Diagnosing and Managing Interstitial Cystitis
Chronic pelvic pain (CPP) is commonly encountered in the primary care office, affecting nearly 1 in 7 women in the United States.1 Interstitial cystitis is one of the causes of chronic pelvic pain and may be more common than previously thought. In the past, IC has been labeled a diagnosis of exclusion: urinary urgency/frequency and/or pelvic pain in the absence of any other definable cause. In fact, IC can be readily identified from its symptom complex and therefore, should be diagnosed without numerous tests or procedures. The characteristic symptoms and patterns of IC presentation are listed in Table 1.
This article has been written from a dual-specialty prespective as the authors include a primary care physician and a gynecologist. Collaboration on this article resulted from the mutual belief that early intervention by a primary care clinician can significantly impact patient outcomes. Referral to a specialist may be avoided if primary care clinicians understand that a large number of patients in the primary care population may have IC, and that these patients can be diagnosed and treated successfully. The goal of managing IC is finding and treating the disease in its early stages, thereby reducing the number of advanced cases, which tend to be resistant to current therapies.
An Overview of the Pathogenesis of CPP
Pain serves as an important alarm that warns us of threatened or ongoing tissue damage. However, chronic pain can become the true pathology — the “disease” that can be disabling. The neuropathology of chronic pelvic pain has been nicely reviewed by others and is beyond the scope of this article.2,3
Key points include the fact that a prolonged barrage of noxious stimuli can result in changes in the sensory processing of all stimuli entering the dorsal horn and this results in allodynia (when a non painful stimulus is perceived as painful).4 This is an example of the neuroplasticity of the dorsal horn and is a key component in the pathogenesis of visceral pain syndromes such as endometriosis, irritable bowel syndrome and interstitial cystitis.
This up-regulated state within the dorsal horn also results in neurogenic inflammation in neighboring organ systems (this “cross-talk” is referred to as viscero-visceral hyperalgesia) and in the pelvic floor musculature becoming hypertonic and tender (this is referred to as pelvic floor tension myalgia).5
Chronic pelvic pain syndromes and especially visceral pain syndromes involve neurogenic inflammation, afferent overactivity and central sensitization, which interact to perpetuate pain. This model of chronic pain explains why therapeutic approaches must involve the treatment of all pain generators because all of these new pain generators project their noxious stimuli into the same dorsal horn segments. It has been shown that approximately 75% of women seen by a gynecologist for complaints of a variety of chronic pain syndromes also have symptoms of urgency, frequency or irritative voiding symptoms.6 Therefore there is an obvious overlap of IC and CPP syndromes that the clinician must be aware of and be prepared to identify and treat.
The Suspected Pathogenesis of IC
The basic role of the bladder is to hold and void urine.7 The bladder is not intended to be an absorptive organ, nor should it possess any sensory component of its contents beyond pressure. Normally, urothelium is shielded from the urine by a glycosaminoglycan (GAG)-containing mucous layer.8 IC is thought to occur when the protective GAG layer becomes defective, therein allowing irritative substances from the urine to aggravate the urothelium and cause inflammation and neurgenic upregulation in the bladder wall.9 The resultant disease process is marked by symptoms of urinary urgency, frequency, pelvic pain, and occasional urinary hesitancy.
Studies suggest potassium may be the urinary constituent primarily responsible for evoking the symptoms of IC.9 Various other factors have also been investigated for their potential roles in the pathogenesis of IC including lymphatic, infectious, neurologic, psychologic, autoimmune, and vasculitic. These factors have not yet been proven to be pertinent to this disease process.
Familiarity with disease presentation facilitates easy recognition of IC by the primary care clinician. The general pattern of IC symptoms is quite unique, though an affected patient may report some variance from day to day.
|Therapeutic Approach||% of
|Biofeedback (relaxation phase)||63%|
|*Oral agents including Amitriptyline: 59%, PPS: 54%, NSAID: 54%|
As previously mentioned, a patient with IC generally suffers from urinary urgency/frequency and pelvic pain. However, the disease should not be dismissed in the absence of one or two of these symptoms. A study by Parsons et al of 466 women and men with IC found that 9% had pain alone, and 8% only had urgency.10