Department of Family Medicine, Brooklyn Hospital Center, NY (Dr. Rosen); Brooklyn Hospital Center, NY (Dr. Baptista); Psychiatry Residency Program, Cape Fear Valley Hospital, Fayetteville, NC (Dr. Klenzak) drpaulie2000@hotmail.com
The authors reported no potential conflict of interest relevant to this article.
An incorrect initial diagnostic path often triggers a cascade of subsequent errors. The physician orders additional unhelpful and expensive tests in an effort to characterize the suspected GI pathology. This then leads the physician to prematurely terminate the work-up and accept the most favored diagnosis. Lastly, sunk-cost fallacy comes into play: The physician has “invested” time and energy investigating a particular diagnosis and rather than abandon the presumed diagnosis, continues to put more time and effort in going down an incorrect diagnostic path.
A series of failures.These biases and miscues have been observed in several studies. For example, a survey of 1725 women by Goff and colleagues30 sought to identify factors related to delayed OC diagnosis. The authors found that the following factors were significantly associated with a delayed diagnosis: omission of a pelvic exam at initial presentation, a separate exploration of a multitude of collateral symptoms, a failure to order ultrasound/computed tomography/CA-125 test, and a failure to consider age as a factor (especially if the patient was outside the norm).
Responses from the survey also revealed that physicians initially ordered work-ups related to GI etiology and only later considered a pelvic work-up. This suggests that well-known presenting signs and symptoms or a constellation of typical and atypical symptoms of OC often failed to trigger physician recognition. Understandably, patients presenting with menorrhagia or gynecologic complaints are more likely to have OC detected at an earlier stage than patients who present with GI or abdominal signs alone.31table 27 summarizes some of the cognitive biases seen in the diagnostic path of OC.
Case 3
A 56-year-old man is brought to the ED by his wife and children for evaluation of odd behavior and episodes of confusion. The patient recently had a negative neurologic work-up for transient ischemic attack and cerebrovascular accident and is admitted for further work-up. He reports visual hallucinations to nursing staff. Screening for memory problems shows no significant deficits. The patient in fact scored a 27 on the Mini–Mental State Examination, well within the normal range. The family notes that the patient has had difficulty with planning over the previous year and has not seemed like his “old self.” The patient has no history of psychosis, schizophrenia, bipolar disorder, or any other psychiatric illness.
While in the hospital, he becomes acutely upset by the hallucinations and is given haloperidol and lorazepam by house staff. In the morning, the patient exhibits severe signs of Parkinson disease that include rigidity and masked facies.
Given the patient’s poor response to haloperidol and continued confusion, the team consulted Neurology and Psychiatry. Gathering a more detailed history from the patient and family, the patient is given a diagnosis of classic LBD. The antipsychotic medications are stopped. The patient and his family receive education about LBD treatment and management, and the patient is discharged to outpatient care.
Psychiatric symptoms can be an early “misdirect” in cases of Lewy body disease
LBD, the second leading neurodegenerative dementia after Alzheimer disease (AD), affects 1.5 million Americans,32 representing about 10% of all dementia cases. LBD and AD overlap in 25% of dementia cases.33 In patients older than 85 years, the prevalence jumps to 5% of the general population and 22% of all cases of dementia.33 Despite its prevalence, a recent study showed that only 6% of PCPs correctly identified LBD as the primary diagnosis when presented with typical case examples.32