Every now and then I come across journal entries that just fascinate me. This case I am sharing with you here is one such case. I love psychology. If you think about it, all of us that perform sedation or especially anesthesia are battling psychology upfront. Fortunately, the drugs we can safely administer usually allow us to control the patient’s state of response among other things. But what about the times we interact with patients that we don’t have any drugs on board? Or should we even care? I’m sure all of you were trained similar to me that setting correct expectations for all treatment is key BEFORE any treatment is performed. We all know how our positive disposition and reassuring words to a patient can have a positive effect, but is it possible that a patient have negative physiologic responses based off of psychological influence? I think you’ll find this interesting.
This is a case published in General Hospital Psychiatry describing a clinical scenario that is both unusual and highly instructive especially for those of us who routinely manage patients undergoing sedation, anesthesia, or invasive procedures.
A 26-year-old male presented to the emergency department after intentionally ingesting 29 capsules from a bottle of study medication as part of a suicide attempt. The patient had responded to an ad seeking patients to be treated for depression in a drug trial. Four years prior this patient had been treated for depression with amitriptyline but had stopped taking it as he found it to “induce intolerable sedation and numbness of his body and felt it was too strong for him.” The patient was experiencing a two-month stent of depression due to a breakup and he thought the new drug was likely a breakthrough medication. The patient was enrolled in a double-blind clinical trial being held at a large university evaluating a new antidepressant. Since the study was double-blind, neither the patient nor the treating physicians knew whether he had been assigned to the active drug or placebo arm of the study. Interestingly, during the first month of the trial, the patient had stated that his mood had improved and he was not experiencing no adverse effects from the capsules. At the beginning of the second month, a fight with his previous girlfriend escalated to him choosing to take all remaining 29 capsules in his prescription bottle. He soon regretted his decision and feared he would die from his overdose and checked himself into an emergency department.
On presentation, the patient complained of dizziness, weakness, and lightheadedness. Initial vital signs demonstrated hypotension with a blood pressure of approximately 80/40 mmHg, along with tachycardia with a heart rate near 110 beats per minute. He appeared pale, diaphoretic and fatigued but remained mostly alert and oriented. Intravenous fluids were initiated due to concern for drug-induced cardiovascular depression, and the treating team prepared for possible complications related to antidepressant overdose, including arrhythmia, CNS depression, or vasodilatory shock.
Because the identity of the ingested medication was unknown, management was limited to supportive care while attempts were made to contact the research investigators to determine the patient’s assignment within the study.
After the study coordinators were reached, the blind was broken.
The patient had been assigned to the placebo group, and the capsules he ingested contained only inert filler with no pharmacologically active compound.
The clinical course that followed was striking. After the patient was informed that he had taken placebo rather than an antidepressant, his symptoms rapidly improved. Over the next several minutes, his blood pressure increased to within normal limits, his heart rate normalized, and his subjective complaints resolved. Within approximately 15 minutes, his vital signs had returned to acceptable baseline values without any pharmacologic intervention that could account for the change.
The authors concluded that the episode represented a classic example of the nocebo effect, defined as the development of adverse physiologic symptoms caused by negative expectation rather than by a pharmacologic agent.
The placebo effect we all recognize as improvement resulting from belief in treatment. The nocebo effect represents the opposite phenomenon — deterioration resulting from belief in harm. Documented effects may include hypotension, tachycardia, syncope, nausea, dyspnea, and measurable alterations in autonomic tone mediated through sympathetic and parasympathetic pathways.
For clinicians involved in sedation and anesthesia, this case has direct relevance. Patient expectation itself is capable of producing clinically significant physiologic instability, even in the absence of pharmacologic effect.
It is tempting to think of physiologic changes as being driven primarily by pharmacology, but cases like this remind us that expectation itself can be a powerful physiologic stimulus.
This has direct implications for sedation and procedural safety.
How we present treatment matters.
How we describe risk matters.
How we speak to patients matters.
We often focus on drug selection, dosing, monitoring, and technique — and we should. But this case is a reminder that safety and patient management begins earlier than that.
I hope you found this as interesting as I did. The mind is a beautiful and mysterious thing. I encourage you to read the full article. If you’d like to discuss further, reach out. Until then, keep doing high quality safe work my friends!
Dr. Travis V. Coulter, DDS
Clinical Director
Xchart.com
Reeves RR, Ladner ME.
Nocebo effects with antidepressant clinical drug trial placebos.
Gen Hosp Psychiatry. 2007;29(3):275-277.
PubMed PMID: 17484949.