Diagnosis

Diagnosis

  • Primarily a diagnosis of exclusion
  • Symptoms of unremitting frequency, sensory urgency, and/or pelvic pain associated with the bladder in the absence of other causes suggest IC.
  • Bladder biopsy is necessary only if needed to rule out other etiologies of the patient's symptoms.
  • Bladder distention to 80cm water pressure under anesthesia can be helpful in confirming the diagnosis
    • Glomerulations, while not specific for IC, are suggestive of diagnosis
    • Provides short-term symptom relief in one-third of patients
    • May effect treatment algorithm if Hunner's ulcer is identified upon distention (approximately 10% of cases), or bladder capacity under anesthesia is less than 200mL.
    • Need for cystoscopy in the absence of microhematuria is controversial.
  • Urodynamics can differentiate sensory from motor urgency.

Etiology

  • May be multifactorial, and a syndrome or symptom complex rather than specific disease
  • Infection
    • Not considered a likely etiologic factor
    • No evidence of bacterial, viral, or fungal infection
  • Abnormality in bladder lining
    • Possible deficiency or abnormality of glycosaminoglycan layer allowing molecular leaks of urinary constituents into the bladder wall
      • Intravesical potassium instillation causes significantly more pain in the following conditions compared to controls: IC, urinary infection, radiation cystitis, and in 25% of patients with detrusor instability
  • A toxic component in the urine may be responsible
    • Pain in augmented bladders and neobladders as well as pouches can develop years after diversion for IC
    • An antiprolilferative factor in the urine of IC patients has been identified that appears to be made or activated in the distal ureter or urinary bladder. Such a factor, that inhibits normal bladder epithelial regeneration, could be causally related to IC and may prove to be a reliable marker for the disorder in the near future.
  • Mast cell release of vasoactive and nociceptive substances with secondary sentization of sensory neurons -- may be a primary or secondary etiologic agent
  • Autoimmunity
    • Suggested by relationship of systemic problems including Sjogrens syndrome, inflammatory bowel disease, systemic lupus in a minority of patients

References

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