Past teaching sessions and blog posts
Subarachnoid Haemorrhage or: How I Learned to Stop Worrying and Love Lumbar Puncture.
Like a lot of people, when I read this article in the BMJ that claimed a 100% sensitivity of CT for SAH within 6 hours of onset of headache, I was pretty excited. Finally we don’t have to do the LP anymore! I posted the paper on this blog here, without much comment, hoping smarter people than me would start to talk about it. Well they did, and a lot of people are excited about it. But good old Jerry Hoffman has taken the paper apart on the January 2012 Emergency Medicine Abstracts tape. His expert analysis is well worth a listen if you are a subscriber (if you are not you should be or you should make friends with someone who is). After the jump is a summary of all the reasons this paper doesn’t tell us that we don’t need to do LPs anymore (with thanks to Rick Bukata and Jerry Hoffman).
ARISE and sepsis
Today we had A/Prof Sandy Peake, the lead investigator of the ARISE trial, come and talk about the trial and then Dr Jason Fletcher from ICU. The website for the study is here. Some more details from the session after the jump...
Trauma Outside the Major Trauma Centre
Here is a link to the powerpoint of the talk we gave at the regional teaching day at St Vincent's Hospital on 14th Dec 2011.
After the jump is some stuff that I wanted to get across in the Thoracic Trauma section but which I don't think the slides tell you. All the rest of the slides are pretty good for getting the main messages across. At the end of the page are some other useful links. If you have any please send them to us and we'll add them on.
Quetiapine in the ED
Quetiapine (Seroquel TM)
Quetiapine is a relatively new "atypical" antipsychotic agent. By "atypical" it is meant that it does not act predominantly as a dopamine antagonist and therefore can be expected to be free of extra-pyramidal side effects.
Due to fairly intense marketing it is being used for a wide range of off license indications, particularly as a calmative agent for impulsive or ill-tempered patients with personality disorders, as a mood stabiliser for bipolar affective disorder, and as a sleeping tablet for patients in whom it is judged best not to use an addictive agent. The evidence for its use in these situations is parlous at best.
Primary Exam Stuff
Quetiapine acts at serotonin, alpha adrenergic, histamine and dopamine receptors but its potency at dopamine receptors is a lot less than that of other agents. The mechanism of its activity is opaque.
Effects include sedation and decrease in psychosis.
Side effects include weight gain and hypertriglyceridemia, increased risk of type 2 diabetes and lowering of arrhythmia threshold.
Oral bioavailability is high. Protein binding his high.
Metabolism is largely hepatic and excretion of metabolites is mostly renal.
Half life is 7 hours (and 12 for the active metabolite) so once daily dosing is effective.
In small overdoses quetiapine is a fairly safe agent causing only a low grade tachycardia without QT or QRS prolongation and sedation.
Neurotoxic effects occur in large doses with the familiar pattern of agitation/sedation, seizures and coma occurring at doses over 3g in an adult.
Likewise, cardiotoxicity is dose dependant but is much less of an issue than with antidepressants. Most people will get some tachycardia. In doses of over 3g hypotension can be expected. In massive doses arrhythmias have been reported in a handful of patients only (and co-ingestants might have had a role to play).
Delirium may respond well to physostigmine but this may be at the risk of seizures and arrhythmias.
Both sedation and cardiotoxicity may be significantly potentiated by co-ingestants especially antidepressants but also benzodiazepines and alcohol.
This blog post from The Poison Review looks at an article reporting a case series of massive overdoses.
According to Dr Shaun Greene, Emergency Physician and Toxicologist, quetiapine overdose is fast becoming one of the most common overdoses in Australia so you better get used to it.
Vital signs are vital, and respiratory rate more than any other. Abnormal vital signs and particularly RESPIRATORY RATE predict who is going to have an arrest! Link to MJA article.
O2 Saturation is not a replacement for respiratory rate! Learn to count the respiratory rate properly and when someone presents a case to you make sure they give you a respiratory rate.
And while we are on the topic, this article in The Lancet provides quality data on the normal ranges of vital signs in chldren of different ages and calls into question the established numbers taught in APLS. It is taken from a metanalysis of a large amount observational data of normal children of different ages. Click here for the centile charts generated from that review.