Acute dural venous sinus injuries: Imaging and challenges

Abstract

Dural venous sinus injury (DVSI) can occur after traumatic brain injury and lead to impaired cerebral venous outflow through extrinsic compression, intraluminal thrombosis, or mixed mechanisms. It can progress to a sinus tear or transection with hemorrhage. On noncontrast-enhanced head CT, DVSI may be subtle and can be confounded by adjacent fractures, extra-axial blood products, and filling defects such as arachnoid granulations. Although the reported incidence of severe head injury is 1–4%, modern trauma imaging has revealed a substantially higher burden of DVSI and dural venous sinus thrombosis (DVST) in patients with skull base and calvarial fractures, particularly when fractures cross or overlie major sinuses or the jugular bulb. This narrative review focuses on acute post-traumatic dural venous sinus injury and synthesizes current knowledge on the angiographic anatomy. We also highlight the strengths and limitations of CT venography (CTV), MR venography (MRV), and adjunctive digital subtraction angiography in detecting DVSI, differentiating intraluminal thrombus from extrinsic compression, and characterizing collateral pathways. Finally, we review management strategies, including neurosurgical decompression for mechanically compressed sinuses, the non-standardized use of systemic anticoagulation for DVST in the presence of a hemorrhage, and the role of detailed venographic mapping for operative planning. Timely recognition of these injuries and their complications, guided by a systematic venographic approach, is essential for mechanism-based management that may reduce the risk of serious sequelae including venous infarction.

Keywords

dural venous sinus injury traumatic dural venous sinus thrombosis CT venography MR venography traumatic brain injury

Introduction

The dural venous sinuses are channels formed where the periosteal and meningeal layers of the dura mater separate. They are essential for the venous drainage of blood from the brain to the internal jugular veins.^1,2 Dural venous sinus injuries (DVSIs) typically occur secondary to acute traumatic head injuries (TBIs).^3,4 DVSI is a term that can include a spectrum of injury mechanisms including extrinsic sinus compression, intraluminal thrombosis (dural venous sinus thrombosis; DVST), and frank sinus laceration or transection.^3,5,6 The reported incidence of traumatic DVSI varies substantially by population and injury type.^4,7 Post-traumatic DVST appears to occur in about 4% of all-comer TBI populations. In higher-risk patients with skull fractures adjacent to or traversing a dural venous sinus, reported prevalence is substantially higher, including 13.9% in a recent prospective intensive care unit (ICU) cohort, 23% to 40.7% in retrospective computed tomography venography (CTV) cohorts, and 26.2% in a meta-analysis.^7–11 However, detection of these injuries is increasing due to the use of dedicated venographic imaging in acute trauma settings.^7,8 Dural venous sinus thrombosis (DVST) is a thrombotic manifestation of DVSI that is also being diagnosed with a consistently increasing frequency in patients with skull fractures, regardless of age group or brain injury severity.^7,11,12 Outcomes for DVSI are variable and depend on the injury site and extent, with injuries in the posterior third of the sinus system having the highest mortality rates.^8,13 Early imaging-based diagnosis of DVSIs is crucial for addressing potentially treatable complications and improving patient outcomes.¹⁴ Additionally, DVSI on initial noncontrast CT can be obscured by adjacent trauma and unrecognized outflow obstruction can rapidly progress to venous infarction or hemorrhage.^3,5,15,16 This narrative review focuses on acute post-traumatic dural venous sinus injury, excluding non-traumatic and spontaneous cerebral venous thrombosis, and summarizes the angiographic anatomy of the major dural venous sinuses, highlights the role of CTV in diagnosing DVSI, describes key radiologic signs, discusses the anatomic basis and proposed pathophysiology of these injuries, outlines management considerations, and presents illustrative cases of DVSI secondary to TBI.

Methods

A literature search was conducted using PubMed and Google Scholar using keywords such as dural venous sinus injury, traumatic dural venous sinus thrombosis, cerebral venous thrombosis, traumatic brain injury, skull fracture, depressed skull fracture, CT venography, MR venography (MRV), digital subtraction angiography, superior sagittal sinus, transverse sinus, sigmoid sinus, cavernous sinus, jugular bulb, torcular Herophili, venous sinus compression, venous sinus occlusion, venous infarction, anticoagulation, blunt cerebrovascular injury, epidural hematoma, arachnoid granulation, sinus thrombosis classification, and venographic anatomy. Illustrative cases were selected from institutional teaching files if they demonstrated acute post-traumatic dural venous sinus injury on CT venography, including examples of extrinsic compression, intraluminal thrombosis, mixed injury patterns, or associated complications such as venous infarction. Cases were excluded if dedicated venographic imaging was unavailable, if the imaging findings were non-diagnostic or indeterminate, or if the injury pattern did not illustrate a distinct mechanism or teaching point relevant to the scope of this review.

Anatomic considerations

The dural venous sinus (DVS) and venous plexuses are endothelium-lined channels located between the periosteal and meningeal layers of the dura mater.^1,17 Together with the cerebral veins, they compose the cerebral venous drainage system.^1,17 The sinuses and plexuses are often fenestrated and have multiple channels, particularly within the cavernous sinus.^1,17 Unlike systemic veins, cerebral veins and the dural sinuses are valveless, allowing bidirectional flow, and they contain arachnoid (Pacchioni) granulations, which are filled with cerebrospinal fluid that drains into the venous circulation.^1,17,18 These arachnoid granulations can often appear as filling defects on imaging.^1,17,18 On CTV, arachnoid granulations are typically distinguished from intraluminal thrombus by their focal rounded or ovoid morphology, smooth margins, short extent along the sinus, cerebrospinal fluid (CSF)-like attenuation on CT, and characteristic anatomic distribution, most often in the lateral lacunae of the superior sagittal sinus and in the transverse sinuses, particularly near the insertion of the vein of Labbe; they may also occur in the straight sinus.^1,16,19 On magnetic resonance imaging (MRI), they are often, but not invariably, CSF-isointense.^18,19 In contrast, intraluminal thrombus more often produces irregular, elongated filling defects that extend along the axis of the sinus lumen.^1,18,19 The DVS also communicates with the extracranial venous system via emissary and diploic veins, which contribute to collateral drainage pathways.^1,16,20,21 Normal anatomic variants, including torcular/transverse sinus asymmetry and intrasinus septations or fenestrations, can make interpreting the DVS on venographic imaging challenging.^1,19,22 Intrasinus septations can appear as linear filling defects within the dural venous sinuses and may mimic intraluminal thrombus; however, CT venography, especially with multiplanar reformations and 3D reconstructions, helps distinguish these normal variants from true dural sinus thrombosis by demonstrating venous continuity and the absence of a true occlusive thrombus.^19,23,24 In contrast to other vascular beds, the dural venous sinus drainage territories do not mirror the arterial distribution, further complicating their characterization and venographic interpretation.^1,17 Given this anatomic variability, the dural venous sinuses are often described in terms of major functional groups and divided into two groups, the posterosuperior and the anteroinferior, with the posterosuperior group being larger and more susceptible to injury.^1,17 A comprehensive summary of the major dural venous sinuses by functional group, including their principal connections, anatomic variants, and clinical relevance in trauma, is provided in Table 1.

Table 1.

Major dural venous sinuses by functional group, with principal tributaries and connections, common anatomic variants, and clinical relevance in acute traumatic injury.

Group	Sinus/structure	Major tributaries and connections	Common anatomic variants	Clinical relevance in trauma
Anteroinferior	Cavernous sinus (CS)	Receives: superior and inferior ophthalmic veins, sphenoparietal sinus	Variable septation and trabeculation	Skull base fractures, orbital trauma propagation, post-traumatic carotid-cavernous fistula
		Drains via: superior and inferior petrosal sinuses, basilar venous plexus	Variable presence of vein of Vesalius/foramen of Vesalius
		Connects to pterygoid venous plexus via foramen ovale ± vein of Vesalius	Variable sphenoparietal drainage
	Clival venous plexus	Plexiform multichannel network along clivus; connects CS with posterior fossa venous outflow	Highly variable plexiform anatomy	Important collateral pathway when other anteroinferior sinuses injured
	Superior petrosal sinus (SPS)	Drains CS to sigmoid sinus along the petrous ridge	Variable caliber and course	Petrous bone fractures
	Inferior petrosal sinus (IPS)	Drains CS to internal jugular vein via jugular foramen	Frequent right-left asymmetry	Skull base fractures involving jugular foramen
	Sphenoparietal sinus	Drains middle cranial fossa structures; commonly empties into anterior CS	Variable Sylvian/paracavernous drainage pattern	Anterior temporal trauma
	Anterior condylar confluence (ACC)	Connects CS with posterior fossa sinuses and posterior cervical venous outflow; tributaries include anterior and lateral condylar veins, IPS, internal jugular vein	Anatomic variability in size and tributary pattern	Occipital condyle fractures; relevant collateral pathway
Posterosuperior	Superior sagittal sinus (SSS)	Receives: ascending frontal veins, multiple superficial bridging veins	Caliber increases from anterior to posterior	Vertex/midline fractures; bridging vein avulsion → subdural hematoma; arachnoid granulation can mimic thrombus
		Connects to Sylvian system via vein of Trolard	Parasagittal venous lacunae often contain arachnoid granulations
		Drains to torcular Herophili
	Inferior sagittal sinus (ISS)	Receives falx tributaries; joins vein of Galen to form straight sinus	Small caliber; often subtle on venography	Less commonly injured in isolation
	Straight sinus	Formed by ISS + vein of Galen at falcotentorial junction; drains to torcular	Persistent falcine sinus (rare; embryological remnant) associated with other venous anomalies	Falcotentorial trauma
	Confluence of sinuses (torcular Herophili)	Posterior midline junction of SSS, straight sinus, and paired transverse sinuses	Right- vs left-dominant drainage	Occipital fractures; recognized pitfall for false-positive thrombosis
			Bifurcating or septated confluence
			Pseudo-empty-delta appearance—common mimic of thrombosis
	Transverse sinus (TS)	Drains torcular toward sigmoid sinus along tentorium attachment	Right-dominant in the majority	Temporal/occipital fractures; granulations and hypoplasia are the two most common false-positives
			Hypoplasia or aplasia common (especially left)—pitfall vs occlusion: correlate with bony groove on bone-window CT
			Arachnoid granulations near vein of Labbé insertion
	Sigmoid sinus	Continuation of TS toward internal jugular vein; communicates with extracranial venous system via mastoid emissary vein	Variable mastoid emissary prominence; asymmetric size mirroring TS dominance	Mastoid and temporal bone fractures; transverse-sigmoid complex injuries
	Jugular bulb	Dilation at origin of internal jugular vein, exiting via jugular foramen	High-riding jugular bulb	Skull base/jugular foramen fractures; mimicry of glomus tumor on middle-ear imaging
			Jugular bulb dehiscence
			Jugular bulb diverticulum
			Each may present as vascular retrotympanic mass

Abbreviations: ACC, anterior condylar confluence; CS, cavernous sinus; CTV, CT venography; IPS, inferior petrosal sinus; ISS, inferior sagittal sinus; SPS, superior petrosal sinus; SSS, superior sagittal sinus; TS, transverse sinus.

Anteroinferior dural venous sinus group

The anteroinferior group of dural venous sinuses includes the cavernous sinus (CS), the clival venous plexus (CVP), the superior and inferior petrosal sinuses (SPS and IPS), and the sphenoparietal sinus (SpPS) (Figure 1).^25,26 The paired set of cavernous sinuses surrounds the pituitary fossa and communicates via the anterior and posterior intercavernous channels (Figure 1(B)).^1,25,26 The CVP is a plexiform, fenestrated, multichannel venous network along the clivus that provides critical collateral pathways by connecting the CS with posterior fossa venous outflow at the skull base.^1,25–27 The CS is a significant part of the anteroinferior dural venous sinus group, as it receives orbital, facial, meningeal, and skull base venous drainage.^25,26

Figure 1.

A. DSA AP view, B. Petrosal venogram, and C. lateral DSA demonstrating structures of the anteroinferior group of dural sinuses including the cavernous sinus (CS), superior petrosal sinus (SPS), inferior petrosal sinus (IPS), clival venous plexus (CVP), and the intercavernous (IC) sinus connecting both CSs. The sphenoid emissary vein (vein of Vesalius, V) can be seen draining the cavernous sinus (C) into the pterygoid venous plexus (PVP). Other structures demonstrated in the images include the internal jugular veins (IJV), the jugular bulb (J), the sigmoid sinus (SigS), transverse sinus (TS), and vertebral artery (VA).

Anteriorly, orbital and facial drainage reaches the CS predominantly via the superior and inferior ophthalmic veins; inferiorly, the CS communicates with the pterygoid venous plexus through emissary veins traversing the skull base foramina, most often the foramen ovale and, when present, the foramen of Vesalius (Figures 2 and 3).^3,25,26,28 Posteriorly, the CS drains via the superior and inferior petrosal sinuses toward the sigmoid sinuses and internal jugular veins, with additional collateral pathways through the basilar venous plexus and the anterior condylar confluence (ACC).^1,14,25,26

Figure 2.

Axial head CT depicting a corticated foramen of Vesalius (red arrow).

Figure 3.

A, B. Coronal head CT angiogram showing the venous plexus (red arrow) contained within the foramen ovale that drain into the pterygoid venous plexus (PVP) (white arrow).

Posterosuperior dural venous sinus group

Another important group of the dural venous sinuses is the posterosuperior group, which includes the superior sagittal sinus (SSS), inferior sagittal sinus (ISS), straight sinus (SS), sinus confluence (torcular Herophili [TH]), transverse sinuses (TS), sigmoid sinuses (SigS), and jugular bulbs (J) (Figure 4).¹⁷ The SSS is a large midline dural venous sinus that originates anteriorly from the ascending frontal veins and travels along the superior margin of the falx cerebri, which parallels the inner calvarial vault.¹⁷ The caliber of the SSS increases along its course from the anterior cranial fossa to the confluences of sinuses in the posterior skull.¹⁷ Along its course, the SSS receives venous drainage from numerous small superficial (bridging) veins.¹⁷ Adjacent to the SSS are parasagittal venous lacunae that can contain arachnoid granulations.^29,30 These arachnoid granulations participate in CSF resorption and can be seen as physiologic filling defects on venography.^29,30 The SSS is also connected to the superior middle cerebral (Sylvian) venous system by major superficial anastomotic pathways, such as the superior anastomotic vein of Trolard (Figure 5).¹⁷

Figure 4.

Sagittal cross-section illustration of the skull demonstrating the posterosuperior dural venous sinus group including the superior sagittal sinus (SSS), inferior sagittal sinus (ISS), straight sinus (SS), sinus confluence (torcular Herophili [TH]), transverse sinuses (TS), sigmoid sinuses (SigS), and jugular bulbs (J).

Figure 5.

Digital subtraction angiography (DSA) during the venous phase depicting the superior sagittal sinus (SSS) and superior anastomotic vein of Trolard (T), that is connected to the superficial middle cerebral vein or Sylvian vein (SV).

The ISS is relatively small when compared to the SSS and lies midline, coursing along the inferior margin of the falx cerebri.¹⁷ Venous blood from the internal cerebral and basal veins drains into the great cerebral vein (vein of Galen), which anastomoses with the ISS at the falcotentorial junction to form the straight sinus (Figure 6(A)).^1,17 The straight sinus then travels posteroinferiorly along the junction of the falx cerebri and tentorium cerebelli.¹⁷ The straight sinus can receive numerous small tributaries from the falx and tentorium and later drain towards the confluence of sinuses (torcular Herophili [TH]), where it interfaces with the transverse sinus system.¹⁷

Figure 6.

A. Lateral and B. posterior view digital subtraction angiography (DSA) in the venous phase depicting the transverse sinuses (TS), the sinus confluence (TH) (white arrow), sigmoid sinus (SigS), jugular bulbs (J), and internal jugular veins (IJV).

The confluence of sinuses is the posterior midline venous junction where the superior sagittal sinus and straight sinus connect with the pair of transverse sinuses.^1,21,24,31 The confluence of sinuses has several anatomical variants, including asymmetry due to right- or left-dominance and bifurcating or septated confluence patterns. From the torcular, the transverse sinuses travel laterally along the margin of the tentorium cerebelli toward the petrous temporal bone, where they turn inferiorly in the sigmoid sulcus and become the sigmoid sinuses.¹⁷ The transverse and sigmoid sinus systems can also communicate with the extracranial venous system through emissary veins, such as the mastoid emissary vein.^20,32 The sigmoid sinuses are the inferior continuation of the transverse sinuses, which descend posterior to the petrous temporal bone and terminate by becoming the internal jugular veins (Figure 6(B)).¹⁷ The jugular bulbs are superior dilatations at the origin of the internal jugular veins, which can exhibit several anatomic variants (e.g., high-riding jugular bulb, dehiscence, or a diverticulum), which are essential to recognize because they can present as vascular retrotympanic masses and be misdiagnosed as a glomus tumor or other vascular middle-ear or internal auditory canal lesions.^19,31,33

Imaging of dural venous sinus injuries

Currently, there is no universally accepted algorithm for the imaging evaluation of acute post-traumatic dural venous sinus injury (DVSI), and practices vary between institutions and clinical scenarios.^15,30,34 In traumatic brain injury, a skull fracture or epidural hematoma overlying a dural venous sinus increases the risk for developing DVST and should prompt evaluation with venographic imaging.^15,35,36 Because thrombosis and occlusive sinus injury are challenging to identify on noncontrast-enhanced CT imaging alone, venographic imaging is often required for adequate characterization and differentiation.^37,38 When DVSI is suspected, CTV or MRV are the primary imaging modalities used to define the extent of injury and detect thrombosis.^1,9,39 Patterns of non-opacification on CTV/MRV can help differentiate between the mechanism of injury, including intraluminal thrombosis, extrinsic compression/stenosis, or a combination of both.^3,5,40 In the setting of acute trauma, CTV is often favored over MRV because it offers fast image acquisition and can be integrated into pre-existing CT-based trauma protocols.^9,24,41 Furthermore, CTV post-processing with thin-section multiplanar reformats, maximum-intensity projections, and 3D renderings can improve anatomic depiction and help define the length and severity of injury.^24,28,31 Additionally, advanced CT post-processing techniques, including dual-energy bone-removal CT venography, may further enhance diagnostic confidence by improving separation of contrast-opacified dural venous sinuses from adjacent skull base bone.^28,31 Distinguishing true intraluminal thrombosis from adjacent extra-axial hemorrhagic compression still relies primarily on multiplanar venographic assessment.⁴²

CT venography has a reported sensitivity ranging from 75% to 95% for detecting dural venous sinus thrombosis and has shown high specificity compared with digital subtraction angiography.^30,39,43 MR venography can also be used for the diagnosis of major dural sinus thrombosis, with MRI offering the added ability to show the thrombus itself and to detect parenchymal lesions with more sensitivity than CT.^23,30,39 A combination of routine or conventional MRI sequences has reported sensitivity of 79.2% with specificity of 89.9% in one study, while a meta-analysis reported sensitivity of 0.82 and specificity of 0.92.^39,44 Table 2 summarizes the major imaging modalities used in the evaluation of acute post-traumatic DVSI.

Table 2.

Comparison of imaging modalities for evaluation of acute post-traumatic dural venous sinus injury.

Modality	Advantages	Limitations	Preferred when
CT venography (CTV)	Rapid acquisition; integrates with CT trauma protocols; no flow-related artifact; excellent bone anatomy correlation; widely available	Ionizing radiation; IV contrast required; lower sensitivity for isolated cortical vein thrombosis; limited parenchymal evaluation	First-line in acute trauma; when rapid diagnosis is needed; critical illness; MRI contraindicated
MR venography (MRV)	Direct thrombus visualization on T1/T2/DWI; parenchymal injury assessment; no ionizing radiation; contrast-enhanced MRV distinguishes low-flow from hypoplastic sinus	Slower acquisition; motion artifact; flow-related artifacts on TOF sequences; less available acutely	Non-acute setting; contrast contraindicated; pediatric patients; parenchymal assessment needed
Digital subtraction angiography (DSA)	Allows for dynamic flow assessment; platform for endovascular therapy	Invasive; radiation; IV contrast; high cost; not first-line in acute trauma	Inconclusive CTV/MRV; endovascular intervention planning; persistent diagnostic uncertainty

Abbreviations: CTV, CT venography; MRV, MR venography; DSA, digital subtraction angiography; TOF, time-of-flight; TBI, traumatic brain injury; IV, intravenous.

MRI/MRV can be used to characterize parenchymal sequelae and cortical vein involvement.^1,39,41 However, time-of-flight and phase-contrast MRV sequences can be susceptible to flow-related artifacts.^1,22,45 Contrast-enhanced MRV can better depict accurate luminal filling and help distinguish decreased flow from a hypoplastic sinus.^1,22,45 MRV can be suited for long-term follow-up imaging and may be preferred in cases where contrast administration or ionizing radiation is undesirable, especially in pediatric patients.^{15,23,39,46,47}

Additional imaging with digital subtraction angiography (DSA) is usually reserved for cases in which venographic imaging is inconclusive or for planning/performing endovascular interventions.^19,39,45 Ultimately, venographic imaging helps distinguish intraluminal thrombus from extrinsic compression and detect complications, including venous congestion, infarction, or hemorrhage.^3,6,11

Radiologic signs of acute traumatic dural venous sinus injury

The diagnosis of acute traumatic dural venous sinus injury relies on identifying specific signs through imaging, with noncontrast-enhanced CT and CTV serving as the primary diagnostic modalities.^48,49 The radiologic findings of DVSI should be interpreted in the clinical and anatomic context of trauma.^5,40 Imaging findings of DVSI can be classified as direct signs of injury to the vessel wall and lumen or indirect signs related to extrinsic compression and associated fractures.^5,40 A comprehensive summary of these direct and indirect radiologic signs, including their optimal imaging modalities and common interpretive pitfalls, is provided in Table 3.

Table 3.

Direct and indirect radiologic signs of acute traumatic dural venous sinus injury, with the best imaging modality for detection and the most clinically relevant mimics or interpretive pitfalls.

Category	Sign	Best modality	Imaging description	Pitfalls and mimics
Direct	Intraluminal hyperattenuation	NCCT	Spontaneously dense clot within the sinus lumen; comparison to other dural sinuses helpful	High hematocrit; dehydration; small sinus caliber; reconstruction artifact
	Filling defect within sinus	CTV; MRV when CTV is equivocal or for selected follow-up/problem-solving	Irregular, elongated non-opacified region tracking along the sinus lumen axis	Arachnoid granulation: rounded/ovoid, CSF-isodense on CT, CSF-isointense on MRI, smooth margins, characteristic location (lateral SSS recesses, TS near vein of Labbé, straight sinus)
	Filling defect within sinus			Pseudo-empty-delta from septated confluence
	Abrupt contrast cutoff/non-opacification	CTV; MRV may help in selected cases or follow-up	Complete absence of contrast opacification of a sinus segment; “claw sign” of acute thrombosis describes acute-angle contrast surrounding the filling defect	Hypoplastic/aplastic sinus: uniformly diminutive throughout, with correspondingly small bony groove on bone windows
	Abrupt contrast cutoff/non-opacification	CTV; MRV may help in selected cases or follow-up		Flow-related artifact on TOF MRV
	“Empty delta” sign	CTV (contrast-enhanced)	Triangular central filling defect surrounded by enhancing dural walls, classically described in the posterior superior sagittal sinus but conceptually reflecting enhancing dura/collaterals around thrombus	Pseudo-empty-delta from right- or left-dominant or septated confluence (anatomic variant, not thrombosis)
	Morphologic abnormality—narrowing, tapered occlusion, irregular contour	CTV	Focal caliber change, tapered occlusion, or irregular intraluminal contour at the injury site	Hypoplastic sinus (uniform, not focal); incidental anatomic variation
	Intraluminal gas	NCCT, CTV	Rare but specific; air within the sinus lumen associated with skull fracture involving or adjacent to the sinus; suggests sinus injury and higher DVST risk	Postoperative or post-intervention state; severe pneumocephalus with mass effect
	Contrast extravasation	CTV	Active contrast extravasation from sinus wall injury, indicating venous laceration/transection; acute AVF should be considered if early venous filling is present	Adjacent arterial active extravasation (correlate with CTA timing)
Indirect	Vessel displacement	CTV	Sinus pushed away from its expected position by an adjacent mass (typically EDH or depressed bone fragments)	Adjacent EDH/posterior fossa epidural hemorrhage can compress/displace the sinus and mimic thrombus; correlate on multiplanar CTV/MRV
	Extrinsic compression by adjacent epidural hematoma	CTV	EDH along sinus trajectory narrowing or effacing the lumen	Differentiate from secondary thrombosis (look for intraluminal filling defect)
	Fracture crossing or paralleling sinus	NCCT, CTV (bone window)	Calvarial or skull base fracture line overlying, crossing, or paralleling the expected sinus position; major risk marker for venous sinus compromise, thrombosis, compression, or operative bleeding risk	Asymptomatic fractures still warrant venographic evaluation if sinus trajectory crossed
	Asymmetric collateral channels	CTV, MRV	Prominent collateral venous channels, including emissary/diploic/scalp or cortical pathways, suggesting altered venous drainage from sinus obstruction	Congenital sinus asymmetry can produce baseline collateral prominence—compare with pre-injury imaging if available
	Venous congestion, infarction, or hemorrhage	NCCT, MRI (DWI, T2/FLAIR, SWI)	Parenchymal edema, restricted diffusion, infarction, or hemorrhage in a venous distribution downstream of a suspected or confirmed sinus injury	Arterial infarction (different territory pattern); contusion (corticospinal junction, coup-contrecoup pattern)

Abbreviations: CTA, CT angiography; CTV, CT venography; DVST, dural venous sinus thrombosis; DWI, diffusion-weighted imaging; EDH, epidural hematoma; FLAIR, fluid-attenuated inversion recovery; MRV, MR venography; NCCT, noncontrast CT; SSS, superior sagittal sinus; SWI, susceptibility-weighted imaging; TOF, time-of-flight; TS, transverse sinus.

Direct signs of DVSIs can manifest as abnormalities in blood flow (opacifications) and vessel morphology.^5,39 A key finding associated with venous injury is the lack of filling or complete occlusion of a sinus segment, which may appear as an abrupt cutoff of contrast on CTV (Figure 7).⁵ For example, an intraluminal thrombosis may present as a hyperattenuating clot within the sinus on noncontrast CT and as a filling defect on CTV (classically described as an “empty delta” appearance in some cases).^48,50 Furthermore, morphologic changes such as narrowing, tapered occlusion, and an irregular contour are additional direct indicators of venous injury (Figure 8).^5,43 Another rare but specific sign of venous injury is the presence of intraluminal gas (Figure 9).^48,49

Figure 7.

A. Axial noncontrast-enhanced CT demonstrating a hyperattenuating clot (red arrow). B. CT venogram demonstrating the corresponding filling defect (red arrows) and associated diastatic fracture (yellow arrow).

Figure 8.

A–C. CT venogram demonstrating a change in caliber and narrowing (blue arrow), tapered occlusion (yellow arrow), and irregular contour (red arrows) with vessel displacement (asterisks).

Figure 9.

Axial CT venogram demonstrating intraluminal gas (arrow).

Indirect signs of DVSIs reflect secondary effects on the dural sinuses from injury to surrounding structures.⁵ Vessel displacement and extrinsic compression are significant indirect findings that are frequently caused by an adjacent epidural hematoma due to a calvarial fracture overlying the sinus (Figures 10 and 11).^5,51 The presence of a diastatic or depressed skull fracture that crosses or lies parallel to a dural sinus is another critical indirect finding and primary risk factor for both laceration and secondary thrombotic or compressive injury.^50–52 When present, asymmetric collateral venous channels or distal reconstitution can further support a focal traumatic abnormality rather than a global timing or technique issue.^11,51

Figure 10.

A. Axial CT venogram and B. 3D reconstruction demonstrating vessel displacement (red arrows) by venous epidural hematoma (white arrows).

Figure 11.

A. Sagittal CT venogram, B. axial head CT, and C. 3D reconstruction demonstrating a calvarial fracture (yellow arrows) with epidural hematoma (EDH) (white arrow in panel A) causing extrinsic compression and narrowing of the superior sagittal sinus (SSS).

There are two important imaging pitfalls: arachnoid (Pacchionian) granulations and congenital transverse sinus hypoplasia or atresia. First, arachnoid (Pacchionian) granulations typically appear as focal rounded filling defects with CSF-like attenuation on CT and signal intensity similar to CSF on MRI.^1,16,18,19 Giant arachnoid granulations may not parallel CSF on all MRI sequences. They are commonly seen in the transverse sinus, especially laterally near the vein of Labbe or lateral tentorial sinus.^1,16,18,19 Giant arachnoid granulations have also been described in the superior sagittal and straight sinuses.^1,16,18,19 In contrast, an intraluminal thrombus typically appears elongated or irregular, extending along the sinus rather than forming a short rounded defect.^1,5,18 An acute venous thrombosis may appear as an elongated hyperattenuating clot on noncontrast CT, and intrinsic thrombus on CTV may produce an acute-angle “claw sign” of contrast partially or completely surrounding the thrombus.^1,5,18 Second, a hypoplastic or atretic transverse sinus can simulate sinus occlusion, particularly on time-of-flight MR venography, where stagnation of blood flow in a normal but small nondominant transverse sinus may mimic thrombosis.^1,16 Correlation with bone-window CT helps differentiate congenital hypoplasia from thrombosis.^5,19,31 One important distinction is that congenitally small transverse or sigmoid sinuses are expected to have small jugular foramina or sigmoid sinus grooves, whereas thrombosed sinuses may be discrepant with the osseous anatomy and show intraluminal thrombus or absent contrast filling on CTV.^5,19,31 Contrast-enhanced MR venography and CT venography can also help resolve this limitation because they are less susceptible to time-of-flight (TOF) flow gaps, and CT venography may directly show a patent hypoplastic transverse sinus.^16,23

Classification and pathophysiology of dural venous sinus injuries

DVSIs can be classified by mechanism of injury.⁵ Type A injuries are due to external compression from blood, air, or bone fragments, leading to a nonocclusive luminal narrowing.⁵ Type B injuries involve a thrombosis of the venous sinus.⁵ Finally, type C injuries are considered mixed, involving both compression and thrombus formation.⁵ DVSI can also be classified by the extent of flow limitation.⁵ Type 1 DVSI is non-occlusive and characterized by a narrowed but patent venous sinus. In contrast, type 2 DVSI occurs when there is complete luminal occlusion without contrast filling in the injured segment of the sinus.⁵ Finally, type 3 injuries involve a transection or tear of the venous sinus with contrast extravasation and can cause the formation of an acute arteriovenous fistula.⁵ This two-axis classification system was introduced by Schwartz et al. as a standardized radiologic grading scheme for traumatic dural venous sinus injury on CT venography.⁵ However, the Schwartz grading scheme has not yet been externally validated or widely adopted into standard clinical practice, and other classification approaches remain in use.⁵ Nevertheless, the system provides a descriptive structure: Type A (extrinsic compression), Type B (intrinsic thrombosis), and Type C (mixed). In selected cases compression or occlusion of the sinus may warrant neurosurgical evaluation, whereas thrombotic injury may raise consideration of anticoagulation, with treatment individualized to balance hematoma expansion against thrombus propagation or venous infarction.^5,9,30,50,53

Acute post-traumatic dural venous sinus thrombosis (DVST) is a potentially fatal complication of traumatic brain injury and can be associated with venous congestion, hemorrhage, and worse clinical outcomes.⁷ DVST more commonly occurs when depressed skull fractures or epidural hematomas are near a dural venous sinus, leading to a mechanical disruption of venous outflow and promoting thrombus formation.^7,54 Overall, the risk of DVST is highest when a fracture extends to the dural sinus or jugular bulb.¹¹ Fractures of the petrous bone that extend towards the transverse sinus, sigmoid sinus, or jugular bulb have also been associated with the formation of DVST.^11,55 When venous outflow obstruction is substantial, the resulting venous congestion can progress to edema, venous infarction, and hemorrhage.¹⁵

Although the exact mechanism of DVST formation has not been fully defined, it may parallel Virchow’s triad: (1) endothelial injury from direct damage to the sinus wall, (2) hypercoagulability after trauma/TBI, and (3) venous stasis when depressed fracture fragments and/or an epidural hematoma compress the sinus.⁷ One potential complication of DVST is venous hypertension, which can have a nonspecific clinical presentation and be masked by coexisting traumatic brain injury and other intracranial hemorrhage symptoms, making early imaging-based recognition important.⁵⁶ Because traumatic DVSI can present with intraluminal thrombus, external compression, or both, distinguishing these mechanisms is essential for subsequent monitoring and management.^5,35

Several anatomic injury patterns are associated with increased risk of DVSI/DVST and other associated complications. In blunt head trauma, skull base fractures that extend to the dural venous sinus or the jugular bulb/foramen carry a high risk for developing post-traumatic dural venous sinus thrombosis or occlusion.^10,11,54 Similarly, comminuted fractures of the mastoid, temporal, and adjacent occipital bone can damage the transverse-sigmoid sinus complex, especially when the fracture line (or associated epidural hematoma) overlies the dural venous sinus.^3,9,40 Furthermore, temporal bone fractures can involve the otic capsule and are clinically significant because they can be associated with a higher likelihood of complications such as facial nerve injury and CSF leak.^48,57,58 Compared with fractures that spare the otic capsule, otic capsule-violating fractures are more often associated with otologic and neurologic complications and therefore require early recognition.^48,57,58

Penetrating cranial trauma can injure a dural venous sinus along the projectile path, leading to sinus wall disruption, intraluminal thrombosis, or extrinsic compression from adjacent hemorrhage.^8,12,59,60 Projectile-related injuries, such as gunshot wounds, to the cranial sinuses are classically associated with severe hemorrhage and sinus thrombosis, warranting prompt evaluation due to the risk of massive blood loss and high perioperative mortality risk.^8,12,59,60

Trauma causing midline/parasagittal calvarial fractures (especially depressed fractures) or vertex/parasagittal extra-axial hematomas overlying the sinus can lead to superior sagittal sinus injuries.^8,13 Extensive venous outflow occlusion, particularly involving the middle or posterior third of the SSS, can be associated with venous congestion or infarction.^50,60 Therefore, a targeted venographic assessment is warranted in cases of midline fractures with suspected dural sinus involvement to identify potential complications.^11,40,41

Illustrative cases of dural venous sinus injuries: Imaging patterns

The following cases illustrate possible traumatic DVSI patterns across the skull base, transverse, sigmoid, and superior sagittal sinus locations, emphasizing the importance of distinguishing thrombosis from extrinsic compression and recognizing potential complications. A summary of the key teaching points for each case, organized by their respective Schwartz classification types, is provided in Table 4.

Table 4.

Teaching points for illustrative cases of acute post-traumatic dural venous sinus injury.

Case	Key Teaching Points
Case 1 Skull base & temporal bone trauma	• Temporal bone and skull base fractures that cross a dural venous sinus are associated with increased risk of traumatic dural venous sinus thrombosis.
	• Skull base fractures that extend to a dural venous sinus, jugular bulb, or carotid canal should prompt targeted vascular imaging based on the suspected injury pattern.
	• Arterial and venous injuries can coexist in skull base trauma; additional vascular imaging should be guided by fracture trajectory and the specific structure at risk.
Case 2 Transverse sinus injury with suspected extrinsic compression	• Preserved contralateral sinus opacification is essential to confirm a focal traumatic abnormality rather than a global technique or timing artifact.
	• Downstream collateral filling of the sigmoid sinus via small venous channels supports a focal venous outflow abnormality, but correlation with the site morphology is needed to distinguish compressive from thrombotic injury and non-occlusive from occlusive injury.
	• Thin-section CTV reformats targeted to the sinus are essential for detecting subtle opacification deficits adjacent to epidural hematomas.
Case 3 Occlusive transverse-sigmoid injury with venous infarction	• Complete absence of contrast filling within the injured sinus segment classifies the lesion as occlusive; occlusive DVST can be associated with venous infarction.
	• Mastoid air cell opacification on noncontrast CT is an indirect sign of fracture trajectory and should prompt dedicated evaluation of the ipsilateral transverse-sigmoid complex.
	• Complete occlusion without downstream reconstitution warrants urgent clinical assessment given high risk of venous infarction.
Case 4 Penetrating injury affecting the transverse sinus	• Intraluminal gas within a dural sinus suggests traumatic sinus injury and is associated with a higher likelihood of concurrent DVST, prompting consideration of CTV.
Case 4 Penetrating injury affecting the transverse sinus	• Comprehensive CTV delineation of occlusion extent and collateral pathways is essential before operative planning in penetrating DVSI.
Case 5 Blunt head trauma affecting the superior sagittal sinus	• Depressed frontal calvarial fractures overlying the SSS require CTV evaluation even for short injury segments, given the SSS’s role as the dominant parasagittal outflow structure.
	• Intact collateral venous pathways should be communicated to the surgical team because they document rerouted venous drainage across the injured segment.

Case 1: Skull base and temporal bone trauma

In this case, a male patient was involved in a motor vehicle accident (Figure 12). CT imaging demonstrates a temporal bone fracture that violates the otic capsule with associated fracture through the jugular fossa, including otologic complications, venous outflow injury, and concomitant arterial injury (Figure 13; blue arrows, Figures 14 and 15). Because skull base fractures can meet screening criteria for blunt cerebrovascular injury (BCVI), a computed tomography angiogram (CTA) can be used to identify concomitant arterial injury, such as an internal carotid artery pseudoaneurysm (BCVI grade III) (Figure 16).^4,52,61 This case highlights the importance of targeted venography and arterial screening when fracture trajectories involve the skull base.

Figure 12.

Head CT 3D reconstruction demonstrating the skull and skull base fractures traversing the jugular foramen (red arrow).

Figure 13.

A–E Temporal bone CT demonstrating otic capsule violating temporal bone fracture (blue arrows) with an associated fracture through the jugular fossa (red arrows).

Figure 14.

A–D. CT venogram demonstrating absence of filling of the sigmoid sinus and jugular bulb on the right (red arrows) with normal filling of the left sigmoid sinus and jugular bulb (yellow arrows).

Figure 15.

CT venogram 3D reconstructions demonstrating a tapered occlusion at the distal right transverse sinus and sigmoid sinus with lack of filling of the jugular bulb (red arrows).

Figure 16.

CT angiography with 3D reconstruction demonstrating a small pseudoaneurysm of the distal left internal carotid artery (ICA) representative of a grade III arterial injury (red arrow).

Case 2: Transverse sinus injury with suspected extrinsic compression

In this case, a 29-year-old male suffered blunt head trauma after being hit with a baseball bat and was run over by a vehicle. Noncontrast-enhanced CT imaging demonstrates a fracture of the left mastoid portion of the temporal bone with an associated occipital fracture (Figure 17) and coexisting traumatic intracranial hemorrhagic injuries, including bilateral frontal hemorrhagic contusions and a right convexity epidural hematoma (Figure 18). CTV with thin-section reformats and targeted post-processing reveals a lack of opacification and possible occlusion of the left transverse sinus with downstream filling of the left sigmoid sinus via small venous collaterals (Figure 19; white arrow). This imaging pattern supports a mechanical compression of the transverse sinus in the region of the epidural hematoma.

Figure 17.

A. 3D rendering of maxillofacial CT showing a displaced fracture of the mastoid segment of the left temporal bone (black arrows). B. Temporal bone CT demonstrating comminuted fractures of the left mastoid with widened fracture lines (white arrows) with another fracture present in the adjacent occipital bone (yellow arrow).

Figure 18.

A–B. Axial brain CT showing hemorrhagic contusions in the bilateral inferior frontal lobes (yellow arrows) with an epidural hematoma along the right convexity (red arrow).

Figure 19.

A. CT venogram and B. CT with curve planar reformation depicting lack of opacification of the left transverse sinus (white arrows) with an epidural hematoma (EDH) obliterating the left transverse sinus. There is filling of the left sigmoid sinus (L SigS) from venous collaterals (V). There is also an irregularity and narrowing at the posterior segment of the superior sagittal sinus (arrowheads) extending to the torcular (TH). The right transverse sinus (R TS) and right sigmoid sinus (R Sigs) demonstrate normal filling. Asterisks delineate a fracture in the occipital bone and mastoid bone.

Case 3: Occlusive transverse-sigmoid sinus injury with venous infarction

In this case, a 42-year-old male sustained head injuries after jumping out of a moving vehicle. CT imaging demonstrates a fracture of the left mastoid bone with opacification of the mastoid air cells (Figure 20; yellow arrows). Imaging with CTV reveals lack of opacification of the left transverse-sigmoid sinus complex, consistent with an occlusive injury (Figure 21; red arrows). The CTV also depicts a lack of distal reconstitution of venous flow, leading to the development of a venous infarct (Figure 22 A - B; red arrows; Figure 22 C; yellow arrows).

Figure 20.

Axial temporal bone CT showing comminuted fracture and opacification (blood) of the left mastoid air cells (yellow arrows).

Figure 21.

A–C. CT venogram showing lack of opacification (occlusion) of the left transverse-sigmoid sinus complex (red arrows) and a filling defect in the right transverse sinus (R TS) which represent an arachnoid granulation (asterisk).

Figure 22.

A. Curved Planar Reformation (CPR) and B. 3D volume rendering showing occlusion of the left transverse-sigmoid sinus complex (red arrows) without distal collateral reconstitution. C. MRI demonstrating a secondary venous infarct on the adjacent left cerebellum (yellow arrow).

Case 4: Penetrating injury affecting the transverse sinus

In the following case, a 22-year-old presented with a gunshot wound to the head. The CT images show multiple comminuted skull base and facial fractures along the projectile’s trajectory, affecting the right mastoid and right occipital calvarium (Figure 23). The CTV demonstrates abnormal right transverse sinus opacification with intraluminal filling defects compatible with clot/thrombus formation (Figure 24; white arrows), intraluminal gas, and distal tapered cutoff/occlusion, best appreciated with thin-section curved planar reformats (“pancake view”) and 3D volume rendering (Figure 25; blue arrows).

Figure 23.

Axial head CT demonstrating multiple comminuted fractures of the skull base and facial bones, along the projectile trajectory (dashed line), involving the right mastoid (M) and right occipital bone (O).

Figure 24.

CT venogram showing irregular opacification and filling defects (white arrows) within the right transverse sinus with distal cutoff of flow (yellow arrow).

Figure 25.

A. CT venogram depicting irregular opacification with filling defects representative of clot formation within the right transverse sinus (white arrows), intraluminal gas (blue arrows), distal tapered occlusion (yellow arrow), and a venous epidural hematoma (red arrows) slightly displacing the right transverse sinus away from the calvarium. B. 3D reconstruction demonstrating fractures through the skull base and calvarium (asterisks). L TS, left transverse sinus; R TS, right transverse sinus; L SigS, left sigmoid sinus.

Case 5: Blunt head trauma affecting the superior sagittal sinus

In this case, a 26-year-old male was assaulted with a crowbar. Noncontrast CT with 3D surface rendering demonstrates comminuted, depressed bilateral frontal calvarial fractures with small adjacent extra-axial hematomas (Figure 26; yellow arrows). CTV shows abrupt vessel caliber change with focal narrowing and discontinuity involving a short segment of the anterior SSS, consistent with traumatic injury/occlusion in the setting of a direct calvarial impact (Figure 27; yellow and red arrows). 3D post-processing with “external view” demonstrates the fracture configuration, while the “internal view” highlights collateral venous pathways that bypass the injured segment (Figure 28). The “internal view” reconstruction is helpful when the damaged segment is short and partially obscured by adjacent bone or hematoma on standard planar views.

Figure 26.

A. Axial CT head showing comminuted, depressed fractures of the bilateral frontal calvarium with subjacent small subdural hematomas (yellow arrows).

Figure 27.

A–B. CT venogram demonstrating change in caliber (yellow arrows) with narrowing and slight displacement of the anterior segment of the superior sagittal sinus (SSS) and focal discontinuity of the SSS (red arrows).

Figure 28.

A. 3D surface rendering (“external view”) showing comminuted, depressed fractures of the bilateral frontal calvarium. B. CT venogram with 3D volume rendering (“internal view”) showing venous collaterals (V) reconstituting the occluded, damaged short segment (arrows) of the anterior portion of the superior sagittal sinus.

Management of dural venous sinus injuries

The management of acute traumatic DVSI should begin by identifying the principal mechanism of injury that is causing the impaired venous outflow leading to sinus compromise.⁷ Essential mechanisms of injury of DVSI include extrinsic compression or stenosis due to depressed skull fractures or hematomas, intramural thrombosis, and a combination of both.⁷ A mechanism-based management summary is outlined in Table 5. When venographic imaging suggests mechanical extrinsic compression, patients may benefit from neurosurgical evaluation and decompression to relieve venous outflow obstruction.⁷ Factors to consider when evaluating mechanical compression include the size and location of the compressing lesion (hematoma) and whether the affected vessels are patent or thrombosed.^3,10,14 In a surgical series of compound depressed fractures overlying the superior sagittal sinus, 50% of patients were found to have an intact sinus, 44% had a small tear which was controlled with Gelfoam or a piece of muscle with added dural tenting and compression for several minutes, and 5.8% had a complete tear of the sinus with massive bleeding that ended with sinus ligation.⁶⁰ In contrast, when the primary mechanism of obstruction is acute post-traumatic DVST, management guidelines become less clear.⁶²

Table 5.

Proposed mechanism-based management approach for acute post-traumatic dural venous sinus injury.

Mechanism	Imaging pattern on CTV/MRV	First-line management	Anticoagulation approach	Follow-up imaging
Extrinsic compression/stenosis	Smooth luminal narrowing or focal stenosis at the level of a depressed skull fracture or extra-axial hematoma; no intraluminal filling defect	Neurosurgical evaluation for decompression of the compressing lesion (elevation of depressed fracture, evacuation of hematoma). Consider venography to confirm patency after decompression	Anticoagulation not indicated unless concurrent thrombosis is identified. Periprocedural DVT prophylaxis per standard TBI protocols	CTV or MRV within 24–48 h after decompression to confirm restored flow. If the sinus remains compressed, repeat imaging in 1–2 weeks
Intraluminal thrombosis (DVST)	Intraluminal filling defect (nonocclusive or occlusive) on CTV/MRV; absent flow-related enhancement; may involve single or multiple sinuses	Medical management: ICP monitoring, seizure prophylaxis, maintenance of euvolemia and normotension. Consider neurosurgical consultation if mass effect or venous infarction	Anticoagulation should be individualized based on hemorrhage stability, thrombus location, occlusion, and clinical course. LMWH is commonly favored when considered safe	Repeat CTV or MRV based on clinical status and treatment plan. If anticoagulated venography at 1–2 weeks and about 3 months is reasonable, with duration adjusted to recanalization and bleeding risk
Mixed compression + thrombosis	Combination of extrinsic narrowing and intraluminal filling defect at the same sinus segment	Individualized management. Address the dominant mechanism first: decompress if significant compression; initiate medical management for the thrombotic component. Multidisciplinary discussion (neurosurgery, neurointervention, neurocritical care)	Compressive lesion should be addressed first if urgent surgical evacuation is needed. Start or resume anticoagulation only after hemorrhage stability is confirmed, often with reduced-dose LMWH initially; timing should be individualized by neurosurgery/neurocritical care	Early post-decompression venous imaging if surgery is performed, then repeat CTV/MRV based on clinical course and anticoagulation plan; 1–2 weeks and 3 months are reasonable follow-up points when anticoagulated
Transection/tear with active extravasation	Frank extravasation of contrast on CTV/MRV; discontinuity of the sinus wall; may be associated with massive extra-axial hematoma	Emergent surgical exploration. Sinus repair options include Gelfoam or muscle patch with dural tenting and compression (15 min), primary suture repair, or sinus ligation (if complete transection). Obtain vascular (open or endovascular) control prior to definitive repair	Anticoagulation contraindicated in the acute phase due to active hemorrhage. After hemostasis is achieved, reassess for residual thrombosis using CTV before considering anticoagulation	Postoperative CTV within 24–48 h. If sinus ligation was performed, monitor for venous hypertension/infarction with serial imaging
Endovascular rescue (any mechanism, refractory)	Persistent or progressive thrombus on CTV despite adequate medical therapy; clinical deterioration	Reserve endovascular therapy for selected refractory cases with progressive thrombosis, venous congestion, or intracranial hypertension despite standard medical and/or surgical measures. Evidence is limited to case reports and small series	Use peri-procedural antithrombotic therapy after multidisciplinary risk assessment. Post-procedure anticoagulation is commonly considered, but timing, agent, and dose should be individualized because trauma-related hemorrhage risk remains substantial	Perform early post-procedure CTV/MRV or angiographic follow-up to confirm patency and then repeat venous imaging according to clinical course, commonly around 1–3 months if ongoing thrombosis treatment is used

Abbreviations: CTV, CT venography; DVT, deep vein thrombosis; DVST, dural venous sinus thrombosis; ICP, intracranial pressure; LMWH, low-molecular-weight heparin; MRV, MR venography; TBI, traumatic brain injury; UFH, unfractionated heparin.

Currently, there is limited data about the management of DVST, and no consensus has been reached regarding optimal treatment strategies.⁶² One challenge when managing DVST is that it often presents in conjunction with cerebral contusions, parenchymal hemorrhages, and subdural and epidural hematomas.⁵⁴ General practice favors systemic anticoagulation with low-molecular-weight heparin (LMWH) to prevent clot propagation, even in the presence of intracranial hemorrhage.⁵⁴ The 2024 American Heart Association scientific statement and the European Stroke Organization guidelines similarly recommend LMWH over unfractionated heparin in the acute phase of cerebral venous thrombosis, noting that venous hemorrhage is not a contraindication to anticoagulation; however, these recommendations are based on spontaneous cerebral venous thrombosis (CVT) populations, and specific guidelines for traumatic DVST are lacking.^15,39,45 In the traumatic setting, limited observational data suggest that delaying anticoagulation until interval CT documents stability of hemorrhagic lesions may reduce the risk of hemorrhagic complications.¹⁵ One adult series had 58% of patients with DVST treated with anticoagulation.^30,63 Of these, 50% demonstrated thrombus resolution at 3 months.^30,63 However, the study reported a rate of complications of 14% including gastrointestinal bleeding, and an additional 14% developed new or worsening intracranial hemorrhage with a mortality of 4.5%.^30,63 A United Kingdom and Ireland survey of neurosurgical and critical care practice found substantial variation: 73.2% of clinicians used anticoagulation in selected cases only, 17.1% used no anticoagulation, and 9.8% used anticoagulation in all cases, with no respondents reporting an established departmental protocol for traumatic cerebral venous sinus thrombosis (tCVST) management.³⁴ It is important to note that there are no standardized guidelines for the timing, dosing, or duration of anticoagulation therapy for DVST.¹² Moreover, the benefits of anticoagulation therapy must be weighed against the risk of progression of hemorrhagic parenchymal contusions and epidural and subdural hematomas.^42,54 Follow-up CT venography at 1 to 2 weeks and at 3 months after injury may be considered to assess recanalization and guide treatment duration; complete recanalization in adult or all-age TBI series has been reported in 41–80% of cases across published series.¹⁵ Endovascular intervention, such as intrasinus thrombolysis or mechanical thrombectomy, is reserved as a rescue option for patients with clinical deterioration despite adequate medical therapy, and current evidence does not support routine endovascular treatment over standard anticoagulation.^39,64

Conclusion

Systematic evaluation of the dural venous sinuses should be part of the diagnostic algorithm in head trauma, particularly when fractures or extra-axial hematomas occur along sinus trajectories (e.g., temporal/mastoid–transverse-sigmoid region, or vertex/frontal-parietal injuries near the superior sagittal sinus). Because DVSI and DVST can present subtly (or not at all) in noncontrast CT, the use of CTV/MRV with thin-section and targeted post-processing can aid diagnosis. Venographic imaging can distinguish between thrombus and extrinsic compression, characterize lesion extent, and define collateral pathways and downstream patency. Ultimately, timely recognition of these injuries, guided by a systematic venographic approach, is important for directing mechanism-based management and reducing the risk of severe sequelae such as venous infarction. However, prospective multicenter studies with standardized imaging protocols are needed to define anticoagulation strategies for traumatic DVST with intracranial hemorrhage and to establish the role of follow-up imaging in assessing recanalization and guiding treatment duration.

Footnotes

ORCID iD

Ruben Gabriel Ortiz Cordero

Ethical consideration

This is a review article for educational purposes.

Funding

The authors received no financial support for the research, authorship, or publication of this article.

Declaration of conflicts of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

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