Keywords
anorectal - benign - anal - abscess - fistula - incontinence
Anal Abscess
Etiology
Several hypotheses of the origin of anal abscesses have been published throughout
the years. Generally, the most accepted hypothesis states that obstruction of the
mucous anal gland outlet duct is the initial stage of anal abscess formation, which
occurs due to fecal material or local trauma. This later leads to stasis and infection.[1] Afterward, pus may generate and traverse through the paths of least resistance along
muscular fibers between the internal and external anal sphincters or through the external
anal sphincter into the ischioanal fossa.[1]
[2] Parks published a study in 1961, which reported that 70% of specimens of anal fistula
tracts that had been excised presented with anal gland epithelium and 25% of those
samples showed cystic dilation of an anal gland.[3] Parks' cryptoglandular theory has been broadly accepted ever since. Less frequent
noncryptoglandular causes of anorectal abscess occur in approximately 10% of cases
and include inflammatory bowel disease (Crohn's disease and ulcerative colitis), infection
(tuberculosis, actinomycosis, lymphogranuloma venereum [LGV]), trauma (impalement,
surgery, foreign body), and malignancy (carcinoma, leukemia, lymphoma, radiation).[4]
Classification
Anal abscesses are classified according to the anorectal space that they occupy[5]: (1) subcutaneous abscess (perianal), (2) intersphincteric abscess, (3) ischioanal
abscess, and (4) supralevator abscess. Superficial types, including perianal and ischioanal
abscesses, are the most common, consisting of approximately 80% of cases ([Table 1]).[4]
[5]
[6]
Table 1
Common benign anorectal disorders[54]
|
Benign anorectal disorders
|
|
• Anal abscess
|
|
• Anal fissure
|
|
• Pilonidal disease
|
|
• Sexually transmitted diseases
|
|
• Hemorrhoids
|
|
• Anal fistula
|
|
• Fecal incontinence
|
|
• Proctalgia
|
Diagnosis and Barriers to Care
Although superficial forms of anorectal abscesses are usually easy to diagnose through
patient's history and physical exam as there tends to be local swelling and pain,
and less frequently fever and suppuration,[7] in low-income settings a prompt diagnosis may be delayed due to poor access to medical
care, lack of patient's medical insurance due to economic limitations, and saturation
of medical services in available local hospitals or clinics. Mexico, for example,
is situated far behind other Organization for Economic Cooperation and Development
(OECD) countries in health status and availability.[8] On the other hand, deeper abscesses (supralevator or high ischiorectal) may be more
difficult to diagnose as swelling tends not to be readily visible on physical exam
and pain may occur in a less specific pattern in the perineum, lower back, or buttocks.[9]
[10]
[11] Thus, these deeper abscesses may have a further delay in diagnosis and treatment.
For those patients in whom diagnosis is not possible through physical exam, computed
tomography (CT) scan, endoanal ultrasound (EAUS), or magnetic resonance imaging (MRI)
should be considered.[7] However, these studies are commonly difficult to afford and sometimes not readily
available for patients in the low-resource setting. In Mexico alone, there are only
2.9 MRI units and 6 CT scanners per 1,000,000 inhabitants,[12]
[13] far less than those available in many first-world countries.
Management and Outcomes
Antibiotics are indicated when cellulitis occurs if there is failure to improve after
proper incision and drainage of the abscess or in immunosuppressed patients.[4] Otherwise, antibiotics are not routinely used, as some studies have found that they
also do not prevent fistula formation.[14] Incision and drainage remains the mainstay of treatment for anal abscesses. Depending
on the type of anal abscess, the site for drainage will be chosen; as a general rule,
“outward” drainage is recommended whenever an abscess enters or passes through skeletal
muscle (levator ani or external anal sphincter), whereas all other types must be drained
internally through the rectum or anal canal.[15] Recurrence occurs in up to 44% of cases, most commonly during the first year after
initial drainage.[16]
[17]
[18]
[19]
[20]
[21] An alternative method for ischioanal abscesses is to make an incision, drain the
abscess, and place a Malecot or Pezzer drain under local anesthesia, which is later
removed when suppuration ceases and there is cavity closure around the drain (usually
3–10 days).[22] Horseshoe abscesses, which most commonly originate in the deep postanal space and
later extend to one or both ischioanal spaces, may be drained utilizing the modified
Hanley technique entailing partial sphincterotomy combined with seton placement.[23]
[24] Abscess drainage with simultaneous fistulotomy may be considered. A Cochrane review
of six randomized controlled trials showed that this approach was associated with
a significant decrease in abscess recurrence, fistula or abscess persistence, and
need for subsequent surgery (relative risk, 0.13; 95% confidence interval [CI], 0.07–0.24)
without a statistically significant increase in incontinence.[25] All of the above-mentioned treatment options are usually readily available and not
costly; thus, they are generally applicable in a low-income setting.
Anal Fissure
Definition and Etiology
An anal fissure is a tear in the epithelial lining of the distal anal canal.[26] Despite many theories, the exact cause remains uncertain. Although unclear if it
is the cause or effect of anal fissures, sphincter hypertonicity, a common finding
in this disease, has been documented by anal manometry in several studies and is the
leading hypothesis behind the pathogenesis.[26]
[27]
[28] Another theory states that relative ischemia exists in the anoderm at the posterior
midline. This has been demonstrated by arteriography and laser Doppler flow studies,
and it is thought to be what generates the proper setting for fissure formation.[29]
[30] Although local trauma (large stool, anorectal intercourse, surgical procedures)
has been associated with many cases of anal fissures, these can occur in the absence
of trauma or constipation and may even occur in patients with diarrhea or sphincter
hypotonia.[26]
Classification and Clinical Features
Symptoms, especially in acute fissures, are sharp, burning, tearing pain or spasms
that can last for hours after defecation and bright red bleeding with bowel movements.
Fissures are classified as acute versus chronic and typical versus atypical.
Diagnosis and Barriers to Care
A thorough history and physical exam will usually suffice to establish the diagnosis
of anal fissure in most patients.[31] The patient may lie in lateral decubitus or prone jackknife position, and by gently
separating the buttocks, inspection should be done first at the posterior midline,
where most fissures are found ([Fig. 1A, B]). Assessment of anal resting pressures through digital rectal exam may be performed,
and if tolerated, office anoscopy may be performed selectively with previous application
of anesthetic lubricant to confirm diagnosis when needed.[4] The above-mentioned methods usually lead to a straightforward diagnosis. Nevertheless,
access to medical care and an experienced colorectal surgeon is not easily obtained
in low-resource settings. In Latin America, this in part is related to the limited
expenditure allotted to health care in many countries. For example, in Mexico and
Brazil (the countries of residence of the authors), health spending amounts to $1,198
and $1,514 USD per capita, respectively, whereas in countries such as Japan, the United
Kingdom, and the United States, health expenditure reaches $4,691, $5,268, and $10,948
USD per capita, respectively.[32] Fortunately, around 93% of acute fissures cure spontaneously.[33] However, chronic anal fissures represent approximately 10% of office visits in proctologic
clinics[34]; nevertheless, their real incidence might be underestimated because more than 80%
of patients with benign anorectal diseases do not seek medical care.[35]
Fig. 1 (A, B) Anorectal fissure in the posterior midline of the anal verge.
Management and Outcomes
Nonoperative treatment is safe, with few side effects, and should be the first-line
treatment. Nonoperative measures such as sitz baths and use of psyllium fiber or other
bulking agents will resolve the symptoms of almost 50% of patients with an acute anal
fissure.[36] Topical nitric oxide donors are associated with healing in approximately 50% of
chronic anal fissures[37]; however, a common side effect in up to 30% of patients is headache,[37]
[38] which may lead to treatment cessation in up to 20% of patients.[39] In some countries, nitroglycerine is not commercially available and may need to
be created at a compounding pharmacy. An alternative for topical treatment is the
use of calcium channel blocking agents, such as diltiazem or nifedipine, which have
been associated with healing rates of anal fissures of 65 to 95%.[40] Some prospective studies have reported healing rates ranging from 18 to 71% with
botulinum toxin application (20–60 units) within 9 weeks of treatment, with results
comparable to or slightly better than topical therapies.[41]
[42] Thus, botulinum toxin application provides similar results compared with topical
treatment as first-line therapy for chronic anal fissures; however, it provides only
modest improvement in healing rates as second-line therapy following treatment with
topical therapies.[36] Nevertheless, botulinum toxin might be expensive and difficult to obtain in certain
areas. For example, in Mexico a bottle of 100U of botulinum toxin may range in cost
from $3,600 to $4,600 pesos (the equivalent of $180 to $230 USD). Lateral internal
sphincterotomy (LIS) is superior when compared with nitrates, calcium channel blockers,
or botulinum toxin, with healing rates of 88 to 100% and with fecal incontinence rates
ranging from 8 to 30%, as shown by multiple randomized trials; for this reason, current
guidelines of the American Society of Colon and Rectal Surgeons (ASCRS) advocate LIS
as the surgical treatment of choice for chronic anal fissures and state that it may
be even offered in select patients without first confirming failure of pharmacological
treatment.[36] Treatment of atypical fissures should focus in identifying the etiology to provide
specific disease-directed therapy.
Pilonidal Disease
Etiology
It is thought that pilonidal disease (PD) occurs secondary to trauma of the skin and
hair follicles in the natal cleft due to trapping of hairs, which are not necessarily
those that originate in this area. Local friction, warmth and moisture, and possibly
local hypoxia lead to local trauma secondary to the barbed texture of hair, which
in time produces a granulomatous foreign body–type reaction. Initially, a sinus that
may drain fluid occurs, but can later progress to multiple sinuses, cystic dilation,
and even abscess formation.[4] Risk factors associated with the development of PD include body mass index > 25,
poor hygiene, family history of PD, hirsutism, deep natal cleft, prolonged sitting,
and excessive sweating.[43]
[44]
[45]
Clinical Features and Diagnosis
During inspection, characteristic midline pits are almost always present in the natal
cleft. In acute cases, patients may present with signs of infection including cellulitis
or an abscess. On the other hand, chronic PD commonly presents with a draining sinus
in the intergluteal fold ([Fig. 2]). Usually, midline pits are connected to subcutaneous tracts that can be easily
misdiagnosed as fistulas.[4] In the majority of cases, simple inspection and palpation during physical exam are
enough to establish diagnosis. Thus, laboratory or radiology examinations are not
routinely required.[46]
Fig. 2 Chronic draining sinus in the intergluteal fold in patient with typical pilonidal
disease.
Barriers to Care
PD affects mostly the working-age population and presents a significant disease burden
worldwide. It is more common in Caucasian males with an incidence of 1.1%.[47] Costs are not widely reported; however, a recent Swedish study reported a cost of
$6,222 EUR per patient for conventional wide excision and closure for pilonidal sinus,
with a 32% recurrence rate at 5 years.[48]
[49] Additionally, the social impact of PD on young people significantly affects their
interpersonal relationships, education, and social activity.[50] In low-resource settings, PD presents quite a challenge as it is a disease associated
with considerable recurrence and complication rates, along with a probability of needing
multiple treatment procedures before achieving adequate healing, which can be quite
costly.
Management and Outcomes
In a low-resource setting, it is particularly important to offer patients a treatment
approach that will effectively resolve the problem while shortening time of recovery.
Thus, whenever excision is advised, primary closure/flap creation should be attempted
(if technically feasible and infection is not present) as healing by secondary intention
would imply a significant economic burden and necessity of reaching medical care for
a longer period. In general, no single procedure is superior to the other.[49] If an abscess is encountered, incision and drainage is indicated. Around 10 to 15%
of patients will have abscess recurrence, and 40 to 60% will progress to develop a
pilonidal sinus requiring excision.[49] With the lay open technique, an incision is made over the pilonidal sinus tract
of the PD and left open for closure under secondary intension. Rates of success for
the initial operation can be as high as 97%, while recurrence may be as low as 8.8%.[51]
[52] Nevertheless, this will require more intense wound care sometimes with need of assistance
and further expense. Primary closure has typically been regarded as having high risk
for local infection; however, a Cochrane review including 26 trials and 2,530 patients
found that there was faster healing with this technique and no difference in infection
rates. In this review, off-midline primary closure reported faster healing and lower
infection rates when compared with midline closure.[53] Primary closure with a flap may be considered, with the objective of excising the
diseased tissue, covering the defect with healthy tissue, and raising the natal cleft
anatomy.[54] A wide variety of flap techniques have been described. The Karydakis flap requires
elliptical incision down to the sacral fascia with the ellipse corners 2 cm off the
midline; after excision of the complete PD, a flap of skin and subcutaneous fat is
created and raised to the opposite side of the midline, with closure in layers of
the wound.[54] Another commonly used flap technique is the Bascom cleft lift, in which the natal
cleft is elevated and closed off the midline ([Fig. 3]). More complex flap techniques have been used especially in cases of wider disease,
for example, the Limberg flap in which a rhomboid flap is created and rotated to cover
larger defects after resection.[54] Other minimally invasive treatments including endoscopic/video-assisted ablation
of pilonidal sinus, laser ablation of pilonidal sinus, and trephination have been
described. In general, the specific resection technique should be chosen on a case-by-case
basis and considering the individual surgeon's expertise. In addition to wound care,
an adjunct to treatment is postoperative hair removal as it has been associated with
a decrease in recurrence rates.[55]
Fig. 3 Bascom cleft repair following excision of a pilonidal cyst.
Sexually Transmitted Infections
Sexually Transmitted Infections
Etiology
Anorectal sexually transmitted infections (STIs) are on the rise, possibly due to
increased practice of receptive anal intercourse. Additionally, other risk factors
are oral–anal sex and contiguous spread from genital infections.[54]
Bacterial STIs
Chlamydia trachomatis
In the United States, it is the most commonly reported STI.[56] Males commonly present with urethritis, with symptoms of pyuria, dysuria, and urinary
frequency, whereas women may commonly have urethritis or cervicitis with cervical
discharge and bleeding. When the rectum is affected, patients present with proctitis
frequently with tenesmus, pain, and discharge.[54] Diagnosis is performed using nucleic acid amplification test (NAAT) with 97% sensitivity
and specificity.[57] Patients should be treated with 1 g of azithromycin or doxycycline 100 mg twice
daily for 7 days. Alternatively, erythromycin or quinolones may be used.
Lymphogranuloma Venereum
It is caused by specific serotypes of C. trachomatis, namely serotypes L1–L3. Unlike other serotypes of C. trachomatis, LGV produces more invasive disease leading to severe proctitis with ulcers that
can initiate the formation of abscesses, fistulas, chronic pain, and strictures. Since
it also affects the lymphatic system, proctitis may be accompanied by usually unilateral
inguinal and femoral lymphadenopathy. Rectal pain, tenesmus, discharge, fever, fatigue,
and weight loss are common manifestations of proctitis. Diagnosis is made by clinical
findings along with rectal or genital swab NAAT to detect C. trachomatis, followed by confirmatory LGV testing. Testing includes cultures, direct immunofluorescence,
or nuclei acid detection.[54] Treatment is doxycycline 100 mg twice daily for 21 days. Erythromycin is an alternative
for allergic patients. Infected lymph nodes may require aspiration or incision and
drainage.[54]
Gonorrhea
Neisseria gonorrhoeae, an intracellular diplococci, is the second most common STI in the United States.[56] Most cases are asymptomatic; however, infection may progress to cervicitis, urethritis,
proctitis, and pelvic inflammatory disease in women and urethritis, epididymitis,
or proctitis in men. Symptoms of urethritis include dysuria and urethral discharge,
and in cases of proctitis tenesmus, hematochezia or purulent discharge may be present.[58]
[59] Anoscopy may show erythema and friable mucosa with mucopurulent discharge. Diagnosis
is made with detection of gonococcus in urogenital, anorectal, pharyngeal, or conjunctival
specimens or in first-catch urine.[60] Definitive testing should be done with NAAT as it has a sensitivity and specificity
of 100%; however, it does not provide susceptibility testing for which culture may
be required in some cases.[54] Treatment consists of ceftriaxone 250 mg given once intramuscularly plus 1 g of
azithromycin. Patients should refrain from sexual intercourse for 7 days after completing
therapy.[54]
Syphilis
It is a systemic disease, caused by the spirochete Treponema pallidum. Syphilis is endemic in developing countries and especially common in patients with
limited access to health care or economic resources.[61] Primary syphilis presents with a commonly painless ulcer 1 to 21 days after infection.
Secondary syphilis presents weeks to months after inoculation with systemic symptoms
such as fever, arthralgias, malaise, lymphadenopathy, a rectal mass, and a rash.[54] If untreated, a latent asymptomatic phase continues, which can last from 1 up to
many years. Tertiary syphilis presents with cardiac affection, gummas, and necrotic
and ulcerated center growths throughout the body. Neurosyphilis can occur at any stage
of the disease.[54] Initial diagnosis is done with venereal disease research laboratory and rapid plasma
reagin; however, confirmatory tests should be performed including antibody testing
such as fluorescent treponemal absorption tests and other enzyme immunoassays and
immunoblots.[57] Penicillin G is the treatment of choice for all stages of the disease, including
a single intramuscular dose of benzathine penicillin G 2.4 million units for early-stage
disease and the same dose once a week for 3 weeks in tertiary syphilis.[62]
Chancroid
This anogenital disease, caused by Haemophilus ducreyi, is characterized by the presence of lesions that start as a papule and later progress
to a pustule and open to form painful ulcerations. Ulcers may be multiple. Unilateral
suppurative inguinal lymphadenopathy may occur. Diagnosis is mainly clinical and is
made by the following criteria: presence of one or more painful genital ulcers, absence
of syphilis infection, regional lymphadenopathy, and an ulcer exudate that is negative
for herpes simplex virus (HSV).[57]
[63] Treatment consists of a single dose of either ceftriaxone 250 mg intramuscularly
or azithromycin 1 g orally.
Donovanosis (Granuloma Inguinale)
Klebsiella granulomatis, an intracellular bacterium, is the cause of the disease. It is more prevalent in
tropical areas of the world and in developing countries. Patients commonly present
with genital papules or subcutaneous nodules that can progress to ulcers, which are
usually painless, granulomatous, snakelike lesions that grow centrifugally. Lesions
can easily bleed and be self-inoculated. Pseudobuboes may also appear.[64] They con also appear in the anorectum manifested as verrucous lesions and/or deep
fissures with fibrotic ulcers. Diagnosis is achieved by identifying Donovan bodies
in mononuclear cells with Giemsa-stained smears obtained from the ulcer. Polymerase
chain reaction (PCR), where available, can aid in the diagnosis.[54] Recommended treatment is azithromycin 1 g orally once a week for 3 weeks or 500 mg
orally once a day for 3 weeks.[57]
Viral STIs
Herpes Simplex Virus
HSV, a DNA virus from the Herpesviridae family, is associated with genital lesions
and proctitis especially in men who have sex with men (MSM).[57]
[65] In the anorectum, lesion are characterized by blistering in the mucosa with symptoms
appearing in 4 to 21 days after receptive anal intercourse including burning sensation,
pain, and pruritus.[66] Initially, lesions may develop as vesicles with surrounding erythema on perianal
skin or in the anal canal. Lesions later rupture and become ulcerated ([Fig. 4]). Proctoscopy may demonstrate a friable mucosa and diffuse ulcerations limited to
the distal 10 cm of the rectum.[54] Serologic PCR assays with nucleic acid amplification of HSV DNA is the gold standard
for diagnosis. Other methods for detection include cell growth culture and Tzanck
preparation with direct immunofluorescence. Oral antiviral medications that have shown
good results on randomized controlled trials and thus are currently used for treatment
include acyclovir, valacyclovir, and famciclovir.[67]
[68]
[69]
[70] Intravenous acyclovir should be considered for severe HSV infection and systemic
or neurologic disease that require hospitalization.[54]
Fig. 4 Ulcerated perianal lesions secondary to herpes simplex virus.
Human Papilloma Virus
Condylomas are common lesions among all sexual orientations; nevertheless, they are
even more so among MSM. Several serotypes exist including subtypes 6 and 11, representing
the most common ones and presenting as condylomas or warts of the genital region,
anus, or rectum. On the other hand, subtypes 16 and 18 are most frequently associated
with anal dysplasia and cancer.[71] Genital lesions appear as gray or pink cauliflowerlike growths that may lead to
bleeding, pruritus, pain, or hygiene difficulty. Anoscopy should be performed to rule
out lesions in the anal canal.[54]
[72] Diagnosis is usually made with physical exam. Dysplastic lesions may be detected
with application of acetic acid, while high-resolution anoscopy is commonly utilized
for ruling out intra-anal disease. Biopsy may be performed when diagnosis is not clear,
whereas anal cytology has been recommended but with limited evidence.[72] A wide variety of treatment options exist, including topical medication, cryotherapy,
fulguration, and excision; however, recurrence rates may range from 4 to 26%.[54]
[73]
[74]
Molluscum Contagiosum
This virus from the poxvirus family produces characteristic pruritic or painful, contagious,
flesh-colored or gray–white skin lesions after direct contact with skin or mucous
membranes containing active lesions. It can also be self-inoculated to several locations
of the body. The disease is commonly self-limiting in nonimmunocompromised patients.
When needed, phenol, trichloroacetic acid, podophyllotoxin, or imiquimod is used for
topical treatment. Additionally, ablation with electrocautery or cryotherapy has shown
to be effective.[54]
[75]
[76]
[77]
Human Immunodeficiency Virus
This RNA retrovirus affects CD4 receptors to enter the cell, which leads to compromised
immune system activation and later to destruction of T lymphocytes. Anal manifestations
include human immunodeficiency virus (HIV)-related anal ulcer, hemorrhoids, fissures,
fistulas, abscesses, or as other conditions related to HIV status (anal condylomas,
herpetic ulcers). When AIDS arises, potential anal manifestations are anal squamous
cell carcinoma, lymphoma, and Kaposi's sarcoma.[78]
[79] Anorectal abscesses should be drained with an incision close to the anal verge,
while fistulas should be managed with setons or sphincter-preserving surgeries. Treatment
for anal fissure is similar as for non-HIV patients; however LIS should be used cautiously
only in those in whom ulcerating disease has been ruled out. Intralesional steroids
have been utilized for treatment of HIV-related anal ulcers with good results; however,
if medical treatment fails, ulcer excision and mucosal advancement flap may be considered.[78]
[80]
Parasitic STIs
Pediculosis Pubis
The parasite Pthirus pubis may produce infestation in the pubic hair and perianal area after sexual contact.
Patients typically present with pruritus, and the infested skin may show flaky or
crusted lesions. Diagnosis is mainly clinical; nevertheless, dermoscopy can be used
to visually detect the parasites in the hair follicles.[81] Treatment with first-line options (permethrin 1% cream or pyrethrins with piperonyl
butoxide) or alternative medications (malathion 0.5% lotion, ivermectin or lindane)
is available. Additionally, combing the affected hair for removing nits and washing
of clothing and bed sheets should be done.
Scabies
This disease is caused by the parasite Sarcoptes scabiei, which can be transmitted through fomites and commonly through sexual contact.[82] Pruritus is the main symptom, and it occurs predominantly nocturnally and is associated
with papules, pustules, and excoriations that appear in a symmetric pattern most frequently
in the interdigital webs, nipples, or genitals.[54] Diagnosis is made by identifying burrows, mites, eggs, or the mites' feces from
affected areas.[83] Recommended treatment for scabies includes permethrin 5% cream or oral/topical ivermectin
or alternatively lindane (lindane should only be used in failure or nontolerance to
the above-mentioned medications due to risk of toxicity).
Limitations and Strategies in the Management of STIs in Low-Resource Settings
The use of state-of-the-art diagnostic tests to establish etiology to provide pathogen-directed
treatment is widely accepted for high-income settings.[84] These include specialized, microscopic, cultural, and serological tests and, more
recently, NAATs. Nevertheless, in a low-resource setting, the cost of setting up laboratory
facilities that can provide such test might be prohibitive; furthermore, patients
may not have access to hospitals or clinics with laboratory facilities at all. Thus,
these constraints have led to empiric treatment approaches (syndromic management)
for STIs based on clinician knowledge as a common form of management in low-resource
areas.[84] For this purpose, point-of-care tests have been developed to provide prompt STI
definitive diagnosis, reducing delay in treatment.[85] To promote the development of simple, accessible, and rapid point-of-care tests,
the World Health Organization (WHO) developed the ASSURED (affordable, sensitive,
specific, user-friendly, rapid and robust, equipment free, and delivered to end users)
benchmark.[86] Point-of-care tests that meet the WHO ASSURED benchmark could bridge the gap for
STI case management and control in these low-resource settings.[85]
Hemorrhoids
Definition and Etiology
Anal cushions or hemorrhoids are part of the normal anatomy of the anal canal. They
contribute 15% to the continence mechanism.[87] Those vessels are a mixture of arteries and veins. In fact, they are formed by anal
mucosa, loose connective tissue, smooth muscle, and arterial and venous vessels, with
the arterial component being more prominent. This anatomical particularity explains
the occurrence of red blood bleeding, the most common symptom of this condition. The
prevalence of hemorrhoids is unknown, although it is one of the most common benign
condition for the colorectal surgeon. To date, the exact causes and the pathophysiology
of this condition is poorly understood. Risk factors for hemorrhoids includes constipation
and straining, and a diet poor in fiber and rich in spices. In addition, pregnancy
and hereditariness are associated with this condition.
Classification
Hemorrhoids can be classified as external and internal hemorrhoids, for which different
approaches are necessary. ([Fig. 5]). External and internal hemorrhoids are located distal and proximal to the dentate
line, respectively. External hemorrhoids are covered by the anoderm or skin.
Fig. 5 Internal and external hemorrhoidal disease.
External hemorrhoids can thrombose and can cause pain, itching, and bleeding, while
internal hemorrhoids are classified and graded according to the size and relation
to the anal verge[88] ([Table 2]).
Table 2
Classification of hemorrhoids
|
Grade I
|
Nonprolapsing hemorrhoids
|
|
Grade II
|
Prolapsing hemorrhoids on straining but reduce spontaneously
|
|
Grade III
|
Prolapsing hemorrhoids requiring manual reduction
|
|
Grade IV
|
Nonreducible prolapsing hemorrhoids, which include acutely thrombosed, incarcerated
hemorrhoids
|
Diagnosis and Barriers to Care
Colorectal surgeons are usually well trained to realize the proctologic examination,
which is the best way to establish the diagnosis. Patients can be examined in the
lateral decubitus position or in the prone position. Inspection is performed with
a good light source and after digital examination, patients underwent anoscopy with
a side-viewing anoscope. However, all patients with a history of mucous discharge
or rectal bleeding should have the colon evaluated through a complete colonoscopy.
In low-income countries, colonoscopy is not available to all patients and many times
a rigid or flexible sigmoidoscopy can be performed to exclude a rectal cancer, the
most feared diagnosis.
Management and Outcomes
Management in any part of the world begins with correction of bowel habits, including
fiber in the diet and fiber supplements to form the stool and facilitate evacuation.
This simple management has level I evidence according to many gastroenterological
colorectal societies.[89] Therefore, in low-resource settings, where a high-fiber diet is facilitated by abundance
of fruits and vegetables, this first conservative measurement represents the main
option, together with warm sitz baths and topical medications, which may be the only
treatment required. In addition, in Brazil and other Latin American countries, coumarin
and other phlebotonic medications are available and frequently utilized, especially
for thrombosed hemorrhoids.[90] Office-based procedures such as sclerotherapy and especially rubber band ligation
are the most utilized methods for grade I and II hemorrhoids. In Brazil, a macro rubber
band equipment was introduced by Reis Neto, with good results[91] ([Fig. 6]). The goal of a rubber band ligature is to promote fibrosis of the submucosa with
subsequent fixation of the anal epithelium to the underlying sphincter. More than
1,500 patients have been treated with the macro ligation, and Reis and colleagues
have demonstrated a better fibrosis and fixation by banding a bigger volume of mucosa.
When grade III and IV piles with mucosal prolapse are present, surgical treatment
is indicated. In fact, the most common excisional procedures, such as the Milligan-Morgan
and the Ferguson operations, remain the first choice and the most indicated procedures
for grade III and IV hemorrhoids.[92] The use of other more recent techniques, such as stapler and Doppler-guided hemorrhoidectomy,
implies having additional cost due to the required equipment, and therefore, these
recent techniques are less utilized in low-resource settings. However, because operations
can cause significant pain, techniques of preemptive analgesia were implemented in
several countries. In Latin America, spinal anesthesia is frequently utilized, and
surgeons are being trained to utilized local anesthesia with pudendal block immediately
after the procedure.
Fig. 6 Equipment used for rubber band ligation.
Anal Fistula
Definition and Etiology
Anal fistula is a benign but frequently complex situation for the patients, due to
both the symptoms associated with inflammation of the tracts and the implications
in terms of preservation of continence mechanism.[93] In the majority of cases, it arises from a previous anal abscess. The prevalence
and incidences of anal fistula are not different from other developed countries. The
main mechanism is related to the cryptoglandular origin, and it is observed more in
male and obese patients.
Classification
Anal fistulas are classified according to the anatomical site of the tracts in relation
to the sphincter muscles.[94] Four main classes of fistulas are described in [Table 3]
Table 3
Anal fistula classification
|
Class
|
Description
|
|
Intersphincteric
|
The internal opening originates in the dentate line and the track in located between
the internal and external sphincter with the external opening in the perianal region
close to the anal verge
|
|
Transsphincteric
|
The tract traverses the internal and external sphincter with the opening in the ischiorectal
fossa
|
|
Suprasphincteric
|
The tract originates at the dentate line more cephalad to the external sphincter mechanism
before opening into the skin at the ischiorectal fossa
|
|
Extrasphincteric
|
The tract is more complex and traverses the muscles including the puborectalis with
the opening proximally at the dentate line or in the lower rectal wall
|
Diagnosis and Barriers to Care
Most patients report a history of previous anal abscess and development of an inflamed
area with purulent discharge. Diagnosis is established with a good history and physical
examination. Once the external opening is visualized, a gentle digital examination
is performed to exclude residual abscess, muscle tenderness, and fecalomas or rectal
tumors. If anal pain is not impeditive for anoscopy, anal canal evaluation can be
performed to look for the internal opening, anal papillae, and associated hemorrhoids.
Imaging methods such as MRI and EAUS are available in most of the important cities
and referenced hospitals.[95] However, these methods are not utilized in small cities, as specialized colorectal
units are not available. Therefore, many complex cases, especially those associated
with inflammatory bowel disease, are sent to the big cities, where specialized surgeons
are more experienced. Imaging methods are especially important in complex, extrasphincteric,
or suprasphincteric fistulas. In South America, portable and more accessible ultrasound
transducers were introduced recently. These transducers can be utilized in the operation
room and fistula tracks can be well demonstrated using oxygen peroxide.[96] This is particularly interesting for cases where sphincter muscles are involved
([Fig. 7]). When comparing MRI with EAUS, sensitivity of both methods is comparable (0.87;
95% CI, 0.70–0.95).[97] However, EAUS is a safe and less expensive preoperative investigation for fistula
surgery.[98]
Fig. 7 Endorectal ultrasound showing fistula involving sphincter complexes.
Management and Outcomes
Surgical treatment is usually necessary. Identification of the tract with probes under
anesthesia is the most common approach, specially performed by general surgeons in
small cities, which place a variety of materials that serves as setons. The most common
technique is a fistulotomy, which allows cutting along the whole length of the fistula
track, leaving it open to heal.[99] According to the Practice Parameters of the ASCRS, fistulotomy has grade of recommendation
1B.[7]
For fistulas with long and complex tracks, when operations are not successful, those
patients are sent to more specialized surgeons, when, in many situations, a fistulotomy
has been already performed, with consequences to the sphincter mechanism. Anal deformities
and asymmetric anus can be the result of a nonspecialized and trained surgeon dealing
with this benign but tricky pathology. For persistent tracks with compromised sphincter
muscles, more advanced techniques such as ligation of intersphincteric fistula tract
and advancement flaps could be other options.[100] Because this pathology is complex, several procedures have been tried, including
the use of glues, video-assisted anal fistula treatment (VAAFT), plugs, and, more
recently, stem cells.[101]
[102] Better results appears to be related to procedures that allow opening of the tracks
and removal of inflammatory tissue. The use of stem cells may improve the outcomes
in the near future.
Anal Incontinence
Definition and Etiology
Anal incontinence is defined as the inability to control the passage of feces or gas
in an individual older than 4 years. It is probably an underestimated condition as
patients are usually embarrassed to report the symptom to the doctors.[103] However, the estimated prevalence in the general population ranges between 2 and
20%.[104] The consequences of losing sphincteric control can be devastating for the affected
individuals, with loss of self-esteem and poor quality of life. The mechanisms that
maintain anal continence are complex and multifactorial, but one of the most common
causes are obstetric injury and surgical trauma to the sphincters.[105] In Brazil and Mexico, medical assistance to the pregnant women can be challenging,
although the incidence of obstetric anal sphincter injuries (OASIS) is around 3.5%,
very acceptable in comparison to the numbers that come from Europe and the United
States.[106] The etiologies are listed in [Table 4].
Table 4
Etiologies of anal incontinence
|
Anal sphincter
|
|
Congenital anorectal malformations
|
|
Dysfunction radiation therapy
|
|
Obstetric anal sphincter injury
|
|
Anal surgery
|
|
Perianal fistulas
|
|
Sexual abuse
|
|
Rectal disorders
|
|
Inflammatory bowel disease
|
|
Radiation proctitis
|
|
Rectocele
|
|
Rectal intussusception
|
|
Rectal prolapse
|
|
Fecal impaction
|
|
Neurological disorders
|
|
Spinal cord lesions
|
|
Stroke
|
|
Multiple sclerosis
|
|
Spina bifida
|
|
Diabetic neuropathy
|
|
Obstetric nerve damage
|
|
Systemic scleroderma
|
|
Rapid colorectal transit
|
|
Chronic diarrhea
|
|
Time irritable bowel syndrome
|
|
Psychological encopresis
|
|
Dementia
|
Classification
There is no widely acceptable classification system for anal incontinence. However,
in a simplified way, we could consider three basic situations: (1) urgency—associated
with damage on the voluntary muscles, especially the external sphincter; (2) passive
incontinence—associated with damage in the internal sphincter; (3) soiling mechanism—when
sensory motor or reflex alterations cause alterations in rectal perception.
Diagnosis and Barriers to Care
Patients should be evaluated with a meticulous and complete clinical examination providing
important information regarding the severity and impact in quality of life. A complete
and structured work-up of patients with fecal incontinence was proposed by Saldana
Ruiz and Kaiser ([Table 5])[107] including some of the validated incontinence scores, such as the Cleveland Clinic
Florida Scoring System (CCFSS).[108] This scoring system is the most utilized around the world and have helped us to
objectively describe the type and severity of incontinence. It is an easy and simple
way to assess incontinence and follow the results of the treatments. In low-income
locations, clinical evaluation is the only way to evaluate patients. Although anal
manometry and EAUS are more available than in the last decade, those methods are not
the reality in many places in the undeveloped world. For patients with fecal incontinence,
evaluation of anal pressures and specific parameters of anal manometry can help in
the evaluation process. For example, in a 56-year-old female patient with incontinence
and urgency, asymmetry and fatigue index are important to evaluate the indication
for biofeedback or the use of a bulking agent[109]([Fig. 8]).
Table 5
Recommended work-up of fecal incontinence
|
Assessment tool
|
Details
|
|
History
|
• Onset
|
|
• Quantification: staining, soilage, seepage, accidents
|
|
• Qualitative assessment: passive incontinence or urge incontinence
|
|
• Obstetric history: pregnancies, vaginal deliveries
|
|
• Previous surgeries: anorectal surgery, hysterectomy, bladder surgery, colon and
rectal surgery, spinal surgery
|
|
• Underlying diseases (diabetes, stroke, etc.)
|
|
• Bowel function and stool quality
|
|
• Incomplete evacuation
|
|
• Stool/gas passage through vagina
|
|
• Medications
|
|
Scoring instruments
|
• Cleveland Clinic Florida Fecal Incontinence Score (CCF-FIS)
|
|
• Fecal Incontinence Quality of Life (FIQoL) score
|
|
• Fecal Incontinence Severity Index (FISI)
|
|
• St. Mark's Incontinence Score
|
|
• EORTEC SF-36
|
|
• Other scoring instruments
|
|
Physical examination
|
• Inspection: patulous anus, folds, perineal body, keyhole, skin irritation, perineal
descent, prolapse, cloaca, rectovaginal fistula (stool in the vagina)
|
|
• Digital exam: sphincter integrity, tone (rest/squeeze), compensatory contraction/discoordination,
rectocele, mass
|
|
• Sensation/anal reflex
|
|
• Instrumentation/visualization: rule out other pathologies (i.e., rectal tumor, proctitis)
|
|
Anorectal physiology testing
|
• Manometry
|
|
• Anorectal sensation and volume tolerance
|
|
• Compliance measurement
|
|
• Nerve studies: PNTML, occasionally EMG
|
|
• Placement of SNS trial electrode (phase I)
|
|
Additional evaluation in select cases
|
• Imaging: anorectal and endovaginal ultrasound and dynamic MRI
|
|
• Defecating proctogram
|
|
• Evaluation by other specialties (urogynecology, urology, gastroenterology, etc.)
|
Abbreviation: MRI, magnetic resonance imaging; EORTEC, European Organization for Research
and Treatment of Cancer; SF 36, The Short Form 36 Health Survey Questionnaire; PNTML,
pudendal nerve terminal motor latency; EMG, electromyography; SNS, sacral nerve stimulation.
Source: Oliveira LCC, Povedano A, Fonseca R. Clinical Evaluation of Continence and
Defecation. In: Oliveira LCC, ed. Anorectal Physiology Textbook: A Clinical and Surgical
Perspective. Springer; 2020:47.
Fig. 8 Measurement of asymmetry and fatigue index as part of work-up for fecal incontinence.
The evaluation of the anal canal with the three-dimensional ultrasound transducers
brought important information regarding sphincter defects.[110] Those methods are complementary and are becoming more available, even in Latin America.
Management and Outcomes
Initial management includes bulking agents and fibers to modify stool consistency.
In addition, loperamide and scopolamine are frequently utilized. When available and
when patients are able to voluntary contract the sphincters, pelvic floor rehabilitation
and biofeedback can be an option. The approach to the patients should be individualized
taking in consideration the particularities of each one. For patients with a poor
quality of life and an anatomical defect, such as a cloaca or patulous anus, some
reconstruction is necessary, mainly with the technique of anterior sphincteroplasty.[111] Unfortunately, the denervated muscle do not sustain the effects of the repair for
a long follow-up.[112]
Therefore, since 2004, a minimally invasive procedure involving neuromodulation of
afferent pathways that connect the pelvic floor with the brain has changed the way
we have been treating patients with fecal incontinence.[113]
Regardless of the etiology, the neurostimulation technique has brought a significant
improvement in quality of life for those patients. The procedure is more expensive
when compared with a sphincter repair, due to the equipment required. However, at
long term, it is cost effective. In Latin America, we performed a multicenter trial
including incontinent patients that were selected to neuromodulation and it was demonstrated
a significant improvement in symptoms and quality of life.[114]
In fact, the results of many series and prospective studies on sacral neuromodulation
have changed the way we manage our patients with fecal incontinence. One of the advantages
of sacral neuromodulation is that it is a reversible technique, with a predictive
positive test and the possibility of improving both fecal and urinary incontinence.[115] Because it also has effects on neuroplasticity, sacral neuromodulation has changed
the algorithm of treatment of fecal incontinence ([Fig. 9]).
Fig. 9 Last proposed fecal incontinence algorithm by the ICS task force on surgical treatment
of fecal incontinence (Knowles et al, 2021)
Proctalgia
Anal and anorectal pain occurs in 7 to 24% of the general population, with most of
the cases without a specific cause.[116] According to the Rome criteria for functional disorders, there are two major situations:
levator ani syndrome and proctalgia fugax.
Levator Ani Syndrome
Levator ani syndrome is a chronic and recurrent anorectal pain with sensation of burning
with irradiation to the gluteal region. It is recurrent and worsens in the seated
position. Usually, it is idiopathic but can be associated with obesity, surgical procedures,
trauma, or childbirth. Digital examination can cause pain and demonstrate a strained
or rigid puborectalis. Treatment includes warm sitz baths, digital massage, analgesics,
antidepressants, and physiotherapy. Surgical treatment is not indicated.
Proctalgia Fugax
It is a typical nocturnal pain, which originates from spastic contractions of the
puborectalis. Located in the anus or lower rectum, it is related to the spasm of the
anal sphincter, associated with stress. It lasts few minutes and is more common in
women. Diagnosis is by exclusion criteria. Patients are treated with a multidisciplinary
team with antispasmodics, oral diazepam, antidepressants, botulin toxin, warm sitz
baths, and sphincter massage.
