Ketamine for Treatment-Resistant OCD
She has heard ketamine works fast for depression and wants to know why it isn't being offered for her OCD — the honest answer is that its OCD evidence is real but far thinner, and the benefit fades in days rather than weeks.
S.N., a 30-year-old woman, works night shifts in a hospital emergency department and has been with her partner for four years; they had been planning to move in together this year before her OCD symptoms worsened enough that she asked to delay it. She is otherwise healthy, with no cardiac or psychiatric history besides her OCD.
Diagnosed six years ago with contamination-themed OCD that intensified noticeably after she began working in the ED, she has since completed two adequate SSRI trials (sertraline 200 mg and fluvoxamine 300 mg, each for at least 12 weeks) and eight months of ERP, with only modest overall improvement; her Y-BOCS today is 27. She raised ketamine herself at this visit, having read about esketamine's approval for treatment-resistant depression and its reputation for working within hours rather than weeks, and wants to know why it isn't being offered to her.
The honest answer is that ketamine's evidence in OCD is real but occupies a genuinely different, much earlier stage than its depression story. Small controlled trials and case series do show a measurable, rapid reduction in obsessions after a single infusion — in the one randomized proof-of-concept crossover trial, in fifteen patients, about half of those given ketamine still met response criteria a week later. But that is the whole of it: single-dose benefit in OCD has generally not been shown to outlast roughly a week, much as in depression, and no maintenance strategy has been demonstrated to sustain it in this diagnosis. Esketamine's FDA approval is specifically for treatment-resistant depression; there is no approved ketamine or esketamine indication for OCD, and no dosing or monitoring protocol has been validated the way it has for TRD. Her genuine treatment-resistant history makes her a reasonable candidate to discuss it with honestly, but "reasonable to discuss" and "reasonable to offer as a real treatment plan right now" are different questions the group needs to answer separately.
What ketamine would and would not offer her
I want to be precise with her about what the OCD trials actually show, because it's a genuinely different shape of result than depression's. NMDA antagonism does produce a measurable, fast drop in obsessive symptoms — but the evidence base is one small randomized crossover trial and some case series, with benefit generally not shown to outlast about a week, and no study has established a maintenance dosing strategy that sustains it in OCD the way repeat esketamine dosing does for TRD. If we offer this, we're offering something closer to a short-lived symptom window than a treatment plan.
Given how transient that benefit is, I don't think a single infusion changes her actual trajectory in any durable way, and I'm wary of offering it as if it does when what we'd really be doing is treating a request, not a documented gap in her care. Her real next steps — augmentation strategy, or considering clomipramine — haven't been exhausted yet, and I don't want ketamine to become a detour around that harder conversation.
I'm not saying never; I'm saying not instead of the next real step in the sequence she hasn't taken yet.
I'd handle this as an honest conversation rather than a flat no. She works in an ED and reads primary literature more critically than most patients who ask about this — she deserves the real distinction between OCD and depression evidence stated plainly, including that no approved indication or validated protocol exists for her diagnosis. If she still wants to pursue it after that, it belongs in a research or specialty ketamine-clinic setting with informed consent naming the transient effect explicitly, not as something we prescribe here today in place of the augmentation step still ahead of her.
Agreed: an antipsychotic augmentation trial added to her current fluvoxamine, as the next evidence-supported step in her actual sequence, with a follow-up Y-BOCS at 8 weeks. Ketamine was discussed with her directly and openly, including the honest distinction between its depression and OCD evidence bases.
Left open rather than closed: whether she should be referred to a research protocol or specialty ketamine clinic if augmentation also proves insufficient. The attending wanted that conversation to wait until augmentation's result is known; the psychiatric pharmacist felt naming it as a named future option, not a vague maybe, respected how carefully she had already researched her own case.