In pregnancy, bacterial and viral lower genital tract infections are common and generally managed medically. Sexually transmitted diseases (STDs) such as gonorrhea, trichomoniasis, and chlamydial infection are treated with antibiotic regimens according to guidelines outlined by the Centers for Disease Control and Prevention (CDC) (Workowski, 2015). Vulvovaginal candidiasis and bacterial vaginosis can also cause symptomatic vaginal discharge during pregnancy. Treatment recommendations for all these are briefly reviewed and interwoven within the specific topics of this chapter.
In contrast, surgical treatment is generally reserved for vulvovaginal abscesses or for condylomata causing marked obstruction. Otherwise, surgery has little role in treating chronic viral or bacterial infections during pregnancy.
The clinical presentation of vulvovaginal infections is probably minimally affected by pregnancy. Host factors such as diabetes mellitus or human immunodeficiency virus (HIV) are evaluated prior to management decisions. Importantly, immunosuppression from HIV and acquired immunodeficiency syndrome (AIDS) may mask clinical and laboratory signs of local infection and bacteremia due to impaired inflammatory response (Berger, 1994).
These usually involve the labia majora, and vulvar abscesses occasionally complicate pregnancy. Acute infections can stem from pyogenic folliculitis, and common risks include local trauma from shaving, obesity, or diabetes mellitus. Chronic or recurrent vulvar abscesses may develop in women with furunculosis, carbuncles, hidradenitis suppurativa, methicillin-resistant Staphylococcus aureus (MRSA) colonization, or less often, with Crohn disease.
Small abscesses may be painful but can often be initially managed conservatively with hot compresses and sitz baths. Most superficial infections will become fluctuant, expand, and then drain spontaneously. After spontaneous emptying, persistent erythema or pain may reflect a surrounding cellulitis. Also, a deeper-seated abscess with a thick wall may not reach the skin surface to drain. Thus, differentiation between cellulitis with marked induration and abscess can be difficult. If the clinical picture is unclear, needle aspiration of the affected area can help distinguish between the two. Additionally, in rare cases with unconventional findings, sonography, if readily available, of the swelling can be considered (Blaivas, 2011).
The involved pathogenic bacteria generally are usual skin flora (staphylococcal and streptococcal species) but may also be composed of a mixed aerobic and anaerobic flora. In complicated infections, culture collection prior to antibiotic initiation may be helpful for later antibiotic regimen adjustment.
Mature, superficial vulvar abscesses are best treated with simple incision and drainage (I & D) (Fig. 12-1). Surgical consent is obtained from the patient, and specific risks include bleeding, recurrent abscess, worsening infection, and scar formation or chronic pain at the incision site.
To begin, the skin overlying the planned I & D site is cleaned with a chlorhexidine or betadine solution. In office settings, a local anesthetic such as 1-percent lidocaine is injected along the planned incision. With a no. 11 scalpel blade oriented perpendicular to the skin surface, a vertical incision, which follows natural Langer cleavage lines, is created. The length is typically dictated by abscess size and the need for wound packing. Specifically, small cavities typically will not require gauze or iodoform packing, but local hydrotherapy may assist healing. Thus, a 0.5- to 1-cm incision may suffice. For larger abscesses, a 1- to 2-cm length is often needed.
Following initial I & D, desired aerobic cultures are obtained. Gentle abscess compression, as tolerated by the patient, aids evacuation. For abscesses larger than 3 cm, a cotton-tip swab can be swept within the cavity to disrupt loculated pockets of pus. Importantly, an abscess may overlie the vascular vestibular bulb, which is shown in Fig. 3-4 (p. 32). In these cases, probing should be gentle to avoid puncture of the posterior abscess wall and laceration of these veins.
Clinicians will often add broad-spectrum oral antimicrobial treatment. In populations with greater risks for MRSA, oral clindamycin may be preferred (Thurman, 2008). However, antibiotics are generally not necessary in the absence of cellulitis or isolation of specific pathogens. If provided, oral antibiotics are suitable for smaller abscesses with mild cellulitis. However, for substantial associated cellulitis or fever, admission for administration is reasonable. Bacterial culture is more strongly recommended in the setting of recurrent or refractory abscesses. Treatment is then guided by antibiotic susceptibility, although most infections are caused by organisms found in skin flora.
Hospitalization for surgical drainage is considered in cases with a large or deep abscess, significant surrounding cellulitis, or suspicion for systemic infection. With a larger abscess, I & D in the operating room may afford adequate patient anesthesia for sufficient disruption of intracavitary loculations and for wound packing.
Following evacuation, packing large cavities with gauze ribbon or placing a passive drain such as a Penrose drain can sustain drainage as infection resolves. Packing is usually changed each day, and premedication with suitable analgesia is typically needed. This may be oral or intravenous sedation depending on wound size and patient tolerance. Most women are ready for discharge after 1 to 2 days, but cases complicated by immunosuppression may require longer stays to manage comorbid conditions.
Necrotizing vulvar infection may present as a cellulitis, fasciitis, or myositis and is a serious polymicrobial process characterized by rapid progression. This is a surgical emergency, and its associated mortality rate ranges between 12 and 60 percent (Horowitz, 2011). Predisposing factors for necrotizing fasciitis include diabetes mellitus most commonly, but prior radiation is also a risk. Clostridial species are classically implicated in this infection. Group A Streptococcus is another important bacteria involved in necrotizing infections that can develop in healthy individuals in any age group (Wong, 2003).
Clinical systemic features include fever and tachycardia, which can evolve to sepsis. Locally, superficial vascular thrombosis develops and gives skin its characteristically dusky appearance (Fig. 12-2). Tissue edema imparts a doughy texture, and a foul odor may be noted. Tissue crepitus or cutaneous bulla formation is frequently caused by toxin production and proliferation of Clostridium species with local gas formation.
FIGURE 12-2
Vulvar necrotizing fasciitis. A. Preoperative photograph shows deceptively minimal erythema, and no fluctuance was appreciated. B. With incision, necrotic tissue and thin watery discharge are noted. C. Extensive debridement was required to reach well-vascularized tissue. (Used with permission from Dr. David Miller.)
Early and aggressive surgical exploration is the key step in managing necrotizing infections. In obvious cases, no imaging is needed, and patients are prepared for surgical debridement. However, tissue destruction is usually far more extensive than is evident by surface examination. Thus, in less-clear cases, the diagnosis may be clarified by identifying gas in affected tissues by radiography or computed tomography if these can be quickly obtained. Otherwise, prompt surgical exploration is preferred, as antibiotic therapy without debridement is associated with high mortality rates that can approach 100 percent (Anaya, 2007).
During debridement, due to poor tissue vascularity, there is little or no bleeding but instead usually a thin, gray transudate. As shown in Figure 12-2, necrotic tissue resection continues until healthy viable tissue is reached at the dissection boundaries. In severe cases, dissection may extend cephalad to the lower anterior abdominal wall, laterally onto the proximal inner thigh, or caudally toward the buttock. Such resection can be disfiguring and may require later reconstructive tissue flaps.
Following excision of necrotic tissues, the wound is packed with moist gauze and covered with a dressing. Wet-to-dry dressing changes are ideally completed twice daily, and additional focal wound debridement is often needed. Debridement is completed at the bedside or in the operating room depending on patient tolerance and the burden of necrotic tissue.
Empiric antibiotic treatment includes antimicrobial activity against gram-positive, gram-negative, and anaerobic organisms, particularly group A Streptococcus and clostridial species. Necrotizing skin and soft-tissue infections may be mono- or polymicrobial, but initial empiric antibiotic therapy should be broad until further culture information can guide therapy. The 2014 Infectious Disease Society of America (IDSA) guidelines recommend broad empiric antibiotic treatment. Acceptable regimens may include: (1) an agent against MRSA (vancomycin, daptomycin, or linezolid) plus piperacillin-tazobactam, (2) an MRSA agent plus a carbapenem, or (3) an MRSA agent plus ceftriaxone and metronidazole (Anaya, 2007; Stevens, 2014). If toxin-elaborating strains of streptococcus are identified as the causative agent, the IDSA recommends penicillin plus clindamycin (Stevens, 2014). Further therapy can be tailored based on Gram stain and on culture and sensitivity results, once available (Table 12-1). Of note, clinicians should be cognizant of the emergence of carbapenemases and betalactamases that may lead to resistance, particularly in gram-negative infections (Vasoo, 2015).
Infection Type | Antimicrobialsa | Bacterial Coverage |
---|---|---|
Mixed | Vancomycin (C) or Daptomycin (B) or Linezolid (C) | MRSA |
PLUS | ||
Piperacillin-tazobactam (B) or Ertapenem (B) or Imipenem (C) or Meropenem (B) | Gram positive Gram negative Anaerobes Group A Streptococcus Clostridium spp | |
Streptococcal | Penicillin (B) PLUS Clindamycin (B) | |
Staphylococcus aureus | Nafcillin (B) or Oxacillin (B) or Cefazolin (B) PLUS Clindamycin (B) |
This chronic pustular disease of apocrine sweat glands can involve axillary, perianal, and genital areas. It often presents as recurrent abscesses with superficial draining sinus tracts. The pathogenesis of hidradenitis suppurativa remains unclear. In histologic studies, sebaceous gland atrophy is followed by early lymphocytic inflammation and hyperkeratosis of the pilosebaceous unit. This leads to subsequent hair-follicle destruction and granuloma formation (Jemec, 2012; Yazdanyar, 2011). Scarring and sinus tracts form during the healing process.
During pregnancy, few indications prompt definitive surgical therapy for chronic hidradenitis suppurativa. That said, lesions may become secondarily infected with staphylococcal, nonhemolytic streptococcal, Escherichia coli, and Proteus species, as well as anaerobes. Additional testing with biopsies and bacterial cultures may be indicated in atypical or refractory cases (Jemec, 2012).
Hidradenitis suppurativa can be difficult to treat, especially when lesions are chronic and extensive. This, in part, stems from the often multiple, deep-seated sites of secondary infection, which antibiotics may not easily penetrate. In general, antibiotics are first-line therapy. With mild superficial lesions, topical 1-percent clindamycin solution applied twice daily is thought to prevent secondary bacterial infections and improve inflammation (Clemmensen, 1983). Oral clindamycin, 300 mg twice daily, may better manage deep-seated lesions (Alhusayen, 2012). As needed, Gram stain and culture can guide antibiotic therapy.
Of other options, in reproductive-aged women, isotretinoin and antiandrogen therapy are used cautiously and require reliable birth control. However, in pregnancy, these two options are avoided because of potential adverse fetal effects (Shirazi, 2015). Extensive surgical management or “unroofing” procedures should be postponed until after delivery.
Cysts and abscess formation are the most common disorders of the Bartholin gland ducts, affecting 2 to 3 percent of women. However, few data are available regarding the specific epidemiology of Bartholin gland duct infection in pregnancy. In one study of 219 women with Bartholin gland duct abscesses, 5.5 percent were pregnant at the time of diagnosis (Kessous, 2013). Affected women may often have prior or concomitant STDs, especially gonorrhea or chlamydial infection. Recurrent abscess may result from a scarred Bartholin gland duct damaged during prior infection. Causative organisms are those of the normal vaginal flora. Thus, potential organisms include gram-negative and gram-positive anaerobic rods, E coli, and staphylococcal or streptococcal species (Kessous, 2013; Tanaka, 2005).
Clinical presentation of a Bartholin gland duct infection is usually an abscess. Ductal infection (bartholinitis) without abscess is unusual. Abscesses are generally unilocular and several centimeters in diameter (Fig. 12-3). Similar to other vulvar abscesses, surrounding erythema, induration, and tenderness may obscure the actual abscess size. Rarely, bacteremia, septic shock, and a toxic-shock-like syndrome can also complicate Bartholin gland duct infections (Honig, 1991; Lopez-Zeno, 1990; Shearin, 1989; Sherer, 2009). Moreover, careful examination for necrotizing fasciitis should precede decisions on the optimal treatment, especially in immunocompromised women. Decisions concerning appropriate therapy depend on underlying immune status and infection severity.
In general, immunocompetent women with early, mild infection or a small abscess can be treated with a broad-spectrum oral antibiotic, analgesics, and local heat by packs or sitz baths. The hope is that warmth will open the obstructed ostium to permit spontaneous evacuation. With such local therapy, abscesses often drain within 1 to 2 days. In abscess management, abscess excision is not indicated. Thus, if the abscess is large and fluctuant, then surgical drainage is appropriate.
Several surgical techniques for Bartholin gland duct abscess include I & D, marsupialization, and catheter drainage. None of these has undergone randomized, prospective evaluation in sufficiently large trials to show differences in outcome. With surgical treatment for Bartholin gland duct abscesses, there are four main goals. First, the infected duct abscess must be adequately emptied. Second, infection complications such as cellulitis or infrequently necrotizing fasciitis and sepsis are identified or prevented. Third, the gland should be preserved, so that it may continue its secretory function. Last, recurrences should be prevented by creation of a new gland duct ostium to replace the function of the presumed damaged or occluded duct. The new opening is actually a cutaneous fistula that may take several weeks to fully epithelialize. Patency of this tract allows continued gland secretion without cyst or recurrent abscess formation.
During patient consenting, several potential complications are discussed. First, following I & D, the Bartholin gland duct can become obstructed again. This is not uncommon, and patients are informed of the possible need to repeat the procedure. Dyspareunia is an infrequent long-term sequela. Rarely, bleeding from vestibular bulb laceration or sepsis may occur. Also rare, chorioamnionitis and sternoclavicular septic arthritis after drainage of a Bartholin gland duct abscess in a pregnant woman has been reported (Kelly, 2014).
The simplest I & D technique involves creating a 1-cm-long vertical stab wound with a no. 11 or 15 scalpel blade into the abscess cavity (Fig. 12-4). The incision is placed just outside and parallel to the hymen at 5 or 7 o’clock (depending on the side involved). This position mimics the normal anatomy of the gland duct opening. If the abscess has drained spontaneously, the opening can be extended as needed to improve evacuation. Wound cultures may be obtained at this time. At our institution, we typically obtain pus samples for aerobic culture and for nucleic acid amplification testing (NAAT) for Neisseria gonorrhoeae and Chlamydia trachomatis.
FIGURE 12-4
Bartholin gland duct incision and drainage (A) followed by Word catheter insertion and balloon insufflation (B). (Reproduced with permission from Hoffman BL, Corton MM: Surgeries for benign gynecologic conditions. In Hoffman BL, Schorge JO, Bradshaw KD, et al: Williams Gynecology, 3rd ed. New York, McGraw-Hill Education, 2016.)
Following drainage, the cavity is explored with a small cotton-tip swab to open potential pus loculations. Probing is gentle to avoid perforation through the duct wall and into the nearby and highly vascular vestibular bulb.
The tip of a self-retaining Word catheter is inserted into the cavity. This flexible latex device has a 10F stem, measures 5 cm long, and has a balloon tip. Once the tip is seated within the cavity, 2 to 5 mL of water or saline is injected into the catheter hub and travels to fill the balloon (Word, 1964). Insufflation with fluid is preferred to air, as the latter is associated with premature balloon deflation. The bulb is inflated sufficiently to prevent spontaneous catheter expulsion through the incision opening. Once in place, the catheter permits pus to drain out around it. The Word catheter stem also serves as the template around which the new fistulous tract forms. The hub end of the Word catheter is then tucked inside the vagina. This prevents it from being dislodged by traction during normal perineal movement and improves catheter comfort.
Following I & D, sitz baths can aid healing and ease pain. The Word catheter may be removed after sufficient epithelialization of the new fistula is complete, usually 2 to 4 weeks. The recurrence rate for this technique ranges from 2 to 25 percent (Marzano, 2004).
Bartholin gland duct abscesses also can be safely drained by marsupialization (Fig. 12-5). The technique has been variously described, but in sum, the abscess is opened, the abscess lining at this incision is isolated, and the lining is tacked to the vestibular skin around the incision using fine absorbable suture. The procedure may require general or regional anesthesia but can be accomplished with local infiltration or pudendal block. Large abscesses usually require greater degrees of anesthesia.
FIGURE 12-5
Bartholin gland duct marsupialization. A. Skin incision reveals abscess wall. B. Following cavity drainage, the cyst walls are grasped with Allis clamps. C. Sutures using fine-gauge absorbable or delayed-absorbable are placed circumferentially around the incision. D. This completed opening will narrow markedly during healing.
To begin, a vertical or elliptical incision is made using a scalpel with a no. 15 blade. Importantly, an ostium of sufficient diameter is created to compensate for wound narrowing, as the healed fistula has an appreciably smaller caliber. An incision measuring 1 to 2 cm is usually adequate (Mayeaux, 2013). The cut is made across the skin overlying the cyst bulge and is placed just outside and parallel to the hymen at 5 or 7 o’clock (depending on the side involved). This position mimics normal anatomy of the gland duct ostium.
A second superimposed vertical incision then opens the underlying cyst wall, and pus under pressure spills out. Pus may be cultured. Allis clamps are then placed on the superior, inferior, right, and left lateral cyst wall edges around the incision and fanned out. The cavity is explored with a small cotton-tip swab to open potential fluid loculations. Again, gentle probing avoids duct wall perforation and vestibular bulb laceration. The edges of the cyst wall are sutured to adjacent skin edges with interrupted sutures using 2-0 or 3-0 gauge absorbable or delayed-absorbable suture.
The abscess cavity can be packed loosely with quarter-inch plain gauze, which may be removed after 24 hours. However, this is not mandatory. Healing is usually completed by 10 days, and recurrence is rare.