Episcleritis and Scleritis

Episcleritis

Background

• Inflammation of the episclera (thin fibroelastic structure that lies between the conjunctiva and sclera)
• Usually mild and self-limiting

Pathophysiology and aetiology

• Most cases are idiopathic
  • Up to a third of patients have an underlying systemic conditions e.g. rheumatoid arthritis, inflammatory bowel disease, SLE, vasculitic disease, dermatological disease etc
• There are two forms of episcleritis
  • Simple episcleritis
    • intermittent bouts of mod-severe inflammation that often recur at 1-3 month intervals.  Usually last 7-10 days
  • Nodular episcleritis (more commonly associated with systemic disease)
    • Often more severe and prolonged attacks
    • Characterised by a discrete, elevated area of inflamed episcleral tissue

Presentation

• General
  • Diffuse or localised, bright red/pink bulbar injection (cf scleritis which is darker/violet)
  • Usually unilateral
  • Some may report other symptoms such as discomfort, photophobia or tenderness
    • Severe pain and discharge are not common
• Simple
  • Often acute redness, occasionally associated with pain (mild-moderate)
    • Usually peaks around 12 hours then slowly resolves over 2-3 days
    • Tends to recur in same or both eyes at the same time
      • With time, attacks become less frequent and can disappear completely
• Nodular
  • Gradual onset redness, noted particularly upon wakening in the morning
  • Worsens over several days, causing discomfort and takes on a nodular appearance
  • Also self-limiting but tends to last longer
  • 

Management

• Supportive management i.e. reassurance is all that is required in most cases
  • NSAIDs may be helpful (ibuprofen tablets), moreso in nodular episcleritis than simple episcleritis

Scleritis

Background

• In contrast with episcleritis, scleritis is potentially blinding and usually requires referral to ophthalmology
• Inflammation of the sclera

Aetiology

• There is a strong link between autoimmunity and scleritis.  In particular, patients with rheumatoid arthritis are at a much higher risk than the general population.
• Also more common in women.

Disease class

• There are two main forms of scleritis which can be further classified as such:
  • Anterior scleritis: inflammation anterior to the extraocular recti muscles
    • Diffuse: anterior scleral oedema is present with dilation of the deep episcleral vessels.  This may be diffuse or localised
    • Nodular: a distinct nodule of scleral oedema is present (can be single or multiple).  They are often tender.
    • Necrotising: most severe form.  Severe pain and scleral tenderness.  Severe vasculitis as well as infarction and necrosis with exposure of the choroid may result.
      • Rarely, necrotising scleritis can occur without inflammation (scleromalacia perforans).  The sclera become very pale, avascular and thin.
  • Posterior scleritis: rare but potentially more serious.  Characterised by flattening of the posterior globe, thickening of the posterior coats of the eye (choroid and sclera) and retrobulbar oedema
    • Can manifest as serious retinal detachment, choroidal folds or both
    • There can also be loss of vision as well as pain on eye movement

Pathophysiology

• Common pathological features include scleral oedema and inflammation, often with a zonal granulomatous (can also necrose) reaction that may be localised or diffuse.  Often mediated by  type III and subsequent type IV autoimmune reactions involving a variety of cell types (T cells, macrophages, B cells, plasma cells etc)

Presentation

• History
  • Redness
    • Gradually increases over several days
    • characteristic violet/blue tinge
  • Pain
    • Most describe severe boring/piercing eye pain over several days
      • may radiate to surrounding facial areas
      • may awaken the patient in the night (cf episcleritis)
      • Tender on movement and palpation
      • Usually not helped by analgesia
  • Tearing may occur secondary to discomfort but discharge is uncommon.
  • PMHx
    • Remember to ask about any autoimmune/ophthalmological conditions 
• Examination
  • Blue hue is best observed under natural light
  • On slit-lamp, inflamed scleral vessels are congested and often have criss-cross pattern and (under green light) there may be areas of capillary non-perfusion and granulation
  • Phenylephrine (constrictor) will only constrict the superficial conjunctival/episclera vessels but the florid appearance of scleritis should remain.

Management

• Main aim is to minimise inflammation and reduce any damage
  • Topical NSAIDs and corticosteroids may be used.  However, ultimately, treatment of any underlying cause may require systemic NSAID/steroid use or even immunomodulatory agents
  • Severe (necrotising) disease will require systemic treatment in any case

 

Viral Conjunctivitis

Background and aetiology

• Very common cause of red-eye, commonly caused by adenovirus
• Risk factors include recent upper respiratory tract infection
• Usually has a longer course than bacterial conjunctivitis (12-21 days cf 7-10 days) and is highly contagious.
• Rarer viral causes include herpes simplex (generally more problematic disease- follicular conjunctivitis)), as well as varicella zoster, HIV and influenza.

Presentation

• History
  • Gritty/uncomfortable eyes (may be one, commonly both)
  • Watery discharge
  • Associated cough/cold
  • Recent association with someone with ‘pink/red eye’
• Examination
  • Red eye with diffuse conjunctival injection
  • Clear discharge
  • Small, white, lymphoid aggregates may be present on the conjunctiva (viral follicles)
  • Small, focal areas of corneal inflammation with erosions and associated opacities may give rise to pronounced symptoms
  • Lymphadenopathy
• Special cases
  • Primary ocular HSV mainly affects young children/infants and presents with a red, irritated, watery eye.  Often the eyelid is also affected with multiple vesicular lesions which can be painful too.

Management

• As with bacterial conjunctivitis, viral conjunctivitis is usually self-limiting and self care (particularly with hygiene and reducing the spread of disease) is all that is recommended.
  • Again, lubricating eye drops may be of benefit.
  • In rare cases where corneal lesions are severe/persistent, steroid drops may be used, but only with ophthalmology supervision, as this carries significant risk of complications (which could ultimately be blinding)

 

 

Bacterial Conjunctivitis

Background

• Bacterial conjunctivitis is an infection of the eye’s mucous membrane, the conjunctiva, which extends from the back surface of the eyelids (palpebral and tarsal conjunctiva), into the fornices, and onto the globe (bulbar conjunctiva) until it fuses with the cornea at the limbus.

Aetiology

• Acute bacterial conjunctivitis is most commonly due to Staph aureus, Strep pneumoniae and H Influenzae
  • More rarely caused by others e.g. pseudomonas aeruginosa; moraxella lacunata; Strep viridans and Proteus mirabilis
  • Hyperacute conjunctivitis is mainly due to Niesseria gonorrhoeae.  This cause is also more likely to occur in neonates whose parents are infected with the STI.  Chlamydia is also another cause of bacterial conjunctivitis.  These bacteria should be considered in patients with chronic disease.  It is important to ask about STI exposure at this point too.
• Risk factors include poor hygiene, contact lens use, other/previous ocular disease e.g. dry eye, blepharitis etc, recent surgery to the eye, foreign body in the eye, immune comprimise

Presentation

• History
  • Painful (stingy) eye, irritated
  • Yellow/white (non-clear) discharge
  • Often begins in one eye and spreads to other
  • Sticky eyes (particularly in the morning) + crusting
  • Redness
  • Blurry vision (usually due to purulent discharge on the cornea- so usually transient and incomplete- i.e. vision should actually be normal)
  • Light sensitivity
• Examination
  • Mucopurulent discharge
  • Uniform engorgement of conjunctival vessels
  • Eyelid may be erythematous and occasionally oedematous
  • Normal cornea, anterior chamber, pupils etc

Investigations

• Usually not necessary
• If disease is chronic and not responding to treatment, discharge cultures may be helpful (conjunctival scrapings can also be done for stain/cultures)

Management

• In most people, infective conjunctivitis is self-limiting and antibiotic treatment has little impact on the time to recovery and carries side-effects
  • Therefore, advice on self-care is all that is required for most patients
    • no contact lenses
    • clean away secretions
    • hand-washing
  • lubrication drops may help to reduce discomfort if this is a problem for the patient
• Consider giving an antibiotic (topical chloramphenicol 1st line- fusidic acid 2nd line) in severe disease (or likely to become severe)
  • NB definition of severe is subjective based on patient distress and clinical experience
  • If the patient requests antibiotics, suggests delay for 1 week to see if it resolves spontaneously
• In cases of gonococcal/chlamydial infection, systemic treatment is usually required (azithromycin 1g once only (+ 500mg ceftriaxone IM for gonorrhoea))

see http://cks.nice.org.uk/conjunctivitis-infective#!topicsummary

 

 

Scrotal Swellings and Examination

Scrotal swellings are not an uncommon presentation, and it is crucial to be able to differentiate the cause of swelling, as some are a lot more serious than others.  Common and important causes include:

• Testicular cancer
• Testicular torsion
• Torsion of a testicular/epididymal appendage
• Varicocele
• Hydrocele
• Haematocele
• Epididymal cyst (spermatocele)

History

• Ask about pain- duration, severity etc
  • usually severe and acute onset in testicular torsion
  • more gradual pain/swelling in epididymo-orchitis
  • episodic pain can be an atypical feature of testicular torsion
• Ask about any associated symptoms
  • e.g. features of UTI/STI (e.g. discharge, pyuria) which might suggest epididymo-orchitis
  • parotid swelling (mumps orchitis)
  • nausea/vomiting (torsion, rarely in epididymo-orchitis)
• Any history of trauma (haematocele, rarely in torsion)
• Also ask about any relevant past medical history: in particular- undescended testes

NB consider the age of the patient: torsion is generally more common in young men, whereas cancer may be more common in older men

Examination

• YOU SHOULD ALWAYS EXAMINE THE SCROTUM IN THE STANDING POSITION
• If there is a normal side, always examine this first to a) make sure it is normal and b) compare to abnormal
• Inspect for
  • Lie (is one testis higher than other?); appearance; scars; oedema; sebaceous cysts, ulcers or swellings; erythema
• Palpate
  • Does the patient have 2 testes? If not, feel the inguinal canal and perineum for an undescended testis.
    • The scrotum should be freely mobile from the testes
  • Feeling the normal side first, palpate the body and poles of the testicle, checking the patient’s face for any pain/tenderness (ask this too)
    • Compare size, shape and consistency (they should be roughly equal, smooth, rubbery and firm)
    • Are there any lumps, changes in consistency, tenderness, swelling etc?
  • Palpate the epididymis along the posterolateral border of the testis, again noting any tenderness or abnormality
  • Palpate up each spermatic cord, whilst gently pulling the respective testis downwards
    • It should feel regular and smooth
• Special tests
  • Cremasteric reflex
    • can be elicited by stroking the superficial aspect of the medial thigh near the testes and the testis should rise on the respective side.
      • may not do so in torsion
  • Prehn’s sign
    • If the patient has pain which is relieved by raising the testes- the pain is suggestive more of epididymitis.
• Assessing scrotal swellings
  • 

Differential Diagnosis

Haematuria

Macroscopic Haematuria- visible blood in the urine

Microscopic Haematuria- not visible but identified by urine microscopy or dipstick test.  This may be symptomatic or asymptomatic.  Defined as >3 red blood cells in the urine.

NB Be wary that dipsticks actually detect haem, and can (in some uncommon situations) be false negative/positive.  Also recognise that it can be normal to have asymptomatic microscopic haematuria, which usually doesn’t require investigation.

• In children and young people, glomerular causes are more predominant.  In older people, this decreases and cancer and stone disease become more common.

Assessment and Investigation

What is significant haematuria?

• Any single episode of macroscopic haematuria
• Any single episode of symptomatic microscopic haematuria in the absence of UTI and other transient causes
• Persistent asymptomatic microscopic haematuria (2 out of 3 separate urinalysis) in the absence of UTI and other transient causes
  • NB the presence of haematuria should NOT be attributed to anti-coagulant/anti-platelet therapy, unless trauma (e.g. traumatic catheterisation) is present.

Characteristics 

• A renal cause such as glomerulonephritis will generally cause persistent microscopic haematuria with or without periods of gross haematuria
• Gross haematuria associated with renal causes will usually be present throughout the stream
  • if haematuria is only present at the start of stream- it is suggestive of a distal urethral cause e.g. urethritis
  • if only present at the end- it is suggestive of upper urethral/prostatic/trigonal cause
    • this said, bladder cancer and other bladder causes can often present as gross haematuria throughout the stream

Associated symptoms

• Pain- usually associated with stone disease or infection
• Rash, arthralgia, fatigue- may be associated with an inflammatory/immune mediated cause
• Fatigue, night sweats and weight loss may be present with neoplastic causes

Investigations

• EXCLUDE UTI- Urine dipstick should always be done first
  • Nitrites and leucocyte markers suggest UTI
  • Protein suggests nephrological cause e.g. glomerulonephritis
  • MSSU should follow any abnormal dipstick to further evaluate findings
• Symptomatic microscopic haematuria and asymptomatic persistent microscopic haematuria should be further investigated:
  • Blood pressure
  • Creatinine/eGFR (renal function)
  • Urine sample for protein/creatinine ratio (normally <50) or albumin/creatinine ratio (normally (<30)
• All macroscopic haematuria should be investigated by urology with some form of imaging
  • Usually Cystoscopy + USS or CT KUB
• All patients with symptomatic haematuria (inc macroscopic haematuria) and all patients >40 years old with any significant haematuria should be referred to urology.  Referal to renal medicine should be made if eGFR/creatinine or PCR/ACR are abnormal and/or a renal cause is suspected.

Potential Causes

• Cancer:
  • Bladder (TCC, Squamous cell carcinoma); Kidney (Renal cell adenocarcinoma); Renal pelvis/ureter (TCC); prostate
• Stones (kidney/ureteric/bladder)
• Infection
  • bacterial, mycobacterial (TB), parasitic (schistosomiasis), infective urethritis
• Inflammation
  • Cyclophosphamide cystitis, interstitial cystitis
• Trauma
  • In particular catheterisation and pelvic fractures
• Renal Cystic disease
• Nephrological causes (consider particularly in children/young adults; or with accompanying significant proteinuria; blood often takes form of red cell casts)-
  • IgA Nephropathy, post-infective glomerulonephritis, membrano-proliferative glomerulonephritis, Henoch-Schonlein purpura, vasculitis, Alport’s syndrome, thin basement membrane disease, Fabry’s disease etc
• Other causes
  • Anticoagulation therapy; sickle cell/hemophilia; renal papillary necrosis

Lower Urinary Tract Symptoms

A collection of symptoms that commonly co-exist.  Most commonly due to prostatic enlargement in men, but this cause is not exclusive and others should be considered where appropriate e.g. with haematuria- consider bladder cancer; chronic retention; rarely due to neurological dysfunction (cauda equina syndrome/spinal tumours.

Symptomology

• Storage
  • Urgency- sudden urge for micturition
  • Frequency
  • Nocturia
  • Urinary incontinence
• Voiding
  • Hesitancy
  • Straining
  • Slow stream
  • Splitting/spraying
  • Intermittency
  • Terminal dribble
• Post-micturition
  • Dribble
  • Feeling of incomplete emptying

Investigation 

• For men with bothersome LUTS, urinary frequency volume chart
• Urine dipstick analysis
• Bloods for U&Es (renal function) plus PSA in men
  • Do a PSA if symptoms suggest bladder outlet obstruction secondary to BPH or if the patient is concerned about prostate cancer
  • Bloods for PSA should be done before a PR exam (although there is little evidence to suggest that PR exam has a significantly large effect on PSE, many doctors practice this way to be safe)
• Flow-rate measurements and residual volume scans are not recommended by NICE but may be carried out depending on local guidelines
• Serum creatinine may be measured if there is any suspicion of associated renal impairment

Differential Diagnosis

• Benign Prostatic Hypertrophy
• Prostate Cancer
• Bladder Cancer
• Chronic retention/overactive bladder
• Neurological deficit

Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

Background

• Tho most common type of reentrant SVT
• Caused by the presence of dual AV nodal pathways

Pathophysiology

• The AV node has two possible pathways for electrical impulses to travel through
  1. A fast pathway (fast conduction)
  2. A slow pathway (slow conduction)
• Normally, impulses from the atria travel to the ventricles only through the fast pathway (they can begin use the slow pathway but cannot travel further as the fast pathway has already reached the end of the AV node and is in a refractory period)
• When an extrapremature atrial impulse reaches the AV node, it encounters a refractory fast pathway and must enter the slow pathway.  By the time this reaches the end of the AV node, the fast pathway has reset, allowing the impulse to travel backwards up the fast pathway
• This creates a reentry circuit which cycles round, activating the ventricles anterogradely and the atria retrogradely.
• 
• The atria are unable to empty contents into the ventricles and so is backed up into the venous system.

Clinical Diagnosis

• Fast, regular small complex tachycardia with a rate of 180-250bpm.  Sudden onset.
  • On ECG- RP distance <100ms; P waves often hidden or immediately after QRS and are usually in opposite direction to QRS
    • May have a notched QRS appearance
• Patient may present with palpitation, syncope, dizziness etc or it may be an incidental finding on ECG/Examination
• Frog sign- Neck vein (JVP) pulsations occur due to simultaneous contraction of atria and ventricles

Management

• If the patient presents acutely, manage as adult tachycardia (ABCDE) approach (see here)
• If the patient is stable, IV adenosine may help acutely to revert the arrhythmia.  If the patient is unstable, synchronised DC shock/amiodarone may be used.
• In the longer term, prophylactic treatment includes beta blockers and calcium channel blockers.

Junctional Rhythm

Background

• In junctional rhythm the electrical impulse starts in the AV node instead of the SA node.
  • NB the AV node does possess autorhythmicity but is usually much slower than the SA node and so is overridden.
• In the context of severe bradycardia, this is an escape mechanism.  In the context of normal/tachycardia, this is abnormal
• Results in electrical impulses travelling simultaneously to the atria and ventricles
  • results in an inverted P wave seen just after or within the QRS complex.  The QRS is usually narrow unless there is co-existent LBBB/RBBB

Aetiology

• Inappropriate slowing of sinus rhythm to 40-60bpm either due to changes in autonomic tone or disease of the sinus node
• Enhanced AV-node automaticity- usually caused by digoxin toxicity, post-op cardiac surgery, during MI or severe calcium dysregulation in the cardiac sarcoplasmic reticulum.

Presentation

• The patient may present with dyspnoea and presyncope

Management

• Depends on the underlying cause
  • If digoxin toxicity- atropine and/or digitoxin immune FAb (digibind) may be given

 

 

 

Atrial Flutter

Background

• Tachycardic arrhythmia characterised by atrial rates usually around 300bpm, producing a ‘saw-tooth’ baseline.  Ventricular activity (QRS) usually occurs every 2 or 3 atrial beats (i.e. 150 or 100bpm) due to an 2:1 or 3:1 AV-node block, respectively.
  • NB AV-node block can be variable

English: A 12 lead ECG showing atrial flutter (Photo credit: Wikipedia)

Pathophysiology

• Atrial flutter can be either ‘typical’ (type I) or ‘atypical’ (type II) depending on the origin of the electrical activity.
  • type I is caused initially by an atrial ectopic beat within the right atrium, causing a reentrant circuit (a neuronal pathway arranged in a circle so that impulses are recycled to cause positive feedback or reverberation) around the tricuspid valve annulus, commonly in an anticlockwise direction
    • results in negatively directed flutter waves in the inferior leads (II, III and aVF)
  • type II is much less common but usually originates from the left atrium and travels in a clockwise direction, causing the opposite picture (often also more variable) on ECG

Aetiology

• PIRATES (also good for atrial fibrillation)
  • P- Pulmonary embolus, pulmonary disease, post-op, pericarditis
  • I- Ischaemic heart disease, idiopathic, IV central line
  • R- Rhuematoid valve disease
  • A- Anaemia, alcohol, age, autonomic tone (vagal mediated AF)
  • T- Thyroid
  • E- elevated BP, electrocution
  • S- Sleep apnoea, sepsis, surgery

Presentation

• Most patients will present with palpitations and associated symptoms e.g. fatigue, dyspnoea, chest pain, dizziness, syncope
  • Occasionally patients can present with TIA/stroke
• Pulse may be regular or irregular, but is almost always rapid
• JVP may show flutter like activity

Investigations

• ECG
  • Narrow complex tachycardia
  • Regular atrial activity at ~300bpm
    • Flutter waves (‘saw-tooth’)- best seen in inferior leads II, III, aVF
    • So rapid that the baseline is lost
    • A QRS usually occurs every 2 flutter waves
      • However, this may be 3/4 or it can be variable

Management

• As with AF, atrial flutter may require immediate rate control or DC shock.
  • Either electrical cardioversion (with anticoagulation; most common method); pharmacological cardioversion (e.g. with amiodarone, sotalol); or ventricular rate control (with calcium channel blocker e.g. verapamil; betablocker or amiodarone)
    • Do not use flecainide on its own as this can risk 1:1 AV nodal conduction (if used, use in combination with a beta-blocker)
• Most cases are secondary to underlying cause, which should be identified and treated appropriately and quickly
• Atrial flutter is more responsive to electrocardioversion than pharmacological.
  • As with AF, patients should be anticoagulated prior to any cardioversion and continue anticoagulation for at least a month.
• For long-term management, either rhythm control (pharmacological tx) or cardiac ablation can be used
  • pharmacological treatment is usually either beta blockers, or second-line: amiodarone or sotalol (which are generally more effective- class III)

Atrial Fibrillation

Background

• In AF, the atria are ‘fibrillating’ at a rate of between 350 and 600bpm, and thus are unable to do so in a synchronised manner.
  • They are unable to properly fill or empty their contents, and thus increase the risk of blood stasis, clot formation and stroke.
  • The disorganised electrical activity of the atria occasionally conduct through the AV node, giving rise to an irregularly irregular rate of QRS complexes.
• It is the most common arrhythmia, particularly found in members of the elderly population.

Scheme of atrial fibrillation (top) and sinus rhythm (bottom). The purple arrow indicates a P wave, which is lost in atrial fibrillation. The baseline is ragged and QRS complexes are ‘irregularly irregular’

Classification

1. Paroxysmal AF
   • Terminates spontaneously, usually within a week
   • By definition is not treated (as such)
2. Persistent AF
   • Usually lasts longer than a week and does not self-terminate (i.e. requires treatment)
3. Permanent AF
   • AF that does not revert to sinus rhythm, despite treatment.  Usually lasts >1 year
   • Whilst it can be possible to regress to persistent/paroxysmal status, it is usually very difficult, and management is mostly symptomatic and risk reduction

Aetiology

• Ischaemic and Hypertensive heart disease
  • Haemodynamic stress (most commonly in mitral valve or tricuspid valve disease and left ventricular dysfunction)
    • NB Aortic stenosis is NOT a cause and if AF is present, mitral regurgitation/prolapse should be considered
  • Atrial ischaemia (following MI or in CAD)
• Inflammation (e.g. endocarditis; Dressler’s syndrome (immune mediated pericarditis which classically appears 4 weeks after an MI))
• Alcohol/drug use (particularly stimulants)
• After surgery
• Endocrine disorders e.g. hyperthyroid, diabetes
• Neurological disorders e.g. SAH, stroke
• Age

Presentation

• In many patients, AF is an incidental finding- either on routine examination or investigation with ECG for another reason
• Patients may present with palpitations; syncope; dizziness; chest discomfort; stroke/TIA; worsening symptoms of heart failure

Investigations

• ECG
  • Irregularly irregular rhythm
  • No P waves- replaced by fibrillatory (disorganised) waves that can be fine or coarse
    • Occasionally mimic P waves
  • Absence of isoelectric baseline
  • Variable ventricular rate
• Other investigations include
  • blood tests e.g. FBC, U&Es, LFTs, TFTs (may identify an underlying cause)
    • Coagulation screen also (especially if planned for anticoagulation)
  • CXR
  • Echocardiography- should be performed
    • if a baseline echocardiogram is important for long-term management (such as in younger patients)
    • if you are considering a rhythm-control strategy that includes electrical or pharmacological cardioversion
    • if you suspect underlying structural or functional heart disease (failure or murmur) that would influence management, such as choice of antiarrhythmic drug
    • where needed to help with stratifying stroke risk for antithrombotic therapy, but only where clinical evidence is needed of left ventricular (LV) dysfunction or valve disease

Management (Based on NICE guidelines)

• Always treat an underlying cause (if it can be identified).
• If the patient is unstable i.e. unconscious and requiring acute care, and AF is thought to be the underlying cause:
  • ABCDE
  • Is the AF known to be permanent?
    • If no/not known, Electrical cardioversion (150J DC shock) should be given.  If this fails, try pharmacological cardioversion with IV amiodarone.
    • If yes, pharmacological rate control with beta blockers or verapamil should be tried (amiodarone- second line).
• If the patient is stable:
  • Paroxysmal AF- Rhythm-control
    • ‘Pill-in-the-pocket’ treatment may be appropriate in a sub-group of patients
    • For others, beta blocker is first line
      • If this fails:
        • If there is no CAD/LVD, flecainide or sotalol; if CAD then sotalol is preferred and if LVD (or if others fail), then amiodarone can be used 3rd line
  • Persistent AF in patients who are symptomatic, younger (<65); presenting for the first time; secondary to a treated/corrected cause; with congestive heart failure- Rhythm Control (often more suitable in older patients where cardiac output may not be as high)
    • If the patient requires cardioversion**- do this
      • Ideally patients will have had an echo prior to cardioversion
    • If the underlying cause cannot be treated (or is unknown)
      • treat with a beta-blocker (e.g. bisoprolol) first line
        • If this fails, then as for paroxysmal AF (class 1c agent then amiodarone or amiodarone only if structural disease present)
        • further cardioversion may also be required

**Cardioversion: Make sure to anticoagulate the patient (usually with heparin).  
If the AF began <48 hours ago, perform electrical or pharmacological cardioversion (with flecainide or amiodarone, depending on heart disease).  
If the AF began >48 hours ago, consider trans-oesophageal echo- guided cardioversion.  
If > 48 hours and high risk of failure (e.g. past failure/recurrence), recommend 4 weeks of sotalol/amiodarone prior to electrical cardioversion.
Remember anticoagulation post-cardioversion (esp if AF >48 hours- 4 weeks minimum).
Patients unsuitable include: marked structural heart disease; prolonged AF (>12 months); previous failed attempts/relapses; or a reversible cause

• Persistent AF in older patients >65, patients with CAD, contraindications to pharmacological treatment or who are unsuitable for cardioversion**.  And Permanent AF- Rate control
  • Assess the need for rate-limiting treatment
    • Target HR <90bpm at rest (110bpm for recent onset AF) and an exercise HR of <110bpm (non-active) and <200-age (active)
  • Again, beta blocker is first line, however an alternative is a rate-limiting calcium antagonist e.g. verapamil/diltiazem can also be used
    • If further rate-limiting therapy needed, consider adding digoxin
      • If this is just with exercise, calcium channel blocker and digoxin is recommended over a beta-blocker and digoxin.
      • If digoxin does not help, particularly in those with no underlying cause or evidence of an electrical disorder e.g. WPWS, other drugs e.g. amiodarone can be consider (specialist)

Thromboprophylaxis

• All patients with AF should be considered for thromboprophylaxis therapy (especially persistent/permanent AF)
• Should be started as soon as possible (note that if the patient is on heparin in the hospital setting, further thromboprophylaxis is not required, but should be initiated on discharge)
• Consider risk of thrombo-embolic event (stroke risk factors)
  • High (CHADS2= 2)
    • Previous stroke/TIA
    • Age >=75 with hypertension, diabetes or vascular disease
    • Clinical evidence of valvular disease or heart failure, or evidence on echo
    • Warfarin unless contraindicated, with target INR 2-3
    • Rivaroxaban, apixaban (Both factor Xa inhibitors) or dabigatran (direct thrombin inhibitor) may be a suitable alternative, particularly in patients who might have trouble managing warfarin monitoring/dosing
  • Moderate (CHADS2 =1)
    • Age >=65 with no risk factors
    • Age <75 with risk factors (above)
    • Consider warfarin or aspirin
  • Low risk (CHADS2 <1)
    • Age <65 with no risk factors
    • Aspirin