Brian Zenger PhD, Sonja Raaum MD
The patient is a 63 y/o male with a PMH of RA on MTX, HTN, and insomnia who presented with agitation, aggression, poor sleep, and chest pain.
HPI: He was challenging to communicate with and, at times, delirious and confused. He notes that he recently started zolpidem 2-3 days ago for insomnia. He also states he has had multiple episodes of intermittent chest and jaw pain. Upon further questioning, he has been unable to sleep longer than 2-3 hours per night, developed new grandiose thinking, and completed many projects around the house. He has a history of occasional alcohol consumption, daily marijuana use for 10-20 years, and a 40-pack year smoking history, quit in 2003. He does not use any other illicit drugs. Physical Abnormalities: Vital signs were notable for hypertension (160s/100s), otherwise hemodynamically stable.
Physical exam was significant for anxious and agitated affect, with grandiose thinking. Neurological exam was unremarkable. No other pertinent exam findings were identified.
Lab/Imaging Results on admission: The patient was found to have hypokalemia, hypernatremia, leukocytosis, and elevated creatinine. High sensitivity troponin was elevated, and TSH was low. The urine tox screen was positive for marijuana and no other substances. Brain CT and MR imaging were unremarkable.
Hospital Course: The patient was initially worked up for neurological causes of agitation and delirium, including LP and viral testing, which all came back negative. Psychiatry was consulted, and he was started on anti-psychotic medications, which seemed to improve his mood overall. However, he remained persistently hypokalemic and developed hypernatremia with persistent hypertension. Chest CT showed a solitary lung nodule unchanged in size since the previous CT. On initial laboratory testing, the Aldosterone level was elevated, possibly suggesting hyperaldosteronism. Endocrine was consulted, and 24-hour urine cortisol is 9948 with ACTH elevated to 226. The diagnosis of ACTH-dependent Cushing's disease secondary to ectopic ACTH production was then established. The patient was started on ketoconazole for profound hypercortisolism and discharged to follow up for definitive management with lung nodule resection.
This is an interesting case presentation of overt hypercortisolism secondary to ectopic ACTH presenting as metabolic disturbances and manic episodes. Furthermore, his poor sleep before admission could also have been secondary to these findings—common psychiatric complaints associated with hypercortisolism range from mild mood disturbances to manic activity. Interestingly, psychiatric symptoms are not always resolved after correcting excess cortisol levels, suggesting possible long-term neurological damage if not quickly treated.
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