High Pressure Chronic Retention

Definitions in Urine Retention

Following definitions can be used to categories urinary retention derived from the Oxford Handbook of Urology

Acute Urine Retention AUR:

Painful inability to void, with a bladder volume between 500-800ml.

Chronic Urine Retention CUR:

Maintenance of voiding function with usually no perceived difficulty in voiding, with high bladder volumes post micturition.

Mitchell 1984 defined the volume threshold for chronic retention as a residual volume greater than the normal bladder capacity, for which 500ml can be an easy and simple number/ threshold to remember.

AUA guidelines define CUR as “elevated PVR of >300 mL that has persisted for at least six months documented on two or more separate occasions”.

National Prostatectomy Audit UK also defined chronic retention as PVR >300ml

Acute on Chronic Retention:

Painful inability to void with volume greater than 800ml.

High Pressure Chronic Retention:

N George & O’Rielly in their original paper titled ‘High Pressure Chronic Retention’ in 1983 credit Mitchell 1972 for identifying the 2 types of chronic retention. In their paper they describe it as “High pressure chronic retention is characterised by late onset enuresis, a tense, palpable bladder, hypertension, and progressive renal impairment associated with bilateral hydronephrosis and hydroureter commonly leading to uraemia and death.”

OHOU defines it as: Bladder volume >800ml with intravesical pressure >30cm H2O accompanied by hydronephrosis. (Why >30cm H2O ? Not sure, but Abrams 1978 in their paper on UDS in chronic retention set the pressure threshold for HPCR at >25cm H2O)

In clinical practise, chronic urinary retention with high intra-vesical pressures causing upper tract deterioration or renal impairment in the absence of any other cause suggests HPCR.

Low Pressure Chronic Retention:

High residual bladder volumes (>300-500ml) without high intravesical pressures, and no hydronephrosis or renal impairment.

Safe PVR

The following are suggested as safe PVRs with low risk of future complications

Men <350ml (quoted from OHOU, ATLESS Study 2006 n= ~1500 reports 2% risk of progression in men with PVR ≥ 350)

Women <150ml (implied from OHOU)

AUA defines chronic retention or raised PCR into High Risk as Low Risk categories and asymptomatic patient’s with no High risk features can be considered for monitoring/ surveillance.

AUA High Risk features in Chronic Retention/ High PVR:

Urine Infections/ Urosepsis

CKD3 or above

Upper tract deterioration on scans

Urine incontinence associated with dependent skin changes or ulcers

OHOU 5th Edition also suggests similar approach in asymptomatic patients without hydronephrosis or renal impairment.

OHOU suggests following as part of surveillance for LPCR:

Monitor renal function (creatinine/ eGFR)

Monitor postvoid residual volumes PVR

Renal USS

Consider TURP

Etiology of HPCR

As the name suggests, High Pressure Chronic Retention refers to Chronic Urinary Retention with high intravesical pressures causing upper tract dilation and/or renal impairment.

Causes of HPCR:

BPH (most common)

Prostate Cancer

Urethral stricture disease

Other causes (such as neuropathic bladders, small capacity non-compliant post radiotherapy bladders)

Red flag signs:

Nocturnal Enuresis

PVR >1L

Typically the residual volumes of >1L are suggested to be a risk factor for developing HPCR.

We also see high pressure retention with upper tract deterioration in patients with neuropathic bladders and also in patient with previous pelvic radiotherapy presenting with small volume non-compliant bladders. These patients understandably do not have the typical >1L residuals.

In contrast the other entity is the Low Pressure Chronic Retention in which you get high residuals volumes (usually <1L) with no upper tract deterioration or renal impairment.

Association between LPCR & HPCR

There is debate regarding the association between LPCR & HPCR.

What we know about progression of BOO/BPH:

In early phases of bladder outflow obstruction, bladder muscle hypertrophies to compensate for this obstruction. This is visible on scans as well as on cytoscopic evaluation of the bladder. Trabeculations are considered an early signs, whereas diverticulae are considered a late sign of this process. Similarly, overactive bladder symptoms (Urgency & Frequency) are considered an early signs of bladder hypertrophy and consequent overactivity secondary to BOO while still being able to maintain good voiding function due to the compensatory hypertrophy, whereas voiding LUTS (such as poor stream, hesitancy and straining) are considered late signs where hypertrophied bladder is unable to overcome the BOO and voiding starts getting effected.

Theory 1: Low pressure as sequel to high pressure retention:

This theory suggests that the hypertrophied bladder generates the high intravesical pressures that cause upper tract deterioration. And that over time the detrusor muscle fails and becomes atonic and thin walled leading to a low pressure system.

However in clinical practice, we do see patients with very large thin walled bladders (volume of >3L) presenting with HPCR and upper tract deterioration.

Theory 2: Low pressure as a prequel high pressure:

This theory is the opposite and is based on the observation that low pressure bladders generally have a low PVR (usually <1L). This suggests that initially a bladder is low pressure however, overtime with chronic BOO, bladder volumes gradually and progressively increase, this leads to decompensation and loss of compliance with resultant upper tract deterioration.

This is similar to the much more well studies cardiac muscle, which hypertrophies in early phases of cardiac outflow disease (such as aortic stenosis, or chronic untreated hypertension), whereas eventually decompensation happen in the form of dilated cardiomyopathy and left ventricular heart failure and back pressure causing pulmonary hypertension.

Theory 3: Low Pressure and High Pressure as separate entities:

George and O’Riely in their paper HPCR in 1983 suggested that perhaps low pressure and high pressure are separate entities altogether.

This is less plausible, as HPCR patients with bladder volumes as high as 3-4 litres surely did not develop those high volumes suddenly. And if this developed gradually, then at some point during this progression they decompensated (from Low pressure to High pressure) and started having renal impairment. If they were alway high pressure, then they would have presented much earlier with renal failure rather than taking time to reach volumes >3L and then presenting with renal impairment.

It is plausible that some patients decompensate earlier then others and that explains the wide variability observed in the bladder volumes of patients presenting with HPCR and renal impairment.

Conclusion on relationship between LPCR & HPCR:

There is no consensus on the relationship of LPCR & HPCR.

I personally feel like low pressure is a prequel to high pressure and there is huge variation in when someone will decompensate from a low pressure system to a high pressure system, as observed in clinical practice with HPCR presenting with volumes <1L to >3L and LPCR generally presenting with volumes <1L.

However clinically, there is also no way to predict if and when a LPCR patient would progress to HPCR. That is the likely reason why OHOU recommends monitoring in LPCR.

Bates et al 2003 reported on 93 men man with PVR between 250-700 managed conservatively and reported PVR remained stable in 50%, reduced in 30% and increased in 20% over a follow-up of 3-10 years. 30% ended up needing intervention (TURP) however they could no identify any predictive factors in the patient’s who eventually required surgery.

Correlation of Prostate size and risk of HPCR

There is no more correlation between prostate size and risk of HPCR, than there is correlation between size of prostate and the degree of bladder outflow obstruction. Patients with small prostates present with symptomatic BOO whereas patients with large prostates can have no bothersome symptoms and void normally. Similarly HPCR can occur in patient with large or small prostates. Prostate size itself is not a predictor of risk of HPCR.

Causes of upper tract deterioration in HPCR

High intra-vesical pressures (>40cm of H2O as per the McGuire studies 1980s or >25cm of H2O as per Abrams 1978)

Dysfunction of anti-reflux mechanism of the intramural ureter secondary to the deformation of the ureterotrigonal complex from overstretching of the bladder (Smith & Tahago Textbook)

Review of Evidence on: Safe Bladder compliance
(The McGuire Principles and Galloway Hostility Score)

40cm of H2O as the safe upper limit for detrusor function is based on the McGuire Principles and the Galloway Hostility Index.

McGuire Principles:

Edward J McGuire was an American Urological, who was trained in Urology at Yale University School of Medicine and also did a fellowship (1970-71) at The Royal London Hospital, England (mentored by Professor Sir John Blandy CBE among others) and joined the faculty at Yales in 1972. In 1983 he joined the University of Michigan as the Head of Urology (successor to the renowned Jack Lapides, who described ISC in 1972). He became a Professor of Urology at the University of Michigan (UM). He retired in 2013. Reed M. Nesbit was the first Section Head of Urology at UM (1930-1968).

1981 McGuire: ‘PROGNOSTIC VALUE OF URODYNAMIC TESTING IN MYELODYSPLASTIC PATIENTS’ by McGuire

This study reported that in patient (n=22) with >40cmH2O intravesical pressure at the time of urethral leakage, (now referrred as Detrusor Leak Point Pressures DLPP), 81% demonstrated signs of upper tract deterioration on IVP whereas in patients (n=20) with Detrusor Leak Point Pressures (DLLP) ≤40cmH2O (n=20) only 10% showed upper tract changes. Mean follow-up 7 years.

The remaining 20% which did not have upper tract dysfunction all developed upper tract deterioration later as reported by McGuire below in 1983.

1983 McGuire: UPPER URINARY TRACT DETERIORATION IN PATIENTS WITH MYELODYSPLASIA AND DETRUSOR HYPERTONIA: A FOLLOWUP STUDY

A follow-up study of this original paper in which long-term outcomes were reviewed in patients who initially had >40cmH2O DLLP but did not have upper tract dilation.

All patients subsequently developed upper Tract dilation, which improved once bladder was appropriately treated.

These findings were confirmed and validated by others as well as McGuire in later larger studies and evolved into the concept of bladder compliance.

Galloway Hostility Score

1984 Bauer: Predictive Value of Urodynamic Evaluation in Newborns With Myelodysplasia

Reported DSD as a risk factor for upper tract deterioration.

Studied 36 infacnts with myelodysplasia. Thirteen (72%) of the group with dyssynergia had or later developed hydroureteronephrosis, as compared to only two (22%) with synergy and one (11%) with absent activity.

1991 Galloway: AN OBJECTIVE SCORE TO PREDICT UPPER TRACT DETERIORATION IN MYELODYSPLASIA

Introduced a 5 point score to risk stratify hostile bladder, which later became known as the Galloway Hostility Score

Reflux

Hyperreflexia

Compliance

Leak Pressure

Sphincter

They reviewed patients who had normal upper tracts at presentation and reported that on follow-up patient with higher hostility scores (>5) were at a higher risk of developing upper tract changes.

1992 Flood & McGuire: OUTCOME OF REFLUX IN CHILDREN WITH MYELODYSPLASIA MANAGED BY BLADDER PRESSURE MONITORING

Reported their 08 year data with 209 children. They self-validated their previous findings and reported high risk of upper tract deterioration above 40cmH20 bladder pressure and improvement in upper tract function once the pressure is treated.

In these early research, the treatment modalities mentioned include ISC, Anti-cholinergics, urethral dilation, urethrolysis, external sphincterotomy or bypass of the urethral sphincter as achieved by vesicostomy or ileal conduit.

Translation to Adult Compliance

1998 Kim Young: BLADDER LEAK POINT PRESSURE: THE MEASURE FOR SPHINCTEROTOMY SUCCESS IN SPINAL CORD INJURED PATIENTS WITH EXTERNAL DETRUSOR-SPHINCTER DYSSYNERGIA

This was a paper from Houston Texas Spinal Injuries Unit, where they studied if urodynamic parameters can predict the success of transurethral resection of external sphincter in patient’s with spinal injuries. 55 patients with mean follow-up ~20years.
They reported even in adults Bladder Leak Point pressure >40 was associated with higher risk of renal damage.
Interestingly it failed to show any statistically significant difference in the occurrence of vesicoureteral reflux, stones, bacteriuria and autonomic dysreflexia in the 2 groups.

Turkish Studies and 75mmH2O as a threshold

2005 Ozkan:

Ozkan et al (from Istanbul Turkey) reported their findings in 39 patients who underwent Augmentation Cystoplasty for Overactive Neurogenic Bladder Dysfunction.
They reported a DLPP of 75mmH2O to be a risk factor for upper urinary tract (UUT) deterioration rather than the conventional 40mmH2O (as suggested by McGuire and later studies)
They also sent full thickness bladder biopsies at the time of the cystoplasty and reported severity of detrusor fibrosis as a significant risk factor for UUT deterioration.

2016 Cetinel:

A larger Turkish retrospective study from the same institute (Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkey).
They reviewed 303 Spinal Cord Injury (SCI) patients and confirmed Ozkan’s 2005 findings and reported detrusor pressures >75mmH2O as a risk factor for UUT deterioration.
They also reported cystometric capacity <200ml as an independent risk factor for UUT deterioration.

Post Obstructive Diuresis POD

Definition:

OHOU defines it as urine output of >200ml/hr for >4hr

Etiology:

Physiological POD: HPCR and it’s consequential renal impairment causes salt and water retention. Once HPCR is relieved by catheterization or nephrostomy insertion, the body gets rid of the excess salt and water in the first few hours and that is physiological POD.

Pathological POD: Persistently high urine output (>200ml/hr for >4hrs) is classed as pathological POD. Following mechanisms have been suggested for this phenomenon;

Loss of corticomedullary concentration gradient

Dysregulation of ANP

Dysregulation of Aquaporin channels and renal response to ADH

Management of POD (OHOU 5th Ed):

Monitor Urine Output and lying standing blood pressure for postural drop (postural drop = 20/10 i.e. >20 in systolic >10 in diastolic)

If persistently high UO >200ml/hr for >4hr or symptomatic postural drop, consider replacement with Normal Saline at a rate of 50% of the hourly urine output.

Effect of Ureteric Obstruction on Renal Function

Animal Studies

Hinman 1959

Recovery of Renal Function After Ureteral Deligation

Hinman refers to a work by Widen which reported permanent loss of renal function to be directly proportional to the duration of the obstruction in animal experiments on dogs.

Vaughan & Gillenwater 1971 & 1973

Vaughan & Gillenwater described their experiments on dogs in 1970s.

They reported completely recovery after 7 days of obstruction and no recovery after 6 weeks of obstruction. They report 6 months post de-obstruction as the time to maximum recovery.

Fink 1980

RENAL IMPAIRMENT AND ITS REVERSlBlLlTY FOLLOWING VARIABLE PERIODS OF COMPLETE URETERIC OBSTRUCTION

A more comprehensive experiment with dogs divided into 7 groups with 5 dogs each. Unilateral ureteric obstruction was produced surgically and corrected after varying durations in the different groups.

Bander 1985

Reported on animal studies on rats. Their findings suggested some degree of permanent loss of functioning nephrons (~15%) even with de-obstruction after only 24hrs of unilateral obstruction. However this is compensated by the remaining functional nephrons and therefore GFR is remains comparable to the other healthy kidney.

Yokoyama - Japan 1994

Animals studies on Rats reported a decline of 50% renal function on DMSA 3 days after complete obstruction. Recovery of renal function was variably depending upon degree of obstruction and the duration of obstruction. Maximum recovery was observed in 7 days after which renal function on DMSA plateaued. In cases of mild partial obstruction, complete recovery was observed in as early as 3 days post release of obstruction.

Human Studies

Shapiro 1976

3 case reports of human patients with ureteric obstruction for 28, 28 and 150 days, having good renal cortex, which showed recovery in renal function after relief of the obstruction.

Jones and O’Reilly 1988

Reviewed recovery of renal function in patients with HPCR. Their findings suggested recovery to be biphasic with an early recovery phase that happens in first 2 weeks (tubular phase) and a later recovery phase that can take upto 3 months (Glomerular phase)

Conclusions

Findings from animal studies are extrapolated to human conditions and complimented by observational data in human disease. Based on this, following clinical judgement can be derived:

Permanent loss of functioning nephrons is possible even with only 24hrs of obstruction (Bander 1985)

Degree of renal impairment from ureteric obstruction depends duration of obstruction (Fink 1980) and the severity of obstruction (Yokoyama 1994)

Significant permanent loss of function can happen (90-100%) from 4-6 weeks of obstruction (Vaughan & Gillenwater 1971/73 & Fink 1980)

Recovery can take up to 4-6 months (Vaughan & Gillenwater 1971/73, Fink 1980 & Jones and O’Reilly 1988)

Renal preservation should be considered even in cases of prolonged obstruction where good renal cortex is observed, as recovery can still be seen in humans (Shapiro 1976)

Super-added infection would aggravate the loss of renal function (clinical reasoning)

Management of HPCR

Long-term Catheter (LTC), if not suitable for surgery.

Offer BOO surgery (guarded prognosis especially with very high bladder volumes).

Intermittent Self Catheterization (ISC) can be considered in exceptional circumstances if patient does not want surgery (or is not suitable) and would like to get rid of the LTC (and is able to do ISC).

Rate of success of surgical management

Abram & George 1978 reported 70% success rate in HPCR whereas only 20% in LPCR cohort. However the sample size is extremely small with n=22 patients in total.

Reynard & Shearer 1999 reported outcomes in 380 TURPs. There reported TWOC failure rate was,

~10% failure in total
Subanalysis: 0% in men with only LUTS (PVR <500ml), 10% failure in AUR (painful retention with <800ml volume), ~40% failure in CUR (PVR >500) , ~40% failure in Acute on Chronic Retention (Painful retention with >800ml volume)
Higher PVR (mean 1.5L) was a risk factor for failure of TWOC
However it is a very old study now. With modern equipment more contemporary data is required

Literature Review in HPCR

Abrams & George 1978 - UDS in Chronic Retention

Study Designs:

Single center prospective observational study

Study Population:

55 consecutive male patients aged 18-77 with chronic retention, 7 excluded and 48 included

LPCR was defined as bladder pressures <25cm H2O at filling cystometry and HPCR as >25cm H2O

Outcome:

Evaluation before and after surgery of patients with CUR

Results:

18 were classified as HPCR and 20 as LPCR

No difference in DRE in the 2 groups

Upper Tract deterioration

70% in HPCR patient (13/18)
20% in LPCR (4/20)
All 4 patients who showed upper tract dilation in the LPCR had unilateral dilation

Surgical Outcome (reported in 22 patients)

90% good outcome in HPCR cohort (9/10)
30% good outcome in LPCR cohort (4/12)

Limitations:

Small sample size

Reynard & Shearer 1999

Failure to void after transurethral resection of the prostate and mode of presentation

Study Design:

Single centre observational study