November 2017

Author: Andy Neill / Codes: / Published: 01/11/2017


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Authors: Dr Andy Neill and Dr Dave McCreary

Codes: CC21

Title: Oxygen Therapy in Suspected Acute Myocardial Infarction

Author: Hoffman, NEJM, Aug 28th 2017


– oxygen has come under some recent criticism for potentially being harmful and the current trend in the guidelines for almost everything is to not mindlessly throw on the 15L O2 non rebreather. The AVOID trial in STEMI and the recent OXYGEN-ICU trial were two recent high profile studies that suggested harm with oxygen use.


– this was an open label of RCT of a bunch of centres in Sweden where patient could be enrolled anywhere from ambulance to cath lab (so they’re not all our patients)

– >30 yrs, sats >90 with symptoms suggestive of ACS and either a +ve trop or +ve ECG

– randomised to either oxygen if required or 6L O2 face mask for 6-12 hours.

– primary outcome was all cause death at 1 year. (all included patients had a unique national Swedish identifier that enabled easy tracking and follow up)

– powered (I think) to find about a 3% difference in mortality (assuming oxygen would be beneficial)


– 6200 enrolled (needed 6000)

– 75% were MI (50% overall STEMI) – angina, pulmonary and non cardiac conditions made up the rest

– mortality at one year was 5% for oxygen and 5.1% for no oxygen

– note that this mortality was hugely lower than that was expected in their power calculations (they assumed 15%) this is really common in trials that overestimate the sickness of the population they’re studying which often makes it harder to detect differences – if nothing bad happens to anyone then it’s hard to show a benefit

Bottom Line

– as EM Lit of Note puts it – oxygen is neither harmful nor beneficial in acute MI according to this large RCT.

– However this is just one cohort of not particularly sick and the physiology of oxygen related harm makes much more sense in the chaotic maelstrom of the post arrest or systemically hyperinflammed patient so I doubt oxygen related harm is dead as a concept quite yet.

Author: Charlotte Davies

Codes: CAP 17

In a lot of places I work, headaches either go home for GP review, or get admitted as a possible SAH. And if they’re a possible SAHs, they get a normal CT in six hours (maybe) and many go home without an LP. This really worries me, as there’s loads of other serious causes of headache I don’t think we exclude thoroughly. In the “old” days, a second doctor generally reviewed the ?SAH to do (or get the results of) a lumbar puncture. So one of the diagnoses we could be missing that worries me is a cerebral venous thrombosis – this is dangerous to miss.

Is there a difference between cerebral venous thrombosis and cavernous venous sinus thrombosis?

CVT and CVST have common underlying etiologies including thrombosis, and terms are occasionally used synonomously. CVST is specifically thrombosis in the cavernous sinus, normally with infection, so cerebral venous thrombosis is a safer term.


If you can’t remember your venous sinus anatomy, check out Andy’s posts on emergency medicine ireland. I can not think of a better way to learn anatomy.

At a very basic level, what happens is you get a clot in one of the veins in the head, which causes problems. At its worst, this can cause death and coma. Middling effects present as a stroke, especially now anyone slightly lopsided seems to get a stroke call. At the “mild” end, a headache may be the only presenting symptom.

There are lots of theories about what is happening to cause these symptoms. It is thought that venous occlusion leads to the development of collateral veins, which combined with altered arachnoid absorption of CSF causes cerebral oedema – which can cause the headache. They can also cause cerebral venous infarction (in 50% of cases) and even haemorrhage.

Risk Factors

  • Excess Oestrogen:
    • oral contraceptive pill: very common cause in female patients <50 years of age
    • pregnancy, IVF
    • puerperium – more common then than in the pregnancy
  • Clotty
    • prothrombotic haematological conditions: 35%
    • g. prothrombin 20210 (factor II) mutation
  • infection: especially mastoid sinus (dural sinus occlusive disease – DSOD)
    • systemic illness
    • dehydration: e.g. gastroenteritis
    • Sepsis
    • Malignancy
    • connective tissue disorders
  • Local Factors
    • skull abnormalities/trauma
    • compressing mass: e.g. meningioma
    • Steroids
  • Idiopathic: ~12% – this is worrying. If you’re going to get a rare disease, being in the rarest bit of rare is unlucky!

Presenting Features

Headache (70-90% of cases)

  • There is no particular “type” of headache, but it is normally persistent. Onset may be sudden, like in sub-arachnoid, or gradual. Most patients present with symptoms that have evolved over days or weeks.
  • Headache is the most frequently (8090%) occurring symptom in cerebral venous thrombosis and often the first symptom reported by patients. The International Classification of Headache Disorders describes the headache as having no specific characteristics[2] but one study found the headache was usually acute or subacute in onset, localised, continuous and moderate to severe.[23] Cases have been reported where headache is the only neurological symptom or sign but this is very rare.


  • Stroke without any typical risk factors, especially in young people may be due to CVT. Up to 75% of cases have focal deficit and headache.
  • Diplopia here (CN VI palsy) is a focal sign here, and should stimulate you to look for papiloedema…and really think hard about CVT.
  • Symptoms are not always classic, but they can be associated with the thrombus location.3,4
    • Cortical vein thrombosis presents with motor and sensory deficits, as well as seizure.
    • Sagittal sinus thrombosis may present with motor deficits, bilateral deficits, and seizures.
    • Patients with thrombus in the lateral sinus may present with intracranial hypertension and headache alone.
    • Thrombosis of the left transverse sinus can present as aphasia.
    • Thrombosis of the deep venous sinus can cause behavioral symptoms due to lesions in the thalamus.
    • Cavernous sinus thrombosis is associated with ocular pain, chemosis, proptosis, and oculomotor palsies.


  • Seizures occur in 30- 50% of presentations, and they are often followed by a Todd’s paresis. Superior sagittal sinus thrombosis (4%) can present with bilateral or alternating neurological deficits.

Coma or encephalopathy

  • This isn’t common, but you can get a rapidly progressive illness with deepening coma, headache, nausea and pyramidal signs, due to extensive involvement of the deep cerebral veins.

More often other clinical manifestations present at onset or develop during the course of the disease. These include papilloedema, focal deficits, altered consciousness, seizures and cranial nerve signs, in particular diplopia caused by sixth nerve palsy. Psychosis, in conjunction with focal neurological signs, has also been reported.[25] The development of symptoms may occur over hours, days or even weeks.

Examination Features

  • Papilloedema
  • Altered vision
  • Neurological symptoms


Examination of the cerebrospinal fluid (CSF) does not necessarily help in establishing the diagnosis as there are no pathognomonic features. Abnormalities are found in up to 84% of cases and include raised CSF pressure, increased protein content, the presence of red blood cells and pleocytosis. D-dimers probably not useful


CT – Often normal, but there may be subtle hyperdensity of the affected sinus or vein for the first 7 – 14 days. May have associated venous haemorrhage or infarction. Haemorrhagic infarcts may be multiple, in no particular location.

String Sign

Seen in 25% of patients with a cavernous sinus thrombosis. It looks like elongated hyperdense image relating to the brain parenchyma.

Dense Triangle

This can be seen in the first two weeks in up to 60% of patients. Fresh, coagulated blood causes a superior sagittal sinus opacification. The opposite of this is the empty delta sign, where contrast is administered highlighting an intraluminal filling deficit. It is not a specific sign.


Anticoagulation – In the last Confidential Enquiries into Maternal Deaths in the United Kingdom report there were four deaths from CVT compared with eight in 200305.[22] The previous report expressed the hope that increasing application of thromboprophylaxis among at-risk women will reduce deaths from both pulmonary embolism and CVT but figures are as yet too small to draw a conclusion.

General measures like proper headboard inclination, adequate oxygenation, and protection of airway due to risk of bronchoaspiration are recommended (although now this has been disproved in stroke, I wonder if its accurate).

Anti-convulsant treatment after even a single seizure is reasonable

Author: Jeff Kline, Andy Neill

Codes: CMP5, HMP4

Jeff Kline is an Emergency Medicine and Thrombosis Physician and Researcher in the USA.

He has a massive research portfolio but is perhaps most famous for the PERC Rule

In this podcast we chat through the thorny issue of reperfusion in PE – what’s the evidence, what are the limitations of that evidence and when should we pull the trigger on lysis.


Authors: Becky Maxwell, Chris Connolly

Codes: CC19, CAP 30

Becky and Chris review RCEM’s recent document outlining the mental capacity act and how it relates to emergency medicine.

Authors: Dave McCreary, Andy Neill

Codes: CC21

Title: Emergency Department use of Apneic Oxygenation versus usual care during rapid sequence intubation: A randomised controlled trial

Author: Nicholas Caputo et al. Academic Emergency Medicine. August 2017.


Apnoeic oxygenation has been an EM and twittersphere hot topic for years. The idea is popular as its a pretty straightforward idea, has physics on its side, and we like the thought of anything that can prevent the dreaded sound of the sats monitor tone telling us our critically ill patient is desaturating. Until now though studies into its effectiveness have been confined to operating theatres and the ICU leaving us to question the relevance of those studies to our practice in the trenches.


  • Single centre RCT
  • Inclusion: All adult patients requiring intubation
  • Exclusion: Patients in cardiac arrest (traumatic or medical) AND patients that didnt have pre-oxygenation
  • Intervention: Apnoeic oxygenation (AO) – nasal cannula at flush rates (15 LPM)
  • Comparison: Usual care (UC) – No supplemental oxygen during laryngoscopy
  • Primary outcome: Average lowest oxygen saturation recorded during apnea period or the two-minutes following intubation
  • Secondary outcomes: Difference in rates of: first pass success rate, saturation <90% and saturation <80%; average time to desaturation; mortality


  • 206 patients enrolled
    • 6 received wrong intervention for their group and observation stopped so excluded
  • Pulmonary pathology most common reason for intubation
  • Primary outcome: no difference in lowest average O2 saturation
    • AO – 92% (95%CI 91-93)
    • UC – 93% (95%CI 92-94)
  • No difference found in rates of moderate (<90%) or severe (<80%) desaturation

Bottom Line

Apnoeic oxygenation may not have an impact on degree or frequency of desaturation in the truly pre-oxygenated group of patients. These are necessarily the patients were most interested in though – what about the crash intubations – or the patients with truly prolonged apnea times (the 15 reported prolonged apnoea times averaged 144 seconds, and in pre-oxygenated patients without a pulmonary pathology) – I dont think this trial answers the question for that population. So yes, for now the jury is still out, but it still seems reasonable to me to use a harmless intervention which hasnt been shown to not be beneficial to the people that may need it most. (Apologies for the wander down Double-negative Lane there).


  • RebelEM have a nice blog on this and on the FELLOW trail if you would like a remind yourself of it

Simon Carley has a great critical look at this paper on the St. Emlyns Journal Club

Authors: Becky Maxwell, Chris Connolly

Codes: CC19, CAP 30

Becky and Chris review RCEMs recent document outlining the mental capacity act and how it relates to emergency medicine.

Emergency Geriatrics – managing pain and agitation

Author: Rosa McNamara, Andy Neill

Codes: HAP 35

Rosa McNamara is an Emergency Physician working in Dublin with a specialist interest in care of the older patient.

We talked in this session about management of the older patient in the ED with agitation. Most of this is non pharmacological and is based on good nursing care and giving older patients the time and attention they need.

Assessing bleeding risk with anti-coagulation

Authors: Kerstin DeWitt, Andy Neill

Codes: HAP 7, CC3

Kerstin De Witt (nee Hogg) is an Emergency Physician and Thrombosis Physician and Researcher in Canada

We talk about some key questions we should ask before we start anticoagulation on VTE patients in the ED.

1) Any history of serious bleeding?

2) What’s the creatinine clearance?

3) What are the other medications?

4) What’s the Hb – is the patient slowly bleeding?

5) How old is the patient?

6) Is there associated cancer?

Authors: Becky Maxwell, Chris Connolly

Codes: CC19, CAP 30

Becky and Chris review RCEMs recent document outlining the mental capacity act and how it relates to emergency medicine.

Authors: Andy Neill, Dave McCreary

Codes: CC21

Title:Short term use of oral corticosteroids and related harms among adults in the United States: population based cohort study

Authors: Waljee, March 2017, BMJ


– we like giving short courses of steroids almost as much as we love polishing off the elderly with NSAIDs. At least for the NSAIDs we know there’s significant harm. But we tend to see steroids as a freebie with only the occasional “roid rage” and high sugar to worry about. This trial is maybe pause for thought.


– this is an insurance company based registry. In the states this is one of the most reliable ways to get data about patients as there’s lots of money involved so people write lots of things down. It’s also not perfect as they tend to write down the more financially relevant things and of course the intended purpose of the data collection is quite different from what we’re currently looking at it for.

– all that said…

– they looked at people aged 18-64 (older than this they joined medicare and left this registry) who got prescriptions for steroids

– they excluded inhaled and lots of chronic steroid users to try and focus on new short term steroid users (this was defined as <30 days which is still fairly long in my book)

– using all kinds of assumptions they then try to link the prescription to the specific physician (this is not easy in the states apparently…)

– they then went looking/fishing for 3 specific steroid complications (sepsis – fair enough, VTE – that was new to me – and fractures – surely more of a long term issue?)


– 1.5 million of whom 20% (330000) got a steroid prescription over 3 years

– roughly half were less than 7 days (what we do) and half were longer than that.

– folk who got steroids were more likely to be older woman with comorbidities (possibly the most important phrase in the paper…)

– highest uses were for chest conditions (fair enough) and low back pain (this is a thing in the states which despite quite a lot of evidence against it seems to persist)

– those who received steroids all had more presence of sepsis, VTE and fractures compared with those who didn’t

– they use something called a “self controlled case study” approach where each individual becomes their own control. Eg for the first year of the study when they didn’t get steroids they looked at outcomes and then for the second year after they got the steroids they looked at the outcomes. The idea being that events since the steroids suggest causality

– the self controlled case study does at least suggest that the steroids were temporally related to the outcomes however the diseases for which they were prescribed steroids were also temporally related to the outcome of interest so it still doesn’t really establish causality.

Bottom Line

– short term steroid use is associated with some adverse outcomes here but unclear if it’s the underlying conditions or the steroids that are the cause.

– kudos to Richard Lehmans weekly review of the literature for this one.

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