|Year : 2020 | Volume
| Issue : 6 | Page : 692-696
Growing skull fracture with leptomeningeal cyst associated with superior sagittal sinus thrombosis
Jay Kantilal Satapara, Hiral Parekh, Nandini Bahri
Department of Radiodiagnosis, Shri MP Shah Government Medical College, Shri Gurugobind Singh Government Hospital, Jamnagar, Gujarat, India
|Date of Submission||30-Aug-2019|
|Date of Decision||14-Nov-2019|
|Date of Acceptance||06-Jan-2020|
|Date of Web Publication||6-Nov-2020|
Jay Kantilal Satapara
Department of Radiodiagnosis, Shri MP Shah Government Medical College, Shri Gurugobind Singh Government Hospital, PN Marg, Jamnagar - 361 008, Gujarat
Source of Support: None, Conflict of Interest: None
Growing skull fracture is a rare complication of head injury usually occurs during the first 3 years of life. It may be associated with cerebral herniation, subdural hygroma, and subgaleal cerebrospinal fluid collection (leptomeningeal cyst). Posttraumatic cerebral venous sinus thrombosis is also an unusual complication of head injury associated with skull fracture extending to a dural sinus or the jugular bulb. It may be associated with ischemic damage to adjacent brain parenchyma. We report the case of growing fracture with leptomeningeal cyst associated with superior sagittal sinus thrombosis. A 2-year-old female child presented to the hospital following head trauma. The patient was drowsy and had hypotonia of all four limbs. Computed tomography was performed which showed a linear fracture of bilateral parietal bone with superior sagittal sinus thrombosis, subgaleal scalp collection in the bilateral parietal region, and ischemic changes in adjacent bilateral parietal lobes. Follow-up magnetic resonance imaging was done after 12 days of conservative treatment which showed similar findings. Surgical correction was done without any intraoperative or postoperative complications. As the delay in treatment may be associated with neurological complications, early diagnosis and prompt treatment are essential to prevent it and imaging modalities help in the early diagnosis.
Keywords: Computed tomography, growing fracture, head, leptomeningeal cyst, magnetic resonance imaging, neuroradiology, subgaleal cerebrospinal fluid collection, superior sagittal sinus thrombosis
|How to cite this article:|
Satapara JK, Parekh H, Bahri N. Growing skull fracture with leptomeningeal cyst associated with superior sagittal sinus thrombosis. Med J DY Patil Vidyapeeth 2020;13:692-6
|How to cite this URL:|
Satapara JK, Parekh H, Bahri N. Growing skull fracture with leptomeningeal cyst associated with superior sagittal sinus thrombosis. Med J DY Patil Vidyapeeth [serial online] 2020 [cited 2021 Mar 1];13:692-6. Available from: https://www.mjdrdypv.org/text.asp?2020/13/6/692/300134
| Introduction|| |
Growing skull fracture is a rare complication of head injury usually occurs during the first 3 years of life. It may be associated with cerebral herniation, subdural hygroma, and subgaleal cerebrospinal fluid (CSF) collection (leptomeningeal cyst). Posttraumatic cerebral venous sinus thrombosis (CVST) is also an unusual complication of head injury associated with skull fracture extending to a dural sinus or jugular bulb. It may be associated with ischemic damage to adjacent brain parenchyma. There have been few reported cases of growing skull fracture with leptomeningeal cyst and few other cases of cranial venous sinus thrombosis following head injury in literature, but until now, there has not been any case report of growing skull fracture with leptomeningeal cyst accompanied by cranial venous sinus thrombosis in literature. This is the first report describing a growing fracture with leptomeningeal cyst associated with superior sagittal sinus thrombosis.
| Case Report|| |
A 2-year-old female child was brought to the hospital with a history of fall an hour back. The patient was drowsy but had no episode of vomiting, seizures, or bleeding from ears or nose. On examination, compressible, tender swelling was present over the bilateral parietal region. There was hypotonia of all four limbs.
The patient underwent contrast-enhanced computed tomography (CT) of the brain with the following findings:
There was a linear displaced fracture of bilateral parietal bones crossing sagittal suture [Figure 1]. Nonenhancing hypodense content was seen in the middle part of the superior sagittal sinus and few adjacent cortical veins adjacent to fracture suggestive of venous sinus thrombosis. A well-defined fluid density hypodense collection was seen in the subgaleal space in the bilateral parietal region. Ill-defined patchy hypodense area was seen in the cortex and subcortical white matter of bilateral high parietal lobe, suggestive of ischemic changes secondary to venous thrombosis [Figure 2].
|Figure 1: Plain computed tomography of the head done after an hour of trauma, showing linear displaced fracture of bilateral parietal bones. (a) Three-dimensional reconstruction. (b) Axial scan bone window. (c) Sagittal scan bone window|
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|Figure 2: Contrast-enhanced computed tomography of the head done after an hour of trauma, coronal view showing. (a) Nonenhancing hypodense content is seen in the superior sagittal sinus (transverse arrow) suggestive of venous sinus thrombosis. A well-defined fluid density hypodense collection is seen in the subgaleal space in the bilateral parietal region (arrow head). (b) Ill-defined patchy hypodense areas are seen in the cortex and subcortical white matter of bilateral high parietal lobe (vertical arrows) suggestive of ischemic changes secondary to venous thrombosis|
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The patient was admitted and given conservative treatment that include mannitol, anticonvulsant, pain-relieving drug, and low-molecular-weight heparin. Follow-up CT scan was performed after 7 days with the following findings:
The distance between the edges of fractured parietal bones was increased as compared to previous CT suggestive of growing nature of the fracture [Figure 3]. Subgaleal scalp collection was increased in size extending mainly within the right parietal region and communicating intracranially with crescentic CSF density hypodense collection in the bilateral frontoparietal region suggestive of subdural hygroma [Figure 4] and [Figure 5].
|Figure 3: Three-dimensional reconstruction of plain computed tomography of head superior view. (a) Done after an hour of trauma. (b) Done after 7 days of trauma, showing increase in the distance between the edges of fracture ends measured along the sagittal suture, suggest growing nature of the fracture|
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|Figure 4: Follow-up plain computed tomography of the head done after 7 days of trauma, showing subgaleal scalp collection (leptomeningeal cyst) increased in size and seen mainly in the right parietal region. (a) Coronal scan. (b) Axial san. (c) Sagittal scan, vertical arrow showing fracture site|
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|Figure 5: Follow-up plain and contrast-enhanced computed tomography scan done after 7 days of trauma, (a) axial view showing subgaleal scalp collection in the right parietal region (transverse arrow) and crescentic cerebrospinal fluid density hypodense collection in bilateral fronto-parietal region suggestive of subdural hygroma (vertical arrow). (b) Coronal view showing nonenhancing hypodense content in the superior sagittal sinus (vertical arrow) suggestive of venous sinus thrombosis and subdural hygroma (transverse arrow). (c) Coronal view showing discontinuity in dura of superior sagittal sinus (vertical arrow)|
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Follow-up magnetic resonance imaging (MRI) was performed after 12 days which showed similar findings.
There was a linear displaced fracture of bilateral parietal bones. Well-defined CSF intensity collection (hypointense on T1 and fluid-attenuated inversion recovery [FLAIR] and hyperintense on T2) was seen in the subgaleal space in the right high parietal region. The collection communicated intracranially with subarachnoid space through the fracture defect suggestive of the leptomeningeal cyst. Altered signal intensity (hypointense on T1 and FLAIR and hyperintense on T2) collection was seen in subdural space in bilateral fronto-parieto-temporal regions suggestive of bilateral posttraumatic subdural hygromas [Figure 6] and [Figure 7]. On postcontrast venography, filling defect was seen in the middle part of superior sagittal sinus suggestive of thrombosis. Focal discontinuity was seen in dura of superior sagittal sinus beneath the fracture site [Figure 8]. The gyral pattern of enhancement was seen within adjacent parenchyma of bilateral high parietal lobe suggestive of ischemic changes secondary to venous thrombosis [Figure 9].
|Figure 6: Magnetic resonance imaging of the head done after 12 days of trauma, axial scan showing well-defined cerebrospinal fluid intensity collection in subgaleal space in the right high parietal region which appears hyperintense on T2 (a) (Transverse arrow), hypointense on T1 (b) and fluid-attenuated inversion recovery. (c) Suggestive of leptomeningeal cyst. Altered signal intensity, hyperintense on T2 (a) (vertical arrow), hypointense on T1 (b) and fluid-attenuated inversion recovery (c), collection in subdural space in bilateral fronto-parieto-temporal regions suggestive of bilateral subdural hygromas|
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|Figure 7: Magnetic resonance imaging of the head done after 12 days of trauma, (a) sagittal scan showing subgaleal cerebrospinal fluid collection communicating intracranially with subarachnoid space through the fracture site defect (transverse arrow). (b) sagittal scan showing focal discontinuity in dura of the superior sagittal sinus beneath the fracture site (vertical arrow). (c) Coronal scan showing discontinuity in dura of the superior sagittal sinus (vertical arrow)|
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|Figure 8: Postcontrast magnetic resonance venography done after 12 days of trauma, showing filling defect in the middle part of the superior sagittal sinus (vertical arrows) suggestive of thrombosis. (a) Sagittal scan, maximum intensity projection reformatted image. (b) Three-dimensional reconstruction venography image|
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|Figure 9: Postcontrast magnetic resonance imaging of the brain done after 12 days of trauma, T1-weighted three-dimensional sequence coronal scan showing the gyral pattern of enhancement within adjacent parenchyma of the bilateral high parietal lobe suggestive of ischemic changes secondary to venous thrombosis|
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The patient was operated for the same without any intraoperative or postoperative complication. The patient was doing fine on follow-up visit.
| Discussion|| |
Growing skull fractures (GSFs) occur after severe head injury during the first 3 years of life, more commonly during infancy and almost never after 8 years of age. The incidence is merely 0.05%–0.1% of skull fractures in childhood.,
The predominant factor in the development of GSF is the laceration of duramater. The brain develops rapidly during the early years of life, and the pulsatile force of the growing brain causes cerebral or subarachnoid herniation through the lacerated dura which causes enlargement of the fracture. This interposition of the tissue prevents osteoblast migration and fracture healing. The continuous pressure from the herniated tissue through the bone gape causes resorption of the adjacent bone and thus further enlargement of the fracture. Skull fractures never increase in size if the underlying dura is intact and also growing fracture does not occur after craniotomy even if watertight closure of dura is not done. Therefore, for growing fractures to develop, a dural laceration along with a fracture line is a must. In our case, both linear fracture and dural laceration along the fracture were present leading to growing fracture.
Other risk factors include severity of underlying trauma and type of fracture. A linear fracture associated with a hemorrhagic contusion of the subjacent brain increases the chance of dural tear. A linear fracture with a diastasis of more than 4 mm increases the risk of developing a GSF. A depressed fracture usually does not become a GSF, but a linear fracture extending from a depressed one can become one.
The brain extrusion can occur through diastatic linear fracture with resultant focal dilatation of the lateral ventricle near the growing fracture. Although GSF may be associated with damage to underlying brain, it is not a prerequisite. Posttraumatic aneurysms and subdural hematomas may accompany GSF.,
Posttraumatic CVST is an unusual complication of traumatic brain injury. Most cases of acute posttraumatic CVST are associated with skull fracture extending to a dural sinus or jugular bulb. In our case, fracture line crosses sagittal suture and underlying superior sagittal sinus, leading to superior sagittal sinus thrombosis.
The pathogenesis of CVST following trauma has not been well established. Various probable hypotheses include skull fractures causing thrombosis by direct compression of the sinus, endothelial injury within the sinus leading to the activation of the coagulation cascade, intramural hemorrhages due to rupture of small sinusoids, extension of the thrombus from injured emissary veins, and compression of the sinuses from intracranial edema.
The patient usually presents with progressive, often pulsatile, scalp swelling that appears sometime after head trauma sustained afterword. The usual site is the parietal region. There may be ocular proptosis or CSF rhinorrhea or otorrhea when a GSF is at the skull base. Most patients with CVST present with symptoms of increased intracranial pressure such as nausea, vomiting, and headache. There may be seizures, hemiparesis, and psychomotor retardation.
A plain radiograph may show a fracture line that crosses a coronal or lambdoid suture. CT scan remains the investigation of choice to define the exact pathology. Based on the CT appearance, growing fracture is subdivided into three types: Type I refers to GSF with a leptomeningeal cyst, which may be seen herniating through the skull defect into the subgaleal space, as seen in our case; Type II fractures are associated with damaged or gliotic brain; and in Type III, a porencephalic cyst can be seen. MRI has an advantage of detecting dural tear immediately following the head trauma, and a timely correction can prevent the growth of the fracture.
CVST can be detected on noncontrast CT (NCCT) by the presence of thrombus or indirectly by ischemic or vascular changes due to venous outflow obstruction. Delta sign, dense vein sign on NCCT, and empty delta sign on contrast CT are the characteristic signs. Magnetic resonance venography has nearly replaced contrast and conventional CT.
In our case, findings of both GSF with leptomeningeal cyst and superior sagittal sinus thrombosis were seen, which have not been reported simultaneously in any case.
The treatment includes maintaining hydration, and the administration of anti-edema agents such as dexamethasone and mannitol and anticonvulsants to prevent seizures. Heparin and urokinase are used to restore the patency of the sagittal sinus. The treatment of GSF consists of surgical reduction of the herniated cerebral tissue and repair of the dural laceration or cranioplasty.
| Conclusion|| |
Possibility of venous sinus thrombosis should always be kept in mind while assessing the imaging of patient with head trauma and possibility of growing skull fracture should not be overlooked while assessing children with head injury. Imaging modalities are useful in the early diagnosis of these conditions. Early diagnosis and prompt treatment are essential to prevent neurological complications.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
DesChamps GT Jr., Blumenthal BI. Radiologic seminar CCXLIX: Growing skull fractures of childhood. J Miss State Med Assoc 1988;29:16-7.
Ramamurthi B, Kalyanaraman S. Rationale for surgery in growing fractures of the skull. J Neurosurg 1970;32:427-30.
Khandelwal S, Sharma GL, Gopal S, Sakhi P. Growing skull fractures/leptomeningeal cyst. Indian J Radiol Imaging 2002;12:485-6. [Full text]
Thompson JB, Mason TH, Haines GL, Cassidy RJ. Surgical management of diastatic linear skull fractures in infants. J Neurosurg 1973;39:493-7.
Arseni C, Ciurea AV. Clinicotherapeutic aspects in the growing skull fracture. A review of the literature. Childs Brain 1981;8:161-72.
Lye RH, Occleshaw JV, Dutton J. Growing fracture of the skull and the role of computerized tomography. Case report. J Neurosurg 1981;55:470-2.
Lende RA, Erickson TC. Growing skull fractures of childhood. J Neurosurg 1961;18:479-89.
Buckingham MJ, Crone KR, Ball WS, Tomsick TA, Berger TS, Tew JM Jr. Traumatic intracranial aneurysms in childhood: Two cases and a review of the literature. Neurosurgery 1988;22:398-408.
Locatelli D, Messina AL, Bonfanti N, Pezzotta S, Gajno TM. Growing fractures: An unusual complication of head injuries in pediatric patients. Neurochirurgia (Stuttg) 1989;32:101-4.
Kumar GS, Chacko AG, Chacko M. Superior sagittal sinus and torcula thrombosis in minor head injury. Neurol India 2004;52:123-4.
] [Full text]
Yi J, Lee YH, Kim SK, Kim SH, Song HT, Shin KH, et al
. Response evaluation of giant-cell tumor of bone treated by denosumab: Histogram and texture analysis of CT images. J Orthop Sci 2018;23:570-7.
Ghuman MS, Salunke P, Sahoo SK, Kaur S. Cerebral venous sinus thrombosis in closed head trauma: A call to look beyond fractures and hematomas! J Emerg Trauma Shock 2016;9:37-8.
Hesselbrock R, Sawaya R, Tomsick T, Wadhwa S. Superior sagittal sinus thrombosis after closed head injury. Neurosurgery 1985;16:825-8.
Parmar RC, Bavdekar SB. Images in radiology: Type III growing skull fracture. J Postgrad Med 2000;46:130-1.
] [Full text]
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]