(Stroke. 1995;26:696-698.)
© 1995 American Heart Association, Inc.
Articles |
Brain Abscess as a Complication of Stroke
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 stroke1 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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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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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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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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References |
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