Presentation
This patient initially presented to an emergency department with coryzal symptoms; dysuria; lower back pain described as muscular; and right testicular pain. Several hours after arrival in emergency department, he developed sudden onset weakness and paresthesias of the right arm. Apart from a history of lymphoma, his history is unremarkable.
Patient Data
Initial NCCT taken shortly after presentation
Unremarkable CT scan of the head.
Two intra-axial lesions are seen in the left cerebral hemisphere. The first is within the left frontal lobe. The second is within the posterior left frontal lobe extending into the parietal lobe. Both lesions demonstrate heterogeneous internal signal intensity suggestive of acute hemorrhage. They have surrounding vasogenic edema. Although diffusion signal is heterogeneous, care must be taken to not over-interpret this in the presence of blood product. No convincing features of dural venous sinus thrombosis. A small area of non-hemorrhagic infarction is also noted inferiorly.
A contrast CT taken approximately 38 hours after presentation
Surgical clips and a left frontal burr hole with associated pneumocephalus is visible within the left anterior frontal lobe.
Two foci of intraaxial hemorrhage in the left frontal and left frontoparietal lobes are noted. Associated mass effect with midline shift which has increased compared to the MRI approximately 14 hours before. No underlying enhancing lesion is demonstrated.
A peripheral wedge-shaped hypodensity in the inferior left frontal lobe demonstrated restricted diffusion on MRI. This likely represents a focus of infarct.
Case Discussion
This patient's initial presentation was not suggestive of neurological pathology. Testicular pathology was excluded by ultrasound.
The subsequent sudden-onset mild subjective right-sided weakness and paresthesia prompted a non-contrast CT. This was unremarkable.
Ongoing deterioration caused a right-sided neuromotor deficit with 0/5 power. GCS was still 15. This lead to a MRI that demonstrated findings consistent with lobar hemorrhages. In the setting of systemic symptoms and Staphylococcus aureus positive blood cultures the possibility of superimposed infection or hemorrhagic cerebritis where considered.
With further deterioration in GCS, urgent neurosurgical intervention with drainage of the cerebral collection was performed. A small amount of blood-stained was fluid aspirated.
The pathology report from the left frontal lesion noted interstitial hemorrhage and acute inflammation with scant Staphylococcus aureus growth. The fluid sample also grew a scant amount of the same species.
A swab from a wound found on the left lateral malleolus grew Staphyloccus aureus. This was thought to be the source of infection.
The final contrast CT demonstrates anatomic correlation to eventual significant neurological deterioration.
It remains unclear what precipitated these lobar hemorrhages and how they relate to sepsis. Possibilities include:
- CT-occult cerebritis that progressed to hemorrhage
- cerebral vein thrombosis (not visualized)
- mycotic aneurysms from sepsis
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