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Found this in an old not in an old app and thought it was still a reasonable summary for EM purposes

Summarised from rosens 8th chapter 116

As always, happy to take comments and more importantly corrections!

Polyarteritis nodosa

  • Digital cyanosis

Takayasu’s

  • initially fever weight loss constitutional symptoms
  •  late followed by pulse differences and limb ischemia

Giant cell

  • affects internal (supplying the eye) and external (supplying masseter and superficial temporal) arteries.
  • if amaurosis fugax think GCA and stroke.

Buergers

  • smoking is key
  • typically lower limb pain and claudication.
  • associated ulceration

Bechet’s

  • chronic relapsing
  • oral ulceration early and essential
  • eye involvement about 70% (iritis)
  • can affect both small and large vessels

Wegener’s

  •  respiratory tract and kidneys
  • commonest manifestations are sinus related so good luck trying to diagnose that
  • can present as glomerulonephritis which will hopefully be easier
  • high (>80% 1 year mortality untreated)

Churg Strauss

  • linked with atopy (part of the diagnosis)
  • usually a couple of years of asthma symptoms prior to diagnosis

Microscopic polyangiitis

  • commonest cause of pulmonary renal syndrome (haemoptysis and glomerulonephritis)
  • mainly seen as rapidly progressive renal impairment

Goodpastures syndrome

  • I struggle to see anything that would clinically help me differentiate this from microscopic polyangiitis
  • both have alveolar bleeding and renal failure

HSP

  •  this is one we actually see fairly commonly
  • Often a preceding URTI
  •  rash arthralgia commonest
  • Abdominal pain and kidney problems too
  • usually self limiting over about 2 months
  • recurs in up to a third

Hypersensitivity vasculitis

  • usually drug related(though hard to prove)
  •  skin findings like HSP but no systemic findings

Mixed cryoglobulinemia

  • cryoglobulins are immune complexes that precipitate at 4 degrees
  • purpura weakness arthralgias
  • viral infections hep b and c EBV and CMV
  • if the cryoglobulins precipitate in the kidneys then there’s problems

Erythema nodosum

  •  inflammation of venules of skin
  •  strep sarcoid and TB are things that should come to mind.
  • Inflammatory bowel disease is a very uncommon cause of nodosum.
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As adapted from a recent local teaching session I prepared.

As a broad topic it appears as a common textbook chapter in EM textbooks and there’s a number of nice #FOAMed posts on the topic (referenced below)

Neutropenic Sepsis

The most common, and I would say the most important one. We a lot of this in pretty much every department I’ve worked in. Because it’s so well recognised it should have almost a knee jerk, protocolised response.

In a nut shell, many chemotherapy agents suppress the bone marrow and suppress neutrophil production (amongst other things). Radiotherapy can do it as well but quite uncommon. Neutrophils form a key part of host response to infection. The chemo also adversely affects many mucous membranes and GI mucosa and barriers that are normally resistant to translocation of bugs (bacteria and fungi) are now open. The combination of the bugs in the wrong places and a deficient host response leads to overwhelming sepsis without appropriate treatment. Finally the underlying malignancy itself can interrupt the immune system (think of haematolgical malignancies destroying bone marrow) leading to their own types of infections.

Clinical Presentation

expect to see someone on chemo either mid cycle or recently finished. Given the bewildering number of potential options it’s hard to say when the nadir of neutrophils will be following the most recent chemo. When I first started 7-14 days post chemo was considered a common danger time.

Patients are well educated to be wary of fevers and present if they have one even if they feel well. You might get lucky and they might have actual symptoms pointing you to a source but a lot of the time all you will have is fever.

We often shoot for the low hanging fruit of urine and chest infections but the key take home is to look in unexpected places. 80% of the bugs are thought to be endogenous to the patient.

  • mucositis can be an entry point for bugs
  • lines
  • pressure areas
  • biposy sites
  • internal metal work (eg biliary stents)

In terms of bugs (adapted from UTD article)

  • Gram-negative bacteria (eg, P. aeruginosa) are generally associated with the most serious infections.
  • S. epidermidis is the most common gram-positive pathogen, accounting for approximately one-half of all infections due to gram-positive infections. It is much less virulent than other bacterial pathogens
  • Although anaerobic bacteria are abundant in the alimentary tract, they are infrequent pathogens isolated from patients with neutropenic fever. However, they can contribute to the pathogenesis of necrotizing mucositis, sinusitis, periodontal cellulitis, perirectal cellulitis, intra-abdominal or pelvic infection, and neutropenic enterocolitis (typhlitis) and can cause anaerobic bacteremia.
  • Polymicrobial infections are infrequent, but their frequency appears to be rising
  • A bug is only identified in about 20-30% of presentations
Investigation

one of the rare instances where blood cultures are really important. try and get them as clean as possible and consider the other sites like wounds and throats.

usual bloods as you would for any septic patient

The definition of neutrpaenia for our purposes is ANC <0.5 (though anywhere under 2 in context would make me twitchy)

Management

Most of the principles of sepsis apply here.

There will almost certainly be a local antibiotic protocol. NICE recommends piperacillin/tazobactam. It does not recommend routine gent but allows this to be modified locally. Importantly they want us to give the antibiotics if we “suspect” neutropenic sepsis – we don’t have to wait for the ANC result.

I find that almost all of the “suspected” patients will get admitted in Irish practice. Even if the ANC comes back at 1.3 – if they’ve had a fever and chemo they almost all will come in overnight.

Of note NICE does allow for out patient management but there’s lot’s of caveats to it and they have to be very low risk.

There are scores available for risk stratifying them so it’s nice to know they exist but I don’t think they’re currently that relevant to local practice. The MASCC (not that one…) or the CISNE score are the key ones to remember.

The one thing to consider is fungal infections. They’re much less common that bacterial. We should think about them in the highest risk patients (stem cell transplant is a good example) and indeed the MASCC score can be used to risk stratify people to the highest risk.

If you’re seeing someone with recurring neutropenic sepsis then the best tips would be to check what bugs they grew last time and again consider antifungals as recurrent neutropenic sepsis should make you think of it.

Viruses are common in the highest risks patients but they are usually already on prophylaxis.

SVC Syndrome

this is rare (I think i’ve seen it once) but very cool in terms of its presentation and pathophysiology. I covered it once before and reproduced it here.

Two main causes

  • malignancy 80%
  • thrombosis 20%

For malignancy think right sided lung and mediastinal masses. Anything that can compress the SVC as it returns to the right atrium

Classically this will be non small cell lung cancer followed by non Hodgkin lymphomas

For thrombotic causes then there’s usually a precipitant in the form of an indwelling line

  • dialysis, port, Hickman, pacer etc…
  • this is the same as for upper limb DVT in general – there’s usually a cause.

A big clot in the major veins returning to the heart would be expected to be a big cause of PE but this seems uncommon. There also seems to be a differentiation between clots on the line (sleeve thrombi) which more commonly cause PE, as opposed to clot on the wall (mural thrombus) which embolises much more rarely.

Presentation

  • dyspnoea the commonest (presumably a mixture of reduced venous return and neck vein distension)
  • usually there are facial changes – swelling, redness, especially with bending forwards
  • Pemberton’s sign is redness in the face on raising the arms, presumably congestion with increased venous return from the arms.

Investigations

  • CXR usually abnormal (though up to date quoted 85% only)
  • ultrasound can usually only view the vessels immediately proximal to the SVC but you can get indirect information by looking at Doppler waveforms with a valsalva (you were all doing that already for your DVT scans weren’t you…)
  • unsurprisingly CT is the best test as the key treatment decision is finding out whether this is a malignant SVC obstruction vs a thrombotic SVC syndrome
  • the next major treatment decision point is biopsy if malignant. The decisions regarding radio and chemo that the oncologist will be driven by this.

I mention the last point to emphasise that while this is an important cancer emergency the time scale is quite different from something like neutropenia sepsis.

In health systems where access to CT at 2am is limited then this is a CT that can wait. SVC is rarely an immediately life threatening emergency and intervention (such as stenting, radio, biopsy and chemo) can all wait till daylight and as a result the CT can probably wait till morning too.

Case courtesy of Dr Henry Knipe, Radiopaedia.org. From the case rID: 28046

Hypercalcaemia

This is common, and also something covered here before.

This is commonly picked up because the person before you randomly ordered some tests and this came back high. Occasionally you might actually suspect it but mostly you’ll just be fishing. The symptoms are typically quite non specific so it’s always worth considering.

Levels about 3 are when it becomes symptomatic and interesting. 2.5-3.0 are still important in terms of a diagnosis but are unlikely to make anyone sick

Once you have a high Ca then consider causes

Malignancies

  • myeloma
  • breast
  • renal
  • lung

A lot of this is due to bone mets which makes sense, however 20% have no bone mets and even in those with bone mets the commonest mechanism of hyper Ca is known as Humoral hypercalcaemia and from the tumour in question producing “parathyroid hormone related peptide”

Other causes

  • hyperparathyroidism
  • paraneoplastic syndromes
  • sarcoid
  • addisson’s
  • dehydration
  • drugs
    • lithium
    • thiazides
  • prolonged cuff time when measuring

There are some ECG changes (which are probably irrelevant but they’d be good as an exam question

  • QT shortening (of note in hypocalcaemia the QT gets longer but that’s about the only ECG change
  • J waves (osborne waves) can happen
  • eventually can have ventricular arrhthmia
  • widening of the QRS
Management

from our point of view it’s primarily fluids. bisphosphonates, calcitonin and diruetics probably all have a role but in the timescale we’re interested fluids and a catheter and good fluid balance is all we need to do.

Cord compression

Hopefully you all know that a history of cancer is a red flag in a back pain presentation. This can be quite a remote history especially if it’s breast cancer where recurrences 10-15 years after treatment are fairly common.

Lung, kidney, breast, prostate and myeloma are common causes here.

Back pain is obviously a common presentation but radicular symptoms and lower limb or bladder issues should also prompt you thinking about it. Any time you have a possible cauda equina patient you should consider malinancy. You might get lucky and see a lesion or a collapse on an xray but ultimately you’re gonna need MRI to see the cord. Be sure to MRI the whole core as multiple levels may well be involved.

The thoracic spine has the most number of vertebra and highest blood supply and therefore gets the most mets followed by the lumbar. You can get mets to the meninges and the cord itself but >90% are external compression from a bony met or collapse.

There’s definitely a role for “emergency” radiotherapy here but be realistic – that means radio within a week… Just because it’s cancer don’t skip orthopaedic invovlement as some of them are grossly unstable needing surgical fixation.

As with any time there’s CNS oedema (think brain mets) then steroids probably have a role. Though by the time you’ve got diagnosis with MRI I suspect someone else will be making that decision.

Further Reading

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Emergency Medicine Ireland by Andy Neill - 6M ago

Just a little heads up.

A few friends are planning a 3 day PoCUS extravaganza in Dublin on June 5th-7th at RCSI.

It’s got something for everyone including a basic level 1 course, a “train the trainer” course for those keen to up their PoCUS education skills and there’s also the return of the great EGLS course for one day only. The third day will be for the advanced learners with a mixture of advanced echo and regional anaesthesia.

You can book just one or even all 3 days, whichever you prefer. There’s a bunch of international faculty on their way so you can be sure you’ll be taught at the highest level.

For all the details and registration check out SonoDub.com.

International candidates are of course very welcome and it’s a great opportunity to see Dublin and the rest of Ireland.

Conflict of interest (in case you’re wondering…)

  • I designed the website but am not paid for that
  • I will be teaching on the EGLS course and will receive payment as an instructor.
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This batch of the tasty morsels series are various pearls and learning points from my most recent 6 months doing paeds EM. I’d done a fair bit of paeds before but never in a dedicated children’s hospital and it was all a long time ago. Turns out there’s always more to learn. These are mainly observations and anecdotes even more so than usual!

Ultrasound for LP

The commonest reason we do LPs in kids is the febrile neonate. This is currently shifting ground and consensus is somewhat lacking but the certainly under 2 months a child with a fever will end up getting an LP whether or not you find a UTI or a bronchiolitis or whatever.

So for now there’ll still be lots of LPs in tiny babies. In general I find them easier than adults. The distance involved from skin to CSF is much shorter and generally the landmarks are fairly easy to identify.

Tips:

  • Sit the child up
    • there are few things that look more awkward than a sitting neonate. They’re just not really built for it. So you need a skilled holder (probably more important than the person with the needle!!!)
    • I only did this for the first time in the past 6 months and found it a massive improvement. Makes finding the mid line and keeping the needle perpendicular to the spinal canal much easier
    • There is an RCT on this that showed no significant difference in lying versus sitting so this one definitely seems to be a personal preference on my part
  • Ultrasound
    • I’ve done this in adults quite a bit and find it useful. Like with a lot of ultrasound things you do need a degree of competence and confidence in interpreting the images otherwise you can just confuse yourself. And it’s still and adjunct, not a magic bullet
    • In kids the anatomy looks beautiful and it allows you to mark the ideal site and have an idea of depth from skin to CSF pocket. That way you don’t put the needle in too far and end up with urine from an LP which is never a good look…
    • The most recent paper I’ve seen on this is this one which we also discussed on the RCEM Learning podcast
      • they had 130 patients randomised to ultrasound guided LP or not
      • ultrasound increased first pass success from 30 (pretty awful) to 60% (acceptable)
      • They were mostly very novice proceduralists
Ultrasound for IV access

This is pretty much my all time favourite ultrasound application and was keen to see how it fitted in with kids. I spent the first month trying to optimise it for the really tiny bubs and it was less than satisfying. Definitely had a few successes but 24G or 26G cannulas are almost impossible to visualise with a standard linear probe and the wriggliness at the ACF just makes it tricky.

My favourite tip was to use it in a similar manner to the ultrasound for LP. Instead of live guidance I’d use an “X marks the spot” on the back of the hand as a guide for where the vein was. This works best in the 6 month old “michelin” baby with rolls of fat. You know there’s probably a vein over the ring finger metacarpal but you just can’t see it. The Ultrasound lets you see it and mark it and then you just proceed with your normal cannulation technique.

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This batch of the tasty morsels series are various pearls and learning points from my most recent 6 months doing paeds EM. I’d done a fair bit of paeds before but never in a dedicated children’s hospital and it was all a long time ago. Turns out there’s always more to learn. These are mainly observations and anecdotes even more so than usual!

Hand, foot & Mouth (& Bum)

  • Should definitely have the “bum” part added as it’s clear that perineum gets a rough time of it in this disease.
  • Expect a variety of lesions in the same patient – some fine macular stuff, some papules and in the mouth and oropharynx look for the vesicles. it’s another one of the rashes for soles and feet which might help clinch it for you.
  • mainly enteroviruses (transmitted through the gut) of which coxsackie A variants are the majority of causes. There are at least 20 different coxsackie types hence the recurring infections that some poor kids get.
  • Can be shed in the stool for 10 weeks hence the almost certain likelihood that someone in your child’s creche is carrying it at some point.
  • Herpangina is HFM’s cousin that presents with oral lesions only.
  • PR diclofenac occasionally works wonders in the child who is dramatically failing their trial of fluids in the department.
  • I warn parents that don’t be surprised if the fingernails fall off after they get better. And reassure them that they grow back. That was more from family experience than reading but it’s definitely a thing.

Roseola

  • I somehow missed that this existed. This is “sixth” disease. Also bizarrely known as baby measles. (think of it in the 6-18 month range mainly)
  • It’s a lovely little diagnosis to make, 3 days fever then bang, fever goes and rash appears. Always makes you look smarter than the doc before who diagnoses some non specific URTI and you come along and make a positive if somewhat obscure and irrelevant diagnosis. It’s the little things…
  • Human herpes virus 6 is the common culprit and we seem to shed that asymptomatically life long so good luck with isolating that one…
  • One report states that 13% during the febrile phase (before the rash) can have sterile pyuria which may well get treated as a UTI pending the culture. It then causes even more confusion when the fever settles (as it should in a UTI on antibiotics) and a rash appears and now you’re blaming an antibiotic reaction.

Urticaria

  • almost always viral and seem to respond really well to antihistamines – as opposed to adults where it seems you see lots of adults with urticaria for whom the antihistamines do little
  • as a result you don’t seem to need steroids in the way we do in adults. (when I say “need” I of course mean the “need” to do something to make the patient feel that we’re doing something for them.)
  • the one I got caught out on was multiforme. Which again is usually benign but it definitely has much clearer edges with the central clearing and has a potentially more serious differential even if it usually isn’t.
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I’m back at the European Society for Emergency Meeting for another couple of talks (older ones can be found here , here and here…).

I have the luxury of getting to pick my topics which gives me the opportunity to express my love of the uncommon but important in emergency medicine.

Cerebral venous thrombosis, or whatever term you wish to call it by, is one of those great and rare diagnoses. It has a myriad of presentations from the ambulatory to the super sick and is frequently missed or delayed in diagnosis.

Spoiler

This is actually something i covered on the AFEM podcast years ago and is worth watching for a quick review

The anatomy here dictates the clinical findings. Non arterial distribution bleeding is a big clue. Most SAH comes from the circle of willis so expect to it there. So if you see blood lying along side the falx cerebri then it may well be venous bleeding from high pressure in the sagittal sinus. In this case the blood is along the left transverse sinus

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org. From the case rID: 5522

You may see non arterial territory infarcts as well. As flow from the cortical veins backs up you can get venous infarcts like this right parietal lobe infarct here.

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org. From the case rID: 5522

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Is it common?

this is a rare disease. I’m still in the single figures for the number i’ve seen personally over 15 years. You will see more strokes, migraines and even sub arachnoid haemorrhages than this.

it’s counted as a stroke but it’s <1% of strokes.

though it remains really important to  be on our differential as it has a specific diagnostic and management pathway that differs from many of the other causes of stroke. they also tend to be much younger patients without the long comorbidity list of the typical stroke patient

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What are the risk factors?

most people seem to forget this but for something like PE, up to 50% have no discernible risk factor for thrombosis in the lungs.

in CVST it seems from the data we have that most people will have some risk factor identified but it’s clear that it is possible to have CVST without any identifiable risk factors. (UTD quotes 85% have a RF)

there’s a female predominance of 3:1 likely reflecting the hormonal risks surrounding OCP and pregnancy

most of the RF are the same as for VTE anywhere else. it’s the venn diagram of hyper coagulability, reduced flow and endothelial trauma

for hyper coagulability think OCP use, pregnancy and particularly the post partum period. things like lupus or factor V leiden also in there.

in terms of tissue trauma or poor flow think recent surgery or even recent concussion type injuries has been reported. the nasty ENT infections show up here too – the invasive mastoiditis sinus infection has been implicated also.

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How do these patients present?

First division is sick/not sick. We’re typically pretty good at this. However we make different kinds of diagnostic errors with each different group.

CVT can present with a number of syndromes. In the lecture I gave 4 case examples:

  • Case 1: The seizure
  • 30 year old female 2 weeks post part from a normal delivery of a beautiful baby girl.
  • she arrives in status epilepticus, quickly settled with some bentos. you notice she’s not moving her right arm. Her CT shows a parietal haemorrhage

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org. From the case rID: 5522

  • Case 2: The Headache
  • in ambulatory care you have a young female with no past history with a severe, thunderclap headache. She’s on no meds apart from the OCP. Your CT looks OK, it’s within 3 hrs. Should you just stop there. Does she need the LP? Something in the back of your head (no pun intended…) tells you you’re missing something

Case courtesy of Dr Andrew Dixon, Radiopaedia.org. From the case rID: 32376

  • Case 3: The head injury
  • a 40 year old man presents a week following a head injury and concussion. His CT showed a linear unrepressed skull fracture and he’s on no anticoagulants. He’s now had increasing right sided weakness over 2 days and worsening of his headache from the head injury. You skip the repeat CT and go straight to MR and you see this in the left cerebellum.

Case courtesy of Dr Hidayatullah Hamidi, Radiopaedia.org. From the case rID: 52813

  • Case 4: The infection
  • This young male attends with a recurrent and worsening right ear pain and discharge. He had surgery a month ago as part of treatment for mastoiditis. He now has numbness in his right hand and difficulty grasping his keys.

Case courtesy of Dr Dalia Ibrahim, Radiopaedia.org. From the case rID: 28971

These cases form a wide range of presentations from the super sick patient to those headaches in your ambulatory care area.

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The super sick

These guys will all be getting imaging and lots of supportive care. We do our ABCs and get a scan and see infarct or blood and that’s the end of our diagnostic reasoning process delaying what might be definitive care and imaging.

the bleeding we’re going to get in CVST is venous typically and so you might see sub arch blood in an unusual place like up at the superior part of the brain along the sagittal sinus. arterial aneurysmal blood should be around the circle of willis and the MCA.

if we see infarct we think stroke but stroke is again an arterial disease and we expect to be in typical arterial territories as shown here.

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org. From the case rID: 10814

Remember the infarcts in CVST are venous typically lying adjacent to the venous drainage and cross arterial territories.

If you have a good radiologist then they’ll probably pick up on this but we rarely give them a good enough clinical picture to do their job properly so go and talk to them and discuss the case

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The not so sick

The typical presentation here is one of severe headache and rightly so top of our list is SAH and we focus our work up on that.

We can make the mistake of going down the routine ED headache pathway to rule out SAH. Either doing the CT early and rightly ruling out SAH and missing the CVT. Or we do the CT and LP but miss or ignore the key features on the LP.

It’s not that the work up we’re doing in the either the sick or not sick patients is wrong it’s just that we don’t keep our differential broad enough to go the extra few steps to make the diagnosis

In terms of LP there’s a few features that might point it out. remember in this not sick patient you’re not expecting the LP to be abnormal, you’re not expecting meningitis here. you’re really doing it as part of your SAH work up. a high opening pressure , a raised lymphocyte pleocytosis and a high protein level are present in various combinations in 50% of CVST

if you’re used to doing your LPs sitting (which i generally find easier) then you’re missing out on opening pressures. get out your manometer and measure the pressure. a high pressure is considered >20cm of CSF.

Idiopathic intracranial hypertension (formerly pseudotumour) is the main differential with a conscious patient with normal CT and high pressure.

Incidentally if it’s low (<6) then you might be looking at a CSF leak headache.

none of these LP features are especially specific for CVST. all they are are prompts to consider expanding your differential.

Jeff Perry’s work in SAH has been brilliant and I think rule out SAH with an early CT is perfectly reasonable. But we’re still not off the hook for all the other causes of SAH and we have to maintain that differential diagnosis.

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Making the diagnosis

you might get lucky and have some findings on the non con CT scan. remember the hyper dense MCA sign that you see in stroke? this is analogous to this for veins. Acute thrombosis can appear hyperdense on CT.  Here on the left you have some hyper density of one of the cortical veins and the post part of the superior sagittal sinus.

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org. From the case rID: 4408

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org. From the case rID: 4408

if you add some contrast and time it right you can get a venogram and here we have the “empty delta sign” with contrast surrounding a clot in the sagittal sinus

In terms of CTV v MRV the AHA guidance on this views CTV and MRV as equivalent. MRI is probably a little better but honestly this will come down to whatever your radiologists are happy with so don’t get too worried about it.

Should we used dimer as part of our diagnostic work up?

Probably not but maybe.

There’s not much out there on it. there have been some small studies but given how badly we’ve used dimer in VTE, I doubt it can be used in a disease state with even more heterogeneity in presentation than PE.

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How do we treat it?

We do all the usual supportive care but definitive treatment (we think) is anticoagulation

most of our job here is considering  the diagnosis early and getting the right test. Once the diagnosis made the clear consensus is that they all need anticoagulated.

there are some studies of interventional clot lysis but they’re small and so far no joy. the mainstay of care remains supportive and anticoagulation

the observational data here is clear as far as observational data goes. but there are two small RCTs but both have big issues

everyone agrees anticoagulation is the way to go. there is little agreement on quite how to do it. In reality most of the options we have from IV heparin to warfarin are all reasonable but it’s low level evidence. DOACs may well be OK,  but there’s no data that i could find.

lots of these patients will have bleeding visible on CT. Surely we don’t anticoagulant them? Well the answer is yes we do and the guidelines all support that 

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References

Radiopaedia Article

Charlotte Davies on RCEM Learning

1. Benabu Y, Mark L, Daniel S, Glikstein R. Cerebral venous thrombosis presenting with subarachnoid hemorrhage. Case report and review. Am J Emerg Med. 2009 Jan;27(1):96–106.

2. Canhao P, Ferro JM, Lindgren AG, Bousser MG, Stam J, Barinagarrementeria F, et al. Causes and Predictors of Death in Cerebral Venous Thrombosis. Stroke. 2005 Jul 27;36(8):1720–5.

3. Ducros A, Bousser M-G. Thunderclap headache. BMJ (Clinical research ed). 2013;346:e8557.

4. Evans RW. Migraine Mimics. Headache: The Journal of Head and Face Pain. 2015 Feb 6;55(2):313–22.

5. Ferro JM. Prognosis of Cerebral Vein and Dural Sinus Thrombosis: Results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke. 2004 Feb 12;35(3):664–70.

6. Fischer C, Goldstein J, Edlow J. Cerebral venous sinus thrombosis in the emergency department: retrospective analysis of 17 cases and review of the literature. 2010 Feb;38(2):140–7.

7. Long B, Koyfman A, Runyon MS. Cerebral Venous Thrombosis: A Challenging Neurologic Diagnosis. Emerg Med Clin North Am. 2017 Nov;35(4):869–78.

8. MD JRP, MD JHK. Basic Neuroanatomy and Stroke Syndromes. Emerg Med Clin North Am. Elsevier Inc; 2012 Aug 1;30(3):601–15.

9. Sayer D, Bloom B, Fernando K, Jones S, Benton S, Dev S, et al. An Observational Study of 2,248 Patients Presenting With Headache, Suggestive of Subarachnoid Hemorrhage, Who Received Lumbar Punctures Following Normal Computed Tomography of the Head. Panagos PD, editor. Academic Emergency Medicine. 2015 Oct 19;22(11):1267–73.

10. Stella CL, Jodicke CD, How HY, Harkness UF, Sibai BM. Postpartum headache: is your work-up complete? Am J Obstet Gynecol. 2007 Apr;196(4):318.e1–7.

11. Tabatabai RR, Swadron SP. Headache in the Emergency Department: Avoiding Misdiagnosis of Dangerous Secondary Causes. Emerg Med Clin North Am. 2016 Nov;34(4):695–716.

12. Thomas G DeLoughery MD F. Venous Thrombotic Emergencies. Emerg Med Clin North Am. Elsevier Ltd; 2009 Aug 1;27(3):445–58.

13. Wilson MH. Monro-Kellie 2.0: The dynamic vascular and venous pathophysiological components of intracranial pressure. Journal of Cerebral Blood Flow & Metabolism. SAGE Publications; 2016 May 12;:1–13.

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I’m back at the European Society for Emergency Meeting for another couple of talks (older ones can be found here , here and here…).

The slide is pinched from Dr Strangelove (via Chris Nickson…)

We all love to hate PE. We can’t seem to stop discussing it or publishing papers on it and there’s even a whole conference just on VTE. We have a similar love hate relationship with the dimer. It’s useful to use when it’s negative (cause we already knew the patient didn’t have a PE…) but it gives us sweats when it’s falsely positive on the patient with minimal symptoms who we never should have ordered it on in the first place.

We are in a position where we know we are both underdiagnosing PE in certain patients and overdiagnosing it in lots of others.

There are 2 new diagnostic strategies available to us.

One involves adjusting the normal level of d dimer based on age and the other modifies the dimer cut off based on clinical probability.

Both strategies apply to the low/intermediate risk patients. High risk patients should be going straight to CT and shocked/hypotensive patients should be trying to get to CT if you can make it and considering lysis. We do OK with this population already and let’s face it they’re not that common.

Age adjusted D dimer

This has been around for a while. I did my CTR for the FRCEM on the topic. The data is all observational and of variable quality

The Righini paper is the big one here.

There is of course a false negative rate – you will miss a very occasional patient by using this strategy. however you will also miss PE with using a convention strategy. In the Righini paper it was 0.1 v 0.3

The major limitation here is that it only applies to the over 50s if you’re 35 your cut off is still 500 in this protocol. if you’re 85 then your cut off is 850 but it’s hard to see the downside of doing a CT on an 85 year old. The contrast nephropathy probably is non existent and the chance of serious pathology (PE or otherwise) is so much higher in this group.

So at its most basic the AADD reduces testing in people who i’m not in a rush to reduce testing in.

It has recently been endorsed by ACEP in their updated VTE policy so you now have a guideline to back you up (it is not as yet endorsed by ACCP or the ESC guidelines)

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The YEARS algorithm

All studies seem to make some horrifically forced acronym out of the title. (PARAMEDIC2 is a good example…) This one is apparently the YEARS study. Though I didn’t see them even make any attempt to explain where the YEARS came from. I suggested this…

They modify the Wells criteria to just 3 questions.

Your d dimer cut off is therefore dependant on your clinical risk.

My big concern with this paper is that the d dimer was done at triage before the assessing doctor answered the 3 questions. You can imagine that knowing the result of the dimer might change how you assign your pre test probability. Say you have a young female with a dimer of 950 and score negative on the other 2 questions of the YEARS protocol. The question “Is PE the most likely diagnosis” could be easily swayed by that knowledge.

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Which should I use?

Honestly i think either are reasonable to use, certainly as part of a departmental protocol you’d be well supported. I think they’re both similar in terms of their evidence base and they both provide safe and modest reductions in current imaging levels.

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What about DVT?

This is an obvious question and the age adjusted dimer is jsut starting to be studied for this. So far it seems the reduction in imaging is even more modest and given the limited harm in just doing it yourself or getting a formal ultrasound then I can’t see it being great benefit.

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References

Douma RA, le Gal G, Sohne M, Righini M, Kamphuisen PW, Perrier A, et al. Potential of an age adjusted D-dimer cut-off value to improve the exclusion of pulmonary embolism in older patients: a retrospective analysis of three large cohorts. BMJ (Clinical research ed). 2010 Mar 30;340(mar30 3):c1475–5.

Whiting PF, Rutjes AWS, Westwood ME, Mallett S, Deeks JJ, Reitsma JB, et al. QUADAS-2: a revised tool for the quality assessment of diagnostic accuracy studies. Ann Intern Med. American College of Physicians; 2011 Oct 17;155(8):529–36.

van Es J, Mos I, Douma R, Erkens P, Durian M, Nizet T, et al. The combination of four different clinical decision rules and an age-adjusted D-dimer cut-off increases the number of patients in whom acute pulmonary embolism can safely be excluded. Thromb Haemost. 2012;107(1):167–71.

Jaffrelot M, Le Ven F, Le Roux P-Y, Tissot V, Rame E, Salaun P-Y, et al. External validation of a D-dimer age-adjusted cut-off for the exclusion of pulmonary embolism. Thromb Haemost. Schattauer Publishers; 2012 Apr 30;107(5):1005–7.

Penaloza A, Roy PM, KLINE J, Verschuren F, le Gal G, Quentin-Georget S, et al. Performance of age-adjusted D-dimer cut-off to rule out pulmonary embolism. Journal of Thrombosis and Haemostasis. 2012 Jul 3;10(7):1291–6.

Schouten HJ, Geersing GJ, Koek HL, Zuithoff NPA, Janssen KJM, Douma RA, et al. Diagnostic accuracy of conventional or age adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis. BMJ (Clinical research ed). 2013 May 3;346(may03 1):f2492–2.

Righini M, Van Es J, Exter Den PL, Roy P-M, Verschuren F, Ghuysen A, et al. Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism. JAMA. 2014 Mar 19;311(11):1117.

Jaconelli T, Crane S. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 2: Should we use an age adjusted D-dimer threshold in managing low risk patients with suspected pulmonary embolism? Emergency Medicine Journal. BMJ Publishing Group Ltd and the British Association for Accident & Emergency Medicine; 2015 Apr;32(4):335–7.

Flores J, de Tena JG, Galipienzo J, García-Avello Á, Pérez-Rodríguez E, Tortuero JI, et al. Clinical usefulness and safety of an age-adjusted D-dimer cutoff levels to exclude pulmonary embolism: a retrospective analysis. Internal and Emergency Medicine. Springer Milan; 2015 Sep 2;11(1):69–75.

Han C, Zhao Y, Cheng W, Yang J, Yuan J, Zheng Y, et al. The performance of age-adjusted D-dimer cut-off in Chinese outpatients with suspected venous thromboembolism. Thrombosis Research. Elsevier Ltd; 2015 Oct 1;136(4):739–43.

Crawford F, Andras A, Welch K, Sheares K, Keeling D, Chappell FM. D-dimer test for excluding the diagnosis of pulmonary embolism. Cochrane Database Syst Rev. 2016 Aug 5;(8):CD010864.

Takach Lapner S, Julian JA, Linkins LA, Bates SM, Kearon C. Questioning the use of an age-adjusted D-dimer threshold to exclude venous thromboembolism: analysis of individual patient data from two diagnostic studies. J Thromb Haemost. 2016 Aug 31;14(10):1953–9.

Monks D, Neill A, D B, Moughty A, A M, Timmons A, et al. Age Adjusted D-Dimer for exclusion of Pulmonary Embolism: a retrospective cohort study. Irish Medical Journal. 2017 Aug 9;110(7):1–6.

Riva N, Camporese G, Iotti M, Bucherini E, Righini M, Kamphuisen PW, et al. Age-adjusted D-dimer to rule out deep vein thrombosis: findings from the PALLADIO algorithm. J Thromb Haemost. 2017 Dec 8;16(2):271–8.

van der Hulle MD T, MD WYC, MD SK, MD LFMB, van Bemmel MD T, van Es MD J, et al. Simplifed diagnostic management of suspected pulmonary embolism (the YEARS study): a prospective, multicentre, cohort study. The Lancet. Elsevier Ltd; 2017 May 22;:1–9.

Kabrhel C, Van Hylckama Vlieg A, Muzikanski A, Singer A, Fermann GJ, Francis S, et al. Multicenter Evaluation of the YEARSCriteria in Emergency Department Patients Evaluated for Pulmonary Embolism. Academic Emergency Medicine. Wiley/Blackwell (10.1111); 2018 Mar 31;:acem.13417–20.

RCEM Learning: Andy Neill & Dan Horner

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