In patients with acute coronary syndrome or obstructive coronary artery disease, stents, especially drug-eluting stents (DESs), are used for percutaneous coronary interventions (PCI). DES prevents abrupt closure of the stented artery. Stent thrombosis is an uncommon but serious complication of PCI, especially with the recent advancement of stent technology. We present a case of a 75-year-old male who initially suffered a non-ST segment elevation myocardial infarction (NSTEMI) treated appropriately with PCI and subsequently developed stent thrombosis after 10 days of initial stent placement. He then underwent emergent repeat PCI with successful replacement of stents overlapping previous stents. The patient did well following the procedure. His clopidogrel was changed to a more potent antiplatelet ticagrelor. He remained stable throughout the hospital stay and was discharged home without any further complications following the next 90 days.
A 48-year-old male presented three days after cocaine use with acute, rapid onset of bilateral lower extremity weakness, bilateral foot numbness, acute urinary retention, and significantly elevated creatinine kinase. Further testing revealed unusual symmetrical edema with contrast enhancement on MRI of the lower extremities. The patient was diagnosed with severe non-traumatic, non-exertional rhabdomyolysis causing lumbosacral plexopathy following cocaine use. The treatment was centered around aggressive fluid resuscitation and electrolyte replacement.
A 69-year-old female with a family history significant for early onset dementia and a past medical history significant for coronary artery disease, primary hypertension, type two diabetes mellitus, and Crohn's disease presents to our facility with rapidly progressive cognitive decline, delusions, hallucinations, and ambulatory dysfunction over the past two months. Neurological examination was remarkable for bilateral horizontal nystagmus, tongue fasciculations, bilateral upper extremity incoordination, and bilateral lower extremity spasticity, atrophy, and weakness. Laboratory and microbiological testing were remarkable for low serum thiamine levels. Computed tomography (CT) of the head without contrast showed significant brain atrophy in the frontal and temporal regions as compared to a CT without contrast of the head 5 years prior. Magnetic resonance imaging (MRI) of the head with and without contrast showed significant atrophy in the frontal and temporal regions as well as the cerebellum. Follow-up electromyography was consistent with lower motor neuron disease. The patient was given adequate thiamine supplementation for her thiamine deficiency and discharged on donepezil with instructions to follow up with the amyotrophic lateral sclerosis clinic for further monitoring and initiation of riluzole.
Encephalitis refers to inflammation of the brain that is most frequently caused by viral infection (particularly herpes simplex virus type 1 [HSV-1]). In some instances, it may be associated with substantial neurological mortality and long-term morbidity. Although HSV-1 is the most common agent involved in producing neurological infections and disorders, herpes simplex virus type 2 (HSV-2) can occasionally affect the central nervous system, particularly in immunocompromised patients. We discuss the case of an immunocompetent male patient with a history of well-controlled diabetes who presented with symptoms of encephalitis. Our patient did not have a history of herpes infection, indicating the presence of subclinical infections. His initial magnetic resonance imaging was inconclusive, but the diagnosis was established following a lumbar puncture and subsequent cerebrospinal fluid analyses.
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