About this blog: information for everyone else

Hi there! I’m a GP and this blog consists of the notes I take on journal articles, as part of my continuing professional development. It is intended purely for my own use in recording and remembering the things I learn so that I can refer back to them in the medical setting. While anyone is welcome to read it, please do not take it as any kind of substitute for seeing your own doctor for any medical-related queries or problems.

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About this blog: information for appraisers

This blog consists of notes made on any learning points I come across in the course of CPD and want to remember/look up later. The two main sources for this are on-line learning modules, and articles which I identify in the course of journal reading as meeting a learning need. Credits for the former are obviously counted elsewhere, so I’ve grouped the latter in a separate category in order to estimate the learning credits I’ve obtained from structured reading. You can find all posts in that category for the 2013 – 14 appraisal year here.

Posted in About this blog, Credits 2016 | 2 Comments

Sports hernia

Yet another one (pretty much the last, for now) from the archives. This article comes from the BJGP of March 2013.

‘Sports hernia’ – also known as sportsman’s hernia, athletic pubalgia, and Gilmore’s groin – is not, in fact, a hernia. It’s a weakness of the posterior wall of the inguinal canal, caused by a set of injuries to the abdominal and pelvic musculature outside the hip joint.

Epidemiology: The typical patient is a young male who actively participates in sport, especially football, hockey or athletics. It’s considerably less common in women and in people who don’t participate in sport (although it can affect both these categories) and is rare in children and older people.

Presentation:

  • Dull, poorly localised groin pain
  • Caused by exertion but can persist for days or weeks following exertion
  • Above the inguinal ligament and radiating towards the scrotum/inner thigh
  • Can cross the midline or be bilateral in nature
  • Absent or mostly so when patient resting from sport; recurs when they take the sport up again
  • Often insidious onset

Examination:

  • Tenderness over pubic symphysis and/or pubic tubercle
  • Exquisite tenderness when the superficial inguinal ring is directly palpated via scrotal inversion with the little finger
  • The ‘direct stress test’ – palpation over the superficial inguinal ring is uncomfortable while the patient is lying supine but pain is increased (and similar to presenting complaint) when the patient straight-leg raises while palpation continues.
  • Resisted sit-ups are painful.

Investigation: Ultrasound or MRI are useful both in helping with the diagnosis and assisting with other pathologies.

Treatment: Start with conservative management for 6 – 12 weeks. This includes rest, NSAIDs, steroid injections and physio. A patient who is pain-free following this should attempt to return to sport.

If this isn’t successful (more often than not it isn’t), move on to surgical management, which consists of reinforcement of the posterior abdominal wall either by open or laparoscopic surgery, followed up by physio. Normally patients can return to full activity between 6 and 12 weeks. Surgery is successful in over 90% of cases.

Plan: If suspicion of a sports hernia is high based on history and examination, start with conservative management. If there is diagnostic uncertainty, arrange scan as above. If symptoms persist and are impacting on the patient’s quality of life, the patient is suitable for surgery, and other causes of groin pain have been ruled out, or if there is diagnostic uncertainty, then refer to a general surgeon with a particular interest in sports hernias.

Posted in Credits 2017, Orthopaedics, Sports medicine | Leave a comment

Snippets

Bits and bobs from the BMJ of 9th September:

A systematic review in PLoS Medicine found gabapentin and pregabalin to be not particularly helpful with chronic low back pain; any benefits from them were outweighed by the risk of side-effects (dizziness, fatigue, visual disturbances). (Minerva)

The pendulum has, kind of, swung back on the issue of prescribing prophylactic antibiotics for high-risk patients undergoing dental procedures; now we’re meant to offer it and discuss risks and benefits. ‘High-risk’, here, includes patients with prosthetic heart valves; patients with a past history of infective endocarditis; and patients with some types of congenital heart disease. Note that, although prophylaxis is known to reduce the incidence of bacteraemia, we do not currently have good evidence as to whether it actually reduces the risk of endocarditis. (Uncertainties)

And a sacred cow appears to have been slain. PURE, an enormous observational study of diet and cardiovascular mortality (five continents and almost 150 000 people, over a median of 7.4 years), found that consumption of fat – even saturated fat – was actually associated with lower cardiovascular disease rates, and saturated fat was also associated with lower stroke risk. Carbohydrate appeared to be the actual problem; high intake was associated with higher total mortality risk. More expectedly, higher fruit, vegetable, and legume intake was associated with lower mortality risk; maximum benefit appeared to occur at 3 – 4 servings (375 – 500g)/day. (Richard Lehman)

Posted in Credits 2017, Medication | Leave a comment

Endometriosis

Some points from a recent BMJ article:

A normal examination and pelvic USS don’t rule out endometriosis. On the other hand, they may not need to; in a lot of cases, you’re only going to be treating the symptoms anyway, and you don’t need a diagnosis of endometriosis to prescribe the COC or NSAIDs for heavy painful periods.

If initial hormonal treatment is contraindicated or is ineffective/not tolerated, refer to gynae (or specialist endometriosis service, if available). Women of 17 or under may be referred to a paed and adolescent gynae service, but it depends on local services (I’m pretty sure we don’t have one).

Hormonal treatment for endometriosis doesn’t improve spontaneous pregnancy rates, so don’t offer it to women looking to conceive.

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COPD algorithm

This is our practice algorithm for COPD treatment:

Treat intermittent symptoms with a SABA.

If more severe, differentiate between low-risk and high-risk patients. Low-risk patients are those with:

  • FEV1 >50%
  • <2 exacerbations/yr

For low-risk patients:

  • First-line treatment: LAMA
  • If symptoms continue: LAMA/LABA combination

For high-risk patients:

  • First-line treatment: LABA/ICS
  • If symptoms continue: add LAMA

The algorithm also listed specific recommended inhalers, but do bear in mind that the brands will have been recommended largely on price grounds: in other words, it’ll mostly be because they’re currently cheaper than other brands rather than because they have any particular clinical difference from others. This therefore isn’t any kind of endorsement. The inhalers currently recommended are as follows:

LAMA

  • MDI: Tiotropium, as Spiriva Respimat 2.5 mg two puffs od.
  • DPI: Aclidinium, as Eklira 322 mcg bd

LAMA/LABA combo

  • MDI: Spiolto via Respimat, once daily (contains Olodaterol + Tiotropium)
  • DPI: Anoro (Umeclidinium/Vilanterol) via Ellipta once daily, or Duaklir (AclidiniumFormoterol) bd

LABA/ICS combo

  • MDI: Fostair 100/6 two puffs bd (Beclometasone + Formoterol)
  • DPI: Relvar 92/2200 (Fluticasone + Vilanterol) or Symbicort 400/12 one puff bd

If one of the above is combined with a LAMA for severe COPD, the guidelines suggest:

  • Fostair – Spiriva, dose as above
  • Relvar – Incruse 55 mg od
  • Symbicort – Eklira, dose as above

I have no idea why. Oh, well, at least now this is all somewhere where I can find it all without having to cart the actual sheet around.

 

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Refractory opioid-induced constipation

As anyone with even a smattering of palliative care knowledge should be aware, opiates typically cause constipation and a laxative should typically be co-prescribed. This week’s BMJ has a useful tip on what to do about opioid-induced constipation that is not responding to laxatives; try targeted antagonism of the peripheral μ-opioids in the gut. Examples include:

  • Methylnaltrexone bromide
  • Prolonged release formulation of oxycodone in fixed dose combination with naloxone
  • Naloxegol oxalate
Posted in Credits 2017, Medication, Palliative care | Leave a comment

Some simplified neuroanatomy

After years of journals and on-line learning programmes it feels quite bizarrely retro to go back to a textbook, but that’s what I did; I’ve been thinking for a while that I really need to refresh my memory on the kind of basic neuroanatomy that’s needed to map symptoms to likely lesion sites. (It’s very depressing how we forget these things, given how much time and effort goes into learning them in the first place.) So I hauled out my good old copy of Wilkinson’s ‘Essential Neurology’. I’ve had this for something like twenty years now and the book itself is even older (published 1988), but I keep it around as it’s so good at expressing hideously complex pathways as this-is-what-you-actualy-need-to-know simple schematics. (And it’s now even better – I just looked up a more recent edition on Amazon and found some really helpful diagrams with the look-inside feature.)

Anyway. Here are some notes on some key points of which I have now reminded myself. They are not very comprehensive and (as always) anyone actually wanting to know something about this subject for themselves would be much better advised to check out a proper expert source.

Motor pathways

  • Start in the cortex
  • Travel through the internal capsule
  • Cross over at the lower end of the medulla
  • Descend in pyramidal tract on the lateral side of the spinal cord, ipsilateral to the muscles they innervate (this is therefore also known as the lateral corticospinal tract)
  • Synapse at the level of their exit from the spinal cord (therefore, spinal cord damage produces upper motor neurone damage)
  • Exit through the ventral root

 

Sensory – pain and temperature

  • Enter spinal cord via the dorsal root (cell body is in dorsal root ganglion, but there’s then a proximal axon of the same nerve that passes into the spinal cord, rather than a synapse in the ganglion)
  • Cross over at the level they enter the spinal cord, after the synapse
  • Ascend in the lateral spinothalamic tract, contralaterally to the side they entered
  • Synapse again in the thalamus

Sensory – proprioception and vibration

  • Again, enter via the dorsal root with body in the dorsal root ganglion, but…
  • The proximal axon then ascends ipsilaterally in the posterior column of the spinal cord, getting all the way to the medulla before synapsing. (For bonus points – synapses are in the gracile or cuneate nucleus.)
  • The pathway crosses in the medulla, after synapsing.
  • Forms a second synapse in the thalamus before passing to the cortex.

 

Autonomic pathways

Less well-defined – can be bilateral.

So, good old Brown-Séquard syndrome gives you ipsilateral upper motor neurone lesions and loss of proprioception/vibration sense and contralateral loss of pain/temperature sensations, below the level of the lesion. (And possibly lower motor neurone lesions at the level of the lesion, depending on how it’s placed.) Bladder and bowels may be spared, although that’s variable.

Anterior lesions of the spinal cord can affect bladder and bowel, pain and temperature, and motor pathways. (The lateral spino-thalamic tracts are anterior to the pyramidal tracts, so I think pain and temperature sensation would be affected first.)

Posterior lesions affect proprioception/vibration sense.

 

Cerebellar control = ipsilateral

Basal ganglia control = contralateral (not sure that’ll ever come up, but there you go)

 

Upper vs. lower motor neurone lesion

Remember that upper motor neurones have an inhibitory effect upon the lower. So, while either upper or lower motor neurone lesions will produce weakness, the other effects are different:

Upper motor neurone lesion:

  • Increased tone
  • Claspknife rigidity
  • No wasting
  • Hyperreflexia
  • Clonus
  • Upgoing plantars

Lower motor neurone lesion

  • Decreased tone
  • Wasting of muscles
  • Reduced or absent reflexes
  • Fasciculation
  • Downgoing or absent plantars

 

Cerebral artery territories

Anterior: Contralateral leg, both sensory and motor

Middle: Contralateral face and arm, both sensory and motor. Also dysphasia, dyslexia, dysgraphia and dyscalculia.

Posterior: Contralateral homonymous hemianopia.

Vertebro-basilar: Cranial nerve lesions, ataxia, bilateral motor and/or sensory loss.

 

Posted in Credits 2017, Neurology | Leave a comment

Treatment of chronic vertigo

There’s a useful article on the BMJ page right now, on chronic vertigo; apparently, first-line treatment for chronic vertigo is vestibular rehabilitation. This involves daily low-intensity exercises for 6 – 12 weeks to stimulate natural vestibular rehabilitation, and has been shown (moderate quality evidence) to be helpful for chronic vertigo. It can be used (on the basis of variable evidence, the details of which I didn’t check) for:

  • Chronic vertigo following vestibular neuronitis
  • Persistent BPPV following Epley manoeuvres
  • Vertigo between attacks of vestibular migraine (weak evidence)
  • Persistent chronic vertigo in Ménière’s disease

The article also cleared up something else for me; although betahistine is only licenced for use in Ménière’s, there is low-quality evidence showing that it works in other chronic vertigo situations. (Actually, there is apparently only low-quality evidence that it works in Ménière’s.)

The authors advised that betahistine has no place in the treatment of chronic vertigo, but, based on what the article itself said, I would disagree with that. There is no doubt, from what they said, that vestibular rehabilitation rather than long-term medication is the way to go for first-line treatment of chronic vertigo. However, like all treatments, it is not going to work for everyone; in fact, the article cited a NNT of 5, which would mean 80% of patients don’t respond. Even allowing for whatever the spontaneous resolution rate is (I didn’t look it up, but I assume there is one), that must still leave a fair number of patients with persistent problems, some of which are going to be disabling. We can’t just leave them with no options. The article says that we have low-quality evidence for the efficacy of betahistine, with a NNT of 8. Low-quality is obviously not great, but it’s still something. It also says that betahistine is generally well tolerated. I know I’d now consider it worth trying if a patient is still having persistent and disabling symptoms even after vestibular rehabilitation (not to mention that I’d have to refer a patient to get vestibular rehabilitation, and they might really want something for symptoms while on the waiting list).

Posted in Credits 2017, ENT, Vertigo | Leave a comment