286
Surg Neurol 1991;35:286-9
Fungal Brain Abscesses (Aspergillosis/Mucormycosis) in Two Immunosuppressed Patients Nancy E. Epstein, M.D., Renee Hollingsworth, P.A., Karen Black, M.D., and Peter Farmer, M.D. Department of Surgery, Division of Neurosurgery, Department of Radiology, Division of Neuroradiology, and Department of Pathology, North Shore University Hospital, Manhasset, and Cornell University Medical College, New York, New York
Epstein NE, Hollingsworth R, Black K, Farmer P. Fungal brain abscesses (aspergillosis/mucormycosis) in two immunosuppressed patients. Surg Neurol 1991;35:286-9.
Although the mortality rate for fungal brain abscesses in immunosuppressed patients remains unacceptably high, this figure may be reduced if computed tomography or magnetic resonance imaging scans are performed more promptly in susceptible individuals with seemingly mild intracranial complaints. Earlier presumptive amphotericin B treatment and more timely surgical debridement may minimize neurological injury and enhance survival. These assumptions were only tentatively supported by the clinical courses of two patients, one an alert patient with promyelocytic leukemia and an aspergillosis brain abscess who survived, and the other, a comatose intravenous drug abuser with mucormycosis who died. KEY WORDS: Aspergillosis; Mucormycosis; Brain abscess; Immunosuppression
The mortality rate for aspergillosis or mucormycosis brain abscesses in immunocompromised patients approaches 8 5 % - 100% [2,6,8,9]. However, if magnetic resonance imaging (MRI) or computed tomography (CT) scans are presumptively performed in patients with seemingly minor cerebral complaints, earlier lesion identification and treatment with amphotericin B and surgery may enhance survival [2,6,8,9]. O f the two cases presented, the survival of the first patient with acute promyelocytic leukemia (APL) and an aspergillosis brain abscess was attributed to the patient's minimal preoperative neurological deficit, the rapid institution of amphotericin B therapy, and surgery, whereas the second patient, an intravenous drug abuser
Address reprint requests to: Nancy E. Epstein, M.D., 410 Lakeville Road #100, New Hyde Park, New York 11042. Received June 18, 1990; accepted August 21, 1990. © 1991 by Elsevier Science PublishingCo., Inc
with mucormycosis who presented in coma, could not be salvaged.
Case R e p o r t s
Case 1 Acute promyelocytic leukemia was diagnosed in a 46year-old white man. One month later, following several courses of chemotherapy [Adriamycin (Adria, Dublin, Ohio), Cyotocan, daunorubicin], profound pancytopenia and immunosuppression contributed to the development of hemoptysis. When a right lower lobe pneumonic infiltrate was identified on plain x-ray film examination, broad spectrum antibiotics (gentamicin, vancomycin, ticarcillin) and amphotericin B (45 mg/day) were presumptively administered. Eight days later, acyclovir was added to the antibiotic regimen to address left ear pain and difficulty in swallowing attributed to herpetic pharyngitis. This diagnosis was changed to external otitis 3 weeks later when an acute left peripheral facial palsy evolved in conjunction with rupture of the tympanic membrane. The serosanguinous drainage that followed showed a fungal species, presumed to be Candida, and amphoteritin B therapy was continued. The noncontrast and constrast-enhanced CT studies confirmed the diagnosis of a middle ear infection, as the left middle ear and mastoid air cells were opacified in the absence of frank bony destruction or intracranial invasion. However, by 5 weeks, confusion and dysphasia prompted the performance of a second contrast-enhanced CT scan and a gadolinium-enhanced MRI study, both of which demonstrated a left temporal cerebritis and destruction of the left petrous bone, mastoid air cells, and external auditory canal complex. At 7 weeks, well-defined multiloculated inferior temporal lobe abscess cavities and progressive lytic changes led to surgical intervention (Figure 1). The operation included resection of the inferior temporal lobe abscesses and debride0090-3019/!) I / $'~ 50
Fungal Brain Abscesses
Surg Neurol 1991;35:286-9
287
Figure 1. Contrast-enhanced CT scan--left temporal aspergillosis abscess-case I. (A) Low axial temporal CT scan. On this contrast-enhanced CT study multiloculated abscesses readily enhanced with contrast in the inferior left temporal lobe (arrow). These well-circumscribedcavities appear contiguous with the petrous pyramid and temporal base below. (B) Mid temporalaxial CT scan. More superiorly, the temporallobeappears diffusely hypodense around well-circumscribed ring-enhancing daughter lesions (arrow~.
ment of the external canal, petrous apex, and mastoid air cells. Of the tissue removed at surgery, the histologic evaluation proved diagnostic for aspergillosis, as the typical large septated dichotomous hyphae with regular angular branching were identified. Alternatively, the Gram stain was negative while the cultures only became positive 3 weeks later. Following surgery, although the patient's confusion and dysphasia rapidly resolved, he was left with a residual partial left peripheral seventh nerve palsy. The CT scans obtained postoperatively over the next 4 months demonstrated continued regression of the left temporal mass effect associated with the fungal cerebritis (Figure 2).
Case 2 A 39-year-old male Vietnam Veteran, a known HIVnegative intravenous drug abuser, insulin-dependent diabetic, and cirrhotic, presented to the emergency room
Figure 2. PostoperativenoncontrastCTscan--lefttemporalabscess--case 1. (A) Low temporal axial CT scan. This secondscan was obtained I week after surgery, which included debridement of the external auditory canal, petrous apex, and mastoid sinus plus removalof the temporal lobeabscesses. Observe the extent of residual hypodense mass effect seen on the low (white arrows) temporal image demonstrated. Also observethe diffuse patchy hemorpostoperative changes. (B) Mid temporal axial CT scan. On the mid temporal axial CT image (black arrows), the large region of temporal hypodensity reflected resolving cerebritis and edema.
Figure 3. Contrast-enhanced CT scan--right ethmoid sinus--case 2. The contrast-enhanced CT scan of the brain through the base of the skull shows mucosal thickening of the right ethmoid air cells consistent with inflammatory changes (white arrows).
in coma following a 1-week history of headache and lethargy. Intubated, without spontaneous respiration, and bilaterally decerebrate to noxious stimuli, the patient exhibited sluggish pupillary and absent oculovestibular responses. Jaundice, periorbital edema, poor dental hygiene, and focal erosion of the hard palate and nasal septum further contributed to his disheveled appearance. Emergent noncontrast and contrast-enhanced CT scans documented opacification of the right ethmoid sinus and a right frontal brain abscess (Figures 3 and 4). The frontal lesion was hypodense and did not enhance with contrast, except at its most inferomedial perimeter, where it became contiguous with the cribiform plate. The marked right to left shift, as indicated by the deformation of the right frontal ventricular horn, resulted in transfalcine herniation. Preoperative correction of the patient's elevated prothrombin time was initiated with the administration of two units of fresh frozen plasma, while thrombocytopenia was similarly addressed with platelet transfusions. Having attempted to reverse the preexisting coagulopathy, an emergency right frontal craniotomy was performed. When the bone flap was elevated, the arachnoid
288
Surg Neurol 1991;35:286-9
Epstein et al
was creamy and discolored. Anteroinferiorly, an encapsulated abscess was excised, whereas posteriorly, the margin between abscess/cerebritis and normal brain became increasingly obscure. Once an adequate frontal decompression had been achieved, meticulous hemostasis was mandated. Despite expeditious surgical debridement and documentation of excellent control of postoperative intracranial pressure using the Cammino fiber optic intracranial pressure monitor placed in the brain parenchyma, the patient never improved. He further exhibited electrolyte imbalance, coagulopathy, leukopenia, anemia, hyperthermia, hypotension, and life-threatening cardiac arrhythmias. Unfortunately, the administration of amphotericin B and attendant discontinuation of ceftriaxone and vancomycin was delayed until the third postoperative day, when murcormycosis was histologically confirmed in the operative specimen based on the degree of angioinvasion demonstrated by nondichotomous, branching, nonseptated hyphae. The patient died on the fifth postoperative day.
Discussion
Figure 4. Contrast-enhanced C T scan--right frontal brain abscess/cerebritis--case 2. (A) Low frontal transsaxial scan of the brain. The axial contrast-enhanced C T scan demonstrates a lucency in the right inferior frontal lobe, contiguous with the right ethmoid sinus below, which extended posteriorly into the right basal ganglia (arrow). (B) Transaxial scan at the mid ventricular level This hypodense lesion is also responsible for the production of significant mass effect on the right lateral ventricle (arrowsJ. When the noncontrast and contrast-enhanced C T scans were compared, there was no evidence of significant focal enhancement. These findings were most suggestive of an inflammatory process, such as a cerebritis, the distribution and lack of enhancement making other diagnoses such as ischemia and neoplasm less likely.
Fungal brain abscesses arise as the result of hematogenous spread from the lung or through direct invasion of adjacent cranial structures [2,6-8]. If infection has already invaded the paranasal sinuses or palate, it may spread across the ethmoid sinuses and cribiform plate, to the intracranial compartment where the meninges, nerves, lymphatic channels, and blood vessels may become involved [2,3,6,9]. In descending order, Candida, Aspergillus, Cryptococcus, and various species in the family of Mucoraceae are reported to be the four fungal organisms most likely to be responsible for brain abscesses in immunosuppressed individuals [ 1-9]. Aspergillosis typically produces large septate hyphae that are dichotomous, branching, nonseptate hyphae with evidence of frank vascular invasion, granuloma formation, and giant cell reaction [ 1 - 3,6,7]. For both aspergillosis and mucormycosis, extension to surrounding neural tissues and blood vessels promotes hemorrhage, thrombosis, infarction, necrosis, meningitis, and ventriculitis [6,7]. Whereas operative specimens may prove sterile in patients who have been receiving amphotericin B, Gram stains and histology should still confirm the two diagnoses [2,7]. Immunosuppressed patients are more likely to acquire aspergillosis or mucormycosis fungal infections. This population includes diabetics, those with poor dental hygiene, patients with tumors on long-term steroid medication or chemotherapy, and intravenous drug abusers. The latter demonstrate a greater susceptibility to cerebral mucormycosis than aspergillosis, frequently
Fungal Brain Abscesses
presenting with precipitous neurological devastation in the absence of systemic or local disease [ 4 , 6 - 8 ] . T h e CT findings for i m m u n o c o m p r o m i s e d patients with cerebral abscesses attributed to aspergillosis or mucormycosis typically include a diffuse hypodense lesion that does not enhance with contrast. T h e lack of contrast enhancement is a p o o r prognostic sign as it indicates failure of the host defense mechanism to isolate or encapsulate the offending organisms, as in the eight patients in the series of Enzmann et al, all of w h o m died [1,3,9]. Although the mortality rate approaches 8 5 % - 1 0 0 % for immunosuppressed patients with cerebral aspergillosis or m u c o r m y c o s i s - - t h e graver prognoses reflecting the greater degrees o f neurological devastation at the time o f p r e s e n t a t i o n - - t h e literature does contain occasional case reports in which patients survived [ 3 - 5 , 9 ] . G o o d m a n and Coffey [2] cited four patients in the literature, and added a fifth of their own, with aspergillosis brain lesions who were treated with success. These authors attributed the survival of their 44-year-old patient with acute myelocytic leukemia and a bilobed occipital lesion to the early presumptive administration of amphotericin B and rapid stereotactic drainage. Such a p r o m p t intervention decompressed the abscess cavity while providing histopathological confirmation of aspergillosis [2]. Unfortunately, even poorer prognoses are observed for immunosuppressed patients with intracranial mucormycosis [9]. W o o d s and H a n n a [9] noted a 100% mortality rate for the four cases of intravenous drug abusers with cerebral mucormycosis reported in the literature. They then introduced a fifth case, an intravenous drug addict with a brain stem lesion, who lived presumably because amphotericin B was administered early in the clinical course. Hamill et al [3] similarly attributed the survival of a diabetic with bifrontal cerebral mucormycosis abscesses to such timely therapy. T h e presumptive administration of amphotericin B in a patient considered at risk for aspergillosis or mucormycosis, either involving the lung or intracranial cavity, appears to increase the chance for survival. Appropriate surgical intervention, including biopsy, craniotomy, or stereotactic drainage, should also accompany antifungal therapy both to establish the diagnosis and to afford needed debridement or decompression. In order to treat immunosuppressed patients with
Surg Neurol 1991;35:286-9
289
aspergillosis or mucormycosis brain abscesses most effectively, those with cranial and/or adnexal complaints should be screened with CT or M R I scans early in the clinical course. Looking for these mycotic infections prior to the onset of neurological deficits, presumptively instituting antifungal therapy (amphotericin B), and performing surgical decompression in a m o r e timely fashion, could enhance survival [3,6,8,9].
Summary Despite more advanced medical and surgical management as aspergillosis and mucormycosis brain abscesses in i m m u n o c o m p r o m i s e d patients, the mortality figures continue to approach 8 5 % - 1 0 0 % [7,9]. I m p r o v e d survival appears contingent on early lesion detection on CT or MRI scans prior to the evolution o f major neurological deficits, the immediate presumptive administration o f amphotericin B, and m o r e timely surgical intervention. The authors wish to express their appreciation to Sherry Lynn Grimm for her assistance in the typing and preparation of this manuscript.
References 1. EnzmannDR, Brant-ZawadzkiM, Britt RH. CT of central nervous system infections in immunocompromised patients. AJR 1980; 135:263-7. 2. Goodman ML, Coffey RJ. Stereotactic drainage of Aspergil/us brain abscess with long-term survival: case report and review. Neurosurgery 1989;24:96-9. 3. Hamill R, Oney LA, Crane LR. Successfultherapy for rhinocerebral mucormycosiswith associated bilateral brain abscesses. Arch Intern Med 1983;13:581-3. 4. Karandanis D, Shulman JA, Factors associated with mortality in brain abscesses. Arch Intern Med 1975;135:1145-50, 5. LevyRM, Rosenbloom S, Perrett LV. Neuroradiologic findings in AIDS: a review of 200 cases. AJR 1986;147:977-83. 6. LoweJ, BradleyJ. Cerebra and orbital Aspergi//us infection due to invasive aspergillosis of ethmoid sinus. J Clin Pathol 1986;39:774-8. 7. Masucci EF, Fabara JA, Saini N, Kurtzke JF. Cerebral mucormycosis (phycomycosis) in a heroin addict. Arch Neurol 1982; 39:304-6. 8. WalshTJ, Hier DB, Caplan LR. Aspergillosisof the central nervous system: clinicopathological analysis of 17 patients. Ann Neurol 1985;18:574-82. 9. WoodsKF, Hanna BJ. Brain stem mucormycosisin a narcotic addict with eventual recovery. Am J Med 1986;80:126-8.
Surg Neurol 1991;35:286-9
Fungal Brain Abscesses (Aspergillosis/Mucormycosis) in Two Immunosuppressed Patients Nancy E. Epstein, M.D., Renee Hollingsworth, P.A., Karen Black, M.D., and Peter Farmer, M.D. Department of Surgery, Division of Neurosurgery, Department of Radiology, Division of Neuroradiology, and Department of Pathology, North Shore University Hospital, Manhasset, and Cornell University Medical College, New York, New York
Epstein NE, Hollingsworth R, Black K, Farmer P. Fungal brain abscesses (aspergillosis/mucormycosis) in two immunosuppressed patients. Surg Neurol 1991;35:286-9.
Although the mortality rate for fungal brain abscesses in immunosuppressed patients remains unacceptably high, this figure may be reduced if computed tomography or magnetic resonance imaging scans are performed more promptly in susceptible individuals with seemingly mild intracranial complaints. Earlier presumptive amphotericin B treatment and more timely surgical debridement may minimize neurological injury and enhance survival. These assumptions were only tentatively supported by the clinical courses of two patients, one an alert patient with promyelocytic leukemia and an aspergillosis brain abscess who survived, and the other, a comatose intravenous drug abuser with mucormycosis who died. KEY WORDS: Aspergillosis; Mucormycosis; Brain abscess; Immunosuppression
The mortality rate for aspergillosis or mucormycosis brain abscesses in immunocompromised patients approaches 8 5 % - 100% [2,6,8,9]. However, if magnetic resonance imaging (MRI) or computed tomography (CT) scans are presumptively performed in patients with seemingly minor cerebral complaints, earlier lesion identification and treatment with amphotericin B and surgery may enhance survival [2,6,8,9]. O f the two cases presented, the survival of the first patient with acute promyelocytic leukemia (APL) and an aspergillosis brain abscess was attributed to the patient's minimal preoperative neurological deficit, the rapid institution of amphotericin B therapy, and surgery, whereas the second patient, an intravenous drug abuser
Address reprint requests to: Nancy E. Epstein, M.D., 410 Lakeville Road #100, New Hyde Park, New York 11042. Received June 18, 1990; accepted August 21, 1990. © 1991 by Elsevier Science PublishingCo., Inc
with mucormycosis who presented in coma, could not be salvaged.
Case R e p o r t s
Case 1 Acute promyelocytic leukemia was diagnosed in a 46year-old white man. One month later, following several courses of chemotherapy [Adriamycin (Adria, Dublin, Ohio), Cyotocan, daunorubicin], profound pancytopenia and immunosuppression contributed to the development of hemoptysis. When a right lower lobe pneumonic infiltrate was identified on plain x-ray film examination, broad spectrum antibiotics (gentamicin, vancomycin, ticarcillin) and amphotericin B (45 mg/day) were presumptively administered. Eight days later, acyclovir was added to the antibiotic regimen to address left ear pain and difficulty in swallowing attributed to herpetic pharyngitis. This diagnosis was changed to external otitis 3 weeks later when an acute left peripheral facial palsy evolved in conjunction with rupture of the tympanic membrane. The serosanguinous drainage that followed showed a fungal species, presumed to be Candida, and amphoteritin B therapy was continued. The noncontrast and constrast-enhanced CT studies confirmed the diagnosis of a middle ear infection, as the left middle ear and mastoid air cells were opacified in the absence of frank bony destruction or intracranial invasion. However, by 5 weeks, confusion and dysphasia prompted the performance of a second contrast-enhanced CT scan and a gadolinium-enhanced MRI study, both of which demonstrated a left temporal cerebritis and destruction of the left petrous bone, mastoid air cells, and external auditory canal complex. At 7 weeks, well-defined multiloculated inferior temporal lobe abscess cavities and progressive lytic changes led to surgical intervention (Figure 1). The operation included resection of the inferior temporal lobe abscesses and debride0090-3019/!) I / $'~ 50
Fungal Brain Abscesses
Surg Neurol 1991;35:286-9
287
Figure 1. Contrast-enhanced CT scan--left temporal aspergillosis abscess-case I. (A) Low axial temporal CT scan. On this contrast-enhanced CT study multiloculated abscesses readily enhanced with contrast in the inferior left temporal lobe (arrow). These well-circumscribedcavities appear contiguous with the petrous pyramid and temporal base below. (B) Mid temporalaxial CT scan. More superiorly, the temporallobeappears diffusely hypodense around well-circumscribed ring-enhancing daughter lesions (arrow~.
ment of the external canal, petrous apex, and mastoid air cells. Of the tissue removed at surgery, the histologic evaluation proved diagnostic for aspergillosis, as the typical large septated dichotomous hyphae with regular angular branching were identified. Alternatively, the Gram stain was negative while the cultures only became positive 3 weeks later. Following surgery, although the patient's confusion and dysphasia rapidly resolved, he was left with a residual partial left peripheral seventh nerve palsy. The CT scans obtained postoperatively over the next 4 months demonstrated continued regression of the left temporal mass effect associated with the fungal cerebritis (Figure 2).
Case 2 A 39-year-old male Vietnam Veteran, a known HIVnegative intravenous drug abuser, insulin-dependent diabetic, and cirrhotic, presented to the emergency room
Figure 2. PostoperativenoncontrastCTscan--lefttemporalabscess--case 1. (A) Low temporal axial CT scan. This secondscan was obtained I week after surgery, which included debridement of the external auditory canal, petrous apex, and mastoid sinus plus removalof the temporal lobeabscesses. Observe the extent of residual hypodense mass effect seen on the low (white arrows) temporal image demonstrated. Also observethe diffuse patchy hemorpostoperative changes. (B) Mid temporal axial CT scan. On the mid temporal axial CT image (black arrows), the large region of temporal hypodensity reflected resolving cerebritis and edema.
Figure 3. Contrast-enhanced CT scan--right ethmoid sinus--case 2. The contrast-enhanced CT scan of the brain through the base of the skull shows mucosal thickening of the right ethmoid air cells consistent with inflammatory changes (white arrows).
in coma following a 1-week history of headache and lethargy. Intubated, without spontaneous respiration, and bilaterally decerebrate to noxious stimuli, the patient exhibited sluggish pupillary and absent oculovestibular responses. Jaundice, periorbital edema, poor dental hygiene, and focal erosion of the hard palate and nasal septum further contributed to his disheveled appearance. Emergent noncontrast and contrast-enhanced CT scans documented opacification of the right ethmoid sinus and a right frontal brain abscess (Figures 3 and 4). The frontal lesion was hypodense and did not enhance with contrast, except at its most inferomedial perimeter, where it became contiguous with the cribiform plate. The marked right to left shift, as indicated by the deformation of the right frontal ventricular horn, resulted in transfalcine herniation. Preoperative correction of the patient's elevated prothrombin time was initiated with the administration of two units of fresh frozen plasma, while thrombocytopenia was similarly addressed with platelet transfusions. Having attempted to reverse the preexisting coagulopathy, an emergency right frontal craniotomy was performed. When the bone flap was elevated, the arachnoid
288
Surg Neurol 1991;35:286-9
Epstein et al
was creamy and discolored. Anteroinferiorly, an encapsulated abscess was excised, whereas posteriorly, the margin between abscess/cerebritis and normal brain became increasingly obscure. Once an adequate frontal decompression had been achieved, meticulous hemostasis was mandated. Despite expeditious surgical debridement and documentation of excellent control of postoperative intracranial pressure using the Cammino fiber optic intracranial pressure monitor placed in the brain parenchyma, the patient never improved. He further exhibited electrolyte imbalance, coagulopathy, leukopenia, anemia, hyperthermia, hypotension, and life-threatening cardiac arrhythmias. Unfortunately, the administration of amphotericin B and attendant discontinuation of ceftriaxone and vancomycin was delayed until the third postoperative day, when murcormycosis was histologically confirmed in the operative specimen based on the degree of angioinvasion demonstrated by nondichotomous, branching, nonseptated hyphae. The patient died on the fifth postoperative day.
Discussion
Figure 4. Contrast-enhanced C T scan--right frontal brain abscess/cerebritis--case 2. (A) Low frontal transsaxial scan of the brain. The axial contrast-enhanced C T scan demonstrates a lucency in the right inferior frontal lobe, contiguous with the right ethmoid sinus below, which extended posteriorly into the right basal ganglia (arrow). (B) Transaxial scan at the mid ventricular level This hypodense lesion is also responsible for the production of significant mass effect on the right lateral ventricle (arrowsJ. When the noncontrast and contrast-enhanced C T scans were compared, there was no evidence of significant focal enhancement. These findings were most suggestive of an inflammatory process, such as a cerebritis, the distribution and lack of enhancement making other diagnoses such as ischemia and neoplasm less likely.
Fungal brain abscesses arise as the result of hematogenous spread from the lung or through direct invasion of adjacent cranial structures [2,6-8]. If infection has already invaded the paranasal sinuses or palate, it may spread across the ethmoid sinuses and cribiform plate, to the intracranial compartment where the meninges, nerves, lymphatic channels, and blood vessels may become involved [2,3,6,9]. In descending order, Candida, Aspergillus, Cryptococcus, and various species in the family of Mucoraceae are reported to be the four fungal organisms most likely to be responsible for brain abscesses in immunosuppressed individuals [ 1-9]. Aspergillosis typically produces large septate hyphae that are dichotomous, branching, nonseptate hyphae with evidence of frank vascular invasion, granuloma formation, and giant cell reaction [ 1 - 3,6,7]. For both aspergillosis and mucormycosis, extension to surrounding neural tissues and blood vessels promotes hemorrhage, thrombosis, infarction, necrosis, meningitis, and ventriculitis [6,7]. Whereas operative specimens may prove sterile in patients who have been receiving amphotericin B, Gram stains and histology should still confirm the two diagnoses [2,7]. Immunosuppressed patients are more likely to acquire aspergillosis or mucormycosis fungal infections. This population includes diabetics, those with poor dental hygiene, patients with tumors on long-term steroid medication or chemotherapy, and intravenous drug abusers. The latter demonstrate a greater susceptibility to cerebral mucormycosis than aspergillosis, frequently
Fungal Brain Abscesses
presenting with precipitous neurological devastation in the absence of systemic or local disease [ 4 , 6 - 8 ] . T h e CT findings for i m m u n o c o m p r o m i s e d patients with cerebral abscesses attributed to aspergillosis or mucormycosis typically include a diffuse hypodense lesion that does not enhance with contrast. T h e lack of contrast enhancement is a p o o r prognostic sign as it indicates failure of the host defense mechanism to isolate or encapsulate the offending organisms, as in the eight patients in the series of Enzmann et al, all of w h o m died [1,3,9]. Although the mortality rate approaches 8 5 % - 1 0 0 % for immunosuppressed patients with cerebral aspergillosis or m u c o r m y c o s i s - - t h e graver prognoses reflecting the greater degrees o f neurological devastation at the time o f p r e s e n t a t i o n - - t h e literature does contain occasional case reports in which patients survived [ 3 - 5 , 9 ] . G o o d m a n and Coffey [2] cited four patients in the literature, and added a fifth of their own, with aspergillosis brain lesions who were treated with success. These authors attributed the survival of their 44-year-old patient with acute myelocytic leukemia and a bilobed occipital lesion to the early presumptive administration of amphotericin B and rapid stereotactic drainage. Such a p r o m p t intervention decompressed the abscess cavity while providing histopathological confirmation of aspergillosis [2]. Unfortunately, even poorer prognoses are observed for immunosuppressed patients with intracranial mucormycosis [9]. W o o d s and H a n n a [9] noted a 100% mortality rate for the four cases of intravenous drug abusers with cerebral mucormycosis reported in the literature. They then introduced a fifth case, an intravenous drug addict with a brain stem lesion, who lived presumably because amphotericin B was administered early in the clinical course. Hamill et al [3] similarly attributed the survival of a diabetic with bifrontal cerebral mucormycosis abscesses to such timely therapy. T h e presumptive administration of amphotericin B in a patient considered at risk for aspergillosis or mucormycosis, either involving the lung or intracranial cavity, appears to increase the chance for survival. Appropriate surgical intervention, including biopsy, craniotomy, or stereotactic drainage, should also accompany antifungal therapy both to establish the diagnosis and to afford needed debridement or decompression. In order to treat immunosuppressed patients with
Surg Neurol 1991;35:286-9
289
aspergillosis or mucormycosis brain abscesses most effectively, those with cranial and/or adnexal complaints should be screened with CT or M R I scans early in the clinical course. Looking for these mycotic infections prior to the onset of neurological deficits, presumptively instituting antifungal therapy (amphotericin B), and performing surgical decompression in a m o r e timely fashion, could enhance survival [3,6,8,9].
Summary Despite more advanced medical and surgical management as aspergillosis and mucormycosis brain abscesses in i m m u n o c o m p r o m i s e d patients, the mortality figures continue to approach 8 5 % - 1 0 0 % [7,9]. I m p r o v e d survival appears contingent on early lesion detection on CT or MRI scans prior to the evolution o f major neurological deficits, the immediate presumptive administration o f amphotericin B, and m o r e timely surgical intervention. The authors wish to express their appreciation to Sherry Lynn Grimm for her assistance in the typing and preparation of this manuscript.
References 1. EnzmannDR, Brant-ZawadzkiM, Britt RH. CT of central nervous system infections in immunocompromised patients. AJR 1980; 135:263-7. 2. Goodman ML, Coffey RJ. Stereotactic drainage of Aspergil/us brain abscess with long-term survival: case report and review. Neurosurgery 1989;24:96-9. 3. Hamill R, Oney LA, Crane LR. Successfultherapy for rhinocerebral mucormycosiswith associated bilateral brain abscesses. Arch Intern Med 1983;13:581-3. 4. Karandanis D, Shulman JA, Factors associated with mortality in brain abscesses. Arch Intern Med 1975;135:1145-50, 5. LevyRM, Rosenbloom S, Perrett LV. Neuroradiologic findings in AIDS: a review of 200 cases. AJR 1986;147:977-83. 6. LoweJ, BradleyJ. Cerebra and orbital Aspergi//us infection due to invasive aspergillosis of ethmoid sinus. J Clin Pathol 1986;39:774-8. 7. Masucci EF, Fabara JA, Saini N, Kurtzke JF. Cerebral mucormycosis (phycomycosis) in a heroin addict. Arch Neurol 1982; 39:304-6. 8. WalshTJ, Hier DB, Caplan LR. Aspergillosisof the central nervous system: clinicopathological analysis of 17 patients. Ann Neurol 1985;18:574-82. 9. WoodsKF, Hanna BJ. Brain stem mucormycosisin a narcotic addict with eventual recovery. Am J Med 1986;80:126-8.
