Broad Complex Tachycardias

Clinical presentation:As with all tachyarrythmias, symptoms depend upon the ventricular rate and pre-existing cardiovascular state.
These symptoms and signs may be mild (consisting of dizziness or light-headedness), moderate (eg. chest pain or shortness of breath), or severe (with cardiovascular collapse or profound shock).

Differential for Wide Complex Regular Tachycardias
    Ventricular Tachycardia
    SVT with aberrant conduction (eg. WPW)
    Atrial flutter with 2:1 & aberrant conduction
    Sinus Tachycardia with aberrant conduction

Ventricular Tachycardia
VT is the most common, and one of the most life threatening causes of a broad complex tachycardia. It is defined as: three or more ventricular extrasystoles in succession at a rate of greater than 120 beats/min.

They most often occur in the context of structural heart disease which makes accessory pathways and re-entrant arrhythmias much more likely. It can easily degenerate into VF, and accounts for 80% of sudden cardiac deaths due to fatal arrhythmia.

VT can be defined according to duration, site of origin (left or right ventricle), or morphology (monomorphic or polymorphic):
-    Ventricular tachycardia lasting for less than 30 seconds is defined as “non-sustained”
-    Right bundle branch block morphology - if the terminal portion of the QRS complex in V1 is positive and suggests activation from the left ventricle or septum
-     Left bundle branch block morphology - if the terminal portion of the QRS complex in V1 is negative and suggests activation from the right ventricle

-        An inferior axis (positive QRS in aVF, negative in V1) - suggests activation from the outflow tracts
-        A superior axis (negative QRS in aVF, positive in V1) - suggests activation from the apex
-        A relatively narrow QRS (100 to 120 ms) implies a septal focus

Wolff-Parkinson-White
If a patient with suspected Wolff-Parkinson-White syndrome develops a broad complex tachycardia, then you should avoid AV nodal blocking drugs. This is because these may increase ventricular activation over the accessory pathway and cause a dangerously fast heart rate. Instead, you should give an intravenous class IC drug such as flecainide, or a class III drug such as amiodarone.

REGULAR tachyarrh. in WPW: Orthodromic - looks like SVT, Antidromic - looks like VTach. Doesn't matter. Manage each as usual. #resus14
— David Marcus (@EMIMDoc) March 29, 2014

Antidromic AVRT
The ventricles are activated directly by an accessory pathway, and the atria are activated retrogradely over the AV node. The management is similar to orthodromic AVRT, and you may be able to use adenosine to terminate the arrhythmia. In patients with atrial fibrillation and Wolff-Parkinson-White syndrome, rapid ventricular conduction across the accessory pathway from the atrium to the ventricle may result in ventricular fibrillation.

Outflow tract ventricular tachycardia
Outflow tract ventricular tachycardia tends to be related to exertion and may respond to adenosine and the Valsalva manoeuvre. It may be haemodynamically well tolerated and less likely to cause sudden cardiac death than other ventricular arrhythmias. You should aim to suppress right ventricular outflow tract tachycardia with the use of beta blockers and verapamil.

Idiopathic left ventricular tachycardia
This ventricular tachycardia originates from the left bundle branches, most commonly the posterior fascicle. It has a relatively narrow morphology.

Polymorphic VT
This is uncommon and rarely sustained. When polymorphic VT is encountered in the acute setting it is frequently the result of an acute cardiac insult and it rapidly deteriorates into ventricular fibrillation. The main features are:
    1.       QRS rate is rapid (200 – 250 beats/min)
    2.       Amplitude of the QRS complexes change in a sinusoidal fashion
    3.       Usually self limiting but may be recurrent
    4.       Between episodes the QT interval is prolonged (see Figure 5)

VT or SVT with aberrant conduction

Most rules are unreliable. If in doubt...treat as VT and shock the patient.

Mattu: Wide regular tachy: Assume VTach, less commonly sinus tach+BBB, or SVT+BBB (dangerous mistake). Err on side of Tx'ing VTach #resus14
— David Marcus (@EMIMDoc) March 28, 2014

VT more likely than SVT:

Mattu: The various wide complex tachycardia diagnostic rules miss 6 - 40% of VTach. #resus14
— David Marcus (@EMIMDoc) March 28, 2014

- Absence of typical RBBB or LBBB morphology
- Extreme axis deviation (“northwest axis”) – QRS is positive in aVR and negative in I + aVF.

“if it’s up in aVR the axis is bizarre!”

- Very broad complexes (>160ms)
- AV dissociation (P and QRS complexes at different rates)
- Capture beats - occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
- Fusion beats - occur when a sinus and ventricular beat coincides to produce a hybrid complex.
- Concordance - all the QRS complexes in the chest leads are either positive or negative. The identification of positive or negative concordance suggests the origin of the VT lies in the posterior ventricular wall or anterior ventricular wall respectively.
- Brugada’s sign –  The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms
- Josephson’s sign – Notching near the nadir of the S-wave
- RSR’ complexes with a taller left rabbit ear. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.

SVT+ Aberrancy more likely than VT
- Age <35
- Rate =150 beats/minute
- Rate >200 beats/minute and patient asymptomatic
- QRS Duration < 0.14 seconds
- Axis normal
- Absence of independent atrial activity or concordance
  

Management

Intravenous amiodarone is the first choice of drug.
In patients with torsades de pointes, correction of serum potassium levels and infusion of intravenous magnesium is needed.

Temporary pacing might be indicated in those patients whose arrhythmia is triggered by bradycardia. Beta blockers may then maintain sinus rhythm and prevent further episodes of polymorphic ventricular tachycardia.

Start with a synchronised DC cardioversion at 200 joules (monophasic) or 120-150 joules (biphasic). If unsuccessful repeat the cardioversion up to a maximum of 3 attempts before giving amiodarone. Changing the paddle position may be helpful in resistant cases.

In patients who are tolerating their arrhythmia, intravenous amiodarone (in a dose of 5mgs/kg up to a maximum of 300mgs) administered over 30 minutes is the treatment of choice. If unsuccessful, DC cardioversion should be considered.

Correction of any underlying abnormalities that might be precipitating the arrhythmia (eg. hypo/hyperkalaemia and hypomagnesaemia) is also required. Consider Calcium gluconate premedication or post treatment if BP falls.

Links
EnlightenMe

http://www.enlightenme.org/knowledge-bank/cempaedia/broad-complex-tachycardias

GoogleFOAM
https://circ.ahajournals.org/content/106/25/e206.full
http://academiclifeinem.com/pv-card-brugada-criteria-svt-aberrancy-vs-vt/
http://bja.oxfordjournals.org/content/92/1/140.full

http://ekgumem.tumblr.com/post/59400445975/wide-complex-tachycardia-vt-vs-svt-with

http://ekgumem.tumblr.com/post/24960326577/wide-complex-tachycardia-episode-40-june-12

http://ekgumem.tumblr.com/post/23993343074/wide-complex-regular-tachycardia-deadly-av

http://hqmeded-ecg.blogspot.co.uk/2014/03/incessant-regular-wide-complex.html

http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/

http://lifeinthefastlane.com/vt-versus-svt-with-aberrancy/

BMJ Learning

Tachycardia - not the best module
Difficult cardiology scenarios
Broad Complex Tachycardias

Doctors.net

http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1535

http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1582

Narrow Complex Tachycardias

Narrow complex tachycardias are also called SVTs or supra-ventricular tachycardia. All narrow complex tachycardias are SVT, but not all SVTs are narrow.

1. Atrial Tachycardias
This is a rare paroxysmal tachycardia with abnormal p waves, having a rate of 130 to 140 beats a minute. It has an abrupt onset and termination, and it can be initiated with programmed electrical stimulation during an electrophysiology study. Normally benign and short lived condition of the elderly.

Atrial tachycardias may cause a dilated cardiomyopathy and heart failure if they are not treated.

Treat with a DC shock.




2. Junctional Tachycardia
These arise from the "junction" in between the atria and the ventricles. Conduction to the ventricles is still normal, but there are more conduction pathways than there should be. P waves are often buried in the QRS.


Atrioventricular nodal re-entry tachyarrhythmias
These are more common in women and are responsible for approximately 60% of narrow complex tachycardias. This arrhythmia occurs when there are two atrial conduction paths into the AV node which triggers a perpetual circuit.
In nodal re-entry tachycardias, atrial (retrograde) and ventricular depolarisation is simultaneous so the p waves are buried in the QRS and hard to identify – look for inverted p waves in inferior leads II, III, AVF, sometimes causing a ‘pseudo’ S wave.

There are normally two paths in the AV node causing this. One of these transmits things quickly (retrograde) and one transmits things slowly (usually antegrade). Atrial and ventricular depolarisation is simultaneous.

 
AV reentry tachycardia
In re-entry tachycardias there is an extra connection between the atria and the ventricles - not more than one pathway in the node. Wolff-Parkinson White syndrome is the best known cause of this, and the accessory pathway is the bundle of Kent.

Wolff-Parkinson White
In sinus rhythm, the ventricles are normally excited by the accessory pathway. This leads to the clinical features of WPW - short PR and slurred upstroke of QRS (delta wave).

Patients may present with syncope, rather than palpitations, when atrial arrhythmias are conducted rapidly over the accessory pathway to the ventricles, bypassing the AV node and resulting in haemodynamic collapse.
For those patients with evidence of ventricular pre-excitation and a delta wave on their ECG, you can use the ECG to find the approximate location of the accessory pathway. Theoretically. you can localise it to the left or right side of the heart by assessing the polarity of the delta wave in lead V1, although how this helps you acutely I'm not sure:

    A left sided pathway may give rise to a positive delta wave in V1 and may cause right bundle branch morphology
    A right sided pathway may give rise to a negative delta wave in V1 and may cause left bundle branch morphology. This is because septal activation is initiated from the right side of the septum.

Conduction may be orthodromic or antidromic

    Orthodromic - anterograde conduction - premature atrial impulse is transmitted via the AV antegradely to the ventricles, then retrogradely back up the accessory pathway, depolarising the atria then passing back via the AV node and down the Bundle of His again antegradely, establishing a re-entry circuit.

P waves are present, but inverted and will follow the QRS, and the delta wave disappears.


    Antidromic - anterograde ventricular activation occurs via the accessory pathway and retrograde atrial activation via the AV node. This causes a regular broad QRS tachycardia but is much less common and occurs in 10% of cases.
Retrograde conduction through the AV node leads to atrial depolarisation and consequently the P waves will be buried in the wide and abnormal shape QRS – this may be indistinguishable from ventricular tachycardia unless a previous ECG is available. One clue is that the re-entry tachycardia will be exactly regular. For more details on this, look at the VT page.

3. Atrial Flutter
This is covered on the AF page. 

Management
If adverse features, go straight to DC cardioversion.
Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower energies: start with 70-120 J biphasic (100 J monophasic).


- Dipyridamole enhances the effect of adenosine.
- May need more adenosine if recently had caffeine.
- In pregnancy adenosine is OK


- Once the arrhythmia has terminated you should start the patient on an AV nodal blocking drug, such as a beta blocker or calcium channel blocker at a low dose. This will need to be continued long term in order to reduce the risk of recurrence of the arrhythmia

- Verapamil is contraindicated in patients receiving beta-blocker therapy.
 Some sources advocate using verapamil first line instead of adenosine, as it is better tolerated.
 Verapamil 5- 10mg IV over 3min.
   
- Troponin isn't so useful in analysing SVT. If you really think there's an ischaemic trigger for the MI, then check a troponin:
    Low risk, prior SVT, feels good after conversion, then NO CARDIAC ENZYMES and outpatient f/u
    Intermediate risk, then DO get CARDIAC ENZYMES; If neg, outpatient follow up but if positive consider admission.
    High risk, older age, or known history of ACS, then DO CARDIAC ENZYMES and admit.

Of note...modified release verapamil has no anti-arrhythmic effects! Check the BNF - MR is only listed in the hypertension section...normal is in anti-arrhythmic too. Don't think you're being too nice by swapping it over!
EnlightenMe
http://www.enlightenme.org/knowledge-bank/cempaedia/supraventricular-tachycardias
http://www.enlightenme.org/emimage/ecg/diagnosis-and-treatment-narrow-complex-tachycardia 
http://www.enlightenme.org/learning-zone/cardioversion-conundrum
http://www.enlightenme.org/learning-zone/tiny-tot%E2%80%99s-ticker-flicker
http://www.enlightenme.org/learning-zone/challenging-case-svt
http://www.enlightenme.org/the-learning-zone/node/6724 


Other
http://ekgumem.tumblr.com/post/17949025577/wpw-orthodromic-and-antidromic-svt-episode

http://pulmccm.org/2012/review-articles/supraventricular-tachycardia-svt-diagnosis-treatment-review-nejm/

http://academiclifeinem.com/svt-are-troponins-necessary/

http://lifeinthefastlane.com/tag/svt/
http://emupdates.com/2009/11/26/calcium-channel-blockers-for-svt/ 
http://www.ems12lead.com/tag/treating-svt-with-adenosine/
http://lifeinthefastlane.com/ecg-library/svt/
http://ekgumem.tumblr.com/post/18378351287/diagnosis-and-treatment-of-svt-episode
http://resus.me/verapamil-vs-adenosine-for-svt/
http://bestbets.org/bets/bet.php?id=1884

http://learning.bmj.com/learning/modules/flow/JIT.html?execution=e2s2&locale=en_GB&action=start&sessionTimeoutInMin=90&moduleId=5003248&status=LIVE&_flowId=JIT&page=1

Atrial Fibrillation

There's so many arrhythmias that can cause palpitations that I was struggling to get through them. It's difficult to separate them out completely - but I had to in the end! So...atrial fibrillation...

Definition
There are many different types of AF and our terminology is always a little loose:
Paroxysmal AF: Discrete episodes that come and go. Episodes of sinus rhythm between.
Persistent AF: When AF lasts longer than a week or doesn’t stop without treatment
Permanent AF: When AF is more longstanding and resistant to therapy, or when no therapy is attempted
The greatest morbidity and mortality associated with AF arises from the thromboembolic sequelae. Up to 25% of all CVAs are attributable to AF-associated thromboembolism. Men are 1.5 times more likely than women to develop atrial fibrillation.




Atrial Flutter is a similar form of re-entry tachycardia where the circuit is almost always confined to the right atrium: rare left atrial cases have been reported. Type 1 or ‘Typical’ atrial flutter will have a rate of around 300/ min (250-350/min) and most commonly produces a negative sawtooth appearance in inferior leads II, III and AVF. ‘Reverse Typical Flutter’ produces a positive sawtooth in the inferior leads at around the same rate, and is due to the electrical impulses passing round the re-entry circuit in the reverse direction.
Type 2 ‘Atypical’ Atrial Flutter is rare, faster, 350-450/min and arises from a different pathway.


Atrial fibrillation looks irregularly irregular on an ECG, with absent P waves. The faster the rate the more regular AF will look but it is always irregularly irregular. An irregularly irregular rhythm isn't always AF- there could be multi-focal atrial tachycardias and atrial flutter present. AF may co-exist with bundle branch block and look like ventricular tachycardias.

Investigations
TFTs
Transthoracic echocardiography if:
    important for long-term management, eg for younger patients
    rhythm-control strategy that includes cardioversion (electrical or pharmacological) possible
    high risk or a suspicion of underlying structural/ functional heart disease (such as heart failure or heart murmur) that will influence their subsequent management (for example, choice of antiarrhythmic drug)

Management
Assess Stroke Risk:
Increase of stroke:
    1.5% for patients aged 50-59 years to
    23.5% for those between 80 and 89 year

The NICE guidelines score patients according to low risk, medium risk, and high risk and advise anticoagulation accordingly.

CHADS2 and CHA2DS2-VASc have been developed as more sophisticated scoring systems. They are not advised to be used in the UK, although an awareness of them is helpful, and there are useful statistics from their use.

The risk of stroke must be balanced against the risk of bleeding. Three main scoring systems for risk of bleeding have been validated in people with atrial fibrillation but I have never seen them used in clinical practice:
HEMORR2HAGES (Hepatic or renal disease, ethanol abuse, malignancy, older (age ≥75 years), Reduced platelet count or function, rebleeding risk, hypertension (uncontrolled), anaemia, genetic factors, excessive fall risk, and stroke)

HAS-BLED (Hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly (eg age >65, frailty, etc), drugs/alcohol concomitantly). This is the score recommended by the ESC.

ATRIA (AnTicoagulation and risk factors in atrial fibrillation).


Chronic:

Treat any identifiable precipitants.
Control the rate









Acute

AFFIRM and RACE trials looked at whether rhythm or rate control is better.

<48 hours = Rhythm Control aka chemical or electrical cardioversion
- If >48 hours needs anticoagulation for six weeks
- If rhythm control unsuccessful, will need rate control instead
- Success rate 65 - 90%
- Relapse high (25- 50% at one month)
- Continue antiarrhythmic drugs afterwards.




Electrical Cardioversion
- More likely to be successful with AP paddles (sternum and left subscapular)
- If permanent pacemaker in place, cardiovert but then interrogate device. Paddles should be as far away as possible from the device.
- More likely to be successful if pre-treated with antiarrhythmic drugs
- For a broad-complex tachycardia or atrial fibrillation, start with 120-150 J biphasic shock (200 J monophasic) and increase in increments if this fails. Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower energies: start with 70-120 J biphasic (100 J monophasic).

And this is how it works (from a cardiologist):
DC cardioversion works by stunning the entire myocardium. The tissues with the shortest refractory period (i.e. recover and start normal electrical service) earliest are the SA node followed by AV node. Therefore DCCV simply stuns everything, and hopefully the tissues that recover soonest determine the rhythm.

We sync to shock on the R wave to avoid the ST-T segment when the ventricular myocardium is repolarising and very vulnerable to VF (this is why long QT syndromes are a problem - if the QT is long enough then risk of ectopic beat hitting the ventricle at that time and becoming VT/VF. If you do shock someone on the ST-T then it's not usually a problem, just turn the sync off and re-shock (although clearly this isn't taught).

Most AF is rate controlled with drugs, but we still do cardiovert a fair number for various reasons (symptoms/can't take warfarin/employment/heart failure etc), the big problem is the recurrence rate (40% back in AF at 6 months, 60% at 1 year). Electrophysiology with ablation is either aimed at pulmonary vein isolation (potentially curative 60-70%) or destroying the AV node and inserting a pacemaker (palliative procedure).

Pharmacological Cardioversion

Class Ib agents (lidocaine) aren't used any more as other agents are more effective. 
Class Ic agents (flecainide and propafenone) are safe in patients who do not have evidence of previous myocardial infarction, acute myocardial ischaemia, or ventricular dysfunction. Their use in the ED is often limited by the poor availability of echo. I can't find any where what happens if you give it and there is a stuctural abnormality, but I guess as it can prolong the QT and cause arrhythmias anyway, you're just more likely to have to sort out a mess. The BNF implies structural problems only cause a problem if they cause haemodynamic compromise.
Class II (metoprolol, propanolol) are used for rate control, not rhythm control.
Class III (sotalol, amiodarone and dronedarone)
- I've never seen sotalol used, possibly because it has dose dependent effects. At low doses, sotalol has only class 2 effects and acts simply as a beta blocker with primarily negative chronotropic effects. It can not be given if there is any sign of heart failure. At high doses, Sotalol exerts class 3 effects and is antidysrhythmic. It can prolong the QT interval.
- Amiodarone is toxic. It has lots of different arrhythmic effects, but is normally put in class III. It is the drug of choice in the presence of heart failure. It can prolong the QT interval.
- The combination of amiodarone and Sotalol is contraindicated as they both prolong the QT interval and can precipitate ventricular dysrhythmias.
Class IV (verapamil, diltiazem)
- Used for rate control

>48hours = Rate Control
There are 3 main options for rate control
1. Beta blockers - metoprolol (IV/PO) or bisoprolol (PO).
The BNF doesn't say, but cardiologists I've worked with say bisoprolol is just as easy as metoprolol, wears off less quickly, and they prefer it. But in the ED we like giving things IV...

2. Calcium channel blockers - diltiazem or verapamil
These should not be used in conjunction with beta blockers

3. Digoxin
Digoxin is not recommended as a first line drug because it does not control the heart rate in ambulant patients. It is positively inotropic, so can be useful.

Emergency Treatment
- Known poor LV function (adequate LV function is dependent upon the 15% of ventricular filling provided by atrial contraction).
- Heart rates (>150 bpm) causing inadequate time for LV filling.

Driving
Do not drive if arrhythmia has, or is likely to cause incapacity
Cause needs to be controlled and identified for four weeks

EnlightenMe
http://www.enlightenme.org/the-learning-zone/node/7515
http://www.enlightenme.org/knowledge-bank/cempaedia/atrial-fibrillation
http://www.enlightenme.org/learning-zone/rate-or-rhythm-control

BMJ Learning
http://learning.bmj.com/learning/module-intro/atrial-fibrillation--diagnosis-and-management.html?moduleId=5003354&searchTerm=%E2%80%9Cvaso-vagal%E2%80%9D&page=1&locale=en_GB

Doctors.net
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1538

Other  
http://emcrit.org/podcasts/crashing-a-fib/    
http://blog.ercast.org/2012/10/should-we-cardiovert-atrial-fibrillation-in-the-ed/
http://guidance.nice.org.uk/CG36
http://calgaryguide.ucalgary.ca/slide.aspx?slide=Atrial%20Flutter.jpg
http://calgaryguide.ucalgary.ca/slide.aspx?slide=Atrial%20Fibrillation%20-%20Clinical%20Findings.jpg
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1163475/
http://circ.ahajournals.org/content/111/23/3141.full
http://academiclifeinem.com/paucis-verbis-card-anticoagulation-in-atrial-fibrillation/
https://www.gov.uk/current-medical-guidelines-dvla-guidance-for-professionals-conditions-a-to-c#arrhythmia
http://www.resus.org.uk/pages/periarst.pdf

UTIs

UTIs are the fourth highest indication for antibiotic prescribing in primary care. They account for approximately 5% of GP consultations. Around a quarter of people will get better whether they take antibiotics or not.

StatisticsMen: incidence <1% between 20 and 60 years of age
Women: 1 in 2 will be treated during their lifetime
 1 in 3 will be treated by 24 years of age

PathophysiologyCommon organisms:
E. coli = 70%
Staph saprophyticus = 15%
Proteus mirabilus = 10%

Proteus, klebsiella, enterobacter and enterococcus are rare.
Pseudomonas and candida are hospital acquired.

Clinical Features
It is important to make sure you ask about all the history features:
-    Frequency
-    Urgency
-    Dysuria - In patients who can explain their symptoms, dysuria is the most diagnostic symptom in older and younger women.
-    Nocturia
-    Haematuria
-    Suprapubic pain
-    Fever

In male patients ask about:
-    Poor stream
-    Terminal dribbling
-    Incomplete voiding
-    Overflow incontinence

Investigations
The role of urinalysis is controversial. Most sources recommend not using urinalysis in patients under 65 years of age, with three or more classic features. 90% of these patients are likely to have a positive urine culture.

For women under 65 years with mild or up to two symptoms, a urine sample is required to:
    Assess its cloudiness
    Consider urinalysis
    Consider a urine culture
Remember that urinalysis requires the sample having enough time to contact the bladder - frequency may affect quality of results.

False-negative nitrite tests are common, but false positives are uncommon
Leukocyte esterase detects the presence of pyuria which can be a non-specific finding.
The absence of both nitrites and leukocyte esterase reliably excludes UTI.
Blood and/or protein in urine are consistent with UTI, but are often non-specific findings

Diagnosis
Most laboratories take 105 colony-forming units per millilitre (cfu/ml) as the threshold for diagnosing significant bacteriuria.

Lower counts such as 103 or 104 of a pure growth of Escherichia coli (E. coli) or Staphylococcus saprophyticus may be significant if women have definitive symptoms of a urinary tract infection and there are white cells present on microscopy.

Epithelial cells with mixed growth may suggest contamination of the specimen.

Sterile pyuria may be due to Chlamydia. Tuberculosis is less likely but still recognised as an important cause of sterile pyuria. Other causes include STIs, renal tumour or calculus, genitourinary tuberculosis, and antibiotic therapy prior to collecting an MSU

No white cells indicates a lack of an immune reaction. This could indicate that bacteriuria is contamination but it also occurs in the immunosuppressed.

Management
Patients with visible haematuria and those over forty years old with microscopic haematuria should be referred for a 2 week wait urology appointment to exclude malignancy.

Antibiotics:
3 days for women, 7 days for men.
In nitrofurantoin, nausea is less likely if you use the modified release formulation (100mg twice daily).
One study suggests that NSAIDs are as effective as antibiotics!

Do not treat asymptomatic bacteriuria, even if catheter associated, which occurs in 25% of women >65years, and 10% of men >65years. A positive urine culture or dipstick test will not differentiate between a urinary tract infection or asymptomatic bacteriuria. Pregnant people should be treated for asymptomatic bacturia, and then have regular urine cultures at each antenatal visit.

Dietary Advice
Cranberry juice might interfere with the attachment of bacterial to uroepithelial cells. It is not useful acutely as treatment of UTIs. Increased oral hydration has little benefit in the acute management of an established UTI and reduced the concentration of antibiotics in the urine. Tea, coffee (caffeine-containing drinks), and alcoholic and citrus drinks should be avoided until symptoms have resolved as they can cause bladder irritation. These drinks should be replaced by water.

Recurrent UTI
- diabetes mellitus
- obesity
- chronic constipation
- poor fluid intake and infrequent voiding of urine
- atrophic vaginitis
- use of tampons

Differential Diagnoses
Atrophic Vaginitis
Presents with superficial stinging and burning on urination and watery non-odourous vaginal discharge. Examination is likely to show mild atrophic vaginal changes only. This is likely due to menopausal changes, and might respond to vaginal oestrogen from cream, pessarys or rings.

Acute ProstatitisCan present similarly to UTIs, but is more likely to also have systemic symptoms such as lower back pain, genital pain and a fever.

Interstitial CystitisOccurs in young people with suprapubic pain and fullness and frequency especially after consuming alcohol. Advise patients to keep a urinary symptom diary, monitor fluid intake and avoid irritants such as caffeine and alcohol.
Need urology follow up.

Purple Bag SyndromeThis is a rare sign of UTI, caused by gram negative bacteria. Treatment is directed towards the underlying bacterial infection and changing the catheter.

DeleriumAcute delirium in elderly patients is a common clinical scenario with protean aetiology, including UTI. Do not treat a positive dipstick in a delirious patient unless there are other indicators of a UTI.

References
http://academiclifeinem.com/paucis-verbis-card-urinary-tract-infection/http://academiclifeinem.com/uncomplicated-urinary-tract-infection-older-adults-diagnosis-treatment-1/
https://jama.jamanetwork.com/article.aspx?articleid=1832516
http://bestbets.org/bets/bet.php?id=1324
http://bestbets.org/bets/bet.php?id=2422http://www.enlightenme.org/learning-zone/spot-diagnosis
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1529
http://www.enlightenme.org/learning-zone/have-you-ever-seen
http://elearning.rcgp.org.uk/course/info.php?id=117
http://www.npc.nhs.uk/therapeutics/common_infections/uti/quiz.php