CASE Light-headed
Mr. M, age 73, is a retired project manager who feels light-headed while walking his dog, causing him to go to the emergency department. His history is significant for hypertension, coronary artery disease (CAD), 3-vessel coronary artery bypass graft surgery (CABG), hyperlipidemia, erectile dysfunction, open-angle glaucoma, hemiretinal vein occlusion, symptoms suggesting rapid eye-movement behavior disorder (RBD), and major depressive disorder (MDD).
The psychiatry consultation-liaison service is asked to help manage Mr. M’s psychiatric medications in the context of orthostatic hypotension and cognitive deficits.
What could be causing Mr. M’s symptoms?
a) drug adverse effect
b) progressive cardiovascular disease
c) MDD
d) all of the above
HISTORY Depression, heart disease
15 years ago. Mr. M experienced his first major depressive episode. His primary care physician (PCP) commented on a history of falling asleep while driving and 1 episode of sleepwalking. His depression was treated to remission with fluoxetine and methylphenidate (dosages were not recorded), the latter also addressed his falling asleep while driving.
5 years ago. Mr. M had another depressive episode characterized by anxiety, difficulty sleeping, and irritability. He also described chest pain; a cardiac work-up revealed extensive CAD, which led to 3-vessel CABG later that year. He also reported dizziness upon standing, which was treated with compression stockings and an increase in sodium intake.
Mr. M continued to express feelings of depression. His cardiologist started him on paroxetine, 10 mg/d, which he took for 2 months and decided to stop because he felt better. He declined psychiatric referral.
4 years ago. Mr. M’s PCP referred him to a psychiatrist for depressed mood, anhedonia, decreased appetite, decreased energy, and difficulty concentrating. Immediate and delayed recall were found to be intact. The psychiatrist diagnosed MDD and Mr. M started escitalopram, 5 mg/d, titrated to 15 mg/d, and trazodone, 50 mg/d.
After starting treatment, Mr. M reported decreased libido. Sustained-release bupropion, 150 mg/d, was added to boost the effects of escitalopram and counteract sexual side effects.
At follow-up, Mr. M reported that his depressive symptoms and libido had improved, but that he had been experiencing unsteady gait when getting out of his car, which he had been noticing “for a while”—before he began trazodone. Mr. M was referred to his PCP, who attributed his symptoms to orthostasis. No treatment was indicated at the time because Mr. M’s lightheadedness had resolved.
3 years ago. Mr. M reported a syncopal attack and continued “dizziness.” His PCP prescribed fludrocortisone, 0.1 mg/d, later to be dosed 0.2 mg/d, and symptoms improved.
Although Mr. M had a history of orthostatic hypotension, he was later noted to have supine hypertension. Mr. M’s PCP was concerned that fludrocortisone could be causing the supine hypertension but that decreasing the dosage would cause his orthostatic hypotension to return.
The PCP also was concerned that the psychiatric medications (escitalopram, trazodone, and bupropion) could be causing orthostasis. There was discussion among Mr. M, his PCP, and his psychiatrist of stopping the psychotropics to see if the symptoms would remit; however, because of concerns about Mr. M’s depression, the medications were continued. Mr. M monitored his blood pressure at home and was referred to a neurologist for work-up of potential autonomic dysfunction.
Shortly afterward, Mr. M reported intermittent difficulty keeping track of his thoughts and finishing sentences. His psychiatrist ordered an MRI, which showed chronic small vessel ischemic changes, and started him on donepezil, 5 mg/d.
Neuropsychological testing revealed decreased processing speed and poor recognition memory; otherwise, results showed above-average intellectual ability and average or above-average performance in measures of language, attention, visuospatial/constructional functions, and executive functions—a pattern typically attributable to psychogenic factors, such as depression.
Mr. M reported to his neurologist that he forgets directions while driving but can focus better if he makes a conscious effort. Physical exam was significant hypotension; flat affect; deficits in concentration and short-term recall; mild impairment of Luria motor sequence (composed of a go/no-go and a reciprocal motor task); and vertical and horizontal saccades.1
Mr. M consulted with an ophthalmologist for anterior iridocyclitis and ocular hypertension, which was controlled with travoprost. He continued to experience trouble with his vision and was given a diagnosis of right inferior hemiretinal vein occlusion, macular edema, and suspected glaucoma. Subsequent notes recorded a history of Posner-Schlossman syndrome (a disease characterized by recurrent attacks of increased intraocular pressure in 1 eye with concomitant anterior chamber inflammation). His vision deteriorated until he was diagnosed with ocular hypertension, open-angle glaucoma, and dermatochalasis.
The authors’ observations
Involvement of multiple specialties in a patient’s care brings to question one’s philosophy on medical diagnosis. Interdisciplinary communication would seem to promote the principle of diagnostic parsimony, or Occam’s razor, which suggests a unifying diagnosis to explain all of the patient’s symptoms. Lack of communication might favor Hickam’s dictum, which states that “patients can have as many diseases as they damn well please.”