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Lateral sinus thrombosis: Complication of minor head injury
International Journal of Pediatric Otorhinolaryngology 73 (2009) 629–635
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International Journal of Pediatric Otorhinolaryngology journal homepage: www.elsevier.com/locate/ijporl
Review article
Lateral sinus thrombosis: Complication of minor head injury Jade Nehme a, Jean-Claude De´carie b, Issam Saliba c,* a
Otorhinolaryngology Department, Centre Hospitalier Universitaire Sainte-Justine (CHU SJ), Montreal University, 3175 Coˆte Sainte-Catherine, Montre´al, Quebec H3T 1C5, Canada Medical Imaging, Centre Hospitalier Universitaire Sainte-Justine (CHU SJ), Montreal University, 3175 Coˆte Sainte-Catherine, Montre´al, Quebec H3T 1C5, Canada c Otorhinolaryngology Department, Otology and Neurotology, Centre Hospitalier Universitaire Sainte-Justine (CHU SJ), Montreal University, 3175 Coˆte Sainte-Catherine, Montre´al, Quebec H3T 1C5, Canada b
A R T I C L E I N F O
S U M M A R Y
Article history: Received 1 July 2008 Received in revised form 27 October 2008 Accepted 30 October 2008 Available online 11 December 2008
Objective: Our review aims: (1) to highlight the suspicion of lateral sinus thrombosis (LST) following a minor head injury in the pediatric population; (2) to discuss the different etiologies of lateral sinus thrombosis; (3) to identify an exact mechanism of the thrombus formation; (4) to clarify the role of each diagnostic tool; (5) to implement an algorithm for the treatment of LST due to a minor head injury. Method: We performed a MEDLINE search for LST following a minor head trauma related articles that were published between 1950 and June 2008. We identified 19 related studies of which 22 patient records were noted. We also added our case to this series. The information from the reports was analyzed to characterize the clinical aspects, the radiologic findings, the treatment, the follow-up, and the management of this disease. Results: Twenty-three cases (20 pediatrics and 3 adults) of LST following a minor head trauma have been published including the new one presented here. The mean pediatric age in this series is 7.8 years. There were 11 cases on the right side and 8 on the left side. Male to female ratio is 1.4:1. Side and sex were not reported in 4 and 6 cases, respectively. Sigmoid and transverse sinuses were the most affected one. Eighty-three percent were treated by observation while the remaining 17% received anticoagulation. The outcome was good in all patients without any notable major complications. The radiological investigation showed that there was a complete recanalization in 9 patients and a partial recanalization in 3 patients with a mean time of 8.3 weeks. Conclusion: Lateral sinus thrombosis seldomly occurs following a minor head injury. This entity is difficult to diagnose and one should exercise a high degree of suspicion when confronted with an ambiguous neurological status following a closed head trauma. The most accurate imaging test according to our experience is a multiple detector row computerized tomography (MDCT) venography completed at the time of the presentation. The indication to proceed with an MRI has to be assessed on a case-by-case basis. Anticoagulation is reserved for patients presenting a papilledema or for patients complaining of persistent headaches, vomiting, or disequilibrium. ß 2008 Elsevier Ireland Ltd. All rights reserved.
Keywords: Sinus thrombosis Head injury Sigmoid sinus Transverse sinus Dural sinus Lateral sinus Anticoagulation Minor injury
Contents 1. 2. 3. 4. 5.
Introduction . . . . . . . . . . . Methods . . . . . . . . . . . . . . 2.1. Case presentation . Results . . . . . . . . . . . . . . . Discussion . . . . . . . . . . . . Conclusion . . . . . . . . . . . . References . . . . . . . . . . . .
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1. Introduction
* Corresponding author. Tel.: +1 514 345 4857; fax: +1 514 737 4822. E-mail address: [email protected] (I. Saliba). 0165-5876/$ – see front matter ß 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijporl.2008.10.025
Lateral sinus thrombosis (LST) following a minor head injury is a very rare presentation; few cases have been reported in the literature [1–7]. LST is a well-recognized complication of an
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otologic infection such as complicated mastoiditis [3] or penetrating head trauma. It could also be triggered by hypercoagulable states. Many theories are possible in the mechanism of the thrombus, but none of them is certain [2,8]. Symptoms could be unspecific and the prognosis unpredictable depending upon many factors such as the dominance of the internal jugular vein (IJV), the venous collateral circulation expansion, and the partial or complete occlusion of the lateral sinus [9]. LST is not the first diagnosis to suspect after a minor head injury. However, a high degree of suspicion should be made earlier in the course of this pathology in order to begin the treatment as well as to prevent complications which could be lethal [4,10,11]. Imagery is the key to the diagnosis and a useful tool in the management of this pathology [1]. Our review aims to highlight the suspicion of LST after a minor head injury in the pediatric population, to discuss the different etiologies of lateral sinus thrombosis, to identify an exact mechanism of the thrombus formation, to clarify the role of each diagnostic tool, and finally, to implement an algorithm for the treatment of LST due to a minor head injury.
He was brought to a local hospital where his neurological exam appeared normal. A mastoid computerized tomography (CT) scan showed a right extradural pneumocephalus displacing the sigmoid sinus (Fig. 1). On the following day, the patient was still complaining of persistent otorrhea and started a fever of 101.3 8F (38.5 8C), as well as nausea, vomiting, and loss of hearing in the right ear. Hematologic exams revealed nothing abnormal, and the lumbar puncture showed no signs of infections within the cerebro-spinal fluid (CSF). Following this new clinical evolution, he was transferred to our tertiary care center for a more advanced analysis. Upon admission,
2. Methods We performed a MEDLINE search for LST following a minor head trauma related articles that were published between 1950 and June 2008. We identified 19 related studies of which 22 patient records were noted. We also added our case to this series. The information from the reports was analyzed to characterize the clinical aspects, the radiologic findings, the treatment, the followup, and the management of this disease. 2.1. Case presentation A 7-year-old male child, with no past history, was transferred to our institution, a pediatric tertiary care center, for a right otorrhea associated with imbalance and fever after a closed head trauma. Two days prior to his referral, he had fallen at school on his right mastoid without any loss of consciousness, but with a lacunar amnesia of what had happened. Following the accident, the child complained about right otalgia with no other symptoms. However, the next morning, he began experiencing a right otorrhea, clear at the beginning, then hemorrhagic later in the afternoon.
Fig. 1. Axial (A) and coronal (B) views of mastoid computerized tomography (CT) Scan showing a right extradural pneumocephalus (white arrow) displacing the sigmoid sinus (SS).
Fig. 2. Axial (A) T1 non-enhanced and coronal (B) T1-weighted gadoliniumenhanced magnetic resonance imaging (MRI) scan showing right epidural hematoma (white arrow) and hyperintense thrombus in the right sigmoid sinus (black arrow). MRI venography view (C) showing a complete thrombosis of the right sigmoid sinus (arrowhead) preventing blood flow to the right internal jugular vein.
Authors
Age/sex
Type of trauma
Skull fracture
Thrombosis extension/ pneumocephalus
Treatment
Time to Recanalization on Radiology
Outcome
Our report Zhao [5] (2008) Zhao [5] (2008) Zhao [5] (2008) Zhao [5] (2008) Shigemori [6] (2007) Yuen [1] (2005) Muthukumar [2] (2005) Stiefel [7] (2000) Stiefel [7] (2000) Stiefel [7] (2000) Stiefel [7] (2000) Stiefel [7] (2000) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Taha [3] (1993) Taha [3] (1993) Taha [3] (1993) Taha [3] (1993)
7.5 y/M 67 y/M 15 y/M 37 y/F 41 y/M 8 y/M 4 y/F 7 y/F 13/F 9/F 10/M 3.5/M 16/F 2 y/13 y/9 y/10 y/8 y/4 y/7 y/M 6 y/M 4 y/M 1 y/F
Fall Fall Fall Car Fall Fall Fall Bicycle Fall Fall Car Fall Car Fall Bicycle Fall Car/mild
Unidentified R temporal L & R temporal R temporal R temporal & orbital Unidentified Unidentified R occipital Vault Vault & basilar Vault & basilar Vault Basilar R occipital L parietal R temporo-parietal R temporo-parietal L temporo-parietal L & R temporal Adjacent to L sigmoid sinus Unidentified Unidentified Adjacent to L sigmoid sinus
R Sig. & Trans./+ R Sig. & Trans. L Sig. & Trans./+ Right Sigmoid R Sig. & Trans. JBT & VI nerve palsy R Sig. & Trans. R Trans. L Trans. R Trans. R Sig. R Sig. & Trans. R Tarns. R Sig. & IJV L Sig. & Trans. Trans. Sigmoid Sigmoid L Trans. & superior Sagittal Left Sig. & Trans. & IJV L Sig. L Sig. L Sig. & Trans.
Observation Anticoagulation Craniotomy + Anticoagulation Observation Observation Anticoagulation Observation Anticoagulation Observation Observation Observation Observation Observation Prophylactic Abt Pneumoc. vaccine Prophylactic Abt Pneumoc. vaccine Prophylactic Abt Prophylactic Abt Pneumoc. vaccine Craniotomy + Hematoma evacuation Hematoma evacuation Observation Observation Observation Observation
2 M/CT C+/partial 4 M/CT C+/partial 3 W/MRA/partial 1 W/MRI/partial 2 W/MRI/partial 4 M/MRI/complete 10 W/MRI/complete 2 M/CT C+/complete 6 W/CT C+/complete 5 M/CT C+/complete 2 M/CT C+/complete 5 W/complete 5 W/complete 5 W/complete 5 W/complete
Normal Left hemiparesis Normal Normal Normal Normal Normal Normal Recurrent Headache Normal Normal Normal Recurrent Headache Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal
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Table 1 Traumatic dural sinus thrombosis reported cases in the literature for mild head injury in the pediatric and adult population. Antibiotic (Abt), computerized tomography with contrast (CT C+), female (F), follow-up (F/U), jugular bulb thrombosis (JBT), left (L), male (M), magnetic resonance angiography (MRA), magnetic resonance imaging (MRI), month (M), Pneumococcal (Pneumoc.), right (R), sigmoid sinus (Sig.), transverse sinus (Trans.), week (W), year (y).
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Table 2 Venous thrombosis predisposing conditions.
Familial venous thrombosis
Hereditary venous thrombosis (not familial) Hypercoagulable states
Pathology
Test
Activated protein C resistance Prothrombin G20210A mutation Protein C deficiency Protein S deficiency Antithrombin deficiency
Activated Protein C resistance assays Prothrombin G20210A mutation test Protein C dosage Protein S dosage Antithrombin dosage
Positive antiphospholipid antibodies
Lupus anticoagulant antibodies Anticardiolipine antibodies
Elevated homocysteine Elevated plasminogene Dysfibrinogenemia (prolonged thrombin time or reptilase time, high fibrinogene levels) Platelet hyperaggregability
Homocysteine assay Plasminogene assay Thrombine time
the child complained about a headache and imbalance. Examination at this time revealed a fully conscious child, with a right middle ear clear effusion on otoscopy. There was an imbalance without true vertigo; no papilledema was denoted. A mastoid CT scan with contrast, done upon his admission, revealed no direct sign of temporal bone fracture, but there was a persistent right pneumocephalus associated with a right sigmoid sinus thrombosis (Fig. 1). The CT scan also revealed a right cerebellar concussion. On the other hand, the audiogram showed a right conductive hearing loss. Clinical and radiological diagnoses of posttraumatic sinus thrombosis were conducted. A magnetic resonance imaging (MRI) and magnetic resonance venogram (MRV) were completed (Fig. 2), confirming a complete right sinus thrombosis with additional data regarding an extradural hematoma compressing the right sigmoid sinus. Since dural sinus thrombosis following a minor head injury is a very rare case, a hypercoagulate panel was done in order to exclude any additional risk factors; results turned out to be normal. The patient was stable upon his admission and showed improvement of his headache on the third day of admission. No criteria to begin anticoagulation were identified. The remaining symptoms subsided on the ninth day of admission with a disappearance of the imbalance as well as the fever. He was discharged and evaluation at the first and third week later was uneventful. 3. Results We found 19 appropriate studies. Twenty-three cases of LST after a minor head trauma have been published including the new one presented here (Table 1). The age of the patients in this series ranged from 1 to 67 years with a mean pediatric age of 7.8 years. Three patients out of 23 were adults. There were 11 cases on the right side and 8 on the left side. There were 10 males and 7 females giving a male to female ratio of 1.4:1. Side and sex were not reported in 4 and 6 cases, respectively. Sigmoid and transverse sinuses were the most affected one. Eighty-three percent were treated by observation and the remaining 17% received anticoagulation. The outcome was good in all patients with no major complication to be noted. Two patients were still suffering from recurrent headaches while 1 patient still presents a left hemiparesis. The radiological investigation showed that there was a complete recanalization in 9 patients and a partial recanalization in 3 patients with a mean time of 8.3 weeks. 4. Discussion Lateral sinus thrombosis which includes the sigmoid and transverse sinuses is a rare entity in childhood, especially in the
Reptilase time, fibrinogene levels
course of a minor head injury. There have been very occasional studies in the literature; it is more often reported as a complication of severe head trauma with a penetrating injury. A minor head injury is usually defined as a blunt injury to the head, after which the patient may briefly lose consciousness, may have short posttraumatic amnesia, or both and may have a normal or minimally altered mental status at presentation (Glasgow Coma Scale [GCS] score of 13–15) [12,13]. Etiologies of dural sinus thrombosis are divided into four categories: traumatic, infectious, systemic conditions, and drugs induced [2,4,14]. Traumatic causes can be divided into a penetrating severe head injury and a minor closed head injury [9]. A basilar skull fracture in the region of the temporal or occipital bone is considered to be a significant risk factor for the development of transverse or sigmoid venous sinus thrombosis [5]. One of the main infectious causes associated with lateral sinus thrombosis is the complication of acute or chronic otitis media [3]. Bacterial or fungal septicemia could also be a predisposing condition for this pathology. Systemic conditions better known as spontaneous sinus thrombosis, such as coagulation disorders (protein C and S deficiencies) and thrombophilia (antiphospholipid syndrome, metastatic malignancies), have been reported to be associated with dural sinus thrombosis (Table 2). Cytotoxic drugs, contraceptive pills, and hormone replacement therapy could be predisposing factors [10,14,15] (Table 3). Iatrogenic causes like middle ear and posterior fossa surgeries are rarely reported in the literature [16]. Localization of the thrombus is variable; transverse sinus (TS), sigmoid sinus (SS), and straight sinus, which have all been described as localizations for thrombosis following a mild head injury [4,5,8]. One case report of Jugular bulb venous thrombosis has been also reported [6]. Extension of the thrombus from the sigmoid sinus can be retrograded occluding the transverse sinus and the cavernous sinus or antegraded involving the jugular vein bulb [4]. Lateral sinus thrombosis has to be differentiated from deep cerebral vein thrombosis, which is not the aim of this study. When a fracture is the cause, sinus thrombosis is commonly attributed to the linear fracture crossing the major dural venous sinus [1,2,5,8]. The exact mechanism of dural sinus thrombosis in a closed head injury is still unknown nowadays, but several theories have been proposed [9]. First, a direct compression of the sinus by adjacent structures such as pneumocephalus or an extradural hematoma can induce progressive thrombosis. Sinus wall trauma with intramural hemorrhage or injury to the lining epithelium could be a cause of SS thrombosis and finally, extension of a thrombus from an injured emissary veins to sigmoid sinus can completely block the sinus. In our case, the mechanism of the thrombosis is thought to be due to an epidural hematoma detected on MRI, compressing and displacing the adjacent sigmoid sinus and inducing a decrease in the venous blood flow. Nevertheless, no
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Table 3 Sinus thrombosis etiologies. Infectious etiologies
Non-infectious etiologies
Local
Penetrating septic trauma Intracranial infections: abscess, meningitis Regional infection: oto-mastoiditis, sinusitis
Head injury (open or close) Post-neurosurgical intervention Tumors: cholesteatoma, meningioma, metastasis, jugular tumors Occlusion of the internal jugular vein
Systemic
Bacterial: septicemia, endocarditis Viral: HIV, herpes Parasitic: malaria, trichinosis, toxoplasmosis Fungal: Aspergillosis, Cryptococcus
Deep vein thrombosis Hypercoagulation disorders: inherited thrombophilia, antiphospholipid syndrome Hyperviscosity: monoclonal gammopathy Malignancies: visceral carcinoma, leukemia Vasculitis: systemic lupus erythematosus, Wegener’s granulomatosis Drugs: contraceptive pills, replacement hormone therapy
fracture line has been identified on the mastoid CT scan, but a small lesion of the intima by a subclinical fracture could be an additional factor. The presence of the pneumocephalus at this site supports the possibility of mastoid and intracranial communication by a subradiological fracture. The mastoid air cells were completely filled with fluid. This decreased the contrast between bone and the surrounding structures, normally air, making the identification of the fracture impossible in the present case. In infectious sinus thrombosis related to oto-mastoiditis, the mechanism of thrombosis is due to the mastoid bone erosion by mastoiditis or cholesteatoma, with the formation of an infected mural thrombus or to an osteothrombophlebitis of the mastoid emissary veins in early acute otitis media [3]. Women, who take contraceptive pills or hormone replacement therapy, have numerous alterations in their coagulation system that promotes a hypercoagulable state. These alterations include hyperaggregable platelets, decreased endothelial fibrinolysis, decreased negative surface charge on vessel walls and blood cells, elevated levels of procoagulants, reduced red blood cells (RBC) filterability, increased blood viscosity secondary to elevated RBC volume, and decreased levels of antithrombin III. An alteration in any of these factors, alone or in combination, may predominate in women who are taking oral contraceptives. The extent of the derangement in the hemostatic system determines whether thrombosis occurs [17]. However, in systemic conditions, the presence of antiphospholipid antibodies or other pro-coagulant factors is not sufficient to cause thrombosis alone; a second factor such as stasis, vascular injury or drugs should be involved as well, much like in antiphospholipid syndrome cases [2]. Risk factors for an unfavorable outcome in deep sinus thrombosis (DST) were identified and included male sex, age above 37 years, coma, mental status disorder, intracranial hemorrhage on admission, thrombosis of the deep cerebral venous system, central nervous system infection, and cancer [10]. In adults, a patient’s history and clinical presentation could lead to the diagnosis of LST. However, clinical signs and symptoms are far less specific in children [4]. Some authors have reported that headaches, neck stiffness and pain have to be considered as specific symptoms, whereas others mentioned spiking temperature as a key factor diagnosis. In our case, the child presented with both a headache and a spiking fever lasting for several days without any sign of an infection. Papilledema and protracted vomiting are particularly described with thrombosis of the sigmoid and transverse sinuses [8]. Papilledema is an optic disc swelling that is secondary to elevated intracranial pressure. In contrast to other causes of optic disc swelling, vision usually is well preserved with acute papilledema. Papilledema almost always presents as a bilateral phenomenon and may develop over hours, even weeks [18]. Upon physical examination swelling over the occiput owing to mastoid emissary vein thrombosis (Greisinger’s sign) and tender-
ness over the sternocleidomastoid area should alert the physicians to LST [3] (Table 4). Our patient began to have a clear otorrhea followed later during the day by a hemorrhagic one; this could be explained by the fact that, following the trauma, a subradiological fracture was creating a clear CSF fistula, followed afterwards by the formation of the subdural pneumocephalus and hemorrhage, forming an otorrhagia and owing to the subdural hematoma. The hematoma and the pneumocephalus compressed the sigmoid sinus and caused a decrease in the venous flow inducing a consecutive thrombosis. Nausea and imbalance in our patient could be explained by a simple contusion of the labyrinth; it should not necessarily lead to further investigations. In our case, these symptoms improved a few days later. Clinical course in these patients is unpredictable and can vary from an asymptomatic route to a fatal one. Variability depends on many factors, such as the site and the extent of the thrombosis, the rate of occlusion, the collateral circulation, the age of the patient as well as the nature of the underlying disease [15]. Untreated sinus thrombus progression may be fatal due to venous congestion and cerebral infarction. Non-dominant sigmoid sinus thrombosis, usually the left one [19], rarely produces neurologic deficit and is associated with a good outcome [1]. The site and extent of the thrombosis are important; when a thrombosis affects a cerebral vein, an infarction will frequently develop with subsequent focal signs, whereas when thrombosis is restricted to the lateral or superior sinus, focal signs are absent and the usual pattern is an isolated intracranial hypertension. The onset of a thrombosis formation is an important factor in the evolution of venous infarction; it may be acute and stroke like, or it may be gradual, allowing time for the development of collateral venous circulation [15]. Symptoms of sinus thrombosis can be classified into two groups: (1) manifestations of an increased intracranial pressure (ICP) such as headache, impaired consciousness and papilledema on ocular fundus and (2) focal signs including convulsive seizures and hemiplegia caused by venous infarction, which is often hemorrhagic. A high degree of suspicion should be maintained in front of atypical neurologic courses, in front of some localized otologic or increased ICP signs, essentially following a trauma. A minor head injury followed by a progressive headache, imbalance, and
Table 4 Clinical presentation of lateral sinus thrombosis. Symptoms
Signs
Headache Nausea/vomiting Diplopia Disequilibrium/vertigo
Spiking fever Neck stiffness Retroauricular edema Greisinger’s sign (mastoid tenderness) Papilledema Ataxia
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vomiting with or without visual disturbance several days after the injury could be suspicious of a traumatic lateral sinus thrombosis [3]. This is the case of the child that we followed: as a matter of fact, facing the persistence of neurological symptoms (headache and imbalance) and despite a first CT scan showing no dural thrombosis, we repeated the CT scan 48 h later. It was positive for LST. Since the clinical presentation is non-specific and the noncontrast CT is not sensitive enough to detect the thrombosis, the diagnosis of DST is difficult to establish. Proper imaging is vital in establishing the diagnosis and assessing the response to treatment. An MRI used to be the recommended imaging test before the advent of multiple detector row CT (MDCT). In our experience, MDCT has many advantages over MRI. It can be performed in the acute setting following the head trauma and the fracture where the thrombosis can be assessed. The need for sedation is much less frequent, the examination time being often under a minute, compared to an MRI examination lasting for at least 30 min as an average time. There are fewer flow artifacts with MDCT venography than with MR venography. Spatial resolution is better with MDCT than with an MRI. An MRI has the advantage of suffering no artifacts secondary to bones and does depict extra-axial collections more accurately. Cerebral and cerebellar parenchymal lesions are assessed with better sensitivity. The indication to complement the MDCT examination with an MRI had to be evaluated on a case-by-case basis. In our case, the CT findings were initially interpreted as showing a right hemorrhagic cortical cerebellar contusion that was proven by the MRI to be an acute epidural hematoma displacing the sigmoid sinus (Fig. 2). Treatment of lateral sinus thrombosis varies depending on the etiology and the symptoms. The role of anticoagulation therapy in traumatic dural sinus thrombosis is still controversial. Because of the small number of patients experiencing sinus thrombosis after a mild head injury, there is no clear answer as to which is the better
therapy. Two ways of thinking have appeared with time. The first one recommends the usage of anticoagulation as soon as possible [20] wherein the second opinion does not see any advantage in anticoagulation unless progressive neurologic deterioration occurs or when the thrombus extends to the jugular vein or cavernous sinus [3]. Taha et al. [3] from a series of 5 cases do not support prophylactic therapy. Holzmann et al. [4] in a series of six children with traumatic dural thrombosis used a conservative way to avoid secondary intracranial hemorrhage. Yuen et al. [1] reported a case of a 4-year-old girl with a spontaneous recanalization of her sigmoid and transverse sinus using a conservative management. Stiefel et al. described 5 cases of dural sinus thrombosis due to a minor head injury. These cases were managed conservatively in all patients and recovery was uneventful. Recanalization of the sinus was documented to occur within 6 weeks to 2 months in three children. One patient showed a residual clot after 5 months and another did not have a radiological follow-up [7] (Table 1). On the opposing side, some authors suggest starting anticoagulation for the following reason; first, systemic anticoagulation therapy seems to be safe as heparin can be titrated to yield a partial thromboplastine time of 60–70 s [20]. Systemic anticoagulation also appears to be effective in limiting clot propagation. The choice of heparin therapy was based on the investigation by Einhaupl et al. [21], who performed a randomized blinded study of heparin therapy with venous sinus thrombosis and presented its advantage; 8 of the heparin-treated patients had a complete clinical recovery 3 months later and two had residual neurological deficits. In the placebo group, only 1 patient had a complete recovery, 6 patients had neurological deficits and 3 patients died. Finally, systemic anticoagulation could allow more rapid recanalization (median of 3 weeks) as in the case presented by Brors et al. [8] where a 32-year-old man with a sigmoid and transverse thrombosis after closed head injury showed a complete recanalization of the sinus 2 weeks after beginning anticoagulation.
Fig. 3. Algorithm of treatment in front of lateral sinus thrombosis (LST) due to a mild head injury. Multiple detector row computerized tomography (MDCT), magnetic resonance venogram (MRV), magnetic resonance imaging (MRI), and rule out (R/O).
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Muthukumar et al. presented another case of a 7-year-old girl with a occipital fracture was discharged 3 days after a conservative treatment, but was readmitted 10 days later for signs of increased intracranial pressure; a magnetic resonance venogram revealed thrombosis of the transverse sinus. The patient improved quickly with 3 weeks of anticoagulation therapy [4]. Twenty-three cases (20 pediatrics and 3 adults) of LST due to a minor head injury are reported in the literature including our case (Table 1). All cases except for 1 patient, who received anticoagulation, did not develop any neurological symptoms or other complications. No cases were surgically treated for thrombus evacuation. Our suggested protocol for LST due to a minor head injury is summarized in Fig. 3. There is no place for surgical embolectomy in these cases of mild trauma. Our child case received no anticoagulation therapy, because he did not meet the criteria for anticoagulation as described in the algorithm in Fig. 3. There were no signs of papilledema, no vomiting, and his headache had improved by the third day. In the setting of a head trauma and especially in a severe injury, anticoagulation is often contraindicated because of the risk of intra-cerebral bleeding. A more aggressive treatment, including endovascular thrombolysis or surgical thrombectomy, is reserved for those patients with either a serious neurological condition or infection. In a study published in 1999, regarding lateral dural sinus thrombosis in childhood [4], all children with a skull base fracture received prophylactic antibiotics and were routinely inoculated against pneumococcal infections. In relation to our practice, we do not think that prophylactic antibiotics should be used, except for cases where there are signs of an infection that must be validated through a workup test. 5. Conclusion Lateral sinus thrombosis occurs rarely following a minor head injury. This entity is difficult to diagnose and one should exercise a high degree of suspicion when confronted with an ambiguous neurological status following a closed head trauma. To the best of our knowledge, the most effective imaging test is MDCT venography completed at the time of the presentation. The indication to proceed to MRI has to be assessed on a case-by-case basis. Tests for hypercoagulation disorders should be done to exclude any underlining pathologies. Observation is our recommended treatment. Anticoagulation is reserved for patients presenting a papilledema or for patients complaining of a persistent headache, vomiting, or disequilibrium.
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References [1] H.W. Yuen, B.K. Gan, W.T. Seow, H.K. Tan, Dural sinus thrombosis after minor head injury in a child, Ann. Acad. Med. Singapore 34 (November (10)) (2005) 639–641. [2] N. Muthukumar, Uncommon cause of sinus thrombosis following closed mild head injury in a child, Childs Nerv. Syst. 21 (January (1)) (2005) 86–88 (Epub. May 27 2004). [3] J.M. Taha, K.R. Crone, T.S. Berger, W.W. Becket, E.C. Prenger, Sigmoid sinus thrombosis after closed head injury in children, Neurosurgery 32 (April (4)) (1993) 541–545 (Discussion 545–6). [4] D. Holzmann, T.A. Huisman, T.E. Linder, Lateral dural sinus thrombosis in childhood, Laryngoscope 109 (April (4)) (1999) 645–651. [5] X. Zhao, A. Rizzo, B. Malek, S. Fakhry, J. Watson, Basilar skull fracture: a risk factor for transverse/sigmoid venous sinus obstruction, J. Neurotrauma 25 (February (2)) (2008) 104–111. [6] Y. Shigemori, M. Koshinaga, T. Suma, S. Nakamura, Y. Murata, T. Kawamata, et al., Jugular bulb venous thrombosis caused by mild head injury: a case report, Surg. Neurol. 68 (December (6)) (2007) 660–664 (Discussion 664). [7] D. Stiefel, G. Eich, P. Sacher, Posttraumatic dural sinus thrombosis in children, Eur. J. Pediatr. Surg. 10 (February (1)) (2000) 41–44. [8] D. Brors, M. Scha¨fers, B. Schick, S. Dazert, W. Draf, G. Kahle, Sigmoid and transverse sinus thrombosis after closed head injury presenting with unilateral hearing loss, Neuroradiology 43 (February (2)) (2001) 144–146. [9] W. Azzi, I. Saliba, V.I. Forest, A. Abela, Lateral sinus thrombosis: serious complication of otitis media, J. Otolaryngol. 34 (December (6)) (2005) 427–431. [10] J.M. Ferro, P. Canha˜o, J. Stam, M.G. Bousser, F. Barinagarrementeria, ISCVT Investigators, Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT), Stroke 35 (March (3)) (2004) 664–670 (Epub. February 19 2004). [11] T.A. Kuether, O. O’Neill, G.M. Nesbit, S.L. Barnwell, Endovascular treatment of traumatic dural sinus thrombosis: case report, Neurosurgery 42 (May (5)) (1998) 1163–1166 (Discussion 1166–7). [12] L.J. Carroll, J.D. Cassidy, L. Holm, J. Kraus, V.G. Coronado, Methodological issues and research recommendations for mild traumatic brain injury: the WHO collaborating centre task force on mild traumatic brain injury, J. Rehabil. Med. 43 (Suppl.) (2004) 113–125. [13] I.G. Stiell, G.A. Wells, K. Vandemheen, C. Clement, H. Lesiuk, A. Laupacis, et al., The Canadian CT head rule for patients with minor head injury, Lancet 357 (9266) (May 2001) 1391–1396. [14] Hypercoagulation panel. Last updated May 29, 2007. [15] V. Biousse, F. Tong, N.J. Newman, Cerebral venous thrombosis, Curr. Treat. Options Neurol. 5 (September (5)) (2003) 409–420. [16] V.A. Shah, G.S. Yang, S. Randhawa, M.R. Hansen, A.G. Lee, Cerebral venous sinus thrombosis following jugular bulb decompression, Semin. Ophthalmol. 21 (January–March (1)) (2006) 41–44. [17] T. Zoltan, M.P. Goldman. Emedicine, Thrombophlebitis, Last updated: May 17, 2007 Available at: [18] J. Giovannini, G. Chrousos. Emedicine, Papilledema, Last updated: June 22, 2005. Available at: [19] H. Ichijo, M. Hosokawa, H. Shinkawa, The relationship between mastoid pneumatization and the position of the sigmoid sinus, Eur. Arch. Otorhinolaryngol. 253 (7) (1996) 421–424. [20] S.W. Soleau, R. Schmidt, S. Stevens, A. Osborn, J.D. MacDonald, Extensive experience with dural sinus thrombosis, Neurosurgery 52 (March (3)) (2003) 534–544 (Discussion 542–4). [21] K.M. Einha¨upl, A. Villringer, W. Meister, S. Mehraein, C. Garner, M. Pellkofer, et al., Heparin treatment in sinus venous thrombosis, Lancet 338 (8767) (September 1991) 597–600 (Erratum in: Lancet 338 (8772) (1991) 958).
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International Journal of Pediatric Otorhinolaryngology journal homepage: www.elsevier.com/locate/ijporl
Review article
Lateral sinus thrombosis: Complication of minor head injury Jade Nehme a, Jean-Claude De´carie b, Issam Saliba c,* a
Otorhinolaryngology Department, Centre Hospitalier Universitaire Sainte-Justine (CHU SJ), Montreal University, 3175 Coˆte Sainte-Catherine, Montre´al, Quebec H3T 1C5, Canada Medical Imaging, Centre Hospitalier Universitaire Sainte-Justine (CHU SJ), Montreal University, 3175 Coˆte Sainte-Catherine, Montre´al, Quebec H3T 1C5, Canada c Otorhinolaryngology Department, Otology and Neurotology, Centre Hospitalier Universitaire Sainte-Justine (CHU SJ), Montreal University, 3175 Coˆte Sainte-Catherine, Montre´al, Quebec H3T 1C5, Canada b
A R T I C L E I N F O
S U M M A R Y
Article history: Received 1 July 2008 Received in revised form 27 October 2008 Accepted 30 October 2008 Available online 11 December 2008
Objective: Our review aims: (1) to highlight the suspicion of lateral sinus thrombosis (LST) following a minor head injury in the pediatric population; (2) to discuss the different etiologies of lateral sinus thrombosis; (3) to identify an exact mechanism of the thrombus formation; (4) to clarify the role of each diagnostic tool; (5) to implement an algorithm for the treatment of LST due to a minor head injury. Method: We performed a MEDLINE search for LST following a minor head trauma related articles that were published between 1950 and June 2008. We identified 19 related studies of which 22 patient records were noted. We also added our case to this series. The information from the reports was analyzed to characterize the clinical aspects, the radiologic findings, the treatment, the follow-up, and the management of this disease. Results: Twenty-three cases (20 pediatrics and 3 adults) of LST following a minor head trauma have been published including the new one presented here. The mean pediatric age in this series is 7.8 years. There were 11 cases on the right side and 8 on the left side. Male to female ratio is 1.4:1. Side and sex were not reported in 4 and 6 cases, respectively. Sigmoid and transverse sinuses were the most affected one. Eighty-three percent were treated by observation while the remaining 17% received anticoagulation. The outcome was good in all patients without any notable major complications. The radiological investigation showed that there was a complete recanalization in 9 patients and a partial recanalization in 3 patients with a mean time of 8.3 weeks. Conclusion: Lateral sinus thrombosis seldomly occurs following a minor head injury. This entity is difficult to diagnose and one should exercise a high degree of suspicion when confronted with an ambiguous neurological status following a closed head trauma. The most accurate imaging test according to our experience is a multiple detector row computerized tomography (MDCT) venography completed at the time of the presentation. The indication to proceed with an MRI has to be assessed on a case-by-case basis. Anticoagulation is reserved for patients presenting a papilledema or for patients complaining of persistent headaches, vomiting, or disequilibrium. ß 2008 Elsevier Ireland Ltd. All rights reserved.
Keywords: Sinus thrombosis Head injury Sigmoid sinus Transverse sinus Dural sinus Lateral sinus Anticoagulation Minor injury
Contents 1. 2. 3. 4. 5.
Introduction . . . . . . . . . . . Methods . . . . . . . . . . . . . . 2.1. Case presentation . Results . . . . . . . . . . . . . . . Discussion . . . . . . . . . . . . Conclusion . . . . . . . . . . . . References . . . . . . . . . . . .
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1. Introduction
* Corresponding author. Tel.: +1 514 345 4857; fax: +1 514 737 4822. E-mail address: [email protected] (I. Saliba). 0165-5876/$ – see front matter ß 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijporl.2008.10.025
Lateral sinus thrombosis (LST) following a minor head injury is a very rare presentation; few cases have been reported in the literature [1–7]. LST is a well-recognized complication of an
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otologic infection such as complicated mastoiditis [3] or penetrating head trauma. It could also be triggered by hypercoagulable states. Many theories are possible in the mechanism of the thrombus, but none of them is certain [2,8]. Symptoms could be unspecific and the prognosis unpredictable depending upon many factors such as the dominance of the internal jugular vein (IJV), the venous collateral circulation expansion, and the partial or complete occlusion of the lateral sinus [9]. LST is not the first diagnosis to suspect after a minor head injury. However, a high degree of suspicion should be made earlier in the course of this pathology in order to begin the treatment as well as to prevent complications which could be lethal [4,10,11]. Imagery is the key to the diagnosis and a useful tool in the management of this pathology [1]. Our review aims to highlight the suspicion of LST after a minor head injury in the pediatric population, to discuss the different etiologies of lateral sinus thrombosis, to identify an exact mechanism of the thrombus formation, to clarify the role of each diagnostic tool, and finally, to implement an algorithm for the treatment of LST due to a minor head injury.
He was brought to a local hospital where his neurological exam appeared normal. A mastoid computerized tomography (CT) scan showed a right extradural pneumocephalus displacing the sigmoid sinus (Fig. 1). On the following day, the patient was still complaining of persistent otorrhea and started a fever of 101.3 8F (38.5 8C), as well as nausea, vomiting, and loss of hearing in the right ear. Hematologic exams revealed nothing abnormal, and the lumbar puncture showed no signs of infections within the cerebro-spinal fluid (CSF). Following this new clinical evolution, he was transferred to our tertiary care center for a more advanced analysis. Upon admission,
2. Methods We performed a MEDLINE search for LST following a minor head trauma related articles that were published between 1950 and June 2008. We identified 19 related studies of which 22 patient records were noted. We also added our case to this series. The information from the reports was analyzed to characterize the clinical aspects, the radiologic findings, the treatment, the followup, and the management of this disease. 2.1. Case presentation A 7-year-old male child, with no past history, was transferred to our institution, a pediatric tertiary care center, for a right otorrhea associated with imbalance and fever after a closed head trauma. Two days prior to his referral, he had fallen at school on his right mastoid without any loss of consciousness, but with a lacunar amnesia of what had happened. Following the accident, the child complained about right otalgia with no other symptoms. However, the next morning, he began experiencing a right otorrhea, clear at the beginning, then hemorrhagic later in the afternoon.
Fig. 1. Axial (A) and coronal (B) views of mastoid computerized tomography (CT) Scan showing a right extradural pneumocephalus (white arrow) displacing the sigmoid sinus (SS).
Fig. 2. Axial (A) T1 non-enhanced and coronal (B) T1-weighted gadoliniumenhanced magnetic resonance imaging (MRI) scan showing right epidural hematoma (white arrow) and hyperintense thrombus in the right sigmoid sinus (black arrow). MRI venography view (C) showing a complete thrombosis of the right sigmoid sinus (arrowhead) preventing blood flow to the right internal jugular vein.
Authors
Age/sex
Type of trauma
Skull fracture
Thrombosis extension/ pneumocephalus
Treatment
Time to Recanalization on Radiology
Outcome
Our report Zhao [5] (2008) Zhao [5] (2008) Zhao [5] (2008) Zhao [5] (2008) Shigemori [6] (2007) Yuen [1] (2005) Muthukumar [2] (2005) Stiefel [7] (2000) Stiefel [7] (2000) Stiefel [7] (2000) Stiefel [7] (2000) Stiefel [7] (2000) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Holzmann [4] (1999) Taha [3] (1993) Taha [3] (1993) Taha [3] (1993) Taha [3] (1993)
7.5 y/M 67 y/M 15 y/M 37 y/F 41 y/M 8 y/M 4 y/F 7 y/F 13/F 9/F 10/M 3.5/M 16/F 2 y/13 y/9 y/10 y/8 y/4 y/7 y/M 6 y/M 4 y/M 1 y/F
Fall Fall Fall Car Fall Fall Fall Bicycle Fall Fall Car Fall Car Fall Bicycle Fall Car/mild
Unidentified R temporal L & R temporal R temporal R temporal & orbital Unidentified Unidentified R occipital Vault Vault & basilar Vault & basilar Vault Basilar R occipital L parietal R temporo-parietal R temporo-parietal L temporo-parietal L & R temporal Adjacent to L sigmoid sinus Unidentified Unidentified Adjacent to L sigmoid sinus
R Sig. & Trans./+ R Sig. & Trans. L Sig. & Trans./+ Right Sigmoid R Sig. & Trans. JBT & VI nerve palsy R Sig. & Trans. R Trans. L Trans. R Trans. R Sig. R Sig. & Trans. R Tarns. R Sig. & IJV L Sig. & Trans. Trans. Sigmoid Sigmoid L Trans. & superior Sagittal Left Sig. & Trans. & IJV L Sig. L Sig. L Sig. & Trans.
Observation Anticoagulation Craniotomy + Anticoagulation Observation Observation Anticoagulation Observation Anticoagulation Observation Observation Observation Observation Observation Prophylactic Abt Pneumoc. vaccine Prophylactic Abt Pneumoc. vaccine Prophylactic Abt Prophylactic Abt Pneumoc. vaccine Craniotomy + Hematoma evacuation Hematoma evacuation Observation Observation Observation Observation
2 M/CT C+/partial 4 M/CT C+/partial 3 W/MRA/partial 1 W/MRI/partial 2 W/MRI/partial 4 M/MRI/complete 10 W/MRI/complete 2 M/CT C+/complete 6 W/CT C+/complete 5 M/CT C+/complete 2 M/CT C+/complete 5 W/complete 5 W/complete 5 W/complete 5 W/complete
Normal Left hemiparesis Normal Normal Normal Normal Normal Normal Recurrent Headache Normal Normal Normal Recurrent Headache Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal
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Table 1 Traumatic dural sinus thrombosis reported cases in the literature for mild head injury in the pediatric and adult population. Antibiotic (Abt), computerized tomography with contrast (CT C+), female (F), follow-up (F/U), jugular bulb thrombosis (JBT), left (L), male (M), magnetic resonance angiography (MRA), magnetic resonance imaging (MRI), month (M), Pneumococcal (Pneumoc.), right (R), sigmoid sinus (Sig.), transverse sinus (Trans.), week (W), year (y).
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Table 2 Venous thrombosis predisposing conditions.
Familial venous thrombosis
Hereditary venous thrombosis (not familial) Hypercoagulable states
Pathology
Test
Activated protein C resistance Prothrombin G20210A mutation Protein C deficiency Protein S deficiency Antithrombin deficiency
Activated Protein C resistance assays Prothrombin G20210A mutation test Protein C dosage Protein S dosage Antithrombin dosage
Positive antiphospholipid antibodies
Lupus anticoagulant antibodies Anticardiolipine antibodies
Elevated homocysteine Elevated plasminogene Dysfibrinogenemia (prolonged thrombin time or reptilase time, high fibrinogene levels) Platelet hyperaggregability
Homocysteine assay Plasminogene assay Thrombine time
the child complained about a headache and imbalance. Examination at this time revealed a fully conscious child, with a right middle ear clear effusion on otoscopy. There was an imbalance without true vertigo; no papilledema was denoted. A mastoid CT scan with contrast, done upon his admission, revealed no direct sign of temporal bone fracture, but there was a persistent right pneumocephalus associated with a right sigmoid sinus thrombosis (Fig. 1). The CT scan also revealed a right cerebellar concussion. On the other hand, the audiogram showed a right conductive hearing loss. Clinical and radiological diagnoses of posttraumatic sinus thrombosis were conducted. A magnetic resonance imaging (MRI) and magnetic resonance venogram (MRV) were completed (Fig. 2), confirming a complete right sinus thrombosis with additional data regarding an extradural hematoma compressing the right sigmoid sinus. Since dural sinus thrombosis following a minor head injury is a very rare case, a hypercoagulate panel was done in order to exclude any additional risk factors; results turned out to be normal. The patient was stable upon his admission and showed improvement of his headache on the third day of admission. No criteria to begin anticoagulation were identified. The remaining symptoms subsided on the ninth day of admission with a disappearance of the imbalance as well as the fever. He was discharged and evaluation at the first and third week later was uneventful. 3. Results We found 19 appropriate studies. Twenty-three cases of LST after a minor head trauma have been published including the new one presented here (Table 1). The age of the patients in this series ranged from 1 to 67 years with a mean pediatric age of 7.8 years. Three patients out of 23 were adults. There were 11 cases on the right side and 8 on the left side. There were 10 males and 7 females giving a male to female ratio of 1.4:1. Side and sex were not reported in 4 and 6 cases, respectively. Sigmoid and transverse sinuses were the most affected one. Eighty-three percent were treated by observation and the remaining 17% received anticoagulation. The outcome was good in all patients with no major complication to be noted. Two patients were still suffering from recurrent headaches while 1 patient still presents a left hemiparesis. The radiological investigation showed that there was a complete recanalization in 9 patients and a partial recanalization in 3 patients with a mean time of 8.3 weeks. 4. Discussion Lateral sinus thrombosis which includes the sigmoid and transverse sinuses is a rare entity in childhood, especially in the
Reptilase time, fibrinogene levels
course of a minor head injury. There have been very occasional studies in the literature; it is more often reported as a complication of severe head trauma with a penetrating injury. A minor head injury is usually defined as a blunt injury to the head, after which the patient may briefly lose consciousness, may have short posttraumatic amnesia, or both and may have a normal or minimally altered mental status at presentation (Glasgow Coma Scale [GCS] score of 13–15) [12,13]. Etiologies of dural sinus thrombosis are divided into four categories: traumatic, infectious, systemic conditions, and drugs induced [2,4,14]. Traumatic causes can be divided into a penetrating severe head injury and a minor closed head injury [9]. A basilar skull fracture in the region of the temporal or occipital bone is considered to be a significant risk factor for the development of transverse or sigmoid venous sinus thrombosis [5]. One of the main infectious causes associated with lateral sinus thrombosis is the complication of acute or chronic otitis media [3]. Bacterial or fungal septicemia could also be a predisposing condition for this pathology. Systemic conditions better known as spontaneous sinus thrombosis, such as coagulation disorders (protein C and S deficiencies) and thrombophilia (antiphospholipid syndrome, metastatic malignancies), have been reported to be associated with dural sinus thrombosis (Table 2). Cytotoxic drugs, contraceptive pills, and hormone replacement therapy could be predisposing factors [10,14,15] (Table 3). Iatrogenic causes like middle ear and posterior fossa surgeries are rarely reported in the literature [16]. Localization of the thrombus is variable; transverse sinus (TS), sigmoid sinus (SS), and straight sinus, which have all been described as localizations for thrombosis following a mild head injury [4,5,8]. One case report of Jugular bulb venous thrombosis has been also reported [6]. Extension of the thrombus from the sigmoid sinus can be retrograded occluding the transverse sinus and the cavernous sinus or antegraded involving the jugular vein bulb [4]. Lateral sinus thrombosis has to be differentiated from deep cerebral vein thrombosis, which is not the aim of this study. When a fracture is the cause, sinus thrombosis is commonly attributed to the linear fracture crossing the major dural venous sinus [1,2,5,8]. The exact mechanism of dural sinus thrombosis in a closed head injury is still unknown nowadays, but several theories have been proposed [9]. First, a direct compression of the sinus by adjacent structures such as pneumocephalus or an extradural hematoma can induce progressive thrombosis. Sinus wall trauma with intramural hemorrhage or injury to the lining epithelium could be a cause of SS thrombosis and finally, extension of a thrombus from an injured emissary veins to sigmoid sinus can completely block the sinus. In our case, the mechanism of the thrombosis is thought to be due to an epidural hematoma detected on MRI, compressing and displacing the adjacent sigmoid sinus and inducing a decrease in the venous blood flow. Nevertheless, no
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Table 3 Sinus thrombosis etiologies. Infectious etiologies
Non-infectious etiologies
Local
Penetrating septic trauma Intracranial infections: abscess, meningitis Regional infection: oto-mastoiditis, sinusitis
Head injury (open or close) Post-neurosurgical intervention Tumors: cholesteatoma, meningioma, metastasis, jugular tumors Occlusion of the internal jugular vein
Systemic
Bacterial: septicemia, endocarditis Viral: HIV, herpes Parasitic: malaria, trichinosis, toxoplasmosis Fungal: Aspergillosis, Cryptococcus
Deep vein thrombosis Hypercoagulation disorders: inherited thrombophilia, antiphospholipid syndrome Hyperviscosity: monoclonal gammopathy Malignancies: visceral carcinoma, leukemia Vasculitis: systemic lupus erythematosus, Wegener’s granulomatosis Drugs: contraceptive pills, replacement hormone therapy
fracture line has been identified on the mastoid CT scan, but a small lesion of the intima by a subclinical fracture could be an additional factor. The presence of the pneumocephalus at this site supports the possibility of mastoid and intracranial communication by a subradiological fracture. The mastoid air cells were completely filled with fluid. This decreased the contrast between bone and the surrounding structures, normally air, making the identification of the fracture impossible in the present case. In infectious sinus thrombosis related to oto-mastoiditis, the mechanism of thrombosis is due to the mastoid bone erosion by mastoiditis or cholesteatoma, with the formation of an infected mural thrombus or to an osteothrombophlebitis of the mastoid emissary veins in early acute otitis media [3]. Women, who take contraceptive pills or hormone replacement therapy, have numerous alterations in their coagulation system that promotes a hypercoagulable state. These alterations include hyperaggregable platelets, decreased endothelial fibrinolysis, decreased negative surface charge on vessel walls and blood cells, elevated levels of procoagulants, reduced red blood cells (RBC) filterability, increased blood viscosity secondary to elevated RBC volume, and decreased levels of antithrombin III. An alteration in any of these factors, alone or in combination, may predominate in women who are taking oral contraceptives. The extent of the derangement in the hemostatic system determines whether thrombosis occurs [17]. However, in systemic conditions, the presence of antiphospholipid antibodies or other pro-coagulant factors is not sufficient to cause thrombosis alone; a second factor such as stasis, vascular injury or drugs should be involved as well, much like in antiphospholipid syndrome cases [2]. Risk factors for an unfavorable outcome in deep sinus thrombosis (DST) were identified and included male sex, age above 37 years, coma, mental status disorder, intracranial hemorrhage on admission, thrombosis of the deep cerebral venous system, central nervous system infection, and cancer [10]. In adults, a patient’s history and clinical presentation could lead to the diagnosis of LST. However, clinical signs and symptoms are far less specific in children [4]. Some authors have reported that headaches, neck stiffness and pain have to be considered as specific symptoms, whereas others mentioned spiking temperature as a key factor diagnosis. In our case, the child presented with both a headache and a spiking fever lasting for several days without any sign of an infection. Papilledema and protracted vomiting are particularly described with thrombosis of the sigmoid and transverse sinuses [8]. Papilledema is an optic disc swelling that is secondary to elevated intracranial pressure. In contrast to other causes of optic disc swelling, vision usually is well preserved with acute papilledema. Papilledema almost always presents as a bilateral phenomenon and may develop over hours, even weeks [18]. Upon physical examination swelling over the occiput owing to mastoid emissary vein thrombosis (Greisinger’s sign) and tender-
ness over the sternocleidomastoid area should alert the physicians to LST [3] (Table 4). Our patient began to have a clear otorrhea followed later during the day by a hemorrhagic one; this could be explained by the fact that, following the trauma, a subradiological fracture was creating a clear CSF fistula, followed afterwards by the formation of the subdural pneumocephalus and hemorrhage, forming an otorrhagia and owing to the subdural hematoma. The hematoma and the pneumocephalus compressed the sigmoid sinus and caused a decrease in the venous flow inducing a consecutive thrombosis. Nausea and imbalance in our patient could be explained by a simple contusion of the labyrinth; it should not necessarily lead to further investigations. In our case, these symptoms improved a few days later. Clinical course in these patients is unpredictable and can vary from an asymptomatic route to a fatal one. Variability depends on many factors, such as the site and the extent of the thrombosis, the rate of occlusion, the collateral circulation, the age of the patient as well as the nature of the underlying disease [15]. Untreated sinus thrombus progression may be fatal due to venous congestion and cerebral infarction. Non-dominant sigmoid sinus thrombosis, usually the left one [19], rarely produces neurologic deficit and is associated with a good outcome [1]. The site and extent of the thrombosis are important; when a thrombosis affects a cerebral vein, an infarction will frequently develop with subsequent focal signs, whereas when thrombosis is restricted to the lateral or superior sinus, focal signs are absent and the usual pattern is an isolated intracranial hypertension. The onset of a thrombosis formation is an important factor in the evolution of venous infarction; it may be acute and stroke like, or it may be gradual, allowing time for the development of collateral venous circulation [15]. Symptoms of sinus thrombosis can be classified into two groups: (1) manifestations of an increased intracranial pressure (ICP) such as headache, impaired consciousness and papilledema on ocular fundus and (2) focal signs including convulsive seizures and hemiplegia caused by venous infarction, which is often hemorrhagic. A high degree of suspicion should be maintained in front of atypical neurologic courses, in front of some localized otologic or increased ICP signs, essentially following a trauma. A minor head injury followed by a progressive headache, imbalance, and
Table 4 Clinical presentation of lateral sinus thrombosis. Symptoms
Signs
Headache Nausea/vomiting Diplopia Disequilibrium/vertigo
Spiking fever Neck stiffness Retroauricular edema Greisinger’s sign (mastoid tenderness) Papilledema Ataxia
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vomiting with or without visual disturbance several days after the injury could be suspicious of a traumatic lateral sinus thrombosis [3]. This is the case of the child that we followed: as a matter of fact, facing the persistence of neurological symptoms (headache and imbalance) and despite a first CT scan showing no dural thrombosis, we repeated the CT scan 48 h later. It was positive for LST. Since the clinical presentation is non-specific and the noncontrast CT is not sensitive enough to detect the thrombosis, the diagnosis of DST is difficult to establish. Proper imaging is vital in establishing the diagnosis and assessing the response to treatment. An MRI used to be the recommended imaging test before the advent of multiple detector row CT (MDCT). In our experience, MDCT has many advantages over MRI. It can be performed in the acute setting following the head trauma and the fracture where the thrombosis can be assessed. The need for sedation is much less frequent, the examination time being often under a minute, compared to an MRI examination lasting for at least 30 min as an average time. There are fewer flow artifacts with MDCT venography than with MR venography. Spatial resolution is better with MDCT than with an MRI. An MRI has the advantage of suffering no artifacts secondary to bones and does depict extra-axial collections more accurately. Cerebral and cerebellar parenchymal lesions are assessed with better sensitivity. The indication to complement the MDCT examination with an MRI had to be evaluated on a case-by-case basis. In our case, the CT findings were initially interpreted as showing a right hemorrhagic cortical cerebellar contusion that was proven by the MRI to be an acute epidural hematoma displacing the sigmoid sinus (Fig. 2). Treatment of lateral sinus thrombosis varies depending on the etiology and the symptoms. The role of anticoagulation therapy in traumatic dural sinus thrombosis is still controversial. Because of the small number of patients experiencing sinus thrombosis after a mild head injury, there is no clear answer as to which is the better
therapy. Two ways of thinking have appeared with time. The first one recommends the usage of anticoagulation as soon as possible [20] wherein the second opinion does not see any advantage in anticoagulation unless progressive neurologic deterioration occurs or when the thrombus extends to the jugular vein or cavernous sinus [3]. Taha et al. [3] from a series of 5 cases do not support prophylactic therapy. Holzmann et al. [4] in a series of six children with traumatic dural thrombosis used a conservative way to avoid secondary intracranial hemorrhage. Yuen et al. [1] reported a case of a 4-year-old girl with a spontaneous recanalization of her sigmoid and transverse sinus using a conservative management. Stiefel et al. described 5 cases of dural sinus thrombosis due to a minor head injury. These cases were managed conservatively in all patients and recovery was uneventful. Recanalization of the sinus was documented to occur within 6 weeks to 2 months in three children. One patient showed a residual clot after 5 months and another did not have a radiological follow-up [7] (Table 1). On the opposing side, some authors suggest starting anticoagulation for the following reason; first, systemic anticoagulation therapy seems to be safe as heparin can be titrated to yield a partial thromboplastine time of 60–70 s [20]. Systemic anticoagulation also appears to be effective in limiting clot propagation. The choice of heparin therapy was based on the investigation by Einhaupl et al. [21], who performed a randomized blinded study of heparin therapy with venous sinus thrombosis and presented its advantage; 8 of the heparin-treated patients had a complete clinical recovery 3 months later and two had residual neurological deficits. In the placebo group, only 1 patient had a complete recovery, 6 patients had neurological deficits and 3 patients died. Finally, systemic anticoagulation could allow more rapid recanalization (median of 3 weeks) as in the case presented by Brors et al. [8] where a 32-year-old man with a sigmoid and transverse thrombosis after closed head injury showed a complete recanalization of the sinus 2 weeks after beginning anticoagulation.
Fig. 3. Algorithm of treatment in front of lateral sinus thrombosis (LST) due to a mild head injury. Multiple detector row computerized tomography (MDCT), magnetic resonance venogram (MRV), magnetic resonance imaging (MRI), and rule out (R/O).
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Muthukumar et al. presented another case of a 7-year-old girl with a occipital fracture was discharged 3 days after a conservative treatment, but was readmitted 10 days later for signs of increased intracranial pressure; a magnetic resonance venogram revealed thrombosis of the transverse sinus. The patient improved quickly with 3 weeks of anticoagulation therapy [4]. Twenty-three cases (20 pediatrics and 3 adults) of LST due to a minor head injury are reported in the literature including our case (Table 1). All cases except for 1 patient, who received anticoagulation, did not develop any neurological symptoms or other complications. No cases were surgically treated for thrombus evacuation. Our suggested protocol for LST due to a minor head injury is summarized in Fig. 3. There is no place for surgical embolectomy in these cases of mild trauma. Our child case received no anticoagulation therapy, because he did not meet the criteria for anticoagulation as described in the algorithm in Fig. 3. There were no signs of papilledema, no vomiting, and his headache had improved by the third day. In the setting of a head trauma and especially in a severe injury, anticoagulation is often contraindicated because of the risk of intra-cerebral bleeding. A more aggressive treatment, including endovascular thrombolysis or surgical thrombectomy, is reserved for those patients with either a serious neurological condition or infection. In a study published in 1999, regarding lateral dural sinus thrombosis in childhood [4], all children with a skull base fracture received prophylactic antibiotics and were routinely inoculated against pneumococcal infections. In relation to our practice, we do not think that prophylactic antibiotics should be used, except for cases where there are signs of an infection that must be validated through a workup test. 5. Conclusion Lateral sinus thrombosis occurs rarely following a minor head injury. This entity is difficult to diagnose and one should exercise a high degree of suspicion when confronted with an ambiguous neurological status following a closed head trauma. To the best of our knowledge, the most effective imaging test is MDCT venography completed at the time of the presentation. The indication to proceed to MRI has to be assessed on a case-by-case basis. Tests for hypercoagulation disorders should be done to exclude any underlining pathologies. Observation is our recommended treatment. Anticoagulation is reserved for patients presenting a papilledema or for patients complaining of a persistent headache, vomiting, or disequilibrium.
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References [1] H.W. Yuen, B.K. Gan, W.T. Seow, H.K. Tan, Dural sinus thrombosis after minor head injury in a child, Ann. Acad. Med. Singapore 34 (November (10)) (2005) 639–641. [2] N. Muthukumar, Uncommon cause of sinus thrombosis following closed mild head injury in a child, Childs Nerv. Syst. 21 (January (1)) (2005) 86–88 (Epub. May 27 2004). [3] J.M. Taha, K.R. Crone, T.S. Berger, W.W. Becket, E.C. Prenger, Sigmoid sinus thrombosis after closed head injury in children, Neurosurgery 32 (April (4)) (1993) 541–545 (Discussion 545–6). [4] D. Holzmann, T.A. Huisman, T.E. Linder, Lateral dural sinus thrombosis in childhood, Laryngoscope 109 (April (4)) (1999) 645–651. [5] X. Zhao, A. Rizzo, B. Malek, S. Fakhry, J. Watson, Basilar skull fracture: a risk factor for transverse/sigmoid venous sinus obstruction, J. Neurotrauma 25 (February (2)) (2008) 104–111. [6] Y. Shigemori, M. Koshinaga, T. Suma, S. Nakamura, Y. Murata, T. Kawamata, et al., Jugular bulb venous thrombosis caused by mild head injury: a case report, Surg. Neurol. 68 (December (6)) (2007) 660–664 (Discussion 664). [7] D. Stiefel, G. Eich, P. Sacher, Posttraumatic dural sinus thrombosis in children, Eur. J. Pediatr. Surg. 10 (February (1)) (2000) 41–44. [8] D. Brors, M. Scha¨fers, B. Schick, S. Dazert, W. Draf, G. Kahle, Sigmoid and transverse sinus thrombosis after closed head injury presenting with unilateral hearing loss, Neuroradiology 43 (February (2)) (2001) 144–146. [9] W. Azzi, I. Saliba, V.I. Forest, A. Abela, Lateral sinus thrombosis: serious complication of otitis media, J. Otolaryngol. 34 (December (6)) (2005) 427–431. [10] J.M. Ferro, P. Canha˜o, J. Stam, M.G. Bousser, F. Barinagarrementeria, ISCVT Investigators, Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT), Stroke 35 (March (3)) (2004) 664–670 (Epub. February 19 2004). [11] T.A. Kuether, O. O’Neill, G.M. Nesbit, S.L. Barnwell, Endovascular treatment of traumatic dural sinus thrombosis: case report, Neurosurgery 42 (May (5)) (1998) 1163–1166 (Discussion 1166–7). [12] L.J. Carroll, J.D. Cassidy, L. Holm, J. Kraus, V.G. Coronado, Methodological issues and research recommendations for mild traumatic brain injury: the WHO collaborating centre task force on mild traumatic brain injury, J. Rehabil. Med. 43 (Suppl.) (2004) 113–125. [13] I.G. Stiell, G.A. Wells, K. Vandemheen, C. Clement, H. Lesiuk, A. Laupacis, et al., The Canadian CT head rule for patients with minor head injury, Lancet 357 (9266) (May 2001) 1391–1396. [14] Hypercoagulation panel. Last updated May 29, 2007.