Asthma management for GPs: ICS–formoterol reliever therapy, fewer oral steroids and biologics — plus a psychiatrist on serotonin syndrome, NMS and lithium

Asthma speaker

Respiratory and sleep physician working on the Gold Coast (self-described: “I’m a respiratory and sleep doctor… up and down the Gold Coast”; works at Pindara and a second hospital whose name the ASR renders as “Jonathan”. Not named in the recording).

Psychiatry speaker

Adult psychiatrist at a private hospital who introduces themselves as “Sandy kale” (name as captured by the ASR, spelling unconfirmed; the hospital name is garbled — “Salesforce special series. Well Private Hospital”).

Others

Several audience members (GPs and others) ask questions and are labelled “Speaker 2–6” or “Unknown Speaker”; none are named. Sponsor: no sponsor or disclosure statement was captured. AstraZeneca and the brand names Ventolin and Symbicort are mentioned in the clinical discussion only.

Session context

Otter title Asthma Management Seminar · id sh0cxY3YerO6UQrVWDfaKoMAw3Y · ~41 min, recorded 21 March 2026 10:17 am AEST. About the first 22 minutes are asthma; from about 22:35 the psychiatrist takes over (“the last bit of the morning”). The Otter title and AI summary mention only asthma in the title, so the psychiatry segment is covered here as a second part. The ASR is poor in places and uncertain wording is flagged.

Key messages for GPs

• Asthma is an inflammatory condition. A reliever that only opens the airways (salbutamol) targets the bronchoconstriction but not the inflammation behind the symptoms.
• Guidelines have shifted: for people who are asthma-naive or have no diagnosis, the speaker said the recent guidance is not to offer a short-acting beta-agonist alone but an inhaled corticosteroid plus formoterol preparation (as captured, “better off preparation”).
• Oral corticosteroids work fast but cost a lot over time — the cumulative metabolic effects “can’t be overstated”. The aim is to minimise systemic steroid.
• Ventolin is not banned — it still has a role, for example in a patient in extremis — but avoid building a patient’s whole plan on it.
• Look beyond the lungs: allergy, reflux, sinus disease/polyps, weight, sleep apnoea, smoking, environment, medications and mood all affect asthma (“treatable traits”).
• Biologics are for the right patient — severe asthma, already on optimised therapy (including good device use), still exacerbating. They are specialist-prescribed, strictly criteria-based and expensive (“40 grand a year”, as stated).
• Asthma is genuinely hard to diagnose: the variability is easy to miss in a well patient, and mimics include vocal cord dysfunction, heart failure and sleep apnoea.
• Part 2 (psychiatry): with serotonin syndrome or neuroleptic malignant syndrome, stop the culprit drug straight away and arrange emergency care if unwell; with lithium plus a diuretic, stop both and check lithium, renal function and potassium. In older patients with agitation, start low and go slow.

Why the reliever is changing: treat the inflammation

The speaker opened by explaining why they chose asthma: “we’re coming into cooler months” (as captured, “cooler lungs”) and more asthma is seen, and there have been “recent paradigm shifts in some of the guidelines” on how acute and long-term asthma are managed — which is “becoming increasingly complicated”.

The main message was the recent change in guidelines about reliever therapy:

• SMART. AstraZeneca has talked about “SMART” therapy — Symbicort maintenance and reliever therapy — for a few years, and the speaker noted that other preparations in the same type of device also have a role as reliever therapy.
• The guideline change. In “last year’s” guidelines (the ASR does not name which; the Otter summary links it to a recommendation against beta-agonists in asthma-naive patients), the recommendation is that patients who are asthma-naive or have no diagnosis should not be given a short-acting reliever alone. Offer them an inhaled corticosteroid plus a long-acting beta-agonist (formoterol) preparation.
• The reasoning is physiological. Asthma is an inflammatory lung condition: a trigger produces bronchoconstriction, and there is also mucus hypersecretion. Salbutamol “only really targets the bronchoconstriction” and is not treating the inflammation that causes symptoms and exacerbations — which matters for chronic asthma. An inhaled corticosteroid used as part of the reliever puts an anti-inflammatory into the airways to treat what is actually causing the asthma.
• Hospital practice. “We’ve been using it in the hospitals for a few years now.” The speaker described a patient with acute asthma on the ward on day one using the combination inhaler several times a day, then tapering over the following days back to their baseline (the exact puffs and frequencies are garbled in the transcript — “two puffs four times a day” is as captured), with the aim of minimising oral corticosteroids.

Keeping oral steroids to a minimum

The speaker called oral corticosteroids “terrible drugs” in the sense that they are very effective anti-inflammatories that work fast — “that’s why it’s a problem” — but whose cumulative metabolic and other effects “can’t be overstated”.

• The arithmetic: a patient with two or three exacerbations a year, each treated with 50 mg of prednisone for three to five days — “do that for 10 years” and there will be long-term consequences (as captured).
• The goal: shift to something that treats the real problem (airway inflammation) and minimise systemic steroid use.
• In the speaker’s own practice: people often do not need a prednisone course. If one is needed, the speaker said they will “often give them just 25 milligrams for two or three days hydrocortisone” (dose and drug exactly as captured — verify against current guidance; the Otter summary reads it as “25 mg hydrocortisone equivalent”). The speaker also made a point about what to tell patients, but the sentence is garbled and is not reported here.
• Fewer admissions: an unidentified speaker remarked that something is not seen “nearly as much” (the ASR says “vaccines”, which is likely a mis-hearing), and the speaker added that “we just don’t see patients being moved to hospital” as often. The speaker credited the range of options now available — medications, how they are applied, long-term management and biologics.

Is Ventolin gone? Not quite

A GP in the audience interrupted with the practical concern that, in an emergency, there is “only a certain number of” puffs that can be given and that “we can go up to 20” (as captured; the rest of the comment is garbled). The speaker’s answer: “it’s not a case of, do not use [Ventolin]. You can still use Ventolin.”

• The speaker described Ventolin as having “minimal, no ceiling” (as captured — meaning unclear) and warned that at high doses you begin to see systemic effects, which are “very unpleasant”, and that palpitations can be dangerous.
• Formoterol is quick-acting, but with repeated use you are also building a cumulative dose of beta-agonist. The transcript here includes figures (“four puffs a day”, “72 micrograms per day”, “eight puffs a day”, “a max dose 1200 a day”) that are garbled and not reliable; check the product information and current guidelines for maximum daily doses.
• Special situations: a patient in extremis, or one who can only manage a nebulised treatment, or someone using a spacer, can still be given a short-acting reliever. But for most patients: optimise maintenance-and-reliever therapy and optimise the acute doses.
• An audience member (Speaker 2) agreed that for some patients “those are the ones we need to give Symbicort”, adding that some are “remote” (the sentence is incomplete).
• The speaker also noted that patients sometimes seem to feel they are “taking away” their ability to cope if they use too much medication — and that patients may not “take it into their own hands” (the passage is heavily garbled). An anecdote about a patient using “two ventilators last week” is as captured.

Look beyond the airways: treatable traits

The speaker described a “treatable traits” approach and said it is discussed in Therapeutic Guidelines and elsewhere in the literature. The question is not just “how do I treat this attack?” but “why are they here in the first place?”

• Type of asthma: is it allergic, or medication-induced (aspirin was named)?
• Outside the airways: reflux (including laryngopharyngeal reflux irritation), sinus disease and nasal polyposis, being overweight, sleep apnoea, smoking, environmental exposures, medications, and mood. The ASR lists “cancer” among these; this is likely a mis-hearing and is not relied on.
• Mood and breathing: depression can worsen asthma (the Otter summary adds anxiety). The speaker’s explanation for patients: when you are anxious you start to breathe quickly and your sympathetic nervous system goes into overdrive. This helps patients understand the link — including those who do not have a firm asthma diagnosis.
• Treat those traits: uncontrolled reflux, nasal polyps and the like “need to be treated” to optimise the patient’s asthma.

Biologics for severe asthma

“Biologics, fantastic drugs for us, fantastic. They’re expensive — 40 grand a year [as stated]. They have to be prescribed by specialists. There’s quite a lot of criteria.” They work very well, but you have to pick the right patient.

• Right patient = severe asthma that has had the right therapy, optimised — including the use of devices (the speaker’s “fifth point” was device use) — and who is still exacerbating. There is no point sending someone for biologics before that.
• How many: there are four biologics (as stated), with a fifth “coming very soon”, each targeting very specific pathways.
• Biomarkers used for applications: peripheral blood eosinophils and IgE (the allergic markers), and FeNO (fractional exhaled nitric oxide — “a measure of airway inflammation”), which can also help guide some biologics. The numeric thresholds in the transcript (“half point three or 1.5”) are garbled and not reproduced as criteria.
• Who to think about: uncontrolled asthma usually on a high-dose inhaled steroid; but also people on a moderate dose who exacerbate two or three times a year, or whose symptoms are not controlled (night-time symptoms, or needing the reliever “multiple times per week”). The speaker did not want it to be a reflex “send them away to consider biologics”, but to look at whether they are clearly still uncontrolled on moderate or high dose.
• The audience question: “What if they have normal eosinophils and normal IgE — would they still be able to get biologics?” Answer: not yet. A new drug (captured as “tepidelumab” — spelling unverified) is “coming out very soon”: TGA-approved but not PBS-listed at the time, with criteria not yet known. It is marketed as working on a different receptor upstream, so it may help people who are not eosinophilic or allergic — though the trials show it works best in those with eosinophilic asthma.
• Beyond asthma: the speaker looks for the same markers in other airway diseases and said “you’re going to see a wave of biologics coming out of COPD very soon”, with “a lot of conjecture” about whether the eosinophil-high COPD in those trials is simply smoking-related COPD.

Why asthma is hard to diagnose

At the table, someone had said asthma is “really easy to diagnose”. The speaker disagreed: “I find it very hard to diagnose.”

• Proving it for biologic criteria needs evidence: a significant bronchodilator response, a positive mannitol challenge, or peak flow variability. “You usually can find it if you go looking for it.”
• A new patient may need to be watched for a few years with lung function on therapy — asthma is by nature variable. If people come when they are well, “you don’t see the variability”.
• Mimics: many patients who say they have asthma may have vocal cord dysfunction, heart failure or sleep apnoea — all of which can cause breathlessness. “The way patients describe their history, I find [it] incredibly difficult.”

When it is not eosinophilic: long-term azithromycin

For patients whose airway inflammation is not eosinophilic or allergic (the speaker described “more neutral” inflammation, with no eosinophilic asthma), the speaker said long-term azithromycin is “actually quite effective”.

• It is also advocated for COPD and bronchiectasis: “in bronchiectasis, in asthma and in COPD, there is data for specific subtypes to benefit.” It is a chronic therapy, usually three times a week — half a tablet three times a week (the 250 mg dose “still works very well”). The speaker said it is not PBS-listed for this use (as captured). Most trials used 500 mg; the ASR gives “three times daily”, which may be a mis-hearing of three times weekly and should not be relied on.
• Who benefits: patients with lots of sputum production and lots of exacerbations — “it just switches it off”. Most patients tolerate it.
• It is not about the antibiotic effect — it is an anti-inflammatory/immune-modulating effect. Doxycycline “doesn’t have the same” effect.
• Origin story: diffuse panbronchiolitis, a rare, progressive airway inflammatory disease seen in Japanese and South-East Asian populations. About 30 years ago, clarithromycin was tried, and it changed outcomes in a disease that had been killing people in their 40s — because of the macrolides’ immune-modulating effect. The speaker’s warning: “Don’t give macrolides out to everyone.”

Part 2: psychiatric emergencies in general practice

About 22 minutes in, the session moved to a psychiatrist who introduced themselves as an adult psychiatrist who sees patients from about age 20 to 100, does general psychiatry and some other work (the ASR lists “TVA”, “workout” — unclear), and said “I don’t do personality”. The talk was run as a case-based quiz on “emergency day”, following one patient — a man with a long history of depression — through three scenarios. Audience members answered along the way.

Case 1: serotonin syndrome

The patient: a man with long-standing depression, on sertraline for years (the dose and duration are garbled) and on amitriptyline 25 mg at night for insomnia. He has severe back, joint and muscle pain; the pain treatments tried (ASR “neurofem” and aspirin) did not help. His wife says another GP gave tramadol a couple of years ago and it helped. The psychiatrist’s message on the idea of giving it again: “that’s very important, because sometimes it can happen.”

• What you’d hear: “everything goes high” — temperature, pulse, blood pressure, respiratory rate, tremor, reflexes (the ASR says “reference line”), even the QT on ECG.
• First step: “just stop” — stop the tramadol straight away.
• If mild: they can stay at home, with a benzodiazepine (ASR: “diazepam, Dora zip” — presumably diazepam or lorazepam, not confirmed) over the next 24–48 hours.
• If unwell: send them to emergency. ED will observe, keep them for about six to eight hours, give fluids if dehydrated and manage blood pressure (the drug named for blood pressure is garbled).

Case 2: neuroleptic malignant syndrome

Same patient, a different problem: now he has been agitated for three days, is not sleeping even with amitriptyline, is not eating, and is anxious all the time. A previous doctor had given something that helped agitation and sleep. The quiz: you give him olanzapine 5 mg because his wife is very concerned. What might happen in a day or two? The point: even a small dose is a risk — “this man is 75”.

• Features: “pretty much similar to serotonin syndrome, but there is a few characteristics”: fluctuating blood pressure, marked confusion, muscle twitches (as captured), CK “through the roof”, a wide QT, and a symptom the ASR renders “Kotha Noria” (unclear, not interpreted).
• Fever: “really, really worse than serotonin” and can reach 40 (°C, as stated).
• Timing: it does not happen straight away — usually a couple of days after oral dosing, up to a week after an injection.
• Risk: it is “about the antipsychotic itself” — worst if you start at a high dose, increase suddenly, or use two antipsychotics together.
• Action: “you don’t negotiate with them” — an emergency. Stop the antipsychotic. They go as a category 1 in ED; they need IV fluids straight away, sometimes a cooling approach (“cold blanket”), sometimes dialysis and ICU. The speaker had seen it once and said the mortality “can feel scary”. (Drug names for the ED treatment are garbled in the ASR — “anthrople”, “homocytes” — and are not interpreted.)

An audience member (Speaker 2) asked whether a drug like tramadol has a similar effect to a neuroleptic; the speaker was unsure and did not answer.

Case 3: lithium and a diuretic

Same man, one step back: on sertraline (as captured, “150”) and amitriptyline 25 mg. This time he went to a specialist because his mood was very low and he was suicidal; the specialist started lithium 250 (units not captured). Two or three weeks later his wife says he has high blood pressure and headaches, and a check shows blood pressure is high. Which class would you avoid? The audience answered correctly: diuretics, especially loop diuretics.

• Why: diuretics can cause dehydration, and the lithium level may rise “even without any changes in the dose”.
• What toxicity looks like: the audience suggested nausea and confusion. The psychiatrist added that before those, patients complain of something “more than usual” despite drinking (the symptom word is not captured; context suggests thirst), then nausea, vomiting and diarrhoea. When you hear that after a diuretic was added, “start thinking straight away”.
• Action: stop both — the diuretic and the lithium, “at least for now”. “They’re not going to die… psychiatry is not going to be upset if you do that.”
• Tests: a lithium level, renal function and potassium.
• If mild: if the lithium is not that high (the speaker gave “maybe one or 1.1” as an example) and the potassium is fine and symptoms are mild, the patient can stay home and hydrate as much as possible; repeat bloods after two days.
• Trough level? In answer to a question about whether it must be a trough: “it doesn’t matter” at this point — you just need to know where you stand now.

Agitation in older people and nursing homes

• Start low and go slow. For someone aged 65 or above, if starting any antipsychotic, the speaker starts at 2.5 mg (the speaker’s example: “take half a tablet” — the drug is not clear in the transcript).
• Try a benzodiazepine first. An audience member (Speaker 6) said that for irritable, aggressive older patients — especially in nursing homes — benzodiazepines should be tried first, and described people being given antipsychotics and dying within two to three days (the passage is garbled). The psychiatrist agreed: “why use an antipsychotic where you can use something like lorazepam and solve the problem?”
• Paranoia in an older man “can be many things”: part of dementia, a primary psychosis, anxiety, personality, or something else. You have to work out which; at the end of the day the treatment may not differ greatly, but if he is anxious, calming the anxiety may settle the paranoia.
• QTc caution: the speaker said to avoid combining a drug captured as “Kotha bee” (the drug name is unclear — not interpreted) with citalopram or escitalopram, because both can increase the QTc; take particular care in the elderly, in ischaemic heart disease, or with a long QTc.
• Nursing-home agitation, dosing: for the commonest scenario the speaker gave a tiny-dose approach — “a quarter of a milligram, two or three times a day, maximum one milligram” — but the drug name is garbled (“User is paid”) so it is not stated which drug. Olanzapine is acceptable “but just go tiny doses”.
• Pressure from staff and family: “You are in the middle like a sandwich. Don’t feel pressure. Just do the right thing.” Tell them exactly what side effects can happen if you go higher, and let them decide with that information. “If you’re not happy, say I’m not going to treat — that’s fine. You have the right to say that.”
• Empathy for GPs: the speaker acknowledged that GPs work in a short consultation time and often cannot be sure of a specific diagnosis: “most likely it’s going to be this; there could be this or that as well.”

GP clinic checklist

Asthma

1. For people with no asthma diagnosis or who are asthma-naive, think about an ICS-containing plus formoterol approach rather than a short-acting reliever alone, and check the current Australian Asthma Handbook / Therapeutic Guidelines for the exact regimens and maximum doses.
2. Treat the inflammation; use oral steroids sparingly and as short as appropriate.
3. Ask why now? — reflux, sinus/polyps, weight, sleep apnoea, smoking, environment, medicines, mood.
4. Check technique and devices before calling asthma “severe”.
5. Consider specialist review for biologics if still exacerbating (or uncontrolled) on moderate–high-dose ICS; blood eosinophils, IgE and FeNO are the markers mentioned.
6. Keep an open mind on the diagnosis: vocal cord dysfunction, heart failure, sleep apnoea.

Psychiatric emergencies

1. Serotonin syndrome or NMS suspected → stop the culprit drug; unwell patients to ED.
2. Lithium patient with a new diuretic and vomiting/diarrhoea/confusion → stop both, check lithium, renal function and potassium; repeat in two days if managed at home.
3. Older patients: start low, go slow; try a benzodiazepine before an antipsychotic where suitable; avoid stacking QT-prolonging drugs.

Transcript caveats

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