NeuroRehabilitation ELSEVIER
NeuroRehabilitation 10 (1998) 61-66
Superior sagittal sinus thrombosis: a complication of gunshot wound injuries to the brain Ross Zafonte*, Kertia Black, Nancy Mann, Shelley Nepa, Thomas Watanabe Rehabilitation Institute of Michigan, Wayne State University, 261 Mack Blvd., Detroit, MI48201, USA
Abstract Superior sagittal sinus thrombosis (SSST) is a rare complication of non-penetrating brain injuries. However, this is not an uncommon event in those patients who have suffered a gun shot wound (GSW) to the head. Disturbances in blood flow, lead to development of SST, endothelial injury and clotting abnormalities. Complications include increased weakness, mental status changes, seizures and potential mortality. The purpose of this paper is to illustrate three cases of SSST and the need to be alert for this entity. Our cases involve three young female patients each of whom suffs:red a GSW to the head, with resultant severe brain injury. In each case, severe disability ensued and imaging studies revealed the presence of the superior sagittal sinus syndrome. The cases demonstrate three different presentations and time courses of this entity, along with the appropriate treatment choices. This condition may appear in the immediate post-injury period, in the post-acute rehabilitation period or even at distant follow-up; therefore, patients with TBI secondary to GSW need to be monitored for an extended time interval for clinical signs which may be indicative of SSST. © 1998 Elsevier Science Ireland Ltd.
Keywords: Superior sagittal sinus thrombosis; Penetrating head injury; Gun shot wound
1. Introduction Craniocerebral gunshot wounds (GSW) constitute a dilemma for clinicians in both the acute and post-acute care environments. There are few studies with long-term follow-up of GSW survivors. Reported series have focused on small
* Corresponding author. Tel.: + 1 313 7459733; fax: + 1 313 7451063; e-mail: [email protected]
numbers of patients and deal mainly with survival [1,2]. Many of the studies are based upon a military population. However, differences exist between civilian and military GSW pathophysiology [3]. For example, Clark [4] reported that civilian GSW are usually associated with smaller caliber weapons traveling at lower velocities than military weapons. Potential late complications of penetrating GSW include cerebrospinal fluid leaks, traumatic intracranial aneurysms, coagulopathies, post-
1053-8135/98/$19.00 © 1998 Elsevier Science Ireland Ltd. All rights reserved.
PIIS1053-8135(97)00045-0
62
R. ZaJonte et al. / NeuroRehabilitation 10 (J998) 61-66
traumatic seizures and dural injuries [5,6]. Superior sagittal sinus thrombosis is an extremely serious complication of penetrating head injury, as life threatening hemorrhage can occur from acute dural venous sinus injuries. Matson [7] has described a classification system for penetrating head injuries which includes injury of dural sinuses Class IV, its most severe category (see Table 1). Depressed skull fractures secondary to gunshot wounds can predispose to late venous sinus thrombosis and venous infarctions most commonly involving the sagittal sinus [8]. The incidence of sagittal sinus thrombosis in traumatic brain injury is unknown but it is most commonly seen after penetrating injury. Mortality is reported to be as a high as 40-50% [9]. The purpose of this paper is to illustrate the variable timing of presentation and the clinical significance of sagittal sinus syndrome. 2. Case report 1 An 18-year-old female without significant past medical history was admitted to a level I trauma center after sustaining a gun shot wound to the left skull and mastoid process during an altercation. Skull films on admission revealed severely comminuted calvarial fractures of the left parietal, temporal and occipital bones with numerous small metallic fragments projecting into the calvarium and adjacent scalp. Initial GCS was 4, with minimal clinical evidence of hypotension. Admission head CT revealed multiple areas of acute brain parenchymal hemorrhage and severe cerebral edema without midline shift. Also seen was a posterior superior sagittal sinus thrombosis (SSST) as well as herniation of brain tissue through the left posterior calvarial defect. Subdural hemorrhage along the left posterior margins of the falx was visualized along with left frontal and parietal extra-axial fluid collections. The symptoms associated with this patient's SSST included spastic quadriparesis and emotional lability. Cerebral angiogram confirmed thrombosis of the posterior superior sagittal sinus, proximal transverse sinus and the straight sinus. The patient underwent surgical debridement of the brain with elevation of the depressed skull fracture. Subse-
Table 1 Matson classification I. Scalp wound II. Skull fracture with our dural penetration III. Skull fracture with penetration of dura/brain 1. Grazing wounds - bone fragments driven in with no retained missile fragments 2. Penetrating wounds - missile fragments retained within the brain 3. Perforating wounds - through and through injuries to the brain IV. Complicating factors 1. Ventricular penetration 2. Fractures of orbit or sinus 3. Injury of dural sinus 4. Intracerebral hematoma
quently the patient was treated with anticoagulation therapy. The patient was transferred to acute in-patient rehabilitation and completed a comprehensive rehabilitation program without neuromedical complication. At the time of discharge from in-patient rehabilitation the patient was ambulating short distances with an assistive device and required minimal assistance for basic activities of daily living. 3. Case report 2 A 16-year-old female without significant past medical history was admitted to a Level I trauma center after sustaining a gun shot wound to the head from a drive-by shooting. The bullet entered through the right external auditory meatus with noted otorrhagia and cerebrospinal fluid otorrhea. Initial GCS at the scene was 3 and in the emergency department was 11 (E4, V2, M5). Head CT on admission revealed a right occipital condyle fracture, small fracture of the right lateral mass of the body of Cl, subarachnoid hemorrhage, intraventricular blood in the basal cisterns, hydrocephalus secondary to fourth ventricle obliteration, diffuse hemorrhages in the left occipital, temporal and parietal lobes as well as pneumocephaly. The patient underwent emergent right cran-
R. ZaJonte et al. / NeuroRehabilitation 10 (J998) 6]-66
iotomy and debridement of the posterior fossa with CSF dura patch. Clinical examination revealed a mild right hemiparesis. Acute hospital course complications included multiple lumbar drains for continued CSF leaks and gram negative meningitis. At 20 days post-injury, the patient was transferred to in-patient rehabilitation. She did well until day 25 post-injury when the patient was noted to have an increase in her right hemiparesis and alteration in her mental status. Head CT suggested and cerebral angiogram confirmed the presence of superior sagittal sinus thrombosis. The patient was anticoagulated with IV heparin and later switched to coumadin. Mter close observation, she was able to resume rehabilitation. Her right hemiparesis improved and she demonstrated considerable functional gains over the course of acute rehabilitation. 4. Case report 3
A 27-year-old female without significant past medical history was admitted to a level I trauma center after sustaining a GSW to the left cerebellar area under unknown circumstances. Initial GCS at the scene was 5. Head CT on admission revealed a left cerebellar/posterior fossa subdural hematoma, fourth ventricle effacement and early hydrocephalus. The patient underwent emergent subdural hematoma evacuation. An acute hospital course included pneumonia, new onset diplopia, generalized weakness and confusion. The patient improved rapidly and was discharged to home from the acute care setting, ambulatory with an assistive device and independent in activities of daily living. The patient was temporally oriented at the time of discharge. Nine months post-discharge, she presented to a rehabilitation neurotrauma clinic with complaints of painless and gradual loss of vision over an 8-month period. MRI revealed superior sagittal sinus thrombosis (SSST). This finding was confirmed by angiography which demonstrated occlusion of the superior sagittal sinus accompanied by extensive venous collateralization. Because the thrombosis was thought to be old, anticoagulation was not indicated. The patient's
63
symptoms gradually improved over the next 6 months and follow-up MRI revealed signs of venous collateralization. S. Discussion The SSS receives blood from the brain via the cerebral veins and CSF flows into the SSS from the arachnoid villi [10]. The most anterior aspect of the SSS is located at the foramen cecum. The sinus courses along the uppermost part of the falx cerebri, then traverses the length of the rostral skull in a boney groove. Blood from the superior cerebral veins flows into this sinus and the contents of the SSS in turn flow into the confluence of dural sinuses at the occipital protuberance. Blood from the entire cerebral venous system drains into the internal jugular vein. Patency of the SSS and easy egress from its confines are essential to the outflow of blood and CSF from the cerebral system. It is easy to imagine that any obstruction of such a sinus could lead to a dangerous accumulation of both blood and CSF in the intracranial space. Multiple factors increase the risk of developing SSST. Trauma may lead to endothelial cell injury and stasis. Post-traumatic dehydration may further predispose the patient to SSST formation [11]. Abnormalities of the clotting mechanism as well as blood flow disturbances are also precipating factors following penetrating trauma [12,13]. SSST formation leads to sinus obstruction and outflow resistance, which results in decreased capillary flow. Retrograde transmission of high pressure into the capillary bed can lead to brain edema, elevations of intracranial pressure and hemorrhagic infarction [14]. SSST obstructs venous drainage into the sinus from the superior and medial surfaces of both cerebral convexities. This results in bilateral lower extremity weakness and sensory changes [15,16]. Mortality is greater in those with complete thrombosis as compared to those with partial sagittal sinus thrombosis. SSST has been associated with homocysteinuria, coagulation disorders, pregnancy, cancer, dehydration, infections, oral contraceptive use, autoimmune disorders and Bechet's disease. None of our patients had been taking oral contraceptive
64
R. Za!of/lc et al. / NClIroRehabilitation 10 (1998) 6/-66
medications. Among traumatic etiologies, SSST is rarely seen outside of the setting of penetrating trauma [17]. SSST may present immediately or several weeks post -penetrating trauma [18,19]. Patients with
SSST may present with headache, seizures, hemiparesis, para or tetraparesis, coma, visual disturbance or nuchal ridgity. Clinical signs of intracranial pressure elevation such as lethargy, coma, papilledema may also be observed (see Table 2)
Fig. I. MRA depicting the classical 'e mpty delta sign' seen with sagittal sinus thrombosis.
R. Zafonte et al. / NeliroRehabilitation 10 (J998) 61-66
Table 2 Clinical signs of superior sagittal sinus thrombosis Coma Seizures Paraparesis Hemiparesis Visual disturbance Altered mental status
nals caring for such patients need to be vigilant for changes which may be indicative of SSST. Acknowledgement
This work was supported in part by a grant (H133A-20016) from the National Institute on Disability and Rehabilitation Research, United Sates Department of Education.
[20]. Definitive diagnosis is established by cerebral angiography, especially if attention is directed towards the venous filling stage. CT or MRI may demonstrate the 'empty delta sign' (a non-enhanced triangular area observed in the posterior region of the sinus, see Fig. 1 [21]. Magnetic resonance angiography may demonstrate incomplete sinus filling or an abrupt cutoff in sinus drainage. Small cortical hemorrhages and cerebral edema are also observed with neuroimaging. Front [22] reported the use of Tc99m-Iabeled nuclear imaging to assess for SSST. A lack of consensus exists regarding the treatment of SSST. Corticosteroids have been used to treat the immediate cerebral edema, however, efficacy is not clear. Anticoagulation is widely advocated although the risk of exacerbating cerebral hemorrhage exists [23]. While initial therapy with heparin and subsequent conversion to warfrain is recommended no clear data regarding duration of anitcoagulant therapy exists. Fibrinolytics have also been described as useful [24]. No clear data exists to support recommendations for optimal duration of anticoagulation. Outcomes for survivors of penetrating brain injuries who receive acute inpatient rehabilitation are comparable to those of patients with brain injuries of other etiologies [25,26]. Physicians should be aware of this potentially devastating complication in patients who demonstrate progression of neurologic deficits following penetrating brain injuries.
[14]
6. Conclusion
[15]
SSST is a severe and significant complication, that may occur within days, weeks or months of a penetrating injury. Those rehabilitation professio-
65
References [1] [2]
[3]
[4]
[5]
[6]
[7] [8]
[9] [10] [11]
[12]
[13]
[16]
Kaufman H. Civilian gunshot wounds to the head. Neurosurgery 1993;32:962-964. Siccardi D, Cavaliere R, Pav A. Penetrating craniocrebral missile injuries in civilians: a retrospective analysis of 314 cases. Surg NeuroI1991;35:455-460. Carey M, Tutton R, Strub R. The correlation between surgical and CT estimates of brain damage following missile wounds. J Neurosurg 1984;60:947-953. Clark M, Mulhbauer M, Watridge C, Ray M. Analysis of 76 civilian craniocerebal gunshot wounds. J Neurosurg 1986;65:9'·14. Nagib M, Rockwold G, Sherman R, Laggard M. Civilian gunshot wounds to the brain: prognosis and management. Neurosurgery 1986;18;533-536. Graham T, Williams F, Harrington T, Spetzler R. Civilian gunshot wounds to the head: a prospective study. Neurosurgery 1990;27;696-700. Matson D. The treatment of acute craniocerebral injuries due to missiles. Springfield, Illinois, 1948. Meier V, Gartner F, Klotzner R, Wolf O. The traumatic dural sinus injury: a clinical study. Acta Neurochir (Wein) 1992;119:91-93. Schnell C, Rathe R. Superior sagittal sinus thrombosis. West J Med 1988;149:304-307. Barker G. Injuries to the superior longitudinal sinus. Br Med J 1949;1:1113-1116. Carrie A, Jaffee F. Thrombosis of the superior sagittal sinus caused by trauma without penetrating injury. J Neurosurg 1954;11 :73-182. Goodknight S, Kenoyer G, Rapaport S, Patch M, Lee J, Kurze T. Defibrination after brain-tissue destruction. N Engl J Med 1974;290:1043-1047. Jaapavan S, Emeis J, Lindman J. Intavascular coagulation: a common phenomenon in minor experimental head injury. J Neurosurg 1981;54:21-25. Gettelfinger D, Kokem E. Superior sagittal sinus thrombosis. Arch Neurol 1977;34:2-6. Martin J. Signs of obstruction of the superior longitudinal sinus following closed head injuries. Br Med J 1955;2:467-470. Awashti D, Rock W, Carey M, Farrell J. Coagulation changes after experimental missile wound to the brain in the cat. Surg Neurol 1991;36:441-446.
66
R. ZaJonte et al.j NeuroRehabilitation 10 (1998) 61-66
[17) Stringer W, Peerless S. Superior sagittal sinus thrombosis after closed head injury. Neurosurgery 1983;12:95-96. (18) Dormont S, Sag K, Biondi AB, Marsault C. Gadolinium-enhanced MR of chronic dural sinus thrombosis. Stroke 1995;26:1196-1199. [19) Valduezna J, Schultz M, Harris L, Einhaupl K. Venous transcranial doppler ultrasound monitoring in acute dural sinus thrombosis. Stroke 1995;26:11196-11199. [20) Karabudak R, Caner H, Oztekin N, Ozcan 0, Zielei T. Thrombosis of intracranial venous sinuses: etiology, clinical findings and prognosis of 56 patients. J Neurosurg Sci 1990;34:117-121. [21] Rippe D, Boyko 0, Spritzer C et al. Demonstration of dural sinus occlusion by the use of MR angiography. Am J Neuroradiol 1990;11:199-201
[22)
[23] [24)
[25)
[26]
Front D, Isreal 0, Even-Sapir E, Feinsaud M. Superior sagittal sinus thrombosis: Assessment with Tc-99 m labeled red blood cells. Radiology 1986;158:453-456. Mohamed A, Mc Leod J, Hallinan J. Superior sagittal sinus thrombosis. Clin Exp Neurol 1991;28;23-36. Eskridge J, Wessbecher F. Thrombolysis for superior sagittal sinus thrombosis. J Vasc Intervent Radiol 1991 ;2:89-93. Valena N, Zafonte R, Mann N, Millis S, Wood D, DeSantis N. Penetrating head injury; a propspective study of outcomes. Am J Phys Med Rehabil 1997;76:163 (abstract). Zafonte R, Mann N, Millis S, Wood D, Black K. Functional outcomes in violent traumatic brain injury. Brain Inj 1997;11:403-407.
NeuroRehabilitation 10 (1998) 61-66
Superior sagittal sinus thrombosis: a complication of gunshot wound injuries to the brain Ross Zafonte*, Kertia Black, Nancy Mann, Shelley Nepa, Thomas Watanabe Rehabilitation Institute of Michigan, Wayne State University, 261 Mack Blvd., Detroit, MI48201, USA
Abstract Superior sagittal sinus thrombosis (SSST) is a rare complication of non-penetrating brain injuries. However, this is not an uncommon event in those patients who have suffered a gun shot wound (GSW) to the head. Disturbances in blood flow, lead to development of SST, endothelial injury and clotting abnormalities. Complications include increased weakness, mental status changes, seizures and potential mortality. The purpose of this paper is to illustrate three cases of SSST and the need to be alert for this entity. Our cases involve three young female patients each of whom suffs:red a GSW to the head, with resultant severe brain injury. In each case, severe disability ensued and imaging studies revealed the presence of the superior sagittal sinus syndrome. The cases demonstrate three different presentations and time courses of this entity, along with the appropriate treatment choices. This condition may appear in the immediate post-injury period, in the post-acute rehabilitation period or even at distant follow-up; therefore, patients with TBI secondary to GSW need to be monitored for an extended time interval for clinical signs which may be indicative of SSST. © 1998 Elsevier Science Ireland Ltd.
Keywords: Superior sagittal sinus thrombosis; Penetrating head injury; Gun shot wound
1. Introduction Craniocerebral gunshot wounds (GSW) constitute a dilemma for clinicians in both the acute and post-acute care environments. There are few studies with long-term follow-up of GSW survivors. Reported series have focused on small
* Corresponding author. Tel.: + 1 313 7459733; fax: + 1 313 7451063; e-mail: [email protected]
numbers of patients and deal mainly with survival [1,2]. Many of the studies are based upon a military population. However, differences exist between civilian and military GSW pathophysiology [3]. For example, Clark [4] reported that civilian GSW are usually associated with smaller caliber weapons traveling at lower velocities than military weapons. Potential late complications of penetrating GSW include cerebrospinal fluid leaks, traumatic intracranial aneurysms, coagulopathies, post-
1053-8135/98/$19.00 © 1998 Elsevier Science Ireland Ltd. All rights reserved.
PIIS1053-8135(97)00045-0
62
R. ZaJonte et al. / NeuroRehabilitation 10 (J998) 61-66
traumatic seizures and dural injuries [5,6]. Superior sagittal sinus thrombosis is an extremely serious complication of penetrating head injury, as life threatening hemorrhage can occur from acute dural venous sinus injuries. Matson [7] has described a classification system for penetrating head injuries which includes injury of dural sinuses Class IV, its most severe category (see Table 1). Depressed skull fractures secondary to gunshot wounds can predispose to late venous sinus thrombosis and venous infarctions most commonly involving the sagittal sinus [8]. The incidence of sagittal sinus thrombosis in traumatic brain injury is unknown but it is most commonly seen after penetrating injury. Mortality is reported to be as a high as 40-50% [9]. The purpose of this paper is to illustrate the variable timing of presentation and the clinical significance of sagittal sinus syndrome. 2. Case report 1 An 18-year-old female without significant past medical history was admitted to a level I trauma center after sustaining a gun shot wound to the left skull and mastoid process during an altercation. Skull films on admission revealed severely comminuted calvarial fractures of the left parietal, temporal and occipital bones with numerous small metallic fragments projecting into the calvarium and adjacent scalp. Initial GCS was 4, with minimal clinical evidence of hypotension. Admission head CT revealed multiple areas of acute brain parenchymal hemorrhage and severe cerebral edema without midline shift. Also seen was a posterior superior sagittal sinus thrombosis (SSST) as well as herniation of brain tissue through the left posterior calvarial defect. Subdural hemorrhage along the left posterior margins of the falx was visualized along with left frontal and parietal extra-axial fluid collections. The symptoms associated with this patient's SSST included spastic quadriparesis and emotional lability. Cerebral angiogram confirmed thrombosis of the posterior superior sagittal sinus, proximal transverse sinus and the straight sinus. The patient underwent surgical debridement of the brain with elevation of the depressed skull fracture. Subse-
Table 1 Matson classification I. Scalp wound II. Skull fracture with our dural penetration III. Skull fracture with penetration of dura/brain 1. Grazing wounds - bone fragments driven in with no retained missile fragments 2. Penetrating wounds - missile fragments retained within the brain 3. Perforating wounds - through and through injuries to the brain IV. Complicating factors 1. Ventricular penetration 2. Fractures of orbit or sinus 3. Injury of dural sinus 4. Intracerebral hematoma
quently the patient was treated with anticoagulation therapy. The patient was transferred to acute in-patient rehabilitation and completed a comprehensive rehabilitation program without neuromedical complication. At the time of discharge from in-patient rehabilitation the patient was ambulating short distances with an assistive device and required minimal assistance for basic activities of daily living. 3. Case report 2 A 16-year-old female without significant past medical history was admitted to a Level I trauma center after sustaining a gun shot wound to the head from a drive-by shooting. The bullet entered through the right external auditory meatus with noted otorrhagia and cerebrospinal fluid otorrhea. Initial GCS at the scene was 3 and in the emergency department was 11 (E4, V2, M5). Head CT on admission revealed a right occipital condyle fracture, small fracture of the right lateral mass of the body of Cl, subarachnoid hemorrhage, intraventricular blood in the basal cisterns, hydrocephalus secondary to fourth ventricle obliteration, diffuse hemorrhages in the left occipital, temporal and parietal lobes as well as pneumocephaly. The patient underwent emergent right cran-
R. ZaJonte et al. / NeuroRehabilitation 10 (J998) 6]-66
iotomy and debridement of the posterior fossa with CSF dura patch. Clinical examination revealed a mild right hemiparesis. Acute hospital course complications included multiple lumbar drains for continued CSF leaks and gram negative meningitis. At 20 days post-injury, the patient was transferred to in-patient rehabilitation. She did well until day 25 post-injury when the patient was noted to have an increase in her right hemiparesis and alteration in her mental status. Head CT suggested and cerebral angiogram confirmed the presence of superior sagittal sinus thrombosis. The patient was anticoagulated with IV heparin and later switched to coumadin. Mter close observation, she was able to resume rehabilitation. Her right hemiparesis improved and she demonstrated considerable functional gains over the course of acute rehabilitation. 4. Case report 3
A 27-year-old female without significant past medical history was admitted to a level I trauma center after sustaining a GSW to the left cerebellar area under unknown circumstances. Initial GCS at the scene was 5. Head CT on admission revealed a left cerebellar/posterior fossa subdural hematoma, fourth ventricle effacement and early hydrocephalus. The patient underwent emergent subdural hematoma evacuation. An acute hospital course included pneumonia, new onset diplopia, generalized weakness and confusion. The patient improved rapidly and was discharged to home from the acute care setting, ambulatory with an assistive device and independent in activities of daily living. The patient was temporally oriented at the time of discharge. Nine months post-discharge, she presented to a rehabilitation neurotrauma clinic with complaints of painless and gradual loss of vision over an 8-month period. MRI revealed superior sagittal sinus thrombosis (SSST). This finding was confirmed by angiography which demonstrated occlusion of the superior sagittal sinus accompanied by extensive venous collateralization. Because the thrombosis was thought to be old, anticoagulation was not indicated. The patient's
63
symptoms gradually improved over the next 6 months and follow-up MRI revealed signs of venous collateralization. S. Discussion The SSS receives blood from the brain via the cerebral veins and CSF flows into the SSS from the arachnoid villi [10]. The most anterior aspect of the SSS is located at the foramen cecum. The sinus courses along the uppermost part of the falx cerebri, then traverses the length of the rostral skull in a boney groove. Blood from the superior cerebral veins flows into this sinus and the contents of the SSS in turn flow into the confluence of dural sinuses at the occipital protuberance. Blood from the entire cerebral venous system drains into the internal jugular vein. Patency of the SSS and easy egress from its confines are essential to the outflow of blood and CSF from the cerebral system. It is easy to imagine that any obstruction of such a sinus could lead to a dangerous accumulation of both blood and CSF in the intracranial space. Multiple factors increase the risk of developing SSST. Trauma may lead to endothelial cell injury and stasis. Post-traumatic dehydration may further predispose the patient to SSST formation [11]. Abnormalities of the clotting mechanism as well as blood flow disturbances are also precipating factors following penetrating trauma [12,13]. SSST formation leads to sinus obstruction and outflow resistance, which results in decreased capillary flow. Retrograde transmission of high pressure into the capillary bed can lead to brain edema, elevations of intracranial pressure and hemorrhagic infarction [14]. SSST obstructs venous drainage into the sinus from the superior and medial surfaces of both cerebral convexities. This results in bilateral lower extremity weakness and sensory changes [15,16]. Mortality is greater in those with complete thrombosis as compared to those with partial sagittal sinus thrombosis. SSST has been associated with homocysteinuria, coagulation disorders, pregnancy, cancer, dehydration, infections, oral contraceptive use, autoimmune disorders and Bechet's disease. None of our patients had been taking oral contraceptive
64
R. Za!of/lc et al. / NClIroRehabilitation 10 (1998) 6/-66
medications. Among traumatic etiologies, SSST is rarely seen outside of the setting of penetrating trauma [17]. SSST may present immediately or several weeks post -penetrating trauma [18,19]. Patients with
SSST may present with headache, seizures, hemiparesis, para or tetraparesis, coma, visual disturbance or nuchal ridgity. Clinical signs of intracranial pressure elevation such as lethargy, coma, papilledema may also be observed (see Table 2)
Fig. I. MRA depicting the classical 'e mpty delta sign' seen with sagittal sinus thrombosis.
R. Zafonte et al. / NeliroRehabilitation 10 (J998) 61-66
Table 2 Clinical signs of superior sagittal sinus thrombosis Coma Seizures Paraparesis Hemiparesis Visual disturbance Altered mental status
nals caring for such patients need to be vigilant for changes which may be indicative of SSST. Acknowledgement
This work was supported in part by a grant (H133A-20016) from the National Institute on Disability and Rehabilitation Research, United Sates Department of Education.
[20]. Definitive diagnosis is established by cerebral angiography, especially if attention is directed towards the venous filling stage. CT or MRI may demonstrate the 'empty delta sign' (a non-enhanced triangular area observed in the posterior region of the sinus, see Fig. 1 [21]. Magnetic resonance angiography may demonstrate incomplete sinus filling or an abrupt cutoff in sinus drainage. Small cortical hemorrhages and cerebral edema are also observed with neuroimaging. Front [22] reported the use of Tc99m-Iabeled nuclear imaging to assess for SSST. A lack of consensus exists regarding the treatment of SSST. Corticosteroids have been used to treat the immediate cerebral edema, however, efficacy is not clear. Anticoagulation is widely advocated although the risk of exacerbating cerebral hemorrhage exists [23]. While initial therapy with heparin and subsequent conversion to warfrain is recommended no clear data regarding duration of anitcoagulant therapy exists. Fibrinolytics have also been described as useful [24]. No clear data exists to support recommendations for optimal duration of anticoagulation. Outcomes for survivors of penetrating brain injuries who receive acute inpatient rehabilitation are comparable to those of patients with brain injuries of other etiologies [25,26]. Physicians should be aware of this potentially devastating complication in patients who demonstrate progression of neurologic deficits following penetrating brain injuries.
[14]
6. Conclusion
[15]
SSST is a severe and significant complication, that may occur within days, weeks or months of a penetrating injury. Those rehabilitation professio-
65
References [1] [2]
[3]
[4]
[5]
[6]
[7] [8]
[9] [10] [11]
[12]
[13]
[16]
Kaufman H. Civilian gunshot wounds to the head. Neurosurgery 1993;32:962-964. Siccardi D, Cavaliere R, Pav A. Penetrating craniocrebral missile injuries in civilians: a retrospective analysis of 314 cases. Surg NeuroI1991;35:455-460. Carey M, Tutton R, Strub R. The correlation between surgical and CT estimates of brain damage following missile wounds. J Neurosurg 1984;60:947-953. Clark M, Mulhbauer M, Watridge C, Ray M. Analysis of 76 civilian craniocerebal gunshot wounds. J Neurosurg 1986;65:9'·14. Nagib M, Rockwold G, Sherman R, Laggard M. Civilian gunshot wounds to the brain: prognosis and management. Neurosurgery 1986;18;533-536. Graham T, Williams F, Harrington T, Spetzler R. Civilian gunshot wounds to the head: a prospective study. Neurosurgery 1990;27;696-700. Matson D. The treatment of acute craniocerebral injuries due to missiles. Springfield, Illinois, 1948. Meier V, Gartner F, Klotzner R, Wolf O. The traumatic dural sinus injury: a clinical study. Acta Neurochir (Wein) 1992;119:91-93. Schnell C, Rathe R. Superior sagittal sinus thrombosis. West J Med 1988;149:304-307. Barker G. Injuries to the superior longitudinal sinus. Br Med J 1949;1:1113-1116. Carrie A, Jaffee F. Thrombosis of the superior sagittal sinus caused by trauma without penetrating injury. J Neurosurg 1954;11 :73-182. Goodknight S, Kenoyer G, Rapaport S, Patch M, Lee J, Kurze T. Defibrination after brain-tissue destruction. N Engl J Med 1974;290:1043-1047. Jaapavan S, Emeis J, Lindman J. Intavascular coagulation: a common phenomenon in minor experimental head injury. J Neurosurg 1981;54:21-25. Gettelfinger D, Kokem E. Superior sagittal sinus thrombosis. Arch Neurol 1977;34:2-6. Martin J. Signs of obstruction of the superior longitudinal sinus following closed head injuries. Br Med J 1955;2:467-470. Awashti D, Rock W, Carey M, Farrell J. Coagulation changes after experimental missile wound to the brain in the cat. Surg Neurol 1991;36:441-446.
66
R. ZaJonte et al.j NeuroRehabilitation 10 (1998) 61-66
[17) Stringer W, Peerless S. Superior sagittal sinus thrombosis after closed head injury. Neurosurgery 1983;12:95-96. (18) Dormont S, Sag K, Biondi AB, Marsault C. Gadolinium-enhanced MR of chronic dural sinus thrombosis. Stroke 1995;26:1196-1199. [19) Valduezna J, Schultz M, Harris L, Einhaupl K. Venous transcranial doppler ultrasound monitoring in acute dural sinus thrombosis. Stroke 1995;26:11196-11199. [20) Karabudak R, Caner H, Oztekin N, Ozcan 0, Zielei T. Thrombosis of intracranial venous sinuses: etiology, clinical findings and prognosis of 56 patients. J Neurosurg Sci 1990;34:117-121. [21] Rippe D, Boyko 0, Spritzer C et al. Demonstration of dural sinus occlusion by the use of MR angiography. Am J Neuroradiol 1990;11:199-201
[22)
[23] [24)
[25)
[26]
Front D, Isreal 0, Even-Sapir E, Feinsaud M. Superior sagittal sinus thrombosis: Assessment with Tc-99 m labeled red blood cells. Radiology 1986;158:453-456. Mohamed A, Mc Leod J, Hallinan J. Superior sagittal sinus thrombosis. Clin Exp Neurol 1991;28;23-36. Eskridge J, Wessbecher F. Thrombolysis for superior sagittal sinus thrombosis. J Vasc Intervent Radiol 1991 ;2:89-93. Valena N, Zafonte R, Mann N, Millis S, Wood D, DeSantis N. Penetrating head injury; a propspective study of outcomes. Am J Phys Med Rehabil 1997;76:163 (abstract). Zafonte R, Mann N, Millis S, Wood D, Black K. Functional outcomes in violent traumatic brain injury. Brain Inj 1997;11:403-407.
