Hyperacute Venous Stroke IV - Clinical Case Summary
Hyperacute Venous Stroke IV - Clinical Case Summary
Hyperacute Venous Stroke IV - Clinical Case Summary
SummaryHistory
53 year old female who presented with confusion, depressed level of consciousnes, fever, and right ear pain. On admission patient had right coalescent otomastoiditis. Her lumbar puncture grew out streptoccus.
Exams performed
Post contrast Temporal bone CT; CTA of the neck; MRV of the head; Delayed post contrast head CT; Post contrast T1-w MR; MR diffusion; MR FLAIR
Prior available imaging reports
CT head
1. There is evidence of aggressive right otomastoiditis with sigmoid plate dehiscence (coalescent otomastoiditis) producing a small volume, epidural abscess, which partiall compresses the adjacent dural sinus. Focal deformity of the sigmoid sinus is evident at the site of epidural abscess, however, the remaining lumen of the right sigmoid sinus and the internal jugular vein are patent. Intraluminal thrombus is present in the torcular herophile, the left transverse/sigmoid sinuses, extending into the high cervical left IJ.
CT perfusion No CT perfusion is available
CTA of the neck
1. Thrombosis of the high cervical left internal jugular vein with collateral drainage into the other left neck veins. 2. The right IJ is patent. No soft tissue abnormality is evident within the cervical soft tissues.
CTA of the head
1. Segmental thromboses in the dural sinuses, especially in the superior sagittal sinus (SSS) and in the left transverse sinus. Major veins in the opacified (non thrombosed) SSS segment are patent and exhibit re-routing patterns. Persistent impression remains adjacent to the small epidural abscess adjacent to the right sigmoid plate.
Post contrast head CT (venocapillary pool analysis)
1.There are known multiple dural sinus thromboses that are underestimated on the delayed post contrast CT. 2. There is no evidence of reduced CT density within the venocapillary pool in either the cerebrum or cerebellum. There is evidence of both optic hydrops and early hydrocephalus related to venous hypertension caused by the dural sinus egress block. It is concievable that the hydrocephalus could be in part related to meningitis associated with the right coalsecent otomasoiditis.
Post contrast T1-w MR
1. Partial improvement In the extent of dural sinus thromboses likely related to improved venous collateral egress and/or progressive recanalization with improved antegrade blood flow. Persistent right otomastoiditis and epidural abscess; the size of the abscess has gotten smaller with treatment. Some reduction in the degree of ventriculomegaly likely related to improved venous egress with reduction in CSF pressure.
MR diffusion dwi
1. There is evidence of positive MR diffuson in the site of coalscent mastoiditis with epidural abscess on the right plus evidence of a very small recent embolic arterial stroke in the left superior vermis.
MR flair
1. There is diffuse meningeal inflammation, likely related to meningitis associated with the aggressive otomastoid infection.
2. There is persistent subtle ventriculomegaly with minimal persistent transependymal fluid migration. Punctate area of positive FLAIR signal in the left vermic area matches the MR diffusion positivity in the same area consistent with stroke. But whether this is a venous or arterial embolic stroke is indeterminate. Interval development of paranasal sinus mucosal thickening, currently without aggressive features.
1. There is evidence of aggressive right otomastoiditis with sigmoid plate dehiscence (coalescent otomastoiditis) producing a small volume, epidural abscess, which partiall compresses the adjacent dural sinus. Focal deformity of the sigmoid sinus is evident at the site of epidural abscess, however, the remaining lumen of the right sigmoid sinus and the internal jugular vein are patent. Intraluminal thrombus is present in the torcular herophile, the left transverse/sigmoid sinuses, extending into the high cervical left IJ.
CT perfusion No CT perfusion is available
CTA of the neck
1. Thrombosis of the high cervical left internal jugular vein with collateral drainage into the other left neck veins. 2. The right IJ is patent. No soft tissue abnormality is evident within the cervical soft tissues.
CTA of the head
1. Segmental thromboses in the dural sinuses, especially in the superior sagittal sinus (SSS) and in the left transverse sinus. Major veins in the opacified (non thrombosed) SSS segment are patent and exhibit re-routing patterns. Persistent impression remains adjacent to the small epidural abscess adjacent to the right sigmoid plate.
Post contrast head CT (venocapillary pool analysis)
1.There are known multiple dural sinus thromboses that are underestimated on the delayed post contrast CT. 2. There is no evidence of reduced CT density within the venocapillary pool in either the cerebrum or cerebellum. There is evidence of both optic hydrops and early hydrocephalus related to venous hypertension caused by the dural sinus egress block. It is concievable that the hydrocephalus could be in part related to meningitis associated with the right coalsecent otomasoiditis.
Post contrast T1-w MR
1. Partial improvement In the extent of dural sinus thromboses likely related to improved venous collateral egress and/or progressive recanalization with improved antegrade blood flow. Persistent right otomastoiditis and epidural abscess; the size of the abscess has gotten smaller with treatment. Some reduction in the degree of ventriculomegaly likely related to improved venous egress with reduction in CSF pressure.
MR diffusion dwi
1. There is evidence of positive MR diffuson in the site of coalscent mastoiditis with epidural abscess on the right plus evidence of a very small recent embolic arterial stroke in the left superior vermis.
MR flair
1. There is diffuse meningeal inflammation, likely related to meningitis associated with the aggressive otomastoid infection.
2. There is persistent subtle ventriculomegaly with minimal persistent transependymal fluid migration. Punctate area of positive FLAIR signal in the left vermic area matches the MR diffusion positivity in the same area consistent with stroke. But whether this is a venous or arterial embolic stroke is indeterminate. Interval development of paranasal sinus mucosal thickening, currently without aggressive features.
Overall impression
1. Right coalescent otomastoiditis with dehiscence of the sigmoid plate producing a small volume epidural empyema.
2. The right otomastoid region empyema causes a partial stenosis of the right transverse-sigmoid segment of the dural sinus.
3. Additionally, there is complete thrombosis of the torcula, the distal segment of the superior sagittal sinus, and of the left transverse sinus. There is functional venous collateral through the dural sinus walls and both the vertex and lateral tentorial pial-dural venous confluences. There is positive DWI in the superior vermis and adjacent tentorial cerebellar parenchyma, likely post ischemic in nature, but whether it proceeds to actual infarction is indeterminate.
4. There is thrombosis of the apex of the straight sinus collateralized via the basal veins of Rosenthal.
5. There is thrombosis of the high cervical segment of the left internal jugular vein, which is collaralized through cervical collateral.
6. There is hyperacute leptomeningitis with evidence of widespread subpial edema and increase sulcal protein.
2. The right otomastoid region empyema causes a partial stenosis of the right transverse-sigmoid segment of the dural sinus.
3. Additionally, there is complete thrombosis of the torcula, the distal segment of the superior sagittal sinus, and of the left transverse sinus. There is functional venous collateral through the dural sinus walls and both the vertex and lateral tentorial pial-dural venous confluences. There is positive DWI in the superior vermis and adjacent tentorial cerebellar parenchyma, likely post ischemic in nature, but whether it proceeds to actual infarction is indeterminate.
4. There is thrombosis of the apex of the straight sinus collateralized via the basal veins of Rosenthal.
5. There is thrombosis of the high cervical segment of the left internal jugular vein, which is collaralized through cervical collateral.
6. There is hyperacute leptomeningitis with evidence of widespread subpial edema and increase sulcal protein.
Lessons to be learned
1. Aggressive otomastoiditis (i.e. coalescent mastoiditis), paranasal sinusitis, and nasopharyngeal infections have a high propensity to develop epidural infections.
2. Epidural and subdural infections secondarily produce phlebothrombosis, which can turn into infectious thrombophlebitis, which can propagate into the dural sinuses and/or cortical veins causing CVT. It is incumbent on the imager to not only recognize CVT, but also to find the initial sites of infection, since they can quickly produce meningitis, ventriculitis, abscess and demise.
3. Coalsecent otomastoiditis and aggressive sinusitis are diagnosed by the presence of bone dehiscence. Hence, bone window viewing is essential, especially on CT.
4. CVT in otomastoiditis/paranasal sinusitis is NOT limited to involvement of the first available venous structure. Notice, in this case of right coalescent otomastoiditis did no cause right transverse sinus thrombosis, but merely deforms the lumen from pressure exerted by a small epidural abscess. However, there is intraluminal thrombus in the distal SSS, the torcula and the left mesial transverse sinus.
2. Epidural and subdural infections secondarily produce phlebothrombosis, which can turn into infectious thrombophlebitis, which can propagate into the dural sinuses and/or cortical veins causing CVT. It is incumbent on the imager to not only recognize CVT, but also to find the initial sites of infection, since they can quickly produce meningitis, ventriculitis, abscess and demise.
3. Coalsecent otomastoiditis and aggressive sinusitis are diagnosed by the presence of bone dehiscence. Hence, bone window viewing is essential, especially on CT.
4. CVT in otomastoiditis/paranasal sinusitis is NOT limited to involvement of the first available venous structure. Notice, in this case of right coalescent otomastoiditis did no cause right transverse sinus thrombosis, but merely deforms the lumen from pressure exerted by a small epidural abscess. However, there is intraluminal thrombus in the distal SSS, the torcula and the left mesial transverse sinus.
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