Case Report:
A 70-year-old Caucasian male with a past medical history of
hypertension, hyperlipidemia, benign prostatic hyperplasia, dementia,
gastroesophageal reflux disease (GERD), and primary progressive multiple
sclerosis (M.S.) presented to the emergency department from home for
evaluation of progressively worsening dysphagia of one-week duration.
His M.S. was diagnosed with lumbar puncture and MRI 37 years ago and has
been progressing. He was previously on dalfampridine for 3-4 years until
he became bedbound one year prior to this admission; it was at that time
that his treatment was discontinued. He has also been treated in the
past with steroids for multiple M.S. flares. The patient’s wife stated
his ability to swallow food had become severely impaired over the past
week. The patient frequently regurgitated and was also unable to
adequately clear oral secretions on arrival.
His wife noticed an accelerated decline in his neurological status over
the past year to the point that he was now bedbound, dysarthric, and
intermittently cognitively impaired. Since being bed-bound, he also
developed frequent episodes of chronic urinary tract infections
(UTIs). At baseline, he was conversational, able to eat soft
foods, and ingest medications in pureed foods. He did not have issues
with clearing secretions until about 6 days prior to admission. It was 9
days before his presentation to our facility when he was started on
carbamazepine by his neurologist for treatment of trigeminal neuralgia.
The dosing was initiated at 200 mg daily for three days, followed by 200
mg twice daily for the 6 days leading up to presentation.
Upon admission, he was noted to have altered mental status as he was
only oriented to person and place but not time or situation. He was
afebrile and hemodynamically stable. Physical exam was notable for
crackles in the upper and lower lobes of the right lung. His laboratory
testing was unremarkable except for pre-renal acute kidney injury.
Imaging was significant for a chest x-ray that showed a small volume
parenchymal opacity in the right lower lobe and suggested possible
pneumonia (Figure 1). Brain CT did not show any new evidence for acute
intracranial pathology (Figure 2). Brain MRI showed white matter disease
in the periventricular areas, with no new changes in comparison to prior
imaging (Figure 3). Echocardiogram showed normal systolic function, no
regional wall motion abnormalities, with mild diastolic dysfunction and
a moderately dilated left atrium.