Initiating ketamine/esketamine for treatment-resistant depression (MEQ)

(i) TRD and offer. Treatment-resistant depression: inadequate response after at least two adequate antidepressant trials with adherence documented; exclude bipolar, substances, organic depression, under-dosing. She has three lines including augmentation — meets pragmatic TRD threshold for considering rapid-acting options. IV racemic ketamine has RCT support from Zarate onward; esketamine nasal spray has phase 3 TRD evidence with oral antidepressant (TRANSFORM-2 flexible dose). Justify supervised programme access, not informal take-home use.[1][2][4][5]

(ii) Pre-treatment. Confirm diagnosis and failed trials; MSE and suicide risk assessment; substance history; pregnancy test if relevant; baseline BP/HR; cardiovascular history (uncontrolled HTN, aneurysm, AVM, prior ICH are major red flags); capacity/consent; service readiness for observation. Document concurrent oral antidepressant plan.[4][5]

(iii) Esketamine induction scaffold. Supervised clinic dosing commonly 56 or 84 mg nasal; induction often twice weekly for four weeks then weekly/biweekly maintenance; concurrent oral AD; ~2-hour observation with BP checks; no driving until the next day after a dose; crisis plan written. If response achieved, discuss SUSTAIN-1 continuation logic to reduce relapse.[2][3][5]

(iv) Adverse effects. Expect dissociation, dizziness, nausea, sedation, transient BP rise — usually session-limited. Monitor BP pre/post, mental state, and recovery before discharge. Counsel that chronic recreational misuse carries bladder toxicity risk; clinic control reduces diversion.[7]

(v) vs ECT. ELEKT-D: IV ketamine noninferior to ECT in nonpsychotic TRD on primary response endpoint — relevant shared-decision data. ECT still preferred or first-line somatic option in psychotic depression, catatonia, and many perinatal severe cases. Discuss access, cognitive AE of ECT, session burden of both, and patient values without guaranteeing cure.[6][5]