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- •Preface to the Third Edition
- •Dedications and Acknowledgments
- •Contents
- •Contributors
- •Perineal Body
- •Anococcygeal Ligament
- •Pelvic Floor Muscles
- •Puborectalis Muscle
- •Iliococcygeus Muscle
- •Pubococcygeus Muscle
- •Introduction
- •Anal Canal Epithelium
- •Internal Anal Sphincter
- •Conjoined Longitudinal Muscle
- •External Anal Sphincter
- •Mesorectum
- •Presacral Fascia
- •Retrosacral Fascia
- •Waldeyer’s Fascia
- •Denonvilliers’ Fascia
- •Anorectal Spaces
- •Perianal Space
- •Intersphincteric Space
- •Submucous Space
- •Ischioanal/Ischiorectal Space
- •Supralevator Space
- •Retrorectal Space
- •Lateral Ligaments
- •Rectal Blood Supply
- •Superior Rectal Artery
- •Middle Rectal Artery
- •Inferior Rectal Artery
- •Physiology
- •Colonic Absorption
- •Colonic Motility
- •Rectal Function
- •The Pelvic Floor
- •The Anal Sphincter Complex
- •Internal Anal Sphincter (IAS)
- •Conjoined Longitudinal Muscle
- •References
- •2: Patient Evaluation
- •Introduction
- •Anatomy
- •History
- •Chief Complaint
- •Bowel Habits
- •Personal History
- •Common Complaints
- •Bleeding
- •Pain
- •Itching
- •Incontinence
- •Constipation
- •Physical Examination
- •Abdominal Examination
- •Anorectal Examination
- •Visual Inspection
- •External Palpation
- •Digital Rectal Examination
- •Diagnostic Studies
- •Anoscopy
- •Proctoscopy
- •Flexible Sigmoidoscopy
- •Endoluminal Ultrasound
- •Computed Tomography
- •Magnetic Resonance Imaging
- •Physiologic Testing
- •Summary
- •References
- •3: Anorectal Physiology Testing
- •Introduction
- •Techniques
- •Anorectal Manometry
- •Balloon Expulsion
- •Electromyography
- •Needle Electrode EMG
- •Surface Electrode EMG
- •Rectal Pressure Testing (Manometry)
- •Cinedefecography
- •Magnetic Resonance Defecography
- •Pudendal Nerve Terminal Motor Latency Testing (PNTML)
- •Clinical Considerations
- •Hirschsprung’s Disease
- •Low Anterior Resection Syndrome (LARS)
- •Anismus
- •Perineal Descent
- •Fecal Incontinence
- •Summary
- •References
- •Introduction
- •Anorectal Malformations
- •Embryology
- •Associated Anomalies
- •Presentation
- •Management
- •Divided Colostomy
- •Posterior Sagittal Anorectoplasty
- •Bowel Management
- •Hirschsprung’s Disease
- •Pathophysiology
- •Presentation
- •Neonatal Obstruction
- •Childhood Constipation
- •Hirschsprung’s-Associated Enterocolitis (HAEC)
- •Diagnosis
- •Contrast Enema
- •Anorectal Manometry
- •Rectal Biopsy
- •Suction vs. Full-Thickness
- •Management
- •Surgical Approaches
- •Swenson
- •Duhamel
- •Soave
- •Modern Approach
- •Long-Segment Disease
- •Complications
- •Incontinence
- •Constipation
- •HAEC
- •Reoperation
- •Laparoscopic-Associated Anorectoplasty (LAARP)
- •Fistula-in-ano/Perianal Abscess
- •Anal Fissure
- •Rectal Prolapse
- •Solitary Rectal Ulcer Syndrome (SRUS)
- •Sexual Abuse
- •References
- •5: Perioperative Management
- •Introduction
- •Preoperative Care
- •Patient Education
- •Aspirin Use
- •Bowel Preparation
- •Perioperative Care
- •Antibiotic Prophylaxis
- •Deep Vein Thrombosis (DVT) Prophylaxis
- •Perioperative Intravenous Fluids
- •Postoperative Care
- •Enhanced Recovery
- •Patient Education
- •Antibiotics
- •Sitz Baths
- •Wound Care
- •Diet
- •Bowel Regimen
- •Pain Management
- •Topical Analgesia
- •Outpatient Follow-Up
- •Ambulatory Surgery Outcomes
- •Complications After Anorectal Surgery
- •Acute Complications
- •Infection
- •Urinary Retention
- •Hemorrhage
- •Chronic Complications
- •Fecal Incontinence
- •Anal Stenosis
- •Chronic Pain
- •Summary
- •References
- •Introduction
- •Positioning
- •Anesthetic Techniques
- •General Anesthesia
- •Regional Anesthesia
- •Monitored Anesthetic Care (MAC)
- •Local Anesthesia
- •Lighting
- •Instrumentation
- •Anoscopes
- •Speculums
- •Retractors
- •Supporting Material
- •References
- •7: Functional Anorectal Disorders
- •Introduction
- •Anismus
- •Perineal Descent Syndrome
- •Solitary Rectal Ulcer Syndrome
- •Sigmoidocele
- •References
- •Introduction
- •Abdominal Approaches
- •Open Rectopexy
- •Laparoscopic Rectopexy
- •Mesh Techniques
- •Laparoscopic Mesh Rectopexy
- •Results of Mesh Rectopexy
- •Ventral Mesh Rectopexy
- •Resection Rectopexy
- •Perineal Approaches
- •Perineal Rectosigmoidectomy
- •Delorme
- •Anal Encirclement
- •Recurrent Rectal Prolapse
- •Rectal Intussusception
- •References
- •9: Fecal Incontinence
- •Introduction
- •Normal Continence
- •Evaluation
- •Treatment
- •Conservative Management
- •Non-surgical Devices
- •Surgical Management
- •Sphincter Augmentation
- •Malone Antegrade Continence Enema
- •Colostomy
- •References
- •10: Anorectal Abscess and Fistula in Ano
- •Introduction
- •Anatomy
- •Abscess
- •Etiology and Pathophysiology
- •Evaluation
- •Symptoms
- •Physical Examination
- •Diagnostic Imaging
- •Treatment
- •General Principles
- •Operative Management
- •Catheter Drainage
- •Primary Fistulotomy
- •Antibiotics
- •Postoperative Care
- •Complications
- •Recurrent Abscess
- •Incontinence
- •Special Considerations
- •Necrotizing Anorectal Infection
- •Treatment
- •Management
- •Fistula-in-Ano
- •Pathophysiology
- •Etiology
- •Evaluation
- •Symptoms
- •Physical Examination
- •Imaging
- •Treatment
- •General Principles
- •Operative Management
- •Fistulotomy
- •Staged Fistulotomy
- •Endoanal Advancement Flap
- •Anal Fistula Plug
- •Fibrin Glue
- •Stem Cells
- •Summary
- •References
- •11: Rectovaginal Fistula
- •Introduction
- •Etiology
- •History
- •Medical Management
- •Crohn’s-Related RVF
- •Surgical Management
- •Simple Fistula Repair
- •Endorectal Advancement Flap
- •Biologic Repairs
- •Overlapping Sphincteroplasty (OS)
- •Perineoproctotomy (PP)
- •Complex Fistula Repair
- •Bulbocavernosus Muscle Flap
- •Gracilis Muscle Transposition Flap (GMTF)
- •Transperineal Omental Flap (TPOF)
- •Resection Repair
- •Bricker Patch Repair
- •Stent Repair
- •Crohn’s-Related RVF Repair
- •Ileoanal Pouch–Vaginal Fistula (IPVF) Repair
- •Diversion
- •References
- •Introduction
- •Rectocele
- •Diagnosis
- •Physical Examination
- •Imaging/Anorectal Physiologic Tests
- •Treatment
- •Nonoperative
- •Operative
- •Transvaginal (Posterior Colporrhaphy)
- •Transperineal
- •Transanal
- •Laparoscopic Rectocele Repair Technique
- •Diagnosis
- •Treatment
- •Medical
- •Surgical
- •Apical Prolapse
- •Enteroceles
- •Perineal Hernia
- •Primary Perineal Hernia
- •Secondary Perineal Hernia
- •Transabdominal Repair
- •Laparoscopic Repair
- •Perineal Repair
- •Summary
- •References
- •13: Pruritus Ani
- •Introduction
- •Etiology
- •Idiopathic Pruritus Ani
- •Dietary Factors
- •Secondary Pruritus Ani
- •Infectious Agents
- •Viruses
- •Parasites
- •Organic Colorectal Conditions
- •Dermatologic
- •Neoplastic Disease
- •Systemic Diseases
- •Psychological
- •Drugs
- •Patient Evaluation
- •History
- •Physical Examination
- •Treatment
- •Recent Advances
- •Summary
- •References
- •Anal Fissure
- •Introduction
- •Pathogenesis
- •Presentation
- •Medical Therapy
- •Operative Therapy
- •PLIS Operative Techniques
- •Alternative Treatment Concepts
- •Subcutaneous Fissurotomy
- •Dilation
- •Flaps
- •Simple Cutaneous Advancement Flap
- •V-Y Advancement Flap
- •Unique Situations
- •Post-PLIS Fissure
- •Hypotonic Fissure
- •Extreme Pain
- •HIV-Related Fissure
- •Non-healing Wounds
- •Anal Stenosis
- •Introduction
- •Pathogenesis
- •Presentation
- •Medical Treatment
- •Dilation
- •Operative Therapy
- •Stricturoplasty
- •Flaps
- •Mucosal Advancement Flap
- •Y-V Advancement Flap
- •V-Y Advancement Flap
- •House Flap
- •Diamond-Shaped Flap
- •Rotational “S” Flaps
- •References
- •15: Pilonidal Disease
- •Background
- •Etiology
- •Clinical Presentation/Diagnosis
- •Treatment
- •Non-operative Management
- •Operative/Excisional Management
- •Basic Procedures
- •Complex Procedures
- •Karydakis Flap
- •Cleft Lift Procedure
- •Rhomboid/Limberg Flap
- •Disease Recurrence
- •References
- •16: Perianal Hidradenitis Suppurativa
- •Introduction
- •Pathogenesis
- •Bacteria
- •Imaging
- •Medical Treatment
- •Antibiotics
- •Steroids
- •Anti-TNF Agents
- •Surgical Treatment
- •Squamous Cell Carcinoma
- •References
- •17: Hemorrhoidal Disease
- •Introduction
- •Anatomy
- •Pathophysiology
- •Etiology
- •Evaluation
- •Symptoms
- •Examination
- •Treatment
- •General Principles
- •Internal Hemorrhoids
- •Flavonoids
- •Rubber Band Ligation
- •Infrared Photocoagulation
- •Sclerotherapy
- •Cryotherapy
- •Electrocautery
- •Dilatation
- •Internal Anal Sphincterotomy
- •Transanal Hemorrhoidal Dearterialization (THD)
- •External Hemorrhoids
- •Acute Thrombosis
- •Operative Hemorrhoidectomy
- •Alternate Energy Sources
- •Special Considerations
- •Summary
- •References
- •Introduction
- •History
- •Physical Examination
- •Anoscopy/Rigid Proctoscopy
- •Imaging/Testing
- •Acute Pelvic Pain
- •Thrombosed External Hemorrhoid
- •Anal Fissure
- •Anorectal Abscess
- •Pruritus Ani
- •Hidradenitis Suppuritiva
- •Infectious
- •Gonorrhea
- •Chlamydia
- •Herpes Simplex/Zoster
- •Syphilis (Treponema Pallidum)
- •Chancroid (Haemophilus Ducreyi)
- •Granuloma Inguinale (Calymmatobacterium Granulomatis)
- •Perianal Crohn’s Disease
- •Proctitis/Pouchitis
- •Radiation
- •Anal Stricture
- •Anal/Rectal Cancer
- •Rectal Prolapse
- •Retrorectal Tumors
- •Prostatitis
- •Gynecological Causes
- •Neurogenic Pain
- •Chronic Pelvic Pain
- •Urogynecological Causes
- •Pelvic Floor Pain Syndrome
- •Levator Ani Syndrome
- •Proctalgia Fugax
- •Coccygodynia
- •Pudendal Neuralgia
- •Summary
- •References
- •19: Anal Neoplasms
- •Introduction
- •Anatomy
- •Anal Squamous Cell Cancer
- •Etiology
- •Diagnosis
- •Staging
- •Treatment
- •Salvage Treatment
- •Functional Results After Radiotherapy
- •Anal Adenocarcinoma
- •Anal Melanoma
- •Sarcoma/Gastrointestinal Stromal Tumor (GIST)
- •Paget’s Disease
- •High-Grade Squamous Intraepithelial Lesion
- •Anal Margin Squamous Cell Cancer
- •Anal Margin Basal Cell Cancer
- •References
- •20: Anal Intraepitheial Neoplasia
- •Introduction
- •Prevention
- •Screening
- •Diagnosis
- •Treatment
- •Expectant Management
- •Ongoing Surveillance
- •Summary
- •References
- •21: Rectal Carcinoma: Imaging for Staging
- •Introduction
- •Imaging Modalities
- •Endorectal Ultrasound
- •Lymph Node Involvement
- •Magnetic Resonance Imaging
- •MRI Technique
- •Lymph Node Involvement
- •Pelvic Side Wall Lymph Nodes
- •Extramural Vascular Invasion
- •Evaluating Tumour Response
- •Hepatic Metastases
- •Pulmonary Metastases
- •Peritoneal Metastases
- •Summary
- •References
- •22: Rectal Carcinoma: Operative Treatment, Transanal
- •Local Approaches to Rectal Cancer
- •Transanal Excision (TAE)
- •Transanal Endoscopic Surgery
- •Intraoperative Complications
- •Peritoneal Entry
- •Conversion
- •Positive Margins
- •Postoperative Complications
- •Functional Outcomes
- •Future Directions: Transanal TME (TATME)
- •Summary
- •References
- •23: Rectal Cancer: Operative Treatment Transabdominal
- •Overview
- •Preoperative Evaluation
- •Preoperative Imaging Studies
- •Staging
- •T2N0 Rectal Cancer
- •Locally Advanced Rectal Cancer
- •Distant Metastatic (M1) Disease
- •Surgical Considerations
- •Radical Resection
- •Total Mesorectal Excision
- •Circumferential Resection Margin
- •Distal Resection Margin
- •Reconstruction Options Following Low Anterior Resection
- •Temporary Diversion Following Low Anterior Resection
- •Abdominoperineal Resection
- •Abdominal Dissection: Minimally Invasive Versus Open Technique
- •Perineal Dissection: Prone Versus Lithotomy Positioning
- •Perineal Reconstruction Options
- •Surgical Technique
- •Blood Supply
- •Autonomic Pelvic Nervous System
- •Open Abdominal Dissection
- •Robotic Total Mesorectal Excision
- •Transanal Extraction Techniques
- •Postoperative Care
- •References
- •Introduction
- •Locally Advanced Rectal Cancer
- •Total Mesorectal Excision
- •Neoadjuvant Therapy
- •Chemoradiation
- •Intraoperative Radiation Therapy
- •Endoluminal Brachytherapy
- •Surgery Related Outcomes Post Chemoradiation
- •Adjuvant Therapy
- •Adjuvant Chemotherapy
- •Induction vs. Adjuvant Chemotherapy
- •Adjuvant Chemotherapy Following PCR
- •Adjuvant Radiotherapy
- •Chemoradiation
- •Metastatic (Stage IV) Rectal Cancer
- •Recurrent Rectal Cancer
- •Summary
- •References
- •Introduction
- •Benign
- •Adenomatous Polyps
- •Treatment
- •Natural History
- •Malignant Polyps
- •Large Rectal Villous Tumors
- •Hyperplastic Polyps
- •Juvenile Polyps
- •Cronkhite-Canada Syndrome
- •Hamartomatous Polyps
- •Lipomas
- •Hemangiomas
- •Solitary Rectal Ulcer Syndrome/Colitis Cystica Profunda
- •Leiomyomas
- •Malignant
- •Leiomyosacrcoma
- •Gastrointestinal Stromal Tumors (GIST)
- •Carcinoid Tumors
- •Carcinoid Carcinomas
- •Lymphoma
- •Retrorectal/Presacral Tumors
- •Melanoma
- •References
- •26: Retrorectal (Presacral) Tumors
- •Introduction
- •Anatomy
- •Congenital Lesions
- •Cystic Lesions
- •Developmental Cysts
- •Duplication Cysts (Enterogenous)
- •Tail Gut Cysts (Cystic Harmatomas)
- •Anterior Sacral Meningocele
- •Solid Lesions
- •Sacrococcygeal Chordomas
- •Neurogenic Tumors
- •Osseous Tumors
- •Miscellaneous Tumors
- •Imaging
- •Preoperative Biopsy
- •Management
- •Surgical Approach
- •Posterior Approach
- •Outcomes
- •Malignant Lesions
- •Benign Lesions
- •References
- •Introduction
- •Sexually Transmitted Anorectal Disorders
- •Bacterial Infections
- •Gonorrhea
- •Chlamydia Trachomatis: Lymphogranuloma Venereum (LGV)
- •Chancroid
- •Granuloma Inguinale
- •Syphilis
- •Viral Infections
- •Herpes Simplex

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Pruritus Ani
BradleyR.Davis
13
Introduction
Pruritus ani is a cutaneous sensation characterized
by unpleasant itching and burning of the perianal
skin. Acutely it may be protective but chronically
it causes distress and is maladaptive. Patients
often delay seeking medical attention, and their
unsupervised attempts at treatment, including
aggressive repetitive cleaning and the use of overthe-counter creams or ointments, typically only
worsens the symptoms and can make it more
difcult to manage [1]. This condition affects up
to 5% of the general population on a daily basis,
with a male predominance of 4:1 [2, 3]. Pruritus
ani may be localized or diffuse in the perianal
region. The onset of symptoms is typically gradual and is often worse at night or in warm, moist
climates. It can be subdivided into two categories
based on etiology—idiopathic (primary) pruritus
ani and secondary pruritus ani. Idiopathic pruritus
ani is a diagnosis of exclusion, while secondary
pruritus ani is attributed to a specic cause [4].
It is difcult to assign a value as to the percent of
patients with secondary versus idiopathic pruritus
ani as the literature assigns ranges between 20 and
75% and is largely dated and of variable quality. If
B. R. Davis (*)
Section of Colon and Rectal Surgery, Carolinas
Medical Center, Charlotte, NC, USA
e-mail: bradley.r.davis@carolinas.org
a patient presents with the sole complaint of anal
itching particularly if it wakens him or her at night
and there is no cutaneous evidence of a dermatologic condition then initial management should
focus on idiopathic pruritus ani. In those patients
in whom therapy is not effective after 4–6weeks,
attention should be given to excluding the multiple potential causes of secondary pruritus ani,
which can be divided into several broad categories: infectious, dermatologic, systemic, local
irritants, and colorectal or anal causes. Potential
causes of irritation include moisture from sweat,
stool and mucus; fecal factors such as bile salts
and stool pH; inadequate hygiene, as well as
overzealous hygiene with introduction of irritating soaps, lotions, and scents; certain food products; as well as topical compounds used by the
patient to obtain relief have all been implicated.
Diagnosis, patient education, and treatment often
simultaneously proceed.
Etiology
Itch is an unpleasant sensation that leads to the
desire to scratch and is mediated by C nerve bers
in the dermis that is referred to as pruritoceptive
itching. These nerve endings may become chronically active with the repetitive trauma of scratching over months to years. Itching can also be
neuropathic, due to disorders of the afferent pathways (e.g. post herpetic neuralgia) neurogenic as
© Springer International Publishing AG, part of Springer Nature 2019
D. E. Beck et al. (eds.), Fundamentals of Anorectal Surgery,
https://doi.org/10.1007/978-3-319-65966-4_13
227

228
B. R. Davis
a result of centrally mediated stimuli (e.g. morphine induced itching) and psychogenic [5, 6].
The sensation of itch can be caused by various
stimuli with histamine release as a potential neuronal mechanism of itch; however, it is not the
only substance that produces itching. Kallikrein,
bradykinin, papain, and trypsin are all itch-mediating substances that are not responsive to blockades with classic histamine antagonists, such as
diphenhydramine. As a consequence, antihistamines have proven ineffective in treating pruritus
in many instances.
Scratching the affected skin provides inadequate feedback to inhibit itching and prolonged
itching can cause damaging excoriations and
infections, which provides additional itching
stimuli. Thus, scratching results in a vicious cycle
of itching and scratching that is difcult to break.
The major contributors to secondary pruritus ani
are listed in Table13.1.
Idiopathic Pruritus Ani
The symptom of pruritus is common to many anorectal conditions second only to bleeding as a presenting complaint [7, 8]. While the pathogenesis
of idiopathic pruritus is not entirely understood
the unifying theory is the presence of an irritative
secretion usually feces emanating from the anal
canal causing itching [9]. Anorectal physiology
studies also support this theory. They demonstrated that patients with pruritus have a more pronounced relaxation of the internal anal sphincter
with rectal distention compared with control subjects and leak sooner on a saline infusion test [10,
11]. Studies have also shown that patients with
pruritus ani are more likely to have loose stools,
drink more water, and have weekly fecal soiling
compared to patients without this condition [12].
Several factors have been implicated in idiopathic pruritus ani, including local irritants,
excess moisture and repeated trauma from wiping. Fecal contamination is particularly noxious
to the perianal skin and leads to local irritation.
Fecal matter contains allergens, bacteria, and
bacterial enzymes capable of activating C-type
nerve bers within the dermis. Caplan reported
Table 13.1 Selected causes of secondary pruritis ani
Infectious Bacterial infection (Staphylococcus,
Anorectal Hemorrhoids (external, prolapsing
Dermatologic Contact dermatitis
Malignant Anal canal cancer
Systemic
disease
Streptococcus, erythrasma)
Sexually-transmitted infection
(Gonococcus, Chlamydia)
Fungal infection (Candida,
dermatophytes)
Parasites (pinworms, scabies)
Viral infection (herpes virus,
condylomata, Molluscum)
internal)
Fistula-in-ano
Anal ssures
Hidradenitis suppurativa
Fecal incontinence
Perianal Crohn’s disease
Skin tags
Chronic diarrhea
Pilonidal disease
Atopic dermatitis
Perianal psoriasis
Lichen sclerosus
Seborrheic dermatitis
Anal margin cancer
Rectal cancer
Bowen’s disease
Extramammary Paget’s disease
Diabetes mellitus
Leukemia
Lymphoma
Chronic renal failure
Iron-deciency anemia
Hyperthyroidism
Hyperbilirubinemia
that 44% of 27 subjects who were patch tested
with autogenous fresh feces, developed pruritus.
Of these 12 symptomatic patients, only 4 had a
previous history of anal pruritus. The authors
concluded that the quickly developing symptoms
were compatible with an irritant rather than an
allergic effect [9]. Marks conrmed that, in pruritic patients, the perianal skin pH paralleled the
stool pH. The authors attributed the excessive
alkalinity of the perianal skin in pruritus patients
to lysozyme, a component of intestinal mucosecretions [13]. The anoderm, in particular, has
been shown to be more sensitive to fecal matter
when compared with other areas of the body [9].
In pruritoceptive itching, the repetitive trauma
of scratching over time stimulates release of local

13 Pruritus Ani
229
pro-inammatory cytokines, leading to chronic
activation of C-type nerve bers. This is also
referred to as the itch-scratch cycle, and is well
described in dermatology literature [6].
Poor anal hygiene is a common factor among
patients presenting with perianal pruritus, but
overzealous hygiene has also been implicated
in its pathogenesis. Patient’s often attribute
the symptom to being dirty and use excessive
amounts of toilet paper and often feel moist following bowel movements a symptom of incomplete evacuation. As a result they often shower,
bath or perform elaborate cleansing routines after
every bowel movement or when symptoms occur.
This, in addition to the use of topical steroids, can
destroy the natural barriers and traumatize the
anoderm and anal margin skin and exacerbate the
problem.
Dietary Factors
In addition, dietary factors have been associated
with the development of perianal pruritus [14].
Diet may incite symptoms through three major
pathways. First, it will affect the consistency of
the stool, which in turn can lead to fecal soiling. Second, the components of the diet may
lead to direct irritation secondary to their chemical composition. Third, if an excessive volume
of liquid is consumed, it could directly lead to
more watery stools and pruritus as a result of
frequent contact irritation. These so-called pruritogenic foods include coffee, colas, citrus fruits,
chocolate, tea, energy drinks, and spicy foods.
Proposed mechanisms by which pruritogenic
foods trigger symptoms include local irritation,
alteration of stool pH, histamine release, and
inappropriate relaxation of the internal sphincter.
Coffee can elicit pruritus when it is ingested in
any form (fresh, instant, decaffeinated, or when
used as a avor additive to other foods, such as
sodas). An apparent threshold for coffee drinkers usually varies between 2 and 4 cups per day.
In an observational study evaluating the inuence
of diet on pruritus Smith etal. noted an average
drop in anal sphincter pressures of 11 mmHg
in 8 of 11 patients who drank 3 cups of coffee
[12]. A similar threshold, noted in milk-drinking
patients, arises at ingestion of between 6 and
10 oz. daily. Pruritus caused by chocolate, tea
and cola is believed to be related to the xanthine
content of these substances. Although beer has
been implicated in eliciting pruritus ani, Smith
and associates [12] found no correlation between
alcohol ingestion and pruritus in their group of
75 patients. Patients with vitamin A and vitamin
D deciencies are also believed to be predisposed
to pruritus ani.
Secondary Pruritus Ani
Secondary pruritus ani, which is pruritus induced
by an underlying cause, can be divided into the
following categories: inammatory, nonsexual
infectious, systemic, premalignant and malignant,
and anorectal causes (Table13.1). As is the case
with idiopathic pruritus ani, secondary causes of
perianal pruritus are also exacerbated by pruritoceptive itching and the itch-scratch cycle.
Infectious Agents
Infectious agents must be considered in the differential diagnosis of secondary pruritus ani. The
etiologic agents may be viral, bacterial, mycotic,
or parasitic. Primary bacterial infections are an
unusual occurrence, and when documented are
usually superimposed on preexisting perianal
skin trauma.
Bacterial offenders include Staphylococcus
aureus, beta-hemolytic Streptococcus pyogenes,
and Corynebacterium minutissimum (erythrasma)
[15]. Baral successfully cultured Staphylococcus
aureus from a small patient population with pruritis ani and reported that 100% of patients had
resolution of symptoms after appropriate antibiotic therapy was instituted [16]. Streptococcus
infection can result in perianal eczema and while
it is more often seen in children it can affect
adults. Culture swabs of the perianal skin can be
obtained in patients who have failed more conservative measures to evaluate for streptococcus
particularly in those patients with an eczemoid

230
Fig. 13.1 Perianal streptococcus
skin reaction (Fig. 13.1). Treatment is initiated
when cultures are positive, usually consisting of
amoxicillin 1g three times daily for 14days [15].
Hidradenitis suppurativa may also cause pruritus
(Fig.13.2). Erythrasma is an uncommon bacterial infection caused by Corynebacterium minutissimum [17], lesions which initially present as a
reddish scaly area that is well demarcated, eventually change to a tan color during the course of
the disease. The diagnosis can be conrmed by
using a Woods ultraviolet lamp, which allows the
examiner to observe the characteristic red uorescence of these lesions. Bowyer and McColl
diagnosed erythrasma in 15 of their 81 patients
with pruritus ani but were only able to culture the
organism in 3 patients. A 10-day course of erythromycin usually relieves the symptoms, but the
condition sometimes recurs.
Sexually transmitted infections have also
been implicated, including Neisseria gonorrhoeae (gonorrhea), Chlamydia trachomatis,
and Treponema pallidum (syphilis); though
these are rarely responsible for chronic symptoms. Syphilitic lesions in their primary or secondary stages may have an associated exudate.
Continued local irritation secondary to moisture
may lead to maceration and pruritic complaints.
In the secondary stage of syphilis, a maculopapular rash is seen to convert to a red, indurated
lesion that may or may not lead to pruritus. When
syphilis is suspected, appropriate laboratory tests
should be performed to conrm the diagnosis,
and one should be especially suspicious of sexu-
B. R. Davis
Fig. 13.2 Hidradenitis suppurativa
ally transmitted diseases in patients practicing
anal intercourse. The drug of choice for the treatment of syphilis remains penicillin, or tetracycline in penicillin-allergic patients [18].
Viruses
Pruritis ani may be associated with three major
sexually transmitted viruses: herpes simplex
virus (anogenital herpes), papillomavirus (condyloma accuminatum) and cytomegalovirus
(CMV). Patients with herpes simplex virus present with painful small vesicles surrounded by an
erythematous areola (Fig.13.3). The vesicles usu-
ally rupture at approximately 48h, then progress
over weeks to scaly eschars; the diagnosis can be
conrmed by viral culture. Oral acyclovir is the
current treatment of choice; recent studies have
indicated the prophylactic use of this medication
is successful in patients known to have frequent
recurrences [19]. Condylomata accuminata are
wart-like lesions found in the perianal region and
the anal canal (Fig.13.4). Patients often present
with perineal moistness and irritation. Lesions
on the anal margin skin should prompt the clini-

13 Pruritus Ani
231
Fig. 13.3 Herpes simplex virus with painful small vesicles surrounded by an erythematous areola
cian to evaluate the anal canal especially in men
that have sex with men. Biopsy of these lesions
can conrm the diagnosis. Unfortunately, these
organisms are notoriously resistant to antiviral
therapy but a trial of imiquimod may be warranted for immunocompetent patients [20].
According to literature, Candida is responsible for up to 15% of secondary pruritus ani [21].
Fungal infections with Candida species and other
dermatophytes often proliferate in diabetics, or
after treatment with antibiotics or immunosuppressant medications, such as steroids. This fungal infection tends to occur in moist or sweaty
environments, including in the deeper folds of
obese or elderly patients. It can also be associated with tight-tting clothing. Patients often
present with diffuse, erythematous, and often
macerated plaques erythematous plaques, often
accompanied by satellite lesions. In the setting of
pruritus ani, the presence of any dermatophytes
should be considered pathologic and treated with
Fig. 13.4 Condylomata accuminata
either topical or systemic antifungal medications
Antifungal powder or lotion can be used, depending on the moisture level of the perianal region.
Oral antifungal agents such as uconazole can
also be used for severe infections [22]. Viral
agents include herpes simplex virus (HSV) and
human papillomavirus (HPV), the latter of which
may manifest as condyloma acuminata. Herpes
zoster, also referred to as singles, can also affect
the perineal region in a dermatomal pattern.
Herpes zoster can only occur in people who were
previously infected with the virus and although
the disease can occur at any age, it typically presents in patients older than the age of 50. The rash
has a distinct appearance and can usually be diagnosed visually. Herpes zoster causes a deep red
rash with blisters that do not cross the midline
of the body. Treatment options include antiviral
medications including valacyclovir hydrochloride [23].
Parasites
Nocturnal symptoms in the pediatric population
should alert suspicion towards a parasitic infec-

232
B. R. Davis
tion with Enterobius vermicularis (pinworms)
[24]. Other parasites that induce pruritic symptoms include Sarcoptes scabei (scabies) and
Pediculosis pubis (crabs).
Pinworms (Enterobius vermicularis) are the
most common cause of perianal itching in the
pediatric age group. Jillson challenged the common belief that pinworms elicit pruritus and
proposed that symptoms are an uneasy crawling
sensation and not itching [25]. The diagnosis can
be made by microscopically evaluating perianal
skin samples collected on cellulose tape. It is
imperative that other family members be evaluated so that they can be treated and recontamination does not occur. The symptoms usually occur
in the evening, when these 6-mm long parasites
migrate to the perianal skin. Pinworm infestation is generally treated with a single dose of
mebendazole [26]. Scabies is a contagious skin
infestation due to the mite Sarcoptes scabiei
that can elicit severe pruritus. Although usually
found on the nger webs or sides of the ngers,
these lesions can often be identied in the perianal region. The diagnosis of scabies can be conrmed by demonstrating the mite or its products,
such as ova or feces, from scrapings prepared on
a slide with one drop of 10% potassium hydroxide [27]. Lesions appear initially as vesicles as
the mite burrows its way into the stratum corneum. Treatment consists of the application of
an appropriate scabeticide such as Kwell R lotion
(Reed & Carnrick, Jersey City, NJ). The parasite
Pediculosis pubis (crab or louse) can often be
found grasping the base of a hair shaft and is noted
to produce macular steel-gray spots, especially
on the thighs and chest. With careful examination under magnication this parasite strikingly
resembles a crab. Management requires the treatment of all infected family members, appropriate
delousing of all fomites such as clothes, bedding
and upholstery and showering with an appropriate pediculocide such as permethrin [28].
Organic Colorectal Conditions
A variety of anorectal diseases are associated
with pruritus ani, including external hemorrhoids,
prolapsing internal hemorrhoids, stula-in-ano,
anal ssures, hidradenitis suppurativa, perianal
Crohn’s disease, skin tags, pilonidal disease, and
chronic diarrhea.
Anorectal conditions resulting in pruritus can
be divided into two broad categories based on
their pathophysiologic mechanism: fecal contamination and local inammation.
In a study by Daniel et al. of 109 patients
with pruritus ani whose sole complaint was itching, 52% had anorectal disease as the cause.
Conditions found in this study included hemorrhoids, anal ssure, anal condyloma, ulcerative
proctitis, stula, and abscess [29]. In another
study of 82 patients presenting with hemorrhoids Murie etal. found that pruritus was more
common than in age- and gender-linked control
subjects. They also reported that treatment of
hemorrhoidal prolapse reduced the incidence
of pruritus, and soiling [30]. In a study of 200
patients with pruritus ani by Bowyer et al., 43
were noted to have hemorrhoids that were contributory and in 16 cases were the sole cause. The
study also revealed that ssure treatment in ve
patients, skin tag removal in ve patients, and
treatment of spasm in four patients led to complete relief of their pruritus. They postulated that
skin tags trap fecal matter in the perianal region,
which induces the irritant process [31]. Fistulain-ano results in chronic drainage of fecal matter
onto the perianal skin (Fig.13.5). Other common
factors resulting in fecal contamination include
fecal incontinence due to impaired sphincter tone
(Fig. 13.6), decreased stool bulk, and chronic
diarrhea. Hidradenitis and perianal Crohn’s disease, on the other hand, are examples of pruritus
mediated by inammatory mechanisms.
Dermatologic
The most common dermatologic conditions
resulting in chronic pruritus ani include contact
dermatitis, allergic dermatitis, atopic dermatitis, psoriasis, and lichen sclerosus. Contact dermatitis results from local irritants, commonly
deodorants, perfumes, soaps, and certain foods.
A detailed history focusing on post-defecation

13 Pruritus Ani
Fig. 13.5 Fistula-in-ano
Fig. 13.6 Anal incontinence due to impaired sphincter
tone
cleansing habits and anal hygiene can elucidate
whether or not irritants may be involved [32].
Atopic dermatitis is a chronic, relapsing pruritic
dermatitis, which usually occurs in adults and
is localized to the exural surfaces of the face,
neck, cubital or popliteal fossa and hands. The
dermatitis usually occurs in patients with a personal or family history of atopy or hay fever/
asthma/urticaria; lesions may present as papular,
scaly or chronic lichenied plaques. The etiology is unknown, but is believed to be IgE mediated. Some researchers support food allergies
and proteinaceous aeroallergens as possible etiologies. Patients with atopic dermatitis are likely
233
to acquire both bacterial and viral infections.
Treatment is directed at skin hydration, corticosteroid administration, immunotherapy and antibiotics if secondary infections are present [33].
Lichen sclerosus is a poorly understood condition that commonly affects perimenopausal
women. Most patients suffering from lichen
sclerosus present with vulvovaginal pruritus,
though perianal symptoms are also common [21].
Typical lesions are porcelain-white papules and
plaques. These patients respond well to topical
steroids. Chronic nonresponders, however, carry
a 5% risk of malignant degeneration into squamous cell carcinoma, and should have biopsies
performed should symptoms persist. Women with
lichen sclerosis have a 300-fold increased risk of
developing cancer compared with those without
the disease [34]. Treatment of the condition does
not reduce this risk. Short term (6–8weeks) treatment with a potent topical steroid, such as clobetasol, is effective in reducing symptoms [35].
Retinoids, testosterone creams, and tacrolimus
ointment have also been described [36].
Psoriasis frequently involves the scalp and
exor surfaces of the knees and elbows, but can
less frequently involve the perianal skin. Psoriasis
has been shown in numerous studies to be a prevalent underlying cause of pruritus ani. Psoriasis
present in the anus, groin, genitals, and axillae
is referred to as “inverse psoriasis” because it
presents as the inverse of the normal distribution.
Although the exact incidence is unknown, one
study found that a signicant portion of patients
(54%) with inverse psoriasis had involvement of
the anus [37]. Psoriasis is incurable but symptoms can be treated with short-term use of a lowto-mid potency steroid for up to 4weeks. After
the induction of remission the patient should
switch to a nonsteroidal topical treatment, such
as calcipotriene, for maintenance [38].
Radiation dermatitis can also involve the
perineum, though it is less commonly seen since
the development of high- and medium-energy
accelerators. In addition, radiation proctitis leads
to diarrhea, which further exacerbates local
perianal skin irritation. Radiation proctitis can
be managed with dietary measures and bulking
agents or a trial of hydrocortisone retention ene-

234
mas. The standard of care for radiation-induced
dermatitis involves topical steroids and routine
skin care with mild, unscented soap.
Neoplastic Disease
Neoplastic diseases should be considered in the
differential diagnosis of any patient with perianal
pruritus. While these maladies could include anal
canal cancer, anal margin cancer and rectal cancer
it is far more likely that pruritus as a presenting
symptoms would be found in anal intraepithelial
neoplasia (Bowen’s Disease) and extramammary
Paget’s disease (cutaneous adenocarcinoma in
situ). The clinician must be cognizant of these
potential etiologies and should exclude them by
performing a careful physical examination and
biopsy if necessary. In the setting of malignancy,
pruritic symptoms will often be more severe and
persistent in comparison to idiopathic pruritus
ani. If malignancy is suspected, biopsies and
endoscopic evaluation is crucial to the work-up.
Polypoid tumors of the anorectum may lead to
soiling which may be secondary to changes in the
normal anatomy or mucous secretions, as seen in
the case of villous lesions.
Extramammary Paget’s disease is an intraepidermal neoplasm with a cellular composition
similar to Paget’s disease of the breast. Although
the cell type of this lesion is still undened, it
is believed to be a pluripotential epithelial cell
that borders on differentiation into sweat gland
tissue. The lesions are usually red, indurated,
scaling plaques often confused with eczema.
Approximately 15% of such lesions are associated with an underlying cutaneous carcinoma or a
breast or urogenital tumor [39]. A 60year review
of Paget’s Disease at Memorial Sloan Kettering
demonstrate that pain and pruritus were the most
common presenting symptom [40]. The condition typically manifests itself as an erythematous, eczematoid plaque in the perianal region
(Fig. 13.7). Paget disease is most common in
the seventh decade of life. A wide excision is the
treatment of this condition [41] (see Chapter 19).
Bowen’s disease is a unique form of squamous
cell carcinoma-in-situ. This squamous carcinoma
B. R. Davis
Fig. 13.7 Erythematous, eczematoid plaque in the perianal region caused by Paget’s disease
usually resides solely in the epidermal region but
has invasive potential, seen in up to 5% of cases
[42, 43]. The disease can present as pruritus or
may be found incidentally in an anorectal surgical
specimen. The lesion is characteristically an erythematous, hyperkeratotic plaque sharply demarcated from the surrounding skin (Fig.13.8). The
size of the lesions ranges from a few millimeters to
several centimeters. Small lesions may be treated
successfully with topical 5-uorouracil, while
larger lesions have been managed with either surgery (wide local excision) or more recently photodynamic therapy [43] (see Chapter 19).
Systemic Diseases
Systemic diseases associated with perianal pruritus
include diabetes mellitus, leukemia, lymphoma,
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