Urinary tract obstruction

Urinary tract obstruction Victor Federico B. Acepcion, MD, FPUA

The Kidney 

Basic function: 



formation of ultrafiltrate that is free of protein with appropriate amount of water, electrolytes, and end products of metabolic pathways to maintain homeostasis.

Remaining portion of UT 

Eliminate and/or store urine

Urine production 





Pressure gradient from glomerulus to Bowman capsule Peristalsis of renal pelvis and ureter Effects of gravity

Urinary tract obstruction • •

Common cause of acute and chronic renal failure Potentially curable form of kidney disease

Definition of terms   

Obstructive uropathy Obstructive nephropathy Hydronephrosis

Objectives      

Define urinary tract obstruction Incidence Etiology/pathophysiology Clinical presentation Diagnosis Treatment and management 

Pre-hospital/emergency department care

Incidence •

Frequency – – –

•

Sex – –

•

No data available in unselected populations 20-35% prevalence in large survey among elderly men 3.8% (adults); 2.0% (children) postmortem examinations No gender difference until 20 years Women 20-60; Men > 60

Age –

Special considerations in pediatric patients

Etiology 

Types of obstruction 

Mechanical blockade  

 

Intrinsic extrinsic

Functional defects Congenital

Common Mechanical Causes of Urinary Tract Obstruction Ureter

Bladder Outlet

Urethra

Bladder neck obstruction

Posterior urethral valves

CONGENITAL Ureteropelvic junction narrowing or obstruction

Ureterovesical Ureterocele junction narrowing or obstruction and reflux

Ureterocele

Damage to S2- Stricture 4

Retrocaval ureter VUR

Anterior urethral valves

Meatal stenosis 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

Retroperitoneal fibrosis

trauma

Aortic aneurysm Uterine leiomyomata Carcinoma of uterus, prostate, bladder, colon, rectum

lymphoma Pelvic inflammatory disease, endometriosis

Accidental surgical ligation

trauma

Pathophysiology    

Unilateral (UUO)? Bilateral (BUO)? Obstruction relieved or not? Time

Global Renal Function Changes  

Obstruction can affect hemodynamic variables and GFR GFR= Kf(PGC-PT-PGC) 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 P- the oncotic pressure of the proteins in the glomerular capillary and efferent arteriolar blood



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 PGC

Triphasic pattern of UUO

Bilateral urinary obstruction (BUO) • • • •

No triphasic pattern Modest increase in RBF after 90 min but between 90 min to 7 hours, RBF is significantly lower than UUO. Increase renal vascular resistance (RVR) After 24 hours, low RBF, high RVR same as UUO

Bilateral urinary obstruction (BUO)   

Ureteral pressure higher than in UUO Effective RBF is markedly decreased after 48 hours GFR is significantly decreased after 48 hours

Summary of UUO and BUO

Pathophysiology Obstructive Uropathy Obstructive Nephropathy

Pathophysiology of Bilateral Ureteral Obstruction

Hemodynamic Effects

Tubule Effects

Clinical Features

ureteral and tubular pressures

pain

Acute Renal Blood Flow GFR Medullary Blood Flow

azotemia reabsorption of Na, urea, water

Oliguria or anuria

Vasodilator PGs Chronic

Renal Blood Flow GFR vasoconstrictor PGs

medullary osmolarity

azotemia

concentrating ability

hypertension

Structural damage; parenchymal atrophy

renin-angiotensin pdn

transport fxn for Na,K, H

ADH-insensitive polyuria Hyperkalemic, hyperchloremic acidosis

Pathophysiology of Bilateral Ureteral Obstruction Release of Obstruction Slow in GFR (variable)

Tubular pressure

solute load per nephron (urea, NaCl)

Natriuretic factors present

Postobstructive diuresis

Potential for volume depletion and electrolyte imbalance due to losses of Na, K, PO4, Mg and water

Consequences of urinary tract obstruction •

Reduced glomerular filtration rate

•

Reduced renal blood flow (after initial rise)

•

Impaired renal concentrating ability

•

Impaired distal tubular function

•

•

Nephrogenic diabetes insipidus

•

Renal salt wasting

•

Renal tubular acidosis

•

Impaired potassium concentration

Postobstructive diuresis

Consequences of urinary tract obstruction 

Progressive and permanent changes to the kidney occur   

Tubulointerstitial fibrosis Tubular atrophy and apoptosis Interstitial inflammation

Diagnosis •

History – – – –

– – –

Pain, renal colic Inability to void effectively Alteration in pattern of micturition (anuria, polyuria, nocturia) Recurrent UTI New-onset or poorly controlled hypertension Polycythemia Recent gynecologic or abdominal surgery

•

History –

–

Medication history • Antihistamines, antipsychotics, antidepressants • Ethylene glycol, indinavir, methotrexate, phenylbutazone, or sulfunamides • Methysergide or other natural-occurring ergotamines Occupational exposure history • Textile manufacturers, shipyard workers, roofers or asbestos miners (retroperitoneal fibrosis) • Textile workers, rubber manufacturing workers, leather workers, painters, hairdressers, drill press workers (bladder cancer)



Physical Examination     

Signs of dehydration and intravascular volume depletion Peripheral edema, hypertension, signs of congestive heart failure Palpable kidney or bladder Enlargement of pelvic organs (eg. Prostate, uterus) Examination of external urethra for phimosis, meatal stenosis

Normal kidney

Treatment and management 

Prehospital Care   

Pulmonary edema Salt and water retention hypovolemia

Treatment and management 

Emergency department care 

Investigate and begin treatment of potentially life-threatening complications    

Pulmonary edema Hypovolemia Urosepsis Hyperkalemia

Treatment and management • –

Overriding goal of treatment: reestablishment of urinary flow Transurethral bladder catheterization • •

Diagnostic and therapeutic No urine output = investigate upper tract

Treatment and management 

Large PVR = obstruction below the bladder 

Fractionating urine removal (?) 



Hematuria and bladder spasm 

 

Christensen, et al. concluded that fractionating urine removal in bladder obstruction is unjustified Gould, et al. : hematuria correlated strongly with degree of bladder wall damage prior to relief of obstruction and not with rate of bladder emptying

Urine should be drained completely and rapidly from an obstructed bladder Prolonged urine stasis only predisposes to UTI, urosepsis and renal failure

Treatment and management 

Calculi – most common causes of unilateral ureteral obstruction   

90% pass spontaneously (calculi