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.

Your first patient has an INR of 10

“Was the INR really 10?” asked the CT2 as we left the handover meeting.
“Yeah. It actually said >10 which means its probably 20.”
“Or 100”
“Or she’s just a pool of blood now.”

The patient was sitting up in her chair, doing puzzles. I was relieved. The single biggest cause of death from warfarin is intracranial bleeding, following by GI bleeding. I saw the job ahead of me as:

1. Working out if she’s having any major or minor bleeds
2. Working out a cause for the INR to shoot up
3. Finding out about why she is on warfarin, her usual dosing and targets
4. Screening for any other urgent medical problems.

Major bleeds are intracranial, gastrointestinal and interarticular, or any bleed that causes haemodynamic instability. Minor bleeds are all the others.

She had no features of raised ICP. This means no headache, no vomiting, no focal neurology, no seizures, normal neurological examination including cranial nerves and pupils. There was no Cushing’s reflex apparent in her obs (which I think of as the brain being so shocked it does the opposite of shock: high blood pressure with a low pulse). I did not check for papilloedema. Those last two signs are pretty late.

She had no features of a GI bleed, although she had bleeding haemorrhoids. The blood was fresh, and was only present on the tissue.

She had no pain or stiffness in her joints. No joint swelling on examination.

In terms of minor bleeds, she had a couple of oldish bruises. She had the haemarrhoids as mentioned earlier, but no mucous membrane bleeding e.g. when brushing teeth. No haematuria or epistaxis.

This was a patient with an INR > 8 without any significant bleed (haemarrhoids alone do not count). You could now look up what to do in the BNF:

The main adverse effect of all oral anticoagulants is haemorrhage. Checking the INR and omitting doses when appropriate is essential; if the anticoagulant is stopped but not reversed, the INR should be measured 2–3 days later to ensure that it is falling. The cause of an elevated INR should be investigated. The following recommendations (which take into account the recommendations of the British Society for Haematology(2)) are based on the result of the INR and whether there is major or minor bleeding; the recommendations apply to patients taking warfarin:

Major bleeding—stop warfarin; give phytomenadione (vitamin K1) 5 mg by slow intravenous injection; give dried prothrombin complex (factors II, VII, IX, and X—section 2.11) 25–50 units/kg (if dried prothrombin complex unavailable, fresh frozen plasma 15 mL/kg can be given but is less effective); recombinant factor VIIa is not recommended for emergency anticoagulation reversal

INR > 8.0, minor bleeding—stop warfarin; give phytomenadione (vitamin K1) 1–3 mg by slow intravenous injection; repeat dose of phytomenadione if INR still too high after 24 hours; restart warfarin when INR <5.0

INR > 8.0, no bleeding—stop warfarin; give phytomenadione (vitamin K1) 1–5 mg by mouth using the intravenous preparation orally [unlicensed use]; repeat dose of phytomenadione if INR still too high after 24 hours; restart warfarin when INR <5.0

INR 5.0–8.0, minor bleeding—stop warfarin; give phytomenadione (vitamin K1) 1–3 mg by slow intravenous injection; restart warfarin when INR <5.0
INR 5.0–8.0, no bleeding—withhold 1 or 2 doses of warfarin and reduce subsequent maintenance dose

Unexpected bleeding at therapeutic levels—always investigate possibility of underlying cause e.g. unsuspected renal or gastro-intestinal tract pathology

So my options were vitamin K orally (1-5mg) or intravenously (0.5mg). I preferred the oral option, as I would rather not put a needle in a patient with an INR of 10 if it were not necessary. Of course, this meant that there were no oral versions available on AMU. I had to go to maternity, where they keep ampoules for prophylaxis and treatment of haemorrhagic disease of the newborn. These ampoules can be given IV, IM or oral.

Vitamin K takes a while to work its magic, as the clotting factors have to be made all over again now that vitamin K is back. The onset of action is slower if given orally, but even when given IV, it takes 2 hours to have any effect and a maximum effect within 6–12 h, compared with 12–24 h for oral vitamin K. This means that if the patient is having a major bleed, you need to replace the clotting factors (prothrombin complex, or fresh frozen plasma if none available) to have an immediate effect and then give vitamin K. Put another way, minor bleeds are distinguished from major bleeds in that a minor bleed won’t kill you in the time it takes for IV vitamin K to have its effect.

So far, so textbook. It was more interesting trying to work out why a compliant lady, who had been on warfarin for at least 20 years and never missed a dose or anticoagulation clinic, had suddenly developed this INR. She denied any alcohol over the past week. She did mention a recent diagnosis of “colitis” 3 weeks ago but was unable to elaborate further. This week she had had diarrhoea for 6 days, initially passing stools 6 times a day with urge inconitenence, but now just 4 times with plenty of warning and feeling much better in herself.

I figured this must be mild UC which was resolving, given she was down to 4 stools daily. I stopped the metronidazole she had been prescribed the day before as the most common cause of a deranged INR is a drug interaction, and metronidazole is a well known inhibitor of the enzymes that metabolise warfarin.

The INR the next day corrected to 2.1 and she was discharged with close INR monitoring in the community.