Scabies - so what's new?

Linda Scott - Tuesday, April 11, 2017

Being a GP is all about glamour isn’t it? That’s why we do this job. For the drama, the George Clooney-esq colleagues, the expensive shoes that never get muddy on home visits and our beautifully coiffed hair that we all have hours each day to perfect. Well, not really. We know because all our ‘Hot ‘Topics team are in the same boat as you. So we’ve parked the blogs on how to make sure your fake tan looks natural and what the latest superfood is and gone for this one instead.

Scabies. Lovely. Because it’s not a sexy condition, there isn’t much in the way of new research on its treatment, the latest being from Clinical Evidence in 2014.

Remember scabies is an infestation of the skin by the mite Sarcoptes scabei. The incubation period is long (8 weeks). It’s spread through skin to skin contact, but it is thought to be possible to be passed by sharing bedding, and towels too. It’s most common in institutionalised communities (e.g. nurseries, schools and care homes) and amongst the most vulnerable – the very young, the very old and those with immune-deficiency. Outbreaks most commonly occur in the winter.

Typical sites of the infestation are between the fingers and wrists but also skin folds (buttocks, breast creases, genitals) and flexor surfaces where visible burrows may be seen. It causes intense itching driving patients mad, especially at night. More widespread eczema-like eruptions may occur. The burrows typically appear as small, greyish lines in the web spaces and flexor surfaces of hands, wrists, ankles and feet. The secondary eczema-like rash spreads over all the skin. In older people it may present as a diffuse truncal eruption, in infants and children the face, scalp, palms and soles are most commonly affected. Some good pictures here on Dermnet New Zealand http://www.dermnetnz.org/topics/scabies-images/

Despite these helpful photos, the main challenge with scabies is thinking of it in the differential in the first place. We see a lot of random rashes and itching in primary care, but if you see either in the very young or elderly, think scabies. The discomfort and itching is much worse in immunocompromised people. Severe, persistent itch and secondary infections can be debilitating. Occasionally, crusted (‘Norwegian’) scabies may develop which is then resistant to routine treatment. Look out for this in patients in nursing homes with dementia who aren’t able to communicate the itching and discomfort typically seen.

Best way to get rid of it? Topical permethrin is the most effective treatment (1a evidence) and highly effective at increasing cure rate at 28 days. Topical crotamiton is less effective than permethrin, but there is evidence that it is an effective treatment. Both of these preparations are better than topical malathion and benzyl benzoate which are often used as second-line agents but lack evidence of efficacy.

Although not based on RCT evidence, treating family members and close contacts at the same time as the index case is advised. Clothing and bed linen belonging to the index case should also be washed. Making sure patients apply the treatment correctly is the other challenge as it can be a faff. There are good patient information leaflets on NHS choices http://www.nhs.uk/conditions/Scabies/Pages/Introduction.aspx and on the British Association of Dermatology http://www.bad.org.uk/for-the-public/patient-information-leaflets/scabies

For patients who have treatment failure, are immunocompromised with severe symptoms, or those with crusted scabies, there is some RCT evidence that oral ivermectin is effective. This drug is only available on a named patient basis’ and is usually given as two doses taken one week apart. Consider referral for these cases of treatment resistant or severe cases (e.g. crusted scabies in patients with HIV/AIDs) for consideration of this.

Zoe Norris

"Metformin - What's not to like then?"

Linda Scott - Wednesday, April 05, 2017

Don’t forget the simple things in life. The joy of a biscuit with your morning cup of tea, a new pair of socks and those nice familiar drugs we prescribe all the time without really knowing that much about them…. Or is that just me?

Like good old metformin - the medication equivalent of your favourite pair of slippers; it’s been around seemingly for ever. We have started it so many times, it’s easy to forget in the whirl of new jazzy treatments, that it’s just as important to be up to speed on metformin as it is on newer drugs.

So how does it work? Well, we aren’t sure… (good start) but we do know it increases the effect of insulin and also makes skeletal muscles take up more glucose. It reduces insulin resistance too!

It’s good, because it works, with a decent effect on HbA1c. It’s cheap, and it doesn’t have any effect on patients’ weight (maybe even a bit of weight loss!)

When used in overweight and obese patients, it improves their short term microvascular outcomes like retinopathy and neuropathy. In the long term, it improves macrovascular disease outcomes such as Cardiovascular disease and mortality.

It doesn’t cause hypos (unless you are also using insulin or sulphonylureas with it). Metformin has no impact on driving and as an added bonus, there is no increased risk of cancer!

What’s not to like then? Well, a couple of things.

The side effects can be a pain. Patients usually get a temporary loss of appetite, nausea, diarrhoea, abdominal pain and sometimes vomiting and diarrhoea. Some patients might notice a weird metallic taste in their mouth. The axiom when commencing metformin is “start low, go slow” to avoid the above GI side-effects. Last year’s diabetes guidelines from NICE recommends if patients struggle with GI side effects on standard release metformin, we should try the slow release preparation.

It can reduce absorption of B12, possibly leading to b12 deficiency.

The big one is lactic acidosis, although the number of cases are actually very low (9 cases per 100,000 person-years of exposure), and actually a Cochrane review revealed no cases of fatal or nonfatal lactic acidosis in over 70,000 patient years of metformin use. The symptoms are nausea, vomiting, abdominal pain, lethargy, hyperventilation and hypotension. However, NICE advise that metformin dose should be reduced to 500mg bd with an eGFR<45 and then stopped if eGFR<30.

Like a number of other drugs, remember to temporarily stop metformin, if the patient has any intercurrent illness, dehydration, acute kidney injury, shock, sepsis or acute heart failure. (Stop the DAMN drugs – Diuretics, ACEI & ARBS, Metformin and NSAIDS. Oh, and the new SGLT-2 inhibitors, but DAMNSGLT-2 isn’t as catchy).

A common mistake is stop to metformin when insulin is introduced; as long as the patients kidney function is sufficient, metformin should be continued to continue to help insulin sensitivity.

A last point not to forget, the NICE T1DM August 2015 guidance recommended metformin as a treatment option in T1DM for the first time. NICE suggest we consider adding metformin to insulin therapy in those with T1DM and BMI>25 (BMI>23 in high risk populations e.g. South Asian), who want to improve their glycaemic control and minimise future increases in insulin dosing.

We want everyone in primary care to feel included – so if you are a practice nurse, or have nurses in your team, then share this with them. This is one of the areas we cover on our new Primary Care Nurse course. This, plus everything from asthma and COPD, to minor illness and more diabetes. All in one neat package, all in one day. Or on the sofa in your pyjamas with our webcast – we aren’t judging.

Zoe Norris

Locum Organiser