Intern

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Authors: Sandeep Jauhar
expressionless. His movements were slow and listless. When he spoke, he slurred his words.
    He denied using drugs and said he didn’t have any previous medical problems. He vaguely recalled taking a medication, but given his current state, he couldn’t remember what it was. I asked his mother to bring in the bottle.
    Meanwhile, I asked him a few standard questions. He knew where he was and the year, but not the month or the president. I asked him to count backwards from one hundred by seven, a test of attentiveness, but he stopped at ninety-three. I asked him to spell “world” backwards, but he started and stopped at “w.” The mental status tests I had learned in class were useless on a patient with such poor mental status.
    The differential diagnosis of his delirium was almost impossibly long. Some of the usual suspects had already been ruled out. He wasn’t intoxicated or hypoglycemic. A CAT scan of his brain revealed no stroke, tumor, or bleeding. Seizures could explain the lethargy and confusion, but his mother had never seen him shake.
    Of all the diagnostic possibilities, infections were probably themost serious. AIDS could cause a kind of premature dementia, but he didn’t have the usual risk factors. Lyme disease was unlikely;
Ixodes
ticks weren’t endemic to St. Louis. What about meningitis, I thought, or, worse, syphilis? Untreated syphilis could infect the spinal cord and brain, causing severe nerve damage and dementia. Syphilis was one of the “great masqueraders,” along with tuberculosis and lupus, diseases with such protean manifestations that they could almost never be excluded with certainty. In fact, syphilis was enjoying a resurgence in urban areas like St. Louis. The only way to rule it out was to do a spinal tap.
    With help from another resident, I had the man sit on the side of his bed, leaning forward onto a table. I scrubbed his lower back with antiseptic soap and then injected local anesthetic into the tissue between the third and fourth vertebrae. It was my first spinal tap, and I gingerly pushed the needle and trocar through the soft tissue, worrying that I was going to pierce the spinal cord. My hands shook in a fine tremor; beads of perspiration wet my brow. I advanced the needle in micron-size increments. It must have taken ten minutes to go an inch. When the needle finally perforated the sac around the spinal column, clear fluid bubbled back through the hub. The resident congratulated me on a “champagne tap,” free of blood. We sent the fluid off to the laboratory.
    Later that evening, test results started coming back. Blood tests for kidney and liver disease were negative. The spinal fluid was clean, ruling out an infection. But when the level of thyroid-stimulating hormone came back, it was off the scale. My patient had the worst case of hypothyroidism the doctors had ever seen.
    The next day, his mother brought in a brown bag. Inside it was an empty prescription bottle. Sure enough, it was for thyroid hormone; he had been taking the medicine at home but had stopped six months earlier after it ran out, slowly sinking into an amnesiac delirium that made him forget he needed it, a lapse that almost cost him his life. Hypothyroid coma has a 20 percent mortality rate even if diagnosed and treated appropriately.
    As in physics, everything fit together nicely. His condition had been a puzzle, but through logic and judicious testing, I had solved it. I felt proud of myself.
    The next morning I ran into my resident and told him I had made the diagnosis. “Let me guess,” he said.
    â€œHypothyroidism.”
    â€œHow did you know?” I asked in disbelief.
    â€œI tapped on his knee,” he replied; the tap had elicited the slow reflex that is a classic sign of the disease. I had been taught this clinical pearl in class, but as with most of what I learned during the first two years of medical school, I had forgotten it. The lapse had

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