Guest guest Posted July 23, 2001 Report Share Posted July 23, 2001 Hi all I'm sending this on again for 'newbie's' but it is a pay fee for site, so I'll just send the whole article, really sorry for the length, but hope it helps. Dee~ ----- Original Message ----- Interesting as they mention RSD (reflex sympathetic dystrophy), They also mention the Low Oxylate diet, Surgery, Dilators, Estrace,Bartholin glands, etc, much much more. Dee Vulvodynia: New Treatments L. lin, MD Vulvodynia is characterized by intractable burning pain and acquired introital dyspareunia, for which no obvious cause can be found. Mild to moderate cases of vulvodynia are associated with persistent vulvar burning and loss of sexual pleasure. In more severe cases, patients cannot have intercourse. Finally, a percentage of women have constant, disabling vulvar pain, bad enough to dominate daily life and cause withdrawal from normal activities. Is Vulvodynia a Sympathetically Maintained Pain? The questions haunting the management of vulvar pain syndromes are still the most basic ones--what establishes these chronic pain loops and how are they maintained? The answers probably lie in considering vulvodynia as a sympathetically maintained pain (rather than a conventional somatic pain). The established model for such a phenomenon is a group of chronic pain syndrome(s) now known as reflex sympathetic dystrophy (RSD). In essence, RSD is a combination--refractory, poorly localized pain and an exaggeration of the local inflammation. The first clinical example of an RSD was S. Wier 's observations made on soldiers who suffered partial gunshot transections of major peripheral nerves during the American Civil War. Writing several decades before the autonomic nervous system had been defined, recognized all of the essential elements: namely, (1) the burning nature of this pain; (2) spread beyond the distributions of the injured peripheral nerve; (3) the seemingly bizarre phenomena of allodynia (perception of non-noxious stimuli as pain); (4) hyperalgesia (exquisite pain from light touch), and the accompanying vasomotor instability, edema, and disrupted sweating; (5) the tendency toward impaired motor function in the regional musculature; (6) the eventual onset of dystrophic contracture with osteoporosis; and (7) the associated emotional lability. In this last regard, 's observations remain classic: The clinical features of vulvodynia fit the model of a sympathetically maintained pain (SMP). Specifically, vulvodynia begins as a sudden exaggerated response to any of a variety of tissue insults (e.g., yeast infection, childbirth trauma, hysterectomy, or a CO2 laser burn). Once established, the syndrome manifests as a disabling, regionalized, burning pain. Examination readily demonstrates that the pain and tenderness emanate from discrete foci of dysesthetic erythema, generally located proximal to Hart's line. Allodynia is reflected in the discomfort produced by wearing jeans or sometimes even normal underwear. Hyperalgesia is reflected in the exquisite tenderness evoked by gentle palpation with a cotton swab. Vasomotor instability is a prominent feature of vulvodynia, especially in areas that rebound after vestibulectomy or CO2 laser treatment. Minor trophic changes are common, such as hymenal fibrosis, clitoral obliteration, and eventual contracture of the fourchette. Histologic changes within biopsies from the hyperalgesic Skene's and Bartholin's ducts are completely nonspecific, until severe dystrophic fibrosis develops. Because of the absence of the usual structural or biochemical lesions, vulvodynia responds poorly to drugs aimed at blocking the peripheral pain cascade (steroids, nonsteroidals, and even opiates). Characteristically, once established, the pain loop of vulvodynia continues after the initiating insult is removed. Finally, vulvodynia sometimes responds to selective serotonin reuptake inhibitors (Paxil, Zoloft) or traditional tricyclic antidepressants (Elavil, Pamelor). Each of these features is characteristic of sympathetically mediated pains (e.g., RSD), but atypical for a somatic pain (e.g., broken limb, heart attack). Medical Treatments for Vulvodynia Within clinics specializing in vulvar pain, treatment of vulvodynia has been a challenge in the past 15 years. Traditionally, vulvodynia has been subdivided according to patterns of redness. The term vulvar vestibulitis syndrome describes the triad of introital dyspareunia, painful erythema at the hymenal sulcus (visible with the naked eye), and severe tenderness on gentle palpation with a cotton swab. Pruritic papillomatosis describes women with similar complaints but without visible inflammation. At colposcopy, however, both types of patients display the same vascular ectasia and irritated acetowhite epithelium. Whether these patterns have distinct causes or are just differences in severity within a single disease spectrum still is unresolved. In our experience, a more important distinction is whether the Bartholin's glands are involved. Most patients have pain only on the surface, which could arise either from focal hypervascularity (visible with the naked eye) or from diffuse hypervascularity (best seen with the aid of the colposcope). Most important, in this group, direct palpation of the Bartholin's fossae when the patient stands does not cause pain. Conversely, the group with deep pain report bruising, lancinating pain in the Bartholin's fossae, sometimes more severe than the burning discomfort produced by palpation of the inflamed duct orifice on the mucosal surface. Regardless of disease pattern, the efficacy of symptom-relieving agents is poor. Medical regimens can be curative, but results are unpredictable and limited. For example, topical 5FU cream may cure pruritic papillomatosis, but it rarely relieves established vestibulitis. In uncontrolled trials, interferon alpha injected into the vulvar connective tissues three times a week for over 4 weeks has relieved symptoms. Such injections are painful and benefits often transient, however. Finally, evidence from a controlled trial suggests that topical Estrace cream had a definite beneficial effect on the mucosal soreness component of vulvodynia. (as well as Lichen Sclerosus) In one case of episodic hyperoxaluria accompanied by mucosal soreness, the patient received calcium citrate to reduce crystal formation in the urine and was advised to avoid oxalate-rich foods, which led to a relief of the pain syndrome. Five years have lapsed since this case report, but the efficacy of this regimen has not yet been established by randomized clinical trial. Considering that a low oxalate diet has been promoted 'misleadingly' by a lay support group as an established treatment for vulvodynia, this hiatus in the scientific literature is a serious omission. Beyond the question of efficacy, myriad other important issues still await systematic investigation. We, at Sinai Hospital, radiographed 56 Bartholin's glands excised from patients with severe vestibulitis. Fifty-five of these glands were radiologically negative, but a pattern consistent with equivocal calcification was seen in one specimen. On microscopic reanalysis under polarized light, however, this sample also proved to be negative (Sonaglia: Unpublished data, 1994). Given the paucity of reliable information on this subject, should practicing physicians continue to prescribe this protocol in routine clinical situations or wait for answers to these questions? If future studies support the initial observations, then reduction of dietary oxalate and ingestion of calcium citrate tablets should be recommended to all suitable vulvodynia patients. Until and unless firm scientific evidence is found, however, manipulation of urinary oxalate levels should be accurately identified for what it is--an interesting but completely unconfirmed anecdote. Vestibulectomy for Vulvodynia Given the limitations of medical therapy, patients in the visible foci of perihymenal erythema generally have been treated by cold-knife resection of the minor vestibular glands and the adjacent hymen, with closure by downward advancement of the vaginal mucosa. This approach has an estimated 50% success rate, but drawbacks include disfigurement and scarring. Unfortunately, some patients are made worse by such surgery because of vascular rebound at the incision or obstruction of the Bartholin's ducts. Although vestibulectomy can produce good results, surgical removal of the hymenal ring and closure by vaginal advancement should be used as a last resort. Even when resective surgery is appropriate, reactive hyperemia surrounding the healed incision is a risk for which the flashlamp excited dye laser (FEDL) represents the only solution. More important, in patients not cured by vestibulectomy, subsequent therapy is complicated significantly by the resulting vestibular skin deficit, and often by Bartholin's duct obstruction. We believe there should be a reevaluation of the role of these operations. As a first surgical option, vestibulectomy is more invasive and perhaps less effective than selective photothermolysis. In refractory cases, vestibulectomy is probably insufficient because the removal of hyperemic surface mucosa does not address the problem of chronically painful Bartholin's glands (Fig. 37) (Figure Not Available) . The presence or absence of deep pain is the major prognostic determinant. In the surface-only group, final response rate to sequential dye laser therapy was 93% (complete response = 63%; partial response = 30%). In contrast, there were only two (4%) complete responses in the surface-plus-deep group. Of the 50 dye laser failures, 40 occurred in women with severe Bartholin's fossa pain. The major complication of dye laser therapy was acute mixed bacterial cellulitis severe enough to require treatment with intravenous antibiotics (ampicillin, clindamycin, and gentamicin). During the first 8 months, 17.2% of dye laser treatments were followed by bacterial cellulitis in the first postoperative week. We reduced the bacterial cellulitis rate to < 1% by following these preventive measures: Pretreatment with topical intravaginal antibiotics, using either 2% clindamycin phosphate suppositories in polyethylene glycol (taken for 3 days before surgery) or 100 mg oxytetracycline HCl in vaginal capsules taken 5 days before and 5 days after surgery)Intraoperative medications with corticosteroids, antihistamines, and anti-inflammatory drugs to reduce the already small component of thermal damage to the surface epithelium Intravaginal instillation of 30 g of polymyxin/bacitracin ointment at the end of surgery Application of specially formulated zinc oxide paste 3× per day (bacitracin powder, 1.7 g; polymyxin B powder, 0.32 g; xylocaine powder, 4.8 g; zinc oxide to 240 g) Selective Photothermolysis with Visible Light Lasers We have explored a variety of laser therapies in search of a more reliable and less mutilating approach. In the mid-1980s we treated 36 patients with vulvodynia with the CO2 laser. Two strategies were used: (1) irritative acetowhite vestibular epithelium, showing low-grade koilocytotic atypia on biopsy, was photovaporized to the second surgical plane; (2) erythematous lamina propria surrounding painful vestibular and Skene's glands were "cylinderized" to a depth of about 1 cm. Lasting clinical remission was achieved in 22 (61.1%) instances. These successes were overshadowed, however, by the onset of exquisitely painful vestibular hyperemia in 9 (25%) women. It is again emphasized that (1) the irritative acetowhitening seen in vulvodynia is not caused by HPV infection, and (2) CO2 laser photovaporization is a fundamental error, which often leads to litigation. In 1987, foci of proliferating telangiectatic surface blood vessels were eradicated by argon laser photocoagulation in five such patients. CW blue-green argon energy has poor selectivity for hemoglobin, however. Damage to the adjacent stroma was almost as severe as that within the ectatic vessels, leading to severe postoperative pain, protracted healing, and considerable vulvovaginal cicatrization. Nonetheless, this observation had one important corollary. Long-term control in these five patients suggested that the blood vessels within these fields of reactive erythema were actual mediators of the chronic pain rather than nonspecific sentinels of some other underlying process. On the basis of these observations we hypothesized that the FEDL (an instrument designed specifically for the photocoagulation of small blood vessels within the superficial dermis of facial and upper body port-wine stains) might offer an efficacious but nonmorbid alternative to the bare fiber argon laser. A single FEDL surgery essentially stopped painful vestibular hypervascularity in 42 (29%) of the 168 women whose therapy began with selective photothermolysis. Further dye laser treatments were given to 126 women. In both instances, the likelihood of success was independent of visual pattern but was profoundly affected by the presence or absence of deep pain. Role of Resective Surgery Our findings indicated that in the presence of deep pain we had to address the problem of angry vessels radiating out of the Bartholin's fossa before surface hypervascularity could be controlled (Fig. 38) (Figure Not Available) . We therefore removed the Bartholin's gland using a microsurgically adapted CO2 laser through paired 15-mm vestibular incisions. Gland removal alone produced clinical remission in 12% (6/52 patients) and marked partial response in another 13 patients (25%). Serial FEDL treatment after gland removal raised response rates to 81% in the refractory surface-plus-deep group. We since have learned that most of our patients with persistent pain after Bartholin's gland removal have associated fibromyalgia within the levator ani muscles. This levator myalgia almost always can be cured by a program of biofeedback-controlled pelvic floor exercises. Comparing cumulative success rates with the number of surgeries performed, our surface-plus-deep group responded almost as well as the surface-only group, provided that the Bartholin's glands were removed. The importance of Bartholin's gland involvement also was reflected in our regression analyses of daily pain severity and dyspareunia scores. During the study period, the major complication of microsurgical Bartholin's gland resection was dyspareunia on stretching an otherwise well-healed scar (29.6%). This problem was treated successfully with steroid injection and local scar-releasing incision. We subsequently learned, however, that this problem could be prevented by use of a dilator from the fourth postoperative week. Other complications (hematoma, 1.9%; wound breakdown, 3.7%) reflected the learning curve, and we seldom see them today. Current Protocol for Managing Vulvodynia The data in our studies were collected primarily between 1989 and 1991. Throughout the years, we found marked Bartholin's fossa pain the pivotal prognostic determinant in our therapy for vulvodynia. Since that time, many practical advances have been made. Essentials of Diagnostic Assessment Because of the poor efficacy of pelvic floor exercises and initial photothermolysis in patients with extreme Bartholin's gland pain, different protocols are now used. Hence, the initial diagnostic workup addresses several important issues. To set landmarks that will define progress (or lack thereof), we first quantify dyspareunia and daily pain. This is best done by using semiobjective scales (see Table 13) (Table Not Available) . We measure pain intensity on the McGill visual analogue scale and gauge functional impairment from an ordinal list of activity disruptions. Through examination, we can map the severity and topography of any symptomatic hypervascularity, evaluate the levator muscles for hyperirritability, and establish whether there are associated dystrophic tissue changes (e.g., hymenal rigidity or posterior contracture). Most important, we examine the Bartholin's fossae with the patient in a standing position to establish the presence and severity of any deep pain loop.Surface-Only Vulvodynia At first, patients with deep pain responded poorly to serial FEDL therapy. Now, we use different protocols based on the presence and severity of Bartholin's fossa tenderness. Patients with surface-only pain or surface pain plus mild to moderate gland tenderness are started on biofeedback-controlled pelvic floor exercises and myofascial release of perineal trigger points in the hope that breaking the levator myalgia pain loop also will break the vulvodynia pain loop. We also offer tricyclic agents or selective serotonin reuptake inhibitors to patients with a causalgia-like component to their pain, and for those with symptoms of depression. Topical estrogen creams are generally tried. Nonresponders receive serial photothermolysis to break the sympathetically mediated pain reflex. Selective destruction of symptomatic subepithelial blood vessels and their accompanying sympathetic fibers is thought to reduce local norepinephrine levels, thus allowing the sensitized nociceptors (pain receptors) to reset back to a "normal" pain threshold.Vulvodynia With Severe Bartholin's Gland Pain Patients with surface-plus-deep pain need remedial pelvic floor exercises and serial photothermolysis as much as do the surface-only group. Because a fully established deep pain reflex seems to nullify the effectiveness of both biofeedback and laser therapy, however, we save these measures until after Bartholin's gland resection. The surgical protocol begins with a single FEDL or Hexascan surgery, aimed at reducing the risk of postoperative rebound hypervascularity during healing of the gland removal incisions. At first surgery, any dystrophic contracture of the posterior vulva is relaxed with a YV advancement flap, both to improve surgical access and to correct future dyspareunia. Because the hymen generally shows dystrophic fibrosis, microsurgical resections of Bartholin's glands are always combined with prophylactic hymenectomy. The patients begin using a No. 4 dilator 4 weeks after surgery, and when able, they graduate to a No. 5 dilator. Resumption of coitus also is encouraged from this point. At the same visit, intensive pelvic floor exercises are prescribed to treat any residual perineal burning and introital dyspareunia emanating from chronic fibromyalgia of the levator ani muscles. Quote Link to comment Share on other sites More sharing options...
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