Attribution error in a patient with colon cancer

Zahia Esber, ACP Associate Member, who practices at McKenzie-Willamette Medical Center in Eugene, Ore., told us about a case of a 71-year-old obese woman whose mental status deteriorated rapidly while in the hospital.

The patient had undergone a sigmoid resection in December 2009 for colon cancer. At that time, her mental status was intact. Three weeks after surgery, she returned to the hospital because of nausea and anorexia. She told the admitting physician that her symptoms began about two weeks after surgery.

A gastroenterologist consulted on the case. Detailed evaluation did not yield a clear diagnosis. He thought that the patient might be depressed from her diagnosis of colon cancer. She was discharged on an anti-emetic and an antidepressant medication.

Symptoms persist

The patient was readmitted several weeks later for persistent symptoms of nausea and anorexia. While in the hospital she was noted to have an abrupt decline in mental status. She developed dysarthria and after several days barely spoke at all. A neurological consult was obtained. In addition to the impaired mental status, the neurologist noted a symmetrical peripheral neuropathy and tenderness to palpation of the lower extremities. There were no focal motor deficits.

Initially the presumptive diagnosis was stroke or brain metastases. However, imaging, including CT scan and MRI/A, were unrevealing. EEG showed no seizure activity. Lumbar puncture was performed, and no abnormalities were noted in the cerebral spinal fluid. Because of the history of colon cancer, a screen for antibodies related to paraneoplastic syndrome was obtained with negative results.

Dr. Esber took over the care of this patient one week after admission. She was concerned that the patient’s neurologic symptoms had developed while in the hospital. Her first thought was that one of the prescribed medications might have caused the decline in mental status. However, once all possibly causal medications were withheld, the patient’s condition continued to deteriorate. Dr. Esber went back over the medical record in detail, but found no clues.

Checking the history

“I tried to make sure that nothing had been missed,” she told us. The record was unclear about the patient’s condition at home, so Dr. Esber contacted and interviewed several family members. “Too often, we are so busy that we have no time, and we rely only on the history from the chart.” She learned from the patient’s son that the patient had hardly been eating for months and had lost a substantial amount of weight, although she was still obese.

“I stayed late after my shift and met up with the neurologist, who graciously sat down with me to go over the case after all of the workup,” Dr. Esber said. The neurologist and Dr. Esber returned to the differential diagnosis of metabolic encephalopathy. Dr. Esber was struck by the history of poor food intake reported by the patient’s family. She wondered whether a nutritional deficiency had been prematurely discounted in evaluating a woman who was so overweight.

If the patient was thiamine deficient, then the decline in mental status might have been precipitated by glucose in the patient’s intravenous fluids. The patient, whose condition was progressively deteriorating, was empirically treated with parenteral thiamine. Within days, she became alert and her dysarthria improved. “Her son, who came to visit from California, was the first to hear her speaking clearly,” Dr. Esber said. Her leg pain improved. The patient was discharged to a skilled nursing facility with instructions to provide thiamine replacement until she could resume an adequate diet.

This case was not classic for thiamine deficiency. We usually consider the diagnosis in an alcoholic patient. It has also been described in patients with anorexia nervosa, cancer and AIDS. In most cases there is obvious malnutrition. Typical findings of Wernicke’s encephalopathy include the triad of mental status changes, oculomotor dysfunction and gait ataxia. This woman was not an alcoholic or obviously malnourished and had no eye findings on exam.

Attribution error

The assumption that an obese woman would not be nutritionally deficient is a form of attribution error. The stereotype in our mind of an overweight person is one who eats to excess, and therefore we may fail to attribute symptoms to the lack of an essential nutrient. The possibility of a vitamin deficiency was reconsidered after obtaining a detailed dietary history from the patient’s family. After obtaining this information, Dr. Esber and the neurologist systematically reviewed the long list of etiologies for metabolic encephalopathy, winnowing the differential diagnosis by linking it to the peripheral neuropathy and thereby arriving at the diagnosis of thiamine deficiency.

Thiamine deficiency is not reliably diagnosed by laboratory tests, although these can be helpful. The recommendation is to empirically treat any patient suspected of thiamine deficiency, as was done in this case. Improvement in symptoms and signs can occur rapidly and dramatically after administration of the vitamin, as seen in this patient.

During her training at Henry Ford Hospital in Detroit, Dr. Esber cared for many patients with poor nutrition and chronic alcoholism, but she had never seen a case before of thiamine deficiency. “I had to keep digging for the diagnosis,” Dr. Esber told us. “Here, the history was very important.” Her careful attention to the medical history helped her avoid making an attribution error related to the patient’s obesity, and allowed Dr. Esber to arrive at the correct diagnosis and provide essential treatment.

Jerome Groopman, a hematologist-oncologist and endocrinologist, and Pamela Hartzband are staff physicians at Boston’s Beth Israel Deaconess Medical Center. They are authors of Your Medical Mind: How to Decide What Is Right for You. This article was originally published in ACP Internist.

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  • Polyonyma

    I am obese and suffered with digestive symptoms for years, which at times looked like ulcerative colitis. And then neurological symptoms, leading to a tentative diagnosis of MS. Turned out: I had a severe B-12 deficiency, I believe caused by diphyllobothriasis and gluten intolerance. I was told flatly by one gastroenterologist that I could not have gluten intolerance because I was too fat. Both digestive and neurological symptoms are banished following praziquantel (one dose) and careful adherence to a gluten-free diet and vitamin supplements. I am still fat, but much healthier.

  • Matt S

    Attribution error or post hoc ergo propter hoc?

    Sounds like the patient may have just been healing herself while the doctors gave her thiamine, especially with all this talk of atypical presentations.

    Could this article just be trading one error for another?

  • http://www.davisliumd.blogspot.com Davis Liu, MD

    This story demonstrates powerfully to both patients and doctors a very simple but important concept that despite all of our tests, imaging studies, and technology, in the end it’s taking a thoughtful history and thinking that matters. Patients with higher copays and deductibles are demanding testing not realizing that tests and imaging studies don’t typically provide answers. Doctors do. http://bit.ly/aYrgHg

    Davis Liu, MD
    Author of Stay Healthy, Live Longer, Spend Wisely: Making Intelligent Choices in America’s Healthcare System
    (available in hardcover, Kindle, and iPad / iBooks)
    Website: http://www.davisliumd.com
    Blog: http://www.davisliumd.blogspot.com
    Twitter: davisliumd

  • http://alchemipedia.blogspot.com Alchemipedia

    Nothing particularly startling in this case. Just reinforces the importance of attention to detail as well as the proper practice of medicine.

    The case was probably not simple thiamine deficiency though. Maybe more a polynutritient deficiency – Strachan’s syndrome might be a better label.

  • ClinRD

    As a clinical dietitian I see this “attribution error” often. I cannot count the times I have heard from an MD that the patient cannot be malnourished as they are “too fat”. Unfortunately, in a setting of inflammation, it is muscle mass that is catabolized and used for energy and/or to support the acute phase response and not the excess fat mass (and admittedly nutrition support does completely reverse this, but can help mitigate some protein losses). Micronutrient deficiencies are common in a hospital setting when patients are anorexic (usually prior to admit) or appropriate enteral feeds are not ordered after prolonged inadequate intake.

    I worked just two years on a neurology floor and saw 5 diagnosed thiamine deficiencies (all with the classic symptoms). Two were alcohol-related, one starvation (anorexia/bulimia), and the last two were secondary to gastric bypass. I anticipate as more gastric bypasses are performed, cases like this will increase.

  • ClinRD

    Correction: and admittedly nutrition support does NOT completely reverse this, but can help mitigate some protein losses).

  • Anonymous

     I’m also fat with a gluten intolerance. Numerous doctors refused to test and/or told me it was impossible to have a food intolerance with my size. I’ve got lots of nutritional deficiencies and debilitating symptoms, and only recently figured out my gluten intolerance. I’m lucky to be alive because of doctors’ sizeism and ignorance.