23: Anal Conditions: STDs

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Anal Conditions: STDs

CindyKin

Refer to Algorithm in Fig. 23.1

Anal Conditions: Sexually Transmitted Diseases

A. Screening for asymptomatic high-risk

patients: Patients at high risk for contracting sexually transmitted diseases include men who have sex with men (MSM), anyone in high-risk sexual networks including prostitutes and swingers, and anyone with a current sexually transmitted disease. These patients should be universally tested for chlamydia and gonorrhea annually at anorectal, oropharyngeal, and urogenital sites (Fig.23.1).

B. Screening and management for symptomatic

patients (Fig.23.1) (a) Perianal and/or genital lesions: Patients

presenting with perianal or genital lesions are often misdiagnosed with stulas, abscesses, hemorrhoids, or pruritus ani. Painful genital or perianal lesions in young sexually active patients are most likely due to infection with herpes or syphilis. Serologic testing for syphilis and HIV, and HSV culture or PCR should be performed. Empiric treatment should be started for the most likely pathogen.

C. Kin (*) Department ofSurgery, Stanford University School ofMedicine, Stanford, CA, USA e-mail: cindykin@stanford.edu

Painless lesions are likely to be condyloma. Pruritus lesions may be due to molluscum contagiosum.

(b) Proctitis: Patients presenting with ano-

rectal pain, tenesmus, and discharge should undergo testing for gonorrhea, chlamydia, syphilis, and herpes. Proctoscopy may not be possible due to patient discomfort, but intra-anal swabs should be taken before doing a rectal exam with lubricant. Empiric treatment for gonorrhea, chlamydia, and herpes simplex virus should be started, as well as symptomatic management with topical anesthetics and stool softeners.

C. Gonorrhea: Symptoms of gonococcal infec-

tion include dysuria, anorectal pain, anal discharge, or tenesmus. Nucleic acid amplication tests (NAATs) are recommended by the Centers for Disease Control (CDC) for detection of gonorrhea, except in cases of potential treatment failure in which cultures are required. Routine screening of all sexually active MSM and other high-risk populations at oropharyngeal, anorectal, and urogenital sites is recommended. Uncomplicated gonococcal infections should be treated with one intramuscular dose of ceftriaxone 250mg, plus either one oral dose of azithromycin 1g or a 7-day course of oral doxycycline 100mg twice daily. Re-testing for gonorrhea should be performed at 3 months, and any sexual partners from the preceding 2months should

https://doi.org/10.1007/978-3-319-65942-8_23

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Fig. 23.1 Algorithm for testing and empiric treatment for symptomatic STDs (A&B); MSM men who have sex with men

C. Kin

Fig. 23.2 Management of gonococcal infection (C); NAAT nucleic acid amplication test

also undergo empiric treatment. Chlamydia and HIV testing at the time of gonorrhea detection and 3–6months later should also be performed (Fig. 23.2). Suspected treatment failures require culture for antimicrobial susceptibility testing, and conrmed treatment failures must be reported.

D. Chlamydia: As most infected patients are

asymptomatic, screening of high-risk patients is critical to control this infection, which can cause the sequelae of pelvic inammatory disease including infertility, chronic pelvic pain, and ectopic pregnancy. The CDC recommends NAATs using rst catch urine or urethral swab for men, vaginal swab or

endocervical swab for women, and also rectal and oropharyngeal specimens. Screening should be performed in sexually active women 24years of age and younger, as well as highrisk older women. Screening may also be considered for high-risk men, which includes men in STD clinics, National Job Training Programs, juvenile detention facilities, the military, jail, men with infected partners, and MSM reporting anoreceptive intercourse. Treatment is a single oral dose of azithromycin 1 g, or a 7-day course of doxycycline 100mg twice a day. Patients should be counseled against engaging in sexual intercourse for a minimum of 7days after treatment, and

23 Anal Conditions: STDs

Fig. 23.3 Management of chlamydia infection (D); NAAT nucleic acid amplication test; LGV Lymphogranuloma venereum

until after their partners have also been treated. Sexual partners from the prior 2 months should also be tested (Fig.23.3).

E. Lymphogranuloma venereum is caused by

Chlamydia trachomatis serovars L1, L2, and L3, and presents with severe inammation which can manifest as unilateral painful inguinal or femoral lymphadenopathy (buboes), genital ulcers, ulcerative proctocolitis or proctitis, or systemic constitutional symptoms. Untreated LGV may have serious sequelae including stulas, strictures, infertility, pelvic brosis, and elephantiasis. The treatment is doxycycline 100 mg PO bid for 3 weeks. Buboes may require drainage. Sexual partners from the prior 2months should be treated.

F. Syphilis, (Fig. 23.4) caused by Treponema

pallidum, has experienced a resurgence among young men, MSM, black men, and Hispanic men. It can present as a solitary nontender genital chancre, multiple chancres, or proctitis. Screening is performed with nontreponemal tests (VDRL and RPR); if this is positive, then a conrmatory treponemal test should be performed. All sexually active MSM and all patients with HIV should be screened at least annually for syphilis. Treatment is a single intramuscular dose of penicillin benzathine 2.4 million units (Table23.1). Sexual contacts should be treated empirically. Repeat testing should be performed at 6 and 12months after treatment.

G. Chancroid, caused by Haemophilus ducreyi,

causes multiple painful purulent genital ulcers with regional lymphadenopathy and bubo formation. It is diagnosed based on

185

Fig. 23.4 Syphilis caused by Treponema pallidum

symptoms and by ruling out syphilis and Herpes. Treatment consists of one dose of ceftriaxone 250 mg intramuscular, one dose of azithromycin 1 g orally, ciprooxacin 500 mg twice a day orally for 3 days, or erythromycin base 500 mg 4 times a day orally for 7days.

H. Granuloma inguinale (donovanosis), caused

by Klebsiella granulomatis, causes painless genital ulcers. Disseminated disease can cause cervical ulceration, pelvic lymphadenopathy, and septic arthritis; HIV-positive patients may experience malignant transformation. It is diagnosed with tissue smears that show Donovan bodies, or PCR.Treatment consists of three-week regimens of doxycycline, cipro-

186

C. Kin

Table 23.1 Management of syphilis infection (F)

Treatment Alternative treatment

Primary, secondary, early latent syphilis

Tertiary or late latent syphilis, syphilis of unknown duration, or relapse of syphilis infection

Neurosyphilis, or patients co-infected with HIV and syphilis

Penicillin G benzathine 2.4 million units IM×1

Penicillin G benzathine 2.4 million units IM weekly×3weeks

Aqueous crystalline penicillin G 18–24 million units daily (given as 3–4 million units IV q4h, OR continuous infusion)×10–14days

oxacin, erythromycin base, or trimethoprim/ sulfamethoxazole.

I. Herpes simplex virus 1 and 2 both cause ano-

genital infection (Fig. 23.5), and 90% of those infected are unaware that they have it. Symptoms include painful vesicular ulcers and/or proctitis, and systemic symptoms especially with the rst clinical episode. Cell culture, PCR, and serologic tests are available. Treatment with antiviral therapy (acyclovir, famciclovir, valacyclovir) can shorten the course of outbreaks, and suppressive therapy can be used in patients with frequent recurrences (≥4 per year) or in those whose sexual partners are negative for HSV.

J. Human papillomavirus infection may occur

in up to 50% of sexually active individuals who are not vaccinated. Low-risk types are HPV 6 and 11 and cause genital warts; highrisk types are HPV 16, 18, 31, 33, and 35 and may cause high-grade dysplasia or squamous cell carcinoma of the anus, cervix, penis, vulva, and vagina. The risk for cancer is higher in immunosuppressed patients, especially in HIV-positive patients. Screening for high-grade dysplasia of the anus is performed with liquid-based anorectal cytology; positive or suspicious ndings should be followed up with anoscopy or high-resolution anoscopy. Treatment options for external genital warts, anal canal warts, and highgrade dysplasia are detailed in Table23.2.

Doxycycline 100mg PO bid×2weeks OR Tetracycline 500mg QID×2weeks

Fig. 23.5 Herpes simplex virus

K. HIV infection may cause painful anal s-

sures and ulcers, and also predispose patients to cryptoglandular disease. Fistulas and abscesses in patients with AIDS should be treated with smaller incisions and drain or seton placement rather than large incisions. Screening for HIV antibodies should be performed in all patients presenting for STD testing. A nucleic acid test may be required to diagnose an acute HIV infection.

23 Anal Conditions: STDs

187

Table 23.2 Management of HPV related lesions (J)

External genital warts

Anal canal warts

High-grade anal dysplasia

Patient-applied therapies:

Podolox 0.5% solution or gel: apply bid × 3days, then 4days without therapy; can repeat cycle up to 4 times OR Imiquimod 5% cream: apply 3 times per week up to 16weeks. Wash treated area with soap and water 6–10h afterwards OR Sinecatechins 15% ointment: apply tid for up to 16weeks

Provider-administered therapies:

Cryotherapy with liquid nitrogen or cryoprobe OR Podophyllin resin 10%–25% OR Trichloroacetic acid (TCA) or Bichloroacetic acid (BCA) OR Surgical fulguration or excision

Cryotherapy with liquid nitrogen OR Trichloroacetic acid (TCA) or Bichloroacetic acid (BCA)- can be applied weekly as needed OR Surgical fulguration or excision Consider high-resolution anoscopy to inspect for high-grade dysplasia

Consider high-resolution anoscopy with ablation and/or excision of aceto-white lesions

L. Molluscum contagiosum, caused by the

Molluscipox virus, results in small, waxy, dome- shaped umbilicated papules that may become secondarily infected due to scratching of the lesions. Treatment consists of curettage excision and cryotherapy and should only be done in immunocompetent patients. Topical treatment with imiquimod 5% cream can be given to immunosuppressed patients.

Anal Considerations: Fournier’s Gangrene

VanessaW.Hui andRahulNarang

Refer to Algorithm in Fig. 24.1

The term “necrotizing soft tissue infection” (NSTI) is a fairly new clinical phrase coined in the 1950s to describe life-threatening infections leading to fulminant tissue destruction associated with sepsis and high death rates. Hippocrates rst described the condition as early as 500 BC as a rapidly progressive bacterial infection that affects any soft tissue from any part of the body, causing cellulitis, myositis and/or fasciitis and associated gangrene. Generally, such infections are divided into two groups based on bacteriology. Type I NSTIs, responsible for 80–90% of all NSTIs, are a polymicrobial infection of mixed aerobic and anaerobic bacteria and more commonly affect patients with immunocompromise or those with chronic disease. Type II NSTIs are less common, occur more commonly in healthy individuals, and typically present as a more severe infection. They are usually monomicrobial (typically involving group A Streptococcus, Aeromonas in freshwater, or Vibrio vulnicus in seawater).

Fournier’s gangrene (FG), most famously

described by the eponymous French venereal

V. W. Hui Department of Surgery, University of Miami, Miami, FL, USA

R. Narang (*) NYU Rangone Health, New York, NY, USA e-mail: rnarang@monteore.org

dermatologist in the nineteenth century, is a NSTI that infects the perineum and/or external genitalia. Similar to most NSTIs, FG infections are polymicrobial, with Streptococcus and Staphylococcus as the main aerobic bacteria involved and with Bacteroides fragilis and Escherichia coli being the main contributing anaerobic counterparts. Recently, several case series have highlighted the emergence of monomicrobial infections with Candida as well as antibiotic-resistant organisms such as methicillinresistant Staphylococcus aureus. Working in syn- ergy, aerobes aggregate thrombocytes while anaerobes produce heparinase to activate localized blood vessel thrombosis, leading to ischemia, necrosis, and gangrene. Sources for FG-causing bacteria include the local skin ora and lower urinary tract, with those infections from the anorectum carrying a worse prognosis and a higher potential for death.

FG usually occurs in people ages 50–60. While it can occur in women, most populationbased studies demonstrate that males are disproportionally affected at a rate of 10 to one and an increasing incidence with older age, plateauing to

3.3 cases per annum by age 50. Children are rarely affected. FG is only responsible for only

0.02% all hospital admissions. Though the mortality for patients with FG had ranged from 20–88% in cases series, recent pooled data from State Inpatient Databases suggest that it is lower at 5–16% per year, though this still remains a signicant mortality rate.

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V. W. Hui and R. Narang

Fig. 24.1 Algorithm for management of Fournier’s gangrene. Timely recognition and treatment for Fournier’s gangrene (FG) begins with a suspicion as well as a combination of history and physical exam, laboratory tests, and/ or imaging workup. If there is no cancer, timing of

Risk factors for FG include baseline comorbidities such as diabetes, human immunodeciency virus (HIV), leukemia, malnutrition and other conditions that can also lead to immunosuppression. Obesity and alcohol abuse have also been associated with an increased incidence of FG.Trauma, surgery, burns, and childbirth are potential inciting factors for FG.

Predictors for mortality include increasing age, hypertension, congestive heart failure, renal failure, and coagulopathy. A one-point increase in the Charlson comorbidity score has been associated with a 50% increase in mortality risk. Hospital admission requiring transfer to teaching hospitals has also been shown to increase the mortality rate and each procedure can potentially increase the patient’s unadjusted odds of death by 27%. Both ndings most likely reect the true severity of the patient’s disease process. Certain interventions also put patients at increased risk of death including need for mechanical ventilation, hemodialysis, colostomy, or penectomy. However,

debridement depends on the hemodynamic stability of the patient, with the possibility of fecal diversion by ostomy. The management in the setting of cancer will depend on patient stability and the status of the cancer in regards to perforation

orchiectomy itself has been associated with a 70% decreased mortality risk. The Fournier’s Gangrene Severity Index (FGSI) has been utilized as a prognostic indicator for survival (Table24.1). Though initially developed from a small sample size, larger retrospective validation studies have demonstrated that this simple index has been highly reliable in predicting survival. A FGSI of eight or less has been associated with a survival rate of 96% while a score of nine or above has been associated with a 46% mortality rate.

Recognition is the key to commencing prompt and appropriate treatment for FG. Symptoms associated with FG may include a prodrome of fevers, chills, malaise, and fatigue. Findings on physical exam may include:

• Pain out of proportion to exam.

• Edema and/or tenderness beyond margin of

erythema.

• Vesicles and/or bullae.

• Thin gray drainage.

24 Anal Considerations: Fournier’s Gangrene

Table 24.1 Fournier’s Gangrene Severity Index (FGSI)

Physiological variable/point assignment High abnormal values Normal

+4 +3 +2 +1 0 +1 +2 +3 +4

Temperature (C)

Heart rate More

Respiration rate

Scrum sodium (mmol/L)

Serum potassium (mmol/L)

Serum creatinine (mg/100mL, ×2 for acute renal failure)

Hematocrit (%)

White blood count (total/

×1000)

Serum bicarbonate (venous, mmol/L)

Reprinted with permission from Laor E, Palmer LS, Tolia BM, Reid RE, Winter HI.Outcome prediction in patients with Fournier’s gangrene. The Journal of urology. 1995 Jul;154 (1):89–92. © Elsevier

More than 41

than 180 More

than 50 More

than 180

More than 7

More than 3.5

More than 60

More than 40

More than 52

39–40.9 – 38.5–38.9 36–38.4 34–35.9 32–33.9 30–31.9 Less

140–179 110–139 – 70–109 – 56–69 40–54 Less

35–49 25–34 12–24 10–11 6–9 Less

160–179 155–159 150–154 130–149 – 120–129 111–119 Less

6–6.9 – 5.5–5.9 3.5–5.4 3–3.4 2.5–2.9 – Less

2–3.4 1.5–1.9 0.6–1.4 Less

than 0.6

– 50–59.9 46–49.0 30–45.9 20–29.9 – Less

– 20–39.9 15–19.9 3–14.9 – 1–2.9 – Less

41–51.9 – 32–40.9 22–31.9 – 18–21.9 15–17.9 Less

Low abnormal values

– –

191

than

29.9

than 39

than 5

than 110

than 25

than 20

than 1

than 15

• Malodor.

• Crepitus.

• Cutaneous anesthesia.

• Ecchymosis and/or necrosis.

Several criteria have been used to distinguish NSTI from non-NSTI including the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) (Table24.2). There should be a clinical suspicion for NSTI and FG if a score is greater than six, with a 92% positive predictive value. Imaging by plain radiography, ultrasonography, or computed tomography may be helpful in cases where a denitive diagnosis cannot be made on physical exam, as 90% of FG soft tissue inltration has subcutaneous emphysema that may be visualized on radiography.

Serial surgical debridement remains the mainstay therapy and serves to eradicate all necrotic tissue that may potentially be a nidus for ongoing infection, along with the concomitant use of broad-spectrum intravenous antibiotics. Typical combination of antibiotics includes carbapenem or beta-lactam-beta-lactamase inhibitor with clindamycin for antitoxin effects against toxin- elaborating strains of Staphylococcus and Streptococcus with an additional antibiotic with activity against methicillin-resistant Staphylococcus aureus. As always, management of the sequelae of sepsis requires aggressive resuscitation with intravenous uid and/or blood products and appropriate level of intensive care support. Adjunctive treatments to consider include hyperbaric oxygen to increase

192

V. W. Hui and R. Narang

Table 24.2 Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC)

Variable, Units β Score C-Reactive protein, mg/L <150 0 0

≥150 Total white cell count, per mm <15 0 0 15–25 0.5 1 >25 2.1 2 Hemoglobin, g/dL >13.5 0 0 11–13.5 0.6 1 <11 1.8 2 Sodium, mmol/L

≥135 <135 1.8 2

Creatinine, μmol/L

≤141 >141 1.8 2 Glucose, mmol/L

≤10 >10 1.2 1

This was a reprint from Reprinted with permission from Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Critical care medicine. 2004 Jul;32(7):1535–41. © Wolters Kluwer Final model constructed using factors found to be independently predictive of necrotizing fasciitis on multivariate analysis. β values are the regression coefcients of our model after adjusting for a shrinkage factor of .89. The maximum score is 13: a score of ≤6 should raise the suspicion of necrotizing fasciitis and a score of ≥18 is strongly predictive of this disease. To convert the values of glucose to mg/dL, multiply by 18.015. To convert the values of creatinine to md/dL, multiply by p0.01131

3.5 4

0 0

tissue oxygen tension and neutrophil function in order to inhibit the thrombotic effects of anaerobes, curb exotoxin production, and limit the degree of necrosis. Nutrition, preferably enteral, should be optimized in order to promote wound healing.

Fecal diversion may be necessary for severe perineal FG in order to minimize the ongoing bacterial contamination in the wound. Indications for fecal diversion include involvement of the anal sphincter as well as fecal incontinence. Diverting colostomies are more often necessary in patients whose FG originates from an anorec-

tal source. The use of a colostomy should be judicious and highly individualized, as it has not been shown to improve overall survival. In addition, patients with ostomies typically suffer longer hospitalizations, higher nancial burden from hospital costs, increased risk for abdominal wall hernia, and lower quality of life. Rectal tubes may be an adequate method for fecal diversion without the added burden of colostomies, with the caveat that they are a relative contraindication in those with colon or anorectal cancer, anorectal trauma, and anal stula.

A. The anorectum is the most common origin of

FG. However, anorectal cancer as the causative agent of FG is rare, encompassing only 0–3% of all anorectal-related FG.The management algorithm for anorectal cancers in the setting of FG depends on patient hemodynamics, the severity of FG, and the presence of a cancer-associated perforation (Fig.24.1). Dependent on the location of the anorectal source and whether the anal sphincter is involved, the infection may have the potential to travel toward (1) the supercial fascia of the perineum to the scrotum and/or penis and superiorly along the anterior abdominal wall, (2) posteriorly into the presacral space and into retroperitoneum, or (3) into the ischiorectal fossa.

B. Pelvic imaging may be necessary to delineate

the extent of debridement necessary to eradicate disease. While perforation is an indicator of cancer aggressiveness, it is difcult to determine whether cancer itself is a poor prognostic indicator for survival given the rarity of such cases.

C. At times, resection of the primary cancer,

in the form of either a low anterior resection for upper to mid-rectal tumors or an abdominoperineal resection for low rectal cancers, at the time of debridement may be necessary in the setting of a frank perforation.

D. If an abdominoperineal resection is per-

formed, the perineal wound should be left open. If primary resection is not technically feasible or if the patient is too hemo-