Manual of Urodynamics

Dr.Sunil Shroff,   Dr. S.Venkat Ramanan 

Department of Urology & Renal Transplantation
Sri Ramachandra Medical College & Research Institute Porur, Chennai – 600116
www.srmcurology.com, [email protected],
Tel: 044-24761546, Fax: 044-24761540.

• Uroflowmetry and types of curves
• Terminology
• Procedure
• Overactive bladder
• Stress urinary incontinence
• Urodynamics in children
• Glossary

PRESSURES

Measuring pressure correctly

• Step 1: Setting zero Zero pressure is the surrounding atmospheric pressure
• Step 2: Calibration of transducers.
• Step 3: Establishing reference level

When external transducers are used, the reference point is the superior edge of the pubic symphysis

• Crucial that there be no air bubbles in any of the transducers or tubing

Ensuring high quality trace:

• Quality control ensured by:
1. Feasible initial pressure recording
ICS values
• Pves (cm H2O)
• Supine 10-20
• Sitting 15-40
• Standing 30-50
• Pdet 0-6 cm H20


2. Cough every minute during filling

Filling Rate
• Slow fill < 10 ml/min ("physiologic")
  Medium fill 10 to 100 ml/min
  Rapid fill > 100 ml/min
  
• Faster the bladder is filled, lower the bladder compliance and not representative physiologically
• Fluid used – saline
• Temperature of fluid – Room temperature

FILLING PHASE

Detrusor activity

• Normal activity: Detrusor quiescent during filling. End filling pressure 10 cm H2O
• Detrusor overactivity: Phasic involuntary detrusor contractions which may be spontaneous or provoked. Abnormal only when it produces symptoms

Bladder sensation

• First sensation (50% of cystometric capacity)
• Normal desire to void (75% of cystometric capacity)
• Strong desire to void (90% of cystometric capacity)
• Urgency
• Abnormal sensation

Compliance:

Defined as the change in bladder pressure for a given change in volume.

• Reduced in infection, inflammation, scarring, chronic indwelling catheter, rapid fill rate.
• High compliance in diabetes, spinal shock.

Urethral function:

• Leak/ no leak

Bladder capacity

• Cystometric capacity: Bladder capacity at end of filling when patient has normal desire to void.
• Maximum cystometric capacity: Patient feels he cannot delay voiding

VOIDNG PHASE

• Detrusor activity Normal
  Underactive
  Acontractile
  
• Urethral function
  Various Indices calculated during Urodynamics
  BCI = Bladder contractility index:
  PdetQmax+5Qmax
  
  
  
  BOOI = Bladder outlet obstruction index:
  PdetQmax-2Qmax

OVERACTIVE BLADDER (OAB)

Definitions:

Overactive bladder is a symptom complex consisting of urgency, with or without urge incontinence, usually with frequency and nocturia. There should be no proven infection or other obvious pathology.

The diagnosis of OAB requires presence of Urgency and at least one other symptom.

The other names for OAB are Urgency syndrome and Urgency-Frequency syndrome.

Urgency is a complaint of sudden compelling desire to pass urine which is difficult to defer.

Urgency incontinence is a complaint of involuntary leakage accompanied or immediately preceded by urgency.

Detrusor overactivity (DO) is the urodynamic study (UDS) finding in patients with OAB.

Limitation of OAB Terminology

• OAB - Some patients have all the Symptoms, but there are no Involuntary Detrusor Contractions on conventional cystometry
• 10-45% of individuals with unstable Detrusor contractions may be asymptomatic.
• The term OAB – Does not indicate –
  – A specific condition
  – Nor is the cause obvious
  (Ref- Eckhardt et al .Urology 2001;58:966-971)
  

Types of OAB:

“OAB wet” – OAB with urgency incontinence
“OAB dry” – OAB without urgency incontinence

Types of Detrusor Overactivity:

Idiopathic detrusor overactivity (IDO) – This is the commonest cause of Detrusor overactivity. It is the same as the earlier description of Detrusor Instability.

Neurogenic detrusor overactivity (NDO) – This is DO as a result of disturbance of nervous control mechanisms. This is the newer terminology for Detrusor Hyperreflexia. In this condition the objective evidence of neurological disorder is a must.

Few examples of NDO are Multiple Sclerosis, Cerebrovascular disease, meningomyelocoele, spinal cord trauma.

Mechanism of OAB/DO:

OAB is considered to be a premature activation of micturition reflex. In case of OAB with incontinence, the following events take place :

1) Increased bladder pressure overcomes the combined resistance of intrinsic urethral muscles and pelvic floor muscles.
2) Urethra may relax along with increased bladder pressure as part of the premature reflex.

In case of “OAB dry”, the pelvic floor musculature is effective enough to prevent the leak. It does so by increasing the outflow resistance above the bladder pressure. Increased pelvic floor activity triggers a reflex inhibition of micturition reflex. These findings are especially prominent in nulliparous women with OAB symptoms. This group of patients do not present with incontinence as they are able to prevent the leak with the help of good pelvic floor musculature.

OAB – Etiopathogenesis

Etiology of OAB is poorly understood

Altered responsiveness of the smooth muscle, nerves, and urothelium plays an important role in its pathogenesis. Causes of O.A.B

1. Idiopathic
2. Myogenic
3. Neuropathic
Examination of various models of OAB due to different etiology, reveal some common features:

1. Patchy denervation of bladder
2. Enlarged sensory neurons
3. Hypertrophic Dorsal Root Ganglion cells
4. Enhanced spinal micturition reflex

Stable Vs Unstable Detrusor

• Normal detrusor is not well coupled electrically – Normally transmission of electrical activity in a cell occurs without it spreading to adjoining muscle cell.
• Unstable bladders are well coupled allowing spread of electrical activity leading to synchronous contraction of detrusor causing tetanic contraction.
• Thus unstable bladders have better connectivity leading to propagation of uninhibited contraction.

Neuroplasticity and OAB

• Neuroplasticity means the ability of nervous system to change - transmitters, reflexes or synaptic transmission with disease , injury or any change in the environment
• Ischemia to nerves leads to neuroplasticity and leads to Detrusor hyperactivity with impaired contractility (DHIC)
• Irreversible neuronal damage causing OAB also seen with Urinary Obstruction and Ageing

Bladder Outflow Obstruction & OAB

In hypertrophied detrusor following obstruction ( BPH, Stricture , DESD) there is –

• an increase in metabolic demand with reduced blood flow to detrusor leading to anoxia and neuronal death
• There is an increase in Nerve Growth Factors (NGF) content in the detrusor muscles
• Increased NGF – leads to increase in size of efferent neurons in the pelvic plexus - causing urinary frequency
• NGF presence also leads to de-novo development of spinal micturition reflex leading to subsequent OAB.
• NGF is responsible for growth of sympathetic and sensory neurons
• With inflammation there is an increase in NGF content in bladder
• Repeated inflammatory stimuli of the bladder also leads to enlargement of bladder DRG ( dorsal root ganglion ) neurons of the spinal cord
• Relief of obstruction can lead to reversal of these neural changes

Association of Depression, Anxiety, Attention Defect Disorder and OAB

• These conditions lead to disturbance in brain circuits using serotonin (5-HT) neurotransmitter.
• 5-HT function is diminished in these conditions, causing low volume threshold for voiding with unstable bladder contractions.
• Reduced 5-HT neurotransmission in the CNS enhances bladder activity.

Females Vs Males & OAB

• OAB more common in females than males.
• Males have 52% higher rate of synthesis of 5-HT as compared to females.
• Women may be predisposed to both OAB and depression in part because levels of 5-HT in the brain are substantially lower in women than in men.

Urodynamics in overactive bladder:

Detrusor overactivity is said to be present if the UDS shows the finding of involuntary phasic detrusor contraction, producing a rise and fall in Pdet during filling phase.

It can occur either spontaneously or on provocation (Provocative measures –
rapid filling, coughing, postural change, hand washing etc.)

A typical patient with Urgency urinary incontinence has been shown to have Detrusor overactivity in 2/3rd of cases. However if Ambulatory urodynamics (AUDS) is performed almost all patients will be found to have DO. Hence patients with typical symptoms of OAB are treated conservatively first.

Indications for UDS in OAB:

(1) Urodynamics is indicated only if the conservative treatment fails after a trial for 6-8 weeks and further invasive or surgical management is contemplated.

(2) UDS is also done in research settings (eg- trials of new drugs)
DO was previously diagnosed only if Pdet increased by greater than 15cmH2O during filling phase. However, the ICS standardization committee makes it clear that any phasic contraction with rise and fall in Pdet is diagnostic of DO. The ICS definition does not specify a minimum change in Pdet , although waves of an amplitude less than 5cmH2O are difficult to detect.

Detrusor overactivity diagnosed by Urodynamics is not always clinically significant. Indeed most of us will have an occasional DO which will be asymptomatic or may be felt as the normal desire to void.

A clinically significant DO is one that produces troublesome symptom which mimics the urgency noticed in everyday life.

There are various patterns of detrusor overactivity. Two important patterns are:

Phasic DO: characteristic phasic wave form which may or may not lead to urinary incontinence.

Terminal DO: single, involuntary detrusor contraction, occurring at cystometric capacity, which cannot be suppressed and results in incontinence or bladder emptying.

“OAB dry”: This is usually common in men and nulliparous women who present with irritative voiding symptoms without incontinence. This condition is also called “Frequency-Urgency syndrome”. It needs to be differentiated from bladder hypersensitivity and painful bladder syndrome.

Bladder Hypersensitivity: It is a urodynamic diagnosis. These patients have increased bladder sensations with early first sensation and first desire. The desire to void persists from first desire quickly to normal desire and strong desire without a break. (In normal individuals, there is absence of sensations between first sensation and desire to void). The usual bladder capacity is less than 250ml.

In patients with this UDS finding, the bladder diary reveals a larger volume voided in early morning sample and volumes during the day are consistently below 250ml.

Painful bladder syndrome: In this condition, patients complain of suprapubic pain related to bladder filling. This is accompanied by increased daytime and night time frequency. Patients with this complaint require further evaluation with urine microscopy, urine cytology and cystoscopy.

Inappropriate Urethral relaxation Incontinence:

This is a very rare and unusual cause for incontinence. Here incontinence occurs without detrusor contraction. It is due to sudden urethral relaxation during filling phase. It leads to a flooding incontinence without any prior warning, such as a feeling of urgency. This condition was previously termed as “Unstable Urethra.”

Management of Overactive bladder :

The initial management of OAB consists of simple conservative measures like fluid restriction to less than 2.5 liters per day, avoidance of excessive caffeine containing fluids (like coffee, tea, coke etc.). Bladder retraining and pelvic floor exercises also help.

Drugs which are useful in OAB are anticholinergics such as Oxybutinin, Tolterodine, Solifenacin.

If these measures fail after a trial for 6-8 weeks, Urodynamics is done to provide an objective diagnosis of OAB. Further management consists of Botulinum toxin injection in bladder. The final surgical management in intractable cases consists of Augmentation or substitution cystoplasty.