Unfortunately, she was too agitated and did not allow the EEG techs to connect the scalp electrodes overnight. She kept trying to pull her lines out. However, you reexamine her the next morning, and at this point, her mentation has improved. She's finally connected to cEEG. This runs for 24 hours, with the results shown below. Based on these results, you recommend discontinuing it.
On day 3 of admission, she develops more severe head and neck pain. Acetaminophen and oxycodone were given. Three hours later, her left pupil becomes dilated, and she becomes less responsive. At this point, both you and the neurosurgery resident are paged to the bedside.
The combination of new decline in mentation with anisocoria suggests an acute process that localizes well. The decline in mentation indicates that the lesion affects the ascending reticular activating system-- anywhere from the dorsal pons, dorsal midbrain, bilateral thalami, or bilateral cerebral hemispheres. With the left pupil being larger, the left midbrain may be compressed, whether by the primary lesion itself or by a lesion more rostral to that. In terms of etiologies for such a hyperacute/acute change, a vascular cause such as a hemorrhage definitely must be ruled out. Melanoma metastases are notorious for bleeding. Perhaps her ependymal metastasis bled into her ventricles to cause a non-obstructive hydrocephalus. Seizure could also be considered, but it's important not to anchor on this diagnosis.
A focal finding such as anisocoria makes a toxic-metabolic process less likely. The patient did receive oxycodone, which can cause somnolence, but would not explain the anisocoria.
She does have leptomeningeal disease, so melanoma that's coating her CN III and brainstem could be responsible. Is there anything else that the leptomeningeal disease can do?
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