Hay Fever vs GCSEs

A 16 year old boy has his GCSEs coming up and feels his hayfever is stopping him from concentrating. He has tried antihistamines before with some success, but he is worried they might make him drowsy and worsen his focus.

This is a real problem. A case-control study found students were more likely to drop GCSE grades between a mock in winter and the real one in summer if they had allergic rhinitis – https://www.ncbi.nlm.nih.gov/pubmed/17560637

“In this study, young people with reported allergic rhinitis symptoms on an examination day were, in comparison with their fellow students without symptoms, 40% more likely to drop a grade between their practice and final GCSE examinations, and 70% more likely to drop a grade if they reported taking sedating antihistamines at the time of their examinations.”

“The significant effect of sedating medications on examination performance observed in this study should encourage prescribers to recommend the use of non-sedating alternatives in routine practice.”


Q. How far do I have to explore other differentials when someone says its their typical hayfever? I find it a little awkward to keep asking patients ‘what do you mean by hayfever?’ when they clearly have hayfever.

A. Hayfever = seasonal rhinitis +/- conjunctivitis

Rhinitis = nasal discharge +/- nasal obstruction (sneezing and itching too, especially in allergic forms)

Sinusitis = facial pain in sinus area +/- rhinitis

After confirming the patient has rhinitis, the next thing to establish is allergic vs infectious vs obstructive.

The red flags for something nasty are unilateral rhinitis symptoms, especially with obstructive/blood stained/smoker/drinker/Chinese origin/CN III-VII abnormalities. It’s also worth examining for polyps / hypertrophied turbinates if this hasn’t been done before. That’s about as far as I normally go in someone who is known to have to have hayfever with a good seasonal history.

Q. Are the non sedating antihistamines really non sedating? Which one would you pick?

From the BNF:

Drowsiness is a significant side-effect with most of the older antihistamines although paradoxical stimulation may occur rarely, especially with high doses or in children and the elderly. Drowsiness may diminish after a few days of treatment and is considerably less of a problem with the newer antihistamines.

From BMJ Learning:

“Cetirizine has a faster onset of action than loratadine, and a meta analysis found it to be more effective for treating allergic rhinitis compared with loratadine, montelukast, and desloratadine. It has also been shown to be more effective than fexofenadine at relieving the symptoms of SAR at five to 12 hours following administration.”

So, non-sedatings are better for this patient. In terms of the choice of non sedating, our local allergy clinic loves cetirizine first line. That said, fexofenadine does not carry drowsiness warning labels in the US, but cetirizine does carry labels stating may cause drowsiness may occur and to avoid heavy machinery/alcohol. Perhaps in this patient fexofenadine could be second line after cetirizine if drowsiness / impaired concentration is still a problem.

Q. What other non-pharmaceutical treatments would you use?

Allergen avoidance and a saline rinse (like Neil Med). The saline rinse seems to be loved by ENT for pretty much all types of nasal congestion. It’s pretty safe, and you can use it once to three times a day.

Q Anything else?

NICE CKS have the following table:

Screen Shot 2017-07-25 at 11.02.40

Oral steroids are occasionally used short term for ridiculously severe symptoms or if something important is coming up, like GCSEs or the Lego Batman movie.

Most of the time I use intranasal corticosteroids next. NICE CKS suggest they can be used for moderate and severe hayfever.

It’s important to demonstrate to the patient how to use them. I’ve often found when I ask a patient to demonstrate how they use the spray, it’s often a deep sniff to the back of the throat preventing oesophageal hayfever. I like this video:

This is how I say it:

To spray the right nostril – a poem by Dr Crunch

Shake it.
Look slightly down.
Hold the spray in your left hand.
Place the spray in the right nostril.
Angle it towards your right ear.
Spray with a gentle inhalation.
Smile.

Q. They aren’t getting better and now they came back to see me instead of someone else and I have to deal with it and help.

A. According to BMJ Learning (http://learning.bmj.com/learning/module-intro/ask-an-expert-hay-fever.html?moduleId=10056477), it’s probably one of the following three things:

• They are using the spray incorrectly
• They are using the spray only “as needed”
• They are not using the spray for long enough.

What were the patient’s expectations about the nasal spray? It takes 8-12 hours to see an effect from the spray, and really at least two weeks to judge if its working. It needs to be used regularly, not PRN. In fact, if someone is known to have bad hayfever each year, then it’s worth using the spray for 2 weeks prior to the start of hayfever season.

Q. Won’t we stunt his growth?

A. The older nasal corticosteroids did have significant systemic absorbtion, especially beclomethasone, which is the most likely one they would purchase over the counter.

The newer ones, like momentasone and fluticasone, basically have <0.5% systemic absorbtion. Neither you or the patient have to worry about this. The BNF is chilled with momentasone 50mcg/day for children from 6 years up.

Q. So just to summarise, what did you do for this patient?

A. GCSE performance may be worsened by poorly controlled hayfever. It was important to get on top of it.

Nasal corticosteroids were the next line after non sedating antihistamines, allergen avoidance and sinus rinse. The patient responded nicely to this, having been advised about the timeframes for response and the technique.

Hb 65, ESR 110. Differentials?

ESR-01
What ESR really measures

A 67 year old woman had an unexplained Hb of 65 g/L. The only previous Hb result was 103 g/L from over four years ago. She felt generally tired with achy muscles most of the day for the past few months. An ESR had been sent, and came back as 110.

Q. Arrgh! PMR! Myeloma! Anaemia of chronic (rheumatological disease) of some kind!

A. Possibly. But it’s still quite likely that the ESR is a result of the anaemia, which raises the Rate at which Erythrocyte Sedimentate (sedimentate is totally a word).

Q. Dammit. We can only use CRP in these situations reliably.

A. You could measure plasma viscosity directly instead of ESR. This is expensive and not done in the NHS generally, and anyway you don’t usually need to unless you are a rheumatologist. And if you are, you probably know more about the merits of CRP vs ESR vs PV than me so I’ll shut up.

Q. Is this your shortest post yet?

A. Yes.

Q. Why?

A. Because if you can’t get a reliable ESR result, it doesn’t matter. Most of the conditions which benefit from ESR over CRP can be reviewed by a rheumatologist later. The only emergency where an ESR changes management is GCA; if you suspect this in a patient with an unreliable ESR, you can discuss with an on-call rheumatologist or treat now and await the formal biopsy.

Aortic Regurgitation: My favourite valvulopathy

This may seem like a very sad title for a blog post. That’s because it is. My last 6 month rota in A&E (working 3 in 4 weekends, with stretches of 5 days followed immediately by 4 nights) was like having my circadian rhythm controlled by a Geiger counter. I found myself waking at random hours, worried about what happened to patients I had seen. Real life and sleep rolled into one. I was probably GCS 14/15 most of the time. In short, I became sad and could only really think medicine. I was routinely staying past my hours because I didn’t want to hand over complex cases to the overstretched night staff. It wasn’t a great time for certain health ministers to imply junior doctors lack vocation or are killing patients by not working more weekends. I think it was these suggestions by Jeremy Hunt more than the details of the new contract that turned junior doctors so overwhelmingly against him and by extension his contract.

Now that I’m on a medical firm, my enthusiasm for geeky medicine has returned. Here’s something I heard recently at the left lower sternal edge of an otherwise well 85 year old woman.

 

The patient had a blood pressure of 156/89 and a regular pulse of 74.

Q. Classic aortic regurgitation. Early diastolic left lower sternal edge, loudest in expiration and on leaning forward. Love it. That’s typical.

A. Actually, mixed aortic valve (i.e. stenosis and regurgitation) disease is probably at least as common than pure AR. The management of mixed aortic valve disease depends on which valve problem is the dominant pathology.

Q. How do you tell that then?

A. Stenosis decompensates into a pressure overload situation, with a narrow pulse pressure. Regurgitation causes a volume overload sitation, with a wide pulse pressure and a hyperdynamic circulation. Echo can help distinguish which is the dominant effect. What matters isn’t so much the gradients/surface areas (although that it relevant), but how much functional impact each valve problem is having on the heart itself.

Q. Water hammer pulses, eh?

A. Yes. I used to get really confused about all the quirky signs of aortic regurgitation as a medical student. They all boil down to a hyperdynamic, superficial-ish arterial-ish vessel leading to a pulsing of something. The water hammer pulse is quite simple:

-> low diastolic pressure in AR, so

-> raising arm means gravitational force pushing blood back down the arm to the body is greater than the rubbish diastolic pressure, so

-> blood drains rapidly during diastole, so you get a sharp high volume pulse in systole which then quickly disappears, so

-> the pulse is ‘tapping’ like a woodpecker in slow motion. Or, if you prefer, water hammer (see the waveform):

Classic video for a classic valvulopathy.

Q. What is the Austin Flint?

Austin Flint = AF = Aortic is Farting back to the mitral valve. Sorry if it’s crude, but it helps me visualise blood flowing back down the aortic valve with such passion and speed that it flows all the way back to the mitral, causing a mid-diastolic murmur as jets flow onto the anterior leaflets of the mitral valve.

The seven month itch

perma-01

A 7 month old boy has suffered with eczema for at least three months. It was all over his body, including the trunk, all four limbs and face. There was no flexural surface preference. On examination, there were areas of dry, lichenified skin. There were no blisters, crusts or vesicles.

He was initially managed on aqueous cream as an emollient, with Oilantum Jr as a soap substitute. His flares were managed on eumovate BD for up to 2 weeks at a time for everywhere apart from the face, where hydrocortisone was used instead. After the two weeks of steroid would finish, his condition rapidly returned.

During the flares, he would itch frequently so was given chlorphenamine for night time relief.

The parents arrived at the GP clinic wondering what else could be done. I’ve tried to find the ICE behind the questions in true GP VTS reflectionophilia.

 

Every time the steroids stop it comes back. It’s not getting anywhere is it? Do you think we should see a specialist?

Likely patient expectation: Eczema can be cured if only we used the right treatment. A dermatologist could offer the treatment to cure it.

Message to get across: Eczema is a relapsing remitting condition. The aims of treatment are to reduce the frequency of flares and also to treat flares quickly.

It’s pretty hard to cure it altogether, but the good news is that most children tend to outgrow it as they get older.

 

I heard Aveeno is really good from my friends. Can we have that?

Likely patient idea: Aveeno is better than the other emollients.

Factors likely driving patient’s idea: Peer recommendation. Also, Aveeno markets itself a bit like the ‘Apple’ of the emollient world i.e. a premium product. It also scents the emollient whereas other companies do not. This means parents get a different feel when they use Aveeno compared to the other emollients.

Message to get across: The emollients are pretty much the same. The most significant difference is in the type of emollient e.g. ointment, cream etc. As long as you use it regularly and liberally, it won’t make a difference.

One exception: don’t use aqueous cream as a leave on emollient. It probably makes eczema worse. You can use it as a soap substitute though.

 

But why is this happening?

Likely patient concerns: My child may have eczema that will never go away because we don’t know what’s causing it.

Message to get across: A lot of childhood eczema is now believed to be worsened by staph aureus, both in acute infection flares and by long term colonisation.

Eczematous skin is generally more prone to infection (the barrier function is not quite as good as normal). The latest thinking in eczema pathophysiology suggests a role of staph aureus toxins producing crazy levels of IL-31, which drives itch. It may be the case that persistent staph aureus colonisation mediates the development of chronic eczema. For persistent eczema that does not respond well to steroids, or relapses rather readily, look carefully for signs of bacterial infection (blisters, weeping and crusting). This is often the cause of ‘resistant’ eczema.

Eczema herpeticum is a different ball game. Refer same day if you see this. (And also to ophthalmology if it’s around the eyes)

 

A previous GP suggested washing the child in bleach. I hope you aren’t as crazy. (*not the actual words used)

Even if the patient is not showing signs of infection right now, decolonisation may help. At a GP masterclass run by a dermatologist, I learnt that bleach baths are very much in vogue in the US. The instructions are straightforward – about twice a week,for 10-15 minutes at a time. Use ½ cup in a full bath tub (=0.0005% bleach / sodium hypochlorite). It’s best to apply steroids/emollients before the bath, and then emollients again afterwards.

The dermatologist who gave this talk herself bleach bathes twice a week simply because it seems to help her skin generally. Read into that what you will.

 

They also said to keep the emollients in the fridge. Is that right?

OK, the patient didn’t ask this but let’s say they did to help the Q&A format. As many as 53% of emollient containers may be colonised with staph aureus in a typical paediatric eczema setting. Given that infection (with blisters, crusts and weeping) and colonisation (long term immune response) probably both contribute to worsening of eczema in children, it is worth keeping the emollient clean. If the parents understand this, they are more likely to comply with treatment. I’m going to advise patients to treat it a little bit like contact lens solution i.e. nothing should touch the actual substance in the container. A clean spoon should be used to take it out, and once opened the container should be kept in the fridge.

Coping with tired all the time (GPVTS)

IMG_0154

Four facts to get things in perspective:

  1. 75% of all complaints of ‘tired all the time’ self resolve in 4 weeks,
  2. Two thirds of ‘tired all the time’ presentations are triggered by acute life stresses.
  3. At least 50% of the time, you won’t find a diagnosis.
  4. Fatigue is rarely the sole presenting complaint of malignancy

Strategy for sifting out the physical causes

Step 1: Define the type of tiredness
If you can identify the type, this will help lead the rest of your history.

Is it drowsiness? (Think sleep apnea and insomnia)

Is it muscular fatigue? (Think neurology)

Is it shortness of breath? (Think cardio, respiratory and anaemia)

Step 2: How is it affecting the patient?

Tiredness is really common in the general population. Only 1 out of 400 people who have tiredness actually see their GP. It is important to find out what brought this patient in. The tipping point is often a change in functional status e.g. struggling at work, unable to go to gym, sleeping in all morning etc. Documenting the functional status allows you to monitor progress.

Step 3: “It’s probably not physical, but…”

It is reasonable to wait 4 weeks to allow tiredness to self resolve before investigating provided there are no red flags.

It is also reasonable to attribute the tiredness to a well defined life stress event provided there are no red flags and the patient has a defined time frame for returning.

The red flags are:

  1. Lymphadenopathy
  2. Weight loss – and if so, take a full GI history in case of malabsorbption
  3. Specific malignancy features. The cancers to consider are the common ones – lung, breast, GI and gyane. This means you would actively ask for haemoptysis, cough, dysphagia, change in bowel habits/bleeding, breast lumps and unexpected PV bleeding. In fact, a good menstrual history is essential in all women – menorrhagia leading to anaemia and amenorrhea from pregnancy are both significant causes of tiredness.
  4. Joint pains – is there a rheumatological or vasculitic problem?
  5. Focal neurology – MS or tumour
  6. Systemic infection – is there TB, glandular fever (or post glandular fever) or perhaps Lyme disease (which does exist in England!)

Step 4: What non physical elements could be driving this?

Social history is the next thing after the red flags. The advantage of doing red flags/physical symptoms first is that the patient is more likely to feel you are taking them seriously than if you go straight to ‘Are you stressed?’

Once you have rapport, explore life events at work and home. Take a depression history when it is appropriate – perhaps after hearing about a life event, you could mention that a lot of people might feel down after that, and has this patient noticed anything like that?

Make sure you have identified alcohol and drug use, especially cannabis use in young people (demotivation is a common effect of cannabis).

Step 5: Examination

This will be focused on the leads from your history, but should always include pulse, blood pressure and BMI.

Step 6: The plan

Less than 3% of tests of anaemia and thyroid function for tiredness are positive. The other physical causes are even rarer e.g. Addison’s, coeliac, diabetes etc.

If you are going to investigate, the first line panel can be FBC, ESR, TFTs and random glucose. There is a fuller panel suggested on NICE CKS, but according to the BMJ article on primary care investigations these four tests are almost as good. And it’s worth bearing in mind that nearly 5% of all tests ordered by GPs are for tiredness. That’s a pretty big use of resources for tests that are rarely positive.

NICE guidelines do also suggest coeliac screening for unexplained tiredness.

If there is no resolution by 3 months, you can send off the second line panel (http://cks.nice.org.uk/tirednessfatigue-in-adults#!diagnosissub:4)

If there is no resolution by 4-6 months, consider chronic fatigue syndrome.

Step 7: Management

I’ll write this next week. I’m too tired.

Sources:

1. BMJ – http://www.bmj.com/content/341/bmj.c4259?sso=

2. Patient UK – http://patient.info/doctor/fatigue-and-tatt

3. NICE CKS – http://cks.nice.org.uk/tirednessfatigue-in-adults#!backgroundsub:4

3. BMJ Learning – http://learning.bmj.com/learning/modules/flow/expired.html?moduleId=10030395&status=LIVE&locale=en_GB&_flowId=JIT&page=5&action=start&shouldStartAtQuestionSection=false&sessionTimeoutInMin=90

Urine dipstick atheism

Worshipping the urine dipstick

I’ve seen the light. I had been worshipping the urine dipstick a wee bit too much.

To summarise everything that’s about to follow, you can rank the usefulness of urine dipsticks like this: (top is useful, bottom is useless)

  1. Young child
  2. Young adult with semi convincing symptoms
  3. Everything else
  4. Acutely confused and elderly patients
  5. Young adult with convincing symptoms

Here are five real life cases that made me think twice about how I use the urine dipstick.

Case 1: The typical UTI

A 39 year old lady presented with dysuria, urgency and frequency for the past 3 days. There is suprapubic tenderness on examination.

Q.1 Is there a point in doing a urine dipstick?

For any test you perform, you need to know what you would you if the test were positive and what you would do if it were negative. Let’s imagine what we would do with the results of the urine in this case:

Dipstick positive Treat as UTI
Dipstick negative Um…look closely…isn’t that actually maybe 1 + nitrite…?

For women suspected of having a UTI in primary care who have a urine dipstick that is negative for leucocytes, nitrites and haematuria, 24% will still have a UTI. A negative result didn’t give you a reason not to treat the symptoms as a UTI; it just left you in a mess. So don’t do it.

There are actually incredibly helpful guidelines endorsed by the HPA and RCCP for managing UTIs in primary care.

The main take home message from these guidelines was that good going UTI symptoms are treated empirically without a urine dipstick. Good going means three typical clinical features, such as dysuria, urgency, frequency, nocturia, suprapubic tenderness or haematuria.

Q2. Is there a point in sending a MSU?

In this case, no. And in most cases no.

You can split UTIs into complicated and uncomplicated.

A UTI in an adult woman < 65 years is by default uncomplicated.

All other UTIs are complicated.

There are also 4 Ps that make an otherwise uncomplicated UTI complicated – pregnant, persistent UTI, pyelonephritis, and problem with the tract.

Complicated ones go for MC&S. Uncomplicated ones do not.

Q3. What else could it be?

The main differential in women is vaginitis or cervicitis. If there is vaginal discharge or other GUM risk factors/symptoms, do the needful.

Q4. What if the patient has had cystitis before, and tells you this is like one of her usual UTIs? Does that make it more likely to be a UTI? Do we have to worry about interstitial cystitis in patients with ‘recurrent UTIs’ that are culture negative?  

Pay attention to her. There is an 84-92% chance that the patient is right if she has had cystitis before and feels this is another episode.

Persistent culture negative UTI like symptoms are often attributed to interstitial cystitis.

There’s a full differential of infection, gynae, neurological, urological and even GI pathologies you should consider – see Patient UK.

Q5. What treatment should we use in this case?

Trimethoprim or nitrofurantoin for 3 days. There is about 20% national resistance to trimethoprim, but be guided by your local resistance pattern. Nowadays you may find a one –off dose of fosfomycin being recommended after discussion with your microbiologist when you are faced with a urine culture teeming with super-resistant bugs.

Case 2 – The non specific child

A 3 year old boy presented with abdominal pain, vomiting and fever for the past 2 days.

Q6. Is there a point in doing a urine dipstick?

Yes. Above 3 (and until they are old enough to have an adult type presentation), use a dipstick as they can present so non specifically.

Below 3 years old, forget the urine dipstick and send the MSU directly. Below 3 months you’d probably refer any suspected UTI to the paeds team.

Q7. Is there a point in sending a MSU?

This is a situation where we are guided more by the urine dipstick than in any other situation. If there are nitrites, that is good enough to treat as UTI and send for culture. If there are leucocytes but no nitrites, look at is holistically. Are the patient’s symptoms better explained by anything else? If UTI is your best explanation, treat as UTI and send culture. If UTI is not the best explanation, explore the other diagnoses and send the culture.

And if its negative for everything, forget the UTI. (It’s the opposite of what I said earlier about the young adult. There is evidence that the NPV of a negative urine dipstick in children aged 2-10 approaches 100%. )

Q8. What else could it be?

Literally anything. Most of the time the child will have had an unexplained fever, or vomiting/loss of appetite which prompted the urine dipstick. Don’t forget appendicitis.

Q9. Does this patient need imaging?

A great dinner table conversation. NICE have guidance and you can memorise those tables however you wish. The basic principles are that:

  1. If the child has a bad/atypical infection right now (not responding to Abx within 48hr, non-E Coli organism, seriously unwell), you do an US now. Now is too late. You need to have already done one, is that possible? (ah, IT Crowd )
  2. If the child has recurrent UTIs, you do an US within 6 weeks
  3. A child below 6 months is a prince. He is having a scan no matter what.If it’s a typical UTI, it’s just a follow up US by 6 weeks. If that is abnormal or it were a recurrent/atypical UTI, do a DMSA (for scarring) at 4-6 months and MCUG (especially good for picking up posterior valves).
  4. The older you are, the less you get scanned.

Case 3 – Pregnancy pickle

A 10 week pregnant 29 year old lady presents with increased frequency for the past 5 days. It is her first pregnancy and she was told this is normal in pregnancy, but just wanted to make sure it wasn’t a urine infection.

Q10. Urine dip here too?

There is physiological pyuria in pregnancy. The nitrite test however does perform well in pregnancy and is highly specific. If it is positive, treat regardless of symptoms and send an MSU. Again, if there are clear symptoms, forget the dipstick, treat empirically and send the MSU.

It can be trickier in pregnancy to elucidate UTI symptoms as the bladder gets progressively more and more messed up through the pregnancy. Increases in urinary frequency can start from 6 weeks gestation

Q11. What is the treatment of choice?

7 days of nitrofurantoin. You try to avoid trimethoprim, especially in the first trimester. If you must give it, add in folic acid 5mg.

Nitrofurantoin is generally considered safe in pregnancy, with the caveat that if given near term there is a risk of haemolysis in the newborn.

You will always send a MSU and check that the bacteriuria has been cleared after your treatment course (see NICE CKS for pregnancy)

Q12. Why are we so paranoid about bacteriuria in pregnancy?

This is because of the risk of pyelonephritis and pre-term labour.

There is a 2% prevalence of pyelonephritis in pregnancy. This increase to nearly 25% if there is bacteriuria, and drops to 3% if this is treated.

Case 4 – Confused about confusion

A 79 year old is brought into A&E acutely confused. Her care home says she smells strongly of urine. Her observations are normal except for a temperature of 35.0.

Q13. Is there a point in doing a urine dipstick?

God no.

SIGN specifically say ‘Do not use dipsticks to diagnose UTI in older patients’.

Asymptomatic bacteruria in the elderly is very common. The urinary tract gets colonised. Especially women. Especially from nursing homes (over 50%).

Treating a positive urine culture or dipstick in the absence of symptoms attributable to a urinary tract infection in an older person is like taking a skin swab from normal skin, growing staph aureus and then treating for cellulitis.

It means jack all if she has bacteria in the urinary tract. Treating bystanding bacteria has no benefit and only risks.

What does matter is whether or not these bacteria are causing her confusion. There may not be a clear history of UTI symptoms, but if there is fever (or hypothermia, as in this case) and/or other signs of inflammation such as a raised CRP and no other explanation, then you should treat as UTI.

Q14. What exactly is the role of CRP here?

CRP increase with age, so it can be difficult to know how much to read into a moderately raised CRP. As a guide, a cut-off of 60mg/l gave a positive predictive value of 91.9% and a negative predictive value of 89.8% for a bacterial infection in patients over 70 admitted to an aged care ward.

There is a great case in the BMJ.  It would be so easy to attribute a strong smelling urine with a positive urine dip and culture in a confused patient to a UTI. In reality, this patient was dehydrated and had too much opiate.

Case 5 – False negatives when it matters most

A 21 year old is admitted in DKA. Infection is actively sought. A urine dipstick is negative for nitrites and leucocytes, but positive for glucose and ketones.

Q15. Is there a point in doing this urine dipstick?

Not for looking for infection. For a quick diagnosis of ketonuria, yes. For monitoring ketones, I’d only do it if capillary ketones were not available. The drop in ketones is a key marker of response to treatment.

Ketones and glucose in the urine are associated with higher rates of false negative nitrites and leucocytes. If you are doing a septic screen in a DKA patient, go for MSU and do not be guided by the urine dipstick. MSU is listed as a routine investigation in Box 1 of the Management of Diabetic Ketoacidosis in Adults.

But it’s really strong smelling.

Doesn’t matter. The smell is irrelevant. Dehydrated urine smells more.

On the other hand, the appearance of the urine is useful. The NPV of non cloudy urine is 97%, which is a better NPV than a completely negative urine dipstick.

My A&E “go away” story

thank you for sharing this – I’m a junior doctor and it has made me think about what kind of message we give patients based on the manner in which we discharge them from a&e.

Betabetic

I’m normally a fan of Resilient GP but today’s blogpost on how to manage ‘inappropriate demand’ in acute services filled me with dismay. It makes many points that I nodded along with, but then slips further and further into patient-blaming, culminating in:

“Patients who attend A&E or OOH inappropriately need to be told to go away.”

Please don’t.

Two years ago, I had a series of A&E attendances where my primary complaint was asthma that was objectively moderate-to-severe, and subjectively not-normal-for-me.

The first time, my GP sent me in. My breathing improved after a couple of nebs, but a senior consultant was concerned by the fact that it wasn’t my standard pattern, and noted my unusually low blood-pressure. He admitted me for 24 hours for monitoring. I spent a night in MAU and went home the next day – under strict instructions to come sooner next time and never to hesitate…

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