Altered Mental State: The Clue in the Blue Bottle

Psychiatric TimesVol 31 No 2
Volume 31
Issue 2

Here's the story of a man with long-standing diabetes -- a pillar of the community-- who had been behaving strangely. He taught his physicians to look past the obvious clues and ultimately learn a lesson they never forgot.

It was a cold Chicago Sunday. Harsh winds rattled the windows. Tree branches, covered in ice, tapped on the glass, like the raven in Poe’s poem. This was not the day to stroll outside for a study break. Instead, I reached for an article about medicine and art, a gift from a biochemistry grad student who was also enthused by Goya’s lead poisoning and its impact on his paintings.

According to the article, artist Francisco Goya unwittingly ingested lead-based paint. His once-polished artwork became bizarre as lead encephalopathy progressed. Goya went deaf. Hand tremors loosened his brushstrokes. His horrific visual hallucinations were perfect for portraying Spain’s bloody wars. Goya’s Black Paintings signaled the start of art’s Romantic Era. They outshone his court portraits, done earlier in his career.

[[{"type":"media","view_mode":"media_crop","fid":"22968","attributes":{"alt":"","class":"media-image media-image-right","id":"media_crop_5637633427403","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"1742","media_crop_rotate":"0","media_crop_scale_h":"124","media_crop_scale_w":"160","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right;","title":" ","typeof":"foaf:Image"}}]]Reading about Goya’s neuropsychiatric problems was the next best thing to visiting a museum, and about as much leisure as a medical student could expect. Mountains of reading for my endocrinology elective awaited-but I chose to take the scenic route to studying that Sunday, to learn more about heavy metals such as lead and related poisonings.

This detour was easy to rationalize. Lead was big news in the early 1970s. Debates about leaded gasoline raged. In 1977, scientists linked high levels of lead in the blood to children’s learning disorders. In 1979, lead paint in residences was outlawed. In pediatrics rotation, we inspected gums for lead lines, knowing that peeling leaded house paint was a tasty treat for toddlers.

The rest of the chapter wasn’t as relevant as the lead entry, but it was intriguing. There was a section on “manganese madness” that strikes manganese miners. I made a mental note about manganese-related micrographia and parkinsonism. There was a blurb about arsenic, as expected. I flipped through pages on selenium, cadmium, and more, before coming across bromine, which was once prescribed for epilepsy and “nerves.” Then I pushed myself to prepare for the endocrine case conference.

Many Mondays later, none of us was prepared for what happened. We got word that a regular patient, a man with long-standing diabetes and a pillar of the community, had been behaving strangely. He was brought in by his wife, aided by several strong relatives.

As the clerk greeted Mr T at the nursing station, the intern grabbed the chart to check the last labs and consults. Mr T’s heart was bad; his kidneys were worse. Because of diabetic retinopathy, his vision was failing. Yet his insulin dose remained stable.

Diabetes wasn’t the problem, according to his family. Mr T wandered the streets at night, as if midnight was daytime. He said he saw ghosts. When I flipped through the chart, I saw no mention of prior psychiatric problems or substance use-just lots of renal, cardiology, and ophthalmology consults. Judging by his overflowing chart, the endocrine ward was his home away from home.

On hearing the history, the intern’s eyes lit up. It was his chance to review the differential diagnosis of altered mental states. I perked up also, because this was my chance to witness this workup.

“Check the lytes right away,” the intern said. “And the glucose. . . . Also, UTI and pneumonia can alter mental status in the elderly.” Mr T was pushing 60, which was “old” in that era. He pattered on as the nurse prepared the IV and the orderly struggled to slip a bathrobe onto the distracted patient. Nurses who knew him from his many past stays said that Mr T typically looked distinguished; this Monday, his coiffed silver hair was coming undone. He stared into space, apparently intrigued by images in the window.

The intern was convinced that Mr T was hypoglycemic and was not willing to delay treatment. “Untreated hypoglycemia can cause permanent brain damage. . . . Besides, even if he turns out to be hyperglycemic, that’s reversible. Untreated hypoglycemia isn’t.” He had a point.

With IV in place, a huge bolus of dextrose was pushed into his vein. Vials of blood were rushed to the lab. The portable x-ray machine arrived in short order, to find signs of infection that could contribute to his decompensation. That’s when big problems arose.

As the x-ray machine approached, Mr T shrieked about alien invaders. It was the most coherent sentence he had uttered since his arrival. Then he punched the intern, accusing him of inviting the alien spaceship. Shockingly, the intern stayed calm and continued to explain the relationship between hypoglycemia and aggression. What Mr T needed was more treatment for hypoglycemia, he hypothesized.

Soon, neurology and psychiatry residents arrived, each espousing different opinions. “Organic brain syndrome,” said the psychiatrist-in-training. “Plus possible paranoid schizophrenia,” countered the neurologist, who based his “rule-out” diagnosis on “bizarre delusions” about aliens and ghosts.

By then, the stat lab results returned. The all-critical potassium was fine. The elevated chloride was dismissed as a lab error. Renal function was compromised, as usual, but there was no suggestion of renal failure or uremia, which also cause brain syndromes. The kicker? The patient was hyperglycemic, with blood sugar level nearing 400. He was approaching ketoacidosis. Treatment was adjusted, and fluids were pushed. Blood sugars were drawn again and again, and the levels dropped lower. That was a good sign.

More IV bottles emptied. Hydration continued. There was still no answer about his strange mental status, but ketoacidosis was now the most pressing problem. Day turned into evening, and evening turned into night. His wife stood by silently, looking more and more worried. As the medical student, and the lowest person on the totem pole, it was my job to speak with the wife, to reassure her (of what?) and get any history that might have been missed. I was running out of questions, when I heard him burping, and burping, and burping.

Not knowing what else to ask, I quizzed the wife about the burping. She assured me that he always burped a lot, and pulled a blue bottle out of her purse. It was Bromo-Seltzer. The same blue bottle stood on the nightstand. “How much does he use?” I queried, falling back on the standard medical dictum of asking about quantities and qualifiers.

When she said, “six or seven bottles a day,” I gasped. I was no expert on Bromo-Seltzer (not yet), but that sounded excessive. I looked at the label on the bottle and thought about his compromised kidney function. Then my mind flashed back to my weekend reading about heavy metals and minerals.

There was a Cecil and Loeb Textbook of Medicine1 in the residents’ room. I pushed the pages to the bromine section-and gasped again. Could bromine poisoning be responsible for his altered mental state? I carried the tome to the intern, who was intrigued. Together, we calculated the dose of bromine in each blue bottle. Initially, it didn’t seem probable-until we read that impaired renal excretion increases toxicity risk. We sent a bromine level to the lab-and rejoiced when we reached the last paragraph, the one that said that bromine displaces chloride and that saline loading relieves bromine toxicity. In other words, his treatment for ketoacidosis would undo bromism-if this theory were correct.

Over the next few days, we continued to hydrate Mr T, monitoring labs, ECGs, and mental status. He showed no signs of infection. The first bromine labs were lost. By day 2, his bromine levels dropped to the high 30s (when they should have been zero). Blood sugar stabilized. (We later learned that labs can misread bromine as chloride, so high chloride levels can suggest bromism.) His kidneys were no worse for the wear. Best of all, he started to sound more lucid. The ghosts near the windowsill disappeared. Mr T made no mention of alien invaders. His visual impairment became more apparent, making me wonder if diabetes-related eye problems made his illusions seem more real.

His wife looked relieved. She smiled a smile that could melt Chicago snow. I, too, was relieved. It was distressing to think that Mr T could be institutionalized indefinitely, and dismissed as dangerous, because he encountered aliens and assaulted the intern. Those were the days when Ken Kesey’s novel One Flew Over the Cuckoo’s Nest informed our impressions of chronic psychiatric care.2

In 1975, the bromine in the Bromo-Seltzer disappeared. Bromo-Seltzer is still sold in its signature blue bottle, minus the sedating bromides. Once a mainstay of “nerve treatments” and a common cause of psychiatric hospital admissions, this outdated cure had faded from memory. However, my memories of Mr T, and these lessons learned in med school, remain. This unexpected event educated everyone present. As trying as it was, I feel fortunate for that opportunity and feel sorry for those who believe that memorizing psychotropic drug names and dosages is sufficient for proper psychiatric practice.


1. Cecil RL, Loeb RF. Textbook of Medicine. 13th ed. Philadelphia: Saunders; 1971.

2. Kesey K. One Flew Over the Cuckoo’s Nest. New York: Signet; 1963.

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