Fascinomas- Fascinating Medical Mysteries

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by Clifton K Meador

I turned to the nurse and said, “Mr. Williams is dead.”

  She looked at me with a dour expression. “Well, aren’t you going to pronounce him?”

  I was taken completely off guard. What did she mean by “pronounce him?” Here I was in New York City in the inner sanctum of the rich and famous trying to assert myself — and feeling clueless. What strange culture had I landed in? I even wondered if I had missed something in medical school.

  I stood up as tall as I could, turned to the nurse, looked at the chart to be sure I had the correct name, and said, “Mr. Jonathan S. Williams is dead.”

  She didn’t budge. “I mean, aren’t you going to pronounce him?” Her tone and demeanor were calm like I had omitted some routine step.

  Now I was really puzzled. What did she want? What custom or ritual did she mean? Was calling someone dead in New York so different from that in the South? Was this some old world custom?

  Finally, I looked around the room to be sure I was alone with the nurse and the dead patient. I then raised my arm and held my hand out over the dead body like some strange priestly ritual and said in my most official voice, “I pronounce Mr. Jonathan S. Williams dead.”

  With that, the nurse said, “Thank you.” She turned and walked out of the room.

  I followed her to the nurses’ station and entered my note in the chart, carefully documenting all the signs of death I had observed. If somehow Mr. Williams did wake up in the morgue, at least I had made sure I had documented his death.

  To this day, I remain mystified by the events of that night. I have never encountered another nurse in more than 50 years who wanted a patient officially pronounced dead. I have told the story to many colleagues, and no one has ever had the same experience or offered a plausible explanation. Was she some strangely religious person? From some obscure cult?

  Or worse, in the following years, did she tell her story over and over of the night she got some green intern from the South to actually stick his arm out over a patient and say, “I pronounce this patient dead.” I can even imagine her collapsing into laughter as she told the story, repeating the punch line.

  Chalk it up to yet another “medical mystery.” I will never know the truth about the night I made my first diagnosis of death, nor will I ever forget it.

  *Story told by Clifton K. Meador, M.D.

  Chapter Nine

  Medicine Can Be a

  Humbling Profession *

  Ed Clemons had enjoyed a long career as an educator and administrator. Now 58, he had risen to become principal of his local county high school. He also coached the football team as an assistant and taught physics to seniors.

  When Dr. Paul Barnett saw Clemons in his office, he found nothing of note in the medical history. But his physical examination revealed a large, pulsating mass in the lower abdomen. Barnett ordered an ultrasound, which showed an aneurysm of the abdominal aorta. An aortic aneurysm is a ballooning and enlargement of the artery leading to the arteries to each leg. This aneurysm measured 8 centimeters in diameter; the normal aorta is around 2 centimeters in diameter. In other words, the aneurysm was quite large and in danger of rupturing.

  A vascular surgeon saw Clemons that day and recommended immediate surgery to repair the aneurysm. If it ruptured, they told him, it would likely be fatal even if he were to get to an emergency room.

  But Clemons would have none of it. He refused the surgery, despite all efforts to convince him otherwise. Instead, he asked what symptoms he could expect if the aneurysm ruptured. Barnett described the pain, weakness and nausea and told him to come in immediately if any such symptoms occurred.

  A few months went by before Clemons called Barnett. He said he was feeling really bad, pain all over his body, very weak and maybe a bit feverish. Barnett told him to come to the ER immediately.

  The vascular surgeon and Barnett met him there. Clemons looked acutely ill, sighing and making slight soft moaning sounds when he exhaled. They did a physical exam, which showed no changes from the months prior. As before, there was no abdominal tenderness. But his temperature was a little over 100, and there was a rash over his legs, arms and abdomen.

  Tests were ordered to check on organ function and to re-examine the ultrasound status of the aneurysm. Taking no chances, the team began prepping Clemons for emergency surgery. The one piece of the puzzle that didn’t fit was the rash, but because time was of the essence both ignored it and moved forward. “You always have to throw out something,” Barnett thought to himself.

  As the doctors and staff had been examining and prepping Clemons, an old woman had come into the room quietly several times to clean. She had obviously overheard all of what was going on. Just as Barnett was about to leave the exam room for the last time, she came up to him.

  “Excuse me, Doctor,” she said gently, “I got 22 grandchildren and dat man got de chicken pox.” She pointed at Clemons.

  Surely not, Barnett thought, but a good doctor leaves no stone unturned. He went back to look at the rash. She was right. Clemons was about to have complex surgery for the chicken pox.

  Barnett says he realized several things in that moment: the need for humility, the importance of remembering that each of us can learn from anyone and that the dismissed symptom can be the key. He thanked the woman and called off the surgery. Clemons recovered uneventfully from the chicken pox.

  Clemons returned a month later for an elective repair of his abdominal aneurysm.

  *Case shared by:

  Paul Barnett, M.D.

  Associate Clinical Professor of Medicine

  Department of Medicine

  Vanderbilt University School of Medicine

  Chapter Ten

  Mysterious Mammaries *

  “Herman, you will love this case. It’s right down your path,” Dr. Steve Stevens said, just returning from the OR after finishing a morning of plastic surgery.

  “The man is 38 years old. Has huge breasts. Wants them off. Can you see him?”

  Dr. Herman Waring, a consulting endocrinologist, immediately wanted to know more. His role in this case would be to determine why this man’s breasts enlarged.

  “Look Herman, that’s why I am sending him to you,” Dr. Stevens interrupted. “I can’t sit around asking questions. All I know is his boobs grew over the past few years.”

  Robert Mac Carter was sitting on the exam table when Dr. Waring came in. Mac Carter was a large man with a dark, full beard. His arms and legs were unusually heavy and hairy. Given this increase in his breast size, Waring immediately began looking for any signs of feminization: a higher pitched voice, feminized hips, loss of body hair. He found none.

  In fact, Mac Carter was the opposite of what Waring expected. The man had the size and demeanor of an NFL tight end — big and tough. When he spoke, his answers were simply “yes,” “no,” or just a few words. It was obvious he did not relish seeing a doctor for this complaint. Waring couldn’t help but be struck by the incongruity of this ultra-masculine man with 44D-cup size breasts.

  Waring took a long and careful medical history from Mac Carter. There was nothing remarkable in his early life. These days, he was an aeronautical engineer traveling the world as a contractor for several major airlines. He had lived on nearly every continent during the past five years, with most of his time spent in the Philippines.

  Yes, he had erections. Yes, he had orgasms. Yes, he had a normal sex drive. Yes, he was heterosexual. No, he had never been married. No, he did not smoke marijuana, which can cause male breasts to grow. None of Mac Carter’s actions or body positions were the least bit feminine.

  Waring then focused on the endocrine causes for breast growth in a man. Tumors of the adrenals and testicles can secrete estrogens, as can some lung and other cancers. Taking estrogens by mouth will also have this effect. Mac Carter denied taking any medicines at all and, when asked specifically about estrogen tablets, seemed offended. “Of course not,” he replied curtly.

  Next came the physical examination which revealed
large pendulous breasts, at least a D cup. There were no masses. The tissue was quite firm, as sometimes is found in women with unusually large breasts. The chest x-ray showed dense breast tissue with normal lungs. The external genitalia were mature male with no masses felt in the testicles. The remainder of the exam was normal.

  Waring ordered all tests measuring estrogen and other hormones controlling sexual development. Results were normal. He thought there had to be some mistake, so he repeated the tests. Again, all normal levels. There was no endocrine explanation for the breast enlargement.

  Waring called Dr. Stevens. “Steve, I’m stumped. I have no idea why Mac Carter grew breasts.”

  “Well, I am taking them off next week,” Stevens said. “Will let you know when I get the path report.”

  The next week, Waring got an urgent call from Stevens. “If you can, get up to the OR. You have got to see this.”

  Waring prepped quickly, putting scrubs on over his suit. He entered the operating room and stood behind Stevens. When he looked into the open breast tissue, he saw a white substance oozing out onto the surgical drapes.

  “What the hell is that?’ Waring asked.

  “It’s paraffin,” Stevens said. “Very waxy feeling. Both breasts are filled with the stuff.”

  Both doctors were completely mystified. After the anesthesia wore off, they began to question Mac Carter about how paraffin could have gotten into his breasts. But as before, Mac Carter remained a man of few words. He wasn’t talking. The only thing he did say was that he would answer no questions, not now, not ever. No response, no explanation. End of story.

  Paraffin injection for breast augmentation was common in the early 20th century but was abandoned because of painful complications. It is still practiced in some Asian countries. Could Mac Carter have been some sort of transgender variant who got breast enlargements with paraffin but then changed his mind? Was there some weird event when he was in Asia that led to the paraffin injections? Neither Stevens nor Waring, even in retrospect, suspected anything unusual about this patient’s behavior or demeanor that would lead to such a strange finding.

  Two days after surgery, Mac Carter left the hospital. Neither doctor ever saw him again. The mystery was sealed.

  *Case shared by

  Lawrence K. Wolfe, M.D., FACP, FACE

  Clinical Professor of Medicine

  Division of Diabetes, Endocrinology and Metabolism

  Department of Medicine

  Vanderbilt University School of Medicine

  Chapter Eleven

  The eye does not see what the mind is not prepared to know. *

  The high school state football championship game was scheduled for the coming weekend between the Black Bears and the Crimson Tigers. Football was big in this Southern state, and excitement was growing. The game would be played on a neutral field in the state’s capitol city, about 70 miles from each competing team.

  Claude Akin, placekicker for the Black Bears, was warming up during the final practice that Friday. He was getting a feel for the championship stadium’s turf and kicking well. After putting a number of balls right through the uprights, however, he was hit by a pain in his lower right leg. It was so sharp, he collapsed to the ground and lay there writhing. It subsided a bit in a few minutes and he managed to get up and walk back to the bench. But no more practice. Something was wrong. The coach told him to ice down the leg below the knee, hoping that would do the trick.

  The ice offered temporary relief, but later that afternoon the pain had become so severe that Akin — now crying and moaning continuously — was taken to the ER. The physician there examined it thoroughly, but could find no explanation for the pain.

  The teenager couldn’t sleep that night, his leg hurt so much. At 3:00 a.m., he woke his parents in the adjoining hotel room and said he had to go back to the ER, but wanted to try a different hospital in hope of answers. By the time the three of them arrived at that ER, Akin was screaming with pain and began to vomit. His parents were anxious and puzzled, given the severity of the pain with absolutely no sign of injury. There was neither redness nor swelling.

  The ER physician examined Akin and found no cause for the pain either. A plain x-ray of Claude’s leg was normal. All joints in the leg showed full range of motion. The ER physician began to wonder if this could simply be another teenager trying to con drugs, so he asked the Akins if their son was a known user. They were horrified and insulted. They immediately checked their son out of the ER and drove across town to a third ER.

  By the time Akin arrived at the third ER, he was prostrate with pain and had to be wheeled inside. Again, the ER physician failed to find a cause and refused to give the young man any narcotic or strong pain medications. He told the parents these extreme “histrionics” coupled with the negative findings suggested malingering and faking.

  Angered by the insensitivity of yet another ER physician and frustrated by the failure to get relief, Akin’s parents called their family physician back home and described the situation. Dr. Richard Snow had been their family doctor for many years. He had known Claude Akin since childhood — and knew instantly what was wrong with that leg.

  “Can only be one thing,” he told Akin’s father. “He may need immediate surgery. Can you get back here quickly?”

  The answer was an unequivocal, “Yes.’’

  “Good,” Snow replied. “I’ll have Dr. Taylor Wilson, who’s an orthopedist, meet you in the ER at St. Paul’s.”

  The Akins rushed the 70 miles back to their hometown hospital. It had been more than 36 hours since the onset of pain in the place-kicker’s leg. As they drove, their son lay in the back seat, trying in vain to find a position of his body or leg that relieved the excruciating pain.

  After Dr. Wilson examined Akin, he said, “This is an anterior compartment syndrome, and we need to do surgery immediately. I am afraid we may be a bit late to save muscle and nerve function in this leg.”

  The anterior compartment of the lower leg runs down beside the long bone of the shin called the Tibia. The bone, four muscles, nerves, vessels and fascia form a tightly enclosed compartment. Injury to the compartment sets up a vicious cycle of tightly enclosed swelling, occlusion of the veins, compression of the nerves and necrosis (death) of the muscles. All of the factors increase in intensity, eventually leading to death and destruction of all the contents of the tight compartment.

  A review of the literature reveals an urgent time window of three to five hours after injury if nerve and muscle function are to be protected. Akin’s injury was more than 36 hours old, far too late to save his muscles and nerves. Unfortunately, the young kicker was left with a permanent foot drop and no longer able to play active sports.

  The anterior compartment syndrome is relatively rare. Often, its only physical finding is a complaint of severe pain in the leg with little or no visible signs early on. It’s one of those diagnoses that must be memorized and remembered in the absence of the common signs of injury like swelling. Only the alert and informed physician will make the diagnosis and see that surgical incisions are made the entire length of the compartment to relieve the swelling and pressure.

  In Akin’s case, three different ER physicians missed the diagnosis, leading to critical time delays and irreversible muscle and nerve death.

  *Case shared by:

  Robert Foote, M.D.

  Director, Nuclear Cardiology Diagnostic Laboratory

  Dartmouth Hitchcock Medical Center

  Assistant Professor of Medicine and Radiology

  Dartmouth Medical School

  Chapter Twelve

  A Drug to Prevent a Complication Causes the Complication. *

  Jason McKnight had been seeing Dr. Paul Barnett for nearly 10 years. He had adult onset diabetes, now called Type 2.

  McKnight was head of a small accounting firm. His compulsive attention to numbers led him to keep meticulous records of his treatment and blood sugar levels, which he measured daily. He also recorded his exercise
sessions and his caloric intake and body weight. Nearly all the numbers were very close to normal. The only medicine he was taking was one Metformin tablet daily, which is one of the oral medications for control of blood sugar levels.

  Dr. Barnett thought of McKnight as the perfect patient with diabetes. He had never seen anyone take better care of himself. Even McKnight’s hemoglobin A1C levels were normal. Hemoglobin A1C is a measure of the average blood sugar level for several months. It is the gold standard for measuring results of treatment in patients with diabetes.

  When McKnight called in for an early appointment, Barnett was surprised to hear him describe having symptoms of nerve damage in his legs and feet, called peripheral neuropathy. This is common in many diabetics, but not usually in those who manage their blood sugars as meticulously as McKnight. Examination did, in fact, show a decreased sense of touch and some loss of pain sensation in both feet. Despite excellent management of his blood sugars, McKnight had somehow developed nerve damage.

  Nerve damage comes from continued high blood sugars and results from damage to the small blood vessels supplying blood to the nerves in both legs. Tight control of blood sugar usually prevents the damage, but apparently not in McKnight’s case. Yet all of his blood tests were again normal, except for a vitamin B12 level that registered at the lower limits of normal.

  Dr. Barnett, puzzled by McKnight’s developing this complication of diabetes while under good control, referred him to a neurologist, Michael Kaminski. Dr. Kaminski was well known for his diagnostic abilities.

  After examining McKnight, Kaminski called Barnett to tell him what he thought might be going on. Kaminski had just read an article describing peripheral neuropathy caused by Metformin, and he referred Barnett to several journal articles.

  The articles reported studies of diabetic patients receiving Metformin. Somewhere between 6 and 30 percent of these patients developed low vitamin B12 blood levels. Further studies concluded that Metformin blocks the absorption of vitamin B12 in the intestines. A deficiency of vitamin B12 is usually called pernicious anemia, caused by a lack of absorption of the vitamin. In that sense, the effect of Metformin resembled pernicious anemia.

 

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