Neuropathic pain in Guillain-Barre-Syndrome

We use the case of a mildly affected GBS patient with severe neuropathic pain to discuss the latter’s pathophysiology in general and the treatment for neuropathic pain in particular.
There is an excellent review article in BMJ 2014 which hints at the various drugs on the horizon, including some known substances whose application in neuropathic pain seems feasible (see below).

Neuropathic pain

  • Prophylaxis: in order to reduce the occurrence of neuropathic pain there is a good rationale for prophylactic treatment in certain cases, such as amputation, Zoster and nerve surgery, although not much good data has been published.
  • Classify: distinguish NP with autonomic features from that without, central versus peripheral (the latter often with autonomous signs)
  • Diagnosis: recognize the core features of pain character with good PPV (radiation, allodynia, hyperalgesia, autonomous sign if present, distribution along affected nerve structures)
  • Basic treatment
    • Stick to the basics: Despite the fact, that we Neurologists tend to think that NP is so special, we forget that basic nonsteroidal analgesics do work in NP; there is even a good pathophysiologic reason for that, since local cytokine production is influenced by at least the antiinflammatory substances (not acetaminophen, though).
    • Opiates: next is opiates, most often as a bridge to other approaches – still highly effective and reasonably well tolerated
    • alpha 2 delta blockers (gabapentinoids) work on the dorsal root ganglion and have been shown to be effective in many prototypical diseases
    • Na blockers (carbamazepine, phenytoin, lidocaine, lamotrigine)
    • NASRIs including tri- and tetracyclics and mirtazapin, as well as venlafaxine and duloxetine
  • Local treatment: only if the pathophysiological proces is focal – capsaicin and lidocain patch
  • Advanced treatment: for more advanced NP, ketamine seems to be the agent of choice as an NMDA blocker with all the problems arising. Further ideas could be: Baclofen, Clonidin. Many anticonvulsants (apart from those above) have been tested, not many survived, except in some diseases (trigeminal neuralgia for instance -> topiramate)
  • Experimental or future therapies: Allopurinol (ADP antagonist), Aprepipant (NK1 blocker), Memantine, Amantadine (both mild NMDA blockers), Cannabinoids (good preclinical data, moderate effect), cytokine inhibitors, NGF blockers

Pain in Guillain-Barré-Syndrome

I hesitate to repeat all the information to be found in the literature. Still it has to be said that pain is very prevalent, often preceding and also often following GBS, can take several forms (backache, interscapular, distal, skin, myalgia, …) and is often severe enough to run through the above list. Here is a good review article in Neurologia on this from 2015. The best case series has been published in Neuroloy in 2010.

On Spencer’s curve

2000px-znak_a-1-svg1In our recent ultrasound refresher course, I tried to give a talk on the vagaries of stenosis graduation (mainly) for extracranial stenoses. The gist of the talk is outlined in the following notes.

The Bernoulli principle

While Bernoulli’s equation is rather intricate, the underlying principle of conservation of flow along a stenosed tube is simple. Consider a tube with a short stenosis with laminar flow of a Newton fluid. Then the bigger area A1 multiplied with the flow  velocity v1 (take psv for simplicity, although this is not really correct) should be the same as the smaller area A2 multiplied with v2. Thus the increase of flow is proportional of A1 / A2, so that the reduction to a third of the area leads to an increase by the factor 3 of the flow velocity, a reduction to a tenth leads to ten times the flow velocity in the stenosis.img_7579

Adding friction

Since we usually don’t observe velocities higher than 5 m/sec, there must be a limiting principle and this is the resistance offered by the stenosis, which reduces flow in the whole vessel. This resistance can be approximated by the law of Hagen-Poiseuille and is proportional to the length of the stenosis, the inverse of r^4 and the inverse of viscosity. Again, this only holds for laminar flow and the case of blood offers some more complications, but the core message is: the longer the stenosis the higher the flow reduction. Also the flow reduction grows much more with decreasing vessel diameter than the flow velocity increase by Bernoulli’s principle can compensate. Very tight and long stenoses show a flow velocity reduction despite there high grade. If you  find a psv of only 2,4m/sec this might therefore mean either a mere medium grade stenosis or a very tight stenosis (near occlusion).img_7578

Spencer’s curve

Taking these two principles into account, Spencer and Reid (in their brilliant 1979 stroke article) deduced the famous curve now known as Spencer’s curve (see Alexandrov’s papers for a more detailled exposition).

Since at the time duplex sonography was technically not feasible, the Spencer curve is based on the theoretical assumption of a 2 mm stenosis and thus does not correct for the length of the stenosis (as well as the other factors mentioned below). This explains why the cw-doppler-data in their paper does not really fit the theoretical model. Still it is the best approximation we have to a theoretical foundation of stenosis quantification.

Measuring diameters

Diameter instead of area

Most of the studies have been done with angiographic imaging of stenoses or ultrasound measurements of the stenosis diameter rather than the area. Of course, the area could easily be calculated from the diameter (r^2 pi) if it were a circle, but then it isn’t. In ultrasound we could measure the area itself (if no shadowing artifacts are present), yet no one does really. Therefore you should remember that most of calculations of the stenosis area from the diameter are systematically invalid.

Where, when and how to measure diameters

For some absurd reason, Europeans kept to the local stenosis degree (i.e., diameter of perfused lumen divided by the original vessel diameter), at least in their ECST trial, while the NASCET trial used the more reasonable distal stenosis degree (i.e., minimal lumen diameter divided by non-stenosed distal ICA diameter). Since the ICA bulb varies in its bulbiness and distends with age and blood pressure (and with stenosis degree), the local stenosis degree is usually a shot in the dark. The distal (NASCET) degree suffers from pseudoocclusion, i.e., collapse of the distal vessel in very high grade stenosis. All attempts to calculate the NASCET stenosis degree from ECST and vice versa are irrational.

Being faithful to both traditions, I measure all the lumina (minimal lumen, original vessel lumen, distal lumen). The only really interesting number is the residual diameter (combined with the length of the minimal lumen), because this determines the hemodynamic compromise.

Other important factors


Neither is blood a Newton fluid, nor is all the viscosity (rarely measured today) explained by the hematocrit alone. Yet the hematocrit is an important number to factor into your interpretation of ultrasound data. You should note it.


Every vessel wall abnormality leads to small perturbations of flow and thus turbulence. Turbulence reduces anterograde flow and thus reduces the distal pressure after a stenosis. While very hard to quantify it is essential to mention turbulent flow when you see it. Remember that to distinguish retrograde (i.e. turbulent) flow from flow increase with aliasing you need to look at the color bar on the side of your duplex image, noting that flow increase jumps over the upper limit of the color spectrum while retrograd flow (usually) passes the black zero flow region.


decreases over the lifetime, even more if severe hypertension or calcification of vessel walls is present. This, again, is very hard to quantify, but often easy to recognize qualitatively in your duplex image, when you recognize the pulsation of the vessel wall. Reduced elasticity has to lead to increased flow velocities.


Since blood flow is not continuous but pulsatile and this in varying shapes, we should really be using mean flows in our stenosis calculations. This has historically not been done. As a consequence, valve abnormalities (aortic stenosis, insufficiency) have to be factored in, when we try to calculate the stenosis degree from peak systolic velocities.

Blood pressure and atrial fibrillation

The (pulsating) blood pressure is the driving force of cerebral blood flow, trying to overcome venous and intracerebral pressure as well as the distal blood pressure offered by collaterals (see below). At least, you should note the blood pressure and relativize your stenosis graduation in cases of extreme values. When the patient has atrial fibrillation, you probably should use an “average” heartbeat rather than the extreme values. But bear in mind that absolute arrhythmia is a risk factor for arterioarterial embolization in itself.

The geometry of the stenosis

usually is far from being that of a tube. Rather, the blood flow curves around plaques, rotating and hitting small plaques on the distal wall. Again, the effects are impossible to quantify, but at least the geometry should be noted. The shape of the stenosis area should be remarked upon, if it isn’t circular.

The role of collaterals

The pressure difference along a stenosis is not only determined by the resistance of the stenosis itself, but also by the collateral blood flow which leads to an increase of distal pressure (mostly but not only in diastole). This leads to a reduction of the blood flow velocity in the case of good collateralization, thus also reduced flow velocities.

The danger of a stenosis

In the neurovascular clinic, I try to estimate four risks of a stenosis: the hemodynamic risk (what happens if the stenosis were to increase?), the embolic risk (how high is the risk of an embolic event from the stenosis?), risk factors and other risks.

Hemodynamic risk

The hemodynamic risk is determined by

  • the current hemodynamic compromise (jet flow velocity, CCA flow vs. ICA flow, pulsatilities, MCA flow, CO2 reserve)
  • the dynamics of the stenosis (how long has this been going on? was there time to develop collaterals?)
  • the completeness of the circle of Willis (variations such as A1 hypoplasia, Pcomm hypoplasia)
  • secondary stenoses in the collateral circulation.

The problem is that we cannot foresee whether the stenosis will be slowly progressive or suddenly close up (as in plaque rupture). At least in asymptomatic stenoses I require CT- or MR-angiography to determine the completeness of the circle of Willis.

Embolic risk

The embolic risk is determined by

  • Plaque morphology and
  • Plaque type
  • Whether the atherosclerotic process is active or burnt out.
    As in coronaries, it is not reasonable to revascularise every severe asymptomatic stenosis. But in a patient where the overall atherosclerotic process is currently active (after an NSTEMI, say), we can expect the plaques to rupture.
  • Previous embolic events can be noted on MRI.
  • Emboli detection
  • Is the anti-platelet medication working? Multiplate or similar tests.

Risk factors

  • Did the patient stop smoking? How long ago?
  • Can we use high dose statins in this patient? Statins are highly effective against plaque deterioration, but also have serious side effects (less exercise tolerance, diabetes, muscle problems), especially in the high doses we like to use for severe stenosis.
  • Is the patient’s blood pressure controllable? Note that severe stenosis lead to very labile blood pressures as one of the most important sensors of the system is damped.
  • Exercise? Although this has not been studied properly in carotid artery stenosis, I surmise that health by fitness should improve the prognosis of carotid artery stenosis.

Other risks

  • Central or mixed sleep apnea syndrome – very prevalent among ICA stenosis patients, leading to a bag of systemic problems, not the least being poor blood pressure control.
  • Bad blood pressure control (see above)
  • Development of secondary stenoses in the collateral vessels (contralateral, ECA, …)
  • Development of a collateral rete with its danger of bleeding


I don’t see any better physical theories coming. Also, we can never expect better data than NASCET and this is a bad foundation. Therefore you have to tackle all the complexities outlined above and refrain from simplifying an ICA stenosis to a mere number (always the worst approach).




An algorithm for starting oral anticoagulants after stroke

Once you identified the heart as the emboligenic source of your stroke unit patient’s stroke, the question arises of why, when and how you institute anticoagulation. This hasn’t gotten any easier with all the new drug options, Big Pharma push and the resulting trust we are supposed have in DOACs.

In this short blog entry, I will list my 6-step program for starting oral anticoagulants after an ischemic event. Thanks to the great acronym creator, here is the mnemonic for it: SHuTOFF DOAC.

  • Stroke risk
  • Hemorrhage risk
  • Timing
  • Oral agents
  • Formulary
  • Follow-up

Stroke risk

Calculate the risk of recurrent stroke, if you find data.

  • Atrial fibrillation: 12% vs 1-3%/a under OAC, use a CHADSVASC-calculator for individualized data, bearing in mind that most of the underlying studies were in a primary prevention setting.
  • Atrial thrombus: An atrial thrombus is essentially just a sign of (possibly undetected) afib and insufficient anticoagulation, although it can occur in otherwise bad hearts (see this huge collection of TEE+ pts). Still, we would like to know how more acute the danger of recurrent stroke is, if you find an atrial thrombus on TEE. Or – as increasingly happens – on CTA, when you stumble on a left atrial appendage filling deficit by chance. Does it double or triple? Or stay the same? No proper data found on this. 
  • Ventricular thrombus: Apart from the fact that those are easier to find (TTE suffices) and that ventricular thrombi are due to bad hearts (large MI, severe cardiomyopathy) in general, no data can be found on the rate of acute stroke recurrence in this setting. In the long run (1/2a) it is very impressive (50%) according to very old studies, seemingly lowered by anticoagulation (to 30% in this analysis).
  • Mechanical heart valves: Few studies exist, since everyone thinks these patients absolutely have to be anticoagulated. Only part of the embolic risk is due to the valve itself, the rest comes from afib, especially with mitral valve replacement.
    This 1994 review finds a risk of 4 per 100 pt. years without anticoagulation, reduced to 2,2 by ASS and 1 by VKA. This newer analysis of pts. with St. Jude valves finds similar rates of embolism with OAC.
  • Bioprosthetic heart valves carry a significantly lower risk, about half the number of embolic events seems a good estimate.
  • Low EF: Although we left routine anticoagulation for low EF in primary prophylaxis after the WATCH and WARCEF studies (where a reduction in embolic strokes was offset by the increased bleeding risk for OAC as compared with ASS), a cardioembolic stroke in the setting of severely reduced EF and sinus rhythm should probably trigger oral anticoagulation. I could not find proper data for the stroke risk after an embolic event happened.
  • PFO plus/minus ASA: The risk is extremely low, if no proof of the paradoxical mechanism can be established (no pulmonary embolism, no DVT). Otherwise the risk should be roughly the same as the risk of recurrent venous thrombosis (determined by genetics, mobility, triggers and so on) times the cross-embolism-factor (how many of those embolisms cross over through the PFO, can be measured semiquantitatively in the bubble test, this is my personal invention :-)).

Hemorrhage risk

Risk for spontaneous ICH under OAC

Find and optimize risk factors for hemorrhagic complications under OAC, in particular ICH. For atrial fibrillation there is the simplified  HASBLED-score, but some particular risk factors might benefit from more intensive workup.

  • The A4F complex of the elderly
    • Age
    • Alzheimer’s
    • Apolipoprotein ε2, ε4
    • Amyloid angiopathy
    • Falls
  • Alcohol
  • Altered coagulation (cirrhosis and the like, low platelets)
  • Adherence problems
  • Diabetes
  • Hypertension
  • Interacting medication
    Obviously, the more drugs a patient takes, the higher the risk. With antiplatelet comedication, you double the risk with monotherapy and triple it with dual therapy (or even worse with the newer antiplatelets ticagrelor, cangrelor)
  • Liver and kidney problems
  • MRI markers: leukoaraiosis (no proper gold standard for quantification, may use Fazekas score or volume of white matter hyperintensities, no cutoff established) and number of microbleeds (no proper cutoff because the sensitivity depends on the MRI sequence used and field strength)

Risk for hemorrhagic transformation of the stroke

The acute setting of a stroke raises the obvious concern of bleeding into the stroke (either minor as hemorrhagic transformation or as parenchematous hematoma). Since the detection of hemorrhagic transformation is a matter of the sensitivity of your imaging technique (proportional to the field strength of your scanner, SWI outperforming T2*), only parenchematous hematoma (as can be seen with any old CT or even on ultrasound) should be used to judge the danger of anticoagulation and the reported rates vary between 10 and 30% of cardioembolic strokes. It is unclear, though, whether this rate increases with oral anticoagulation (it does with heparin and LMWH, but those are way more intense) and for how long the danger persists – see next step.


The 1-3-6-12 rule

There is practically no data on when to start OACs after stroke, so we use the guidelines (ESC 2016) with their practical 1-3-6-12d rule (TIA/NIHSS 0, NIHSS < 8, 8-15, > 15), although they don’t regulate the case of hemorrhagically transformed or parenchymatous hematoma in stroke.


And in the meantime?

  • It is unclear whether ASS makes sense for bridging until OAC in afib – it seems to not hurt much after cardioembolic stroke, though. The guidelines recommend ASS bridging.
  • Heparin or OAC bridging (at least with Warfarin) confers no benefit in the huge studies analyzed in Sandercock’s Cochrane analysis. Whether (lower dosed) DOACs could be used in this setting (analogous to, say, half-hearted LMWH treatment) is also an open question.

Bear in mind that the risk for recurrent stroke during the inpatient period is extremely low (around 3% in simple afib patients – old data, but replicated in modern case series such as this one). It is a daunting question when to bridge in the higher risk groups, such as mechanical heart valves. Most reviews recommend 7-14 days (without proper data to back that recommendation).

Oral anticoagulant

In the next step you have to choose among the 5 options. Consider the acronym DOAC:

  • Drugs: what other drugs is the patient on, what are the possible interactions?
  • Organs: is the patient at risk for renal insufficiency or liver failure?
  • Age: since the lightweight elderly are prone to renal failure even with borderline creatinine, age is a risk factor for all DOACs.
  • Compliance: DOACs aren’t very forgiving, if you forget some doses, VKA usually are.


Lookup the dose according to all of the above (most of the DOACs have a low and high dose regime, according to risk factors among the above)


Do you have to ensure lab checks? This is obvious and well established for VKAs. It should also be reasonable to check creatinines in patients at risk for renal failure. Rarely, if ever, are drug levels or anti-Xa-activity needed for standard therapy. When it comes to acute surgery, tPA or in case of bleeding, having drug levels at hand is, well, handy.

Drop attacks

splash-water-1362224788t1gMedical terminology knows 5 reasons for people to fall unaided: common fall, syncope, collapse, seizure and drop attack.

A drop attack consist of the loss of lower extremity tone, leading to collapse, but decidedly without disturbance of consciousness (as opposed to syncopes) and without accompanying neurological or other signs or symptoms, in particular without dizziness or faintness, diplopia etc. Peculiarly, the attacks occur while walking, not standing or sitting. They seem to be quite prevalent, constituting a significant percentage of falls in the elderly.

The concept of drop attacks is very old and yet, there is not much published about it. As far as I got in my literature review, a 1986 series in Neurology has the most modern data (an astonishing 108 patients!). Apart from that you have to work through case reports and chapters in neurology textbooks, such as Neurological Differential Diagnosis – a cased-based approach.

The prototypical patient is a woman over forty who reports falling forward while hurriedly walking on the pavement, as if someone had pushed her, without warning, the legs giving way. She might even have injured herself. Once down, she could get up again after a few seconds, without feeling dizzy, nauseus or unsteady.

The differential diagnosis is huge, since so many diseases have been associated with drop attacks, and in some cases falsely so.

Hemodynamic ischemia

Take vertebrobasilar ischemia, for instance. Before the advent of MRI and CTA, many anomalies in the posterior circulation were interpreted as evidence of pathology, such as hypoplastic posterior communicating arteries, asymmetry of one vertebral artery or hypoplastic V4 segments. In practice, it seems to be nearly impossible to get isolated drop attacks (without vertigo!) from a hemodynamic basilar compromise. In a series of 83 proven basilar artery occlusions from basilar stenoses, prodromi included “drop attacks” in only 4 cases and these were accompanied by vertigo in 3 (Ferbert, Stroke 1990). Similarly rare, yet pathophysiologically more reasonable, is the case of a high grade carotid artery stenosis with contralateral hypoplastic A1-segment – when the compromised ICA supplies both anterior cerebral arteries.

It is interesting to note that the stroke rate of people with drop attacks was not increased as compared to age-matched controls in the 1986 series.

Systemic hypoperfusion (aka syncope without dizziness)

The classical mechanisms of syncope (orthostatic, neurocardiogenic etc., aortic stenosis) practically always lead to disturbance of consciousness or at least dizziness. There is just one exception: rhythmogenic drop attacks (Adam-Stokes attacks). In the above mentioned case series this constituted a sizable percentage (13%). Although I would think that a careful reevaluation reduce that number considerably, I concede that an event recorder is a reasonable investment for recurring drop attacks, not the least, because the gadgets have become so simple to implant.

A special case is carotid hypersensitivity syndrome, where a vagal mechanism due to head rotation or local pressure is usually hypothesized. To be honest, I haven’t seen many cases of this, despite the fact that I am working in a neurovascular lab much of my spare time, so it can’t be that frequent.


Atonic (or astatic) seizures are well-known phenomena in pediatric neurology, arising in Lennox-Gastaut-syndrome, Doose syndrome and other epilepsies. It is rare as a manifestation of adult onset epilepsy, all the less in the elderly, yet the classical temporal lobe epilepsy can lead to temporal lobe syncopes or temporal lobe drop attacks in this age group as in any. 

In these modern times of weird autoimmune encephalitis variants, LGI1-antibody encephalitis has been reported to cause drop attacks even before it’s more typical facio-brachio-crural dystonic seizures.

Movement disorders

In (advanced) Parkinson’s you can be attacked by drops, usually with polypharmacy and fluctuating clinical course (on/off phenomena, freezing). Patients with Progressive Supranuclear Palsy tend to fall backward rather than forward, yet this can be described as a drop attack as well. Both diseases should present with clinical hints at the movement disorder.

Paroxysmal kinesiogenic dystonia has been proposed as an imitator of epilepsy and you could assume that this can lead to drop attacks as well, although I could not find a case report of this. At any rate of occurrence, a family history should help.

Negative myoclonus

This can be an expression of epilepsy (particularly, if focal as in benign partial epilepsy, see above) or a more generalized encephalopathy such as hepatic or toxic, leading to Asterixis (think of Pregabalin, Oxcarbazepine and toxic doses of any central acting drug). History, a hunt for the “flapping tremor” and lab works should rule this out.

Vestibular drop attacks

An acute and temporary disturbance in otolith function can lead to drop attacks. This has been eponymized by Tumarkin who coined the term otolith crisis in the thirties. The attacks are not the correlate of an acute Meniere’s endolymphatic hydrops, but due to unstable otolith function. In contrast to most other drop attacks there ought to be a sensation of vertigo, i.e., of movement of the outer world, yet only few patients can actually report this.

Theoretically, other vestibular disorders, in particular superior canal dehiscence syndrome, should be able to provoke vestibular drop attacks as well, yet there are no case reports.

(Cranio-)Cervical dysfunction

Quite a few diseases of the cervical myelon and the craniocervical junction can lead to temporary compression or dysfunction of either the pyramidal tract or the dorsal column afferent fibres, thus leading to either loss of tone or loss of feeling in the legs, hence the drop attack.

  • Posterior fossa tumors
  • Subacute combined degeneration (Vitamin B12)
  • Chiari Type I
  • Cervical spinal canal stenosis and other causes of cord compression

Other rare causes

  • Third ventricle tumors (colloid cyst, pineal cyst) – usually with postural headache
  • Isolated cataplexy as an abortive variant of narcolepsy
  • Coffin-Lowry-syndrome – stimulus-induced drop events

How to do a presentation

Academically, Iclimbing_through_the_yellow_band_mt-_everest_-may_2007_a was raised in Mathematics, where a lecture is in fact a development of ideas on the black- or whiteboard. In the Mathematics research community things then went downhill with presentations in LaTeX trying to imitate Powerpoints horrible themes.

In Medicine, the situation has been disastrous even before Powerpoint – medical talks have always been boring with lots of facts and no investment into the choreography of the talk itself. Prezi took this even further, emphasizing the structure of the content rather than the talk.

For me it was the fascination with SMACC talks such as Vic Brazil’s famous Timing, Tribes and STEMIs and of course Cliff Reid’s impressive resuscitation talks, that led me first to the theory (Presentation zen, Nancy Duarte and the like) and then the practice (TED talks) of modern presentation creation.

This blog entry serves to collect the most helpful references for creating presentations. It also captures the basic steps I recommend for giving a small 20 min talk on a current topic in our departments’ continued education rounds.

5 steps for creating presentations

While three seems to play an important role in structuring you talk, I prefer rules of 5 for mnemonics, so here are my presentation creation 5.

  1. What
  2. So what?
  3. How
  4. Practice
  5. Present


Choose a topic that interests you and your audience, priority on the latter. Don’t let the topic be dictated. Read up and become an expert. Helpful is Scott Weingarts tip to create a folder with a ppt-template, a note-file (eg mindmap), lots of subfolders (images, articles, videos, recordings) way ahead of the talk to let your subconscious work on the talk all those weeks, collecting articles, noting ideas.

So what?

Why should this topic be interesting for your audience? How do you want to change them? Write an elevator pitch for that.


Choose one of three formats to structure your talk:

  •  Problem/solution: most frequent in medicine
  •  Narrative: most effective – use drama theory, suspense curves and the like
  •  Chronologic: most diffficult – take the audience through a historic tour

Now write the basic steps for Intro, Story, Closing on yellow postits and thus create the structure as a modifiable lattice.


I recommend 5 rehearsals for simple and 6 rehearsals for important talks

  1. Ad hoc: starting from your postits, talk the talk standing in front of an empty chair, then note necessary changes to your structure, write down good formulations as segues in differently coloured postits, fill in the missing data, examples etc.
  2. W/o slides: run through the talk again immediately and note at which point you need visual aids, the flipchart, videos etc to improve the talk. Use differently coloured postits as placeholders. Use the following weeks’ break to search for this stuff and take your time, letting it stew.
  3. To a person: give the talk with slides to a good friend or colleague, gathering as much feedback as you can – this is the first time you give the talk to an audience; make sure you achieve what you planned for, change the talk radically otherwise and start with 2 again. Work through each formulation, each slide. It helps to record the talk on video.
  4. Preparation: give the talk again in private at least a week ahead of the date. You might record this (audio only) Then give your subconscious time to improve the talk even further.
  5. Rehearsal: This is the final rehearsal 1-2 days before your talk. If you give the talk to a big audience, you should repeat this as a dress rehearsal to a small group, such as your peers, gathering feedback.


Annouce and advocate your talk. Go to the venue and check everything out, if possible, 1 day before the talk. Get a clicker (not a pointer). Get to the talk on time. Be well-dressed and smart. Have someone announce your talk to make sure everyone is quiet. Stand before the audience and talk to them, not to the slides, looking them into the eyes, reacting. After the talk, get feedback and improve your talk.

5 steps for creating slides

  1. Not a teleprompter
  2. Not a handout
  3. Don’t distract
  4. Good design
  5. Good images

Not a teleprompter

Using your practice runs, you don’t need the slides as notes. Whenever the information on the slide is just for you to remember what to say, move it to the notes. Only citations may be read verbatim to the audience (it is always so cool, if you can cite by heart facing the audience).

Not a handout

If you feel the audience needs information to take home, prepare a handout. Your slides are not your handout. Every word on the slide needs to be checked whether it is inspirational or handout material. Long lists are handout material.

Don’t distract

Remove everything, every word, every object, every colour, every footer, every logo, everything that doesn’t serve your story. No template. Black background. No animations. No transitions.

Each slide should contain one thing, either a supporting image (fotos for emotions, graphs for illustration) or a slogan, maybe both.

If you absolutely need lists, keep them short, so that the eye can grasp the whole list in one glance (max. 5-6 entries)

Good design

Use all the theory of design (golden cut, font design, clear lines, few words) to improve your slides. Use a professional, if possible. Make it simple. Look at Apple’s advertisements and presentations to get the idea.

If you feel you have to excuse a busy slide, throw it out, redesign it. Most complex slides are better developed on the whiteboard.

Good images

Images are used to create emotions. Use good real fotos in high resolution, not artificial cartoons. You judt have to evoke the feeling. Make sure you have the right to use the images.


Obviously, I did not develop these concepts on my own. Here is an annotated list of useful links and references.


Life’s simple 3

When a stroke patient with symptomatic intracranial stenosis has been worked up, we SAMMPRIS him, by which we mean ASS, Clopidogrel and high dose statin. This is, of course, not the whole story – more important than drugs are the necessary lifestyle adjustments. We use this example to develop a system for stepwise improvement of risk factors and health behaviour.

In my view, the standard risk factors (pressure, sugar, fat and weight) can all be improved by concentrating on the simple three:

  1. Get active and work out
  2. Eat healthy
  3. Don’t smoke

This sounds reasonable, although the science behind 1 and 2 is not so simple. Just staying active (e.g. walking every day for at least 30 mins or running for 3 x 25 mins) might be healthy but need not really lower your blood pressure. Vastly more efficient are more intense workouts such as muscle strengthening (resistance) exercises or even high intensity interval training. The evidence for these measures is quite good. With regard to healthy eating, there seems to be no golden way to a good diet (in fact, most diets studied have been harmful), yet the mere fact that you are trying to be conscious about your food has a proven health promoting effect.

The current decade is probably the best to initiate health promoting behaviour, as smartphone/smartwatch/fitness bands abound and make it easier to watch your health without investing too much time. In particular these applications

  • can help to find out what improves weight or fitness
  • introduce a gamification factor to the otherwise boring issue
  • might lead to more insight about how your blood pressure, sugar or cholesterol react to specific measures
  • might allow to identify those patients where high dose statins are harmful by reducing fitness effects


Defining away sepsis

Why do we need new definitions for sepsis? We want the term to denote a syndrome with serious consequences, something that needs the full force of an ICU to recover.

No simple infections. So not a young girl with viral feverish URI (who happens to have leucocytes < 4). Neither a simple pneumonia. Maybe the myriad of negative sepsis studies stem from the fact that they included too many simple infections. What used to constitute severe sepsis, the endangered endorgans should become requisite in the definition of sepsis.

High sensitivity. What about the 90 yo dehydrated nursing home resident with positive nitrite stick and altered mental status? He might recover with some fluids and antibiotics, but then he also might not and deteriorate, so that he needs treatment response monitoring – he could be septic, but he also could just be cured in 2 hours.

I see the recent initiative to improve our definition of sepsis (dubbed Sepsis 3.0 by the FOAMED community) in this light. While the new definitions sound a bit esoteric, they are actually very practical, focussing on two situations:

  • Non-ICU: The normal ward, private practice or ER, where we need to recognize those patients with suspected infection that might deteriorate and need close monitoring, while ressources are not that good, that every patient can have an arterial blood or extensive lab works. Sepsis 3.0 recommends to use the qSOFA, also known as BAT score, where 2 out of 3 criteria suffice.
    • Blood pressure < 100
    • Altered mental status
    • Tachypnea 22 breaths/min
  • In ICU, we should screen with the daily labs we already have, using the SOFA score (routinely computed in electronic charts, also called CAR-LOG = coagulation-arterial pressure-renal-liver-oxygenation-GCS) and use a 2 point change as a threshold for sepsis, if infection is suspected. Septic shock is defined by need for noradrenaline to keep the MAP above 65 with remaining lactate geq 2 mmol/l, provided that enough fluids have been given.

Who is suspected? The beauty of the old and new definition of sepsis that “suspected infection” is not further specified. You might be warned by fever, CRP or leucocytosis, but also by a good story for an infection (postoperative patient, smelly urine). While some folks find this too vague, I think we always know when to suspect infection.

Think of sepsis when organs bail out. The article reminds us to think of sepsis (and thus suspect infection), whenever any organ failure occurs.