It is really tough to come up with a good case for polio that I could have experienced in order to talk about this disease that dominated much of the 20th century, led to the practice of mechanical ventilation, the invention of ICUs (somehow, at least) and showed that the WHO is more than a toothless tiger.

I use a case of suspected post-polio-syndrome to discuss the epidemiology, pathophysiology and sequelae of polio, then spend some time on the eradication program and it’s successes so far and finally cover the post polio discussion.


Information management

I always was a fierce defendant of evidence-based medicine. After all, what harm is there in finding, using and being able to reject the available evidence for a particular question. Although we never learned it in medical school, I did some postgrad courses on medical literature appraisal, ploughed through the User’s Guide and tried to understand the mechanics of metaanalysis. I also follow most of the relevant Neurology journals. Still, I am unable to answer any given bedside clinical question in the way EBM would have it. It just takes too long and I am too dumb. Properly reading a study takes hours and then I am not able to find all weaknesses that internet blogs find in it.

So either I am unsuited for  EBM or it does not work. Also, it just explains how to answer questions, not how to raise them.

With these fears in the background, I stumbled upon this paper and this talk, explaining a basic approach to what I would call informed medicine. I would add to the information in the article some core principles of work with medical literature:

  1. Try to stay current with the big journals (because they matter), but beware of their pharma influence.
  2. Try to stay current with some more independent and small journals (such as in PMC and the British journals).
  3. Follow informed discussions on the web (such as CCML, emcrit, …) in places where you reliably found good doctors.
  4. Don’t be an early adopter, unless a study has very small NNTs and has been replicated.
  5. Mistrust studies with thousands of participants, unless their (so-called scientific) results have been replicated in clinical practice.
  6. If facing a patient with a problem, read up in good textbooks written by people you trust and who are too old to be influenced by every small whiff of medical wind.
  7. Then confront this with something like uptodate.
  8. Finally read some reviews.

As a final remark, I offer the following strategy for finding a treatment for your patient: do a search on RCT with limits to 1970-1990 on your subject – you will find many rightfully abandoned approaches, but also some gems to be recovered.

The 5 fingers of stroke

Did you get the stroke etiology right?

I love checklists with 5 items – 5 things to ask for in CHF, 2 x 5 things to remember in delirium. By looking at any of your hands, you can understand and work down the checklist. So here is my 5 item checklist for acute stroke care – designed for handovers.

  1. Stroke characteristics:
    1. syndrome
    2. localization
    3. imaging results
    4. pattern
    5. confidence (couldn’t it be a mimic?)
  2. Acute stroke treatment: tPA? endovascular therapy? Any early neurological deterioration?
  3. Etiology: determines secondary prevention measures. I use ASCO
    1. risk factors
    2. atherosclerosis (big vessels – ultrasound results? CTA/MRA?),
    3. small vessels aka microangiopathy (CT/MRI)
    4. cardiac (ECG, monitor, further results)
    5. other etiologies
  4. Complications: the big 5 are
    1. infection
    2. cardiac (rhythm, troponin)
    3. pressure
    4. gut problems
    5. thrombosis
  5. Rehabilitation
    1. physiotherapy
    2. ergotherapy
    3. logopedic (aka SLT) therapy
    4. social services?
    5. rehabilitation planned?

Strong acid base

Peter Stewart – the inventor of the quantitative (“ignore H+”) approach to acid base

I grew up with the German approach to acid base (“no clue – ask someone else”), then learned the Boston way (with all their compensation formulas). In parallel I tried to understand the Stewart style of quantitative acid base treatment, always missing the easy rule-of-thumb calculations I so loved in the anion gap calculations. So I really enjoyed the developments of the last years, where simple formulas for the strong ion gap proved to be adequate.

I will not delve into the discussion of the pros and cons of Stewart’s “H+ is not the point of acid base”, but happily accept that the old anion gap (if corrected for albumin) and the physicochemical approach yield the same results, if by different means. Scott Weingart at emcrit.org has devised a simple algorithm to deal with metabolic acid base disturbances, that I have adopted – you can enter all that stuff into acidbase.org’s calculator.

  1. Labs: BGA (Na, Cl, K, pH, pCO2, base deficit = -base excess, lactate) plus albumin
  2. Determine the sum effect of all acid base disorders:
    • pH < 7,35 = acidosis
    • pH > 7,45 = alkalosis
  3. Determine the respiratory effect (might be compensation)
    • pCO2 > 45 = respiratory acidosis
    • pCO2 < 35 = respiratory alkalosis
  4. Determine the strong ion effect: SID = Na – Cl
    • SID < 38 = low SID acidosis: get urinary anion gap (UAG) = urine Na + K – Cl
      • fluid administration with low SID fluids (saline, D5W)
      • renal tubular acidosis if UAG > 0
        • type I: urinary pH > 5,55
        • type II: urinary pH < 5,55
        • type IV: hyperkalemic, pH < 5,55
    • SID > 38 = high SID alkalosis (nasogastric suction, diuretics, hyperaldosteronism, fluid depletion)
  5. Determine the lactate effect (due to hypoxia or toxicity with Metformin, Propofol, Linezolid, amphetamines, Valproate, HIV drugs, …)
  6. Determine the albumine effect: 2,5 * (4,2 – [Alb in g/dl])
  7. Add all the metabolic components into the Strong Ion Gap:
    • SIG = base deficit + SID – 38 + Albumine effect – Lactate
    • SIG > 2 = SIG metabolic acidosis: calculate osmolar gap = measured – 2 * Na + Gluc/18 + Urea/2,8 (> 10 is pathological)
      • Uremia, diabetic ketoacidosis, alcoholic ketoacidosis
      • Toxins: ASS, alcohols (methanol, mannitol, propylene glycol as in benzo or dilantin preparations), iron
      • Short gut syndrome (D-Lactate)
    • SIG < 0 = overdose with cations (Lithium, Bromide, Hyper-K, Hyper-Mg, Hyper-Ca, Nitrates, Immunoglobulins)
  8. Check adequacy of compensation for chronic primary acid base disorders
    • In respiratory: expected delta SID = 0,4 * delta CO2
    • In metabolic acidosis: delta CO2 = base deficit
    • In metabolic alkalosis: delta CO2 = 0,6 * base excess

Recommended reading

A manifest checklist

We had a few near misses and annoyed team members the last weeks, so we did some probing, asked around and tried to identify what went wrong. It turns out – as so often – that team communication had deteriorated over the last months, so that the various members did not understand eachother anymore. This led to exchanges about our communication culture and to the project of a team timeout with a stroke team “preflight checklist” that we go through for each patient in the morning:

  • What is the disease of the patient?
  • Is he stable?
  • What is the plan for today?
  • Are all drugs ordered and ready?
  • Have all labs been drawn?
  • Is there any impediment to mobilization or oral nutrition?

We learned a lot from projects like the Provonost study and the surgical safety checklist. As far as I understand the author of “The checklist manifesto” – a Brigham and Women’s surgeon named Atul Gawande – checklists form the condensation point for interdisciplinary communication, allowing all team members to contribute to and understand the common goals and prioritize their work.

Of course, we will see how it works out but I have been fascinated by Gawande’s exposition and expect great results…

Stroke prevention – what patients can or should do

An aspirine a day, some statin, maybe more drugs (controlling BP, cholesterol, sugar) – we have a lot of ideas what to prescribe patients after their stroke. So what should they themselves do to prevent the next stroke?

I preach the five columns of stroke prevention behavior

  1. Lose weight 
  2. Move around (5 times 30 minutes a week)
  3. Eat healthy (see recommendations by our German Nutritional Society)
  4. Don’t smoke
  5. Take your drugs (aka adherence)

This all sounds very well and we all suspect that properly following these instructions will reduce stroke risk in high risk situations (such as intracranial stenosis – see SAMMPRIS). Still, the evidence is scarce – as far as I know every attempt at showing that a particular diet is helpful for mortality failed. Studies for sports are rare. Even smoking studies are hard to come by.

We discuss the evidence and then develop a plan for a given patient.

The neurosurgical implications of PICA strokes

If your big PICA stroke gets worse, there are plenty of possible causes – here is a list:

  1. Direct brainstem compression
    – typically affects the contralateral corticospinal tract, often above it’s crossin, so that an ipsilateral hemiparesis occurs
    – pontomedullary motor cranial nerves might be affected
    – vertigo, oculomotor abnormalities
  2. Hydrocephalus from
    – Compression of the IIIrd ventricle
    – Compression of the aqueduct
    – Compression of the IVth ventricle
  3. Ascending transtentorial herniation
    – Somnolence
    – Vertical oculomotor abnormalities
    – Vertigo
  4. Transforaminal herniation
    – Vertigo
    – Nystagmus
    – Medullary brainstem signs