Complications of Urinary
Diversion
By
Peter Tran, D.O.
Garden City Hospital
Resident Talk
12/17/2008
Overview
Classification of urinary diversions
 Factors influencing complications
 Complications according to bowel
segments
 Metabolic/physiologic complications
 Surgical complications: early and late

Clasification of Diversions
Orthotopic
 Heterotopic

◦ Continent cutaneous
◦ Non-continent cutaneous
◦ Diversion to GIT
Examples of Orthotopic
Neobladders
Figure 82-2 Construction of the modified Camey II. A, The ileal loop is folded three times (Z shaped) and incised on the antimesenteric border. B, The reservoir is closed with a running
suture to approximate the incised ileum. C, The urethroenteric anastomosis is performed.
Examples of Orthotopic
Neobladders
Figure 82-3 Construction of the Hautmann ileal neobladder. A, A 70-cm portion of terminal ileum is selected. Note that the isolated segment of ileum is incised on the antimesenteric
border. B, The ileum is arranged into an M or W configuration with the four limbs sutured to one another. C, After a buttonhole of ileum is removed on an antimesenteric portion of
the ileum, the urethroenteric anastomosis is performed. The ureteral implants (Le Duc) are performed and stented, and the reservoir is then closed in a side-to-side manner.
Examples of Orthotopic
Neobladders
Figure 82-4 Construction of the ileal
neobladder (Studer pouch) with an
isoperistaltic afferent ileal limb. A, A 60- to
65-cm distal ileal segment is isolated
(approximately 25 cm proximal to the
ileocecal valve) and folded into a U
configuration. Note that the distal 40 cm of
ileum constitutes the U shape and is opened
on the antimesenteric border; the more
proximal 20 to 25 cm of ileum remains intact
(afferent limb). B, The posterior plate of the
reservoir is formed by joining the medial
borders of the limbs with a continuous
running suture. The ureteroileal anastomoses
are performed in a standard end-to-side
technique to the proximal portion (afferent
limb) of the ileum. Ureteral stents are used
and brought out anteriorly through separate
stab wounds. C, The reservoir is folded and
oversewn (anterior wall). D, Before
complete closure, a buttonhole opening is
made in the most dependent (caudal)
portion of the reservoir. E, The
urethroenteric anastomosis is performed. F,
A cystostomy tube is placed, and the
reservoir is closed completely.
Examples of Orthotopic
Neobladders
Figure 82-5 Construction of the Kock ileal
reservoir. A, A total of 61 cm of terminal ileum is
isolated. Two 22-cm segments are placed in a U
configuration and opened adjacent to the
mesentery. Note that the more proximal 17-cm
segment of ileum will be used to make the afferent
intussuscepted nipple valve. B, The posterior wall
of the reservoir is then formed by joining the
medial portions of the U with a continuous
running suture. C, A 5- to 7-cm antireflux valve is
made by intussusception of the afferent limb with
the use of Allis forceps clamps. D, The afferent
limb is fixed with two rows of staples placed
within the leaves of the valve. E, The valve is fixed
to the back wall from outside the reservoir. F,
After completion of the afferent limb, the
reservoir is completed by folding the ileum on
itself and closing it (anterior wall). Note that the
most dependent portion of the reservoir becomes
the neourethra. The ureteroileal anastomosis is
performed first, and the urethroenteric
anastomosis is completed in a tension-free,
mucosa-to-mucosa fashion.
Examples of Orthotopic
Neobladders
Figure 82-8 Construction of the Mainz ileocolonic orthotopic reservoir. A, An isolated 10 to
15 cm of cecum in continuity with 20 to 30 cm of ileum is isolated. B, The entire bowel
segment is opened along the antimesenteric border. Note that an appendectomy is performed.
C, The posterior plate of the reservoir is constructed by joining the opposing three limbs
together with a continuous running suture. D, An antireflux implantation of the ureters
through a sub-mucosal tunnel is performed and stented. E, A buttonhole incision in the
dependent portion of the cecum is made that provides for the urethroenteric anastomosis.
Note that the ureterocolonic anastomoses are performed before closure of the reservoir. F,
The reservoir is closed side to side with a cystostomy tube and the stents exiting.
Examples of Orthotopic
Neobladders
Figure 82-9 Construction of Le Bag (ileocolonic) orthotopic reservoir. A, A total of 20 cm of ascending cecum and colon, with a corresponding length of adjacent
terminal ileum, is isolated. The bowel is opened along the entire antimesenteric border, and the two incised segments are then sewn to one another. This forms the
posterior plate of the reservoir. B, This reservoir is folded and rotated 180 degrees into the pelvis with the most proximal portion of the ileum (2 cm nondetubularized) anastomosed to the urethra. C, Modification is performed with complete detubularization of the bowel segment, which is then anastomosed to the
urethra.
Examples of Heterotopic
Cutaneous Diversion
Continent/catherizable Pouch
◦ Indiana Pouch
 Segment of ascending colon with terminal ileum and IC valve as
continence mechanism.
◦ Penn Pouch
 Same as Indiana pouch except appendix used based on Mitrofanoff
principle in which continence mechanism is the appendix.
◦ Gastric Pouch
 Segment of stomach and ileum recreated in to a reservoir
 Non-Continent
◦ Most popular - ileal loop
 Excretion of urine by means of evacuation
◦ Ureterosigmoidostomy
◦ Rectal bladder
◦ Sigmoid hemi-Kock

Factors Influencing Complications
Patient factors
 Bowel factors

Patient Factors
Performance status/co-morbidities
 Pt/caregiver compliance with CIC
 Mobility
 Previous XRT
 Renal function
 Liver function
 Body habitus
 BMI

Bowel Factors/Technical Factors
Type of intestinal segment used
 Length of intestinal segment
 Continent vs. incontinent
 Method/extend of detubularization
 Capacity
 Compliance
 Refluxing/non-refluxing uretero-enteric
anastomosis
 Type of diversion chosen

Gastric Complications
Hypochloremic, hypokalemic metabolic
alkalosis
 Hyper-gastrinemia
 Hematuria-dysuria syndrome

Jejunum Complications
Most severe metabolic complications
 Hyponatremia
 Hyperkalemic, hypochloremic metabolic
acidosis
 Severe dehydration

Ileal Complications
Hyperchloremic, hypokalemic metabolic
acidosis
 Vit B12 deficiency

Colonic Complications

Hyperchloremic, hypokalemic metabolic
acidosis
Metabolic/Physiologic Complications











Renal deterioration
Electrolyte disturbance
Hypertension
Altered sensorium
Abnormal drug metabolism
Osteomalacia
Abnormal growth/development
Vit deficiency
Anemia
Chronic diarrhea
Hyper-gastrinemia
Electrolyte Disturbance

Colon/Ileum
◦ Hyperchloremic, hypokalemic metabolic acidosis

Stomach
◦ Hypochloremic, hypokalemic metabolic alkalosis

Jejunum
◦ Hyperchloremic, hyperkalemic, hyponatremic metabolic acidosis

Hyperammonemia

Hypomagnesemia

Hypocalcemia
Colon and Ileum

Hyperchloremic, hypokalemic metabolic
acidosis
◦ 15% of ileal conduits
 10% severe enough to require Tx
◦ 20% of colon conduits
 15% require Tx
◦ 50% ileal or colonic pouches
 40% require Tx
◦ 80% of ureterosigmoidostomy
Hyperchloremic, hypokalemic
metabolic acidosis

Symptoms
◦
◦
◦
◦
◦
Easy fatigability
Anorexia/weight loss
Polydipsia
Lethargy
Exacerbation of diarrhea in GI diversions
Hyperchloremic, hypokalemic
metabolic acidosis: MOA

Net absorption of ammonium + chloride

Increased secretion of HCO3

Impaired distal tubular secretion of hydrogen

Physiologic Response
◦ Increased acid secretion by kidneys
◦ Bone demineralization to buffer acidosis
Hyperchloremic, hypokalemic
metabolic acidosis: Treatment


Alkalinizing agent
◦ NaHCO3
◦ K-Citrate
◦ Na-Citrate
Blockers of Cl transport
◦ Chlorpromazine
◦ Nicotinic acid
Gastric Complications

Hypochloremic, hypokalemic metabolic alkalosis
◦ Rare unless comcomitant renal failure
◦ Severe dehydration, often triggered by vomiting or GI illness
◦ High serum gastrin levels
 Overdistension of gastric segment triggers gastrin release
Gastric Complications

Symptoms
◦
◦
◦
◦
◦
Lethargy
Weakness
Respiratory insufficiency
Seizures
Ventricular arrhythmia
Gastric Complications: MOA
H+, K+, and Cl- loss in gastric segment
 Net addition of HCO3
 Serum gastrin levels correlate with
systemic HCO3 concentration

Gastric Complications: Tx

Acute severe metabolic alkalosis
◦
◦
◦
◦
◦
◦
Empty bladder
NaCl volume replacement
H2 blocker
PPI
Arginine HCl
Surgical removal of gastric segment
Gastric Complications: Tx

Mild/prophylaxis
◦ Oral Na/K supplementation
◦ H2 blockers
Hypokalemia - Incidence

Colonic diversions
◦ 30% reduction in total body K

Ileal diversions
◦ 0-15% reduction
Hypokalemia: MOA

Colonic/Ileal diversions
◦ Ileum may passively reabsorb some K blunting
the loss
◦ Chronic metabolic acidosis
◦ Renal K wasting
Hypokalemia

Symptoms
◦ Typically no symptoms
◦ At most severe
 Muscle weakness
 Paralysis
Hypokalemia: Tx

Correct the acidosis
◦ Beware of acutely worsening K as in moves
backto intracellular stores
◦ Oral K supplementation
Altered Sensorium: MOA
Hypomagnesemia
 Drug reabsorption
 Ammonia encephalopathy

Altered Sensorium:
Hypomagnesemia
Renal loss
 Chronic diarrhea
 Decreased absorption

Altered Sensorium:
Hypomagnesemia

Symptoms
◦
◦
◦
◦

Cardiac arrhythmias
Tremor
Tetany
Seizures
Treament
◦ Mg replacement
Ammoniogenic Encephalopathy
Ammonium secreted by the kidney
 Ammonia is produced by urease splitting
bacteria
 Reabsorbed and transferred to liver by
portal circulation
 Nomally liver copes and coverts ammonia
to urea

Ammoniogenic Encephalopathy

Risk Factors
◦ Typically in pre-existing or acquired liver disease
◦ Ureterosigmoidostomy>Colon or ileal conduits
◦ Triggers in setting of liver disease
 Constipation
 Increased protein load
 GI bleed
 UTI with ammonia producer
 Co-existing CNS depressant use
 Renal failure
◦ Normal liver
◦ Bacterial endotoxin – liver dysfunction with normal LFT
Ammoniogenic Encephalopathy:
Symptoms
Apathy
 Restlessness
 Sleep disturbance
 Impaired intellectual abililites
 Asterixis and lethargy
 Stupor
 Coma

Ammoniogenic Encephalopathy: Tx

Decrease nitrogen load/remove precipitants
◦ Drain urine diversion
◦ Limit dietary protein intake
◦ Treat any systemic or UTI
◦ Lactulose
 Lowers gut pH so more NH4 than NH3
 Promotes non-urease producing bacteria
 Decreases transit time of fecal matter
 Complexes the ammonia
◦ Neomycin/tetracycline
 Eliminate ammonia producing bacteria from the GIT
◦ Arginine glutamate
 Complexes ammonia
Abnormal Drug Metabolism
Drugs absorbs in GIT
 Drugs excreted unchanged in urine
 Reabsorbed in intestinal segment

Abnormal Drug Metabolism

List of drugs
◦ Dilantin
◦ Methotrexate/chemo
◦ Theophylline
◦ Abx (beta-lactams, nitrofurantoin, aminoglycosides)

ChemoTx
◦ Ensure pt well hydrated
◦ Drain diversion with catheter
◦ Consider leukovorin administration with methotrexate
Osteomalacia
Potential long-term complication
 Affects children and adults
 Bone demineralization
 Mineralized component of bone is replace
with osteoid

Osteomalacia


Risk Factors
◦ Bowel segment used
 Ureterosig most commonly
 Colon or ileal cystoplasties
 Colon or ileal conduits/neobladders
◦ Renal failure
Chronic untreated metabolic acidosis
Osteomalacia: MOA





Bone buffering of chronic metabolic acidosis
Vit D resistance – less Ca absorption by GIT
Vit D deficiency – acidosis limits vit D production
Sulphate in urine inhibits Ca and Mg re-absorption
Resitance to PTH
◦ = Ca loss
Osteomalacia

Symptoms
◦
◦
◦
◦
◦
Diffuse skeletal pain
Bone tenderness
Fractures
Gait disturbance
Proximal muscle weakness
Osteomalacia

Prevention
◦ Particularly important in postmenopausal
women and children
◦ Tx underlying metabolic acidosis
Vit C
 Vit D
 Activated Vit D metabolite

◦ 1-alpha-hydroxycholecalciferol
◦ Ca supplementation
Vitamin Deficiency
ADEK – fat soluble lost in malabsorption
of fat
 Vit B12 – absorbed in distal ileum

Vitamin B12 Deficiency: Etiology








Not synthesized by mammals – only dietary source
B12 released from food by enzymes in stomach
Bound to IF in duodenum
Absorbed in terminal ileum
Stored mainly in liver
Total body stores of 2-5mg, loss of 0.1% daily
Takes 2-4 years for defeciency to take effect
3-20% incidence after terminal ileum resection
Vitamin B12 Deficiency: Symptoms
Neurologic
◦ Peripheral neuropathy
◦ Degenerative changes/demyelination in spinal cord
◦ Voiding dysfunction
◦ Optic neuropathy
 Hematologic
◦ Megaloblastic anemia
 Inflammation of tongue/mouth
 Psychiatric disturbances

Vitamin B12 Deficiency: Labs
MCV > 120
 Often neutropenia and thrombocytopenia
 Hypersegmented neutrophils
 Low serum B12 levels

Vitamin B12 Deficiency: Bowel
Segment

Continent diversion increased risk
◦ Larger bowel segment used
◦ TI/IC junction resection
◦ Resection of > 50cm appears to be a major
risk factor
Vitamin B12 Deficiency: Tx

Prevention
◦ Replace with 100ug cobalamin IM monthly
starting 1 year after surgery if > 50cm ileum
resected

Treatment
◦ Neurologic symptoms may precede other
◦ Treat if the least bit concered
◦ Treat if lab values are abnormal but
asymptomatic
Surgical Complications

Early
◦
◦
◦
◦
◦
◦
◦
◦
◦
Wound infection
Intra-abdominal abscess
Pyelonephritis
Hemorrhage
Urine leak/fistula
Bowel leak/fistula
Ileus
Bowel obstruction
Stomal bleeding/necrosis
Surgical Complications

Late
◦
◦
◦
◦
◦
◦
◦
◦
Wound hernia or dehiscence
Bowel obstruction
Ureteral stricture
UTI/pyelo
Urinary stones
Renal deterioration
Stomal stenosis/parastomal hernia
Hematuria dysuria syndrome
Stomal Complications

Early
◦ Bleeding
◦ Necrosis

Late
◦
◦
◦
◦
◦
Dermatitis
Retraction
Prolapse
Parastomal hernia
Stenosis
Stomal Bleeding

Early
◦ Conservative Tx
◦ Most will stop with pressure/time

Late
◦
◦
◦
◦
Liver disease due to dilated veins
Correct coagulopathy
Ligation
Porto-systemic shunting
Parastomal Hernia

Incidence
◦ 10% ileal conduit
◦ 20% colon conduit

Risk Factors
◦
◦
◦
◦
◦
◦
◦
Wound infection
Steriod use
Malnutrition
Obesity
Chronic cough/COPD
Advanced age
Stomal not brought out through rectus muscle
Stomal Stenosis

Incidence
◦ 3-25% of ileal conduits
◦ 10-20% of colon conduits
◦ Catherizable stoma – 50%

Brooke > Turnbull loop
Stomal Stenosis

Risk Factors
◦ Catherizable > end > loop
◦ Technical
 Protruding better and flushed for non-continent
 Insufficient fascial opening
◦
◦
◦
◦
◦
Muscle spasm
Ischemia
Infection
Poor stomal hygiene
Poor fitting appliance
Stomal Stenosis

Symptoms
◦ Suspect in




Metabolic disturbance
Infection/pyelo/sepsis
Stones
Renal decline
Stomal Stenosis


Work-up
◦ Conduit residual urine
◦ Loopogram
 Elongation
 Reflux with upper tract dilation
 Segment stenosis
Tx
◦ Requires surgical repair
Ureteroenteric Stricture

Risk Factors
◦ Technical
 Tension
 Stripping ureteric blood supply
 Insufficient window through colon mesentery
 No mucosal to mucosal apposition
◦ Infection
◦ Stone passage
◦ Radiation
◦ IBD
◦ Previous urine leak
Ureteroenteric Stricture

Symptom
◦ Stones
◦ Back pain
◦ Infection/sepsis

DDx
◦ Ureteral stone
◦ TCC recurrence
Ureteroenteric Stricture
Imaging
 US
 Loopogram
 CT/IVP
 Renogram
 Antegrade Nephrostogram

◦ Most useful
◦ Diagnostic/therapeutic
◦ Tract for antegrade procedure
Ureteroenteric Stricture

Tx
◦ Endoscopic
 Antegrade vs retrograde
 Balloon dilation
 Cold knife
 Laser incision
◦ Open
Ureteroenteric Stricture

Advantages of Endoscopic
◦
◦
◦
◦
◦
◦

Reasonable 1st line Tx
Less morbidity
Less OR time
Less blood loss
Shorter hospital stay
Pt. with metastatic disease
Disadvantages
◦ High failure rate
◦ May complicate open repair
Ureteroenteric Stricture

Factors associated with failure of
endoscopic repair
◦ Length > 1cm
◦ Stricture presenting < 6 months since surgery
◦ Left sided stricture
Ureteroenteric Anastomosis
Ureteroenteric Stricture
Procedure
Stricture
Colon
Leadbetter-Clarke
14%
Strickler
14%
Pagano
7%
Small Bowel
Bricker
7%
Wallace
3%
Nipple
8%
Le Duc
18%