Benign Prostatic Hyperplasia (BPH)

Aetiology

• Occurs in men over 50 years; by age 60, 50% have histological BPH
• Most common cause of bladder outflow obstruction (BOO) in men >70 years
• Hormonal theory: declining testosterone with relatively preserved oestrogen levels promotes growth; intermediate peptide growth factors also play a role
• Metabolic syndrome and hereditary factors are also implicated

Pathology

Fig 84.1 - Enlargement of lateral and median lobes of the prostate with hypertrophy of the trigone

Effects of BPH

On the Urethra

• Prostatic urethra is lengthened (sometimes doubled), but not narrowed anatomically
• Posterior curve may be so exaggerated that a curved catheter is needed

On the Bladder

• If BOO results, bladder musculature hypertrophies - appears trabeculated
• Increased blood flow - veins at base of bladder may cause haematuria

Fig 84.3 - Bladder with trabeculae and diverticula, bilateral hydroureter and hydronephrosis from BOO due to BPH

Consequences of BPH (Summary Box 84.2)

Lower Urinary Tract Symptoms (LUTS)

Voiding (Obstructive) Symptoms

• Hesitancy (worse if bladder very full)
• Poor flow (unimproved by straining)
• Intermittent stream (stops and starts)
• Dribbling (including post-micturition)
• Sensation of poor bladder emptying
• Episodes of near retention

Storage (Irritative) Symptoms

• Frequency
• Nocturia
• Urgency
• Urge incontinence

Complications of BOO

1. Acute retention - sometimes the first presentation
2. Chronic retention - residual volume >250 mL leads to high-pressure chronic retention, bilateral hydronephrosis, upper tract infection, and renal impairment; presents with overflow incontinence, enuresis, renal insufficiency
3. Urinary infection and calculi - from impaired bladder emptying
4. Post-obstructive diuresis - after catheter release in uraemic chronic retention (loss of tubular reabsorption due to chronic back pressure)

Investigations

Urinary Flow Rates

Voiding Pressures (Urodynamics)

Other Investigations

• Urine: dipstick (glucose, leucocyte esterase, blood), MSU for culture; cytology if CIS suspected
• Blood: serum creatinine, electrolytes, haemoglobin; PSA in appropriate patients (life expectancy >10 years)
• Imaging: Ultrasound for post-void residual; upper tract imaging (USS/CT urography) if haematuria or infection present
• Cystourethroscopy: done immediately before prostatectomy to exclude urethral stricture, bladder carcinoma, non-opaque vesical calculus
• Pressure-flow urodynamics: for suspected neuropathy, dominant irritative symptoms, borderline flow rates, young men (<50) or elderly (>80)
• IPSS (International Prostate Symptom Score): validated questionnaire used to quantify symptom severity

Management

Strong Indications for Surgery (Prostatectomy)

1. Acute retention in fit men (accounts for ~25% of prostatectomies)
2. Chronic retention with renal impairment - residual urine ≥200 mL + hydronephrosis/uraemia (accounts for ~15%)
3. Complications of BOO - stones, infection, diverticulum formation
4. Recurrent haematuria from a very vascular prostate

Treatment Options (Summary Box 84.4)

• Fluid manipulation (avoid fluid bingeing and late-night intake)
• Reduce caffeine and alcohol intake
• Suitable for mild symptoms

TURP - Key Facts

• Resectoscope inserted transurethrally; electric current via diathermy loop resects tissue
• Success rate: 90% for urodynamically proven BOO; only 65% for mild symptoms or weak detrusor
• Mortality: <0.5%
• Retrograde ejaculation: 75-80%
• Erectile dysfunction: 5-10%
• Incontinence: ~1%
• Severe sepsis: ~6%
• Severe haematuria requiring transfusion: ~3%
• Re-operation rate: ~15% after 8-10 years
• TURP syndrome: dilutional hyponatraemia from absorption of hypotonic irrigating fluid - now largely avoided with bipolar/saline-based systems

Chronic Retention - Special Considerations

• Uraemic patients must have urgent catheterisation before surgery - wait at least 6 weeks for renal function to recover before prostatectomy
• Risk of post-obstructive diuresis after catheter placement - requires careful IV fluid replacement (0.45% saline or D5W based on urine output)
• Haematuria commonly follows catheterisation due to bladder/upper tract decompression - usually settles within days

Achalasia Cardia

Definition and Aetiology

• Loss of inhibitory ganglion cells in the myenteric (Auerbach's) plexus of the oesophagus
• Postulated mechanism: virus-induced autoimmune destruction (evidence points to latent HSV-1 infection in genetically susceptible individuals with specific HLA alleles)
• Histology shows reduced ganglion cells with variable chronic inflammatory infiltrate (predominantly cytotoxic T cells)
• Key neurotransmitter deficit: loss of inhibitory neurons (NO and VIP) that mediate LOS relaxation and propagated peristalsis
• The excitatory cholinergic pathway is partially preserved, which explains why botulinum toxin has some effect

• Chagas disease - Trypanosoma cruzi destroys the myenteric plexus (South America)
• Cancer of the gastric cardia - must always be excluded
• Allgrove syndrome - rare genetic triad of familial adrenal insufficiency, alacrima, and achalasia

Chicago Classification (HRM Types)

• Degree of ganglion cell loss parallels disease duration: likely progression from EGJ outflow obstruction → Type II → Type I → end-stage achalasia (megaoesophagus)
• Type III has unique pathogenesis - myenteric inflammation + altered function, without destruction

Clinical Features

Symptoms

• Dysphagia (to both solids AND liquids - hallmark distinguishing from mechanical obstruction) - gradual onset, often present for years
• Regurgitation - nonbilious, nonacid, mixed with saliva; food from hours/days previously
• Retrosternal chest pain / odynophagia - common early, especially in type III; may improve spontaneously
• Heartburn - paradoxically common; actually due to fermentation of retained food (not true acid reflux)
• Halitosis - from fermentation of food residues
• Weight loss - variable; patients often adapt diet to maintain weight
• Aspiration pneumonia / respiratory symptoms - up to 10% with advanced disease

Eckardt Score (Clinical Severity Scoring)

Diagnosis

1. Endoscopy (OGD)

• Frothy saliva pooling in oesophagus
• Food residue in oesophagus
• Oesophagus dilated or tortuous
• OGJ appears tight/spastic but usually allows scope passage with gentle pressure
• 30-40% of endoscopies are normal - does not exclude achalasia
• Critical to exclude pseudo-achalasia (carcinoma of gastric cardia)

2. Barium Contrast Study (Barium Swallow)

• Dilatation of oesophageal body
• Abnormal/absent peristaltic contractions
• "Bird's beak" / "Rat's tail" appearance - smooth tapering at the distal oesophagus/OGJ

Fig 66.25 - Barium contrast showing the typical "rat's tail" / "bird's beak" appearance at the OGJ

• Timed barium oesophagogram - quantifies contrast column height at fixed time intervals to assess disease severity
• Progressive dilatation leads to sigmoid-shaped / megaoesophagus (end-stage)
• Note: In normal individuals, no air-fluid level is seen in the stomach in achalasia on erect plain X-ray (no air passes through the LOS)

3. High-Resolution Manometry (HRM) - Gold Standard for Definitive Diagnosis

• Elevated Integrated Relaxation Pressure (IRP) across OGJ
• Aperistalsis in smooth muscle oesophagus
• Classifies into Type I, II, III
• Mandatory before any intervention

Complications

1. Aspiration pneumonia - from retained food
2. Oesophageal carcinoma - chronic retention oesophagitis/fermentation predisposes (squamous cell carcinoma; ~10-33x increased risk)
3. Megaoesophagus / sigmoid oesophagus - end-stage with grossly dilated, tortuous oesophagus
4. Malnutrition and weight loss

Treatment

Treatment is palliative - there is no therapy to reverse neuronal degeneration. All therapies target LOS reduction.

1. Medical Therapy (Limited Role)

• Calcium channel blockers (nifedipine), nitrates, PDE5 inhibitors - reduce LOS pressure
• Significant side effects (headache, oedema, hypotension)
• Reserved for patients unfit for endoscopic or surgical treatment

2. Botulinum Toxin Injection

• Inhibits presynaptic ACh release, paralyses LOS cholinergic excitatory neurons
• Symptom relief: ~70% at 3 months → ~40% at 1 year
• Effect is temporary - repeated injections required
• Repeated injections may cause scarring, making subsequent treatments more difficult
• Not first-line in patients who are good surgical candidates
• Useful when: diagnosis is in doubt, elderly or high-comorbidity patients

3. Pneumatic Dilatation (PD)

• Non-compliant balloon (30-40 mm) inserted over guidewire to disrupt LOS muscle fibres
• Graded serial dilatation: 30 mm → 35 mm → 40 mm
• Efficacy similar to surgical myotomy in selected patients
• Predictors of good response: age >45 years, female sex, undilated oesophagus, type II achalasia, response to first dilatation
• Complication: perforation (~1.9% average; <0.5% with 30-mm balloon; increases with larger balloons)
• Requires experienced endoscopist and surgical backup

4. Heller's Myotomy (Standard Surgical Treatment)

• Cutting the muscle of the lower oesophagus and gastric cardia (anterior myotomy)
• Extent: ≥6 cm proximally on oesophageal side + 2-3 cm distally into gastric cardia
• Standard approach: laparoscopic (transabdominal)
• Major complication: GORD in up to 40% of patients
• Therefore combined with partial fundoplication:
  • Anterior Dor fundoplication or posterior Toupet fundoplication - reduces GORD incidence
  • Nissen (360°) fundoplication is CONTRAINDICATED - increases outflow resistance against an aperistaltic oesophagus → postoperative dysphagia
• Laparoscopic myotomy is superior to single pneumatic dilatation in efficacy and durability
• Better outcomes in Type I and II achalasia; Type III needs longer extended proximal myotomy

5. POEM (Peroral Endoscopic Myotomy)

• Mucosa opened proximal to intended myotomy site
• Submucosal tunnel extended to ~2-3 cm into gastric cardia
• Circular ± longitudinal muscles cut with ESD instruments
• Myotomy: minimum 6 cm proximally + 2 cm into gastric cardia
• Mucosal entry site closed with endoclips
• Advantages:
  • Equivalent efficacy to PD and Heller's myotomy in RCTs for dysphagia relief
  • Can extend myotomy proximally - ideal for Type III achalasia (spastic component)
  • Can treat distal oesophageal spasm and hypercontractile oesophagus
• Disadvantage: Higher rate of GORD (no antireflux procedure):
  • Oesophagitis at 3 months post-POEM: up to 57%
  • May require lifelong PPI or subsequent antireflux surgery

6. Oesophagectomy

• Reserved for end-stage achalasia with sigmoid/megaoesophagus not responding to other methods
• High operative risk vs. risk of aspiration complications must be balanced
• Option for surgically fit patients with grossly dilated oesophagus predisposing to aspiration pneumonia

Comparison of Treatment Options

Follow-up

• Treatment success assessed by Eckardt score (target ≤3)
• Counsel on post-treatment diet - oesophageal body motility remains defective
• Surveillance endoscopy for oesophageal carcinoma risk (long-standing achalasia)
• Patients with POEM require monitoring for GORD and possible acid suppression therapy