Detrusor Underactivity (Underactive Bladder): Causes, Symptoms & Management [Bethanechol]

Mayta
Nov 27
5 min read

1. Definition

Detrusor underactivity (DU) or Underactive Bladder (UAB) is a condition where the bladder muscle (detrusor) contracts too weakly and/or too briefly to empty the bladder completely during voiding.

Formal urodynamic definition (ICS – International Continence Society): “A contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or failure to achieve complete bladder emptying within a normal time span.”

Clinically, you will see:

Slow urinary stream
Straining to void
Feeling of incomplete emptying
High post-void residual (PVR)
Sometimes overflow incontinence or acute urinary retention

2. Normal Physiology of Voiding

To understand DU, you must first know normal physiology.

During storage phase:
- Detrusor muscle is relaxed.
- Bladder outlet (internal sphincter, external sphincter, pelvic floor) is contracted.
- Sympathetic system (hypogastric nerve) and somatic (pudendal nerve) dominate.
During voiding phase:
- Parasympathetic system (pelvic nerve) releases acetylcholine.
- Acetylcholine stimulates muscarinic M3 receptors on detrusor → strong contraction.
- Bladder outlet relaxes (decreased sympathetic and somatic tone).
- Coordination between detrusor contraction and sphincter relaxation is essential.

In detrusor underactivity, the “pump” (detrusor contraction) is too weak or absent.

3. Etiology and Risk Factors

Detrusor underactivity is usually multifactorial. Common causes:

3.1 Neurogenic causes

Diabetes mellitus (diabetic cystopathy)
Spinal cord injury or myelopathy
Multiple sclerosis
Parkinson disease
Stroke
Peripheral neuropathies

Mechanism: Damage to sensory or motor pathways → impaired afferent signaling and/or efferent parasympathetic output to the bladder.

3.2 Myogenic causes

Chronic bladder outlet obstruction (e.g., long-standing BPH in men) → detrusor hypertrophy → then decompensation and fibrosis → weak muscle
Aging-related detrusor muscle degeneration
Ischemia of bladder wall

3.3 Iatrogenic / pharmacologic

Anticholinergic drugs (e.g., oxybutynin, TCA, many antihistamines)
Opioids
Benzodiazepines
Botulinum toxin injections in the bladder (used for overactive bladder but can overshoot)

3.4 Postoperative / transient

Post-anaesthesia urinary retention
Post pelvic or spine surgery

3.5 Idiopathic

No clear cause, especially in older women.

4. Clinical Presentation

Symptoms are usually those of voiding difficulty and storage consequences.

4.1 Voiding symptoms

Slow stream
Hesitancy
Intermittent stream
Straining to void
Feeling of incomplete emptying
Prolonged voiding time

4.2 Storage symptoms (from chronic retention)

Frequency
Nocturia
Urgency
Urgency incontinence
Overflow incontinence (small continuous dribbling)

4.3 Complications

Recurrent urinary tract infection (UTI)
Bladder stones
Hydronephrosis and renal impairment (from chronic high residual volumes)
Acute urinary retention

In severe cases, patients present with:

Lower abdominal pain
Palpable distended bladder
No urine output (anuria) despite adequate hydration

5. Physical Examination

Key findings:

Suprapubic fullness (distended bladder)
Possibly reduced perineal sensation or anal tone (if neurogenic cause)
Neurological signs (depending on lesion: spine, brain, peripheral nerve)
In male: coexisting signs of prostate enlargement
In female: pelvic organ prolapse may coexist but is not the primary problem in pure DU

6. Investigations

6.1 Basic tests

Urinalysis and urine culture: to exclude infection
Serum creatinine, BUN: assess renal function
Ultrasound KUB:
- Measure post-void residual (PVR)
- Check for hydronephrosis, stones, bladder wall thickening

A PVR > 100–200 mL is commonly considered abnormal; very high PVR raises strong suspicion of DU or obstruction.

6.2 Urodynamic study (gold standard)

This is essential for a definite diagnosis.

Findings in detrusor underactivity:

Low detrusor pressure during voiding
Reduced or absent detrusor contraction
Intermittent/weak flow
High residual volume
No significant outlet resistance (if pure DU without obstruction)

It is important to distinguish:

DU (weak pump)vs.
Bladder outlet obstruction (BOO, high resistance at outlet)

Sometimes both coexist, especially in older men or post-pelvic surgery.

6.3 Additional tests depending on suspected cause

MRI spine (if spinal cord lesion suspected)
Nerve conduction studies (if peripheral neuropathy suspected)
HbA1c, fasting glucose (for diabetic neuropathy)

7. Diagnosis

The diagnosis of Detrusor Underactivity / Underactive Bladder is based on:

Symptoms of voiding difficulty ± overflow.
High PVR on ultrasound or catheterization.
Urodynamic demonstration of low-pressure, weak detrusor contraction with or without prolonged voiding and incomplete emptying.
Exclusion or identification of bladder outlet obstruction and neurogenic causes.

8. Management Principles

Management focuses on:

Protecting the kidneys.
Preventing infection and bladder damage.
Improving emptying (if possible).
Maintaining quality of life.

Immediate management of acute urinary retention

If the patient presents with no urine and suprapubic discomfort:

Insert a Foley catheter urgently.
Decompress bladder; record drained volume.
Assess for hematuria, infection, and post-obstructive diuresis if chronic retention.

If large volumes (>800–1000 mL) are drained, this supports chronic retention.

9. Long-term Management

9.1 Behavioral and conservative measures

Timed voiding (e.g., every 3–4 hours)
Double voiding (void, wait, then try again)
Avoid excessive fluid intake before bedtime
Manage constipation (stool burden can aggravate bladder dysfunction)
Review and stop drugs that impair bladder contraction (anticholinergics, opioids, etc.)

These methods help but are rarely sufficient alone in true DU.

9.2 Catheter-based strategies

Because DU is often chronic and only partially reversible, catheterization is central to management.

9.2.1 Clean Intermittent Catheterization (CIC)

Gold standard for chronic underactive bladder.
The patient or caregiver uses a catheter several times per day (e.g., every 4–6 hours) to empty the bladder.
Advantages:
- Lower infection risk than long-term indwelling catheter.
- Better bladder dynamics and quality of life.
Widely recommended in guidelines for neurogenic bladder and DU.

9.2.2 Indwelling catheter

Foley catheter or suprapubic catheter.
Reserved for patients unable to perform CIC (e.g., poor hand function, lack of caregiver, severe cognitive impairment).
Higher risk of UTI, stones, urethral trauma.

9.3 Pharmacologic treatment

Evidence for drugs is limited, but there are some options.

9.3.1 Parasympathomimetics

Bethanechol
Muscarinic agonist (M3) → increases detrusor contraction.
Typical dose: 25 mg orally 3–4 times daily.
Side effects: diarrhea, salivation, sweating, flushing, bronchospasm, bradycardia.
Works best in patients with partial residual parasympathetic function and no significant outlet obstruction.
Distigmine / Neostigmine
Acetylcholinesterase inhibitors → increase acetylcholine.
Distigmine is sometimes used orally in chronic DU.
Neostigmine is mostly for acute or perioperative urinary retention, not long-term therapy.

Important: In many patients, pharmacologic response is modest. CIC often remains necessary.

9.3.2 Alpha-blockers

These drugs (e.g., tamsulosin, silodosin) relax the bladder neck and prostate.
They do NOT increase detrusor contraction.
They are useful only when DU coexists with bladder outlet obstruction, mostly in men.
In women with pure DU, they are usually not beneficial and can worsen retention.

So:

Detrusor underactivity alone → alpha-blockers are not primary therapy.
DU + BOO (e.g., BPH) → treat outlet obstruction plus consider DU management.

9.4 Neuromodulation and surgery

In selected patients:

Sacral neuromodulation (e.g., S3 nerve stimulation) can improve bladder emptying in some DU/neurogenic bladder cases.
Bladder augmentation or urinary diversion procedures may be used when conservative and medical therapy fail and the upper urinary tract is at risk.

These are specialized procedures in tertiary centers.

10. Special Considerations in Women

Women do not have a prostate, so outlet obstruction is less common, except from pelvic organ prolapse, urethral stricture, or iatrogenic causes.
Many women with UAB have idiopathic or neurogenic DU.
Use of prostate-centric alpha-blockers (e.g., silodosin) is generally inappropriate unless there is clear functional outlet obstruction confirmed by urodynamics.
Clean intermittent catheterization and, where appropriate, parasympathomimetics form the core of management.

11. Prognosis

Prognosis depends on the cause:

Diabetic cystopathy: progression can be slowed by good glycemic control but may not fully reverse.
Post-obstructive myogenic failure (e.g., after years of BPH): sometimes partially reversible if obstruction is relieved early; late-stage often permanent.
Neurogenic causes (spinal cord injury, MS): often chronic and require long-term bladder management strategies.
Idiopathic DU in older adults: usually chronic, with management focused on symptom control and renal protection.

The key determinant of long-term outcome is:

Preservation of renal function.
Adequate bladder emptying (often via CIC).
Prevention of recurrent UTIs.

12. Key Exam Pearls

Underactive bladder = problem with the “pump” (detrusor), not primarily with the “pipe” (outlet).
High PVR + low detrusor pressure on urodynamics = DU.
First priority in acute retention: catheterization and decompression.
Long-term: CIC is the gold standard for many DU patients.
Parasympathomimetics (bethanechol, distigmine) may help, but evidence is limited; always monitor side effects.
Alpha-blockers are mainly for outlet obstruction (BPH) and are not primary treatment for pure DU.
Always search for reversible causes: diabetes, medications, spinal pathology, chronic obstruction.