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COMPLICATIONS OF CATARACT SURGERY

1. Operative (happen during surgery)
2. Acute Post-operative (happen shortly after surgery)
3. Late Post-operative (happen weeks to months later)

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PART 1 - OPERATIVE COMPLICATIONS

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1. POSTERIOR CAPSULAR RUPTURE (PCR)

Why does it happen? (Causes)

• Incomplete hydrodissection - In cataract surgery, water is injected to separate the lens from its capsule. If this step is done incorrectly, the suction machine accidentally sucks in the capsule along with the lens material. This tears the back wall.
• Defective nuclear fragmentation - The hard central part of the lens (nucleus) is broken into pieces using ultrasound (phacoemulsification). If this is done poorly, the instruments can poke through and rupture the capsule.

What problems does PCR cause?

• Implantation disturbance - The artificial lens (IOL = Intraocular Lens) cannot be placed in its normal position (inside the capsular bag) because the bag is torn.
• Fall of IOL into the vitreous - The artificial lens can fall into the jelly-like substance at the back of the eye (vitreous). This is a serious complication.
  • Solution: The IOL is then placed at alternative positions - either in the sulcus (the groove just behind the iris) or in the anterior chamber (the space in front of the lens).
• Vitreous in the anterior segment - The jelly from the back comes forward into the front part of the eye, which can cause inflammation and raise eye pressure.

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2. UGH SYNDROME

• U - Uveitis (inflammation inside the eye)
• G - Glaucoma (raised eye pressure)
• H - Hyphema (collection of blood in the anterior chamber - the space between the cornea and the iris)

Why does UGH syndrome happen?

• Irritation and inflammation
• Tiny blood vessels in the iris get damaged and bleed
• Pigment (color) gets scraped off the iris and floats around in the eye fluid

Three complications from iris chafing:

1. Inflammation → Uveitis: The constant rubbing irritates the eye tissues, causing inflammation (uveitis).
2. Glaucoma: The scraped-off pigment from the iris (which is a pigmented/colored tissue) floats in the eye fluid and blocks the trabecular meshwork (the drainage channel of the eye). When drainage is blocked, eye pressure rises → glaucoma.
3. Hyphema: The iris has a rich blood supply. Constant rubbing damages blood vessels → blood leaks between the cornea and the iris (anterior chamber) → hyphema.

Management of UGH syndrome:

• Steroids - to reduce inflammation
• Antiglaucoma agents - to lower eye pressure
• Explant ACIOL - remove the artificial lens in severe cases
• Recovery is slower than normal - takes 7-10 days to regain vision (normally after eye surgery vision returns in 24 hours)

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3. EXPULSIVE CHOROIDAL HAEMORRHAGE

What is it?

Why does it happen?

• Posterior (back) part of the sclera and choroid
• Outer 4 layers of the retina

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4. DESCEMET MEMBRANE DETACHMENT

What is it?

Why does it happen?

Treatment:

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PART 2 - ACUTE POST-OPERATIVE COMPLICATIONS

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1. IRIS PROLAPSE

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2. ENDOPHTHALMITIS (EO) - THE MOST IMPORTANT ONE FOR EXAMS

Which organisms cause which type?

Symptoms:

• Pain
• Redness
• Loss of vision

Signs:

• In the anterior chamber (front of eye):
  • Hypopyon/pus - a white-yellow layer of pus settling at the bottom of the anterior chamber (seen as a white layer at the bottom of the colored eye)
  • Hazy cornea - cornea becomes cloudy
  • Congestion/hyperemia - blood vessel engorgement, making the eye very red
• In the posterior segment (back of eye):
  • Yellowish exudates in the vitreous - pus-like material in the jelly of the eye

Management (Treatment):

• Evisceration - surgical removal of all contents of the eyeball EXCEPT the sclera (the white coat is kept; everything inside is removed).

• Give both:
  • Intravitreal antibiotics (injected directly into the jelly of the eye):
    • Vancomycin 1 mg in 0.1 mL (covers gram positive bacteria)
    • Ceftazidime 2.2 mg in 0.1 mL (covers gram negative bacteria)
  • Topical antibiotics (eye drops)
  • Pars plana vitrectomy - surgical procedure to remove the infected vitreous (jelly)

IMPORTANT NOTE (Exam favourite!):

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3. FLAT / SHALLOW ANTERIOR CHAMBER (AC)

1. Wound leak - fluid leaking out from the surgical wound
2. Malignant glaucoma - aqueous fluid is misdirected posteriorly into the vitreous instead of flowing forward
3. Pupillary block glaucoma - the artificial lens blocks the flow of aqueous fluid through the pupil, raising pressure
4. Cilio-choroidal detachment - the ciliary body (which produces eye fluid) detaches, reducing fluid production

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4. Other Acute Complications (briefly):

• Uveitis - inflammation inside the eye
• Retinal detachment - the retina peels away from the back of the eye
• Astigmatism - irregular curvature of the cornea due to the surgical wound

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PART 3 - LATE POST-OPERATIVE COMPLICATIONS

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1. POSTERIOR CAPSULAR OPACIFICATION (PCO) - MOST IMPORTANT LATE COMPLICATION

Why does it happen?

Types of PCO (from the diagram):

• Elschnig's pearls (90% of cases) - the epithelial cells multiply and form clusters that look like pearls/bubbles on the posterior capsule. This is the most common type.
• Sommering's ring (10%) - cells accumulate at the equator (edge) of the capsule, forming a ring shape.
• Capsular wrinkling - the capsule wrinkles and becomes irregular.

Prevention:

• Square-edged IOL - Using an artificial lens with sharp, square edges. This acts as a physical barrier and prevents the epithelial cells from migrating across to the posterior capsule.

Treatment:

• Nd:YAG Laser Posterior Capsulotomy - A laser is used to make a hole in the opacified posterior capsule.
• Mechanism: Photodisruption - the laser creates a small explosion that blasts a hole in the membrane, allowing light to pass through again.
• This is a quick, painless, outpatient procedure.

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2. ANTERIOR CAPSULE PHIMOSIS

• Result: IOL decentration - the lens is no longer centred in front of the pupil, causing blurry or distorted vision.

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3. IRVINE-GASS SYNDROME

1. Cystoid Macular Edema (CME) - Swelling at the central part of the retina (macula) with cyst-like spaces filled with fluid. This causes blurred central vision.
2. Bullous Keratopathy - The cornea develops blisters (bullae) due to damage to the inner lining cells (endothelium), causing the cornea to swell and become opaque.
3. Vitreous Strand touching the cornea (Vitreous Wick) - A strand of vitreous (the jelly) gets caught in the surgical wound and acts like a "wick" - it pulls on the macula and the cornea, contributing to both CME and keratopathy.

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4. IOL DISLOCATION

Causes of Lost Lens Syndrome:

• Due to PCR (Posterior Capsular Rupture) - the bag that holds the lens tears during surgery, so the lens falls back into the vitreous.
• Spontaneous (no apparent cause) - called Hallerman-Streiff syndrome (a connective tissue disorder where lens zonules are weak).

• Sunrise = lens goes UP (like the sun rising)
• Sunset = lens goes DOWN (like the sun setting)

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QUICK SUMMARY TABLE FOR EXAM

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CARDIOLOGY: ECTOPIC BEATS, TACHYCARDIA, ATRIAL FIBRILLATION & ATRIAL FLUTTER

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PART 1 - ECTOPIC BEATS (EXTRASYSTOLES / PREMATURE BEATS)

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WHAT IS AN ECTOPIC BEAT?

• Feeling of extra beats - "my heart skipped a beat"
• Thumping sensation in the chest
• Sensation of missed beats

• Irregularity in rhythm
• Missing beats on palpation
• After the ectopic beat, the next normal beat feels extra forceful (postectopic bounding beat)
• Cannon waves on JVP (Jugular Venous Pulse) - visible pulsations in the neck veins

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CLASSIFICATION OF ECTOPIC BEATS

1. Supraventricular (above the ventricles):
   • Atrial ectopics - arising from the atrium
   • Atrial Premature Beats
2. Junctional:
   • Arising from the AV (atrioventricular) junction - the junction between the atria and ventricles
3. Ventricular:
   • Arising from the ventricular muscle (the pumping chambers)

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PART 2 - SUPRAVENTRICULAR ECTOPICS (ATRIAL ECTOPICS / ATRIAL PREMATURE BEATS - APCs)

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WHAT ARE APCs?

• Found in over 60% of normal adults on 24-hour Holter monitoring (ambulatory ECG)
• They are usually asymptomatic (no symptoms) and benign (harmless)

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CAUSES OF APCs

• Idiopathic - found in healthy individuals with no cause
• Anxiety
• Excessive coffee, tea, or tobacco
• Ischemic heart disease (reduced blood supply to heart)
• Valvular heart disease (problems with heart valves)

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ECG FEATURES OF APCs

• Shows early abnormal P waves (P waves appear before the expected time)
• The P wave has a different morphology (different shape/direction) compared to normal sinus P waves
• P wave may be inverted if the ectopic beat arises near the AV node
• R-R interval (time between beats) preceding and following the ectopic beat is less than twice the basal R-R interval
  • This means the pause after an APC is NOT fully compensatory (incomplete compensatory pause)

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WHAT PROBLEMS CAN APCs CAUSE?

• Atrial tachycardia (fast atrial rhythm)
• Atrial flutter (rapid, regular flutter of atria)
• Atrial fibrillation (chaotic, irregular atrial activity)

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TREATMENT OF APCs

• Treatment is only needed if they cause palpitations (uncomfortable awareness of heartbeat)
• Identify and eliminate the trigger (alcohol, tobacco, coffee, adrenergic stimulants)
• If no trigger is found - mild sedation or a beta-blocker may be tried
• Trigger for paroxysmal SVT (sudden-onset tachycardia): treat the underlying cause

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PART 3 - VENTRICULAR PREMATURE COMPLEXES (VPCs) / VENTRICULAR ECTOPICS / PVCs

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WHAT ARE VPCs?

• Also called: VPBs (Ventricular Premature Beats), PVCs (Premature Ventricular Contractions)
• Over 60% of adult males will show VPCs on 24-hour Holter monitoring
• In patients with previous MI (heart attack), if VPCs are frequent (>10 per hour) or complex, they are associated with increased mortality

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CAUSES OF VPCs

• Idiopathic (in healthy individuals)
• Excessive tea, coffee, alcohol
• Acute myocardial infarction (MI) - heart attack
• Myocardial ischemia (reduced blood flow)
• Myocarditis (inflammation of heart muscle)
• Digitalis toxicity (digoxin drug side effect)
• Hypokalemia (low potassium in blood)
• Mitral valve prolapse (a valve defect)

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ECG FEATURES OF VPCs

• Wide, bizarre QRS complex - QRS duration >0.12 seconds (3 small squares on ECG paper)
• No preceding P wave - because the beat starts in the ventricle, not from the SA node
• The beat arises from an abnormal (ectopic) site in the ventricular myocardium

Important ECG Concepts for VPCs:

• The AV node or ventricle is still "refractory" (unresponsive) to the next normal sinus impulse
• The pause is fully compensated, meaning: R-R before VPC + R-R after VPC = 2 × normal R-R interval

Terminology for Multiple VPCs:

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TREATMENT OF VPCs

• In the absence of cardiac disease, isolated asymptomatic VPCs (even frequent or complex) do NOT require treatment
• Beta-blockers are useful for symptomatic VPCs
• Beta-blockers are also helpful for conditions that worsen VPCs (e.g., thyrotoxicosis, mitral valve prolapse)
• ICD (Implantable Cardioverter-Defibrillator) placement improves prognosis in patients with:
  • Inducible VT (ventricular tachycardia) AND
  • LV (left ventricular) dysfunction

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PART 4 - TACHYCARDIA

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DEFINITION

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CLASSIFICATION

By Origin:

1. Supraventricular Tachycardia (SVT):
   • Utilizes atrial or AV nodal tissue as part of its mechanism
   • Originates above the bundle of His (the electrical pathway connecting atria to ventricles)
2. Ventricular Tachycardia (VT):
   • Originates below the level of bundle of His

By QRS Shape on ECG:

1. Narrow-complex tachycardia (QRS < 0.12 sec):
   • Usually originates from or above the AV node
   • The AV node generally produces narrow QRS complexes
2. Wide-complex tachycardia (QRS > 0.12 sec):
   • Usually originates below the AV node (i.e., in the ventricles)
   • Tachycardias originating below AV node produce wide QRS complexes

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TYPES OF SUPRAVENTRICULAR TACHYCARDIA (SVT)

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PART 5 - SINUS TACHYCARDIA

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DEFINITION

CAUSES

• Exercise, emotion, pregnancy

• Anemia (low RBC/hemoglobin)
• Thyrotoxicosis (overactive thyroid)
• Anxiety, fever
• Heart failure
• Pheochromocytoma (adrenal tumor)
• Drugs (beta-agonists like salbutamol/bronchodilators)
• Pulmonary embolism (blood clot in lung)
• Shock

TREATMENT

• Identify and treat the underlying cause
• If tachycardia causes myocardial ischemia (chest pain due to fast rate), treat with beta-blockers

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PART 6 - AV NODE RE-ENTRY TACHYCARDIA (AVNRT)

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WHAT IS AVNRT?

• AVNRT is the most common cause of paroxysmal (sudden-onset) supraventricular tachycardia (PSVT)
• It produces a regular tachycardia at 120-240 beats/minute

MECHANISM (How it happens)

1. Fast pathway: Has a LONGER effective refractory period but conducts FASTER
2. Slow pathway: Has a SHORTER effective refractory period but conducts SLOWER

• Imagine an early atrial beat (APC) arrives at the AV node when the fast pathway is still "asleep" (refractory)
• The impulse takes the slow pathway down to the ventricles
• By the time it reaches the other end, the fast pathway has "woken up" and is ready again
• The impulse then travels BACK UP through the fast pathway to the atrium
• This creates a circular loop (circuit) → this keeps repeating → tachycardia!
• This is the most common "slow-fast" or "typical" AVNRT

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CLINICAL FEATURES

• More common in women (Female:Male = 2:1)
• Occurs suddenly without any structural heart disease or obvious cause
• Exertion, coffee, tea, and alcohol may aggravate or induce it
• Episodes may last seconds to hours and may stop spontaneously
• Patient feels a rapid, very forceful, regular heartbeat
• May also feel chest discomfort, lightheadedness, breathlessness
• Sometimes causes polyuria (excessive urination) - due to release of atrial natriuretic peptide (ANP) from the distended atria during fast rate

ECG FEATURES

• Regular tachycardia at 140-240/minute
• Normal regular QRS complexes
• Occasionally, bundle branch block pattern (wide QRS) may appear

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MANAGEMENT OF AVNRT

Step 1: Vagal maneuvers (to slow AV node conduction)

• Carotid sinus pressure - pressing on the carotid artery in the neck (increases vagal tone → slows AV node)
• Valsalva maneuver - forced expiration against a closed glottis (like blowing into a thumb), increases intrathoracic pressure → vagal response → slows AV node

Step 2: If vagal maneuvers fail - give DRUGS

• Adenosine (3-12 mg rapidly IV in incremental doses until tachycardia stops) - DRUG OF CHOICE for acute termination
  • Mechanism: Blocks AV node conduction briefly
  • It works within seconds
• Verapamil (5 mg IV over 1 min) - calcium channel blocker that slows AV node
• IV beta-blocker or flecainide may also be used

Step 3: If there is severe hemodynamic compromise (patient is very unwell)

• DC cardioversion (electric shock to the heart to reset normal rhythm)

Long-term Prevention

• Catheter ablation permanently prevents SVT in >90% of cases - this is the definitive cure
  • A catheter is inserted and the slow pathway is ablated (destroyed) using radiofrequency energy

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PART 7 - ATRIAL FIBRILLATION (AF)

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DEFINITION

• Disorganized atria producing multiple atrial foci firing impulses at a rate of 350-600/minute
• There is NO atrial contraction - only fibrillation (chaotic quivering)
• The ventricles respond at 100-140/minute in an irregularly irregular pattern
• It is the most common cause of sustained cardiac arrhythmia

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ETIOLOGY (CAUSES)

• Hypertensive heart disease (high blood pressure damaging the heart)
• Valvular heart disease (e.g., rheumatic heart disease, especially mitral stenosis)
• Ischemic heart disease (blocked coronary arteries)
• Heart failure
• Cardiomyopathy (disease of heart muscle)
• Pericarditis (inflammation of pericardium)
• Congenital heart disease
• Post-cardiac surgery

• Pulmonary (lung) causes: Pneumonia, COPD, pulmonary embolism
• Hyperthyroidism/thyrotoxicosis - a very important cause
• Excess catecholamine/sympathetic activity
• Drugs and alcohol
• Significant electrolyte imbalance

• Younger patients (<60 years)
• No underlying cause
• Usually no symptoms
• Normal heart structure
• No associated co-morbidities

• Acute upper respiratory tract infection (URTI), chest infection
• Acute myocardial infarction (AMI)
• Pericarditis, thyrotoxicosis
• Pulmonary embolism
• After CABG (coronary artery bypass grafting)
• Holiday heart syndrome - excessive alcohol intake causing temporary AF (e.g., after a party)

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MECHANISMS OF AF (How AF Happens)

1. Triggered activity from ectopic foci - rapid bursts of depolarizing automatic ectopic beats arising from the pulmonary veins or from diseased atrial tissue. The atria respond at this rapid rate. Many impulses reach the AV node during its refractory period and are blocked (hence not all reach ventricles).
2. Multiple re-entry circuits (the main sustaining mechanism) - AF is maintained by continuous, rapid activation of the atria by multiple re-entrant conduction circuits looping around the atria. Re-entry occurs in enlarged atria or when conduction is slow (common in heart disease).

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CLINICAL FEATURES

• Palpitations (most common)
• Fatigue
• Syncope (fainting)
• Angina (chest pain)
• Symptoms of cardiac failure
• Symptoms of thromboembolism (stroke - from blood clots)

1. Irregularly irregular pulse - the key feature. The rhythm is completely irregular. Also, the pulse volumes vary (varying volumes of pulse)
2. Pulse deficit (apex pulse deficit) - heart rate counted at apex is faster than pulse felt at wrist, because some beats are too weak to be felt at wrist
3. Blood pressure: Hypotension (low BP). Take mean of 3 recordings
4. Absence of 'a' waves on JVP - normally the atria contract and produce 'a' waves in the jugular vein. In AF there is no atrial contraction → no 'a' waves
5. Varying intensity of first heart sound - because ventricular filling varies with each cycle
6. Disappearance of 4th heart sound (which requires atrial contraction)
7. Disappearance of the pre-systolic murmur of mitral stenosis in some patients

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INVESTIGATIONS

1. ECG (most important - see Box 1.50 below)
2. 2D ECHO - to check LA (left atrium) size, look for thrombus (blood clot), assess LV (left ventricle) function
3. Holter monitoring - for paroxysmal (intermittent) AF
4. Exercise stress test - to look for ischemic heart disease
5. Catheterization - before ablation procedure
6. Thyroid function tests - always check! Thyroid disease is a reversible cause
7. Serum electrolytes - check K+, Mg2+
8. Chest X-ray
9. Fasting lipid profile

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ECG CHANGES IN ATRIAL FIBRILLATION (Box 1.50)

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COMPLICATIONS OF ATRIAL FIBRILLATION

1. Thromboembolism - THE MOST DANGEROUS. Blood pools in the non-contracting atrium → clot forms in the left atrial appendage → clot can break off → travels to brain → STROKE. This is why anticoagulation is so important.
2. Precipitation/worsening of cardiac failure - fast irregular rate reduces cardiac output
3. Syncope (fainting)
4. Hypotension (low blood pressure)
5. Angina (chest pain from fast rate)
6. Precipitation of pulmonary edema in mitral stenosis

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MANAGEMENT OF ATRIAL FIBRILLATION

Goals of Treatment:

1. Hemodynamic stabilization
2. Heart rate control OR restoration of sinus rhythm (rhythm control)
3. Minimize symptoms
4. Prevent tachycardia-associated cardiomyopathy (heart damage from prolonged fast rate)
5. Prevention of recurrent AF
6. Reduce risk of thromboembolism (anticoagulation)
7. Treat underlying cause

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STRATEGY 1: RATE CONTROL

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STRATEGY 2: RHYTHM CONTROL (CARDIOVERSION)

• Quinidine, ibutilide, flecainide, propafenone, or amiodarone
• Amiodarone dose: 5-7 mg/kg IV over 1 hour, followed by 1.2-1.8 g/24-hour infusion

• Used when drugs fail
• Done after 3 weeks of warfarin therapy
• Anticoagulation continued for another 4 weeks after cardioversion (because stunning of atria can still form clots after cardioversion)

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CLINICAL CLASSIFICATION OF AF AND TREATMENT (Table 1.89)

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ANTICOAGULATION IN AF (CHA₂DS₂-VASc SCORE)

• 0 points = Low risk → No anticoagulation needed
• 1-2 points = Moderate risk → Oral anticoagulant OR aspirin recommended
• ≥3 points = High risk → Oral anticoagulant STRONGLY recommended

• Warfarin - INR should be maintained between 2.0-3.0 (2.5-3.5 if rheumatic valvular disease or mechanical heart valve)
• Newer oral anticoagulants (NOACs):
  • Dabigatran (direct thrombin inhibitor) - 150 mg BD
  • Apixaban - 5 mg BD
  • Rivaroxaban - 20 mg OD
• Aspirin 325 mg/day - used as alternative when warfarin is contraindicated in:
  • Patients <75 years with no previous stroke/TIA without hypertension, diabetes, or heart failure

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PREVENTION OF RECURRENCE

• After restoring sinus rhythm - use quinidine, amiodarone, or dronedarone (dronedarone is safer than amiodarone)
• If cardioversion fails → allow patient to remain in AF + reduce ventricular rate with digitalis, diltiazem, verapamil, or propranolol
• Chronic anticoagulation - to prevent stroke
• Reduction of stroke risk by warfarin or antiplatelet agents

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RADIOFREQUENCY (RF) ABLATION THERAPY

• Very symptomatic patients who refuse antiarrhythmic drugs
• Young patients where only effective drug is amiodarone
• Patients with significant bradycardia for whom antiarrhythmic drugs would require pacemaker

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PART 8 - ATRIAL FLUTTER

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DEFINITION

• Organized, regular, rapid atrial rate between 250-350/minute
• The ventricles respond to every 2nd, 3rd, or 4th atrial impulse → 2:1, 3:1, or 4:1 AV block
• Typical ventricular rate: If 2:1 block → ~150/min; if 4:1 block → ~75/min

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CAUSES OF ATRIAL FLUTTER

• Organic heart diseases (ischemic, rheumatic, congenital)
• Pericarditis
• After open heart surgery (1st week post-op)

• Acute respiratory failure

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ECG FEATURES OF ATRIAL FLUTTER

• Characteristic saw-toothed flutter waves ("F" waves) between QRS complexes - these look like the teeth of a saw on ECG
• No clear P waves
• Flutter waves at 300/minute
• QRS complexes are regular (unlike AF where they are irregular)
• The most common ratio is 2:1 AV block → ventricular rate of ~150/min

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MANAGEMENT OF ATRIAL FLUTTER

1. Restoration to sinus rhythm:
   • Symptomatic acute paroxysm → Direct electrical cardioversion (first choice)
   • Flutter lasting >1-2 days → anticoagulate for 3 weeks before cardioversion (similar to AF)
2. Control of ventricular rate (if not cardioverting):
   • Digoxin, beta-blockers, or verapamil/diltiazem - to slow AV conduction
   • Then convert to sinus rhythm using quinidine, amiodarone, disopyramide, or flecainide
3. Prevention of recurrences:
   • Class III antiarrhythmic agents: quinidine, amiodarone, disopyramide, or flecainide
   • Treatment of CHOICE for recurrent atrial flutter = Catheter ablation (destroys the flutter circuit)
4. Prevention of stroke:
   • Risk of stroke is similar to AF
   • Management is almost identical to AF
   • Anticoagulants may be stopped earlier after successful ablation

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QUICK SUMMARY TABLE FOR EXAM

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