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

Degenerative cervical myelopathy

This is the new name for the conditon formerly known as cervical spondylotic myelopathy, and is spinal cord dysfunction from compression in the neck due to degenerative change (disc herniation, ligament hypertrophy/ossification, osteophyte formation).


Gradual onset and worsening of symptoms, which vary and may include:

  • Neck pain and/or stiffness
  • Limb or body pain; unilateral or bilateral
  • Upper limb weakness, numbness, or loss of dexterity; may be unilateral or bilateral.
  • Lower limb weakness, sensory loss, or stiffness; may be unilateral or bilateral.
  • Paraesthesia
  • Autonomic symptoms; bowel or bladder incontinence, erectile dysfunction, or difficulty PUing
  • Unsteadiness/poor balance, sometimes leading to falls.
  • Atypical symptoms; headaches, muscle cramps.

Symptoms can be insidious and the course, although generally downhill, is variable; patients may have mild stable symptoms for long periods of time, or a more rapid decline. Patients will typically have increasing loss of dexterity (difficulty with tasks such as doing up buttons, writing, using mobile phones) and/or mobility (may need walking aids/have frequent falls).



  • Pyramidal weakness (UL worse in extensors, LL worse in flexors)
  • Limb hyperreflexia
  • Spasticity (claspknife sign)
  • Clonus – esp Achilles tendon
  • Babinski’s (upgoing plantars)
  • Hoffman’s sign (flick the nail of the middle finger to flex it sharply, see whether there is any reflex contraction of the thumb and/or index on that hand)
  • Segmental weakness at the level of compression
  • Sensory loss (limb and/or trunk)
  • Lhermitte’s sign (neck flexion or extension causes electric shock sensation down the spine/into the limbs – this is an indication that the problem is quite severe)
  • Gait disturbance



Requires MRI of the cervical spine, not surprisingly. This may be routine in patients with mild stable symptoms, but needs to be urgent in patients with progressive symptoms and/or symptoms substantially affecting quality of life. If MRI can’t be ordered directly, refer to neurology first if needed.

Note that scan findings do not correlate well with disease severity; mild compression can cause severe disease.



Spinal decompression (although a wait-and-see approach may be appropriate for patients with mild, stable DCM).

Maximal recovery has usually taken place by around 6 – 12 months post-op; residual symptoms at this point are likely to be permanent.


DCM as an incidental finding

This is quite common, and does not need any treatment if asymptomatic; however, patients should be reviewed for symptoms and made aware of symptoms that need prompt reporting in the future.


BMJ: Degenerative cervical myelopathy

Posted in Credits 2018, Don't miss, Neurology, Orthopaedics | Leave a comment

Cutaneous horns

I’ve just spent a bit of time refreshing my memory on these, after seeing a lesion I wasn’t sure about. After looking at several photos I do believe the patient I saw does have a small cutaneous horn, and the Dermnetnz article confirmed that these need excision to exclude premalignant or even malignant cells at the base, which occur in about 50% of cases (which is a higher percentage than I thought). The article also had a list of features associated with a higher risk of malignancy in these lesions:

  • Pain
  • Large size
  • Wide base, or wide base compared to the length
  • Induration at the base
  • Redness at the base
  • Site: lesions on the nose, ears, scalp, face, forearms, or backs of hands are more likely to be malignant, which is not surprising given that these will be the high-risk areas for sun exposure. Lesions on the penis are also more likely to be malignant, which is more surprising; I don’t know the explanation for this.
  • Lack of terrace formation. ‘Terrace formation’ apparently refers to a pattern of horizontal ridges on the side of the horn – lack of this can be a sign of rapid unorganised growth.

This is reassuring as my patient’s lesion was small and not painful with a narrow base and no inflammation. However, it’s important to note that there is no single sign that can reliably confirm or exclude malignancy; only excision and histology will do that. This confirms that, as I suspected, I need to refer this patient as a two week wait.

Posted in Credits 2018, Dermatology, Skin lesions | Leave a comment

Slow initiation of warfarin protocol.

We’re all familiar with the usual 5mg warfarin initiation protocol (and many of us have distant memories of the 10-10-5 regimes started in hospital, or at least that’s what was being done when I was a junior doctor, back in the Dark Ages second half of the ’90s). I had, however, heard that it’s possible to initiate warfarin even more slowly, and that has obvious benefits in elderly people being started on it for AF, who don’t need the anticoagulation urgently and are at more risk if they’re overanticoagulated. So, when I had a patient fitting that description, I went looking for a protocol.

I found what I was looking for on the site GP Notebook, which directed me to two studies, of which this one looked like the best bet. The protocol here is to start patients on a 3 mg loading dose daily, and check on Day 8 and Day 15. I’ll try the 3 mg and checking on Day 8, and take it from there.

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Recovery after laparascopic surgery

Pain: Abdominal cramps and bloating, and shoulder tip pain, are common in the first 24 hours. Worsening pain after this period can be a sign of complications.

Other symptoms of complications: Loss of appetite for food or fluids, reluctance to mobilise, N&V, poor urine output.

Possible signs of complications: Pyrexia, tachycardia, abdominal tenderness or distension.

Time off work: There are no clear guidelines; play it by ear according to the person’s occupation, procedure, and recovery. As a rough rule of thumb, smaller procedures such as lap chol or appendicectomy typically only require a couple of weeks off. Larger procedures are likely to require more time off/more gradual return to work.

Return to driving: Requires the ability not just to do emergency stops, but to turn around enough to check blind spots and to react quickly. Might take one or two weeks for lap chol or appendicectomy and longer for groin surgery or more major procedures.

Heavy lifting: Not that much data. The advice is to avoid lifting anything heavier than a kettle/a shopping bag, and also to avoid pushing and pulling activities such as vacuuming, mowing the lawn, and hanging up heavy washing. One or two weeks should be enough for smaller procedures and four weeks for larger procedures.

Eating and drinking: Normally no restrictions, although a few procedures (gastric banding, anti-reflux surgery, surgery for oesophagogastric cancer) can require a liquid-only diet initially.

Recovery generally: Patients should expect to notice an almost daily increase in how much they can do without pain or discomfort.

Travel: Patients are advised not to fly for 24 hours after laparoscopy because of the possibility of expansion of carbon dioxide in the abdominal cavity. It’s considered sensible to use thromboembolic stockings if flying within the first month.

Swelling at the site: Might be due to haematoma, abscess, or seroma; important as seromas may be treatable conservatively, but abscesses and large haematomas are usually going to require surgical intervention.

  • Haematoma: Usually shows up within 24 – 48 hours of surgery. May be painful and there may be bruising present. Overlying skin temperature is normal.
  • Abscess: Typically 3 – 7 days after surgery. Likely to be very tender with hot, red overlying skin and sometimes visible purulent discharge.
  • Seroma: Usually show up over a week post-op and cause only slight discomfort. Skin colour and temperature are normal.

Note that superficial wound infections can probably be treated in general practice, but contact surgery if there is any concern about possible deeper infection.

Thromboprophylaxis: In cancer patients, and normally in patients who’ve had bariatric surgery for morbid obesity, this is continued for a month.


BMJ: Management of patients after laparoscopic procedures.

Posted in Credits 2018, Surgery | Leave a comment

Prophylaxis of recurrent UTI in women

Background: No official definition, but generally defined by most people as two or more episodes in six months or three or more per year. The only recommended prophylactic treatment currently is low-dose prophylactic antibiotics, which, based on one systematic review/meta-analysis, has a very good success rate with a NNT of 1.85 over a 6 – 12 month period (though unfortunately the studies on which this was based seem to have been of poor quality). The problem, of course, is our old bugbear of antibiotic resistance. This BMJ article discusses other methods.

Short version: Currently we don’t have much evidence to say that anything else works for prophylaxis. However, methenamine hippurate is looking promising, and topical vaginal oestrogens are probably helpful in post-menopausal women.

Methods discussed were:

Urinary alkalisation: No evidence as to whether or not it works because, in a recent review, none of 172 RCTs of the matter were good enough quality to include, which is a pretty scary comment on the state of our medical research today. Side-effects include nausea, flatulence, and mild diuresis. In practice, probably comes under the heading of ‘Might be worth a try’, but isn’t anything we can medically vouch for at this point.

Probiotics: Don’t seem to help, according to a recent Cochrane review, but again we have the problem of all the research being fairly poor quality, which means there may possibly be benefits that have been missed. Side-effects showed up in <5% of the women and included vaginal discharge, genital irritation, and diarrhoea. I’d file this as ‘Can’t hurt, but don’t expect too much’.

Chinese herbal medicine: Does seem to work according to a Cochrane review, but, again, problems with poor research; also, the existing research seems to have been in post-menopausal women and won’t necessarily apply to the pre-menopausal population. Not much work done on side-effects and, unfortunately, Chinese herbal medicine¬†does have more potential for harm than the two above methods, so this is not one I’d recommend unless a lot more work gets done.

Methenamine hippurate: One trial of 30 people with recurrent UTI found this to be associated with a relative risk of UTI of 0.46, and several studies have found very low rates of adverse events; out of 2032 people in all studies in one Cochrane review, twelve had nausea, one had rash, one had diarrhoea, one had sore throat, and one had bladder ‘stinging’. Therefore, while there is not currently enough evidence to say this works, there is enough to be cautiously optimistic. Results of an ongoing multicentre RCT are awaited. Watch this space.

Cranberry juice: Seems, alas, to have been discredited; previous studies that showed benefits had a high dropout rate, and an updated Cochrane review did not see a statistically significant benefit. Another one bites the dust.

Oral immunostimulants: I’m not even sure what these are. Whatever they are, a meta-analysis of four RCTs found they helped, a further double-blind RCT found no effect, and the European Association of Urology supports their use, so overall it sounds as though they’re worth finding out about.

Topical vaginal oestrogen: In post-menopausal women, obviously. An analysis of two small RCTs did find a benefit, with a minority experiencing side-effects related to either hormonal (breast tenderness, vaginal bleeding, change in discharge) or local (vaginal irritation, burning or itching) effects.

Coming soon: Research papers on intravesical agents, vaccines, and D-mannose.



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Migraine in pregnancy

The good news is that pre-existing migraine often gets better in pregnancy, especially migraine without aura and premenstrual migraine. However, it’s important to know a) how to treat it when it occurs and b) how to avoid confusing more dangerous causes of headache with migraine.

Treatment of pain

  • Paracetamol should be used first-line
  • Ibuprofen can be considered but has less safety data than paracetamol and should be avoided in the third trimester (risk of premature closure of the ductus arteriosus)
  • Opiates are considered safe in pregnancy, but can exacerbate nausea/reduce gastric mobility, so the article advises avoiding them, although frankly I think that may be too strong a piece of advice given that you may well end up without other safe options for treating someone in pain.

Treatment of nausea

The choice is better here. Cyclizine is first-line, but other acceptable choices include prochlorperazine, domperidone, ondansetron and metoclopramide (although avoid long-term use of the latter due to its extrapyramidal SEs).

Prophylactic treatment

  • Aspirin 75 mg od. Often helpful for migraine prevention in pregnancy (which makes me wonder whether it’s been tried as a prophylactic outside of pregnancy, since it would surely have a role there) and has been used safely up to 36 weeks gestation in a recent RCT.
  • Beta-blockers, such as propranolol 10 – 40 mg tds or the equivalent dose once daily. Studies did not find use in the first trimester to be associated with an increase in rate of congenital anomalies.
  • Low dose TCAs; e.g. amitriptyline 10 – 25 mg nocte.


Red flags

  • Sudden-onset headache reaching maximal intensity in <1 minute – could be a bleed
  • New onset severe headache or significant change in headache type.
  • Headaches progressively worsening over time
  • Features of meningitis
  • Features of RICP
  • Orthostatic headache (changes with posture)
  • New-onset focal neurological deficit
  • Visual disturbance or visual field defect
  • New-onset seizures or cognitive dysfunction
  • Impaired consciousness
  • Personality changes
  • Head or neck trauma in the past 3 months (and, unlike most of the others, this is one I wouldn’t have known to be a problem)
  • Unusual aura (e.g. >1 hr duration, associated motor weakness)
  • Symptoms of GCA
  • Symptoms of glaucoma
  • Raised BP/symptoms of pre-eclampsia

Also consider:

  • History of neurological conditions
  • History of pituitary problems
  • History of immunocompromise
  • History of malignancy
  • History of conditions associated with procoagulable state
  • FH of ICH

And, less urgently:

  • Medication that might contribute to the headache: e.g. CCBs.
  • Possible medication overuse headache.

BMJ 2018;360:k80

Posted in Credits 2018, Medication in pregnancy, Migraine, Pregnancy and Childbirth | Leave a comment

Peripheral arterial disease

Most patients are asymptomatic; however, note that this usually reflects more sedentary lifestyle rather than lesser severity, and asymptomatic patients with PAD are at just as much risk of complication. (Note that coexisting diabetic neuropathy also increases the chances of the leg being asymptomatic.)


Risk factors

  • Smoking probably causes about half of all cases.
  • Diabetes carries a similar risk level to smoking.
  • Increasing age increases prevalence.
  • Tends to show up in men at younger ages, but difference in prevalence levels is similar between men and women.
  • High cholesterol, hypertension, and CKD each increase risk by a factor of 1.5x.
  • Remember to check for AF as a risk factor for acute ischaemia.



May be with claudication, acute limb-threatening ischaemia, or chronic limb-threatening ischaemia:


Aching or burning in leg muscles, reliably reproduced at a set distance on walking, relieved within minutes on rest, not exacerbated by position, not present at rest. Pain is usually in the calf, but can be in the thigh if the iliac artery is affected.

Acute limb-threatening ischaemia

ALTI is thromboembolic in nature. Embolic ALTI is typically in a normal artery (most usually a result of AF) and comes on very suddenly; this is the one that presents with one or more of the 6 Ps, as per medical school teaching, and needs treatment within hours, including embolectomy. Cases caused by thrombus typically form in an artery with existing arteriosclerosis; they tend to be more gradual onset and (due to pre-existing collateral arterial formation) less severe than the embolic ones. Cases due to thrombus can often be medically managed.

Chronic limb-threatening ischaemia

Caused by narrowing of multiple arteries to the point where the foot becomes severely ischaemic. Presents with rest pain and/or tissue loss. Although it’s less dramatic than ALTI, it’s a serious condition with a high risk of limb loss or death and requires same-day discussion with a vascular surgeon.

Rest pain: note that this is usually in the forefoot/toes rather than the leg muscles. Typically, this is continuous and worse when the foot is elevated – hence patients will get more severe pain at night, hang their foot over the side of the bed to relieve pain, and often sleep in a chair to relieve pain. The latter, unfortunately, tends to start up a vicious circle as sleeping with dependent feet leads to an increase in foot oedema which can reduce the arterial circulation further.

Tissue loss: May be ulceration (usually over pressure areas; hence the toes, the heel, or the metatarsal heads) or gangrene (usually of the toes).

CLTI often presents without prior symptoms of claudication. This is partly because patients may not walk far enough to get claudication, and partly because coexisting diabetic neuropathy is, for obvious reasons, common in CLTI patients.

CLTI usually requires a revascularisation procedure (or, in 15%, amputation) but can be managed conservatively in about 20% of patients. However, always discuss with a vascular surgeon.

Note that CLTI is easily missed. (In fact, the article I’m taking this information from is in the ‘Easily Missed’ section of the BMJ.) It often presents insidiously and is easily mistaken for cellulitis, gout, or plantar fasciitis. The patient may still have foot pulses (not common, but it happens, even in cases of embolisation in the early stages) or may feel as though they have foot pulses when they don’t (there is a substantial false positive as well as false negative rate for palpation of foot pulses – even when vascular surgeons do it, which is reassuring or worrying depending on your point of view). ABPIs can be misleading, partly due to collaterals and partly due to arterial wall calcification (see below). The foot may look lovely and pink if the patient is sitting in a chair and hence getting lots of downward blood flow. Moral of the story? Have a high index of suspicion, and do Buerger’s test (see below).



  • Check peripheral pulses, obviously, going proximal to distal (I don’t know why or whether it matters which way you go, actually, but this is what the article says).
  • Look for hidden tissue loss on the heel and between toes.
  • Don’t bother too much with capillary refill, hair loss, or colour (I assume suspected acute ischaemia is an exception to the last) as they are of little diagnostic importance.
  • If CLTI is suspected at all, then do Buerger’s test; the foot turns pale on elevation due to ischaemia and red on dependency due to reactive hyperaemia.

ABPI of 0.9 or less is diagnostic of PAD and 0.5 or less suggests critical limb ischaemia. However, beware arterial calcification; this can cause falsely elevated ABPI values due to arterial incompressibility. Tends to show up in people with diabetes and/or CKD.

Also check:

  • Pulse (you still remember that Finals question, right?)*
  • BP
  • FBC/E&C/glucose or HbA1c/lipids
  • If patient under 50 yrs, thrombophilia screen
  • ECG


Indications for referral

Referral is not always necessary; asymptomatic patients and those with claudication only can be managed in primary care. (Document the ET at presentation in order to monitor whether progress is being made.) Note the following three situations:

1. Limb-threatening ischaemia, whether acute or chronic, requires urgent admission under the vascular team.

2. Diabetic foot ulcers in patients with PAD need urgent referral to the diabetic foot multidisciplinary team.

3. Patients with claudication symptoms that are affecting their quality of life and not improving after three months of supervised exercise therapy (see below) should be routinely referred to the vascular clinic for consideration of revascularisation.



  • Stop smoking. Smoking cessation, for a PAD patient, not only reduces their risk of amputation, it also doubles their chance of surviving the next five years.
  • Antiplatelet treatment. Clopidogrel is first choice (best risk of harms/benefits), aspirin is second choice. Don’t use both, though – the bleeding risk with dual therapy is too high. Warfarin is normally only used in cases of arterial emboli (or AF, I assume). NOACs weren’t mentioned; don’t know offhand whether or not any of them are licenced for arterial emboli in PAD.
  • Exercise. There is apparently excellent evidence that supervised exercise programmes work significantly better than unsupervised exercise, but unfortunately the article didn’t clarify what ‘supervised’ was meant to mean here; I’m guessing I’m not actually meant to go out and watch all my patients with PAD walk several times a week. Anyway, the goal to aim for is walking for >30 minutes to near-maximal pain, at least three times a week for at least six months. Supervised exercise therapy actually works as well as angioplasty at improving both walking distance and quality of life. Interestingly, the improvement can occur even when ABPI remains the same.
  • Naftidrofuryl oxalate can be effective and is a possible second-line treatment in patients who are no better with walking therapy but don’t want secondary care referral. It should be tried for 3 – 6 months but stopped if not making a difference at that time. Cilostazol is also an option, but naftidrofuryl is both the most efficacious (up to 60% improvement) and the most cost-effective.
  • Advise weight loss if BMI >25, including giving ‘an optimal diet plan and a goal’. The article didn’t say what evidence there was for this.

Also, of course, PAD is a marker for other arteriopathy, so there are other things that aren’t particularly helpful for the PAD symptoms or risks but that are important to do anyway:

  • Statins. Reduce both CVA and all-cause mortality (OR 0.77 in each case) but not clear whether they affect walking distance. It’s secondary prevention, not primary; use Atorvastatin 80 mg od as first choice and aim to reduce non-HDL concentration by 40%.
  • Hypertension management. Ramipril is recommended as first-line therapy; the BMJ article says on page 202 that it doesn’t improve claudication symptoms (symptomatic review and meta-analysis) and on page 203 that ACE inhibitors improve walking distance in patients with claudication by an average of 86m. So, make what you will of that; maybe if I have time I’ll haul out the studies and try to figure it out. However, treatment of hypertension does of course improve overall cardiovascular risk, so worth going for anyway. Target is <140/90 in the under-80s and <150/90 in the over-80s.
  • Work for good glycaemic control in diabetes; it doesn’t seem to reduce amputation risk, but it does reduce the risk of microvascular complications. Target is <48mmol/l.



At five years from diagnosis of PAD:

  • Most patients with claudication will have stable or improved symptoms.
  • Between 1 and 3.3% will have progressed to amputation.
  • 20% will have died (I assume due to the association with other vasculopathies – MI, CVA, renovascular disease, vascular dementia, and mesenteric disease).

For patients with critical limb ischaemia the prognosis, not surprisingly, is a lot worse. By one year 30% will have had an amputation, and by five years 50% will be dead.


*In surgical finals, I was examining someone with possible PAD and started my presentation of examination findings by reeling off the pulse rate and rhythm. The examiner asked me why I mentioned that it was regular; turned out he was hoping I’d thought to exclude AF due to the increase in arterial thrombosis risk. Sadly, I wasn’t nearly that savvy and had simply been going through the standard list without thinking, so I missed a chance to impress him. It was a useful lesson, though (and I did pass, so I suppose that’s what matters).

Articles used in writing:

https://doi.org/10.1136/bmj.j5842 – PAD generally

https://doi.org/10.1136/bmj.j5460 – CLTI/ALTI

Posted in BMJ, Credits 2018, PAD, Vascular | Leave a comment