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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

Pilonidal Disease
P. N. Joshi and Shekhar Suradkar
6
6.1 Introduction
In its more usual form, this disease consists of a
sinus situated a short distance behind the anus
and generally contains hair. It was fi rst described
by Anderson in 1847 in a paper entitled “Hair
extracted from an Ulcer.” Warren in 1854 reported
an “Abscess containing Hair on Nates,” and
Hodges in 1880 termed it as a pilonidal sinus
(pilus for hair and nidus for nest) (Aird 1952 ;
Goligher 1970 ; Turrel 1959 ).
It is a disease of the second and third decade.
It is rare after 40 years of age. Men are more commonly affected than women, and majority are
dark hairy subjects. Surprisingly, the condition is
rare in Negroes. Trauma or infection is an exciting factor in precipitating the symptoms. Second
World War focused attention on sudden outburst
of this disease in soldiers who were subjected to
stress of driving trucks, tanks, jeeps, and so on,
for which it came to be known as jeep disease.
Other sites of this disease are fi nger webs, axilla,
perineum, amputation stump, umbilicus, supra-
P. N. Joshi
Department of Proctology ,
Grant Medical College , Mumbai, Maharashtra , India
drpnjoshi@rediffmail.com
e-mail:
S. Suradkar (*)
Department of Surgery, WIALS centre, Highway
Hospital and Multi-specialitycentre, Marathon Square,
Thane (West), Mumbai 400 0604, Maharashtra, India
highwayhospital@gmail.com
e-mail:
pubic region, presternal region, neck, nipple,
groin, and anal canal (Aird 1952 ; Buie Practical
et al. 1960 ; Crosby 1962 ; Currie et al. 1953 ).
6.2 Etiology
Various theories of its origin are described by
different authors based upon their observation.
6.2.1 Theory of Acquired Origin
Patey and Scarff ( 1946 ) suggested that the sinus
was of acquired origin (Goligher 1970 ). Brearly
( 1955 ) who is also of the same view suggested
that the rolling movement which normally takes
place between contiguous surfaces of buttocks at
the cleft may result in hair still attached to the
skin, being twisted into a bundle which lies along
the cleft and drills its way obliquely headward
through the skin. Further penetration may be
assisted by a suction mechanism. He pointed out
that separation of buttocks in sitting or bending
down renders the skin of internatal cleft and tends
to lift it off the underlying sacrococcygeal fascia
with creation of negative pressure. It is implied
that eventually the hairs lose their attachment and
become entirely free of the skin and get buried
inside. The other factors which support acquired
origin of the disease are recurrence after complete excision and higher recurrence and risk in
© 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_6
71

72
P.N. Joshi and S. Suradkar
hirsute, those with increased sweating, obesity
(50 %), local trauma and irritation (34 %), sedentary habits (38 %), and folliculitis. High body
mass index has been reported as a possible risk
factor for pilonidal disease in adolescents
(Clothier and Haywood 1984 ; Akinci et al 1999 ;
Arda 2005 .
6.2.2 Theory of Sequestration
Dermoid
Joshi PN (Joshi 1978 ) asserted that the pilonidal
disease is either a sequestration dermoid or
implantation dermoid, depending on its situation.
The pilonidal sinuses are seen at the site of
fusion, e.g., midline. The common sites are
sacrococcygeal region, umbilical region, presternal region, suprapubic region, etc.; the sinuses
which develop in webs of fi nger or amputation
stumps can be explained on the basis of implantation dermoid. The other facts favoring this view
are as follows:
1. The disease manifests in the second and early
part of the third decade which coincides with
the development of secondary sexual charac-
ter when growth of hair with increased seba-
ceous secretion occurs. It is rarely seen before
puberty.
2. The primary opening of the sinus is in mid-
line, and its lining is continuous with the lin-
ing of the skin.
3. Cyst when present contains hair and epithelial
debris. Its lining is that of the skin unless
destroyed by infection.
4. Sinus which leads to terminal cavity toward
headword direction is usually one to two inches
away from it. The cavity contains hair which is
sometimes larger than the one in the vicinity,
and the luster of hair is also different.
5. It is common experience of all surgeons that if
radical excision of sinus is done, recurrence
does not occur. This also shows that though
the primary factor or rolling movement still
persists, sinus does not recur.
6. If pilonidal sinus was due to acquired origin,
they should occur more frequently in the
regions of the axilla, groin, and behind the ear
where ideal condition for its occurrence exists.
It should also occur at any age instead of being
seen after puberty.
7. Very rarely pilonidal sinus and perianal fi stula
may be seen simultaneously in the same patient.
6.3 Clinical Features
Pilonidal disease may be asymptomatic or present as a simple disease, chronic discharging sinus,
an abscess, or a recurrent and complex disease. It
seldom presents till infection has supervened.
Patient is usually a young adult who develops an
abscess at the base of the spine which either
bursts on its own or is incised by his doctor (Doll
et al. 2008 ). The discharge then ceases after few
days, and patient may remain comfortable till
another episode of infection occurs. On examination, fi ndings in the postanal region are very characteristic. The sinus is situated in the midline
some two inches above and behind the anus
(Fig. 6.1 ). There may be a single opening or
series of openings placed close together or spread
out over a distance. Sometimes the openings are
so that they have a smooth edge unlike that of an
ordinary fi stula, and hair may project from the
opening. In addition, majority of patients may
have another sinus opening 1 or 2 in away toward
the head end on one or the other side of midline
with granulation tissue projecting from it. On pal-
Fig. 6.1 Classical position for pilonidal sinus

6 Pilonidal Disease
73
pation, irregular areas of induration around the
orifi ces can be felt, and on pressure, pus or purulent discharge comes out. Occasionally, if the
sinus openings are closed, a cyst may be felt. The
operative fi ndings of this sinus are quite characteristic. The primary tract commences in the skin
lined orifi ce or orifi ces and extends in subcutaneous tissue in a cranial direction for a distance of 1
or 2 in. It may have sidetracks and may expand
into a small cavity. Hair is seen projecting from
the sinus opening or lying in the sinus tract when
it is laid open (Fig. 6.2 ). They may be lying
Fig. 6.2 Hair from pilonidal sinus (courtesy of Pankaj
Garg, India)
loose or may still be attached to the cyst wall.
In addition, it may also contain sebaceous material. The secondary tracts are connected to the
primary tract, and they are lined by granulation
tissue. Endoanal pilonidal sinus, a rare variety,
presents circumferentially around the anus
(Wilson et al. 1971 ; Taylor and Hughes 1984 .
6.4 Differential Diagnosis
Furuncle, carbuncle, anal fi stula (Fig. 6.3a, b ),
hidradenitis suppurativa, specifi c granuloma, and
osteomyelitis of the sacrum should be considered in
differential diagnosis (Solla and Rotherberger 1990 ).
Squamous cell carcinoma and basal cell carci-
noma have been reported to develop in the longstanding pilonidal sinus.
6.5 Investigations
Apart from routine test, USG may tell about the
status of abscess. Simple sinograms do not give
much information. On the other hand, methylene
blue injection on table will help to delineate the
cavity and the side tracts. MRI sinogram is
reserved for recurrent and complicated disease.
a b
Fig. 6.3 ( a , b ) Perianal pilonidal sinus mimicking fi stula in ano (( a ) before and ( b ) after excision)

74
P.N. Joshi and S. Suradkar
6.6 Treatment
Asymptomatic patients need lifestyle modifi cations like weight reduction, regular (fortnight)
shaving in the natal cleft area for about 2 in.
around, and local hygiene. These patients should
be followed and treated if they become symptomatic. Otherwise, there is no role of any kind of
treatment. Symptomatic disease should be treated
either by conservative or surgical methods,
depending on the nature of the disease.
6.6.1 Conservative Treatment
80 % phenol liquid is injected through the tiny
openings of the sinus slowly and without pressure
until fl uid is seen coming through other openings
(Stansby and Greatorex 1989 ). Then the needle is
withdrawn and sinus is gently pressed upon to
squeeze out debris and hair. The procedure is
repeated, and then dressing is applied. The healing
occurs in 3–6 weeks in 60–90 % of patients. Cure
rate of 92 % was reported with pit excision and
phenol injection at day 1, and 7. 10 % of patients
developed skin necrosis (Olmez et al. 2013 ).
Conservative treatment is indicated in those
unwilling for surgery, with associated medical
comorbidity, mild disease, and if patient cannot
take rest for recovery. Disease usually dies after
40 years of age and should be kept in mind while
deciding about treatment (Maurice 1964 ).
a
b
Fig. 6.4 ( a , b ) Simple unroofi ng and curettage (( a ) before
and ( b ) after surgery) (courtesy of Pankaj Garg, India)
is more. Relying on these results, Kepenekci
advocated unroofi ng and curettage as the procedure of choice in the management of pilonidal
disease (Kepenekci et al.
2010 ).
6.6.2 Operative Procedures
6.6.2.1 Simple Incision of Abscess
This is done for acute infection to drain the pus
and debris (Joshi 1978 ).
6.6.2.2 Unroofi ng and Curettage
Unroofi ng and curettage for pilonidal sinus disease is an easy and effective technique (Fig. 6.4a, b ).
The vast majority of the patients, including those
with abscess as well as those with chronic disease, will heal with this simple procedure, after
which even recurrences can be managed successfully
with the same procedure. However, healing time
6.6.2.3 Excision With or Without Wound Closure
Excision of sinus and primary wound closure
with or without drain is performed when the disease is quiescent (Fig. 6.5a, b ). The entire sinus
tract is excised, and the wound is closed in layers
or left open (saucerization/marsupialization) for
secondary healing. Trephining alone may be adequate for simple, superfi cial, and single sinus.
In saucerization, wound is left open to heal by
secondary intention in about 6–8 weeks. It is done
for sinuses with cellulitis around. It gives broad
fl at and hairless scar, thereby less risk of friction,
hair penetration, and follicle infection. Recurrence
rate is from 8 to 21 % (Sondenaa et al. 1996 ).

6 Pilonidal Disease
75
a
Area of induration
in chronic abscess
b
Fig. 6.6 Bascom I technique
Incision
Area of debridement
under skin
Anus
endangers signifi cant skin loss. The hair follicles
are relocated and thereby friction forces avoided.
The midline scar is also avoided.
Fig. 6.5 ( a , b ) Excision and primary closure of pilonidal
sinus
(a) Bascom II Cleft Lift Technique . The proce-
dure unlike other fl ap techniques does not
excise normal subcutaneous tissue. The skin
In marsupialization, wound edges are sutured
to deep tissue, thereby reducing the raw area and
healing time with low recurrence rate (4–8 %)
(Solla and Rotherberger 1990 ).
with thin rim of fat of gluteal cleft is detached
from underlying subcutaneous tissue on
either side. The unhealthy tissue or tract is
excised. Subcutaneous fat is approximated in
the midline. The skin fl ap from normal side is
6.6.2.4 Bascom I Technique
This procedure has been recommended in patients
with chronic abscess in whom it has shown excellent results without midline scar. The abscess cavity is curetted through a liberal lateral incision.
The overlying skin is undermined, and the secondary tracts curetted out to communicate with the
main incision. The midline pits are excised with a
small-diamond-shaped incision and closed with
vertical mattress sutures. The lateral incision is left
open to heal by secondary intention. The gluteal
cleft is maintained without excising normal tissue
(Fig.
6.6 ) (Jeffery et al. 2009 ).
brought across midline and sutured to skin
fl ap of opposite side after excision of diseased
skin. This creates primary closure of the midline and obliterating glutted cleft at the same
time (Fig. 6.7a–d ). No recurrence has been
reported by Bascom though duplication of
results is awaited (Jeffery et al 2009 ).
(b) Karydakis Advancement Flap . Elliptical
eccentric incision with one limb off the midline and other adjacent to sinus openings on
the opposite side is made. The sinus with vulnerable tissue is excised eccentrically. The
defect is closed by a full-thickness fl ap raised
on the opposite side and advanced for pri-
6.6.2.5 Excision of Sinus with Flap
Closure
Flap closure is reserved for recurrent and complex disease with multiple draining sinuses
around the midline and when complete excision
mary closure of the midline (Fig. 6.8 ). The
Karydakis procedure has been reported to be
superior to simple midline closure in patients
with recurrent disease (Lesalneiks 2013 ). The
technique has been used even as a primary

76
a
Sinuses and
Skin to be
excised
c
P.N. Joshi and S. Suradkar
b
Undermined
skin flap to be
advanced to
opposite side
Skin flap suture line
Sacrum
d
Gluteal flaps
sutured in
centre
Final Scar
off midline
Sacrum
Fig. 6.7 ( a – d ) Bascom II cleft left technique
Skin flap to be
undermined and
advanced to the
opposite side
b
Fig. 6.8 Karydakis advancement fl ap technique
Assymetric defect
after excision
a
procedure with a recurrence rate of 1.3 %
(Kulacoglu 2008 ).
(c) Rhomboid (Limberg Flap) . This fl ap is indi-
cated when we expect a large defect after
b
a
Final Scar
off midline
excision of pilonidal sinus with multiple openings. It should not be routinely used as it endangers sacrifi ce of normal tissue and the fl ap
necrosis due to compromised vascularity. 5 %

6 Pilonidal Disease
Fig. 6.9 Design for rhomboid
fl a p
77
Flap
Defect
Final picture after Transposition of Flap
Area to be
excised
Fig. 6.10 V-Y advancement fl a p
Fig. 6.11 Lazy S-fl a p
Fig. 6.12 Z-plasty
V Flap to be raised and
advanced medially
Area to be
excised
Final Scar
Final Scar
recurrence rates have been reported (Fig. 6.9 )
(Abu Galala et al. 1999 ; Azad et al. 1984 ).
(d) Other Local Flaps . V-Y advancement, lazy
S-plasty, and Z-plasty procedures are aimed
at asymmetric closure and are useful in situations where closure under tension is anticipated by simpler techniques (Figs. 6.10 ,
6.11 , and 6.12 ). However, issue of fl ap necro-
sis and shape of defect restricts the use of
these fl aps (Sharma 2006 ; Jeffery et al. 2009 ;
Morrison 1985 ).
(e) Myocutaneous Flaps. These are reserved for
large deep wounds and where simple methods of fl ap cover have failed. These fl aps

78
P.N. Joshi and S. Suradkar
have predictable vascularity and are less susceptible to infections and necroses. However,
it requires long operation time and hospitalization. Recurrence rates have been reported
from 6 to 20 % (Senapati and Cripps 2000 ) .
One should make sure that the vascularity of
fl aps is maintained while raising fl aps, keeping
intact adequate base and pedicle.
6.6.2.6 Vacuum-Assisted Closure (VAC)
As for wounds in other parts of the body, VAC
has been used for large defects after excision of
complex pilonidal disease for rapid wound healing (Jenny et al. 2004 ).
6.6.2.7 Endoscopic Pilonidal Sinus
Treatment (EPSIT)
This is a minimally invasive procedure which is
being evaluated for pilonidal sinus disease. Initial
results have shown minimal pain without any signifi cant complication (Meinero et al. 2014 ).
6.7 Prevention of Recurrence
Local hygiene should be maintained, weight
reduced, and sitting for long periods of time
should be avoided. Postoperative irradiation,
depilation by electrolysis, regular use of depilatory cream, and regular shaving of the area are
used to prevent recurrences.
6.8 Summary
Despite the increasing volume of data on the treatment of pilonidal disease, the optimal treatment is
yet to be established. Asymptomatic patients need
no treatment except lifestyle modifi cations. Acute
abscess should be drained by lateral incision and
followed. Simple disease should be treated by
simple techniques without sacrifi cing normal tissue like excision with or without primary closure
or lazy S-plasty. Recurrent disease needs wider
excisions with reconstruction using various types
of fl aps depending on the situation.
Bibliography
Abu Galala KH, Salam IM, et al. Treatment of pilonidal
sinus by primary closure with a transposed rhomboid
fl ap compared with deep suturing: a prospective
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468–72.
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Rectovaginal Fistulas
Fazl Q. Parray
7
7.1 Introduction
A rectovaginal fi stula (RVF) is by defi nition an
epithelial-lined tract between the rectum and
vagina. Most RVFs are located at or just above
the dentate line. Fistulas below the dentate line
are not true RVFs but are instead anovaginal
fi stulas.
From time immemorial, women suffered on
self-esteem, intimacy, and long-term relationship
because of the distressing symptoms generated
by RVF. Even though the present modalities of
management have markedly decreased the suffering of the patients, but still they can be quite
bothersome to both the patient and the surgeon
due to their irritating and embarrassing symptoms and high failure rates after repair. A small
percentage still cannot be corrected because of
patient comorbidity or disease-related factors. In
such patients, the only help which can be offered
is fecal diversion (Galandiuk et al.
individualized systematic approach to these fi stulas based on their size, location, and etiology provides a more concise treatment plan.
F. Q. Parray , MS, FICS, FMAS, FACRSI, FACS
Department of Colorectal Surgery ,
Sher-I-Kashmir Institute of Medical Sciences ,
Soura Srinagar , Jammu and Kashmir 190011 , India
fazlparray@rediffmail.com;
e-mail:
fazlparray@gmail.com
2005 ). An
7.2 Etiology
Fistulas can be broadly classifi ed into congenital
or acquired varieties.
7.2.1 Congenital
This variety may at times present for the fi rst time
in life. This variety usually follows relatively
minor anorectal vestibular anomalies where even
a trivial trauma results in a rectovaginal fi stula.
7.2.2 Acquired
These are secondary to infective, infl ammatory,
neoplastic, radiation, and post-traumatic causes.
7.2.2.1 Child Birth
RVFs may be caused by childbirth. Main contributory factors are:
• Prolonged labor with necrosis of the rectovaginal septum
• Obstetric injury with a third- or fourth-degree
perineal tear
• Episiotomy
• Inadequate repair, breakdown of the repair, or
infection
• Infectious processes within the rectovaginal septum
• Cryptoglandular anorectal abscesses and
Bartholin gland infections
© 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_7
81
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