The Iatrogenic Potential of the Physician’s Words
JAMA. Published online October 31, 2017. doi:10.1001/jama.2017.16216
Some of the information
that physicians convey to their patients can inadvertently amplify
patients’ symptoms and become a source of heightened somatic distress,
an effect that must be understood by physicians to ensure optimal
management of patient care. This effect illustrates the iatrogenic
potential of information, as opposed to the iatrogenic potential of
drugs and procedures.
Somatic symptoms and underlying disease do not have a
fixed, invariable, one-to-one equivalence. Symptoms can occur in the
absence of demonstrable disease, “silent” disease occurs without
symptoms, and there is substantial interindividual variability in the
symptoms resulting from the same pathology or pathophysiology. One
mediator of this variability between symptoms and disease is the
patient’s thoughts, beliefs, and ideas. These cognitions can amplify
symptoms and bodily distress. Although cognitions may not cause
symptoms, they can amplify, perpetuate, and exacerbate them, making
symptoms more salient, noxious, intrusive, and bothersome.
Several common clinical scenarios exemplify the
iatrogenic potential of the physician’s words—for example, instituting a
new medication regimen, reviewing an informed consent document,
presenting ambiguous laboratory test information, and preparing patients
for painful procedures.
Knowledge of the nonspecific, diffuse, ambiguous adverse
effects of a drug (such as fatigue, difficulty concentrating, nausea,
dizziness, headache) increases the frequency with which they are
experienced and reported.1
Whether the information is imparted through discussion with the
physician or when obtaining informed consent, patients who learn about
the common, nonspecific adverse effects of β-blockers, statins,
estrogen-containing oral contraceptives, and agents for obstructive
urinary symptoms report more of these putative adverse effects than
comparable patients not informed of them. For example, in a study of 76
patients who received β-blocker treatment for hypertension, erectile
dysfunction occurred in 32% of the 38 patients explicitly informed of
this adverse effect and in 13% of the 38 patients not specifically
warned about it.2
Likewise, in a double-blind trial of statins, the incidence of
muscle-related adverse effects increased from 1.00% per year to 1.26%
per year when patients (n = 9899) were subsequently unblinded and given
the active drug.3
The nocebo phenomenon (the development of adverse
effects to placebo) strongly supports that patient knowledge of adverse
effects influences the reported incidence of these symptoms. Thus, the
frequency and profile of adverse effects manifested by patients
randomized to receive placebo in controlled, double-blind clinical
trials are similar to those they have been told may occur with the
active comparator drug.
Providing test results of dubious clinical significance
also can lead to increased symptoms. For example, in a randomized study
of acute low back pain, one group (n = 210) underwent spine imaging,
whereas the other group (n = 211) did not. A treatment plan of
conservative medical management was implemented in both groups. At
3-month follow-up, the former group had significantly more pain, greater
functional impairment, and more physician visits.4
The problems involved in conveying equivocal test results or anatomical
abnormalities of unknown clinical significance (“incidentalomas”) are
likely to increase in importance as the volume and resolution of
diagnostic testing accelerate.
Pain is particularly sensitive to the beliefs, thoughts,
and expectations of patients. The specific language used in describing
and preparing patients for painful procedures can affect the pain
experience. For example, in a randomized study of women receiving
epidural anesthesia or spinal anesthesia (n = 140) for childbirth, those
told that the intradermal injection of a local anesthetic would “feel
like a bee sting: this is the worst part of the procedure” reported
significantly more pain than did those told “the local anesthetic…will
numb the area and you will be comfortable during the procedure.”5
The importance of cognitions in the experience of pain is particularly
timely, given the current crisis in opiate treatment for chronic,
nonmalignant pain.
The Mechanism of Viscerosomatic Amplification
Viscerosomatic amplification has been proposed as an
explanatory mechanism whereby information can affect the perception of
symptoms.6
The information conveyed by the physician does not cause somatic
symptoms but rather amplifies symptoms—symptoms that may be due to the
underlying medical condition or to normal physiology (eg, ectopy,
orthostatic hypotension), common benign dysfunctions (hoarseness,
bloating, cramps), transient and self-limited ailments (rashes, upper
respiratory tract infections), stressful life events, lack of exercise,
insufficient sleep, or dietary indiscretion.
New medical information can initiate a self-perpetuating and self-validating cycle of symptom amplification (eFigure in the Supplement).
Learning that a symptom may be more noteworthy or medically significant
amplifies it. Reattributing the symptom to a new and more serious and
more concerning source then causes the patient to monitor and scrutinize
the symptom more closely, and this heightened attentional focus
amplifies the symptom, making it more intense and intrusive, more
disturbing and distressing.6,7
The misattribution also launches a selective search for additional
symptoms to corroborate the suspicion that something is wrong, resulting
in a heightened awareness of other diffuse, transient, or ambiguous
symptoms that were previously ignored, minimized, or dismissed as
insignificant. The seeming emergence of these “new” symptoms (along with
dismissal of observations that do not confirm the suspected cause) is
taken as further evidence of seriousness. The cycle of amplification is
also fueled by mounting anxiety: Increasing worry and concern about the
symptom’s medical significance, and its apparent worsening, make it more
threatening and ominous.
Modulating Symptom Amplification and Minimizing Undue Distress
Careful attention to what and how information is
conveyed can minimize the inadvertent fostering of excessive,
disproportionate, and unduly bothersome symptoms. The initial
therapeutic step is an exploration of the patient’s ideas about the
symptoms: What is the suspected cause of the symptoms and their putative
significance, what is the future course expected to be, what is most
worrisome and troubling about them? The answers to these questions can
lead to more realistic and reassuring discussion of the patients’
specific concerns.
Explaining the process of viscerosomatic amplification
can be beneficial. Understanding that the interpretation of medical
information can exacerbate and perpetuate symptoms, and learning about
the processes of misattribution, selective attention, increased bodily
scrutiny, and secondary anxiety, can have a palliative effect by
providing patients with a more benign and reassuring explanation for
their discomfort. The reassurance that the symptoms, however bothersome,
are not medically harmful makes them less intrusive and more tolerable.
The nocebo phenomenon provides a vivid, helpful, and nonpejorative
illustration of the power of beliefs to amplify symptoms. This
discussion also helps by emphasizing and encouraging adaptive coping to
increase the tolerance of discomfort. It may be useful to prospectively
identify patients at increased risk of disproportionate or undue
nonspecific medication adverse effects, so that the amplification
process can be explained to them in advance. This can be done with the
Perceived Sensitivity to Medicines scale,8 a 5-item self-report questionnaire with demonstrated validity and reliability.
In addition to exploring the patient’s ideas and
explaining the process of amplification, physicians need to use care in
their choice of words. For example, in discussing potentially painful
procedures, physicians can emphasize what will be done to alleviate the
pain (such as simple relaxation techniques), use neutral language to
describe the experience, and give the patient as much choice and control
over the analgesic regimen as is medically feasible. Likewise, language
is important in discussing nonspecific drug adverse effects, for
example, focusing on the proportion of patients who do not have the
adverse effects being enumerated, rather than on the proportion who do,
and closely coupling information about benefits with information about
adverse effects.
When obtaining informed consent, physicians must
absolutely provide complete and truthful information and must avoid
fostering a “paternalistic” patient-physician relationship. But
balancing the requirement for full and complete disclosure with the
iatrogenic potential of some information is problematic. “Contextualized
informed consent” has been proposed as an ethical way of balancing
these competing imperatives.9
When prescribing a medication, all serious and medically significant
adverse effects are of course described, and the patient is instructed
to report all adverse effects; however, if the patient agrees, benign,
nonspecific symptoms are not enumerated in advance because it is
explained that doing so makes them more likely.
Unusually distressing symptoms may point to difficulties
in the patient-physician relationship, because symptoms can be a
nonconfrontational and less explicit way of expressing doubts or
concerns that patients feel and are unable or too embarrassed to voice
openly. Symptoms can then become a covert, nonverbal communication of
anxiety about pain, misgivings about medications, concerns about the
meaning of a diagnostic test result, or concerns about the physician’s
care or expertise.1
Conclusions
Information is an important mediator of the variability
in the relationship between disease and symptoms. Some nonspecific drug
adverse effects, undue pain from procedures, and symptoms exacerbated by
learning about test results of unclear medical significance can be
understood to share similar pathogenic mechanisms and respond to similar
strategies of medical management.
Article Information
Corresponding Author: Arthur J. Barsky, MD, Department of Psychiatry, Brigham and Women’s Hospital, 60 Fenwood Rd, Boston, MA 02115 (abarsky@bwh.harvard.edu).
Published Online: October 31, 2017. doi:10.1001/jama.2017.16216
Conflict of Interest Disclosures: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
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