Paeds Vivas · acute-care-resuscitation-and-toxicology
Opioid, sedative and recreational-drug toxicity — branching viva
A branching viva following one adolescent from the recognition of opioid and recreational-drug toxicity through an ABCDE primary survey, naloxone titrated to effective ventilation with an infusion for a long-acting agent, the flumazenil caution for a co-ingested benzodiazepine, sympathomimetic and serotonergic management of MDMA toxicity, and disposition with safeguarding and mental-health follow-up.
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Target exams
Branching cross-examination
This is a MedVellum formative viva. It is not an official RACP, MRCPCH, ABP, ACGME or RCPSC station, mark scheme, duration or pass standard. Release each update only after the candidate states the failing system, the immediate action and the reassessment endpoint. [1]
Candidate brief
You are the senior paediatric clinician in the emergency department. Speak as you would during resuscitation. Recognise the toxidrome from the bedside pattern, state the change you expect from each action, and say what you will reassess. This is one continuous case. Each escalation branch leads to the next update. [1]
Question 1 — Recognition and the first 60 seconds
Stimulus update. A 16-year-old is carried in by friends who say the adolescent collapsed at a party after taking something. The adolescent is unconscious with slow, shallow breathing. Question: What do you say and do now? [1]
Consultant-level model answer. "I am immediately concerned. The first impression is a life-threatening poisoning until proved otherwise. I call the senior paediatric and resuscitation teams and the Poisons Information Centre, name a leader, allocate roles, and bring age-appropriate equipment and monitoring. I begin the ABCDE survey at once: open and protect the airway, give high-flow oxygen, and start bag-mask ventilation because the breathing is slow and shallow. The pupils, the mental state and the vital signs will tell me the toxidrome within a minute." [1] [2]
Probing follow-up. "Why start ventilation before giving an antidote?" A strong answer is: "Because respiratory depression is the common pathway to death in opioid and sedative toxicity, and ventilation protects the brain while I identify and treat the cause. The antidote is given in parallel, not as a substitute for protecting the airway and breathing." [2]
Common weak answer. "I will take a full history from the friends and order a drug screen before treating." This delays life-saving ventilation in a child who is not breathing adequately. [1]
Escalation branch. If the candidate ventilates and surveys, release the toxidrome findings in Question 2. If they anchor on a drug name, ask which bedside pattern they are treating. [1]
Question 2 — The opioid toxidrome and naloxone titration
Stimulus update. The pupils are pinpoint at 1 millimetre, the respiratory rate is 8 and shallow, and the friend now reports the adolescent had access to a relative's sustained-release morphine and may also have taken a benzodiazepine. Question: Identify the toxidrome and describe your naloxone strategy. [2]
Consultant-level model answer. "This is the opioid toxidrome: pinpoint pupils, slow shallow breathing and reduced conscious level from mu-receptor agonism. I titrate naloxone to effective ventilation, not to full wakefulness, because over-reversal precipitates withdrawal, vomiting, aspiration and rarely pulmonary oedema. I give an initial 10 micrograms per kilogram intravenously and repeat every two to three minutes until ventilation is effective; in the apnoeic child up to 100 micrograms per kilogram per dose to a maximum of 2 mg. Because the agent is a sustained-release opioid, I expect recurrence, and I will start a naloxone infusion once the effective bolus is found." [2]
Probing follow-up. "What is the infusion principle?" A strong answer is: "Naloxone has a short half-life of roughly 60 to 90 minutes, shorter than the opioid. After the effective bolus dose is found, I infuse about two-thirds of that effective dose per hour, titrated to keep ventilation adequate, and observe for many hours." [2]
Common weak answer. "Give a single naloxone bolus and discharge once awake." This ignores the recurrence of a long-acting opioid and the principle of titration to ventilation. [2]
Escalation branch. If the candidate titrates naloxone and plans an infusion, move to Question 3 on the benzodiazepine co-ingestion. If they reverse to full wakefulness, ask what harm that risks. [2]
Question 3 — The flumazenil caution for the co-ingested benzodiazepine
Stimulus update. The friend confirms the adolescent may have taken a benzodiazepine as well, and the registrar asks whether flumazenil should be given to reverse the benzodiazepine component. Question: What is your answer, and why? [8]
Consultant-level model answer. "I would not give flumazenil here. Flumazenil is not a routine reversal agent in the poisoned patient, because removing GABA-mediated inhibition can precipitate seizures in chronic benzodiazepine users, in mixed or unknown overdoses, and where a proconvulsant may have been co-ingested — exactly this patient's profile. The contraindications are chronic benzodiazepine use, mixed or unknown overdose, co-ingestion of a proconvulsant such as a tricyclic antidepressant, and a known seizure disorder. The default is supportive airway and ventilatory care. I reserve flumazenil for the narrow case of an isolated, known benzodiazepine ingestion in a benzodiazepine-naive patient, or iatrogenic reversal of procedural sedation." [8] [9]
Probing follow-up. "What if the benzodiazepine is the sole agent in a naive patient?" A strong answer is: "Even then, flumazenil is reserved for significant respiratory depression that cannot be managed supportively, given in titrated increments of 10 micrograms per kilogram to a maximum of 500 micrograms per dose, with resuscitation equipment and a seizure plan to hand. Supportive care remains the default." [8]
Common weak answer. "Give flumazenil to reverse the sedation and avoid intubation." This ignores the seizure risk in mixed overdose. [9]
Escalation branch. If the candidate declines flumazenil appropriately, release in Question 4 the evolving MDMA features. If they reach for flumazenil, ask what the seizure risk is. [8]
Question 4 — Evolving MDMA hyperthermia and serotonin features
Stimulus update. As the opioid component reverses, the adolescent becomes agitated, rigid, with clonus in the lower limbs, a heart rate of 140, a temperature of 39.5 degrees Celsius, and a sodium of 124 millimoles per litre. The friend now mentions MDMA as well. Question: Interpret this and describe your management. [10]
Consultant-level model answer. "This is evolving sympathomimetic and serotonergic toxicity from MDMA, with the rigidity and clonus signalling serotonin syndrome, the hyperthermia a life-threatening feature, and the hyponatraemia a recognised complication of water intoxication with inappropriate antidiuretic hormone release. I give titrated benzodiazepines first line to control agitation and reduce heat generation, cool actively with evaporative measures and cooled intravenous fluids, give isotonic fluids to protect the kidney from rhabdomyolysis, send a creatine kinase and renal function, restrict free water, and consider cyproheptadine for severe serotonin syndrome with toxicology input. I avoid beta-blocker monotherapy, and I escalate to intensive care." [10] [12]
Probing follow-up. "Why avoid a beta-blocker?" A strong answer is: "Because blocking beta-2 vasodilation leaves unopposed alpha-mediated vasoconstriction, which can paradoxically worsen hypertension and coronary vasospasm. Benzodiazepines are first line; a direct vasodilator such as phentolamine is used for refractory hypertension." [12]
Common weak answer. "Give a beta-blocker for the tachycardia and hypertension." This risks unopposed alpha vasoconstriction. [12]
Escalation branch. If the candidate manages the MDMA features correctly, move to Question 5 on disposition and follow-up. [10]
Question 5 — Disposition, safeguarding and mental-health follow-up
Stimulus update. The adolescent stabilises on benzodiazepines, cooling and fluids, with the sodium corrected and the creatine kinase trending down. Question: Describe your disposition, safeguarding and mental-health plan. [10]
Consultant-level model answer. "The disposition is high-dependency or intensive care observation until the temperature, agitation, sodium and cardiovascular state are controlled and the creatine kinase is reassuring. I take a confidential, non-judgemental history that respects adolescent autonomy while securing safety, because an intentional or recreational presentation is a marker of ongoing risk. I arrange a mental-health and social assessment before discharge, give a clear safety net, harm-reduction advice and follow-up, and I apply local safeguarding and confidentiality provisions. The family receives poison-prevention advice and the access route for return." [10]
Probing follow-up. "What is the one principle you most want the team to carry forward?" A strong answer is: "Recognise the toxidrome, lead the ABCDE survey, titrate naloxone to ventilation, never reach for flumazenil in the mixed overdose, treat sympathomimetic toxicity with benzodiazepines first, and escalate early — and never let the confidentiality of the adolescent history delay safety." [1]
Common weak answer. "Discharge once the adolescent is awake." This ignores the recurrence risk, the hyponatraemia, the rhabdomyolysis, and the psychosocial risk. [10]
References
- [1]Hoffman, Robert J Toxidromes and a general approach to poisoning Archives of disease in childhood, 2025.PMID 39978865
- [2]Boyer, Edward W Management of opioid analgesic overdose The New England journal of medicine, 2012.PMID 22784117
- [8]Kreshak, Angela A Flumazenil administration in poisoned pediatric patients Pediatric emergency care, 2012.PMID 22531190
- [9]McDuffee, Andrew T Seizure after flumazenil administration in a pediatric patient Pediatric emergency care, 1995.PMID 7651879
- [10]Levine, Mark New Designer Drugs Emergency medicine clinics of North America, 2021.PMID 34215409
- [12]Lucyk, Sarah N Acute Cardiovascular Toxicity of Cocaine The Canadian journal of cardiology, 2022.PMID 35697321