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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1199_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword for Benign Anorectal Disorders
- •Preface 1
- •Preface 2
- •1.5 Nerve Supply of Anal Canal and Rectum
- •1.6 Anorectal Spaces
- •Bibliography
- •2: Physiology of Defecation
- •2.1 Normal Defecation
- •2.1.2 Reservoir
- •Contents
- •1: Surgical Anatomy of Anal Canal and Rectum
- •1.1 Rectum
- •1.1.1 Relations
- •1.2 Anal Canal
- •1.2.1 Inner Lining
- •Bibliography
- •3: Hemorrhoids
- •3.1 Introduction
- •3.3.1 Vascular Hemorrhoids
- •3.3.2 Mucosal Hemorrhoids
- •3.3.3 Internal Hemorrhoids
- •3.3.4 External Hemorrhoids
- •3.4 Symptoms
- •3.4.1 Bleeding
- •3.4.2 Protrusion
- •3.4.3 Pain
- •3.4.4 Discharge and Irritation
- •3.4.5 Anemia
- •3.4.6 Painful Mass in the Anal Region
- •3.5 Clinical Examination
- •3.5.1 Digital Rectal Examination
- •3.5.2 Endoscopic Examination
- •3.6 Treatment
- •3.6.2 Medical Treatment
- •3.6.3.1 Injection Sclerotherapy
- •3.6.3.2 Rubber Band Ligation
- •3.6.3.3 Cryotherapy
- •3.6.3.4 Infrared Coagulation (IRC)
- •3.6.3.4.1 Complications
- •3.6.3.6 Direct Current Therapy
- •3.6.4 Surgical Treatment
- •3.6.4.2 Closed Hemorrhoidectomy (Ferguson)
- •3.6.4.3 White Head (Submucosal) Hemorrhoidectomy
- •3.6.4.4 Laser Hemorrhoidectomy
- •3.6.4.5 LigaSure Hemorrhoidectomy
- •3.6.4.6 Hemorrhoidectomy by Ultrasonic Scalpel (HUS)
- •3.6.4.6.1 Mechanism
- •3.6.4.6.2 Coaptive Coagulation
- •3.6.4.6.3 Cavitation Effect
- •3.6.4.6.4 Technique
- •3.6.4.8 Doppler-Guided Hemorrhoidal Artery Ligation (DGHAL)
- •3.6.4.8.1 Procedure
- •3.6.4.8.2 Postoperative Complications
- •3.6.4.8.3 Results
- •3.7.1 Pain
- •3.7.2 Urinary Retention
- •3.7.3 Postoperative Bleeding
- •3.7.4 Wound Infection
- •3.7.5 Fecal Impaction
- •3.7.6 Stenosis
- •3.7.7 Recurrence
- •3.7.8 Incontinence
- •3.7.9 Other Late Complications
- •3.8 Special Situations
- •3.8.1 Thrombosed Hemorrhoids
- •3.8.2 Strangulated Hemorrhoids
- •3.8.3 Anorectal Varices and Portal Hypertension
- •3.8.4 Pregnancy
- •3.8.5 Crohn’s Disease and Ulcerative Colitis
- •3.8.6 Immunocompromised Patients
- •3.8.7 Coagulation Disorders
- •3.8.8 Fissure
- •3.8.9 Sepsis
- •Conclusion
- •Bibliography
- •4: Anal Fissure
- •4.1 Introduction
- •4.2 Epidemiology
- •4.4 Pathology
- •4.5 Etiopathogenesis
- •4.5.1 Microtrauma to Anal Canal Mucosa
- •4.5.2 Anal Sphincteric Spasm
- •4.5.3 Anal Mucosal Ischemia
- •4.5.4 Trauma During Childbirth
- •4.5.5 Other Causes of Secondary Anal Fissure
- •4.6 Clinical Features
- •4.7 Differential Diagnosis
- •4.8 Management
- •4.8.2.1 Medical Management
- •4.8.2.2.3 Fissurectomy
- •4.8.2.2.4 Anal Dilatation or Stretch (Lord’s Procedure)
- •4.8.2.2.5 V-Y Mucosal Advancement Flap
- •4.8.2.2.6 Internal Anal Sphincterolysis
- •4.8.2.2.7 Direct Current Treatment
- •4.8.3 Recurrence
- •4.8.4 Special Situations
- •4.9 Prevention
- •Conclusion
- •Bibliography
- •5: Perianal Sepsis and Fistula
- •5.1 Introduction
- •5.2 Anatomy
- •5.3 Epidemiology and Etiology
- •5.4.1 Anorectal Abscess
- •5.4.2 Anal Fistula
- •5.5 Diagnosis
- •5.5.1 Anorectal Abscess
- •4.8.2.1.1 Chemical Sphincterotomy
- •4.8.2.1.2 Topical Nitroglycerine
- •4.8.2.1.3 Topical Diltiazem (2 %)
- •4.8.2.1.4 Topical Nifedipine (0.3 %)
- •4.8.2.1.5 Topical Bethanechol
- •4.8.2.1.6 Botulinum Toxin
- •4.8.2.1.8 Minoxidil
- •4.8.2.2 Surgical Management
- •4.8.2.2.1 Internal Sphincterotomy
- •4.8.2.2.2 Fissurotomy and Posterior Sphincterotomy
- •5.5.2 Anal Fistulas
- •5.5.3 Special Studies
- •5.5.3.1 Sigmoidoscopy and Colonoscopy
- •5.5.3.2 Fistulography
- •5.5.3.3 Endoanal Ultrasonography
- •5.5.3.4 Computed Tomography (CT) Scan
- •5.5.3.5 Magnetic Resonance Imaging (MRI)
- •5.5.3.6 Anorectal Manometry
- •5.5.3.7 Fistuloscopy
- •5.6 Treatment
- •5.6.1 Anorectal Abscess
- •5.6.2 Horseshoe Abscess
- •5.6.3 Abscess and Primary Fistulotomy
- •5.6.4 Fistula-in-Ano
- •5.6.4.1 Advancement Flap
- •5.6.4.2 Fibrin Glue
- •5.6.4.3 Seton
- •5.6.4.4 Anal Fistula Plug
- •5.6.4.5 Ligation of Intersphincteric Fistula Tract (LIFT)
- •5.6.4.6 Video-Assisted Anal Fistula Treatment (VAAFT)
- •5.6.4.7 Autologous Adipose-Derived Stem Cell
- •5.6.4.8 Fistulectomy and Fistulotomy
- •5.6.4.9 Fistulectomy with Primary Sphincter Reconstruction
- •5.6.5 Intersphincteric Fistula-in-Ano
- •Conclusion
- •Bibliography
- •6: Pilonidal Disease
- •6.1 Introduction
- •6.2 Etiology
- •6.2.1 Theory of Acquired Origin
- •6.3 Clinical Features
- •6.4 Differential Diagnosis
- •6.5 Investigations
- •6.6 Treatment
- •6.6.1 Conservative Treatment
- •6.6.2 Operative Procedures
- •6.6.2.1 Simple Incision of Abscess
- •6.6.2.3 Excision With or Without Wound Closure
- •6.6.2.4 Bascom I Technique
- •6.6.2.6 Vacuum-Assisted Closure (VAC)
- •6.7 Prevention of Recurrence
- •6.8 Summary
- •Bibliography
- •7: Rectovaginal Fistulas
- •7.1 Introduction
- •7.2 Etiology
- •7.2.1 Congenital
- •7.2.2 Acquired
- •7.2.2.1 Child Birth
- •7.2.2.2 Diverticular Disease
- •7.2.2.4 Malignancies
- •7.2.2.5 Radiation Therapy
- •7.2.2.6 Operative Trauma
- •7.3.1 Size
- •7.3.2 Location and Etiology
- •7.3.3 Anatomy
- •7.3.3.1 Pelvic Enterovaginal Fistula
- •7.3.3.2 High Rectovaginal Fistula
- •7.3.3.3 Midzone Rectovaginal Fistula
- •7.3.3.4 Low Rectovaginal Fistula
- •7.3.3.5 Suprasphincteric and Transsphincteric Anovaginal Fistula
- •7.4 Clinical Presentation
- •7.5 Diagnosis
- •7.5.2 Anorectal Manometry
- •7.5.3 Neurophysiologic Testing
- •7.5.4 Vaginography
- •7.5.5 Barium Enema
- •7.5.6 Computed Tomography (CT) Scan
- •7.5.7 Endoanal Ultrasonography (EAUS)
- •7.5.8 Magnetic Resonance Imaging (MRI)
- •7.5.9 Endoanal MRI
- •7.6 Management
- •7.6.1 Medical Management
- •7.6.2 Surgical Treatment
- •7.6.2.1 Transanal Approaches
- •7.6.2.1.1 Mucosal Advancement Flap Repair
- •7.6.2.1.2 Transanal Sleeve Advancement Flap (TSAF)
- •7.6.2.2 Transvaginal Approaches
- •7.6.2.2.1 Transvaginal Inversion Repair
- •7.6.2.3 Transperineal Approaches
- •7.6.2.3.1 Simple Fistulotomy
- •7.6.2.3.2 Fistulotomy with Perineoproctotomy with Layered Closure
- •7.6.2.3.3 Perineal Repair with Levatoroplasty
- •7.6.2.4 Transsphincteric Approach
- •7.6.2.5 Repair with Biological Agents
- •7.6.2.6 Tissue Transfer Procedures
- •7.6.2.6.1 Gracilis Transfer
- •7.6.2.6.2 Martius Flap Repair
- •7.6.2.7 Transabdominal Approaches
- •7.6.2.8 Fistula Division
- •7.6.2.8.1 Coloanal Sleeve Reconstruction
- •7.6.2.8.2 Bricker Patch
- •7.6.2.8.3 Stoma
- •7.6.2.9 Laparoscopic Repair
- •7.7 Complications
- •7.7.1 Complications of Local Repairs
- •7.7.1.1 Bleeding
- •7.7.1.2 Infection
- •7.7.1.3 Urinary Retention
- •7.7.1.4 Recurrence
- •7.7.2 Complications of Abdominal Repairs
- •7.7.2.1 Bleeding
- •7.7.2.2 Infection
- •7.7.2.3 Enterocutaneous Fistula
- •7.7.2.4 Recurrence
- •Bibliography
- •8: Anorectal Injuries
- •8.1 Introduction
- •8.2 Etiology
- •8.2.1 Trauma
- •8.2.1.1 Blunt Anorectal Trauma
- •8.2.1.2 Penetrating Anorectal Trauma
- •8.2.1.3 Blast Injury
- •8.2.2 Anorectal Foreign Bodies
- •8.2.3 Obstetric Injury
- •8.2.4 Iatrogenic Injuries
- •8.2.5 Sexual Assault
- •8.3 Diagnosis of Anorectal Trauma
- •8.3.1 Unstable Patient
- •8.3.2 Stable Patient
- •8.4 Grade of Injury
- •8.5 Surgical Strategy
- •8.5.1 Technical Points in Surgery
- •8.5.2 Anorectal Foreign Bodies
- •8.5.4 Iatrogenic Anorectal Injuries
- •8.5.5 Closure of Colostomy
- •8.6 Outcome
- •8.6.1 Complications
- •8.6.2 Mortality
- •Conclusion
- •Bibliography
- •9: Anal Incontinence
- •9.1 Introduction
- •9.2 Anatomy of the Anal Sphincter Complex
- •9.3 Causes of Incontinence
- •9.3.1 Trauma
- •9.3.2 Neurological Conditions
- •9.3.3 Diarrheal States
- •9.3.4 Congenital Disease
- •9.3.5 Pelvic Floor Denervation
- •9.3.6 Aging
- •9.3.7 Miscellaneous
- •9.4 Clinical Evaluation
- •9.4.1 Medical History
- •9.4.2 Examination
- •9.4.3 Investigations
- •9.4.3.1 Manometry
- •9.4.3.2 Measurement of Sphincter Strength
- •9.4.3.3 Anal Sphincter Electromyography (EMG)
- •9.4.3.4 Anal Ultrasound
- •9.4.3.5 Balloon Proctography and Defecography
- •9.4.3.7 Endoscopy
- •9.4.3.8 Pudendal Nerve Motor Latency (PNML)
- •9.5.1 Conservative Treatment
- •9.5.1.1 Diet
- •9.5.1.2 Pharmacological Treatment
- •9.5.1.3 Bowel Management
- •9.5.1.4 Physical Treatment
- •9.5.1.5 Biofeedback
- •9.5.1.6 Faradic Stimulation
- •9.5.2 Surgical Treatment
- •9.5.2.1 Thiersch Operation
- •9.5.2.2 Repair of Obstetrical Injuries
- •9.5.2.4 Restoration of the Anorectal Angle
- •9.5.2.5 Muscular Graft
- •9.5.2.5.1 Gluteoplasty
- •9.5.2.5.2 Graciloplasty
- •9.5.2.5.2.1 Adynamic Graciloplasty
- •9.5.2.5.2.2 Dynamic Graciloplasty
- •9.5.2.6 Sacral Nerve Stimulation (SNS)
- •9.5.2.8 The FENIX™ Continence Restoration System
- •9.5.2.9 Miscellaneous Procedures
- •9.5.2.9.1 Smooth Muscle Plasty
- •9.5.2.9.2 Reinforcement of the Occlusion Mechanism
- •9.5.2.9.3 Secca Procedure
- •9.5.2.9.4 Injectable Agents
- •9.5.2.9.5 Colostomy
- •Bibliography
- •10: Complete Rectal Prolapse in Adults
- •10.1 Introduction
- •10.2 Etiology
- •10.3 Clinical Features
- •10.4 Diagnosis
- •10.5 Treatment
- •10.5.1 Abdominal Procedure
- •10.5.1.1 Suture Rectopexy
- •10.5.1.2 Prosthetic or Mesh Rectopexy
- •10.5.1.3 Posterior Mesh Rectopexy
- •10.5.1.4 Ripstein Procedure (Anterior Sling Rectopexy)
- •10.5.1.5 Rectopexy with Resection
- •10.5.1.6 Ventral Rectopexy
- •10.5.1.7 Laparoscopic Rectopexy
- •10.5.2 Perineal Procedure
- •10.5.2.1 Thiersch Procedure
- •10.5.2.2 Delorme Operation
- •10.5.2.3 Perineal Rectosigmoidectomy (Altemeier’s Procedure)
- •10.6 Comparison of Different Procedures and Approaches
- •10.7 Choice of Operation
- •10.8 Recurrent Prolapse
- •10.9 Summary
- •Bibliography
- •11: Pelvic Floor Dysfunction
- •11.1 Introduction
- •11.2 Anatomical Footprint for Pelvic Floor Surgical Navigation
- •11.3 Clinical Features
- •11.3.1 Urinary Continence
- •11.3.2 Bladder Storage/Sensation Symptoms
- •11.3.3 Voiding/Micturition Symptoms
- •11.3.4 Pelvic Organ Prolapse Symptoms
- •11.3.5 Sexual Dysfunction Symptoms
- •11.3.6 Anorectal Dysfunction Symptoms
- •11.3.7 Pelvic Pain Syndrome/Pudendal Neuralgia (Nantes Criteria)
- •11.3.8 Erectile Tissue Denervation (S2–S4) Symptoms
- •11.4 Evaluation for Pelvic Floor Dysfunction
- •11.4.1 Examination for Pelvic Organ Prolapse
- •11.4.2 Evaluation for Anorectal Dysfunction
- •11.4.3 Evaluation for Anorectal Incontinence
- •11.4.4 Evaluation for Functional Defecation Syndromes
- •11.4.4.4 Rule Out Slow-Transit Constipation
- •11.4.4.5 Imaging for Pelvic Floor Dysfunction with ODS
- •11.4.4.5.1 Dynamic Fluoroscopic Defecography
- •11.4.4.5.2 Anal Endosonography
- •11.4.4.5.3 Dynamic MRI Defecography
- •11.5 Causes of Anorectal Outlet Obstruction
- •11.5.1 Paradoxical Puborectalis Syndrome (PPR) or Anismus
- •11.5.2 Rectal Intussusception
- •11.5.3 Rectocele
- •11.5.4 Idiopathic Megarectum
- •11.6 Management of Pelvic Floor Dysfunction
- •11.6.1 Surgery for ODS: Stapled Transanal Resection Rectopexy (STARR)
- •11.6.1.1 Operative Procedure
- •11.6.2 Pelvic Organ Prolapse Surgery with STARR (POPSTARR)
- •11.7 Descending Perineum Syndrome
- •11.8 Functional Pelvic Pain Disorders
- •11.8.1 Levator Ani Syndrome
- •11.8.2 Proctalgia Fugax
- •Bibliography
- •12: Perianal Dermatology
- •12.1 Introduction
- •12.3.1 Contact Dermatitis
- •12.3.2 Danthron Contact Dermatitis
- •12.3.4 Seborrheic Dermatitis
- •12.3.5 Atopic Dermatitis
- •12.3.6 Psoriasis
- •12.3.7 Lichen Simplex Chronicus
- •12.3.9 Hidradenitis Suppurativa
- •12.3.10 Crohn’s Disease (Synonym: Regional Ileitis)
- •12.3.12.1 Anal Fissures
- •12.3.12.2 Anal Fistula
- •12.3.12.3 Pilonidal Cyst/Sinus
- •12.3.12.4 Pruritus Ani
- •12.4 Infections
- •12.4.1 Folliculitis and Furunculosis
- •12.4.2 Streptococcal Dermatitis/Perianal Cellulitis
- •12.4.3 Perianal Abscess
- •12.4.4 Ecthyma Gangrenosum
- •12.4.5 Necrotizing Infections
- •12.4.6 Common Mycoses
- •12.4.7 Thread/Pinworms
- •12.4.8 Sexually Transmitted Diseases (STDs)
- •12.4.9 Miscellaneous Infections
- •12.5 Benign Tumors
- •12.5.1 Hemorrhoids
- •12.6 Premalignant Dermatoses and Frank Malignancies
- •12.6.1 Porokeratosis
- •12.6.2 Anal Intraepithelial Neoplasia
- •12.6.3 Carcinoma of the Anus
- •12.6.5 Miscellaneous Malignancies
- •12.8 Trauma in the Perianal Area
- •Conclusion
- •References
- •13: Benign Ulcers of the Anorectum
- •13.1 Introduction
- •13.2 Etiology
- •13.3 Signs and Symptoms
- •13.3.1 Diarrhea
- •13.3.2 Pain
- •13.3.3 Hemorrhage
- •13.3.4 Discharges
- •13.3.5 Pruritis or Itching
- •13.4 Diagnosis and Investigation
- •13.4.1 Endoscopy (Macroscopic and Microscopic Appearance)
- •13.4.2 Anorectal Function Tests
- •13.4.3 Radiological Investigation
- •13.4.3.1 Defecography
- •13.4.3.2 Barium Enema
- •13.4.3.3 Transrectal Ultrasound
- •13.4.4 Differential Diagnosis
- •13.5 Special Anorectal Ulcers
- •13.5.1 Anal Fissure
- •13.5.2 Hemorrhoidal Ulcer
- •13.5.3 Varicose Ulcer
- •13.5.4 Tubercular Ulcer
- •13.5.5 Syphilitic Ulcers
- •13.5.6 Dysenteric Ulceration
- •13.5.7 AIDS-Associated Anorectal Ulcers
- •13.5.8.1 Introduction
- •13.5.8.2 Clinical Features
- •13.5.8.4 Investigations
- •13.5.8.4.1 Sigmoidoscopy
- •13.5.8.4.2 Defecography
- •13.5.8.4.3 Barium Enema
- •13.5.8.4.4 Transrectal Ultrasonography (TRUS)
- •13.5.8.4.5 Anorectal Manometry
- •13.5.8.5 Differential Diagnosis
- •13.5.8.6 Management of SRUS
- •13.5.8.6.1 Conservative Treatment
- •13.5.8.6.2 Surgery
- •13.5.9 Suppository-Related Ulcers
- •13.5.10 Nicorandil-Induced Ulcers
- •13.6 Radiation-Induced Anorectal Ulcers
- •Bibliography
- •14: Benign Strictures of Anorectum
- •14.1 Introduction
- •14.2 Diagnosis
- •14.3 Etiology
- •14.3.1 Amoebic Proctocolitis
- •14.3.2 Tuberculous Stricture
- •14.3.3 Lymphogranuloma Venereum
- •14.3.4 Actinomycosis
- •14.3.6 Ischemic Colitis
- •14.3.7 Stricture Following Bowel Anastomosis
- •14.3.8 Stricture Following Anorectal Surgery
- •14.3.9 Strictures Following Traumatic Injuries
- •14.3.10 Postradiation Stricture
- •14.3.11 Endometriosis
- •14.4 Treatment Options
- •14.4.1 Diet and Medical Treatment
- •14.4.2 Dilatations
- •14.4.3 Surgical Treatment
- •14.4.3.1 Sphincterotomy
- •14.4.3.2 Anoplasty (Stricturoplasty)
- •14.4.3.3 Surgery for Rectal Strictures
- •14.4.3.4 Colostomy
- •14.5 Summary
- •Bibliography
- •15: Benign Tumors of the Anorectum
- •15.1 Introduction
- •15.2 Benign Tumors of Epithelial Origin
- •15.2.2 Keratoacanthoma
- •15.2.3.1 Etiopathogenesis
- •15.2.3.2 Epidemiological Facts
- •15.2.3.4 Investigations
- •15.2.3.5 Treatment
- •15.2.4 Preventive Measures
- •15.2.5.1 Serrated Polyps and Adenoma
- •15.2.6 Nonneoplastic Adenomas
- •15.2.6.1 Hyperplastic Polyp
- •15.2.6.3 Hamartomatous Polyps, Juvenile Polyp, and Retention Polyp
- •15.2.6.4 Lymphoid Hyperplasia and Lymphoid Polyp
- •15.3 Benign Mesenchymal Tumors
- •15.3.1 Lipoma
- •15.3.2 Fibroma
- •15.3.4 Leiomyoma
- •15.3.7 Hemangioma
- •15.3.8 Lymphangioma
- •15.4 Benign Exogenous, Extrinsic, and Miscellaneous Tumors
- •15.4.1 Barium Granuloma
- •15.4.2 Endometriosis
- •15.4.4 Sarcoidosis
- •15.4.5 Tuberculosis
- •Conclusion
- •Bibliography

174
I. Hassan and P.A. Rather
A periorifi cial form of Langerhans’ cell histiocytosis/eosinophilic granuloma may cause ulcerating and vegetating lesions within the anal canal
and in the perianal skin (Tzung and Wu 2005 ).
12.7 Congenital
and Developmental
Abnormalities
Developmental abnormalities such as hemangioma, pigmented nevi, etc., may be seen in the
region. Developmental cysts, fi stulae, sinuses,
and tumors are not uncommon and may become
infected and cause confusion with clinical diagnosis of hidradenitis suppurativa or furuncles.
Dermoid cysts may occur on or adjacent to the
perineal raphe, and cloacal sinuses may form fi stulae from the anus to the adjoining skin.
Chordoma cutis presenting as single or multiple, smooth, skin-colored, non-tender nodules
arises from the embryonic precursor of notochord
and can involve the skin of perianal area by direct
extension or metastasis (Su et al. 1993 ). Because
of preceding sacrococcygeal pain of a persistent
nature, it may mimic sacral cysts, and scanning
procedures may be required to differentiate
between them (Van Kleft and Van Vyve 1991 ).
Congenital hypertrichosis over the midline in
the lumbosacral area (faun tail) is a sign of underlying spinal dysraphism (e.g., spina bifi da
occulta). Pilonidal sinus may also be considered
an important developmental defect.
12.8 Trauma in the Perianal Area
Unilateral skin necrosis of the perianal area
has been reported following indwelling umbilical
artery catheterization from thrombosis and occlusion of the inferior gluteal artery (Mann 1980 ).
12.9 Chronic Perianal Pain
and the “Perineal Syndrome”
A number of names have been given to sensations of pain localized to the perianal region in
the absence of evident organic cause (Neill and
Swash 1982 ). These include proctalgia fugax,
“coccygodynia,” “descending perineum syndrome,” and “chronic idiopathic anal pain.” The
pain is described as dull and throbbing, often precipitated by sitting. Attacks occur without warning but may be brought about by a full rectum,
and the skin is entirely normal. The patients are
usually stressed individuals. The exact mechanism is unknown, although cholinergic mechanism is proposed.
Conclusion
Knowledge about various dermatological con-
ditions in the perianal area or in other words
perianal dermatology is mandatory for the clini-
cians in order to differentiate between simple
less serious conditions from the more severe
devastating ones. This can aid in earlier diagno-
sis and prompt treatment of diseases with more
serious pathology, for example, carcinomas.
This also highlights the importance of liaison
and cooperation between medical professionals,
especially dermatologists, surgeons, gastroen-
terologists, and oncologists, so as to identify
and treat the various perianal dermatoses.
Anal trauma is not uncommon and it is one of the
most common causes of ulceration in the area.
This may occur because of insertion of foreign
bodies occasionally into the rectum and anogenital tattooing which has become a commonplace.
Pressure sores (decubitus ulcers) in the sacral
area are common especially in elderly, debilitated, or bedridden patients. It often starts as persistent patch of erythema on the sacral or ischial
region, which leads to impending ulceration.
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Akdamar K, Martin RJ, Ichinose H. Syphilitic proctitis.
Am J Dig Dis. 1977;22:701.
Alexander RM, Kaminsky DB. Giant condyloma acumi-
natum (Buschke–Löwenstein tumour) of the anus. Dis
Colon Rectum. 1979;22:561–5.

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Alexander-Williams J. Pruritus ani. BMJ. 1983;287:
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Benign Ulcers of the Anorectum
Ahmad Abdul Hai and Niharika Roy
1 3
13.1 Introduction
An ulcer is a break in the continuity of the lining
surface, either the skin or mucous membrane.
Multiple isolated areas on the wall of the anorectal region may be affected by ulcers. Ulcerations
at the anorectal region are not limited to any age,
sex, or environment but may be more common
where attention to hygiene and cleanliness is not
much observed. These ulcers may be superfi cial or
deep, large or small, single or multiple, acute or
chronic, and circular or irregular in shape and may
cause slight or most excruciating pain.
13.1.1 Pathophysiology of Benign
Anorectum Ulcer
The rectum although part of a large gut lacks in
cardinal features such as taeniae, appendices epiploicae, and sacculations. It extends from the rectosigmoid junction to the anorectal sling; it starts
at the level of third sacral vertebrae and ends in
front of the tip of the coccyx (12 cm). In surgical
A. A. Hai (*)
Department of General Surgery,
Hai Medicare and Research Institute ,
Raja Bazar, Bailey Road , Patna 800 014 , India
draahai@gmail.com
e-mail:
N . R o y
Gen Surgery , PARAS HMRI Hospital , Patna , India
drniharika.mail@gmail.com
e-mail:
practice, it is taken from the sacral promontory to
the puborectal sling (18 cm long). It is doubly
curved in the anterior-posterior and lateral planes
2004 ). It is narrow at its two extremes, i.e.,
(Hai
the sigmoid fl exure at the proximal end and the
anal canal at the distal end.
The ampulla of the rectum which is the largest
part is movable. It extends from the rectosigmoid
junction to the crossing of levator ani muscle. In
normal empty state, the anterior and posterior
wall remains in contact, presenting a transverse
slit. In the portion below the levator ani, in empty
state, the lateral walls are in contact presenting as
anterior-posterior slit. The length and tortuosity
of the anorectum increase with age. This again is
a factor which explains higher incidence of
mucosal ulceration in the elderly.
Microscopically, it has four layers, peritoneum (partial), muscular, submucous, and
mucous. The muscular layer is thicker and
stronger than other parts of the large intestine
and has a circular inner layer and a longitudinal
outer layer. This produces a higher intraluminal
pressure. The submucosa is a collection of
dense connective tissue, with blood vessels,
nerves, and lymphatics. It is lax to permit free
gliding of the mucous membrane over it. In
infl ammatory diseases, the layer becomes
thickened, indurated, and rigid, adhering to
muscular wall, and interferes with mobility of
the mucous membrane; therefore, the gliding
movement of the mucosa is lost and this makes
© Springer India 2016
N.A. Chowdri, F.Q. Parray (eds.), Benign Anorectal Disorders:
A Guide to Diagnosis and Management, DOI 10.1007/978-81-322-2589-8_13
177

178
A.A. Hai and N. Roy
it more prone to trauma by the descending fecal
stream which is further aggravated by the rising
intraluminal pressure. The mucous membrane
of the rectum is much more thicker and has a
more generous blood supply. The mucous cells
are much more plentiful here.
The anorectum is very frequently the seat of
various types of ulceration which may extend
into the sigmoid proximally and perineal skin
distally. The hard fecal mass bruises the anorectum. In straining, the force is exerted against
an immovable and resistant wall. The sliding of
the fecal mass causes obstruction of the circulation and congestion that further leads to
ulceration.
The superior hemorrhoidal veins, draining the
upper rectum, are a part of portal circulation. The
collateral circulation below is so feeble that it
predisposes the rectum to constant congestion
and ulceration.
The anal glands drain into the base of the
crypts and may extend submucosally to reach the
internal anal sphincter. These anal glands when
infl amed or blocked are the most common leading cause for anal abscess and fi stula.
The anorectum forms the fi nal portion of the
intestinal tract and serves as a transit station for
the rough and indigestible refuse. They are subjected to continued pressure by the scabula,
which causes abrasions and wounds. Whenever
the accumulation of feces remains for a protracted period in the rectum or sigmoid, it
becomes very hard, and by its constant pressure
and to-and-fro movements, caused by peristalsis
and intra-abdominal pressure changes, it is likely
to produce congestion, abrasion, and sloughing
of the mucous membrane, causing ulceration.
The fact that there are numerous bacteria and
bacilli always present in the intestinal canal,
especially at the lower end, further predisposes
these organs to ulceration, as they become easily
infected when they are injured due to any cause.
The large variety of parasitic agents found in the
intestinal tract, such as amebae, Trichomonas
intestinalis , Strongyloides , etc., further predispose to infection and ulceration in this region.
Aside from the specifi c diseases, such as tuberculosis, syphilis, HIV, etc., certain other constitutional and organic diseases like Crohn’s ulcerative
colitis predispose anorectal region to ulceration.
In general, one may say whatever enfeebles the
circulation will predispose to congestion and
ulceration of the anorectum.
From a pathological point of view, and for
convenience of description, anorectal ulcers may
be divided into simple, specifi c, and systemic
ulcerations:
• The simple ulcerations are those due to trauma
or any other cause followed by infection from
the bacteria present in the intestinal canal.
• The specifi c ulcers are those due to infection
by bacilli or other pathogens not normally
present in the human, e.g., tubercular and
syphilitic ulcers.
• The systemic types are constitutional or
organic diseases, e.g., ulcerative colitis and
Crohn’s diseases.
Some of these divisions show overlap as both
pathological conditions may be present in the
same individual. Thus, there may be simple
ulceration of the mucous membrane along with
malignant involvement of the rectum at a higher
point. A simple traumatic ulcer may become
infected by tuberculosis or syphilis, and its nature
will be entirely changed from what it was when
fi rst observed.
13.2 Etiology
Ulcers of the anorectal region are very variable in
etiology and morphology. The different causes of
ulcers of the anorectum are as follows:

13 Benign Ulcers of the Anorectum
(i) Anal fi ssures (xvi) Rectal endometriosis
(ii) Hemorrhoidal and varicose ulcer (xvii) Injury:
(iii) Ulcer with mucosal prolapse Self-infl icted
(iv) Crohn’s disease and ulcerative colitis Iatrogenic
(v) Proctitis: Anal intercourse
Toxic (xviii) Suppositories:
Bacterial Paracetamol
Radiogenic Ergot
Not classifi able (xix) Drugs (nicorandil)
(vi) Vascular: (xx) Ulcers associated with
proximal malignancy
Ischemic colitis (xxi) Idiopathic
Varicose ulcer
(vii) Necrotizing enterocolitis
(viii) Pseudomembranous colitis
(ix) Pyoderma gangrenosum
(x) Tropical infection:
Amebiasis
Giardiasis
Shigella, salmonella
(xi) Fungal
(xii) Actinomycosis
(xiii) Viral infection:
HIV
Herpes
(xiv) Syphilis
(xv) Tuberculosis
179
13.3 Signs and Symptoms
The symptoms of ulceration of the anorectum
are very similar in many respects for all varieties
and all causes. The size of the ulcer as a rule
bears no relationship to the severity of symptoms. Extensive ulceration well above the internal sphincter may cause very slight and indefi nite
symptoms, whereas a very small ulcer situated
low down may have great pain, muscular spasm,
nervous irritability, and refl ex disturbances in
nearly all the organs of the body.
The most prominent clinical features of
benign anorectal ulceration are:
• Diarrhea
• Pain
• Bleeding
• Discharge of pus and mucus
• Pruritis

180
A.A. Hai and N. Roy
13.3.1 Diarrhea
Patient presents with this condition not knowing that the underlying cause is ulceration.
Stool may vary from 3 to 20 per day, accompanied by great straining and tenesmus, exhausting the patient and causing rapid loss of weight.
The cause is due to the contact of feces with
exposed nerve terminals, which excites and
increases peristalsis. One peculiar characteristic of the diarrhea in ulceration of the rectum is
that it is generally quiescent at night, whereas
during daytime, the patient suffers from frequent calls to stool.
13.3.2 Pain
Pain is a very unreliable and indefi nite symptom in ulceration of the rectum. Patient may
have no, little, or severe pain, depending on the
site and cause of ulceration. If the ulceration is
high up in the rectum, a sense of heaviness and
aching in the sacral region is the chief discomfort of which most patients complain. If it is
situated lower down within the sphincters and
involves the mucocutaneous area where the
sensitive nerve ends enter, pain of a sharp, lancinating, or burning character will be the chief
symptom.
Painful ulceration is usually due to recurrent
genital herpes, syphilis (in endemic areas), or
trauma. Severe pain is seen in perianal herpes
simplex infection (usually interstitial) or perianal abscess. More recently, lymphogranuloma
venereum has emerged as a major cause in
Western countries. Painless ulcers are associated with syphilitic chancre, although HSV and
trauma must be kept in mind (Russell
The pain of anal fi ssure may be constant or
intermittent, usually most severe during or
immediately after stool passage. In the intervals
of defecation, there is a dull aching, which may
be confi ned to the rectum or extend up to the
back and down the limbs. The patient may prefer standing during consultation or sit gingerly
and walk with a wide-based, tentative gait.
2011 ).
13.3.3 Hemorrhage
Hemorrhage is always present in a greater or lesser
degree, depending upon the location and the extent
of the ulceration. It may be slight so that the
discharges may only be tinged with a streak of
blood. On the other hand, it may be profuse, if a
large vein or artery is attacked by the ulcer.
13.3.4 Discharges
Besides blood, there is discharge of mucus and
pus in varying quantities. Discharge increases as
ulcers increase in size and number. The discharge
is sticky, reddish in color, and of the consistency
of pus with fragments of necrosed tissue and constantly oozes out of the anus.
13.3.5 Pruritis or Itching
In case of long-standing ulcers, there will invariably be pruritis around the anal margin. This may
extend in any direction until many deep fi ssures
are to be seen. It usually subsides when the ulceration has been cured.
13.4 Diagnosis and Investigation
The diagnosis of anorectal ulceration in most
cases can be easily made when a correct history
is obtained and a careful examination has been
made. Normally, a diagnosis of anorectal ulceration will be made from the macroscopic appearances of the rectum either at sigmoidoscopy or
radiologically at barium enema. Only in certain
circumstances will an ulcer be palpable.
13.4.1 Endoscopy (Macroscopic and Microscopic Appearance)
Endoscopic appearance of most of the ulcer is
nonspecifi c, and histopathology provides the
only means of defi nitive diagnosis.

13 Benign Ulcers of the Anorectum
181
The number, size, and location of the ulcers
can be seen by proctoscope or fl exible sigmoidoscope. An ulcer may be shallow or deep and is
often not initially apparent, being concealed
under the radiating mucous folds. It can be clearly
seen only by drawing back the skin of the perianal region.
Morphologically tubercular ulcer presents in
seven forms: fi stula in ano, ulcer with sharply
defi ned undermined edges, rectal stricture,
multiple small mucosal ulcer, lupoid form of
submucosal nodule, mucosal ulcer, and verrucous form with multiple warty lesions.
The macroscopic appearance of typical SRUS
ulcer is a small, shallow lesion with white slough
or a hyperemic mucosal patch, usually on the
anterior wall of the rectum. Endoscopic spectrum
of SRUS varies from hyperemic mucosal patch to
small or giant ulcers to broad-based polypoid
lesions of different sizes. Usually the lesion is
5–10 cm from the anal verge. The ulcers may
range from 0.5 to 4.0 cm in diameter but usually
are 1–1.5 cm in diameter.
Syphilitic and chancroid ulcers are initially
superfi cial and multiple situated anteriorly at
mucocutaneous junction and are painful. These
are generally smooth, sloping, and non- indurated.
In late stages, there may be mucosal fi ssure which
may heal with fi brosis and stricture formation.
The varicose ulcers appear as sharply defi ned,
irregular depressions in the mucous membrane of
the rectum. The edges are slightly elevated, and
the bases are covered with a yellowish pus,
beneath which are bright-red granulation tissues.
The veins of the rectum surrounding the ulcerated portion and, in general, all over the rectum
are varicose, and when the patient strains, they
become largely dilated.
Hemorrhoidal ulcers are entirely distinct from
varicose ulcerations. The hemorrhoidal ulcerations are usually fi ssure-like cracks or splits
through their center, in a protruding stump from
which the hemorrhoid partly sloughed away due
to thrombosis, trauma, or corrosive injections.
Ulcers in acute hemorrhagic rectal ulcer syndrome (AHRUS) are small, shallow, and irregular
or circumferential and situated in the terminal
rectum immediately proximal to the dentate line,
occupying from one-third to the entire circumference of the rectum.
On examination, AIDS ulcers are differentiated by their location proximal to the dentate line
with a broad based which may dissect between
tissue planes.
Ulcerative colitis patients have diffuse
erythema, attenuated vascular pattern, friability,
erosions, and multiple superfi cial ulcers.
Crohn’s disease patients have aphthous ulcers
which are longitudinal with normal intervening
mucosa, cobblestone appearance, stricture,
fi stula, or pseudodiverticular formation.
Traumatic ulcers consist of simple granulations, neither nodular nor proliferating bathed in
thick white milky secretions containing pus cells
and bacteria.
13.4.2 Anorectal Function Tests
Anorectal function tests have been performed,
but the results are variable, and the tests do not
help in establishing the diagnosis or predicting
therapeutic response.
13.4.3 Radiological Investigation
13.4.3.1 Defecography
Defecography (also known as proctography, defecating/defecation proctography, evacuating/
evacuation proctography, or dynamic rectal
examination) is a type of medical radiological
imaging in which the mechanics of a patient’s
defecation are visualized in real time using a fl uoroscope. The anatomy and function of the anorectum and pelvic fl oor can be dynamically
studied at various stages during defecation. It is
used mainly for prolapsed ulcer.
13.4.3.2 Barium Enema
Nodularity of the rectal mucosa, thickening of
the rectal folds, stricture formation, polypoid
lesions, and ulceration may be seen in a barium
enema. This is however not a specifi c and

182
A.A. Hai and N. Roy
defi nitive diagnostic fi nding, because these features cannot be differentiated from those of sinister conditions.
13.4.3.3 Transrectal Ultrasound
Transrectal ultrasound is easy to perform and
well tolerated and can be repeated as a follow-up
examination. Mucosal ulceration and changes in
the rectal wall architecture should be easily
detected and eventually measured.
The entire rectal wall consists of fi ve layers.
The mucosa is defi ned as the hypoechoic layer
nearest the probe and the muscularis propria as the
outer most hypoechoic layer. The three remaining
hyperechoic layers are considered as interfaces.
Normally, the individual layers are distinct from
each other and are not interrupted. An ulcer is
characterized as a hyperechoic spot or zone that
interrupts the continuity of the layer on ultrasonography; marked thickening of the internal anal
sphincter is the most striking feature, although
thickening of the submucosa and external anal
sphincter may be present. The rectal wall can be
thickened, especially the muscularis propria.
Fading of the borders between mucosa and muscularis propria can be seen. All of these features
probably are secondary to chronic straining.
Anal sphincter and puborectalis muscle at rest
and in dynamic condition can be assessed, and
the puborectalis muscle is clearly visualized by
rotating the probe in lateral direction. During
squeezing, contraction of the muscle is observed
with an upward movement of the pelvic fl oor in
healthy individuals. The lack of relaxation of the
puborectalis muscle during straining is accompanied by craniocaudal intussusceptions of the rectum with the formation of typical “onion-like”
structure created by superposition of different
layers of the proximal into distal part of the rectal
wall, observed especially in SRUS.
infl ammatory bowel disease and anal fi ssure on
macroscopic appearances alone can at times be
diffi cult as both give rise to (i) shallow ulceration,
(ii) granular appearances, (iii) hemorrhagic friable mucosa, and (iv) edematous mucosa. The
presence of pseudopolyps is most likely due to
ulcerative colitis, but this feature is seen more in
colonic disease rather than in the rectum. The
symptoms of ulcerative colitis develop over a
more prolonged period of time, and patients
rarely complain of abdominal pain. The presence
of multiple yellowish plaques of few millimeters
to 2 cm size is suggestive of pseudomembranous
or antibiotic-associated colitis, which is due to
toxin-mediated disease induced by Clostridium
diffi cile following exposure to antibiotics.
In the early stages of infl ammatory disease, the
diagnosis can be helped by bacteriology of stool.
The appearance of granulomas, fi ssures, and transmural infl ammation of anal lesion indicates
Crohn’s disease. A nonspecifi c infl ammation is a
feature of ulcerative colitis or postirradiation proctitis, which may be distinguished by history alone.
If rare organisms are cultured, such as cryptosporida or viruses, the possibility of immune disease
(e.g., HIV or leukemia) should be considered. The
history of sodomy and anal intercourse should be
elicited. These sometimes present with multiple
fi ssures and anal abscess.
Ischemia rarely affects the rectum but when
present is usually in older age groups and is of
sudden onset and associated with profuse bleeding and abdominal pain. The ulcers of SRUS are
palpable and feel indurated with fi xity to extrarectal tissues. Biopsy is essential to distinguish it
from malignant causes (Ellis
part is not to miss a malignant rectal ulcer in its
early stages, and even few “unwanted” biopsies
may be indicated.
2011 ). The crucial
13.4.4 Differential Diagnosis
The macroscopic appearance of various ulcers
has been discussed in endoscopy section of this
chapter. The clinical distinction between an anal
fi ssure and a rectal ulcer secondary to an
13.5 Special Anorectal Ulcers
13.5.1 Anal Fissure
Anal fi ssure is a longitudinal ulcer in the anoderm extending proximally to the dentate line
and distally to the anal verge. It may present as

13 Benign Ulcers of the Anorectum
183
acute fi ssure with severe excruciating pain or
may present in the chronic form, characterized by
a skin tag distally (sentinel piles), hypertrophied
papilla proximally, and the base of ulcer showing
the transverse fi bers of the sphincter. The pain is
exaggerated on defecation and may be accompanied with streaks of blood. Blood is scanty and
bright red. The topic is described in detail in a
separate chapter of this book.
13.5.2 Hemorrhoidal Ulcer
This type of anorectal ulcer is caused by sloughing and ulceration of a well-defi ned hemorrhoidal
mass. This may be due to thrombosis followed by
necrosis, trauma from the passage of hard fecal
masses or foreign bodies, or strangulation. It may
also be produced by the application of ice in
order to relieve congestion and by the action of
corrosive substances applied to the surface or
injected into the body of the hemorrhoid for the
purpose of curing it. The symptoms of this variety of ulceration are a history of the existence of
hemorrhoids either internal or external and of
prolapse, strangulation, efforts at reduction, and
the application of ice or cauterizing agents.
Morning diarrhea may or may not be present, but
the patient is frequently awakened at night by the
spasmodic contraction of the sphincter and the
desire to defecate.
Treatment is absolutely and unequivocally
surgical. The sphincter is dilated, and the ulcerated hemorrhoidal mass is taken away either by
crushing the clamp and cautery or by ligation.
The clamp-and-cautery operation by its stimulating effect and bactericidal action seems to be
as near a specifi c as one can desire.
13.5.3 Varicose Ulcer
This is a chronic, intractable ulcer which occurs in
patients with varicosity of the rectal mucous membrane. Their chronicity is due to varicosities of the
superior hemorrhoidal veins. This is different from
the ulceration of the hemorrhoids in the fact that it
is chronic. Exciting cause is some wound or injury
to the mucous membrane or rupture of one of the
varicose veins. Infection takes place and causes the
ulceration. Heavy eaters and drinkers who do little
exercise and are inclined to constipation are predisposed to this type of ulceration.
The ulcers occur above the mucocutaneous
border and produce few symptoms other than the
frequent desire to defecate, more marked during
daytime. There is always an inclination to defecate immediately upon rising in the morning,
which generally results in the passage of small
quantities of mucus and pus, with or without
blood. Occasionally these patients suffer from
quite severe hemorrhages. There is a dull aching
pain, but when the ulcers invade the mucocutaneous tissue at the margin of the anus, the patient
may suffer from acute pain. In this condition,
spasm of the sphincter will also complicate the
ulceration.
The treatment of varicose ulcers of the rectum
is very tedious and unsatisfactory. At the same
time, it is almost impossible for these ulcers to
heal without absolute rest in bed. The diet should
be regulated so as to contain as little refuse material as possible.
13.5.4 Tubercular Ulcer
Extrapulmonary tuberculosis (TB) accounts for
less than 15 % of all cases of tuberculosis, while
the intestinal one alone constitutes less than 1 %
of extrapulmonary forms of the disease. The most
common morphological form of anal TB is the
ulcerative form which typically presents as a
superfi cial ulceration, with a hemorrhagic
necrotic base that is granular and covered with
thick purulent secretions of mucus.
The postulated mechanisms by which the
tubercle bacilli reach the gastrointestinal tract are
(i) hematogenous spread from the primary lung
focus in childhood, with later reactivation; (ii)
ingestion of bacilli in sputum from active pulmonary focus; (iii) direct spread from adjacent
organs; and (iv) through lymph channels from
infected nodes.
The chief complaints are fever, anorexia, and
weight loss. The fever is low grade, intermittent,
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