Urinary Obstruction : Common Diagnosis and Management

三軍總醫院泌尿外科學科

李俊德醫師

2018-03-21

Urinary Obstruction : Common Diagnosis and Management

Outline

I. Background

II. Pathophysiology and pathological changes with urinary tract obstruction

III. Patient work-up and management

IV. Causes of urinary tract obstruction

I. Background




Definitions

Hydronephrosis- Dilation of the renal pelvis or calyces

Obstructive uropathy- functional or anatomic obstruction of urine flow at any level of the urinary tract

Obstructive nephropathy- when obstruction causes functional or anatomic renal damage

Prevalence

3.1% in autopsy series

No gender differences until 20 years

Females more common 20-60

Males more common older than 60

2-2.5% of children at autopsy

I. Background




Etiology

Types of obstruction

Mechanical blockade

Intrinsic

extrinsic

Functional defects

Congenital

Common Mechanical Causes of Urinary

Tract Obstruction

Ureter Bladder

Outlet

Urethra

CONGENITAL

Ureteropelvic

junction

narrowing or

obstruction

Bladder neck

obstruction

Posterior

urethral valves

Ureterovesical

junction

narrowing or

obstruction

and reflux

Ureterocele Anterior

urethral valves

Ureterocele Damage to

S2-4

Stricture

Retrocaval

ureter

Meatal

stenosis

VUR VUR Phimosis

Ureter Bladder Outlet Urethra

Acquired Intrinsic Defects

Calculi Benign prostatic

hyperplasia

stricture

Inflammation Cancer of the

prostate

tumor

Infection Cancer of the

bladder

calculi

Trauma Calculi trauma

Sloughed

Papillae

Diabetic

neuropathy

phimosis

Tumor Spinal cord

disease

Blood Clots Anticholinergic

drugs and alpha

adrenergic

antagonists

Uric acid

crystals

Ureter Bladder

Outlet

Urethra

Acquired Extrinsic Defects

Pregnant uterus Carcinoma of

cervix, colon

trauma

Retroperitoneal

fibrosis

trauma

Aortic aneurysm

Uterine

leiomyomata

Carcinoma of

uterus, prostate,

bladder, colon,

rectum

lymphoma

Pelvic

inflammatory

disease,

endometriosis

Accidental

Global Renal Functional Changes

Obstruction can affect hemodynamic variables and GFR Degree of affect depends on extent and severity of obstruction, whether UUO

or BUO, and whether it has been relieved or not

GFR= Kf(PGC-PT-πGC) Need to understand in order to comprehend the relationships between

changes in renal hemodynamics and alterations in GFR during and after obstruction

RPF= (aortic pressure-renal venous pressure)renal vascular resistance

Influences PGC Constriction of the afferent arteriole will result in a decrease of PGC and GFR An increase in efferent arteriolar resistance will increase PGCPS: UUO：unilateral ureteral obstruction; BUO: bilateral ureteral obstruction

Kf- glomerular ultrafiltration coeffecient related to the surface area

and permeability of the capillary membrane

PGC- glomerular capillary pressure. Influenced by renal plasma

flow and the resistance of the afferent and efferent arterioles

PT- Hydraulic pressure of fluid in the tubule

π- the oncotic pressure of the proteins in the glomerular capillary

and efferent arteriolar blood

Hemodynamic Changes with UUO

Triphasic pattern of renal blood flow and ureteral pressure changes

1. RBF increases during the first 1-2 hours and is accompanied by a high PT and collecting system pressure

2. For another 3-4 hours, the pressures remains elevated but the RBF begins to decline

3. 5 hours after obstruction, further decline in RBF occurs. A decrease in PT and collecting system pressure also occurs

PS: PT- Hydraulic pressure of fluid in the tubule

Triphasic pattern of UUO

Hemodynamic Changes with UUO

Alterations in flow dynamics within the kidney occur dye to changes in the biochemical and hormonal milieu regulating renal resistance Phase I- The increased PT is counterbalanced by an

increase in renal blood flow via net renal vasodilation, which limits the fall of GFR PGE2, NO – Contribute to net renal vasodilation early in UUO

Phase II and III- An increase in afferent arteriolar resistance occurs causing a decrease RPF. A shift in RBF from the outer cortex to the inner cortex also occurs all reducing GFR Angiotensin II, TXA2, Endothelin - mediators of the preglomerular

vasoconstriction during the 2nd and 3rd phase of UUO

Hemodynamic Changes with BUO Only a modest increase in RBF lasting 90 minutes

followed by a prolonged and profound decrease in RBF that is even more than with UUO

The intrarenal distribution of blood flow changes from the inner to the outer cortex (opposite from UUO)

Accumulation of vasoactive substances (ANP) in BUO that contributes to preglomerular vasodilation and postglomerular vasoconstriction with UUO, these substances would be excreted by the normal kidney

When obstruction is released, GFR and RBF remain depressed due to persisent vasoconstriction of the afferent arteriole the post-obstructive diuresis is much greater than with UUO

Summary of UUO and BUO

Partial Ureteral Occlusion

Changes in renal hemodynamics and tubular function are similar to complete models of obstruction Develop more slowly

Animal Studies- Difficult to initate partial obstruction 14 days- normal functional recovery

28 days- recover 31% of function

60 days- recovery 8% of function

Effects of Obstruction on Tubular Function

Dysregulation of aquaporin water channels in the proximal tubule, thin descending loop, and collecting tubule Lead to polyuria and impaired concentrating capacity

Sodium Transport Decreased which leads to a role in the postobstructed kidney’s

impaired ability to concentrate and dilute urine Much greater sodium and water excretion after release of BUO than

UUO due to the retention of Na, water, urea nitrogen and increased ANP, all which

stimulate a profound naturesis

Potassium and phosphate excretions follow changes in sodium Decreased with UUO Increased transiently with BUO in parallel with the massive diuresis

Deficit in urinary acidification

Magnesium excretion is increased after release of UUO or BUO

Changes in peptide excretion mark renal damage

Cellular and Molecular Changes Lead to Fibrosis and Tubular Cell Death

Obstruction leads to biochemical, immunologic, hemodynamic, and functional changes of the kidney

A cascade of events occur which lead to release of angiotensin II, cytokines, and growth factors (TGF-B, TNF-a, NFkB) Some mediators are produced directly from the renal tubular and

interstitial cells

Others are generated by way of fibroblasts and macrophages

Progressive and permanent changes to the kidney occur

Tubulointerstitial fibrosis Tubular atrophy and apoptosis

Interstitial inflammation

Pathologic Changes of Obstruction in porcine model

Gross Pathologic Changes 42 hours- Dilation of the pelvis and ureter and blunting of the

papillary tips. Kidney also heavier

7days- Increased pelviureteric dilation and weight. Parenchyma is edematous

21-28 days- External dimensions of kidneys are similar but the cortex and medullary tissue is diffusely thinned

6 weeks- Enlarged, cystic appearing, weighs less than non-obstructed kidney

did not see such differences in partially obstructed kidneys

Microscopic Pathologic Findings

42 hours- lymphatic dilation, interstitial edema, tubular and glomerular preservation

7 days- collecting duct and tubular dilation, widening of Bowman’s space, tubular basement membrane thickening, cell flattening

12 days- papillary tip necrosis, regional tubular destruction, inflammatory cell response

5-6 weeks- widespread glomeular collapse and tubular atrophy, interstitial fibrosis, proliferation of connective tissue in the collecting system

Pathologic Changes of Obstruction in porcine model

Compensatory Renal Growth

Enlargement of the contralateral kidney with unilateral hydronephrosis or renal agenesis

A reduction in compensatory growth occurs with age

An increase in the number of nephrons or glomeruli does not occur, despite enlargement

Renal Recovery after Obstruction

Degree of obstruction, age, and baseline renal function affect chance of recovery Two phases of recovery may occur

Tubular function recovery GFR recovery

Duration has a significant influence Full recovery of GFR seen with relief of acute

complete obstruction Longer periods of complete obstruction are

associated with diminished return of GFR

DMSA scan is predicative of renal recovery

Pathophysiology

民國前/通用格式民國前/通用格式民國前/通用格式民國前/通用格式

Ureteric and tubular pressure

Renal blood flow (RBF)

GFR

Baseline

HOURS

Obstructive Uropathy

Obstructive Nephropathy

Pathophysiology of Bilateral Ureteral Obstruction

Hemodynamic Effects Tubule Effects Clinical Features

Acute

Renal Blood Flow ureteral and tubular

pressures

pain

GFR azotemia

Medullary Blood Flow reabsorption of Na,

urea, water

Oliguria or anuria

Vasodilator PGs

Chronic

Renal Blood Flow medullary osmolarity azotemia

GFR concentrating ability hypertension

vasoconstrictor PGs Structural damage;

parenchymal atrophy

ADH-insensitive polyuria

renin-angiotensin pdn transport fxn for Na,K,

H

Hyperkalemic,

hyperchloremic acidosis

Pathophysiology of Bilateral Ureteral Obstruction

Release of

Obstruction

Slow in GFR

(variable)

Tubular pressure Postobstructive

diuresis

solute load per

nephron (urea, NaCl)

Potential for volume

depletion and

electrolyte imbalance

due to losses of Na, K,

PO4, Mg and water

Natriuretic factors

present

I. Background




Management of Patients with Obstructiondiagnostic imaging

Renal US Safe in pregnant and pediatric patients

Good initial screening test

No need for IV contrast

May have false negative in acute obstruction (35%)

Hydronephrosis= anatomic diagnosis caliectasis or pelviectasis in an unobstructed system

Doppler- measures renal arterial resistive index (RI), an assessment of obstruction RI= (PSV-EDV)/PSV

PSV: peak systolic velocity; EDV: end diastolic velocity RI > 0.7 is suggestive elevated resistance to blood flow

suggesting obstructive uropathy

Diagnostic Imaging

Excretory Urography

applies anatomic and functional information

limited use in patients with renal insufficiencyincreased risk of contrast-

induced nephropathy

cannot use in patients with contrast allergy

Retrograde Pyelography

accurate details of ureteral and collecting system anatomy

renal insufficiency or other risks for contrast

Loopogram- use for evaluation of patients with cutaneous diversions

Antegrade Pyelography

RP is not possible and other imaging doesn’t offer enough details

Diagnostic Imaging

Whitaker Test

“True pressure” within the pelvis = Collecting system pressure – intravesicle presure Saline or contrast though a percutaneous needle or

nephrostomy tube at a rate of 10mL/ min

Catheter in bladder to monitor intravesicle pressure

Invasiveness and discordant results limit clinical usefulness

Normal < 15 cm H2O

Indeterminate = 15-22 cm H2O

Obstruction > 22 cm H2O

Diagnostic Imaging

Nuclear Renography

Provides functional assessment without contrastObstruction is measured by the clearance curves

Tc 99m DTPA- glomerular agent ( GFR)

Tc 99m MAG3 – tubular agent ( ERPF)

Diuretic renogram- maximizes flow and distinguishes true obstruction from dilated and unobstructed

Normal = T ½ < 10 min

Indeterminate = T ½ 10-20 min

Obstructed T ½ > 20 min

Diagnostic Imaging

CT most accurate study to

diagnose ureteral calculi more sensitive to identify

cause of obstruction helpful in surgical

planning preferred initial imaging

study in those with suspected ureteral obstruction

MRI identify hydronephrosis but

unable to identify calculi and ureteral anatomy of unobstructed systems

diuretic MRU can demonstrate obstructionespecially accurate with strictures or

congential abnormalities

gadopentetate-DTPA allows functional assessment of collecting system while providing anatomic detail GFR assessment

Renal clearance

still several limitations in use

Diagnostic Imaging

Issues in Patient Management

Hypertension

Can be caused by ureteral obstruction Especially BUO or obstruction of a solitary kidney

Less common with UUO

Volume-mediated Increased ANP with obstruction which normalizes after

drainage

Decreased plasma renin activity

Renal Drainage⚫ endourologic or IR(Interventional Radiology) procedures

allow prompt temporary and occasionally permanent drainage⚫ no statistically significant difference in HRQL(health-related quality

of life) between the two techniques⚫ extrinsic compression causing obstruction have a high risk of

ureteral stent failure 42-56.4 % failure rate at 3 months 43% failed within 6 days of placement in one study high failure rate at even getting placement(27%) stent diameter did not predict risk of failure

ultrasound guided percutaneous drainage should be initial consideration in pregnant patients

percutaneous placement with suspected pyonephrosis⚫ large diameter ureteral stents

Issues in Patient Management

Reconstruction endoscopic, open and laparoscopic techniques

should be considered

Nephrectomy? allow 6-8 weeks for adequate drainage before

proceeding

nuclear imaging provides accurate functional information< 10% contribution to global renal function is considered

threshold for nephrectomy

Issues in Patient Management in surgical intervention

increases in collecting system pressure and ureteral wall tension contribute to renal colic

results in spinothalamic tract C-fiber excitation

treating Pain narcotics

rapid onset, nausea, sedation, abuse

NSAIDS targets the inflammatory basis of pain by inhibiting

prostaglandin synthesis reduces collecting system pressure by decreasing renal

blood flow avoid in patients with renal insufficiency, GI bleeding

Issues in Patient Management in pain

usually with BUO or solitary kidney urine output > 200ml/hour a normal physiologic response to volume

expansion and solute accumulation elimination of sodium, urea, and free water diuresis ends when homeostasis returns

postobstructive diuresis (POD) impaired concentating abilility or sodium absorption

down-regulation of sodium transporters and re-absorption in the thick ascending loop of Henle

increased production and regulation of ANP poor response of collecting system to ADH

Issues in Patient Management in postobstructive diuresis

Management monitor BUO or UUO in solitary kidney for POD

electrolytes, Mg, BUN, Cr

intensity of monitoring depends on clinical factors if no signs of POD→ If alert, no fluid overload, normal renal

function, normal electrolytes, → discharge and follow up if signs of POD → If alert, able to consume fluids, normal vital

sign→ continue in-patient observation, free access to oral fluids, and daily labs until diuresis resolves (No IV Fluids)

if signs of POD and signs of fluid overload, poor renal function, hypovolemia, or mental status changes→ Frequent vital signs and urine output records, labs q 12 hrs (or more), urinary osmolarity, restrict oral hydration (Minimal IV fluid hydration) most have self-limiting physiologic diuresis if pathologic diuresis occurs- very intense monitoring is

indicated

Issues in Patient Management in postobstructive diuresis

I. Background




Retroperitoneal Fibrosis an inflammatory mass, a fibrous whitish plaque,

envelops and potentially obstructs retroperitoneal structures

usually extends from the renal hilum to pelvic brimmay involve the mediastinum and the pelvis

2 phases lead to its developmenta)autoimmune reaction thought to occur due to

leakage of ceroid from the atheromatous plaques in the aorta

b)fibrotic maturation with development of homogeneous fibrous tissue with limited cellularity

1: 200,000, 3:1 Male: Female, Age 50

2/3s of Cases are “idiopathic” 8-10% of cases have underlying malignancy

Other causes: Medications (methysergide, hydralazine, Haldol, Beta-Blockers, LSD, Phenacetin, Amphetamines), Retroperitoneal hemorrhage, urinary extravasation, trauma, radiation, Inflammatory Bowel Disease (IBD), Gonorrhea, collagen disease, peri-aneurysmal inflammation

symptoms- dull, non-colicky pain in a “girdle” distribution, ureteral or vascular obstruction (late)

Retroperitoneal Fibrosis

Diagnosis

IVP- medial deviation of the uretersseen in 18% of normal subjects

CT – well demarcated mass that is isodense with muscle (non-contrast study)

MRI- allows superior soft tissue discrimination and can more accurately distinguish the plaque from the great vessels



Treatment1. correct obstructive uropathy2. biopsy to exclude malignancy3. if biopsy is negative, medical therapy is preferred

– Discontinue any offending medications– Corticosteroids- prednisolone 60mg qod x 2 mos, tapered to 5mg daily over the

next 2 months, then continue 5mg daily for 2 years– Tamoxifen– Immunotherapy

4. ureterolysis- if patient not a candidate for medical therapy or if it fails- May do open or laparoscopic- Bilateral treatment is recommended even if unilateral

disease- To prevent recurrent ureteral involvement→ bring ureter

intraperitoneal, or wrap in omentum- Stents can usually be removed 6-8 wks after ureterolysis

Experimental


Pelvic Lipomatosis Rare benign proliferative disease involving

the mature fatty tissues of the pelvic retroperitoneum

18:1 Male to female

More common in African American men

Unknown etiology

Obesity?

Genetic?

Pelvic Lipomatosis Patient Presentation and Diagnosis

LUTS (lower urinary tract symptoms), Constipation, non-specific pain, HTN

Physical Exam- suprapubic mass, high riding prostate, indistinct pelvic mass

Younger patients are thought to have a more progressive course than older patients who have a more indolent course

Pelvic Lipomatosis Imaging

KUB- Pelvic lucency

IVP- Bladder is pear-shaped and elevated, hydronephrosis may be evident

CT- pelvic fat is readily demonstrated

Pelvic Lipomatosis

Other evaluation Cystoscopy- cystitis cystica, cystitis glandular (40%),

adenocarcinoma, chronic UTIHigh bladder neck, pelvic fixation, and elongated prostatic urethra may impair rigid cystoscopy

Treatment Exploration is not recommended due to the

obliteration of normal planes and increased vascularity of the mass

In patients with obstructive uropathy→ stents,

PCNs, ureteral reimplanation, urinary diversion

Pregnancy Reported to occur in 43-100%

Right > Left

Etiology

Hormonal- progesterone thought to promote ureteral dilation

Mechanical – increased degree of dilation after 20 weeks when the uterus reaches the pelvic brim

Pregnancy Diagnosis

Usually asymptomatic If symptoms, may have flank pain or pyelonephritis

US will show dilation to the pelvic brim If it extends below this, consider other etiologies (stone)

Limited IVU or MRI to diagnose

Treatment Most respond to conservative treatment

IVF, analgesics, antibiotics

If signs of sepsis or compromised renal function may need ureteral stents or nephrostomy tubes

Endometriosis GU tract involvement

Bladder 70-80%

Ureter 15-20%

May be intrinsic or extrinsic (80%)

Cyclical flank pain, dysuria, urgency, UTI, hematuria, or no GU symptoms (silent loss of renal function may occur)

Recommended to image the Upper tracts in all patients with pelvic endometriosis (RUS or EXU)

Endometriosis Treatment

Hormone therapy- if normal renal function with mild hydro and no functional obstruction seen on renogram GnRH agonists

Surgery- treatment of choice for patients with significant disease TAH with BSO

Unilateral oopherectomy

Ureterolysis if extrinsic disease

Distal ureterectomy with re-implantation

Vascular Causes of Ureteral Obstruction

Abdominal Aortic Aneurysm Ureteral obstruction may be the first sign

Medial deviation of the ureters associated with the desmoplastic reaction of inflammatory AAA (IAAA) more likely to cause obstruction than lateral deviation

Stent placement usually recommended prior to aneurysmal repair (CVS) Ureterolysis usually not needed and obstruction resolves

with correction of the aneurysm

Circumcaval Ureter Anomalous course of the ureter to the IVC

leading to extrinsic obstruction

Due to the persistence of the subcardinal vein as the infrarenal IVC, causing medial migration and compression of the right ureter Other theories involve persistence of the posterior

cardinal vein as the infrarenal cava

Both, theories note failure of the supracardinal vein to develop into the infrarenal IVC

Circumcaval Ureter

Circumcaval Ureter Treatment is performed only in presence of

obstruction

Divide ureter proximally and at the distal point it emerges lateral to the IVC

Spatulated ureterostomy performed

Thanks For You Attention

Campbell-Walsh UROLOGY

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Urinary Obstruction : Common Diagnosis and Management