and Filippo Murina2
(1)
Center of Gynecology and Medical Sexology, San Raffaele Resnati Hospital, Milan, Italy
(2)
Lower Genital Tract Disease Unit V. Buzzi Hospital, University of Milan, Milan, Italy
Physicians and healthcare providers (HCPs) can contribute to vulvar pain with different pathophysiologic pathways and responsibilities. They seem to be often unaware of a dramatic truth, valid in every field of medicine: doctors can be cofactors in the pathogenesis of a disease (Graziottin 2006; Norian and Stratton 2008; Esparaz et al. 2015). Specifically, HCPs may contribute to cause vulvar pain, acting as:
Predisposing factor, with two leading mechanisms:
First, when they increase the vulnerability of the vulvar organ, or the afferent nerves and muscle, to precipitating factors and/or of the emotional attitude toward genital pain, during diagnostic or therapeutic maneuvers (Graziottin 2006)
Second, when they do not recognize and diagnose conditions that may prelude, precipitate, or perpetuate vulvar pain (Graziottin 2015)
Precipitating factors, with two other mechanisms:
First, through the inappropriate prescription of medications, the negative outcome of surgery, obstetrics, and/or chemotherapy, hormonotherapy, or radiotherapy (Graziottin 2011, 2014 Graziottin and Serafini 2012; Graziottin and Lukasiewicz 2016a, b; Lukasiewicz and Graziottin 2015; McDonald et al. 2015).
Second, when HCPs do not respect the professional boundaries in the clinician-patient relationship, with sexually abusive behaviors. This is another neglected precipitating cofactor of vulvar pain and sexual dysfunctions, especially for women who sought professional help in a vulnerable moment of their life (Gabbard et Anderson 1995; Plait 2003; Stewart et al. 2009). It is a problem still dramatically underdiagnosed and underreported, persisting in the shadow of medical misconducts (Stewart et al. 2009).
Perpetuating factors, through the most frequent mistake in the field of vulvar pain: the lack of diagnostic recognition of its biological truth. Furthermore, the diagnostic omission encompasses occasional or systematic diagnostic neglects, particularly in the area of biological/medical etiology of vulvar pain. Typical omissions include:
Lack of diagnostic attention to:
Vulvar pain, when even the name is missing, such as in vulvar pain in childhood or after female genital mutilation/cutting (FGM/C) (please see the dedicated chapters).
Vestibulodynia/vulvodynia complaint: the average diagnostic delay between the onset of symptoms and the correct diagnosis is of about 4 years in the author’s personal series (Graziottin, unpublished data).
Sexual pain, and specifically introital dyspareunia, a persistently neglected complaint from adolescence onward and particularly after delivery (Glazener 1997; McDonald et al. 2015).
Hyperactive pelvic floor, as a predisposing, precipitating, and perpetuating factor of vestibular pain and introital dyspareunia (Graziottin 2015).
Comorbidities between vulvar pain and other medical conditions.
Lack of appropriate treatment of all the abovementioned conditions. Conditions specifically critical for perpetuating vulvar pain include:
Pelvic floor hyperactivity that can be associated to vaginismus and introital dyspareunia and may turn into a serious perpetuating factor (Graziottin and Gambini 2015).
Sexual pain disorders.
Comorbidities between medical conditions, sexual problems, and vulvar pain. For example, the abuse of antibiotics in recurrent cystitis alters the intestinal and vaginal microbiota vaginal, predisposing and precipitating recurrent Candida infections, with consequent increased vulnerability to vulvar vestibulitis and provoked vestibulodynia (Graziottin 2014; Graziottin and Zanello 2015) (please see Chap. 6 for more details).
Key Point
“Iatrogenic” is not only what an HCP actively does, which causes vulvar damage (and sometimes sexual damage), but also what the HCP omits to diagnose and treat. In consequence of that, it causes one or more damages, as vulvar pain becomes chronic and/or because the natural course of the disease will not be changed due to the omitted diagnosis and treatment.
This chapter will discuss a few critical aspects in these three major areas of iatrogenic disorders, as a paradigm, to open a mental window that physicians all too often omit to consider.
9.1 Iatrogenic Factors Predisposing to Vulvar Pain in the Lifespan
It is difficult to provide an effective intervention, if there is no mention of a problem (Graziottin 2006). The omission of a frank and respectful discussion about sexual pain issues may contribute to vulvar pain with different dynamics, which will be briefly reviewed with a lifespan perspective.
9.1.1 Vulvar Pain in Childhood
The diagnostic omission is amazing as even the name of vulvar pain is omitted (please see the Chap. 4).
9.1.2 Vulvar Pain in Adolescents
In a retrospective case series of vulvodynia in preadolescent girls, Reed and Cantor found similar pain characteristics as in adulthood (Reed et Cantor 2008). The girls had many years of pain without a correct diagnosis and without an adequate physical examination.
In adolescence, causes of recurrent vulvovaginal pain have been associated with intercourse. The association with sexual activity and vulvodynia compromises future sexual functioning, psychological well-being, and quality of life. It was suggested that 30–50 % of adult women with provoked vestibulodynia experienced primary, i.e., lifelong, introital dyspareunia. It is often associated with undiagnosed lifelong vaginismus, not severe enough to prevent penetration, but sufficient to determine both fear of intercourse, poor/inadequate/absent arousal due to the phobic attitude, and a tightening/squeezing of the vaginal entrance, due to the associated hyperactive pelvic floor that predisposes to introital microtraumas with recurrent pain and vestibular inflammation at every sexual attempt, contributing to intermittent/chronic vulvar vestibulitis (Graziottin 2006). This neglected inflammation, gradually shifting from physiologic to pathologic, finally may contribute to the shift to pathologic/neuropathic inflammation, genital and in the brain, the hallmark of provoked vestibulodynia.
Vulvovaginal pain in adolescents was associated not only with intercourse but also with the nonsexual contextual factor such as the impossibility to tampon insertion in virginal adolescents. Vulvovaginal insertional pain is a red alert on a hyperactive pelvic floor (Graziottin 2006, 2015). It has been linked to chronic dyspareunia, as a powerful predisposing factor. Severe pain at first tampon insertion use was associated with a fourfold risk of reporting dyspareunia (Landry and Bergeron 2009).
The practical tip is just one: when a girl tells the HCPs (usually a “she”) that she cannot use tampons, the correct answer must not be: “Well, use the external protection instead” but “Why she cannot?”, to make the appropriate diagnosis. It is essential to examine gently the perineum and evaluate the contraction of the levator ani around the vaginal entrance and the condition of the hymen while thinking: “Is there an hyperactive pelvic floor? Is there a fibrous, cribrous, thick, tightened hymen? Are there signs of recurrent Candida vaginitis and inflammation?” (please see Chap. 6 for more details).
Key Point
In adolescents, the difficulty in using tampons for the menstrual protection is one of the first (neglected) signs of hyperactivity of the pelvic floor, predicting dyspareunia and vulvodynia.
9.1.3 After Female Genital Mutilation/Cutting (FMG/C)
Vulvar pain is not even mentioned in the majority of papers on FGM/C, in spite of the fact that the vulva itself is cut and sutured, often with primitive means. So an excruciating pain, due the extremely rich nervous vulvar network, goes totally unrecognized and undiagnosed. This neglect persists in spite of more than 20 % of women with FGM reporting severe introital dyspareunia with a subset that cannot accept/have penetration at all (“apareunia”) because of pain (Berg et al. 2014) (see the chapter on vulvar pain in women with FGM/C for the analysis of the many implications of this diagnostic omission).
A serious issue is when HCPs perform FGM/C themselves. Medicalization of FGM/C refers to situations in which FGM/C is practiced by any category of healthcare provider, in a public or a private clinic, at home, or elsewhere (Abdulcadir et al. 2015). It also includes reinfibulation at any point of time in a woman’s life. Medicalization of FGM/C has been condemned by WHO and medical associations, including the International Federation of Gynecology and Obstetrics (FIGO), United Nations agencies, international agencies, nongovernmental organizations (NGOs), and governments (Abdulcadir et al. 2015).
The practice of FGM/C by HCPs should be considered as a serious misconduct, violating the basic, essential medical principle of not harming first, more so when the intervention implies involving partial or total removal of the external female genitalia or other injury to the female genital organs for nonmedical reasons. The serious responsibility of HCPs in causing permanent iatrogenic health and sexual damages when performing FGM/C should be more rigorously stigmatized and condemned by health organizations.
Ambiguities and controversies assimilating FGM/C to female genital cosmetic surgery (FGCS) deserve careful consideration and a more definite clear-cut position by scientific societies and health agencies.
9.1.4 In Pregnancy and After Delivery
9.1.5 After the Menopause
After the menopause, a general lack of communication about female sexual health issues and specifically about vulvovaginal atrophy (VVA) in the clinical setting has been reported in many researches (please see Chap. 8 for a detailed discussion). In the recent Real Women’s Views of Treatment Options for Menopausal Vaginal Changes (REVIVE) survey, postmenopausal women reported that only 19 % of healthcare professionals addressed their sexual lives and only 13 % specifically raised the issue of genitourinary symptoms, despite the fact that 40 % of women expected their HCPs to initiate discussions related to menopausal symptoms (Kingsberg et al. 2013).
9.2 Iatrogenic Factors Precipitating Vulvar Pain in the Lifespan
Physicians may not only predispose women to vulvar pain, but they may actively precipitate or worsen a preexisting unrecognized vulvar disease, in their daily practice.
This negative effect may be due to the known, but not completely avoidable, side effects of a necessary treatment, medical and surgical, or to mistakes, negligence, and overall malpractice.
9.2.1 Pharmacologic Effects
Chemotherapy has a complex effect: in prepubertal and fertile women, it may cause a permanent ovarian damage with, respectively, primary hypergonadotropic amenorrhea or premature menopause. This prolonged deprivation of sexual hormones, especially in women with hormone-dependent cancers, where hormone therapy is currently contraindicated, may negatively affect the whole sexual response, the younger the woman, the worse the effect, for the negative impact of the menopause on general and sexual health. When not adequately treated, particularly in women after breast cancer, when vaginal estrogens are still contraindicated, vulvovaginal atrophy (VVA) may become a critical predisposing and precipitating effect of vestibular pain, vaginal dryness, and introital dyspareunia (Graziottin 2001, 2006; Graziottin et Lukasiewicz 2016a; Lukasiewicz et Graziottin 2015). Peripheral neuropathies consequent to chemotherapy may affect the pudendal nerve (Graziottin et al. 2015).
Hormonotherapy: estrogenic receptor-positive breast cancer has been treated with tamoxifen for almost three decades. Although reasonably well tolerated, this worldwide used drug may specifically affect sexual function. Studies indicate that during tamoxifen therapy the most frequent complaints are hot flushes (85 %), disturbed sleep (55 %), vaginal dryness and/or dyspareunia (47 %), decreased sexual desire (44 %), and muscular-skeletal symptoms (43 %). Disturbed sleep correlates with hot flushes (P < 0.0005) and concentration problems (P < 0.05). Decreased sexual interest correlates with vaginal dryness (P < 0.0005) and/or dyspareunia (P < 0.0005). This is clinically obvious, as sexual pain is a major killer of sexual intimacy. After discontinuation of tamoxifen, symptoms decreased significantly (Merits et al. 2002; Graziottin e Lukasiewicz 2016a; Graziottin 2006, 2016).
More recent treatments with aromatize inhibitors such as anastrozole, which inhibits the conversion of androgens to estrogens, may as well have a negative impact on the whole sexual response, specifically contributing to VVA and vestibular pain and, consequently, to introital dyspareunia (Derzko et al. 2007; Graziottin 2016)
9.2.2 Negative Outcomes of Surgery in Oncology
Cervical carcinoma may require radical surgery, radiotherapy, and chemotherapy in the most aggressive and/or advanced stages. Radical surgery may shorten the vagina, thus reducing its “habitability,” i.e., receptiveness, which may be further reduced by radiotherapy, unless early psychosexual rehabilitation and at least topical hormonal treatment are timely started. Cervical adenocarcinoma, being hormone dependent, is the only contraindication to hormonal treatment for 5 years after surgery.
Assessment and treatment of a hyperactive, defensive pelvic floor, more frequent in nulliparous women or women who had cesarean section, is mandatory (Graziottin 2006, 2015; Graziottin and Gambini 2015, 2016). The sooner, the better.
Dyspareunia is the most frequent complaint related to vaginal shortening, while loss of desire, arousal difficulties, and vaginal dryness may be related to the loss of estrogens and testosterone concomitant to oophorectomy and cancer-related problems (Graziottin 2001, 2006; Graziottin and Lukasiewicz, 2016a, b). This includes the severity and duration of neuroinflammation, which recognizes a multifactorial etiology. After cancer diagnosis and treatment, neuroinflammation is the leading contributor to sickness behavior, fatigue, and depression and major neglected contributor to loss of desire and global female sexual dysfunction. Concomitant bladder symptoms, if the nerve sparing technique has not been made or has not been adequate, may further negatively impact on the sexual outcomes (Graziottin 2001, 2006; Graziottin and Lukasiewicz 2016a, b).
Vulvar cancer. Treatment modalities for vulvar carcinoma have greatly improved over the last three decades by providing improved cure rates with more conservative surgery. This carries decreased risk of morbidity (e.g., lymphedema, disfigurement, and sexual dysfunction) (Aerts et al. 2012).
Surgical requirements for removal of clitoral areas and stenosis of the vaginal opening along with local pain from scarring create different patterns of sexual dysfunction post therapy (Graziottin 2006; Lukasiewicz et Graziottin 2015; Graziottin e Lukasiewicz 2016b).
Surgical management of vulvar carcinoma must be individualized and tailored to the extent of disease. By optimizing care to the individual patient, psychological, sexual, and physical morbidity will be minimized (Graziottin e Lukasiewicz 2016b).
However, these surgeries remain a major psychological trauma for women. Clinical attention, openness to discussing sexual and psychological functioning, and timely rehabilitative intervention, hormonal and physical, before and after surgery, can definitely improve the outcomes of vulvar cancer.
9.2.3 Negative Outcomes of Radiotherapy
Total body radiotherapy may specifically damage sexuality through two major mechanisms:
Associated with bone marrow transplant, it may be associated with sexual dysfunction because of associated premature menopause, with the cohort of climacteric symptoms (Graziottin and Basson 2004; Graziottin et Lukasiewicz 2016a).
The negative impact on sexuality may be worsened by asthenia, fatigue, and immunodepression due to the primary neoplastic disease and the need of immunodepressants, when inadequate host/donor compatibility leading to graft versus host reaction requires chronic immunomodulating treatment (Graziottin and Basson 2004).
9.2.4 In Gynecology: For Benign Conditions
Women are seeking care for pelvic organ prolapse (POP) in increasing numbers. A significant proportion of them will undergo a second repair for recurrence (Ellington and Richter 2013). This has initiated interest by both surgeons and industry to utilize and design prosthetic mesh materials to help augment longevity of prolapse repairs. Unfortunately, the introduction of transvaginal synthetic mesh kits for use in women was done without the benefit of level 1 data to determine its utility compared to native tissue repair (Ellington et Richter 2013).
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