2. Urinary retention is as an inability to pass urine. It can be
divided into either acute or chronic urinary retention.
Acute urinary retention is defined as a new onset inability to
pass urine, which subsequently leads to pain and discomfort,
with significant residual volumes.
The condition is most prevalent in older male patients,
typically due to an enlarged prostate leading to bladder
outflow obstruction, however there are a wide array of
potential causes.
3. The most common cause in men is BPH. Other common
obstructive causes include urethral strictures or prostate cancer.
UTI can cause the urethral sphincter to close. Constipation can
also cause acute retention, through compression on the urethra.
Neurological causes can include peripheral neuropathy, iatrogenic
nerve damage during pelvic surgery, upper motor neurone disease
(such as Multiple Sclerosis, Parkinson’s disease), or Bladder
Sphincter Dyssinergia.
Severe pain can often cause patients to enter acute retention.
Medications, such as anti-muscarinics or spinal or epidural
anaesthesia, can affect innervation to the bladder, resulting in
acute retention.
4. Bladder Sphincter Dysinergy is the lack of co-ordination
of detrusor muscle contraction with urethral sphincter
relaxation, leading to contraction against a closed
sphincter, often seen with spinal cord pathology or
traumatic injury.
5. Urinary retention causing such high intra-vesicular pressures
that the anti-reflux mechanism of the bladder and ureters is
overcome and ‘backs up’ into the upper renal tract leading to
hydroureter and hydronephrosis, impairing the kidneys’
clearance levels.
Repeat episodes of high-pressure chronic retention can cause
permanent renal scarring and chronic kidney disease (CKD).
By contrast, low pressure retention occurs in patients with
retention with the upper renal tract unaffected due competent
urethral valves or reduced detrusor muscle contractility or
complete detrusor failure.
6. Acute suprapubic pain and an inability to micturate.
This may be associated with symptoms suggestive of the
predisposing cause, such as a urinary tract infection, change to
medication, or worsening voiding LUTS.
Any associated fevers/rigors or lethargy may suggest an infective
cause. Ensure to perform a PR examination, especially in elderly
patients, to assess for any prostate enlargement or constipation.
7. On examination, the patient will have
a palpable distended bladder, with
suprapubic tenderness
8. All patients require routine bloods, especially a FBC, CRP, and
U&Es . Post-catheterisation, a CSU (Catheterised Specimen of
Urine) should also be sent to assess for the presence of infection.
Patients with features of high-pressure retention will require an
ultrasound scan of their urinary tract to assess for the presence of
associated hydronephrosis. If this is confirmed, follow-up repeat
imaging will be required.
A post-void bedside bladder scan
will show the volume of retained urine
helping to confirm the diagnosis.
10. Patients will warrant immediate urethral catheterisation to resolve
the retention. Ensure to measure the volume drained post-
catheterisation.
The underlying causes should then be treated accordingly.
Ensure to check for any evidence of infection and treat with
antibiotics if needed.
Patients who have a large retention volume (arbitrarily around
>1000ml) need to be monitored post-catheterisation for evidence
of post-obstructive diuresis.
11. • Patients who have high-pressure urinary retention will have to keep
their catheters in-situ until definitive management can be arranged
(e.g. TURP), due to risk of which may lead to renal scarring and
CKD.
• If patients have no evidence of renal impairment, a TWOC (Trial
WithOut Catheter) will be attempted, whereby the catheter is
removed 24-48hrs after insertion. If the patient voids successfully,
with a minimal residual volume, the TWOC is considered
successful.
Complications include Chronic urinary retention, UTIs and Renal
stones.
12. Following resolution of the retention through catheterisation,
the kidneys can often over-diurese due to the loss of their
medullary concentration gradient, which can take time to re-
equilibrate.
This over-diuresis can lead to a worsening AKI.
Consequently, those patients at risk should have their urine
output monitored over the following 24 hours post-
catheterisation.
Patients producing >200ml/hr urine output should have
around 50% of their urine output replaced with intravenous
fluids to avoid any worsening AKI.