Psychopharmacology and psychotropic medicines in children and adolescents — formative SAQs

SAQ 1 — Starting an SSRI in adolescent depression (10 marks)

A 15-year-old girl presents with moderate major depressive disorder (PHQ-A in the moderate-severe range), four weeks of low mood, anhedonia, sleep and appetite disturbance, and declining school attendance. She has no current suicidal intent but has had fleeting passive thoughts. There is no history of mania or psychosis. Her mother asks whether she needs tablets, and what the risks are. [1] [8]

Questions

1. Justify your pharmacological choice and outline the starting dose, the role of cognitive-behavioural therapy, and the evidence you would cite. (5 marks) [1]
2. Explain the FDA black-box suicidality warning, how you would counsel the family, and the review schedule you would set in the first month. (5 marks) [8] [9]

Model answer

Choice, dose, therapy and evidence (5). My first-line SSRI is fluoxetine, ideally combined with cognitive-behavioural therapy (CBT). Fluoxetine has the strongest paediatric evidence base and is the SSRI approved for paediatric depression down to age 8. The pivotal TADS trial showed that fluoxetine, CBT and their combination all beat placebo for adolescent depression, but combination therapy gave the best outcomes and lowered suicidality compared with fluoxetine alone — so medication plus therapy is safer and better than medication alone. I would start at about half the typical adult dose, taken in the morning, confirm the exact dose against the BNF for Children / AMH Children's Dose, and titrate after 4 to 6 weeks if response is partial. I would explicitly not use paroxetine first-line, because the Restoring Study 329 reanalysis showed its benefit was overstated and its harms understated. [1] [2] [10]

Suicidality warning, counselling and review (5). The FDA black-box warning covers all antidepressants in people under 25: paediatric antidepressant trials showed an increased rate of reported suicidal ideation and attempts (Bridge meta-analysis). The Gibbons reanalysis argues the absolute risk is low and that effective treatment itself protects against suicide, so the defensible position is close monitoring plus treatment, not avoidance of treating real depression, because untreated depression carries its own substantial suicide risk. I would counsel the family that the SSRI takes 4 to 6 weeks to work, that early agitation or worsening should prompt immediate contact, and that the main monitoring obligation is suicidality. My review schedule would be at 1 week, 2 weeks and 4 weeks, and at every dose change, with explicit suicidality assessment, a safety plan, removal of access to means, and an open-access pathway. [8] [9]

SAQ 2 — Antipsychotic monitoring and an emergency (10 marks)

An 8-year-old boy with autism and severe, persistent irritability and aggression is started on risperidone by the CAMHS team after structured behavioural and educational intervention failed. He is reviewed by you in general paediatric clinic at week 4. [21]

Questions

1. Outline the baseline and ongoing metabolic monitoring this antipsychotic exposure requires, and the evidence that justifies it. (5 marks) [21]
2. Three months later, while also taking an SSRI for comorbid anxiety, he presents with agitation, tremor, hyperreflexia, clonus and fever. What is the diagnosis, the immediate management, and how do you distinguish it from neuroleptic malignant syndrome? (5 marks) [19]

Model answer

Metabolic monitoring and evidence (5). Second-generation antipsychotics require baseline and ongoing metabolic monitoring because of their weight-gain, dyslipidaemia and hyperglycaemia burden. At baseline I would record weight, height, BMI and waist circumference, blood pressure, fasting glucose or HbA1c, and a fasting lipid profile; consider a baseline prolactin and an ECG when relevant. I would repeat weight and BMI at least quarterly, fasting glucose and lipids at around 12 weeks and then at least annually, and blood pressure at every visit. The justification is the Correll first-use study, which showed substantial weight gain and metabolic change in the first 11 weeks of paediatric antipsychotic use, with olanzapine highest and aripiprazole among the lower — so even metabolically safer agents carry real risk. The Marcus and Owen trials established aripiprazole for autism irritability, but risperidone (RUPP) is also evidence-based; both demand monitoring. [19] [21]

Serotonin syndrome and NMS distinction (5). The combination of agitation, tremor, hyperreflexia, clonus and fever in a child on an SSRI (with or without an antipsychotic) is serotonin syndrome. Immediate management is to stop all serotonergic agents, give benzodiazepines for agitation and rigidity, cool actively, hydrate, and escalate; cyproheptadine is used in severe cases. The distinction from neuroleptic malignant syndrome is that serotonin syndrome produces neuromuscular hyperactivity (hyperreflexia, clonus, myoclonus) while NMS produces lead-pipe rigidity and bradyreflexia with marked rigidity; both have fever and autonomic instability. NMS management is to stop the antipsychotic, cool, hydrate, give benzodiazepines, supportive or ICU care, and dantrolene in severe cases. Because he is on both an SSRI and an antipsychotic, both diagnoses must be actively considered, and the hyperreflexia and clonus point to serotonin syndrome as the primary emergency while the team also excludes NMS. [21]