acute stroke, developed an abscess in the previous
hemorrhage
or infarction area after an infectious complication.
The patient in case 1 suffered from a left putaminal hemorrhage that
was considered hypertensive in nature. The patient's initial episode
of fever was due to sepsis caused by K pneumoniae and was
controlled with antibiotic treatment. In the second febrile episode,
the patient had headache and meningeal signs. A repeat CT scan showed a
localized mass with a ring enhancement. Although a uniform, thin-ring
enhancement is an important sign for the diagnosis of brain abscess by
CT,5 6 7 the finding is by no means specific. A similar ring
enhancement can also be observed around a hematoma from 1 to 8 weeks
after stroke.8 In our case 1, it was difficult to
differentiate a partially resorbed hematoma from an abscess on the
basis of the second CT performed 5 weeks after stroke. Moreover, a
marked CSF pleocytosis with predominance of neutrophils and a very low
level of CSF glucose favored the diagnosis of bacterial
meningitis.9 The third episode of fever occurred 9 weeks
after stroke. The diagnosis of brain abscess at this time became clear
because the contrast CT still showed a strong ring enhancement with
prominent mass effect, which is incompatible with a hematoma of more
than 2 months old.
The clinical course of the patient in case 2 was also complicated by an
infectious episode. The second CT study in this case revealed two
contiguous hypodense areas with ring enhancement in the previously
infarcted area. After 1 week from stroke, contrast enhancement may
appear in the infarcted area and may last up to a month or
longer.8 Thus, contrast CT done in this period may show a
pattern similar to that of an abscess. However, contrast enhancement of
an infarct is usually in the form of small, patchy, scattered areas or
curvilinear bands, and the distribution is mostly in the gray
matter.8 Brain abscess was diagnosed in our case 2 before
surgery because in this patient the CT findings of thin-ring
enhancement, multiloculation, and involvement of both gray and white
matters all indicate a brain abscess5 6 rather than a
subacute infarct.
In case 1, K pneumoniae was isolated from the pus culture.
Although the microorganism has been recognized as an uncommon pathogen
causing central nervous system infection, it accounted for 13% of 317
patients with culture-proven bacterial meningitis between 1981 and 1991
in our recent study.10 The pathogen in case 2 was not
known. Nevertheless, the typical CT findings and the puslike fluid
aspirated by surgery established the diagnosis. Treatment with surgical
aspiration and a third-generation cephalosporin was successful in case
1. The case 2 patient had a fatal outcome, which was probably due to
the inability to recognize the process of abscess formation and the
delay of appropriate treatment until uncal herniation occurred.
These two cases document that a cerebral hematoma or infarct can be
transformed into an abscess when systemic infection complicates an
acute or subacute stroke. Intact brain is quite resistant to infection.
However, it is conceivable that disruption of the blood-brain barrier
caused by hemorrhage or infarction may predispose the affected brain
tissue to infection and thus abscess formation. Advances in
neurosurgical techniques and antibiotic treatment have greatly
reduced the mortality of brain abscess to as low as 4% to
9.7%.11 12 Awareness of the possible risk of
transformation of a hematoma or infarct into an abscess after a
systemic infection may lead to better management of stroke
patients.
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Footnotes
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Reprint requests to Sien-Tsong Chen, MD, Department of Neurology,
Chang Gung Memorial Hospital, 199 Tung Hwa North Rd, Taipei,
Taiwan.
Received November 7, 1994;
revision received January 25, 1995;
accepted January 25, 1995.
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