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Empyema of the cavum septum pellucidum
Empyema of the Cavum Septum Pellucidum Sung-Tse Li, MD*, Nan-Chang Chiu, MD*, Chyong-Hsin Hsu, MD*, and Ming-Fu Chiang, MD† The cavum septum pellucidum is not a part of the brain’s ventricular system and does not communicate with the lateral ventricles. However, under conditions of increased intraventricular pressure, cerebrospinal fluid may penetrate the septum and cause formation of a cavity. We report a neonate with pus accumulation in the cavum septum pellucidum after an episode of ventriculitis. The cavum septum pellucidum disappeared after medical and surgical management of the infection and increased intracranial pressure. © 2002 by Elsevier Science Inc. All rights reserved. Li S-T, Chiu N-C, Hsu C-H, Chiang M-F. Empyema of the cavum septum pellucidum. Pediatr Neurol 2002;26: 391-393.
Introduction Cavum septum pellucidum refers to a space within the septum pellucidum, a midline structure separating the frontal horns of the lateral ventricles. It is a normal variant and usually asymptomatic. The roof of the septum pellucidum is the body of the corpus callosum, rostrum of the corpus callosum located anteroinferiorly, and columns of the fornix located posteroinferiorly. If the space extends posteriorly above the third ventricle and is bounded by the splenium posteriorly, it is called a cavum vergae. Under usual conditions, the cavum septum pellucidum and cavum vergae do not communicate with the lateral ventricles. Accumulation of pus in the cavum septum pellucidum is rare. We report a neonate with increased intracranial pressure who developed an empyema in the cavum septum pellucidum that communicated with the ventricles.
From the *Department of Pediatrics and the †Department of Neurosurgery; Mackay Memorial Hospital; Taipei, Taiwan.
© 2002 by Elsevier Science Inc. All rights reserved. PII S0887-8994(01)00399-X ● 0887-8994/02/$—see front matter
Case Report A male infant was born to a gravida 4 para 3 mother at a gestation of 31 weeks. His birth weight was 1,646 gm. Rupture of the membranes had been evident for 3 months before delivery. He was admitted to the hospital because of prematurity, low birth weight, and respiratory distress. No bacteria were isolated from the cerebrospinal fluid or peripheral blood during the first hospitalization. A group B streptococcus antigen test in the urine was negative. The initial brain echo was normal. He was discharged 35 days after admission. Twelve days after discharge, the infant developed mild fever and irritable crying and was brought to our hospital again. On admission, his temperature was 38.2oC. Blood pressure was 87/48 mmHg. Physical examination was unremarkable. The anterior fontanel was flat at rest but bulged mildly when he cried. A septic evaluation, including blood, cerebrospinal fluid, and urine cultures was performed to determine the origin of the fever. The hemoglobin was 12.8 gm/dL initially, and the peripheral leukocyte count was 16,550/mm3 with 9% band forms, 72% neutrophils, 4% monocytes, and 15% lymphocytes. A lumbar puncture yielded turbid cerebrospinal fluid with more than 10,000 leukocytes (79% neutrophils and 21% lymphocytes), an extremely low glucose (0 mg/dL), and a markedly increased protein (1038 mg/dL). Urinalysis was normal. Because of seizures, hypothermia (35.6°C), and a decreased hemoglobin level (9.3 gm/dL) on the second hospital day, he was transferred to the intensive care unit. Brain echo revealed wall enhancement of the cavum septum pellucidum and internal debris (Fig 1). The result of magnetic resonance imaging also demonstrated abscess formation within the cavum septum pellucidum. Proteus mirabilis was isolated from the cerebrospinal fluid. Fourteen days after admission and treatment with antibiotics, the debris in the cavum septum pellucidum disappeared on sonographic examination, although the size of lateral ventricles increased. Another lumbar puncture performed 2 weeks after the initial puncture revealed leukocytes 44/mm3 (38 neutrophils and 6 lymphocytes), a persistently low glucose (28 mg/dL), and increased protein level (426 mg/dL). However, no bacteria were isolated. Progressive hydrocephalus was monitored by serial brain sonography (Fig 2). Finally a ventriculoperitoneal shunt was placed. The ventricular size returned to normal and the cavum septum pellucidum gradually disappeared (Fig 3). Ampicillin (300 mg/kg/day) and cefotaxime (200 mg/kg/day) were administered initially to treat the Proteus mirabilis meningitis. Ampicillin was then discontinued, and cefotaxime was administered for a total of 6 weeks. Phenobarbital was added to control seizures. Electroencephalogram performed 1 month after admission revealed no epileptiform discharge. Auditory evoked potential was normal. Bilateral mild visualcortical pathway dysfunction was evident on visual-evoked potential. The infant was clinically well on follow-up.
Discussion The cavum septum pellucidum is a normal anatomic structure during fetal growth. It forms during the fourth month of gestation and is present in nearly 100% of premature infants and 15% of 6-month-old infants [1-4]. The septum pellucidum forms from the banks of the
Communications should be addressed to: Dr. Chiu; Department of Pediatrics; 92, Sec 2, Chung Shan N. Road; Taipei 10449, Taiwan. Received October 12, 2001; accepted November 12, 2001.
Li et al: Cavum Septum Pellucidum Empyema 391
Figure 1. Brain sonography of coronal (A) and midline sagittal (B) sections are evident on the first day of the second hospitalization demonstrating high echogenicity of the wall and accumulation of pus in the cavum septum pellucidum.
median groove of the massa commissuralis, which become the lamellae of the septum at 12-20 weeks of gestation [5-7]. The cavum septum pellucidum begins to close posteriorly, with the cavum vergae beginning to narrow at approximately 6 months of gestation. The cavum septum pellucidum begins to disappear just before term and decreases rapidly in size 2 months after delivery. The incidence at 6 months of age is almost equal to that in adults [1]. The cavum septum pellucidum and cavum vergae are sometimes called the fifth and sixth ventricles, but they are actually not part of the ventricular system. Their embryologic origin differs from that of the ventricular system and they are not lined with ependymal or choroid plexus cells [8,9]. Under normal conditions, they do not communicate with the ventricles. The cava contain fluid, but its source is unclear [1]. Cysts forming in the septum pellucidum have been considered to be caused by mechanical occlusion of the foramen of Monro and by hydrocephalus.
However, without communication with the lateral ventricles, enlargement of the cyst is still not well explained. Sam [10] reported a patient with empyema of the cavum septum pellucidum and the cavum vergae who was injured in a car accident 3 years previously. No fracture of the base of the skull was visible on imaging studies. He underwent surgical drainage and medical treatment of the empyema. The causative microorganism was Streptococcus pneumoniae. Although the head injury was trivial, the author still felt it was the accident that had triggered invasion of the pathogen. A noncommunicating cyst might end up in continuity with the ventricle if the septum pellucidum were to rupture spontaneously. Fenestration of the thin wall might be caused by stretching beyond its elastic limit or an imbalance of pressure between the two sides of the septum [1,10-13]. In some cases of hydrocephalus the pressure of the ventricles is so high that the cavum is more likely to be compressed than expanded.
Figure 2. Brain sonography 2 weeks after the second admission. (A) The cavum septum pellucidum is still visible on the coronal view but becoming clearer. (B) Progressively enlarging size of the lateral ventricles was evident on the parasagittal view.
392
PEDIATRIC NEUROLOGY
Vol. 26 No. 5
Figure 3. Brain sonography after ventriculoperitoneal shunt is presented. (A) The coronal view demonstrates disappearance of the cavum septum pellucidum. (B) The parasagittal view reveals resolution of the dilated lateral ventricles.
In our patient, the first brain sonogram after delivery did not reveal a cavum septum pellucidum or hydrocephalus. Although no bacteria were isolated on the first admission, the infant might have had occult infection at that time. The pathogen apparently passed through the blood– brain barrier and caused ventriculitis. Subsequently, increased intraventricular pressure could have caused fenestration of the membrane of the septum pellucidum, allowing the pathogen to invade the cavum and form an abscess. The inflammatory process itself might also have contributed to permeability of the septum. The later onset of hydrocephalus resulted from occlusion of the aqueduct by debris. The ventriculoperitoneal shunt not only improved the hydrocephalus but also led to a decrease in size and, finally, disappearance of the cavum septum pellucidum. The above-proposed process assumes communication between the cavum septum pellucidum and ventricular system. This report illustrated that pus may accumulate in a potential space. The small space and deep location of the cavum septum pellucidum made a surgical approach difficult. Antibiotics may have been helpful in controlling progression of the infection. However, the development of hydrocephalus mandated surgical shunting to relieve the increased intracranial pressure. Medical and surgical management thus both played important roles in the treatment of this patient.
References [1] Shaw CM, Alvord EC. Cava septi pellucidi et vergae: Their normal and pathologic states. Brain 1969;92:213-224. [2] Mott S, Bodensteiner JB, Allan W. The cavum septum pellucidum in preterm and term infants. Ann Neurol 1990;28:452. [3] Dooling EC, Barlow JF, Murphy JV, Richardson EP. Cyst of the cavum septi pellucidi. Arch Neurol 1972;27:79-88. [4] Heiskan O. Cyst of the cavum septum pellucidum causing increased intracranial pressure and hydrocephalus. J Neurosurg 1973;38: 771-3. [5] Rakic P, Yakovlev PI. Development of the corpus callosum and cavum septi in man. J Comp Neurol 1968;132:45-72. [6] Leech RW, Shuman RM. Holoprosencephaly and related midline cerebral anomalies: A review. J Child Neurol 1986;1:3-18. [7] Bodensteiner JB, Schaefer GB. Wide cavum septum pellucidum: A maker of disturbed brain development. Pediatr Neurol 1990;6: 391-394. [8] Silbert PL, Gubbay SS, Vaughan RJ. Cavum septum pellucidum and obstructive hydrocephalus. J Neurosurg Psychiatry 1993;56:820822. [9] Bruyn GW. Agenesis septi pellucidi, cavum septi pellucidi, cavum vergae, and cavum veli interposti. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol 30. Amsterdam: North Holland Publishing Company, 1997:299-337. [10] Sam M. Empyema of the septum pellucidum et vergae. S Afr J Surg 1994;32:109-111. [11] Ciric I, Zivin I. Neuroepithelial (colloid) cysts of the septum pellucidum. J Neurosurg 1975;43:69-73. [12] Assam NI, Timperley WR. Intracerebral cyst due to ectopic choroid plexus. J Neurosurg 1981;55:651-653. [13] Dandy WE. Congenital cerebral cyst of the cavum septi pellucidi (fifth ventricle) and cavum vergae (sixth ventricle). Arch Neurol Psychiatry 1931;25:44-66.
Li et al: Cavum Septum Pellucidum Empyema 393
Introduction Cavum septum pellucidum refers to a space within the septum pellucidum, a midline structure separating the frontal horns of the lateral ventricles. It is a normal variant and usually asymptomatic. The roof of the septum pellucidum is the body of the corpus callosum, rostrum of the corpus callosum located anteroinferiorly, and columns of the fornix located posteroinferiorly. If the space extends posteriorly above the third ventricle and is bounded by the splenium posteriorly, it is called a cavum vergae. Under usual conditions, the cavum septum pellucidum and cavum vergae do not communicate with the lateral ventricles. Accumulation of pus in the cavum septum pellucidum is rare. We report a neonate with increased intracranial pressure who developed an empyema in the cavum septum pellucidum that communicated with the ventricles.
From the *Department of Pediatrics and the †Department of Neurosurgery; Mackay Memorial Hospital; Taipei, Taiwan.
© 2002 by Elsevier Science Inc. All rights reserved. PII S0887-8994(01)00399-X ● 0887-8994/02/$—see front matter
Case Report A male infant was born to a gravida 4 para 3 mother at a gestation of 31 weeks. His birth weight was 1,646 gm. Rupture of the membranes had been evident for 3 months before delivery. He was admitted to the hospital because of prematurity, low birth weight, and respiratory distress. No bacteria were isolated from the cerebrospinal fluid or peripheral blood during the first hospitalization. A group B streptococcus antigen test in the urine was negative. The initial brain echo was normal. He was discharged 35 days after admission. Twelve days after discharge, the infant developed mild fever and irritable crying and was brought to our hospital again. On admission, his temperature was 38.2oC. Blood pressure was 87/48 mmHg. Physical examination was unremarkable. The anterior fontanel was flat at rest but bulged mildly when he cried. A septic evaluation, including blood, cerebrospinal fluid, and urine cultures was performed to determine the origin of the fever. The hemoglobin was 12.8 gm/dL initially, and the peripheral leukocyte count was 16,550/mm3 with 9% band forms, 72% neutrophils, 4% monocytes, and 15% lymphocytes. A lumbar puncture yielded turbid cerebrospinal fluid with more than 10,000 leukocytes (79% neutrophils and 21% lymphocytes), an extremely low glucose (0 mg/dL), and a markedly increased protein (1038 mg/dL). Urinalysis was normal. Because of seizures, hypothermia (35.6°C), and a decreased hemoglobin level (9.3 gm/dL) on the second hospital day, he was transferred to the intensive care unit. Brain echo revealed wall enhancement of the cavum septum pellucidum and internal debris (Fig 1). The result of magnetic resonance imaging also demonstrated abscess formation within the cavum septum pellucidum. Proteus mirabilis was isolated from the cerebrospinal fluid. Fourteen days after admission and treatment with antibiotics, the debris in the cavum septum pellucidum disappeared on sonographic examination, although the size of lateral ventricles increased. Another lumbar puncture performed 2 weeks after the initial puncture revealed leukocytes 44/mm3 (38 neutrophils and 6 lymphocytes), a persistently low glucose (28 mg/dL), and increased protein level (426 mg/dL). However, no bacteria were isolated. Progressive hydrocephalus was monitored by serial brain sonography (Fig 2). Finally a ventriculoperitoneal shunt was placed. The ventricular size returned to normal and the cavum septum pellucidum gradually disappeared (Fig 3). Ampicillin (300 mg/kg/day) and cefotaxime (200 mg/kg/day) were administered initially to treat the Proteus mirabilis meningitis. Ampicillin was then discontinued, and cefotaxime was administered for a total of 6 weeks. Phenobarbital was added to control seizures. Electroencephalogram performed 1 month after admission revealed no epileptiform discharge. Auditory evoked potential was normal. Bilateral mild visualcortical pathway dysfunction was evident on visual-evoked potential. The infant was clinically well on follow-up.
Discussion The cavum septum pellucidum is a normal anatomic structure during fetal growth. It forms during the fourth month of gestation and is present in nearly 100% of premature infants and 15% of 6-month-old infants [1-4]. The septum pellucidum forms from the banks of the
Communications should be addressed to: Dr. Chiu; Department of Pediatrics; 92, Sec 2, Chung Shan N. Road; Taipei 10449, Taiwan. Received October 12, 2001; accepted November 12, 2001.
Li et al: Cavum Septum Pellucidum Empyema 391
Figure 1. Brain sonography of coronal (A) and midline sagittal (B) sections are evident on the first day of the second hospitalization demonstrating high echogenicity of the wall and accumulation of pus in the cavum septum pellucidum.
median groove of the massa commissuralis, which become the lamellae of the septum at 12-20 weeks of gestation [5-7]. The cavum septum pellucidum begins to close posteriorly, with the cavum vergae beginning to narrow at approximately 6 months of gestation. The cavum septum pellucidum begins to disappear just before term and decreases rapidly in size 2 months after delivery. The incidence at 6 months of age is almost equal to that in adults [1]. The cavum septum pellucidum and cavum vergae are sometimes called the fifth and sixth ventricles, but they are actually not part of the ventricular system. Their embryologic origin differs from that of the ventricular system and they are not lined with ependymal or choroid plexus cells [8,9]. Under normal conditions, they do not communicate with the ventricles. The cava contain fluid, but its source is unclear [1]. Cysts forming in the septum pellucidum have been considered to be caused by mechanical occlusion of the foramen of Monro and by hydrocephalus.
However, without communication with the lateral ventricles, enlargement of the cyst is still not well explained. Sam [10] reported a patient with empyema of the cavum septum pellucidum and the cavum vergae who was injured in a car accident 3 years previously. No fracture of the base of the skull was visible on imaging studies. He underwent surgical drainage and medical treatment of the empyema. The causative microorganism was Streptococcus pneumoniae. Although the head injury was trivial, the author still felt it was the accident that had triggered invasion of the pathogen. A noncommunicating cyst might end up in continuity with the ventricle if the septum pellucidum were to rupture spontaneously. Fenestration of the thin wall might be caused by stretching beyond its elastic limit or an imbalance of pressure between the two sides of the septum [1,10-13]. In some cases of hydrocephalus the pressure of the ventricles is so high that the cavum is more likely to be compressed than expanded.
Figure 2. Brain sonography 2 weeks after the second admission. (A) The cavum septum pellucidum is still visible on the coronal view but becoming clearer. (B) Progressively enlarging size of the lateral ventricles was evident on the parasagittal view.
392
PEDIATRIC NEUROLOGY
Vol. 26 No. 5
Figure 3. Brain sonography after ventriculoperitoneal shunt is presented. (A) The coronal view demonstrates disappearance of the cavum septum pellucidum. (B) The parasagittal view reveals resolution of the dilated lateral ventricles.
In our patient, the first brain sonogram after delivery did not reveal a cavum septum pellucidum or hydrocephalus. Although no bacteria were isolated on the first admission, the infant might have had occult infection at that time. The pathogen apparently passed through the blood– brain barrier and caused ventriculitis. Subsequently, increased intraventricular pressure could have caused fenestration of the membrane of the septum pellucidum, allowing the pathogen to invade the cavum and form an abscess. The inflammatory process itself might also have contributed to permeability of the septum. The later onset of hydrocephalus resulted from occlusion of the aqueduct by debris. The ventriculoperitoneal shunt not only improved the hydrocephalus but also led to a decrease in size and, finally, disappearance of the cavum septum pellucidum. The above-proposed process assumes communication between the cavum septum pellucidum and ventricular system. This report illustrated that pus may accumulate in a potential space. The small space and deep location of the cavum septum pellucidum made a surgical approach difficult. Antibiotics may have been helpful in controlling progression of the infection. However, the development of hydrocephalus mandated surgical shunting to relieve the increased intracranial pressure. Medical and surgical management thus both played important roles in the treatment of this patient.
References [1] Shaw CM, Alvord EC. Cava septi pellucidi et vergae: Their normal and pathologic states. Brain 1969;92:213-224. [2] Mott S, Bodensteiner JB, Allan W. The cavum septum pellucidum in preterm and term infants. Ann Neurol 1990;28:452. [3] Dooling EC, Barlow JF, Murphy JV, Richardson EP. Cyst of the cavum septi pellucidi. Arch Neurol 1972;27:79-88. [4] Heiskan O. Cyst of the cavum septum pellucidum causing increased intracranial pressure and hydrocephalus. J Neurosurg 1973;38: 771-3. [5] Rakic P, Yakovlev PI. Development of the corpus callosum and cavum septi in man. J Comp Neurol 1968;132:45-72. [6] Leech RW, Shuman RM. Holoprosencephaly and related midline cerebral anomalies: A review. J Child Neurol 1986;1:3-18. [7] Bodensteiner JB, Schaefer GB. Wide cavum septum pellucidum: A maker of disturbed brain development. Pediatr Neurol 1990;6: 391-394. [8] Silbert PL, Gubbay SS, Vaughan RJ. Cavum septum pellucidum and obstructive hydrocephalus. J Neurosurg Psychiatry 1993;56:820822. [9] Bruyn GW. Agenesis septi pellucidi, cavum septi pellucidi, cavum vergae, and cavum veli interposti. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol 30. Amsterdam: North Holland Publishing Company, 1997:299-337. [10] Sam M. Empyema of the septum pellucidum et vergae. S Afr J Surg 1994;32:109-111. [11] Ciric I, Zivin I. Neuroepithelial (colloid) cysts of the septum pellucidum. J Neurosurg 1975;43:69-73. [12] Assam NI, Timperley WR. Intracerebral cyst due to ectopic choroid plexus. J Neurosurg 1981;55:651-653. [13] Dandy WE. Congenital cerebral cyst of the cavum septi pellucidi (fifth ventricle) and cavum vergae (sixth ventricle). Arch Neurol Psychiatry 1931;25:44-66.
Li et al: Cavum Septum Pellucidum Empyema 393