DundeeChest 3.0

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I know this has nothing to do with respiratory medicine, but it’s really good… So good, I’m starting a new category for related posts. I’m the admin, I can do what I like!

Cross posted from my Doc-2-Doc blog.

I did a post take ward round on Monday. The usual mixture of general medicine, with little to excite the respiratory physician. A student commented that I had reviewed a whole bay of patients without the need for a stethoscope. This got me thinking – has the ancient art of auscultation died with my generation of physicians?

Does it matter if we can tell the difference between various murmurs when a portable echo can give us not only qualitative, but quantitative information with one bedside test. We hear fine crackles, an echo an an HRCT tell us what we need to know. 25 years ago our cardiologists taught us how to determine reverse splitting of the second heart sound, and to judge the severity of mitral stenosis from the delay before the opening snap. When was the last time you relied on that kind of clinical finding? Last month I saw a patient with a 5 cm pericardial effusion; there was no clinical indication of that diagnosis at all.
So what’s the point of all this? A senior colleague of mine has long said we should stop teaching our students auscultation, and teach them all bedside ultrasound rom an early stage. I have to agree with him about the ultrasound: we should be definitely be teaching these skills, and I have started teaching all our registrars, and ST grades the basics of thoracic ultrasound. But should we throw away our ‘tubes’? I don’t think so.
Rene Laennec invented the stethoscope on 1816, and it has served us well for nearly 200 years. Although the echocardiogram may have made listening to heard sounds “so last century”, there’s no test to detect bronchospasm, no scan to detect a pleural rub. So as chest physicians, we still need the ‘scope.

A non-physician friend of mine worked with HEMS in the 90’s – he tells me that the real reason we carry stethoscopes is for photo opportunities. What would Laennec say?

Amy, regular DC3.0 user asks:

Hi,
Do we need to know the side effects of the TB drugs…at this stage?
thanks!

It is important to know the drugs routinely used to treat TB, and their side effects.

Rifampicin – Causes orange colouration of tears, urine, and other secretions.
Isoniazid – Can cause a peripheral neuropathy. Co-prescription of pyridoxine reduces this risk.
Ethambutol – Can cause optic atrophy. All patients should have their colour vision checked prior to commencing ethambutol, and advised to seek medical attention if their colour vision begins to deteriorate.
Pyrazinamide – All the anti-TB drugs can cause gastrointestinal upset, but pyrazinamide is the most likely to give significant symptoms.

Rifampicin, Isoniazid and ethambutol can all affect liver function – we accept a 5 fold increase in ALT as being acceptable when on treatment; as long as the patient remains asymptomatic. For further side effects, refer to the BNF (www.bnf.org)

Remember that the standard regimen for proven MTB in Ninewells is Rifampicin, Isoniazid, Pyrazinamide and Ethambutol for 2 months, stepping down to Rifampicin and Isoniazid for a further 4 months if clinical and radiological improvement is seen at 2 month review.

Drug resistance is uncommon in the indigenous population of Scotland, however multi drug resistance is increasingly common in the immigrant population. We have seen only 1 case of extended spectrum drug resistant TB in Scotland thus far.

The commonest cause of treatment failure in Scotland is poor concordance with medication.

Thanks to everyone who made the effort to come along to the revision lecture on Wednesday – I appreciate that the week before the exams is a precious time, and two hours of me waving my arms about at the front of the class, being grumpy about hypoxic drive might not be your first choice of entertainment for Wednesday.

I have been told I was a little bit *too* grumpy, which is probably a fair piece of feedback – I was disappointed that the issues of Respiratory Failure, CO2 retention, and oxygen therapy remain the biggest stumbling blocks for you all, despite me having put in a lot of personal effort to explain these concepts to you all during the respiratory block.

After the lecture I taught a small group of 4th years on arterial blood gas analysis and respiratory failure. A small number of 2nd years tagged along (This is hugely rewarding for me, that 2nd years want to join in with 4th year teaching, so thanks) and it was during this session that I think I’m expecting too much regarding the respiratory failure, hypoxic drive issues: the 4th years have no more grasp of the concepts than the 2nd years. These *are* difficult concepts, and it is likely that the lack of understanding is due to poor teaching, rather than a global misunderstanding on the students part.

This has made me think about how I have been teaching these concepts. i have posted on DC1 and DC3.0 the definitions and explanations of the concepts of both CO2 retention in hypoventilatory states, the concepts of V/Q mismatch, and respiratory failure a couple of times, and each time I’ve tried to make them more understandable, and more straightfoward. I have had little feedback from the students regarding these posts. The videos are helpful, I’m sure, but the students are not getting it.

We have opportunities for students to do fellowships, SSCs, 4th year projects, and extra curricular work developing new learning materials, if anyone is interested.

So the revision lecture on Wednesday? My initial thoughts were of disappointment, and a small amount of despair. When I heard the feedback from a student that I was grumpy during the session, it has made me think more about not just the lecture, but how we teach these difficult concepts. Now? I’m hopeful that someone out there is encouraged enough to come to see me with an idea for a way to teach these topics in a more engaging way.

And I’m allowed to be grumpy occasionally – 365 days a year of manic enthusiasm takes it out on a person, even me!

Confused 2nd year student, Anna, says:

Hi – I’m struggling to comprehend the management of acute asthma. I was just looking in a textbook and at the BTS Guidelines management of acute asthma – but I’m still a little confused.

What do you give and in what order and how much?

I know you give O2 to maintain sats at 94-98% and nebulised Salbutamol – but how much? What is the dose for Ipratropium? – Inregards to steroids again BTS simply mentions “Give steroids in adequate doses in all cases of acute asthma. Continue Pred. 40-50mg daily for at least 5/7 or until recovery” – what is the starting dose? and what is the clinical indication/point at which IV magnesium is considered?
Is there a Tayside Protocol? I’m sure there must be one, but I can’t find it.
Thanks – I’m probably confused over something really simple, but I’d really appreciate the clarification as I don’t want to mistreat a patient one day!

In order:

Oxygen – yes, you have it right.
Salbutamol – 5 mg, nebulised, driven by oxygen, not air
Ipratropium- 500 mcg nebulised, driven by oxygen, not air
Steroids – 50 mg prednisolone PO, or 200 mg hydrocortisone IV. Locally we give 25 mg prednisolone BD for the acute phase, and swap to 50 mg OD for discharge. We usually give 5 to 7 days, or until they get better.
IV Magnesium – it’s on the protocol, and we do use it. 1.2 – 2 g MgSO4 given IV over about 20 minutes. We say to give it if there are any life threatening features. The evidence for it is mixed, but anecdotal evidence is striking. Don’t let IV magnesium administration delay calling the anaesthetists when the patient begins to develop type 2 respiratory failure.

The Tayside protocol is stuck on the wall in ward 15, it’s in the protocol book in ward 15, and it’s on the intra-net somewhere. I’ll try to dig out an electronic version and post it up here.

Laura, stalwart member of PRN, and long time DundeeChest user, has asked about how to make the diagnosis of asthma.

There’s a guideline for that! And in it is has a nice diagram suggesting the signs and symptoms that suggest a diagnosis of asthma, and those which do not suggest a diagnosis of asthma.

Is asthma a likely diagnosis?

When you’ve weighed up the pro and con probabilities, you can determine whether asthma is of high, low, or intermediate probability. If it is highly probable, give a trial of treatment and assess response. If it is of low probability, seek alternative diagnosis. If it is of intermediate probability, spirometry might be helpful, or might not, and a PEF diary might be useful too. A trial of treatment, and early review is usually the most useful test.

Start pharmacological management appropriate to the severity of symptoms, but aim for control of asthma, regardless of severity.

The respiratory sounds lecture I put up on the old DC site has mysteriously vanished!

So, after some shenanigans with FTP uploads, it’s here instead.

Someone has asked me to put up the respiratory revision lecture! I think it was more of a chat than a lecture I can actually put up. I can put up a summary of what we talked about, if you like?

Inhaler technique is clearly important – we can give the patient any drug we please, but it they can’t use the inhaler device properly, they might as well be sticking it up their….

So it begs the question, how good is *our* inhaler technique? Are we the blind, leading the blind? In the kingdom of the blind, the one eyed man is king, lest we forget.

In the Asthma and Allergy Research Group (AARG) the Asthma and Allergy Research Fellows (AARFs) are embarking on a research project to test the inhaler technique of various grades of various health care professionals. They were down at the educational meeting last Friday to test out the consultants (Professor Lipworth assures us that the machine he was using was “Broken, obviously”), and now they want to roll it out to a wider audience. The idea is to do a baseline screen of technique, intervene, and then close the loop. There’s bound to be a poster in it, probably a short paper for a journal. Anyone out there interested in taking part in the research, getting their name on a poster, or even writing a paper?

I have been asked to deliver a revision course to the 2nd years on the whole of respiratory medicine. I have an hour, maybe an hour and a half, following my team roles session at 12:30 on Wednesday. The team roles session should be over by 1:30, and we can decant to a lecture theatre then, and do some learning.

Post your questions in reply to this post, so I can prepare the session – you ask, I answer. Hopefully.

So, tirez.

EDIT: The lecture will now be in LT2, starting at 1pm, as the interest in the team roles session has been, erm, 1 person, so I’ve cancelled it.

Inquisitive user El on the AskDundeeChest page has asked another question!

Would you be able to explain the difference between types 1 and 2 respiratory failure and the pink puffers and blue bloaters?Books are very unclear about this!

Here’s my response, as it might be of use to more students out there:

OK. This is the question I get asked about the most, the concept people get wrong most often, and is consistently poorly understood.

Type 1 respiratory failure is hypoxaemia. The pO2 is low, the pCO2 may be low (due to hyper-ventilation to compensate for hypoxaemia) or normal.

Acute type 2 respiratory failure is hypoxaemia with hypercarbia. The pO2 is low, the pCO2 is high. pH is usually low. This follows type 1 failure, usually because of exhaustion, and consequent hypoventilation.

Chronic type 2 respiratory failure is hypoxaemia, long standing hypercarbia with metabolic compensation. The pO2 is low, the pCO2 is high, the HCO3 is high. pH is normal. This can occur in any disease that causes chronic hypoventilation.

Acute on chronic type 2 respiratory failure is hypoxaemia, long standing hypercarbia with metabolic compensation, and an acute event leading to a further hypercarbia, and consequently, acidaemia. The pO2 is low, the pCO2 is very high, HCO3 is high, the pH is low. Think acute exacerbation of any cause of chronic type 2 respiratory failure.

Forget blue bloaters and pink puffers, the concept is not useful, to my mind.

I hope that helps you all out there!