Wk 3, Case 28 - Review

Report


CLINICAL INDICATION: Trauma.

TECHNIQUE: Routine brain MRI exam using standard pulse sequences pre- and post- intravenous administration of Gadolinium contrast 9.4 cc Gadovist. Noncontrast enhanced 3D time-of-flight MRA of the brain as well as pre-and post-contrast 2D and 3D MRA exam of the neck also performed with review of axial raw data and 3D/MIP images.

COMPARISON: None available

FINDINGS:

Brain MRI:
On the FLAIR sequence, diffuse increased signal intensity in the subarachnoid space bilateral cerebral hemispheres and infratentorial posterior fossa subarachnoid space demonstrated. Those hyperintensities are compatible with a subarachnoid hemorrhage. Part of those signal intensities could also be caused by hyperoxygenation intubation.

Blood product also seen in the bilateral lateral ventricles especially on the right side layering in the occipital horn. Small subdural hemorrhage along the posterior cerebral falx extending along the superior surface of the left cerebellar tentorium leaflet present with maximum thickness
measuring 4 mm. Minimal blood product also seen in the suprasellar cistern along the vermis of the cerebellum localized hemorrhagic contusion or focal hematoma involving the anterior aspect of the genu of the splenium of corpus callosum also present. Additional scattered hemorrhagic foci in the bilateral frontal and left parietal lobes also present in the gray-white matter junction. FLAIR sequences demonstrate also increased signal intensity involving the splenium of the corpus callosum. Those findings are compatible with diffuse axonal injury.

Diffusion scan demonstrates no evidence of territorial cerebral infarction, noting signal changes associated with the blood products. There is generalized cerebral edema with sweating of the cortex, for example in the right to frontal superior frontal gyrus. There is no midline shift or hydrocephalus. Ventricular size within normal range for patient's age. Edema which could represent contusion also involving the posterior midbrain bilaterally more on the left side. The central aquduct of Sylvius is patent. The postcontrast images demonstrate no enhancing mass. Mild linear meningeal enhancement in the cerebral convexity noted which could be related to the subarachnoid hemorrhage.

The cervicocranial junction is anatomic. There is no evidence of transtentorial or tonsillar herniation. Slight prominent bilateral frontal subdural CSF signal is seen measuring up to 4 mm, a nonspecific finding. However, this is within normal range. Mucoperiosteal thickening and minimal fluid in the ethmoid and sphenoid sinuses could represent underlying sinus inflammatory disease but could also be related to intubation. Mastoid air cells junction no significant fluid opacification. Multiple areas of the scalp edema from the trauma present without harsh hematoma.


IMPRESSION:
1. Intracranial hemorrhages including small subdural hematoma, subarachnoid hemorrhage, intraventricular blood, and possible hemorrhagic contusion to the posterior corpus callosum. The involvement of the corpus callosum and multiple hemorrhagic foci at the gray-white matter junction is compatible with diffuse axonal injury.
2. Mild generalized cerebral edema present with no evidence of herniation or midline shift. No evidence of hydrocephalus. No evidence of acute territorial cerebral infarction.