[Triage Note: shortness of breath, can’t eat, abdominal pain and bloating in RUQ (right upper quadrant) after eating]
John Grover is a nice guy. He’s fifty-five, short, a little chubby, and he has a neatly trimmed red beard. He’s the kind of guy whose eyes light up the moment you walk into the room; The kind of guy who remembers your kids names, their ages, and their interests. I’d met him a few times before. He’d come in once to refill his blood pressure medication because he couldn’t get into his family doctor’s office in time. I’d also seen him a week after his heart surgery the previous year. His wound was a little inflamed and he wanted to make sure it wasn’t infected, and that everything was healing alright.
This day, however, he isn’t his jovial self. He’s a little pale – ‘sallow,’ according to my clinical note, or, according to dictionary.com, “of a sickly yellowish color. “Oh, man,” he says, putting a fist into his upper abdomen. “I sure hope you can figure out what’s wrong with my stomach,” he says. “I can’t eat anything. I can’t eat anything at all. One bite and I feel bloated and sick.”
“How long have you felt like this?” I ask.
“Days or weeks?”
“Weeks,” he says, his lips sour. “Two or three for sure.”
“Have you had it looked at?”
“No,” he says, his eyes apologetic. “I thought it was indigestion.”
“Where does it hurt?”
He looks toward his stomach and stretches out a finger. He plants it on the right side of his upper abdomen. “Right here.”
I question him. The pain has been there for a few weeks – worse after eating, occasionally associated with nausea and shortness of breath. There’s no vomiting, no diarrhea. His bowels are moving fine. He’s had some fatigue, but he’s otherwise fine – no fever, no chills.
He’s just recently returned to work as a machinist after a year off. Two years prior, he began to notice progressive shortness of breath on exertion. After weeks of testing, he was found to have severe aortic valve stenosis – a narrowing of the heart’s outflow tract that impairs blood flow into the aorta. His heart began to work harder and harder, causing worsening breathlessness, dizziness, and fatigue. Weeks before surgery to replace the defective valve was scheduled, John went into heart failure. His heart could no longer pump blood effectively beyond the constricted passage. Fluid backed up into his legs, and eventually, into his lungs.
“That’s all fine now,” he says. “It’s my stomach now. I haven’t eaten in days.” He moves slowly to the examining table, lying onto his back and unbuttoning his shirt.
I put a stethoscope above his nipple. The mechanical valve clicks like an amplified wristwatch. He notices my fascination and smiles: “I can hear it when I’m falling asleep sometimes.” His lungs are clear and his bowel sounds normal. There ‘s only a trace of fluid in ankles that were once so badly swollen, he couldn’t even wear shoes.
I push just below the right side of his rib cage. He groans and grabs my wrist, holding his breath as if he’s been punched in the gut. “Have you ever been told you have gallstones?” I ask. He shakes no. “Anyone in your family have gallstones?” No again.
Twenty minutes later, as I wait for his blood results to return, his belly is still sore from the exam. Morphine and Gravol settle him, and we chat about our weekend plans. The blood work confirms my suspicion: His white count is mildly elevated, indicating infection. His liver enzymes are markedly high, characteristic of a stone blocking the passage of bile from the liver and gallbladder. “I can’t get an ultrasound tonight,” I say, “but I think you need to come in to hospital to see a surgeon.”
The following day, an ultrasound shows no stones. In fact, other than some mild, non-specific thickening of the gallbladder wall, the ultrasound is normal. In reviewing the clinical picture and lab results, the radiologist recommends a HIDA scan – a special test in which a radioactive marker is injected into a vein, then tracked as it flows from the liver, into the gallbladder, and then into the surrounding ducts. By following the radioactive tracer, blockages can easily be seen. Like many specialized tests, however, HIDA scans are difficult to arrange. John is started on antibiotics, and kept on clear fluids, as daily liver enzymes are ordered and tracked. As the days progress, many tests are performed, all coming back negative: His hepatitis A, B, and C serology are negative. There’s no reason to believe alcohol is the culprit, as he’d stopped drinking a half-decade earlier. There are no signs of familial or acquired liver disease. However, his liver enzymes continue to rise, and eventually, his red blood cell count drops. He still can’t eat, and now, he’s vomiting.
A week after admission, the HIDA scan is performed. It too is negative: radioactive markers flow freely from liver, to gallbladder, to gut. No blockage. A day later, jaundice sets in: John’s eyes and skin are as yellow as a banana popsicle. A CT scan of the abdomen is ordered and suggests early pancreatitis – another condition that can result from gallstones and duct blockage. Despite the normal HIDA scan, an emergent ERCP is booked. An ERCP is an invasive test in which a camera is fed into the patients gut (through the mouth), in an effort to find a blocked bile duct. Once the blockage is found, a stent can be placed to bypass the disruption.
His condition worsens. He develops increasing shortness of breath. His liver enzymes continue to rise. And then, a day before the ERCP, his legs swell dramatically, fluid rising to his hips, and eventually, seeping into his lungs. Supplemental oxygen is given, and the need for a ventilator is considered. John is in heart failure once again.
In his discharge summary, the specialist wrote: “Presented with abdominal pain, an enlarged liver, abnormal liver function tests, and the possibility of gallstones. In retrospect, all symptoms were secondary to heart failure.” An echocardiogram showed leakage of fluid at the site of John’s prosthetic aortic valve. This had been the culprit all along; The fluid backed up to the liver, and the ensuing congestion caused symptoms and signs that almost exactly mimicked gallstones.
Fixation error can be deadly in medicine, as well as in other industries. On December 29, 1972 the experienced crew of an Eastern Air Lines flight en route from New York City to Miami became preoccupied with a landing gear problem. While resting in a holding pattern on autopilot, the crew became fixated over a malfunctioning light – studying it, wiggling it, taping it – failing to recognized that the plane was, in fact, slowly descending. Shortly before reaching its destination, it crashed in the Everglades, killing 103 of the 176 people on board.
In medicine, fixation error occurs when physicians concentrate on a single aspect of care to the detriment of other, more relevant aspects. In John’s case, there was an ongoing failure to revisit his diagnosis; each physician kept John on the erroneous path upon which I had initially embarked. His physical examination, blood work, and imaging studies were all interpreted to fit the initial diagnosis of an obstructed bile duct. This was despite John’s extensive, recent cardiac history, as well as his shortness of breath, which was incorrectly attributed to his abdominal pain.
Two months after surgery to revise the failing valve, John and I are both lucky enough to chat about his ordeal. “Looking back,” I tell him. “I can’t believe so many of us missed it. It seems so obvious now.”
“If it happens again,” he says, “at least we’ll know what it is.”
“Sure,” I say. “Next time it will be gallstones.”