Andrew Robb1 / Holly Weaver and Nikesh Thiruchelvam2, 3, 4, 5, 6 / Suzanne Biers3
Urological emergencies in childhood are common. In this chapter we discuss a number of the more common emergencies encountered.
Acute scrotum in childhood
Defined as an acute onset of painful swelling of the scrotum or its contents. It is the commonest urological emergency encountered in children. The causes of an acute scrotum are listed in Box 6.1. Irreversible damage to the testicle can be observed after 4 hours of ischaemia; therefore, testicular torsion and incarcerated inguinal hernia must be rapidly identified and treated.
Box 6.1 Differential diagnosis of the acute scrotum in children.
•Idiopathic scrotal oedema.
•Incarcerated inguinal hernia.
Although testicular torsion has a bimodal incidence it may present at any time in childhood. The peak incidence occurs during:
•The perinatal period (neonatal torsion).
Testicular torsion often presents in a manner similar to that in adults (see page 69). In children it can also have an atypical presentation, with the child complaining of abdominal or loin pain. Abdominal examination in all paediatric patients should include examination of the external genitalia for this reason.
The use of ultrasonography is controversial. It may be helpful in establishing or excluding a diagnosis in difficult cases. However, it may cause undue delay in getting a patient to theatre for treatment of the torsion.
Treatment is emergency scrotal exploration (see also page 71). A midline (median raphe) incision or transverse scrotal incision may be employed. The tunica vaginalis (sac of tissue around the testis) is opened to expose the affected testicle. If a testicular torsion is identified, it should be untwisted and left for several minutes in a warm saline-soaked gauze and reassessed for viability. For proven cases of torsion, both testes should be fixed (bilateral orchidopexy) to prevent further episodes of torsion (and ischaemia) on either the affected side or the contralateral ‘normal’ side. The contralateral testis may be particularly susceptible to torsion due to cord insertion in the interpolar region of the testis leading to a ‘bell-clapper’ configuration. If the testis is no longer viable due to prolonged torsion, removal of the testis is required (orchidectomy), along with fixation of the other testis. Manual attempts to try to untwist the testis directly through the scrotal skin (scrotal detorsion) has no role in the management of testicular torsion.
Neonatal testicular torsion
In this clinical scenario, the torsion event happens before or around the time of birth. The presentation will depend on the time before birth that the torsion occurred:
•Prolonged period before birth: the infant may be born with an absent testis, and should be managed as a patient with an impalpable testis.
•Weeks before birth: the infant may present with a regular, firm, painless mass that is smaller than the normal contralateral testis. The mass is attached to the scrotal wall and there is no evidence of acute inflammation.
•Days or hours before birth: a painful enlarged testis with overlying inflammatory changes in the scrotal wall is seen.
•If the torsion occurs after birth, the scrotum will appear normal on initial inspection, but acute inflammatory signs will develop later.
Management is controversial. Some surgeons explore all neonates with evidence of torsion; others manage all patients conservatively except for neonates who present with acute symptoms after birth. The option of a contralateral orchidopexy should be discussed with the parents.
Torted testicular appendage
This is the commonest reason for scrotal exploration in childhood, particularly in pre-pubertal boys. The testicular appendage (also known as the hydatid of Morgagni) is a small tissue remnant found at the superior pole of the testis in most males. It is often pedunculated and therefore prone to torsion. If it twists it causes oedema and venous congestion, leading to ischaemia and infarction of the appendage, which manifests as pain.
On clinical examination, a blue spot (Figure 4.2, page 72) may be visible through the scrotum (in around a third of cases), and the clinician may be able to elicit point tenderness over the upper pole of the testis.
It is a self-limiting condition with resolution of symptoms typically after 3–5 days. It can therefore be managed conservatively with rest and analgesia. Alternatively, scrotal exploration can be performed with immediate resolution of symptoms.
Epididymitis or orchitis can occur in both pre- and post-pubertal boys. Presentation is similar to that seen in adults. A urine dipstick should be performed and urine culture sent. Doppler ultrasound may reveal an enlarged testis with increased blood flow to the epididymis or testicle compared to the contralateral side.
If any doubt regarding the diagnosis exists, scrotal exploration is mandatory. Following diagnosis, treatment is with appropriate antibiotics.
Scrotal trauma is relatively common in boys and may be caused by a direct blow or a straddle injury. Trauma may precipitate testicular torsion, so it is important not to overlook this diagnosis.
Assessment by ultrasonography may demonstrate the presence of haematoma or testicular rupture. A haematoma can be managed conservatively, whilst a ruptured testicle should be repaired.
Idiopathic scrotal oedema
Idiopathic scrotal oedema is a condition seen in pre-pubertal males. The peak incidence occurs between 5 and 6 years of age. As the name suggests, the cause is unknown. It is characterised by swelling of the scrotum and redness (Figure 6.1). This may occur unilaterally or bilaterally, and it may extend upward into the inguinal region or to the perineum (often seen as a red inverted triangle in the perineum). Importantly the testes themselves are not tender on examination.
Figure 6.1 Idiopathic scrotal oedema.
The condition resolves spontaneously, often within 24–48 hours. No specific treatment is required. Antihistamines or antibiotics are sometimes prescribed, but there is no good evidence to support their use.
Henoch–Schönlein purpura (HSP)
This is an acute immunoglobulin-A (IgA)-mediated vasculitis that presents with a typical rash on the legs. Involvement of the scrotum and testis in HSP is a well-documented complication. It gives rise to acute tenderness, swelling and scrotal discolouration. Scrotal exploration is not required.
Penile and foreskin problems in children
Complications following circumcision are common, and include:
•Bleeding. Initially, circumferential pressure around the penis should be applied. If this fails then exploration and revision of circumcision under general anaesthesia (GA) is needed. The patient should also be investigated for a bleeding diathesis.
•Retained PlastiBell® (plastic device used for neonatal circumcision). This may require a short GA to remove the retained device.
•Glans trauma. This should be referred to a paediatric urologist for further management, as it may require specialist repair under GA.
•Excess skin removed. This should be referred to a paediatric urologist for further management, as it may need formal reconstruction.
Paraphimosis is caused by the foreskin being retracted and cannot then return to its normal position (Figure 6.2). It can result in injury or necrosis of the foreskin (and the glans). It may present with pain or acute urinary obstruction. The diagnosis should be obvious on examination.
Figure 6.2 Paraphimosis.
The foreskin should be reduced as soon as possible. Manual reduction is achieved by reducing the oedema from the foreskin. It is then replaced by using the thumbs to push down on the glans while the other fingers pull the foreskin forwards into its anatomical position. Adequate analgesia should be given prior to reduction.
It may be necessary to perform this under GA in children. If manual reduction under GA fails, then a dorsal slit can be employed. Although it is an option in an adult patient, circumcision should not be performed in the acute setting if possible due to the high complication rate.
Voiding problems in children
Urinary retention in childhood is uncommon. There are a large number of causes (Box 6.2). Urinary retention should be looked at as a symptom that requires identification of the underlying cause. Dependent on the aetiology, urinary retention may be painful or painless.
Box 6.2 Causes of urinary retention in childhood.
•Urinary tract infection (UTI).
•Balanitis xerotica obliterans.
•Bladder outlet obstruction.
Assessment includes a full history, full physical examination including neurological examination, assessment of the spine and sacrum, and examination of external genitalia. A rectal examination should also be considered where clinically appropriate, preferably after paediatric urology review, and deferred where possible to be performed under GA if the child is also having a cystoscopy or other intervention.
Treatment involves ensuring adequate drainage of the bladder and treating the underlying cause of the retention. Options for achieving drainage of the bladder include:
•Getting the child to relax (playing in the bath is a good strategy).
•Benzodiazepines may help.
Balanitis xerotica obliterans (BXO) is a benign, scarring condition that can affect the foreskin, glans of the penis and urethra (Figure 6.3). Most commonly it causes a pathological phimosis (tightening) of the foreskin, but it can also cause narrowing of the external urethral meatus and urethral strictures. If BXO is identified as the cause of urinary retention, then an emergency circumcision is required (with further treatment of any associated meatal stenosis or urethral stricture disease if identified).
Figure 6.3 Balanitis xerotica obliterans as a cause of acute urinary retention.
In all cases of urinary retention the case should be discussed with a specialist paediatric urologist.
•Testicular torsion in children can have an atypical presentation, necessitating examination of genitalia in all paediatric patients with abdominal pain.
•Procedures in children may require general anaesthesia.
•Urinary retention in childhood requires specialist paediatric urology input.
Although pregnant women may seek medical attention for a range of pregnancy-related problems, they can still be affected by the full range of urological diseases that may affect them in their non-pregnant state. Several important factors must be taken into consideration when approaching urological disease in the pregnant woman. Firstly, awareness of the stage of pregnancy and ongoing dialogue with the obstetric team are crucial. This is particularly pertinent when deciding management options, to ensure medical treatments and surgical interventions are safe in pregnancy. This also means the range of investigations and management options are limited compared to the non-pregnant patient, as the well-being of the fetus is paramount. Secondly, interpretation of investigation results must be done with the knowledge of the physiological and anatomical changes affecting the urinary system in pregnancy, to best inform management decisions (Box 6.3). Of particular note, there is progressive dilatation of the renal collecting system known as a physiological hydronephrosis. This is classically more pronounced on the right side than the left (Figure 6.4), which can make the diagnosis of new pathological hydronephrosis difficult to identify.
Pyelonephritis in pregnancy
Pyelonephritis occurs in up to 1 in every 50 pregnancies with recognised obstetric complications including pre-term labour, pre-eclampsia and low birth weight. The prevalence of asymptomatic bacteriuria is comparable with the non-pregnant population, but more pregnant women go on to develop symptoms and upper UTI (pyelonephitis), due to a dilated collecting system and urinary stasis promoting bacterial growth. Women should be screened for asymptomatic bacteriuria frequently in pregnancy, and treated where positive. They should also be treated quickly and effectively if pyelonephritis is suspected. The physiological changes of pregnancy can mask signs of sepsis, and as pregnant women can deteriorate very rapidly, any delay in treatment may have harmful consequences.
Box 6.3 Changes to the urinary system in pregnancy.
•Kidneys enlarge due to increased intravascular volume.
•Dilatation of the renal pelvis (physiological hydronephrosis) and hydroureter due to hormonal muscle relaxants and pressure from the gravid uterus.
•Glomerular filtration rate increases by up to half, so urea and creatinine levels will be lower than the reference range for the non-pregnant woman.
•Bladder tone decreases and capacity increases.
•With uterine growth, urinary frequency, urgency, nocturia and incontinence become more common.
Figure 6.4 Physiological hydronephrosis of pregnancy. T2-weighted magnetic resonance imaging with sagittal view (a) showing a right-sided hydronephrosis and hydroureter due to compression of the ureter at the pelvic brim as a result of the gravid uterus (arrow). Axial images also show the right hydronephrosis and dilated upper ureter (b) and dilated right ureter below the kidney (c).
•Stage of pregnancy with an up-to-date obstetric history.
•Onset and nature of symptoms: loin tenderness, dysuria, fever.
•Screen for obstetric complications: discharge or bleeding per vagina.
Depending on the stage of pregnancy, the gravid uterus may make examination more difficult, but a thorough examination is still important, particularly to elicit any flank tenderness.
Ensure appropriate obstetric support for the antenatal mother and fetal checks.
•Bloods: as for non-pregnant cases of suspected pyelonephritis, taking into account the physiological change in blood result parameters (creatinine and urea lower due to a higher GFR).
•Urine dip and culture.
•Imaging: an ultrasound scan of the kidneys, ureters, bladder (USS KUB) can be performed, but interpretation needs to account for the physiological hydronephrosis of pregnancy. Computed tomography (CT) is avoided due to the radiation exposure risk to the fetus.
•Aggressive intravenous (IV) fluid resuscitation.
•Timely and safe IV antibiotics after cultures are taken. Discuss with both the obstetric team and microbiology to use an effective antibiotic that is safe for the stage of pregnancy and/or consult your national drug formulary. Empirical antibiotics are started until the urine culture results are known.
•Ongoing assessment and management of both the mother and the fetal parameters are needed throughout with obstetric input.
•Once the infection is controlled (i.e. temperature and other observations have settled with IV antibiotics), the patient should complete a prolonged course of oral antibiotics (typically to complete a total of 10 days therapy), guided by the urine cultures.
•For the duration of the pregnancy, a repeat urine dipstick and/or cultures should be regularly checked at antenatal visits.
Acute kidney injury in pregnancy
Causes of acute kidney injury (AKI) in pregnancy can be classified as pre-renal, intrinsic or post-renal in origin, as for the non-pregnant population (Box 6.4). However, assessment and management must take into consideration causes specific to pregnancy, such as the glomerular injury of pre-eclampsia, or the hypovolaemic state induced by obstetric haemorrhage. It is also important to remember the adjusted reference ranges for laboratory values in the pregnant population, whereby what is a slightly elevated creatinine or urea for the non-pregnant state, may actually indicate a significant deterioration in renal function in pregnancy.
•An up-to-date obstetric history, including any history of pre-eclampsia or hypertensive disorders in previous pregnancies.
•Any new symptoms, vomiting or hyperemesis gravidarum or other causes of volume depletion.
Box 6.4 Causes of AKI specific to pregnancy.
•Pre-renal: intravascular volume depletion secondary to haemorrhage, sepsis or vomiting.
•Intrinsic: pre-eclampsia, HELLP* syndrome.
•Post-renal: any cause of urinary tract obstruction in single kidney function or affecting urinary tracts bilaterally if normal function.
*HELLP (H, haemolysis; EL, elevated liver enzymes; LP, low platelets) syndrome is a life-threatening emergency encountered in the later stages of pregnancy, and considered a variant of pre-eclampsia. Common presentations include headache, nausea and vomiting, abdominal tenderness, and it is commonly associated with hypertension and proteinuria.
•Assess for evidence of bleeding (obstetric or otherwise) as part of the initial fluid balance assessment that could cause hypovolaemia.
•Any signs of sepsis causing intravascular fluid depletion.
•Consider pre-eclampsia as a cause of renal dysfunction: should be suspected in any hypertensive state in pregnancy and diagnosis usually involves evidence of proteinuria; may also see pitting, non-dependent oedema.
•Bloods: note the importance of adjusted normal parameters in pregnancy; the reference range for creatinine and urea is lower than in the non-pregnant state, especially in the first trimester, so be careful not to overlook clinically significant rises.
•Imaging: USS KUB can be performed, but interpretation needs to account for the physiological hydronephrosis of pregnancy.
•Urine dipstick (look for proteinuria as well as evidence of infection).
Urolithiasis in pregnancy
The formation of calculi in the urinary tract (or urolithiasis) is a common cause for hospital admissions in pregnancy, with most presenting in the second or third trimesters. Overall, the incidence of renal colic is reported to be the same in pregnant and non-pregnant women; however, there are several factors that can contribute to stone formation in pregnancy including hypercalciuria and an increased excretion of urinary citrate (which is normally protective against stone formation). Most patients will present with flank pain. Other possible differential diagnoses also need to be checked and excluded, including pyelonephritis, appendicitis and placental complications. Stones are associated with an increased risk of pre-term labour.
•Stage of pregnancy with an up-to-date obstetric history.
•Onset and nature of symptoms.
•Fevers or rigors.
•Evidence of UTI/infection.
•Surgical history: remember other surgical emergencies like appendicitis can present atypically in pregnancy.
•Personal or family history of ureteric calculi.
•Abdominal exam: renal angle tenderness; check whether abdominal distension is consistent with stage of pregnancy, with obstetric input to assess mother and fetal well-being.
•Close monitoring of observations for haemodynamic instability and temperature.
•Urinalysis and culture.
•Bloods including full blood count (FBC), C-reactive protein (CRP), renal function. Note that biochemistry reference ranges can be altered in pregnancy.
•Septic screen if febrile, hypotensive or tachycardic.
•Imaging: first-line imaging is USS. It will be able to demonstrate a non-physiological hydronephrosis and can provide a safe modality to monitor the clinical situation. It can also identify the presence of ureteric jets (if there is concern regarding an obstructed renal system). USS has a poor sensitivity for ureteric stones, but it avoids the risks of teratogenicity and childhood malignancy associated with CT.
•Any other imaging needs discussion with radiology, urology, obstetrics and the patient. Options for second-line imaging may include magnetic resonance imaging without contrast. Low-dose CT has a high sensitivity and specificity for stones, but is best avoided due to radiation exposure risk, as is single-shot intravenous pyelography.
•Multi-disciplinary approach: needs ongoing discussion with obstetrics in light of potential complications and the need for intervention.
•Conservative management is the preferred first-line option with a trial of spontaneous stone passage with hydration and analgesia. Spontaneous stone passage is encouraged by ureteric smooth muscle relaxation due to higher progesterone levels. Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided in pregnancy.
•Intervention is indicated if there is evidence of:
›Sepsis (fever, infection).
›Renal insufficiency, bilateral obstruction, or problems in a solitary kidney.
›Obstetric complications relating to the stone.
›Refractory pain, nausea and vomiting and a large stone.
Temporary drainage versus definitive treatment
•Urgent temporary drainage is indicated if fever and infection are associated with a ureteric stone (indicating an infected, obstructed system). This can be achieved with ureteric stent insertion in theatre or ultrasound-guided nephrostomy insertion.
•Ureteric stent placement demands ongoing management through pregnancy due to accelerated rates of encrustation due to hypercalciuria, and thus requires replacement every 4–6 weeks. The same applies for nephrostomy insertion.
•Intervention with ureteroscopy and removal of the stone with a basket or laser fragmentation. This avoids the need for regular stent exchanges but can be challenging.
Often it is difficult to make an accurate diagnosis because of the inability to use ionising radiation. As such, it is acceptable to offer nephrostomy drainage or ureteric stenting without a definite diagnosis of a ureteric stone until pregnancy is complete.
•Asymptomatic bacteriuria should be tested for during pregnancy and treated.
•Before administering antibiotics check your national formulary for which drugs are safe in the different trimesters of pregnancy.
•Biochemical reference ranges are altered in pregnancy, with the GFR increased and creatinine and urea values lower compared to non-pregnant women.
•Beware of patients with hypertension and proteinuria – involve obstetrics early.
•USS is the safest imaging modality in pregnancy but has a limited ability to diagnose a ureteric stone.
•Ureteric stents and nephrostomies in pregnancy require regular exchanges as they are at higher risk of encrustation (and blockage).
This describes dysfunction of the urinary bladder due to disease of the central or peripheral nervous system involved in the control of micturition.
Micturition depends on the integration of neuronal pathways between the cerebral cortex, brainstem and sacral spinal cord. Therefore, causes of a neurogenic bladder encompass both traumatic and atraumatic insults at varying levels, including the cerebral cortex and spinal cord. Those that affect the spinal cord above the sacral level produce an upper motor neuron pattern of injury. Insults at the level of the sacrum and lower result in a lower motor neuron deficit.
When evaluating the effect of a spinal cord injury (SCI) on bladder function, consider the level affected, as this alters the clinical presentation and will guide bladder management (Table 6.1). This is particularly important in supra-sacral spinal cord level injuries where urgent intervention may be required for a high-pressure urinary tract in order to protect renal function. The primary concern for long-term management of the neurogenic bladder is to preserve kidney function, and secondarily, to treat symptomatic lower urinary tract symptoms.
Note that patients with complete or partial SCI at the same level can present differently. Also, patients can have defects at multiple levels (such as in multiple sclerosis), and clinical presentation may be variable.
Level of lesion
Example of neurological problem
Effect on the urinary tract
Parkinson’s disease, stroke, MS, tumours, dementia
(Safe, low-pressure bladder)
Supra-sacral spinal cord (between the pons and L5 level)
SCI, spina bifida, disc prolapse (upper motor neuron pattern of injury)
Overactive bladder/detrusor hyperreflexia
Stiffer bladder (poor compliance)
(Dangerous bladder; high pressure, risk to kidneys)
Conus (sacral spinal cord from S1 to S5 or peripheral nerves)
Cauda equina, SCI, peripheral neuropathy (including causes such as diabetes)
(lower motor neuron pattern of injury)
Underactive bladder (urinary retention)
Weak external urethral sphincter (causing incontinence)
(Safe, low-pressure bladder)
DSD: detrusor sphincter dyssynergia; MS: multiple sclerosis; SCI: spinal cord injury.
Urological emergencies that may present to the emergency department in patients with underlying neurological causes include the following as outlined below.
This is a significant acute medical emergency characterised by severe uncontrolled peripheral hypertension, which can occur in patients with SCI at or above the level of the 6th thoracic vertebrae (T6). A significant sensory stimulus entering the spinal cord via intact peripheral nerves induces a large sympathetic output from thoracolumbar sympathetic nerves, resulting in widespread vasoconstriction (particularly splanchnic vascular bed). Due to the level of injury, descending inhibitory impulses are unable to exert an effect at sympathetic outflow sites, and compensatory increased parasympathetic vagal cardiac input (bradycardia) is inadequate, thereby uncontrolled peripheral arterial hypertension ensues.
The stimulus is usually bladder or bowel in origin. Urological triggers include bladder distension (Figure 6.5), urinary tract calculus, urological intervention (such as catheterisation or cystoscopy) and UTI.
Figure 6.5 Axial pelvic CT image of a high-pressure ‘unsafe’ neuropathic bladder. Note multiple bladder diverticulae, a thickened bladder wall and bilaterally dilated distal ureters. These appearances are sometimes referred to as a ‘fir-tree’ or ‘pine cone’ bladder.
Complications of stroke, seizure, cardiac complications and death can occur if autonomic dysreflexia is left unresolved.
A high index of suspicion is required and you should look out for the following features:
›Profuse sweating around the face and neck.
›Rise in systolic and diastolic blood pressure (BP) above baseline (note BP baseline is often low in spinal cord injury).
›Skin changes above the level of the lesion = parasympathetic responses: flushing and sweating.
›Skin changes below the level of the lesion = sympathetic responses: pale, cool skin with piloerection.
•Sit the patient upright (and loosen tight clothing or belts).
•Examine for a distended bladder and treat.
•If a catheter is present, ensure it is draining. If it is blocked, change the catheter.
•Perform a rectal exam to exclude faecal impaction as a cause.
•Ensure BP is monitored; a short-acting antihypertensive may be indicated for BP control, but this will not resolve a hypertensive crisis if the underlying stimulus is not removed.
This is caused by compression on the spinal roots. It can be due to benign causes such as lumbar disc rupture, spinal infection, spinal fracture, spinal haematoma, spinal canal stenosis, blunt and penetrating spinal trauma or arteriovenous malformation. Malignant causes include spinal cord tumours or metastases – this is covered in full on pages 125–126. Patients present acutely with lower back pain, lower limb weakness and numbness, and sudden-onset bladder, bowel and sexual dysfunction. An emergency magnetic resonance imaging (MRI) of the spine is required. If the diagnosis is confirmed, steroids and decompressive surgery to relieve pressure on the nerves is required urgently, under the care of spinal or neurological surgeons. Antibiotics are given for any infective processes.
Acute spinal cord injury
This can be caused by blunt or penetrating trauma resulting in injury to the spinal vertebrae, discs or ligaments of the vertebral column or to the spinal cord directly, and can be complicated by haematoma. Injuries can be complete or incomplete, and the manifestations on the urinary tract will depend on the level of the injury and nerves directly affected (motor, sensory and autonomic nerves can be involved).
Spinal shock is the sudden loss of spinal reflex activity below the level of the SCI. This causes passive bladder filling and subsequent overflow incontinence. The duration of this areflexia depends on the level of the lesion. It may last weeks, particularly if the injury affects sacral segments causing a sacral areflexia, typified by flaccid paraplegia, reduced anal tone and loss of sensation in the sacral dermatomes. Awareness of this can allow prompt catheter insertion that will form the basis of acute management.
An urethral indwelling catheter should be inserted immediately for the acute phase of resuscitation and to mitigate the problem of passive bladder filling causing distension in spinal shock. Care should be taken to prevent traction on the catheter with placement of a catheter restrainer. Once the spinal injury is stable, aim for removal of the indwelling catheter and start clean intermittent self-catheterisation (CISC) if required. A suprapubic catheter can be used when patients cannot perform CISC.
Assessment of other general problems relating to the urinary tract in neuropathic patients
•Clarify the underlying neurological disorder or injury and at what level the spinal cord is affected.
•How does the condition affect other organs (e.g. bowel incontinence, sexual dysfunction, mobility, manual dexterity)?
•Is the neurological problem stable or progressive?
›Stable – SCI, spina bifida.
›Progressive – stroke, multiple sclerosis, Parkinson’s disease.
•Any previous urinary tract surgery? (Patients with long-term conditions such as spina bifida may have had several operations already for bladder problems or incontinence).
•Is there new disruption to storage and/or emptying of the bladder?
•Drug and treatment history – is the patient on any drugs that might affect their bladder function (i.e. anticholinergic medication is used for an overactive bladder, but has a risk of urinary retention)?
•Inspection – the patient may have scars from previous neurological surgery relating to their neurological problems or complications associated with their condition which they may not have told you about (ventriculoperitoneal shunt, Mitrofanoff, colostomy).
•Standard examination of the abdomen, perineum with vaginal or rectal examination, assessing for a palpable bladder, prolapse, an enlarged or suspicious prostate.
•Neurological assessment, including assessment of the lower limbs, back and rectal examination to establish if there is normal peri-anal sensation and anal tone (where clinically appropriate). Be vigilant for signs of an undiagnosed neurological disorder (i.e. sacral agenesis, spina bifida occulta).
•Urinalysis and culture: to assess for infection. Proteinuria and haematuria may also be an indicator of renal impairment, and requires further assessment.
•Bloods, including urea and creatinine for renal function testing.
•USS KUB to assess for any evidence of upper tract obstruction and to assess if the bladder empties adequately. If patients have high-pressure bladders or if they retain urine (chronic retention) they are at risk of upper tract dilatation and renal deterioration.
•Appropriate neurological imaging dependent on first or recurrent presentation of neurological sequelae. If the patient presents acutely with new-onset lower limb weakness and urinary retention, an MRI of the spine is required to rule out spinal cord or cauda equina compression or injury.
•Urodynamic studies may be offered in the outpatient setting.
Treatment decisions will depend on neurological aetiology, whether the neurological disorder is stable or progressive, its effect on associated organ function and the individual patient’s wishes. The main aims to achieve are outlined below.
Protection of the upper renal tracts:
•Overactive bladder – reduce pressure in the bladder by CISC. Alternative interventions include:
›Bladder augmentation – using a bowel patch to relieve the pressure build up, e.g. clam ileocystoplasty.
›Disruption of micturition reflex arc – via dorsal rhizotomy (dorsal sacral nerve roots surgically divided) with implantation of a sacral root stimulator.
›Botulinum toxin (botox) – injected intravesically to relax the muscle of the bladder, which increases its capacity and lowers its pressure.
›Sacral root neuromodulation – achieved via implantation of an S3 sacral root stimulator.
›Urinary diversion – formation of an ileal conduit for refractory cases.
•Chronic retention – may require a catheter (often suprapubic) if urodynamic studies reveal a high-pressure bladder. CISC is preferable to an indwelling catheter if the patient has appropriate manual dexterity and cognitive function, as there is a lower risk of UTI.
•Detrusor sphincter dyssynergia (DSD) – this is discoordinated synchronous contraction of both the bladder and urethral sphincter at the same time, which causes problems passing urine and can lead to high pressures in the bladder (which can be transmitted to the upper tracts). This can be treated with regular CISC or the use of catheters, injection of botox into the external sphincter, surgical division of the external sphincter or sacral nerve neuromodulation.
Management of stress incontinence (i.e. due to sphincter weakness).
Conservative management options include an indwelling catheter or using a condom sheath drainage device, e.g. Conveen®, in males. Surgical management in women includes: urethral bulking agents, midurethral tapes, pubovaginal slings and colposuspension. Insertion of an artificial urinary sphincter can be offered to both women and men. Bladder neck closure can be performed in intractable cases, but will require formation of a catheterisable continent channel (such as a Mitrofanoff) to drain the bladder via an alternative route. Finally, urinary diversion with an ileal conduit could be considered.
Prevention of recurrent lower urinary tract infections
Address any chronic retention, and treat any reversible causes for UTIs. Prophylactic low-dose antibiotics are sometimes considered (see page 63).
•Be aware of the risk of autonomic dysreflexia in spinal cord injuries at or above T6 and treat triggers such as a distended bladder quickly.
•Cauda equina compression manifests with urinary retention along with back pain and lower limb weakness, and needs an urgent MRI, steroids and spinal decompression surgery.
•After spinal cord injury, there is a period of spinal shock that can cause bladder dysfunction – so catheterise the bladder in the early stages.
•In cases of neurogenic bladder, protection of the upper urinary tracts is a priority, whilst minimising infection risk