Every Patient Tells a Story (12 page)

“Can you feel this?” She nodded. “Is it the same on both legs?” Again she nodded. He worked his way up her legs. Sensation was normal. He lifted her left knee with one hand and struck it with a rubber arrowhead hammer. Nothing. He repeated the move on the right. The leg jerked and swung upward. He tried again on the left and again there was no response at all.

He stared at the left leg, then called Zawahir over. “Look at this,” he said, pointing to the patient’s leg. Tiny patches of skin on Gayle’s leg appeared to
be moving, jerking, twisting. There was no movement of the leg itself—just the skin and the muscles of the thigh. Small groups of muscles were contracting spontaneously, independently. It looked as if there were little worms inching along under the skin.

“Fasciculations,” said Sadigh in his soft accented voice; little uncoordinated bursts of activity from a group of muscle fibers powered by a single nerve fiber. He knew he had found an important clue.

Outside the room, Sadigh reviewed what he thought were the important characteristics of the patient and her illness: First, she had been very healthy until now and had spent a lot of time outdoors. She had a profound weakness that affected both legs, but one much more than the other. It was only the thigh and hip muscles that were involved—the muscles of the lower leg and upper body were spared. Only the nerves that power the muscles were affected. Sensation, which is carried on different nerve fibers and connects to a different part of the spinal cord, was normal. And she had fasciculations. Those little muscle jerks were the clincher. The fasciculations and the sparing of sensation suggested that a single type of cell in the spinal cord was affected: the cells that control the muscles of the body, known as the anterior horn cells—a description based on where they are located in the spinal cord.

“I’ve seen this before—but not so much in this country. This is what polio looks like,” he said—then added: “But I do not think this is polio.” There is another disease, he explained, a disease new to this country. A disease that can look just like polio. A disease that can cause the same devastating paralysis. He paused. “I think she has the West Nile virus.”

West Nile had burst into the news four years earlier in the summer of 1999, when it ravaged a small community in Queens, New York. It was a disease well known in Africa, where it originated, and localized epidemics had been reported throughout Europe and parts of Russia, but until that summer, it had never been seen in the United States. The distinctive presentation of the disease—with its polio-like paralysis and its preference for those over fifty—had helped the Health Department doctors in New York recognize it as a new entity and move rapidly and aggressively to contain the
epidemic. Nevertheless, sixty-two people were hospitalized with the virus that summer; seven of them—all over fifty—had died. Despite aggressive measures to wipe out the mosquitoes that spread the disease, by 2003 cases had been reported in every state in the continental United States.

Sadigh remembered the events of the summer of 1999 clearly. The poliolike quality of the disease had been much discussed at the time. Seeing Delacroix, Sadigh was certain this is what she had. A sample of Gayle Delacroix’s spinal fluid had to be sent to the state lab in Hartford to confirm the diagnosis. It would be days—maybe weeks—before the results would be available. In the meantime they would make sure that it wasn’t some other entity that they would need to treat.

After discussing the likelihood of West Nile virus with Dr. Sadigh, Zawahir returned to the patient’s bedside to tell her the news. Gayle and Kathy had heard about West Nile virus. Who in Connecticut had not? But they didn’t know much about it. Zawahir made the parallel to polio that Sadigh had made. When she heard that, the patient’s eyes filled with tears. The very word brought up images of children in iron lungs or walking with metal braces and crutches. Was that her future? Zawahir tried to reassure her but she didn’t know. This was one of the first cases seen in the state. They’d simply have to wait and see what happened.

“The hardest part was not knowing what was going on or where this would take me,” Gayle told me. The diagnosis of West Nile virus wasn’t reassuring, but for someone relatively young and exceptionally healthy it was survivable. She and her partner found themselves in a whole new world. It wasn’t where they wanted to be, but it was where they were, and so they threw themselves into the work of learning a new language, mastering a new landscape.

Kathy read up on West Nile virus and polio, hungry for strategies to help her partner fight back. By her third day in the hospital, though still febrile and weak, Gayle insisted on trying to get out of bed and stand. She did it, though she needed help. By the end of the week she had taken a few unsteady steps braced with a walker and monitored by the physical therapist. Meanwhile, the test results slowly trickled in. It wasn’t Lyme; it wasn’t Rocky
Mountain spotted fever. It wasn’t tuberculosis, sarcoidosis, syphilis, or HIV. Antibiotics given in the hope of a treatable infection were stopped. Finally they received the confirmation of what they already knew. She had been infected with the West Nile virus.

“We hoped against hope that it wasn’t West Nile, but the doctors seemed pretty sure right from the start,” Gayle told me. Just knowing what she was up against—as scary as it was—was unexpectedly comforting and gave her a direction to focus her considerable energy to get well.

No Time for a Physical

In the case of Gayle Delacroix and the West Nile virus, the physical exam led directly to an extraordinary diagnosis. More commonly, the physical exam can provide not a diagnosis but an essential clue to direct further testing—a shortcut to the right answer. Ordering a slew of studies to evaluate a patient might get you the answer eventually, but time is often short in the care of a very sick patient. In many cases a careful exam can focus the search and help the physician find the problem faster. Where such an advantage would be most helpful, naturally, is among those patients who are critically ill. But even here—maybe especially here—the physical exam is becoming as obsolete as the doctor’s black bag.

The sicker the patient, the greater the temptation to skip the fundamentals—like the physical examination—and to rely on the available technology to provide us with answers. It’s a temptation that can sometimes prove fatal—as Charlie Jackson almost discovered.

For most of his adult life Charlie Jackson didn’t go to doctors. That changed when he had a massive stroke at age sixty-two. The stroke rendered his right leg and arm nearly motionless, his face crooked, and his speech slurred. Still, his beautiful cockeyed smile and gallant manner—he frequently showed up for his appointments toting a basket of peaches or a bag of pecans from back home in his native Carolina—made him a favorite at our office. He had been doing well, so I was shocked when I got a call from the staff saying that Charlie was dying.

He’d come to the office for a regular follow-up appointment with Sue, our nurse-practitioner. As soon as she saw him that morning, she knew that there was something very wrong. His walk, always a little ungainly after his stroke, was barely a shuffle. His slender frame was bent over his walker as if he couldn’t hold himself up.

“What’s the matter, Charlie?” she asked as she hurried to his side. “I … can’t … walk.” He choked out the words. His voice was strange in a new way, too—as if he were speaking in slow motion. She reached down and felt his pulse. It was slow—very slow. Too slow to keep even this slender reed of a man alive. She didn’t do any more of an examination. She knew he needed to be in a hospital.

The EMT team burst through the emergency room doors, pushing Charlie into the throng of the crowded room. The triage nurse directed them straight into an empty cubicle as they barked out what they knew. “Sixty-four-year-old man … history of a stroke … complaints of weakness and belly pain.” His heart was slow, they reported; his blood pressure too low to be measured. The monitor showed a heart rate in the twenties—normal is over sixty. Dr. Ralph Warner strode in and quickly assessed the situation. “Get me an amp of atropine,” he snapped, calling for the medicine used to speed up the heart.

After injecting the medicine, he watched as the monitor continued its flat yellow line, broken far too rarely by the spike indicating another heartbeat. But slowly the patient’s heart rate and blood pressure began to rise.

With the usual chaos of the emergency room boiling around them, Warner forced himself to sit and focus as Charlie described his symptoms. It had started the night before, he told the doctor in his new, strange slur. He felt weak, could barely move. That morning his stomach began to ache. Any chest pain? Warner broke in. Shortness of breath? Fever or chills? Vomiting? The patient shook his head no. He was taking medications to lower his blood pressure and cholesterol. He had not smoked or drunk alcohol since his stroke. A brief exam showed Warner the results of the stroke but he saw nothing else.

Why was his heart beating so slowly? the doctor wondered. Had he taken too much of one of his medications? Had he suffered a heart attack that
affected the natural pacemaker in his heart? The EKG, although abnormal, didn’t suggest a heart attack. Warner called the cardiologist, who rushed in to place a temporary pacemaker. Charlie was being prepped for this potentially life-saving treatment when the lab called with part of the answer.

Blood work done in the emergency room showed that the patient’s kidneys weren’t working. And his potassium—an essential element in body chemistry, regulated by the kidneys—was dangerously high. Potassium controls how easily a cell responds to the body’s commands. Too little potassium, and the cells overreact to any stimulation; too much, and the body slows down. If the elevated potassium was slowing his heart, then getting rid of the mineral would allow his heart to pump at a normal rate. The patient was given a medicine to get the potassium out of his system and then transferred to the ICU for monitoring.

If the potassium was high because of his kidney failure, what had caused his kidneys to fail? Dr. Peter Sands, the intern on call in the ICU, gnawed at this question as he reviewed the chart and results of all the tests that had been done. It wasn’t a drug error. The patient’s medication box showed the correct number of pills. And it hadn’t been a heart attack; a blood test proved that. Sands looked for the results of the urinalysis to see if there was any clue there but he couldn’t find it. Somehow no one had sent any urine to the lab. Were his kidneys too damaged to produce urine? That would be critical to know.

Sands asked the nurse to get some urine from the patient. She returned empty-handed. The patient couldn’t urinate; he told her he hadn’t been able to since the night before. The nurse hadn’t been able to insert a Foley catheter, a rubber tube that is passed through the urethra into the bladder to collect urine. Was something blocking the urethra? A urology resident finally managed to get a catheter into the bladder and immediately urine gushed out of the tube—nearly half a gallon of it. A full bladder comfortably holds a little over a cup of urine. Charlie’s bladder had held just under eight. The urology resident looked at the intern: “I guess now we know why his kidneys weren’t working.”

The urethra
was
blocked—by the prostate gland. The prostate surrounds
the urethra, and when it enlarges, as it often does with age, it can impinge on the narrow outlet, obstructing and ultimately blocking it so that no urine can pass. As the trapped liquid filled the bladder, stretching it far beyond its normal capacity, the pressure shut down the patient’s kidneys. Just hours after the obstruction was relieved, Charlie’s potassium began to drop as the kidneys went back to work. Four hours later, his heart rate was up over sixty. By the next morning, the abdominal pain, probably caused by his hugely distended bladder, had eased. When he left the hospital three days later, his potassium and heart rate were normal and his kidneys nearly so. He would have to keep the tube in his bladder until the obstructed tube could be opened.

In the hours before his diagnosis, Charlie was seen by at least two nurses and three doctors. He had complained of abdominal pain. How is it possible that none of these doctors or nurses noticed that his bladder, normally the size of a hockey puck, was the size of a football? Charlie’s a slender man, over six feet tall and weighing only 140 pounds. His belly is normally flat. I didn’t see him that day, but I’m guessing it was distended and tender. No one noticed, I suspect, because no one looked.

No one examined Charlie Jackson—until it was almost too late.

The Delirious Doctor

As a practicing physician, I understand the temptation to skip the physical exam. A sick patient comes in and you are so focused on the thing that you are certain might kill him that you don’t think of looking at anything else. There’s a kind of anxiety, a controlled adrenaline-fed panic, when facing a patient who could die before your eyes. You pore over the labs and the studies. You get the consult. You send him to the ICU. But you don’t examine him. That’s not what doctors do anymore, in part because they no longer know how.

So thoroughly has this lesson been absorbed that doctors—those in training and out—often don’t even notice when the loss of this creaky old
antique makes a classic diagnosis impossible. I frequently attend medical conferences with the hope of finding cases for my newspaper column. I ran across a perfect example of this at a recent conference of the Society of General Internal Medicine, a gathering of academic physicians.

Judy Reemsma, a third-year resident, stood by her poster in the rabbit warren of partitions that make up the display halls where residents and medical students display research and case reports. She spoke with confidence about the case presented in her poster. She should—in this case she was both the doctor who made the diagnosis and the patient.

During her second year of medical school Reemsma became ill and was taken to the emergency room by her fiancé, David DiSilva. Assigned to the case was Dr. Jack McFarland, an emergency medicine resident and close friend of Judy’s.