Bladder carcinoma- augmentation cystoplasty complications

Bladder carcinoma- augmentation cystoplasty complications

1. Dept of Urology
GovtRoyapettahHospital and KilpaukMedical College
Chennai
Complications of Augmentation
Cystoplasty
1

2. Moderators:
Professors:
Prof. Dr. G. Sivasankar, M.S., M.Ch.,
Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
Dr. J. Sivabalan, M.S., M.Ch.,
Dr. R. Bhargavi, M.S., M.Ch.,
Dr. S. Raju, M.S., M.Ch.,
Dr. K. Muthurathinam, M.S., M.Ch.,
Dr. D. Tamilselvan, M.S., M.Ch.,
Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC, Chennai.
2

3. Indications
Neuropathic
Spinal cord injury
Multiple sclerosis
Myelodysplasia
Tethered spinal cord
Non neuropathic
Tuberculosis and
Schistosomiasis
Detrusorinstability
Interstitial cystitis
Radiation cystitis
Cloacalexstrophy
Certain complications noted may be specific to patients with neurologic disease
Creatinineclearance of < 15 ml/minute can be considered as a contraindication
(Kusset al)
3
Dept of Urology, GRH and KMC, Chennai.

4. Usual Scenario
1.Non compliant ,contracted bladder
not responded to non operative
management
2.Capacity of < 100 ml
3. Intolerable symptoms
4
Dept of Urology, GRH and KMC, Chennai.

5. Bowel is the gold standard for bladder augmentation
5
Dept of Urology, GRH and KMC, Chennai.

6. Limitations
The gastrointestinal tract is a relatively poor substitute for
urothelium
Semi-permeability permits nonphysiologicalfluid and
electrolyte absorption, leading to metabolic abnormalities.
The loss of various portions of the gastrointestinal tract can
interfere with normal gastrointestinal function, resulting in
metabolic complications such as chronic diarrhea
6
Dept of Urology, GRH and KMC, Chennai.

7. 7
Dept of Urology, GRH and KMC, Chennai.

8. Early Complications
Cardiovascular, pulmonary, gastrointestinal and thrombo
embolic perioperative events
A mortality rate as high as 2.7% -in older literature
Greenwell et al(2001) -no deaths in 267 patients undergoing
bladder augmentation (follow up ≥5 yrs)
Other noted early surgical complications include-
1.9% to 5.7% risk of bowel obstruction requiring intervention
Risk of a significant wound infection of ≤6.4%
Bleeding requiring blood transfusion is seen in ≤3%
8
Dept of Urology, GRH and KMC, Chennai.

9. Early bladder anastomoticleak
Incidence low
Prevented by
optimal bladder drainage -achieved with use of both urethral
and suprapubiccatheter
Adequate drainage of perivesicalspace
Regular irrigation to evacuate mucus
9
Dept of Urology, GRH and KMC, Chennai.

10. Cystogram
Early post operative leak 10
Dept of Urology, GRH and KMC, Chennai.

11. Management
Small anastomoticleaks heal on their own with adequate
drainage
When conservative therapy fails to heal clinically significant
anastomoticleaks-percutaneousdrainage of both kidneys
and drainage of urinoma, if one is present
Rarely, anastomoticleak caused by an ischemic bowel
segment-Laparotomywith resection of the nonviable
segment and repeat anastomosis
11
Dept of Urology, GRH and KMC, Chennai.

12. Long term complications
Specific to bowel segment
Metabolic
Mechanical
Neoplastic
12
Dept of Urology, GRH and KMC, Chennai.

13. Ileum
Advantages
abundant supply of small bowel,
predictable and abundant mesenteric blood supply,
compliance relative to that of other bowel segments
moderate mucous production compared to colon
Less severe associated metabolic complications compared to
stomach or colon
13
Dept of Urology, GRH and KMC, Chennai.

14. Contraindications
History of
short gut syndrome,
inflammatory bowel disease
pelvic and abdominal irradiation
significant renal insufficiency
14
Dept of Urology, GRH and KMC, Chennai.

15. Ileocystoplasty
Mcguiremodification
15
Dept of Urology, GRH and KMC, Chennai.

16. Colon
Shorter mesenteries can make mobilization and
reconfiguration of the large bowel more difficult.
Colon is associated with a greater degree of mucus formation
16
Dept of Urology, GRH and KMC, Chennai.

17. Coloplasty
Mainz cystoplasty
Sigmoid cystoplasty
17
Dept of Urology, GRH and KMC, Chennai.

18. Acidosis
In intestinal urinary diversion
the net absorption of NH4 is the major contributor to
increased acid load and metabolic acidosis
To a lesser extent
bicarbonate losses,
the use of bicarbonate to titrate endogenous and ingested acids,
inability of the kidneys to secrete acid
18
Dept of Urology, GRH and KMC, Chennai.

19. 19
Dept of Urology, GRH and KMC, Chennai.

20. Incidence
50% of patients with ilealbladder
More than 50% with a colonic reservoir have hyperchloremic
metabolic acidosis
Ureterosigmoidostomieshave even higher rates of metabolic
acidosis-80%
Mucosal atrophy and decreased villous height-mechanism for
decreased intestinal absorptive capacity
20
Dept of Urology, GRH and KMC, Chennai.

21. Incidence
In older series, hyperchloremicacidosis was reported in up
to 68% of patients with an ilealconduit, major problem in
18%
Symptoms-easy fatiguability, anorexia, weight loss,
polydipsiaand lethargy
21
Dept of Urology, GRH and KMC, Chennai.

22. Treatment
Alkalinizationwith
Oral Sodium bicarbonate-1meq/kg/day ;not tolerated due to
excess gas , 325-650 mg tablets given 4-6 times/d
Sodium citrate and Citric acid solutions-taste unpalatable
Chlorpromazine or Nicotinic acid may limit the degree of
acidosis and decrease the need for alkalinizing agents-
Mechanism-Inhibiting cyclic AMP and impeding chloride
transport
Side Effects-Tardivedyskinesia, liver disease, g.i. bleed
22
Dept of Urology, GRH and KMC, Chennai.

23. Hypokalemia
Renal potassium wasting
Chronic metabolic acidosis causing intracellular potassium
depletion
Ilealsegments -greater capacity for potassium reabsorption
compared to colon segments
Continent colon urinary diversions and uretero
sigmoidostomiescarry an increased risk of hypokalemia
compared to ilealneobladders
23
Dept of Urology, GRH and KMC, Chennai.

24. Treatment
Replacing potassium in addition to correcting acidosis with
bicarbonate
Care must be taken since the correction of acidosis results in
an intracellular potassium shift and can lead to profound
hypokalemia, flaccid paralysis
24
Dept of Urology, GRH and KMC, Chennai.

25. Hypocalcemia
Uncommon
Chronic metabolic acidosis results in the loss of calcium
stores from bone as phosphates and sulfates are used to buffer
the acids
Symptoms include tetany, tremors, irritability and in
extremely severe cases death
Treatment is based on calcium repletion
25
Dept of Urology, GRH and KMC, Chennai.

26. Hypomagnesemia
Magnesium malabsorption
Renal loss
Decreased renal tubular absorption secondary to acidosis
Symptoms are similar to those that occur with low calcium
levels
Treatment consists of exogenous replacement
26
Dept of Urology, GRH and KMC, Chennai.

27. Stomach
Metabolic benefits of gastric cystoplasty
intestinal sparing
prevention of short bowel syndrome,
decreased occurrence of hyperchloremicmetabolic acidosis
decreased mucus production
Translates into lower rates of urine infection and stone
formation
Helps those with renal failure/ chronic acidosis
27
Dept of Urology, GRH and KMC, Chennai.

28. Gastrocystoplaty
28
Dept of Urology, GRH and KMC, Chennai.

29. Complications
Acute gastrointestinal illness -precipitate severe metabolic
alkalosis requiring hospitalization, particularly in patients
with baseline renal insufficiency
Resulting in severe dehydration and hypochloremic,
hypokalemicmetabolic alkalosis
Clinical presentation-ranging from lethargy and mental
status changes to intractable seizures
In severe cases-respiratory compromise related to the
compensatory respiratory acidosis seen
29
Dept of Urology, GRH and KMC, Chennai.

30. Treatment
Normal saline infusion and potassium repletion
Minimal alkalosis-histamine-2 blockers and anticholinergic
therapy
In severe cases of alkalosis that are not responsive to more
standard therapy omeprazolecan be used to inhibit K/H ion
exchange
30
Dept of Urology, GRH and KMC, Chennai.

31. Hematuria–Dysuriasyndrome
Dysuria, genital skin irritation and excoriation, bladder spasms,
suprapubicand/or urethral pain and gross hematuria-30% cases
Etiology -Chemical irritation of the urothelium
Treatment includes
Increased fluid intake,
Correction of potassium abnormalities,
Use of histamine-2 blockers,
Anticholinergicagents and omeprazole
Rarely removal of the gastric segment
Less frequent after antralcystoplasty(smaller load of parietal
cells)
31
Dept of Urology, GRH and KMC, Chennai.

32. Jejunum
Should not be used for enterocystoplastybecause of the
metabolic cost
Electrolyte abnormalities
increased secretion of sodium and chloride
increased reabsorptionof potassium and hydrogen ions,
resulting
Hyponatremic, hypochloremic, hyperkalemic, azotemic
metabolic acidosis
The excess loss of sodium chloride causes osmotic diuresis,
resulting in severe water loss and dehydration and
stimulation of the renin-angiotensin-aldosteronesystem
32
Dept of Urology, GRH and KMC, Chennai.

33. Metabolic Problems
Aldosteronemay also increase secondary to hyperkalemia.
The high levels of reninand aldosteronefacilitate renal
sodium reabsorptionand potassium loss, producing urine
low in sodium and high in potassium
Favorable concentration gradient for sodium loss and
potassium reabsorptionby the jejunum, thus perpetuating
electrolyte abnormalities
33
Dept of Urology, GRH and KMC, Chennai.

34. Jejunalsyndrome
Symptoms -lethargy, nausea, vomiting, dehydration,
muscular weakness and fever.
More commonly seen when the proximal jejunum is used
Incidence is directly related to the length of segment used
34
Dept of Urology, GRH and KMC, Chennai.

35. Hyperammonemia
Urinary ammonium excreted by the kidneys is reabsorbed by
the intestinal segment
NORMALLY returned to the liver through the portal
circulation and then metabolized to urea through the
ornithinecycle
In liver dysfunction the metabolic reserve may be exceeded-
lead to ammoniagenicencephalopathy and coma
Systemic bacteremiaand urinary tract infections with urea-
splitting organisms can impair the hepatic metabolism -
hyperammonemiasyndrome, even with normal hepatic
function
35
Dept of Urology, GRH and KMC, Chennai.

36. Treatment
Maximizing urinary drainage from the diversion to minimize
the time with which ammonia is in contact with mucosa
Systemic antibiotics are indicated in the presence of infection
Neomycin or Lactulose-bind ammonia and decrease
gastrointestinal absorption
36
Dept of Urology, GRH and KMC, Chennai.

37. Vitamin B 12 deficiency
15 cm of ileum proximal to the ileocecaljunction should be
spared
B12-intrinsic factor complex binds to intrinsic factor
receptor in the distal ileum
Vitamin B12 is stored in the liver and reserves last
approximately 3 years
Megaloblasticanemia and neurological consequences,
including peripheral neuropathies, optic atrophy,
degenerative changes in the spinal cord involving the
dorsolateralcolumns and dementia
Axonal degeneration is a late and irreversible manifestation
37
Dept of Urology, GRH and KMC, Chennai.

38. Treatment
The incidence is from 3% to 20% when ileum is used
Continent urinary diversion increases the risk because larger
sections of ileum are needed and the ileocecaljunction may
be incorporated into the diversion
Panneket al reported that 50 cm ileum -critical limit of
length used in diversions
To prevent vitamin B12 deficiency they recommended
beginning intramuscular injections of 100 µg
hydroxycobalaminmonthly 1 year following surgery
38
Dept of Urology, GRH and KMC, Chennai.

39. Renal function
Direct detrimental effect on long-term renal function has not
been well defined
Fountaineet al studied 53 patients with intestinal urinary
reservoirs in a 10-year period using the creatinineEDTA
measured glomerularfiltration rate(GFR)
Mean GFR decreased from 97.9 to 92.9 ml per minute per
1.72 m^2
Jonsson et al-long-term decrease in GFR measured in 126
patients with continent urinary diversion was similar to that
observed normally with aging
39
Dept of Urology, GRH and KMC, Chennai.

40. Steatorrhoea
Removal of more than 100 cm of ileum results in bile acid
and lipid malabsorption, even in the presence of an intact
terminal ileum and ileocecalvalve
When fecal losses of bile acids exceed hepatic production-
Steatorrheaoccurs with impaired absorption of fat and
consequently fat soluble vitamins (A, D, E and K)
The secretorydiarrhea -severe chemical irritation of the
colon -results in excessive loss of chloride and water
40
Dept of Urology, GRH and KMC, Chennai.

41. Steatorrhoea
Treated with oral cholestyramine(anion exchange resin) and
a low fat diet
Diarrhea secondary to removal of the ileocecalvalve -
managed by codeine or diphenoxylateand atropine in an
attempt to decrease the intrinsic transit time
Long-term complications of fat malabsorption
Hyper triglyceridemia
Increased risk for gallstones
41
Dept of Urology, GRH and KMC, Chennai.

42. Bone disease
Chronic acidosis can result in bone demineralization after
enterocytoplasty, resulting in rickets in children and
osteomalaciain adults
Bone releases carbonate and phosphate into circulation to
buffer excess hydrogen ions
Skeletal calcium content is decreased
Bone mineral is replaced with osteoid, resulting in decrease
in bone strength-fractures
42
Dept of Urology, GRH and KMC, Chennai.

43. Bone disease
Acidosis appears to
inhibit the conversion of 25OH cholecalciferolto 1,25-
(OH)cholecalciferolby the kidney
activate osteoclasts
Most patients are asymptomatic;haveNormal PTH and
vitamin D levels
Initial treatment –correction of acidosis
In the setting of failed re-mineralization -calcium and
vitamin D supplements used
43
Dept of Urology, GRH and KMC, Chennai.

44. Growth
Mundy et al noted a halving of growth rate in 20% of
children undergoing colocystoplasty
Recent data with confounding factors removed suggest that
urinary intestinal diversion is not associated with growth
retardation
Vajdaet al prospectively study-
Metabolic acidosis greater with Cecum/Asc. colon 58% vs31%
Linear Growth retardation more with sigmoid (56%)
Ileum, as opposed to colon is able to reabsorb calcium
44
Dept of Urology, GRH and KMC, Chennai.

45. Bacteruria
Asymptomatic bacteriuriaand colonization of the urinary
tract common-65 to 100%
Recurrent symptomatic urinary infections occurred in
23% of patients after ileocystoplasty
17% after sigmoid cystoplasty
13% after cecocystoplasty
8% after gastrocystoplasty
Febrile UTI occurred in 13% of patients
Asymptomatic bacteriuriashould not be treated with
antibiotic
Risk factors-mucus production, urinary stasis, PVR, CIC
45
Dept of Urology, GRH and KMC, Chennai.

46. Infection
Cannot rely on the typical symptoms of UTI such as
frequency, urgency, and dysuria
Patients with NGB may have vague symptoms such as an
increase in spasticity, malodorous or cloudy urine, symptoms
of concomitant autonomic dysreflexia
Patients have fewer instances of postoperative UTI related to
secretion of immunoglobulin A by the bowel
Urine cultures positive for urea splitting organisms-treat to
prevent stones
46
Dept of Urology, GRH and KMC, Chennai.

47. Management
Imaging of the upper and lower urinary tract -to rule out
potential sources of infection
Irrigate the bladder regularly during CIC-to remove mucus
Change to sterile CIC with one-time use catheter kits
Hydrophilic catheters may be helpful in decreasing the risk of
recurrent UTI
47
Dept of Urology, GRH and KMC, Chennai.

48. Calculus Disease
Incidence 18-30%
Risk 5 times if CIC through the native urethra and
10 times if CIC through a continent urinary stoma
Risk factors-chronic dehydration, urine stasis, mucus
production, colonization with urea-splitting organisms, use
of CIC, exposed staples
In addition, enteric hyperoxaluria; hypocitraturiasecondary
to chronic acidosis, increased mobilization of calcium from
bone stores and impaired reabsorptionin the distal renal
tubule-hypercalciuria-CALCIUM OXALATE STONES
48
Dept of Urology, GRH and KMC, Chennai.

49. Calculus Disease
Lower incidence of stone with gastrocystoplasty-due to
Lower urinary pH,
Less mucus production,
Lower incidence of bacteriuria
Symptoms of stones include hematuria, recurrent UTI and
deterioration of urinary continence
Diagnosed mostly during routine radiographic
follow-up/USG
49
Dept of Urology, GRH and KMC, Chennai.

50. Management
Large stones –open removal
Percutaneouscystolithotomyshould be considered in
pediatric patients small urethra
Remove all the stone material because any remaining
fragments can serve as a nidusof recurrent stone formation
Potential risk of unidentified perforation through the much
thinner bowel-always drain with catheter
50
Dept of Urology, GRH and KMC, Chennai.

51. Stones in augmentation
X-KUB showing calculi51
Dept of Urology, GRH and KMC, Chennai.

52. Prevention
Fluid intake, adequate drainage , frequent irrigations,
antibiotics for infection
Low fat diet, avoid oxalates
Calcium citrate supplements
Prophylactic irrigation protocol -43% versus 7%; (P < .001)
in the incidence of stone formation --240 mLsaline solution
twice a week and 120 to 240 mLgentamicinsulfate solution
(240-480 mg/L)
52
Dept of Urology, GRH and KMC, Chennai.

53. Tumors
Incidence-56 such tumors reported, including 31 involving
ilealsegments and 25 in colonic segments
• Most of the cancers occurred in patients that had
tuberculosis or chronic cystitis
• Anastomoticsuture line at greatest risk
• “Lag time” greater than tenyears
•Adenocarcinoma, TCC, carcinoid,sarcoma
15 to 25 years after diversion
30% patients die due to tumors
53
Dept of Urology, GRH and KMC, Chennai.

54. TUMORS
INDIANA SERIES -
• 260 cases
• All with greater than 10 year follow up
• 3 patients with Metastatic TCC
• Mean time from augmentation 19 years
• Overall cancer risk 1.2%
•Augmentation-Independent risk factor for subsequent TCC
Soergelet al, 2004
54
Dept of Urology, GRH and KMC, Chennai.

55. Pathogenesis
Risk factors-chronic inflammation of the augment patch,
recurrent UTI, and urinary stasis
Nitrosamines have been implicated in tumors associated with
urinary conduits and ureterosigmoidostomies
Cytologicexamination is often unreliable secondary to a
chronically infected state
55
Dept of Urology, GRH and KMC, Chennai.

56. Management
Cystoscopicevaluation and surveillance regimen starting
annually after 5 or 10 years
Treatment requires radical cystectomy, removal of the
augment segment and reconstruction
56
Dept of Urology, GRH and KMC, Chennai.

57. Perforation
• Life threatening complication
• 7-15%, Indiana Univ-10%
30% recurrent perforation
• Risk factors -
Overdistensionsecondary to poor patient compliance
Bladder hyperreflexia
Chronic infections
Traumatic catheterization
Chronic bowel wall ischemia secondary to chronic over distention
Competent bladder outlet that does not allow for a “pop-off” of
urine
57
Dept of Urology, GRH and KMC, Chennai.

58. Evaluation
Acute Abdominal pain, distension, nausea, vomiting,
shoulder pain, oliguriaand fever
Insensate patients are at greater risk and typically present
later-high index of suspicion is necessary
Use of ileum decreased the risk of perforation
Cystogrammay show extravasation; however, ≤24% of
patients may have normal study results
CT urogrammay be superior to a cystogramin identifying a
perforation
58
Dept of Urology, GRH and KMC, Chennai.

59. Treatment
Most common site -is either the junction
between the bowel and the bladder wall or the
augment segment
Treatment -abdominal exploration
Conservative management-catheter drainage
of the bladder and percutaneousdrainage of any
intra-abdominal fluid collections-stable patient
who do not show signs of progression or
worsening of their symptoms
59
Dept of Urology, GRH and KMC, Chennai.

60. Hour glass stricture
Bladder has a great
tendency to reform itself,
turning the augmentation
into a diverticulumwith a
relatively small opening
60
Dept of Urology, GRH and KMC, Chennai.

61. Prevention
Bladder should be bivalved
(‘clamshelled’) from the
bladder neck ventrally to
the trigoneposteriorly
If bladder is small and thick
walled, the ‘star’
modification
Preserve urothelium,
shorter catheter duration
61
Dept of Urology, GRH and KMC, Chennai.

62. Incontinence
Nocturnal incontinence
decreased urethral resting pressure,
increased urinary output at night
failure of the sphincter to increase its resting tone in response to
bladder contractions
Incompetent outlet preoperatively can lead to symptoms of stress
urinary incontinence
Leak secondary to inadequate bladder augmentation
inadequately small piece of intestine,
an impaired blood supply to the augment segment that leads to
decreased capacity or compliance,
the presence of bowel mass contractions
62
Dept of Urology, GRH and KMC, Chennai.

63. Management
Evaluation -voiding diary and urodynamicstudy
Rule out excessive fluid intake and infrequent CIC
Inadequate sphincter -pubovaginalsling, bladder neck
reconstruction, bladder neck closure and artificial urinary
sphincter
Anticholinergics, Botulinumtoxin
Repeat bladder augmentation with ileum-if colon, stomach
used previously
63
Dept of Urology, GRH and KMC, Chennai.

64. Pregnancy
Problems -UTI or pyelonephritis, renal deterioration,
ureteralobstruction and premature labor
Hill and Kramer-15cases-pyelonephritisin 60% and
premature labor in 25% of patients
Vaginal delivery is safe for all patients who had prior bladder
augmentation
Cesarean section through a classic upper segment approach
It may be helpful to have a urologist available to understand
reconstructive anatomy
64
Dept of Urology, GRH and KMC, Chennai.

65. Infection of a ventriculoperitoneal
shunt
Unusual issue that should be specifically watched for-eg.
myelomeningocele
Prevention
Appropriate perioperativeantibiotics
minimize any risk of intestinal spillage
use of the extraperitonealaugment
Symptoms-fever, headaches,lethargy,changein vision and
mental status, seizures
Treat with broad spectrum antibiotics, neurosurgeon
consultation
65
Dept of Urology, GRH and KMC, Chennai.

66. Latex Allergy
Most commonly seen in patients with myelomeningocele
Wear nonlatexsurgical gloves and use latex-free catheters
and latex-free surgical drains
Symptom -Precipitous fall in BP
Treatment-instant interruption of contact with possible
antigens, copious irrigation of the field, expeditious
completion or termination of the surgical procedure
Volume expansion, resuscitation and management of
anaphylaxis
66
Dept of Urology, GRH and KMC, Chennai.

67. Where are we ?
67
Dept of Urology, GRH and KMC, Chennai.

68. Ureterocystoplasty
68
Dept of Urology, GRH and KMC, Chennai.

69. Autoaugmentation
69
Dept of Urology, GRH and KMC, Chennai.

70. 70
Dept of Urology, GRH and KMC, Chennai.

71. SeromuscularEnterocystoplasty
71
Dept of Urology, GRH and KMC, Chennai.

72. 72
Dept of Urology, GRH and KMC, Chennai.

73. The ideal technique
Will be one that:
' removes the need for intraperitonealsurgery ; prevents the risk
of intestinal adhesions;
' stops the development of intestinal mucus and stone formation;
' prevents the metabolic complications and potential bony
complications during adolescence;
' at the same time improves the patient's resistance to UTI;
' maintains the same degree of long-term, good, low pressure
urine storage
73
Dept of Urology, GRH and KMC, Chennai.

74. 74
Dept of Urology, GRH and KMC, Chennai.