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Multiple bilateral cerebral abscesses with hemorrhage.


Spontaneous hemorrhage is a well-recognized complication in brain tumors.[15] Brain abscesses rarely present with hemorrhage. Only three reports of hemorrhage into a single brain abscess have been reported in adults.[2,17,13] Two reports of a single brain abscess with hemorrhage was found in early infancy.[11,16] A case of seven brain abscesses with hemorrhage in both cerebral hemispheres is herein reported.

Case History

A sixty-three year old right-handed male business administrator previously in good health presented to his physician with flu-like symptoms and generalized fatigue that was treated with ampicillin. His symptoms persisted and two weeks later he became lethargic, unable to concentrate or remember names of people and what he was supposed to do. He also experienced bifrontal headaches that awakened him from sleep and bothered him intermittently throughout the day. He was oriented to person, place and time. However, he had dyslexia (difficulty reading words) and dysnomia (difficulty naming objects). He was admitted directly to the hospital. Magnetic resonance imaging (MRI) of his brain revealed seven individual ring-enhancing lesions varying in size from 5 mm to 1.7 cm in diameter located throughout both cerebral hemispheres. Each lesion showed hemosiderin deposition (presence of blood resulting from hemorrhage within the lesion).

Past medical history revealed a five-year history of stable angina, coronary artery disease, organic heart disease, hypercholesteremia and spinal arthritis. He smoked cigarettes for thirty-five years but had not smoked for seven years prior to admission. Routine hematological and biochemistry examinations were within normal limits including white blood cell count and sedimentation rate. Medications upon admission included diltiazem hydrochloride (Cardizem CD) 240 mg daily and nitroglycerin sublingually as needed.

To search for a possible metastatic or infectious cause for the MRI findings, multiple tests were performed. Chest radiography revealed a left hilar calcification. Transesophageal echocardiography, bone scan and panorex were negative. Computed tomography (CT) of the chest revealed a 1.5 cm mass within the pretracheal region. A bronchoscopy was performed which was negative for cytology, acid-fast bacilli and fungus. CT scans of the sinuses and pelvis were negative. Blood cultures and human immunodeficiency virus (HIV) testing were negative. A stool specimen was guiac negative. He was given prophylactic phenytoin (Dilantin) and dexamethasone (Decadron).

Neurosurgical intervention was deemed necessary to obtain a diagnosis after this extensive evaluation.[20] The neurosurgeon elected to perform surgery utilizing MRI guidance that required placement of scalp fiducials (markers). The left temporal lesion was selected for removal to obtain a tissue diagnosis as it was easily accessible and the probability of neurological complications was felt to be lower.

Preoperatively, the patient was transported to the MRI suite. A neurosurgical clinical nurse specialist placed nine indelible ink marks around the circumference of the head of the patient. Small fiducials that are detectable by MRI were taped directly over the indelible ink marks. Scalp fiducial placement was chosen based upon knowledge of patient position during surgery and the area where the incision would be made. Each fiducial was positioned in a different plane and at least 2.5 centimeters apart to maximize accuracy. A volumetric MRI study consisting of 124 axial images of the brain using 1.3 mm slice thickness without and with gadopentetate dimeglumine (Magnevist) was obtained. After completion of the MRI, the fiducials were removed and a small piece of transparent tape was placed over each indelible ink mark. The MRI revealed multiple contrast enhancing circular lesions involving both cerebral hemispheres (Figs 1-6). MRI after the administration of Magnevist has been chosen to illustrate the contrast enhancing nature of the pathology.


The next day the patient was transported to the operating room, intubated and positioned for surgery with the head supported in a Mayfield head clamp. A reference arc, equipped with multiple light emitting diodes (LEDs), was attached to the head rest (Fig 7). The indelible ink marks where the fiducials had been placed during the MRI were touched with a registration probe equipped with LEDs.[9,10] The LEDs on the handle of the registration probe are tracked by an overhead camera array (Fig 8). By touching the marks on the scalp and stepping on a foot pedal, the marks where the fiducials had been placed were entered into the computer of the Stealth Station (Sofamor Danek, Memphis, TN, Fig 9) that was developed at St. Louis University Health Sciences Center.


After the patient was prepped and draped, the neurosurgeon used a bayonet forceps equipped with three LEDs (Fig 10) to identify location of the lesion before making the incision.[7,8] Localization of the lesion using the forceps equipped with LEDs showed the lesion to be 1.5 cm beneath the cortex. A curvilinear skin incision approximately 6 cm in length was made above the left ear directly over the lesion. A craniectomy approximately 2 cm x 2 cm was made with a high speed drill and enlarged slightly with the use of a manual bone bitting instrument. The aura was opened using a T-style incision. The underlying brain had a normal appearance. At this time, the localizing forceps was used to confirm location of the lesion.[6] The lesion was encountered 1.5 cm beneath the cortex as expected. Upon direct visualization, purulent necrotic tissue within a firm capsule was found and removed. Prior to removal of the lesion, aerobic, anaerobic and fungal cultures as well as acid fast bacillus culture and gram stain were obtained and sent to the laboratory.


Pathological findings confirmed blood clot and necrotic cell debris. No neoplasm was present. Since purulent material was seen at the time of surgery, the patient was immediately started on a broad-spectrum antibiotic, cefotaxime (Claforan), 2 grams intravenously every six hours and metronidazole (Flagyl) 500 mg intravenously every eight hours until results of the cultures taken during surgery were available. The patient was monitored overnight in the neurosurgical intensive care unit and transferred to the neurosurgical floor the following day.

Forty-eight hours after surgery, results of the cultures showed growth of Streptococcus intermedius. Claforan was discontinued. The patient was started on four million units of intravenous penicillin every four hours and remained on the same dose of Flagyl. Complete blood counts were frequently performed as long-term antibiotic treatment can lower the white blood cell count.

Hospital Course

While hospitalized, an MRI of the brain was obtained at weeks two, three and four after diagnosis of multiple cerebral abscesses had been confirmed to determine response to intravenous antimicrobial therapy. Gradual decrease in size of the lesions was observed. The MRI taken at week four demonstrated one persistent lesion in the left temporal lobe that was the slowest--to decreased in size.

Four days after surgery, the patient developed eructations and bloating and a stool specimen was guiac positive. Another source of Streptococcus intermedius is lower gastrointestinal cancer. Bacteremic septic emboli were suspected. Results of blood cultures were negative. A CT of the pelvis with oral and intravenous dye was performed which was negative. The patient developed a reaction to the dye manifested by a macular and papular skin rash with pruritus treated with diphenhydramine (Benadryl), 50 mg by mouth every eight hours and allergic diverticulitis treated with simethicone (Mylanta), 40 mg four times a day until resolution.

Eight days after surgery, the patient developed deep vein thrombosis of the left calf manifested by calf tenderness and swelling. A doppler study showed bilateral venous thrombosis involving both legs without progression to the popliteal level on either side. Intravenous heparin and oral warfarin sodium were started. Heparin was discontinued after the prothrombin time reached 18 seconds with an International Normalization Ratio (INR) of 2 which is within the acceptable ratio of 1.7-2.5 for patients receiving therapy for venous thromboembolism.

Eleven days after surgery, the patient developed forearm phlebitis secondary to rotation of intravenous sites. Length of intravenous therapy was unknown and the patient underwent placement of a single lumen Hickman catheter using a local anesthetic. The patient was monitored by an anesthesiologist during the surgery. The procedure was well tolerated.

Eighteen days after surgery, the patient experienced pain in his left leg. Ultrasound confirmed the presence of multiple deep vein thrombosis. Heparin was restarted. The reason for his tendency to develop thrombosis and his hypercoagulable state was unknown. He was placed on bedrest with his left leg elevated 45 degrees. Four days later he was able to ambulate with assistance. Coumadin was restarted the following day.

During the next two weeks, the patient continued to physically improve. A faint rash remained on his chest and back without pruritus. White blood count was stable. Slight pedal edema persisted without leg pain, tenderness or swelling. He participated in physical therapy and occupational therapy. He was discharged to his home five weeks after surgery when extensive tests revealed no apparent residual source of infection. At time of discharge, the patient could repeat sentences, read most of the given words and sentences but had difficulty reading complex words. He could name most of the given objects however; naming detailed objects remained unchanged from admission and speech was occasionally interrupted by inability to name words.

Arrangements were made for a visiting nurse to continue his intravenous penicillin and Flagyl therapy for an additional two weeks at home and to monitor his vital signs. A complete blood count, chemistry and prothrombin time were obtained and monitored biweekly. He remained on 5 mg of Coumadin every day for three months. Repeat cranial MRIs were obtained at week three, nine and twelve after hospital discharge to assure that the intracranial lesions continued to resolve. Over time and with daily speech therapy, the patient's symptoms dramatically improved.


MRI is invaluable in the initial assessment of a patient presenting with a history of mental status changes. Although a ring-enhancing lesion suggests a pyogenic process, ring-enhancement with cerebral edema is also seen in patients with gliomas, metastatic lesions, hematomas and hemorrhagic infarcts.[3,12,14,18,19,21] This case was complicated by the presence of hemorrhage and multiple lesions.

Evolution of brain abscess can be divided into four stages based on histological criteria: early and late cerebritis and early and late capsule formation.[5] In non-immunocompromised patients, cerebritis is characterized on MRI by an area that has a dark center representing necrosis surrounded by a white circular area (known as enhancement) which is thick and diffuse and seen after administration of gadopentetate dimeglumine intravenously. Histologically, a few small scattered blood vessels are present. In the capsule formation stage, a well-defined thin-circular enhancing collagen capsule is seen. Surrounding edematous brain is usually seen in patients at least two weeks after symptoms onset.[1]

History and physical findings are vital to correlate abnormalities found on MRI scans. Although a preoperative diagnosis of brain abscesses was considered in this patient, the MRI findings were felt to be more consistent with multiple strokes. However, in patients with a stroke, simultaneous hemorrhage inside multiple lesions has not been reported.

Usual predisposing factors for intracranial abscess include congenital heart disease, intrathoracic infection and chronic otitis or mastoiditis.[17] Previous history of upper respiratory tract infection was unknown at time of hospital admission and would have been beneficial in diagnosis of the patient. Information that he had been treated two weeks before admission for flu-like symptoms with an antibiotic was discovered incidentally two days postoperatively.

Presence of hemorrhage into the lesions made diagnosis difficult. Intracranial hemorrhage is uncommon but may be seen in the presence of a brain tumor. Brain abscess with hemorrhage is an even less occurrence and has only been reported in two previous cases involving a single abscess.[2,17]

Pathogenesis of hemorrhage into an abscess is not completely understood. It has been postulated that developing thin-walled vessels may become distorted because of increased intracranial pressure. When hemorrhage occurs, blood is directed to the area of least resistance that is the necrotic center of the abscess.[1,17]

Serial follow-up MRI or CT scans are invaluable in monitoring therapy response. After initial diagnosis, scans are performed frequently to determine if the patient is responding to antimicrobial therapy. Frequency of scans depends on the patient's response to therapy. Persistent ring-enhancement that was documented by MRIs on this patient, has been observed after discontinuance of steroid therapy.[21] Increase in enhancement after discontinuation of steroids may represent a loss of steroid effect on the blood-brain barrier. Loss of steroid suppression of inflammatory cell response is also seen.

A residual ring-enhancement focus has numerous causes. Serial scans have shown that the enhancing focus usually resolves within three to four months but may take as long as eight months to dissipate. However, the patient should be monitored closely for recurrence or other disease entities such as cerebral infarction.


Brain abscess with hemorrhage is rare and has only been reported in cases involving hemorrhage into a single lesion. An extensive review of the literature revealed that no previous case documentation of multiple brain abscesses in both cerebral hemispheres with hemorrhage exists.

This patient matches the typical profile of how a person can develop cerebral abscess. His symptoms began with flu-like manifestations involving the upper respiratory tract. Frequently an associated sinus infection is present.

Although examinations were performed in anticipation of identifying a reason to explain and treat the patient without resorting to craniotomy, it was impossible in his case. Utilizing MRI computer guidance, a minimally invasive craniotomy was performed to obtain the necessary tissue to determine a diagnosis. Material submitted for culture at time of surgery resulted in identifying Streptococcus intermedius as the organism responsible for his multiple abscesses. Penicillin is the drug of choice in treating streptococcus intermedius and is what this patient received along with Flagyl.[4]

Serial MRIs were used to follow resolution of this patient's multiple cerebral abscesses because MRI was the imaging modality first used to diagnose the problem and MRI-guided craniotomy was used to remove one lesion for diagnosis. Switching to a different imaging modality such as CT, was not done because accurate comparison of lesions using two different imaging modalities is impossible.

Recovery from brain abscess is normally seen in three to four months, but may take as long as eight months before the organism is irradiated. Confirmation of abscess resolution in this patient was documented at month five with an outpatient MRI using 5 mm slice thicknesses. After administration of gadopentetate dimeglumine, figures 11-16 show resolution and/or disappearance of lesions indicating positive response to therapy.



The author gratefully acknowledges Richard D. Bucholz, MD, FACS, Professor and Director of the Jean H. Bakewell Section of Image Guided Surgery at St. Louis University Health Sciences Center for his review and recommendations in preparation of this manuscript. The author is thankful to Karen Engdorf, MHA, PhD of the Biomedical Communications Department at St. Louis University Health Sciences Center for her assistance and creativity of the artwork provided for this manuscript.


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[3.] Blaquiere RM: The computed tomographic appearances of intra- and extracerebral abscesses. Br J Radiol 1983; 56:171-181.

[4.] Brewer NS, MacCarty CS, Wellman WE: Brain abscess: A review of recent experience. Ann of Intern Med 1975; 82:571-576.

[5.] Britt R, Enzmann D: Clinical stages of human brain abscess on serial CT scans after contrast infusion. J Neurosurg 1983; 59:972-989.

[6.] Bucholz RD: Image Guidance for Infections and Trauma. Neurosurgery Clinics of North America, Macuinas R (editor). WB Saunders Company, in press.

[7.] Bucholz RD, Smith KR: A comparison of sonic versus light emitting diode based localization. Pages 179-200 in: Interactive Image-Guided Neurosurgery, Macunias R (editor). The American Association of Neurological Surgeons, 1993.

[8.] Bucholz RD, Smith KR, Baumann CK, McDurmont L, Schultz D: Intraoperative localization with an optical digitizer. Proceedings of the XIth meeting of the World Society for Stereotactic and Functional Neurosurgery 1994; 63(1-4):100.

[9.] Bucholz RD, Smith KR, Henderson J, McDurmont L, Schultz D: Clinical Applications of Modern Imaging Technology. Society of Photo-Optical Instrumentation Engineers (SPIE) Proceedings, Intraoperative Localization Using a Three Dimensional Optical Digitizer. 1993; 1894:312-322.

[10.] Henderson JM, Bucholz RD: Accurate and ergonomic method of registration for image-guided neurosurgery. Computer Medical Imaging and Graphics 1994; 18(4):273-277.

[11.] Hoffman HJ, Hendrick EB, Hiscox JL: Cerebral abscess in early infancy. J Neurosurg 1970; 33:172-177.

[12.] Holtas S, Tornquist C, Cronqvist S: Diagnostic difficulties in computed tomography of brain abscesses. J Comp Assist Tomogr 1982; 6:683-688.

[13.] Jamjoom AB, Atasoy M, Coakham HB: Spontaneous haemorrhage in a cerebellar abscess: A unique complication. Br J Neurosurg 1990; 4:231-236.

[14.] Kandalaft N, Diehl J, Neuwelt EA: Nonneoplastic intracranial lesions simulating neoplasms on computed tomographic scan. JAMA 1982; 248:2166-2168.

[15.] Kase CS: Intracerebral haemorrhage: Non-hypertensive causes. Stroke 1986; 17:590-595.

[16.] Nakagawa Y, Shinno K, Akaike Y, Fujimoto N, Okajima K, Matsumoto K Neurol Med Chir (Tokyo) 1989;29:861-863.

[17.] Orita T, Fujii M, Hayashi M, Fudaba H, Aoki H: Brain abscess with haemorrhage. Neuroradiology 1987; 29:576-577.

[18.] Salzman C, Tuazon C: Value of the ring-enhancing sign in differentiating intracerebral hematomas and brain abscesses. Arch Intern Med 1987; 147:951-52.

[19.] Stevens EA, Norman D, Kramer RA et al: Computed tomographic brain scanning in intraparenchymal pyogenic abscesses. AJR 1978; 130:111-114.

[20.] Smith KR, Bucholz RD: Computer methods for improved diagnostic image display applied to stereotactic neurosurgery. Automedica 1992; 14:371-382.

[21.] Whelan MA, Hilal SK: Computed tomography as a guide in the diagnosis and follow-up of brain abscess. Radiology 1980; 135:663-671.

Questions or comments about this article may be directed to: Carol K. Baumann, RN, MSN(R), CNOR, Division of Neurosurgery, Bakewell Section of Image Guided Surgery, 1320 South Grand, St. Louis, Missouri 63104-1087. She is a clinical nurse specialist in the Division of Neurosurgery.
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Author:Baumann, Carol K.
Publication:Journal of Neuroscience Nursing
Date:Feb 1, 1997
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