Introduction
Pediatric and adolescent patients frequently present to the office with vulvar or vaginal concerns. The most common concerns include prepubertal and postpubertal vulvovaginitis, lichen sclerosus, labial adhesions, and vulvar ulcers ( Table 15.1 ).
Etiology | Evaluation | |
Prepubertal vulvovaginitis | Nonspecific | Exam, possible vaginal culture |
Postpubertal vulvovaginitis | Nonspecific | Exam, vaginal cultures |
Lichen sclerosus | Unknown | Exam |
Labial adhesions | Inflammation of vulvar skin in hypoestrogenic environment | Exam |
Aphthous vulvar ulcers | Idiopathic, nonspecific inflammatory response to systemic bacterial, viral, and fungal illnesses | Exam, HSV testing, varies across practices, refer to section below on aphthous ulcers |
Differential Diagnosis | Treatment | |
Prepubertal vulvovaginitis | Foreign body vaginitis, vaginitis caused by chlamydia or gonorrhea, pinworm infection, dermatoses, precocious puberty, urinary pathology | Improved genital hygiene, hypoallergenic vulvar care, topical barrier emollients, estrogen, antibiotics if specific pathogen is found on vaginal culture, evaluation and treatment of constipation |
Postpubertal vulvovaginitis | Physiologic leukorrhea, foreign objects, dermatoses, infections (yeast, bacterial vaginosis, sexually transmitted infections) | Improved genital hygiene, hypoallergenic vulvar care, topical emollients, antibiotics if specific pathogen is found on vaginal culture |
Lichen sclerosus | Vitiligo, can have subtle and early skin changes, trauma/injury, lichen simplex chronicus | Hypoallergenic vulvar care, topical corticosteroids, topical calcineurin inhibitors |
Labial adhesions | Vulvar-vaginal variants such as lower vaginal outlet obstruction | Topical estrogen or topical betamethasone 0.05% |
Aphthous vulvar ulcers | HSV ulcers, Behcet disease, inflammatory bowel disease (i.e., Crohn disease), trauma | Symptomatic treatment |
Prepubertal vulvovaginitis
Prepubertal vulvovaginitis is a term used to describe vulvar and vaginal inflammation in females before puberty. It is a common complaint causing parents to seek medical attention, but the exact prevalence is not well understood. In one study of 191 premenarchal females surveyed at the time of their well-child visit, 2% reported current vulvovaginal symptoms, with 49% reporting any history of vulvovaginal symptoms not associated with urinary tract infections or trauma.
The most common etiology of prepubertal vulvovaginitis is nonspecific and is thought to be the result of many factors. Prepubertal females have smaller perineal bodies and underdeveloped labia minora with hairless, less fatty labia majora compared with postpubertal females. This difference in anatomy increases the risk of traumatic irritation to the labia and the risk of exposure to enteric bacteria. In addition, some females are exposed to contact irritants such as harsh soaps and bubble baths, which can cause genital irritation.
Frequently, prepubertal females struggle with personal hygiene. When cleaning after bowel movements, children frequently wipe “back to front” or not as carefully as adults. This can result in exposure of fecal bacteria to the vagina. In addition, prepubertal females may not take the time to void completely or spread their legs far enough apart, which results in the urine refluxing into the vagina. This is termed vaginal voiding, and this urine collection in the vagina can act as a medium for bacteria to grow. Other hygiene concerns for prepubertal females include poor handwashing, nose picking, thumb sucking, or scratching, which can introduce oropharyngeal and skin bacteria to the vagina. Beyond concerns for poor hygiene, the pH of the prepubertal vagina is alkaline because of the presence of less lactobacilli and hypoestrogenic compared with the postpubertal vagina, which allows pathogenic bacteria to grow.
The clinical presentation of prepubertal vulvovaginitis involves genital discomfort (itching, irritation, and/or burning), erythema, and abnormal vaginal discharge. A detailed history can be taken to determine symptoms, the length of time symptoms have been present, questions about hygiene ( Table 15.2 ), and treatments that have already been attempted to relieve symptoms.
How frequently does the patient take a bath or shower? |
What type of soaps are used for bathing? For detergents? |
Does the patient take bubble baths? |
Is the child toilet trained? |
How does the child sit on the toilet when voiding? |
How does the patient wipe in the restroom? Front to back? Or back to front? |
Does the patient experience urine dribbling or urinary incontinence? |
Does the patient wear loose-fitting clothes? |
A physical examination should be performed to assess pubertal development, any abnormalities of the genital anatomy, skin changes, presence of vaginal discharge, and presence of vaginal voiding. A vaginal culture can be obtained. When collecting the vaginal culture, care should be made to avoid direct contact of the swab with the hymen, causing discomfort. If the vagina cannot be swabbed, a vaginal lavage with normal saline can be used to aid in the collection of vaginal culture. If symptoms are persistent despite treatment or there is concern for a foreign body, further assessment of the vagina with vaginoscopy can be performed. In the setting of pruritus, an evaluation for pinworms can be performed by putting tape around the anus first thing in the morning. Finally, if there is concern for sexual abuse, testing can be performed for gonorrhea and chlamydia.
The differential diagnosis of prepubertal vulvovaginitis includes foreign body vaginitis, vaginitis caused by chlamydia or gonorrhea, pinworm infection, dermatologic conditions, precocious puberty, and urinary pathology ( Table 15.3 ). If gonorrhea or chlamydia is detected, a careful evaluation for sexual abuse should be undertaken. Prepubertal vulvovaginitis is frequently treated with yeast medications, but it is important to note that Candida is not commonly found in the vagina of prepubertal females. , Candida is a common cause of diaper dermatitis but is rarely found on vaginal culture of prepubertal females with vulvovaginitis unless risk factors are present, including immunosuppression, diabetes, or recent antibiotic use. ,
Nonspecific Vulvovaginitis | Bacterial Vulvovaginitis |
---|---|
Vaginitis caused by gonorrhea or chlamydia | Psoriasis |
Lichen sclerosus | Vaginitis caused by foreign body |
Allergic contact dermatitis | Voiding dysfunction |
Eczema | Ectopic ureter |
Precocious puberty | Pinworms |
Studies have shown that the majority of prepubertal vulvovaginitis is nonspecific with no specific pathogen found. In only about 25% to 40% of cultures, a pathogen can be found associated with symptoms of vulvovaginitis. , , As a result, the vaginal culture should only be treated if the bacteria are isolated and growing extensively on culture. Because of hygiene factors in prepubertal females, the most common pathogens found on vaginal culture are from enteric and respiratory organisms ( Table 15.4 ).
Organism | Treatment |
---|---|
Group A streptococci beta-hemolytic (S. pyogenes) | Penicillin family |
Group B streptococci beta-hemolytic (S. agalactiae) | Penicillin family |
Staphylococcus coagulase positive (S. aureus) | Penicillin family |
Haemophilus influenza | Penicillin family |
Escherichia coli | Azithromycin |
Enterococcus faecalis | Penicillin family |
Enterobiasis vermicularis | Mebendazole or pyrantel pamoate |
Nonspecific prepubertal vulvovaginitis is treated by encouraging improved hygiene measures ( Table 15.5 ). Topical emollients can provide symptomatic relief. In severe cases of prepubertal vulvovaginitis where the patient has vulvar inflammation and irritation, a low-potency topical steroid such as triamcinolone acetonide ointment 1% can be applied to the affected area, such as the labia majora, twice a day until symptoms improve. If a specific pathogen is found on vaginal culture, a susceptible antibiotic should be used.
Bathe every day with warm water for a short period |
Eliminate bubble baths |
Avoid contact irritants by using fragrance-free soaps and detergents |
Wipe from front to back when using the restroom |
When using the restroom to void, sit with legs wide on the toilet seat and lean forward to avoid vaginal voiding; sitting backward on the toilet may make spreading the legs easier |
Wear loose-fitting underwear and clothes |
Avoid sitting in wet, tight underwear or bathing suits for long periods |
Postpubertal vulvovaginitis
Postpubertal vulvovaginitis is a term used to describe vulvar and vaginal inflammation in females after puberty. Postpubertal vulvovaginitis is a common complaint in adolescents. This section will focus on nonsexually acquired postpubertal vulvovaginitis, as sexually transmitted infections are discussed in Chapter 20 .
After puberty, the epithelium in postpubertal adolescents is more resistant to infection compared with that of the prepubertal female. This is because of increasing estrogen levels and a decrease in vaginal pH, caused in part by the increased presence of lactobacilli. Two of the most common nonsexually acquired causes of postpubertal vulvovaginitis are yeast infections and bacterial vaginosis. The majority of women (75%) will experience at least one vaginal yeast infection and almost half will have two or more infections. Vaginal yeast infections are typically associated with Candida albicans, although recurrent infections can be caused by Candida glabrata . There is a greater risk of vaginal yeast infection after treatment with broad-spectrum antibiotics and in the presence of immunodeficiency such as human immunodeficiency virus (HIV) and diabetes mellitus.
Bacterial vaginosis is considered the most common cause of vaginal irritation and discharge in women, and prevalence among adolescents ages 14 to 19 has been reported at 23%. Bacterial vaginosis is caused by a shift in vaginal flora, with a decrease in peroxidase-producing Lactobacillus and an increase in the presence of anaerobic gram-negative rods, particularly Gardnerella vaginalis . This shift causes the vaginal pH to rise.
Postpubertal vulvovaginitis presents with vulvovaginal complaints such as genital discomfort (itching, irritation, and/or burning), erythema, and abnormal vaginal discharge. Vaginal yeast infections are typically associated with a thick, white, odorless vaginal discharge associated with genital discomfort. Bacterial vaginosis is not a vaginitis but is a vaginosis, so signs of inflammation are typically absent, but it does present with a thin white/gray discharge that is adherent to the vagina.
A detailed history should assess for hygiene, possible foreign objects such as tampons/condoms, use of over-the-counter feminine products such as douches, symptoms of genital discomfort and features of any vaginal discharge (color, odor, association with menses), the length of the time the symptoms have been present, and treatments that have already been attempted to relieve symptoms.
Specific features on physical examination to assess include any skin changes, presence of vaginal discharge, vulvar itching, and/or presence of vaginal voiding. If a pelvic examination is performed, the cervix should be examined for inflammation, lesions, and any cervical motion or adnexal tenderness. Swabs can be obtained of vaginal fluid and, if needed, of the endocervix. If the patient is not sexually active, the physical examination can be limited to an external genital examination with only blind vaginal swab collection if discharge is seen.
A wet preparation of any vaginal discharge can be made using saline and 10% potassium hydroxide (KOH) on two separate samples. Vaginal yeast infections can be diagnosed on KOH wet preparation when either budding yeast, hyphae, or pseudohyphae are seen ( Fig. 15.1 ). A yeast culture is not recommended unless the infection is recurrent.
Bacterial vaginosis is diagnosed based on a wet preparation ( Fig. 15.2 ) using the Amsel criteria ( Table 15.6 ).
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Gram staining of the vaginal fluid has been considered the gold standard of diagnosing bacterial vaginosis but is rarely done clinically. Newer commercial testing for both vaginal yeast infections and bacterial vaginosis is available with high sensitivity and specificity compared with traditional wet preparation but has not been well studied in the adolescent population.
The differential diagnosis of postpubertal vulvovaginitis includes physiologic leukorrhea, foreign objects, dermatoses, and vaginal infections (caused by yeast, bacterial vaginosis, and sexually transmitted infections). , The management options for these patients depends on the diagnosis. Patients with physiologic leukorrhea, an asymptomatic clear to white vaginal discharge, can be reassured that the discharge is normal. Patients with retained foreign objects such as tampons and condoms will often present with a foul-smelling vaginal discharge, with symptoms resolving with removal of the foreign object. Vulvar inflammation and irritation can result from chemical irritants found in feminine hygiene products, soaps, detergents, perfumed products, and bubble baths. Sitz baths and barrier emollients can be useful in reducing symptoms along with counseling patients on good genital hygiene ( Table 15.7 ). Similar to nonspecific prepubertal vulvovaginitis, in severe cases of vulvar inflammation and irritation, a low-potency topical steroid such as triamcinolone acetonide ointment 1% can be applied to the affected area twice a day until symptoms improve.
Consistent condom use |
Avoid the use of feminine hygiene products such as douches |
Wear loose cotton underwear |
Use mild and unscented soaps and detergents |
Avoid bubble baths |
Wipe front to back when using the restroom |
Avoid tight-fitting clothes |
Vaginal yeast infections can be treated with either over-the-counter intravaginal creams or suppositories such as clotrimazole, miconazole, terconazole, and tioconazole. Dosing is based on the formulation and strength. Oral fluconazole is also used in the treatment of vaginal yeast infections. Patients can elect for either option, as topical or oral treatment of vaginal yeast infections is equally effective. Bacterial vaginosis is treated with either oral metronidazole or vaginal preparations of metronidazole or clindamycin. Treatment of sexual partners is not recommended.
Vulvar lichen sclerosus
Lichen sclerosus is an inflammatory dermatologic condition causing hypopigmentation that commonly affects the anogenital region. The exact prevalence of lichen sclerosus is not known, but a report from a general adult gynecology practice estimated a prevalence of 1.7%. Vulvar lichen sclerosus can be diagnosed at any age but is typically diagnosed either in prepubertal or menopausal females. Pediatric vulvar lichen sclerosus accounts for ∼7% to 15% of all cases diagnosed. The average age of diagnosis of pediatric vulvar lichen sclerosus is 6 to 7 years. ,
The etiology of lichen sclerosus is unknown. Patients with the condition are more likely to suffer from autoimmune conditions and have higher levels of autoantibodies compared with controls; however, this does not confirm it is an autoimmune disease. Lichen sclerosus can run in families, which has led to research on human leukocyte antigen (HLA) association but further studies are needed.
The most common symptoms of lichen sclerosus at presentation are pruritus, vulvar pain, dysuria, constipation, and bleeding. The classic feature of vulvar lichen sclerosus is a well-defined plaque of hypopigmentation with sclerosus in a figure of eight configuration (surrounding the vulva, perineum, and perianal skin) , ( Fig. 15.3 ). It is rare for lichen sclerosus to occur in the proper vagina (superior to the hymen). Other skin changes can occur such as ecchymoses, petechiae, fissures, erosions, and hemorrhagic blisters. As most adults are not familiar with this skin condition, children can be mistakenly referred to child protective services because of the ecchymoses of lichen sclerosus. Vulvar vitiligo is another inflammatory dermatologic condition that causes hypopigmentation that can also occur in patients with lichen sclerosus, which can make diagnosis challenging.
Lichen sclerosus can progress to vulvar structural distortion, resulting in atrophy of the labia minora, adhesions of the clitoral hood, and/or introital stenosis, all of which may be permanent and require surgical correction. A recent study found 25% of pediatric patients with lichen sclerosus had vulvar structural distortion.
Unlike in adults, vulvar biopsy is not typically performed in the diagnosis of pediatric vulvar lichen sclerosus. It should be reserved for cases with uncertain diagnosis or lack of response to treatment. If biopsy is undertaken, it should be from the most hypopigmented area affected, and the histopathology is distinctive, occurring in all age groups.
Most clinical recommendations divide the treatment of lichen sclerosus into two phases: induction of remission and maintenance ( Table 15.8 ). Since 1991, the gold standard of treatment of lichen sclerosus has been topical corticosteroids. , No single regimen exists for induction of remission, but the mainstays of therapy include topical high-potency corticosteroids such as clobetasol propionate, mometasone furoate, and betamethasone dipropionate. , , Ointments are the preferred vehicle because they have a low rate of contact dermatitis and good penetrance. , After improvement in symptoms and skin changes, patients can be transitioned to lower-potency corticosteroids such as triamcinolone acetonide, methylprednisolone aceponate, or hydrocortisone. , , Maintenance treatment should be continued and decreased in potency until the patient has long-term control of the disease with no symptoms and normal skin findings. Patients should be followed closely initially then can be moved to less frequent follow-up if the disease is well controlled. If the disease worsens, the potency of corticosteroid can be retitrated as needed. The most common side effects of the use of topical corticosteroids include superimposed Candida infection, erythema, and stinging from application of the steroid (see Table 15.8 ). Prolonged use of topical steroids can be associated with thinning of the dermis and, rarely, hypothalamic-pituitary-adrenal axis suppression, though this has not been reported in long-term studies of corticosteroid treatment of lichen sclerosus. ,