Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1199_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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

30
P. Sivalingam et al.
Intake of diet high in fi ber and fl uid helps to minimize pain. Oral metronidazole (Carapeti et al.
1998 ), topical diltiazem (Silverman et al. 2005 ),
and injection of botulinum toxin (Patti et al.
2006 ) have been found to have marginal benefi t.
3.7.2 Urinary Retention
Retention of the urine occurs in about 10–32 %
patients. The contributing factors for urinary retention include the use of spinal anesthesia, fl uid overload, rectal packing, rectal spasm, and refl ex spasm.
Retention of urine responds to simple measures in
most cases. Hot water bags and injection carbachol
may help to relieve the retention. Some patients
may need catheterization. In older people, benign
prostate enlargement should be excluded.
3.7.3 Postoperative Bleeding
Postoperative hemorrhage may be early or late.
Early hemorrhage occurs as reactionary hemorrhage from the skin wound or the pedicle. It is
rare when the wound is sutured during surgery.
Early bleeding from the pedicle may be due to
loose ligature of the pedicle or slippage of ligature. The patient may have to be taken to the
operation theater for controlling of the bleeding.
Secondary hemorrhage is more serious, for
the bleeding may be considerable and the blood
may accumulate in the rectum and missed for
some time. It is due to sepsis occurring in the
pedicle resulting in softening of the wall of the
main artery. It usually occurs between 7–10th
postoperative days. Inspection may show trickling of dark blood from the anus. Rectal examination may reveal large soft clot, and on withdrawal
of fi nger, blood comes out. During proctoscopy,
blood clot may extrude through the lumen.
Delayed bleeding is usually not a preventable
condition. The patient is examined under anesthesia. Any clot is removed by a combination of
swabs and irrigation with saline. The bleeding
point is looked for, and if present, the bleeder is
under run using Vicryl in a small half circle or 5/8
needle. Bleeding can be controlled by passing a
Foley’s catheter, and traction of the catheter
brings the balloon into contact with the bleeding
area. Patient is given a proper antibiotic later.
3.7.4 Wound Infection
Infection is inevitable in a wound in such a contaminated area. But it is surprising that even
suturing of the skin wound does not lead to clinical infection. Still rarely, perianal and ischiorectal abscess have been reported. Any patient with
severe pain, fever, and urinary retention after
anorectal surgery should be examined carefully.
If the initial examination indicates the presence
of septic focus, the patient should be examined
under anesthesia. The treatment of sepsis in the
local area consists of drainage, debridement of
necrotic tissue, and parental antibiotics.
3.7.5 Fecal Impaction
Fecal impaction follows incomplete bowel action.
Though the bowel opens every day, it is incomplete.
Fecal material remains within the rectum and
becomes a large hard mass. The patient has a continued sensation of rectal fullness. In severe cases,
anesthesia may be required for digital evacuation.
3.7.6 Stenosis
The cause of postoperative anal stricture is excision of considerable portion of the anal mucosa
and anoderm. The fi brous tissue proliferation
leads to scarring and contraction of the anal orifi ce and narrowing of anal outlet.
The stenosis may be in the anal verge or may
be within the anal canal. Stenosis in anal verge is
due to excessive removal of skin below the dentate line. With each bowel, action skin splits and
a chronic fi ssure forms. The anal orifi ce is scarred
and contracted.
Stenosis within the anal canal is due to generous excision of anal canal mucosa during surgery.
The stricture is usually short and continued to the
mucosa and submucosa. In severe cases, the
lumen may not even admit the tip of the fi nger. If
the stenosis is within the reach of the fi nger, regu-

3 Hemorrhoids
31
lar dilatation with fi nger or Hagar dilator may
provide good result. Surgically, the strictures are
corrected by anoplasty to have a permanent cure.
An anoplasty should be considered for an anal
stenosis if medical treatment by bulk laxatives,
suppositories, dilatation, and enema has failed.
3.7.7 Recurrence
Nonsurgical therapy for hemorrhoid disease has a
recurrence rate of as high as 20 %, but after surgery it is only 2 %. Patients with nonsurgical
therapy will readily accept to have repeat therapy
because recurrence occurs 1–3 years after the
fi rst therapy. Recurrence after surgery is usually
in an accessory hemorrhoid, and the treatment is
decided on individual basis.
3.7.8 Incontinence
Anal leakage or soiling is common during the early
postoperative period, but frank incontinence of liquid and stool is rare. After 6–8 weeks, most patients
with imperfect continence regain full control. Anal
dilatation at the time of hemorrhoidectomy may
result in some loss of control for motion or fl atus.
The other cause for defective continence after hemorrhoidectomy is the loss of anal canal sensation
due to removal of sensory bearing anal canal epithelium and replacement by scar tissue. In closed
technique, this complication never occurs.
3.7.9 Other Late Complications
Anal fi stula, skin tags, ectropion, and mucosal
prolapse are some of the rare late complications
following haemorrhoid surgery.
constipation or diarrhea. The pain reaches its
peak 48 h and starts subsiding from fourth day.
The overlying skin may necrose and ulcerate
leading to discharge, bleeding, and infection. If
the patient presents with severe pain or onset of
the condition within 48 h, excision is the preferred
treatment. It can be done under local anesthesia
as outpatient procedure (0.5 % lidocaine mixed
with equal amount of 0.25 % bupivacaine containing 1:2,00,000 adrenaline). A short radial
incision is made over the swelling and the underlying clot is evacuated. The wound is left open. If
there is only discomfort and patient presents in a
resolving stage, conservative treatment in the
form of sitz baths, stool softeners, bulk-forming
fi ber supplement, and analgesics should be initiated. Proctoscopy should be postponed when the
patient is pain-free.
Thrombosed internal hemorrhoids are often
attributed to prolapse of the internal component
with inadequate reduction, resulting in venous
stasis and thrombosis of the vascular cushion.
Powerful sustained straining at defecation may
lead to thrombosis of internal hemorrhoids.
When this occurs the haemorrhoid prolapses
with edema of the corresponding perianal area.
If the patient has had trouble with internal hemorrhoid prior to this episode of thrombosis, the
correct treatment is early surgical intervention.
Emergency hemorrhoidectomy for thrombosed
hemorrhoids is technically easy and the patient
is relieved from pain remarkably. The management of acute thrombosed internal haemorrhoid
is usually nonoperative because pain is not a
frequent complaint. Even though conservative
treatment is practiced, the continued discomfort, prolonged disability, and fi nancial burden may warrant urgent operation for all such
individuals.
3.8 Special Situations
3.8.1 Thrombosed Hemorrhoids
Thrombosed external hemorrhoids usually present as a painful, pea size, tender mass in the perianal region, frequently following an episode of
3.8.2 Strangulated Hemorrhoids
Prolonged swelling of prolapsed third- or fourthdegree hemorrhoids can make it irreducible,
leading to incarceration and strangulation. If not
treated, it can lead to necrosis or gangrene and
ulcerations. The presence of gangrene, prolapse,
and edematous hemorrhoids usually causes

32
P. Sivalingam et al.
severe pain, swelling, bleeding, and foul- smelling
discharge. The treatment is reduction of the hemorrhoids into the anal canal under local anesthesia. Ideally, the patient should be admitted and
hemorrhoidectomy preferably by open technique
done on the following day. In the past, there has
been reluctance to treat the ulcerated and gangrenous hemorrhoids by immediate surgery for fear
of causing serious septic complications.
3.8.3 Anorectal Varices and Portal Hypertension
Varices are quite common in patients with portal
hypertension but are implicated in less than 1 %
of massive bleeding episodes in such patients.
Bleeding from anorectal varices is usually profuse and dark in color as compared to hemorrhoidal bleeding which is bright red in color
(Jacobs et al. 1980 ).
3.8.4 Pregnancy
Hemorrhoidal disease is usually exaggerated
during pregnancy, but the symptoms usually
resolve after delivery. The conservative method is
usually preferred. Surgery is only indicated for
acute thrombosed and prolapsed piles. The surgery should be preferably done under local
anesthesia with patient in left anterolateral position to push the uterus off the major abdominal
vessels. Sclerotherapy is strictly contraindicated.
3.8.6 Immunocompromised Patients
The hemorrhoidal disease in these patients should
be treated with extreme caution because of high
risk of delayed wound healing and septic complications though human immunocompromised
virus (HIV) disease is not an absolute contraindication to surgery. It cannot be recommended for
patients with acquired immunocompromised
disease syndrome (AIDS) because of high risk of
complications except under well-controlled
circumstances.
3.8.7 Coagulation Disorders
Patients receiving anticoagulants or having any
coagulation disorder should be preferably
treated with conservative methods. All precautions should be taken to prevent bleeding if any
surgical intervention is warranted.
3.8.8 Fissure
Primary treatment is directed to fi ssure. Fissure
with grade I or II piles are treated with LIS and
sclerotherapy or rubber band ligation for
hemorrhoids. Associated III and IV degree piles
are dealt by LIS and hemorrhoidectomy.
3.8.9 Sepsis
3.8.5 Crohn’s Disease and Ulcerative Colitis
Hemorrhoids in patients with Crohn’s disease
should preferably managed by conservative
methods. Hemorrhoidectomy should be reserved
only for those who do not respond to conservative
treatment. Postoperative complication rate is substantially high in these patients and can sometimes
warrant proctectomy. If indicated, hemorrhoidectomy in patients with ulcerative colitis should be
performed when disease is in remission.
Suppuration is dealt fi rst. Surgical intervention
for hemorrhoids should be avoided in the same
sitting.
Conclusion
The consensus is that most of the patients with
hemorrhoidal disease can be managed with
simple lifestyle adaptations, including dietary
and bowel habit modifi cations. The method
of treatment to be used should be selected
after proper judgment in order to achieve best
results. Grade I, II, and sometimes III hemorrhoids can be treated successfully in a large

3 Hemorrhoids
33
proportion of patients by offi ce-based procedures, either rubber band ligation or injection
sclerotherapy, depending on the clinician’s
usual practice. Grade IV and some grade III
hemorrhoids, together with those that fail to
respond to offi ce-based procedures, are most
effectively treated by traditional hemorrhoidectomy, although there is increasingly compelling evidence to support the use of stapled
hemorrhoidectomy. It should be used selectively for circumferential prolapse and in the
absence of external tags for best outcome.
Other less common procedures have their
advocates, but further evidence is required
before their use becomes more widespread.
Bibliography
Abo-hashem AA, Sarhan A, Aly AM. Egypt Harmonic
Scalpel Compared with bipolar electro-cautery
hemorrhoidectomy: a randomized controlled trial. Int
J Surg. 2010;8(3):243–7.
Agbo SP. Surgical management of haemorrhoids. J. Surg
Tech Case Rep. 2011;3(2):68–75.
Aigner F, Bodner G, Conrad F, et al. The Superior rectal
artery and its branching pattern with regards to its
clinical infl uence on ligation techniques for internal
haemorrhoids. Am J Surg. 2004;187:102–8.
Alonso-Coello P, Mills E, Heels-Ansdell D, et al. Fiber
for the treatment of hemorrhoid complications: a systematic review and meta-analysis. Am J Gastroenterol.
2006;101:181–8.
Armstrong DN, Ambroze WL, Schertzer ME, et al.
Harmonic Scalpel vs. electrocautery hemorrhoidectomy: a prospective evaluation. Dis Colon Rectum.
2001;44(4):558–64.
Baron J. Offi ce ligation treatment of hemorrhoids. Dis
Colon Rectum. 1963;6:109–13.
Bulus H, Tas A, Coskun A, et al. Evaluation of two
haemorrhoidectomy techniques: harmonic scalpel and
Ferguson’s with electrocautery. Asian J Surg. 2014;
37(1):20–3.
Burkitt DP. Varicose veins, deep vein thrombosis and
haemorrhoids: epidemiology and suggested aetiology.
Br Med J. 1972;2(5813):556–61.
Burkitt DP. Dietary fi bre and pressure disease. J.R Coll.
Physicians Lond. 1975;9(2):138–46.
Bursics A, Morvay K, Kupcsulik P, et al. Comparison of
early and 1-year follow-up results of conventional
hemorrhoidectomy and hemorrhoid artery ligation: a
randomized study. Int J Colorectal Dis. 2004;19:
176–80.
Carapeti EA, Kamm MA, McDonald PJ, et al. Double-
blind randomized controlled trial of effect of
metronidazole on pain after day-case haemorrhoidectomy. Lancet. 1998;351:169–72.
Chau NG, Bhatia S, Raman M. Pylephlebitis and pyo-
genic liver abscesses: a complication of hemorrhoidal
banding. Can J Gastroenterol. 2007;21:601–3.
Chung CC, Ha JP, Tai YP, et al. Double-blind randomized
trial comparing Harmonic Scalpel hemorrhoidectomy,
bipolar scissors haemorrhoidectomy and scissors excision: ligation technique. Dis Colon Rectum.
2002;45(6):789–94.
Chung CC, Cheung HY, Chan ES, et al. Stapled haemor-
rhoidopexy vs Harmonic Scalpel hemorrhoidectomy:
a randomized trial. Dis Colon Rectum. 2005;48(6):
1213–9.
Dal Monte PP, Tagariello C, Sarago M, et al. Transanal
haemorrhoidal dearterialisation: nonexcisional surgery for the treatment of haemorrhoidal disease. Tech
Coloproctol. 2007;11(4):333–8.
Faucheron JL, Gangner Y. Doppler-guided hemorrhoidal
artery ligation for the treatment of symptomatic hemorrhoids: early and three-year follow-up results in 100
consecutive patients. Dis Colon Rectum. 2008;51:
945–9.
Giordano P, Overton J, Madeddu F, et al. Transanal hem-
orrhoidal dearterialization: a systematic review. Dis
Colon Rectum. 2009;52(9):1665–71.
Guy RJ, Soew-Choen F. Septic complications after treat-
ment of haemorrhoids. Br J Surg. 2003;90:147–56.
Ho YH, Soew-Choen F, Tan M, et al. Randomized con-
trolled trial of open and closed haemorrhoidectomy.
Br J Surg. 1997;84:1729–30.
Hoffman G. Stapled haemorrhoidopexy: a new device
and method of performance without using a pursestring suture. Dis Colon Rectum. 2005;49:
135–42.
Infantino A, Bellomo R, Dal Monte PP, et al. Transanal
haemorrhoidal artery echodoppler ligation and anopexy (THD) is effective for II and III degree haemorrhoids: a prospective multicentric study. Colorectal
Dis. 2010;12(8):804–9.
Ivanou D, Babovic S, Selesi D, et al. Harmonic Scalpel
haemorrhoidectomy; a painless procedure. Med Pregl.
2007;60(9–10):421–6.
Jacobs DM, Bubrick MP, Onstad GR, et al. The relation-
ship of haemorrhoids to portal hypertension. Dis
Colon Rectum. 1980;23:567–9.
Johanson JF, Sonnenberg A. The prevalence of haemor-
rhoids and chronic constipation. Gastroenterology.
1990;98:380–6.
Kaider–Person O, Person B, Wexner SD. Haemorrhoidal
disease a comprehensive review. J Am Coll Surg.
2007;204:102–17.
Khan S, Pawlak SE, Eggenberger JC, et al. Surgical
treatment of haemorrhoids: prospective randomized
trial comparing closed excisional haemorrhoidectomy
and the Harmonic Scalpel technique of excisional
haemorrhoidectomy. Dis Colon Rectum. 2001;44(6):
845–9.
Kwok SY, Chung CC, Tsui KK, et al. A double blind ran-
domized trial comparing ligasure and Harmonic

34
P. Sivalingam et al.
Scalpel haemorrhoidectomy. Dis Colon Rectum.
2005;48(2):344–8.
Longo A. Stapled anopexy and stapled haemorrhoidec-
tomy: two opposite concepts and procedures. Dis
Colon Rectum. 2002;45:571–2.
Longo A. Treatment of haemorrhoidal disease by reduc-
tion of mucosa and haemorrhoidal prolapse with a
circular suturing device: a new procedure. In: 6th
World congress of endoscopic surgery (IFES).
Mundozzi Editore; 1998. p. 777–84.
MacRae HM, McLeod RS. Comparison of haemorrhoidal
treatment modalities. A meta-analysis. Dis Colon
Rectum. 1995;38:687–94.
Morinaga K, Hasuda K, Ikeda T, et al. A novel therapy for
internal hemorrhoids. Ligation of the haemorrhoidal
artery with newly devised instrument (Moricorn) in
conjunction with a Doppler fl ow meter. Am J
Gastroenterol. 1995;90:610–3.
Neiger A. Haemorrhoids in every day practice. Procto-
cology. 1979;2;22–8.
O’Hara VS. Fatal clostridial infection following haemor-
rhoidal banding. Dis Colon Rectum. 1980;23:570–1.
Parks AG. A note on the anatomy of the anal canal. Proc
R Doc Med. 1954;47:997–8.
Park AG. The surgical treatment of haemorrhoids. Br. J
Surg. 1956;43:337–51.
Patti R, Almasio PL, Arcara M, et al. Botulinum toxin vs
topical glyceryl trinitrate ointment for pain control in
patients undergoing haemorrhoidectomy: a randomized trial. Dis Colon Rectum. 2006;49:1741–8.
Poon GP, Chu KW, Lau WY, et al. Conventional vs. triple
band ligation for haemorrhoids: a prospective,
randomized trial. Dis Colon Rectum. 1986;29:836–8.
Rama Kant AA. A journey from piles to smiles. J Surg
Sci. 2010;1:14–8.
Ratto C, Donisi L, Parello A, et al. Evaluation of transanal
hemorrhoidal dearterialization as a minimally invasive
therapeutic approach to hemorrhoids. Dis Colon
Rectum. 2010;53(5):803–11.
Scheyer M, Antonietti E, Rollinger G, et al. Doppler
guided haemorrhoidal artery ligation. Am J Surg.
2006;191:80–3.
Senapati A, Nicholls RJ. A randomized trial to compare
the results of injection sclerotherapy with bulk laxative
alone in the treatment of bleeding haemorrhoids. Int J
Colorectal Dis. 1988;3:124–6.
Shanmugam V, Thaha MA, Rabindranath KS, et al.
Systematic review of randomized trails comparing
rubber bands ligation with excisional haemorrhoidectomy. Br J Surg. 2005;92:1481–7.
Shao WJ, Li GC, Zhang ZH, et al. Systematic review and
meta analysis of randomized controlled trials
comparing stapled haemorrhoidectomy with conventional haemorrhoidectomy. Br J Surg. 2008;95:
147–60.
Silverman R, Bendick PJ, Wasvary HJ. A randomized,
prospective, double-blind, placebo controlled trial of
the effect of a calcium channel blocker ointment on
pain after hemorrhoidectomy. Dis Colon Rectum.
2005;48:1913–6.
Smith LE, Goodreau JJ, Fouty WJ. Operative haemor-
rhoidectomy versus cryo destruction. Dis Colon
Rectum. 1979;22:10–6.
Sohn N, Aronoff JS, Cohen FS, et al. Transanal hemor-
rhoidal dearterialization is an alternative to operative
hemorrhoidectomy. Am J Surg. 2001;182(5):
515–9.
Sohn VY, Martin MJ, Mullenix PS, et al. A comparison of
open versus closed techniques using the Harmonic
Scalpel in outpatient haemorrhoid surgery. Mil Med.
2008;173(7):689–92.
Thomson WH. The nature of haemorrhoids. Br J Surg.
1975;62:542–52.
Thomson JPS, Leicester RJ, Smith LE. Haemorrhoids.
MM Henry and M Swash (eds), Coloproctology and
the pelvic fl oor. London: Butterworth – Heinemann.
2nd ed. 1992. p. 373–93.
Tjandra JJ, Chan MK. Systematic review on the proce-
dure for prolapse and haemorrhoids. (Stapled
haemorrhoidopexy). Dis Colon Rectum. 2007;50:
878–92.
Tsunoda A, Sada H, Sugimoto T, et al. Randomized
controlled trial of bipolar diathermy vs ultrasonic
scalpel for closed haemorrhoidectomy. World J
Gastrointest Surg. 2011;3(10):147–52.
Wang JY, Chang-Chien CR, Chen JS, et al. The role of
lasers in haemorrhoidectomy. Dis Colon Rectum.
1991;34(1):78–82.
Whitehead W. The surgical treatment of haemorrhoids. Br
Med J. 1882;1:148–50.
Wolff BG, Culp CE. The whitehead haemorrhoidectomy.
An unjustly maligned procedure. Dis Colon Rectum.
1988;31:587–90.
You SY, Kim SH, Chung CS, et al. Open vs closed
haemorrhoidectomy. Dis Colon Rectum. 2005;48:
108–13.

Anal Fissure
Benjamin Perakath and Niranjan Agarwal
4
4.1 Introduction
Anal fi ssure or fi ssure in ano is a longitudinal tear
or split in the skin covering the distal anal canal
below the level of the dentate line, overlying the
lower half of the internal sphincter (Fig. 4.1 ). It
usually presents as a linear superfi cial ulcer in the
anoderm and is characterized by excruciating
sharp perianal pain associated with passage of
small amounts of bright red blood per rectum
and/or pruritus (Zaghiyan and Fleshner 2011 ).
4.2 Epidemiology
Fissure in ano is one of the common benign anorectal conditions and can occur at any age. It
commonly affects the younger and middle age
groups but is sometimes seen at other ages,
including infancy and early childhood and has no
sex predilection. Ninety percent of anal fi ssures
occur in the posterior midline of the anoderm and
are solitary. Ten percent of women and one
percent of men may have fi ssures in the anterior
midline (Fig. 4.2 ). Women who develop symp-
toms during pregnancy or after childbirth usually
Fig. 4.1 Typical chronic anal fi ssure
B. Perakath , MS, FRCS(G)
Department of Surgery Unit 2 ,
Christian Medical College , Vellore 632004 , India
benjamin@cmcvellore.ac.in
e-mail:
N. Agarwal , MS (MUM), DNB, FACRSI (*)
Department of General Surgery,
Bombay Hospital Institute of Medical Sciences
Mumbai – 20 , Mumbai , India
drndagarwal@hotmail.com
e-mail:
© 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_4
Fig. 4.2 Anterior anal fi ssure
35

36
Figs. 4.3 and 4.4 Atypical positions of anal fi ssure
B. Perakath and N. Agarwal
have anterior fi ssure in ano (Jonas et al. 2001 ).
Atypical positions of fi ssure or multiple fi ssures
(Figs. 4.3 and 4.4 ) should raise the suspicion of
uncommon causes like infl ammatory bowel disease, tuberculosis, anal intercourse and anal
malignancy, or immunodefi ciency syndromes.
4.3 Classifi cation
Fissures may be classifi ed as primary idiopathic,
which is the most common and secondary, based
on the etiology. It has also been classifi ed arbitrarily as acute fi ssure in ano and chronic fi ssure
in ano based on the duration of symptoms and
healing. Typically acute anal fi ssures are those
which heal within 6 weeks of duration spontaneously or with medical management. They are
superfi cial and may deepen to expose the underlying internal sphincter. Fissures which have not
healed in 6 weeks and developed secondary
changes in the form of sentinel tag, hypertrophied anal papilla (Fig.
lateral edges of the fi ssure, relative stenosis secondary to spasm, or fi brosis of the internal
sphincter are labeled as chronic, and these often
require surgical management (Zaghiyan and
Fleshner 2011 ; Madalinski 2011 ). Based on
location, fi ssure is classifi ed as typical or atypical. Among the typical sites, posterior fi ssures
are the most common (90 %), while anterior ones
are uncommon. Atypical fi ssures are located at
any other site and usually due to some secondary
pathology.
4.5 ), induration of the
Fig. 4.5 Hypertrophied papillae and sentinel pile
4.4 Pathology
In its early stages, a fi ssure is a simple split in the
skin of the anal canal, but there soon develop in
connection with it certain secondary changes. One
of the most striking of these is a swelling of the
skin at the lower end of the fi ssure, actually at the
level of the anal orifi ce, so that it forms a tag – like
swelling the so-called sentinel pile. This is presumably due to low-grade infection and lymphatic
edema, and often the tag has a very infl amed,
tense, and edematous appearance (Fig. 4.6 ); later it
may undergo fi brosis and persist as a permanent
fi brous skin tag even after the fi ssure has healed.
Quite frequently, the anal valve immediately
above the fi ssure also becomes swollen due to
edema and fi brosis and forms a hypertrophied
anal papilla . Another feature in a long-standing

4 Anal Fissure
37
Fig. 4.6 Infl amed, edematous sentinel pile
4.5 Etiopathogenesis
The etiology and pathogenesis of this condition is
poorly understood and hence the confusion in the
choice of optimal modality of treatment. It was
known for a long time that the tear in anal fi ssure
is caused by passage of hard fecal mass. In 1994, a
theory of inverse relationship of anodermal blood
fl ow in the posterior commissure of the anoderm
to the internal sphincter resting pressure was postulated by Schouten et al. ( 1996 ). The blood sup-
ply to the posterior midline of the anal canal has
been demonstrated to be signifi cantly lower using
Laser Doppler Flowmetry than anywhere else in
the anal canal (Klosterhalfen et al. 1989 ) and
hence the increased propensity of occurrence of
anal fi ssures in this region. It has also been found
that there is a decrease in the normal spontaneous
cyclical anal sphincter relaxation in patients with
anal fi ssure. No single factor can be attributed to
the etiopathogenesis of anal fi ssures, and a combination of factors may be contributory. These can
be discussed under the following subheadings:
Fig. 4.7 Fissure fi stula complex
case is the development of fi brous induration in
the lateral edges of the fi ssure. At any stage, frank
suppuration may occur and extend into the surrounding tissues to form a perianal abscess,
which may discharge through the fi ssure into the
anal canal or may burst externally to produce a
low anal fi stula: fi ssure fi stula complex (Fig.
4.7 ).
Usually the external opening of this fi stula lies in
or close to the midline, a short distance behind
the anus, and an anal fi ssure should always be
thought of as the most common cause of such a
median low dorsal anal fi stula. When the fi ssure
is relatively superfi cial, the sphincter usually
undergoes a tight spasm, but when the fi ssure
deepens and bares the sphincter fi bers, this
becomes even more pronounced. Eventually after
several months, the muscle may become fi brosed
in its spastic condition so that a rather fi brotic,
tightly contracted, internal sphincter may result.
4.5.1 Microtrauma to Anal Canal Mucosa
Passage of a hard fecal mass causes a tear in the
anoderm distal to the dentate line which is sensitive to pain. This causes severe pricking pain in the
anal canal which in turn results in severe anal
sphincteric spasm. This vicious cycle perpetuates
and progresses to chronic fi ssure in ano, which is
characterized by deep fi ssure, associated with
hypertrophy of split mucosal edges, external skin
tag at the distal end, and hypertrophied anal papillae at the proximal end.
4.5.2 Anal Sphincteric Spasm
The resting anal pressure is a function of the
internal anal sphincter and is mediated by both
alpha-adrenergic nerve fi bers and inherent muscle tone. Relaxation of internal anal sphincter on
rectal distension automatically is called rectoanal
inhibitory refl ex (RAIR). It has been observed
that in patients with chronic fi ssure in ano, there

38
B. Perakath and N. Agarwal
is abnormal rectoanal inhibitory refl ex along with
hypertonicity of the internal anal sphincter and a
long high pressure zone (HPZ). The application
of pharmacological preparations that relax
internal anal sphincter is effective in healing of
chronic fi ssure in ano.
4.5.3 Anal Mucosal Ischemia
It has been demonstrated in cadaveric angiographic studies that there is paucity of vascular
supply to the posterior commissure of the anal
canal mucosa in patients with fi ssure. Any mucosal microtrauma in this region has delayed healing and progresses to a chronic condition if the
causative factor is not eliminated (Schouten et al.
1996 ; Klosterhalfen et al. 1989 ).
4.5.4 Trauma During Childbirth
A small number of women develop chronic anal
fi ssure following traumatic childbirth which is
either attributed to indirect shearing forces during
vaginal birth or due to tethering of anal mucosa to
the underlying internal sphincter due to fi brosis,
rendering it susceptible to further trauma.
4.5.5 Other Causes of Secondary Anal Fissure
Rare causes of anal fi ssure include infl ammatory
bowel disease like Crohn’s disease, tuberculosis,
sexually transmitted diseases like syphilis, anal
malignancy, human immunodefi ciency syndrome,
and anal trauma due to unnatural sexual intercourse
or fi nger digitation. Fissures in these patients may
be located anywhere including atypical sites.
the stools. Subsequently, it may continue as a
severe burning discomfort for few minutes to
hours after defecation. To some patients with an
anal fi ssure, the pain is so agonizing that they are
frightened to have a motion and may remain in a
constipated condition. Some patients complain of
perianal pruritus and feeling of wetness in the
perianal region. Some patients with a large sentinel tag may become aware of this as a lump at the
anus and may complain of having a painful external pile. Sometimes patients with a painful anal
fi ssure develop disturbances of micturition, either
dysuria and retention or increased frequency.
During examination, it is essential that extreme
gentleness is displayed since fi ssure in ano is an
extremely painful condition and the patient suffering from it is usually very apprehensive of rectal examination. Examination of the perianal
region on careful inspection typically shows a
superfi cial mucosal split in acute fi ssure. This
requires gentle parting of the buttocks suffi cient
to open the anal orifi ce. A chronic fi ssure will
have raised edges of the mucosal split with varying depth mostly in the posterior midline, exposing the pale-colored internal sphincter at the fl oor.
The induration at the edges gives an impression
that of a button hole on palpation. There is often a
skin tag at the distal end and a hypertrophied anal
papilla at the proximal end (Gupta 2004 ).
Proctoscopy may have to be deferred especially in
an acute case in view of pain. The sphincter spasm
and the fi brosis may be appreciated during palpation. Occasionally, a fi stula may be demonstrated
with an infected fi ssure in ano (Fig.
locations and multiplicity should raise a suspicion, and attempts must be made to rule out specifi c causes for the occurrence of fi ssure in ano as
described above. Crohn’s fi ssures are multiple,
asymptomatic, and eccentric in location. HIVdisease-related fi ssures are deep, broad based, or
cavitating ulcers with poor sphincter function.
4.7 ). Abnormal
4.6 Clinical Features
The most common symptom of fi ssure in ano is
excruciating tearing anal pain after passage of
stools associated with passage of minimal
amounts of bright red blood which usually lines
4.7 Differential Diagnosis
(a) Idiopathic stenosis of internal sphincter:
It is a defi nite clinical entity. It occurs in
certain older patients, usually women, who

4 Anal Fissure
39
have been accustomed to taking aperients
over many years so that the anal canal has for
a long time been spared the regular dilating
action of a normal solid motion. As a consequence, the internal sphincter undergoes
contraction and may become fi xed in this
contracted condition by fi brosis, as in a case
of chronic anal fi ssure. There may be no
symptoms, or when the contraction becomes
extreme, the patient may fi nd diffi culty in
passing motions. The condition is easily recognized by fi nding a tightly contracted internal sphincter on palpation, without any
evidence of a past or present fi ssure. If
required, it can be treated by internal sphincterotomy exactly as for chronic anal fi ssure.
(b) Pruritus ani with superfi cial cracks of the
anal skin.
(c) Tuberculous ulcer.
(d) Infl ammatory bowel disease with anal
ulceration.
(e) Squamous cell carcinoma of the anus or ade-
nocarcinoma of the rectum invading the anal
canal or anus.
(f) Syphilitic fi ssures.
(g) Secondary fi ssures may be caused by previ-
ous anal operations that result in scarring,
stenosis, and loss of anoderm. Individuals
who have undergone intestinal bypass proce-
dures for obesity may develop anal stenosis
associated with a fi ssure.
(h) Atypical fi ssures other than in the classical
position or multiple fi ssures warrant detailed
history and examination to rule out causes
like tuberculosis, infl ammatory bowel dis-
ease, malignancy, sexually transmitted dis-
ease, or unnatural sexual practices.
4.8.1 Management of Acute
Superfi cial Anal Fissure
Conservative measures to treat superfi cial fi ssure
involves breaking the vicious cycle of tear, pain,
and anal sphincteric spasm. This includes:
(a) Measures to soften stools like high-fi ber diet,
adequate oral fl uid intake, and consumption
of bulk-forming agents like Isphagula and
laxatives (Jensen 1987 ).
(b) Warm water sitz baths help to soothen the
perianal region and relieve sphincter spasm
(Dodi et al. 1986 ).
(c) Measures to relieve anal pain like local appli-
cation of local anesthetic agents like lignocaine cream before the act of defecation and
after (Gupta 2004 ).
(d) Antibiotics, anti-amoebic, and antihelmintics
are prescribed in presence of infections.
Fortunately, most of the acute fi ssures respond
well to these measures itself, but the rest may
require some form of medical treatment which is
no different from that advised for chronic fi ssure
and described below:
4.8.2 Management of Persistent
Acute Fissure In Ano
and Chronic Anal Fissure
4.8.2.1 Medical Management
Medical management aims at eliminating the
factors involved in the etiopathogenesis of anal
fi ssure and consists of facilitating passage of
soft stools, anal sphincteric relaxation, and adequate pain relief and thereby promoting fi ssure
healing.
4.8 Management
Management strategies are decided based
on the acuteness or chronicity of the fi ssure
clubbed with the patients presenting complaints.
Etiological factors and complications of fi ssures also determine the choice of the treatment
offered.
(a) Warm water sitz baths promote healing by
soothening the area and aid in relaxing the
sphincter (Dodi et al. 1986 ).
(b) High dietary fi ber intake as maintenance
therapy has shown to decrease recurrence
rates (Jensen 1987 ). Recurrence ranges from
30 to 70 % if the high-fi ber diet is abandoned
after fi ssure is healed. This rate is reduced to
Соседние файлы в папке Библиотека им академика М.И. Перельмана
