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:

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?

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

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)

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

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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Red fright or green light? | A child with fever

A 14 month year old boy has a fever for the past 4 days. The fever peaked at 38.5°C as measured at home. The child has been irritable and clingy since arriving at the GPs, but has not shown any obvious pain. There is no photophobia, neck stiffness or rash. There has been a non-productive cough for two days, which is worse at night. There is no history suggesting stridor, respiratory distress or wheeze. He has had a runny nose over this time. He is tolerating food and drink, although he is eating less than normal. He sometimes vomits after eating. There have been no changes to his bowel habits and he is producing about 6 wet nappies a day.

Examination is difficult. He cries at the slightest intrusion of his personal space by anyone other than his mother. His temperature is 37.2, although mum tells you he just had calpol about thirty minutes ago. His pulse is 120. There is subcostal and intercostal recession when he is crying, but none when the crying settles. His respiratory rate when he is settled is 40. His saturations are 96% on air. The anterior fontanelle is neither bulging nor sunken.

An ENT examination is almost impossible. You eventually find it to be normal. There is no rash top to toe. His chest sounds clear. His abdomen is soft.

You go to write up your findings to give yourself time to think whilst mum dresses the child. You have not found the source for the fever. You look at the PMH – he was a preterm baby at 34/40 weeks but has been generally well since. His development has been fine. All his vaccinations have been up to date. He is an only child, and no household contacts have been unwell.

But it’s only a ‘fever’ of 37.2 – that’s not significant

You only have a snapshot of the child’s temperature. You cannot discount the parental concerns about fever over the past four days based on a one-off reading just now. NICE state:

“Reported parental perception of a fever should be considered valid and taken seriously by healthcare professionals”

Then it’s a feverish child with no source! Admit, admit!

There are basically two things that mean a feverish child may need admission –a) suspicion of a serious bacterial infection or b) not coping with the illness itself e.g. dehydration, first ever/complex febrile convulsion, respiratory distress etc.

Regarding a) – the majority (>80-90%) of fevers in children will be self-limiting viral infections.

Regarding b) – the majority of children will cope absolutely fine with a febrile illness.

Our task is to identify the minority who have a problem with a) or b) for further assessment. We should advise the remainder to self-care at home with safety netting. Sometimes you cannot quite 100% pin down the source; this in itself does not necessarily require an urgent assessment.

How do you interpret the fever in light of the fact that the child took calpol?

It does not matter. The height of the fever in a child over 6 months does not predict a serious bacterial infection, nor does it tell you how the child is coping with the illness. The height of the fever is therefore not going to alter your management plan.

In infants less than 3 months, a fever greater than 38°C should be seen urgently by a paediatrician (red flag in NICE guidelines).

In infants between 3 and 6 months, a fever greater than 39°C is an amber flag in NICE guidelines.

Isn’t it great that NICE guidelines are perfect! We don’t have to think, just use the table!

The traffic light system is helpful. It does not replace clinical judgment. This reflects the fact it is difficult (?impossible) to create a rigid scoring system for something as complex and nuanced as assessing a feverish children. The most common bacterial infection the traffic light system misses is a UTI – in fact, about one fifth of the time a child with a UTI will score green. There has been a suggestion to add urinalysis to the NICE traffic light assessment of the feverish child (http://www.bmj.com/content/346/bmj.f866). However, there are also some who feel that this study considered only the traffic light system in isolation, without considering the NICE guideline’s holistically. The purpose of the traffic light system was not to diagnose but to help with the initial triage of feverish children. (http://www.bmj.com/content/348/bmj.g2056/rr/691345)

So what is this magical table?

Have a look: traffic light system for identifying risk of serious illness

The main thing to emphasise is that NICE states that if the child appears unwell to you, refer urgently. Your clinical gestalt is valuable, no matter your level of experience with children ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458229/).

What happened in this case?

It’s a fever of unknown source. There are some suggestions of a viral source (runny nose, non productive cough) but nothing definitive. There is no way you can predict what will happen in 4, 8 or 24 hours. The mother was told to contact us if the child remained clingy/crying frequently at home. Given the child had green flags at the time of assessment, and the mother knew when to come back or when to go to A&E, the child could be watched at home with appropriate safety nets.

Cool. Alternating paracetamol and tepid sponging then to keep T < 38.

NO! That is so 2008. You treat fever only so the child doesn’t feel distressed. You do not give antipyretics to target a temperature.

And you only give ibuprofen or paracetamol (at least initially). Alternating doses leads to frequent dosing errors. If the fever is not controlled with either agent alone, and the child is distressed, then maybe you could alternate them – but ask the parents to keep a written record of what they have given and when. And forget tepid sponging. Just dress the child in clothes which are appropriate for the room temperature.

Any specific advice for the parents?

NICE CKS mentions the following:

 

• Look for signs of dehydration including poor urine output, dry mouth, sunken anterior fontanelle (usually closed by 18 months), absence of tears, sunken eyes, and poor overall appearance).
• Offer regular fluids (if breastfeeding, continue this as normal) and encourage a higher intake if signs of dehydration develop.
• Dress the child appropriately for their surroundings, with the aim of preventing overheating or shivering.
• Avoid using tepid sponging (using cool water) to cool the child.
• Check the child regularly, including during the night (how often depends on the situation).
• Keep the child away from nursery or school while the fever persists, and notify the nursery or school of the illness.

• Advise parents and carers to seek medical help if:
  • The child is getting dehydrated.
  • The child has a fit.
  • The child develops a non-blanching rash.
  • The fever lasts longer than 5 days.
  • The child is becoming more unwell.
  • They are distressed or concerned that they are unable to look after the child.

 

3kg baby replaced by 3kg of urine

3.2 L of urine replaces 3.2kg of baby. 

I’m going to have a withdrawal bleed once I leave O&G’s hormonal fuelled adventures behind. It has been a mix of the high (on entanox) and the low (lying placenta). I’m no longer scared of the concept of pregnancy (even if the BNF seems to be – “no evidence of harm but what the hell – manufacturers advise avoid”). I’m glad I did it, but I’m more glad it’s over.

That said, it just wouldn’t be O&G without one last not-normal-fluid-out-an-orifice scenario to work through. Towards the end of the placement, I noticed several women who had normal vaginal deliveries developed urinary retention. Post op C section retention is nothing new; pretty much any major surgery has this risk. However, I was unaware of how frequent retention is post vaginal delivery, and how best to recognise/manage it.

Before we dive in, there’s a little analogy I find helpful. I used to think urinary retention must be absolute i.e. if the patient is passing something, it can’t be retention. I now think of it more like faecal impaction than full-on bowel obstruction. Just like you can have some overflow with faecal impaction, you can pass little overflow-y voids with retention. If the voiding volume is small and/or there’s voiding difficulty and/or suprapubic pain and/or there’s a high residual, treat it as potential retention even if there is some urine output.

A woman has a normal delivery. There was a second degree tear which was sututred. She had difficulty passing urine post delivery, passing 50ml then 60 ml in 6 hours post delivery. She complains of lower abdominal pain. She is a little tachycardic. The team assume she is dry and give her 3.5L orally over the next 24 hours. The urine output does not pick up, and her observations remain the same.

Our super SHO (not me) does a thorough examination discovers that there is suprapubic tenderness combined with the urge to pass urine. The patient feels really uncomfortable. A urinary catheter is passed. It drains 3.2L.

How did this happen?

During pregnancy (especially the third trimester), the bladder tone decreases and bladder capacity enlarges. Before she gives birth, the pressure of the gravid uterus compressing the bladder helps maintain voiding pressure. After delivery, the bladder expands and intravesical pressure drops. In 1.7-17.9% of women who have a vaginal delivery, this leads to retention.

So it’s kinda normal then. When do I worry about it? 

It can take up to 6 hours after a normal delivery for bladder sensation to return to normal (more if an epidural was used). If a woman has not passed urine within 4 hours after delivery despite adequate fluid intake, she should be given every opportunity to pass urine naturally. This means controlling pain, keeping her mobile, giving her privacy and perhaps trying a warm bath. If it reaches 6 hours, it’s time to catheterise.

But this woman passed a little. Does that count?

One void less than 200ml could still be consistent with retention (especially if accompanied with voiding symptoms such as suprapubic pain, poor stream, leaking/passing urine without the urge etc.)

OK, so now that we catheterised her, she had a residual of 3.2L. How you gonna deal with that?

There is no formal guideline. A ‘normal’ adult bladder distends up to 400-600ml. Distension beyond this volume should be uncomfortable. The fact it drained 3.2L means her bladder has been significantly distended.

That said, immediately post partum the bladder is naturally a little distended.

The urge to pass urine starts at around 150-250ml. If there’s a post-void residual of more than 150ml, it suggests a voiding issue.

You didn’t answer my question.

Fine. I found several approaches used by different midwife units. Nottingham’s guidelines specifically talk about how variable the guidelines from various units are. One approach for symptomatic retention that I found intuitive was from a New Zealand. With some slight modification to fit in with what I generally saw being done in the UK, we’ve got the following plan for overt (i.e. symptomatic) retention:

Once the 6 hour deadline has elapsed, you re-catheterise the patient. If there’s a small residual (<150ml) it’s fine – it’s not retention (maybe she was a bit dry). If it’s medium (150-700ml) keep it in for 24 hours and repeat the TWOC then. If it’s big (past 700ml), keep it in for 48 hours. This gives more time for the bladder to be unfull and hence hopefully return to its normal size.

On the second TWOC, if she does a good void (>200ml) within 6 hours, you check the residual. If the residual is less than 150ml, it’s all good. If it’s bigger, or she doesn’t do a good void in the new 6 hour deadline, then she failed the second TWOC which usually means a 7 day in dwelling catheter before a re TWOC. Another approach is intermittent self catheterisation.

If the volume for the first TWOC is bloody ridiculous like 3.2L, go straight for re-TWOC in 7 days.

Covert retention (post voiding residual >150ml without symptoms) is nicely covered by the same New Zealand guidelines. It seemed similar to what I see in the UK.

How is it going to resolve?

Postpartum retention is usually a short-term problem that resolves over weeks. It can lead to a persistent hypotonic bladder if poorly managed.

Unsweetened vomit

Pregnant women vomit a lot. I don’t just mean morning sickness. Pregnancy can result in altered taste and smell, which means certain foods and smells make them feel violently sick. Although most cases of pregnancy induced vomiting get better after 20 weeks, there are some unlucky ladies who feel sick every single day until the birth of their you-are-lucky-you-look-cute-otherwise-I’d-bloody little bundle of joy.

A lady in her mid 30s was admitted at 39/40 with persistent vomiting. It had been going for two days and she was vomiting nearly every hour. There was no change in bowel habits. There was upper abdominal tightening that occurred with the vomiting, but no other abdominal pain. No one else was affected at home and she had not been travelling or eating unusual foods. She had no vertigo or hearing problems. She had a throbbing headache of about 5/10 severity, especially on being upright. There were no visual symptoms or other neurology.

She was unable to keep anything down, including fluids, for the past 24 hours.

On examination she was dehydrated, with dry mucous membranes. Her urine showed 5+ ketones. Her observations were stable. Her urine was dark, but the output was adequate. There was no abdominal tenderness.

During the admission, she was persistently hypoglycemic. Her BMs were around 3-3.5 despite 5% dextrose being used as rehydrating fluid.

There was no PMH of anything, and no access she could have had to antidiabetic medications/insulin.

Her U&Es, lactate, TFTs, LFTs and calcium were all normal.

Would it be reasonable to attribute her low glucose to 36 hours fasting in the absence of any other medical problems?

I’m thinking no. Here’s why:

• The body responds to low glucose by first switching off insulin and increasing glucagon production. This has the effect of increasing gluconeogenesis and glycogenolysis in the liver.
• Catecholamines are also released as the glucose continues to drop. Biochemically, this causes glycogenolysis in the liver and muscle and gluconeogenesis in the liver and kidney. Clinically, this produces the cathecholamine excess symptoms – sweats, tremors, tachycardia and a sense of hunger (and anxiety).
• Finally, growth hormone is stimulated (which stimulate lipolysis) as well as ACTH (which increases lipolysis and muscle breakdown).
• If glucose continues to stay low, the patient may develop neuroglycopenic symptoms (dizziness, inappropriate behaviour, poor concentration, confusion, blurred vision, stroke-like symptoms and eventually coma/death). The body prioritises glucose for the brain. If the body can’t supply the brain with glucose, this means something is failing in a big way.

So, in a patient with an otherwise intact endocrine system, a healthy liver and a decent glycogen store, fasting alone will rarely produce hypoglycemia. Hypoglycemia from malnutrition usually occurs when at least one of those three things are out e.g. Addison’s disease, liver disease or prolonged malnutrition depleting the glycogen stores.

What else could cause hypoglycaemia?

Hypoglycemia causes can be split into fasting (occurring at least 6 hours after a meal) and non-fasting. I’m just going to focus on the fasting ones for today.

The fasting hypoglycemias can be split into those with an appropriately low insulin level and those with an inappropriately high insulin level.

Appropriately low insulin

Alcohol – independent of any effect on liver function, alcohol inhibits hepatic gluconeogenesis

Endocrine – usually a problem in the CRH-ACTH-cortistol axis, but also rarely growth hormone deficiencies.

Liver disease – loss of gluconeogenesis ability and/or inability to store glycogen

Renal disease – the kidney does do some gluconeogenesis, but not as much as the liver. The most common clinical application of this is end stage diabetic nephropathy reducing kidney function and therefore a decrease in the insulin/antidiabetic dose requirements.

Sepsis – can lead to impaired gluconeogenesis. However, more commonly hypergylcemia. One of the SIRS criteria is actually raised glucose in a non diabetic.

Pregnancy – the foetus takes priority over resources. Mum’s stores are depleted. This leaves her at risk of hypoglycaemia.

Rare stuff – inborn errors of metabolism.

Inappropriately high insulin

Diabetic meds – by far the commonest. The body can’t ‘switch off’ insulin that is pushed into it. Insulin secretagogues can also cause hypogylcemia. A clinical possibility: An elderly diabetic patient with decreasing renal function has been on a sulfonylurea for ages. The sulfonylurea has reduced clearance because of the reducing renal function, so the patient ends up developing hypoglycaemia.

Insulinoma – classic MRCP case. A prolonged fast for 72 hours is the key test. Normally insulin should switch off. However, if the patient is hypogylcemia with a high insulin level (and raised C peptide to show it was endogenous insulin) then you are a diagnostic machine for spotting an insulinoma.

Bottom line: My patient probably had depleted glycogen stores from her baby which meant when she got into a fasting state, she didn’t have the reserves.